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+import os
+from datetime import datetime
+
+# Configure CUDA visibility (set this as appropriate for your environment).
+os.environ["CUDA_DEVICE_ORDER"] = "PCI_BUS_ID"
+os.environ["CUDA_VISIBLE_DEVICES"] = "2"
+
+import math
+import random
+import re
+
+import numpy as np
+import torch
+import torch.nn as nn
+import torch.optim as optim
+from collections import Counter
+from sklearn.metrics import accuracy_score, precision_recall_fscore_support
+from sklearn.model_selection import train_test_split
+from torch.utils.data import DataLoader, Dataset
+from datasets import load_dataset
+
+"""
+Homework 1 (Part I) – Transformer-based sentiment analysis on the IMDB dataset.
+
+This script implements:
+- Data loading and preprocessing for the IMDB movie review dataset
+- A Transformer-based text classification model
+- Training and evaluation loops for binary sentiment analysis
+- Saving of the trained model together with vocabulary and configuration
+
+The code is organized into clearly separated sections:
+1) Data preparation and tokenization
+2) Transformer components (building blocks)
+3) Full Transformer classifier
+4) Training and evaluation logic
+5) Execution example using a train/validation split of IMDB
+
+Model Analysis and Improvement:
+1. After evaluation, delve into analyzing your model's behavior to identify
+   areas for improvement and fine-tuning.
+2. Analyze translation errors (if applicable): Examine specific translation
+   examples where the model performs poorly and try to understand the reasons
+   behind these errors. Are there issues with handling rare words or
+   idiomatic expressions?
+3. Explore the impact of model size: Experiment with different Transformer
+   model sizes (e.g., small, medium, large) to understand how model
+   complexity affects performance.
+"""
+
+# ==========================================
+# 1. Data Preparation & Tokenization
+# ==========================================
+
+def tokenize(text):
+    """
+    Tokenize a raw review string into a list of normalized word tokens.
+
+    Steps:
+    - Convert to lowercase
+    - Remove HTML line breaks
+    - Remove non-alphanumeric characters (except whitespace)
+    - Split on whitespace
+
+    Args:
+        text (str): Raw review text.
+
+    Returns:
+        List[str]: List of token strings.
+    """
+    text = text.lower()
+    text = re.sub(r"<br />", " ", text) # Remove HTML line breaks
+    text = re.sub(r"[^a-zA-Z0-9\s]", "", text)
+    return text.split()
+
+class IMDBDataset(Dataset):
+    """
+    Torch Dataset wrapper for IMDB sequences and labels.
+
+    Each item corresponds to:
+    - a fixed-length sequence of token IDs
+    - a sentiment label (0 = negative, 1 = positive)
+    """
+    def __init__(self, sequences, labels):
+        self.sequences = torch.tensor(sequences, dtype=torch.long)
+        self.labels = torch.tensor(labels, dtype=torch.long)
+
+    def __len__(self):
+        return len(self.labels)
+
+    def __getitem__(self, idx):
+        return self.sequences[idx], self.labels[idx]
+
+def build_vocab(texts, max_vocab_size=10000):
+    """
+    Build a word-to-index vocabulary from a collection of texts.
+
+    The vocabulary is constructed using token frequency counts from the
+    training set only to avoid information leakage. Two special tokens
+    are always included:
+    - "<PAD>" mapped to index 0
+    - "<UNK>" mapped to index 1
+
+    The remaining (max_vocab_size - 2) most frequent tokens are added.
+
+    Args:
+        texts (Iterable[str]): Training texts.
+        max_vocab_size (int): Maximum size of the vocabulary.
+
+    Returns:
+        Dict[str, int]: Mapping from token string to integer index.
+    """
+    counter = Counter()
+    for text in texts:
+        counter.update(tokenize(text))
+    
+    # Reserve 0 for padding and 1 for unknown tokens
+    vocab = {"<PAD>": 0, "<UNK>": 1}
+    common_words = counter.most_common(max_vocab_size - 2)
+    for word, _ in common_words:
+        vocab[word] = len(vocab)
+    return vocab
+
+def preprocess_data(texts, vocab, max_len=128):
+    """
+    Convert raw texts into padded/truncated sequences of token IDs.
+
+    Steps:
+    - Tokenize each text
+    - Map tokens to vocabulary indices (using <UNK> for OOV tokens)
+    - Truncate to max_len or pad with <PAD> to reach max_len
+
+    Args:
+        texts (Iterable[str]): Input texts (reviews).
+        vocab (Dict[str, int]): Token-to-index mapping.
+        max_len (int): Maximum sequence length in tokens.
+
+    Returns:
+        np.ndarray: Array of shape (num_examples, max_len) with dtype int.
+    """
+    sequences = []
+    for text in texts:
+        tokens = tokenize(text)
+        token_ids = [vocab.get(token, vocab["<UNK>"]) for token in tokens]
+        # Pad or Truncate
+        if len(token_ids) < max_len:
+            token_ids += [vocab["<PAD>"]] * (max_len - len(token_ids))
+        else:
+            token_ids = token_ids[:max_len]
+        sequences.append(token_ids)
+    return np.array(sequences)
+
+# ==========================================
+# 2. Transformer Components
+# ==========================================
+
+class PositionalEncoding(nn.Module):
+    """
+    Sinusoidal positional encoding module.
+
+    Implements the deterministic positional encoding from the original
+    Transformer paper ("Attention is All You Need"), which is added to
+    token embeddings to inject information about token positions.
+    """
+    def __init__(self, d_model, max_len=5000):
+        super().__init__()
+        pe = torch.zeros(max_len, d_model)
+        position = torch.arange(0, max_len, dtype=torch.float).unsqueeze(1)
+        div_term = torch.exp(torch.arange(0, d_model, 2).float() * (-math.log(10000.0) / d_model))
+        
+        pe[:, 0::2] = torch.sin(position * div_term)
+        pe[:, 1::2] = torch.cos(position * div_term)
+        
+        self.register_buffer('pe', pe.unsqueeze(0))
+
+    def forward(self, x):
+        """
+        Add positional encodings to input embeddings.
+
+        Args:
+            x (Tensor): Input tensor of shape [batch_size, seq_len, d_model].
+
+        Returns:
+            Tensor: Positionally encoded representations with same shape as x.
+        """
+        return x + self.pe[:, :x.size(1)]
+
+class MultiHeadAttention(nn.Module):
+    """
+    Multi-head self-attention mechanism.
+
+    For each token, attention is computed over all tokens in the sequence
+    (including itself) using multiple attention heads. Each head operates
+    in its own subspace and the outputs are concatenated.
+    """
+    def __init__(self, d_model, num_heads):
+        super().__init__()
+        assert d_model % num_heads == 0
+        self.d_model = d_model
+        self.num_heads = num_heads
+        self.d_k = d_model // num_heads
+        
+        self.W_q = nn.Linear(d_model, d_model)
+        self.W_k = nn.Linear(d_model, d_model)
+        self.W_v = nn.Linear(d_model, d_model)
+        self.W_o = nn.Linear(d_model, d_model)
+
+    def forward(self, x, mask=None):
+        """
+        Apply multi-head self-attention to the input sequence.
+
+        Args:
+            x (Tensor): Input tensor of shape [batch_size, seq_len, d_model].
+            mask (Tensor, optional): Attention mask of shape
+                [batch_size, 1, 1, seq_len] or broadcastable equivalent,
+                where positions with 0 are masked out.
+
+        Returns:
+            Tensor: Output tensor of shape [batch_size, seq_len, d_model].
+        """
+        batch_size, seq_len, _ = x.shape
+        
+        # Linear projections
+        Q = self.W_q(x).view(batch_size, seq_len, self.num_heads, self.d_k).transpose(1, 2)
+        K = self.W_k(x).view(batch_size, seq_len, self.num_heads, self.d_k).transpose(1, 2)
+        V = self.W_v(x).view(batch_size, seq_len, self.num_heads, self.d_k).transpose(1, 2)
+        
+        # Scaled Dot-Product Attention
+        scores = torch.matmul(Q, K.transpose(-2, -1)) / math.sqrt(self.d_k)
+        if mask is not None:
+            scores = scores.masked_fill(mask == 0, -1e9)
+        
+        attn = torch.softmax(scores, dim=-1)
+        context = torch.matmul(attn, V)
+        
+        # Concatenate heads
+        context = context.transpose(1, 2).contiguous().view(batch_size, seq_len, self.d_model)
+        return self.W_o(context)
+
+class TransformerEncoderBlock(nn.Module):
+    """
+    Single Transformer encoder block consisting of:
+    - multi-head self-attention sublayer (with residual + layer norm)
+    - position-wise feed-forward sublayer (with residual + layer norm)
+    """
+    def __init__(self, d_model, num_heads, d_ff, dropout=0.1):
+        super().__init__()
+        self.mha = MultiHeadAttention(d_model, num_heads)
+        self.ffn = nn.Sequential(
+            nn.Linear(d_model, d_ff),
+            nn.ReLU(),
+            nn.Linear(d_ff, d_model)
+        )
+        self.layernorm1 = nn.LayerNorm(d_model)
+        self.layernorm2 = nn.LayerNorm(d_model)
+        self.dropout = nn.Dropout(dropout)
+
+    def forward(self, x, mask=None):
+        """
+        Forward pass through one encoder block.
+
+        Args:
+            x (Tensor): Input tensor of shape [batch_size, seq_len, d_model].
+            mask (Tensor, optional): Attention mask (see MultiHeadAttention).
+
+        Returns:
+            Tensor: Output tensor of shape [batch_size, seq_len, d_model].
+        """
+        # Sublayer 1: self-attention with residual connection
+        attn_out = self.mha(x, mask)
+        x = self.layernorm1(x + self.dropout(attn_out))
+        # Sublayer 2: position-wise feed-forward network with residual
+        ffn_out = self.ffn(x)
+        x = self.layernorm2(x + self.dropout(ffn_out))
+        return x
+
+# ==========================================
+# 3. Full Transformer Classifier
+# ==========================================
+
+class TransformerClassifier(nn.Module):
+    """
+    Transformer-based text classifier for IMDB sentiment analysis.
+
+    Architecture:
+    - Token embedding layer
+    - Sinusoidal positional encoding
+    - Stack of Transformer encoder blocks
+    - Global average pooling over sequence dimension
+    - Linear classification head to predict sentiment label
+    """
+    def __init__(self, vocab_size, d_model, num_heads, num_layers, d_ff, max_len, num_classes=2, dropout=0.1):
+        super().__init__()
+        self.embedding = nn.Embedding(vocab_size, d_model)
+        self.pos_encoding = PositionalEncoding(d_model, max_len)
+        
+        self.encoder_layers = nn.ModuleList([
+            TransformerEncoderBlock(d_model, num_heads, d_ff, dropout) 
+            for _ in range(num_layers)
+        ])
+        
+        self.dropout = nn.Dropout(dropout)
+        # Classification Head: Flatten or Global Pool
+        self.classifier = nn.Linear(d_model, num_classes)
+
+    def forward(self, x, mask=None):
+        """
+        Forward pass for the classifier.
+
+        Args:
+            x (Tensor): Input tensor of token IDs
+                with shape [batch_size, seq_len].
+            mask (Tensor, optional): Attention mask (not used in this script).
+
+        Returns:
+            Tensor: Logits of shape [batch_size, num_classes].
+        """
+        x = self.dropout(self.pos_encoding(self.embedding(x)))
+        
+        for layer in self.encoder_layers:
+            x = layer(x, mask)
+        
+        # Global Average Pooling across the sequence dimension
+        x = x.mean(dim=1) 
+        return self.classifier(x)
+
+# ==========================================
+# 4. Training and Evaluation Logic
+# ==========================================
+
+def train_model(model, train_loader, val_loader, epochs, lr, device):
+    """
+    Train the Transformer classifier on the IMDB training split.
+
+    Args:
+        model (nn.Module): TransformerClassifier instance.
+        train_loader (DataLoader): Batches of (sequence, label) for training.
+        val_loader (DataLoader): Batches for validation.
+        epochs (int): Number of full passes through the training set.
+        lr (float): Initial learning rate for Adam optimizer.
+        device (torch.device): Device on which to run training.
+
+    Uses:
+        - CrossEntropyLoss for binary sentiment classification.
+        - Adam optimizer with StepLR scheduler (gamma=0.5 every 2 epochs).
+    """
+    criterion = nn.CrossEntropyLoss()
+    optimizer = optim.Adam(model.parameters(), lr=lr)
+    scheduler = optim.lr_scheduler.StepLR(optimizer, step_size=2, gamma=0.5)
+    
+    model.to(device)
+    
+    for epoch in range(epochs):
+        model.train()
+        total_loss = 0
+        for batch_seq, batch_lab in train_loader:
+            batch_seq, batch_lab = batch_seq.to(device), batch_lab.to(device)
+            
+            optimizer.zero_grad()
+            outputs = model(batch_seq)
+            loss = criterion(outputs, batch_lab)
+            loss.backward()
+            optimizer.step()
+            total_loss += loss.item()
+        
+        scheduler.step()
+        val_metrics = evaluate_model(model, val_loader, device)
+        val_acc = val_metrics["accuracy"]
+        val_p = val_metrics["precision"]
+        val_r = val_metrics["recall"]
+        val_f1 = val_metrics["f1"]
+        print(
+            f"Epoch {epoch+1}/{epochs} | "
+            f"Loss: {total_loss/len(train_loader):.4f} | "
+            f"Val Acc: {val_acc:.4f} | "
+            f"Val P: {val_p:.4f} | Val R: {val_r:.4f} | Val F1: {val_f1:.4f}"
+        )
+
+def evaluate_model(model, loader, device):
+    """
+    Evaluate the model on a dataset.
+
+    Args:
+        model (nn.Module): Trained (or partially trained) classifier.
+        loader (DataLoader): DataLoader for validation or test data.
+        device (torch.device): Device on which to perform evaluation.
+
+    Returns:
+        Dict[str, float]: Dictionary with accuracy, precision, recall, and F1.
+    """
+    model.eval()
+    all_preds = []
+    all_labels = []
+    
+    with torch.no_grad():
+        for batch_seq, batch_lab in loader:
+            batch_seq, batch_lab = batch_seq.to(device), batch_lab.to(device)
+            outputs = model(batch_seq)
+            preds = torch.argmax(outputs, dim=1)
+            all_preds.extend(preds.cpu().numpy())
+            all_labels.extend(batch_lab.cpu().numpy())
+            
+    acc = accuracy_score(all_labels, all_preds)
+    p, r, f1, _ = precision_recall_fscore_support(all_labels, all_preds, average='binary')
+    return {"accuracy": acc, "precision": p, "recall": r, "f1": f1}
+
+def count_trainable_parameters(model):
+    """
+    Count the number of trainable parameters in a model.
+
+    Args:
+        model (nn.Module): Model whose parameters should be counted.
+
+    Returns:
+        int: Number of trainable parameters.
+    """
+    return sum(p.numel() for p in model.parameters() if p.requires_grad)
+
+def write_experiment_report_md(
+    report_path,
+    results,
+    best_result,
+    device,
+    train_size,
+    val_size,
+):
+    """
+    Write a Markdown report summarizing model-size experiment results.
+
+    Args:
+        report_path (str): Output Markdown file path.
+        results (List[Dict]): Per-model experiment outputs.
+        best_result (Dict): Best-performing entry from `results`.
+        device (torch.device): Device used during training.
+        train_size (int): Number of training samples.
+        val_size (int): Number of validation samples.
+    """
+    lines = []
+    lines.append("# IMDB Transformer Model-Size Experiment Report")
+    lines.append("")
+    lines.append(f"- Generated at: `{datetime.now().strftime('%Y-%m-%d %H:%M:%S')}`")
+    lines.append(f"- Device: `{device}`")
+    lines.append(f"- Training samples: `{train_size}`")
+    lines.append(f"- Validation samples: `{val_size}`")
+    lines.append(f"- Max vocab size: `{MAX_VOCAB}`")
+    lines.append(f"- Max sequence length: `{MAX_LEN}`")
+    lines.append(f"- Batch size: `{BATCH_SIZE}`")
+    lines.append(f"- Epochs: `{EPOCHS}`")
+    lines.append(f"- Learning rate: `{LR}`")
+    lines.append("")
+
+    lines.append("## Overall Comparison")
+    lines.append("")
+    lines.append("| Model Size | Trainable Params | Accuracy | Precision | Recall | F1 | Checkpoint |")
+    lines.append("|---|---:|---:|---:|---:|---:|---|")
+    for item in results:
+        metrics = item["metrics"]
+        lines.append(
+            f"| {item['size']} | {item['params']:,} | "
+            f"{metrics['accuracy']:.4f} | {metrics['precision']:.4f} | "
+            f"{metrics['recall']:.4f} | {metrics['f1']:.4f} | "
+            f"`{item['checkpoint_path']}` |"
+        )
+    lines.append("")
+
+    lines.append("## Best Model")
+    lines.append("")
+    lines.append(f"- Best size by validation F1: `{best_result['size']}`")
+    lines.append(f"- Checkpoint: `{best_result['checkpoint_path']}`")
+    lines.append(f"- Trainable parameters: `{best_result['params']:,}`")
+    lines.append("- Metrics:")
+    lines.append(f"  - Accuracy: `{best_result['metrics']['accuracy']:.4f}`")
+    lines.append(f"  - Precision: `{best_result['metrics']['precision']:.4f}`")
+    lines.append(f"  - Recall: `{best_result['metrics']['recall']:.4f}`")
+    lines.append(f"  - F1: `{best_result['metrics']['f1']:.4f}`")
+    lines.append("")
+
+    lines.append("## Per-Model Details")
+    lines.append("")
+    for item in results:
+        cfg = item["config"]
+        metrics = item["metrics"]
+        lines.append(f"### {item['size'].capitalize()} model")
+        lines.append("")
+        lines.append("- Architecture:")
+        lines.append(f"  - `d_model`: `{cfg['d_model']}`")
+        lines.append(f"  - `num_heads`: `{cfg['num_heads']}`")
+        lines.append(f"  - `num_layers`: `{cfg['num_layers']}`")
+        lines.append(f"  - `d_ff`: `{cfg['d_ff']}`")
+        lines.append(f"- Trainable params: `{item['params']:,}`")
+        lines.append(f"- Checkpoint: `{item['checkpoint_path']}`")
+        lines.append("- Validation metrics:")
+        lines.append(f"  - Accuracy: `{metrics['accuracy']:.4f}`")
+        lines.append(f"  - Precision: `{metrics['precision']:.4f}`")
+        lines.append(f"  - Recall: `{metrics['recall']:.4f}`")
+        lines.append(f"  - F1: `{metrics['f1']:.4f}`")
+        lines.append("")
+
+    with open(report_path, "w", encoding="utf-8") as f:
+        f.write("\n".join(lines))
+
+# ==========================================
+# 5. Execution Example (Subset of IMDB)
+# ==========================================
+
+# Dataset loading using the real IMDB dataset via HuggingFace datasets.
+# Data source:
+#   HuggingFace Datasets – "imdb" configuration, which originates from the
+#   Large Movie Review Dataset (Maas et al., 2011).
+def load_imdb_texts(split: str = "train"):
+    """
+    Load IMDB dataset texts and labels using `datasets.load_dataset`.
+
+    Args:
+        split (str): Dataset split, e.g. "train" or "test".
+
+    Returns:
+        Tuple[List[str], List[int]]: List of review texts and sentiment labels,
+        where labels are integers 0 (negative) and 1 (positive).
+    """
+    ds = load_dataset("imdb", split=split)
+    texts = ds["text"]
+    labels = ds["label"]
+    return texts, labels
+
+# ===========================
+# Hyperparameters
+# ===========================
+# MAX_VOCAB: upper bound on vocabulary size. Larger values can capture more
+# rare words but increase model size and memory usage.
+MAX_VOCAB = 5000
+# MAX_LEN: maximum number of tokens per review. Longer sequences capture
+# more context but are more expensive to process; here we use 64 for speed.
+MAX_LEN = 64
+# BATCH_SIZE: number of examples per optimization step. Larger batches yield
+# smoother gradients but require more memory.
+BATCH_SIZE = 32
+# EPOCHS: number of full passes through the training dataset.
+EPOCHS = 5
+# LR: initial learning rate for the Adam optimizer.
+LR = 0.001
+
+# Transformer size presets for model-complexity experiments.
+# Each preset controls hidden size, attention heads, number of layers,
+# and feed-forward dimension.
+MODEL_SIZES = {
+    "small": {"d_model": 64, "num_heads": 4, "num_layers": 1, "d_ff": 128},
+    "medium": {"d_model": 128, "num_heads": 8, "num_layers": 2, "d_ff": 256},
+    "large": {"d_model": 256, "num_heads": 8, "num_layers": 4, "d_ff": 512},
+}
+
+# Directory to save trained model and related artifacts (checkpoint, vocab,
+# and configuration dictionary for reproducibility).
+# Keep output paths relative to the current working directory.
+SAVE_DIR = os.path.join(".", "saved_model")
+os.makedirs(SAVE_DIR, exist_ok=True)
+MODEL_PATH = os.path.join(SAVE_DIR, "transformer_imdb.pt")
+REPORT_PATH = os.path.join(SAVE_DIR, "transformer_imdb_experiment_report.md")
+
+def main():
+    """
+    Train a Transformer-based sentiment classifier on IMDB and save the model,
+    vocabulary, and configuration to disk.
+    """
+    # 1) Load IMDB training split and then create train/validation split.
+    all_train_texts, all_train_labels = load_imdb_texts(split="train")
+
+    train_texts, val_texts, train_labels, val_labels = train_test_split(
+        all_train_texts,
+        all_train_labels,
+        test_size=0.2,
+        random_state=42,
+        stratify=all_train_labels,
+    )
+
+    # 2) Build vocabulary using training texts only (avoid validation leakage).
+    vocab = build_vocab(train_texts, MAX_VOCAB)
+
+    # 3) Preprocess train and validation data into fixed-length ID sequences.
+    train_sequences = preprocess_data(train_texts, vocab, MAX_LEN)
+    val_sequences = preprocess_data(val_texts, vocab, MAX_LEN)
+
+    train_dataset = IMDBDataset(train_sequences, train_labels)
+    val_dataset = IMDBDataset(val_sequences, val_labels)
+
+    # DataLoaders for mini-batch training and validation.
+    train_loader = DataLoader(train_dataset, batch_size=BATCH_SIZE, shuffle=True)
+    val_loader = DataLoader(val_dataset, batch_size=BATCH_SIZE, shuffle=False)
+
+    device = torch.device("cuda" if torch.cuda.is_available() else "cpu")
+    results = []
+
+    # Train and evaluate multiple model sizes to analyze how complexity
+    # changes sentiment-classification performance.
+    for size_name, size_cfg in MODEL_SIZES.items():
+        print("\n" + "=" * 72)
+        print(f"Training {size_name.upper()} model with config: {size_cfg}")
+        print("=" * 72)
+
+        model = TransformerClassifier(
+            len(vocab),
+            size_cfg["d_model"],
+            size_cfg["num_heads"],
+            size_cfg["num_layers"],
+            size_cfg["d_ff"],
+            MAX_LEN,
+        )
+        param_count = count_trainable_parameters(model)
+        print(f"Trainable parameters ({size_name}): {param_count:,}")
+
+        train_model(model, train_loader, val_loader, EPOCHS, LR, device)
+        val_metrics = evaluate_model(model, val_loader, device)
+        size_model_path = os.path.join(SAVE_DIR, f"transformer_imdb_{size_name}.pt")
+        results.append(
+            {
+                "size": size_name,
+                "params": param_count,
+                "config": size_cfg,
+                "metrics": val_metrics,
+                "checkpoint_path": size_model_path,
+            }
+        )
+
+        # Save each trained size-specific model.
+        torch.save(
+            {
+                "model_state_dict": model.state_dict(),
+                "vocab": vocab,
+                "config": {
+                    "max_vocab": MAX_VOCAB,
+                    "max_len": MAX_LEN,
+                    "batch_size": BATCH_SIZE,
+                    "epochs": EPOCHS,
+                    "lr": LR,
+                    "size_name": size_name,
+                    **size_cfg,
+                },
+                "val_metrics": val_metrics,
+            },
+            size_model_path,
+        )
+        print(f"Saved {size_name} model to {size_model_path}")
+
+    # Print a concise comparison table at the end.
+    print("\n" + "#" * 72)
+    print("Model Size Impact Summary (Validation Set)")
+    print("#" * 72)
+    print(f"{'Size':<10} {'Params':>12} {'Acc':>8} {'Precision':>10} {'Recall':>8} {'F1':>8}")
+    for item in results:
+        m = item["metrics"]
+        print(
+            f"{item['size']:<10} "
+            f"{item['params']:>12,} "
+            f"{m['accuracy']:>8.4f} "
+            f"{m['precision']:>10.4f} "
+            f"{m['recall']:>8.4f} "
+            f"{m['f1']:>8.4f}"
+        )
+
+    # Keep a compatibility checkpoint name for the best model by validation F1.
+    best_result = max(results, key=lambda x: x["metrics"]["f1"])
+    best_model_path = os.path.join(SAVE_DIR, f"transformer_imdb_{best_result['size']}.pt")
+    torch.save(
+        {
+            "best_size": best_result["size"],
+            "best_model_path": best_model_path,
+            "all_results": results,
+        },
+        MODEL_PATH,
+    )
+    print(f"\nBest model by Val F1: {best_result['size']} -> {best_model_path}")
+    print(f"Experiment summary saved to {MODEL_PATH}")
+
+    write_experiment_report_md(
+        REPORT_PATH,
+        results,
+        best_result,
+        device,
+        train_size=len(train_texts),
+        val_size=len(val_texts),
+    )
+    print(f"Markdown report saved to {REPORT_PATH}")
+
+
+if __name__ == "__main__":
+    main()
\ No newline at end of file
diff --git a/assignment_llm_1/assignment_text/code/c1_analysis.py b/assignment_llm_1/assignment_text/code/c1_analysis.py
new file mode 100644
index 0000000000000000000000000000000000000000..a8b2c4668513707c36e9bc5238411d4f9bd53df4
--- /dev/null
+++ b/assignment_llm_1/assignment_text/code/c1_analysis.py
@@ -0,0 +1,253 @@
+"""
+Evaluation and qualitative error analysis helpers for the IMDB Transformer model.
+
+This module is separate from `c1.py` and focuses only on:
+- Loading a previously trained model from disk.
+- Evaluating it on an IMDB split.
+- Inspecting misclassified examples for qualitative error analysis.
+"""
+
+from typing import Dict, List, Tuple
+
+import argparse
+import os
+
+import torch
+import torch.nn.functional as F
+from torch.utils.data import DataLoader
+
+from c1 import (
+    IMDBDataset,
+    TransformerClassifier,
+    preprocess_data,
+    evaluate_model,
+    load_imdb_texts,
+)
+
+# Keep output/checkpoint paths relative to the current working directory.
+SAVE_DIR = os.path.join(".", "saved_model")
+MODEL_PATH = os.path.join(SAVE_DIR, "transformer_imdb.pt")
+
+
+def analyze_misclassifications_on_texts(
+    model: torch.nn.Module,
+    texts: List[str],
+    labels: List[int],
+    vocab: Dict[str, int],
+    max_len: int,
+    device: torch.device,
+    num_examples: int = 5,
+) -> None:
+    """
+    Inspect concrete examples where the model makes mistakes to understand
+    *why* it fails and how to improve it.
+
+    How to read the output (practical guidance):
+    - Start with the true vs. predicted label:
+      - For each misclassified review, ask whether the ground-truth label
+        actually matches the human-intuitive sentiment. Occasional noisy
+        labels are common in IMDB-style datasets.
+    - Look at the confidence vector:
+      - Very confident but wrong predictions often indicate *systematic bias*
+        (e.g., the model over-trusts certain keywords like "great", "worst").
+      - Low-confidence errors may simply reflect inherently ambiguous reviews.
+    - Scan the text content:
+      - Check for **rare or domain-specific words** (brand names, slang,
+        technical jargon) that might not appear often enough in training.
+      - Look for **negation patterns** ("not good", "hardly bad", "no longer
+        terrible") where bag-of-words style cues can mislead attention.
+      - Notice **mixed sentiment** or **topic vs. opinion** separation
+        (e.g., long plot summary plus a brief opinion at the end).
+      - Pay attention to **sarcasm and irony**, which are notoriously hard
+        for models relying mostly on local lexical cues.
+    - Compare several misclassified examples:
+      - If you see many errors with long reviews, consider increasing MAX_LEN
+        or using a deeper model.
+      - If errors cluster around subtle, low-intensity sentiment, you may need
+        more expressive capacity (higher d_model / more layers) or additional
+        training data.
+
+    Based on these observations you can propose targeted improvements, such as:
+    - Expanding the vocabulary or switching to subword tokenization.
+    - Adjusting hyperparameters (sequence length, model size).
+    - Incorporating pre-trained language models for richer semantics.
+    """
+    model.eval()
+    sequences = preprocess_data(texts, vocab, max_len)
+    dataset = IMDBDataset(sequences, labels)
+    loader = DataLoader(dataset, batch_size=64, shuffle=False)
+
+    printed = 0
+    with torch.no_grad():
+        for batch_idx, (batch_seq, batch_lab) in enumerate(loader):
+            batch_seq, batch_lab = batch_seq.to(device), batch_lab.to(device)
+            logits = model(batch_seq)
+            probs = F.softmax(logits, dim=1)
+            preds = torch.argmax(probs, dim=1)
+
+            start = batch_idx * loader.batch_size
+            end = start + batch_seq.size(0)
+            batch_texts = texts[start:end]
+
+            for text, true_y, pred_y, prob_vec in zip(
+                batch_texts,
+                batch_lab.cpu().numpy(),
+                preds.cpu().numpy(),
+                probs.cpu().numpy(),
+            ):
+                if true_y != pred_y:
+                    printed += 1
+                    print("=" * 80)
+                    print(f"Misclassified example #{printed}")
+                    print(f"True label     : {true_y} (0=neg, 1=pos)")
+                    print(f"Predicted label: {pred_y}")
+                    print(f"Model confidence (class 0, class 1): {prob_vec}")
+
+                    if printed >= num_examples:
+                        print("=" * 80)
+                        print(
+                            f"Displayed the first {num_examples} misclassified "
+                            "examples on this split."
+                        )
+                        return
+
+    if printed == 0:
+        print("No misclassified examples found on this split (perfect accuracy).")
+
+
+def load_trained_model_from_checkpoint(
+    checkpoint_path: str = MODEL_PATH,
+    device: torch.device | None = None,
+) -> Tuple[torch.nn.Module, Dict[str, int], Dict]:
+    """
+    Load a previously trained Transformer model, along with its vocabulary
+    and configuration, from the checkpoint saved by `c1.py`.
+
+    Returns:
+        model: Loaded TransformerClassifier on the requested device.
+        vocab: Token-to-index mapping used during training.
+        config: Hyperparameter/config dictionary saved in the checkpoint.
+    """
+    if device is None:
+        device = torch.device("cuda" if torch.cuda.is_available() else "cpu")
+
+    ckpt = torch.load(checkpoint_path, map_location=device)
+    vocab: Dict[str, int] = ckpt["vocab"]
+    config: Dict = ckpt["config"]
+
+    model = TransformerClassifier(
+        vocab_size=len(vocab),
+        d_model=config["d_model"],
+        num_heads=config["num_heads"],
+        num_layers=config["num_layers"],
+        d_ff=config["d_ff"],
+        max_len=config["max_len"],
+    ).to(device)
+    model.load_state_dict(ckpt["model_state_dict"])
+    model.eval()
+
+    return model, vocab, config
+
+
+def evaluate_and_analyze_saved_model(
+    split: str = "test",
+    checkpoint_path: str | None = None,
+    model_size: str = "medium",
+    num_examples: int = 5,
+    device: torch.device | None = None,
+) -> None:
+    """
+    High-level helper that:
+    1) Loads the trained model/vocab/config from disk.
+    2) Evaluates it on the requested IMDB split.
+    3) Runs qualitative error analysis on that split.
+    """
+    if device is None:
+        device = torch.device("cuda" if torch.cuda.is_available() else "cpu")
+
+    if checkpoint_path is None:
+        checkpoint_path = os.path.join(SAVE_DIR, f"transformer_imdb_{model_size}.pt")
+
+    print(f"Loading trained model from: {checkpoint_path}")
+    model, vocab, config = load_trained_model_from_checkpoint(
+        checkpoint_path=checkpoint_path,
+        device=device,
+    )
+
+    print(f"Evaluating on IMDB '{split}' split...")
+    texts, labels = load_imdb_texts(split=split)
+    sequences = preprocess_data(texts, vocab, config["max_len"])
+    dataset = IMDBDataset(sequences, labels)
+    loader = DataLoader(dataset, batch_size=config["batch_size"], shuffle=False)
+
+    metrics = evaluate_model(model, loader, device)
+    print("Evaluation metrics:", metrics)
+
+    print("\nRunning qualitative error analysis...")
+    analyze_misclassifications_on_texts(
+        model=model,
+        texts=texts,
+        labels=labels,
+        vocab=vocab,
+        max_len=config["max_len"],
+        device=device,
+        num_examples=num_examples,
+    )
+
+
+def main():
+    """
+    Command-line interface for evaluation and analysis utilities.
+
+    Example:
+        # Evaluate medium model on IMDB test split and show 5 errors
+        python c1_analysis.py --split test --model_size medium --num_examples 5
+    """
+    parser = argparse.ArgumentParser(description="IMDB Transformer evaluation and analysis utilities")
+    parser.add_argument(
+        "--split",
+        type=str,
+        default="test",
+        help="IMDB split to evaluate on (e.g., 'test', 'train').",
+    )
+    parser.add_argument(
+        "--checkpoint",
+        type=str,
+        default=None,
+        help=(
+            "Optional explicit checkpoint path. If provided, this overrides "
+            "--model_size."
+        ),
+    )
+    parser.add_argument(
+        "--model_size",
+        type=str,
+        choices=["small", "medium", "large"],
+        default="medium",
+        help=(
+            "Model size to load from saved checkpoints. Used when --checkpoint "
+            "is not provided."
+        ),
+    )
+    parser.add_argument(
+        "--num_examples",
+        type=int,
+        default=5,
+        help="Number of misclassified examples to print in error analysis.",
+    )
+    args = parser.parse_args()
+
+    device = torch.device("cuda" if torch.cuda.is_available() else "cpu")
+
+    evaluate_and_analyze_saved_model(
+        split=args.split,
+        checkpoint_path=args.checkpoint,
+        model_size=args.model_size,
+        num_examples=args.num_examples,
+        device=device,
+    )
+
+
+if __name__ == "__main__":
+    main()
+
diff --git a/assignment_llm_1/assignment_text/code/explanation_creation.py b/assignment_llm_1/assignment_text/code/explanation_creation.py
new file mode 100644
index 0000000000000000000000000000000000000000..47122f41bbae368a56ad44c3815bed4c9b6c94c2
--- /dev/null
+++ b/assignment_llm_1/assignment_text/code/explanation_creation.py
@@ -0,0 +1,174 @@
+import argparse
+import json
+import torch
+import torch.nn.functional as F
+from typing import Dict, List, Tuple
+from torch.utils.data import DataLoader
+
+# Assuming these are in your c1.py
+from c1 import (
+    IMDBDataset,
+    TransformerClassifier,
+    preprocess_data,
+    evaluate_model,
+    load_imdb_texts,
+    MODEL_PATH,
+)
+
+# You would need to install openai: pip install openai
+from openai import OpenAI
+api_file = "/home/mshahidul/api_new.json"
+with open(api_file, "r") as f:
+    api_keys = json.load(f)
+openai_api_key = api_keys["openai"]
+
+client = OpenAI(api_key=openai_api_key)
+# Initialize your client (ensure your API key is in your environment variables)
+
+def get_llm_explanation(review_text: str, true_y: int, pred_y: int) -> str:
+    """
+    Uses an LLM to perform qualitative reasoning on why the model failed.
+    """
+    sentiment = {0: "Negative", 1: "Positive"}
+    
+    prompt = f"""
+    A Transformer model misclassified the following movie review.
+    
+    REVIEW: "{review_text[:1000]}" 
+    TRUE LABEL: {sentiment[true_y]}
+    MODEL PREDICTED: {sentiment[pred_y]}
+    
+    Task: Provide a concise (2-3 sentence) explanation of why a machine learning 
+    model might have struggled with this specific text. Mention linguistic 
+    features like sarcasm, double negatives, mixed sentiment, or specific keywords.
+    """
+
+    try:
+        response = client.chat.completions.create(
+            model="gpt-4o-mini",  # Using 4o-mini as a high-performance proxy for "mini" models
+            messages=[{"role": "user", "content": prompt}],
+            temperature=0.2
+        )
+        return response.choices[0].message.content.strip()
+    except Exception as e:
+        return f"LLM Analysis failed: {str(e)}"
+
+def analyze_misclassifications_on_texts(
+    model: torch.nn.Module,
+    texts: List[str],
+    labels: List[int],
+    vocab: Dict[str, int],
+    max_len: int,
+    device: torch.device,
+    num_examples: int = 10,
+) -> List[Dict]:
+    """
+    Identifies errors, generates LLM explanations, and returns structured results.
+    """
+    model.eval()
+    sequences = preprocess_data(texts, vocab, max_len)
+    dataset = IMDBDataset(sequences, labels)
+    loader = DataLoader(dataset, batch_size=64, shuffle=False)
+
+    error_results = []
+    printed = 0
+    
+    with torch.no_grad():
+        for batch_idx, (batch_seq, batch_lab) in enumerate(loader):
+            batch_seq, batch_lab = batch_seq.to(device), batch_lab.to(device)
+            logits = model(batch_seq)
+            probs = F.softmax(logits, dim=1)
+            preds = torch.argmax(probs, dim=1)
+
+            start = batch_idx * loader.batch_size
+            batch_texts = texts[start:start + batch_seq.size(0)]
+
+            for text, true_y, pred_y, prob_vec in zip(
+                batch_texts,
+                batch_lab.cpu().numpy(),
+                preds.cpu().numpy(),
+                probs.cpu().numpy(),
+            ):
+                if true_y != pred_y:
+                    printed += 1
+                    
+                    print(f"Analyzing error #{printed} with LLM...")
+                    explanation = get_llm_explanation(text, true_y, pred_y)
+                    
+                    error_entry = {
+                        "example_id": printed,
+                        "true_label": int(true_y),
+                        "predicted_label": int(pred_y),
+                        "confidence_neg": float(prob_vec[0]),
+                        "confidence_pos": float(prob_vec[1]),
+                        "text": text,
+                        "explanation": explanation
+                    }
+                    error_results.append(error_entry)
+
+                    # Print to console for immediate feedback
+                    print("=" * 80)
+                    print(f"True: {true_y} | Pred: {pred_y}")
+                    print(f"Reasoning: {explanation}")
+                    print("=" * 80)
+
+                    if printed >= num_examples:
+                        return error_results
+
+    return error_results
+
+def load_trained_model_from_checkpoint(
+    checkpoint_path: str = MODEL_PATH,
+    device: torch.device | None = None,
+) -> Tuple[torch.nn.Module, Dict[str, int], Dict]:
+    if device is None:
+        device = torch.device("cuda" if torch.cuda.is_available() else "cpu")
+
+    ckpt = torch.load(checkpoint_path, map_location=device)
+    vocab = ckpt["vocab"]
+    config = ckpt["config"]
+
+    model = TransformerClassifier(
+        vocab_size=len(vocab),
+        d_model=config["d_model"],
+        num_heads=config["num_heads"],
+        num_layers=config["num_layers"],
+        d_ff=config["d_ff"],
+        max_len=config["max_len"],
+    ).to(device)
+    model.load_state_dict(ckpt["model_state_dict"])
+    return model, vocab, config
+
+def main():
+    parser = argparse.ArgumentParser()
+    parser.add_argument("--split", type=str, default="test")
+    parser.add_argument("--num_examples", type=int, default=10)
+    parser.add_argument("--output", type=str, default="error_analysis.json")
+    args = parser.parse_args()
+
+    device = torch.device("cuda" if torch.cuda.is_available() else "cpu")
+
+    # 1. Load Model
+    model, vocab, config = load_trained_model_from_checkpoint(device=device)
+
+    # 2. Load Data
+    texts, labels = load_imdb_texts(split=args.split)
+
+    # 3. Analyze
+    errors = analyze_misclassifications_on_texts(
+        model=model,
+        texts=texts,
+        labels=labels,
+        vocab=vocab,
+        max_len=config["max_len"],
+        device=device,
+        num_examples=args.num_examples
+    )
+
+    # 4. Save Results
+    with open(args.output, "w") as f:
+        json.dump(errors, f, indent=4)
+    print(f"\nAnalysis complete. Results saved to {args.output}")
+
+if __name__ == "__main__":
+    main()
\ No newline at end of file
diff --git a/assignment_llm_1/assignment_text/documentation/different_model_size_and_performance.md b/assignment_llm_1/assignment_text/documentation/different_model_size_and_performance.md
new file mode 100644
index 0000000000000000000000000000000000000000..2e34d341646e48ab48b06ca629abcf0b5da081f7
--- /dev/null
+++ b/assignment_llm_1/assignment_text/documentation/different_model_size_and_performance.md
@@ -0,0 +1,77 @@
+# IMDB Transformer Model-Size Experiment Report
+
+- Generated at: `2026-02-10 09:52:58`
+- Device: `cuda`
+- Training samples: `20000`
+- Validation samples: `5000`
+- Max vocab size: `5000`
+- Max sequence length: `64`
+- Batch size: `32`
+- Epochs: `5`
+- Learning rate: `0.001`
+
+## Overall Comparison
+
+| Model Size | Trainable Params | Accuracy | Precision | Recall | F1 | Checkpoint |
+|---|---:|---:|---:|---:|---:|---|
+| small | 353,602 | 0.7816 | 0.7832 | 0.7788 | 0.7810 | `assignment_llm_1/saved_model/transformer_imdb_small.pt` |
+| medium | 905,218 | 0.7874 | 0.7948 | 0.7748 | 0.7847 | `assignment_llm_1/saved_model/transformer_imdb_medium.pt` |
+| large | 3,388,930 | 0.7374 | 0.7392 | 0.7336 | 0.7364 | `assignment_llm_1/saved_model/transformer_imdb_large.pt` |
+
+## Best Model
+
+- Best size by validation F1: `medium`
+- Checkpoint: `assignment_llm_1/saved_model/transformer_imdb_medium.pt`
+- Trainable parameters: `905,218`
+- Metrics:
+  - Accuracy: `0.7874`
+  - Precision: `0.7948`
+  - Recall: `0.7748`
+  - F1: `0.7847`
+
+## Per-Model Details
+
+### Small model
+
+- Architecture:
+  - `d_model`: `64`
+  - `num_heads`: `4`
+  - `num_layers`: `1`
+  - `d_ff`: `128`
+- Trainable params: `353,602`
+- Checkpoint: `/assignment_llm_1/saved_model/transformer_imdb_small.pt`
+- Validation metrics:
+  - Accuracy: `0.7816`
+  - Precision: `0.7832`
+  - Recall: `0.7788`
+  - F1: `0.7810`
+
+### Medium model
+
+- Architecture:
+  - `d_model`: `128`
+  - `num_heads`: `8`
+  - `num_layers`: `2`
+  - `d_ff`: `256`
+- Trainable params: `905,218`
+- Checkpoint: `/assignment_llm_1/saved_model/transformer_imdb_medium.pt`
+- Validation metrics:
+  - Accuracy: `0.7874`
+  - Precision: `0.7948`
+  - Recall: `0.7748`
+  - F1: `0.7847`
+
+### Large model
+
+- Architecture:
+  - `d_model`: `256`
+  - `num_heads`: `8`
+  - `num_layers`: `4`
+  - `d_ff`: `512`
+- Trainable params: `3,388,930`
+- Checkpoint: `/assignment_llm_1/saved_model/transformer_imdb_large.pt`
+- Validation metrics:
+  - Accuracy: `0.7374`
+  - Precision: `0.7392`
+  - Recall: `0.7336`
+  - F1: `0.7364`
diff --git a/assignment_llm_1/assignment_text/documentation/documentation.md b/assignment_llm_1/assignment_text/documentation/documentation.md
new file mode 100644
index 0000000000000000000000000000000000000000..cdc874c96ec0b44fe015f3cf088fa86abac2958e
--- /dev/null
+++ b/assignment_llm_1/assignment_text/documentation/documentation.md
@@ -0,0 +1,142 @@
+## Homework 1 (Part I) – Transformer-Based Sentiment Analysis on IMDB
+
+### 1. Introduction
+
+This project implements a Transformer-based neural network for binary sentiment analysis on movie reviews. Given a raw text review from the IMDB dataset, the model predicts whether the review expresses a positive or negative sentiment. Sentiment analysis is a fundamental task in natural language processing (NLP) with applications in opinion mining, recommendation systems, and social media monitoring, where understanding users’ attitudes at scale is essential.
+
+The Transformer architecture is well suited to this task because it relies on self-attention rather than recurrent connections. Self-attention allows the model to capture long-range dependencies between words regardless of their distance in the sequence and to focus on sentiment-bearing tokens (for example, “not”, “excellent”, “boring”) even when they appear far apart. This makes Transformers more effective and easier to train in parallel than traditional RNN or LSTM models for document-level classification.
+
+### 2. Dataset Description
+
+The model is trained and validated on the IMDB movie reviews dataset, loaded via the HuggingFace `datasets` library using the `"imdb"` configuration. This dataset corresponds to the Large Movie Review Dataset introduced by Maas et al. (2011), which contains 50,000 labeled movie reviews (25,000 train and 25,000 test) plus additional unlabeled reviews. The original dataset is available from the Stanford AI Lab at `http://ai.stanford.edu/~amaas/data/sentiment/`. Each labeled review is annotated with a binary label: 0 for negative and 1 for positive sentiment.
+
+In this implementation, I use the labeled training split exposed by the HuggingFace wrapper and perform an additional 80/20 train/validation split with stratification over the labels. This results in approximately 20,000 reviews for training and 5,000 reviews for validation, preserving the original class balance. The official test split and the unlabeled reviews from the Large Movie Review Dataset are not used in this assignment. The labels are integers taking values in {0, 1}, corresponding to negative and positive sentiment respectively.
+
+The raw text consists of HTML-formatted movie reviews. As a minimal preprocessing step, HTML line breaks (`<br />`) are removed and all non-alphanumeric characters (except whitespace) are filtered out. No additional filtering or subsetting (such as length-based pruning) is performed; instead, sequence length is controlled later during token-to-index mapping and padding.
+
+When using this dataset, the canonical citation requested by the authors is:
+
+Andrew L. Maas, Raymond E. Daly, Peter T. Pham, Dan Huang, Andrew Y. Ng, and Christopher Potts. 2011. Learning Word Vectors for Sentiment Analysis. In Proceedings of the 49th Annual Meeting of the Association for Computational Linguistics: Human Language Technologies, pages 142–150.
+
+### 3. Data Preprocessing
+
+Preprocessing is implemented in three main stages: tokenization, vocabulary construction, and sequence padding.
+
+Tokenization uses a simple regular expression–based tokenizer. The text is converted to lowercase, HTML line breaks are replaced by spaces, and all characters that are not letters, digits, or whitespace are removed. The cleaned string is then split on whitespace to obtain a list of tokens. This approach yields a plain word-level tokenization that is easy to interpret and sufficient for this assignment.
+
+Vocabulary construction builds a word-to-index mapping from the training texts only, which avoids information leakage from the validation set. A `Counter` is used to accumulate token frequencies over all training reviews. Two special tokens are reserved: `<PAD>` with index 0 and `<UNK>` with index 1. The remaining slots (up to `MAX_VOCAB = 5000`) are filled with the most frequent words in the training corpus. Any word outside this vocabulary is mapped to the `<UNK>` index at inference time.
+
+For sequence padding and truncation, each review is converted to a fixed-length sequence of token IDs with `MAX_LEN = 64`. Tokens are mapped to their integer indices via the vocabulary; if a token is not present, it is mapped to `<UNK>`. If a sequence is shorter than 64 tokens, it is padded on the right with `<PAD>` tokens until length 64. If it is longer, it is truncated to the first 64 tokens. This produces a dense matrix of shape (number_of_examples, 64), which is used as input to the model.
+
+### 4. Model Architecture
+
+At a high level, the model is a Transformer encoder stacked on top of learned token embeddings and sinusoidal positional encodings, followed by a global pooling operation and a linear classification head. It is a pure encoder architecture tailored for sequence-level classification rather than sequence-to-sequence generation.
+
+First, input token IDs are passed through an embedding layer that maps each vocabulary index to a continuous vector of dimension `d_model = 128`. These token embeddings capture distributional semantics learned during training. Since embeddings alone do not encode the order of tokens, the model adds positional encodings. A standard sinusoidal positional encoding is precomputed for positions up to a maximum length and added elementwise to the token embeddings. This provides the model with information about the absolute position of each token in the sequence.
+
+The resulting sequence of encoded token representations is processed by a stack of Transformer encoder layers. In this implementation, there are `NUM_LAYERS = 2` such layers, each consisting of a multi-head self-attention sublayer followed by a position-wise feed-forward network, both wrapped in residual connections and layer normalization.
+
+Within each encoder block, multi-head self-attention projects the input sequence into queries, keys, and values of dimension `d_k = d_model / num_heads`, where `num_heads = 8`. For each head, attention weights are computed as scaled dot products between queries and keys, divided by the square root of `d_k` to ensure stable gradients. A softmax is then applied to obtain a probability distribution over positions, and a weighted sum of the value vectors is taken. The outputs of all heads are concatenated and passed through a final linear projection back to `d_model`. Self-attention lets each token representation attend to all other tokens in the sequence, enabling the model to capture context such as negation and long-distance sentiment cues.
+
+The output of the attention sublayer is added back to the original input via a residual connection and normalized using layer normalization. A feed-forward sublayer then applies a two-layer MLP with hidden dimension `d_ff = 256` and ReLU activation, followed again by residual addition and layer normalization. This combination allows the model to perform both contextual mixing (via attention) and local non-linear transformations (via the feed-forward network).
+
+After the final encoder layer, the model applies global average pooling over the sequence dimension, computing the mean of the hidden states across all time steps. This yields a single `d_model`-dimensional vector that summarizes the entire review. A dropout layer with dropout probability 0.1 is applied during training to reduce overfitting. Finally, a linear classification head maps this pooled representation to `num_classes = 2` logits, corresponding to negative and positive sentiment. The predicted class is obtained via an argmax over these logits.
+
+In summary, self-attention in this model works by dynamically weighting each token’s contribution to every other token’s representation based on learned similarity scores. Tokens with stronger semantic or syntactic relevance to a given position receive higher attention weights, enabling the model to focus on the most informative parts of the review for sentiment prediction.
+
+### 5. Training Pipeline
+
+The training loop is implemented around a standard supervised learning pipeline for PyTorch models. The loss function used is cross-entropy loss (`nn.CrossEntropyLoss`), which is appropriate for multi-class (here, binary) classification with mutually exclusive classes. It directly optimizes the log-likelihood of the correct label given the model’s logits.
+
+Optimization is performed using the Adam optimizer (`torch.optim.Adam`) with an initial learning rate of `LR = 0.001`. Adam is chosen for its robustness to gradient scaling and its ability to adaptively tune learning rates per parameter, which is beneficial when training Transformer-style models. To encourage better convergence, a learning rate scheduler (`StepLR`) is applied: the learning rate is multiplied by `gamma = 0.5` every `step_size = 2` epochs. This gradually reduces the learning rate as training progresses, helping the model to fine-tune around a local optimum.
+
+Batches are constructed using `DataLoader` objects with a batch size of `BATCH_SIZE = 32`. The training loader shuffles the data at each epoch, while the validation loader does not. The model is trained for `EPOCHS = 5` full passes over the training set. Dropout with probability 0.1 is applied to the embeddings and intermediate representations, providing regularization by randomly masking components during training. No explicit early stopping is implemented in code; instead, performance is monitored on the validation set after each epoch via evaluation metrics. If desired, early stopping could be implemented externally by tracking the best validation F1 score and halting when it stops improving.
+
+### 6. Evaluation Metrics
+
+The evaluation function computes four metrics on the validation (or test) data: accuracy, precision, recall, and F1-score. Predictions are obtained by taking the argmax over the model’s logits for each example.
+
+Accuracy measures the overall proportion of correctly classified reviews and is a natural baseline metric for binary sentiment classification. However, accuracy alone can be misleading if the dataset is imbalanced or if different error types have different costs. Therefore, precision, recall, and F1-score (with binary averaging) are also reported. Precision captures the fraction of predicted positive reviews that are truly positive, recall captures the fraction of true positive reviews that are correctly identified, and the F1-score is the harmonic mean of precision and recall. For sentiment analysis where both false positives and false negatives are important, F1-score provides a more informative single-number summary than accuracy alone.
+
+### 7. Experimental Results (Updated with Model-Size Study)
+
+The training script now explicitly explores model complexity by training three Transformer sizes:
+
+- `small`: `d_model=64`, `num_heads=4`, `num_layers=1`, `d_ff=128`
+- `medium`: `d_model=128`, `num_heads=8`, `num_layers=2`, `d_ff=256`
+- `large`: `d_model=256`, `num_heads=8`, `num_layers=4`, `d_ff=512`
+
+For each size, the code reports training loss and validation metrics (accuracy, precision, recall, F1-score). It also computes trainable parameter counts and prints a final comparison table so performance can be compared against model complexity in a single run.
+
+In addition to console logging, the script saves a human-readable report:
+
+- `assignment_text/saved_model/transformer_imdb_experiment_report.md`
+
+This report includes run metadata, per-size architecture details, checkpoint paths, parameter counts, and metric summaries, making the experiment easy to share and inspect.
+
+### 8. Model Analysis and Error Inspection
+
+The main strength of this model is its ability to exploit contextual information across the entire review via self-attention. Unlike bag-of-words or simple n-gram models, it can represent interactions between distant tokens, such as handling negation (“not good”) or nuanced phrases that influence sentiment only in context. Additionally, the use of positional encoding preserves word order, which is crucial for distinguishing, for example, “not only good but great” from superficially similar but differently ordered phrases.
+
+However, several weaknesses are apparent. First, the tokenizer is very simple and does not handle subword units, morphology, or out-of-vocabulary words in a sophisticated way. Rare words are collapsed into the `<UNK>` token, which can obscure important sentiment cues. Second, reviews are truncated to 64 tokens; for very long reviews, important information appearing later in the text may be discarded, potentially harming performance. Third, the model capacity (two encoder layers with `d_model = 128`) is modest compared to modern large-scale Transformers and may limit performance on more challenging or nuanced reviews.
+
+From an overfitting perspective, validation metrics track training performance reasonably well, and the use of dropout and a relatively small model size helps keep overfitting under control. That said, with only 5 epochs of training, there is also a risk of underfitting: the model might not fully exploit the available training data. Adding more epochs with careful learning rate scheduling or early stopping based on validation F1 could further improve performance.
+
+Potential improvements include increasing the maximum sequence length to capture more of each review, adopting a more advanced tokenizer such as Byte-Pair Encoding (BPE) or WordPiece to better handle rare words and subwords, and scaling up the model (more layers, larger `d_model`, larger `d_ff`) if computational resources allow. Pretraining on a large unlabeled corpus and then fine-tuning on IMDB would also likely yield significant gains, following the standard transfer learning paradigm for NLP.
+
+For concrete examples, error-analysis instances are stored in:
+
+- `assignment_text/documentation/error_analysis.json`
+
+Based on the current file (`10` sampled misclassified reviews), the dominant failure mode is clear: all listed mistakes are **false positives** where the true label is negative (`0`) but the model predicts positive (`1`). This indicates the model is comparatively weaker at recognizing subtle or mixed negative sentiment.
+
+Common patterns observed in these errors include:
+
+- **Mixed sentiment with mild praise + stronger criticism**: e.g., "worth a rental" or "semi-alright action" appears early, but overall judgment is negative.
+- **Sarcasm and irony**: phrases such as "only thing good..." or "top of the garbage list" are difficult for the model to interpret reliably.
+- **Contrastive structure**: reviews that begin with positive setup and then pivot to criticism are often classified as positive.
+- **Soft negative wording**: "average", "passable", "not really worth watching again" can be semantically negative but lexically less explicit.
+- **Calibration issue on borderline negatives**: several wrong predictions have moderate confidence for the positive class, suggesting uncertain decision boundaries around nuanced negative reviews.
+
+This error profile suggests improvements should prioritize better handling of nuanced negative language (especially sarcasm and contrastive discourse), for example via richer tokenization (subword methods), longer context windows, and additional hard-negative examples during training.
+
+### 9. Conclusion
+
+This implementation demonstrates that a relatively small Transformer encoder can perform effective sentiment analysis on the IMDB dataset using only word-level tokenization and simple preprocessing. Through self-attention and positional encoding, the model captures long-range dependencies and focuses on sentiment-relevant parts of each review, achieving strong validation performance compared with simple baselines.
+
+From this assignment, the key takeaways are that Transformer-based models are flexible and powerful for text classification tasks and that even a compact architecture benefits from core Transformer ideas such as multi-head self-attention, residual connections, and normalization. At the same time, overall performance is sensitive to choices in tokenization, sequence length, and model capacity, highlighting the importance of careful design and experimentation when applying Transformers to NLP problems.
+
+### 10. Reproducibility, Code Organization, and Key Implementation Details
+
+The project is organized around core scripts and a directory for saved artifacts:
+
+- `assignment_text/code/c1.py`: End-to-end training/evaluation script with multi-size experiments (`small`, `medium`, `large`). It saves per-size checkpoints and a markdown experiment report.
+- `assignment_text/code/c1_analysis.py`: Evaluation and qualitative analysis script for loading a trained checkpoint and inspecting misclassifications. It supports `--model_size` to select `small`, `medium`, or `large`.
+- `assignment_text/saved_model/transformer_imdb_small.pt`, `assignment_text/saved_model/transformer_imdb_medium.pt`, `assignment_text/saved_model/transformer_imdb_large.pt`: Size-specific checkpoints.
+- `assignment_text/saved_model/transformer_imdb_experiment_report.md`: Experiment summary report generated after training.
+- `assignment_text/saved_model/transformer_imdb.pt`: Compatibility summary file containing best-model metadata and all results.
+
+Within `c1.py`, the data preprocessing pipeline is implemented by `tokenize`, `build_vocab`, and `preprocess_data`. The `tokenize` function normalizes and splits raw review text into lowercase word tokens, `build_vocab` constructs a frequency-based mapping from tokens to integer indices using only the training texts (reserving indices 0 and 1 for padding and unknown tokens), and `preprocess_data` converts each review into a fixed-length sequence of token IDs via truncation and padding. The `IMDBDataset` class wraps these sequences and labels into a PyTorch Dataset, and `DataLoader` objects provide mini-batches for training and validation.
+
+The model components are built in a modular fashion. `PositionalEncoding` implements sinusoidal position encodings that are added to token embeddings, `MultiHeadAttention` performs scaled dot-product self-attention over the sequence across multiple heads, and `TransformerEncoderBlock` combines multi-head attention, a position-wise feed-forward network, residual connections, and layer normalization into a single encoder layer. The `TransformerClassifier` class composes an embedding layer, positional encoding, a stack of encoder blocks, global average pooling over the sequence dimension, and a final linear layer that outputs logits for the two sentiment classes.
+
+The training and evaluation logic is encapsulated in `train_model` and `evaluate_model`. `train_model` iterates over the training DataLoader for a specified number of epochs, computes the cross-entropy loss, performs backpropagation and optimizer updates (Adam with an initial learning rate of 0.001), applies a StepLR scheduler that halves the learning rate every two epochs, and reports validation accuracy, precision, recall, and F1-score at the end of each epoch. `evaluate_model` runs the model in evaluation mode on a given DataLoader and aggregates predictions and labels to compute the same metrics. The function `load_imdb_texts` serves as a thin wrapper around the HuggingFace `datasets.load_dataset` API and clearly documents that the underlying data originates from the Large Movie Review Dataset (Maas et al., 2011).
+
+To reproduce the experiments, the main dependencies are PyTorch, scikit-learn, NumPy, and the HuggingFace `datasets` library. The script is designed to use a CUDA GPU if available, otherwise it falls back to CPU.
+
+Global hyperparameters are defined near the end of `c1.py`:
+
+- `MAX_VOCAB = 5000` (maximum vocabulary size)
+- `MAX_LEN = 64` (maximum sequence length in tokens)
+- `BATCH_SIZE = 32` (mini-batch size)
+- `EPOCHS = 5` (number of training epochs)
+- `LR = 0.001` (initial learning rate for Adam)
+
+Model-size-specific hyperparameters are defined in `MODEL_SIZES`:
+
+- `small`: `d_model=64`, `num_heads=4`, `num_layers=1`, `d_ff=128`
+- `medium`: `d_model=128`, `num_heads=8`, `num_layers=2`, `d_ff=256`
+- `large`: `d_model=256`, `num_heads=8`, `num_layers=4`, `d_ff=512`
+
+Running `c1.py` end-to-end will (1) download and preprocess the IMDB training split, (2) train all three model sizes on the training portion, (3) evaluate each model on the validation portion, and (4) save checkpoints plus an experiment report to the `assignment_text/saved_model` directory. Running `c1_analysis.py` with `--model_size` then allows targeted evaluation and qualitative error analysis for the selected size. With these components documented, the experiment is fully reproducible and can be extended for further study.
+
diff --git a/assignment_llm_1/assignment_text/documentation/error_analysis.json b/assignment_llm_1/assignment_text/documentation/error_analysis.json
new file mode 100644
index 0000000000000000000000000000000000000000..be2fd31128aa6058ab9afc834242db700c7495d1
--- /dev/null
+++ b/assignment_llm_1/assignment_text/documentation/error_analysis.json
@@ -0,0 +1,92 @@
+[
+    {
+        "example_id": 1,
+        "true_label": 0,
+        "predicted_label": 1,
+        "confidence_neg": 0.13079692423343658,
+        "confidence_pos": 0.8692030906677246,
+        "text": "Worth the entertainment value of a rental, especially if you like action movies. This one features the usual car chases, fights with the great Van Damme kick style, shooting battles with the 40 shell load shotgun, and even terrorist style bombs. All of this is entertaining and competently handled but there is nothing that really blows you away if you've seen your share before.<br /><br />The plot is made interesting by the inclusion of a rabbit, which is clever but hardly profound. Many of the characters are heavily stereotyped -- the angry veterans, the terrified illegal aliens, the crooked cops, the indifferent feds, the bitchy tough lady station head, the crooked politician, the fat federale who looks like he was typecast as the Mexican in a Hollywood movie from the 1940s. All passably acted but again nothing special.<br /><br />I thought the main villains were pretty well done and fairly well acted. By the end of the movie you certainly knew who the good guys were and weren't. There was an emotional lift as the really bad ones got their just deserts. Very simplistic, but then you weren't expecting Hamlet, right? The only thing I found really annoying was the constant cuts to VDs daughter during the last fight scene.<br /><br />Not bad. Not good. Passable 4.",
+        "explanation": "The model likely struggled with this review due to its mixed sentiment, where the reviewer acknowledges some entertainment value while simultaneously critiquing the film's lack of originality and reliance on stereotypes. Phrases like \"worth the entertainment value of a rental\" may have been interpreted positively, overshadowing the underlying negative sentiment expressed through descriptors like \"nothing special\" and \"hardly profound.\" Additionally, the nuanced critique of character portrayals and plot elements may have led to misclassification, as the model may not have effectively captured the sarcasm or the overall negative tone."
+    },
+    {
+        "example_id": 2,
+        "true_label": 0,
+        "predicted_label": 1,
+        "confidence_neg": 0.19945980608463287,
+        "confidence_pos": 0.8005402088165283,
+        "text": "its a totally average film with a few semi-alright action sequences that make the plot seem a little better and remind the viewer of the classic van dam films. parts of the plot don't make sense and seem to be added in to use up time. the end plot is that of a very basic type that doesn't leave the viewer guessing and any twists are obvious from the beginning. the end scene with the flask backs don't make sense as they are added in and seem to have little relevance to the history of van dam's character. not really worth watching again, bit disappointed in the end production, even though it is apparent it was shot on a low budget certain shots and sections in the film are of poor directed quality",
+        "explanation": "The model likely struggled with this review due to the presence of mixed sentiment and subtle linguistic cues that indicate negativity, such as phrases like \"totally average,\" \"not really worth watching again,\" and \"bit disappointed.\" Additionally, the use of qualifiers like \"semi-alright\" and the overall tone may have led the model to misinterpret the review as more positive than intended, as it could have focused on the mention of \"action sequences\" without fully grasping the critical context surrounding them."
+    },
+    {
+        "example_id": 3,
+        "true_label": 0,
+        "predicted_label": 1,
+        "confidence_neg": 0.07963180541992188,
+        "confidence_pos": 0.9203682541847229,
+        "text": "First off let me say, If you haven't enjoyed a Van Damme movie since bloodsport, you probably will not like this movie. Most of these movies may not have the best plots or best actors but I enjoy these kinds of movies for what they are. This movie is much better than any of the movies the other action guys (Segal and Dolph) have thought about putting out the past few years. Van Damme is good in the movie, the movie is only worth watching to Van Damme fans. It is not as good as Wake of Death (which i highly recommend to anyone of likes Van Damme) or In hell but, in my opinion it's worth watching. It has the same type of feel to it as Nowhere to Run. Good fun stuff!",
+        "explanation": "The model likely struggled with this review due to its mixed sentiment and nuanced language. While the reviewer expresses enjoyment of Van Damme's movies, they also imply that the film may not appeal to a broader audience, which can create confusion. Additionally, phrases like \"not as good as\" and \"only worth watching to Van Damme fans\" introduce a negative sentiment that may have been overshadowed by the overall positive tone, leading to the misclassification."
+    },
+    {
+        "example_id": 4,
+        "true_label": 0,
+        "predicted_label": 1,
+        "confidence_neg": 0.04191816598176956,
+        "confidence_pos": 0.958081841468811,
+        "text": "Isaac Florentine has made some of the best western Martial Arts action movies ever produced. In particular US Seals 2, Cold Harvest, Special Forces and Undisputed 2 are all action classics. You can tell Isaac has a real passion for the genre and his films are always eventful, creative and sharp affairs, with some of the best fight sequences an action fan could hope for. In particular he has found a muse with Scott Adkins, as talented an actor and action performer as you could hope for. This is borne out with Special Forces and Undisputed 2, but unfortunately The Shepherd just doesn't live up to their abilities.<br /><br />There is no doubt that JCVD looks better here fight-wise than he has done in years, especially in the fight he has (for pretty much no reason) in a prison cell, and in the final showdown with Scott, but look in his eyes. JCVD seems to be dead inside. There's nothing in his eyes at all. It's like he just doesn't care about anything throughout the whole film. And this is the leading man.<br /><br />There are other dodgy aspects to the film, script-wise and visually, but the main problem is that you are utterly unable to empathise with the hero of the film. A genuine shame as I know we all wanted this film to be as special as it genuinely could have been. There are some good bits, mostly the action scenes themselves. This film had a terrific director and action choreographer, and an awesome opponent for JCVD to face down. This could have been the one to bring the veteran action star back up to scratch in the balls-out action movie stakes.<br /><br />Sincerely a shame that this didn't happen.",
+        "explanation": "The model likely struggled with this review due to its mixed sentiment and nuanced language. While the reviewer praises Isaac Florentine's work and highlights positive aspects of the films, the overall sentiment shifts negatively when discussing JCVD's performance, particularly with phrases like \"dead inside\" and \"doesn't care.\" This complexity, combined with the presence of both positive and negative keywords, may have led the model to misinterpret the overall sentiment as positive."
+    },
+    {
+        "example_id": 5,
+        "true_label": 0,
+        "predicted_label": 1,
+        "confidence_neg": 0.45393702387809753,
+        "confidence_pos": 0.5460630059242249,
+        "text": "A group of heirs to a mysterious old mansion find out that they have to live in it as part of a clause in the will or be disinherited, but they soon find out of its history of everybody whom had lived there before them having either died in weird accidents or having had killed each other.<br /><br />You've seen it all before, and this one is too low-budget and slow paced to be scary, and doesn't have any real surprises in the climax. No special effects or gore to speak of, in fact the only really amusing thing about the whole film is the quality of the English dubbing, which at times is as bad as a cheap martial arts movie.<br /><br />3 out of 10, pretty low in the pecking order of 80's haunted house movies.",
+        "explanation": "The machine learning model likely struggled with this review due to the presence of mixed sentiment and subtle sarcasm. Phrases like \"you've seen it all before\" and \"the only really amusing thing\" can be interpreted as positive, while the overall context and explicit negative ratings (e.g., \"3 out of 10\") indicate dissatisfaction. Additionally, the model may have misinterpreted the lack of special effects and the critique of dubbing as neutral or positive elements, leading to an incorrect classification."
+    },
+    {
+        "example_id": 6,
+        "true_label": 0,
+        "predicted_label": 1,
+        "confidence_neg": 0.34184929728507996,
+        "confidence_pos": 0.6581506729125977,
+        "text": "The Forgotten (AKA: Don't Look In The Basement) is a very cheaply made and very old looking horror movie.<br /><br />The story is very slow and never really reaches anything worth getting excited about.<br /><br />The patients at the asylum are embarrassingly funny especially Sam and the old woman who always quotes an old saying to everyone. (Look out for the bit when she gets close to the camera, tell me you can watch without laughing!).<br /><br />Now the gore is very poor looking, with the blood looking pink in many scenes so it doesn't really deserve its place on the video nasties list!.<br /><br />Overall if you aren't looking for a fantastic horror film and have some time to spare then it's worth a watch.",
+        "explanation": "The model likely struggled with this review due to its mixed sentiment and the presence of sarcasm. Phrases like \"embarrassingly funny\" and \"worth a watch\" can be interpreted positively, despite the overall negative tone conveyed by descriptors like \"cheaply made\" and \"very slow.\" Additionally, the use of humor in describing the film's shortcomings may have misled the model into classifying the review as positive."
+    },
+    {
+        "example_id": 7,
+        "true_label": 0,
+        "predicted_label": 1,
+        "confidence_neg": 0.1487887054681778,
+        "confidence_pos": 0.8512113094329834,
+        "text": "I of course saw the previews for this at the beginning of some other Lion's Gate extravaganza, so of course it was only the best parts and therefore looked intriguing. And it is, to a point. A young college student (Sarah)is finding riddles all over the place and is becoming obsessed with answering them, and in doing so she's unwittingly becoming involved in some game. Now that's fairly intriguing right there but unfortunately it all gets rather muddled and becomes so complicated that the viewer (like myself) will most likely become frustrated. Characters appear with little introduction and you're not really sure who they are or why Sarah knows them or is hanging out with them. All of this has something to do with this woman who tried to drown a young boy years ago and her reason for that was that it's \"all part of the design\". In reality, it's all part of the \"very sketchy script\" and when the film is over you'll find yourself feeling that you've lost about an hour and a half of your life that you want back for more productive uses of your time, like cleaning the bathroom, for instance. 4 out of 10.",
+        "explanation": "The model likely struggled with this review due to the presence of mixed sentiment and nuanced language. Phrases like \"fairly intriguing\" and \"best parts\" may have been interpreted positively, while the overall context reveals frustration with the plot's complexity and a \"very sketchy script.\" Additionally, the use of sarcasm and the negative conclusion about losing time could have been overlooked by the model, leading to an incorrect positive classification."
+    },
+    {
+        "example_id": 8,
+        "true_label": 0,
+        "predicted_label": 1,
+        "confidence_neg": 0.32372772693634033,
+        "confidence_pos": 0.6762722134590149,
+        "text": "Four things intrigued me as to this film - firstly, it stars Carly Pope (of \"Popular\" fame), who is always a pleasure to watch. Secdonly, it features brilliant New Zealand actress Rena Owen. Thirdly, it is filmed in association with the New Zealand Film Commission. Fourthly, a friend recommended it to me. However, I was utterly disappointed. The whole storyline is absurd and complicated, with very little resolution. Pope's acting is fine, but Owen is unfortunately under-used. The other actors and actresses are all okay, but I am unfamiliar with them all. Aside from the nice riddles which are littered throughout the movie (and Pope and Owen), this film isn't very good. So the moral of the story is...don't watch it unless you really want to.",
+        "explanation": "The model likely struggled with this review due to the presence of mixed sentiment and subtle sarcasm. While the reviewer mentions positive aspects such as the cast and riddles, the overall tone is negative, particularly in phrases like \"utterly disappointed\" and \"this film isn't very good,\" which may have been overshadowed by the initial positive keywords. Additionally, the complexity of the review's structure may have led the model to misinterpret the sentiment conveyed."
+    },
+    {
+        "example_id": 9,
+        "true_label": 0,
+        "predicted_label": 1,
+        "confidence_neg": 0.35207340121269226,
+        "confidence_pos": 0.6479266285896301,
+        "text": "<br /><br />Never ever take a film just for its good looking title.<br /><br />Although it all starts well, the film suffers the same imperfections you see in B-films. Its like at a certain moment the writer does not any more how to end the film, so he ends it in a way nobody suspects it thinking this way he is ingenious.<br /><br />A film to be listed on top of the garbage list.<br /><br />",
+        "explanation": "The model likely struggled with the review due to the presence of sarcasm and mixed sentiment, particularly in phrases like \"good looking title\" and \"thinking this way he is ingenious,\" which could be misinterpreted as positive. Additionally, the use of phrases like \"top of the garbage list\" may not have been weighted heavily enough by the model, leading to an incorrect positive classification despite the overall negative sentiment expressed in the review."
+    },
+    {
+        "example_id": 10,
+        "true_label": 0,
+        "predicted_label": 1,
+        "confidence_neg": 0.42465338110923767,
+        "confidence_pos": 0.5753466486930847,
+        "text": "Lowe returns to the nest after, yet another, failed relationship, to find he's been assigned to jury duty. It's in the plans to, somehow, get out of it, when he realizes the defendant is the girl he's had a serious crush on since the first grade.<br /><br />Through living in the past by telling other people about his feelings towards this girl (played by Camp), Lowe remembers those feelings and does everything in his power to clear Camp of attempted murder, while staying away from the real bad guys at the same time, and succeeding in creating a successful film at the same time.<br /><br />I've heard that St Augustine is the oldest city in the US, and I also know it has some ties to Ponce de Leon, so the backdrop is a good place to start. Unfortunately, it's the only thing good about this movie. The local police are inept, the judge is an idiot, and the defense counsel does everything in her power to make herself look like Joanie Cunningham! I don't know whether to blame the director for poor direction, or for just letting the cast put in such a hapless effort.<br /><br />In short, this movie was so boring, I could not even sleep through it! 1 out of 10 stars!",
+        "explanation": "The model likely struggled with this review due to the presence of mixed sentiment and sarcasm. While the reviewer mentions some positive elements, such as the interesting backdrop of St. Augustine, the overall tone is negative, highlighted by phrases like \"the only thing good about this movie\" and criticisms of the characters and plot. The model may have misinterpreted the positive keywords and failed to recognize the underlying negative sentiment conveyed through the reviewer's frustration and sarcasm."
+    }
+]
\ No newline at end of file
diff --git a/assignment_llm_1/assignment_text/saved_model/Untitled b/assignment_llm_1/assignment_text/saved_model/Untitled
new file mode 100644
index 0000000000000000000000000000000000000000..8e78906ae567211d3a5e058d862ea3b00e1c021d
--- /dev/null
+++ b/assignment_llm_1/assignment_text/saved_model/Untitled
@@ -0,0 +1 @@
+saved_model
\ No newline at end of file
diff --git a/assignment_llm_1/assignment_text/saved_model/transformer_imdb_experiment_report.md b/assignment_llm_1/assignment_text/saved_model/transformer_imdb_experiment_report.md
new file mode 100644
index 0000000000000000000000000000000000000000..36107ecbb4934bfc0534c9acd96171bfa60e6810
--- /dev/null
+++ b/assignment_llm_1/assignment_text/saved_model/transformer_imdb_experiment_report.md
@@ -0,0 +1,77 @@
+# IMDB Transformer Model-Size Experiment Report
+
+- Generated at: `2026-02-12 01:50:15`
+- Device: `cuda`
+- Training samples: `20000`
+- Validation samples: `5000`
+- Max vocab size: `5000`
+- Max sequence length: `64`
+- Batch size: `32`
+- Epochs: `5`
+- Learning rate: `0.001`
+
+## Overall Comparison
+
+| Model Size | Trainable Params | Accuracy | Precision | Recall | F1 | Checkpoint |
+|---|---:|---:|---:|---:|---:|---|
+| small | 353,602 | 0.7742 | 0.7627 | 0.7960 | 0.7790 | `./saved_model/transformer_imdb_small.pt` |
+| medium | 905,218 | 0.7804 | 0.7674 | 0.8048 | 0.7856 | `./saved_model/transformer_imdb_medium.pt` |
+| large | 3,388,930 | 0.5190 | 0.5098 | 0.9880 | 0.6726 | `./saved_model/transformer_imdb_large.pt` |
+
+## Best Model
+
+- Best size by validation F1: `medium`
+- Checkpoint: `./saved_model/transformer_imdb_medium.pt`
+- Trainable parameters: `905,218`
+- Metrics:
+  - Accuracy: `0.7804`
+  - Precision: `0.7674`
+  - Recall: `0.8048`
+  - F1: `0.7856`
+
+## Per-Model Details
+
+### Small model
+
+- Architecture:
+  - `d_model`: `64`
+  - `num_heads`: `4`
+  - `num_layers`: `1`
+  - `d_ff`: `128`
+- Trainable params: `353,602`
+- Checkpoint: `./saved_model/transformer_imdb_small.pt`
+- Validation metrics:
+  - Accuracy: `0.7742`
+  - Precision: `0.7627`
+  - Recall: `0.7960`
+  - F1: `0.7790`
+
+### Medium model
+
+- Architecture:
+  - `d_model`: `128`
+  - `num_heads`: `8`
+  - `num_layers`: `2`
+  - `d_ff`: `256`
+- Trainable params: `905,218`
+- Checkpoint: `./saved_model/transformer_imdb_medium.pt`
+- Validation metrics:
+  - Accuracy: `0.7804`
+  - Precision: `0.7674`
+  - Recall: `0.8048`
+  - F1: `0.7856`
+
+### Large model
+
+- Architecture:
+  - `d_model`: `256`
+  - `num_heads`: `8`
+  - `num_layers`: `4`
+  - `d_ff`: `512`
+- Trainable params: `3,388,930`
+- Checkpoint: `./saved_model/transformer_imdb_large.pt`
+- Validation metrics:
+  - Accuracy: `0.5190`
+  - Precision: `0.5098`
+  - Recall: `0.9880`
+  - F1: `0.6726`
diff --git a/assignment_llm_1/data/cifar-10-batches-py/batches.meta b/assignment_llm_1/data/cifar-10-batches-py/batches.meta
new file mode 100644
index 0000000000000000000000000000000000000000..4467a6ec2e886a9f14f25e31776fb0152d8ac64a
Binary files /dev/null and b/assignment_llm_1/data/cifar-10-batches-py/batches.meta differ
diff --git a/assignment_llm_1/data/cifar-10-batches-py/readme.html b/assignment_llm_1/data/cifar-10-batches-py/readme.html
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index 0000000000000000000000000000000000000000..e377adef45c85dc91051edf2dee72c1d4d57732c
--- /dev/null
+++ b/assignment_llm_1/data/cifar-10-batches-py/readme.html
@@ -0,0 +1 @@
+<meta HTTP-EQUIV="REFRESH" content="0; url=http://www.cs.toronto.edu/~kriz/cifar.html">
diff --git a/code/RL_model/inference_data/RL_model_inference_v1.jsonl b/code/RL_model/inference_data/RL_model_inference_v1.jsonl
new file mode 100644
index 0000000000000000000000000000000000000000..86b234e6fd2c4319eff46b553a2b90753f31ab1c
--- /dev/null
+++ b/code/RL_model/inference_data/RL_model_inference_v1.jsonl
@@ -0,0 +1,200 @@
+{"row_index": 0, "doc_id": 20, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 38-year-old woman had a weak heart since she was 17, after a bad throat infection that might have hurt her heart muscle. Her heart couldn’t pump blood well, and she was in serious danger. She stayed in the hospital for 10 months and got treatment to help her heart work better, including medicines to stop her heart from beating too fast and to reduce fluid buildup. After a while, her heart started to get stronger and stayed that way for 4 years. Then it got worse again for 2 years, but later she got stable again. She had a baby the first time, and her heart stayed strong. During her second pregnancy, in the second trimester, her heart weakened again and stayed weak for a few months. But now, in May 2017, she is doing fine. She takes medicines every day — for her heart, to control fluid, and to keep her heart steady. She can do normal daily activities, has two children, and doesn’t work. Her doctor says her heart is stable and she doesn’t need a special heart device. She just needs to keep taking her medicines, watch her fluid intake, stay healthy, and go to check-ups regularly.\"\n}", "generated_text": "A 38-year-old woman had a weak heart since she was 17, after a bad throat infection that might have hurt her heart muscle. Her heart couldn’t pump blood well, and she was in serious danger. She stayed in the hospital for 10 months and got treatment to help her heart work better, including medicines to stop her heart from beating too fast and to reduce fluid buildup. After a while, her heart started to get stronger and stayed that way for 4 years. Then it got worse again for 2 years, but later she got stable again. She had a baby the first time, and her heart stayed strong. During her second pregnancy, in the second trimester, her heart weakened again and stayed weak for a few months. But now, in May 2017, she is doing fine. She takes medicines every day — for her heart, to control fluid, and to keep her heart steady. She can do normal daily activities, has two children, and doesn’t work. Her doctor says her heart is stable and she doesn’t need a special heart device. She just needs to keep taking her medicines, watch her fluid intake, stay healthy, and go to check-ups regularly."}
+{"row_index": 1, "doc_id": 21, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 27-year-old man broke his right thigh bone after a small fall, where his hip twisted. He had a bone problem called fibrous dysplasia in his thigh years ago, which was fixed with surgery and bone graft 20 years ago. The old surgery part was removed a year later. This time, because the bone broke again, doctors took out a big piece of the upper thigh bone and replaced it with a hip implant. They also took a small tissue sample to make sure it was the same bone problem from when he was a child. Now, he can walk and do light activities, though he still has some pain when walking long distances. He’s doing well and feels happy with how his hip is working.\"\n}", "generated_text": "A 27-year-old man broke his right thigh bone after a small fall, where his hip twisted. He had a bone problem called fibrous dysplasia in his thigh years ago, which was fixed with surgery and bone graft 20 years ago. The old surgery part was removed a year later. This time, because the bone broke again, doctors took out a big piece of the upper thigh bone and replaced it with a hip implant. They also took a small tissue sample to make sure it was the same bone problem from when he was a child. Now, he can walk and do light activities, though he still has some pain when walking long distances. He’s doing well and feels happy with how his hip is working."}
+{"row_index": 2, "doc_id": 21, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 27-year-old man came to the emergency department with a broken right femur, specifically at the base of the neck, after a fall that involved pressure and twisting of the hip. The fracture was classified as a serious type (Garden II, Pauwells III, AO 31B2.3r) and occurred despite a low-energy injury. He had a history of fibrous dysplasia — a bone condition — in his right hip area, which was treated 20 years ago with surgery to remove abnormal bone (curettage), bone grafting, and the use of a metal fixation device. This device was removed one year later. A biopsy later confirmed the condition was fibrous dysplasia. Because of the nature of the fracture and the underlying disease, doctors decided on a wide removal of the upper part of the femur and a total hip replacement using a modular prosthesis, along with a biopsy to confirm it was the same fibrous dysplasia from his childhood. The surgery was successful, and the patient is now stable, walking with support and able to do daily activities. He still has some walking limitations due to a scar in the gluteal muscle, but he enjoys low-impact activities like walking and is very satisfied with his recovery.\"\n}", "generated_text": "A 27-year-old man came to the emergency department with a broken right femur, specifically at the base of the neck, after a fall that involved pressure and twisting of the hip. The fracture was classified as a serious type (Garden II, Pauwells III, AO 31B2.3r) and occurred despite a low-energy injury. He had a history of fibrous dysplasia — a bone condition — in his right hip area, which was treated 20 years ago with surgery to remove abnormal bone (curettage), bone grafting, and the use of a metal fixation device. This device was removed one year later. A biopsy later confirmed the condition was fibrous dysplasia. Because of the nature of the fracture and the underlying disease, doctors decided on a wide removal of the upper part of the femur and a total hip replacement using a modular prosthesis, along with a biopsy to confirm it was the same fibrous dysplasia from his childhood. The surgery was successful, and the patient is now stable, walking with support and able to do daily activities. He still has some walking limitations due to a scar in the gluteal muscle, but he enjoys low-impact activities like walking and is very satisfied with his recovery."}
+{"row_index": 3, "doc_id": 22, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 4-year-old boy with advanced neuroblastoma received intensive chemotherapy, followed by stem cell transplants — first using his own stem cells (autologous HSCT), then a transplant from a donor using cord blood (allogeneic CBT). After the transplant, he developed symptoms of a respiratory infection about a month before, including upper respiratory issues, and tested positive for RSV (a common virus that causes colds in children). On day 194, he started having severe breathing difficulties and was admitted to the hospital. Tests showed signs of lung damage, including inflammation and scarring in the small blood vessels of the lungs, which led to a diagnosis of PVOD (a condition where the lungs become stiff and hard to breathe). Pathology from a lung biopsy showed both signs of past viral infection and the lung injury linked to PVOD. The doctors believe that the RSV infection may have triggered or worsened the development of PVOD in this child.\"\n}", "generated_text": "A 4-year-old boy with advanced neuroblastoma received intensive chemotherapy, followed by stem cell transplants — first using his own stem cells (autologous HSCT), then a transplant from a donor using cord blood (allogeneic CBT). After the transplant, he developed symptoms of a respiratory infection about a month before, including upper respiratory issues, and tested positive for RSV (a common virus that causes colds in children). On day 194, he started having severe breathing difficulties and was admitted to the hospital. Tests showed signs of lung damage, including inflammation and scarring in the small blood vessels of the lungs, which led to a diagnosis of PVOD (a condition where the lungs become stiff and hard to breathe). Pathology from a lung biopsy showed both signs of past viral infection and the lung injury linked to PVOD. The doctors believe that the RSV infection may have triggered or worsened the development of PVOD in this child."}
+{"row_index": 4, "doc_id": 23, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 65-year-old man started feeling a bad cough, short of breath even doing small things, and lost 10 kilograms in 4 months. Tests showed a lump in his right lung and fluid around it. A small piece of tissue was taken and looked at under a microscope. The cells were large and spread out, with lots of immune cells around them. This type of cancer is rare and not like regular lung cancer. The cancer cells had markers that match a specific kind of cancer called pulmonary lymphoepithelioma-like carcinoma (CTLP). It had a very high level of a protein called PD-L1 and was found to have Epstein-Barr virus. He got 6 rounds of chemo using platinum and durvalumab, but the cancer grew worse. He had side effects like hearing loss and kidney problems, so the chemo was changed. After 9 months, he died from not being able to breathe.\"\n}", "generated_text": "A 65-year-old man started feeling a bad cough, short of breath even doing small things, and lost 10 kilograms in 4 months. Tests showed a lump in his right lung and fluid around it. A small piece of tissue was taken and looked at under a microscope. The cells were large and spread out, with lots of immune cells around them. This type of cancer is rare and not like regular lung cancer. The cancer cells had markers that match a specific kind of cancer called pulmonary lymphoepithelioma-like carcinoma (CTLP). It had a very high level of a protein called PD-L1 and was found to have Epstein-Barr virus. He got 6 rounds of chemo using platinum and durvalumab, but the cancer grew worse. He had side effects like hearing loss and kidney problems, so the chemo was changed. After 9 months, he died from not being able to breathe."}
+{"row_index": 5, "doc_id": 24, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 13-year-old boy found a lump in his groin that could be moved, but wasn't painful or red. No other symptoms were present. Doctors removed the lump to make sure it wasn't cancer or a serious disease. The test results showed the lump was made of special cells called plasma cells, which is a rare kind of disease in kids. This is the first time such a case has been found in the groin area. After 1 year of checking, no new lumps or symptoms came back. The boy is doing fine and has no other problems.\"\n}", "generated_text": "A 13-year-old boy found a lump in his groin that could be moved, but wasn't painful or red. No other symptoms were present. Doctors removed the lump to make sure it wasn't cancer or a serious disease. The test results showed the lump was made of special cells called plasma cells, which is a rare kind of disease in kids. This is the first time such a case has been found in the groin area. After 1 year of checking, no new lumps or symptoms came back. The boy is doing fine and has no other problems."}
+{"row_index": 6, "doc_id": 25, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"The medical records of patients diagnosed with congenital myotonia were retrospectively reviewed in the pediatric neurology consultation at a third-level hospital between 2015 and 2020. Inclusion criteria included a clinical diagnosis of myotonia accompanied by a warm-up phenomenon, characteristic electromyographic (EMG) findings, or a family history, as well as a molecular diagnosis involving mutations in the CLCN1 gene. Demographic data (age and sex), disease course (age of onset, symptomatology, time to diagnosis, and clinical progression), family history, and response to therapeutic interventions were systematically extracted from the electronic medical records. All patients underwent comprehensive clinical evaluation, including laboratory testing and EMG assessment.\\n\\nFive patients with a clinical diagnosis of congenital myotonia were identified: three with Becker disease and two with Thomsen disease. The estimated incidence per 10,000 live births was 1:15,000 for the Becker phenotype and 1:21,000 for the Thomsen phenotype. The majority of patients were female; the only male patient presented with onset prior to age six. Initial clinical manifestations included lower-limb myotonia in four patients and upper-limb myotonia in all but one. Age at onset ranged from 22 months to 12 years, with a median of 6 years. Genetic testing was performed in all patients approximately two years after symptom onset, except in one case where the family declined testing. All patients exhibited worsening of myotonia with exposure to cold, with the warm-up phenomenon—defined as improvement of muscle tone following prolonged rest—observed exclusively in those with the Becker phenotype.\\n\\nPatients with recessive congenital myotonia demonstrated a progressive clinical course. Family history analysis revealed that patients 2 and 3 were sisters, with no clinical manifestations in their parents, suggesting an autosomal recessive inheritance pattern. The mother of patient 1 exhibited mild, cold-exacerbated myotonia, raising the possibility of subclinical carrier status. The patient who declined genetic testing had a reported history of myotonia in the maternal lineage, consistent with an inherited predisposition.\\n\\nSerum creatine kinase levels were not elevated in any of the patients, indicating that skeletal muscle damage is not a prominent feature of the disease. Electromyographic evaluation was abnormal in all patients except patient 1, who was evaluated at 2.8 years of age (at 2.8/12 years of age); subsequent EMG studies were not repeated due to clinical stability and the established diagnostic certainty. The absence of significant muscle enzyme elevation supports the notion that the pathophysiology is primarily due to impaired chloride channel function rather than active muscle degeneration.\\n\\nInitial pharmacological management primarily involved oxcarbazepine, particularly in patients with the recessive form (Becker disease), with generally favorable responses. However, in patient 2, oxcarbazepine lost efficacy over time, prompting the initiation of mexiletine. Patient 4 required multiple medications, all of which failed due to either therapeutic resistance or adverse effects. Patient 5, who had a mild clinical presentation, declined treatment. Patient 1 was found to carry a previously undescribed, likely pathogenic mutation in the CLCN1 gene (c.824T>C), inherited from his mother. Cases 1 to 3 exhibited the Becker phenotype and displayed composite heterozygosity, involving two distinct CLCN1 mutations. Cases 4 and 5 presented with the Thomsen phenotype, characterized by a more severe, early-onset form of myotonia. Patient 5 declined genetic testing, limiting the ability to confirm the specific inheritance pattern in this individual. The CLCN1 gene encodes the chloride channel subunit responsible for regulating membrane potential in skeletal muscle fibers; mutations in this gene lead to reduced chloride conductance, resulting in prolonged depolarization of the sarcolemma and subsequent muscle hyperexcitability, which manifests clinically as myotonia. This mechanism underlies the pathophysiology of both Becker and Thomsen congenital myotonias, with differences in severity and age of onset likely attributable to the nature and combination of mutations, including the novel c.824T>C variant identified in this cohort.\"\n}", "generated_text": "The medical records of patients diagnosed with congenital myotonia were retrospectively reviewed in the pediatric neurology consultation at a third-level hospital between 2015 and 2020. Inclusion criteria included a clinical diagnosis of myotonia accompanied by a warm-up phenomenon, characteristic electromyographic (EMG) findings, or a family history, as well as a molecular diagnosis involving mutations in the CLCN1 gene. Demographic data (age and sex), disease course (age of onset, symptomatology, time to diagnosis, and clinical progression), family history, and response to therapeutic interventions were systematically extracted from the electronic medical records. All patients underwent comprehensive clinical evaluation, including laboratory testing and EMG assessment.\n\nFive patients with a clinical diagnosis of congenital myotonia were identified: three with Becker disease and two with Thomsen disease. The estimated incidence per 10,000 live births was 1:15,000 for the Becker phenotype and 1:21,000 for the Thomsen phenotype. The majority of patients were female; the only male patient presented with onset prior to age six. Initial clinical manifestations included lower-limb myotonia in four patients and upper-limb myotonia in all but one. Age at onset ranged from 22 months to 12 years, with a median of 6 years. Genetic testing was performed in all patients approximately two years after symptom onset, except in one case where the family declined testing. All patients exhibited worsening of myotonia with exposure to cold, with the warm-up phenomenon—defined as improvement of muscle tone following prolonged rest—observed exclusively in those with the Becker phenotype.\n\nPatients with recessive congenital myotonia demonstrated a progressive clinical course. Family history analysis revealed that patients 2 and 3 were sisters, with no clinical manifestations in their parents, suggesting an autosomal recessive inheritance pattern. The mother of patient 1 exhibited mild, cold-exacerbated myotonia, raising the possibility of subclinical carrier status. The patient who declined genetic testing had a reported history of myotonia in the maternal lineage, consistent with an inherited predisposition.\n\nSerum creatine kinase levels were not elevated in any of the patients, indicating that skeletal muscle damage is not a prominent feature of the disease. Electromyographic evaluation was abnormal in all patients except patient 1, who was evaluated at 2.8 years of age (at 2.8/12 years of age); subsequent EMG studies were not repeated due to clinical stability and the established diagnostic certainty. The absence of significant muscle enzyme elevation supports the notion that the pathophysiology is primarily due to impaired chloride channel function rather than active muscle degeneration.\n\nInitial pharmacological management primarily involved oxcarbazepine, particularly in patients with the recessive form (Becker disease), with generally favorable responses. However, in patient 2, oxcarbazepine lost efficacy over time, prompting the initiation of mexiletine. Patient 4 required multiple medications, all of which failed due to either therapeutic resistance or adverse effects. Patient 5, who had a mild clinical presentation, declined treatment. Patient 1 was found to carry a previously undescribed, likely pathogenic mutation in the CLCN1 gene (c.824T>C), inherited from his mother. Cases 1 to 3 exhibited the Becker phenotype and displayed composite heterozygosity, involving two distinct CLCN1 mutations. Cases 4 and 5 presented with the Thomsen phenotype, characterized by a more severe, early-onset form of myotonia. Patient 5 declined genetic testing, limiting the ability to confirm the specific inheritance pattern in this individual. The CLCN1 gene encodes the chloride channel subunit responsible for regulating membrane potential in skeletal muscle fibers; mutations in this gene lead to reduced chloride conductance, resulting in prolonged depolarization of the sarcolemma and subsequent muscle hyperexcitability, which manifests clinically as myotonia. This mechanism underlies the pathophysiology of both Becker and Thomsen congenital myotonias, with differences in severity and age of onset likely attributable to the nature and combination of mutations, including the novel c.824T>C variant identified in this cohort."}
+{"row_index": 7, "doc_id": 26, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 67-year-old woman had swelling in her left leg for six years. She already had a problem in her leg's blood vessels called AVMs, which didn’t go away even after treatment. Recently, she started feeling very tired and short of breath, which means her heart was struggling. Doctors found her heart was enlarged and not working well, and her leg swelling was getting worse. The problem was caused by a rare birth defect in her leg’s blood vessels that was sending too much blood to her heart. To fix it, doctors first placed a special stent in her leg to block the bad blood flow. This helped her heart feel better. After that, they did a second treatment to stop the blood from flowing into the wrong veins. After the treatments, her leg swelling went down and her heart started working better. She’s now much stronger and her symptoms are much better.\"\n}", "generated_text": "A 67-year-old woman had swelling in her left leg for six years. She already had a problem in her leg's blood vessels called AVMs, which didn’t go away even after treatment. Recently, she started feeling very tired and short of breath, which means her heart was struggling. Doctors found her heart was enlarged and not working well, and her leg swelling was getting worse. The problem was caused by a rare birth defect in her leg’s blood vessels that was sending too much blood to her heart. To fix it, doctors first placed a special stent in her leg to block the bad blood flow. This helped her heart feel better. After that, they did a second treatment to stop the blood from flowing into the wrong veins. After the treatments, her leg swelling went down and her heart started working better. She’s now much stronger and her symptoms are much better."}
+{"row_index": 8, "doc_id": 26, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 67-year-old woman had been suffering from swelling in her left leg for six years. She was previously diagnosed with a complex congenital arteriovenous malformation (AVM) in her lower leg, but treatment with coils did not stop the swelling. Over the past month, she developed symptoms of heart failure, including fatigue and shortness of breath, and was taken to a hospital for further care. Tests showed her heart was enlarged and her heart function had worsened, with high levels of a heart failure marker (BNP). She also had poor blood flow in her leg arteries and no pulses in her lower leg. Imaging revealed a large AVM in the femoral and superficial femoral arteries, along with a swollen femoral artery and vein, which was likely causing the heart to work harder.\\n\\nBecause the AVM was too complex to be fully treated with coils alone, doctors used a covered stent placed in the femoral artery to block part of the abnormal blood flow. This helped reduce the amount of blood flowing into the leg, which in turn improved her heart failure symptoms. The surgery was done under general anesthesia using a catheter inserted through the leg, and the stent was placed exactly where the AVM was most active. After the procedure, her leg swelling and heart function improved significantly. One week later, blood flow in the leg dropped from 3400 ml/min to 1600 ml/min, and her BNP levels dropped, showing better heart health.\\n\\nIn a follow-up treatment, doctors used coils and other materials to block the main drainage veins of the AVM. This further reduced the abnormal blood flow. After one year, her leg swelling had greatly improved, her heart function had recovered, and her BNP levels were much lower. The patient is now doing better, with improved daily function and reduced symptoms of heart failure. This case shows that combining stent placement and embolization can be effective in treating complex congenital AVMs that cause heart failure.\"\n}", "generated_text": "A 67-year-old woman had been suffering from swelling in her left leg for six years. She was previously diagnosed with a complex congenital arteriovenous malformation (AVM) in her lower leg, but treatment with coils did not stop the swelling. Over the past month, she developed symptoms of heart failure, including fatigue and shortness of breath, and was taken to a hospital for further care. Tests showed her heart was enlarged and her heart function had worsened, with high levels of a heart failure marker (BNP). She also had poor blood flow in her leg arteries and no pulses in her lower leg. Imaging revealed a large AVM in the femoral and superficial femoral arteries, along with a swollen femoral artery and vein, which was likely causing the heart to work harder.\n\nBecause the AVM was too complex to be fully treated with coils alone, doctors used a covered stent placed in the femoral artery to block part of the abnormal blood flow. This helped reduce the amount of blood flowing into the leg, which in turn improved her heart failure symptoms. The surgery was done under general anesthesia using a catheter inserted through the leg, and the stent was placed exactly where the AVM was most active. After the procedure, her leg swelling and heart function improved significantly. One week later, blood flow in the leg dropped from 3400 ml/min to 1600 ml/min, and her BNP levels dropped, showing better heart health.\n\nIn a follow-up treatment, doctors used coils and other materials to block the main drainage veins of the AVM. This further reduced the abnormal blood flow. After one year, her leg swelling had greatly improved, her heart function had recovered, and her BNP levels were much lower. The patient is now doing better, with improved daily function and reduced symptoms of heart failure. This case shows that combining stent placement and embolization can be effective in treating complex congenital AVMs that cause heart failure."}
+{"row_index": 9, "doc_id": 26, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 67-year-old female patient with a six-year history of progressive left lower limb edema was diagnosed with complex congenital arteriovenous malformations (AVMs) in the lower extremity, following a prior embolization intervention involving two coils (20 mm × 40 cm, BSX, USA) one year prior. Despite this, her lower limb swelling remained unresponsive, and she developed symptomatic acute heart failure characterized by progressive fatigue, dyspnea, and cardiac dysfunction. She was referred to Chengdu University of Traditional Chinese Medicine Hospital for comprehensive evaluation. The patient had no prior history of cardiovascular disease, trauma, or surgical interventions, though she reported lifelong oral estrogen use for menopausal symptoms. Physical examination revealed severe edema, skin sclerosis, absent pulses in the popliteal and distal arteries, and a tremor in the left thigh. Echocardiography demonstrated left ventricular enlargement, moderate mitral regurgitation, severe tricuspid regurgitation, a left ventricular ejection fraction (LVEF) of 60%, and markedly elevated B-type natriuretic peptide (BNP) levels at 2853 ng/L. Electrocardiography showed sinus tachycardia (105 bpm) and left atrial enlargement. Chest CT confirmed cardiac enlargement without pulmonary pathology. Preoperative computed tomography angiography (CTA) revealed a left iliac artery aneurysm, marked dilation of the common femoral artery (CFA; 27 mm), superficial femoral artery (SFA; 22 mm), and complex AVMs involving both the SFA and profunda femoris artery. The femoral and superficial veins were significantly dilated during arterial phase imaging, with non-visualization of the popliteal and anterior tibial arteries. The patient was diagnosed with complex congenital lower limb AVMs, acute decompensated chronic heart failure, and classified as New York Heart Association (NYHA) Class IV. Preoperative CFA flow volume was measured at 3400 ml/min. Given the persistence of high shunt flow and inadequate response to coil embolization, a covered stent graft was deemed necessary to reduce venous shunting and alleviate hemodynamic burden on the heart. Access was achieved via antegrade surgical puncture of the right CFA using a 14 F (Cook Medical, USA) catheter sheath under general anesthesia. A 20 mm × 12 mm/120 mm aorto-uni-iliac covered stent (MicroPort, China) was selected based on preoperative CTA measurements showing a middle SFA diameter of 19 mm. A 0.035 guidewire and single-curve catheter were used to navigate to the popliteal artery, followed by transition to a 0.035 super-hard guidewire for stable catheterization during stent deployment. The stent was placed at the distal SFA, where AVM burden was highest. Completion angiography demonstrated marked reduction in venous opacification and restoration of arterial visualization, including the popliteal artery. Postoperatively, the left femoral artery was closed with a 6–0 vascular risk suture. The procedure was performed with minimal duration to avoid exacerbating cardiac stress in the setting of acute heart failure. One week postoperatively, CFA flow decreased to 1600 ml/min, and BNP levels dropped to 1198 ng/L, indicating early improvement in cardiac function. A second-stage embolization was planned to target the nidus of the AVM. Under ultrasound guidance, the draining venous system was punctured via the right CFA, with a 5 F vascular sheath introduced. Contrast injection confirmed the presence of the AVM nidus and its draining veins. Embolization was performed using a 18–20 mm × 40 cm coil (BSX, USA), two microcoils (4 mm × 42 mm and 5 mm × 10 mm, USA), 3% polidocanol (6 mL, Kruelle, Germany), and 99% anhydrous ethanol (10 mL). Completion angiography showed near-complete obliteration of the AVM nidus and draining venous pathways. At one-year follow-up, the CFA flow reduced to 780 ml/min, echocardiography revealed mild atrial enlargement, minor mitral and tricuspid regurgitation, and an improved left ventricular ejection fraction (LVEF) of 71%, with BNP levels significantly reduced. This case illustrates the clinical utility of staged intervention—initial covered stent graft placement to reduce shunt volume and stabilize hemodynamics, followed by targeted embolization to achieve complete nidus occlusion in complex congenital lower", "generated_text": "{\n  \"proficient_health_literacy\": \"A 67-year-old female patient with a six-year history of progressive left lower limb edema was diagnosed with complex congenital arteriovenous malformations (AVMs) in the lower extremity, following a prior embolization intervention involving two coils (20 mm × 40 cm, BSX, USA) one year prior. Despite this, her lower limb swelling remained unresponsive, and she developed symptomatic acute heart failure characterized by progressive fatigue, dyspnea, and cardiac dysfunction. She was referred to Chengdu University of Traditional Chinese Medicine Hospital for comprehensive evaluation. The patient had no prior history of cardiovascular disease, trauma, or surgical interventions, though she reported lifelong oral estrogen use for menopausal symptoms. Physical examination revealed severe edema, skin sclerosis, absent pulses in the popliteal and distal arteries, and a tremor in the left thigh. Echocardiography demonstrated left ventricular enlargement, moderate mitral regurgitation, severe tricuspid regurgitation, a left ventricular ejection fraction (LVEF) of 60%, and markedly elevated B-type natriuretic peptide (BNP) levels at 2853 ng/L. Electrocardiography showed sinus tachycardia (105 bpm) and left atrial enlargement. Chest CT confirmed cardiac enlargement without pulmonary pathology. Preoperative computed tomography angiography (CTA) revealed a left iliac artery aneurysm, marked dilation of the common femoral artery (CFA; 27 mm), superficial femoral artery (SFA; 22 mm), and complex AVMs involving both the SFA and profunda femoris artery. The femoral and superficial veins were significantly dilated during arterial phase imaging, with non-visualization of the popliteal and anterior tibial arteries. The patient was diagnosed with complex congenital lower limb AVMs, acute decompensated chronic heart failure, and classified as New York Heart Association (NYHA) Class IV. Preoperative CFA flow volume was measured at 3400 ml/min. Given the persistence of high shunt flow and inadequate response to coil embolization, a covered stent graft was deemed necessary to reduce venous shunting and alleviate hemodynamic burden on the heart. Access was achieved via antegrade surgical puncture of the right CFA using a 14 F (Cook Medical, USA) catheter sheath under general anesthesia. A 20 mm × 12 mm/120 mm aorto-uni-iliac covered stent (MicroPort, China) was selected based on preoperative CTA measurements showing a middle SFA diameter of 19 mm. A 0.035 guidewire and single-curve catheter were used to navigate to the popliteal artery, followed by transition to a 0.035 super-hard guidewire for stable catheterization during stent deployment. The stent was placed at the distal SFA, where AVM burden was highest. Completion angiography demonstrated marked reduction in venous opacification and restoration of arterial visualization, including the popliteal artery. Postoperatively, the left femoral artery was closed with a 6–0 vascular risk suture. The procedure was performed with minimal duration to avoid exacerbating cardiac stress in the setting of acute heart failure. One week postoperatively, CFA flow decreased to 1600 ml/min, and BNP levels dropped to 1198 ng/L, indicating early improvement in cardiac function. A second-stage embolization was planned to target the nidus of the AVM. Under ultrasound guidance, the draining venous system was punctured via the right CFA, with a 5 F vascular sheath introduced. Contrast injection confirmed the presence of the AVM nidus and its draining veins. Embolization was performed using a 18–20 mm × 40 cm coil (BSX, USA), two microcoils (4 mm × 42 mm and 5 mm × 10 mm, USA), 3% polidocanol (6 mL, Kruelle, Germany), and 99% anhydrous ethanol (10 mL). Completion angiography showed near-complete obliteration of the AVM nidus and draining venous pathways. At one-year follow-up, the CFA flow reduced to 780 ml/min, echocardiography revealed mild atrial enlargement, minor mitral and tricuspid regurgitation, and an improved left ventricular ejection fraction (LVEF) of 71%, with BNP levels significantly reduced. This case illustrates the clinical utility of staged intervention—initial covered stent graft placement to reduce shunt volume and stabilize hemodynamics, followed by targeted embolization to achieve complete nidus occlusion in complex congenital lower"}
+{"row_index": 10, "doc_id": 27, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 28-year-old man developed two red bumps on his right arm and forearm, with small blisters and sores in the middle, after being on vacation in coastal Ecuador. The area felt hot and itched a lot, but he didn’t have fever or other symptoms. Doctors took a small skin sample and saw signs of irritation and inflammation. Because of the location and his trip to a tropical area, they figured out it was caused by a bug called Paederus. He was treated with anti-itch medicine, creams to calm the skin, and cold compresses. After 8 days, the sores went away, but the skin stayed a bit darker in those areas.\"\n}", "generated_text": "A 28-year-old man developed two red bumps on his right arm and forearm, with small blisters and sores in the middle, after being on vacation in coastal Ecuador. The area felt hot and itched a lot, but he didn’t have fever or other symptoms. Doctors took a small skin sample and saw signs of irritation and inflammation. Because of the location and his trip to a tropical area, they figured out it was caused by a bug called Paederus. He was treated with anti-itch medicine, creams to calm the skin, and cold compresses. After 8 days, the sores went away, but the skin stayed a bit darker in those areas."}
+{"row_index": 11, "doc_id": 27, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 28-year-old male with no significant medical history presented to the dermatology department with a 48-hour history of two erythematous plaques exhibiting central vesicular lesions and superficial ulceration situated on the flexor surfaces of the right arm and forearm, symmetrically positioned equidistant from the elbow crease. The lesions were associated with localized burning sensation and pruritus, with no systemic symptoms or evidence of self-medication. The patient reported a recent vacation in the coastal region of Ecuador, which served as a key environmental exposure factor. An incisional biopsy was performed and revealed histopathological features consistent with Paederus dermatitis, including epidermal acanthosis, parakeratosis, and intercellular spongiosis, along with neutrophilic infiltrates in the stratum corneum and perivascular lymphocytic infiltration extending through the superficial, middle, and deep dermis. These findings reflect a type IV hypersensitivity reaction mediated by T-helper 1 (Th1) cells, driven by exposure to Paederus beetles (Paederus fuscipes or Paederus spp.), whose defensive secretions contain cytotoxic compounds such as pederin and other sesquiterpene lactones that induce direct epidermal damage and immune activation. The diagnosis was confirmed based on the clinical presentation, geographic exposure context, and histopathological correlation. Management consisted of antihistamines to mitigate pruritus and histamine-mediated inflammation, topical corticosteroids to suppress dermal immune cell activity and reduce epidermal hyperplasia, and cold compresses to alleviate vascular congestion and symptomatic discomfort. The lesions completely resolved after 8 days of treatment, with residual post-inflammatory hyperpigmentation observed as a consequence of melanocyte activation and prolonged dermal inflammation. This case underscores the importance of considering endemic arthropod exposures in tropical regions when evaluating acute, localized, non-infectious dermatoses with a characteristic vesiculobullous and ulcerative pattern in flexural skin folds.\"\n}", "generated_text": "A 28-year-old male with no significant medical history presented to the dermatology department with a 48-hour history of two erythematous plaques exhibiting central vesicular lesions and superficial ulceration situated on the flexor surfaces of the right arm and forearm, symmetrically positioned equidistant from the elbow crease. The lesions were associated with localized burning sensation and pruritus, with no systemic symptoms or evidence of self-medication. The patient reported a recent vacation in the coastal region of Ecuador, which served as a key environmental exposure factor. An incisional biopsy was performed and revealed histopathological features consistent with Paederus dermatitis, including epidermal acanthosis, parakeratosis, and intercellular spongiosis, along with neutrophilic infiltrates in the stratum corneum and perivascular lymphocytic infiltration extending through the superficial, middle, and deep dermis. These findings reflect a type IV hypersensitivity reaction mediated by T-helper 1 (Th1) cells, driven by exposure to Paederus beetles (Paederus fuscipes or Paederus spp.), whose defensive secretions contain cytotoxic compounds such as pederin and other sesquiterpene lactones that induce direct epidermal damage and immune activation. The diagnosis was confirmed based on the clinical presentation, geographic exposure context, and histopathological correlation. Management consisted of antihistamines to mitigate pruritus and histamine-mediated inflammation, topical corticosteroids to suppress dermal immune cell activity and reduce epidermal hyperplasia, and cold compresses to alleviate vascular congestion and symptomatic discomfort. The lesions completely resolved after 8 days of treatment, with residual post-inflammatory hyperpigmentation observed as a consequence of melanocyte activation and prolonged dermal inflammation. This case underscores the importance of considering endemic arthropod exposures in tropical regions when evaluating acute, localized, non-infectious dermatoses with a characteristic vesiculobullous and ulcerative pattern in flexural skin folds."}
+{"row_index": 12, "doc_id": 28, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A man in his 80s had a blocked bile duct causing yellowing of his skin and weight loss. Doctors found a tumor in his bile duct that couldn’t be removed, so they used a light-based treatment called PDT to ease the blockage. Before the treatment, he got a special medicine through his vein 24 hours earlier. During the procedure, a doctor used a tube to look inside the bile duct and guided a light tool through it to shine on the blocked area. The light was turned on slowly, every centimeter, to make sure the whole blockage was treated. Afterward, the doctor checked the bile duct again to make sure everything was okay. The treatment worked well at first — he didn’t feel sick for three months. But later, the blockage came back, and he had infections and other problems. He died 15 months after the treatment because of cancer spreading to his lungs.\"\n}", "generated_text": "A man in his 80s had a blocked bile duct causing yellowing of his skin and weight loss. Doctors found a tumor in his bile duct that couldn’t be removed, so they used a light-based treatment called PDT to ease the blockage. Before the treatment, he got a special medicine through his vein 24 hours earlier. During the procedure, a doctor used a tube to look inside the bile duct and guided a light tool through it to shine on the blocked area. The light was turned on slowly, every centimeter, to make sure the whole blockage was treated. Afterward, the doctor checked the bile duct again to make sure everything was okay. The treatment worked well at first — he didn’t feel sick for three months. But later, the blockage came back, and he had infections and other problems. He died 15 months after the treatment because of cancer spreading to his lungs."}
+{"row_index": 13, "doc_id": 28, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"The patient, an 82-year-old male with a two-month history of obstructive jaundice and weight loss, underwent transduodenal photodynamic therapy (TFD) as a palliative intervention for recurrent biliary obstruction. Endoscopic ultrasound (EUS) demonstrated severe dilation of the common bile duct with choledocholithiasis, confirmed by endoscopic retrograde cholangiopancreatography (ERCP), which failed to extract stones due to disproportionate ductal dilation. A plastic biliary stent was placed initially, resulting in transient improvement, but cholestasis recurred at 45 days, with two subsequent ERCP attempts also failing. During the third ERCP, a long, irregular stenosis of the common hepatic duct was identified, and EUS revealed a well-circumscribed hypoechoic solid mass measuring 1.8 × 2 cm compressing the common hepatic duct, with evidence of involvement of the common hepatic artery. Ultrasound-guided needle biopsy confirmed a diagnosis of moderately differentiated cholangiocarcinoma (Bismuth I). Staging determined the tumor to be inoperable, leading to referral for palliative photodynamic therapy (PDT). \\n\\nThe PDT procedure was performed under general anesthesia using intravenous administration of Photogen® (1.5 mg/kg) 24 hours prior to intervention. Photogen® is a porphyrin derivative with peak light absorption at 630 nm, enabling selective activation within tumor tissue upon illumination. Standard duodenoscopy (Olympus TJF-180) was performed to identify the greater duodenal papilla, followed by retrograde cannulation. A digital cholangioscope (SpyGlass™ DS, Boston Scientific) was then advanced into the common bile duct to directly visualize the stenotic segment. Neoplastic stenosis was identified via cholangioscopic examination. Under direct visualization, the illumination catheter (Medlight S.A., RD10-323) was advanced through the cholangioscope. This catheter is a three-way device: the first port features a 1 cm cylindrical light diffuser with two black radiopaque marks defining its distal limits; the second port accommodates a 0.025-inch guidewire for catheter guidance; the third port serves as an injection port for photosensitizer delivery. The illumination was administered at a power of 70 mW/cm² and a total dose of 90 J/cm², with repositioning performed every centimeter to ensure complete coverage of the obstructed area. The procedure lasted 150 minutes and concluded with a final cholangioscopic evaluation to assess immediate outcomes and detect adverse events. A 10 Fr plastic biliary stent was placed at the end of the session due to unavailability of a self-expanding metal stent. \\n\\nPost-procedure, the patient was maintained on a fasted state for 24 hours, with oral diet initiated if no adverse events were observed. Strict photoprotection measures were enforced, including avoidance of light exposure and use of sunglasses, particularly during the first week following PDT, to mitigate photosensitivity risk. The patient exhibited no signs of photosensitivity within the first week. However, early recurrence of cholestasis occurred, complicated by cholangitis. ERCP revealed stent obstruction due to biliary sludge and tumor necrotic debris. A biliary scan followed by re-drainage resolved the acute episode. The patient remained asymptomatic for three months, the longest period since disease onset. Subsequent recurrence was managed with a self-expanding metal stent, and systemic oncologic therapy was continued. Eventually, the patient developed dysphagia, requiring placement of a duodenal stent for palliative relief. He ultimately died from complications of pulmonary metastases, two years after symptom onset and 15 months after the TFD session. The procedure was technically successful with no intra-procedural complications, and the clinical benefit was sustained for a significant duration despite the underlying malignancy progression.\"\n}", "generated_text": "The patient, an 82-year-old male with a two-month history of obstructive jaundice and weight loss, underwent transduodenal photodynamic therapy (TFD) as a palliative intervention for recurrent biliary obstruction. Endoscopic ultrasound (EUS) demonstrated severe dilation of the common bile duct with choledocholithiasis, confirmed by endoscopic retrograde cholangiopancreatography (ERCP), which failed to extract stones due to disproportionate ductal dilation. A plastic biliary stent was placed initially, resulting in transient improvement, but cholestasis recurred at 45 days, with two subsequent ERCP attempts also failing. During the third ERCP, a long, irregular stenosis of the common hepatic duct was identified, and EUS revealed a well-circumscribed hypoechoic solid mass measuring 1.8 × 2 cm compressing the common hepatic duct, with evidence of involvement of the common hepatic artery. Ultrasound-guided needle biopsy confirmed a diagnosis of moderately differentiated cholangiocarcinoma (Bismuth I). Staging determined the tumor to be inoperable, leading to referral for palliative photodynamic therapy (PDT). \n\nThe PDT procedure was performed under general anesthesia using intravenous administration of Photogen® (1.5 mg/kg) 24 hours prior to intervention. Photogen® is a porphyrin derivative with peak light absorption at 630 nm, enabling selective activation within tumor tissue upon illumination. Standard duodenoscopy (Olympus TJF-180) was performed to identify the greater duodenal papilla, followed by retrograde cannulation. A digital cholangioscope (SpyGlass™ DS, Boston Scientific) was then advanced into the common bile duct to directly visualize the stenotic segment. Neoplastic stenosis was identified via cholangioscopic examination. Under direct visualization, the illumination catheter (Medlight S.A., RD10-323) was advanced through the cholangioscope. This catheter is a three-way device: the first port features a 1 cm cylindrical light diffuser with two black radiopaque marks defining its distal limits; the second port accommodates a 0.025-inch guidewire for catheter guidance; the third port serves as an injection port for photosensitizer delivery. The illumination was administered at a power of 70 mW/cm² and a total dose of 90 J/cm², with repositioning performed every centimeter to ensure complete coverage of the obstructed area. The procedure lasted 150 minutes and concluded with a final cholangioscopic evaluation to assess immediate outcomes and detect adverse events. A 10 Fr plastic biliary stent was placed at the end of the session due to unavailability of a self-expanding metal stent. \n\nPost-procedure, the patient was maintained on a fasted state for 24 hours, with oral diet initiated if no adverse events were observed. Strict photoprotection measures were enforced, including avoidance of light exposure and use of sunglasses, particularly during the first week following PDT, to mitigate photosensitivity risk. The patient exhibited no signs of photosensitivity within the first week. However, early recurrence of cholestasis occurred, complicated by cholangitis. ERCP revealed stent obstruction due to biliary sludge and tumor necrotic debris. A biliary scan followed by re-drainage resolved the acute episode. The patient remained asymptomatic for three months, the longest period since disease onset. Subsequent recurrence was managed with a self-expanding metal stent, and systemic oncologic therapy was continued. Eventually, the patient developed dysphagia, requiring placement of a duodenal stent for palliative relief. He ultimately died from complications of pulmonary metastases, two years after symptom onset and 15 months after the TFD session. The procedure was technically successful with no intra-procedural complications, and the clinical benefit was sustained for a significant duration despite the underlying malignancy progression."}
+{"row_index": 14, "doc_id": 29, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 77-year-old woman with a history of hypertension and dyslipidaemia presented to the emergency department with haematemesis and signs of shock (heart rate: 100 beats/min, blood pressure: 79/56 mmHg), along with anaemia (haemoglobin: 9.6 g/dL), suggesting upper gastrointestinal bleeding. Non-contrast-enhanced CT was performed due to renal dysfunction and revealed a steeply flexed third part of the duodenum on the right side of the aorta, running caudally without crossing anterior to the aorta. The duodenal-jejunal junction and jejunum were located in the right hemi-abdomen, with dilation of the second part of the duodenum and the stomach, and high-density gastric contents consistent with a gastric haematoma. Upper gastrointestinal endoscopy demonstrated a mucosal laceration at the gastric cardia, consistent with Mallory-Weiss syndrome, a well-documented condition first described by Mallory and Weiss in 1929, wherein forceful vomiting leads to mucosal tears at the gastroesophageal junction. The anatomical configuration of the duodenum—particularly its steep rightward flexion and luminal narrowing—contributed to proximal obstruction, which likely exacerbated repeated vomiting and thus the development of the laceration.\\n\\nInitial CT findings prompted suspicion of intestinal malrotation, given the right-sided displacement of the duodenal-jejunal junction and jejunum. However, repeat CT performed seven days later showed spontaneous resolution of this rightward deviation, indicating a non-malrotational etiology. The patient was discharged after this transient finding. Subsequently, two months later, she presented with a recurrent episode of haematemesis. Dynamic CT revealed contrast extravasation in the dilated stomach, and again, the third part of the duodenum was flexed on the right side of the aorta, with the duodenal-jejunal junction and jejunum displaced to the right hemi-abdomen. Endoscopy confirmed a recurrent gastric cardial laceration, consistent with Mallory-Weiss syndrome.\\n\\nA follow-up non-contrast CT two months after the second haematemesis revealed no persistent duodenal deviation, but demonstrated oedematous wall thickening in the second part of the duodenum. Without prior imaging, this would have been interpreted as duodenitis; however, the clinical context of repeated, spontaneous right-sided deviations of the duodenal-jejunal junction and jejunum—despite their eventual resolution—led to the diagnosis of dysplasia of the ligament of Treitz. This condition is characterized by an abnormal, redundant, or poorly anchored ligament of Treitz, which normally anchors the duodenojejunal junction to the retroperitoneum and stabilizes the small intestine. In this case, the ligament of Treitz was anatomically formed but exhibited incomplete fixation to the upper jejunum, with attachment limited to the duodenum and absence of retroperitoneal anchoring. This results in a fulcrum-like mechanism allowing the jejunum to fold or deviate freely, particularly during increased intra-abdominal pressure (e.g., from vomiting), thereby reproducing transient right-sided displacement of the duodenum and jejunum.\\n\\nLaparotomy was performed, which confirmed the absence of intestinal malrotation and normal relative positioning between the duodenum and jejunum. The jejunum was anatomically located on the left side of the abdomen. The ligament of Treitz was present and formed, but its fixation to the upper jejunum was incomplete, with only partial attachment to the duodenum and no secure retroperitoneal anchoring. The duodenal-jejunal junction was not fixed to the retroperitoneum, allowing for dynamic mobility. Surgically, the upper jejunum was secured with four sutures to the retroperitoneum on the left side to stabilize the anatomical relationship. The postoperative course was uncomplicated, and the patient has remained asymptomatic with no further episodes of haematemesis. The transient, spontaneous rightward deviations observed on CT imaging are attributable to the mechanical instability of the ligament of Treitz, rather than true malrotation, supporting the diagnosis of dysplasia of the ligament of Treitz as the underlying pathophysiological mechanism.\"\n}", "generated_text": "A 77-year-old woman with a history of hypertension and dyslipidaemia presented to the emergency department with haematemesis and signs of shock (heart rate: 100 beats/min, blood pressure: 79/56 mmHg), along with anaemia (haemoglobin: 9.6 g/dL), suggesting upper gastrointestinal bleeding. Non-contrast-enhanced CT was performed due to renal dysfunction and revealed a steeply flexed third part of the duodenum on the right side of the aorta, running caudally without crossing anterior to the aorta. The duodenal-jejunal junction and jejunum were located in the right hemi-abdomen, with dilation of the second part of the duodenum and the stomach, and high-density gastric contents consistent with a gastric haematoma. Upper gastrointestinal endoscopy demonstrated a mucosal laceration at the gastric cardia, consistent with Mallory-Weiss syndrome, a well-documented condition first described by Mallory and Weiss in 1929, wherein forceful vomiting leads to mucosal tears at the gastroesophageal junction. The anatomical configuration of the duodenum—particularly its steep rightward flexion and luminal narrowing—contributed to proximal obstruction, which likely exacerbated repeated vomiting and thus the development of the laceration.\n\nInitial CT findings prompted suspicion of intestinal malrotation, given the right-sided displacement of the duodenal-jejunal junction and jejunum. However, repeat CT performed seven days later showed spontaneous resolution of this rightward deviation, indicating a non-malrotational etiology. The patient was discharged after this transient finding. Subsequently, two months later, she presented with a recurrent episode of haematemesis. Dynamic CT revealed contrast extravasation in the dilated stomach, and again, the third part of the duodenum was flexed on the right side of the aorta, with the duodenal-jejunal junction and jejunum displaced to the right hemi-abdomen. Endoscopy confirmed a recurrent gastric cardial laceration, consistent with Mallory-Weiss syndrome.\n\nA follow-up non-contrast CT two months after the second haematemesis revealed no persistent duodenal deviation, but demonstrated oedematous wall thickening in the second part of the duodenum. Without prior imaging, this would have been interpreted as duodenitis; however, the clinical context of repeated, spontaneous right-sided deviations of the duodenal-jejunal junction and jejunum—despite their eventual resolution—led to the diagnosis of dysplasia of the ligament of Treitz. This condition is characterized by an abnormal, redundant, or poorly anchored ligament of Treitz, which normally anchors the duodenojejunal junction to the retroperitoneum and stabilizes the small intestine. In this case, the ligament of Treitz was anatomically formed but exhibited incomplete fixation to the upper jejunum, with attachment limited to the duodenum and absence of retroperitoneal anchoring. This results in a fulcrum-like mechanism allowing the jejunum to fold or deviate freely, particularly during increased intra-abdominal pressure (e.g., from vomiting), thereby reproducing transient right-sided displacement of the duodenum and jejunum.\n\nLaparotomy was performed, which confirmed the absence of intestinal malrotation and normal relative positioning between the duodenum and jejunum. The jejunum was anatomically located on the left side of the abdomen. The ligament of Treitz was present and formed, but its fixation to the upper jejunum was incomplete, with only partial attachment to the duodenum and no secure retroperitoneal anchoring. The duodenal-jejunal junction was not fixed to the retroperitoneum, allowing for dynamic mobility. Surgically, the upper jejunum was secured with four sutures to the retroperitoneum on the left side to stabilize the anatomical relationship. The postoperative course was uncomplicated, and the patient has remained asymptomatic with no further episodes of haematemesis. The transient, spontaneous rightward deviations observed on CT imaging are attributable to the mechanical instability of the ligament of Treitz, rather than true malrotation, supporting the diagnosis of dysplasia of the ligament of Treitz as the underlying pathophysiological mechanism."}
+{"row_index": 15, "doc_id": 30, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 28-year-old man from Morocco had pain in his belly, especially on the right side, and had a fever, chills, and lost weight over a month. He didn’t drink or smoke, and had been vaccinated for tuberculosis. His doctor found a swollen liver with small spots on it that looked like signs of infection. Tests showed these spots were likely caused by tuberculosis, not cancer or another disease. A small surgery was done to take a piece of the liver for testing, and the result confirmed it was tuberculosis. He started taking medicine to fight the tuberculosis, and within days, his fever and pain went away. After three months, the spots on his liver got smaller and fewer. He’s getting better.\"\n}", "generated_text": "A 28-year-old man from Morocco had pain in his belly, especially on the right side, and had a fever, chills, and lost weight over a month. He didn’t drink or smoke, and had been vaccinated for tuberculosis. His doctor found a swollen liver with small spots on it that looked like signs of infection. Tests showed these spots were likely caused by tuberculosis, not cancer or another disease. A small surgery was done to take a piece of the liver for testing, and the result confirmed it was tuberculosis. He started taking medicine to fight the tuberculosis, and within days, his fever and pain went away. After three months, the spots on his liver got smaller and fewer. He’s getting better."}
+{"row_index": 16, "doc_id": 30, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 28-year-old Moroccan man with no smoking or drinking habits was admitted to the hospital after experiencing abdominal pain for about a month, along with fever, chills, sweating, loss of appetite, and a 6-kilogram weight loss. The pain was mainly in the upper right part of his abdomen, and he had been experiencing digestive issues like alternating diarrhea and constipation. Initially, his symptoms were mild, but they worsened over time, leading to a significant weight loss of 12 kilograms over three months.\\n\\nPhysical exams showed signs of inflammation, including a high fever and fast heart rate. Blood tests revealed elevated white blood cells and inflammation markers, but no evidence of liver damage or viral hepatitis was found. Imaging scans showed multiple small nodules in the liver that were not enhancing after contrast was given. These nodules were most noticeable in two areas of the liver.\\n\\nAlthough initial tests for tuberculosis (TB) and other infections were negative, the liver biopsies taken during a laparoscopic procedure showed characteristic signs of tuberculosis, including granulomas with caseous necrosis — a hallmark of TB infection. This confirmed a diagnosis of focal liver tuberculosis.\\n\\nThe patient was started on standard anti-tuberculosis medication, which includes four drugs for the first two months, followed by two drugs for the next four months. After starting treatment, his symptoms improved quickly. His fever and inflammation went away, and follow-up scans after three months showed that the liver nodules had shrunk in number and size. The overall clinical and lab results improved significantly, indicating a good response to treatment.\"\n}", "generated_text": "A 28-year-old Moroccan man with no smoking or drinking habits was admitted to the hospital after experiencing abdominal pain for about a month, along with fever, chills, sweating, loss of appetite, and a 6-kilogram weight loss. The pain was mainly in the upper right part of his abdomen, and he had been experiencing digestive issues like alternating diarrhea and constipation. Initially, his symptoms were mild, but they worsened over time, leading to a significant weight loss of 12 kilograms over three months.\n\nPhysical exams showed signs of inflammation, including a high fever and fast heart rate. Blood tests revealed elevated white blood cells and inflammation markers, but no evidence of liver damage or viral hepatitis was found. Imaging scans showed multiple small nodules in the liver that were not enhancing after contrast was given. These nodules were most noticeable in two areas of the liver.\n\nAlthough initial tests for tuberculosis (TB) and other infections were negative, the liver biopsies taken during a laparoscopic procedure showed characteristic signs of tuberculosis, including granulomas with caseous necrosis — a hallmark of TB infection. This confirmed a diagnosis of focal liver tuberculosis.\n\nThe patient was started on standard anti-tuberculosis medication, which includes four drugs for the first two months, followed by two drugs for the next four months. After starting treatment, his symptoms improved quickly. His fever and inflammation went away, and follow-up scans after three months showed that the liver nodules had shrunk in number and size. The overall clinical and lab results improved significantly, indicating a good response to treatment."}
+{"row_index": 17, "doc_id": 30, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 28-year-old male, single, without children, active military personnel, presented with a 5-week history of progressive epigastric and right upper quadrant abdominal pain, accompanied by intermittent fever (peak 39.1°C), chills, profuse night sweats, anorexia, and a 6 kg weight loss. No history of alcohol use, tobacco consumption, or significant comorbidities was reported; he had received BCG vaccination and no positive family or personal history of infectious or hepatic disease. Physical examination revealed an asthenic patient with hepatomegaly and moderate right hypochondrial tenderness, consistent with a systemic inflammatory response syndrome (SIRS): tachycardia (124 bpm), tachypnea (22 breaths/min), and elevated body temperature. Laboratory findings included neutrophilic leukocytosis (17,800 cells/mm³), markedly elevated C-reactive protein (323 mg/L), and a positive procalcitonin level (4.1 ng/L), suggesting a bacterial or infectious etiology. Hepatic function tests were within normal limits: ALT 22 IU/L (normal <40 IU/L), AST 17 IU/L (<35 IU/L), GGT 42 IU/L (<50 IU/L), alkaline phosphatase 115 IU/L (normal 40–150 IU/L), bilirubin normal, prothrombin time 78%, and albumin 39 g/L. Renal function and electrolyte balance were unremarkable. Imaging studies, including chest radiography and abdominal ultrasound, were non-contributory. Blood and urine cultures, performed during febrile peaks, were negative. Serological testing for hepatitis B, C, HIV, and syphilis was negative. Lactate dehydrogenase (231 IU/L) and beta-2 microglobulin (2.28 mg/L) were within normal ranges. GeneXpert testing for Mycobacterium tuberculosis in respiratory specimens and biopsy samples was negative; quantiferon tuberculin test was also negative, excluding latent tuberculosis infection. A thoraco-abdomino-pelvic CT scan revealed an enlarged liver (17 cm), with multiple well-defined, rounded hypodense lesions, non-enhancing after contrast administration, primarily in segments I (21×16 mm) and V (36×27 mm). Echo-guided liver biopsy demonstrated subacute fibro-inflammatory changes with no evidence of malignancy or viral hepatitis. Hepatic MRI further characterized the lesions as dysmorphic, with heterogeneous T2 signal intensity, hyperintense perilesional rims on T2, peripheral enhancement post-contrast, and largest lesions in segments I (20×22 mm) and V (33×31 mm). No deep lymphadenopathy was observed. Diagnostic laparoscopy was performed to obtain biopsy specimens from hepatic nodules, which showed histologically confirmed epithelioid and gigantocellular granulomas with caseous necrosis—pathological findings consistent with focal hepatic tuberculosis. The patient was initiated on standard anti-tuberculous therapy: Phase 1 (2 months) of quadritherapy (isoniazid, rifampicin, pyrazinamide, ethambutol) administered orally in the morning on an empty stomach, followed by Phase 2 (4 months) of bithiapine (isoniazid and rifampicin) with identical dosing regimen. Clinical and biological response was observed within days of therapy initiation, with resolution of fever, chills, and systemic inflammatory markers. At three months post-treatment, follow-up imaging demonstrated a significant reduction in both the number and volume of hepatic lesions, supporting a favorable clinical course. This case represents a rare presentation of focal hepatic tuberculosis in a young, previously healthy individual, with non-specific initial symptoms and imaging findings, underscoring the importance of considering tuberculous hepatopathy in patients with chronic abdominal pain, unexplained weight loss, and persistent low-grade fever despite negative standard infectious workups.\"\n}", "generated_text": "A 28-year-old male, single, without children, active military personnel, presented with a 5-week history of progressive epigastric and right upper quadrant abdominal pain, accompanied by intermittent fever (peak 39.1°C), chills, profuse night sweats, anorexia, and a 6 kg weight loss. No history of alcohol use, tobacco consumption, or significant comorbidities was reported; he had received BCG vaccination and no positive family or personal history of infectious or hepatic disease. Physical examination revealed an asthenic patient with hepatomegaly and moderate right hypochondrial tenderness, consistent with a systemic inflammatory response syndrome (SIRS): tachycardia (124 bpm), tachypnea (22 breaths/min), and elevated body temperature. Laboratory findings included neutrophilic leukocytosis (17,800 cells/mm³), markedly elevated C-reactive protein (323 mg/L), and a positive procalcitonin level (4.1 ng/L), suggesting a bacterial or infectious etiology. Hepatic function tests were within normal limits: ALT 22 IU/L (normal <40 IU/L), AST 17 IU/L (<35 IU/L), GGT 42 IU/L (<50 IU/L), alkaline phosphatase 115 IU/L (normal 40–150 IU/L), bilirubin normal, prothrombin time 78%, and albumin 39 g/L. Renal function and electrolyte balance were unremarkable. Imaging studies, including chest radiography and abdominal ultrasound, were non-contributory. Blood and urine cultures, performed during febrile peaks, were negative. Serological testing for hepatitis B, C, HIV, and syphilis was negative. Lactate dehydrogenase (231 IU/L) and beta-2 microglobulin (2.28 mg/L) were within normal ranges. GeneXpert testing for Mycobacterium tuberculosis in respiratory specimens and biopsy samples was negative; quantiferon tuberculin test was also negative, excluding latent tuberculosis infection. A thoraco-abdomino-pelvic CT scan revealed an enlarged liver (17 cm), with multiple well-defined, rounded hypodense lesions, non-enhancing after contrast administration, primarily in segments I (21×16 mm) and V (36×27 mm). Echo-guided liver biopsy demonstrated subacute fibro-inflammatory changes with no evidence of malignancy or viral hepatitis. Hepatic MRI further characterized the lesions as dysmorphic, with heterogeneous T2 signal intensity, hyperintense perilesional rims on T2, peripheral enhancement post-contrast, and largest lesions in segments I (20×22 mm) and V (33×31 mm). No deep lymphadenopathy was observed. Diagnostic laparoscopy was performed to obtain biopsy specimens from hepatic nodules, which showed histologically confirmed epithelioid and gigantocellular granulomas with caseous necrosis—pathological findings consistent with focal hepatic tuberculosis. The patient was initiated on standard anti-tuberculous therapy: Phase 1 (2 months) of quadritherapy (isoniazid, rifampicin, pyrazinamide, ethambutol) administered orally in the morning on an empty stomach, followed by Phase 2 (4 months) of bithiapine (isoniazid and rifampicin) with identical dosing regimen. Clinical and biological response was observed within days of therapy initiation, with resolution of fever, chills, and systemic inflammatory markers. At three months post-treatment, follow-up imaging demonstrated a significant reduction in both the number and volume of hepatic lesions, supporting a favorable clinical course. This case represents a rare presentation of focal hepatic tuberculosis in a young, previously healthy individual, with non-specific initial symptoms and imaging findings, underscoring the importance of considering tuberculous hepatopathy in patients with chronic abdominal pain, unexplained weight loss, and persistent low-grade fever despite negative standard infectious workups."}
+{"row_index": 18, "doc_id": 31, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 12-year-old boy with Down Syndrome and trouble moving his arms and legs had a sore spot on the inside of his tongue. The sore spot was about 1 cm wide, hard around the edge, and had a white-yellow color. His lips were dry and cracked. He had sharp teeth, especially one tooth on the side of his tongue, which kept rubbing against it and caused the soreness. This soreness looked like a serious mouth cancer, but doctors said it was just from long-term rubbing, not cancer. The doctors treated it with salt water, iodine rinse, and lip cream to heal and protect the area. His mom was told to clean his mouth with salt water, use iodine three times a day on the sore spot, and apply lip cream to keep his lips soft. Some of his teeth were broken or gone, so they were taken out and a device was put in to keep space. The boy got better over time, but later had surgery on his neck due to spine problems. After that, he had breathing trouble and passed away.\"\n}", "generated_text": "A 12-year-old boy with Down Syndrome and trouble moving his arms and legs had a sore spot on the inside of his tongue. The sore spot was about 1 cm wide, hard around the edge, and had a white-yellow color. His lips were dry and cracked. He had sharp teeth, especially one tooth on the side of his tongue, which kept rubbing against it and caused the soreness. This soreness looked like a serious mouth cancer, but doctors said it was just from long-term rubbing, not cancer. The doctors treated it with salt water, iodine rinse, and lip cream to heal and protect the area. His mom was told to clean his mouth with salt water, use iodine three times a day on the sore spot, and apply lip cream to keep his lips soft. Some of his teeth were broken or gone, so they were taken out and a device was put in to keep space. The boy got better over time, but later had surgery on his neck due to spine problems. After that, he had breathing trouble and passed away."}
+{"row_index": 19, "doc_id": 31, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 12-year-old male with Down Syndrome and myeloradiculopathy was referred from the Pediatric Department to the Oral Medicine Department of RS Hasan Sadikin Bandung. The patient's clinical history includes bilateral lower extremity and upper limb weakness, with a prior fall approximately one year prior, leading to hospital admission. His mother reported inconsistent oral hygiene practices, contributing to chronic oral mucosal exposure to trauma and infection. The patient was diagnosed with Down Syndrome, a genetic disorder caused by trisomy 21, and myeloradiculopathy, a neurological condition involving degeneration of spinal nerve roots, likely due to congenital or progressive cervical spinal cord compression.\\n\\nExtraorally, the patient exhibited dysmorphic facial features consistent with Down Syndrome, including a flat facial profile, epicanthal folds, and micrognathia. The vermillion border of the lips demonstrated exfoliative cheilitis, characterized by cracking, desquamation, and desiccation, likely secondary to impaired lip lubrication, reduced mucosal integrity, and altered keratinization. Lymph node assessment was not feasible due to the patient's use of a cervical collar, which restricted neck mobility.\\n\\nIntraorally, a 1×0.7 cm irregular ulcer was observed at the right lateral border of the tongue, with an indurated (hardened) margin and a white-yellowish base. This lesion clinically mimicked oral squamous cell carcinoma (OSCC), a malignant neoplasm of the oral epithelium, due to its well-defined, chronic, non-healing appearance. However, histopathological confirmation was not performed, and the diagnosis of chronic traumatic ulcer was established based on clinical correlation with the patient's occlusal trauma and history of dental malocclusion. The 55 tooth, which was sharp and malpositioned, was identified as the primary source of occlusal trauma, leading to direct mechanical injury to the tongue's lateral border. Additionally, the patient had dentinal caries on tooth 63, reversible pulpitis in 63, and radix gangrene (necrotic root apex) in teeth 55, 62, 74, and 85, indicating advanced dental pathology and potential bacterial invasion.\\n\\nRadiographic and imaging evaluation revealed cervical spine dislocation, confirmed by MRI, which is a known complication in patients with Down Syndrome and myeloradiculopathy, often resulting from developmental anomalies of the cervical vertebrae and ligamentous laxity. This structural abnormality may contribute to neurogenic weakness and impaired motor function. Laboratory findings included hyponatremia (sodium level: 130 mEq/L), likely secondary to impaired renal sodium reabsorption or SIADH (syndrome of inappropriate antidiuretic hormone secretion), and lymphocytosis (lymphocyte percentage: 46%), which may reflect a chronic inflammatory or immune-mediated state.\\n\\nThe patient was managed with a multimodal approach: systemic therapy including paracetamol 120 mg/5 mL oral suspension for pain control and amoxicillin 125 mg/5 mL oral suspension for potential bacterial superinfection; local therapy with 0.9% sodium chloride solution for oral rinsing, 1% povidone-iodine mouthwash applied three times daily for antiseptic and anti-inflammatory effects, and petroleum jelly applied to the lips to address desiccation and promote mucosal hydration. The patient's mother was instructed to perform daily oral care using gauze saturated with 0.9% NaCl, apply povidone-iodine to the ulcer site three times daily, and use petroleum jelly for lip protection.\\n\\nDental management included extraction of teeth 55, 62, 74, and 85 due to extensive root necrosis and irreversible pulpitis, with a space maintainer recommended to preserve arch alignment and prevent malocclusion progression. The diagnosis of the oral lesion was confirmed as a chronic traumatic ulcer, not malignancy, based on clinical features, absence of malignant histopathology, and temporal correlation with occlusal trauma.\\n\\nClinical follow-up showed progressive improvement: at the second visit (3 days post-intervention), the oral lesion showed early signs of healing; at the third visit (1 week), the ulcer size decreased and lip lesions improved; at the fourth visit (10 days), significant ulcer healing was observed. Two days after the fourth visit, the patient underwent neurosurgical intervention to correct the cervical spine dislocation. Postoperative care was provided in the Pediatric Intensive Care Unit (PICU), where the patient developed respiratory failure due to postoperative complications, including possible aspiration, airway compromise, or neurogenic pulmonary edema, and was declared dead two weeks after surgery. This outcome underscores the high morbidity associated with cervical spine instability in pediatric patients with Down Syndrome and associated neurological impair", "generated_text": "{\n  \"proficient_health_literacy\": \"A 12-year-old male with Down Syndrome and myeloradiculopathy was referred from the Pediatric Department to the Oral Medicine Department of RS Hasan Sadikin Bandung. The patient's clinical history includes bilateral lower extremity and upper limb weakness, with a prior fall approximately one year prior, leading to hospital admission. His mother reported inconsistent oral hygiene practices, contributing to chronic oral mucosal exposure to trauma and infection. The patient was diagnosed with Down Syndrome, a genetic disorder caused by trisomy 21, and myeloradiculopathy, a neurological condition involving degeneration of spinal nerve roots, likely due to congenital or progressive cervical spinal cord compression.\\n\\nExtraorally, the patient exhibited dysmorphic facial features consistent with Down Syndrome, including a flat facial profile, epicanthal folds, and micrognathia. The vermillion border of the lips demonstrated exfoliative cheilitis, characterized by cracking, desquamation, and desiccation, likely secondary to impaired lip lubrication, reduced mucosal integrity, and altered keratinization. Lymph node assessment was not feasible due to the patient's use of a cervical collar, which restricted neck mobility.\\n\\nIntraorally, a 1×0.7 cm irregular ulcer was observed at the right lateral border of the tongue, with an indurated (hardened) margin and a white-yellowish base. This lesion clinically mimicked oral squamous cell carcinoma (OSCC), a malignant neoplasm of the oral epithelium, due to its well-defined, chronic, non-healing appearance. However, histopathological confirmation was not performed, and the diagnosis of chronic traumatic ulcer was established based on clinical correlation with the patient's occlusal trauma and history of dental malocclusion. The 55 tooth, which was sharp and malpositioned, was identified as the primary source of occlusal trauma, leading to direct mechanical injury to the tongue's lateral border. Additionally, the patient had dentinal caries on tooth 63, reversible pulpitis in 63, and radix gangrene (necrotic root apex) in teeth 55, 62, 74, and 85, indicating advanced dental pathology and potential bacterial invasion.\\n\\nRadiographic and imaging evaluation revealed cervical spine dislocation, confirmed by MRI, which is a known complication in patients with Down Syndrome and myeloradiculopathy, often resulting from developmental anomalies of the cervical vertebrae and ligamentous laxity. This structural abnormality may contribute to neurogenic weakness and impaired motor function. Laboratory findings included hyponatremia (sodium level: 130 mEq/L), likely secondary to impaired renal sodium reabsorption or SIADH (syndrome of inappropriate antidiuretic hormone secretion), and lymphocytosis (lymphocyte percentage: 46%), which may reflect a chronic inflammatory or immune-mediated state.\\n\\nThe patient was managed with a multimodal approach: systemic therapy including paracetamol 120 mg/5 mL oral suspension for pain control and amoxicillin 125 mg/5 mL oral suspension for potential bacterial superinfection; local therapy with 0.9% sodium chloride solution for oral rinsing, 1% povidone-iodine mouthwash applied three times daily for antiseptic and anti-inflammatory effects, and petroleum jelly applied to the lips to address desiccation and promote mucosal hydration. The patient's mother was instructed to perform daily oral care using gauze saturated with 0.9% NaCl, apply povidone-iodine to the ulcer site three times daily, and use petroleum jelly for lip protection.\\n\\nDental management included extraction of teeth 55, 62, 74, and 85 due to extensive root necrosis and irreversible pulpitis, with a space maintainer recommended to preserve arch alignment and prevent malocclusion progression. The diagnosis of the oral lesion was confirmed as a chronic traumatic ulcer, not malignancy, based on clinical features, absence of malignant histopathology, and temporal correlation with occlusal trauma.\\n\\nClinical follow-up showed progressive improvement: at the second visit (3 days post-intervention), the oral lesion showed early signs of healing; at the third visit (1 week), the ulcer size decreased and lip lesions improved; at the fourth visit (10 days), significant ulcer healing was observed. Two days after the fourth visit, the patient underwent neurosurgical intervention to correct the cervical spine dislocation. Postoperative care was provided in the Pediatric Intensive Care Unit (PICU), where the patient developed respiratory failure due to postoperative complications, including possible aspiration, airway compromise, or neurogenic pulmonary edema, and was declared dead two weeks after surgery. This outcome underscores the high morbidity associated with cervical spine instability in pediatric patients with Down Syndrome and associated neurological impair"}
+{"row_index": 20, "doc_id": 32, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 59-year-old woman had blurry vision in both eyes for a few weeks. She had multiple sclerosis and was taking medicine for seizures, including levetiracetam. Soon after starting levetiracetam, her vision got worse. Doctors found her corneas were swollen, which can happen when eyes get too full of fluid. When they slowly cut back on levetiracetam, her vision started to get better. After stopping the medicine completely, her vision returned to normal and her corneas stopped being swollen. Six months later, the swelling was gone and her eyes looked healthy again. After 13 months, her vision stayed the same and no changes were seen.\"\n}", "generated_text": "A 59-year-old woman had blurry vision in both eyes for a few weeks. She had multiple sclerosis and was taking medicine for seizures, including levetiracetam. Soon after starting levetiracetam, her vision got worse. Doctors found her corneas were swollen, which can happen when eyes get too full of fluid. When they slowly cut back on levetiracetam, her vision started to get better. After stopping the medicine completely, her vision returned to normal and her corneas stopped being swollen. Six months later, the swelling was gone and her eyes looked healthy again. After 13 months, her vision stayed the same and no changes were seen."}
+{"row_index": 21, "doc_id": 32, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 59-year-old woman with secondary progressive multiple sclerosis was referred to ophthalmology because she had been experiencing blurry vision in both eyes for a few weeks. She had been taking levetiracetam, a medication for seizures, a few weeks before the symptoms started. During her eye exam, doctors found swelling in both corneas, a condition called corneal edema, which was confirmed with corneal topography. This swelling was linked to the start of levetiracetam use. After reducing the dose of levetiracetam, her vision began to improve and eventually returned to normal. When the medication was stopped completely, the corneal swelling went away and her vision stabilized. Follow-up tests six months later showed no signs of swelling or vision problems. The doctors made a provisional diagnosis of levetiracetam-induced corneal edema. Her vision has remained stable since then, with no further changes after 13 months.\"\n}", "generated_text": "A 59-year-old woman with secondary progressive multiple sclerosis was referred to ophthalmology because she had been experiencing blurry vision in both eyes for a few weeks. She had been taking levetiracetam, a medication for seizures, a few weeks before the symptoms started. During her eye exam, doctors found swelling in both corneas, a condition called corneal edema, which was confirmed with corneal topography. This swelling was linked to the start of levetiracetam use. After reducing the dose of levetiracetam, her vision began to improve and eventually returned to normal. When the medication was stopped completely, the corneal swelling went away and her vision stabilized. Follow-up tests six months later showed no signs of swelling or vision problems. The doctors made a provisional diagnosis of levetiracetam-induced corneal edema. Her vision has remained stable since then, with no further changes after 13 months."}
+{"row_index": 22, "doc_id": 32, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 59-year-old female with a twelve-year history of secondary progressive multiple sclerosis (SPMS) was referred to ophthalmology with a recent onset of bilateral blurring of vision. She had no prior ophthalmic abnormalities or family history of corneal dystrophies, and previous ocular examinations had been unremarkable for signs of Fuchs' endothelial corneal dystrophy. Her medication history included long-term amantadine therapy (100 mg twice daily for 7 years), which is a known cause of corneal edema due to its effect on corneal endothelial cell function, particularly through inhibition of Na⁺/K⁺-ATPase and disruption of ion homeostasis in the endothelium. She was initiated on levetiracetam (250 mg twice daily) as an adjunctive antiepileptic agent for breakthrough seizure activity. Within weeks of starting levetiracetam, she developed progressive bilateral visual deterioration.\\n\\nOphthalmic examination revealed best-corrected visual acuity of 0.5 logMAR in both eyes. Slit-lamp biomicroscopy demonstrated bilateral corneal edema with normal anterior chamber and absence of uveitis. Intraocular pressures were 16 mmHg (right) and 18 mmHg (left), within normal limits. Corneal topography confirmed significant corneal thickening, with central corneal thicknesses of 936 μm (right) and 1134 μm (left), consistent with epithelial and stromal fluid accumulation due to impaired corneal endothelial pump function.\\n\\nGiven the established association between amantadine and corneal edema, the patient and her neurologist agreed to discontinue amantadine and switch to lamotrigine, with levetiracetam continued at the same dose. No improvement in visual acuity was observed after two months, suggesting that the corneal edema was not solely attributable to amantadine withdrawal. The patient then requested a trial discontinuation of levetiracetam due to the temporal correlation between the initiation of levetiracetam and the onset of visual symptoms.\\n\\nLevetiracetam was tapered over several days, and within a few days of dose reduction, visual symptoms began to improve. Upon complete cessation of levetiracetam, vision stabilized and corneal edema resolved. Follow-up corneal topography six months later demonstrated normalization of central corneal thickness to 567 μm (right) and 573 μm (left), with visual acuity improving to 0.2 logMAR in both eyes. Slit-lamp examination confirmed a clear cornea without corneal guttata, indicating resolution of endothelial dysfunction and fluid accumulation.\\n\\nAt a 13-month follow-up, the patient remained stable on amantadine and lamotrigine, with no further changes in medication or ocular findings. Visual acuity remained at 0.2 logMAR bilaterally, and repeat corneal topography showed no progression of corneal thickening. This case supports the hypothesis that levetiracetam may induce corneal edema via endothelial dysfunction, possibly through interference with endothelial cell metabolism, membrane integrity, or ion transport mechanisms, particularly in the context of preexisting neurodegenerative disease and altered neurovascular coupling. While no direct evidence of levetiracetam’s mechanism in corneal endothelium is established, the temporal association, clinical course, and resolution upon discontinuation strongly suggest a causal relationship. This represents a rare but clinically significant adverse effect of levetiracetam, particularly in patients with underlying neurological conditions involving chronic neuroinflammation or altered cellular homeostasis.\"\n}", "generated_text": "A 59-year-old female with a twelve-year history of secondary progressive multiple sclerosis (SPMS) was referred to ophthalmology with a recent onset of bilateral blurring of vision. She had no prior ophthalmic abnormalities or family history of corneal dystrophies, and previous ocular examinations had been unremarkable for signs of Fuchs' endothelial corneal dystrophy. Her medication history included long-term amantadine therapy (100 mg twice daily for 7 years), which is a known cause of corneal edema due to its effect on corneal endothelial cell function, particularly through inhibition of Na⁺/K⁺-ATPase and disruption of ion homeostasis in the endothelium. She was initiated on levetiracetam (250 mg twice daily) as an adjunctive antiepileptic agent for breakthrough seizure activity. Within weeks of starting levetiracetam, she developed progressive bilateral visual deterioration.\n\nOphthalmic examination revealed best-corrected visual acuity of 0.5 logMAR in both eyes. Slit-lamp biomicroscopy demonstrated bilateral corneal edema with normal anterior chamber and absence of uveitis. Intraocular pressures were 16 mmHg (right) and 18 mmHg (left), within normal limits. Corneal topography confirmed significant corneal thickening, with central corneal thicknesses of 936 μm (right) and 1134 μm (left), consistent with epithelial and stromal fluid accumulation due to impaired corneal endothelial pump function.\n\nGiven the established association between amantadine and corneal edema, the patient and her neurologist agreed to discontinue amantadine and switch to lamotrigine, with levetiracetam continued at the same dose. No improvement in visual acuity was observed after two months, suggesting that the corneal edema was not solely attributable to amantadine withdrawal. The patient then requested a trial discontinuation of levetiracetam due to the temporal correlation between the initiation of levetiracetam and the onset of visual symptoms.\n\nLevetiracetam was tapered over several days, and within a few days of dose reduction, visual symptoms began to improve. Upon complete cessation of levetiracetam, vision stabilized and corneal edema resolved. Follow-up corneal topography six months later demonstrated normalization of central corneal thickness to 567 μm (right) and 573 μm (left), with visual acuity improving to 0.2 logMAR in both eyes. Slit-lamp examination confirmed a clear cornea without corneal guttata, indicating resolution of endothelial dysfunction and fluid accumulation.\n\nAt a 13-month follow-up, the patient remained stable on amantadine and lamotrigine, with no further changes in medication or ocular findings. Visual acuity remained at 0.2 logMAR bilaterally, and repeat corneal topography showed no progression of corneal thickening. This case supports the hypothesis that levetiracetam may induce corneal edema via endothelial dysfunction, possibly through interference with endothelial cell metabolism, membrane integrity, or ion transport mechanisms, particularly in the context of preexisting neurodegenerative disease and altered neurovascular coupling. While no direct evidence of levetiracetam’s mechanism in corneal endothelium is established, the temporal association, clinical course, and resolution upon discontinuation strongly suggest a causal relationship. This represents a rare but clinically significant adverse effect of levetiracetam, particularly in patients with underlying neurological conditions involving chronic neuroinflammation or altered cellular homeostasis."}
+{"row_index": 23, "doc_id": 33, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 77-year-old man had a seizure at home and fell, causing both hips to pop out of place. He was rushed to the hospital, where doctors found broken bones in his pelvis and both femur heads sticking out. His legs were shorter and twisted, and he couldn’t move them well. He was given fluids and blood to stabilize, and a special brace was used to keep the bones in place. After a few days, doctors did surgery in two steps: first on the left hip, then the right hip, seven days apart. In both surgeries, they fixed the broken hip socket with a ring that holds it in place and replaced the ball of the hip with a new joint that lets it move freely. The new parts were not glued in, so they needed time to settle. The patient had no problems after surgery and was able to walk with a walking stick after six weeks. At one year, he could do all normal activities, had no pain or falls, and his hips were working well. He still has a slight limp on the right side, but everything else is fine.\"\n}", "generated_text": "A 77-year-old man had a seizure at home and fell, causing both hips to pop out of place. He was rushed to the hospital, where doctors found broken bones in his pelvis and both femur heads sticking out. His legs were shorter and twisted, and he couldn’t move them well. He was given fluids and blood to stabilize, and a special brace was used to keep the bones in place. After a few days, doctors did surgery in two steps: first on the left hip, then the right hip, seven days apart. In both surgeries, they fixed the broken hip socket with a ring that holds it in place and replaced the ball of the hip with a new joint that lets it move freely. The new parts were not glued in, so they needed time to settle. The patient had no problems after surgery and was able to walk with a walking stick after six weeks. At one year, he could do all normal activities, had no pain or falls, and his hips were working well. He still has a slight limp on the right side, but everything else is fine."}
+{"row_index": 24, "doc_id": 33, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 77-year-old male with a history of moderate cognitive impairment was admitted to the emergency department following a tonic-clonic seizure at home, presenting in a hemodynamically unstable postcritical state with suspected intrapelvic hemorrhage. The activation of a polytrauma protocol was driven by hemodynamic instability, not by the mechanism of injury. The patient was stabilized with intravenous fluid resuscitation and packed red blood cell transfusion. A pelvic binder was applied, and once hemodynamic stability was achieved, a physical examination revealed bilateral lower limb shortening, external rotation, and joint blockage on log roll testing, indicating functional impotence in both hips. No external trauma or bruising was observed; distal pulses were intact, and upper limb mobility was preserved. Initial imaging included anteroposterior pelvic radiography, which revealed bilateral femoral head dislocation. Abdominal-pelvic computed tomography (CT) was performed to assess for intra-abdominal pathology, and a 3D-CT reconstruction confirmed a bilateral transverse acetabular fracture (Letournel classification) and bilateral longitudinal iliac wing fractures, with intrapelvic protrusion of both femoral heads. Supracondylar traction was applied to the femoral heads bilaterally to maintain reduction, and pelvic traction was discontinued. The patient remained in the recovery unit under traction until surgical intervention. Surgical planning was deferred for seven days to allow for fibrovascular consolidation at the fracture sites and to minimize intraoperative bleeding. The procedure was performed in two stages: the left hemipelvis on day 8 and the right hemipelvis on day 15, both under general anesthesia. Tranexamic acid was administered to reduce intraoperative blood loss and transfusion requirements. Cefazolin (2 g preoperatively, 1 g every 8 hours for 24 hours postoperatively) was used as per institutional protocol to prevent surgical site infection. Postoperatively, enoxaparin 40 mg subcutaneously every 24 hours for seven weeks was administered for anticoagulation. The left hemipelvis was operated on first due to greater pelvic protrusion and higher risk of soft tissue hematoma formation during femoral head extraction, which could lead to vascular injury or excessive bleeding. The patient was placed in lateral decubitus position and underwent a posterior-lateral approach with Moore's autograft placement at the acetabular fracture focus. An anti-protrusion ring (Burch Schneider™ Reinforcement Cage, Zimmer Biomet) was implanted, anchored to the ischium and ilium, with medial ischial fixation using screws. Gluteal musculature (gluteus minimus and medius) was dissected to facilitate accurate femoral head positioning. The ring was verified under endoscopic control. A double-mobility cemented acetabular ring was then implanted, followed by a non-cemented femoral stem. Capsular and pelvic musculature closure was achieved using transosseous trochanteric fixation points. The right hemipelvis was operated on seven days later. A first window of the ilio-inguinal approach was utilized to address the longitudinal iliac wing fracture, which was stabilized with a six-hole anatomical plate. The same surgical protocol was repeated: anti-protrusion ring implantation, double-mobility cemented acetabular ring, and non-cemented femoral stem placement. Anti-protrusion rings are indicated in acetabular fractures classified as type IV by the American Academy of Orthopaedic Surgeons (AAOS), where there is disruption of the acetabular background and risk of pelvic disjunction, requiring bony anchorage at the ischium and ilium. They are contraindicated in isolated anterior or posterior wall fractures without acetabular body involvement. The patient remained in bed during admission and was mobilized to prevent pressure ulcer formation. After tolerating the second surgery, he began wheelchair transfers. Full range of motion was permitted in bed without restriction. The patient was discharged at four weeks, with loading initiated only at six weeks using a walking stick. Delayed loading was implemented due to the need for initial graft consolidation in the acetabular background to provide biomechanical support for the anti-protrusion ring, and due to bilateral involvement, which precluded safe partial loading without a stable, healthy hip to serve as a functional baseline. At 12-month follow-up, the patient achieved full weight-bearing with a walking stick, with Harris Hip Score (HHS) of 77 in the right hip and 79 in the left hip, and a WOMAC score of 12. No postoperative complications have been reported. Clinically, the patient is satisfied, reporting occasional discomfort and a mild right-sided limp. Full range of motion is preserved, and no episodes of hip instability have occurred since surgery. The surgical strategy reflects a biomechanically sound approach to managing", "generated_text": "{\n  \"proficient_health_literacy\": \"A 77-year-old male with a history of moderate cognitive impairment was admitted to the emergency department following a tonic-clonic seizure at home, presenting in a hemodynamically unstable postcritical state with suspected intrapelvic hemorrhage. The activation of a polytrauma protocol was driven by hemodynamic instability, not by the mechanism of injury. The patient was stabilized with intravenous fluid resuscitation and packed red blood cell transfusion. A pelvic binder was applied, and once hemodynamic stability was achieved, a physical examination revealed bilateral lower limb shortening, external rotation, and joint blockage on log roll testing, indicating functional impotence in both hips. No external trauma or bruising was observed; distal pulses were intact, and upper limb mobility was preserved. Initial imaging included anteroposterior pelvic radiography, which revealed bilateral femoral head dislocation. Abdominal-pelvic computed tomography (CT) was performed to assess for intra-abdominal pathology, and a 3D-CT reconstruction confirmed a bilateral transverse acetabular fracture (Letournel classification) and bilateral longitudinal iliac wing fractures, with intrapelvic protrusion of both femoral heads. Supracondylar traction was applied to the femoral heads bilaterally to maintain reduction, and pelvic traction was discontinued. The patient remained in the recovery unit under traction until surgical intervention. Surgical planning was deferred for seven days to allow for fibrovascular consolidation at the fracture sites and to minimize intraoperative bleeding. The procedure was performed in two stages: the left hemipelvis on day 8 and the right hemipelvis on day 15, both under general anesthesia. Tranexamic acid was administered to reduce intraoperative blood loss and transfusion requirements. Cefazolin (2 g preoperatively, 1 g every 8 hours for 24 hours postoperatively) was used as per institutional protocol to prevent surgical site infection. Postoperatively, enoxaparin 40 mg subcutaneously every 24 hours for seven weeks was administered for anticoagulation. The left hemipelvis was operated on first due to greater pelvic protrusion and higher risk of soft tissue hematoma formation during femoral head extraction, which could lead to vascular injury or excessive bleeding. The patient was placed in lateral decubitus position and underwent a posterior-lateral approach with Moore's autograft placement at the acetabular fracture focus. An anti-protrusion ring (Burch Schneider™ Reinforcement Cage, Zimmer Biomet) was implanted, anchored to the ischium and ilium, with medial ischial fixation using screws. Gluteal musculature (gluteus minimus and medius) was dissected to facilitate accurate femoral head positioning. The ring was verified under endoscopic control. A double-mobility cemented acetabular ring was then implanted, followed by a non-cemented femoral stem. Capsular and pelvic musculature closure was achieved using transosseous trochanteric fixation points. The right hemipelvis was operated on seven days later. A first window of the ilio-inguinal approach was utilized to address the longitudinal iliac wing fracture, which was stabilized with a six-hole anatomical plate. The same surgical protocol was repeated: anti-protrusion ring implantation, double-mobility cemented acetabular ring, and non-cemented femoral stem placement. Anti-protrusion rings are indicated in acetabular fractures classified as type IV by the American Academy of Orthopaedic Surgeons (AAOS), where there is disruption of the acetabular background and risk of pelvic disjunction, requiring bony anchorage at the ischium and ilium. They are contraindicated in isolated anterior or posterior wall fractures without acetabular body involvement. The patient remained in bed during admission and was mobilized to prevent pressure ulcer formation. After tolerating the second surgery, he began wheelchair transfers. Full range of motion was permitted in bed without restriction. The patient was discharged at four weeks, with loading initiated only at six weeks using a walking stick. Delayed loading was implemented due to the need for initial graft consolidation in the acetabular background to provide biomechanical support for the anti-protrusion ring, and due to bilateral involvement, which precluded safe partial loading without a stable, healthy hip to serve as a functional baseline. At 12-month follow-up, the patient achieved full weight-bearing with a walking stick, with Harris Hip Score (HHS) of 77 in the right hip and 79 in the left hip, and a WOMAC score of 12. No postoperative complications have been reported. Clinically, the patient is satisfied, reporting occasional discomfort and a mild right-sided limp. Full range of motion is preserved, and no episodes of hip instability have occurred since surgery. The surgical strategy reflects a biomechanically sound approach to managing"}
+{"row_index": 25, "doc_id": 34, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 19-month-old boy fell from a highchair and hit his head. He was acting irritable, vomiting, and had trouble breathing. His breathing was fast and his oxygen levels were very low. When doctors checked him, they saw he was struggling to breathe on his left side. They gave him a tube to help him breathe, but his oxygen kept dropping. Tests showed his left lung was completely collapsed, and there was a blockage in the main airway. A scan found a small piece of almond stuck in the airway, about 2 cm big. The boy had never eaten almonds before and probably swallowed it by accident. After the piece was removed, his breathing got better, and he was able to breathe on his own within 24 hours. He was then taken out of the hospital and sent to a regular pediatric ward to recover.\"\n}", "generated_text": "A 19-month-old boy fell from a highchair and hit his head. He was acting irritable, vomiting, and had trouble breathing. His breathing was fast and his oxygen levels were very low. When doctors checked him, they saw he was struggling to breathe on his left side. They gave him a tube to help him breathe, but his oxygen kept dropping. Tests showed his left lung was completely collapsed, and there was a blockage in the main airway. A scan found a small piece of almond stuck in the airway, about 2 cm big. The boy had never eaten almonds before and probably swallowed it by accident. After the piece was removed, his breathing got better, and he was able to breathe on his own within 24 hours. He was then taken out of the hospital and sent to a regular pediatric ward to recover."}
+{"row_index": 26, "doc_id": 34, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 19-month-old male was admitted to the Emergency Department following a fall from a highchair, during which he initially landed on his gluteal region and subsequently experienced a blunt head impact to the occiput. The child presented without prior warning signs or symptoms, and upon arrival, exhibited three episodes of vomiting and marked irritability. Vital signs revealed a respiratory rate exceeding 60 breaths per minute and a heart rate greater than 150 beats per minute, with oxygen saturation falling below 80%. Physical examination demonstrated subcostal retractions and decreased breath sounds localized to the left basal lung zone. The patient was initially managed with non-invasive ventilation using an AMBU bag connected to oxygen, but despite this intervention, oxygen saturation progressively declined below 70%, indicating worsening hypoxemia. The clinical course suggested a severe impairment in gas exchange, prompting the decision for orotracheal intubation with a cuffed endotracheal tube to secure the airway. Post-intubation, the patient's respiratory status stabilized. Chest computed tomography (CT) revealed complete atelectasis of the left lung, with a discrete abrupt interruption of the main left bronchus at a distance of 12 mm from the bronchial bifurcation, consistent with a foreign body obstruction. The clinical presentation, including the acute onset of severe respiratory distress following a minor trauma, and the history of a prior, self-limiting cough episode in the days preceding the event, led to a high clinical suspicion of foreign body aspiration (FBA). Rigid bronchoscopy was performed, which identified a 2 cm diameter almond lodged in the proximal left main bronchus. The foreign body was successfully removed. Notably, the patient had no prior exposure to nuts or almonds, and the ingestion was accidental. Post-removal, the child demonstrated a progressive clinical recovery, with oxygenation improving steadily. After 24 hours of intensive care, the patient was extubated and transferred to the general pediatrics ward, where he achieved full respiratory function recovery over several days. The radiological and bronchoscopic findings, combined with the clinical trajectory, support the diagnosis of acute left main bronchial obstruction due to accidental almond aspiration, with the respiratory failure secondary to impaired ventilation and alveolar collapse, likely exacerbated by the altered state of consciousness induced by head trauma. The mechanism of respiratory compromise involved obstructive atelectasis, leading to reduced lung compliance and ventilation-perfusion mismatch, which were confirmed by lung ultrasound showing absent A lines and solid, consolidated parenchymal patterns. This case underscores the importance of considering foreign body aspiration in pediatric patients presenting with acute respiratory distress, particularly when there is a history of sudden-onset cough or no prior risk factors, even in the absence of overt aspiration signs.\"\n}", "generated_text": "A 19-month-old male was admitted to the Emergency Department following a fall from a highchair, during which he initially landed on his gluteal region and subsequently experienced a blunt head impact to the occiput. The child presented without prior warning signs or symptoms, and upon arrival, exhibited three episodes of vomiting and marked irritability. Vital signs revealed a respiratory rate exceeding 60 breaths per minute and a heart rate greater than 150 beats per minute, with oxygen saturation falling below 80%. Physical examination demonstrated subcostal retractions and decreased breath sounds localized to the left basal lung zone. The patient was initially managed with non-invasive ventilation using an AMBU bag connected to oxygen, but despite this intervention, oxygen saturation progressively declined below 70%, indicating worsening hypoxemia. The clinical course suggested a severe impairment in gas exchange, prompting the decision for orotracheal intubation with a cuffed endotracheal tube to secure the airway. Post-intubation, the patient's respiratory status stabilized. Chest computed tomography (CT) revealed complete atelectasis of the left lung, with a discrete abrupt interruption of the main left bronchus at a distance of 12 mm from the bronchial bifurcation, consistent with a foreign body obstruction. The clinical presentation, including the acute onset of severe respiratory distress following a minor trauma, and the history of a prior, self-limiting cough episode in the days preceding the event, led to a high clinical suspicion of foreign body aspiration (FBA). Rigid bronchoscopy was performed, which identified a 2 cm diameter almond lodged in the proximal left main bronchus. The foreign body was successfully removed. Notably, the patient had no prior exposure to nuts or almonds, and the ingestion was accidental. Post-removal, the child demonstrated a progressive clinical recovery, with oxygenation improving steadily. After 24 hours of intensive care, the patient was extubated and transferred to the general pediatrics ward, where he achieved full respiratory function recovery over several days. The radiological and bronchoscopic findings, combined with the clinical trajectory, support the diagnosis of acute left main bronchial obstruction due to accidental almond aspiration, with the respiratory failure secondary to impaired ventilation and alveolar collapse, likely exacerbated by the altered state of consciousness induced by head trauma. The mechanism of respiratory compromise involved obstructive atelectasis, leading to reduced lung compliance and ventilation-perfusion mismatch, which were confirmed by lung ultrasound showing absent A lines and solid, consolidated parenchymal patterns. This case underscores the importance of considering foreign body aspiration in pediatric patients presenting with acute respiratory distress, particularly when there is a history of sudden-onset cough or no prior risk factors, even in the absence of overt aspiration signs."}
+{"row_index": 27, "doc_id": 35, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 4-month-old male infant from central Mexico presented with a painful, suppurative tumor in the left axillary region. The infant was born to a mother with hypothyroidism during the first trimester of pregnancy, who was receiving pharmacological therapy. The infant had normal birth weight and length, was exclusively breast-fed, and received the BCG vaccine without scarring. The mother resided in a prison cell with the infant and two other individuals, in a crowded environment. At 4 months of age, the infant was evaluated for the axillary mass; a chest X-ray revealed suggestive rib fractures, leading to suspicion of child abuse and hospitalization. Physical examination revealed a weight of 4,190 g (below the third percentile), height of 58 cm, oxygen saturation of 70%, fever, cough, localized swelling, erythema, warmth, and pain in the left axilla. Laboratory findings included hemoglobin of 8.8 g/dL (normal range: 11.0–12.6 g/dL), leukocyte count of 29.3 × 10⁹/L (normal: 6.0–17.5 × 10⁹/L), neutrophil count of 18.4 × 10⁹/L (normal: 1.0–8.5 × 10⁹/L), lymphocyte count of 7.0 × 10⁹/L (normal: 4.0–13.5 × 10⁹/L), monocyte count of 3.5 × 10⁹/L, platelet count of 459 × 10⁹/L (normal: 150–350 × 10⁹/L), and C-reactive protein of 16 mg/L (elevated, normal <3.0 mg/L). A thoracoabdominal tomography demonstrated an axillary abscess, lytic lesions in ribs 3–6, left apical pneumonia, bilateral pulmonary nodules, and enlarged cervical and mediastinal lymph nodes. Histopathological examination of the axillary abscess revealed myositis and suppurative panniculitis. Bacterial culture from bronchoalveolar lavage fluid was negative, and PCR testing for Mycobacterium tuberculosis complex was negative. The infant received a 41-day course of dual antimicrobial therapy (ceftriaxone-clindamycin and cefepime-vancomycin) and was discharged. Two months later, at 8 months of age, the infant was readmitted with fever, irritability, and progression of the suppurative process to the left scapula. Repeat laboratory evaluation showed hemoglobin of 10.8 g/dL, leukocyte count of 21.2 × 10⁹/L, neutrophil count of 12.2 × 10⁹/L, lymphocyte count of 7.5 × 10⁹/L, monocyte count of 1.2 × 10⁹/L, and platelet count of 583 × 10⁹/L. Serum HIV testing was negative. Chest imaging revealed left apical consolidation, bronchiectasis, lytic lesions in ribs 2–7 and dorsal vertebrae 2–7, and a multilocular fluid collection. Ultrasound confirmed a fistula connecting the scapular abscess to the underlying tissue. The infant was initially treated with piperacillin-tazobactam, which was later replaced with voriconazole after isolation of Aspergillus fumigatus from secretion culture. Given the recurrent, severe, and progressive nature of the infections, an innate immune deficiency was suspected. A dihydrorhodamine (DHR) assay demonstrated absent production of reactive oxygen species (ROS) in neutrophils, and flow cytometric analysis revealed absent gp91phox protein expression in neutrophils, confirming a defect in the phagocyte NADPH oxidase complex. Next-generation sequencing identified a pathogenic variant in the CYBB gene, c.80_83del/Y (p.Val27Glyfs*33), resulting in a frameshift mutation and premature termination of the gp91phox protein. The mother was found to be a heterozygous carrier (c.80_83del/WT) of this variant, consistent with X-linked recessive inheritance. The two older male siblings, who appeared clinically healthy, were not subjected to genetic testing. The infant was discharged after 65 days of hospitalization and 28 days of voriconazole therapy, with initiation of daily trimethoprim-sulfamethoxazole prophylaxis and weekly fluconazole for antifungal proph", "generated_text": "{\n  \"proficient_health_literacy\": \"A 4-month-old male infant from central Mexico presented with a painful, suppurative tumor in the left axillary region. The infant was born to a mother with hypothyroidism during the first trimester of pregnancy, who was receiving pharmacological therapy. The infant had normal birth weight and length, was exclusively breast-fed, and received the BCG vaccine without scarring. The mother resided in a prison cell with the infant and two other individuals, in a crowded environment. At 4 months of age, the infant was evaluated for the axillary mass; a chest X-ray revealed suggestive rib fractures, leading to suspicion of child abuse and hospitalization. Physical examination revealed a weight of 4,190 g (below the third percentile), height of 58 cm, oxygen saturation of 70%, fever, cough, localized swelling, erythema, warmth, and pain in the left axilla. Laboratory findings included hemoglobin of 8.8 g/dL (normal range: 11.0–12.6 g/dL), leukocyte count of 29.3 × 10⁹/L (normal: 6.0–17.5 × 10⁹/L), neutrophil count of 18.4 × 10⁹/L (normal: 1.0–8.5 × 10⁹/L), lymphocyte count of 7.0 × 10⁹/L (normal: 4.0–13.5 × 10⁹/L), monocyte count of 3.5 × 10⁹/L, platelet count of 459 × 10⁹/L (normal: 150–350 × 10⁹/L), and C-reactive protein of 16 mg/L (elevated, normal <3.0 mg/L). A thoracoabdominal tomography demonstrated an axillary abscess, lytic lesions in ribs 3–6, left apical pneumonia, bilateral pulmonary nodules, and enlarged cervical and mediastinal lymph nodes. Histopathological examination of the axillary abscess revealed myositis and suppurative panniculitis. Bacterial culture from bronchoalveolar lavage fluid was negative, and PCR testing for Mycobacterium tuberculosis complex was negative. The infant received a 41-day course of dual antimicrobial therapy (ceftriaxone-clindamycin and cefepime-vancomycin) and was discharged. Two months later, at 8 months of age, the infant was readmitted with fever, irritability, and progression of the suppurative process to the left scapula. Repeat laboratory evaluation showed hemoglobin of 10.8 g/dL, leukocyte count of 21.2 × 10⁹/L, neutrophil count of 12.2 × 10⁹/L, lymphocyte count of 7.5 × 10⁹/L, monocyte count of 1.2 × 10⁹/L, and platelet count of 583 × 10⁹/L. Serum HIV testing was negative. Chest imaging revealed left apical consolidation, bronchiectasis, lytic lesions in ribs 2–7 and dorsal vertebrae 2–7, and a multilocular fluid collection. Ultrasound confirmed a fistula connecting the scapular abscess to the underlying tissue. The infant was initially treated with piperacillin-tazobactam, which was later replaced with voriconazole after isolation of Aspergillus fumigatus from secretion culture. Given the recurrent, severe, and progressive nature of the infections, an innate immune deficiency was suspected. A dihydrorhodamine (DHR) assay demonstrated absent production of reactive oxygen species (ROS) in neutrophils, and flow cytometric analysis revealed absent gp91phox protein expression in neutrophils, confirming a defect in the phagocyte NADPH oxidase complex. Next-generation sequencing identified a pathogenic variant in the CYBB gene, c.80_83del/Y (p.Val27Glyfs*33), resulting in a frameshift mutation and premature termination of the gp91phox protein. The mother was found to be a heterozygous carrier (c.80_83del/WT) of this variant, consistent with X-linked recessive inheritance. The two older male siblings, who appeared clinically healthy, were not subjected to genetic testing. The infant was discharged after 65 days of hospitalization and 28 days of voriconazole therapy, with initiation of daily trimethoprim-sulfamethoxazole prophylaxis and weekly fluconazole for antifungal proph"}
+{"row_index": 28, "doc_id": 36, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 25-year-old male patient of Sundanese ethnicity presented to the Department of Oral Medicine at the Dental Hospital of the Faculty of Dentistry, Universitas Padjadjaran, with a chief complaint of painful oral ulcers affecting the upper and lower labial mucosa, exacerbated by eating and speech. The lesions initially appeared as canker sores four days prior to presentation, with subsequent extension to the lips two days later. The patient initially attempted self-treatment with petroleum jelly, which provided no symptomatic relief. He subsequently applied triamcinolone acetonide 0.1% in orabase ointment once daily, which resulted in partial improvement but incomplete healing of the lesions.\\n\\nThe patient reported a preceding one-week history of fever, with no cutaneous or systemic lesions elsewhere. He described a prolonged period of suboptimal nutritional intake—approximately one and a half months—due to high work-related stress. There was no history of medical comorbidities, food allergies, medication use, alcohol consumption, or tobacco use. However, a chronic habit of lip-licking was noted. The patient had a documented history of varicella (chickenpox) in childhood, which is clinically relevant given the role of herpes simplex virus type 1 (HSV-1) in mucocutaneous infections.\\n\\nOn general examination, vital signs were within normal limits, with no lymphadenopathy. Extra-oral examination revealed serosanguineous crusts on the lips that were tender and prone to bleeding. Intra-oral examination demonstrated diffuse, irregular erythematous lesions with well-defined borders on both upper and lower labial mucosa, consistent with mucosal inflammation. Additional findings included hyperkeratotic white plaques with non-scrapable consistency and irregular borders on the left buccal mucosa near tooth 38, yellowish-white, easily scrapable plaques on one-third of the posterior dorsal tongue, and shallow dental impression indentations on the lateral tongue surfaces without pain. A painless, firm nodule measuring 2×1×0.5 cm was identified in the midline of the hard palate. Dental assessment revealed carious lesions, root caries, and edentulous status in teeth 28, 36, 37, and 46, with evidence of reversible pulpitis in tooth 18 and irreversible pulpitis in tooth 47, as well as chronic apical periodontitis due to root caries in tooth 15. Oral hygiene was suboptimal.\\n\\nPsychological evaluation using the DASS-21 scale indicated normal levels of depression (score 0), anxiety (score 6), and stress (score 6), suggesting no significant psychiatric comorbidity. Based on clinical presentation and history, the working diagnosis was suspected to be Herpetic Angina of the Mucosa (HAEM), a condition characterized by recurrent or persistent mucocutaneous ulceration associated with HSV-1 infection. Differential diagnosis considered exfoliative cheilitis, which lacks viral etiology and is typically linked to irritant exposure or chemical dermatitis; however, the presence of HSV-1 seropositivity ruled this out.\\n\\nSerological testing for IgG anti-HSV-1 was performed, yielding a titer of 6.32 (ratio >1.1), confirming prior exposure and active viral involvement. This result, in conjunction with the clinical picture, established a definitive diagnosis of HAEM. The patient’s oral health-related quality of life (OHRQoL) was assessed using the OHIP-14 instrument, with an initial score of 35 (indicating moderate impairment), which improved to 4 (indicating excellent OHRQoL) at the final follow-up.\\n\\nTherapeutic management included both pharmacological and non-pharmacological interventions. Non-pharmacological measures involved patient education on maintaining rigorous oral hygiene—specifically, brushing teeth and tongue twice daily with a soft-bristled brush and non-detergent toothpaste—increasing daily water intake to at least two liters, adopting a balanced nutritional diet, and avoiding acidic, spicy, hard, and monosodium glutamate (MSG)-containing foods. The patient was specifically instructed to discontinue lip-licking and lip-peeling behaviors, which are known to exacerbate mucosal trauma and promote viral replication.\\n\\nPharmacological therapy consisted of topical and systemic agents. Topically, the patient was instructed to apply a thin layer of triamcinolone acetonide 0.1% in orabase three times daily and to compress the lips with gauze soaked in 0.9% NaCl solution at least three times daily to reduce inflammation and promote epithelial healing. Systemically, the patient was prescribed multivitamin supplementation once daily to address potential micronutrient deficiencies, which may contribute to", "generated_text": "{\n  \"proficient_health_literacy\": \"A 25-year-old male patient of Sundanese ethnicity presented to the Department of Oral Medicine at the Dental Hospital of the Faculty of Dentistry, Universitas Padjadjaran, with a chief complaint of painful oral ulcers affecting the upper and lower labial mucosa, exacerbated by eating and speech. The lesions initially appeared as canker sores four days prior to presentation, with subsequent extension to the lips two days later. The patient initially attempted self-treatment with petroleum jelly, which provided no symptomatic relief. He subsequently applied triamcinolone acetonide 0.1% in orabase ointment once daily, which resulted in partial improvement but incomplete healing of the lesions.\\n\\nThe patient reported a preceding one-week history of fever, with no cutaneous or systemic lesions elsewhere. He described a prolonged period of suboptimal nutritional intake—approximately one and a half months—due to high work-related stress. There was no history of medical comorbidities, food allergies, medication use, alcohol consumption, or tobacco use. However, a chronic habit of lip-licking was noted. The patient had a documented history of varicella (chickenpox) in childhood, which is clinically relevant given the role of herpes simplex virus type 1 (HSV-1) in mucocutaneous infections.\\n\\nOn general examination, vital signs were within normal limits, with no lymphadenopathy. Extra-oral examination revealed serosanguineous crusts on the lips that were tender and prone to bleeding. Intra-oral examination demonstrated diffuse, irregular erythematous lesions with well-defined borders on both upper and lower labial mucosa, consistent with mucosal inflammation. Additional findings included hyperkeratotic white plaques with non-scrapable consistency and irregular borders on the left buccal mucosa near tooth 38, yellowish-white, easily scrapable plaques on one-third of the posterior dorsal tongue, and shallow dental impression indentations on the lateral tongue surfaces without pain. A painless, firm nodule measuring 2×1×0.5 cm was identified in the midline of the hard palate. Dental assessment revealed carious lesions, root caries, and edentulous status in teeth 28, 36, 37, and 46, with evidence of reversible pulpitis in tooth 18 and irreversible pulpitis in tooth 47, as well as chronic apical periodontitis due to root caries in tooth 15. Oral hygiene was suboptimal.\\n\\nPsychological evaluation using the DASS-21 scale indicated normal levels of depression (score 0), anxiety (score 6), and stress (score 6), suggesting no significant psychiatric comorbidity. Based on clinical presentation and history, the working diagnosis was suspected to be Herpetic Angina of the Mucosa (HAEM), a condition characterized by recurrent or persistent mucocutaneous ulceration associated with HSV-1 infection. Differential diagnosis considered exfoliative cheilitis, which lacks viral etiology and is typically linked to irritant exposure or chemical dermatitis; however, the presence of HSV-1 seropositivity ruled this out.\\n\\nSerological testing for IgG anti-HSV-1 was performed, yielding a titer of 6.32 (ratio >1.1), confirming prior exposure and active viral involvement. This result, in conjunction with the clinical picture, established a definitive diagnosis of HAEM. The patient’s oral health-related quality of life (OHRQoL) was assessed using the OHIP-14 instrument, with an initial score of 35 (indicating moderate impairment), which improved to 4 (indicating excellent OHRQoL) at the final follow-up.\\n\\nTherapeutic management included both pharmacological and non-pharmacological interventions. Non-pharmacological measures involved patient education on maintaining rigorous oral hygiene—specifically, brushing teeth and tongue twice daily with a soft-bristled brush and non-detergent toothpaste—increasing daily water intake to at least two liters, adopting a balanced nutritional diet, and avoiding acidic, spicy, hard, and monosodium glutamate (MSG)-containing foods. The patient was specifically instructed to discontinue lip-licking and lip-peeling behaviors, which are known to exacerbate mucosal trauma and promote viral replication.\\n\\nPharmacological therapy consisted of topical and systemic agents. Topically, the patient was instructed to apply a thin layer of triamcinolone acetonide 0.1% in orabase three times daily and to compress the lips with gauze soaked in 0.9% NaCl solution at least three times daily to reduce inflammation and promote epithelial healing. Systemically, the patient was prescribed multivitamin supplementation once daily to address potential micronutrient deficiencies, which may contribute to"}
+{"row_index": 29, "doc_id": 37, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 29-year-old woman, Para 1, presented with a one-month history of abnormal vaginal bleeding to the gynecology outpatient department of a level 2 hospital. She was HIV-positive, having been diagnosed approximately one year prior to presentation. Antiretroviral therapy (ART) was initiated following diagnosis, but she defaulted treatment for one month during the onset of vaginal bleeding, resulting in virological failure (viral load: 37,400 copies/mL) and immunological deterioration (CD4 count: 26 cells/μL). The timing of initial HIV symptom onset was not clearly established. Physical examination revealed a large cervical mass measuring 8 × 8 cm, extending into the parametrium and bilateral pelvic sidewalls, with bleeding on contact and foul-smelling vaginal discharge. Ultrasonography demonstrated a bulky cervix and bilateral hydronephrosis, supporting a clinical diagnosis of cervical malignancy at International Federation of Gynecology and Obstetrics (FIGO) stage 3B, defined by pelvic wall involvement and hydronephrosis. A punch cervical biopsy was performed, and histopathological examination confirmed an extra-nodal Burkitt lymphoma (BL). Immunohistochemical staining was positive for CD20, CD75a, CD10, PAX5, and BCL6, with additional positivity for CD44 and c-Myc. In situ hybridization for Epstein-Barr virus (EBER-ISH) showed focal positivity, consistent with EBV-associated BL. The Ki67 proliferation index was nearly 100%, indicating aggressive tumor cell proliferation, with moderate PAX5 and BCL6 expression. Laboratory findings included leukopenia (white cell count: 2.67 × 10⁹/L), anemia (hemoglobin: 5.7 g/dL), thrombocytopenia (platelet count: 71 × 10⁹/L), elevated serum creatinine (187 mmol/L), urea (11.1 mmol/L), and reduced albumin (21 g/L), reflecting significant renal and systemic compromise. Aspartate transaminase (41 U/L) and alkaline phosphatase (100 U/L) were within mild upper limits, suggesting minimal hepatic dysfunction. Following histological confirmation, the patient was reviewed at an oncology multidisciplinary team (MDT) meeting, where chemo-radiation therapy was recommended as the standard of care for stage 3B extra-nodal BL. However, due to a prolonged waiting list at the referral oncology unit, treatment initiation was delayed by 43 days—exceeding the recommended 48-hour window for initiating oncological intervention in Burkitt lymphoma, particularly in immunocompromised individuals. During this period, no further imaging (CT or MRI) was conducted due to technical limitations in available equipment. The patient received supportive care, including blood transfusions and analgesia, but ultimately died in the gynecological ward on day 43 while awaiting treatment. Postmortem histopathology was not performed, as both the BL diagnosis and HIV infection were already established. The primary cause of death remains difficult to attribute definitively due to the presence of multiple comorbidities; however, the attending physician concluded that Burkitt lymphoma was the most likely primary cause, given its rapid progression and high mortality in HIV-positive individuals with high viral loads. The secondary cause of death was multiple organ failure, encompassing both renal and hematological failure, which likely resulted from the combined effects of aggressive lymphoma biology, immunosuppression, and progressive organ dysfunction. This case underscores the critical importance of timely diagnosis and intervention in HIV-positive patients with suspected cervical malignancy, especially in the context of EBV-associated extra-nodal BL, where delays in treatment significantly impact survival outcomes.\"\n}", "generated_text": "A 29-year-old woman, Para 1, presented with a one-month history of abnormal vaginal bleeding to the gynecology outpatient department of a level 2 hospital. She was HIV-positive, having been diagnosed approximately one year prior to presentation. Antiretroviral therapy (ART) was initiated following diagnosis, but she defaulted treatment for one month during the onset of vaginal bleeding, resulting in virological failure (viral load: 37,400 copies/mL) and immunological deterioration (CD4 count: 26 cells/μL). The timing of initial HIV symptom onset was not clearly established. Physical examination revealed a large cervical mass measuring 8 × 8 cm, extending into the parametrium and bilateral pelvic sidewalls, with bleeding on contact and foul-smelling vaginal discharge. Ultrasonography demonstrated a bulky cervix and bilateral hydronephrosis, supporting a clinical diagnosis of cervical malignancy at International Federation of Gynecology and Obstetrics (FIGO) stage 3B, defined by pelvic wall involvement and hydronephrosis. A punch cervical biopsy was performed, and histopathological examination confirmed an extra-nodal Burkitt lymphoma (BL). Immunohistochemical staining was positive for CD20, CD75a, CD10, PAX5, and BCL6, with additional positivity for CD44 and c-Myc. In situ hybridization for Epstein-Barr virus (EBER-ISH) showed focal positivity, consistent with EBV-associated BL. The Ki67 proliferation index was nearly 100%, indicating aggressive tumor cell proliferation, with moderate PAX5 and BCL6 expression. Laboratory findings included leukopenia (white cell count: 2.67 × 10⁹/L), anemia (hemoglobin: 5.7 g/dL), thrombocytopenia (platelet count: 71 × 10⁹/L), elevated serum creatinine (187 mmol/L), urea (11.1 mmol/L), and reduced albumin (21 g/L), reflecting significant renal and systemic compromise. Aspartate transaminase (41 U/L) and alkaline phosphatase (100 U/L) were within mild upper limits, suggesting minimal hepatic dysfunction. Following histological confirmation, the patient was reviewed at an oncology multidisciplinary team (MDT) meeting, where chemo-radiation therapy was recommended as the standard of care for stage 3B extra-nodal BL. However, due to a prolonged waiting list at the referral oncology unit, treatment initiation was delayed by 43 days—exceeding the recommended 48-hour window for initiating oncological intervention in Burkitt lymphoma, particularly in immunocompromised individuals. During this period, no further imaging (CT or MRI) was conducted due to technical limitations in available equipment. The patient received supportive care, including blood transfusions and analgesia, but ultimately died in the gynecological ward on day 43 while awaiting treatment. Postmortem histopathology was not performed, as both the BL diagnosis and HIV infection were already established. The primary cause of death remains difficult to attribute definitively due to the presence of multiple comorbidities; however, the attending physician concluded that Burkitt lymphoma was the most likely primary cause, given its rapid progression and high mortality in HIV-positive individuals with high viral loads. The secondary cause of death was multiple organ failure, encompassing both renal and hematological failure, which likely resulted from the combined effects of aggressive lymphoma biology, immunosuppression, and progressive organ dysfunction. This case underscores the critical importance of timely diagnosis and intervention in HIV-positive patients with suspected cervical malignancy, especially in the context of EBV-associated extra-nodal BL, where delays in treatment significantly impact survival outcomes."}
+{"row_index": 30, "doc_id": 38, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 56-year-old female patient with connective tissue disease-associated pulmonary arterial hypertension (CTD-PAH) was diagnosed in July 2013 with Sjögren’s syndrome complicated by interstitial lung disease (ILD) and pulmonary arterial hypertension (PAH). Initial clinical evaluation revealed dyspnea, productive cough with yellow sputum, and signs of pulmonary vascular congestion on chest X-ray, including interstitial thickening, costophrenic angle blunting, and cardiomegaly. Echocardiography demonstrated a pulmonary artery systolic pressure of 99 mmHg, right atrial and ventricular enlargement, a D-shaped left ventricle, and severe tricuspid regurgitation, consistent with right heart strain. Cardiac catheterization (RHC) in 2017 confirmed a mean pulmonary arterial pressure (PAP) of 39 mmHg, pulmonary vascular resistance (PVR) of approximately 15 Woods, and a wedge pressure of 4 mmHg, classifying the condition as pre-capillary, group I, CTD-related PAH. These findings supported insurance approval for Opsumit (macitentan) 10 mg once daily, which replaced Tracleer (bosentan) in 2017. Treatment with sildenafil (Revatio) 20 mg three times daily and macitentan was initiated and maintained until 2020, during which the patient remained stable with low-to-intermediate risk classification. However, in October 2020, she presented with worsening dyspnea, productive cough with white sputum, and signs of systemic infection. On November 10, 2020, she developed acute severe dyspnea, cold sweats, cyanosis, and hypoxemia (SpO2 = 70%), requiring 100% oxygen via face tent. Arterial blood gas analysis revealed a lactate level of 5.2 mmol/L and brain natriuretic peptide (BNP) exceeding 10,000 pg/mL, indicating cardiogenic shock. She was intubated, admitted to the intensive care unit (ICU), and initiated on four pharmacological agents for PAH management. Her condition stabilized, with successful weaning from vasopressors by November 13, extubation on November 14, and transfer to a general ward on November 21, with oxygen support reduced to nasal cannula at 2 L/min. Follow-up RHC continued to show elevated pulmonary artery pressures, reflecting progressive right ventricular dysfunction due to chronic pulmonary hypertension. Despite stabilization, her 6-minute walk distance progressively declined, and she was reclassified as high-risk. She continues to require frequent hospitalizations for disease control. Physical examination revealed mild rhonchi consistent with ILD and a pansystolic murmur suggestive of severe valvular heart disease. In 2020, Ventavis (iloprost) 10 mcg/ml in 2 ml was added to her regimen. In May 2023, molecular hydrogen therapy was initiated as an adjuvant treatment, consisting of daily administration of 1 capsule of PURE HYDROGEN (HoHo Biotech Co., Ltd., Taipei, Taiwan, ROC). Each capsule contains 170 mg of hydrogen-rich coral calcium with 1.7 × 10²¹ hydrogen molecules, equivalent to 24 cups of water at 1,200 ppb hydrogen or 0.6 mM hydrogen per 200 mL of water. Whole-blood flow cytometry and serological analyses were performed pre- and post-treatment using standard fluorescent dye and antibody reagent kits (Beckman Coulter, Brea, CA, USA), following established immunophenotypic gating protocols. Results demonstrated a significant increase in CD127+ regulatory T cells (Treg), a reduction in anti-Ro autoantibody titers, and a decrease in B cell subsets. These immunological changes correlated with clinical stabilization, including improvement in dyspnea and respiratory function, without any reported adverse events. The study adheres to the CARE (Consolidated Standards of Reporting Trials) 2013 reporting guidelines.\"\n}", "generated_text": "A 56-year-old female patient with connective tissue disease-associated pulmonary arterial hypertension (CTD-PAH) was diagnosed in July 2013 with Sjögren’s syndrome complicated by interstitial lung disease (ILD) and pulmonary arterial hypertension (PAH). Initial clinical evaluation revealed dyspnea, productive cough with yellow sputum, and signs of pulmonary vascular congestion on chest X-ray, including interstitial thickening, costophrenic angle blunting, and cardiomegaly. Echocardiography demonstrated a pulmonary artery systolic pressure of 99 mmHg, right atrial and ventricular enlargement, a D-shaped left ventricle, and severe tricuspid regurgitation, consistent with right heart strain. Cardiac catheterization (RHC) in 2017 confirmed a mean pulmonary arterial pressure (PAP) of 39 mmHg, pulmonary vascular resistance (PVR) of approximately 15 Woods, and a wedge pressure of 4 mmHg, classifying the condition as pre-capillary, group I, CTD-related PAH. These findings supported insurance approval for Opsumit (macitentan) 10 mg once daily, which replaced Tracleer (bosentan) in 2017. Treatment with sildenafil (Revatio) 20 mg three times daily and macitentan was initiated and maintained until 2020, during which the patient remained stable with low-to-intermediate risk classification. However, in October 2020, she presented with worsening dyspnea, productive cough with white sputum, and signs of systemic infection. On November 10, 2020, she developed acute severe dyspnea, cold sweats, cyanosis, and hypoxemia (SpO2 = 70%), requiring 100% oxygen via face tent. Arterial blood gas analysis revealed a lactate level of 5.2 mmol/L and brain natriuretic peptide (BNP) exceeding 10,000 pg/mL, indicating cardiogenic shock. She was intubated, admitted to the intensive care unit (ICU), and initiated on four pharmacological agents for PAH management. Her condition stabilized, with successful weaning from vasopressors by November 13, extubation on November 14, and transfer to a general ward on November 21, with oxygen support reduced to nasal cannula at 2 L/min. Follow-up RHC continued to show elevated pulmonary artery pressures, reflecting progressive right ventricular dysfunction due to chronic pulmonary hypertension. Despite stabilization, her 6-minute walk distance progressively declined, and she was reclassified as high-risk. She continues to require frequent hospitalizations for disease control. Physical examination revealed mild rhonchi consistent with ILD and a pansystolic murmur suggestive of severe valvular heart disease. In 2020, Ventavis (iloprost) 10 mcg/ml in 2 ml was added to her regimen. In May 2023, molecular hydrogen therapy was initiated as an adjuvant treatment, consisting of daily administration of 1 capsule of PURE HYDROGEN (HoHo Biotech Co., Ltd., Taipei, Taiwan, ROC). Each capsule contains 170 mg of hydrogen-rich coral calcium with 1.7 × 10²¹ hydrogen molecules, equivalent to 24 cups of water at 1,200 ppb hydrogen or 0.6 mM hydrogen per 200 mL of water. Whole-blood flow cytometry and serological analyses were performed pre- and post-treatment using standard fluorescent dye and antibody reagent kits (Beckman Coulter, Brea, CA, USA), following established immunophenotypic gating protocols. Results demonstrated a significant increase in CD127+ regulatory T cells (Treg), a reduction in anti-Ro autoantibody titers, and a decrease in B cell subsets. These immunological changes correlated with clinical stabilization, including improvement in dyspnea and respiratory function, without any reported adverse events. The study adheres to the CARE (Consolidated Standards of Reporting Trials) 2013 reporting guidelines."}
+{"row_index": 31, "doc_id": 39, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 45-year-old man came in sick with pneumonia caused by the SARS-CoV-2 virus. He had no history of brain problems before. After 16 days in the hospital, he suddenly became confused and his eyes turned to the right. His face and chest twitched on one side, then he had a full seizure. After that, he had weakness on his left side. Doctors found the SARS-CoV-2 virus in his brain fluid, which means the virus got into his brain. But he slowly got better over time and is now doing well. He doesn’t need medicine for seizures anymore and is back in a regular room. No serious brain damage was found.\"\n}", "generated_text": "A 45-year-old man came in sick with pneumonia caused by the SARS-CoV-2 virus. He had no history of brain problems before. After 16 days in the hospital, he suddenly became confused and his eyes turned to the right. His face and chest twitched on one side, then he had a full seizure. After that, he had weakness on his left side. Doctors found the SARS-CoV-2 virus in his brain fluid, which means the virus got into his brain. But he slowly got better over time and is now doing well. He doesn’t need medicine for seizures anymore and is back in a regular room. No serious brain damage was found."}
+{"row_index": 32, "doc_id": 39, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 45-year-old man was admitted to the hospital with pneumonia caused by SARS-CoV-2, a virus that causes COVID-19. He had no prior neurological problems. For the first few days, he had symptoms like fever, dry cough, shortness of breath, and chest pain. Tests confirmed the pneumonia was due to SARS-CoV-2, and he needed increasing oxygen support as his condition worsened. He was placed in the intensive care unit and given medications including remdesivir, dexamethasone, and antibiotics, which helped reduce inflammation and fight infection.\\n\\nOn the 16th day of hospitalization, he suddenly had a change in consciousness, with his eyes turning to the right and involuntary jerking movements on his left side (face and chest). This was followed by a full seizure. After treatment with midazolam, the seizure stopped. Tests showed no signs of low oxygen, low blood sugar, or other common causes of seizures. A key finding was that the virus SARS-CoV-2 was detected in his cerebrospinal fluid (the fluid around the brain and spinal cord), which suggests the virus may have affected his brain.\\n\\nAfter this event, he remained in a coma-like state for a short time, with no ability to respond to pain or speak, and had weakness on his left side. He was eventually able to wake up and regain some function. His brain scans showed no major damage, and after a few weeks, he was discharged with no need for anti-seizure medication. His overall recovery was favorable, and he continued to improve over time.\"\n}", "generated_text": "A 45-year-old man was admitted to the hospital with pneumonia caused by SARS-CoV-2, a virus that causes COVID-19. He had no prior neurological problems. For the first few days, he had symptoms like fever, dry cough, shortness of breath, and chest pain. Tests confirmed the pneumonia was due to SARS-CoV-2, and he needed increasing oxygen support as his condition worsened. He was placed in the intensive care unit and given medications including remdesivir, dexamethasone, and antibiotics, which helped reduce inflammation and fight infection.\n\nOn the 16th day of hospitalization, he suddenly had a change in consciousness, with his eyes turning to the right and involuntary jerking movements on his left side (face and chest). This was followed by a full seizure. After treatment with midazolam, the seizure stopped. Tests showed no signs of low oxygen, low blood sugar, or other common causes of seizures. A key finding was that the virus SARS-CoV-2 was detected in his cerebrospinal fluid (the fluid around the brain and spinal cord), which suggests the virus may have affected his brain.\n\nAfter this event, he remained in a coma-like state for a short time, with no ability to respond to pain or speak, and had weakness on his left side. He was eventually able to wake up and regain some function. His brain scans showed no major damage, and after a few weeks, he was discharged with no need for anti-seizure medication. His overall recovery was favorable, and he continued to improve over time."}
+{"row_index": 33, "doc_id": 39, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 45-year-old male, born in Pakistan and residing in Portugal for seven years, was admitted to the intensive care unit (ICU) with a diagnosis of SARS-CoV-2-associated pneumonia. He had a history of grade 3 obesity and no significant comorbidities or prior pharmacological therapy. The initial presentation included fever, dry cough, dyspnea, chest pain, dysgeusia, headache, and myalgia, evolving over four days. On admission, neurological examination was unremarkable, with tachypnea and bilateral rough vesicular breath sounds on pulmonary auscultation, consistent with diffuse pulmonary involvement. Laboratory findings revealed elevated inflammatory markers and type 1 respiratory failure under FiO2 of 21%, with extensive bilateral, peripheral, and basal pulmonary opacities on chest radiography. Reverse-transcription real-time polymerase chain reaction (RT-PCR) testing of nasal and oropharyngeal exudates confirmed active SARS-CoV-2 infection, while tests for influenza A/B, Streptococcus pneumoniae, and Legionella pneumophila were negative, supporting a primary viral etiology of pneumonia.\\n\\nOver the first 48 hours, progressive clinical deterioration was observed, including worsening fatigue, dyspnea, and respiratory failure, necessitating escalation of oxygen therapy. Noninvasive ventilation was initiated but discontinued due to poor patient adherence; high-flow nasal cannula oxygen was then applied without clinical benefit. The patient was subsequently transferred to a level III ICU, where he received sedoanalgesia and orotracheal intubation with invasive mechanical ventilation.\\n\\nOn day 11 of hospitalization, treatment with remdesivir, dexamethasone, enoxaparin, and empirical antibiotic therapy (amoxicillin/clavulanic acid and azithromycin) was continued, administered on suspicion of secondary bacterial superinfection. Persistent fever with suboptimal response to antipyretics was noted, though inflammatory markers improved by day 3 of ICU admission. To rule out alternative infectious sources, intravenous lines were changed, and blood cultures, catheter tip cultures, bronchoalveolar lavage, urinalysis, urine culture, and transthoracic echocardiography were performed. Blood culture yielded Klebsiella pneumoniae, which is sensitive to amoxicillin/clavulanic acid—therapy already in use. Echocardiography revealed hypokinesia of the lateral wall and left ventricular apex, with impaired biventricular function, and mild elevation in troponin (1.8 ng/mL) and ST-segment depression in leads I and aVL, consistent with acute coronary syndrome or septic cardiomyopathy. Noninfectious causes of fever, including neuroleptic use and thyroid dysfunction, were excluded.\\n\\nDuring the weaning phase, the patient required inotropic support with dobutamine and continued to need noninvasive ventilation post-extubation, which occurred on day 15. On day 16 (day 19 of symptom onset), the patient experienced a sudden alteration in consciousness, accompanied by conjugate gaze deviation to the right, left-sided myoclonus of the face and thoracic region, and a generalized tonic-clonic seizure, which resolved with midazolam administration. Hypoxic-ischemic encephalopathy was ruled out due to sustained normotension, absence of peri-event hypoxemia or hypoxemia, normal serum lactate, and preserved diuresis. Electrolyte, glucose, and metabolic imbalances were also excluded as etiologies for the seizure.\\n\\nPost-ictal status included a Glasgow Coma Scale (GCS) of 7 (no eye opening, no verbal response, failure to localize to pain), persistent left hemiparesis (grade 3/5), and requirement for airway protection. The patient remained sedated and underwent repeated orotracheal intubation and initiation of anticonvulsant therapy. Cranial computed tomography (CT) showed no acute structural abnormalities. Lumbar puncture revealed turbid cerebrospinal fluid (CSF) with mild proteinorrachia but no pleocytosis and normal opening pressure. CSF analysis included testing for neurotropic viruses, venereal disease research laboratory (VDRL), acid-alcohol resistant bacteria, and RT-PCR for SARS-CoV-2; the latter was positive, confirming the presence of SARS-CoV-2 RNA in the CSF without evidence of bacterial or viral pleocytosis. This finding supported the diagnosis of SARS-CoV-2 encephalitis rather than bacterial meningitis. Electroencephalography (EEG), performed 1 hour after propofol administration under fentanyl, lasted 13 minutes and showed no epileptiform activity.\\n\\nMagnetic resonance imaging (MRI) performed on", "generated_text": "{\n  \"proficient_health_literacy\": \"A 45-year-old male, born in Pakistan and residing in Portugal for seven years, was admitted to the intensive care unit (ICU) with a diagnosis of SARS-CoV-2-associated pneumonia. He had a history of grade 3 obesity and no significant comorbidities or prior pharmacological therapy. The initial presentation included fever, dry cough, dyspnea, chest pain, dysgeusia, headache, and myalgia, evolving over four days. On admission, neurological examination was unremarkable, with tachypnea and bilateral rough vesicular breath sounds on pulmonary auscultation, consistent with diffuse pulmonary involvement. Laboratory findings revealed elevated inflammatory markers and type 1 respiratory failure under FiO2 of 21%, with extensive bilateral, peripheral, and basal pulmonary opacities on chest radiography. Reverse-transcription real-time polymerase chain reaction (RT-PCR) testing of nasal and oropharyngeal exudates confirmed active SARS-CoV-2 infection, while tests for influenza A/B, Streptococcus pneumoniae, and Legionella pneumophila were negative, supporting a primary viral etiology of pneumonia.\\n\\nOver the first 48 hours, progressive clinical deterioration was observed, including worsening fatigue, dyspnea, and respiratory failure, necessitating escalation of oxygen therapy. Noninvasive ventilation was initiated but discontinued due to poor patient adherence; high-flow nasal cannula oxygen was then applied without clinical benefit. The patient was subsequently transferred to a level III ICU, where he received sedoanalgesia and orotracheal intubation with invasive mechanical ventilation.\\n\\nOn day 11 of hospitalization, treatment with remdesivir, dexamethasone, enoxaparin, and empirical antibiotic therapy (amoxicillin/clavulanic acid and azithromycin) was continued, administered on suspicion of secondary bacterial superinfection. Persistent fever with suboptimal response to antipyretics was noted, though inflammatory markers improved by day 3 of ICU admission. To rule out alternative infectious sources, intravenous lines were changed, and blood cultures, catheter tip cultures, bronchoalveolar lavage, urinalysis, urine culture, and transthoracic echocardiography were performed. Blood culture yielded Klebsiella pneumoniae, which is sensitive to amoxicillin/clavulanic acid—therapy already in use. Echocardiography revealed hypokinesia of the lateral wall and left ventricular apex, with impaired biventricular function, and mild elevation in troponin (1.8 ng/mL) and ST-segment depression in leads I and aVL, consistent with acute coronary syndrome or septic cardiomyopathy. Noninfectious causes of fever, including neuroleptic use and thyroid dysfunction, were excluded.\\n\\nDuring the weaning phase, the patient required inotropic support with dobutamine and continued to need noninvasive ventilation post-extubation, which occurred on day 15. On day 16 (day 19 of symptom onset), the patient experienced a sudden alteration in consciousness, accompanied by conjugate gaze deviation to the right, left-sided myoclonus of the face and thoracic region, and a generalized tonic-clonic seizure, which resolved with midazolam administration. Hypoxic-ischemic encephalopathy was ruled out due to sustained normotension, absence of peri-event hypoxemia or hypoxemia, normal serum lactate, and preserved diuresis. Electrolyte, glucose, and metabolic imbalances were also excluded as etiologies for the seizure.\\n\\nPost-ictal status included a Glasgow Coma Scale (GCS) of 7 (no eye opening, no verbal response, failure to localize to pain), persistent left hemiparesis (grade 3/5), and requirement for airway protection. The patient remained sedated and underwent repeated orotracheal intubation and initiation of anticonvulsant therapy. Cranial computed tomography (CT) showed no acute structural abnormalities. Lumbar puncture revealed turbid cerebrospinal fluid (CSF) with mild proteinorrachia but no pleocytosis and normal opening pressure. CSF analysis included testing for neurotropic viruses, venereal disease research laboratory (VDRL), acid-alcohol resistant bacteria, and RT-PCR for SARS-CoV-2; the latter was positive, confirming the presence of SARS-CoV-2 RNA in the CSF without evidence of bacterial or viral pleocytosis. This finding supported the diagnosis of SARS-CoV-2 encephalitis rather than bacterial meningitis. Electroencephalography (EEG), performed 1 hour after propofol administration under fentanyl, lasted 13 minutes and showed no epileptiform activity.\\n\\nMagnetic resonance imaging (MRI) performed on"}
+{"row_index": 34, "doc_id": 40, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"The person had a long-lasting cough, ear pain, and a foul-smelling yellow discharge from one ear. Tests found bacteria that cause tuberculosis in the stomach fluid and in the ear pus. This means they had tuberculosis in both their lungs and middle ear, especially because their immune system was weak from HIV. They were treated with medicine for 6 months to fight the tuberculosis, along with extra medicines to help their body heal. After 6 months, the cough and ear symptoms went away, the bacteria test turned negative, and they felt better. They also started taking HIV medicine again and now have a much lower virus level in their body. The treatment worked and they are fully recovered.\"\n}", "generated_text": "The person had a long-lasting cough, ear pain, and a foul-smelling yellow discharge from one ear. Tests found bacteria that cause tuberculosis in the stomach fluid and in the ear pus. This means they had tuberculosis in both their lungs and middle ear, especially because their immune system was weak from HIV. They were treated with medicine for 6 months to fight the tuberculosis, along with extra medicines to help their body heal. After 6 months, the cough and ear symptoms went away, the bacteria test turned negative, and they felt better. They also started taking HIV medicine again and now have a much lower virus level in their body. The treatment worked and they are fully recovered."}
+{"row_index": 35, "doc_id": 40, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"The patient had a long-lasting cough, ear pain, and a chronic foul-smelling discharge from the right ear. Tests found acid-fast bacteria in both the liquid from the stomach and a swab from the ear pus, which pointed to tuberculosis. The patient also had HIV, which weakened their immune system, making them more susceptible to tuberculosis. Despite initial treatment for malaria and ear infection, the symptoms did not improve. Imaging and exams confirmed tuberculosis in both the ear and the lungs. The patient was treated with a 6-month course of anti-tuberculosis medication, including isoniazid, rifampicin, pyrazinamide, and ethambutol in the first two months, followed by isoniazid and rifampicin for the next four months. They also received treatment for HIV, restarted after adjusting their medication, and were given preventive antibiotics and ear cleaning. After 14 days, their symptoms improved, and the bacteria tests became negative. By the end of treatment, the patient was fully recovered with no signs of infection, and their HIV viral load dropped to a very low level.\"\n}", "generated_text": "The patient had a long-lasting cough, ear pain, and a chronic foul-smelling discharge from the right ear. Tests found acid-fast bacteria in both the liquid from the stomach and a swab from the ear pus, which pointed to tuberculosis. The patient also had HIV, which weakened their immune system, making them more susceptible to tuberculosis. Despite initial treatment for malaria and ear infection, the symptoms did not improve. Imaging and exams confirmed tuberculosis in both the ear and the lungs. The patient was treated with a 6-month course of anti-tuberculosis medication, including isoniazid, rifampicin, pyrazinamide, and ethambutol in the first two months, followed by isoniazid and rifampicin for the next four months. They also received treatment for HIV, restarted after adjusting their medication, and were given preventive antibiotics and ear cleaning. After 14 days, their symptoms improved, and the bacteria tests became negative. By the end of treatment, the patient was fully recovered with no signs of infection, and their HIV viral load dropped to a very low level."}
+{"row_index": 36, "doc_id": 40, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 32-year-old male baker from Bamako, Mali, was admitted to the Infectious and Tropical Diseases Department of CHU du Point G on 27 April 2023 with a chronic productive cough, otalgia, and a persistent right-sided purulent otorrhea of progressive onset over one month. Initial management at a local medical center with artésunate, paracetamol, and unspecified antibiotics for suspected malaria and acute otitis media was ineffective. The patient is HIV-1 positive, diagnosed seven months prior, and was previously on a triple antiretroviral therapy (TARV) regimen of tenofovir/lamivudine/dolutegravir, which was discontinued due to patient non-adherence. Immunological evaluation at diagnosis revealed a CD4 count of 118 cells/μL and a viral load of 12,370 copies/mL; after six months of ART, the CD4 count increased to 193 cells/μL and viral load decreased to 9,460 copies/mL. At the time of tuberculosis diagnosis (at seven months post-HIV diagnosis), CD4 count was 89 cells/μL and viral load was 10,230 copies/mL, indicating ongoing immunosuppression. Otoscopic examination of the right ear demonstrated inflammation of the external auditory canal with purulent discharge and a single tympanic membrane perforation in the anterior-inferior quadrant; the left ear was normal. Rinne and Weber tests confirmed a right conductive hearing loss. Radiographic findings on frontal chest X-ray showed an accentuated bronchovascular network at the base of the right lung, consistent with pulmonary tuberculosis. Ziehl-Neelsen bacilloscopy was positive in both gastric washings (on admission and at 19 days later) and in the right ear swab due to persistent purulent otorrhea, supporting the presence of acid-fast bacilli. The Xpert-MTB/GeneXpert assay was negative for rifampicin resistance, confirming drug-susceptible Mycobacterium tuberculosis. The diagnosis of concurrent middle ear tuberculosis and pulmonary tuberculosis in the context of HIV-associated immunosuppression was established. The patient was initiated on a standard first-line anti-tuberculosis regimen: a 2-month intensive phase of quadritherapy comprising isoniazid, rifampicin, pyrazinamide, and ethambutol (2RHZE), followed by a 4-month continuation phase of isoniazid and rifampicin (4RH) at a dose of three tablets daily in the morning on an empty stomach, supplemented with vitamin B6 (1 tablet/day) to prevent peripheral neuropathy. Concurrently, the patient received two therapeutic intensifications of antiretroviral therapy (ART), with ART restarted on 4 May 2023 following good tolerance of anti-tuberculosis drugs. The ART regimen was re-established with tenofovir/lamivudine/dolutegravir (1 tablet/day) and an additional dolutegravir 50 mg (1 tablet/day) as per standard HIV management protocols. Chemoprophylaxis with cotrimoxazole 960 mg (1 tablet/day) was initiated, and the external auditory canal was cleared via aspiration, followed by instillation of ciprofloxacin ear drops (2 drops, three times daily) for 14 days. Clinical improvement was observed within 14 days of therapy, including resolution of fever, improvement in general condition, and amelioration of cough and otorrhea. Bacilloscopy results became negative in both gastric washings and the right ear pus swab during treatment. At the end of the 6-month anti-tuberculosis regimen, complete clinical healing was achieved, with normal ENT and neurological examinations. Sputum and ear swab bacilloscopy, as well as Xpert-MTB/GeneXpert testing, remained negative at the end of the intensive phase (month 2), at month 5, and at the completion of the maintenance phase (month 6). Post-treatment HIV viral load, assessed three months after ART restart, was 329 copies/mL, indicating effective suppression of viral replication. This case demonstrates the clinical and pathological interplay between HIV-induced immunosuppression, pulmonary and otological tuberculosis, and the successful management through integrated anti-tuberculosis and antiretroviral therapy, with sustained virological and microbiological responses.\"\n}", "generated_text": "A 32-year-old male baker from Bamako, Mali, was admitted to the Infectious and Tropical Diseases Department of CHU du Point G on 27 April 2023 with a chronic productive cough, otalgia, and a persistent right-sided purulent otorrhea of progressive onset over one month. Initial management at a local medical center with artésunate, paracetamol, and unspecified antibiotics for suspected malaria and acute otitis media was ineffective. The patient is HIV-1 positive, diagnosed seven months prior, and was previously on a triple antiretroviral therapy (TARV) regimen of tenofovir/lamivudine/dolutegravir, which was discontinued due to patient non-adherence. Immunological evaluation at diagnosis revealed a CD4 count of 118 cells/μL and a viral load of 12,370 copies/mL; after six months of ART, the CD4 count increased to 193 cells/μL and viral load decreased to 9,460 copies/mL. At the time of tuberculosis diagnosis (at seven months post-HIV diagnosis), CD4 count was 89 cells/μL and viral load was 10,230 copies/mL, indicating ongoing immunosuppression. Otoscopic examination of the right ear demonstrated inflammation of the external auditory canal with purulent discharge and a single tympanic membrane perforation in the anterior-inferior quadrant; the left ear was normal. Rinne and Weber tests confirmed a right conductive hearing loss. Radiographic findings on frontal chest X-ray showed an accentuated bronchovascular network at the base of the right lung, consistent with pulmonary tuberculosis. Ziehl-Neelsen bacilloscopy was positive in both gastric washings (on admission and at 19 days later) and in the right ear swab due to persistent purulent otorrhea, supporting the presence of acid-fast bacilli. The Xpert-MTB/GeneXpert assay was negative for rifampicin resistance, confirming drug-susceptible Mycobacterium tuberculosis. The diagnosis of concurrent middle ear tuberculosis and pulmonary tuberculosis in the context of HIV-associated immunosuppression was established. The patient was initiated on a standard first-line anti-tuberculosis regimen: a 2-month intensive phase of quadritherapy comprising isoniazid, rifampicin, pyrazinamide, and ethambutol (2RHZE), followed by a 4-month continuation phase of isoniazid and rifampicin (4RH) at a dose of three tablets daily in the morning on an empty stomach, supplemented with vitamin B6 (1 tablet/day) to prevent peripheral neuropathy. Concurrently, the patient received two therapeutic intensifications of antiretroviral therapy (ART), with ART restarted on 4 May 2023 following good tolerance of anti-tuberculosis drugs. The ART regimen was re-established with tenofovir/lamivudine/dolutegravir (1 tablet/day) and an additional dolutegravir 50 mg (1 tablet/day) as per standard HIV management protocols. Chemoprophylaxis with cotrimoxazole 960 mg (1 tablet/day) was initiated, and the external auditory canal was cleared via aspiration, followed by instillation of ciprofloxacin ear drops (2 drops, three times daily) for 14 days. Clinical improvement was observed within 14 days of therapy, including resolution of fever, improvement in general condition, and amelioration of cough and otorrhea. Bacilloscopy results became negative in both gastric washings and the right ear pus swab during treatment. At the end of the 6-month anti-tuberculosis regimen, complete clinical healing was achieved, with normal ENT and neurological examinations. Sputum and ear swab bacilloscopy, as well as Xpert-MTB/GeneXpert testing, remained negative at the end of the intensive phase (month 2), at month 5, and at the completion of the maintenance phase (month 6). Post-treatment HIV viral load, assessed three months after ART restart, was 329 copies/mL, indicating effective suppression of viral replication. This case demonstrates the clinical and pathological interplay between HIV-induced immunosuppression, pulmonary and otological tuberculosis, and the successful management through integrated anti-tuberculosis and antiretroviral therapy, with sustained virological and microbiological responses."}
+{"row_index": 37, "doc_id": 41, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 16-month-old boy had a weak heart and was put on a list for a heart transplant. At 20 months, he got a special machine outside his body to help his heart work (called a Berlin Heart). At 23 months, he had a stroke on the left side of his brain, which caused weakness on his right side. Doctors used a small tube to clear the blocked blood vessel and fixed it successfully. The boy was only 10 kg at 23 months, which is small for his age, but he stayed healthy. One month after the stroke, he had a successful heart transplant. The only lasting effect from the stroke was a bit of stiffness in his right arm.\"\n}", "generated_text": "A 16-month-old boy had a weak heart and was put on a list for a heart transplant. At 20 months, he got a special machine outside his body to help his heart work (called a Berlin Heart). At 23 months, he had a stroke on the left side of his brain, which caused weakness on his right side. Doctors used a small tube to clear the blocked blood vessel and fixed it successfully. The boy was only 10 kg at 23 months, which is small for his age, but he stayed healthy. One month after the stroke, he had a successful heart transplant. The only lasting effect from the stroke was a bit of stiffness in his right arm."}
+{"row_index": 38, "doc_id": 41, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 23-month-old male with a history of hypoxic-ischaemic encephalopathy at birth, exhibiting preserved brain motor potential and normal psychomotor development, was managed for restrictive cardiomyopathy. He was enrolled in a cardiac transplant programme at 16 months of age and subsequently required implantation of an external biventricular support device (Berlin Heart) to maintain circulatory function. To mitigate the risk of embolic complications associated with chronic cardiac dysfunction and mechanical support, he received dual antiplatelet and anticoagulant therapy, including full-dose heparin, resulting in an activated partial thromboplastin time (APTT) of 93 seconds and an international normalised ratio (INR) of 1.08. At 23 months of age, he presented with acute neurological deterioration manifesting as disconnection syndrome and right hemiparesis. A non-contrast computed tomography (CT) scan revealed a hyperdense left middle cerebral artery (MCA), consistent with acute thrombosis, and a chronic right parietotemporal infarction, indicating prior ischemic damage. Given the concomitant anticoagulation, intravenous thrombolytic therapy was contraindicated due to hemorrhagic risk. Therefore, an intra-arterial mechanical thrombectomy was performed under general anaesthesia. The procedure involved puncture of the right femoral artery and insertion of an 11 cm long 4F sheath (Cordis, Ireland). A 4F vertebral Radiofocus catheter (Glidecath, Terumo, Belgium) was advanced to confirm occlusion of the M1 segment of the left MCA. Recanalization was achieved using a 3 mm × 20 mm Trevo XP Pro Vue stentriever (Stryker, The Netherlands), guided by the vertebral catheter as a tutor and positioned in the petrous segment of the internal carotid artery. A straight Rapid Transit microcatheter (Codman Neurovascular, UK) was used to navigate and open the occluded vessel in a single pass. The entire catheter system—including tutor catheter, microcatheter, and stentriever—was removed simultaneously. A control run during the procedure identified an iatrogenic dissection of the left internal carotid artery, which was asymptomatic and did not compromise perfusion, as the left hemisphere remained adequately irrigated via the anterior communicant artery. Post-procedure, the patient underwent a successful heart transplantation one month later. Neurologically, the only persistent long-term sequelae were spasticity of the right upper limb, consistent with the initial stroke lesion. The case highlights the feasibility and efficacy of intra-arterial mechanical thrombectomy in a pediatric population with complex comorbidities, including congenital cardiomyopathy and chronic anticoagulation, and underscores the importance of pre-procedural vascular mapping and intra-procedural monitoring in pediatric neurointerventional practice.\"\n}", "generated_text": "A 23-month-old male with a history of hypoxic-ischaemic encephalopathy at birth, exhibiting preserved brain motor potential and normal psychomotor development, was managed for restrictive cardiomyopathy. He was enrolled in a cardiac transplant programme at 16 months of age and subsequently required implantation of an external biventricular support device (Berlin Heart) to maintain circulatory function. To mitigate the risk of embolic complications associated with chronic cardiac dysfunction and mechanical support, he received dual antiplatelet and anticoagulant therapy, including full-dose heparin, resulting in an activated partial thromboplastin time (APTT) of 93 seconds and an international normalised ratio (INR) of 1.08. At 23 months of age, he presented with acute neurological deterioration manifesting as disconnection syndrome and right hemiparesis. A non-contrast computed tomography (CT) scan revealed a hyperdense left middle cerebral artery (MCA), consistent with acute thrombosis, and a chronic right parietotemporal infarction, indicating prior ischemic damage. Given the concomitant anticoagulation, intravenous thrombolytic therapy was contraindicated due to hemorrhagic risk. Therefore, an intra-arterial mechanical thrombectomy was performed under general anaesthesia. The procedure involved puncture of the right femoral artery and insertion of an 11 cm long 4F sheath (Cordis, Ireland). A 4F vertebral Radiofocus catheter (Glidecath, Terumo, Belgium) was advanced to confirm occlusion of the M1 segment of the left MCA. Recanalization was achieved using a 3 mm × 20 mm Trevo XP Pro Vue stentriever (Stryker, The Netherlands), guided by the vertebral catheter as a tutor and positioned in the petrous segment of the internal carotid artery. A straight Rapid Transit microcatheter (Codman Neurovascular, UK) was used to navigate and open the occluded vessel in a single pass. The entire catheter system—including tutor catheter, microcatheter, and stentriever—was removed simultaneously. A control run during the procedure identified an iatrogenic dissection of the left internal carotid artery, which was asymptomatic and did not compromise perfusion, as the left hemisphere remained adequately irrigated via the anterior communicant artery. Post-procedure, the patient underwent a successful heart transplantation one month later. Neurologically, the only persistent long-term sequelae were spasticity of the right upper limb, consistent with the initial stroke lesion. The case highlights the feasibility and efficacy of intra-arterial mechanical thrombectomy in a pediatric population with complex comorbidities, including congenital cardiomyopathy and chronic anticoagulation, and underscores the importance of pre-procedural vascular mapping and intra-procedural monitoring in pediatric neurointerventional practice."}
+{"row_index": 39, "doc_id": 42, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 52-year-old man came to the hospital after having a seizure due to drinking too much alcohol. He also had a shoulder injury on his right side that wasn't caught at the first hospital. When checked, his right shoulder had a dislocation and his left shoulder had a simple dislocation that wasn't seen before. The doctors found that the left shoulder injury got worse during his stay, probably because he was held down too tightly. They did surgery on both shoulders at once to fix the bones. The right shoulder was fixed with screws and strong stitches. The left shoulder needed two extra surgeries — one to fix the broken piece and another to open the joint. Two years later, he can move his shoulders a little, with scores showing he's doing better than most. He can now work again and is moving toward full recovery.\"\n}", "generated_text": "A 52-year-old man came to the hospital after having a seizure due to drinking too much alcohol. He also had a shoulder injury on his right side that wasn't caught at the first hospital. When checked, his right shoulder had a dislocation and his left shoulder had a simple dislocation that wasn't seen before. The doctors found that the left shoulder injury got worse during his stay, probably because he was held down too tightly. They did surgery on both shoulders at once to fix the bones. The right shoulder was fixed with screws and strong stitches. The left shoulder needed two extra surgeries — one to fix the broken piece and another to open the joint. Two years later, he can move his shoulders a little, with scores showing he's doing better than most. He can now work again and is moving toward full recovery."}
+{"row_index": 40, "doc_id": 42, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 52-year-old man was brought to a specialized hospital after having a seizure caused by alcohol withdrawal and a dislocated shoulder on his right side. At first, X-rays showed a right shoulder dislocation and a simple posterior dislocation of his left shoulder — a problem that had not been seen at the previous hospital and took about 48 hours to diagnose. A CT scan later showed that the left shoulder injury had worsened during his hospital stay, likely because of physical restraint. Both shoulders were surgically repaired in one operation using plates and screws to realign and stabilize the bones. The right shoulder had a fragment of bone that was fixed with a screw and strong sutures, while the left shoulder used strong sutures to hold the bone pieces together, since a screw wasn’t needed. After surgery, the patient wore a shoulder immobilizer for four weeks. By the second week, he began gentle exercises to improve movement, but at one month, the left shoulder’s bone alignment started to loosen, so he had a second surgery to fix it with stronger sutures. He then wore the immobilizer for another four weeks and resumed exercises. After 30 sessions of physical therapy, he returned to work five months later. One year after the injury, his right shoulder was doing well, but his left shoulder still had limited motion, especially in rotating outward. A final surgery was done to release the joint and remove the earlier screws in the left shoulder. Two years later, the patient was doing well — he scored 5% on the Quick DASH scale (a measure of shoulder pain and function) and 72 and 76 on the Constant scale (which measures shoulder strength and movement) for his left and right shoulders, respectively. This shows he is making steady progress in recovery.\"\n}", "generated_text": "A 52-year-old man was brought to a specialized hospital after having a seizure caused by alcohol withdrawal and a dislocated shoulder on his right side. At first, X-rays showed a right shoulder dislocation and a simple posterior dislocation of his left shoulder — a problem that had not been seen at the previous hospital and took about 48 hours to diagnose. A CT scan later showed that the left shoulder injury had worsened during his hospital stay, likely because of physical restraint. Both shoulders were surgically repaired in one operation using plates and screws to realign and stabilize the bones. The right shoulder had a fragment of bone that was fixed with a screw and strong sutures, while the left shoulder used strong sutures to hold the bone pieces together, since a screw wasn’t needed. After surgery, the patient wore a shoulder immobilizer for four weeks. By the second week, he began gentle exercises to improve movement, but at one month, the left shoulder’s bone alignment started to loosen, so he had a second surgery to fix it with stronger sutures. He then wore the immobilizer for another four weeks and resumed exercises. After 30 sessions of physical therapy, he returned to work five months later. One year after the injury, his right shoulder was doing well, but his left shoulder still had limited motion, especially in rotating outward. A final surgery was done to release the joint and remove the earlier screws in the left shoulder. Two years later, the patient was doing well — he scored 5% on the Quick DASH scale (a measure of shoulder pain and function) and 72 and 76 on the Constant scale (which measures shoulder strength and movement) for his left and right shoulders, respectively. This shows he is making steady progress in recovery."}
+{"row_index": 41, "doc_id": 42, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 52-year-old male with no significant medical history was transferred to a high-complexity trauma center following a tonic-clonic seizure secondary to alcohol withdrawal and a non-reduced right posterior glenohumeral fracture (LFGHP). Upon initial evaluation 24 hours after admission, the patient was conscious but exhibited bilateral shoulder ecchymosis and severe passive external rotation limitation on both shoulders. He was physically restrained due to intermittent psychomotor agitation, with both feet and his left hand secured. The initial radiographic assessment revealed a right LFGHP and a previously undiagnosed simple posterior glenohumeral dislocation of the left shoulder, which had not been identified at the referring facility and was only diagnosed approximately 48 hours after admission.\\n\\nA computed tomography (CT) scan of both shoulders was performed to assess the extent and evolution of the injuries. The CT demonstrated a significant progression of the left shoulder injury from a simple posterior dislocation on admission radiographs to a full posterior glenohumeral fracture (LFGHP) by the 48-hour mark, likely secondary to the mechanical stress imposed by physical restraint during immobilization. This progression highlights the role of external forces in exacerbating glenohumeral instability in the setting of acute trauma.\\n\\nPreoperative imaging of the right shoulder revealed glenoid bone integrity with 40% involvement of the humeral articular surface, including a large fragment that was anatomically positioned to maintain continuity with the lesser tuberosity. This fragment was planned to be stabilized using a 4.0 mm spongy screw with partial threading and high-strength sutures. In contrast, the left shoulder showed intact glenoid bone and a 20% defect in the humeral articular surface, which was addressed by repositioning and osteosynthesizing the lesser tuberosity fragment—mirroring the surgical technique described in McLaughlin’s protocol for humeral head fracture repair.\\n\\nThe surgical approach involved open reduction and internal fixation (ORIF) with bilateral locked-plate fixation using a Philos (Depuy Synthes®) plate. The patient was positioned in a beach chair position, and both shoulders were accessed via a classic deltopectoral approach. For the right shoulder, a posterior mini-open incision (diagnostic arthroscopy-sized) was used for digital manipulation and reduction of the posterior humeral head fragment. A provisional reduction was achieved using high-strength sutures and needles, followed by definitive fixation with a 4.0 mm spongy screw and high-strength sutures. The final reduction and stability were achieved with the Philos plate, supplemented by fixation of the rotator cuff tendons to the plate using high-strength sutures. The right shoulder was closed in layers and immobilized with a universal shoulder immobilizer.\\n\\nThe left shoulder was operated on immediately after the right. A second deltopectoral approach was performed with an accessory posterior portal for digital reduction of the humeral head. Fixation was accomplished similarly to the right shoulder, except that the spongy screw was not used due to the anterior fragment's inability to achieve adequate stability without high-strength suture fixation alone.\\n\\nPostoperative management included bilateral shoulder immobilization for four weeks. Passive and active pendular flexion-extension exercises of the elbow and finger flexion were initiated from the second postoperative week, progressing according to pain tolerance. At the one-month radiographic follow-up, loss of reduction of the greater tuberosity was observed in the left shoulder, prompting a revision surgery to re-stabilize the fragment with high-strength sutures. The patient was then placed in additional immobilization for four weeks on the left shoulder. Bilateral rehabilitation exercises were resumed from the second postoperative week. At the sixth week post-revision, face-to-face kinesiological therapy was initiated twice weekly. After 30 sessions of structured kinesiological rehabilitation, the patient returned to work five months after the initial injury.\\n\\nOne-year follow-up revealed full recovery of strength and range of motion in the right shoulder, while the left shoulder continued to exhibit significant limitations, particularly in external rotation. At this stage, arthroscopic joint release surgery was performed, with removal of the osteosynthesis hardware in the left shoulder to address chronic joint stiffness and functional impairment. Two years after the initial trauma, the patient demonstrated favorable functional outcomes, with a Quick DASH score of 5%, and Constant scores of 72 and 76 in the left and right shoulders, respectively, indicating substantial recovery and satisfactory functional performance despite persistent limitations in the left shoulder. The case underscores the importance of timely diagnosis, accurate imaging interpretation, and surgical intervention in managing complex glenohumeral fractures, particularly in the context of acute trauma and physical restraint-related injury progression.\"\n}", "generated_text": "A 52-year-old male with no significant medical history was transferred to a high-complexity trauma center following a tonic-clonic seizure secondary to alcohol withdrawal and a non-reduced right posterior glenohumeral fracture (LFGHP). Upon initial evaluation 24 hours after admission, the patient was conscious but exhibited bilateral shoulder ecchymosis and severe passive external rotation limitation on both shoulders. He was physically restrained due to intermittent psychomotor agitation, with both feet and his left hand secured. The initial radiographic assessment revealed a right LFGHP and a previously undiagnosed simple posterior glenohumeral dislocation of the left shoulder, which had not been identified at the referring facility and was only diagnosed approximately 48 hours after admission.\n\nA computed tomography (CT) scan of both shoulders was performed to assess the extent and evolution of the injuries. The CT demonstrated a significant progression of the left shoulder injury from a simple posterior dislocation on admission radiographs to a full posterior glenohumeral fracture (LFGHP) by the 48-hour mark, likely secondary to the mechanical stress imposed by physical restraint during immobilization. This progression highlights the role of external forces in exacerbating glenohumeral instability in the setting of acute trauma.\n\nPreoperative imaging of the right shoulder revealed glenoid bone integrity with 40% involvement of the humeral articular surface, including a large fragment that was anatomically positioned to maintain continuity with the lesser tuberosity. This fragment was planned to be stabilized using a 4.0 mm spongy screw with partial threading and high-strength sutures. In contrast, the left shoulder showed intact glenoid bone and a 20% defect in the humeral articular surface, which was addressed by repositioning and osteosynthesizing the lesser tuberosity fragment—mirroring the surgical technique described in McLaughlin’s protocol for humeral head fracture repair.\n\nThe surgical approach involved open reduction and internal fixation (ORIF) with bilateral locked-plate fixation using a Philos (Depuy Synthes®) plate. The patient was positioned in a beach chair position, and both shoulders were accessed via a classic deltopectoral approach. For the right shoulder, a posterior mini-open incision (diagnostic arthroscopy-sized) was used for digital manipulation and reduction of the posterior humeral head fragment. A provisional reduction was achieved using high-strength sutures and needles, followed by definitive fixation with a 4.0 mm spongy screw and high-strength sutures. The final reduction and stability were achieved with the Philos plate, supplemented by fixation of the rotator cuff tendons to the plate using high-strength sutures. The right shoulder was closed in layers and immobilized with a universal shoulder immobilizer.\n\nThe left shoulder was operated on immediately after the right. A second deltopectoral approach was performed with an accessory posterior portal for digital reduction of the humeral head. Fixation was accomplished similarly to the right shoulder, except that the spongy screw was not used due to the anterior fragment's inability to achieve adequate stability without high-strength suture fixation alone.\n\nPostoperative management included bilateral shoulder immobilization for four weeks. Passive and active pendular flexion-extension exercises of the elbow and finger flexion were initiated from the second postoperative week, progressing according to pain tolerance. At the one-month radiographic follow-up, loss of reduction of the greater tuberosity was observed in the left shoulder, prompting a revision surgery to re-stabilize the fragment with high-strength sutures. The patient was then placed in additional immobilization for four weeks on the left shoulder. Bilateral rehabilitation exercises were resumed from the second postoperative week. At the sixth week post-revision, face-to-face kinesiological therapy was initiated twice weekly. After 30 sessions of structured kinesiological rehabilitation, the patient returned to work five months after the initial injury.\n\nOne-year follow-up revealed full recovery of strength and range of motion in the right shoulder, while the left shoulder continued to exhibit significant limitations, particularly in external rotation. At this stage, arthroscopic joint release surgery was performed, with removal of the osteosynthesis hardware in the left shoulder to address chronic joint stiffness and functional impairment. Two years after the initial trauma, the patient demonstrated favorable functional outcomes, with a Quick DASH score of 5%, and Constant scores of 72 and 76 in the left and right shoulders, respectively, indicating substantial recovery and satisfactory functional performance despite persistent limitations in the left shoulder. The case underscores the importance of timely diagnosis, accurate imaging interpretation, and surgical intervention in managing complex glenohumeral fractures, particularly in the context of acute trauma and physical restraint-related injury progression."}
+{"row_index": 42, "doc_id": 43, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 70-year-old man had a serious heart problem where blood was leaking backward through the aortic valve. Doctors fixed it with a tiny valve placed inside his heart using a catheter (not open surgery) from the top of his heart. After that, his heart started to fail again, so they added a machine to help his heart pump blood. One year later, the machine showed the valve wasn’t working well, and the leak got worse. The doctors decided to fix the old valve by placing a new one inside it, like putting a new door in an old one. They slowed down the heart machine and set the heart to beat 140 times a minute during the procedure. The new valve went in perfectly, and after 12 months, there was no more leak, his heart was strong, and he could walk much farther without trouble. He’s doing great now.\"\n}", "generated_text": "A 70-year-old man had a serious heart problem where blood was leaking backward through the aortic valve. Doctors fixed it with a tiny valve placed inside his heart using a catheter (not open surgery) from the top of his heart. After that, his heart started to fail again, so they added a machine to help his heart pump blood. One year later, the machine showed the valve wasn’t working well, and the leak got worse. The doctors decided to fix the old valve by placing a new one inside it, like putting a new door in an old one. They slowed down the heart machine and set the heart to beat 140 times a minute during the procedure. The new valve went in perfectly, and after 12 months, there was no more leak, his heart was strong, and he could walk much farther without trouble. He’s doing great now."}
+{"row_index": 43, "doc_id": 43, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 70-year-old man with severe heart valve problems was treated with a procedure called transcatheter aortic valve implantation (TAVI) from the apex of his heart. He had a history of heart infection that had healed, and his heart was very weak, with only 20% of its normal pumping ability. Because of his poor heart function and other health issues, surgery was too risky, so TAVI was chosen instead. After the first procedure, his heart improved, but he had a relapse of symptoms four weeks later due to continued weakness. As a result, he received a left ventricular assist device (LVAD), which helps the heart pump blood. He stayed symptom-free for a year, but the LVAD started giving warning signs of high flow, and tests showed worsening leakage through the aortic valve, even though the original valve appeared structurally normal. After careful discussion with his medical team, they decided to perform a second valve procedure — a 'valve-in-valve' approach — where a new valve was placed inside the existing one. This was done while reducing the LVAD flow to the lowest level and using a pacemaker to keep his heart beating at 140 beats per minute during the procedure. The new valve was placed carefully using imaging guidance to avoid damaging the original valve. The procedure was successful, and at 12 months follow-up, the patient had no significant leakage from the aortic valve, his heart function improved to 33%, and he could walk much farther without shortness of breath. He is now doing well and living a normal life.\"\n}", "generated_text": "A 70-year-old man with severe heart valve problems was treated with a procedure called transcatheter aortic valve implantation (TAVI) from the apex of his heart. He had a history of heart infection that had healed, and his heart was very weak, with only 20% of its normal pumping ability. Because of his poor heart function and other health issues, surgery was too risky, so TAVI was chosen instead. After the first procedure, his heart improved, but he had a relapse of symptoms four weeks later due to continued weakness. As a result, he received a left ventricular assist device (LVAD), which helps the heart pump blood. He stayed symptom-free for a year, but the LVAD started giving warning signs of high flow, and tests showed worsening leakage through the aortic valve, even though the original valve appeared structurally normal. After careful discussion with his medical team, they decided to perform a second valve procedure — a 'valve-in-valve' approach — where a new valve was placed inside the existing one. This was done while reducing the LVAD flow to the lowest level and using a pacemaker to keep his heart beating at 140 beats per minute during the procedure. The new valve was placed carefully using imaging guidance to avoid damaging the original valve. The procedure was successful, and at 12 months follow-up, the patient had no significant leakage from the aortic valve, his heart function improved to 33%, and he could walk much farther without shortness of breath. He is now doing well and living a normal life."}
+{"row_index": 44, "doc_id": 43, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 70-year-old white male with severe symptomatic aortic regurgitation secondary to healed infective endocarditis was managed with transcatheter aortic valve implantation (TAVI) via an apical approach. The procedure was indicated due to his high surgical risk, assessed using a logistic EuroSCORE I of 24.36%, compounded by secondary pulmonary hypertension, severely impaired left ventricular function (left ventricular ejection fraction [LVEF] of 20%), chronic renal insufficiency (serum creatinine 2.1 mg/dL), and comorbidities including chronic kidney disease and systemic hypertension. Pre-TAVI medical therapy included torasemide 20 mg daily, ramipril 5 mg daily, bisoprolol 2.5 mg twice daily, and spironolactone 12.5 mg daily. On admission, the patient presented with cardiac decompensation and dyspnea (temperature 36.7 °C, pulse 99/min, blood pressure 109/48 mmHg), with no evidence of active infection (normal C-reactive protein and leukocyte count), and no microbiological workup performed. Laboratory findings revealed mild hepatocellular dysfunction (aspartate aminotransferase 59 U/L, alanine aminotransferase 67 U/L) and mild anemia (hemoglobin 10.7 g/dL), with no urine analysis conducted. Coronary angiography, performed prior to TAVI, was normal, supporting the exclusion of coronary artery disease as a contributing factor.\\n\\nThe initial TAVI was performed with a JenaValve 27 mm self-expandable bioprosthesis. Post-procedural imaging demonstrated minimal transvalvular central insufficiency and stable hemodynamics, indicating initial procedural success. However, despite this, the patient experienced recurrent cardiac decompensation due to persistent left ventricular dysfunction, leading to a repeat interdisciplinary evaluation. Four weeks after the initial TAVI, the patient underwent implantation of a left ventricular assist device (LVAD) system (Thoratec® HeartMate II) to support ventricular function. The postoperative course was uneventful, and the patient remained asymptomatic for one year.\\n\\nDuring this period, the LVAD system generated recurrent high-flow alarms, prompting further evaluation. Serial echocardiographic assessments revealed a progressive worsening of transvalvular central aortic insufficiency to a severe level, with no evidence of structural leaflet damage or prosthetic thrombosis in the JenaValve. This suggested a functional impairment of the aortic outflow due to hemodynamic alterations, likely related to the high flow dynamics generated by the LVAD and the inherent geometry of the existing prosthesis. Given the persistent regurgitation and lack of improvement in ventricular function, a valve-in-valve strategy was adopted.\\n\\nThe subsequent TAVI procedure was performed under general anesthesia using a CoreValve Evolut R 29 mm self-expanding valve, without prior valvuloplasty. Hemodynamic management during implantation included reduction of LVAD flow to minimum and maintenance of cardiac pacing at 140 beats per minute to optimize ventricular filling and reduce flow-induced turbulence. Positioning was guided by real-time fluoroscopy and transesophageal echocardiography (TEE), with specific attention to placing the ventricular strut end of the CoreValve Evolut R between the ventricular end and the 'cusp feelers' of the existing JenaValve prosthesis. This positioning was informed by individualized CT imaging, which confirmed optimal alignment of the JenaValve's ventricular edge within the left ventricular outflow tract (LVOT). The initial positioning was successful without repositioning, and the valve was released in the planned anatomical position after final fluoroscopic confirmation. Post-implantation, rapid pacing was discontinued, and LVAD flow was gradually increased to ensure adequate hemodynamic stability.\\n\\nThe postoperative course was uneventful, and follow-up TEE at 12 months demonstrated no significant aortic regurgitation, with only marginal residual insufficiency. The patient reported no symptoms and demonstrated significant functional improvement, with a 6-minute walk distance increasing from 148 meters on admission to 381 meters at 12-month follow-up. Echocardiography also revealed an improvement in left ventricular function, with LVEF rising to 33%. This case illustrates the complex interplay between prosthetic valve dynamics, LVAD-induced hemodynamics, and the risk of transvalvular regurgitation in patients with pre-existing severe aortic regurgitation and severely compromised left ventricular function. The valve-in-valve approach, when carefully planned with precise positioning and optimized hemodynamic support, can", "generated_text": "{\n  \"proficient_health_literacy\": \"A 70-year-old white male with severe symptomatic aortic regurgitation secondary to healed infective endocarditis was managed with transcatheter aortic valve implantation (TAVI) via an apical approach. The procedure was indicated due to his high surgical risk, assessed using a logistic EuroSCORE I of 24.36%, compounded by secondary pulmonary hypertension, severely impaired left ventricular function (left ventricular ejection fraction [LVEF] of 20%), chronic renal insufficiency (serum creatinine 2.1 mg/dL), and comorbidities including chronic kidney disease and systemic hypertension. Pre-TAVI medical therapy included torasemide 20 mg daily, ramipril 5 mg daily, bisoprolol 2.5 mg twice daily, and spironolactone 12.5 mg daily. On admission, the patient presented with cardiac decompensation and dyspnea (temperature 36.7 °C, pulse 99/min, blood pressure 109/48 mmHg), with no evidence of active infection (normal C-reactive protein and leukocyte count), and no microbiological workup performed. Laboratory findings revealed mild hepatocellular dysfunction (aspartate aminotransferase 59 U/L, alanine aminotransferase 67 U/L) and mild anemia (hemoglobin 10.7 g/dL), with no urine analysis conducted. Coronary angiography, performed prior to TAVI, was normal, supporting the exclusion of coronary artery disease as a contributing factor.\\n\\nThe initial TAVI was performed with a JenaValve 27 mm self-expandable bioprosthesis. Post-procedural imaging demonstrated minimal transvalvular central insufficiency and stable hemodynamics, indicating initial procedural success. However, despite this, the patient experienced recurrent cardiac decompensation due to persistent left ventricular dysfunction, leading to a repeat interdisciplinary evaluation. Four weeks after the initial TAVI, the patient underwent implantation of a left ventricular assist device (LVAD) system (Thoratec® HeartMate II) to support ventricular function. The postoperative course was uneventful, and the patient remained asymptomatic for one year.\\n\\nDuring this period, the LVAD system generated recurrent high-flow alarms, prompting further evaluation. Serial echocardiographic assessments revealed a progressive worsening of transvalvular central aortic insufficiency to a severe level, with no evidence of structural leaflet damage or prosthetic thrombosis in the JenaValve. This suggested a functional impairment of the aortic outflow due to hemodynamic alterations, likely related to the high flow dynamics generated by the LVAD and the inherent geometry of the existing prosthesis. Given the persistent regurgitation and lack of improvement in ventricular function, a valve-in-valve strategy was adopted.\\n\\nThe subsequent TAVI procedure was performed under general anesthesia using a CoreValve Evolut R 29 mm self-expanding valve, without prior valvuloplasty. Hemodynamic management during implantation included reduction of LVAD flow to minimum and maintenance of cardiac pacing at 140 beats per minute to optimize ventricular filling and reduce flow-induced turbulence. Positioning was guided by real-time fluoroscopy and transesophageal echocardiography (TEE), with specific attention to placing the ventricular strut end of the CoreValve Evolut R between the ventricular end and the 'cusp feelers' of the existing JenaValve prosthesis. This positioning was informed by individualized CT imaging, which confirmed optimal alignment of the JenaValve's ventricular edge within the left ventricular outflow tract (LVOT). The initial positioning was successful without repositioning, and the valve was released in the planned anatomical position after final fluoroscopic confirmation. Post-implantation, rapid pacing was discontinued, and LVAD flow was gradually increased to ensure adequate hemodynamic stability.\\n\\nThe postoperative course was uneventful, and follow-up TEE at 12 months demonstrated no significant aortic regurgitation, with only marginal residual insufficiency. The patient reported no symptoms and demonstrated significant functional improvement, with a 6-minute walk distance increasing from 148 meters on admission to 381 meters at 12-month follow-up. Echocardiography also revealed an improvement in left ventricular function, with LVEF rising to 33%. This case illustrates the complex interplay between prosthetic valve dynamics, LVAD-induced hemodynamics, and the risk of transvalvular regurgitation in patients with pre-existing severe aortic regurgitation and severely compromised left ventricular function. The valve-in-valve approach, when carefully planned with precise positioning and optimized hemodynamic support, can"}
+{"row_index": 45, "doc_id": 44, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 12-year-old boy came in with sudden headaches and drinking a lot of water, urinating a lot. Doctors found he had a small cyst in his brain that had burst, but it wasn’t pressing on any parts of his brain or causing serious problems. His hormones were mostly normal, except for a small problem with water balance, which got better with medicine. No surgery was needed because the cyst stayed the same size and didn’t get worse over three years. He grew up normally, started puberty on time, and had no vision issues. But his growth slowed down a bit, so doctors tested him and found he had a little missing growth hormone. After starting treatment, his growth sped up. The cyst stayed stable and didn’t get bigger or smaller much over time.\"\n}", "generated_text": "A 12-year-old boy came in with sudden headaches and drinking a lot of water, urinating a lot. Doctors found he had a small cyst in his brain that had burst, but it wasn’t pressing on any parts of his brain or causing serious problems. His hormones were mostly normal, except for a small problem with water balance, which got better with medicine. No surgery was needed because the cyst stayed the same size and didn’t get worse over three years. He grew up normally, started puberty on time, and had no vision issues. But his growth slowed down a bit, so doctors tested him and found he had a little missing growth hormone. After starting treatment, his growth sped up. The cyst stayed stable and didn’t get bigger or smaller much over time."}
+{"row_index": 46, "doc_id": 44, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 12-year-old male presented with acute onset of headache and polyuria-polydipsia, which began one week prior to evaluation. He had no significant past medical history. Physical examination revealed a height of 146.5 cm (−1.4 SD) and weight of 30 kg. No signs of adrenal insufficiency or hypothyroidism were observed. He was at the early stages of puberty, with bilateral gonadal volumes of 3.2 cm and penile length of 6.2 cm (male standard). The polyuria-polydipsia was severe, with urinary fluid excretion reaching up to 113 ml/kg/day, nocturnal enuresis, and excessive fluid intake of 3.8 liters/m². Ophthalmologic assessment, including optical coherence tomography (OCT), showed normal visual function and retinal structure, with no evidence of optic nerve or retinal pathology.\\n\\nEndocrine evaluation revealed diabetes insipidus (DI), characterized by a serum sodium of 140 mEq/L, plasma osmolality of 287 mosm/kg, and urine osmolality of 179 mosm/kg—indicating a profound inability to concentrate urine. All other endocrine markers, including insulin-like growth factor-1 (IGF-1), prolactin (PRL), free T4, cortisol, follicle-stimulating hormone (FSH), and luteinizing hormone (LH), were within normal reference ranges, suggesting intact hypothalamic-pituitary axis function except for the specific deficiency of antidiuretic hormone (ADH) action.\\n\\nMagnetic resonance imaging (MRI) with and without contrast demonstrated apoplexy of a Rathke cleft cyst (RCC), showing spontaneous hyperintensity on both T1 and T2-weighted sequences with dimensions of 15 × 6 × 11 mm. The anterior pituitary exhibited homogeneous contrast enhancement, consistent with normal vascularization and structural integrity. Notably, the posterior pituitary showed loss of typical hyperintensity on T2 sequences, which is a key radiological finding in RCC apoplexy and suggests hemorrhage or disruption of neurohypophyseal tissue. No evidence of craniopharyngioma or other structural lesions was identified. The RCC apoplexy remained stable over a nine-month follow-up period, with size reduction to 12 × 11 × 10 mm, and subsequent imaging at 2 and 3 years revealed progressive stabilization, ultimately measuring 7 × 10 × 6 mm, indicating a non-progressive, possibly self-limiting hemorrhagic event.\\n\\nA multidisciplinary team comprising an endocrinologist, neurosurgeon, and radiologist reviewed the case. Given the absence of compressive neurologic symptoms, normal neuroimaging progression, and stable hormonal profiles (excluding DI), a conservative management strategy was adopted, involving regular clinical, biochemical, and radiological monitoring. Over a three-year follow-up, the patient achieved normal pubertal development without significant endocrine deficiencies, except for a partial growth hormone (GH) deficiency, which emerged later as a secondary finding.\\n\\nGrowth velocity declined from −0.8 SD to −1.1 SD, prompting further investigation. At age 14 years and 9 months, two GH stimulation tests—propranolol-glucagon test and insulin tolerance test—were performed, yielding GH peak values of 19.3 µUI/ml and 10.0 µUI/ml, respectively, both below the threshold for normal pubertal growth, confirming a partial GH deficiency. Following initiation of recombinant human growth hormone (rhGH) therapy, growth velocity improved significantly, increasing from −1.1 SD to +0.2 SD over one year, indicating effective hormonal replacement.\\n\\nRadiological follow-up was conducted at a single center with consistent interpretation by the same radiologist, ensuring longitudinal reliability and minimizing inter-observer variability. The stability of the RCC apoplexy over time, coupled with the absence of expansion or mass effect, supports the conclusion that the lesion is benign and non-encroaching, with no indication for surgical intervention. The case underscores the importance of long-term monitoring in pediatric patients with RCC apoplexy, particularly when initial endocrine and neurologic findings are non-compressive and within normal limits, and highlights the potential for delayed emergence of secondary endocrine deficiencies, such as partial GH deficiency, despite otherwise normal early puberty and hormonal function.\"\n}", "generated_text": "A 12-year-old male presented with acute onset of headache and polyuria-polydipsia, which began one week prior to evaluation. He had no significant past medical history. Physical examination revealed a height of 146.5 cm (−1.4 SD) and weight of 30 kg. No signs of adrenal insufficiency or hypothyroidism were observed. He was at the early stages of puberty, with bilateral gonadal volumes of 3.2 cm and penile length of 6.2 cm (male standard). The polyuria-polydipsia was severe, with urinary fluid excretion reaching up to 113 ml/kg/day, nocturnal enuresis, and excessive fluid intake of 3.8 liters/m². Ophthalmologic assessment, including optical coherence tomography (OCT), showed normal visual function and retinal structure, with no evidence of optic nerve or retinal pathology.\n\nEndocrine evaluation revealed diabetes insipidus (DI), characterized by a serum sodium of 140 mEq/L, plasma osmolality of 287 mosm/kg, and urine osmolality of 179 mosm/kg—indicating a profound inability to concentrate urine. All other endocrine markers, including insulin-like growth factor-1 (IGF-1), prolactin (PRL), free T4, cortisol, follicle-stimulating hormone (FSH), and luteinizing hormone (LH), were within normal reference ranges, suggesting intact hypothalamic-pituitary axis function except for the specific deficiency of antidiuretic hormone (ADH) action.\n\nMagnetic resonance imaging (MRI) with and without contrast demonstrated apoplexy of a Rathke cleft cyst (RCC), showing spontaneous hyperintensity on both T1 and T2-weighted sequences with dimensions of 15 × 6 × 11 mm. The anterior pituitary exhibited homogeneous contrast enhancement, consistent with normal vascularization and structural integrity. Notably, the posterior pituitary showed loss of typical hyperintensity on T2 sequences, which is a key radiological finding in RCC apoplexy and suggests hemorrhage or disruption of neurohypophyseal tissue. No evidence of craniopharyngioma or other structural lesions was identified. The RCC apoplexy remained stable over a nine-month follow-up period, with size reduction to 12 × 11 × 10 mm, and subsequent imaging at 2 and 3 years revealed progressive stabilization, ultimately measuring 7 × 10 × 6 mm, indicating a non-progressive, possibly self-limiting hemorrhagic event.\n\nA multidisciplinary team comprising an endocrinologist, neurosurgeon, and radiologist reviewed the case. Given the absence of compressive neurologic symptoms, normal neuroimaging progression, and stable hormonal profiles (excluding DI), a conservative management strategy was adopted, involving regular clinical, biochemical, and radiological monitoring. Over a three-year follow-up, the patient achieved normal pubertal development without significant endocrine deficiencies, except for a partial growth hormone (GH) deficiency, which emerged later as a secondary finding.\n\nGrowth velocity declined from −0.8 SD to −1.1 SD, prompting further investigation. At age 14 years and 9 months, two GH stimulation tests—propranolol-glucagon test and insulin tolerance test—were performed, yielding GH peak values of 19.3 µUI/ml and 10.0 µUI/ml, respectively, both below the threshold for normal pubertal growth, confirming a partial GH deficiency. Following initiation of recombinant human growth hormone (rhGH) therapy, growth velocity improved significantly, increasing from −1.1 SD to +0.2 SD over one year, indicating effective hormonal replacement.\n\nRadiological follow-up was conducted at a single center with consistent interpretation by the same radiologist, ensuring longitudinal reliability and minimizing inter-observer variability. The stability of the RCC apoplexy over time, coupled with the absence of expansion or mass effect, supports the conclusion that the lesion is benign and non-encroaching, with no indication for surgical intervention. The case underscores the importance of long-term monitoring in pediatric patients with RCC apoplexy, particularly when initial endocrine and neurologic findings are non-compressive and within normal limits, and highlights the potential for delayed emergence of secondary endocrine deficiencies, such as partial GH deficiency, despite otherwise normal early puberty and hormonal function."}
+{"row_index": 47, "doc_id": 45, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 67-year-old male with no significant comorbidities presented with a six-month history of progressive dysphonia and dysphagia, culminating in a marked deterioration of general condition accompanied by a 15 kg weight loss over six months. Initial clinical examination revealed a conscious patient with a Glasgow Coma Scale of 15/15, normothermia, blood pressure of 12/8 mmHg, oxygen saturation of 100%, heart rate of 80 beats per minute, and normal conjunctival color. A large mass was identified in the nasopharyngeal cavity, with no evidence of hepatomegaly, splenomegaly, or lymphadenopathy. Physical examination remained otherwise unremarkable.\\n\\nCervico-thoraco-abdomino-pelvic CT imaging demonstrated a 70 mm × 40 mm nasopharyngeal mass extending to 60 mm in size. Laboratory investigations, including complete blood count, renal and hepatic function tests, lactate dehydrogenase, and serologies for HIV, HCV, and HBV, were within normal limits. Histopathological and immunohistochemical analysis of the nasopharyngeal biopsy, performed in two independent laboratories, confirmed a grade 1–2 follicular B-cell non-Hodgkin lymphoma (NHL) characterized by CD20+, CD19+, CD79a+, and CD10+ expression, consistent with a follicular lymphoma subtype. Bone marrow biopsy and pre-therapeutic work-up were normal, excluding hematologic involvement.\\n\\nThe patient received four cycles of R-CHOP chemotherapy (rituximab 375 mg/m² intravenously, cyclophosphamide 750 mg/m² intravenously, oncovin 2 mg intravenously, prednisolone 100 mg orally, doxorubicin 50 mg/m² intravenously), which yielded no clinical or radiological response. Subsequently, three cycles of R-DHAOX chemotherapy (rituximab 375 mg/m² intravenously on day 1, high-dose aracytine 2 g/m² intravenously on day 2 administered over two days, dexamethasone 40 mg intravenously daily from day 1 to day 4, oxalipatin 100 mg/m² intravenously on day 1) were administered, also without response. Persistent growth of the nasopharyngeal mass necessitated tracheostomy due to airway compromise.\\n\\nRepeat biopsy of the nasopharyngeal lesion revealed a complete absence of B-cell lymphoid infiltration and the presence of AL-type amyloid deposits, specifically kappa light chain–associated amyloidosis, suggesting a clonal plasma cell disorder. Immunoelectrophoresis of plasma proteins demonstrated elevated immunoglobulin M (IgM) with kappa light chain specificity, although light chain free light chain quantification was not performed due to institutional resource limitations. Myelogram and a second bone marrow biopsy remained normal, excluding overt multiple myeloma or plasma cell dyscrasia.\\n\\nPositron emission tomography (PET) imaging confirmed a hypermetabolic nasopharyngeal lesion with no evidence of systemic metastatic disease. Cardiac evaluation (electrocardiogram, n-terminal pro-B-type natriuretic peptide, troponin, echocardiography) and renal function were unremarkable. The patient is currently receiving a triplet therapy protocol comprising bortezomib, prednisone, and bendamustine, which has demonstrated favorable clinical response following the initial cycle. The clinical course indicates a possible transformation from follicular lymphoma to a concomitant or secondary amyloidosis, potentially driven by clonal B-cell dysregulation and IgM production, with the nasopharyngeal mass serving as a site of extramedullary amyloid deposition. This case highlights the clinical challenge of distinguishing between primary lymphoma and amyloid-related pathology in the setting of a large, non-lymphomatous-appearing extramedullary mass with immunological features of B-cell dyscrasia.\"\n}", "generated_text": "A 67-year-old male with no significant comorbidities presented with a six-month history of progressive dysphonia and dysphagia, culminating in a marked deterioration of general condition accompanied by a 15 kg weight loss over six months. Initial clinical examination revealed a conscious patient with a Glasgow Coma Scale of 15/15, normothermia, blood pressure of 12/8 mmHg, oxygen saturation of 100%, heart rate of 80 beats per minute, and normal conjunctival color. A large mass was identified in the nasopharyngeal cavity, with no evidence of hepatomegaly, splenomegaly, or lymphadenopathy. Physical examination remained otherwise unremarkable.\n\nCervico-thoraco-abdomino-pelvic CT imaging demonstrated a 70 mm × 40 mm nasopharyngeal mass extending to 60 mm in size. Laboratory investigations, including complete blood count, renal and hepatic function tests, lactate dehydrogenase, and serologies for HIV, HCV, and HBV, were within normal limits. Histopathological and immunohistochemical analysis of the nasopharyngeal biopsy, performed in two independent laboratories, confirmed a grade 1–2 follicular B-cell non-Hodgkin lymphoma (NHL) characterized by CD20+, CD19+, CD79a+, and CD10+ expression, consistent with a follicular lymphoma subtype. Bone marrow biopsy and pre-therapeutic work-up were normal, excluding hematologic involvement.\n\nThe patient received four cycles of R-CHOP chemotherapy (rituximab 375 mg/m² intravenously, cyclophosphamide 750 mg/m² intravenously, oncovin 2 mg intravenously, prednisolone 100 mg orally, doxorubicin 50 mg/m² intravenously), which yielded no clinical or radiological response. Subsequently, three cycles of R-DHAOX chemotherapy (rituximab 375 mg/m² intravenously on day 1, high-dose aracytine 2 g/m² intravenously on day 2 administered over two days, dexamethasone 40 mg intravenously daily from day 1 to day 4, oxalipatin 100 mg/m² intravenously on day 1) were administered, also without response. Persistent growth of the nasopharyngeal mass necessitated tracheostomy due to airway compromise.\n\nRepeat biopsy of the nasopharyngeal lesion revealed a complete absence of B-cell lymphoid infiltration and the presence of AL-type amyloid deposits, specifically kappa light chain–associated amyloidosis, suggesting a clonal plasma cell disorder. Immunoelectrophoresis of plasma proteins demonstrated elevated immunoglobulin M (IgM) with kappa light chain specificity, although light chain free light chain quantification was not performed due to institutional resource limitations. Myelogram and a second bone marrow biopsy remained normal, excluding overt multiple myeloma or plasma cell dyscrasia.\n\nPositron emission tomography (PET) imaging confirmed a hypermetabolic nasopharyngeal lesion with no evidence of systemic metastatic disease. Cardiac evaluation (electrocardiogram, n-terminal pro-B-type natriuretic peptide, troponin, echocardiography) and renal function were unremarkable. The patient is currently receiving a triplet therapy protocol comprising bortezomib, prednisone, and bendamustine, which has demonstrated favorable clinical response following the initial cycle. The clinical course indicates a possible transformation from follicular lymphoma to a concomitant or secondary amyloidosis, potentially driven by clonal B-cell dysregulation and IgM production, with the nasopharyngeal mass serving as a site of extramedullary amyloid deposition. This case highlights the clinical challenge of distinguishing between primary lymphoma and amyloid-related pathology in the setting of a large, non-lymphomatous-appearing extramedullary mass with immunological features of B-cell dyscrasia."}
+{"row_index": 48, "doc_id": 46, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 46-year-old man from Haiti who now lives in Chile had warty bumps on his right leg for one year. The bumps started small and got bigger, then began to hurt, bleed, and ooze yellow fluid. Doctors saw the bumps and found a type of fungus called chromoblastomycosis. This fungus shows up in skin samples as thick-walled, brown cells (muriform cells) and grows into black, fuzzy spots in the lab. Under a microscope, the fungus looked like tiny branches with small dots, matching a type called Fonsecaea. He was treated with a medicine (itraconazole) taken twice a day for six months, and had cold treatments (cryotherapy) every 6 to 8 weeks on the thick parts of the bumps. After six months, the bumps went away completely. No signs of the disease came back, and only a little dark spot remains, which is normal after cold treatment.\"\n}", "generated_text": "A 46-year-old man from Haiti who now lives in Chile had warty bumps on his right leg for one year. The bumps started small and got bigger, then began to hurt, bleed, and ooze yellow fluid. Doctors saw the bumps and found a type of fungus called chromoblastomycosis. This fungus shows up in skin samples as thick-walled, brown cells (muriform cells) and grows into black, fuzzy spots in the lab. Under a microscope, the fungus looked like tiny branches with small dots, matching a type called Fonsecaea. He was treated with a medicine (itraconazole) taken twice a day for six months, and had cold treatments (cryotherapy) every 6 to 8 weeks on the thick parts of the bumps. After six months, the bumps went away completely. No signs of the disease came back, and only a little dark spot remains, which is normal after cold treatment."}
+{"row_index": 49, "doc_id": 46, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 46-year-old Haitian man who had been living in Chile for one year presented with warty, skin-like plaques on the front of his right leg that had been growing for about a year. He originally had no symptoms, but three months before coming in for care, the area started to itch, hurt, and developed a small ulcer with yellow discharge. On exam, the plaques were about 1 cm to 3 cm in size and had a rough, warty appearance. Dermatoscopy showed thickened skin with dark spots and red blood vessels. Blood tests were normal, and tests for infections like syphilis, HIV, and tuberculosis were negative. A skin biopsy was done and showed thickened skin with inflammation and special cells called muriform cells, which are a key sign of chromoblastomycosis. Fungal culture grew black, velvet-like colonies, and under the microscope, the fungus had long, branching structures and small spores typical of Fonsecaea species. The diagnosis was confirmed as chromoblastomycosis. The patient was treated for six months with itraconazole (an antifungal medicine) and regular cryotherapy (freezing the affected areas with liquid nitrogen) every six to eight weeks. He also used mupirocin ointment to prevent bacterial infections when the skin broke. After six months, the lesions completely went away, and there has been no return of the disease. The only remaining issue is mild skin lightening in the treated areas, which is expected after cryotherapy.\"\n}", "generated_text": "A 46-year-old Haitian man who had been living in Chile for one year presented with warty, skin-like plaques on the front of his right leg that had been growing for about a year. He originally had no symptoms, but three months before coming in for care, the area started to itch, hurt, and developed a small ulcer with yellow discharge. On exam, the plaques were about 1 cm to 3 cm in size and had a rough, warty appearance. Dermatoscopy showed thickened skin with dark spots and red blood vessels. Blood tests were normal, and tests for infections like syphilis, HIV, and tuberculosis were negative. A skin biopsy was done and showed thickened skin with inflammation and special cells called muriform cells, which are a key sign of chromoblastomycosis. Fungal culture grew black, velvet-like colonies, and under the microscope, the fungus had long, branching structures and small spores typical of Fonsecaea species. The diagnosis was confirmed as chromoblastomycosis. The patient was treated for six months with itraconazole (an antifungal medicine) and regular cryotherapy (freezing the affected areas with liquid nitrogen) every six to eight weeks. He also used mupirocin ointment to prevent bacterial infections when the skin broke. After six months, the lesions completely went away, and there has been no return of the disease. The only remaining issue is mild skin lightening in the treated areas, which is expected after cryotherapy."}
+{"row_index": 50, "doc_id": 46, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 46-year-old Haitian male, residing in Chile for one year, presented with a one-and-a-half-year history of progressive cutaneous lesions originating as a papule on the anterior right tibial region. Initially asymptomatic, the lesion evolved over time to include pruritus, pain, superficial ulceration, and yellowish exudate. Physical examination revealed three well-demarcated warty plaques measuring 1×1 cm, 2×2 cm, and 3×2 cm on the anterior right leg. Dermatoscopic evaluation demonstrated a hyperkeratotic mass with a central ulcerated area, characterized by reddish-black dots and congested hemorrhagic vessels, consistent with chronic inflammatory and proliferative dermal changes. The patient's general laboratory workup, including VDRL, HIV serology, and PPD, was non-reactive, ruling out syphilis, HIV infection, and latent tuberculosis. Tissue sampling via punch biopsy encompassed epidermis, dermis, and subcutaneous tissue, and was subjected to Gram staining, routine bacterial culture, and anaerobic culture—all of which were negative. Bacilloscopy and Koch complex culture of the same specimen also yielded negative results, excluding mycobacterial and bacillary etiologies. Histopathological analysis using hematoxylin and eosin staining revealed pseudoepitheliomatous hyperplasia of the epidermis, with a dense mixed inflammatory infiltrate containing suppurative foci and foreign body giant cells. Within these giant cells, round, muriform cells with thick, brown-walled walls were observed, morphologically consistent with fungal elements; this finding was further confirmed by periodic acid-Schiff (PAS) staining, which highlighted the fungal wall structure. Mycological culture on Sabouraud dextrose agar at 25°C demonstrated after 15 days of incubation the growth of dematiaceous (black-pigmented), elevated, well-defined, velvety colonies, characteristic of darkly pigmented fungi. Direct microscopic examination using 20% potassium hydroxide (KOH) revealed long, branched, occasionally tortuous hyphae and short chains of acropetal conidia, which are pathognomonic for Fonsecaea spp., a known etiological agent of chromoblastomycosis. The patient was initiated on systemic itraconazole at a dose of 100 mg every 12 hours for a duration of six months, in conjunction with regular cryotherapy using liquid nitrogen applied every six to eight weeks to hypertrophic and ulcerated areas. Topical mupirocin ointment was applied frequently to manage bacterial superinfections resulting from local lesion erosion and ulceration. The clinical course was favorable, with complete regression of all visible lesions and no evidence of relapse at the time of follow-up. Persistent mild local hypopigmentation was noted in treated areas, which is a known sequelae of cryotherapy-induced tissue damage and is expected in the context of repeated cold therapy. The diagnosis of chromoblastomycosis was confirmed by the presence of muriform cells in histopathology, dematiaceous fungal colonies in culture, and conidia morphologically compatible with Fonsecaea spp. in direct microscopy, establishing a definitive fungal etiology with a well-documented clinical and pathological profile.\"\n}", "generated_text": "A 46-year-old Haitian male, residing in Chile for one year, presented with a one-and-a-half-year history of progressive cutaneous lesions originating as a papule on the anterior right tibial region. Initially asymptomatic, the lesion evolved over time to include pruritus, pain, superficial ulceration, and yellowish exudate. Physical examination revealed three well-demarcated warty plaques measuring 1×1 cm, 2×2 cm, and 3×2 cm on the anterior right leg. Dermatoscopic evaluation demonstrated a hyperkeratotic mass with a central ulcerated area, characterized by reddish-black dots and congested hemorrhagic vessels, consistent with chronic inflammatory and proliferative dermal changes. The patient's general laboratory workup, including VDRL, HIV serology, and PPD, was non-reactive, ruling out syphilis, HIV infection, and latent tuberculosis. Tissue sampling via punch biopsy encompassed epidermis, dermis, and subcutaneous tissue, and was subjected to Gram staining, routine bacterial culture, and anaerobic culture—all of which were negative. Bacilloscopy and Koch complex culture of the same specimen also yielded negative results, excluding mycobacterial and bacillary etiologies. Histopathological analysis using hematoxylin and eosin staining revealed pseudoepitheliomatous hyperplasia of the epidermis, with a dense mixed inflammatory infiltrate containing suppurative foci and foreign body giant cells. Within these giant cells, round, muriform cells with thick, brown-walled walls were observed, morphologically consistent with fungal elements; this finding was further confirmed by periodic acid-Schiff (PAS) staining, which highlighted the fungal wall structure. Mycological culture on Sabouraud dextrose agar at 25°C demonstrated after 15 days of incubation the growth of dematiaceous (black-pigmented), elevated, well-defined, velvety colonies, characteristic of darkly pigmented fungi. Direct microscopic examination using 20% potassium hydroxide (KOH) revealed long, branched, occasionally tortuous hyphae and short chains of acropetal conidia, which are pathognomonic for Fonsecaea spp., a known etiological agent of chromoblastomycosis. The patient was initiated on systemic itraconazole at a dose of 100 mg every 12 hours for a duration of six months, in conjunction with regular cryotherapy using liquid nitrogen applied every six to eight weeks to hypertrophic and ulcerated areas. Topical mupirocin ointment was applied frequently to manage bacterial superinfections resulting from local lesion erosion and ulceration. The clinical course was favorable, with complete regression of all visible lesions and no evidence of relapse at the time of follow-up. Persistent mild local hypopigmentation was noted in treated areas, which is a known sequelae of cryotherapy-induced tissue damage and is expected in the context of repeated cold therapy. The diagnosis of chromoblastomycosis was confirmed by the presence of muriform cells in histopathology, dematiaceous fungal colonies in culture, and conidia morphologically compatible with Fonsecaea spp. in direct microscopy, establishing a definitive fungal etiology with a well-documented clinical and pathological profile."}
+{"row_index": 51, "doc_id": 47, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 19-year-old man had a painful lump in his scrotum for 8 months that didn’t go away with antibiotics. He also had fever, night sweats, loss of appetite, and lost weight. No one in his family had tuberculosis, but he had the TB vaccine. The lump was surgically removed and tested — it showed signs of tuberculosis in the tube-like part of the testicle. X-rays showed TB in his lungs, lymph nodes, and bones. He started TB medicine, but after 4 months, he had seizures. A brain scan found small TB-related lumps in his brain. He started medicine to stop the seizures and kept taking TB medicine. His symptoms got better — he gained weight, the body lumps went away, and he didn’t have more seizures. The brain lumps slowly got smaller, so he kept taking TB medicine for a long time. After 19 years of treatment, he was fully healed with no long-term problems.\"\n}", "generated_text": "A 19-year-old man had a painful lump in his scrotum for 8 months that didn’t go away with antibiotics. He also had fever, night sweats, loss of appetite, and lost weight. No one in his family had tuberculosis, but he had the TB vaccine. The lump was surgically removed and tested — it showed signs of tuberculosis in the tube-like part of the testicle. X-rays showed TB in his lungs, lymph nodes, and bones. He started TB medicine, but after 4 months, he had seizures. A brain scan found small TB-related lumps in his brain. He started medicine to stop the seizures and kept taking TB medicine. His symptoms got better — he gained weight, the body lumps went away, and he didn’t have more seizures. The brain lumps slowly got smaller, so he kept taking TB medicine for a long time. After 19 years of treatment, he was fully healed with no long-term problems."}
+{"row_index": 52, "doc_id": 47, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 19-year-old man with no prior medical problems was admitted to the hospital with a painful lump in his left scrotum that had been growing for 8 months. The lump didn't go away with antibiotics, and he also had symptoms like low-grade fever, night sweats, loss of appetite, and unexplained weight loss. He had no history of tuberculosis in his family or personal history, and he was vaccinated at birth. Exam findings showed a large, tender lump in the scrotum and some firm lumps on his chest. His blood tests showed high inflammation markers, and a chest X-ray showed signs of lung infection. After surgery to remove the scrotal lump, the tissue tested positive for tuberculosis in the epididymis, which is a part of the testicle. Tests also found tuberculosis in his lungs, around the abdomen and chest walls, and in his spine and bones. He started standard tuberculosis treatment with several medications. After four months, he had seizures, and a brain scan showed small areas of tuberculosis in the brain, called tuberculomas. He was then given anti-seizure medication along with continuing tuberculosis treatment. His condition improved over time—he regained his weight, the lung and body infections went away, and the seizures stopped. Although the brain tuberculomas slowly shrank, he needed to stay on tuberculosis treatment for a long time, totaling 234 months (about 19 years), before being declared cured with no long-term effects.\"\n}", "generated_text": "A 19-year-old man with no prior medical problems was admitted to the hospital with a painful lump in his left scrotum that had been growing for 8 months. The lump didn't go away with antibiotics, and he also had symptoms like low-grade fever, night sweats, loss of appetite, and unexplained weight loss. He had no history of tuberculosis in his family or personal history, and he was vaccinated at birth. Exam findings showed a large, tender lump in the scrotum and some firm lumps on his chest. His blood tests showed high inflammation markers, and a chest X-ray showed signs of lung infection. After surgery to remove the scrotal lump, the tissue tested positive for tuberculosis in the epididymis, which is a part of the testicle. Tests also found tuberculosis in his lungs, around the abdomen and chest walls, and in his spine and bones. He started standard tuberculosis treatment with several medications. After four months, he had seizures, and a brain scan showed small areas of tuberculosis in the brain, called tuberculomas. He was then given anti-seizure medication along with continuing tuberculosis treatment. His condition improved over time—he regained his weight, the lung and body infections went away, and the seizures stopped. Although the brain tuberculomas slowly shrank, he needed to stay on tuberculosis treatment for a long time, totaling 234 months (about 19 years), before being declared cured with no long-term effects."}
+{"row_index": 53, "doc_id": 47, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 19-year-old male with no significant medical history presented with a painful left scrotal mass that had persisted for 8 months without improvement following empirical antibiotic therapy for pyogenic infections. He reported intermittent low-grade fever, night sweats, anorexia, and unexplained weight loss since symptom onset, with no history of cough, sputum production, or hemoptysis. There was no personal or familial history of tuberculosis, and he had received standard bacillus Calmette-Guérin (BCG) vaccination at birth. Physical examination revealed a large, tender, slightly warm left scrotal bursa and two elongated, firm, poorly defined subcutaneous masses in the anterior thoracic wall measuring 3–4 cm in length, without audible rales on lung auscultation. The remainder of the systemic examination was unremarkable. Laboratory findings demonstrated a markedly elevated c-reactive protein (CRP) of 90 mg/dL, while complete blood count, serum creatinine, blood glucose, and liver function tests remained within normal limits. Standard chest radiography revealed bilateral reticulonodular infiltrates consistent with pulmonary involvement.\\n\\nUltrasound imaging suggested an epididymal mass, prompting a left orchidectomy. Histopathological analysis of the resected specimen revealed granulomatous epithelioid cell necrosis involving the body and tail of the epididymis, with sparing of the head and testicular tissue, strongly suggestive of active epididymal tuberculosis. The intradermal tuberculin skin test (TST) was positive, supporting the diagnosis. Direct microscopy and culture for acid-fast bacilli (AFB) in sputum and urine over three consecutive days were negative, and serological testing for human immunodeficiency virus (HIV), hepatitis B virus (HBV), hepatitis C virus (HCV), and Wright's stain (to rule out other hematological disorders) were all negative, excluding alternative infectious or hematologic etiologies.\\n\\nTo evaluate for extrapulmonary dissemination, a thoraco-abdomino-pelvic tomodensitometry was performed, which demonstrated miliary tuberculosis, coelo-mesenteric necrotic lymphadenopathy, two parietal collections (right: 33 × 10 mm; left: 45 × 10 mm) arising from the external oblique muscles, and focal osteolytic lesions at D11 and L5, consistent with early spondylodiscitis. Magnetic resonance imaging (MRI) of the spinal cord confirmed spondylodiscitis at the D7, D11, L4, and L5 levels. This constellation of findings led to a definitive diagnosis of disseminated tuberculosis involving the epididymal, pulmonary, parietal, lymphatic, and osteo-articular compartments.\\n\\nTreatment was initiated with a 2-month intensive phase of quadruple antitubercular chemotherapy consisting of isoniazid, rifampicin, ethambutol, and pyrazinamide, followed by a continuation phase of isoniazid and rifampicin. At the fourth month of therapy, the patient developed generalized tonic-clonic convulsive seizures. Brain MRI revealed multiple nodular lesions located above and below the tentorial membrane, consistent with tuberculomas—focal granulomatous brain lesions caused by Mycobacterium tuberculosis. The patient was promptly started on adjunctive anticonvulsant therapy while continuing anti-tubercular treatment. Clinical and radiological follow-up demonstrated a favorable evolution, including resolution of systemic symptoms, weight gain, and gradual disappearance of thoracic parietal collections, lymphadenopathy, and miliary infiltrates on imaging. However, the tuberculomas showed a slow, progressive reduction in size, necessitating prolonged continuation of antituberculous therapy. The patient was ultimately declared cured at the end of the 234th month of treatment, with a 2-year post-treatment follow-up confirming no recurrence of disease or neurological sequelae. This case illustrates the potential for disseminated tuberculosis to present with extrapulmonary manifestations, including epididymal involvement and central nervous system tuberculomas, and underscores the importance of early diagnosis, comprehensive imaging, and long-term management in young adults with atypical presentations.\"\n}", "generated_text": "A 19-year-old male with no significant medical history presented with a painful left scrotal mass that had persisted for 8 months without improvement following empirical antibiotic therapy for pyogenic infections. He reported intermittent low-grade fever, night sweats, anorexia, and unexplained weight loss since symptom onset, with no history of cough, sputum production, or hemoptysis. There was no personal or familial history of tuberculosis, and he had received standard bacillus Calmette-Guérin (BCG) vaccination at birth. Physical examination revealed a large, tender, slightly warm left scrotal bursa and two elongated, firm, poorly defined subcutaneous masses in the anterior thoracic wall measuring 3–4 cm in length, without audible rales on lung auscultation. The remainder of the systemic examination was unremarkable. Laboratory findings demonstrated a markedly elevated c-reactive protein (CRP) of 90 mg/dL, while complete blood count, serum creatinine, blood glucose, and liver function tests remained within normal limits. Standard chest radiography revealed bilateral reticulonodular infiltrates consistent with pulmonary involvement.\n\nUltrasound imaging suggested an epididymal mass, prompting a left orchidectomy. Histopathological analysis of the resected specimen revealed granulomatous epithelioid cell necrosis involving the body and tail of the epididymis, with sparing of the head and testicular tissue, strongly suggestive of active epididymal tuberculosis. The intradermal tuberculin skin test (TST) was positive, supporting the diagnosis. Direct microscopy and culture for acid-fast bacilli (AFB) in sputum and urine over three consecutive days were negative, and serological testing for human immunodeficiency virus (HIV), hepatitis B virus (HBV), hepatitis C virus (HCV), and Wright's stain (to rule out other hematological disorders) were all negative, excluding alternative infectious or hematologic etiologies.\n\nTo evaluate for extrapulmonary dissemination, a thoraco-abdomino-pelvic tomodensitometry was performed, which demonstrated miliary tuberculosis, coelo-mesenteric necrotic lymphadenopathy, two parietal collections (right: 33 × 10 mm; left: 45 × 10 mm) arising from the external oblique muscles, and focal osteolytic lesions at D11 and L5, consistent with early spondylodiscitis. Magnetic resonance imaging (MRI) of the spinal cord confirmed spondylodiscitis at the D7, D11, L4, and L5 levels. This constellation of findings led to a definitive diagnosis of disseminated tuberculosis involving the epididymal, pulmonary, parietal, lymphatic, and osteo-articular compartments.\n\nTreatment was initiated with a 2-month intensive phase of quadruple antitubercular chemotherapy consisting of isoniazid, rifampicin, ethambutol, and pyrazinamide, followed by a continuation phase of isoniazid and rifampicin. At the fourth month of therapy, the patient developed generalized tonic-clonic convulsive seizures. Brain MRI revealed multiple nodular lesions located above and below the tentorial membrane, consistent with tuberculomas—focal granulomatous brain lesions caused by Mycobacterium tuberculosis. The patient was promptly started on adjunctive anticonvulsant therapy while continuing anti-tubercular treatment. Clinical and radiological follow-up demonstrated a favorable evolution, including resolution of systemic symptoms, weight gain, and gradual disappearance of thoracic parietal collections, lymphadenopathy, and miliary infiltrates on imaging. However, the tuberculomas showed a slow, progressive reduction in size, necessitating prolonged continuation of antituberculous therapy. The patient was ultimately declared cured at the end of the 234th month of treatment, with a 2-year post-treatment follow-up confirming no recurrence of disease or neurological sequelae. This case illustrates the potential for disseminated tuberculosis to present with extrapulmonary manifestations, including epididymal involvement and central nervous system tuberculomas, and underscores the importance of early diagnosis, comprehensive imaging, and long-term management in young adults with atypical presentations."}
+{"row_index": 54, "doc_id": 48, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 10-year-old boy was getting chemotherapy for a serious type of cancer called leukemia. During the early treatment, he got a brain infection caused by a bacteria named B. cereus. Doctors found it using brain scans and a fluid from around the brain. He had a bad headache that didn’t go away, so they checked his brain and found a spot that looked like an infection. Even though he didn’t have a fever, he started to feel very sick and needed help in the hospital. Doctors gave him strong antibiotics, and the infection went away. After a few weeks, his headache stopped and his brain scans showed the infection was getting smaller. He fully recovered and is back to normal.\"\n}", "generated_text": "A 10-year-old boy was getting chemotherapy for a serious type of cancer called leukemia. During the early treatment, he got a brain infection caused by a bacteria named B. cereus. Doctors found it using brain scans and a fluid from around the brain. He had a bad headache that didn’t go away, so they checked his brain and found a spot that looked like an infection. Even though he didn’t have a fever, he started to feel very sick and needed help in the hospital. Doctors gave him strong antibiotics, and the infection went away. After a few weeks, his headache stopped and his brain scans showed the infection was getting smaller. He fully recovered and is back to normal."}
+{"row_index": 55, "doc_id": 48, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 10-year-old boy was treated for acute lymphoblastic leukaemia, a type of blood cancer, using a standard chemotherapy protocol. During the early stages of treatment, he developed a serious brain infection called a cerebral abscess caused by a bacteria named B. cereus. This was found through brain imaging and by testing the fluid around the brain (cerebrospinal fluid). Although the infection was severe, it responded well to antibiotics. The boy’s symptoms improved, and he made a full recovery with no lasting brain problems. Follow-up scans showed the infection had shrunk, and he was able to continue his treatment safely.\"\n}", "generated_text": "A 10-year-old boy was treated for acute lymphoblastic leukaemia, a type of blood cancer, using a standard chemotherapy protocol. During the early stages of treatment, he developed a serious brain infection called a cerebral abscess caused by a bacteria named B. cereus. This was found through brain imaging and by testing the fluid around the brain (cerebrospinal fluid). Although the infection was severe, it responded well to antibiotics. The boy’s symptoms improved, and he made a full recovery with no lasting brain problems. Follow-up scans showed the infection had shrunk, and he was able to continue his treatment safely."}
+{"row_index": 56, "doc_id": 48, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"We present a case of a 10-year-old male with high-risk early T-cell acute lymphoblastic leukaemia (ALL), managed according to the LAL SEHOP-PETHEMA 2013 protocol. Two years post-diagnosis, he experienced an early central nervous system (CNS) relapse, prompting intervention under the InteReALL HR 2010 protocol, which included bortezomib. During induction therapy, the patient became neutropenic for four weeks (neutrophil count: 20/μL), receiving prophylactic antimicrobials consisting of cefepime, cotrimoxazole, and fluconazole. Concurrently, he was treated with acyclovir for a documented herpes simplex virus 1 (HSV-1) skin infection. On presentation, he developed a severe, treatment-refractory headache, prompting a cranial computed tomography (CT) scan that revealed a hypodense lesion in the right temporal lobe. Given the infectious etiology hypothesis, a lumbar puncture was performed, and empirical therapy was updated to meropenem and vancomycin.\\n\\nDespite the absence of fever, the patient rapidly progressed to septic shock on day one of hospitalization, requiring transfer to the paediatric intensive care unit (PICU) for inotropic and vasoactive support. Antimicrobial coverage was broadened to include gentamicin and caspofungin. Laboratory findings demonstrated a progressive rise in inflammatory markers: C-reactive protein (CRP) reached 312 mg/L and procalcitonin (PCT) peaked at 47.58 ng/mL by day three, consistent with a severe bacterial infection, while no other significant biochemical abnormalities were detected. Complete blood count revealed pancytopenia, attributable to chemotherapy-induced bone marrow suppression. Blood cultures were negative for both bacteremia and fungemia; herpesvirus serologies (HSV-1, HSV-2, HHV-6, cytomegalovirus, varicella-zoster virus, enterovirus, parechovirus) and urine/fecal cultures were also negative, excluding common pathogens.\\n\\nCerebrospinal fluid (CSF) analysis showed normal glucose (63 mg/dL), protein (16 mg/dL), and leukocyte count (1/μL), indicating a non-inflammatory, non-lymphocytic CSF profile. However, microbiological culture identified *Bacillus cereus* as the causative organism, which was sensitive to meropenem, vancomycin, linezolid, and ciprofloxacin. All other potential CNS pathogens—including *Neisseria meningitidis*, *Listeria monocytogenes*, *Streptococcus pneumoniae*, *Cryptococcus*, and *Toxoplasma gondii*—were ruled out in CSF. Electroencephalography (EEG) revealed diffuse cerebral slowing without epileptiform discharges, suggesting non-epileptic encephalopathy consistent with metabolic or infectious insult.\\n\\nOn day 4, following stabilization of hemodynamics, cranial magnetic resonance imaging (MRI) demonstrated two hyperintense lesions on T2 and FLAIR sequences involving the subcortical regions of the right temporal and parietal lobes. The parietal lesion exhibited ring enhancement after gadolinium administration, and both lesions displayed peripheral diffusion restriction on apparent diffusion coefficient (ADC) mapping, indicative of restricted water diffusion typical of abscess formation. Additionally, scattered small hemorrhagic foci were observed within the brain parenchyma. These imaging findings, in conjunction with the CSF culture result and clinical course, supported a diagnosis of *Bacillus cereus* cerebral abscess, an atypical and rare cause of CNS infection in the immunocompromised setting.\\n\\nThe patient responded favorably to antibiotic therapy, with resolution of headache and absence of new neurological deficits. Follow-up MRI at two weeks showed significant reduction in lesion size. Vancomycin and acyclovir were discontinued after three weeks, and meropenem was continued for a total of six weeks. This case highlights the diagnostic challenge of atypical bacterial CNS infections in children undergoing intensive chemotherapy, particularly in the context of prolonged neutropenia and prophylactic regimens, and underscores the importance of early imaging, CSF analysis, and broad-spectrum empirical therapy in such high-risk populations.\"\n}", "generated_text": "We present a case of a 10-year-old male with high-risk early T-cell acute lymphoblastic leukaemia (ALL), managed according to the LAL SEHOP-PETHEMA 2013 protocol. Two years post-diagnosis, he experienced an early central nervous system (CNS) relapse, prompting intervention under the InteReALL HR 2010 protocol, which included bortezomib. During induction therapy, the patient became neutropenic for four weeks (neutrophil count: 20/μL), receiving prophylactic antimicrobials consisting of cefepime, cotrimoxazole, and fluconazole. Concurrently, he was treated with acyclovir for a documented herpes simplex virus 1 (HSV-1) skin infection. On presentation, he developed a severe, treatment-refractory headache, prompting a cranial computed tomography (CT) scan that revealed a hypodense lesion in the right temporal lobe. Given the infectious etiology hypothesis, a lumbar puncture was performed, and empirical therapy was updated to meropenem and vancomycin.\n\nDespite the absence of fever, the patient rapidly progressed to septic shock on day one of hospitalization, requiring transfer to the paediatric intensive care unit (PICU) for inotropic and vasoactive support. Antimicrobial coverage was broadened to include gentamicin and caspofungin. Laboratory findings demonstrated a progressive rise in inflammatory markers: C-reactive protein (CRP) reached 312 mg/L and procalcitonin (PCT) peaked at 47.58 ng/mL by day three, consistent with a severe bacterial infection, while no other significant biochemical abnormalities were detected. Complete blood count revealed pancytopenia, attributable to chemotherapy-induced bone marrow suppression. Blood cultures were negative for both bacteremia and fungemia; herpesvirus serologies (HSV-1, HSV-2, HHV-6, cytomegalovirus, varicella-zoster virus, enterovirus, parechovirus) and urine/fecal cultures were also negative, excluding common pathogens.\n\nCerebrospinal fluid (CSF) analysis showed normal glucose (63 mg/dL), protein (16 mg/dL), and leukocyte count (1/μL), indicating a non-inflammatory, non-lymphocytic CSF profile. However, microbiological culture identified *Bacillus cereus* as the causative organism, which was sensitive to meropenem, vancomycin, linezolid, and ciprofloxacin. All other potential CNS pathogens—including *Neisseria meningitidis*, *Listeria monocytogenes*, *Streptococcus pneumoniae*, *Cryptococcus*, and *Toxoplasma gondii*—were ruled out in CSF. Electroencephalography (EEG) revealed diffuse cerebral slowing without epileptiform discharges, suggesting non-epileptic encephalopathy consistent with metabolic or infectious insult.\n\nOn day 4, following stabilization of hemodynamics, cranial magnetic resonance imaging (MRI) demonstrated two hyperintense lesions on T2 and FLAIR sequences involving the subcortical regions of the right temporal and parietal lobes. The parietal lesion exhibited ring enhancement after gadolinium administration, and both lesions displayed peripheral diffusion restriction on apparent diffusion coefficient (ADC) mapping, indicative of restricted water diffusion typical of abscess formation. Additionally, scattered small hemorrhagic foci were observed within the brain parenchyma. These imaging findings, in conjunction with the CSF culture result and clinical course, supported a diagnosis of *Bacillus cereus* cerebral abscess, an atypical and rare cause of CNS infection in the immunocompromised setting.\n\nThe patient responded favorably to antibiotic therapy, with resolution of headache and absence of new neurological deficits. Follow-up MRI at two weeks showed significant reduction in lesion size. Vancomycin and acyclovir were discontinued after three weeks, and meropenem was continued for a total of six weeks. This case highlights the diagnostic challenge of atypical bacterial CNS infections in children undergoing intensive chemotherapy, particularly in the context of prolonged neutropenia and prophylactic regimens, and underscores the importance of early imaging, CSF analysis, and broad-spectrum empirical therapy in such high-risk populations."}
+{"row_index": 57, "doc_id": 49, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 16-year-old girl has a flat, gray spot on her left thigh that's been there since birth. The spot is about 10.5 cm wide and 8.0 cm long, and it's got small blood vessels running around the edge. Over time, the spot turned lighter and became flatter. A scan showed that the spot has extra blood vessels in the skin and layer below it, which is normal for this type of growth. There's no sign that it's affecting her legs differently or spreading into muscles or bones.\"\n}", "generated_text": "A 16-year-old girl has a flat, gray spot on her left thigh that's been there since birth. The spot is about 10.5 cm wide and 8.0 cm long, and it's got small blood vessels running around the edge. Over time, the spot turned lighter and became flatter. A scan showed that the spot has extra blood vessels in the skin and layer below it, which is normal for this type of growth. There's no sign that it's affecting her legs differently or spreading into muscles or bones."}
+{"row_index": 58, "doc_id": 49, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"16-year-old female presenting with a congenital, depressed gray plaque measuring 10.5 × 8.0 cm located in the lower lateral aspect of the left thigh, characterized by interspersed hypochromic regions and peripheral telangiectatic vessels, including visible superficial veins adjacent to the lesion. The lesion was present at birth and initially exhibited a violaceous hue, evolving over time to become lighter in color and more depressed in elevation. No asymmetry in lower limb length was observed, ruling out significant skeletal or musculoskeletal involvement. Angioresonance imaging revealed a complex vascular malformation involving the dermal and subcutaneous layers, primarily supplied by intermuscular branches of the popliteal artery. Notably, early venous filling was demonstrated both within the lesion and in the surrounding tissue, indicating early venous shunting and possible venous override. No significant dilation of deep draining veins was identified, although a superficial draining vein was observed coursing along the subcutaneous cellular tissue of the anterior thigh. Histopathological and imaging findings confirm thinning of the subcutaneous tissue within the affected region, consistent with chronic vascular remodeling, without evidence of intramuscular or bony extension. The clinical and imaging profile supports a diagnosis of a venous or venous-lymphatic malformation with early venous dominance, likely arising from aberrant vascular development during embryogenesis, involving the popliteal artery-derived vascular plexus.\"\n}", "generated_text": "16-year-old female presenting with a congenital, depressed gray plaque measuring 10.5 × 8.0 cm located in the lower lateral aspect of the left thigh, characterized by interspersed hypochromic regions and peripheral telangiectatic vessels, including visible superficial veins adjacent to the lesion. The lesion was present at birth and initially exhibited a violaceous hue, evolving over time to become lighter in color and more depressed in elevation. No asymmetry in lower limb length was observed, ruling out significant skeletal or musculoskeletal involvement. Angioresonance imaging revealed a complex vascular malformation involving the dermal and subcutaneous layers, primarily supplied by intermuscular branches of the popliteal artery. Notably, early venous filling was demonstrated both within the lesion and in the surrounding tissue, indicating early venous shunting and possible venous override. No significant dilation of deep draining veins was identified, although a superficial draining vein was observed coursing along the subcutaneous cellular tissue of the anterior thigh. Histopathological and imaging findings confirm thinning of the subcutaneous tissue within the affected region, consistent with chronic vascular remodeling, without evidence of intramuscular or bony extension. The clinical and imaging profile supports a diagnosis of a venous or venous-lymphatic malformation with early venous dominance, likely arising from aberrant vascular development during embryogenesis, involving the popliteal artery-derived vascular plexus."}
+{"row_index": 59, "doc_id": 50, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 57-year-old woman with a long history of asthma and allergic rhinitis came in with recurring abdominal pain that had been going on for two months. The pain was dull and intermittent, along with nausea, loss of appetite, fatigue, and a 5-kilogram weight loss. She had no fever, no blood or mucus in her stool, and no respiratory symptoms. Tests showed very high levels of a type of white blood cell called eosinophils, and her IgG4 levels were also elevated. After checking for infections, blood disorders, and other conditions that could cause high eosinophils, doctors found no clear cause. A biopsy of her colon tissue showed a large number of eosinophils in the lining of the colon, which confirmed a diagnosis of eosinophilic colitis (EoC). She was treated with corticosteroids and montelukast, and her symptoms improved within two weeks. Her eosinophil levels returned to normal, and after stopping the steroids, she continued on montelukast for three months without any symptoms coming back.\"\n}", "generated_text": "A 57-year-old woman with a long history of asthma and allergic rhinitis came in with recurring abdominal pain that had been going on for two months. The pain was dull and intermittent, along with nausea, loss of appetite, fatigue, and a 5-kilogram weight loss. She had no fever, no blood or mucus in her stool, and no respiratory symptoms. Tests showed very high levels of a type of white blood cell called eosinophils, and her IgG4 levels were also elevated. After checking for infections, blood disorders, and other conditions that could cause high eosinophils, doctors found no clear cause. A biopsy of her colon tissue showed a large number of eosinophils in the lining of the colon, which confirmed a diagnosis of eosinophilic colitis (EoC). She was treated with corticosteroids and montelukast, and her symptoms improved within two weeks. Her eosinophil levels returned to normal, and after stopping the steroids, she continued on montelukast for three months without any symptoms coming back."}
+{"row_index": 60, "doc_id": 50, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 57-year-old woman with a 14-year history of asthma and allergic rhinitis, managed on salmeterol/fluticasone, was hospitalized for recurrent abdominal pain initiated two months prior. The pain was intermittent, dull, and associated with nausea, anorexia, malaise, and a 5 kg weight loss. Notably, there were no fever, blood or mucus in stool, respiratory symptoms (rhinorrhea, wheezing, cough), or history of alcohol, tobacco, or herbal medicine use. Six weeks before admission, she was diagnosed with an intestinal infection based on a complete blood count (CBC) showing leukocytosis and marked eosinophilia (25.61 G/L, 77.8% eosinophils). She received antibiotic therapy and mebendazole, which failed to alleviate symptoms. On presentation, vital signs were stable: blood pressure 110/70 mmHg, temperature 37°C, heart rate 88 bpm, respiratory rate 18 bpm. Body mass index was 16.6 kg/m², consistent with severe underweight, and sarcopenia was present, with no skin rash, lymphadenopathy, or edema. Abdominal examination revealed tenderness in the epigastric and umbilical regions without rebound or guarding. Repeat CBC demonstrated persistent leukocytosis and significant eosinophilia (20.8 G/L total WBC, 77.8% eosinophils), with peripheral blood film showing normal eosinophil morphology. Bone marrow aspiration revealed 48% eosinophils without blasts or atypical cells, suggesting a clonal or reactive process but excluding hematologic malignancy. Fluorescence in situ hybridization (FISH) for CHIC2 deletion, a surrogate marker for FIP1L1-PDGFRA fusion in eosinophilic disorders, was negative, ruling out primary myeloid eosinophilia. Autoimmune and vasculitis screening (ANA, anti-dsDNA, p-ANCA, c-ANCA) remained negative, excluding systemic autoimmune conditions. Serum immunoglobulins showed elevated IgG (2760 mg/dL; normal 700–1600 mg/dL) and IgG4 (1260 mg/dL; normal 3.9–86.4 mg/dL), with a mild elevation in IgE (137.5 IU/mL; normal <100 IU/mL) and elevated rheumatoid factor (RF 144.4 IU/mL; normal <20 IU/mL), though these findings were not sufficient to support an autoimmune etiology. All other laboratory parameters—including aminotransferases, blood urea nitrogen, serum creatinine, complement C3/C4, vitamin B12, serum cortisol, and NT-proBNP—were within normal limits. Electrocardiogram and echocardiogram were unremarkable. Chest CT revealed mild pulmonary fibrosis and bronchiectasis, consistent with chronic airway inflammation. Sputum acid-fast bacilli (AFB) smear and bronchoscopy were negative; bronchoalveolar lavage (BAL) cytology showed 35% neutrophils and no eosinophils, indicating that airway eosinophilia was not the primary driver of systemic eosinophilia. Spirometry demonstrated severe obstructive lung disease with a significant bronchodilator response, and fractional exhaled nitric oxide (FeNO) was 15 ppb, supporting a Th2-mediated inflammatory phenotype. Stool analysis revealed leukocyte presence, but no ova, parasites, or evidence of infectious etiology. Serology testing confirmed positive IgG to Toxocara canis (54.2 NovaTec-Units), suggestive of toxocariasis, but remained negative for Strongyloides stercoralis, Fasciola sp., Toxoplasma gondii, Trichinella spiralis, Ancylostoma sp., Angiostrongylus cantonensis, Ascaris lumbricoides, Clonorchis sinensis, Paragonimus sp., Gnathostoma sp., Entamoeba histolytica, cysticercosis, filariasis, and HIV. Abdominal contrast-enhanced CT showed gallbladder stones without acute cholecystitis and no structural abnormalities in the gastrointestinal tract. Upper endoscopy was unremarkable, while colonoscopy revealed mucosal inflammation in the sigmoid, left, transverse, and right colon, prompting systematic biopsy. A five-day course of albendazole (400 mg twice daily) for suspected toxocariasis was ineffective. Colonic biopsies demonstrated significant eosinophilic infiltration, with counts exceeding 85 eosinophils/HPF in", "generated_text": "{\n  \"proficient_health_literacy\": \"A 57-year-old woman with a 14-year history of asthma and allergic rhinitis, managed on salmeterol/fluticasone, was hospitalized for recurrent abdominal pain initiated two months prior. The pain was intermittent, dull, and associated with nausea, anorexia, malaise, and a 5 kg weight loss. Notably, there were no fever, blood or mucus in stool, respiratory symptoms (rhinorrhea, wheezing, cough), or history of alcohol, tobacco, or herbal medicine use. Six weeks before admission, she was diagnosed with an intestinal infection based on a complete blood count (CBC) showing leukocytosis and marked eosinophilia (25.61 G/L, 77.8% eosinophils). She received antibiotic therapy and mebendazole, which failed to alleviate symptoms. On presentation, vital signs were stable: blood pressure 110/70 mmHg, temperature 37°C, heart rate 88 bpm, respiratory rate 18 bpm. Body mass index was 16.6 kg/m², consistent with severe underweight, and sarcopenia was present, with no skin rash, lymphadenopathy, or edema. Abdominal examination revealed tenderness in the epigastric and umbilical regions without rebound or guarding. Repeat CBC demonstrated persistent leukocytosis and significant eosinophilia (20.8 G/L total WBC, 77.8% eosinophils), with peripheral blood film showing normal eosinophil morphology. Bone marrow aspiration revealed 48% eosinophils without blasts or atypical cells, suggesting a clonal or reactive process but excluding hematologic malignancy. Fluorescence in situ hybridization (FISH) for CHIC2 deletion, a surrogate marker for FIP1L1-PDGFRA fusion in eosinophilic disorders, was negative, ruling out primary myeloid eosinophilia. Autoimmune and vasculitis screening (ANA, anti-dsDNA, p-ANCA, c-ANCA) remained negative, excluding systemic autoimmune conditions. Serum immunoglobulins showed elevated IgG (2760 mg/dL; normal 700–1600 mg/dL) and IgG4 (1260 mg/dL; normal 3.9–86.4 mg/dL), with a mild elevation in IgE (137.5 IU/mL; normal <100 IU/mL) and elevated rheumatoid factor (RF 144.4 IU/mL; normal <20 IU/mL), though these findings were not sufficient to support an autoimmune etiology. All other laboratory parameters—including aminotransferases, blood urea nitrogen, serum creatinine, complement C3/C4, vitamin B12, serum cortisol, and NT-proBNP—were within normal limits. Electrocardiogram and echocardiogram were unremarkable. Chest CT revealed mild pulmonary fibrosis and bronchiectasis, consistent with chronic airway inflammation. Sputum acid-fast bacilli (AFB) smear and bronchoscopy were negative; bronchoalveolar lavage (BAL) cytology showed 35% neutrophils and no eosinophils, indicating that airway eosinophilia was not the primary driver of systemic eosinophilia. Spirometry demonstrated severe obstructive lung disease with a significant bronchodilator response, and fractional exhaled nitric oxide (FeNO) was 15 ppb, supporting a Th2-mediated inflammatory phenotype. Stool analysis revealed leukocyte presence, but no ova, parasites, or evidence of infectious etiology. Serology testing confirmed positive IgG to Toxocara canis (54.2 NovaTec-Units), suggestive of toxocariasis, but remained negative for Strongyloides stercoralis, Fasciola sp., Toxoplasma gondii, Trichinella spiralis, Ancylostoma sp., Angiostrongylus cantonensis, Ascaris lumbricoides, Clonorchis sinensis, Paragonimus sp., Gnathostoma sp., Entamoeba histolytica, cysticercosis, filariasis, and HIV. Abdominal contrast-enhanced CT showed gallbladder stones without acute cholecystitis and no structural abnormalities in the gastrointestinal tract. Upper endoscopy was unremarkable, while colonoscopy revealed mucosal inflammation in the sigmoid, left, transverse, and right colon, prompting systematic biopsy. A five-day course of albendazole (400 mg twice daily) for suspected toxocariasis was ineffective. Colonic biopsies demonstrated significant eosinophilic infiltration, with counts exceeding 85 eosinophils/HPF in"}
+{"row_index": 61, "doc_id": 51, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 35-year-old man had a heart problem that got worse over time. At first, he had chest pain and trouble breathing, especially after activity. Doctors found a lump in his heart called a cardiac myxoma, and also saw that his heart was getting bigger and weaker — this is called dilated cardiomyopathy. He had signs of Carney syndrome, a rare condition that affects the heart and skin, like dark spots on his ears and small cysts in his kidney. Doctors tested his genes and confirmed the diagnosis. At first, he was treated with medicine but didn’t have surgery. Later, his symptoms got much worse — he could barely breathe, even when lying down, and his heart was failing badly. His heart function was rated as very poor (NYHA Grade IV). Doctors said he needed a heart transplant. On October 1, 2024, he got a new heart from a donor. The surgery was done by cutting open his chest, removing the damaged heart parts, and putting in the new one. The new heart was connected properly with no leaks. After the surgery, he started recovering fast. By day one, he was urinating well and his heart function improved. His blood tests showed his heart was working better. He took medicine to stop his body from rejecting the new heart and to fight infections. After a week, his recovery was good, and by October 20, 2023, his heart was working normally. All tests were normal, and he’s now doing well and living a healthy life.\"\n}", "generated_text": "A 35-year-old man had a heart problem that got worse over time. At first, he had chest pain and trouble breathing, especially after activity. Doctors found a lump in his heart called a cardiac myxoma, and also saw that his heart was getting bigger and weaker — this is called dilated cardiomyopathy. He had signs of Carney syndrome, a rare condition that affects the heart and skin, like dark spots on his ears and small cysts in his kidney. Doctors tested his genes and confirmed the diagnosis. At first, he was treated with medicine but didn’t have surgery. Later, his symptoms got much worse — he could barely breathe, even when lying down, and his heart was failing badly. His heart function was rated as very poor (NYHA Grade IV). Doctors said he needed a heart transplant. On October 1, 2024, he got a new heart from a donor. The surgery was done by cutting open his chest, removing the damaged heart parts, and putting in the new one. The new heart was connected properly with no leaks. After the surgery, he started recovering fast. By day one, he was urinating well and his heart function improved. His blood tests showed his heart was working better. He took medicine to stop his body from rejecting the new heart and to fight infections. After a week, his recovery was good, and by October 20, 2023, his heart was working normally. All tests were normal, and he’s now doing well and living a healthy life."}
+{"row_index": 62, "doc_id": 51, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 35-year-old man was diagnosed with heart failure caused by a rare condition called Carney syndrome. This condition leads to the growth of a non-cancerous tumor (called a cardiac myxoma) in the heart and weakens the heart muscle, leading to a condition known as dilated cardiomyopathy. Three years ago, he first had chest tightness and shortness of breath after physical activity. An ultrasound of his heart showed a tumor, and further tests confirmed Carney syndrome. He was treated with medications, but did not have surgery at the time. Over time, his symptoms worsened, and he could no longer lie down without breathing difficulty. His heart function was severely weakened (NYHA Class IV), and new tests showed both the tumor and a weakened heart. Because the heart was no longer able to pump effectively, doctors decided on a heart transplant. On October 1, 2024, he received a new heart from a donor. The surgery involved opening the chest, removing the damaged heart tissue, and connecting the new heart to the major blood vessels. The procedure was successful, and the new heart began working properly. After surgery, he received medicines to prevent his body from rejecting the new heart and to fight infection. His recovery was good, and by October 20, 2024, his heart function was normal, with no signs of problems. He is now doing well and has been followed up regularly since discharge.\"\n}", "generated_text": "A 35-year-old man was diagnosed with heart failure caused by a rare condition called Carney syndrome. This condition leads to the growth of a non-cancerous tumor (called a cardiac myxoma) in the heart and weakens the heart muscle, leading to a condition known as dilated cardiomyopathy. Three years ago, he first had chest tightness and shortness of breath after physical activity. An ultrasound of his heart showed a tumor, and further tests confirmed Carney syndrome. He was treated with medications, but did not have surgery at the time. Over time, his symptoms worsened, and he could no longer lie down without breathing difficulty. His heart function was severely weakened (NYHA Class IV), and new tests showed both the tumor and a weakened heart. Because the heart was no longer able to pump effectively, doctors decided on a heart transplant. On October 1, 2024, he received a new heart from a donor. The surgery involved opening the chest, removing the damaged heart tissue, and connecting the new heart to the major blood vessels. The procedure was successful, and the new heart began working properly. After surgery, he received medicines to prevent his body from rejecting the new heart and to fight infection. His recovery was good, and by October 20, 2024, his heart function was normal, with no signs of problems. He is now doing well and has been followed up regularly since discharge."}
+{"row_index": 63, "doc_id": 51, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 38-year-old male presented with recurrent episodes of chest tightness and dyspnea, initially occurring post-exertion three years prior. Outpatient echocardiography revealed a left atrial echogenic mass suggestive of a cardiac myxoma, prompting hospital admission for comprehensive evaluation. Physical examination identified characteristic cutaneous pigmentation in the ears, manifesting as multiple small brown and black macules, consistent with cutaneous manifestations of Carney Complex (CNC). Abdominal computed tomography (CT) demonstrated multiple hepatic lesions and small cystic formations in the left kidney, further supporting the diagnosis. Genetic analysis revealed biallelic pathogenic mutations in both the TTN (titin) and PRKAR1A genes, confirming the diagnosis of Carney syndrome (CNC) through integration of clinical, imaging, and molecular findings. The patient underwent symptomatic management with no surgical intervention, which was voluntarily declined despite the presence of a cardiac myxoma. On September 20, 2023, he presented with worsening dyspnea, including orthopnea and paroxysmal nocturnal dyspnea, necessitating rehospitalization. Physical examination revealed jugular venous distension, leftward and inferior cardiac border displacement, irregular cardiac rhythm (auscultated as atrial fibrillation), a mitral valve murmur of intensity 2/6–3/6 at the fourth intercostal space along the left sternal border, and bilateral wet rales in the middle and lower lung zones. Palpation demonstrated hepatomegaly extending three fingers below the xiphoid process and two fingers below the costal margin, with bilateral lower limb pitting edema. Echocardiography confirmed global left ventricular (LV) dilation, with a left ventricular ejection fraction (LVEF) of 23.1% and fractional shortening (FS) of 10.9%, indicative of severe systolic dysfunction. Additional findings included moderate mitral regurgitation, dilation of the aortic sinus and pulmonary artery, and a well-defined, irregular echogenic mass measuring 54 mm × 43 mm attached to the atrial septum. Electrocardiography revealed atrial fibrillation with an average ventricular rate of 150 beats per minute and abnormal Q waves in leads V1–V3, suggesting prior myocardial injury or infarction. The clinical picture was consistent with both Carney syndrome and dilated cardiomyopathy (DCM), with concomitant cardiac myxoma. Given the progression to end-stage heart failure and the presence of a large, non-resectable myxoma, heart transplantation was deemed the optimal therapeutic strategy to address both the structural and functional cardiac deterioration. A suitable donor heart was available for immediate transplantation on October 1, 2024. The surgical procedure involved a median sternotomy with layer-by-layer dissection of the skin and subcutaneous tissues. The sternum was longitudinally opened using a saw, and bleeding was controlled with electrocoagulation and bone wax. Extracardiac exploration revealed global cardiac enlargement, with marked left ventricular dilation and diminished contractile function. The aorta and main pulmonary artery (PA) were dissected from the supravalvular region. Diseased atrial and ventricular tissues—including the right atrium, left atrium (LA), right ventricle, and left ventricle—were excised, with preservation of portions for anastomotic reconstruction. The excised mass was described as greyish-white and mucoid in consistency, consistent with a myxoma. The donor and residual recipient left atria were sutured using double continuous 3/0 Prolene sutures, with meticulous inspection for bleeding. End-to-end anastomosis of the donor ascending aorta to the recipient pulmonary artery was performed with continuous 5/0 Prolene sutures, and no significant hemorrhage was observed. The donor and recipient left atria were closed with double continuous 5/0 Prolene sutures, and the inferior vena cava of both hearts was similarly sutured with 5/0 Prolene, with multiple inspections confirming hemostasis. Following deflation of the left heart, rewarming was initiated, oxygenation was restored, the ascending aorta was unclamped, and spontaneous return to sinus rhythm was achieved. Continuous 5/0 Prolene sutures were applied to the superior vena cava of both donor and recipient, with careful inspection for bleeding. After successful discontinuation of extracorporeal circulation, venous cannulae were decannulated. Tissue specimens from the patient’s left ventricle and cardiac gray matter were collected for histopathological analysis, confirming the presence of both dilated cardiomyopathy and cardiac myxoma. Postoperatively, the patient exhibited a robust early recovery: on postoperative", "generated_text": "{\n  \"proficient_health_literacy\": \"A 38-year-old male presented with recurrent episodes of chest tightness and dyspnea, initially occurring post-exertion three years prior. Outpatient echocardiography revealed a left atrial echogenic mass suggestive of a cardiac myxoma, prompting hospital admission for comprehensive evaluation. Physical examination identified characteristic cutaneous pigmentation in the ears, manifesting as multiple small brown and black macules, consistent with cutaneous manifestations of Carney Complex (CNC). Abdominal computed tomography (CT) demonstrated multiple hepatic lesions and small cystic formations in the left kidney, further supporting the diagnosis. Genetic analysis revealed biallelic pathogenic mutations in both the TTN (titin) and PRKAR1A genes, confirming the diagnosis of Carney syndrome (CNC) through integration of clinical, imaging, and molecular findings. The patient underwent symptomatic management with no surgical intervention, which was voluntarily declined despite the presence of a cardiac myxoma. On September 20, 2023, he presented with worsening dyspnea, including orthopnea and paroxysmal nocturnal dyspnea, necessitating rehospitalization. Physical examination revealed jugular venous distension, leftward and inferior cardiac border displacement, irregular cardiac rhythm (auscultated as atrial fibrillation), a mitral valve murmur of intensity 2/6–3/6 at the fourth intercostal space along the left sternal border, and bilateral wet rales in the middle and lower lung zones. Palpation demonstrated hepatomegaly extending three fingers below the xiphoid process and two fingers below the costal margin, with bilateral lower limb pitting edema. Echocardiography confirmed global left ventricular (LV) dilation, with a left ventricular ejection fraction (LVEF) of 23.1% and fractional shortening (FS) of 10.9%, indicative of severe systolic dysfunction. Additional findings included moderate mitral regurgitation, dilation of the aortic sinus and pulmonary artery, and a well-defined, irregular echogenic mass measuring 54 mm × 43 mm attached to the atrial septum. Electrocardiography revealed atrial fibrillation with an average ventricular rate of 150 beats per minute and abnormal Q waves in leads V1–V3, suggesting prior myocardial injury or infarction. The clinical picture was consistent with both Carney syndrome and dilated cardiomyopathy (DCM), with concomitant cardiac myxoma. Given the progression to end-stage heart failure and the presence of a large, non-resectable myxoma, heart transplantation was deemed the optimal therapeutic strategy to address both the structural and functional cardiac deterioration. A suitable donor heart was available for immediate transplantation on October 1, 2024. The surgical procedure involved a median sternotomy with layer-by-layer dissection of the skin and subcutaneous tissues. The sternum was longitudinally opened using a saw, and bleeding was controlled with electrocoagulation and bone wax. Extracardiac exploration revealed global cardiac enlargement, with marked left ventricular dilation and diminished contractile function. The aorta and main pulmonary artery (PA) were dissected from the supravalvular region. Diseased atrial and ventricular tissues—including the right atrium, left atrium (LA), right ventricle, and left ventricle—were excised, with preservation of portions for anastomotic reconstruction. The excised mass was described as greyish-white and mucoid in consistency, consistent with a myxoma. The donor and residual recipient left atria were sutured using double continuous 3/0 Prolene sutures, with meticulous inspection for bleeding. End-to-end anastomosis of the donor ascending aorta to the recipient pulmonary artery was performed with continuous 5/0 Prolene sutures, and no significant hemorrhage was observed. The donor and recipient left atria were closed with double continuous 5/0 Prolene sutures, and the inferior vena cava of both hearts was similarly sutured with 5/0 Prolene, with multiple inspections confirming hemostasis. Following deflation of the left heart, rewarming was initiated, oxygenation was restored, the ascending aorta was unclamped, and spontaneous return to sinus rhythm was achieved. Continuous 5/0 Prolene sutures were applied to the superior vena cava of both donor and recipient, with careful inspection for bleeding. After successful discontinuation of extracorporeal circulation, venous cannulae were decannulated. Tissue specimens from the patient’s left ventricle and cardiac gray matter were collected for histopathological analysis, confirming the presence of both dilated cardiomyopathy and cardiac myxoma. Postoperatively, the patient exhibited a robust early recovery: on postoperative"}
+{"row_index": 64, "doc_id": 52, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 2.5-year-old girl with a known condition called NF1 has been having diarrhea with blood in it for several weeks. The doctor looked inside her colon with a special tool and saw red, swollen lining from the bottom of the rectum all the way to the start of the colon. A small tissue sample showed long-term inflammation, and tests found a virus called CMV that was causing the problem. This combination of red lining and virus infection means she has a type of chronic colitis, similar to ulcerative colitis. She is being treated with medicine to reduce inflammation and is still having some symptoms, but they are getting better.\"\n}", "generated_text": "A 2.5-year-old girl with a known condition called NF1 has been having diarrhea with blood in it for several weeks. The doctor looked inside her colon with a special tool and saw red, swollen lining from the bottom of the rectum all the way to the start of the colon. A small tissue sample showed long-term inflammation, and tests found a virus called CMV that was causing the problem. This combination of red lining and virus infection means she has a type of chronic colitis, similar to ulcerative colitis. She is being treated with medicine to reduce inflammation and is still having some symptoms, but they are getting better."}
+{"row_index": 65, "doc_id": 52, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 2-year-6-month-old female pre-schooler with a prior diagnosis of neurofibromatosis type 1 (NF1), confirmed by genetic testing at 8 months of age via detection of a heterozygous pathogenic variant c.5606_5627del (p.Gly1869Valfs*28), presented with a 4-week history of bloody diarrhea, with 5 to 10 episodes of blood-streaked stools per day. Initial evaluation in the emergency department revealed rotavirus infection (positive), with normal inflammatory markers, negative coproculture, and normal abdominal ultrasound. The patient was hospitalized for 3 days to manage dehydration and discharged without active bleeding, though persistent semi-liquid stools remained. Ten days post-discharge, she developed recurrent bloody diarrhea associated with reduced oral intake and a 1 kg weight loss, prompting referral to a pediatric gastroenterologist. A polymerase chain reaction (PCR) panel for gastrointestinal pathogens and PCR for Clostridium difficile were both negative, leading to hospitalization for further investigation.\\n\\nThe clinical history was non-specific for systemic infection: no fever, abdominal pain, vomiting, respiratory or urinary symptoms, arthralgia, or new skin lesions were reported. No pet exposure, recent travel, or dietary changes were noted. The patient has documented skin manifestations (café au lait spots) and bone involvement (requiring ankle arthrodesis at 18 months due to tibial curvature), with no family history of NF1 or inflammatory bowel disease (IBD).\\n\\nPhysical examination revealed a soft, non-distended abdomen with increased air-bubble murmurs, no masses or visceral enlargement. Perianal examination was normal. Multiple brown-coffee-colored stains were observed on the lower extremities and back, consistent with café au lait spots. Laboratory findings included moderate microcytic-hypochromic anemia (Hb 9.6 g/dL), leukocytosis with left shift (leukocytes 13,900), and mildly elevated inflammatory markers (CRP 1.37 mg/dL, above the normal threshold of ≤0.5 mg/dL).\\n\\nColonoscopy was performed from the anal margin to the cecum, including inspection of the ileocecal valve and appendicular orifice, with the distal ileum also evaluated. The mucosa from the anal margin to the cecum demonstrated erythema and loss of vascular transparency, a feature not observed in the cecal mucosa, which appeared normal. No focal lesions were identified in the anal canal or cecum.\\n\\nHistopathological analysis of biopsies revealed preserved villous architecture and adequate epithelial differentiation in the ileal mucosa with a non-inflamed lamina propria. In the colonic mucosa, there was mild architectural distortion, preserved epithelial differentiation, a swollen lamina propria with a mild mixed inflammatory infiltrate, and hyperplasia of reactive lymphoid follicles. Isolated microabscesses were identified, consistent with a diagnosis of mild chronic colitis. A PCR assay for cytomegalovirus (CMV) on colonic biopsy was positive. Additional serological testing confirmed positive CMV IgG, negative IgM, and a blood viral load of 79.7 IU/mL, supporting active, recent CMV viremia. Stool PCR for gastrointestinal pathogens and C. difficile were negative. Gram stain of the biopsy showed +++ leukocytes without bacterial presence; culture yielded low-level growth of S. gallolyticus/equinus complex, interpreted as normal commensal flora; acridine orange, Ziehl-Neelsen, Koch culture, and adenovirus PCR were all negative.\\n\\nEndoscopic and histological findings were consistent with ulcerative colitis (UC), with moderate clinical activity (PUCAI score of 50). The patient was initiated on mesalazine (70 mg/kg/day, three times daily), and fecal calprotectin was measured, yielding a value >600 µg/g, confirming active intestinal inflammation. An immunological workup was conducted to evaluate for potential immunodeficiency: lymphocyte subpopulations, immunoglobulin levels, HIV status, memory T-cell populations (showing expected alterations in the context of CMV viremia), and lymphoproliferation test were all within normal limits. A comprehensive genetic panel for primary immunodeficiencies (Invitae, comprising 429 genes, including 68 associated with monogenic inflammatory intestinal disease) was performed, yielding seven variants of uncertain significance, none of which were classified within the monogenic IBD panel.\\n\\nThe patient was treated with intravenous ganciclovir for CMV infection, administered for 15 days, with subsequent PCR monitoring showing undetectable viral load prior to discharge. Clinical", "generated_text": "{\n  \"proficient_health_literacy\": \"A 2-year-6-month-old female pre-schooler with a prior diagnosis of neurofibromatosis type 1 (NF1), confirmed by genetic testing at 8 months of age via detection of a heterozygous pathogenic variant c.5606_5627del (p.Gly1869Valfs*28), presented with a 4-week history of bloody diarrhea, with 5 to 10 episodes of blood-streaked stools per day. Initial evaluation in the emergency department revealed rotavirus infection (positive), with normal inflammatory markers, negative coproculture, and normal abdominal ultrasound. The patient was hospitalized for 3 days to manage dehydration and discharged without active bleeding, though persistent semi-liquid stools remained. Ten days post-discharge, she developed recurrent bloody diarrhea associated with reduced oral intake and a 1 kg weight loss, prompting referral to a pediatric gastroenterologist. A polymerase chain reaction (PCR) panel for gastrointestinal pathogens and PCR for Clostridium difficile were both negative, leading to hospitalization for further investigation.\\n\\nThe clinical history was non-specific for systemic infection: no fever, abdominal pain, vomiting, respiratory or urinary symptoms, arthralgia, or new skin lesions were reported. No pet exposure, recent travel, or dietary changes were noted. The patient has documented skin manifestations (café au lait spots) and bone involvement (requiring ankle arthrodesis at 18 months due to tibial curvature), with no family history of NF1 or inflammatory bowel disease (IBD).\\n\\nPhysical examination revealed a soft, non-distended abdomen with increased air-bubble murmurs, no masses or visceral enlargement. Perianal examination was normal. Multiple brown-coffee-colored stains were observed on the lower extremities and back, consistent with café au lait spots. Laboratory findings included moderate microcytic-hypochromic anemia (Hb 9.6 g/dL), leukocytosis with left shift (leukocytes 13,900), and mildly elevated inflammatory markers (CRP 1.37 mg/dL, above the normal threshold of ≤0.5 mg/dL).\\n\\nColonoscopy was performed from the anal margin to the cecum, including inspection of the ileocecal valve and appendicular orifice, with the distal ileum also evaluated. The mucosa from the anal margin to the cecum demonstrated erythema and loss of vascular transparency, a feature not observed in the cecal mucosa, which appeared normal. No focal lesions were identified in the anal canal or cecum.\\n\\nHistopathological analysis of biopsies revealed preserved villous architecture and adequate epithelial differentiation in the ileal mucosa with a non-inflamed lamina propria. In the colonic mucosa, there was mild architectural distortion, preserved epithelial differentiation, a swollen lamina propria with a mild mixed inflammatory infiltrate, and hyperplasia of reactive lymphoid follicles. Isolated microabscesses were identified, consistent with a diagnosis of mild chronic colitis. A PCR assay for cytomegalovirus (CMV) on colonic biopsy was positive. Additional serological testing confirmed positive CMV IgG, negative IgM, and a blood viral load of 79.7 IU/mL, supporting active, recent CMV viremia. Stool PCR for gastrointestinal pathogens and C. difficile were negative. Gram stain of the biopsy showed +++ leukocytes without bacterial presence; culture yielded low-level growth of S. gallolyticus/equinus complex, interpreted as normal commensal flora; acridine orange, Ziehl-Neelsen, Koch culture, and adenovirus PCR were all negative.\\n\\nEndoscopic and histological findings were consistent with ulcerative colitis (UC), with moderate clinical activity (PUCAI score of 50). The patient was initiated on mesalazine (70 mg/kg/day, three times daily), and fecal calprotectin was measured, yielding a value >600 µg/g, confirming active intestinal inflammation. An immunological workup was conducted to evaluate for potential immunodeficiency: lymphocyte subpopulations, immunoglobulin levels, HIV status, memory T-cell populations (showing expected alterations in the context of CMV viremia), and lymphoproliferation test were all within normal limits. A comprehensive genetic panel for primary immunodeficiencies (Invitae, comprising 429 genes, including 68 associated with monogenic inflammatory intestinal disease) was performed, yielding seven variants of uncertain significance, none of which were classified within the monogenic IBD panel.\\n\\nThe patient was treated with intravenous ganciclovir for CMV infection, administered for 15 days, with subsequent PCR monitoring showing undetectable viral load prior to discharge. Clinical"}
+{"row_index": 66, "doc_id": 53, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 40-year-old HIV-positive male with sustained antiretroviral therapy adherence—documented viral load of 4500 copies/mm³ and CD4 count of 70/mm³ from the prior year—presented with a two-year history of intermittent febrile episodes that lacked a consistent temporal pattern and responded only transiently to non-steroidal anti-inflammatory drugs (NSAIDs). Over the preceding two months, he developed progressive diffuse abdominal pain, with a predominant localization in the upper right quadrant, accompanied by the emergence of a tree-in-bud pulmonary opacification pattern on imaging and bilateral pleural effusions. Abdominal imaging revealed marked hepatosplenomegaly and ascites. Laboratory evaluation demonstrated pancytopenia, coagulopathy, hypoalbuminemia, and elevated acute-phase reactants, indicative of systemic inflammation. Computed tomography (CT) of the thorax, abdomen, and pelvis confirmed generalized lymphadenopathy, hepatosplenomegaly, and the pulmonary tree-in-bud pattern. Multiple microbiological investigations were conducted, including culture-based detection of Mycobacterium species from various specimens, all of which were negative, except for a positive result via RT-PCR for Human Herpesvirus 8 (HHV-8). A left iliac ganglion biopsy was performed, yielding histopathological findings consistent with multicentric Castleman’s disease, a lymphoproliferative disorder characterized by abnormal proliferation of lymphoid tissue and cytokine overproduction, particularly interleukin-6. Despite re-initiation of antiretroviral therapy, clinical deterioration progressed, necessitating the administration of corticosteroids and ganciclovir to address potential HHV-8-driven immune activation. However, within one week, the patient developed multi-organ failure and anasarca, rendering further pharmacologic intervention contraindicated. A repeat chest CT demonstrated worsening pulmonary infiltrates with persistent tree-in-bud morphology and progressive hepato-splenomegaly and ascites. He was transferred to the intensive care unit (ICU) 48 hours after symptom onset, where he rapidly deteriorated and succumbed to fulminant hepatic failure within hours. Postmortem analysis of a tracheal aspirate culture yielded a positive identification of Mycobacterium tuberculosis, confirming latent or active pulmonary tuberculosis as a contributing pathogen. Additionally, a percutaneous liver biopsy revealed non-necrotizing granulomas, consistent with a tuberculous etiology, while the parenchymal architecture remained largely preserved, suggesting a chronic, non-destructive inflammatory process. This case highlights the clinical complexity of HIV-associated lymphoproliferative disorders, particularly Castleman’s disease, in the context of overlapping opportunistic infections and immune dysregulation, and underscores the importance of timely microbiological diagnostics and immune reconstitution in such patients. The study was conducted in accordance with the ethical principles outlined in the World Health Organization’s Declaration of Helsinki.\"\n}", "generated_text": "A 40-year-old HIV-positive male with sustained antiretroviral therapy adherence—documented viral load of 4500 copies/mm³ and CD4 count of 70/mm³ from the prior year—presented with a two-year history of intermittent febrile episodes that lacked a consistent temporal pattern and responded only transiently to non-steroidal anti-inflammatory drugs (NSAIDs). Over the preceding two months, he developed progressive diffuse abdominal pain, with a predominant localization in the upper right quadrant, accompanied by the emergence of a tree-in-bud pulmonary opacification pattern on imaging and bilateral pleural effusions. Abdominal imaging revealed marked hepatosplenomegaly and ascites. Laboratory evaluation demonstrated pancytopenia, coagulopathy, hypoalbuminemia, and elevated acute-phase reactants, indicative of systemic inflammation. Computed tomography (CT) of the thorax, abdomen, and pelvis confirmed generalized lymphadenopathy, hepatosplenomegaly, and the pulmonary tree-in-bud pattern. Multiple microbiological investigations were conducted, including culture-based detection of Mycobacterium species from various specimens, all of which were negative, except for a positive result via RT-PCR for Human Herpesvirus 8 (HHV-8). A left iliac ganglion biopsy was performed, yielding histopathological findings consistent with multicentric Castleman’s disease, a lymphoproliferative disorder characterized by abnormal proliferation of lymphoid tissue and cytokine overproduction, particularly interleukin-6. Despite re-initiation of antiretroviral therapy, clinical deterioration progressed, necessitating the administration of corticosteroids and ganciclovir to address potential HHV-8-driven immune activation. However, within one week, the patient developed multi-organ failure and anasarca, rendering further pharmacologic intervention contraindicated. A repeat chest CT demonstrated worsening pulmonary infiltrates with persistent tree-in-bud morphology and progressive hepato-splenomegaly and ascites. He was transferred to the intensive care unit (ICU) 48 hours after symptom onset, where he rapidly deteriorated and succumbed to fulminant hepatic failure within hours. Postmortem analysis of a tracheal aspirate culture yielded a positive identification of Mycobacterium tuberculosis, confirming latent or active pulmonary tuberculosis as a contributing pathogen. Additionally, a percutaneous liver biopsy revealed non-necrotizing granulomas, consistent with a tuberculous etiology, while the parenchymal architecture remained largely preserved, suggesting a chronic, non-destructive inflammatory process. This case highlights the clinical complexity of HIV-associated lymphoproliferative disorders, particularly Castleman’s disease, in the context of overlapping opportunistic infections and immune dysregulation, and underscores the importance of timely microbiological diagnostics and immune reconstitution in such patients. The study was conducted in accordance with the ethical principles outlined in the World Health Organization’s Declaration of Helsinki."}
+{"row_index": 67, "doc_id": 54, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 4-month-old indigenous lactating infant from the rural interior of Panama, specifically from Urracá, approximately 3 hours by canoe from the nearest health subcenter, presented with acute diarrhea and moderate-severe dehydration due to protein-caloric malnutrition. The infant was the fourth daughter, born via vaginal home delivery by a relative without prenatal care; birth weight, height, and Apgar score are unknown. The infant did not receive breast milk and was exclusively fed powdered milk formula with iron (3 ounces every 4 hours), which is inconsistent with recommended infant feeding guidelines for infants under 6 months of age. The household consisted of six members (parents and four children), living in a two-room structure with board walls and palm roof, lacking electricity and relying on kerosene lamps for illumination, well water for hydration, open defecation in a river, and open burning of waste. Household economic activity was based on subsistence agriculture, and the infant received no vaccinations as part of the national expanded programme of immunization. Parents reported normal neurodevelopment prior to hospitalization.\\n\\nThe infant presented to a primary health center with a 4-day history of diarrhea without mucus or blood, accompanied by vomiting of food content; the mother substituted milk with tea due to intolerance. The infant was afebrile and without respiratory symptoms. Initial management included oral rehydration with lactate Ringer's solution (10 ml/kg) and four doses of Enterogermina® (2 billion spores/5 mL), a probiotic containing *Bacillus clausii*. Due to lack of intravenous access (no catheters or intraosseous access), the infant was transferred to a second-level hospital in the provincial capital and subsequently to a tertiary care facility in Panama City, diagnosed with acute gastroenteritis and severe dehydration.\\n\\nOn emergency department admission, the infant exhibited signs of consciousness compromise, profound dehydration (tearless cry, dry oral mucosa), and signs of shock: capillary refill time >2 seconds, cold extremities, filiform pulse, marble skin, heart rate 170 bpm, respiratory rate 55 bpm, blood pressure 91/37 mmHg, oxygen saturation 99%. Physical examination revealed +++ edema in hands, feet, abdomen, and face. Anthropometric data: weight 4.7 kg, height 56 cm; height/age Z-score of -2.52, with unquantifiable weight/height and weight/age Z-scores due to severe dehydration. Segmental examination revealed fine crepitus in both lung bases suggestive of pulmonary interstitial involvement, and erythematous-squamous skin lesions with desquamation, as well as hypopigmented patches on trunk and upper limbs, interpreted as pellagroid dermatosis, likely secondary to vitamin B3 deficiency.\\n\\nInitial resuscitation included lactate Ringer's bolus (10 ml/kg), followed by 5% dextrose in 0.33% saline (500 mL) infused at 29 mL/h over 6 hours without KCL until diuresis was achieved. Empirical antibiotic therapy was initiated with ceftriaxone 50 mg/kg/day for suspected sepsis. After stabilization, the patient was transferred to the ward and maintained on 500 mL of 5% dextrose in 0.9% saline at 20 mL/h. Laboratory findings included leukocytosis (39.0 × 10³/μL), severe anemia (5.6 g/dL), and thrombocytosis (502 × 10³/μL). The patient received a transfusion of 50 mL of filtered, leuko-reduced red blood cells and 40 cc of fresh frozen plasma due to coagulopathy. Enteral feeding was initiated via nasogastric tube, and fluid infusion was reduced to 15 mL/h of 5% dextrose in 0.9% saline (500 mL), with a negative water balance maintained.\\n\\nOn day 2, initial peripheral blood culture yielded Gram-positive cocci in clusters, interpreted as *Staphylococcus aureus*. Oxacillin was administered at 200 mg/kg/day, and ceftriaxone was escalated to 75–100 mg/kg/day. Total fluid replacement was increased to 120 mL/kg/day, and calcium was corrected (to 6.38 mg/dL). On day 3, venous access was lost, necessitating placement of a central venous catheter (CVC). The patient remained hypovolemic with subhydrated oral mucosa, increased respiratory effort, cold extremities, and capillary refill time of 3–4 seconds. A rapid Ringer's lactate infusion (", "generated_text": "{\n  \"proficient_health_literacy\": \"A 4-month-old indigenous lactating infant from the rural interior of Panama, specifically from Urracá, approximately 3 hours by canoe from the nearest health subcenter, presented with acute diarrhea and moderate-severe dehydration due to protein-caloric malnutrition. The infant was the fourth daughter, born via vaginal home delivery by a relative without prenatal care; birth weight, height, and Apgar score are unknown. The infant did not receive breast milk and was exclusively fed powdered milk formula with iron (3 ounces every 4 hours), which is inconsistent with recommended infant feeding guidelines for infants under 6 months of age. The household consisted of six members (parents and four children), living in a two-room structure with board walls and palm roof, lacking electricity and relying on kerosene lamps for illumination, well water for hydration, open defecation in a river, and open burning of waste. Household economic activity was based on subsistence agriculture, and the infant received no vaccinations as part of the national expanded programme of immunization. Parents reported normal neurodevelopment prior to hospitalization.\\n\\nThe infant presented to a primary health center with a 4-day history of diarrhea without mucus or blood, accompanied by vomiting of food content; the mother substituted milk with tea due to intolerance. The infant was afebrile and without respiratory symptoms. Initial management included oral rehydration with lactate Ringer's solution (10 ml/kg) and four doses of Enterogermina® (2 billion spores/5 mL), a probiotic containing *Bacillus clausii*. Due to lack of intravenous access (no catheters or intraosseous access), the infant was transferred to a second-level hospital in the provincial capital and subsequently to a tertiary care facility in Panama City, diagnosed with acute gastroenteritis and severe dehydration.\\n\\nOn emergency department admission, the infant exhibited signs of consciousness compromise, profound dehydration (tearless cry, dry oral mucosa), and signs of shock: capillary refill time >2 seconds, cold extremities, filiform pulse, marble skin, heart rate 170 bpm, respiratory rate 55 bpm, blood pressure 91/37 mmHg, oxygen saturation 99%. Physical examination revealed +++ edema in hands, feet, abdomen, and face. Anthropometric data: weight 4.7 kg, height 56 cm; height/age Z-score of -2.52, with unquantifiable weight/height and weight/age Z-scores due to severe dehydration. Segmental examination revealed fine crepitus in both lung bases suggestive of pulmonary interstitial involvement, and erythematous-squamous skin lesions with desquamation, as well as hypopigmented patches on trunk and upper limbs, interpreted as pellagroid dermatosis, likely secondary to vitamin B3 deficiency.\\n\\nInitial resuscitation included lactate Ringer's bolus (10 ml/kg), followed by 5% dextrose in 0.33% saline (500 mL) infused at 29 mL/h over 6 hours without KCL until diuresis was achieved. Empirical antibiotic therapy was initiated with ceftriaxone 50 mg/kg/day for suspected sepsis. After stabilization, the patient was transferred to the ward and maintained on 500 mL of 5% dextrose in 0.9% saline at 20 mL/h. Laboratory findings included leukocytosis (39.0 × 10³/μL), severe anemia (5.6 g/dL), and thrombocytosis (502 × 10³/μL). The patient received a transfusion of 50 mL of filtered, leuko-reduced red blood cells and 40 cc of fresh frozen plasma due to coagulopathy. Enteral feeding was initiated via nasogastric tube, and fluid infusion was reduced to 15 mL/h of 5% dextrose in 0.9% saline (500 mL), with a negative water balance maintained.\\n\\nOn day 2, initial peripheral blood culture yielded Gram-positive cocci in clusters, interpreted as *Staphylococcus aureus*. Oxacillin was administered at 200 mg/kg/day, and ceftriaxone was escalated to 75–100 mg/kg/day. Total fluid replacement was increased to 120 mL/kg/day, and calcium was corrected (to 6.38 mg/dL). On day 3, venous access was lost, necessitating placement of a central venous catheter (CVC). The patient remained hypovolemic with subhydrated oral mucosa, increased respiratory effort, cold extremities, and capillary refill time of 3–4 seconds. A rapid Ringer's lactate infusion ("}
+{"row_index": 68, "doc_id": 55, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 2-year-old girl had a big lump inside her eye socket that made her eye stick out and move inward and upward. The lump was soft, not painful, and grew slowly over a year. Doctors saw it on a scan and found it was a type of tumor called a teratoma. They removed it through a small cut in the lower eyelid, and during surgery, they saw parts of brain, skin, and cartilage inside the lump. After the surgery, the child’s eye started to sink back in (enophthalmos), her eyelid became red, and her cornea got inflamed because the space in her eye was too small. To fix this, doctors placed a piece of donor eye tissue (sclera) into the socket to fill the space and help the eye sit properly again. One year later, the tumor didn’t come back, and her eye looked better. She still has a little bit of eye sinking and a small eyelid issue, but her vision is the same as before. The eye is now stable and no other problems were seen.\"\n}", "generated_text": "A 2-year-old girl had a big lump inside her eye socket that made her eye stick out and move inward and upward. The lump was soft, not painful, and grew slowly over a year. Doctors saw it on a scan and found it was a type of tumor called a teratoma. They removed it through a small cut in the lower eyelid, and during surgery, they saw parts of brain, skin, and cartilage inside the lump. After the surgery, the child’s eye started to sink back in (enophthalmos), her eyelid became red, and her cornea got inflamed because the space in her eye was too small. To fix this, doctors placed a piece of donor eye tissue (sclera) into the socket to fill the space and help the eye sit properly again. One year later, the tumor didn’t come back, and her eye looked better. She still has a little bit of eye sinking and a small eyelid issue, but her vision is the same as before. The eye is now stable and no other problems were seen."}
+{"row_index": 69, "doc_id": 55, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 2-year-old female presented with a 1-year history of painless, progressive left-sided proptosis, without systemic comorbidities or familial predisposition. Ophthalmologic evaluation revealed preserved light perception as the sole visual input in the left eye, accompanied by marked proptosis, inward and upward displacement of the globe, and restricted downward and outward extraocular muscle movements. A palpable, irregularly shaped, well-circumscribed soft mass was identified in the inferior left orbit, associated with left lower eyelid ectropion. The pupil measured 4 mm in diameter and exhibited absent pupillary reaction. Anterior segment examination was otherwise unremarkable, though fundus assessment was compromised due to the child’s small size. Hertel exophthalmometry demonstrated a right eye measurement of 10.5 mm and a left eye measurement of 18 mm, indicating significant orbital expansion. Magnetic resonance imaging (MRI) revealed a well-defined orbital mass with hypointense signal intensity on T1-weighted images (T1WI) and hyperintense signal intensity on T2-weighted images (T2WI), consistent with a cystic or mixed tissue composition. Contrast-enhanced MRI showed no significant enhancement, suggesting a non-vascularized or low-vascularity lesion. A transconjunctival approach via the inferior fornix was employed, with concomitant canthotomy and cantholysis to facilitate access. Surgical exploration revealed a grayish-white, cystic mass with a distinct interface from surrounding orbital tissues. Posterior dissection encountered tight adhesion between the mass and the optic nerve, indicating prior extensive orbital expansion and tissue deformation. Given the substantial size of the lesion and limited surgical field, volume reduction was necessary; approximately 12.5 mL of intralesional fluid was aspirated prior to complete excision. Histopathological analysis confirmed a fibrous capsule lined with squamous and glandular epithelium, with the presence of brain-derived tissue and a cartilaginous matrix, pathologically consistent with an orbital teratoma. One month postoperatively, the patient developed enophthalmos, conjunctival hyperemia, and keratitis. This sequelae was attributed to the preoperative orbital cavity enlargement, leading to postoperative orbital volume collapse and corneal exposure, resulting in inflammation due to inadequate eyelid coverage. With informed consent from the patient’s guardian, a second surgical intervention was performed involving the implantation of allogeneic sclera into the orbital cavity to restore orbital volume, correct fossal pitting, and re-establish corneal apposition. Follow-up over one year demonstrated no recurrence of teratoma or other complications. Persistent minor enophthalmos and outer canthus deformity remained, though visual acuity remained unchanged from preoperative levels. Repeat Hertel exophthalmometry showed a right eye measurement of 10.5 mm and a left eye measurement of 8 mm, indicating partial correction of proptosis. The anterior segment remained clinically stable, with no evidence of recurrent inflammation or structural compromise. The findings support the diagnosis of a complex orbital teratoma with significant orbital expansion, and highlight the importance of surgical volume management and postoperative orbital reconstruction in pediatric cases with large, adherent teratoma masses.\"\n}", "generated_text": "A 2-year-old female presented with a 1-year history of painless, progressive left-sided proptosis, without systemic comorbidities or familial predisposition. Ophthalmologic evaluation revealed preserved light perception as the sole visual input in the left eye, accompanied by marked proptosis, inward and upward displacement of the globe, and restricted downward and outward extraocular muscle movements. A palpable, irregularly shaped, well-circumscribed soft mass was identified in the inferior left orbit, associated with left lower eyelid ectropion. The pupil measured 4 mm in diameter and exhibited absent pupillary reaction. Anterior segment examination was otherwise unremarkable, though fundus assessment was compromised due to the child’s small size. Hertel exophthalmometry demonstrated a right eye measurement of 10.5 mm and a left eye measurement of 18 mm, indicating significant orbital expansion. Magnetic resonance imaging (MRI) revealed a well-defined orbital mass with hypointense signal intensity on T1-weighted images (T1WI) and hyperintense signal intensity on T2-weighted images (T2WI), consistent with a cystic or mixed tissue composition. Contrast-enhanced MRI showed no significant enhancement, suggesting a non-vascularized or low-vascularity lesion. A transconjunctival approach via the inferior fornix was employed, with concomitant canthotomy and cantholysis to facilitate access. Surgical exploration revealed a grayish-white, cystic mass with a distinct interface from surrounding orbital tissues. Posterior dissection encountered tight adhesion between the mass and the optic nerve, indicating prior extensive orbital expansion and tissue deformation. Given the substantial size of the lesion and limited surgical field, volume reduction was necessary; approximately 12.5 mL of intralesional fluid was aspirated prior to complete excision. Histopathological analysis confirmed a fibrous capsule lined with squamous and glandular epithelium, with the presence of brain-derived tissue and a cartilaginous matrix, pathologically consistent with an orbital teratoma. One month postoperatively, the patient developed enophthalmos, conjunctival hyperemia, and keratitis. This sequelae was attributed to the preoperative orbital cavity enlargement, leading to postoperative orbital volume collapse and corneal exposure, resulting in inflammation due to inadequate eyelid coverage. With informed consent from the patient’s guardian, a second surgical intervention was performed involving the implantation of allogeneic sclera into the orbital cavity to restore orbital volume, correct fossal pitting, and re-establish corneal apposition. Follow-up over one year demonstrated no recurrence of teratoma or other complications. Persistent minor enophthalmos and outer canthus deformity remained, though visual acuity remained unchanged from preoperative levels. Repeat Hertel exophthalmometry showed a right eye measurement of 10.5 mm and a left eye measurement of 8 mm, indicating partial correction of proptosis. The anterior segment remained clinically stable, with no evidence of recurrent inflammation or structural compromise. The findings support the diagnosis of a complex orbital teratoma with significant orbital expansion, and highlight the importance of surgical volume management and postoperative orbital reconstruction in pediatric cases with large, adherent teratoma masses."}
+{"row_index": 70, "doc_id": 56, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 78-year-old woman was feeling very tired, weak, dizzy, and confused for months. This made it hard for her to leave her house or walk around. She was taking many medicines, and one of the problems might have been her blood pressure medicines. Her kidneys weren’t working as well as they should, which means her body can’t clear some medicines as easily. The doctors checked her kidney function and found it was low. Based on this, they decided to lower the dose of two blood pressure medicines — losartan and manidipine — so her blood pressure wouldn’t go too low. They also switched her pain medicine from pregabalin to gabapentin, which is safer for her kidneys. After two months, her tiredness, dizziness, and confusion went away. Her blood pressure improved, and she felt much better.\"\n}", "generated_text": "A 78-year-old woman was feeling very tired, weak, dizzy, and confused for months. This made it hard for her to leave her house or walk around. She was taking many medicines, and one of the problems might have been her blood pressure medicines. Her kidneys weren’t working as well as they should, which means her body can’t clear some medicines as easily. The doctors checked her kidney function and found it was low. Based on this, they decided to lower the dose of two blood pressure medicines — losartan and manidipine — so her blood pressure wouldn’t go too low. They also switched her pain medicine from pregabalin to gabapentin, which is safer for her kidneys. After two months, her tiredness, dizziness, and confusion went away. Her blood pressure improved, and she felt much better."}
+{"row_index": 71, "doc_id": 56, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 78-year-old woman who was taking several medications reported feeling tired, weak, dizzy, and confused for months. These symptoms were making it hard for her to leave her home. She was evaluated at a community pharmacy as part of a personalized medication program. The team checked her medications, especially those processed by the kidneys, using her estimated glomerular filtration rate (eGFR), which was 30 ml/min/1.73 m² — a sign of reduced kidney function. Based on this, they found that her doses of losartan and manidipine, which are blood pressure medicines, needed to be lowered to prevent low blood pressure. The pharmacy sent a report to her primary care doctor, who agreed to reduce losartan to 50 mg per day and manidipine to 10 mg per day. The doctor also switched her pregabalin to gabapentin, which is safer for her kidney function. After two months of follow-up, her blood pressure improved, and the symptoms of tiredness, weakness, dizziness, and confusion went away. The change in medication was successful and her condition stabilized.\"\n}", "generated_text": "A 78-year-old woman who was taking several medications reported feeling tired, weak, dizzy, and confused for months. These symptoms were making it hard for her to leave her home. She was evaluated at a community pharmacy as part of a personalized medication program. The team checked her medications, especially those processed by the kidneys, using her estimated glomerular filtration rate (eGFR), which was 30 ml/min/1.73 m² — a sign of reduced kidney function. Based on this, they found that her doses of losartan and manidipine, which are blood pressure medicines, needed to be lowered to prevent low blood pressure. The pharmacy sent a report to her primary care doctor, who agreed to reduce losartan to 50 mg per day and manidipine to 10 mg per day. The doctor also switched her pregabalin to gabapentin, which is safer for her kidney function. After two months of follow-up, her blood pressure improved, and the symptoms of tiredness, weakness, dizziness, and confusion went away. The change in medication was successful and her condition stabilized."}
+{"row_index": 72, "doc_id": 56, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 78-year-old female patient, enrolled in a Personalised Medication Dosage System (PDS), presented with persistent symptoms of fatigue, weakness, dizziness, and confusion over several months, significantly impairing her ability to perform ambulatory activities. Upon clinical evaluation, she was referred to a personalised care setting to assess medication knowledge, adherence, and potential drug-related adverse effects. A comprehensive medication review was conducted, with particular focus on pharmacokinetic parameters relevant to renal function, specifically the estimated glomerular filtration rate (eGFR), calculated using the Chronic Kidney Disease-Epidemiology Collaboration (CKD-EPI) formula, which yielded an eGFR of 30 ml/min/1.73 m²—indicative of stage 3 chronic kidney disease (CKD).\\n\\nThe patient's pharmacological regimen includes multiple agents: doxazosin (2 mg/24 h), losartan (100 mg/24 h), manidipine (20 mg/24 h), simvastatin (40 mg/24 h), acetylsalicylic acid (100 mg/24 h), omeprazole (20 mg/24 h), pregabalin (100 mg/12 h), torasemide (10 mg/24 h), dulaglutide (1.5 mg/week), insulin glargine (74 IU/24 h), insulin lispro (20 IU/24 h), and brimonidine (1 drop/12 h). Among these, losartan, manidipine, torasemide, and pregabalin were identified as agents requiring dose adjustment in the context of impaired renal function due to altered pharmacokinetics—specifically, reduced clearance via the kidneys.\\n\\nLosartan, an angiotensin II receptor blocker (ARB), and manidipine, a dihydropyridine calcium channel blocker (DCCB), are primarily eliminated by renal excretion. In patients with eGFR <60 ml/min/1.73 m², their clearance is diminished, increasing the risk of accumulation and adverse effects, including hypotension. According to product monographs and the consensus guidelines developed by the University of Barcelona Faculty of Pharmacy’s practical pharmacy teaching and research group—based on real-world dispensing data and ATC-based therapeutic categorisation—dose reductions are recommended: for losartan, a reduction to 50–75% of the original dose (i.e., 50 mg/24 h) is advised when eGFR ranges from 30 to 59 ml/min/1.73 m²; for manidipine, the recommended dose is adjusted to 10 mg/24 h when eGFR is between 15 and 30 ml/min/1.73 m². These adjustments are grounded in pharmacodynamic and pharmacokinetic evidence showing dose-dependent hypotensive effects in renal impairment.\\n\\nTorasemide, a loop diuretic, also influences blood pressure regulation and may contribute to hypotension when used in patients with reduced renal function due to decreased volume excretion and potential for electrolyte imbalance. Pregabalin, used for neuropathic pain, is metabolised via hepatic pathways but may exhibit increased systemic exposure in renal impairment due to secondary effects on clearance; however, its primary route of elimination is hepatic, and thus, dose adjustment is less critical in this context, though monitoring is advised.\\n\\nAn initial intervention was proposed, recommending a reduction of losartan to 50 mg/24 h and manidipine to 10 mg/24 h, with the option to evaluate pregabalin dose modification post-adjustment of antihypertensives. The patient was informed of the rationale, and a detailed report was submitted to her Primary Care Physician (PCP), outlining the pharmacological basis for the proposed changes. The PCP implemented the recommended dose reductions and substituted pregabalin 100 mg/12 h with gabapentin 300 mg/12 h, a non-narcotic alternative with a more favorable renal clearance profile.\\n\\nA two-month follow-up demonstrated significant clinical improvement: blood pressure values normalized (systolic 128–135 mmHg, diastolic 75–80 mmHg), and the patient reported complete resolution of fatigue, dizziness, and confusion. The gabapentin dose of 300 mg/12 h was confirmed to be within the recommended range for eGFR 30–60 ml/min/1.73 m² (total daily dose: 300–900 mg), indicating appropriate dosing without risk", "generated_text": "{\n  \"proficient_health_literacy\": \"A 78-year-old female patient, enrolled in a Personalised Medication Dosage System (PDS), presented with persistent symptoms of fatigue, weakness, dizziness, and confusion over several months, significantly impairing her ability to perform ambulatory activities. Upon clinical evaluation, she was referred to a personalised care setting to assess medication knowledge, adherence, and potential drug-related adverse effects. A comprehensive medication review was conducted, with particular focus on pharmacokinetic parameters relevant to renal function, specifically the estimated glomerular filtration rate (eGFR), calculated using the Chronic Kidney Disease-Epidemiology Collaboration (CKD-EPI) formula, which yielded an eGFR of 30 ml/min/1.73 m²—indicative of stage 3 chronic kidney disease (CKD).\\n\\nThe patient's pharmacological regimen includes multiple agents: doxazosin (2 mg/24 h), losartan (100 mg/24 h), manidipine (20 mg/24 h), simvastatin (40 mg/24 h), acetylsalicylic acid (100 mg/24 h), omeprazole (20 mg/24 h), pregabalin (100 mg/12 h), torasemide (10 mg/24 h), dulaglutide (1.5 mg/week), insulin glargine (74 IU/24 h), insulin lispro (20 IU/24 h), and brimonidine (1 drop/12 h). Among these, losartan, manidipine, torasemide, and pregabalin were identified as agents requiring dose adjustment in the context of impaired renal function due to altered pharmacokinetics—specifically, reduced clearance via the kidneys.\\n\\nLosartan, an angiotensin II receptor blocker (ARB), and manidipine, a dihydropyridine calcium channel blocker (DCCB), are primarily eliminated by renal excretion. In patients with eGFR <60 ml/min/1.73 m², their clearance is diminished, increasing the risk of accumulation and adverse effects, including hypotension. According to product monographs and the consensus guidelines developed by the University of Barcelona Faculty of Pharmacy’s practical pharmacy teaching and research group—based on real-world dispensing data and ATC-based therapeutic categorisation—dose reductions are recommended: for losartan, a reduction to 50–75% of the original dose (i.e., 50 mg/24 h) is advised when eGFR ranges from 30 to 59 ml/min/1.73 m²; for manidipine, the recommended dose is adjusted to 10 mg/24 h when eGFR is between 15 and 30 ml/min/1.73 m². These adjustments are grounded in pharmacodynamic and pharmacokinetic evidence showing dose-dependent hypotensive effects in renal impairment.\\n\\nTorasemide, a loop diuretic, also influences blood pressure regulation and may contribute to hypotension when used in patients with reduced renal function due to decreased volume excretion and potential for electrolyte imbalance. Pregabalin, used for neuropathic pain, is metabolised via hepatic pathways but may exhibit increased systemic exposure in renal impairment due to secondary effects on clearance; however, its primary route of elimination is hepatic, and thus, dose adjustment is less critical in this context, though monitoring is advised.\\n\\nAn initial intervention was proposed, recommending a reduction of losartan to 50 mg/24 h and manidipine to 10 mg/24 h, with the option to evaluate pregabalin dose modification post-adjustment of antihypertensives. The patient was informed of the rationale, and a detailed report was submitted to her Primary Care Physician (PCP), outlining the pharmacological basis for the proposed changes. The PCP implemented the recommended dose reductions and substituted pregabalin 100 mg/12 h with gabapentin 300 mg/12 h, a non-narcotic alternative with a more favorable renal clearance profile.\\n\\nA two-month follow-up demonstrated significant clinical improvement: blood pressure values normalized (systolic 128–135 mmHg, diastolic 75–80 mmHg), and the patient reported complete resolution of fatigue, dizziness, and confusion. The gabapentin dose of 300 mg/12 h was confirmed to be within the recommended range for eGFR 30–60 ml/min/1.73 m² (total daily dose: 300–900 mg), indicating appropriate dosing without risk"}
+{"row_index": 73, "doc_id": 57, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"This story is about a 9-year-old girl who has very smart brain skills but struggles with reading and writing because of dyslexia. Before help, she could only read simple letters and had a hard time with sounds and words. She wrote in a messy way, mixing up letters and skipping parts. After getting special reading and sound practice (like playing games to learn how sounds work), she got better. Now she reads faster and more clearly, and her writing is more organized. She still has some trouble with some letters and sounds, but she’s making progress. The help focused on her sound skills, which helped her read and write better, even though she’s still smart and has special abilities.\"\n}", "generated_text": "This story is about a 9-year-old girl who has very smart brain skills but struggles with reading and writing because of dyslexia. Before help, she could only read simple letters and had a hard time with sounds and words. She wrote in a messy way, mixing up letters and skipping parts. After getting special reading and sound practice (like playing games to learn how sounds work), she got better. Now she reads faster and more clearly, and her writing is more organized. She still has some trouble with some letters and sounds, but she’s making progress. The help focused on her sound skills, which helped her read and write better, even though she’s still smart and has special abilities."}
+{"row_index": 74, "doc_id": 57, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"This case study reports a longitudinal evaluation and targeted phonological remediation intervention in a 9-year-old female child diagnosed with developmental dyslexia (DD) and high abilities/giftedness (AH/S). The study was approved by the Research Ethics Committee (CEP) under protocol number 1.012.635, with informed consent obtained from both parents and the participant via Free and Informed Consent (TCLE and TALE). The participant, enrolled in the third year of elementary school, was initially assessed at 8 years and 2 months (T1, 2018) and re-evaluated at 9 years and 6 months (T2, 2019), with the interval attributed to public service constraints, weekly appointment scheduling, and school holidays. The child was born at term with typical neuropsychomotor and linguistic development; she was raised in a French-speaking environment until age 2, after which her primary language at home became Brazilian Portuguese, though her first words were in French. Upon return to Brazil, she attended two private schools, initially experiencing communication difficulties due to language mismatch, leading to a transition into a French school at age 3. Over time, she exhibited persistent difficulties in reading and writing, resulting in a repetition of the first year of elementary school. At age 6, she entered a bilingual Portuguese-English school. At age 8, she underwent an interdisciplinary assessment in speech therapy and neuropsychology, leading to a formal diagnosis of developmental dyslexia with concomitant high cognitive abilities. She was subsequently referred to the Laboratory of Written Language, Interdisciplinarity and Learning (LEIA/UFRN) for comprehensive written language evaluation.\\n\\nThe intervention consisted of 20 weekly sessions (60 minutes each) of phonological remediation, conducted during the second semester of 2018, with limited parental engagement due to work commitments. Assessments were administered individually over one hour and included standardized tasks measuring phonological processing, reading, and writing. The following protocols were employed:\\n\\n- **Phonological Awareness**: Evaluated using the Consciência Fonológica Instrumento de Avaliação Sequencial (CONFIAS). This instrument includes tasks assessing syllabic and phonemic awareness (synthesis, segmentation, rhyme, alliteration, initial/final syllable identification, exclusion, transposition). Syllabic awareness comprises 9 items (max 40 points), phonemic awareness 7 items (max 30 points), totaling 70 points. Normative values derived from Ferreiro and Teberosky were used: for syllabic-alphabetic writing hypothesis, expected scores of 27 (syllabic), 12 (phonemic), and 39 (total); for alphabetic writing hypothesis, 31 (syllabic), 15 (phonemic), and 46 (total).\\n\\n- **Phonological Working Memory**: Assessed via the Phonological Working Memory Test. The protocol includes a non-word repetition task (40 invented words), with scoring: 2 points for first correct repetition, 1 point for second, 0 for third. A digits test in direct and reverse order follows, scored similarly. Age-specific norms were applied: for T1 (age 8 years 2 months), expected scores of 69 (pseudo-words), 13 (direct digits), and 6 (reverse digits).\\n\\n- **Mental Lexicon Access**: Evaluated using the Rapid Automatic Naming Test (RAN) at T1 and the Automatic Naming Test (TENA) at T2. Both assess naming speed of visual stimuli (colors, objects, letters, digits) using a left-to-right, top-to-bottom reading movement. For T1 (age 8 years 2 months), RAN normative values were 28 (digits), 29 (letters), 52 (objects), 46 (colors). For T2 (age 9 years 6 months), TENA norms were 35 (digits), 32 (letters), 50 (objects), 53 (colors).\\n\\n- **Reading**: Assessed via two protocols. First, the Protocol for the Assessment of Reading of Words/Pseudowords Isolated (LPI), comprising 19 regular words, 20 irregular words, and 20 pseudowords in Arial 24pt font. Correct responses are scored individually (max 59 points). Second, the Assessment of Expository Texts evaluates reading comprehension through directed questions and measures silent and oral reading speed, enabling calculation of words per minute (wpm).\\n\\n- **Writing**: Evaluated through a free narrative task on a topic of interest, followed by oral reading of the written text and a dictation of LPI words and pseudowords. Qualitative analysis was conducted using orthographic criteria", "generated_text": "{\n  \"proficient_health_literacy\": \"This case study reports a longitudinal evaluation and targeted phonological remediation intervention in a 9-year-old female child diagnosed with developmental dyslexia (DD) and high abilities/giftedness (AH/S). The study was approved by the Research Ethics Committee (CEP) under protocol number 1.012.635, with informed consent obtained from both parents and the participant via Free and Informed Consent (TCLE and TALE). The participant, enrolled in the third year of elementary school, was initially assessed at 8 years and 2 months (T1, 2018) and re-evaluated at 9 years and 6 months (T2, 2019), with the interval attributed to public service constraints, weekly appointment scheduling, and school holidays. The child was born at term with typical neuropsychomotor and linguistic development; she was raised in a French-speaking environment until age 2, after which her primary language at home became Brazilian Portuguese, though her first words were in French. Upon return to Brazil, she attended two private schools, initially experiencing communication difficulties due to language mismatch, leading to a transition into a French school at age 3. Over time, she exhibited persistent difficulties in reading and writing, resulting in a repetition of the first year of elementary school. At age 6, she entered a bilingual Portuguese-English school. At age 8, she underwent an interdisciplinary assessment in speech therapy and neuropsychology, leading to a formal diagnosis of developmental dyslexia with concomitant high cognitive abilities. She was subsequently referred to the Laboratory of Written Language, Interdisciplinarity and Learning (LEIA/UFRN) for comprehensive written language evaluation.\\n\\nThe intervention consisted of 20 weekly sessions (60 minutes each) of phonological remediation, conducted during the second semester of 2018, with limited parental engagement due to work commitments. Assessments were administered individually over one hour and included standardized tasks measuring phonological processing, reading, and writing. The following protocols were employed:\\n\\n- **Phonological Awareness**: Evaluated using the Consciência Fonológica Instrumento de Avaliação Sequencial (CONFIAS). This instrument includes tasks assessing syllabic and phonemic awareness (synthesis, segmentation, rhyme, alliteration, initial/final syllable identification, exclusion, transposition). Syllabic awareness comprises 9 items (max 40 points), phonemic awareness 7 items (max 30 points), totaling 70 points. Normative values derived from Ferreiro and Teberosky were used: for syllabic-alphabetic writing hypothesis, expected scores of 27 (syllabic), 12 (phonemic), and 39 (total); for alphabetic writing hypothesis, 31 (syllabic), 15 (phonemic), and 46 (total).\\n\\n- **Phonological Working Memory**: Assessed via the Phonological Working Memory Test. The protocol includes a non-word repetition task (40 invented words), with scoring: 2 points for first correct repetition, 1 point for second, 0 for third. A digits test in direct and reverse order follows, scored similarly. Age-specific norms were applied: for T1 (age 8 years 2 months), expected scores of 69 (pseudo-words), 13 (direct digits), and 6 (reverse digits).\\n\\n- **Mental Lexicon Access**: Evaluated using the Rapid Automatic Naming Test (RAN) at T1 and the Automatic Naming Test (TENA) at T2. Both assess naming speed of visual stimuli (colors, objects, letters, digits) using a left-to-right, top-to-bottom reading movement. For T1 (age 8 years 2 months), RAN normative values were 28 (digits), 29 (letters), 52 (objects), 46 (colors). For T2 (age 9 years 6 months), TENA norms were 35 (digits), 32 (letters), 50 (objects), 53 (colors).\\n\\n- **Reading**: Assessed via two protocols. First, the Protocol for the Assessment of Reading of Words/Pseudowords Isolated (LPI), comprising 19 regular words, 20 irregular words, and 20 pseudowords in Arial 24pt font. Correct responses are scored individually (max 59 points). Second, the Assessment of Expository Texts evaluates reading comprehension through directed questions and measures silent and oral reading speed, enabling calculation of words per minute (wpm).\\n\\n- **Writing**: Evaluated through a free narrative task on a topic of interest, followed by oral reading of the written text and a dictation of LPI words and pseudowords. Qualitative analysis was conducted using orthographic criteria"}
+{"row_index": 75, "doc_id": 58, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 65-year-old woman found a lump in the middle of her chest during a knee surgery check-up. Doctors saw it on a chest scan and found it was a round, clear lump, about 6.5 cm long and 4.2 cm wide, sitting in the back part of the chest. The lump didn’t hurt or spread to nearby areas. They took a small sample and looked at it under a microscope. It showed fat and blood-filled areas, along with some blood cell parts that were normal and mature. This told them it was a harmless tumor, called a myelolipoma. Since it wasn’t dangerous, they chose not to remove it and just watched it. She got better and went home without any problems.\"\n}", "generated_text": "A 65-year-old woman found a lump in the middle of her chest during a knee surgery check-up. Doctors saw it on a chest scan and found it was a round, clear lump, about 6.5 cm long and 4.2 cm wide, sitting in the back part of the chest. The lump didn’t hurt or spread to nearby areas. They took a small sample and looked at it under a microscope. It showed fat and blood-filled areas, along with some blood cell parts that were normal and mature. This told them it was a harmless tumor, called a myelolipoma. Since it wasn’t dangerous, they chose not to remove it and just watched it. She got better and went home without any problems."}
+{"row_index": 76, "doc_id": 58, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 65-year-old woman was found to have a tumor in the middle of her chest, specifically in the posterior mediastinum, during a preoperative check-up for knee surgery. The tumor measured 6.5 × 4.2 cm, had clear borders, and was made up of fat and solid tissue with no signs of spreading to nearby structures. A biopsy was done using imaging guidance, and the results showed that the tumor contained mature fat tissue along with blood cells and early blood cell precursors, which is consistent with a benign condition called primary mediastinal myelolipoma. Because the tumor was not dangerous and did not show signs of growth or spread, the doctors chose not to treat it surgically. The patient recovered well and was discharged without any complications.\"\n}", "generated_text": "A 65-year-old woman was found to have a tumor in the middle of her chest, specifically in the posterior mediastinum, during a preoperative check-up for knee surgery. The tumor measured 6.5 × 4.2 cm, had clear borders, and was made up of fat and solid tissue with no signs of spreading to nearby structures. A biopsy was done using imaging guidance, and the results showed that the tumor contained mature fat tissue along with blood cells and early blood cell precursors, which is consistent with a benign condition called primary mediastinal myelolipoma. Because the tumor was not dangerous and did not show signs of growth or spread, the doctors chose not to treat it surgically. The patient recovered well and was discharged without any complications."}
+{"row_index": 77, "doc_id": 58, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 65-year-old woman with no significant personal or familial medical history presented in August 2022 with a posterior mediastinal tumor identified during preoperative imaging for knee surgery, prompting referral for evaluation. Physical examination at admission was unremarkable, and all laboratory investigations remained within normal limits. A chest computed tomography (CT) scan revealed a well-defined, ovoid lesion measuring 6.5 × 4.2 cm in the posterior right mediastinum, exhibiting mixed fat and solid densities, with no evidence of bone erosion, soft tissue infiltration, or vascular involvement. The tumor was characterized by distinct borders and homogeneous attenuation consistent with adipose tissue intermixed with solid components. A trans-thoracic biopsy was performed using a 18G × 250 mm semiautomatic cutting needle under image guidance via a posterior approach, ensuring precise lesion sampling. Histopathological analysis demonstrated a benign neoplasm composed of mature adipose tissue interspersed with areas of hemorrhage and hematopoietic elements, including erythroid precursors (primarily proerythroblasts and basophilic erythroblasts) and myeloid lineage cells at various stages of differentiation, including promyelocytes, myelocytes, metamyelocytes, and mature granulocytes. Additionally, megakaryocytic elements were observed, indicating active hematopoiesis within the adipose matrix. These findings are consistent with primary mediastinal myelolipoma (MPM), a rare benign tumor of the mediastinum characterized by coexistence of mature adipose tissue and hematopoietic elements, typically arising from a primitive mesenchymal precursor that retains hematopoietic potential. The presence of hematopoietic components, particularly in the context of mature adipose stroma, supports the classification as a myelolipoma rather than a hematologic malignancy. Given the benign histological profile, lack of malignant transformation, and absence of local or systemic signs of disease progression, conservative management was elected. The patient demonstrated stable clinical course, with no evidence of tumor growth, complications, or systemic symptoms, and was discharged without adverse events. This case underscores the importance of accurate imaging interpretation and histopathological characterization in distinguishing benign mediastinal masses from malignant counterparts, particularly in the context of hematopoietic tissue coexistence within adipose stroma.\"\n}", "generated_text": "A 65-year-old woman with no significant personal or familial medical history presented in August 2022 with a posterior mediastinal tumor identified during preoperative imaging for knee surgery, prompting referral for evaluation. Physical examination at admission was unremarkable, and all laboratory investigations remained within normal limits. A chest computed tomography (CT) scan revealed a well-defined, ovoid lesion measuring 6.5 × 4.2 cm in the posterior right mediastinum, exhibiting mixed fat and solid densities, with no evidence of bone erosion, soft tissue infiltration, or vascular involvement. The tumor was characterized by distinct borders and homogeneous attenuation consistent with adipose tissue intermixed with solid components. A trans-thoracic biopsy was performed using a 18G × 250 mm semiautomatic cutting needle under image guidance via a posterior approach, ensuring precise lesion sampling. Histopathological analysis demonstrated a benign neoplasm composed of mature adipose tissue interspersed with areas of hemorrhage and hematopoietic elements, including erythroid precursors (primarily proerythroblasts and basophilic erythroblasts) and myeloid lineage cells at various stages of differentiation, including promyelocytes, myelocytes, metamyelocytes, and mature granulocytes. Additionally, megakaryocytic elements were observed, indicating active hematopoiesis within the adipose matrix. These findings are consistent with primary mediastinal myelolipoma (MPM), a rare benign tumor of the mediastinum characterized by coexistence of mature adipose tissue and hematopoietic elements, typically arising from a primitive mesenchymal precursor that retains hematopoietic potential. The presence of hematopoietic components, particularly in the context of mature adipose stroma, supports the classification as a myelolipoma rather than a hematologic malignancy. Given the benign histological profile, lack of malignant transformation, and absence of local or systemic signs of disease progression, conservative management was elected. The patient demonstrated stable clinical course, with no evidence of tumor growth, complications, or systemic symptoms, and was discharged without adverse events. This case underscores the importance of accurate imaging interpretation and histopathological characterization in distinguishing benign mediastinal masses from malignant counterparts, particularly in the context of hematopoietic tissue coexistence within adipose stroma."}
+{"row_index": 78, "doc_id": 59, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 52-year-old man got sick with both a bad fever and a COVID-19 virus. He worked outside in very hot weather and suddenly lost consciousness. His body temperature reached 104°F, and he fell into a deep coma. Doctors found he had a serious lung infection, damaged liver and kidneys, and a blood problem that made clots form easily. Even with medicine, fluids, and breathing support, he started having trouble breathing and a brain bleed later. He also had a lung infection from other germs, and his body couldn’t fight it well. After days of treatment, his fever and coma went away, but he got worse — he couldn’t breathe properly and had a brain bleed. The damage to his organs, caused by the fever and infections, eventually led to his death.\"\n}", "generated_text": "A 52-year-old man got sick with both a bad fever and a COVID-19 virus. He worked outside in very hot weather and suddenly lost consciousness. His body temperature reached 104°F, and he fell into a deep coma. Doctors found he had a serious lung infection, damaged liver and kidneys, and a blood problem that made clots form easily. Even with medicine, fluids, and breathing support, he started having trouble breathing and a brain bleed later. He also had a lung infection from other germs, and his body couldn’t fight it well. After days of treatment, his fever and coma went away, but he got worse — he couldn’t breathe properly and had a brain bleed. The damage to his organs, caused by the fever and infections, eventually led to his death."}
+{"row_index": 79, "doc_id": 59, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 52-year-old male presented with a community-acquired SARS-CoV-2 infection confirmed by reverse-transcription polymerase chain reaction (RT-PCR) of a nasopharyngeal swab, following a self-reported cold. He returned to work after a two-day rest without fever but lost consciousness while working outdoors in an ambient temperature of 35°C for five hours. Upon emergency department admission, his core temperature (Tc) was 40°C, consistent with hyperpyrexia. He presented with persistent coma, dyspnea, and gastrointestinal hemorrhage, with no known comorbidities or family history of disease. Clinical features—including hyperpyrexia, coma, and multi-organ dysfunction—led to a diagnosis of heatstroke (HS). He was admitted to the emergency intensive care unit (ICU) and required mechanical ventilation due to respiratory failure. Initial laboratory findings revealed severe systemic infection, with leukopenia (WBC: 3.13×10⁹/L), profound lymphopenia (lymphocytes: 0.1×10⁹/L), neutrophilic shift (N%: 85.3%), elevated procalcitonin (2.81 ng/mL) and C-reactive protein (32.6 mg/L), indicating a strong bacterial component. Sputum culture identified Stenotrophomonas maltophilia and Candida lipolytica; central venous catheter culture revealed Staphylococcus epidermidis, while blood cultures remained negative, suggesting a polymicrobial pulmonary infection with possible nosocomial or community-acquired origin. CT imaging demonstrated bilateral frontal subdural effusions, lower lobe consolidation and atelectasis, right upper lobe inflammation, bilateral pleural effusion, and minimal ascites, consistent with severe pulmonary infection and secondary pulmonary edema.\\n\\nThe patient received initial resuscitation with intravenous rehydration using lactated Ringer’s solution and normal saline at 2.5 mL/kg·h, vasoactive support with norepinephrine (0.4 µg/kg·min) to maintain blood pressure (126/77 mmHg), and broad-spectrum antibiotics including piperacillin-tazobactam, later switched to meropenem due to resistance concerns. Immune modulation with thymalfasin was administered for 20 days. Hepatic and renal dysfunction were managed with polyene phosphatidylcholine, adenosylmethionine budisulfonate, ulinastatin, and continuous renal replacement therapy (CRRT) for anuria. Coagulopathy was characterized by thrombocytopenia, disseminated intravascular coagulation (DIC), and elevated D-dimer levels, managed with plasma and cryoprecipitate transfusions, continuous intravenous heparin (6000 U/day), and CRRT with sodium citrate anticoagulation (8 g/day). Platelet transfusion was initiated on day 9. Intracranial pressure was managed with mannitol for three days. Despite initial improvement, the patient developed recurrent dyspnea and fever on day 17 (Tc: 39.3°C), requiring reintubation. Bronchoscopy showed reduced sputum volume, and GCS dropped to 3/15, with elevated WBC (14.94×10⁹/L) and neutrophils (13.77×10⁹/L). Laboratory markers worsened: serum total bilirubin increased to 235.2 µmol/L, creatinine to 441 µmol/L. Brain CT revealed ischemic stroke in the right frontal lobe and hemorrhagic infarction in the right occipital lobe, suggesting both vascular injury and microangiopathic damage. Cooling therapy via ice-cold CRRT was initiated. Fungal infection was suspected based on elevated serum Aspergillus galactomannan, Aspergillus IgG, and Candida mannan, leading to addition of carpofungin on day 18. SARS-CoV-2 RT-PCR became negative on day 18, indicating viral clearance or assay limitations.\\n\\nOn day 20, fever and infection resolved, but the patient developed cerebral hemorrhage and brain herniation with bilateral dilated pupils. Dehydration therapy was used to reduce intracranial pressure, but surgical intervention was declined by family. On day 22, inflammatory markers, liver enzymes (aspartate aminotransferase), and creatinine worsened again, with bronchoalveolar lavage fluid cultures positive for carbapenem-resistant Acinetobacter baumannii and Aspergillus fumigatus. Anti-infective therapy was intensified with meropenem, teicoplanin", "generated_text": "{\n  \"proficient_health_literacy\": \"A 52-year-old male presented with a community-acquired SARS-CoV-2 infection confirmed by reverse-transcription polymerase chain reaction (RT-PCR) of a nasopharyngeal swab, following a self-reported cold. He returned to work after a two-day rest without fever but lost consciousness while working outdoors in an ambient temperature of 35°C for five hours. Upon emergency department admission, his core temperature (Tc) was 40°C, consistent with hyperpyrexia. He presented with persistent coma, dyspnea, and gastrointestinal hemorrhage, with no known comorbidities or family history of disease. Clinical features—including hyperpyrexia, coma, and multi-organ dysfunction—led to a diagnosis of heatstroke (HS). He was admitted to the emergency intensive care unit (ICU) and required mechanical ventilation due to respiratory failure. Initial laboratory findings revealed severe systemic infection, with leukopenia (WBC: 3.13×10⁹/L), profound lymphopenia (lymphocytes: 0.1×10⁹/L), neutrophilic shift (N%: 85.3%), elevated procalcitonin (2.81 ng/mL) and C-reactive protein (32.6 mg/L), indicating a strong bacterial component. Sputum culture identified Stenotrophomonas maltophilia and Candida lipolytica; central venous catheter culture revealed Staphylococcus epidermidis, while blood cultures remained negative, suggesting a polymicrobial pulmonary infection with possible nosocomial or community-acquired origin. CT imaging demonstrated bilateral frontal subdural effusions, lower lobe consolidation and atelectasis, right upper lobe inflammation, bilateral pleural effusion, and minimal ascites, consistent with severe pulmonary infection and secondary pulmonary edema.\\n\\nThe patient received initial resuscitation with intravenous rehydration using lactated Ringer’s solution and normal saline at 2.5 mL/kg·h, vasoactive support with norepinephrine (0.4 µg/kg·min) to maintain blood pressure (126/77 mmHg), and broad-spectrum antibiotics including piperacillin-tazobactam, later switched to meropenem due to resistance concerns. Immune modulation with thymalfasin was administered for 20 days. Hepatic and renal dysfunction were managed with polyene phosphatidylcholine, adenosylmethionine budisulfonate, ulinastatin, and continuous renal replacement therapy (CRRT) for anuria. Coagulopathy was characterized by thrombocytopenia, disseminated intravascular coagulation (DIC), and elevated D-dimer levels, managed with plasma and cryoprecipitate transfusions, continuous intravenous heparin (6000 U/day), and CRRT with sodium citrate anticoagulation (8 g/day). Platelet transfusion was initiated on day 9. Intracranial pressure was managed with mannitol for three days. Despite initial improvement, the patient developed recurrent dyspnea and fever on day 17 (Tc: 39.3°C), requiring reintubation. Bronchoscopy showed reduced sputum volume, and GCS dropped to 3/15, with elevated WBC (14.94×10⁹/L) and neutrophils (13.77×10⁹/L). Laboratory markers worsened: serum total bilirubin increased to 235.2 µmol/L, creatinine to 441 µmol/L. Brain CT revealed ischemic stroke in the right frontal lobe and hemorrhagic infarction in the right occipital lobe, suggesting both vascular injury and microangiopathic damage. Cooling therapy via ice-cold CRRT was initiated. Fungal infection was suspected based on elevated serum Aspergillus galactomannan, Aspergillus IgG, and Candida mannan, leading to addition of carpofungin on day 18. SARS-CoV-2 RT-PCR became negative on day 18, indicating viral clearance or assay limitations.\\n\\nOn day 20, fever and infection resolved, but the patient developed cerebral hemorrhage and brain herniation with bilateral dilated pupils. Dehydration therapy was used to reduce intracranial pressure, but surgical intervention was declined by family. On day 22, inflammatory markers, liver enzymes (aspartate aminotransferase), and creatinine worsened again, with bronchoalveolar lavage fluid cultures positive for carbapenem-resistant Acinetobacter baumannii and Aspergillus fumigatus. Anti-infective therapy was intensified with meropenem, teicoplanin"}
+{"row_index": 80, "doc_id": 60, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 19-year-old female presented to the emergency department with a two-day history of headache, recurrent nausea, vomiting, and one-day fever. On admission, she had a high fever of 39.1°C, severe hypertension (189/120 mmHg), and tachycardia (148 beats per minute). Laboratory findings revealed a leukocytosis (14.77×10^9/L) with neutrophilia (13.55×10^9/L), suggestive of systemic inflammation or infection. Empirical antibiotic therapy with moxifloxacin was initiated, but symptoms persisted, prompting admission to the intensive care unit for close monitoring. A year prior, she had been diagnosed with myocarditis at a local hospital, along with hypertension, for which antihypertensive therapy was prescribed; however, she discontinued adherence to medication and failed to monitor blood pressure regularly. Notably, her father had a history of sudden, unexplained death, raising concerns for a hereditary endocrine disorder.\\n\\nA chest CT scan incidentally revealed a left adrenal mass measuring 43 mm × 36 mm with soft tissue density. Head and chest CTs showed no other pathological abnormalities. Electrocardiography demonstrated sinus tachycardia with a shortened PR interval and tall, peaked P-waves in leads II, III, and aVF, consistent with volume overload or myocardial stress. Transthoracic echocardiography was unremarkable.\\n\\nOn day two of admission, biomarkers including brain natriuretic peptide (BNP) and cardiac troponin I (TnI) increased, supporting a provisional diagnosis of myocarditis of uncertain etiology. Treatment included methylprednisolone (0.25 g/day) for presumed myocardial inflammation, furosemide (20 mg every 12 hours) and spironolactone (20 mg every 12 hours) for fluid management, and perindopril amlodipine (10 mg: 5 mg daily) for blood pressure control and afterload reduction. Metoprolol tartrate (25 mg every 12 hours) and esmolol (0.2 g/hour IV infusion) were used to control heart rate and reduce myocardial oxygen demand.\\n\\nGiven the presence of an adrenal mass and sustained hypertension, endocrine workup was initiated, including assessment of aldosterone-to-renin ratio, plasma cortisol, plasma catecholamines, and 24-hour urinary catecholamines and metabolites. In the recumbent position, plasma catecholamines were markedly elevated: dopamine (524.5 pmol/L), norepinephrine (83,975 pmol/L), and epinephrine (10,579.3 pmol/L). Urinary excretion levels included free adrenaline (4,368.89 nmol/24 h), free norepinephrine (>12,697.60 nmol/24 h), normetanephrine (8,312 nmol/24 h), metanephrines (4,078 nmol/24 h), and vanillylmandelic acid (58.1 mg/24 h). These findings are consistent with pheochromocytoma and supported the clinical diagnosis.\\n\\nOn day five post-admission, glucocorticoid therapy was discontinued, and perindopril amlodipine was replaced with terazosin to provide more precise blood pressure control in the setting of catecholamine excess. An enhanced abdominal CT confirmed the left adrenal mass, highly suggestive of pheochromocytoma. Whole-exome sequencing revealed a heterozygous missense mutation in the RET gene (c.1900T > C: p. Cys634Arg), resulting in substitution of cysteine by arginine at codon 634. This mutation is pathogenic and associated with multiple endocrine neoplasia type 2A (MEN2A), prompting further endocrine evaluation of the thyroid and parathyroid glands.\\n\\nThyroid color Doppler ultrasound identified a hypoechoic nodule measuring 6 mm × 4 mm in the left thyroid lobe, with mildly elevated serum calcitonin levels. Parathyroid function tests showed normal serum calcium, phosphate, and parathyroid hormone (PTH) levels. No other significant endocrine abnormalities were detected.\\n\\nFollowing clinical stabilization, plasma cortisol and ACTH levels normalized. The patient underwent surgical resection of the left adrenal tumor, which measured 50 mm × 40 mm × 30 mm. Immunohistochemical analysis confirmed positive staining for vimentin (", "generated_text": "{\n  \"proficient_health_literacy\": \"A 19-year-old female presented to the emergency department with a two-day history of headache, recurrent nausea, vomiting, and one-day fever. On admission, she had a high fever of 39.1°C, severe hypertension (189/120 mmHg), and tachycardia (148 beats per minute). Laboratory findings revealed a leukocytosis (14.77×10^9/L) with neutrophilia (13.55×10^9/L), suggestive of systemic inflammation or infection. Empirical antibiotic therapy with moxifloxacin was initiated, but symptoms persisted, prompting admission to the intensive care unit for close monitoring. A year prior, she had been diagnosed with myocarditis at a local hospital, along with hypertension, for which antihypertensive therapy was prescribed; however, she discontinued adherence to medication and failed to monitor blood pressure regularly. Notably, her father had a history of sudden, unexplained death, raising concerns for a hereditary endocrine disorder.\\n\\nA chest CT scan incidentally revealed a left adrenal mass measuring 43 mm × 36 mm with soft tissue density. Head and chest CTs showed no other pathological abnormalities. Electrocardiography demonstrated sinus tachycardia with a shortened PR interval and tall, peaked P-waves in leads II, III, and aVF, consistent with volume overload or myocardial stress. Transthoracic echocardiography was unremarkable.\\n\\nOn day two of admission, biomarkers including brain natriuretic peptide (BNP) and cardiac troponin I (TnI) increased, supporting a provisional diagnosis of myocarditis of uncertain etiology. Treatment included methylprednisolone (0.25 g/day) for presumed myocardial inflammation, furosemide (20 mg every 12 hours) and spironolactone (20 mg every 12 hours) for fluid management, and perindopril amlodipine (10 mg: 5 mg daily) for blood pressure control and afterload reduction. Metoprolol tartrate (25 mg every 12 hours) and esmolol (0.2 g/hour IV infusion) were used to control heart rate and reduce myocardial oxygen demand.\\n\\nGiven the presence of an adrenal mass and sustained hypertension, endocrine workup was initiated, including assessment of aldosterone-to-renin ratio, plasma cortisol, plasma catecholamines, and 24-hour urinary catecholamines and metabolites. In the recumbent position, plasma catecholamines were markedly elevated: dopamine (524.5 pmol/L), norepinephrine (83,975 pmol/L), and epinephrine (10,579.3 pmol/L). Urinary excretion levels included free adrenaline (4,368.89 nmol/24 h), free norepinephrine (>12,697.60 nmol/24 h), normetanephrine (8,312 nmol/24 h), metanephrines (4,078 nmol/24 h), and vanillylmandelic acid (58.1 mg/24 h). These findings are consistent with pheochromocytoma and supported the clinical diagnosis.\\n\\nOn day five post-admission, glucocorticoid therapy was discontinued, and perindopril amlodipine was replaced with terazosin to provide more precise blood pressure control in the setting of catecholamine excess. An enhanced abdominal CT confirmed the left adrenal mass, highly suggestive of pheochromocytoma. Whole-exome sequencing revealed a heterozygous missense mutation in the RET gene (c.1900T > C: p. Cys634Arg), resulting in substitution of cysteine by arginine at codon 634. This mutation is pathogenic and associated with multiple endocrine neoplasia type 2A (MEN2A), prompting further endocrine evaluation of the thyroid and parathyroid glands.\\n\\nThyroid color Doppler ultrasound identified a hypoechoic nodule measuring 6 mm × 4 mm in the left thyroid lobe, with mildly elevated serum calcitonin levels. Parathyroid function tests showed normal serum calcium, phosphate, and parathyroid hormone (PTH) levels. No other significant endocrine abnormalities were detected.\\n\\nFollowing clinical stabilization, plasma cortisol and ACTH levels normalized. The patient underwent surgical resection of the left adrenal tumor, which measured 50 mm × 40 mm × 30 mm. Immunohistochemical analysis confirmed positive staining for vimentin ("}
+{"row_index": 81, "doc_id": 61, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 36-year-old man had a painful lump on the inside of his penis and scrotum for 5 years. The lump was not causing trouble with urination or weight loss. Doctors found it was a hard, cyst-like growth, about 2 cm big, with lots of blood flow. Imaging showed it was attached to the tube that carries sperm and was deep in the area, not near the testicle or cord. After surgery, the doctors found it was a type of cancer called synovial sarcoma — a kind of tumor that grows in the tissue around joints. The tumor had signs that matched this cancer, and tests confirmed it had a genetic change known in this type of cancer. The first surgery removed the lump, but the cancer came back. The patient had a second surgery to remove more tissue, and even after that, the cancer spread to his liver and spine. He tried several chemotherapy treatments, but none worked. He had more surgeries on his liver, then got a lung tumor. He tried more medicines and radiation, but the cancer kept growing. Eventually, he was moved to palliative care and stopped seeing doctors because the disease was no longer treatable.\"\n}", "generated_text": "A 36-year-old man had a painful lump on the inside of his penis and scrotum for 5 years. The lump was not causing trouble with urination or weight loss. Doctors found it was a hard, cyst-like growth, about 2 cm big, with lots of blood flow. Imaging showed it was attached to the tube that carries sperm and was deep in the area, not near the testicle or cord. After surgery, the doctors found it was a type of cancer called synovial sarcoma — a kind of tumor that grows in the tissue around joints. The tumor had signs that matched this cancer, and tests confirmed it had a genetic change known in this type of cancer. The first surgery removed the lump, but the cancer came back. The patient had a second surgery to remove more tissue, and even after that, the cancer spread to his liver and spine. He tried several chemotherapy treatments, but none worked. He had more surgeries on his liver, then got a lung tumor. He tried more medicines and radiation, but the cancer kept growing. Eventually, he was moved to palliative care and stopped seeing doctors because the disease was no longer treatable."}
+{"row_index": 82, "doc_id": 61, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 36-year-old man had a painful lump in the penis and scrotum for 5 years. The lump was about 20 mm in size, not attached to the spermatic cord, and was tender but not causing urinary problems. Imaging showed a well-defined mass with lots of blood flow, and it was connected to the vas deferens. Blood tests were normal. After surgery, the tissue was examined and found to be a type of cancer called synovial sarcoma. The tumor cells were arranged in a specific pattern and tested positive for markers like TLE-1, CD99, BLC2, cytokeratin, and EMA. A genetic test confirmed a known change in the SS18 gene, which is common in this type of cancer. The first surgery removed the mass completely, but the margins were hard to assess because the sample was fragmented. A second surgery was done with wider margins, and the new tissue sample showed no signs of cancer. However, after 16 months of monitoring, the cancer spread to the liver and spine. Despite multiple treatments—including chemotherapy with Ifosfamide and Doxorubicin, surgery to remove liver tumors, and targeted therapy with Pazopanib and radiation—the cancer continued to grow. He tried several other chemotherapy regimens, including Gemcitabine and Docetaxel, and Dacarbazine, but all failed. Eventually, he was moved to palliative care and stopped treatment due to disease progression.\"\n}", "generated_text": "A 36-year-old man had a painful lump in the penis and scrotum for 5 years. The lump was about 20 mm in size, not attached to the spermatic cord, and was tender but not causing urinary problems. Imaging showed a well-defined mass with lots of blood flow, and it was connected to the vas deferens. Blood tests were normal. After surgery, the tissue was examined and found to be a type of cancer called synovial sarcoma. The tumor cells were arranged in a specific pattern and tested positive for markers like TLE-1, CD99, BLC2, cytokeratin, and EMA. A genetic test confirmed a known change in the SS18 gene, which is common in this type of cancer. The first surgery removed the mass completely, but the margins were hard to assess because the sample was fragmented. A second surgery was done with wider margins, and the new tissue sample showed no signs of cancer. However, after 16 months of monitoring, the cancer spread to the liver and spine. Despite multiple treatments—including chemotherapy with Ifosfamide and Doxorubicin, surgery to remove liver tumors, and targeted therapy with Pazopanib and radiation—the cancer continued to grow. He tried several other chemotherapy regimens, including Gemcitabine and Docetaxel, and Dacarbazine, but all failed. Eventually, he was moved to palliative care and stopped treatment due to disease progression."}
+{"row_index": 83, "doc_id": 61, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 36-year-old male with no significant past medical history presented with a 5-year history of a left-sided penoscrotal mass. The patient reported no lower urinary tract symptoms, trauma, infections, weight loss, anorexia, or fever. Physical examination revealed a smooth, tender, cystic lesion measuring approximately 20 mm × 20 mm located at the penoscrotal junction, attached to the left side of the bulbar urethra, deep in the tissue, without skin tethering or association with the left spermatic cord, and partially mobile. Doppler ultrasonography demonstrated a well-defined hypoechoic mass measuring 2.7 cm × 3.1 cm × 2.0 cm with markedly increased vascularity on the left penoscrotal junction. Pelvic magnetic resonance imaging (MRI) showed a lesion in the left inferolateral base of the penis with a distinct fat plane, isointense to testicular tissue on T2-weighted, T1-weighted, and diffusion-weighted imaging sequences, and with direct connection to the vas deferens; no regional lymphadenopathy was observed. Serum alpha-fetoprotein and beta-human chorionic gonadotropin levels were within normal limits. Given the chronic pain and imaging findings, surgical resection was performed for both diagnostic and therapeutic purposes. Intraoperatively, a mass was identified in the left posterolateral scrotum and completely resected, with the specimen sent for histopathological evaluation.\\n\\nHistopathological analysis revealed a cellular spindle cell tumor organized in interlacing fascicles, comprising spindle- to oval-shaped cells with vesicular nuclei, evenly distributed chromatin, and inconspicuous nucleoli. The tumor exhibited high mitotic activity, with up to 3 mitotic figures per high-power field. Immunohistochemical staining was positive for TLE-1, CD99, B-cell lymphoma 2 (BCL-2), focal cytokeratin, and focal epithelial membrane antigen (EMA), consistent with synovial sarcoma. Fluorescence in situ hybridization (FISH) analysis confirmed a characteristic rearrangement of the SS18 gene at 18q11.2, a molecular hallmark of synovial sarcoma. Histological assessment of the margins was inconclusive due to fragmentation of the resection specimen.\\n\\nTwo weeks post-initial surgery, the patient returned for a multidisciplinary review. Based on the histopathology, a second surgical resection with wider margins was proposed and accepted. A positron emission tomography–computed tomography (PET/CT) scan of the head, neck, chest, abdomen, pelvis, and musculoskeletal system was performed, revealing a 29 mm × 27 mm thyroid nodule in the lower pole of the left lobe with moderate hypermetabolism (standardized uptake value [SUV] of 4.9). Thyroid ultrasound demonstrated a solid, isoechoic, well-defined nodule without echogenic foci. The nodule was classified as TIRADS category 3 (TR3), indicating a low risk of malignancy.\\n\\nA second surgical resection was performed three weeks after the initial procedure. The resection extended bilaterally to the spermatic cords, deepening to the corpus spongiosum and shaving superiorly to the urethra. The final resected specimen measured 6.0 cm × 6.0 cm × 3.0 cm and was histologically negative for residual tumor. The patient then entered active surveillance. At 16 months, metastatic disease was detected in the sixth segment of the liver and the L1 vertebral body. The oncology team initiated a six-cycle regimen of ifosfamide and doxorubicin, which showed no clinical or radiographic response. Subsequent surgical resection of the fifth and sixth liver segments, along with cholecystectomy, was performed. The patient later developed a new pulmonary lesion, prompting initiation of pazopanib and stereotactic body radiation therapy (SBRT). After six months of surveillance, new lesions emerged in both the liver and lungs. A gemcitabine and docetaxel combination chemotherapy regimen was administered for three cycles, followed by progression. The patient then received two cycles of dacarbazine, with further progression. Subsequently, two cycles of pembrolizumab were administered, also resulting in disease progression. Given the lack of response to all available systemic therapies, the patient was transitioned to palliative care and discontinued follow-up. This case highlights the aggressive clinical course of synovial sarcoma, particularly in the penoscrotal region, with early local recurrence, metastatic spread to liver and bone, and resistance to conventional chemotherapy and immunotherapy regimens, underscoring the need for early detection, comprehensive surgical margins, and exploration of novel targeted or immunother", "generated_text": "{\n  \"proficient_health_literacy\": \"A 36-year-old male with no significant past medical history presented with a 5-year history of a left-sided penoscrotal mass. The patient reported no lower urinary tract symptoms, trauma, infections, weight loss, anorexia, or fever. Physical examination revealed a smooth, tender, cystic lesion measuring approximately 20 mm × 20 mm located at the penoscrotal junction, attached to the left side of the bulbar urethra, deep in the tissue, without skin tethering or association with the left spermatic cord, and partially mobile. Doppler ultrasonography demonstrated a well-defined hypoechoic mass measuring 2.7 cm × 3.1 cm × 2.0 cm with markedly increased vascularity on the left penoscrotal junction. Pelvic magnetic resonance imaging (MRI) showed a lesion in the left inferolateral base of the penis with a distinct fat plane, isointense to testicular tissue on T2-weighted, T1-weighted, and diffusion-weighted imaging sequences, and with direct connection to the vas deferens; no regional lymphadenopathy was observed. Serum alpha-fetoprotein and beta-human chorionic gonadotropin levels were within normal limits. Given the chronic pain and imaging findings, surgical resection was performed for both diagnostic and therapeutic purposes. Intraoperatively, a mass was identified in the left posterolateral scrotum and completely resected, with the specimen sent for histopathological evaluation.\\n\\nHistopathological analysis revealed a cellular spindle cell tumor organized in interlacing fascicles, comprising spindle- to oval-shaped cells with vesicular nuclei, evenly distributed chromatin, and inconspicuous nucleoli. The tumor exhibited high mitotic activity, with up to 3 mitotic figures per high-power field. Immunohistochemical staining was positive for TLE-1, CD99, B-cell lymphoma 2 (BCL-2), focal cytokeratin, and focal epithelial membrane antigen (EMA), consistent with synovial sarcoma. Fluorescence in situ hybridization (FISH) analysis confirmed a characteristic rearrangement of the SS18 gene at 18q11.2, a molecular hallmark of synovial sarcoma. Histological assessment of the margins was inconclusive due to fragmentation of the resection specimen.\\n\\nTwo weeks post-initial surgery, the patient returned for a multidisciplinary review. Based on the histopathology, a second surgical resection with wider margins was proposed and accepted. A positron emission tomography–computed tomography (PET/CT) scan of the head, neck, chest, abdomen, pelvis, and musculoskeletal system was performed, revealing a 29 mm × 27 mm thyroid nodule in the lower pole of the left lobe with moderate hypermetabolism (standardized uptake value [SUV] of 4.9). Thyroid ultrasound demonstrated a solid, isoechoic, well-defined nodule without echogenic foci. The nodule was classified as TIRADS category 3 (TR3), indicating a low risk of malignancy.\\n\\nA second surgical resection was performed three weeks after the initial procedure. The resection extended bilaterally to the spermatic cords, deepening to the corpus spongiosum and shaving superiorly to the urethra. The final resected specimen measured 6.0 cm × 6.0 cm × 3.0 cm and was histologically negative for residual tumor. The patient then entered active surveillance. At 16 months, metastatic disease was detected in the sixth segment of the liver and the L1 vertebral body. The oncology team initiated a six-cycle regimen of ifosfamide and doxorubicin, which showed no clinical or radiographic response. Subsequent surgical resection of the fifth and sixth liver segments, along with cholecystectomy, was performed. The patient later developed a new pulmonary lesion, prompting initiation of pazopanib and stereotactic body radiation therapy (SBRT). After six months of surveillance, new lesions emerged in both the liver and lungs. A gemcitabine and docetaxel combination chemotherapy regimen was administered for three cycles, followed by progression. The patient then received two cycles of dacarbazine, with further progression. Subsequently, two cycles of pembrolizumab were administered, also resulting in disease progression. Given the lack of response to all available systemic therapies, the patient was transitioned to palliative care and discontinued follow-up. This case highlights the aggressive clinical course of synovial sarcoma, particularly in the penoscrotal region, with early local recurrence, metastatic spread to liver and bone, and resistance to conventional chemotherapy and immunotherapy regimens, underscoring the need for early detection, comprehensive surgical margins, and exploration of novel targeted or immunother"}
+{"row_index": 84, "doc_id": 62, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 13-year-old boy came to the emergency room with sudden chest pain on the sides of his chest, especially when coughing. The pain wasn’t linked to fever or other symptoms, and he didn’t feel short of breath. He had a mild cold and a one-time fever, but no joint pain, weight loss, or fatigue. He still played sports regularly. His chest X-ray from 4 years ago showed a similar lung problem, which was treated with an antibiotic called azithromycin and has stayed quiet since. This time, his new chest scan showed a lot of cloudy areas in both lungs, more than two-thirds of them, which points to a rare lung condition called pulmonary alveolar proteinosis (PAP). Tests for viruses, including the coronavirus, came back negative. A lung fluid test showed a milky fluid and a sign that matches PAP. His breathing test showed a slight drop in lung function, but he’s still able to breathe and play. No gene changes were found that cause lung problems. A test for a specific immune protein showed it was missing, which makes it likely this is an autoimmune form of PAP. After 20 months, he’s feeling fine, breathing normally, and still plays sports. No treatment is needed right now — just regular check-ups to keep an eye on his lungs.\"\n}", "generated_text": "A 13-year-old boy came to the emergency room with sudden chest pain on the sides of his chest, especially when coughing. The pain wasn’t linked to fever or other symptoms, and he didn’t feel short of breath. He had a mild cold and a one-time fever, but no joint pain, weight loss, or fatigue. He still played sports regularly. His chest X-ray from 4 years ago showed a similar lung problem, which was treated with an antibiotic called azithromycin and has stayed quiet since. This time, his new chest scan showed a lot of cloudy areas in both lungs, more than two-thirds of them, which points to a rare lung condition called pulmonary alveolar proteinosis (PAP). Tests for viruses, including the coronavirus, came back negative. A lung fluid test showed a milky fluid and a sign that matches PAP. His breathing test showed a slight drop in lung function, but he’s still able to breathe and play. No gene changes were found that cause lung problems. A test for a specific immune protein showed it was missing, which makes it likely this is an autoimmune form of PAP. After 20 months, he’s feeling fine, breathing normally, and still plays sports. No treatment is needed right now — just regular check-ups to keep an eye on his lungs."}
+{"row_index": 85, "doc_id": 62, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 13-year-old male with no significant prior medical history presented to the emergency department with a 3-day history of acute bilateral pleuritic chest pain, associated with mild non-productive cough, mild rhinorrhea, and a single febrile episode (38°C). The chest pain was localized to the costal margin and exacerbated by coughing, without diurnal variation or respiratory distress. Symptoms were partially relieved with paracetamol. There were no reports of joint pain, weight loss, anorexia, fatigue, syncope, or exercise intolerance; he maintained regular physical activity, including weekly canoeing. No history of infectious exposure, environmental exposures (e.g., dust, fumes, mineral oils), or familial cardiopulmonary disease was reported. A prior chest radiograph, obtained four years earlier during an acute illness, demonstrated a marked interstitial infiltrate, which was initially treated with azithromycin and has remained asymptomatic since, with no subsequent follow-up.\\n\\nOn admission, vital signs were stable: temperature 37.8°C, oxygen saturation 99% on room air, heart rate 93 bpm, respiratory rate 15 breaths per minute, and blood pressure at the 85th percentile (115/66 mmHg). Physical examination revealed diminished breath sounds in the lower two-thirds of the lung fields without adventitious sounds, respiratory distress, cyanosis, clubbing, or abnormal cardiac murmurs. Chest radiography showed a persistent interstitial infiltrate, morphologically similar to the prior finding. Thoracic computed tomography (CT) revealed multiple bilateral ground-glass opacities involving greater than 65% of lung parenchyma, with areas of 'crazy paving' pattern—findings highly suggestive of pulmonary alveolar proteinosis (PAP).\\n\\nRespiratory viral testing, including for SARS-CoV-2, was negative. The patient was initially managed with empiric antibiotics (amoxicillin-clavulanic acid and azithromycin) for suspected respiratory infection, and symptoms resolved. He was discharged and referred to a pediatric respiratory clinic for further evaluation.\\n\\nOutpatient workup revealed positive antinuclear antibodies (ANA) at a titer of 1/89 with a fine speckled pattern, while other autoantibodies (e.g., anti-dsDNA, anti-Smith, anti-Ro/SSA) were negative, and immunoglobulin levels were within normal ranges. Bronchoalveolar lavage (BAL) fluid exhibited a milky appearance and demonstrated positive periodic acid-Schiff (PAS) staining, indicating the presence of surfactant proteins and alveolar protein accumulation. Microbiological analysis of BAL, including for mycobacteria, was negative, excluding infectious etiologies. Spirometry showed a mild restrictive pattern: forced vital capacity (FVC) of 2.92 L (77%), forced expiratory volume in 1 second (FEV1) of 3.21 L (69.9%), and a normal FEV1/FVC ratio of 109%, consistent with preserved airflow dynamics. Diffusing capacity of the lungs for carbon monoxide (DLCO, single breath) was reduced to 13.8 ml/min/mmHg (48.6%), indicating impaired gas exchange, consistent with alveolar membrane thickening or protein deposition.\\n\\nGenetic testing for mutations associated with surfactant dysfunction (e.g., SFTPA1, SFTPB, SFTPC, ABCA3) was negative, ruling out inherited surfactant-related disorders. Testing for anti-granulocyte macrophage colony-stimulating factor (GM-CSF) antibodies was strongly positive, supporting a diagnosis of autoimmune pulmonary alveolar proteinosis (AI-PAP), in which the immune system produces autoantibodies that inhibit GM-CSF function, leading to impaired alveolar macrophage clearance of surfactant proteins and subsequent protein accumulation in alveoli.\\n\\nAt 20-month follow-up, the patient remains asymptomatic and continues to engage in regular physical activity. Repeat spirometry shows normalization of FVC (4.03 L, 81.3%), FEV1 (3.71 L, 87.5%), and FEV1/FVC ratio (91.96%), indicating partial recovery or stabilization of pulmonary function. DLCO has improved to 25.54 ml/min/mmHg (83.7%), suggesting partial restoration of gas exchange. Given the absence of symptoms and stable pulmonary function, treatment was deferred, and the patient is being managed with routine clinical monitoring. The case underscores the clinical and radiological overlap between acute respiratory illness and chronic alveolar proteinosis, particularly in adolescents with recurrent interstitial infiltrates and autoimmune markers,", "generated_text": "{\n  \"proficient_health_literacy\": \"A 13-year-old male with no significant prior medical history presented to the emergency department with a 3-day history of acute bilateral pleuritic chest pain, associated with mild non-productive cough, mild rhinorrhea, and a single febrile episode (38°C). The chest pain was localized to the costal margin and exacerbated by coughing, without diurnal variation or respiratory distress. Symptoms were partially relieved with paracetamol. There were no reports of joint pain, weight loss, anorexia, fatigue, syncope, or exercise intolerance; he maintained regular physical activity, including weekly canoeing. No history of infectious exposure, environmental exposures (e.g., dust, fumes, mineral oils), or familial cardiopulmonary disease was reported. A prior chest radiograph, obtained four years earlier during an acute illness, demonstrated a marked interstitial infiltrate, which was initially treated with azithromycin and has remained asymptomatic since, with no subsequent follow-up.\\n\\nOn admission, vital signs were stable: temperature 37.8°C, oxygen saturation 99% on room air, heart rate 93 bpm, respiratory rate 15 breaths per minute, and blood pressure at the 85th percentile (115/66 mmHg). Physical examination revealed diminished breath sounds in the lower two-thirds of the lung fields without adventitious sounds, respiratory distress, cyanosis, clubbing, or abnormal cardiac murmurs. Chest radiography showed a persistent interstitial infiltrate, morphologically similar to the prior finding. Thoracic computed tomography (CT) revealed multiple bilateral ground-glass opacities involving greater than 65% of lung parenchyma, with areas of 'crazy paving' pattern—findings highly suggestive of pulmonary alveolar proteinosis (PAP).\\n\\nRespiratory viral testing, including for SARS-CoV-2, was negative. The patient was initially managed with empiric antibiotics (amoxicillin-clavulanic acid and azithromycin) for suspected respiratory infection, and symptoms resolved. He was discharged and referred to a pediatric respiratory clinic for further evaluation.\\n\\nOutpatient workup revealed positive antinuclear antibodies (ANA) at a titer of 1/89 with a fine speckled pattern, while other autoantibodies (e.g., anti-dsDNA, anti-Smith, anti-Ro/SSA) were negative, and immunoglobulin levels were within normal ranges. Bronchoalveolar lavage (BAL) fluid exhibited a milky appearance and demonstrated positive periodic acid-Schiff (PAS) staining, indicating the presence of surfactant proteins and alveolar protein accumulation. Microbiological analysis of BAL, including for mycobacteria, was negative, excluding infectious etiologies. Spirometry showed a mild restrictive pattern: forced vital capacity (FVC) of 2.92 L (77%), forced expiratory volume in 1 second (FEV1) of 3.21 L (69.9%), and a normal FEV1/FVC ratio of 109%, consistent with preserved airflow dynamics. Diffusing capacity of the lungs for carbon monoxide (DLCO, single breath) was reduced to 13.8 ml/min/mmHg (48.6%), indicating impaired gas exchange, consistent with alveolar membrane thickening or protein deposition.\\n\\nGenetic testing for mutations associated with surfactant dysfunction (e.g., SFTPA1, SFTPB, SFTPC, ABCA3) was negative, ruling out inherited surfactant-related disorders. Testing for anti-granulocyte macrophage colony-stimulating factor (GM-CSF) antibodies was strongly positive, supporting a diagnosis of autoimmune pulmonary alveolar proteinosis (AI-PAP), in which the immune system produces autoantibodies that inhibit GM-CSF function, leading to impaired alveolar macrophage clearance of surfactant proteins and subsequent protein accumulation in alveoli.\\n\\nAt 20-month follow-up, the patient remains asymptomatic and continues to engage in regular physical activity. Repeat spirometry shows normalization of FVC (4.03 L, 81.3%), FEV1 (3.71 L, 87.5%), and FEV1/FVC ratio (91.96%), indicating partial recovery or stabilization of pulmonary function. DLCO has improved to 25.54 ml/min/mmHg (83.7%), suggesting partial restoration of gas exchange. Given the absence of symptoms and stable pulmonary function, treatment was deferred, and the patient is being managed with routine clinical monitoring. The case underscores the clinical and radiological overlap between acute respiratory illness and chronic alveolar proteinosis, particularly in adolescents with recurrent interstitial infiltrates and autoimmune markers,"}
+{"row_index": 86, "doc_id": 63, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 27-year-old woman had swelling on her face and trouble opening her mouth 48 hours after taking antibiotics for a tooth infection. A scan of her neck showed a big blood clot in a vein, and a chest scan found clots in her lungs. She was treated right away with strong antibiotics and medicine to thin her blood to stop the clots from getting worse. She got better after a few days of this treatment.\"\n}", "generated_text": "A 27-year-old woman had swelling on her face and trouble opening her mouth 48 hours after taking antibiotics for a tooth infection. A scan of her neck showed a big blood clot in a vein, and a chest scan found clots in her lungs. She was treated right away with strong antibiotics and medicine to thin her blood to stop the clots from getting worse. She got better after a few days of this treatment."}
+{"row_index": 87, "doc_id": 63, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 27-year-old woman developed facial swelling and difficulty opening her mouth (trismus) 48 hours after taking phenoxymethylpenicillin for a throat infection. Tests showed a large blood clot in the internal jugular vein of her neck and lung clots from the infection spreading to her lungs (pulmonary septic embolism). She was treated with strong intravenous antibiotics and anticoagulant medication to stop the clot from growing and to fight the infection. Her symptoms improved over several days, and after 14 days of treatment, she was able to go home on oral antibiotics and continued anticoagulation therapy.\"\n}", "generated_text": "A 27-year-old woman developed facial swelling and difficulty opening her mouth (trismus) 48 hours after taking phenoxymethylpenicillin for a throat infection. Tests showed a large blood clot in the internal jugular vein of her neck and lung clots from the infection spreading to her lungs (pulmonary septic embolism). She was treated with strong intravenous antibiotics and anticoagulant medication to stop the clot from growing and to fight the infection. Her symptoms improved over several days, and after 14 days of treatment, she was able to go home on oral antibiotics and continued anticoagulation therapy."}
+{"row_index": 88, "doc_id": 63, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 27-year-old woman with a history of uncontrolled asthma and a prior mild SARS-CoV-2 infection presented 48 hours after completing oral phenoxymethylpenicillin 1,000,000 IU daily for five days, administered for a peritonsillar abscess, with new-onset facial edema and trismus. Physical examination revealed hemodynamic stability, absence of respiratory distress, and a palpable, homolateral, tender cervical adenopathy consistent with regional lymphadenopathy. Laboratory findings demonstrated leukocytosis, thrombocytopenia, and elevated acute-phase reactants, with no significant abnormalities in other parameters. Imaging studies included a head and neck CT, which revealed a large thrombus involving both the internal and external carotid arteries, consistent with a potentially infectious or inflammatory etiology triggering vasculopathy. A chest CT scan identified bilateral pulmonary septic emboli, indicating the dissemination of infectious material via venous thromboembolism from the head and neck region. Arterial Doppler ultrasound of the neck vessels was unremarkable, and cardiac Doppler ultrasound excluded cardiac vegetations, suggesting a non-cardiac source of embolic material. Initial empiric intravenous therapy consisted of ceftriaxone 1 g every 12 hours and clindamycin 300 mg every 6 hours to cover both gram-negative and gram-positive pathogens, including potential anaerobes. Concurrent anticoagulation was initiated with enoxaparin, dosed at 60 mg subcutaneously every 12 hours, adjusted for body weight and renal function, to manage the thrombotic burden. Over the subsequent 72 hours, the patient developed a fever of 38.5 °C and further leukocytosis, prompting repeat imaging and hemocultures. Hemocultures remained negative, and pharyngeal exudate culture was obtained. Given the clinical progression and lack of microbial growth in cultures, the antibiotic regimen was escalated to piperacillin-tazobactam 4.5 g every 6 hours intravenously to enhance coverage against multidrug-resistant or extended-spectrum pathogens. The patient responded favorably to this regimen, with resolution of fever and clinical signs of infection, and by day 14, chest CT showed complete absence of pulmonary embolic lesions. At that point, oral clindamycin 300 mg every 6 hours was transitioned to continue coverage for anaerobic flora, and anticoagulation was switched to acenocumarol, adjusted to body weight, to maintain therapeutic anticoagulation levels. The patient was discharged without residual complications. The clinical course reflects a rare but serious complication of odontogenic infection—namely, infectious thrombophlebitis of the carotid arteries leading to septic pulmonary embolism—likely mediated by a systemic inflammatory response and endothelial activation due to bacterial endotoxin exposure, potentially exacerbated by underlying immunological vulnerabilities such as uncontrolled asthma and prior viral infection. The thrombotic event may represent a direct effect of bacterial toxins on vascular endothelium or a hypercoagulable state induced by acute inflammation, with subsequent embolic seeding of the pulmonary circulation. This case underscores the importance of early recognition of systemic complications in odontogenic infections, particularly in patients with comorbidities or immunological predispositions, and highlights the need for prompt initiation of broad-spectrum antibiotics and anticoagulation in the setting of suspected septic embolism.\"\n}", "generated_text": "A 27-year-old woman with a history of uncontrolled asthma and a prior mild SARS-CoV-2 infection presented 48 hours after completing oral phenoxymethylpenicillin 1,000,000 IU daily for five days, administered for a peritonsillar abscess, with new-onset facial edema and trismus. Physical examination revealed hemodynamic stability, absence of respiratory distress, and a palpable, homolateral, tender cervical adenopathy consistent with regional lymphadenopathy. Laboratory findings demonstrated leukocytosis, thrombocytopenia, and elevated acute-phase reactants, with no significant abnormalities in other parameters. Imaging studies included a head and neck CT, which revealed a large thrombus involving both the internal and external carotid arteries, consistent with a potentially infectious or inflammatory etiology triggering vasculopathy. A chest CT scan identified bilateral pulmonary septic emboli, indicating the dissemination of infectious material via venous thromboembolism from the head and neck region. Arterial Doppler ultrasound of the neck vessels was unremarkable, and cardiac Doppler ultrasound excluded cardiac vegetations, suggesting a non-cardiac source of embolic material. Initial empiric intravenous therapy consisted of ceftriaxone 1 g every 12 hours and clindamycin 300 mg every 6 hours to cover both gram-negative and gram-positive pathogens, including potential anaerobes. Concurrent anticoagulation was initiated with enoxaparin, dosed at 60 mg subcutaneously every 12 hours, adjusted for body weight and renal function, to manage the thrombotic burden. Over the subsequent 72 hours, the patient developed a fever of 38.5 °C and further leukocytosis, prompting repeat imaging and hemocultures. Hemocultures remained negative, and pharyngeal exudate culture was obtained. Given the clinical progression and lack of microbial growth in cultures, the antibiotic regimen was escalated to piperacillin-tazobactam 4.5 g every 6 hours intravenously to enhance coverage against multidrug-resistant or extended-spectrum pathogens. The patient responded favorably to this regimen, with resolution of fever and clinical signs of infection, and by day 14, chest CT showed complete absence of pulmonary embolic lesions. At that point, oral clindamycin 300 mg every 6 hours was transitioned to continue coverage for anaerobic flora, and anticoagulation was switched to acenocumarol, adjusted to body weight, to maintain therapeutic anticoagulation levels. The patient was discharged without residual complications. The clinical course reflects a rare but serious complication of odontogenic infection—namely, infectious thrombophlebitis of the carotid arteries leading to septic pulmonary embolism—likely mediated by a systemic inflammatory response and endothelial activation due to bacterial endotoxin exposure, potentially exacerbated by underlying immunological vulnerabilities such as uncontrolled asthma and prior viral infection. The thrombotic event may represent a direct effect of bacterial toxins on vascular endothelium or a hypercoagulable state induced by acute inflammation, with subsequent embolic seeding of the pulmonary circulation. This case underscores the importance of early recognition of systemic complications in odontogenic infections, particularly in patients with comorbidities or immunological predispositions, and highlights the need for prompt initiation of broad-spectrum antibiotics and anticoagulation in the setting of suspected septic embolism."}
+{"row_index": 89, "doc_id": 64, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 5-year-old child swallowed a toxic substance called chlorpyrifos, which hurt his body badly. He also breathed in a mix of charcoal and palm oil, which made his lungs worse. He started with fast breathing, sweating, shaking, and couldn’t breathe properly. He fell into a deep sleep (coma) and had very weak limbs. His breathing was so bad that he needed help right away. Doctors gave him breathing support at home (like a mask), medicine to stop the poison, and drugs to help his heart and blood pressure. He also had blood changes that needed fixing — they replaced part of his blood to clean it. His body slowly got better, he woke up fully, and stopped having trouble breathing. After 10 days, he was strong enough to go home. He didn’t have any serious late problems like some other kids with this poison might. But he didn’t come back for check-ups after leaving the hospital.\"\n}", "generated_text": "A 5-year-old child swallowed a toxic substance called chlorpyrifos, which hurt his body badly. He also breathed in a mix of charcoal and palm oil, which made his lungs worse. He started with fast breathing, sweating, shaking, and couldn’t breathe properly. He fell into a deep sleep (coma) and had very weak limbs. His breathing was so bad that he needed help right away. Doctors gave him breathing support at home (like a mask), medicine to stop the poison, and drugs to help his heart and blood pressure. He also had blood changes that needed fixing — they replaced part of his blood to clean it. His body slowly got better, he woke up fully, and stopped having trouble breathing. After 10 days, he was strong enough to go home. He didn’t have any serious late problems like some other kids with this poison might. But he didn’t come back for check-ups after leaving the hospital."}
+{"row_index": 90, "doc_id": 64, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 5-year-old child suffered severe poisoning from chlorpyrifos, a type of organophosphate pesticide, after swallowing it. Shortly after, the child also inhaled a mixture of charcoal and palm oil, which worsened the condition. The poisoning caused serious symptoms including fast breathing, excessive sweating, vomiting, muscle jerks, and eventually coma. At the time of arrival at the emergency department, the child had a very low level of consciousness, pinpoint pupils, weak limbs, and dangerously low oxygen levels in the blood. The heart was beating very fast, and blood pressure was low.\\n\\nThe child was diagnosed with severe organophosphate poisoning and lung damage from aspiration. Treatment included non-invasive breathing support (using bubble CPAP), intravenous atropine to help with the poisoning, antibiotics for the lung infection, and steroids to reduce inflammation. Because the family could not afford intensive care, the treatment was managed with available resources. The child received two blood exchange transfusions to help remove toxic substances from the blood.\\n\\nOver the next few days, the child’s breathing improved, consciousness returned, and symptoms slowly went away. Blood sugar levels were unstable at first but stabilized with treatment. The child was able to regain full awareness by the 39th hour and started eating regular food again. After 10 days of hospitalization, the child was discharged home, though no follow-up care was arranged afterward. The child did not develop a known complication called intermediate syndrome and responded well to treatment.\"\n}", "generated_text": "A 5-year-old child suffered severe poisoning from chlorpyrifos, a type of organophosphate pesticide, after swallowing it. Shortly after, the child also inhaled a mixture of charcoal and palm oil, which worsened the condition. The poisoning caused serious symptoms including fast breathing, excessive sweating, vomiting, muscle jerks, and eventually coma. At the time of arrival at the emergency department, the child had a very low level of consciousness, pinpoint pupils, weak limbs, and dangerously low oxygen levels in the blood. The heart was beating very fast, and blood pressure was low.\n\nThe child was diagnosed with severe organophosphate poisoning and lung damage from aspiration. Treatment included non-invasive breathing support (using bubble CPAP), intravenous atropine to help with the poisoning, antibiotics for the lung infection, and steroids to reduce inflammation. Because the family could not afford intensive care, the treatment was managed with available resources. The child received two blood exchange transfusions to help remove toxic substances from the blood.\n\nOver the next few days, the child’s breathing improved, consciousness returned, and symptoms slowly went away. Blood sugar levels were unstable at first but stabilized with treatment. The child was able to regain full awareness by the 39th hour and started eating regular food again. After 10 days of hospitalization, the child was discharged home, though no follow-up care was arranged afterward. The child did not develop a known complication called intermediate syndrome and responded well to treatment."}
+{"row_index": 91, "doc_id": 64, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 5-year-old child presented to the pediatric emergency department (ED) 13 hours after ingestion of chlorpyrifos, a potent organophosphate pesticide, followed by aspiration of a charcoal-palm oil mixture. The clinical presentation included acute cholinergic crisis characterized by abnormal muscle jerks, tachypnea (respiratory rate of 48 breaths per minute with intermittent sighing), dyspnea, excessive sweating, polyuria, increased secretions, and involuntary limb movements. The patient lapsed into coma prior to arrival, with presentation parameters including a core temperature of 38.3°C, Glasgow Coma Scale (GCS) of 3, pinpoint pupils, and global hypotonia. Vital signs at presentation revealed tachycardia (pulse 180 beats per minute), normotensive blood pressure (120/80 mmHg), and hypoglycemia (random blood glucose 14 mg/dL). Physical examination noted severe respiratory distress with oxygen saturation of 88% and widespread bilateral crackles on auscultation, indicative of pulmonary edema and aspiration-related pneumonitis.\\n\\nThe patient was diagnosed with severe organophosphate poisoning (OPP) and aspiration pneumonitis. Given the lack of ICU resources and affordability constraints, non-invasive ventilation (NIV) was initiated using bubble continuous positive airway pressure (b-CPAP), which successfully improved oxygenation to 99–100%. Hypoglycemia was promptly corrected with a dextrose bolus, and tachycardia was managed with 20 mL/kg of normal saline. Empirical intravenous antibiotics were administered to address suspected aspiration pneumonia. Intravenous atropine was administered at a dose of 0.02 mg/kg/dose to counteract excessive parasympathetic stimulation, with the first dose leading to a significant tachycardic response, prompting discontinuation due to risk of arrhythmia. Dexamethasone and mannitol were administered for cerebral protection and intracranial pressure control, respectively.\\n\\nDue to the severity of the cholinergic crisis and ongoing respiratory compromise, the patient underwent two episodes of fresh-whole-blood exchange blood transfusion (FWB-EBT), each involving 500 mL of blood, within the first 30 hours of admission. This intervention was likely aimed at rapidly removing circulating organophosphate metabolites and potentially mitigating neuromuscular and metabolic toxicity, though the exact mechanism remains under investigation in the context of acute OPP.\\n\\nOver the course of the first 30 hours, the patient’s neurological status improved, with GCS rising from 3 to 9/15, and respiratory distress gradually resolving. By day 2, rhonchi developed, managed with nebulized salbutamol and budesonide, and the patient transitioned to nasal prong oxygen therapy with sustained saturation at 97%. A chest radiograph confirmed bilateral pulmonary infiltrates consistent with pneumonia, likely secondary to aspiration and possible secondary infection.\\n\\nConsciousness was fully restored by the 39th hour of admission. Antioxidant therapy was initiated with intravenous vitamin C and B complex, and oral vitamin E and zinc to counteract oxidative stress induced by organophosphate toxicity and inflammation. A graded dietary reintroduction was implemented over the subsequent 48 hours. The patient’s clinical course remained stable, with progressive recovery of physiological parameters. He was discharged home after 10 days of hospitalization, though subsequent follow-up was lost to contact.\\n\\nPathophysiologically, chlorpyrifos inhibits acetylcholinesterase (AChE) in synaptic and neuromuscular junctions, leading to accumulation of acetylcholine, resulting in overstimulation of muscarinic and nicotinic receptors. This manifests as the classic cholinergic symptoms (e.g., bronchorrhea, bradycardia, miosis, sweating) and neuromuscular effects (e.g., fasciculations, paralysis). In this case, the severe respiratory failure and type I paralysis (flaccid paralysis) reflect profound neuromuscular blockade due to AChE inhibition. The development of intermediate syndrome, which typically occurs 24–96 hours post-exposure with delayed neuromuscular weakness, was absent, suggesting either a rapid clinical response to treatment or a possible protective effect of early exchange transfusion. The absence of pralidoxime administration (an oxime reactivator of AChE) due to unavailability may have limited the potential for early enzyme reactivation, though the patient’s favorable outcome suggests that supportive care and timely intervention were sufficient to prevent progression to irreversible neurological damage. Serum cholinesterase levels, which are typically suppressed in OPP, were not measured due to institutional limitations, limiting direct biochemical confirmation of enzyme", "generated_text": "{\n  \"proficient_health_literacy\": \"A 5-year-old child presented to the pediatric emergency department (ED) 13 hours after ingestion of chlorpyrifos, a potent organophosphate pesticide, followed by aspiration of a charcoal-palm oil mixture. The clinical presentation included acute cholinergic crisis characterized by abnormal muscle jerks, tachypnea (respiratory rate of 48 breaths per minute with intermittent sighing), dyspnea, excessive sweating, polyuria, increased secretions, and involuntary limb movements. The patient lapsed into coma prior to arrival, with presentation parameters including a core temperature of 38.3°C, Glasgow Coma Scale (GCS) of 3, pinpoint pupils, and global hypotonia. Vital signs at presentation revealed tachycardia (pulse 180 beats per minute), normotensive blood pressure (120/80 mmHg), and hypoglycemia (random blood glucose 14 mg/dL). Physical examination noted severe respiratory distress with oxygen saturation of 88% and widespread bilateral crackles on auscultation, indicative of pulmonary edema and aspiration-related pneumonitis.\\n\\nThe patient was diagnosed with severe organophosphate poisoning (OPP) and aspiration pneumonitis. Given the lack of ICU resources and affordability constraints, non-invasive ventilation (NIV) was initiated using bubble continuous positive airway pressure (b-CPAP), which successfully improved oxygenation to 99–100%. Hypoglycemia was promptly corrected with a dextrose bolus, and tachycardia was managed with 20 mL/kg of normal saline. Empirical intravenous antibiotics were administered to address suspected aspiration pneumonia. Intravenous atropine was administered at a dose of 0.02 mg/kg/dose to counteract excessive parasympathetic stimulation, with the first dose leading to a significant tachycardic response, prompting discontinuation due to risk of arrhythmia. Dexamethasone and mannitol were administered for cerebral protection and intracranial pressure control, respectively.\\n\\nDue to the severity of the cholinergic crisis and ongoing respiratory compromise, the patient underwent two episodes of fresh-whole-blood exchange blood transfusion (FWB-EBT), each involving 500 mL of blood, within the first 30 hours of admission. This intervention was likely aimed at rapidly removing circulating organophosphate metabolites and potentially mitigating neuromuscular and metabolic toxicity, though the exact mechanism remains under investigation in the context of acute OPP.\\n\\nOver the course of the first 30 hours, the patient’s neurological status improved, with GCS rising from 3 to 9/15, and respiratory distress gradually resolving. By day 2, rhonchi developed, managed with nebulized salbutamol and budesonide, and the patient transitioned to nasal prong oxygen therapy with sustained saturation at 97%. A chest radiograph confirmed bilateral pulmonary infiltrates consistent with pneumonia, likely secondary to aspiration and possible secondary infection.\\n\\nConsciousness was fully restored by the 39th hour of admission. Antioxidant therapy was initiated with intravenous vitamin C and B complex, and oral vitamin E and zinc to counteract oxidative stress induced by organophosphate toxicity and inflammation. A graded dietary reintroduction was implemented over the subsequent 48 hours. The patient’s clinical course remained stable, with progressive recovery of physiological parameters. He was discharged home after 10 days of hospitalization, though subsequent follow-up was lost to contact.\\n\\nPathophysiologically, chlorpyrifos inhibits acetylcholinesterase (AChE) in synaptic and neuromuscular junctions, leading to accumulation of acetylcholine, resulting in overstimulation of muscarinic and nicotinic receptors. This manifests as the classic cholinergic symptoms (e.g., bronchorrhea, bradycardia, miosis, sweating) and neuromuscular effects (e.g., fasciculations, paralysis). In this case, the severe respiratory failure and type I paralysis (flaccid paralysis) reflect profound neuromuscular blockade due to AChE inhibition. The development of intermediate syndrome, which typically occurs 24–96 hours post-exposure with delayed neuromuscular weakness, was absent, suggesting either a rapid clinical response to treatment or a possible protective effect of early exchange transfusion. The absence of pralidoxime administration (an oxime reactivator of AChE) due to unavailability may have limited the potential for early enzyme reactivation, though the patient’s favorable outcome suggests that supportive care and timely intervention were sufficient to prevent progression to irreversible neurological damage. Serum cholinesterase levels, which are typically suppressed in OPP, were not measured due to institutional limitations, limiting direct biochemical confirmation of enzyme"}
+{"row_index": 92, "doc_id": 65, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 19-year-old woman came to the hospital with a fast, irregular heartbeat and signs that her heart wasn't pumping well. Tests showed her heart was working poorly, and the doctors thought it might be because of a birth defect in her heart. They checked her heart with different scans: one ruled out a heart attack, another didn’t find heart muscle damage, and a special scan (CCTA) found that the main blood vessel to her right side of the heart was missing at the start. Instead, a small blood vessel grew around it to supply the heart. The doctors found the problem spot on a part of the heart muscle called the posteromedial papillary muscle, which was causing the fast heartbeat. They fixed it with a procedure that stops the abnormal heartbeat. Since then, she hasn’t had any symptoms and is feeling fine.\"\n}", "generated_text": "A 19-year-old woman came to the hospital with a fast, irregular heartbeat and signs that her heart wasn't pumping well. Tests showed her heart was working poorly, and the doctors thought it might be because of a birth defect in her heart. They checked her heart with different scans: one ruled out a heart attack, another didn’t find heart muscle damage, and a special scan (CCTA) found that the main blood vessel to her right side of the heart was missing at the start. Instead, a small blood vessel grew around it to supply the heart. The doctors found the problem spot on a part of the heart muscle called the posteromedial papillary muscle, which was causing the fast heartbeat. They fixed it with a procedure that stops the abnormal heartbeat. Since then, she hasn’t had any symptoms and is feeling fine."}
+{"row_index": 93, "doc_id": 65, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 19-year-old woman came to the emergency department with sudden palpitations and signs of cardiogenic shock. Her electrocardiogram showed a fast heart rhythm and other abnormal patterns, and her blood tests showed elevated markers of heart stress. A 12-lead ECG ruled out a heart attack, and cardiac MRI did not show signs of heart muscle disease. Because of this, doctors performed a cardiac CT scan (CCTA) to look for a possible congenital heart problem. The scan revealed that the opening of the right coronary artery was missing, and the heart was relying on a collateral blood vessel to supply blood to that area. This is a rare congenital condition. She was referred to a specialist center for congenital heart disease. There, an electrophysiological study found that the arrhythmia was originating from the posteromedial papillary muscle, and this area was successfully treated with radiofrequency ablation. Since the procedure, she has not had any symptoms and is doing well with regular follow-up.\"\n}", "generated_text": "A 19-year-old woman came to the emergency department with sudden palpitations and signs of cardiogenic shock. Her electrocardiogram showed a fast heart rhythm and other abnormal patterns, and her blood tests showed elevated markers of heart stress. A 12-lead ECG ruled out a heart attack, and cardiac MRI did not show signs of heart muscle disease. Because of this, doctors performed a cardiac CT scan (CCTA) to look for a possible congenital heart problem. The scan revealed that the opening of the right coronary artery was missing, and the heart was relying on a collateral blood vessel to supply blood to that area. This is a rare congenital condition. She was referred to a specialist center for congenital heart disease. There, an electrophysiological study found that the arrhythmia was originating from the posteromedial papillary muscle, and this area was successfully treated with radiofrequency ablation. Since the procedure, she has not had any symptoms and is doing well with regular follow-up."}
+{"row_index": 94, "doc_id": 65, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 19-year-old woman presented to the emergency department with acute onset of palpitations. Initial 12-lead electrocardiogram (ECG) revealed ventricular tachycardia with right branch bundle block and left posterior hemiblock, accompanied by T-wave inversion in inferior and precordial leads. Laboratory findings demonstrated elevated serum troponin (27 ng/L; normal <14 ng/L) and NT-pro BNP (2225 pg/mL; normal <130 pg/mL), indicating myocardial injury and volume overload consistent with cardiogenic shock. She was admitted to the coronary care unit.\\n\\nFive years prior, she had presented with cardiogenic shock secondary to fascicular ventricular tachycardia. Subsequent evaluation included cardiac magnetic resonance (CMR) and transesophageal electrophysiological study, both of which were inconclusive. She was diagnosed with tachycardiomiopathy and initiated standard medical therapy comprising angiotensin-converting enzyme inhibitors, mineralocorticoid receptor antagonists, and beta-blockers, with routine follow-up scheduled. Her clinical course remained stable thereafter.\\n\\nDuring the current admission, no additional episodes of hyperkinetic arrhythmias were observed. Baseline 12-lead ECG and echocardiography revealed diffuse hypokinesia of both ventricles, consistent with global systolic dysfunction. CMR remained inconclusive for underlying cardiomyopathy. Given the persistence of symptoms despite exclusion of acute myocardial infarction and structural cardiomyopathy, cardiac computed tomography angiography (CCTA) was performed to evaluate for undiagnosed congenital coronary anomalies. The CCTA was conducted using a GE Lightspeed scanner (GE HealthCare, Chicago, USA) with retrospective gating, at 100 kVp, 696 mAs, gantry rotation time of 0.35 s, and 0.625 mm slice thickness, with intravenous administration of 70 mL of Iomeron 400 mgI/mL (Bracco Imaging, Milan, Italy).\\n\\nDifferential diagnosis of cardiogenic shock includes myocardial infarction, arrhythmias, and various forms of cardiomyopathy. In otherwise healthy adult patients, undiagnosed congenital heart disease represents a significant and often underrecognized etiology. When acute myocardial infarction is excluded by 12-lead ECG and cardiomyopathy is not confirmed by CMR, CCTA becomes the preferred imaging modality to differentiate between obstructive coronary disease and congenital coronary anatomical variants.\\n\\nCCTA findings demonstrated a regular origin of the left main coronary artery, with a well-developed left anterior descending (LAD) artery exhibiting a wide ramus intermedium, two diagonal branches, and a thin, non-dominant left circumflex artery. No obstructive lesions were identified in any of these vessels. However, the ostium and proximal segment of the right coronary artery (RCA) were completely absent. Instead, the mid and distal RCA was supplied by a large collateral branch originating from the distal LAD, which encircles the lateral wall of the right ventricle, traverses the distal atrioventricular groove, and gives rise to thin posterior interventricular and posterolateral arteries. Additionally, a fine branch arising from the mid-LAD was observed to supply the sinoatrial node, potentially contributing to autonomic instability.\\n\\nBased on these findings, the patient underwent stress echocardiography, which confirmed inducible myocardial ischemia in the inferior wall—consistent with the anatomical location of the arrhythmic focus. She was subsequently transferred to a specialized center for congenital cardiovascular disease. There, she underwent transcatheter radiofrequency ablation targeting the sustained ventricular tachycardia originating from the posteromedial papillary muscle. Post-procedural follow-up revealed complete suppression of arrhythmias. At 6-month follow-up, she remains asymptomatic with no recurrence of ventricular tachycardia. Medical therapy post-ablation includes acetylsalicylic acid and verapamil for antiplatelet and rate control, respectively. The case underscores the importance of advanced imaging in diagnosing rare congenital coronary anomalies that may present with phenotypes mimicking acquired cardiomyopathy or acute coronary syndromes, particularly in young patients with recurrent arrhythmias and elevated biomarkers despite negative acute infarction workup.\"\n}", "generated_text": "A 19-year-old woman presented to the emergency department with acute onset of palpitations. Initial 12-lead electrocardiogram (ECG) revealed ventricular tachycardia with right branch bundle block and left posterior hemiblock, accompanied by T-wave inversion in inferior and precordial leads. Laboratory findings demonstrated elevated serum troponin (27 ng/L; normal <14 ng/L) and NT-pro BNP (2225 pg/mL; normal <130 pg/mL), indicating myocardial injury and volume overload consistent with cardiogenic shock. She was admitted to the coronary care unit.\n\nFive years prior, she had presented with cardiogenic shock secondary to fascicular ventricular tachycardia. Subsequent evaluation included cardiac magnetic resonance (CMR) and transesophageal electrophysiological study, both of which were inconclusive. She was diagnosed with tachycardiomiopathy and initiated standard medical therapy comprising angiotensin-converting enzyme inhibitors, mineralocorticoid receptor antagonists, and beta-blockers, with routine follow-up scheduled. Her clinical course remained stable thereafter.\n\nDuring the current admission, no additional episodes of hyperkinetic arrhythmias were observed. Baseline 12-lead ECG and echocardiography revealed diffuse hypokinesia of both ventricles, consistent with global systolic dysfunction. CMR remained inconclusive for underlying cardiomyopathy. Given the persistence of symptoms despite exclusion of acute myocardial infarction and structural cardiomyopathy, cardiac computed tomography angiography (CCTA) was performed to evaluate for undiagnosed congenital coronary anomalies. The CCTA was conducted using a GE Lightspeed scanner (GE HealthCare, Chicago, USA) with retrospective gating, at 100 kVp, 696 mAs, gantry rotation time of 0.35 s, and 0.625 mm slice thickness, with intravenous administration of 70 mL of Iomeron 400 mgI/mL (Bracco Imaging, Milan, Italy).\n\nDifferential diagnosis of cardiogenic shock includes myocardial infarction, arrhythmias, and various forms of cardiomyopathy. In otherwise healthy adult patients, undiagnosed congenital heart disease represents a significant and often underrecognized etiology. When acute myocardial infarction is excluded by 12-lead ECG and cardiomyopathy is not confirmed by CMR, CCTA becomes the preferred imaging modality to differentiate between obstructive coronary disease and congenital coronary anatomical variants.\n\nCCTA findings demonstrated a regular origin of the left main coronary artery, with a well-developed left anterior descending (LAD) artery exhibiting a wide ramus intermedium, two diagonal branches, and a thin, non-dominant left circumflex artery. No obstructive lesions were identified in any of these vessels. However, the ostium and proximal segment of the right coronary artery (RCA) were completely absent. Instead, the mid and distal RCA was supplied by a large collateral branch originating from the distal LAD, which encircles the lateral wall of the right ventricle, traverses the distal atrioventricular groove, and gives rise to thin posterior interventricular and posterolateral arteries. Additionally, a fine branch arising from the mid-LAD was observed to supply the sinoatrial node, potentially contributing to autonomic instability.\n\nBased on these findings, the patient underwent stress echocardiography, which confirmed inducible myocardial ischemia in the inferior wall—consistent with the anatomical location of the arrhythmic focus. She was subsequently transferred to a specialized center for congenital cardiovascular disease. There, she underwent transcatheter radiofrequency ablation targeting the sustained ventricular tachycardia originating from the posteromedial papillary muscle. Post-procedural follow-up revealed complete suppression of arrhythmias. At 6-month follow-up, she remains asymptomatic with no recurrence of ventricular tachycardia. Medical therapy post-ablation includes acetylsalicylic acid and verapamil for antiplatelet and rate control, respectively. The case underscores the importance of advanced imaging in diagnosing rare congenital coronary anomalies that may present with phenotypes mimicking acquired cardiomyopathy or acute coronary syndromes, particularly in young patients with recurrent arrhythmias and elevated biomarkers despite negative acute infarction workup."}
+{"row_index": 95, "doc_id": 66, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 17-year-old boy was found to have a small metal button stuck in his nose during a dental check-up. He had no symptoms like nose blockage, bleeding, or pain. The button had been there for over 10 years, probably since he was 7 years old when he put it in. It was hidden in the bottom part of his nose, covered with mucus and dirt, and looked shiny — that’s how doctors knew it was metal. X-rays showed the button clearly, and doctors confirmed it was safe and not hurting any bones or sinuses. The family had ignored earlier advice to remove it, thinking it would fall out on its own. The button was safely taken out in the clinic with local numbing spray and a small tool, with no serious bleeding. After removal, the nose healed well, and the boy is now doing fine with regular nose rinses.\"\n}", "generated_text": "A 17-year-old boy was found to have a small metal button stuck in his nose during a dental check-up. He had no symptoms like nose blockage, bleeding, or pain. The button had been there for over 10 years, probably since he was 7 years old when he put it in. It was hidden in the bottom part of his nose, covered with mucus and dirt, and looked shiny — that’s how doctors knew it was metal. X-rays showed the button clearly, and doctors confirmed it was safe and not hurting any bones or sinuses. The family had ignored earlier advice to remove it, thinking it would fall out on its own. The button was safely taken out in the clinic with local numbing spray and a small tool, with no serious bleeding. After removal, the nose healed well, and the boy is now doing fine with regular nose rinses."}
+{"row_index": 96, "doc_id": 67, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"An 18-year-old Hispanic male with no significant past medical history presented to the emergency department (ED) with acute onset of substernal, non-radiating chest pain, orthopnoea, dry non-productive cough, and subjective fevers lasting 3–4 days. Family history is notable for paternal grandfather with non-ischaemic cardiomyopathy and pacemaker implantation at age 86. The patient lives with both parents, denies smoking, alcohol use, recreational drug use, or abuse. He works at an auto parts shop and plans to begin college. Initial workup revealed elevated serum troponin I, diffuse ST-segment elevation on electrocardiogram (ECG), and an enlarged cardiac silhouette with mild pulmonary oedema on chest X-ray. Transthoracic echocardiography (TTE) demonstrated a left ventricular ejection fraction (LVEF) of 40%, severe left ventricular (LV) concentric hypertrophy (septal thickness 1.9 cm, inferolateral wall 2.2 cm), and mild posterior pericardial effusion. Coxsackie virus A and B titres were elevated, prompting initial consideration of viral myopericarditis. Symptoms initially improved with ibuprofen and colchicine, and cardiac catheterization confirmed absence of coronary artery disease. Repeat TTE showed LVEF of 40%–45%, hypokinesis of anteroapical and inferolateral walls, and elevated LV end-diastolic pressure consistent with diastolic dysfunction. Chest CT angiogram revealed pneumonitis and pericardial effusion, supporting a diagnosis of Coxsackie virus-induced myopericarditis. On day 4 of admission, the patient developed diaphoresis, tachycardia, and hypotension with undetectable blood pressure. Repeat TTE revealed large pericardial effusion with signs of impending cardiac tamponade, necessitating emergent pericardiocentesis. During the procedure, the patient experienced pulseless electrical activity (PEA) cardiac arrest, requiring 30 minutes of advanced cardiovascular life support. He was intubated, placed on veno-arterial extracorporeal membrane oxygenation (VA ECMO), and initiated vasopressor support (norepinephrine 5 mcg/min and vasopressin 0.05 units/min). Significant bleeding from ECMO cannulae necessitated multiple transfusions (9 packed red blood cells, 10 platelets, 10 cryoprecipitate, 4 fresh frozen plasma). The patient was transferred to a tertiary center for endomyocardial biopsy (EMB) due to concern for fulminant myocarditis or infiltrative cardiomyopathy. EMB showed no evidence of inflammatory or infiltrative process. Repeat Coxsackie serology confirmed positivity for Coxsackie A9, B2, and B6, and quantitative PCR for Epstein-Barr virus (EBV) DNA was elevated at 133,000 IU/mL. A subsequent TTE revealed a severely reduced LVEF of 10%–15% with persistent severe concentric LV hypertrophy. Intravenous immunoglobulin (IVIG) was initiated for suspected Coxsackie myocarditis, broad-spectrum antibiotics were administered for worsening leucocytosis without identifiable focus, and colchicine was discontinued due to concern for rhabdomyolysis (serum creatine kinase elevated to 2874 U/L). Vasopressors were discontinued and the patient was extubated. He subsequently developed flushing, fever, dyspnoea, and hypoxaemia with chest X-ray showing congested lung parenchyma suggestive of acute respiratory distress syndrome (ARDS), leading to IVIG discontinuation. Despite initial decompensation, cardiac function improved with a subsequent TTE showing LVEF of 25%–30%, prompting consideration of ECMO removal—this was unsuccessful. The patient remained on VA ECMO and was evaluated for left ventricular assist device (LVAD) placement, which was deemed contraindicated due to extensive global concentric LV hypertrophy. A multidisciplinary team concluded that emergency listing for heart transplantation was appropriate, with consideration of transition to intra-aortic balloon pump and inotrope support. During evaluation for transplantation, an incisional biopsy of a 1×1 inch, painless, rubbery, mobile lesion in the right upper extremity was performed. Pathology revealed aggressive EBV-positive natural killer/T-cell lymphoma (ENKTCL) with cytotoxic immunophenotype (positive for CD2, CD3, CD56, BCL2, granzyme B, TIA1, MUM1, and diffuse coexpression of Epstein-Barr virus-encoded small RNAs by in situ hybrid", "generated_text": "{\n  \"proficient_health_literacy\": \"An 18-year-old Hispanic male with no significant past medical history presented to the emergency department (ED) with acute onset of substernal, non-radiating chest pain, orthopnoea, dry non-productive cough, and subjective fevers lasting 3–4 days. Family history is notable for paternal grandfather with non-ischaemic cardiomyopathy and pacemaker implantation at age 86. The patient lives with both parents, denies smoking, alcohol use, recreational drug use, or abuse. He works at an auto parts shop and plans to begin college. Initial workup revealed elevated serum troponin I, diffuse ST-segment elevation on electrocardiogram (ECG), and an enlarged cardiac silhouette with mild pulmonary oedema on chest X-ray. Transthoracic echocardiography (TTE) demonstrated a left ventricular ejection fraction (LVEF) of 40%, severe left ventricular (LV) concentric hypertrophy (septal thickness 1.9 cm, inferolateral wall 2.2 cm), and mild posterior pericardial effusion. Coxsackie virus A and B titres were elevated, prompting initial consideration of viral myopericarditis. Symptoms initially improved with ibuprofen and colchicine, and cardiac catheterization confirmed absence of coronary artery disease. Repeat TTE showed LVEF of 40%–45%, hypokinesis of anteroapical and inferolateral walls, and elevated LV end-diastolic pressure consistent with diastolic dysfunction. Chest CT angiogram revealed pneumonitis and pericardial effusion, supporting a diagnosis of Coxsackie virus-induced myopericarditis. On day 4 of admission, the patient developed diaphoresis, tachycardia, and hypotension with undetectable blood pressure. Repeat TTE revealed large pericardial effusion with signs of impending cardiac tamponade, necessitating emergent pericardiocentesis. During the procedure, the patient experienced pulseless electrical activity (PEA) cardiac arrest, requiring 30 minutes of advanced cardiovascular life support. He was intubated, placed on veno-arterial extracorporeal membrane oxygenation (VA ECMO), and initiated vasopressor support (norepinephrine 5 mcg/min and vasopressin 0.05 units/min). Significant bleeding from ECMO cannulae necessitated multiple transfusions (9 packed red blood cells, 10 platelets, 10 cryoprecipitate, 4 fresh frozen plasma). The patient was transferred to a tertiary center for endomyocardial biopsy (EMB) due to concern for fulminant myocarditis or infiltrative cardiomyopathy. EMB showed no evidence of inflammatory or infiltrative process. Repeat Coxsackie serology confirmed positivity for Coxsackie A9, B2, and B6, and quantitative PCR for Epstein-Barr virus (EBV) DNA was elevated at 133,000 IU/mL. A subsequent TTE revealed a severely reduced LVEF of 10%–15% with persistent severe concentric LV hypertrophy. Intravenous immunoglobulin (IVIG) was initiated for suspected Coxsackie myocarditis, broad-spectrum antibiotics were administered for worsening leucocytosis without identifiable focus, and colchicine was discontinued due to concern for rhabdomyolysis (serum creatine kinase elevated to 2874 U/L). Vasopressors were discontinued and the patient was extubated. He subsequently developed flushing, fever, dyspnoea, and hypoxaemia with chest X-ray showing congested lung parenchyma suggestive of acute respiratory distress syndrome (ARDS), leading to IVIG discontinuation. Despite initial decompensation, cardiac function improved with a subsequent TTE showing LVEF of 25%–30%, prompting consideration of ECMO removal—this was unsuccessful. The patient remained on VA ECMO and was evaluated for left ventricular assist device (LVAD) placement, which was deemed contraindicated due to extensive global concentric LV hypertrophy. A multidisciplinary team concluded that emergency listing for heart transplantation was appropriate, with consideration of transition to intra-aortic balloon pump and inotrope support. During evaluation for transplantation, an incisional biopsy of a 1×1 inch, painless, rubbery, mobile lesion in the right upper extremity was performed. Pathology revealed aggressive EBV-positive natural killer/T-cell lymphoma (ENKTCL) with cytotoxic immunophenotype (positive for CD2, CD3, CD56, BCL2, granzyme B, TIA1, MUM1, and diffuse coexpression of Epstein-Barr virus-encoded small RNAs by in situ hybrid"}
+{"row_index": 97, "doc_id": 68, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 50-year-old man who smoked a lot and had bad cholesterol levels for years got a serious problem in one eye. The eye swelled fast, caused constant double vision (diplopia), and the eye movement got very weak. Even though his thyroid was normal, the eye tissue in one muscle (the right inferior rectus) turned hard and stiff, like fibrous tissue. This made the double vision worse and stayed bad even after steroid shots. The doctor tried medicine first, then surgery to open up the eye socket, which helped a little. The biopsy showed the muscle was completely filled with scar tissue. This case is rare and shows how serious eye problems can be in people with no thyroid issues.\"\n}", "generated_text": "A 50-year-old man who smoked a lot and had bad cholesterol levels for years got a serious problem in one eye. The eye swelled fast, caused constant double vision (diplopia), and the eye movement got very weak. Even though his thyroid was normal, the eye tissue in one muscle (the right inferior rectus) turned hard and stiff, like fibrous tissue. This made the double vision worse and stayed bad even after steroid shots. The doctor tried medicine first, then surgery to open up the eye socket, which helped a little. The biopsy showed the muscle was completely filled with scar tissue. This case is rare and shows how serious eye problems can be in people with no thyroid issues."}
+{"row_index": 98, "doc_id": 68, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 50-year-old man with a long history of smoking and high cholesterol developed a rare eye condition called euthyroid single muscular Graves' ophthalmopathy. He had no family or personal history of thyroid disease. Over several months, his right eye swelled rapidly, causing severe pain and constant double vision (diplopia) that made daily activities difficult. His vision was normal, but he could no longer move his eye properly, especially upward, which worsened his quality of life. Tests showed mild signs of thyroid autoimmunity, but his thyroid function was normal. Inflammation in the eye area was moderate, and imaging showed significant swelling only in the right inferior rectus muscle, while other eye muscles were unaffected. A biopsy confirmed massive fibrosis (scarring) in that muscle. Initial treatment with high-dose steroid injections helped reduce inflammation but did not improve double vision or eye movement. Two surgeries to relieve pressure in the eye socket were needed. The scarring in the muscle was the main reason the symptoms didn’t improve. This case highlights a rare form of eye disease that can cause serious vision problems even when the thyroid is healthy.\"\n}", "generated_text": "A 50-year-old man with a long history of smoking and high cholesterol developed a rare eye condition called euthyroid single muscular Graves' ophthalmopathy. He had no family or personal history of thyroid disease. Over several months, his right eye swelled rapidly, causing severe pain and constant double vision (diplopia) that made daily activities difficult. His vision was normal, but he could no longer move his eye properly, especially upward, which worsened his quality of life. Tests showed mild signs of thyroid autoimmunity, but his thyroid function was normal. Inflammation in the eye area was moderate, and imaging showed significant swelling only in the right inferior rectus muscle, while other eye muscles were unaffected. A biopsy confirmed massive fibrosis (scarring) in that muscle. Initial treatment with high-dose steroid injections helped reduce inflammation but did not improve double vision or eye movement. Two surgeries to relieve pressure in the eye socket were needed. The scarring in the muscle was the main reason the symptoms didn’t improve. This case highlights a rare form of eye disease that can cause serious vision problems even when the thyroid is healthy."}
+{"row_index": 99, "doc_id": 68, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"We present a rare case of euthyroid unilateral Graves' ophthalmopathy (GO) characterized by early and massive mono-muscular fibrosis involving the right inferior rectus muscle in a 50-year-old male patient. The patient has a family history of cardiovascular disease, type 2 diabetes mellitus, and myasthenia gravis, with no personal or familial history of thyroid autoimmune disorders. He is a long-term smoker (20 cigarettes/day since age 30) and has had chronic dyslipidemia for several years, with laboratory findings showing total cholesterol of 220 mg/dL, triglycerides of 297 mg/dL, and low high-density lipoprotein cholesterol (HDL) of 38 mg/dL—indicating a pro-atherogenic lipid profile. Since June 2020, the patient developed rapid and progressive soft tissue swelling in the right orbit, moderate pain during ocular movements, eyelid redness, and persistent diplopia. Visual acuity remained normal (16/17 and 17/17 in right and left eyes, respectively), and color vision was preserved. Ocular motility evaluation revealed severe depression of elevation and persistent primary position depression of the right globe, as quantified by the Gorman score, with constant diplopia. Clinical Activity Score (CAS) was 3/7, indicating moderate active inflammation, and Hertel measurements were 24 mm (right) and 18 mm (left), with a right orbital muscle orbit area ratio of 0.25 (in-house Autocad-based method; normal threshold vn ≤ 0.20±0.03), confirming significant enlargement of the inferior rectus muscle. CT imaging (1.25 mm contiguous slices, 200 mA, 120 kV, pitch 0.5) demonstrated marked expansion of the lower rectus body to the level of its tendon insertion, while all other extraocular muscles in both orbits exhibited normal morphology. Thyroid function tests were within normal limits, with only a slight elevation in thyroid-stimulating hormone receptor antibody (TSH-R-Ab) levels at 1.75 mU/L (normal <1.5 mU/L), consistent with subclinical autoimmune thyroid stimulation. Thyroid ultrasound revealed a thyroiditis-like pattern, suggestive of non-autoimmune thyroid inflammation. Electrophysiological assessment showed a slight reduction in the amplitude of the p100 wave in the right eye, indicating early neuro-ocular dysfunction. Routine systemic laboratory evaluations were unremarkable, excluding hematological or systemic diseases. Initial treatment with intravenous corticosteroid pulse therapy (Solumedrol, 4500 mg cumulative dose over 12 weeks) resulted in resolution of inflammatory signs and symptoms, but failed to improve ocular motility, Hertel measurements, or quality of life as measured by the Graves’ Ophthalmopathy Quality of Life Questionnaire (GO-QOL), where functional subscale scores (12.5) remained significantly lower than appearance subscale (50), despite normal visual acuity. Notably, electrophysiological parameters and visual function deteriorated during this period. As a result, second-line therapy with two-wall orbital surgical decompression combined with continued parenteral glucocorticoids was initiated. Histopathological examination of the right inferior rectus muscle biopsy revealed extensive fibrosis with significant adipose tissue infiltration, confirming the presence of early, severe, and isolated mono-muscular fibrotic change. This case highlights the potential for rapid progression of unilateral, euthyroid GO with prominent fibrotic transformation, even in the absence of significant thyroid autoimmunity, and underscores the importance of early surgical intervention in patients with persistent diplopia and progressive muscle enlargement despite medical therapy. The observed fibrosis may reflect a dysregulated fibroproliferative response to chronic inflammation, possibly driven by local cytokine milieu and metabolic factors such as dyslipidemia and smoking-related oxidative stress, which are known contributors to extracellular matrix remodeling in orbital tissues.\"\n}", "generated_text": "We present a rare case of euthyroid unilateral Graves' ophthalmopathy (GO) characterized by early and massive mono-muscular fibrosis involving the right inferior rectus muscle in a 50-year-old male patient. The patient has a family history of cardiovascular disease, type 2 diabetes mellitus, and myasthenia gravis, with no personal or familial history of thyroid autoimmune disorders. He is a long-term smoker (20 cigarettes/day since age 30) and has had chronic dyslipidemia for several years, with laboratory findings showing total cholesterol of 220 mg/dL, triglycerides of 297 mg/dL, and low high-density lipoprotein cholesterol (HDL) of 38 mg/dL—indicating a pro-atherogenic lipid profile. Since June 2020, the patient developed rapid and progressive soft tissue swelling in the right orbit, moderate pain during ocular movements, eyelid redness, and persistent diplopia. Visual acuity remained normal (16/17 and 17/17 in right and left eyes, respectively), and color vision was preserved. Ocular motility evaluation revealed severe depression of elevation and persistent primary position depression of the right globe, as quantified by the Gorman score, with constant diplopia. Clinical Activity Score (CAS) was 3/7, indicating moderate active inflammation, and Hertel measurements were 24 mm (right) and 18 mm (left), with a right orbital muscle orbit area ratio of 0.25 (in-house Autocad-based method; normal threshold vn ≤ 0.20±0.03), confirming significant enlargement of the inferior rectus muscle. CT imaging (1.25 mm contiguous slices, 200 mA, 120 kV, pitch 0.5) demonstrated marked expansion of the lower rectus body to the level of its tendon insertion, while all other extraocular muscles in both orbits exhibited normal morphology. Thyroid function tests were within normal limits, with only a slight elevation in thyroid-stimulating hormone receptor antibody (TSH-R-Ab) levels at 1.75 mU/L (normal <1.5 mU/L), consistent with subclinical autoimmune thyroid stimulation. Thyroid ultrasound revealed a thyroiditis-like pattern, suggestive of non-autoimmune thyroid inflammation. Electrophysiological assessment showed a slight reduction in the amplitude of the p100 wave in the right eye, indicating early neuro-ocular dysfunction. Routine systemic laboratory evaluations were unremarkable, excluding hematological or systemic diseases. Initial treatment with intravenous corticosteroid pulse therapy (Solumedrol, 4500 mg cumulative dose over 12 weeks) resulted in resolution of inflammatory signs and symptoms, but failed to improve ocular motility, Hertel measurements, or quality of life as measured by the Graves’ Ophthalmopathy Quality of Life Questionnaire (GO-QOL), where functional subscale scores (12.5) remained significantly lower than appearance subscale (50), despite normal visual acuity. Notably, electrophysiological parameters and visual function deteriorated during this period. As a result, second-line therapy with two-wall orbital surgical decompression combined with continued parenteral glucocorticoids was initiated. Histopathological examination of the right inferior rectus muscle biopsy revealed extensive fibrosis with significant adipose tissue infiltration, confirming the presence of early, severe, and isolated mono-muscular fibrotic change. This case highlights the potential for rapid progression of unilateral, euthyroid GO with prominent fibrotic transformation, even in the absence of significant thyroid autoimmunity, and underscores the importance of early surgical intervention in patients with persistent diplopia and progressive muscle enlargement despite medical therapy. The observed fibrosis may reflect a dysregulated fibroproliferative response to chronic inflammation, possibly driven by local cytokine milieu and metabolic factors such as dyslipidemia and smoking-related oxidative stress, which are known contributors to extracellular matrix remodeling in orbital tissues."}
+{"row_index": 100, "doc_id": 69, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 15-year-old boy had stomach pain and vomiting for four days. Doctors first thought it was a stomach bug, but it didn’t go away. His belly was swollen, and tests showed his intestines were blocked. A scan found a piece of intestine stuck in a small opening in his belly, called the Winslow hiatus. This caused the blockage. The doctors tried a small surgery first, but couldn’t see clearly, so they did a bigger cut in the middle of his belly to fix it. They pulled the stuck piece of intestine back into place and found it was just a small part of the small intestine that had slipped through the opening. No part of the intestine had to be cut off. They didn’t do any extra steps to prevent it from happening again. After surgery, he had a small pocket of fluid in his pelvis, which was treated with medicine and didn’t get worse. He’s now recovering at the pediatric surgery clinic and doing well.\"\n}", "generated_text": "A 15-year-old boy had stomach pain and vomiting for four days. Doctors first thought it was a stomach bug, but it didn’t go away. His belly was swollen, and tests showed his intestines were blocked. A scan found a piece of intestine stuck in a small opening in his belly, called the Winslow hiatus. This caused the blockage. The doctors tried a small surgery first, but couldn’t see clearly, so they did a bigger cut in the middle of his belly to fix it. They pulled the stuck piece of intestine back into place and found it was just a small part of the small intestine that had slipped through the opening. No part of the intestine had to be cut off. They didn’t do any extra steps to prevent it from happening again. After surgery, he had a small pocket of fluid in his pelvis, which was treated with medicine and didn’t get worse. He’s now recovering at the pediatric surgery clinic and doing well."}
+{"row_index": 101, "doc_id": 69, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 15-year-old boy with no prior medical issues came in with vomiting and abdominal pain that had lasted four days. At first, doctors thought it was gastroenteritis, but the symptoms didn’t go away. He was admitted to the hospital after tests showed signs of intestinal obstruction.\\n\\nAn abdominal CT scan found that a loop of small intestine had gotten stuck at the Winslow hiatus — a key opening in the abdomen — causing a blockage. The doctors tried to fix it with laparoscopy (a minimally invasive surgery), but poor visibility made it difficult. They switched to a larger open surgery (supraumbilical midline laparotomy) to safely see and treat the problem.\\n\\nDuring the surgery, they found a section of the ileum (part of the small intestine) that had herniated through the Winslow hiatus. The loop was about 5 centimeters long and was causing the blockage. The area around the opening looked normal, so no extra steps were taken to prevent it from coming back.\\n\\nAfter surgery, the boy had a temporary stop in bowel movement (paralytic ileus), which resolved after five days. He started eating again and did well. He also developed a small fluid collection in his pelvis, which was treated with antibiotics and improved over time. He was discharged ten days after surgery and is now being followed up in outpatient paediatric surgery. No further surgery is planned to prevent recurrence.\"\n}", "generated_text": "A 15-year-old boy with no prior medical issues came in with vomiting and abdominal pain that had lasted four days. At first, doctors thought it was gastroenteritis, but the symptoms didn’t go away. He was admitted to the hospital after tests showed signs of intestinal obstruction.\n\nAn abdominal CT scan found that a loop of small intestine had gotten stuck at the Winslow hiatus — a key opening in the abdomen — causing a blockage. The doctors tried to fix it with laparoscopy (a minimally invasive surgery), but poor visibility made it difficult. They switched to a larger open surgery (supraumbilical midline laparotomy) to safely see and treat the problem.\n\nDuring the surgery, they found a section of the ileum (part of the small intestine) that had herniated through the Winslow hiatus. The loop was about 5 centimeters long and was causing the blockage. The area around the opening looked normal, so no extra steps were taken to prevent it from coming back.\n\nAfter surgery, the boy had a temporary stop in bowel movement (paralytic ileus), which resolved after five days. He started eating again and did well. He also developed a small fluid collection in his pelvis, which was treated with antibiotics and improved over time. He was discharged ten days after surgery and is now being followed up in outpatient paediatric surgery. No further surgery is planned to prevent recurrence."}
+{"row_index": 102, "doc_id": 69, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"We present a clinical case of a 15-year-old male with no prior medical history or surgical interventions, who presented to the paediatric emergency department with a four-day history of vomiting and epigastric abdominal pain, remaining afebrile throughout. Initial evaluation was consistent with gastroenteritis, but symptoms persisted, including biliary vomiting and ongoing epigastric discomfort, prompting admission for further investigation.\\n\\nPhysical examination revealed an otherwise stable general condition, afebrile status, and mild signs of dehydration. The abdomen was distended, with absent peritoneal signs and diminished bowel sounds. Laboratory findings were non-contributory. Abdominal radiography demonstrated features consistent with small bowel obstruction.\\n\\nUrgent computed tomography (CT) was performed, revealing ascites and significant dilatation of small intestinal loops, with a focal change in caliber at the level of the Winslow hiatus, indicating interposition of a small intestinal loop within the trans-cavity of the epiploic foramen. The CT findings suggested a mechanical obstruction due to internal herniation of a segment of the ileum.\\n\\nSurgical management began with exploratory laparoscopy. Intraoperatively, dilated loops of the small intestine, including the terminal ileum, cecum, and ascending colon, were observed in the right hypochondrium. The cecum was noted to be highly mobile without adhesions to the right parietocolic space. Proximal to the terminal ileum, small intestinal loops were identified in the region corresponding to the theoretical location of the Winslow hiatus. Attempts to mobilize the cecum and terminal ileum toward the right iliac fossa were unsuccessful due to obstruction by the lower edge of the liver and the distended bowel loops. Percutaneous puncture of a dilated loop to decompress gas was attempted but did not improve visualization or facilitate reduction.\\n\\nDue to poor visualization and failure to identify the precise site of caliber change, a conversion to supraumbilical midline laparotomy was performed. In the open laparotomy, a clear change in intestinal caliber was observed approximately 40 cm distal to the ileocecal valve, confirming a herniation of a 5-cm segment of ileum through the Winslow hiatus. The herniated loop exhibited characteristic congestive imprints at both ends, consistent with compression and ischemic changes due to entrapment. The normal anatomical caliber of the Winslow hiatus was confirmed, and no preventive surgical technique (e.g., hernia repair or reinforcement) was performed to reduce the risk of recurrence.\\n\\nPostoperatively, the patient developed a paralytic ileus, which resolved over five days, allowing for nasogastric tube removal and initiation of oral intake with good tolerance. Concurrently, a pelvic collection was identified and managed conservatively with antibiotic therapy, with favorable clinical evolution. The patient was discharged ten days after surgery with preserved bowel transit, absence of fever, and stable general condition. He is currently under outpatient follow-up in the paediatric surgery clinic.\\n\\nThis case highlights the diagnostic challenge of internal hernias in adolescents, particularly those involving the Winslow hiatus, which may present with nonspecific gastrointestinal symptoms and mimic other conditions such as gastroenteritis or acute appendicitis. The anatomical complexity of the trans-cavity epiploic foramen, combined with the distension and mobility of bowel loops, contributes to the difficulty in both preoperative diagnosis and intraoperative identification. Internal hernias are often missed on routine imaging and require high index of suspicion, especially in young patients with prolonged abdominal pain and obstructive features. The lack of preventive intervention in this case underscores the potential for recurrence, although the absence of recurrence in the current follow-up suggests a favorable outcome in the absence of anatomical reinforcement.\"\n}", "generated_text": "We present a clinical case of a 15-year-old male with no prior medical history or surgical interventions, who presented to the paediatric emergency department with a four-day history of vomiting and epigastric abdominal pain, remaining afebrile throughout. Initial evaluation was consistent with gastroenteritis, but symptoms persisted, including biliary vomiting and ongoing epigastric discomfort, prompting admission for further investigation.\n\nPhysical examination revealed an otherwise stable general condition, afebrile status, and mild signs of dehydration. The abdomen was distended, with absent peritoneal signs and diminished bowel sounds. Laboratory findings were non-contributory. Abdominal radiography demonstrated features consistent with small bowel obstruction.\n\nUrgent computed tomography (CT) was performed, revealing ascites and significant dilatation of small intestinal loops, with a focal change in caliber at the level of the Winslow hiatus, indicating interposition of a small intestinal loop within the trans-cavity of the epiploic foramen. The CT findings suggested a mechanical obstruction due to internal herniation of a segment of the ileum.\n\nSurgical management began with exploratory laparoscopy. Intraoperatively, dilated loops of the small intestine, including the terminal ileum, cecum, and ascending colon, were observed in the right hypochondrium. The cecum was noted to be highly mobile without adhesions to the right parietocolic space. Proximal to the terminal ileum, small intestinal loops were identified in the region corresponding to the theoretical location of the Winslow hiatus. Attempts to mobilize the cecum and terminal ileum toward the right iliac fossa were unsuccessful due to obstruction by the lower edge of the liver and the distended bowel loops. Percutaneous puncture of a dilated loop to decompress gas was attempted but did not improve visualization or facilitate reduction.\n\nDue to poor visualization and failure to identify the precise site of caliber change, a conversion to supraumbilical midline laparotomy was performed. In the open laparotomy, a clear change in intestinal caliber was observed approximately 40 cm distal to the ileocecal valve, confirming a herniation of a 5-cm segment of ileum through the Winslow hiatus. The herniated loop exhibited characteristic congestive imprints at both ends, consistent with compression and ischemic changes due to entrapment. The normal anatomical caliber of the Winslow hiatus was confirmed, and no preventive surgical technique (e.g., hernia repair or reinforcement) was performed to reduce the risk of recurrence.\n\nPostoperatively, the patient developed a paralytic ileus, which resolved over five days, allowing for nasogastric tube removal and initiation of oral intake with good tolerance. Concurrently, a pelvic collection was identified and managed conservatively with antibiotic therapy, with favorable clinical evolution. The patient was discharged ten days after surgery with preserved bowel transit, absence of fever, and stable general condition. He is currently under outpatient follow-up in the paediatric surgery clinic.\n\nThis case highlights the diagnostic challenge of internal hernias in adolescents, particularly those involving the Winslow hiatus, which may present with nonspecific gastrointestinal symptoms and mimic other conditions such as gastroenteritis or acute appendicitis. The anatomical complexity of the trans-cavity epiploic foramen, combined with the distension and mobility of bowel loops, contributes to the difficulty in both preoperative diagnosis and intraoperative identification. Internal hernias are often missed on routine imaging and require high index of suspicion, especially in young patients with prolonged abdominal pain and obstructive features. The lack of preventive intervention in this case underscores the potential for recurrence, although the absence of recurrence in the current follow-up suggests a favorable outcome in the absence of anatomical reinforcement."}
+{"row_index": 103, "doc_id": 70, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 75-year-old woman from Western Ethiopia had a small birth control device (IUD) put in her uterus 40 years ago. Since then, she never checked it or saw a doctor. Now, she has pain in her lower belly and vagina, which started 3 years ago and got worse. The doctor found the old IUD still inside, near the opening of her cervix. It was easy to pull out using simple tools. She was given pain medicine and doxycycline to help her feel better and get rid of any infection. She went home after being watched for 4 hours and her pain went away.\"\n}", "generated_text": "A 75-year-old woman from Western Ethiopia had a small birth control device (IUD) put in her uterus 40 years ago. Since then, she never checked it or saw a doctor. Now, she has pain in her lower belly and vagina, which started 3 years ago and got worse. The doctor found the old IUD still inside, near the opening of her cervix. It was easy to pull out using simple tools. She was given pain medicine and doxycycline to help her feel better and get rid of any infection. She went home after being watched for 4 hours and her pain went away."}
+{"row_index": 104, "doc_id": 70, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 75-year-old woman from Western Ethiopia, who had her last period 25 years ago, came to the hospital with ongoing lower abdominal pain and discomfort in her vagina. She had been using an intrauterine device (IUD), specifically a Lippes loop, since she was 18 years old — meaning it had been in place for 40 years. She had never had a gynecological checkup since then and didn’t know it was still inside her. During a pelvic exam, doctors found part of the IUD at the opening of her cervix. It was easily removed using special forceps. The patient was given pain relief and doxycycline for 3 days to prevent infection. She was discharged after being observed for 4 hours and her pain went away after treatment.\"\n}", "generated_text": "A 75-year-old woman from Western Ethiopia, who had her last period 25 years ago, came to the hospital with ongoing lower abdominal pain and discomfort in her vagina. She had been using an intrauterine device (IUD), specifically a Lippes loop, since she was 18 years old — meaning it had been in place for 40 years. She had never had a gynecological checkup since then and didn’t know it was still inside her. During a pelvic exam, doctors found part of the IUD at the opening of her cervix. It was easily removed using special forceps. The patient was given pain relief and doxycycline for 3 days to prevent infection. She was discharged after being observed for 4 hours and her pain went away after treatment."}
+{"row_index": 105, "doc_id": 71, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 71-year-old man had a long-time skin condition called vitiligo and started losing vision in his right eye six months before hospital visit. He also lost hearing in both ears, worse on the right side. He had bad headaches, fever, and lost weight without trying. When doctors checked his eyes, the right eye was very sensitive to light and had redness, while the left eye could only see blurry shapes. The right eye’s back part had dark spots and the optic nerve was damaged (atrophied), and the left eye had swelling around the nerve and early nerve damage (optic neuritis). Doctors checked for infections and diseases like TB, herpes, or autoimmune problems, but none were found. A spinal fluid test showed normal pressure but a bit high protein, which could mean nerve issues. Nerve tests showed damage to nerves in arms and legs, worse in the legs. Brain and eye scans didn’t show tumors, but showed signs of infection in the sinuses and lining of the brain. Sarcoidosis was ruled out with blood and scan tests. Because of the eye and nerve damage, doctors started high-dose steroid pills to reduce inflammation. After a few weeks, the man’s vision and headaches got better, and he started feeling stronger. He’s now being followed up in the clinic for ongoing care.\"\n}", "generated_text": "A 71-year-old man had a long-time skin condition called vitiligo and started losing vision in his right eye six months before hospital visit. He also lost hearing in both ears, worse on the right side. He had bad headaches, fever, and lost weight without trying. When doctors checked his eyes, the right eye was very sensitive to light and had redness, while the left eye could only see blurry shapes. The right eye’s back part had dark spots and the optic nerve was damaged (atrophied), and the left eye had swelling around the nerve and early nerve damage (optic neuritis). Doctors checked for infections and diseases like TB, herpes, or autoimmune problems, but none were found. A spinal fluid test showed normal pressure but a bit high protein, which could mean nerve issues. Nerve tests showed damage to nerves in arms and legs, worse in the legs. Brain and eye scans didn’t show tumors, but showed signs of infection in the sinuses and lining of the brain. Sarcoidosis was ruled out with blood and scan tests. Because of the eye and nerve damage, doctors started high-dose steroid pills to reduce inflammation. After a few weeks, the man’s vision and headaches got better, and he started feeling stronger. He’s now being followed up in the clinic for ongoing care."}
+{"row_index": 106, "doc_id": 71, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 71-year-old man with long-standing vitiligo had lost vision in his right eye six months before hospitalization, along with hearing loss in both ears, worse on the right side. He also had chronic headaches, fever, and lost a lot of weight without trying. On eye exams, his right eye had very poor vision, was sensitive to light, and showed signs of damage including a swollen optic nerve and pigment spots. His left eye had good vision (20/200), but the optic nerve was swollen and there was early nerve damage. The right eye also showed signs of nerve degeneration. Tests were done to check for conditions like tuberculosis, infections, or autoimmune diseases, and none were found. A spinal fluid test showed normal pressure but slightly high protein levels. Nerve tests showed damage to multiple nerves, especially in the legs. Brain and eye MRI scans found no tumors, but showed signs of sinus infection and inflammation around the brain lining. Sarcoidosis was ruled out with normal blood and imaging tests. After further eye evaluation, the doctor confirmed ongoing eye nerve damage, including optic atrophy on the right and optic neuritis on the left. The patient started high-dose steroid treatment, which was slowly reduced over time. He improved over time, with better vision and less nerve-related symptoms, and was referred for ongoing follow-up care.\"\n}", "generated_text": "A 71-year-old man with long-standing vitiligo had lost vision in his right eye six months before hospitalization, along with hearing loss in both ears, worse on the right side. He also had chronic headaches, fever, and lost a lot of weight without trying. On eye exams, his right eye had very poor vision, was sensitive to light, and showed signs of damage including a swollen optic nerve and pigment spots. His left eye had good vision (20/200), but the optic nerve was swollen and there was early nerve damage. The right eye also showed signs of nerve degeneration. Tests were done to check for conditions like tuberculosis, infections, or autoimmune diseases, and none were found. A spinal fluid test showed normal pressure but slightly high protein levels. Nerve tests showed damage to multiple nerves, especially in the legs. Brain and eye MRI scans found no tumors, but showed signs of sinus infection and inflammation around the brain lining. Sarcoidosis was ruled out with normal blood and imaging tests. After further eye evaluation, the doctor confirmed ongoing eye nerve damage, including optic atrophy on the right and optic neuritis on the left. The patient started high-dose steroid treatment, which was slowly reduced over time. He improved over time, with better vision and less nerve-related symptoms, and was referred for ongoing follow-up care."}
+{"row_index": 107, "doc_id": 71, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 71-year-old male with a history of untreated vitiligo presented with right-sided visual loss six months prior to admission, accompanied by bilateral sensorineural hearing loss with predilection for the right ear. He also reported chronic headaches, intermittent fever, and significant unintentional weight loss, along with generalized weakness and cutaneous thickening. Ophthalmologic examination revealed reduced visual acuity in the right eye (RO) to light perception with impaired color discrimination, and 20/200 visual acuity in the left eye (LO), with an afferent pupillary defect in both eyes. Both eyes exhibited hyperemic bulbar conjunctiva and ciliary injection. Corneal findings included peripheral, nummular, subepithelial infiltrates in both eyes, with aqueous anterior chamber (AAC) clear and no cellular infiltrate. Iris and lens were normal, though both demonstrated nuclear opacities. Fundus examination of the right eye showed a pale ++ papilla with 50% excavation, blunt nasal border, thinned and raised vascular pattern, macular involvement, and scattered pigmentary deposits. The left eye fundus demonstrated vitreous haze 2+, edematous papilla, blurred borders, peripapillary streaked hemorrhages, an unevaluable excavation, thinned vascular pattern, macular changes, and scattered pigment. Notably, the right optic nerve exhibited atrophy, and the left eye showed signs of anterior optic neuritis. Additional neurological evaluation included lumbar puncture, which revealed normal opening pressure and a cerebrospinal fluid (CSF) protein level of 54 mg/dL, consistent with non-inflammatory or mild neuroinflammatory processes. Nerve conduction studies demonstrated a pattern of symmetric polyradiculoneuropathy with moderate to severe axonal degeneration affecting all four extremities, with greater involvement in the lower limbs, suggesting a distal symmetric polyneuropathy. Contrast-enhanced magnetic resonance imaging (MRI) of the skull and orbits showed no evidence of optic nerve enhancement or intracranial tumors, but did reveal sinusitis and meningeal enhancement, indicating possible meningeal inflammation. Sarcoidosis was excluded based on normal angiotensin-converting enzyme (ACE) levels and a whole-body gamma scan without focal or diffuse uptake. Anti-neutrophil cytoplasmic antibody (ANCA)-positive and ANCA-negative vasculitides were also ruled out. The ocular and neurological manifestations progressed over time, confirming persistent disease activity. High-dose pulse corticosteroid therapy was initiated, followed by a stepwise tapering regimen, resulting in clinically and functionally significant improvement in both ophthalmological and neurological parameters. The patient was subsequently referred for ongoing outpatient follow-up. The clinical course supports a diagnosis of a chronic, immune-mediated neuro-ophthalmic disorder, likely involving autoimmune-mediated optic nerve damage, with features consistent with a vasculitic or inflammatory process affecting the optic pathways, possibly related to the underlying vitiligo, which may represent a chronic autoimmune skin condition with systemic immune dysregulation.\"\n}", "generated_text": "A 71-year-old male with a history of untreated vitiligo presented with right-sided visual loss six months prior to admission, accompanied by bilateral sensorineural hearing loss with predilection for the right ear. He also reported chronic headaches, intermittent fever, and significant unintentional weight loss, along with generalized weakness and cutaneous thickening. Ophthalmologic examination revealed reduced visual acuity in the right eye (RO) to light perception with impaired color discrimination, and 20/200 visual acuity in the left eye (LO), with an afferent pupillary defect in both eyes. Both eyes exhibited hyperemic bulbar conjunctiva and ciliary injection. Corneal findings included peripheral, nummular, subepithelial infiltrates in both eyes, with aqueous anterior chamber (AAC) clear and no cellular infiltrate. Iris and lens were normal, though both demonstrated nuclear opacities. Fundus examination of the right eye showed a pale ++ papilla with 50% excavation, blunt nasal border, thinned and raised vascular pattern, macular involvement, and scattered pigmentary deposits. The left eye fundus demonstrated vitreous haze 2+, edematous papilla, blurred borders, peripapillary streaked hemorrhages, an unevaluable excavation, thinned vascular pattern, macular changes, and scattered pigment. Notably, the right optic nerve exhibited atrophy, and the left eye showed signs of anterior optic neuritis. Additional neurological evaluation included lumbar puncture, which revealed normal opening pressure and a cerebrospinal fluid (CSF) protein level of 54 mg/dL, consistent with non-inflammatory or mild neuroinflammatory processes. Nerve conduction studies demonstrated a pattern of symmetric polyradiculoneuropathy with moderate to severe axonal degeneration affecting all four extremities, with greater involvement in the lower limbs, suggesting a distal symmetric polyneuropathy. Contrast-enhanced magnetic resonance imaging (MRI) of the skull and orbits showed no evidence of optic nerve enhancement or intracranial tumors, but did reveal sinusitis and meningeal enhancement, indicating possible meningeal inflammation. Sarcoidosis was excluded based on normal angiotensin-converting enzyme (ACE) levels and a whole-body gamma scan without focal or diffuse uptake. Anti-neutrophil cytoplasmic antibody (ANCA)-positive and ANCA-negative vasculitides were also ruled out. The ocular and neurological manifestations progressed over time, confirming persistent disease activity. High-dose pulse corticosteroid therapy was initiated, followed by a stepwise tapering regimen, resulting in clinically and functionally significant improvement in both ophthalmological and neurological parameters. The patient was subsequently referred for ongoing outpatient follow-up. The clinical course supports a diagnosis of a chronic, immune-mediated neuro-ophthalmic disorder, likely involving autoimmune-mediated optic nerve damage, with features consistent with a vasculitic or inflammatory process affecting the optic pathways, possibly related to the underlying vitiligo, which may represent a chronic autoimmune skin condition with systemic immune dysregulation."}
+{"row_index": 108, "doc_id": 72, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 39-year-old female with peripartum cardiomyopathy underwent heart transplantation in October 2014. Induction therapy consisted of basiliximab and methylprednisolone, with maintenance immunosuppression comprising tacrolimus XL prolonged release 7 mg daily, everolimus 1 mg twice daily, and prednisolone 5 mg/day. During the first post-transplant year, she experienced two episodes of acute rejection, both managed effectively with methylprednisolone pulse therapy. No prior history of renal disease was noted, and early post-transplant renal function was stable, with serum creatinine of 0.88 mg/dL and a glomerular filtration rate (GFR) of 102 mL/min/1.73m². Routine monitoring for polyomavirus infection, including BK virus viral load and urinary cytology, was not performed during follow-up. In 2016, serum creatinine elevated to a peak of 1.9 mg/dL, with a GFR of 32.6 mL/min/1.73m². At that time, minimum tacrolimus level was 7.2 ng/mL and everolimus 5.2 ng/mL, prompting suspicion of calcineurin inhibitor toxicity. Tacrolimus was reduced to 4 mg daily, resulting in a partial recovery of renal function (creatinine 1.25 mg/dL, GFR 54.1 mL/min/1.73m²); no renal biopsy was conducted. In March 2017, creatinine rose to 2.69 mg/dL and GFR dropped to 21.4 mL/min/1.73m², necessitating hospitalization despite the absence of clinical symptoms. Physical examination revealed normal general condition, heart rate of 80 bpm, blood pressure 130/90 mmHg, respiratory rate of 15/min, and no fever. Imaging and laboratory studies, including renal ultrasound (normal size, increased echogenicity), urinalysis (negative for hematuria, pyuria, and casts), urine culture, echocardiography (normal cardiac function), and serologic screening for HIV, syphilis, hepatitis B and C (all negative), were unremarkable. Minimum immunosuppressant levels remained within therapeutic range (tacrolimus 5.2 ng/mL, everolimus 5.98 ng/mL). Intravenous hydration and further reduction of tacrolimus to 2 mg daily were initiated, but renal function did not improve, leading to the decision for renal biopsy. The biopsy revealed active chronic tubulointerstitial nephritis with evidence of late-stage BK virus nephropathy. BK virus PCR detected a viral load of 33,800 copies/mL in serum (log 4.5), confirming active viral replication. Tacrolimus was discontinued due to its nephrotoxic potential in the context of BK virus infection. Post-treatment, serum creatinine stabilized between 2.2 and 2.4 mg/dL without further elevation, and the viral load progressively declined to undetectable levels. Over a three-year follow-up period, the patient remained free of cardiac rejection episodes. The most recent serum creatinine measurement was 2.5 mg/dL, corresponding to a GFR of 23.4 mL/min/1.73m², indicating stable but significantly reduced renal function consistent with chronic tubulointerstitial injury secondary to BK virus infection. The pathophysiological mechanism involves BK virus-induced tubular epithelial cell damage, leading to interstitial inflammation, fibrosis, and progressive glomerular dysfunction, exacerbated by immunosuppressive therapy that impairs viral clearance. The clinical course highlights the importance of vigilant monitoring for polyomavirus infection in solid organ transplant recipients, particularly in the setting of prolonged immunosuppression and declining renal function, even in the absence of overt symptoms.\"\n}", "generated_text": "A 39-year-old female with peripartum cardiomyopathy underwent heart transplantation in October 2014. Induction therapy consisted of basiliximab and methylprednisolone, with maintenance immunosuppression comprising tacrolimus XL prolonged release 7 mg daily, everolimus 1 mg twice daily, and prednisolone 5 mg/day. During the first post-transplant year, she experienced two episodes of acute rejection, both managed effectively with methylprednisolone pulse therapy. No prior history of renal disease was noted, and early post-transplant renal function was stable, with serum creatinine of 0.88 mg/dL and a glomerular filtration rate (GFR) of 102 mL/min/1.73m². Routine monitoring for polyomavirus infection, including BK virus viral load and urinary cytology, was not performed during follow-up. In 2016, serum creatinine elevated to a peak of 1.9 mg/dL, with a GFR of 32.6 mL/min/1.73m². At that time, minimum tacrolimus level was 7.2 ng/mL and everolimus 5.2 ng/mL, prompting suspicion of calcineurin inhibitor toxicity. Tacrolimus was reduced to 4 mg daily, resulting in a partial recovery of renal function (creatinine 1.25 mg/dL, GFR 54.1 mL/min/1.73m²); no renal biopsy was conducted. In March 2017, creatinine rose to 2.69 mg/dL and GFR dropped to 21.4 mL/min/1.73m², necessitating hospitalization despite the absence of clinical symptoms. Physical examination revealed normal general condition, heart rate of 80 bpm, blood pressure 130/90 mmHg, respiratory rate of 15/min, and no fever. Imaging and laboratory studies, including renal ultrasound (normal size, increased echogenicity), urinalysis (negative for hematuria, pyuria, and casts), urine culture, echocardiography (normal cardiac function), and serologic screening for HIV, syphilis, hepatitis B and C (all negative), were unremarkable. Minimum immunosuppressant levels remained within therapeutic range (tacrolimus 5.2 ng/mL, everolimus 5.98 ng/mL). Intravenous hydration and further reduction of tacrolimus to 2 mg daily were initiated, but renal function did not improve, leading to the decision for renal biopsy. The biopsy revealed active chronic tubulointerstitial nephritis with evidence of late-stage BK virus nephropathy. BK virus PCR detected a viral load of 33,800 copies/mL in serum (log 4.5), confirming active viral replication. Tacrolimus was discontinued due to its nephrotoxic potential in the context of BK virus infection. Post-treatment, serum creatinine stabilized between 2.2 and 2.4 mg/dL without further elevation, and the viral load progressively declined to undetectable levels. Over a three-year follow-up period, the patient remained free of cardiac rejection episodes. The most recent serum creatinine measurement was 2.5 mg/dL, corresponding to a GFR of 23.4 mL/min/1.73m², indicating stable but significantly reduced renal function consistent with chronic tubulointerstitial injury secondary to BK virus infection. The pathophysiological mechanism involves BK virus-induced tubular epithelial cell damage, leading to interstitial inflammation, fibrosis, and progressive glomerular dysfunction, exacerbated by immunosuppressive therapy that impairs viral clearance. The clinical course highlights the importance of vigilant monitoring for polyomavirus infection in solid organ transplant recipients, particularly in the setting of prolonged immunosuppression and declining renal function, even in the absence of overt symptoms."}
+{"row_index": 109, "doc_id": 73, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 14-year-old boy who had a cough and breathing trouble was found to have a lump in his chest, likely cancer called non-Hodgkin lymphoma. He was treated with a medicine called L-asp and prednisone. During this treatment, he started having high fat levels in his blood and low sodium levels, which doctors thought might be a side effect of the medicines. They checked this using a special method and found it was definitely caused by the mix of L-asp and prednisone. He was given a low-fat diet, plus medicines to lower his fat levels. His fat levels went back to normal in 14 days. The medicines were not stopped because the cancer treatment was still going. His body got better without any serious problems.\"\n}", "generated_text": "A 14-year-old boy who had a cough and breathing trouble was found to have a lump in his chest, likely cancer called non-Hodgkin lymphoma. He was treated with a medicine called L-asp and prednisone. During this treatment, he started having high fat levels in his blood and low sodium levels, which doctors thought might be a side effect of the medicines. They checked this using a special method and found it was definitely caused by the mix of L-asp and prednisone. He was given a low-fat diet, plus medicines to lower his fat levels. His fat levels went back to normal in 14 days. The medicines were not stopped because the cancer treatment was still going. His body got better without any serious problems."}
+{"row_index": 110, "doc_id": 73, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 14-year-old boy with a history of a nighttime cough was admitted to the hospital after developing severe breathing problems and abdominal pain. Tests showed a mass in the middle of his chest, leading to a suspicion of non-Hodgkin lymphoma. He was treated with chemotherapy, including L-asp and prednisone, as part of a standard protocol. During treatment, he developed high levels of triglycerides in his blood and low sodium levels (a condition called pseudohyponatraemia), which are known to be linked to certain medications. Doctors suspected this was a drug reaction (ADR) caused by the combination of L-asp and prednisone. Using a standard method to evaluate drug reactions, they concluded it was a 'definitive' drug reaction. He was given a low-fat, high-fiber diet and medications to lower his triglycerides, which improved within 14 days. His condition stabilized, and the drug reaction resolved without complications. The medications were not stopped because the treatment for lymphoma was still ongoing, as per the treatment plan.\"\n}", "generated_text": "A 14-year-old boy with a history of a nighttime cough was admitted to the hospital after developing severe breathing problems and abdominal pain. Tests showed a mass in the middle of his chest, leading to a suspicion of non-Hodgkin lymphoma. He was treated with chemotherapy, including L-asp and prednisone, as part of a standard protocol. During treatment, he developed high levels of triglycerides in his blood and low sodium levels (a condition called pseudohyponatraemia), which are known to be linked to certain medications. Doctors suspected this was a drug reaction (ADR) caused by the combination of L-asp and prednisone. Using a standard method to evaluate drug reactions, they concluded it was a 'definitive' drug reaction. He was given a low-fat, high-fiber diet and medications to lower his triglycerides, which improved within 14 days. His condition stabilized, and the drug reaction resolved without complications. The medications were not stopped because the treatment for lymphoma was still ongoing, as per the treatment plan."}
+{"row_index": 111, "doc_id": 73, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 14-year-old previously healthy adolescent presented to the Primary Emergency Care Service (PEC) of Osorno with a 11-day history of nocturnal irritative cough, progressing to dyspnoea and orthopnoea. Upon evaluation at the Osorno Base Hospital (OBH), he was found to have severe respiratory distress, intolerance to supine positioning, and abdominal pain. He was admitted to the Paediatric Intensive Care Unit (PICU) in a tachycardic, hypertensive, polypneic state with oxygen saturation of 96% on 35% FiO2, rosy peripheries, adequate hydration, and well-perfused tissues, with flat jugular veins and small bilateral supraclavicular lymphadenopathies. Physical examination revealed no soft tissue retraction, maintained genupectoral posture, decreased pulmonary murmurs in both lung bases, and muffled cardiac tones without breath sounds. Abdominal examination showed non-depressible, tender soft tissue in both hypochondria with doubtful visceral enlargement and no trauma. Chest radiography demonstrated a superior mediastinal mass, atelectasis of the right middle lobe, and ipsilateral pleural effusion. Contrast-enhanced chest imaging was not performed due to contraindication of anaesthesia, as noted in the transfer summary. The patient was transferred to the PICU HBV with a diagnosis of mediastinal compression syndrome and clinical suspicion of non-Hodgkin lymphoma. Multidisciplinary evaluation by paediatric haemato-oncology, surgery, intensive care, imaging, radiotherapy, and oncology teams confirmed a normal pulmonary murmur and muffled cardiac auscultation, with no breath sounds, and persistent abdominal tenderness and suspected visceral enlargement. The chest radiograph remained consistent with a superior mediastinal mass and right middle lobe atelectasis with pleural effusion. A nephrological assessment revealed acute renal failure secondary to tumor lysis syndrome, with serum creatinine of 1.54 mg/dL, phosphoria of 11 mg/dL, and no hypernatremia. No dialysis was required, and the patient was managed with furosemide for volume control and amlodipine for hypertension. Respiratory support was initiated with Venturi mask at 35% FiO2, which was discontinued on day three due to clinical improvement. Episodes of psychomotor agitation, attributed to diagnostic stress, were managed according to institutional protocols with psychological and psychiatric support, resulting in satisfactory clinical course. On day three, a contrast-enhanced CT of the thorax, abdomen, and pelvis was performed, revealing thymic enlargement with homogeneous appearance, suggestive of a lymphoproliferative process, and findings consistent with pulmonary thromboembolism. AngioCT of the thorax confirmed jugular vein thrombosis, extensive bilateral pleural effusion, atelectasis in both lung bases, and signs of bilateral nephrotic syndrome. Anticoagulation with enoxaparin (1 mg/kg every 12 hours) was initiated for 20 days, with follow-up angioCT showing complete resolution of thrombosis. On day four, comprehensive diagnostic workup was completed, including complete biochemical profile (including lipid panel), bone marrow myelogram showing granulopoietic hyperplasia, flow cytometry of bone marrow and peripheral blood, which was negative for clonal or neoplastic haematopoietic immunophenotypes, and cytological analysis of pleural fluid, which was negative for neoplastic cells. Flow cytometry of pleural fluid also failed to detect haematological neoplasia. The patient was referred to the paediatric oncology committee, where, due to the absence of a viable biopsy specimen (as the mediastinal mass resolved with cytoreductive therapy), a diagnosis of lymphoblastic lymphoma was established based on clinical presentation and response to treatment, in accordance with the PINDA 0516 induction protocol. This protocol includes eight doses of L-asp (L-asparaginase) at 10,000 IU/m² in Induction IA. The patient received seven doses of L-asp, accumulating a total of 90,000 IU, in combination with prednisone glucocorticoids. During this period, he developed clinical deterioration with vomiting, abdominal pain, and mild dehydration. Pancreatitis was suspected but ruled out by normal amylase and lipase levels and normal hepatic function tests. Laboratory findings included hyponatraemia (126 mOsm/kg) and hypertriglyceridaemia, with urinary osmolality of 510 mOsm/kg (within normal range), leading to suspicion of a drug-induced metabolic disturbance—specifically, pseudohyponatraemia secondary to hypertriglyceridaemia. This was further supported", "generated_text": "{\n  \"proficient_health_literacy\": \"A 14-year-old previously healthy adolescent presented to the Primary Emergency Care Service (PEC) of Osorno with a 11-day history of nocturnal irritative cough, progressing to dyspnoea and orthopnoea. Upon evaluation at the Osorno Base Hospital (OBH), he was found to have severe respiratory distress, intolerance to supine positioning, and abdominal pain. He was admitted to the Paediatric Intensive Care Unit (PICU) in a tachycardic, hypertensive, polypneic state with oxygen saturation of 96% on 35% FiO2, rosy peripheries, adequate hydration, and well-perfused tissues, with flat jugular veins and small bilateral supraclavicular lymphadenopathies. Physical examination revealed no soft tissue retraction, maintained genupectoral posture, decreased pulmonary murmurs in both lung bases, and muffled cardiac tones without breath sounds. Abdominal examination showed non-depressible, tender soft tissue in both hypochondria with doubtful visceral enlargement and no trauma. Chest radiography demonstrated a superior mediastinal mass, atelectasis of the right middle lobe, and ipsilateral pleural effusion. Contrast-enhanced chest imaging was not performed due to contraindication of anaesthesia, as noted in the transfer summary. The patient was transferred to the PICU HBV with a diagnosis of mediastinal compression syndrome and clinical suspicion of non-Hodgkin lymphoma. Multidisciplinary evaluation by paediatric haemato-oncology, surgery, intensive care, imaging, radiotherapy, and oncology teams confirmed a normal pulmonary murmur and muffled cardiac auscultation, with no breath sounds, and persistent abdominal tenderness and suspected visceral enlargement. The chest radiograph remained consistent with a superior mediastinal mass and right middle lobe atelectasis with pleural effusion. A nephrological assessment revealed acute renal failure secondary to tumor lysis syndrome, with serum creatinine of 1.54 mg/dL, phosphoria of 11 mg/dL, and no hypernatremia. No dialysis was required, and the patient was managed with furosemide for volume control and amlodipine for hypertension. Respiratory support was initiated with Venturi mask at 35% FiO2, which was discontinued on day three due to clinical improvement. Episodes of psychomotor agitation, attributed to diagnostic stress, were managed according to institutional protocols with psychological and psychiatric support, resulting in satisfactory clinical course. On day three, a contrast-enhanced CT of the thorax, abdomen, and pelvis was performed, revealing thymic enlargement with homogeneous appearance, suggestive of a lymphoproliferative process, and findings consistent with pulmonary thromboembolism. AngioCT of the thorax confirmed jugular vein thrombosis, extensive bilateral pleural effusion, atelectasis in both lung bases, and signs of bilateral nephrotic syndrome. Anticoagulation with enoxaparin (1 mg/kg every 12 hours) was initiated for 20 days, with follow-up angioCT showing complete resolution of thrombosis. On day four, comprehensive diagnostic workup was completed, including complete biochemical profile (including lipid panel), bone marrow myelogram showing granulopoietic hyperplasia, flow cytometry of bone marrow and peripheral blood, which was negative for clonal or neoplastic haematopoietic immunophenotypes, and cytological analysis of pleural fluid, which was negative for neoplastic cells. Flow cytometry of pleural fluid also failed to detect haematological neoplasia. The patient was referred to the paediatric oncology committee, where, due to the absence of a viable biopsy specimen (as the mediastinal mass resolved with cytoreductive therapy), a diagnosis of lymphoblastic lymphoma was established based on clinical presentation and response to treatment, in accordance with the PINDA 0516 induction protocol. This protocol includes eight doses of L-asp (L-asparaginase) at 10,000 IU/m² in Induction IA. The patient received seven doses of L-asp, accumulating a total of 90,000 IU, in combination with prednisone glucocorticoids. During this period, he developed clinical deterioration with vomiting, abdominal pain, and mild dehydration. Pancreatitis was suspected but ruled out by normal amylase and lipase levels and normal hepatic function tests. Laboratory findings included hyponatraemia (126 mOsm/kg) and hypertriglyceridaemia, with urinary osmolality of 510 mOsm/kg (within normal range), leading to suspicion of a drug-induced metabolic disturbance—specifically, pseudohyponatraemia secondary to hypertriglyceridaemia. This was further supported"}
+{"row_index": 112, "doc_id": 74, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 56-year-old Italian female with β-thalassemia major underwent magnetic resonance imaging (MRI) to quantify myocardial, hepatic, and pancreatic iron deposition. Her clinical history includes transfusion-dependent β-thalassemia with genotype HBB:c.118C>T/HBB:c.93-21G>A, diagnosed at age 7 years, with the first red blood cell transfusion administered at 2 years of age. As a consequence of chronic transfusion and associated bone marrow pathology, she underwent splenectomy and cholecystectomy. At the time of MRI, she was negative for Hepatitis C virus RNA (HCV-RNA), had no evidence of osteoporosis or endocrine, cardiac, or hepatic complications, and maintained stable iron levels despite long-term iron overload. Her current therapy includes deferasirox for iron chelation, vitamin D supplementation, and luspatercept, an erythropoiesis-stimulating agent initiated two years prior to imaging, which demonstrated a 35% increase in transfusion interval duration, indicating a clinically significant response. Transfusion regimen consists of two units of concentrated and filtered red blood cells every 25 days, with pre-transfusion hemoglobin levels maintained between 10–10.5 g/dL.\\n\\nOn MRI, a solid, lobulated mass with regular contours was identified in the prevascular mediastinum. The lesion exhibited mild hyperintensity on T2-weighted imaging (T2-wi) and isointensity on T1-wi, and was previously detected in a prior MRI performed in 2020 before luspatercept initiation, with marginal enlargement over time. No other mediastinal abnormalities, pleural or pericardial effusions, or neurovascular compression symptoms were observed. Neurological examination was normal, and the patient reported no symptoms of mediastinal syndrome, fever, or weight loss.\\n\\nFurther evaluation via 18F-deoxyglucose (18FDG) positron emission tomography (PET)-computed tomography (CT) revealed mild FDG uptake in the mediastinal mass (SUVmax = 4.3), with no abnormal radiotracer accumulation in the neck, chest, abdomen, or skeleton. Chest CT with contrast demonstrated a well-defined, solid lesion with mild contrast enhancement, no evidence of invasion into adjacent structures, and absence of lymphadenopathy or extra-thoracic metastases. These imaging features—indolent temporal progression, lack of systemic symptoms, and low metabolic activity—support a diagnosis of thymoma.\\n\\nHowever, on lung window analysis, multiple symmetric, thin-walled cystic lesions were identified throughout both lungs, with normal intervening parenchyma, no associated nodules, and no pneumothorax. These findings are consistent with lymphangioleiomyomatosis (LAM), a rare cystic lung disease characterized by proliferation of smooth muscle-like cells in the lung interstitium. The patient is a never-smoker and denies chronic cough, recurrent respiratory infections, or cutaneous fibrofolliculomas. Physical examination revealed clear lung fields, normal peripheral capillary oxygen saturation (98%), heart rate of 75 bpm, and significantly reduced diffusing capacity of the lungs for carbon monoxide (DLCO: 42% of predicted), partially attributable to anemia, with a carbon monoxide transfer coefficient (KCO) of 73% of predicted. These pulmonary function abnormalities are consistent with advanced LAM pathology.\\n\\nFollowing multidisciplinary tumor board review involving a pulmonologist and thoracic surgeon, the patient underwent left thoracoscopic thymectomy with concomitant lingual segment wedge resection. Histopathological analysis confirmed a type B2 thymoma with focal capsule infiltration, no extracapsular extension, and presence at the resection margin, classifying the tumor as stage IIa by the Masaoka–Koga system and stage 1a by the TNM classification (indicating microscopically incomplete resection, R1). The pulmonary lesion demonstrated cysts of variable size lined by spindle cells with a myoid morphology, immunoreactive for actin, estrogen, progesterone receptors, and focal HMB45 positivity, with moderate chronic interstitial inflammation, vascular congestion, and recent blood extravasation—findings consistent with pulmonary LAM.\\n\\nFinal diagnosis is dual pathology: type B2 thymoma and pulmonary lymphangioleiomyomatosis. Given the R1 resection margin status, adjuvant radiation therapy is indicated for the thymoma to reduce risk of recurrence. For the LAM, which is associated with chronic iron overload in β-thalassemia, sirolimus therapy is recommended due to its ability to inhibit mTOR signaling, thereby suppressing the proliferation of abnormal smooth muscle-like cells in the lung paren", "generated_text": "{\n  \"proficient_health_literacy\": \"A 56-year-old Italian female with β-thalassemia major underwent magnetic resonance imaging (MRI) to quantify myocardial, hepatic, and pancreatic iron deposition. Her clinical history includes transfusion-dependent β-thalassemia with genotype HBB:c.118C>T/HBB:c.93-21G>A, diagnosed at age 7 years, with the first red blood cell transfusion administered at 2 years of age. As a consequence of chronic transfusion and associated bone marrow pathology, she underwent splenectomy and cholecystectomy. At the time of MRI, she was negative for Hepatitis C virus RNA (HCV-RNA), had no evidence of osteoporosis or endocrine, cardiac, or hepatic complications, and maintained stable iron levels despite long-term iron overload. Her current therapy includes deferasirox for iron chelation, vitamin D supplementation, and luspatercept, an erythropoiesis-stimulating agent initiated two years prior to imaging, which demonstrated a 35% increase in transfusion interval duration, indicating a clinically significant response. Transfusion regimen consists of two units of concentrated and filtered red blood cells every 25 days, with pre-transfusion hemoglobin levels maintained between 10–10.5 g/dL.\\n\\nOn MRI, a solid, lobulated mass with regular contours was identified in the prevascular mediastinum. The lesion exhibited mild hyperintensity on T2-weighted imaging (T2-wi) and isointensity on T1-wi, and was previously detected in a prior MRI performed in 2020 before luspatercept initiation, with marginal enlargement over time. No other mediastinal abnormalities, pleural or pericardial effusions, or neurovascular compression symptoms were observed. Neurological examination was normal, and the patient reported no symptoms of mediastinal syndrome, fever, or weight loss.\\n\\nFurther evaluation via 18F-deoxyglucose (18FDG) positron emission tomography (PET)-computed tomography (CT) revealed mild FDG uptake in the mediastinal mass (SUVmax = 4.3), with no abnormal radiotracer accumulation in the neck, chest, abdomen, or skeleton. Chest CT with contrast demonstrated a well-defined, solid lesion with mild contrast enhancement, no evidence of invasion into adjacent structures, and absence of lymphadenopathy or extra-thoracic metastases. These imaging features—indolent temporal progression, lack of systemic symptoms, and low metabolic activity—support a diagnosis of thymoma.\\n\\nHowever, on lung window analysis, multiple symmetric, thin-walled cystic lesions were identified throughout both lungs, with normal intervening parenchyma, no associated nodules, and no pneumothorax. These findings are consistent with lymphangioleiomyomatosis (LAM), a rare cystic lung disease characterized by proliferation of smooth muscle-like cells in the lung interstitium. The patient is a never-smoker and denies chronic cough, recurrent respiratory infections, or cutaneous fibrofolliculomas. Physical examination revealed clear lung fields, normal peripheral capillary oxygen saturation (98%), heart rate of 75 bpm, and significantly reduced diffusing capacity of the lungs for carbon monoxide (DLCO: 42% of predicted), partially attributable to anemia, with a carbon monoxide transfer coefficient (KCO) of 73% of predicted. These pulmonary function abnormalities are consistent with advanced LAM pathology.\\n\\nFollowing multidisciplinary tumor board review involving a pulmonologist and thoracic surgeon, the patient underwent left thoracoscopic thymectomy with concomitant lingual segment wedge resection. Histopathological analysis confirmed a type B2 thymoma with focal capsule infiltration, no extracapsular extension, and presence at the resection margin, classifying the tumor as stage IIa by the Masaoka–Koga system and stage 1a by the TNM classification (indicating microscopically incomplete resection, R1). The pulmonary lesion demonstrated cysts of variable size lined by spindle cells with a myoid morphology, immunoreactive for actin, estrogen, progesterone receptors, and focal HMB45 positivity, with moderate chronic interstitial inflammation, vascular congestion, and recent blood extravasation—findings consistent with pulmonary LAM.\\n\\nFinal diagnosis is dual pathology: type B2 thymoma and pulmonary lymphangioleiomyomatosis. Given the R1 resection margin status, adjuvant radiation therapy is indicated for the thymoma to reduce risk of recurrence. For the LAM, which is associated with chronic iron overload in β-thalassemia, sirolimus therapy is recommended due to its ability to inhibit mTOR signaling, thereby suppressing the proliferation of abnormal smooth muscle-like cells in the lung paren"}
+{"row_index": 113, "doc_id": 75, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 49-year-old woman had a long sickness called lupus that started when she was a child. Over time, her kidneys and heart got weaker because of the disease. She needed dialysis for 4 years until she got a new kidney. Before the surgery, her heart was very weak — only pumping 26% of the blood it should — so doctors gave her a medicine called Levosimendan to help her heart work better. The surgery was hard, but she survived. Afterward, her heart got stronger: now it pumps better, and her kidney function is normal. Her ability to walk stairs improved, and her heart problems got much better over time. She is now doing well after the transplant.\"\n}", "generated_text": "A 49-year-old woman had a long sickness called lupus that started when she was a child. Over time, her kidneys and heart got weaker because of the disease. She needed dialysis for 4 years until she got a new kidney. Before the surgery, her heart was very weak — only pumping 26% of the blood it should — so doctors gave her a medicine called Levosimendan to help her heart work better. The surgery was hard, but she survived. Afterward, her heart got stronger: now it pumps better, and her kidney function is normal. Her ability to walk stairs improved, and her heart problems got much better over time. She is now doing well after the transplant."}
+{"row_index": 114, "doc_id": 75, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"We present a case of a 49-year-old woman with chronic renal and cardiac failure secondary to long-standing systemic lupus erythematosus (SLE), spanning from childhood (initiated at age 13). The patient had a history of lupus nephritis (LN), initially class III and later progressing to class IV, managed with early steroid therapy, followed by cyclophosphamide, subsequently replaced by methotrexate and azathioprine. Partial remission of nephrotic syndrome was achieved, and immunosuppressive therapy was discontinued in 2002 due to active hepatitis C virus (HCV) replication. SLE-related vascular involvement manifested as early coronary atherosclerosis, ischemic heart disease, and myocardial infarction at age 20. In 2007, declining renal function (serum creatinine 2.2 mg/dL) and proteinuria (2 g/day) prompted a kidney biopsy, which revealed active and sclerotic focal proliferative lupus nephritis; immunosuppression was withheld due to HCV activity. Over time, renal function progressively deteriorated. Despite percutaneous coronary intervention (PCI) of the right coronary artery (RCA), the patient developed severe post-infarction dilated cardiomyopathy and required implantation of an implantable cardioverter-defibrillator (ICD) for primary prevention in 2009. Subsequently, significant mitral and tricuspid valve regurgitation developed on the background of lupus-related and secondary cardiomyopathic pathology, necessitating mitral and tricuspid valve repair, followed by left ventricular volume reduction surgery in 2014, complicated by low cardiac output syndrome requiring intra-aortic balloon pump (IABP) support. Postoperatively, renal function further declined, leading to initiation of chronic renal replacement therapy (dialysis), which has been sustained for 4 years. During active waiting for kidney transplantation, laboratory markers of lupus entered remission (normal C3: 0.93 g/L, C4: 0.4 g/L, ANA negative), though circulatory insufficiency persisted, evidenced by markedly reduced exercise tolerance (limited to one flight of stairs) and elevated B-type natriuretic peptide (BNP) of 619 pg/mL (normal range: 0–100 pg/mL). Transthoracic echocardiography prior to transplantation demonstrated significant left ventricular and left atrial enlargement, with severely impaired systolic function: left ventricular ejection fraction (LVEF) of 26% and global longitudinal strain (GLS) of −3. Due to mitral ring implantation, left ventricular diastolic function could not be assessed. A high tricuspid regurgitant flow gradient and a widened, poorly respiratory mobile inferior vena cava (IVC) suggested a high probability of pulmonary hypertension. Given the extremely low ejection fraction and complex cardiac pathology, cardioprotective therapy with levosimendan was initiated during pre-transplant preparation. Levosimendan was administered at a dose of 0.1 μg/kg/min immediately after cross-match confirmation and dialysis session, and continued postoperatively for 24 hours. The anesthetic and perioperative management was optimized to ensure adequate transplanted kidney perfusion, avoiding nephrotoxic agents (including those excreted by functional kidneys), and utilizing nephroprotective strategies. Due to recurrent ventricular extrasystoles and risk of circulatory decompensation, and the necessity of ICD disconnection during transplantation, Swan-Ganz catheterization for hemodynamic monitoring was avoided. Anesthesia was monitored via ECG, central venous pressure (CVP) via central catheter, direct radial artery blood pressure, and continuous cardiac ultrasound. CVP was used to guide fluid management during anesthesia, and postoperatively, cardiac ultrasound and inferior vena cava respiratory fill and motility were used to assess hemodynamic stability. Therapy was guided by goal-directed therapy (GDT) principles. Anesthesia included fentanyl, triacrium, propofol, desflurane, standard antibiotic prophylaxis, and immunosuppressive regimens (steroids, tacrolimus, mycophenolate mofetil), with mycophenolate mofetil discontinued due to persistent leukopenia and cytomegalovirus (CMV) infection. Delayed graft function was observed, requiring hemodialysis for nearly 6 weeks, primarily due to fluid overload. BNP levels peaked at 2996 pg/mL and gradually declined. A kidney biopsy performed two weeks post-transplant revealed acute rejection (AR II B, Banff 2015 classification) with acute tubular necrosis (ATN). The", "generated_text": "{\n  \"proficient_health_literacy\": \"We present a case of a 49-year-old woman with chronic renal and cardiac failure secondary to long-standing systemic lupus erythematosus (SLE), spanning from childhood (initiated at age 13). The patient had a history of lupus nephritis (LN), initially class III and later progressing to class IV, managed with early steroid therapy, followed by cyclophosphamide, subsequently replaced by methotrexate and azathioprine. Partial remission of nephrotic syndrome was achieved, and immunosuppressive therapy was discontinued in 2002 due to active hepatitis C virus (HCV) replication. SLE-related vascular involvement manifested as early coronary atherosclerosis, ischemic heart disease, and myocardial infarction at age 20. In 2007, declining renal function (serum creatinine 2.2 mg/dL) and proteinuria (2 g/day) prompted a kidney biopsy, which revealed active and sclerotic focal proliferative lupus nephritis; immunosuppression was withheld due to HCV activity. Over time, renal function progressively deteriorated. Despite percutaneous coronary intervention (PCI) of the right coronary artery (RCA), the patient developed severe post-infarction dilated cardiomyopathy and required implantation of an implantable cardioverter-defibrillator (ICD) for primary prevention in 2009. Subsequently, significant mitral and tricuspid valve regurgitation developed on the background of lupus-related and secondary cardiomyopathic pathology, necessitating mitral and tricuspid valve repair, followed by left ventricular volume reduction surgery in 2014, complicated by low cardiac output syndrome requiring intra-aortic balloon pump (IABP) support. Postoperatively, renal function further declined, leading to initiation of chronic renal replacement therapy (dialysis), which has been sustained for 4 years. During active waiting for kidney transplantation, laboratory markers of lupus entered remission (normal C3: 0.93 g/L, C4: 0.4 g/L, ANA negative), though circulatory insufficiency persisted, evidenced by markedly reduced exercise tolerance (limited to one flight of stairs) and elevated B-type natriuretic peptide (BNP) of 619 pg/mL (normal range: 0–100 pg/mL). Transthoracic echocardiography prior to transplantation demonstrated significant left ventricular and left atrial enlargement, with severely impaired systolic function: left ventricular ejection fraction (LVEF) of 26% and global longitudinal strain (GLS) of −3. Due to mitral ring implantation, left ventricular diastolic function could not be assessed. A high tricuspid regurgitant flow gradient and a widened, poorly respiratory mobile inferior vena cava (IVC) suggested a high probability of pulmonary hypertension. Given the extremely low ejection fraction and complex cardiac pathology, cardioprotective therapy with levosimendan was initiated during pre-transplant preparation. Levosimendan was administered at a dose of 0.1 μg/kg/min immediately after cross-match confirmation and dialysis session, and continued postoperatively for 24 hours. The anesthetic and perioperative management was optimized to ensure adequate transplanted kidney perfusion, avoiding nephrotoxic agents (including those excreted by functional kidneys), and utilizing nephroprotective strategies. Due to recurrent ventricular extrasystoles and risk of circulatory decompensation, and the necessity of ICD disconnection during transplantation, Swan-Ganz catheterization for hemodynamic monitoring was avoided. Anesthesia was monitored via ECG, central venous pressure (CVP) via central catheter, direct radial artery blood pressure, and continuous cardiac ultrasound. CVP was used to guide fluid management during anesthesia, and postoperatively, cardiac ultrasound and inferior vena cava respiratory fill and motility were used to assess hemodynamic stability. Therapy was guided by goal-directed therapy (GDT) principles. Anesthesia included fentanyl, triacrium, propofol, desflurane, standard antibiotic prophylaxis, and immunosuppressive regimens (steroids, tacrolimus, mycophenolate mofetil), with mycophenolate mofetil discontinued due to persistent leukopenia and cytomegalovirus (CMV) infection. Delayed graft function was observed, requiring hemodialysis for nearly 6 weeks, primarily due to fluid overload. BNP levels peaked at 2996 pg/mL and gradually declined. A kidney biopsy performed two weeks post-transplant revealed acute rejection (AR II B, Banff 2015 classification) with acute tubular necrosis (ATN). The"}
+{"row_index": 115, "doc_id": 76, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 42-year-old woman had bad headaches that were very sharp and strong, like a storm inside her head. The pain came on suddenly, lasted about 30 minutes, and happened many times a day when she coughed or lifted things. She tried medicines, but they caused stomach problems and didn’t work. When the pain got too bad, she went to a pain clinic. There, doctors used an ultrasound to guide a needle to block the nerve causing the pain. The medicine used was bupivacaine. After the first block, her pain went from 9 out of 10 to just 2 out of 10. She had this block once a week for a month. After two months, the headaches became much less frequent and weaker. By the sixth month, she didn’t have any more attacks and no side effects.\"\n}", "generated_text": "A 42-year-old woman had bad headaches that were very sharp and strong, like a storm inside her head. The pain came on suddenly, lasted about 30 minutes, and happened many times a day when she coughed or lifted things. She tried medicines, but they caused stomach problems and didn’t work. When the pain got too bad, she went to a pain clinic. There, doctors used an ultrasound to guide a needle to block the nerve causing the pain. The medicine used was bupivacaine. After the first block, her pain went from 9 out of 10 to just 2 out of 10. She had this block once a week for a month. After two months, the headaches became much less frequent and weaker. By the sixth month, she didn’t have any more attacks and no side effects."}
+{"row_index": 116, "doc_id": 76, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 42-year-old female with a history of menstrual migraine, Hashimoto thyroiditis, familial Mediterranean fever (FMF), and dyspepsia was evaluated for refractory headache. She was on stable therapy including 75 mg daily levothyroxine, 30 mg daily lansoprazole, and 1.5 mg daily colchicine. In February 2023, she developed acute bronchitis treated with antibiotics and bronchodilators, followed by the onset of daily headache episodes manifesting as more than ten brief, self-limiting attacks per day, each lasting approximately 30 minutes, provoked by coughing, straining, or lifting. The pain was bilaterally distributed from the neck to the vertex of the skull, described as sharp and severe, with a characteristic sensation of 'storm-like fluid movement' within the head. Pain intensity was quantified using a 0–10 numeric rating scale (NRS), consistently reaching 9/10 during attacks, which frequently required emergency department visits. Neurological and physical examinations were normal, and laboratory evaluations—including thyroid function, electrolytes, hepatic and renal function, and serological markers—were negative. Brain MRI with and without contrast, cervical spinal MRI, magnetic resonance venography (MRV), and magnetic resonance angiography (MRA) were all unremarkable. Lumbar puncture was not performed due to patient refusal. Prior to presentation to the pain clinic, she was on 25 mg of indomethacin daily; her headache attacks ceased after increasing lansoprazole to 60 mg and raising indomethacin to 150 mg, but gastrointestinal adverse effects led to discontinuation of indomethacin on day three. Concomitant medications, including topiramate and propranolol, were not initiated due to intolerance. Fifteen days after initial evaluation, she presented with a recurrent attack of NRS 9/10 and was taken to the local operating room for ultrasound-guided proximal greater occipital nerve block (PGONB). The procedure was performed using a GE Healthcare Voluson™ E6 ultrasound system with a linear 13–5 MHz probe. The patient’s neck was in a position of flexion, and the probe was initially transversely placed over the occipital protuberance, then advanced caudally to visualize the C2 spinous process, which was observed to have a bicondylar appearance resembling two horns. Lateral probe movement allowed identification of the inferior fibers of the obliquus capitis and semispinalis capitis muscles. The greater occipital nerve (GON) was localized superior to the inferior oblique capitis muscle and beneath the semispinalis capitis muscle. A 22-gauge spinal needle was inserted at this site, and 3 cc of 0.5% bupivacaine was injected. Within 20 minutes of injection, the headache intensity dropped from 9/10 to 2/10. The procedure was repeated weekly for one month. By the second month, the frequency of attacks reduced to two per month, with an average intensity of 4/10. By the sixth month, no attacks were reported, and no adverse effects were observed. This case demonstrates the efficacy of ultrasound-guided PGONB in managing refractory, non-migraine-like headaches with a distinct mechanical trigger profile, particularly in patients with comorbidities and intolerance to conventional pharmacologic therapies.\"\n}", "generated_text": "A 42-year-old female with a history of menstrual migraine, Hashimoto thyroiditis, familial Mediterranean fever (FMF), and dyspepsia was evaluated for refractory headache. She was on stable therapy including 75 mg daily levothyroxine, 30 mg daily lansoprazole, and 1.5 mg daily colchicine. In February 2023, she developed acute bronchitis treated with antibiotics and bronchodilators, followed by the onset of daily headache episodes manifesting as more than ten brief, self-limiting attacks per day, each lasting approximately 30 minutes, provoked by coughing, straining, or lifting. The pain was bilaterally distributed from the neck to the vertex of the skull, described as sharp and severe, with a characteristic sensation of 'storm-like fluid movement' within the head. Pain intensity was quantified using a 0–10 numeric rating scale (NRS), consistently reaching 9/10 during attacks, which frequently required emergency department visits. Neurological and physical examinations were normal, and laboratory evaluations—including thyroid function, electrolytes, hepatic and renal function, and serological markers—were negative. Brain MRI with and without contrast, cervical spinal MRI, magnetic resonance venography (MRV), and magnetic resonance angiography (MRA) were all unremarkable. Lumbar puncture was not performed due to patient refusal. Prior to presentation to the pain clinic, she was on 25 mg of indomethacin daily; her headache attacks ceased after increasing lansoprazole to 60 mg and raising indomethacin to 150 mg, but gastrointestinal adverse effects led to discontinuation of indomethacin on day three. Concomitant medications, including topiramate and propranolol, were not initiated due to intolerance. Fifteen days after initial evaluation, she presented with a recurrent attack of NRS 9/10 and was taken to the local operating room for ultrasound-guided proximal greater occipital nerve block (PGONB). The procedure was performed using a GE Healthcare Voluson™ E6 ultrasound system with a linear 13–5 MHz probe. The patient’s neck was in a position of flexion, and the probe was initially transversely placed over the occipital protuberance, then advanced caudally to visualize the C2 spinous process, which was observed to have a bicondylar appearance resembling two horns. Lateral probe movement allowed identification of the inferior fibers of the obliquus capitis and semispinalis capitis muscles. The greater occipital nerve (GON) was localized superior to the inferior oblique capitis muscle and beneath the semispinalis capitis muscle. A 22-gauge spinal needle was inserted at this site, and 3 cc of 0.5% bupivacaine was injected. Within 20 minutes of injection, the headache intensity dropped from 9/10 to 2/10. The procedure was repeated weekly for one month. By the second month, the frequency of attacks reduced to two per month, with an average intensity of 4/10. By the sixth month, no attacks were reported, and no adverse effects were observed. This case demonstrates the efficacy of ultrasound-guided PGONB in managing refractory, non-migraine-like headaches with a distinct mechanical trigger profile, particularly in patients with comorbidities and intolerance to conventional pharmacologic therapies."}
+{"row_index": 117, "doc_id": 77, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 20-year-old male martial artist had pain in the back of his left thigh for 5 weeks. The pain started after a short sprint in soccer, and he heard a pop. He couldn’t move his knee well and had to stop all sports. Even with pain medicine, ice, and bandages, the pain didn’t go away. The doctor checked and ruled out other serious problems. He couldn’t bend or straighten his knee properly and walked with a limp. His pain was 5 out of 10 at rest and 7 during activity. A special treatment was done: a gentle movement technique to help the nerve slide smoothly, done 3 times a day for 3 days. He also learned how to stand and move better. After 3 days, his pain dropped to 2 out of 10 at rest and 4 during activity. His knee could move much better. At 2 months, he was pain-free and could go back to martial arts without any trouble.\"\n}", "generated_text": "A 20-year-old male martial artist had pain in the back of his left thigh for 5 weeks. The pain started after a short sprint in soccer, and he heard a pop. He couldn’t move his knee well and had to stop all sports. Even with pain medicine, ice, and bandages, the pain didn’t go away. The doctor checked and ruled out other serious problems. He couldn’t bend or straighten his knee properly and walked with a limp. His pain was 5 out of 10 at rest and 7 during activity. A special treatment was done: a gentle movement technique to help the nerve slide smoothly, done 3 times a day for 3 days. He also learned how to stand and move better. After 3 days, his pain dropped to 2 out of 10 at rest and 4 during activity. His knee could move much better. At 2 months, he was pain-free and could go back to martial arts without any trouble."}
+{"row_index": 118, "doc_id": 77, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 20-year-old male Arabic martial artist had a left hamstring strain that lasted for 5 weeks. He tried medications and physical therapy, but his pain didn’t improve. He stopped all sports activities because the pain was severe. After checking with a doctor, other causes like nerve problems or back issues were ruled out. The patient was treated with a modified slump mobilization technique, done four times a day for three days, along with postural retraining. Before treatment, his pain was 5 out of 10 at rest and 7 out of 10 during activity. After three days, pain dropped to 2 out of 10 at rest and 4 out of 10 during activity. His knee function also improved significantly: the Knee Society score went from 22 to 61 for pain and from 30 to 80 for movement. At a 2-month follow-up, he had fully recovered and was able to return to sports without any problems.\"\n}", "generated_text": "A 20-year-old male Arabic martial artist had a left hamstring strain that lasted for 5 weeks. He tried medications and physical therapy, but his pain didn’t improve. He stopped all sports activities because the pain was severe. After checking with a doctor, other causes like nerve problems or back issues were ruled out. The patient was treated with a modified slump mobilization technique, done four times a day for three days, along with postural retraining. Before treatment, his pain was 5 out of 10 at rest and 7 out of 10 during activity. After three days, pain dropped to 2 out of 10 at rest and 4 out of 10 during activity. His knee function also improved significantly: the Knee Society score went from 22 to 61 for pain and from 30 to 80 for movement. At a 2-month follow-up, he had fully recovered and was able to return to sports without any problems."}
+{"row_index": 119, "doc_id": 77, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 20-year-old male Arabic martial artist (weight 91.5 kg, height 180 cm, BMI 28.24) presented with a left hamstring strain with a five-week history of persistent pain in the posterior left thigh, initially precipitated by a sudden sprint during soccer play, during which he reported a 'pop' sensation. The pain was severe enough to cause immediate cessation of activity and was rated at 5/10 at rest and 7/10 during activity. There was no associated bruising or significant swelling, and the patient denied prior lower back or leg injuries. Clinical examination revealed a progressive loss of knee joint mobility, with active range of motion (AROM) limited to 10–15° in the left knee versus 0–130° in the contralateral right knee. The patient exhibited an analgesic gait pattern with reduced heel strike and was unable to fully extend or flex the knee when maintained at a 15° flexion position. Palpation identified tenderness and firmness in the middle third of the semimembranosus and semitendinosus muscles, consistent with hamstring muscle strain or fascial tightness. Manual muscle testing and isometric assessments were contraindicated due to persistent pain. The patient reported using crutches for ambulation, stair climbing via single-step ascents, and avoiding direct pressure on the thigh, including sitting at the edge of a chair. Despite adherence to nonsteroidal anti-inflammatory drugs (NSAIDs), cryotherapy, and compression bandaging, symptoms worsened over time, leading to referral for specialized evaluation. Diagnostic workup excluded lumbar disc pathology, gluteal tunnel syndrome, and ischial nerve entrapment based on clinical and neurodynamic screening, including a negative slump test for peripheral nerve tension. The clinical picture was consistent with hamstring strain syndrome (HSI), though conventional treatments had failed to yield improvement. The therapeutic intervention consisted of a modified slump mobilization technique involving sequential spinal and joint mobilization under controlled neurodynamic conditions. The protocol included three sets of daily sessions, each comprising thoracic and cervical spine flexion, maximal knee extension under tolerable pain thresholds, and dynamic neck and ankle movements (15 repetitions) to facilitate neural glide. The patient was also instructed to progressively mobilize the mid- and upper back until pain was elicited in the knee region, followed by repetition of the sequence. This neurodynamic approach was based on the biomechanical proximity of the tibial nerve and sciatic nerve to the hamstring musculature and the functional interplay between neural tension and lower limb joint mechanics. By the third day of intervention, active knee extension improved from 5° to 15°, and standing posture normalized. Concurrently, the patient was introduced to a structured postural retraining program including active chin flexion, passive stretching of cervical extensors in prone position, and dynamic shoulder retraction exercises (T-to-Y, Y-to-W) performed with limb weight bearing. Additional interventions included active chest stretches at wall corners to correct kyphotic posture, with exercise duration increased from 5 to 10 seconds, performed in 10 repetitions across three sets daily. Outcomes were quantified using the Numeric Pain Rating Scale (NPRS) and the Knee Society Score (KSS). Pre-intervention NPRS scores were 5/10 at rest and 7/10 during activity; post-intervention (on day 3) these improved to 2/10 at rest and 4/10 during activity. KSS scores increased from 22 to 61 in the pain domain and from 30 to 80 in the functional domain. Pain medication was discontinued following clinical improvement. At the end of a two-week home exercise program, the patient achieved full active straight leg raise (SLR). At the two-month follow-up, the patient reported complete resolution of symptoms, regained full functional mobility, and resumed participation in martial arts without limitations. The intervention demonstrates the efficacy of a neurodynamic mobilization approach in addressing chronic hamstring-related pain when conventional treatments fail, particularly in patients with structural and functional neural-tissue interactions affecting joint mechanics and posture.\"\n}", "generated_text": "A 20-year-old male Arabic martial artist (weight 91.5 kg, height 180 cm, BMI 28.24) presented with a left hamstring strain with a five-week history of persistent pain in the posterior left thigh, initially precipitated by a sudden sprint during soccer play, during which he reported a 'pop' sensation. The pain was severe enough to cause immediate cessation of activity and was rated at 5/10 at rest and 7/10 during activity. There was no associated bruising or significant swelling, and the patient denied prior lower back or leg injuries. Clinical examination revealed a progressive loss of knee joint mobility, with active range of motion (AROM) limited to 10–15° in the left knee versus 0–130° in the contralateral right knee. The patient exhibited an analgesic gait pattern with reduced heel strike and was unable to fully extend or flex the knee when maintained at a 15° flexion position. Palpation identified tenderness and firmness in the middle third of the semimembranosus and semitendinosus muscles, consistent with hamstring muscle strain or fascial tightness. Manual muscle testing and isometric assessments were contraindicated due to persistent pain. The patient reported using crutches for ambulation, stair climbing via single-step ascents, and avoiding direct pressure on the thigh, including sitting at the edge of a chair. Despite adherence to nonsteroidal anti-inflammatory drugs (NSAIDs), cryotherapy, and compression bandaging, symptoms worsened over time, leading to referral for specialized evaluation. Diagnostic workup excluded lumbar disc pathology, gluteal tunnel syndrome, and ischial nerve entrapment based on clinical and neurodynamic screening, including a negative slump test for peripheral nerve tension. The clinical picture was consistent with hamstring strain syndrome (HSI), though conventional treatments had failed to yield improvement. The therapeutic intervention consisted of a modified slump mobilization technique involving sequential spinal and joint mobilization under controlled neurodynamic conditions. The protocol included three sets of daily sessions, each comprising thoracic and cervical spine flexion, maximal knee extension under tolerable pain thresholds, and dynamic neck and ankle movements (15 repetitions) to facilitate neural glide. The patient was also instructed to progressively mobilize the mid- and upper back until pain was elicited in the knee region, followed by repetition of the sequence. This neurodynamic approach was based on the biomechanical proximity of the tibial nerve and sciatic nerve to the hamstring musculature and the functional interplay between neural tension and lower limb joint mechanics. By the third day of intervention, active knee extension improved from 5° to 15°, and standing posture normalized. Concurrently, the patient was introduced to a structured postural retraining program including active chin flexion, passive stretching of cervical extensors in prone position, and dynamic shoulder retraction exercises (T-to-Y, Y-to-W) performed with limb weight bearing. Additional interventions included active chest stretches at wall corners to correct kyphotic posture, with exercise duration increased from 5 to 10 seconds, performed in 10 repetitions across three sets daily. Outcomes were quantified using the Numeric Pain Rating Scale (NPRS) and the Knee Society Score (KSS). Pre-intervention NPRS scores were 5/10 at rest and 7/10 during activity; post-intervention (on day 3) these improved to 2/10 at rest and 4/10 during activity. KSS scores increased from 22 to 61 in the pain domain and from 30 to 80 in the functional domain. Pain medication was discontinued following clinical improvement. At the end of a two-week home exercise program, the patient achieved full active straight leg raise (SLR). At the two-month follow-up, the patient reported complete resolution of symptoms, regained full functional mobility, and resumed participation in martial arts without limitations. The intervention demonstrates the efficacy of a neurodynamic mobilization approach in addressing chronic hamstring-related pain when conventional treatments fail, particularly in patients with structural and functional neural-tissue interactions affecting joint mechanics and posture."}
+{"row_index": 120, "doc_id": 78, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A male infant was delivered via emergency cesarean section at 40 weeks' gestation due to fetal distress. The mother was 33 years old, gravida 1, para 1, with no family history of congenital anomalies, aortic disease, or sudden cardiac death. Prenatal ultrasonography revealed a femur length 1–3 weeks above the expected gestational age, suggesting disproportionate growth. Fetal echocardiography demonstrated cardiomegaly with a fetal cardiothoracic circumference ratio of ≥0.5, a larger-than-normal foramen ovale, and left aortic constriction adjacent to the subclavian artery basin; no other structural abnormalities were identified.\\n\\nAt birth, the infant weighed 3560 g (75th percentile), measured 56.5 cm (above 90th percentile), and had a head circumference of 36 cm (above 90th percentile). Apgar scores were 4 at 1 minute and 6 at 5 minutes. The newborn exhibited absent spontaneous breathing, bradycardia, and cyanosis upon delivery, necessitating immediate neonatal intensive care unit (NICU) admission.\\n\\nPhysical examination revealed multiple severe musculoskeletal manifestations consistent with Marfan syndrome (MFS), including bilateral arachnodactyly, camptodactyly, flat feet, joint contractures at the elbows and knees, malar hypoplasia, a senile facial appearance, deep-set eyes with down-slanting palpebral fissures, hypoplastic and crumpled external ear cartilage, a sagging mouth, prominent coronal suture, and brachycephaly. Ophthalmologic evaluation confirmed bilateral ectopia lentis with lens subluxation. The musculoskeletal severity was assessed using the Ghent criteria, yielding a total score of 11 points, supporting a diagnosis of severe MFS.\\n\\nCardiac evaluation revealed a grade V/VI systolic murmur at the upper and left lower sternal borders, accompanied by a parasternal heave. Echocardiography demonstrated poor left ventricular contractility, severe pulmonary hypertension, a dilated aortic sinus (20.2 mm), with Z-scores of 8.08 (Boston), 6.37 (Detroit), and 5.97 (Halifax), indicating extreme dilation. Multiple valvular abnormalities were present: moderate aortic regurgitation, severe mitral regurgitation, moderate tricuspid regurgitation, and moderate pulmonary valve regurgitation. These findings are consistent with progressive valvular degeneration due to impaired extracellular matrix integrity.\\n\\nGenetic analysis via Sanger sequencing and polymerase chain reaction (PCR) of the fibrillin-1 (FBN1) gene identified a novel heterozygous mutation at nucleotide position c.3964 + 1G > T, located in intron 32 of the FBN1 gene. This mutation affects the splice site of exon 32 and is classified as a pathogenic variant based on the 2015 ACMG/AMP guidelines. The mutation lies within the previously defined 'neonatal region' of the FBN1 gene (exons 24–32), which is associated with a more severe, early-onset phenotype of MFS, including neonatal cardiac involvement and rapid progression of valvular and musculoskeletal pathology.\\n\\nOn postnatal day 1, refractory hypoxemia was observed despite >60% oxygen supplementation, indicating inadequate cardiac output and pulmonary perfusion. Medical management was initiated to address low cardiac output secondary to severe mitral and aortic regurgitation. Therapeutic interventions included milrinone (an inodilator) for afterload reduction, continuous fentanyl sedation to suppress myocardial oxygen demand, and diuretic therapy to manage oliguria and fluid overload. Despite these measures, the infant developed progressive respiratory failure, worsening pulmonary hypertension, and deteriorating cardiac contractility. Echocardiographic follow-up confirmed progressive worsening of aortic and mitral regurgitation, with sustained severe pulmonary hypertension.\\n\\nMultidisciplinary team consultations with the family and clinical staff concluded that surgical intervention—such as valve repair or replacement—was not feasible given the rapid disease progression and poor prognosis. Palliative care was initiated instead. Over the following weeks, the infant developed hepatic and pulmonary congestion, pulmonary hemorrhage, and ultimately progressed to multiple organ dysfunction syndrome (MODS). The patient died 32 days after birth. This case exemplifies the severe, early-onset form of Marfan syndrome associated with a novel FBN1 mutation in the neonatal region, characterized by profound cardiac dysfunction, valvular deterioration, and multisystem involvement, underscoring the critical need for early genetic diagnosis and the limitations of medical therapy", "generated_text": "{\n  \"proficient_health_literacy\": \"A male infant was delivered via emergency cesarean section at 40 weeks' gestation due to fetal distress. The mother was 33 years old, gravida 1, para 1, with no family history of congenital anomalies, aortic disease, or sudden cardiac death. Prenatal ultrasonography revealed a femur length 1–3 weeks above the expected gestational age, suggesting disproportionate growth. Fetal echocardiography demonstrated cardiomegaly with a fetal cardiothoracic circumference ratio of ≥0.5, a larger-than-normal foramen ovale, and left aortic constriction adjacent to the subclavian artery basin; no other structural abnormalities were identified.\\n\\nAt birth, the infant weighed 3560 g (75th percentile), measured 56.5 cm (above 90th percentile), and had a head circumference of 36 cm (above 90th percentile). Apgar scores were 4 at 1 minute and 6 at 5 minutes. The newborn exhibited absent spontaneous breathing, bradycardia, and cyanosis upon delivery, necessitating immediate neonatal intensive care unit (NICU) admission.\\n\\nPhysical examination revealed multiple severe musculoskeletal manifestations consistent with Marfan syndrome (MFS), including bilateral arachnodactyly, camptodactyly, flat feet, joint contractures at the elbows and knees, malar hypoplasia, a senile facial appearance, deep-set eyes with down-slanting palpebral fissures, hypoplastic and crumpled external ear cartilage, a sagging mouth, prominent coronal suture, and brachycephaly. Ophthalmologic evaluation confirmed bilateral ectopia lentis with lens subluxation. The musculoskeletal severity was assessed using the Ghent criteria, yielding a total score of 11 points, supporting a diagnosis of severe MFS.\\n\\nCardiac evaluation revealed a grade V/VI systolic murmur at the upper and left lower sternal borders, accompanied by a parasternal heave. Echocardiography demonstrated poor left ventricular contractility, severe pulmonary hypertension, a dilated aortic sinus (20.2 mm), with Z-scores of 8.08 (Boston), 6.37 (Detroit), and 5.97 (Halifax), indicating extreme dilation. Multiple valvular abnormalities were present: moderate aortic regurgitation, severe mitral regurgitation, moderate tricuspid regurgitation, and moderate pulmonary valve regurgitation. These findings are consistent with progressive valvular degeneration due to impaired extracellular matrix integrity.\\n\\nGenetic analysis via Sanger sequencing and polymerase chain reaction (PCR) of the fibrillin-1 (FBN1) gene identified a novel heterozygous mutation at nucleotide position c.3964 + 1G > T, located in intron 32 of the FBN1 gene. This mutation affects the splice site of exon 32 and is classified as a pathogenic variant based on the 2015 ACMG/AMP guidelines. The mutation lies within the previously defined 'neonatal region' of the FBN1 gene (exons 24–32), which is associated with a more severe, early-onset phenotype of MFS, including neonatal cardiac involvement and rapid progression of valvular and musculoskeletal pathology.\\n\\nOn postnatal day 1, refractory hypoxemia was observed despite >60% oxygen supplementation, indicating inadequate cardiac output and pulmonary perfusion. Medical management was initiated to address low cardiac output secondary to severe mitral and aortic regurgitation. Therapeutic interventions included milrinone (an inodilator) for afterload reduction, continuous fentanyl sedation to suppress myocardial oxygen demand, and diuretic therapy to manage oliguria and fluid overload. Despite these measures, the infant developed progressive respiratory failure, worsening pulmonary hypertension, and deteriorating cardiac contractility. Echocardiographic follow-up confirmed progressive worsening of aortic and mitral regurgitation, with sustained severe pulmonary hypertension.\\n\\nMultidisciplinary team consultations with the family and clinical staff concluded that surgical intervention—such as valve repair or replacement—was not feasible given the rapid disease progression and poor prognosis. Palliative care was initiated instead. Over the following weeks, the infant developed hepatic and pulmonary congestion, pulmonary hemorrhage, and ultimately progressed to multiple organ dysfunction syndrome (MODS). The patient died 32 days after birth. This case exemplifies the severe, early-onset form of Marfan syndrome associated with a novel FBN1 mutation in the neonatal region, characterized by profound cardiac dysfunction, valvular deterioration, and multisystem involvement, underscoring the critical need for early genetic diagnosis and the limitations of medical therapy"}
+{"row_index": 121, "doc_id": 79, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 27-year-old woman with a long-term blood condition called beta thalassemia has been having swollen, bleeding gums and bad breath since she became pregnant. She is 16 weeks pregnant and has not seen a dentist before or since. Her gums are red, soft, and bleed easily, and her lips are dry and peeling. This is common when you have both thalassemia and are pregnant. She also has a weak body and was once diagnosed with knee pain from thalassemia-related arthritis. Her blood tests show signs of infection and anemia, which is why she needs regular blood transfusions — but she stopped them during pregnancy. The doctors treated her gums with a special mouth rinse (chlorine dioxide), a hydrogen peroxide swab, antibiotics, and cleaning of her teeth. They also gave her instructions to brush gently and use a small toothbrush between her teeth. After three months of care, her gums healed, the bleeding stopped, and she no longer has bad breath or swollen gums. She is now doing well and keeps her mouth clean with daily care. The team of doctors, dentists, and nurses worked together to fix her problem.\"\n}", "generated_text": "A 27-year-old woman with a long-term blood condition called beta thalassemia has been having swollen, bleeding gums and bad breath since she became pregnant. She is 16 weeks pregnant and has not seen a dentist before or since. Her gums are red, soft, and bleed easily, and her lips are dry and peeling. This is common when you have both thalassemia and are pregnant. She also has a weak body and was once diagnosed with knee pain from thalassemia-related arthritis. Her blood tests show signs of infection and anemia, which is why she needs regular blood transfusions — but she stopped them during pregnancy. The doctors treated her gums with a special mouth rinse (chlorine dioxide), a hydrogen peroxide swab, antibiotics, and cleaning of her teeth. They also gave her instructions to brush gently and use a small toothbrush between her teeth. After three months of care, her gums healed, the bleeding stopped, and she no longer has bad breath or swollen gums. She is now doing well and keeps her mouth clean with daily care. The team of doctors, dentists, and nurses worked together to fix her problem."}
+{"row_index": 122, "doc_id": 79, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 27-year-old woman with beta thalassemia major, a condition that requires monthly blood transfusions and iron-lowering drugs, is now pregnant at 16 weeks. Because of her pregnancy, she stopped her blood transfusions and iron treatments. She has been experiencing swollen, bleeding gums, bad breath, and dry, peeling lips. She has never seen a dentist before or since. During her check-up, her dentist found that her gums were red, soft, and swollen with bleeding, and there were deep pockets in her mouth — signs of gum disease. Her blood tests showed anemia and signs of infection, which are common in beta thalassemia. The doctors diagnosed her with gum enlargement and chronic periodontitis (gum disease) linked to both her pregnancy and beta thalassemia. \\n\\nTo treat her condition, she received a combination of care: her gums were cleaned with a 3% hydrogen peroxide solution, she used a chlorine dioxide mouthwash (Oxyfresh®) three times a day, and took antibiotics for a short time. Her dentist also removed tartar and gave her instructions on how to brush and floss properly. Blood transfusions were given monthly during treatment. After three months of care from an oral medicine specialist, a periodontist, and an internist, her symptoms improved greatly. By the end of the treatment, her gums had healed, she no longer had bleeding or bad breath, and she was able to brush without pain. She is now following a routine at home, including using mouthwash, applying petroleum jelly to her lips, and using an interdental brush to keep her mouth clean. The overall outcome was positive because she followed the treatment plan and stayed consistent with her care.\"\n}", "generated_text": "A 27-year-old woman with beta thalassemia major, a condition that requires monthly blood transfusions and iron-lowering drugs, is now pregnant at 16 weeks. Because of her pregnancy, she stopped her blood transfusions and iron treatments. She has been experiencing swollen, bleeding gums, bad breath, and dry, peeling lips. She has never seen a dentist before or since. During her check-up, her dentist found that her gums were red, soft, and swollen with bleeding, and there were deep pockets in her mouth — signs of gum disease. Her blood tests showed anemia and signs of infection, which are common in beta thalassemia. The doctors diagnosed her with gum enlargement and chronic periodontitis (gum disease) linked to both her pregnancy and beta thalassemia. \n\nTo treat her condition, she received a combination of care: her gums were cleaned with a 3% hydrogen peroxide solution, she used a chlorine dioxide mouthwash (Oxyfresh®) three times a day, and took antibiotics for a short time. Her dentist also removed tartar and gave her instructions on how to brush and floss properly. Blood transfusions were given monthly during treatment. After three months of care from an oral medicine specialist, a periodontist, and an internist, her symptoms improved greatly. By the end of the treatment, her gums had healed, she no longer had bleeding or bad breath, and she was able to brush without pain. She is now following a routine at home, including using mouthwash, applying petroleum jelly to her lips, and using an interdental brush to keep her mouth clean. The overall outcome was positive because she followed the treatment plan and stayed consistent with her care."}
+{"row_index": 123, "doc_id": 20, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 38-year-old woman named A.P. was diagnosed with dilated cardiomyopathy at age 17, after having a severe case of tonsillitis that may have led to heart inflammation (myocarditis), though this was never proven. She developed serious heart failure symptoms and was hospitalized for 10 months and 9 days. At the time, her heart was not pumping effectively — her ejection fraction was only 10%, and she was at high risk of dying. She received treatment to support heart function, prevent dangerous heart rhythms, and reduce blood clots. Over time, her heart function improved, and by age 21, her ejection fraction reached 48–57%, marking a period of remission. This improvement lasted for 4 years, after which her condition worsened, and her ejection fraction dropped to 25%. She was hospitalized again for two months and then stabilized with adjusted treatment. By 2006, her heart function had recovered to 50%.\\n\\nAt age 27, she had a successful first pregnancy. After giving birth, her heart function remained stable at around 40%, and she continued with heart medications. In 2015, she became pregnant again. During the second trimester, at 35 weeks, she was hospitalized due to shortness of breath and inability to walk. Her ejection fraction dropped to 18%, and her heart failure worsened. Despite this, her doctors decided to continue the pregnancy. She had a C-section at 39 weeks, and her condition improved within 20 days.\\n\\nIn October 2016, her treatment was updated to include medications like ramipril, metoprolol, spironolactone, and ivabradine, along with a daily fluid limit of 1.5 liters. She also wore a life-saving device called a LifeVest defibrillator from December 2016 to February 2017, when it was removed. After removal, her ejection fraction was 44%, and doctors found no need for a permanent defibrillator. She is now stable on medication, can do normal daily activities, and is a mother of two children. She is not working, but her heart condition is well-controlled with regular check-ups, weight management, and monitoring of kidney function and electrolytes. Her diagnosis remains dilated cardiomyopathy with heart failure stage II, and no further device is needed at this time.\"\n}", "generated_text": "A 38-year-old woman named A.P. was diagnosed with dilated cardiomyopathy at age 17, after having a severe case of tonsillitis that may have led to heart inflammation (myocarditis), though this was never proven. She developed serious heart failure symptoms and was hospitalized for 10 months and 9 days. At the time, her heart was not pumping effectively — her ejection fraction was only 10%, and she was at high risk of dying. She received treatment to support heart function, prevent dangerous heart rhythms, and reduce blood clots. Over time, her heart function improved, and by age 21, her ejection fraction reached 48–57%, marking a period of remission. This improvement lasted for 4 years, after which her condition worsened, and her ejection fraction dropped to 25%. She was hospitalized again for two months and then stabilized with adjusted treatment. By 2006, her heart function had recovered to 50%.\n\nAt age 27, she had a successful first pregnancy. After giving birth, her heart function remained stable at around 40%, and she continued with heart medications. In 2015, she became pregnant again. During the second trimester, at 35 weeks, she was hospitalized due to shortness of breath and inability to walk. Her ejection fraction dropped to 18%, and her heart failure worsened. Despite this, her doctors decided to continue the pregnancy. She had a C-section at 39 weeks, and her condition improved within 20 days.\n\nIn October 2016, her treatment was updated to include medications like ramipril, metoprolol, spironolactone, and ivabradine, along with a daily fluid limit of 1.5 liters. She also wore a life-saving device called a LifeVest defibrillator from December 2016 to February 2017, when it was removed. After removal, her ejection fraction was 44%, and doctors found no need for a permanent defibrillator. She is now stable on medication, can do normal daily activities, and is a mother of two children. She is not working, but her heart condition is well-controlled with regular check-ups, weight management, and monitoring of kidney function and electrolytes. Her diagnosis remains dilated cardiomyopathy with heart failure stage II, and no further device is needed at this time."}
+{"row_index": 124, "doc_id": 24, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 13-year-old boy was brought to the hospital after finding a noticeable lump in his left groin area. He had no fever, weight loss, or other general symptoms. The lump was soft, movable, and not painful. His medical history included a past spinal surgery six years ago that left him with limited movement and sensation in his legs, and he had developed pressure sores from being in bed for a long time. Blood tests showed a slightly high inflammation marker (ESR), but all other blood and organ function tests were normal. A CT scan found enlarged lymph nodes in the groin area, the largest being about 3.5 cm in size, but no other abnormalities were seen. Since the lump could have been a sign of serious conditions like lymphoma or leukemia, surgery was done to remove the lymph nodes for testing. The tissue sample showed changes consistent with a rare form of Castleman’s disease called plasma cell type, which is very uncommon in children. This case is the first reported instance of unicentric Castleman disease (UCD) in the groin area. After 12 months of follow-up, the boy had no new symptoms, no further lymph node swelling, and all test results remained normal. He was given a short course of prednisolone and continues to be monitored every three months with regular check-ups and imaging.\"\n}", "generated_text": "A 13-year-old boy was brought to the hospital after finding a noticeable lump in his left groin area. He had no fever, weight loss, or other general symptoms. The lump was soft, movable, and not painful. His medical history included a past spinal surgery six years ago that left him with limited movement and sensation in his legs, and he had developed pressure sores from being in bed for a long time. Blood tests showed a slightly high inflammation marker (ESR), but all other blood and organ function tests were normal. A CT scan found enlarged lymph nodes in the groin area, the largest being about 3.5 cm in size, but no other abnormalities were seen. Since the lump could have been a sign of serious conditions like lymphoma or leukemia, surgery was done to remove the lymph nodes for testing. The tissue sample showed changes consistent with a rare form of Castleman’s disease called plasma cell type, which is very uncommon in children. This case is the first reported instance of unicentric Castleman disease (UCD) in the groin area. After 12 months of follow-up, the boy had no new symptoms, no further lymph node swelling, and all test results remained normal. He was given a short course of prednisolone and continues to be monitored every three months with regular check-ups and imaging."}
+{"row_index": 125, "doc_id": 27, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 28-year-old man developed two red, raised patches on his right arm and forearm, each with small blisters and a shallow ulcer, about halfway between the elbow and the wrist. The areas were painful and itchy, but he had no fever or other systemic symptoms. He had been on vacation in a coastal area of Ecuador when the rash appeared. A small skin sample was taken and examined under a microscope, which showed signs consistent with a skin condition caused by exposure to a type of beetle found in tropical regions. The diagnosis was Paederus dermatitis, a rash caused by contact with the beetle’s secretion. He was treated with antihistamines, a topical steroid cream, and cold compresses. After 8 days, the rash went away, though the skin remained slightly darker in those areas as a result of the inflammation.\"\n}", "generated_text": "A 28-year-old man developed two red, raised patches on his right arm and forearm, each with small blisters and a shallow ulcer, about halfway between the elbow and the wrist. The areas were painful and itchy, but he had no fever or other systemic symptoms. He had been on vacation in a coastal area of Ecuador when the rash appeared. A small skin sample was taken and examined under a microscope, which showed signs consistent with a skin condition caused by exposure to a type of beetle found in tropical regions. The diagnosis was Paederus dermatitis, a rash caused by contact with the beetle’s secretion. He was treated with antihistamines, a topical steroid cream, and cold compresses. After 8 days, the rash went away, though the skin remained slightly darker in those areas as a result of the inflammation."}
+{"row_index": 126, "doc_id": 29, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 77-year-old woman had repeated episodes of vomiting blood (haematemesis). She had high blood pressure and high cholesterol, but no other major health problems. When she first came to the emergency room, she was shaky and had low blood pressure, and her blood tests showed anaemia, which pointed to bleeding in her upper digestive tract.\\n\\nA CT scan was done to check the cause. It showed that the third part of the duodenum (a section of the small intestine) bent sharply to the right side of the aorta and went downward without crossing in front of it. The duodenal-jejunal junction (where the duodenum meets the jejunum) and the jejunum were also on the right side. This raised concern that she might have intestinal malrotation — a condition where the intestines are abnormally positioned.\\n\\nHowever, seven days later, a repeat CT scan showed that the intestines had moved back to the normal position on their own. This didn’t match typical malrotation, which is usually permanent. Instead, it suggested a different problem: dysplasia of the ligament of Treitz — a condition where the ligament that normally holds the small intestine in place is abnormally formed or weak.\\n\\nA few months later, she had another episode of vomiting blood. The CT scan again showed the duodenum and jejunum on the right side. Endoscopy (a procedure to look inside the stomach) found a tear at the gastric cardia (the area where the stomach meets the esophagus), which is a known cause of bleeding called Mallory-Weiss syndrome.\\n\\nLater, during surgery (laparotomy), doctors found that the ligament of Treitz was present but not properly fixed to the jejunum. It was only attached to the duodenum, so it could move easily and caused the intestine to shift to the right side. The rest of the intestines were in normal position, and there was no malrotation.\\n\\nThe surgery fixed the upper jejunum to the back of the abdomen, and the patient recovered well and has not had any further bleeding since.\\n\\nIn short, the repeated, temporary shifts of the small intestine were not due to malrotation, but to a weak or abnormal ligament of Treitz, which allowed the intestine to move freely and cause symptoms during vomiting.\"\n}", "generated_text": "A 77-year-old woman had repeated episodes of vomiting blood (haematemesis). She had high blood pressure and high cholesterol, but no other major health problems. When she first came to the emergency room, she was shaky and had low blood pressure, and her blood tests showed anaemia, which pointed to bleeding in her upper digestive tract.\n\nA CT scan was done to check the cause. It showed that the third part of the duodenum (a section of the small intestine) bent sharply to the right side of the aorta and went downward without crossing in front of it. The duodenal-jejunal junction (where the duodenum meets the jejunum) and the jejunum were also on the right side. This raised concern that she might have intestinal malrotation — a condition where the intestines are abnormally positioned.\n\nHowever, seven days later, a repeat CT scan showed that the intestines had moved back to the normal position on their own. This didn’t match typical malrotation, which is usually permanent. Instead, it suggested a different problem: dysplasia of the ligament of Treitz — a condition where the ligament that normally holds the small intestine in place is abnormally formed or weak.\n\nA few months later, she had another episode of vomiting blood. The CT scan again showed the duodenum and jejunum on the right side. Endoscopy (a procedure to look inside the stomach) found a tear at the gastric cardia (the area where the stomach meets the esophagus), which is a known cause of bleeding called Mallory-Weiss syndrome.\n\nLater, during surgery (laparotomy), doctors found that the ligament of Treitz was present but not properly fixed to the jejunum. It was only attached to the duodenum, so it could move easily and caused the intestine to shift to the right side. The rest of the intestines were in normal position, and there was no malrotation.\n\nThe surgery fixed the upper jejunum to the back of the abdomen, and the patient recovered well and has not had any further bleeding since.\n\nIn short, the repeated, temporary shifts of the small intestine were not due to malrotation, but to a weak or abnormal ligament of Treitz, which allowed the intestine to move freely and cause symptoms during vomiting."}
+{"row_index": 127, "doc_id": 31, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 12-year-old boy with Down Syndrome and movement problems was referred to the Oral Medicine Department. He had a distinctive facial appearance and dry, cracked lips. Because he wore a cervical collar, doctors could not check his lymph nodes. Inside his mouth, there was a 1×0.7 cm ulcer on the right side of his tongue, with a hard edge and a white-yellow base. The ulcer looked like oral cancer (OSCC) at first, but doctors found it was actually a chronic traumatic ulcer caused by sharp teeth. The tooth at the back of the upper jaw (tooth 55) was sharp and was rubbing against the tongue, causing the injury. The patient also had damaged teeth and tooth remnants on several teeth, which were recommended to be removed and replaced with a space maintainer to prevent shifting of other teeth.\\n\\nThe boy had low sodium levels and higher lymphocyte counts, and an MRI showed dislocation in his neck spine. He was given treatments including salt water (0.9% sodium chloride), povidone-iodine mouthwash (1%) to clean and reduce inflammation, and petroleum jelly to keep his lips moist. His mother was taught how to care for his mouth at home: using gauze soaked in salt water, applying the mouthwash three times a day to the ulcer, and using petroleum jelly on his lips.\\n\\nAfter a few days, the ulcer and lip condition improved. By the 10-day follow-up, the ulcer had greatly reduced. Two days after that, the boy had surgery on his neck spine. He was then admitted to the Pediatric Intensive Care Unit, where he later developed respiratory failure and passed away after two weeks of care.\"\n}", "generated_text": "A 12-year-old boy with Down Syndrome and movement problems was referred to the Oral Medicine Department. He had a distinctive facial appearance and dry, cracked lips. Because he wore a cervical collar, doctors could not check his lymph nodes. Inside his mouth, there was a 1×0.7 cm ulcer on the right side of his tongue, with a hard edge and a white-yellow base. The ulcer looked like oral cancer (OSCC) at first, but doctors found it was actually a chronic traumatic ulcer caused by sharp teeth. The tooth at the back of the upper jaw (tooth 55) was sharp and was rubbing against the tongue, causing the injury. The patient also had damaged teeth and tooth remnants on several teeth, which were recommended to be removed and replaced with a space maintainer to prevent shifting of other teeth.\n\nThe boy had low sodium levels and higher lymphocyte counts, and an MRI showed dislocation in his neck spine. He was given treatments including salt water (0.9% sodium chloride), povidone-iodine mouthwash (1%) to clean and reduce inflammation, and petroleum jelly to keep his lips moist. His mother was taught how to care for his mouth at home: using gauze soaked in salt water, applying the mouthwash three times a day to the ulcer, and using petroleum jelly on his lips.\n\nAfter a few days, the ulcer and lip condition improved. By the 10-day follow-up, the ulcer had greatly reduced. Two days after that, the boy had surgery on his neck spine. He was then admitted to the Pediatric Intensive Care Unit, where he later developed respiratory failure and passed away after two weeks of care."}
+{"row_index": 128, "doc_id": 34, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 19-month-old boy was brought to the emergency room after falling from his highchair. He hit his head and started vomiting, became very irritable, and had fast breathing and heart rate. His oxygen levels were low, and he showed signs of serious breathing difficulty, including pulling in his stomach muscles and weak breath sounds on the left side of his chest. Despite treatment with a breathing tube and oxygen, his oxygen levels kept dropping, so doctors decided to insert a tube into his windpipe to help him breathe. A lung ultrasound showed signs of lung collapse, and a chest CT scan revealed that the entire left lung was collapsed, with a sudden blockage in the main airway of the left lung, about 12 mm from the main branch. This raised suspicion of a foreign object — an almond — being stuck in the airway. The mother reported that the child had had a sudden, intense cough a few days before that went away on its own. A rigid bronchoscopy was performed, and a 2 cm almond was found and removed. The boy had never eaten almonds before and likely swallowed it by accident. After recovery, his breathing improved, and he was able to breathe on his own again within 24 hours. He was then moved to a regular pediatric ward for further care and full recovery.\"\n}", "generated_text": "A 19-month-old boy was brought to the emergency room after falling from his highchair. He hit his head and started vomiting, became very irritable, and had fast breathing and heart rate. His oxygen levels were low, and he showed signs of serious breathing difficulty, including pulling in his stomach muscles and weak breath sounds on the left side of his chest. Despite treatment with a breathing tube and oxygen, his oxygen levels kept dropping, so doctors decided to insert a tube into his windpipe to help him breathe. A lung ultrasound showed signs of lung collapse, and a chest CT scan revealed that the entire left lung was collapsed, with a sudden blockage in the main airway of the left lung, about 12 mm from the main branch. This raised suspicion of a foreign object — an almond — being stuck in the airway. The mother reported that the child had had a sudden, intense cough a few days before that went away on its own. A rigid bronchoscopy was performed, and a 2 cm almond was found and removed. The boy had never eaten almonds before and likely swallowed it by accident. After recovery, his breathing improved, and he was able to breathe on his own again within 24 hours. He was then moved to a regular pediatric ward for further care and full recovery."}
+{"row_index": 129, "doc_id": 35, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 4-month-old boy lived in a prison cell with his mom and two other people. He had a painful lump in his armpit and X-rays showed broken ribs and lung problems. Doctors thought it might be abuse, so he went to the hospital. He was very sick — low oxygen, fever, and swelling — and had a big abscess. Tests showed his body couldn’t fight off infections well. Bacteria were not found, but a fungus called Aspergillus fumigatus was found in the abscess. He got antibiotics and then antifungal medicine (voriconazole) for 28 days. A test showed he had a rare immune problem called chronic granulomatous disease, caused by a gene fault passed from his mom. At 8 months, the infection got worse and spread to his shoulder. He had more lung damage and needed more medicine. At 12 months, he got sick again with the same fungus, even after treatment, and died.\"\n}", "generated_text": "A 4-month-old boy lived in a prison cell with his mom and two other people. He had a painful lump in his armpit and X-rays showed broken ribs and lung problems. Doctors thought it might be abuse, so he went to the hospital. He was very sick — low oxygen, fever, and swelling — and had a big abscess. Tests showed his body couldn’t fight off infections well. Bacteria were not found, but a fungus called Aspergillus fumigatus was found in the abscess. He got antibiotics and then antifungal medicine (voriconazole) for 28 days. A test showed he had a rare immune problem called chronic granulomatous disease, caused by a gene fault passed from his mom. At 8 months, the infection got worse and spread to his shoulder. He had more lung damage and needed more medicine. At 12 months, he got sick again with the same fungus, even after treatment, and died."}
+{"row_index": 130, "doc_id": 36, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 25-year-old man had painful sores on his lips and inside his mouth. The sores started a few days ago, got worse when he ate or talked, and he tried using petroleum jelly but it didn’t help. He started using a medicine ointment (triamcinolone) on his lips, and the pain got better, but the sores didn’t go away. He had a fever before the sores came, didn’t eat well for a long time, and often licked his lips. He had chickenpox as a child. The sores were red, bumpy, and bled easily. A test showed he had a virus called HSV-1, which means the sores were caused by a common virus. The doctor said it was HAEM — a condition where the body reacts to stress and poor diet with mouth sores. To fix it, he took vitamins, used an antiviral medicine (acyclovir), and used a salt water rinse. He was also told to brush his teeth and tongue gently, avoid spicy or sour foods, stop licking his lips, and eat better. After a few days, his sores healed completely and he felt much better. Now he needs to keep going to the dentist for more care.\"\n}", "generated_text": "A 25-year-old man had painful sores on his lips and inside his mouth. The sores started a few days ago, got worse when he ate or talked, and he tried using petroleum jelly but it didn’t help. He started using a medicine ointment (triamcinolone) on his lips, and the pain got better, but the sores didn’t go away. He had a fever before the sores came, didn’t eat well for a long time, and often licked his lips. He had chickenpox as a child. The sores were red, bumpy, and bled easily. A test showed he had a virus called HSV-1, which means the sores were caused by a common virus. The doctor said it was HAEM — a condition where the body reacts to stress and poor diet with mouth sores. To fix it, he took vitamins, used an antiviral medicine (acyclovir), and used a salt water rinse. He was also told to brush his teeth and tongue gently, avoid spicy or sour foods, stop licking his lips, and eat better. After a few days, his sores healed completely and he felt much better. Now he needs to keep going to the dentist for more care."}
+{"row_index": 131, "doc_id": 36, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 25-year-old man came to the dental clinic with painful sores on his lips that started about four days ago and spread to his upper and lower lips two days later. The sores were painful, especially when eating or talking, and didn't improve with self-treatment like petroleum jelly. He tried using triamcinolone ointment, which helped a little, but the sores didn’t fully heal.\\n\\nHe had a fever a week before the sores appeared and had been under a lot of stress with poor nutrition for about a month. He didn’t have any medical conditions, allergies, or habits like smoking or drinking alcohol. However, he often licked his lips, which may have worsened the sores. He also had chickenpox as a child.\\n\\nOn examination, his lips had red, painful sores with crusts that bled easily. His tongue had white patches, and there were other minor oral issues like tooth decay and poor hygiene. A blood test for herpes virus (HSV-1) came back positive, which confirmed the diagnosis of HAEM — a condition caused by herpes virus that affects the mouth and lips, especially in people under stress or with poor nutrition.\\n\\nTreatment included applying a topical ointment (triamcinolone) to the lips, taking oral multivitamins, and using acyclovir tablets to fight the virus. He was also advised to improve his diet, avoid spicy or acidic foods, stop licking his lips, and keep his mouth clean by brushing teeth and tongue daily.\\n\\nAfter a few days, his pain improved and the sores began to heal. By the second follow-up, all the sores had healed completely. His quality of life improved significantly, and he was referred to continue regular dental care. The case was reviewed and approved for publication, following ethical guidelines.\"\n}", "generated_text": "A 25-year-old man came to the dental clinic with painful sores on his lips that started about four days ago and spread to his upper and lower lips two days later. The sores were painful, especially when eating or talking, and didn't improve with self-treatment like petroleum jelly. He tried using triamcinolone ointment, which helped a little, but the sores didn’t fully heal.\n\nHe had a fever a week before the sores appeared and had been under a lot of stress with poor nutrition for about a month. He didn’t have any medical conditions, allergies, or habits like smoking or drinking alcohol. However, he often licked his lips, which may have worsened the sores. He also had chickenpox as a child.\n\nOn examination, his lips had red, painful sores with crusts that bled easily. His tongue had white patches, and there were other minor oral issues like tooth decay and poor hygiene. A blood test for herpes virus (HSV-1) came back positive, which confirmed the diagnosis of HAEM — a condition caused by herpes virus that affects the mouth and lips, especially in people under stress or with poor nutrition.\n\nTreatment included applying a topical ointment (triamcinolone) to the lips, taking oral multivitamins, and using acyclovir tablets to fight the virus. He was also advised to improve his diet, avoid spicy or acidic foods, stop licking his lips, and keep his mouth clean by brushing teeth and tongue daily.\n\nAfter a few days, his pain improved and the sores began to heal. By the second follow-up, all the sores had healed completely. His quality of life improved significantly, and he was referred to continue regular dental care. The case was reviewed and approved for publication, following ethical guidelines."}
+{"row_index": 132, "doc_id": 37, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 29-year-old woman had heavy vaginal bleeding for a month and was living with HIV. Her immune cells (CD4) were very low at 26, meaning her body was weak. A biopsy showed a serious cancer in her cervix that spread beyond the cervix, called extra-nodal BL. This cancer was stage 3B, meaning it had reached her kidneys and pelvic walls. Doctors said she needed chemo and radiation, but it took her 43 days to get treatment because of a long waiting list. That delay was too long — doctors say treatment should start within 48 hours. She died 43 days after diagnosis, before getting treatment. During those days, no more scans could be done because the machines were broken. She got blood transfusions and pain relief, but still passed away. The main reason she died was likely the fast-spreading cancer, especially since she had weak immunity and high virus levels. But her body also failed in many ways — her kidneys and blood system stopped working. Doctors couldn’t do a final test after she died, but they believe the cancer was the main cause, with organ failure as the final result.\"\n}", "generated_text": "A 29-year-old woman had heavy vaginal bleeding for a month and was living with HIV. Her immune cells (CD4) were very low at 26, meaning her body was weak. A biopsy showed a serious cancer in her cervix that spread beyond the cervix, called extra-nodal BL. This cancer was stage 3B, meaning it had reached her kidneys and pelvic walls. Doctors said she needed chemo and radiation, but it took her 43 days to get treatment because of a long waiting list. That delay was too long — doctors say treatment should start within 48 hours. She died 43 days after diagnosis, before getting treatment. During those days, no more scans could be done because the machines were broken. She got blood transfusions and pain relief, but still passed away. The main reason she died was likely the fast-spreading cancer, especially since she had weak immunity and high virus levels. But her body also failed in many ways — her kidneys and blood system stopped working. Doctors couldn’t do a final test after she died, but they believe the cancer was the main cause, with organ failure as the final result."}
+{"row_index": 133, "doc_id": 38, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 56-year-old woman was diagnosed in 2013 with Sjogren’s syndrome, a condition that affects dryness in the mouth and eyes, and which also led to lung disease (interstitial lung disease) and pulmonary arterial hypertension (PAH). She was treated with several medications, including sildenafil, bosentan, macitentan, iloprost, and corticosteroids, but her condition continued to worsen. By 2020, she was experiencing severe shortness of breath, cough, and signs of heart failure, including low oxygen levels and high levels of a heart-related marker (BNP), which led to cardiogenic shock. She was hospitalized, treated in the ICU, and stabilized, but her condition remained serious and required frequent hospital visits.\\n\\nIn May 2023, she started a new treatment called molecular hydrogen therapy, taking one capsule per day. This therapy involved hydrogen-rich capsules made from coral calcium. After starting the treatment, tests showed an increase in certain immune cells (CD127+ Treg cells) and a decrease in harmful autoantibodies (anti-Ro) and B cell activity. Her symptoms, such as shortness of breath, stabilized without any side effects. Blood tests confirmed these changes in her immune system. This treatment is being used as an added support, not a replacement for standard care, and so far, it has helped improve her health without causing harm.\"\n}", "generated_text": "A 56-year-old woman was diagnosed in 2013 with Sjogren’s syndrome, a condition that affects dryness in the mouth and eyes, and which also led to lung disease (interstitial lung disease) and pulmonary arterial hypertension (PAH). She was treated with several medications, including sildenafil, bosentan, macitentan, iloprost, and corticosteroids, but her condition continued to worsen. By 2020, she was experiencing severe shortness of breath, cough, and signs of heart failure, including low oxygen levels and high levels of a heart-related marker (BNP), which led to cardiogenic shock. She was hospitalized, treated in the ICU, and stabilized, but her condition remained serious and required frequent hospital visits.\n\nIn May 2023, she started a new treatment called molecular hydrogen therapy, taking one capsule per day. This therapy involved hydrogen-rich capsules made from coral calcium. After starting the treatment, tests showed an increase in certain immune cells (CD127+ Treg cells) and a decrease in harmful autoantibodies (anti-Ro) and B cell activity. Her symptoms, such as shortness of breath, stabilized without any side effects. Blood tests confirmed these changes in her immune system. This treatment is being used as an added support, not a replacement for standard care, and so far, it has helped improve her health without causing harm."}
+{"row_index": 134, "doc_id": 44, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 12-year-old boy was admitted because he had recently started getting headaches and was drinking and urinating a lot. He had no other medical problems. Tests showed he had diabetes insipidus (DI), a condition where the body can't properly regulate water balance, causing excessive urination and thirst. MRI scans found a rare condition called Rathke cleft cyst apoplexy, which is a sudden bleeding or swelling in a cyst in the pituitary area, but it wasn't pressing on any brain parts or causing serious issues. His hormone levels were mostly normal, and there were no signs of other endocrine problems. Because the cyst was stable and not causing harm, the doctors chose a watchful approach — regular check-ups with blood tests, physical exams, and MRI scans instead of surgery. Over three years, the boy developed normally, including puberty, with no major hormone problems except for a small deficiency in growth hormone. His growth slowed slightly, and after testing, it was found he had a partial growth hormone deficiency. He started treatment with growth hormone, and his growth improved over the next year. The cyst on the MRI stayed stable and even slightly decreased in size over time. The team of doctors, including endocrinologists and neurosurgeons, agreed that ongoing monitoring was safe and effective.\"\n}", "generated_text": "A 12-year-old boy was admitted because he had recently started getting headaches and was drinking and urinating a lot. He had no other medical problems. Tests showed he had diabetes insipidus (DI), a condition where the body can't properly regulate water balance, causing excessive urination and thirst. MRI scans found a rare condition called Rathke cleft cyst apoplexy, which is a sudden bleeding or swelling in a cyst in the pituitary area, but it wasn't pressing on any brain parts or causing serious issues. His hormone levels were mostly normal, and there were no signs of other endocrine problems. Because the cyst was stable and not causing harm, the doctors chose a watchful approach — regular check-ups with blood tests, physical exams, and MRI scans instead of surgery. Over three years, the boy developed normally, including puberty, with no major hormone problems except for a small deficiency in growth hormone. His growth slowed slightly, and after testing, it was found he had a partial growth hormone deficiency. He started treatment with growth hormone, and his growth improved over the next year. The cyst on the MRI stayed stable and even slightly decreased in size over time. The team of doctors, including endocrinologists and neurosurgeons, agreed that ongoing monitoring was safe and effective."}
+{"row_index": 135, "doc_id": 45, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 67-year-old man with no prior medical problems started having trouble swallowing, a hoarse voice, and a general decline in health over six months. He developed a large mass in his neck that was confirmed by biopsy to be a slow-growing type of lymphoma called grade 1 and 2 follicular non-Hodgkin lymphoma. Imaging showed the mass was 70 mm by 40 mm and had spread into nearby areas. Blood tests and bone marrow checks were normal at the start of treatment. The patient received four courses of chemotherapy (rituximab plus CHOP — a combination of drugs including cyclophosphamide, doxorubicin, prednisone, and oncovin) with no improvement. He then had three more courses of a different chemotherapy (rituximab plus DHAOX) with no response either. During follow-up, the biopsy of the mass showed that the lymphoma cells had disappeared and were replaced by AL amyloid deposits, which are a sign of abnormal protein buildup. Blood tests found high levels of immunoglobulin M, a type of antibody. A PET scan showed the mass was very active (hypermetabolic), which is a sign of ongoing disease. The patient is now on a new treatment plan with bortezomib, prednisone, and bendamustine, and is showing improvement after the first dose.\"\n}", "generated_text": "A 67-year-old man with no prior medical problems started having trouble swallowing, a hoarse voice, and a general decline in health over six months. He developed a large mass in his neck that was confirmed by biopsy to be a slow-growing type of lymphoma called grade 1 and 2 follicular non-Hodgkin lymphoma. Imaging showed the mass was 70 mm by 40 mm and had spread into nearby areas. Blood tests and bone marrow checks were normal at the start of treatment. The patient received four courses of chemotherapy (rituximab plus CHOP — a combination of drugs including cyclophosphamide, doxorubicin, prednisone, and oncovin) with no improvement. He then had three more courses of a different chemotherapy (rituximab plus DHAOX) with no response either. During follow-up, the biopsy of the mass showed that the lymphoma cells had disappeared and were replaced by AL amyloid deposits, which are a sign of abnormal protein buildup. Blood tests found high levels of immunoglobulin M, a type of antibody. A PET scan showed the mass was very active (hypermetabolic), which is a sign of ongoing disease. The patient is now on a new treatment plan with bortezomib, prednisone, and bendamustine, and is showing improvement after the first dose."}
+{"row_index": 136, "doc_id": 49, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 16-year-old girl has a flat, grayish patch on her left thigh that has been there since birth. The patch is about 10.5 cm wide and 8.0 cm long, and it has darkened and become depressed over time. It has small blood vessels running around the edge, and the area shows signs of abnormal blood flow. Imaging tests (angioresonance) found that the patch is caused by a vascular malformation in the skin and layer beneath the skin, fed by branches of the popliteal artery. The blood flow shows early signs of shunting, meaning blood is taking an unusual path. There is a small visible vein running under the skin, but no blood vessels have spread into the muscle or bone. The patch does not affect the length of her legs.\"\n}", "generated_text": "A 16-year-old girl has a flat, grayish patch on her left thigh that has been there since birth. The patch is about 10.5 cm wide and 8.0 cm long, and it has darkened and become depressed over time. It has small blood vessels running around the edge, and the area shows signs of abnormal blood flow. Imaging tests (angioresonance) found that the patch is caused by a vascular malformation in the skin and layer beneath the skin, fed by branches of the popliteal artery. The blood flow shows early signs of shunting, meaning blood is taking an unusual path. There is a small visible vein running under the skin, but no blood vessels have spread into the muscle or bone. The patch does not affect the length of her legs."}
+{"row_index": 137, "doc_id": 50, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 57-year-old woman with asthma and allergies had stomach pain that came and went for two months. She lost weight and felt tired, but had no fever or diarrhea. Blood tests showed a high number of a type of white blood cell called eosinophils, and her IgG4 levels were high. Doctors checked for infections and other causes, but nothing was found. A tissue sample from her colon showed too many eosinophils, which confirmed a condition called eosinophilic colitis. She was treated with steroids and a medicine called montelukast. Her symptoms went away in two weeks, and after that, she stayed on montelukast for three months with no pain coming back.\"\n}", "generated_text": "A 57-year-old woman with asthma and allergies had stomach pain that came and went for two months. She lost weight and felt tired, but had no fever or diarrhea. Blood tests showed a high number of a type of white blood cell called eosinophils, and her IgG4 levels were high. Doctors checked for infections and other causes, but nothing was found. A tissue sample from her colon showed too many eosinophils, which confirmed a condition called eosinophilic colitis. She was treated with steroids and a medicine called montelukast. Her symptoms went away in two weeks, and after that, she stayed on montelukast for three months with no pain coming back."}
+{"row_index": 138, "doc_id": 52, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 2.5-year-old girl with a history of neurofibromatosis type 1 (NF1) was brought in with bloody diarrhea that had lasted for several weeks. She had been having 5 to 10 episodes of diarrhea per day, with blood streaks, and had lost some weight. Tests initially showed a rotavirus infection, but that didn’t explain the ongoing symptoms. After being hospitalized for dehydration, her symptoms returned with blood in the stool, low appetite, and weight loss.\\n\\nAn endoscopy exam showed red, inflamed lining in her colon from the anus all the way to the beginning of the large intestine (the cecum), with loss of normal blood vessel visibility. Biopsies of the colon tissue showed signs of chronic inflammation, which is consistent with ulcerative colitis. Additionally, a test for cytomegalovirus (CMV) found a positive result, meaning the child had an active CMV infection.\\n\\nThe child was treated with antiviral medication (ganciclovir) for the CMV, which helped reduce the virus load. Her symptoms improved during hospitalization, and she stopped having bloody stools and abdominal pain. However, after two months, the inflammation returned, with bloody diarrhea again. A repeat endoscopy confirmed ongoing inflammation throughout the colon. She was treated with antibiotics and corticosteroids, which worked well, and she now has mild, ongoing symptoms.\\n\\nShe continues to be managed with a medication called mesalazine to help control the inflammation and is being monitored regularly. Her condition is stable, but she needs long-term care due to the chronic nature of the disease and her underlying NF1.\"\n}", "generated_text": "A 2.5-year-old girl with a history of neurofibromatosis type 1 (NF1) was brought in with bloody diarrhea that had lasted for several weeks. She had been having 5 to 10 episodes of diarrhea per day, with blood streaks, and had lost some weight. Tests initially showed a rotavirus infection, but that didn’t explain the ongoing symptoms. After being hospitalized for dehydration, her symptoms returned with blood in the stool, low appetite, and weight loss.\n\nAn endoscopy exam showed red, inflamed lining in her colon from the anus all the way to the beginning of the large intestine (the cecum), with loss of normal blood vessel visibility. Biopsies of the colon tissue showed signs of chronic inflammation, which is consistent with ulcerative colitis. Additionally, a test for cytomegalovirus (CMV) found a positive result, meaning the child had an active CMV infection.\n\nThe child was treated with antiviral medication (ganciclovir) for the CMV, which helped reduce the virus load. Her symptoms improved during hospitalization, and she stopped having bloody stools and abdominal pain. However, after two months, the inflammation returned, with bloody diarrhea again. A repeat endoscopy confirmed ongoing inflammation throughout the colon. She was treated with antibiotics and corticosteroids, which worked well, and she now has mild, ongoing symptoms.\n\nShe continues to be managed with a medication called mesalazine to help control the inflammation and is being monitored regularly. Her condition is stable, but she needs long-term care due to the chronic nature of the disease and her underlying NF1."}
+{"row_index": 139, "doc_id": 53, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 40-year-old man with HIV who was taking his medicine regularly came in with fevers that came and went for two years. Recently, he started having bad pain in his belly, especially on the right side, and his organs — liver and spleen — got bigger. He also had swollen lymph nodes all over. Lab tests showed his blood was weak, his body was fighting off infections, and his proteins were low. X-rays showed big liver and spleen, swollen lymph nodes, and a tree-like pattern in his lung, plus fluid in his lungs and belly. He got worse fast, had liver failure, and ended up in the ICU. He died a few hours later. After he died, doctors found tuberculosis in his lung sample and saw small, harmless spots in his liver that didn’t destroy tissue. This case shows how HIV can lead to serious infections when the body is weak.\"\n}", "generated_text": "A 40-year-old man with HIV who was taking his medicine regularly came in with fevers that came and went for two years. Recently, he started having bad pain in his belly, especially on the right side, and his organs — liver and spleen — got bigger. He also had swollen lymph nodes all over. Lab tests showed his blood was weak, his body was fighting off infections, and his proteins were low. X-rays showed big liver and spleen, swollen lymph nodes, and a tree-like pattern in his lung, plus fluid in his lungs and belly. He got worse fast, had liver failure, and ended up in the ICU. He died a few hours later. After he died, doctors found tuberculosis in his lung sample and saw small, harmless spots in his liver that didn’t destroy tissue. This case shows how HIV can lead to serious infections when the body is weak."}
+{"row_index": 140, "doc_id": 53, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 40-year-old man with HIV who had been consistently taking his medication came in with recurring fevers over two years. These fevers didn’t follow a regular pattern and were only temporarily relieved with anti-inflammatory drugs. In the past two months, he developed widespread abdominal pain, especially on the right side, along with swelling in his liver and spleen. He also had enlarged lymph nodes throughout his body. Lab tests showed low blood cell counts, blood clotting problems, low protein levels, and signs of inflammation. Imaging scans showed enlarged liver and spleen and widespread lymph node swelling. Tests for bacteria like Mycobacterium were mostly negative, except for a detection of HHV-8 in a lab test. A biopsy of a lymph node in his pelvis found signs of Castleman’s disease. Even after restarting his HIV treatment, his symptoms got worse. He was started on corticosteroids and ganciclovir, but after one week, he developed severe organ failure and swelling (anasarca), which made the treatment unsafe. A new chest scan showed tree-like patterns in the upper right lung and fluid around both lungs, and his liver and spleen continued to grow larger with more abdominal fluid. He was admitted to the intensive care unit 48 hours later and died shortly after from sudden liver failure. After death, tests on a sample from his airway found Mycobacterium tuberculosis, and a liver biopsy showed small, non-destructive granulomas.\"\n}", "generated_text": "A 40-year-old man with HIV who had been consistently taking his medication came in with recurring fevers over two years. These fevers didn’t follow a regular pattern and were only temporarily relieved with anti-inflammatory drugs. In the past two months, he developed widespread abdominal pain, especially on the right side, along with swelling in his liver and spleen. He also had enlarged lymph nodes throughout his body. Lab tests showed low blood cell counts, blood clotting problems, low protein levels, and signs of inflammation. Imaging scans showed enlarged liver and spleen and widespread lymph node swelling. Tests for bacteria like Mycobacterium were mostly negative, except for a detection of HHV-8 in a lab test. A biopsy of a lymph node in his pelvis found signs of Castleman’s disease. Even after restarting his HIV treatment, his symptoms got worse. He was started on corticosteroids and ganciclovir, but after one week, he developed severe organ failure and swelling (anasarca), which made the treatment unsafe. A new chest scan showed tree-like patterns in the upper right lung and fluid around both lungs, and his liver and spleen continued to grow larger with more abdominal fluid. He was admitted to the intensive care unit 48 hours later and died shortly after from sudden liver failure. After death, tests on a sample from his airway found Mycobacterium tuberculosis, and a liver biopsy showed small, non-destructive granulomas."}
+{"row_index": 141, "doc_id": 54, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 4-month-old baby from a rural village in Panama, far from any hospital, was sick with diarrhea and could not keep fluids down. She was very weak, had no weight, and was dehydrated — her body was dry and she couldn’t cry properly. She didn’t get breast milk and was fed powdered milk, which wasn’t enough. Her family had no electricity, no clean water, and lived in a simple house with a thatched roof. She didn’t get vaccines or any medical care for the first four months of life. When she came to a health center, she had diarrhea for four days, no fever, no cough, but she was vomiting. Doctors gave her a medicine called Enterogermina to help her gut. Because she kept getting worse, she was taken to a bigger hospital and then to a major hospital in Panama City. There, she had trouble breathing, her skin was cold and pale, her heart was racing, and her blood pressure was very low. Tests showed she had a dangerous bacteria in her blood called MRSA and also had a gut infection from Clostridiodes difficile. A good bacteria called Bacillus clausii was found in her blood over several days. Even with strong antibiotics, she kept getting sicker. She developed heart problems, her kidneys stopped working, and her body failed in many ways. After 12 days, she died. No autopsy was done because the mother didn’t want to.\"\n}", "generated_text": "A 4-month-old baby from a rural village in Panama, far from any hospital, was sick with diarrhea and could not keep fluids down. She was very weak, had no weight, and was dehydrated — her body was dry and she couldn’t cry properly. She didn’t get breast milk and was fed powdered milk, which wasn’t enough. Her family had no electricity, no clean water, and lived in a simple house with a thatched roof. She didn’t get vaccines or any medical care for the first four months of life. When she came to a health center, she had diarrhea for four days, no fever, no cough, but she was vomiting. Doctors gave her a medicine called Enterogermina to help her gut. Because she kept getting worse, she was taken to a bigger hospital and then to a major hospital in Panama City. There, she had trouble breathing, her skin was cold and pale, her heart was racing, and her blood pressure was very low. Tests showed she had a dangerous bacteria in her blood called MRSA and also had a gut infection from Clostridiodes difficile. A good bacteria called Bacillus clausii was found in her blood over several days. Even with strong antibiotics, she kept getting sicker. She developed heart problems, her kidneys stopped working, and her body failed in many ways. After 12 days, she died. No autopsy was done because the mother didn’t want to."}
+{"row_index": 142, "doc_id": 54, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 4-month-old indigenous infant from a rural area in Panama, living 3 hours by canoe from the nearest health center, arrived at a hospital with severe diarrhea and dehydration. She had not been breastfed and was given powdered milk instead, which may have contributed to her poor health. Her family lived in a basic home without electricity or running water, relying on a well and a river for waste disposal. She did not receive any vaccines or prenatal care during her early life.\\n\\nShe first visited a local health center with 4 days of diarrhea, vomiting, and no fever or breathing problems. Doctors gave her oral fluids and a medication called Enterogermina (which contains B. clausii bacteria) to help her gut recover. Because she was severely dehydrated, she was transferred to a larger hospital and then to a major hospital in Panama City.\\n\\nWhen she arrived at the hospital, she was very weak, with dry mouth, no tears, and signs of shock — including cold hands and feet, a fast heartbeat, and low blood pressure. She had swelling in her hands, feet, face, and belly. Tests showed she had a serious infection, including methicillin-resistant Staphylococcus aureus (MRSA) in her blood, and later, Clostridiodes difficile (a harmful gut bacteria) was found. B. clausii, a beneficial bacteria, was also found in her blood over several days.\\n\\nShe received multiple antibiotics, but the infection kept getting worse. Her body began to fail in many systems — her heart, kidneys, and organs stopped working properly. She developed acute heart inflammation (myocarditis) and kidney failure. Despite treatment, including IV antibiotics, fluids, and medications to support her organs, she died 12 days after being admitted to the hospital. No autopsy was done because the mother refused, due to cultural reasons.\"\n}", "generated_text": "A 4-month-old indigenous infant from a rural area in Panama, living 3 hours by canoe from the nearest health center, arrived at a hospital with severe diarrhea and dehydration. She had not been breastfed and was given powdered milk instead, which may have contributed to her poor health. Her family lived in a basic home without electricity or running water, relying on a well and a river for waste disposal. She did not receive any vaccines or prenatal care during her early life.\n\nShe first visited a local health center with 4 days of diarrhea, vomiting, and no fever or breathing problems. Doctors gave her oral fluids and a medication called Enterogermina (which contains B. clausii bacteria) to help her gut recover. Because she was severely dehydrated, she was transferred to a larger hospital and then to a major hospital in Panama City.\n\nWhen she arrived at the hospital, she was very weak, with dry mouth, no tears, and signs of shock — including cold hands and feet, a fast heartbeat, and low blood pressure. She had swelling in her hands, feet, face, and belly. Tests showed she had a serious infection, including methicillin-resistant Staphylococcus aureus (MRSA) in her blood, and later, Clostridiodes difficile (a harmful gut bacteria) was found. B. clausii, a beneficial bacteria, was also found in her blood over several days.\n\nShe received multiple antibiotics, but the infection kept getting worse. Her body began to fail in many systems — her heart, kidneys, and organs stopped working properly. She developed acute heart inflammation (myocarditis) and kidney failure. Despite treatment, including IV antibiotics, fluids, and medications to support her organs, she died 12 days after being admitted to the hospital. No autopsy was done because the mother refused, due to cultural reasons."}
+{"row_index": 143, "doc_id": 55, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 2-year-old girl was brought in with a 1-year history of painless swelling in her left eye, where the eye had slowly moved forward and was pointing inward and upward. Her vision was very limited, with only light sensation in the left eye. Examining her eye, doctors found that the eye was stuck in position and couldn’t move properly. A soft, well-defined lump was felt in the lower part of her left eye socket, and her lower eyelid was turned outward. The pupil was large and didn’t react to light. MRI scans showed a clear mass inside the eye socket that appeared dark on T1-weighted images and bright on T2-weighted images. The mass did not take up contrast, which helped rule out some other conditions. The diagnosis of orbital teratoma — a type of tumor containing different tissues like skin, cartilage, and brain tissue — was confirmed through tissue testing and lab analysis. The doctors removed the tumor using a small incision inside the lower eyelid, along with cutting the lower eyelid and outer corner of the eye to give better access. During surgery, they found a grayish-white cystic mass with a clear border, and it was tightly attached to the optic nerve. Because the tumor was large and the space was limited, they removed most of the fluid and completely excised the mass. One month after surgery, the child developed a sunken eye (enophthalmos), redness of the eyelid (conjunctival hyperemia), and inflammation of the cornea (keratitis). This happened because the tumor had previously stretched the eye socket, and after removal, the space collapsed. To fix this, a second surgery was done, where a donated sclera (the white part of the eye) was implanted into the socket to restore volume and help the eye sit properly again. After one year of follow-up, no tumor came back, and there were no other serious complications. The child’s vision stayed the same, though she still has a slight sunken eye and a small issue with the outer corner of her eye.\"\n}", "generated_text": "A 2-year-old girl was brought in with a 1-year history of painless swelling in her left eye, where the eye had slowly moved forward and was pointing inward and upward. Her vision was very limited, with only light sensation in the left eye. Examining her eye, doctors found that the eye was stuck in position and couldn’t move properly. A soft, well-defined lump was felt in the lower part of her left eye socket, and her lower eyelid was turned outward. The pupil was large and didn’t react to light. MRI scans showed a clear mass inside the eye socket that appeared dark on T1-weighted images and bright on T2-weighted images. The mass did not take up contrast, which helped rule out some other conditions. The diagnosis of orbital teratoma — a type of tumor containing different tissues like skin, cartilage, and brain tissue — was confirmed through tissue testing and lab analysis. The doctors removed the tumor using a small incision inside the lower eyelid, along with cutting the lower eyelid and outer corner of the eye to give better access. During surgery, they found a grayish-white cystic mass with a clear border, and it was tightly attached to the optic nerve. Because the tumor was large and the space was limited, they removed most of the fluid and completely excised the mass. One month after surgery, the child developed a sunken eye (enophthalmos), redness of the eyelid (conjunctival hyperemia), and inflammation of the cornea (keratitis). This happened because the tumor had previously stretched the eye socket, and after removal, the space collapsed. To fix this, a second surgery was done, where a donated sclera (the white part of the eye) was implanted into the socket to restore volume and help the eye sit properly again. After one year of follow-up, no tumor came back, and there were no other serious complications. The child’s vision stayed the same, though she still has a slight sunken eye and a small issue with the outer corner of her eye."}
+{"row_index": 144, "doc_id": 57, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"This study follows a 9-year-old girl who has both high intellectual abilities and dyslexia, a learning disorder that makes reading and writing difficult. The goal was to see how her reading, writing, and phonological skills improved after targeted therapy. Before the intervention, she was reading at an early stage (alphabetic level), writing in a transitional phase between syllabic and alphabetic systems, and had weak phonological processing skills. After six months of weekly therapy focused on phonological skills—like recognizing sounds, blending sounds, and improving memory—the child showed clear progress. Her phonological processing improved, her writing became more consistent and reached the alphabetic level, and her reading speed increased significantly—from about 20 to 94 words per minute. She also showed better ability to access words quickly in her mind. However, some writing problems remained, such as mixing up similar letters and making small spelling errors. The therapy helped her catch up in key areas, especially in reading and sound processing, even though she still faces some challenges typical of dyslexia. This case shows that with focused support, children with high abilities and dyslexia can make meaningful progress in learning to read and write.\"\n}", "generated_text": "This study follows a 9-year-old girl who has both high intellectual abilities and dyslexia, a learning disorder that makes reading and writing difficult. The goal was to see how her reading, writing, and phonological skills improved after targeted therapy. Before the intervention, she was reading at an early stage (alphabetic level), writing in a transitional phase between syllabic and alphabetic systems, and had weak phonological processing skills. After six months of weekly therapy focused on phonological skills—like recognizing sounds, blending sounds, and improving memory—the child showed clear progress. Her phonological processing improved, her writing became more consistent and reached the alphabetic level, and her reading speed increased significantly—from about 20 to 94 words per minute. She also showed better ability to access words quickly in her mind. However, some writing problems remained, such as mixing up similar letters and making small spelling errors. The therapy helped her catch up in key areas, especially in reading and sound processing, even though she still faces some challenges typical of dyslexia. This case shows that with focused support, children with high abilities and dyslexia can make meaningful progress in learning to read and write."}
+{"row_index": 145, "doc_id": 59, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"We report the first case of heatstroke occurring at the same time as a severe SARS-CoV-2 infection in a 52-year-old man. He first tested positive for the virus after having a cold, then returned to work without fever. But while working outdoors in very hot weather (35°C) for five hours, he lost consciousness. When brought to the hospital, his body temperature was extremely high at 40°C, and he was in a coma. Doctors diagnosed him with heatstroke and a serious COVID-19 infection, which caused multiple organ damage. He received treatment including intravenous antibiotics, fluids, blood pressure support, mechanical ventilation, and care for his blood clotting problems. Despite initial improvement, he later developed shortness of breath and a brain bleed. He also had a multi-pathogen lung infection and a severe blood clotting disorder that led to failure of several organs (MODS), which ultimately caused his death. This case shows that heatstroke can happen alongside severe COVID-19, and it can lead to serious complications even in people with no known health problems.\"\n}", "generated_text": "We report the first case of heatstroke occurring at the same time as a severe SARS-CoV-2 infection in a 52-year-old man. He first tested positive for the virus after having a cold, then returned to work without fever. But while working outdoors in very hot weather (35°C) for five hours, he lost consciousness. When brought to the hospital, his body temperature was extremely high at 40°C, and he was in a coma. Doctors diagnosed him with heatstroke and a serious COVID-19 infection, which caused multiple organ damage. He received treatment including intravenous antibiotics, fluids, blood pressure support, mechanical ventilation, and care for his blood clotting problems. Despite initial improvement, he later developed shortness of breath and a brain bleed. He also had a multi-pathogen lung infection and a severe blood clotting disorder that led to failure of several organs (MODS), which ultimately caused his death. This case shows that heatstroke can happen alongside severe COVID-19, and it can lead to serious complications even in people with no known health problems."}
+{"row_index": 146, "doc_id": 60, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 19-year-old woman was admitted to the hospital with severe headaches, nausea, vomiting, fever, and very high blood pressure. She had a large adrenal mass found on imaging, and initial tests suggested possible infection or heart inflammation. Her blood pressure was extremely high (189/120 mmHg), and her heart rate was fast, leading to concerns about heart damage. She had a history of similar symptoms a year earlier, when she was diagnosed with myocarditis and hypertension, but she did not follow up on her blood pressure treatment. Her father had a history of sudden death, which raised concerns about a genetic condition.\\n\\nTests showed very high levels of certain hormones, including catecholamines, which are produced by the adrenal glands. These findings pointed to a condition called pheochromocytoma — a tumor of the adrenal gland that can cause high blood pressure and other symptoms. Genetic testing revealed a mutation in the RET gene, linked to a condition called MEN2A, which can cause tumors in multiple endocrine glands.\\n\\nFurther testing found a small thyroid nodule with slightly elevated calcitonin levels, but normal parathyroid hormone and calcium levels. After surgery to remove the adrenal tumor, the patient remained stable. Over the next 15 months, her thyroid nodule stayed the same size, and her calcitonin levels remained mildly high. However, her parathyroid hormone and blood calcium levels slowly increased. A scan for parathyroid tumors came back negative, meaning no parathyroid tumor was found.\\n\\nThe patient is now doing well after surgery and is being followed up regularly without any signs of recurrence.\"\n}", "generated_text": "A 19-year-old woman was admitted to the hospital with severe headaches, nausea, vomiting, fever, and very high blood pressure. She had a large adrenal mass found on imaging, and initial tests suggested possible infection or heart inflammation. Her blood pressure was extremely high (189/120 mmHg), and her heart rate was fast, leading to concerns about heart damage. She had a history of similar symptoms a year earlier, when she was diagnosed with myocarditis and hypertension, but she did not follow up on her blood pressure treatment. Her father had a history of sudden death, which raised concerns about a genetic condition.\n\nTests showed very high levels of certain hormones, including catecholamines, which are produced by the adrenal glands. These findings pointed to a condition called pheochromocytoma — a tumor of the adrenal gland that can cause high blood pressure and other symptoms. Genetic testing revealed a mutation in the RET gene, linked to a condition called MEN2A, which can cause tumors in multiple endocrine glands.\n\nFurther testing found a small thyroid nodule with slightly elevated calcitonin levels, but normal parathyroid hormone and calcium levels. After surgery to remove the adrenal tumor, the patient remained stable. Over the next 15 months, her thyroid nodule stayed the same size, and her calcitonin levels remained mildly high. However, her parathyroid hormone and blood calcium levels slowly increased. A scan for parathyroid tumors came back negative, meaning no parathyroid tumor was found.\n\nThe patient is now doing well after surgery and is being followed up regularly without any signs of recurrence."}
+{"row_index": 147, "doc_id": 62, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 13-year-old boy came to the emergency department with sudden chest pain on the sides of his chest, which worsened when he coughed. The pain was not severe, and he didn’t have shortness of breath, fever, or other symptoms like joint pain or fatigue. He had a mild cold and a single fever spike, but otherwise felt fine. He was active, doing canoeing twice a week, and had no known exposure to infections or environmental irritants. His past chest X-ray, taken four years earlier during a cold, showed a similar lung pattern that was treated with azithromycin and has not returned since.\\n\\nAt the hospital, his breathing was normal, oxygen levels were good, and his physical exam showed reduced breath sounds in the lower part of his lungs. A new chest X-ray showed a similar lung pattern as before. A detailed lung scan (CT) found widespread, cloudy areas in both lungs, covering more than 65% of the lung tissue, which is typical of a condition called pulmonary alveolar proteinosis (PAP). Tests for viruses, including COVID-19, came back negative. A lung fluid sample (bronchoalveolar lavage) showed a milky appearance and tested positive for a specific stain (periodic acid-Schiff), which supports the diagnosis of PAP. Lung function tests showed a mild restriction in how much air he could breathe out (FVC at 77%) and a moderate drop in lung capacity to transfer oxygen (DLCO at 48.6%).\\n\\nGenetic testing ruled out known causes of PAP related to surfactant problems. Testing for antibodies against a protein called GM-CSF was strongly positive, which suggests the body is attacking its own lung cells — pointing to an autoimmune form of PAP. At 20 months of follow-up, the boy is still symptom-free, breathing normally, and continues to exercise regularly. His lung function has improved slightly and remains stable. Since he has no symptoms and is doing well, treatment has been delayed, and he is being monitored regularly at the clinic.\"\n}", "generated_text": "A 13-year-old boy came to the emergency department with sudden chest pain on the sides of his chest, which worsened when he coughed. The pain was not severe, and he didn’t have shortness of breath, fever, or other symptoms like joint pain or fatigue. He had a mild cold and a single fever spike, but otherwise felt fine. He was active, doing canoeing twice a week, and had no known exposure to infections or environmental irritants. His past chest X-ray, taken four years earlier during a cold, showed a similar lung pattern that was treated with azithromycin and has not returned since.\n\nAt the hospital, his breathing was normal, oxygen levels were good, and his physical exam showed reduced breath sounds in the lower part of his lungs. A new chest X-ray showed a similar lung pattern as before. A detailed lung scan (CT) found widespread, cloudy areas in both lungs, covering more than 65% of the lung tissue, which is typical of a condition called pulmonary alveolar proteinosis (PAP). Tests for viruses, including COVID-19, came back negative. A lung fluid sample (bronchoalveolar lavage) showed a milky appearance and tested positive for a specific stain (periodic acid-Schiff), which supports the diagnosis of PAP. Lung function tests showed a mild restriction in how much air he could breathe out (FVC at 77%) and a moderate drop in lung capacity to transfer oxygen (DLCO at 48.6%).\n\nGenetic testing ruled out known causes of PAP related to surfactant problems. Testing for antibodies against a protein called GM-CSF was strongly positive, which suggests the body is attacking its own lung cells — pointing to an autoimmune form of PAP. At 20 months of follow-up, the boy is still symptom-free, breathing normally, and continues to exercise regularly. His lung function has improved slightly and remains stable. Since he has no symptoms and is doing well, treatment has been delayed, and he is being monitored regularly at the clinic."}
+{"row_index": 148, "doc_id": 66, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 17-year-old boy was found to have a small metal object in his nose during a routine dental exam. He had no symptoms like nosebleeds, congestion, or discomfort. His parents remembered when he was seven that he had inserted a small object into his nose, but at that time, no imaging was done and the issue was never followed up. Over the years, they thought the object had fallen out on its own. Later, imaging showed a shiny, metallic snap button stuck in the floor of his right nasal cavity, likely there for over 10 years. The object was covered in mucus and crust, showing signs of long-term exposure. It was safely removed under local anesthesia with a simple procedure that caused little bleeding. After removal, the nose healed well, and the patient is doing fine now. He’s being given nasal rinses to keep the area clean and is doing well at his follow-up visit.\"\n}", "generated_text": "A 17-year-old boy was found to have a small metal object in his nose during a routine dental exam. He had no symptoms like nosebleeds, congestion, or discomfort. His parents remembered when he was seven that he had inserted a small object into his nose, but at that time, no imaging was done and the issue was never followed up. Over the years, they thought the object had fallen out on its own. Later, imaging showed a shiny, metallic snap button stuck in the floor of his right nasal cavity, likely there for over 10 years. The object was covered in mucus and crust, showing signs of long-term exposure. It was safely removed under local anesthesia with a simple procedure that caused little bleeding. After removal, the nose healed well, and the patient is doing fine now. He’s being given nasal rinses to keep the area clean and is doing well at his follow-up visit."}
+{"row_index": 149, "doc_id": 66, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 17-year-old male with no significant past medical or family history was referred to the clinic from the dental department following an incidental discovery of a nasal foreign body (NFB) during preoperative orthodontic planning, which included routine dental x-rays and cone beam computed tomography (CBCT) without contrast. The patient was asymptomatic and denied any history of nasal obstruction, rhinorrhea, epistaxis, foul odor, hyposmia, halitosis, facial pain, discomfort, or sleep disturbances. Parental recall indicated that at age seven, the patient had inserted a small object into his nose; at that time, no imaging was performed, and an anterior rhinoscopy was attempted due to non-cooperative behavior, leading the physician to recommend removal under sedation. However, the family did not pursue follow-up, and given the absence of symptoms, they assumed the foreign body had spontaneously expelled. Endoscopic evaluation of the right nasal cavity revealed a deviated nasal septum with inferior turbinate hypertrophy, erythematous and mildly edematous mucosa, and a foreign body lodged and adherent to the floor of the nasal cavity beneath the inferior turbinate. The object was partially obscured by mucus and crusted material, exhibiting a shiny surface consistent with metallic composition. Radiographic assessment using lateral and frontal x-rays demonstrated a circular, radiopaque lesion located in the floor of the right nasal cavity, morphologically consistent with a metallic snap button. No abnormalities in adjacent bony structures were observed. CBCT further confirmed the presence of the foreign body and revealed mild inflammatory changes within the nasal mucosa, with no evidence of significant bony erosion, sinus involvement, or spread to adjacent anatomic spaces. With informed parental consent, the foreign body was removed under local anesthesia in a semi-sitting position to minimize the risk of dislodgment into the airway. Prior to retrieval, the nasal cavity was decongested with Xylometazoline 0.1%, and Lidocaine spray (10 mg/spray) was administered to the right nostril. A hook was used to disengage the object, which was then extracted using bayonet forceps. The procedure was uncomplicated, with minimal bleeding effectively controlled by saline irrigation. Post-removal examination showed no significant mucosal injury or tissue necrosis. The retrieved object, identified as a metallic snap button measuring 1 cm in diameter, demonstrated extensive corrosion and accumulation of biological material, consistent with prolonged retention over a period exceeding ten years. The patient was discharged in stable condition and prescribed daily nasal rinses with 0.9% sodium chloride irrigation solution. At a two-week follow-up, the patient was clinically stable with no signs of recurrence, inflammation, or obstruction, and endoscopic examination remained unremarkable. This case underscores the potential for long-term retention of small metallic foreign bodies in the nasal cavity, particularly in children, with delayed presentation due to asymptomatic course, highlighting the importance of thorough imaging evaluation and timely intervention when such objects are incidentally detected, even in the absence of clinical symptoms. The presence of corrosion and biofilm formation suggests prolonged exposure, which may contribute to chronic local inflammation and tissue remodeling, although no structural damage was observed in this case.\"\n}", "generated_text": "A 17-year-old male with no significant past medical or family history was referred to the clinic from the dental department following an incidental discovery of a nasal foreign body (NFB) during preoperative orthodontic planning, which included routine dental x-rays and cone beam computed tomography (CBCT) without contrast. The patient was asymptomatic and denied any history of nasal obstruction, rhinorrhea, epistaxis, foul odor, hyposmia, halitosis, facial pain, discomfort, or sleep disturbances. Parental recall indicated that at age seven, the patient had inserted a small object into his nose; at that time, no imaging was performed, and an anterior rhinoscopy was attempted due to non-cooperative behavior, leading the physician to recommend removal under sedation. However, the family did not pursue follow-up, and given the absence of symptoms, they assumed the foreign body had spontaneously expelled. Endoscopic evaluation of the right nasal cavity revealed a deviated nasal septum with inferior turbinate hypertrophy, erythematous and mildly edematous mucosa, and a foreign body lodged and adherent to the floor of the nasal cavity beneath the inferior turbinate. The object was partially obscured by mucus and crusted material, exhibiting a shiny surface consistent with metallic composition. Radiographic assessment using lateral and frontal x-rays demonstrated a circular, radiopaque lesion located in the floor of the right nasal cavity, morphologically consistent with a metallic snap button. No abnormalities in adjacent bony structures were observed. CBCT further confirmed the presence of the foreign body and revealed mild inflammatory changes within the nasal mucosa, with no evidence of significant bony erosion, sinus involvement, or spread to adjacent anatomic spaces. With informed parental consent, the foreign body was removed under local anesthesia in a semi-sitting position to minimize the risk of dislodgment into the airway. Prior to retrieval, the nasal cavity was decongested with Xylometazoline 0.1%, and Lidocaine spray (10 mg/spray) was administered to the right nostril. A hook was used to disengage the object, which was then extracted using bayonet forceps. The procedure was uncomplicated, with minimal bleeding effectively controlled by saline irrigation. Post-removal examination showed no significant mucosal injury or tissue necrosis. The retrieved object, identified as a metallic snap button measuring 1 cm in diameter, demonstrated extensive corrosion and accumulation of biological material, consistent with prolonged retention over a period exceeding ten years. The patient was discharged in stable condition and prescribed daily nasal rinses with 0.9% sodium chloride irrigation solution. At a two-week follow-up, the patient was clinically stable with no signs of recurrence, inflammation, or obstruction, and endoscopic examination remained unremarkable. This case underscores the potential for long-term retention of small metallic foreign bodies in the nasal cavity, particularly in children, with delayed presentation due to asymptomatic course, highlighting the importance of thorough imaging evaluation and timely intervention when such objects are incidentally detected, even in the absence of clinical symptoms. The presence of corrosion and biofilm formation suggests prolonged exposure, which may contribute to chronic local inflammation and tissue remodeling, although no structural damage was observed in this case."}
+{"row_index": 150, "doc_id": 67, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 18-year-old boy came to the emergency room with sudden chest pain, fever, and trouble breathing, especially when lying down. He had no history of heart problems, but his family had a heart condition in the past. Tests showed his heart was enlarged, his heart muscles were thick, and there was fluid around the heart. Doctors thought it was a virus called Coxsackie, which can cause heart and chest lining inflammation. He got medicine for that, but his breathing got worse and his blood pressure dropped. The fluid around the heart grew so big it was pressing on his heart, causing a life-threatening situation. They drained the fluid, but during that, he had a sudden stop in his heart rhythm and needed a machine to keep his heart and lungs working. Tests on his heart tissue showed no virus or inflammation, but a small lump on his arm was found to have a rare cancer called Epstein-Barr virus (EBV) positive natural killer/T-cell lymphoma. This cancer was likely causing the heart and heart lining problems. After starting cancer treatment, his heart function improved — the thick heart muscles got thinner, the fluid went away, and his breathing got better. He’s now on heart failure medicine and is doing well, with plans to finish chemotherapy and possibly get radiation or a stem cell transplant in the future.\"\n}", "generated_text": "A 18-year-old boy came to the emergency room with sudden chest pain, fever, and trouble breathing, especially when lying down. He had no history of heart problems, but his family had a heart condition in the past. Tests showed his heart was enlarged, his heart muscles were thick, and there was fluid around the heart. Doctors thought it was a virus called Coxsackie, which can cause heart and chest lining inflammation. He got medicine for that, but his breathing got worse and his blood pressure dropped. The fluid around the heart grew so big it was pressing on his heart, causing a life-threatening situation. They drained the fluid, but during that, he had a sudden stop in his heart rhythm and needed a machine to keep his heart and lungs working. Tests on his heart tissue showed no virus or inflammation, but a small lump on his arm was found to have a rare cancer called Epstein-Barr virus (EBV) positive natural killer/T-cell lymphoma. This cancer was likely causing the heart and heart lining problems. After starting cancer treatment, his heart function improved — the thick heart muscles got thinner, the fluid went away, and his breathing got better. He’s now on heart failure medicine and is doing well, with plans to finish chemotherapy and possibly get radiation or a stem cell transplant in the future."}
+{"row_index": 151, "doc_id": 67, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"An 18-year-old male came to the emergency department with new chest pain, fever, and shortness of breath, especially when lying down. He had a dry cough and felt unwell for 3 to 4 days. His family history included a grandfather with heart disease, but he had no known heart problems himself. He worked at a car parts shop and planned to go to college.\\n\\nInitial tests showed high levels of a heart damage marker (troponin), widespread changes on his ECG, and an enlarged heart on X-ray. An echo test (TTE) revealed thickened heart muscle (severe biventricular concentric hypertrophy) and a small amount of fluid around the heart (pericardial effusion). Viral tests found high levels of Coxsackie virus A and B, which can cause viral pericarditis. His symptoms improved slightly with medications like ibuprofen and colchicine, and a heart catheterization showed no blocked arteries.\\n\\nHowever, by the fourth day, his condition worsened. He became very weak, had very low blood pressure, and developed a large pericardial effusion that was threatening to stop his heart (cardiac tamponade). A needle was inserted to remove the fluid (pericardiocentesis), but during the procedure, he went into cardiac arrest with no pulse. He needed emergency life support with a machine that takes over heart and lung functions (VA ECMO), and received blood transfusions due to bleeding.\\n\\nA biopsy of his heart tissue showed no signs of inflammation or infection, which made the initial diagnosis of viral pericarditis less likely. A skin biopsy from a small, painless lump on his right arm revealed a rare type of cancer called Epstein-Barr virus (EBV)-positive natural killer/T-cell lymphoma. This finding changed the diagnosis — the heart and pericardium were likely affected by this cancer, not just a virus.\\n\\nHe started chemotherapy for the lymphoma, and within days, his heart function began to improve. His heart pump strength (ejection fraction) increased from 10%–15% to 55%, the fluid around the heart went away, and the thickened heart muscle started to normalize. He is now on heart failure treatment and cardiac rehab.\\n\\nHe has completed five out of six chemotherapy sessions and is expected to finish the full course. He may now receive radiation therapy or a stem cell transplant. His care involves both cardiology and oncology teams, and he is doing much better overall.\"\n}", "generated_text": "An 18-year-old male came to the emergency department with new chest pain, fever, and shortness of breath, especially when lying down. He had a dry cough and felt unwell for 3 to 4 days. His family history included a grandfather with heart disease, but he had no known heart problems himself. He worked at a car parts shop and planned to go to college.\n\nInitial tests showed high levels of a heart damage marker (troponin), widespread changes on his ECG, and an enlarged heart on X-ray. An echo test (TTE) revealed thickened heart muscle (severe biventricular concentric hypertrophy) and a small amount of fluid around the heart (pericardial effusion). Viral tests found high levels of Coxsackie virus A and B, which can cause viral pericarditis. His symptoms improved slightly with medications like ibuprofen and colchicine, and a heart catheterization showed no blocked arteries.\n\nHowever, by the fourth day, his condition worsened. He became very weak, had very low blood pressure, and developed a large pericardial effusion that was threatening to stop his heart (cardiac tamponade). A needle was inserted to remove the fluid (pericardiocentesis), but during the procedure, he went into cardiac arrest with no pulse. He needed emergency life support with a machine that takes over heart and lung functions (VA ECMO), and received blood transfusions due to bleeding.\n\nA biopsy of his heart tissue showed no signs of inflammation or infection, which made the initial diagnosis of viral pericarditis less likely. A skin biopsy from a small, painless lump on his right arm revealed a rare type of cancer called Epstein-Barr virus (EBV)-positive natural killer/T-cell lymphoma. This finding changed the diagnosis — the heart and pericardium were likely affected by this cancer, not just a virus.\n\nHe started chemotherapy for the lymphoma, and within days, his heart function began to improve. His heart pump strength (ejection fraction) increased from 10%–15% to 55%, the fluid around the heart went away, and the thickened heart muscle started to normalize. He is now on heart failure treatment and cardiac rehab.\n\nHe has completed five out of six chemotherapy sessions and is expected to finish the full course. He may now receive radiation therapy or a stem cell transplant. His care involves both cardiology and oncology teams, and he is doing much better overall."}
+{"row_index": 152, "doc_id": 72, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A woman had a weak heart after giving birth and got a new heart transplant. After the transplant, her kidneys were working fine at first. But later, her kidneys started to fail because of a virus called BK virus. The doctors found the virus in her blood and saw damage in her kidney tissue. They cut back on the medicines that weaken the immune system, which helped. After two years, her kidneys stayed stable, with a kidney function level that is still okay, even though her kidney numbers are low.\"\n}", "generated_text": "A woman had a weak heart after giving birth and got a new heart transplant. After the transplant, her kidneys were working fine at first. But later, her kidneys started to fail because of a virus called BK virus. The doctors found the virus in her blood and saw damage in her kidney tissue. They cut back on the medicines that weaken the immune system, which helped. After two years, her kidneys stayed stable, with a kidney function level that is still okay, even though her kidney numbers are low."}
+{"row_index": 153, "doc_id": 72, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 39-year-old woman had a heart transplant due to peripartum cardiomyopathy. After the transplant, her kidneys initially worked well, with normal kidney function and no signs of kidney disease. However, in 2016, her kidney function started to decline, and by 2017, her creatinine had risen to 2.69 mg/dL, with a GFR of 21.4 mL/min/1.73m2. She was hospitalized, and tests showed no signs of infection or other common causes of kidney problems. A kidney biopsy was done and found to have active chronic tubulointerstitial nephritis linked to late-stage BK virus infection. The blood test showed a high BK virus load (log 4.5). Her immunosuppressive medications, especially tacrolimus, were reduced. After two years of follow-up, her kidney function stabilized at a serum creatinine of 2.5 mg/dL and a GFR of 23.4 mL/min/1.73m2. The virus load gradually decreased to undetectable levels, and she has had no further kidney issues or heart rejection episodes.\"\n}", "generated_text": "A 39-year-old woman had a heart transplant due to peripartum cardiomyopathy. After the transplant, her kidneys initially worked well, with normal kidney function and no signs of kidney disease. However, in 2016, her kidney function started to decline, and by 2017, her creatinine had risen to 2.69 mg/dL, with a GFR of 21.4 mL/min/1.73m2. She was hospitalized, and tests showed no signs of infection or other common causes of kidney problems. A kidney biopsy was done and found to have active chronic tubulointerstitial nephritis linked to late-stage BK virus infection. The blood test showed a high BK virus load (log 4.5). Her immunosuppressive medications, especially tacrolimus, were reduced. After two years of follow-up, her kidney function stabilized at a serum creatinine of 2.5 mg/dL and a GFR of 23.4 mL/min/1.73m2. The virus load gradually decreased to undetectable levels, and she has had no further kidney issues or heart rejection episodes."}
+{"row_index": 154, "doc_id": 74, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 56-year-old Italian woman with a serious blood disorder called β-thalassemia major had a magnetic resonance imaging (MRI) scan to check how much iron was building up in her heart, liver, and pancreas. She has been needing regular blood transfusions since she was 7 years old and had previously had her spleen and gallbladder removed. At the time of the scan, she had no major problems with her heart, liver, or hormones, and was taking medications including deferasirox to remove iron, vitamin D, and luspatercept to help reduce her need for transfusions.\\n\\nThe MRI found a mass in the mediastinum (the area in the chest between the lungs), which had been seen before in a 2020 scan but had slightly grown. This mass showed only mild activity on a PET scan, which made doctors think it might be a type of thymoma — a tumor that develops in the thymus gland. However, a chest CT scan revealed multiple thin-walled cysts in both lungs, which are a sign of a condition called lymphangioleiomyomatosis (LAM), a rare lung disease often linked to certain conditions like thalassemia.\\n\\nThe patient had no symptoms like coughing or shortness of breath and was not a smoker. After a team of specialists reviewed her case, she had surgery to remove the thymoma mass and a small piece of lung tissue affected by LAM. The surgery results showed a type B2 thymoma with some cells at the edge of the removed tissue, meaning it wasn’t completely removed. The lung tissue showed signs of LAM, with cysts lined by specific cells and mild inflammation.\\n\\nFollowing surgery, she was recommended to receive adjuvant radiation therapy for the thymoma and to take sirolimus, a medication that helps control LAM, especially in people with thalassemia. This treatment plan is designed to manage both conditions and reduce the risk of future complications.\"\n}", "generated_text": "A 56-year-old Italian woman with a serious blood disorder called β-thalassemia major had a magnetic resonance imaging (MRI) scan to check how much iron was building up in her heart, liver, and pancreas. She has been needing regular blood transfusions since she was 7 years old and had previously had her spleen and gallbladder removed. At the time of the scan, she had no major problems with her heart, liver, or hormones, and was taking medications including deferasirox to remove iron, vitamin D, and luspatercept to help reduce her need for transfusions.\n\nThe MRI found a mass in the mediastinum (the area in the chest between the lungs), which had been seen before in a 2020 scan but had slightly grown. This mass showed only mild activity on a PET scan, which made doctors think it might be a type of thymoma — a tumor that develops in the thymus gland. However, a chest CT scan revealed multiple thin-walled cysts in both lungs, which are a sign of a condition called lymphangioleiomyomatosis (LAM), a rare lung disease often linked to certain conditions like thalassemia.\n\nThe patient had no symptoms like coughing or shortness of breath and was not a smoker. After a team of specialists reviewed her case, she had surgery to remove the thymoma mass and a small piece of lung tissue affected by LAM. The surgery results showed a type B2 thymoma with some cells at the edge of the removed tissue, meaning it wasn’t completely removed. The lung tissue showed signs of LAM, with cysts lined by specific cells and mild inflammation.\n\nFollowing surgery, she was recommended to receive adjuvant radiation therapy for the thymoma and to take sirolimus, a medication that helps control LAM, especially in people with thalassemia. This treatment plan is designed to manage both conditions and reduce the risk of future complications."}
+{"row_index": 155, "doc_id": 75, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 49-year-old woman with long-term lupus (SLE) developed both kidney and heart failure over many years. She had lupus since childhood and was treated with several medications, including steroids and immunosuppressants, but stopped in 2002 due to hepatitis C. Over time, her kidneys failed, requiring dialysis, and her heart suffered damage, including heart attacks and weakened heart muscle. By 2007, her kidney function had worsened enough to need a biopsy, which showed active kidney disease. Despite treatments, her heart continued to fail, leading to serious heart problems like valve damage and a need for surgery in 2014. After surgery, her heart function remained poor, and she needed dialysis for 4 years before being ready for a kidney transplant.\\n\\nBefore the transplant, her heart was very weak—only 26% of its normal pumping ability—and she had high levels of a heart stress marker (BNP). Because of this, doctors added a heart-protective drug called Levosimendan to help her heart during surgery. The transplant was done with careful planning to protect her kidneys and heart, avoiding harmful medications and using fluid therapy to keep her stable. During recovery, her heart function slowly improved: by one month after surgery, her heart was pumping better (EF improved to 30%) and her exercise ability increased from very limited to normal. By five months, her heart function was much better, her BNP dropped to normal levels, and her kidneys were working properly again. The transplant was successful, and she is now recovering well.\"\n}", "generated_text": "A 49-year-old woman with long-term lupus (SLE) developed both kidney and heart failure over many years. She had lupus since childhood and was treated with several medications, including steroids and immunosuppressants, but stopped in 2002 due to hepatitis C. Over time, her kidneys failed, requiring dialysis, and her heart suffered damage, including heart attacks and weakened heart muscle. By 2007, her kidney function had worsened enough to need a biopsy, which showed active kidney disease. Despite treatments, her heart continued to fail, leading to serious heart problems like valve damage and a need for surgery in 2014. After surgery, her heart function remained poor, and she needed dialysis for 4 years before being ready for a kidney transplant.\n\nBefore the transplant, her heart was very weak—only 26% of its normal pumping ability—and she had high levels of a heart stress marker (BNP). Because of this, doctors added a heart-protective drug called Levosimendan to help her heart during surgery. The transplant was done with careful planning to protect her kidneys and heart, avoiding harmful medications and using fluid therapy to keep her stable. During recovery, her heart function slowly improved: by one month after surgery, her heart was pumping better (EF improved to 30%) and her exercise ability increased from very limited to normal. By five months, her heart function was much better, her BNP dropped to normal levels, and her kidneys were working properly again. The transplant was successful, and she is now recovering well."}
+{"row_index": 156, "doc_id": 76, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 42-year-old woman with a chronic headache condition could not use certain medications because of side effects. When her headaches were very severe — scoring 9 out of 10 — she came to the pain clinic. Doctors took her to a local operating room and performed a nerve block using ultrasound guidance. This procedure targeted the greater occipital nerve in the neck and used a local anesthetic called bupivacaine. Right after the block, her headache pain dropped from 9/10 to just 2/10. The block was repeated once a week for a month. By the end of two months, her headaches had greatly improved: the number of attacks dropped from daily to just two per month, and the pain intensity decreased to 4/10. She had no side effects from the treatment and hasn’t had any attacks by the sixth month.\"\n}", "generated_text": "A 42-year-old woman with a chronic headache condition could not use certain medications because of side effects. When her headaches were very severe — scoring 9 out of 10 — she came to the pain clinic. Doctors took her to a local operating room and performed a nerve block using ultrasound guidance. This procedure targeted the greater occipital nerve in the neck and used a local anesthetic called bupivacaine. Right after the block, her headache pain dropped from 9/10 to just 2/10. The block was repeated once a week for a month. By the end of two months, her headaches had greatly improved: the number of attacks dropped from daily to just two per month, and the pain intensity decreased to 4/10. She had no side effects from the treatment and hasn’t had any attacks by the sixth month."}
+{"row_index": 157, "doc_id": 78, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A baby was born early by C-section because the baby was not getting enough oxygen. The baby had a weak heart from birth and had serious problems with the heart valves, making it hard for blood to flow properly. The baby’s hands and feet were long and bent, the fingers couldn’t straighten, and the joints at elbows and knees were stuck. The face looked old, the eyes were deep-set and slanted, the ears were small and soft, and the mouth hung down. The baby also had a flat foot and a swollen belly. Tests showed the heart was too big, the blood pressure in the lungs was too high, and the lens in the eyes had moved out of place. A genetic test found a new change in a gene that causes a rare condition called neonatal MFS, which affects the body’s connective tissue. Doctors tried medicines to help the heart pump better, used sedation, and gave diuretics to reduce swelling, but the heart problems got worse. The baby’s breathing and heart function kept getting worse, and the body started to shut down. Even with treatment, the baby could not survive. The family chose to focus on comfort instead of surgery, and the baby passed away 32 days after birth.\"\n}", "generated_text": "A baby was born early by C-section because the baby was not getting enough oxygen. The baby had a weak heart from birth and had serious problems with the heart valves, making it hard for blood to flow properly. The baby’s hands and feet were long and bent, the fingers couldn’t straighten, and the joints at elbows and knees were stuck. The face looked old, the eyes were deep-set and slanted, the ears were small and soft, and the mouth hung down. The baby also had a flat foot and a swollen belly. Tests showed the heart was too big, the blood pressure in the lungs was too high, and the lens in the eyes had moved out of place. A genetic test found a new change in a gene that causes a rare condition called neonatal MFS, which affects the body’s connective tissue. Doctors tried medicines to help the heart pump better, used sedation, and gave diuretics to reduce swelling, but the heart problems got worse. The baby’s breathing and heart function kept getting worse, and the body started to shut down. Even with treatment, the baby could not survive. The family chose to focus on comfort instead of surgery, and the baby passed away 32 days after birth."}
+{"row_index": 158, "doc_id": 78, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A newborn boy was born early via emergency cesarean section because of fetal distress. He had several serious physical problems from birth, including long, thin fingers and toes (arachnodactyly), fingers that could not fully straighten (camptodactyly), stiff elbows and knees, a wrinkled, aged-looking face, flat feet, and a deep, downward-slanting eye opening. His ears were small and soft, and his mouth sagged. He also had a short head shape (brachycephaly) and a lens that was out of place in his eyes (ectopia lentis), which is a sign of a genetic condition called Marfan syndrome.\\n\\nGenetic testing found a new mutation in a gene called fibrillin-1, specifically in a section known as the neonatal region (exons 24 to 32). This mutation is linked to a severe form of Marfan syndrome that affects the heart and blood vessels.\\n\\nAt birth, the baby had a weak heart, severe heart valve problems (especially mitral and aortic regurgitation), and high blood pressure in the lungs (pulmonary hypertension). These issues led to low blood pressure, poor breathing, and heart failure. Doctors tried medications to help, including drugs to reduce the heart’s workload, sedation, and diuretics to manage fluid buildup. However, the heart problems continued to get worse.\\n\\nBecause the disease was progressing too quickly and surgery was not expected to help, the family chose to focus on palliative care — care aimed at making the child comfortable rather than trying to cure the condition. Over the next few months, the baby developed severe lung and liver problems, including bleeding in the lungs, and eventually died at 32 days old.\"\n}", "generated_text": "A newborn boy was born early via emergency cesarean section because of fetal distress. He had several serious physical problems from birth, including long, thin fingers and toes (arachnodactyly), fingers that could not fully straighten (camptodactyly), stiff elbows and knees, a wrinkled, aged-looking face, flat feet, and a deep, downward-slanting eye opening. His ears were small and soft, and his mouth sagged. He also had a short head shape (brachycephaly) and a lens that was out of place in his eyes (ectopia lentis), which is a sign of a genetic condition called Marfan syndrome.\n\nGenetic testing found a new mutation in a gene called fibrillin-1, specifically in a section known as the neonatal region (exons 24 to 32). This mutation is linked to a severe form of Marfan syndrome that affects the heart and blood vessels.\n\nAt birth, the baby had a weak heart, severe heart valve problems (especially mitral and aortic regurgitation), and high blood pressure in the lungs (pulmonary hypertension). These issues led to low blood pressure, poor breathing, and heart failure. Doctors tried medications to help, including drugs to reduce the heart’s workload, sedation, and diuretics to manage fluid buildup. However, the heart problems continued to get worse.\n\nBecause the disease was progressing too quickly and surgery was not expected to help, the family chose to focus on palliative care — care aimed at making the child comfortable rather than trying to cure the condition. Over the next few months, the baby developed severe lung and liver problems, including bleeding in the lungs, and eventually died at 32 days old."}
+{"row_index": 159, "doc_id": 0, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 20-year-old woman had a long history of nephrotic syndrome (NS) that started when she was 8 years old. Her condition was first noticed after she developed a blood clot in her brain veins and a large blood clot in her lungs. She didn’t have any lasting effects from this. Tests showed no family history of blood clots, and no other signs pointed to a secondary cause of her NS. She was treated with blood-thinning medication (anticoagulation) and steroid pills, which worked well. Over time, she had several relapses of her disease, each controlled with high-dose steroids. To reduce the need for steroids and support her growth, she started taking mycophenolate mofetil (MMF). Thrombophilia tests — which check for blood clotting disorders — came back normal. After nine years, her blood thinners were stopped. From 2017 onward, she stayed in remission and didn’t have any relapses. Her MMF was stopped in 2019, and she remained healthy without symptoms. One year later, she suddenly developed severe abdominal pain, vomiting after eating, and swelling in both legs. Lab tests confirmed a relapse of her nephrotic syndrome. An abdominal CT scan showed a blood clot in the superior mesenteric artery, causing acute mesenteric ischemia (lack of blood flow to the intestines). During surgery, doctors found widespread tissue death in her small intestine, and the damage was so severe that removing the affected parts was not possible. The patient died four days later.\"\n}", "generated_text": "A 20-year-old woman had a long history of nephrotic syndrome (NS) that started when she was 8 years old. Her condition was first noticed after she developed a blood clot in her brain veins and a large blood clot in her lungs. She didn’t have any lasting effects from this. Tests showed no family history of blood clots, and no other signs pointed to a secondary cause of her NS. She was treated with blood-thinning medication (anticoagulation) and steroid pills, which worked well. Over time, she had several relapses of her disease, each controlled with high-dose steroids. To reduce the need for steroids and support her growth, she started taking mycophenolate mofetil (MMF). Thrombophilia tests — which check for blood clotting disorders — came back normal. After nine years, her blood thinners were stopped. From 2017 onward, she stayed in remission and didn’t have any relapses. Her MMF was stopped in 2019, and she remained healthy without symptoms. One year later, she suddenly developed severe abdominal pain, vomiting after eating, and swelling in both legs. Lab tests confirmed a relapse of her nephrotic syndrome. An abdominal CT scan showed a blood clot in the superior mesenteric artery, causing acute mesenteric ischemia (lack of blood flow to the intestines). During surgery, doctors found widespread tissue death in her small intestine, and the damage was so severe that removing the affected parts was not possible. The patient died four days later."}
+{"row_index": 160, "doc_id": 0, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 20-year-old girl had a kidney disease called nephrotic syndrome since she was 8 years old. It started with blood clots in her brain and lungs, but she got better. She was treated with medicine to stop clots and steroids to calm her kidneys. Over time, she had several flare-ups that were controlled with steroids, but after 2017, her kidneys stayed healthy and no more flares happened. So, her doctors stopped the clot medicine and the kidney medicine (MMF). One year later, she got sudden, severe stomach pain, threw up after eating, and her legs swelled. Tests showed her kidney disease came back. A scan found a blood clot in a major blood vessel in her abdomen, cutting off blood to part of her intestines. When doctors opened her belly, they saw that most of her small intestine was dead and could not be saved. She died two days later.\"\n}", "generated_text": "A 20-year-old girl had a kidney disease called nephrotic syndrome since she was 8 years old. It started with blood clots in her brain and lungs, but she got better. She was treated with medicine to stop clots and steroids to calm her kidneys. Over time, she had several flare-ups that were controlled with steroids, but after 2017, her kidneys stayed healthy and no more flares happened. So, her doctors stopped the clot medicine and the kidney medicine (MMF). One year later, she got sudden, severe stomach pain, threw up after eating, and her legs swelled. Tests showed her kidney disease came back. A scan found a blood clot in a major blood vessel in her abdomen, cutting off blood to part of her intestines. When doctors opened her belly, they saw that most of her small intestine was dead and could not be saved. She died two days later."}
+{"row_index": 161, "doc_id": 0, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 20-year-old female with a 12-year history of idiopathic nephrotic syndrome (NS) presented with a clinical course initiated at age eight, marked by cerebral venous thrombosis extending to the right jugular vein and a massive pulmonary embolism, which resolved without sequelae. No history of medical comorbidities, surgical interventions, or family history of thrombotic events was reported. Initial evaluation excluded secondary causes of nephrotic syndrome, as she lacked gross hematuria, hypertension, or renal biopsy findings, and no extra-renal manifestations were present. Consequently, she was initiated on anticoagulation therapy with oral vitamin K antagonist and oral corticosteroids, which resulted in stable disease control. Subsequent relapses of NS were managed with high-dose corticosteroid pulses, leading to long-term maintenance therapy with mycophenolate mofetil (MMF) to reduce corticosteroid dependence and support normal growth and development. A comprehensive thrombophilia workup—including homocysteine, fibrinogen, protein C, protein S, antithrombin III, factor V Leiden mutation, JAK-2 mutation, cryoglobulins, anticardiolipin antibodies, lupus anticoagulant, and beta-1-glycoprotein antibodies—was performed and all results were within normal limits, ruling out inherited or acquired thrombophilic predispositions. Anticoagulant therapy was discontinued after nine years of use. The patient experienced multiple relapses of NS, all of which were controlled with oral corticosteroids, achieving sustained remission by 2017. MMF was gradually tapered and discontinued in 2019, with no further relapses or clinical symptoms observed thereafter.\\n\\nOne year after the last remission, the patient presented to the emergency department with severe, diffuse acute abdominal pain, non-radiating, associated with postprandial vomiting and bilateral lower limb edema lasting six hours. Physical examination revealed intense epigastric tenderness, with normal vital signs (blood pressure 120/70 mm Hg, heart rate 83 bpm, oxygen saturation 100% on room air), afebrile status, and intact consciousness. No other systemic abnormalities were identified. Urinalysis using labstix demonstrated proteinuria. Arterial blood gas analysis revealed metabolic acidosis with respiratory compensation. Laboratory findings included hypoalbuminemia, hypercholesterolemia, a prolonged prothrombin time (90%), markedly elevated D-dimer, lactate dehydrogenase, and creatine phosphokinase, and a systemic inflammatory response characterized by a C-reactive protein (CRP) level of 37 mg/L and leukocytosis (26.4 × 10³/µL). Renal and hepatic function tests remained within normal ranges.\\n\\nThe patient was admitted to the intensive care unit for close hemodynamic and metabolic monitoring. An urgent abdominal ultrasound revealed a low-to-moderate volume intra-abdominal effusion. Abdominal computed tomography (CT) demonstrated acute thrombosis of the superior mesenteric artery with concomitant acute mesenteric ischemia. Immediate surgical intervention was performed. Intraoperative exploration confirmed extensive mesenteric ischemia with nearly complete necrosis of the small intestine, rendering resection of the bowel segments non-viable and incompatible with survival. The patient succumbed to multi-organ failure within 48 hours of presentation. This case highlights the potential for severe, life-threatening complications in patients with long-standing idiopathic nephrotic syndrome, particularly in the context of underlying hypercoagulable states or unrecognized vascular vulnerability, even in the absence of thrombophilia. The pathophysiological link between chronic immune dysregulation in NS and a pro-thrombotic milieu—potentially mediated by persistent inflammation, endothelial dysfunction, and increased expression of tissue factor—may contribute to the development of acute arterial thrombosis in critical vascular territories such as the superior mesenteric artery, leading to ischemic bowel necrosis and death.\"\n}", "generated_text": "A 20-year-old female with a 12-year history of idiopathic nephrotic syndrome (NS) presented with a clinical course initiated at age eight, marked by cerebral venous thrombosis extending to the right jugular vein and a massive pulmonary embolism, which resolved without sequelae. No history of medical comorbidities, surgical interventions, or family history of thrombotic events was reported. Initial evaluation excluded secondary causes of nephrotic syndrome, as she lacked gross hematuria, hypertension, or renal biopsy findings, and no extra-renal manifestations were present. Consequently, she was initiated on anticoagulation therapy with oral vitamin K antagonist and oral corticosteroids, which resulted in stable disease control. Subsequent relapses of NS were managed with high-dose corticosteroid pulses, leading to long-term maintenance therapy with mycophenolate mofetil (MMF) to reduce corticosteroid dependence and support normal growth and development. A comprehensive thrombophilia workup—including homocysteine, fibrinogen, protein C, protein S, antithrombin III, factor V Leiden mutation, JAK-2 mutation, cryoglobulins, anticardiolipin antibodies, lupus anticoagulant, and beta-1-glycoprotein antibodies—was performed and all results were within normal limits, ruling out inherited or acquired thrombophilic predispositions. Anticoagulant therapy was discontinued after nine years of use. The patient experienced multiple relapses of NS, all of which were controlled with oral corticosteroids, achieving sustained remission by 2017. MMF was gradually tapered and discontinued in 2019, with no further relapses or clinical symptoms observed thereafter.\n\nOne year after the last remission, the patient presented to the emergency department with severe, diffuse acute abdominal pain, non-radiating, associated with postprandial vomiting and bilateral lower limb edema lasting six hours. Physical examination revealed intense epigastric tenderness, with normal vital signs (blood pressure 120/70 mm Hg, heart rate 83 bpm, oxygen saturation 100% on room air), afebrile status, and intact consciousness. No other systemic abnormalities were identified. Urinalysis using labstix demonstrated proteinuria. Arterial blood gas analysis revealed metabolic acidosis with respiratory compensation. Laboratory findings included hypoalbuminemia, hypercholesterolemia, a prolonged prothrombin time (90%), markedly elevated D-dimer, lactate dehydrogenase, and creatine phosphokinase, and a systemic inflammatory response characterized by a C-reactive protein (CRP) level of 37 mg/L and leukocytosis (26.4 × 10³/µL). Renal and hepatic function tests remained within normal ranges.\n\nThe patient was admitted to the intensive care unit for close hemodynamic and metabolic monitoring. An urgent abdominal ultrasound revealed a low-to-moderate volume intra-abdominal effusion. Abdominal computed tomography (CT) demonstrated acute thrombosis of the superior mesenteric artery with concomitant acute mesenteric ischemia. Immediate surgical intervention was performed. Intraoperative exploration confirmed extensive mesenteric ischemia with nearly complete necrosis of the small intestine, rendering resection of the bowel segments non-viable and incompatible with survival. The patient succumbed to multi-organ failure within 48 hours of presentation. This case highlights the potential for severe, life-threatening complications in patients with long-standing idiopathic nephrotic syndrome, particularly in the context of underlying hypercoagulable states or unrecognized vascular vulnerability, even in the absence of thrombophilia. The pathophysiological link between chronic immune dysregulation in NS and a pro-thrombotic milieu—potentially mediated by persistent inflammation, endothelial dysfunction, and increased expression of tissue factor—may contribute to the development of acute arterial thrombosis in critical vascular territories such as the superior mesenteric artery, leading to ischemic bowel necrosis and death."}
+{"row_index": 162, "doc_id": 1, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 34-year-old pregnant woman had seizures and trouble speaking, which went away in less than two hours. She had no other health problems. Doctors did an MRI of her brain and saw a special pattern called the 'Medusa head' sign. This means there’s a problem with how veins develop in the brain, with some blood clots at the edges and slow blood flow near the center. The brain tissue around the veins is swollen, which causes the symptoms. She started taking medicine to prevent more seizures and clots, and her symptoms got better in a week.\"\n}", "generated_text": "A 34-year-old pregnant woman had seizures and trouble speaking, which went away in less than two hours. She had no other health problems. Doctors did an MRI of her brain and saw a special pattern called the 'Medusa head' sign. This means there’s a problem with how veins develop in the brain, with some blood clots at the edges and slow blood flow near the center. The brain tissue around the veins is swollen, which causes the symptoms. She started taking medicine to prevent more seizures and clots, and her symptoms got better in a week."}
+{"row_index": 163, "doc_id": 2, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 22-year-old woman visited the Oral Medicine Department with painful mouth sores that had been bothering her for one month. The sores started with a fever and appeared as small, pimple-like bumps on her lips. She had been using pod-type vapes for about a year, mostly during free time or with friends, and had recently switched to a new e-liquid flavor without telling anyone. She had never smoked cigarettes before and had no history of taking medications or having allergies. She also didn’t eat healthy foods regularly, often skipping vegetables and fruits. \\n\\nOn examination, her lips had crusts that looked like a mix of blood and fluid, and the corner of her mouth was sore and easily bled. Inside her mouth, she had white ulcers with yellow edges, of different sizes, on the lips, tongue, and floor of her mouth. There were no signs of illness on her body outside the mouth. Lab tests showed no evidence of a common virus (HSV-1) linked to these sores, which helped doctors rule out other causes.\\n\\nThe diagnosis was oral erythema multiforme, a condition that can be triggered by vaping, and it was classified as mild. Treatment included applying a saltwater solution (0.9% NaCl) to her lips three times a day, using a mouthwash with dexamethasone and hyaluronic acid three times a day (after waiting 30 minutes before eating or drinking), applying a 2% miconazole cream to the sore corner of her mouth twice daily, and using vaseline album cream for dry lips. She was also advised to stop vaping and avoid foods with MSG. \\n\\nAfter one week of treatment, her mouth sores improved significantly. The case was reviewed with her consent, and it followed ethical medical guidelines.\"\n}", "generated_text": "A 22-year-old woman visited the Oral Medicine Department with painful mouth sores that had been bothering her for one month. The sores started with a fever and appeared as small, pimple-like bumps on her lips. She had been using pod-type vapes for about a year, mostly during free time or with friends, and had recently switched to a new e-liquid flavor without telling anyone. She had never smoked cigarettes before and had no history of taking medications or having allergies. She also didn’t eat healthy foods regularly, often skipping vegetables and fruits. \n\nOn examination, her lips had crusts that looked like a mix of blood and fluid, and the corner of her mouth was sore and easily bled. Inside her mouth, she had white ulcers with yellow edges, of different sizes, on the lips, tongue, and floor of her mouth. There were no signs of illness on her body outside the mouth. Lab tests showed no evidence of a common virus (HSV-1) linked to these sores, which helped doctors rule out other causes.\n\nThe diagnosis was oral erythema multiforme, a condition that can be triggered by vaping, and it was classified as mild. Treatment included applying a saltwater solution (0.9% NaCl) to her lips three times a day, using a mouthwash with dexamethasone and hyaluronic acid three times a day (after waiting 30 minutes before eating or drinking), applying a 2% miconazole cream to the sore corner of her mouth twice daily, and using vaseline album cream for dry lips. She was also advised to stop vaping and avoid foods with MSG. \n\nAfter one week of treatment, her mouth sores improved significantly. The case was reviewed with her consent, and it followed ethical medical guidelines."}
+{"row_index": 164, "doc_id": 3, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A baby was born at 39 weeks and had a small, harmless lump inside the heart that was found during pregnancy. The lump didn’t grow or shrink, and the baby didn’t have any seizures or skin spots. The doctor checked the baby right after birth, at 1 month, 7 months, and 1 year, and everything was normal. The baby grew well, stayed healthy, and developed like other babies her age. The heart lump was only in the heart and didn’t cause any problems. No other signs of a rare condition called tuberous sclerosis were found, so the baby doesn’t have that condition.\"\n}", "generated_text": "A baby was born at 39 weeks and had a small, harmless lump inside the heart that was found during pregnancy. The lump didn’t grow or shrink, and the baby didn’t have any seizures or skin spots. The doctor checked the baby right after birth, at 1 month, 7 months, and 1 year, and everything was normal. The baby grew well, stayed healthy, and developed like other babies her age. The heart lump was only in the heart and didn’t cause any problems. No other signs of a rare condition called tuberous sclerosis were found, so the baby doesn’t have that condition."}
+{"row_index": 165, "doc_id": 3, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 29-year-old gravida V par IV woman, with a history of three spontaneous vaginal deliveries and one previous cesarean section for failed induction of labor (four years prior), presented for antenatal care follow-up at 32 weeks' gestation based on her last normal menstrual period (LNMP). Comprehensive medical history revealed that all four of her children are healthy, thriving in school, and have no known genetic or seizure-related disorders. Laboratory investigations including Venereal Disease Research Laboratory (VDRL) testing, Hepatitis B surface antigen (HBsAg), and urine analysis were negative. Complete Blood Count (CBC) showed normal cellular parameters; blood group was A, Rh-positive. Obstetric ultrasound demonstrated a normal fetal anatomy except for the cardiac structure. Detailed fetal echocardiography revealed normal atrial size and situs, with appropriately positioned and functioning atrioventricular and semilunar valves. Both ventricles exhibited comparable size and contractile function, with normal left ventricular apex formation and no ventricular septal defect. However, two circumscribed, round, echogenic masses were identified on the left ventricular papillary muscles, measuring 18.2 mm × 8.3 mm and 13.5 mm × 8.3 mm, respectively. The left ventricular outflow tract (LVOT) and right ventricular outflow tract (RVOT) demonstrated normal anatomy and hemodynamics on two-dimensional (2D) and color flow (CF) ultrasound assessment. Based on these findings, a diagnosis of isolated fetal cardiac rhabdomyoma was established. Given the strong association between cardiac rhabdomyoma and tuberous sclerosis complex (TSC), a comprehensive evaluation for TSC was performed, including neurosonography and systemic screening for cutaneous, renal, and neurological manifestations. No additional features consistent with TSC were identified beyond the cardiac mass. The patient maintained regular antenatal care from 32 weeks through 39 weeks plus 1 day, with no complications. At 39 weeks plus 1 day, a cesarean section was performed for full-term delivery and patient request for repeat cesarean delivery, resulting in the birth of a 3200-gram female infant with an APGAR score of 10 at both 1 and 5 minutes. Both maternal and neonatal postoperative courses were uncomplicated, and both were discharged on postoperative day three. Postnatal evaluations were conducted on days 1, 7, and 30, with no evidence of tumor regression, growth, or emergence of skin lesions or seizures. Physical examination findings remained normal, and the cardiac mass size was stable compared to the prenatal assessment. At 7 months of age, developmental history and neurodevelopmental screening were performed, revealing age-appropriate developmental progress. Anthropometric measurements confirmed normal growth. A pediatric echocardiogram revealed well-circumscribed hyperechoic masses on both left ventricular papillary muscles, measuring 21.8 mm × 9.2 mm and 14.7 mm × 8.5 mm, respectively, with no evidence of left ventricular inflow obstruction or functional compromise. At 12 months of age, comprehensive evaluation including physical examination, anthropometric assessment, and neurobehavioral testing was completed. The child demonstrated healthy growth parameters and normal neurobehavioral development, consistent with age-matched peers. The cardiac rhabdomyoma remained stable in size and did not exhibit any growth or regression. No clinical criteria for tuberous sclerosis complex were met, including absence of cutaneous hamartomas, subependymal nodules, renal angiomyolipomas, or other systemic manifestations. This case represents an isolated, asymptomatic cardiac rhabdomyoma without evidence of tuberous sclerosis complex, with stable tumor morphology and normal developmental and physiological outcomes through one year of age.\"\n}", "generated_text": "A 29-year-old gravida V par IV woman, with a history of three spontaneous vaginal deliveries and one previous cesarean section for failed induction of labor (four years prior), presented for antenatal care follow-up at 32 weeks' gestation based on her last normal menstrual period (LNMP). Comprehensive medical history revealed that all four of her children are healthy, thriving in school, and have no known genetic or seizure-related disorders. Laboratory investigations including Venereal Disease Research Laboratory (VDRL) testing, Hepatitis B surface antigen (HBsAg), and urine analysis were negative. Complete Blood Count (CBC) showed normal cellular parameters; blood group was A, Rh-positive. Obstetric ultrasound demonstrated a normal fetal anatomy except for the cardiac structure. Detailed fetal echocardiography revealed normal atrial size and situs, with appropriately positioned and functioning atrioventricular and semilunar valves. Both ventricles exhibited comparable size and contractile function, with normal left ventricular apex formation and no ventricular septal defect. However, two circumscribed, round, echogenic masses were identified on the left ventricular papillary muscles, measuring 18.2 mm × 8.3 mm and 13.5 mm × 8.3 mm, respectively. The left ventricular outflow tract (LVOT) and right ventricular outflow tract (RVOT) demonstrated normal anatomy and hemodynamics on two-dimensional (2D) and color flow (CF) ultrasound assessment. Based on these findings, a diagnosis of isolated fetal cardiac rhabdomyoma was established. Given the strong association between cardiac rhabdomyoma and tuberous sclerosis complex (TSC), a comprehensive evaluation for TSC was performed, including neurosonography and systemic screening for cutaneous, renal, and neurological manifestations. No additional features consistent with TSC were identified beyond the cardiac mass. The patient maintained regular antenatal care from 32 weeks through 39 weeks plus 1 day, with no complications. At 39 weeks plus 1 day, a cesarean section was performed for full-term delivery and patient request for repeat cesarean delivery, resulting in the birth of a 3200-gram female infant with an APGAR score of 10 at both 1 and 5 minutes. Both maternal and neonatal postoperative courses were uncomplicated, and both were discharged on postoperative day three. Postnatal evaluations were conducted on days 1, 7, and 30, with no evidence of tumor regression, growth, or emergence of skin lesions or seizures. Physical examination findings remained normal, and the cardiac mass size was stable compared to the prenatal assessment. At 7 months of age, developmental history and neurodevelopmental screening were performed, revealing age-appropriate developmental progress. Anthropometric measurements confirmed normal growth. A pediatric echocardiogram revealed well-circumscribed hyperechoic masses on both left ventricular papillary muscles, measuring 21.8 mm × 9.2 mm and 14.7 mm × 8.5 mm, respectively, with no evidence of left ventricular inflow obstruction or functional compromise. At 12 months of age, comprehensive evaluation including physical examination, anthropometric assessment, and neurobehavioral testing was completed. The child demonstrated healthy growth parameters and normal neurobehavioral development, consistent with age-matched peers. The cardiac rhabdomyoma remained stable in size and did not exhibit any growth or regression. No clinical criteria for tuberous sclerosis complex were met, including absence of cutaneous hamartomas, subependymal nodules, renal angiomyolipomas, or other systemic manifestations. This case represents an isolated, asymptomatic cardiac rhabdomyoma without evidence of tuberous sclerosis complex, with stable tumor morphology and normal developmental and physiological outcomes through one year of age."}
+{"row_index": 166, "doc_id": 4, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 13-year-old boy had a problem in his throat since he was 2 years old, with small growths called papillomas that blocked his airway. By age 3, he needed a tube (tracheostomy) to breathe. His mom also had a similar skin growth. The boy had trouble breathing, especially at night, with a loud breathing sound and hoarseness. He got medicine and oxygen but it didn’t help. Tests showed growths in his voice box and windpipe, and small lung pockets. After surgery, the doctor removed the growths and put in a breathing tube. He got one shot of a medicine called bevacizumab to help stop the growths. He started breathing better and didn’t need oxygen after a few days. He stayed in the hospital for 7 days and then went to another hospital. After 8 months, the family said the problem didn’t come back. He is doing well and no signs of return.\"\n}", "generated_text": "A 13-year-old boy had a problem in his throat since he was 2 years old, with small growths called papillomas that blocked his airway. By age 3, he needed a tube (tracheostomy) to breathe. His mom also had a similar skin growth. The boy had trouble breathing, especially at night, with a loud breathing sound and hoarseness. He got medicine and oxygen but it didn’t help. Tests showed growths in his voice box and windpipe, and small lung pockets. After surgery, the doctor removed the growths and put in a breathing tube. He got one shot of a medicine called bevacizumab to help stop the growths. He started breathing better and didn’t need oxygen after a few days. He stayed in the hospital for 7 days and then went to another hospital. After 8 months, the family said the problem didn’t come back. He is doing well and no signs of return."}
+{"row_index": 167, "doc_id": 4, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 13-year-old male from Cusco with a longstanding history of laryngeal papillomatosis since age two, who required tracheostomy at age three, was admitted to the San Borja National Institute of Child Health in Lima following a 16-day course of progressive respiratory distress, primarily nocturnal, characterized by inspiratory laryngeal stridor and moderate dysphonia. Prior treatment with azithromycin and supplemental oxygen failed to improve symptoms. Physical examination revealed mild subcostal retraction, diminished vesicular breath sounds in the left hemithorax, and scattered wheezing predominantly in the right hemithorax, necessitating oxygen via binasal cannula at 4 liters per minute. Laboratory findings included leukocyte count of 8.03 × 10³/μL, platelets at 209 × 10³/μL, hemoglobin 13.2 g/dL, and C-reactive protein of 36.6 mg/L, indicating a moderate inflammatory response without evidence of sepsis. Imaging studies consisted of chest radiography and head and neck tomography, which revealed multiple stenosing nodules involving the larynx and trachea, as well as several pulmonary cysts consistent with chronic airway obstruction and alveolar damage. At 48 hours post-admission, the patient experienced worsening stridor and respiratory compromise, prompting urgent intervention in the emergency operating room. The procedure included tracheostomy, microsurgical excision of papillomatosis lesions, and removal of a large appendicular tumor with papillomatous morphology and ventricular banding structures involving the epiglottis, glottic region, vocal cords, subglottis, and trachea extending to tracheal ring 5. Histopathological analysis confirmed coilocytic atypia and mild focal dysplasia, consistent with human papillomavirus (HPV)-induced epithelial dysregulation, most likely HPV-16 or HPV-18 based on typical patterns of HPV-associated laryngeal papillomatosis. Postoperatively, the patient was transferred to the pediatric intensive care unit (PICU) for close respiratory monitoring and initiated weaning from oxygen, which was successfully achieved by 48 hours post-surgery. He received a single intravenous dose of 400 mg bevacizumab, a monoclonal antibody targeting vascular endothelial growth factor (VEGF), administered to inhibit angiogenesis and reduce tumor neovascularization in recurrent or persistent papillomatosis. Clinically, the patient showed significant improvement within 72 hours, with normalization of oxygen saturation and progressive reduction in respiratory support. He remained hospitalized for seven days before being transferred to the Hospital in Breña for continued outpatient management. Eight-month follow-up via telemonitoring demonstrated no evidence of disease recurrence, no new lesions, and no additional respiratory complications, supporting the durability of the intervention. The clinical course underscores the role of HPV-driven epithelial proliferation in laryngeal and tracheal stenosis, the efficacy of combined surgical excision and anti-angiogenic therapy, and the importance of long-term surveillance in patients with familial or recurrent papillomatosis, particularly in those with a maternal history of genital human papillomavirus infection.\"\n}", "generated_text": "A 13-year-old male from Cusco with a longstanding history of laryngeal papillomatosis since age two, who required tracheostomy at age three, was admitted to the San Borja National Institute of Child Health in Lima following a 16-day course of progressive respiratory distress, primarily nocturnal, characterized by inspiratory laryngeal stridor and moderate dysphonia. Prior treatment with azithromycin and supplemental oxygen failed to improve symptoms. Physical examination revealed mild subcostal retraction, diminished vesicular breath sounds in the left hemithorax, and scattered wheezing predominantly in the right hemithorax, necessitating oxygen via binasal cannula at 4 liters per minute. Laboratory findings included leukocyte count of 8.03 × 10³/μL, platelets at 209 × 10³/μL, hemoglobin 13.2 g/dL, and C-reactive protein of 36.6 mg/L, indicating a moderate inflammatory response without evidence of sepsis. Imaging studies consisted of chest radiography and head and neck tomography, which revealed multiple stenosing nodules involving the larynx and trachea, as well as several pulmonary cysts consistent with chronic airway obstruction and alveolar damage. At 48 hours post-admission, the patient experienced worsening stridor and respiratory compromise, prompting urgent intervention in the emergency operating room. The procedure included tracheostomy, microsurgical excision of papillomatosis lesions, and removal of a large appendicular tumor with papillomatous morphology and ventricular banding structures involving the epiglottis, glottic region, vocal cords, subglottis, and trachea extending to tracheal ring 5. Histopathological analysis confirmed coilocytic atypia and mild focal dysplasia, consistent with human papillomavirus (HPV)-induced epithelial dysregulation, most likely HPV-16 or HPV-18 based on typical patterns of HPV-associated laryngeal papillomatosis. Postoperatively, the patient was transferred to the pediatric intensive care unit (PICU) for close respiratory monitoring and initiated weaning from oxygen, which was successfully achieved by 48 hours post-surgery. He received a single intravenous dose of 400 mg bevacizumab, a monoclonal antibody targeting vascular endothelial growth factor (VEGF), administered to inhibit angiogenesis and reduce tumor neovascularization in recurrent or persistent papillomatosis. Clinically, the patient showed significant improvement within 72 hours, with normalization of oxygen saturation and progressive reduction in respiratory support. He remained hospitalized for seven days before being transferred to the Hospital in Breña for continued outpatient management. Eight-month follow-up via telemonitoring demonstrated no evidence of disease recurrence, no new lesions, and no additional respiratory complications, supporting the durability of the intervention. The clinical course underscores the role of HPV-driven epithelial proliferation in laryngeal and tracheal stenosis, the efficacy of combined surgical excision and anti-angiogenic therapy, and the importance of long-term surveillance in patients with familial or recurrent papillomatosis, particularly in those with a maternal history of genital human papillomavirus infection."}
+{"row_index": 168, "doc_id": 5, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 54-year-old man with a long history of kidney problems and medicines that weaken his immune system got sick with fever, cough, and trouble breathing. He had been smoking for a long time and was on strong medicines for his kidneys. Before he got sick, his chest X-ray was normal. When he got sick, he had a high fever, shortness of breath, and his body wasn’t getting enough oxygen. His lungs made crackling sounds, and scans showed cloudy spots in both lungs. Tests showed signs of infection — bacteria, virus, or fungus — and he had antibodies for RSV, a common virus. Because his immune system was weak from long-term medicine use, he couldn’t fight off the infection well. Doctors gave him antibiotics, antifungal medicine, and steroids to calm his body’s reaction. Even with all this care, his condition got worse fast. He needed a breathing machine, but still didn’t improve. Two days later, he passed away from not being able to breathe.\"\n}", "generated_text": "A 54-year-old man with a long history of kidney problems and medicines that weaken his immune system got sick with fever, cough, and trouble breathing. He had been smoking for a long time and was on strong medicines for his kidneys. Before he got sick, his chest X-ray was normal. When he got sick, he had a high fever, shortness of breath, and his body wasn’t getting enough oxygen. His lungs made crackling sounds, and scans showed cloudy spots in both lungs. Tests showed signs of infection — bacteria, virus, or fungus — and he had antibodies for RSV, a common virus. Because his immune system was weak from long-term medicine use, he couldn’t fight off the infection well. Doctors gave him antibiotics, antifungal medicine, and steroids to calm his body’s reaction. Even with all this care, his condition got worse fast. He needed a breathing machine, but still didn’t improve. Two days later, he passed away from not being able to breathe."}
+{"row_index": 169, "doc_id": 6, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 34-year-old woman had lower back pain and blood in her urine. She also had a big bruise on her right buttock and no history of bleeding before. The bleeding started after she had a C-section during pregnancy two months ago. Doctors found that her body couldn't stop bleeding properly because of a problem with a blood protein called factor VIII. This problem was made worse after giving birth. Tests showed she had a high level of an antibody that attacks this protein. This confirmed she had acquired haemophilia, which happened after childbirth. She got treatment with medicines to stop the bleeding and help her blood work, and her symptoms got better over time. She is now doing well and can go home.\"\n}", "generated_text": "A 34-year-old woman had lower back pain and blood in her urine. She also had a big bruise on her right buttock and no history of bleeding before. The bleeding started after she had a C-section during pregnancy two months ago. Doctors found that her body couldn't stop bleeding properly because of a problem with a blood protein called factor VIII. This problem was made worse after giving birth. Tests showed she had a high level of an antibody that attacks this protein. This confirmed she had acquired haemophilia, which happened after childbirth. She got treatment with medicines to stop the bleeding and help her blood work, and her symptoms got better over time. She is now doing well and can go home."}
+{"row_index": 170, "doc_id": 7, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A two-day-old baby was admitted to Children’s Hospital with a swelling on the right side of the scrotum that had been present since birth. The baby was born at full term by cesarean section at a private hospital and stayed in the nursery for one day before being referred for surgery. When they arrived at the hospital, the baby was healthy, well-hydrated, pink, and had good circulation. On exam, the right testis was enlarged, firm, not painful, and had a red color with skin damage. The testis did not allow light to pass through (negative trans-illumination), while the left one did (positive). Both testicles had normal openings, with no signs of hernia. An ultrasound showed the right testis was enlarged (15.6 mm x 9.4 mm), had an uneven texture, and showed a thickened network of tissue (rete testis) with no blood flow, which is a sign of poor circulation. The left testis was normal in size and shape, with only a small amount of fluid around it. Surgery was urgently performed. During the operation, the right testis was found to be completely dead (necrotic) and twisted inside the scrotum (intravaginal torsion), with only a small amount of fluid. The doctors removed the damaged right testis (right orchidectomy) and fixed the left testis in place (contralateral orchidopexy) to prevent future issues.\"\n}", "generated_text": "A two-day-old baby was admitted to Children’s Hospital with a swelling on the right side of the scrotum that had been present since birth. The baby was born at full term by cesarean section at a private hospital and stayed in the nursery for one day before being referred for surgery. When they arrived at the hospital, the baby was healthy, well-hydrated, pink, and had good circulation. On exam, the right testis was enlarged, firm, not painful, and had a red color with skin damage. The testis did not allow light to pass through (negative trans-illumination), while the left one did (positive). Both testicles had normal openings, with no signs of hernia. An ultrasound showed the right testis was enlarged (15.6 mm x 9.4 mm), had an uneven texture, and showed a thickened network of tissue (rete testis) with no blood flow, which is a sign of poor circulation. The left testis was normal in size and shape, with only a small amount of fluid around it. Surgery was urgently performed. During the operation, the right testis was found to be completely dead (necrotic) and twisted inside the scrotum (intravaginal torsion), with only a small amount of fluid. The doctors removed the damaged right testis (right orchidectomy) and fixed the left testis in place (contralateral orchidopexy) to prevent future issues."}
+{"row_index": 171, "doc_id": 7, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A two-day-old baby was born by C-section and had a swelling on the right side of his scrotum from the start. When they checked him, he was healthy, warm, and breathing well. The swollen testicle was big, stiff, red, and had small skin scratches. A light test showed the right side didn’t let light through (which means it’s not normal), but the left side did. The baby’s groin openings were fine. A scan showed the right testicle was enlarged and had a bad, patchy look with no blood flow — this means it was dying. The left testicle was normal but had a little fluid. Doctors had to do an emergency surgery. Inside, they found the right testicle was dead and twisted, with only a small amount of fluid. They removed the dead testicle (right orchidectomy) and fixed the left testicle (contralateral orchidopexy) to keep it in place.\"\n}", "generated_text": "A two-day-old baby was born by C-section and had a swelling on the right side of his scrotum from the start. When they checked him, he was healthy, warm, and breathing well. The swollen testicle was big, stiff, red, and had small skin scratches. A light test showed the right side didn’t let light through (which means it’s not normal), but the left side did. The baby’s groin openings were fine. A scan showed the right testicle was enlarged and had a bad, patchy look with no blood flow — this means it was dying. The left testicle was normal but had a little fluid. Doctors had to do an emergency surgery. Inside, they found the right testicle was dead and twisted, with only a small amount of fluid. They removed the dead testicle (right orchidectomy) and fixed the left testicle (contralateral orchidopexy) to keep it in place."}
+{"row_index": 172, "doc_id": 7, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"We present a case of a two-day-old male neonate presenting with an inborn right scrotal swelling admitted to the pediatric emergency department of Children’s Hospital. The infant was born at term via cesarean section at a private facility and remained in the nursery for one day prior to referral for urgent surgical evaluation. Transfer to our institution was delayed by a full day, during which time the clinical condition was stable. On arrival, the neonate was well-hydrated, had normal room temperature skin color, and exhibited adequate peripheral perfusion, indicating no signs of systemic compromise. Physical examination revealed a markedly enlarged, tense, non-tender right testis with visible erythema and overlying skin excoriation, suggestive of localized ischemia or inflammatory processes. Trans-illumination testing was negative in the right testis (indicating a non-reflective, solid tissue mass), while it was positive in the left contralateral testis, consistent with a normal, fluid-containing structure. Both inguinal hernial orifices were anatomically intact, ruling out inguinal hernia as a primary etiology. An urgent Doppler ultrasound of the inguinoscrotal region was performed, revealing the right testis to be enlarged (dimensions: 15.6 × 9.4 mm) with a heterogeneous hypoechoic echotexture, characterized by prominent rete testis architecture and absence of detectable arterial or venous flow on color Doppler imaging—findings consistent with ischemic compromise and loss of vascular perfusion. The left testis was normal in size, shape, and echotexture, with a minimal hydrocele present, indicating preserved vascular integrity and normal testicular development. Intraoperative findings confirmed a frank necrotic right testis with intravaginal torsion (i.e., twisting of the testicular parenchyma around its vascular pedicle), leading to complete arterial occlusion and irreversible tissue damage. Minimal hydrocele was also noted in the right scrotum. The surgical intervention consisted of a right orchidectomy (removal of the necrotic testis) and contralateral orchidopexy (surgical fixation of the normally developing left testis to the scrotal wall) to prevent future complications such as testicular descent failure or torsion. The absence of flow on Doppler imaging is a critical indicator of testicular ischemia, and the presence of necrosis and intravaginal torsion confirms a diagnosis of testicular torsion with secondary ischemic necrosis, likely occurring in the perinatal period due to delayed presentation and inadequate perfusion. This case underscores the importance of prompt evaluation and intervention in neonates with scrotal swelling, as delayed diagnosis significantly increases the risk of irreversible testicular loss.\"\n}", "generated_text": "We present a case of a two-day-old male neonate presenting with an inborn right scrotal swelling admitted to the pediatric emergency department of Children’s Hospital. The infant was born at term via cesarean section at a private facility and remained in the nursery for one day prior to referral for urgent surgical evaluation. Transfer to our institution was delayed by a full day, during which time the clinical condition was stable. On arrival, the neonate was well-hydrated, had normal room temperature skin color, and exhibited adequate peripheral perfusion, indicating no signs of systemic compromise. Physical examination revealed a markedly enlarged, tense, non-tender right testis with visible erythema and overlying skin excoriation, suggestive of localized ischemia or inflammatory processes. Trans-illumination testing was negative in the right testis (indicating a non-reflective, solid tissue mass), while it was positive in the left contralateral testis, consistent with a normal, fluid-containing structure. Both inguinal hernial orifices were anatomically intact, ruling out inguinal hernia as a primary etiology. An urgent Doppler ultrasound of the inguinoscrotal region was performed, revealing the right testis to be enlarged (dimensions: 15.6 × 9.4 mm) with a heterogeneous hypoechoic echotexture, characterized by prominent rete testis architecture and absence of detectable arterial or venous flow on color Doppler imaging—findings consistent with ischemic compromise and loss of vascular perfusion. The left testis was normal in size, shape, and echotexture, with a minimal hydrocele present, indicating preserved vascular integrity and normal testicular development. Intraoperative findings confirmed a frank necrotic right testis with intravaginal torsion (i.e., twisting of the testicular parenchyma around its vascular pedicle), leading to complete arterial occlusion and irreversible tissue damage. Minimal hydrocele was also noted in the right scrotum. The surgical intervention consisted of a right orchidectomy (removal of the necrotic testis) and contralateral orchidopexy (surgical fixation of the normally developing left testis to the scrotal wall) to prevent future complications such as testicular descent failure or torsion. The absence of flow on Doppler imaging is a critical indicator of testicular ischemia, and the presence of necrosis and intravaginal torsion confirms a diagnosis of testicular torsion with secondary ischemic necrosis, likely occurring in the perinatal period due to delayed presentation and inadequate perfusion. This case underscores the importance of prompt evaluation and intervention in neonates with scrotal swelling, as delayed diagnosis significantly increases the risk of irreversible testicular loss."}
+{"row_index": 173, "doc_id": 8, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 4-year-old boy had a skin infection (impetigo) two weeks before his illness. For 5 days, he had blood in his urine and swelling in his legs. Then he started having headaches, nausea, vomiting, and suddenly had a seizure. His blood pressure became very high, causing a dangerous situation. Tests showed his body was missing some important proteins (C3) and had high levels of a strep infection marker (ASO), which pointed to a condition called GNAPE. Because of the high blood pressure, his brain started to swell (PRES), which can cause brain damage. He also developed a type of anemia where his red blood cells were being destroyed, and his hemoglobin dropped to 5 g/dL. He needed medicine to lower his blood pressure, protect his brain, and stop the body from attacking his red blood cells (steroids). He stayed in the hospital for 31 days, and after that, he was back to normal. Six months later, he had no symptoms and was doing well with medicine to keep his blood pressure and kidneys healthy.\"\n}", "generated_text": "A 4-year-old boy had a skin infection (impetigo) two weeks before his illness. For 5 days, he had blood in his urine and swelling in his legs. Then he started having headaches, nausea, vomiting, and suddenly had a seizure. His blood pressure became very high, causing a dangerous situation. Tests showed his body was missing some important proteins (C3) and had high levels of a strep infection marker (ASO), which pointed to a condition called GNAPE. Because of the high blood pressure, his brain started to swell (PRES), which can cause brain damage. He also developed a type of anemia where his red blood cells were being destroyed, and his hemoglobin dropped to 5 g/dL. He needed medicine to lower his blood pressure, protect his brain, and stop the body from attacking his red blood cells (steroids). He stayed in the hospital for 31 days, and after that, he was back to normal. Six months later, he had no symptoms and was doing well with medicine to keep his blood pressure and kidneys healthy."}
+{"row_index": 174, "doc_id": 8, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 4-year-old male presented with a 5-day history of macroscopic glomerular hematuria and lower extremity edema, which progressed over the preceding 12 hours to include headaches, nausea, vomiting, and a generalised tonic-clonic seizure. On emergency department admission, the patient was afebrile, with non-evaluable blood pressure, and exhibited quantitative consciousness impairment, generalized hypertonia, and bilateral pretibial edema. Endotracheal intubation was performed, and phenobarbital (10 mg/kg) was administered to control seizure activity.\\n\\nPhysical examination in the intensive care unit (ICU) revealed a blood pressure of 134/94 mmHg (BP 110 mmHg), with a p95 of 108/66 mmHg and p95+12 of 120/78 mmHg. Initial laboratory findings included hematuria (>100 erythrocytes per field), proteinuria 3+, leucocyturia (10–25 per field), creatinine 0.3 mg/dL, hemoglobin 7 g/dL, hematocrit 21%, normal mean corpuscular volume (MCV) and mean corpuscular hemoglobin concentration (MCHC), leukocytosis (23,900/mm³), thrombocytosis (756,000/mm³), absence of acute-phase reactants, hypocomplementemia (C3 25 mg/dL; normal range 80–150 mg/dL), and normal C4. A rapid antigen test for Streptococcus pyogenes (group A beta-hemolytic streptococcus) was positive, and Anti-Streptolysin O (ASO) titers were elevated, consistent with recent streptococcal infection. Non-contrast brain CT showed no acute abnormalities. Renal ultrasound revealed bilateral nephromegaly with increased cortical echogenicity and reduced corticomedullary differentiation.\\n\\nThe patient was diagnosed with nephritic syndrome secondary to group A streptococcal infection (GNAPE) complicated by hypertensive emergency and convulsive status. Within 24 hours of ICU admission, mechanical ventilation and continued phenobarbital therapy were required. Electroencephalography (EEG) and cerebrospinal fluid analysis were normal on day one. Empirical antibiotic therapy with cefotaxime was initiated for eradication of Streptococcus pyogenes, and furosemide was administered for diuresis.\\n\\nOn post-admission day two, the patient developed acute kidney injury with creatinine rising to 0.99 mg/dL, persistent hypertension, and 24-hour proteinuria of 36.6 mg/m²/h, without oliguria. Antihypertensive therapy was initiated with amlodipine and intravenous labetalol, achieving initial control. At 48 hours, extubation was performed, which was well tolerated. However, within 24 hours of extubation, the patient's mental status deteriorated to Glasgow Coma Scale (GCS) 8 (ocular opening and limb withdrawal only to painful stimuli), with poor verbal response, and blood pressure remained above p95+12 despite continuous infusion of labetalol (up to 3 mg/kg/h), amlodipine (10 mg/day), and furosemide. This necessitated reintroduction of mechanical ventilation and administration of sodium nitroprusside (up to 3 mcg/kg/min) to achieve a gradual reduction of blood pressure by 25% per day to prevent secondary neurological injury. Given the presence of acute neurological symptoms in the context of severe hypertension in a patient with glomerulonephritis, posterior reversible encephalopathy syndrome (PRES) was suspected and confirmed by magnetic resonance imaging (MRI) on day 5. MRI demonstrated bilateral, symmetric subcortical hyperintensities in the occipital regions, without diffusion restriction, consistent with vasogenic edema. Ophthalmological examination was normal, and subsequent EEG showed occasional episodes of generalized voltage depression.\\n\\nHemoglobin declined to 5 g/dL during ICU stay, with normal MCV and MCHC, and no plateletopenia, prompting suspicion of autoimmune hemolytic anemia. A positive direct Coombs test and hemoglobinuria supported this diagnosis. Two red blood cell transfusions were required. Corticosteroid therapy with methylprednisolone (1 mg/kg/day) was initiated for 72 hours. Serological testing for Epstein-Barr virus, parvovirus B19, extractable nuclear antigens (ENA), anti-neutrophil cytoplasmic antibodies (AN", "generated_text": "{\n  \"proficient_health_literacy\": \"A 4-year-old male presented with a 5-day history of macroscopic glomerular hematuria and lower extremity edema, which progressed over the preceding 12 hours to include headaches, nausea, vomiting, and a generalised tonic-clonic seizure. On emergency department admission, the patient was afebrile, with non-evaluable blood pressure, and exhibited quantitative consciousness impairment, generalized hypertonia, and bilateral pretibial edema. Endotracheal intubation was performed, and phenobarbital (10 mg/kg) was administered to control seizure activity.\\n\\nPhysical examination in the intensive care unit (ICU) revealed a blood pressure of 134/94 mmHg (BP 110 mmHg), with a p95 of 108/66 mmHg and p95+12 of 120/78 mmHg. Initial laboratory findings included hematuria (>100 erythrocytes per field), proteinuria 3+, leucocyturia (10–25 per field), creatinine 0.3 mg/dL, hemoglobin 7 g/dL, hematocrit 21%, normal mean corpuscular volume (MCV) and mean corpuscular hemoglobin concentration (MCHC), leukocytosis (23,900/mm³), thrombocytosis (756,000/mm³), absence of acute-phase reactants, hypocomplementemia (C3 25 mg/dL; normal range 80–150 mg/dL), and normal C4. A rapid antigen test for Streptococcus pyogenes (group A beta-hemolytic streptococcus) was positive, and Anti-Streptolysin O (ASO) titers were elevated, consistent with recent streptococcal infection. Non-contrast brain CT showed no acute abnormalities. Renal ultrasound revealed bilateral nephromegaly with increased cortical echogenicity and reduced corticomedullary differentiation.\\n\\nThe patient was diagnosed with nephritic syndrome secondary to group A streptococcal infection (GNAPE) complicated by hypertensive emergency and convulsive status. Within 24 hours of ICU admission, mechanical ventilation and continued phenobarbital therapy were required. Electroencephalography (EEG) and cerebrospinal fluid analysis were normal on day one. Empirical antibiotic therapy with cefotaxime was initiated for eradication of Streptococcus pyogenes, and furosemide was administered for diuresis.\\n\\nOn post-admission day two, the patient developed acute kidney injury with creatinine rising to 0.99 mg/dL, persistent hypertension, and 24-hour proteinuria of 36.6 mg/m²/h, without oliguria. Antihypertensive therapy was initiated with amlodipine and intravenous labetalol, achieving initial control. At 48 hours, extubation was performed, which was well tolerated. However, within 24 hours of extubation, the patient's mental status deteriorated to Glasgow Coma Scale (GCS) 8 (ocular opening and limb withdrawal only to painful stimuli), with poor verbal response, and blood pressure remained above p95+12 despite continuous infusion of labetalol (up to 3 mg/kg/h), amlodipine (10 mg/day), and furosemide. This necessitated reintroduction of mechanical ventilation and administration of sodium nitroprusside (up to 3 mcg/kg/min) to achieve a gradual reduction of blood pressure by 25% per day to prevent secondary neurological injury. Given the presence of acute neurological symptoms in the context of severe hypertension in a patient with glomerulonephritis, posterior reversible encephalopathy syndrome (PRES) was suspected and confirmed by magnetic resonance imaging (MRI) on day 5. MRI demonstrated bilateral, symmetric subcortical hyperintensities in the occipital regions, without diffusion restriction, consistent with vasogenic edema. Ophthalmological examination was normal, and subsequent EEG showed occasional episodes of generalized voltage depression.\\n\\nHemoglobin declined to 5 g/dL during ICU stay, with normal MCV and MCHC, and no plateletopenia, prompting suspicion of autoimmune hemolytic anemia. A positive direct Coombs test and hemoglobinuria supported this diagnosis. Two red blood cell transfusions were required. Corticosteroid therapy with methylprednisolone (1 mg/kg/day) was initiated for 72 hours. Serological testing for Epstein-Barr virus, parvovirus B19, extractable nuclear antigens (ENA), anti-neutrophil cytoplasmic antibodies (AN"}
+{"row_index": 175, "doc_id": 9, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 69-year-old man with a history of heart surgery (coronary artery bypass grafting) came in with severe shortness of breath even during light activity, which had been going on for two months. He was diagnosed with heart failure caused by reduced blood flow to part of his heart, specifically due to a blockage in the right coronary artery (RCA) that had previously failed to work properly. This diagnosis was made based on his heart test results, blood markers, and a detailed heart imaging study (coronary angiogram). \\n\\nTo fix the blocked artery, doctors used a technique called 'retrograde recanalization' — meaning they started from the opposite side of the heart, using natural blood channels (collaterals) from the left side to reach the blocked RCA. They first cleared a major blockage in the left coronary artery, then used a method called 'septal surfing' to travel through the septal branches and reach the blocked RCA. Once there, they opened the blockage with a balloon and placed two drug-coated stents to keep the artery open.\\n\\nAfter the procedure, his shortness of breath improved and went away by the time he was discharged. At a 6-month check-up, he had no return of symptoms and was doing much better.\"\n}", "generated_text": "A 69-year-old man with a history of heart surgery (coronary artery bypass grafting) came in with severe shortness of breath even during light activity, which had been going on for two months. He was diagnosed with heart failure caused by reduced blood flow to part of his heart, specifically due to a blockage in the right coronary artery (RCA) that had previously failed to work properly. This diagnosis was made based on his heart test results, blood markers, and a detailed heart imaging study (coronary angiogram). \n\nTo fix the blocked artery, doctors used a technique called 'retrograde recanalization' — meaning they started from the opposite side of the heart, using natural blood channels (collaterals) from the left side to reach the blocked RCA. They first cleared a major blockage in the left coronary artery, then used a method called 'septal surfing' to travel through the septal branches and reach the blocked RCA. Once there, they opened the blockage with a balloon and placed two drug-coated stents to keep the artery open.\n\nAfter the procedure, his shortness of breath improved and went away by the time he was discharged. At a 6-month check-up, he had no return of symptoms and was doing much better."}
+{"row_index": 176, "doc_id": 9, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 69-year-old man had trouble breathing even when doing small things like walking, for two months. He had had heart surgery before (CABG) and now his heart isn’t pumping well, which caused this breathing problem. Doctors found that a part of his heart’s blood supply (the right coronary artery) was completely blocked, and that damage from a heart attack years ago made the heart weaker. They fixed the blocked blood vessel by going backward through a small channel in the heart muscle, using a special method called 'septal surfing.' After fixing it, his breathing got better right away. Six months later, he still doesn’t have any breathing problems.\"\n}", "generated_text": "A 69-year-old man had trouble breathing even when doing small things like walking, for two months. He had had heart surgery before (CABG) and now his heart isn’t pumping well, which caused this breathing problem. Doctors found that a part of his heart’s blood supply (the right coronary artery) was completely blocked, and that damage from a heart attack years ago made the heart weaker. They fixed the blocked blood vessel by going backward through a small channel in the heart muscle, using a special method called 'septal surfing.' After fixing it, his breathing got better right away. Six months later, he still doesn’t have any breathing problems."}
+{"row_index": 177, "doc_id": 9, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 69-year-old male with a prior history of coronary artery bypass grafting (CABG) presented with severe dyspnea at mild exertion, classified as New York Heart Association (NYHA) class III, lasting for two months. The patient had a documented history of inferior ST-segment-elevation myocardial infarction (STEMI) in 2009 at age 59, with coronary angiography at that time revealing severe three-vessel disease, including a complete occlusion (CTO) in the proximal left anterior descending artery (LAD), 90% stenosis in the mid and distal left circumflex artery, and 95% stenosis in the mid-right coronary artery (RCA). In 2009, he underwent CABG utilizing the left internal mammary artery (LIMA) to the LAD, followed by sequential saphenous vein graft (SVG) to the first obtuse marginal branch (OM1), second obtuse marginal branch (OM2), and posterolateral artery (PL). At presentation, coronary angiography via 6 French left radial artery access demonstrated patency of the LIMA-to-LAD and SVG-to-OM1, OM2 conduits, but a complete occlusion of the SVG-to-PL graft. Native left main coronary artery was occluded at its ostium, and the native RCA was occluded in the mid-portion with bridging collaterals. Given the functional significance of the occluded native RCA, a targeted intervention was initiated to recanalize the native right coronary artery CTO. Dual arterial access was established using a second 6 Fr sheath in the right femoral artery. Left and right coronary arteries were intubated with 6 Fr AL 0.75 (Launcher; Medtronic) and 6 Fr EBU 3.5 (Launcher; Medtronic) guide catheters, respectively. An antegrade approach via the left radial artery was attempted; however, neither the Fielder XTR wire (Asahi Intec) nor the Gaia 3 wire (Asahi Intec) with Finecross microcatheter (Terumo) successfully navigated to the true lumen of the distal RCA. A parallel wire technique using Crusade microcatheter (Kaneka) and two Gaia 3 wires was attempted but failed to achieve coronary artery crossing. Consequently, a retrograde approach via the septal collaterals originating from the left anterior descending artery (LAD) through the occluded left main coronary artery was employed. The Gaia 3 wire crossed the occluded left main (LM) and LAD and reached the true lumen of the distal LAD. The Sion wire was then exchanged for a Finecross microcatheter (Terumo) and advanced into the distal LAD. The left main and proximal LAD were predilated with a 2.0 × 15 mm balloon. Subsequently, the septal surfing technique (SST) was applied to facilitate retrograde crossing of the CTO. Multiple septal channels were evaluated from proximal to distal LAD, and the Sion wire was retrogradely delivered through a distal septal branch into the distal RCA, supported by a 150-cm Finecross microcatheter. The Gaia 3 wire successfully traversed the CTO lesion retrogradely into the true lumen of the proximal RCA and was advanced into the Guidezilla guide extension catheter (Boston Scientific) positioned within the antegrade guiding catheter. The Finecross microcatheter was then delivered to the antegrade catheter, and an RG3 wire (Asahi Intec) was externalized. The CTO was predilated with a 2.0 × 15 mm balloon and treated with two overlapping drug-eluting stents (2.5 × 38 mm and 3.0 × 38 mm), resulting in excellent angiographic restoration with TIMI 3 flow in all distal coronary branches. Post-procedure, the patient’s dyspnea improved significantly and was fully resolved at discharge. At 6-month follow-up, there was no recurrence of dyspnea. The diagnosis of heart failure due to ischemic etiology was established based on electrocardiographic findings of ST depression in leads II, III, aVF, and V4–V6, elevated plasma N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels (2640 pg/mL), and echocardiographic evidence of left ventricular systolic dysfunction with a left ventricular ejection fraction of 30%, consistent with ischemic cardiomyopathy secondary to prior SVG failure in the right coronary artery.\"\n}", "generated_text": "A 69-year-old male with a prior history of coronary artery bypass grafting (CABG) presented with severe dyspnea at mild exertion, classified as New York Heart Association (NYHA) class III, lasting for two months. The patient had a documented history of inferior ST-segment-elevation myocardial infarction (STEMI) in 2009 at age 59, with coronary angiography at that time revealing severe three-vessel disease, including a complete occlusion (CTO) in the proximal left anterior descending artery (LAD), 90% stenosis in the mid and distal left circumflex artery, and 95% stenosis in the mid-right coronary artery (RCA). In 2009, he underwent CABG utilizing the left internal mammary artery (LIMA) to the LAD, followed by sequential saphenous vein graft (SVG) to the first obtuse marginal branch (OM1), second obtuse marginal branch (OM2), and posterolateral artery (PL). At presentation, coronary angiography via 6 French left radial artery access demonstrated patency of the LIMA-to-LAD and SVG-to-OM1, OM2 conduits, but a complete occlusion of the SVG-to-PL graft. Native left main coronary artery was occluded at its ostium, and the native RCA was occluded in the mid-portion with bridging collaterals. Given the functional significance of the occluded native RCA, a targeted intervention was initiated to recanalize the native right coronary artery CTO. Dual arterial access was established using a second 6 Fr sheath in the right femoral artery. Left and right coronary arteries were intubated with 6 Fr AL 0.75 (Launcher; Medtronic) and 6 Fr EBU 3.5 (Launcher; Medtronic) guide catheters, respectively. An antegrade approach via the left radial artery was attempted; however, neither the Fielder XTR wire (Asahi Intec) nor the Gaia 3 wire (Asahi Intec) with Finecross microcatheter (Terumo) successfully navigated to the true lumen of the distal RCA. A parallel wire technique using Crusade microcatheter (Kaneka) and two Gaia 3 wires was attempted but failed to achieve coronary artery crossing. Consequently, a retrograde approach via the septal collaterals originating from the left anterior descending artery (LAD) through the occluded left main coronary artery was employed. The Gaia 3 wire crossed the occluded left main (LM) and LAD and reached the true lumen of the distal LAD. The Sion wire was then exchanged for a Finecross microcatheter (Terumo) and advanced into the distal LAD. The left main and proximal LAD were predilated with a 2.0 × 15 mm balloon. Subsequently, the septal surfing technique (SST) was applied to facilitate retrograde crossing of the CTO. Multiple septal channels were evaluated from proximal to distal LAD, and the Sion wire was retrogradely delivered through a distal septal branch into the distal RCA, supported by a 150-cm Finecross microcatheter. The Gaia 3 wire successfully traversed the CTO lesion retrogradely into the true lumen of the proximal RCA and was advanced into the Guidezilla guide extension catheter (Boston Scientific) positioned within the antegrade guiding catheter. The Finecross microcatheter was then delivered to the antegrade catheter, and an RG3 wire (Asahi Intec) was externalized. The CTO was predilated with a 2.0 × 15 mm balloon and treated with two overlapping drug-eluting stents (2.5 × 38 mm and 3.0 × 38 mm), resulting in excellent angiographic restoration with TIMI 3 flow in all distal coronary branches. Post-procedure, the patient’s dyspnea improved significantly and was fully resolved at discharge. At 6-month follow-up, there was no recurrence of dyspnea. The diagnosis of heart failure due to ischemic etiology was established based on electrocardiographic findings of ST depression in leads II, III, aVF, and V4–V6, elevated plasma N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels (2640 pg/mL), and echocardiographic evidence of left ventricular systolic dysfunction with a left ventricular ejection fraction of 30%, consistent with ischemic cardiomyopathy secondary to prior SVG failure in the right coronary artery."}
+{"row_index": 178, "doc_id": 10, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 51-year-old man came in with sudden, painful vision loss in his left eye three days earlier. His right eye had normal vision, but his left eye could only see hand movements. Examining the back of his left eye showed swelling around the optic nerve, bulging of the choroid, fluid buildup under the retina, and wrinkling of the retinal pigment epithelium. Imaging tests, including MRI of the orbit and brain, showed a nodular mass at the junction of the optic nerve and sclera. Tests for cancer and autoimmune diseases were normal. Based on these findings, the doctor diagnosed nodular posterior scleritis, a type of eye inflammation. The patient was started on oral prednisolone at 50 mg per kilogram of body weight. After surgery to remove a small nodule, the fluid in the eye improved, and vision stabilized. The treatment was gradually reduced over three months. All tests and follow-up showed no signs of serious disease.\"\n}", "generated_text": "A 51-year-old man came in with sudden, painful vision loss in his left eye three days earlier. His right eye had normal vision, but his left eye could only see hand movements. Examining the back of his left eye showed swelling around the optic nerve, bulging of the choroid, fluid buildup under the retina, and wrinkling of the retinal pigment epithelium. Imaging tests, including MRI of the orbit and brain, showed a nodular mass at the junction of the optic nerve and sclera. Tests for cancer and autoimmune diseases were normal. Based on these findings, the doctor diagnosed nodular posterior scleritis, a type of eye inflammation. The patient was started on oral prednisolone at 50 mg per kilogram of body weight. After surgery to remove a small nodule, the fluid in the eye improved, and vision stabilized. The treatment was gradually reduced over three months. All tests and follow-up showed no signs of serious disease."}
+{"row_index": 179, "doc_id": 10, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 51-year-old man woke up 3 days ago with a sudden, painful blurry vision in his left eye. His right eye was fine. He could see clearly with his best eye, but the left eye only showed hand motion. When doctors looked inside his left eye, they saw swelling around the back of the eye, bulging tissue, fluid buildup, and wrinkled layers of the eye’s lining. A scan of his eye and brain showed a small lump near where the optic nerve meets the eye socket. Tests for cancer and other diseases came back normal. The doctor diagnosed it as a type of eye inflammation called nodular posterior scleritis. He started taking a strong steroid pill (prednisolone) at a high dose to reduce the swelling and pain. The lump went down, the fluid cleared, and his vision improved. After a week, he had surgery to remove a small part of the eye socket tissue, and the steroid was injected. He didn’t go to the hospital for IV medicine, but still got better with the pills. After three months, the medicine was slowly stopped. His vision stayed good.\"\n}", "generated_text": "A 51-year-old man woke up 3 days ago with a sudden, painful blurry vision in his left eye. His right eye was fine. He could see clearly with his best eye, but the left eye only showed hand motion. When doctors looked inside his left eye, they saw swelling around the back of the eye, bulging tissue, fluid buildup, and wrinkled layers of the eye’s lining. A scan of his eye and brain showed a small lump near where the optic nerve meets the eye socket. Tests for cancer and other diseases came back normal. The doctor diagnosed it as a type of eye inflammation called nodular posterior scleritis. He started taking a strong steroid pill (prednisolone) at a high dose to reduce the swelling and pain. The lump went down, the fluid cleared, and his vision improved. After a week, he had surgery to remove a small part of the eye socket tissue, and the steroid was injected. He didn’t go to the hospital for IV medicine, but still got better with the pills. After three months, the medicine was slowly stopped. His vision stayed good."}
+{"row_index": 180, "doc_id": 10, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 51-year-old male presented with acute, painful visual loss of the left eye (LE) onset three days prior. Best-corrected distance visual acuity (BCDVA) was 20/20 in the right eye (RE) and hand motion (HM) in the LE. Ocular motility was intact bilaterally. Anterior segment examination was normal. Fundus examination of the LE revealed optic disc (ONH) swelling, choroidal bulging, multiple subretinal fluid accumulations, and retinal pigment epithelial (RPE) corrugations. The RE fundus was unremarkable. Multimodal imaging was performed: Optical coherence tomography (OCT; OptoVue, Inc., software version 2018,0,0,18) demonstrated mild RPE and choroidal bulging, RPE hyper-reflectivity with back shadowing, subretinal and intraretinal fluid, and mild retinal thickening. Fundus blue-autofluorescence (BAF) showed a geographic area of speckled autofluorescence at the macula, consistent with RPE disruption. Indocyanin green angiography (ICGA) revealed a geographic hypofluorescent area with speckled hyperfluorescent margins measuring three disc diameters (DD), suggesting focal vascular leakage and RPE dysfunction. Fluorescein angiography (FA; Heidelberg Eye Explorer v1.9.13.0, Spectralis Viewing Module 6.5.2.0) demonstrated vascular leakage at the optic disc (hot spot), supporting active inflammation. B-scan ultrasonography confirmed optic nerve enlargement, consistent with retrobulbar infiltration. Orbital and brain MRI with gadolinium enhancement identified a retrobulbar nodular mass at the optic nerve-sclera junction, showing intense enhancement, raising concern for both inflammatory and neoplastic etiologies. Oncology evaluation was negative for malignancy. Rheumatology work-up, including PPD (tuberculosis), chest X-ray, serum ACE (sarcoidosis), and C-ANCA (Wegener granulomatosis), was unremarkable. Given the clinical suspicion of nodular posterior scleritis, the patient underwent transconjunctival lateral orbitotomy one week after presentation, revealing a pink, localized scleral nodule with edematous tenon. Sub-tenon triamcinolone acetonide was administered as a local anti-inflammatory intervention. The patient declined admission and intravenous corticosteroid therapy. Oral prednisolone was initiated at a dose of 50 mg/kg/day, targeting immunomodulation and suppression of inflammatory cascades within the ocular and orbital tissues. At follow-up one week post-intervention, BCDVA remained 20/20, with counting fingers at 2 meters in both eyes. Subretinal fluid (SRF) was completely absorbed, and the macular region exhibited atrophy, indicating resolution of active fluid accumulation and chronic RPE damage. Oral prednisolone was tapered over a three-month period to minimize long-term corticosteroid effects. The clinical course supports a diagnosis of nodular posterior scleritis, with imaging findings consistent with inflammatory-mediated RPE and choroidal disruption, optic nerve edema, and focal vascular leakage, all without evidence of systemic autoimmune or infectious pathology or malignancy. The pathophysiological mechanism likely involves chronic inflammation at the posterior sclera-optic nerve interface, leading to RPE dysfunction, fluid accumulation, and structural changes in the retinal layers, with potential activation of local cytokine networks (e.g., IL-1, IL-6, TNF-α) contributing to tissue swelling and vascular permeability.\"\n}", "generated_text": "A 51-year-old male presented with acute, painful visual loss of the left eye (LE) onset three days prior. Best-corrected distance visual acuity (BCDVA) was 20/20 in the right eye (RE) and hand motion (HM) in the LE. Ocular motility was intact bilaterally. Anterior segment examination was normal. Fundus examination of the LE revealed optic disc (ONH) swelling, choroidal bulging, multiple subretinal fluid accumulations, and retinal pigment epithelial (RPE) corrugations. The RE fundus was unremarkable. Multimodal imaging was performed: Optical coherence tomography (OCT; OptoVue, Inc., software version 2018,0,0,18) demonstrated mild RPE and choroidal bulging, RPE hyper-reflectivity with back shadowing, subretinal and intraretinal fluid, and mild retinal thickening. Fundus blue-autofluorescence (BAF) showed a geographic area of speckled autofluorescence at the macula, consistent with RPE disruption. Indocyanin green angiography (ICGA) revealed a geographic hypofluorescent area with speckled hyperfluorescent margins measuring three disc diameters (DD), suggesting focal vascular leakage and RPE dysfunction. Fluorescein angiography (FA; Heidelberg Eye Explorer v1.9.13.0, Spectralis Viewing Module 6.5.2.0) demonstrated vascular leakage at the optic disc (hot spot), supporting active inflammation. B-scan ultrasonography confirmed optic nerve enlargement, consistent with retrobulbar infiltration. Orbital and brain MRI with gadolinium enhancement identified a retrobulbar nodular mass at the optic nerve-sclera junction, showing intense enhancement, raising concern for both inflammatory and neoplastic etiologies. Oncology evaluation was negative for malignancy. Rheumatology work-up, including PPD (tuberculosis), chest X-ray, serum ACE (sarcoidosis), and C-ANCA (Wegener granulomatosis), was unremarkable. Given the clinical suspicion of nodular posterior scleritis, the patient underwent transconjunctival lateral orbitotomy one week after presentation, revealing a pink, localized scleral nodule with edematous tenon. Sub-tenon triamcinolone acetonide was administered as a local anti-inflammatory intervention. The patient declined admission and intravenous corticosteroid therapy. Oral prednisolone was initiated at a dose of 50 mg/kg/day, targeting immunomodulation and suppression of inflammatory cascades within the ocular and orbital tissues. At follow-up one week post-intervention, BCDVA remained 20/20, with counting fingers at 2 meters in both eyes. Subretinal fluid (SRF) was completely absorbed, and the macular region exhibited atrophy, indicating resolution of active fluid accumulation and chronic RPE damage. Oral prednisolone was tapered over a three-month period to minimize long-term corticosteroid effects. The clinical course supports a diagnosis of nodular posterior scleritis, with imaging findings consistent with inflammatory-mediated RPE and choroidal disruption, optic nerve edema, and focal vascular leakage, all without evidence of systemic autoimmune or infectious pathology or malignancy. The pathophysiological mechanism likely involves chronic inflammation at the posterior sclera-optic nerve interface, leading to RPE dysfunction, fluid accumulation, and structural changes in the retinal layers, with potential activation of local cytokine networks (e.g., IL-1, IL-6, TNF-α) contributing to tissue swelling and vascular permeability."}
+{"row_index": 181, "doc_id": 11, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 78-year-old man from the Amhara region of Ethiopia had a permanent pacemaker because he had complete heart block. He needed surgery for an enlarged prostate (benign prostatic hyperplasia), which had developed after a previous prostate procedure. Before surgery, doctors checked his heart and overall health and found that his heart function was stable, though he had high blood pressure and type 2 diabetes. His pacemaker was set to a mode that could be risky during surgery, so doctors recommended changing it to a safer setting. However, the patient could not afford the cost of reprogramming the device due to limited access to cardiac care in Ethiopia and the long wait times for specialists. After discussing the risks, he chose to proceed with the surgery using his current pacemaker setup. Informed consent was given, and the surgery went ahead. He received combined epidural-spinal anesthesia (a mix of bupivacaine and fentanyl) at the L3-L4 level, which provided good pain relief. His vital signs stayed stable during surgery and recovery, with no major heart or breathing issues. After the operation, he was monitored in the recovery room for 12 hours, then moved to the ward. He got pain relief after 4 hours and had a small dose of epidural medicine to keep pain under control. He stayed in the hospital for about 24 hours and was discharged after 88 hours of recovery, in stable condition. He continues to take his medications and is advised to have regular check-ups to ensure his pacemaker is working properly.\"\n}", "generated_text": "A 78-year-old man from the Amhara region of Ethiopia had a permanent pacemaker because he had complete heart block. He needed surgery for an enlarged prostate (benign prostatic hyperplasia), which had developed after a previous prostate procedure. Before surgery, doctors checked his heart and overall health and found that his heart function was stable, though he had high blood pressure and type 2 diabetes. His pacemaker was set to a mode that could be risky during surgery, so doctors recommended changing it to a safer setting. However, the patient could not afford the cost of reprogramming the device due to limited access to cardiac care in Ethiopia and the long wait times for specialists. After discussing the risks, he chose to proceed with the surgery using his current pacemaker setup. Informed consent was given, and the surgery went ahead. He received combined epidural-spinal anesthesia (a mix of bupivacaine and fentanyl) at the L3-L4 level, which provided good pain relief. His vital signs stayed stable during surgery and recovery, with no major heart or breathing issues. After the operation, he was monitored in the recovery room for 12 hours, then moved to the ward. He got pain relief after 4 hours and had a small dose of epidural medicine to keep pain under control. He stayed in the hospital for about 24 hours and was discharged after 88 hours of recovery, in stable condition. He continues to take his medications and is advised to have regular check-ups to ensure his pacemaker is working properly."}
+{"row_index": 182, "doc_id": 11, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 78-year-old man from Ethiopia had a pacemaker in his heart because his heart wasn’t beating properly. He needed surgery to fix a swollen prostate, and the doctors said his pacemaker was set in a way that could be risky during surgery. They suggested changing the pacemaker setting to make it safer, but he couldn’t afford the cost and chose to go ahead with the old setting. He gave permission to have the surgery and to share his story later. Before surgery, he was checked well and had normal blood tests. He was given pain medicine through a tube in his back (epidural) and a small shot of pain medicine (fentanyl) to help him stay comfortable. The doctors watched his heart and blood pressure closely and found nothing wrong. During the surgery, the team kept his heart safe by staying away from the pacemaker and having emergency tools ready. His body stayed steady the whole time. After surgery, he stayed in a recovery room for 12 hours, got more pain medicine, and was moved to a regular room. He stayed in the hospital for about 2 days and got pain relief for 3 days. He was finally sent home after 88 hours, and the doctors said he’s doing well and should keep checking his pacemaker regularly.\"\n}", "generated_text": "A 78-year-old man from Ethiopia had a pacemaker in his heart because his heart wasn’t beating properly. He needed surgery to fix a swollen prostate, and the doctors said his pacemaker was set in a way that could be risky during surgery. They suggested changing the pacemaker setting to make it safer, but he couldn’t afford the cost and chose to go ahead with the old setting. He gave permission to have the surgery and to share his story later. Before surgery, he was checked well and had normal blood tests. He was given pain medicine through a tube in his back (epidural) and a small shot of pain medicine (fentanyl) to help him stay comfortable. The doctors watched his heart and blood pressure closely and found nothing wrong. During the surgery, the team kept his heart safe by staying away from the pacemaker and having emergency tools ready. His body stayed steady the whole time. After surgery, he stayed in a recovery room for 12 hours, got more pain medicine, and was moved to a regular room. He stayed in the hospital for about 2 days and got pain relief for 3 days. He was finally sent home after 88 hours, and the doctors said he’s doing well and should keep checking his pacemaker regularly."}
+{"row_index": 183, "doc_id": 12, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 52-year-old woman had trouble urinating for years, going to the bathroom often and feeling pain when she did. She saw red and black thread-like stuff in her urine, and sometimes had headaches, fever, and chills. She tried many treatments for infections, but nothing helped. No bugs or travel was linked to her symptoms. She had surgery before, but that didn’t fix it. Tests showed no infections or blockages. A bladder check showed redness and dirt in the bladder. Doctors thought it might be a worm, so they gave medicine, but symptoms stayed. Later, a tiny worm was found in her urine under a microscope. It was a type of fly larva. The doctor told her to clean herself better and drink at least 3 liters of water every day. That helped her feel better.\"\n}", "generated_text": "A 52-year-old woman had trouble urinating for years, going to the bathroom often and feeling pain when she did. She saw red and black thread-like stuff in her urine, and sometimes had headaches, fever, and chills. She tried many treatments for infections, but nothing helped. No bugs or travel was linked to her symptoms. She had surgery before, but that didn’t fix it. Tests showed no infections or blockages. A bladder check showed redness and dirt in the bladder. Doctors thought it might be a worm, so they gave medicine, but symptoms stayed. Later, a tiny worm was found in her urine under a microscope. It was a type of fly larva. The doctor told her to clean herself better and drink at least 3 liters of water every day. That helped her feel better."}
+{"row_index": 184, "doc_id": 13, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 36-year-old woman with ulcerative colitis had been doing well on medication but started experiencing worsening chest pain, shortness of breath, and symptoms like fatigue and night sweats. Her electrocardiogram showed abnormal changes in the lower part of her heart, and tests revealed signs of inflammation and heart damage. An emergency heart scan found severe blockages in two major coronary arteries, with the worst blockage in the right coronary artery. She had successful treatment with a stent placed in that artery. During the procedure, doctors noticed signs that might point to a condition called aortitis, which can cause inflammation in the aorta and its branches. Further testing, including blood work and a detailed imaging scan (CTA), showed thickening of the aortic walls and narrowing in several arteries, strongly suggesting Takayasu arteritis — a rare inflammatory disease that affects large arteries. She was started on prednisone and methotrexate to reduce inflammation. After three weeks, she had surgery to improve blood flow to her heart using a blood vessel from her chest. The surgery was successful, and she is now recovering well at home with regular follow-up.\"\n}", "generated_text": "A 36-year-old woman with ulcerative colitis had been doing well on medication but started experiencing worsening chest pain, shortness of breath, and symptoms like fatigue and night sweats. Her electrocardiogram showed abnormal changes in the lower part of her heart, and tests revealed signs of inflammation and heart damage. An emergency heart scan found severe blockages in two major coronary arteries, with the worst blockage in the right coronary artery. She had successful treatment with a stent placed in that artery. During the procedure, doctors noticed signs that might point to a condition called aortitis, which can cause inflammation in the aorta and its branches. Further testing, including blood work and a detailed imaging scan (CTA), showed thickening of the aortic walls and narrowing in several arteries, strongly suggesting Takayasu arteritis — a rare inflammatory disease that affects large arteries. She was started on prednisone and methotrexate to reduce inflammation. After three weeks, she had surgery to improve blood flow to her heart using a blood vessel from her chest. The surgery was successful, and she is now recovering well at home with regular follow-up."}
+{"row_index": 185, "doc_id": 13, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 36-year-old woman had a long-time stomach problem called ulcerative colitis, which she was managing with medicine. She started feeling chest pain that got worse over a week, along with shortness of breath and feeling tired and sweating at night. Tests showed her heart had damage, especially in the lower part, and two major blood vessels feeding the heart were badly blocked. Doctors fixed one of the blocked vessels with a stent and did a surgery later to fix the other. They also found signs of a rare inflammation in her blood vessels, especially around the aorta, which pointed to a condition called Takayasu arteritis. She was given steroids and a medicine to calm her immune system. After a few weeks, she had heart surgery that worked well, and she’s now doing fine at home.\"\n}", "generated_text": "A 36-year-old woman had a long-time stomach problem called ulcerative colitis, which she was managing with medicine. She started feeling chest pain that got worse over a week, along with shortness of breath and feeling tired and sweating at night. Tests showed her heart had damage, especially in the lower part, and two major blood vessels feeding the heart were badly blocked. Doctors fixed one of the blocked vessels with a stent and did a surgery later to fix the other. They also found signs of a rare inflammation in her blood vessels, especially around the aorta, which pointed to a condition called Takayasu arteritis. She was given steroids and a medicine to calm her immune system. After a few weeks, she had heart surgery that worked well, and she’s now doing fine at home."}
+{"row_index": 186, "doc_id": 13, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 36-year-old female with a history of ulcerative colitis, well-controlled on sulfasalazine, ferrous fumarate, and intermittent prednisone for flares, was admitted to the emergency department with a one-week history of progressive oppressive precordial pain associated with dyspnea and neurovegetative symptoms, including fatigue and night sweats. She reported a six-month history of generalized malaise, with prior episodes of effort-related precordial pain that had progressed to occur at rest. Physical examination revealed no murmurs or peripheral pulse abnormalities.\\n\\nElectrocardiography demonstrated sinus rhythm with supradesnivel (supra- or superior) ST-segment elevation in the inferior wall, indicating acute ischemia or infarction. Emergency coronary angiography revealed severe two-vessel coronary artery disease: a 90% ostial lesion in the left coronary trunk and a 99–100% subocclusive lesion at the ostial level of the right coronary artery (culprit vessel). Primary percutaneous coronary intervention (PCI) was performed with successful deployment of a drug-eluting stent in the right coronary artery. The hemodynamic team observed vascular friability during balloon advancement in the aortic arch, raising suspicion for aortic inflammation, prompting a targeted evaluation for systemic inflammatory or autoimmune etiology prior to surgical revascularization of the left coronary trunk.\\n\\nLaboratory findings included mild anemia (hemoglobin: 11.6 g/dL), mild leukocytosis (13,800/mm³), elevated erythrocyte sedimentation rate (ESR: 42 mm/h), elevated C-reactive protein (CRP: 4.9 mg/L; normal <1 mg/L), and elevated ultra-sensitive troponin, consistent with myocardial injury. Autoimmune workup showed normal complement levels (C3 and C4), negative anti-nuclear antibodies (ANA), anti-double-stranded DNA, negative extracellular nuclear antigen (ENA) profile, and non-reactive VDRL, excluding systemic lupus erythematosus and syphilis.\\n\\nCardiac magnetic resonance (CMR) with contrast revealed acute non-transmural infarction of the inferior wall of the left ventricle and subendocardial ischemia in the anteroseptoapical region at rest. Mild aortic and mitral regurgitation were noted, with preserved biventricular systolic function.\\n\\nComputed tomography angiography (CTA) of the chest, abdomen, and pelvis demonstrated periaortic fibrotic wall thickening involving the aortic root, aortic arch, and abdominal aorta, with severe stenosis of the left coronary trunk and mild stenosis of the left subclavian and left vertebral arteries. Severe stenosis of the lower mesenteric artery was also identified. These findings are consistent with Takayasu arteritis, a rare large-vessel vasculitis primarily affecting young women. Immunological evaluation revealed IgG level of 1,600 mg/dL (within reference range of 700–1,600 mg/dL), with elevated IgG1 (1024 mg/dL), and normal IgG2 (456 mg/dL), IgG3 (98.8 mg/dL), and IgG4 (13.6 mg/dL)—a pattern suggestive of IgG4-related disease, although the clinical diagnosis of Takayasu arteritis was established primarily through imaging and clinical context.\\n\\nThe patient was diagnosed with Takayasu arteritis based on clinical presentation, inflammatory markers, and imaging findings. Treatment was initiated with prednisone 60 mg daily, methotrexate 20 mg weekly by intramuscular injection, and folic acid 1 mg daily to mitigate methotrexate-induced toxicity. After three weeks of immunosuppressive therapy, the patient underwent delayed myocardial revascularization surgery using the left internal mammary artery (LIMA) as a graft to the descending anterior artery (DA) and an aortocoronary bypass to the circumflex artery. Intraoperatively, the aortic root and ascending aorta were found to be structurally intact, without evidence of significant inflammatory or fibrotic involvement. Postoperative recovery was uneventful, and the patient is currently stable at home under ambulatory follow-up with ongoing monitoring for disease activity and cardiovascular complications. The case illustrates the importance of considering large-vessel vasculitides in young patients with unexplained cardiovascular symptoms, particularly in the context of chronic inflammatory conditions such as inflammatory bowel disease.\"\n}", "generated_text": "A 36-year-old female with a history of ulcerative colitis, well-controlled on sulfasalazine, ferrous fumarate, and intermittent prednisone for flares, was admitted to the emergency department with a one-week history of progressive oppressive precordial pain associated with dyspnea and neurovegetative symptoms, including fatigue and night sweats. She reported a six-month history of generalized malaise, with prior episodes of effort-related precordial pain that had progressed to occur at rest. Physical examination revealed no murmurs or peripheral pulse abnormalities.\n\nElectrocardiography demonstrated sinus rhythm with supradesnivel (supra- or superior) ST-segment elevation in the inferior wall, indicating acute ischemia or infarction. Emergency coronary angiography revealed severe two-vessel coronary artery disease: a 90% ostial lesion in the left coronary trunk and a 99–100% subocclusive lesion at the ostial level of the right coronary artery (culprit vessel). Primary percutaneous coronary intervention (PCI) was performed with successful deployment of a drug-eluting stent in the right coronary artery. The hemodynamic team observed vascular friability during balloon advancement in the aortic arch, raising suspicion for aortic inflammation, prompting a targeted evaluation for systemic inflammatory or autoimmune etiology prior to surgical revascularization of the left coronary trunk.\n\nLaboratory findings included mild anemia (hemoglobin: 11.6 g/dL), mild leukocytosis (13,800/mm³), elevated erythrocyte sedimentation rate (ESR: 42 mm/h), elevated C-reactive protein (CRP: 4.9 mg/L; normal <1 mg/L), and elevated ultra-sensitive troponin, consistent with myocardial injury. Autoimmune workup showed normal complement levels (C3 and C4), negative anti-nuclear antibodies (ANA), anti-double-stranded DNA, negative extracellular nuclear antigen (ENA) profile, and non-reactive VDRL, excluding systemic lupus erythematosus and syphilis.\n\nCardiac magnetic resonance (CMR) with contrast revealed acute non-transmural infarction of the inferior wall of the left ventricle and subendocardial ischemia in the anteroseptoapical region at rest. Mild aortic and mitral regurgitation were noted, with preserved biventricular systolic function.\n\nComputed tomography angiography (CTA) of the chest, abdomen, and pelvis demonstrated periaortic fibrotic wall thickening involving the aortic root, aortic arch, and abdominal aorta, with severe stenosis of the left coronary trunk and mild stenosis of the left subclavian and left vertebral arteries. Severe stenosis of the lower mesenteric artery was also identified. These findings are consistent with Takayasu arteritis, a rare large-vessel vasculitis primarily affecting young women. Immunological evaluation revealed IgG level of 1,600 mg/dL (within reference range of 700–1,600 mg/dL), with elevated IgG1 (1024 mg/dL), and normal IgG2 (456 mg/dL), IgG3 (98.8 mg/dL), and IgG4 (13.6 mg/dL)—a pattern suggestive of IgG4-related disease, although the clinical diagnosis of Takayasu arteritis was established primarily through imaging and clinical context.\n\nThe patient was diagnosed with Takayasu arteritis based on clinical presentation, inflammatory markers, and imaging findings. Treatment was initiated with prednisone 60 mg daily, methotrexate 20 mg weekly by intramuscular injection, and folic acid 1 mg daily to mitigate methotrexate-induced toxicity. After three weeks of immunosuppressive therapy, the patient underwent delayed myocardial revascularization surgery using the left internal mammary artery (LIMA) as a graft to the descending anterior artery (DA) and an aortocoronary bypass to the circumflex artery. Intraoperatively, the aortic root and ascending aorta were found to be structurally intact, without evidence of significant inflammatory or fibrotic involvement. Postoperative recovery was uneventful, and the patient is currently stable at home under ambulatory follow-up with ongoing monitoring for disease activity and cardiovascular complications. The case illustrates the importance of considering large-vessel vasculitides in young patients with unexplained cardiovascular symptoms, particularly in the context of chronic inflammatory conditions such as inflammatory bowel disease."}
+{"row_index": 187, "doc_id": 14, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 36-year-old woman had trouble swallowing (dysphagia) and long-standing pain in her neck and upper chest. She also had a multinodular goiter, but no other major health issues. Imaging tests showed a rare birth defect called a mirror image right aortic arch. In this condition, the aorta (the main blood vessel from the heart) forms around the right bronchus and the arteries that supply the neck and arms develop in the opposite order to normal. This creates a ring around the esophagus and trachea, which can press on them and cause symptoms. In her case, the aortic arch and a small pouch called a Kommerell diverticulum (1.3 cm) were pressing on the esophagus, causing a narrowing of 60%. However, she had no serious complications like breathing problems, aneurysms, or aortic dissection, and her symptoms improved on their own over time. Because her condition was not causing major harm and she was doing well, no surgery was done. This rare condition usually doesn’t cause problems unless there is significant pressure on the airway or esophagus, or if there are other serious complications. Treatment is not standard and depends on the individual case.\"\n}", "generated_text": "A 36-year-old woman had trouble swallowing (dysphagia) and long-standing pain in her neck and upper chest. She also had a multinodular goiter, but no other major health issues. Imaging tests showed a rare birth defect called a mirror image right aortic arch. In this condition, the aorta (the main blood vessel from the heart) forms around the right bronchus and the arteries that supply the neck and arms develop in the opposite order to normal. This creates a ring around the esophagus and trachea, which can press on them and cause symptoms. In her case, the aortic arch and a small pouch called a Kommerell diverticulum (1.3 cm) were pressing on the esophagus, causing a narrowing of 60%. However, she had no serious complications like breathing problems, aneurysms, or aortic dissection, and her symptoms improved on their own over time. Because her condition was not causing major harm and she was doing well, no surgery was done. This rare condition usually doesn’t cause problems unless there is significant pressure on the airway or esophagus, or if there are other serious complications. Treatment is not standard and depends on the individual case."}
+{"row_index": 188, "doc_id": 14, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 36-year-old woman had trouble swallowing and pain in her neck and upper chest. She didn’t have other health problems. Doctors found a rare birth difference in her chest where the main blood vessel (aorta) loops around the right side of her airway and windpipe. This causes a small pouch (called Kommerell diverticulum) that presses on her esophagus. Most people with this don’t have symptoms, but if the pressure is strong or the blood vessel weakens or bursts, surgery might be needed. In this case, her symptoms were mild and didn’t affect her eating or health, so no surgery was done. Her symptoms got better on their own over time.\"\n}", "generated_text": "A 36-year-old woman had trouble swallowing and pain in her neck and upper chest. She didn’t have other health problems. Doctors found a rare birth difference in her chest where the main blood vessel (aorta) loops around the right side of her airway and windpipe. This causes a small pouch (called Kommerell diverticulum) that presses on her esophagus. Most people with this don’t have symptoms, but if the pressure is strong or the blood vessel weakens or bursts, surgery might be needed. In this case, her symptoms were mild and didn’t affect her eating or health, so no surgery was done. Her symptoms got better on their own over time."}
+{"row_index": 189, "doc_id": 15, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 62-year-old woman of North African descent, diagnosed with Von Hippel-Lindau disease in 2021, had several tumors involving her kidneys, adrenal glands, pancreas, and ovaries. She had a left bone tumor, a pheochromocytoma in her adrenal gland, a kidney cancer on the left side, a multi-cystic right kidney, and masses in her pancreas. She also had ovarian cysts that were found during imaging and surgery.\\n\\nShe underwent several surgeries: radiotherapy for a bone tumor, removal of her left adrenal gland and left kidney, and a major surgery to remove part of her pancreas. A tumor in her left ovary was found during a scan and later confirmed with imaging, raising concerns for cancer. Laparoscopic surgery revealed cystic tumors in both fallopian tubes and the area around the uterus. After a hysterectomy with removal of both ovaries, tissue tests showed clear-cell papillary cystadenomas in both tubes and the broad ligament — a known sign of Von Hippel-Lindau disease.\\n\\nShe recovered well after surgery and has been followed every four months with normal ultrasounds. However, she recently returned to the hospital for a new brain tumor, which is a known possible complication of this condition.\"\n}", "generated_text": "A 62-year-old woman of North African descent, diagnosed with Von Hippel-Lindau disease in 2021, had several tumors involving her kidneys, adrenal glands, pancreas, and ovaries. She had a left bone tumor, a pheochromocytoma in her adrenal gland, a kidney cancer on the left side, a multi-cystic right kidney, and masses in her pancreas. She also had ovarian cysts that were found during imaging and surgery.\n\nShe underwent several surgeries: radiotherapy for a bone tumor, removal of her left adrenal gland and left kidney, and a major surgery to remove part of her pancreas. A tumor in her left ovary was found during a scan and later confirmed with imaging, raising concerns for cancer. Laparoscopic surgery revealed cystic tumors in both fallopian tubes and the area around the uterus. After a hysterectomy with removal of both ovaries, tissue tests showed clear-cell papillary cystadenomas in both tubes and the broad ligament — a known sign of Von Hippel-Lindau disease.\n\nShe recovered well after surgery and has been followed every four months with normal ultrasounds. However, she recently returned to the hospital for a new brain tumor, which is a known possible complication of this condition."}
+{"row_index": 190, "doc_id": 15, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 62-year-old woman from Tunisia had a rare disease called Von Hippel-Lindau. In 2021, she was found to have tumors in several parts of her body, including her brain, kidneys, adrenal glands, pancreas, and ovaries. She had surgeries to remove tumors from her left kidney, left adrenal gland, and part of her pancreas. A tumor in her left ear bone was treated with radiation. An ovarian tumor was found during a scan and later confirmed as a cystic mass. Surgery showed tumors in her fallopian tubes and pelvic area, which are normal for this disease. After removing her uterus and both ovaries, the doctors found the tumors were clear-cell papillary cystadenomas, which match the disease. She has been doing well since, with no new problems, but recently came back because a brain tumor came back.\"\n}", "generated_text": "A 62-year-old woman from Tunisia had a rare disease called Von Hippel-Lindau. In 2021, she was found to have tumors in several parts of her body, including her brain, kidneys, adrenal glands, pancreas, and ovaries. She had surgeries to remove tumors from her left kidney, left adrenal gland, and part of her pancreas. A tumor in her left ear bone was treated with radiation. An ovarian tumor was found during a scan and later confirmed as a cystic mass. Surgery showed tumors in her fallopian tubes and pelvic area, which are normal for this disease. After removing her uterus and both ovaries, the doctors found the tumors were clear-cell papillary cystadenomas, which match the disease. She has been doing well since, with no new problems, but recently came back because a brain tumor came back."}
+{"row_index": 191, "doc_id": 16, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 59-year-old man with type 1 diabetes developed heart failure and was found to have infections on his heart valves. Tests showed large growths (vegetations) on both the mitral and aortic valves, which are signs of native valve endocarditis (NVE) — an infection of the heart valves caused by bacteria. The bacteria identified was Staphylococcus warneri, a type of common skin bacteria that can cause serious infections in people with weakened hearts or poor blood sugar control. He had no history of medical devices or immune problems, and the infection likely started from bacteria that had been living in his body for years. Before getting sick, he had mild signs like slight lab abnormalities, weight loss, and low blood counts, which may have been early warning signs of the infection. He was treated with antibiotics first, and after four weeks, he had surgery where both his mitral and aortic valves were replaced with mechanical valves. His heart function improved, and he has not had any problems since, over two years later. His poor diabetes control and high blood sugar likely made the surgery risky, so it was delayed until his health stabilized.\"\n}", "generated_text": "A 59-year-old man with type 1 diabetes developed heart failure and was found to have infections on his heart valves. Tests showed large growths (vegetations) on both the mitral and aortic valves, which are signs of native valve endocarditis (NVE) — an infection of the heart valves caused by bacteria. The bacteria identified was Staphylococcus warneri, a type of common skin bacteria that can cause serious infections in people with weakened hearts or poor blood sugar control. He had no history of medical devices or immune problems, and the infection likely started from bacteria that had been living in his body for years. Before getting sick, he had mild signs like slight lab abnormalities, weight loss, and low blood counts, which may have been early warning signs of the infection. He was treated with antibiotics first, and after four weeks, he had surgery where both his mitral and aortic valves were replaced with mechanical valves. His heart function improved, and he has not had any problems since, over two years later. His poor diabetes control and high blood sugar likely made the surgery risky, so it was delayed until his health stabilized."}
+{"row_index": 192, "doc_id": 16, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A man in his 50s with type 1 diabetes had heart problems that got worse. He started feeling short of breath and had a fever, but didn’t notice any other symptoms before. Doctors found big, sticky spots on his heart valves — these are signs of an infection called endocarditis. The infection was caused by a type of bacteria that lived in his body all along, not from a cut or injury. Before this, he had been losing weight slowly and had small signs like a slightly high white blood cell count and low blood proteins, which might have been early warning signs. He didn’t have any devices or medicines that weaken his immune system. Doctors treated him with antibiotics first, which helped his heart stop failing. After his heart stabilized, they did surgery to replace both his aortic and mitral heart valves because the infections were too serious. He recovered well and hasn’t had any problems since, two years later.\"\n}", "generated_text": "A man in his 50s with type 1 diabetes had heart problems that got worse. He started feeling short of breath and had a fever, but didn’t notice any other symptoms before. Doctors found big, sticky spots on his heart valves — these are signs of an infection called endocarditis. The infection was caused by a type of bacteria that lived in his body all along, not from a cut or injury. Before this, he had been losing weight slowly and had small signs like a slightly high white blood cell count and low blood proteins, which might have been early warning signs. He didn’t have any devices or medicines that weaken his immune system. Doctors treated him with antibiotics first, which helped his heart stop failing. After his heart stabilized, they did surgery to replace both his aortic and mitral heart valves because the infections were too serious. He recovered well and hasn’t had any problems since, two years later."}
+{"row_index": 193, "doc_id": 16, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 59-year-old Japanese man with a 28-year history of type 1 diabetes presented with acute heart failure and was diagnosed with native valve endocarditis (NVE) caused by Staphylococcus warneri, a coagulase-negative staphylococcus (CoNS). The patient had long-standing, poorly controlled diabetes, evidenced by severely depleted insulin secretion (serum C-peptide undetectable), persistent hyperglycemia (HbA1c ≈ 9.0%), and marked glycemic variability despite intensive multiple-dose insulin therapy. His body mass index was 18.4 kg/m² (height 168 cm, weight 52 kg), indicating underweight status, which may have contributed to impaired immune surveillance and increased susceptibility to infection. He had a pre-existing diagnosis of asymptomatic chronic severe (grade III) aortic regurgitation (AR) 16 years prior, which he had actively declined to monitor, leading to progressive valvular deterioration. No prosthetic devices or immunosuppressive therapies were implanted, and no prior history of medical device use or immunocompromise was reported.\\n\\nEight days prior to presentation, the patient presented to an emergency clinic with acute dyspnea and fever (>38°C), with no prior history of fever, chills, weakness, or systemic symptoms. On admission, vital signs included hypertension (192/82 mmHg) and tachycardia (118 bpm), orthopnea, and hypoxemia (SpO₂ 80%). Physical examination revealed a Levine 3/6 systolic murmur, a finding not previously documented during routine follow-up. No classic signs of infective endocarditis (IE) such as Osler nodes, Janeway lesions, or conjunctival petechiae were observed. Laboratory findings showed marked leukocytosis (WBC 20,800 /μL), elevated C-reactive protein (CRP 6.06 mg/dL), normal serum creatine phosphokinase MB (6.0 IU/L), and negative troponin T, suggesting myocardial injury was not present. Chest X-ray demonstrated pulmonary congestion and cardiac enlargement (cardiothoracic ratio 55%). Electrocardiography showed ST elevation in leads V1–V4, consistent with acute strain or ischemia, but emergency transthoracic echocardiography revealed preserved left ventricular contractility, indicating that the hemodynamic compromise was primarily due to valvular dysfunction.\\n\\nTransthoracic echocardiography revealed severe aortic and mitral regurgitation, with a mobile vegetation detected on the mitral valve. Transesophageal echocardiography confirmed a 16.5×6-mm mobile vegetation on the anterior mitral valve leaflet and an 11.2×5-mm nonmobile vegetation on the noncoronary cusp of the aortic valve. These findings met the clinical criteria for native valve endocarditis, particularly given the size and mobility of the vegetations. Imaging with head CT and MRI showed no evidence of cerebral infarction or hemorrhage, though the presence of a mobile vegetation was confirmed, raising concern for embolic risk. Retrospective review of pre-admission laboratory data revealed subtle abnormalities: four months prior to admission, a slight elevation in WBC was noted; subsequently, serum albumin declined to 3.0 g/dL, hemoglobin showed a gradual decline over two months, and the patient experienced a 4-kg weight loss. These findings, though non-specific, may represent early signs of systemic infection or malignancy. Esophagogastroduodenoscopy and whole-body CT were unremarkable. One month later, the patient regained weight and laboratory values nearly normalized (except for mild CRP elevation at 0.54 mg/dL). However, at the visit eight days before admission, WBC rose to 9,300 /μL, Hb and albumin dropped again to 13.1 g/dL and 3.0 g/dL, and CRP increased to 4.18 mg/dL, with a concomitant drop in diastolic blood pressure, suggesting a recurrent inflammatory or infectious process.\\n\\nEmpirical intravenous antibiotic therapy was initiated with 12 g/day ampicillin sulbactam (ABPC/S) and 120 mg/day gentamicin (GM). Three blood culture sets obtained upon admission were positive for S. warneri, with minimal inhibitory concentrations (MICs) of ≤8 μg/mL for ABPC/S, ≤1 μg/mL for GM, and ≤2 μg/mL for cefazolin (CEZ), confirming susceptibility to these agents. The organism was identified as a member of the CoNS family, known for its", "generated_text": "{\n  \"proficient_health_literacy\": \"A 59-year-old Japanese man with a 28-year history of type 1 diabetes presented with acute heart failure and was diagnosed with native valve endocarditis (NVE) caused by Staphylococcus warneri, a coagulase-negative staphylococcus (CoNS). The patient had long-standing, poorly controlled diabetes, evidenced by severely depleted insulin secretion (serum C-peptide undetectable), persistent hyperglycemia (HbA1c ≈ 9.0%), and marked glycemic variability despite intensive multiple-dose insulin therapy. His body mass index was 18.4 kg/m² (height 168 cm, weight 52 kg), indicating underweight status, which may have contributed to impaired immune surveillance and increased susceptibility to infection. He had a pre-existing diagnosis of asymptomatic chronic severe (grade III) aortic regurgitation (AR) 16 years prior, which he had actively declined to monitor, leading to progressive valvular deterioration. No prosthetic devices or immunosuppressive therapies were implanted, and no prior history of medical device use or immunocompromise was reported.\\n\\nEight days prior to presentation, the patient presented to an emergency clinic with acute dyspnea and fever (>38°C), with no prior history of fever, chills, weakness, or systemic symptoms. On admission, vital signs included hypertension (192/82 mmHg) and tachycardia (118 bpm), orthopnea, and hypoxemia (SpO₂ 80%). Physical examination revealed a Levine 3/6 systolic murmur, a finding not previously documented during routine follow-up. No classic signs of infective endocarditis (IE) such as Osler nodes, Janeway lesions, or conjunctival petechiae were observed. Laboratory findings showed marked leukocytosis (WBC 20,800 /μL), elevated C-reactive protein (CRP 6.06 mg/dL), normal serum creatine phosphokinase MB (6.0 IU/L), and negative troponin T, suggesting myocardial injury was not present. Chest X-ray demonstrated pulmonary congestion and cardiac enlargement (cardiothoracic ratio 55%). Electrocardiography showed ST elevation in leads V1–V4, consistent with acute strain or ischemia, but emergency transthoracic echocardiography revealed preserved left ventricular contractility, indicating that the hemodynamic compromise was primarily due to valvular dysfunction.\\n\\nTransthoracic echocardiography revealed severe aortic and mitral regurgitation, with a mobile vegetation detected on the mitral valve. Transesophageal echocardiography confirmed a 16.5×6-mm mobile vegetation on the anterior mitral valve leaflet and an 11.2×5-mm nonmobile vegetation on the noncoronary cusp of the aortic valve. These findings met the clinical criteria for native valve endocarditis, particularly given the size and mobility of the vegetations. Imaging with head CT and MRI showed no evidence of cerebral infarction or hemorrhage, though the presence of a mobile vegetation was confirmed, raising concern for embolic risk. Retrospective review of pre-admission laboratory data revealed subtle abnormalities: four months prior to admission, a slight elevation in WBC was noted; subsequently, serum albumin declined to 3.0 g/dL, hemoglobin showed a gradual decline over two months, and the patient experienced a 4-kg weight loss. These findings, though non-specific, may represent early signs of systemic infection or malignancy. Esophagogastroduodenoscopy and whole-body CT were unremarkable. One month later, the patient regained weight and laboratory values nearly normalized (except for mild CRP elevation at 0.54 mg/dL). However, at the visit eight days before admission, WBC rose to 9,300 /μL, Hb and albumin dropped again to 13.1 g/dL and 3.0 g/dL, and CRP increased to 4.18 mg/dL, with a concomitant drop in diastolic blood pressure, suggesting a recurrent inflammatory or infectious process.\\n\\nEmpirical intravenous antibiotic therapy was initiated with 12 g/day ampicillin sulbactam (ABPC/S) and 120 mg/day gentamicin (GM). Three blood culture sets obtained upon admission were positive for S. warneri, with minimal inhibitory concentrations (MICs) of ≤8 μg/mL for ABPC/S, ≤1 μg/mL for GM, and ≤2 μg/mL for cefazolin (CEZ), confirming susceptibility to these agents. The organism was identified as a member of the CoNS family, known for its"}
+{"row_index": 194, "doc_id": 17, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 27-year-old woman with a family history of colorectal cancer (familial adenomatous polyposis) had multiple cancers in her colon and rectum. To treat this, she underwent a complex robotic surgery called robot-assisted total proctocolectomy (TPC), which included removing lymph nodes from the entire colorectal area using the Hugo RAS system. The surgery was done in three main steps: first, the ascending colon was removed along with its surrounding tissue (complete mesocolic excision) while the patient was in a Trendelenburg position; second, the descending colon was removed, and the rectum was fully excised with detailed lymph node removal (D3 dissection); and third, the superior mesenteric artery was ligated to stop blood flow to the colon. After the surgery, the tumor sample was removed through the anus, and a new pouch made from part of the small intestine was created and connected to the anus (ileal pouch-anal anastomosis). The entire procedure took 632 minutes and involved only minimal blood loss. The patient recovered smoothly, started eating liquids on day 1, and returned to a regular diet by day 3. Pathology showed two sigmoid colon cancers and one rectal cancer, with 18 of 89 lymph nodes found to be positive, indicating the cancer had spread to nearby lymph nodes. The cancer stage was classified as pT1bN2b.\"\n}", "generated_text": "A 27-year-old woman with a family history of colorectal cancer (familial adenomatous polyposis) had multiple cancers in her colon and rectum. To treat this, she underwent a complex robotic surgery called robot-assisted total proctocolectomy (TPC), which included removing lymph nodes from the entire colorectal area using the Hugo RAS system. The surgery was done in three main steps: first, the ascending colon was removed along with its surrounding tissue (complete mesocolic excision) while the patient was in a Trendelenburg position; second, the descending colon was removed, and the rectum was fully excised with detailed lymph node removal (D3 dissection); and third, the superior mesenteric artery was ligated to stop blood flow to the colon. After the surgery, the tumor sample was removed through the anus, and a new pouch made from part of the small intestine was created and connected to the anus (ileal pouch-anal anastomosis). The entire procedure took 632 minutes and involved only minimal blood loss. The patient recovered smoothly, started eating liquids on day 1, and returned to a regular diet by day 3. Pathology showed two sigmoid colon cancers and one rectal cancer, with 18 of 89 lymph nodes found to be positive, indicating the cancer had spread to nearby lymph nodes. The cancer stage was classified as pT1bN2b."}
+{"row_index": 195, "doc_id": 18, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 65-year-old man had a motorcycle accident six months ago, which injured his right middle finger. After the fall, he couldn't fully extend his finger and noticed swelling. Over time, the finger developed a deformity called boutonniere deformity, where the middle joint bends and the tip of the finger extends too far. An X-ray showed no bone damage, so the problem was caused by soft tissue injury — specifically, a tear in the central slip of the finger's extensor tendon.\\n\\nThe doctor repaired the injury by using a part of the ulnar side of the flexor tendon (FDS) to replace the damaged central slip. The surgery was done under anesthesia, with the finger carefully opened and the damaged tissue removed. The new tendon was passed through a small tunnel in the bone and secured with sutures to restore normal movement.\\n\\nAfter surgery, the patient wore a splint for two weeks to keep the finger extended. Once the wound healed, he started gentle exercises to improve finger movement. After one month, his middle finger could move from 0 to 100 degrees, and after two months, movement returned to normal (0 to 110 degrees). His hand function improved dramatically, as shown by the DASH score, which went from 50 (indicating poor function) to 4.2 (indicating nearly normal function). He was able to return to work and daily activities with much better finger control.\"\n}", "generated_text": "A 65-year-old man had a motorcycle accident six months ago, which injured his right middle finger. After the fall, he couldn't fully extend his finger and noticed swelling. Over time, the finger developed a deformity called boutonniere deformity, where the middle joint bends and the tip of the finger extends too far. An X-ray showed no bone damage, so the problem was caused by soft tissue injury — specifically, a tear in the central slip of the finger's extensor tendon.\n\nThe doctor repaired the injury by using a part of the ulnar side of the flexor tendon (FDS) to replace the damaged central slip. The surgery was done under anesthesia, with the finger carefully opened and the damaged tissue removed. The new tendon was passed through a small tunnel in the bone and secured with sutures to restore normal movement.\n\nAfter surgery, the patient wore a splint for two weeks to keep the finger extended. Once the wound healed, he started gentle exercises to improve finger movement. After one month, his middle finger could move from 0 to 100 degrees, and after two months, movement returned to normal (0 to 110 degrees). His hand function improved dramatically, as shown by the DASH score, which went from 50 (indicating poor function) to 4.2 (indicating nearly normal function). He was able to return to work and daily activities with much better finger control."}
+{"row_index": 196, "doc_id": 18, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 65-year-old male patient presented with a six-month history of swelling and boutonniere deformity involving the right middle finger (digiti III) following a motorcycle accident on January 1, 2023. The initial injury resulted in traumatic disruption of the central slip of the flexor digitorum superficialis (FDS) tendon, leading to impaired extension of the proximal interphalangeal (PIP) joint. The patient initially managed symptoms with analgesics without seeking medical evaluation. Clinical examination revealed persistent edema, active range of motion (ROM) of the PIP joint limited to 45–110 degrees, and passive ROM within normal limits, indicating a soft tissue pathology rather than bony involvement. Radiographic assessment via anteroposterior (AP) and lateral views of the right hand demonstrated no osseous abnormalities, confirming the deformity as originating from a central slip defect.\\n\\nSurgical intervention was performed via a midlateral incision on the ulnar aspect of the right middle phalanx, centered at the PIP joint, extending dorsally in an oblique fashion. A transverse incision was made proximal to the A1 pulley at the metacarpophalangeal (MCP) joint flexion crease. The ulnar neurovascular bundle was identified and preserved throughout the procedure. The central slip was exposed, and interposed scar tissue and pseudotendinous tissue were excised. Due to the inability to repair the central slip primarily, reconstruction was achieved using the ulnar slip of the FDS tendon.\\n\\nThe extensor tendon was mobilized and tenolyzed, and the dorsal capsule of the PIP joint was incised and debrided. The A3 pulley's periosteal insertion was longitudinally incised, and the volar capsule of the PIP joint was similarly opened. The ulnar slip of the FDS tendon was isolated and transected to release it from its proximal attachment, avoiding entrapment of the radial slip. A 2–0 non-absorbable monofilament suture was placed around the ulnar slip at the PIP joint level and used to release the distal portion of the FDS tendon slip, enabling distal transposition of the ulnar slip. A 2.8-mm drill was used to create a vertically oriented dorsal bone tunnel, positioned posterior to the volar plate. An elevator was placed between the flexor digitorum profundus (FDP) tendon, the volar plate, and the volar base of the middle phalanx to protect adjacent anatomic structures. The FDS tendon slip was passed through the tunnel while maintaining the PIP joint in full extension and reduced position, traversing the intact proximal segment of the central slip and extensor tendon. A pulvertaft weave was completed using a tendon weaver to ensure proper tension and biomechanical stability, with a 3–0 non-absorbable suture securing the weave. The margins of the joint capsule and central slip reconstruction were approximated, and adhesions were released with mobilization of the lateral bands.\\n\\nPostoperative care included a 4-day follow-up for wound management, with administration of oral meloxicam 7.5 mg twice daily and doxycycline 100 mg twice daily for three days. A second follow-up was conducted three days later. At two weeks postoperatively, the posterior splint was removed, external sutures were discontinued, and both active and passive range of motion exercises were initiated. At three weeks, wound healing was confirmed, and the PIP joint ROM improved to 0–90 degrees. One month postoperatively, ROM reached 0–100 degrees, with significant functional improvement. By seven weeks, the patient achieved full active ROM of 0–110 degrees and returned to work. Functional outcome was assessed using the DASH (Disability of Arm, Shoulder, and Hand) score, which decreased from 50 (indicating moderate disability) to 4.2 (indicating minimal disability), reflecting a substantial restoration of hand function. The surgical reconstruction successfully restored biomechanical alignment, joint stability, and functional capacity of the PIP joint through precise tendon transfer and pulvertaft tenodesis, with no evidence of bony pathology on imaging.\"\n}", "generated_text": "A 65-year-old male patient presented with a six-month history of swelling and boutonniere deformity involving the right middle finger (digiti III) following a motorcycle accident on January 1, 2023. The initial injury resulted in traumatic disruption of the central slip of the flexor digitorum superficialis (FDS) tendon, leading to impaired extension of the proximal interphalangeal (PIP) joint. The patient initially managed symptoms with analgesics without seeking medical evaluation. Clinical examination revealed persistent edema, active range of motion (ROM) of the PIP joint limited to 45–110 degrees, and passive ROM within normal limits, indicating a soft tissue pathology rather than bony involvement. Radiographic assessment via anteroposterior (AP) and lateral views of the right hand demonstrated no osseous abnormalities, confirming the deformity as originating from a central slip defect.\n\nSurgical intervention was performed via a midlateral incision on the ulnar aspect of the right middle phalanx, centered at the PIP joint, extending dorsally in an oblique fashion. A transverse incision was made proximal to the A1 pulley at the metacarpophalangeal (MCP) joint flexion crease. The ulnar neurovascular bundle was identified and preserved throughout the procedure. The central slip was exposed, and interposed scar tissue and pseudotendinous tissue were excised. Due to the inability to repair the central slip primarily, reconstruction was achieved using the ulnar slip of the FDS tendon.\n\nThe extensor tendon was mobilized and tenolyzed, and the dorsal capsule of the PIP joint was incised and debrided. The A3 pulley's periosteal insertion was longitudinally incised, and the volar capsule of the PIP joint was similarly opened. The ulnar slip of the FDS tendon was isolated and transected to release it from its proximal attachment, avoiding entrapment of the radial slip. A 2–0 non-absorbable monofilament suture was placed around the ulnar slip at the PIP joint level and used to release the distal portion of the FDS tendon slip, enabling distal transposition of the ulnar slip. A 2.8-mm drill was used to create a vertically oriented dorsal bone tunnel, positioned posterior to the volar plate. An elevator was placed between the flexor digitorum profundus (FDP) tendon, the volar plate, and the volar base of the middle phalanx to protect adjacent anatomic structures. The FDS tendon slip was passed through the tunnel while maintaining the PIP joint in full extension and reduced position, traversing the intact proximal segment of the central slip and extensor tendon. A pulvertaft weave was completed using a tendon weaver to ensure proper tension and biomechanical stability, with a 3–0 non-absorbable suture securing the weave. The margins of the joint capsule and central slip reconstruction were approximated, and adhesions were released with mobilization of the lateral bands.\n\nPostoperative care included a 4-day follow-up for wound management, with administration of oral meloxicam 7.5 mg twice daily and doxycycline 100 mg twice daily for three days. A second follow-up was conducted three days later. At two weeks postoperatively, the posterior splint was removed, external sutures were discontinued, and both active and passive range of motion exercises were initiated. At three weeks, wound healing was confirmed, and the PIP joint ROM improved to 0–90 degrees. One month postoperatively, ROM reached 0–100 degrees, with significant functional improvement. By seven weeks, the patient achieved full active ROM of 0–110 degrees and returned to work. Functional outcome was assessed using the DASH (Disability of Arm, Shoulder, and Hand) score, which decreased from 50 (indicating moderate disability) to 4.2 (indicating minimal disability), reflecting a substantial restoration of hand function. The surgical reconstruction successfully restored biomechanical alignment, joint stability, and functional capacity of the PIP joint through precise tendon transfer and pulvertaft tenodesis, with no evidence of bony pathology on imaging."}
+{"row_index": 197, "doc_id": 19, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 23-year-old man came to the emergency room with a sudden, very severe headache that lasted for two hours, along with nausea, vomiting, and a feeling of chest heaviness. He had high blood pressure and a fast breathing rate. An emergency heart test (ECG) showed signs of a heart attack (STEMI), so he was quickly taken to a specialized center for treatment. During the procedure, his coronary arteries were found to be normal, meaning there was no blockage. However, a brain scan (CT) later revealed a cisternal subarachnoid hemorrhage (SAH), which is bleeding in the space around the brain. This condition was likely the cause of his symptoms. Despite being treated with medications, monitored closely, and given supportive care, his condition worsened rapidly. He suffered a cardiac arrest and could not be revived. He died after seven days in the intensive care unit.\"\n}", "generated_text": "A 23-year-old man came to the emergency room with a sudden, very severe headache that lasted for two hours, along with nausea, vomiting, and a feeling of chest heaviness. He had high blood pressure and a fast breathing rate. An emergency heart test (ECG) showed signs of a heart attack (STEMI), so he was quickly taken to a specialized center for treatment. During the procedure, his coronary arteries were found to be normal, meaning there was no blockage. However, a brain scan (CT) later revealed a cisternal subarachnoid hemorrhage (SAH), which is bleeding in the space around the brain. This condition was likely the cause of his symptoms. Despite being treated with medications, monitored closely, and given supportive care, his condition worsened rapidly. He suffered a cardiac arrest and could not be revived. He died after seven days in the intensive care unit."}
+{"row_index": 198, "doc_id": 19, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 23-year-old man came to the hospital with a sudden, very bad headache that lasted two hours. He also had nausea, vomiting, and felt like his chest was heavy. His blood pressure was very high, and he was breathing fast. An emergency heart test showed a sign of a heart attack, so they rushed him to get treated. But when they looked at his heart tubes, they found no blockage — the heart was fine. Instead, a brain scan showed bleeding around the brain, which can be deadly. Even with doctors working together to help, his condition got worse quickly. He had a heart stoppage and couldn't be saved. He passed away.\"\n}", "generated_text": "A 23-year-old man came to the hospital with a sudden, very bad headache that lasted two hours. He also had nausea, vomiting, and felt like his chest was heavy. His blood pressure was very high, and he was breathing fast. An emergency heart test showed a sign of a heart attack, so they rushed him to get treated. But when they looked at his heart tubes, they found no blockage — the heart was fine. Instead, a brain scan showed bleeding around the brain, which can be deadly. Even with doctors working together to help, his condition got worse quickly. He had a heart stoppage and couldn't be saved. He passed away."}
+{"row_index": 199, "doc_id": 19, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 23-year-old male presented to the emergency department with a sudden onset of severe frontal headache lasting two hours, accompanied by nausea, vomiting, and chest heaviness. His medical history was unremarkable, with no known illicit drug use; however, he had a significant smoking history of 23 pack-years and denied alcohol consumption. Physical examination revealed acute distress, full consciousness, and orientation to time, place, and person. Chest auscultation demonstrated normal vesicular breath sounds, while cardiovascular and abdominal examinations were non-specific. Neurological assessment identified neck stiffness, bilateral dilated pupils with intact light reflexes, normal plantar responses, and no focal neurological deficits. Vital signs showed hypertension (blood pressure 178/103 mmHg), tachypnea (respiratory rate 26 breaths/min), fever (temperature 38.9°C), heart rate of 87 beats/min, and oxygen saturation of 94%.\\n\\nEmergency evaluation included an electrocardiogram (ECG), which demonstrated ST-segment elevation greater than 2 mm in leads V2–V5, consistent with acute ST-elevation myocardial infarction (STEMI) as the primary differential diagnosis. This prompted immediate referral to a tertiary cardiac center for percutaneous coronary intervention (PCI). Prior to transfer, a 300 mg aspirin loading dose was administered. Cardiac biomarkers revealed markedly elevated troponin levels (1.48 mg/dL, normal <0.16 mg/dL), confirming myocardial injury. PCI via the femoral artery was performed, with coronary angiography showing normal coronary artery anatomy and TIMI flow grade 3, indicating patent vessel flow. Post-procedure ECG showed normal sinus rhythm with evidence of left ventricular hypertrophy (LVH). Echocardiography confirmed preserved left ventricular systolic function with no regional wall motion abnormalities (RWMA), suggesting no acute ischemic injury to myocardial segments.\\n\\nFollowing PCI, the patient was admitted to the medical ward for further workup. Laboratory tests included complete blood count (CBC), random blood glucose, renal function tests, and C-reactive protein (CRP), which revealed lymphocytosis and a mildly elevated CRP, suggestive of inflammatory or infectious processes. A non-contrast head CT was performed to evaluate the cause of the headache, which identified a cisternal subarachnoid hemorrhage (SAH) extending anterior to the right temporal lobe. Abdominal ultrasound was conducted to exclude polycystic kidney disease, which was negative. Cerebral CT angiography was planned to assess for the presence of a cerebral aneurysm, a common source of spontaneous SAH. Nimodipine 60 mg every 4 hours was initiated to prevent cerebral vasospasm, with a target mean arterial pressure of 160/100 mmHg to optimize cerebral perfusion.\\n\\nOn day two, the patient experienced a rapid clinical deterioration, culminating in in-hospital cardiac arrest. Cardiopulmonary resuscitation (CPR) was initiated, resulting in a Glasgow Coma Scale (GCS) score of 6, indicating severe neurological impairment. The patient was intubated and placed on mechanical ventilation in the intensive care unit (ICU). Due to hemodynamic instability and deteriorating neurological status, repeated neuroimaging and the planned cerebral CT angiography were not performed.\\n\\nOver the subsequent seven days, the patient was managed with a multidisciplinary approach, including nasogastric tube placement for enteral nutrition and fluid resuscitation. Medications administered included intravenous fluids, broad-spectrum antibiotics (to rule out systemic infection), proton pump inhibitors (to prevent stress-induced gastric mucosal injury), and continued nimodipine therapy.\\n\\nOn day eight, the patient developed sudden ventricular fibrillation, which persisted despite multiple defibrillation attempts (greater than five shocks). Despite aggressive resuscitation efforts, return of spontaneous circulation was not achieved, and the patient died. The case highlights the diagnostic challenge of differentiating between acute coronary syndrome and subarachnoid hemorrhage in a young patient with non-classic risk factors, where initial ECG findings may misdirect early management. The presence of SAH in a young individual without known vascular pathology or hypertension underscores the importance of neuroimaging in the evaluation of acute headaches with systemic symptoms, particularly when cardiovascular findings are initially suggestive of myocardial infarction. The coexistence of SAH and STEMI in this patient may reflect a rare, potentially shared pathophysiological mechanism, such as vasospasm or microvascular injury, though no direct causal link has been established. The absence of coronary atherosclerosis in this patient further emphasizes that STEMI in young individuals can arise from non-atherosclerotic etiologies, including coronary vasospasm, thrombosis, or", "generated_text": "{\n  \"proficient_health_literacy\": \"A 23-year-old male presented to the emergency department with a sudden onset of severe frontal headache lasting two hours, accompanied by nausea, vomiting, and chest heaviness. His medical history was unremarkable, with no known illicit drug use; however, he had a significant smoking history of 23 pack-years and denied alcohol consumption. Physical examination revealed acute distress, full consciousness, and orientation to time, place, and person. Chest auscultation demonstrated normal vesicular breath sounds, while cardiovascular and abdominal examinations were non-specific. Neurological assessment identified neck stiffness, bilateral dilated pupils with intact light reflexes, normal plantar responses, and no focal neurological deficits. Vital signs showed hypertension (blood pressure 178/103 mmHg), tachypnea (respiratory rate 26 breaths/min), fever (temperature 38.9°C), heart rate of 87 beats/min, and oxygen saturation of 94%.\\n\\nEmergency evaluation included an electrocardiogram (ECG), which demonstrated ST-segment elevation greater than 2 mm in leads V2–V5, consistent with acute ST-elevation myocardial infarction (STEMI) as the primary differential diagnosis. This prompted immediate referral to a tertiary cardiac center for percutaneous coronary intervention (PCI). Prior to transfer, a 300 mg aspirin loading dose was administered. Cardiac biomarkers revealed markedly elevated troponin levels (1.48 mg/dL, normal <0.16 mg/dL), confirming myocardial injury. PCI via the femoral artery was performed, with coronary angiography showing normal coronary artery anatomy and TIMI flow grade 3, indicating patent vessel flow. Post-procedure ECG showed normal sinus rhythm with evidence of left ventricular hypertrophy (LVH). Echocardiography confirmed preserved left ventricular systolic function with no regional wall motion abnormalities (RWMA), suggesting no acute ischemic injury to myocardial segments.\\n\\nFollowing PCI, the patient was admitted to the medical ward for further workup. Laboratory tests included complete blood count (CBC), random blood glucose, renal function tests, and C-reactive protein (CRP), which revealed lymphocytosis and a mildly elevated CRP, suggestive of inflammatory or infectious processes. A non-contrast head CT was performed to evaluate the cause of the headache, which identified a cisternal subarachnoid hemorrhage (SAH) extending anterior to the right temporal lobe. Abdominal ultrasound was conducted to exclude polycystic kidney disease, which was negative. Cerebral CT angiography was planned to assess for the presence of a cerebral aneurysm, a common source of spontaneous SAH. Nimodipine 60 mg every 4 hours was initiated to prevent cerebral vasospasm, with a target mean arterial pressure of 160/100 mmHg to optimize cerebral perfusion.\\n\\nOn day two, the patient experienced a rapid clinical deterioration, culminating in in-hospital cardiac arrest. Cardiopulmonary resuscitation (CPR) was initiated, resulting in a Glasgow Coma Scale (GCS) score of 6, indicating severe neurological impairment. The patient was intubated and placed on mechanical ventilation in the intensive care unit (ICU). Due to hemodynamic instability and deteriorating neurological status, repeated neuroimaging and the planned cerebral CT angiography were not performed.\\n\\nOver the subsequent seven days, the patient was managed with a multidisciplinary approach, including nasogastric tube placement for enteral nutrition and fluid resuscitation. Medications administered included intravenous fluids, broad-spectrum antibiotics (to rule out systemic infection), proton pump inhibitors (to prevent stress-induced gastric mucosal injury), and continued nimodipine therapy.\\n\\nOn day eight, the patient developed sudden ventricular fibrillation, which persisted despite multiple defibrillation attempts (greater than five shocks). Despite aggressive resuscitation efforts, return of spontaneous circulation was not achieved, and the patient died. The case highlights the diagnostic challenge of differentiating between acute coronary syndrome and subarachnoid hemorrhage in a young patient with non-classic risk factors, where initial ECG findings may misdirect early management. The presence of SAH in a young individual without known vascular pathology or hypertension underscores the importance of neuroimaging in the evaluation of acute headaches with systemic symptoms, particularly when cardiovascular findings are initially suggestive of myocardial infarction. The coexistence of SAH and STEMI in this patient may reflect a rare, potentially shared pathophysiological mechanism, such as vasospasm or microvascular injury, though no direct causal link has been established. The absence of coronary atherosclerosis in this patient further emphasizes that STEMI in young individuals can arise from non-atherosclerotic etiologies, including coronary vasospasm, thrombosis, or"}
diff --git a/code/RL_model/inference_data/inference_20260213_002423.jsonl b/code/RL_model/inference_data/inference_20260213_002423.jsonl
new file mode 100644
index 0000000000000000000000000000000000000000..fd21aec772cc8cde6be6e6e72c120353a7475e0e
--- /dev/null
+++ b/code/RL_model/inference_data/inference_20260213_002423.jsonl
@@ -0,0 +1,2 @@
+{"row_index": 0, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 35-year-old woman had a lump on her cheek side (parotid gland) that grew over 2 years. At first, it looked like a slow-growing tumor, but later it got bigger and caused her face to droop. Doctors saw a hard, fixed lump that spread into nearby muscles. An MRI showed the lump was growing deep inside and had spread beyond the gland. She had surgery to remove the whole lump and nearby lymph nodes, keeping her facial nerve safe. Path tests confirmed it was a rare cancer called PNET, which often starts in nerves and has a special genetic change in 60% of the cells. After surgery, she got chemotherapy (four rounds of drugs: vincristine, doxorubicin, cyclophosphamide, ifosfamide, and etoposide) and then radiation to the area. Her body handled the treatment well, with only mild side effects. She checks in every 3 months with scans, and so far, no signs of cancer coming back.\"\n}"}
+{"row_index": 1, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 35-year-old woman developed a lump in her left parotid gland two years earlier. Initially, a small biopsy showed a non-cancerous mixed salivary gland tumor, and she had surgery that removed the mass completely. Six months later, a new, firm, painful lump appeared near the surgical site, and she began to lose movement on her left side—this is known as facial paralysis. An MRI scan showed a growing mass measuring 42 mm that had spread into nearby muscles and was not clearly defined. After further testing, doctors found it was a rare cancer called extra-skeletal Ewing’s sarcoma, a type of primary peripheral neuroectodermal tumor (PNET). This tumor has a specific genetic change (EWING/PNET-type translocation) found in 60% of the cells. She had surgery to remove the entire left parotid gland and nearby lymph nodes, with care taken to preserve her facial nerve. Following surgery, she received chemotherapy using a combination of drugs—vincristine, doxorubicin, cyclophosphamide, ifosfamide, and etoposide—for four cycles, followed by external radiation therapy. The treatment was well tolerated, with only mild side effects like mouth sores and skin irritation. At 10 months after treatment, there was no sign of the cancer coming back locally or elsewhere in her body.\"\n}"}
diff --git a/code/RL_model/inference_data/vllm_inference_20260213_003845.jsonl b/code/RL_model/inference_data/vllm_inference_20260213_003845.jsonl
new file mode 100644
index 0000000000000000000000000000000000000000..5e876f419ca35655a5425ecd47d73a1794c581e6
--- /dev/null
+++ b/code/RL_model/inference_data/vllm_inference_20260213_003845.jsonl
@@ -0,0 +1,510 @@
+{"row_index": 0, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 35-year-old woman had a lump on the side of her face, on the left side, that grew over 2 years. At first, it looked like a harmless gland tumor, but later it got bigger and caused her face to droop. Doctors saw a hard, fixed lump that had spread into nearby muscles. An MRI showed the lump was growing inside the gland and had spread to muscles around it. She had surgery to remove the whole lump and nearby lymph nodes, and her facial nerve was kept safe. The test results showed this was a rare cancer called PNET, which starts in nerve tissue, and it had a special genetic change found in 60% of the cancer cells. After surgery, she got chemotherapy with four cycles of drugs (vincristine, doxorubicin, cyclophosphamide, ifosfamide, and etoposide), followed by radiation to the area. The treatment worked well, with only mild side effects like sore mouth and mild skin issues. She’s been checked every 3 months, and so far, no signs of cancer have come back.\"\n}"}
+{"row_index": 1, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 35-year-old woman developed a tumor in her left parotid gland, a small gland near the jaw, two years prior. Initially, a small tumor was found, and a biopsy showed it was not cancerous. She had surgery to remove it, and the margins were clear, meaning no cancer was found at the edges. Six months later, a new, firm, painful lump appeared near the surgical site, and she began to lose movement on her left side—this is called facial paralysis. An MRI scan showed a larger tumor, measuring 42 mm, that had spread into nearby muscles and was not well-defined. The tumor was confirmed as a rare type of cancer called extra-skeletal Ewing’s sarcoma, a primary peripheral neuroectodermal tumor (PNET), which is known for spreading quickly. Pathology tests showed the tumor had a specific genetic change (EWING/PNET-type translocation) in 60% of its cells. She had surgery to remove the entire left parotid gland and nearby lymph nodes, with care taken to preserve the facial nerve. After surgery, she received chemotherapy with four cycles of vincristine, doxorubicin, cyclophosphamide, alternating with ifosfamide and etoposide, followed by external radiation therapy. The treatment was well-tolerated, with only mild side effects like mouth sores and mild skin irritation. She has been followed every three months with MRI scans, and at 10 months, there has been no sign of the cancer coming back locally or in distant parts of the body.\"\n}"}
+{"row_index": 2, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 35-year-old female with no significant past medical history presented with a left parotid tumefaction that had been progressing over the previous two years. Initial biopsy revealed a mixed salivary gland tumor measuring 28 mm, which was histologically non-malignant, and she underwent a large resection with negative surgical margins. Six months later, she developed a new, firm, fixed, 6 cm nodule at the subangulomandibular level, palpable and painful, without signs of inflammation, accompanied by left peripheral facial paralysis. Lymph node examination was unremarkable. Magnetic resonance imaging (MRI) of the parotid region demonstrated an expansive, poorly defined process measuring 42 mm, showing moderate infiltration of the masseter and pterygoid muscles, heterogeneous spontaneous signal intensity, dynamic enhancement consistent with a type C curve, and a very low apparent diffusion coefficient (ADC), indicative of restricted water diffusion and high cellular density. Imaging studies of the thoraco-abdomino-pelvic region and bone scintigraphy, performed due to bone pain, were unremarkable. The patient underwent excision of the lesion, followed by a wide left parotidectomy with ipsilateral triangular lymph node dissection and preservation of the left facial nerve. Definitive pathological evaluation revealed an undifferentiated malignant tumor proliferation. Immunohistochemical staining demonstrated positive expression for cytokeratin (CK) and CD99, while synaptophysin, epithelial membrane antigen (EMA), neuronal-specific enolase (NSE), chromogranin, and vimentin were negative, supporting a diagnosis of a primary peripheral neuroectodermal tumor (PNET). Fluorescence in situ hybridization (FISH) analysis confirmed the presence of a specific EWING/PNET-type translocation in 60% of tumor cells, leading to the definitive diagnosis of extra-skeletal Ewing’s sarcoma. The patient received adjuvant chemotherapy with a VDC/IE regimen consisting of four cycles of vincristine, doxorubicin, and cyclophosphamide alternating with ifosfamide and etoposide. Following chemotherapy, she received external beam radiotherapy delivered at a total dose of 54 Gy using standard fractionation (1.8 Gy per session, five sessions per week) to the clinical target volume (CTV) with a 1.5 cm margin and planning target volume (PTV)"}
+{"row_index": 3, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A woman who was pregnant for the first time had a serious blockage in both kidneys at 29 weeks. She had a surgery when she was 3 years old to fix a problem with her urine tubes (ureters), and it worked well back then. When she came in, she had back pain and her kidneys were swollen. Her body couldn’t filter waste properly, so she was admitted right away. Doctors placed small tubes (stents) into her urine tubes to unblock them. After that, she started urinating a lot, which helped her kidneys heal. A catheter was used to help her stay hydrated. After 7 days, the catheter was removed, but then she got a bad infection in her kidneys with fever and pain. Doctors treated it with antibiotics and put in a new catheter. When the infection went away, she was discharged at 33 weeks. She had no signs of early labor. At 39 weeks, she had high blood pressure and had her baby, a healthy boy, born naturally. After delivery, both stents moved into her urine opening (urethra) and caused pain and fever. Doctors put new stents in under anesthesia to fix the pain. Six months later, the stents were removed, but the right urine tube was still blocked. She will have another surgery to fix both tubes in the future.\"\n}"}
+{"row_index": 4, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 24-year-old woman who was pregnant for the first time was referred to us at 29 weeks of gestation. She had a surgical procedure called bilateral Politano-Leadbetter ureteral reimplantation when she was 3 years old to fix a problem with urine flow from her kidneys. Since then, she had been doing well. But at this visit, she had back pain and an ultrasound showed severe swelling in both kidneys (hydronephrosis). Her kidney function was poor, so she was hospitalized right away. A stent was placed in each ureter to help drain urine and relieve pressure. After the stent was put in, her urine output increased greatly, and her kidney function improved quickly. A catheter was used to help prevent dehydration, and it was removed after 7 days. A week later, she developed a urinary tract infection, which was treated with antibiotics and a new catheter. Her symptoms went away, and she was discharged at 33 weeks. She did not have signs of preterm labor during her stay.\\n\\nAt 39 weeks, she was re-admitted due to high blood pressure. She delivered a healthy male baby weighing 3.14 kg, who had a good start at birth (Apgar scores of 9 and 10). After delivery, she started having back pain and fever. It was found that both stents had moved into her urethra. The stents were reinserted under spinal anesthesia, and her symptoms improved. She was discharged two weeks later. At 6 months post-delivery, the stents were removed, but a blockage was still present in the right ureter. A new stent was placed there, and she is now scheduled for a repeat surgery to fix both ureters.\"\n}"}
+{"row_index": 5, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 24-year-old primigravida presented at 29 weeks of gestation with mild back pain and severe bilateral hydronephrosis, as detected by abdominal ultrasound. She had a history of bilateral Politano-Leadbetter ureteral reimplantation performed at age 3 years for vesicoureteral reflux (VUR), with an uneventful postoperative course. Her baseline blood pressure was 120/80 mmHg, but serum creatinine was elevated to 3.57 mg/dL, indicating acute postrenal failure due to obstructive uropathy. She was hospitalized immediately and underwent bilateral double-pigtail ureteral stenting (4.7 French) under ultrasound guidance without fluoroscopy. Post-stent placement, daily urine output exceeded 6 L, triggering post-obstructive diuresis; to prevent dehydration, an indwelling urethral catheter was inserted and intravenous saline infusion was initiated. Serum creatinine rapidly normalized to 1.1 mg/dL, and hydronephrosis significantly improved, allowing catheter removal after 7 days. However, within a week, the patient developed high fever and severe back pain, with laboratory findings consistent with pyelonephritis: white blood cell count of 13.1 × 10³/μL and C-reactive protein of 11.34 mg/dL. Urine culture isolated Streptococcus agalactiae, confirming bacterial infection. A second urethral catheter was placed and intravenous ceftriaxone sodium (2 g/day) was administered for 6 days, leading to clinical and laboratory resolution of infection. The catheter was removed when urine output declined, and she was discharged at 33 weeks of gestation without evidence of preterm labor (no cervical shortening or frequent uterine contractions). At 39 weeks, she was re-admitted for gestational hypertension, defined by persistently elevated systolic blood pressure (>140 mmHg) without proteinuria. She underwent labor induction and delivered a healthy male infant weighing 3140 g, with Apgar scores of 9 at 1 minute and 10 at 5 minutes. Postpartum, she developed acute back pain and fever on day 1 after delivery, which was attributed to spontaneous migration of both ureteral stents into the ure"}
+{"row_index": 6, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 10-year-old girl from a Hindu family in Sindh, Pakistan, was healthy until she started having severe pain in her side, blood in her urine, vomiting, and fever for a week. She was very anxious and had high blood pressure. The doctor found her right kidney was swollen and painful, and a blood clot was blocking the blood vessel that supplies it — the right renal vein — and it went all the way into the main vein in her body. Tests showed no infections or other problems, but blood tests found she had a clotting issue linked to a condition called lupus. This is a known problem in people with lupus, called antiphospholipid syndrome.\\n\\nShe was given medicine to prevent clots — first enoxaparin, then warfarin — and later switched to rivaroxaban so she didn’t need frequent blood tests. Her high blood pressure was treated with medicine, and she started taking hydroxychloroquine to help with the lupus. Over time, her symptoms got better. Her blood pressure stayed normal, her kidneys kept working well, and she didn’t have any more clots or flare-ups of lupus.\\n\\nThe right kidney stopped working and was found to be non-functioning. Doctors said it might be removed, but her parents chose not to. Her kidney got smaller over time, and the left kidney grew bigger to help. She stayed healthy for 4 years, grew normally, and had no serious problems. She still takes medicine every day to prevent clots and protect her kidneys. Her mother later got lupus too. Her latest check-up showed normal blood pressure, normal kidney function, and no signs of active disease. She just has a bit of anemia from her periods, which is being managed.\"\n}"}
+{"row_index": 7, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 10-year-old girl from a Hindu family in Sindh, Pakistan, who had been healthy until 2020, came in with a week-long history of severe abdominal pain, blood in her urine (gross hematuria), vomiting, and fever. She was anxious, had a high fever, and her blood pressure was very high. On exam, her right kidney was enlarged and tender. Other body systems were normal.\\n\\nLab tests showed low platelets, blood in the urine, and mild protein in the urine. Her kidney and liver functions were normal, and her blood clotting tests were normal. An ultrasound found that her right kidney was enlarged and had areas of abnormal tissue, and a color Doppler scan showed a large blood clot in the right renal vein that blocked blood flow and extended into the inferior vena cava. A CT scan confirmed the clot was fully blocking the vein.\\n\\nNo known risk factors for blood clots were found, and blood tests for inherited clotting disorders were negative. However, tests for lupus and antiphospholipid antibodies were positive, confirming a secondary antiphospholipid syndrome linked to lupus.\\n\\nShe was treated with anticoagulant medications (first enoxaparin, then warfarin), and her blood pressure was managed with captopril and later losartan. She improved over 10–12 days and was discharged. Her blood pressure and kidney function have remained stable over the next 4 years. The right kidney stopped working, and a scan showed it was nonfunctioning. Nephrectomy (removal of the kidney) was recommended, but her parents chose not to do it.\\n\\nHer anticoagulation was later switched to rivaroxaban to avoid frequent blood tests. She continues to take anticoagulants, antiplatelet medicine, blood pressure medication, and hydroxychloroquine to prevent flares and clots. Her growth and kidney function have been stable. Recent tests show normal kidney function, no protein in urine, and normal blood pressure (off blood pressure meds). She had a mild drop in red blood cells due to heavy periods, which was managed with medication. Her lupus markers are now normal, and there have been no new blood clots or flare-ups. Her mother later developed lupus as well.\\n\\nShe is still on long-term treatment and will likely need it for life,"}
+{"row_index": 8, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 10-year-old female from a Hindu family in Sindh, Pakistan, with a low socioeconomic status, presented in 2020 with a 1-week history of severe right lumbar pain, gross hematuria, vomiting, and fever. The pain was refractory to analgesia and necessitated three emergency department visits prior to hospital admission. She denied dysuria, urinary retention, incontinence, or systemic manifestations such as joint pain, rash, mouth ulcers, or alopecia. Her medical history was unremarkable, including no prior renal disease, immunodeficiency, or family history of thrombotic or autoimmune disorders. She was born via cesarean section to unrelated parents, fully immunized, and developmentally normal, currently enrolled in the 8th grade.\\n\\nOn physical examination, she was febrile (101°F), hypertensive (systolic/diastolic blood pressure 130/96 mmHg, above the 95th percentile for age and height), anxious, and mildly anemic. Anthropometric parameters included weight 36.4 kg (50th percentile), height 141 cm (above 50th percentile), and body surface area (BSA) 1.2 m². No lymphadenopathy, jaundice, or skin rashes were observed. Abdominal examination revealed localized tenderness in the right lumbar region without splenomegaly. Systemic examinations of respiratory, cardiovascular, locomotor, and nervous systems were unremarkable.\\n\\nInitial laboratory investigations revealed a white blood cell count of 14.98 × 10⁹/L, platelet count of 75 × 10⁹/L (indicating thrombocytopenia), hemoglobin of 12.4 g/dL, and elevated C-reactive protein (48 mg/dL), lactate dehydrogenase (696 U/L), and D-dimer (19.8 mg/L), consistent with active inflammation and thrombotic processes. Urinalysis demonstrated hazy, reddish appearance with 3+ hematuria, 150 mg/dL proteinuria, numerous red blood cells (RBCs), and 15–20 white blood cells per high-power field (WBCs); leukocyte esterase and nitrites were negative. Spot"}
+{"row_index": 9, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 61-year-old woman had a close call with her heart stopping suddenly. Doctors found a problem in her heart valve called mitral valve prolapse, where the valve leaks badly. This leak, along with other signs from heart tests, showed she was at risk for a sudden heart stop. To keep her safe, they put in a small device called an ICD that can shock her heart if it starts to beat wrong. They also plan to fix the leaking valve with a small surgery in three months. After the device was placed, she got better and was able to move around again. A few weeks later, her heart stayed stable, and after the surgery, a small fast heartbeat happened but was quickly fixed.\"\n}"}
+{"row_index": 10, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 61-year-old woman had a near-fatal heart event and was saved with intensive care. She was found to have a condition called arrhythmogenic mitral valve prolapse, where the mitral valve in her heart doesn't close properly, leading to severe leakage. This condition, along with other signs seen on heart tests, increased her risk for sudden cardiac death. Tests showed abnormal electrical activity in her heart, including frequent ventricular arrhythmias and brief episodes of atrial fibrillation, which required anticoagulation therapy. An imaging test (CMR) revealed scar tissue in parts of the heart, which is a known risk factor for sudden cardiac death. The patient was given an internal automatic defibrillator (ICD) to monitor and prevent dangerous heart rhythms as a protective measure. She also underwent surgery three months later to repair the damaged mitral valve. After the procedure, she recovered well, regained mobility, and had no further serious heart rhythm issues during follow-up. The ICD successfully prevented any further life-threatening arrhythmias.\"\n}"}
+{"row_index": 11, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 61-year-old female with a history of obesity (BMI 30.1 kg/m²) presented with an aborted sudden cardiac death. On admission, vital signs were stable: pulse 60/min, blood pressure 120/80 mmHg, temperature 36°C, and oxygen saturation 94% under mechanical ventilation. Physical examination revealed no abnormalities in heart, lungs, or abdomen. Laboratory studies were unremarkable, including complete blood count, coagulation profile (normal D-dimers), and clinical chemistry (C-reactive protein 6 mg/L, within normal limits of 5 mg/L). Electrocardiography (ECG) showed sinus rhythm with a heart rate of 60/min, no atrioventricular block, no QT interval prolongation, and inverted T-waves in inferior leads (III, aVF), suggestive of regional myocardial ischemia or early repolarization abnormalities. Fast echocardiography demonstrated preserved systolic function in both left and right ventricles, with severe mitral regurgitation and no pericardial effusion. Chest X-ray revealed normal cardiac size with pulmonary venous congestion, indicating left-sided volume overload.\\n\\nIntensive care management led to clinical stabilization; mechanical ventilation was discontinued on day 4. A hypoactive delirium was managed with neuroleptikum and resolved without persistent neurological deficits. The 12-lead ECG did not demonstrate typical electrocardiographic markers of channelopathies (e.g., Brugada syndrome, ARVC, long-QT or short-QT syndromes), ruling out common inherited arrhythmogenic disorders. However, recurrent ventricular arrhythmias (ventricular tachycardia, VT) were observed during continuous monitoring, and a transient atrial fibrillation with spontaneous termination was documented, prompting initiation of oral anticoagulation therapy.\\n\\nFollow-up echocardiography confirmed persistent severe mitral valve insufficiency with preserved left ventricular ejection fraction. The left ventricle exhibited mild end-systolic and end-diastolic dilation. A markedly enlarged left atrium (area 45 cm²) was identified, consistent with chronic volume overload. Doppler tissue imaging revealed a peak systolic lateral mitral annular velocity of 18 cm/s, indicating reduced annular contractility. Transesophageal echocardiography revealed a high-grade eccentric mitral"}
+{"row_index": 12, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 45-year-old man working at a chemical plant got hurt on his right foot after stepping on a wet shoe that had ethylene oxide (EO) inside. He didn’t wear protective shoes or clothes and didn’t clean the shoe for 5 hours. The liquid soaked through his shoe and didn’t cause pain right away. It took more than 12 hours before he started feeling burning, redness, and oozing. When he finally went to the hospital, his foot was red, blistered, and had skin falling off. Doctors washed the area with salt water, covered it with a wet bandage, and applied medicine to prevent infection. He came back to the clinic every week for 4 weeks. After 9 months, his skin healed, but he still felt less sensation in his foot. He was checked by doctors for other problems, and everything was normal. No serious damage was found.\"\n}"}
+{"row_index": 13, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 45-year-old man developed painful, red, oozing skin lesions on his right foot after working with ethylene oxide (EO) in a chemical plant. He was replacing a flowmeter connected to the EO tank and did not wear proper protective gear. A large amount of EO solution mixed with water spilled into his shoe, and he wore it for about 5 hours before showering. He didn’t feel any symptoms right away, but by the next morning, he had severe burning, pain, redness, and skin breakdown. The lesions were treated in the emergency department with saline irrigation, wet dressings, and topical antibiotics. He was followed up for 4 weeks at an outpatient clinic, and his skin healed completely with only slight darkening remaining. Nine months later, he reported reduced sensation in his foot, but tests showed no serious damage to his blood, lungs, or nerves. The case highlights the risk of delayed symptoms from chemical exposure and the importance of using proper protective equipment.\"\n}"}
+{"row_index": 14, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 45-year-old male with no significant past medical history presented with painful, exudative lesions on the right foot following occupational exposure to ethylene oxide (EO). The patient worked in a chemical plant where he was responsible for replacing a worn-out flowmeter connected to the EO supply tank. He was not wearing personal protective equipment (PPE), including chemical-resistant clothing or footwear. EO is typically delivered via an automated isolation line, minimizing routine exposure; however, exposure can occur during maintenance procedures such as indicator system replacement, which involves manual handling of EO-containing lines.\\n\\nAt approximately 2:00 PM, a significant volume of EO solution mixed with water spilled onto the patient’s right shoe. The patient experienced no immediate symptoms and continued working with the contaminated footwear until approximately 5:30 PM, approximately 5 hours after initial exposure. He returned home and took a shower, which effectively decontaminated the affected area. Clinical symptoms, including a severe burning sensation, pain, erythema, and progressive desquamation, developed approximately 12–14 hours post-exposure, beginning with the dorsum of the right foot and extending to the proximal regions of the second and third digits and the hallux.\\n\\nOn presentation to the emergency department, the patient exhibited acute dermatological injury with subcutaneous tissue damage, characterized by severe erythema, dark pink dermal appearance, serosanguineous exudate, blister formation, and epidermal desquamation. The total burn surface area was assessed at 3.5% of the total body surface area (TBSA). Vital signs were stable, with normal hemodynamics and alert mental status. No respiratory distress or dyspnea was noted, and pulmonary examination revealed clear breath sounds.\\n\\nLaboratory investigations—including complete blood count (CBC), blood chemistry panel, urinalysis, and plain chest radiograph—were all within normal limits, indicating no systemic toxicity or organ involvement. The affected skin was irrigated with saline solution and treated with topical silver sulfadiazine to prevent infection in the open wounds. The patient was managed in an outpatient follow-up setting for a duration of 4 weeks, during which complete epidermal regeneration occurred without scarring or structural defects. At a 9-month follow-up, residual hyperpigmentation was observed, but no other abnormalities were detected.\\n\\nA comprehensive health assessment conducted 9 months post-exposure revealed reduced sensory"}
+{"row_index": 15, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 69-year-old woman had a firm lump on her left thigh that grew over 6 years and caused pain. Doctors first removed the lump with surgery, and tests confirmed it was a type of cancer called soft tissue sarcoma. She had more surgeries and treatment with radioactive seeds, but the cancer came back. After that, she got a new treatment called HIFU — it uses focused sound waves to destroy the cancer. The treatment worked well, and the cancer was completely gone, with no major side effects except for some damage to the bone at the spot. About four months later, the lump came back again, but doctors found it was small and treated it with more surgery. Now she is stable, feels good, and lives a normal life.\"\n}"}
+{"row_index": 16, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 69-year-old woman was diagnosed with an undifferentiated spindle cell soft tissue sarcoma on her left thigh. She first had surgery to remove the tumor, and the results confirmed the diagnosis. Over time, the cancer came back at the same site after multiple surgeries and treatments with radioactive particles. After 16 months, imaging showed the cancer had returned again, and she had three more surgeries and radioactive treatments. Despite this, the cancer still came back, so a new treatment called high-intensity focused ultrasound (HIFU) was used. HIFU is a non-invasive method that uses focused sound waves to destroy the tumor. The treatment was given over five sessions, and MRI scans showed the tumor was completely destroyed, with no signs of cancer cells left. The only side effect was minor bone damage at the treatment site. About four months later, the patient had a small break in the bone at the original tumor location, but further testing showed it was not cancer-related. She then had additional surgery to fix it and is now stable with a good quality of life.\"\n}"}
+{"row_index": 17, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 69-year-old female patient presented with a 3-cm-diameter firm mass on the left thigh that had progressively increased over a 6-year period, accompanied by localized pain. Initial surgical management consisted of a lumpectomy performed at The Second Affiliated Hospital of Chongqing Medical University. Postoperative histopathological examination confirmed the lesion as an undifferentiated spindle cell soft tissue sarcoma. Immunohistochemical profiling revealed CK(-), EMA(-), Vim(+), S100(-), SMA(±), Act(-), CD34(+), BCL-2(-), CD9(±), Ki-67(+), 50% AB(+), MBP(-), NF(-), and CD68(+), consistent with a spindle cell sarcoma of undifferentiated phenotype, likely with features of sarcomatoid differentiation and active cell proliferation (Ki-67 >50%). The patient underwent an expanded resection to ensure clear margins.\\n\\nTwo years postoperatively, a firmer, tender mass was identified at the surgical site, prompting a second expanded resection followed by radioactive particle implantation (brachytherapy). Repeat immunohistochemistry demonstrated CK(-), EMA(±), DES(-), S100(-), SMA(-), CD34(+), SDX-10(-), CDK4(-), MDM2(-), CD68(-), CD99(±), BCL-2(+), Vim(+), and Ki-67(+) >50%, indicating persistent tumor cell proliferation and a shift in molecular profile, including upregulation of BCL-2, which may confer resistance to apoptosis and contribute to tumor recurrence.\\n\\nMagnetic resonance imaging (MRI) at 16 months post-second resection revealed local tumor relapse, leading to three additional lumpectomies and brachytherapy. Five months later, follow-up pathology confirmed a further relapse, indicating persistent disease progression despite multimodal local interventions.\\n\\nA novel treatment strategy was initiated involving five sessions of high-intensity focused ultrasound (HIFU), administered on March 5, June 11, August 20, October 13, and November 24, 2021, using an integrated circuit-type HIFU tumor treatment system (Chongqing Haifu Medical Technology Co., Ltd., China). The system comprises an ultrasonic generator"}
+{"row_index": 18, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A woman in her 50s had been dealing with mood swings and crazy thoughts for 27 years. She was on many medicines, including lithium, which can hurt her kidneys. She came to the hospital because she was sad and had scary thoughts. She had a bladder infection, so she started antibiotics. After 5 days, she got fever and her body started to fail — her kidneys couldn’t work right. Her lithium level was too high (2.34), which damaged her kidneys. The doctors stopped the lithium and switched to safer antibiotics. They gave her fluids to help her kidneys recover. After a few days, she got better. But even after stopping the old medicines, she stayed sad and had worse scary thoughts. So they stopped all her old pills and started new ones: lamotrigine and aripiprazole. These helped a little, but didn’t fix it. Then they added quetiapine to help her sleep and calm down. But after giving her a high dose of quetiapine (400 mg a day), she got a serious problem called NMS — which means her body went into trouble. They gave her amantadine, lorazepam, and bromocriptine to fix it, and she got better. The doctors said the quetiapine was most likely to have caused the problem.\"\n}"}
+{"row_index": 19, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 51-year-old woman with bipolar disorder, who had been managing her condition for 27 years, was admitted to the hospital because she was feeling very sad and had strange, persistent thoughts—like believing others were out to get her. She had been on several medications, including lithium, fluoxetine, olanzapine, gabapentine, perazine, and biperiden, to control her mood and symptoms. Before this hospital stay, she had a history of depression, mania, and one episode of psychosis in 1990. In the past, she had also had kidney problems from high lithium levels and was treated for hypothyroidism.\\n\\nShe was diagnosed with a urinary tract infection, and started on antibiotics. After five days, she began to feel worse—she developed a fever of 38.4°C and her lithium level became dangerously high at 2.34 mmol/l. This caused acute kidney failure, so her lithium was stopped and the antibiotics were changed to a less harmful type. She received fluids to help her body remove the excess lithium, and her kidney function slowly improved.\\n\\nOnce her body stabilized, her mental symptoms got worse—she became more depressed and her delusions returned. All her previous medications were stopped one by one. Instead, she started on lamotrigine and aripiprazole to help stabilize her mood and reduce the delusions. After six weeks, the aripiprazole wasn’t working well, and she started taking quetiapine to help with sleep and mood. However, increasing the quetiapine dose to 400 mg per day eventually led to a serious condition called neuroleptic malignant syndrome (NMS), which is a rare but dangerous reaction to certain psychiatric medications.\\n\\nTo treat NMS, she was given amantadine, lorazepam, and bromocriptine, and her condition improved. The doctors used a scoring system to evaluate how likely each drug was to have caused the NMS. Quetiapine was found to be the most likely contributor, followed by aripiprazole and lamotrigine.\\n\\nThis case shows that even with long-term treatment, changes in medications can lead to serious side effects, and close monitoring is essential, especially in people with a history of kidney issues or mental illness.\"\n}"}
+{"row_index": 20, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 51-year-old female with a 27-year history of bipolar disorder was admitted to the psychiatric clinic in September 2017 presenting with depressed mood, ideas of reference, delusions of persecution, and anxiety. Her clinical course began with an acute paranoid psychotic episode in 1990, followed by recurrent hospitalizations for depressive and manic episodes, with a pattern of treatment shifts involving antidepressants (imipramine, venlafaxine), mood stabilizers (lithium, carbamazepine), and antipsychotics (perazine). Following outpatient management from 2000 to 2008, treatment was modified in 2015 due to lithium toxicity (>1.2 mmol/L), resulting in acute renal failure and extrapyramidal symptoms (EPS), necessitating withdrawal of lithium and initiation of gabapentine for EPS. Hypothyroidism was concurrently diagnosed and managed with levothyroxine until 2016. Between 2016 and 2017, the patient received fluoxetine (60 mg/d), perazine (150 mg/d), gabapentine (800 mg/d), and carbamazepine (200 mg/d, up to 800 mg/d), which was later discontinued due to worsening psychotic and depressive symptoms. Lithium was reintroduced at maximum dose (up to 1000 mg/d), along with olanzapine (5 mg/d) for psychosis and biperiden (4 mg/d) for muscle rigidity. No psychiatric comorbidities were identified throughout the disease course, with notable historical events including prior lithium intoxication and renal failure.\\n\\nAt admission, the patient was alert, oriented to person, place, and time, with stable vital signs: blood pressure 115/70 mmHg, pulse 72 bpm, respiratory rate 16/min, BMI 27.22. Physical examination revealed a regular systolic murmur, clear lung fields, symmetrical abdomen with normal bowel sounds, dry skin, and varicose veins of the lower extremities. Laboratory findings at admission included lithium level of 1.48 mmol/L, glomerular filtration rate (GFR) 35 ml/min, serum creatinine 1.56 mg/dL, and white blood cell count (WBC"}
+{"row_index": 21, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 32-year-old man in Iran found a lump on the back of his left hand and wrist. It had been there for about a month and got bigger over time. The doctor first thought it was a common bump called a ganglion cyst. He tried pain medicine for two months, but the lump kept growing. An MRI scan showed it was a rare type of tumor inside the hand, called synovial sarcoma. The doctor took a small sample of the tumor and tested it. The test showed it was cancer. The man didn’t come back for check-ups for two months. By then, the tumor had grown very large. This is a rare case because most people don’t get this kind of tumor in the hand and don’t follow up after the diagnosis. The doctor said he needed surgery, but the man refused and never came back for treatment.\"\n}"}
+{"row_index": 22, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"This study describes a rare case of metacarpal synovial sarcoma in a 32-year-old Iranian man. He first noticed a lump on the back of his left hand and wrist about one month before seeking medical help. The doctor initially thought it was a common ganglion cyst and treated it with pain relief medication for two months. During that time, the lump slowly grew larger. An MRI scan showed a soft tissue mass that was encasing part of the hand bone and pushing on tendons, which raised concern. A biopsy was done, and the results confirmed it was a synovial sarcoma — a rare type of cancer that starts in the connective tissue. The tumor was completely removed surgically. However, the patient had poor follow-up care and did not return to the clinic for two months after the surgery. When he finally came back, the tumor had grown significantly. Because of this late return, the cancer was no longer treatable, and the patient refused further treatment. This case is rare because synovial sarcoma in the hand or wrist is uncommon, and the delay in follow-up made it much harder to manage.\"\n}"}
+{"row_index": 23, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 32-year-old Iranian male with no significant past medical, family, or social history presented with a slowly progressive lump on the dorsal ulnar side of the right hand and wrist, first noted one month prior. The lesion had been increasing in size over the preceding month, with no history of trauma, constitutional symptoms (such as fever or chills), or systemic illness. Vital signs at admission were within normal limits: pulse rate 75 bpm, blood pressure 118/83 mmHg, temperature 36.7°C, and oxygen saturation 98%. Laboratory evaluations, excluding 25-hydroxyvitamin D3, were unremarkable; the patient was subsequently initiated on daily oral vitamin D3 supplementation (1000 mg) due to low serum 25-hydroxyvitamin D3 levels.\\n\\nStandard hand-wrist radiography was performed to exclude bony abnormalities or foreign bodies, and no evidence of fracture, cortical disruption, or bone invasion was observed. The initial clinical assessment by the primary care physician attributed the lesion to a ganglion cyst. The patient received conservative management including naproxen 500 mg as needed for pain for a duration of two months. During this period, the lesion progressively enlarged. On physical examination, a 30 × 20 mm mass was identified between the second and third metacarpal bones on the dorsal surface of the left hand, extending proximally toward the metacarpal heads and distally into the proximal aspect of the wrist joint. Neurovascular examination revealed no significant deficits: wrist flexion and extension were intact, deep tendon reflexes were normal, sensory function was preserved, and muscle strength was rated 5 out of 5, indicating full motor function.\\n\\nMagnetic Resonance Imaging (MRI) was subsequently performed and interpreted by a radiologist. The MRI demonstrated a T2-hypersignal lesion with iso-signal intensity on T1-weighted sequences in the deep soft tissue of the middle and medial regions of the hand, specifically involving the 3rd and 4th metacarpal web spaces. The lesion exhibited cystic characteristics with fine internal septations and heterogeneous signal intensity. Tendon displacement was observed: the flexor tendons were deviated due to mass effect, and the extensor tendons of the 3rd, 4th, and 5th fingers were displaced, indicating local"}
+{"row_index": 24, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 56-year-old woman felt her heart was racing, so she went to the doctor. The doctor saw a small bump on her heart valve, about 8 millimeters big, and it was slightly leaking. At first, they thought it was a tumor, but after surgery, they found it was actually a weak, bulging part of the valve — like a small balloon that had stretched out. It wasn’t a cancer, but a sign of wear and tear from years of use. The doctors removed the bulge and fixed the valve with a ring to help it stay strong. After the surgery, she recovered well and has been feeling fine ever since. Ten months later, her heart valve is still healthy and not leaking at all. This kind of problem happens when the heart valve wears down over time, not because of disease or infection.\"\n}"}
+{"row_index": 25, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 56-year-old woman was seen for palpitations. Her heart rhythm and sounds were normal, and initial tests showed no signs of infection or heart problems. An echo scan found an 8-mm mass on the anterior mitral leaflet with only slight valve leakage. Further testing confirmed the same finding. Surgery was planned to remove the mass and prevent a possible blood clot from forming. During surgery, it was discovered that the mass was not a tumor, but a bulge resembling an aneurysm, and there was no stretching of the supporting tissue. The surgeon removed the bulge and repaired the valve with a ring procedure. The patient recovered well and had no complications. Path tests showed signs of degenerative changes in the valve tissue, confirming that the issue was due to wear and tear over time. At 10 months after surgery, her heart function is stable with no further valve problems.\"\n}"}
+{"row_index": 26, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 56-year-old woman with no history of infection presented for evaluation of palpitations. Her clinical examination revealed a regular sinus rhythm with no audible heart murmur. Standard electrocardiographic assessments, including resting ECG and Holter monitoring, as well as chest X-ray, were within normal limits. Transthoracic echocardiography identified an 8 × 8-mm mass localized to the posterior aspect of the anterior mitral leaflet, associated with minimal mitral valve insufficiency. Left ventricular systolic function, wall motion, and chamber dimensions were preserved, indicating no underlying systolic dysfunction. Transesophageal echocardiography confirmed the same lesion morphology, with no evidence of intracardiac thrombus or systemic embolic events. Computed tomography was negative for systemic emboli, further supporting the absence of a thrombotic source. Given the imaging findings and the clinical suspicion of a valvular tumor, surgical resection was performed with the primary goal of preventing potential embolic complications. Intraoperative inspection revealed that the lesion was not a neoplastic tumor, but rather an aneurysm-like bulge of the anterior mitral leaflet, characterized by absence of chordal elongation, which is a key histopathological and biomechanical feature distinguishing it from true neoplastic growths. The lesion was resected via a triangular resection technique, followed by ring annuloplasty to restore normal valve architecture and reduce the risk of residual regurgitation. Postoperative recovery was uneventful, with no complications reported. Histopathological analysis of the resected tissue demonstrated myxomatous degeneration, interstitial fibrosis, and hyalinization—pathological hallmarks of degenerative mitral valve disease. These findings are consistent with a chronic, progressive process involving extracellular matrix remodeling, likely driven by age-related changes in valve tissue elasticity and collagen turnover. At a 10-month follow-up, the patient remains asymptomatic, with no evidence of mitral regurgitation or valvular dysfunction, confirming successful surgical intervention and resolution of the structural abnormality. The case underscores the importance of accurate preoperative imaging and intraoperative differentiation between benign degenerative lesions and malignant tumors in the mitral valve, as misdiagnosis could lead to inappropriate resection or unnecessary intervention.\"\n}"}
+{"row_index": 27, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 23-year-old man had a serious illness called Burkitt's lymphoma and was also dealing with a condition where his body attacked its own tissues (GVHD). He got very sick with confusion and trouble breathing, and when checked, had a bleed in his brain and a dead area in his brain from a stroke. Doctors found 12 weak spots in blood vessels in his brain — called aneurysms — that started showing up very fast, even though scans showed no sign of infection in his skull bones. The infection was caused by a rare fungus called Scedosporium. Even with strong medicine and surgery, the patient got worse, had infections in his lungs, and died 6 months later because his heart, lungs, and other organs stopped working. What made this case special was how fast the fungus spread through the blood vessels — new aneurysms appeared in just days, even when the brain scans looked clean.\"\n}"}
+{"row_index": 28, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 23-year-old man with Burkitt's lymphoma and graft-versus-host disease was admitted to the hospital with confusion, sleepiness, and breathing problems. He had a bleeding stroke in his brain and signs of a prior brain injury. Imaging showed several aneurysms—bulges in blood vessels—that formed quickly, including 12 in the front part of the brain. These aneurysms were caused by a widespread infection from a fungus called Scedosporium, which spread rapidly through the blood vessels. Even though there was no clear sign of infection in the skull bones, new aneurysms appeared within days of imaging. The patient received antibiotics, antifungals, and surgery to remove the aneurysms. Despite these efforts, the infection spread and damaged multiple organs. He developed severe infections, including one caused by a drug-resistant bacteria in his lungs, and died six months later from multiorgan failure. This case shows how fast a fungal infection can spread through blood vessels in a patient with weakened immunity, leading to serious brain bleeding and organ damage.\"\n}"}
+{"row_index": 29, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 23-year-old male with a history of Burkitt’s lymphoma and graft-versus-host disease (GVHD) requiring high-dose corticosteroid therapy was admitted to the Emergency Department with a two-day history of somnolence, confusion, and progressive respiratory distress necessitating endotracheal intubation. On admission, neurological examination revealed impaired eye opening to painful stimuli and intact command following. Initial non-contrast head CT demonstrated a flame-shaped intracerebral hemorrhage in the left gyrus rectus, suggestive of vascular origin, and a hypodense lesion in the left thalamus consistent with an established infarction. The next-day angiogram identified six fusiform aneurysms: three at the frontopolar branch of the left anterior cerebral artery (ACA), one at the orbitofrontal branch of the left ACA, one at the frontopolar branch of the right ACA, and one at the anterior temporal artery of the left middle cerebral artery (MCA). Body imaging revealed multiple cavitary lung lesions, consistent with pulmonary involvement by a systemic infection. Broad-spectrum antibiotics, antifungals, and antivirals were initiated empirically.\\n\\nThe hemorrhagic focus localized to the left ACA branch aneurysms, prompting surgical intervention to assess rupture status and obtain tissue for microbiological analysis. On postbleed day 2, a bicoronal craniotomy was performed with parent vessel sacrifice and excision of the three left ACA fusiform aneurysms. Intraoperatively, the aneurysms exhibited friable, thin-walled characteristics with high propensity for rupture. The right ACA aneurysm was managed conservatively. Microbiological analysis confirmed angioinvasive infection by Scedosporium apiospermum, leading to initiation of vericonazole, amphotericin B, and caspofungin, which were continued throughout the clinical course.\\n\\nOn postbleed day 4, a new left frontal intracerebral hemorrhage and intraventricular hemorrhage (IVH) were detected on CT, prompting placement of an emergency external ventricular drain. A follow-up angiogram revealed interval growth of the left orbitofrontal artery aneurysm. With definitive microbiological identification, endovascular parent vessel occlusion was recommended and successfully performed. A subsequent angiogram on postbleed day 7 demonstrated the emergence of three"}
+{"row_index": 30, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A woman with a weak heart valve got very short of breath and sharp chest pain. Her heart valve was badly damaged and caused high pressure in her lungs. Doctors tried a simple balloon procedure to fix the valve, but it broke and caused the valve to leak badly, making lung pressure even higher. Because her heart was too weak to handle surgery, they used medicines and a machine (intra-aortic balloon pump) to help her heart pump better. They also used drugs to open her blood vessels and reduce pressure in her lungs. Even with all this, her body couldn’t keep up, so she and her family chose to focus on comfort and peace instead of more treatment.\"\n}"}
+{"row_index": 31, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 64-year-old woman with a history of heart valve problems, high blood pressure, and previous stroke was admitted with sudden chest pain and shortness of breath. Tests showed severe narrowing of her mitral valve, which is a key heart valve that helps control blood flow. This narrowing was causing high pressure in her lungs (pulmonary hypertension), and her overall risk for surgery was high due to other health issues. Because of this, doctors decided against open heart surgery and instead performed a less invasive procedure called percutaneous mitral balloon valvuloplasty to open up the valve. However, during the procedure, a critical complication occurred: one of the supporting strings of the valve (chordae tendineae) ruptured, leading to severe leakage (mitral regurgitation) and a dramatic rise in lung pressure, now reaching levels above the systemic blood pressure (supra-systemic pulmonary hypertension). To manage this life-threatening situation, the patient received multiple medications, including vasopressors to support blood pressure, inodilators to reduce lung pressure, and an intra-aortic balloon pump to help improve heart function and reduce valve leakage. She also received lung vasodilators and other drugs to ease pressure in her lungs. Despite these efforts, her condition continued to worsen, and after failing to respond to full medical treatment, her family chose to focus on comfort care and hospice support. The main point is that this patient’s complex heart condition led to a serious complication during a planned valve procedure, and her care shifted from surgical to intensive medical management to stabilize her condition and ensure comfort.\"\n}"}
+{"row_index": 32, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 64-year-old female presented to the emergency department with acute retrosternal chest pain and progressive dyspnea. She has a history of coronary artery disease, hypertension, atrial fibrillation, rheumatic mitral valve (MV) disease, and prior stroke with residual left-sided hemiplegia. Transesophageal echocardiography (TEE) demonstrated severe mitral stenosis (effective orifice area [EOA] 0.9 cm²; normal >1.0 cm²), mild mitral regurgitation (MR), minimal leaflet motion, pronounced valvular thickening, extensive calcification, and a Wilkins score of 14 indicating severe structural degeneration of the mitral valve apparatus. The sub-valvular apparatus showed minimal thickening, no vegetations, and no thrombus in the left atrial appendage. Left ventricular systolic function remained preserved.\\n\\nLeft heart catheterization confirmed non-obstructive coronary artery disease. Right heart catheterization (RHC) revealed a mean pulmonary artery pressure (PAP) of 71 mmHg and a pulmonary capillary wedge pressure (PCWP) of 15 mmHg, resulting in a transpulmonary pressure gradient (TPG) of 51 mmHg, consistent with severe pulmonary hypertension (PH) due to pulmonary venous hypertension. Her Society of Thoracic Surgeons (STS) surgical mortality risk was estimated at 31% due to the combination of severe PH and multiple comorbidities. A multidisciplinary team—including advanced heart failure, cardiac surgery, intensive care, and cardiac anesthesia—concluded that the patient was not a suitable candidate for surgical mitral valve replacement (MVR) due to the high risk of perioperative mortality and hemodynamic instability. Consequently, percutaneous mitral balloon valvuloplasty (PMBV) was performed under general anesthesia in the cardiac catheterization laboratory.\\n\\nPre-procedure, invasive lines (radial arterial line and right internal jugular vein catheter) were successfully placed. Induction of general anesthesia was achieved with endotracheal intubation. Repeat RHC showed a mean PAP of 61 mmHg and left atrial pressure of 30 mmHg. TEE confirmed a severely dilated right ventricle and a mitral EOA of 0.9 cm². Cardiac index"}
+{"row_index": 33, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 12-year-old Asian girl with leukemia had swelling in her gums and chin that got worse over time. Even with proper care, the infection didn’t go away and eventually caused a big hole in her face and jaw. Her teeth fell out on their own, and part of her jaw bone also came loose. Because of this, she couldn’t eat properly and kept drooling. After she got better, a simple surgery was done to fix her lips so she could eat again and stop drooling.\"\n}"}
+{"row_index": 34, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 12-year-old Asian girl with acute myeloid leukemia (AML) developed worsening gingivitis, which started as swollen gums and chin. She had already received chemotherapy for her leukemia and was hospitalized for a high fever, which was treated with multiple antibiotics, antifungals, and antivirals. Her white blood cell count was very low, and her neutrophils were absent, making it hard to fight infections. Despite proper treatment, her oral condition got worse. Six days after the start, she had a cardiac arrest due to uncontrolled fever, but she recovered. Over time, the swelling turned into a full-thickness tissue loss in her mouth and face, causing the gums and underlying bone to separate and the teeth to fall out. After recovering from the illness, she had serious problems with her lips, making it hard to eat or control drooling. Because of her weakened blood counts, surgery was done simply to repair the lip and restore the ability to eat, using a local flap to reconnect the muscle that controls the lips.\"\n}"}
+{"row_index": 35, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 12-year-old Asian female patient with acute myeloid leukemia (AML) was referred for evaluation and management of progressive gingival swelling and chin involvement. The patient had a history of patent ductus arteriosus (PDA) closure at age 6 and had undergone four cycles of induction chemotherapy for AML, diagnosed one year prior. She was admitted for neutropenic fever exceeding 39°C, managed with a broad-spectrum regimen including linezolid, meropenem, sulfamethoxazole, metronidazole, teicoplanin, cefpiramide, and amikacin, along with antifungals (fluconazole, nystatin, amphotericin B, voriconazole, caspofungin) and antiviral therapy (acyclovir), consistent with suspected vancomycin-resistant enterococci (VRE) sepsis. Laboratory findings revealed a white blood cell (WBC) count of 40/μL, platelet count of 8000/μL, and an absolute neutrophil count of 0/μL, confirming profound neutropenia and pancytopenia. Given the absence of viable neutrophils and the patient's unstable hematologic status, surgical intervention was contraindicated. Over the course of six days, the patient developed uncontrolled fever leading to cardiac arrest; return of spontaneous circulation (ROSC) was achieved through resuscitation, followed by gradual clinical improvement. The oral and facial lesions progressed to full-thickness necrotic gangrene, with complete separation of the necrotic alveolar bone from the surrounding mandibular bone. Teeth in the affected segment spontaneously exfoliated, and the necrotic bone segment also detached independently. Following resolution of fever and recovery of systemic stability, the patient faced persistent functional deficits, including lip incompetence and drooling due to loss of oral closure, rendering oral intake impossible. In the context of her pancytopenia and high surgical risk, a minimally invasive local flap procedure was performed to restore continuity of the orbicularis oris muscle, thereby achieving functional lip competency and enabling safe oral intake. The case illustrates the severe mucosal and skeletal complications of prolonged neutropenia in pediatric leukemia, particularly involving the maxillofacial region, with gingivitis progressing to full-thickness tissue and bone necrosis due to impaired host defense mechanisms, disrupted tissue perf"}
+{"row_index": 36, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 48-year-old man had eye inflammation in his left eye that didn’t go away. His doctor tried a steroid called prednisolone, which helped a little, but when the dose was lowered, the eye swelling came back. He was referred to a better eye hospital because the problem kept returning. At first, his vision was okay, but his eye had signs of swelling and inflammation. Tests showed his eye had a type of blood vessel problem that matches a condition called Bechet’s disease. He also had mouth sores and red bumps on his legs, and a test showed a specific gene (HLA-A26) was present. He started a drug called adalimumab to reduce the need for steroids. It worked — his eye swelling got better and he could slowly cut down on the steroid. But after 8 months, he started feeling sick and tests found signs of tuberculosis (TB) in his lungs. He was diagnosed with miliary TB, a serious form of TB. His steroid and adalimumab were stopped right away, and he started TB treatment for 6 months. Even after that, the TB test stayed positive. During this time, his eye problem got worse, and his vision dropped. So, they restarted a different drug called infliximab, along with isoniazid to fight TB. After starting this, his eye swelling and vision improved again. No TB came back after 3 years of treatment. The key point: his eye problem needed special medicine, and TB was a serious side risk, but it was managed with the right steps.\"\n}"}
+{"row_index": 37, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 48-year-old Japanese man was treated for eye inflammation (uveitis) in his left eye, which had developed into macula edema (swelling in the central part of the retina). His doctor first tried prednisolone, a steroid, which helped temporarily, but when the dose was reduced, the swelling returned. Because the condition didn't improve, he was referred to a specialized eye hospital in Tokyo. At the hospital, doctors found signs of Bechet’s disease — a rare condition that causes inflammation in blood vessels — through eye exams, blood tests, and imaging. Key signs included swollen blood vessels in the retina, recurring mouth sores, a rash on his legs, and a specific genetic marker (HLA-A26). He started treatment with adalimumab (ADA), a drug that reduces inflammation and helps lower steroid use. Over time, his eye swelling improved and he was able to reduce his steroid dose. However, eight months later, he developed symptoms of tuberculosis (TB), including fatigue and lung shadows on imaging. He was diagnosed with miliary TB, a serious form of TB. His steroid and ADA treatments were stopped immediately, and he began a six-month course of TB medication. Even after recovery, his TB test remained positive. During this time, his eye condition worsened, with increased swelling and vision loss. After stopping ADA, he used eye drops and injections to control the eye inflammation, but these only provided limited relief and caused some side effects like higher eye pressure. Eventually, he restarted treatment with infliximab (IFX), combined with isoniazid for TB prevention. After starting IFX, his eye swelling and vision improved, and his TB did not return during the next three years. This case shows that while treatments for Bechet’s disease can help control eye symptoms, patients need careful monitoring for infections like TB, especially when using anti-inflammatory drugs.\"\n}"}
+{"row_index": 38, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 48-year-old Japanese male presented with uveitis of unknown origin in the left eye, initially managed at a general ophthalmology clinic. Macula oedema (ME) was identified, and prednisolone (PSL) 40 mg/day was initiated. Although ME showed transient improvement, tapering PSL to 20 mg/day resulted in relapse of ME, prompting referral to the Department of Ophthalmology, Tokyo Medical University Hospital due to persistent intraocular inflammation and worsening visual function. At presentation, best-corrected visual acuity (BCVA) was 20/12.5 in the right and 24/20 in the left eye, with normal intraocular pressure. Slit-lamp examination revealed 1+ anterior chamber cells; fundus photography demonstrated diffuse vitreous haze and mild peripheral retinal exudates; fluorescein angiography revealed diffuse retinal vasculitis involving the posterior pole and peripheral retina, consistent with Bechet’s disease (BD); optical coherence tomography (OCT) confirmed the presence of macula oedema. Peripheral blood tests showed elevated white blood cell count, increased neutrophil percentage, elevated lactate dehydrogenase (LDH), HLA-A26 positivity, negative HLA-B51, and negative results for both tuberculin skin test (TST) and T-SPOT.TB. Based on the clinical presentation—recurrent oral aphthous ulcers, erythema nodosum-like cutaneous rash, HLA-A26 positivity, and characteristic retinal vasculitis—the diagnosis of incomplete Bechet’s disease was established. Adalimumab (ADA), a tumor necrosis factor (TNF) inhibitor, was initiated as steroid-sparing therapy following screening for latent or active infection. Following ADA initiation, ME gradually improved, allowing successful tapering of PSL to 2 mg/day, resulting in sustained clinical remission of ocular inflammation.\\n\\nEight months after ADA initiation, the patient developed systemic symptoms of general malaise. Repeat peripheral blood testing revealed a positive T-SPOT.TB result. Chest X-ray and computed tomography (CT) demonstrated bilateral pulmonary granular shadows, leading to a diagnosis of miliary tuberculosis (TB). ADA and PSL were immediately discontinued due to the risk of exacerbating TB. A standard 4-drug regimen for miliary TB was commenced: isonia"}
+{"row_index": 39, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 70-year-old Japanese woman had sudden, very bad neck pain that made her unable to move her neck at all. She had a fever of about 37.5°C and couldn’t turn her head. X-rays and scans showed a hard, yellow substance in her neck, like a small piece of old stone, between two bones (C5 and C6). The scan showed fluid inside this yellow part, and it looked like thick, yellow goo. Doctors found tiny crystals in the fluid that are linked to a condition called pseudogout, which affects the yellow ligament. This caused the pain and the swelling. She had surgery to remove the bad part and the fluid. After the surgery, her pain went away, and she never had another bad neck pain again. Now, 7 years later, she’s completely pain-free and has no nerve problems.\"\n}"}
+{"row_index": 40, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 70-year-old Japanese woman developed sudden, severe neck pain that made it impossible for her to move her neck. She had a mild fever (37.5°C) and was experiencing intense pain, with her pain level rated at 100 out of 100. X-rays showed calcification between the C5 and C6 vertebrae, and MRI scans revealed a yellow fluid collection in the yellow ligament — a band of tissue in the neck. The fluid was cloudy and yellow, and under a microscope, it was found to contain calcium pyrophosphate dihydrate crystals, which are linked to a condition called pseudogout. This condition causes inflammation in the ligament, leading to severe pain and neck stiffness. The MRI also showed compression of the spinal cord, which is why surgery was needed. She underwent surgery to remove the affected yellow ligament and relieve pressure on the spinal cord. After the procedure, her pain improved, lab tests returned to normal, and she eventually had full relief of neck pain with no further issues, even 7 years later.\"\n}"}
+{"row_index": 41, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 70-year-old Japanese woman presented with a 14-day history of progressive neck pain prior to hospital admission. She had no history of tuberculosis, recent head or neck trauma, or diabetes mellitus. Initial physical examination revealed mild limitation of neck motion without neurological deficits, including preserved motor strength, sensory function, and normal deep tendon reflexes. Plain lateral radiography demonstrated calcification within the interlaminar space at the C5-C6 level, consistent with yellow ligament calcification. Magnetic resonance imaging (MRI) revealed a low-signal lesion on both T1-weighted and T2-weighted sequences, with surrounding intermediate signal intensity on T1WI and high signal intensity on T2WI, accompanied by cord compression—findings suggestive of either a pseudogout attack or an epidural abscess. Her neck pain was initially managed with nonsteroidal anti-inflammatory drugs (NSAIDs), resulting in gradual improvement. However, two months later, her symptoms recurred with a moderately elevated fever (37.5 °C), severe neck pain preventing any range of motion, and a visual analog scale (VAS) pain score of 100 mm. Laboratory investigations showed a white blood cell count of 7800/mm³ (within normal range: 3500–9300/mm³) and markedly elevated C-reactive protein (5.13 mg/dL, normal: 0–0.3 mg/dL), indicating acute inflammation. Computed tomography (CT) confirmed a high-density area between the C5 and C6 laminae, consistent with calcification of the yellow ligament. Repeat MRI demonstrated persistent T1- and T2-low signal central region with surrounding intermediate and high signal intensity, confirming ongoing inflammatory or crystalline process with spinal cord compression. Despite continued NSAID therapy, pain remained uncontrolled. Surgical intervention was performed two weeks after the second admission, consisting of C6 laminectomy and resection of the C5-C6 yellow ligament. Intraoperative findings included a turbid, yellow fluid collection within the yellow ligament, visible calcifications, and dural adhesions to the ligament. Histopathological analysis of the fluid revealed calcium pyrophosphate dihydrate (CPPD) crystals, confirming the diagnosis of pseudogout (calcium pyrophosphate deposition disease) involving the yellow ligament. Postoperatively, her clinical course was uneventful; pain"}
+{"row_index": 42, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 68-year-old woman had heart problems for a long time. Her heart couldn’t pump blood well, and doctors found a buildup of protein in her heart muscle called amyloidosis. After 3 years, she got a small device in her chest to help her heart beat better. For 7 years, she stayed quiet, but then at age 78, she started having shortness of breath and her heart was much bigger than normal. A scan showed a big lump in her liver and a tumor that had spread from the liver through blood vessels all the way to her heart’s upper chamber. This tumor was diagnosed as liver cancer (hepatocellular carcinoma). Her blood test showed very high levels of a cancer marker. Even though she was on medicine to prevent blood clots, her body still had clots for months. The cancer in her liver and the blood clot were likely what made her heart problems worse. Her symptoms got better with medicine that helps remove extra fluid from her body.\"\n}"}
+{"row_index": 43, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 68-year-old woman was first admitted to the hospital with heart failure caused by a type of protein buildup in her heart called AL type primary cardiac amyloidosis. After three years, she had a device implanted to help her heart beat more effectively — this is called cardiac resynchronization therapy (CRT). The device was used because her heart was not pumping well, with a left ventricular ejection fraction of only 34%, and she had severe heart failure symptoms (NYHA class III). She remained stable for seven years after the device was implanted. At age 78, she returned with worsening heart failure symptoms, including shortness of breath and an enlarged heart seen on chest X-ray. An ultrasound and CT scan revealed a large tumor in her liver — specifically, hepatocellular carcinoma (HCC) — and a tumor that had spread from the liver through blood vessels into her heart, filling the right atrium. The tumor was confirmed with a contrast CT, and her alpha-fetoprotein level was extremely high, which is a sign of liver cancer. Even though she was on blood-thinning medication, her blood had been abnormally clotting for more than six months before her symptoms returned. Her heart failure symptoms improved with standard diuretics. Doctors believe the tumor and its spread caused the heart problems in this case. The patient’s specialty care was in cardiology.\"\n}"}
+{"row_index": 44, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 68-year-old female was initially admitted to the hospital due to symptomatic heart failure, which was ultimately diagnosed as AL type primary cardiac amyloidosis, confirmed by endomyocardial biopsy. Following a 3-year period of clinical follow-up, she underwent implantation of a cardiac resynchronization therapy (CRT) device for biventricular pacing, due to recurrent heart failure episodes (New York Heart Association class III), a left ventricular ejection fraction of 34%, and a wide QRS complex of 143 ms indicative of complete left bundle branch block. She remained clinically stable for seven years post-implantation. At age 78, she presented with a recurrence of heart failure symptoms, including progressive shortness of breath, physical examination findings consistent with decompensated heart failure, and significant cardiomegaly evidenced by an extended cardiothoracic ratio of 74% on chest radiography. Echocardiographic evaluation revealed a large echogenic mass occupying the right atrium. Sixty-four multi-detector computed tomography (CT) imaging demonstrated a lobulated, heterogeneously enhancing mass in the right upper lobe of the liver, consistent with hepatocellular carcinoma (HCC), and a continuous tumor thrombus extending from the portal vein and hepatic vein through the inferior vena cava to the right atrium. Alpha-fetoprotein levels were markedly elevated at >20,000 ng/mL (reference range: 0.0–10.0 ng/mL), supporting the diagnosis of HCC. The presence of persistent hypercoagulability was documented for more than six months prior to the clinical deterioration, despite concomitant anticoagulant therapy, suggesting a prothrombotic state that likely contributed to the formation and propagation of the tumor thrombus. The extensive tumor thrombus was deemed the primary hemodynamic contributor to the decompensated heart failure, leading to impaired cardiac filling and outflow. The patient's symptoms were initially managed with standard diuretic therapy, which provided partial relief. This case illustrates a rare and severe complication in which advanced hepatocellular carcinoma with portal and hepatic venous invasion leads to systemic venous obstruction and right-sided heart dysfunction, likely mediated by both tumor-induced thrombosis and chronic hemodynamic stress in the context of pre-existing cardiac amyloidosis and CRT device use. The interplay between cardiac amyloidosis, chronic left"}
+{"row_index": 45, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"An 80-year-old woman had a liver problem from hepatitis C, which caused scar tissue in her liver and a cancer in her liver (HCC). She had a small tumor treated with a procedure called RFA in two sessions, one 25 months ago and another 3 months later. A year before she got sick, a scan showed no signs of cancer or a hole in her diaphragm. Then, suddenly, she had a sharp pain in her belly. A chest X-ray showed part of her small intestine stuck in her chest. Doctors found that the intestine was trapped and not getting enough blood — this is called a strangulated diaphragmatic hernia. The hole where the intestine slipped through was about 2 cm wide. The doctors did emergency surgery to push the intestine back, cut out the damaged part, and fixed the hole with strong, dissolvable stitches. She recovered well and was out of the hospital in 10 days. Five months after surgery, no signs of the hole coming back were found.\"\n}"}
+{"row_index": 46, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"An 80-year-old woman with liver damage from hepatitis C and a history of liver cancer (HCC) was admitted to the hospital with sudden, severe pain in her upper abdomen. She had previously received radiofrequency ablation (RFA) treatment for HCC in segments 6 and 7 of her liver, a procedure that uses heat to destroy cancer cells. Twenty-two months before her admission, she had a second RFA session. A follow-up CT scan done a month before admission showed no signs of cancer or a diaphragmatic hernia (DH). However, on the day of admission, she developed intense abdominal pain, and a chest X-ray showed gas in the chest area, suggesting the small intestine had pushed through the diaphragm into the chest. Emergency laparoscopic surgery was performed. The surgery found that the small intestine had herniated through a hole in the diaphragm, and part of it was damaged due to lack of blood supply (ischaemic). The damaged section was removed, and the hole was closed with absorbable stitches. The patient recovered well and was discharged on day 10. At her 15-month follow-up, no signs of hernia recurrence were found.\"\n}"}
+{"row_index": 47, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"An 80-year-old woman with a history of hepatitis C-induced liver cirrhosis and hepatocellular carcinoma (HCC) involving segment 6 of the liver was admitted due to acute, sudden-onset epigastric pain. Prior to admission, she had undergone two ultrasonography-guided percutaneous radiofrequency ablation (RFA) procedures using the LeVeen Super Slim 3.0 device (Boston Scientific, Marlborough, Massachusetts, US). The first RFA session, performed 25 months earlier, targeted HCC in segment 6 and lasted 114 minutes, without the use of artificial pleural effusion or ascites. Three months later, a second RFA procedure was conducted for recurrent HCC in segment 6/7, again using the same device, this time with artificial pleural effusion, and lasted 125 minutes. A follow-up contrast-enhanced computed tomography (CT) scan performed one month prior to admission (21 months after the second RFA) showed no evidence of HCC recurrence or diaphragmatic hernia (DH). No history of trauma was present. On the day of presentation, she experienced acute, severe epigastric pain and was evaluated by her family physician. Chest radiography revealed a massive accumulation of intestinal gas above the right lobe of the liver, suggestive of intestinal herniation. She was transferred to our institution for further assessment. Vital signs at admission were stable: blood pressure 100/70 mmHg, pulse 80 beats per minute, and oxygen saturation 94% on room air. Physical examination revealed mild umbilical tenderness without signs of peritoneal irritation or trauma. Laboratory studies, including white blood cell count and C-reactive protein, were within normal limits. Hepatic function was impaired, with Child–Pugh Class B classification, mild hypoalbuminemia (3.2 g/dL), and a significantly prolonged prothrombin time (63% increase above baseline). Contrast-enhanced CT imaging demonstrated herniation of the small intestine into the right thoracic cavity, with congestion and haziness of the surrounding mesenteric fat, indicating ischemic changes; however, no evidence of bowel perforation was observed. Emergency laparoscopic surgery was performed under general anesthesia in the supine position using the open Hasson technique. A 12-mm port was placed above the umbilicus, followed"}
+{"row_index": 48, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 41-year-old man had long-term joint pain from rheumatoid arthritis, which he didn’t properly treat for a year. His body started showing signs of damage — red, non-blanching rashes on his legs and fingers, swelling, and lots of protein in his urine. Doctors found a kidney problem called membranous nephropathy, where tiny blood clots formed in the kidney’s filters. Even after stopping pain medicines and arthritis drugs, the protein in his urine stayed high. He also developed blood vessel inflammation (vasculitis) and lung disease (sarcoidosis), both of which improved with steroids. But the kidney problem only got better a little, not fully. He tried a special medicine called Rituximab, which helped at first, but the protein in his urine slowly went back up. His skin and joint issues completely went away after starting strong steroids, but the kidney problem still isn’t fully fixed. His blood tests show he still has cryoglobulins, meaning the problem is ongoing.\"\n}"}
+{"row_index": 49, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 41-year-old man with chronic rheumatoid arthritis had worsening symptoms, including skin rashes, swelling in his legs, and high protein in his urine, leading to a diagnosis of nephrotic syndrome. A kidney biopsy showed membranous nephropathy with blood clots inside the kidney's tiny blood vessels (intracapillary thrombi), which is linked to his autoimmune condition. Despite stopping his usual arthritis medications like NSAIDs and DMARDs, his proteinuria did not improve. He also developed cryoglobulinemic vasculitis and pulmonary sarcoidosis, both of which improved with high-dose steroids. Rituximab, a drug used to reduce immune system activity, helped reduce proteinuria initially, but only partially. After restarting the treatment, proteinuria gradually returned to higher levels, showing only partial response. His skin and joint symptoms fully resolved with treatment, but the underlying kidney issue remained difficult to fully control. His cryoglobulin levels stayed positive, suggesting ongoing immune system problems.\"\n}"}
+{"row_index": 50, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 41-year-old Hispanic man with a 2-year history of rheumatoid arthritis (RA) and type 2 diabetes mellitus presented to the emergency department with newly developed bilateral lower extremity purpuric rash and edema following a 1-year period of lost follow-up. RA was initially diagnosed two years prior, characterized by polyarthritis and markedly elevated serum immunologic markers: rheumatoid factor titer of 1220 IU/ml (normal <20 IU/ml) and anti-cyclic citrullinated peptide (anti-CCP) titer of 240.05 U/ml (normal <20 U/ml; strongly positive >60 U/ml). Prior therapy with methotrexate, low-dose prednisone, and sulfasalazine achieved disease control, but the patient discontinued DMARDs and was intermittently managed with ibuprofen 800 mg every 8 hours for joint pain for approximately one month.\\n\\nOn admission (day 0), physical examination revealed non-tender, non-blanching purpuric macules coalescing into large patches on the left leg, with smaller lesions on the right, in a dependent, flexor-surface distribution. Polyarticular arthritis was present with pain and swelling in the right 2nd and 3rd metacarpophalangeal (MCP) joints and left 3rd MCP joint. Boutonniere deformities were observed bilaterally, with greater severity on the left. Subcutaneous nodules were present at the elbows. Significant pitting edema was noted in the lower extremities. Urinalysis showed 21 red blood cells/high power field (hpf) and 7 white blood cells/hpf. Creatinine was 0.9 mg/dL, with an estimated glomerular filtration rate (eGFR) of 93 mL/min by the MDRD equation. Nephrotic syndrome was diagnosed based on proteinuria of 11 g/gm, hypoalbuminemia (2.2 g/dL), and peripheral edema.\\n\\nSerologic evaluation revealed low complement levels: C3 (86, normal 88–201), C4 (24, normal 16–47), positive cryoglobulin qualitative test (<1% cryocrit), and negative c-ANCA, p-ANCA,"}
+{"row_index": 51, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 79-year-old woman had a small hole in her heart’s left side that was still letting blood leak after surgery. Doctors used a tiny device (WATCHMAN) to close it. The device fit perfectly, stayed in place, and sealed the hole well. There was just 1.4 mm of tiny leak left, which is very small. After the procedure, she kept taking two pills: aspirin and apixaban. Six weeks later, the leak was still very small (1.49 mm) and there was no blood clot. So, her doctors stopped the apixaban pill and switched her to taking aspirin and another pill called clopidogrel. She hasn’t had any more bleeding, and they plan to stop the clopidogrel in 6 months, but she will keep taking aspirin forever.\"\n}"}
+{"row_index": 52, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 79-year-old woman had a procedure to close off a small pocket in her left atrium (LAA) using a device called the WATCHMAN™. She had previously had surgery to fix her heart valves and had been on blood thinners because of a high risk of stroke, but she had trouble with bleeding in her stomach due to diverticulosis. Before the procedure, her heart was stable and her kidneys were working well, though she had mild anemia. During the procedure, imaging showed that the LAA was still open, with only 1.4 mm of leak (PDL), and the device was placed successfully, meeting all key safety and placement standards. After the procedure, she continued on apixaban and aspirin. At 6 weeks, a follow-up scan showed the leak had slightly increased to 1.49 mm but no blood clots were found. Her doctors decided to stop apixaban and switch her to aspirin and clopidogrel instead. She has not had any major bleeding since, and her team plans to stop clopidogrel after 6 months, while continuing aspirin forever.\"\n}"}
+{"row_index": 53, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 79-year-old Black female with a history of mitral regurgitation, tricuspid regurgitation, and persistent atrial fibrillation complicated by recurrent significant gastrointestinal hemorrhage on anticoagulation due to diverticulosis was referred for percutaneous left atrial appendage occlusion (LAAO). Five months prior, she underwent surgical mitral and tricuspid valve repair, along with LAA ligation using a 35 mm AtriClip, driven by a high stroke risk (CHA2DS2-VASc score of 5) and intolerance to oral anticoagulation. Pre-procedural evaluation revealed a hemodynamically stable patient with regular heart rate and irregular rhythm, normal renal function (serum creatinine 0.81 mg/dL), and mild anemia (hemoglobin 10.8 g/dL, reference range 12.0–15.0 g/dL). Intra-procedural transesophageal echocardiography (TEE) confirmed complete closure of the left atrial appendage at the time of surgery. However, 40-day follow-up TEE and cardiac computed tomography (CT) demonstrated a persistent anatomic communication between the left atrium and the left atrial appendage, with no evidence of thrombus formation, indicating incomplete occlusion. Given this finding, a percutaneous LAAO device was considered to achieve definitive occlusion of the residual LAA pouch. Trans-septal puncture was performed under fluoroscopic and TEE guidance, with intracardiac ultrasound confirming mid-septal access. Intra-procedural TEE was utilized for precise LAA sizing, leading to the selection and deployment of a 27 mm WATCHMAN™ device. Deployment was successful, with all P.A.S.S. (Position, Anchor, Size, and Seal) criteria met. The residual patent left atrial appendage (PDL) measured 1.4 mm at the time of device placement. Post-procedural management included apixaban 5 mg twice daily and aspirin 81 mg daily. At 6-week follow-up TEE, a trivial PDL of 1.9 mm was identified along the posterior aspect of the appendage, with no detectable thrombus. The anticoagulation regimen was adjusted to"}
+{"row_index": 54, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A man in his 40s had a swollen belly and belly pain for months. His doctor couldn't find the cause at first, even after checking for cancer or liver problems. Tests showed no signs of infection or cancer, but later, his belly fluid had high levels of a substance linked to tuberculosis. When the doctor looked inside his belly with a small camera, they found a thick, fibrous layer wrapping around his small intestine, full of old infection signs. Biopsy samples proved it was tuberculosis, not cancer. After starting medicine to fight the TB, the swelling went down a lot and he started feeling better. He’s been back to normal for years with no more problems.\"\n}"}
+{"row_index": 55, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 47-year-old man had a 3-month history of abdominal swelling, pain, and nausea. Even though he lost some weight, he didn’t have fever, cough, or night sweats. He had no history of liver disease or abdominal surgery, but had had tuberculous pleurisy about 20 years earlier. Tests showed no signs of cancer, infection, or liver problems, and imaging didn’t show obvious causes. His abdominal fluid was clear and contained no bacteria or cancer cells. After two months, his symptoms worsened, with more fatigue, weight loss, and increased abdominal swelling. New tests showed higher levels of markers linked to infection and inflammation. Imaging revealed a thick membrane covering his small intestine and small nodules in the abdominal lining, which raised concern for either cancer or tuberculosis. A laparoscopy was done and found a dense fibrous membrane wrapping the small bowel, with small nodules that tested positive for tuberculosis. Biopsies confirmed tuberculous infection. The surgery tried to remove the membrane and release the trapped bowel, but it was very difficult due to the thick, fibrous tissue. The patient was then treated with anti-tuberculosis medication for six months. After treatment, his abdominal fluid greatly decreased, his symptoms improved, and he returned to normal function. He has remained symptom-free for six years without needing further surgery.\"\n}"}
+{"row_index": 56, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 47-year-old male presented with a three-month history of progressive abdominal distension, intermittent abdominal pain, and nausea, despite a 4 kg weight loss. He reported no fever, chronic cough, or night sweats, and had no prior history of abdominal surgery, liver cirrhosis, or chronic hepatitis virus infection. Notably, he had a history of tuberculous pleurisy approximately 20 years earlier. Physical examination revealed gross abdominal distension with ascitic fluid of unknown etiology, but no tenderness. Laboratory evaluation, including serum tumor markers, erythrocyte sedimentation rate (ESR), adenosine deaminase (ADA) activity, and anti-tuberculosis antibody (TB-Ab), was within normal limits. The tuberculin skin test was negative, and HIV serology was negative. Chest radiography showed no evidence of pulmonary tuberculosis. Plain upright abdominal X-ray demonstrated colonic air without air-fluid levels or free intraperitoneal gas, suggesting a non-obstructive fluid collection. Contrast-enhanced computed tomography (CT) of the abdomen revealed duodenal dilatation and congestion of small bowel loops trapped within a large volume of ascitic fluid, surrounded by a dense, fibrous membrane. Gastroscopy excluded gastrointestinal malignancy. Two paracenteses were performed, yielding blood-stained ascitic fluid without detection of malignant cells, acid-fast bacilli (AFB), or tuberculosis organisms. The ascitic fluid was classified as exudative, with ADA levels within the normal range (4–18 U/L), consistent with a non-infectious or non-tuberculous exudate. The patient declined laparoscopy and was discharged without a definitive diagnosis.\\n\\nTwo months later, the patient returned with worsening symptoms, including increased fatigue, emaciation, and a 10-kg weight loss over the prior two months. Repeat laboratory testing revealed elevated serum ADA (21 U/L, above the normal range of 4–18 U/L), elevated ESR (28 mm/h, normal 0–15 mm/h), and negative TB-Ab. Paracentesis fluid remained negative for bacteria, AFB, and malignant cells, but ascitic ADA increased significantly to 41 U/L, supporting an infectious etiology. Serum CA-125 was markedly elevated (97.39 U/mL, normal <35 U/mL), suggesting per"}
+{"row_index": 57, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 45-year-old man had high blood sugar for six months and was hospitalized. Tests showed a big tumor in his abdomen, but his blood pressure was normal. Doctors found the tumor was benign (not cancer), and they removed it using a small surgery (laparoscopy) with no major problems. After surgery, his hormone levels (which were high before) went back to normal, but his blood sugar stayed high. Tests on the tumor’s genes showed no changes that would mean it was cancerous. He’s doing well now, but his sugar level still needs attention.\"\n}"}
+{"row_index": 58, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 45-year-old man was hospitalized due to high blood sugar (hyperglycemia). He didn't have symptoms like headaches, high blood pressure, or heart palpitations. Tests showed his blood pressure was normal, but his serum and urine had high levels of catecholamines, which are chemicals linked to certain tumors. An abdominal CT scan found a 7.2 × 6.5 cm mass in the right area near the aorta, and the adrenal glands were normal. This led to a diagnosis of a large paraganglioma (PGL), a type of tumor that can cause high sugar levels. Because of financial reasons and lack of equipment, he didn't get a MIBG scan, which is often used to confirm such tumors. He was then treated with laparoscopic surgery — a minimally invasive procedure — where the tumor was safely removed. During surgery, his blood pressure stayed stable, and the procedure took 120 minutes with only about 50 mL of blood loss. He recovered well and was discharged on day 5. Pathology confirmed the tumor was benign, and DNA tests for SDHB and SDHD genes showed no mutations. Six months after surgery, his catecholamine levels returned to normal, but his blood sugar remained high, suggesting that the cause of his high sugar levels is still not fully explained.\"\n}"}
+{"row_index": 59, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 45-year-old male presented with a six-month history of hyperglycemia. He denied symptoms of episodic headache, hypertension, palpitations, or diaphoresis. Initial evaluation included 24-hour electrocardiographic monitoring and serial blood pressure measurements, both of which remained within normal limits. Glycemic control was achieved with insulin therapy, with serum glucose levels returning to baseline. Laboratory investigations were otherwise unremarkable, except for elevated serum and urinary catecholamine levels, suggesting possible pheochromocytoma or paraganglioma (PGL). Abdominal-pelvic computed tomography (CT) with contrast revealed a 7.2 × 6.5 cm inhomogeneous mass in the right para-aortic region, at the level of the inferior mesenteric artery, with no evidence of adrenal parenchymal involvement. This finding supported a diagnosis of paraganglioma, specifically a large para-aortic paraganglioma (POZ). Despite the absence of hypertension or autonomic symptoms, the elevated catecholamines indicated a functional tumor. Preoperative management included intravascular volume expansion and alpha-adrenergic blockade with phenoxybenzamine for two weeks, even in the absence of elevated blood pressure, to mitigate potential intraoperative catecholamine surges. Given the tumor's size, location, and potential for vascular involvement, a comprehensive surgical strategy was implemented, with full contingency planning for conversion to open surgery in the event of acute hemorrhage, limited operative field, malignant tumor invasion, or vascular injury. A laparoscopic approach was adopted, with the patient positioned in 70° left lateral decubitus. Trocars were placed at the umbilicus (10 mm), right costal margin (10 mm), right anterior axillary line (10 mm), and subxiphoid (5 mm). A steep Trendelenburg position was utilized to displace the small bowel and omentum away from the mass. Dissection began with ultrasonic shearing of the hepatic triangular ligament and hepatocolic ligament to mobilize the liver and expose the upper pole of the right kidney. The ascending mesocolon was longitudinally incised and expanded to visualize the right kidney and renal vein, with the descending and horizontal duodenal segments separated to expose the tumor's vascular supply. The tumor was found to be well-encapsulated"}
+{"row_index": 60, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 12-year-old boy from Syria came to the hospital because he was bleeding from his nose, not eating, losing weight, and sweating at night. When doctors checked him, they found swollen lymph nodes in the neck and under the jaw. There was also a lump on the roof of his mouth that pushed his uvula to one side, making it hard for him to swallow and breathe. Blood tests showed high white blood cells and a very high inflammation level. An ultrasound showed a slightly enlarged spleen, and chest X-ray was normal. A CT scan found many swollen lymph nodes on the right side of his neck. A small piece of tissue from a neck lump was taken and tested. At first, doctors thought it was a type of cancer called Classical Hodgkin Lymphoma. But later, tests showed it was actually a different kind of cancer — ALK-negative Anaplastic Large Cell Lymphoma — because the cancer cells had certain markers that matched this type. The boy got chemotherapy, but after 5 months, his condition didn’t improve, so doctors retested. The new test confirmed the cancer type. He got 5 rounds of chemo, but sadly, he passed away six months later.\"\n}"}
+{"row_index": 61, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 12-year-old Syrian boy was admitted to the hospital with bleeding from the nose (epistaxis), loss of appetite, weight loss, and night sweats. On exam, doctors found enlarged lymph nodes in the neck and under the jaw, with one node about 3 to 5 cm in size. A mass on the hard palate pushed the uvula to the right, causing trouble swallowing and breathing. Blood tests showed high white blood cells and elevated inflammation markers. An ultrasound showed a slightly enlarged spleen, and chest X-ray was normal. A CT scan found multiple enlarged lymph nodes on the right side of the neck. A biopsy of one of the lymph nodes showed abnormal cells that looked like Reed-Sternberg cells, leading to a preliminary diagnosis of Classical Hodgkin Lymphoma. However, because the lab tests needed to confirm the diagnosis were not available at the time, the exact type could not be confirmed. The boy started chemotherapy with the ABVD protocol, but after five months, there was no improvement, so the diagnosis was questioned. Later, immunohistochemistry tests confirmed the presence of CD30 and CD3 positive cells, but no ALK, CD15, or CD20, which led to the final diagnosis of ALK-negative Anaplastic Large Cell Lymphoma (ALCL). He received five cycles of chemotherapy, but unfortunately passed away six months after starting treatment.\"\n}"}
+{"row_index": 62, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 12-year-old Syrian boy was admitted to our hospital with symptoms of epistaxis, anorexia, weight loss, and night sweats. Medical and family history were unremarkable. Physical examination revealed preauricular, postauricular, and submandibular lymphadenopathy, with the largest node measuring approximately 3 × 5 cm. A hard palate mass was identified, deviating the uvula to the right, resulting in dysphagia and dyspnea. Laboratory findings included a white blood cell count of 35,380/μL, hemoglobin of 10.1 g/dL, platelets of 641 × 10³/μL, and an erythrocyte sedimentation rate (ESR) of 124 mm/hr, indicating systemic inflammation. Abdominal ultrasound demonstrated mild splenomegaly without focal lesions. Chest radiography was normal, with no mediastinal widening. A computed tomography (CT) scan revealed multiple enlarged lymph nodes on the right side of the neck. An excisional biopsy of a cervical lymph node (3 × 4 cm) was performed. Histopathological examination showed complete effacement of lymph node architecture, with proliferation of medium to large-sized anaplastic cells resembling Reed-Sternberg cells located in the interfollicular zones and subcapsular sinuses, admixed with histiocytes, small lymphocytes, and sparse eosinophils. The neoplastic cells exhibited a cohesive growth pattern, abundant cytoplasm, wreath-like or multiple nuclei, multiple nucleoli, and occasional mitotic figures, consistent with a large B-cell lymphoma. Bone marrow aspiration revealed hypercellularity with reactive inflammatory changes, but no evidence of neoplastic infiltration was detected. Based on routine histological staining, the initial diagnosis was Classical Hodgkin Lymphoma (CHL), with a recommendation for immunohistochemical confirmation. At the time, immunohistochemistry was not available at our institution. The patient was initiated on ABVD chemotherapy (doxorubicin, bleomycin, vinblastine, and dacarbazine). Five months later, the patient presented with no clinical improvement, prompting a re-evaluation of the diagnosis. Immunohistochemical analysis confirmed strong CD30 positivity in large Reed-Sternberg-like cells and CD3 positivity, while ALK, CD15, and CD20"}
+{"row_index": 63, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 6-year-old boy was brought to the emergency room because he suddenly couldn’t breathe after eating popcorn. At first, he was okay, but then he started coughing and had trouble breathing. He became very tired and hard to wake up. Doctors saw no blockage in his throat, but one side of his lung wasn’t working. A small bubble of air showed up under his skin on the right neck, which meant something was wrong with his breathing.\\n\\nHe was put to sleep with medicine to help him breathe, and a tube was put into his windpipe. A chest X-ray showed that air was trapped on the left side, and a small piece of popcorn was stuck in the main airway. Doctors knew it had to be removed right away.\\n\\nThey went into the operating room and used a special tool to look inside his airway. They found a piece of popcorn stuck in the trachea, right at the main split of the airway. They also saw a rare extra airway on the right side — it’s not normal, but it’s part of his body now.\\n\\nThe popcorn was safely taken out using a small tool. After that, the airway cleared up, and his breathing improved. He stayed in the hospital for a day, got medicine to help his airway heal, and was able to play and eat normally. He went home the next day feeling fine, with no more breathing problems.\"\n}"}
+{"row_index": 64, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 6-year-old boy who had no prior medical or surgical issues was brought to the Emergency Department with severe shortness of breath after accidentally swallowing a piece of popcorn. At first, his oxygen levels were okay, but soon he became very distressed and could not breathe properly. He was quickly intubated (a tube placed into his airway) and taken to the operating room for a procedure called direct laryngobronchoscopy, which allows doctors to see the airway and remove a foreign object.\\n\\nDuring the procedure, the doctors found a piece of popcorn stuck in the trachea (the main airway), blocking airflow. They successfully removed it using special tools. While doing this, they also discovered that the boy had a rare condition called a tracheal bronchus — a small extra airway that connects the trachea to a bronchus, which can sometimes cause breathing problems.\\n\\nAfter the foreign body was removed, the boy’s breathing improved, and his oxygen levels stabilized. He was moved to the pediatric intensive care unit (PICU) and stayed there until he was fully awake and able to breathe on his own. He was given medicine to reduce airway swelling and was able to eat and play normally. He was discharged the next day in good health with no further treatment needed.\"\n}"}
+{"row_index": 65, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 6-year-old male, medically and surgically free, with a body weight of 22 kg and height of 122 cm, was admitted to the emergency department (ED) by his teacher following sudden onset of severe shortness of breath after ingestion of popcorn. The clinical presentation began with acute respiratory distress, characterized by agitation, drowsiness, and semi-consciousness. Physical examination revealed no overt upper airway obstruction, but auscultation demonstrated absent air entry in the left lung, with subcutaneous emphysema noted on the right neck. Oxygen saturation remained stable with supplemental oxygen.\\n\\nShortly thereafter, the patient experienced a rapid deterioration in respiratory status and was intubated using a combination of midazolam, ketamine, and succinylcholine. Post-intubation chest radiography revealed proper endotracheal tube (ETT) placement, a hyperlucent left hemithorax, flattening of the left hemidiaphragm, rightward mediastinal shift, and a radiopaque lesion within the left main bronchus. Auscultation post-intubation showed minimal airflow in the left lung, with intermittent desaturation episodes.\\n\\nOtolaryngology–Head and Neck Surgery was consulted for urgent direct laryngoscopy and bronchoscopy (DLB). After stabilization, the patient was transferred to the operating room for DLB and foreign body removal, with informed consent obtained for potential complications including hemorrhage, infection, failure of foreign body extraction, pneumothorax, and dental injury.\\n\\nIn the operating room, the patient was intubated via bag-mask ventilation. Bilateral air entry was diminished, with scattered wheezing; significant chest wall expansion was observed on the left side, indicating impaired ventilation. Initial end-tidal CO₂ was 104 mm Hg. Arterial blood gas analysis revealed a pH of 6.87, PaCO₂ of 181 mm Hg (indicating severe respiratory acidosis), and PaO₂ of 231 mm Hg (mild hypoxemia).\\n\\nGeneral anesthesia was maintained with continuous propofol infusion at 250 mcg/kg/min and dexmedetomidine at 1 mcg/kg/hr. A single dose of dexamethasone (0.5 mg/kg"}
+{"row_index": 66, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 37-year-old woman started feeling weak in her hands about 5 years ago, first in her left hand, then later in her right. The weakness got worse over time, making it hard to write, hold chopsticks, or make a fist. By the time she came to the hospital, her hands were very weak and had shriveled. She didn’t get proper care before this. Tests showed that her hands were weak, but her sense of touch and thinking were normal. The nerves in her arms were damaged, especially the ones that control hand movement, and the damage was seen in the median, ulnar, and radial nerves. There was no damage to her nerves that carry feeling. She also has a condition called Hashimoto’s thyroiditis, which means her body is attacking its own thyroid gland. Even though her thyroid hormones were normal, the antibodies were high, showing the immune system is active. She was treated with medicine that helps calm the immune system, and after a month, her hand strength improved a lot. She will keep coming back for check-ups.\"\n}"}
+{"row_index": 67, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 37-year-old woman came to our hospital complaining of weakness in both hands. Five years ago, she first noticed mild weakness in her left hand, which slowly got worse. Two years later, her right hand also started to weaken. The weakness gradually progressed, making it hard for her to write, use chopsticks, or make a fist. She visited local clinics but wasn't properly evaluated. When she came to our hospital, her hands were severely weak and had noticeable muscle shrinkage, but she had no numbness or pain. Her mental abilities and brain function were normal, and there were no signs of problems in her face, eyes, or neck.\\n\\nNeurological tests showed severe weakness in the muscles of her hands, especially in the fingers and wrist areas, with poor muscle strength and visible muscle wasting. Her legs were not affected. Her reflexes in her arms were reduced, but her sense of touch and other sensory functions were normal.\\n\\nLab tests showed that her thyroid function (levels of hormones) was normal, but her immune system was active against the thyroid, which led to a diagnosis of Hashimoto's thyroiditis — a common autoimmune condition where the body attacks its own thyroid gland.\\n\\nElectrical tests of her nerves (nerve conduction studies) showed a specific pattern of weakness in the nerves that control hand movement, particularly in the median, ulnar, and radial nerves. This pattern is typical of a condition called Miller-Fisher-like neuropathy (MMN), which affects motor nerves without affecting sensation. Even though she didn’t have antibodies to certain nerve-related proteins, the clinical signs and test results clearly supported the diagnosis of MMN.\\n\\nA thyroid biopsy confirmed the presence of Hashimoto's thyroiditis. She was treated with high-dose intravenous immunoglobulin for five days, and one month later, her hand weakness and muscle deformities had improved significantly, with better nerve function. She is now being followed up regularly at our outpatient clinic.\"\n}"}
+{"row_index": 68, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 37-year-old woman presented with progressive distal upper-limb weakness, initially noted in the left hand five years prior with insidious onset, followed by symmetric progression to the right hand two years later. The weakness evolved gradually, impairing fine motor functions such as writing, chopstick handling, and fist formation. Clinical evaluation revealed severe motor weakness in both hands, with Medical Research Council (MRC) grades ranging from 2/5 to 3/5 across multiple intrinsic hand muscles, including flexor digitorum profundus and sublimis, flexor pollicis longus, extensor digitorum communis, and abductor digiti minimi, with notable muscle atrophy and distal deformities. Motor function in the lower extremities was preserved, and deep tendon reflexes were reduced in the upper limbs. Sensory examination was intact, with normal cortical sensation, cranial nerve function, cerebellar signs, and no evidence of sensory neuropathy. Neurological examination confirmed alertness, intact orientation, and absence of cognitive impairment. No abnormal findings were observed in the cervical spine on magnetic resonance imaging (MRI), which showed only mild disc protrusions at C5-6 and C6-7 levels.\\n\\nLaboratory investigations revealed normal hemogram, electrolytes, renal function, cerebrospinal fluid, and autoimmune markers for systemic vasculitides including rheumatoid factor, anti-dsDNA, lupus anticoagulant, anticardiolipin, antithrombin III, ANCA, anti-SSA/SSB, complement 3/4, anti-Jo-1, cryoglobulin, immunofixation, and anti-GM1/GD1b antibodies. A mildly elevated fluorescent antinuclear antibody titer (1:40) was detected, but no evidence of systemic autoimmune disease was found. Tumor markers (alpha-fetoprotein, carcinoembryonic antigen, CA-19-9, CA-125) and enzymatic markers (hexosaminidases A and B, creatine kinase) were within normal limits. Notably, thyroid function tests showed normal levels of T3, free T4, and TSH, but significantly elevated antithyroglobulin antibody (794 U/mL; normal: 0–100 U/mL) and antimicrosomal antibody (26,030 U/mL"}
+{"row_index": 69, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A man in his 60s got serious burns over 35% of his body after setting himself on fire. The burns were on his chest, arms, neck, and face. He also had smoke in his nose and throat, which meant his airway was burned. He got a bad infection in his blood, called bacteremia, and needed antibiotics to fight it. While on antibiotics, a red rash started on his chest and arms and spread fast to his hands and legs. This rash wasn’t on the burned areas, which means it didn’t start where the burns were. Doctors thought it was a reaction to the medicine, called TEN. They stopped the antibiotics and gave him a strong steroid medicine for 3 days. The rash got better after that. After a few days, the redness faded and he started feeling better. He didn’t get any new infections and was finally able to go home after 41 days in the hospital.\"\n}"}
+{"row_index": 70, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 68-year-old man suffered severe burns covering 35% of his body after setting himself on fire while trying to commit suicide. He had second- and third-degree burns, and his burns were so severe that he needed hospitalization. During treatment, he developed a blood infection (bacteremia) caused by a resistant bacteria, leading to antibiotic use. However, after stopping the antibiotics, a rash appeared on his trunk and arms and quickly spread to his limbs. This rash was later diagnosed as TEN (toxic epidermal necrolysis), a serious skin reaction that usually occurs outside of burn areas. The rash improved after stopping the antibiotics and starting a short course of high-dose steroid medication (methylprednisolone, 1,000 mg per day for 3 days). The skin reaction was only on non-burned parts, which suggests that TEN did not start at the burn sites. After recovery, he received several skin grafts over time and was eventually discharged from the ICU on day 41. No specific cause for the TEN was found, but the treatment was successful and he fully recovered.\"\n}"}
+{"row_index": 71, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 68-year-old male presented with extensive thermal burns resulting from a self-inflicted fire incident involving the application of 10 liters of gasoline to his head and body, followed by ignition on a riverbed. He had a history of insomnia and anxiety but no known allergies or smoking history. On admission, his Glasgow Coma Scale was 15, body temperature 35.8°C, heart rate 98 bpm, blood pressure 170/85 mm Hg, respiratory rate 20 bpm, and oxygen saturation 100% on 10-liter mask. Clinical examination revealed erythema and bullae involving the auricular to mandibular neck, thorax, abdomen, occiput, right upper arm, right dorsal hand, and left forearm. The anterior chest and posterior neck were covered with soot, with corresponding grayish-white skin discoloration, indicating deep dermal and epidermal destruction. Soot was also present in the nasal cavity, pharynx, and larynx, confirming upper airway burn injury. Bronchoscopy demonstrated soot adhesion, peripheral edema, and mucosal erythema from the vocal cords to the pharynx, consistent with thermal injury to the upper respiratory tract. Total body surface area (TBSA) burned was 35%, comprising 20% second-degree and 15% third-degree burns, with a revised BAUX score of 120, indicating severe burn severity. Initial wound management included daily washing with warm water, application of dimethyl isopropylazulene and gentamicin sulfate ointment, and coverage with moist wound care pads. Due to lack of guarantor consent, aggressive initial interventions such as surgical debridement and skin grafting were withheld.\\n\\nOn day 8, the patient developed a high fever (38–40°C) with a marked systemic inflammatory response, and blood culture identified methicillin-resistant *Staphylococcus aureus* (MRSA). Empirical therapy with vancomycin and ampicillin/sulbactam was initiated to manage the burn-associated infection. Once infection control was achieved, first split-thickness skin grafts (STSG) were performed on day 17 using a 0.01-inch graft harvested from both thighs via electric dermatome, meshed at a 1:3 expansion ratio. Following this,"}
+{"row_index": 72, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 50-year-old man had pain in his right eye, blurry vision, headaches, and trouble walking because he was unbalanced. Doctors found a fluid-filled sac inside his brain stem that was pressing on important parts of his brain. This sac was causing the symptoms. He had surgery to fix it. A small hole was made in his skull, and a tiny camera was used to drain the fluid from the sac and create a new path for brain fluid to flow. After the surgery, the fluid-filled sac got smaller, the brain’s fluid spaces shrank, and the fluid could now move freely through the brain’s tunnels. His walking, eye problems, and headaches all got better over time. Now he walks normally and feels much better.\"\n}"}
+{"row_index": 73, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 50-year-old man came in with pain in his right eye, blurry vision, headaches, and trouble walking due to balance issues. He had no numbness or weakness in his arms or legs. He also had a history of diabetes, high blood pressure, and high cholesterol.\\n\\nOn exam, he was alert and his mental status was normal. His right eye had reduced vision and he had double vision when looking to the sides. He showed slight eye shaking (nystagmus) but other brain nerve functions were normal. His strength and sensation were normal, and although his gait was slightly unsteady, he didn’t have a Romberg sign, which means his balance wasn't due to loss of coordination.\\n\\nMRI scans showed three cysts in the right part of his midbrain, totaling about 2.2 cm in size, with one large cyst measuring up to 1.7 cm. This cyst was pressing on the narrow passage (aqueduct) that carries cerebrospinal fluid, causing mild buildup of fluid in the brain ventricles (hydrocephalus).\\n\\nHe had surgery to relieve the pressure. Under general anesthesia, two small holes (burr holes) were made in his skull. One was in the right front part of the skull to access the third ventricle and create a new opening (endoscopic third ventriculostomy or ETV) to let fluid flow properly. The second hole was used to reach the brainstem cyst. Using a small camera (endoscope), the surgeon opened the cyst (fenestration) and drained its fluid, which was found to be pure cerebrospinal fluid. An external drain was placed to monitor pressure after surgery.\\n\\nAfter the procedure, the patient recovered well. His intracranial pressure stayed normal, and the drain was removed the next day. He could walk without help and perform daily tasks independently. His thinking and memory were unchanged.\\n\\nFollow-up scans showed that the brain ventricles had shrunk and fluid was now flowing through the aqueduct and the new opening. The brainstem cysts also decreased in size. By one month, his balance and double vision had improved. By five months, his headaches and double vision had almost completely gone, and imaging showed the cysts and ventricles were well decompressed.\"\n}"}
+{"row_index": 74, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 50-year-old male presented to the inpatient neurosurgical service with a progressive neurological syndrome characterized by right eye pain, blurred vision, occasional diplopia, headache, and gait imbalance with frequent falls. He denied peripheral sensory deficits or motor weakness. His medical history included type II diabetes mellitus, hypertension, and hyperlipidemia, all of which may contribute to cerebrovascular and neurodegenerative risk factors. On neurological examination, he was alert and oriented to person, place, and time. He exhibited decreased visual acuity in the right eye and diplopia on extreme lateral gaze, with subtle horizontal nystagmus. Cranial nerve examination beyond the ocular motor nerves was grossly intact, and all four extremities demonstrated normal strength and sensation. The Romberg sign was negative, though his gait was mildly ataxic, consistent with cerebellar or brainstem dysfunction.\\n\\nMagnetic resonance imaging (MRI) without contrast revealed a stable cluster of three cystic lesions localized within the tegmentum of the right midbrain, measuring 2.2 cm × 1.4 cm × 1.4 cm in aggregate. The largest cyst, located dorsomedially, reached a maximum dimension of 1.7 cm and demonstrated significant compression of the adjacent cerebral aqueduct. This compression was associated with mild hydrocephalus, evidenced by distention of both the lateral and third ventricles, indicating impaired cerebrospinal fluid (CSF) dynamics and impaired flow through the aqueduct.\\n\\nThe patient underwent an endoscopic third ventriculostomy (ETV) with cyst fenestration under general anesthesia. He was secured in a Mayfield head holder and stereotactic navigation was used to guide instrument placement. Two burr holes were created: a posterior burr hole in the right frontal region near the coronal suture for ETV access, and an anterior burr hole positioned anterior to the first to provide access to the brainstem cyst and posterior third ventricle. The endoscope was introduced via the posterior burr hole into the lateral ventricle and advanced through the foramen of Monro into the third ventricle. A conventional ETV was performed in the floor of the third ventricle, anterior to the mammillary bodies, establishing a new pathway for CSF flow.\\n\\nSubsequently, the endoscope was repositioned through the anterior burr hole and advanced posterior"}
+{"row_index": 75, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 69-year-old man had cancer in his left breast back in the 1990s. The tumor was big, over 6 cm, and spread to nearby lymph nodes. He had surgery to remove the breast and the lymph nodes. After surgery, he got chemotherapy, but two months later, cancer spread to his lungs. He then started treatment for the breast cancer, including pills that stop estrogen. Two years later, he started having trouble going to the bathroom often. Tests found he also had prostate cancer — a cancer in the prostate gland — with a high PSA level of 40.5. He got radiation to the prostate, and later took a medicine called Estracyt® that stayed in the prostate and helped lower the PSA. The PSA went back to normal, and he kept taking it for three years. But after five years, he got a blood clot in his leg, which happened because of the cancer medicines. Later, when he stopped breast cancer treatment, the breast cancer came back and spread to his liver. Even though he tried other medicines for the prostate cancer, the breast cancer kept getting worse and he passed away five years after getting prostate cancer. This case shows that men can get breast cancer, and they need special care for both cancers at the same time.\"\n}"}
+{"row_index": 76, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 69-year-old man was diagnosed with breast cancer in the 1990s. He had a large lump in his left breast, and tests showed it was a serious type of cancer (stage IIIC). He had a mastectomy and surgery to remove lymph nodes in his armpit. After surgery, he received chemotherapy, but two months later, the cancer spread to his lungs. He then started treatment for metastatic breast cancer using anti-estrogen therapy and 5-fluorouracil. Two years later, he started having trouble with urination, and tests found that he also had prostate cancer (stage III) with a high PSA level of 40.5 ng/mL. He received radiation therapy for the prostate cancer and later started using Estracyt® to control it. His PSA levels dropped and stayed normal for a few years. However, after five years, he developed a blood clot in his leg, which was linked to the hormone treatments. When he stopped breast cancer treatment, the breast cancer returned and spread to his liver. He continued prostate cancer treatment with other medications, but he eventually died from breast cancer progression five years after his prostate cancer diagnosis. This case shows that men can get breast cancer, and when they have both breast and prostate cancer, they need careful, ongoing care from a team of specialists.\"\n}"}
+{"row_index": 77, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 69-year-old male presented to the Department of Breast Surgery at Shiga General Hospital (Moriyama, Shiga, Japan) in the 1990s with a palpable lump in the left breast. Physical examination revealed a mass exceeding 6 cm in the upper-lateral quadrant, without evidence of skin invasion, and associated axillary lymphadenopathy. The patient had a comorbid history of type 2 diabetes mellitus, hypertension, cerebral infarction, and a previously managed brain schwannoma, treated with oral glimepiride 0.5 mg, nifedipine 40 mg, and aspirin 100 mg. No significant family history of cancer was reported.\\n\\nUltrasonographic evaluation confirmed a solid breast mass and right-sided axillary lymph node enlargement. Core needle biopsy demonstrated a high histological grade invasive ductal carcinoma, characterized by estrogen receptor (ER)-positive, progesterone receptor (PgR)-negative, human epidermal growth factor receptor 2 (HER2)-negative, and androgen receptor (AR)-positive status (detected using anti-AR rabbit monoclonal antibody SP107; Roche Tissue Diagnostics, Ltd.), with a Ki-67 labeling index of 10%, indicating a moderately proliferative tumor. Based on the Union for International Cancer Control (UICC) 8th edition TNM classification, the tumor was staged as cT3N3M0, stage IIIC breast cancer.\\n\\nDue to the absence of preoperative systemic therapy, the patient underwent mastectomy with axillary lymph node dissection. Final pathological assessment confirmed pt3N3a (36/39) M0, consistent with stage IIIC disease. Postoperative adjuvant chemotherapy was administered with a CEF regimen: epirubicin 40 mg/m², 5-fluorouracil (5-FU) 500 mg/m² every 2 weeks, and oral cyclophosphamide 100 mg daily. Following two cycles of chemotherapy, a computed tomography (CT) scan revealed pleural metastasis in the right lung, indicating early dissemination. The patient was then initiated on first-line endocrine therapy with high-dose toremifene (TOR) 120 mg twice daily and oral 5-FU/5’DFUR (doxif"}
+{"row_index": 78, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 45-year-old woman found a lump in her thyroid during a check-up and also had a blood clot in a vein near her thyroid. She didn’t feel sick or have any symptoms. The doctor saw nothing wrong during the exam. Tests showed her thyroid levels were normal. An ultrasound found a solid lump in her left thyroid and a clot in the middle thyroid vein. A small sample taken from the lump showed some cells that were growing, but it wasn’t clear if it was cancer. The doctor decided to remove part of her thyroid, the middle piece, and the lymph nodes near the neck to be safe. After surgery, the tissue test showed a very small type of thyroid cancer, and the clot was found to be part of the cancer spreading into the vein.\"\n}"}
+{"row_index": 79, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 45-year-old woman was found to have a thyroid mass and a blood clot in the middle thyroid vein during a routine physical exam. She had no symptoms and the exam showed no signs of illness. An ultrasound revealed a solid nodule in her left thyroid and a clot in the middle thyroid vein. A biopsy of the nodule showed an atypical lesion with some cells that were growing (classified as TBSRTC III), and no BRAFV600E mutation was found. Because of these findings, she had surgery, including removal of the left thyroid, part of the middle thyroid (isthmus), and nearby lymph nodes. A procedure was also done to remove the blood clot. After surgery, the pathologist found a small papillary thyroid cancer (microcarcinoma) in the left thyroid, and the clot was confirmed to be a tumor thrombus, meaning it had spread from the thyroid cancer.\"\n}"}
+{"row_index": 80, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 45-year-old woman presented with a thyroid mass and thrombosis in the middle thyroid vein identified during a routine physical examination. The thyroid mass was detected three months prior to presentation, with no associated symptoms. The patient reported undergoing surgery due to psychological stress related to the discovery, despite having no prior medical history of thyroid disease or familial predisposition to thyroid carcinoma. There was no history of childhood radiation exposure. Physical examination findings were unremarkable, with no signs of thyroid enlargement, neck tenderness, or other systemic abnormalities. Laboratory evaluation of thyroid function—specifically triiodothyronine (T3), free triiodothyronine (FT3), thyroxine (T4), thyroglobulin, and thyroid-stimulating hormone (TSH)—revealed normal values, indicating euthyroidism and ruling out overt thyroid dysfunction. Ultrasound imaging demonstrated a solid nodule in the left thyroid lobe, characterized by a medially echoic lesion, and concurrently revealed a thrombotic occlusion within the middle thyroid vein. Subsequent ultrasonography-guided fine-needle aspiration biopsy yielded a cytological diagnosis of an atypical lesion of ambiguous significance (TBSRTC III), exhibiting the presence of some actively proliferating cells, consistent with a biologically aggressive but non-malignant growth pattern. Notably, the BRAFV600E mutation, a well-established driver mutation commonly associated with papillary thyroid carcinoma, was not detected in the biopsy sample. The patient underwent a left thyroidectomy with isthmus lobectomy and prophylactic central neck lymph node dissection to ensure complete removal of potentially involved tissue. Additionally, thromboembolectomy was performed to remove the tumor thrombus from the middle thyroid vein. Final pathological examination confirmed the presence of a papillary microcarcinoma (pT1a) in the left thyroid, measuring less than 1 cm in greatest dimension, with no evidence of lymph node metastasis or extrathyroidal extension. The thrombus in the middle thyroid vein was histologically confirmed as a tumor-derived thrombus, consistent with extension of the papillary thyroid carcinoma into the venous system, a known phenomenon in certain subtypes of thyroid malignancy, particularly those with high vascularity or invasive growth patterns. This case illustrates the importance of imaging and biopsy in evaluating thyroid nodules with venous involvement, as well as the role of molecular testing in refining the biological characterization of thyroid lesions, even"}
+{"row_index": 81, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 22-year-old woman went to the hospital after having diarrhea for 5 days. She started taking clindamycin to treat an infection from a tooth problem. After that, her diarrhea got worse and turned into a serious condition called toxic megacolon, where her colon became swollen and burst. This led to a dangerous infection in her blood, called sepsis. Doctors found a harmful bacteria in her stool, called C. difficile (type 087), and another bacteria, Klebsiella pneumoniae, in her blood. She was treated with antibiotics like metronidazole and ceftriaxone, but she still got worse. Even with treatment, she died 10 days after coming to the hospital. The doctors found yellow spots in her colon during autopsy, which is a sign of pseudomembranous colitis. This case shows that even young, healthy people can get very serious infections from antibiotics, especially if they don’t get the right treatment fast. The infection spread quickly because the bacteria made a lot of harmful toxins. This strain (087) is common in Hungary but rare elsewhere. The patient had no hospital visits before, but her college life was stopped by this illness. She needed surgery, but it wasn’t done in time. This case warns doctors: young people can get severe colitis, and fast action is key to saving lives.\"\n}"}
+{"row_index": 82, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 22-year-old female university student was admitted to University Hospital of the West Indies, Jamaica with a 5-day history of diarrhea. The diarrhea started after she took clindamycin for a tooth infection. Despite stopping the antibiotic and starting other treatments, her condition worsened. She developed toxic megacolon, a severe swelling of the colon, which eventually led to a bowel perforation and blood infection (sepsis) caused by Gram-negative bacteria. Tests found that the diarrhea was due to Clostridium difficile (C. difficile) strain NAP1/ribotype 087, and blood cultures showed Klebsiella pneumoniae. She was treated with metronidazole and antibiotics to clear the bacteria, but her condition did not improve. She died 10 days after admission. An autopsy confirmed pseudomembranous colitis (PMC), a serious form of C. difficile infection, and found signs of severe inflammation in her large intestine. The case is unusual because it happened in a young person without prior hospital stays or health care exposure. While such severe complications are more common in older adults, this case shows that young people can also develop life-threatening forms of the infection. The doctors did not use recommended treatments like intracolonic vancomycin or surgery when needed, which may have contributed to the poor outcome. This highlights the importance of early recognition and proper treatment of C. difficile infections, even in younger patients.\"\n}"}
+{"row_index": 83, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 22-year-old female university student was admitted to the University Hospital of the West Indies, Jamaica with a presumptive diagnosis of pseudomembranous colitis (PMC) following a 5-day history of diarrhoea and fever that began 5 days after initiation of clindamycin therapy for a dental abscess requiring tooth extraction. Despite discontinuation of clindamycin and initiation of empiric therapy with chloramphenicol and metronidazole, her diarrhoea and fever persisted. Physical examination revealed a febrile patient with severe cardiopulmonary distress, tachycardia (heart rate 150 beats/min), and hypertension (blood pressure 150/100 mmHg). Laboratory findings included haemoglobin 10.4 g/dL, leukopenia (white cell count 2.1 × 10⁹/L), and platelet count 182 × 10⁹/L. Clinical deterioration progressed to toxic megacolon, bowel perforation, and Gram-negative sepsis. Blood cultures collected in brain heart infusion and thioglycollate broths grown from all four bottles after 24-hour incubation at 37°C yielded Klebsiella pneumoniae. Stool specimens collected the day after admission tested positive for Clostridium difficile toxin A and B using ELISA (Alexon Inc., Sunnyvale, CA), and the organism was isolated on cycloserine, cefoxitin, fructose agar (CCFA).  \\n\\nSusceptibility testing of K. pneumoniae via Kirby Bauer disc diffusion demonstrated susceptibility to ceftriaxone, co-trimoxazole, ceporin, amikacin, gentamicin, ceftazidine, and augmentin, with resistance to chloramphenicol, piperacillin, and ampicillin. The patient received intravenous metronidazole, followed by ceftriaxone and gentamicin, which resulted in fever resolution and sterile blood cultures. However, persistent hypotension, pulmonary oedema, leucopenia, and thrombocytopenia required intensive care management, and the patient died 10 days after admission. Autopsy revealed florid pseudomembranous colitis with multiple discrete yellowish exudative plaques throughout the large bowel mucosa, confirming PMC. Additional pathologic findings included markedly"}
+{"row_index": 84, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 58-year-old woman had a brain tumor before, called a meningioma, and had surgery for it when she was 31. She had more surgeries later, 16 and 26 years later. While treating a broken bone, doctors found a big lump in the back part of her pancreas. This lump looked scary, so they did scans and found it had blood vessels and was not normal. At first, they thought it might be a type of cancer or a rare tumor, but the test results showed it was actually a type of tumor called SFT, which started in her brain tumor. The doctors removed the pancreas part with the tumor safely, and she recovered well. Later, 4 years after surgery, the tumor came back in her brain, but no new tumors have come back in her belly. She is now being treated for the brain problem.\"\n}"}
+{"row_index": 85, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 58-year-old woman with a history of brain tumors (diagnosed as meningioma) was seen for a cystic tumor in the tail of her pancreas. The tumor was found during a CT scan done for a bone fracture. Imaging showed a complex, blood-rich mass that could have been a type of pancreatic cancer or a rare tumor like a neuroendocrine neoplasm or solid pseudopapillary neoplasm. However, after surgery, the pathologist found it was a malignant hemangiopericytoma (SFT) of the pancreas, a type of tumor that originates from connective tissue. Importantly, the brain tumor she had before was found to be the same type as this pancreatic tumor, meaning the pancreatic tumor likely came from the brain lesion. The surgery was successful with no complications, and she recovered well. Four years after the surgery, she developed a recurrence of brain disease, but no new tumors have appeared in her abdomen. She is currently being treated for the brain recurrence.\"\n}"}
+{"row_index": 86, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 58-year-old woman with a history of recurrent meningioma, initially resected at age 31 and subsequently reoperated at ages 16 and 26 years post-initial resection, was referred for evaluation of a cystic lesion in the pancreas tail. During admission for femoral fracture management, incidental detection via computed tomography (CT) revealed a 5.5-cm cystic mass in the pancreatic tail. Laboratory findings at presentation included a slightly elevated serum lipase (56 IU/L; normal range: 13–55 IU/L) and gamma-glutamyl transpeptidase (47 IU/L; normal range: 9–32 IU/L), with all tumor markers—carcinoembryonic antigen, carbohydrate antigen 19-9, and DUPAN-2—within normal limits. Endoscopic ultrasonography (EUS) demonstrated a well-encapsulated, circumscribed cystic mass with prominent intratumoral vascularity, including a hypervascular region resembling collateral vessels. Dynamic contrast-enhanced CT revealed a heterogeneously enhancing mass adjacent to the splenic hilum, characterized by strong arterial-to-portal phase enhancement of the solid components' rim and edge, with a large central non-enhancing area. During the portal to delayed phase, the solid components gradually isoattenuated relative to surrounding pancreatic parenchyma, with the non-enhancing region remaining distinct. Magnetic resonance imaging (MRI) confirmed low signal intensity on T1-weighted sequences and slightly higher signal intensity on T2-weighted sequences compared to normal pancreatic tissue, consistent with the presence of solid components. The large non-enhancing region on CT corresponded to a hyperintense signal on T2-weighted MRI, indicating cystic or necrotic transformation. Differential diagnoses included pancreatic neuroendocrine neoplasm, solid pseudopapillary neoplasm, hemangioma, and mucinous cystic neoplasm (due to patient sex and anatomical location), with invasive pancreatic carcinoma excluded based on imaging features. EUS-guided fine-needle aspiration was avoided due to the risk of cystic rupture and hemorrhage. The patient underwent distal pancreatectomy with regional lymph node dissection, with resection extending above the left edge of the superior mesenteric artery. The pancreatic stump was free of residual disease, with a margin of approximately 3 cm including stap"}
+{"row_index": 87, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 70-year-old woman had trouble moving her right side, which started 4 months ago. Doctors used a brain scan and a blood vessel test to check her brain. They found a small, old damage in her brain that could explain the weakness. They also found a strange blood vessel problem under the brain’s cover, called a TDAVF. This problem was feeding from two small blood vessels on the back of the brain and was sending blood backward (like water going uphill), which is dangerous. To fix it, doctors used a special glue to block the main leaky spot. After that, a small new leak appeared — it wasn’t seen before and came from a hidden blood vessel. But one week later, this new leak went away on its own. The patient had no more problems, no more weakness, and no signs of the leak coming back. She’s back to normal and doing fine.\"\n}"}
+{"row_index": 88, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 70-year-old woman had right-side weakness that had been present for 4 months. MRI showed a small area of damage (chronic infarction) in the left corona radiata, which likely caused her weakness. During the imaging, a vascular abnormality was found beneath the cerebellar tentorium. This abnormality was an arteriovenous fistula (TDAVF) supplied by the bilateral posterior meningeal arteries. It had a shunting point under the tentorium with blood flowing backward (retrograde flow), which is a type known as Borden III and Cognard III. This kind of abnormality can lead to bleeding, so it was treated with endovascular embolization using a special glue called n-butyl-2-cyanoacrylate (NBCA) to block the shunting point. After the procedure, the main shunt disappeared, but a small, new shunt was found that was not seen before. This new shunt was supplied by a blood vessel called the AWW, which was not visible on the preoperative scans. One week later, follow-up imaging showed that this residual shunt disappeared on its own. The patient had no further issues, no neurological problems, and no recurrence of the fistula after 6 months of follow-up. The treatment was successful in preventing complications.\"\n}"}
+{"row_index": 89, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 70-year-old woman presented with a 4-month history of right hemispheric motor weakness, which was evaluated with magnetic resonance imaging (MRI). Fluid-attenuated inversion recovery (FLAIR) sequences revealed chronic lacunar infarction in the left corona radiata, consistent with a contributing pathophysiological mechanism for her right-sided motor deficit. No edema or acute infarct was observed in either supratentorial or infratentorial regions. MRI angiography (MRA) identified a vascular lesion located beneath the cerebellar tentorium on constructive interference in steady-state (CISS) images, suggesting an arteriovenous shunt. Cerebral angiography confirmed the presence of a dural arteriovenous fistula (TDAVF) supplied by the bilateral posterior meningeal arteries (PMAs), with no other identifiable feeders detected. The shunting point was situated on the inferior surface of the cerebellar tentorium, exhibiting retrograde venous flow into the tentorial sinus and ultimately the transverse sinus, consistent with Borden type III and Cognard type III classification. The left vertebral angiogram demonstrated venous congestion with no retrograde flow in the basal vein of Rosenthal, while the internal carotid and bilateral posterior cerebral arteries exhibited fetal-type vasculature. The straight sinus demonstrated anterograde flow, and no arterial feeders were observed in the internal carotid or vertebral systems. The arteriovenous shunt was primarily fed by the PMAs, with drainage via the superior vermian vein to the petrosal vein and superior petrosal sinus, and alternatively through the inferior hemispheric vein, inferior hemispheric vein, and tentorial sinus. A selective angiogram of the mastoid branch of the occipital artery confirmed the PMA as the primary arterial supply, with bilateral involvement observed in both left and right occipital territories. The shunting point was precisely localized beneath the cerebellar tentorium on maximum intensity projection (MIP) images, with venous drainage converging into the transverse sinus. Transarterial endovascular embolization was performed under general anesthesia using two Envoy 5F 90 cm microcatheters (MPD, Codman Neuro) introduced into the bilateral occipital arteries. A Masters HF 2.8-Fr/3.2-Fr 125 cm"}
+{"row_index": 90, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 11-year-old girl had a serious bone cancer in her leg. Doctors removed the cancer and put in a fake joint (prosthesis) to replace the broken part. Six months later, the joint got infected, so they had to take it out and clean the area deeply. They used a temporary spacer with medicine to fight the infection. After healing, the girl broke a small bone in her thigh because she started walking too soon. This stopped her leg from growing longer. Her leg was now 5 cm shorter than the other. To fix this, they used a special growing prosthesis that can stretch over time. This device added 8 cm of bone length, helping her leg grow to the right size. The girl now walks without pain, carries her full weight, and plays sports again. There’s no sign of infection or cancer coming back. The leg is almost the same length now, and she’s doing well after all the surgeries.\"\n}"}
+{"row_index": 91, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"This report shares a case of a 11-year-old girl who had a serious bone cancer in her left leg, called high-grade osteosarcoma, which required surgery to remove the affected part of her femur. After the initial surgery, she developed a deep infection six months later, which required a two-stage revision. In the first stage, the infected implant was removed, the infection was treated with antibiotics, and the area was cleaned thoroughly. During recovery, she accidentally broke a bone in her tibia (the shin bone) because she started walking too early, which stopped her leg from growing properly. This caused a 5 cm difference in leg length.\\n\\nBecause the infection had already damaged the bone and growth plates, doctors chose a special bio-expandable prosthesis called MUTARS® BioXpand to fix the leg length. This device can grow longer over time by using a motorized nail that gently stretches the bone. It was designed to add 8 cm of bone length without needing to remove more bone or use a large implant. The prosthesis was placed, and the leg was gradually lengthened over several months. However, the family did not follow the required care schedule, which led to a small bony bridge forming at the break site. After adjusting the care plan, the lengthening was resumed safely.\\n\\nOnce the leg reached its full length, the temporary prosthesis was replaced with a permanent one. The new implant was stable and well-integrated. At the final follow-up, the girl was pain-free, walking without any support, and able to do all her normal activities, including sports. There was no sign of infection or cancer coming back. Although her knee joint is now slightly uneven due to the growth stoppage, she has excellent movement and function. Her outcomes were rated very well by medical scoring systems, showing a full return to daily life.\"\n}"}
+{"row_index": 92, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"An 11-year-old female presented with high-grade osteosarcoma of the left distal femur, undergoing wide resection followed by initial prosthetic reconstruction with a conventional endoprosthesis. Six months postoperatively, during the final cycle of adjuvant chemotherapy, she developed septic shock secondary to acute deep infection characterized by extensive pus formation and skin necrosis on the anteromedial knee, exposing the implant. Microbiological analysis revealed polymicrobial flora including Staphylococcus epidermidis, Neisseria mucosa, Cutibacterium acnes, and Bacillus sp., with no detectable genetic markers of antibiotic resistance; sensitivity testing confirmed standard susceptibility to empiric agents.\\n\\nFirst-stage revision involved explantation of the infected endoprosthesis, followed by thorough debridement of soft tissues and intramedullary canals using high-pressure lavage irrigation. A reinforced temporary antibiotic cement spacer (containing Vancomycin-loaded calcium phosphate beads, STIMULAN®) was implanted to maintain joint space and deliver localized antimicrobial therapy. The surgical site was covered with a vacuum-assisted closure device. Empiric therapy with ciprofloxacin and metronidazole was initiated, subsequently switched to linezolid and cefixime upon culture confirmation. Clinical improvement was observed with wound healing and normalization of inflammatory markers.\\n\\nDespite infection control, the patient independently transitioned to full weight-bearing, resulting in a Salter-Harris type V-like fracture of the proximal tibia physis. This fracture formed a bony bridge across the lateral half of the physis, resulting in irreversible loss of growth potential in the proximal tibia. The combined resection of the distal femur and proximal tibia physeal structures resulted in a 5 cm leg length discrepancy at the time of planned second-stage reconstruction. The initial cement spacer measured 10 cm, which is insufficient for an expandable prosthesis due to the minimum required implant length of 18 cm for distal femoral endoprostheses.\\n\\nGiven the anticipated end-growth discrepancy of 10 cm, which would be unmanageable without a lengthening implant, and considering the prior deep infection and compromised bone quality, a bioexpandable MUTARS® BioXpand endoprosthesis (Implantcast, Germany) was selected. This system comprises a 10 cm-long femoral component"}
+{"row_index": 93, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A man in his 60s had trouble remembering things, had poor brain function, and had problems with his nerves and eyes. He had diabetes, but his blood sugar was well controlled. He also had trouble with his bladder, blood pressure, and hearing. Doctors thought it might be a rare nerve or brain problem, so they checked his genes. They found a gene mutation in WFS1 that has been seen before in a person with Wolfram syndrome — a rare condition that causes memory loss, eye problems, and nerve issues. The test also found missing pieces in his energy-producing parts of the cells, which supports this diagnosis. Even though he had a normal diet, he was missing thiamine (a vitamin), which likely hurt his brain and nerves. Treatment for the vitamin didn’t help much. The doctors now believe he has Wolfram syndrome, and this explains most of his problems.\"\n}"}
+{"row_index": 94, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 61-year-old man with diabetes, memory problems, brain and nerve damage, and vision issues was initially diagnosed with a condition called multiple system atrophy. However, further testing showed that he had multiple problems in his mitochondria — the energy-producing parts of cells — and a severe lack of thiamine (a vitamin needed for brain function), even though he had a normal diet and no alcohol use. Tests found several mutations in his mitochondrial DNA, and while some genetic tests were negative, targeted exome sequencing revealed a specific mutation in the WFS1 gene. This mutation has been seen before in people with Wolfram syndrome, a rare disorder that affects the brain, eyes, pancreas, and nerves. The patient’s symptoms — including memory loss, vision problems, nerve damage, and diabetes — match what is seen in Wolfram syndrome. Although thiamine treatment had little effect, the genetic finding confirms the diagnosis. The patient now has a clear explanation for his condition and is being managed accordingly.\"\n}"}
+{"row_index": 95, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 61-year-old man with a history of diabetes mellitus (DM), autonomic neuropathy, diffuse brain atrophy, optic nerve atrophy (OA), and severe amnestic syndrome was referred for neurologic evaluation. Initially diagnosed with multiple system atrophy-cerebellar type (MSAc) based on MRI findings of severe cerebellar and brainstem atrophy, the clinical picture raised significant diagnostic concerns due to the absence of cerebellar motor signs and the prominent, progressive anterograde amnesia. The patient's early history included childhood bedwetting and urinary urgency in early adulthood, followed by bladder dysfunction requiring intermittent catheterization and erectile dysfunction in his 20s. At age 33, he was diagnosed with type 1 diabetes, with a random C-peptide level of 0.6 ng/mL (reference range 0.9–4.3 ng/mL) at a blood glucose of 83 mg/dL, indicating significant insulin deficiency. Despite good long-term glycemic control (HbA1c 6.5–7.2%), he had no evidence of microvascular or macrovascular complications, and polyuria/polydipsia resolved with insulin therapy.\\n\\nIn his 30s, he began wearing unusual clothing, later diagnosed with color blindness. At age 53, ophthalmologic examination revealed bilateral optic atrophy with preserved vision, and brain MRI demonstrated severe atrophy of the cerebellar hemispheres, vermis, pons, and middle cerebellar peduncles, along with moderate cerebral atrophy—findings that worsened at age 61 with more pronounced cerebral atrophy. Notably, he reported no gait instability or upper extremity incoordination, which is inconsistent with typical cerebellar atrophy.\\n\\nNeuropsychological assessment revealed profound anterograde amnesia, with additional deficits in cognitive flexibility, executive function, naming, and high-order visual processing. Attention, mental tracking, verbal abstract reasoning, complex auditory instructions, and visual spatial functions remained intact. Psychiatric evaluation identified depression, which responded to sertraline. Concurrently, progressive autonomic neuropathy developed, manifesting as gastroparesis and severe postural hypotension—exceeding the expected severity given his well-controlled diabetes and absence of diabetic complications. Bladder dysfunction progressed to the need for suprapubic catheterization at age 6"}
+{"row_index": 96, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 35-year-old housewife had sudden paralysis in her legs and trouble controlling her bladder after giving birth. She had back pain and couldn’t feel her legs properly, even though she was otherwise fine. Doctors found a growth outside her spine (in the middle back) that was pressing on her spinal cord. This growth, called an angiolipoma, was removed with surgery. The surgery worked well, and she recovered fully.\"\n}"}
+{"row_index": 97, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 35-year-old housewife developed sudden paralysis in her lower limbs and loss of bladder control one month after giving birth. She also had back pain. Upon examination, she had no weakness or reflex issues in her upper body, but her lower limbs showed no muscle strength, stiff muscles, overactive reflexes, and a positive Babinski sign. Sensory tests showed she lost feeling below the umbilicus, and there was tenderness in the middle back. Blood tests were normal. An MRI scan revealed a tumor outside the spinal cord, between the fifth and eighth thoracic vertebrae (D5 to D8), pressing on the spinal cord. The tumor appeared similar to fat on imaging and showed signs of being made of blood vessels and fat (angiolipoma). It was surgically removed through a back approach with no major complications. The surgery was successful, and the patient recovered well. The diagnosis was confirmed through tissue testing after surgery.\"\n}"}
+{"row_index": 98, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 35-year-old female presented to the emergency department with a sudden onset of bilateral lower limb paralysis lasting one month following vaginal delivery. The onset was acute and was accompanied by severe back pain and complete loss of sphincteric control, including urinary incontinence. On clinical examination, the patient was otherwise generally well with normal vital signs and a Glasgow Coma Scale (GCS) of 15/15. Cranial nerve function was intact, and upper limb motor strength, tone, and reflexes were normal, with preserved sensation to all modalities. In contrast, lower limb motor examination revealed complete paralysis (motor power grade 0), hypertonia, hyperreflexia (grade 4), and a positive Babinski sign, indicating upper motor neuron pathology. Sensory assessment demonstrated impaired vibration and position sense extending to the level of the umbilicus, consistent with a sensory level at T10. Mid-dorsal tenderness was noted, particularly at the D5–D8 region.\\n\\nHematological investigations were unremarkable, excluding hematologic causes of spinal cord compression. A dorsal lumbar MRI was performed, revealing a T1-weighted extradural hyperintense lesion extending from D5 to D8, posteriorly compressing the spinal cord. On T2-weighted imaging, the lesion exhibited hyperintensity relative to the spinal cord and was nearly isointense with normal adipose tissue, suggesting a lipid-rich composition. The lesion demonstrated characteristic myelopathic changes in the surrounding cord, consistent with acute compressive injury. Contrast-enhanced MRI showed focal, slightly inhomogeneous contrast uptake, indicating partial vascular permeability and possible active angiogenesis within the lesion.\\n\\nThe diagnosis was confirmed as a thoracic spinal extradural angiolipoma, a rare benign neoplasm composed of adipocytes and blood vessels, typically arising in the extradural space of the spinal column. Surgical intervention was performed via a posterior approach, involving dorsal decompressive laminectomy and complete resection of the lesion. The procedure was uncomplicated, with no intraoperative complications. The resected specimen was sent for histopathological analysis, which confirmed the presence of mature adipocytes, vascular channels, and a well-differentiated angiolipomatous tissue consistent with a benign angiolipoma. Postoperative recovery was excellent, with full restoration of motor and sensory function and resolution of sphincter dysfunction, indicating successful decompression and complete removal of the"}
+{"row_index": 99, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 46-year-old man got very sick with fever, cough, and chest tightness. Doctors tested his lung fluid and did a lung scan to find out if it was COVID-19. The test came back positive. He got medicine to fight the virus, like interferon and ribavirin, and other medicines to calm his body, clear mucus, protect his liver, and stop his lungs from scarring. He used a machine that gives him extra oxygen through his nose and mouth to help breathe easier. His breathing got better over time, his lungs healed, and he was finally able to go home. He fully recovered.\"\n}"}
+{"row_index": 100, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 46-year-old man was hospitalized with severe symptoms of fever, cough, and chest tightness that had lasted for about 11 days. He had recently traveled to several cities in China and had been in close contact with someone from Wuhan. Tests showed he had severe pneumonia, and although initial tests did not find the virus, a later test on his lung fluid (BALF) confirmed he had SARS-CoV-2 infection. To treat the virus, he received a combination of antiviral medications, including interferonalfa-1b and ribavirin, as well as lopinavir and ritonavir at different stages of his illness. He also got medicines to reduce inflammation, protect his liver, clear mucus, and support healthy gut bacteria. Because he was having trouble breathing, he was given oxygen through a BIPAP machine and later switched to high-flow humidified oxygen. His oxygen levels improved over time, and by early February, his symptoms had greatly improved. CT scans showed that the pneumonia was getting better. He was diagnosed with a mild liver issue possibly caused by the virus, and received treatment to protect his liver. To prevent long-term lung damage, he took a medication to support lung healing. By February 12, his lungs showed clear signs of recovery, and he was discharged from the hospital fully recovered.\"\n}"}
+{"row_index": 101, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 46-year-old male from Yili Development Zone, Xinjiang, China, was admitted to the University of Hong Kong-Shenzhen Hospital on 19 January 2020 with an 11-day history of fever (38 °C), dry cough, muscle ache, and fatigue. He reported close contact with an individual from Wuhan on 10 January and traveled from Yili to Shanghai (16 January), Shanghai to Ningbo (17 January), and Ningbo to Shenzhen (19 January), with no exposure to Wuhan. On 18 January, symptoms progressed to chest tightness without chest pain or hemoptysis. Initial testing excluded influenza A/B, respiratory syncytial virus (RSV), Mycoplasma pneumoniae, Cryptococcus haemolyticus, Aspergillus, Epstein-Barr virus (EBV) IgM and DNA, and Cytomegalovirus (CMV) DNA/antigen. Blood gas analysis on admission revealed a pH of 7.445, PaCO₂ of 4.72 kPa, and PaO₂ of 7.82 kPa, indicating hypoxemia. The patient was isolated in a single ward and initially treated with levofloxacin for suspected bacterial pneumonia. On 22 January, BALF testing was negative for Aspergillus, Legionella, Pneumocystis carinii, acid-fast bacilli, and Mycobacterium tuberculosis, leading to a diagnosis of severe bilateral community-acquired pneumonia (not excluding COVID-19) with hypoxemia. Levofloxacin was discontinued and replaced with a combination of amoxicillin-clavulanate and doxycycline for broad-spectrum coverage. On 23 January, the patient was transferred to the Third People’s Hospital of Shenzhen for further management. He had no comorbidities, allergies, or gastrointestinal or renal abnormalities.\\n\\nDuring hospitalization, the patient received a multimodal therapeutic regimen. Interferon-alpha-1b (60 μg via inhalation, administered twice daily) was used for antiviral activity against RNA viruses. Bio-Three tablets (0.4 g orally, three times daily) and Bifid-triple viable capsules (420 mg, three times daily) were administered to modulate intestinal microbiota. Mucosolvan ("}
+{"row_index": 102, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 60-year-old woman from Eritrea had a lump coming out of her left eye for 3 months, and her vision in that eye got worse. When doctors checked her, her left eye was bulging out a lot, her vision was very poor, and the back of her eye was swollen. Blood tests were normal, and a scan showed a fluid-filled cyst in her eye socket, which looked like a hydatid cyst. She took medicine for 2 weeks to help shrink it. Then, the doctors cut into her eye socket to remove the cyst. During surgery, the cyst broke and clear fluid came out, and the lining was taken out carefully. The tissue was tested and confirmed it was a hydatid cyst. After surgery, she had some swelling and trouble moving her eye slightly, but these improved over a week. Her vision and eye swelling got better. However, she moved back to Eritrea and we couldn’t check on her after that.\"\n}"}
+{"row_index": 103, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 60-year-old Eritrean woman had a 3-month history of painless swelling in her left eye, along with slowly worsening vision. On exam, her left eye was noticeably bulging, her vision was very poor, and there was swelling in the back of the eye (papilledema). Blood tests were normal, and a CT scan showed a fluid-filled cyst in her orbital area, which is typical of a hydatid cyst. She was treated with two weeks of oral albendazole, a medication that helps fight the cyst. After that, she had surgery where the cyst was removed through an incision in the eye socket. During surgery, the cyst ruptured and was carefully removed, and the tissue was sent for testing. The biopsy confirmed it was a hydatid cyst. After surgery, she had mild swelling of the eyelid and some difficulty moving her eye inward (adduction), but these improved over time. Her vision and eye swelling also improved. However, she moved back to Eritrea and we were unable to monitor her condition further.\"\n}"}
+{"row_index": 104, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 60-year-old female sheep herder from Eritrea presented to the St. Paul’s Hospital Millennium Medical College ophthalmology department with a three-month history of painless left eye proptosis accompanied by progressive decline in left eye visual acuity. Right eye visual acuity was 6/18, while left eye acuity was reduced to counting fingers at the front of the eye. Physical examination demonstrated a 4 mm exophthalmometric discrepancy between the eyes, with a proptosis measurement of 21 mm on the left side. Fundus examination revealed a tortuous temporal arcade and grade 4 papilledema in the left eye, indicating significant intracranial pressure due to optic nerve compression. Laboratory investigations, including a complete blood count, were within normal limits. A computed tomography (CT) scan of the brain and orbit demonstrated a well-defined, thin-walled, non-enhancing cystic lesion measuring 2.6 cm × 2.0 cm × 1.9 cm located in the left orbital cavity, exhibiting compression and lateral displacement of the globe and stretching of the optic nerve. The left medial rectus muscle was not distinctly delineated from the lesion, suggesting intimate adhesion. No osseous lytic or sclerotic changes were observed in the bony orbit, further supporting a non-invasive, soft-tissue origin. The imaging findings were consistent with a hydatid cyst of the orbit, a parasitic infection caused by *Echinococcus granulosus*. Abdominal ultrasound and chest X-ray were unremarkable, excluding extra-orbital hydatid disease or pulmonary involvement.\\n\\nThe patient was initiated on oral albendazole 400 mg twice daily for two weeks, a standard antihelminthic regimen targeting the larval stage of *Echinococcus*, with the goal of reducing cyst viability and preventing further growth. Following this medical phase, she underwent anterior medial orbitotomy for surgical excision of the cystic mass. Intraoperatively, a cystic lesion attached to the inferior aspect of the medial rectus muscle was identified. During manipulation, the cyst ruptured, releasing a clear fluid. The cyst wall, described as paper-white and laminated, was removed in piecemeal fashion, with careful preservation of the medial rectus muscle to avoid functional compromise. The external capsule was excised with meticulous dissection to prevent irreversible damage to the extraocular"}
+{"row_index": 105, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 43-year-old man from Asia had cancer in his penis that had been growing for 3 years. The cancer spread to his right eye, where it damaged the inside of the eye and made him lose his vision. Doctors saw signs of cancer in the eye using scans — the cancer looked bright on one type of scan and dark on another. Because the eye pain was severe and vision couldn't be saved, they removed the entire right eye. After checking the tissue from the eye, they found it was cancer that started in the penis and had spread to the eye. This cancer was not very aggressive but still dangerous. The man got treatment with chemo and radiation, but later the cancer spread to his brain and he passed away.\"\n}"}
+{"row_index": 106, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 43-year-old Asian man with a 3-year history of penile cancer developed cancer that spread to his right eye. He had been diagnosed with advanced cancer (stage T4N3M1) and had already lost vision in his right eye more than a month before. Imaging tests showed that the cancer had spread to the inside of his right eye, including the retina, optic nerve, and surrounding structures. On MRI, the tumor appeared bright on T1-weighted images and dark on T2-weighted images, which are signs of metastatic cancer. After removing the affected eye (enucleation) due to severe pain and no chance of recovery, pathologist tests confirmed it was metastatic, moderately differentiated penile squamous cell carcinoma. The cancer had spread into the eye's layers, including the sclera, choroid, and retina. He received chemotherapy and radiation for six months, but eventually died from brain metastasis.\"\n}"}
+{"row_index": 107, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 43-year-old Asian male with a three-year history of progressively invasive penile carcinoma (PC) presented on January 31, 2015, with acute pain in the right eye and irreversible vision loss, with best-corrected visual acuity of no light perception in the right eye and 20/20 in the left eye. The patient was previously staged as T4N3M1 according to the TNM classification, indicating advanced local invasion (T4), regional lymph node involvement (N3), and distant metastasis (M1). Prior to ocular metastasis, he had developed bilateral inguinal lymph node and ipsilateral iliac node metastases, followed by systemic dissemination to the liver and lungs. His medical history included multiple prior surgical interventions, with no reported family history of hereditary disorders or psychiatric conditions.\\n\\nOphthalmological examination revealed mild proptosis and intact ocular motility in all directions. The right eye demonstrated a dilated pupil (5 mm) with absent pupillary reflex, and fundus examination showed post-equatorial retinal detachment with a black eminence and a pale optic disc. B-scan ultrasonography confirmed retinal detachment with intraretinal hemorrhage. Orbital magnetic resonance imaging (MRI) demonstrated thickening and structural strengthening of the right lateral orbital wall, consistent with metastatic tumor infiltration. The internal rectus and lateral rectus muscles were also thickened and hardened, with a 2-cm-long optic nerve exhibiting significant thickening and invasion at its stump. MRI sequences revealed hyperintensity on T1-weighted imaging and hypointensity on T2-weighted imaging, indicative of tumor-associated signal characteristics. Contrast-enhanced MRI showed inhomogeneous enhancement of the posterior orbital wall, supporting active tumor vascularity and cellular infiltration. Histopathological evidence confirmed invasion of the optic nerve, choroid, sclera, retina, and external intraocular structures by metastatic cells.\\n\\nIntraoperative evaluation of the enucleated right eye revealed complete tumor involvement of the globe. Histopathological analysis, performed using hematoxylin-and-eosin (H&E) staining, identified keratin pearls and sheets of keratinized squamous carcinoma cells with intercellular bridges, consistent with moderately differentiated penile squamous cell carcinoma. The tumor demonstrated infiltrative growth patterns, with extensive spread into the deep layers of the eye, including the choroid, which is a"}
+{"row_index": 108, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 33-year-old man had belly pain and vomiting. Doctors found a 45-mm lump in his small intestine (ileum) that had some calcium inside it. The lump wasn’t blocking or twisting, so they didn’t think it was an emergency. After checking it with a scan, they knew it was a tumor. They did a small surgery through just one spot on his belly to remove part of the small intestine. The tumor looked like a soft, white growth with lots of thick, stiff tissue and tiny calcium spots. It had some immune cells inside. Tests showed that a certain protein (factor XIIIa) was present, but other tumor markers were missing. This pattern matched a type of rare tumor called CFT. The man got better after the surgery and hasn’t had any problems in 6 months. No signs of it coming back.\"\n}"}
+{"row_index": 109, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 33-year-old man came in with abdominal pain and vomiting. His physical exam showed lower abdominal tenderness, but blood tests and imaging like ultrasound and X-ray were normal. A CT scan found a 45-mm mass in the ileum (a part of the small intestine) with some calcification, but no signs of blockage or twisting. The tumor was suspected, and after further testing with MRI, doctors considered several possibilities, including a gastrointestinal stromal tumor (GIST), a chronic hematoma, a leiomyoma, or a CFT (cystic fibrosis-related tumor — actually, in this case, a CFT refers to a specific type of tumor called IgG4-related fibrosis). The patient underwent laparoscopic surgery using a single small incision in the belly button. During the procedure, a white, pedunculated tumor was found in the ileum, and only that tumor was seen. A partial resection (removal) of the ileum was done, and the ends were reconnected. Pathology showed a tumor made up of spindle-shaped cells, dense collagen, and scattered calcifications, with some lymphoplasmacytic cells present. Key test results showed that factor XIIIa was positive, while other markers for common tumors were negative. Over 40% of the immune cells in the tumor were IgG4 positive, which is a key sign of CFT. Based on these findings, the tumor was finally diagnosed as a CFT. The patient recovered well, was discharged on day 7, and has had no signs of recurrence in the 6 months since surgery.\"\n}"}
+{"row_index": 110, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 33-year-old man with no prior medical or surgical history presented with acute abdominal pain and vomiting. Physical examination revealed localized tenderness in the lower abdomen, while laboratory investigations were unremarkable: C-reactive protein at 0.16 mg/dL, white blood cell count of 9600 /μL, neutrophil percentage 91.3%, and lymphocyte count 5.4%. Initial imaging with ultrasonography and radiography failed to identify a source of pain. Contrast-enhanced computed tomography (CT) revealed a 45-mm-sized mass in the ileum with partial calcification, showing no signs of invagination, obstruction, or volvulus, and no other radiological findings suggestive of underlying pathology. The patient was clinically diagnosed with an ileal tumor, and his symptoms resolved spontaneously. Subsequently, magnetic resonance imaging (MRI) was performed to characterize the lesion, demonstrating hypointensity on both T1-weighted and T2-weighted images, with isointense enhancement on gadolinium-enhanced T1WI, which supported a differential diagnosis including gastrointestinal stromal tumor (GIST), chronic distending hematoma, leiomyoma, and carcinoid tumor of the gastrointestinal tract (CFT).\\n\\nLaparoscopic surgical intervention was performed for both diagnostic and therapeutic purposes using a single-port technique via a vertical 4-cm umbilical incision with EZ access and Lap Protector (Hakko Medical, Nagano, Japan), employing two 5-mm ports. Intraoperatively, a white-colored tumor was identified in the ileum at 100 cm from the terminal ileum. No additional tumors, lymph node metastases, or evidence of systemic dissemination were detected in the abdominal cavity. The tumor was extracorporeally retrieved and a partial resection of the ileum was carried out, followed by a functional end-to-end anastomosis. Macroscopically, the tumor was pedunculated and located on the antimesenteric side. Microscopically, it extended from the muscularis propria to the subserosa, exhibiting a hypocellular architecture composed of spindle cells embedded in dense hyalinized collagen with interspersed calcification and focal infiltration of lymphoplasmacytic cells. Immunohistochemical analysis showed negative or nearly negative staining for CD34, c-kit, DOG-1, desmin, S100"}
+{"row_index": 111, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 24-year-old man from Somalia had a fever, headache, stomach pain, nausea, vomiting, and lost weight over two months. He had been treated before with medicine and a blood transfusion, but it didn’t help. When he came to the hospital, he looked very weak and pale, and his belly was swollen. His blood tests showed very low red blood cells, white blood cells, and platelets — this means his body wasn’t making enough blood cells. The test for malaria was positive, but after three days of anti-malarial medicine, his symptoms didn’t go away and his belly got worse. Other tests ruled out HIV, hepatitis, and infections like Brucella or Leishmania. Blood and bone marrow checks showed no infection or cancer. A small piece of the spleen was taken and tested — it confirmed the cause was visceral leishmaniasis. He was given a special medicine mix (sodium stibogluconate and paromomycin) for 17 days. After a few weeks, his symptoms got better, and by the end, he was fully back to normal. A second test of his spleen showed no more signs of the disease, and he was sent home.\"\n}"}
+{"row_index": 112, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 24-year-old man from a rural area in Somalia, who recently moved from Yemen, came to the hospital with a two-month history of fever, headache, abdominal pain, nausea, vomiting, and weight loss. He had previously been treated at a local clinic with antibiotics, fever-reducers, and a blood transfusion, which gave only temporary relief. When he returned with worsening symptoms, he was found to be pale, weak, and had an enlarged spleen and liver. Blood tests showed low levels of red blood cells, white blood cells, and platelets (a condition called pancytopenia), and a rapid test for malaria was positive. However, after three days of anti-malarial treatment, his symptoms did not improve and his spleen continued to grow larger. Other tests for infections like HIV, hepatitis, and Brucella were negative, and blood and bone marrow exams showed no signs of infection or cancer. A biopsy of the spleen confirmed the diagnosis of visceral leishmaniasis, a serious parasitic infection. The patient was treated with a combination of sodium stibogluconate and paromomycin for 17 days. After four weeks, his symptoms improved significantly, and by the fifth week, he was fully recovered. A follow-up spleen biopsy showed normal results, and he was discharged.\"\n}"}
+{"row_index": 113, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 24-year-old male patient from Sa’ada, northwest Yemen, recently relocated to Burhakaba, Somalia, was referred to our hospital with a complaint of a left upper hypochondrial mass. He presented with a two-month history of high-grade fever, headache, abdominal pain, nausea, vomiting, anorexia, and progressive weight loss. He reported a prior episode of similar symptoms three months earlier. Prior to hospital admission, he had been evaluated at a local health facility where he received symptomatic management with antipyretics, broad-spectrum antibiotics, and two units of whole blood transfusion, resulting in transient clinical improvement. However, symptoms recurred two months later, now accompanied by generalized weakness and further weight loss.\\n\\nOn presentation, the patient exhibited signs of chronic illness: pallor, fever (temperature 38.9°C), tachycardia (pulse 110 beats/minute), and splenomegaly. Vital signs included blood pressure 110/78 mmHg, respiratory rate 16 breaths/minute, blood glucose 110 mg/dL. Laboratory findings revealed profound pancytopenia: white blood cell count of 1.03 × 10⁹/L (normal 4.00–10.00 × 10⁹/L), hemoglobin 6.6 g/dL (normal 12.0–16.0 g/dL), hematocrit 0.203 (normal 0.400–0.540), and platelet count 70 × 10⁹/L (normal 100–300 × 10⁹/L). Inflammatory markers were elevated: C-reactive protein 45.73 mg/L (normal 2.5–10 mg/L), with significant hepatocellular enzyme elevation—ast 104.5 U/L (normal 6–38 U/L) and alt 112.5 U/L (normal 6–40 U/L). Renal function parameters were mildly impaired: serum creatinine 1.4 mg/dL (normal 0.4–1.4 mg/dL) and serum urea 54.3 mg/dL (normal 10–50 mg/dL).\\n\\nA rapid diagnostic"}
+{"row_index": 114, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 34-year-old man felt short of breath when walking, had swelling in his legs, lost 50 pounds without trying, and was tired all the time. He had small spots in his lungs and fluid building up around his heart and lungs. Tests showed fluid pressing on his heart, which made it hard to pump blood. A drain was put in to remove the fluid, and after a while, the fluid came back and his heart stopped working properly. Doctors did an emergency surgery to open up the space around his heart to let the fluid go out. Later, scans showed the tissue around his heart was stiff and not moving right, which means his heart was being squeezed. Tests confirmed this was due to a disease called sarcoidosis, which causes small lumps in the lungs, lining of the lungs, and the sac around the heart. The surgery removed the stiff tissue, and the tissue tested showed small lumps, proving the disease was in the heart sac. Now he’s doing better, no more swelling, no shortness of breath, and he’s on medicine to keep it from coming back.\"\n}"}
+{"row_index": 115, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 34-year-old man with a five-month history of shortness of breath when active, swelling in his legs, unexplained weight loss, and fatigue was evaluated. He had a cough and felt tired easily. Tests showed lung nodules, especially in the upper lungs, and fluid buildup in his lungs and around his heart. His heart was showing signs of pressure problems due to fluid around it, which led to a temporary drain being placed. After the drain was removed, the fluid returned and caused a serious heart condition called cardiogenic shock, requiring an emergency procedure to relieve the pressure. Imaging tests showed that the fluid around the heart was thickening and not moving normally, which is a sign of constrictive pericarditis. A procedure called pericardiectomy was done, and the tissue samples showed small, non-necrotizing granulomas, confirming that the condition was sarcoidosis affecting his lungs, pleura, and heart. He was started on steroids and later switched to a lower dose with methotrexate. Over time, his symptoms improved, his breathing got better, and his heart function returned to normal. Follow-up tests showed no ongoing issues and he was able to return to a stable condition.\"\n}"}
+{"row_index": 116, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 34-year-old Caucasian male presented with a five-month history of progressive exertional dyspnea, productive cough, lower extremity edema, unintentional 50-pound weight loss, fatigue, and early satiety. His medical history included controlled hypertension managed with hydrochlorothiazide and carvedilol, with recent initiation of furosemide for peripheral edema. He was a non-smoker with no recent travel or environmental exposures. Physical examination revealed diaphoresis, pallor, diminished cardiac sounds, markedly reduced breath sounds in the right thorax, and 2+ pitting edema of the lower extremities. Vital signs showed oxygen saturation of 92% on 2 L/min supplemental oxygen and mild tachycardia.\\n\\nPulmonary function testing revealed an intrinsic restrictive ventilatory defect: forced vital capacity (FVC) of 4.03 L (59% of predicted) and diffusion capacity of the lung for carbon monoxide (DLCO) of 23.3 mL/min/mmHg (55% of predicted). Arterial blood gas analysis demonstrated hypoxemia with a partial pressure of oxygen (PaO₂) of 60 mmHg. High-resolution chest computed tomography (HRCT) showed diffuse pulmonary nodules with upper lobe predominance and perilymphatic distribution, diffuse partially calcified mediastinal and hilar lymphadenopathy, moderate to large right pleural effusion, and moderate to large pericardial effusion with pericardial thickening.\\n\\nTransthoracic echocardiography revealed preserved left ventricular systolic function, a large circumferential pericardial effusion, and evidence of respiratory variation in mitral and tricuspid inflow, along with paradoxical septal shift—findings consistent with early tamponade physiology. The patient was admitted and underwent urgent pericardiocentesis, during which 500 mL of serosanguinous fluid was removed, resulting in immediate clinical improvement. The fluid was monocyte-dominant, culture-negative, and showed no evidence of infection or malignancy. The pericardial drain was removed after several days of minimal output.\\n\\nDiagnostic workup included thoracentesis, fiberoptic bronchoscopy with bronchoalveolar lavage (BAL), transbronchial biopsy, and endobronchial ultrasound-guided"}
+{"row_index": 117, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 62-year-old woman had high CA125 levels in her blood for a year. At first, doctors thought it was a harmless cyst called a chocolate cyst, but after checking with ultrasound and special imaging, they saw signs of a serious tumor. A test using contrast ultrasound showed the tumor had solid parts and blood flow, which made doctors think it might be cancer. The final test on the tumor tissue confirmed it was high-grade serous adenocarcinoma, a type of ovarian cancer. She had surgery to remove the tumor and then received chemotherapy, which worked well. Her CA125 levels went back to normal, and she is now doing well.\"\n}"}
+{"row_index": 118, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 62-year-old woman had rising CA125 levels in her blood for one year, which raised concern for ovarian cancer. At a local hospital, her ultrasound showed a large mass in her pelvis, but the doctors initially thought it was a chocolate cyst—a common type of benign ovarian cyst. To get a clearer picture, she was referred to our hospital for further testing. Contrast CT and MRI scans showed a complex cystic mass in her right ovary, with features that could suggest either a benign or malignant condition. A transvaginal ultrasound combined with contrast-enhanced ultrasound (CEUS) revealed signs of a malignant tumor, leading doctors to suspect cystadenocarcinoma. After surgery, the tumor was found to be a high-grade serous adenocarcinoma, a type of aggressive ovarian cancer. Pathology confirmed the diagnosis, and the patient underwent chemotherapy with carboplatin and paclitaxel. Her CA125 levels dropped to normal after treatment, and she is now doing well with no signs of recurrence.\"\n}"}
+{"row_index": 119, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 62-year-old woman presented with a progressively rising serum CA125 level, initially elevated to 50 U/ml (normal < 35 U/ml) in November 2018, which increased to 75 U/ml by November 2019. Her serum CEA and CA19-9 levels remained within normal limits, and initial transvaginal ultrasound (TUS) revealed no obvious abnormalities. Subsequent TUS at the local hospital demonstrated a large pelvic mass, prompting referral to our institution for further evaluation. Laboratory investigations, including tumor markers, reproductive hormone assays, and routine blood work, were within normal ranges. The patient was asymptomatic, with no palpable abdominal mass on physical examination. A positive family history was noted, as her mother had died of ovarian cancer.\\n\\nAbdominal computed tomography (CT) revealed a well-circumscribed, hypodense mass in the right adnexa. Contrast-enhanced CT demonstrated mild enhancement of the lesion and a fluid–fluid level sign. Magnetic resonance imaging (MRI) showed a well-defined, lobulated, cystic mass measuring 4.9 × 4.8 cm in the right pelvic cavity. On T2-weighted imaging (T2WI) and T1-weighted imaging (T1WI), the mass exhibited mixed signal intensity, with nodular hypointensity observed on both sequences. Diffusion-weighted imaging (DWI) revealed severe hyperintensity, consistent with restricted diffusion, and a fluid–fluid level sign was present. Based on these imaging features, the lesion was initially suspected to represent a chocolate cyst (endometriotic cyst), a benign condition commonly associated with endometriosis.\\n\\nPreoperative TUS revealed a right adnexal mass measuring approximately 5.6 × 4.4 × 5.5 cm, characterized by a well-defined cystic structure with mural and septal nodules. The largest internal papillary excrescences measured 3.0 × 1.4 × 1.7 cm. Doppler ultrasound detected blood flow within the internal septations, cystic wall, and papillary projections, with a resistive index of 0.9—indicative of vascular resistance consistent with a neoplastic process. Given the presence of papillary structures and abnormal vascularity, a primary diagnosis of malignant neoplasm was established.\\n\\nTo further characterize"}
+{"row_index": 120, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 63-year-old woman had very bad kidney disease and couldn’t walk or move. She was confused for 5 days and had been on dialysis for months. She also had liver problems, high blood sugar, and a lung infection. A type of fungus called Candida guilliermondii was found in her blood and in the tube that goes into her vein. Even after changing her medicine, the fungus stayed in her blood. A small lump was found on her heart valve, but the family said no surgery because she had too many serious health problems. She was given medicine for the fungus, but it didn’t work. After 8 weeks, her condition got worse — the lump grew bigger and she had lung and spleen problems. She was given hospice care and sent home on a daily antifungal pill. She died a few weeks later from liver problems and being in a deep sleep.\"\n}"}
+{"row_index": 121, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 63-year-old woman with end-stage kidney disease was admitted to the hospital after being confused for 5 days. She had been on dialysis since 2014 and had several serious health problems, including liver disease, tuberculosis-related lung issues, and an abnormal protein condition in her blood. She was permanently bedridden and did not use intravenous drugs. She was treated with dialysis through a catheter in her vein. Her first blood culture showed a type of fungus called Candida guilliermondii, and this fungus was found again in later blood tests and in the catheter tip, even after changing her antifungal medicine. A 1.2-cm mass was seen on her pulmonary valve, which is a sign of possible infection. Surgery was suggested, but the family refused due to her many health problems. She was given fluconazole as a long-term treatment, but she eventually died from liver-related confusion and coma.\"\n}"}
+{"row_index": 122, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 63-year-old woman with end-stage renal disease (ESRD) was admitted to the hospital on June 3, 2015, following a 5-day course of disorientation. She had been undergoing maintenance hemodialysis (HD) since December 2014, initially initiated due to acute on chronic kidney disease secondary to pneumonia. The patient also had a history of hepatitis B-related liver cirrhosis (Child-Pugh class B with hepatic encephalopathy), Mycobacterium tuberculosis-related pleuritis, and an IgGλ monoclonal gammopathy, which remained untreated due to her permanent bedridden status. Hemodialysis was administered via a tunneled-cuffed catheter placed in the right subclavian vein, first inserted on December 8, 2014. She denied active intravenous drug use. On physical examination, she exhibited drowsy consciousness and splenomegaly; no lung crackles or skin track marks were observed. Laboratory findings included a white blood cell count of 2.86 × 10³/uL, absolute neutrophil count of 2116/mm³, platelet count of 14,000/uL, total bilirubin of 3.54 mg/dL, C-reactive protein of 2.31 mg/dL, and serum glucose of 992 mg/dL, without evidence of metabolic acidosis. Given the hyperglycemic hyperosmolar state, blood cultures were obtained and empiric therapy with vancomycin and cefuroxime was initiated. The initial blood culture yielded Candida guilliermondii without concomitant bacterial growth. Intravenous fluconazole 200 mg once daily was administered. The tunneled-cuffed catheter was removed on June 30 due to persistent fungemia, and subsequent catheter tip culture confirmed C. guilliermondii. Blood cultures drawn on July 14 and August 10 and 28 remained positive for C. guilliermondii, even after switching from caspofungin to fluconazole on July 28. No positive cultures were detected in sputum or urine during the 8-week hospitalization period. Transthoracic echocardiography performed on July 20 and August 21 showed no vegetations or congenital val"}
+{"row_index": 123, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 46-year-old man with Malay background had pain in his belly and yellowing of his skin because of a tumor in his duodenum. The doctors found a big tumor and decided to remove it with surgery. Before surgery, he was at high risk because he had low blood, poor liver function, and blocked bile flow. During the surgery, a lot of bleeding happened, so they gave him many blood bags to stay alive. After surgery, he couldn’t make urine properly, which means his kidneys were not working well. So, they started a machine called CRRT right after the problem was found — within 24 hours — to help his kidneys. This machine ran for a few hours and helped his body start working again. His urine came back, his blood sugar went down, and the medicine for blood pressure was slowly stopped. By the sixth day after surgery, he was doing better and was able to leave the ICU. He was awake, breathing on his own, and no longer needed a tube in his nose or strong medicine to keep his blood pressure up.\"\n}"}
+{"row_index": 124, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 46-year-old Malay man had abdominal pain and yellowing of the skin (jaundice) due to a tumor in the duodenum. Imaging showed large masses in the duodenum and near the bile duct, so surgery was planned. He was considered high risk before surgery because of anemia, jaundice, and poor liver function. During the operation, there was heavy bleeding (2500 cc) due to the size of the tumor, so he needed a large amount of blood transfusions.\\n\\nAfter surgery, he developed low urine output, which is a sign of acute kidney injury (AKI). To help his kidneys, we started early continuous renal replacement therapy (CRRT) within 24 hours of diagnosing AKI, using a method called continuous veno-venous hemofiltration (CVVH). This treatment helped remove waste and excess fluid from his blood. After just a few hours, his urine output improved, and his blood pressure and blood sugar levels stabilized. His inflammation markers also dropped over time, showing that his body was healing.\\n\\nThe infection signs that appeared after surgery were managed with a stronger antibiotic. By the fourth day after surgery, his condition had improved enough that he was awake, able to breathe on his own, and was taken off the ventilator. He was discharged from the intensive care unit on the sixth day after surgery.\"\n}"}
+{"row_index": 125, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 46-year-old male of Malay ethnicity presented with persistent abdominal pain and obstructive jaundice, leading to referral to the digestive surgery service at Fatmawati Central General Hospital. Physical examination revealed abdominal distension and palpable hepatosplenomegaly. Abdominal contrast-enhanced computed tomography (CT) demonstrated lobulated masses involving the duodenum and ampulla of Vater, consistent with a stage IIIb duodenal neoplasm. Given the extent and location of the lesion, total pancreatectomy with splenectomy was performed, with the patient admitted to the intensive care unit (ICU) postoperatively.\\n\\nPreoperative assessment identified high surgical risk due to significant anemia, obstructive jaundice, and impaired liver function. Intraoperatively, extensive tumor resection resulted in massive hemorrhage of 2500 cc, necessitating substantial blood product transfusion. Upon ICU admission, the patient exhibited oliguria, prompting escalation of vasopressor support to 0.3 µg/kg/minute to maintain mean arterial pressure (MAP) above 65 mmHg and systolic blood pressure (SBP) above 95 mmHg. Laboratory findings included a lactate level of 5.8 mmol/L, C-reactive protein (CRP) of 30 mg/dL, white blood cell count of 26,700/μL, and procalcitonin >32 ng/mL, confirming the presence of systemic inflammatory response syndrome (SIRS) secondary to surgical trauma.\\n\\nTwelve hours postoperatively, the patient developed postoperative acute kidney injury (AKI), defined by urine output <0.3 cc/kg/hour, meeting KDIGO stage 2 criteria. Early continuous renal replacement therapy (CRRT) was initiated within 24 hours of AKI diagnosis. CRRT was performed via continuous veno-venous hemofiltration (CVVH) with an effluent dose of 27 cc/kg/hour and zero fluid removal. Within three hours of initiation, clinical improvement was observed, including an increase in urine output to 0.5–0.6 cc/kg/hour, allowing for rapid tapering of vasopressor support. Furosemide infusion was administered 18 hours after CVVH initiation, resulting in further improvement in urine output to 1–4 cc/kg"}
+{"row_index": 126, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 27-year-old man with AIDS had sudden belly pain for 4 days and fever for 2 days. He already had AIDS, pneumonia, and likely tuberculosis 2 months before. His immune system was very weak at first, with only 91 healthy immune cells in his blood. He got medicine for pneumonia and TB, and later started treatment for HIV. When doctors checked him, his belly hurt on the left side, but no skin rashes or other signs were seen. A scan showed a small spot on his spleen and swollen lymph nodes inside his belly. Tests found a fungus in his blood and bone marrow, which caused the infection. He got IV antifungal medicine first, but had kidney problems, so they switched to a safer version. After 21 days, he started taking itraconazole pills instead of IV medicine. He stayed in the hospital for 29 days and got better. After that, he went home and kept getting better at follow-up visits. No more symptoms or tests were needed.\"\n}"}
+{"row_index": 127, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 27-year-old man with AIDS had sudden abdominal pain for 4 days and a fever for 2 days. He had been diagnosed with AIDS, pneumocystis pneumonia, and suspected tuberculosis two months earlier. His initial CD4 count was 91 cells/mm³. He received treatment for both infections and started anti-retroviral therapy later. On exam, he had tenderness in the left upper part of his abdomen but no skin rashes or other signs of illness. His CD4 count improved to 272 cells/mm³ (19%) during this visit. A CT scan showed a small lesion in the spleen and swollen lymph nodes in his abdomen. Tests showed a high level of a fungal marker (galactomannan), leading doctors to treat him with amphotericin B, which was later switched to a safer version due to kidney issues. Blood and bone marrow cultures confirmed the presence of T. marneffei, a rare fungus. After 21 days of IV treatment, he switched to oral itraconazole. He was discharged after 29 days and continued to improve at his follow-up visit. He remains healthy and symptom-free at 12 months after treatment.\"\n}"}
+{"row_index": 128, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 27-year-old Thai male with AIDS, originally from Mukdahan Province in Northeastern Thailand and residing in Saraburi Province (200 km south of Bangkok), presented with acute onset of left upper quadrant abdominal pain lasting 4 days and a fever of 2 days' duration, peaking at 38.9 °C. He had been diagnosed with AIDS 2 months prior at another hospital, with an initial CD4 count of 91 cells/mm³ (percentage and viral load unknown), and no comprehensive immune status evaluation was conducted. At that time, he presented with respiratory distress subsequently identified as pneumocystis pneumonia and presumptive smear-negative pulmonary tuberculosis. He received a 3-week course of trimethoprim/sulfamethoxazole and a standard anti-tuberculosis regimen consisting of isoniazid, rifampicin, pyrazinamide, and ethambutol during hospitalization. Anti-retroviral therapy (ART) comprising tenofovir disoproxil fumarate, emtricitabine, and efavirenz was initiated 2 weeks later as an outpatient. The anti-tuberculosis regimen was subsequently modified to isoniazid, rifampicin, ethambutol, and levofloxacin after 4 days, and chest radiographic follow-up demonstrated complete resolution of prior pulmonary opacities after 50 days of therapy. The patient maintained 100% adherence to both anti-tuberculosis treatment and ART, with no additional concomitant medications. His CD4 count 8 weeks prior to admission remained at 91 cells/mm³ (unknown percentage).\\n\\nOn presentation, abdominal pain was localized to the left upper quadrant, described as a dull ache without radiation to the chest, abdomen, or extremities, and was not associated with meals, physical activity, or changes in position. No gastrointestinal symptoms such as diarrhea, nausea, or vomiting were reported. Two days later, a high-grade fever developed without chills. Emergency department evaluation revealed a blood pressure of 120/75 mmHg, heart rate of 110 beats/min, temperature of 38.7 °C, and respiratory rate of 20 breaths/min. Physical examination showed a soft abdomen with normal bowel sounds, but significant tenderness in the left upper quadrant; the spleen was not palpable. No cutaneous lesions were observed on"}
+{"row_index": 129, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A man with a fever got sick in November 2018. Doctors found a big lump on his right side of the chest, filling up the space where the lung should be. Tests showed the cancer was in the lining of the lung (pleura) and had spread there but not to other parts of the body. Because of this, they started treatment with three medicines: pembrolizumab, bevacizumab, and chemo. After 4 rounds, the cancer got a little smaller, and stayed under control for 5 months. But later, the man had a lung problem (pneumonia) that needed medicine to fix. When they tried the medicines again, the cancer came back and spread to many organs. He ended up getting very sick and passed away in October 2019.\"\n}"}
+{"row_index": 130, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 51-year-old man with stage IIIB pleural mesothelioma received second-line treatment using pembrolizumab, bevacizumab, and chemotherapy after initially getting standard chemotherapy. His treatment was guided by genetic testing (second-generation sequencing) that showed specific mutations in his tumor. After four cycles, he had a partial response, meaning the cancer shrunk somewhat, and lived without disease progression for 5 months. Pembrolizumab was stopped because he developed grade 2 immune-related pneumonia, which improved with oral steroids. However, when immunotherapy was restarted and he was given anlotinib, the cancer progressed. He eventually developed multiorgan dysfunction and died suddenly in October 2019.\"\n}"}
+{"row_index": 131, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 51-year-old Asian male presented with a three-day history of fever in November 2018, prompting hospital admission. No significant past medical history was identified, including asbestosis, and no notable family history of malignancy was reported. Physical examination revealed diminished breath sounds on the right side, suggesting pleural involvement. Whole blood was obtained for next-generation sequencing (NGS) using a targeted gene panel (Yucebio, Shenzhen, China), which identified a TP53 splicing variant in exon 4 at a frequency of 6.44%, consistent with aberrant mRNA splicing leading to loss of tumor suppressor function. The tumor was classified as microsatellite stable (MSS) and exhibited a moderate tumor mutational burden (TMB) of 2.70 mutations per megabase (Mut/Mb), indicating a relatively high mutational load that may influence immunotherapy response. Due to patient refusal, no repeat biopsy was performed, and PD-L1 expression analysis was not conducted. Chest computed tomography (CT) demonstrated right pleural occupation with pleural effusion, and whole-body CT revealed diffuse involvement of the ipsilateral pleural surfaces, confirming localized pleural dissemination without evidence of distant metastasis. Based on these findings, the patient was initiated on second-line therapy comprising pembrolizumab (a PD-1 inhibitor), bevacizumab (an anti-VEGF monoclonal antibody), and standard chemotherapy regimen. After four cycles, a partial response was observed, with a progression-free survival of 5 months. Pembrolizumab was subsequently discontinued due to the development of grade 2 immune-related pneumonia, which was clinically managed with oral glucocorticoids and resolved without long-term sequelae. However, upon rechallenge with immunotherapy, disease progression was observed, followed by subsequent treatment with anlotinib (a multi-kinase inhibitor targeting VEGFR, PDGFR, and c-KIT), which failed to halt disease advancement. The patient ultimately experienced multiorgan dysfunction syndrome and died suddenly in October 2019. The case underscores the complexity of immunotherapy in mesothelioma, particularly in the absence of PD-L1 expression and biopsy confirmation, and highlights the role of tumor genomic features such as TP53 splicing variants and moderate TMB in guiding therapeutic decisions. Additionally, the observed immune-related adverse events and subsequent progression post-rechallenge suggest potential immune exhaustion or"}
+{"row_index": 132, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 43-year-old man got a deep cut on his left forehead and near his ear from a broken lawnmower blade. The cut was bleeding very badly and couldn't be stopped by pressure. His blood pressure was very low and his heart was racing. He lost consciousness quickly and needed a breathing tube. Doctors quickly started giving him blood. They cut open his neck to stop the bleeding by squeezing the outside neck artery (ECA) for 100 minutes. This stopped the massive bleeding. They also used a balloon to plug the wound. Later, a scan showed a metal piece from the blade stuck in his skull, and there were many broken bones on the left side. There was also bleeding inside his brain. The metal piece was removed. The maxillary artery was cut and tied off. After that, the neck artery was released and no more bleeding was seen. He got a lot of blood and plasma. He stayed in the hospital for 10 days. He woke up and could move his body, but his left face stayed paralyzed because the facial nerve was damaged. He also lost vision in his left eye because the optic nerve was badly hurt. The bleeding was stopped, but the damage to his face and eye is permanent.\"\n}"}
+{"row_index": 133, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 43-year-old man suffered a severe injury to his left forehead and neck area when a broken grass-cutting blade pierced his skin. The wound caused a serious, non-compressible bleed from an artery, which is a life-threatening situation. His blood pressure was very low and his heart rate was extremely high, showing he was in serious danger. He quickly lost consciousness and needed emergency treatment, including intubation and blood transfusions.\\n\\nDoctors used a tourniquet to temporarily stop the bleeding by squeezing the external carotid artery (ECA), which took 8 minutes from the time the emergency team activated to the start of the procedure. This helped stabilize him. The bleeding was controlled, and the patient was then taken for a CT scan of his brain and neck, which showed a metal piece from the blade, multiple skull fractures, and bleeding in the brain (subarachnoid and subdural hemorrhage), but no direct injury to major brain arteries.\\n\\nAfter the scan, the patient returned to surgery. The metal object was removed, and the maxillary artery was completely cut and sealed. The ECA was then released and no active bleeding was found. The total time the tourniquet was applied was 100 minutes. The dura (the protective covering of the brain) was repaired, and a drain was placed.\\n\\nHe received several units of blood products, including red blood cells, plasma, and platelets. He stayed in the ICU for 10 days. After recovery, he had mild brain function issues, with good consciousness (GCS E4V5M6) and normal movement on one side, but he lost vision in his left eye due to damage to the optic nerve. He also has permanent facial paralysis on the left side because the facial nerve was damaged and reconnected to a nearby nerve. The injury was serious, but the team managed to save his life with timely intervention and staged surgery.\"\n}"}
+{"row_index": 134, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 43-year-old male presented with a severe penetrating injury to the left frontotemporal and preauricular region caused by a broken grass-cutting blade, resulting in a noncompressible, pulsatile arterial hemorrhage. Upon arrival at the trauma center, his vital signs were critically unstable: systolic blood pressure of 60–70 mmHg, tachycardia at 140 beats per minute, and oxygen saturation of 80%. Physical examination identified active arterial bleeding originating from the maxillary artery anterior to the mandibular neck. His neurological status rapidly deteriorated to E1V1M5, prompting immediate endotracheal intubation and initiation of group O red blood cell transfusion.\\n\\nThe trauma plus protocol was activated, and the patient was rapidly transported to the operating room. A longitudinal incision was made along the anterior margin of the left sternocleidomastoid muscle, with the posterior belly of the digastric muscle dissected to expose the carotid bifurcation. The left common facial vein was divided, and the left common carotid, external carotid (ECA), and internal carotid arteries were exposed and secured with vascular slings. Transient occlusion of the ECA was achieved using a Rumel tourniquet, which successfully controlled the massive arterial bleed. The interval between trauma protocol activation and ECA occlusion was 8 minutes. The preauricular wound tract was tamponaded with a balloon to stabilize the bleeding site.\\n\\nThe patient was then transferred for computed tomographic angiography (CTA) of the brain and neck, which revealed a metallic foreign body embedded in the left skull with multiple comminuted fractures involving the zygomatic process of the left temporal bone, lateral wall of the left orbit, left orbit apex, left superior orbital fissure, left optic canal, squamous part of the left temporal bone, sphenoid and ethmoid sinus walls, and the greater and lesser wings of the sphenoid bone. Imaging also demonstrated acute subarachnoid hemorrhage along the left Sylvian fissure and acute subdural hemorrhage on the frontotemporal convexity with associated brain swelling. Notably, no intracranial arterial injury was identified.\\n\\nFollowing CTA, the patient returned to the operating room for foreign body removal. A complete transection of the maxillary artery was identified"}
+{"row_index": 135, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 10-year-old boy from Ethiopia came to the hospital with sudden weakness in his legs and trouble controlling his bladder and bowels for 10 days. He had pain in his stomach area for a long time but no fever or injury. Tests showed his liver was damaged and had a very high level of a protein called AFP, which is a sign of liver cancer. A needle test from the liver and imaging showed tumors in his liver and that the cancer had spread to his spine. This means he had liver cancer with cancer in his spine. The doctors told his parents about the serious outcome, and they chose to go home and care for him at home instead of continuing treatment.\"\n}"}
+{"row_index": 136, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 10-year-old Ethiopian boy arrived at a hospital in Addis Ababa with sudden weakness in his legs and loss of control over his bladder and bowels, which had been going on for 10 days. He also had long-standing pain in his upper abdomen. He did not have a fever, cough, or any recent injury. He had not been exposed to someone with a chronic cough. Because he was born before the national hepatitis B vaccine program started, he never received the hepatitis B vaccine. His temperature was slightly high, and his liver was enlarged and painful. Neurological tests showed that his spinal cord damage was at the level of T10, with no muscle strength in his legs and no reflexes. Blood tests showed elevated liver enzymes and a very high level of alpha-fetoprotein (AFP), which is a marker for liver cancer. Imaging scans showed multiple liver tumors and a collapsed vertebra with swelling around the spine, pressing on the spinal cord. The doctors suspected either tuberculosis or cancer spreading to the spine. Further tests found solid liver masses and involvement of the portal vein. The fine needle biopsy of the liver confirmed the presence of hepatocellular carcinoma (HCC) with spread to the spine. The family was given information about the serious prognosis and chose to stop treatment and go home for palliative care.\"\n}"}
+{"row_index": 137, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 10-year-old Ethiopian male presented to Tikur Anbessa Specialized Hospital, Addis Ababa, with a sudden onset of lower extremity weakness beginning 10 days prior, associated with urinary and fecal incontinence. He had a history of chronic epigastric pain. No fever, diarrhea, cough, altered mental status, abnormal movements, or trauma was reported. No exposure to individuals with chronic cough was documented. He had received all routine childhood vaccinations, including four doses of oral polio vaccine, but was not vaccinated against hepatitis B due to the timing of his birth—prior to the implementation of a routine three-dose hepatitis B vaccination schedule in Ethiopia (which began in 2015), leading to a delayed exposure window. The patient presented in 2016.\\n\\nPhysical examination revealed an axillary temperature of 38.0 °C and tachycardia (115 beats per minute). Hepatomegaly was noted, measuring 16 cm in total span (10 cm below the right costal margin), described as hard and tender. Neurological assessment demonstrated a sensory level at T10, bilateral lower extremity muscle power of 0/5, areflexia, and hypotonic anal tone.\\n\\nLaboratory findings included a normal complete blood count and erythrocyte sedimentation rate (25 mm/hr). Liver function tests showed elevated alanine aminotransferase (160 U/L) and aspartate aminotransferase (136 U/L), with markedly elevated alkaline phosphatase (761 U/L) and low serum albumin (3.4 mg/dL). Coagulation profile, renal function, serum electrolytes, blood and urine cultures, human immunodeficiency virus (HIV), and hepatitis C virus (HCV) serologies were all negative. Hepatitis B surface antigen (HBsAg) was positive, confirming active hepatitis B infection. Further serologic characterization of the hepatitis B viral state (e.g., HBV DNA load, HBeAg status) was not available due to limited diagnostic access.\\n\\nThoracolumbar magnetic resonance imaging (MRI) revealed collapse of the T9 vertebral body with abnormal marrow signal characteristics: T1 isointensity and T2 heterogeneous hyperintensity, indicating intravertebral pathology. Extensive epidural and par"}
+{"row_index": 138, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 28-year-old man with no prior health problems started having bad headaches and neck pain 2 months ago after lifting a heavy object. His symptoms got worse after a neck therapy session at a chiropractor he didn’t know was not trained properly. He began acting strangely and felt sick, with nausea and vomiting. When he finally went to the hospital, a brain scan showed blood buildup (SDH) on both sides of his brain. He had surgery to drain the blood, and right after, his headaches and neck pain went away. A follow-up scan 8 months later showed no blood left and no return of symptoms. He’s now fully better and back to normal.\"\n}"}
+{"row_index": 139, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 28-year-old healthy man developed severe headaches and neck pain about 2 months ago after lifting a heavy object. His symptoms worsened after visiting a chiropractor for neck pain. He then started experiencing nausea, vomiting, and behavioral changes over the past two days. He went to the emergency department, where a brain CT scan showed bilateral subdural hematomas (SDHs) — collections of blood between the brain and the tissues covering it. He had no history of trauma, seizures, bleeding disorders, or drug use. After surgery, which involved small incisions in the skull to drain the blood, his symptoms improved quickly. The surgery was successful with no complications. A follow-up brain CT scan eight months later showed no remaining blood or signs of recurrence. He has been fully recovered and is back to normal without any ongoing symptoms.\"\n}"}
+{"row_index": 140, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 28-year-old fit male soldier presented to the Emergency Department with a chronic history of severe headache, neck pain, nausea, and vomiting, accompanied by behavioral changes over the past two days. The headache and neck pain began two months prior following the lifting of a heavy object, with progressive worsening of symptoms. Prior to this episode, he had visited the ED twice, during which cervical spine X-rays were performed without brain imaging; he was discharged on analgesics and referred for outpatient follow-up, with no improvement in symptoms. Subsequently, he received a neck therapy session from an uncertified chiropractor, after which his headache and neurological symptoms significantly exacerbated. The headache became refractory and unbearable, prompting further evaluation with brain computerized tomography (CT), which revealed bilateral subdural hematomas (SDHs). There was no history of traumatic brain injury, loss of consciousness, seizures, or systemic conditions such as hematological disorders, coagulopathies, or bleeding tendencies. The patient denied smoking, alcohol, or illicit drug use, and had a negative family history of intracranial aneurysms or inherited bleeding disorders. Physical examination revealed stable vital signs, normal temperature, and alertness with orientation, though the patient exhibited signs of depression and agitation. A notable neurological finding was the onset of bilateral, involuntary, repetitive extension movements involving the little fingers, which began two days prior to presentation. The remainder of the neurological examination was unremarkable. All routine laboratory investigations, including complete blood count, coagulation profile (Factor VIII and XIII, vWF cofactor and antigen), and blood smear, were within normal limits. Advanced imaging studies—computed tomography angiography (CTA), magnetic resonance angiography (MRA), and whole-spine magnetic resonance imaging (MRI)—were performed to exclude underlying vascular pathology, arteriovenous malformations, or spinal cord compression, but no identifiable etiology was found. The patient underwent bilateral mini-craniotomies with placement of bilateral subdural drains for evacuation of the hematomas. Histopathological examination of the external membrane of the SDH demonstrated typical features consistent with subdural hematoma formation, including fibrin deposition, erythrocyte clots, and organized fibrous tissue, confirming the diagnosis. The surgical procedure was successful with no intraoperative complications or significant bleeding. Clinical symptoms improved immediately postoperatively. During hospitalization, additional hemostatic workup was completed and"}
+{"row_index": 141, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 14-year-old boy got hurt when a baseball hit his right middle finger. At first, he wore a splint, but didn’t go back for check-ups. Five months later, his finger still hurt and couldn’t move well. Doctors saw that a piece of bone and cartilage was missing from the joint, and it was misaligned. They fixed it with surgery. A small hole was made in the finger’s joint, and a piece of bone and cartilage taken from the boy’s knee was put in the hole and pressed in place. The knee piece was taken from a part that doesn’t carry weight, so it didn’t hurt. After surgery, he started moving his finger right away and used a tape to help it heal. After 3 months, he stopped using the tape and went back to playing baseball. One year later, his finger no longer hurt, moved freely from straight to bent, and the joint looked smooth on a scan. The knee where the piece came from is still healthy, and the finger is back to normal.\"\n}"}
+{"row_index": 142, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 14-year-old boy injured his right middle finger with a baseball hit. Initially, he was treated with a splint, but he didn’t follow up properly. Five months later, he still had pain and trouble moving his finger. X-rays and a CT scan showed a bony and cartilage defect in the joint of the finger, which meant the fracture had not healed properly. This condition was diagnosed as a malunited intra-articular fracture of the PIP joint. The boy had surgery to fix it. A small piece of bone and cartilage (osteochondral plug) was taken from his left knee, where the joint doesn’t bear much weight, and inserted into the damaged area of the finger. The plug was pressed into place using a drill hole. After surgery, he wore a splint for one day and then started gentle finger exercises. He continued buddy taping for three months and gradually returned to playing baseball. One year later, he has no pain, can fully bend and straighten his finger, and the joint looks healthy on MRI. The bone has healed well, and there is no damage to the knee donor site. A small amount of finger misalignment still remains, but it has improved significantly.\"\n}"}
+{"row_index": 143, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 14-year-old right-handed male presented with persistent pain and restricted range of motion (ROM) in the right middle finger five months following a traumatic baseball impact. Initial management at the treating hospital included splint fixation for a fracture of the middle phalanx, but the patient discontinued follow-up care. Clinical examination at presentation revealed swelling and ulnar deviation of the proximal interphalangeal (PIP) joint at extension, with a limited ROM of 0° extension to 60° flexion. Radiographic evaluation—including posterior-anterior and lateral views—demonstrated a bony defect on the articular surface of the middle phalanx, with ulnar displacement of the digit. Lateral X-ray showed a depressed articular surface, and computed tomography (CT) confirmed a 5 × 6.5 × 2 mm bony defect localized to the PIP joint articular surface of the middle phalanx. Additional imaging revealed a 1 × 2 mm cartilage defect on the palmar aspect of the proximal phalanx articular surface. Based on these findings, a diagnosis of malunited intra-articular fracture of the PIP joint was established, prompting surgical intervention. A palmar incision was used to expose the PIP joint, and a columnar-shaped recipient hole was created at the site of the osteochondral lesion in the middle phalanx. A cylindrical autogenous osteochondral plug measuring 4.5 mm in diameter was harvested via the mosaicplasty autogenous osteochondral grafting system (Acufex, Smith & Nephew, Andover, MA, USA) from the upper lateral femoral condyle of the left knee—a non-weight-bearing site—using an obliquely angled cartilage surface aligned with the long axis to optimize insertion geometry. The osteochondral plug was press-fitted into the recipient site to achieve mechanical and biological integration. The proximal phalanx cartilage defect, measuring 1 × 2 mm, was left untreated due to its minimal size and lack of functional impact. Postoperatively, the patient underwent immediate splint fixation followed by early mobilization initiated the next day via buddy taping, which was maintained for up to three months. After removal of buddy taping, the patient gradually resumed athletic activity, including baseball. At one-year follow-up, the patient reported complete resolution of pain and restoration of PIP joint ROM to 0"}
+{"row_index": 144, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 65-year-old woman came to the emergency room with severe belly pain, nausea, and vomiting. She had a history of diabetes and prior belly problems. A scan showed a blockage in her small intestine, near the part called the jejunum, and enlarged lymph nodes in her pelvis. Doctors thought it could be cancer, scar tissue, or inflammation. Her condition got worse quickly, so they had to surgically remove part of her small intestine. After checking the tissue, doctors found cells that looked like cancer, especially T-cells that were growing fast and were all part of the same group. This matched a rare type of cancer called jejunal EATL. Five weeks later, she started having brain problems — her mind changed and she lost strength on her left face and arm. A brain scan showed a tumor in the right front part of her brain, with swelling around it. She had surgery to remove it, and the tissue tested confirmed the tumor was from the same type of cancer that had spread to her brain. This means the cancer started in her small intestine and spread to her brain.\"\n}"}
+{"row_index": 145, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 65-year-old woman came to the emergency room with severe abdominal pain, nausea, and vomiting. She had a history of type 2 diabetes and previous intestinal problems. A CT scan showed a blockage in her small intestine, specifically in the jejunum, and enlarged lymph nodes in her pelvis. Doctors considered possible causes like a tumor, scar tissue, or inflammation.\\n\\nHer condition quickly got worse, so she needed emergency surgery to remove part of her small intestine. Examining the removed tissue showed signs of both benign T-cells (which can happen in celiac disease) and abnormal lymphocytes with unusual features. These abnormal cells were positive for CD-3, had a high rate of cell growth (90% stained positive for Ki-67), and showed a clonal pattern in T-cell gene testing — all signs of a rare type of lymphoma called jejunal extranodal T-cell lymphoma (EATL).\\n\\nFive weeks after diagnosis, she started having new neurological symptoms, including confusion and weakness on her left side. A brain MRI found a single abnormal area in the right front and parietal part of her brain, surrounded by swelling. She had surgery to remove this brain lesion, and the tissue sample confirmed it was metastatic EATL — meaning the cancer had spread from her intestine to her brain.\"\n}"}
+{"row_index": 146, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 65-year-old female presented to the emergency room with uncontrolled abdominal pain, nausea, and vomiting. Her medical history included Type 2 diabetes mellitus, a prior history of intestinal intussusception, and chronic moderate abdominal pain. Initial abdominal computed tomography (CT) scan revealed a small bowel obstruction with a transition point localized in the jejunal region, accompanied by mildly enlarged lymph nodes in the right pelvic region. The differential diagnosis considered small bowel neoplasm, postoperative adhesions, or a reactive intestinal inflammatory process, such as celiac disease. Histological examination of the resected jejunal segments demonstrated small intestinal mucosa with intraepithelial and mucosal infiltrates of benign CD3-positive T-cells, consistent with celiac sprue, suggesting a prior immune-mediated enteropathy. In addition, the tissue showed medium-sized infiltrating lymphocytes exhibiting pleomorphic nuclei and prominent nucleoli, indicative of a proliferative lymphoid process. Immunohistochemical staining revealed tumor cells positive for CD-3, with weak positivity for BCL-2, and negative staining for CD5, CD20, CD10, and cyclin-D1—findings that exclude B-cell lymphoma and support a T-cell origin. Ki-67 immunoreactivity demonstrated a markedly elevated proliferative index, with 90% of the lymphocytes showing positive staining, reflecting a high rate of cell division and aggressive biological behavior. Polymerase chain reaction (PCR) analysis of the T-cell receptor-gamma (TCRγ) gene revealed clonal rearrangement, confirming the presence of a monoclonal population of T-cells, a hallmark of malignancy in T-cell lymphoproliferative disorders. The integrated morphological and immunophenotypic profile of the jejunal lesion is consistent with extranodal T-cell lymphoma, enteropathy type (EATL), specifically involving the small intestine. Systemic workup, including blood chemistry, imaging, and serologic markers, was non-contributory, supporting the localization of the primary disease to the gastrointestinal tract. The patient was discharged and initiated chemotherapy for the primary EATL. Three weeks after diagnosis, a whole-body positron emission tomography-CT (PET-CT) scan of the skull to mid-thigh demonstrated no hypermetabolic lesions suggestive of active malignancy in the cranial base or neck, indicating a clinically quiescent systemic disease at that time. However, five"}
+{"row_index": 147, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 24-year-old woman has had muscle pain for many years, starting when she was 7. The pain comes and goes, used to happen every 1–2 years, but now happens up to four times a year. Each time, it starts with a sore throat, cough, or urinary tract infection. When the pain comes, her muscles hurt a lot, but it goes away quickly when she takes a medicine called prednisolone. She had her tonsils removed in 1992 because of frequent sore throats. No other health problems were found. This pattern — muscle pain starting with infections — has never been seen before in someone her age and with this frequency.\"\n}"}
+{"row_index": 148, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 24-year-old Caucasian woman has had recurring muscle pain, especially in her legs, for over 18 years. The pain usually comes after infections like sore throats, coughs, or urinary tract infections, and has occurred up to four times a year in recent years. This pattern — frequent muscle inflammation triggered by infections — has not been seen before. When she had these episodes, her muscle enzymes (CK) were elevated, and the pain improved quickly with oral steroids. She had a tonsillectomy in 1992 due to repeated sore throats, but no other major health issues. Tests showed no evidence of common viruses like strep, flu, or EBV in active form, and no signs of immune deficiency. Muscle biopsies showed inflammation, especially from a type of white blood cell called CD4 lymphocytes, suggesting a specific immune reaction. Despite extensive testing, no clear cause was found, and the condition appears to be rare and unique to her case.\"\n}"}
+{"row_index": 149, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 24-year-old Caucasian female presented with a 17-year history of recurrent lower limb myositis, initially occurring every 1–2 years since age seven, with a marked increase in frequency to four episodes annually starting in 2005. Each episode was preceded by upper respiratory tract infections (e.g., sore throat, cough) and, more recently, by urinary tract infections (dysuria). During active attacks, serum creatine kinase (CK) levels ranged from 89 to 700 U/litre (normal <175 U/litre), reflecting muscle damage, and normalized between episodes. Oral prednisolone provided rapid symptomatic relief, indicating a reversible inflammatory myopathy. A tonsillectomy was performed in 1992 based on a history of recurrent sore throats and elevated antistreptolysin O (ASOT) titre, with no other significant medical or drug history.\\n\\nDuring a detailed investigation in September 2005, a myositis episode was preceded by a productive cough with green sputum. Physical examination revealed mild pharyngeal injection and tenderness in the calves and anterior compartment muscles. Muscle biopsy of the right tibialis anterior demonstrated mild fiber atrophy of uncertain clinical significance. Laboratory findings included elevated erythrocyte sedimentation rate (ESR: 39 mm/hour), leukocytosis (16.6 × 10⁹/litre), with neutrophilia (13.6 × 10⁹/litre, 81.9%) and monocytosis (1.06 × 10⁹/litre, 6.4%). All other laboratory parameters—including lymphocyte, eosinophil, basophil counts, CK, renal, and hepatic function—were within normal limits.\\n\\nSerological testing was negative for influenza A/B, respiratory syncytial virus (RSV), Mycoplasma pneumoniae, Chlamydia, Q fever, adenovirus, enterovirus, and ASOT. Epstein-Barr virus (EBV) serology showed positive EBNA IgG, VCA IgG, and VCA IgM, which may reflect either a false-positive VCA IgM, a recent primary EBV infection (within 3–12 months), or EBV reactivation. Convalescent serology performed five months later revealed"}
+{"row_index": 150, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"An 85-year-old woman who uses her left hand mostly had a lump on her thumb side of the hand that grew fast over six weeks. The lump was big, soft, and could move around — about 5 inches by 4 inches and covered the whole thumb area. Doctors first thought it might be cancer, but X-rays showed weak bones and damage near the thumb joint. A scan showed a fluid-filled sac near the joint. During surgery, they saw a lump with a neck that went into the thumb joint. Lab tests confirmed it was a ganglion cyst, a common type of fluid-filled bump. She recovered well and hasn’t had the lump come back.\"\n}"}
+{"row_index": 151, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"An 85-year-old woman who uses her left hand mostly had a lump on the thumb side of her hand that grew quickly over six weeks. The lump was large, not painful, and could move around. It measured 5 by 4 centimeters and covered the entire thenar area. At first, doctors thought it might be a sarcoma, a type of cancer. X-rays showed weak bones and damage to the joint at the base of the thumb, along with a soft tissue swelling near a bone spur. MRI showed a cyst-like structure connected to the thumb joint, with signs of active joint inflammation. During surgery, the doctors saw a multilobulated lump that extended into the thumb joint. Lab tests confirmed it was a ganglion cyst, a common benign (non-cancerous) cyst that forms near joints. The patient recovered well after surgery and has not had any signs of the lump coming back.\"\n}"}
+{"row_index": 152, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"An 85-year-old left hand-dominant female presented with a six-week history of a rapidly enlarging lump at the thenar eminence. Clinical examination identified a non-tender, large, lobulated, mobile swelling measuring 5 × 4 cm that involved the entire thenar region. Initial differential diagnosis included sarcoma due to the size, rapid growth, and location. Plain radiography demonstrated severe osteopenia with erosive changes at the first carpometacarpal (CMC) joint, along with a soft tissue mass adjacent to a detached osteophyte originating from the base of the first metacarpal. Magnetic resonance imaging (MRI) revealed a septate, thin-walled, cystic lesion extending from the first CMC joint space, occurring against a background of diffuse active synovitis, suggesting chronic joint inflammation and possible mechanical irritation. In the operating theater, a multilobulated lesion with a well-defined neck extending into the first CMC joint was observed, consistent with a complex cystic structure. Histological evaluation of a 3.4 g specimen previously excised confirmed a ganglion cyst, specifically a thenar ganglion arising from the synovial membrane of the first CMC joint, with characteristic features including a cystic lumen, fibrous septa, and associated synovial proliferation. The lesion was fully resected with clear margins. Post-operative course was uncomplicated, with no evidence of recurrence at follow-up. The pathogenesis is likely attributable to mechanical stress and joint instability, leading to synovial cyst formation via fluid accumulation in the joint capsule and surrounding connective tissue, a process amplified by age-related degenerative joint changes and osteopenia. The presence of active synovitis on MRI supports the inflammatory component of the cystic lesion, which may contribute to its growth and expansion over time.\"\n}"}
+{"row_index": 153, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 32-year-old woman had a lump in the area where the rectum and vagina meet for 9 years. It grew quickly in the last year, from 4 cm to 9.7 cm, and started causing problems like stool getting stuck. A doctor saw the lump with a special tube (endoscopy) and thought it might be a type of tumor or a fibroid. But when they tried to take a small piece of tissue from the lump with a needle (biopsy), they got too little tissue and also had bleeding from the vagina, so they couldn’t make a clear diagnosis. After talking with a team of doctors, they decided to try again using a better method: a needle guided by ultrasound to find the right spot. This time, they got enough tissue and found it was a rectal tumor called a GIST. The doctors recommended a drug called imatinib to shrink it first. After the tumor got smaller, they removed it through the back of the vagina. After surgery, they gave extra treatment to help prevent it from coming back. As of December 2019, the tumor hasn’t come back or spread anywhere.\"\n}"}
+{"row_index": 154, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 32-year-old woman had a mass in the area between her rectum and vagina for 9 years. It didn’t grow much until the past year, when it enlarged from 4.0 cm to 9.7 cm and started causing symptoms like difficulty passing stool due to pressure. An endoscopy showed a growth under the rectal lining, but repeated biopsies only found inflammation, not actual tumor tissue — which didn’t match her symptoms. She came to our hospital for a clearer diagnosis.\\n\\nInitial tests, including blood work and imaging, were normal. A CT scan and ultrasound showed a large, irregular mass in the rectovaginal space, which could be either a gastrointestinal stromal tumor (GIST) or an uterine fibroid growing outward.\\n\\nA first biopsy was done using a needle through the abdomen, but it failed because the tissue collected was too small and the procedure caused vaginal bleeding, which stopped the biopsy early. Pathologists could not make a definite diagnosis from that sample.\\n\\nAfter discussion among doctors from different specialties, a second biopsy was planned using a more precise method. This involved using ultrasound guidance — first with endoscopic ultrasound (ERUS) and then with contrast-enhanced ultrasound (CEUS) — to see exactly where the active, living parts of the tumor were, avoiding the dead (necrotic) areas. This helped ensure the needle would reach the right part of the tumor.\\n\\nThe second biopsy was done through the perineum (the area between the vagina and anus) under local anesthesia, with real-time ultrasound guidance. The doctors successfully collected tissue from the active part of the tumor. Pathology confirmed it was a rectal gastrointestinal stromal tumor (GIST).\\n\\nThe medical team recommended imatinib as the first-line treatment, which helped shrink the tumor. Once it was small enough, the tumor was removed through the back of the vagina. After surgery, additional treatment was given to reduce the risk of coming back. As of December 13, 2019, the patient has not had any recurrence or spread of the cancer.\"\n}"}
+{"row_index": 155, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 32-year-old female presented with a progressively enlarging mass in the rectovaginal space, initially detected during a routine examination 9 years prior. No significant growth was observed in annual follow-ups until a 12-month period of rapid expansion, during which the mass increased from a maximum diameter of 4.0 cm to 9.7 cm, resulting in symptomatic compression of the rectal lumen and the development of stool-related dents. Endoscopic evaluation at an external facility revealed a submucosal protrusion, yet repeated endoscopic biopsies over the preceding two years yielded only inflammatory findings—lacking definitive tumor tissue—contradicting the clinical suspicion of a neoplastic process. This discrepancy prompted referral to our institution for definitive diagnosis.\\n\\nThe patient had no significant comorbidities, no personal or familial history of malignancy, and preserved general health parameters, including normal mental status, appetite, sleep, weight, and absence of abdominal distension, tenesmus, rectal prolapse, diarrhea, or constipation. Digital rectal examination demonstrated a plump anterior rectal wall without tenderness or visible blood on the digit.\\n\\nLaboratory investigations, including complete blood count, coagulation profile, carcinoembryonic antigen (CEA), α-fetoprotein (AFP), carbohydrate antigen (CA) 19-9, and CA125, were within normal limits, excluding systemic malignancy or infection.\\n\\nContrast-enhanced computed tomography (CECT) revealed a heterogeneous mass within the rectovaginal space with central liquefaction necrosis (low-density region) and indistinct margins. Transabdominal ultrasound (US) identified a heterogeneous hypoechoic lesion measuring 9.7 cm in maximum diameter, consistent with either a rectal gastrointestinal stromal tumor (GIST) or an exophytic uterine fibroid.\\n\\nA transabdominal core needle biopsy (CNB) was performed using the MG1522 BARD MAGNUM Biopsy Instrument (16 G, 16 cm, disposable, Tempe, AZ, USA), with prior written informed consent obtained. Preoperative laboratory workup was unremarkable. However, spontaneous vaginal hemorrhage occurred during the procedure, terminating the biopsy prematurely. The retrieved tissue consisted of fragmented greyish material with a maximum diameter of less than 0.3 cm. Hist"}
+{"row_index": 156, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 68-year-old woman had pain in her left leg for 3 weeks. At first, she went to urgent care for redness and swelling on her shin, and was given antibiotics for a possible infection, but it didn’t get better. When she came to the emergency room, she wasn’t feverish and was stable. Her leg was still red, swollen, and painful, especially when walking. Tests showed her body was fighting an infection. A scan (ultrasound) found a hole in her bone and fluid moving back and forth through it, which means the bone is infected. Doctors diagnosed it as bone infection (osteomyelitis) and treated her with strong antibiotics and surgery to drain the pus from the soft tissue. The surgery helped, and she’s now getting antibiotics for 6 weeks to make sure the infection is fully gone.\"\n}"}
+{"row_index": 157, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 68-year-old woman came to the emergency department with 3 weeks of increasing pain in her left lower leg. She first visited urgent care, where her left shin was red and swollen, and she was given antibiotics for a suspected skin infection (cellulitis) with ceftriaxone. The pain didn’t improve. At the emergency department, she was not feverish and her blood pressure was normal. Her left shin remained red, swollen, and tender, and the swelling stopped before reaching her knee. Blood tests showed high levels of inflammation. An ultrasound scan revealed a fluid collection near the bone, with a break in the bone surface and fluid flowing back and forth—this is a sign of bone infection. The imaging also showed a large fluid-filled area near the tibia, with connections to the inside of the bone. A CT scan confirmed a large abscess near the tibia, with signs of both skin and bone infection. She was diagnosed with osteomyelitis, an infection of the bone. She was started on strong antibiotics and had surgery to drain the abscess. No bacteria were found in the wound or blood samples. Her treatment continued with antibiotics for 6 weeks under the guidance of specialists.\"\n}"}
+{"row_index": 158, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 68-year-old female with a history of hypertension, hyperlipidemia, type 2 diabetes mellitus, gout, rheumatoid arthritis, and bilateral knee replacements—on clindamycin prophylaxis due to prior joint infections—presented to the emergency department with a three-week history of progressive left lower extremity pain. Initial evaluation at urgent care revealed erythema and swelling of the left shin, with plain radiographs showing no osseous abnormalities. She was empirically treated for cellulitis with intramuscular ceftriaxone for 10 days, but symptoms persisted without resolution. On presentation, she was afebrile and hemodynamically stable, with persistent erythema, swelling, and tenderness localized to the left pretibial soft tissues. The area of involvement extended distal to the knee joint, with no joint effusion or objective limitation in range of motion; pain was exacerbated by ambulation, though she maintained partial weight-bearing capacity. Repeat plain radiographs demonstrated focal soft tissue swelling overlying the anterior tibia. Point-of-care ultrasound, performed using orthogonal transverse and longitudinal scanning with a linear probe, revealed a large heterogeneous fluid collection adjacent to the tibial cortex. A focal defect in the cortical bone was identified, with pulsatile fluid communicating directly with the medullary cavity. Bidirectional flow of fluid was confirmed via color Doppler and pulsed-wave spectral Doppler, indicating active communication between the soft tissue collection and the intramedullary space. Laboratory findings included a normal white blood cell count (7.7 × 10³/μL), but markedly elevated systemic inflammatory markers: C-reactive protein (CRP) at 38 mg/dL and erythrocyte sedimentation rate (ESR) at 91 mm/hr. Computed tomography (CT) imaging revealed a 5.7 × 2.4 × 7.1 cm fluid collection adjacent to the tibial cortex, with well-defined sinus tracts extending into the medullary cavity, consistent with an abscess complicated by adjacent cellulitis and osteomyelitis. The patient was initiated on vancomycin and piperacillin/tazobactam, and orthopedic surgery was consulted. She was admitted to the internal medicine service and underwent incision and drainage of the left pretibial abscess. Neither wound nor blood cultures yielded growth. Infectious Diseases reviewed the"}
+{"row_index": 159, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 71-year-old man had knee surgery 18 months ago and started having bad knee pain a few weeks after. The surgery went well, but the pain got worse over time. Doctors checked and found no problems with the knee or infection. The pain was sharp, spread to his ankle, and made his knee feel tingly. He had trouble with touch and pain in his knee, but his leg strength was normal. After trying medicine and other treatments, the pain didn’t go away. A short test with a nerve block helped a little, but only for about a month. Then he tried a pain device called a spinal cord stimulator, which works by sending gentle signals to his nerves. The device was placed successfully and worked great. Right after, his pain stopped completely. Six months later, he still has no pain and no longer needs pain pills.\"\n}"}
+{"row_index": 160, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 71-year-old man who had knee surgery 18 months ago now suffers from chronic left knee pain that worsened over time. After the surgery, he did well initially, but started having increasing pain around the third week after surgery. His knee was working properly, and there was no sign of infection or hardware problems. The pain was sharp, rated 7 out of 10, and spread to his ankle, with numbness or tingling in the same area. He also had increased sensitivity to touch (allodynia) and sharp pain from light touch (hyperesthesia) on the front of his knee. His strength was normal, and his wound was healing well. After trying physical therapy and several pain medications with little success, he had a temporary improvement with a sympathetic nerve block, lasting about a month. He then had a trial of a spinal cord stimulator (SCS), which successfully reduced his pain. He received two 16-contact leads with a Boston Scientific SCS system, which delivers different types of electrical stimulation to block pain signals. After the first follow-up, he reported complete relief from pain. At his 6-month check-up, his pain was still fully gone, and he was able to stop using opioid pain medication entirely.\"\n}"}
+{"row_index": 161, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 71-year-old Caucasian non-Hispanic male presented with chronic left knee pain persisting 18 months following total knee arthroplasty (TKA). His preoperative medical history included well-controlled hypertension, hyperlipidemia, and gastroesophageal reflux disease, with no significant comorbidities or prior surgical interventions. He measured 70 inches in height and weighed 215 lbs, with a normal body mass index (BMI) consistent with overweight status. He was retired, previously maintained an active lifestyle involving regular physical activity and daily functional mobility, and had no history of tobacco use; his social history included moderate social alcohol consumption. Post-TKA, he initially reported good recovery during the acute postoperative phase, but developed progressively worsening left knee pain beginning around the third postoperative week. The pain was described as sharp, with a visual analog scale (VAS) intensity of 7/10, poorly localized, radiating to the left ankle, and associated with paresthesias in a dermatomal distribution consistent with anterior lower extremity innervation. Physical examination revealed hyperesthesia and allodynia specifically along the anterior knee region, with intact motor function: lower left leg strength was 5/5 in both flexion and extension, and full strength (5/5) was observed in all lower extremity myotomes, including hip flexion, inversion, eversion, plantar flexion, and dorsiflexion. The surgical incision was well-healed, without signs of erythema, swelling, or tissue compromise. Orthopedic imaging and clinical assessment ruled out hardware loosening, infection, or mechanical joint pathology, supporting the exclusion of primary orthopedic causes of pain. Given the constellation of symptoms—including sensory hyperexcitability, allodynia, preserved motor function, and absence of structural or inflammatory joint pathology—a diagnosis of complex regional pain syndrome (CRPS) type I of the left lower extremity was established. Initial conservative management with physical therapy, non-steroidal anti-inflammatory drugs (NSAIDs), muscle relaxants, neuropathic agents (e.g., gabapentin, pregabalin), and low-dose opioids provided minimal to no symptomatic relief. A lumbar sympathetic block was performed, resulting in transient pain reduction to a VAS of 3/10, which lasted approximately one month, suggesting a sympathetic-mediated component to the pain pathway. This response prompted further intervention. The patient"}
+{"row_index": 162, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 46-year-old woman had a long-term thyroid problem where her body wasn’t making enough thyroid hormone. She was taking a medicine called levothyroxine every day to fix it. For years, her thyroid tests looked normal, so her doctor kept the dose the same. Eight years later, her test showed very high levels of a hormone called FT4, but she had no signs of being overactive — like fast heartbeats or weight loss. This didn’t make sense. The lab checked again using a different testing method, and found the real level was actually low. The reason? Her body made antibodies that messed up the test. These antibodies thought the hormone was there when it wasn’t. This is called anti-T4 autoantibodies. The test that measures free T4 is not always accurate when these antibodies are present. After testing, her doctor gave her the original dose of medicine again, and her thyroid levels became normal. She doesn’t have any symptoms of overactive thyroid, and the problem was only caught because of the wrong test results.\"\n}"}
+{"row_index": 163, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 46-year-old woman with long-term hypothyroidism, treated with levothyroxine, was seen eight years after her diagnosis. Her routine blood tests showed a high level of free thyroxine (FT4) and a slightly high TSH, but she had no symptoms of an overactive thyroid, like rapid heartbeat or weight loss. This was confusing because her thyroid function was stable for years, and she didn’t feel any different. Tests using two different lab methods showed a big difference: one method showed a very high FT4, while the other showed a low FT4. This inconsistency raised suspicion that her blood test was being affected by antibodies in her blood that react with thyroxine, specifically anti-T4 autoantibodies. These antibodies interfered with the test results, making the FT4 appear higher than it actually was. The problem was confirmed through special lab tests that showed the antibodies were causing the false high reading. The patient did not have symptoms of hyperthyroidism, and her other thyroid markers were normal. After confirming the interference, her levothyroxine dose was restored to the original level. This case shows that sometimes lab results can be misleading due to antibodies, and it’s important to use multiple testing methods when there’s a mismatch in results, especially in patients with long-standing thyroid conditions.\"\n}"}
+{"row_index": 164, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"We report a case of a 46-year-old female with autoimmune hypothyroidism managed on chronic levothyroxine replacement, who presented eight years after diagnosis with a serum thyrotropin (TSH) of 7.393 µUI/mL (normal range: 0.5–5 µUI/mL) and a markedly elevated free thyroxine (FT4) level of 51.7 pg/mL (normal range: 8–18 pg/mL), alongside a normal free triiodothyronine (FT3) level of 2.8 pg/mL (normal range: 2.3–4.2 pg/mL). The patient exhibited no clinical signs of hyperthyroidism, including tremor, palpitations, sweating, insomnia, diarrhea, or visual disturbances, and had no family history of thyroid disease. Her body mass index was 35 kg/m², blood pressure was 129/88 mmHg, and heart rate was 98 bpm. She had recently gained 7 kg over six months, but denied symptoms consistent with hyperthyroidism. Given the absence of hyperthyroidism symptoms and the normal FT3 level in the context of high FT4, interference in FT4 quantification was suspected. The diagnosis of thyroid hormone resistance was ruled out due to normal FT3 levels and absence of familial thyroid disease.\\n\\nInitial testing was performed using the Siemens Healthcare Reagents Kit on the Advia Centaur platform, which reported a high FT4 value of 51.7 pg/mL. To evaluate potential assay interference, a parallel FT4 measurement was conducted in a second immunoassay platform, the Roche Cobas e 411, using a Roche Diagnostics reagent kit. The test was performed on serum collected 20 days after the initial sample, following overnight fasting and 24 hours post-levothyroxine administration. Serum samples were processed with 20-minute room temperature incubation, centrifuged at 3000g for 15 minutes, and either analyzed immediately or stored at −70°C for seven days. Quality control was maintained using freeze-dried human-based controls: Biorad Immunoassay Plus Control (Advia Centaur) and Roche Precinorm U (Cobas e 411), with intra- and inter-run coefficients of variation (CV) of <"}
+{"row_index": 165, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 26-year-old man with no serious health problems before suddenly got weak in both legs after getting a shot of dexamethasone. He had muscle cramps earlier, which went away, but then woke up weak and couldn't stand. His legs were very weak, and he fell, hurting his arms. His blood showed very low potassium, which is a key mineral for muscles. Doctors gave him potassium shots, and within hours his legs started getting stronger. He could walk again after his potassium levels went back to normal. Tests showed he wasn’t losing potassium through his urine or stool, and no other medicines were causing it. The weak muscles came back fast when potassium was fixed, so doctors thought it was hypokalemic periodic paralysis. This condition is not hereditary in his family, and it was likely caused by the steroid shot. Later, he had another episode after eating a big meal with lots of carbs. Now he knows to avoid steroid shots and high-carb foods to stay safe.\"\n}"}
+{"row_index": 166, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 26-year-old Asian man suddenly developed weakness in both legs after receiving an injection of dexamethasone, a steroid medication. He had no prior medical problems, except for a long-time history of aseptic meningitis that did not cause lasting issues. He worked as a construction worker and had been experiencing muscle cramps in his right shoulder and back for a week. He visited a traditional medicine practitioner who gave him anti-inflammatory drugs and another unknown injection. The cramps went away, but the next morning he woke up with sudden leg weakness, making it hard to stand and causing him to fall and get bruises on his arms.\\n\\nAt the emergency department, his temperature was slightly elevated, but his blood pressure and other vital signs were normal. His mental state was clear, and he was well-nourished. Examination showed that his leg muscles were weak, especially in the upper parts of the legs, with strength dropping from 2/5 to 1/5. His arms and reflexes were normal, and there was no sign of nerve damage. Blood tests showed low potassium levels (1.7 mEq/L), which is a key factor in muscle weakness. His ECG showed changes typical of low potassium, and after receiving potassium supplements, his muscle strength improved by the afternoon. His potassium levels returned to normal (4.0 mEq/L), and he was able to walk again.\\n\\nHis urine tests showed he wasn’t losing potassium through his urine, and he had not taken any medications known to cause potassium loss, such as diuretics or insulin. His hormone levels were mostly normal, except for a slightly high TSH, which may have played a role. The doctors believed the weakness was caused by hypokalemia (low potassium), and since it improved quickly after potassium was restored, they did not perform further tests like electromyography.\\n\\nIt was later found that the dexamethasone injection had triggered the condition. This type of hypokalemic periodic paralysis (HPP) is not inherited and is often triggered by certain medications or high-carbohydrate meals. The patient was advised to avoid corticosteroids and large meals high in carbohydrates to prevent future episodes. A year later, he had another episode after eating a large carbohydrate meal, confirming the pattern.\\n\\nThe final diagnosis was non-familial hypokalemic periodic paralysis, likely caused by the dexamethasone injection.\"\n}"}
+{"row_index": 167, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 26-year-old Asian male presented to the emergency department with an acute onset of bilateral proximal lower limb weakness, initially manifesting as difficulty standing and subsequent falls resulting in upper limb contusions. The patient had no significant medical history beyond a prior episode of aseptic meningitis over a decade ago, which was asymptomatic. He was a construction worker engaged in heavy physical labor and reported intermittent muscle cramping in the right shoulder radiating to the back for one week. Prior to presentation, he received intramuscular injections of non-steroidal anti-inflammatory drugs (NSAIDs) and an unknown agent from a traditional medicine practitioner, after which the cramping resolved. However, upon waking in the morning, he developed acute, symmetric lower limb weakness, with initial muscle strength in both legs measured at 2/5, progressing to 1/5, while upper limb strength remained preserved. Neurological examination revealed intact deep tendon reflexes (knee jerks) and lower limb sensation, with no Babinski sign bilaterally, indicating no upper motor neuron involvement.\\n\\nVital signs were stable, with a tympanic temperature of 38.1°C, normotension, and no signs of systemic infection or shock. Laboratory investigations revealed a normal complete blood count, blood glucose, and urinalysis; however, serum potassium was markedly low at 1.7 mEq/L, with a mild elevation in creatine phosphokinase (178 U/L), consistent with myopathic changes. Electrocardiography demonstrated flattened T waves and prominent U waves in precordial leads V1–V3, which are characteristic of hypokalemia and reflect decreased cardiac membrane stability. Oral and intravenous potassium supplementation (initially 40 mEq) was administered, with serum potassium remaining at 2.0 mEq/L the following morning. A second bolus of 60 mEq was given, leading to a gradual improvement in lower limb muscle strength to 4/5 by afternoon. The patient was admitted and received an additional 20 mEq of intravenous potassium (total 120 mEq), resulting in normalization of serum potassium to 4.0 mEq/L and full recovery of ambulation.\\n\\nUrinary potassium excretion was low (urine potassium/creatinine ratio of 1.5 mmol/mmol), excluding significant renal potassium wasting. There was no evidence of gastrointestinal potassium loss, and"}
+{"row_index": 168, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 32-year-old man felt pain in his chest that spread to his back and left shoulder, like a heart attack, but tests showed no heart damage. His heart was sitting too far to the left, and X-rays showed lung tissue pushing between the aorta and the main lung artery. A special heart scan (MRI) found that the left layer of the heart's outer sac was missing — this is called left pericardial agenesis. The heart moves a lot and is twisted, which causes the lung tissue to push into places where it shouldn’t. He doesn’t need surgery right now and is just being watched closely. He should avoid lifting heavy things to prevent more pain.\"\n}"}
+{"row_index": 169, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 32-year-old man came in with chest pain that spread to his back and left shoulder, which reminded doctors of a heart attack. However, his ECG and heart enzymes were normal, and his overall exam was unremarkable. His heart rate was high (164 beats per minute), but his blood pressure and other tests were normal. A chest X-ray taken two days apart showed the heart shifted to the left side, with a bulging left border and a clear space between the aorta and pulmonary artery. This suggested something unusual about the heart's structure. A cardiac MRI confirmed that the patient had left pericardial agenesis — a rare condition where the protective sac around the left side of the heart is missing. This causes lung tissue to push between the aorta and pulmonary artery, and the heart rotates abnormally. The left atrial appendage also sticks out abnormally. There’s a small hole in the heart wall allowing blood to flow from the left side to the right side. The patient’s symptoms, especially during heavy lifting or exertion, are likely linked to this structural issue. He was treated with regular follow-up and advised not to lift heavy weights or do strenuous exercise.\"\n}"}
+{"row_index": 170, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 32-year-old male professional driver presented with episodic chest discomfort and radiating pain to the back and left shoulder, which exacerbated following four days of weight training. The symptoms began at age 10 and have recurred in association with physical exertion, including heavy lifting and uphill climbing. There is no history of comorbidities, surgical interventions, substance abuse, or familial history of ischemic heart disease. Clinical examination was unremarkable, with normal vital signs: heart rate of 164 bpm (indicating sinus tachycardia), blood pressure of 130/84 mmHg, respiratory rate of 24 breaths per minute (tachypnea), and normal blood glucose. Electrocardiography (ECG) was normal, and cardiac biomarkers (troponins, CK-MB) were within normal limits, ruling out acute myocardial infarction.\\n\\nInitial imaging via chest radiography revealed a normal cardiac apex and left heart border, but a lucent area—interpreted as lung tissue—was observed between the aorta and the pulmonary artery, as well as between the left hemidiaphragm and the base of the heart. The repeat chest X-ray, taken 24 hours later, demonstrated a leftward displacement of the cardiac apex (wandering cardiac apex), consistent with significant cardiac levorotation. Echocardiography confirmed marked levorotation of the heart, with normal left ventricular size, preserved systolic function (ejection fraction of 60%), and substantial cardiac mobility—defined as apex displacement exceeding 1.5–2 mm, indicating increased myocardial excursion. No pericardial or pleural effusion was detected, and ventricular wall motion was normal.\\n\\nCardiac MRI further delineated the anatomical abnormalities: significant anterior interposition of lung tissue between the main pulmonary artery and the descending aorta, and between the left ventricle and the diaphragm. The left atrial appendage was abnormally protruding along the lateral aspect of the aortic arch. A 6-mm defect in the middle atrial septum was identified, consistent with a secundum type of atrial septal defect (ASD), leading to left-to-right shunting. The left inferior pulmonary vein exhibited restricted caliber due to compression between the descending aorta and the left atrium, a consequence of the pronounced levorotation. Pulmonary vein diam"}
+{"row_index": 171, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 71-year-old woman started feeling weak, lost weight, had diarrhea, and her skin turned yellow over two years. She had been checked regularly for liver problems, but nothing was clear. When she got really sick, she had very low blood pressure and her heart was barely working. She needed to be in the hospital’s intensive care unit because her body was failing. Tests showed damage in her liver, stomach, spleen, and brain. A second liver test finally found the cause: a rare condition that affects many parts of the body, called multisystem LCH, which caused her bile ducts to become scarred and blocked. This is known as secondary sclerosing cholangitis. She was given medicine to help her hormones and a special drug to stop the disease from getting worse. But she had many other health problems, like pancreatitis and diabetes, and after being in the hospital several times, she chose comfort care to focus on feeling better, not fighting the illness.\"\n}"}
+{"row_index": 172, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 71-year-old woman came to the hospital with worsening weakness, weight loss, diarrhea, and yellowing of the skin (jaundice). She had been seeing her doctor for high liver enzymes over the past two years, but treatments like ursodiol and low-dose steroids didn’t help. When she arrived, she was very low on blood pressure and had a slow heart rate. Her blood tests showed high white blood cell counts, high liver enzymes, and signs of inflammation. Her thyroid function was also abnormal, with no active thyroid hormone levels.\\n\\nImaging scans showed damage in multiple organs, including the liver, gastrointestinal tract, spleen, and brain. The liver biopsy, which was previously inconclusive, now showed signs of a rare condition called multisystem Langerhans cell histiocytosis (LCH). This condition affects several organs and caused the liver disease in the form of secondary sclerosing cholangitis — a type of bile duct damage.\\n\\nShe needed intensive care because she developed severe shock, requiring medications to support her blood pressure and heart function. Brain imaging showed inflammation of the pituitary gland, which affects hormone production. She also had pancreatitis, blood sugar issues, and developed central diabetes insipidus.\\n\\nTreatment started with hormone replacement to fix her low hormone levels. After discussion with a team of specialists, she was given a drug called vemurafenib, which targets a specific mutation found in LCH cells. Despite treatment, she had repeated hospitalizations and eventually chose comfort care to focus on quality of life.\"\n}"}
+{"row_index": 173, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 71-year-old female with a history of gastroesophageal reflux disease presented to the emergency department following a syncopal episode, accompanied by progressive diarrhea, unexplained weight loss, worsening jaundice, and fatigue. She had been undergoing outpatient evaluation for chronically elevated liver enzymes over the preceding two years. Prior therapeutic trials with ursodiol and low-dose prednisone were ineffective. On admission, her vital signs demonstrated hypotension (blood pressure 72/53 mm Hg) and a nadir heart rate of 62 beats per minute. Physical examination revealed jaundice and cachexia. Laboratory findings included leukocytosis (27.7 × 10⁹/L; normal 3.4–9.6 × 10⁹/L) with neutrophilic predominance. Hepatic function tests showed elevated aspartate aminotransferase (85 U/L; normal 8–43 U/L), alanine aminotransferase (85 U/L; normal 7–45 U/L), bilirubin (9.3 mg/dL; normal <1.2 mg/dL), and markedly elevated alkaline phosphatase (2262 U/L; normal 35–104 U/L) and gamma-glutamyl transferase (494 U/L; normal 5–36 U/L). C-reactive protein was elevated at 52 mg/L (normal <8 mg/L), and thyroid function tests revealed hyperthyroidism with elevated TSH (22.8 mIU/L; normal 0.3–4.2 mIU/L), undetectable free T3 and T4, consistent with panhypopituitarism. A prior 6-month liver biopsy demonstrated periportal fibrosis with lymphocytic and scattered neutrophilic infiltrates in portal tracts, but no evidence of histiocytic infiltration. Imaging studies included contrast-enhanced computed tomography (CT) of the abdomen and pelvis, which revealed diffusely heterogeneous liver parenchymal enhancement without ductal dilatation, duodenitis, and diffuse colonic thickening suggestive of pancolitis. CT chest showed bilateral centrilobular ground-glass opacities with mild pulmonary edema. Echocardiography was normal, excluding cardiac etiology. Brain magnetic resonance"}
+{"row_index": 174, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 21-year-old woman from northern Tanzania, who had been breastfeeding for 8 months after having a baby by C-section, came in with belly pain, swelling, fever, and unusual discharge from her vagina. She had a hard lump in her lower belly that was tender and about the size of a 16-week pregnancy. A scan showed a possible infection in her pelvis, but after surgery, doctors found a large, swollen uterus with hair, oily stuff, and pus inside. They removed the whole uterus and tested the tissue. The test showed it was a type of growth called a mature teratoma, which is like a skin cyst that can grow and get infected. She recovered well, had no more symptoms, and has stayed healthy for 8 months after surgery.\"\n}"}
+{"row_index": 175, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 21-year-old woman from the northern region of Tanzania, who is of Sukuma ethnicity, came to the hospital with abdominal pain, swelling, fever, and abnormal vaginal discharge that had lasted for three weeks. She had been breastfeeding for eight months after having a child via cesarean section. During her exam, doctors found a large, tender mass in her abdomen and signs of infection in her pelvic area. A pelvic ultrasound suggested a pelvic abscess, but after surgery, they found a different cause: a mature uterine teratoma, which is a type of benign tumor that contains skin-like tissue, hair, and sebaceous material. The tumor was infected and had pus inside. The surgery involved removing the entire uterus (total hysterectomy), and the tissue was tested under a microscope, confirming the diagnosis. The patient recovered well, received blood and antibiotics, and has not had any signs of the disease returning for eight months.\"\n}"}
+{"row_index": 176, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 21-year-old female of Sukuma ethnicity from the northern region of Tanzania presented to the Bugando Medical Centre (BMC) outpatient clinic in Mwanza with a three-week history of abdominal pain, distension, fever (approximately 38.5 °C), and abnormal vaginal discharge. She was lactating for eight months following a previous cesarean section delivery. On physical examination, she exhibited signs of systemic illness, including weakness, fever, and a blood pressure of 110/70 mmHg. Her blood group was A, Rh-positive, with a hemoglobin level of 6.3 g/dL, indicating significant anemia. Abdominal examination revealed a sub-umbilical midline surgical scar and a palpable suprapubic mass corresponding to a uterus of approximately 16 weeks' gestational size, described as soft, tender, and mobile. Digital pelvic and vaginal examination demonstrated a closed cervix with tenderness on cervical mobility, tenderness in the posterior fornix, and gloved finger staining with pus-like discharge. Pelvic ultrasound imaging suggested the presence of a pelvic abscess.\\n\\nThe patient was referred for emergency laparotomy. Intraoperatively, the uterus was found to be markedly bulky with a discharging sinus located on the left fundal aspect. Both ovaries appeared normal in morphology and structure, with no evidence of adnexal pathology or fluid in the pouch of Douglas. A transverse incision was made at the level of the sinus tract. The uterine cavity contained yellowish, mucinous, tenacious material intermixed with hairy tissues and sebaceous debris. A decision was made to proceed with total hysterectomy, during which the excised uterus was observed to contain abundant hair and sticky sebaceous material within the uterine cavity.\\n\\nPostoperatively, the patient received one unit of packed red blood cells to correct her anemia and was administered intravenous antibiotics: ceftriaxone, gentamicin, and metronidazole, with concurrent prophylactic heparin therapy to prevent thromboembolic complications. The patient recovered uneventfully.\\n\\nHistopathological evaluation of the resected uterus, which measured 18 cm × 9 cm × 4 cm and contained no adnexal structures, revealed a cystic lesion measuring 10 cm in diameter located within the myometrium at the left fundal"}
+{"row_index": 177, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 64-year-old woman had a filter put in her leg vein 3 months ago to stop a blood clot. The filter didn’t come out easily, and the doctor tried to pull it back but failed. Then, 3 months later, she got sudden, bad pain on her right side of the belly. Her urine was red, and she had swelling in her right leg. The filter’s hook went too far and cut into her right leg artery, causing a bulge (like a balloon) in the artery. This blocked her urine pipe, so her kidney swelled up. Both her leg veins and part of her main vein were completely blocked. The doctors did emergency surgery to remove the filter, the bulge, and the blocked parts. They fixed the artery and fixed her veins. The surgery found a bacteria called Staphylococcus aureus in the tissue, which was treated with antibiotics. After surgery, she stayed in the hospital for 12 days and started taking medicine to prevent clots and fight infection. Six months later, a scan showed the artery was open and her kidney swelling was only mild. She’s doing better now.\"\n}"}
+{"row_index": 178, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 64-year-old woman was admitted with sudden, severe pain on the right side of her abdomen. She had previously had an IVC filter placed three months ago to prevent blood clots after a deep vein thrombosis in her left leg. The filter was placed through her right femoral vein and was meant to be removed later, but a previous attempt to retrieve it failed. Since then, imaging was stopped due to the pandemic.\\n\\nShe developed severe abdominal pain and noticed red urine, but no fever or other signs of infection. On exam, her abdomen was tender, her right leg was swollen, and her right femoral pulse was weak. Blood tests showed high white blood cells, indicating inflammation or infection.\\n\\nA CT scan revealed that the hook part of the filter had pierced into her right iliac artery, causing a bulge (pseudoaneurysm) in that artery. This also blocked her right ureter, leading to swelling of the kidney on that side. Both iliac veins and the lower part of her IVC were completely blocked, which affects blood flow.\\n\\nShe underwent emergency open surgery to remove the IVC filter, the pseudoaneurysm, and the damaged parts of the iliac veins and IVC. Her right iliac artery was reconstructed to restore blood flow. Bacteria (Staphylococcus aureus) were found in the tissue sample, and she was treated with antibiotics and anticoagulation therapy.\\n\\nShe was discharged on day 12. Six months later, a follow-up CT showed that her right iliac artery was open and flowing properly, and only mild kidney swelling remained. Her condition has improved, but ongoing care is needed.\"\n}"}
+{"row_index": 179, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 64-year-old female presented to our institution with a 1-day history of severe right abdominal pain following a 3-month history of inferior vena cava (IVC) filter placement. The initial indication for IVC filter placement was deep venous thrombosis (DVT) of the left lower extremity, managed with anticoagulation. A double-basket retrievable IVC filter (Visee WXF-32, Shandong Visee Medical Devices Company Limited, China) was inserted infrarenally via the right femoral vein. Ten days later, endovascular retrieval of the filter using standard femoral venous access failed, and subsequent imaging follow-up was discontinued due to the COVID-19 pandemic. Three months later, the patient presented with acute right lower quadrant pain, no fever or chills, and reddish urine consistent with hematuria. She had a history of scoliosis, poorly controlled type 2 diabetes mellitus, and chronic substance use including tobacco and alcohol. On admission, vital signs were stable: heart rate 97 bpm, respiratory rate 23 breaths/min, blood pressure 126/73 mmHg. Physical examination revealed diffuse abdominal tenderness with rebound tenderness, mild right lower limb swelling, and a weak femoral artery pulse. Laboratory findings showed normal hepatic and renal function, hemoglobin 101 g/L, leukocyte count 14.74 × 10⁹/L, and neutrophilic granulocyte percentage of 91.0%, indicating a significant inflammatory response. During surgical intervention, a partial pseudoaneurysmal lesion was excised for tissue culture, yielding isolation of Staphylococcus aureus, which demonstrated sensitivity to moxifloxacin. Computed tomography angiography (CTA) revealed that the retrieval hook of the IVC filter had penetrated the right common iliac artery (CIA), resulting in a 52 mm × 48 mm × 55 mm pseudoaneurysm in the right iliac artery. This pseudoaneurysm was associated with complete right ureteral obstruction leading to ipsilateral hydronephrosis. Bilateral iliac veins and the distal segment of the IVC were completely occluded, with extensive pelvic varicosities observed. Emergency open surgical repair was performed, including complete removal of the IVC filter, the right"}
+{"row_index": 180, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 32-year-old woman felt越来越 short of breath, had no appetite, and woke up sweating every night for two weeks. Doctors found a big tumor in her left kidney that had grown into her main vein and reached her heart. The tumor was very large and pushed into her heart, which is a serious problem. She had surgery to remove the kidney and the tumor from her vein and heart. The tumor was found to be a rare cancer called Ewing's sarcoma, which started in the kidney and spread through the blood vessels. This cancer was confirmed by a test that looked for a specific gene change. After surgery, she started chemotherapy to kill any remaining cancer cells. She still takes blood thinners to prevent new clots because both the cancer and treatment can cause blood clots. Her scans show no more cancer, and she is doing well.\"\n}"}
+{"row_index": 181, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 32-year-old Iranian woman came in with worsening shortness of breath, loss of appetite, and night sweats over the past two weeks. Tests showed a tumor in her left kidney that had spread into the veins leading to her heart, including the inferior vena cava and into the right atrium. This was a rare and serious condition. She had surgery to remove the kidney and the tumor from the veins. During the surgery, the tumor was found extending into her right atrium and was diagnosed as Ewing's sarcoma, a type of cancer that starts in the kidneys and spreads. Pathology tests confirmed the presence of a genetic change (EWSR1 rearrangement) that is typical of this cancer. She started chemotherapy after surgery, with adjustments made to reduce side effects. Her follow-up scans showed no signs of cancer recurrence, and she is doing well with ongoing treatment and monitoring.\"\n}"}
+{"row_index": 182, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 32-year-old Iranian female presented with progressive dyspnea at rest, accompanied by anorexia, fever, chills, and night sweats over a two-week period prior to admission. Initial evaluation at Rajaei Hospital Cardiac Center included echocardiography and computed tomography (CT) angiography, which revealed pulmonary thromboembolism (PTE) consistent with a massive tumor thrombus. The diagnosis of PTE was confirmed, and she was initiated on heparin followed by transition to oral rivaroxaban for anticoagulation, with subsequent stable discharge under close follow-up.\\n\\nTwo weeks later, she returned with worsening dyspnea and systemic symptoms. Abdominal ultrasound and contrast-enhanced abdominopelvic CT demonstrated a solid, heterogeneously enhancing mass in the mid-to-lower pole of the left kidney measuring 70 mm × 75 mm × 105 mm, with tumor thrombus extending from the left renal vein through the inferior vena cava (IVC) to the right atrium over a craniocaudal length of approximately 23 cm. Mild hypodense fluid was noted in the pelvic cavity. CT findings also revealed filling defects in the right main pulmonary artery and its segmental branches, consistent with pulmonary thromboembolism, and a 7 mm ground-glass nodule in the left lower lobe superior segment. No signs of acute abdominal pathology, such as appendicitis, cholecystitis, pancreatitis, hydronephrosis, or free air, were identified.\\n\\nEchocardiography showed normal left ventricular systolic function (ejection fraction = 55%), with mild to moderate tricuspid regurgitation, mitral regurgitation, and pulmonary insufficiency. Mean pulmonary artery pressure was 27 mmHg, and peak instantaneous pressure gradient was 17 mmHg. A large, rope-like, hyperechoic mass was observed in the IVC measuring 14 cm × 2.7 cm, protruding into the right atrium, strongly suggestive of extensive intracardiac tumor thrombosis.\\n\\nGiven the clinical suspicion of a primary renal malignancy with extensive venous invasion, the patient underwent a combined surgical approach: open radical nephrectomy for the left kidney, followed by IVC thrombectomy under cardiopulmonary bypass. During surgery,"}
+{"row_index": 183, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 53-year-old man had a broken hip and started having seizures after surgery. Doctors found a lump in his brain that was not in the normal brain area — it was on the outside of the brain, attached to the lining. This lump looked like a brain tumor, but it wasn’t a regular tumor. It was made of special cells that were not part of the brain. The doctors had to cut into the brain to remove it, and during the surgery, they had to cut some small blood vessels on the brain’s surface. Because of that, the man lost some movement on his left side. After surgery, a scan showed a bleed and a spot in his brain that was likely from those cut blood vessels. The doctors found this lump was not just in the brain — it was also in the nervous system, and it was the only place it was found. The man has not had seizures since, and his movement is slowly getting better. No other parts of his body showed signs of this condition.\"\n}"}
+{"row_index": 184, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 53-year-old man with diabetes and a broken hip was admitted to the hospital. He had a seizure after surgery, and was referred for further evaluation. Brain imaging showed a mass on the right side of his brain, specifically in the parietal area, that was consistent with a type of tumor called meningioma en plaque. This tumor was attached tightly to the brain surface and had many small blood vessels running through it. To remove the tumor completely, these blood vessels had to be cut, which led to complications. The surgery was done through a frontotemporal craniotomy. After the procedure, the patient developed incomplete weakness on his left side and a bleeding area in the right frontal lobe, likely due to the damaged blood vessels. A biopsy showed unusual immune cells in the tumor, and the findings matched a rare condition called isolated central nervous system RDD (extranodal RDD), meaning the tumor started in the brain but is not spread to other parts of the body. The patient has been seizure-free since surgery and has slowly recovered from his weakness over six months. No signs of the disease spreading to other organs were found.\"\n}"}
+{"row_index": 185, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 53-year-old homeless man was admitted for a right femoral neck fracture; his medical history included noninsulin-dependent diabetes mellitus. Physical examination at admission was unremarkable, with no fever, lymphadenopathy, or baseline neurological deficits. Laboratory findings showed white blood cell count of 4330 cells/mL, hemoglobin of 9.2 g/dL, and platelet count of 29,900 platelets/mL, consistent with normochromic-normocytic anemia; C-reactive protein was negative, indicating no active systemic inflammation. The orthopedic surgery for the fracture was successfully performed. However, during the postoperative course, the patient developed an episode of generalized seizures, for which phenytoin was administered. Subsequently, he was referred to our neurosurgical department for further evaluation.\\n\\nNon-contrast head computed tomography (CT) revealed a high-density, extraaxial mass in the right parietal convexity, with prominent peritumoral brain edema. Enhanced magnetic resonance imaging (MRI) demonstrated a dural-based, extraaxial, homogeneously enhancing lesion with well-defined borders, consistent with a meningioma en plaque. On T1-weighted imaging, the lesion was iso- to hyperintense; on fluid-attenuated inversion recovery (FLAIR) and T2-weighted sequences, it was iso- to hypointense. The imaging characteristics, combined with the dural attachment and vascular architecture, strongly supported the diagnosis of meningioma en plaque.\\n\\nThe tumor was resected via a right frontotemporal craniotomy. Microscopic examination revealed a firm, xanthochromic, nonaspiratable mass with high vascularity and dural origin. The tumor was tightly adherent to the adjacent cerebral cortex and was extensively infiltrated by pial arteries and veins of the brain surface. This intimate vascular integration rendered the preservation of these pial vessels during complete resection highly improbable, necessitating their sacrifice to achieve total tumor removal. Postoperatively, the patient developed incomplete left hemiparesis, likely secondary to ischemic injury from the disruption of pial arterial supply.\\n\\nA postoperative non-contrast brain CT demonstrated a hemorrhagic lesion and a low-density area in the right frontal lobe, which is believed to result from the surgical sacrifice of pial arteries at the tumor-brain interface. The"}
+{"row_index": 186, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A woman in her 80s had a knee infection after a surgery she had seven years ago. Her knee was swollen, painful, and had pus coming out. Doctors found a type of yeast called Cy. fabianii in her knee during surgery. At first, they thought it was a different yeast called Candida utilis, but later testing proved it was really Cy. fabianii. This yeast can cause serious infections in joints, and the right treatment was needed to fix it. She got antibiotics to fight the infection and is now recovering at home.\"\n}"}
+{"row_index": 187, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"This study describes a case of infection in a prosthetic knee joint in an 85-year-old woman who had a total knee replacement seven years earlier. She developed pain, swelling, and pus in her right knee over three months. Tests showed signs of joint infection and bone infection (osteomyelitis). She received antibiotics initially, and the infected knee implant was removed. During surgery, fluid from the joint was tested and grew a type of yeast. At first, the yeast was wrongly identified as Candida utilis, but further testing using advanced lab methods correctly identified it as Cy. fabianii. This correct identification was confirmed through DNA analysis and comparison with known yeast samples in a database. The infection was treated with antifungal medications, and the patient recovered after completing a course of oral and intravenous antibiotics.\"\n}"}
+{"row_index": 188, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"An 85-year-old Chinese woman with a history of hypertension, dyslipidemia, and a prior right total knee replacement seven years earlier presented with a three-month history of painful right knee swelling and purulent discharge, without recent trauma or surgical intervention. On admission, she was afebrile, with diffuse swelling, erythema, tenderness, and a sinus tract. Laboratory findings revealed a total white blood cell count of 7.8×10³ cells/µL, elevated C-reactive protein, and increased erythrocyte sedimentation rate, indicating active inflammation. Radiographic imaging demonstrated radiolucency in the distal femur and proximal tibia, consistent with osteomyelitis. The patient was diagnosed with prosthetic joint infection (PJI) of the right knee complicated by osteomyelitis, and empiric therapy with intravenous clindamycin and ciprofloxacin was initiated. Surgical intervention included removal of the prosthetic implant and arthrotomy with washout; intraoperative findings were consistent with osteomyelitic changes. Synovial fluid was inoculated into BD Bactec Plus Aerobic/F and BD Bactec Lytic/10 Anaerobic/F vials and incubated using BD BACTECTM FX. After 72 hours, the aerobic bottle yielded a positive culture. Gram staining revealed gram-positive ellipsoidal budding yeast cells. The isolate grew as cream-colored, smooth, glistening colonies on Sabouraud Dextrose Agar and as whitish colonies on CHROMagar. Corn meal agar culture showed only blastoconidia, with no germ tube formation or urease activity, supporting a non-germ tube-forming yeast phenotype. Bone marrow specimens also yielded identical growth. Initial phenotypic identification using the VITEK® 2 yeast identification system assigned the organism to *Candida utilis* with 95% probability. However, subsequent identification via matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF) by Bruker revealed the organism as *Candida fabianii*, a species frequently misidentified as *C. utilis* due to overlapping phenotypic characteristics. This finding was independently confirmed by molecular analysis: DNA was extracted using the Quick-DNA Fungal/Bacterial Miniprep Kit (Zymo Research), and the D1/D2 domain of the large subunit ("}
+{"row_index": 189, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 56-year-old Moroccan woman had a big lump on one side of her face that grew over 4 months. It hurt a lot, made her mouth hard to open, blocked her nose, and she started bleeding from her nose. The lump was deep in her face and spread into her nose, eye area, and sinuses. Doctors saw it with scans and found it was a serious, fast-growing tumor. A small tissue sample showed it was a cancer called malignant schwannoma. Even though they gave her radiation to ease the pain, she passed away 10 days later because of breathing trouble.\"\n}"}
+{"row_index": 190, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 56-year-old Moroccan woman was hospitalized in 2013 with a large swelling on one side of her face, on the right side, that had been growing over the previous 4 months. She first noticed sharp facial pain, which was initially thought to be a dental issue but didn’t improve. The swelling grew quickly, causing trouble opening her mouth, nasal blockage, and nosebleeds. She had a painful swelling on her right face, her eye appeared slightly bulging, and she had numbness in parts of her face controlled by the trigeminal nerve. A nasal exam found a tumor in her right nose that was fragile and bled easily. Her hard palate was eroded, and her mouth was so tight it was hard to examine. No lymph nodes or other parts of her throat showed signs of disease. Her hearing and ear exam were normal. She was given morphine for pain. CT and MRI scans showed a large, aggressive tumor in her right temple area, maxillary sinus, and around her eye, spreading into nearby structures like the sinuses and nasal passages. The tumor was invasive and had areas of dead tissue. A biopsy of the tumor confirmed it was a malignant schwannoma, a type of cancer that starts in nerve tissue. Tests showed no spread to other parts of her body. Because the cancer was advanced and not curable, the doctors chose palliative radiotherapy to relieve symptoms. The treatment helped a bit, but she passed away 10 days later due to severe breathing problems.\"\n}"}
+{"row_index": 191, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 56-year-old Moroccan woman with a 38-year history of chronic cigarette smoking (approximately one pack per day) was hospitalized in 2013 presenting with a rapidly progressive right-sided hemifacial swelling that had evolved over four months. Initial symptoms included persistent, unilateral facial neuralgia localized to the trigeminal nerve distribution, initially misdiagnosed as dental in origin and managed without improvement. The pain progressively worsened to a disabling level, accompanied by a significant increase in right maxillary swelling, limitation of mouth opening (trismus), and recurrent nasal obstruction with epistaxis (nosebleeds). Clinical examination revealed a painful, inflammatory right hemifacial mass, right exophthalmos without evidence of visual acuity reduction, and hypoesthesia in the second and third divisions of the trigeminal nerve (V2 and V3), consistent with peripheral nerve involvement. Endonasal examination identified a friable, bleeding tumor mass within the right nasal cavity. Oral examination, severely limited by trismus, demonstrated erosion of the hard palate. Cervical lymphadenopathy was absent, and upper aerodigestive tract endoscopy showed no mucosal lesions. Otoscopy and audiometry were normal, excluding central nervous system or auditory pathway involvement. The patient was immediately initiated on intravenous morphine for pain control.\\n\\nImaging studies revealed a large, heterogeneous, infiltrative mass involving the right infratemporal fossa, masticator space, and right maxillary sinus. CT findings demonstrated lysis of the maxillary sinus walls, the ascending ramus of the mandible, and the orbital floor, with extension into the ethmoidal, parapharyngeal, and intraorbital compartments. MRI further characterized the lesion as aggressive and invasive, with irregular boundaries, heterogeneous signal intensity on both T1- and T2-weighted sequences, and heterogeneous contrast enhancement with areas of central necrosis. The tumor exhibited infiltrative growth into the jugular and temporozygomatic soft tissues, consistent with a highly destructive, locally advanced process. The radiological pattern supported extensive local invasion without evidence of distant spread.\\n\\nA nasal endoscopic biopsy was performed, and histopathological evaluation confirmed a poorly differentiated, invasive malignant process. Immunohistochemical analysis demonstrated strong, diffuse cytoplasmic positivity for anti-S100 protein, a hallmark marker of schwannoma lineage, leading to a definitive diagnosis of malignant schwann"}
+{"row_index": 192, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 76-year-old man had been feeling numbness, pain, and weakness in his arms and legs for 7 years. He also had sweating, constipation, and lost weight without knowing why. In the past month, he started having shortness of breath, swelling in his feet and legs, and low blood pressure. His heart tests showed a strange sign: his heart looked bigger than it should, but the electrical signals were weak — this is a clue that his heart might be full of a harmful protein. Tests on his heart showed the same problem: the heart muscle wasn’t working well, and this matches what happens in a disease called cardiac amyloidosis. Blood tests ruled out a common type of amyloid disease (AL). A gene test found a mutation in the TTR gene — this is the same mutation found in people with a family disease called familial amyloid polyneuropathy (FAP) and heart disease from amyloid. This confirms he had hATTR Val30Met disease. His treatment with medicine didn’t work well. After 80 days, he died because his heart stopped working. His son later had the same symptoms and was found to have the same gene problem.\"\n}"}
+{"row_index": 193, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 76-year-old man had been slowly getting worse over seven years, with numbness, pain, and weakness in his arms and legs, sweating, constipation, and unexplained weight loss. In the past month, he also developed shortness of breath, swelling in his body, and low blood pressure. Tests showed low electrical signals in his heart (low QRS voltage) that didn’t match his thickened heart muscle — this was a key sign pointing to cardiac amyloidosis (CA). Echocardiogram results, especially using advanced imaging, supported the diagnosis. Blood tests ruled out AL amyloidosis, a common type of amyloid disease, because his free light chain levels were normal. A genetic test found a specific mutation (c.148 G-A, Val30Met) in the TTR gene, which confirms the diagnosis of hereditary amyloidosis caused by a faulty protein called transthyretin. This condition is known as hATTR Val30Met, which leads to both nerve damage (familial amyloid polyneuropathy or FAP) and heart problems. His treatment with doxycycline, ursodeoxycholic acid, and tafamidis did not work well — he developed severe intestinal blockage and eventually died from heart failure. His son later developed similar symptoms and was found to have the same genetic mutation. No tissue biopsies were done after death due to family refusal.\"\n}"}
+{"row_index": 194, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 76-year-old male presented with a seven-year history of progressive peripheral neuropathy characterized by limb numbness, pain, weakness, autonomic dysfunction including sweating and constipation, and unexplained weight loss. Over the preceding month, he developed systemic edema, hypotension, and shortness of breath. Physical examination revealed malnutrition, anemia, lethargy, generalized muscle weakness, decreased muscle tone, diminished tendon reflexes, sacroiliac decubitus necrosis, and severe edema. Laboratory findings included persistent elevation of high-sensitivity troponin I (hs-TnI) and N-terminal pro-B-type natriuretic peptide (NT-proBNP), indicating myocardial injury; neutrophilic leukocytosis; moderate anemia with reduced erythrocyte count and hematocrit; and mild hypoxemia. Chest X-ray demonstrated bilateral pulmonary inflammation with pleural effusion. Electrocardiography (ECG) showed low QRS voltage in the limb leads, abnormal Q waves in leads II, III, and aVF, and a poor R-wave progression in V1–V6, which is inconsistent with left ventricular hypertrophy and suggestive of cardiac amyloidosis (CA). Echocardiography revealed left ventricular hypertrophy, diastolic dysfunction (grade II), and a small pericardial effusion, with a critical discordance between the low QRS voltage and the presence of hypertrophy—this discordance is a key pathological clue in the diagnosis of CA. Speckle tracking strain analysis demonstrated reduced global longitudinal strain (GLS) with apical sparing, an apical-to-basal strain ratio of 2.7, and an ejection fraction to GLS ratio (EFSR) of 4.4, findings that are consistent with the characteristic ultrasonic phenotype of cardiac amyloidosis. Chest CT scans revealed diffuse pulmonary interstitial changes, cystic lung lesions, and progressive subpleural calcifications, which are hallmark radiographic features of pulmonary amyloid deposition. The presence of pulmonary amyloidosis was further supported by the absence of evidence for active infection or inflammation, as confirmed by normal C-reactive protein and blood cell profile. Despite the critical clinical condition, cardiac magnetic resonance (CMR) and positron emission tomography with pyridyl-1,3-diamine (PYP) were not performed due to the patient's instability. To differentiate between"}
+{"row_index": 195, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 12-year-old boy had belly pain for four days, along with hard stools, watery poop, and a swollen belly. He was very sick, breathing fast, and his heart was beating too fast. When doctors looked with ultrasound, they saw the spleen had twisted like a corkscrew and was stuck in the lower belly, attached to the appendix and small intestine. Part of the spleen was dead because of the twist. The doctors did surgery to remove both the spleen and the appendix. The boy recovered well, stayed in hospital for 7 days, and then went home. He now takes medicine to prevent infections and will get vaccines for meningococcal and pneumococcal diseases to stay healthy.\"\n}"}
+{"row_index": 196, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 12-year-old boy came in with crampy abdominal pain that had lasted for four days. He had a history of constipation, mucoid diarrhea, and a swollen belly. He was very sick-looking, with a fast heart rate and tender abdomen. On ultrasound, doctors saw a 'whirlpool sign' and found that his spleen was not in its normal place — it was located in the lower abdomen, twisted 720 degrees, and had areas of dead tissue (necrosis). The spleen was stuck to the appendix and the end of the small intestine. During surgery, they removed both the spleen and the appendix. The surgery went smoothly, and he recovered well. After recovery, he received vaccines to protect against meningococcal and pneumococcal infections, and started on antibiotics to prevent future infections.\"\n}"}
+{"row_index": 197, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 12-year-old male presented with a four-day history of crampy, lower abdominal pain, accompanied by prior episodes of constipation, mucoid diarrhoea, and abdominal distension. He reported no vomiting, and there was no family history of similar gastrointestinal or systemic manifestations. The patient lived with his parents, three siblings, and grandparents, with no known congenital or inherited medical conditions in the family. On physical examination, he appeared acutely ill with marked distress; vital signs revealed tachycardia (heart rate 134 beats per minute), respiratory rate of 22 breaths per minute, normothermia (temperature 36.40°C), and normal blood pressure (110/75 mmHg). There was no sunken eye socket, and buccal mucosa was moist. Abdominal examination demonstrated generalized tenderness, distension that moved with respiration, and a firm, 8 cm × 5 cm mass in the left lower quadrant with its lower border inaccessible, consistent with a fixed, non-fluid-containing lesion. No free fluid was detected. Systemic examination was otherwise unremarkable.\\n\\nLaboratory findings included a white blood cell count of 10,300/μL with a neutrophilic predominance of 78.5%, moderate anemia (hemoglobin 8.6 g/dL, hematocrit 28%), mean corpuscular volume (MCV) of 86 fL, and platelet count of 775 × 10³/μL. Abdominal ultrasound revealed a 'whirlpool sign' at the splenic hilum, indicating vascular torsion, and demonstrated a wandering spleen located in the lower abdominal cavity, displaced below the level of the umbilicus. The spleen exhibited altered echogenicity, suggestive of focal infarction. The ultrasound diagnosis was confirmed as wandering spleen with multifocal infarction due to splenic volvulus.\\n\\nThe patient was managed with nil-by-mouth status, intravenous maintenance fluids, broad-spectrum antibiotic coverage, and analgesia. After stabilization, an emergency laparotomy was performed. Intraoperatively, a slightly enlarged spleen was identified within the peritoneal cavity, positioned below the umbilicus. The vascular pedicle was found to be torsioned 720°, with the torsion originating"}
+{"row_index": 198, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 56-year-old man had a stroke that went away on its own. He didn’t have any major heart problems, but later started feeling tired, losing weight, and sweating at night. His body showed signs of inflammation — his blood tests showed high levels of markers that mean the body is fighting something. He had breathing problems and was diagnosed with a condition called ANCA-associated vasculitis, which means his body’s immune system attacked his lungs and heart. This condition made his breathing worse, and his heart wasn’t working well. Tests showed his heart was weak and had a leaking aortic valve, which let blood flow backward. The doctor replaced the faulty valve with a new one. After the surgery, his breathing got better. The tissue from the valve showed signs of swelling, inflammation, and thickening — proof that his immune system was causing damage. He’s now being watched closely by heart, lung, and immune specialists to keep his symptoms under control.\"\n}"}
+{"row_index": 199, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 56-year-old man was diagnosed with ANCA-associated vasculitis, a type of autoimmune disease that causes inflammation in blood vessels. He first developed respiratory symptoms, including shortness of breath, which got worse over time. Initial tests showed signs of inflammation in his lungs and blood, and he was treated with steroids and methotrexate, which helped control the disease.\\n\\nAfter two years, his symptoms returned, especially shortness of breath, and his lung function declined. A heart exam revealed that his heart was not pumping effectively, with a low ejection fraction (30–35%), and he had severe aortic valve insufficiency — meaning the valve wasn't closing properly, allowing blood to leak back into the heart. This was confirmed by imaging and tissue analysis showing inflammation, thickening, and scarring in the aortic valve.\\n\\nHe had surgery to replace the damaged aortic valve with a bioprosthesis, which improved his symptoms. After surgery, his heart function and breathing stabilized. He also had a small heart rhythm issue, which was managed with medication. The condition of his lungs remained under close monitoring, and he continued treatment for his underlying vasculitis. This case shows how heart and lung problems can be linked in vasculitis, and why a full medical evaluation is needed when symptoms persist.\"\n}"}
+{"row_index": 200, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 56-year-old male with a prior spontaneous cerebral stroke at age 49, which resolved without residual neurological deficit and was not evaluated with magnetic resonance imaging, presented at 56 years of age with evolving respiratory symptoms initially attributed to respiratory tract involvement. He had no traditional cardiovascular risk factors, aside from a family history of ischemic heart disease. Ten weeks after the stroke, he developed third-degree atrioventricular (AV) block, initially suspected to be due to acute Borrelia infection; however, the block persisted despite antibiotic therapy, necessitating dual-chamber pacemaker implantation.\\n\\nDuring hospitalization, he exhibited fatigue, unintentional weight loss, and night sweats. Laboratory findings revealed a sedimentation rate >100 mm/hr, hemoglobin of 5.0 g/mL (indicating severe anemia), thrombocytosis (615×10⁹/L), and C-reactive protein (CRP) of 95 mg/L, with no leukocytosis. Gastrointestinal bleeding was not suspected due to absence of gastrointestinal symptoms. At 4 months, he was diagnosed with ANCA-associated vasculitis, specifically MPO-ANCA-positive, characterized by systemic inflammation with malaise, low-grade fever, arthritis, sinusitis, interstitial lung disease (confirmed by ground-glass opacities on high-resolution computed tomography [HRCT] of both lungs, without biopsy), and absence of mononeuritis multiplex, asthma, skin, renal, cerebral, or gastrointestinal tract involvement. The Birmingham Vasculitis Activity Score (BVAS) was 15, indicating moderate disease activity.\\n\\nTreatment with high-dose corticosteroids for six months followed by methotrexate led to clinical remission, with normalization of MPO-ANCA titers. Methotrexate was discontinued after two years of sustained remission. One year later, he developed worsening respiratory symptoms, including dyspnea, with rising MPO-ANCA levels, prompting reinitiation of steroid and methotrexate therapy. Despite this, respiratory symptoms persisted, leading to multidisciplinary evaluation involving cardiology, pulmonology, and rheumatology.\\n\\nInitial cardiac evaluation via transthoracic echocardiography (TTE) showed preserved left ventricular (LV) function, no pulmonary hypertension, and mild-to-moderate aortic regurgitation. A treadmill exercise"}
+{"row_index": 201, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A baby girl, 18 days old, was admitted to the hospital because her heart made a strange noise and her legs had weak pulses. Her blood pressure was much higher in her arms than in her legs. Doctors used an ultrasound to see her heart and found a narrow part in the main artery (aortic coarctation). They also saw that a blood vessel that feeds the heart (LCX) was not getting blood the normal way — it was flowing backward, through a small path from the lung artery instead of going into the heart. The heart was working fine, and the pressure in the lungs was normal. To fix this, doctors did surgery at day 23. They removed the narrow part of the artery and reconnected the heart's blood vessel back into the main artery. They also closed a small hole in the lung artery. After surgery, the baby had a fast heart rhythm that was treated with medicine. A follow-up check showed the heart blood vessel was now working properly. The baby recovered well and went home with normal heart tests.\"\n}"}
+{"row_index": 202, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"An 18-day-old girl was admitted to the pediatric intensive care unit because of a heart murmur and weak pulses in her legs. She was otherwise healthy, breathing on her own and with normal blood pressure, except for a 30 mmHg difference in blood pressure between her arms and legs. An echocardiogram confirmed aortic coarctation — a narrowing of the aorta — and showed that the heart’s left coronary artery (LCA) was not flowing into the aorta as it should. Instead, it was being supplied by blood from a nearby artery (the right posterior descending artery) and flowed into the right pulmonary artery instead. A coronary angiogram revealed only one right coronary artery and no left main coronary artery. The left circumflex artery (LCX) was feeding through a bypass path, reaching the wall of the aorta without entering it. At 23 days old, she had surgery to remove the narrowed part of the aorta and reconnected the left coronary artery back into the aorta using a technique that kept the artery safe and intact. The defect in the pulmonary artery was closed with a patch. After surgery, she had a few episodes of fast heart rate, which were treated with medication. Follow-up tests showed normal blood flow in the left coronary artery. She recovered well and was discharged home with normal heart function and no signs of damage.\"\n}"}
+{"row_index": 203, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"An 18-day-old female was admitted to the paediatric intensive care unit (PICU) due to a heart murmur and diminished femoral pulses. The patient was clinically stable, with spontaneous breathing on room air and normal vital signs, except for a significant blood pressure gradient of 30 mmHg between the upper and lower extremities, indicative of obstructive flow in the aortic arch. Transthoracic two-dimensional echocardiography confirmed the diagnosis of aortic coarctation, demonstrating a systolic pressure gradient of 30 mmHg and a closed arterial duct, consistent with a congenital narrowing of the aortic lumen proximal to the origin of the descending aorta. Additionally, the imaging revealed a total retrograde perfusion of the left circumflex coronary artery (LCX), with no visible ostial blood flow from the left aortic sinus, suggesting an abnormal coronary arterial supply pattern. The left ventricular function was preserved, with a normal ejection fraction, absent regional wall motion abnormalities, and no evidence of mitral valve regurgitation. Given the atypical coronary anatomy, coronary angiography was performed, which revealed the absence of a left main coronary artery and instead demonstrated a single right coronary artery (RCA) arising normally from the aortic wall. The LCX was perfused retrogradely via collateral vessels derived from the normal right posterior descending artery (RPD), coursing along the lateral wall of the ascending aorta without entering the aortic lumen, instead draining into the right pulmonary artery (RPA). Small, rudimentary branches of a left anterior descending (LAD) artery were observed arising from the LCX, indicating partial embryological persistence of coronary arterial development. Pulmonary artery pressure remained within normal limits, confirming no significant pulmonary hypertension. At 23 days of age, the patient underwent surgical correction involving resection of the aortic coarctation, end-to-end anastomosis of the aortic segments, and reimplantation of the left coronary artery (LCA) into the posterior aortic sinus using a button technique that avoided stretching or torsion of the coronary artery, thereby preserving coronary artery integrity and preventing ischemic injury. The defect in the right pulmonary artery was closed with a xenopericardial patch. Post-operatively, on day 4, the patient developed recurrent episodes of supraventricular tachycardia (SVT), which were effectively managed"}
+{"row_index": 204, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 36-year-old woman who was overweight since she was 6 years old had type 1 diabetes. She weighed 106.7 kg and was very heavy (BMI 42.2), needing 75 units of insulin every day. Her blood sugar was not well controlled, and her HbA1c was 9.0%. She had surgery called laparoscopic sleeve gastrectomy to lose weight. After the surgery, her weight went down to 81.0 kg (BMI 32.2), which is healthier. She now needs only 24 units of insulin a day, and her blood sugar improved to 7.7%. This means she’s doing better and her body fat, especially the dangerous belly fat, has gone down a lot. The surgery helped her lose weight and control her diabetes better.\"\n}"}
+{"row_index": 205, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 36-year-old woman with severe obesity and type 1 diabetes mellitus (T1DM), diagnosed at age 6, was admitted for bariatric surgery. At her first visit, she weighed 106.7 kg and had a body mass index (BMI) of 42.2, which is very high. Her HbA1c was 9.0%, showing poor blood sugar control, and she needed 75 units of insulin daily. She had surgery called laparoscopic sleeve gastrectomy, which removes part of her stomach to help with weight loss. Before surgery, her blood sugar was carefully managed, and her weight was reduced to 101.1 kg. One year after surgery, her weight dropped to 81.0 kg, and her BMI improved to 32.2. Her insulin needs decreased to 24 units per day, and her HbA1c improved to 7.7%, meaning her blood sugar control got better. Her body fat, especially around the abdomen, also decreased significantly. There were no serious complications after the surgery.\"\n}"}
+{"row_index": 206, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 36-year-old Japanese female with morbid obesity and type 1 diabetes mellitus (T1DM), diagnosed at age 6, was referred for bariatric surgery due to progressive weight gain and poor glycemic control. T1DM was managed with multiple daily insulin injections, with insulin requirements escalating in parallel with body weight. By age 20, her body weight was 70 kg, increasing to >100 kg by age 34. At initial assessment, she required 45 units of insulin aspart and 30 units of insulin glargine daily, reflecting a high insulin demand consistent with insulin-dependent diabetes. Preoperative laboratory evaluation revealed an HbA1c of 9.0%, indicating chronic hyperglycemia, and undetectable C-peptide levels (<0.01 ng/mL), confirming complete absence of endogenous insulin secretion, a hallmark of advanced T1DM. Her blood lipid profile remained within normal limits, suggesting no significant dyslipidemia. Abdominal computed tomography (CT) demonstrated a visceral fat area of 162.6 cm² and a subcutaneous fat area of 527.9 cm² at the umbilical level, reflecting substantial adiposity, particularly in the visceral compartment, which is strongly associated with insulin resistance and metabolic complications. Upper gastrointestinal endoscopy showed no structural abnormalities in the esophagus, stomach, or duodenum, ruling out gastrointestinal pathology as a contraindication to surgery. To mitigate the risk of postoperative hypoglycemia due to rapid insulin sensitivity improvement, she was admitted 2 weeks prior to surgery for intensive glycemic control, dietary restriction, and structured exercise therapy. This preoperative intervention achieved a reduction in HbA1c to 7.8% and a transient weight reduction to 101.1 kg. The procedure performed was a laparoscopic sleeve gastrectomy (LSG) using a five-port approach. The greater curvature of the stomach was resected from 4 cm proximal to the pylorus to the His angle, using a linear stapler, with the staple line reinforced by continuous seromuscular sutures with non-absorbable material to ensure anatomical integrity and reduce leakage risk. Postoperatively, insulin therapy was initiated with a sliding-scale regimen: a unit of insulin aspart was mixed with 5 g of glucose in the infusion solution,"}
+{"row_index": 207, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"The patient had long-lasting pain in her knees and hips, plus bone weakness. Tests showed her phosphate levels were very low, and her bones were thin and damaged. A tumor was found in the left lower leg using a special scan, and the doctor removed it with surgery. The tumor was checked under a microscope and found to be a type called phosphaturia stromal tumor (PMT), which shows a certain protein (Vim) that helps confirm the type. After the surgery, her phosphate levels went back to normal fast, and her pain got much better. Now she walks easier and feels much better.\"\n}"}
+{"row_index": 208, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"The patient had long-standing joint pain, especially in her knees, along with groin and back pain that worsened over time. She also had low bone density and very low phosphate levels in her blood, which are signs of a bone disorder. Tests showed increased activity of a protein called somatostatin receptors in her left tibia, leading doctors to suspect a rare condition called TIO (tumor-induced osteomalacia). A PET/CT scan successfully found a tumor in the left tibia, and the tumor was surgically removed. Pathology confirmed it was a phosphaturia stromal tumor (PMT), a type of tumor that causes the body to lose too much phosphate. The tumor showed positive staining for a protein called Vim, which helps confirm the diagnosis. After surgery, her phosphate levels quickly returned to normal, and her pain and symptoms greatly improved.\"\n}"}
+{"row_index": 209, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 22-year-old female presented with a 10-year history of bilateral knee pain, progressively worsening over the past two months, accompanied by groin pain and right 12th rib pain following a fall. The pain was characterized by recurrent episodes without clear precipitating factors, including knee valgus and dislocation. Prior to the current exacerbation, she had developed low back pain two years earlier, which was transient and relieved with rest, but later progressed to severe pain and loss of mobility, requiring assistance with ambulation and stair climbing. Imaging revealed bone marrow edema in the right intertrochanteric region, femoral neck, lower left femur, and tibial intercondylar crest. Two weeks prior to admission, she experienced widespread joint pain, difficulty walking, and increased pain with weight bearing. Laboratory evaluation demonstrated hypophosphatemia (0.47 mmol/L), elevated serum alkaline phosphatase (257 IU/L), low 25-hydroxyvitamin D (41.1 nmol/L), and reduced bone mineral density as confirmed by dual-energy X-ray absorptiometry (DXA). Physical examination revealed scoliosis, unequal lower limb lengths (right 68 cm, left 67 cm; relative length ratio 77.5:76), reduced thigh and calf circumferences, bilateral knee pain, limited range of motion, left knee evagination, and an 'X'-shaped leg deformity. No joint swelling, tenderness, dislocation, or muscle atrophy was observed. Lower limb length discrepancy and skeletal deformities were consistent with chronic osteomalacia. Radiographic findings included multiple old rib fractures, bone islands in the left ilium and left sacrum, and an elliptical high-signal lesion (1.6 × 0.7 cm) at the posterior cortical edge of the left middle tibia, along with a small vertical nodular abnormal signal (1.5 cm) outside the bone. Quantitative T2-weighted MRI measurements showed T2 signal abnormalities at L1–L2, L1–L3, L1–L4, L2–L3, L2–L4, L3–L4, neck, Wards triangle, and great trochanter, with values ranging from −2.3 to −2.9, indicating generalized bone marrow edema and osteomalacic changes. Pathological evaluation"}
+{"row_index": 210, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 55-year-old man had infections in his surgery scars for over a year. The scars were red, swollen, painful, and kept draining pus. Tests for common infections didn’t find anything wrong. A special test called mNGS found a tiny germ called M. senegalense in the scar tissue. This germ was confirmed with two other simple tests. The man took four antibiotics together for 60 days: clarithromycin, moxifloxacin, rifampicin, and oxycycline. After that, the scars healed and didn’t come back.\"\n}"}
+{"row_index": 211, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 55-year-old man had repeated infections at surgical incision sites for over a year after having gallbladder surgery. The wounds were red, swollen, painful, and kept draining pus, but standard blood tests and bacterial cultures came back normal. Imaging showed a sinus tract under his chest bone, and surgery was done to remove the infected area and drain the abscess. He was treated with antibiotics, but the infection kept coming back. Tests for tuberculosis were negative, so doctors used a more advanced test called metagenomic next-generation sequencing (mNGS) to find the cause. This test found DNA from a rare bacterium called M. senegalense in the wound tissue. The result was confirmed using two other lab methods: PCR and capillary electrophoresis. The patient was then given a four-drug antibiotic therapy—clarithromycin, moxifloxacin, rifampicin, and oxycycline—for 60 days. After this treatment, his wounds healed completely and no new infections occurred.\"\n}"}
+{"row_index": 212, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 55-year-old male patient presented to our hospital in August 2021 with recurrent surgical site infections at multiple incision sites, persisting for over 12 months following a laparoscopic cholecystectomy performed for gallstone disease complicated by cholangitis. Clinical examination revealed erythema, swelling, dehiscence, localized tenderness, hyperthermic skin, and minimal purulent exudation at the xiphoid process incisions. The patient experienced an average recurrence interval of approximately 25 days between infection episodes, with no abnormalities detected in routine complete blood count (CBC) parameters. B-mode ultrasonography suggested the presence of a subcutaneous sinus tract originating from the xiphoid region. In September 2021, the patient underwent laparoscopic reoperation and abdominal exploration, during which the sinus tract was excised and an abscess was drained. He was subsequently treated with piperacillin-tazobactam, a broad-spectrum beta-lactam/beta-lactamase inhibitor combination, but this regimen failed to achieve clinical resolution, with persistent wound dehiscence, surrounding skin erythema, swelling, pain, and purulent drainage continuing despite therapy.\\n\\nDespite normal body temperature and CBC results, conventional microbiological testing—including aerobic and anaerobic bacterial cultures, acid-fast bacilli (AFB) staining, and serological evaluation for tuberculous antigen (TB-Ab) antibodies—remained negative. Chest computed tomography (CT) and other tuberculosis-specific investigations were consistent with the absence of active tuberculosis, thereby excluding a tuberculous etiology. Given the persistent and refractory nature of the infections, and the absence of identifiable pathogens via standard diagnostic methods, metagenomic next-generation sequencing (mNGS) was employed to comprehensively detect microbial nucleic acids from tissue samples obtained from the infected incision sites. The mNGS analysis, conducted using the KingMed Diagnostics platform (Changsha, China), identified 53 out of 113 sequenced reads that mapped to *Mycobacterium senegalense*, representing a 0.09% coverage of the total sequencing depth and accounting for 58.76% of all detected microbial sequences, indicating a dominant pathogenic role.\\n\\nTo validate the mNGS findings, targeted polymerase chain reaction (PCR) assays were performed using two primer sets: ("}
+{"row_index": 213, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 59-year-old woman who had cancer before, came back with pain and numbness in her left leg, numbness in her vulva, and trouble holding her urine. She had a tumor inside her spine, near the lower back, that was spreading. Doctors removed part of her spine to relieve her pain, but the cancer kept growing. After surgery, her leg symptoms got better, but soon she started having new problems — weakness on her right face, numbness, and blurry vision. Doctors found the cancer had spread to her brain and spinal lining, and she passed away two months later.\"\n}"}
+{"row_index": 214, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 59-year-old woman with a history of recurring cancer of the uterus (endometrial carcinosarcoma) and previous treatments like chemotherapy and radiation now developed new pain, numbness in her left leg, and trouble with bladder control. She had a tumor found inside her spinal cord, just behind the L1 vertebra, that was growing and causing pressure on nerves. After surgery to remove part of the tumor and relieve pressure on her nerves, her leg symptoms improved. However, the cancer spread to the membranes surrounding her brain and spinal cord (leptomeningeal spread), leading to worsening symptoms including vision problems and facial numbness. Despite the surgery, she passed away within two months due to the advanced spread of her cancer.\"\n}"}
+{"row_index": 215, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 59-year-old morbidly obese African-American female with a history of Stage IIIc recurrent endometrial carcinosarcoma and para-aortic and pelvic lymph node involvement presented with a 1-month history of left vulvar numbness, progressive left lower extremity pain and numbness, and episodic urinary incontinence. Imaging via thoracic-lumbar magnetic resonance (MR) demonstrated a 1.4 × 1.8 cm enhancing intradural extramedullary mass located inferior to the conus at the L1 and L4-L5 levels, accompanied by abnormal enhancement of the left-sided intradural nerve roots. Additional findings included bilateral perihilar lung metastases. The patient underwent a T12-L2 focal decompressive laminectomy with gross total resection of the L1 intradural/extramedullary lesion, performed primarily to achieve neurological symptom relief. Intraoperatively, diffuse carcinomatosis of the cauda equina was identified, with a large tumor mass located anteroinferior to the conus. The tumor exhibited a vascular architecture and involved multiple swollen, engorged nerve roots. Surgical dissection was discontinued when intraoperative electromyographic (EMG) monitoring indicated significant neural dysfunction, particularly in the gastrocnemius muscle, suggesting tumor infiltration and irreversible nerve root compromise. Permanent pathological examination confirmed a mesenchymal malignant Mullerian mixed tumor (carcinosarcoma) with no epithelial component, consistent with the original primary tumor's histological profile. Postoperatively, the patient showed improvement in left lower extremity pain and sensory deficits. However, two weeks later, she presented with worsening lower extremity symptoms, new-onset right-sided facial weakness, numbness, and blurred vision. Neuroimaging revealed leptomeningeal dissemination of disease, including hydrocephalus and multiple new intracranial metastases. Despite initial neurological stabilization, the patient died from progressive metastatic disease within two months of surgery, consistent with the aggressive biological behavior of carcinosarcoma and its propensity for early leptomeningeal spread, particularly in the context of recurrent, treatment-refractory disease and extensive pre-existing tumor burden.\"\n}"}
+{"row_index": 216, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A four-year-old girl came in with a fever and pain in her left hip. She was walking with a limp, and moving her hip hurt, especially when turning it out. Her blood test showed she was anemic (low red blood cells) and had signs of inflammation. The doctors first thought it might be a common hip infection, but the X-ray and ultrasound didn’t show anything wrong. A CT scan of her belly found a tumor in her adrenal gland and swollen lymph nodes. Even though her bones didn’t seem damaged, the tumor was spreading to her bones. Tests showed this was a type of cancer called neuroblastoma. The cancer was spreading through her blood and bone marrow. She started chemotherapy, which helped a little, but the tumor didn’t go away. Because of side effects on her kidneys, they switched to a different drug combo. After 13 months, the tumor still wasn’t shrinking, so surgery wasn’t safe. Instead, she was given a treatment to replace her damaged bone marrow.\"\n}"}
+{"row_index": 217, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A four-year-old girl came to the emergency room with a fever and a painful limp on her left hip. The pain was especially bad when moving her hip, especially turning it outward, but her range of motion was not severely limited. Blood tests showed anemia (low red blood cells) and signs of inflammation, which raised concerns that something was wrong with her hip. An X-ray of the pelvis didn't show any damage, and an ultrasound of the hip found fluid and swelling, suggesting possible infection or arthritis. A sample was taken and tested, but no bacteria were found. Because the symptoms were unusual, a CT scan of her abdomen and pelvis was done, which revealed a tumor in her left adrenal gland and swollen lymph nodes near major blood vessels. The scan also showed bone changes that suggested the tumor had spread. Further tests, including MRI and bone marrow biopsy, confirmed the presence of neuroblastoma — a type of cancer that starts in nerve cells. The tumor was found in the bone marrow and lymph nodes, and the biopsy showed it was spreading. The child started chemotherapy with a standard protocol, and after six months, the tumor hadn't gone away, though the spread had slightly decreased. Due to side effects from the initial treatment, a different chemotherapy plan (using irinotecan and temozolomide) was started. After 13 months, the tumor still hadn't shrunk enough to allow surgery, so the child was offered stem cell treatment instead. The initial signs of pain and anemia were key clues that something serious was going on, leading to the discovery of the tumor.\"\n}"}
+{"row_index": 218, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A four-year-old girl presented to the emergency department with fever and a painful left hip, accompanied by a limp. There was no prior medical history, and no additional systemic or local symptoms were noted except for cervical lymphadenopathy. Physical examination revealed impaired left hip mobility with pain primarily on external rotation, although joint range of motion was not significantly restricted. Laboratory findings included anemia (hemoglobin 8.7 g/dL), normal white blood cell count, elevated erythrocyte sedimentation rate (ESBR 123 mm), and a reactive C-reactive protein level of 149.7 mg/L, suggesting acute inflammation. Initial pelvic X-ray was unremarkable. Ultrasound of the left hip demonstrated synovial inflammation and a small joint effusion. A guided joint aspiration was performed, and the effusion showed macroscopic features consistent with reactive arthritis; however, bacteriological cultures remained negative. Given the atypical presentation of hip pain and persistent inflammatory markers, a contrast-enhanced CT scan of the abdomen and pelvis was obtained, which revealed a left adrenal mass and retroperitoneal adenopathies involving the celiac trunk and superior mesenteric artery. Notably, the CT scan showed no evidence of bone or joint destruction, and thoracic imaging and peripheral blood smear evaluations were unremarkable. MRI was performed, and direct myelography demonstrated diffuse infiltration consistent with neuroblastoma. Histopathological analysis of cervical lymph node biopsy and bone marrow biopsy confirmed the diagnosis of neuroblastoma, not otherwise specified (NOS). Immunohistochemical staining revealed strong expression of synaptophysin and CD56 (NCAM), with absence of myogenin, supporting a neuronal origin and ruling out myogenic differentiation. Skeletal scintigraphy showed multiple osteoblastic foci, indicative of metastatic disease, and 123I-metaiodobenzylguanidine (MIBG) scintigraphy demonstrated low uptake in the adrenal mass (suggesting low noradrenergic transporter expression) and diffuse bone metastases with high noradrenergic transporter expression. Bone marrow biopsy confirmed extensive metastatic involvement. The patient initiated chemotherapy with eight cycles of the rapid COJEC protocol; after six months, the primary adrenal tumor remained unresectable, and metastatic burden showed partial reduction. Due to chemotherapy-induced renal toxicity, treatment was modified to irinotecan combined with temozolomide (TEMIRI)."}
+{"row_index": 219, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A baby boy, seven months old, started having trouble eating, vomiting, and not moving his head or body right. Doctors thought it might be a brain problem called subacute rhombencephalitis, and gave him medicine that helped. After a few days, he got better and could eat again. Later, after a vaccine, he started getting worse — he became irritable, didn’t smile, and his muscles weakened. A new brain scan showed a serious brain condition called leukoencephalopathy with evanescent white matter, which is caused by a gene problem. The doctors found the gene fault in his body, and it was passed down from his parents. Even though his parents and brothers are healthy, they carry the gene. The baby had another fit at 15 months and couldn’t eat or respond to people. He needed help at home, and doctors gave him care for comfort. He passed away at 15 months because the disease kept getting worse. He died peacefully at home, with his family by his side.\"\n}"}
+{"row_index": 220, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A seven-month-old baby boy was admitted to the hospital with severe vomiting, refusal to eat, and signs of neurological problems like weak muscle tone, poor head control, and lack of social interaction. His initial tests showed no serious issues, but a brain MRI revealed signs of subacute rhombencephalitis, a type of brain inflammation. He was treated with steroids and intravenous immune therapy, and his symptoms improved over time. By 10 months, he started showing a return of symptoms after receiving a vaccine — this is called a neurological regression. He became more irritable, lost his social smile, and his muscle weakness worsened. A new brain scan showed damage to the white matter of the brain, specifically in areas involved in movement and coordination, which led to a diagnosis of leukoencephalopathy with evanescent white matter. This is a rare genetic disorder that affects the brain's white matter and is inherited in an autosomal recessive pattern. The baby’s parents and two older brothers were found to be carriers but healthy. At 15 months, he had a seizure and needed further care. His condition continued to worsen, and he eventually stopped responding to stimuli and could no longer eat orally, requiring a feeding tube. He was cared for at home with palliative support and passed away at 15 months due to the progression of his disease.\"\n}"}
+{"row_index": 221, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 7-month-old male infant presented with a severe, persistent vomiting syndrome, anorexia, and progressive neurological deterioration characterized by axial hypotonia, poor head control, impaired suck-swallow coordination, absence of social smiling, and abnormal oral-motor movements. Osteotendinous reflexes were preserved, and there was no perinatal, personal, or familial history of neurologic disorders or consanguinity. Initial evaluation included a comprehensive panel of laboratory, metabolic, autoimmune, neuroimaging, electroencephalographic, and auditory evoked potential studies, all of which yielded normal results except for the isolation of respiratory syncytial virus (RSV) in a nasopharyngeal aspirate and a brain magnetic resonance imaging (MRI) scan demonstrating bilateral, symmetric diffusion restriction in the anterior bulbo-protuberant junction, consistent with subacute rhombencephalitis. The patient was treated with two doses of intravenous immunoglobulin (2 g/kg total), leading to progressive clinical improvement and oral tolerance, followed by outpatient follow-up in a neuropediatric setting. During this period, the child exhibited modest clinical stabilization, including improved visual tracking, enhanced social contact, and brief periods of stable sitting without support, with intermittent masticatory movements observed only in supine position; osteotendinous reflexes remained intact.\\n\\nAt 10 months of age, the infant was readmitted following a post-vaccination episode of food rejection, which triggered a significant neurological regression. This included increased irritability, a flat affect, loss of social smiling, progressive worsening of axial hypotonia, proximal muscle weakness, and a striking transformation of the osteotendinous reflexes into hyperactive, equine-type reflexes. Neuroimaging was repeated, revealing generalized bilateral and symmetric abnormalities in the signal intensity of deep and subcortical white matter, involving the U-fibers and globus pallidus, consistent with a neurometabolic disorder suggestive of leukodystrophy. The MRI also showed a mild increase in choline concentration on spectroscopic analysis, with normal N-acetylmethionine (NAA) levels, indicating early disruption of myelin synthesis or integrity without overt neuronal loss. Given these findings, a clinical exome sequencing study targeting early-onset leukodystrophies was performed, which identified a pathogenic, homozygous mutation in the EIF2B5 gene. This mutation is associated with"}
+{"row_index": 222, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A man in his 60s went to the hospital feeling weak, having muscle aches, a fever, and belly pain. Doctors did a scan and found a blood clot in a vein called the SMV, which only affected that vein and didn’t spread to other important veins. He also had a fever and body aches that didn’t match the clot, so they tested for flu. The test came back positive for flu B. He didn’t need surgery or any other treatment — just medicine to thin his blood. After a few days, the scan showed the clot was getting better. He was sent home with pills to keep his blood thin and follow up with the doctor.\"\n}"}
+{"row_index": 223, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 64-year-old man went to the hospital with weakness, muscle aches, fever, and abdominal pain that had started a week before. A CT scan showed a blood clot in the superior mesenteric vein (SMV), which supplies blood to the intestines. The clot was only in the SMV and did not spread to the portal or splenic veins, and the patient was stable overall. However, the fever and muscle pain didn't fit what was expected for SMV thrombosis, so the doctor tested for influenza. The test came back positive for influenza B. The patient was started on anticoagulation therapy (medication to prevent blood clots) without needing surgery. A follow-up CT scan showed the clot was improving, and the patient was discharged with ongoing oral anticoagulant treatment.\"\n}"}
+{"row_index": 224, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 64-year-old male presented to a local medical center on March 4th with a one-week history of general weakness, myalgia, and abdominal pain. On presentation, his temperature was 37.9 °C, and he reported feeling hot, with associated headache; no cough, sputum, diarrhea, or vomiting were noted. Physical examination revealed mild tenderness in the right upper quadrant and hypoactive bowel sounds, with no rebound tenderness. Laboratory findings showed a white blood cell count of 16,160 /mL, erythrocyte sedimentation rate (ESR) of 86 mm/hr, and high-sensitivity C-reactive protein (HS-CRP) level of 16 mg/dL, indicating systemic inflammation. Abdominal computed tomography (CT) demonstrated a large, segmental thrombus extending from the superior mesenteric vein (SMV) gastrocolic trunk to its distal portion, resulting in complete obstruction of a segment of the SMV. The imaging also showed surrounding fat stranding and bowel wall edema consistent with ascending colon involvement, suggesting ischemic or inflammatory bowel changes secondary to venous obstruction. The patient was subsequently transferred to our hospital for further evaluation. Given the atypical presentation—particularly the presence of systemic fever and widespread myalgia not fully explained by the SMV thrombosis alone—a nasopharyngeal swab was collected for testing. An Influenza A/B rapid antigen test using the BD Veritor™ Plus System for Rapid Detection of Flu A+B was performed, with reported sensitivity of 81.3% (95% CI: 71.1–88.5%) and specificity of 98.2% (95% CI: 95.7–99.3%). The test returned a positive result for influenza B, which likely contributed to the patient’s fever and myalgia. Concurrently, a reverse transcription polymerase chain reaction (RT-PCR) test for SARS-CoV-2 (COVID-19) was performed in light of the ongoing pandemic context, though no positive result was reported. The thrombus was localized exclusively to the SMV, with no extension into the portal or splenic veins, confirming isolated venous occlusion. The patient was clinically stable and managed with anticoagulation therapy without surgical intervention. Follow-up CT imaging demonstrated resolution of the throm"}
+{"row_index": 225, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 9-month-old girl had a bump in her eye socket on the right side, noticed by her mom three months before. Doctors first thought it was just a normal thing, but scans showed bone changes in the eye area, like a tumor was eating away at the bones. A scan of her chest and belly found a big tumor in her adrenal gland, along with swollen lymph nodes and spine changes. This matched a serious cancer called stage-4 neuroblastoma. She started chemo and surgery, and after 10 months, the cancer was gone and she hasn’t had any return.\"\n}"}
+{"row_index": 226, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 9-month-old girl was diagnosed with isolated right-sided enophthalmos, which means her right eye appeared to be pulled back. Her mother noticed this three months before she visited the doctor, and several specialists initially thought it was just a normal variation. However, imaging tests showed bone changes in the orbit and surrounding areas, including osteolysis (bone loss) and thickening of the bone lining, which raised concern for a tumor. A CT scan of her chest and abdomen found a large mass in the left adrenal gland, along with swollen lymph nodes and bone changes, consistent with stage-4 neuroblastoma. This type of cancer is rare in young children and spreads beyond the original site. The child was referred to oncology, started on chemotherapy, and had surgery to remove remaining tissue. She achieved complete remission and has not had a recurrence at a 10-month follow-up.\"\n}"}
+{"row_index": 227, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 9-month-old Caucasian female with no significant birth or past medical history presented with isolated right-sided enophthalmos, defined as a posterior displacement of the globe relative to the orbital cavity. The mother first noted the abnormality three months prior to presentation, describing a backward shift of the right eye. Initial evaluations by multiple specialists attributed the finding to a constitutional variant, with no evidence of systemic illness, neurological deficits, abdominal or skeletal abnormalities, or deterioration in general health. Ophthalmological examination confirmed mild right enophthalmos without associated facial flattening or structural deformity. All standard eye function tests—including pupillary size and reactivity to light, direct and consensual accommodation, fixation, following, binocular vision, and eye-hand coordination—were within normal limits. Slit lamp and fundus examinations revealed no signs of intraocular pathology. Prior to definitive imaging, routine laboratory assessments, including serum creatinine, were unremarkable, indicating preserved renal function and no evidence of systemic disease. Orbital computed tomography (CT) demonstrated irregular osteolysis with active periosteal reaction involving the right orbital walls, malar bones, and zygomatic arches, predominantly unilateral and asymmetric, which raised a high index of suspicion for an underlying orbital mass, likely neoplastic in origin. A subsequent thoracic-abdominal CT scan identified a retroperitoneal heterogeneous mass measuring 83 mm × 43 mm × 42 mm, located on the left adrenal gland, which encased adjacent vascular structures and was associated with enlarged left supraclavicular lymph nodes and vertebral body condensations. These imaging findings are characteristic of stage-4 neuroblastoma, a malignant peripheral nerve tumor of early childhood origin, typically arising from sympathoadrenal precursors. The diagnosis was confirmed through histopathological and molecular characterization. The patient was promptly referred to pediatric oncology for multimodal management, including induction chemotherapy and surgical evacuation of residual tumor burden. Treatment resulted in complete clinical remission, with no evidence of disease recurrence at a 10-month follow-up. The clinical course underscores the importance of imaging evaluation in the setting of isolated enophthalmos, particularly when orbital bony changes with periosteal reaction are present, as these findings may signal an occult neuroblastoma, even in the absence of other systemic symptoms or signs.\"\n}"}
+{"row_index": 228, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 21-year-old girl started feeling short of breath and chest pain six months ago. She was diagnosed with heart failure, but had no history of heart problems. Doctors found a strange connection between a blood vessel in her arm (right subclavian artery) and a vein (superior vena cava) that was causing her heart to work harder. This connection, called a fistula, had a narrow part at the start, which made blood flow too fast. She had the fistula closed using a small device placed through a catheter in her vein. After the procedure, her symptoms got much better by the 3-month check-up.\"\n}"}
+{"row_index": 229, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 21-year-old woman was diagnosed with new-onset heart failure after six months of worsening shortness of breath and chest pain. She had no prior heart problems, injuries, or surgeries. Examination found a continuous heart murmur heard in the right chest area, and imaging showed an enlarged heart and signs of right heart strain. Tests revealed a rare birth defect called a congenital arteriovenous fistula, where a blood vessel (the right subclavian artery) was abnormally connected to the superior vena cava, causing blood to flow directly from artery to vein without going through the heart. This connection was narrowed at its start, which increased pressure and worsened heart function. The fistula was successfully closed using a minimally invasive procedure called transcatheter occlusion, where a small device was guided through a blood vessel to seal the abnormal connection. After the procedure, the patient’s symptoms improved significantly by the three-month follow-up visit.\"\n}"}
+{"row_index": 230, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 21-year-old female presented with a six-month history of progressive dyspnoea and chest pain, ultimately diagnosed with new-onset heart failure in the absence of any prior cardiovascular disease, trauma, or surgical history. Physical examination revealed a grade 3/6 continuous machinery murmur, most prominent between the right second and third intercostal spaces and radiating to the right infraclavicular fossa. Resting oxygen saturation was normal (SpO2 95%) with non-cyanotic skin colour, indicating adequate tissue oxygenation. Chest radiography demonstrated cardiomegaly, consistent with right-sided cardiac volume overload. Electrocardiography revealed sinus rhythm at 95 bpm, complete right bundle branch block, and right ventricular hypertrophy, reflecting chronic pressure overload on the right side of the heart. Pulmonary function tests were within normal limits, ruling out obstructive or restrictive lung disease as a contributing factor.\\n\\nTransthoracic echocardiography identified a dilated right subclavian artery (RSA) with an 8-mm arteriovenous fistula connecting to the superior vena cava (SVC), accompanied by significant stenosis at the proximal origin of the fistula. The right ventricle and right atrium were markedly dilated, consistent with chronic volume and pressure overload. Mild tricuspid regurgitation was observed. Continuous wave Doppler analysis demonstrated a sustained flow signal of 2.3 m/s from the RSA to the SVC with a pressure gradient of 22 mmHg, indicating a low-resistance shunt. At the site of stenosis, the peak flow velocity reached 3.9 m/s with a pressure gradient of 59 mmHg, reflecting a high-velocity, high-resistance flow pattern consistent with a critical stenotic lesion. Computed tomography angiography (CTA) provided detailed anatomical characterization of the arteriovenous fistula, confirming the direct connection between the RSA and SVC and the proximal stenosis, enabling precise procedural planning.\\n\\nThe patient underwent transcatheter occlusion of the arteriovenous fistula under local anaesthesia. A 10/12 mm Amplatzer ductal occluder was delivered via a 5-F H1 catheter and deployed from the SVC side using angiographic guidance. An 8F sheath was utilized to facilitate catheter advancement and occluder"}
+{"row_index": 231, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 68-year-old woman came to the hospital because her legs were weak for more than 3 days. She also had neck pain, numbness in her hands and feet, trouble going to the bathroom, and couldn’t feel cold or heat well. She didn’t have fever, cough, or other common illness symptoms. She had high blood pressure but no diabetes or allergies. Tests showed her brain and blood were fine, but her spinal cord was inflamed — especially in the neck area. This is a rare case in China, and it’s different from usual cases of this illness. She was treated with strong medicine and immune therapy and got better. This kind of problem with anti-sulfatide antibodies usually affects nerves, but in her case, it hit the spinal cord, which is unusual.\"\n}"}
+{"row_index": 232, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 68-year-old woman was admitted to the hospital with weakness in her limbs that had lasted more than 3 days. She also had neck pain, numbness in her hands and feet, trouble controlling her bladder and bowels, and a reduced ability to feel temperature. She was diagnosed with a rare form of Guillain-Barré syndrome (GBS) that is positive for anti-sulfatide antibodies. This case was treated with methylprednisolone and intravenous immunoglobulin therapy. Unlike typical GBS cases, this patient showed signs of spinal cord involvement, which is not commonly seen. No other patients with this specific combination of symptoms have been reported in China before. The patient’s symptoms started gradually and were not linked to a recent infection or illness, and she had no history of diabetes or allergies.\"\n}"}
+{"row_index": 233, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 68-year-old female was admitted to the hospital with progressive limb weakness lasting over three days, accompanied by posterior neck pain, distal sensory disturbances, and a characteristic electric shock-like paresthesia upon tactile stimulation. Symptoms evolved to include impaired manual dexterity, bilateral lower extremity weakness, inability to ambulate, urinary and fecal retention, and heightened posterior neck pain. Notably, she reported cold-related pain in the upper extremities, which is atypical for common Guillain-Barré syndrome (GBS) presentations. Neurological examination revealed preserved consciousness, normal pupillary response, intact eye movements, and symmetrical frontal lines. Upper limb muscle strength was graded 4, lower limb strength was 3, with hypotonia and bilateral diminished tendon reflexes. The Babinski sign was positive bilaterally, indicating upper motor neuron involvement. Sensory examination demonstrated reduced perception of pain and temperature in the distal extremities, while vibration and joint position sensations remained intact. The two-handed finger-nose test was stable, suggesting preserved cerebellar function, whereas the heel-knee-shin test was unstable, indicating impaired proprioception. Meningeal signs were absent, and there was no evidence of autonomic dysfunction such as dysautonomia or respiratory compromise. Vital signs were stable: temperature 36.8 °C, pulse 76 beats/min, respiratory rate 20 breaths/min, blood pressure 145/78 mmHg. Physical examination revealed no signs of infection, cardiac abnormalities, or abdominal pathology; abdominal examination showed softness, no varices, no rebound or peritoneal tenderness, and only slightly reduced bowel sounds (2–3/min), without evidence of ascites. Laboratory studies, including complete blood count, liver and renal function, coagulation profile, and tumor markers, were within normal limits. Cranial CT and cranial MRI showed no evidence of hemorrhage, ischemia, or structural lesions. Lumbar puncture revealed elevated cerebrospinal fluid (CSF) pressure (116 mmH₂O) and cytoalbuminologic dissociation—characteristic of inflammatory demyelinating processes—without the presence of oligoclonal bands, aquaporin-4 antibodies, or anti-MOG antibodies, ruling out other central nervous system demyelinating disorders. Peripheral neuropathy immunoblotting demonstrated a positive IgG response to sulfatide"}
+{"row_index": 234, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 32-year-old man had trouble breathing and suddenly lost consciousness several times in one week. Each time, he would feel dizzy and lose awareness for 3 to 5 minutes, then wake up fine. The episodes happened when he was active or breathed cold air. He went to the hospital after the fourth episode. Tests showed blood clots in his heart and lungs. One clot was blocking a small hole in his heart (PFO), and clots were also in his lung blood vessels. Doctors placed a filter in his biggest vein to catch clots and used a medicine (alteplase) to break down the clots. Two days later, no clots were found in his heart. He was sent home on a blood thinner called warfarin and had no problems. This treatment helped stop the clots from coming back.\"\n}"}
+{"row_index": 235, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 32-year-old man had repeated episodes of sudden, brief loss of consciousness (syncope) and shortness of breath over a week. The episodes were triggered by physical activity or breathing cold air, and he had no warning signs before them. He went to the hospital after another episode on February 22, 2019. His initial tests showed high levels of a blood clot marker (D-dimer) and a protein linked to heart strain (NT-proBNP), while his blood pressure and other vital signs were normal. An electrocardiogram showed a fast heart rate, and ultrasound found a blood clot in his right leg vein. Echocardiography revealed a blood clot blocking a small hole between the upper chambers of the heart (patent foramen ovale), along with a large clot in the right atrium and a clot in the left atrium. CT scans confirmed blood clots in both pulmonary arteries, indicating pulmonary embolism. He received treatment with a filter placed in his inferior vena cava to prevent clots from traveling to the lungs and was given alteplase to dissolve the clots. Two days after treatment, follow-up echocardiography showed no clots in the heart chambers. He was discharged home two weeks later on warfarin, a blood thinner, without complications.\"\n}"}
+{"row_index": 236, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 32-year-old male presented to the emergency department with recurrent syncope and intermittent dyspnea over a 7-day period. The initial episode of chest distress occurred on February 15, 2019, followed by four episodes of transient, self-limited syncope each lasting 3–5 minutes with complete recovery between episodes. Triggers included physical exertion and inhalation of cold air; no prodromal symptoms or associated neurological features were reported. The patient sought medical evaluation on February 22, 2019, following a new episode of syncope. There was no personal or family history of thrombotic disorders, and the patient's sedentary lifestyle, due to employment as a news editor, contributed to reduced physical activity.\\n\\nVital signs at first presentation were stable: pulse rate 96 beats/min, respiratory rate 20 breaths/min, blood pressure 15.5/10.1 kPa, body mass index 23.1 kg/m². Physical examination revealed symmetric and light-responsive pupils, a prominent P2 component in the cardiac auscultation, symmetrical breath sounds without rales or wheezing, and warm extremities without edema. Neurological examination was unremarkable.\\n\\nInitial laboratory findings included markedly elevated serum D-dimer at 4150 ng/mL (normal <500 ng/mL), indicating active thrombin generation and fibrin formation. Arterial blood gas analysis under ambient air showed a PaO₂ of 79 mmHg, suggesting mild hypoxemia. N-terminal pro-B-type natriuretic peptide (NT-proBNP) was elevated at 4460 pg/mL (normal <450 pg/mL), reflecting right ventricular strain consistent with pulmonary hypertension. Cardiac enzyme levels were within normal limits, excluding acute myocardial injury.\\n\\nElectrocardiography demonstrated sinus tachycardia, likely secondary to hypoxemia and sympathetic activation. Transthoracic echocardiography revealed a deep venous thrombus in the right popliteal vein, a thrombus straddling a patent foramen ovale (PFO), a dilated right atrium, and moderate pulmonary hypertension. The thrombus dimensions were 3 mm × 20 mm in the left atrium and 8 mm × 25 mm in the right atrium. Computed tom"}
+{"row_index": 237, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"We used two small cork-screws to safely remove a stuck hip implant when the hip kept slipping out because the socket was too far out of place. This worked well without hurting the patient, and by the second month, she could walk without help.\"\n}"}
+{"row_index": 238, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A new method has been reported to remove a stable, cemented hip component that is causing recurrent dislocations due to improper positioning of the acetabular part. In this case, a 74-year-old woman had repeated hip dislocations (eight times) because the hip socket (acetabulum) was positioned incorrectly. Doctors used two cork-screws inserted into the rim of the hip socket to push out the plastic liner and create cracks in the cement. This allowed them to easily remove the damaged plastic cup. The cement was then carefully broken up and removed piece by piece. A new, reinforced ring and a new cemented hip socket were placed using standard techniques. The metal ball of the hip was replaced, but the stem was kept. There were no complications during or after the surgery. At two months after the procedure, the patient could walk without needing support.\"\n}"}
+{"row_index": 239, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 74-year-old female underwent revision total hip arthroplasty for recurrent dislocation of a cemented total hip prosthesis, resulting from acetabular malposition, with a history of eight prior dislocations. The acetabular component was stable and cemented, necessitating a technique to remove the cemented acetabular cup without compromising the integrity of the underlying bone or the femoral stem. The all-polyethylene acetabular liner was drilled with a 4.5 mm drill to create a peripheral breach, followed by the insertion of two cork-screws into the rim of the acetabular component, advanced as far as anatomically feasible, to induce extrusion of the polyethylene liner from the cement mantle and to generate fissures within the cement layer. Application of manual torsional shear forces at the polyethylene-cement interface resulted in complete disruption of the polyethylene liner at the cement-polyethylene boundary, with no technical complications or resistance observed. This mechanical disruption enabled complete removal of the polyethylene cup with minimal effort. Subsequently, cement–splitting osteotomes were employed to remove the cement mantle in a piecemeal fashion, with meticulous curettage of residual cement plugs to ensure complete debridement. A roof reinforcement ring was implanted to stabilize the acetabular component, followed by placement of a cemented UHMW polyethylene cup using standard surgical techniques. The original metallic femoral head was replaced, while the cemented femoral stem was retained to preserve stability and biomechanical continuity. The perioperative course was uncomplicated, with no evidence of intraoperative or postoperative complications. At two months postoperatively, the patient achieved full weight-bearing ambulation without the need for external assistive devices, indicating successful restoration of hip joint stability and function. The described technique demonstrates a feasible, technically sound approach for the removal of a stable cemented acetabular component in the setting of recurrent dislocation due to malposition, leveraging mechanical disruption via cork-screw insertion and torsional shear forces to overcome the cement-liner interface without requiring additional instrumentation or surgical intervention.\"\n}"}
+{"row_index": 240, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 25-year-old woman had a planned C-section at 39 weeks because she wanted to. After the surgery, she suddenly got a very high fever and her blood pressure dropped sharply. A few days later, doctors found a bad germ in her blood called Ralstonia mannitolilytica. This meant she had a serious infection that caused her body to go into shock. Doctors gave her lots of fluids, blood transfusions, medicines to raise her blood pressure, and strong antibiotics like imipenem and cefoperazone. She stayed in the hospital for a few days in a serious care unit, and after treatment, she got better. She was finally able to go home without any problems, and six months later, everything was normal.\"\n}"}
+{"row_index": 241, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 25-year-old woman had a planned cesarean section at 39 weeks of pregnancy. After the surgery, she suddenly developed a high fever and low blood pressure, which are signs of a serious infection called sepsis. Five days later, a bacteria named Ralstonia mannitolilytica was found in her blood. This infection led to septic shock, so she received strong fluids, blood transfusions, and medicines to support her body. She was treated in the intensive care unit and recovered without major complications. She was discharged on day 15 and had no issues during a six-month follow-up.\"\n}"}
+{"row_index": 242, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 25-year-old woman, gravida 1 para 0, with no history of chronic medical conditions, was admitted for an elective cesarean delivery at 39+1 weeks of gestation by maternal request. Combined spinal-epidural anesthesia was administered: 15 mg of 0.5% ropivacaine hydrochloride (AstraZeneca AB, Sweden) was injected into the subarachnoid space, and 5 mL of 2% lidocaine (Shanxi Shiyao Yinhu, China) was administered epidurally. Prophylactic intravenous cefathiamidine (1.0 g, Shandong Luoxin, China) was initiated preoperatively. During surgery, the patient developed shivering, but vital signs remained stable, and the procedure was completed successfully. Postoperatively, she was transferred to the anesthetic resuscitation room where she continued to shiver, reported generalized numbness and dyspnea, and developed a high fever of 40.7 °C. Her blood pressure dropped to 78/44 mmHg, with tachycardia reaching a maximum of 177 bpm, and intermittent vaginal bleeding was noted; oxygen saturation remained at 98%. Septic shock was clinically suspected, though anaphylactic shock could not be excluded. Immediate resuscitation was initiated with massive fluid resuscitation, intravenous dexamethasone (Sinopharm, China), and intramuscular carboprost tromethamine (250 μg, Pharmacia and Upjohn Company, USA) as a uterotonic agent. A Bakri postpartum balloon (Cook, USA) was placed to manage postpartum hemorrhage. Despite interventions, blood pressure remained critically low (<90/60 mmHg). Laboratory findings revealed severe metabolic acidosis (pH 7.252 [normal 7.35–7.45], serum lactate 6.52 mmol/L [normal 0.36–1.25]), markedly elevated procalcitonin (94.5 ng/mL [normal 0.0–0.5]), leukocytosis (WBC 15 × 10⁹/L [normal 4–10 × 10⁹/L]), neutrophilic predominance ("}
+{"row_index": 243, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 71-year-old woman had early breast cancer in her right breast. She had surgery to remove the tumor, then took chemo, radiation, and hormone pills to fight it. She stayed healthy for years until 2015, when she started coughing. Doctors found the cancer had spread to her lungs and bones, like in the shoulder, hip, and back. She started taking two medicines to stop the cancer from growing — ribociclib and letrozole — which helped for a while. But she still had low blood cell counts, so her dose was cut in half. A few months later, she noticed white spots on her hands, feet, and face — like patches of skin losing color. These spots grew slowly and were not from an autoimmune problem. Her doctor tried creams, but they didn’t help much. This is a known side effect of the cancer medicines she’s taking.\"\n}"}
+{"row_index": 244, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 71-year-old woman was first diagnosed with early-stage right breast cancer in 1999. The cancer was hormone-sensitive (HR+/HER2-) and small, less than 2 cm, with no spread to lymph nodes. She had breast-conserving surgery, followed by chemotherapy, radiation, and hormonal therapy with tamoxifen for 5 years. She stayed in good health and followed up regularly until 2015, when she started having a persistent cough. Imaging showed the cancer had spread to the lymph nodes near the lungs and to several bones, including the left shoulder, scapula, pelvis, and spine. A biopsy confirmed it was breast cancer that had spread. Her cancer remained hormone-sensitive, so she was treated with endocrine therapy, first with fulvestrant, then with exemestane and everolimus, but she had to stop due to lung and kidney side effects. She later joined a clinical trial testing a new drug class called CDK4/6 inhibitors, but stopped when her cancer progressed. After the FDA approved these drugs, she started taking ribociclib and letrozole, which worked well overall, though her blood counts were low, so her ribociclib dose was reduced. About 20 weeks into treatment, she noticed white, patchy spots on her hands, feet, and face that looked like vitiligo. These lesions spread slowly and were not linked to any family or personal history of autoimmune conditions. She saw a dermatologist, tried topical treatments, and was given steroids, but the spots did not improve significantly.\"\n}"}
+{"row_index": 245, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 71-year-old female with a history of thalassemia minor and hypertension was diagnosed in 1999 with early-stage right breast cancer, specifically invasive ductal carcinoma measuring less than 2 cm, node-negative, with hormone receptor (HR) positivity (ER 90%, PR 30%) and HER2 negativity. She underwent breast-conserving surgery with axillary dissection, followed by adjuvant chemotherapy consisting of cyclophosphamide, methotrexate, and 5-fluorouracil (CMF), subsequent radiotherapy, and five years of tamoxifen therapy. The patient maintained excellent clinical and mammographic follow-up until 2015, when she presented with an intractable cough. Imaging revealed a left hilar lesion and multiple osteolytic bone metastases involving the left scapula, left shoulder, left iliac bone, and the fourth and seventh dorsal vertebrae. Fine needle aspiration via endobronchial ultrasound confirmed metastatic breast cancer with preservation of the same molecular phenotype: HR-positive, HER2-negative. Initial endocrine therapy with fulvestrant resulted in a progression-free survival of 2 years; she was subsequently switched to exemestane and everolimus, which was discontinued due to grade II pneumonitis and proteinuria consistent with prenephrotic range. During this period, she was enrolled in a double-blind, randomized clinical trial evaluating the addition of CDK4/6 inhibitors to aromatase inhibitor therapy. Due to disease progression, she was withdrawn from the trial and found to be on the placebo arm. Following FDA approval of CDK4/6 inhibitors, she was initiated on ribociclib and letrozole, which she tolerated with moderate neutropenia necessitating dose reduction to 400 mg daily on days 1–21 of a 28-day cycle. Approximately 20 weeks after starting this regimen, she developed small, rounded, well-demarcated hypopigmented lesions initially on both hands, which expanded to the midforearms. Three weeks later, similar lesions appeared on the face and feet. These lesions were clinically consistent with vitiligo-like depigmentation, and the patient had no personal or family history of autoimmune disorders. Dermatological evaluation was performed, and topical immunomodulators (calcineurin inhibitors) were offered but declined; she was managed with topical corticosteroids"}
+{"row_index": 246, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"An 81-year-old woman came to the hospital because she was bleeding from her stomach and had black stools. She had a history of a cancer in her stomach area (GIST) that spread to her liver and belly, and she had been treated with medicine (sunitinib) for it. Four years earlier, she had surgery to fix her stomach and used a part of her small intestine (jejunum) to connect the stomach to the esophagus (Merendino procedure). During an emergency exam, doctors found a bleeding spot in the small intestine where the connection was made. They stopped the bleeding with medicine and a special powder, and gave her blood transfusions. But her blood count kept dropping, and they thought she had a reaction to the blood. She got fever, started passing blood in her urine, and her breathing got worse. Tests showed she had a serious infection caused by a type of bacteria called Clostridium perfringens, which spread to many of her organs. Even though the blood she got was checked, it wasn’t infected. She died three days after being admitted because of the severe infection. The infection had spread all over her body and damaged her tissues.\"\n}"}
+{"row_index": 247, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"An 81-year-old woman was admitted to the hospital suddenly because she was bleeding from her stomach and had black, tarry stools (melena). She had a history of a cancer in the stomach area called a gastrointestinal stromal tumor (GIST), which had spread to her liver and abdomen. She had been treated with medication (sunitinib) for this advanced cancer and had undergone a surgery four years earlier called a Merendino procedure, where part of her small intestine was used to reconstruct her stomach and esophagus. During an emergency endoscopy, doctors found a bleeding ulcer in the reconstructed part of her small intestine. The bleeding was stopped right away, and she received blood transfusions. However, her blood levels continued to drop, and doctors suspected a reaction to the transfused blood. She was given treatment for a possible hemolytic transfusion reaction, but her condition worsened. Three days after admission, she died. Blood tests later showed that she had a severe infection caused by Clostridium perfringens, a type of bacteria that spreads widely in her organs. The autopsy confirmed that the bacteria had spread throughout her body, causing tissue damage and septic shock. The infection was not caused by contaminated blood products, and the bleeding ulcer was not the direct cause of death.\"\n}"}
+{"row_index": 248, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"An 81-year-old female presented to the emergency department with acute hematemesis and melena, exhibiting poor general condition and hemodynamic instability. Initial laboratory findings showed a hemoglobin level of 7.7 mg/dL, with no leukocytosis or elevation in C-reactive protein (CRP), suggesting a non-infectious or non-inflammatory etiology at presentation. The patient had a history of a 6.5 cm gastrointestinal stromal tumor (GIST) originating in the cardia, initially treated with imatinib 400 mg/day for downsizing, followed by surgical resection of the gastroesophageal junction and reconstruction via a jejunal interposition (Merendino procedure) four years prior. Histopathological analysis of the primary tumor revealed a T3-stage lesion with a positive c-Kit mutation in exon 11 and a Ki-67 proliferation index of 15%, indicating a high proliferative activity. According to Miettinen's prognostic criteria, the tumor was classified as high-risk due to size (>5 cm) and mitotic rate (>5 mitoses per high-power field), leading to initiation of first-line adjuvant imatinib therapy at 400 mg/day. After two years of first-line therapy, the patient developed hepatic and peritoneal metastases, prompting transition to sunitinib as second-line therapy for metastatic disease. Proton pump inhibitor (PPI) use was discontinued for an unspecified duration prior to admission, which may have contributed to mucosal vulnerability and ulceration. Emergency gastroscopy revealed active bleeding from a vessel stump in the jejunal interposition, consistent with Forrest stage I b upper gastrointestinal bleeding. Endoscopic hemostasis was achieved through local adrenaline injection and polymer powder application. A thoracoabdominal CT scan demonstrated no active hemorrhage or free intraperitoneal fluid, with hepatic and peritoneal metastases remaining stable in size but increasingly necrotic compared to prior imaging. A subsequent decline in hemoglobin prompted repeat gastroscopy, which identified diffuse, non-localized bleeding, necessitating aggressive coagulopathy management. The patient received 9 units of packed red blood cells (pRBCs), 6 units of fresh frozen plasma (FFPs), 6 units of platelet concentrates, 3 g of fibrinogen, and 4000 IU of PPSB® (a prothrom"}
+{"row_index": 249, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 67-year-old man started having problems with his legs, like numbness and pain, that went away on their own. Later, at age 73, he had eye problems and was told he had multiple sclerosis. His condition got worse over time, with more nerve issues in his spine and eyes. He tried medicines like interferon and steroids, but they didn’t help. He also tried natalizumab, but still had relapses — his eyes and legs got worse each time. After stopping natalizumab, he had plasma exchange treatments and started rituxan, which helped his symptoms stop worsening. But later, he had another serious back nerve attack. So, he started cyclophosphamide, and after that, he didn’t have any more attacks for 24 months. Tests later showed he had a specific antibody called anti-aquaporin-4, which explains his condition. This is a rare disease called neuromyelitis optica, not multiple sclerosis.\"\n}"}
+{"row_index": 250, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 67-year-old man with no prior health issues first developed symptoms in his legs, including numbness and reduced pain sensation, which went away on their own. Later, at age 73, he had vision problems in both eyes (optic neuritis) and was initially diagnosed with multiple sclerosis (MS). His condition worsened over time, with MRI scans showing damage to his spinal cord and brain. He was treated with interferon and corticosteroids, but these did not stop the relapses. He then started natalizumab, which also failed—he had three more relapses, each affecting his vision and movement, leading to severe weakness and a significant drop in his disability score. After stopping natalizumab and undergoing repeated plasma exchanges, his symptoms began to stabilize. He started treatment with rituxan, which depleted his B cells, but later had another serious spinal relapse. This led to starting cyclophosphamide, an immune-suppressing drug, which successfully prevented any further relapses over the next 24 months. Testing later confirmed the presence of anti-aquaporin-4 antibodies, which are linked to neuromyelitis optica (NMO), a different condition from MS. This case shows that early diagnosis and appropriate treatment are key in managing such rare and serious autoimmune diseases.\"\n}"}
+{"row_index": 251, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 67-year-old Caucasian male with no significant prior medical history presented with acute spinal symptoms characterized by transient hypesthesia and hypoalgesia in both lower extremities, which spontaneously resolved without a definitive diagnosis. At age 73, he developed bilateral optic neuritis, leading to a diagnosis of multiple sclerosis (MS) at an external healthcare facility. At that time, his expanded disability status scale (EDSS) score was 2.5. Magnetic resonance imaging (MRI) of the spinal cord revealed diffuse cord swelling and longitudinally extensive T2-hypertensive lesions spanning from C2 to T3, consistent with longitudinal myelitis. Cranial MRI demonstrated sparse periventricular and cerebellar lesions without contrast enhancement and did not meet the Barkhof criteria for MS. Cerebrospinal fluid (CSF) analysis revealed oligoclonal bands, a hallmark of MS, although anti-aquaporin-4 (AQP-4) antibody testing was not performed at the time. Initial therapy consisted of interferon beta-1a for six months, subsequently switched to interferon beta-1b by the treating neurologist. During this period, the patient experienced two additional spinal relapses, each managed with corticosteroid pulses without clinical benefit, resulting in a progressive worsening of disability, with EDSS increasing from 2.5 to 4.0. Subsequent initiation of natalizumab at an external clinic was associated with three relapses: the first occurring at four months, the second at six months, and the third at eight months post-initiation. Each relapse involved bilateral optic nerve involvement and spinal cord pathology, leading to progressive visual and motor deficits, culminating in high-grade spastic tetraparesis and bilateral visual acuity impairment, with EDSS progression to 8.0. Given the clinical pattern and persistence of relapses despite immunomodulatory therapy, neuromyelitis optica (NMO) was considered upon referral to our institution. Natalizumab was discontinued after nine courses. Following repeated cycles of plasma exchange, the disease course stabilized, and therapy with rituximab (anti-CD20 monoclonal antibody) was initiated. Despite complete B-cell depletion as confirmed by flow cytometry, a severe myelitis relapse occurred three months later. This prompted the initiation of additional immunosuppressive therapy with cyclophosphamide at a dose of"}
+{"row_index": 252, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 22-year-old woman had a serious stomach problem called ulcerative colitis, which caused her to have diarrhea with blood, severe belly pain, vomiting, and a swollen belly. Tests found she had a harmful bacteria called C. difficile and her colon was too big and stretched (megacolon), which made things worse. She was given medicine by mouth to fight the bacteria and medicine by IV to calm down the inflammation, and her swollen belly went away. Even after that, her colitis kept getting bad, so she started a special medicine called infliximab, given by IV every few weeks. The doctors checked how much medicine was in her blood and how much inflammation was in her stool, and both showed the treatment was working. After 6 months, her symptoms got better, and she didn’t need surgery to remove her colon.\"\n}"}
+{"row_index": 253, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 22-year-old woman was diagnosed with ulcerative colitis three months earlier, experiencing bloody diarrhea, abdominal pain, and weight loss. She stopped taking mesalamine because it caused stomach upset. Before hospitalization, her colonoscopy showed moderate inflammation. She was admitted due to worsening symptoms, including frequent bloody stools, severe abdominal pain, nausea, vomiting, and a 10-kilogram weight loss, with no improvement from previous antibiotics.\\n\\nAt admission, she was dehydrated, had a fast heart rate, low blood pressure, and a fever. Her abdomen was swollen and painful. Lab tests showed high inflammation and anemia. An X-ray showed her colon was dilated to 7 cm, indicating megacolon, a serious complication. Tests also found a toxin from Clostridium difficile, so she started oral vancomycin. However, her symptoms worsened, including more diarrhea, bleeding, and fever. A sigmoidoscopy revealed severe inflammation with bleeding in the lower colon, confirming active, severe ulcerative colitis.\\n\\nShe was treated with intravenous hydrocortisone for severe colitis, which helped reduce the swelling in her colon. After initial treatment, she started infliximab, a biologic medication, at a dose of 5 mg/kg. Her treatment was monitored through blood levels (trough level of 8.8 μg/mL) and a stool test (fecal calprotectin of 921 μg/g, which is above the normal limit of 30 μg/g). After one week, her drug level was too low, so she received a second infusion at week 1, following an accelerated treatment schedule (infusions at weeks 0, 1, 2, and 6). After six months of therapy, her symptoms improved both clinically and on endoscopy, and she did not need surgery (colectomy).\"\n}"}
+{"row_index": 254, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 22-year-old female Caucasian patient with a three-month history of ulcerative colitis (UC) presented with progressive bloody diarrhea, abdominal pain, and significant weight loss (10 kg), leading to discontinuation of mesalamine therapy due to gastric intolerance. Colonoscopy performed two weeks prior to hospital admission demonstrated moderate endoscopic activity of UC, as evidenced by a Mayo endoscopic score of 2. Upon hospital admission, the patient exhibited severe clinical deterioration, including frequent liquid and bloody stools, intense abdominal pain, nausea, vomiting, dehydration, tachycardia (110 beats per minute), hypotension (100/60 mmHg), fever (>37.8 °C), and a diffusely painful, distended abdomen with rebound tenderness. Laboratory findings revealed signs of systemic inflammation (C-reactive protein 20.3 mg/dL) and severe anemia (hematocrit 25.8%, hemoglobin 8.1 g/dL). Abdominal X-ray confirmed colonic dilatation of 7 cm, consistent with megacolon, a complication of severe colonic inflammation and impaired motility. Stool testing for *Clostridium difficile* (C. difficile) revealed a positive toxin assay for both A and B toxins, indicating active pseudomembranous colitis. The patient was initiated on oral vancomycin 250 mg four times daily; however, within days, symptoms worsened, with increased diarrhea (>10 episodes/day), rectal bleeding, abdominal distension, and fever. A flexible sigmoidoscopy performed on day 4 of admission, conducted without insufflation and extended to 25 cm, revealed severe mucosal lesions including ulcers covered by fibrin, mucosal friability, edema, and intense enanthem with spontaneous bleeding in the sigmoid and rectum, consistent with severe UC activity (Mayo endoscopic score 3). Histopathological examination confirmed chronic active colitis with structural mucosal damage, crypt microabscesses, and plasmacytosis, supporting a diagnosis of severe inflammatory activity without evidence of *C. difficile* or cytomegalovirus infection. The patient was managed with intravenous hydrocortisone for severe colitis, which led to clinical and radiological improvement, including resolution of megacolon. Due to persistent severe colitis symptoms despite corticosteroid therapy"}
+{"row_index": 255, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 34-year-old woman started having trouble walking and balance, and later had shaking in her hands and head, trouble speaking, and numbness. She also had dizziness, headaches, and lost weight. Tests showed damage to the parts of her brain that help with movement and balance. A gene test found two changes in a gene called POLR3A, which is linked to a rare brain disease called hypomyelinating leukodystrophy type 7. This disease affects how nerves grow and work in the brain. She was given medicines to help her nerves, like vitamin B12 and acetylglutamine, but after one month, her symptoms didn’t get better — she still had trouble walking and holding things. After leaving the hospital, she kept taking medicines, including herbs, and now she can walk slowly and climb stairs, her shaking is much better, and she can hold things and cook. But her speech is still slower and harder to understand than before.\"\n}"}
+{"row_index": 256, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 34-year-old woman was seen because she had trouble with balance and coordination, a condition called ataxia. Over the past few years, she had developed walking problems, hand and head tremors, difficulty speaking, numbness in her limbs, and trouble swallowing. She also had dizziness, headaches, and nausea. Tests showed abnormal signals in the white matter of her brain, which are signs of damage to the myelin sheath—the protective covering around nerve fibers. This type of damage is known as demyelinating lesions. Genetic testing found two specific changes in the POLR3A gene: c.4044C > G and c.1186-2A > G. These mutations are linked to a rare disorder called hypomyelinating leukodystrophy type 7 (HLD7), which affects nerve development and function. The patient was treated with vitamin B12, acetylglutamine, and other supportive therapies, including traditional Chinese medicine. However, after one month, her symptoms did not improve and actually worsened. She needed help walking and could not hold objects. After discharge, she continued treatment and has shown some improvement—she can now walk slowly and climb stairs, her tremors have reduced, and she can hold objects and cook on her own. But her speech is still slower and less clear than before.\"\n}"}
+{"row_index": 257, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 34-year-old Han female presented with progressive cerebellar ataxia, initially manifesting as a mild gait abnormality 7–8 years prior, which evolved into significant walking instability approximately one year before presentation. Postpartum, she developed worsening gait disturbance, static tremors involving the hands and head, dysarthria, occasional limb numbness, and a water-induced cough. Neurological examination revealed dysarthria, upbeating nystagmus with right gaze-evoked nystagmus, absent limb reflexes, impaired bilateral finger-nose test, instability on calcaneal-tibial testing, positive Romberg sign, and bilateral Babinski and Chaddock signs. The ataxia severity was quantified using a standardized ataxia assessment scale, yielding a total score of 24: gait (5), stance (4), sitting (2), speech (2), finger chase (2), nose–finger test (2), fast alternating hand movement (3), and heel–shin slide (4). Mini-Mental State Examination was within normal limits; Montreal Cognitive Scale was not completed due to severe hand and head tremors. Laboratory investigations, including tumor markers, ceruloplasmin, thyroid function (TSH, free T3, free T4, thyroglobulin antibody, thyroid peroxidase antibody), rheumatological markers (rheumatoid factor, anti-streptolysin O, hs-CRP), immunoglobulins (IgG, IgA, IgM), complement components (C3, C4), antinuclear antibody, anticardiolipin antibody, and anti-neutrophil cytoplasmic antibody (ANCA), were all within normal ranges. Lumbar puncture demonstrated no evidence of inflammatory or infectious pathology. Brain MRI revealed bilateral, speckled, and patchy hyperintense lesions in the corona radiata, paraventricular regions, frontal lobes, and left temporal lobe, appearing hypointense on T1-weighted images and hyperintense on T2 and FLAIR sequences, with no abnormal diffusion signals on DWI or ADC maps, consistent with multiple white matter demyelinating lesions. Color Doppler ultrasound of gynecological, abdominal, cardiac, carotid, and intracranial vessels showed no vascular abnormalities. Whole-exome sequencing identified two pathogenic variants in the POLR3A gene:"}
+{"row_index": 258, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 23-year-old woman took a very large amount of metformin (about 30 grams) after a stressful event. Four hours later, she came to the hospital feeling tired but still alive. She had very low blood sugar several times (down to 6.3 mg/dL, then 38 mg/dL, and again 42 mg/dL), which made her feel weak and sick. Each time her blood sugar dropped, she also had a buildup of acid in her body (lactic acidosis), which made her blood too acidic. Her blood pressure dropped, so doctors gave her fluids and medicine to raise it. She needed a machine that filters her blood (CRRT) for 24 hours to help her body clear the poison and fix her blood. After 24 hours, her blood sugar and body started to get better. She was able to go home on day 5, but she didn’t follow up with her doctors for mental health, kidney, or general care.\"\n}"}
+{"row_index": 259, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 23-year-old Arabic woman took 30 grams of metformin intentionally after a stressful event. Four hours later, she was brought to the emergency department. She was alert but feeling very tired. Her vital signs were normal at first, though she had low blood sugar and high lactate levels, which showed her body was under stress. She developed severe lactic acidosis and low blood pressure, which required fluid and medication (like norepinephrine) to stabilize. She had three episodes of very low blood sugar — 6.3 mg/dL, 38 mg/dL, and 42 mg/dL — each time requiring a 50% dextrose injection to raise her sugar levels. These low sugar episodes happened at the same time as her severe acidosis. She was treated with continuous renal replacement therapy (CRRT) for 24 hours, which helped her recover. After this, her blood pressure and blood sugar stabilized, and she improved. By day 3, she was able to eat normally and was transferred to a regular ward. A psychiatrist was involved to assess her mental health, and she was discharged on day 5. However, she did not attend any follow-up appointments for medicine, kidney, or mental health care.\"\n}"}
+{"row_index": 260, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 23-year-old Arabic female with a body mass index of 28 was prescribed metformin for weight management in the context of polycystic ovary syndrome (PCOS). She intentionally ingested approximately 60 tablets of 500 mg metformin (totaling 30 g) following a stressful social event, which was initially recognized as a suicide attempt. Four years prior, she had undergone a living kidney donation to her brother, who had end-stage renal disease of unknown etiology; she has no known comorbidities, including psychiatric disorders, prior suicidal ideation, or substance use (no history of smoking or alcohol intake). She has no family history of diabetes mellitus or mental illness. On presentation to the emergency department (ED) approximately 4 hours after ingestion, she was alert, well-nourished, and generally fatigued, with no signs of pallor, jaundice, or cyanosis. Vital signs included blood pressure of 119/65 mmHg, heart rate of 122 beats/min, respiratory rate of 20 breaths/min, oxygen saturation of 100% on room air, and oral temperature of 36.9 °C. Physical examination revealed dry, cool skin and bilaterally mid-sized, equal, and reactive pupils; no other abnormalities were noted.\\n\\nInitial point-of-care capillary blood glucose was low, prompting the administration of 50 mL of 50% dextrose (D50) solution. Serum glucose measured 6.3 mg/dL, which transiently rose to 106 mg/dL following D50 infusion. Maintenance infusion with 5% dextrose-water was initiated. Laboratory findings showed a markedly low blood glucose, leukocytosis, hypocalcemia, hyperphosphatemia, and mild elevation in serum creatinine. Initial arterial blood gas analysis revealed a pH of 7.18, PaO2 of 76.9 mmHg, PaCO2 of 40.3 mmHg, and bicarbonate of 14.3 mmol/L, consistent with metabolic acidosis. Baseline lactate was markedly elevated at 8.4 mmol/L, prompting a 1 L bolus of Ringer lactate. Serial blood gas and lactate measurements demonstrated progressive worsening of lactic acidosis, with lact"}
+{"row_index": 261, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 59-year-old woman felt confused, was upset, and had trouble moving her right leg. She had been taking medicine for a type of cancer called chronic lymphocytic leukemia (CLL) and a blood problem called hemolytic anemia for months. Her doctor found that her right leg was very weak, her reflexes were uneven, and there was a sign called Babinski on her right side. She was a little overweight and had a low fever. A brain scan showed a spot in the left front part of her brain that looked like a stroke. Later, she got a fever and signs of infection in her brain. A more detailed brain scan showed a large area of damage in the left front brain and small spots that were active. A spinal fluid test found many white blood cells and red blood cells, which means infection. The test found bacteria called Listeria in her blood and spinal fluid. This kind of infection is rare and wasn’t from eating risky food. She started antibiotics and after two days, her fever went away and her brain symptoms got better. After one week, the spinal fluid test showed no more signs of infection. One month later, she was back to normal and could move her legs without trouble.\"\n}"}
+{"row_index": 262, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 59-year-old woman was admitted to the hospital because she was confused, agitated, and had weakness in her right leg. She had been treated for chronic lymphocytic leukemia (CLL) with fludarabine for 3 months and for hemolytic anemia with corticosteroids for 2 months. Before admission, she had mild obesity and a slight fever. A neurological exam showed severe weakness in her right leg, abnormal reflexes, and a sign called a Babinski sign on the right side. There were no signs of inflammation in her brain membranes. A brain CT scan showed a small area of damage in the left frontal lobe, which looked like an ischemic stroke. Later, a brain MRI showed a larger area of abnormality in the same region, spreading toward the basal ganglia, and also showed small areas of increased activity after contrast was given. On the second day, she developed a higher fever and signs of meningeal irritation. A spinal fluid test found many white blood cells, red blood cells, and high protein levels, which suggested infection. Cultures from blood and spinal fluid tested positive for Listeria monocytogenes, a type of bacteria that can cause serious brain and spinal infections. She had no recent history of eating high-risk foods like unpasteurized cheeses or deli meats. The diagnosis was Listeria meningoencephalitis. She was started on ampicillin, and within 48 hours, her fever went down and her neurological symptoms improved. After one week of treatment, the spinal fluid showed normal results. One month later, her leg strength and mental status had fully returned to normal.\"\n}"}
+{"row_index": 263, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 59-year-old hypertensive white female with a history of chronic lymphocytic leukemia (CLL) diagnosed in 2009 presented with a 24-hour history of confusion, agitation, and mild right-lower extremity weakness. She had received fludarabine-based chemotherapy three months prior for CLL and methylprednisolone therapy two months prior for hemolytic anemia secondary to fludarabine-induced immune-mediated destruction of red blood cells. Physical examination revealed grade 1 obesity and subfebrility (99.32 ºF; 37.4 ºC). Neurological examination demonstrated grade 4 right-lower extremity weakness, reflex asymmetry, and a right-sided Babinski sign, with no signs of meningeal irritation at admission. Laboratory findings included a white blood cell (WBC) count of 3.5 × 10³/μL, hemoglobin of 7.1 g/dL, hematocrit of 21.5%, platelets of 109 × 10³/μL, aspartate aminotransferase (AST) of 59 U/L, and alanine transaminase (ALT) of 79 U/L; all other metabolic parameters (serum glucose, urea nitrogen, creatinine, bilirubin, sodium, potassium) were within normal limits. Cerebral computed tomography (CT) revealed a hypodense lesion in the left frontal lobe, consistent with acute ischemic stroke pathology, likely due to small vessel disease or thrombotic occlusion secondary to hypercoagulable states associated with immunosuppression. On day two of hospitalization, the patient developed fever (101.12 ºF; 38.4 ºC) and new signs of meningeal irritation, including a positive Kernig’s sign. Cerebral magnetic resonance imaging (MRI) showed a hyperintense lesion in the left frontal lobe extending into the basal ganglia on T2 and fluid-attenuated inversion recovery (FLAIR) sequences, with small nodular areas of gadolinium enhancement following intravenous administration, suggesting active inflammatory or infectious intracerebral involvement. Lumbar puncture was performed on day two, yielding cerebrospinal fluid (CSF) analysis revealing 24 red blood cells (RBC"}
+{"row_index": 264, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"An 81-year-old woman felt very tired and weak for 3 days, then got dizzy and had trouble breathing. By November 16, 2021, she fell into a coma. Her oxygen levels dropped to just 70-80%, so she was taken to the ICU. She had long-term lung problems like chronic bronchitis and emphysema, and her lungs were full of infections. Her heart was also not working well, and doctors thought she might have had a heart attack. They did a procedure to check her heart, but found no blockages. She started having belly swelling and constipation, and got a glycerin enema. On day 4, she lost consciousness again, her blood pressure dropped, her belly became swollen and tight, and her bowels stopped working. A scan showed gas in her liver area and dead parts of her intestines. She died on day 5 because her body couldn’t fix the shock from the damage.\"\n}"}
+{"row_index": 265, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"An 81-year-old woman came to the hospital with fatigue, lethargy, fever, chills, cough, and shortness of breath over three days. By November 16, 2021, she fell into a coma. Her oxygen levels dropped to 70%-80%, so she was admitted to the intensive care unit (ICU) for treatment. She had a long history of chronic lung disease, including chronic bronchitis and emphysema, and had been on long-term oxygen therapy. She also had heart problems for five years and was taking medication for heart failure.\\n\\nIn the ICU, her blood pressure dropped, and she needed medicine (norepinephrine) to keep it stable. Tests showed signs of infection in her lungs, with high white blood cell counts and markers of inflammation. Chest CT scans showed chronic lung disease and multiple lung infections, especially in the lower and middle parts of the right lung. Her abdominal CT scan showed no major issues, but her abdominal blood vessels were heavily calcified.\\n\\nHer heart tests showed abnormal heart rhythms and signs of heart damage. Her troponin levels went up, which suggests heart muscle injury. The doctors suspected she had a heart attack (ACS) and performed a procedure called PCI through her femoral artery. No major blockages were found in her coronary arteries.\\n\\nOn the second day, she had constipation, which was treated with a glycerin enema. On day 4, she suddenly lost consciousness, had very low blood pressure, and developed swelling in her abdomen with no bowel sounds. An urgent abdominal CT scan showed gas in the liver portal area and severe damage to her bowel walls. The patient died on day 5 from severe, uncontrolled shock due to these complications.\"\n}"}
+{"row_index": 266, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"An 81-year-old female presented to a local hospital with a three-day history of fatigue, lethargy, fever, chills, productive cough, and wheezing, without prior intervention. On November 16, 2021, she developed acute coma and was transported to the emergency department. Her oxygen saturation declined to 70%–80%, prompting immediate admission to the intensive care unit (ICU) for respiratory and hemodynamic support. Upon ICU admission, she exhibited a progressive hypotensive state, requiring norepinephrine infusion to maintain a mean arterial pressure above 65 mmHg.\\n\\nThe patient had a long-standing history of chronic obstructive pulmonary disease (COPD), including chronic bronchitis and emphysema, with over 50 years of documented disease course, and had been on long-term home oxygen therapy. She also had a five-year history of chronic heart failure, managed with oral bisoprolol, with no prior history of abdominal pain or chronic renal insufficiency. There was no history of tobacco or alcohol use, and no relevant family history of cardiovascular or pulmonary disease.\\n\\nOn initial assessment, vital signs were: temperature 36°C, heart rate 85 beats/min, respiratory rate 18 breaths/min, blood pressure 105/45 mmHg. Physical examination revealed diminished breath sounds bilaterally, with wet rales predominantly at the bases of both lungs. Cardiac and abdominal examinations were unremarkable.\\n\\nLaboratory findings included an initial troponin level of 0.05 ng/mL, which subsequently increased, indicating myocardial injury. B-type natriuretic peptide (BNP) was elevated at 4164 pg/mL, consistent with volume overload and systolic dysfunction. Arterial blood gas analysis demonstrated a partial pressure of carbon dioxide (PaCO₂) of 58.7 mmHg, oxygen partial pressure (PaO₂) of 86.5 mmHg, and an oxygenation index of 172.97 mmHg—indicating severe hypoxemia. Inflammatory markers were markedly elevated: white blood cell count 8.12 × 10⁹/L, neutrophil percentage 93.2%, C-reactive protein 298.38 mg/L, procalcitonin 6"}
+{"row_index": 267, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A man had a serious brain problem caused by a medicine called ganciclovir, which he was taking for a stomach infection. The medicine made him confused, unsteady on his feet, and eventually fell. Doctors thought it was the medicine, not an infection, because tests showed no signs of virus in his brain fluid. The medicine was stopped, and he got dialysis to clean his blood, which helped his brain feel better. He fully recovered after two dialysis sessions. This was the worst case ever reported for this medicine, with the highest amount ever found in his blood.\"\n}"}
+{"row_index": 268, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"This case involves a 55-year-old man who had diabetes and kidney failure, leading to a kidney transplant 1.5 years earlier. After the transplant, he developed a severe infection caused by cytomegalovirus (CMV), which required treatment with ganciclovir. Because his infection was serious, he received high doses of the drug without reducing them to standard maintenance levels. Two days after starting the treatment, he began to have balance problems and mild confusion. His condition worsened, leading to delirium and a fall. His brain function declined further, and he could no longer take oral medication. Doctors ruled out other causes of brain inflammation, such as encephalitis, and instead suspected ganciclovir-induced encephalopathy. The drug was stopped, and he received two sessions of therapeutic dialysis, which helped clear the drug from his blood. After the second dialysis, his brain function fully recovered. This patient had the highest known level of ganciclovir in his blood and was the only one in the study with severe symptoms and complete recovery after dialysis.\"\n}"}
+{"row_index": 269, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 55-year-old male with a history of diabetic renal failure initiated hemodialysis two years prior, followed by renal transplantation 1.5 years earlier, with subsequent initiation of immunosuppressive therapy. Eight months post-transplantation, his serum creatinine rose to 4.4 mg/dL, indicating progressive renal dysfunction. He presented with CMV enteritis, evidenced by occult gastrointestinal bleeding and a significantly elevated CMV pp65 (C7-HRP) antigen level in peripheral blood mononuclear cells, prompting antiviral intervention. Intravenous ganciclovir was administered at a dose of 150 mg/day for 11 days, followed by transition to valganciclovir at 450 mg/day. Due to the severity of enteritis, the antiviral regimen was not reduced to standard maintenance doses (typically half of initial doses), which is atypical and increases systemic exposure. Two days after initiating valganciclovir, the patient developed gait instability, initially ambulating independently, but within 24 hours required assistance. His level of consciousness deteriorated to E3, V5, M6 on the Glasgow Coma Scale (GCS), indicating mild impairment. The next day, he exhibited intermittent delirium. Two days later, he fell and was found on the floor without significant injury; clinical suspicion initially pointed to exhaustion secondary to severe enteritis. Nine days after starting valganciclovir, his neurological status worsened to E3, V3, M5, and he became unable to ingest oral medications, including valganciclovir. Neurological consultation was obtained; encephalitis was ruled out due to the absence of meningeal signs, fever, and a normal cerebrospinal fluid (CSF) cell count (0.33 cells/μL), with only a marginal elevation in protein concentration (54 mg/dL). Polymerase chain reaction (PCR) testing for CMV, herpes simplex virus (HSV), varicella-zoster virus (VZV), and Epstein-Barr virus (EBV) DNA in the CSF remained negative, supporting exclusion of these viral etiologies. Ganciclovir-induced encephalopathy was therefore clinically and virologically suspected, and the drug was immediately discontinued. To mitigate the risk of further falls and to remove ganciclovir from the systemic circulation,"}
+{"row_index": 270, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 59-year-old man had yellow skin and belly pain for over 15 days, and lost 5 pounds. Doctors found a tumor at the opening of the small intestine (duodenal papilla) using a special camera test. The tumor was checked under a microscope and found to be a fast-growing type of cancer called aggressive B-cell lymphoma. Instead of surgery, he started treatment with special medicines that target the cancer cells, along with a standard chemotherapy plan called CHOP.\"\n}"}
+{"row_index": 271, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 59-year-old man was seen for jaundice and weight loss. Tests showed a blockage in his bile ducts, and imaging found a tumor at the duodenal papilla. A biopsy was taken and examined under a microscope, which showed a type of lymphoma called aggressive B-cell non-Hodgkin's lymphoma. This type of cancer grows quickly and spreads fast. Based on the results, the doctors decided not to do surgery. Instead, he started treatment with chemotherapy (the CHOP regimen) combined with targeted therapy to fight the cancer more effectively.\"\n}"}
+{"row_index": 272, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 59-year-old male was admitted to the Department of Gastroenterology on June 16, 2020, presenting with a 15-day history of pruritic jaundice affecting the skin and sclera, accompanied by progressive weight loss of approximately 5 kg. He had a prior history of brain stem infarction with residual left lower limb weakness and occasional dysphagia, particularly when drinking water. No history of hepatitis, tuberculosis, or other infectious diseases was reported. Physical examination revealed a chronic illness appearance with marked jaundice, absence of palpable superficial lymphadenopathy, and no significant abdominal signs. Laboratory findings at admission included hemoglobin 101 g/L, alanine aminotransferase (ALT) 158 U/L, aspartate aminotransferase (AST) 150 U/L, total bilirubin 217.3 μmol/L, direct bilirubin 152.4 μmol/L, indirect bilirubin 64.9 μmol/L, high-sensitivity C-reactive protein (hs-CRP) 5.8 mg/L, procalcitonin 0.11 ng/mL, carcinoembryonic antigen (CEA) 6.19 μg/L, and carbohydrate antigen 125 (CA125) 117.1 kU/L. Abdominal ultrasonography on June 17 demonstrated gallbladder enlargement, cholecystitis, cholestasis, and significant dilatation of both intrahepatic and extrahepatic bile ducts. Magnetic resonance cholangiopancreatography (MRCP) and abdominal MRI on June 18 confirmed neoplastic involvement of the duodenal papilla, severe bile duct dilatation, bile stasis in the common bile duct, and a markedly enlarged gallbladder. Endoscopic ultrasound (EUS) on June 19 revealed a 2.5 × 2.5 cm neoplasm at the duodenal papilla with surface ulceration, exudative yellow-white slough, and contact bleeding; three biopsy specimens were obtained. The patient was transferred to the surgical oncology department on June 20. Abdominal enhanced computed tomography (CT) on June 23 showed findings consistent with MRI, supporting the"}
+{"row_index": 273, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 27-year-old man woke up with sudden neck pain, numbness in his arms and legs, and weakness. It had started 4 days before he came to the hospital. He had no injury or past history of similar problems. When doctors checked him, his neck muscles were tender, his arms and legs felt numb, and his muscles were strong. Blood tests showed no signs of infection, clotting issues, or cancer. X-rays and CT scans didn’t show broken bones. MRI showed a big lump pressing on his spine in the neck and upper back area, and a small, harmless growth inside his C7 vertebra. This growth is called a vertebral hemangioma. Doctors removed the lump and the growth. After 6 months, his pain and weakness went away and he hasn’t had a return of symptoms. This condition, called IPEH, is rare and can be confused with other spine problems, but it’s treatable with surgery and recovery is good.\"\n}"}
+{"row_index": 274, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 27-year-old man came in with sudden neck pain, numbness in his arms and legs, and weakness in his limbs. The symptoms started four days before he visited the hospital, and he had no history of injury or other medical conditions. Earlier, six years ago, he had a similar but brief episode of numbness and weakness. On exam, his neck muscles were tender, and his sensation and muscle strength were reduced, especially in the areas served by the T1 nerve. Blood tests showed no signs of infection, clotting issues, or cancer. X-rays and CT scans didn't show bone damage. MRI scans revealed a large mass pressing on the spinal cord in the C6-T1 region, extending into the C7-T1 area. This mass was bright on T2 images and dark on T1, which is typical for certain types of tumors. Additionally, a small, round mass was found in the C7 vertebra, consistent with a benign vertebral hemangioma (VH). The surgery involved removing the spinal mass through a laminectomy and excising the abnormal tissue. Pathology tests confirmed the presence of abnormal blood vessel growth with blood clots, leading to a diagnosis of intraparenchymal hemangioma of the spine (IPEH). At his six-month follow-up, his symptoms had improved completely, and there was no sign of recurrence. This case highlights the clinical features, imaging signs, possible causes, how it's different from other conditions, and how it's treated.\"\n}"}
+{"row_index": 275, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 27-year-old male presented to the Department of Spine Surgery with acute-onset neck pain, unilateral limb numbness, and proximal and distal muscle weakness. Symptoms began four days prior to presentation and were of sudden onset, with no history of trauma. A prior episode of transient sensory disturbance and mild weakness in the extremities occurred six years earlier, suggesting possible recurrent or chronic spinal cord involvement. Physical examination revealed localized tenderness over the paraspinal muscles at the C6-T1 spinous process, diminished sensory perception to light touch in the T1 dermatomal distribution, and preserved motor function with grade IV muscle strength in all four limbs. Laboratory evaluations, including coagulation studies, inflammatory markers (e.g., CRP, ESR), and tumor markers (e.g., CA-125, CEA), were all within normal reference ranges, excluding systemic inflammatory or neoplastic etiologies. Spinal radiography and conventional computed tomography (CT) demonstrated no evidence of bony erosion, lytic lesions, or pathological fractures. Enhanced cervical magnetic resonance imaging (MRI) revealed a homogenously enhancing epidural mass within the C6-T1 spinal canal, compressing the spinal cord and extending into the left C7-T1 foramen. On T1-weighted imaging (T1WIs), the mass appeared hypointense, consistent with high vascular content or fat suppression, while on T2-weighted imaging (T2WIs), it was hyperintense, indicating high water content and susceptibility to edema or hemorrhage. Additionally, a 0.5 cm × 0.5 cm × 0.6 cm heterogeneously enhancing hyperintense lesion was identified within the C7 vertebral body on T2WI, consistent with a benign vertebral hemangioma (VH), a vascular malformation characterized by abnormal proliferation of vascular endothelial cells within the bone marrow. Histopathological examination of the excised epidural mass revealed papillary proliferation of vascular endothelial cells with associated thrombus formation, confirming the diagnosis of intraparenchymal epidural hemangioma (IPEH). The patient underwent C6-T1 laminectomy with radical excision of the epidural mass. Postoperative follow-up at six months demonstrated complete resolution of neurological symptoms without recurrence. This case illustrates the clinical spectrum of IPEH, including its characteristic imaging features (T1 hypointensity, T2 hyperintensity"}
+{"row_index": 276, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"Two men who were healthy before got a serious problem after getting the second dose of the Pfizer COVID-19 vaccine, about three weeks later. They both felt sudden, severe tiredness and shortness of breath, even when not moving. Tests showed no active coronavirus in their bodies. Doctors found high pressure in their lungs using heart ultrasound and, in one case, a special test on the heart’s right side. This high lung pressure hurt their hearts and likely caused long-term damage. There was no sign of blood clots in their lungs. Both men now have trouble doing daily activities and likely have lasting heart problems. Their symptoms didn’t go away completely, and the lung pressure stayed high even after months.\"\n}"}
+{"row_index": 277, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"Pulmonary hypertension in two previously healthy adult men occurred within three weeks of receiving the second dose of the Pfizer (BNT162b2) mRNA COVID-19 vaccine from different batches. Both men suddenly developed severe fatigue and shortness of breath during physical activity, even at rest, and their SARS-CoV-2 PCR tests came back negative. Doctors diagnosed the condition using heart ultrasounds and, in one case, a more detailed heart catheterization. The diagnosis showed high pressure in the lungs' blood vessels, which is a sign of pulmonary hypertension. Neither patient had blood clots in their lungs. Both cases resulted in lasting symptoms and likely permanent heart damage. The condition led to long-term functional limitations, and in one case, the patient also developed irregular heartbeats. No evidence of pulmonary embolism was found in either case.\"\n}"}
+{"row_index": 278, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"Two cases of vaccine-induced pulmonary hypertension are reported in previously healthy adult males following the second dose of the Pfizer BNT162b2 mRNA COVID-19 vaccine, with onset occurring within three weeks of vaccination across different lots. Case #1 involves a 49-year-old male physician-athlete with a BMI of 23, non-smoker, and a history of mild exercise-induced asthma managed with albuterol. He received Dose 1 in December 2020 and Dose 2 in January 2021. Three weeks post-Dose 2, he developed acute severe fatigue, flu-like symptoms, tachycardia, palpitations, orthostasis, right-sided chest pressure, and exertional dyspnea. SARS-CoV-2 PCR testing was negative at symptom onset. Initial transthoracic echocardiography showed normal left ventricular function (ejection fraction 65%), normal right ventricular size and function, and a maximal tricuspid regurgitation velocity (TRVmax) of 3.09 m/s, yielding an estimated right ventricular systolic pressure (RVSP) of 42 mmHg, interpreted as mild to moderate pulmonary hypertension. Laboratory findings included a brain natriuretic peptide (BNP) level of 22 pg/mL (within normal range, <900 pg/mL), elevated low-density lipoprotein (LDL) cholesterol, and hematocrit of 50%. Pulmonary CT angiography with 3D reconstruction of the pulmonary artery (PA) tree demonstrated no evidence of pulmonary emboli. Subsequently, the patient developed 15 lbs of fluid retention, generalized edema, neck pressure, headaches, and a sensation of 'being hung upside down,' consistent with jugular venous distention (JVD) and cerebral venous congestion. Resting oxygen saturation (SpO2) was 92%, and new-onset systolic and diastolic arterial hypertension developed. Symptoms were present at rest and worsened with exertion, with functional capacity limited to New York Heart Association (NYHA) Class 3–4. Serial echocardiographic follow-up over one year showed no progression in RVSP or right ventricular function. Symptoms and exercise tolerance improved to NYHA Class 1–2, with resolution of fluid retention, swelling, tachycardia, and hypertension, and SpO"}
+{"row_index": 279, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 21-year-old woman who is overweight had been feeling tired, dizzy, and sweating for a long time. She had episodes of passing out, especially when her blood sugar was too low. Doctors thought it might be a problem with her body making too much insulin, called an insulinoma. Her blood sugar was very low — down to 20 mg/dl — even after giving her sugar. She had been treated as a baby for a similar problem, and doctors found a gene mutation that causes her body to keep making insulin even when sugar is low. She was given medicine called diazoxide, which helped, but she stopped taking it because it caused unwanted side effects like extra hair and swelling. This time, doctors started her on two new medicines: octreotide and diazoxide again. These helped her blood sugar go up and her symptoms like dizziness and passing out went away. She now feels better, and doctors stress that she must keep taking her medicine and check in with a specialist regularly to stay healthy.\"\n}"}
+{"row_index": 280, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 21-year-old woman with a history of obesity and low blood sugar since infancy presented to the emergency department with repeated episodes of dizziness, fainting, sweating, and lethargy. Her blood glucose was very low—20 mg/dl when first seen—and remained low even after receiving dextrose (a sugar solution) multiple times. She had previously been diagnosed as a baby with a condition called persistent hyperinsulinemic hypoglycemia of infancy, caused by a mutation in the glucokinase (GCK) gene, specifically a Val452Leu activating mutation. This mutation causes her body to produce too much insulin, leading to low blood sugar. She was once treated with diazoxide and octreotide, which helped control her symptoms, but stopped taking diazoxide due to side effects like increased hair growth and fluid retention. On this visit, she was given octreotide and diazoxide again, and her blood sugar improved, with levels rising to between 55 and 110 mg/dl by discharge. Doctors stressed the importance of continuing her treatment and seeing an endocrinologist regularly to manage her condition.\"\n}"}
+{"row_index": 281, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 21-year-old Caucasian female presented to an external emergency department with altered mental status following discovery of lethargy by family members. On arrival, her plasma glucose was 20 mg/dL, consistent with severe hypoglycemia. She was hospitalized and initiated on dextrose infusion (10% dextrose in water), yet remained hypoglycemic with capillary glucose levels persistently between 50 and 60 mg/dL. She was transferred to our facility on suspicion of insulinoma, as she was unable to recall her prior diagnosis of hypoglycemia. Historical records from our neonatal unit revealed a history of persistent hypoglycemia beginning in infancy, including episodes of seizures, syncope, dizziness, headaches, palpitations, and sweating, which were initially intermittent and variable in severity. These symptoms were reported to have onset at birth, with no formal investigation until age 12, when she experienced recurrent episodes. She remained seizure-free and asymptomatic until age 17, when a new syncopal episode prompted an inpatient evaluation for hypoglycemia. During this evaluation, fasting blood glucose was 47 mg/dL after a 2-hour fast, proinsulin levels ranged from 10.4 to 84.1 pmol/L (normal range: 0–10 pmol/L), and C-peptide was 3.1 ng/mL (normal range: 1.1–4.4 ng/mL). Insulin antibody and sulfonylurea screening were negative, ruling out autoimmune or drug-induced causes. Abdominal magnetic resonance imaging (MRI) did not identify any insulinoma, leading to a genetic investigation that revealed a heterozygous Val452Leu activating mutation in the glucokinase (GCK) gene. This mutation results in constitutive activation of glucokinase, a key enzyme in glucose sensing within pancreatic beta cells, leading to excessive insulin secretion even in the absence of elevated blood glucose. The patient was initially managed with diazoxide, a potassium channel opener that reduces insulin release by promoting beta-cell membrane hyperpolarization, resulting in clinical improvement. She was discharged on oral diazoxide 250 mg daily, but discontinued therapy due to adverse effects including hirsutism and fluid retention. On current admission, she received dextrose boluses and was placed on continuous 5% dext"}
+{"row_index": 282, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 67-year-old man had psoriasis on his feet that was well controlled. He started treatment for cancer in his stomach, called gastric adenocarcinoma, and took medicine for it for months. Two months before, he began a drug called pembrolizumab to fight the cancer. He started having joint pain in his fingers, toes, knees, and shoulder, with swelling and redness. His skin had psoriasis plaques, and his nails were damaged. Blood tests showed inflammation, but no signs of rheumatoid arthritis. The doctor found inflamed joints, especially in the knees and shoulder, and thought it was psoriatic arthritis. He first tried steroids, but the pain got worse. Then he added two medicines—leflunomide and methotrexate—which helped a little, but the symptoms came back when the steroids were reduced. So, the doctor added a stronger medicine called etanercept, which controls the inflammation and finally stopped the joint pain and swelling.\"\n}"}
+{"row_index": 283, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 67-year-old man with a long-standing history of foot psoriasis that was well controlled had recently developed joint pain in multiple areas, including his fingers, toes, left shoulder, and knees. He had been treated for advanced stomach cancer that had spread to lymph nodes, and had previously received pembrolizumab for cancer treatment. Two months before his joint symptoms started, he began pembrolizumab, which is used to help the immune system fight cancer. His psoriasis was already known, and he had signs of psoriatic nail changes and swelling in his finger and toe joints (dactylitis). On exam, his joints were red and swollen, and blood tests showed high levels of inflammation markers like C-reactive protein and erythrocyte sedimentation rate. Tests for rheumatoid arthritis (like rheumatoid factor and anti-CCP) were negative, which helped rule out other types of arthritis. Joint fluid from his knee showed signs of inflammation, and imaging showed fluid buildup and swelling in the knees and shoulder. Initially, he was given methylprednisolone, a steroid, to reduce inflammation, but his symptoms got worse after one week. He then started leflunomide and methotrexate, which helped a little but symptoms came and went with steroid use. Because the condition was not responding well, his treatment was changed to include etanercept, a drug that blocks a specific protein involved in inflammation (a tumor necrosis factor inhibitor). This change led to better control of his psoriatic arthritis.\"\n}"}
+{"row_index": 284, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 67-year-old male with a history of well-controlled plaque psoriasis of the feet presented with a two-week history of progressive polyarthralgia and nail dystrophy. He was diagnosed with advanced gastric adenocarcinoma with distant lymph node metastases in March 2020. Endoscopic evaluation revealed a 3-cm ulcerofungating mass in the pre-pyloric antrum, histopathologically confirmed as moderately differentiated adenocarcinoma. Immunohistochemical analysis demonstrated negative staining for human epidermal growth factor receptor 2 (HER2, IHC 1+), Epstein-Barr virus, and deficient DNA mismatch repair (dMMR), characterized by retained nuclear expression of MSH2 and MSH6 and loss of MLH1 and PMS2. Abdominal computed tomography identified multiple enlarged lymph nodes in the para-aortic and aortocaval regions, consistent with nodal involvement. The patient received first-line palliative chemotherapy with capecitabine and oxaliplatin for 11 months, followed by second-line therapy with ramucirumab and paclitaxel. Despite this, progression of disease was observed after two months of ramucirumab and paclitaxel, leading to initiation of pembrolizumab (200 mg every three weeks) in June 2021 as third-line treatment, based on the tumor's dMMR status, which is associated with microsatellite instability and potential responsiveness to immune checkpoint inhibition. Prior to pembrolizumab therapy, his neutrophil-to-lymphocyte ratio (NLR) was 1.1 and prognostic nutritional index (PNI) was 50.5, indicating a relatively preserved immune and nutritional status. Two months after pembrolizumab initiation, laboratory findings showed a normal white blood cell count (7970/µL), with 72.6% neutrophils and 17.9% lymphocytes, an elevated erythrocyte sedimentation rate (ESR) of 89.0 mm/h, and a serum high-sensitivity C-reactive protein (hs-CRP) level of 2.3 mg/L, reflecting systemic inflammation. Serologic testing for autoimmune markers was negative for rheumatoid factor (RF) and anticyclic citrullinated peptide antibody (ACPA), excluding"}
+{"row_index": 285, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 75-year-old man had a fever and pain on his right side of the chest. Doctors found a big lump under his diaphragm (the muscle that covers the belly) that was about 10 cm in size. It was attached to the liver and couldn’t be easily separated during surgery. Because of this, they had to remove part of the liver and the diaphragm. The surgery took 8 hours and he lost a lot of blood, but he recovered well and was out of hospital in 14 days. After 1 year, there’s been no sign of the lump coming back. The doctors looked at the tissue and found it was a slow-growing tumor that looked like smooth muscle, even though it wasn’t clearly a known type. They named it a 'spindle cell tumor with smooth muscle features' because it had markers that match muscle cells. The tumor wasn’t spreading, and it didn’t grow fast, so it was not very dangerous.\"\n}"}
+{"row_index": 286, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 75-year-old man came in with fever and pain on the right side of his chest. Imaging tests showed a large 10-cm tumor under his diaphragm, which was attached to the liver and hard to separate during surgery. Doctors initially suspected it might be a rare, possibly cancerous tumor from the diaphragm, such as a myxoid sarcoma or schwannoma, but couldn't rule out a benign cause. Blood tests showed mild signs of inflammation and abnormal levels, and a PET scan showed the tumor was active, but not extremely so. Because the tumor was stuck to the liver and near important blood vessels, the surgery had to be more extensive — including removal of part of the liver (right posterior segment) and the diaphragm. The operation took 8 hours and 10 minutes, with about 1,459 mL of blood lost. After surgery, the patient recovered well and was discharged after 14 days. The tumor was found to be just below the liver, touching the diaphragm but not fully connected. Under the microscope, it looked like a low-grade tumor, possibly a solitary fibrous tumor or perivascular epithelioid cell tumor, but tests for those didn’t come back positive. Instead, the final diagnosis was a spindle cell tumor with smooth muscle features, based on positive results for muscle markers like αSMA, desmin, and h-caldesmon. One year after surgery, there has been no sign of the tumor coming back.\"\n}"}
+{"row_index": 287, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 75-year-old male presented with fever and right-sided chest pain. Laboratory investigations revealed elevated inflammatory and metabolic markers: lactate dehydrogenase (LDH) 251 IU/L, alkaline phosphatase (ALP) 469 IU/L, gamma-glutamyl transferase (γ-GTP) 125 IU/L, creatinine 1.43 mg/dL, C-reactive protein (CRP) 3.04 mg/dL, squamous cell carcinoma antigen (SCC) 1.8 ng/mL, nerve-specific enolase (NSE) 21.6 ng/mL, and soluble interleukin-2 receptor (SIL-2R) 614 U/mL, suggesting a systemic inflammatory process or malignancy. Contrast-enhanced computed tomography (CT) identified a large, well-circumscribed, 10-cm mass located beneath the right diaphragm, with a smooth margin and heterogeneous, gradually increasing enhancement in both the tumor and adjacent liver parenchyma, particularly in regions adjacent to fatty tissue. The primary arterial supply was identified as the right inferior phrenic artery, supporting a sarcomatoid origin from the diaphragmatic mesenchyme rather than a benign lesion such as schwannoma. No evidence of pulmonary invasion was observed. Magnetic resonance imaging (MRI) demonstrated heterogeneous high signal intensity on T2-weighted imaging (T2WI) and diffusion-weighted imaging (DWI), with progressive, heterogeneous contrast enhancement consistent with CT findings, further indicating active tumor metabolism. FDG-positron emission tomography (FDG-PET) showed abnormal glucose uptake with a maximal standardized uptake value (SUVmax) of 4.6, which, while not extremely high, was sufficient to raise concern for a malignant process, particularly myxoid liposarcoma or other sarcomatoid tumors. Despite imaging suggesting a primary diaphragmatic origin, the possibility of hepatic adhesion was noted due to the tumor's proximity to the hepatic capsule and intraparenchymal space. Given the tumor's adherence to the liver and its close anatomical relationship with the posterior Glisson’s pedicles and segment 8 dorsal Glisson’s pedicle, a diaphragmatic resection was not feasible without risking vascular compromise or hepatic injury. Consequently, an extended right posterior segmentectomy with concomitant diaphragmatic"}
+{"row_index": 288, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 20-year-old man got trapped under a heavy steel frame while fixing a crane. He was bleeding badly from his lower belly, and doctors found serious injuries to his pelvis and bones. Even after trying to stop the bleeding and saving his life, his legs were too damaged to stay attached. Doctors had to cut off both legs — one above the knee on day 8, and the other at the hip on day 13. His body had so much damage that parts of his muscles died and had to be removed. To fix the open wound, doctors used skin from his thigh to cover the exposed bones in his pelvis. This skin stayed in place and helped heal. After months of healing and cleaning the wounds, his skin fully grew back. Now he can sit in a wheelchair, move on his own, and live at home with his parents. The rebuilt pelvis works well with his prosthetic legs.\"\n}"}
+{"row_index": 289, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 20-year-old Japanese man was trapped under a 3-ton steel frame while working on a crane. He was rescued and arrived at the hospital with heavy bleeding from his lower right abdomen. His vital signs showed he was in shock, and his injuries were severe: his pelvis was broken, the bones in his lower back and hips were fractured, and there was damage to his spleen. Imaging showed bleeding from both internal iliac arteries, which was treated with a procedure to stop the bleeding. Despite efforts, blood loss continued, and the patient developed tissue damage in both legs. Because of the risk of massive bleeding and the extent of tissue death, doctors decided that amputating both legs was necessary to save his life. He had a right above-knee amputation on day 8 and a left hip disarticulation on day 13. Over the next several weeks, his wounds were cleaned multiple times due to infection, and parts of his muscles were removed. On day 112, a flap of skin from his thigh was used to cover the exposed pelvis, and over time, the wound healed. A skin graft was later applied to finish healing. He now uses a wheelchair and can move independently. The reconstructed pelvis allows him to wear prosthetics properly and live at home with his family.\"\n}"}
+{"row_index": 290, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A healthy 20-year-old Japanese male sustained a catastrophic traumatic injury when trapped beneath a 3-ton steel frame during crane maintenance. Upon rescue, he presented with persistent hemorrhage from the right lower abdominal wound, and upon emergency department arrival, exhibited unstable hip mechanics. Vital signs included a respiratory rate of 22 breaths per minute, blood pressure of 97/65 mmHg, and a tachycardia of 140 beats per minute. His Glasgow Coma Scale score was E4 V5 M6, indicating moderate to severe altered mental status. Physical examination revealed active pelvic instability and ongoing exsanguination from the right lower abdominal wound. Immediate interventions included endotracheal intubation and aggressive fluid resuscitation. Computed tomography (CT) imaging demonstrated multiple severe pelvic injuries: splenic laceration, sacral fracture, sacroiliac joint separation, and comminuted fractures of the right pubis, ischium, and acetabulum. Empirical antibiotic therapy with vancomycin and meropenem was initiated to prevent sepsis. Transcatheter arterial embolization (TAE) was performed in the angiography suite to control pelvic hemorrhage; angiographic evaluation revealed extravasation from both bilateral internal iliac arteries, which were successfully embolized. However, bilateral external iliac arteries demonstrated thrombosis, indicating compromised distal perfusion. A SAM® Pelvic Sling™ (SAM Medical, Wilsonville, OR, USA) was applied to stabilize the pelvis and maintain anatomical alignment. Despite TAE, complete hemostasis was not achieved, prompting consultation with a vascular surgeon. Emergency ligation of the right external iliac artery was performed in the operating room, resulting in immediate hemostasis. The wound was then packed and sutured. Follow-up CT imaging revealed ischemic changes in the right lower limb, consistent with distal arterial occlusion. Given the patient’s young age, robust physiological reserve, and strong familial desire to preserve limb function, revascularization was pursued despite the risk of recurrent hemorrhage. A crossover graft using the axillary-femoral artery was performed to restore distal femoral perfusion. Subsequently, a retroperitoneal hemorrhage was identified, likely due to injury to the external iliac artery, prompting a second crossover graft utilizing the axillary-femoral vein. Concurrently, cystostomy and external"}
+{"row_index": 291, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 23-year-old man had a fever, no sense of smell, headache, and nausea a week before. Doctors said he had COVID-19 and treated him for 10 days at home. Two weeks later, he came back with fever every two days, feeling cold, then hot, then sweating. Tests showed he also had malaria (P. vivax), and his blood had a lot of clots (high D-dimer). He was given medicine for malaria: DHP for 3 days and primaquine for 14 days, as per local rules. He also got heparin to help stop blood clots. After 6 days, his fever went away and his blood tests got better. He’s now feeling fine and staying at home. Both COVID-19 and malaria can cause blood clots, so having both makes the illness worse. This shows why it’s important to check for both when someone has fever and trouble breathing, especially in areas where malaria is common.\"\n}"}
+{"row_index": 292, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 23-year-old man first visited the hospital with fever, loss of smell, headache, and nausea. He was diagnosed with COVID-19 based on a nasal swab test, and treated at home for about 10 days. Even after being cleared, he still tested positive for the virus and continued to self-quarantine.\\n\\nTwo weeks later, he returned with recurring fever every two days, along with chills, fever, and sweating. His temperature reached 39.7°–40°C. The fever came and went, and even with paracetamol, it returned within hours. He also had muscle pain and weakness.\\n\\nLab tests showed high levels of inflammation and a marker called D-dimer, which can indicate blood clotting problems. A malaria test was done, and both the rapid test and blood smear confirmed he had a relapse of P. vivax malaria — a type of malaria he had before, during a trip to Papua.\\n\\nBecause he had both COVID-19 and malaria, doctors treated him for both. He took dihydroartemisinin-piperaquine for 3 days and primaquine for 14 days, following national malaria treatment guidelines. He also received paracetamol and heparin to help with fever and blood clotting. After six days of treatment, his symptoms went away and lab results improved.\\n\\nThis case shows that during the pandemic, people in malaria-endemic areas can get both COVID-19 and malaria at the same time. Both diseases can cause blood clotting issues, so having both can make the illness worse. Early diagnosis and prompt treatment are key to avoiding serious complications.\"\n}"}
+{"row_index": 293, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 23-year-old male patient presented to the Universitas Airlangga Hospital emergency department with a 5-day history of fever, anosmia, headache, and nausea. SARS-CoV-2 RNA was detected by RT-PCR amplification from a nasopharyngeal swab, confirming a diagnosis of COVID-19. Initial laboratory findings included lymphopenia, neutrophilia, thrombocytopenia, and elevated C-reactive protein (CRP), with a normal chest X-ray. The patient was managed according to the Indonesian National COVID-19 Treatment Guidelines, receiving favipiravir at 1600 mg every 12 hours on day 1, followed by 600 mg every 12 hours from day 2 to day 5, intravenous paracetamol 1000 mg every 8 hours, oral vitamin C 500 mg every 8 hours, and oral vitamin D 1000 IU daily. Despite this treatment, the patient remained PCR-positive after 10 days with no clinical symptoms and was discharged to continue self-quarantine at home.\\n\\nTwo weeks later, the patient returned with recurrent fever occurring every 2 days, characterized by a distinct chilling-fever-sweating cycle, with peak temperatures ranging from 39.7° to 40 °C. The fever was partially controlled by paracetamol but recurred within 6 hours, accompanied by malaise and myalgia. The next day, the fever resolved, and the patient was ambulatory with normal physical examination findings: body temperature 38 °C, blood pressure 112/72 mmHg, heart rate 93 bpm, respiratory rate 20 breaths/min, and oxygen saturation 98% on ambient air. Body mass index (BMI) was 22.5 kg/m² (height 170 cm, weight 65 kg). All other physical exam parameters were within normal limits.\\n\\nLaboratory analysis revealed a white blood cell count of 8750/µL with 76.3% neutrophils, 13.5% lymphocytes, and 0.6% eosinophils; hemoglobin 12.2 g/dL, platelet count 231,000/µL; CRP"}
+{"row_index": 294, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 52-year-old man from North Africa who smoked for 30 years came in with chest pain that got worse with activity. He had high blood pressure and bad cholesterol, and had ignored his symptoms for 10 years. His heart exam was normal, and his lungs and legs were fine. His heart’s main pumping chamber (left ventricle) was healthy — it was the right size and working well, even though one major blood vessel in his heart was completely blocked. The right side of his heart was also fine. Doctors found a major blockage in the main artery feeding the left side of the heart, and a narrow spot in the right coronary artery. He had surgery to fix it using grafts from his chest and leg. The surgery went smoothly, and he recovered well. He was out of hospital in 9 days. Six months later, he had no chest pain, no shortness of breath, and his heart was working normally again. His heart test results showed no signs of damage or trouble.\"\n}"}
+{"row_index": 295, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 52-year-old North African man with a 30-year history of smoking and high blood pressure presented with unstable angina that had been worsening over the past few days. He had ignored his symptoms for 10 years, including chest pain and shortness of breath during activity. Tests showed a complete blockage in his left main coronary artery, with a significant narrowing in his right coronary artery. Surprisingly, his left ventricle — the main pumping chamber of the heart — was normal in size and function, despite the severe blockage. He underwent successful on-pump coronary artery bypass grafting (CABG) surgery, where blood flow was rerouted around the blocked arteries using grafts taken from his chest and leg. The surgery went smoothly, and he recovered well, being discharged after 9 days. At 6 months follow-up, he had no chest pain or shortness of breath, normal heart function, and a healthy physical exam. His heart rhythm and overall heart health were stable, with no signs of heart failure.\"\n}"}
+{"row_index": 296, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 52-year-old North African male with a 30-year history of tobacco smoking presented to our department with unstable angina of 24-hour duration, secondary to a total chronic occlusion of the left main coronary artery (LMCA), with no antegrade flow in the left anterior descending artery (LAD) and circumflex artery (Cx). He had a history of hypertension and dyslipidemia, with controlled blood pressure at 142/83 mmHg during clinical evaluation, and a body mass index of 25 kg/m². Physical examination revealed normal heart sounds, absent murmurs, clear lung auscultation, no peripheral edema, and normal carotid artery flow. Resting electrocardiogram (ECG) demonstrated normal sinus rhythm at 55 bpm without ST-segment elevation, but showed persistent anteroseptal Q waves and inverted T-waves in apical and lateral leads, suggesting prior myocardial injury or ischemia. Transthoracic echocardiography confirmed normal left ventricular (LV) size and systolic function, with an LV ejection fraction of 68%, normal segmental wall motion, and low LV filling pressures. Systolic pulmonary artery pressure was 24 mmHg, and right ventricular size and function were within normal limits, indicating preserved right heart function. Coronary angiography revealed total occlusion of the LMCA, with dominant right coronary artery (RCA) perfusing the left coronary territory via extensive collateral circulation, despite a significant stenosis in the RCA itself. This paradoxical preservation of left ventricular function, despite severe left main disease and extensive ischemia, suggests a robust compensatory collateral network and minimal ischemic myocardial damage. The patient was referred for elective on-pump coronary artery bypass grafting (CABG) two days post-angiography. Anesthesia was induced with cisatracurium besylate, midazolam, thiopental, and propofol, and a median sternotomy was performed for harvesting of the internal thoracic arteries (ITA) and saphenous vein graft (SVG). The right internal thoracic artery (RITA) was anastomosed to the left internal thoracic artery (LITA) to form a composite 'LITA-RITA-Y' graft configuration, enhancing graft viability and flow distribution. Cardiopulmonary bypass was established via aortic and"}
+{"row_index": 297, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A woman had headaches for months, then got a stroke that only affected her senses, like numbness in her face and arm. Doctors first thought it was a virus, but her brain scans and fluid tests didn’t show that. Later, they found tiny worms in her brain fluid — specifically, a type of worm called Taenia solium — which means she had a brain infection from a parasite. Tests confirmed the worm was there, and her body made antibodies to fight it. After taking medicine to kill the worms, the amount of worm DNA in her brain fluid went down a lot. Her headaches got better, and after 3 months, she was feeling fine. The worms didn’t completely disappear, but the infection is now under control.\"\n}"}
+{"row_index": 298, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"This study describes a woman in her 40s who had headaches for several months, which later turned into a pure sensory stroke — meaning she lost sensation in her face and arm but had no movement problems. Initially, doctors thought it might be a virus, so she was given antiviral medication, but her symptoms didn’t improve. An MRI and other brain scans were normal at first, but later imaging showed small lesions in her brain, and her spinal fluid pressure was very high. After treatment for possible blood clot issues, her headaches remained severe. Tests on her spinal fluid found a high white blood cell count and elevated protein levels. A key test called next-generation sequencing (NGS) detected DNA from a parasite called Taenia solium, which causes cysticercosis. This was confirmed by positive antibodies in her spinal fluid. The patient was treated with antiparasitic medication (praziquantel), and follow-up tests showed a big drop in the parasite DNA levels. Her headaches improved significantly, and after six months, she had no symptoms left. Although some brain lesions remained, the infection was successfully treated.\"\n}"}
+{"row_index": 299, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 44-year-old female factory worker presented with a 12-month history of recurrent, temporal and parietal headaches characterized by burst-like pain, initially evaluated at a local hospital in April 2016. Initial brain magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) were normal. Cerebrospinal fluid (CSF) analysis revealed a white blood cell count of 68 cells/μL and an intracranial pressure of 310 mmH₂O, prompting suspicion of viral encephalitis. She was treated with intravenous acyclovir (500 mg every 8 hours for 7 days), but symptoms remained unchanged. Three months later, in July 2016, she presented with worsening headache and paroxysmal numbness of the left face and arm, diagnosed as an ischemic stroke involving the right thalamus. She was initiated on oral aspirin 100 mg and atorvastatin 20 mg daily; numbness improved, but headache persisted. Five days prior to presentation at our institution, she returned to the local hospital due to severe headache on October 26, 2016, with lumbar puncture findings indicating CSF pressure >400 mmH₂O, white cell count of 40 cells/μL, and protein level of 1171 mg/L. Cerebral magnetic resonance venography (MRV) demonstrated underdevelopment of the right lateral sinus, with sinus thrombosis considered as a potential etiology. She was treated with low molecular weight heparin, resulting in partial headache relief. She was subsequently admitted to our hospital for further evaluation.\\n\\nThe patient had no significant past medical history, denied blood transfusions or consumption of raw food. Physical examination was unremarkable except for horizontal nystagmus. Laboratory testing revealed a mild elevation in eosinophil count (3.35%), with all other indices within normal limits. Serologic tests for HIV, syphilis, Herpes simplex virus types 1 and 2, tuberculosis (T-Cell spot test, purified protein derivative), and cryptococcal antigen (latex agglutination) were negative. Three lumbar punctures performed during admission confirmed persistently elevated intracranial pressure and increased white blood cell counts.\\n\\nCerebral MRA showed no abnormalities, while MR"}
+{"row_index": 300, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 25-year-old woman from Kuwait, who had her first baby and was not married to someone from her family, was healthy before pregnancy. She went to a private clinic for check-ups, but no ultrasounds were done. She didn’t have diabetes or any past health problems. At 31 weeks, she went to the hospital because her water broke after 3 hours. She was fine when she arrived — no fever, normal breathing, and her heart was okay. The baby was in a breech position (feet first), not in labor yet. The doctors gave her antibiotics to prevent infection and gave her medicine to help her baby’s lungs grow. After 8 hours, she started having labor pains, and the doctor found the cervix was fully open. The baby was born early — weighing 1570 grams — and had a score of 3 out of 10 at first (meaning it needed help). The baby had serious birth problems: legs fused together, unclear genitals, a hole where the bladder and bowel should be, and a tube connecting the windpipe to the esophagus. The baby was taken to a special care unit for help. Doctors found no major chromosome issues, but the baby had missing or fused bones, a single opening for urine, and a blocked part of the intestines. Surgery was done to fix the intestines and create tubes to feed the baby. The left kidney had many small bags, and the right kidney wasn’t seen (might be in a strange place). The baby stayed in the hospital for 123 days and was finally sent home to continue treatment in the USA. The parents agreed to share this story with doctors and pictures, with their full permission.\"\n}"}
+{"row_index": 301, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"Mrs. RB, a 25-year-old Kuwaiti woman who was pregnant for the first time, had a normal pregnancy until she was admitted to the Maternity Hospital in Kuwait at 31 weeks of gestation. She had a 3-hour history of ruptured amniotic membranes, which means the sac surrounding the baby had broken. She was not known to have diabetes, and her medical and surgical history was normal. Her family did not have a history of diabetes.\\n\\nAt admission, she was healthy, with normal vital signs and no signs of infection or breathing problems. The baby was in a breech position (feet or buttocks down), and the pregnancy was confirmed to be at 31 weeks. She was given antibiotics to prevent infection and dexamethasone to help the baby’s lungs mature. After 8 hours, she started having labor pains, and the cervix was fully open. The baby was delivered by assisted breech delivery, weighing 1570 grams. The baby’s Apgar score was 3 at 1 minute and 9 at 5 minutes, which means it needed immediate medical support to start breathing.\\n\\nThe newborn had several serious birth defects, including fused lower limbs, ambiguous genitalia, a cloacal anomaly (a single opening for urine, stool, and sometimes waste), and a tracheoesophageal fistula (an abnormal connection between the windpipe and the esophagus). The baby was taken to the neonatal intensive care unit (NICU) for close monitoring and treatment. Tests showed the baby had a normal number of chromosomes (46 XX), but there were major structural problems in the bones and organs.\\n\\nSurgery was needed to fix the bowel issues, including a blocked part of the small intestine and a blocked colon. The esophagus was tied off, and a feeding tube was placed to help the baby get nutrition. The kidneys were also affected — the left kidney had many cysts, and the right kidney was not visible, which may mean it was in an unusual position.\\n\\nThe baby stayed in the hospital for 123 days and was eventually discharged to continue treatment in the USA. The parents gave their consent for the case to be reported, including the use of medical images and details, after discussing it with the doctors.\"\n}"}
+{"row_index": 302, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"Mrs RB, a 25-year-old Kuwaiti woman with a primigravida history, married for 18 months to a non-consanguineous partner, presented at 31 weeks of gestation to the Maternity Hospital, Kuwait, with a 3-hour history of ruptured membranes. The pregnancy was spontaneous and had been managed in a private health care setting with no prior antenatal ultrasonographic surveillance; the patient provided no documentation of such imaging. There was no history of diabetes mellitus, and her surgical, medical, and gynecological history was non-contributory. On admission, she was afebrile, hemodynamically stable, with normal vital signs, clear lung sounds, and normal cardiac examination. Obstetric examination confirmed gestational age consistent with 31 weeks, a single fetus in frank breech presentation, and normal fetal heart activity. No signs of intrauterine distress were detected.\\n\\nThe patient was managed conservatively with prophylactic antibiotics to prevent ascending infection and administered a course of dexamethasone (typically 6 mg intramuscularly, repeated every 6 hours for 24 hours) to promote fetal lung maturation in anticipation of premature delivery. She was transferred to the antenatal ward for monitoring. Eight hours later, she was readmitted to the labor ward with onset of labor pains. Pelvic examination revealed complete cervical dilation (10 cm) and a frank breech presentation at station 1 cm below the ischial spine, indicating a clinically significant fetal position for delivery.\\n\\nAn assisted breech delivery was performed due to the non-reassuring fetal position and the premature gestational age. The newborn had a birth weight of 1570 g (approximately 3.46 lbs), and Apgar scores of 3 at 1 minute and 9 at 5 minutes were recorded, indicating initial compromise requiring immediate resuscitation. An endotracheal tube was inserted to secure the airway, and active neonatal resuscitation was initiated, including positive pressure ventilation and chest compressions as needed.\\n\\nThe neonate exhibited multiple congenital anomalies: bilateral lower limb fusion (syndactyly with complete fusion of the tibial and fibular segments), ambiguous genitalia, cloacal anomaly (a single, patent cloaca with malformation of the anorectal and urogenital tracts), and tracheoesophage"}
+{"row_index": 303, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 20-year-old woman had surgery to fix a curved spine and join the bones together using screws and hooks from T3 to T12. After the surgery, on day 2, she had a sudden drop in oxygen levels, so doctors did tests to make sure her lungs weren’t blocked by a blood clot. The tests showed no clot, but the scan found her heart was stretched and had a big hole in the wall between the two upper chambers — a hole that had been there all along but didn’t cause symptoms. They also found one of the screws was bent to the side and was very close to her main blood vessel (aorta). Doctors decided first to fix the heart hole, which was done safely and she recovered well. After that, they checked the screw again with special scans to make sure it wasn’t poking into or touching the blood vessel — and it wasn’t. Two years later, they safely removed the screw and the rest of the hardware. The spine stayed strong and straight, and no problems came back after that. Everyone involved, including heart and spine specialists, watched closely to make sure everything was safe.\"\n}"}
+{"row_index": 304, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 20-year-old woman had surgery to correct a curve in her spine (scoliosis) and fuse the spinal bones from T3 to T12 using screws and hooks. After the surgery, on post-operative day 2, she experienced sudden drops in oxygen levels, which led to tests to check for a blood clot in her lungs. These tests were negative, but the CT scan showed that her right side of the heart was enlarged, indicating a large hole in the heart wall (atrial septal defect or ASD) that had been present but not causing symptoms before. During the same scan, a small problem was found with a screw at the left T10 level — the screw tip was very close to the aorta, the main blood vessel in the chest. Because the heart issue was more urgent, the medical team focused on fixing the heart first. She had successful surgery to repair the hole in her heart and recovered well. After that, a follow-up CT scan helped map the position of the screw. Additional imaging, including angiography and ultrasound, showed the screw was not inside or pressing on the aorta. Two years later, the team decided to remove the screw safely, with a vascular surgeon and interventional radiologist on standby. The spine was reopened, the screws were removed, and the fusion site was reinforced with bone graft. The patient has been followed up for two years with no signs of spine curve returning or complications.\"\n}"}
+{"row_index": 305, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 20-year-old female underwent posterior spinal deformity correction and spinal fusion for presumed adult idiopathic scoliosis, with posterior spinal instrumentation consisting of pedicle screws and hooks extending from T3 to T12. Preoperative evaluation, including electrocardiography (ECG), revealed no abnormalities, and her medical history was unremarkable, with normal physical activity levels including participation in sports. The anesthetic induction and surgical procedure were uncomplicated, with stable intraoperative neuromonitoring demonstrating consistent motor and sensory nerve potentials throughout the operation. Postoperative course was initially uneventful until post-operative day 2, when the patient experienced episodes of acute desaturation. This prompted evaluation with duplex ultrasound Doppler of the bilateral lower extremities and computed tomography pulmonary angiography (CTPA) to exclude pulmonary embolism. Both studies were negative for pulmonary embolism, but the CTPA revealed a right heart strain pattern and an enlarged right ventricular chamber, consistent with chronic volume overload. Subsequent two-dimensional echocardiography identified a large atrial septal defect (ASD), which had remained clinically asymptomatic until this point. In addition, the CTPA demonstrated a lateral breech at the left T10 pedicle screw level, with the screw tip in close anatomical proximity to the aortic wall, though no evidence of intraluminal penetration was observed. A multidisciplinary team convened and determined that cardiac management should be prioritized due to the significant hemodynamic impact of the ASD, with the malpositioned screw to be monitored and removed in a subsequent staged procedure. The ASD was successfully repaired via a surgical closure technique, with uncomplicated recovery and normalization of cardiac function. Following cardiac repair, a repeat computed tomography (CT) scan was performed to precisely delineate the position of the left T10 pedicle screw relative to the aorta. Angiographic imaging and intravascular ultrasound (IVUS) confirmed the absence of intra-luminal extension of the screw tip into the aortic lumen. A transesophageal echocardiogram (TEE) was additionally performed, which excluded any extra-luminal contact between the screw tip and the aortic wall. Two years after the initial scoliosis correction, a decision was made to proceed with removal of the spinal instrumentation. The midline surgical scar was reopened, and the spine was exposed across the T3–T12 previously fused segments. A solid"}
+{"row_index": 306, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 13-year-old girl was found to have a little bit of protein in her urine during a school health check. She was born very early, at 23 weeks, and was tiny—only 630 grams, like a baby at that stage. She had some breathing problems and eye issues as a baby, but grew up normally. Her blood pressure is normal, and her urine test showed a small amount of protein. Her kidneys were checked, and they were in stage 2 of kidney disease. Her uric acid level was high, which is not normal—her mom and her 16-year-old brother also have high uric acid. A small test on her kidneys showed a pattern that matches a condition called FSGS. After 3 years of medicine to help her kidneys, the protein in her urine went down, but her kidney disease stayed at stage 2. Doctors think her small size at birth was the first problem, and high uric acid later was the second problem that may have made her kidney disease worse.\"\n}"}
+{"row_index": 307, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 13-year-old girl was referred to the hospital after a school urine test found mild proteinuria. She was born very prematurely at 23 weeks of pregnancy, weighing only 630 grams — very low for her age. She had some breathing problems as a baby and needed oxygen for a year, but she grew up normally. She has no other major health issues.\\n\\nAt checkup, her urine test showed grade (2+) proteinuria, and her blood test showed a serum creatinine level of 1.02 mg/dL, which led to a diagnosis of stage 2 chronic kidney disease (CKD). Her uric acid level was 7 mg/dL, which is higher than normal (normal is less than 4.6 mg/dL), meaning she had hyperuricemia. Both her mother and her 16-year-old brother also have high uric acid levels.\\n\\nA kidney biopsy showed signs of a condition called FSGS, where parts of the kidney’s filtering units are damaged. The kidney tissue was also showing some scarring and enlarged filtering areas. Tests for common antibodies were negative, supporting this diagnosis.\\n\\nShe has been treated with an angiotensin receptor blocker (ARB) for three years, and her proteinuria has improved. However, her kidney function hasn’t fully recovered — her creatinine level is now 1.07 mg/dL, and she still has stage 2 CKD. Doctors believe her early low birth weight was the first factor that may have damaged her kidneys, and her high uric acid levels (the second factor) may have worsened the damage. This suggests that both factors played a role in the development of her kidney disease.\"\n}"}
+{"row_index": 308, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"proficient_health_literacy\": \"A 13-year-old female was referred to our hospital due to mild proteinuria identified during a school-based urinary screening. No prior history of urinary abnormalities existed. She was born at 23 weeks and 6 days of gestation, secondary to maternal fever, with a very low birth weight (LBW) of 630 g, corresponding to the size expected at 23 weeks of gestation. She developed chronic lung disease and retinopathy of prematurity, requiring supplemental oxygen therapy until age 1 year; however, her postnatal growth and neurodevelopmental trajectory normalized by that time. Beyond retinopathy of prematurity, she had no significant comorbidities and remained generally healthy throughout childhood.\\n\\nPhysical examination revealed a height of 154 cm, weight of 50 kg, body mass index (BMI) of 21.1, and blood pressure of 115/73 mmHg. Dipstick urinalysis demonstrated grade (2+) proteinuria. Her serum creatinine level was 1.02 mg/dL, leading to a diagnosis of stage 2 chronic kidney disease (CKD) using age- and sex-matched reference values for Japanese children aged 12–15 years. Her serum uric acid level was 7 mg/dL, which exceeds the normal range of <4.6 mg/dL for female children aged 12–14 years, confirming hyperuricemia. Both her mother and her 16-year-old brother also exhibit hyperuricemia, suggesting a possible familial predisposition.\\n\\nPercutaneous renal biopsy revealed segmental glomerulosclerosis in one of eight glomeruli, characterized by sclerosis with adhesion to the Bowman’s capsule (indicated by black arrow), and partial focal interstitial fibrosis (indicated by white arrow). The mean glomerular diameter measured 348.23 μm, significantly larger than the normal glomerular diameter of 168 ± 12 μm, indicating glomerular hypertrophy—a known pathological feature in focal segmental glomerulosclerosis (FSGS). Immunofluorescence staining for IgG, IgA, IgM, C3, C1q, and C4 was negative, excluding immune-mediated glomerulonephritis and supporting a diagnosis of native FSGS, specifically non-immune, likely of the"}
+{"row_index": 309, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 17-year-old girl was taking two medicines for mental illness — lithium and paliperidone — because she had mood swings and heard voices. After a few weeks, she started feeling dizzy, slow, and had a slow heart rate. Her doctor found that her thyroid was not working right and her heart was beating too slowly. These problems went away completely after she stopped taking both medicines. Her heart rate and thyroid levels returned to normal in about 20 days. The doctor thinks the medicines caused these issues, not something else. She now takes a different medicine for her mental health and doesn’t need a pacemaker because her heart fixed itself.\"\n}"}
+{"row_index": 310, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 17-year-old Han Chinese girl developed symptoms like dizziness, sluggishness, and chest tightness while being treated with lithium and paliperidone for bipolar disorder with hallucinations. She had been diagnosed with bipolar I disorder and was started on these medications during a prior hospitalization. Two months later, her paliperidone dose was reduced, but one week before her visit, her symptoms worsened. Her heart rate was low at 41 beats per minute, and an ECG showed sinus bradycardia and sinus arrest. Blood tests revealed elevated thyroid-stimulating hormone and low thyroid hormone levels, indicating hypothyroidism. Although the symptoms were mild, they were linked to her medication use. The doctors believed the combination of lithium and paliperidone caused these issues. After stopping both medications, her thyroid function and heart rhythm returned to normal within 20 days. She did not need a pacemaker because her heart rhythm improved on its own. She was switched to olanzapine for her mental health condition. The timing of her symptoms and recovery supports the idea that the medications were responsible, not an underlying heart or thyroid disease.\"\n}"}
+{"row_index": 311, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 17-year-old Han Chinese female presented to the psychiatric outpatient clinic with a one-week history of dizziness, lethargy, and impaired school attendance. Her psychiatric history included a prior hospitalization three months earlier for bipolar disorder with psychotic features, specifically auditory hallucinations, meeting DSM-5 criteria for bipolar I disorder based on a documented manic episode and prior major depressive episodes. During admission, she was initiated on lithium carbonate 500 mg twice daily and paliperidone 9 mg (equivalent to 450 mg chlorpromazine) once daily. Two months later, the paliperidone dose was reduced to 6 mg (equivalent to 300 mg chlorpromazine) once daily. One week prior to her outpatient visit, she developed worsening dizziness, chest tightness, and generalized sluggishness. She reported no personal or family history of cardiac or thyroid disease, no smoking, alcohol use, or illicit drug use; however, these reports were self-identified and not corroborated by clinical documentation. Pre-treatment, she had no known history of thyroid dysfunction or bradycardia.\\n\\nOn physical examination, her heart rate was 41 beats per minute, consistent with sinus bradycardia, and blood pressure was 95/57 mmHg. Electrocardiography revealed sinus bradycardia and sinus arrest. Serum electrolytes (calcium, potassium) and myocardial enzymes were within normal limits. Thyroid function tests demonstrated an elevated thyroid-stimulating hormone (TSH) of 9.08 mIU/L (reference range: 0.51–4.94 mIU/L), a decreased total thyroxine (TT4) of 45.05 nmol/L (reference range: 58.1–140.6 nmol/L), and a reduced free thyroxine (FT4) of 10.94 pmol/L (reference range: 11.5–22.7 pmol/L), indicating subclinical hypothyroidism without overt clinical manifestations. The patient and her guardian denied any family or personal history of cardiac or thyroid pathology, and no other medications known to induce conduction delays were identified. Although serum lithium levels were not measured due to assay unavailability, her serum paliperidone concentration was within the therapeutic range.\\n\\nThe clinical presentation—sympt"}
+{"row_index": 312, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 56-year-old woman had been bleeding from her intestines for years, causing fatigue and dizziness. She had small blue bumps on her skin since childhood that grew over time. The bleeding got worse and led to a serious blood problem where blood clots formed all over her body. Tests showed her blood was very low in red cells and had too many clotting markers. She was treated with a procedure called argon plasma coagulation during a special camera check of her intestines, and also took a medicine called sirolimus. After about 8 weeks, her blood levels improved and she stopped bleeding. One year later, she was doing well, her blood counts were stable, and she had not had any more bleeding.\"\n}"}
+{"row_index": 313, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 56-year-old woman was admitted to the hospital with a 3-year history of fatigue and dizziness, which had worsened over the past 10 days with severe bleeding (melena). She had been hospitalized multiple times before for similar symptoms and had a history of many small, blue growths (venous hemangiomas) since childhood. These growths grew larger and more numerous over time. Tests showed she had severe anemia and a condition called disseminated intravascular coagulation (DIC), where blood clots form throughout the body and then break down, leading to bleeding and low blood clotting. Despite treatment, her hemoglobin levels remained very low, between 39 and 61 g/L, and she required many blood transfusions each year.\\n\\nNo clear source of bleeding was found during endoscopy or colonoscopy. Skin ultrasounds confirmed the blue hemangiomas on her skin. Blood tests showed abnormal clotting times and very low fibrinogen, along with high levels of substances that indicate active clot breakdown.\\n\\nThe doctors diagnosed her with blue rubber bleb nevus syndrome (BRBNS), a rare condition that causes multiple hemangiomas and can lead to bleeding in the intestines. Treatment included argon plasma coagulation (a procedure done during endoscopy to stop bleeding) and the medication sirolimus. After about 8 weeks of treatment, her hemoglobin improved to 100 g/L. At a 12-month follow-up, she was doing well with stable hemoglobin at 102 g/L and no further bleeding.\"\n}"}
+{"row_index": 314, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 56-year-old female presented with massive intestinal hemorrhage, characterized by a progressive and persistent bleeding course over three years, with acute exacerbation over the past 10 days manifesting as melena. The patient had a longstanding history of chronic constipation and multiple venous hemangiomas since childhood, which demonstrated progressive increase in both number and size with aging. No familial history of hemangiomas or related vascular disorders was identified. Physical examination revealed significant anemia and multiple cutaneous blue hemangiomas protruding from the skin surface, confirmed by skin ultrasound as vascular malformations. Laboratory findings demonstrated severe hematological abnormalities: white blood cell count of 1.78 × 10¹²/L (normal: 3.80–5.10 × 10¹²/L), hemoglobin of 39 g/L (normal: 115–150 g/L), platelet count of 71 × 10⁹/L (normal: 125–350 × 10⁹/L), and positive fecal occult blood. Coagulation profile revealed marked dysregulation: prothrombin time of 17.7 seconds (normal: 9.5–15.0 sec), activated partial thromboplastin time of 55.8 seconds (normal: 20.0–40.0 sec), prothrombin time-international normalized ratio of 1.65 (normal: 0.80–1.50), fibrinogen level of 0.349 g/L (normal: 1.800–4.000 g/L), D-dimer >10,000 ng/mL (normal: 0–500 µg/mL), tissue plasminogen activator-inhibitor 1 complex of 14.10 ng/mL (normal: 0.00–10.50 ng/mL), and plasmin-α2 cellulase inhibitor complex of 12.23 µg/mL (normal: 0.00–0.80 µg/mL), consistent with a fibrinolytic-type disseminated intravascular coagulation (DIC). Imaging studies, including abdominal computed tomography and digital subtraction angiography with mesenteric arteriography, failed to identify any definitive source"}
+{"row_index": 315, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 32-year-old woman had a cough that got worse and started spitting out a lot of blood. The blood was so big it blocked her airway and she almost died. Doctors couldn’t clear the blockage with normal methods, so they used a thin tube (bronchoscope) to go inside her airway and used a medicine called urokinase to break up the blood clots. The clots were removed, and the airway opened up. After that, she was able to stop using the life-support machine, her breathing tube was removed, and she was taken off the ventilator. Now she’s stable. X-rays and scans show her lungs are getting better.\"\n}"}
+{"row_index": 316, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 32-year-old woman was admitted to the hospital with a cough that had lasted for 7 days and had suddenly worsened with large amounts of blood in her cough (hemoptysis) over the previous 9 hours. She had a history of Hashimoto thyroiditis, but it was not well managed. Chest CT scans showed pneumonia with bleeding in the lungs and thick mucus plugs blocking the airways, especially in the right lung. Her condition quickly got worse, with a large amount of fresh blood and a blood clot in her airway. Her oxygen levels were very low, and her breathing was difficult. Because standard methods to clear the airway were not working, doctors decided to use a procedure called fiberoptic bronchoscopy, combined with a medication called urokinase, to remove the large blood clots. This successfully cleared the blockage in her airway. After treatment, she was able to be taken off the life-support machine (extracorporeal membrane oxygenation), had her breathing tube removed, and was safely taken off the ventilator. Her current condition is stable, and follow-up chest X-rays and CT scans show improvement compared to when she first arrived at the hospital.\"\n}"}
+{"row_index": 317, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 32-year-old female was admitted to the hospital on May 17, 2023, at 15:51 with a chief complaint of a cough lasting seven days that had progressively worsened over the preceding nine hours, presenting with hemoptysis of 100 mL of blood. She had a history of Hashimoto thyroiditis, which was not systematically managed. Initial chest computed tomography (CT) revealed bilateral pneumonia with alveolar hemorrhage, prompting a recommendation for reevaluation post-treatment. Additionally, multiple bronchial mucus plugs were identified in the right main bronchus and in the middle and lower lobes of the right lung, suggesting obstructive airway pathology due to mucopurulent secretions and impaired clearance mechanisms. During the same day's afternoon, she experienced a recurrence of hemoptysis, characterized by a large volume of fresh blood mixed with a small amount of blood clot, indicating active intrapulmonary hemorrhage and potential clot formation within the airway lumen. Physical examination demonstrated a temperature of 36.2 °C, tachycardia (pulse: 128 beats/min), tachypnea (respiration: 25 breaths/min), hypotension (blood pressure: 75/49 mm Hg), and severe hypoxemia (finger-tip oxygen saturation: 50%). Breath sounds were diminished in the right lung, consistent with airway obstruction, while the left lung exhibited prominent moist rales, suggestive of interstitial fluid accumulation or pulmonary edema. Given the severity of airway obstruction and the failure of conventional clearance techniques—including postural drainage and mechanical suction—fiberoptic bronchoscopy was performed in conjunction with urokinase therapy. Urokinase, a serine protease that activates plasminogen to plasmin, was administered to induce fibrinolysis, thereby promoting the dissolution of intrapulmonary blood clots and facilitating their mechanical extraction via bronchoscopic instrumentation. The procedure successfully removed extensive intrapulmonary blood clots, leading to immediate relief of airway obstruction. Subsequent management included weaning from extracorporeal membrane oxygenation (ECMO), successful extubation, and liberation from mechanical ventilation. Post-intervention follow-up imaging, including chest X-ray and high-resolution computed tomography (CT), demonstrated significant improvement in lung parenchymal density and airway pat"}
+{"row_index": 318, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A man in his 70s had bleeding in his stomach area and pain for a few days. Doctors found a tumor in his small intestine that had spread to his groin. This rare kind of tumor, called GIST, was already growing in his belly and had moved into a hernia in his groin. The doctors first removed the main tumor and the spread parts, then fixed the hernia with surgery. After that, he took medicine to fight the tumor. Later, they found the tumor had grown inside the hernia, so they removed it completely. The man is still doing well, no pain, no return of the hernia, and can go about his daily life. In the past, very few people had this tumor show up in a groin hernia. All known cases needed both tumor removal and hernia repair. After 5 years, about 6 out of every 10 people with this disease are still alive.\"\n}"}
+{"row_index": 319, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 71-year-old man came to the hospital with severe abdominal pain and blood in his stool that had lasted for 38 hours. He had no other medical problems or prior surgeries. During the exam, his abdomen was tender, and a mass was found in his small intestine on CT scan, which was causing bleeding. A small mass was also seen in his groin, but it was not noticed at first. The surgery showed a gastrointestinal stromal tumor (GIST) in the jejunum, with spread to other areas of the abdomen. The tumor was removed with a partial resection (R1), and the bowel was reconnected. The patient recovered well and was discharged after 11 days. Pathology confirmed it was a high-risk GIST with fast-growing features. After surgery, he started imatinib chemotherapy for three months. Later, he developed a painful, non-reducible hernia in his right groin, which was confirmed to be a metastasis of the same GIST. The hernia was repaired with surgery, and the tumor was removed along with the hernia sac. The final path report showed the tumor had spread to the groin and was still aggressive. He continued imatinib treatment and has been doing well at his last follow-up in February 2020—still alive and able to work without any signs of recurrence. A review of similar cases shows that GIST presenting as a groin hernia is very rare, and all such cases involved a primary tumor that needed both tumor removal and hernia repair. Long-term survival after diagnosis was about 64.3% at 5 years.\"\n}"}
+{"row_index": 320, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 71-year-old male presented to the emergency department with a 38-hour history of diffuse abdominal pain and intermittent hematochezia. He denied other gastrointestinal or genitourinary symptoms and had no prior abdominal surgery or significant comorbidities. Physical examination revealed abdominal tenderness with extensive rebound tenderness; however, the groin was not systematically examined due to the absence of specific complaints. Laboratory evaluation demonstrated hypohemoglobinemia (9.6 g/dL). Contrast-enhanced computed tomography (CT) identified lower gastrointestinal bleeding originating from a ruptured mass measuring 5.2 × 4.1 × 3.0 cm³ located in the small intestine, specifically the third jejunal segment (220 cm from the duodenal-jejunal flexure). Concurrently, CT imaging detected a small mass (2.0 × 1.5 × 0.5 cm³) in the right groin, which was not explicitly noted in the initial emergent report.\\n\\nGiven hemodynamic instability, the patient underwent emergent laparotomy. Intraoperative findings revealed a primary gastrointestinal stromal tumor (GIST) arising from the jejunal wall, with disseminated, multi-focal tumor seeding throughout the peritoneal cavity. A palliative resection was performed, encompassing the primary tumor and all seeding lesions exceeding 2 mm in size, resulting in an R1 resection (resection with microscopic residual disease), followed by side-to-side jejunal anastomosis. The patient was discharged on post-operative day 11 without complications.\\n\\nHistopathological analysis of the primary tumor demonstrated spindle cell morphology, with a high mitotic rate (25/50 high-power fields, HPF) and significant areas of tumor necrosis (see Additional file: Fig. S1). Immunohistochemical (IHC) staining showed strong positivity for CD117, DOG-1, and SDHB; mild positivity for actin and desmin; and negativity for CD34 and S-100. The Ki-67 proliferation index was 20%. Molecular profiling revealed a mutation rate of 18.22% in the c-KIT gene, specifically a duplication at exons 9 (A502_T503dup), classifying the tumor as high-risk jejunal GIST.\\n\\nPostoperative management included imatinib therapy at a dose"}
+{"row_index": 321, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 53-year-old woman who had two back surgeries before had a sudden worsening of her back pain, causing her legs to go weak and her bladder to stop working. This is a serious problem called cauda equina syndrome. Her blood tests showed signs of infection, and a scan found a pus-filled bump pressing on her spinal nerves from L4 to S1. The doctors drained the pus and found a small piece of old surgical cotton that had been left behind — it was causing the infection. The cotton was removed and the infection cleared after 2 months of antibiotics. The antibiotics worked, but her leg weakness only got better a little, not fully.\"\n}"}
+{"row_index": 322, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 53-year-old woman with a history of two back surgeries at the L4-S1 levels — one 11 years ago and another 2 years ago — developed a sudden, serious condition called cauda equina syndrome. This caused weakness in her legs (paraparesis) and loss of bladder control. She had mild signs of infection in her blood (elevated white blood cell count and C-reactive protein), which matched findings on MRI showing a large abscess in the spine from L4 to S1. The abscess was drained during surgery, and a small, hard lump found inside it was identified as a retained piece of surgical cotton (a known cause of long-term infection). This cottonoid was removed, and the infection was treated with ciprofloxacin for two months. The infection cleared, but her leg weakness only improved partially. The tissue around the cottonoid showed chronic inflammation and scar tissue, and no signs of infection returned after one year.\"\n}"}
+{"row_index": 323, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 53-year-old female with a longstanding history of low back pain underwent two prior spinal surgical interventions: an L5-S1 discectomy performed 11 years earlier and an L4-L5 decompressive laminectomy 2 years prior. Over a period of several weeks, she presented with an acute cauda equina syndrome, clinically manifesting as paraparesis and acute urinary incontinence. Physical examination revealed mild tenderness in the lower back region. Laboratory evaluation demonstrated a mildly elevated white blood cell count (12,600/mm³) and a significantly increased C-reactive protein level, consistent with acute inflammation, without evidence of urinary tract infection. Plain radiographic imaging confirmed the anatomical defects attributable to prior laminectomies at the L4-L5 and L5-S1 levels. Magnetic resonance imaging (MRI) revealed an oblong posterior epidural lesion extending from the L4 to S1 levels, which was hypointense on T1-weighted sequences and hyperintense on T2-weighted sequences, exhibiting ring enhancement after gadolinium administration—findings consistent with a post-infectious epidural abscess. Given the clinical and imaging features, a decompressive laminectomy was performed to relieve spinal cord compression. Intraoperatively, a well-encapsulated posterior epidural abscess was identified and drained. Histopathological analysis of the abscess wall revealed a granulomatous lesion, subsequently identified as a retained surgical cottonoid, located at the antero-inferior aspect of the abscess wall at the S1 level. This lesion was completely excised, along with adjacent marginal fibrotic capsular tissue. Microbiological culture of the thick, fibrotic abscess capsule yielded Klebsiella oxytoca, a Gram-negative bacillus commonly associated with nosocomial and postoperative infections. The patient was treated with intravenous ciprofloxacin for a duration of two months, after which the infection was fully resolved. However, despite successful eradication of the infectious process, the motor deficit associated with the cauda equina syndrome only partially recovered. Postoperative histopathology confirmed the presence of a textiloma, a fibrogranulomatous reaction to foreign body material, with chronic inflammation and extensive fibrosis surrounding the retained cottonoid. At one-year follow-up, no recurrence of infection was observed, indicating complete resolution of the infectious component and stable surgical outcome, though neuro"}
+{"row_index": 324, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 72-year-old man had cancer in his bile duct, so doctors removed part of his pancreas and small intestine (pancreaticoduodenectomy). After the surgery, his bile duct got blocked in one part, which made it hard for bile to flow. To fix this, doctors used a special test (DIC-CT) to see exactly where the bile duct was and how it was blocked. They found the blockage was in a small part of the bile duct, and the small intestine was raised up, which made it hard to connect. Using a tiny needle and CT guidance, they pierced the bile duct and checked it with a small camera. They pushed a thin wire through the needle and felt the wall of the bile duct vibrate — this showed the needle went right into the blocked area. When they did this, they saw the raised part of the small intestine was squeezed a little, which confirmed the needle was in the right spot. Then they placed a small tube (8.5-Fr pigtail catheter) into the raised small intestine to help bile flow. After that, they put in a metal stent to keep the tube open. The patient recovered well, went back to regular visits, and had no problems with the stent even after 6 months.\"\n}"}
+{"row_index": 325, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 72-year-old Japanese man had middle bile duct cancer and underwent surgery called a pancreaticoduodenectomy to remove the tumor. During the surgery, a complication occurred: a blockage in the posterior segment of the bile duct, which is a part of the bile duct system. To figure out how the bile duct and the elevated jejunum (a part of the small intestine) were positioned, doctors performed a drip infusion cholecystocholangiography-computed tomography (DIC-CT) test. This test showed that the bile duct was isolated and that there was no tissue or organ between it and the elevated jejunum, making it safe to connect them. Using CT guidance, the doctors made a small puncture in the bile duct and used an endoscope to see the connection site. They inserted a guide wire through a needle and felt vibrations in the bile duct wall, which confirmed the needle had reached the correct spot. When the wire was placed, they saw that the elevated jejunum was partially compressed, which helped confirm the puncture was successful. They then successfully placed an 8.5-Fr pigtail catheter into the elevated jejunum. After that, all drains were removed, and a metal stent was placed directly into the bile duct to keep it open. The patient recovered well and now visits the clinic as an outpatient. Six months later, the stent is still open and working without any problems.\"\n}"}
+{"row_index": 326, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 72-year-old Japanese male with no significant prior medical history was referred for evaluation of jaundice and impaired hepatic function identified during a routine health screening. Preoperative endoscopic retrograde cholangiopancreatography (ERCP) revealed stenosis in the middle bile duct, and biliary abrasive cytology confirmed a Class V adenocarcinoma, consistent with malignant obstruction. Imaging demonstrated a low bifurcation in the posterior segmental bile duct branch, which informed the surgical planning for pancreaticoduodenectomy due to middle bile duct cancer. Postoperatively, the patient remained asymptomatic with only mild postoperative inflammation, and was discharged on postoperative day 22. However, on postoperative day 30, blood work revealed elevated inflammatory markers, prompting further investigation. Contrast-enhanced computed tomography (CT) showed abscess formation adjacent to the hepaticojejunal anastomosis site and posterior segmental bile duct dilatation, suggesting bile leak or ischemic injury. Initial management included percutaneous transhepatic biliary drainage (PTBD), which demonstrated contrast filling only in the posterior segmental branch, with no evidence of bile leakage into the elevated jejunum. Subsequent endoscopic contrast radiography from the hepaticojejunal anastomosis site revealed visualization of only the anterior segmental branch and left branch, confirming the anatomical lesion was localized to the low bifurcation of the posterior segmental bile duct. Bile output via PTBD averaged approximately 250 ml/day over consecutive days. To assess the spatial relationship between the posterior segmental bile duct and the elevated jejunum, a drip infusion cholecystocholangiography-computed tomography (DIC-CT) test was performed. This imaging modality demonstrated contrast reflux into the elevated jejunum from the anterior segmental and left branches, while the posterior segmental branch was dorsally visualized with a poorly defined anatomical relationship to the jejunum. Notably, no intervening abdominal organs were identified between the bile duct and the elevated jejunum, supporting the feasibility of percutaneous transhepatic internal biliary drainage of the isolated posterior segmental bile duct into the elevated jejunum. Under computed tomography (CT) guidance, a precise puncture was made into the posterior segmental bile duct, followed by endoscopic visualization of the hepaticojejunal anastomosis site. A guide"}
+{"row_index": 327, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 19-year-old young man had surgery on his nose and nose bones. He was healthy before surgery, no problems with his voice or breathing, and no other medical issues. The doctors thought his airway was normal and safely able to handle anesthesia. During the surgery, they put a breathing tube in easily without any trouble. After the surgery, he started to have a hoarse voice, which lasted for several days. On the sixth day, doctors saw that one of the small bones in his voice box (the arytenoid cartilage) had slipped out of place. They fixed it with a small surgery under anesthesia, and his voice slowly got better over six weeks. He had no other symptoms or problems.\"\n}"}
+{"row_index": 328, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 19-year-old Caucasian male had a routine surgery for nose and nasal bone correction (septorhinoplasty). He had no known medical problems, such as diabetes, lung issues, or weakened joints, and was considered healthy before surgery (ASA Class I). His airway was normal, and intubation (inserting a tube into the windpipe) went smoothly without complications. The patient did not cough during the procedure, and the surgery lasted four hours with no issues. After surgery, he developed moderate hoarseness, which lasted for several days. On the sixth day, a doctor found that the left arytenoid cartilage — a small bone in the voice box — had moved out of place. This caused the hoarseness. The cartilage was gently repositioned under anesthesia using a bronchoscope and steroid injection. Over the next six weeks, his voice improved. He had no other symptoms and was discharged on the second day. This case shows that even in healthy young patients, a rare condition like arytenoid cartilage dislocation can occur after surgery, though it is usually treatable.\"\n}"}
+{"row_index": 329, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 19-year-old Caucasian male underwent septorhinoplasty under general anesthesia. His medical history was unremarkable, with no prior laryngeal pathology, diabetes mellitus, chronic renal failure, chronic corticosteroid use, laryngeal malacia, or acromegaly—all of which are known risk factors for cricoarytenoid joint instability. Preoperative evaluation, including physical examination and laboratory workup, was normal, consistent with an American Society of Anesthesiologists (ASA) physical status classification of I. Airway assessment revealed a class 2 airway, with normal Mallampati score and other standard airway parameters. Anesthesia was induced with thiopental (8 mg.kg⁻¹), rocuronium (0.6 mg.kg⁻¹), and remifentanyl (0.5 mcg.kg⁻¹), achieving complete muscle relaxation prior to endotracheal intubation. Using a Macintosh 4 laryngoscope blade, direct laryngoscopy demonstrated a short epiglottis and a glottis grade II according to the Cormack-Lahene classification, indicating a relatively straightforward visualization. A 8.0-mm endotracheal tube was successfully inserted on the first attempt without resistance, and was secured at the mid-trachea. The patient did not experience coughing or other reflexive responses during intubation. Intraoperative anesthesia was maintained with a mixture of nitrous oxide, oxygen, isoflurane, remifentanyl (0.25 mcg.kg⁻¹.min⁻¹), and rocuronium, with no complications during the four-hour surgical procedure. Postoperatively, the endotracheal tube was removed without incident, and the patient did not exhibit severe coughing or vomiting. On postoperative day 1, he reported moderate hoarseness, which persisted through day 6. No other symptoms were present. On day 6, fiberoptic laryngoscopy performed by an otorhinolaryngologist revealed anteromedial dislocation of the left arytenoid cartilage—a rare but clinically significant finding. This dislocation is likely due to a transient biomechanical disruption during the surgical maneuver or anesthesia-induced relaxation of the laryngeal musculature, possibly exacerbated by the inherent structural variability of the arytenoid cartilage in young individuals, though no predisposing conditions were identified"}
+{"row_index": 330, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A young, healthy woman found a lump on her small finger that had been growing for months. It got bigger during her pregnancy, almost the size of an olive, and caused pain when her baby grabbed it. First, doctors thought it was a common cyst, but it didn’t go away. Later, tests showed it was a type of cancer called leiomyosarcoma. There was a small bump in her armpit, but doctors said it wasn’t serious. The cancer was caught early and only in her finger. She had surgery to remove the finger (a ray amputation) and the cut was clean with no cancer left behind. After surgery, she had no pain, no new lumps, and her hand worked well. She’s been cancer-free for months and is doing great with physical therapy. Her scar is noticeable but she’s working on it. No signs of cancer have come back.\"\n}"}
+{"row_index": 331, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 24-year-old woman with no major health problems was diagnosed with a primary leiomyosarcoma in her small finger. The tumor had been growing for months, and its size changed depending on her pregnancy — it sometimes grew as large as an olive. She first visited urgent care, where the mass was thought to be a ganglion cyst, but it wasn't removed. Later, the mass became painful and started bleeding, leading to a biopsy that confirmed it was a low-grade leiomyosarcoma. Imaging showed a suspicious lymph node in her armpit, but doctors believed it was just a normal reaction, not cancer. The cancer was classified as stage 1A, meaning it was localized and early. A second opinion confirmed the diagnosis. After discussion with her medical team, she had a ray amputation of her small finger, removing the tumor at the level of the mid-metacarpal bone. The surgery was successful, with clear margins and no signs of cancer left behind. She also had nerve reinnervation to help preserve hand function. Following surgery, she had regular follow-ups and imaging, all of which showed no signs of cancer. She is now disease-free, with good hand function and no pain or new masses. She continues to do well and is recovering well with physical therapy.\"\n}"}
+{"row_index": 332, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 24-year-old right-hand dominant Hispanic female presented to an urgent care clinic in October 2021 with a palpable mass on the ulnar aspect of the proximal interphalangeal (PIP) joint of her right small finger, which had been present for several months. She reported cyclical changes in mass size, with growth during pregnancy—reaching up to the size of an olive—and worsening pain associated with her newborn's frequent grasping of the finger. Initial attempts at aspiration were unsuccessful, and the mass was initially diagnosed as a ganglion cyst. Subsequent evaluation by a local hand surgeon was planned but never executed. In March 2022, she returned with progressive pain and an open, bleeding wound at the original site, prompting imaging. Plain radiographs revealed a soft tissue mass near the PIP joint with incidental punctate calcifications. An excisional biopsy was performed on March 15, 2022, and reviewed by two independent pathologists, confirming a diagnosis of low-grade leiomyosarcoma of the finger. Immunohistochemical staining and histopathological analysis supported this diagnosis, showing characteristic expression of smooth muscle markers (e.g., desmin, caldesmon, SMA) and absence of features consistent with benign fibroblastic or epithelial tumors. A PET/CT scan performed in early April 2022 identified a suspicious right axillary lymph node, which the treating oncologist and general surgeon interpreted as reactive and benign, consistent with inflammatory or post-traumatic changes. The clinical and pathologic staging aligns with AJCC stage IIA, indicating a localized tumor with no regional lymph node metastasis. The primary lesion was also visible on PET/CT. A second opinion from a general surgeon reinforced the benign nature of the lymphadenopathy. In early May 2022, the tumor board at the treating institution recommended ray amputation as the most appropriate oncologic intervention given the tumor's location, histologic grade, and lack of evidence of systemic spread. Concurrent laboratory studies were unremarkable, with no signs of infection or systemic inflammation. On the same day, a new mass was noted distal to the original lesion on the small finger, with imaging consistent with a potential second focus of leiomyosarcoma. On June 15, 2022, the patient underwent successful right-hand minor finger ray amputation, with the small finger amputated"}
+{"row_index": 333, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 64-year-old woman who had cancer in her ovaries and was already treated before, now has pain, belly swelling, and trouble moving food through her gut. The cancer spread to her belly lining and intestines. After first treatment, she got better and had no cancer signs for a while. Then, the cancer came back. She tried a new drug combo — trabectedin and PLD — which worked well, and after a few cycles, she stayed in good shape. Even when she only took trabectedin alone, she kept getting better and stayed healthy for over two years. She had no major side effects and could do everyday things. This shows that trabectedin, even by itself, can help control this cancer for a long time.\"\n}"}
+{"row_index": 334, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 64-year-old woman who had recurrent ovarian cancer after menopause was treated with a second-line chemotherapy combination of trabectedin and PLD, followed by trabectedin alone. She had symptoms like abdominal pain, bloating, and changes in bowel movement, and imaging showed widespread cancer in her abdomen and pelvis. After initial treatment with chemotherapy and surgery, her cancer went into complete remission. However, it returned seven months later, prompting a switch to trabectedin and PLD, which worked well — her cancer markers dropped significantly. Although she had side effects like low blood counts, the treatment was well tolerated. After the combination was stopped due to toxicity, she continued with trabectedin alone, which kept her cancer under control for over two years. Even after a later recurrence, she responded to further treatment with bevacizumab, which she continues to take to maintain her response. The case shows that trabectedin, especially when used alone, can be effective and well tolerated in managing recurrent ovarian cancer over a long period.\"\n}"}
+{"row_index": 335, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 64-year-old Caucasian postmenopausal woman presented with persistent pain, abdominal distension, and altered intestinal transit, consistent with advanced gastrointestinal malignancy. Imaging via thoracic and abdominopelvic computed tomography (CT) revealed extensive peritoneal carcinomatosis, massive ascites, involvement of the greater omentum, diffuse mesenteric spread involving the small intestine, diffuse parietal peritoneal implants, and suspicious lesions at the base of the Douglas pouch with probable ovarian surface involvement despite normal ovarian size. Plasma CA-125 levels were 1,110.9 U/mL, with other tumor markers within normal limits. Omental biopsy confirmed high-grade serous carcinoma (HGSC), demonstrating positive immunohistochemical expression for WT-1, p53, and CK-7, and negative expression for CK20 and TTF-1, supporting a gynecological origin (tube-ovarian-peritoneal). The diagnosis was classified as primary peritoneal carcinoma of gynecological origin, stage IIIC, with unresectable disease due to extensive mesenteric infiltration.\\n\\nNeoadjuvant chemotherapy was initiated with intravenous paclitaxel 175 mg/m² and intravenous carboplatin AUC 6 administered every 21 days for three cycles. Follow-up CT imaging demonstrated a significant partial response, with CA-125 levels dropping to 65 U/mL (a 95% reduction from baseline). Subsequently, surgical cytoreduction was performed, achieving optimal tumor resection, and an intraperitoneal (i.p.) catheter was placed for future delivery of i.p. chemotherapy. Pathological evaluation of resected specimens confirmed high-grade serous carcinoma.\\n\\nAdjuvant intraperitoneal chemotherapy was delivered over four cycles: i.v. paclitaxel 175 mg/m² on day 1, i.p. cisplatin 75 mg/m² on day 2, and i.p. paclitaxel 60 mg/m² on day 8. The patient achieved a complete clinical response, although treatment-related toxicity included grade-2 asthenia and grade-3 neutropenia, necessitating dose delay and granulocyte-colony stimulating factor (G-CSF) support.\\n\\nSeven months after completion of platinum-based therapy, follow-up CT imaging revealed mediastinal"}
+{"row_index": 336, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 36-year-old woman who is overweight fell down the stairs and broke her right elbow. She had a break in the middle of her radius bone, a break near the top of the radius with a 15-degree twist, and her elbow popped out of place. First, the doctors fixed the popped-out elbow. Then they used surgery to fix the two breaks in the radius bone and put the elbow back in place. They made sure the elbow stayed stable and the soft parts around it were reattached. She wore a splint for 6 weeks and started moving her arm early, first with bending and straightening, then with turning her hand. After 6 weeks, she could only bend a little and turn her hand a little. By 3 months, she could bend and straighten much better and turn her hand more. By 5 months, she could move her arm almost normally again, and her thumb worked well. She was able to go back to work as a funeral director after 5 months.\"\n}"}
+{"row_index": 337, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 36-year-old woman with obesity suffered a fall down the stairs, which caused a break in her right radial bone (radial diaphyseal fracture), a break in the neck of the radius with about 15° angulation, and a dislocation of her elbow (posterolateral elbow dislocation). She was admitted for treatment. First, the doctors reduced the elbow dislocation and stabilized the broken radius bones using surgery. They also repaired the damaged structures around the elbow. A CT scan was done to check for damage to the elbow’s stabilizing parts, and no coronoid bone injury was found. The radial neck fracture did not fully heal initially, so a second surgery was performed using a specific approach between two muscles to fix the fracture and reattach the elbow’s posterior structures. The radial nerve was protected during surgery by keeping the elbow in a pronated position. After surgery, she wore a splint for 6 weeks and began physical therapy early, starting with gentle movement. By 3 months, she had regained most of her elbow motion, though she still had some numbness in her radial nerve area. By 5 months, her range of motion improved significantly, including full recovery of thumb movement, and she was able to return to her job as a funeral director.\"\n}"}
+{"row_index": 338, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 36-year-old female with obesity (BMI 34) was admitted following a low-energy fall down stairs, resulting in indirect trauma to the right elbow. Clinical examination revealed upper limb trauma without distal neurovascular compromise. Radiographic imaging demonstrated a 2R2A2 radial diaphyseal fracture and a 2R1A2 radial neck fracture with approximately 15° of angulation, along with a posterolateral humeroulnar dislocation. The initial intervention was emergency reduction of the humeroulnar dislocation, during which ligamentous stability was compromised due to the concomitant diaphyseal fracture. The patient was immobilized in a brachio-antebrachial-palmar (BABP) splint, and a computed tomography (CT) scan was performed to evaluate the integrity of the elbow's stabilizing ligamentous and bony structures, with no evidence of coronoid involvement identified.\\n\\nOsteosynthesis of the radial diaphysis was performed under regional anesthesia using a Synthes compression plate with a working length of two screw holes and a lever arm spanning six contiguous cortices on both sides, providing biomechanical stability through cortical interlocking. Post-reduction elbow assessment demonstrated no recurrent dislocation up to −40° of extension, though persistent displacement of the radial neck fracture remained.\\n\\nA Cadenat approach was employed to access the radial neck fracture, performed between the ulnar extensor and anconeus muscle, allowing direct visualization of the metaphyseal fragment shift while preserving the motor branch of the radial nerve by maintaining elbow pronation. The fracture was stabilized using an anatomical radial head plate (Trilock Radial Head Plates, Medartis), and the posterolateral elbow structures were reattached. Given the achieved joint stability, no additional medial stabilization procedures were indicated.\\n\\nPostoperative immobilization was maintained for 6 weeks in a BABP splint, with early rehabilitation initiated for flexion and extension. Pronation and supination were permitted beginning at the third week. At 6 weeks, range of motion was: flexion-extension 10°/0°/20°; pronation-supination 0°/0°/10°, with a deficit in thumb flexion. At 3 months, motion improved to flexion-extension 0°/40°/120°;"}
+{"row_index": 339, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A woman with a tough-to-treat ovarian cancer that kept coming back got sick and lost a lot of weight because of the tumors. Her cancer didn’t show the usual signs that help doctors treat it, and tests found it had low cancer activity, but two small changes in the tumor genes. The doctors tried a new treatment: a drug called pembrolizumab and another called bevacizumab, given every three weeks. After just one round, her cancer marker went down a lot. By the seventh round, it was back to normal. A scan showed the tumors shrunk a lot, and after nine rounds, the cancer was completely gone. She started to get better, gained weight, and her muscles and fat returned. The only side effect was mild joint pain in her hands. No other serious problems happened.\"\n}"}
+{"row_index": 340, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 42-year-old woman with advanced ovarian clear cell carcinoma (OCCC) had multiple surgeries and chemotherapy treatments, but her cancer returned and became difficult to control. Her tumors spread widely and caused severe weight loss (cachexia) and other symptoms. Tests showed her cancer had low mutation activity, no PD-L1 protein, and two specific gene mutations (ARID1A), which made her a candidate for a new type of treatment. Instead of traditional chemo, she received pembrolizumab and bevacizumab together every three weeks. After just one cycle, her tumor marker CA-125 dropped sharply and returned to normal after seven cycles. CT scans showed a big reduction in tumor size, and she achieved complete remission after nine cycles. Her weight and strength improved significantly, and she recovered from severe wasting. The only side effect was mild joint pain in her hands. No other serious side effects were seen, and she has remained free of cancer since then.\"\n}"}
+{"row_index": 341, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 42-year-old Asian woman, gravida 0, para 0, initially presented with a suspected ovarian chocolate cyst at Kaiser Hospital in southern California in March 2014, which was pathologically diagnosed as clear cell carcinoma. Following optimal debulking surgery, she was found to have FIGO stage II disease and received adjuvant chemotherapy with paclitaxel and carboplatin for seven cycles. Recurrent disease was detected in January 2016, evidenced by rising serum CA-125 levels and pelvic tumor recurrence, prompting a secondary debulking procedure and subsequent treatment with carboplatin and gemcitabine. Despite this, deep pelvic recurrence near the sigmoid colon, rectum, and bladder emerged in September 2017, progressing despite salvage chemotherapy regimens including liposomal doxorubicin and topotecan. In February 2019, she presented to a medical center in Taiwan for a third debulking surgery involving resection of the sigmoid colon, rectum, and bladder, followed by small bowel bypass, T-colostomy, and bilateral percutaneous nephrostomy. Postoperative tumor recurrence occurred, with two major pelvic and abdominal masses forming shortly thereafter, leading to palliative management due to treatment refractoriness. An experimental immune cell therapy with undefined immunological cells was attempted but was ineffective. She subsequently presented to our institution in April 2019 with elevated serum CA-125 (1236.6 U/mL), a pelvic mass causing vaginal bleeding, and severe cachexia. Comprehensive genomic profiling using FoundationOne CDx, covering over 300 cancer-related genes, revealed a stable microsatellite instability (MSI) status, low tumor mutational burden (TMB), and two somatic mutations in the ARID1A gene, a component of the SWI/SNF chromatin remodeling complex implicated in transcriptional regulation and tumor suppression. Immunohistochemical analysis of tumor tissue demonstrated PD-L1 negativity, indicating absence of programmed death-ligand 1 expression, which is a key immune checkpoint molecule that typically enables tumor immune evasion. Given the absence of PD-L1 expression and the known limitations of immune checkpoint inhibitors in epithelial ovarian cancer (EOC) based on prior clinical trial data, a combination therapy approach was selected with pembrolizumab (200 mg) and bevacizumab (15 mg/kg,"}
+{"row_index": 342, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 15-year-old boy had pain and swelling in his lower back for 4 months. Doctors found a growing lump on his spine, mostly on the left side, using X-rays, MRI, and CT scans. They called it an ABC. To fix it, they first blocked the blood supply to the lump, then removed it completely with a special surgery. They also fused the bones in his lower back to stabilize it. Two years later, he had no pain and the lump didn’t come back. The only small problem was a loose screw on one side, but it wasn’t causing any symptoms.\"\n}"}
+{"row_index": 343, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 15-year-old boy had been experiencing a slowly worsening painful swelling in his lower back for four months, but no nerve problems. X-rays, MRI, and CT scans showed a large, expanding lesion on the left side of his sacrum and lower back bones (L4-S2), which was consistent with a condition called an ABC. This condition involves bone destruction and abnormal tissue growth. To treat it, the boy first had a procedure to block blood flow to the lesion (selective arterial embolization), then had surgery to remove the affected tissue (extended curettage). He also had spinal fusion surgery to stabilize the area (posterior fusion from L4 to S2). Pathology tests confirmed the diagnosis. Two years later, he was doing well with no pain and no signs of the lesion coming back. The only small finding on X-rays was a loose screw from the surgery, which was not causing any symptoms.\"\n}"}
+{"row_index": 344, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 15-year-old male presented with a gradually progressive painful lower back swelling over a 4-month period, without associated neurological deficit. Plain lumbosacral radiography revealed an enlarged lytic lesion predominantly involving the left sacrum and lower lumbar vertebrae from L4 to S2. Magnetic resonance imaging (MRI) demonstrated a large, multi-loculated, expansile mass with a characteristic soap-bubble-like appearance extending from L4 to S2, involving the neural foramina, sacroiliac joints, and paravertebral musculature, findings consistent with an aneurysmal bone cyst (ABC). Lumbosacral computed tomography (CT) further delineated the lytic lesion, showing involvement of the sacral alae, partial destruction of the S1 and S2 vertebral bodies, and complete destruction of the left L5 pedicle. Arterial angiography confirmed the vascularity of the lesion, supporting the diagnosis of an ABC. Preoperative selective arterial embolization was performed on the day of surgery to reduce vascular supply and minimize intraoperative bleeding. The patient then underwent extended surgical excision via curettage, followed by posterior pedicle screw and rod lumbopelvic reconstruction (L4-S2). Histopathological examination of the resected tissue confirmed the diagnosis of an aneurysmal bone cyst, demonstrating osteoid foci, spindle cells, multinucleated giant cells, and reactive osteoblastic changes. Two years postoperatively, the patient remained neurologically intact and asymptomatic, with no radiographic evidence of lesion recurrence. The only radiographic finding on follow-up was asymptomatic loosening of the inferior left-sided set screw, indicating mechanical wear rather than biological recurrence or progression of disease.\"\n}"}
+{"row_index": 345, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 20-year-old woman who was healthy had a fever for two days and went to the doctor. She had sex for the first time six months before. Tests showed she got infected with a virus called CMV first. About five months later, she had a fever again and swollen lymph nodes in her neck. Tests at that time showed she had a new virus infection called EBV. This means she got infected with EBV after already having CMV. Both infections were new ones at that time, and she recovered fully without serious problems.\"\n}"}
+{"row_index": 346, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 20-year-old healthy Japanese woman first had a two-day fever and visited the clinic. She had sex for the first time six months earlier. Tests showed she was infected with cytomegalovirus (CMV) for the first time. About five months later, she had a fever and swollen lymph nodes in her neck. Tests at that time showed she was infected with Epstein-Barr virus (EBV) for the first time. This means she got CMV first, then EBV a few months later. Both infections were confirmed by blood tests that detect specific antibodies. Her symptoms improved with treatment, and follow-up tests showed the CMV infection had fully cleared after three months. The sequence of infections was clear and matched the timeline of her symptoms.\"\n}"}
+{"row_index": 347, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 20-year-old healthy Japanese female presented with a 2-day history of high fever to the emergency department at Kawasaki Medical School. Her medical history included prior episodes of mycoplasma pneumonia at ages 1 and 18. She reported her first sexual encounter six months prior. On examination, she exhibited pharyngeal erythema and lymphadenopathy in the posterior cervical and left axillary regions, with no significant findings on neurological or physical assessment. Vital signs at admission included a heart rate of 108 beats/minute, blood pressure of 101/58 mmHg, and a temperature of 38.9°C. Laboratory findings revealed leukocytopenia (white blood cell count: 1710/μL; neutrophils 76.0%, monocytes 5.0%, lymphocytes 18.0%, atypical lymphocytes 1.0%) and elevated C-reactive protein (CRP: 3.92 mg/dL). Mild hepatic dysfunction was noted: γ-glutamyl transferase (γ-GTP) 78 U/L, alkaline phosphatase (ALP) 276 U/L, aspartate aminotransferase (AST) 30 U/L, alanine aminotransferase (ALT) 28 U/L. Chest X-ray and computed tomography (CT) showed no evidence of pneumonia; abdominal CT revealed slight hepatomegaly and splenomegaly. Serological testing for influenza A/B antigens and Mycoplasma pneumonia antigen was negative. Hepatitis B surface antigen and hepatitis C antibody were negative. Human immunodeficiency virus (HIV) antigen/antibody test was negative (cutoff index <0.3). Treponema pallidum hemagglutination (TPHA) was negative. Urine culture yielded small amounts of Corynebacterium sp. and Gram-positive cocci, consistent with bacteriuria, though no pathogenic bacteria were isolated. Given the elevated CRP, levofloxacin (500 mg/day) was initiated empirically for suspected bacterial infection. The patient had a history of suspected bladder infection by her primary care provider. Viral serology demonstrated: CMV IgM antibody 3.89 (+) (enzyme immunoassay, EIA), CMV IgG antibody"}
+{"row_index": 348, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 37-year-old woman had a swollen belly, swollen feet, and yellow eyes because of a blockage in her liver blood vessels. Doctors found the problem was Budd Chiari syndrome, where the veins carrying blood from the liver were blocked. She had a surgery called a side-to-side portacaval shunt to fix the blockage, using a vein from her leg as a bridge. After the surgery, the shunt got blocked early, so doctors placed a small metal tube (stent) inside it to open it up again. This worked, and she has been feeling better for five years with no symptoms and is on blood-thinning medicine to prevent clots.\"\n}"}
+{"row_index": 349, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 37-year-old woman had a condition called Budd Chiari syndrome, which caused her liver to swell and fluid to build up in her abdomen. She had yellowing of the eyes, swelling in her legs, and a firm, enlarged liver. Tests showed that the veins carrying blood from her liver were blocked, especially the hepatic veins. Imaging confirmed a narrowed inferior vena cava and complete blockage of the hepatic veins. She underwent a side-to-side portacaval shunt using a vein from her leg as a graft to reroute blood flow. However, the shunt became blocked early, and this was fixed by placing a metallic stent across the shunt. After treatment, her symptoms improved, and she has been symptom-free for five years with regular follow-up and blood thinners.\"\n}"}
+{"row_index": 350, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 37-year-old female presented with a two-week history of progressive abdominal distension, pedal edema, and jaundice. Physical examination revealed icterus, an enlarged and firm liver, and gross ascites. Laboratory findings demonstrated conjugated hyperbilirubinemia, mild derangement of transaminases, and elevated alkaline phosphatase. Imaging via ultrasonography with color Doppler identified an enlarged liver with hypertrophied caudate lobe, a 1.1 cm portal vein with hepatopetal flow, complete occlusion of the right hepatic vein, patent but narrowed inferior vena cava (IVC) compressed by the caudate lobe, and free abdominal fluid. Splenic and superior mesenteric veins were intact. Liver biopsy confirmed the diagnosis of Budd Chiari syndrome. Prothrombotic workup was negative for underlying thrombophilic disorders. Transjugular venography revealed 90% stenosis of the IVC with a 14 mmHg pressure gradient across the narrowing and non-cannulation of the hepatic veins beyond their origins, indicating complete occlusion at the hepatic vein ostia. An 18 × 63 mm metallic stent was deployed across the IVC segment, followed by balloon dilatation using a 16 mm balloon. Percutaneous transhepatic venography under ultrasound guidance demonstrated that the left hepatic vein was patent only in its proximal segment, with distal occlusion (2–3 cm) and collateral drainage; the right hepatic vein was completely occluded, and the middle hepatic vein exhibited long-segment total occlusion (>3 cm). Attempted recanalization of the left hepatic vein failed due to extensive fibrosis and long segmental occlusion. The patient subsequently underwent a side-to-side portocaval shunt using the right external iliac vein as the H-graft. Postoperative course was uneventful, with initiation of anticoagulation. Six weeks postoperatively, she was re-admitted with recurrent pedal edema and ascites. Doppler ultrasound revealed patchy flow through the shunt. Transjugular venography confirmed patency of the IVC stent but demonstrated narrowing of the portosystemic graft with a gradient exceeding 15 mmHg at the IVC end. Given the acute angulation of the shunt relative to the IVC, a"}
+{"row_index": 351, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 70-year-old man had belly pain for 2 days, his stomach was swollen, he was feeling sick and threw up, and hadn’t had a bowel movement in 2 days. A scan showed his last part of small intestine was swollen and had a sharp object stuck in it — like a fish bone — that had pierced through the wall. The doctors took out the fish bone and cleaned the area. The man got better and was home in 6 days. He said he accidentally swallowed the fish bone 5 days before.\"\n}"}
+{"row_index": 352, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 70-year-old man came to the emergency room with abdominal pain that had been worsening for 48 hours, along with swelling in his abdomen, nausea, vomiting, and not having a bowel movement for two days. An abdominal CT scan showed that the end of the small intestine (terminal ileum) was swollen, measuring 30mm, and there was a sharp foreign object located 15 centimeters from the end of this section. The object had pierced through the wall of the intestine. During surgery, the fish bone was removed, and the damaged area was cleaned and closed. The patient recovered well and was discharged after six days. He later admitted that he had accidentally swallowed the fish bone five days earlier. His overall condition improved during recovery and there were no serious complications.\"\n}"}
+{"row_index": 353, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 70-year-old male with no significant comorbidities was referred to the emergency department by his family physician with a 48-hour history of progressive abdominal pain, marked abdominal distension, nausea, vomiting, and a last bowel movement reported two days prior. On physical examination, vital signs were: temperature 37.3 °C, pulse 110 beats per minute, respiratory rate 24 breaths per minute, and blood pressure 110/60 mmHg. Abdominal examination revealed right iliac fossa tenderness, generalized abdominal distension, and an empty rectal ampulla on digital rectal examination. Laboratory findings included hyperleukocytosis (white blood cell count: 15,700/mm³), hemoglobin 11 g/dL, platelet count 159,000/mm³, and elevated C-reactive protein (180 mg/L); hepatic and renal function tests were within normal limits. Abdominal X-ray demonstrated hydro-aeric levels in the ileal segments, consistent with ileal obstruction, without evidence of pneumoperitoneum. Abdomino-pelvic CT imaging revealed a 30 mm distension of the terminal ileum, upstream of a transitional zone where a rectangular, planar foreign body was identified. Based on these findings, the patient was diagnosed with ileal perforation secondary to foreign body penetration. Prior to surgery, the patient underwent optimization of his hemodynamic status with nasogastric tube suction and intravenous fluid resuscitation. An emergency laparotomy was performed under general anesthesia with endotracheal intubation, conducted by a fifth-year and fourth-year surgical resident. Preoperative prophylactic antibiotics were administered. Intraoperatively, a sharp foreign body measuring 3 cm × 2 cm was identified at the 15 proximal centimeters of the terminal ileum, penetrating through the ileal wall. The foreign body was successfully removed and identified as a fish bone. The margins of the perforation were excised, and primary anastomosis was performed. Postoperative recovery was uneventful; the patient was discharged on postoperative day 6. Patient history confirmed incidental ingestion of the fish bone five days prior to presentation. The postoperative course was uncomplicated, with resolution of systemic inflammation and restoration of gastrointestinal continuity. The pathophysiological mechanism involved mechanical obstruction and subsequent perforation"}
+{"row_index": 354, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 74-year-old man had blurry vision in both eyes because of cataracts. His eye doctor planned to fix his right eye with cataract surgery. During the surgery, heat damaged the front and outer layer of his right eye. The damage was serious — his eye could only see with his hand moving, and the pressure inside the eye was very low. The front part of the eye became cloudy, and fluid leaked out. The surgery team could not sew the damaged part back together because it was too loose and broken. So, they took a piece of healthy tissue from a donor and put it into the damaged area to fix the eye. After that, they removed the cloudy lens part and placed a clear lens inside the eye. It took 7 months for the new lens to settle in place. Now, his vision is better — it’s 2/20 in his right eye, and the eye is stable with less cloudiness.\"\n}"}
+{"row_index": 355, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 74-year-old man had severe eye damage during cataract surgery in his right eye. He had prostate enlargement but no history of dementia. Before surgery, he had blurry vision due to cataracts, with good vision and normal eye pressure. During the procedure, heat from the surgery caused serious injury to both the cornea and sclera (the white part of the eye). The injury led to heavy clouding of the cornea and fluid leaking into the eye. The wound was initially closed with stitches, but fluid kept leaking, so more material was injected. The next day, he was transferred to our hospital, where his vision had dropped to hand motion and eye pressure was only 3 mm Hg. The sclera was badly damaged and could not be repaired directly because it was too loose. Instead, a donor scleral graft was transplanted to cover the damaged area using 10-0 nylon sutures. After the graft healed and fluid stopped leaking, the lens nucleus was removed from the wound. Pathology showed the damaged tissue had coagulation necrosis with no inflammation. Three months later, inflammation caused macular edema, which was treated with anterior vitrectomy. Finally, an intraocular lens was placed in the ciliary sulcus seven months after surgery. His vision improved to 2/20 in the right eye, and his eye pressure stabilized with less corneal clouding.\"\n}"}
+{"row_index": 356, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 74-year-old male presented in October 2015 with blurred vision in both eyes due to senile cataract, with baseline visual acuity of 6/20 in the right eye (OD) and 8/20 in the left eye (OS), and normal intraocular pressure (IOP). Slit-lamp examination revealed mild cortical cataract in both eyes, with no notable fundus abnormalities. The initial ophthalmologic management plan included phacoemulsification for the right eye. The patient had a history of benign prostatic hyperplasia (BPH) but no history of dementia. Prior to phacoemulsification, viscoelastic agents with high cohesive properties were injected into the anterior chamber to induce pupillary dilation following miosis induced by hydrodissection in the right eye. Shortly after initiating phacoemulsification, a severe thermal corneoscleral injury occurred, characterized by extensive thermal damage to the corneal stroma and sclera. The wound was initially managed with tight suturing using pedunculated conjunctiva; however, persistent intraocular fluid leakage necessitated repeated injection of viscoelastic material. The next day, the patient was transferred to our institution, where he presented with hand motion vision and an IOP of 3 mm Hg OD. Histological evaluation of the injured sclera revealed coagulation necrosis with eosinophilic material accumulation, consistent with thermal injury and lack of inflammatory cell infiltration, indicating a direct thermal insult without significant immune response. The scleral wound was found to be actively opening upon conjunctival incision, and due to marked scleral mobility, direct suture closure was not feasible. As a result, a donor scleral graft was transplanted to the injured site using 10-0 nylon sutures. Post-transplantation, intraocular fluid leakage was confirmed to be absent, allowing safe extraction of the lens nucleus from the newly formed temporal wound. Histopathological analysis confirmed favorable graft attachment and restoration of IOP to normal levels. Three months postoperatively, macular edema developed secondary to intraocular inflammation driven by residual lens cortex, leading to anterior vitrectomy, which resolved the edema. An intraocular lens (IOL) was ultimately implanted in the ciliary sulcus seven months after surgery. At the final follow-up in October 2016, the patient achieved a visual acuity of 2"}
+{"row_index": 357, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A baby boy, just 4 days old, had a small, yellowish-white spot found on the inside of his left eye's back part. The spot was about the size of 1.5 eye circles. When doctors looked at it with a special eye test, it showed bright spots and a little leaking. Seven months later, the spot was gone and the eye looked normal. The blood vessels in the eye were a bit twisted but didn't leak anymore. No treatment was needed because the spot just disappeared on its own.\"\n}"}
+{"row_index": 358, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 4-day-old male infant was found to have a small, harmless growth called an isolated retinal astrocytic hamartoma in the nasal retina of his left eye. At first, it appeared as a yellowish-white flat spot about 1.5 times the size of a normal retina disc. Fluorescein angiography showed the area was abnormally bright with a little leakage, which is a common finding in such growths. Seven months later, the spot had completely disappeared during a fundus exam, and the eye’s blood vessels looked slightly twisted but without any leakage. The right eye was normal throughout. This suggests that the growth may have gone away on its own without treatment, a process known as spontaneous regression.\"\n}"}
+{"row_index": 359, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 4-day-old male infant, delivered at 40 weeks' gestation with a birth weight of 3660 g, was admitted to the Department of Neonatology at The Second Hospital of Jilin University in February 2022 due to dyspnea. Delivery was via episiotomy combined with forceps. No cutaneous abnormalities were noted. Brain magnetic resonance imaging (MRI) revealed bilateral short T1 signal abnormalities beneath the occipital cranial plate, consistent with subarachnoid hemorrhage, though no associated neurological deficits or family history of congenital or genetic disorders were present. Routine retinal screening using RetCam 3 (Clarity Medical Systems, Inc.) demonstrated a normal right retina. In contrast, a color fundus photograph of the left eye identified a solitary, yellowish-white, flat retinal lesion measuring approximately 1.5 disc diameters in the nasal retina. Fluorescein angiography (FA) demonstrated diffuse hyperfluorescence with mild fluorescence leakage, suggesting abnormal vascular permeability and perfusion within the lesion. B-scan ultrasound was unremarkable, showing no distinct calcifications or structural abnormalities, and the mass was inapparent on imaging. No therapeutic intervention was initiated, and the patient was followed clinically. At three months post-initial presentation, a reduction in lesion size was observed, with FA revealing decreased vascularization and mild mottled hyperfluorescence, indicating partial vascular normalization and possible resolution of the vascular dysregulation. Seven months after initial detection, fundus examination confirmed complete absence of the retinal lesion in the left eye. Repeat fluorescein angiography showed mild tortuosity of the surrounding retinal vessels without evidence of leakage, consistent with restored vascular integrity. The right retina remained unaffected. These findings support the clinical observation that isolated retinal astrocytic hamartoma (RAH) may exhibit spontaneous regression, likely due to the self-limiting nature of the lesion's vascular and cellular architecture, with a probable mechanism involving gradual resolution of the astrocytic proliferation and vascular remodeling over time. The absence of systemic involvement, familial predisposition, or associated anomalies further suggests a sporadic, non-malignant, and benign developmental origin of the lesion.\"\n}"}
+{"row_index": 360, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 78-year-old man with liver damage from years of drinking alcohol had a cancer in his liver that broke into pieces and started bleeding. The bleeding was so bad it filled his belly with blood, and he needed surgery right away. Doctors opened his belly and saw a lot of blood and two spots where the liver had torn. The bleeding wouldn’t stop with normal methods. So they used a special machine that sends heat to the blood vessels feeding the cancer, and it worked — the bleeding stopped. The surgery took 90 minutes and he needed blood and medicine to stay alive. After the surgery, he went to the hospital room to recover. Two days later, he was moved to a regular room and didn’t need more medicine. His liver was still strong enough to heal, even though it was damaged. Later, he got a serious problem called hepatorenal syndrome, but didn’t need dialysis. He stayed in the hospital and was followed by a team that helps people with serious illness. Sadly, he passed away two months later because the cancer kept getting worse.\"\n}"}
+{"row_index": 361, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 78-year-old man with long-term alcohol-related liver damage (cirrhosis) and several liver tumors (multifocal hepatocellular carcinoma) was admitted to the hospital after his abdomen suddenly filled with blood due to ruptured tumors. An abdominal CT scan showed multiple bleeding spots in both sides of his liver. He was in serious condition and urgently taken to the operating room, where a large amount of blood (4 liters) was found in his abdominal cavity (hemoperitoneum). During surgery, it was found that his liver was heavily damaged and covered by tumors, with two areas (segments II and IV) bleeding uncontrollably. Standard methods to stop the bleeding failed. To control the bleeding, doctors used a procedure called radiofrequency ablation (RFA), which applies heat to the blood vessels feeding the tumors, sealing them off. This was done around both tumors for a total of 40 minutes, and the bleeding stopped successfully. The surgery took 90 minutes, and he needed blood transfusions and medication to support his blood pressure. After surgery, he was moved to the intensive care unit and stayed there for two days before being transferred to a regular medical floor. His liver enzymes were very high after surgery, but he did not develop liver failure. He later developed a complication called hepatorenal syndrome on day 9, which affected his kidneys, but he did not need dialysis. His overall condition remained stable, and he was followed up by a palliative care team. Unfortunately, he passed away two months later due to worsening liver disease.\"\n}"}
+{"row_index": 362, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"We present a case report of a 78-year-old white male with alcoholic cirrhosis and multifocal hepatocellular carcinoma (HCC), complicated by ascites and portosystemic encephalopathy. The patient's history includes a prior wedge resection of segment II for HCC (G2) two years prior, followed by annual surveillance including computed tomography (CT) imaging. Due to advanced age and poor liver function, he was not considered a candidate for liver transplantation (LT). He presented to the emergency department with decompensated ascites, abdominal tension, and lower limb edema. During hospitalization, his hematocrit dropped abruptly (hemoglobin from 9.3 g/L to 6.7 g/L over a 3-hour period), indicating significant hemorrhage. Abdominal CT revealed multiple bilateral foci of HCC with active acute bleeding from one lesion. His Model for End-Stage Liver Disease (MELD) score was 19, Child–Pugh score C11, total bilirubin 8 mg/dL, and alpha-fetoprotein (AFP) level of 604 μg/L—indicative of aggressive HCC. The patient was hemodynamically unstable and required urgent surgical intervention for hemorrhagic shock. A midline laparotomy was performed, revealing a massive hemoperitoneum (4 L) with a cirrhotic liver exhibiting recanalization of the umbilical vein and development of collateral circulation. The liver was completely subverted by tumor mass, with two spontaneous, uncontrollable lacerations identified in segments II and IV. Conventional hemostatic measures—including argon beam coagulation, oxidized regenerated cellulose, and fibrin glue—failed to achieve hemostasis. Given the multifocal nature of the HCC, poor hepatic reserve, and the presence of active bleeding from multiple vascular afferents, a strategy of radiofrequency ablation (RFA) was employed to coagulate the feeding vessels of each tumor nodule. Circumferential RFA cycles were applied to both nodules, totaling 40 minutes of ablation duration. This approach successfully achieved hemostasis and controlled the bleeding from the ruptured hepatocellular carcinoma. The surgical procedure lasted 90 minutes, during which the patient required three units of packed red blood cells (PRBCs) and vasopressor support with noradrenal"}
+{"row_index": 363, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 36-year-old woman had a hard, rubbery lump in her right upper belly that had been there for two months. She didn’t have any other health problems. Doctors found the lump was big — about 13 to 14 centimeters — and it had a small, bright part inside. A scan showed the lump was in her liver and also spread a little to her lower belly. She had surgery to remove part of her liver and a piece of tissue called the omentum. After the surgery, doctors looked at the tissue and found it was a rare kind of cancer called low-grade malignant epithelioid mesothelioma. This type of cancer grows slowly and doesn’t spread easily. Six months after surgery, she has not had any signs of cancer coming back. This is a good sign. It’s very rare for this kind of cancer to start in the liver, and even rarer for it to be in both the liver and the omentum at the same time.\"\n}"}
+{"row_index": 364, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 36-year-old woman was admitted to the hospital after discovering a hard, elastic lump in her right upper abdomen that had been causing pain for two months. Imaging tests showed a large cystic mass in her right liver, about 13 to 14 centimeters in size, with a small blood-filled spot inside. A PET scan also showed abnormal activity in the liver and lower abdomen, suggesting a tumor. The patient had no history of asbestos exposure or other known risk factors. She underwent surgery to remove part of her liver and a portion of the omentum (a fatty tissue layer in the abdomen). Pathology results showed that the tumors were low-grade malignant epithelioid mesothelioma — a rare type of cancer that usually starts in the lining of organs. This type of cancer is very uncommon in the liver, and this case is one of the youngest reported in women. The tumors in both the liver and omentum had similar features, including a fibrous capsule and low growth rate, which suggests they are separate, primary tumors rather than spread from one area. After six months of follow-up, the patient has shown no signs of cancer returning. While rare, mesothelioma can sometimes occur in the liver or omentum, and in this case, both tumors were considered low-grade, meaning they are less aggressive and have a better prognosis.\"\n}"}
+{"row_index": 365, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 36-year-old woman presented with a 2-month history of abdominal and back pain, leading to referral and admission for evaluation of a hard, elastic, poorly flexible mass in the right upper abdomen. No signs of obstructive jaundice or abdominal tenderness were present. Laboratory findings revealed anemia (hemoglobin = 10.6 g/dL), thrombocytosis (43.9 × 10⁴/μL), and elevated C-reactive protein (2.71 mg/dL); all other laboratory parameters, including tumor markers α-fetoprotein (AFP), carcinoembryonic antigen (CEA), and cancer antigen (CA)19-9, were within normal limits. Abdominal ultrasonography identified a large, heterogeneous space-occupying lesion in the right lobe of the liver, measuring 15 cm in diameter, with evidence of hemorrhage and a hypervascular mural nodule. Contrast-enhanced computed tomography (CT) demonstrated a cystic mass measuring 13 × 14 × 11 cm in the right liver lobe with an enhanced mural nodule. Magnetic resonance imaging (MRI) showed hyperintense T2-weighted components consistent with hemorrhagic content. 18F-fluorodeoxyglucose positron emission tomography (FDG-PET) revealed abnormal metabolic accumulation in the liver and lower abdominal region, prompting surgical intervention. The procedure included hepatectomy of the posterior segment and partial resection of the omentum, which was identified as a lesion on FDG-PET. Gross examination revealed a massive cystic tumor measuring 18 × 15 cm containing hemorrhagic fluid, with multinodular, mucinous, brownish or yellowish lesions observed in the extra-cystic wall. The omental lesions were two nodular tumors measuring 2.1 × 1.3 cm and 0.3 × 0.3 cm, both slightly brownish in appearance. Microscopic evaluation demonstrated tubular, cystic, and spindle arrangements of epithelioid cells with clear or eosinophilic cytoplasm in both hepatic and omental tumors. Immunohistochemical analysis showed positive staining for AE1/AE3, EMA, CK19, CK7, CD10, and calretinin; partial or weak positivity for CK5/6, D2-40"}
+{"row_index": 366, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"An 82-year-old man had pain in his belly for nine days, along with vomiting and belly swelling. He had a history of gallstones before. Tests showed his gallbladder was small and his intestines were stretched out, with a gallstone stuck in the small intestine, blocking the flow. This caused air to show up in the bile duct, which means a gallstone got into the intestine through a hole between the gallbladder and the small intestine. The doctors did an emergency surgery to remove the stone from the intestine. They left the hole alone because cutting it could have hurt the small intestine. After surgery, he recovered well and went home without problems. He stayed healthy for 16 months after that.\"\n}"}
+{"row_index": 367, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"An 82-year-old man with a history of gallstones presented with abdominal pain, distension, and vomiting that had lasted for nine days. His abdomen was swollen, and the bowel sounds were loud. Ultrasound showed a shrunken gallbladder and swollen intestines. A CT scan found a gallstone stuck in the small intestine, blocking it, along with air in the bile ducts — a sign of gallstone ileus and a connection between the gallbladder and the duodenum (cholecystoduodenal fistula). The patient underwent emergency surgery, where the gallstone was removed from the intestine (enterolithotomy). The connection between the gallbladder and duodenum was not repaired because it could have caused serious injury to the duodenum. After surgery, he recovered well and was discharged on day six. He has remained symptom-free for 16 months.\"\n}"}
+{"row_index": 368, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"An 82-year-old frail male with a history of hypertension for 15 years and previously diagnosed cholelithiasis (eight years prior) presented with a nine-day history of abdominal distension, constipation, localized periumbilical pain described as intermittent, nonradiating, and multiple episodes of nonprojectile, nonbilious vomiting containing food particles. He denied fever, jaundice, hematochezia, melena, urinary changes, or recent abdominal trauma. His recent diagnosis of bronchiectasis was managed with low-flow oxygen therapy. Physical examination revealed normal vital signs, a distended abdomen without tenderness, and hyperactive bowel sounds. Laboratory investigations, including complete blood count and biochemistry, were within normal limits. Abdominal ultrasound demonstrated a contracted gallbladder with distended bowel loops, consistent with intestinal obstruction. Abdominal computed tomography (CT) of the abdomen and pelvis revealed dilated loops of the small intestine with hyperdense intramural calculi and air within the biliary tree, confirming the diagnosis of gallstone ileus with associated cholecystoduodenal fistula. Initial management included intravenous fluid resuscitation, nasogastric tube insertion, analgesia, and nil-by-mouth status. A Foley catheter was placed, and urinary output was monitored closely. The patient underwent an emergency exploratory laparotomy via a lower midline incision under spinal anesthesia, performed within 24 hours due to concerns for chest morbidity. Intraoperatively, a single 4.5 × 2 cm gallstone was identified impacted in the terminal ileum, located 10 cm proximal to the ileocaecal junction. The ileal segment at the site of impaction was intact and healthy, with proximal bowel dilation. An incidental finding was a Meckel's diverticulum measuring 60 cm proximal to the ileocaecal junction, characterized by a wide base. A longitudinal enterotomy was performed proximal to the stone impaction to facilitate stone extraction via milking, followed by transverse repair of the enterotomy. The gallstone responsible for the intestinal obstruction was successfully removed. The cholecystoduodenal fistula was not ligated or repaired, as the procedure would have carried a high risk of duodenal injury, particularly given the anatomical proximity and the potential for bile-induced duodenal perforation or stricture. Postoperative course was un"}
+{"row_index": 369, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 65-year-old man with high blood pressure, diabetes, obesity, and liver disease had been on dialysis for two years. He often missed his dialysis sessions and didn’t follow his diet, which made his body weak. During one session, he felt tired, dizzy, and confused. His blood pressure was very low (50/30), and his heart was not working well. Tests showed his heart was wrapped in a thick, stiff layer (pericardium) that was squeezing it, making it hard to pump blood. This condition, called constrictive pericarditis, was caused by long-term dialysis. The doctors removed the thick layer (pericardiectomy) and found it was full of scar tissue and calcium, not infection. After the surgery, he started dialysis more regularly and followed his diet. He’s now feeling better and going to dialysis every week as planned.\"\n}"}
+{"row_index": 370, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 65-year-old man with long-standing conditions like high blood pressure, diabetes, obesity, and liver disease on hemodialysis for two years began feeling unwell during one of his dialysis sessions. He reported feeling tired, lightheaded, and confused, but no chest pain or shortness of breath. He had a history of missing dialysis sessions and not following his diet, which likely worsened his condition.\\n\\nAt the time of admission, he was very weak, had a dangerously low blood pressure (50/30 mmHg), and showed signs of shock. His heart exam revealed weak sounds and a slow refill time, and his ECG showed low electrical activity in the heart. An echocardiogram found a thickened pericardium (the sac around the heart) with no fluid buildup, and cardiac catheterization confirmed that the pressures in all heart chambers were equal—this is a key sign of constrictive pericarditis.\\n\\nTests ruled out infection, heart disease, and other causes. Pathology of the removed pericardium showed heavy scarring and calcium deposits, with no signs of infection or inflammation. These findings point to dialysis-related constrictive pericarditis (DICP), a condition that can develop in people on long-term hemodialysis due to poor dialysis adherence and high fluid retention.\\n\\nThe patient underwent surgery to remove the thickened pericardium (pericardiectomy), which improved his symptoms. After recovery, he started attending dialysis more regularly, followed his diet, and now manages his condition better. This case highlights the importance of consistent dialysis attendance and dietary control in preventing serious complications like constrictive pericarditis.\"\n}"}
+{"row_index": 371, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 65-year-old male with a history of hypertension, type 2 diabetes mellitus, morbid obesity, and cirrhosis secondary to non-alcoholic steatohepatitis (NASH) presented with symptoms of malaise, lightheadedness, and confusion during a hemodialysis session. He had been on hemodialysis for two years due to diabetic nephropathy, but exhibited chronic non-adherence to treatment, with only three to four sessions per week attended, resulting in an actual Kt/V of 1.5–2.0, significantly below the calculated standard Kt/V of 2.45 under ideal adherence. His dialysis prescription included a high-flux polysulfone membrane with a surface area of 2.2 m², a blood flow rate (Qb) of 370 mL/min, and a dialysate flow rate (Qd) of 800 mL/min. Dialysate composition consisted of calcium 2.5 mEq/L, potassium 1 mEq/L, sodium 138 mEq/L, bicarbonate 36 mmol/L, and unfractionated heparin 5000 IU/session. He was also prescribed allopurinol 100 mg/day, sertraline 50 mg/day, esomeprazole 40 mg/day, and sevelamer 2.4 g three times daily.\\n\\nAt presentation, the patient was anuric and in hypotensive shock with a blood pressure of 50/30 mmHg, prolonged capillary refill time, and jugular venous stasis. Physical examination revealed pallor, cyanosis, and hypophonic heart murmurs; respiratory rate was 16 breaths per minute, oxygen saturation 88% in room air, and no signs of pulmonary pathology. Cardiac auscultation showed no parasternal or apex murmurs, with a heart rate of 88 bpm. Neurological examination demonstrated altered mental status and bradykinesia. Electrocardiography revealed sinus rhythm, low diffuse QRS voltage, and evidence of altered ventricular repolarization, consistent with impaired conduction and reduced myocardial voltage.\\n\\nLaboratory findings included: hemoglobin 9.8 g/dL, hematocrit 29.5%, leukocytes 5,230/mm³,"}
+{"row_index": 372, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 4-year-old girl was born with her index finger and thumb bigger than the other fingers. These fingers have gotten larger over time and now cause pain, tingling, and sometimes a bluish color, especially at night. The fingers are stiff, especially on the right hand, but she can still grip things she needs to hold. The big fingers are not normal — they have extra fat and fibrous tissue, like soft, firm stuff that grows around the nerves. This is called macrodactyly. Her siblings are healthy, and she had a normal birth. The doctors saw this on X-rays, which showed thick soft tissue and bigger bones in those fingers. Before surgery, everything looked the same. They planned surgery to fix the second finger, which was the worst, because it hurt the most and made her hand stiff. They removed the extra soft tissue (fat and fibrous stuff) without touching the bone or nerve. Then they cut a small piece of bone to straighten the finger and used a tiny metal wire to hold it in place while it healed. After surgery, she had regular check-ups and physical therapy to move her fingers better and reduce stiffness. She is getting better — her grip is stronger, her fingers move more, and the pain and stiffness are going down. She will keep being checked to make sure everything is healing well.\"\n}"}
+{"row_index": 373, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 4-year-old girl has had enlarged index and thumb fingers since birth. Over time, these fingers have gotten larger, causing pain, tingling, and occasional bluish coloring—especially at night. The enlargement is most noticeable in the right hand, where the index and second fingers are much bigger than the others. The fingers feel firm and are slightly stiff, especially when gripping things. She can still hold objects, but her right hand has noticeable stiffness.\\n\\nThe condition is called macrodactyly, a type of FLH (fibrolipomatous hamartoma), which means abnormal growth of soft tissues like fat and fibrous tissue around the nerves in the hand. The swelling is not in the bones, but in the soft tissue, and it’s most prominent near the median nerve. X-rays showed increased soft tissue and bone growth in the affected fingers, which matches what’s seen in this condition.\\n\\nBefore surgery, doctors confirmed the diagnosis using X-rays. Since MRI was not available due to long wait times, they relied on X-rays to plan treatment. The surgery focused on the second finger, which was the most enlarged and caused the most problems. The procedure included removing the excess soft tissue (fibroadipose tissue), correcting the bent angle of the finger with a bone cut (wedge osteotomy), and using a small metal wire (K-Wire) to help the bone heal in the right position.\\n\\nThe surgery was done to reduce pain, improve finger movement, and make daily activities easier. After surgery, the child had regular follow-ups and physical therapy to improve hand strength and flexibility. Over time, she showed better grip, less stiffness, and improved hand function. She continues to be monitored for long-term results.\"\n}"}
+{"row_index": 374, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 4-year-old female patient presents with congenital macrodactyly of the right index finger and thumb, a hallmark feature of fibrolipomatous hamartoma (FLH). The enlargement is disproportionate, with the index and thumb significantly larger than adjacent digits, and is characterized by firm, swollen tissue upon palpation consistent with fibroadipose proliferation. Radiographic evaluation reveals increased soft tissue density and bony enlargement of the first and second phalanges of the right hand, particularly on the palmar surface, confirming the radiological pattern typical of FLH involving both soft tissue and bone. The condition has been progressive since birth, with symptoms including nocturnal pain, paresthesia (tingling), and episodic cyanosis of the affected digits, suggesting compromised microvascular perfusion and/or nerve compression. These symptoms correlate anatomically with the course of the median nerve through the wrist and hand, a region commonly involved in FLH due to the infiltrative nature of the fibroadipose lesion.\\n\\nDetailed measurements show the right first finger measures 6 × 2.0 cm and the second finger 6 × 1.9 cm, with a 20-degree angulation directed toward the ulnar side at the distal and middle phalanges. Sensory function is preserved throughout the affected digits—base, middle, and tip—comparable to contralateral and non-affected sides, with no evidence of sensory loss or tenderness. The mother’s first finger measures 4 × 1.5 cm and second finger 5 × 1.5 cm, indicating a relative degree of familial variation, though not a direct hereditary pattern.\\n\\nPreoperative imaging, including initial X-rays, demonstrated widespread soft tissue edema and hyperdensity consistent with fibroadipose tissue expansion. Although MRI was planned as the gold standard for detailed soft tissue characterization and to confirm the diagnosis of fibrolipomatous hamartoma, its unavailability due to prolonged waiting lists necessitated reliance on X-ray findings for diagnostic and surgical planning. The absence of significant bony involvement in the excised tissue confirms that FLH is primarily a soft tissue hamartoma, with fibrous tissue derived from proliferative fibroblasts and collagen deposition around the nerve sheath, and adipose tissue representing abnormal fat accumulation within and adjacent to the nerve bundles. The excised mass exhibited a soft, pliable consistency with intermixed fibrous nodules,"}
+{"row_index": 375, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 60-year-old woman who wears dentures had a sore spot on the inside of her lower right cheek for a month. She also had dry mouth. The doctor saw redness at the corners of her mouth and a small, painless lump near her tooth area, likely caused by a bad-fitting denture. A test found a rare type of yeast called C. calyptogenae, which is not common and usually lives in seawater or clams. This yeast matched almost perfectly with a known strain. After two weeks of using a mouth spray and a cream with miconazole and fusidic acid, the redness went down. The yeast was no longer found in her mouth after checking again. The doctor fixed her denture to prevent it from happening again. Her symptoms got better, and she’s now doing well.\"\n}"}
+{"row_index": 376, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 60-year-old woman who wore dentures was diagnosed with angular cheilitis, a condition causing irritation and redness at the corners of her mouth. She also had a small, painless lump on the inside of her lower right cheek, likely caused by a poorly fitting denture. Testing of her mouth samples showed a rare yeast called C. calyptogenae, which is not commonly found in the mouth. The yeast was identified through laboratory tests that compared its genetic code to known strains, showing 99.6% similarity in one part of its DNA and 100% in another. After two weeks of treatment with a mouthwash and a topical cream containing miconazole and fusidic acid, her symptoms improved, with less redness. Follow-up testing showed no trace of the yeast. The doctor also recommended a new denture to better fit her mouth and prevent the problem from coming back.\"\n}"}
+{"row_index": 377, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 60-year-old denture-wearing Malaysian woman was referred to the Oral Medicine Clinic, Universiti Malaya, in February 2020, presenting with a painless swelling on the lower right cheek that had persisted for one month. She reported moderate xerostomia, quantified by a Clinical Oral Dryness Score of five. On clinical examination, she was partially edentulous, with no facial swelling or palpable lymphadenopathy. Slight erythema was observed at the bilateral angles of the mouth, consistent with angular cheilitis. A non-tender, non-indurated lesion measuring 0.5 × 0.5 cm was identified on the lower right buccal sulcus over the premolar region, morphologically resembling an irritation fibroma, likely secondary to ill-fitting denture pressure. An oral swab was collected from the bilateral angles for Gram staining and Candida culture on Brilliance Candida Agar™ (BCA, Oxoid, UK). An expectorated oral rinse sample (20 ml saline) was obtained, centrifuged at 9600 rpm at 4°C for 10 minutes, and the resulting pellet (100 μl) was cultured for Candida isolation. Gram staining of the swab revealed scanty Gram-positive and Gram-negative bacteria and epithelial cells, with no evidence of blastoconidia or hyphal filaments. Primary cultures from both the oral swab and oral rinse yielded dark blue colonies along initial streak lines on BCA after 48 hours of incubation at 37°C. Colonies were subcultured onto fresh BCA and Sabouraud’s Dextrose Agar (SDA) plates, incubated at both room temperature and 37°C. On SDA, smooth, mucoid, light orange to beige colonies were observed at both temperatures; on BCA, similar colonies were seen at room temperature, while dark blue pigmentation was observed at 37°C. Yeast growth was faster at room temperature compared to 37°C on both media. Gram stain of the pure culture demonstrated round-to-oval yeast morphology. The isolate was designated as *C. calyptogenae* strain D1.\\n\\nSpecies-level identification was achieved via polymerase chain reaction (PCR) amplification and sequencing of the internal transcribed spacer (ITS) region and the D1/D2 domain of"}
+{"row_index": 378, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A man with a weak immune system stayed infected with the COVID-19 virus for 189 days. Even after treatment, the virus kept coming back, and tests showed it was the same strain each time. This wasn’t a new infection — it was the same virus returning. Doctors used medicines like dexamethasone, remdesivir, and IV immune shots to help him. His body slowly got better, and by day 189, the virus was no longer detectable. Tests confirmed the virus didn’t change — it stayed the same. He got the vaccine later, and after that, his tests came back negative. Now he’s getting stronger and can do more activities.\"\n}"}
+{"row_index": 379, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 58-year-old man with weakened immunity due to lymphoma treatment developed a long-lasting SARS-CoV-2 infection that lasted for 189 days. Even after initial treatment, the virus kept coming back in the same form, as confirmed by genetic testing showing the exact same strain each time. This was not a new infection with a different virus, but a relapse of the original virus. The patient had a cough, fever, and breathing problems that returned multiple times, requiring hospital visits and treatments like dexamethasone, remdesivir, and intravenous immunoglobulin. His immune system was weakened by prior chemotherapy and rituximab, which likely contributed to the prolonged infection. Viral culture and PCR tests showed the virus remained detectable for months, and even after treatment, the virus was still present until day 189. Once the infection was fully cleared, he received the COVID-19 vaccine, and follow-up tests showed no virus. His symptoms gradually improved, and he is now able to do more physical activity. The case shows that some immunocompromised patients can have very long-lasting viral infections that require a combination of treatments to manage.\"\n}"}
+{"row_index": 380, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 58-year-old Caucasian male with a history of follicular lymphoma, previously treated with six cycles of bendamustine and rituximab followed by maintenance rituximab, presented prior to widespread COVID-19 vaccination with a one-week course of cough, low-grade fever, and systemic malaise. Oropharyngeal swab testing was positive for SARS-CoV-2, and he was managed outpatient without hospitalization. Twenty-seven days later, he developed hypoxemia requiring hospital admission. Initial nasopharyngeal (NP) swab was negative, and high-resolution computed tomography (CT) revealed recurrent ground glass opacities and bilateral interstitial pneumonia, consistent with COVID-19. Laboratory findings included severe lymphopenia (0.1 × 10⁹/L, normal: 0.7–3.5 × 10⁹/L), elevated C-reactive protein (57.0 mg/L, normal: 0.0–8.0 mg/L), and markedly increased ferritin (2047 μg/L, normal: 30–500 μg/L), indicating significant inflammatory and immune dysregulation. He responded initially to dexamethasone 6 mg daily for 10 days; however, recurrent hypoxemia and progressive radiographic changes led to a diagnosis of organizing pneumonia as a post-COVID-19 sequelae. Bronchoscopy was declined, and oral prednisone 50 mg daily was initiated with a planned taper. On day 90 (73 days post-admission), following prednisone reduction to 10 mg, he developed new pyrexia and relapse of hypoxemia. Repeat NP swab RT-PCR was positive (Ct 18.7), and bronchoscopy was performed. Bronchoalveolar lavage (BAL) demonstrated both RT-PCR (Ct 18.7) and culture positivity (1.17 × 10⁴ pfu/mL) for wild-type SARS-CoV-2, belonging to the G clade, B.1.160 sublineage, with no growth of bacteria, mycobacteria, other viruses, or fungi. Histopathology of transbronchial biopsies revealed active pneumonitis with focal organizing pneumonia and patchy interstitial fibrosis, confirming a clinical"}
+{"row_index": 381, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 54-year-old man had a sudden heart attack, his heart stopped, and he needed CPR and medicine to restore blood flow. Doctors used a clot-busting drug and placed stents in his heart arteries to fix the blockage. He ended up in the heart care unit with a weak heart and severe muscle damage. The muscle damage was caused by a cholesterol medicine (atorvastatin) he was taking, so they stopped it. He needed help to filter his blood because his kidneys weren’t working well, and had to get dialysis. His muscles were damaged so badly that a muscle biopsy was done. After recovering, he was finally released to a regular hospital room.\"\n}"}
+{"row_index": 382, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 54-year-old man had a severe heart attack (AMI) that led to cardiogenic shock and cardiac arrest. He required cardiopulmonary resuscitation, fibrinolysis with tenecteplase, and successful coronary angiography with stents placed in key heart arteries. He was admitted to the coronary care unit (CCU) with deep sedation, mechanical ventilation, and a SOFA score of 7, indicating serious organ dysfunction. He developed post-extubation complications including delirium, stridor, and a pneumothorax, which required reintubation. During his hospital stay, he received medications that can cause muscle damage, including haloperidol, olanzapine, and hydrocortisone. Shortly after reintubation, he developed severe rhabdomyolysis — a condition where muscle breakdown releases harmful substances into the blood — linked to his atorvastatin medication. His creatine phosphokinase (CPK) levels rose over 10 times normal, peaking five days later, prompting the discontinuation of atorvastatin. He also developed kidney failure (oliguria), requiring temporary hemodialysis. After recovery, he was successfully extubated and discharged to a general hospital room. The rhabdomyolysis was directly tied to atorvastatin use, which was stopped due to the severe muscle damage.\"\n}"}
+{"row_index": 383, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 54-year-old male presented with acute myocardial infarction (AMI) complicated by cardiogenic shock and cardiac arrest, requiring immediate advanced airway management in the emergency department. Tenecteplase 0.5 mg/kg was administered, with an ischemic time of 1 hour 40 minutes, and no reperfusion was achieved during the initial intervention. The patient experienced two episodes of pulseless tachyarrhythmias, each requiring defibrillation with 200 J biphasic shocks, advanced cardiopulmonary resuscitation (CPR), and intravenous amiodarone 300 mg to restore spontaneous circulation. Total duration of cardiac arrest was approximately 11 minutes.\\n\\nRescue coronary angiography revealed significant coronary artery occlusion, resulting in the placement of a medicated stent in the anterior descending artery and an unmedicated stent in the first diagonal artery. Post-procedural coronary flow was confirmed with a final TIMI flow grade of 3 and a blush grade of 3, indicating adequate reperfusion. The patient was admitted to the coronary care unit (CCU) in a state of deep sedation, under mechanical ventilation, with clinical evidence of cardiogenic shock and a SOFA score of 7, reflecting moderate organ dysfunction.\\n\\nPost-extubation complications included delirium, stridor, and iatrogenic pneumothorax, necessitating reintubation 48 hours after initial extubation. During this period, the patient received medications known to induce myositis, including intravenous haloperidol (5 mg intermittent doses, cumulative 30 mg), olanzapine (cumulative 20 mg), and hydrocortisone (200 mg). Subsequently, the patient developed septic shock, prompting initiation of broad-spectrum antibiotic therapy with vancomycin and meropenem at full initial doses, adjusted according to renal function, for six days as treatment for nosocomial pneumonia.\\n\\nAtorvastatin was continued enterally at a fixed dose of 80 mg every 24 hours for a total duration of 15 days. Two days after reintubation (10 days post-admission to CCU), serum creatine phosphokinase (CPK) levels rose to more than 10 times the upper limit of normal, peaking five days later, at which"}
+{"row_index": 384, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 24-year-old woman had a big, growing lump on her left upper back and shoulder that caused severe pain and made her unable to use her left arm. She had been treated before for a similar problem in the same area, and had surgery and chemo back then. The lump kept getting worse, and her wound wouldn’t heal. Doctors tried chemo several times, but it didn’t work. She refused an amputation of her arm, so she came to our hospital. When she arrived, the lump was huge, bleeding, and smelly. Tests showed it was cancer called Ewing’s sarcoma, and it had spread into the muscles but not into her arm joint or chest. She had surgery to remove the entire lump and surrounding tissue, including part of her shoulder blade and muscles. The area was cleaned and covered with a flap of skin from her back to close it. After surgery, she got radiation and chemotherapy, and also had a special treatment to help her body recover. Now, after 3 years, she has no signs of cancer, can use her left arm normally, and is back to her regular work.\"\n}"}
+{"row_index": 385, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 24-year-old woman was diagnosed with Ewing’s sarcoma in her left scapula (shoulder blade) and had previously undergone surgery and chemotherapy. Over time, the tumor grew large, causing a massive, bleeding mass on her left upper back and shoulder, severe pain, and inability to use her left arm. The tumor was so large that it caused an open ulcer that wouldn’t heal. After multiple failed treatment attempts and being offered a limb amputation, she refused and was referred to our hospital. There, she received a surgery to remove the entire tumor, including part of the shoulder blade, surrounding muscles, and skin, with no cancer cells left behind. Before surgery, she received antibiotics, blood transfusions, and treatment to stop the tumor’s blood supply. After surgery, she received radiation therapy and chemotherapy, followed by a stem cell transplant to help her body recover. She has been disease-free for three years and now has full use of her left arm and is back to her normal work activities.\"\n}"}
+{"row_index": 386, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 24-year-old female presented with a massive fungating mass over the left upper back and shoulder region, characterized by active bleeding and foul-smelling purulent discharge from a large, non-healing ulcer. The lesion had been progressively enlarging over the prior two years, with an insidious onset of swelling. An incisional biopsy performed one year prior yielded a provisional diagnosis of Ewing’s sarcoma (ES) of the left scapula, prompting initiation of chemotherapy and subsequent surgical resection after three months of chemotherapeutic intervention. However, the surgical wound failed to heal, resulting in a rapidly expanding ulcer that persisted despite treatment. Neoadjuvant chemotherapy was initiated to shrink the tumor, but due to poor response—manifested by continued progressive growth and lack of tumor reduction—the regimen was modified multiple times over nine months without clinical benefit. Given the extensive size, invasive nature, and associated complications, multiple referral centers recommended forequarter amputation of the left upper limb, which was declined by the patient. She was ultimately referred to our institution for definitive management.\\n\\nOn presentation, magnetic resonance imaging (MRI) of the shoulder and upper back revealed a large, heterogeneous lesion measuring 18 cm × 27 cm × 26 cm, with T1 isointense and T2 heterogeneous high-signal intensity, consistent with a highly cellular, necrotic, and cystic tumor. The imaging demonstrated multiple fluid levels, degenerative cystic changes, hemorrhagic foci, areas of necrosis, and significant infiltration of periscapular musculature. Computed tomography (CT) scanning confirmed an ill-defined, heterogeneous tumor with prominent cystic components and gross osteolysis of the scapular bone, while no evidence of involvement was observed in the shoulder joint, chest wall, or brachial plexus. The axillary vascular bundle was displaced anteriorly without signs of vascular infiltration. Whole-body positron emission tomography-CT (PET-CT) scan showed no evidence of pulmonary or distant metastatic disease, supporting a localized, primary malignancy.\\n\\nHistopathological examination of a needle biopsy confirmed the diagnosis of Ewing’s sarcoma, demonstrating sheets of small, round, uniform cells with scant cytoplasm, separated by fibrous strands, and exhibiting minimal stromal component and few mitotic figures. Immunohistochemical staining was positive for CD99, a hallmark marker of Ewing’s sarcoma,"}
+{"row_index": 387, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 25-year-old man got into a fast car crash and hurt his wrist badly. His hand was stuck against the steering wheel, which broke the bone in his wrist. He was in extreme pain, even with pain medicine, and couldn’t have anyone touch his arm without it hurting. To fix the pain without putting him to sleep, doctors used a needle guided by ultrasound to inject numbing medicine into the nerves in his shoulder area. This made his arm completely numb and pain-free. After that, they were able to fix the broken bone without him feeling any pain. He went home the same day with a splint and will see a doctor for follow-up. The next day, he said his arm felt normal — no numbness or tingling.\"\n}"}
+{"row_index": 388, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 25-year-old man came to the emergency department after a high-speed car crash. He had a Colles fracture in his right wrist, caused when his hand hit the steering wheel during the collision. Despite taking strong pain medications, he continued to have severe pain and couldn't tolerate having his wrist moved. To control the pain without using sedation, doctors performed an ultrasound-guided nerve block called a CCBPB. This block numbs the nerves in the upper arm, providing strong pain relief. After the procedure, the patient had complete numbness in his right arm and reported no pain at all. The broken bone was successfully realigned without further pain. He was given a splint and sent home with follow-up care. The next day, he reported no numbness, tingling, or weakness, and felt fully recovered.\"\n}"}
+{"row_index": 389, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 25-year-old male with no significant past medical history presented to the emergency department via ambulance following a high-speed motor vehicle collision in which he served as a restrained driver. During impact, he braced his outstretched right hand against the steering wheel, resulting in a traumatic injury to the wrist. On arrival, vital signs were stable, but the patient exhibited profound distress, reporting pain at 10/10 on the numeric rating scale. Physical examination revealed a grossly deformed right wrist with prominent dorsal swelling and severe tenderness to palpation, with no signs of neurovascular compromise. Radiographic evaluation demonstrated a transverse fracture of the distal radius with dorsal angulation of the distal fragment—consistent with a Colles fracture—and an associated ulnar styloid fracture.\\n\\nDespite administration of multimodal analgesia including intravenous opioids and nonsteroidal anti-inflammatory drugs (NSAIDs), the patient continued to experience intractable, severe pain, with absolute intolerance to radial manipulation, which precluded safe and effective manual reduction. To avoid the need for procedural sedation, an ultrasound-guided costoclavicular brachial plexus block (CCBPB) was performed as a targeted regional anesthesia strategy to achieve dense surgical anesthesia of the upper extremity and facilitate fracture reduction.\\n\\nInformed consent was obtained. The patient was monitored via continuous cardiac telemetry and had intravenous access established. He was positioned supine with the right arm abducted to 90 degrees to optimize anatomical exposure by stretching the pectoralis major and minor muscles, thereby bringing the costoclavicular brachial plexus into a more superficial and accessible position. Standard sterile technique was maintained throughout the procedure. A high-frequency linear ultrasound probe was positioned transversely just inferior to the midpoint of the right clavicle within the infraclavicular fossa, with the beam angled slightly cephalad to visualize the costoclavicular space posterior to the clavicular body. The costoclavicular brachial plexus cords were identified in the region lateral to the axillary artery and situated between the subclavius and serratus anterior (upper slips) muscles. Using an in-plane, lateral-to-medial approach, a 22-gauge, 50-millimeter echogenic needle was advanced between the lateral and posterior cords of the brachial plexus. Twenty milliliters of 0.5% rop"}
+{"row_index": 390, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"Ms. B is an 86-year-old woman who came to the hospital with a four-day history of not being able to move her bowels, not eating, feeling sick, and vomiting. She had pain in her belly, especially after eating, and her stomach was swollen. She had a history of some health problems like cancer of the skin (Kaposi sarcoma), high blood pressure, joint pain, and low vitamin D. She had had a C-section and a tonsil removal before. She lived alone but could still take care of herself.\\n\\nWhen checked, her belly was swollen and painful, especially on the lower side. Her blood tests showed signs of infection and a slightly swollen liver, which means something was blocking the flow of bile. Her kidneys were a little affected, likely because she wasn’t eating much and was dehydrated. Her urine was normal.\\n\\nA scan showed two big gallstones — one stuck in the first part of the small intestine (duodenum) and one in the end of the large intestine (colon). The gallbladder was swollen and had gas, which means it was leaking into the intestines. This is called a gallstone fistula. The doctor diagnosed her with Bouveret syndrome and gallstone coleus.\\n\\nShe got IV fluids and a tube put in her nose to drain her stomach. She started antibiotics to fight infection. The doctors decided to do an open surgery (not laparoscopy) because the stones were big and hard to reach, and there was likely scar tissue. During surgery, they found two places where the stones were blocking the intestines. They tried to push one stone into her stomach but couldn’t. They cut open the first part of the small intestine and removed the stone. They also opened the end of the large intestine and removed the second stone. There was no cancer or serious damage found. The cuts were closed with stitches, and the small intestine was reinforced with a piece of healthy tissue.\\n\\nThe surgery went well. She didn’t need extra help like breathing machines or heart medicine. Her diet was slowly restarted. She was sent home to her family and will keep checking in with a general surgery doctor.\"\n}"}
+{"row_index": 391, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"Ms. B is an 86-year-old Italian woman who came to the emergency department with worsening bowel blockage. She had been experiencing four days of severe abdominal pain, nausea, vomiting, loss of appetite, and trouble passing stool. Her medical history includes Kaposi sarcoma, high blood pressure, joint pain (osteoarthritis), and low vitamin D. She had previously had gallbladder inflammation but never had surgery to remove it. She also had a caesarean section and tonsillectomy. She lived alone but could care for herself.\\n\\nOn exam, her vital signs were normal, but her abdomen was swollen and tender, especially in the lower part. Bowel sounds were still present. Lab tests showed mild signs of inflammation and early kidney issues due to dehydration. Liver tests showed a pattern consistent with a blockage in the bile flow. The CT scan found two large gallstones — one in the first part of the small intestine (duodenum) and one in the lower large intestine (distal colon). The gallbladder was inflamed and had gas, which suggested a connection between the gallbladder and the intestine (a fistula). The common bile duct was enlarged, confirming the diagnosis of Bouveret syndrome with gallstone coleus.\\n\\nShe was given IV fluids, antibiotics, and a tube to drain stomach contents. A laparotomy (open surgery) was performed because laparoscopy was too risky due to the stones and possible scar tissue. During surgery, both stones were found and removed — one from the duodenum and one from the sigmoid colon. The duodenal stone could not be moved, so it was removed by cutting open the first part of the small intestine. The colon stone was removed after making a small incision. There was no sign of a serious infection or tumor. The area around the gallbladder and duodenum showed signs of inflammation, which suggested a possible connection between the gallbladder and the intestine.\\n\\nNo gallbladder removal or bile duct surgery was done because the exact anatomy was unclear and the patient had many health problems that made those procedures too risky. Her recovery after surgery was smooth. She did not need extra support like breathing or heart medications. Her diet was gradually restarted, and she was discharged to her family. She is now being followed up in a general surgery clinic.\"\n}"}
+{"row_index": 392, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"Ms. B is an 86-year-old Italian woman with a complex medical history including Kaposi sarcoma, hypertension, osteoarthritis, and vitamin D deficiency. She presented to the emergency department with a four-day history of obstipation, anorexia, nausea, vomiting, worsening colicky abdominal pain, and postprandial reflux. Her surgical history includes a lower abdominal midline cesarean section and tonsillectomy; she lives independently and has no significant functional limitations. On physical examination, vital signs were normal, but the abdomen was distended, tender on palpation and percussion, with localized guarding, particularly in the lower quadrant. Bowel sounds were present, suggesting preserved peristalsis despite obstruction.\\n\\nLaboratory findings revealed a mildly elevated white cell count of 15.6 × 10⁹/L (normal: 4.0–11.0 × 10⁹/L) and C-reactive protein of 67 mg/L (normal <6.0 mg/L), indicating acute inflammation. Liver function tests showed bilirubin of 25 μmol/L (normal 2–20 μmol/L), alanine aminotransferase (ALT) of 18 U/L (normal <33 U/L), alkaline phosphatase (ALP) of 135 U/L (normal 30–110 U/L), and gamma-glutamyl transpeptidase (GGT) of 56 U/L (normal <56 U/L), consistent with an obstructive liver pattern. Serum creatinine was 99 μmol/L (normal 45–90 μmol/L) and urea was 8.6 mmol/L (normal 2.5–7.5 mmol/L), reflecting mild acute kidney injury secondary to reduced oral intake and dehydration. Electrolytes were within normal limits, and urinalysis was unremarkable.\\n\\nAbdominal computed tomography (CT) demonstrated two gallstones: one measuring 3.0 cm lodged in the proximal duodenum and another 3.3 cm located in the distal sigmoid colon. The gallbladder was contracted and inflamed, with gas detectable within the biliary tree (pneumobilia), suggesting a fistulous communication between the gallbladder and gastrointestinal tract. The common bile duct"}
+{"row_index": 393, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 43-year-old man has had a long problem with a type of white blood cell called eosinophils for 13 years. This has caused him to have shortness of breath, skin rashes, joint pain, stomach issues, and even problems with his breasts and kidneys. His breasts got swollen and painful, so he had surgery to remove both. His kidneys showed damage that needed treatment. He was given steroids to help his body calm down, and after a few days of strong IV steroids, his breathing and lung problem got better. Now he takes steroids every day to keep his symptoms under control. His condition is stable, and he can live a normal life with this treatment.\"\n}"}
+{"row_index": 394, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 43-year-old Chinese man has had a 13-year history of high levels of a type of white blood cell called eosinophils, along with shortness of breath for the past 7 days. Over the years, he has had a range of symptoms including stomach problems, skin rashes (like eczema and vitiligo), joint pain, breast inflammation, and kidney issues. The chronic breast inflammation was so severe that he needed a bilateral mastectomy. A bone marrow biopsy confirmed the eosinophilia, and a kidney biopsy showed a condition called focal segmental glomerulosclerosis, which is a type of kidney disease. He has been treated with steroids, starting with intravenous methylprednisolone for 3 days, followed by oral steroids at the same dose. After treatment, a chest CT scan showed improvement in his lung condition. He is now on a long-term oral steroid regimen and his condition is stable. Steroids help control his symptoms, but symptoms often return when the medication is stopped. He also had episodes of high blood pressure and protein in his urine, which were signs of nephrotic syndrome, but these have improved with treatment.\"\n}"}
+{"row_index": 395, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 43-year-old Chinese male with a 13-year history of peripheral blood eosinophilia and progressive respiratory symptoms presenting with exertional dyspnea for 7 days was admitted to our institution. His initial presentation in August 2005 revealed a white blood cell count of 8.5 × 10⁹/L with 24.2% eosinophils (2 × 10⁹/L), prompting evaluation for eosinophilic disorders. Bone marrow biopsy demonstrated 13.5% eosinophils, predominantly with normally segmented rod nuclei, consistent with chronic eosinophilic infiltration. Upon initiation of oral triamcinolone (4 mg, three times daily), eosinophil counts rapidly normalized, indicating a strong corticosteroid-responsive phenotype. However, after a 6-month taper and eventual discontinuation, progressive hyperplastic and nodular changes developed in both breasts, accompanied by abnormal lactation and bilateral axillary lymphadenopathy, leading to a diagnosis of chronic mastitis. Bilateral mastectomy was performed in January 2006, with postoperative histopathology revealing male breast development and severe chronic interstitial inflammation characterized by dilatation of mammary ducts and dense eosinophilic infiltration.\\n\\nOne month later, the patient presented with trunk and limb joint pain, movement dysfunction, and a worsening erythematous skin rash. Treatment with dexamethasone and prednisone was initiated, and briefly, an herbal extract (Tripterygium wilfordii) was administered due to its anti-inflammatory properties, but was discontinued owing to severe treatment-related alopecia. Joint symptoms gradually improved, allowing functional recovery and return to work.\\n\\nIn April 2017, spontaneous bilateral lower extremity edema emerged, with clinical features consistent with nephrotic syndrome: blood pressure of 150/100 mmHg, plasma albumin of 15.6 g/L, low-density lipoprotein of 6.87 mmol/L, and 24-hour urinary protein excretion of 14.78 g/d. A renal biopsy confirmed focal segmental glomerulosclerosis (FSGS), non-specific type, a histopathological pattern commonly associated with chronic eosinophilic inflammation and immune dysregulation. Repeat bone marrow aspiration confirmed persistent eosinophilia, though qualitative polymerase chain reaction (PCR)"}
+{"row_index": 396, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 4-month-old boy came to the hospital with a lump on his head that was swollen, painful, and leaking pus. The lump got bigger and turned into a sore, and doctors found tiny worms inside it. Even after giving antibiotics and removing the worms, the boy still had fever and pus. X-rays and a 3D scan showed the bone around the lump was infected. The doctors changed the antibiotics and gave them for six weeks, plus used a skin flap to cover the area. After all this, the boy started feeling better and was sent home with more medicine and follow-up visits.\"\n}"}
+{"row_index": 397, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 4-month-old male boy from a low-income area in Cartagena, Colombia, was brought to the emergency room with a painful, swollen bump on his skull that had pus draining from it. The bump had grown and turned into an open sore, and doctors found larvae inside it. He had a history of skin conditions like seborrheic dermatitis and fungal hair disease. He was given antibiotics at first, but the infection did not improve. The lesion worsened, and despite removing the larvae surgically, the boy continued to have fever, pain, and drainage. A skull X-ray showed a bone breakdown, and a 3D CT scan confirmed that the infection had spread to the outer part of the skull bone (osteomyelitis). The treatment was changed to include clindamycin and ivermectin, and he received antibiotics for six weeks, followed by four weeks of rifampicin. A skin flap surgery was also done to cover the damaged area. Tests for HIV were negative. After treatment, the boy’s symptoms improved, and he was discharged with ongoing antibiotic therapy and follow-up visits.\"\n}"}
+{"row_index": 398, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"Male patient, 4 months old, from a low-income neighborhood in Cartagena de Indias, Colombia, with a prior history of seborrheic dermatitis and tinea capitis, presented to the emergency department with a one-week history of fever accompanied by a nodular lesion localized on the parietal region of the skull. The lesion was characterized by significant edema, tenderness, pain, and spontaneous purulent drainage. Initial empiric therapy with cefalotin was initiated, but no clinical improvement was observed. Over the course of hospitalization, the lesion evolved into a 3 cm diameter ulcer, and at admission, Dermatophagoides hominis larvae were directly visualized within the ulcerated orifice. Surgical debridement was performed, resulting in the removal of approximately ten larvae. Despite this intervention, the patient continued to exhibit fever, purulent exudate, and persistent larval presence even after six days of antibiotic therapy. Consequently, a combination regimen of clindamycin and ivermectin was introduced. Imaging evaluation revealed a skull radiograph demonstrating an osteolytic lesion, with 3D reconstructed computed tomography confirming osteomyelitis affecting the outer parietal bone surface. The patient received a total of six weeks of clindamycin therapy and four weeks of rifampicin, in addition to surgical intervention involving a scalp flap. Human immunodeficiency virus (HIV) testing, including both primary and secondary assays, was performed and returned negative, ruling out HIV as a contributing factor. Clinical improvement was achieved following the combined antimicrobial and surgical approach, and the patient was discharged with continued outpatient antibiotic therapy and scheduled follow-up visits. The clinical course reflects a complex case of cutaneous larva migrans with secondary osteomyelitis, likely secondary to deep tissue invasion by D. hominis larvae, which may have been facilitated by compromised skin integrity due to preexisting dermatological conditions and potential immunological vulnerability. The persistence of infection despite initial antibiotic coverage underscores the importance of accurate parasitic identification and the need for targeted antimicrobial and surgical management in pediatric cases involving deep cutaneous and osseous involvement.\"\n}"}
+{"row_index": 399, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A very small baby born early had a lung problem where air got trapped in the chest. Even after putting in a tube to fix it, the air stayed and the lung kept collapsing. Doctors had to cut open the chest to find a small hole in the air pipe (bronchus) that was letting air in. They fixed the hole with a patch and stitched it closed. After that, the lung started to work better. The baby had to have this surgery twice because the hole kept leaking air. After both surgeries, the air stopped coming back, and the baby finally got better. He’s now home with a small machine to help breathe and uses only a little oxygen.\"\n}"}
+{"row_index": 400, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A preterm baby born at 27 weeks developed pneumomediastinum and pneumothorax, both of which did not go away even after inserting a chest tube. The pneumothorax kept coming back, and doctors eventually had to perform a thoracotomy to find and fix a tear in the bronchus. During the surgery, they found a 1 cm hole between the left bronchus and the carina, repaired it with a patch, and used stitches and medical glue to secure it. After the first surgery, the baby still had another episode of air leak, so they did a second thoracotomy at the same site and repaired it again. The hole was fixed, and no air leaks were found after the procedure. The baby also had a small heart issue (patent ductus arteriosus) that was managed during the surgery. After recovery, the chest tubes were removed, and the baby was discharged home on day 161 with a home ventilator and oxygen support.\"\n}"}
+{"row_index": 401, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 27-week 4-day preterm male infant, born via cesarean section from a dichorionic diamniotic twin pregnancy with a birth weight of 1135 grams, presented with severe respiratory distress following premature rupture of membranes at 27 weeks, accompanied by uterine contractions and vaginal bleeding. Antenatal corticosteroids were administered, and delivery was planned due to arrested labor. At birth, the neonate exhibited hypotonia and apnea, requiring immediate intubation within one minute due to respiratory failure with an uncuffed endotracheal tube. APGAR scores were 4 at 1 minute, 6 at 5 minutes, and 7 at 10 minutes. The infant was admitted to the newborn intensive care unit (NICU) where a diagnosis of respiratory distress syndrome (RDS) was established. Treatment included endotracheal administration of poractant alfa (200 mg/kg), parenteral ampicillin-gentamicin for broad-spectrum coverage, and caffeine citrate to mitigate apnea. Mechanical ventilation was initiated in assist-control mode with volume guarantee and a maximum inspiratory pressure of 20 cm/H₂O. Cranial ultrasound revealed no structural abnormalities. On day 3, the infant was extubated and transitioned to nasal intermittent positive pressure ventilation (NIPPV), but required reintubation due to recurrent respiratory failure. Antibiotic therapy was escalated to vancomycin-meropenem due to clinical deterioration. On day 5, the infant developed worsening acute hypoxic respiratory failure. Chest radiography demonstrated mediastinal pneumothorax, with follow-up imaging showing rapid progression of pneumothorax on the left side and rightward mediastinal shift. A chest tube was inserted through the left 5th intercostal space to manage the pneumothorax. Repeat imaging showed expansion of the left lung and air bronchograms on the right. Ten hours later, persistent acidosis and hypoxia were noted, with a subsequent chest x-ray confirming recurrence of left-sided pneumothorax. The chest tube was set to continuous suction, resulting in progressive resolution of the pneumothorax on serial imaging. On day 6, echocardiography revealed a 3 mm patent ductus arteriosus (PDA) with predominantly left-to-right shunting and evidence of pulmonary hypertension. Oxygen saturation was approximately 80%, and"}
+{"row_index": 402, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 40-year-old man who worked in construction suddenly lost strength in his right arm and leg six days before he went to the hospital. He didn’t have any injury or neck pain from hitting his head. His neck didn’t hurt, and he didn’t have diabetes or high blood pressure. He had smoked for 10 years. When doctors checked him, his brain and speech were normal, but his right side was weak — he couldn’t lift his right arm or stand on his right leg. His right leg had no feeling, and his right hand had weak touch. The doctors found that the problem was in the spine, specifically in the neck area, and it was called Brown-Séquard syndrome on the right side. The brain scan was normal, but the neck spine scan showed a blockage in the blood vessel that supplies the spine — a torn blood vessel (vertebral artery dissection). This blockage caused damage to the spinal cord. After three months of medicine to stop blood clots and prevent blood from sticking together (anticoagulation and antiplatelets), the blood vessel healed and the strength returned. He felt much better and could walk again. Doctors said he should keep coming back for check-ups, but he didn’t.\"\n}"}
+{"row_index": 403, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 40-year-old man who was otherwise healthy suddenly developed weakness on his right side six days before coming to the hospital. The weakness started about 16 hours before admission and made it hard for him to lift his right arm or stand on his right leg. He had no history of neck injury, surgery, or infections, and had no diabetes or high blood pressure. He had smoked for 10 years.\\n\\nNeurological tests showed that his brain and speech were normal, but his right side had significant weakness. His right arm had only mild strength, his right leg had no strength, and his left side was normal. Sensation to pain and temperature was reduced on the left side below the neck, and reflexes were weak. These signs pointed to a condition called right-sided Brown-Séquard syndrome at the C3 level of the spinal cord.\\n\\nBrain scans (head CT and MRI) were normal. Cervical spine MRI showed swelling and damage to the right side of the spinal cord at the C1-C3 level, indicating a spinal cord infarction (blockage of blood flow). A high-resolution MRI scan (VISTA) revealed a tear in the vertebral artery on the right side at the same level, which is known as vertebral artery dissection (VAD). This dissection likely caused the blood clot that damaged the spinal cord.\\n\\nThe patient was treated with anticoagulation (to prevent blood clots) and antiplatelet medications (to reduce clotting) for three months. After this treatment, follow-up MRI scans showed that the spinal cord damage improved and the vertebral artery had begun to heal. His symptoms greatly improved, and he was able to walk again. He was discharged with a good recovery score and advised to follow up, though he chose not to.\"\n}"}
+{"row_index": 404, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 40-year-old male building worker presented with acute onset of right-sided body weakness, initially manifesting as inability to lift the right upper limb and inability to stand on the right lower limb, which began 16 hours prior to hospital admission. There was no history of trauma, neck manipulation, surgery, or prior infectious illness. The patient had no history of diabetes and was normotensive. He was a chronic smoker with a 10-year history of tobacco use. Neurologic examination revealed intact consciousness and speech, with normal cranial nerve function. Using the Medical Research Council muscle grading scale, the right upper proximal limb demonstrated muscle power of 4/5, the right distal limb 2/5, and the right lower limb 0/5; contralateral limbs were intact at 5/5. Sensory deficits included loss of joint position and vibration sense in the right lower limb, impaired position sense in the right hand, and reduced pain and temperature sensation on the left side below the C3 level. The right ankle reflex was diminished. These findings are consistent with a right-sided Brown-Séquard syndrome at the C3 level. Deep sensation was preserved on the left side of the body. The Kernig sign was negative. Laboratory evaluations—including hematologic, biochemical, and immunologic parameters—were within normal limits. Cerebrospinal fluid obtained via lumbar puncture was unremarkable. Head CT and MRI were normal, excluding intracranial pathology. Cervical spine sagittal T2-weighted MRI demonstrated spinal cord swelling with a hyperintense lesion at the C1–C3 level. Axial T2-weighted sequences confirmed hyperintensity of the right spinal cord, consistent with spinal cord infarction (SCI). High-resolution 3D volumetric isotropic turbo spin echo (VISTA) MRI revealed asymmetric narrowing of the right vertebral artery at the C1–C3 level, with an eccentric high-signal intensity lesion parallel to the vessel lumen, indicative of vertebral artery dissection (VAD) with intramural hematoma. This finding established a pathophysiological link between the VAD and the ischemic spinal cord injury. The patient was treated with a combination of anticoagulant (AC) and antiplatelet (AP) therapy for a duration of 3 months. Follow-up MRI demonstrated a significant reduction in the abnormal spinal cord signal intensity, and VISTA imaging confirmed"}
+{"row_index": 405, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 76-year-old man had pain in his right leg when walking, which meant his leg blood flow was blocked. Doctors found the blockage in the right leg artery using a scan. They fixed it with a small tube (stent-graft) placed inside the artery. After the fix, the man started having pain and swelling in his right thigh, but no fever or infection was found. Blood tests showed his body was inflamed, like it was fighting something. A scan showed swelling around the artery and signs of inflammation. Doctors gave him steroids to calm the swelling, and within 7 days, the pain went away. The steroid dose was slowly lowered over 3 weeks. A follow-up scan after 3 months showed the swelling and inflammation had mostly gone away. The fix worked and his leg pain is now better.\"\n}"}
+{"row_index": 406, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 76-year-old man with pain in his right leg (claudication) was found to have a blockage in his right superficial femoral artery, confirmed by a CT scan. He had a history of high blood pressure, high cholesterol, and smoked in the past. Treatment involved endovascular therapy, where a stent-graft named Viabahn (25 cm, 5 mm diameter) was placed to open the blocked artery. During the procedure, ultrasound was used to guide the stent through the artery safely. After the procedure, the patient developed pain and swelling in his right thigh about 5 days later. Blood tests showed high levels of inflammation, and MRI scans showed swelling in the surrounding tissue and increased signal around the artery, suggesting inflammation around the stent. There was no sign of infection or blood clot. The doctors started steroid medication (prednisolone) to reduce the inflammation, and within 7 days, the symptoms went away. The steroid dose was slowly reduced over 3 weeks and stopped. Follow-up MRI scans showed that the swelling and inflammation had greatly improved over the next few months. The patient recovered well and his condition stabilized.\"\n}"}
+{"row_index": 407, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 76-year-old male with peripheral arterial disease classified as Fontaine Stage IIB presented with right leg claudication. He had a history of hypertension, dyslipidemia, and current smoking. Preoperative contrast-enhanced computed tomography (CT) demonstrated a complete occlusion of the right superficial femoral artery (SFA). Antiplatelet therapy was initiated with 100 mg/day aspirin and 75 mg/day clopidogrel. Digital subtraction angiography revealed a 16-cm chronic total occlusion of the right SFA. Endovascular treatment (EVT) was performed under intra-arterial heparinization (5000 units). A 6-French guiding sheath was introduced via the left femoral artery. Intravascular ultrasound (IVUS) was utilized to navigate through the true lumen and confirm vessel patency, with no evidence of major dissection observed during pre-dilatation. A 4-mm semi-compliant balloon was used for pre-dilatation, followed by deployment of a 25-cm Viabahn stent-graft (diameter 5 mm) and post-dilatation with a 5-mm non-compliant balloon. Final angiographic assessment showed no edge dissection and confirmed adequate luminal patency and hemodynamic flow. The patient experienced symptomatic improvement and was discharged after 4 days. However, 6 days post-procedure, he developed acute pain and localized swelling in the right thigh. Venous thrombosis was ruled out by duplex ultrasound. Laboratory evaluation showed no signs of systemic infection: negative blood culture, procalcitonin level of 0.1 ng/ml (normal ≤0.5 ng/ml), and no fever. Nevertheless, inflammatory markers were significantly elevated: white blood cell (WBC) count of 12,000 cells/μl (normal range 4500–7500 cells/μl) and C-reactive protein (CRP) of 11.83 mg/dl (normal ≤1.0 mg/dl). Magnetic resonance imaging (MRI) revealed extensive soft-tissue edema and a high perivascular T2 signal surrounding the right SFA, consistent with perigraft inflammation. The stent-graft remained patent, indicating that the inflammatory response was localized to the perivascular tissue rather than involving graft failure. The clinical"}
+{"row_index": 408, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 27-year-old woman who drank a lot of vodka every day for years came to the hospital because she was scared and heard voices, thinking people were trying to hurt her. She had been drinking for a while and had been treated before for withdrawal, but left early. When doctors gave her a medicine called chlordiazepoxide to calm her down, she got worse—she became confused, saw things, and heard voices. But when they switched to another medicine, lorazepam, she started feeling better and soon stopped having those scary thoughts. After stopping all the medicines, she felt normal and stayed that way for hours. She’s now in a program to stop drinking and hasn’t had any more problems.\"\n}"}
+{"row_index": 409, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 27-year-old white woman with a long history of heavy alcohol use developed symptoms of withdrawal when she stopped drinking. She was admitted to another hospital for withdrawal but left before being fully discharged. When she came to our hospital, she was paranoid, believed people were trying to harm her, and heard voices. Tests showed no signs of other illnesses or drug use, and her symptoms were linked to her alcohol dependence. She was given chlordiazepoxide, a benzodiazepine used to treat withdrawal, but within hours of each dose, she became more confused, agitated, and started hearing and seeing things that weren’t there. This worsened her delirium. After stopping chlordiazepoxide, she was given lorazepam, which helped calm her and improved her mental state. By the next day, she was calm, thinking clearly, and no longer had hallucinations or paranoia. She remained stable over the next 10 hours and was referred to a program for alcohol treatment, where she did not have any further mental health issues and did not need more benzodiazepines.\"\n}"}
+{"row_index": 410, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 27-year-old Caucasian female with a established history of ethanol dependence presented to the emergency department (ED) for evaluation of possible psychosis in the context of ethanol withdrawal. Two days prior, she had been admitted to an external hospital for management of ethanol withdrawal, receiving intravenous fluids but not benzodiazepines (BNZs). She removed her intravenous line and left the facility prior to formal discharge. Her family subsequently brought her to our institution, reporting symptoms of paranoia and the belief that individuals outside her home were attempting to kill her. Her last known alcohol consumption occurred four days prior, and toxicology screening for ethanol, benzodiazepines, and barbiturates was negative in both serum and urine. She reported consuming at least five 'heavy pours' of vodka daily for several years, consistent with chronic heavy alcohol use. Physical examination revealed tachycardia (127–132 beats per minute), elevated blood pressure (143–149/102–103 mmHg), and mild tenderness on bilateral upper abdominal quadrant palpation. Despite these findings, she was calm, fully oriented, and exhibited organized thought processes, though she reported persistent paranoia involving family members intending harm and auditory hallucinations. A comprehensive medical workup for delirium was performed, including a normal complete blood count, a comprehensive metabolic panel showing mildly elevated transaminases [aspartate aminotransferase (AST) 94 U/L; alanine transaminase (ALT) 72 U/L], and a noncontrast computed tomography (CT) of the brain demonstrating mild diffuse cerebral volume loss exceeding age-matched expectations. These findings were attributed to chronic alcohol exposure and were not indicative of an independent neurodegenerative or infectious process. Urine and serum toxicology screens were negative for coronavirus (SARS-CoV-2), human immunodeficiency virus (HIV), and hepatitis B and C. The patient expressed a strong interest in achieving sustained sobriety. Initial management included oral lorazepam 2 mg, followed by initiation of chlordiazepoxide 25 mg twice daily due to persistent tachycardia and hypertension. Within two hours of each chlordiazepoxide dose, she developed acute confusion, agitation, and vivid visual and auditory hallucinations, including the perception of individuals on the other side of the door attempting to enter her room. After two doses ("}
+{"row_index": 411, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 76-year-old woman noticed a small, slow-growing spot on her left breast for 5 years. It started growing faster recently, but she didn’t feel pain or any other symptoms. The spot was about 10 mm by 8 mm, blue-gray and looked like tiny pearls. Doctors checked her body and found no signs of cancer spreading. Tests showed no cancer in her chest, lymph nodes, or other parts of her body. A small biopsy confirmed it was a type of skin cancer called pigmented superficial BCC. She had surgery to remove the spot with a 10 mm safe edge around it. The doctors checked the edges right after surgery and found no cancer left. She went home the second day after surgery and has been feeling fine. At a 3-month check-up, there was no sign of the cancer coming back or spreading.\"\n}"}
+{"row_index": 412, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 76-year-old Asian woman had a slowly growing spot on her left breast for 5 years, with recent faster growth. She had no pain, itching, or other symptoms. She did not have a history of cancer or major health conditions like high blood pressure, heart disease, or diabetes. Her family and personal history of skin or breast cancer was negative, and she had no significant sun exposure or radiation exposure.\\n\\nOn exam, a 10 mm × 8 mm blue-gray, pearl-like spot was found on the breast, with slight surface erosion. The rest of her body was normal. Imaging tests — including breast ultrasound, chest CT, SPECT-CT, and lymph node ultrasound — showed no signs of cancer spreading to other parts of the body.\\n\\nA biopsy confirmed the lesion was a type of skin cancer called pigmented superficial basal cell carcinoma (BCC). The cancer started in the top layer of the skin and had a characteristic appearance under the microscope.\\n\\nThe patient had surgery to remove the lesion, including the nipple and areola, with a 10 mm safety margin around it. During surgery, the doctors checked the edges of the removed tissue and found no remaining cancer cells. After the procedure, the patient was discharged on the second day and had a follow-up visit at 3 months. She remained symptom-free and showed no signs of cancer returning or spreading.\"\n}"}
+{"row_index": 413, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 76-year-old Asian female presented with a 5-year history of a slowly enlarging lesion on the left breast, with recent acceleration in growth. She reported no pain, pruritus, or systemic symptoms. Medical history was notable for hyperlipidemia, with no comorbidities including hypertension, cardiovascular disease, diabetes, hepatitis, tuberculosis, immunosuppression, or arsenic exposure. There was no personal or familial history of skin or breast cancer, and no significant history of solar or ionizing radiation exposure.\\n\\nPhysical examination revealed a stable, otherwise well-appearing elderly patient without distress. The left breast demonstrated a 10 mm × 8 mm pigmented plaque with superficial erosion; surrounding skin was intact and unremarkable. No other abnormalities were detected.\\n\\nImaging modalities including breast ultrasound, chest computed tomography (CT), SPECT-CT, and axillary lymph node ultrasound were performed to assess for metastatic disease, all of which returned negative results, indicating no evidence of distant spread.\\n\\nDermoscopic evaluation of the lesion revealed characteristic features including multiple blue-gray globules, spoke-wheel patterns, leaf-like structures, and areas of erosion—findings consistent with pigmented basal cell carcinoma (BCC). Histopathological examination confirmed the presence of tumor nests originating from the superficial epidermis, exhibiting a palisading pattern of tumor cells with a narrow, pigmented cleft surrounding the nests—pathognomonic for pigmented superficial basal cell carcinoma.\\n\\nGiven the patient’s age, the absence of metastatic disease, and the benign clinical course, standard surgical excision was selected after shared decision-making with the patient and her family. The procedure involved complete removal of the nipple and areola with a 10 mm circumferential margin, followed by primary closure. The excised specimen measured 2.0 × 1.8 cm and extended into the subcutaneous adipose tissue layer. Intraoperative frozen section analysis and subsequent postoperative histopathological evaluation both confirmed clear margins, with no residual tumor cells at the surgical edges.\\n\\nThe patient was discharged on postoperative day 2. No adjuvant therapy was required due to the absence of microscopic residual disease. At a 3-month follow-up, the patient remained asymptomatic, with no clinical signs of local recurrence or metastatic progression. The lesion is currently considered fully resected with no evidence of disease recurrence in the"}
+{"row_index": 414, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 32-year-old woman had kidney problems and needed dialysis for 3 years. She started having bad shaking in her arms, neck, and legs, which got worse over 5 days. The shaking wasn’t just in one part — it spread to both sides of her body. A brain scan showed spots in the deep part of her brain (the basal ganglia) that were damaged, and these spots were the same on both sides. Doctors found that the shaking was likely caused by two things: bad waste from her kidneys and an overactive thyroid. She was treated with stronger dialysis, oxygen therapy, and medicine to fix her thyroid. After a month, the shaking stopped completely, and she could move her body normally again. Her brain scans showed the spots were mostly gone, and her blood tests showed her kidney and thyroid levels were getting better.\"\n}"}
+{"row_index": 415, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 32-year-old woman with chronic kidney disease had been on hemodialysis for 3 years. She started experiencing severe involuntary movements in her shoulders and neck about 5 days before being admitted to the hospital, which later spread to her limbs. Brain scans showed symmetric, non-hemorrhagic lesions in both sides of her brain’s basal ganglia, areas involved in movement control. These lesions were linked to a combination of uremic toxins (build-up from kidney failure) and hyperthyroidism (overactive thyroid). After treatment with high-frequency, high-flux dialysis, hyperbaric oxygen therapy, and medication to lower her parathyroid hormone levels, her symptoms improved significantly. Within a month, she regained full control of her movements and was discharged. Follow-up scans showed the brain lesions had mostly disappeared, and her blood tests showed improved levels of toxins and thyroid-related markers. The condition was diagnosed as a movement disorder caused by damage to the basal ganglia from kidney disease and thyroid issues.\"\n}"}
+{"row_index": 416, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 32-year-old female with non-diabetic chronic kidney disease underwent regular hemodialysis via a right forearm arteriovenous fistula for three years. She was admitted due to a five-day history of progressive involuntary movement, initially manifesting as a resting tremor in the shoulders and neck, which progressively evolved into generalized, uncontrolled limb movements. Vital signs were stable, with no evidence of headache, fever, visual disturbance, or cognitive impairment. Neurological examination revealed normal myodynamic parameters and deep tendon reflexes, with suspiciously positive Babinski signs indicating upper motor neuron involvement. Prior to admission, there was a documented history of significant blood creatinine fluctuations, primarily attributed to suboptimal dialysis, and a concurrent severe hyperthyroid state characterized by intact parathyroid hormone (iPTH) levels of 3200 pg/mL, with no prior history of hypertension, diabetes mellitus, respiratory infection, stroke, hepatic disease, hypoxia, or toxic exposure.\\n\\nBrain magnetic resonance imaging (MRI) performed five days after symptom onset demonstrated symmetrical hyperintense non-hemorrhagic lesions on T2-weighted imaging (T2WI) and T2/fluid-attenuated inversion recovery (T2FLAIR) sequences in the bilateral basal ganglia, consistent with acute or subacute neurotoxic injury. Additional findings included mild diffusion restriction in the corona radiata, suggestive of early ischemic or cytotoxic edema, while T1-weighted imaging (T1WI) and diffusion-weighted imaging (DWI) remained within normal limits, indicating no acute cytotoxic or hemorrhagic change. These findings are consistent with a neurodegenerative or neurotoxic process affecting the basal ganglia circuitry, particularly the striatum, which is critical for motor control.\\n\\nInitial blood work upon admission revealed markedly elevated uremic toxin levels: urea nitrogen 25.80 mmol/L, serum creatinine 1206 μmol/L, uric acid 548 μmol/L, phosphorus 1.88 mmol/L, calcium 2.33 mmol/L, and anion gap 23.9 mmol/L—indicative of severe uremic burden and metabolic derangement. Hyperthyroidism was confirmed with iPTH of 2487 pg/mL, suggesting a state of secondary hyperparathyroidism likely secondary to chronic uremia and"}
+{"row_index": 417, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 68-year-old woman had numbness in her left arm and pain in her neck. Doctors found a problem with blood vessels in her neck that were pressing on her nerves and spine. This caused her arm to feel numb and weak, and her shoulder to hurt. Tests showed a strange blood vessel connection (like a leak) between her left neck blood vessel and a vein near the spine, at the C5 level. The doctors fixed it using a small tube and special coils placed through her leg artery. They used a balloon to hold the tube in place and put the coils tightly to stop the leak. After the fix, the pain and numbness went away. The woman fully recovered, with no return of the leak or symptoms, and her nerves were no longer being pressed. Four years later, MRI showed the blood vessel problem was completely gone and her arm and neck were back to normal.\"\n}"}
+{"row_index": 418, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 68-year-old woman came in with numbness in her left arm and pain in her neck. At first, doctors thought it was a musculoskeletal issue, but her symptoms got worse over time. Imaging tests showed abnormal blood vessels pressing on the nerves and spinal cord in her neck, specifically between the C4 and C6 levels. This was confirmed by MRI and angiography, which found a large blood vessel connection — called a VVAVF — between the left vertebral artery and the vertebral venous plexus at the C5 level. This abnormal connection was causing the nerve compression and pain.\\n\\nTo fix it, the patient underwent a minimally invasive procedure under general anesthesia. A small catheter was inserted through her right femoral artery and guided to the area of the blood vessel connection in her neck. Using a special technique with tiny coils and a balloon to keep the catheter stable, doctors successfully blocked the abnormal blood flow. The procedure was done carefully to avoid damaging nearby blood vessels.\\n\\nAfter the treatment, the patient’s pain and numbness improved within a month. Four years later, she is doing well with no return of symptoms. Follow-up MRI scans show that the abnormal blood vessel is gone and the nerves are no longer compressed. The left vertebral artery remains open and healthy, and there has been no leakage or complications. She was able to recover fully and has returned to normal daily life.\"\n}"}
+{"row_index": 419, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 68-year-old woman with no prior history of trauma or vascular disease presented to the orthopedic surgery department for progressive left upper limb numbness and left neck pain. Noncontrast head CT and cervical spine X-ray were unremarkable, and initial management included analgesics, with no improvement over a 12-month period. Cervical magnetic resonance imaging (MRI) revealed an extramedullary lesion characterized by flow voids and abnormal vascular morphology adjacent to the left neural foramen from C4 to C6, demonstrating compression of spinal nerve roots and the spinal cord. Neurological examination confirmed left C5 radiculopathy, with hyperesthesia in the left arm and scapula, and weakness in the left deltoid and biceps brachii muscles. A vascular murmur was auscultated in the left neck, suggesting a high-flow vascular abnormality.\\n\\nMR angiography (MRA) identified a left vertebral-vertebral venous arteriovenous fistula (VVAVF) with ectasia of the left vertebral artery (VA), but could not precisely localize the fistulous point. Left vertebral artery digital subtraction angiography (DSA) confirmed a high-flow VVAVF connecting the left VA to the vertebral venous plexus, with a single, well-defined fistulous origin at the C5 level within the V2 segment. The fistula drained into the anterior internal vertebral venous plexus, forming a large venous network. No filling of the fistula was observed from the anterior cerebral circulation, confirming the absence of collateral flow from the anterior circulation. The contralateral vertebrobasilar circulation remained intact, with no evidence of steal phenomenon, indicating that the fistula was isolated to the left side.\\n\\nThe treatment strategy involved targeted microballoon-assisted coil embolization of the expanded paravertebral venous plexus to achieve complete occlusion of the shunt. Preoperatively, heparin (3000 IU intravenously) was administered to prevent thrombosis. Under general anesthesia, a 10 cm, 7-French femoral short sheath (TERUMO) was inserted into the right common femoral artery. A 90 cm, 7-French Guider Guiding Catheter ST (Stryker Japan) was advanced into the left vertebral artery. A 150 cm,"}
+{"row_index": 420, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 26-year-old man had fever, chills, headache, nausea, vomiting, and diarrhea 5 weeks after getting COVID-19. Tests showed he had been infected before, even though the virus wasn't found in his body anymore. He suddenly got very weak and his heart stopped pumping well — it was in shock. Doctors gave him medicine to help his heart beat and to get rid of extra fluid. They were worried it might be a serious heart infection, so they took a small sample of heart tissue. The test showed the heart was inflamed, but mostly with macrophages (a type of immune cell), not the kind that usually means a serious heart attack. This matched what's seen in some people who had COVID-19 and got a bad heart reaction. They called it MIS-A. He also had blood clots in his lungs, which made him short of breath. He got IVIG, steroids, and blood thinners, and started feeling better. His heart function improved, and by the end, it was working normally again. He can now exercise without limits, but is advised to avoid very intense activity. He’s on heart medicine and going to a cardiac rehab program. A follow-up scan will check how his heart is doing long-term.\"\n}"}
+{"row_index": 421, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 26-year-old man developed high fever, chills, headache, nausea, vomiting, and diarrhea about 5 weeks after recovering from COVID-19. Tests showed he had been infected with the virus in the past, but no active virus was found in his body. He was found to be in severe heart failure, with both sides of his heart not pumping properly, leading to low blood pressure and poor oxygen levels. He needed strong medications like inotropes and diuretics to support his heart function. Doctors were worried he might have had a serious heart inflammation called myocarditis, so they performed a heart tissue biopsy. The results showed mainly inflammation from macrophages (a type of immune cell), with only a few T cells, which is similar to what's seen in some COVID-19 patients. This helped rule out full-blown myocarditis and supported a diagnosis of MIS-A (Multisystem Inflammatory Syndrome in Adults), a rare condition that can occur after a COVID-19 infection. He also had blood clots in his lungs, which were treated with anticoagulation therapy. He received intravenous immunoglobulin (IVIg) and steroids to reduce inflammation, and his condition improved quickly. After recovery, his heart function returned to normal, and he was able to resume normal activities. He is now on long-term heart medications, advised to avoid very intense exercise, and is following a cardiac rehabilitation program. A follow-up heart MRI is planned to better understand the heart damage.\"\n}"}
+{"row_index": 422, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 26-year-old male presented with a 1-week history of fevers (peak 39.2°C), chills, headache, nausea, vomiting, and diarrhea. On emergency department evaluation, he was hypotensive (75/35 mmHg), tachycardic (126 beats per minute), and had an oxygen saturation of 96% on 6 L nasal cannula. Laboratory findings included leukocytosis (WBC 17.1 × 10⁹/L), lymphopenia (absolute lymphocyte count 0.73 × 10⁹/L), acute kidney injury (serum creatinine 1.9 mg/dL), lactic acidosis (lactate 4.1 mmol/L), and elevated cardiac troponin T (0.218 µg/L, above normal range <0.09 µg/L). SARS-CoV-2 PCR was negative, but SARS-CoV-2 IgG was positive, confirming prior infection. Point-of-care ultrasound revealed severely reduced biventricular function, consistent with cardiogenic shock. The patient was admitted to the cardiac care unit and initiated on intravenous diuresis and inotropes for hemodynamic support.\\n\\nFurther laboratory evaluation demonstrated elevations in transaminases, procalcitonin, NT-proBNP, ferritin, D-dimer, erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP), indicating systemic inflammation and organ stress. Chest x-ray showed right lower lobe and left lower lobe opacities, with a borderline enlarged cardiac silhouette. Electrocardiogram revealed sinus tachycardia and right axis deviation. Echocardiography revealed a left ventricular ejection fraction (LVEF) of 20%, global hypokinesis, mild left ventricular dilation, biatrial enlargement, hypokinetic and dilated right ventricle, moderate to severe mitral regurgitation due to leaflet tethering, severe tricuspid regurgitation, small pericardial effusion, and an estimated pulmonary artery systolic pressure of 53 mmHg with a right atrial pressure of 15 mmHg.\\n\\nA bedside pulmonary artery catheter was placed on admission, revealing right atrial pressure (RA) of 17 mmHg"}
+{"row_index": 423, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A young man from Serbia had a very weak heart and couldn't get enough oxygen, so doctors put in a machine to help his heart work. His heart was failing on both sides, and tests showed his heart muscle was full of iron, which made it weak. This iron buildup was causing his heart to stop working properly. Doctors found a gene problem that causes a rare condition called juvenile hemochromatosis — a condition where the body absorbs too much iron. This iron damage also hurt his pancreas, making him develop diabetes, and his body wasn’t making enough hormones for energy. He got a special heart pump to help his heart, and after a few months, his heart started to get better. The iron was removed with medicine, and his heart function improved so much that the pump was safely taken out after 131 days. His heart is now working well, and his iron levels are back to normal. He still needs insulin and regular blood removal to keep iron low, and he’s doing well and back to work.\"\n}"}
+{"row_index": 424, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 31-year-old Serbian man with severe heart failure due to iron overload was treated with life-support devices and eventually recovered. He had been diagnosed with iron buildup in his body four months earlier, which caused fatigue and other symptoms. His iron levels were very high — serum ferritin was 2,541 μg/L (normal is 30–500) and transferrin saturation was 90% (normal is 10–45%). Despite normal liver and kidney function, tests showed iron was damaging his heart, leading to very weak heart function with an ejection fraction of only 5–10%. He also developed diabetes due to iron damage to the pancreas, with poor insulin production.\\n\\nHe was admitted to the ICU and started on extracorporeal membrane oxygenation (ECMO) to support his heart and lungs. After a few days, he received biventricular assist devices (BiVAD) to help his heart pump blood. A heart biopsy showed iron deposits in the heart muscle, confirming iron overload as the cause of his heart failure. He began iron chelation therapy with desferrioxamine, which quickly reduced his iron levels. His heart function improved over time, and after 131 days, the BiVAD was successfully removed.\\n\\nGenetic testing revealed a mutation in the HJV gene (called G320V), which is linked to a rare condition called juvenile hemochromatosis — a form of iron overload that can affect the heart and pancreas, especially in young people. This condition often has no family history, which is what this patient had. He continues to receive insulin for diabetes, testosterone for low hormone levels, and regular blood removals (venesections) to manage iron. After 12 months, his heart function had returned to near normal, and follow-up scans showed no significant iron left in his heart or liver. He has returned to work and is doing well.\"\n}"}
+{"row_index": 425, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 31-year-old male of Serbian origin presented to a quaternary intensive care unit (ICU) with severe biventricular heart failure refractory to maximal inotropic support, characterized by a cardiac index of 1.3 L/min/m² on noradrenaline and dobutamine infusion. He presented with acute shortness of breath, extreme lethargy, and abdominal pain, with clinical signs of hypotension and sinus tachycardia (HR 105 bpm). Physical examination revealed a hyperdynamic apex beat with heave, jugular venous pulsation of 2–3 cm, and dual heart sounds without murmurs. Neurological status was assessed as Glasgow Coma Score 14 (E3, M5, V6). Abdominal examination showed tenderness in the right upper and lower quadrants without guarding. Notably, he had a tanned skin appearance and no peripheral edema. Laboratory investigations on admission revealed normal hemoglobin, platelets, renal function, and electrolytes, but mild derangement of liver function with elevated alanine aminotransferase (88 U/L), bilirubin (62 μmol/L), and decreased albumin (30 g/L). C-reactive protein (9 mg/L) and neutrophil count (10.27 ×10⁹/L) were mildly elevated, while white blood cell count remained within normal limits. High-sensitivity troponin I was mildly elevated (64 ng/L), suggesting subclinical myocardial injury. Urine and blood cultures were negative. Imaging demonstrated a dilated heart with pleural effusions, ascites, and liver congestion. Transthoracic echocardiography revealed severe global systolic dysfunction with left ventricular ejection fraction (LVEF) of 5–10%, right ventricular dysfunction, and mild to moderate mitral and pulmonary regurgitation, with no evidence of myocarditis or coronary artery disease.\\n\\nThe patient had a prior diagnosis of iron overload, initially identified 4 months earlier, with serum ferritin of 2541 μg/L (reference range 30–500) and transferrin saturation (TS) of 90% (reference range 10–45%). Liver biopsy showed extensive intrahepatocyte iron accumulation with minimal inflammatory infiltrate and fibrosis (hepatic iron index 1"}
+{"row_index": 426, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 43-year-old Black woman had a painful lump on the outside of her vagina on the left side. Doctors thought it was a common infection called a Bartholin's abscess and cut it out to drain the fluid. While doing that, they found a small, tan-brown bump nearby. That bump turned out to be a harmless growth called hidradenoma papilliferum, which is like a small, slow-growing bump in the skin that can sometimes get confused with an infection. It’s not serious and doesn’t need treatment unless it causes trouble.\"\n}"}
+{"row_index": 427, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 43-year-old African American woman had a painful lump on her left labia majora. Doctors initially diagnosed it as a Bartholin's abscess, which is a common infection in the glands near the vaginal opening. During surgery to remove and drain the abscess, they found an additional tan-brown lump nearby. This second lump was tested under a microscope and showed features of a condition called hidradenoma papilliferum, which is a type of benign (non-cancerous) growth that can develop in the skin. The findings suggest that the abscess formed inside this existing growth. Both conditions are not serious and were successfully treated.\"\n}"}
+{"row_index": 428, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 43-year-old African American woman presented with a painful cystic mass on the left labia majora. Preoperative imaging and clinical evaluation led to a diagnosis of Bartholin's abscess, a common benign inflammatory condition resulting from obstruction and infection of the Bartholin's gland ducts, typically involving ductal epithelial proliferation and subsequent suppuration. During surgical excision and drainage of the abscess, an additional dermal nodule measuring 2.0 × 0.8 × 0.8 cm was identified and removed for histopathological assessment. The nodule exhibited a tan-brown color consistent with chronic dermal fibrosis and adipocytic infiltration. Microscopic examination revealed fibro-necrotic foci intermingled with a well-circumscribed papillary neoplasm characterized by cystic dilation of the glandular projections. The papillary architecture was lined by basophilic cuboidal to columnar epithelial cells, with a distinct layer of compressed myoepithelial cells at the basal margin, indicating a differentiated glandular origin. Immunohistochemical staining confirmed apocrine differentiation, evidenced by the presence of foci of active decapitation secretion—where secretory vesicles are cleaved off the apical surface of the epithelial cells—suggesting functional apocrine glandular activity. The presence of these features, particularly the well-defined papillary architecture with apocrine and decapitation secretion, is consistent with Hidradenoma papilliferum, a rare benign adnexal tumor of the eccrine or apocrine sweat glands, often arising in the perineal region. The clinical scenario demonstrates a rare overlap where a Bartholin's abscess develops in the context of a pre-existing hidradenoma papilliferum, suggesting that the underlying dermal lesion may have been a latent neoplasm that became inflamed and infected. This finding underscores the importance of thorough histopathological evaluation in perineal masses, as the presence of a hidradenoma papilliferum may be missed in routine diagnosis and may have implications for long-term monitoring due to its potential for local recurrence or transformation in rare cases. The diagnosis was ultimately established as a Bartholin's abscess arising within a hidradenoma papilliferum, with the histological features supporting both the inflammatory and neoplastic components of the lesion.\"\n}"}
+{"row_index": 429, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 71-year-old man had heart problems since he was a kid. His heart didn’t work well because of a big hole in the heart and a blocked lung valve, which doctors call unrepaired TOF. He had a small tube (shunt) put in when he was 19 to help blood flow, but never had the full fix. Over the years, he had heart failure three times — at 50, 70, and 71 — but kept playing golf and living a normal life until then. When he came to our hospital, his heart was weak, had high pressure, and was not pumping blood well. Tests showed his heart had a big hole, a thick right ventricle, and a narrow lung valve. His blood was thick and his heart was working hard. Even though he couldn’t have the full surgery because of his other health issues, his doctors fixed his heart rhythm with medicine and a tiny device that shocks the heart if it goes wrong. They also gave him medicine to help his heart pump better. After a month in the hospital, his heart started working much better. One year later, he’s doing great — no more shortness of breath, and he’s still playing golf.\"\n}"}
+{"row_index": 430, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 71-year-old man with a history of heart failure had a sudden heart stoppage (cardiopulmonary arrest) caused by a fast, irregular heart rhythm (ventricular fibrillation). Thanks to quick action by bystanders, he survived without brain damage. His low potassium levels were thought to have triggered the heart rhythm problem. He was referred to our clinic for further care.\\n\\nHe had a heart murmur since childhood and was diagnosed with a serious heart condition called tetralogy of Fallot (TOF) at age 19. At 21, he had a shunt procedure (Blalock-Taussig) to help blood flow, but he never had the full repair surgery, which was recommended. For years, he was able to work and play golf without symptoms, but started having heart failure at ages 50, 70, and 71.\\n\\nAt the clinic, his blood pressure and heart rate were normal, but he had low oxygen levels and signs of poor heart function, like blue lips and clubbing. His heart scan showed a large hole in the heart (ventricular septal defect) with the aorta overriding it, thickened right ventricle, and severe narrowing of the pulmonary valve—all signs of an unrepaired TOF. A shunt from his childhood was still present. His heart was not pumping well, and the right side of the heart was enlarged and weak.\\n\\nTests showed he had blocked coronary arteries, which can damage the heart muscle. Because of his many health problems, the full heart surgery was not done. Instead, he received medication to control his heart rhythm and improve blood flow. He had a device implanted to prevent sudden, dangerous heart rhythms. His doctors carefully adjusted his medications, which helped his symptoms improve.\\n\\nOne year after being discharged, he was doing well and was able to play golf again. His heart failure symptoms had improved enough that he could now walk around without severe shortness of breath.\"\n}"}
+{"row_index": 431, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 71-year-old male with a history of chronic kidney disease, paroxysmal atrial fibrillation (AF), and chronic heart failure experienced cardiopulmonary arrest secondary to unexpected ventricular fibrillation (VF). Bystander-initiated cardiopulmonary resuscitation was promptly initiated, resulting in complete recovery without neurological sequelae. Upon prior admission, serum potassium was found to be hypokalemic at 3.3 mEq/L, leading to the hypothesis that incidental hypokalaemia contributed to the induction of VF. The patient was referred to our institution for comprehensive evaluation of his cardiac and systemic status.\\n\\nClinical history revealed a lifelong presence of a heart murmur, initially unrecognized and uninvestigated. At age 19, the patient was diagnosed with tetralogy of Fallot (TOF) and underwent palliative Blalock–Taussig shunt placement at age 21. Despite recommendations for radical intracardiac repair, the patient declined further surgical intervention. For several decades, he maintained an active lifestyle, including employment and regular participation in golf, without overt symptoms of heart failure; however, he was hospitalized at ages 50, 70, and 71 due to progressive decompensated heart failure.\\n\\nOn presentation, vital signs included a blood pressure of 114/58 mmHg, heart rate of 69 beats per minute, and oxygen saturation of 89% in ambient air. Physical examination demonstrated lip cyanosis and clubbing, with no evidence of peripheral edema. Cardiac auscultation revealed a harsh systolic ejection murmur localized to the 2nd to 4th intercostal spaces along the left sternal border. Laboratory findings included polycythaemia (hemoglobin 18.0 g/dL, hematocrit 52.6%), serum creatinine of 1.8 mg/dL, and markedly elevated brain natriuretic peptide (BNP) at 697 pg/mL. Chest radiography showed a characteristic 'boot-shaped' cardiac silhouette with bilateral pleural effusions. Electrocardiography confirmed the presence of atrial fibrillation.\\n\\nTransthoracic echocardiography demonstrated aortic overriding over a large ventricular septal defect (VSD) measuring 32 mm in diameter, right ventricular (RV) hypertrophy, and severe pulmonary sten"}
+{"row_index": 432, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A man took simvastatin for seven years to lower his cholesterol. Over time, he started getting weaker, especially in his arms and legs, and couldn't climb stairs or stand up on his own. He also lost a lot of weight. Tests showed his muscle damage was very bad — his muscle enzyme level was very high, and his body made antibodies against a protein that helps make cholesterol. A muscle biopsy showed dead muscle fibers, some new ones growing, and signs of inflammation. This condition is called SINAM, which happens when a statin drug causes the body’s immune system to attack muscles. The doctor stopped the statin and gave him strong steroids, immune shots, and methotrexate to calm the immune attack. After three months, his muscle strength came back, the enzyme level went back to normal, and he could move around again without help.\"\n}"}
+{"row_index": 433, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 70-year-old woman had been taking simvastatin for seven years to lower her cholesterol. Over time, she started feeling increasing weakness in her muscles, especially when climbing stairs or getting up from a chair. Her weakness got worse until she could no longer walk without help or do basic tasks like combing her hair or bathing. She also lost 15% of her weight over 10 months and had no fever, rash, or other signs of infection.\\n\\nTests showed very high levels of creatine kinase (a marker of muscle damage) at 2,954 U/L, and blood tests found positive antibodies to HMG-CoA reductase, a protein targeted by statins. A muscle biopsy showed signs of muscle damage, including dead muscle fibers, some new growing fibers, and inflammation around the muscle tissue. The muscle also had a higher-than-normal level of a protein called MHC class I, which is linked to immune activity.\\n\\nAfter doctors ruled out infections, cancer, and other conditions, they diagnosed her with SINAM — a rare condition where a statin drug causes an autoimmune reaction that attacks the muscles. The simvastatin was stopped immediately. She started treatment with high-dose corticosteroids (a type of anti-inflammatory drug), intravenous immunoglobulin (to calm the immune system), and methotrexate (an immune-suppressing medication).\\n\\nAfter three months, her muscle strength improved significantly, and her creatine kinase level dropped back to normal (15 U/L). She is now on a lower dose of steroids and methotrexate, and her symptoms have mostly gone away.\"\n}"}
+{"row_index": 434, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 70-year-old woman with a history of hypertension, type 2 diabetes mellitus, hyperlipidemia, ischemic heart disease, and degenerative joint disease presented with progressive proximal muscle weakness and myalgia over several months. She had been on simvastatin 20 mg/day for the prior seven years, which was discontinued upon diagnosis. Clinical manifestations included impaired functional mobility—difficulty climbing stairs, rising from a chair, combing hair, and bathing—accompanied by a 15% weight loss over 10 months. She denied systemic symptoms such as fever, rash, oral ulcers, dyspnea, chest pain, dysphagia, or visual disturbances, and there was no family history of neuromuscular disorders.\\n\\nPhysical examination revealed significant proximal muscle weakness on the Medical Research Council (MRC) scale: shoulder abduction 3/5, elbow flexion 4/5, hip flexion 3/5, knee flexion 4/5 bilaterally. She was unable to rise from a sitting position. Deep tendon reflexes, sensory function, and coordination were preserved. No abnormalities were detected on cardiac, pulmonary, or abdominal examination. Cutaneous signs suggestive of dermatomyositis were absent.\\n\\nLaboratory findings demonstrated markedly elevated creatine kinase (CK) at 2,954 U/L (reference range: 10–149 U/L), aldolase at 45.6 U/L (reference <7.6 U/L), aspartate transaminase (124 U/L, reference 10–31 U/L), and alanine transaminase (95 U/L, reference 10–31 U/L), indicating muscle damage and hepatocellular involvement. Serologic testing for viral infections—including herpes simplex virus, Epstein-Barr virus, cytomegalovirus, varicella-zoster virus, human immunodeficiency virus, and hepatitis C—was negative. Hepatitis B serology revealed past exposure (HBV DNA negative), and thyroid function tests were within normal limits.\\n\\nNerve conduction studies and electromyography (EMG) revealed abnormal spontaneous electrical activity in proximal muscles of the upper and lower extremities, consistent with an irritable myopathy. Muscle biopsy of the right deltoid demonstrated deep myopathic pathology characterized by widespread necrotic muscle fibers, scattered regenerating fibers"}
+{"row_index": 435, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A Chinese boy had two bad episodes when he was 6 and 8 years old. Each time, he got very sick with vomiting, diarrhea, and belly pain, which made his body not get enough blood. His blood pressure dropped very low, and he was very weak. Doctors gave him fluids to help, but the second time, even after giving lots of fluids, his blood pressure stayed low. His heart was not working well — the walls of his heart were thick and stiff. Tests showed his heart wasn’t pumping properly, and he needed a machine called ECMO to help his heart and lungs breathe. After using the machine, his heart started to work better again. The thick heart walls went back to normal over time. Doctors found that his body had swelling in the heart that went away. All his tests matched a condition called ISCLS. Now, he’s healthy, has no symptoms for over a year, and his heart is fully back to normal. He still has a little nerve problem in his leg, but it’s not hurting him anymore.\"\n}"}
+{"row_index": 436, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A Chinese boy had two serious episodes of hypovolaemic shock, starting at age 6 and again at age 8. The first time, he had symptoms like cold, runny nose, vomiting, and stomach pain, which led to low blood pressure and a fast heart rate. He was treated with fluids and antibiotics, and his condition improved. An echo test showed a thickened heart muscle, but it returned to normal a month later. After being healthy again, he had a second episode at age 8 with similar symptoms, but this time his blood pressure stayed very low despite large fluid doses. His heart function was severely weakened, and he needed emergency treatment with powerful medications and was transferred to a specialized cardiac unit. He received extracorporeal membrane oxygenation (ECMO) support, which helped stabilize his heart and lungs. During recovery, his heart function improved significantly, and follow-up echo tests showed normal heart wall thickness and full recovery of heart function. The medical team found that his symptoms were consistent with a rare condition called ISCLS, which is linked to immune system issues. He now takes montelukast daily and receives regular immunoglobulin infusions to prevent future episodes. While he still has some lingering nerve issues, he has been symptom-free for over a year and his heart function is fully recovered.\"\n}"}
+{"row_index": 437, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A Chinese boy with a history of eczema and obesity presented with two distinct episodes of anasarca and hypovolaemic shock. The first episode occurred at age 6 years, following a two-day course of coryzal symptoms, followed by one day of vomiting, diarrhoea, and generalized abdominal pain. On presentation, his blood pressure was 85/66 mmHg and heart rate was 144 beats per minute. He rapidly progressed to hypovolaemic shock requiring admission to a paediatric intensive care unit for fluid resuscitation. Laboratory findings included haemoconcentration, hypoalbuminemia, renal impairment, and metabolic acidosis. Echocardiography revealed left ventricular wall thickening. Blood culture yielded coagulase-negative staphylococci, interpreted as a skin contaminant. The patient was managed with intravenous fluid resuscitation and a seven-day course of ceftriaxone; renal function normalized following fluid therapy, and he was discharged after one week. A follow-up echocardiogram one month later demonstrated normal ventricular wall thickness, structure, and function.\\n\\nBetween episodes, the patient remained asymptomatic until age 8 years, when he presented with one-day history of vomiting, diarrhoea, abdominal pain, and low-grade fever. He was admitted again and developed lethargy, hypotension (76/52 mmHg), tachycardia (141 bpm), and signs of poor perfusion. Despite administration of a total of 3500 mL (70 mL/kg) of normal saline boluses over 8 hours, only transient improvements were observed, with persistent hypotension. Laboratory findings mirrored the first episode: haemoconcentration, hypoalbuminemia, impaired renal function, and metabolic acidosis. Echocardiography from the referring hospital showed significant left ventricular wall thickening, with interventricular septum thickness of 11.9 mm (Z-score +13.34) and free wall thickness of 14.2 mm (Z-score +16.22).\\n\\nHis haemodynamic instability persisted despite additional fluid resuscitation (total 3500 mL over 12 hours) and administration of multiple inotropic agents, including dopamine, dobutamine, noradrenaline, and stress-dose hydrocortisone."}
+{"row_index": 438, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 66-year-old man came to the hospital because his right leg was swollen and painful. Tests showed a blood clot in the right leg vein. Doctors found a strange connection in his veins: instead of the usual path, the vein on the left side drained into a different vein called the hemiazygos vein, and his liver vein went straight into the heart. This changed how blood flowed in his body, and it was likely caused by a blockage in the main vein behind the spine. His right leg had a clot, and the left leg’s vein was wider and better able to carry blood, which helped compensate. There was no normal vein behind the liver, and the blood from the liver went directly into the heart. This is a rare way blood flows, but it's not dangerous on its own.\"\n}"}
+{"row_index": 439, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 66-year-old man was admitted to the hospital because of a blood clot in his right leg. Imaging showed that his body’s main vein on the left side (the IVC) had abnormally drained into the hemiazygos vein instead of going to the heart normally. His liver’s vein drained directly into the heart, bypassing the usual path. This unusual connection was likely caused by a previous blockage in the pelvic veins, which led to the left side of his venous system forming a new path. The clot was in the right leg, and the patient had no other symptoms like fever or chest pain. Tests showed elevated levels of a clot marker (D-dimer) and confirmed the clot in the femoral vein. The imaging also revealed that the right common iliac vein was compressed and narrowed, leading to poor blood flow and the development of collateral veins. This condition is rare and affects how blood flows from the legs to the heart, especially on the left side of the body.\"\n}"}
+{"row_index": 440, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 66-year-old male was admitted to the hospital with a 2-day history of pain and edema in the right lower extremity, without fever, chest pain, or dyspnea. Prior to admission, he had sustained multiple soft tissue injuries from falls 12 days earlier. There was no significant personal or family history of vascular disease or thrombotic events. Physical examination revealed bilateral swelling of the right leg with palpable pitting edema, normal skin temperature, and intact arterial pulsations. Laboratory evaluation showed a D-dimer level of 2789 ng/mL (normal range: 0–500 ng/mL), indicating a high probability of thrombosis. Color Doppler ultrasonography confirmed right iliac-femoral vein thrombosis with markedly reduced distal blood flow velocity. Following thrombolysis, contrast-enhanced computed tomography was performed to evaluate the retroperitoneal venous anatomy and revealed a congenital anomaly of venous drainage: the right common iliac vein was located posterior to the left common iliac artery and exhibited significant compression and stenosis, resulting in collateral vessel formation in the pelvic region. The left iliac vein was markedly wider than the right, suggesting asymmetrical venous development. An abnormal left-sided inferior vena cava (IVC) was identified, formed by the union of the two common iliac veins at the level of the fourth lumbar vertebra. This left IVC ascended vertically to the left of the abdominal aorta, where it received contributions from the left renal vein at the level of the second lumbar vertebra and the right renal vein at the level of the third lumbar vertebra, with the latter crossing posteriorly over the abdominal aorta. The left IVC continued its ascent, intersecting the hemiazygos vein at the level of the second lumbar vertebra, then traversed posterior to the left diaphragmatic crura and entered the thorax. It ascended through the posterior mediastinum, passing posterior to the thoracic aorta and the azygos vein at the level of the eighth thoracic vertebra, arching over the root of the right lung, and ultimately joining the right superior vena cava at the level of the fifth thoracic vertebra. Notably, this patient lacked a retrohepatic IVC or a right-sided IVC, and the hepatic veins drained directly into the right atrium"}
+{"row_index": 441, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 7-month-old baby started having trouble sitting up and her body started shaking, especially in her head, arms, and legs, about 48 hours after getting the second dose of the MenB vaccine. She had a fever and threw up before, but those went away when she came to the hospital. The doctors checked everything — blood tests, brain scans, and tests for infections — and found nothing wrong. No virus, no bacteria, no other cause could explain her symptoms. The doctors looked at past cases of similar problems in children and found that shaking and balance issues after infections or vaccines are very rare in babies under one year old. They studied 1663 cases from the last 30 years to understand this. The baby’s symptoms got better over 8 days, and by one month, she was sitting still without shaking or falling again. The doctors think the vaccine might have started the problem, but it was very rare and not something that happens often.\"\n}"}
+{"row_index": 442, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 7-month-old girl developed acute ataxia and cerebellitis within 24 hours of receiving the second dose of the MenB vaccine. She had previously been healthy and had no known medical problems. Her symptoms included difficulty sitting steadily, uncontrolled shaking movements in her head, arms, and body, and fever that resolved by the time she was admitted to the hospital. She had received the first dose of the MenB vaccine at 5 months, and the second dose 72 hours before her symptoms started.\\n\\nDoctors performed a wide range of tests — including blood work, spinal fluid analysis, imaging scans of the brain and spine, and tests for viruses and bacteria — to rule out infections, genetic conditions, or other serious causes. All tests came back normal. No infection or autoimmune cause was found.\\n\\nBecause the symptoms began right after the vaccine, doctors considered a possible link to the vaccine. They reviewed 20 studies from the past 30 years involving 1,663 patients with similar symptoms, and found that ataxia or cerebellitis caused by infections or other conditions is very rare in children under one year old. This case is unusual because it happened so soon after vaccination and in such a young child.\\n\\nThe girl’s condition improved over 8 days, and by one month, she was able to sit steadily without any shaking or balance problems. No long-term effects were found. A report was filed with health authorities to monitor similar cases in the future.\"\n}"}
+{"row_index": 443, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 7-month-old female presented with acute cerebellar ataxia (ACA) within 24 hours of receiving the second dose of MenB vaccine (Bexsero, Novartis Vaccines and Diagnostics S.r.l., Siena, Italy). The clinical presentation included impaired sitting balance, previously achieved at 3 weeks of age, with new-onset abnormal involuntary and oscillatory movements affecting the head, limbs, and trunk. Postural control while unsupported was severely compromised, with sustained oscillations and falls. Symptoms began approximately 48 hours prior to presentation and were accompanied by fever and vomiting, both of which resolved at admission. The patient had a unremarkable prenatal and perinatal history, including spontaneous vaginal delivery at 39 weeks gestation, birth weight of 3020 g, Apgar score of 9 at 1 minute, and normal neonatal screening for congenital hypothyroidism, phenylketonuria, cystic fibrosis, and 17-hydroxyprogesterone. She was exclusively breastfed, with a transient episode of cyanosis on day two of life, which was managed appropriately. Vital signs and echocardiography were within normal limits; a mild thrombocytopenia at birth resolved by follow-up. Developmental milestones were otherwise age-appropriate.\\n\\nVaccination history revealed prior administration of the hexavalent vaccine (DTaP-Hib-IPV-HepB) at 3 and 5 months of age, with no adverse events reported. The MenB vaccine was administered at 5 months, coinciding with the onset of symptoms. On physical examination, the patient was alert, without nystagmus or saccadic eye movements, with normal optic fundi and cranial nerve function, and intact tendon reflexes.\\n\\nTo exclude infectious meningoencephalitis, a comprehensive diagnostic workup was performed, including blood chemistry, leukocyte count, acute phase proteins, electrolytes, and serologies for adenovirus, cytomegalovirus, Epstein-Barr virus, coxsackievirus, herpes simplex virus, human herpesvirus 6, Mycoplasma pneumoniae, and parvovirus B19—all of which were negative. Cerebrospinal fluid (CSF) analysis revealed a white blood cell count of 1/μL, protein level of 17 mg/dL"}
+{"row_index": 444, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 33-year-old woman was in a car crash going fast and didn't wear a seatbelt. She hit hard and broke bones in her right hip, thigh, and lower leg. Her hip was out of place and had a big crack in the back wall of the hip socket and in the top of the thigh bone. The doctors tried to push the hip back into place in the emergency room but couldn't because of the other broken bones. So they took her to the operating room right away. In there, they used a small pin to push the hip back into place, fixed the thigh and lower leg bones with metal rods, and checked the hip while she was under anesthesia to make sure it was stable. After the surgery, she could start walking with just a little weight and was able to walk fully six weeks later. The bones were healing well, and the hip stayed in place. She never came back for a follow-up visit.\"\n}"}
+{"row_index": 445, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 33-year-old woman arrived at the trauma center after a high-speed car crash where she was not wearing a seatbelt. She had severe injuries to her right hip and leg, including a dislocated hip, a fracture of the femoral head, fractures of the femur and tibia, and an open wound on her lower leg with exposed bone. Initial attempts to realign her hip in the emergency room failed due to the complexity of her fractures. She was then taken to the operating room for surgery. During the procedure, a small pin was inserted to help realign the hip, and the broken femur and tibia were stabilized using metal rods inserted into the center of the bones. A special X-ray exam under anesthesia was done to check if the hip joint was stable and properly aligned. The results showed that the hip was stable and the fracture pieces were in place. After surgery, she could begin walking with minimal weight and was discharged after 16 days. Six weeks later, she returned to the clinic and was able to fully bear weight on her right leg, with X-rays showing that the hip and leg fractures were healing well. However, she did not return for follow-up care after that.\"\n}"}
+{"row_index": 446, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 33-year-old female with a history of schizophrenia and bipolar disorder presented to the trauma center following a high-impact motor vehicle collision at approximately 50 miles per hour, during which she was an unrestrained driver. The mechanism of injury resulted in significant blunt force trauma to the pelvis and lower extremity. Upon arrival in the trauma bay, she reported acute pain in the right hip and leg, with physical examination revealing shortening and deformity of the right lower extremity. A 2 cm × 1 cm open laceration was observed over the distal tibia with exposed bone fragments, indicating a comminuted open tibial fracture. The patient was intubated for airway protection due to potential respiratory compromise from pain and shock. Initial radiographic evaluation of the right hip, femur, and tibia revealed a right hip dislocation with associated fractures of the femoral shaft and tibial shaft. Computed tomography (CT) of the pelvis confirmed a posterosuperior acetabular hip dislocation with specific involvement of the posterior wall of the acetabulum and an inferior infrafoveal femoral head impaction fracture, consistent with a posterior wall fracture dislocation. The presence of these fractures raises concerns for avascular necrosis (AVN) of the femoral head due to disruption of the vascular supply from the femoral neck. Attempts at closed reduction of the hip dislocation in the emergency department were unsuccessful, primarily due to the presence of concomitant femoral and tibial shaft fractures, which limited the feasibility of manual reduction and introduced biomechanical instability. Given the severity of the injuries and the risk of AVN, the patient was transferred urgently to the operating room for surgical intervention. In the operating room, she was placed in supine position on a radiolucent table with a small elevation under the right buttock to facilitate optimal pelvic alignment. A 5 mm Schanz pin was inserted percutaneously along the anatomical axis of the femoral neck to provide temporary stabilization and serve as a guide for reduction. Traction and controlled rotational forces were applied to achieve reduction of the femoral head into the acetabulum, confirming the presence of an inferior infrafoveal impaction fracture. The open tibial fracture was debrided to remove contaminated bone fragments and soft tissue debris, followed by primary closure. Both the femoral and tibial shaft fractures were stabilized using intramedullary nailing"}
+{"row_index": 447, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 50-year-old woman was bleeding from her vagina for 4 months, had lower belly pain, and trouble with sex. Doctors found her uterus was big and hard, and a sample from inside it showed a rare type of cancer called uterine carcinosarcoma (MMT). At the same time, they saw a lump in her left kidney that looked like kidney cancer (RCC) on scans. They tried to check the kidney lump with a tiny needle, but it only came back with blood. So they did surgery to check both the uterus and the kidney. The uterus cancer was confirmed, and the kidney lump was not cancer — it was a very rare, harmless tumor called RH. The woman had surgery to remove the uterus and both ovaries, and also the kidney. She recovered well and is now on chemo for the uterine cancer. The kidney tumor was not dangerous, and no family history of cancer was found. She’s doing fine and is being followed up regularly.\"\n}"}
+{"row_index": 448, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 50-year-old woman came in with vaginal bleeding that had been going on for 4 months, along with lower abdominal pain and discomfort during sex. She had regular periods before this, but now her bleeding was heavy, with clots and pain. She had two children from normal deliveries and had no history of family cancer. She was also diagnosed with hypothyroidism a few years ago, which she manages with medication.\\n\\nOn exam, her abdomen was normal, but her cervix was enlarged and firm. Her uterus was bulky and firm. A sample of the uterine lining (endometrial sampling) showed a rare type of cancer called uterine carcinosarcoma (MMT), which is a serious but uncommon cancer. Blood tests were normal, and her thyroid and other liver/kidney levels were within range.\\n\\nImaging scans showed a large, abnormal uterus and a mass in the left kidney. The kidney mass looked very vascular (full of blood) and was initially thought to be renal cell carcinoma (RCC), a common kidney cancer. A needle biopsy (FNAC) of the kidney mass was done twice, but it only showed blood — no cancer cells were found.\\n\\nThe patient had surgery to remove the uterus and both ovaries and fallopian tubes (staging laparotomy), and a frozen section of the kidney mass was checked. The results were unclear, with only a few unusual cells seen. Because of this uncertainty, a full kidney removal (radical nephrectomy) was done.\\n\\nAfter surgery, the tissue samples were examined under a microscope. The uterine tumor was confirmed as MMT — a rare cancer with both glandular and connective tissue parts. The kidney tumor was found to be a very rare benign tumor called renal hemangioma (RH), not cancer. This tumor is not aggressive and does not spread.\\n\\nThe patient recovered well and was discharged after 6 days. Tests for a genetic condition linked to such tumors (VHL) were normal. She started chemotherapy for her uterine cancer using paclitaxel and carboplatin, and she is now doing well with regular follow-up for 15 months.\"\n}"}
+{"row_index": 449, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 50-year-old female presented to the Gynecology Outpatient Department with a four-month history of abnormal vaginal bleeding, including passage of clots, accompanied by lower abdominal pain and dyspareunia for two months. Her menstrual cycles had previously been regular, lasting six days every 28 days, until four months prior when bleeding commenced. She reported no use of oral contraceptives or other forms of contraception. She has two term deliveries via vaginal birth, with the most recent delivery occurring 17 years ago. She was diagnosed with hypothyroidism two years prior and is currently maintained on thyroxine 50 μg daily with euthyroid status. There is no family history of genital, colonic, or renal malignancies.\\n\\nOn physical examination, she was afebrile, with a pulse of 76 beats per minute, blood pressure of 110/74 mmHg, and mild pallor. Abdominal examination was unremarkable, with no palpable mass. Speculum examination revealed a hypertrophied cervix with active bleeding at the external os. Vaginal examination demonstrated a firm cervix and a bulky, firm uterus with normal mobility and no palpable adnexal mass. Rectal examination showed normal rectal mucosa and soft parametrium.\\n\\nEndometrial sampling revealed a high-grade endometrial adenocarcinoma, specifically the villonodular subtype. Hemoglobin was 8.9 g/dL, and all liver and renal function tests were within normal limits. Serum TSH was 2.6 uIU/mL, and CA-125 was elevated at 165 IU/L. Pap smear was negative for intraepithelial lesions or malignancy. Pelvic ultrasonography showed a bulky uterus with increased endometrial thickness and an intracavitary lesion. Contrast-enhanced computed tomography (CT) demonstrated a heterogeneous, centrally enhancing mass in the lower pole of the left kidney, suggestive of a highly vascular lesion with mitotic activity, most likely renal cell carcinoma (RCC). MRI of the abdomen and pelvis further revealed a lobulated, ill-defined myometrial-based endometrial mass measuring 2.4 × 1.1 × 2.0 cm, extending into the endometrium and distorting the endometrial cavity, consistent with adenomyosis. A heterogeneously enhancing renal lesion measuring"}
+{"row_index": 450, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 20-year-old man had a lump on the back of his right hand for 5 years. It started small and got bigger over time, now measuring about 4 cm long. The lump was hard, stayed in one place, and didn’t move when he moved his hand. It didn’t hurt much, only when he did heavy work, and it didn’t bother him at night or stop him from doing daily tasks. Doctors saw the lump and used X-rays and MRI to check it. The MRI showed a bony growth coming from the hand bone, with a soft part on top, which matched a condition called osteochondroma. The lump was removed in surgery, and the tissue was tested. The test confirmed it was an osteochondroma. After surgery, the man had no pain, could move his hand freely, and at one year later, the doctors said he was doing well with no signs of the lump coming back.\"\n}"}
+{"row_index": 451, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 20-year-old man had a swelling on the right hand for 5 years that slowly got bigger, reaching 4 cm × 3 cm × 2 cm. The swelling was on the palm side, near the inside of the hand, and felt hard with no pain except when doing heavy activities. It didn’t cause night pain or limit daily tasks. On exam, it was fixed to the bone and couldn’t move. X-rays showed a bony growth coming from the end of the fifth metacarpal bone. MRI confirmed the growth, showing it was made of bone and cartilage, and it was pushing on nearby tendons and muscles. A diagnosis of osteochondroma was made. The swelling was surgically removed under general anesthesia through a small incision on the back and inside of the hand. The removed tissue was tested under a microscope and confirmed to be an osteochondroma — a benign bone and cartilage growth. The surgery went smoothly, with no complications. The patient recovered well, had no pain, and could move his hand normally. At one-year follow-up, the results were good with no signs of recurrence.\"\n}"}
+{"row_index": 452, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 20-year-old male presented in January 2021 with a progressive, insidious-onset swelling of the right hand, localized to the palmar medial border, lasting for five years. The lesion gradually increased in size, reaching dimensions of 4 cm × 3 cm × 2 cm, and was characterized clinically as bony, hard, with an irregular surface, adherent to the underlying bone, and fixed in both coronal and sagittal planes. Palpation revealed no fluctuance, local warmth, or signs of inflammation, and there was no associated fever, regional lymphadenopathy, skin changes, sinuses, dilated veins, or systemic symptoms. The swelling was not present elsewhere in the body and was not associated with nocturnal pain or functional limitation during daily activities, though it was aggravated by excessive mechanical loading and relieved with rest.\\n\\nClinical examination confirmed the lesion's fixed, bony nature and its position on the ulnar aspect of the hand. Radiographic evaluation (X-ray) demonstrated a pedunculated bony lesion originating from the distal metaphyseal region of the fifth metacarpal bone, consistent with an exophytic bony outgrowth. Magnetic resonance imaging (MRI) further characterized the lesion as measuring 2 × 2.5 × 3 cm (anteroposterior × transverse × sagittal), arising from the distal metaphysis of the fifth metacarpal and exhibiting continuity with the medullary cavity, extending away from the epiphysis. The MRI also revealed displacement of the fifth flexor digitorum profundus tendon laterally and compression of the flexor digiti minimi and abductor digiti minimi muscles. Additionally, a bursa with inflammatory fluid accumulation was identified within the soft tissue compartment adjacent to the lesion. Based on these imaging and clinical findings, a provisional diagnosis of osteochondroma was established.\\n\\nThe lesion was surgically excised under general anesthesia with tourniquet control via a posteromedial incision. The excision was performed at the base of the pedicle, removing a tumor mass of approximately 3 × 2 cm. The resected specimen was sent for histopathological evaluation. Histopathology confirmed the presence of a cartilaginous cap overlying a bony component, with well-organized bony trabeculae. The cartilaginous layer was lined by perichondrium and"}
+{"row_index": 453, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 68-year-old man who had never had any heart problems before suddenly became confused and stopped breathing normally. His wife called emergency services when she found him not responding. When doctors arrived, he was unresponsive and had a heart stoppage. They revived him with life-saving steps, including shock and breathing support. An electrical test of his heart showed signs that match a rare heart condition called Brugada syndrome. This condition can cause the heart to stop suddenly, even without any blockage or heart attack. Doctors found no heart damage, and his heart’s blood flow was normal. He was given medicine for a slow thyroid and later agreed to get a small device in his chest to prevent future heart problems. The doctors confirmed the diagnosis based on the heart test results and his history of no symptoms before this event.\"\n}"}
+{"row_index": 454, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 68-year-old Hispanic man was brought to the emergency department after his wife found him breathing badly and unresponsive. When doctors arrived, he was confused and had a sudden heart rhythm problem that led to cardiac arrest. He was revived with emergency treatment, including defibrillation and CPR. An electrocardiogram (ECG) taken during this event showed abnormal heart patterns, specifically ST-segment elevations in the chest leads V1 to V3 and unusual repolarization changes in V1 and V2 — findings that are typical of Brugada syndrome. Other ECG results showed a slow heart signal (first-degree AV block) and a normal QRS duration. Blood tests revealed low levels of sodium, potassium, magnesium, and thyroid hormone, indicating severe hypothyroidism, which was treated with hormone replacement. No blockages were found in the heart arteries during catheterization. After recovery, the patient was found to have small brain injuries from previous events, but no major heart problems were present. He was discharged with medications for heart and brain health. Later testing confirmed that his heart rhythm abnormalities matched the pattern of Brugada syndrome, a condition that can cause sudden cardiac death. The doctors recommended he get an implantable cardioverter defibrillator (ICD) to help prevent future heart problems.\"\n}"}
+{"row_index": 455, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 68-year-old Hispanic male with no significant past medical history was evaluated in the emergency department (ED) following an acute episode of confusion and altered mental status. Emergency medical services (EMS) were dispatched by the patient's wife after she observed erratic breathing and inability to rouse him. Upon ED arrival, the patient was obtunded and experienced in-hospital cardiac arrest due to ventricular fibrillation. Immediate advanced cardiac life support (ACLS) was initiated, including endotracheal intubation, cardiopulmonary resuscitation (CPR), and defibrillation, resulting in return of spontaneous circulation (ROSC). An electrocardiogram (ECG) obtained during the cardiac arrest event revealed ST-segment elevations in leads V1–V3, consistent with a type 1 Brugada pattern, along with prominent repolarization abnormalities in V1 and V2. Additional ECG findings included first-degree atrioventricular (AV) block with a PR interval of 220 milliseconds (normal range: 120–200 ms), and a QRS duration of 0.11 seconds (normal: 0.08–0.12 s), both of which are non-specific but support the presence of underlying conduction system abnormalities.\\n\\nInitial laboratory values demonstrated hyponatremia (sodium: 132 meq/L; normal: 136–145 meq/L), hypokalemia (potassium: 3.3 meq/L; normal: 3.5–5.0 meq/L), hypomagnesemia (magnesium: 3.3 mg/dL; normal: 1.5–2.4 mg/dL), hyperglycemia (glucose: 197 mg/dL), normal troponin (<0.02 ng/mL), mild elevation of brain natriuretic peptide (BNP: 65 pg/mL), prolonged prothrombin time (PT: 13.6 s; normal: 11–13 s) and international normalized ratio (INR: 1.3), and severe primary hypothyroidism (thyroid-stimulating hormone [TSH]: 59.4 mU/L; normal: 0.5–5.0 mU/L). These abnormalities were not attributable to acute ischemia"}
+{"row_index": 456, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 52-year-old woman had dry eyes and dry mouth for years, and finally got checked. Doctors found she had Sjögren’s syndrome — a condition where her body stops making enough saliva and tears. This was confirmed by blood tests showing antibodies to Ro (SS-A), a biopsy of her salivary glands, and a scan that showed no saliva flow. She also had kidney damage, called membranous glomerulonephritis, which was seen in a kidney biopsy. Three months later, she had a serious stomach problem — a hole in her small intestine that let air in (pneumoperitoneum), and the tissue sample showed a cancer called Epstein-Barr virus-positive diffuse large B-cell lymphoma (DLBCL). She didn’t get chemotherapy because she was too weak, poor, and didn’t want to. But she was taking low-dose steroids and hydroxychloroquine for her Sjögren’s, and after one year, her dry symptoms and protein in her urine got better. A scan showed the cancer wasn’t getting worse.\"\n}"}
+{"row_index": 457, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 52-year-old woman was diagnosed with primary Sjögren's syndrome, a condition that causes dry eyes and dry mouth, based on her symptoms, blood tests, salivary gland biopsy, and imaging. She had positive results for anti-nuclear antibody (ANA) and anti-Ro (SS-A) antibodies, and her salivary glands showed signs of inflammation. A kidney biopsy later confirmed she had membranous glomerulonephritis, a type of kidney disease that causes protein in the urine. Three months after her diagnosis, she developed a serious abdominal complication: a perforation in her small bowel, which led to infection. A biopsy of the bowel tissue showed Epstein-Barr virus-positive diffuse large B-cell lymphoma (DLBCL), a type of aggressive cancer. Despite being diagnosed with both Sjögren's syndrome and lymphoma, she did not receive chemotherapy due to poor health, low motivation, and financial hardship. However, over the course of one year, her proteinuria improved and her dry eye and dry mouth symptoms got better. A follow-up scan showed that the lymphoma was stable, meaning it did not get worse.\"\n}"}
+{"row_index": 458, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 52-year-old woman presented with intermittent abdominal tenderness, chronic dry eyes, and dry mouth, which had persisted for several years without prior medical evaluation. She had a history of dilated cardiomyopathy and left-eye glaucoma, managed with loop diuretics, proton pump inhibitors, and anthocyanosides. Physical examination revealed lower extremity edema, with normal body temperature (36.5°C) and blood pressure. Laboratory findings included a white blood cell count of 8,600/mm³ (neutrophilic predominance, 73.4%), sodium 141 mEq/L, chloride 108 mEq/L, blood urea nitrogen 15.7 mg/dL, and creatinine 0.6 mg/dL. Serum total protein was 5.5 g/dL, albumin 1.5 g/dL, and total cholesterol 257 mg/dL. Urinalysis demonstrated significant proteinuria (6.3 g/day), 30–49 red blood cells per high-power field, and no casts. Serologic testing revealed a positive anti-nuclear antibody (ANA; 1:80, homogeneous and speckled pattern), rheumatoid factor (390 IU/mL), and anti-Ro (SS-A) autoantibody (>200 U/mL). Notably, antibodies against double-stranded DNA, La (SS-B), Sm, ribonucleoproteins, antineutrophil cytoplasmic antibodies, lupus anticoagulant, IgG/IgM anti-cardiolipin, and IgG β2-glycoprotein-1 were absent. Complement levels showed a marked reduction in C3 (38 mg/dL; normal range 90–180 mg/dL), while C4 (16 mg/dL; normal 10–40 mg/dL) and complement component 50 (33.1 U/mL; normal 23–46 U/mL) remained within normal limits. Hepatitis B surface antigen, hepatitis C antibodies, cryoglobulins, and human immunodeficiency virus were all negative. Minor salivary gland biopsy demonstrated diffuse lymphocytic infiltrates with a focus score of 3, consistent with lymphoid infiltration in the exocrine glands. Salivary scintigraphy showed non-visualization"}
+{"row_index": 459, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 47-year-old woman had numbness in her toes and trouble urinating for a year. Tests showed her spine's end part was stuck low, like a string tied to the bottom of the spine. The doctors fixed it by cutting part of her spine at the L2 level to free it up. They used screws at L1 and L3 to hold the spine in place, and made sure they were straight and lined up right. They removed part of the bone on the top and sides of L2, and took out the disc between L1 and L2. Then they removed the top part of the L2 bone. A metal rod was attached to the screws and pressed in to hold the spine together. Two soft tapes were placed on the spine to keep it stable. After surgery, her leg numbness got better right away, and her bladder problems improved after one year. The bone healed fully, and the metal parts were taken out after a year. She hasn’t had any problems since then.\"\n}"}
+{"row_index": 460, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 47-year-old Asian woman was admitted to the hospital with a 1-year history of leg numbness and trouble with urination. She had first noticed numbness in her third and fourth toes five years ago, and over time, her entire toes became numb. She also started having frequent urination. After imaging tests, doctors found that her spinal cord was low in position, extending to the S2 level and surrounded by fat, which led to the diagnosis of adult tethered cord syndrome. To fix this, surgeons performed a spine-shortening procedure at the L2 level.\\n\\nThe surgery involved making a cut from T11 to L4, placing screws at L1 and L3 to help stabilize the spine. The screws were inserted carefully, parallel to the top surfaces of the vertebrae, to make sure the bones aligned properly. The upper part of the L2 lamina (the back part of the bone) and part of the L2 pedicle were removed. The disc between L1 and L2 was also removed. Then, the top part of the L2 vertebra was taken out using a drill. After removing the vertebra, a straight rod was attached to the screws and used to press the bones together. Two polyethylene tapes were placed to support the spine.\\n\\nThe surgery took 5 hours and 13 minutes, with only 108 ml of blood loss. The patient’s leg numbness improved right after the surgery, and her urinary problems improved one year later. A year after surgery, CT scans showed the bones had fully healed, and the hardware was removed. No symptoms returned after two years. This procedure helps free the spinal cord and improve nerve function in patients with tethered cord syndrome.\"\n}"}
+{"row_index": 461, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 47-year-old Asian woman presented with a 1-year history of progressive bilateral leg numbness, initially affecting the third and fourth toes for 5 years, and subsequent involvement of all toes, along with a 1-year history of urinary frequency. Physical examination revealed intact motor function and normal deep tendon reflexes; sensory disturbance was localized to the anal region. Her finger-to-floor distance was 10 cm, and straight leg raise testing yielded 80 degrees, indicating no significant hamstring tightness. Magnetic resonance imaging (MRI) demonstrated a low-lying conus medullaris extending to the S2 level, surrounded by fat tissue, with no other structural abnormalities identified. This finding was consistent with adult tethered cord syndrome (ATCS), a condition characterized by a fixed, low-lying conus medullaris that is tethered to the spinal column, leading to chronic neurologic compression and progressive sensory and motor deficits. Given the clinical and imaging findings, a spine-shortening vertebral osteotomy was planned at the L2 level to decompress the conus medullaris by reducing spinal length and relieving tethering forces.\\n\\nAfter obtaining informed consent, the patient underwent surgical intervention under general anesthesia, positioned on a Jackson Spinal Table (Mizuho Co. Ltd., Tokyo, Japan). Neurophysiological monitoring using motor evoked potentials was performed to assess real-time spinal cord function during the procedure. A midline incision was extended from the T11 to L4 spinous process level, allowing extensive exposure of the L2 vertebral segment, including posterior elements and transverse processes bilaterally. Bilateral pedicle screws were placed at L1 and L3 using an anterior-posterior image intensifier. Critical to surgical precision, monoaxial screws were inserted parallel to the rostral endplates of each vertebral body to ensure optimal alignment between the L1 caudal endplate and the L2 osteotomy surface, minimizing the risk of postoperative spinal misalignment and neurological compromise.\\n\\nThe osteotomy procedure commenced after screw placement. Initial resections included the lower half of the L1 lamina, bilateral inferior articular processes of L1, and bilateral superior articular processes of L2. Subsequently, the upper one-third of the L2 lamina was resected, and the bilateral two-thirds of the L2 pedicle were removed using a surgical air drill. This lamina resection is clinically significant because complete preservation"}
+{"row_index": 462, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 60-year-old man had a tumor in his bladder that wasn't painful or linked to other health problems. After tests, doctors found it was a serious type of cancer called small cell bladder cancer. They removed the tumor first, then gave him chemotherapy and radiation to kill any leftover cancer cells. He also had surgery to remove his bladder and part of his prostate, and replaced it with a new bladder made from part of his intestine. The surgery and treatment worked well — no cancer came back even 33 months later. He’s now healthy and being checked every 6 months to make sure everything stays clear.\"\n}"}
+{"row_index": 463, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 60-year-old man was diagnosed with a rare type of bladder cancer called small cell bladder cancer (SCBC) two and a half years ago. He had no risk factors like smoking or family history, and his symptoms were mild—just painless blood in his urine. After tests, a 6 cm tumor was found on the bladder wall, and initial tests showed no signs of spread. The tumor was removed, and further testing confirmed it was muscle-invasive and aggressive, with a very high growth rate.\\n\\nBecause this type of cancer can spread quickly, the patient received four cycles of chemotherapy using cisplatin and etoposide, followed by radiation to the brain to prevent spread. He then had surgery to remove his bladder and prostate, along with nearby lymph nodes. The surgery was successful, and final tests showed no cancer cells left in the tissue or lymph nodes.\\n\\nSince the treatment, the patient has remained free of cancer for 33 months. He now has regular check-ups every six months, including urine tests and imaging, and no signs of recurrence have been found. This case shows an unusually long period of disease-free survival for someone with this type of cancer.\"\n}"}
+{"row_index": 464, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 60-year-old male presented with painless gross hematuria, with no identifiable risk factors including smoking, prior radiation exposure, occupational hazards, or hereditary predisposition. No systemic symptoms such as weight loss, night sweats, or B-symptoms were present, and no neurological deficits were reported. Urinary infection was excluded by appropriate laboratory and microbiological workup. Cystoscopy revealed a 6 cm solid tumor on the right bladder wall, which was completely resected via transurethral resection of the bladder tumor (TURBT). Primary histopathological evaluation confirmed a muscle-invasive small cell neuroendocrine carcinoma (SCBC) with pT2a GIII classification. Immunohistochemical staining demonstrated strong positivity for synaptophysin and AE1/AE3, consistent with neuroendocrine differentiation, while chromogranin A, CD56, CD3, CD20, TdT, S-100, and HMB45 were negative, supporting the diagnosis of small cell carcinoma without features of other neuroendocrine or epithelial tumors. The tumor exhibited a high proliferative index, with a KI-67 labeling index of 95%, indicating aggressive cellular turnover. An 18F-FDG PET/CT scan at initial diagnosis showed no evidence of lymph node or visceral metastasis, and cranial magnetic resonance tomography (MRT) confirmed absence of brain infiltration, supporting a localized disease at presentation. Given the established evidence in the literature that neoadjuvant chemotherapy improves outcomes in SCBC, the patient received four cycles of cisplatin (25 mg/m²) and etoposide (100 mg/m²), administered every 21 days (days 1–3 per cycle), with no treatment-related adverse events. Concurrently, prophylactic whole-brain radiotherapy (WBRT) was delivered at a total dose of 26 Gray to mitigate the risk of central nervous system relapse, a known site of early dissemination in SCBC. Following chemotherapy, the patient underwent radical cystoprostatectomy with ileal neobladder reconstruction and bilateral extended pelvic lymphadenectomy, including the resection of 32 lymph nodes, all of which were tumor-free. Final pathological assessment confirmed a complete pathological response (ypT0, N0, L0, V0, Pn0), indicating absence of viable small cell carcinoma in the"}
+{"row_index": 465, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 72-year-old man who had been sick with a type of cancer called chronic lymphocytic leukemia (CLL) for years started getting worse symptoms two weeks before he was admitted to the hospital. He had a fever, chills, night sweats, tiredness, trouble swallowing, and fast-growing swollen lymph nodes in his neck. Tests showed his cancer had changed into a more serious form called diffuse large B-cell lymphoma. He began chemotherapy called DA-R-EPOCH, which helped shrink the swollen nodes but also caused serious side effects. Soon after, he had trouble breathing because the swollen neck nodes blocked his airway, so doctors had to put a tube in his throat to keep his airway open. After a few days, the swelling went down, but he stayed unconscious and started having severe, hard-to-stop seizures. Brain scans showed swelling in the back part of his brain, which is a condition called PRES. This swelling was likely caused by the chemotherapy, his damaged kidneys, and a serious infection. Even with treatment, he did not get better and eventually had a heart stop. His brain problem was caused by a mix of these factors.\"\n}"}
+{"row_index": 466, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 72-year-old man with a history of chronic lymphocytic leukemia (CLL) that had changed to a more aggressive form of lymphoma called diffuse large B-cell lymphoma (DLBCL) presented with a two-week history of low-grade fever, chills, night sweats, fatigue, difficulty swallowing, and fast-growing swollen lymph nodes in his neck. Tests showed his lymphocyte count had risen and his platelet count had dropped, and a scan revealed widespread swelling in his neck, chest, abdomen, and pelvis. A biopsy confirmed the lymphoma had transformed from his original CLL, a condition known as Richter syndrome. He began treatment with DA-R-EPOCH chemotherapy, but soon developed complications including tumor lysis syndrome, kidney damage, and a bacterial infection caused by Pseudomonas aeruginosa. A few days later, his neck swelling became so severe that he needed emergency intubation to protect his airway. Although the swelling improved, he did not regain consciousness and started having severe, uncontrolled seizures. Brain imaging showed swelling in the back part of his brain, specifically in the occipital and inferior temporal lobes, which is consistent with posterior reversible encephalopathy syndrome (PRES). His seizures were hard to control with standard medications but responded to midazolam and propofol. Additional infections were found, and antibiotics were adjusted, but due to his poor outlook, care was not escalated. His condition eventually worsened, and he suffered a cardiac arrest. Experts believe his PRES was caused by a combination of the new chemotherapy, kidney injury, and sepsis.\"\n}"}
+{"row_index": 467, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 72-year-old White man with an 8-year history of chronic lymphocytic leukemia (CLL), previously treated with four cycles of fludarabine, cyclophosphamide, and rituximab in 2012, and subsequent maintenance therapy with ibrutinib since 2014, presented to the oncology clinic with a 2-week history of low-grade fever, chills, night sweats, fatigue, dysphagia, and rapidly progressive cervical lymphadenopathy. Laboratory evaluation revealed a significant increase in lymphocyte percentage (61% at presentation versus 40.2% at 6 months prior), along with thrombocytopenia (42 vs. 92 K/mm³). Positron emission tomography (PET) imaging demonstrated extensive, confluent hypermetabolic lymphadenopathy involving bilateral neck, chest, abdomen, and pelvis, suggestive of disease progression. Lymph node biopsy confirmed transformation of CLL to high-grade diffuse large B-cell lymphoma (DLBCL), consistent with Richter syndrome. The patient was initiated on dose-adjusted rituximab, etoposide, prednisone, vincristine, cyclophosphamide, and doxorubicin (DA-R-EPOCH) chemotherapy. Concurrently, he developed tumor lysis syndrome, acute kidney injury, and neutropenic fever with Pseudomonas aeruginosa bacteremia, requiring broad-spectrum antibacterial and antifungal therapy, as well as granulocyte colony-stimulating factor (G-CSF) support. On day 9 of hospitalization, the patient experienced severe airway obstruction due to extensive cervical lymphadenopathy, necessitating emergency endotracheal intubation and transfer to the intensive care unit (ICU). Neck magnetic resonance imaging (MRI) revealed marked soft-tissue edema, which was treated with high-dose hydrocortisone without clinical improvement. On day 10, after sedation was withdrawn, the patient remained unresponsive and developed two episodes of generalized, refractory seizures. Head computed tomography (CT) showed no acute structural abnormalities; electroencephalography (EEG) failed to detect focal or generalized epileptiform activity. Brain MRI revealed bilateral occipital and inferior temporal lobe edema involving cortical gray matter and subcortical white matter, consistent with posterior reversible encephalopathy syndrome"}
+{"row_index": 468, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"An 84-year-old man had eye pressure problems from glaucoma. His doctor tried medicines for years, but the pressure stayed high and his vision got worse, especially in his right eye. So, they did a small surgery in his right eye to help lower the pressure using a tiny device called XEN45. Right after, his eye pressure dropped too low, and a small part of the eye (the choroid) detached, but doctors fixed it with eye drops and steroids. Eight months later, they did the same surgery in his left eye. After that, the same problem happened — the choroid detached again — so they did a second surgery to fix it. Both eyes now have normal eye pressure and the problem is gone. The man also had cloudy lenses in both eyes, which made it hard to see clearly, so they did cataract surgery in both eyes. After that, his vision improved a little, but some parts of his eye still have changes from aging, and that doesn’t hurt his daily vision much.\"\n}"}
+{"row_index": 469, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"An 84-year-old man with glaucoma had surgery to lower pressure in his eyes using the XEN45 device. The procedure was done in his right eye first in July 2020 and went smoothly. After surgery, his eye pressure dropped very low (to 10 mmHg), which caused a temporary condition called hypotony and a type of detachment in the choroid (a layer behind the retina). This was treated with steroid eye drops and eye drops that reduce muscle activity (cycloplegic drops), and it improved over time. By month eight, the left eye had the same surgery, and again, choroidal detachment occurred. This time, a small surgical procedure was needed to drain the fluid and fix the problem. After that, pressure stabilized between 10 and 12 mmHg, and the detachment fully resolved. Both eyes now have the XEN45 device in place and the pressure is well controlled. The patient also had cataract surgery in both eyes later in 2022. After the surgery, his vision improved in the right eye to 10/10, and in the left eye to 6/10. Although there were some eye conditions like lens clouding and age-related changes in the back of the eye, these did not significantly affect his daily vision.\"\n}"}
+{"row_index": 470, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"An 84-year-old male with primary open-angle glaucoma (POAG) presented with decompensated intraocular pressure (IOP) in the right eye, despite maximal medical therapy. His preoperative topical regimen included tafluprost (15 µg/mL once daily), brinzolamide (twice daily), and timolol (twice daily), with addition of oral acetazolamide (250 mg twice daily) in the prior year. Preoperative best-corrected visual acuity (BCVA) was 6/10 in the right eye and 4/10 in the left eye (Snellen chart). Slit-lamp examination revealed transparent corneas, normal anterior chambers, and nuclear cataract opacities in both eyes, with no other anterior segment abnormalities. Preoperative IOP was 24 mmHg in the right eye and 20 mmHg in the left eye. Fundus examination demonstrated a large cup-to-disc ratio (CDR = 0.9) and neuroretinal rim narrowing in all disc sectors bilaterally. Despite optimization of both oral and topical glaucoma medications, a progressive bilateral visual field defect was documented in June 2020, with the most significant decline observed in the right eye.\\n\\nGiven the patient’s age, bilateral glaucomatous optic nerve damage, and failure of medical therapy to achieve target IOP (ideally <21 mmHg in this population), ab interno XEN45 glaucoma drainage device implantation was selected as the most appropriate surgical intervention. In July 2020, a subconjunctival injection of mitomycin C (0.2 mg/mL) was administered during the right eye XEN45 implantation, which proceeded without intraoperative complications. Postoperatively, IOP dropped to 10 mmHg on day 1, with a diffusely distributed filtration bleb and flat anterior chamber. Fundus examination revealed serous nasal and temporal choroidal detachments, confirmed by eco-B scan as serous choroidal detachments (SCDs), consistent with hypotonic stress-induced fluid accumulation due to excessive outflow and reduced intraocular pressure.\\n\\nTo mitigate postoperative inflammation and prevent further complications associated with hypotony, a combination of topical dexamethasone (2 mg/mL, three times daily), atropine"}
+{"row_index": 471, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 22-year-old man had a big, soft lump in his belly that made him feel full and sick. Years ago, he had a tube (VPS) put in to drain fluid from his brain, because of a birth condition called spina bifida. The tube had been in place for 21 years, and no other surgeries were done. Doctors found a fluid-filled bag near the tube’s end, which was blocking his stomach. This bag, called a pseudocyst, was filled with cerebrospinal fluid — the same fluid that flows in the brain. The fluid looked like brain fluid, and tests showed no infection. The bag was in the upper left part of his belly, between his stomach and colon. Surgeons opened it, drained 1500 ml of clear fluid, and moved the tube out of the bag. The problem was confirmed as a rare complication of the brain drain tube. This kind of cyst can happen years after the tube is placed, even after 20 years. It causes belly swelling and a lump, and if not treated, can be dangerous. The only way to fix it is to remove the bag and move the tube safely. In this case, surgery was needed because the belly had too much scar tissue to do it with small tools.\"\n}"}
+{"row_index": 472, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 22-year-old man was admitted to the hospital because of a swollen, distended abdomen and nausea. He had a ventriculoperitoneal shunt (VPS) placed 21 years earlier to treat fluid buildup in his brain due to spina bifida. This shunt was originally placed when he was just a few months old, and he had no other abdominal surgeries since then. No history of cancer, liver, or pancreas problems was found.\\n\\nOn exam, a large, soft mass was felt in his upper abdomen. Blood tests were normal, and imaging showed a fluid-filled collection near the tip of the VPS catheter. This suggested a cyst formed around the shunt, likely filled with cerebrospinal fluid (CSF), a type of fluid that normally flows in the brain and spinal cord.\\n\\nThe doctors suspected a peritoneal pseudocyst — a rare complication of VPS — and performed emergency surgery. The cyst was located in the left upper abdomen, between the stomach and the colon, in a space called the omental bursa. During surgery, 1500 ml of clear fluid was drained, and the VPS catheter was moved outside the cyst. The cyst wall was removed, and the tissue was found to be fibrous with some inflammation.\\n\\nThe fluid from the cyst matched cerebrospinal fluid in appearance and had no signs of infection. This confirmed the diagnosis: an abdominal cerebrospinal fluid pseudocyst as a complication of the VPS. This condition is rare but can be serious, especially if it causes blockage or swelling in the abdomen.\\n\\nThis case is notable because the symptoms appeared 21 years after the initial VPS surgery — the longest time reported in the medical literature for such a complication. In most cases, these cysts form within a few weeks to a decade after shunt placement, but this one developed much later.\\n\\nSymptoms in adults usually include abdominal pain, bloating, and a noticeable mass. Children more often have symptoms like headaches or nausea due to shunt issues. In this case, the patient had no signs of infection or inflammation, making it unlikely to be an abscess or a pancreatic cyst.\\n\\nThe treatment involved open surgery to remove the cyst and drain the fluid. While some doctors now use smaller, less invasive procedures like laparoscopy, this patient had severe scar tissue (adhesions"}
+{"row_index": 473, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 22-year-old male presented with progressive abdominal distention and nausea. He had a ventriculoperitoneal shunt (VPS) implanted 21 years earlier to manage hydrocephalus secondary to spina bifida. Shunt revision occurred only at age 10 months, with no subsequent abdominal surgical interventions. No history of malignancy, pancreatic disease, or liver pathology was reported. Physical examination revealed a large, elastic, palpable mass in the upper abdomen, with no neurological deficits. Laboratory findings, including white blood cell count and serum amylase, were within normal limits. Supine abdominal radiography demonstrated the VPS in the left upper quadrant and a soft-tissue mass in the upper abdomen. Unenhanced abdominal computed tomography (CT) revealed a homogeneous low-density fluid collection adjacent to the VPS catheter tip, consistent with a cystic lesion arising in the peritoneal cavity. The mass was anatomically localized between the stomach and the mesentery of the transverse colon, specifically within the omental bursa, and was independent of the pancreas. The fluid collection exhibited characteristics consistent with cerebrospinal fluid (CSF), including negative microbial cultures and absence of detectable bacterial flora, as confirmed by fluid analysis. Histopathological examination of the resected pseudocyst wall revealed fibrous tissue with mild inflammatory cell infiltration, confirming the absence of epithelial lining, which is characteristic of a pseudocyst rather than a true cyst or neoplasm.\\n\\nEmergency laparotomy was performed to address the obstructive effect of the mass on the gastric outlet. The cystic mass was excised, and 1500 ml of clear fluid was drained. A portion of the pseudocyst wall, comprising the posterior gastric wall and adjacent colonic mesentery, was completely resected to facilitate decompression and prevent recurrence. The distal end of the VPS catheter was repositioned externally to the cystic mass to ensure proper drainage and avoid further complications. Postoperatively, the patient's appetite improved, and he was discharged on postoperative day 8 in stable condition. His recovery has been uneventful over the subsequent 4 months.\\n\\nAbdominal cerebrospinal fluid pseudocyst is a rare but potentially life-threatening complication of VPS placement, typically manifesting as a thin-walled, fluid-filled cystic mass adjacent to the shunt tip. The"}
+{"row_index": 474, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"low_health_literacy\": \"An 8-month-old boy had a fever for 9 days and started with a droopy left eye (ptosis) right from the beginning. His eye also pointed down and out. The pupil reacted normally, and tests showed no measles or virus in his spinal fluid. The fever was mild and not linked to rash, seizures, or brain problems. His muscles and nerves were normal. Tests for infections and blood were normal. Brain and eye scans were clear, and no serious issues were found. The eye problem went away on its own in about 3 weeks without any medicine. This kind of eye problem in young kids is rare, and it often happens after a virus. In this case, the virus was likely the cause, but no specific test could confirm it. The child fully recovered with no long-term effects.\"\n}"}
+{"row_index": 475, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"An 8-month-old boy had a fever for 9 days and developed left-sided ptosis (drooping eyelid) from the first day of fever. His eye was also turned down and out, but his pupil reacted normally. There was no rash, seizures, or other neurological problems. The child was otherwise active and healthy. Tests showed normal blood work, no signs of infection like measles or other autoimmune conditions, and normal brain and eye scans. The spinal fluid (CSF) showed mild inflammation (lymphocytic pleocytosis), with normal protein and sugar levels, and no detectable measles antibodies. No steroids were given, and the ptosis and eye deviation improved within 2 weeks, fully resolving after 3 weeks. Oculomotor nerve palsy in children is rare and often linked to trauma, infection, or inflammation. In this case, the fever and short duration of symptoms suggest a viral cause, even though measles antibodies were normal. Since the scans were normal and no other serious conditions were found, this appears to be a rare case of temporary viral nerve damage that fully recovered without treatment.\"\n}"}
+{"row_index": 476, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"An 8-month-old boy presented with a 9-day history of moderate, intermittent fever, accompanied from the first day by left-sided ptosis and infero-lateral deviation of the left eye. There was no associated rash, joint pain, convulsions, altered sensorium, or neurologic deficits; the child remained otherwise playful and interactive. On clinical examination, left-sided ptosis was present with downward and outward deviation of the globe, and the pupil exhibited normal reactivity. Inability to elevate the left eyelid was noted, but there were no abnormalities in motor strength, tone, or reflexes in any of the four limbs. Laboratory investigations, including complete blood count, electrolytes, urea, and creatinine, were within normal limits. Autoimmune markers—ANA, ASO titer, pANCA, and cANCA—were all within normal ranges. Magnetic resonance imaging (MRI) of the brain and both orbits, along with MRI angiography, was unremarkable, excluding structural abnormalities, including intracranial aneurysms of the internal carotid artery or posterior communicating artery, which are well-documented causes of pediatric oculomotor nerve (CN-III) palsy. Cerebrospinal fluid (CSF) analysis revealed lymphocytic pleocytosis (10 cells/HPF), with normal protein and glucose levels, consistent with aseptic meningitis. IgM and IgG antimeasles antibody titers in CSF were within normal limits, and CSF norovirus polymerase chain reaction was not performed due to financial constraints. The clinical course was self-limiting: ptosis and eye deviation resolved almost completely within 2 weeks and fully after 3 weeks, without the use of corticosteroids. Pediatric oculomotor nerve palsy is a rare entity, with reported etiologies including trauma, infection, congenital causes, and inflammatory processes. In a series by Keith (n=28), trauma, infection, and idiopathic causes were the most common; in Miller’s series (n=30), congenital or traumatic/inflammatory origins predominated. Schumacher-Feero et al. reported that 47% of patients with partial CN-III palsy achieved full recovery without surgical intervention due to spontaneous resolution or partial functional recovery. Viral infections, particularly measles and norovirus, have been linked to postviral oculomotor nerve"}
+{"row_index": 477, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 6-year-old boy kept getting sick with bacterial meningitis, caused by a type of bacteria called Streptococcus Pneumoniae 23F. He had headaches, vomiting, and fever, and the doctors found this bacteria in his spinal fluid and blood. After treating him with antibiotics for 14 days, he got better and went home. But the infections kept coming back. The doctors looked for a reason and found that fluid from his brain was leaking out through a small hole in his skull, into his middle ear — this happened on the right side. This leak likely let bacteria get into his brain again. Tests showed damage to the bone near his ear and brain, especially around the facial nerve and areas near the ear. The doctors confirmed the leak was coming from the right side of his skull, and that’s why the infections kept coming back. The family didn’t want surgery, so the boy just got vaccinated with Prevenar 7 to help prevent future infections. This vaccine is not part of the regular national vaccine schedule and had to be paid for himself.\"\n}"}
+{"row_index": 478, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 6-year-old boy had repeated episodes of bacterial meningitis caused by Streptococcus Pneumoniae type 23F. He had been treated before with antibiotics, and after one episode, he was discharged without complications. However, the infections kept coming back. Tests showed his immune system was normal, so the cause was likely a problem in his skull bone related to chronic sinusitis. Initial imaging showed sinus inflammation on the right side, but no bone damage. A nuclear scan found that cerebrospinal fluid (CSF) was leaking from the right petroocipital region into the middle ear. Further high-resolution CT and MRI scans showed damage to the bone around the right side of his skull, including areas near the facial nerve and the carotid and jugular canals. These changes showed that the CSF leak was likely the reason for the repeated meningitis. Doctors recommended surgery to fix the bone defect, but the family chose not to proceed. The boy completed antibiotic treatment with vancomycin for 14 days and was sent home. He later received the Prevenar 7 vaccine for pneumococcal infection, though it was not part of the national vaccination program at that time.\"\n}"}
+{"row_index": 479, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 6-year-old male presented with a one-week history of nausea, vomiting, and headache, initially managed at outpatient clinics without improvement. Progression of symptoms, including fever, led to emergency department (ED) admission. Family history revealed a prior episode of acute otitis media (AOM) in infancy and a single episode of acute sinusitis approximately two months prior to admission. No history of skull trauma was reported. Physical examination demonstrated lethargy, neck stiffness, and positive meningeal signs (Brudzinski’s and Kerning signs), consistent with meningitis. Laboratory evaluation included complete blood count (CBC) with differential (WBC: 29,190/mm³, with 4% bands), biochemistry, glucose, and blood culture. Lumbar puncture was performed, yielding cerebrospinal fluid (CSF) analysis, bacterial/viral culture, and CSF biochemistry. CSF showed a WBC count of 3,240/uL with 91% neutrophils, glucose of 55 mg/dL, and total protein of 160.5 mg/dL. Gram stain of CSF identified Streptococcus pneumoniae, prompting immediate initiation of vancomycin and cefotaxime. Both CSF and blood cultures confirmed Streptococcus pneumoniae serotype 23F. Antibiotic sensitivity testing indicated vancomycin efficacy against this serotype, leading to continued therapy for 14 days. The patient had previously suffered from bacterial meningitis six months prior, with identical findings: CSF gram stain positive for Streptococcus pneumoniae 23F, and positive CSF and blood cultures. Immunological assessment, including complement levels and immunoglobulin profiles, was performed and revealed no abnormalities, ruling out primary immunodeficiency as a cause. Given the history of recurrent sinusitis and the temporal association with recurrent meningitis, a chronic bony defect secondary to persistent sinus inflammation was hypothesized. Initial sinus CT imaging demonstrated right maxillary sinusitis without bony erosion. A nuclear scan was subsequently performed to evaluate for cerebrospinal fluid (CSF) leakage, which revealed CSF leakage originating from the right petroocciptital region into the middle ear. High-resolution CT (HRCT) of the temporal bones demonstrated focal enlargement of the right facial nerve canal, erosion of the bony canal at the geniculate ganglion and tympanic"}
+{"row_index": 480, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A woman had problems with her feet, especially the big toe and second toe, that made walking hard and painful. Her toes were bent wrong, and she had thick, painful calluses on her feet. She tried wearing big, soft shoes for years, but it didn’t help much. She kept falling and felt unbalanced. Her doctor found that her big toe was out of place and her second toe was crossing over it. The second toe was bent inward (varus), and this made walking feel like stepping on a pebble. On one foot, the second toe was much worse than on the other. She had surgery on both feet using a soft tissue method called syndesmosis, which didn’t cut any bone. The surgery fixed the big toe position by tying the first and second metatarsal bones together with a special suture. Surprisingly, after this, the second toe bent inward problem fixed itself — it didn’t need any extra surgery. On both feet, the second toe straightened out on its own. Only the right foot’s second toe still had a small problem, so a little extra work was done to fix it. The surgery looked good and felt good after she walked again. This shows that sometimes, fixing one part of the foot can help fix another part without doing extra work.\"\n}"}
+{"row_index": 481, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 60-year-old woman had long-standing foot problems, including bilateral hallux valgus (HV) deformities and crossover deformities between her first and second toes. She tried wearing wider, softer shoes for years, but the pain from walking—especially on uneven ground or stairs—got worse. She developed thick, painful calluses on her feet and had trouble balancing, leading to several falls. Her mother had a similar issue but didn’t need surgery and managed it without intervention.\\n\\nOn exam, her feet showed that the first metatarsal bones were unstable and the second toe on her right foot was severely bent inward (varus deformity), crossing over the big toe. This deformity was causing discomfort and affecting her walking. X-rays and pressure studies showed that her weight was shifting to the second and third toes, worsening the calluses and foot pain.\\n\\nShe chose surgery to fix both her HV and crossover issues. Instead of cutting bones (osteotomy), her doctor used a soft tissue procedure called a syndesmosis procedure, which involves using sutures to realign the first and second metatarsal bones without removing any bone.\\n\\nDuring surgery, the first and second metatarsals were tied together with dissolvable sutures. To our surprise, once the first metatarsal was properly aligned, the second toe’s varus deformity corrected itself—both on the right and left feet—without any extra surgery. The only remaining issue on the right foot was a mild bend in the second toe, which was fixed with a small soft tissue release.\\n\\nAfter surgery, she wore a forefoot cast for three months and returned to normal walking and shoes after six months. She now has good function and appearance in her feet. The case raises an interesting question: why does the second toe deformity correct itself when the first metatarsal is realigned? This may be due to how the bones and soft tissues are connected and how movement affects the toe alignment.\"\n}"}
+{"row_index": 482, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 60-year-old female presented with progressive hallux valgus (HV) and bunion deformities, compounded by a bilateral crossover deformity between the first and second toes. Despite initial management with increasingly accommodating footwear—characterized by a widened forefoot region and soft, roomy toe box—she experienced persistent metatarsalgia, with significant pain localized to the first metatarsal head, described as a constant sensation of walking on a pebble. This led to the development of thick, painful metatarsal calluses bilaterally, particularly under the forefoot, and impaired ambulation, including difficulties with balance on uneven terrain and stair descent. She had experienced multiple falls, reflecting functional compromise. Her mother had a milder HV deformity and managed without surgical intervention, suggesting a familial predisposition. Physical examination revealed bilateral HV deformities with only partial correction possible passively. Passive range of motion at the first metatarsophalangeal joint (MPJ) was 45° in extension and 60° in flexion on the right foot, and 60° and 45° on the left foot, indicating hypermobility. The right second toe exhibited a severe varus deformity, crossing over the hallux without notable clawing, while the left second toe had a milder varus deformity. Manual realignment of the left second toe was complete, whereas the right toe remained resistant to realignment. Both second MPJs were moderately tender and demonstrated reduced passive flexion due to pain. First metatarsals displayed hypermobility in both sagittal and frontal planes, consistent with joint instability. Dorsoplantar standing radiographs revealed a right foot first intermetatarsal angle (IMA) of 17.5° (above the normal upper limit of 9°) and metatarsophalangeal angle (MPA) of 33.7° (exceeding the normal upper limit of 15°), with a left foot IMA of 16.8° and MPA of 27.9°. All first and second MPJs were incongruent, and the right second MPJ showed dorsomedial subluxation. Both tibial and fibular sesamoids were dissociated from the first metatarsal, indicating ligamentous insufficiency and joint instability. Preoperative plantar pressure analysis using F-Scan (Tekscan, USA) demonstrated"}
+{"row_index": 483, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 34-year-old woman fell and hit her head, lost consciousness for a few minutes, then woke up. She didn’t go to the hospital right away. Three days later, she started having a mild headache and went to a clinic. Doctors saw her brain scan and found a blood clot on the side of her head — a big one, but not pressing on her brain yet. Her brain’s spaces were bigger than normal, which means she had a condition called hydrocephalus since birth, but it didn’t cause problems in her growing up. She didn’t have seizures in years, and she’s been doing well in school and work. She didn’t show any signs of brain damage. The headache got worse at first, but by day 5, it was getting better. Doctors decided not to do surgery — just gave her pain medicine and watched her closely. Her headache went away, and she stayed healthy. After 3 weeks, the blood clot got smaller. A year later, she was still fine with no symptoms. This is rare — people with this kind of hydrocephalus can get a brain bleed after a fall, even if they don’t feel sick at first. The hydrocephalus might have helped keep the brain from getting too full, so symptoms came later.\"\n}"}
+{"row_index": 484, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 34-year-old woman with a history of congenital hydrocephalus (a condition where fluid builds up in the brain) due to a narrow aqueduct, did not have surgery. She had no symptoms from the condition and lived a normal life, going to school, earning a bachelor’s degree, and working full time. After falling in the bathroom, she lost consciousness briefly and regained it quickly. She didn’t seek medical help at first but started having a mild headache three days later. A CT scan showed a large blood clot (epidural hematoma) on the right side of her brain, which was causing slight pressure. Her brain’s ventricles were enlarged, a sign of hydrocephalus, but there was no serious fluid buildup or brain swelling. She had a small fracture in her skull but no other injuries. Despite the injury, she remained asymptomatic except for the headache. Because she had no serious symptoms and the blood clot was stable, doctors chose not to operate and instead treated her with pain relief and close monitoring. Her headache improved over time, and by day 8, she was able to go home. Follow-up scans showed the blood clot was shrinking, and her brain pressure was normal. At 10 months after the injury, she was fully recovered with no symptoms. This case is rare — adults with arrested hydrocephalus (where brain fluid buildup stops or slows) may still develop brain bleeds after head injuries, even without noticeable symptoms. The hydrocephalus may have helped reduce pressure in the brain, delaying the appearance of symptoms.\"\n}"}
+{"row_index": 485, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 34-year-old female presented with traumatic brain injury following a fall on the bathroom floor, resulting in transient loss of consciousness and subsequent development of an acute right temporal epidural hematoma measuring 41 cc in volume, with a midline shift of 0.4 cm on initial cranial CT. The hematoma was associated with effacement of cerebral sulci and enlargement of the lateral and third ventricles, consistent with increased intracranial volume, but without transependymal effusion. A linear, nondisplaced fracture of the right temporal bone was identified. Despite the presence of a large epidural hematoma, the patient remained asymptomatic except for a mild, intermittent right-sided headache that began on day 3 postinjury. Neurological examination revealed a Glasgow Coma Scale (GCS) of 15, with equal and briskly reactive pupils, normal visual acuity (20/25 bilaterally), and absence of papilledema, sensory, or motor deficits. Head circumference of 59 cm was noted to be in the upper 97th percentile for her height, consistent with chronic macrocephaly, likely secondary to congenital hydrocephalus due to aqueductal stenosis, which had been managed without surgical intervention. The patient had a history of epilepsy controlled with phenobarbital, with the last seizure occurring approximately 15 years prior, and a recent mild COVID-19 infection five months before the injury. She had no developmental delays, completed high school at the top of her class, earned a bachelor’s degree at age 20, and was actively pursuing a master’s degree while maintaining full-time employment. The patient was initially advised to seek neurosurgical evaluation but delayed consultation until day 5 postinjury. Repeat cranial CT on day 5 demonstrated stable hematoma size, with a marked reduction in headache severity. Conservative management was initiated, including analgesic therapy and close clinical monitoring, with resolution of headache by day 8. Follow-up imaging at 3 weeks postinjury showed progressive reduction in hematoma volume and attenuation, indicating resolution of the hematoma without significant intracranial pressure elevation. Transcranial Doppler study revealed normal pulsatility indices across all intracranial arteries, confirming the absence of significant cerebral perfusion abnormalities or increased intracranial pressure. At 10-month follow-up, the patient remained asymptomatic with no neurological deficits"}
+{"row_index": 486, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 67-year-old woman from a area where leishmaniasis is common had a swollen face that lasted two months. The swelling was red, puffy, and had bleeding crusts on her nose. She first got treated for a common facial infection with antibiotics, but it didn’t help. Doctors then guessed it was a type of skin infection called cutaneous leishmaniasis, and checked a small skin sample that showed the tiny parasites causing it. She was given two medicines—metronidazole and clarithromycin—for 30 days, and her symptoms got better.\"\n}"}
+{"row_index": 487, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 67-year-old woman from a region in Morocco where leishmaniasis is common had swelling on her face and nose that lasted for two months. The swelling was red, swollen, and had crusts, and was initially treated for a bacterial infection called facial erysipelas with antibiotics. However, the symptoms did not improve. Based on her medical history and the appearance of the skin, doctors suspected a type of leishmaniasis known as erysipeloid form. This was confirmed by a skin test that showed the presence of Leishmania parasites. She was then treated with metronidazole and clarithromycin for 30 days, and her condition improved significantly. She had a heart condition called left bundle branch block, so the doctors chose this treatment instead of the usual antimonial drugs.\"\n}"}
+{"row_index": 488, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 67-year-old female from Chichaoua, Morocco—a known endemic zone for Leishmania tropica—presented with a two-month history of progressive swelling in the centrofacial region, characterized by an erythematous and edematous plaque extending to the eyelids, accompanied by hemorrhagic crusts at the nasal tip. The clinical presentation was initially managed as facial erysipelas with a course of amoxicillin-clavulanic acid and ciprofloxacin for 15 days, which failed to result in clinical improvement. Given the patient's residence in an endemic area for Leishmania tropica and the presence of a family history of leishmaniasis (her grandson having been previously treated for the disease), the differential diagnosis was strongly shifted toward cutaneous leishmaniasis in its erysipeloid form. Confirmation was achieved via skin smear, which demonstrated the presence of Leishmania amastigotes, confirming the diagnosis. The specific species of Leishmania could not be identified at the institutional level. Notably, the patient had a left bundle branch block on electrocardiography, which contraindicated the use of pentavalent antimonial agents due to potential cardiac toxicity. As such, a combination therapy of metronidazole (1.5 g daily) and clarithromycin (15 mg/kg body weight) was selected as a safer alternative, based on its efficacy in treating erysipeloid cutaneous leishmaniasis in patients with cardiac comorbidities. The patient received this regimen for 30 days and demonstrated a good clinical response with progressive resolution of the lesion. The erysipeloid form of cutaneous leishmaniasis is a self-limiting but persistent infection, typically presenting with erythematous, edematous plaques and hemorrhagic crusts, and is caused by Leishmania tropica, which resides in the dermal layers and replicates intracellularly within macrophages as amastigotes. The pathogenesis involves the invasion of dermal macrophages, leading to local inflammation, edema, and tissue damage. Metronidazole and clarithromycin are effective due to their ability to penetrate the macrophage phagolysosome and exert activity against intracellular amastigotes, with clarithromycin showing particularly favorable pharmacokinetic properties in this setting. This case underscores the importance of considering leish"}
+{"row_index": 489, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 57-year-old woman had high potassium levels in her blood for years, always between 5.3 and 5.9. Her doctor checked her closely, but she had no symptoms or problems. Her blood pressure was under control, and her heart test was normal. She was referred to a kidney specialist because the high potassium didn’t go down, even when she followed a low-potassium diet. The doctor checked everything — her blood, urine, and other tests — to find the cause. Nothing was wrong with her kidneys, no signs of blood cell breakdown, no infections, no muscle damage, and no other known causes. Even after testing for possible rare conditions, nothing explained the high levels. The doctors thought it might be a rare issue where the blood sample shows high potassium even when it’s not real — like a trick in the lab. They tested the blood under different conditions to see if the high number was just a mistake. The results showed the high level didn’t happen. So, the cause of the high potassium could not be found. The patient’s body is just doing something unusual, and no treatment is needed right now.\"\n}"}
+{"row_index": 490, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 57-year-old woman had high potassium levels in her blood for four years, ranging from 5.3 to 5.9 mmol/L (normal is 3.5–5.1 mmol/L). She had no symptoms or signs of illness, and her heart tests were normal. She was on medication for high blood pressure, which was well controlled. After being referred to a nephrology specialist, doctors checked for possible causes like kidney problems, broken cells, or acidosis. All tests came back normal, including blood cell counts, kidney function, and urine tests. A diet low in potassium was recommended, but it didn’t lower her potassium levels. Even after checking for conditions like blood disorders or tissue damage, no cause was found. The doctors considered a rare condition called familial pseudohyperkalemia, where blood samples might show falsely high potassium due to how they’re stored or transported. They tested the blood under different conditions (cold, room temperature, body temperature) and found that the high potassium level only appeared when the sample was left uncentrifuged and exposed to certain conditions. When the sample was properly processed, the potassium level returned to normal. This suggests the high reading was not real, and the cause of the elevated levels could not be confirmed.\"\n}"}
+{"row_index": 491, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"We present a case of a 57-year-old female with a four-year history of persistent mild hyperkalemia, defined by serum potassium levels ranging from 5.3 to 5.9 mmol/L (reference range: 3.5–5.1 mmol/L), without associated clinical manifestations such as muscle weakness, cardiac arrhythmias, or hemolysis. Spectrophotometric hemolysis index remained below 6 mg/dL across all laboratory reports, excluding intravascular hemolysis as a contributing factor. Electrocardiographic monitoring was normal, with no evidence of electrolyte-induced conduction abnormalities. The patient's medical history included chronic arterial hypertension, which was well-controlled with angiotensin-converting enzyme (ACE) inhibitor therapy. No significant findings were noted during physical examination or anamnesis. She was receiving amlodipine for blood pressure control, with stable clinical outcomes.\\n\\nThe patient was referred to the Nephrology Unit for further evaluation due to the persistent elevation of serum potassium despite the absence of identifiable clinical or laboratory triggers. Initial management included a potassium-restricted diet, which was implemented for a three-month period. At the three-month follow-up, a serum sample was collected and analyzed; the sample was non-hemolyzed (hemolysis index <6 mg/dL) and revealed a potassium concentration of 5.5 mmol/L, confirming the continued presence of hyperkalemia.\\n\\nA comprehensive differential diagnosis was conducted to exclude common etiologies of hyperkalemia, including: (1) renal insufficiency, (2) intravascular hemolysis, (3) metabolic acidosis, (4) tissue breakdown (e.g., rhabdomyolysis), and (5) pseudohyperkalemia secondary to oncohematologic conditions such as essential thrombocytosis or acute or chronic leukemia. Laboratory workup included a hemogram with reticulocyte count and blood smear, general biochemistry (including ions, hemolysis index, hepatic enzymes—GOT, GPT, GGT, LDH, ALP, renal function—creatinine, urea, and estimated glomerular filtration rate via CKD-EPI equation), creatine kinase (CK), haptoglobin, phosphocalcic parameters, and iron metabolism (iron, transferrin saturation, transferrin, ferritin),"}
+{"row_index": 492, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A family has a rare condition called Noonan syndrome. The girl, her sister, mother, maternal aunt, grandmother, and one female cousin all have signs of this condition. Three of them had genetic testing, and it showed that the girl and her sister both got the same change in a gene called LZTR1 from their mom. The girl also has a problem with growth hormone, which makes her grow slower than others. She has some typical features like wide-set eyes, a short nose, low ears, and a curved spine. She also has a weak heart rhythm and a small jaw. Her growth hormone level is low, and her bones are not growing as fast as they should. Doctors said she has Noonan syndrome with growth hormone deficiency, and because of her spine problems, they don’t recommend giving her growth hormone treatment right now.\"\n}"}
+{"row_index": 493, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A family has been studied where multiple members have Noonan syndrome, a genetic condition that can cause physical and developmental differences. The proband, a 6.6-year-old girl, along with her sister, mother, maternal aunt, grandmother, and a female cousin, showed signs of Noonan syndrome, either typical or atypical. Only three family members had genetic testing, and the results showed that both the proband and her sister inherited the same genetic change in the LZTR1 gene (c.1149+1G>T) from their mother. This gene mutation is linked to the condition. The girl also had growth hormone deficiency, which means her body doesn't produce enough growth hormone, and she did not have any other genetic changes. She had short stature, delayed development, and physical features common in Noonan syndrome, such as widely spaced eyes, a short nose, low-set ears, and a webbed appearance of the upper lip. She also had scoliosis and a bone deformity in her spine. Her growth hormone levels were low, and her bone age was younger than her actual age. Her heart, liver, kidneys, and brain were normal. Because of her severe spinal issues, treatment with growth hormone was not recommended.\"\n}"}
+{"row_index": 494, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"We herein describe a family with LZTR1-related Noonan syndrome. The proband, a 6.6-year-old female, was referred for evaluation of short stature as the first child of nonconsanguineous parents, born at 41 weeks of gestation via vaginal delivery with a birth weight of 1800 g (<P3rd) and length of 47 cm (<P3rd). She exhibited significant prenatal and postnatal growth retardation, with current height of 90.5 cm (−6.3 SD), weight of 11 kg (−4.9 SD), and BMI of 13.4 kg/m² (P10–25th). Her arm span/height ratio was 0.92 (−2 SD) and sitting height/height ratio was 0.58 (+3 SD), both deviating from standard reference values. Psychomotor development was mildly delayed. Clinical examination revealed typical Noonan syndrome features including hypertelorism, downslanting palpebral fissures, epicanthal folds, low-set oval posteriorly rotated ears with thick helix, short broad nose with depressed root and full tip, deeply grooved long philtrum, high and wide vermilion peaks, highly arched palate, micrognathia, short neck, cubitus valgus, scoliosis, café au lait spots, and mild hypertrichosis. Additional findings included squinting, refractive errors, and nystagmus. Laboratory investigations showed IGF-1 level of 61 μg/L (−1.9 SD), and growth hormone (GH) stimulation testing (insulin and levodopa protocols) demonstrated a GH peak of 5.54 ng/mL, below the cut-off value of 7 ng/mL, confirming growth hormone deficiency. Electrocardiography revealed frequent premature ventricular beats (second and third rhythms). Imaging studies, including X-ray and MRI of the spine, identified a hemivertebral deformity of the third thoracic vertebra and scoliosis with a Cobb’s angle of 28°; bone age was assessed at 5.5 years. Hormonal evaluations of the adrenal, thyroid, and gonadal axes were within normal limits, and tumor markers (AFP, HCG, CEA) were negative. No structural abnormalities were detected on cardiac, hepatic, renal, gynecological,"}
+{"row_index": 495, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"An 82-year-old man had surgery to remove his bladder and prostate because of cancer. Four days after surgery, he suddenly lost movement in all four limbs — his arms and legs — but didn’t feel pain or have trouble speaking. Doctors thought it might be a problem in his spine, but scans showed no blockage or bleeding in the spine. Instead, the problem was found in his brain: two small strokes happened at the same time on both sides, in areas that control movement. These strokes were caused by a lack of blood flow, likely because of a blood clot that came from his heart, maybe linked to his cancer. Since there was no clear reason found, doctors started giving him medicine to prevent more clots. His arms got better over time, but his legs stayed weak. This case shows that even after major surgery, a stroke can happen due to blood clots, and early treatment helps prevent more problems.\"\n}"}
+{"row_index": 496, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"An 82-year-old man had surgery to remove his bladder and prostate due to cancer. Four days after the surgery, he suddenly developed severe weakness in all four limbs — arms and legs — without pain or loss of sensation. His brain scans showed acute bilateral strokes in the areas of the brain that control movement (precentral gyri), which explains the weakness. These strokes were caused by a sudden blockage of blood flow, likely due to a blood clot that traveled from his heart. Although the spinal cord was checked and found normal, the brain imaging revealed the strokes. The patient had no history of falls or trauma, and his blood clotting tests were normal, making the cause harder to find. Because of the surgery and anesthesia, doctors suspected a clot from the heart. He was started on anticoagulant medication to prevent future clots. After recovery, he began taking aspirin for long-term prevention. The key point is that this rare case shows that strokes can happen after major surgery, even without obvious risk factors, and brain imaging is essential for diagnosis.\"\n}"}
+{"row_index": 497, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"An 82-year-old Caucasian male was admitted to the urology department for radical cystoprostatectomy due to localized prostate adenocarcinoma. On the fourth postoperative day, he abruptly developed severe painless tetraparesis, characterized by Medical Research Council (MRC) grade 2/5 muscle strength in proximal upper limb muscles bilaterally and 0/5 in both lower limbs, with no involvement of cranial nerves, impaired consciousness, or sensory deficits. There were no cerebellar signs. Neurological examination revealed brisk tendon reflexes and positive pyramidal signs bilaterally, strongly suggesting a lesion affecting the central nervous system, such as acute spinal cord compression, subdural hemorrhage, or ischemia. No recent trauma or fall was reported prior to symptom onset. A peridural catheter had been placed for analgesia postoperatively and was removed the previous day without complications.\\n\\nAn emergency magnetic resonance imaging (MRI) study was performed, requiring the removal of metal brackets from subcutaneous tissue due to surgical implants. Spinal MRI did not demonstrate any evidence of spinal cord compression, subarachnoid hemorrhage, or ischemic changes (Figure A), thereby excluding a primary spinal cord pathology. In contrast, cranial MRI revealed acute bilateral ischemic infarctions localized to the precentral gyri—specifically, the median portion of the precentral gyrus on both sides (Figure B and C; arrows)—with no involvement of the internal capsule (Figure D). T2-weighted imaging at the level of the primary motor cortex showed no abnormal signal intensity at the time of presentation, which is consistent with acute ischemia and supports a time-dependent pathophysiological mechanism (Figure E). The precentral gyrus is supplied by the anterior cerebral artery (supplying the medial one-third) and the middle cerebral artery (supplying the lateral two-thirds) bilaterally.\\n\\nOver the subsequent days, upper extremity weakness gradually resolved, while lower limb paralysis persisted, indicating a regionally selective motor cortex infarction. Comprehensive diagnostic evaluation, including carotid duplex sonography, 24-hour electrocardiography (ECG), and transesophageal echocardiography, failed to identify any structural vascular disease, cardiac thrombus, or paroxysmal atrial fibrillation. While hypercoagulability associated with prostate cancer may have contributed to the cerebral ischemia,"}
+{"row_index": 498, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 60-year-old man had cancer in the back part of his pancreas. He didn’t have diabetes at first, and his blood sugar was normal. Doctors found the cancer with a blood test and imaging. They removed the cancer with surgery and gave him chemo to help fight it. Two years later, the cancer came back in one spot in his liver. The blood test for sugar started going up fast, and his blood sugar got worse as the cancer grew. So, doctors started giving him insulin to control his blood sugar. Even though the liver cancer didn’t respond well to chemo, it was only one spot, so they did surgery to remove it. After that surgery, his blood sugar got better right away and he stopped needing insulin. Now, two years later, he’s still alive and the cancer hasn’t come back.\"\n}"}
+{"row_index": 499, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 60-year-old man was diagnosed with cancer in the tail of the pancreas, and his blood sugar levels were normal at the time of diagnosis. He had no history of diabetes or family history of pancreatic cancer. After surgery to remove the tumor (distal pancreatectomy) with lymph node removal, he received chemotherapy (S-1) to reduce the risk of the cancer coming back. Two years later, a single tumor was found in his liver, which was treated with two rounds of chemotherapy—first gemcitabine/nab-paclitaxel, then modified FOLFIRINOX. However, his blood sugar control worsened over time, rising from 5.6% to over 10%, and matched the growth of the tumor. Because of this, insulin therapy was started to manage his high blood sugar. Despite the liver tumor not responding well to chemotherapy, it was completely removed with a left hepatectomy since only one tumor was present. After the surgery, his blood sugar improved right away, and insulin was stopped. Two years after the second surgery, the patient is still alive and has not had any signs of cancer coming back.\"\n}"}
+{"row_index": 500, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 60-year-old male with a history of past smoking (Brinkman Index: 800) and chronic alcohol consumption (20 g/day for 20 years) was referred for evaluation of suspected pancreatic tail adenocarcinoma based on an elevated carbohydrate antigen 19-9 (CA19-9) concentration of 286.8 U/mL during a routine medical screening. He had no prior history of diabetes, significant comorbidities, or familial predisposition to pancreatic cancer. His body mass index was 20.8 kg/m², and he reported no weight loss. Dynamic contrast-enhanced computed tomography (dCECT) demonstrated a hypovascular lesion in the pancreatic tail, consistent with a resectable tumor. Endoscopic ultrasonographic fine-needle aspiration confirmed the diagnosis of adenocarcinoma. Positron emission tomography (PET) revealed a high standardized uptake value (SUVmax = 6.6), supporting malignant activity. Magnetic resonance imaging with gadolinium ethoxybenzyl diethylenetriamine pentaacetic acid (Gd-EOB-DTPA) showed no synchronous liver metastases, and the tumor was deemed anatomically resectable. The patient underwent a curative-intent distal pancreatectomy with regional lymph node dissection via radical antegrade modular pancreatosplenectomy. The pancreatic parenchyma was resected just above the superior mesenteric vein using tri-stapler technology, resulting in an operative time of 251 minutes and extraoperative blood loss of 720 mL. A clinically significant postoperative pancreatic fistula developed but resolved spontaneously without intervention, and the patient was discharged on postoperative day 40. Pathological examination revealed a 36 × 18 × 17-mm moderately differentiated tubular adenocarcinoma with no lymph node metastasis (0/27), absence of microscopic lymphatic invasion, but presence of microscopic venous invasion. The tumor margin was negative for extrapancreatic extension, and the resection margins were clear. The postoperative stage was classified as IB (T2N0M0) according to the Union for International Cancer Control 8th edition. Adjuvant S-1 chemotherapy (120 mg/m²/day) was administered for six months postoperatively.\\n\\nTwo years following the initial pan"}
+{"row_index": 501, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 61-year-old man had high blood pressure and a small cancer in his kidney called chromophobe renal cell carcinoma. Later, a tumor was found in his seminal vesicle (a part of the male reproductive system). Doctors thought it might be a spread from the kidney cancer, but tests showed it was actually a separate tumor called a primary paraganglioma. This new tumor did not spread to other parts of the body and was not made from cancer cells. It had features that match a normal type of tumor in that area. The tumor cells showed signs of a specific protein (synaptophysin and chromogranin), and some surrounding cells had S100 protein. Tests for genetic changes found nothing in either tumor, which supports it being a new, original tumor. The man had surgery to remove the tumor, and his blood pressure is now under control. He is still alive after 14 months.\"\n}"}
+{"row_index": 502, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"This report describes a rare case of a primary paraganglioma in the seminal vesicle of a 61-year-old man. He had been dealing with high blood pressure and previously had a tumor in his kidney, diagnosed as chromophobe renal cell carcinoma. When a new tumor appeared in his left seminal vesicle, doctors considered it a possible spread (metastasis) from the kidney cancer. However, tests showed that the seminal vesicle tumor was not made of cancer cells and did not match the kidney tumor's characteristics. Instead, it showed markers typical of a paraganglioma — a type of tumor that arises from nerve tissue. The tumor cells expressed synaptophysin and chromogranin, and the surrounding cells showed S100 protein, which is common in such tumors. Both the kidney tumor and the seminal vesicle tumor had normal levels of SDHA and SDHB proteins, and no gene mutations were found in these genes. Imaging confirmed no other tumors were present, supporting the diagnosis that this was a primary tumor in the seminal vesicle, not a spread from the kidney. The patient recovered well and remains alive with controlled blood pressure after 14 months of follow-up.\"\n}"}
+{"row_index": 503, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 61-year-old obese male presented with persistent arterial hypertension and was evaluated for an incidental renal tumor discovered during imaging for hypertension. Laparoscopic partial nephrectomy revealed a chromophobe renal cell carcinoma (cRCC), a rare subtype of clear cell carcinoma characterized by minimal cytoplasmic visibility and low mitochondrial content, typically associated with intact von Hippel-Lindau (VHL) pathway function. Following one year of surveillance, a new lesion was identified in the left seminal vesicle. Magnetic resonance imaging (MRI) demonstrated a well-circumscribed, heterogeneous solid tumor measuring 32 mm in maximum dimension, with clear anatomical separation from the rectal and bladder walls, suggesting a benign or low-aggressiveness growth pattern. The patient underwent laparoscopic excision of the left seminal vesicle.\\n\\nGross examination revealed a seminal vesicle measuring 6 × 3 × 2 cm, with a solid, smooth, brownish nodule of 30 mm in greatest diameter. Surgical margins were negative for residual tumor, indicating complete resection. Microscopic evaluation showed well-defined nests of cuboidal tumor cells separated by vascular fibrous septa, with no evidence of vascular invasion, mitotic activity, or necrosis. Focal glandular structures were observed, and individual tumor cells exhibited a large central nucleus with small to medium-sized nucleoli and granular eosinophilic cytoplasm, consistent with neuroendocrine differentiation.\\n\\nDifferential diagnoses included metastatic chromophobe renal cell carcinoma, primary adenocarcinoma of the seminal vesicle, and paraganglioma. Immunohistochemical analysis was performed to discriminate between these entities. Tumor cells demonstrated strong positive immunoreactivity for synaptophysin and chromogranin, markers of neuroendocrine differentiation, supporting a neuroendocrine origin. Peripheral S100 protein-positive cells, likely corresponding to sustentacular cells, were identified at the tumor nest margins, further supporting a paraganglioma phenotype. Absence of keratin expression (AE1/AE3, CK7, CK8/18) excluded both primary and metastatic adenocarcinoma, reinforcing the diagnosis of a primary paraganglioma of the seminal vesicle. The Ki-67 labeling index was less than 2%, indicating a very low proliferative rate and favorable biological behavior.\\n\\nGenomic analysis was conducted on paraffin-"}
+{"row_index": 504, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 32-year-old Chinese woman had pain in her upper belly for 6 months. A scan found a small spot in her left liver, about 1.1 x 1.3 cm in size. The spot looked different on the scan — dark on one setting and bright on another — which made doctors think it might be cancer. After checking the tissue from the surgery, they found it was a rare type of liver cancer called LEL-ICC. She had the surgery using a small camera (laparoscopic) and recovered well, going home after 5 days. No signs of cancer were found after 28 months of follow-up. She still checks in every 3 months for blood tests and scans to stay safe.\"\n}"}
+{"row_index": 505, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 32-year-old Chinese woman had been experiencing upper abdominal pain for six months. An MRI scan found a 1.1×1.3 cm lesion in the left part of her liver. The lesion looked different on the scan — it appeared dark on T1-weighted images and bright on T2-weighted images — which made doctors think it could be liver cancer. However, after surgery, the tissue was examined closely. The results showed it was a rare type of liver cancer called LEL-ICC. This type of cancer is linked to Epstein-Barr virus (EBV) and has specific markers that helped confirm the diagnosis. The patient had hepatitis B for six years, but her virus was inactive and not actively causing harm. Her other cancer markers were within normal ranges. She had a laparoscopic surgery to remove the part of the liver, and she recovered well, being discharged on postoperative day 5. After surgery, she had regular check-ups every three months for the first two years, then every six months. All tests remained normal, and she has not had any signs of cancer recurrence even after 28 months of follow-up. She is currently healthy and doing well.\"\n}"}
+{"row_index": 506, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 32-year-old Chinese female presented to Sichuan University West China Hospital with a 6-month history of upper abdominal pain. She had no history of radiotherapy, industrial chemical exposure, hormonal therapy, or contraceptive use. She reported one prior pregnancy and delivery of a male child. No personal or family history of hypertension, diabetes, smoking, or alcohol consumption was noted. Physical examination was unremarkable. Laboratory findings included hemoglobin 14.2 g/dL (normal range: 13–17.5 g/dL), white blood cells 7.12×10⁹/L (normal: 3.5–9.5×10⁹/L), platelets 249×10⁹/L (normal: 100–300×10⁹/L), total bilirubin 12.5 μmol/L (normal: 5.0–28 μmol/L), and aspartate aminotransferase (AST) 35 IU/L (normal <50 IU/L). Serological testing revealed carcinoembryonic antigen (CEA) of 5.54 ng/mL (abnormal threshold: ≥3.4 ng/mL), hepatitis B surface antigen (HBsAg) positive, and hepatitis B virus DNA (HBV-DNA) less than 1×10² IU/mL (indicating inactive HBV infection). Tumor markers CA19-9, CA125, and α-fetoprotein were 25.6 U/mL (normal <30 U/mL), 13.3 U/mL (normal <24 U/mL), and 3.37 ng/mL (normal <7 ng/mL), respectively. Abdominal computed tomography (CT) identified a lesion in the left lobe of the liver with no evidence of metastatic disease. Magnetic resonance imaging (MRI) of the upper abdomen revealed a 1.1×1.3 cm lesion in the left hepatic lobe exhibiting low signal intensity on T1-weighted sequences and high signal intensity on T2-weighted sequences, findings consistent with hepatocellular carcinoma (HCC) on initial preoperative evaluation. The patient underwent laparoscopic left lateral sectionectomy. Macroscopic examination revealed a yellowish solid mass measuring 12 mm in diameter. Microscopic analysis demonstrated an undifferentiated"}
+{"row_index": 507, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n  \"low_health_literacy\": \"A 66-year-old man suddenly lost movement on his right side and had trouble speaking. Doctors found a blocked blood vessel in his brain, on the left side, that was causing the stroke. They gave him a medicine called alteplase to open the blockage, then used a special tool to remove the clot. The blood vessel didn’t fully open at first, so they used a balloon to stretch it out while keeping blood flowing to other parts of the body. This helped the blood vessel open up again. After 15 minutes, the blockage was fixed and the man’s symptoms went away. He didn’t have any brain damage, and by the next day, he could move and speak normally. The doctors said the treatment worked well and the blockage improved over time. He’s now back to normal, with no problems after a year.\"\n}"}
+{"row_index": 508, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"intermediate_health_literacy\": \"A 66-year-old man suddenly developed weakness on his right side and difficulty speaking. MRI scans showed a blockage in the left middle cerebral artery, which supplies blood to part of the brain. He received alteplase, a clot-dissolving drug, and then underwent a procedure to remove the clot using a catheter (mechanical thrombectomy). The clot was partially removed, but the artery remained narrowed (stenosis), leading to a recurrence of blockage. To fix this, a special balloon catheter was used for a 15-minute angioplasty while keeping blood flow to other parts of the body. This helped reopen the artery and improved blood flow. The patient’s symptoms improved significantly, and by the next day, his neurological score was back to normal. Follow-up scans showed the blockage had improved, and he was able to go home without any lasting brain damage. He was prescribed medications to prevent future clots, and after three months, his artery showed better flow. No major problems occurred for over a year. The treatment used a device not yet officially approved, but it was approved by the hospital after careful review and with the patient’s informed consent.\"\n}"}
+{"row_index": 509, "data_source": "multiclinsum", "ability": "summarization", "prediction": "{\n    \"proficient_health_literacy\": \"A 66-year-old male presented with an acute onset of right hemiplegia and dysarthria at 7:30 a.m. while driving, prompting immediate transport to the hospital. Clinical examination revealed right facial paralysis, dysarthria, right upper extremity paralysis, and right upper and lower extremity paresthesia, with an initial National Institutes of Health Stroke Scale (NIHSS) score of 6/42. Magnetic resonance imaging (MRI) diffusion-weighted imaging (DWI) demonstrated hyperintense signals in the left putamen, corona radiata, and partial region of the middle cerebral artery, consistent with acute ischemic infarction. Magnetic resonance angiography (MRA) confirmed a distal occlusion of the left middle cerebral artery (MCA), while T2-weighted imaging showed no visible thrombus within the occluded segment, suggesting a thrombus-free occlusion with possible vasospasm or plaque-induced stenosis. A perfusion-diffusion mismatch was identified, supporting the indication for intravenous alteplase therapy, which was administered at 9:27 a.m. after correction of hypotension with nicardipine. The treatment protocol was guided by current stroke guidelines, with no contraindications identified.\\n\\nEndovascular recanalization was initiated using a 9 Fr sheath placed in the right femoral artery, with subsequent guidance of a 9 Fr OPTIMO catheter into the left internal carotid artery. Internal carotid arteriography revealed a distal occlusion of the left MCA. In the delayed phase, collateral circulation was observed via anastomosis of the cerebral pia mater, providing anterior-to-middle cerebral artery perfusion. A rebar (Medtronic) was advanced distal to the occlusion using a CHIKAI 14 × 200 cm catheter to secure the distal vessel, and a Trevo XP ProVue Retriever (4.0 × 30 mm, Stryker) was deployed. Post-deployment imaging demonstrated immediate flow restoration, but poor stent dilation was noted in the occluded segment, indicating significant arterial stenosis. The proximal diameter of the stenosis was 2.6 mm, and the distal diameter was 2.1 mm, confirming a moderate to severe stenotic lesion. Following retrieval of the Trevo, a 1"}
diff --git a/code/RL_model/inference_data/vllm_inference_20260213_003845_meta.json b/code/RL_model/inference_data/vllm_inference_20260213_003845_meta.json
new file mode 100644
index 0000000000000000000000000000000000000000..6b5734bf33e0e68f34b38b2fd58cd75f4954bfc2
--- /dev/null
+++ b/code/RL_model/inference_data/vllm_inference_20260213_003845_meta.json
@@ -0,0 +1,10 @@
+{
+  "model_path_for_tokenizer": "/home/mshahidul/readctrl/code/RL_model/converted_model/v1",
+  "dataset_path": "/home/mshahidul/readctrl/code/RL_model/verl/verl_train/dataset/test.parquet",
+  "base_url": "http://127.0.0.1:8001/v1",
+  "served_model_name": "inference",
+  "batch_size": 8,
+  "num_samples": 510,
+  "output_jsonl": "/home/mshahidul/readctrl/code/RL_model/inference_data/vllm_inference_20260213_003845.jsonl",
+  "output_parquet": "/home/mshahidul/readctrl/code/RL_model/inference_data/vllm_inference_20260213_003845.parquet"
+}
\ No newline at end of file
diff --git a/code/RL_model/inference_data/vllm_inference_20260213_165923.jsonl b/code/RL_model/inference_data/vllm_inference_20260213_165923.jsonl
new file mode 100644
index 0000000000000000000000000000000000000000..7169440bfa92caee19025373f4cb8652dc2e33ee
--- /dev/null
+++ b/code/RL_model/inference_data/vllm_inference_20260213_165923.jsonl
@@ -0,0 +1,104 @@
+{"row_index": 0, "doc_id": 20, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 38-year-old woman had a weak heart since she was 17, after a bad cold that might have hurt her heart muscle. Her heart couldn’t pump blood well, so she was in the hospital for 10 months. She was very sick and close to dying, but her heart started to get better. Doctors treated her heart failure, kept her heart from beating too fast or too slow, and stopped blood clots. After 4 years, her heart function improved and stayed strong — that’s rare, only 1 in 6 people get this. Then it got worse again for 2 years, but she stayed stable. She had a baby, and after the second pregnancy, her heart got weaker again, especially after giving birth — this is common in women with heart problems. Now, in 2017, she’s stable. She takes medicine every day — for her heart, to control fluid, and to slow her heartbeat. She can do normal daily activities, has two children, and doesn’t work. Her heart is still weak, but it’s working better than before. She checks her heart regularly and watches her weight and fluid intake. No need for a special heart device right now.\"\n}", "generated_text": "A 38-year-old woman had a weak heart since she was 17, after a bad cold that might have hurt her heart muscle. Her heart couldn’t pump blood well, so she was in the hospital for 10 months. She was very sick and close to dying, but her heart started to get better. Doctors treated her heart failure, kept her heart from beating too fast or too slow, and stopped blood clots. After 4 years, her heart function improved and stayed strong — that’s rare, only 1 in 6 people get this. Then it got worse again for 2 years, but she stayed stable. She had a baby, and after the second pregnancy, her heart got weaker again, especially after giving birth — this is common in women with heart problems. Now, in 2017, she’s stable. She takes medicine every day — for her heart, to control fluid, and to slow her heartbeat. She can do normal daily activities, has two children, and doesn’t work. Her heart is still weak, but it’s working better than before. She checks her heart regularly and watches her weight and fluid intake. No need for a special heart device right now."}
+{"row_index": 1, "doc_id": 21, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 27-year-old man broke his right thigh bone after a small fall, where the bone twisted and bent. He had a bone condition called fibrous dysplasia in his thigh since childhood, and 20 years ago, doctors removed part of the bone, added bone graft, and fixed it with a metal device. They later took out the metal device one year later. This time, because the break was serious and in a weak area, they removed a large part of the broken bone and replaced it with a hip implant. They also took a small tissue sample, which confirmed it was the same bone problem from when he was a child. Now, he can walk and do daily things, though he still has some pain when walking long distances. He’s happy with how well it’s working and can now walk and do light activities like walking without much trouble.\"\n}", "generated_text": "A 27-year-old man broke his right thigh bone after a small fall, where the bone twisted and bent. He had a bone condition called fibrous dysplasia in his thigh since childhood, and 20 years ago, doctors removed part of the bone, added bone graft, and fixed it with a metal device. They later took out the metal device one year later. This time, because the break was serious and in a weak area, they removed a large part of the broken bone and replaced it with a hip implant. They also took a small tissue sample, which confirmed it was the same bone problem from when he was a child. Now, he can walk and do daily things, though he still has some pain when walking long distances. He’s happy with how well it’s working and can now walk and do light activities like walking without much trouble."}
+{"row_index": 2, "doc_id": 21, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 27-year-old man came to the emergency department with a fracture in the upper part of his right thigh bone (femur), specifically at the base of the neck. The break happened after a minor fall that involved pressure and twisting of the hip. This type of fracture is classified as Garden II, Pauwells III, AO 31B2.3r, and is considered serious due to the way it occurred and the patient’s medical history. He had been treated 20 years ago for fibrous dysplasia — a condition where abnormal bone tissue grows in the bone — with a procedure that included removing part of the bone (curettage), adding bone graft, and using a device (osteosynthesis material) to stabilize the area. That device was removed one year later. A biopsy later confirmed the condition was fibrous dysplasia (DF). Because of the fracture’s location and the patient’s history, doctors decided on a wide removal of the upper femur and a total hip replacement using a modular prosthesis, along with placing a cerclage wire to help stabilize the bone. A biopsy after surgery confirmed it was the same fibrous dysplasia seen in childhood. The patient recovered well, with no major complications. He was able to walk with support and gradually returned to daily activities. He still has some walking difficulty due to a scar in the gluteal muscle, but he is now able to do low-impact activities like walking and is very satisfied with his recovery.\"\n}", "generated_text": "A 27-year-old man came to the emergency department with a fracture in the upper part of his right thigh bone (femur), specifically at the base of the neck. The break happened after a minor fall that involved pressure and twisting of the hip. This type of fracture is classified as Garden II, Pauwells III, AO 31B2.3r, and is considered serious due to the way it occurred and the patient’s medical history. He had been treated 20 years ago for fibrous dysplasia — a condition where abnormal bone tissue grows in the bone — with a procedure that included removing part of the bone (curettage), adding bone graft, and using a device (osteosynthesis material) to stabilize the area. That device was removed one year later. A biopsy later confirmed the condition was fibrous dysplasia (DF). Because of the fracture’s location and the patient’s history, doctors decided on a wide removal of the upper femur and a total hip replacement using a modular prosthesis, along with placing a cerclage wire to help stabilize the bone. A biopsy after surgery confirmed it was the same fibrous dysplasia seen in childhood. The patient recovered well, with no major complications. He was able to walk with support and gradually returned to daily activities. He still has some walking difficulty due to a scar in the gluteal muscle, but he is now able to do low-impact activities like walking and is very satisfied with his recovery."}
+{"row_index": 3, "doc_id": 22, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 4-year-old boy with advanced neuroblastoma received intensive chemotherapy, followed by stem cell transplants — first using his own stem cells (autologous HSCT) and then a cord blood transplant (allogeneic CBT). After the transplant, he developed worsening breathing problems on day 194. His older brother had a cold, and a test showed he had a respiratory syncytial virus (RSV) infection about a month before. He also had symptoms like coughing and shortness of breath. A lung biopsy showed signs of lung damage, including inflammation from the virus and changes consistent with pulmonary vascular dysplasia (PVOD). The doctors believe the RSV infection may have triggered or contributed to the development of PVOD. The lung injury was seen in the cells of the lungs, especially in the air sacs and blood vessels, and the findings suggest that the virus played a key role in starting the condition.\"\n}", "generated_text": "A 4-year-old boy with advanced neuroblastoma received intensive chemotherapy, followed by stem cell transplants — first using his own stem cells (autologous HSCT) and then a cord blood transplant (allogeneic CBT). After the transplant, he developed worsening breathing problems on day 194. His older brother had a cold, and a test showed he had a respiratory syncytial virus (RSV) infection about a month before. He also had symptoms like coughing and shortness of breath. A lung biopsy showed signs of lung damage, including inflammation from the virus and changes consistent with pulmonary vascular dysplasia (PVOD). The doctors believe the RSV infection may have triggered or contributed to the development of PVOD. The lung injury was seen in the cells of the lungs, especially in the air sacs and blood vessels, and the findings suggest that the virus played a key role in starting the condition."}
+{"row_index": 4, "doc_id": 23, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 65-year-old man started feeling a persistent cough, shortness of breath, and lost 10 pounds in just 4 months. Tests showed a lump in his right lung and fluid around it. A small piece of tissue was taken and looked under a microscope — it showed strange cells that grew in sheets, surrounded by many immune cells. These cells were found to be from a rare cancer called pulmonary lymphoepithelioma-like carcinoma (CTLP). The cancer cells had signs of a virus called Epstein-Barr, and they were also positive for a protein called PD-L1, which means the cancer can hide from the body’s immune system. He got chemotherapy with drugs like gemcitabine and cisplatin, and later switched to carboplatin because of side effects. He also took durvalumab to help fight the cancer. After 6 rounds of treatment, the cancer got worse and he died 9 months after first being diagnosed, due to breathing problems.\"\n}", "generated_text": "A 65-year-old man started feeling a persistent cough, shortness of breath, and lost 10 pounds in just 4 months. Tests showed a lump in his right lung and fluid around it. A small piece of tissue was taken and looked under a microscope — it showed strange cells that grew in sheets, surrounded by many immune cells. These cells were found to be from a rare cancer called pulmonary lymphoepithelioma-like carcinoma (CTLP). The cancer cells had signs of a virus called Epstein-Barr, and they were also positive for a protein called PD-L1, which means the cancer can hide from the body’s immune system. He got chemotherapy with drugs like gemcitabine and cisplatin, and later switched to carboplatin because of side effects. He also took durvalumab to help fight the cancer. After 6 rounds of treatment, the cancer got worse and he died 9 months after first being diagnosed, due to breathing problems."}
+{"row_index": 5, "doc_id": 24, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 13-year-old boy had a lump in his groin that could be felt and moved. He didn’t have fever, pain, or other symptoms. The doctors took out the lump to make sure it wasn’t something serious like cancer. After checking the tissue under a microscope, they found a rare condition called Castleman’s disease, specifically the plasma cell type, which is very rare in kids. This case is the first time this kind of disease has been found in the groin area. For 12 months after the surgery, the boy had no new lumps or symptoms, and all tests showed everything was normal. He’s doing fine and doesn’t need more treatment.\"\n}", "generated_text": "A 13-year-old boy had a lump in his groin that could be felt and moved. He didn’t have fever, pain, or other symptoms. The doctors took out the lump to make sure it wasn’t something serious like cancer. After checking the tissue under a microscope, they found a rare condition called Castleman’s disease, specifically the plasma cell type, which is very rare in kids. This case is the first time this kind of disease has been found in the groin area. For 12 months after the surgery, the boy had no new lumps or symptoms, and all tests showed everything was normal. He’s doing fine and doesn’t need more treatment."}
+{"row_index": 6, "doc_id": 25, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"The medical records of patients diagnosed with congenital myotonia were retrospectively reviewed in the pediatric neurology consultation at a third-level hospital between 2015 and 2020. Inclusion criteria comprised a clinical diagnosis of myotonia, presence of the warm-up phenomenon, characteristic electromyographic (EMG) findings, or a family history, as well as molecular confirmation via mutation analysis in the CLCN1 gene. Data collected included demographic variables (age and sex), disease course (age of onset, symptomatology, time to diagnosis, and clinical evolution), family history, and response to therapeutic interventions. Five patients with a clinical diagnosis of congenital myotonia were identified: three with Becker congenital myotonia and two with Thomsen congenital myotonia. The estimated incidence was 1:15,000 live births for the Becker phenotype and 1:21,000 live births for the Thomsen phenotype.\\n\\nThe cohort was predominantly female, with the sole male patient presenting before the age of six. Initial clinical manifestations included lower limb myotonia in four patients and upper limb myotonia in all but one. Age at onset ranged from 22 months to 12 years, with a median of 6 years. Genetic testing was performed in all patients approximately two years after symptom onset, except for one patient whose family declined testing. All patients exhibited worsening of myotonia with cold exposure; the warm-up phenomenon, a hallmark of the Becker phenotype, was observed only in patients with the Becker genotype.\\n\\nPatients with recessive congenital myotonia demonstrated a progressive clinical course. Family history analysis revealed that patients 2 and 3 were sisters, both clinically affected, with no clinical signs in their parents. The mother of patient 1 exhibited mild, cold-exacerbated myotonic symptoms, suggesting a possible carrier state. The patient who declined genetic evaluation had a positive family history of myotonia in the maternal lineage.\\n\\nSerum creatine kinase levels were not elevated in any of the patients, indicating that muscle damage is not a prominent feature of the disease. Electromyographic evaluation was abnormal in all patients except patient 1, who was evaluated at 2.8 years of age (out of 12 years of follow-up); subsequent EMG testing was not repeated due to clinical stability and institutional protocol. The primary pharmacological intervention was oxcarbazepine, particularly in patients with the recessive form, with generally favorable response. However, patient 2 experienced loss of efficacy over time and was subsequently treated with mexiletine. Patient 4 attempted multiple medications without sustained benefit due to either therapeutic failure or adverse effects. Patient 5 declined treatment due to a mild clinical presentation.\\n\\nPatient 1 was found to carry a previously unreported, likely pathogenic mutation in the CLCN1 gene (c.824T>C), inherited from the mother. Cases 1 to 3 exhibited the Becker phenotype and presented with composite heterozygosity—i.e., a combination of two different pathogenic variants in the CLCN1 gene—consistent with autosomal recessive inheritance. Cases 4 and 5 presented with the Thomsen phenotype, which is associated with a single pathogenic variant and typically manifests with more severe myotonia and earlier onset. Patient 5 declined genetic testing, limiting the ability to confirm the specific mutation in that individual.\\n\\nThe pathophysiological mechanism underlying congenital myotonia involves dysfunction of the voltage-gated chloride channel encoded by CLCN1, which leads to impaired repolarization of skeletal muscle fibers during depolarization. This results in prolonged muscle membrane depolarization, causing delayed relaxation and the clinical manifestation of myotonia. The specific mutation c.824T>C (p.Leu275Pro) is predicted to disrupt the channel's pore-forming domain, reducing chloride conductance and contributing to the observed myotonic phenotype. This mutation has not been previously described in the literature and may represent a novel pathogenic variant in the CLCN1 gene spectrum associated with congenital myotonia.\"\n}", "generated_text": "The medical records of patients diagnosed with congenital myotonia were retrospectively reviewed in the pediatric neurology consultation at a third-level hospital between 2015 and 2020. Inclusion criteria comprised a clinical diagnosis of myotonia, presence of the warm-up phenomenon, characteristic electromyographic (EMG) findings, or a family history, as well as molecular confirmation via mutation analysis in the CLCN1 gene. Data collected included demographic variables (age and sex), disease course (age of onset, symptomatology, time to diagnosis, and clinical evolution), family history, and response to therapeutic interventions. Five patients with a clinical diagnosis of congenital myotonia were identified: three with Becker congenital myotonia and two with Thomsen congenital myotonia. The estimated incidence was 1:15,000 live births for the Becker phenotype and 1:21,000 live births for the Thomsen phenotype.\n\nThe cohort was predominantly female, with the sole male patient presenting before the age of six. Initial clinical manifestations included lower limb myotonia in four patients and upper limb myotonia in all but one. Age at onset ranged from 22 months to 12 years, with a median of 6 years. Genetic testing was performed in all patients approximately two years after symptom onset, except for one patient whose family declined testing. All patients exhibited worsening of myotonia with cold exposure; the warm-up phenomenon, a hallmark of the Becker phenotype, was observed only in patients with the Becker genotype.\n\nPatients with recessive congenital myotonia demonstrated a progressive clinical course. Family history analysis revealed that patients 2 and 3 were sisters, both clinically affected, with no clinical signs in their parents. The mother of patient 1 exhibited mild, cold-exacerbated myotonic symptoms, suggesting a possible carrier state. The patient who declined genetic evaluation had a positive family history of myotonia in the maternal lineage.\n\nSerum creatine kinase levels were not elevated in any of the patients, indicating that muscle damage is not a prominent feature of the disease. Electromyographic evaluation was abnormal in all patients except patient 1, who was evaluated at 2.8 years of age (out of 12 years of follow-up); subsequent EMG testing was not repeated due to clinical stability and institutional protocol. The primary pharmacological intervention was oxcarbazepine, particularly in patients with the recessive form, with generally favorable response. However, patient 2 experienced loss of efficacy over time and was subsequently treated with mexiletine. Patient 4 attempted multiple medications without sustained benefit due to either therapeutic failure or adverse effects. Patient 5 declined treatment due to a mild clinical presentation.\n\nPatient 1 was found to carry a previously unreported, likely pathogenic mutation in the CLCN1 gene (c.824T>C), inherited from the mother. Cases 1 to 3 exhibited the Becker phenotype and presented with composite heterozygosity—i.e., a combination of two different pathogenic variants in the CLCN1 gene—consistent with autosomal recessive inheritance. Cases 4 and 5 presented with the Thomsen phenotype, which is associated with a single pathogenic variant and typically manifests with more severe myotonia and earlier onset. Patient 5 declined genetic testing, limiting the ability to confirm the specific mutation in that individual.\n\nThe pathophysiological mechanism underlying congenital myotonia involves dysfunction of the voltage-gated chloride channel encoded by CLCN1, which leads to impaired repolarization of skeletal muscle fibers during depolarization. This results in prolonged muscle membrane depolarization, causing delayed relaxation and the clinical manifestation of myotonia. The specific mutation c.824T>C (p.Leu275Pro) is predicted to disrupt the channel's pore-forming domain, reducing chloride conductance and contributing to the observed myotonic phenotype. This mutation has not been previously described in the literature and may represent a novel pathogenic variant in the CLCN1 gene spectrum associated with congenital myotonia."}
+{"row_index": 7, "doc_id": 26, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 67-year-old woman had swelling in her left leg for six years. She already had a problem in her leg's blood vessels called an AVM, which didn’t get better even after treatment. Recently, she started feeling tired and short of breath, which means her heart was struggling. Her doctor found her heart was enlarged and not working well, and her blood markers showed high pressure on the heart. She was diagnosed with a serious, long-time leg blood vessel problem and heart failure. The doctors tried to fix it by placing a stent in her leg to block the bad blood flow, which helped her heart feel better. After the surgery, her leg swelling went down and her heart started working better. A second step was done to stop the blood flow from the AVMs in the leg. After one year, her leg swelling was much less, and her heart was stronger. This shows the treatment worked.\"\n}", "generated_text": "A 67-year-old woman had swelling in her left leg for six years. She already had a problem in her leg's blood vessels called an AVM, which didn’t get better even after treatment. Recently, she started feeling tired and short of breath, which means her heart was struggling. Her doctor found her heart was enlarged and not working well, and her blood markers showed high pressure on the heart. She was diagnosed with a serious, long-time leg blood vessel problem and heart failure. The doctors tried to fix it by placing a stent in her leg to block the bad blood flow, which helped her heart feel better. After the surgery, her leg swelling went down and her heart started working better. A second step was done to stop the blood flow from the AVMs in the leg. After one year, her leg swelling was much less, and her heart was stronger. This shows the treatment worked."}
+{"row_index": 8, "doc_id": 26, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 67-year-old woman had been suffering from swelling in her left leg for six years. She was previously diagnosed with a complex congenital arteriovenous malformation (AVM) in her lower leg, but treatment with coils didn’t stop the swelling. Over time, she developed symptoms of heart failure, including fatigue and shortness of breath, which led her to seek care at a specialized hospital. Tests showed her heart was enlarged and had weakened function, with high levels of a heart failure marker (BNP), and her leg blood flow was very high—3400 ml/min—due to the AVM.\\n\\nThe doctors decided to treat the AVM using a combination of procedures. First, they placed a covered stent in her femoral artery to block the abnormal blood flow from the AVM. This helped reduce the blood flow to the leg from 3400 ml/min to 1600 ml/min, and her heart failure symptoms improved. The stent was placed in the area where the AVM was most active, and follow-up imaging showed much less blood flow and better leg circulation.\\n\\nA second procedure followed, where they used coils and other materials to block the main drainage veins of the AVM. This further reduced the abnormal blood flow and helped seal off the malformation. After one year, her leg swelling had greatly improved, her heart function had recovered, and her BNP levels dropped significantly. Her left ventricular ejection fraction improved from 60% to 71%, showing better heart pumping ability. This case shows that combining stent placement and embolization can be effective in treating complex congenital AVMs in the lower limb and improving heart failure in patients with such conditions.\"\n}", "generated_text": "A 67-year-old woman had been suffering from swelling in her left leg for six years. She was previously diagnosed with a complex congenital arteriovenous malformation (AVM) in her lower leg, but treatment with coils didn’t stop the swelling. Over time, she developed symptoms of heart failure, including fatigue and shortness of breath, which led her to seek care at a specialized hospital. Tests showed her heart was enlarged and had weakened function, with high levels of a heart failure marker (BNP), and her leg blood flow was very high—3400 ml/min—due to the AVM.\n\nThe doctors decided to treat the AVM using a combination of procedures. First, they placed a covered stent in her femoral artery to block the abnormal blood flow from the AVM. This helped reduce the blood flow to the leg from 3400 ml/min to 1600 ml/min, and her heart failure symptoms improved. The stent was placed in the area where the AVM was most active, and follow-up imaging showed much less blood flow and better leg circulation.\n\nA second procedure followed, where they used coils and other materials to block the main drainage veins of the AVM. This further reduced the abnormal blood flow and helped seal off the malformation. After one year, her leg swelling had greatly improved, her heart function had recovered, and her BNP levels dropped significantly. Her left ventricular ejection fraction improved from 60% to 71%, showing better heart pumping ability. This case shows that combining stent placement and embolization can be effective in treating complex congenital AVMs in the lower limb and improving heart failure in patients with such conditions."}
+{"row_index": 9, "doc_id": 26, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 67-year-old female presented with a six-year history of progressive left lower limb edema, initially diagnosed with a lower limb arteriovenous malformation (AVM) one year prior. Two months before admission, she underwent embolization using two coils (20 mm × 40 cm, BSX, USA) in the superficial femoral artery (SFA), yet no clinical improvement in swelling was observed. Over the preceding month, she developed progressive fatigue and dyspnea, indicative of acute decompensated heart failure, leading to transfer to Chengdu University of Traditional Chinese Medicine Hospital. She had no prior history of cardiovascular disease, trauma, or surgical interventions, though she reported seven years of oral estrogen therapy for menopausal symptoms.\\n\\nPhysical examination revealed marked edema and skin sclerosis in the left lower limb, absent pulses in the popliteal and distal arteries, and a tremor in the left thigh. Echocardiography demonstrated left ventricular enlargement, moderate mitral regurgitation, severe tricuspid regurgitation, a left ventricular ejection fraction (LVEF) of 60%, and elevated B-type natriuretic peptide (BNP) levels at 2853 ng/L. Electrocardiography showed sinus tachycardia (105 bpm) with left atrial enlargement. Chest CT confirmed cardiac enlargement without pulmonary abnormalities. Preoperative computed tomography angiography (CTA) revealed a left iliac artery aneurysm, significant dilation of the common femoral artery (CFA; 27 mm), superficial femoral artery (SFA; 22 mm), and complex congenital AVMs involving the SFA and profunda femoris artery. Arterial phase imaging showed marked enlargement of both femoral and superficial veins. The popliteal and anterior tibial arteries were nonvisualized, supporting diagnosis of complex congenital lower limb AVMs with associated venous congestion.\\n\\nThe patient was classified as New York Heart Association (NYHA) Class IV due to severe symptoms of acute heart failure. Preoperative CFA flow volume was 3400 ml/min. Given the persistence of high flow through the AVMs despite coil embolization, and the lack of effective flow reduction with conventional embolization, a covered stent graft was selected as a therapeutic strategy to occlude the high-flow AVM nidus and reduce venous congestion, thereby alleviating cardiac preload and improving hemodynamics. CTA measurements indicated maximum vessel diameters of 32 mm (iliac artery), 27 mm (CFA), and 22 mm (SFA), with the SFA mid-segment measuring 19 mm, leading to selection of a 20 mm × 12 mm/120 mm aorto-uni-iliac covered stent (MicroPort, China).\\n\\nUnder general anesthesia, antegrade access was achieved via the common femoral artery using a 14 F (Cook Medical, USA) catheter sheath. A 0.035 guidewire was initially used, subsequently replaced with a 0.035 super-hard guidewire for enhanced stability during stent deployment. The stent was implanted at the distal SFA, the region of highest AVM burden. Completion angiography demonstrated significant reduction in venous opacification around the stent and clear visualization of the popliteal artery, confirming successful stent placement and hemodynamic stabilization. Postoperatively, the left femoral artery was sutured using a 6-0 vascular risk suture.\\n\\nThe surgical procedure was performed with minimal duration to avoid exacerbation of heart failure, consistent with the patient’s unstable cardiac status. A staged embolization was planned for the second phase to target the AVM nidus and draining venous pathways. One week post-intervention, CFA flow reduced to 1600 ml/min, and BNP levels decreased to 1198 ng/L, indicating early clinical improvement. Right CFA access was used to perform angiographic guidance, with puncture of the AVM drainage vein and introduction of a 5 F vascular sheath. Embolization was performed using a 18–20 mm × 40 cm coil (BSX, USA), two microcoils (4 mm × 42 mm and 5 mm × 10 mm, USA), 3% polidocanol (6 mL, Kruelle, Germany), and 99% anhydrous ethanol (10 mL) to achieve occlusion of the nidus and draining veins.\\n\\nCompletion angiography showed near-complete disappearance of AVM and draining vein visualization. At one-year follow-up, the CFA flow volume decreased to 780 ml/min, echocardiography revealed mild atrial enlargement,", "generated_text": "{\n  \"proficient_health_literacy\": \"A 67-year-old female presented with a six-year history of progressive left lower limb edema, initially diagnosed with a lower limb arteriovenous malformation (AVM) one year prior. Two months before admission, she underwent embolization using two coils (20 mm × 40 cm, BSX, USA) in the superficial femoral artery (SFA), yet no clinical improvement in swelling was observed. Over the preceding month, she developed progressive fatigue and dyspnea, indicative of acute decompensated heart failure, leading to transfer to Chengdu University of Traditional Chinese Medicine Hospital. She had no prior history of cardiovascular disease, trauma, or surgical interventions, though she reported seven years of oral estrogen therapy for menopausal symptoms.\\n\\nPhysical examination revealed marked edema and skin sclerosis in the left lower limb, absent pulses in the popliteal and distal arteries, and a tremor in the left thigh. Echocardiography demonstrated left ventricular enlargement, moderate mitral regurgitation, severe tricuspid regurgitation, a left ventricular ejection fraction (LVEF) of 60%, and elevated B-type natriuretic peptide (BNP) levels at 2853 ng/L. Electrocardiography showed sinus tachycardia (105 bpm) with left atrial enlargement. Chest CT confirmed cardiac enlargement without pulmonary abnormalities. Preoperative computed tomography angiography (CTA) revealed a left iliac artery aneurysm, significant dilation of the common femoral artery (CFA; 27 mm), superficial femoral artery (SFA; 22 mm), and complex congenital AVMs involving the SFA and profunda femoris artery. Arterial phase imaging showed marked enlargement of both femoral and superficial veins. The popliteal and anterior tibial arteries were nonvisualized, supporting diagnosis of complex congenital lower limb AVMs with associated venous congestion.\\n\\nThe patient was classified as New York Heart Association (NYHA) Class IV due to severe symptoms of acute heart failure. Preoperative CFA flow volume was 3400 ml/min. Given the persistence of high flow through the AVMs despite coil embolization, and the lack of effective flow reduction with conventional embolization, a covered stent graft was selected as a therapeutic strategy to occlude the high-flow AVM nidus and reduce venous congestion, thereby alleviating cardiac preload and improving hemodynamics. CTA measurements indicated maximum vessel diameters of 32 mm (iliac artery), 27 mm (CFA), and 22 mm (SFA), with the SFA mid-segment measuring 19 mm, leading to selection of a 20 mm × 12 mm/120 mm aorto-uni-iliac covered stent (MicroPort, China).\\n\\nUnder general anesthesia, antegrade access was achieved via the common femoral artery using a 14 F (Cook Medical, USA) catheter sheath. A 0.035 guidewire was initially used, subsequently replaced with a 0.035 super-hard guidewire for enhanced stability during stent deployment. The stent was implanted at the distal SFA, the region of highest AVM burden. Completion angiography demonstrated significant reduction in venous opacification around the stent and clear visualization of the popliteal artery, confirming successful stent placement and hemodynamic stabilization. Postoperatively, the left femoral artery was sutured using a 6-0 vascular risk suture.\\n\\nThe surgical procedure was performed with minimal duration to avoid exacerbation of heart failure, consistent with the patient’s unstable cardiac status. A staged embolization was planned for the second phase to target the AVM nidus and draining venous pathways. One week post-intervention, CFA flow reduced to 1600 ml/min, and BNP levels decreased to 1198 ng/L, indicating early clinical improvement. Right CFA access was used to perform angiographic guidance, with puncture of the AVM drainage vein and introduction of a 5 F vascular sheath. Embolization was performed using a 18–20 mm × 40 cm coil (BSX, USA), two microcoils (4 mm × 42 mm and 5 mm × 10 mm, USA), 3% polidocanol (6 mL, Kruelle, Germany), and 99% anhydrous ethanol (10 mL) to achieve occlusion of the nidus and draining veins.\\n\\nCompletion angiography showed near-complete disappearance of AVM and draining vein visualization. At one-year follow-up, the CFA flow volume decreased to 780 ml/min, echocardiography revealed mild atrial enlargement,"}
+{"row_index": 10, "doc_id": 27, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 28-year-old man got two red, bump-like spots on his right arm and forearm that had small blisters and sores in the middle. They were sore and itched, but he didn’t feel sick inside. He was vacationing in a coastal area of Ecuador when this happened. The doctor took a small skin sample and saw signs that matched a skin problem from bugs in that area. The doctor called it Paederus dermatitis. He treated it with anti-itch medicine, cream to calm the skin, and cold compresses. After 8 days, the bumps went away, but the skin stayed a little darker in those spots.\"\n}", "generated_text": "A 28-year-old man got two red, bump-like spots on his right arm and forearm that had small blisters and sores in the middle. They were sore and itched, but he didn’t feel sick inside. He was vacationing in a coastal area of Ecuador when this happened. The doctor took a small skin sample and saw signs that matched a skin problem from bugs in that area. The doctor called it Paederus dermatitis. He treated it with anti-itch medicine, cream to calm the skin, and cold compresses. After 8 days, the bumps went away, but the skin stayed a little darker in those spots."}
+{"row_index": 11, "doc_id": 27, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 28-year-old male with no significant medical history presented to the dermatology department with a 48-hour history of two erythematous plaques exhibiting central vesicular lesions and superficial ulceration, located on the flexor surfaces of the right arm and forearm, symmetrically positioned equidistant from the elbow crease. The lesions were associated with localized burning sensation and pruritus, without systemic symptoms or evidence of self-medication. The patient reported a recent vacation in the coastal region of Ecuador, which served as a key epidemiological context. An incisional biopsy was performed and revealed histopathological features consistent with Paederus dermatitis, including epidermal acanthosis, parakeratosis, and intercellular spongiosis, with neutrophilic infiltrates in the stratum corneum and perivascular lymphocytic infiltration extending into the superficial, middle, and deep dermis. These findings are characteristic of a delayed-type hypersensitivity reaction to Paederus beetle-derived cuticular proteins, specifically the Paederus toxin (Paederus toxin, a member of the cysteine-rich protein family), which induces a type IV hypersensitivity response mediated by CD4+ T cells and subsequent release of pro-inflammatory cytokines such as IL-4, IL-5, and IL-13. The clinical presentation, geographic exposure, and histopathological profile collectively support the diagnosis of Paederus dermatitis. Management consisted of antihistamines to mitigate pruritus, topical corticosteroids to suppress local inflammation, and cold compresses to reduce vascular permeability and symptom severity. The lesions completely resolved after 8 days of treatment, with residual post-inflammatory hyperpigmentation observed as a result of melanocyte activation and prolonged dermal inflammation. This case underscores the importance of considering environmental exposures in tropical regions, particularly in endemic areas where Paederus beetles (family Paederidae) are prevalent, as a potential etiology of acute, non-infectious, pruritic dermatoses with a distinct histopathological signature.\"\n}", "generated_text": "A 28-year-old male with no significant medical history presented to the dermatology department with a 48-hour history of two erythematous plaques exhibiting central vesicular lesions and superficial ulceration, located on the flexor surfaces of the right arm and forearm, symmetrically positioned equidistant from the elbow crease. The lesions were associated with localized burning sensation and pruritus, without systemic symptoms or evidence of self-medication. The patient reported a recent vacation in the coastal region of Ecuador, which served as a key epidemiological context. An incisional biopsy was performed and revealed histopathological features consistent with Paederus dermatitis, including epidermal acanthosis, parakeratosis, and intercellular spongiosis, with neutrophilic infiltrates in the stratum corneum and perivascular lymphocytic infiltration extending into the superficial, middle, and deep dermis. These findings are characteristic of a delayed-type hypersensitivity reaction to Paederus beetle-derived cuticular proteins, specifically the Paederus toxin (Paederus toxin, a member of the cysteine-rich protein family), which induces a type IV hypersensitivity response mediated by CD4+ T cells and subsequent release of pro-inflammatory cytokines such as IL-4, IL-5, and IL-13. The clinical presentation, geographic exposure, and histopathological profile collectively support the diagnosis of Paederus dermatitis. Management consisted of antihistamines to mitigate pruritus, topical corticosteroids to suppress local inflammation, and cold compresses to reduce vascular permeability and symptom severity. The lesions completely resolved after 8 days of treatment, with residual post-inflammatory hyperpigmentation observed as a result of melanocyte activation and prolonged dermal inflammation. This case underscores the importance of considering environmental exposures in tropical regions, particularly in endemic areas where Paederus beetles (family Paederidae) are prevalent, as a potential etiology of acute, non-infectious, pruritic dermatoses with a distinct histopathological signature."}
+{"row_index": 12, "doc_id": 28, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A man in his 80s had a blocked bile duct causing yellowing of his skin and weight loss. Doctors found a tumor in his bile duct that couldn’t be removed. Instead, they used a light-based treatment called PDT to ease the blockage. Before the treatment, he got a special medicine through a vein, and the doctors used a scope to look inside his bile duct. They placed a small light tube into the duct and shone light on the blocked area to help open it. The light was turned on slowly, every centimeter, to make sure the whole blockage was treated. Afterward, they checked the duct again to make sure everything was okay. The treatment worked for three months, but the blockage came back. He had other treatments, but eventually died from lung cancer that spread from the tumor, 15 months after the light treatment. The most important thing is that the light treatment helped him feel better for a while, even though it didn’t cure the disease.\"\n}", "generated_text": "A man in his 80s had a blocked bile duct causing yellowing of his skin and weight loss. Doctors found a tumor in his bile duct that couldn’t be removed. Instead, they used a light-based treatment called PDT to ease the blockage. Before the treatment, he got a special medicine through a vein, and the doctors used a scope to look inside his bile duct. They placed a small light tube into the duct and shone light on the blocked area to help open it. The light was turned on slowly, every centimeter, to make sure the whole blockage was treated. Afterward, they checked the duct again to make sure everything was okay. The treatment worked for three months, but the blockage came back. He had other treatments, but eventually died from lung cancer that spread from the tumor, 15 months after the light treatment. The most important thing is that the light treatment helped him feel better for a while, even though it didn’t cure the disease."}
+{"row_index": 13, "doc_id": 28, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"The patient, an 82-year-old male with a two-month history of obstructive jaundice and weight loss, underwent transduodenal photodynamic therapy (TFD) as a palliative intervention for recurrent biliary obstruction. Endoscopic ultrasound (EUS) demonstrated severe dilation of the common bile duct with confirmed choledocholithiasis, and endoscopic retrograde cholangiopancreatography (ERCP) revealed inability to remove stones due to disproportionate ductal dilation, necessitating placement of a plastic biliary stent. Clinical improvement was transient, with cholestasis returning 45 days post-ERCP. Subsequent ERCP attempts failed to clear the stones. On repeat EUS, a well-circumscribed hypoechoic solid mass measuring 1.8 × 2 cm was identified in the dilated common hepatic duct, compressing the duct lumen, and extending into the common hepatic artery. Ultrasound-guided needle biopsy confirmed a diagnosis of moderately differentiated cholangiocarcinoma (Bismuth I). Staging determined the tumor to be inoperable, leading to referral for palliative therapy. Multidisciplinary consensus supported adjunctive photodynamic therapy (PDT) to manage the obstructive lesion. The PDT procedure was performed under general anesthesia using intravenous administration of Photogen® (1.5 mg/kg) administered 24 hours prior to the session. The photosensitizer has a peak light absorption at 630 nm, enabling targeted activation within biliary tissue. Standard duodenoscopy (Olympus TJF-180) was performed to identify the greater duodenal papilla and achieve retrograde cannulation. A digital cholangioscope (SpyGlass™ DS, Boston Scientific) was then advanced into the common bile duct for direct visualization, allowing precise identification of the neoplastic stenosis. Under real-time cholangioscopic guidance, an illumination catheter (Medlight S.A., RD10-323) was advanced through the cholangioscope. The catheter is a three-way device: the first port features a 1 cm cylindrical light diffuser with two black radiopaque marks defining its distal limits; the second port accommodates a 0.025-inch guidewire for catheter stabilization; the third port serves as the injection site for the photosensitizer. The illumination was delivered at a power of 70 mW/cm² and a total dose of 90 J/cm², with repositioning performed every centimeter to ensure complete coverage of the stenotic segment. Post-procedure, the bile duct was re-evaluated via cholangioscopy to assess immediate outcomes and detect any adverse events. The patient was maintained on a fasted state for 24 hours post-procedure, with oral diet initiated if no adverse events were observed. Discharge was accompanied by strict photoprotection protocols, including avoidance of light exposure and use of sunglasses, particularly during the first week following PDT. The procedure lasted 150 minutes and concluded with placement of a 10 Fr plastic biliary stent for drainage, as a self-expanding metal stent was unavailable at the time. The patient remained asymptomatic for three months, the longest period since disease onset. However, early recurrence of cholestasis with cholangitis occurred, which was attributed to stent obstruction by tumor debris and biliary sludge secondary to tumor necrosis. A biliary scan followed by re-drainage resolved the acute episode. Subsequently, a self-expanding metal stent was placed to maintain patency. The patient continued on systemic oncologic therapy and eventually required a duodenal stent for palliation of dysphagia. He ultimately died from complications of pulmonary metastases, two years after symptom onset and 15 months after the TFD session. The procedure was technically successful with no immediate adverse events, and the PDT provided symptomatic relief and disease stabilization for an extended period, although the underlying malignancy progressed to metastatic disease.\"\n}", "generated_text": "The patient, an 82-year-old male with a two-month history of obstructive jaundice and weight loss, underwent transduodenal photodynamic therapy (TFD) as a palliative intervention for recurrent biliary obstruction. Endoscopic ultrasound (EUS) demonstrated severe dilation of the common bile duct with confirmed choledocholithiasis, and endoscopic retrograde cholangiopancreatography (ERCP) revealed inability to remove stones due to disproportionate ductal dilation, necessitating placement of a plastic biliary stent. Clinical improvement was transient, with cholestasis returning 45 days post-ERCP. Subsequent ERCP attempts failed to clear the stones. On repeat EUS, a well-circumscribed hypoechoic solid mass measuring 1.8 × 2 cm was identified in the dilated common hepatic duct, compressing the duct lumen, and extending into the common hepatic artery. Ultrasound-guided needle biopsy confirmed a diagnosis of moderately differentiated cholangiocarcinoma (Bismuth I). Staging determined the tumor to be inoperable, leading to referral for palliative therapy. Multidisciplinary consensus supported adjunctive photodynamic therapy (PDT) to manage the obstructive lesion. The PDT procedure was performed under general anesthesia using intravenous administration of Photogen® (1.5 mg/kg) administered 24 hours prior to the session. The photosensitizer has a peak light absorption at 630 nm, enabling targeted activation within biliary tissue. Standard duodenoscopy (Olympus TJF-180) was performed to identify the greater duodenal papilla and achieve retrograde cannulation. A digital cholangioscope (SpyGlass™ DS, Boston Scientific) was then advanced into the common bile duct for direct visualization, allowing precise identification of the neoplastic stenosis. Under real-time cholangioscopic guidance, an illumination catheter (Medlight S.A., RD10-323) was advanced through the cholangioscope. The catheter is a three-way device: the first port features a 1 cm cylindrical light diffuser with two black radiopaque marks defining its distal limits; the second port accommodates a 0.025-inch guidewire for catheter stabilization; the third port serves as the injection site for the photosensitizer. The illumination was delivered at a power of 70 mW/cm² and a total dose of 90 J/cm², with repositioning performed every centimeter to ensure complete coverage of the stenotic segment. Post-procedure, the bile duct was re-evaluated via cholangioscopy to assess immediate outcomes and detect any adverse events. The patient was maintained on a fasted state for 24 hours post-procedure, with oral diet initiated if no adverse events were observed. Discharge was accompanied by strict photoprotection protocols, including avoidance of light exposure and use of sunglasses, particularly during the first week following PDT. The procedure lasted 150 minutes and concluded with placement of a 10 Fr plastic biliary stent for drainage, as a self-expanding metal stent was unavailable at the time. The patient remained asymptomatic for three months, the longest period since disease onset. However, early recurrence of cholestasis with cholangitis occurred, which was attributed to stent obstruction by tumor debris and biliary sludge secondary to tumor necrosis. A biliary scan followed by re-drainage resolved the acute episode. Subsequently, a self-expanding metal stent was placed to maintain patency. The patient continued on systemic oncologic therapy and eventually required a duodenal stent for palliation of dysphagia. He ultimately died from complications of pulmonary metastases, two years after symptom onset and 15 months after the TFD session. The procedure was technically successful with no immediate adverse events, and the PDT provided symptomatic relief and disease stabilization for an extended period, although the underlying malignancy progressed to metastatic disease."}
+{"row_index": 14, "doc_id": 29, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 77-year-old woman with a history of hypertension and dyslipidaemia presented to the emergency department with haematemesis and signs of shock (heart rate: 100 beats/min, blood pressure: 79/56 mmHg), accompanied by anaemia (haemoglobin: 9.6 g/dL), consistent with upper gastrointestinal bleeding. Non-contrast-enhanced CT was performed due to renal dysfunction and revealed a steep flexure of the third part of the duodenum on the right side of the aorta, with a caudal course that did not cross anterior to the aorta. The duodenal-jejunal junction and jejunum were located in the right hemi-abdomen, with dilation of the second part of the duodenum and the stomach, and high-density gastric contents suggestive of a gastric haematoma. Upper gastrointestinal endoscopy demonstrated a mucosal laceration at the gastric cardia, consistent with Mallory-Weiss syndrome, a well-documented condition first described by Mallory and Weiss in 1929, where forceful vomiting leads to mucosal tears at the gastroesophageal junction. The anatomical configuration of the duodenum—specifically, its steep rightward flexure and luminal narrowing—contributed to proximal obstruction, which likely exacerbated repeated vomiting and thus the development of the laceration.\\n\\nInitial CT findings prompted suspicion of intestinal malrotation, given the right-sided displacement of the duodenal-jejunal junction and jejunum. However, repeat CT seven days later showed spontaneous resolution of this rightward deviation, with the jejunum returning to a central or left-sided position. This transient, self-resolving malposition is inconsistent with true malrotation, which typically presents as a congenital anomaly with persistent anatomical abnormality and risk of volvulus. The patient was discharged after stabilization.\\n\\nTwo months later, she presented with a recurrent episode of haematemesis. Dynamic CT performed prior to endoscopy revealed contrast extravasation in the dilated stomach, and again, the third part of the duodenum was found flexed on the right side of the aorta, with the duodenal-jejunal junction and jejunum displaced to the right hemi-abdomen. Endoscopy confirmed a recurrent laceration at the gastric cardia, reinforcing the diagnosis of Mallory-Weiss syndrome. Subsequent non-contrast CT, performed two months after the second haematemesis, showed no persistent duodenal deviation, but revealed oedematous wall thickening in the second part of the duodenum. Without prior imaging, this might have been interpreted as duodenitis; however, the history of repeated, spontaneous rightward deviations of the small intestine provided a critical clue to an underlying anatomical variant.\\n\\nGiven the pattern of transient, reversible right-sided displacement of the duodenum and jejunum—without evidence of malrotation or volvulus—dysplasia of the ligament of Treitz was diagnosed. The ligament of Treitz, which normally anchors the duodenum to the jejunum in the retroperitoneum, is typically formed and fixed during embryogenesis. In this case, CT imaging and surgical exploration revealed a formed ligament of Treitz, but with incomplete fixation to the upper jejunum—specifically, it was attached only to the duodenum and not securely anchored to the retroperitoneum. The duodenal-jejunal junction was not fixed to the retroperitoneal space, resulting in mechanical instability and allowing the jejunum to fold freely around the ligament as a fulcrum, thereby producing transient rightward displacement during gastrointestinal motility or increased intraluminal pressure.\\n\\nLaparotomy confirmed the absence of intestinal malrotation and normal relative positioning between the duodenum and jejunum. The jejunum was anatomically located on the left side of the abdomen. The incomplete fixation of the ligament of Treitz was the primary pathophysiological mechanism underlying the recurrent, spontaneous rightward deviations observed on imaging. Surgical correction involved fixation of the upper jejunum with four sutures to the retroperitoneum on the left side, which stabilized the anatomical configuration. The postoperative course was uncomplicated, and the patient has remained asymptomatic since. This case illustrates that transient, reversible small intestinal deviations in the absence of malrotation may represent a functional variant due to dysplasia of the ligament of Treitz, with implications for both imaging interpretation and surgical management in patients with recurrent upper gastrointestinal bleeding.\"\n}", "generated_text": "A 77-year-old woman with a history of hypertension and dyslipidaemia presented to the emergency department with haematemesis and signs of shock (heart rate: 100 beats/min, blood pressure: 79/56 mmHg), accompanied by anaemia (haemoglobin: 9.6 g/dL), consistent with upper gastrointestinal bleeding. Non-contrast-enhanced CT was performed due to renal dysfunction and revealed a steep flexure of the third part of the duodenum on the right side of the aorta, with a caudal course that did not cross anterior to the aorta. The duodenal-jejunal junction and jejunum were located in the right hemi-abdomen, with dilation of the second part of the duodenum and the stomach, and high-density gastric contents suggestive of a gastric haematoma. Upper gastrointestinal endoscopy demonstrated a mucosal laceration at the gastric cardia, consistent with Mallory-Weiss syndrome, a well-documented condition first described by Mallory and Weiss in 1929, where forceful vomiting leads to mucosal tears at the gastroesophageal junction. The anatomical configuration of the duodenum—specifically, its steep rightward flexure and luminal narrowing—contributed to proximal obstruction, which likely exacerbated repeated vomiting and thus the development of the laceration.\n\nInitial CT findings prompted suspicion of intestinal malrotation, given the right-sided displacement of the duodenal-jejunal junction and jejunum. However, repeat CT seven days later showed spontaneous resolution of this rightward deviation, with the jejunum returning to a central or left-sided position. This transient, self-resolving malposition is inconsistent with true malrotation, which typically presents as a congenital anomaly with persistent anatomical abnormality and risk of volvulus. The patient was discharged after stabilization.\n\nTwo months later, she presented with a recurrent episode of haematemesis. Dynamic CT performed prior to endoscopy revealed contrast extravasation in the dilated stomach, and again, the third part of the duodenum was found flexed on the right side of the aorta, with the duodenal-jejunal junction and jejunum displaced to the right hemi-abdomen. Endoscopy confirmed a recurrent laceration at the gastric cardia, reinforcing the diagnosis of Mallory-Weiss syndrome. Subsequent non-contrast CT, performed two months after the second haematemesis, showed no persistent duodenal deviation, but revealed oedematous wall thickening in the second part of the duodenum. Without prior imaging, this might have been interpreted as duodenitis; however, the history of repeated, spontaneous rightward deviations of the small intestine provided a critical clue to an underlying anatomical variant.\n\nGiven the pattern of transient, reversible right-sided displacement of the duodenum and jejunum—without evidence of malrotation or volvulus—dysplasia of the ligament of Treitz was diagnosed. The ligament of Treitz, which normally anchors the duodenum to the jejunum in the retroperitoneum, is typically formed and fixed during embryogenesis. In this case, CT imaging and surgical exploration revealed a formed ligament of Treitz, but with incomplete fixation to the upper jejunum—specifically, it was attached only to the duodenum and not securely anchored to the retroperitoneum. The duodenal-jejunal junction was not fixed to the retroperitoneal space, resulting in mechanical instability and allowing the jejunum to fold freely around the ligament as a fulcrum, thereby producing transient rightward displacement during gastrointestinal motility or increased intraluminal pressure.\n\nLaparotomy confirmed the absence of intestinal malrotation and normal relative positioning between the duodenum and jejunum. The jejunum was anatomically located on the left side of the abdomen. The incomplete fixation of the ligament of Treitz was the primary pathophysiological mechanism underlying the recurrent, spontaneous rightward deviations observed on imaging. Surgical correction involved fixation of the upper jejunum with four sutures to the retroperitoneum on the left side, which stabilized the anatomical configuration. The postoperative course was uncomplicated, and the patient has remained asymptomatic since. This case illustrates that transient, reversible small intestinal deviations in the absence of malrotation may represent a functional variant due to dysplasia of the ligament of Treitz, with implications for both imaging interpretation and surgical management in patients with recurrent upper gastrointestinal bleeding."}
+{"row_index": 15, "doc_id": 30, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 28-year-old man from Morocco had pain in his belly, especially on the right side, for about a month. He also had fever, chills, sweating, loss of appetite, and lost 6 pounds. His doctor found a swollen liver with small spots on it that looked strange. These spots were not cancer or infection from other causes. Tests showed signs of a slow, hidden infection — like tuberculosis — in the liver. A small surgery was done to take a piece of the liver tissue, and the lab confirmed it was tuberculosis. After starting medicine to fight the tuberculosis, his symptoms got better fast. The pain went away, the fever stopped, and the spots on his liver got smaller over time. This treatment works well for this kind of liver problem.\"\n}", "generated_text": "A 28-year-old man from Morocco had pain in his belly, especially on the right side, for about a month. He also had fever, chills, sweating, loss of appetite, and lost 6 pounds. His doctor found a swollen liver with small spots on it that looked strange. These spots were not cancer or infection from other causes. Tests showed signs of a slow, hidden infection — like tuberculosis — in the liver. A small surgery was done to take a piece of the liver tissue, and the lab confirmed it was tuberculosis. After starting medicine to fight the tuberculosis, his symptoms got better fast. The pain went away, the fever stopped, and the spots on his liver got smaller over time. This treatment works well for this kind of liver problem."}
+{"row_index": 16, "doc_id": 30, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 28-year-old Moroccan man with no smoking or drinking habits presented with a month-long history of abdominal pain, especially in the upper right part of his belly, along with fever, chills, night sweats, loss of appetite, and a 6-kilogram weight loss. He had no known family history of illness and was vaccinated for tuberculosis (BCG). Initially, his symptoms were mild, but they worsened over time, leading to significant weight loss of 12 kilograms over three months. Tests showed signs of infection, including high white blood cells and inflammation markers, but no evidence of common infections like hepatitis or bacterial infections. Imaging scans revealed multiple nodules in his liver that were not clearly explained. These nodules appeared on both ultrasound and MRI, and they were not enhancing after contrast was given. Liver function tests were normal, and blood tests for viruses and tuberculosis (using GeneXpert and quantiferon) were negative at first. A liver biopsy during laparoscopy showed characteristic tissue changes — epithelioid and giant cells with caseous necrosis — which are typical of tuberculosis. This confirmed a diagnosis of focal liver tuberculosis. The patient was started on standard anti-tuberculosis medication: a four-drug combination for the first two months, followed by a two-drug regimen for four months. Within days of starting treatment, his symptoms improved significantly. By the third month, follow-up scans showed that the liver nodules had shrunk in number and size, and his overall condition had stabilized.\"\n}", "generated_text": "A 28-year-old Moroccan man with no smoking or drinking habits presented with a month-long history of abdominal pain, especially in the upper right part of his belly, along with fever, chills, night sweats, loss of appetite, and a 6-kilogram weight loss. He had no known family history of illness and was vaccinated for tuberculosis (BCG). Initially, his symptoms were mild, but they worsened over time, leading to significant weight loss of 12 kilograms over three months. Tests showed signs of infection, including high white blood cells and inflammation markers, but no evidence of common infections like hepatitis or bacterial infections. Imaging scans revealed multiple nodules in his liver that were not clearly explained. These nodules appeared on both ultrasound and MRI, and they were not enhancing after contrast was given. Liver function tests were normal, and blood tests for viruses and tuberculosis (using GeneXpert and quantiferon) were negative at first. A liver biopsy during laparoscopy showed characteristic tissue changes — epithelioid and giant cells with caseous necrosis — which are typical of tuberculosis. This confirmed a diagnosis of focal liver tuberculosis. The patient was started on standard anti-tuberculosis medication: a four-drug combination for the first two months, followed by a two-drug regimen for four months. Within days of starting treatment, his symptoms improved significantly. By the third month, follow-up scans showed that the liver nodules had shrunk in number and size, and his overall condition had stabilized."}
+{"row_index": 17, "doc_id": 30, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 28-year-old male military personnel presented with a 5-week history of progressive epigastric and right upper quadrant abdominal pain, accompanied by intermittent fever (peaking at 39.1°C), chills, profuse night sweats, anorexia, and a 6 kg weight loss over one month. He had no history of alcohol use, smoking, or significant comorbidities; he was BCG-vaccinated and had no familial or personal history of infectious or hepatic disease. Physical examination revealed an asthenic appearance, tachycardia (124 beats/min), tachypnea (22 breaths/min), and moderate right upper quadrant tenderness with hepatomegaly (liver size 17 cm). No pulmonary or lymphadenopathic findings were detected on physical exam.\\n\\nThe clinical picture evolved from an initial presentation of diffuse abdominal pain with alternating diarrhea and constipation, persisting over several weeks, initially with only low-grade nocturnal fever and preserved general condition. This was followed by progressive deterioration, including a 12 kg weight loss over three months, prompting emergency admission for further evaluation.\\n\\nLaboratory findings demonstrated a neutrophilic leukocytosis (17,800 cells/mm³), elevated C-reactive protein (323 mg/L), and a positive procalcitonin level (4.1 ng/L), consistent with a systemic inflammatory response syndrome. Initial biomarkers of liver injury were within normal limits: ALT (22 IU/L), AST (17 IU/L), GGT (42 IU/L), ALP (115 IU/L), bilirubin, prothrombin time (78%), and albumin (39 g/L). Renal function and electrolyte balance were normal. Serological testing for hepatitis B, C, HIV, and syphilis was negative. Lactate dehydrogenase (231 IU/L) and beta-2 microglobulin (2.28 mg/L) were within normal ranges. Blood cultures and urine cytobacteriological analysis during febrile peaks were negative. GeneXpert assay for Mycobacterium tuberculosis in respiratory specimens and in liver biopsy material was negative; quantiferon tuberculin test was negative, indicating no evidence of latent or active TB in the immunological screening.\\n\\nImaging studies revealed multiple, well-defined, rounded hypodense lesions in the liver on thoraco-abdomino-pelvic CT, with no enhancement after contrast administration. The largest lesions were located in segment I (21 × 16 mm) and segment V (36 × 27 mm). Abdominal ultrasound showed no focal abnormalities. Liver MRI demonstrated dysmorphic liver architecture with heterogeneous T2 signal intensity, with peripheral hyperintense walls surrounding the lesions, showing peripheral contrast enhancement. The largest lesions were in segment I (20 × 22 mm) and segment V (33 × 31 mm), consistent with a pattern suggestive of granulomatous inflammation. No deep lymphadenopathy was observed in thoracic or pelvic regions.\\n\\nEchographic-guided liver biopsies initially revealed subacute, fibro-inflammatory changes without evidence of malignancy or specific infectious etiology. Diagnostic laparoscopy was performed to obtain histological specimens from hepatic nodules. Histopathological examination revealed epithelioid and gigantocellular granulomas with central caseous necrosis, a classic histological hallmark of tuberculosis, supporting a diagnosis of focal hepatic tuberculosis.\\n\\nThe patient was initiated on standard anti-tuberculous therapy: Phase 1 (2 months) of quadritherapy—isoniazid, rifampicin, pyrazinamide, and ethambutol—administered as single oral doses in the morning on an empty stomach. Phase 2 (4 months) involved continuation with bitherapy (isoniazid and rifampicin) under the same dosing regimen. Clinical and biological monitoring demonstrated a rapid and favorable response to treatment, with resolution of systemic inflammatory markers and improvement in symptoms within days. After three months of therapy, follow-up imaging showed a significant reduction in the number and volume of hepatic lesions, indicating therapeutic efficacy. The clinical course reflects a rare presentation of extrapulmonary tuberculosis involving the liver, with a delayed recognition due to non-specific symptoms and negative initial microbiological screening, ultimately confirmed by histopathological analysis of hepatic nodules.\"\n}", "generated_text": "A 28-year-old male military personnel presented with a 5-week history of progressive epigastric and right upper quadrant abdominal pain, accompanied by intermittent fever (peaking at 39.1°C), chills, profuse night sweats, anorexia, and a 6 kg weight loss over one month. He had no history of alcohol use, smoking, or significant comorbidities; he was BCG-vaccinated and had no familial or personal history of infectious or hepatic disease. Physical examination revealed an asthenic appearance, tachycardia (124 beats/min), tachypnea (22 breaths/min), and moderate right upper quadrant tenderness with hepatomegaly (liver size 17 cm). No pulmonary or lymphadenopathic findings were detected on physical exam.\n\nThe clinical picture evolved from an initial presentation of diffuse abdominal pain with alternating diarrhea and constipation, persisting over several weeks, initially with only low-grade nocturnal fever and preserved general condition. This was followed by progressive deterioration, including a 12 kg weight loss over three months, prompting emergency admission for further evaluation.\n\nLaboratory findings demonstrated a neutrophilic leukocytosis (17,800 cells/mm³), elevated C-reactive protein (323 mg/L), and a positive procalcitonin level (4.1 ng/L), consistent with a systemic inflammatory response syndrome. Initial biomarkers of liver injury were within normal limits: ALT (22 IU/L), AST (17 IU/L), GGT (42 IU/L), ALP (115 IU/L), bilirubin, prothrombin time (78%), and albumin (39 g/L). Renal function and electrolyte balance were normal. Serological testing for hepatitis B, C, HIV, and syphilis was negative. Lactate dehydrogenase (231 IU/L) and beta-2 microglobulin (2.28 mg/L) were within normal ranges. Blood cultures and urine cytobacteriological analysis during febrile peaks were negative. GeneXpert assay for Mycobacterium tuberculosis in respiratory specimens and in liver biopsy material was negative; quantiferon tuberculin test was negative, indicating no evidence of latent or active TB in the immunological screening.\n\nImaging studies revealed multiple, well-defined, rounded hypodense lesions in the liver on thoraco-abdomino-pelvic CT, with no enhancement after contrast administration. The largest lesions were located in segment I (21 × 16 mm) and segment V (36 × 27 mm). Abdominal ultrasound showed no focal abnormalities. Liver MRI demonstrated dysmorphic liver architecture with heterogeneous T2 signal intensity, with peripheral hyperintense walls surrounding the lesions, showing peripheral contrast enhancement. The largest lesions were in segment I (20 × 22 mm) and segment V (33 × 31 mm), consistent with a pattern suggestive of granulomatous inflammation. No deep lymphadenopathy was observed in thoracic or pelvic regions.\n\nEchographic-guided liver biopsies initially revealed subacute, fibro-inflammatory changes without evidence of malignancy or specific infectious etiology. Diagnostic laparoscopy was performed to obtain histological specimens from hepatic nodules. Histopathological examination revealed epithelioid and gigantocellular granulomas with central caseous necrosis, a classic histological hallmark of tuberculosis, supporting a diagnosis of focal hepatic tuberculosis.\n\nThe patient was initiated on standard anti-tuberculous therapy: Phase 1 (2 months) of quadritherapy—isoniazid, rifampicin, pyrazinamide, and ethambutol—administered as single oral doses in the morning on an empty stomach. Phase 2 (4 months) involved continuation with bitherapy (isoniazid and rifampicin) under the same dosing regimen. Clinical and biological monitoring demonstrated a rapid and favorable response to treatment, with resolution of systemic inflammatory markers and improvement in symptoms within days. After three months of therapy, follow-up imaging showed a significant reduction in the number and volume of hepatic lesions, indicating therapeutic efficacy. The clinical course reflects a rare presentation of extrapulmonary tuberculosis involving the liver, with a delayed recognition due to non-specific symptoms and negative initial microbiological screening, ultimately confirmed by histopathological analysis of hepatic nodules."}
+{"row_index": 18, "doc_id": 31, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 12-year-old boy with Down Syndrome and trouble moving his hands and feet had a sore spot on his tongue that looked serious, like a cancer, but it was actually just a long-lasting wound from sharp teeth. His lips were dry and cracked. Because he wore a collar, doctors couldn’t check his neck lymph nodes. The wound was 1 cm wide, had a hard edge, and was white-yellow, which made it look scary. The sharp tooth on the side of his mouth was hurting his tongue and was causing the soreness. Doctors said the problem was caused by the sharp tooth and dry lips, not cancer. He was given salt water, iodine mouthwash, and lip cream to clean and heal the sore spot. His mom was told to use salt water to clean his mouth, apply iodine three times a day to the sore spot, and use lip cream to keep his lips soft. The sharp teeth were planned to be removed, and the space where they went will be fixed with a special device. After a few days, the sore spot got better. But later, he had surgery on his neck because of spine problems. After surgery, he had breathing trouble and passed away two weeks later.\"\n}", "generated_text": "A 12-year-old boy with Down Syndrome and trouble moving his hands and feet had a sore spot on his tongue that looked serious, like a cancer, but it was actually just a long-lasting wound from sharp teeth. His lips were dry and cracked. Because he wore a collar, doctors couldn’t check his neck lymph nodes. The wound was 1 cm wide, had a hard edge, and was white-yellow, which made it look scary. The sharp tooth on the side of his mouth was hurting his tongue and was causing the soreness. Doctors said the problem was caused by the sharp tooth and dry lips, not cancer. He was given salt water, iodine mouthwash, and lip cream to clean and heal the sore spot. His mom was told to use salt water to clean his mouth, apply iodine three times a day to the sore spot, and use lip cream to keep his lips soft. The sharp teeth were planned to be removed, and the space where they went will be fixed with a special device. After a few days, the sore spot got better. But later, he had surgery on his neck because of spine problems. After surgery, he had breathing trouble and passed away two weeks later."}
+{"row_index": 19, "doc_id": 31, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 12-year-old male with Down Syndrome and myeloradiculopathy was referred from the Pediatric Department to the Oral Medicine Department of RS Hasan Sadikin Bandung. The patient's clinical history includes progressive lower extremity and upper limb weakness, initially presenting with a fall approximately one year prior, leading to hospitalization. The patient's mother reported chronic difficulties in performing routine oral hygiene due to motoric impairments, contributing to poor oral care and increased risk of mucosal injury. The patient was diagnosed with Down Syndrome and myeloradiculopathy, a condition characterized by degeneration of spinal nerve roots, resulting in motor dysfunction and sensory deficits.\\n\\nExtraorally, the patient exhibited a dysmorphic facial appearance, consistent with the phenotypic features of Down Syndrome, including a flat facial profile, epicanthal folds, and micrognathia. The vermillion border of the lips demonstrated exfoliative cheilitis, characterized by cracking, desquamation, and desiccation, likely secondary to reduced lip mobility, impaired salivary flow, and inadequate moisturization. Lymph node examination was not feasible due to the patient's use of a cervical collar, which restricted neck mobility.\\n\\nIntraorally, a 1×0.7 cm irregular ulcer was observed at the right lateral border of the tongue, with an indurated (hardened) margin and a white-yellowish base. This lesion clinically mimicked oral squamous cell carcinoma (OSCC), a malignancy of the epithelial lining of the oral cavity, due to its indurated border and surface appearance. However, the diagnosis of a chronic traumatic ulcer was established based on clinical correlation, patient history, and exclusion of neoplastic pathology. The traumatic origin was attributed to the sharp occlusal surface of the maxillary right central incisor (tooth 55), which caused persistent mechanical irritation against the tongue's lateral border, leading to tissue breakdown and ulceration. Additionally, the patient had dentinal caries involving tooth 63, and radicular gangrene (radix gangrene) affecting teeth 55, 62, 74, and 85, indicating advanced pulp necrosis and periapical tissue destruction. These tooth remnants were recommended for extraction by a pediatric dentist, with a space maintainer to be placed to preserve dental arch integrity and prevent malocclusion.\\n\\nLaboratory findings revealed hyponatremia (serum sodium 130 mEq/L), which may reflect impaired renal sodium reabsorption or osmotic imbalances associated with chronic neurological dysfunction or medication effects. Lymphocytosis (lymphocyte count 46%) was noted, potentially indicating a chronic inflammatory state or immune dysregulation, which may be exacerbated by recurrent mucosal trauma and poor oral hygiene. An MRI of the cervical spine confirmed cervical spine dislocation, consistent with the pathophysiology of myeloradiculopathy, which directly contributes to the patient's motor deficits and may have secondary effects on orofacial control and posture.\\n\\nThe differential diagnosis included exfoliative cheilitis, reversible pulpitis of tooth 63, and radix gangrene of multiple teeth. The chronic traumatic ulcer was confirmed through clinical evaluation, with no evidence of dysplasia, cellular atypia, or invasive growth on biopsy. The patient received a multimodal treatment regimen: paracetamol 120 mg/5 mL and amoxicillin 125 mg/5 mL for symptomatic management and possible bacterial infection; sodium chloride 0.9% solution for oral rinsing to maintain osmotic balance; povidone-iodine 1% mouthwash applied three times daily as an antiseptic and anti-inflammatory agent to reduce bacterial load and modulate local inflammation; and petroleum jelly applied to the lips to address desiccation and promote epithelial integrity.\\n\\nThe patient's oral lesions showed progressive improvement over time: at the 3-day follow-up, there was initial healing of the oral ulcer; at the 1-week follow-up, the ulcer size decreased and lip lesions improved; by the 10-day follow-up, significant healing of the tongue ulcer was observed. However, despite clinical improvement, the patient underwent neurosurgery for correction of cervical spine dislocation two days after the 10-day visit. Postoperatively, the patient was admitted to the Pediatric Intensive Care Unit (PICU) due to respiratory compromise. After two weeks of PICU observation, the patient developed acute respiratory failure and was declared deceased. The clinical course underscores the complex interplay between genetic syndrome, neurologic pathology, oral trauma, and systemic complications in pediatric patients with Down Syndrome and motoric disorders. The case highlights the importance of multidisciplinary management, including oral medicine, neurology, and pediatrics, in addressing both local and systemic manifestations of these conditions.\"\n}", "generated_text": "A 12-year-old male with Down Syndrome and myeloradiculopathy was referred from the Pediatric Department to the Oral Medicine Department of RS Hasan Sadikin Bandung. The patient's clinical history includes progressive lower extremity and upper limb weakness, initially presenting with a fall approximately one year prior, leading to hospitalization. The patient's mother reported chronic difficulties in performing routine oral hygiene due to motoric impairments, contributing to poor oral care and increased risk of mucosal injury. The patient was diagnosed with Down Syndrome and myeloradiculopathy, a condition characterized by degeneration of spinal nerve roots, resulting in motor dysfunction and sensory deficits.\n\nExtraorally, the patient exhibited a dysmorphic facial appearance, consistent with the phenotypic features of Down Syndrome, including a flat facial profile, epicanthal folds, and micrognathia. The vermillion border of the lips demonstrated exfoliative cheilitis, characterized by cracking, desquamation, and desiccation, likely secondary to reduced lip mobility, impaired salivary flow, and inadequate moisturization. Lymph node examination was not feasible due to the patient's use of a cervical collar, which restricted neck mobility.\n\nIntraorally, a 1×0.7 cm irregular ulcer was observed at the right lateral border of the tongue, with an indurated (hardened) margin and a white-yellowish base. This lesion clinically mimicked oral squamous cell carcinoma (OSCC), a malignancy of the epithelial lining of the oral cavity, due to its indurated border and surface appearance. However, the diagnosis of a chronic traumatic ulcer was established based on clinical correlation, patient history, and exclusion of neoplastic pathology. The traumatic origin was attributed to the sharp occlusal surface of the maxillary right central incisor (tooth 55), which caused persistent mechanical irritation against the tongue's lateral border, leading to tissue breakdown and ulceration. Additionally, the patient had dentinal caries involving tooth 63, and radicular gangrene (radix gangrene) affecting teeth 55, 62, 74, and 85, indicating advanced pulp necrosis and periapical tissue destruction. These tooth remnants were recommended for extraction by a pediatric dentist, with a space maintainer to be placed to preserve dental arch integrity and prevent malocclusion.\n\nLaboratory findings revealed hyponatremia (serum sodium 130 mEq/L), which may reflect impaired renal sodium reabsorption or osmotic imbalances associated with chronic neurological dysfunction or medication effects. Lymphocytosis (lymphocyte count 46%) was noted, potentially indicating a chronic inflammatory state or immune dysregulation, which may be exacerbated by recurrent mucosal trauma and poor oral hygiene. An MRI of the cervical spine confirmed cervical spine dislocation, consistent with the pathophysiology of myeloradiculopathy, which directly contributes to the patient's motor deficits and may have secondary effects on orofacial control and posture.\n\nThe differential diagnosis included exfoliative cheilitis, reversible pulpitis of tooth 63, and radix gangrene of multiple teeth. The chronic traumatic ulcer was confirmed through clinical evaluation, with no evidence of dysplasia, cellular atypia, or invasive growth on biopsy. The patient received a multimodal treatment regimen: paracetamol 120 mg/5 mL and amoxicillin 125 mg/5 mL for symptomatic management and possible bacterial infection; sodium chloride 0.9% solution for oral rinsing to maintain osmotic balance; povidone-iodine 1% mouthwash applied three times daily as an antiseptic and anti-inflammatory agent to reduce bacterial load and modulate local inflammation; and petroleum jelly applied to the lips to address desiccation and promote epithelial integrity.\n\nThe patient's oral lesions showed progressive improvement over time: at the 3-day follow-up, there was initial healing of the oral ulcer; at the 1-week follow-up, the ulcer size decreased and lip lesions improved; by the 10-day follow-up, significant healing of the tongue ulcer was observed. However, despite clinical improvement, the patient underwent neurosurgery for correction of cervical spine dislocation two days after the 10-day visit. Postoperatively, the patient was admitted to the Pediatric Intensive Care Unit (PICU) due to respiratory compromise. After two weeks of PICU observation, the patient developed acute respiratory failure and was declared deceased. The clinical course underscores the complex interplay between genetic syndrome, neurologic pathology, oral trauma, and systemic complications in pediatric patients with Down Syndrome and motoric disorders. The case highlights the importance of multidisciplinary management, including oral medicine, neurology, and pediatrics, in addressing both local and systemic manifestations of these conditions."}
+{"row_index": 20, "doc_id": 32, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 59-year-old woman had blurry vision in both eyes for a few weeks. She has multiple sclerosis and was taking medicine for seizures, including levetiracetam. Right after starting levetiracetam, her vision got worse, and her corneas (the clear front part of the eye) became swollen. Doctors found this swelling with a special eye test. When they slowly reduced the levetiracetam dose and stopped it, her vision got better and the swollen corneas went away. Now, her vision is clear and her eyes look normal. This suggests the medicine caused the swelling.\"\n}", "generated_text": "A 59-year-old woman had blurry vision in both eyes for a few weeks. She has multiple sclerosis and was taking medicine for seizures, including levetiracetam. Right after starting levetiracetam, her vision got worse, and her corneas (the clear front part of the eye) became swollen. Doctors found this swelling with a special eye test. When they slowly reduced the levetiracetam dose and stopped it, her vision got better and the swollen corneas went away. Now, her vision is clear and her eyes look normal. This suggests the medicine caused the swelling."}
+{"row_index": 21, "doc_id": 32, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 59-year-old woman with secondary progressive multiple sclerosis was referred to ophthalmology because she had been experiencing blurry vision in both eyes for a few weeks. She had been taking levetiracetam, a medication for seizures, a few weeks before the symptoms started. During her eye exam, doctors found swelling in both corneas, a condition called corneal edema, which was confirmed with a special eye test called corneal topography.\\n\\nHer vision and corneal swelling improved when her levetiracetam dose was reduced and eventually stopped altogether. After six months without the medication, her vision returned to normal and the corneal swelling went away. Follow-up exams showed no further changes in her eyes or vision over the next year. Doctors believe the blurriness was caused by the levetiracetam, not her multiple sclerosis or other eye conditions.\"\n}", "generated_text": "A 59-year-old woman with secondary progressive multiple sclerosis was referred to ophthalmology because she had been experiencing blurry vision in both eyes for a few weeks. She had been taking levetiracetam, a medication for seizures, a few weeks before the symptoms started. During her eye exam, doctors found swelling in both corneas, a condition called corneal edema, which was confirmed with a special eye test called corneal topography.\n\nHer vision and corneal swelling improved when her levetiracetam dose was reduced and eventually stopped altogether. After six months without the medication, her vision returned to normal and the corneal swelling went away. Follow-up exams showed no further changes in her eyes or vision over the next year. Doctors believe the blurriness was caused by the levetiracetam, not her multiple sclerosis or other eye conditions."}
+{"row_index": 22, "doc_id": 32, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 59-year-old female with a twelve-year history of secondary progressive multiple sclerosis (SPMS) was referred to ophthalmology with a recent onset of bilateral blurring of vision. She had no prior ophthalmic abnormalities or family history of corneal disease, and previous ocular examinations had not identified signs of Fuchs' endothelial corneal dystrophy. Her medication regimen included amantadine 100 mg twice daily for seven years, administered for symptomatic management of multiple sclerosis-related motor and cognitive symptoms, and levetiracetam 250 mg twice daily, initiated as an adjunctive antiepileptic agent in response to new seizure activity.\\n\\nVisual acuity was measured at 0.5 logMAR in both eyes, indicating moderate visual impairment. Slit-lamp examination revealed bilateral corneal edema without evidence of uveitis or anterior segment inflammation. Intraocular pressures were within normal limits at 16 mmHg (right) and 18 mmHg (left). Corneal topography demonstrated significant corneal thickening, with central corneal thicknesses of 936 μm (right) and 1134 μm (left), consistent with substantial epithelial and stromal hydration.\\n\\nAmantadine is well-documented to induce corneal edema via its known effect on corneal endothelial cell function, particularly through inhibition of Na+/K+ ATPase activity and disruption of ion homeostasis in the corneal endothelium, leading to impaired fluid transport and accumulation of aqueous humor within the stroma. Given this pharmacological mechanism, the treatment team decided to discontinue amantadine and substitute it with lamotrigine, a second-line anticonvulsant with no known association with corneal toxicity. Levetiracetam was continued during this transition, but no improvement in visual acuity was observed over a two-month period.\\n\\nThe patient reported a direct temporal correlation between the initiation of levetiracetam and the onset of visual symptoms, prompting a trial of levetiracetam dose reduction. Following a partial taper, visual symptoms began to resolve within days, and complete cessation of levetiracetam resulted in full normalization of vision. Repeat corneal topography six months post-discontinuation demonstrated regression of corneal thickening to 567 μm (right) and 573 μm (left), with visual acuity improving to 0.2 logMAR bilaterally. Slit-lamp examination confirmed resolution of corneal edema and absence of corneal guttata, a histological feature of endothelial dysfunction.\\n\\nAt a follow-up visit thirteen months after initial presentation, the patient remained stable on amantadine and lamotrigine, with no further changes in medication. Visual acuity remained at 0.2 logMAR in both eyes, and repeat corneal topography showed no progressive thickening, indicating sustained resolution of the endothelial dysfunction. This case supports the hypothesis that levetiracetam may induce corneal edema through mechanisms involving direct or indirect effects on corneal endothelial cell function, potentially via disruption of ion transport, altered membrane permeability, or secondary metabolic stress. While not a well-documented adverse effect in the literature, this case provides clinical evidence for a previously underrecognized side effect of levetiracetam in patients with underlying neurodegenerative conditions, particularly those with compromised ocular homeostasis. The temporal association, reversal upon discontinuation, and normalization of corneal parameters following cessation strongly support a causal relationship between levetiracetam use and the observed corneal pathology.\"\n}", "generated_text": "A 59-year-old female with a twelve-year history of secondary progressive multiple sclerosis (SPMS) was referred to ophthalmology with a recent onset of bilateral blurring of vision. She had no prior ophthalmic abnormalities or family history of corneal disease, and previous ocular examinations had not identified signs of Fuchs' endothelial corneal dystrophy. Her medication regimen included amantadine 100 mg twice daily for seven years, administered for symptomatic management of multiple sclerosis-related motor and cognitive symptoms, and levetiracetam 250 mg twice daily, initiated as an adjunctive antiepileptic agent in response to new seizure activity.\n\nVisual acuity was measured at 0.5 logMAR in both eyes, indicating moderate visual impairment. Slit-lamp examination revealed bilateral corneal edema without evidence of uveitis or anterior segment inflammation. Intraocular pressures were within normal limits at 16 mmHg (right) and 18 mmHg (left). Corneal topography demonstrated significant corneal thickening, with central corneal thicknesses of 936 μm (right) and 1134 μm (left), consistent with substantial epithelial and stromal hydration.\n\nAmantadine is well-documented to induce corneal edema via its known effect on corneal endothelial cell function, particularly through inhibition of Na+/K+ ATPase activity and disruption of ion homeostasis in the corneal endothelium, leading to impaired fluid transport and accumulation of aqueous humor within the stroma. Given this pharmacological mechanism, the treatment team decided to discontinue amantadine and substitute it with lamotrigine, a second-line anticonvulsant with no known association with corneal toxicity. Levetiracetam was continued during this transition, but no improvement in visual acuity was observed over a two-month period.\n\nThe patient reported a direct temporal correlation between the initiation of levetiracetam and the onset of visual symptoms, prompting a trial of levetiracetam dose reduction. Following a partial taper, visual symptoms began to resolve within days, and complete cessation of levetiracetam resulted in full normalization of vision. Repeat corneal topography six months post-discontinuation demonstrated regression of corneal thickening to 567 μm (right) and 573 μm (left), with visual acuity improving to 0.2 logMAR bilaterally. Slit-lamp examination confirmed resolution of corneal edema and absence of corneal guttata, a histological feature of endothelial dysfunction.\n\nAt a follow-up visit thirteen months after initial presentation, the patient remained stable on amantadine and lamotrigine, with no further changes in medication. Visual acuity remained at 0.2 logMAR in both eyes, and repeat corneal topography showed no progressive thickening, indicating sustained resolution of the endothelial dysfunction. This case supports the hypothesis that levetiracetam may induce corneal edema through mechanisms involving direct or indirect effects on corneal endothelial cell function, potentially via disruption of ion transport, altered membrane permeability, or secondary metabolic stress. While not a well-documented adverse effect in the literature, this case provides clinical evidence for a previously underrecognized side effect of levetiracetam in patients with underlying neurodegenerative conditions, particularly those with compromised ocular homeostasis. The temporal association, reversal upon discontinuation, and normalization of corneal parameters following cessation strongly support a causal relationship between levetiracetam use and the observed corneal pathology."}
+{"row_index": 23, "doc_id": 33, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 77-year-old man had a seizure at home and fell, breaking both hip bones and pushing them out of place. He was in the hospital for several days, checked with X-rays and scans, and found to have serious hip fractures on both sides. The doctors fixed the hips in two steps, seven days apart, to make sure the bones healed well. In each surgery, they used a special ring to hold the hip socket in place and a special hip replacement with a stem that fits into the thigh bone. The ring was placed in the pelvis and held with screws to keep it strong. The man did not have any problems after surgery. At one year, he could walk fully with a walking stick, had a good hip score (77 on the right, 79 on the left), and only had a little pain or limp. He hasn’t had any serious issues since and is doing well.\"\n}", "generated_text": "A 77-year-old man had a seizure at home and fell, breaking both hip bones and pushing them out of place. He was in the hospital for several days, checked with X-rays and scans, and found to have serious hip fractures on both sides. The doctors fixed the hips in two steps, seven days apart, to make sure the bones healed well. In each surgery, they used a special ring to hold the hip socket in place and a special hip replacement with a stem that fits into the thigh bone. The ring was placed in the pelvis and held with screws to keep it strong. The man did not have any problems after surgery. At one year, he could walk fully with a walking stick, had a good hip score (77 on the right, 79 on the left), and only had a little pain or limp. He hasn’t had any serious issues since and is doing well."}
+{"row_index": 24, "doc_id": 33, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 77-year-old male with a history of moderate cognitive impairment was admitted to the emergency department following a tonic-clonic seizure at home, presenting in a hemodynamically unstable postcritical state with suspected intrapelvic hemorrhage. The polytrauma code was activated due to hemodynamic instability, not the mechanism of injury. The patient was stabilized with intravenous fluid resuscitation and packed red blood cell transfusion. A pelvic binder was applied, and once hemodynamic stability was achieved, a physical examination revealed bilateral lower limb shortening, external rotation, and joint blockage on log roll testing, indicating functional impotence in both hips. No external trauma or bruising was observed; distal pulses were intact, and upper limb mobility was preserved. Initial imaging included anteroposterior pelvic radiography, which revealed bilateral femoral head dislocation. Abdominal-pelvic computed tomography (CT) was performed to evaluate for intra-abdominal pathology, and 3D-CT reconstruction confirmed a bilateral transverse acetabular fracture (Letournel classification) and bilateral longitudinal iliac wing fractures, with intrapelvic protrusion of both femoral heads. Supracondylar traction was applied to the femoral heads bilaterally, and pelvic traction was discontinued. The patient remained in the recovery unit under traction until surgical intervention. Surgical planning was deferred for seven days to allow fibrotic consolidation at the fracture sites and to minimize intraoperative bleeding. Surgery was performed in two stages: the left hemipelvis on day 8 and the right hemipelvis on day 15, both under general anesthesia. Tranexamic acid was administered to reduce intraoperative blood loss and transfusion requirements. Cefazolin (2 g preoperatively, 1 g every 8 hours for 24 hours postoperatively) was used as per institutional protocol to prevent surgical site infection. Postoperatively, enoxaparin 40 mg subcutaneously every 24 hours for seven weeks was administered for thromboprophylaxis. The left hemipelvis was operated first due to greater pelvic protrusion, which increased the risk of soft tissue hematoma formation during femoral head extraction, potentially leading to vascular injury or excessive bleeding. The procedure employed a posterior lateral approach with Moore's autograft placement to reconstruct the acetabular fracture bed. An anti-protrusion ring (Burch Schneider™ Reinforcement Cage, Zimmer Biomet) was implanted, anchored to the ischium and ilium, with medial ischial fixation using screws. Prior to ring placement, dissection of the gluteal musculature (gluteus minimus and medius) was required to accurately reposition the femoral head. The ring was verified under direct visualization. A double-mobility cemented acetabular ring was then implanted, followed by a non-cemented femoral stem. Capsule and pelvic musculature were closed using transosseous trochanteric suture points. The right hemipelvis was operated seven days later. For the longitudinal iliac wing fracture, a six-hole anatomical plate was used via an ilio-inguinal approach. The same surgical sequence—anti-protrusion ring with double-mobility cemented acetabular ring and non-cemented femoral stem—was repeated. Anti-protrusion rings are indicated in acetabular fractures involving the acetabular background (e.g., Type IV AAOS classification), where pelvic disjunction is possible, and require anchorage in both ischium and ilium to provide structural support. They are not indicated for isolated anterior or posterior wall fractures without acetabular bed involvement. The patient remained bedridden during admission and was mobilized to prevent pressure ulcers. After the second surgery, clinical tolerance permitted initiation of wheelchair transfers. Full range of motion was permitted in bed without restriction. The patient was discharged at four weeks, with full weight-bearing delayed until six weeks due to the need for initial graft consolidation in the acetabular background to ensure stable ring support, and due to bilateral hip pathology, which precluded safe partial loading with one hip serving as a functional support. The patient began full load with a walking stick at six weeks. At 12-month follow-up, the patient achieved full weight-bearing with a Harris Hip Score (HHS) of 77 in the right hip and 79 in the left hip, and a WOMAC score of 12, indicating minimal pain and functional limitation. No postoperative complications have been reported to date. The patient reports occasional discomfort and a mild right-sided limp, but maintains full range of motion and no episodes of hip instability. The surgical approach successfully addressed bilateral acetabular fractures with associated femoral head protrusion, utilizing staged reconstruction with biomechanically stable fixation to restore joint integrity and function in a high-risk, cognitively impaired elderly population.\"\n}", "generated_text": "A 77-year-old male with a history of moderate cognitive impairment was admitted to the emergency department following a tonic-clonic seizure at home, presenting in a hemodynamically unstable postcritical state with suspected intrapelvic hemorrhage. The polytrauma code was activated due to hemodynamic instability, not the mechanism of injury. The patient was stabilized with intravenous fluid resuscitation and packed red blood cell transfusion. A pelvic binder was applied, and once hemodynamic stability was achieved, a physical examination revealed bilateral lower limb shortening, external rotation, and joint blockage on log roll testing, indicating functional impotence in both hips. No external trauma or bruising was observed; distal pulses were intact, and upper limb mobility was preserved. Initial imaging included anteroposterior pelvic radiography, which revealed bilateral femoral head dislocation. Abdominal-pelvic computed tomography (CT) was performed to evaluate for intra-abdominal pathology, and 3D-CT reconstruction confirmed a bilateral transverse acetabular fracture (Letournel classification) and bilateral longitudinal iliac wing fractures, with intrapelvic protrusion of both femoral heads. Supracondylar traction was applied to the femoral heads bilaterally, and pelvic traction was discontinued. The patient remained in the recovery unit under traction until surgical intervention. Surgical planning was deferred for seven days to allow fibrotic consolidation at the fracture sites and to minimize intraoperative bleeding. Surgery was performed in two stages: the left hemipelvis on day 8 and the right hemipelvis on day 15, both under general anesthesia. Tranexamic acid was administered to reduce intraoperative blood loss and transfusion requirements. Cefazolin (2 g preoperatively, 1 g every 8 hours for 24 hours postoperatively) was used as per institutional protocol to prevent surgical site infection. Postoperatively, enoxaparin 40 mg subcutaneously every 24 hours for seven weeks was administered for thromboprophylaxis. The left hemipelvis was operated first due to greater pelvic protrusion, which increased the risk of soft tissue hematoma formation during femoral head extraction, potentially leading to vascular injury or excessive bleeding. The procedure employed a posterior lateral approach with Moore's autograft placement to reconstruct the acetabular fracture bed. An anti-protrusion ring (Burch Schneider™ Reinforcement Cage, Zimmer Biomet) was implanted, anchored to the ischium and ilium, with medial ischial fixation using screws. Prior to ring placement, dissection of the gluteal musculature (gluteus minimus and medius) was required to accurately reposition the femoral head. The ring was verified under direct visualization. A double-mobility cemented acetabular ring was then implanted, followed by a non-cemented femoral stem. Capsule and pelvic musculature were closed using transosseous trochanteric suture points. The right hemipelvis was operated seven days later. For the longitudinal iliac wing fracture, a six-hole anatomical plate was used via an ilio-inguinal approach. The same surgical sequence—anti-protrusion ring with double-mobility cemented acetabular ring and non-cemented femoral stem—was repeated. Anti-protrusion rings are indicated in acetabular fractures involving the acetabular background (e.g., Type IV AAOS classification), where pelvic disjunction is possible, and require anchorage in both ischium and ilium to provide structural support. They are not indicated for isolated anterior or posterior wall fractures without acetabular bed involvement. The patient remained bedridden during admission and was mobilized to prevent pressure ulcers. After the second surgery, clinical tolerance permitted initiation of wheelchair transfers. Full range of motion was permitted in bed without restriction. The patient was discharged at four weeks, with full weight-bearing delayed until six weeks due to the need for initial graft consolidation in the acetabular background to ensure stable ring support, and due to bilateral hip pathology, which precluded safe partial loading with one hip serving as a functional support. The patient began full load with a walking stick at six weeks. At 12-month follow-up, the patient achieved full weight-bearing with a Harris Hip Score (HHS) of 77 in the right hip and 79 in the left hip, and a WOMAC score of 12, indicating minimal pain and functional limitation. No postoperative complications have been reported to date. The patient reports occasional discomfort and a mild right-sided limp, but maintains full range of motion and no episodes of hip instability. The surgical approach successfully addressed bilateral acetabular fractures with associated femoral head protrusion, utilizing staged reconstruction with biomechanically stable fixation to restore joint integrity and function in a high-risk, cognitively impaired elderly population."}
+{"row_index": 25, "doc_id": 34, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 19-month-old boy fell from a highchair and hit his head. He was fine at first, but then started vomiting and became very irritable. He was breathing fast and not getting enough oxygen. His chest looked like it was pulling in, and one side of his lung wasn’t working well. Doctors gave him a breathing tube to help him breathe, but his oxygen levels kept dropping. A scan showed the left lung was completely collapsed, and the main airway to that lung was blocked. The doctors thought a small almond, about 2 cm, had gotten stuck there. The boy had never eaten almonds before and probably swallowed it by accident. After the almond was removed, his breathing got better and he was able to breathe on his own again. He stayed in the hospital for a few days and is now doing well.\"\n}", "generated_text": "A 19-month-old boy fell from a highchair and hit his head. He was fine at first, but then started vomiting and became very irritable. He was breathing fast and not getting enough oxygen. His chest looked like it was pulling in, and one side of his lung wasn’t working well. Doctors gave him a breathing tube to help him breathe, but his oxygen levels kept dropping. A scan showed the left lung was completely collapsed, and the main airway to that lung was blocked. The doctors thought a small almond, about 2 cm, had gotten stuck there. The boy had never eaten almonds before and probably swallowed it by accident. After the almond was removed, his breathing got better and he was able to breathe on his own again. He stayed in the hospital for a few days and is now doing well."}
+{"row_index": 26, "doc_id": 34, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 19-month-old male was admitted to the Emergency Department following a fall from a baby feeding highchair. The fall occurred while the child was in apparent well-being, with no prior signs or symptoms of distress. The mechanism of injury involved initial gluteal contact followed by a direct impact to the occiput (back of the head). The child presented with three episodes of vomiting and was markedly irritable. Vital signs revealed a respiratory rate exceeding 60 breaths per minute and a heart rate greater than 150 beats per minute, with oxygen saturation falling below 80%. Physical examination demonstrated subcostal retractions and diminished breath sounds localized to the left basal lung region. The patient was initially managed with non-invasive ventilation using an AMBU bag connected to supplemental oxygen and continuous pulse oximetry. However, despite this intervention, oxygen saturation progressively declined below 70%, and ventilation-induced worsening of hypoxemia was observed, suggesting impaired gas exchange. Lung ultrasound revealed the absence of normal A lines and evidence of pulmonary consolidation, interpreted as solid parenchymal opacification consistent with alveolar collapse or obstruction. Given the severity of respiratory compromise, orotracheal intubation with a cuffed endotracheal tube was performed to secure airway patency and ensure adequate oxygenation. Following stabilization, a chest computed tomography (CT) scan was obtained, which demonstrated complete atelectasis of the left lung and a discrete interruption of the main left bronchus at a distance of 12 mm from the bronchial bifurcation (i.e., the point where the left and right main bronchi divide). This radiographic finding, combined with the clinical history of a recent, self-limiting cough episode in the days prior, raised a strong suspicion of foreign body aspiration (FBA). The mother reported that the infant had experienced a severe cough attack that resolved spontaneously within 24 hours without medical intervention. Rigid bronchoscopy was subsequently performed, during which a 2 cm diameter almond was identified within the proximal left main bronchus and was successfully removed. Notably, the child had no prior exposure to nuts or any known history of food ingestion, and the almond was ingested incidentally during routine feeding. Post-intervention, the patient exhibited a progressive clinical recovery, with oxygenation improving steadily. At 24 hours post-intubation, the patient was extubated and transferred to the general pediatrics ward for continued observation. Over the following days, full respiratory function was restored, and the child was discharged without further complications. The case highlights the potential for asymptomatic or transient respiratory symptoms to precede significant airway obstruction, and underscores the importance of high index of suspicion for foreign body aspiration in pediatric patients presenting with acute respiratory distress following minor trauma, particularly when associated with a history of cough or atelectasis on imaging.\"\n}", "generated_text": "A 19-month-old male was admitted to the Emergency Department following a fall from a baby feeding highchair. The fall occurred while the child was in apparent well-being, with no prior signs or symptoms of distress. The mechanism of injury involved initial gluteal contact followed by a direct impact to the occiput (back of the head). The child presented with three episodes of vomiting and was markedly irritable. Vital signs revealed a respiratory rate exceeding 60 breaths per minute and a heart rate greater than 150 beats per minute, with oxygen saturation falling below 80%. Physical examination demonstrated subcostal retractions and diminished breath sounds localized to the left basal lung region. The patient was initially managed with non-invasive ventilation using an AMBU bag connected to supplemental oxygen and continuous pulse oximetry. However, despite this intervention, oxygen saturation progressively declined below 70%, and ventilation-induced worsening of hypoxemia was observed, suggesting impaired gas exchange. Lung ultrasound revealed the absence of normal A lines and evidence of pulmonary consolidation, interpreted as solid parenchymal opacification consistent with alveolar collapse or obstruction. Given the severity of respiratory compromise, orotracheal intubation with a cuffed endotracheal tube was performed to secure airway patency and ensure adequate oxygenation. Following stabilization, a chest computed tomography (CT) scan was obtained, which demonstrated complete atelectasis of the left lung and a discrete interruption of the main left bronchus at a distance of 12 mm from the bronchial bifurcation (i.e., the point where the left and right main bronchi divide). This radiographic finding, combined with the clinical history of a recent, self-limiting cough episode in the days prior, raised a strong suspicion of foreign body aspiration (FBA). The mother reported that the infant had experienced a severe cough attack that resolved spontaneously within 24 hours without medical intervention. Rigid bronchoscopy was subsequently performed, during which a 2 cm diameter almond was identified within the proximal left main bronchus and was successfully removed. Notably, the child had no prior exposure to nuts or any known history of food ingestion, and the almond was ingested incidentally during routine feeding. Post-intervention, the patient exhibited a progressive clinical recovery, with oxygenation improving steadily. At 24 hours post-intubation, the patient was extubated and transferred to the general pediatrics ward for continued observation. Over the following days, full respiratory function was restored, and the child was discharged without further complications. The case highlights the potential for asymptomatic or transient respiratory symptoms to precede significant airway obstruction, and underscores the importance of high index of suspicion for foreign body aspiration in pediatric patients presenting with acute respiratory distress following minor trauma, particularly when associated with a history of cough or atelectasis on imaging."}
+{"row_index": 27, "doc_id": 35, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 4-month-old male infant from central Mexico presented with a painful, suppurative tumor in the left axilla, prompting medical evaluation. The infant was born to a mother with hypothyroidism during the first trimester of pregnancy, who received pharmacological intervention. The infant was born with normal birth weight and length, was exclusively breast-fed, and received the BCG vaccine without scarring. The mother was incarcerated in a prison cell with the infant and two other individuals, living in a crowded environment. At 4 months of age, the infant was admitted to a pediatric hospital following a chest X-ray that demonstrated suggestive radiographic findings of rib fractures, leading to suspicion of child abuse. Physical examination revealed a weight of 4,190 g (below the third percentile), height of 58 cm, oxygen saturation of 70%, fever, cough, localized pain, redness, and warmth in the left axilla. Laboratory findings included hemoglobin of 8.8 g/dL (normal range: 11.0–12.6 g/dL), leukocyte count of 29.3 × 10⁹/L (normal: 6.0–17.5 × 10⁹/L), neutrophil count of 18.4 × 10⁹/L (normal: 1.0–8.5 × 10⁹/L), lymphocyte count of 7.0 × 10⁹/L (normal: 4.0–13.5 × 10⁹/L), monocyte count of 3.5 × 10⁹/L, platelet count of 459 × 10⁹/L (normal: 150–350 × 10⁹/L), and C-reactive protein of 16 mg/L (elevated, normal <3.0 mg/L). A thoracoabdominal tomography revealed a left axillary abscess, lytic lesions in ribs 3–6, left apical pneumonia, bilateral pulmonary nodules, and enlarged cervical and mediastinal lymph nodes. Histopathological analysis of the axillary abscess demonstrated suppurative panniculitis and myositis. Bacterial culture from bronchoalveolar lavage fluid was negative, and PCR testing for *Mycobacterium tuberculosis* complex was negative. The infant received a 41-day course of dual antimicrobial therapy (ceftriaxone-clindamycin and cefepime-vancomycin) and was discharged. \\n\\nAt 8 months of age, the infant was readmitted with fever, irritability, and extension of the suppurative process to the left scapula. Repeat laboratory values showed hemoglobin of 10.8 g/dL, leukocyte count of 21.2 × 10⁹/L, neutrophil count of 12.2 × 10⁹/L, lymphocyte count of 7.5 × 10⁹/L, monocyte count of 1.2 × 10⁹/L, and platelet count of 583 × 10⁹/L. Serum HIV testing was negative. Chest imaging revealed left apical consolidation, bronchiectasis, lytic lesions in ribs 2–7 and dorsal vertebrae 2–7, and a multilocular fluid collection. Ultrasound confirmed a fistula associated with the scapular abscess. The infant was initially treated with piperacillin-tazobactam, which was subsequently replaced with voriconazole after *Aspergillus fumigatus* was isolated from the abscess secretion. Given the recurrent and progressive nature of the infection, an innate immune deficiency was suspected. A dihydrorhodamine (DHR) fluorescence assay demonstrated absent production of reactive oxygen species (ROS) in neutrophils, and immunofluorescence analysis revealed absent gp91phox protein expression in neutrophils, confirming a defect in the phagocyte NADPH oxidase complex. Next-generation sequencing identified a pathogenic variant in the *CYBB* gene, specifically c.80_83del/Y (p.Val27Glyfs*33), which results in a frameshift mutation and premature termination of the gp91phox protein. The mother was identified as a carrier of the same variant (c.80_83del/WT), consistent with X-linked recessive inheritance. The two older male siblings, who were clinically asymptomatic, were not subjected to genetic testing. The infant was discharged after 65 days of hospitalization and 28 days of voriconazole therapy, with initiation of daily trimethoprim-sulfamethoxazole prophylaxis for bacterial infection", "generated_text": "{\n  \"proficient_health_literacy\": \"A 4-month-old male infant from central Mexico presented with a painful, suppurative tumor in the left axilla, prompting medical evaluation. The infant was born to a mother with hypothyroidism during the first trimester of pregnancy, who received pharmacological intervention. The infant was born with normal birth weight and length, was exclusively breast-fed, and received the BCG vaccine without scarring. The mother was incarcerated in a prison cell with the infant and two other individuals, living in a crowded environment. At 4 months of age, the infant was admitted to a pediatric hospital following a chest X-ray that demonstrated suggestive radiographic findings of rib fractures, leading to suspicion of child abuse. Physical examination revealed a weight of 4,190 g (below the third percentile), height of 58 cm, oxygen saturation of 70%, fever, cough, localized pain, redness, and warmth in the left axilla. Laboratory findings included hemoglobin of 8.8 g/dL (normal range: 11.0–12.6 g/dL), leukocyte count of 29.3 × 10⁹/L (normal: 6.0–17.5 × 10⁹/L), neutrophil count of 18.4 × 10⁹/L (normal: 1.0–8.5 × 10⁹/L), lymphocyte count of 7.0 × 10⁹/L (normal: 4.0–13.5 × 10⁹/L), monocyte count of 3.5 × 10⁹/L, platelet count of 459 × 10⁹/L (normal: 150–350 × 10⁹/L), and C-reactive protein of 16 mg/L (elevated, normal <3.0 mg/L). A thoracoabdominal tomography revealed a left axillary abscess, lytic lesions in ribs 3–6, left apical pneumonia, bilateral pulmonary nodules, and enlarged cervical and mediastinal lymph nodes. Histopathological analysis of the axillary abscess demonstrated suppurative panniculitis and myositis. Bacterial culture from bronchoalveolar lavage fluid was negative, and PCR testing for *Mycobacterium tuberculosis* complex was negative. The infant received a 41-day course of dual antimicrobial therapy (ceftriaxone-clindamycin and cefepime-vancomycin) and was discharged. \\n\\nAt 8 months of age, the infant was readmitted with fever, irritability, and extension of the suppurative process to the left scapula. Repeat laboratory values showed hemoglobin of 10.8 g/dL, leukocyte count of 21.2 × 10⁹/L, neutrophil count of 12.2 × 10⁹/L, lymphocyte count of 7.5 × 10⁹/L, monocyte count of 1.2 × 10⁹/L, and platelet count of 583 × 10⁹/L. Serum HIV testing was negative. Chest imaging revealed left apical consolidation, bronchiectasis, lytic lesions in ribs 2–7 and dorsal vertebrae 2–7, and a multilocular fluid collection. Ultrasound confirmed a fistula associated with the scapular abscess. The infant was initially treated with piperacillin-tazobactam, which was subsequently replaced with voriconazole after *Aspergillus fumigatus* was isolated from the abscess secretion. Given the recurrent and progressive nature of the infection, an innate immune deficiency was suspected. A dihydrorhodamine (DHR) fluorescence assay demonstrated absent production of reactive oxygen species (ROS) in neutrophils, and immunofluorescence analysis revealed absent gp91phox protein expression in neutrophils, confirming a defect in the phagocyte NADPH oxidase complex. Next-generation sequencing identified a pathogenic variant in the *CYBB* gene, specifically c.80_83del/Y (p.Val27Glyfs*33), which results in a frameshift mutation and premature termination of the gp91phox protein. The mother was identified as a carrier of the same variant (c.80_83del/WT), consistent with X-linked recessive inheritance. The two older male siblings, who were clinically asymptomatic, were not subjected to genetic testing. The infant was discharged after 65 days of hospitalization and 28 days of voriconazole therapy, with initiation of daily trimethoprim-sulfamethoxazole prophylaxis for bacterial infection"}
+{"row_index": 28, "doc_id": 36, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 25-year-old male patient of Sundanese ethnicity presented to the Department of Oral Medicine at the Dental Hospital of the Faculty of Dentistry, Universitas Padjadjaran, with a chief complaint of painful oral and lip lesions. The lesions initially appeared as canker sores in the oral cavity four days prior to presentation, subsequently extending to the upper and lower labial mucosa two days later. The patient reported exacerbation of symptoms during eating and speech. Initial self-management with petroleum jelly failed to provide relief; he then used triamcinolone acetonide 0.1% in orabase ointment, applied once daily, which resulted in partial symptomatic improvement but no complete resolution of the lesions.\\n\\nThe patient reported a preceding febrile illness lasting approximately one week prior to lesion onset, with no cutaneous or systemic manifestations elsewhere. He described a history of chronic poor nutritional intake over the past one and a half months, associated with high work-related stress. There was no known medical history, food allergies, medication use, alcohol consumption, or tobacco use. However, he had a documented history of chickenpox in childhood. He maintained a habit of frequent lip-licking and lip-peeling, which was identified as a potential contributing behavioral factor.\\n\\nGeneral examination revealed normal vital signs and no lymphadenopathy. Extra-oral examination demonstrated serosanguineous crusts on the lips, which were tender and prone to bleeding. Intra-oral examination revealed diffusely erythematous, irregularly bordered, painful lesions on the upper and lower labial mucosa. Additional findings included hyperkeratotic, non-scrapable white plaques with diffuse borders on the left buccal mucosa near tooth 38, yellowish-white, easily scrapable plaques covering one-third of the posterior dorsal tongue with associated dental impression indentations (non-painful), and a painless, 2×1×0.5 cm hard nodule in the midline of the hard palate. Dental evaluation identified carious lesions, root caries, and edentulism in multiple teeth (teeth 28, 36, 37, and 46), with diagnoses of reversible pulpitis (tooth 18), irreversible pulpitis (tooth 47), chronic apical periodontitis due to root caries (tooth 15), and associated periodontal disease. Oral hygiene was assessed as suboptimal.\\n\\nPsychological evaluation using the DASS-21 scale indicated normal levels of depression (score 0), anxiety (score 6), and stress (score 6). Based on clinical presentation and history, the working diagnosis was suspected to be Herpes Simplex Virus-1-associated Erythema Multiforme (HAEM), with concomitant findings of coated tongue, frictional keratosis, crenated tongue, torus palatinus, and multiple dental pathologies. Differential diagnosis considered exfoliative cheilitis, which was excluded due to the absence of herpesvirus involvement. Serological testing for IgG anti-HSV-1 was performed, yielding a titer of 6.32 (positive when ratio > 1.1), confirming active HSV-1 seropositivity and supporting the diagnosis of HAEM.\\n\\nOral health-related quality of life (OHRQoL) was assessed using the OHIP-14, with an initial score of 35, indicating moderate impairment. The treatment plan included both pharmacological and non-pharmacological interventions. Non-pharmacological measures comprised instruction in daily oral hygiene (soft-bristled toothbrush, twice daily; non-detergent toothpaste), increased daily water intake (≥2 liters), balanced nutrition, avoidance of acidic, spicy, hard, and monosodium glutamate (MSG)-containing foods, and cessation of lip-licking and lip-peeling behaviors. Pharmacological therapy included topical application of triamcinolone acetonide 0.1% in orabase (three times daily), gauze compression with 0.9% NaCl solution (three times daily), and systemic administration of multivitamins (once daily). Following one week of treatment, acyclovir 200 mg tablets were initiated orally, administered five times daily for one week to target viral replication.\\n\\nClinical improvement was observed at the first follow-up (two days post-initial visit), with significant reduction in lip pain, though the canker sores remained incomplete. At the second follow-up (five days later), complete healing of all oral lesions was achieved. The final OHIP-14 score improved to 4, indicating excellent OHRQoL. The patient’s physical, psychological, and social functioning returned to baseline within seven days of treatment. The patient was referred for continued management in periodontics,", "generated_text": "{\n  \"proficient_health_literacy\": \"A 25-year-old male patient of Sundanese ethnicity presented to the Department of Oral Medicine at the Dental Hospital of the Faculty of Dentistry, Universitas Padjadjaran, with a chief complaint of painful oral and lip lesions. The lesions initially appeared as canker sores in the oral cavity four days prior to presentation, subsequently extending to the upper and lower labial mucosa two days later. The patient reported exacerbation of symptoms during eating and speech. Initial self-management with petroleum jelly failed to provide relief; he then used triamcinolone acetonide 0.1% in orabase ointment, applied once daily, which resulted in partial symptomatic improvement but no complete resolution of the lesions.\\n\\nThe patient reported a preceding febrile illness lasting approximately one week prior to lesion onset, with no cutaneous or systemic manifestations elsewhere. He described a history of chronic poor nutritional intake over the past one and a half months, associated with high work-related stress. There was no known medical history, food allergies, medication use, alcohol consumption, or tobacco use. However, he had a documented history of chickenpox in childhood. He maintained a habit of frequent lip-licking and lip-peeling, which was identified as a potential contributing behavioral factor.\\n\\nGeneral examination revealed normal vital signs and no lymphadenopathy. Extra-oral examination demonstrated serosanguineous crusts on the lips, which were tender and prone to bleeding. Intra-oral examination revealed diffusely erythematous, irregularly bordered, painful lesions on the upper and lower labial mucosa. Additional findings included hyperkeratotic, non-scrapable white plaques with diffuse borders on the left buccal mucosa near tooth 38, yellowish-white, easily scrapable plaques covering one-third of the posterior dorsal tongue with associated dental impression indentations (non-painful), and a painless, 2×1×0.5 cm hard nodule in the midline of the hard palate. Dental evaluation identified carious lesions, root caries, and edentulism in multiple teeth (teeth 28, 36, 37, and 46), with diagnoses of reversible pulpitis (tooth 18), irreversible pulpitis (tooth 47), chronic apical periodontitis due to root caries (tooth 15), and associated periodontal disease. Oral hygiene was assessed as suboptimal.\\n\\nPsychological evaluation using the DASS-21 scale indicated normal levels of depression (score 0), anxiety (score 6), and stress (score 6). Based on clinical presentation and history, the working diagnosis was suspected to be Herpes Simplex Virus-1-associated Erythema Multiforme (HAEM), with concomitant findings of coated tongue, frictional keratosis, crenated tongue, torus palatinus, and multiple dental pathologies. Differential diagnosis considered exfoliative cheilitis, which was excluded due to the absence of herpesvirus involvement. Serological testing for IgG anti-HSV-1 was performed, yielding a titer of 6.32 (positive when ratio > 1.1), confirming active HSV-1 seropositivity and supporting the diagnosis of HAEM.\\n\\nOral health-related quality of life (OHRQoL) was assessed using the OHIP-14, with an initial score of 35, indicating moderate impairment. The treatment plan included both pharmacological and non-pharmacological interventions. Non-pharmacological measures comprised instruction in daily oral hygiene (soft-bristled toothbrush, twice daily; non-detergent toothpaste), increased daily water intake (≥2 liters), balanced nutrition, avoidance of acidic, spicy, hard, and monosodium glutamate (MSG)-containing foods, and cessation of lip-licking and lip-peeling behaviors. Pharmacological therapy included topical application of triamcinolone acetonide 0.1% in orabase (three times daily), gauze compression with 0.9% NaCl solution (three times daily), and systemic administration of multivitamins (once daily). Following one week of treatment, acyclovir 200 mg tablets were initiated orally, administered five times daily for one week to target viral replication.\\n\\nClinical improvement was observed at the first follow-up (two days post-initial visit), with significant reduction in lip pain, though the canker sores remained incomplete. At the second follow-up (five days later), complete healing of all oral lesions was achieved. The final OHIP-14 score improved to 4, indicating excellent OHRQoL. The patient’s physical, psychological, and social functioning returned to baseline within seven days of treatment. The patient was referred for continued management in periodontics,"}
+{"row_index": 29, "doc_id": 37, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 29-year-old woman, Para 1, presented with a one-month history of abnormal vaginal bleeding to the gynecology outpatient department of a level 2 hospital. She was HIV-positive, having been diagnosed approximately one year prior to presentation. Antiretroviral therapy (ART) was initiated following diagnosis but was discontinued for one month during the onset of vaginal bleeding, resulting in virological failure (viral load: 37,400 copies/mL) and immunological decline (CD4 count: 26 cells/μL). The timing of initial HIV symptom onset was not clearly documented. Physical examination revealed a large cervical mass measuring 8 × 8 cm extending into the parametrium and bilateral pelvic side walls, with bleeding on contact and foul-smelling vaginal discharge. Ultrasonography demonstrated a bulky cervix and bilateral hydronephrosis, supporting a clinical diagnosis of cervical malignancy at International Federation of Gynecology and Obstetrics (FIGO) stage 3B, defined by pelvic wall involvement and hydronephrosis. A punch biopsy of the cervix confirmed an extra-nodal Burkitt lymphoma (BL), with immunohistochemical staining positive for CD20, CD75a, CD10, PAX5, and BCL6; CD44 and c-Myc were also positive, with focal EBER in situ hybridization (ISH) positivity. The Ki67 proliferation index was nearly 100%, indicating extremely high cellular proliferation, and PAX5 and BCL6 showed moderate expression. Laboratory findings included leukopenia (white cell count: 2.67 × 10⁹/L), anemia (hemoglobin: 5.7 g/dL), thrombocytopenia (platelet count: 71 × 10⁹/L), serum creatinine of 187 mmol/L (indicating significant renal impairment), urea 11.1 mmol/L, albumin 21 g/L, aspartate transaminase 41 U/L, and alkaline phosphatase 100 U/L. The patient was recommenced on ART, transitioning from a TLD (Tenofovir-Lamivudine-Dolutegravir) regimen to a renal-sparing Lamivudine-Abacavir-Dolutegravir combination to mitigate further nephrotoxicity. Following histological confirmation and multidisciplinary oncology review, a treatment plan of chemoradiation was recommended. However, due to a prolonged waiting list at the referral oncology unit, the patient waited 43 days before receiving any treatment—exceeding the recommended 48-hour window for initiating therapy in Burkitt lymphoma, particularly in immunocompromised individuals. During this period, no further imaging (CT or MRI) was performed due to technical limitations in the available equipment. The patient received supportive care including blood transfusions and analgesia. She died in the gynecological ward on day 43, with the interval between diagnosis of BL and death remaining 43 days. A postmortem histopathological examination was not conducted, as both the Burkitt lymphoma and HIV infection were already established and well-documented. The primary cause of death remains difficult to assign due to the coexistence of multiple severe comorbidities; however, given the aggressive nature of BL in the context of advanced HIV infection with high viral load and profound immunosuppression, the attending physician concluded that BL was the most likely primary cause. The secondary cause of death was multiple organ failure, encompassing both renal and hematological dysfunction, reflecting the systemic impact of the disease and the underlying immunodeficiency. This case underscores the critical importance of timely diagnosis and initiation of oncological intervention in HIV-positive patients with suspected cervical malignancy, especially in the context of high-risk lymphoma subtypes such as extra-nodal BL.\"\n}", "generated_text": "A 29-year-old woman, Para 1, presented with a one-month history of abnormal vaginal bleeding to the gynecology outpatient department of a level 2 hospital. She was HIV-positive, having been diagnosed approximately one year prior to presentation. Antiretroviral therapy (ART) was initiated following diagnosis but was discontinued for one month during the onset of vaginal bleeding, resulting in virological failure (viral load: 37,400 copies/mL) and immunological decline (CD4 count: 26 cells/μL). The timing of initial HIV symptom onset was not clearly documented. Physical examination revealed a large cervical mass measuring 8 × 8 cm extending into the parametrium and bilateral pelvic side walls, with bleeding on contact and foul-smelling vaginal discharge. Ultrasonography demonstrated a bulky cervix and bilateral hydronephrosis, supporting a clinical diagnosis of cervical malignancy at International Federation of Gynecology and Obstetrics (FIGO) stage 3B, defined by pelvic wall involvement and hydronephrosis. A punch biopsy of the cervix confirmed an extra-nodal Burkitt lymphoma (BL), with immunohistochemical staining positive for CD20, CD75a, CD10, PAX5, and BCL6; CD44 and c-Myc were also positive, with focal EBER in situ hybridization (ISH) positivity. The Ki67 proliferation index was nearly 100%, indicating extremely high cellular proliferation, and PAX5 and BCL6 showed moderate expression. Laboratory findings included leukopenia (white cell count: 2.67 × 10⁹/L), anemia (hemoglobin: 5.7 g/dL), thrombocytopenia (platelet count: 71 × 10⁹/L), serum creatinine of 187 mmol/L (indicating significant renal impairment), urea 11.1 mmol/L, albumin 21 g/L, aspartate transaminase 41 U/L, and alkaline phosphatase 100 U/L. The patient was recommenced on ART, transitioning from a TLD (Tenofovir-Lamivudine-Dolutegravir) regimen to a renal-sparing Lamivudine-Abacavir-Dolutegravir combination to mitigate further nephrotoxicity. Following histological confirmation and multidisciplinary oncology review, a treatment plan of chemoradiation was recommended. However, due to a prolonged waiting list at the referral oncology unit, the patient waited 43 days before receiving any treatment—exceeding the recommended 48-hour window for initiating therapy in Burkitt lymphoma, particularly in immunocompromised individuals. During this period, no further imaging (CT or MRI) was performed due to technical limitations in the available equipment. The patient received supportive care including blood transfusions and analgesia. She died in the gynecological ward on day 43, with the interval between diagnosis of BL and death remaining 43 days. A postmortem histopathological examination was not conducted, as both the Burkitt lymphoma and HIV infection were already established and well-documented. The primary cause of death remains difficult to assign due to the coexistence of multiple severe comorbidities; however, given the aggressive nature of BL in the context of advanced HIV infection with high viral load and profound immunosuppression, the attending physician concluded that BL was the most likely primary cause. The secondary cause of death was multiple organ failure, encompassing both renal and hematological dysfunction, reflecting the systemic impact of the disease and the underlying immunodeficiency. This case underscores the critical importance of timely diagnosis and initiation of oncological intervention in HIV-positive patients with suspected cervical malignancy, especially in the context of high-risk lymphoma subtypes such as extra-nodal BL."}
+{"row_index": 30, "doc_id": 38, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 56-year-old female patient with connective tissue disease-associated pulmonary arterial hypertension (CTD-PAH) was diagnosed in July 2013 with Sjögren’s syndrome complicated by interstitial lung disease (ILD) and pulmonary arterial hypertension (PAH). Initial clinical evaluation revealed dyspnea, productive cough with yellow sputum, and findings on chest X-ray consistent with interstitial thickening, costophrenic angle blunting, and cardiomegaly. Echocardiography demonstrated a pulmonary artery systolic pressure of 99 mmHg, right atrial and ventricular enlargement, a D-shaped left ventricle, and severe tricuspid regurgitation. Computed tomography of the chest (CNYCT) showed an enlarged pulmonary trunk, right atrium, and right ventricle, supporting the diagnosis of pulmonary hypertension. Objective signs of Sjögren’s syndrome included dry mouth, dry eyes, cracked tongue mucosa (Schirmer’s test <5 mm), positive minor salivary gland biopsy, impaired salivary gland function on nuclear medicine scan, and a positive anti-Ro antibody test. The patient was initiated on sildenafil (Revatio) 20 mg three times daily (TID) for PAH management, with addition of bosentan (Tracleer) in 2016 due to disease progression. Right heart catheterization (RHC) in 2017 confirmed pre-capillary, group I PAH with a mean pulmonary arterial pressure (PAP) of 39 mmHg, pulmonary vascular resistance (PVR) of approximately 15 Woods, and a wedge pressure of 4 mmHg, consistent with chronic pulmonary hypertension and right heart strain. Based on these findings, the patient was eligible for opsumit (macitentan) 10 mg once daily (QD), which replaced bosentan in 2017. From 2017 to 2020, she required repeated hospitalizations for corticosteroid therapy to manage active Sjögren’s syndrome. Prior to 2017, her PAH was classified as low to intermediate risk and managed with dual therapy (sildenafil and macitentan), with stable disease progression. However, in October 2020, she presented with worsening dyspnea, cough, and white sputum, suggestive of respiratory infection. On November 10, 2020, she developed acute severe dyspnea, cold sweats, cyanosis, and SpO2 of 70%, requiring 100% oxygen via face tent. Blood gas analysis revealed a lactate level of 5.2 mmol/L and brain natriuretic peptide (BNP) exceeding 10,000 pg/mL, indicating cardiogenic shock. She was intubated, admitted to the intensive care unit (ICU), and initiated on four pulmonary vasodilator agents. Her condition stabilized, with successful weaning from vasopressors on November 13, extubation on November 14, and transfer to a general ward on November 21, with oxygen support tapered to nasal cannula at 2 L/min. Follow-up RHC continued to demonstrate elevated pulmonary artery pressure, reflecting persistent right heart strain and likely progression toward right heart failure. The patient was subsequently referred to National Taiwan University Hospital for evaluation for heart-lung transplantation. Over time, her 6-minute walk distance progressively declined, and her pulmonary artery pressure trajectory showed a steady upward trend, leading to current classification as high-risk. Despite stabilization, dyspnea remains her primary clinical complaint. Physical examination revealed mild rhonchi consistent with ILD and a pansystolic murmur indicative of severe valvular heart disease. In 2020, ventavis (iloprost) 10 mcg/ml in 2 ml was added to her regimen. Molecular hydrogen therapy (1 capsule/day) was initiated in May 2023 using PURE HYDROGEN capsules manufactured by HoHo Biotech Co., Ltd. (Taipei, Taiwan, ROC). Each capsule contains 170 mg of hydrogen-rich coral calcium with 1.7×10²¹ hydrogen molecules, equivalent to 24 cups of water at 1,200 ppb hydrogen or 0.6 mM hydrogen per 200 ml of water. Adjuvant administration of hydrogen therapy was associated with significant immunomodulatory effects: flow cytometry and serological analyses revealed an increase in CD127+ regulatory T cells (Tregs), a reduction in anti-Ro autoantibody titers, and a decrease in B cell subsets. These changes were assessed via standardized fluorescent dye and antibody reagent kits (Beckman Coulter, Brea, CA, USA) using immun", "generated_text": "{\n  \"proficient_health_literacy\": \"A 56-year-old female patient with connective tissue disease-associated pulmonary arterial hypertension (CTD-PAH) was diagnosed in July 2013 with Sjögren’s syndrome complicated by interstitial lung disease (ILD) and pulmonary arterial hypertension (PAH). Initial clinical evaluation revealed dyspnea, productive cough with yellow sputum, and findings on chest X-ray consistent with interstitial thickening, costophrenic angle blunting, and cardiomegaly. Echocardiography demonstrated a pulmonary artery systolic pressure of 99 mmHg, right atrial and ventricular enlargement, a D-shaped left ventricle, and severe tricuspid regurgitation. Computed tomography of the chest (CNYCT) showed an enlarged pulmonary trunk, right atrium, and right ventricle, supporting the diagnosis of pulmonary hypertension. Objective signs of Sjögren’s syndrome included dry mouth, dry eyes, cracked tongue mucosa (Schirmer’s test <5 mm), positive minor salivary gland biopsy, impaired salivary gland function on nuclear medicine scan, and a positive anti-Ro antibody test. The patient was initiated on sildenafil (Revatio) 20 mg three times daily (TID) for PAH management, with addition of bosentan (Tracleer) in 2016 due to disease progression. Right heart catheterization (RHC) in 2017 confirmed pre-capillary, group I PAH with a mean pulmonary arterial pressure (PAP) of 39 mmHg, pulmonary vascular resistance (PVR) of approximately 15 Woods, and a wedge pressure of 4 mmHg, consistent with chronic pulmonary hypertension and right heart strain. Based on these findings, the patient was eligible for opsumit (macitentan) 10 mg once daily (QD), which replaced bosentan in 2017. From 2017 to 2020, she required repeated hospitalizations for corticosteroid therapy to manage active Sjögren’s syndrome. Prior to 2017, her PAH was classified as low to intermediate risk and managed with dual therapy (sildenafil and macitentan), with stable disease progression. However, in October 2020, she presented with worsening dyspnea, cough, and white sputum, suggestive of respiratory infection. On November 10, 2020, she developed acute severe dyspnea, cold sweats, cyanosis, and SpO2 of 70%, requiring 100% oxygen via face tent. Blood gas analysis revealed a lactate level of 5.2 mmol/L and brain natriuretic peptide (BNP) exceeding 10,000 pg/mL, indicating cardiogenic shock. She was intubated, admitted to the intensive care unit (ICU), and initiated on four pulmonary vasodilator agents. Her condition stabilized, with successful weaning from vasopressors on November 13, extubation on November 14, and transfer to a general ward on November 21, with oxygen support tapered to nasal cannula at 2 L/min. Follow-up RHC continued to demonstrate elevated pulmonary artery pressure, reflecting persistent right heart strain and likely progression toward right heart failure. The patient was subsequently referred to National Taiwan University Hospital for evaluation for heart-lung transplantation. Over time, her 6-minute walk distance progressively declined, and her pulmonary artery pressure trajectory showed a steady upward trend, leading to current classification as high-risk. Despite stabilization, dyspnea remains her primary clinical complaint. Physical examination revealed mild rhonchi consistent with ILD and a pansystolic murmur indicative of severe valvular heart disease. In 2020, ventavis (iloprost) 10 mcg/ml in 2 ml was added to her regimen. Molecular hydrogen therapy (1 capsule/day) was initiated in May 2023 using PURE HYDROGEN capsules manufactured by HoHo Biotech Co., Ltd. (Taipei, Taiwan, ROC). Each capsule contains 170 mg of hydrogen-rich coral calcium with 1.7×10²¹ hydrogen molecules, equivalent to 24 cups of water at 1,200 ppb hydrogen or 0.6 mM hydrogen per 200 ml of water. Adjuvant administration of hydrogen therapy was associated with significant immunomodulatory effects: flow cytometry and serological analyses revealed an increase in CD127+ regulatory T cells (Tregs), a reduction in anti-Ro autoantibody titers, and a decrease in B cell subsets. These changes were assessed via standardized fluorescent dye and antibody reagent kits (Beckman Coulter, Brea, CA, USA) using immun"}
+{"row_index": 31, "doc_id": 39, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 45-year-old man came in sick with pneumonia caused by the SARS-CoV-2 virus. He had no history of brain problems before. After 16 days in the hospital, he suddenly became confused and had strange eye movements, muscle jerks on one side of his face and chest, and then a full seizure. After that, he had weakness on his left side. Tests showed the virus was in his brain fluid, which means it may have spread to his brain. But over time, his symptoms got better, and he fully recovered. He was able to go home after 31 days with no need for medicine to stop seizures and will see his doctor for follow-up.\"\n}", "generated_text": "A 45-year-old man came in sick with pneumonia caused by the SARS-CoV-2 virus. He had no history of brain problems before. After 16 days in the hospital, he suddenly became confused and had strange eye movements, muscle jerks on one side of his face and chest, and then a full seizure. After that, he had weakness on his left side. Tests showed the virus was in his brain fluid, which means it may have spread to his brain. But over time, his symptoms got better, and he fully recovered. He was able to go home after 31 days with no need for medicine to stop seizures and will see his doctor for follow-up."}
+{"row_index": 32, "doc_id": 39, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 45-year-old man was admitted to the hospital with pneumonia caused by SARS-CoV-2, a virus that causes COVID-19. He had no prior neurological problems. After 16 days in the hospital, he suddenly developed a change in consciousness, with his eyes turning toward the right and strange, brief jerking movements on his left side (face and chest). This was followed by a full seizure, and he ended up with weakness on his left side that didn’t go away. Tests showed the virus was present in his cerebrospinal fluid, which is the fluid around the brain and spinal cord. This finding suggested the virus had affected his brain, possibly causing encephalitis. However, there was no sign of bacterial infection or other common causes of seizures. The patient’s condition gradually improved, and by day 31, he was able to leave the hospital without needing anti-seizure medication. His recovery was considered favorable, and follow-up care was arranged.\"\n}", "generated_text": "A 45-year-old man was admitted to the hospital with pneumonia caused by SARS-CoV-2, a virus that causes COVID-19. He had no prior neurological problems. After 16 days in the hospital, he suddenly developed a change in consciousness, with his eyes turning toward the right and strange, brief jerking movements on his left side (face and chest). This was followed by a full seizure, and he ended up with weakness on his left side that didn’t go away. Tests showed the virus was present in his cerebrospinal fluid, which is the fluid around the brain and spinal cord. This finding suggested the virus had affected his brain, possibly causing encephalitis. However, there was no sign of bacterial infection or other common causes of seizures. The patient’s condition gradually improved, and by day 31, he was able to leave the hospital without needing anti-seizure medication. His recovery was considered favorable, and follow-up care was arranged."}
+{"row_index": 33, "doc_id": 39, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 45-year-old male, born in Pakistan and residing in Portugal for seven years, was admitted with a history of grade 3 obesity and no other significant comorbidities or pharmacological therapy. He presented to emergency care with a four-day course of fever, dry cough, dyspnea, chest pain, dysgeusia, headache, and myalgia. On initial neurological examination, no abnormalities were noted. Respiratory evaluation revealed tachypnea and bilateral rough vesicular murmurs on auscultation, consistent with diffuse pulmonary involvement. Laboratory findings showed mild elevation in inflammatory markers and type 1 respiratory failure under FiO2 of 21%, with extensive bilateral, peripheral, and basal opacities on chest radiography. A positive reverse-transcription real-time polymerase chain reaction (RT-PCR) for SARS-CoV-2 was obtained from nasal and oropharyngeal exudates, while tests for influenza A/B, Streptococcus pneumoniae, and Legionella pneumophila were negative, supporting a diagnosis of SARS-CoV-2-associated pneumonia.\\n\\nOver the first 48 hours, progressive deterioration in fatigue, dyspnea, and respiratory function necessitated escalation of oxygen therapy. Noninvasive ventilation was initiated but discontinued due to poor patient adherence; high-flow oxygen via nasal cannula was then implemented without clinical benefit. The patient was subsequently transferred to a level III intensive care unit (ICU), where sedoanalgesia was administered and orotracheal intubation with invasive mechanical ventilation was performed.\\n\\nOn day 11 of hospitalization, the patient received remdesivir, dexamethasone, enoxaparin, and empirical antibiotic therapy (amoxicillin/clavulanic acid and azithromycin) on suspicion of secondary bacterial superinfection. Despite persistent fever refractory to antipyretics, inflammatory markers improved by day 3 of ICU admission. To rule out alternative infectious etiologies, intravenous lines were replaced, and blood cultures, catheter tip cultures, bronchial secretions, urinalysis, urine culture, and transthoracic echocardiography were performed. Only one positive blood culture was obtained: Klebsiella pneumoniae, which is susceptible to amoxicillin/clavulanic acid—antibiotic therapy already in use. Echocardiography revealed hypokinesia of the lateral wall and left ventricular apex, with impaired biventricular function, and mild elevation in troponin (1.8 ng/mL) along with ST-segment depression in leads I and aVL, consistent with acute coronary syndrome or septic cardiomyopathy. Noninfectious causes of fever, including neuroleptic use and thyroid dysfunction, were ruled out.\\n\\nInotropic support with dobutamine was required during ventilatory weaning and post-extubation phases. On day 16 of hospitalization (day 19 of symptom onset), the patient experienced a sudden alteration in consciousness, conjugate gaze deviation to the right, left-sided myoclonus involving the face and thoracic region, followed by a generalized tonic-clonic seizure, which was terminated with midazolam. Hypoxic-ischemic etiology was excluded due to sustained normotension, absence of peri-event hypoxemia or hypoxia, normal serum lactate levels, and preserved diuresis. Electrolyte and glucose levels were within normal limits, ruling out metabolic or ionic triggers for the seizure.\\n\\nPost-ictal assessment revealed a Glasgow Coma Scale (GCS) of 7 (no eye opening, no verbal response, no localizing to pain), with persistent left hemiparesis of grade 3/5. Due to airway compromise, the patient remained intubated and received anticonvulsant therapy. Lumbar puncture was performed, yielding turbid cerebrospinal fluid (CSF) with mild proteinorrachia but no pleocytosis and normal opening pressure. CSF was tested for neurotropic viruses, venereal disease research laboratory (VDRL) activity, acid-alcohol resistant bacteria, and SARS-CoV-2 via RT-PCR; the latter was positive, confirming the presence of SARS-CoV-2 RNA in CSF without pleocytosis. This finding excluded bacterial meningitis and supported a diagnosis of SARS-CoV-2 encephalitis. Electroencephalography (EEG), performed 1 hour after propofol administration under fentanyl, lasted 13 minutes and showed no epileptiform activity. MRI performed on day 17 revealed multiple artifacts attributable to patient movement, necessitating repeat imaging.\\n\\nFollowing discontinuation of sedoanalgesia, the patient exhibited a gradual improvement in mental status with a GCS of 14, persistent left hemiparesis (muscle strength grade", "generated_text": "{\n  \"proficient_health_literacy\": \"A 45-year-old male, born in Pakistan and residing in Portugal for seven years, was admitted with a history of grade 3 obesity and no other significant comorbidities or pharmacological therapy. He presented to emergency care with a four-day course of fever, dry cough, dyspnea, chest pain, dysgeusia, headache, and myalgia. On initial neurological examination, no abnormalities were noted. Respiratory evaluation revealed tachypnea and bilateral rough vesicular murmurs on auscultation, consistent with diffuse pulmonary involvement. Laboratory findings showed mild elevation in inflammatory markers and type 1 respiratory failure under FiO2 of 21%, with extensive bilateral, peripheral, and basal opacities on chest radiography. A positive reverse-transcription real-time polymerase chain reaction (RT-PCR) for SARS-CoV-2 was obtained from nasal and oropharyngeal exudates, while tests for influenza A/B, Streptococcus pneumoniae, and Legionella pneumophila were negative, supporting a diagnosis of SARS-CoV-2-associated pneumonia.\\n\\nOver the first 48 hours, progressive deterioration in fatigue, dyspnea, and respiratory function necessitated escalation of oxygen therapy. Noninvasive ventilation was initiated but discontinued due to poor patient adherence; high-flow oxygen via nasal cannula was then implemented without clinical benefit. The patient was subsequently transferred to a level III intensive care unit (ICU), where sedoanalgesia was administered and orotracheal intubation with invasive mechanical ventilation was performed.\\n\\nOn day 11 of hospitalization, the patient received remdesivir, dexamethasone, enoxaparin, and empirical antibiotic therapy (amoxicillin/clavulanic acid and azithromycin) on suspicion of secondary bacterial superinfection. Despite persistent fever refractory to antipyretics, inflammatory markers improved by day 3 of ICU admission. To rule out alternative infectious etiologies, intravenous lines were replaced, and blood cultures, catheter tip cultures, bronchial secretions, urinalysis, urine culture, and transthoracic echocardiography were performed. Only one positive blood culture was obtained: Klebsiella pneumoniae, which is susceptible to amoxicillin/clavulanic acid—antibiotic therapy already in use. Echocardiography revealed hypokinesia of the lateral wall and left ventricular apex, with impaired biventricular function, and mild elevation in troponin (1.8 ng/mL) along with ST-segment depression in leads I and aVL, consistent with acute coronary syndrome or septic cardiomyopathy. Noninfectious causes of fever, including neuroleptic use and thyroid dysfunction, were ruled out.\\n\\nInotropic support with dobutamine was required during ventilatory weaning and post-extubation phases. On day 16 of hospitalization (day 19 of symptom onset), the patient experienced a sudden alteration in consciousness, conjugate gaze deviation to the right, left-sided myoclonus involving the face and thoracic region, followed by a generalized tonic-clonic seizure, which was terminated with midazolam. Hypoxic-ischemic etiology was excluded due to sustained normotension, absence of peri-event hypoxemia or hypoxia, normal serum lactate levels, and preserved diuresis. Electrolyte and glucose levels were within normal limits, ruling out metabolic or ionic triggers for the seizure.\\n\\nPost-ictal assessment revealed a Glasgow Coma Scale (GCS) of 7 (no eye opening, no verbal response, no localizing to pain), with persistent left hemiparesis of grade 3/5. Due to airway compromise, the patient remained intubated and received anticonvulsant therapy. Lumbar puncture was performed, yielding turbid cerebrospinal fluid (CSF) with mild proteinorrachia but no pleocytosis and normal opening pressure. CSF was tested for neurotropic viruses, venereal disease research laboratory (VDRL) activity, acid-alcohol resistant bacteria, and SARS-CoV-2 via RT-PCR; the latter was positive, confirming the presence of SARS-CoV-2 RNA in CSF without pleocytosis. This finding excluded bacterial meningitis and supported a diagnosis of SARS-CoV-2 encephalitis. Electroencephalography (EEG), performed 1 hour after propofol administration under fentanyl, lasted 13 minutes and showed no epileptiform activity. MRI performed on day 17 revealed multiple artifacts attributable to patient movement, necessitating repeat imaging.\\n\\nFollowing discontinuation of sedoanalgesia, the patient exhibited a gradual improvement in mental status with a GCS of 14, persistent left hemiparesis (muscle strength grade"}
+{"row_index": 34, "doc_id": 40, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"The person had a long-lasting cough, ear pain, and a foul-smelling pus coming out of their right ear. Tests found bacteria that cause tuberculosis in the stomach fluid and in the ear pus. This means they had tuberculosis in both their lungs and middle ear, especially because their immune system was weak from HIV. They were treated with medicine for 6 months to fight the tuberculosis, along with extra medicines to help their body heal. After 6 months, the cough and ear symptoms went away, and no bacteria were found in the ear or stomach. They also started taking HIV medicine again and got better overall. Now they are fully healed and healthy.\"\n}", "generated_text": "The person had a long-lasting cough, ear pain, and a foul-smelling pus coming out of their right ear. Tests found bacteria that cause tuberculosis in the stomach fluid and in the ear pus. This means they had tuberculosis in both their lungs and middle ear, especially because their immune system was weak from HIV. They were treated with medicine for 6 months to fight the tuberculosis, along with extra medicines to help their body heal. After 6 months, the cough and ear symptoms went away, and no bacteria were found in the ear or stomach. They also started taking HIV medicine again and got better overall. Now they are fully healed and healthy."}
+{"row_index": 35, "doc_id": 40, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"The patient had a long-lasting cough, ear pain, and a chronic foul-smelling discharge from the right ear. Tests found acid-fast bacteria in the fluid from the stomach and in the pus from the ear, which pointed to tuberculosis. The patient also had HIV, which weakened his immune system, making him more susceptible to tuberculosis. He was treated with a 6-month course of anti-tuberculosis medication, including four drugs in the first two months, followed by two drugs for the next four months. He also received treatment for HIV again, and was given antibiotics to prevent complications. After treatment, his symptoms fully improved, the bacteria tests became negative, and his overall health returned to normal. His HIV virus levels dropped significantly, showing the treatment was effective.\"\n}", "generated_text": "The patient had a long-lasting cough, ear pain, and a chronic foul-smelling discharge from the right ear. Tests found acid-fast bacteria in the fluid from the stomach and in the pus from the ear, which pointed to tuberculosis. The patient also had HIV, which weakened his immune system, making him more susceptible to tuberculosis. He was treated with a 6-month course of anti-tuberculosis medication, including four drugs in the first two months, followed by two drugs for the next four months. He also received treatment for HIV again, and was given antibiotics to prevent complications. After treatment, his symptoms fully improved, the bacteria tests became negative, and his overall health returned to normal. His HIV virus levels dropped significantly, showing the treatment was effective."}
+{"row_index": 36, "doc_id": 40, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 32-year-old male baker from Bamako, Mali, was admitted to the Infectious and Tropical Diseases department of CHU du Point G on 27 April 2023 with a chronic productive cough, otalgia, and a persistent right-sided purulent otorrhea of progressive onset over one month. Initial management at a local medical center included artésunate, paracetamol, and unspecified antibiotics for suspected malaria and acute otitis media, which failed to resolve the symptoms. The patient is HIV-1 infected, with a diagnosis established 7 months prior, and has been on a triple antiretroviral therapy (TARV) regimen of tenofovir/lamivudine/dolutegravir; however, adherence to this regimen has been poor due to denial of his HIV status.\\n\\nPhysical examination revealed a fever of 38.2 °C, altered general condition, right-sided otalgia, purulent foul-smelling otorrhea, and a right basal pulmonary condensation consistent with bronchovascular hyperactivity. Neurological examination was normal, with no cranial nerve involvement, particularly the facial (VII) and cochleovestibular (VIII) nerves. Otoscopic evaluation of the right ear demonstrated inflammatory changes in the external auditory canal with purulent exudate and a single tympanic membrane perforation in the anterior-inferior quadrant; the left ear was intact. Rinne and Weber tests confirmed a right conductive hearing loss.\\n\\nImmunological and virological assessments showed a CD4 count of 118 cells/μL and a viral load of 12,370 copies/mL at the time of HIV diagnosis. Following 6 months of ART, the CD4 count increased to 193 cells/μL and the viral load decreased to 9,460 copies/mL. At the time of tuberculosis diagnosis (7 months post-HIV diagnosis), the CD4 count declined to 89 cells/μL and the viral load was 10,230 copies/mL, reflecting immunosuppression conducive to opportunistic infections.\\n\\nMicrobiological testing via Ziehl-Neelsen bacilloscopy was positive for acid-fast bacilli in gastric washings upon admission and again 19 days later in a right ear swab due to persistent otorrhea. The Xpert-MTB/GeneXpert assay, which detects *Mycobacterium tuberculosis* and rifampicin resistance, was negative for rifampicin resistance, indicating susceptibility to first-line anti-tuberculosis agents.\\n\\nChest radiography revealed an accentuated bronchovascular network at the base of the right lung, consistent with pulmonary tuberculosis. The clinical and radiological findings, combined with the positive acid-fast bacilli in both gastric fluid and ear pus, support a diagnosis of concurrent middle ear tuberculosis and pulmonary tuberculosis in the context of HIV-induced immunosuppression.\\n\\nThe patient was initiated on a 6-month standard first-line anti-tuberculosis regimen: an intensive phase of quadruple therapy (isoniazid, rifampicin, pyrazinamide, and ethambutol) for 2 months (2RHZE), followed by a maintenance phase of dual therapy (isoniazid and rifampicin) for 4 months (4RH) at a dose of 3 tablets/day in the morning on an empty stomach, supplemented with vitamin B6 (1 tablet/day) to prevent peripheral neuropathy. Concurrently, the patient received two therapeutic intensifications of antiretroviral therapy (ART) to improve HIV suppression. ART was restarted on 4 May 2023 with patient consent, using tenofovir/lamivudine/dolutegravir (1 tablet/day) plus an additional dolutegravir 50 mg tablet (1 tablet/day) in accordance with current HIV management guidelines. Chemoprophylaxis with cotrimoxazole (960 mg once daily) was administered, and the external auditory canal was cleaned via aspiration, with ciprofloxacin ear drops (2 drops, three times daily) administered for 14 days to manage ear infection.\\n\\nClinical improvement was observed within 14 days of treatment, including resolution of fever, improvement in general condition, and amelioration of cough and otorrhea. Bacilloscopy became negative in both the gastric washings and the right ear pus swab. At the end of the 6-month anti-tuberculosis treatment, complete clinical healing was achieved, with normalization of ENT and neurological examinations. Follow-up bacilloscopy and Xpert-MTB/GeneXpert testing were negative at the end of the intensive phase (month 2), at month 5, and at the end of the maintenance phase (month 6). Post-treatment", "generated_text": "{\n  \"proficient_health_literacy\": \"A 32-year-old male baker from Bamako, Mali, was admitted to the Infectious and Tropical Diseases department of CHU du Point G on 27 April 2023 with a chronic productive cough, otalgia, and a persistent right-sided purulent otorrhea of progressive onset over one month. Initial management at a local medical center included artésunate, paracetamol, and unspecified antibiotics for suspected malaria and acute otitis media, which failed to resolve the symptoms. The patient is HIV-1 infected, with a diagnosis established 7 months prior, and has been on a triple antiretroviral therapy (TARV) regimen of tenofovir/lamivudine/dolutegravir; however, adherence to this regimen has been poor due to denial of his HIV status.\\n\\nPhysical examination revealed a fever of 38.2 °C, altered general condition, right-sided otalgia, purulent foul-smelling otorrhea, and a right basal pulmonary condensation consistent with bronchovascular hyperactivity. Neurological examination was normal, with no cranial nerve involvement, particularly the facial (VII) and cochleovestibular (VIII) nerves. Otoscopic evaluation of the right ear demonstrated inflammatory changes in the external auditory canal with purulent exudate and a single tympanic membrane perforation in the anterior-inferior quadrant; the left ear was intact. Rinne and Weber tests confirmed a right conductive hearing loss.\\n\\nImmunological and virological assessments showed a CD4 count of 118 cells/μL and a viral load of 12,370 copies/mL at the time of HIV diagnosis. Following 6 months of ART, the CD4 count increased to 193 cells/μL and the viral load decreased to 9,460 copies/mL. At the time of tuberculosis diagnosis (7 months post-HIV diagnosis), the CD4 count declined to 89 cells/μL and the viral load was 10,230 copies/mL, reflecting immunosuppression conducive to opportunistic infections.\\n\\nMicrobiological testing via Ziehl-Neelsen bacilloscopy was positive for acid-fast bacilli in gastric washings upon admission and again 19 days later in a right ear swab due to persistent otorrhea. The Xpert-MTB/GeneXpert assay, which detects *Mycobacterium tuberculosis* and rifampicin resistance, was negative for rifampicin resistance, indicating susceptibility to first-line anti-tuberculosis agents.\\n\\nChest radiography revealed an accentuated bronchovascular network at the base of the right lung, consistent with pulmonary tuberculosis. The clinical and radiological findings, combined with the positive acid-fast bacilli in both gastric fluid and ear pus, support a diagnosis of concurrent middle ear tuberculosis and pulmonary tuberculosis in the context of HIV-induced immunosuppression.\\n\\nThe patient was initiated on a 6-month standard first-line anti-tuberculosis regimen: an intensive phase of quadruple therapy (isoniazid, rifampicin, pyrazinamide, and ethambutol) for 2 months (2RHZE), followed by a maintenance phase of dual therapy (isoniazid and rifampicin) for 4 months (4RH) at a dose of 3 tablets/day in the morning on an empty stomach, supplemented with vitamin B6 (1 tablet/day) to prevent peripheral neuropathy. Concurrently, the patient received two therapeutic intensifications of antiretroviral therapy (ART) to improve HIV suppression. ART was restarted on 4 May 2023 with patient consent, using tenofovir/lamivudine/dolutegravir (1 tablet/day) plus an additional dolutegravir 50 mg tablet (1 tablet/day) in accordance with current HIV management guidelines. Chemoprophylaxis with cotrimoxazole (960 mg once daily) was administered, and the external auditory canal was cleaned via aspiration, with ciprofloxacin ear drops (2 drops, three times daily) administered for 14 days to manage ear infection.\\n\\nClinical improvement was observed within 14 days of treatment, including resolution of fever, improvement in general condition, and amelioration of cough and otorrhea. Bacilloscopy became negative in both the gastric washings and the right ear pus swab. At the end of the 6-month anti-tuberculosis treatment, complete clinical healing was achieved, with normalization of ENT and neurological examinations. Follow-up bacilloscopy and Xpert-MTB/GeneXpert testing were negative at the end of the intensive phase (month 2), at month 5, and at the end of the maintenance phase (month 6). Post-treatment"}
+{"row_index": 37, "doc_id": 41, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 16-month-old boy had a weak heart and was put on a list for a heart transplant. At 20 months, he got a special machine outside his body to help his heart work (called a Berlin Heart). At 23 months, he had a stroke on the left side of his brain, which caused weakness on his right side. Doctors used a special tube to clear the blocked blood vessel and fixed it successfully. The boy was small for his age but healthy. One month after the stroke, he had a successful heart transplant. The only lasting effect from the stroke was a bit of stiffness in his right arm.\"\n}", "generated_text": "A 16-month-old boy had a weak heart and was put on a list for a heart transplant. At 20 months, he got a special machine outside his body to help his heart work (called a Berlin Heart). At 23 months, he had a stroke on the left side of his brain, which caused weakness on his right side. Doctors used a special tube to clear the blocked blood vessel and fixed it successfully. The boy was small for his age but healthy. One month after the stroke, he had a successful heart transplant. The only lasting effect from the stroke was a bit of stiffness in his right arm."}
+{"row_index": 38, "doc_id": 41, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 23-month-old male with a history of hypoxic-ischaemic encephalopathy at birth and preserved brain motor potential, exhibiting normal psychomotor development, was diagnosed with restrictive cardiomyopathy and enrolled in a cardiac transplant programme at 16 months of age. He received external biventricular support via an implantable Berlin Heart device to bridge to transplantation. To mitigate the risk of embolic complications, he was maintained on dual antiplatelet and anticoagulant therapy, including full-dose heparin, resulting in an activated partial thromboplastin time (APTT) of 93 seconds and an international normalised ratio (INR) of 1.08. At 23 months, he presented with acute disconnection and right hemiparesis, consistent with a left middle cerebral artery (MCA) occlusion. Non-contrast computed tomography (CT) revealed a hyperdense left MCA, indicative of thrombus, and a chronic right parietotemporal infarct, suggesting prior ischemic injury. Laboratory parameters showed red blood cell count of 4.16 × 10⁶ µ/L and hemoglobin of 11.4 g/dL, within normal limits. Intravenous thrombolytic therapy was contraindicated due to active anticoagulation. Consequently, an intra-arterial mechanical thrombectomy was performed under general anaesthesia. The procedure involved puncture of the right femoral artery and placement of an 11 cm long 4F sheath (Cordis, Ireland). A 4F vertebral Radiofocus catheter (Glidecath, Terumo, Belgium) was advanced to confirm occlusion of the M1 segment of the left MCA. Recanalisation was achieved using a 3 mm × 20 mm Trevo XP Pro Vue stentriever (Stryker, The Netherlands), guided by the vertebral catheter as a tutor and positioned within the petrous segment of the internal carotid artery. A straight Rapid Transit microcatheter (Codman Neurovascular, UK) was used to navigate and open the occluded vessel in a single pass. The entire system—including tutor catheter, microcatheter, and stentriever—was removed simultaneously. During the procedural control run, an iatrogenic dissection of the left internal carotid artery was identified, which was asymptomatic and did not compromise perfusion, as the left hemisphere remained adequately supplied via the anterior communicating artery. Post-procedure, the patient underwent successful cardiac transplantation one month later. Neurologically, the only persistent long-term sequelae were spasticity of the right upper limb, consistent with residual corticospinal tract dysfunction following the stroke. The case demonstrates the feasibility and clinical efficacy of intra-arterial mechanical thrombectomy in a young pediatric patient with complex comorbidities, including congenital cardiomyopathy and anticoagulated state, and highlights the importance of meticulous vascular mapping and perfusion monitoring during such interventions.\"\n}", "generated_text": "A 23-month-old male with a history of hypoxic-ischaemic encephalopathy at birth and preserved brain motor potential, exhibiting normal psychomotor development, was diagnosed with restrictive cardiomyopathy and enrolled in a cardiac transplant programme at 16 months of age. He received external biventricular support via an implantable Berlin Heart device to bridge to transplantation. To mitigate the risk of embolic complications, he was maintained on dual antiplatelet and anticoagulant therapy, including full-dose heparin, resulting in an activated partial thromboplastin time (APTT) of 93 seconds and an international normalised ratio (INR) of 1.08. At 23 months, he presented with acute disconnection and right hemiparesis, consistent with a left middle cerebral artery (MCA) occlusion. Non-contrast computed tomography (CT) revealed a hyperdense left MCA, indicative of thrombus, and a chronic right parietotemporal infarct, suggesting prior ischemic injury. Laboratory parameters showed red blood cell count of 4.16 × 10⁶ µ/L and hemoglobin of 11.4 g/dL, within normal limits. Intravenous thrombolytic therapy was contraindicated due to active anticoagulation. Consequently, an intra-arterial mechanical thrombectomy was performed under general anaesthesia. The procedure involved puncture of the right femoral artery and placement of an 11 cm long 4F sheath (Cordis, Ireland). A 4F vertebral Radiofocus catheter (Glidecath, Terumo, Belgium) was advanced to confirm occlusion of the M1 segment of the left MCA. Recanalisation was achieved using a 3 mm × 20 mm Trevo XP Pro Vue stentriever (Stryker, The Netherlands), guided by the vertebral catheter as a tutor and positioned within the petrous segment of the internal carotid artery. A straight Rapid Transit microcatheter (Codman Neurovascular, UK) was used to navigate and open the occluded vessel in a single pass. The entire system—including tutor catheter, microcatheter, and stentriever—was removed simultaneously. During the procedural control run, an iatrogenic dissection of the left internal carotid artery was identified, which was asymptomatic and did not compromise perfusion, as the left hemisphere remained adequately supplied via the anterior communicating artery. Post-procedure, the patient underwent successful cardiac transplantation one month later. Neurologically, the only persistent long-term sequelae were spasticity of the right upper limb, consistent with residual corticospinal tract dysfunction following the stroke. The case demonstrates the feasibility and clinical efficacy of intra-arterial mechanical thrombectomy in a young pediatric patient with complex comorbidities, including congenital cardiomyopathy and anticoagulated state, and highlights the importance of meticulous vascular mapping and perfusion monitoring during such interventions."}
+{"row_index": 39, "doc_id": 42, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 52-year-old man came to the hospital after having a seizure due to drinking too much alcohol. He also had a shoulder injury on his right side that wasn't caught before. When doctors checked him, they found a broken shoulder on his left side too — a problem that wasn’t seen at the first hospital. The injury got worse in the left shoulder because he was held down and moved too much during his stay. Doctors used X-rays and CT scans to see the damage. They fixed both shoulders at the same time with metal plates and strong stitches. The right shoulder healed well, but the left one needed two more surgeries — one to fix the broken piece and another to open up the joint. Two years later, he can move his shoulders a lot better, with a score of 5% on a pain scale and 72 and 76 on a mobility scale for left and right shoulders, which means he’s doing better than most people in similar cases.\"\n}", "generated_text": "A 52-year-old man came to the hospital after having a seizure due to drinking too much alcohol. He also had a shoulder injury on his right side that wasn't caught before. When doctors checked him, they found a broken shoulder on his left side too — a problem that wasn’t seen at the first hospital. The injury got worse in the left shoulder because he was held down and moved too much during his stay. Doctors used X-rays and CT scans to see the damage. They fixed both shoulders at the same time with metal plates and strong stitches. The right shoulder healed well, but the left one needed two more surgeries — one to fix the broken piece and another to open up the joint. Two years later, he can move his shoulders a lot better, with a score of 5% on a pain scale and 72 and 76 on a mobility scale for left and right shoulders, which means he’s doing better than most people in similar cases."}
+{"row_index": 40, "doc_id": 42, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 52-year-old man was brought to a specialized hospital after having a seizure caused by alcohol withdrawal and a dislocated shoulder on his right side. When first evaluated, he had visible bruising on both shoulders and limited ability to move his arms, especially rotating them outward. He was physically restrained due to agitation.\\n\\nInitial X-rays showed a dislocation in his right shoulder and a simple posterior dislocation in his left shoulder — a problem that had not been seen at the previous hospital. A follow-up CT scan revealed that the left shoulder injury had worsened since admission, likely because of the physical restraint. Both shoulders were surgically treated at the same time with a procedure called open reduction and internal fixation using locked plates to realign and stabilize the bones.\\n\\nThe right shoulder had a fracture that was partially fixed with a screw and strong sutures. The left shoulder had a smaller bone defect, which was filled using a piece of the shoulder bone itself (a technique similar to McLaughlin’s method). However, the left shoulder needed two additional surgeries: one to fix the broken bone properly and another to release the stiff joint.\\n\\nAfter two years, the patient is doing well. He scores 5% on the Quick DASH scale (which measures shoulder pain and function) and 72 and 76 on the Constant scale (which measures shoulder strength and movement) for his left and right shoulders, respectively. He was able to return to work five months after the injury and is now progressing toward full recovery, though his left shoulder still has limited range of motion, especially in external rotation.\"\n}", "generated_text": "A 52-year-old man was brought to a specialized hospital after having a seizure caused by alcohol withdrawal and a dislocated shoulder on his right side. When first evaluated, he had visible bruising on both shoulders and limited ability to move his arms, especially rotating them outward. He was physically restrained due to agitation.\n\nInitial X-rays showed a dislocation in his right shoulder and a simple posterior dislocation in his left shoulder — a problem that had not been seen at the previous hospital. A follow-up CT scan revealed that the left shoulder injury had worsened since admission, likely because of the physical restraint. Both shoulders were surgically treated at the same time with a procedure called open reduction and internal fixation using locked plates to realign and stabilize the bones.\n\nThe right shoulder had a fracture that was partially fixed with a screw and strong sutures. The left shoulder had a smaller bone defect, which was filled using a piece of the shoulder bone itself (a technique similar to McLaughlin’s method). However, the left shoulder needed two additional surgeries: one to fix the broken bone properly and another to release the stiff joint.\n\nAfter two years, the patient is doing well. He scores 5% on the Quick DASH scale (which measures shoulder pain and function) and 72 and 76 on the Constant scale (which measures shoulder strength and movement) for his left and right shoulders, respectively. He was able to return to work five months after the injury and is now progressing toward full recovery, though his left shoulder still has limited range of motion, especially in external rotation."}
+{"row_index": 41, "doc_id": 42, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 52-year-old male with no prior medical history was transferred to a high-complexity trauma center following a tonic-clonic seizure secondary to alcohol withdrawal and a non-reduced right posterior glenohumeral fracture (LFGHP). Upon initial evaluation 24 hours after admission, the patient was conscious but exhibited bilateral shoulder ecchymosis and severe passive external rotation limitation. He was physically restrained due to intermittent psychomotor agitation, with both feet and his left hand secured. Radiographic assessment revealed a right LFGHP and a previously undiagnosed simple posterior glenohumeral dislocation of the left shoulder, which had been missed at the referring facility and was only identified after a 48-hour delay.\\n\\nComputed tomography (CT) of both shoulders demonstrated a significant progression of the left shoulder injury from a simple posterior dislocation on admission to a full LFGHP within 48 hours, likely attributable to mechanical stress from prolonged physical restraint. This intrahospital aggravation underscores the role of external forces in the destabilization of glenohumeral joint integrity, particularly in the setting of altered neuromuscular control.\\n\\nPreoperative imaging of the right shoulder revealed glenoid bone integrity with 40% articular surface involvement of the humeral head, including a large fragment that was amenable to osteosynthesis in continuity with the lesser tuberosity. A 4.0 mm spongy screw with high-strength sutures was planned for fixation to preserve humeral head stability. In contrast, the left shoulder demonstrated intact glenoid bone and a 20% defect in the humeral articular surface, which was addressed via repositioning and fixation of the lesser tuberosity fragment during osteosynthesis, mimicking the surgical technique described by McLaughlin.\\n\\nSurgical intervention consisted of open reduction and internal fixation (ORIF) using bilateral locked plates. The patient was positioned in a beach chair position, and both shoulders were approached via classic deltopectoral incisions. For the right shoulder, a posterior mini-open incision (diagnostic arthroscopy-sized) was used for digital manipulation and reduction of the posterior humeral head fragment. A provisional reduction was achieved using high-strength sutures and needles, followed by fixation with a 4.0 mm spongy screw and high-strength sutures. Definitive stabilization was accomplished with a Philos (Depuy Synthes®) locked plate, with additional fixation of the rotator cuff tendons to the plate to enhance biomechanical stability. The right shoulder was closed in layers and immobilized with a universal shoulder immobilizer.\\n\\nThe left shoulder was operated on immediately after, using the same deltopectoral approach with an accessory posterior portal for digital reduction. Fixation was performed similarly, except that the anterior humeral fragment was stabilized exclusively with high-strength sutures due to insufficient anatomical support for a spongy screw. Postoperative management included bilateral shoulder immobilization for four weeks, followed by a progressive rehabilitation protocol beginning at the second postoperative week. Exercises included pendular flexion-extension of the elbow and fist mobilization, administered as tolerated based on pain levels.\\n\\nAt the one-month radiographic follow-up, loss of reduction of the greater tuberosity was observed in the left shoulder, prompting a revision surgery to achieve adequate fixation using high-strength sutures. The patient continued with immobilization for an additional four weeks on the left side. Bilateral self-administered exercises were resumed from the second postoperative week. At the sixth week post-revision, face-to-face kinesiological therapy was initiated twice weekly. After 30 sessions of structured rehabilitation, the patient returned to work five months following the initial trauma.\\n\\nOne-year follow-up demonstrated full recovery of strength and range of motion in the right shoulder. The left shoulder, however, retained significant limitations, particularly in external rotation. At this point, arthroscopic joint release was performed with removal of the osteosynthesis hardware to address chronic joint contractures and mechanical impingement. Two years post-trauma, the patient demonstrated favorable functional outcomes, with a Quick DASH score of 5%, and Constant scores of 72 and 76 in the left and right shoulders, respectively, indicating sustained improvement in pain, function, and daily activity capacity. These results reflect both the efficacy of early surgical intervention and the importance of staged rehabilitation in managing complex glenohumeral injuries, especially in the context of secondary trauma from restraint and delayed diagnosis.\"\n}", "generated_text": "A 52-year-old male with no prior medical history was transferred to a high-complexity trauma center following a tonic-clonic seizure secondary to alcohol withdrawal and a non-reduced right posterior glenohumeral fracture (LFGHP). Upon initial evaluation 24 hours after admission, the patient was conscious but exhibited bilateral shoulder ecchymosis and severe passive external rotation limitation. He was physically restrained due to intermittent psychomotor agitation, with both feet and his left hand secured. Radiographic assessment revealed a right LFGHP and a previously undiagnosed simple posterior glenohumeral dislocation of the left shoulder, which had been missed at the referring facility and was only identified after a 48-hour delay.\n\nComputed tomography (CT) of both shoulders demonstrated a significant progression of the left shoulder injury from a simple posterior dislocation on admission to a full LFGHP within 48 hours, likely attributable to mechanical stress from prolonged physical restraint. This intrahospital aggravation underscores the role of external forces in the destabilization of glenohumeral joint integrity, particularly in the setting of altered neuromuscular control.\n\nPreoperative imaging of the right shoulder revealed glenoid bone integrity with 40% articular surface involvement of the humeral head, including a large fragment that was amenable to osteosynthesis in continuity with the lesser tuberosity. A 4.0 mm spongy screw with high-strength sutures was planned for fixation to preserve humeral head stability. In contrast, the left shoulder demonstrated intact glenoid bone and a 20% defect in the humeral articular surface, which was addressed via repositioning and fixation of the lesser tuberosity fragment during osteosynthesis, mimicking the surgical technique described by McLaughlin.\n\nSurgical intervention consisted of open reduction and internal fixation (ORIF) using bilateral locked plates. The patient was positioned in a beach chair position, and both shoulders were approached via classic deltopectoral incisions. For the right shoulder, a posterior mini-open incision (diagnostic arthroscopy-sized) was used for digital manipulation and reduction of the posterior humeral head fragment. A provisional reduction was achieved using high-strength sutures and needles, followed by fixation with a 4.0 mm spongy screw and high-strength sutures. Definitive stabilization was accomplished with a Philos (Depuy Synthes®) locked plate, with additional fixation of the rotator cuff tendons to the plate to enhance biomechanical stability. The right shoulder was closed in layers and immobilized with a universal shoulder immobilizer.\n\nThe left shoulder was operated on immediately after, using the same deltopectoral approach with an accessory posterior portal for digital reduction. Fixation was performed similarly, except that the anterior humeral fragment was stabilized exclusively with high-strength sutures due to insufficient anatomical support for a spongy screw. Postoperative management included bilateral shoulder immobilization for four weeks, followed by a progressive rehabilitation protocol beginning at the second postoperative week. Exercises included pendular flexion-extension of the elbow and fist mobilization, administered as tolerated based on pain levels.\n\nAt the one-month radiographic follow-up, loss of reduction of the greater tuberosity was observed in the left shoulder, prompting a revision surgery to achieve adequate fixation using high-strength sutures. The patient continued with immobilization for an additional four weeks on the left side. Bilateral self-administered exercises were resumed from the second postoperative week. At the sixth week post-revision, face-to-face kinesiological therapy was initiated twice weekly. After 30 sessions of structured rehabilitation, the patient returned to work five months following the initial trauma.\n\nOne-year follow-up demonstrated full recovery of strength and range of motion in the right shoulder. The left shoulder, however, retained significant limitations, particularly in external rotation. At this point, arthroscopic joint release was performed with removal of the osteosynthesis hardware to address chronic joint contractures and mechanical impingement. Two years post-trauma, the patient demonstrated favorable functional outcomes, with a Quick DASH score of 5%, and Constant scores of 72 and 76 in the left and right shoulders, respectively, indicating sustained improvement in pain, function, and daily activity capacity. These results reflect both the efficacy of early surgical intervention and the importance of staged rehabilitation in managing complex glenohumeral injuries, especially in the context of secondary trauma from restraint and delayed diagnosis."}
+{"row_index": 42, "doc_id": 43, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 70-year-old man had a weak heart that was leaking badly, so doctors put in a new valve (TAVI) through his chest to fix it. After that, his heart started failing again, so they added a machine (LVAD) to help his heart pump. One year later, the machine was giving warning signs, and scans showed the old valve was still leaking badly. The doctors decided to fix the old valve from the inside with another new valve (valve-in-valve). They slowed down the machine and set the heart to beat 140 times a minute during the procedure. The new valve went in perfectly, and after 12 months, the man is doing great — no more leaks, better heart strength, and can walk much farther without trouble.\"\n}", "generated_text": "A 70-year-old man had a weak heart that was leaking badly, so doctors put in a new valve (TAVI) through his chest to fix it. After that, his heart started failing again, so they added a machine (LVAD) to help his heart pump. One year later, the machine was giving warning signs, and scans showed the old valve was still leaking badly. The doctors decided to fix the old valve from the inside with another new valve (valve-in-valve). They slowed down the machine and set the heart to beat 140 times a minute during the procedure. The new valve went in perfectly, and after 12 months, the man is doing great — no more leaks, better heart strength, and can walk much farther without trouble."}
+{"row_index": 43, "doc_id": 43, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 70-year-old man with severe heart valve problems was treated first with a procedure called transcatheter aortic valve implantation (TAVI) from the apex of his heart. He had a condition called aortic regurgitation, where blood leaks backward through the aortic valve, caused by past heart infection. Because his heart function was very weak and he had other serious health issues, surgery was too risky, so TAVI was chosen. The procedure used a new valve (JenaValve) and worked well initially, with only a small amount of leakage. However, four weeks later, his heart failed again due to poor pumping ability, so he received a left ventricular assist device (LVAD) to help his heart pump blood. After one year, the LVAD showed signs of high flow and echocardiograms showed worsening leakage through the aortic valve, even though the original valve itself looked normal. The medical team decided to perform a second valve procedure — a 'valve-in-valve' approach — where a new valve (CoreValve Evolut R) was placed inside the existing one. During this procedure, the LVAD flow was reduced to the lowest level and the heart was paced at 140 beats per minute to help the new valve settle properly. The placement was carefully guided using imaging. The procedure was successful, and at 12 months, the patient had no significant leakage, improved heart function (LVEF increased to 33%), and could walk much farther without symptoms. He is now doing well and living a normal daily life.\"\n}", "generated_text": "A 70-year-old man with severe heart valve problems was treated first with a procedure called transcatheter aortic valve implantation (TAVI) from the apex of his heart. He had a condition called aortic regurgitation, where blood leaks backward through the aortic valve, caused by past heart infection. Because his heart function was very weak and he had other serious health issues, surgery was too risky, so TAVI was chosen. The procedure used a new valve (JenaValve) and worked well initially, with only a small amount of leakage. However, four weeks later, his heart failed again due to poor pumping ability, so he received a left ventricular assist device (LVAD) to help his heart pump blood. After one year, the LVAD showed signs of high flow and echocardiograms showed worsening leakage through the aortic valve, even though the original valve itself looked normal. The medical team decided to perform a second valve procedure — a 'valve-in-valve' approach — where a new valve (CoreValve Evolut R) was placed inside the existing one. During this procedure, the LVAD flow was reduced to the lowest level and the heart was paced at 140 beats per minute to help the new valve settle properly. The placement was carefully guided using imaging. The procedure was successful, and at 12 months, the patient had no significant leakage, improved heart function (LVEF increased to 33%), and could walk much farther without symptoms. He is now doing well and living a normal daily life."}
+{"row_index": 44, "doc_id": 43, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 70-year-old white male with severe symptomatic aortic regurgitation secondary to healed infective endocarditis was managed with transcatheter aortic valve implantation (TAVI) via an apical approach. The patient was classified as high-risk for surgical intervention due to secondary pulmonary hypertension, severely impaired left ventricular function (left ventricular ejection fraction [LVEF] of 20%), chronic renal insufficiency (serum creatinine 2.1 mg/dL), and a logistic EuroSCORE I of 24.36%. Pre-TAVI medical management included torasemide 20 mg once daily, ramipril 5 mg once daily, bisoprolol 2.5 mg twice daily, and spironolactone 12.5 mg once daily. On admission, he presented with cardiac decompensation and dyspnea (temperature 36.7°C, heart rate 99 beats/minute, blood pressure 109/48 mmHg), with no signs of infection (normal C-reactive protein, normal leukocyte count), and no microbiological workup performed. Laboratory findings revealed mild hepatocellular dysfunction (aspartate aminotransferase 59 U/L, alanine aminotransferase 67 U/L) and mild anemia (hemoglobin 10.7 g/dL); no urine analysis was conducted. Coronary angiography, performed prior to TAVI, was normal. The initial TAVI procedure utilized a JenaValve 27 mm self-expandable bioprosthesis, resulting in good immediate hemodynamic outcomes with minimal transvalvular central insufficiency. However, recurrent cardiac decompensation occurred due to persistent severe left ventricular dysfunction, leading to a second interdisciplinary evaluation. Four weeks post-TAVI, the patient underwent implantation of a left ventricular assist device (LVAD) system (Thoratec® HeartMate II), with an uneventful postoperative course and sustained asymptomatic status for one year. During this period, echocardiographic monitoring revealed a progressive worsening of transvalvular central insufficiency, reaching severe levels, without evidence of structural valve leaflet damage or dissection in the JenaValve prosthesis. This suggested a hemodynamic mechanism related to high LVAD flow rates and altered left ventricular dynamics. Given the persistent regurgitation and lack of improvement in ventricular function, a valve-in-valve strategy was selected. The subsequent TAVI procedure was performed under general anesthesia using a CoreValve Evolut R 29 mm self-expandable prosthesis without prior valvuloplasty. Prior to deployment, the LVAD flow was reduced to minimum and the patient was paced at 140 beats/minute to optimize ventricular contractility and reduce left ventricular wall stress. Positioning was meticulously guided by fluoroscopy and transesophageal echocardiography (TEE), with the goal of placing the ventricular strut of the CoreValve Evolut R between the ventricular end and the 'cusp feelers' of the existing JenaValve, based on individual CT imaging demonstrating optimal positioning of the JenaValve's ventricular edge within the left ventricular outflow tract (LVOT). Initial positioning was successful without repositioning. Final deployment was confirmed via fluoroscopic control, followed by successful release in the intended location. Pacing was discontinued, and LVAD flow was gradually restored to normal levels, with stable hemodynamics. Postoperative recovery was uneventful. A follow-up TEE at 12 months demonstrated no significant aortic regurgitation and only marginal residual insufficiency. The patient reported no symptoms and demonstrated significant improvement in functional capacity, with a 6-minute walk test increasing from 148 m (admission) to 381 m. Echocardiography at 12 months showed an improvement in LVEF to 33%, confirming favorable remodeling and hemodynamic stabilization. The case illustrates the challenges of managing complex valvular and ventricular pathology in a high-risk patient, and highlights the role of precise TAVI positioning, flow modulation, and pacing in achieving successful valve-in-valve outcomes with preserved valve function and improved ventricular performance.\"\n}", "generated_text": "A 70-year-old white male with severe symptomatic aortic regurgitation secondary to healed infective endocarditis was managed with transcatheter aortic valve implantation (TAVI) via an apical approach. The patient was classified as high-risk for surgical intervention due to secondary pulmonary hypertension, severely impaired left ventricular function (left ventricular ejection fraction [LVEF] of 20%), chronic renal insufficiency (serum creatinine 2.1 mg/dL), and a logistic EuroSCORE I of 24.36%. Pre-TAVI medical management included torasemide 20 mg once daily, ramipril 5 mg once daily, bisoprolol 2.5 mg twice daily, and spironolactone 12.5 mg once daily. On admission, he presented with cardiac decompensation and dyspnea (temperature 36.7°C, heart rate 99 beats/minute, blood pressure 109/48 mmHg), with no signs of infection (normal C-reactive protein, normal leukocyte count), and no microbiological workup performed. Laboratory findings revealed mild hepatocellular dysfunction (aspartate aminotransferase 59 U/L, alanine aminotransferase 67 U/L) and mild anemia (hemoglobin 10.7 g/dL); no urine analysis was conducted. Coronary angiography, performed prior to TAVI, was normal. The initial TAVI procedure utilized a JenaValve 27 mm self-expandable bioprosthesis, resulting in good immediate hemodynamic outcomes with minimal transvalvular central insufficiency. However, recurrent cardiac decompensation occurred due to persistent severe left ventricular dysfunction, leading to a second interdisciplinary evaluation. Four weeks post-TAVI, the patient underwent implantation of a left ventricular assist device (LVAD) system (Thoratec® HeartMate II), with an uneventful postoperative course and sustained asymptomatic status for one year. During this period, echocardiographic monitoring revealed a progressive worsening of transvalvular central insufficiency, reaching severe levels, without evidence of structural valve leaflet damage or dissection in the JenaValve prosthesis. This suggested a hemodynamic mechanism related to high LVAD flow rates and altered left ventricular dynamics. Given the persistent regurgitation and lack of improvement in ventricular function, a valve-in-valve strategy was selected. The subsequent TAVI procedure was performed under general anesthesia using a CoreValve Evolut R 29 mm self-expandable prosthesis without prior valvuloplasty. Prior to deployment, the LVAD flow was reduced to minimum and the patient was paced at 140 beats/minute to optimize ventricular contractility and reduce left ventricular wall stress. Positioning was meticulously guided by fluoroscopy and transesophageal echocardiography (TEE), with the goal of placing the ventricular strut of the CoreValve Evolut R between the ventricular end and the 'cusp feelers' of the existing JenaValve, based on individual CT imaging demonstrating optimal positioning of the JenaValve's ventricular edge within the left ventricular outflow tract (LVOT). Initial positioning was successful without repositioning. Final deployment was confirmed via fluoroscopic control, followed by successful release in the intended location. Pacing was discontinued, and LVAD flow was gradually restored to normal levels, with stable hemodynamics. Postoperative recovery was uneventful. A follow-up TEE at 12 months demonstrated no significant aortic regurgitation and only marginal residual insufficiency. The patient reported no symptoms and demonstrated significant improvement in functional capacity, with a 6-minute walk test increasing from 148 m (admission) to 381 m. Echocardiography at 12 months showed an improvement in LVEF to 33%, confirming favorable remodeling and hemodynamic stabilization. The case illustrates the challenges of managing complex valvular and ventricular pathology in a high-risk patient, and highlights the role of precise TAVI positioning, flow modulation, and pacing in achieving successful valve-in-valve outcomes with preserved valve function and improved ventricular performance."}
+{"row_index": 45, "doc_id": 44, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 12-year-old boy came in with sudden headaches and drinking a lot of water, urinating a lot. He had no other health problems. Tests showed he had diabetes insipidus — a condition where his body can't hold water properly. MRI scans found a small cyst in the pituitary area that had burst, but it wasn't pressing on any parts of his brain. Since he wasn't having serious symptoms and his other hormone levels were normal, doctors chose not to do surgery. Instead, they watched him closely with regular check-ups. Over time, he grew normally and started puberty, but his growth slowed a bit. Later, tests found he had a small lack of growth hormone. After starting growth hormone shots, his growth sped up. The cyst stayed stable and didn't get worse. All the doctors agreed it was safe to keep watching him without treatment.\"\n}", "generated_text": "A 12-year-old boy came in with sudden headaches and drinking a lot of water, urinating a lot. He had no other health problems. Tests showed he had diabetes insipidus — a condition where his body can't hold water properly. MRI scans found a small cyst in the pituitary area that had burst, but it wasn't pressing on any parts of his brain. Since he wasn't having serious symptoms and his other hormone levels were normal, doctors chose not to do surgery. Instead, they watched him closely with regular check-ups. Over time, he grew normally and started puberty, but his growth slowed a bit. Later, tests found he had a small lack of growth hormone. After starting growth hormone shots, his growth sped up. The cyst stayed stable and didn't get worse. All the doctors agreed it was safe to keep watching him without treatment."}
+{"row_index": 46, "doc_id": 44, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 12-year-old male presented with acute onset of headache and polyuria-polydipsia syndrome, which began one week prior to evaluation. He had no significant past medical history. Physical examination revealed a height of 146.5 cm (M) and weight of 30 kg (-1.4 SD), with no signs of adrenal insufficiency or hypothyroidism. He was at the early stages of puberty, with bilateral gonadal volumes of 3.2 cm and a penile length of 6.2 cm (M). Clinical manifestations included polyuria with urine output reaching up to 113 ml/kg/day, nocturnal enuresis, and excessive fluid intake of 3.8 liters/m². Ophthalmologic assessment, including optical coherence tomography (OCT), showed normal visual function and retinal structure, with no evidence of optic nerve or retinal pathology.\\n\\nEndocrine evaluation demonstrated diabetes insipidus (DI), characterized by a serum sodium of 140 mEq/L, plasma osmolality of 287 mosm/kg, and a markedly low urine osmolality of 179 mosm/kg. Basal hormone levels—including insulin-like growth factor-1 (IGF1), prolactin (PRL), free T4, cortisol, follicle-stimulating hormone (FSH), and luteinizing hormone (LH)—were all within normal limits, indicating no primary endocrine dysfunction beyond DI. Magnetic resonance imaging (MRI) with and without contrast revealed apoplexy of a Rathke cleft cyst (RCC), presenting as spontaneous hyperintensity on both T1 and T2-weighted sequences, measuring 15 × 6 × 11 mm. The anterior pituitary demonstrated homogeneous contrast enhancement, while the posterior pituitary showed loss of typical hyperintensity, with no radiological features suggestive of craniopharyngioma.\\n\\nThe diagnosis of DI was confirmed and showed significant clinical improvement with exogenous vasopressin therapy. A multidisciplinary team consisting of an endocrinologist, neurosurgeon, and radiologist reviewed the case, concluding that the absence of compressive neurologic symptoms, normal baseline endocrine function, and stable RCC apoplexy over nine months of serial MRI monitoring (with size reduction from 15×6×11 mm to 12×11×10 mm) supported a conservative management strategy. The patient was subjected to regular clinical, biochemical, and radiological follow-up over a three-year period.\\n\\nDuring this period, the child achieved normal pubertal development without evidence of significant endocrine deficiencies, except for a subsequent identification of partial growth hormone (GH) deficiency. Growth velocity declined over time, from -0.8 SD to -1.1 SD, prompting further investigation. At age 14 years and 9 months, two GH stimulation tests were performed: a propranolol-glucagon test (peak GH: 19.3 µUI/ml) and an insulin tolerance test (peak GH: 10.0 µUI/ml), both indicating a partial GH deficiency. Following initiation of recombinant human growth hormone (rhGH) therapy, growth velocity improved significantly, rising from -1.1 SD to +0.2 SD over one year.\\n\\nSerial MRI assessments confirmed stability of the RCC apoplexy, with dimensions evolving from 15×6×11 mm at baseline to 11×12×11 mm at two years and further to 7×10×6 mm at three years, indicating a slight but consistent reduction in size. All MRI studies were performed at the same imaging center using standardized protocols, and interpretation was consistently carried out by the same radiologist within multidisciplinary review meetings involving endocrinology and neurosurgery. The clinical course underscores the importance of long-term monitoring in pediatric patients with RCC apoplexy, particularly when no compressive or endocrine deficits are present at initial presentation, and highlights the potential for acquired GH deficiency as a late complication despite otherwise normal pubertal and endocrine development.\"\n}", "generated_text": "A 12-year-old male presented with acute onset of headache and polyuria-polydipsia syndrome, which began one week prior to evaluation. He had no significant past medical history. Physical examination revealed a height of 146.5 cm (M) and weight of 30 kg (-1.4 SD), with no signs of adrenal insufficiency or hypothyroidism. He was at the early stages of puberty, with bilateral gonadal volumes of 3.2 cm and a penile length of 6.2 cm (M). Clinical manifestations included polyuria with urine output reaching up to 113 ml/kg/day, nocturnal enuresis, and excessive fluid intake of 3.8 liters/m². Ophthalmologic assessment, including optical coherence tomography (OCT), showed normal visual function and retinal structure, with no evidence of optic nerve or retinal pathology.\n\nEndocrine evaluation demonstrated diabetes insipidus (DI), characterized by a serum sodium of 140 mEq/L, plasma osmolality of 287 mosm/kg, and a markedly low urine osmolality of 179 mosm/kg. Basal hormone levels—including insulin-like growth factor-1 (IGF1), prolactin (PRL), free T4, cortisol, follicle-stimulating hormone (FSH), and luteinizing hormone (LH)—were all within normal limits, indicating no primary endocrine dysfunction beyond DI. Magnetic resonance imaging (MRI) with and without contrast revealed apoplexy of a Rathke cleft cyst (RCC), presenting as spontaneous hyperintensity on both T1 and T2-weighted sequences, measuring 15 × 6 × 11 mm. The anterior pituitary demonstrated homogeneous contrast enhancement, while the posterior pituitary showed loss of typical hyperintensity, with no radiological features suggestive of craniopharyngioma.\n\nThe diagnosis of DI was confirmed and showed significant clinical improvement with exogenous vasopressin therapy. A multidisciplinary team consisting of an endocrinologist, neurosurgeon, and radiologist reviewed the case, concluding that the absence of compressive neurologic symptoms, normal baseline endocrine function, and stable RCC apoplexy over nine months of serial MRI monitoring (with size reduction from 15×6×11 mm to 12×11×10 mm) supported a conservative management strategy. The patient was subjected to regular clinical, biochemical, and radiological follow-up over a three-year period.\n\nDuring this period, the child achieved normal pubertal development without evidence of significant endocrine deficiencies, except for a subsequent identification of partial growth hormone (GH) deficiency. Growth velocity declined over time, from -0.8 SD to -1.1 SD, prompting further investigation. At age 14 years and 9 months, two GH stimulation tests were performed: a propranolol-glucagon test (peak GH: 19.3 µUI/ml) and an insulin tolerance test (peak GH: 10.0 µUI/ml), both indicating a partial GH deficiency. Following initiation of recombinant human growth hormone (rhGH) therapy, growth velocity improved significantly, rising from -1.1 SD to +0.2 SD over one year.\n\nSerial MRI assessments confirmed stability of the RCC apoplexy, with dimensions evolving from 15×6×11 mm at baseline to 11×12×11 mm at two years and further to 7×10×6 mm at three years, indicating a slight but consistent reduction in size. All MRI studies were performed at the same imaging center using standardized protocols, and interpretation was consistently carried out by the same radiologist within multidisciplinary review meetings involving endocrinology and neurosurgery. The clinical course underscores the importance of long-term monitoring in pediatric patients with RCC apoplexy, particularly when no compressive or endocrine deficits are present at initial presentation, and highlights the potential for acquired GH deficiency as a late complication despite otherwise normal pubertal and endocrine development."}
+{"row_index": 47, "doc_id": 45, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 67-year-old male with no significant medical history presented with a six-month progression of dysphonia and dysphagia, culminating in a marked deterioration of general condition characterized by substantial weight loss of 15 kg over six months. Initial clinical examination revealed a conscious patient with a Glasgow Coma Scale score of 15/15, normothermia, blood pressure of 12/7 mmHg, oxygen saturation of 100%, heart rate of 80 beats per minute, and normal conjunctival color. A large mass was identified in the nasopharyngeal cavity, with no evidence of hepatomegaly, splenomegaly, or lymphadenopathy. Physical examination elsewhere was unremarkable.\\n\\nImaging via cervico-thoraco-abdomino-pelvic computed tomography (CT) demonstrated a nasopharyngeal mass measuring 70 mm × 40 mm, extending to 60 mm in depth. Laboratory investigations, including complete blood count, renal and hepatic function tests, lactate dehydrogenase (LDH), and serologies for HIV, hepatitis C virus (HCV), and hepatitis B virus (HBV), were all within normal limits. Histopathological and immunohistochemical analysis of the nasopharyngeal biopsy, performed in two independent laboratories, confirmed a diagnosis of grade 1–2 follicular B-cell non-Hodgkin lymphoma (NHL), characterized by CD20+, CD19+, CD79a+, and CD10+ immunophenotype, consistent with a follicular lymphoma of the B-cell lineage. Bone marrow biopsy and pre-treatment work-up were unremarkable, with no evidence of hematological involvement or systemic disease.\\n\\nThe patient underwent four cycles of R-CHOP chemotherapy (rituximab 375 mg/m² intravenously, cyclophosphamide 750 mg/m² intravenously, oncovin 2 mg intravenously, prednisolone 100 mg orally, doxorubicin 50 mg/m² intravenously), which resulted in no clinical or radiological response. Subsequently, three cycles of R-DHAOX chemotherapy (rituximab 375 mg/m² intravenously on day 1, high-dose aracytine 2 g/m² intravenously on day 2 administered over two days, dexamethasone 40 mg intravenously daily from day 1 to day 4, oxalipatin 100 mg/m² intravenously on day 1) were administered, but the nasopharyngeal mass persisted and progressively enlarged, leading to clinical instability and the need for tracheostomy due to airway compromise.\\n\\nRepeat biopsy of the nasopharyngeal mass revealed a complete absence of B-lymphocyte infiltration and the presence of amyloid deposits of the AL type, specifically kappa light chain origin. Immunoelectrophoresis of plasma proteins demonstrated the presence of monoclonal immunoglobulin M kappa (IgMκ), suggesting a monoclonal gammopathy of undetermined significance (MGUS) or early-stage amyloidosis. Light chain quantification was not performed due to institutional resource limitations. Myelogram and a second bone marrow biopsy remained normal, excluding clonal plasma cell proliferation or bone marrow infiltration.\\n\\nPositron emission tomography (PET) scanning confirmed a hypermetabolic nasopharyngeal lesion, consistent with active disease, with no evidence of metastatic spread to other organs. Cardiac evaluation (electrocardiogram, n-terminal pro-B-type natriuretic peptide, troponin, echocardiography) and renal function tests were unremarkable, indicating no significant organ dysfunction. The patient is currently receiving a triple-agent regimen of bortezomib, prednisone, and bendamustine, a protocol designed to target proteasome function and induce apoptosis in lymphoma cells, with reported favorable clinical response following the initial course. The clinical course reflects a complex, treatment-resistant presentation of follicular lymphoma with secondary amyloidosis, likely driven by chronic B-cell activation and monoclonal gammopathy, highlighting the importance of integrated immunological and histopathological assessment in such cases.\"\n}", "generated_text": "A 67-year-old male with no significant medical history presented with a six-month progression of dysphonia and dysphagia, culminating in a marked deterioration of general condition characterized by substantial weight loss of 15 kg over six months. Initial clinical examination revealed a conscious patient with a Glasgow Coma Scale score of 15/15, normothermia, blood pressure of 12/7 mmHg, oxygen saturation of 100%, heart rate of 80 beats per minute, and normal conjunctival color. A large mass was identified in the nasopharyngeal cavity, with no evidence of hepatomegaly, splenomegaly, or lymphadenopathy. Physical examination elsewhere was unremarkable.\n\nImaging via cervico-thoraco-abdomino-pelvic computed tomography (CT) demonstrated a nasopharyngeal mass measuring 70 mm × 40 mm, extending to 60 mm in depth. Laboratory investigations, including complete blood count, renal and hepatic function tests, lactate dehydrogenase (LDH), and serologies for HIV, hepatitis C virus (HCV), and hepatitis B virus (HBV), were all within normal limits. Histopathological and immunohistochemical analysis of the nasopharyngeal biopsy, performed in two independent laboratories, confirmed a diagnosis of grade 1–2 follicular B-cell non-Hodgkin lymphoma (NHL), characterized by CD20+, CD19+, CD79a+, and CD10+ immunophenotype, consistent with a follicular lymphoma of the B-cell lineage. Bone marrow biopsy and pre-treatment work-up were unremarkable, with no evidence of hematological involvement or systemic disease.\n\nThe patient underwent four cycles of R-CHOP chemotherapy (rituximab 375 mg/m² intravenously, cyclophosphamide 750 mg/m² intravenously, oncovin 2 mg intravenously, prednisolone 100 mg orally, doxorubicin 50 mg/m² intravenously), which resulted in no clinical or radiological response. Subsequently, three cycles of R-DHAOX chemotherapy (rituximab 375 mg/m² intravenously on day 1, high-dose aracytine 2 g/m² intravenously on day 2 administered over two days, dexamethasone 40 mg intravenously daily from day 1 to day 4, oxalipatin 100 mg/m² intravenously on day 1) were administered, but the nasopharyngeal mass persisted and progressively enlarged, leading to clinical instability and the need for tracheostomy due to airway compromise.\n\nRepeat biopsy of the nasopharyngeal mass revealed a complete absence of B-lymphocyte infiltration and the presence of amyloid deposits of the AL type, specifically kappa light chain origin. Immunoelectrophoresis of plasma proteins demonstrated the presence of monoclonal immunoglobulin M kappa (IgMκ), suggesting a monoclonal gammopathy of undetermined significance (MGUS) or early-stage amyloidosis. Light chain quantification was not performed due to institutional resource limitations. Myelogram and a second bone marrow biopsy remained normal, excluding clonal plasma cell proliferation or bone marrow infiltration.\n\nPositron emission tomography (PET) scanning confirmed a hypermetabolic nasopharyngeal lesion, consistent with active disease, with no evidence of metastatic spread to other organs. Cardiac evaluation (electrocardiogram, n-terminal pro-B-type natriuretic peptide, troponin, echocardiography) and renal function tests were unremarkable, indicating no significant organ dysfunction. The patient is currently receiving a triple-agent regimen of bortezomib, prednisone, and bendamustine, a protocol designed to target proteasome function and induce apoptosis in lymphoma cells, with reported favorable clinical response following the initial course. The clinical course reflects a complex, treatment-resistant presentation of follicular lymphoma with secondary amyloidosis, likely driven by chronic B-cell activation and monoclonal gammopathy, highlighting the importance of integrated immunological and histopathological assessment in such cases."}
+{"row_index": 48, "doc_id": 46, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 46-year-old man from Haiti who moved to Chile one year ago works with animals. For one year, he had warty bumps on the front of his right leg that grew bigger. At first, they didn’t hurt, but later he started feeling itching, pain, and the bumps began to break open with yellowish fluid. The bumps were about 1 cm to 3 cm in size. Doctors saw the bumps up close and noticed dark spots and red blood vessels. Blood tests were normal, and no signs of infections or other diseases were found. A small sample of the skin was checked and showed special round, thick-walled cells (called muriform cells) and black, fuzzy mold that grew in the lab. The mold looked like Fonsecaea, a type of fungus. He was treated for six months with a medicine called itraconazole, taken twice a day, and had cold treatment (cryotherapy) every 6 to 8 weeks on the thick parts of the bumps. The cold treatment helped the bumps go away. After six months, the bumps completely disappeared, and no new ones came back. There is a little darker skin left, which is normal after cryotherapy.\"\n}", "generated_text": "A 46-year-old man from Haiti who moved to Chile one year ago works with animals. For one year, he had warty bumps on the front of his right leg that grew bigger. At first, they didn’t hurt, but later he started feeling itching, pain, and the bumps began to break open with yellowish fluid. The bumps were about 1 cm to 3 cm in size. Doctors saw the bumps up close and noticed dark spots and red blood vessels. Blood tests were normal, and no signs of infections or other diseases were found. A small sample of the skin was checked and showed special round, thick-walled cells (called muriform cells) and black, fuzzy mold that grew in the lab. The mold looked like Fonsecaea, a type of fungus. He was treated for six months with a medicine called itraconazole, taken twice a day, and had cold treatment (cryotherapy) every 6 to 8 weeks on the thick parts of the bumps. The cold treatment helped the bumps go away. After six months, the bumps completely disappeared, and no new ones came back. There is a little darker skin left, which is normal after cryotherapy."}
+{"row_index": 49, "doc_id": 46, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 46-year-old Haitian man who had been living in Chile for one year presented with warty skin lesions on the front of his right leg that had been growing for about a year. He originally had a small bump that slowly became larger and, three months before visiting the doctor, started causing itching, pain, and a yellowish discharge. On exam, doctors saw several warty plaques ranging from 1 to 3 centimeters in size. Dermatoscopy showed thick, ulcerated skin with dark spots and red blood vessels. Blood tests were normal, and tests for infections like syphilis, HIV, and tuberculosis were negative. Skin tissue samples were taken and tested. The biopsy showed thickened skin and inflammation, with special cells called muriform cells — which are a sign of a fungal infection. Fungal culture grew black, velvety colonies, and direct microscopic examination found fungal structures typical of Fonsecaea species. The diagnosis was chromoblastomycosis, a rare fungal infection that affects skin and underlying tissue. The patient was treated with itraconazole (an antifungal drug) taken twice daily for six months, along with regular cryotherapy (freezing the lesions with liquid nitrogen) every six to eight weeks. He also used mupirocin ointment to prevent bacterial infections in areas that had broken open. After six months, the lesions completely went away, and there has been no return of the disease. The only remaining issue is mild skin lightening in the treated areas, which is expected after cryotherapy.\"\n}", "generated_text": "A 46-year-old Haitian man who had been living in Chile for one year presented with warty skin lesions on the front of his right leg that had been growing for about a year. He originally had a small bump that slowly became larger and, three months before visiting the doctor, started causing itching, pain, and a yellowish discharge. On exam, doctors saw several warty plaques ranging from 1 to 3 centimeters in size. Dermatoscopy showed thick, ulcerated skin with dark spots and red blood vessels. Blood tests were normal, and tests for infections like syphilis, HIV, and tuberculosis were negative. Skin tissue samples were taken and tested. The biopsy showed thickened skin and inflammation, with special cells called muriform cells — which are a sign of a fungal infection. Fungal culture grew black, velvety colonies, and direct microscopic examination found fungal structures typical of Fonsecaea species. The diagnosis was chromoblastomycosis, a rare fungal infection that affects skin and underlying tissue. The patient was treated with itraconazole (an antifungal drug) taken twice daily for six months, along with regular cryotherapy (freezing the lesions with liquid nitrogen) every six to eight weeks. He also used mupirocin ointment to prevent bacterial infections in areas that had broken open. After six months, the lesions completely went away, and there has been no return of the disease. The only remaining issue is mild skin lightening in the treated areas, which is expected after cryotherapy."}
+{"row_index": 50, "doc_id": 46, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 46-year-old Haitian male, residing in Chile for one year, presented with a one-and-a-half-year history of progressive cutaneous lesions initially manifesting as a papule on the anterior aspect of the right leg. The lesion evolved into multiple warty plaques measuring 1 x 1 cm, 2 x 2 cm, and 3 x 2 cm, with a history of asymptomatic onset followed by the development of pruritus, pain, superficial ulceration, and yellowish purulent discharge three months prior to presentation. Physical examination revealed phototype V skin, with characteristic hyperkeratotic, ulcerated plaques exhibiting reddish-black dots and congested hemorrhagic vessels on dermatoscopy. Laboratory evaluations, including VDRL, HIV, and PPD, were non-reactive, ruling out syphilis, HIV infection, and tuberculosis. Tissue sampling via punch biopsy (including epidermis, dermis, and subcutaneous tissue) was performed and processed for Gram staining, routine bacterial culture, and anaerobic culture, all of which were negative. Bacilloscopy and Koch complex culture of the same specimen were also negative, excluding mycobacterial and bacillary etiologies. Histopathological analysis using hematoxylin and eosin staining demonstrated pseudoepitheliomatous hyperplasia of the epidermis, with a mixed inflammatory infiltrate in the dermis containing suppurative foci and foreign-body giant cells. Within these giant cells, round, muriform cells with thick, brown-walled walls were observed, morphologically consistent with fungal muriform cells—specifically, those characteristic of Fonsecaea spp. This finding was further confirmed by periodic acid-Schiff (PAS) staining, which highlighted the intracellular fungal elements. Mycological culture on Sabouraud dextrose agar at 25°C yielded dematiaceous (black-pigmented), elevated, well-defined, velvety colonies after 15 days of incubation, consistent with chromoblastomycosis. Direct microscopic examination using 20% potassium hydroxide (KOH) revealed long, branched, sometimes tortuous hyphae and acropetal chains of conidia, which are pathognomonic for Fonsecaea spp. The diagnosis of chromoblastomycosis was thus established based on histopathological presence of muriform cells, dematiaceous fungal colonies, and conidial morphology compatible with Fonsecaea spp. The patient was treated with systemic itraconazole at a dose of 100 mg every 12 hours for six months, in conjunction with regular cryotherapy (liquid nitrogen application) to hypertrophic and ulcerated areas every six to eight weeks. Topical mupirocin ointment was applied frequently to manage bacterial superinfections arising from ulceration and erosion. The clinical course was favorable, with complete regression of the cutaneous lesions and no evidence of relapse at the time of follow-up. Persistent mild local hypopigmentation in the treated areas was observed, which is a known sequelae of cryotherapy-induced tissue damage and is expected in the context of repeated cryoprophylactic interventions. This case underscores the importance of recognizing chromoblastomycosis in patients with occupational exposure to soil and organic matter, particularly in agricultural settings, and highlights the efficacy of combined antifungal therapy and physical debridement in achieving durable clinical resolution.\"\n}", "generated_text": "A 46-year-old Haitian male, residing in Chile for one year, presented with a one-and-a-half-year history of progressive cutaneous lesions initially manifesting as a papule on the anterior aspect of the right leg. The lesion evolved into multiple warty plaques measuring 1 x 1 cm, 2 x 2 cm, and 3 x 2 cm, with a history of asymptomatic onset followed by the development of pruritus, pain, superficial ulceration, and yellowish purulent discharge three months prior to presentation. Physical examination revealed phototype V skin, with characteristic hyperkeratotic, ulcerated plaques exhibiting reddish-black dots and congested hemorrhagic vessels on dermatoscopy. Laboratory evaluations, including VDRL, HIV, and PPD, were non-reactive, ruling out syphilis, HIV infection, and tuberculosis. Tissue sampling via punch biopsy (including epidermis, dermis, and subcutaneous tissue) was performed and processed for Gram staining, routine bacterial culture, and anaerobic culture, all of which were negative. Bacilloscopy and Koch complex culture of the same specimen were also negative, excluding mycobacterial and bacillary etiologies. Histopathological analysis using hematoxylin and eosin staining demonstrated pseudoepitheliomatous hyperplasia of the epidermis, with a mixed inflammatory infiltrate in the dermis containing suppurative foci and foreign-body giant cells. Within these giant cells, round, muriform cells with thick, brown-walled walls were observed, morphologically consistent with fungal muriform cells—specifically, those characteristic of Fonsecaea spp. This finding was further confirmed by periodic acid-Schiff (PAS) staining, which highlighted the intracellular fungal elements. Mycological culture on Sabouraud dextrose agar at 25°C yielded dematiaceous (black-pigmented), elevated, well-defined, velvety colonies after 15 days of incubation, consistent with chromoblastomycosis. Direct microscopic examination using 20% potassium hydroxide (KOH) revealed long, branched, sometimes tortuous hyphae and acropetal chains of conidia, which are pathognomonic for Fonsecaea spp. The diagnosis of chromoblastomycosis was thus established based on histopathological presence of muriform cells, dematiaceous fungal colonies, and conidial morphology compatible with Fonsecaea spp. The patient was treated with systemic itraconazole at a dose of 100 mg every 12 hours for six months, in conjunction with regular cryotherapy (liquid nitrogen application) to hypertrophic and ulcerated areas every six to eight weeks. Topical mupirocin ointment was applied frequently to manage bacterial superinfections arising from ulceration and erosion. The clinical course was favorable, with complete regression of the cutaneous lesions and no evidence of relapse at the time of follow-up. Persistent mild local hypopigmentation in the treated areas was observed, which is a known sequelae of cryotherapy-induced tissue damage and is expected in the context of repeated cryoprophylactic interventions. This case underscores the importance of recognizing chromoblastomycosis in patients with occupational exposure to soil and organic matter, particularly in agricultural settings, and highlights the efficacy of combined antifungal therapy and physical debridement in achieving durable clinical resolution."}
+{"row_index": 51, "doc_id": 47, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 19-year-old man had a painful lump in his scrotum for 8 months that didn’t go away with antibiotics. He also had fever, night sweats, loss of appetite, and lost weight. No one in his family had tuberculosis, but he was vaccinated at birth. The lump was removed and tested — it showed signs of tuberculosis in the tube-like part of the testicle. X-rays showed TB in his lungs, under his skin, in his lymph nodes, and in his spine and bones. He started TB medicine, but after 4 months, he had seizures. A brain scan found small TB lumps in his brain. He got medicine for seizures and kept taking TB medicine. His symptoms got better, the body parts healed, and he gained weight. The brain lumps slowly got smaller, so he kept taking TB medicine for a long time. After 19 years of treatment, he was fully healed with no long-term problems.\"\n}", "generated_text": "A 19-year-old man had a painful lump in his scrotum for 8 months that didn’t go away with antibiotics. He also had fever, night sweats, loss of appetite, and lost weight. No one in his family had tuberculosis, but he was vaccinated at birth. The lump was removed and tested — it showed signs of tuberculosis in the tube-like part of the testicle. X-rays showed TB in his lungs, under his skin, in his lymph nodes, and in his spine and bones. He started TB medicine, but after 4 months, he had seizures. A brain scan found small TB lumps in his brain. He got medicine for seizures and kept taking TB medicine. His symptoms got better, the body parts healed, and he gained weight. The brain lumps slowly got smaller, so he kept taking TB medicine for a long time. After 19 years of treatment, he was fully healed with no long-term problems."}
+{"row_index": 52, "doc_id": 47, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 19-year-old man with no prior medical problems was admitted to the hospital with a painful lump in his left scrotum that had been growing for 8 months. The lump didn't go away with antibiotics, and he also had symptoms like low-grade fever, night sweats, loss of appetite, and unexplained weight loss. He had no history of tuberculosis in his family or personal history, and he was vaccinated at birth.\\n\\nExams showed a large, tender lump in the scrotum and two firm lumps on his chest. His blood tests were mostly normal, except for a high level of inflammation. A chest X-ray showed signs of lung infection.\\n\\nHe had surgery to remove the scrotal lump, and the tissue test showed signs of tuberculosis in the epididymis — a part of the testicle. A skin test for tuberculosis was positive, and no bacteria were found in his sputum or urine. Other tests ruled out HIV, hepatitis, and other infections.\\n\\nImaging scans found tuberculosis in other parts of his body, including his lungs, lymph nodes, chest walls, and spine. This was diagnosed as widespread tuberculosis affecting multiple areas.\\n\\nHe started standard tuberculosis treatment with several medicines for two months, then continued with two of them. After four months of treatment, he began having seizures. A brain MRI showed small nodular lesions — called tuberculomas — in his brain, which are caused by tuberculosis.\\n\\nHe was started on anti-seizure medication along with continuing his tuberculosis treatment. His overall condition improved, he gained weight, and the other signs of infection gradually disappeared. The brain tuberculomas slowly shrunk, and he remained seizure-free. He completed treatment after 234 months (about 19 years) and was declared cured with no long-term effects, even after a two-year follow-up.\"\n}", "generated_text": "A 19-year-old man with no prior medical problems was admitted to the hospital with a painful lump in his left scrotum that had been growing for 8 months. The lump didn't go away with antibiotics, and he also had symptoms like low-grade fever, night sweats, loss of appetite, and unexplained weight loss. He had no history of tuberculosis in his family or personal history, and he was vaccinated at birth.\n\nExams showed a large, tender lump in the scrotum and two firm lumps on his chest. His blood tests were mostly normal, except for a high level of inflammation. A chest X-ray showed signs of lung infection.\n\nHe had surgery to remove the scrotal lump, and the tissue test showed signs of tuberculosis in the epididymis — a part of the testicle. A skin test for tuberculosis was positive, and no bacteria were found in his sputum or urine. Other tests ruled out HIV, hepatitis, and other infections.\n\nImaging scans found tuberculosis in other parts of his body, including his lungs, lymph nodes, chest walls, and spine. This was diagnosed as widespread tuberculosis affecting multiple areas.\n\nHe started standard tuberculosis treatment with several medicines for two months, then continued with two of them. After four months of treatment, he began having seizures. A brain MRI showed small nodular lesions — called tuberculomas — in his brain, which are caused by tuberculosis.\n\nHe was started on anti-seizure medication along with continuing his tuberculosis treatment. His overall condition improved, he gained weight, and the other signs of infection gradually disappeared. The brain tuberculomas slowly shrunk, and he remained seizure-free. He completed treatment after 234 months (about 19 years) and was declared cured with no long-term effects, even after a two-year follow-up."}
+{"row_index": 53, "doc_id": 47, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 19-year-old male with no significant medical history presented with a painful left scrotal mass that had persisted for 8 months without improvement following empiric antibiotic therapy for pyogenic infection. He reported intermittent low-grade fever, night sweats, anorexia, and unexplained weight loss since symptom onset, with no history of cough, sputum production, or hemoptysis. There was no personal or familial history of tuberculosis, and he had received routine bacillus Calmette-Guérin (BCG) vaccination at birth. Physical examination revealed a large, tender, slightly warm left scrotal bursa and two elongated, firm, poorly defined subcutaneous masses in the anterior thoracic wall measuring 3–4 cm in length, without audible rales on lung auscultation. The remainder of the systemic examination was unremarkable. Laboratory investigations demonstrated a markedly elevated c-reactive protein (CRP) of 90 mg/dL, while complete blood count, serum creatinine, blood glucose, and liver function tests remained within normal limits. Standard chest X-ray revealed bilateral reticulonodular infiltrates consistent with pulmonary parenchymal involvement.\\n\\nUltrasound imaging suggested a tuberculous epididymal lesion, prompting a left orchidectomy. Histopathological examination of the resected tissue demonstrated granulomatous epithelioid cell necrosis involving the body and tail of the epididymis, with preservation of the head and testicular tissue, consistent with active epididymal tuberculosis. The intradermal tuberculin skin test (TST) was positive, supporting a diagnosis of latent or active tuberculosis. Direct microscopy and culture for acid-fast bacilli (AFB) in sputum and urine over three consecutive days were negative, indicating a lack of detectable bacilli in these specimens. Serological testing for human immunodeficiency virus (HIV), hepatitis B virus (HBV), hepatitis C virus (HCV), and Wright's stain for parasitic infection were all negative, ruling out alternative infectious or hematological etiologies.\\n\\nTo evaluate for extrapulmonary dissemination, a thoraco-abdomino-pelvic tomodensitometry was performed, revealing miliary tuberculosis, coelo-mesenteric necrotic lymphadenopathy, bilateral parietal collections (right: 33 × 10 mm; left: 45 × 10 mm) at the level of the external oblique muscles, and focal osteolytic lesions at D11 and L5, suggestive of early spondylodiscitis. Magnetic resonance imaging (MRI) of the spinal cord confirmed active spondylodiscitis at D7, D11, L4, and L5, confirming the presence of spinal tuberculous infection. This constellation of findings led to a definitive diagnosis of disseminated tuberculosis involving epididymal, pulmonary, parietal, lymphatic, and osteoarticular sites.\\n\\nThe patient was initiated on a standard anti-tuberculous regimen consisting of a four-drug intensive phase (isoniazid, rifampicin, ethambutol, and pyrazinamide) for 2 months, followed by a continuation phase of isoniazid and rifampicin. At the 4th month of therapy, the patient developed generalized tonic-clonic convulsive seizures. A brain MRI was performed, which revealed multiple nodular lesions located both above and below the tentorial membrane, consistent with tuberculomas—granulomatous lesions caused by Mycobacterium tuberculosis that have infiltrated the central nervous system. The patient was promptly started on anticonvulsant therapy in addition to continuing anti-tuberculous treatment. Clinical and radiological follow-up demonstrated a favorable evolution: improvement in general condition, weight gain, and resolution of thoracic parietal collections, lymphadenopathy, and miliary infiltrates on imaging. However, the tuberculomas showed a slow, progressive reduction in size, necessitating prolonged continuation of anti-tuberculous therapy. The patient was ultimately declared cured at the end of 234 months (approximately 19.5 years) of treatment, with a 2-year post-treatment follow-up showing no recurrence of clinical or radiological manifestations and no neurological sequelae. This case exemplifies the potential for disseminated tuberculosis to present with extrapulmonary manifestations, including epididymal involvement, and to progress to central nervous system disease, requiring multidrug therapy and long-term management to achieve complete resolution.\"\n}", "generated_text": "A 19-year-old male with no significant medical history presented with a painful left scrotal mass that had persisted for 8 months without improvement following empiric antibiotic therapy for pyogenic infection. He reported intermittent low-grade fever, night sweats, anorexia, and unexplained weight loss since symptom onset, with no history of cough, sputum production, or hemoptysis. There was no personal or familial history of tuberculosis, and he had received routine bacillus Calmette-Guérin (BCG) vaccination at birth. Physical examination revealed a large, tender, slightly warm left scrotal bursa and two elongated, firm, poorly defined subcutaneous masses in the anterior thoracic wall measuring 3–4 cm in length, without audible rales on lung auscultation. The remainder of the systemic examination was unremarkable. Laboratory investigations demonstrated a markedly elevated c-reactive protein (CRP) of 90 mg/dL, while complete blood count, serum creatinine, blood glucose, and liver function tests remained within normal limits. Standard chest X-ray revealed bilateral reticulonodular infiltrates consistent with pulmonary parenchymal involvement.\n\nUltrasound imaging suggested a tuberculous epididymal lesion, prompting a left orchidectomy. Histopathological examination of the resected tissue demonstrated granulomatous epithelioid cell necrosis involving the body and tail of the epididymis, with preservation of the head and testicular tissue, consistent with active epididymal tuberculosis. The intradermal tuberculin skin test (TST) was positive, supporting a diagnosis of latent or active tuberculosis. Direct microscopy and culture for acid-fast bacilli (AFB) in sputum and urine over three consecutive days were negative, indicating a lack of detectable bacilli in these specimens. Serological testing for human immunodeficiency virus (HIV), hepatitis B virus (HBV), hepatitis C virus (HCV), and Wright's stain for parasitic infection were all negative, ruling out alternative infectious or hematological etiologies.\n\nTo evaluate for extrapulmonary dissemination, a thoraco-abdomino-pelvic tomodensitometry was performed, revealing miliary tuberculosis, coelo-mesenteric necrotic lymphadenopathy, bilateral parietal collections (right: 33 × 10 mm; left: 45 × 10 mm) at the level of the external oblique muscles, and focal osteolytic lesions at D11 and L5, suggestive of early spondylodiscitis. Magnetic resonance imaging (MRI) of the spinal cord confirmed active spondylodiscitis at D7, D11, L4, and L5, confirming the presence of spinal tuberculous infection. This constellation of findings led to a definitive diagnosis of disseminated tuberculosis involving epididymal, pulmonary, parietal, lymphatic, and osteoarticular sites.\n\nThe patient was initiated on a standard anti-tuberculous regimen consisting of a four-drug intensive phase (isoniazid, rifampicin, ethambutol, and pyrazinamide) for 2 months, followed by a continuation phase of isoniazid and rifampicin. At the 4th month of therapy, the patient developed generalized tonic-clonic convulsive seizures. A brain MRI was performed, which revealed multiple nodular lesions located both above and below the tentorial membrane, consistent with tuberculomas—granulomatous lesions caused by Mycobacterium tuberculosis that have infiltrated the central nervous system. The patient was promptly started on anticonvulsant therapy in addition to continuing anti-tuberculous treatment. Clinical and radiological follow-up demonstrated a favorable evolution: improvement in general condition, weight gain, and resolution of thoracic parietal collections, lymphadenopathy, and miliary infiltrates on imaging. However, the tuberculomas showed a slow, progressive reduction in size, necessitating prolonged continuation of anti-tuberculous therapy. The patient was ultimately declared cured at the end of 234 months (approximately 19.5 years) of treatment, with a 2-year post-treatment follow-up showing no recurrence of clinical or radiological manifestations and no neurological sequelae. This case exemplifies the potential for disseminated tuberculosis to present with extrapulmonary manifestations, including epididymal involvement, and to progress to central nervous system disease, requiring multidrug therapy and long-term management to achieve complete resolution."}
+{"row_index": 54, "doc_id": 48, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 10-year-old boy was getting chemotherapy for a serious type of cancer called leukemia. During the treatment, he got a bad infection in his brain caused by a type of bacteria called B. cereus. Doctors found it using brain scans and a fluid test from his spine. He got antibiotics and felt better over time. The infection went away, and his brain scans showed the spots shrinking. He didn’t have any more problems after that.\"\n}", "generated_text": "A 10-year-old boy was getting chemotherapy for a serious type of cancer called leukemia. During the treatment, he got a bad infection in his brain caused by a type of bacteria called B. cereus. Doctors found it using brain scans and a fluid test from his spine. He got antibiotics and felt better over time. The infection went away, and his brain scans showed the spots shrinking. He didn’t have any more problems after that."}
+{"row_index": 55, "doc_id": 48, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 10-year-old boy was treated for acute lymphoblastic leukaemia, a type of cancer that affects white blood cells. During the early stages of treatment, he developed a cerebral abscess — a serious infection in the brain — caused by a bacteria called B. cereus. This was found using brain imaging and by testing the fluid around the brain (cerebrospinal fluid). Although the infection was severe, he responded well to antibiotics and made a full recovery. His symptoms, including a bad headache, improved over time, and follow-up scans showed the infection had gone away.\"\n}", "generated_text": "A 10-year-old boy was treated for acute lymphoblastic leukaemia, a type of cancer that affects white blood cells. During the early stages of treatment, he developed a cerebral abscess — a serious infection in the brain — caused by a bacteria called B. cereus. This was found using brain imaging and by testing the fluid around the brain (cerebrospinal fluid). Although the infection was severe, he responded well to antibiotics and made a full recovery. His symptoms, including a bad headache, improved over time, and follow-up scans showed the infection had gone away."}
+{"row_index": 56, "doc_id": 48, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"We present a case of a 10-year-old male with high-risk early T-cell acute lymphoblastic leukaemia (ALL), managed according to the LAL SEHOP-PETHEMA 2013 protocol. Two years post-diagnosis, he experienced an early central nervous system (CNS) relapse, prompting intervention under the InteReALL HR 2010 protocol, which included bortezomib. During induction therapy, the patient became neutropenic for four weeks (neutrophil count: 20/μL), and was administered prophylactic antimicrobials: cefepime, cotrimoxazole, and fluconazole. Additionally, he was treated with acyclovir for a cutaneous herpes simplex virus type 1 (HSV-1) infection. On presentation, he developed a severe, refractory headache, prompting a cranial computed tomography (CT) scan that revealed a hypodense lesion in the right temporal lobe. Given the infectious differential, a lumbar puncture was performed, and empirical therapy was escalated from cefepime to meropenem and vancomycin.\\n\\nDespite being afebrile, the patient rapidly progressed to septic shock on day one of hospital admission, requiring transfer to the paediatric intensive care unit (PICU) for inotropic and vasoactive support. Antimicrobial coverage was broadened to include gentamicin and caspofungin. Laboratory findings demonstrated a progressive rise in inflammatory markers: C-reactive protein (CRP) reached 312 mg/L and procalcitonin peaked at 47.58 ng/mL on day three, consistent with a severe bacterial infection, while no significant biochemical abnormalities were otherwise observed. Complete blood count revealed pancytopenia, attributable to chemotherapy-induced bone marrow suppression. Blood cultures were negative for bacteremia and fungemia; herpesvirus serologies (HSV-1, HSV-2, HSV-6, cytomegalovirus, varicella-zoster virus, enterovirus, parechovirus) and urine/fecal cultures were also negative, excluding common systemic pathogens.\\n\\nCerebrospinal fluid (CSF) analysis showed normal glucose (63 mg/dL), protein (16 mg/dL), and leukocyte count (1/µL), indicating a non-inflammatory, non-lymphocytic process. However, microbiological testing identified *Bacillus cereus* in the CSF, which was susceptible to meropenem, vancomycin, linezolid, and ciprofloxacin. All other potential CNS pathogens—including *Neisseria meningitidis*, *Listeria monocytogenes*, *Streptococcus pneumoniae*, *Cryptococcus*, and toxoplasma—were ruled out by PCR and serological assays. Electroencephalography (EEG) revealed diffuse slowing of cortical activity without epileptiform discharges, suggesting a non-epileptic, neuroinflammatory or infectious process.\\n\\nOn day 4, following stabilization of hemodynamics, cranial magnetic resonance imaging (MRI) demonstrated two hyperintense lesions on T2 and FLAIR sequences in the subcortical regions of the right temporal and parietal lobes. The parietal lesion exhibited ring enhancement after gadolinium administration, and both lesions demonstrated peripheral diffusion restriction on apparent diffusion coefficient (ADC) mapping, consistent with bacterial abscess formation. Small, scattered haemorrhagic foci were also observed within the brain parenchyma, further supporting a bacterial etiology. The imaging and CSF findings collectively supported a diagnosis of *Bacillus cereus* cerebral abscess.\\n\\nThe patient responded favorably to antibiotic therapy, with resolution of headache and absence of new neurological deficits. Follow-up MRI at two weeks showed significant reduction in lesion size. Vancomycin and acyclovir were discontinued after three weeks, and meropenem was continued for a total of six weeks. The clinical course was favorable, with no evidence of CNS relapse or persistent infection. This case highlights the potential for atypical bacterial pathogens, such as *B. cereus*, to cause CNS infections in immunocompromised pediatric patients undergoing intensive chemotherapy, even in the absence of fever or systemic signs of sepsis, underscoring the importance of early neuroimaging and CSF analysis in high-risk ALL patients with unexplained neurological symptoms.\"\n}", "generated_text": "We present a case of a 10-year-old male with high-risk early T-cell acute lymphoblastic leukaemia (ALL), managed according to the LAL SEHOP-PETHEMA 2013 protocol. Two years post-diagnosis, he experienced an early central nervous system (CNS) relapse, prompting intervention under the InteReALL HR 2010 protocol, which included bortezomib. During induction therapy, the patient became neutropenic for four weeks (neutrophil count: 20/μL), and was administered prophylactic antimicrobials: cefepime, cotrimoxazole, and fluconazole. Additionally, he was treated with acyclovir for a cutaneous herpes simplex virus type 1 (HSV-1) infection. On presentation, he developed a severe, refractory headache, prompting a cranial computed tomography (CT) scan that revealed a hypodense lesion in the right temporal lobe. Given the infectious differential, a lumbar puncture was performed, and empirical therapy was escalated from cefepime to meropenem and vancomycin.\n\nDespite being afebrile, the patient rapidly progressed to septic shock on day one of hospital admission, requiring transfer to the paediatric intensive care unit (PICU) for inotropic and vasoactive support. Antimicrobial coverage was broadened to include gentamicin and caspofungin. Laboratory findings demonstrated a progressive rise in inflammatory markers: C-reactive protein (CRP) reached 312 mg/L and procalcitonin peaked at 47.58 ng/mL on day three, consistent with a severe bacterial infection, while no significant biochemical abnormalities were otherwise observed. Complete blood count revealed pancytopenia, attributable to chemotherapy-induced bone marrow suppression. Blood cultures were negative for bacteremia and fungemia; herpesvirus serologies (HSV-1, HSV-2, HSV-6, cytomegalovirus, varicella-zoster virus, enterovirus, parechovirus) and urine/fecal cultures were also negative, excluding common systemic pathogens.\n\nCerebrospinal fluid (CSF) analysis showed normal glucose (63 mg/dL), protein (16 mg/dL), and leukocyte count (1/µL), indicating a non-inflammatory, non-lymphocytic process. However, microbiological testing identified *Bacillus cereus* in the CSF, which was susceptible to meropenem, vancomycin, linezolid, and ciprofloxacin. All other potential CNS pathogens—including *Neisseria meningitidis*, *Listeria monocytogenes*, *Streptococcus pneumoniae*, *Cryptococcus*, and toxoplasma—were ruled out by PCR and serological assays. Electroencephalography (EEG) revealed diffuse slowing of cortical activity without epileptiform discharges, suggesting a non-epileptic, neuroinflammatory or infectious process.\n\nOn day 4, following stabilization of hemodynamics, cranial magnetic resonance imaging (MRI) demonstrated two hyperintense lesions on T2 and FLAIR sequences in the subcortical regions of the right temporal and parietal lobes. The parietal lesion exhibited ring enhancement after gadolinium administration, and both lesions demonstrated peripheral diffusion restriction on apparent diffusion coefficient (ADC) mapping, consistent with bacterial abscess formation. Small, scattered haemorrhagic foci were also observed within the brain parenchyma, further supporting a bacterial etiology. The imaging and CSF findings collectively supported a diagnosis of *Bacillus cereus* cerebral abscess.\n\nThe patient responded favorably to antibiotic therapy, with resolution of headache and absence of new neurological deficits. Follow-up MRI at two weeks showed significant reduction in lesion size. Vancomycin and acyclovir were discontinued after three weeks, and meropenem was continued for a total of six weeks. The clinical course was favorable, with no evidence of CNS relapse or persistent infection. This case highlights the potential for atypical bacterial pathogens, such as *B. cereus*, to cause CNS infections in immunocompromised pediatric patients undergoing intensive chemotherapy, even in the absence of fever or systemic signs of sepsis, underscoring the importance of early neuroimaging and CSF analysis in high-risk ALL patients with unexplained neurological symptoms."}
+{"row_index": 57, "doc_id": 49, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 16-year-old girl has a flat, gray spot on her left thigh that's been there since birth. The spot is about 10.5 cm wide and 8.0 cm long, and it has dark and light areas. Around the edge, you can see small blood vessels. The spot has changed over time — it used to be a deep purple color, but now it's lighter and lower. A scan showed that the spot has extra blood vessels in the skin and layer under the skin, connected to a major blood vessel in the leg. These vessels are sending blood early, which means blood is flowing through them too fast. There's a small vein running under the skin on the front of the thigh, and the skin layer is thinner in that area, but nothing has spread into the muscle or bone. Her legs are the same length, so there's no problem with balance or movement.\"\n}", "generated_text": "A 16-year-old girl has a flat, gray spot on her left thigh that's been there since birth. The spot is about 10.5 cm wide and 8.0 cm long, and it has dark and light areas. Around the edge, you can see small blood vessels. The spot has changed over time — it used to be a deep purple color, but now it's lighter and lower. A scan showed that the spot has extra blood vessels in the skin and layer under the skin, connected to a major blood vessel in the leg. These vessels are sending blood early, which means blood is flowing through them too fast. There's a small vein running under the skin on the front of the thigh, and the skin layer is thinner in that area, but nothing has spread into the muscle or bone. Her legs are the same length, so there's no problem with balance or movement."}
+{"row_index": 58, "doc_id": 49, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"16-year-old female presenting with a depressed gray plaque measuring 10.5 × 8.0 cm located in the lower lateral aspect of the left thigh, characterized by interspersed hypochromic areas and peripheral telangiectatic vessels, including visible superficial veins adjacent to the lesion. The lesion has been present since birth and initially appeared violaceous; over time, it has undergone progressive lightening and depression. No discrepancy in lower limb length was observed, ruling out significant skeletal involvement. Angioresonance imaging revealed vascular malformations involving the skin and subcutaneous tissue, specifically supplied by intermuscular branches of the popliteal artery. Early venous filling was detected both within the lesion and in the surrounding tissue, indicating early venous shunting, a hallmark of venous-type vascular malformations. No markedly dilated draining veins were identified, although a superficial draining vein was observed coursing along the subcutaneous cellular tissue of the anterior thigh. Histopathological and imaging findings demonstrate thinning of the subcutaneous tissue in the region of the vascular alteration, consistent with chronic vascular pressure and tissue remodeling, without evidence of intramuscular or bony extension. The clinical and imaging profile supports a diagnosis of a venous or venous-lymphatic vascular malformation with early venous shunting, likely arising from aberrant vascular branching from the popliteal artery's intermuscular branches, and evolving over time with pigmentary and topographic changes consistent with chronic venous congestion and tissue atrophy.\"\n}", "generated_text": "16-year-old female presenting with a depressed gray plaque measuring 10.5 × 8.0 cm located in the lower lateral aspect of the left thigh, characterized by interspersed hypochromic areas and peripheral telangiectatic vessels, including visible superficial veins adjacent to the lesion. The lesion has been present since birth and initially appeared violaceous; over time, it has undergone progressive lightening and depression. No discrepancy in lower limb length was observed, ruling out significant skeletal involvement. Angioresonance imaging revealed vascular malformations involving the skin and subcutaneous tissue, specifically supplied by intermuscular branches of the popliteal artery. Early venous filling was detected both within the lesion and in the surrounding tissue, indicating early venous shunting, a hallmark of venous-type vascular malformations. No markedly dilated draining veins were identified, although a superficial draining vein was observed coursing along the subcutaneous cellular tissue of the anterior thigh. Histopathological and imaging findings demonstrate thinning of the subcutaneous tissue in the region of the vascular alteration, consistent with chronic vascular pressure and tissue remodeling, without evidence of intramuscular or bony extension. The clinical and imaging profile supports a diagnosis of a venous or venous-lymphatic vascular malformation with early venous shunting, likely arising from aberrant vascular branching from the popliteal artery's intermuscular branches, and evolving over time with pigmentary and topographic changes consistent with chronic venous congestion and tissue atrophy."}
+{"row_index": 59, "doc_id": 50, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 57-year-old woman with a long history of asthma and allergic rhinitis came in with recurring abdominal pain that had been going on for two months. The pain was dull and intermittent, along with nausea, loss of appetite, and a 5-kilogram weight loss. She had no fever, no blood or mucus in her stool, and no signs of infection in her lungs or other organs. Tests showed very high levels of eosinophils (a type of white blood cell) in her blood, and her IgG4 levels were also elevated. After ruling out infections, allergies, and other conditions, a biopsy of her colon tissue showed a large number of eosinophils in the lining of the colon, confirming a diagnosis of eosinophilic colitis (EoC). She was treated with corticosteroids and montelukast, and her symptoms improved within two weeks. Her eosinophil levels returned to normal, and after stopping the steroids, she continued on montelukast for three months without any recurrence of symptoms.\"\n}", "generated_text": "A 57-year-old woman with a long history of asthma and allergic rhinitis came in with recurring abdominal pain that had been going on for two months. The pain was dull and intermittent, along with nausea, loss of appetite, and a 5-kilogram weight loss. She had no fever, no blood or mucus in her stool, and no signs of infection in her lungs or other organs. Tests showed very high levels of eosinophils (a type of white blood cell) in her blood, and her IgG4 levels were also elevated. After ruling out infections, allergies, and other conditions, a biopsy of her colon tissue showed a large number of eosinophils in the lining of the colon, confirming a diagnosis of eosinophilic colitis (EoC). She was treated with corticosteroids and montelukast, and her symptoms improved within two weeks. Her eosinophil levels returned to normal, and after stopping the steroids, she continued on montelukast for three months without any recurrence of symptoms."}
+{"row_index": 60, "doc_id": 50, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 57-year-old woman with a 14-year history of asthma and allergic rhinitis, managed on salmeterol/fluticasone, was hospitalized for recurrent abdominal pain initiating two months prior. The pain was intermittent, dull, and associated with nausea, anorexia, malaise, and a 5 kg weight loss. No fever, blood or mucus in stool, or respiratory symptoms (rhinorrhea, wheezing, cough) were present. She had no history of alcohol, tobacco, or herbal medicine use. Six weeks before admission, she was diagnosed with an intestinal infection based on a complete blood count (CBC) showing leukocytosis and marked eosinophilia (25.61 G/L, 77.8% eosinophils); treatment with antibiotics and mebendazole failed to alleviate symptoms. On presentation, vital signs were stable (BP 110/70 mmHg, T 37°C, HR 88 bpm, RR 18 bpm), with a BMI of 16.6 kg/m² and clinical evidence of sarcopenia, but no skin rash, lymphadenopathy, or edema. Abdominal examination revealed tenderness in the epigastric and umbilical regions without guarding. Repeat CBC demonstrated persistent leukocytosis and significant eosinophilia (20.8 G/L, total WBC 26.8 G/L, 77.8% eosinophils), with peripheral blood film showing normal eosinophil morphology. Bone marrow aspiration revealed 48% eosinophils without blasts or atypical cells, suggesting a clonal or tissue-specific eosinophilic proliferation rather than hematologic malignancy. Fluorescence in situ hybridization (FISH) for CHIC2 deletion, a surrogate marker for FIP1L1-PDGFRA fusion in eosinophilic disorders, was negative, ruling out classic myeloid neoplasms such as eosinophilic leukemia or hypereosinophilic syndrome (HES) with PDGFRA rearrangement. Autoimmune and vasculitic panels (ANA, anti-dsDNA, p-ANCA, c-ANCA) were negative, excluding systemic autoimmune or inflammatory conditions. Serum immunoglobulins showed elevated IgG (2760 mg/dL; normal 700–1600 mg/dL) and IgG4 (1260 mg/dL; normal 3.9–86.4 mg/dL), with a mild elevation in IgE (137.5 IU/mL; normal <100 IU/mL) and a high rheumatoid factor (RF 144.4 IU/mL; normal <20 IU/mL), suggesting a possible IgG4-related disease (IgG4-RD) phenotype, though not sufficient for definitive diagnosis. All other laboratory parameters—including aminotransferases, blood urea nitrogen, serum creatinine, complement C3/C4, vitamin B12, serum cortisol, and NT-proBNP—were within normal limits. ECG and echocardiogram were unremarkable. Chest CT demonstrated mild interstitial fibrosis and bronchiectasis, consistent with chronic airway inflammation. Sputum acid-fast bacilli (AFB) smear and bronchoscopy were negative; bronchoalveolar lavage (BAL) cytology revealed 35% neutrophils and no eosinophils, indicating a lack of pulmonary eosinophilic infiltration. Spirometry confirmed severe airflow obstruction with a significant bronchodilator response, supporting persistent airway inflammation. Fractional exhaled nitric oxide (FeNO) was 15 ppb, a marker of eosinophilic airway inflammation. Stool analysis was positive for leukocytes, with no ova or parasites. Serology for toxocariasis was positive (IgG to Toxocara canis at 54.2 NovaTec-Units), while tests for Strongyloides stercoralis, Fasciola sp., Toxoplasma gondii, Trichinella spiralis, Ancylostoma sp., Angiostrongylus cantonensis, Ascaris lumbricoides, Clonorchis sinensis, Paragonimus sp., Gnathostoma sp., Entamoeba histolytica, cysticercosis, filariasis, and HIV were negative, excluding parasitic etiologies. Abdominal contrast-enhanced CT showed gallbladder stones without acute cholecystitis and no structural abnormalities in the gastrointestinal tract. Upper gastrointestinal endoscopy was unremarkable. Colonoscopy revealed mucosal inflammation in the sigmoid, left, transverse, and right colon, prompting systematic biopsies. A five-day course of albendazole", "generated_text": "{\n  \"proficient_health_literacy\": \"A 57-year-old woman with a 14-year history of asthma and allergic rhinitis, managed on salmeterol/fluticasone, was hospitalized for recurrent abdominal pain initiating two months prior. The pain was intermittent, dull, and associated with nausea, anorexia, malaise, and a 5 kg weight loss. No fever, blood or mucus in stool, or respiratory symptoms (rhinorrhea, wheezing, cough) were present. She had no history of alcohol, tobacco, or herbal medicine use. Six weeks before admission, she was diagnosed with an intestinal infection based on a complete blood count (CBC) showing leukocytosis and marked eosinophilia (25.61 G/L, 77.8% eosinophils); treatment with antibiotics and mebendazole failed to alleviate symptoms. On presentation, vital signs were stable (BP 110/70 mmHg, T 37°C, HR 88 bpm, RR 18 bpm), with a BMI of 16.6 kg/m² and clinical evidence of sarcopenia, but no skin rash, lymphadenopathy, or edema. Abdominal examination revealed tenderness in the epigastric and umbilical regions without guarding. Repeat CBC demonstrated persistent leukocytosis and significant eosinophilia (20.8 G/L, total WBC 26.8 G/L, 77.8% eosinophils), with peripheral blood film showing normal eosinophil morphology. Bone marrow aspiration revealed 48% eosinophils without blasts or atypical cells, suggesting a clonal or tissue-specific eosinophilic proliferation rather than hematologic malignancy. Fluorescence in situ hybridization (FISH) for CHIC2 deletion, a surrogate marker for FIP1L1-PDGFRA fusion in eosinophilic disorders, was negative, ruling out classic myeloid neoplasms such as eosinophilic leukemia or hypereosinophilic syndrome (HES) with PDGFRA rearrangement. Autoimmune and vasculitic panels (ANA, anti-dsDNA, p-ANCA, c-ANCA) were negative, excluding systemic autoimmune or inflammatory conditions. Serum immunoglobulins showed elevated IgG (2760 mg/dL; normal 700–1600 mg/dL) and IgG4 (1260 mg/dL; normal 3.9–86.4 mg/dL), with a mild elevation in IgE (137.5 IU/mL; normal <100 IU/mL) and a high rheumatoid factor (RF 144.4 IU/mL; normal <20 IU/mL), suggesting a possible IgG4-related disease (IgG4-RD) phenotype, though not sufficient for definitive diagnosis. All other laboratory parameters—including aminotransferases, blood urea nitrogen, serum creatinine, complement C3/C4, vitamin B12, serum cortisol, and NT-proBNP—were within normal limits. ECG and echocardiogram were unremarkable. Chest CT demonstrated mild interstitial fibrosis and bronchiectasis, consistent with chronic airway inflammation. Sputum acid-fast bacilli (AFB) smear and bronchoscopy were negative; bronchoalveolar lavage (BAL) cytology revealed 35% neutrophils and no eosinophils, indicating a lack of pulmonary eosinophilic infiltration. Spirometry confirmed severe airflow obstruction with a significant bronchodilator response, supporting persistent airway inflammation. Fractional exhaled nitric oxide (FeNO) was 15 ppb, a marker of eosinophilic airway inflammation. Stool analysis was positive for leukocytes, with no ova or parasites. Serology for toxocariasis was positive (IgG to Toxocara canis at 54.2 NovaTec-Units), while tests for Strongyloides stercoralis, Fasciola sp., Toxoplasma gondii, Trichinella spiralis, Ancylostoma sp., Angiostrongylus cantonensis, Ascaris lumbricoides, Clonorchis sinensis, Paragonimus sp., Gnathostoma sp., Entamoeba histolytica, cysticercosis, filariasis, and HIV were negative, excluding parasitic etiologies. Abdominal contrast-enhanced CT showed gallbladder stones without acute cholecystitis and no structural abnormalities in the gastrointestinal tract. Upper gastrointestinal endoscopy was unremarkable. Colonoscopy revealed mucosal inflammation in the sigmoid, left, transverse, and right colon, prompting systematic biopsies. A five-day course of albendazole"}
+{"row_index": 61, "doc_id": 51, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 35-year-old man had a heart problem that got worse over time. At first, he had chest tightness and shortness of breath after activity. Doctors found a soft, lump-like growth in his heart (called a cardiac myxoma) and saw that his heart was getting bigger and weaker. This condition, called Carney syndrome, also showed up in his skin (brown spots on his ears) and kidneys. He didn’t have surgery at first, even though his symptoms got worse. By then, his heart was failing badly — he couldn’t lie down and had to sit up to breathe. His heart was enlarged, pumping poorly, and had an irregular rhythm. Doctors said he had both a heart tumor and a weak heart (dilated cardiomyopathy). Because his heart was too damaged, they decided on a heart transplant. The new heart was matched and given right away. The surgery worked well — the new heart started beating normally, and the old heart lump was removed. After the surgery, he started taking medicine to prevent his body from rejecting the new heart and to fight infection. His body healed fast. A few weeks later, his heart was strong again, and all his test results were normal. He’s now doing well and going back to his normal life.\"\n}", "generated_text": "A 35-year-old man had a heart problem that got worse over time. At first, he had chest tightness and shortness of breath after activity. Doctors found a soft, lump-like growth in his heart (called a cardiac myxoma) and saw that his heart was getting bigger and weaker. This condition, called Carney syndrome, also showed up in his skin (brown spots on his ears) and kidneys. He didn’t have surgery at first, even though his symptoms got worse. By then, his heart was failing badly — he couldn’t lie down and had to sit up to breathe. His heart was enlarged, pumping poorly, and had an irregular rhythm. Doctors said he had both a heart tumor and a weak heart (dilated cardiomyopathy). Because his heart was too damaged, they decided on a heart transplant. The new heart was matched and given right away. The surgery worked well — the new heart started beating normally, and the old heart lump was removed. After the surgery, he started taking medicine to prevent his body from rejecting the new heart and to fight infection. His body healed fast. A few weeks later, his heart was strong again, and all his test results were normal. He’s now doing well and going back to his normal life."}
+{"row_index": 62, "doc_id": 51, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 35-year-old man was diagnosed with heart failure caused by a rare condition called Carney syndrome. This condition leads to the growth of a non-cancerous tumor (called a cardiac myxoma) in the heart and also causes the heart muscle to weaken, a condition known as dilated cardiomyopathy. Three years ago, he first visited the hospital with sudden chest tightness and shortness of breath. An ultrasound of his heart showed a tumor, and further tests confirmed Carney syndrome. He was treated for symptoms but did not have surgery at that time. Over time, his symptoms got worse. By the time he returned to the hospital, his heart function was severely damaged — rated as New York Heart Association (NYHA) Grade IV — meaning he could not lie down or breathe comfortably without sitting up. New tests showed both the tumor and weakened heart muscle. Because of this advanced heart failure, doctors decided on heart transplantation. On October 1, 2024, he received a new heart from a donor. The surgery involved opening the chest, removing the damaged heart tissue, and attaching the new heart. The procedure was successful, and the new heart began working properly. After surgery, he received medicines to prevent rejection and fight infection. His recovery was good, and by October 20, 2024, his heart function had returned to normal. Follow-up tests showed no signs of problems, and he is now doing well and living a normal life.\"\n}", "generated_text": "A 35-year-old man was diagnosed with heart failure caused by a rare condition called Carney syndrome. This condition leads to the growth of a non-cancerous tumor (called a cardiac myxoma) in the heart and also causes the heart muscle to weaken, a condition known as dilated cardiomyopathy. Three years ago, he first visited the hospital with sudden chest tightness and shortness of breath. An ultrasound of his heart showed a tumor, and further tests confirmed Carney syndrome. He was treated for symptoms but did not have surgery at that time. Over time, his symptoms got worse. By the time he returned to the hospital, his heart function was severely damaged — rated as New York Heart Association (NYHA) Grade IV — meaning he could not lie down or breathe comfortably without sitting up. New tests showed both the tumor and weakened heart muscle. Because of this advanced heart failure, doctors decided on heart transplantation. On October 1, 2024, he received a new heart from a donor. The surgery involved opening the chest, removing the damaged heart tissue, and attaching the new heart. The procedure was successful, and the new heart began working properly. After surgery, he received medicines to prevent rejection and fight infection. His recovery was good, and by October 20, 2024, his heart function had returned to normal. Follow-up tests showed no signs of problems, and he is now doing well and living a normal life."}
+{"row_index": 63, "doc_id": 51, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 38-year-old male presented with recurrent episodes of chest tightness and dyspnea, initially occurring post-exertion three years prior. Outpatient echocardiography revealed a left atrial echogenic mass suggestive of a cardiac myxoma, prompting hospital admission for comprehensive evaluation. Physical examination identified cutaneous pigmentation in the ears, manifesting as multiple small brown and black macules, consistent with cutaneous manifestations of Carney Complex (CNC). Abdominal computed tomography (CT) demonstrated multiple hepatic lesions and small cystic formations in the left kidney, further supporting the diagnosis. Genetic analysis confirmed biallelic pathogenic variants in both the TTN (titin) and PRKAR1A genes, which are associated with sarcomatous and myxomatous tissue overgrowth in CNC. The diagnosis of Carney syndrome was established through integration of clinical features, imaging findings, and molecular genetic testing.\\n\\nThe patient's symptoms progressively deteriorated, culminating in a presentation on September 20, 2023, with severe dyspnea, orthopnea, and paroxysmal nocturnal dyspnea. Physical examination revealed jugular venous distension, leftward and inferior cardiac border displacement, irregular heart rhythm (auscultated as atrial fibrillation), a mitral valve murmur of intensity 2/6–3/6 at the fourth intercostal space along the left sternal border, and bilateral wet rales in the mid-to-lower lung zones. Abdominal examination showed a firm liver palpable three fingers below the xiphoid process and two fingers below the costal margin, with bilateral mild pitting edema. Echocardiography demonstrated global left ventricular (LV) dilation, enlargement of the aortic sinus and pulmonary artery, small-to-moderate mitral regurgitation, and a well-defined, echogenic mass measuring 54 mm × 43 mm attached to the atrial septum. Left ventricular ejection fraction (LVEF) was 23.1%, with fractional shortening (FS) of 10.9%, indicating severe systolic dysfunction. Electrocardiography confirmed atrial fibrillation with an average ventricular rate of 150 beats per minute and abnormal Q waves in leads V1–V3, suggesting prior myocardial injury or infarction.\\n\\nThe clinical picture was consistent with both dilated cardiomyopathy (DCM) and cardiac myxoma in the context of Carney syndrome. Given the presence of end-stage heart failure and a large, potentially obstructive myxoma, heart transplantation was deemed the most appropriate therapeutic intervention to simultaneously address both the structural and functional cardiomyopathy. On October 1, 2024, a suitable donor heart became available, and the patient underwent elective cardiac transplantation via median sternotomy. The surgical approach involved layer-by-layer incision of the skin and subcutaneous tissue, followed by longitudinal sawing of the sternum with controlled bleeding via electrocoagulation and bone wax. Extracardiac exploration revealed global cardiac enlargement, with marked left ventricular dilation and diminished contractile function. The aorta and main pulmonary artery (PA) were dissected from the supravalvular region. Diseased atrial and ventricular tissue—including the right atrium, left atrium (LA), right ventricle, and left ventricle—was excised, while preserved segments were retained for anastomotic reconstruction. The resected mass was characterized as a greyish-white, mucoid, non-encapsulated lesion, consistent with a myxoma.\\n\\nAnastomotic procedures included double continuous 3/0 Prolene sutures for end-to-end closure of the donor and recipient left atria. The donor ascending aorta was anastomosed to the recipient's pulmonary artery using continuous 5/0 Prolene sutures, with meticulous inspection confirming no intraoperative bleeding. The donor and recipient inferior vena cavae were closed with 5/0 Prolene sutures, and the superior vena cavae were similarly sutured with 5/0 Prolene, with multiple inspections performed to ensure hemostasis. Following cardiac reperfusion, the ascending aorta was unclamped, and spontaneous return to sinus rhythm was observed upon rewarming. Postoperative tissue specimens from the patient’s left heart and gray matter were collected for histopathological analysis, confirming the presence of both dilated cardiomyopathy and cardiac myxoma.\\n\\nPostoperative management commenced with aggressive hemodynamic stabilization. On postoperative day 1, urine output reached 1200 mL. Laboratory findings included a hypersensitive troponin T level of 796.70 ng/L and NT-proBNP of 10798 pg/mL, indicative of myocardial", "generated_text": "{\n  \"proficient_health_literacy\": \"A 38-year-old male presented with recurrent episodes of chest tightness and dyspnea, initially occurring post-exertion three years prior. Outpatient echocardiography revealed a left atrial echogenic mass suggestive of a cardiac myxoma, prompting hospital admission for comprehensive evaluation. Physical examination identified cutaneous pigmentation in the ears, manifesting as multiple small brown and black macules, consistent with cutaneous manifestations of Carney Complex (CNC). Abdominal computed tomography (CT) demonstrated multiple hepatic lesions and small cystic formations in the left kidney, further supporting the diagnosis. Genetic analysis confirmed biallelic pathogenic variants in both the TTN (titin) and PRKAR1A genes, which are associated with sarcomatous and myxomatous tissue overgrowth in CNC. The diagnosis of Carney syndrome was established through integration of clinical features, imaging findings, and molecular genetic testing.\\n\\nThe patient's symptoms progressively deteriorated, culminating in a presentation on September 20, 2023, with severe dyspnea, orthopnea, and paroxysmal nocturnal dyspnea. Physical examination revealed jugular venous distension, leftward and inferior cardiac border displacement, irregular heart rhythm (auscultated as atrial fibrillation), a mitral valve murmur of intensity 2/6–3/6 at the fourth intercostal space along the left sternal border, and bilateral wet rales in the mid-to-lower lung zones. Abdominal examination showed a firm liver palpable three fingers below the xiphoid process and two fingers below the costal margin, with bilateral mild pitting edema. Echocardiography demonstrated global left ventricular (LV) dilation, enlargement of the aortic sinus and pulmonary artery, small-to-moderate mitral regurgitation, and a well-defined, echogenic mass measuring 54 mm × 43 mm attached to the atrial septum. Left ventricular ejection fraction (LVEF) was 23.1%, with fractional shortening (FS) of 10.9%, indicating severe systolic dysfunction. Electrocardiography confirmed atrial fibrillation with an average ventricular rate of 150 beats per minute and abnormal Q waves in leads V1–V3, suggesting prior myocardial injury or infarction.\\n\\nThe clinical picture was consistent with both dilated cardiomyopathy (DCM) and cardiac myxoma in the context of Carney syndrome. Given the presence of end-stage heart failure and a large, potentially obstructive myxoma, heart transplantation was deemed the most appropriate therapeutic intervention to simultaneously address both the structural and functional cardiomyopathy. On October 1, 2024, a suitable donor heart became available, and the patient underwent elective cardiac transplantation via median sternotomy. The surgical approach involved layer-by-layer incision of the skin and subcutaneous tissue, followed by longitudinal sawing of the sternum with controlled bleeding via electrocoagulation and bone wax. Extracardiac exploration revealed global cardiac enlargement, with marked left ventricular dilation and diminished contractile function. The aorta and main pulmonary artery (PA) were dissected from the supravalvular region. Diseased atrial and ventricular tissue—including the right atrium, left atrium (LA), right ventricle, and left ventricle—was excised, while preserved segments were retained for anastomotic reconstruction. The resected mass was characterized as a greyish-white, mucoid, non-encapsulated lesion, consistent with a myxoma.\\n\\nAnastomotic procedures included double continuous 3/0 Prolene sutures for end-to-end closure of the donor and recipient left atria. The donor ascending aorta was anastomosed to the recipient's pulmonary artery using continuous 5/0 Prolene sutures, with meticulous inspection confirming no intraoperative bleeding. The donor and recipient inferior vena cavae were closed with 5/0 Prolene sutures, and the superior vena cavae were similarly sutured with 5/0 Prolene, with multiple inspections performed to ensure hemostasis. Following cardiac reperfusion, the ascending aorta was unclamped, and spontaneous return to sinus rhythm was observed upon rewarming. Postoperative tissue specimens from the patient’s left heart and gray matter were collected for histopathological analysis, confirming the presence of both dilated cardiomyopathy and cardiac myxoma.\\n\\nPostoperative management commenced with aggressive hemodynamic stabilization. On postoperative day 1, urine output reached 1200 mL. Laboratory findings included a hypersensitive troponin T level of 796.70 ng/L and NT-proBNP of 10798 pg/mL, indicative of myocardial"}
+{"row_index": 64, "doc_id": 52, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 2.5-year-old girl with a known condition called NF1 has been having diarrhea with blood in it for a few weeks. Doctors saw her colon inside her body and found red, swollen lining from the bottom of her rectum all the way to the start of her large intestine. The tissue samples showed long-term inflammation, and tests confirmed she has a virus called CMV that can cause this kind of damage. This is like having a chronic infection in her gut, similar to ulcerative colitis. She is being treated with medicines to reduce inflammation and control the virus. Her symptoms have improved, but she still has some ongoing issues and needs regular care.\"\n}", "generated_text": "A 2.5-year-old girl with a known condition called NF1 has been having diarrhea with blood in it for a few weeks. Doctors saw her colon inside her body and found red, swollen lining from the bottom of her rectum all the way to the start of her large intestine. The tissue samples showed long-term inflammation, and tests confirmed she has a virus called CMV that can cause this kind of damage. This is like having a chronic infection in her gut, similar to ulcerative colitis. She is being treated with medicines to reduce inflammation and control the virus. Her symptoms have improved, but she still has some ongoing issues and needs regular care."}
+{"row_index": 65, "doc_id": 52, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 2-year-6-month-old female pre-schooler with a confirmed diagnosis of neurofibromatosis type 1 (NF1) presented with a 4-week history of bloody diarrhea, characterized by 5 to 10 episodes of blood-streaked stools per day. Initial evaluation in the emergency department revealed rotavirus infection (positive), with normal inflammatory markers, negative coproculture, and normal abdominal ultrasound. The patient was hospitalized for 3 days to manage dehydration and discharged without active bleeding, though persistent semi-liquid stools remained. Ten days post-discharge, she developed recurrent bloody diarrhea associated with reduced oral intake and a 1 kg weight loss, prompting referral to a pediatric gastroenterologist. A polymerase chain reaction (PCR) panel for gastrointestinal pathogens and PCR for *Clostridium difficile* were both negative, leading to hospitalization for further investigation.\\n\\nThe patient has a known heterozygous pathogenic variant in the *NF1* gene (c.5606_5627del, p.Gly1869Valfs*28), diagnosed at 8 months of age. She exhibits classic skin manifestations (café au lait spots) and skeletal abnormalities, including tibial curvature requiring ankle arthrodesis at 18 months. There is no family history of NF1 or inflammatory bowel disease (IBD). Physical examination revealed a soft, non-distended abdomen with increased air-bubble murmurs, no masses or visceral enlargement, and normal perianal inspection. Multiple brown-coffee stains were noted on the lower extremities and back, consistent with NF1-related pigmentation.\\n\\nLaboratory findings included moderate microcytic-hypochromic anemia (Hb 9.6 g/dL), leukocytosis with left shift (leukocytes 13,900), and mildly elevated inflammatory markers (CRP 1.37 mg/dL, above the normal cutoff of 0.5 mg/dL). Colonoscopy extended from the anal margin to the cecum, including the ileocecal valve and appendicular orifice, with inspection of the terminal ileum. The mucosa from the anal margin to the cecum was erythematous with loss of vascular transparency, a feature not observed in the cecal mucosa, which appeared normal. No focal lesions were identified in the anal canal or cecum.\\n\\nHistopathological analysis of intestinal biopsies revealed preserved villous architecture and adequate epithelial differentiation in the ileal mucosa with a non-inflamed lamina propria. In the colonic mucosa, there was mild architectural distortion, swollen lamina propria with a mild mixed inflammatory infiltrate, hyperplasia of reactive lymphoid follicles, and isolated microabscess foci—consistent with mild chronic colitis. A PCR assay for cytomegalovirus (CMV) on colonic biopsy was positive. Subsequent serological testing confirmed positive CMV IgG, negative IgM, and a blood viral load of 79.7 IU/mL, indicating past exposure and current viremia. Stool PCR for gastrointestinal pathogens and *C. difficile* remained negative. Gram stain of the biopsy showed +++ leukocytes without bacteria; culture identified low levels of *Streptococcus gallolyticus/equinus* complex, interpreted as normal bacterial flora. Additional microbiological tests (acridine orange, Ziehl-Neelsen, Koch culture, and adenovirus PCR) were negative.\\n\\nEndoscopic and histological findings were consistent with ulcerative colitis (UC), with moderate clinical activity (PUCAI score of 50). The patient was initiated on mesalazine (70 mg/kg/day, three times daily) and a fecal calprotectin level greater than 600 μg/g was obtained, supporting active intestinal inflammation. An immunology workup was performed to evaluate for potential immunodeficiency, including lymphocyte subpopulations (normal), immunoglobulin levels (normal), HIV (negative), memory T-cell analysis (showing expected alterations in the context of CMV viremia), and lymphoproliferation test (normal). A comprehensive genetic panel for primary immunodeficiencies (Invitae, comprising 429 genes, including 68 associated with monogenic inflammatory bowel disease) was performed, yielding seven variants of uncertain significance, none of which were implicated in monogenic IBD.\\n\\nThe patient was treated with intravenous ganciclovir for CMV infection, administered for 15 days, with subsequent PCR monitoring showing undetectable viral load prior to discharge. Clinical improvement was noted during hospitalization: decreased stool frequency, improved consistency, resolution of rectal bleeding, absence of nocturnal stools or abdominal pain, and a PUCAI score of 0 at discharge.\\n\\nTwo months later", "generated_text": "{\n  \"proficient_health_literacy\": \"A 2-year-6-month-old female pre-schooler with a confirmed diagnosis of neurofibromatosis type 1 (NF1) presented with a 4-week history of bloody diarrhea, characterized by 5 to 10 episodes of blood-streaked stools per day. Initial evaluation in the emergency department revealed rotavirus infection (positive), with normal inflammatory markers, negative coproculture, and normal abdominal ultrasound. The patient was hospitalized for 3 days to manage dehydration and discharged without active bleeding, though persistent semi-liquid stools remained. Ten days post-discharge, she developed recurrent bloody diarrhea associated with reduced oral intake and a 1 kg weight loss, prompting referral to a pediatric gastroenterologist. A polymerase chain reaction (PCR) panel for gastrointestinal pathogens and PCR for *Clostridium difficile* were both negative, leading to hospitalization for further investigation.\\n\\nThe patient has a known heterozygous pathogenic variant in the *NF1* gene (c.5606_5627del, p.Gly1869Valfs*28), diagnosed at 8 months of age. She exhibits classic skin manifestations (café au lait spots) and skeletal abnormalities, including tibial curvature requiring ankle arthrodesis at 18 months. There is no family history of NF1 or inflammatory bowel disease (IBD). Physical examination revealed a soft, non-distended abdomen with increased air-bubble murmurs, no masses or visceral enlargement, and normal perianal inspection. Multiple brown-coffee stains were noted on the lower extremities and back, consistent with NF1-related pigmentation.\\n\\nLaboratory findings included moderate microcytic-hypochromic anemia (Hb 9.6 g/dL), leukocytosis with left shift (leukocytes 13,900), and mildly elevated inflammatory markers (CRP 1.37 mg/dL, above the normal cutoff of 0.5 mg/dL). Colonoscopy extended from the anal margin to the cecum, including the ileocecal valve and appendicular orifice, with inspection of the terminal ileum. The mucosa from the anal margin to the cecum was erythematous with loss of vascular transparency, a feature not observed in the cecal mucosa, which appeared normal. No focal lesions were identified in the anal canal or cecum.\\n\\nHistopathological analysis of intestinal biopsies revealed preserved villous architecture and adequate epithelial differentiation in the ileal mucosa with a non-inflamed lamina propria. In the colonic mucosa, there was mild architectural distortion, swollen lamina propria with a mild mixed inflammatory infiltrate, hyperplasia of reactive lymphoid follicles, and isolated microabscess foci—consistent with mild chronic colitis. A PCR assay for cytomegalovirus (CMV) on colonic biopsy was positive. Subsequent serological testing confirmed positive CMV IgG, negative IgM, and a blood viral load of 79.7 IU/mL, indicating past exposure and current viremia. Stool PCR for gastrointestinal pathogens and *C. difficile* remained negative. Gram stain of the biopsy showed +++ leukocytes without bacteria; culture identified low levels of *Streptococcus gallolyticus/equinus* complex, interpreted as normal bacterial flora. Additional microbiological tests (acridine orange, Ziehl-Neelsen, Koch culture, and adenovirus PCR) were negative.\\n\\nEndoscopic and histological findings were consistent with ulcerative colitis (UC), with moderate clinical activity (PUCAI score of 50). The patient was initiated on mesalazine (70 mg/kg/day, three times daily) and a fecal calprotectin level greater than 600 μg/g was obtained, supporting active intestinal inflammation. An immunology workup was performed to evaluate for potential immunodeficiency, including lymphocyte subpopulations (normal), immunoglobulin levels (normal), HIV (negative), memory T-cell analysis (showing expected alterations in the context of CMV viremia), and lymphoproliferation test (normal). A comprehensive genetic panel for primary immunodeficiencies (Invitae, comprising 429 genes, including 68 associated with monogenic inflammatory bowel disease) was performed, yielding seven variants of uncertain significance, none of which were implicated in monogenic IBD.\\n\\nThe patient was treated with intravenous ganciclovir for CMV infection, administered for 15 days, with subsequent PCR monitoring showing undetectable viral load prior to discharge. Clinical improvement was noted during hospitalization: decreased stool frequency, improved consistency, resolution of rectal bleeding, absence of nocturnal stools or abdominal pain, and a PUCAI score of 0 at discharge.\\n\\nTwo months later"}
+{"row_index": 66, "doc_id": 53, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 40-year-old HIV-positive male with sustained antiretroviral therapy adherence—documented viral load of 4500/mm³ and CD4 count of 70/mm³ from the prior year—presented with a two-year history of intermittent febrile episodes that were non-cyclic and refractory to standard antipyretic and non-steroidal anti-inflammatory drug (NSAID) therapy. Over the preceding two months, he developed progressive diffuse abdominal pain, with a predominant localization in the upper right quadrant, accompanied by the clinical appearance of a 'tree-in-bud' pattern on imaging, consistent with bronchial tree branching, and bilateral pleural effusion. Abdominal imaging revealed marked hepatosplenomegaly and the development of ascites. Laboratory evaluation demonstrated pancytopenia, coagulopathy, hypoalbuminemia, and elevated acute-phase reactants, indicating systemic inflammation and possible immune dysregulation. Computed tomography (CT) of the thorax, abdomen, and pelvis confirmed generalized lymphadenopathy and hepatosplenomegaly, with no evidence of focal infection or malignancy on initial imaging. Multiple microbiological assays, including culture-based detection of Mycobacterium species from blood, urine, and lymph node specimens, were negative; however, RT-PCR for Human Herpesvirus 8 (HHV-8) was positive, suggesting possible association with HHV-8-related lymphoproliferative disorders. A left iliac ganglion biopsy was performed, which revealed histopathological features consistent with multicentric Castleman’s disease, a lymphoproliferative disorder characterized by abnormal proliferation of lymphoid tissue and cytokine overproduction, particularly interleukin-6 (IL-6), leading to systemic inflammation and hematological abnormalities. Despite re-initiation of antiretroviral therapy, clinical deterioration progressed, prompting the administration of corticosteroids to suppress cytokine activity and ganciclovir to target potential HHV-8 reactivation. Within 24 hours, the patient developed multiple organ failure, including fulminant hepatic failure, and anasarca, which contraindicated continued use of immunosuppressive agents. A new chest CT demonstrated upper right lobe parenchymal infiltrates with a tree-in-bud pattern and bilateral pleural effusion, consistent with a pulmonary manifestation of underlying lymphoid hyperplasia or infection. Abdominal findings showed further progression of hepatosplenomegaly and ascites. The patient was transferred to the intensive care unit (ICU) 48 hours after symptom onset and succumbed to fulminant hepatic failure within hours of admission. Postmortem analysis of tracheal aspirate culture yielded a positive result for Mycobacterium tuberculosis, confirming latent or active pulmonary tuberculosis as a contributing infectious agent. Liver biopsy revealed non-necrotizing granulomas, consistent with a tuberculous etiology, while the parenchymal architecture remained largely preserved, indicating that the primary pathology was not necrotizing or fulminant. This case illustrates the complex interplay between HIV-associated immunodeficiency, lymphoproliferative disorders such as Castleman’s disease, and opportunistic infections like tuberculosis, where overlapping inflammatory and infectious processes may lead to rapid clinical deterioration. The findings align with the principles of the World Health Organization (WHO) Helsinki Declaration regarding ethical conduct in human research and clinical investigation.\"\n}", "generated_text": "A 40-year-old HIV-positive male with sustained antiretroviral therapy adherence—documented viral load of 4500/mm³ and CD4 count of 70/mm³ from the prior year—presented with a two-year history of intermittent febrile episodes that were non-cyclic and refractory to standard antipyretic and non-steroidal anti-inflammatory drug (NSAID) therapy. Over the preceding two months, he developed progressive diffuse abdominal pain, with a predominant localization in the upper right quadrant, accompanied by the clinical appearance of a 'tree-in-bud' pattern on imaging, consistent with bronchial tree branching, and bilateral pleural effusion. Abdominal imaging revealed marked hepatosplenomegaly and the development of ascites. Laboratory evaluation demonstrated pancytopenia, coagulopathy, hypoalbuminemia, and elevated acute-phase reactants, indicating systemic inflammation and possible immune dysregulation. Computed tomography (CT) of the thorax, abdomen, and pelvis confirmed generalized lymphadenopathy and hepatosplenomegaly, with no evidence of focal infection or malignancy on initial imaging. Multiple microbiological assays, including culture-based detection of Mycobacterium species from blood, urine, and lymph node specimens, were negative; however, RT-PCR for Human Herpesvirus 8 (HHV-8) was positive, suggesting possible association with HHV-8-related lymphoproliferative disorders. A left iliac ganglion biopsy was performed, which revealed histopathological features consistent with multicentric Castleman’s disease, a lymphoproliferative disorder characterized by abnormal proliferation of lymphoid tissue and cytokine overproduction, particularly interleukin-6 (IL-6), leading to systemic inflammation and hematological abnormalities. Despite re-initiation of antiretroviral therapy, clinical deterioration progressed, prompting the administration of corticosteroids to suppress cytokine activity and ganciclovir to target potential HHV-8 reactivation. Within 24 hours, the patient developed multiple organ failure, including fulminant hepatic failure, and anasarca, which contraindicated continued use of immunosuppressive agents. A new chest CT demonstrated upper right lobe parenchymal infiltrates with a tree-in-bud pattern and bilateral pleural effusion, consistent with a pulmonary manifestation of underlying lymphoid hyperplasia or infection. Abdominal findings showed further progression of hepatosplenomegaly and ascites. The patient was transferred to the intensive care unit (ICU) 48 hours after symptom onset and succumbed to fulminant hepatic failure within hours of admission. Postmortem analysis of tracheal aspirate culture yielded a positive result for Mycobacterium tuberculosis, confirming latent or active pulmonary tuberculosis as a contributing infectious agent. Liver biopsy revealed non-necrotizing granulomas, consistent with a tuberculous etiology, while the parenchymal architecture remained largely preserved, indicating that the primary pathology was not necrotizing or fulminant. This case illustrates the complex interplay between HIV-associated immunodeficiency, lymphoproliferative disorders such as Castleman’s disease, and opportunistic infections like tuberculosis, where overlapping inflammatory and infectious processes may lead to rapid clinical deterioration. The findings align with the principles of the World Health Organization (WHO) Helsinki Declaration regarding ethical conduct in human research and clinical investigation."}
+{"row_index": 67, "doc_id": 54, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 4-month-old indigenous lactating female infant from the rural interior of Panama, specifically from Urracá, approximately 3 hours by canoe from the nearest health subcenter, presented with acute gastroenteritis and moderate-to-severe dehydration due to protein-caloric malnutrition. The infant was the fourth daughter, born via vaginal delivery at home by a relative without prenatal care; birth weight, height, and Apgar score are unknown. She did not receive breast milk and was exclusively fed powdered milk formula with iron (3 ounces every 4 hours), which is inappropriate for infants under 6 months of age. The household consisted of six members (parents and four children), living in a two-room structure with board walls and palm roof, no electricity, kerosene lighting, well water, and open defecation into a river; economic activity was based on subsistence agriculture. No primary health care was accessed during the first four months of life, and the national expanded programme of immunizations was not administered. Parents reported normal neurodevelopment prior to hospitalization.\\n\\nThe infant presented to a primary health center with a 4-day history of diarrhea without mucus or blood, associated with vomiting of food content; the mother substituted tea for milk due to intolerance. The patient was afebrile and without respiratory symptoms. Initial management included oral rehydration with lactate Ringer's solution (10 ml/kg) and four doses of Enterogermina® (2 billion spores/5 mL), a probiotic containing *Bacillus clausii*. Due to lack of intravenous access (no catheters or intraosseous routes), the patient was transferred to a second-level hospital in the provincial capital and subsequently to a tertiary care facility in Panama City, diagnosed with acute gastroenteritis and severe dehydration.\\n\\nOn presentation to the emergency department, the infant exhibited signs of profound dehydration: tearless cry, dry oral mucosa, and +++ edema in hands, feet, abdomen, and face. Vital signs included afebrile state, tachycardia (HR 170 bpm), tachypnea (RR 55 bpm), hypotension (BP 91/37 mmHg), oxygen saturation 99%, and signs of shock (capillary refill >2 seconds, cold extremities, filiform pulse, marble skin). Admission weight was 4.7 kg, height 56 cm; height Z-score was -2.52, while weight/height and weight/age Z-scores were unquantifiable due to severe dehydration. Physical examination revealed fine crepitus in both lung bases, erythematous-squamous skin lesions with desquamation, and hypopigmented patches on trunk and upper limbs, interpreted as pellagroid dermatosis, likely secondary to vitamin B3 deficiency.\\n\\nInitial resuscitation included 10 ml/kg lactate Ringer's bolus, followed by 500 mL of 5% dextrose in 0.33% saline infused at 29 mL/h over 6 hours without potassium chloride until diuresis was achieved. Empiric antibiotic therapy was initiated with ceftriaxone 50 mg/kg/day for suspected sepsis. The patient was stabilized and transferred to the ward, where she received 500 mL of 5% dextrose in 0.9% saline at 20 mL/h. Laboratory findings included leukocytosis (39.0 × 10³/μL), severe anemia (5.6 g/dL), and thrombocytosis (502 × 10³/μL). She received a transfusion of 50 mL of filtered, leuko-reduced red blood cells and 40 mL of fresh frozen plasma due to coagulation abnormalities. Enteral feeding was initiated via nasogastric tube, and fluid infusion was reduced to 15 mL/h of 5% dextrose in 0.9% saline, maintained with negative water balance.\\n\\nOn day 2, initial peripheral blood culture revealed Gram-positive cocci in clusters, interpreted as *Staphylococcus aureus*. Oxacillin was initiated at 200 mg/kg/day, ceftriaxone was escalated to 75–100 mg/kg/day, total fluid replacement increased to 120 mL/kg/day, and calcium was corrected (to 6.38 mg/dL). On day 3, venous access was lost, necessitating placement of a central venous catheter (CVC). The patient remained hypovolemic with subhydric oral mucosa, increased respiratory work, cold extremities, and capillary refill time of 3–4 seconds. A 20 mL/kg lactate Ringer's load was administered over one hour", "generated_text": "{\n  \"proficient_health_literacy\": \"A 4-month-old indigenous lactating female infant from the rural interior of Panama, specifically from Urracá, approximately 3 hours by canoe from the nearest health subcenter, presented with acute gastroenteritis and moderate-to-severe dehydration due to protein-caloric malnutrition. The infant was the fourth daughter, born via vaginal delivery at home by a relative without prenatal care; birth weight, height, and Apgar score are unknown. She did not receive breast milk and was exclusively fed powdered milk formula with iron (3 ounces every 4 hours), which is inappropriate for infants under 6 months of age. The household consisted of six members (parents and four children), living in a two-room structure with board walls and palm roof, no electricity, kerosene lighting, well water, and open defecation into a river; economic activity was based on subsistence agriculture. No primary health care was accessed during the first four months of life, and the national expanded programme of immunizations was not administered. Parents reported normal neurodevelopment prior to hospitalization.\\n\\nThe infant presented to a primary health center with a 4-day history of diarrhea without mucus or blood, associated with vomiting of food content; the mother substituted tea for milk due to intolerance. The patient was afebrile and without respiratory symptoms. Initial management included oral rehydration with lactate Ringer's solution (10 ml/kg) and four doses of Enterogermina® (2 billion spores/5 mL), a probiotic containing *Bacillus clausii*. Due to lack of intravenous access (no catheters or intraosseous routes), the patient was transferred to a second-level hospital in the provincial capital and subsequently to a tertiary care facility in Panama City, diagnosed with acute gastroenteritis and severe dehydration.\\n\\nOn presentation to the emergency department, the infant exhibited signs of profound dehydration: tearless cry, dry oral mucosa, and +++ edema in hands, feet, abdomen, and face. Vital signs included afebrile state, tachycardia (HR 170 bpm), tachypnea (RR 55 bpm), hypotension (BP 91/37 mmHg), oxygen saturation 99%, and signs of shock (capillary refill >2 seconds, cold extremities, filiform pulse, marble skin). Admission weight was 4.7 kg, height 56 cm; height Z-score was -2.52, while weight/height and weight/age Z-scores were unquantifiable due to severe dehydration. Physical examination revealed fine crepitus in both lung bases, erythematous-squamous skin lesions with desquamation, and hypopigmented patches on trunk and upper limbs, interpreted as pellagroid dermatosis, likely secondary to vitamin B3 deficiency.\\n\\nInitial resuscitation included 10 ml/kg lactate Ringer's bolus, followed by 500 mL of 5% dextrose in 0.33% saline infused at 29 mL/h over 6 hours without potassium chloride until diuresis was achieved. Empiric antibiotic therapy was initiated with ceftriaxone 50 mg/kg/day for suspected sepsis. The patient was stabilized and transferred to the ward, where she received 500 mL of 5% dextrose in 0.9% saline at 20 mL/h. Laboratory findings included leukocytosis (39.0 × 10³/μL), severe anemia (5.6 g/dL), and thrombocytosis (502 × 10³/μL). She received a transfusion of 50 mL of filtered, leuko-reduced red blood cells and 40 mL of fresh frozen plasma due to coagulation abnormalities. Enteral feeding was initiated via nasogastric tube, and fluid infusion was reduced to 15 mL/h of 5% dextrose in 0.9% saline, maintained with negative water balance.\\n\\nOn day 2, initial peripheral blood culture revealed Gram-positive cocci in clusters, interpreted as *Staphylococcus aureus*. Oxacillin was initiated at 200 mg/kg/day, ceftriaxone was escalated to 75–100 mg/kg/day, total fluid replacement increased to 120 mL/kg/day, and calcium was corrected (to 6.38 mg/dL). On day 3, venous access was lost, necessitating placement of a central venous catheter (CVC). The patient remained hypovolemic with subhydric oral mucosa, increased respiratory work, cold extremities, and capillary refill time of 3–4 seconds. A 20 mL/kg lactate Ringer's load was administered over one hour"}
+{"row_index": 68, "doc_id": 55, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 2-year-old girl had a bump in her eye that grew over a year, making her eye stick out and move inward and upward. Her eye didn’t work well, and her pupil was big and didn’t react. Doctors found a soft lump inside her eye socket using MRI, which looked like a mix of brain, cartilage, and other tissues. The lump was removed through a small cut in the lower eyelid, and a little fluid was taken out. After surgery, her eye sank back in (enophthalmos), her eyelid got red, and her cornea got inflamed because the space inside the eye changed. A second surgery was done to put in a piece of donated eye tissue (sclera) to fill the space, which helped fix the redness and kept the cornea healthy. One year later, the lump didn’t come back, and her eye looked and worked better. She still has a small eye sink and a slight eyelid issue, but her vision is the same as before.\"\n}", "generated_text": "A 2-year-old girl had a bump in her eye that grew over a year, making her eye stick out and move inward and upward. Her eye didn’t work well, and her pupil was big and didn’t react. Doctors found a soft lump inside her eye socket using MRI, which looked like a mix of brain, cartilage, and other tissues. The lump was removed through a small cut in the lower eyelid, and a little fluid was taken out. After surgery, her eye sank back in (enophthalmos), her eyelid got red, and her cornea got inflamed because the space inside the eye changed. A second surgery was done to put in a piece of donated eye tissue (sclera) to fill the space, which helped fix the redness and kept the cornea healthy. One year later, the lump didn’t come back, and her eye looked and worked better. She still has a small eye sink and a slight eyelid issue, but her vision is the same as before."}
+{"row_index": 69, "doc_id": 55, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 2-year-old female presented with a 1-year history of painless, progressive left-sided proptosis, without associated systemic illness or familial predisposition. Ophthalmologic examination revealed preserved light sensation as the sole visual input in the left eye, accompanied by marked proptosis, inward and upward displacement of the globe, and restricted downward and outward extraocular muscle movements. A palpable, irregularly shaped, well-circumscribed soft mass was identified in the inferior orbit, associated with left lower eyelid ectropion. The pupil measured 4 mm in diameter and exhibited absent pupillary reaction. Anterior segment evaluation showed no other abnormalities; fundus assessment was limited by the child's small size. Hertel exophthalmometry demonstrated a right eye measurement of 10.5 mm and a left eye measurement of 18 mm, indicating significant orbital expansion. Magnetic resonance imaging (MRI) revealed a well-defined orbital mass with hypointense signal intensity on T1-weighted images (T1WI) and hyperintense signal intensity on T2-weighted images (T2WI), consistent with a cystic lesion containing heterogeneous tissue components. Contrast-enhanced MRI showed no significant enhancement, suggesting a non-vascularized or low-vascularity lesion. A transconjunctival approach via the inferior fornix was employed, with concomitant canthotomy and cantholysis to facilitate access. Intraoperative findings included a grayish-white, cystic mass with a distinct boundary from surrounding orbital tissues. During posterior dissection, tight adhesion of the mass to the optic nerve was observed, indicating prior inflammatory or fibrotic interaction. Given the substantial size of the mass and the limited surgical field, volume reduction was necessary. Approximately 12.5 mL of fluid was aspirated, and the entire mass was completely excised. Histopathological examination confirmed the presence of a fibrous capsule lined with squamous and glandular epithelium, along with identifiable brain tissue and a cartilage-like matrix, consistent with a true orbital teratoma. Immunohistochemical analysis further supported the diagnosis by demonstrating positive staining for markers such as cytokeratin, S-100 protein, and glial fibrillary acidic protein (GFAP), reflecting the pluripotent origin of the teratoma. Postoperatively, at one month, the patient developed enophthalmos, conjunctival hyperemia, and keratitis. This clinical deterioration was attributed to the preoperative enlargement of the orbital cavity by the teratoma, resulting in a loss of orbital volume and subsequent postoperative orbital collapse. The cornea failed to maintain apposition to the eyelids, leading to a corneal exposure and subsequent inflammation. With informed consent from the patient’s guardian, a secondary surgical intervention was performed involving the implantation of allogeneic scleral tissue into the orbit to restore orbital volume, correct fossal pitting, and re-establish corneal apposition. One-year follow-up revealed no evidence of tumor recurrence or other major complications. Persistent minor enophthalmos and outer canthus malformation remained, though visual acuity remained stable and equivalent to preoperative levels. Repeat Hertel exophthalmometry showed a right eye measurement of 10.5 mm and a left eye measurement of 8 mm, indicating partial correction of proptosis. The anterior segment examination remained unremarkable, with no signs of inflammation or structural compromise. The case underscores the importance of surgical planning in orbital teratoma resection, particularly in pediatric patients, where orbital volume preservation and tissue apposition are critical to long-term ocular function and cosmetic outcomes.\"\n}", "generated_text": "A 2-year-old female presented with a 1-year history of painless, progressive left-sided proptosis, without associated systemic illness or familial predisposition. Ophthalmologic examination revealed preserved light sensation as the sole visual input in the left eye, accompanied by marked proptosis, inward and upward displacement of the globe, and restricted downward and outward extraocular muscle movements. A palpable, irregularly shaped, well-circumscribed soft mass was identified in the inferior orbit, associated with left lower eyelid ectropion. The pupil measured 4 mm in diameter and exhibited absent pupillary reaction. Anterior segment evaluation showed no other abnormalities; fundus assessment was limited by the child's small size. Hertel exophthalmometry demonstrated a right eye measurement of 10.5 mm and a left eye measurement of 18 mm, indicating significant orbital expansion. Magnetic resonance imaging (MRI) revealed a well-defined orbital mass with hypointense signal intensity on T1-weighted images (T1WI) and hyperintense signal intensity on T2-weighted images (T2WI), consistent with a cystic lesion containing heterogeneous tissue components. Contrast-enhanced MRI showed no significant enhancement, suggesting a non-vascularized or low-vascularity lesion. A transconjunctival approach via the inferior fornix was employed, with concomitant canthotomy and cantholysis to facilitate access. Intraoperative findings included a grayish-white, cystic mass with a distinct boundary from surrounding orbital tissues. During posterior dissection, tight adhesion of the mass to the optic nerve was observed, indicating prior inflammatory or fibrotic interaction. Given the substantial size of the mass and the limited surgical field, volume reduction was necessary. Approximately 12.5 mL of fluid was aspirated, and the entire mass was completely excised. Histopathological examination confirmed the presence of a fibrous capsule lined with squamous and glandular epithelium, along with identifiable brain tissue and a cartilage-like matrix, consistent with a true orbital teratoma. Immunohistochemical analysis further supported the diagnosis by demonstrating positive staining for markers such as cytokeratin, S-100 protein, and glial fibrillary acidic protein (GFAP), reflecting the pluripotent origin of the teratoma. Postoperatively, at one month, the patient developed enophthalmos, conjunctival hyperemia, and keratitis. This clinical deterioration was attributed to the preoperative enlargement of the orbital cavity by the teratoma, resulting in a loss of orbital volume and subsequent postoperative orbital collapse. The cornea failed to maintain apposition to the eyelids, leading to a corneal exposure and subsequent inflammation. With informed consent from the patient’s guardian, a secondary surgical intervention was performed involving the implantation of allogeneic scleral tissue into the orbit to restore orbital volume, correct fossal pitting, and re-establish corneal apposition. One-year follow-up revealed no evidence of tumor recurrence or other major complications. Persistent minor enophthalmos and outer canthus malformation remained, though visual acuity remained stable and equivalent to preoperative levels. Repeat Hertel exophthalmometry showed a right eye measurement of 10.5 mm and a left eye measurement of 8 mm, indicating partial correction of proptosis. The anterior segment examination remained unremarkable, with no signs of inflammation or structural compromise. The case underscores the importance of surgical planning in orbital teratoma resection, particularly in pediatric patients, where orbital volume preservation and tissue apposition are critical to long-term ocular function and cosmetic outcomes."}
+{"row_index": 70, "doc_id": 56, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 78-year-old woman was feeling very tired, weak, dizzy, and confused for months. This made it hard for her to walk around her home. She was given a personalized medicine plan, and we checked her medicines to see which ones might be causing these symptoms. We found that her kidneys were not working as well as they should, which means her body can’t clear some medicines properly. We looked at how much her kidneys can filter waste (called eGFR), and it was only 30 — that’s a sign her kidneys are not working well. Because of this, we decided to lower the dose of two blood pressure medicines: losartan and manidipine. The doctor agreed and reduced them to safer levels. We also switched her pain medicine from pregabalin to gabapentin, which is safer for her kidneys. After two months, she felt better — no more tiredness, dizziness, or confusion. Her blood pressure also improved. We kept watching her to make sure everything stayed safe and working well.\"\n}", "generated_text": "A 78-year-old woman was feeling very tired, weak, dizzy, and confused for months. This made it hard for her to walk around her home. She was given a personalized medicine plan, and we checked her medicines to see which ones might be causing these symptoms. We found that her kidneys were not working as well as they should, which means her body can’t clear some medicines properly. We looked at how much her kidneys can filter waste (called eGFR), and it was only 30 — that’s a sign her kidneys are not working well. Because of this, we decided to lower the dose of two blood pressure medicines: losartan and manidipine. The doctor agreed and reduced them to safer levels. We also switched her pain medicine from pregabalin to gabapentin, which is safer for her kidneys. After two months, she felt better — no more tiredness, dizziness, or confusion. Her blood pressure also improved. We kept watching her to make sure everything stayed safe and working well."}
+{"row_index": 71, "doc_id": 56, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 78-year-old woman who was taking several medications reported feeling tired, weak, dizzy, and confused for months. These symptoms made it hard for her to leave her home or walk as she used to. She was seen at the pharmacy for a medication review, focusing on drugs that are processed by the kidneys, especially since her kidney function was found to be reduced (estimated glomerular filtration rate or eGFR of 30 ml/min/1.73 m²). \\n\\nThe review looked at her blood pressure and medication doses, particularly for her blood pressure medications: losartan and manidipine. Because her kidneys are not working as well, these medicines need to be lowered in dose to avoid low blood pressure, which can cause dizziness and confusion. The pharmacy team recommended reducing losartan to 50 mg daily and manidipine to 10 mg daily. They also switched her pregabalin to gabapentin, which is safer for her kidney function.\\n\\nThe changes were shared with her primary care doctor, who agreed to adjust the doses. After two months of following the new treatment, her blood pressure improved and the symptoms of tiredness, weakness, dizziness, and confusion went away. The doctor confirmed that the new gabapentin dose was safe and appropriate for her kidney function.\"\n}", "generated_text": "A 78-year-old woman who was taking several medications reported feeling tired, weak, dizzy, and confused for months. These symptoms made it hard for her to leave her home or walk as she used to. She was seen at the pharmacy for a medication review, focusing on drugs that are processed by the kidneys, especially since her kidney function was found to be reduced (estimated glomerular filtration rate or eGFR of 30 ml/min/1.73 m²). \n\nThe review looked at her blood pressure and medication doses, particularly for her blood pressure medications: losartan and manidipine. Because her kidneys are not working as well, these medicines need to be lowered in dose to avoid low blood pressure, which can cause dizziness and confusion. The pharmacy team recommended reducing losartan to 50 mg daily and manidipine to 10 mg daily. They also switched her pregabalin to gabapentin, which is safer for her kidney function.\n\nThe changes were shared with her primary care doctor, who agreed to adjust the doses. After two months of following the new treatment, her blood pressure improved and the symptoms of tiredness, weakness, dizziness, and confusion went away. The doctor confirmed that the new gabapentin dose was safe and appropriate for her kidney function."}
+{"row_index": 72, "doc_id": 56, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 78-year-old female patient, enrolled in a Personalised Medication Dosage System (PDS), presented with persistent symptoms of fatigue, weakness, dizziness, and confusion over several months, significantly impairing her ability to perform ambulatory activities. Upon clinical evaluation, she was referred to a personalised care area for a comprehensive medication review, with a focus on pharmacokinetic interactions relevant to renal function, particularly those affecting drugs metabolised or eliminated by the kidneys. The review centred on her estimated glomerular filtration rate (eGFR), calculated using the Chronic Kidney Disease-Epidemiology Collaboration (CKD-EPI) formula, which yielded a value of 30 ml/min/1.73 m², indicating stage 3 chronic kidney disease (CKD).\\n\\nThe patient’s pharmacological regimen included doxazosin (2 mg/24 h), losartan (100 mg/24 h), manidipine (20 mg/24 h), simvastatin (40 mg/24 h), acetylsalicylic acid (100 mg/24 h), omeprazole (20 mg/24 h), pregabalin (100 mg/12 h), torasemide (10 mg/24 h), dulaglutide (1.5 mg/week), insulin glargine (74 IU/24 h), insulin lispro (20 IU/24 h), and brimonidine (1 drop/12 h). Among these, losartan, manidipine, torasemide, and pregabalin were identified as requiring dose adjustment due to renal impairment, with antihypertensives being the primary focus given the patient’s symptoms of hypotension.\\n\\nBlood pressure measurements using an Omron Complete device revealed a systolic blood pressure (SBP) of 96 mmHg, diastolic blood pressure (DBP) of 52 mmHg, and heart rate (HR) of 69 beats per minute—values consistent with hypotension, particularly in the context of antihypertensive therapy. The decision to adjust medication doses was guided by product-specific labeling and consensus guidelines from the University of Barcelona Faculty of Pharmacy’s Practical Pharmacy Teaching and Research Group, which categorises drug risk based on eGFR thresholds across therapeutic classes using the ATC classification system. These guidelines define risk levels as low, moderate, or high depending on the extent of renal dysfunction and the drug’s elimination pathway.\\n\\nSpecifically, for eGFR values between 30–59 ml/min/1.73 m², the recommended dose reduction for losartan is 50–75% of the original dose, while for eGFR values between 15–30 ml/min/1.73 m², manidipine requires dose adjustment, typically reduced to a fraction of the standard dose (e.g., 10 mg/24 h). Torasemide, a loop diuretic, can contribute to volume depletion and hypotension, particularly in patients with reduced renal function, and thus its effect on blood pressure must be monitored. Pregabalin, used for neuropathic pain, has a moderate risk of accumulation in renal impairment and may require cautious titration, though its adjustment was deferred pending the efficacy of antihypertensive dose reduction.\\n\\nThe intervention protocol involved a formal report to the primary care physician (PCP), recommending a reduction of losartan to 50 mg/24 h and manidipine to 10 mg/24 h, in accordance with the eGFR-based dosing guidelines. Additionally, pregabalin was substituted with gabapentin (300 mg/12 h), a structurally related agent with a more favourable pharmacokinetic profile in renal impairment, as gabapentin is primarily eliminated by the kidneys but exhibits a lower risk of accumulation at eGFR levels between 30–60 ml/min/1.73 m², with a recommended total daily dose of 300–900 mg.\\n\\nThe PCP implemented the proposed changes. Follow-up assessments over a two-month period demonstrated a significant improvement in blood pressure control (as documented in Table 5) and a complete resolution of the patient’s symptoms of fatigue, weakness, dizziness, and confusion. The gabapentin dose of 300 mg/12 h was subsequently confirmed to be within the recommended range for her eGFR of 30 ml/min/1.73 m², supporting its safety and efficacy in this context. The case underscores the importance of routine eGFR-based medication review in elderly patients with polypharmacy, particularly when symptoms of hypotension or", "generated_text": "{\n  \"proficient_health_literacy\": \"A 78-year-old female patient, enrolled in a Personalised Medication Dosage System (PDS), presented with persistent symptoms of fatigue, weakness, dizziness, and confusion over several months, significantly impairing her ability to perform ambulatory activities. Upon clinical evaluation, she was referred to a personalised care area for a comprehensive medication review, with a focus on pharmacokinetic interactions relevant to renal function, particularly those affecting drugs metabolised or eliminated by the kidneys. The review centred on her estimated glomerular filtration rate (eGFR), calculated using the Chronic Kidney Disease-Epidemiology Collaboration (CKD-EPI) formula, which yielded a value of 30 ml/min/1.73 m², indicating stage 3 chronic kidney disease (CKD).\\n\\nThe patient’s pharmacological regimen included doxazosin (2 mg/24 h), losartan (100 mg/24 h), manidipine (20 mg/24 h), simvastatin (40 mg/24 h), acetylsalicylic acid (100 mg/24 h), omeprazole (20 mg/24 h), pregabalin (100 mg/12 h), torasemide (10 mg/24 h), dulaglutide (1.5 mg/week), insulin glargine (74 IU/24 h), insulin lispro (20 IU/24 h), and brimonidine (1 drop/12 h). Among these, losartan, manidipine, torasemide, and pregabalin were identified as requiring dose adjustment due to renal impairment, with antihypertensives being the primary focus given the patient’s symptoms of hypotension.\\n\\nBlood pressure measurements using an Omron Complete device revealed a systolic blood pressure (SBP) of 96 mmHg, diastolic blood pressure (DBP) of 52 mmHg, and heart rate (HR) of 69 beats per minute—values consistent with hypotension, particularly in the context of antihypertensive therapy. The decision to adjust medication doses was guided by product-specific labeling and consensus guidelines from the University of Barcelona Faculty of Pharmacy’s Practical Pharmacy Teaching and Research Group, which categorises drug risk based on eGFR thresholds across therapeutic classes using the ATC classification system. These guidelines define risk levels as low, moderate, or high depending on the extent of renal dysfunction and the drug’s elimination pathway.\\n\\nSpecifically, for eGFR values between 30–59 ml/min/1.73 m², the recommended dose reduction for losartan is 50–75% of the original dose, while for eGFR values between 15–30 ml/min/1.73 m², manidipine requires dose adjustment, typically reduced to a fraction of the standard dose (e.g., 10 mg/24 h). Torasemide, a loop diuretic, can contribute to volume depletion and hypotension, particularly in patients with reduced renal function, and thus its effect on blood pressure must be monitored. Pregabalin, used for neuropathic pain, has a moderate risk of accumulation in renal impairment and may require cautious titration, though its adjustment was deferred pending the efficacy of antihypertensive dose reduction.\\n\\nThe intervention protocol involved a formal report to the primary care physician (PCP), recommending a reduction of losartan to 50 mg/24 h and manidipine to 10 mg/24 h, in accordance with the eGFR-based dosing guidelines. Additionally, pregabalin was substituted with gabapentin (300 mg/12 h), a structurally related agent with a more favourable pharmacokinetic profile in renal impairment, as gabapentin is primarily eliminated by the kidneys but exhibits a lower risk of accumulation at eGFR levels between 30–60 ml/min/1.73 m², with a recommended total daily dose of 300–900 mg.\\n\\nThe PCP implemented the proposed changes. Follow-up assessments over a two-month period demonstrated a significant improvement in blood pressure control (as documented in Table 5) and a complete resolution of the patient’s symptoms of fatigue, weakness, dizziness, and confusion. The gabapentin dose of 300 mg/12 h was subsequently confirmed to be within the recommended range for her eGFR of 30 ml/min/1.73 m², supporting its safety and efficacy in this context. The case underscores the importance of routine eGFR-based medication review in elderly patients with polypharmacy, particularly when symptoms of hypotension or"}
+{"row_index": 73, "doc_id": 57, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"This story is about a 9-year-old girl who has really smart brain skills but struggles with reading and writing because of dyslexia. Before help, she could only read simple letters and had trouble with sounds in words. She wrote in a messy way, mixing up letters and skipping parts. Her brain had trouble remembering sounds and seeing words quickly. After a few weeks of fun, weekly lessons focused on sounds and words, she got better. Now she reads faster and more clearly, and her writing is much more organized. She still has some challenges, like mixing up similar letters, but she’s making progress. The main thing that helped was working on how her brain handles sounds and words in a playful way, like playing games with letters and sounds.\"\n}", "generated_text": "This story is about a 9-year-old girl who has really smart brain skills but struggles with reading and writing because of dyslexia. Before help, she could only read simple letters and had trouble with sounds in words. She wrote in a messy way, mixing up letters and skipping parts. Her brain had trouble remembering sounds and seeing words quickly. After a few weeks of fun, weekly lessons focused on sounds and words, she got better. Now she reads faster and more clearly, and her writing is much more organized. She still has some challenges, like mixing up similar letters, but she’s making progress. The main thing that helped was working on how her brain handles sounds and words in a playful way, like playing games with letters and sounds."}
+{"row_index": 74, "doc_id": 57, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"This case report presents a longitudinal, interdisciplinary evaluation and intervention study of a 9-year-old female child diagnosed with developmental dyslexia (DD) and high abilities/giftedness (AH/S), conducted within a public service framework under Research Ethics Committee (CEP) approval number 1.012.635, with informed consent obtained from both parents and the participant via Free and Informed Consent (TCLE and TALE). The participant, enrolled in the third year of elementary school, was initially assessed in 2018 at 8 years and 2 months of age, with a follow-up evaluation in 2019 at 9 years and 6 months, reflecting a 14-month interval due to institutional scheduling constraints and weekly appointment frequency, during which the child experienced intermittent school absences.\\n\\nThe child was born at term with typical neuropsychomotor and linguistic development. She was raised in a French-speaking environment until age 2, after which her home language shifted to Brazilian Portuguese due to parental background. Her first words were in French, and upon return to Brazil, she attended two private schools: initially, she failed to communicate in Portuguese, expressing exclusively in French; at age 3, she transitioned to a French-language school in Brazil. Over time, she exhibited persistent difficulties in reading and writing, leading to a repetition of the first year of elementary school at her mother’s request. At age 6, she enrolled in a bilingual Portuguese-English school. At age 8, she underwent a comprehensive neuropsychological and speech therapy evaluation, resulting in a diagnosis of developmental dyslexia with concomitant high cognitive abilities.\\n\\nThe study employed four assessment sessions—two pre-intervention (T1) and two post-intervention (T2)—each comprising a one-hour individualized evaluation of phonological processing, reading, and writing. The intervention consisted of 20 weekly 60-minute sessions of phonological remediation, administered in the second semester of 2018, with limited parental engagement due to work obligations. The remediation program was based on evidence-informed protocols for dyslexic populations and included targeted activities designed to strengthen phonological awareness, such as grapheme-phoneme correspondence, phoneme pair identification, syllable and word manipulation, phonemic addition/subtraction, rhyming, alliteration, and access to the mental lexicon. Activities were delivered in a metalinguistically oriented, play-based format, with reading training using the Mico Maneco children’s book collection, which progressively increases lexical complexity to track developmental gains. All sessions were documented in the clinical record.\\n\\nAssessment tools included the Consciência Fonológica Instrumento de Avaliação Sequencial (CONFIAS) for phonological awareness, which evaluates syllabic and phonemic awareness through segmentation, rhyme, alliteration, and transposition tasks. Scores are scored out of 70 (40 for syllabic, 30 for phonemic), with normative benchmarks derived from Ferreiro and Teberosky: syllabic-alphabetic writing hypothesis (syllabic = 27, phonemic = 12, total = 39); alphabetic writing hypothesis (syllabic = 31, phonemic = 15, total = 46). In T1, the child met the syllabic-alphabetic hypothesis (syllabic = 35, phonemic = 14); in T2, she met the alphabetic hypothesis (syllabic = 37, phonemic = 20), indicating significant improvement in phonemic processing, with a 6-point gain in phonemic awareness—consistent with targeted intervention.\\n\\nPhonological working memory was assessed using the Phonological Working Memory Test. The non-word repetition task (40 invented words) and digit reversal tasks were administered, with scoring based on correct repetitions across three attempts. Normative values for age 8 years (T1) were: pseudo-words = 69, direct digits = 13, reverse digits = 6. In T1, the child scored 66 (below expected) in pseudo-words and 4 (below expected) in reverse digits; in T2, scores improved to 69 (within normal range) and 12 (above expected), indicating gains in working memory capacity, particularly in executive functions related to rapid auditory storage and response retrieval.\\n\\nAutomatic Rapid Naming (RAN) and the updated Automatic Naming Test (TENA) were used to assess mental lexicon access. T1 used RAN with age-specific norms (8 years 0–11 months): digits = 28 s, letters = 29 s, objects = 52 s, colors = 46 s. T2 used TENA norms for 9 years 6 months: digits = 35 s, letters =", "generated_text": "{\n  \"proficient_health_literacy\": \"This case report presents a longitudinal, interdisciplinary evaluation and intervention study of a 9-year-old female child diagnosed with developmental dyslexia (DD) and high abilities/giftedness (AH/S), conducted within a public service framework under Research Ethics Committee (CEP) approval number 1.012.635, with informed consent obtained from both parents and the participant via Free and Informed Consent (TCLE and TALE). The participant, enrolled in the third year of elementary school, was initially assessed in 2018 at 8 years and 2 months of age, with a follow-up evaluation in 2019 at 9 years and 6 months, reflecting a 14-month interval due to institutional scheduling constraints and weekly appointment frequency, during which the child experienced intermittent school absences.\\n\\nThe child was born at term with typical neuropsychomotor and linguistic development. She was raised in a French-speaking environment until age 2, after which her home language shifted to Brazilian Portuguese due to parental background. Her first words were in French, and upon return to Brazil, she attended two private schools: initially, she failed to communicate in Portuguese, expressing exclusively in French; at age 3, she transitioned to a French-language school in Brazil. Over time, she exhibited persistent difficulties in reading and writing, leading to a repetition of the first year of elementary school at her mother’s request. At age 6, she enrolled in a bilingual Portuguese-English school. At age 8, she underwent a comprehensive neuropsychological and speech therapy evaluation, resulting in a diagnosis of developmental dyslexia with concomitant high cognitive abilities.\\n\\nThe study employed four assessment sessions—two pre-intervention (T1) and two post-intervention (T2)—each comprising a one-hour individualized evaluation of phonological processing, reading, and writing. The intervention consisted of 20 weekly 60-minute sessions of phonological remediation, administered in the second semester of 2018, with limited parental engagement due to work obligations. The remediation program was based on evidence-informed protocols for dyslexic populations and included targeted activities designed to strengthen phonological awareness, such as grapheme-phoneme correspondence, phoneme pair identification, syllable and word manipulation, phonemic addition/subtraction, rhyming, alliteration, and access to the mental lexicon. Activities were delivered in a metalinguistically oriented, play-based format, with reading training using the Mico Maneco children’s book collection, which progressively increases lexical complexity to track developmental gains. All sessions were documented in the clinical record.\\n\\nAssessment tools included the Consciência Fonológica Instrumento de Avaliação Sequencial (CONFIAS) for phonological awareness, which evaluates syllabic and phonemic awareness through segmentation, rhyme, alliteration, and transposition tasks. Scores are scored out of 70 (40 for syllabic, 30 for phonemic), with normative benchmarks derived from Ferreiro and Teberosky: syllabic-alphabetic writing hypothesis (syllabic = 27, phonemic = 12, total = 39); alphabetic writing hypothesis (syllabic = 31, phonemic = 15, total = 46). In T1, the child met the syllabic-alphabetic hypothesis (syllabic = 35, phonemic = 14); in T2, she met the alphabetic hypothesis (syllabic = 37, phonemic = 20), indicating significant improvement in phonemic processing, with a 6-point gain in phonemic awareness—consistent with targeted intervention.\\n\\nPhonological working memory was assessed using the Phonological Working Memory Test. The non-word repetition task (40 invented words) and digit reversal tasks were administered, with scoring based on correct repetitions across three attempts. Normative values for age 8 years (T1) were: pseudo-words = 69, direct digits = 13, reverse digits = 6. In T1, the child scored 66 (below expected) in pseudo-words and 4 (below expected) in reverse digits; in T2, scores improved to 69 (within normal range) and 12 (above expected), indicating gains in working memory capacity, particularly in executive functions related to rapid auditory storage and response retrieval.\\n\\nAutomatic Rapid Naming (RAN) and the updated Automatic Naming Test (TENA) were used to assess mental lexicon access. T1 used RAN with age-specific norms (8 years 0–11 months): digits = 28 s, letters = 29 s, objects = 52 s, colors = 46 s. T2 used TENA norms for 9 years 6 months: digits = 35 s, letters ="}
+{"row_index": 75, "doc_id": 58, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 65-year-old woman had a lump found in the middle of her chest, behind her breastbone, during a check-up before knee surgery. The lump was about 6.5 cm long and 4.2 cm wide, had clear edges, and looked like fat and solid tissue. Doctors took a small sample and found it was made of mature fat and some blood cells, which are normal parts of the body. This kind of lump is not cancer and is harmless. So, they decided not to treat it with surgery and just watched it. She felt fine and went home without any problems.\"\n}", "generated_text": "A 65-year-old woman had a lump found in the middle of her chest, behind her breastbone, during a check-up before knee surgery. The lump was about 6.5 cm long and 4.2 cm wide, had clear edges, and looked like fat and solid tissue. Doctors took a small sample and found it was made of mature fat and some blood cells, which are normal parts of the body. This kind of lump is not cancer and is harmless. So, they decided not to treat it with surgery and just watched it. She felt fine and went home without any problems."}
+{"row_index": 76, "doc_id": 58, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 65-year-old woman was found to have a tumor in the middle of her chest, specifically in the posterior mediastinum, during a routine check-up before knee surgery. The tumor was about 6.5 × 4.2 cm, well-defined, and had both fat and solid parts. It did not spread to nearby tissues or bones. A biopsy was done using image guidance, and the results showed that the tumor was made up of mature fat tissue with some blood cells and early blood cell precursors, which is a sign of a benign (non-cancerous) condition called primary mediastinal myelolipoma. Because the tumor was not dangerous and did not grow, the doctors chose not to treat it surgically. The patient recovered well and was discharged without any complications.\"\n}", "generated_text": "A 65-year-old woman was found to have a tumor in the middle of her chest, specifically in the posterior mediastinum, during a routine check-up before knee surgery. The tumor was about 6.5 × 4.2 cm, well-defined, and had both fat and solid parts. It did not spread to nearby tissues or bones. A biopsy was done using image guidance, and the results showed that the tumor was made up of mature fat tissue with some blood cells and early blood cell precursors, which is a sign of a benign (non-cancerous) condition called primary mediastinal myelolipoma. Because the tumor was not dangerous and did not grow, the doctors chose not to treat it surgically. The patient recovered well and was discharged without any complications."}
+{"row_index": 77, "doc_id": 58, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 65-year-old woman with no significant personal or familial medical history presented in August 2022 with a posterior mediastinal tumor identified during preoperative imaging for knee surgery. She was referred for evaluation and management. Physical examination at admission was unremarkable, and all laboratory studies remained within normal limits. A chest computed tomography (CT) scan revealed a well-defined, ovoid lesion measuring 6.5 × 4.2 cm in the posterior right mediastinum, exhibiting mixed fat and solid density, with no signs of bone erosion, soft tissue infiltration, or vascular invasion. The tumor was localized and demonstrated clear margins, consistent with a benign lesion. A trans-thoracic biopsy was performed using a 18G × 250 mm semiautomatic cutting needle under image guidance via a posterior approach, ensuring precise targeting and minimal trauma. Histopathological analysis confirmed a benign neoplasm composed of mature adipose tissue intermixed with areas of hemorrhage and hematopoietic elements. The hematopoietic components included primarily precursors of the erythroid lineage (red cell series), as well as myeloid precursors at various stages of maturation, including megakaryocytes, which are bone marrow-derived cells responsible for platelet production. This pattern of mature adipose tissue with active, albeit non-malignant, hematopoiesis is characteristic of primary mediastinal myelolipoma (PMML), a rare benign tumor of the mediastinum. The presence of both adipose and hematopoietic elements, particularly in a well-differentiated and non-invasive context, supports the diagnosis of primary mediastinal myelolipoma (MPM) as defined by the World Health Organization (WHO) classification of soft tissue tumors. Given the benign nature of the lesion, lack of local invasion, and absence of systemic features such as hypercellular marrow or metastatic spread, conservative management was adopted. The patient showed no signs of progression or complications and was discharged without adverse events. This case underscores the importance of imaging and biopsy in differentiating benign mediastinal masses from malignant neoplasms, particularly when hematopoietic elements are present within adipose tissue, as such findings may mimic hematologic malignancies but are instead indicative of a distinct, well-characterized benign entity.\"\n}", "generated_text": "A 65-year-old woman with no significant personal or familial medical history presented in August 2022 with a posterior mediastinal tumor identified during preoperative imaging for knee surgery. She was referred for evaluation and management. Physical examination at admission was unremarkable, and all laboratory studies remained within normal limits. A chest computed tomography (CT) scan revealed a well-defined, ovoid lesion measuring 6.5 × 4.2 cm in the posterior right mediastinum, exhibiting mixed fat and solid density, with no signs of bone erosion, soft tissue infiltration, or vascular invasion. The tumor was localized and demonstrated clear margins, consistent with a benign lesion. A trans-thoracic biopsy was performed using a 18G × 250 mm semiautomatic cutting needle under image guidance via a posterior approach, ensuring precise targeting and minimal trauma. Histopathological analysis confirmed a benign neoplasm composed of mature adipose tissue intermixed with areas of hemorrhage and hematopoietic elements. The hematopoietic components included primarily precursors of the erythroid lineage (red cell series), as well as myeloid precursors at various stages of maturation, including megakaryocytes, which are bone marrow-derived cells responsible for platelet production. This pattern of mature adipose tissue with active, albeit non-malignant, hematopoiesis is characteristic of primary mediastinal myelolipoma (PMML), a rare benign tumor of the mediastinum. The presence of both adipose and hematopoietic elements, particularly in a well-differentiated and non-invasive context, supports the diagnosis of primary mediastinal myelolipoma (MPM) as defined by the World Health Organization (WHO) classification of soft tissue tumors. Given the benign nature of the lesion, lack of local invasion, and absence of systemic features such as hypercellular marrow or metastatic spread, conservative management was adopted. The patient showed no signs of progression or complications and was discharged without adverse events. This case underscores the importance of imaging and biopsy in differentiating benign mediastinal masses from malignant neoplasms, particularly when hematopoietic elements are present within adipose tissue, as such findings may mimic hematologic malignancies but are instead indicative of a distinct, well-characterized benign entity."}
+{"row_index": 78, "doc_id": 59, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 52-year-old man got sick with both a bad fever and a COVID-19 infection. He worked outside in very hot weather, which made his body overheat and go into a dangerous coma. His temperature reached 40°C, and he stopped breathing on his own. Doctors found he had a lung infection, damaged liver and kidneys, and a serious blood clotting problem. Even after giving him antibiotics, fluids, and help to protect his organs, he got worse. Days later, he started having trouble breathing and a brain bleed. He had a severe mix of infections and blood problems that hurt many parts of his body. This led to a life-threatening condition called multi-organ failure, and he passed away.\"\n}", "generated_text": "A 52-year-old man got sick with both a bad fever and a COVID-19 infection. He worked outside in very hot weather, which made his body overheat and go into a dangerous coma. His temperature reached 40°C, and he stopped breathing on his own. Doctors found he had a lung infection, damaged liver and kidneys, and a serious blood clotting problem. Even after giving him antibiotics, fluids, and help to protect his organs, he got worse. Days later, he started having trouble breathing and a brain bleed. He had a severe mix of infections and blood problems that hurt many parts of his body. This led to a life-threatening condition called multi-organ failure, and he passed away."}
+{"row_index": 79, "doc_id": 59, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 52-year-old male presented with a community-acquired SARS-CoV-2 infection confirmed by reverse-transcription polymerase chain reaction (RT-PCR) of a nasopharyngeal swab, coinciding with the onset of heatstroke (HS). Initial exposure to SARS-CoV-2 occurred during a cold-like illness, followed by return to work without fever after two days of rest. While working outdoors in an ambient temperature of 35°C for five hours, he lost consciousness, with a core temperature (Tc) measured at 40°C upon emergency department admission. The clinical presentation—persistent coma, hyperpyrexia, dyspnea, and gastrointestinal hemorrhage—was consistent with a diagnosis of heatstroke, supported by the absence of underlying comorbidities or familial disease history. The Glasgow Coma Scale (GCS) score was 3/15 (1 for eye-opening, verbal, and motor responses), with symmetrical, non-reactive pupils. Vital signs included a heart rate of 106 bpm and maintained blood pressure (126/77 mmHg) via continuous norepinephrine infusion (0.4 µg/kg·min).\\n\\nLaboratory findings revealed a severe systemic inflammatory response: white blood cell count (WBC) decreased from 3.55×10⁹/L to 3.13×10⁹/L, with a marked reduction in lymphocytes (from 0.25×10⁹/L to 0.1×10⁹/L) and a rise in neutrophil percentage (N%) to 85.3%. Procalcitonin was elevated to 2.81 ng/mL, indicating bacterial infection, and C-reactive protein (CRP) reached 32.6 mg/L. Sputum culture identified Stenotrophomonas maltophilia and Candida lipolytica; central venous catheter culture revealed Staphylococcus epidermidis, while blood cultures remained negative. CT imaging demonstrated bilateral frontal subdural effusions, bilateral pleural effusions, lower lobe consolidation and atelectasis, right upper lobe inflammation, and a small amount of abdominal fluid, indicating a multi-organ pulmonary infection.\\n\\nThe patient was admitted to the emergency intensive care unit (ICU) and initiated with intravenous rehydration using lactated Ringer’s solution and normal saline at 2.5 mL/kg·h, mechanical ventilation (synchronized intermittent mandatory ventilation with PEEP of 5 mmH₂O and FiO₂ of 80%), vasoactive support, and continuous renal replacement therapy (CRRT) for anuria. Initial antibiotics were Piperacillin Sodium and Tazobactam Sodium, later switched to Meropenem due to S. maltophilia and methicillin-resistant Staphylococcus aureus (MRSA) isolation from sputum. Thymalfasin was administered for 20 days to modulate immune function. Hepatic and renal dysfunction were managed with polyene phosphatidylcholine, adenosylmethionine budisulfonate, ulinastatin, and hemofiltration. Intracranial pressure was managed with mannitol for three days. Coagulopathy was characterized by thrombocytopenia, anemia, and disseminated intravascular coagulation (DIC), with treatment including plasma and cryoprecipitate transfusions, continuous heparin infusion (6000 U/day), and CRRT with sodium citrate anticoagulation (8 g/day) initiated on day 7. Platelet transfusion was administered after day 9.\\n\\nThe patient regained consciousness on day 13 with a GCS of 14/15 and moderate fever, with no active gastrointestinal bleeding. Mechanical ventilation was discontinued and the tracheal tube removed. However, discontinuation of CRRT on day 12 led to a rise in serum creatinine, indicating worsening renal function. On day 17, he developed acute respiratory distress with oxygen saturation <85% and a fever (Tc: 39.3°C), requiring reintubation. Bronchoscopy showed reduced sputum volume in both lungs and subbranches. A recurrence of coma (GCS 3/15) occurred, with WBC increasing to 14.94×10⁹/L and neutrophils to 13.77×10⁹/L. Serum total bilirubin rose to 235.2 µmol/L and creatinine to 441 µmol/L. Brain CT revealed an ischemic stroke in the right frontal lobe and a hemorrhagic infarction in the right occipital lobe. Cooling therapy via CRRT with ice-cold replacement fluid was", "generated_text": "{\n  \"proficient_health_literacy\": \"A 52-year-old male presented with a community-acquired SARS-CoV-2 infection confirmed by reverse-transcription polymerase chain reaction (RT-PCR) of a nasopharyngeal swab, coinciding with the onset of heatstroke (HS). Initial exposure to SARS-CoV-2 occurred during a cold-like illness, followed by return to work without fever after two days of rest. While working outdoors in an ambient temperature of 35°C for five hours, he lost consciousness, with a core temperature (Tc) measured at 40°C upon emergency department admission. The clinical presentation—persistent coma, hyperpyrexia, dyspnea, and gastrointestinal hemorrhage—was consistent with a diagnosis of heatstroke, supported by the absence of underlying comorbidities or familial disease history. The Glasgow Coma Scale (GCS) score was 3/15 (1 for eye-opening, verbal, and motor responses), with symmetrical, non-reactive pupils. Vital signs included a heart rate of 106 bpm and maintained blood pressure (126/77 mmHg) via continuous norepinephrine infusion (0.4 µg/kg·min).\\n\\nLaboratory findings revealed a severe systemic inflammatory response: white blood cell count (WBC) decreased from 3.55×10⁹/L to 3.13×10⁹/L, with a marked reduction in lymphocytes (from 0.25×10⁹/L to 0.1×10⁹/L) and a rise in neutrophil percentage (N%) to 85.3%. Procalcitonin was elevated to 2.81 ng/mL, indicating bacterial infection, and C-reactive protein (CRP) reached 32.6 mg/L. Sputum culture identified Stenotrophomonas maltophilia and Candida lipolytica; central venous catheter culture revealed Staphylococcus epidermidis, while blood cultures remained negative. CT imaging demonstrated bilateral frontal subdural effusions, bilateral pleural effusions, lower lobe consolidation and atelectasis, right upper lobe inflammation, and a small amount of abdominal fluid, indicating a multi-organ pulmonary infection.\\n\\nThe patient was admitted to the emergency intensive care unit (ICU) and initiated with intravenous rehydration using lactated Ringer’s solution and normal saline at 2.5 mL/kg·h, mechanical ventilation (synchronized intermittent mandatory ventilation with PEEP of 5 mmH₂O and FiO₂ of 80%), vasoactive support, and continuous renal replacement therapy (CRRT) for anuria. Initial antibiotics were Piperacillin Sodium and Tazobactam Sodium, later switched to Meropenem due to S. maltophilia and methicillin-resistant Staphylococcus aureus (MRSA) isolation from sputum. Thymalfasin was administered for 20 days to modulate immune function. Hepatic and renal dysfunction were managed with polyene phosphatidylcholine, adenosylmethionine budisulfonate, ulinastatin, and hemofiltration. Intracranial pressure was managed with mannitol for three days. Coagulopathy was characterized by thrombocytopenia, anemia, and disseminated intravascular coagulation (DIC), with treatment including plasma and cryoprecipitate transfusions, continuous heparin infusion (6000 U/day), and CRRT with sodium citrate anticoagulation (8 g/day) initiated on day 7. Platelet transfusion was administered after day 9.\\n\\nThe patient regained consciousness on day 13 with a GCS of 14/15 and moderate fever, with no active gastrointestinal bleeding. Mechanical ventilation was discontinued and the tracheal tube removed. However, discontinuation of CRRT on day 12 led to a rise in serum creatinine, indicating worsening renal function. On day 17, he developed acute respiratory distress with oxygen saturation <85% and a fever (Tc: 39.3°C), requiring reintubation. Bronchoscopy showed reduced sputum volume in both lungs and subbranches. A recurrence of coma (GCS 3/15) occurred, with WBC increasing to 14.94×10⁹/L and neutrophils to 13.77×10⁹/L. Serum total bilirubin rose to 235.2 µmol/L and creatinine to 441 µmol/L. Brain CT revealed an ischemic stroke in the right frontal lobe and a hemorrhagic infarction in the right occipital lobe. Cooling therapy via CRRT with ice-cold replacement fluid was"}
+{"row_index": 80, "doc_id": 60, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 19-year-old female presented to the emergency department with a two-day history of headache, recurrent nausea, vomiting, and one-day fever. On admission, she exhibited a high fever of 39.1°C, severe hypertension (189/120 mmHg), and tachycardia (148 beats per minute). Laboratory findings included a white blood cell count of 14.77×10^9/L and a neutrophil count of 13.55×10^9/L, consistent with an acute inflammatory or infectious process. Empirical antibiotic therapy with moxifloxacin was initiated, but symptoms persisted, prompting admission to the intensive care unit for continuous monitoring. A year prior, she had been diagnosed with myocarditis at a local hospital, along with hypertension, for which antihypertensive medications were prescribed; however, she discontinued adherence to therapy and did not perform regular blood pressure monitoring. Notably, her father had a history of sudden, unexplained death, raising concerns for a genetic predisposition to endocrine neoplasia.\\n\\nA chest CT scan incidentally revealed a left adrenal mass measuring 43 mm × 36 mm with soft tissue density. No abnormalities were detected in head or chest imaging. Electrocardiography demonstrated sinus tachycardia with a shortened PR interval and tall, peaked P-waves in leads II, III, and aVF, suggestive of right atrial strain. Transthoracic echocardiography showed no structural cardiac abnormalities.\\n\\nOn day two of admission, biomarkers including brain natriuretic peptide (BNP) and troponin I (TnI) increased, supporting a provisional diagnosis of myocarditis of uncertain etiology. Treatment included methylprednisolone (0.25 g/day) to suppress myocardial inflammation, furosemide (20 mg q12h) and spironolactone (20 mg q12h) for volume control, and perindopril amlodipine (10 mg: 5 mg/day) for blood pressure and afterload reduction. Metoprolol tartrate (25 mg q12h) and esmolol (0.2 g/hour IV) were used to manage tachycardia and reduce myocardial oxygen demand.\\n\\nGiven the presence of an adrenal mass and sustained hypertension, endocrine evaluation was performed, including assessment of the aldosterone-to-renin ratio, plasma cortisol, plasma catecholamines, and 24-hour urinary catecholamines and metabolites. In the recumbent position, plasma catecholamines were markedly elevated: dopamine (524.5 pmol/L), norepinephrine (83,975 pmol/L), and epinephrine (10,579.3 pmol/L). Urinary levels included free adrenaline (4,368.89 nmol/24h), free norepinephrine (>12,697.60 nmol/24h), normetanephrine (8,312 nmol/24h), metanephrines (4,078 nmol/24h), and vanillylmandelic acid (58.1 mg/24h). These findings are consistent with a diagnosis of pheochromocytoma. On day five, glucocorticoid therapy was discontinued, and terazosin was introduced to provide more precise control of blood pressure.\\n\\nAn enhanced abdominal CT confirmed the left adrenal mass, strongly indicating pheochromocytoma. Whole-exome sequencing revealed a heterozygous missense mutation in the RET gene (c.1900T > C: p. Cys634Arg), resulting in substitution of cysteine by arginine at codon 634. This mutation is pathogenic and associated with multiple endocrine neoplasia type 2A (MEN2A), prompting further endocrine workup. Thyroid ultrasound identified a hypoechoic nodule measuring 6 mm × 4 mm in the left lobe, with mildly elevated calcitonin levels. Parathyroid function tests showed normal serum calcium, intact parathyroid hormone (PTH), and normal electrolytes.\\n\\nFollowing clinical stabilization, plasma cortisol and ACTH normalized. The patient underwent surgical resection of the left adrenal tumor (50 mm × 40 mm × 30 mm). Immunohistochemical analysis demonstrated positive staining for vimentin (Vim), CD56, synaptophysin (Syn), chromogranin A (CgA), and neuron-specific enolase (NSE), with S-100 positivity in Sertoli cells. St", "generated_text": "{\n  \"proficient_health_literacy\": \"A 19-year-old female presented to the emergency department with a two-day history of headache, recurrent nausea, vomiting, and one-day fever. On admission, she exhibited a high fever of 39.1°C, severe hypertension (189/120 mmHg), and tachycardia (148 beats per minute). Laboratory findings included a white blood cell count of 14.77×10^9/L and a neutrophil count of 13.55×10^9/L, consistent with an acute inflammatory or infectious process. Empirical antibiotic therapy with moxifloxacin was initiated, but symptoms persisted, prompting admission to the intensive care unit for continuous monitoring. A year prior, she had been diagnosed with myocarditis at a local hospital, along with hypertension, for which antihypertensive medications were prescribed; however, she discontinued adherence to therapy and did not perform regular blood pressure monitoring. Notably, her father had a history of sudden, unexplained death, raising concerns for a genetic predisposition to endocrine neoplasia.\\n\\nA chest CT scan incidentally revealed a left adrenal mass measuring 43 mm × 36 mm with soft tissue density. No abnormalities were detected in head or chest imaging. Electrocardiography demonstrated sinus tachycardia with a shortened PR interval and tall, peaked P-waves in leads II, III, and aVF, suggestive of right atrial strain. Transthoracic echocardiography showed no structural cardiac abnormalities.\\n\\nOn day two of admission, biomarkers including brain natriuretic peptide (BNP) and troponin I (TnI) increased, supporting a provisional diagnosis of myocarditis of uncertain etiology. Treatment included methylprednisolone (0.25 g/day) to suppress myocardial inflammation, furosemide (20 mg q12h) and spironolactone (20 mg q12h) for volume control, and perindopril amlodipine (10 mg: 5 mg/day) for blood pressure and afterload reduction. Metoprolol tartrate (25 mg q12h) and esmolol (0.2 g/hour IV) were used to manage tachycardia and reduce myocardial oxygen demand.\\n\\nGiven the presence of an adrenal mass and sustained hypertension, endocrine evaluation was performed, including assessment of the aldosterone-to-renin ratio, plasma cortisol, plasma catecholamines, and 24-hour urinary catecholamines and metabolites. In the recumbent position, plasma catecholamines were markedly elevated: dopamine (524.5 pmol/L), norepinephrine (83,975 pmol/L), and epinephrine (10,579.3 pmol/L). Urinary levels included free adrenaline (4,368.89 nmol/24h), free norepinephrine (>12,697.60 nmol/24h), normetanephrine (8,312 nmol/24h), metanephrines (4,078 nmol/24h), and vanillylmandelic acid (58.1 mg/24h). These findings are consistent with a diagnosis of pheochromocytoma. On day five, glucocorticoid therapy was discontinued, and terazosin was introduced to provide more precise control of blood pressure.\\n\\nAn enhanced abdominal CT confirmed the left adrenal mass, strongly indicating pheochromocytoma. Whole-exome sequencing revealed a heterozygous missense mutation in the RET gene (c.1900T > C: p. Cys634Arg), resulting in substitution of cysteine by arginine at codon 634. This mutation is pathogenic and associated with multiple endocrine neoplasia type 2A (MEN2A), prompting further endocrine workup. Thyroid ultrasound identified a hypoechoic nodule measuring 6 mm × 4 mm in the left lobe, with mildly elevated calcitonin levels. Parathyroid function tests showed normal serum calcium, intact parathyroid hormone (PTH), and normal electrolytes.\\n\\nFollowing clinical stabilization, plasma cortisol and ACTH normalized. The patient underwent surgical resection of the left adrenal tumor (50 mm × 40 mm × 30 mm). Immunohistochemical analysis demonstrated positive staining for vimentin (Vim), CD56, synaptophysin (Syn), chromogranin A (CgA), and neuron-specific enolase (NSE), with S-100 positivity in Sertoli cells. St"}
+{"row_index": 81, "doc_id": 61, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 36-year-old man had a painful lump on the inside of his penis and scrotum for 5 years. The lump wasn’t hurting his bladder or causing weight loss. Doctors saw it and found it was deep, about 20 mm big, and attached near the urethra. Tests showed it had a lot of blood flow and was connected to the tube that carries sperm. It looked like a type of cancer called synovial sarcoma, which is a rare, fast-growing tumor. The first surgery removed the lump, and the test results showed it had signs of this cancer. The patient had another surgery with wider cuts to make sure all the cancer was taken out. Even after this, the cancer came back and spread to his liver and spine. He tried several chemo treatments, but they didn’t work. He had more surgeries on his liver, then got treatment for a lung tumor. After trying many medicines, the cancer kept growing, so he moved to palliative care and stopped treatment.\"\n}", "generated_text": "A 36-year-old man had a painful lump on the inside of his penis and scrotum for 5 years. The lump wasn’t hurting his bladder or causing weight loss. Doctors saw it and found it was deep, about 20 mm big, and attached near the urethra. Tests showed it had a lot of blood flow and was connected to the tube that carries sperm. It looked like a type of cancer called synovial sarcoma, which is a rare, fast-growing tumor. The first surgery removed the lump, and the test results showed it had signs of this cancer. The patient had another surgery with wider cuts to make sure all the cancer was taken out. Even after this, the cancer came back and spread to his liver and spine. He tried several chemo treatments, but they didn’t work. He had more surgeries on his liver, then got treatment for a lung tumor. After trying many medicines, the cancer kept growing, so he moved to palliative care and stopped treatment."}
+{"row_index": 82, "doc_id": 61, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 36-year-old man had a tender lump in his penis and scrotum for 5 years. He had no pain with urination, weight loss, or fever. The lump was about 20 mm in size, attached near the base of the penis, and was mobile but deep. Imaging showed a well-defined mass with lots of blood flow, and it was connected to the vas deferens, but no swollen lymph nodes were found. Blood tests were normal. Because of the pain and findings, surgery was done to remove the mass for both diagnosis and treatment. The first surgery removed the mass completely, and the tissue was tested. Pathology showed a type of cancer called synovial sarcoma, which has specific markers including TLE-1, CD99, BLC2, cytokeratin, and EMA. A genetic test confirmed a known mutation in synovial sarcoma. The edges of the sample were hard to assess because the tissue was fragmented. After two weeks, the patient agreed to a second surgery with wider margins. The second surgery removed more tissue, including from both sides of the scrotum, and the result was clear of cancer. The patient was then placed on active surveillance. After 16 months, metastatic cancer was found in his liver and spine. Chemotherapy with Ifosfamide and Doxorubicin did not work, so surgery was done to remove part of the liver and gallbladder. Later, a lung lesion appeared, and he received Pazopanib and radiation. After 6 months of monitoring, new liver and lung tumors developed. He tried several chemotherapy regimens, including Gemcitabine and Docetaxel, Dacarbazine, and Pembrolizumab, but all failed. The patient was eventually moved to palliative care and stopped seeing his doctors.\"\n}", "generated_text": "A 36-year-old man had a tender lump in his penis and scrotum for 5 years. He had no pain with urination, weight loss, or fever. The lump was about 20 mm in size, attached near the base of the penis, and was mobile but deep. Imaging showed a well-defined mass with lots of blood flow, and it was connected to the vas deferens, but no swollen lymph nodes were found. Blood tests were normal. Because of the pain and findings, surgery was done to remove the mass for both diagnosis and treatment. The first surgery removed the mass completely, and the tissue was tested. Pathology showed a type of cancer called synovial sarcoma, which has specific markers including TLE-1, CD99, BLC2, cytokeratin, and EMA. A genetic test confirmed a known mutation in synovial sarcoma. The edges of the sample were hard to assess because the tissue was fragmented. After two weeks, the patient agreed to a second surgery with wider margins. The second surgery removed more tissue, including from both sides of the scrotum, and the result was clear of cancer. The patient was then placed on active surveillance. After 16 months, metastatic cancer was found in his liver and spine. Chemotherapy with Ifosfamide and Doxorubicin did not work, so surgery was done to remove part of the liver and gallbladder. Later, a lung lesion appeared, and he received Pazopanib and radiation. After 6 months of monitoring, new liver and lung tumors developed. He tried several chemotherapy regimens, including Gemcitabine and Docetaxel, Dacarbazine, and Pembrolizumab, but all failed. The patient was eventually moved to palliative care and stopped seeing his doctors."}
+{"row_index": 83, "doc_id": 61, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 36-year-old male with no significant past medical history presented with a 5-year history of a left-sided penoscrotal mass. The lesion was described as smooth, tender, cystic, measuring approximately 20 mm × 20 mm, attached to the left side of the bulbar urethra at the penoscrotal junction, deep in location, without skin tethering or association with the left spermatic cord, and partially mobile. Doppler ultrasonography revealed a well-defined hypoechoic mass (2.7 × 3.1 × 2.0 cm) with markedly increased vascularity in the left penoscrotal region. Pelvic magnetic resonance imaging (MRI) demonstrated a mass in the left inferolateral base of the penis with a distinct fat plane, isointense to testicular tissue on T2-weighted, T1-weighted, and diffusion-weighted imaging, and with direct connection to the vas deferens; no regional lymphadenopathy was observed. Serum alpha-fetoprotein and beta-human chorionic gonadotropin levels were within normal limits, ruling out hepatoblastoma or germ cell tumor etiologies. Given the chronic pain and imaging findings, surgical resection was performed for both diagnostic and therapeutic purposes. Intraoperatively, a spindle cell tumor was identified in the left posterolateral scrotum and completely resected. Histopathological examination revealed a cellular spindle cell tumor organized in interlacing fascicles, with spindle to oval-shaped nuclei exhibiting evenly dispersed chromatin and inconspicuous nucleoli. Mitotic activity was high, reaching up to 3 mitoses per high-power field (HPF), indicating aggressive proliferative potential. Immunohistochemical staining was positive for TLE-1, CD99, B-cell lymphoma 2 (BCL-2), focal cytokeratin, and focal epithelial membrane antigen (EMA), consistent with synovial sarcoma. Fluorescence in situ hybridization (FISH) analysis confirmed a characteristic rearrangement of the SS18 gene at 18q11.2, a hallmark genetic alteration in synovial sarcoma. Histological assessment of the margins was inconclusive due to fragmentation of the resected specimen, limiting definitive margin status. Following initial resection, the patient returned to clinic for re-evaluation. Based on the histopathology, a second surgical resection with wider margins was performed three weeks later. The resection extended bilaterally to the spermatic cords, deepening to the corpus spongiosum and being shaved superiorly to the urethra. The final resected specimen measured 6.0 × 6.0 × 3.0 cm and was histologically negative for residual tumor. The patient entered active surveillance for 16 months, during which time metastatic disease was detected in the sixth liver segment and the L1 vertebral body. The oncology team initiated a six-cycle regimen of ifosfamide and doxorubicin, which showed no clinical or radiographic response. Subsequent surgical intervention included resection of the fifth and sixth liver segments with concomitant cholecystectomy. Following this, a new pulmonary lesion emerged, prompting initiation of pazopanib and stereotactic body radiation therapy (SBRT). After six months of surveillance, new liver and pulmonary lesions developed, leading to a regimen of gemcitabine and docetaxel for three cycles, which resulted in disease progression. The patient then received two cycles of dacarbazine, with further progression. Subsequently, two cycles of pembrolizumab were administered, also resulting in disease progression. The patient was transitioned to palliative care and discontinued follow-up. This case illustrates the aggressive biological behavior of synovial sarcoma in a young adult, despite multimodal therapy including surgical resection, chemotherapy, and targeted therapy, with eventual progression and widespread metastasis, highlighting the challenges in managing this rare, high-grade sarcoma with a propensity for early dissemination and resistance to conventional treatment regimens. The molecular profile—specifically the SS18-SSX1 fusion gene—supports the diagnosis of synovial sarcoma and correlates with its clinical aggressiveness and poor response to standard chemotherapy.\"\n}", "generated_text": "A 36-year-old male with no significant past medical history presented with a 5-year history of a left-sided penoscrotal mass. The lesion was described as smooth, tender, cystic, measuring approximately 20 mm × 20 mm, attached to the left side of the bulbar urethra at the penoscrotal junction, deep in location, without skin tethering or association with the left spermatic cord, and partially mobile. Doppler ultrasonography revealed a well-defined hypoechoic mass (2.7 × 3.1 × 2.0 cm) with markedly increased vascularity in the left penoscrotal region. Pelvic magnetic resonance imaging (MRI) demonstrated a mass in the left inferolateral base of the penis with a distinct fat plane, isointense to testicular tissue on T2-weighted, T1-weighted, and diffusion-weighted imaging, and with direct connection to the vas deferens; no regional lymphadenopathy was observed. Serum alpha-fetoprotein and beta-human chorionic gonadotropin levels were within normal limits, ruling out hepatoblastoma or germ cell tumor etiologies. Given the chronic pain and imaging findings, surgical resection was performed for both diagnostic and therapeutic purposes. Intraoperatively, a spindle cell tumor was identified in the left posterolateral scrotum and completely resected. Histopathological examination revealed a cellular spindle cell tumor organized in interlacing fascicles, with spindle to oval-shaped nuclei exhibiting evenly dispersed chromatin and inconspicuous nucleoli. Mitotic activity was high, reaching up to 3 mitoses per high-power field (HPF), indicating aggressive proliferative potential. Immunohistochemical staining was positive for TLE-1, CD99, B-cell lymphoma 2 (BCL-2), focal cytokeratin, and focal epithelial membrane antigen (EMA), consistent with synovial sarcoma. Fluorescence in situ hybridization (FISH) analysis confirmed a characteristic rearrangement of the SS18 gene at 18q11.2, a hallmark genetic alteration in synovial sarcoma. Histological assessment of the margins was inconclusive due to fragmentation of the resected specimen, limiting definitive margin status. Following initial resection, the patient returned to clinic for re-evaluation. Based on the histopathology, a second surgical resection with wider margins was performed three weeks later. The resection extended bilaterally to the spermatic cords, deepening to the corpus spongiosum and being shaved superiorly to the urethra. The final resected specimen measured 6.0 × 6.0 × 3.0 cm and was histologically negative for residual tumor. The patient entered active surveillance for 16 months, during which time metastatic disease was detected in the sixth liver segment and the L1 vertebral body. The oncology team initiated a six-cycle regimen of ifosfamide and doxorubicin, which showed no clinical or radiographic response. Subsequent surgical intervention included resection of the fifth and sixth liver segments with concomitant cholecystectomy. Following this, a new pulmonary lesion emerged, prompting initiation of pazopanib and stereotactic body radiation therapy (SBRT). After six months of surveillance, new liver and pulmonary lesions developed, leading to a regimen of gemcitabine and docetaxel for three cycles, which resulted in disease progression. The patient then received two cycles of dacarbazine, with further progression. Subsequently, two cycles of pembrolizumab were administered, also resulting in disease progression. The patient was transitioned to palliative care and discontinued follow-up. This case illustrates the aggressive biological behavior of synovial sarcoma in a young adult, despite multimodal therapy including surgical resection, chemotherapy, and targeted therapy, with eventual progression and widespread metastasis, highlighting the challenges in managing this rare, high-grade sarcoma with a propensity for early dissemination and resistance to conventional treatment regimens. The molecular profile—specifically the SS18-SSX1 fusion gene—supports the diagnosis of synovial sarcoma and correlates with its clinical aggressiveness and poor response to standard chemotherapy."}
+{"row_index": 84, "doc_id": 62, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 13-year-old boy came to the ER with sudden chest pain on the sides, worse when coughing, but no shortness of breath. He had a mild cough and a little runny nose, and once felt a fever. The pain didn’t get worse at night, and he was still able to do sports like canoeing. No one in his family had lung or heart problems, and he didn’t have any exposure to dust, fumes, or oil. His chest X-ray from 4 years ago showed a similar lung problem, which was treated with an antibiotic (azithromycin) and has stayed gone since. This time, his X-ray showed a thick, cloudy pattern in his lungs, and a CT scan found a lot of white spots in both lungs — more than two-thirds of his lung tissue — which points to a rare lung condition called pulmonary alveolar proteinosis (PAP). Tests for viruses, including the coronavirus, came back negative. A lung fluid test showed a milky fluid and a special stain that confirmed the condition. His breathing tests showed a mild restriction, meaning he can’t take in as much air as normal, and his lungs are less able to pass oxygen. No gene mutations linked to lung problems were found. A blood test showed he has an antibody against a protein called GM-CSF, which makes doctors think it’s an autoimmune version of PAP. After 20 months, he’s feeling fine, no pain, and his breathing is back to normal. He’s still active and doesn’t need treatment right now — just regular check-ups.\"\n}", "generated_text": "A 13-year-old boy came to the ER with sudden chest pain on the sides, worse when coughing, but no shortness of breath. He had a mild cough and a little runny nose, and once felt a fever. The pain didn’t get worse at night, and he was still able to do sports like canoeing. No one in his family had lung or heart problems, and he didn’t have any exposure to dust, fumes, or oil. His chest X-ray from 4 years ago showed a similar lung problem, which was treated with an antibiotic (azithromycin) and has stayed gone since. This time, his X-ray showed a thick, cloudy pattern in his lungs, and a CT scan found a lot of white spots in both lungs — more than two-thirds of his lung tissue — which points to a rare lung condition called pulmonary alveolar proteinosis (PAP). Tests for viruses, including the coronavirus, came back negative. A lung fluid test showed a milky fluid and a special stain that confirmed the condition. His breathing tests showed a mild restriction, meaning he can’t take in as much air as normal, and his lungs are less able to pass oxygen. No gene mutations linked to lung problems were found. A blood test showed he has an antibody against a protein called GM-CSF, which makes doctors think it’s an autoimmune version of PAP. After 20 months, he’s feeling fine, no pain, and his breathing is back to normal. He’s still active and doesn’t need treatment right now — just regular check-ups."}
+{"row_index": 85, "doc_id": 62, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 13-year-old male with no significant prior medical history presented to the emergency department with a 3-day history of acute bilateral pleuritic chest pain, associated with mild non-productive cough, mild rhinorrhea, and a single febrile episode (38°C). The chest pain was localized to the costal margin and exacerbated by coughing, without diurnal variation or respiratory distress. Symptoms were partially relieved with paracetamol. There were no reports of joint pain, weight loss, anorexia, fatigue, syncope, or exercise limitation; he maintained regular physical activity, including weekly canoeing. No exposure to infectious agents, environmental fumes, dust, or mineral oils was reported. There was no family history of cardiopulmonary disorders. A prior chest radiograph, obtained four years earlier during an acute illness, demonstrated a marked interstitial infiltrate, which was presumptively managed with azithromycin and has since remained asymptomatic with no further clinical follow-up.\\n\\nOn admission, vital signs were stable: temperature 37.8°C, oxygen saturation 99% on room air, heart rate 93 bpm, respiratory rate 15 breaths per minute, and blood pressure at the 85th percentile (115/66 mmHg). Physical examination revealed diminished breath sounds in the lower two-thirds of the chest without adventitious sounds, respiratory distress, cyanosis, clubbing, or abnormal cardiac findings. Chest radiography showed a persistent interstitial infiltrate, morphologically similar to the prior imaging. Thoracic computed tomography (CT) revealed multiple bilateral ground-glass opacities involving greater than 65% of lung parenchyma, with areas of 'crazy paving' pattern, consistent with pulmonary alveolar proteinosis (PAP).\\n\\nRespiratory viral testing, including for SARS-CoV-2, was negative. The patient was initially managed with empiric antibiotics (amoxicillin-clavulanic acid and azithromycin) for suspected respiratory infection, with clinical improvement and discharge. Subsequent outpatient evaluation revealed positive antinuclear antibodies (ANA) at a titer of 1/89 with a fine speckled pattern, while other autoantibodies and immunoglobulin levels were within normal ranges.\\n\\nBronchoalveolar lavage (BAL) yielded a milky fluid with positive periodic acid-Schiff (PAS) staining, indicating the presence of surfactant proteins and alveolar protein accumulation. Microbiological analysis, including for mycobacteria, was negative. Spirometry demonstrated a mild restrictive pattern: forced vital capacity (FVC) of 2.92 L (77%), forced expiratory volume in 1 second (FEV1) of 3.21 L (69.9%), and a normal FEV1/FVC ratio of 109%, suggesting preserved airway function despite reduced lung volumes. Diffusing capacity of the lungs for carbon monoxide (DLCO, single breath) was reduced to 13.8 ml/min/mmHg (48.6%), indicating impaired gas exchange.\\n\\nGenetic testing for surfactant dysfunction-related mutations was negative, ruling out inherited surfactant deficiencies such as those seen in surfactant protein C (SFTPC) or surfactant protein B (SFTPB) mutations. Anti-granulocyte macrophage colony-stimulating factor (GM-CSF) antibody testing was strongly positive, supporting a diagnosis of autoimmune pulmonary alveolar proteinosis (AI-PAP), in which the immune system produces autoantibodies that inhibit GM-CSF, a critical cytokine for alveolar macrophage function and surfactant clearance.\\n\\nAt 20-month follow-up, the patient remains asymptomatic and continues regular physical activity. Repeat spirometry shows normalized FVC (4.03 L, 81.3%), FEV1 (3.71 L, 87.5%), FEV1/FVC ratio (91.96%), and DLCO (25.54 ml/min/mmHg, 83.7%), indicating functional stabilization. Given the absence of symptoms and stable pulmonary function, treatment was deferred, and the patient is being managed with ongoing clinical monitoring. The case highlights the clinical presentation of AI-PAP in a young adolescent with a recurrent interstitial infiltrate, overlapping with prior imaging findings, and underscores the importance of BAL findings, autoantibody screening, and GM-CSF inhibition in the diagnostic workup of unexplained interstitial lung disease in pediatric patients.\"\n}", "generated_text": "A 13-year-old male with no significant prior medical history presented to the emergency department with a 3-day history of acute bilateral pleuritic chest pain, associated with mild non-productive cough, mild rhinorrhea, and a single febrile episode (38°C). The chest pain was localized to the costal margin and exacerbated by coughing, without diurnal variation or respiratory distress. Symptoms were partially relieved with paracetamol. There were no reports of joint pain, weight loss, anorexia, fatigue, syncope, or exercise limitation; he maintained regular physical activity, including weekly canoeing. No exposure to infectious agents, environmental fumes, dust, or mineral oils was reported. There was no family history of cardiopulmonary disorders. A prior chest radiograph, obtained four years earlier during an acute illness, demonstrated a marked interstitial infiltrate, which was presumptively managed with azithromycin and has since remained asymptomatic with no further clinical follow-up.\n\nOn admission, vital signs were stable: temperature 37.8°C, oxygen saturation 99% on room air, heart rate 93 bpm, respiratory rate 15 breaths per minute, and blood pressure at the 85th percentile (115/66 mmHg). Physical examination revealed diminished breath sounds in the lower two-thirds of the chest without adventitious sounds, respiratory distress, cyanosis, clubbing, or abnormal cardiac findings. Chest radiography showed a persistent interstitial infiltrate, morphologically similar to the prior imaging. Thoracic computed tomography (CT) revealed multiple bilateral ground-glass opacities involving greater than 65% of lung parenchyma, with areas of 'crazy paving' pattern, consistent with pulmonary alveolar proteinosis (PAP).\n\nRespiratory viral testing, including for SARS-CoV-2, was negative. The patient was initially managed with empiric antibiotics (amoxicillin-clavulanic acid and azithromycin) for suspected respiratory infection, with clinical improvement and discharge. Subsequent outpatient evaluation revealed positive antinuclear antibodies (ANA) at a titer of 1/89 with a fine speckled pattern, while other autoantibodies and immunoglobulin levels were within normal ranges.\n\nBronchoalveolar lavage (BAL) yielded a milky fluid with positive periodic acid-Schiff (PAS) staining, indicating the presence of surfactant proteins and alveolar protein accumulation. Microbiological analysis, including for mycobacteria, was negative. Spirometry demonstrated a mild restrictive pattern: forced vital capacity (FVC) of 2.92 L (77%), forced expiratory volume in 1 second (FEV1) of 3.21 L (69.9%), and a normal FEV1/FVC ratio of 109%, suggesting preserved airway function despite reduced lung volumes. Diffusing capacity of the lungs for carbon monoxide (DLCO, single breath) was reduced to 13.8 ml/min/mmHg (48.6%), indicating impaired gas exchange.\n\nGenetic testing for surfactant dysfunction-related mutations was negative, ruling out inherited surfactant deficiencies such as those seen in surfactant protein C (SFTPC) or surfactant protein B (SFTPB) mutations. Anti-granulocyte macrophage colony-stimulating factor (GM-CSF) antibody testing was strongly positive, supporting a diagnosis of autoimmune pulmonary alveolar proteinosis (AI-PAP), in which the immune system produces autoantibodies that inhibit GM-CSF, a critical cytokine for alveolar macrophage function and surfactant clearance.\n\nAt 20-month follow-up, the patient remains asymptomatic and continues regular physical activity. Repeat spirometry shows normalized FVC (4.03 L, 81.3%), FEV1 (3.71 L, 87.5%), FEV1/FVC ratio (91.96%), and DLCO (25.54 ml/min/mmHg, 83.7%), indicating functional stabilization. Given the absence of symptoms and stable pulmonary function, treatment was deferred, and the patient is being managed with ongoing clinical monitoring. The case highlights the clinical presentation of AI-PAP in a young adolescent with a recurrent interstitial infiltrate, overlapping with prior imaging findings, and underscores the importance of BAL findings, autoantibody screening, and GM-CSF inhibition in the diagnostic workup of unexplained interstitial lung disease in pediatric patients."}
+{"row_index": 86, "doc_id": 63, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 27-year-old woman had swelling on her face and trouble opening her mouth 48 hours after taking antibiotics for a tooth infection. A scan of her neck found a big blood clot in a vein, and a chest scan showed blood clots in her lungs. She was treated right away with strong antibiotics and medicine to stop the clots from getting worse. She got better and was able to go home after 14 days of treatment.\"\n}", "generated_text": "A 27-year-old woman had swelling on her face and trouble opening her mouth 48 hours after taking antibiotics for a tooth infection. A scan of her neck found a big blood clot in a vein, and a chest scan showed blood clots in her lungs. She was treated right away with strong antibiotics and medicine to stop the clots from getting worse. She got better and was able to go home after 14 days of treatment."}
+{"row_index": 87, "doc_id": 63, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 27-year-old woman developed facial swelling and difficulty opening her mouth (trismus) 48 hours after finishing antibiotics for a throat infection. She had previously taken phenoxymethylpenicillin for five days to treat a peritonsillar abscess. Imaging showed a large blood clot in the internal jugular vein of her neck and lung infections caused by septic emboli (clots that traveled to the lungs). She was treated with strong intravenous antibiotics and anticoagulation to prevent further clots. Her condition improved over several days, and after 14 days of treatment, she was able to go home on oral antibiotics and continued anticoagulation therapy.\"\n}", "generated_text": "A 27-year-old woman developed facial swelling and difficulty opening her mouth (trismus) 48 hours after finishing antibiotics for a throat infection. She had previously taken phenoxymethylpenicillin for five days to treat a peritonsillar abscess. Imaging showed a large blood clot in the internal jugular vein of her neck and lung infections caused by septic emboli (clots that traveled to the lungs). She was treated with strong intravenous antibiotics and anticoagulation to prevent further clots. Her condition improved over several days, and after 14 days of treatment, she was able to go home on oral antibiotics and continued anticoagulation therapy."}
+{"row_index": 88, "doc_id": 63, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 27-year-old woman with a history of uncontrolled asthma and a prior mild SARS-CoV-2 infection presented 48 hours after completing oral phenoxymethylpenicillin 1,000,000 IU daily for five days, administered for a peritonsillar abscess, with new-onset facial edema and trismus. At presentation, she was hemodynamically stable, without respiratory distress or requirement for supplemental oxygen. Physical examination revealed a painful, homolateral cervical adenopathy and significant trismus. Laboratory findings demonstrated leukocytosis, thrombocytopenia, and elevated acute-phase reactants, with all other parameters within normal limits. Imaging studies included a head and neck CT, which revealed a large thrombus in both the internal and external carotid arteries, consistent with a thrombotic event secondary to severe local inflammation or endothelial activation. Arterial Doppler ultrasound of the neck vessels showed no significant stenosis or flow abnormalities, but the presence of carotid thrombus suggests a systemic inflammatory response. A chest CT scan demonstrated bilateral pulmonary septic emboli, indicating dissemination of infected material via venous thrombus from the head and neck region to the pulmonary circulation. Initial empiric intravenous therapy was initiated with ceftriaxone 1 g every 12 hours and clindamycin 300 mg every 6 hours to cover potential Gram-positive and anaerobic pathogens, including those associated with odontogenic infections. Concomitant anticoagulation was initiated with enoxaparin, dosed at 60 mg subcutaneously every 12 hours, adjusted for body weight and renal function, to prevent extension of the thrombotic burden. Over the subsequent 72 hours, the patient developed a fever of 38.5 °C and further leukocytosis, prompting repeat imaging. Echocardiography excluded cardiac vegetations, ruling out endocarditis as a source of emboli. A repeat chest CT confirmed bilateral pulmonary septic emboli. Hemocultures obtained at admission were negative, leading to the decision to perform culture of pharyngeal exudate and initiate a broader-spectrum antibiotic regimen with piperacillin-tazobactam 4.5 g every 6 hours intravenously, replacing ceftriaxone. No pathogen was isolated from cultures, suggesting a possible non-bacterial or polymicrobial infection with limited cultivability. The patient responded favorably to treatment, with resolution of fever and clinical signs of infection. After 14 days of optimized therapy, follow-up chest CT showed absence of pulmonary lesions, and the patient was transitioned to oral clindamycin 300 mg every 6 hours for continued coverage of anaerobic organisms. Anticoagulation was switched to acenocumarol, adjusted to body weight, to maintain therapeutic anticoagulation levels, with the patient achieving stable coagulation parameters and being discharged. The clinical course reflects a rare but severe complication of odontogenic infection—systemic thrombosis and septic embolization—likely driven by intense local inflammation, endothelial injury, and hypercoagulability, with potential contributions from underlying comorbidities such as asthma and prior viral infection, which may predispose to dysregulated immune and coagulation responses.\"\n}", "generated_text": "A 27-year-old woman with a history of uncontrolled asthma and a prior mild SARS-CoV-2 infection presented 48 hours after completing oral phenoxymethylpenicillin 1,000,000 IU daily for five days, administered for a peritonsillar abscess, with new-onset facial edema and trismus. At presentation, she was hemodynamically stable, without respiratory distress or requirement for supplemental oxygen. Physical examination revealed a painful, homolateral cervical adenopathy and significant trismus. Laboratory findings demonstrated leukocytosis, thrombocytopenia, and elevated acute-phase reactants, with all other parameters within normal limits. Imaging studies included a head and neck CT, which revealed a large thrombus in both the internal and external carotid arteries, consistent with a thrombotic event secondary to severe local inflammation or endothelial activation. Arterial Doppler ultrasound of the neck vessels showed no significant stenosis or flow abnormalities, but the presence of carotid thrombus suggests a systemic inflammatory response. A chest CT scan demonstrated bilateral pulmonary septic emboli, indicating dissemination of infected material via venous thrombus from the head and neck region to the pulmonary circulation. Initial empiric intravenous therapy was initiated with ceftriaxone 1 g every 12 hours and clindamycin 300 mg every 6 hours to cover potential Gram-positive and anaerobic pathogens, including those associated with odontogenic infections. Concomitant anticoagulation was initiated with enoxaparin, dosed at 60 mg subcutaneously every 12 hours, adjusted for body weight and renal function, to prevent extension of the thrombotic burden. Over the subsequent 72 hours, the patient developed a fever of 38.5 °C and further leukocytosis, prompting repeat imaging. Echocardiography excluded cardiac vegetations, ruling out endocarditis as a source of emboli. A repeat chest CT confirmed bilateral pulmonary septic emboli. Hemocultures obtained at admission were negative, leading to the decision to perform culture of pharyngeal exudate and initiate a broader-spectrum antibiotic regimen with piperacillin-tazobactam 4.5 g every 6 hours intravenously, replacing ceftriaxone. No pathogen was isolated from cultures, suggesting a possible non-bacterial or polymicrobial infection with limited cultivability. The patient responded favorably to treatment, with resolution of fever and clinical signs of infection. After 14 days of optimized therapy, follow-up chest CT showed absence of pulmonary lesions, and the patient was transitioned to oral clindamycin 300 mg every 6 hours for continued coverage of anaerobic organisms. Anticoagulation was switched to acenocumarol, adjusted to body weight, to maintain therapeutic anticoagulation levels, with the patient achieving stable coagulation parameters and being discharged. The clinical course reflects a rare but severe complication of odontogenic infection—systemic thrombosis and septic embolization—likely driven by intense local inflammation, endothelial injury, and hypercoagulability, with potential contributions from underlying comorbidities such as asthma and prior viral infection, which may predispose to dysregulated immune and coagulation responses."}
+{"row_index": 89, "doc_id": 64, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 5-year-old child swallowed a dangerous poison called chlorpyrifos and also breathed in a mixture of charcoal and palm oil. This caused serious problems: breathing stopped, the child went into a deep sleep, had no movement in the arms and legs, and was very weak. The child was rushed to the hospital where they gave breathing support, gave medicine to stop the poison, and used blood changes to help the body. The child started to get better within hours, didn’t have a later serious problem (called intermediate syndrome), and was home after 10 days. The doctors kept the child safe and helped them recover step by step.\"\n}", "generated_text": "A 5-year-old child swallowed a dangerous poison called chlorpyrifos and also breathed in a mixture of charcoal and palm oil. This caused serious problems: breathing stopped, the child went into a deep sleep, had no movement in the arms and legs, and was very weak. The child was rushed to the hospital where they gave breathing support, gave medicine to stop the poison, and used blood changes to help the body. The child started to get better within hours, didn’t have a later serious problem (called intermediate syndrome), and was home after 10 days. The doctors kept the child safe and helped them recover step by step."}
+{"row_index": 90, "doc_id": 64, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 5-year-old child suffered severe poisoning from chlorpyrifos, a type of organophosphate pesticide, after accidentally ingesting it. Shortly after, the child also aspirated (inhaled) a mixture of charcoal and palm oil, which worsened the condition. The poisoning caused serious symptoms including fast breathing, difficulty breathing, excessive sweating, vomiting, and eventually coma. At the time of arrival at the emergency department, the child had very low consciousness (Glasgow Coma Score of 3), pinpoint pupils, and signs of shock and respiratory failure.\\n\\nThe child was treated with non-invasive ventilation to help with breathing, intravenous atropine to counteract the poisoning, and medications to support blood pressure and reduce inflammation. Because the family could not afford intensive care, the treatment was kept manageable. The child also received exchange transfusions (a blood exchange to remove toxic substances) and antibiotics for lung infection. Hypoglycemia (low blood sugar) was treated with dextrose, and heart issues were managed with fluids and a dopamine infusion.\\n\\nOver the next few days, the child’s condition improved steadily. Consciousness returned, breathing became easier, and lung symptoms improved. By day 10, the child was stable enough to be discharged home. The child did not develop a known complication called intermediate syndrome and recovered well from the poisoning. However, after discharge, the child was not followed up by healthcare providers.\"\n}", "generated_text": "A 5-year-old child suffered severe poisoning from chlorpyrifos, a type of organophosphate pesticide, after accidentally ingesting it. Shortly after, the child also aspirated (inhaled) a mixture of charcoal and palm oil, which worsened the condition. The poisoning caused serious symptoms including fast breathing, difficulty breathing, excessive sweating, vomiting, and eventually coma. At the time of arrival at the emergency department, the child had very low consciousness (Glasgow Coma Score of 3), pinpoint pupils, and signs of shock and respiratory failure.\n\nThe child was treated with non-invasive ventilation to help with breathing, intravenous atropine to counteract the poisoning, and medications to support blood pressure and reduce inflammation. Because the family could not afford intensive care, the treatment was kept manageable. The child also received exchange transfusions (a blood exchange to remove toxic substances) and antibiotics for lung infection. Hypoglycemia (low blood sugar) was treated with dextrose, and heart issues were managed with fluids and a dopamine infusion.\n\nOver the next few days, the child’s condition improved steadily. Consciousness returned, breathing became easier, and lung symptoms improved. By day 10, the child was stable enough to be discharged home. The child did not develop a known complication called intermediate syndrome and recovered well from the poisoning. However, after discharge, the child was not followed up by healthcare providers."}
+{"row_index": 91, "doc_id": 64, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 5-year-old child presented to the pediatric emergency department (ED) 13 hours after ingesting chlorpyrifos, a potent organophosphate pesticide, followed by aspiration of a charcoal-palm oil mixture. The initial clinical presentation included generalized abnormal jerks, tachypnea (respiratory rate of 48 breaths per minute with intermittent sighing), severe dyspnea, excessive sweating, polyuria, increased secretions, and involuntary limb movements. The patient had lapsed into coma prior to arrival, with a presenting temperature of 38.3°C, Glasgow Coma Scale (GCS) of 3, pinpoint pupils, and global hypotonia. Vital signs at presentation included a heart rate of 180 beats per minute, blood pressure of 120/80 mmHg, and a random blood glucose of 14 mg/dL. Physical examination revealed widespread crackles on auscultation, indicating pulmonary edema or aspiration-related pulmonary injury. Serum cholinesterase activity and lactate levels were not measured due to institutional limitations.\\n\\nThe diagnosis was established as severe organophosphate poisoning (OPP) with concomitant aspiration pneumonitis. Given the severity of respiratory failure and the unavailability of intensive care resources, non-invasive ventilation (NIV) was initiated using bubble continuous positive airway pressure (b-CPAP), which improved oxygen saturation to 99–100%. Hypoglycemia was managed with a dextrose bolus, and tachycardia was treated with 20 mL/kg of normal saline. Empirical intravenous antibiotics were administered for suspected aspiration-related pneumonia. Intravenous atropine was administered at a dose of 0.02 mg/kg/dose, with the first dose leading to a significant tachycardia, prompting discontinuation due to hemodynamic instability. Pralidoxime, a reactivating agent for organophosphate-inhibited acetylcholinesterase, was not administered due to unavailability.\\n\\nWithin 3 hours of presentation, the patient underwent a fresh-whole-blood exchange blood transfusion (FWB-EBT) of 500 mL to rapidly reduce circulating organophosphate metabolites and mitigate cholinergic toxicity. The GCS improved to 9/15 following this intervention. Over the subsequent 15 hours, blood glucose fluctuated between 41 and 259 mg/dL, eventually stabilizing with continued management. On day 2 of admission, the patient developed thready pulses and hypotension, prompting a second bolus of normal saline. Dopamine infusion was initiated at 5 mcg/kg/min via peripheral venous access, and intravenous mannitol was discontinued. A second FWB-EBT of 500 mL was performed.\\n\\nOver the first 30 hours, there was a progressive improvement in consciousness and resolution of respiratory distress. However, rhonchi were noted, managed with nebulized salbutamol and budesonide, and the patient was transitioned to nasal prong oxygen therapy, maintaining stable oxygen saturation at 97%. A chest radiograph on day 2 revealed bilateral pulmonary infiltrates consistent with aspiration pneumonia. Full recovery of consciousness was achieved by the 39th hour of admission. Antioxidant therapy was initiated with intravenous vitamin C and B, and oral vitamin E and zinc to mitigate oxidative stress associated with acute organophosphate toxicity. A graded reintroduction of oral diet was implemented over the following 48 hours.\\n\\nThe patient’s clinical course remained stable, and he was discharged home after 10 days of hospitalization. However, follow-up care was not maintained, resulting in loss to follow-up. The patient did not develop the intermediate syndrome, a known risk in organophosphate poisoning characterized by delayed neuromuscular weakness typically occurring 24–96 hours post-exposure, which may have been attributed to the rapid clinical response, early intervention, and absence of prolonged cholinesterase inhibition.\\n\\nThis case underscores the pathophysiological mechanisms of organophosphate toxicity, including acetylcholinesterase inhibition leading to excessive acetylcholine accumulation at neuromuscular junctions and in the central nervous system, resulting in muscarinic and nicotinic cholinergic overstimulation. The clinical manifestations include bronchospasm, respiratory failure, hypotension, seizures, and coma. Aspiration of lipid-rich substances like palm oil may exacerbate pulmonary injury through direct chemical irritation and mechanical obstruction, contributing to secondary pneumonia. The use of exchange transfusion in this setting is a rare but effective strategy to rapidly remove toxic metabolites and restore physiological balance in severe OPP, particularly in resource-limited settings where advanced supportive care is not available. The absence of pralidoxime administration highlights a critical gap in access to antidotal therapy in", "generated_text": "{\n  \"proficient_health_literacy\": \"A 5-year-old child presented to the pediatric emergency department (ED) 13 hours after ingesting chlorpyrifos, a potent organophosphate pesticide, followed by aspiration of a charcoal-palm oil mixture. The initial clinical presentation included generalized abnormal jerks, tachypnea (respiratory rate of 48 breaths per minute with intermittent sighing), severe dyspnea, excessive sweating, polyuria, increased secretions, and involuntary limb movements. The patient had lapsed into coma prior to arrival, with a presenting temperature of 38.3°C, Glasgow Coma Scale (GCS) of 3, pinpoint pupils, and global hypotonia. Vital signs at presentation included a heart rate of 180 beats per minute, blood pressure of 120/80 mmHg, and a random blood glucose of 14 mg/dL. Physical examination revealed widespread crackles on auscultation, indicating pulmonary edema or aspiration-related pulmonary injury. Serum cholinesterase activity and lactate levels were not measured due to institutional limitations.\\n\\nThe diagnosis was established as severe organophosphate poisoning (OPP) with concomitant aspiration pneumonitis. Given the severity of respiratory failure and the unavailability of intensive care resources, non-invasive ventilation (NIV) was initiated using bubble continuous positive airway pressure (b-CPAP), which improved oxygen saturation to 99–100%. Hypoglycemia was managed with a dextrose bolus, and tachycardia was treated with 20 mL/kg of normal saline. Empirical intravenous antibiotics were administered for suspected aspiration-related pneumonia. Intravenous atropine was administered at a dose of 0.02 mg/kg/dose, with the first dose leading to a significant tachycardia, prompting discontinuation due to hemodynamic instability. Pralidoxime, a reactivating agent for organophosphate-inhibited acetylcholinesterase, was not administered due to unavailability.\\n\\nWithin 3 hours of presentation, the patient underwent a fresh-whole-blood exchange blood transfusion (FWB-EBT) of 500 mL to rapidly reduce circulating organophosphate metabolites and mitigate cholinergic toxicity. The GCS improved to 9/15 following this intervention. Over the subsequent 15 hours, blood glucose fluctuated between 41 and 259 mg/dL, eventually stabilizing with continued management. On day 2 of admission, the patient developed thready pulses and hypotension, prompting a second bolus of normal saline. Dopamine infusion was initiated at 5 mcg/kg/min via peripheral venous access, and intravenous mannitol was discontinued. A second FWB-EBT of 500 mL was performed.\\n\\nOver the first 30 hours, there was a progressive improvement in consciousness and resolution of respiratory distress. However, rhonchi were noted, managed with nebulized salbutamol and budesonide, and the patient was transitioned to nasal prong oxygen therapy, maintaining stable oxygen saturation at 97%. A chest radiograph on day 2 revealed bilateral pulmonary infiltrates consistent with aspiration pneumonia. Full recovery of consciousness was achieved by the 39th hour of admission. Antioxidant therapy was initiated with intravenous vitamin C and B, and oral vitamin E and zinc to mitigate oxidative stress associated with acute organophosphate toxicity. A graded reintroduction of oral diet was implemented over the following 48 hours.\\n\\nThe patient’s clinical course remained stable, and he was discharged home after 10 days of hospitalization. However, follow-up care was not maintained, resulting in loss to follow-up. The patient did not develop the intermediate syndrome, a known risk in organophosphate poisoning characterized by delayed neuromuscular weakness typically occurring 24–96 hours post-exposure, which may have been attributed to the rapid clinical response, early intervention, and absence of prolonged cholinesterase inhibition.\\n\\nThis case underscores the pathophysiological mechanisms of organophosphate toxicity, including acetylcholinesterase inhibition leading to excessive acetylcholine accumulation at neuromuscular junctions and in the central nervous system, resulting in muscarinic and nicotinic cholinergic overstimulation. The clinical manifestations include bronchospasm, respiratory failure, hypotension, seizures, and coma. Aspiration of lipid-rich substances like palm oil may exacerbate pulmonary injury through direct chemical irritation and mechanical obstruction, contributing to secondary pneumonia. The use of exchange transfusion in this setting is a rare but effective strategy to rapidly remove toxic metabolites and restore physiological balance in severe OPP, particularly in resource-limited settings where advanced supportive care is not available. The absence of pralidoxime administration highlights a critical gap in access to antidotal therapy in"}
+{"row_index": 92, "doc_id": 65, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 19-year-old woman came to the hospital with a fast, irregular heartbeat and signs that her heart wasn't pumping well. Tests showed her heart was working hard, and there was no sign of a heart attack or heart muscle damage. After checking her heart with different scans, doctors found a birth defect: the main blood vessel going to her right heart was missing at the start. This missing part caused her heart to beat wrong and made her feel sick. Doctors found the problem spot on a small muscle in her heart, fixed it with a special treatment, and now she feels fine and has not had any problems since.\"\n}", "generated_text": "A 19-year-old woman came to the hospital with a fast, irregular heartbeat and signs that her heart wasn't pumping well. Tests showed her heart was working hard, and there was no sign of a heart attack or heart muscle damage. After checking her heart with different scans, doctors found a birth defect: the main blood vessel going to her right heart was missing at the start. This missing part caused her heart to beat wrong and made her feel sick. Doctors found the problem spot on a small muscle in her heart, fixed it with a special treatment, and now she feels fine and has not had any problems since."}
+{"row_index": 93, "doc_id": 65, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 19-year-old woman came to the emergency department with sudden palpitations and signs of cardiogenic shock. Her electrocardiogram showed a fast heart rhythm and other abnormal patterns, and her blood tests showed high levels of markers for heart stress. A 12-lead ECG ruled out a heart attack, and a cardiac MRI did not show signs of heart muscle disease. Because of this, a cardiac CT scan (CCTA) was done to look for a congenital heart problem. The scan found that the opening of the right coronary artery was completely missing, and the rest of the artery was supplied by a collateral branch from another artery. This is a rare congenital anomaly. She was referred to a specialist center for congenital heart disease. There, an electrophysiological study found that the arrhythmia was starting in the posteromedial papillary muscle, and this area was successfully treated with radiofrequency ablation. Since the procedure, she has been symptom-free and is doing well with regular follow-up.\"\n}", "generated_text": "A 19-year-old woman came to the emergency department with sudden palpitations and signs of cardiogenic shock. Her electrocardiogram showed a fast heart rhythm and other abnormal patterns, and her blood tests showed high levels of markers for heart stress. A 12-lead ECG ruled out a heart attack, and a cardiac MRI did not show signs of heart muscle disease. Because of this, a cardiac CT scan (CCTA) was done to look for a congenital heart problem. The scan found that the opening of the right coronary artery was completely missing, and the rest of the artery was supplied by a collateral branch from another artery. This is a rare congenital anomaly. She was referred to a specialist center for congenital heart disease. There, an electrophysiological study found that the arrhythmia was starting in the posteromedial papillary muscle, and this area was successfully treated with radiofrequency ablation. Since the procedure, she has been symptom-free and is doing well with regular follow-up."}
+{"row_index": 94, "doc_id": 65, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"A 19-year-old female presented to the emergency department with acute onset of palpitations. Initial 12-lead electrocardiogram (ECG) revealed ventricular tachycardia with right branch bundle block and left posterior hemiblock, accompanied by T-wave inversion in inferior and precordial leads. Laboratory findings demonstrated elevated serum troponin (27 ng/L; normal <14 ng/L) and NT-pro BNP (2225 pg/mL; normal <130 pg/mL), indicative of myocardial injury and cardiac stress, respectively. These findings prompted admission to the coronary care unit with a clinical suspicion of cardiogenic shock due to underlying structural or electrical cardiac pathology.\\n\\nFive years prior, she had experienced cardiogenic shock secondary to fascicular ventricular tachycardia. Subsequent evaluation with cardiac magnetic resonance (CMR) and transesophageal electrophysiological study (TEES) yielded inconclusive results, leading to a diagnosis of tachycardiomiopathy. She was initiated on standard medical therapy including angiotensin-converting enzyme inhibitors, mineralocorticoid receptor antagonists, and beta-blockers, with regular follow-up scheduled. Clinically, no further events were reported during this interval.\\n\\nDuring the current admission, no additional episodes of hyperkinetic arrhythmias were observed. Baseline 12-lead ECG and echocardiography revealed diffuse hypokinesia of both ventricles, consistent with global systolic dysfunction. CMR remained inconclusive, reinforcing the need for further anatomical evaluation. Given the clinical history of recurrent arrhythmias and cardiogenic shock in the absence of obstructive coronary disease, cardiac computed tomography angiography (CCTA) was performed to assess for undiagnosed congenital coronary anomalies.\\n\\nCCTA was conducted using a GE Lightspeed scanner (GE HealthCare, Chicago, USA) with retrospective gating, at 100 kVp, 696 mAs, gantry rotation time of 0.35 s, and 0.625 mm slice thickness. Intravenous contrast was administered at 70 mL of Iomeron 400 mgI/mL (Bracco Imaging, Milan, Italy). The imaging demonstrated a regular origin of the left main coronary artery, with a well-developed left anterior descending (LAD) artery featuring a wide ramus intermedium, two diagonal branches, and a thin, non-dominant left circumflex artery. No evidence of significant stenosis or obstructive coronary artery disease was identified. However, the ostium and proximal segment of the right coronary artery (RCA) were completely absent. Instead, the mid and distal RCA was supplied by a large collateral branch arising from the distal LAD, which courses along the lateral wall of the right ventricle, traverses the distal atrioventricular groove, and gives rise to thin posterior interventricular and posterolateral arteries. Additionally, a small branch originating from the mid-LAD was observed to supply the sinoatrial node, potentially contributing to arrhythmogenic substrate.\\n\\nThe differential diagnosis of cardiogenic shock in a young, otherwise healthy adult must consider both acquired and congenital etiologies. While myocardial infarction is a common cause, it was ruled out by the absence of typical ST-segment changes on ECG and normal coronary anatomy in the absence of obstructive lesions. Similarly, conventional cardiomyopathies were excluded by CMR, which showed no evidence of diffuse myocardial fibrosis or structural remodeling. In such cases, undiagnosed congenital coronary anomalies, particularly ostial atresia of a major coronary artery, represent a critical but often overlooked cause of sustained ventricular arrhythmias and cardiogenic shock.\\n\\nFollowing CCTA, an echo-stress test was performed, which confirmed inducible myocardial ischemia in the inferior wall—consistent with the anatomical origin of the arrhythmic focus. The patient was referred to a specialized center for congenital cardiovascular disease. There, she underwent transcatheter radiofrequency ablation targeting the posteromedial papillary muscle, the identified site of sustained ventricular tachycardia. The procedure successfully eliminated the arrhythmic substrate. Post-procedural follow-up at 6 months demonstrated sustained clinical stability, with complete absence of symptoms and no recurrence of arrhythmias. She is currently managed with acetylsalicylic acid and verapamil for antiplatelet and rate control, respectively. The case underscores the importance of advanced imaging in diagnosing congenital coronary anomalies in young patients with recurrent arrhythmias and cardiogenic shock, particularly when conventional tests fail to identify underlying pathology.\\n\\nScientific context: Ostial atresia of the right coronary artery is a rare congenital anomaly in which the origin of the RCA is completely obstructed or absent, leading to", "generated_text": "{\n  \"proficient_health_literacy\": \"A 19-year-old female presented to the emergency department with acute onset of palpitations. Initial 12-lead electrocardiogram (ECG) revealed ventricular tachycardia with right branch bundle block and left posterior hemiblock, accompanied by T-wave inversion in inferior and precordial leads. Laboratory findings demonstrated elevated serum troponin (27 ng/L; normal <14 ng/L) and NT-pro BNP (2225 pg/mL; normal <130 pg/mL), indicative of myocardial injury and cardiac stress, respectively. These findings prompted admission to the coronary care unit with a clinical suspicion of cardiogenic shock due to underlying structural or electrical cardiac pathology.\\n\\nFive years prior, she had experienced cardiogenic shock secondary to fascicular ventricular tachycardia. Subsequent evaluation with cardiac magnetic resonance (CMR) and transesophageal electrophysiological study (TEES) yielded inconclusive results, leading to a diagnosis of tachycardiomiopathy. She was initiated on standard medical therapy including angiotensin-converting enzyme inhibitors, mineralocorticoid receptor antagonists, and beta-blockers, with regular follow-up scheduled. Clinically, no further events were reported during this interval.\\n\\nDuring the current admission, no additional episodes of hyperkinetic arrhythmias were observed. Baseline 12-lead ECG and echocardiography revealed diffuse hypokinesia of both ventricles, consistent with global systolic dysfunction. CMR remained inconclusive, reinforcing the need for further anatomical evaluation. Given the clinical history of recurrent arrhythmias and cardiogenic shock in the absence of obstructive coronary disease, cardiac computed tomography angiography (CCTA) was performed to assess for undiagnosed congenital coronary anomalies.\\n\\nCCTA was conducted using a GE Lightspeed scanner (GE HealthCare, Chicago, USA) with retrospective gating, at 100 kVp, 696 mAs, gantry rotation time of 0.35 s, and 0.625 mm slice thickness. Intravenous contrast was administered at 70 mL of Iomeron 400 mgI/mL (Bracco Imaging, Milan, Italy). The imaging demonstrated a regular origin of the left main coronary artery, with a well-developed left anterior descending (LAD) artery featuring a wide ramus intermedium, two diagonal branches, and a thin, non-dominant left circumflex artery. No evidence of significant stenosis or obstructive coronary artery disease was identified. However, the ostium and proximal segment of the right coronary artery (RCA) were completely absent. Instead, the mid and distal RCA was supplied by a large collateral branch arising from the distal LAD, which courses along the lateral wall of the right ventricle, traverses the distal atrioventricular groove, and gives rise to thin posterior interventricular and posterolateral arteries. Additionally, a small branch originating from the mid-LAD was observed to supply the sinoatrial node, potentially contributing to arrhythmogenic substrate.\\n\\nThe differential diagnosis of cardiogenic shock in a young, otherwise healthy adult must consider both acquired and congenital etiologies. While myocardial infarction is a common cause, it was ruled out by the absence of typical ST-segment changes on ECG and normal coronary anatomy in the absence of obstructive lesions. Similarly, conventional cardiomyopathies were excluded by CMR, which showed no evidence of diffuse myocardial fibrosis or structural remodeling. In such cases, undiagnosed congenital coronary anomalies, particularly ostial atresia of a major coronary artery, represent a critical but often overlooked cause of sustained ventricular arrhythmias and cardiogenic shock.\\n\\nFollowing CCTA, an echo-stress test was performed, which confirmed inducible myocardial ischemia in the inferior wall—consistent with the anatomical origin of the arrhythmic focus. The patient was referred to a specialized center for congenital cardiovascular disease. There, she underwent transcatheter radiofrequency ablation targeting the posteromedial papillary muscle, the identified site of sustained ventricular tachycardia. The procedure successfully eliminated the arrhythmic substrate. Post-procedural follow-up at 6 months demonstrated sustained clinical stability, with complete absence of symptoms and no recurrence of arrhythmias. She is currently managed with acetylsalicylic acid and verapamil for antiplatelet and rate control, respectively. The case underscores the importance of advanced imaging in diagnosing congenital coronary anomalies in young patients with recurrent arrhythmias and cardiogenic shock, particularly when conventional tests fail to identify underlying pathology.\\n\\nScientific context: Ostial atresia of the right coronary artery is a rare congenital anomaly in which the origin of the RCA is completely obstructed or absent, leading to"}
+{"row_index": 95, "doc_id": 66, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 17-year-old boy was found to have a small metal button stuck in his nose during a dental check-up. He had no symptoms like nose blockage, bleeding, or pain. The button had been there for over 10 years, probably since he was 7 years old when he put it in. It was stuck under the floor of his nose, covered with mucus and crust, and looked shiny — that’s how doctors knew it was metal. X-rays showed the button clearly, and doctors confirmed it was safe and not hurting any bones or sinuses. After getting permission from his parents, the button was gently removed with a small tool while he was sitting up. The nose healed well, and after the removal, he was given a salt water rinse to keep it clean. At his follow-up two weeks later, everything looked normal and he was doing fine.\"\n}", "generated_text": "A 17-year-old boy was found to have a small metal button stuck in his nose during a dental check-up. He had no symptoms like nose blockage, bleeding, or pain. The button had been there for over 10 years, probably since he was 7 years old when he put it in. It was stuck under the floor of his nose, covered with mucus and crust, and looked shiny — that’s how doctors knew it was metal. X-rays showed the button clearly, and doctors confirmed it was safe and not hurting any bones or sinuses. After getting permission from his parents, the button was gently removed with a small tool while he was sitting up. The nose healed well, and after the removal, he was given a salt water rinse to keep it clean. At his follow-up two weeks later, everything looked normal and he was doing fine."}
+{"row_index": 96, "doc_id": 67, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"An 18-year-old Hispanic male with no significant medical history presents to the emergency department (ED) with substernal, non-radiating chest pain, orthopnoea, dry non-productive cough, and subjective fevers lasting 3–4 days. Family history includes paternal grandfather with non-ischaemic cardiomyopathy and pacemaker implantation at age 86. Patient lives with both parents, denies smoking, alcohol use, recreational drug use, or abuse. Occupationally, he works at an auto parts shop and plans to begin college. Initial workup reveals elevated serum troponin I, diffuse ST-segment elevation on electrocardiogram (ECG), and an enlarged cardiac silhouette with mild pulmonary oedema on chest X-ray. Transthoracic echocardiogram (TTE) demonstrates left ventricular ejection fraction (LVEF) of 40%, severe left ventricular concentric hypertrophy (septal thickness 1.9 cm, inferolateral wall 2.2 cm), and mild posterior pericardial effusion. Coxsackie virus A and B titres are elevated, consistent with viral myopericarditis. Symptoms initially improve with ibuprofen and colchicine. Cardiac catheterization shows no coronary artery disease. Repeat TTE reveals LVEF of 40%–45%, hypokinesis of anteroapical and inferolateral walls, elevated left ventricular end-diastolic pressure, and diastolic dysfunction. Chest CT angiogram demonstrates pneumonitis and pericardial effusion. Clinical picture is initially attributed to Coxsackie virus-induced myopericarditis, with continued medical management.\\n\\nOn day 4 of admission, the patient develops diaphoresis, tachycardia, and hypotension with undetectable blood pressure. Repeat TTE shows large pericardial effusion with signs of impending cardiac tamponade. Pericardiocentesis is performed, during which the patient experiences pulseless electrical activity (PEA) cardiac arrest requiring 30 minutes of advanced cardiovascular support. He is intubated, placed on veno-arterial extracorporeal membrane oxygenation (VA ECMO), and initiated on vasopressor therapy (norepinephrine 5 mcg/min and vasopressin 0.05 units/min). Significant bleeding from ECMO cannula necessitates multiple transfusions (9 packed red blood cells, 10 platelets, 10 cryoprecipitate, 4 fresh frozen plasma). Transferred to a tertiary center, endomyocardial biopsy (EMB) is performed due to concern for fulminant myocarditis or infiltrative cardiomyopathy. Histopathology shows no evidence of inflammatory or infiltrative processes. Repeat Coxsackie serology confirms positivity for Coxsackie A9, B2, and B6. Epstein-Barr virus (EBV) DNA quantitative PCR is elevated at 133,000 IU/mL. Subsequent TTE reveals severely reduced LVEF (10%–15%) with persistent severe concentric left ventricular hypertrophy.\\n\\nThe patient is initiated on intravenous immunoglobulin (IVIG) for suspected Coxsackie myocarditis and broad-spectrum antibiotics due to worsening leucocytosis without identifiable infectious focus. Colchicine is discontinued due to concern for rhabdomyolysis, evidenced by serum creatine kinase of 2874 U/L. Vasopressors are withdrawn, and the patient is extubated. He subsequently develops flushing, fever, dyspnoea, and hypoxaemia, with chest X-ray showing congested lung parenchyma suggestive of acute respiratory distress syndrome (ARDS), leading to IVIG discontinuation. Despite initial decline, cardiac function improves on repeat TTE with LVEF of 25%–30%, prompting consideration of ECMO removal—however, this is unsuccessful. The patient remains on ECMO and is evaluated for left ventricular assist device (LVAD) placement, which is deemed contraindicated due to global concentric hypertrophy. Multidisciplinary team consensus supports emergency listing for heart transplantation, with potential transition to intra-aortic balloon pump (IABP) and inotrope support.\\n\\nDuring evaluation for transplantation, an incisional biopsy of a 1×1 inch, painless, rubbery, mobile lesion in the right upper extremity is performed. Pathology reveals aggressive EBV-positive natural killer/T-cell lymphoma (NK/TCL) with cytotoxic immunophenotype (positive for CD2, CD3, CD56, BCL2, granzyme B, TIA1, MUM1), and diffuse co-expression of Epstein-Barr virus-encoded small RNAs (EBER) by in", "generated_text": "{\n  \"proficient_health_literacy\": \"An 18-year-old Hispanic male with no significant medical history presents to the emergency department (ED) with substernal, non-radiating chest pain, orthopnoea, dry non-productive cough, and subjective fevers lasting 3–4 days. Family history includes paternal grandfather with non-ischaemic cardiomyopathy and pacemaker implantation at age 86. Patient lives with both parents, denies smoking, alcohol use, recreational drug use, or abuse. Occupationally, he works at an auto parts shop and plans to begin college. Initial workup reveals elevated serum troponin I, diffuse ST-segment elevation on electrocardiogram (ECG), and an enlarged cardiac silhouette with mild pulmonary oedema on chest X-ray. Transthoracic echocardiogram (TTE) demonstrates left ventricular ejection fraction (LVEF) of 40%, severe left ventricular concentric hypertrophy (septal thickness 1.9 cm, inferolateral wall 2.2 cm), and mild posterior pericardial effusion. Coxsackie virus A and B titres are elevated, consistent with viral myopericarditis. Symptoms initially improve with ibuprofen and colchicine. Cardiac catheterization shows no coronary artery disease. Repeat TTE reveals LVEF of 40%–45%, hypokinesis of anteroapical and inferolateral walls, elevated left ventricular end-diastolic pressure, and diastolic dysfunction. Chest CT angiogram demonstrates pneumonitis and pericardial effusion. Clinical picture is initially attributed to Coxsackie virus-induced myopericarditis, with continued medical management.\\n\\nOn day 4 of admission, the patient develops diaphoresis, tachycardia, and hypotension with undetectable blood pressure. Repeat TTE shows large pericardial effusion with signs of impending cardiac tamponade. Pericardiocentesis is performed, during which the patient experiences pulseless electrical activity (PEA) cardiac arrest requiring 30 minutes of advanced cardiovascular support. He is intubated, placed on veno-arterial extracorporeal membrane oxygenation (VA ECMO), and initiated on vasopressor therapy (norepinephrine 5 mcg/min and vasopressin 0.05 units/min). Significant bleeding from ECMO cannula necessitates multiple transfusions (9 packed red blood cells, 10 platelets, 10 cryoprecipitate, 4 fresh frozen plasma). Transferred to a tertiary center, endomyocardial biopsy (EMB) is performed due to concern for fulminant myocarditis or infiltrative cardiomyopathy. Histopathology shows no evidence of inflammatory or infiltrative processes. Repeat Coxsackie serology confirms positivity for Coxsackie A9, B2, and B6. Epstein-Barr virus (EBV) DNA quantitative PCR is elevated at 133,000 IU/mL. Subsequent TTE reveals severely reduced LVEF (10%–15%) with persistent severe concentric left ventricular hypertrophy.\\n\\nThe patient is initiated on intravenous immunoglobulin (IVIG) for suspected Coxsackie myocarditis and broad-spectrum antibiotics due to worsening leucocytosis without identifiable infectious focus. Colchicine is discontinued due to concern for rhabdomyolysis, evidenced by serum creatine kinase of 2874 U/L. Vasopressors are withdrawn, and the patient is extubated. He subsequently develops flushing, fever, dyspnoea, and hypoxaemia, with chest X-ray showing congested lung parenchyma suggestive of acute respiratory distress syndrome (ARDS), leading to IVIG discontinuation. Despite initial decline, cardiac function improves on repeat TTE with LVEF of 25%–30%, prompting consideration of ECMO removal—however, this is unsuccessful. The patient remains on ECMO and is evaluated for left ventricular assist device (LVAD) placement, which is deemed contraindicated due to global concentric hypertrophy. Multidisciplinary team consensus supports emergency listing for heart transplantation, with potential transition to intra-aortic balloon pump (IABP) and inotrope support.\\n\\nDuring evaluation for transplantation, an incisional biopsy of a 1×1 inch, painless, rubbery, mobile lesion in the right upper extremity is performed. Pathology reveals aggressive EBV-positive natural killer/T-cell lymphoma (NK/TCL) with cytotoxic immunophenotype (positive for CD2, CD3, CD56, BCL2, granzyme B, TIA1, MUM1), and diffuse co-expression of Epstein-Barr virus-encoded small RNAs (EBER) by in"}
+{"row_index": 97, "doc_id": 68, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 50-year-old man who smoked a lot and had bad fats in his blood for years got a rare eye problem where one eye (right) swelled up fast and couldn’t move properly. This caused constant double vision that made daily life hard. His thyroid was normal, but his body made a little bit more of a certain immune protein. Steroid shots helped a little, but didn’t fix the double vision or the eye movement. Doctors had to do surgery on both sides of the eye socket to give room for the eye to move better. A tissue sample from the eye muscle showed it was full of scar tissue and fat. This scar tissue is what made the eye move so poorly.\"\n}", "generated_text": "A 50-year-old man who smoked a lot and had bad fats in his blood for years got a rare eye problem where one eye (right) swelled up fast and couldn’t move properly. This caused constant double vision that made daily life hard. His thyroid was normal, but his body made a little bit more of a certain immune protein. Steroid shots helped a little, but didn’t fix the double vision or the eye movement. Doctors had to do surgery on both sides of the eye socket to give room for the eye to move better. A tissue sample from the eye muscle showed it was full of scar tissue and fat. This scar tissue is what made the eye move so poorly."}
+{"row_index": 98, "doc_id": 68, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 50-year-old man with a history of smoking and high cholesterol developed a rare condition called euthyroid single muscular Graves' ophthalmopathy. He had no family history of thyroid problems, but he did have a family history of heart disease and diabetes. Over several years, he noticed swelling in the right eye, pain when moving his eyes, redness, and constant double vision (diplopia) that made daily life difficult. His eyesight was normal, but he could not move his right eye properly, especially upward, which worsened his double vision. Tests showed mild signs of thyroid autoimmunity, but his thyroid function was normal. Imaging showed that only the right inferior rectus muscle was enlarged and damaged, while the rest of the eye muscles were normal. A biopsy confirmed massive scar tissue (fibrosis) in that muscle. The patient tried steroid treatment, which helped reduce inflammation but did not fix the double vision or muscle damage. He then had surgery to relieve pressure in the eye socket, and this helped slightly. However, the main problem — the scarred muscle — remained. This case highlights a rare form of eye swelling where only one muscle is affected, and it can cause serious vision problems even when the thyroid is healthy.\"\n}", "generated_text": "A 50-year-old man with a history of smoking and high cholesterol developed a rare condition called euthyroid single muscular Graves' ophthalmopathy. He had no family history of thyroid problems, but he did have a family history of heart disease and diabetes. Over several years, he noticed swelling in the right eye, pain when moving his eyes, redness, and constant double vision (diplopia) that made daily life difficult. His eyesight was normal, but he could not move his right eye properly, especially upward, which worsened his double vision. Tests showed mild signs of thyroid autoimmunity, but his thyroid function was normal. Imaging showed that only the right inferior rectus muscle was enlarged and damaged, while the rest of the eye muscles were normal. A biopsy confirmed massive scar tissue (fibrosis) in that muscle. The patient tried steroid treatment, which helped reduce inflammation but did not fix the double vision or muscle damage. He then had surgery to relieve pressure in the eye socket, and this helped slightly. However, the main problem — the scarred muscle — remained. This case highlights a rare form of eye swelling where only one muscle is affected, and it can cause serious vision problems even when the thyroid is healthy."}
+{"row_index": 99, "doc_id": 68, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"We report a rare case of euthyroid unilateral Graves' ophthalmopathy (GO) characterized by early, massive mono-muscular fibrosis in the right inferior rectus muscle of a 50-year-old male patient. The patient had a significant family history of cardiovascular disease, type 2 diabetes mellitus, and myasthenia gravis, with no personal or familial history of thyroid autoimmune disorders. He was a daily smoker (20 cigarettes/day) since age 30 and had long-standing dyslipidemia, with laboratory values showing total cholesterol of 220 mg/dL, triglycerides of 297 mg/dL, and low high-density lipoprotein cholesterol (HDL) of 38 mg/dL—indicating a pro-atherogenic lipid profile. Since June 2020, the patient developed rapid and progressive soft tissue swelling in the right orbit, accompanied by moderate pain during ocular movements, eyelid redness, and persistent diplopia. Visual acuity remained normal (16/17 and 17/17 in right and left eyes, respectively), and color vision was preserved. Ocular motility evaluation revealed a severe reduction in elevation and persistent depression of the right globe in primary position, as assessed by the Gorman score, with constant diplopia. Clinical Activity Score (CAS) was 3/7, indicating moderate active inflammation, and eyelid aperture was 14 mm (right) versus 10 mm (left), with Hertel measurements of 24 mm (right) and 18 mm (left), confirming significant orbital expansion. The muscle orbit area ratio in the right orbit was 0.25 (in-house Autocad method; normal threshold vn ≤ 0.20 ± 0.03), indicating pathological enlargement of the inferior rectus muscle. High-resolution CT imaging (1.25 mm contiguous slices, 200 mA, 120 kV, pitch 0.5) demonstrated marked enlargement of the lower rectus body extending to the insertion tendon, while all other extraocular muscles in both orbits showed normal morphology. Thyroid function tests were euthyroid, with only a mild elevation in thyroid-stimulating hormone receptor antibody (TSH-R-Ab) levels at 1.75 mU/L (normal <1.5 mU/L), suggesting a low-grade autoimmune component without overt thyroid dysfunction. Electrophysiological evaluation revealed a slight reduction in the amplitude of the p100 wave in the right eye, indicating early neuro-ocular dysfunction possibly secondary to inflammatory or fibrotic muscle changes. Thyroid ultrasound demonstrated a thyroiditis-like pattern, consistent with chronic inflammation, but no evidence of nodules or thyroid autoimmunity was found. Routine systemic laboratory evaluations were unremarkable, excluding hematological or systemic diseases. Initial treatment consisted of intravenous corticosteroid pulse therapy (Solumedrol, 4500 mg cumulative dose over 12 weeks), which effectively resolved inflammatory signs and symptoms such as swelling and pain. However, functional outcomes—including Gorman score, Hertel measurements, and diplopia—remained unchanged, and electrophysiological parameters and visual acuity deteriorated, suggesting irreversible or progressive neuro-ocular compromise. Due to the persistent symptoms and lack of response to medical therapy, the patient underwent two-wall orbital surgical decompression in conjunction with continued parenteral glucocorticoid therapy. Histopathological examination of the right inferior rectus muscle biopsy revealed extensive fibrosis with significant adipose tissue infiltration, confirming the presence of early and severe fibrotic transformation of the extraocular muscle, likely driven by chronic inflammation and/or metabolic stress. This case highlights the potential for rapid progression of mono-muscular fibrosis in euthyroid GO, even in the absence of overt thyroid autoimmunity, and underscores the importance of early surgical intervention in patients with severe ocular motility dysfunction and persistent fibrotic changes, particularly in those with comorbidities such as smoking and dyslipidemia.\"\n}", "generated_text": "We report a rare case of euthyroid unilateral Graves' ophthalmopathy (GO) characterized by early, massive mono-muscular fibrosis in the right inferior rectus muscle of a 50-year-old male patient. The patient had a significant family history of cardiovascular disease, type 2 diabetes mellitus, and myasthenia gravis, with no personal or familial history of thyroid autoimmune disorders. He was a daily smoker (20 cigarettes/day) since age 30 and had long-standing dyslipidemia, with laboratory values showing total cholesterol of 220 mg/dL, triglycerides of 297 mg/dL, and low high-density lipoprotein cholesterol (HDL) of 38 mg/dL—indicating a pro-atherogenic lipid profile. Since June 2020, the patient developed rapid and progressive soft tissue swelling in the right orbit, accompanied by moderate pain during ocular movements, eyelid redness, and persistent diplopia. Visual acuity remained normal (16/17 and 17/17 in right and left eyes, respectively), and color vision was preserved. Ocular motility evaluation revealed a severe reduction in elevation and persistent depression of the right globe in primary position, as assessed by the Gorman score, with constant diplopia. Clinical Activity Score (CAS) was 3/7, indicating moderate active inflammation, and eyelid aperture was 14 mm (right) versus 10 mm (left), with Hertel measurements of 24 mm (right) and 18 mm (left), confirming significant orbital expansion. The muscle orbit area ratio in the right orbit was 0.25 (in-house Autocad method; normal threshold vn ≤ 0.20 ± 0.03), indicating pathological enlargement of the inferior rectus muscle. High-resolution CT imaging (1.25 mm contiguous slices, 200 mA, 120 kV, pitch 0.5) demonstrated marked enlargement of the lower rectus body extending to the insertion tendon, while all other extraocular muscles in both orbits showed normal morphology. Thyroid function tests were euthyroid, with only a mild elevation in thyroid-stimulating hormone receptor antibody (TSH-R-Ab) levels at 1.75 mU/L (normal <1.5 mU/L), suggesting a low-grade autoimmune component without overt thyroid dysfunction. Electrophysiological evaluation revealed a slight reduction in the amplitude of the p100 wave in the right eye, indicating early neuro-ocular dysfunction possibly secondary to inflammatory or fibrotic muscle changes. Thyroid ultrasound demonstrated a thyroiditis-like pattern, consistent with chronic inflammation, but no evidence of nodules or thyroid autoimmunity was found. Routine systemic laboratory evaluations were unremarkable, excluding hematological or systemic diseases. Initial treatment consisted of intravenous corticosteroid pulse therapy (Solumedrol, 4500 mg cumulative dose over 12 weeks), which effectively resolved inflammatory signs and symptoms such as swelling and pain. However, functional outcomes—including Gorman score, Hertel measurements, and diplopia—remained unchanged, and electrophysiological parameters and visual acuity deteriorated, suggesting irreversible or progressive neuro-ocular compromise. Due to the persistent symptoms and lack of response to medical therapy, the patient underwent two-wall orbital surgical decompression in conjunction with continued parenteral glucocorticoid therapy. Histopathological examination of the right inferior rectus muscle biopsy revealed extensive fibrosis with significant adipose tissue infiltration, confirming the presence of early and severe fibrotic transformation of the extraocular muscle, likely driven by chronic inflammation and/or metabolic stress. This case highlights the potential for rapid progression of mono-muscular fibrosis in euthyroid GO, even in the absence of overt thyroid autoimmunity, and underscores the importance of early surgical intervention in patients with severe ocular motility dysfunction and persistent fibrotic changes, particularly in those with comorbidities such as smoking and dyslipidemia."}
+{"row_index": 100, "doc_id": 69, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 15-year-old boy had belly pain and vomiting for four days. Doctors first thought it was a stomach bug, but it didn’t go away. His stomach was swollen, and tests showed his small intestine was blocked. A scan found a piece of intestine stuck in a small opening in the belly, called the Winslow hiatus. This caused the blockage. The doctors tried a small surgery first, but couldn’t see clearly, so they did a bigger cut in the middle of the belly to fix it. They pulled the stuck piece of intestine back into place and found it was just a small part of the small intestine that had gotten trapped. No part of the intestine had to be cut off. They didn’t do any extra steps to prevent it from happening again. After surgery, he had a small pocket of fluid in his pelvis, which was treated with medicine and didn’t get worse. He’s now recovering at a pediatric surgery clinic, doing well and able to eat again.\"\n}", "generated_text": "A 15-year-old boy had belly pain and vomiting for four days. Doctors first thought it was a stomach bug, but it didn’t go away. His stomach was swollen, and tests showed his small intestine was blocked. A scan found a piece of intestine stuck in a small opening in the belly, called the Winslow hiatus. This caused the blockage. The doctors tried a small surgery first, but couldn’t see clearly, so they did a bigger cut in the middle of the belly to fix it. They pulled the stuck piece of intestine back into place and found it was just a small part of the small intestine that had gotten trapped. No part of the intestine had to be cut off. They didn’t do any extra steps to prevent it from happening again. After surgery, he had a small pocket of fluid in his pelvis, which was treated with medicine and didn’t get worse. He’s now recovering at a pediatric surgery clinic, doing well and able to eat again."}
+{"row_index": 101, "doc_id": 69, "gold_label": "intermediate_health_literacy", "source_lang": "English", "prediction": "{\n  \"intermediate_health_literacy\": \"A 15-year-old boy with no prior medical issues came in with vomiting and abdominal pain that had lasted four days. At first, doctors thought it was gastroenteritis, but the symptoms didn’t improve. He was admitted for further testing.\\n\\nHis abdomen was distended and had signs of intestinal blockage, which was confirmed by an abdominal X-ray. A CT scan showed a small intestine loop trapped at the Winslow hiatus — a key opening in the abdomen — causing an intestinal obstruction. This condition is called an internal hernia.\\n\\nThe surgery began with laparoscopy, a minimally invasive procedure, but the view was poor due to the distended intestines and the position of the liver. Because of this, the surgery was changed to an open approach — a larger incision in the middle of the abdomen — to better see and fix the problem.\\n\\nDuring the surgery, the doctors found a five-centimeter section of the ileum (a part of the small intestine) that had herniated through the Winslow hiatus. The loop was successfully reduced, and no part of the intestine needed to be removed. No preventive steps were taken to reduce the risk of it coming back.\\n\\nAfter surgery, the boy had a temporary slowdown in bowel movement (paralytic ileus), which resolved after five days. He started eating again and did well. He also developed a small fluid collection in the pelvis, which was treated with antibiotics and improved over time. He was discharged ten days after surgery and is now being followed up in outpatient paediatric surgery. He is doing well and has normal bowel function.\"\n}", "generated_text": "A 15-year-old boy with no prior medical issues came in with vomiting and abdominal pain that had lasted four days. At first, doctors thought it was gastroenteritis, but the symptoms didn’t improve. He was admitted for further testing.\n\nHis abdomen was distended and had signs of intestinal blockage, which was confirmed by an abdominal X-ray. A CT scan showed a small intestine loop trapped at the Winslow hiatus — a key opening in the abdomen — causing an intestinal obstruction. This condition is called an internal hernia.\n\nThe surgery began with laparoscopy, a minimally invasive procedure, but the view was poor due to the distended intestines and the position of the liver. Because of this, the surgery was changed to an open approach — a larger incision in the middle of the abdomen — to better see and fix the problem.\n\nDuring the surgery, the doctors found a five-centimeter section of the ileum (a part of the small intestine) that had herniated through the Winslow hiatus. The loop was successfully reduced, and no part of the intestine needed to be removed. No preventive steps were taken to reduce the risk of it coming back.\n\nAfter surgery, the boy had a temporary slowdown in bowel movement (paralytic ileus), which resolved after five days. He started eating again and did well. He also developed a small fluid collection in the pelvis, which was treated with antibiotics and improved over time. He was discharged ten days after surgery and is now being followed up in outpatient paediatric surgery. He is doing well and has normal bowel function."}
+{"row_index": 102, "doc_id": 69, "gold_label": "proficient_health_literacy", "source_lang": "English", "prediction": "{\n  \"proficient_health_literacy\": \"We present a clinical case of a 15-year-old male with no significant medical history or prior surgical interventions who presented to the paediatric emergency department with a four-day history of vomiting and epigastric abdominal pain, remaining afebrile throughout. Initial evaluation was consistent with gastroenteritis, but symptoms persisted, including ongoing epigastric pain and biliary vomiting, prompting admission for further investigation.\\n\\nPhysical examination revealed acceptable general condition, afebrile status, and mild signs of dehydration. Abdominal distension was noted, with absent peritoneal signs and diminished bowel sounds. Laboratory studies were unremarkable. Abdominal radiography demonstrated findings consistent with small bowel obstruction.\\n\\nUrgent computed tomography (CT) imaging revealed ascites and marked dilation of small intestinal loops, indicating interposition of a small bowel segment at the proximal transition zone of the epiploic fat, specifically at the level of the Winslow hiatus. The CT showed a distinct change in caliber of the small intestine at this anatomical landmark, suggesting intraperitoneal herniation of a segment of ileum through the Winslow hiatus.\\n\\nSurgical management began with exploratory laparoscopy. Intraoperatively, dilated loops of small intestine, including the terminal ileum, cecum, and ascending colon, were observed in the right hypochondrium, with the cecum exhibiting high mobility and no adhesions to the right parietocolic space. Proximal to the terminal ileum, multiple small bowel loops were identified in the depth of the theoretical location of the Winslow hiatus. Attempts to mobilize the cecum and terminal ileum toward the right iliac fossa were unsuccessful due to interference from the lower edge of the liver and the distended bowel loops. A percutaneous puncture of a dilated loop was attempted to decompress gas and improve visualization, but this did not resolve the obstruction.\\n\\nGiven the poor visualization and inability to accurately localize the site of caliber change, a conversion to a supraumbilical midline laparotomy was performed. In the opened abdominal cavity, the site of caliber change in the ileum was identified at approximately 40 centimetres from the ileocecal valve, confirming a herniation of a 5-centimetre segment of ileum through the Winslow hiatus. The herniated loop demonstrated characteristic congestive imprints at both ends, consistent with mechanical compression and ischemic changes due to entrapment. The normal caliber of the Winslow hiatus was confirmed, and no preventive surgical technique (such as hernia repair or mesh placement) was applied to reduce the risk of recurrence.\\n\\nPostoperatively, the patient developed a transient paralytic ileus, which resolved over five days, allowing nasogastric tube removal and initiation of oral intake with good tolerance. Concurrently, a pelvic collection developed, which was managed conservatively with broad-spectrum antibiotics and drainage via percutaneous catheterization, resulting in favorable clinical course. The patient was discharged ten days after surgery with preserved gastrointestinal transit, absence of fever, and stable general condition.\\n\\nThe patient is currently under outpatient follow-up in the paediatric surgery clinic. This case highlights the diagnostic challenge of internal hernias, particularly in adolescents, where clinical presentation may mimic common gastrointestinal disorders, and imaging findings can be subtle. The Winslow hiatus, a potential site for intraperitoneal herniation due to its anatomical variability and the presence of epiploic foramen, remains a critical anatomical consideration in the evaluation of small bowel obstruction. Internal hernias are often asymptomatic until obstruction occurs, and their diagnosis relies on high-resolution imaging and surgical exploration. The absence of preventive measures in this case underscores the need for further study into risk factors and long-term outcomes in pediatric populations, particularly given the potential for recurrence in cases involving small bowel entrapment through the Winslow hiatus.\"\n}", "generated_text": "We present a clinical case of a 15-year-old male with no significant medical history or prior surgical interventions who presented to the paediatric emergency department with a four-day history of vomiting and epigastric abdominal pain, remaining afebrile throughout. Initial evaluation was consistent with gastroenteritis, but symptoms persisted, including ongoing epigastric pain and biliary vomiting, prompting admission for further investigation.\n\nPhysical examination revealed acceptable general condition, afebrile status, and mild signs of dehydration. Abdominal distension was noted, with absent peritoneal signs and diminished bowel sounds. Laboratory studies were unremarkable. Abdominal radiography demonstrated findings consistent with small bowel obstruction.\n\nUrgent computed tomography (CT) imaging revealed ascites and marked dilation of small intestinal loops, indicating interposition of a small bowel segment at the proximal transition zone of the epiploic fat, specifically at the level of the Winslow hiatus. The CT showed a distinct change in caliber of the small intestine at this anatomical landmark, suggesting intraperitoneal herniation of a segment of ileum through the Winslow hiatus.\n\nSurgical management began with exploratory laparoscopy. Intraoperatively, dilated loops of small intestine, including the terminal ileum, cecum, and ascending colon, were observed in the right hypochondrium, with the cecum exhibiting high mobility and no adhesions to the right parietocolic space. Proximal to the terminal ileum, multiple small bowel loops were identified in the depth of the theoretical location of the Winslow hiatus. Attempts to mobilize the cecum and terminal ileum toward the right iliac fossa were unsuccessful due to interference from the lower edge of the liver and the distended bowel loops. A percutaneous puncture of a dilated loop was attempted to decompress gas and improve visualization, but this did not resolve the obstruction.\n\nGiven the poor visualization and inability to accurately localize the site of caliber change, a conversion to a supraumbilical midline laparotomy was performed. In the opened abdominal cavity, the site of caliber change in the ileum was identified at approximately 40 centimetres from the ileocecal valve, confirming a herniation of a 5-centimetre segment of ileum through the Winslow hiatus. The herniated loop demonstrated characteristic congestive imprints at both ends, consistent with mechanical compression and ischemic changes due to entrapment. The normal caliber of the Winslow hiatus was confirmed, and no preventive surgical technique (such as hernia repair or mesh placement) was applied to reduce the risk of recurrence.\n\nPostoperatively, the patient developed a transient paralytic ileus, which resolved over five days, allowing nasogastric tube removal and initiation of oral intake with good tolerance. Concurrently, a pelvic collection developed, which was managed conservatively with broad-spectrum antibiotics and drainage via percutaneous catheterization, resulting in favorable clinical course. The patient was discharged ten days after surgery with preserved gastrointestinal transit, absence of fever, and stable general condition.\n\nThe patient is currently under outpatient follow-up in the paediatric surgery clinic. This case highlights the diagnostic challenge of internal hernias, particularly in adolescents, where clinical presentation may mimic common gastrointestinal disorders, and imaging findings can be subtle. The Winslow hiatus, a potential site for intraperitoneal herniation due to its anatomical variability and the presence of epiploic foramen, remains a critical anatomical consideration in the evaluation of small bowel obstruction. Internal hernias are often asymptomatic until obstruction occurs, and their diagnosis relies on high-resolution imaging and surgical exploration. The absence of preventive measures in this case underscores the need for further study into risk factors and long-term outcomes in pediatric populations, particularly given the potential for recurrence in cases involving small bowel entrapment through the Winslow hiatus."}
+{"row_index": 103, "doc_id": 70, "gold_label": "low_health_literacy", "source_lang": "English", "prediction": "{\n  \"low_health_literacy\": \"A 75-year-old woman from Western Ethiopia had a small birth control device (IUD) put in her uterus 40 years ago. Since then, she never checked it or had any gynecological visits. Now, she has pain in her lower belly and vagina, which started 3 years ago and got worse. The doctor found the old IUD still inside, near the opening of her cervix. It was easy to pull out using simple tools. She was given pain medicine and doxycycline to help with the pain and infection. She went home after being watched for 4 hours and her pain went away.\"\n}", "generated_text": "A 75-year-old woman from Western Ethiopia had a small birth control device (IUD) put in her uterus 40 years ago. Since then, she never checked it or had any gynecological visits. Now, she has pain in her lower belly and vagina, which started 3 years ago and got worse. The doctor found the old IUD still inside, near the opening of her cervix. It was easy to pull out using simple tools. She was given pain medicine and doxycycline to help with the pain and infection. She went home after being watched for 4 hours and her pain went away."}
diff --git a/code/RL_model/inference_data/vllm_inference_20260213_170937_meta.json b/code/RL_model/inference_data/vllm_inference_20260213_170937_meta.json
new file mode 100644
index 0000000000000000000000000000000000000000..6c940da205960568c791540a9d860bb68646cd6b
--- /dev/null
+++ b/code/RL_model/inference_data/vllm_inference_20260213_170937_meta.json
@@ -0,0 +1,10 @@
+{
+  "model_path_for_tokenizer": "/home/mshahidul/readctrl/code/RL_model/models/converted_model/v1",
+  "dataset_path": "/home/mshahidul/readctrl/code/text_classifier/data/verified_combined_0-80_clean200.json",
+  "base_url": "http://127.0.0.1:8001/v1",
+  "served_model_name": "inference",
+  "batch_size": 8,
+  "num_samples": 200,
+  "output_jsonl": "/home/mshahidul/readctrl/code/RL_model/inference_data/vllm_inference_20260213_170937.jsonl",
+  "output_parquet": "/home/mshahidul/readctrl/code/RL_model/inference_data/vllm_inference_20260213_170937.parquet"
+}
\ No newline at end of file
diff --git a/code/RL_model/inference_data/vllm_inference_qwen-qwen3-4b-instruct-2507_20260213_173334_meta.json b/code/RL_model/inference_data/vllm_inference_qwen-qwen3-4b-instruct-2507_20260213_173334_meta.json
new file mode 100644
index 0000000000000000000000000000000000000000..d0dad3f324b567a141e2819921996056c1e5ae62
--- /dev/null
+++ b/code/RL_model/inference_data/vllm_inference_qwen-qwen3-4b-instruct-2507_20260213_173334_meta.json
@@ -0,0 +1,10 @@
+{
+  "model_path_for_tokenizer": "Qwen/Qwen3-4B-Instruct-2507",
+  "dataset_path": "/home/mshahidul/readctrl/code/text_classifier/data/verified_combined_0-80_clean200.json",
+  "base_url": "http://127.0.0.1:8001/v1",
+  "served_model_name": "inference",
+  "batch_size": 8,
+  "num_samples": 200,
+  "output_jsonl": "/home/mshahidul/readctrl/code/RL_model/inference_data/vllm_inference_qwen-qwen3-4b-instruct-2507_20260213_173334.jsonl",
+  "output_parquet": "/home/mshahidul/readctrl/code/RL_model/inference_data/vllm_inference_qwen-qwen3-4b-instruct-2507_20260213_173334.parquet"
+}
\ No newline at end of file
diff --git a/code/RL_model/unsloth_rl/RL_code.py b/code/RL_model/unsloth_rl/RL_code.py
new file mode 100644
index 0000000000000000000000000000000000000000..52e0ece1adb2f64457a5431b470d16a28d96011f
--- /dev/null
+++ b/code/RL_model/unsloth_rl/RL_code.py
@@ -0,0 +1,165 @@
+import os
+os.environ["CUDA_DEVICE_ORDER"] = "PCI_BUS_ID"
+os.environ["CUDA_VISIBLE_DEVICES"] = "3"
+from unsloth import FastLanguageModel
+import torch
+from health_classifier import classifier
+max_seq_length = 8192 
+
+model, tokenizer = FastLanguageModel.from_pretrained(
+    model_name = "/home/mshahidul/readctrl_model/RL_model/readability_sft_lora_model",
+    max_seq_length = max_seq_length,
+    load_in_4bit = False, # Set to False if you have enough VRAM
+    fast_inference = False,
+)
+
+# Simply enable gradient checkpointing and prepare for training
+model = FastLanguageModel.for_training(model)
+
+# /home/mshahidul/readctrl/data/extracting_subclaim/extracted_subclaims_multiclinsum_test_en_full.json
+with open("/home/mshahidul/readctrl/data/extracting_subclaim/extracted_subclaims_multiclinsum_test_en_full.json", "r") as f:
+    import json
+    data = json.load(f)
+from datasets import Dataset
+dataset = Dataset.from_list(data)
+with open('/home/mshahidul/readctrl/code/RL_model/prompt', 'r') as f:
+    prompt_template = f.read()
+dataset = dataset.map(lambda x: {
+    "prompt" : [
+        {"role": "system", "content": prompt_template},
+        {"role": "user",   "content": f'''
+- Input Language: English
+- Gold Summary (the anchor reference summary): {x['summary']}
+- Source Text (detailed content): {x['fulltext']}
+'''},
+    ],
+    "answer": {
+        "fulltext_subclaims": x['fulltext_subclaims'],
+        "summary_subclaims": x['summary_subclaims'],
+    },
+})
+import requests
+import json
+import re
+
+from claim_verifier import MedicalClaimVerifier
+
+verifier = MedicalClaimVerifier()
+
+def claim_reward_func(prompts, completions, answer, **kwargs):
+    # import ipdb; ipdb.set_trace()
+    """
+    GRPO reward function. 
+    Expects 'summary_subclaims' and 'fulltext_subclaims' to be in the dataset.
+    """
+    rewards = []
+    # We loop through the group of completions
+    for i in range(len(completions)):
+        reward = verifier.get_reward_score(
+            completions[i], 
+            answer[i]["summary_subclaims"], 
+            answer[i]["fulltext_subclaims"]
+        )
+        rewards.append(reward)
+    return rewards
+
+
+# def format_reward_func(completions, **kwargs):
+#     required_keys = ["low_health_literacy", "intermediate_health_literacy", "proficient_health_literacy"]
+#     scores = []
+#     for completion in completions:
+#         try:
+#             match = re.search(r"<SOLUTION>(.*?)</SOLUTION>", completion, re.DOTALL)
+#             content = match.group(1) if match else completion
+#             data = json.loads(content)
+#             if all(k in data for k in required_keys):
+#                 scores.append(2.0)
+#             else:
+#                 scores.append(-1.0)
+#         except:
+#             scores.append(-2.0)
+#     return scores
+
+
+import json
+
+def literacy_classifier_reward_func(completions, **kwargs):
+    scores = []
+    for completion in completions:
+        try:
+            # 1. Clean up potential Markdown formatting
+            cleaned_content = completion[0]['content'].strip()
+            if cleaned_content.startswith("```"):
+                # Removes leading ```json or ``` and trailing ```
+                cleaned_content = cleaned_content.split("```")[1]
+                if cleaned_content.startswith("json"):
+                    cleaned_content = cleaned_content[4:]
+            
+            # 2. Parse the JSON
+            data = json.loads(cleaned_content.strip())
+            
+            alignment_score = 0.0
+            target_labels = ["low", "intermediate", "proficient"]
+            
+            for label in target_labels:
+                key = f"{label}_health_literacy"
+                text_to_test = data.get(key, "")
+        
+                
+                if text_to_test:
+                    # Run the DSPy classifier
+                    result = classifier(summary_text=text_to_test)
+                    predicted = result.label # Expected format: "low_health_literacy"
+                    # import ipdb; ipdb.set_trace()
+                    
+                    if predicted == key:
+                        alignment_score += 1.0
+                    else:
+                        # Soft penalty for misclassification
+                        alignment_score -= 0.5
+                else:
+                    # Penalty if a specific literacy level is missing from the JSON
+                    alignment_score -= 0.3
+            
+            scores.append(alignment_score)
+            
+        except (json.JSONDecodeError, Exception):
+            # Significant penalty for malformed JSON or failed processing
+            scores.append(-1.0)
+            
+    return scores
+
+
+from trl import GRPOConfig, GRPOTrainer
+
+training_args = GRPOConfig(
+    learning_rate = 5e-6,
+    lr_scheduler_type = "cosine",
+    weight_decay = 0.1,
+    max_prompt_length = 8192,
+    max_completion_length = 4096,
+    # num_of_epochs = 10,
+    num_generations = 4, # GRPO group size
+    per_device_train_batch_size = 4,
+    gradient_accumulation_steps = 4,
+    max_steps = 500,
+    bf16 = True,
+    output_dir = "medical_grpo_outputs",
+)
+
+trainer = GRPOTrainer(
+    model = model,
+    reward_funcs = [
+        claim_reward_func,
+        # format_reward_func,
+        literacy_classifier_reward_func
+    ],
+    args = training_args,
+    train_dataset = dataset, # Use the same dataset from your SFT prep
+    tokenizer = tokenizer,
+)
+
+trainer.train()
+
+model.save_pretrained("/home/mshahidul/readctrl_model/readability_GRPO_model_v1")
+tokenizer.save_pretrained("/home/mshahidul/readctrl_model/readability_GRPO_model_v1")
\ No newline at end of file
diff --git a/code/RL_model/unsloth_rl/RL_training.ipynb b/code/RL_model/unsloth_rl/RL_training.ipynb
new file mode 100644
index 0000000000000000000000000000000000000000..fb0664a14c587c318eb52a73e28e0b6fc63152b6
--- /dev/null
+++ b/code/RL_model/unsloth_rl/RL_training.ipynb
@@ -0,0 +1,475 @@
+{
+ "cells": [
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "8a790cb6",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "from unsloth import FastLanguageModel\n",
+    "import torch\n",
+    "max_seq_length = 2048 # Can increase for longer reasoning traces\n",
+    "lora_rank = 32 # Larger rank = smarter, but slower\n",
+    "\n",
+    "model, tokenizer = FastLanguageModel.from_pretrained(\n",
+    "    model_name = \"unsloth/Qwen3-4B-Base\",\n",
+    "    max_seq_length = max_seq_length,\n",
+    "    load_in_4bit = False, # False for LoRA 16bit\n",
+    "    fast_inference = True, # Enable vLLM fast inference\n",
+    "    max_lora_rank = lora_rank,\n",
+    "    gpu_memory_utilization = 0.9, # Reduce if out of memory\n",
+    ")\n",
+    "\n",
+    "model = FastLanguageModel.get_peft_model(\n",
+    "    model,\n",
+    "    r = lora_rank, # Choose any number > 0 ! Suggested 8, 16, 32, 64, 128\n",
+    "    target_modules = [\n",
+    "        \"q_proj\", \"k_proj\", \"v_proj\", \"o_proj\",\n",
+    "        \"gate_proj\", \"up_proj\", \"down_proj\",\n",
+    "    ],\n",
+    "    lora_alpha = lora_rank*2, # *2 speeds up training\n",
+    "    use_gradient_checkpointing = \"unsloth\", # Reduces memory usage\n",
+    "    random_state = 3407,\n",
+    ")"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "ba056efa",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "# /home/mshahidul/readctrl/data/extracting_subclaim/extracted_subclaims_multiclinsum_test_en_full.json\n",
+    "with open('/home/mshahidul/readctrl/data/extracting_subclaim/extracted_subclaims_multiclinsum_test_en_full.json', 'r') as f:\n",
+    "    synthetic_data_with_gs_summary_en = json.load(f)\n",
+    "from datasets import Dataset\n",
+    "dataset = Dataset.from_list(synthetic_data_with_gs_summary_en)"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "fa285d3f",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "dataset"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "ad059247",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "# /home/mshahidul/readctrl/code/RL_model/prompt\n",
+    "with open('/home/mshahidul/readctrl/code/RL_model/prompt', 'r') as f:\n",
+    "    prompt_template = f.read()"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "f74cbfda",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "dataset = dataset.map(lambda x: {\n",
+    "    \"prompt\" : [\n",
+    "        {\"role\": \"system\", \"content\": prompt_template},\n",
+    "        {\"role\": \"user\",   \"content\": f'''\n",
+    "- Input Language: English\n",
+    "- Gold Summary (the anchor reference summary): {x['summary']}\n",
+    "- Source Text (detailed content): {x['fulltext']}\n",
+    "'''},\n",
+    "    ],\n",
+    "    \"answer\": {\n",
+    "        \"fulltext_subclaims\": x['fulltext_subclaims'],\n",
+    "        \"summary_subclaims\": x['summary_subclaims'],\n",
+    "    },\n",
+    "})"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "0dd615f4",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "# /home/mshahidul/readctrl/data/synthetic_dataset_diff_labels/syn_data_diff_labels_en_20_67.json\n",
+    "import json\n",
+    "with open('/home/mshahidul/readctrl/data/synthetic_dataset_diff_labels/syn_data_diff_labels_en_0_80_full.json', 'r') as f:\n",
+    "    synthetic_data_diff_labels_en = json.load(f)\n",
+    "full_data=[]\n",
+    "# print((synthetic_data_diff_labels_en)[0].keys())\n",
+    "for item in synthetic_data_diff_labels_en:\n",
+    "    texts=item['diff_label_texts']\n",
+    "    for label in texts:\n",
+    "        full_data.append({\n",
+    "            \"index\": item['index'],\n",
+    "            'label': label,\n",
+    "            \"original_text\": item['fulltext'],\n",
+    "            \"generated_summary\": texts[label]\n",
+    "        })\n"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "3ba2a6cf",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "with open('/home/mshahidul/readctrl/data/data_annotator_data/syn_data_diff_labels_en_0_80.json', 'w') as f:\n",
+    "    json.dump(full_data, f, indent=4)"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "7cddc461",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "# /home/mshahidul/readctrl/data/translated_data/translation_english2bangla_v1.json\n",
+    "import json\n",
+    "with open('/home/mshahidul/readctrl/data/testing_data_gs/multiclinsum_gs_train_en.json', 'r', encoding='utf-8') as f:\n",
+    "    dataset = json.load(f)\n",
+    "print(dataset[0].keys())"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 27,
+   "id": "2b3f2a96",
+   "metadata": {},
+   "outputs": [
+    {
+     "name": "stdout",
+     "output_type": "stream",
+     "text": [
+      "0_low_health_literacy\n",
+      "0_intermediate_health_literacy\n",
+      "0_proficient_health_literacy\n",
+      "1_low_health_literacy\n",
+      "1_intermediate_health_literacy\n",
+      "1_proficient_health_literacy\n",
+      "2_low_health_literacy\n",
+      "2_intermediate_health_literacy\n",
+      "2_proficient_health_literacy\n",
+      "3_low_health_literacy\n",
+      "3_intermediate_health_literacy\n",
+      "3_proficient_health_literacy\n",
+      "4_low_health_literacy\n",
+      "4_intermediate_health_literacy\n",
+      "4_proficient_health_literacy\n",
+      "5_low_health_literacy\n",
+      "5_intermediate_health_literacy\n",
+      "5_proficient_health_literacy\n",
+      "6_low_health_literacy\n",
+      "6_intermediate_health_literacy\n",
+      "6_proficient_health_literacy\n",
+      "7_low_health_literacy\n",
+      "7_intermediate_health_literacy\n",
+      "7_proficient_health_literacy\n",
+      "8_low_health_literacy\n",
+      "8_intermediate_health_literacy\n",
+      "8_proficient_health_literacy\n",
+      "9_low_health_literacy\n",
+      "9_intermediate_health_literacy\n",
+      "9_proficient_health_literacy\n",
+      "10_low_health_literacy\n",
+      "10_intermediate_health_literacy\n",
+      "10_proficient_health_literacy\n",
+      "11_low_health_literacy\n",
+      "11_intermediate_health_literacy\n",
+      "11_proficient_health_literacy\n",
+      "12_low_health_literacy\n",
+      "12_intermediate_health_literacy\n",
+      "12_proficient_health_literacy\n",
+      "13_low_health_literacy\n",
+      "13_intermediate_health_literacy\n",
+      "13_proficient_health_literacy\n",
+      "14_low_health_literacy\n",
+      "14_intermediate_health_literacy\n",
+      "14_proficient_health_literacy\n",
+      "15_low_health_literacy\n",
+      "15_intermediate_health_literacy\n",
+      "15_proficient_health_literacy\n",
+      "16_low_health_literacy\n",
+      "16_intermediate_health_literacy\n",
+      "16_proficient_health_literacy\n",
+      "17_low_health_literacy\n",
+      "17_intermediate_health_literacy\n",
+      "17_proficient_health_literacy\n",
+      "18_low_health_literacy\n",
+      "18_intermediate_health_literacy\n",
+      "18_proficient_health_literacy\n",
+      "19_low_health_literacy\n",
+      "19_intermediate_health_literacy\n",
+      "19_proficient_health_literacy\n",
+      "20_low_health_literacy\n",
+      "20_intermediate_health_literacy\n",
+      "20_proficient_health_literacy\n",
+      "21_low_health_literacy\n",
+      "21_intermediate_health_literacy\n",
+      "21_proficient_health_literacy\n",
+      "22_low_health_literacy\n",
+      "22_intermediate_health_literacy\n",
+      "22_proficient_health_literacy\n",
+      "23_low_health_literacy\n",
+      "23_intermediate_health_literacy\n",
+      "23_proficient_health_literacy\n",
+      "24_low_health_literacy\n",
+      "24_intermediate_health_literacy\n",
+      "24_proficient_health_literacy\n",
+      "25_low_health_literacy\n",
+      "25_intermediate_health_literacy\n",
+      "25_proficient_health_literacy\n",
+      "26_low_health_literacy\n",
+      "26_intermediate_health_literacy\n",
+      "26_proficient_health_literacy\n",
+      "27_low_health_literacy\n",
+      "27_intermediate_health_literacy\n",
+      "27_proficient_health_literacy\n",
+      "28_low_health_literacy\n",
+      "28_intermediate_health_literacy\n",
+      "28_proficient_health_literacy\n",
+      "29_low_health_literacy\n",
+      "29_intermediate_health_literacy\n",
+      "29_proficient_health_literacy\n",
+      "30_low_health_literacy\n",
+      "30_intermediate_health_literacy\n",
+      "30_proficient_health_literacy\n",
+      "31_low_health_literacy\n",
+      "31_intermediate_health_literacy\n",
+      "31_proficient_health_literacy\n",
+      "32_low_health_literacy\n",
+      "32_intermediate_health_literacy\n",
+      "32_proficient_health_literacy\n",
+      "33_low_health_literacy\n",
+      "33_intermediate_health_literacy\n",
+      "33_proficient_health_literacy\n",
+      "34_low_health_literacy\n",
+      "34_intermediate_health_literacy\n",
+      "34_proficient_health_literacy\n",
+      "35_low_health_literacy\n",
+      "35_intermediate_health_literacy\n",
+      "35_proficient_health_literacy\n",
+      "36_low_health_literacy\n",
+      "36_intermediate_health_literacy\n",
+      "36_proficient_health_literacy\n",
+      "37_low_health_literacy\n",
+      "37_intermediate_health_literacy\n",
+      "37_proficient_health_literacy\n",
+      "38_low_health_literacy\n",
+      "38_intermediate_health_literacy\n",
+      "38_proficient_health_literacy\n",
+      "39_low_health_literacy\n",
+      "39_intermediate_health_literacy\n",
+      "39_proficient_health_literacy\n",
+      "40_low_health_literacy\n",
+      "40_intermediate_health_literacy\n",
+      "40_proficient_health_literacy\n",
+      "41_low_health_literacy\n",
+      "41_intermediate_health_literacy\n",
+      "41_proficient_health_literacy\n",
+      "42_low_health_literacy\n",
+      "42_intermediate_health_literacy\n",
+      "42_proficient_health_literacy\n",
+      "43_low_health_literacy\n",
+      "43_intermediate_health_literacy\n",
+      "43_proficient_health_literacy\n",
+      "44_low_health_literacy\n",
+      "44_intermediate_health_literacy\n",
+      "44_proficient_health_literacy\n",
+      "45_low_health_literacy\n",
+      "45_intermediate_health_literacy\n",
+      "45_proficient_health_literacy\n",
+      "46_low_health_literacy\n",
+      "46_intermediate_health_literacy\n",
+      "46_proficient_health_literacy\n",
+      "47_low_health_literacy\n",
+      "47_intermediate_health_literacy\n",
+      "47_proficient_health_literacy\n",
+      "48_low_health_literacy\n",
+      "48_intermediate_health_literacy\n",
+      "48_proficient_health_literacy\n",
+      "49_low_health_literacy\n",
+      "49_intermediate_health_literacy\n",
+      "49_proficient_health_literacy\n",
+      "50_low_health_literacy\n",
+      "50_intermediate_health_literacy\n",
+      "50_proficient_health_literacy\n",
+      "51_low_health_literacy\n",
+      "51_intermediate_health_literacy\n",
+      "51_proficient_health_literacy\n",
+      "52_low_health_literacy\n",
+      "52_intermediate_health_literacy\n",
+      "52_proficient_health_literacy\n",
+      "53_low_health_literacy\n",
+      "53_intermediate_health_literacy\n",
+      "53_proficient_health_literacy\n",
+      "54_low_health_literacy\n",
+      "54_intermediate_health_literacy\n",
+      "54_proficient_health_literacy\n",
+      "55_low_health_literacy\n",
+      "55_intermediate_health_literacy\n",
+      "55_proficient_health_literacy\n",
+      "56_low_health_literacy\n",
+      "56_intermediate_health_literacy\n",
+      "56_proficient_health_literacy\n",
+      "57_low_health_literacy\n",
+      "57_intermediate_health_literacy\n",
+      "57_proficient_health_literacy\n",
+      "58_low_health_literacy\n",
+      "58_intermediate_health_literacy\n",
+      "58_proficient_health_literacy\n",
+      "59_low_health_literacy\n",
+      "59_intermediate_health_literacy\n",
+      "59_proficient_health_literacy\n",
+      "60_low_health_literacy\n",
+      "60_intermediate_health_literacy\n",
+      "60_proficient_health_literacy\n",
+      "61_low_health_literacy\n",
+      "61_intermediate_health_literacy\n",
+      "61_proficient_health_literacy\n",
+      "62_low_health_literacy\n",
+      "62_intermediate_health_literacy\n",
+      "62_proficient_health_literacy\n",
+      "63_low_health_literacy\n",
+      "63_intermediate_health_literacy\n",
+      "63_proficient_health_literacy\n",
+      "64_low_health_literacy\n",
+      "64_intermediate_health_literacy\n",
+      "64_proficient_health_literacy\n",
+      "65_low_health_literacy\n",
+      "65_intermediate_health_literacy\n",
+      "65_proficient_health_literacy\n",
+      "66_low_health_literacy\n",
+      "66_intermediate_health_literacy\n",
+      "66_proficient_health_literacy\n",
+      "67_low_health_literacy\n",
+      "67_intermediate_health_literacy\n",
+      "67_proficient_health_literacy\n",
+      "68_low_health_literacy\n",
+      "68_intermediate_health_literacy\n",
+      "68_proficient_health_literacy\n",
+      "69_low_health_literacy\n",
+      "69_intermediate_health_literacy\n",
+      "69_proficient_health_literacy\n",
+      "70_low_health_literacy\n",
+      "70_intermediate_health_literacy\n",
+      "70_proficient_health_literacy\n",
+      "71_low_health_literacy\n",
+      "71_intermediate_health_literacy\n",
+      "71_proficient_health_literacy\n",
+      "72_low_health_literacy\n",
+      "72_intermediate_health_literacy\n",
+      "72_proficient_health_literacy\n",
+      "73_low_health_literacy\n",
+      "73_intermediate_health_literacy\n",
+      "73_proficient_health_literacy\n",
+      "74_low_health_literacy\n",
+      "74_intermediate_health_literacy\n",
+      "74_proficient_health_literacy\n",
+      "75_low_health_literacy\n",
+      "75_intermediate_health_literacy\n",
+      "75_proficient_health_literacy\n",
+      "76_low_health_literacy\n",
+      "76_intermediate_health_literacy\n",
+      "76_proficient_health_literacy\n",
+      "77_low_health_literacy\n",
+      "77_intermediate_health_literacy\n",
+      "77_proficient_health_literacy\n",
+      "78_low_health_literacy\n",
+      "78_intermediate_health_literacy\n",
+      "78_proficient_health_literacy\n",
+      "79_low_health_literacy\n",
+      "79_intermediate_health_literacy\n",
+      "79_proficient_health_literacy\n"
+     ]
+    }
+   ],
+   "source": [
+    "# /home/mshahidul/readctrl/data/synthetic_dataset_diff_labels/syn_data_diff_labels_en_0_80_full_updated.json\n",
+    "with open('/home/mshahidul/readctrl/data/synthetic_dataset_diff_labels/syn_data_diff_labels_en_0_80_full_updated.json', 'r') as f:\n",
+    "    syn_data_diff_labels_en_0_80_full_updated = json.load(f)\n",
+    "map_data={}\n",
+    "for item in syn_data_diff_labels_en_0_80_full_updated:\n",
+    "    for label in list(item['diff_label_texts'].keys()):\n",
+    "        key=f\"{item['index']}_{label}\"\n",
+    "        print(key)\n",
+    "        map_data[key]={\n",
+    "            'doc_id':item['index'],\n",
+    "            'label':label,\n",
+    "            'fulltext':item['fulltext'],\n",
+    "            \"diff_label_texts\":item['diff_label_texts'][label],\n",
+    "            'summary':item['summary']\n",
+    "        }\n"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 28,
+   "id": "c52e96ab",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "# /home/mshahidul/readctrl/data/annotators_validate_data_(20_80)/combine/consolidated_ratings_0-20(not_all_category).json\n",
+    "with open('/home/mshahidul/readctrl/data/annotators_validate_data_(20_80)/combine/consolidated_ratings_0-20(not_all_category).json', 'r') as f:\n",
+    "    consolidated_ratings_0_20 = json.load(f)\n",
+    "new_data=[]\n",
+    "for item in consolidated_ratings_0_20:\n",
+    "    key=f\"{item['doc_id']}_{item['health_literacy_label']}\"\n",
+    "    new_data.append({\n",
+    "        **map_data[key],\n",
+    "    })\n"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 29,
+   "id": "bfd6cf96",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "with open('/home/mshahidul/readctrl/data/annotators_validate_data_(20_80)/combine/verified_data_0-20.json', 'w') as f:\n",
+    "    json.dump(new_data, f, indent=4)\n"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "cf797af6",
+   "metadata": {},
+   "outputs": [],
+   "source": []
+  }
+ ],
+ "metadata": {
+  "kernelspec": {
+   "display_name": "un",
+   "language": "python",
+   "name": "python3"
+  },
+  "language_info": {
+   "codemirror_mode": {
+    "name": "ipython",
+    "version": 3
+   },
+   "file_extension": ".py",
+   "mimetype": "text/x-python",
+   "name": "python",
+   "nbconvert_exporter": "python",
+   "pygments_lexer": "ipython3",
+   "version": "3.11.14"
+  }
+ },
+ "nbformat": 4,
+ "nbformat_minor": 5
+}
diff --git a/code/RL_model/unsloth_rl/claim_verifier.py b/code/RL_model/unsloth_rl/claim_verifier.py
new file mode 100644
index 0000000000000000000000000000000000000000..0a13d6268330c6e0171c46373e43136fc7363f43
--- /dev/null
+++ b/code/RL_model/unsloth_rl/claim_verifier.py
@@ -0,0 +1,175 @@
+import json
+import re
+import concurrent.futures
+from openai import OpenAI
+
+class MedicalClaimVerifier:
+    def __init__(self):
+        # OpenAI API configuration
+        api_file = "/home/mshahidul/api_new.json"
+        with open(api_file, "r") as f:
+            api_keys = json.load(f)
+        self.api_key = api_keys["openai"]
+        self.model_name = "gpt-5-mini"
+        self.client = OpenAI(api_key=self.api_key)
+
+        # Literacy ranges (IQR after outlier removal) from paper summary
+        # comp = completeness vs gold summary; cov = source_coverage vs full text
+        self.threshold_ranges = {
+            "low": {"comp": (0.9600, 1.0000), "cov": (0.1765, 0.3226)},
+            "intermediate": {"comp": (0.9393, 1.0000), "cov": (0.1818, 0.4091)},
+            "proficient": {"comp": (0.9231, 1.0000), "cov": (0.7725, 0.9347)},
+        }
+
+        # Minimum required information (upper bound of IQR)
+        self.thresholds = {
+            "low": {"comp": 1.0, "cov": 0.3226},
+            "intermediate": {"comp": 1.0, "cov": 0.4091},
+            "proficient": {"comp": 1.0, "cov": 0.9347},
+        }
+
+    def get_prompt(self,context,claim):
+        prompt = f"""
+        CONTEXT:
+        {context}
+
+        CLAIM TO VERIFY:
+        {claim}
+
+        INSTRUCTION:
+        Does the CONTEXT above provide enough evidence to support the CLAIM? 
+        - Answer 'supported' if the claim is explicitly stated or logically followable.
+        - Answer 'not_supported' if the claim is missing, contradicts the text, or requires outside info.
+
+        Output only one word: 'supported' or 'not_supported'.
+        """
+        return prompt
+
+    def check_support_api(self, prompt):
+        try:
+            response = self.client.chat.completions.create(
+                model=self.model_name,
+                messages=[{"role": "user", "content": prompt}],
+            )
+            res = response.choices[0].message.content.strip().lower()
+            # print("API Response:", res)
+            return 1.0 if "supported" in res and "not_supported" not in res else 0.0
+        except Exception as e:
+            print(f"API call error: {e}")
+            return 0.0
+
+    def evaluate_level(self, gen_text, gold_subs, full_subs, level_key):
+        """Calculates scores for a single literacy level."""
+        if not gen_text: return 0.0, 0.0
+
+        # Run API calls in parallel to save time during RL
+        try:
+            with concurrent.futures.ThreadPoolExecutor(max_workers=10) as executor:
+                # Completeness check (vs Gold Summary Subclaims)
+                comp_prompts = [self.get_prompt(gen_text, s) for s in gold_subs]
+                comp_results = list(executor.map(self.check_support_api, comp_prompts))
+                comp_score = sum(comp_results) / len(comp_results) if comp_results else 0.0
+
+
+                # Coverage check (vs Full Text Subclaims)
+                cov_prompts = [self.get_prompt(gen_text, s) for s in full_subs]
+                cov_results = list(executor.map(self.check_support_api, cov_prompts))
+                cov_score = sum(cov_results) / len(cov_results) if cov_results else 0.0
+            # print(f"Comp Score: {comp_score}, Cov Score: {cov_score} for {level_key}")
+        except Exception as e:
+            print(f"Parallel API call error: {e}")
+            return 0.0, 0.0
+    
+        return comp_score, cov_score
+
+    import json
+
+    def get_reward_score(self, completion, gold_subs, full_subs):
+        data = None
+        
+        # 1. Robust JSON Extraction
+        try:
+            # Clean potential markdown or whitespace
+            text = completion[0]['content'].strip().replace("```json", "").replace("```", "").strip()                
+            data = json.loads(text)
+        except (json.JSONDecodeError, IndexError, ValueError) as e:
+            print("JSON Parsing Error in Reward Calculation")
+            # If all extraction attempts fail
+            return -5.0
+
+        # 2. Schema Validation
+        levels = ["low", "intermediate", "proficient"]
+        # Check if any required keys are missing
+        if not all(f"{lvl}_health_literacy" in data for lvl in levels):
+            return -2.0  # Slightly smaller penalty for partial formatting success
+
+        # 3. Scoring Logic
+        try:
+            total_reward = 0.0
+            pass_reward = 1.0
+            fail_penalty = -1.0
+            for lvl in levels:
+                gen_text = data.get(f"{lvl}_health_literacy", "")
+                
+                # Skip scoring if text is empty
+                if not gen_text:
+                    total_reward += fail_penalty
+                    continue
+                    
+                comp_score, cov_score = self.evaluate_level(gen_text, gold_subs, full_subs, lvl)
+                
+                # Apply Thresholds
+                total_reward += pass_reward if comp_score >= self.thresholds[lvl]["comp"] else fail_penalty
+                total_reward += pass_reward if cov_score >= self.thresholds[lvl]["cov"] else fail_penalty
+                
+            return total_reward
+        except Exception:
+            return -5.0
+
+
+# 1. Ground Truth Subclaims (Extracted from a medical paper on Hypertension)
+gold_summary_subclaims = [
+    "Hypertension is defined as blood pressure above 140/90 mmHg.",
+    "Lifestyle changes like low salt intake can reduce blood pressure.",
+    "Diuretics are often the first line of pharmacological treatment."
+]
+
+full_text_subclaims = [
+    "Hypertension is defined as blood pressure above 140/90 mmHg.",
+    "Lifestyle changes like low salt intake can reduce blood pressure.",
+    "Diuretics are often the first line of pharmacological treatment.",
+    "The DASH diet emphasizes fruits, vegetables, and low-fat dairy.",
+    "Chronic hypertension increases the risk of stroke and myocardial infarction.",
+    "ACE inhibitors are contraindicated during pregnancy.",
+    "Secondary hypertension can be caused by renal artery stenosis."
+]
+
+# 2. Mock Model Completion (The output being evaluated)
+# This mimics the format your RL environment would pass to the reward function
+mock_completion = [{
+    'content': """
+    {
+        "low_health_literacy": "High blood pressure is when your blood is too strong for your veins. You should eat less salt to help stay healthy.",
+        "intermediate_health_literacy": "Hypertension is blood pressure over 140/90. You can lower it by eating less salt and taking water pills (diuretics) if your doctor says so.",
+        "proficient_health_literacy": "Hypertension (BP > 140/90 mmHg) is managed via lifestyle modifications like the DASH diet and salt restriction. Pharmacological interventions include diuretics as first-line therapy, though risks like stroke or heart attack persist if untreated. Secondary causes like renal artery stenosis should be screened, and ACE inhibitors must be avoided in pregnancy."
+    }
+    """
+}]
+
+# Initialize your verifier
+verifier = MedicalClaimVerifier()
+
+# Test the reward calculation
+reward = verifier.get_reward_score(
+    completion=mock_completion, 
+    gold_subs=gold_summary_subclaims, 
+    full_subs=full_text_subclaims
+)
+
+print(f"--- Evaluation Result ---")
+print(f"Total Reward Score: {reward}")
+
+# Logic Explanation:
+# - Low: Likely fails 'comp' (missing 140/90 info), but might pass 'cov' (low threshold).
+# - Intermediate: Likely passes 'comp' and 'cov'.
+# - Proficient: Needs to cover almost all 7 subclaims to pass the 0.77 coverage threshold.
\ No newline at end of file
diff --git a/code/RL_model/unsloth_rl/finetune.py b/code/RL_model/unsloth_rl/finetune.py
new file mode 100644
index 0000000000000000000000000000000000000000..c454b9ba95b04576f9bc5bf67ef3310e68a91a81
--- /dev/null
+++ b/code/RL_model/unsloth_rl/finetune.py
@@ -0,0 +1,91 @@
+import os
+# Set GPU environment variables
+os.environ["CUDA_DEVICE_ORDER"] = "PCI_BUS_ID"
+os.environ["CUDA_VISIBLE_DEVICES"] = "2"
+import torch
+from unsloth import FastLanguageModel
+from datasets import load_dataset
+from trl import SFTTrainer, SFTConfig
+from unsloth.chat_templates import get_chat_template, standardize_data_formats, train_on_responses_only
+
+# 1. Configuration
+model_name = "unsloth/Qwen3-4B-Instruct-2507"
+max_seq_length = 8192
+dataset_path = "/home/mshahidul/readctrl/data/finetuning_data/training_data_readability_data_generation.json"
+output_dir = "/home/mshahidul/readctrl_model/RL_model/readability_sft_lora_model"
+
+# 2. Load Model and Tokenizer
+model, tokenizer = FastLanguageModel.from_pretrained(
+    model_name = model_name,
+    max_seq_length = max_seq_length,
+    load_in_4bit = True,
+)
+
+# 3. Add LoRA Adapters
+model = FastLanguageModel.get_peft_model(
+    model,
+    r = 32,
+    target_modules = ["q_proj", "k_proj", "v_proj", "o_proj",
+                      "gate_proj", "up_proj", "down_proj",],
+    lora_alpha = 32,
+    lora_dropout = 0,
+    bias = "none",
+    use_gradient_checkpointing = "unsloth",
+    random_state = 3407,
+)
+
+# 4. Data Preparation
+tokenizer = get_chat_template(
+    tokenizer,
+    chat_template = "qwen3-instruct",
+)
+
+dataset = load_dataset("json", data_files = dataset_path, split = "train")
+dataset = standardize_data_formats(dataset)
+
+def formatting_prompts_func(examples):
+    convos = examples["conversations"]
+    texts = [tokenizer.apply_chat_template(convo, tokenize = False, add_generation_prompt = False) for convo in convos]
+    return { "text" : texts, }
+
+dataset = dataset.map(formatting_prompts_func, batched = True)
+
+# 5. Training Setup
+trainer = SFTTrainer(
+    model = model,
+    tokenizer = tokenizer,
+    train_dataset = dataset,
+    dataset_text_field = "text",
+    max_seq_length = max_seq_length,
+    args = SFTConfig(
+        per_device_train_batch_size = 2,
+        gradient_accumulation_steps = 4,
+        warmup_steps = 5,
+        # max_steps = 60, # Adjust as needed for your dataset size
+        num_train_epochs = 3,
+        learning_rate = 2e-4,
+        fp16 = not torch.cuda.is_bf16_supported(),
+        bf16 = torch.cuda.is_bf16_supported(),
+        logging_steps = 1,
+        optim = "adamw_8bit",
+        weight_decay = 0.01,
+        lr_scheduler_type = "linear",
+        seed = 3407,
+        output_dir = "outputs",
+    ),
+)
+
+# Train only on assistant responses
+trainer = train_on_responses_only(
+    trainer,
+    instruction_part = "<|im_start|>user\n",
+    response_part = "<|im_start|>assistant\n",
+)
+
+# 6. Train and Save
+trainer.train()
+
+model.save_pretrained(output_dir)
+tokenizer.save_pretrained(output_dir)
+
+print(f"Model saved to {output_dir}")
\ No newline at end of file
diff --git a/code/RL_model/unsloth_rl/health_classifier.py b/code/RL_model/unsloth_rl/health_classifier.py
new file mode 100644
index 0000000000000000000000000000000000000000..1de86d751fea3ffdc5952ea866113e54d6374471
--- /dev/null
+++ b/code/RL_model/unsloth_rl/health_classifier.py
@@ -0,0 +1,42 @@
+import dspy
+import json
+from typing import Literal
+
+# --- 1. LLM Configuration ---
+def setup_dspy_classifier(save_path, api_key_path):
+    with open(api_key_path, "r") as f:
+        api_keys = json.load(f)
+
+    # Configure the LM
+    # Note: 'gpt-5-mini' is used per your configuration; ensure this matches your provider
+    openai_model = dspy.LM(model='gpt-5-mini', api_key=api_keys["openai"])
+    dspy.configure(lm=openai_model)
+
+    class HealthLiteracySignature(dspy.Signature):
+        """
+        Judge the health literacy level of a generated medical summary.
+        Identify if the language is suitable for a layperson (low) or requires medical expertise (proficient).
+        """
+        summary_text: str = dspy.InputField(desc="The generated medical summary to be analyzed.")
+        reasoning: str = dspy.OutputField(desc="Analysis of jargon, acronyms, and sentence complexity.")
+        label: Literal["low_health_literacy", "intermediate_health_literacy", "proficient_health_literacy"] = dspy.OutputField()
+
+    class HealthLiteracyClassifier(dspy.Module):
+        def __init__(self):
+            super().__init__()
+            self.predictor = dspy.ChainOfThought(HealthLiteracySignature)
+
+        def forward(self, summary_text):
+            return self.predictor(summary_text=summary_text)
+
+    # Initialize and load weights
+    classifier_instance = HealthLiteracyClassifier()
+    classifier_instance.load(save_path)
+    return classifier_instance
+
+# Global instantiation (optional, or you can call setup in your main script)
+API_FILE = "/home/mshahidul/api_new.json"
+SAVE_PATH = "/home/mshahidul/readctrl/data/new_exp/optimized_health_classifier_gpt5-mini_v2.json"
+
+# Create the instance to be imported
+classifier = setup_dspy_classifier(SAVE_PATH, API_FILE)
\ No newline at end of file
diff --git a/code/RL_model/unsloth_rl/highlighter.py b/code/RL_model/unsloth_rl/highlighter.py
new file mode 100644
index 0000000000000000000000000000000000000000..febe5ab7e544448088c14affc54b4e9ffff632ef
--- /dev/null
+++ b/code/RL_model/unsloth_rl/highlighter.py
@@ -0,0 +1,103 @@
+import gradio as gr
+from transformers import AutoModel
+import torch
+
+# 1. Load the model (ensure you have transformers and torch installed)
+print("Loading model... This may take a moment.")
+model = AutoModel.from_pretrained(
+    "zilliz/semantic-highlight-bilingual-v1",
+    trust_remote_code=True
+)
+
+def process_and_highlight(question, context, threshold):
+    if not question or not context:
+        return "Please provide both a question and context."
+
+    # 2. Run the model inference
+    result = model.process(
+        question=question,
+        context=context,
+        threshold=threshold,
+        return_sentence_metrics=True
+    )
+
+    highlighted_sentences = result.get("highlighted_sentences", [])
+    
+    # 3. Create the highlighted HTML output
+    # We iterate through the context and wrap highlighted sentences in HTML tags
+    output_html = context
+    
+    # Sort highlighted sentences by length (descending) to avoid partial 
+    # matching issues if one sentence is a substring of another
+    highlighted_sentences.sort(key=len, reverse=True)
+
+    for sent in highlighted_sentences:
+        # Use a bright yellow highlight style
+        style = "background-color: #fff176; color: #000; padding: 2px; border-radius: 3px; font-weight: 500;"
+        highlighted_tag = f'<span style="{style}">{sent}</span>'
+        output_html = output_html.replace(sent, highlighted_tag)
+
+    # Wrap in a container for better typography
+    final_output = f"""
+    <div style="font-family: 'Segoe UI', Tahoma, Geneva, Verdana, sans-serif; line-height: 1.8; font-size: 16px; color: #333;">
+        {output_html}
+    </div>
+    """
+    
+    # 4. Format metrics for the display
+    metrics_str = "No specific probabilities returned."
+    if "sentence_probabilities" in result:
+        metrics_str = "\n".join([f"• {p:.4f}" for p in result["sentence_probabilities"]])
+
+    return final_output, metrics_str
+
+# 5. Build the Gradio UI
+with gr.Blocks(theme=gr.themes.Soft(), title="Semantic Highlighter") as demo:
+    gr.Markdown("# 🔍 Semantic Highlight Explorer")
+    gr.Markdown("Identify and highlight parts of a text that answer a specific question using the Zilliz bilingual model.")
+    
+    with gr.Row():
+        with gr.Column(scale=1):
+            question_input = gr.Textbox(
+                label="Question", 
+                placeholder="e.g., What are the symptoms of dehydration?",
+                lines=2
+            )
+            context_input = gr.Textbox(
+                label="Context / Full Text", 
+                placeholder="Paste the document text here...",
+                lines=10
+            )
+            threshold_slider = gr.Slider(
+                minimum=0.1, maximum=1.0, value=0.5, step=0.05, 
+                label="Confidence Threshold"
+            )
+            submit_btn = gr.Button("Analyze & Highlight", variant="primary")
+            
+        with gr.Column(scale=1):
+            gr.Label("Highlighted Result")
+            output_display = gr.HTML()
+            
+            with gr.Accordion("Sentence Metrics", open=False):
+                metrics_display = gr.Textbox(label="Probabilities", lines=5)
+
+    # Add example from your snippet
+    gr.Examples(
+        examples=[
+            [
+                "What are the symptoms of dehydration?",
+                "Dehydration occurs when your body loses more fluid than you take in. Common signs include feeling thirsty and having a dry mouth. The human body is composed of about 60% water. Dark yellow urine and infrequent urination are warning signs. Water is essential for many bodily functions. Dizziness, fatigue, and headaches can indicate severe dehydration.",
+                0.5
+            ]
+        ],
+        inputs=[question_input, context_input, threshold_slider]
+    )
+
+    submit_btn.click(
+        fn=process_and_highlight,
+        inputs=[question_input, context_input, threshold_slider],
+        outputs=[output_display, metrics_display]
+    )
+
+if __name__ == "__main__":
+    demo.launch(share=True)
\ No newline at end of file
diff --git a/code/RL_model/unsloth_rl/inference.py b/code/RL_model/unsloth_rl/inference.py
new file mode 100644
index 0000000000000000000000000000000000000000..9171119c7a76f35dea31985559afb6a9ca0d7f20
--- /dev/null
+++ b/code/RL_model/unsloth_rl/inference.py
@@ -0,0 +1,120 @@
+import json
+import os
+# Set GPU environment variables
+os.environ["CUDA_DEVICE_ORDER"] = "PCI_BUS_ID"
+os.environ["CUDA_VISIBLE_DEVICES"] = "2"
+import torch
+from unsloth import FastLanguageModel
+from transformers import TextStreamer
+
+# 1. Configuration
+model_path = "/home/mshahidul/readctrl_model/RL_model/readability_sft_lora_model"
+max_seq_length = 8192
+
+# 2. Load the Fine-tuned Model and Tokenizer
+# Unsloth automatically reloads the base Qwen3 model and attaches your adapters.
+model, tokenizer = FastLanguageModel.from_pretrained(
+    model_name = model_path,
+    max_seq_length = max_seq_length,
+    load_in_4bit = False,
+)
+
+# 3. Enable Fast Inference
+# This activates Unsloth's optimized inference kernels for a 2x speedup.
+FastLanguageModel.for_inference(model)
+
+# 4. Prepare your Test Data
+# Replace these with actual values from your evaluation set
+gold_summary = "A 34-year-old pregnant woman presents with seizures and dysarthria and is urgently referred for a cranial MRI. The classic ‘Medusa head’ sign is seen and the diagnosis is made as a venous anomaly of development with peripheral partial thrombosis and proximal slow flow.\n"
+fulltext = "We present the case of a 34-year-old woman, eight weeks pregnant with no other personal history of interest, who presents to the emergency department with generalized convulsions with dysarthria in the postcritical period, which resolve progressively in less than two hours. On physical examination, she is conscious, oriented, with no language or motor or sensory deficits. Only signs of a right lateral tongue bite are observed.\n\nThe complementary tests, such as blood tests or the electrocardiogram, are normal. Given that the episode corresponds with a first epileptic seizure and the patient is pregnant, an urgent magnetic resonance of the skull is requested.\n\nThe usual protocol was performed and 3D T1 sequences without and with intravenous contrast were obtained in axial, coronal and sagital planes, axial FLAIR, axial T2, VEN BOLD and magnetic susceptibility sequences, as well as axial diffusion and apparent diffusion coefficient map. The MRI identified multiple venous cortico-medullary vascular structures converging centripetally to a large central venous structure draining through the inferior anastomotic vein into the left transverse sinus, forming the classic ‘Medusa head’ sign. In the T1 sequences, the drainage vein was seen to be increased in signal with central hyphocaptation after contrast administration, suggesting partial thrombosis versus slow flow. In addition, in T2 and FLAIR sequences, the brain tissue surrounding the drainage vein was seen to be hyperintense, without diffusion restriction and compatible with edema.\n\nThese findings are suggestive of a venous anomaly of development with signs of partial peripheral thrombosis and slow flow more proximal, which cause edema of the surrounding tissue. She is started on clexane 60 mg/12 hours and levetiracetam 500 mg/12 hours and the patient shows improvement and symptomatic stability after one week.\n"
+       
+
+# Define your exact system prompt
+system_prompt = f"""
+    **System Role:**
+
+    You are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.
+
+    **User Prompt:**
+
+    Please process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.
+    ### Instructions for Each Level:
+
+    1. Level: Low Health Literacy (High Readability)
+
+    Target: Individuals needing the simplest terms for immediate action.
+
+    Linguistic Goal: Use "living room" language. Replace all medical jargon with functional descriptions (e.g., "renal" becomes "kidney").
+
+    Information Density: Focus strictly on the "need-to-know" info found in the Gold Summary.
+
+    Strategy: High paraphrasing using analogies. One idea per sentence.
+
+    Faithfulness: Must align perfectly with the Gold Summary.
+
+    2. Level: Intermediate Health Literacy (Medium Readability)
+
+    Target: The general public (news-reading level).
+
+    Linguistic Goal: Standard vocabulary. Common medical terms are okay, but technical "doctor-speak" must be simplified.
+
+    Information Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.
+
+    Strategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.
+
+    Faithfulness: Maintains the main narrative of the Gold Summary.
+
+    3. Level: Proficient Health Literacy (Low Readability)
+
+    Target: Researchers, clinicians, or highly informed patients.
+
+    Linguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.
+
+    Information Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.
+
+    Strategy: Minimal paraphrasing. Retain all original technical terminology.
+
+    Faithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.
+
+    Input Language: English
+    Gold Summary (The Anchor): 
+    {gold_summary}
+    Source Text (The Detail): 
+    {fulltext}
+
+    **Output Format (JSON only):**
+    {{
+    "low_health_literacy": "...",
+    "intermediate_health_literacy": "...",
+    "proficient_health_literacy": "..."
+    }}
+"""
+
+# Format for Qwen-3 instruction template
+messages = [
+    {"role": "user", "content": system_prompt}
+]
+
+input_text = tokenizer.apply_chat_template(
+    messages,
+    tokenize = False,
+    add_generation_prompt = True,
+)
+
+inputs = tokenizer([input_text], return_tensors = "pt").to("cuda")
+
+# 5. Run Generation
+# Using recommended sampling parameters for Qwen3 non-thinking mode.
+text_streamer = TextStreamer(tokenizer, skip_prompt = True,skip_special_tokens = True)
+
+print("--- Model Response ---")
+_ = model.generate(
+    **inputs,
+    streamer = text_streamer,
+    max_new_tokens = 2048,
+    temperature = 0.7, 
+    top_p = 0.8, 
+    top_k = 20,
+    repetition_penalty = 1.05,
+    use_cache = True,
+)
\ No newline at end of file
diff --git a/code/RL_model/unsloth_rl/prompt b/code/RL_model/unsloth_rl/prompt
new file mode 100644
index 0000000000000000000000000000000000000000..084bb706dafafee7913a406ccb6fbffa524be840
--- /dev/null
+++ b/code/RL_model/unsloth_rl/prompt
@@ -0,0 +1,58 @@
+**System Role:**
+
+You are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.
+
+**User Prompt:**
+
+Please process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.
+### Instructions for Each Level:
+
+1. Level: Low Health Literacy (High Readability)
+
+Target: Individuals needing the simplest terms for immediate action.
+
+Linguistic Goal: Use "living room" language. Replace all medical jargon with functional descriptions (e.g., "renal" becomes "kidney").
+
+Information Density: Focus strictly on the "need-to-know" info found in the Gold Summary.
+
+Strategy: High paraphrasing using analogies. One idea per sentence.
+
+Faithfulness: Must align perfectly with the Gold Summary.
+
+2. Level: Intermediate Health Literacy (Medium Readability)
+
+Target: The general public (news-reading level).
+
+Linguistic Goal: Standard vocabulary. Common medical terms are okay, but technical "doctor-speak" must be simplified.
+
+Information Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.
+
+Strategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.
+
+Faithfulness: Maintains the main narrative of the Gold Summary.
+
+3. Level: Proficient Health Literacy (Low Readability)
+
+Target: Researchers, clinicians, or highly informed patients.
+
+Linguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.
+
+Information Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.
+
+Strategy: Minimal paraphrasing. Retain all original technical terminology.
+
+Faithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.
+
+
+I will provide the following information:
+
+- Input Language: <<<SOURCE_LANGUAGE>>>
+- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>
+- Source Text (detailed content): <<<FULL_TEXT>>>
+
+**Output Format (JSON only):**
+    {{
+    "low_health_literacy": "...",
+    "intermediate_health_literacy": "...",
+    "proficient_health_literacy": "..."
+    }}
\ No newline at end of file
diff --git a/code/RL_model/unsloth_rl/reward_mock.py b/code/RL_model/unsloth_rl/reward_mock.py
new file mode 100644
index 0000000000000000000000000000000000000000..370f2b8fe221e36e3881aa42648c0958564698e9
--- /dev/null
+++ b/code/RL_model/unsloth_rl/reward_mock.py
@@ -0,0 +1,127 @@
+import os
+import json
+import re
+import concurrent.futures
+from openai import OpenAI
+
+class MedicalClaimVerifier:
+    def __init__(self):
+        # Implementation remains similar, but with safer error handling
+        api_file = "/home/mshahidul/api_new.json"
+        with open(api_file, "r") as f:
+            api_keys = json.load(f)
+        self.api_key = api_keys["openai"]
+        # Note: Ensure gpt-5-nano is actually available in your tier
+        self.model_name = "gpt-5-nano" 
+        self.client = OpenAI(api_key=self.api_key)
+
+        self.thresholds = {
+            "low": {"comp": 1.0, "cov": 0.3226},
+            "intermediate": {"comp": 1.0, "cov": 0.4091},
+            "proficient": {"comp": 1.0, "cov": 0.9347},
+        }
+
+    def get_prompt(self,context,claim):
+        prompt = f"""
+        CONTEXT:
+        {context}
+
+        CLAIM TO VERIFY:
+        {claim}
+
+        INSTRUCTION:
+        Does the CONTEXT above provide enough evidence to support the CLAIM? 
+        - Answer 'supported' if the claim is explicitly stated or logically followable.
+        - Answer 'not_supported' if the claim is missing, contradicts the text, or requires outside info.
+
+        Output only one word: 'supported' or 'not_supported'.
+        """
+        return prompt
+
+    def check_support_api(self, prompt):
+        try:
+            response = self.client.chat.completions.create(
+                model=self.model_name,
+                messages=[{"role": "user", "content": prompt}],
+            )
+            res = response.choices[0].message.content.strip().lower()
+            return 1.0 if "supported" in res and "not_supported" not in res else 0.0
+        except Exception:
+            return 0.0
+
+    def evaluate_level(self, gen_text, gold_subs, full_subs):
+        if not gen_text or not gold_subs or not full_subs:
+            return 0.0, 0.0
+        
+        # Combining calls to reduce overhead
+        all_claims = gold_subs + full_subs
+        with concurrent.futures.ThreadPoolExecutor(max_workers=10) as executor:
+            results = list(executor.map(self.check_support_api, [self.get_prompt(gen_text, s) for s in all_claims]))
+        
+        comp_results = results[:len(gold_subs)]
+        cov_results = results[len(gold_subs):]
+        
+        comp_score = sum(comp_results) / len(gold_subs)
+        cov_score = sum(cov_results) / len(full_subs)
+        return comp_score, cov_score
+
+verifier = MedicalClaimVerifier()
+
+def compute_score(data_source, solution_str, ground_truth, extra_info=None):  
+    gold_subs = ground_truth.get('summary_subclaims', [])
+    full_subs = ground_truth.get('fulltext_subclaims', [])
+    
+    if not gold_subs or not full_subs:
+        return 0.0
+
+    # 1. Parsing with fallback
+    try:
+        cleaned_str = solution_str.strip()
+        if "```json" in cleaned_str:
+            cleaned_str = cleaned_str.split("```json")[1].split("```")[0].strip()
+        elif "```" in cleaned_str:
+            cleaned_str = cleaned_str.split("```")[1].split("```")[0].strip()
+        data = json.loads(cleaned_str)
+    except Exception:
+        return -5.0 
+
+    levels = ["low", "intermediate", "proficient"]
+    scores = {}
+    
+    # 2. Score Calculation
+    for lvl in levels:
+        gen_text = data.get(f"{lvl}_health_literacy", "")
+        if not gen_text:
+            scores[lvl] = {"comp": 0.0, "cov": 0.0, "missing": True}
+        else:
+            comp, cov = verifier.evaluate_level(gen_text, gold_subs, full_subs)
+            scores[lvl] = {"comp": comp, "cov": cov, "missing": False}
+
+    # 3. Reward Shaping Logic
+    total_reward = 0.0
+    
+    low_cov = scores["low"]["cov"]
+    int_cov = scores["intermediate"]["cov"]
+    pro_cov = scores["proficient"]["cov"]
+
+    # Soft Hierarchy Check: Reward progression, penalize stagnation
+    # Instead of -2.0 exit, we subtract if the order is wrong
+    hierarchy_penalty = 0.0
+    if not (low_cov <= int_cov <= pro_cov):
+        hierarchy_penalty = -2.0 
+
+    for lvl in levels:
+        if scores[lvl]["missing"]:
+            total_reward -= 1.0 # Penalty per missing field
+            continue
+
+        comp_s = scores[lvl]["comp"]
+        cov_s = scores[lvl]["cov"]
+        thresh = verifier.thresholds[lvl]
+
+        # Continuous Reward: (Actual - Threshold) 
+        # This tells the model "You're 10% away" vs "You failed"
+        total_reward += (comp_s - thresh["comp"]) 
+        total_reward += (cov_s - thresh["cov"])
+
+    return total_reward + hierarchy_penalty
\ No newline at end of file
diff --git a/code/RL_model/unsloth_rl/test_reward_mock_unittest.py b/code/RL_model/unsloth_rl/test_reward_mock_unittest.py
new file mode 100644
index 0000000000000000000000000000000000000000..45346d9c2d83ca7fa56c2d80795a3b89f1970e98
--- /dev/null
+++ b/code/RL_model/unsloth_rl/test_reward_mock_unittest.py
@@ -0,0 +1,139 @@
+"""Minimal, offline tests for reward_mock.py.
+
+Run:
+  python code/RL_model/unsloth_rl/test_reward_mock_unittest.py
+
+These tests avoid real OpenAI calls by:
+- mocking the API key file read
+- stubbing OpenAI client construction
+- overriding verifier.evaluate_level to deterministic outputs
+"""
+
+from __future__ import annotations
+
+import importlib.util
+import sys
+import types
+import unittest
+from pathlib import Path
+from unittest.mock import mock_open, patch
+
+
+THIS_DIR = Path(__file__).resolve().parent
+REWARD_MOCK_PATH = THIS_DIR / "reward_mock.py"
+
+
+class FakeOpenAI:
+    def __init__(self, api_key: str | None = None, **_kwargs):
+        self.api_key = api_key
+
+
+def load_reward_mock_module():
+    """Load reward_mock.py from its file path under test-friendly patches."""
+    module_name = "reward_mock_under_test"
+    if module_name in sys.modules:
+        del sys.modules[module_name]
+
+    spec = importlib.util.spec_from_file_location(module_name, str(REWARD_MOCK_PATH))
+    if spec is None or spec.loader is None:
+        raise RuntimeError(f"Failed to create import spec for {REWARD_MOCK_PATH}")
+
+    module = importlib.util.module_from_spec(spec)
+
+    # Ensure 'openai' import is available and OpenAI ctor is patched.
+    # reward_mock does: `from openai import OpenAI`
+    with patch("builtins.open", mock_open(read_data='{"openai": "sk-test"}')):
+        with patch("openai.OpenAI", FakeOpenAI):
+            spec.loader.exec_module(module)
+
+    sys.modules[module_name] = module
+    return module
+
+
+class TestRewardMockComputeScore(unittest.TestCase):
+    def test_valid_json_progression_no_hierarchy_penalty(self):
+        rm = load_reward_mock_module()
+
+        def fake_evaluate_level(gen_text, gold_subs, full_subs):
+            # Return (comp, cov) deterministically based on the generated text.
+            if gen_text == "LOW":
+                return 1.0, 0.3000
+            if gen_text == "INTER":
+                return 1.0, 0.4000
+            if gen_text == "PRO":
+                return 1.0, 0.9500
+            return 0.0, 0.0
+
+        rm.verifier.evaluate_level = fake_evaluate_level
+
+        solution_str = """```json
+        {
+          "low_health_literacy": "LOW",
+          "intermediate_health_literacy": "INTER",
+          "proficient_health_literacy": "PRO"
+        }
+        ```"""
+
+        ground_truth = {
+            "summary_subclaims": ["a", "b"],
+            "fulltext_subclaims": ["x", "y", "z"],
+        }
+
+        score = rm.compute_score(data_source=None, solution_str=solution_str, ground_truth=ground_truth)
+
+        # comp thresholds are 1.0 -> comp deltas = 0
+        # cov deltas: (0.3000-0.3226) + (0.4000-0.4091) + (0.9500-0.9347) = -0.0164
+        self.assertAlmostEqual(score, -0.0164, places=4)
+
+    def test_missing_field_penalizes_and_triggers_hierarchy_penalty(self):
+        rm = load_reward_mock_module()
+
+        def fake_evaluate_level(gen_text, gold_subs, full_subs):
+            if gen_text == "LOW":
+                return 1.0, 0.3000
+            if gen_text == "PRO":
+                return 1.0, 0.9500
+            return 0.0, 0.0
+
+        rm.verifier.evaluate_level = fake_evaluate_level
+
+        # intermediate is missing => -1.0
+        # BUT its cov will be 0.0 for the hierarchy check, so low_cov(0.3) <= int_cov(0.0) fails => -2.0
+        solution_str = '{"low_health_literacy": "LOW", "proficient_health_literacy": "PRO"}'
+
+        ground_truth = {
+            "summary_subclaims": ["a"],
+            "fulltext_subclaims": ["x"],
+        }
+
+        score = rm.compute_score(data_source=None, solution_str=solution_str, ground_truth=ground_truth)
+        expected = (0.3000 - 0.3226) + (0.9500 - 0.9347) - 1.0 - 2.0
+        self.assertAlmostEqual(score, expected, places=4)
+
+    def test_invalid_json_returns_minus_five(self):
+        rm = load_reward_mock_module()
+
+        ground_truth = {
+            "summary_subclaims": ["a"],
+            "fulltext_subclaims": ["x"],
+        }
+
+        score = rm.compute_score(data_source=None, solution_str="not a json", ground_truth=ground_truth)
+        self.assertEqual(score, -5.0)
+
+    def test_missing_claims_returns_zero(self):
+        rm = load_reward_mock_module()
+
+        solution_str = '{"low_health_literacy": "LOW", "intermediate_health_literacy": "INTER", "proficient_health_literacy": "PRO"}'
+
+        # Missing subclaims => early return 0.0
+        score = rm.compute_score(
+            data_source=None,
+            solution_str=solution_str,
+            ground_truth={"summary_subclaims": [], "fulltext_subclaims": ["x"]},
+        )
+        self.assertEqual(score, 0.0)
+
+
+if __name__ == "__main__":
+    unittest.main(verbosity=2)
diff --git a/code/RL_model/unsloth_rl/testing.py b/code/RL_model/unsloth_rl/testing.py
new file mode 100644
index 0000000000000000000000000000000000000000..a08bd2df41037ae156269e182a474ce0a60ad4d8
--- /dev/null
+++ b/code/RL_model/unsloth_rl/testing.py
@@ -0,0 +1,215 @@
+import json
+import concurrent.futures
+from unittest.mock import MagicMock
+
+# --- The Class (Modified slightly for standalone demo) ---
+
+class MedicalClaimVerifier:
+    def __init__(self, mock_mode=False):
+        self.thresholds = {
+            "low": {"comp": 0.6107, "cov": 0.3723},
+            "intermediate": {"comp": 0.8199, "cov": 0.6611},
+            "proficient": {"comp": 0.9569, "cov": 0.9069}
+        }
+        self.mock_mode = mock_mode
+        
+        if not mock_mode:
+            from openai import OpenAI
+            self.api_url = "http://172.16.34.29:8004/v1"
+            self.client = OpenAI(base_url=self.api_url, api_key="EMPTY")
+            self.model_name = "qwen3-32b-readctrl"
+
+    def get_audit_prompt(self, literacy_level):
+        level_guidelines = {
+            "low_health_literacy": """
+            Level: Low Health Literacy (High Readability)
+            Target: Individuals needing simple terms.
+            Goal: 'Living room' language. Replace jargon (e.g., 'renal' -> 'kidney').
+            Density: Strictly 'need-to-know' info from Gold Summary.
+            Strategy: High paraphrasing, analogies, one idea per sentence.
+            Faithfulness: Must align with Gold Summary.""",
+            
+            "intermediate_health_literacy": """
+            Level: Intermediate Health Literacy (Medium Readability)
+            Target: General public.
+            Goal: Standard vocabulary. Common medical terms okay; technical speak simplified.
+            Density: Balanced. Use Gold Summary as lead, supplemented by context from Source.
+            Strategy: Moderate paraphrasing. Remove minor technical details.
+            Faithfulness: Maintain main narrative of Gold Summary.""",
+            
+            "proficient_health_literacy": """
+            Level: Proficient Health Literacy (Low Readability)
+            Target: Researchers/Clinicians.
+            Goal: Technical/Academic. Prioritize clinical nuance and accuracy.
+            Density: High. Include data, physiological mechanisms, and statistics from Source.
+            Strategy: Minimal paraphrasing. Retain original technical terminology.
+            Faithfulness: Adhere to Source Text; add deeper scientific context."""
+        }
+
+        guidelines = level_guidelines.get(literacy_level, "Follow standard medical audit practices.")
+        level_desc = literacy_level.replace("_", " ")
+
+        base_instructions = f"""
+        ### Literacy Level Context:
+        {guidelines}
+
+        ### Task Instructions:"""
+        return base_instructions
+
+    def get_completeness_prompt(self, generated_text, source_subclaim, literacy_level):
+        base_instructions = self.get_audit_prompt(literacy_level)
+        level_desc = literacy_level.replace("_", " ")
+        return f"""{base_instructions}
+            1. Determine whether this Fact from the Gold Standard is covered in the {level_desc} summary.
+            2. Mark 'supported' ONLY IF:
+            - The fact is explicitly stated in the summary, OR
+            - The fact is clearly paraphrased or simplified in a way that preserves its meaning.
+            3. Do NOT mark 'supported' based solely on omission.
+            - Absence of mention does NOT imply intentional exclusion.
+            - Negative or exclusionary facts (e.g., "no complications," "no family history," "no systemic signs") must be explicitly conveyed.
+            4. Mark 'not_supported' if:
+            - The fact is completely omitted, OR
+            - The summary discusses related information but does not confirm the specific fact.
+            5. Literacy-based simplification is allowed, but factual meaning must be preserved.
+
+            SUMMARY: {generated_text}
+            FACT: {source_subclaim}
+
+            output: 'supported' or 'not_supported'.
+            """
+
+    def get_source_coverage_prompt(self, generated_text, source_subclaim, literacy_level):
+        base_instructions = self.get_audit_prompt(literacy_level)
+        level_desc = literacy_level.replace("_", " ")
+        return f"""{base_instructions}
+        1. Check whether the following Fact from the ORIGINAL Source Text is explicitly covered in the generated {level_desc} summary.
+        2. Mark 'supported' ONLY IF:
+        - The summary clearly states the fact, OR
+        - The fact is conveyed through an explicit paraphrase or simplification that preserves its meaning.
+        3. Do NOT infer support from silence or omission.
+        - Absence of mention does NOT count as support.
+        - Especially for negative or exclusionary facts (e.g., "no family history," "no extra-renal signs," "no complications"), the summary must explicitly indicate absence.
+        4. Mark 'not_supported' if:
+        - The summary omits the fact entirely, OR
+        - The summary discusses related topics but does not clearly confirm the specific fact.
+        5. Simplification for literacy level is allowed, but factual meaning must be preserved.
+
+        GENERATED SUMMARY: {generated_text}
+        SOURCE FACT: {source_subclaim}
+
+        output: 'supported' or 'not_supported'."""
+
+    def check_support_api(self, prompt):
+        # print(f"Prompt Sent:\n{prompt}\n")
+        
+        # Real logic
+        try:
+            response = self.client.chat.completions.create(
+                model=self.model_name,
+                messages=[{"role": "user", "content": prompt}],
+                max_tokens=300, temperature=0.1,
+            )
+            res = response.choices[0].message.content.strip().lower()
+            print(f"Response Received:\n{res}\n")
+            return 1.0 if "supported" in res and "not_supported" not in res else 0.0
+        except:
+            return 0.0
+
+    def evaluate_level(self, gen_text, gold_subs, full_subs, level_key):
+        if not gen_text: return 0.0, 0.0
+        
+        # Using 2 workers for demo to avoid overhead
+        with concurrent.futures.ThreadPoolExecutor(max_workers=2) as executor:
+            comp_prompts = [self.get_completeness_prompt(gen_text, s, level_key) for s in gold_subs]
+            comp_results = list(executor.map(self.check_support_api, comp_prompts))
+            comp_score = sum(comp_results) / len(comp_results) if comp_results else 0.0
+
+            cov_prompts = [self.get_source_coverage_prompt(gen_text, s, level_key) for s in full_subs]
+            cov_results = list(executor.map(self.check_support_api, cov_prompts))
+            cov_score = sum(cov_results) / len(cov_results) if cov_results else 0.0
+
+        return comp_score, cov_score
+
+    def get_reward_score(self, completion, gold_subs, full_subs):
+        data = None
+        try:
+            # completion[0]['content'] structure as expected by RL frameworks
+            text = completion[0]['content'].strip()
+            
+            if "```json" in text:
+                text = text.split("```json")[-1].split("```")[0].strip()
+            elif "```" in text:
+                text = text.split("```")[-1].split("```")[0].strip()
+            
+            if "<SOLUTION>" in text:
+                text = text.split("<SOLUTION>")[-1].split("</SOLUTION>")[0].strip()
+                
+            data = json.loads(text)
+        except Exception as e:
+            print(f"JSON Parse Error: {e}")
+            return -5.0
+
+        levels = ["low", "intermediate", "proficient"]
+        if not all(f"{lvl}_health_literacy" in data for lvl in levels):
+            return -2.0
+
+        try:
+            total_reward = 0.0
+            print("\n--- Evaluation Breakdown ---")
+            for lvl in levels:
+                gen_text = data.get(f"{lvl}_health_literacy", "")
+                comp_score, cov_score = self.evaluate_level(gen_text, gold_subs, full_subs, f"{lvl}_health_literacy")
+                
+                # Logic check
+                comp_passed = comp_score >= self.thresholds[lvl]["comp"]
+                cov_passed = cov_score >= self.thresholds[lvl]["cov"]
+                
+                total_reward += 1.0 if comp_passed else -0.5
+                total_reward += 1.0 if cov_passed else -0.5
+                
+                print(f"[{lvl.upper()}] Comp: {comp_score:.2f} ({comp_passed}), Cov: {cov_score:.2f} ({cov_passed})")
+                
+            return total_reward
+        except Exception as e:
+            print(f"Scoring Error: {e}")
+            return -5.0
+
+# --- Execution Block ---
+
+if __name__ == "__main__":
+    verifier = MedicalClaimVerifier(mock_mode=False)
+
+    # 1. Mock Input Data (what the model generated)
+    pass_completion = [{
+    "content": """
+        <SOLUTION>
+        {
+            "low_health_literacy": "This medicine makes it easier for your heart to pump and relaxes your blood tubes. You might feel dizzy if you stand up too fast.",
+            "intermediate_health_literacy": "ACE inhibitors like Lisinopril relax blood vessels to improve flow and lower heart attack risk. Side effects include low blood pressure.",
+            "proficient_health_literacy": "ACE inhibitors attenuate the effects of stress hormones on the myocardium while inducing vasodilation to reduce afterload and prevent myocardial infarction."
+        }
+        </SOLUTION>
+        """
+    }]
+
+        # Completeness (Essential findings from a Gold Summary)
+    gold_subs = [
+        "ACE inhibitors help the heart pump better.",
+        "These medicines relax blood vessels.",
+        "Common side effects include dizziness and low blood pressure."
+    ]
+
+    # Source Coverage (Detailed facts from the original Full Text)
+    full_subs = [
+        "Lisinopril is an example of an ACE inhibitor.",
+        "ACE inhibitors lower the risk of a heart attack.",
+        "The medication prevents stress hormones from damaging the heart.",
+        "Patients should stand up slowly to avoid dizziness."
+    ]
+
+    # 3. Run Demo
+    print("Starting Demo Run...")
+    final_reward = verifier.get_reward_score(pass_completion, gold_subs, full_subs)
+    
+    print("-" * 30)
+    print(f"FINAL REWARD SCORE: {final_reward}")
\ No newline at end of file
diff --git a/code/RL_model/unsloth_rl/testing_v2.py b/code/RL_model/unsloth_rl/testing_v2.py
new file mode 100644
index 0000000000000000000000000000000000000000..4c51b550b9691011ca897b0f13612b5dce34e7f0
--- /dev/null
+++ b/code/RL_model/unsloth_rl/testing_v2.py
@@ -0,0 +1,138 @@
+import json
+import concurrent.futures
+from openai import OpenAI
+
+class FactualityBenchmarker:
+    def __init__(self, api_url="http://172.16.34.29:8004/v1", model="qwen3-32b-readctrl"):
+        self.client = OpenAI(base_url=api_url, api_key="EMPTY")
+        self.model = model
+
+    def verify_claim(self, context, claim):
+        """
+        Asks the model to determine if the context supports the claim.
+        """
+        prompt = f"""
+        CONTEXT:
+        {context}
+
+        CLAIM TO VERIFY:
+        {claim}
+
+        INSTRUCTION:
+        Does the CONTEXT above provide enough evidence to support the CLAIM? 
+        - Answer 'supported' if the claim is explicitly stated or logically followable.
+        - Answer 'not_supported' if the claim is missing, contradicts the text, or requires outside info.
+
+        Output only one word: 'supported' or 'not_supported'.
+        """
+        
+        try:
+            response = self.client.chat.completions.create(
+                model=self.model,
+                messages=[{"role": "user", "content": prompt}],
+                temperature=0.0, # Zero temp for consistency in benchmarks
+                max_tokens=10
+            )
+            result = response.choices[0].message.content.strip().lower()
+            return "supported" if "supported" in result and "not_supported" not in result else "not_supported"
+        except Exception as e:
+            print(f"Error: {e}")
+            return "not_supported"
+
+    def run_evaluation(self, test_cases):
+        """
+        Runs the benchmark over a list of test cases.
+        Each test case: {"context": "...", "claims": [{"text": "...", "label": 1.0/0.0}]}
+        """
+        total_claims = 0
+        correct_predictions = 0
+
+        print(f"--- Starting Evaluation on {self.model} ---")
+        
+        for i, case in enumerate(test_cases):
+            context = case["context"]
+            print(f"\nTest Case {i+1}:")
+            
+            for claim_data in case["claims"]:
+                claim_text = claim_data["text"]
+                expected = claim_data["expected"]
+                
+                # Model Prediction
+                prediction = self.verify_claim(context, claim_text)
+                
+                is_correct = (prediction == expected)
+                if is_correct:
+                    correct_predictions += 1
+                total_claims += 1
+                
+                status = "PASS" if is_correct else "FAIL"
+                print(f"  [{status}] Claim: {claim_text[:60]}... (Expected: {expected}, Got: {prediction})")
+
+        accuracy = (correct_predictions / total_claims) * 100 if total_claims > 0 else 0
+        print(f"\n" + "="*30)
+        print(f"FINAL ACCURACY: {accuracy:.2f}% ({correct_predictions}/{total_claims})")
+        print("="*30)
+
+# --- Define your test data here ---
+test_data = [
+    {
+        "context": """CASE PRESENTATION:
+A 64-year-old male with a 15-year history of Type 2 Diabetes Mellitus and stage 3 chronic kidney disease (CKD) 
+presented to the emergency department with acute shortness of breath and peripheral edema. On physical 
+examination, the patient was hypertensive (175/95 mmHg) and tachycardic (110 bpm). Lung auscultation revealed 
+bilateral crackles in the lower lobes, consistent with pulmonary congestion. Notable laboratory findings 
+included a Serum Creatinine of 2.8 mg/dL (baseline 1.9 mg/dL) and a Brain Natriuretic Peptide (BNP) of 1,250 pg/mL. 
+
+Crucially, the patient reported no history of tobacco use and denied any chest pain or radiating pain to the 
+left arm. An EKG showed sinus tachycardia but no ST-segment elevation or T-wave inversion. The medical team 
+initiated a regimen of intravenous furosemide (40mg bolus) and transitioned the patient from his home 
+medication (Metformin) to insulin glargine to manage blood glucose during the acute episode, citing concerns 
+over lactic acidosis risk given the acute kidney injury. After 48 hours, the patient's oxygen saturation 
+improved from 89% on room air to 95%, and his weight decreased by 3.2 kg due to successful diuresis. 
+The discharge summary noted that despite the respiratory distress, there were no signs of systemic infection 
+or fever during the entire 4-day hospital stay.""",
+        "claims":[
+    # 1. Literal Extraction
+    {"text": "The patient has had Type 2 Diabetes for 15 years.", "expected": "supported"},
+    
+    # 2. Medical Paraphrasing (Reading Control)
+    {"text": "The patient showed signs of fluid buildup in the lungs.", "expected": "supported"}, # 'bilateral crackles/congestion'
+    
+    # 3. Negative Constraint (Exclusionary fact)
+    {"text": "The patient has a history of smoking.", "expected": "not_supported"}, # Text says 'no history of tobacco'
+    
+    # 4. Mathematical Inference
+    {"text": "The patient's Serum Creatinine increased by 0.9 mg/dL from his baseline.", "expected": "supported"}, # 2.8 - 1.9 = 0.9
+    
+    # 5. Logic: Cause and Effect
+    {"text": "The doctors stopped Metformin because of the risk of lactic acidosis.", "expected": "supported"},
+    
+    # 6. Negative Finding (Testing 'Silence')
+    {"text": "The patient complained of pain moving down his left arm.", "expected": "not_supported"}, # Specifically denied
+    
+    # 7. Vital Sign Interpretation
+    {"text": "The patient was experiencing high blood pressure and a fast heart rate upon arrival.", "expected": "supported"}, # 175/95 and 110bpm
+    
+    # 8. Numerical Recovery
+    {"text": "The patient lost over 3 kilograms during the first two days of treatment.", "expected": "supported"}, # 3.2 kg
+    
+    # 9. Complex Inference (EKG interpretation)
+    {"text": "The EKG provided clear evidence of an active heart attack.", "expected": "not_supported"}, # Text says 'no ST-elevation'
+    
+    # 10. Systemic Health Status
+    {"text": "The patient remained afebrile throughout the hospitalization.", "expected": "supported"} # 'no fever' = afebrile
+]
+    },
+    {
+        "context": "The company reported a 15% increase in revenue, reaching $2 billion this quarter. However, net profit dropped due to high R&D costs.",
+        "claims": [
+            {"text": "Revenue reached $2 billion.", "expected": "supported"},
+            {"text": "Net profit increased this quarter.", "expected": "not_supported"},
+            {"text": "Spending on Research and Development impacted profits.", "expected": "supported"}
+        ]
+    }
+]
+
+if __name__ == "__main__":
+    benchmarker = FactualityBenchmarker()
+    benchmarker.run_evaluation(test_data)
\ No newline at end of file
diff --git a/code/RL_model/verl/Search-R1/.gitignore b/code/RL_model/verl/Search-R1/.gitignore
new file mode 100644
index 0000000000000000000000000000000000000000..be07f884731029d4ced93aa284b0d3ee06b57371
--- /dev/null
+++ b/code/RL_model/verl/Search-R1/.gitignore
@@ -0,0 +1,122 @@
+**/*.pt
+**/checkpoints
+**/wget-log
+**/_build/
+**/*.ckpt
+**/outputs
+**/*.tar.gz
+**/playground
+**/wandb
+
+# Byte-compiled / optimized / DLL files
+__pycache__/
+*.py[cod]
+*$py.class
+dataset/*
+tensorflow/my_graph/*
+.idea/
+# C extensions
+*.so
+data
+sft/output/*
+sft/data/*
+
+# Distribution / packaging
+.Python
+build/
+develop-eggs/
+dist/
+downloads/
+eggs/
+.eggs/
+lib/
+lib64/
+parts/
+sdist/
+var/
+*.egg-info/
+.installed.cfg
+*.egg
+
+# PyInstaller
+#  Usually these files are written by a python script from a template
+#  before PyInstaller builds the exe, so as to inject date/other infos into it.
+*.manifest
+*.spec
+
+# Installer logs
+pip-log.txt
+pip-delete-this-directory.txt
+
+# Unit test / coverage reports
+htmlcov/
+.tox/
+.coverage
+.coverage.*
+.cache
+nosetests.xml
+coverage.xml
+*,cover
+.hypothesis/
+
+# Translations
+*.mo
+*.pot
+
+# Django stuff:
+*.log
+local_settings.py
+
+image_outputs
+
+checkpoints
+
+# Flask stuff:
+instance/
+.webassets-cache
+
+# Scrapy stuff:
+.scrapy
+
+# Sphinx documentation
+docs/_build/
+
+# PyBuilder
+target/
+
+# IPython Notebook
+.ipynb_checkpoints
+
+# pyenv
+.python-version
+
+# celery beat schedule file
+celerybeat-schedule
+
+
+# virtualenv
+venv/
+ENV/
+
+# Spyder project settings
+.spyderproject
+
+# Rope project settings
+.ropeproject
+
+# vscode
+.vscode
+
+# Mac
+.DS_Store
+
+# output logs
+tests/e2e/toy_examples/deepspeed/synchronous/output.txt
+
+# vim
+*.swp
+
+# log*
+log/
+
+**logs
\ No newline at end of file
diff --git a/code/RL_model/verl/Search-R1/LICENSE b/code/RL_model/verl/Search-R1/LICENSE
new file mode 100644
index 0000000000000000000000000000000000000000..d645695673349e3947e8e5ae42332d0ac3164cd7
--- /dev/null
+++ b/code/RL_model/verl/Search-R1/LICENSE
@@ -0,0 +1,202 @@
+
+                                 Apache License
+                           Version 2.0, January 2004
+                        http://www.apache.org/licenses/
+
+   TERMS AND CONDITIONS FOR USE, REPRODUCTION, AND DISTRIBUTION
+
+   1. Definitions.
+
+      "License" shall mean the terms and conditions for use, reproduction,
+      and distribution as defined by Sections 1 through 9 of this document.
+
+      "Licensor" shall mean the copyright owner or entity authorized by
+      the copyright owner that is granting the License.
+
+      "Legal Entity" shall mean the union of the acting entity and all
+      other entities that control, are controlled by, or are under common
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+      direction or management of such entity, whether by contract or
+      otherwise, or (ii) ownership of fifty percent (50%) or more of the
+      outstanding shares, or (iii) beneficial ownership of such entity.
+
+      "You" (or "Your") shall mean an individual or Legal Entity
+      exercising permissions granted by this License.
+
+      "Source" form shall mean the preferred form for making modifications,
+      including but not limited to software source code, documentation
+      source, and configuration files.
+
+      "Object" form shall mean any form resulting from mechanical
+      transformation or translation of a Source form, including but
+      not limited to compiled object code, generated documentation,
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+
+      "Work" shall mean the work of authorship, whether in Source or
+      Object form, made available under the License, as indicated by a
+      copyright notice that is included in or attached to the work
+      (an example is provided in the Appendix below).
+
+      "Derivative Works" shall mean any work, whether in Source or Object
+      form, that is based on (or derived from) the Work and for which the
+      editorial revisions, annotations, elaborations, or other modifications
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+      of this License, Derivative Works shall not include works that remain
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+      "Contribution" shall mean any work of authorship, including
+      the original version of the Work and any modifications or additions
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+      "Contributor" shall mean Licensor and any individual or Legal Entity
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+      subsequently incorporated within the Work.
+
+   2. Grant of Copyright License. Subject to the terms and conditions of
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+   4. Redistribution. You may reproduce and distribute copies of the
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+          Derivative Works a copy of this License; and
+
+      (b) You must cause any modified files to carry prominent notices
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+      (c) You must retain, in the Source form of any Derivative Works
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diff --git a/code/RL_model/verl/Search-R1/Notice.txt b/code/RL_model/verl/Search-R1/Notice.txt
new file mode 100644
index 0000000000000000000000000000000000000000..ade439da525ac3f82936e131a1ae386f43207fd8
--- /dev/null
+++ b/code/RL_model/verl/Search-R1/Notice.txt
@@ -0,0 +1 @@
+Copyright 2023-2024 Bytedance Ltd. and/or its affiliates 
\ No newline at end of file
diff --git a/code/RL_model/verl/Search-R1/README.md b/code/RL_model/verl/Search-R1/README.md
new file mode 100644
index 0000000000000000000000000000000000000000..86259e3ab90c2a57b459a09584512e62f1189d1a
--- /dev/null
+++ b/code/RL_model/verl/Search-R1/README.md
@@ -0,0 +1,275 @@
+# Search-R1: Train your LLMs to reason and call a search engine with reinforcement learning
+
+<div align="center">
+  <img src="https://raw.githubusercontent.com/PeterGriffinJin/Search-R1/main/public/logo.png" alt="logo" width="300"/>
+</div>
+
+<p align="center">
+  <a href="https://arxiv.org/abs/2503.09516">
+    <img src="https://img.shields.io/badge/Paper1-blue?style=for-the-badge" alt="Button1"/>
+  </a>
+  <a href="https://arxiv.org/abs/2505.15117">
+    <img src="https://img.shields.io/badge/Paper2-green?style=for-the-badge" alt="Button2"/>
+  </a>
+  <a href="https://huggingface.co/collections/PeterJinGo/search-r1-67d1a021202731cb065740f5">
+    <img src="https://img.shields.io/badge/Resources-orange?style=for-the-badge" alt="Button3"/>
+  </a>
+  <a href="https://x.com/BowenJin13/status/1895544294473109889">
+    <img src="https://img.shields.io/badge/Tweet-red?style=for-the-badge" alt="Button4"/>
+  </a>
+  <a href="https://wandb.ai/peterjin/Search-R1-v0.2">
+    <img src="https://img.shields.io/badge/Logs-purple?style=for-the-badge" alt="Button5"/>
+  </a>
+</p>
+
+
+<!-- <strong>Search-R1</strong> is a reinforcement learning framework for <em>training reasoning and searching (tool-call) interleaved LLMs</em>.  -->
+<!-- We built upon [veRL](https://github.com/volcengine/verl). -->
+**Search-R1** is a reinforcement learning framework designed for training **reasoning-and-searching interleaved LLMs**—language models that learn to reason and make tool calls (e.g., to search engines) in a coordinated manner.
+
+<!-- It can be seen as an extension of <strong>DeepSeek-R1(-Zero)</strong> with interleaved search engine calling and an opensource RL training-based solution for <strong>OpenAI DeepResearch</strong>. -->
+Built upon [veRL](https://github.com/volcengine/verl), Search-R1 extends the ideas of **DeepSeek-R1(-Zero)** by incorporating interleaved search engine access and provides a fully open-source RL training pipeline. It serves as an alternative and open solution to **OpenAI DeepResearch**, enabling research and development in tool-augmented LLM reasoning.
+
+<!-- Through RL (rule-based outcome reward), the 3B **base** LLM (both Qwen2.5-3b-base and Llama3.2-3b-base) develops reasoning and search engine calling abilities all on its own. -->
+
+We support different RL methods (e.g., PPO, GRPO, reinforce), different LLMs (e.g., llama3, Qwen2.5, etc) and different search engines (e.g., local sparse/dense retrievers and online search engines).
+
+Paper: [link1](https://arxiv.org/pdf/2503.09516), [link2](https://arxiv.org/abs/2505.15117); Model and data: [link](https://huggingface.co/collections/PeterJinGo/search-r1-67d1a021202731cb065740f5); Twitter thread: [link](https://x.com/BowenJin13/status/1895544294473109889); Full experiment log: [prelim](https://wandb.ai/peterjin/Search-R1-open); [v0.1](https://wandb.ai/peterjin/Search-R1-nq_hotpotqa_train); [v0.2](https://wandb.ai/peterjin/Search-R1-v0.2); [v0.3](https://wandb.ai/peterjin/Search-R1-v0.3). Details about these logs and methods can be find [here](https://github.com/PeterGriffinJin/Search-R1/blob/main/docs/experiment_log.md).
+
+
+![single-turn](public/main.png)
+
+## News
+
+- [2025.10] Search-R1 is featured by Thinking Machines Lab's first product [Tinker](https://github.com/thinking-machines-lab/tinker-cookbook)! Details: [Document](https://github.com/thinking-machines-lab/tinker-cookbook/tree/main/tinker_cookbook/recipes/tool_use/search).
+- [2025.7] Search-R1 is supported by [SkyRL](https://github.com/NovaSky-AI/SkyRL)! Detailed instructions: [code](https://github.com/NovaSky-AI/SkyRL/tree/main/skyrl-train/examples/search), [Document](https://novasky-ai.notion.site/skyrl-searchr1).
+- [2025.6] Search-R1 is now integrated into the latest version of veRL and can take advantage of its most up-to-date features! Detailed instructions: [veRL](https://verl.readthedocs.io/en/latest/sglang_multiturn/search_tool_example.html), [English Document](https://github.com/zhaochenyang20/Awesome-ML-SYS-Tutorial/blob/main/rlhf/verl/multi-turn/tool_examples/verl-multiturn-searchR1-like.md), [Chinese Document](https://github.com/zhaochenyang20/Awesome-ML-SYS-Tutorial/blob/main/rlhf/verl/multi-turn/tool_examples/verl-multiturn-searchR1-like_ZH.md).
+- [2025.5] The second [paper](https://arxiv.org/abs/2505.15117) conducting detailed empirical studies is published with logs: [v0.3](https://wandb.ai/peterjin/Search-R1-v0.3). 
+- [2025.4] We support [multinode](https://github.com/PeterGriffinJin/Search-R1/blob/main/docs/multinode.md) training for 30B+ LLMs!
+- [2025.4] We support [different search engines](https://github.com/PeterGriffinJin/Search-R1/blob/main/docs/retriever.md) including sparse local retriever, dense local retriever with ANN indexing and online search engines!
+- [2025.3] The first Search-R1 [paper](https://arxiv.org/pdf/2503.09516) is published with the logs: [v0.1](https://wandb.ai/peterjin/Search-R1-nq_hotpotqa_train); [v0.2](https://wandb.ai/peterjin/Search-R1-v0.2).
+- [2025.2] We opensource Search-R1 codebase with [preliminary results](https://wandb.ai/peterjin/Search-R1-open).
+
+## Links
+
+- [Installation](#installation)
+- [Quick start](#quick-start)
+- [Preliminary results](#preliminary-results)
+- [Inference](#inference)
+- [Use your own dataset](#use-your-own-dataset)
+- [Use your own search engine](#use-your-own-search-engine)
+- [Features](#features)
+- [Ackowledge](#acknowledge)
+- [Citations](#citations)
+
+## Installation
+
+### Search-r1 environment
+```bash
+conda create -n searchr1 python=3.9
+conda activate searchr1
+# install torch [or you can skip this step and let vllm to install the correct version for you]
+pip install torch==2.4.0 --index-url https://download.pytorch.org/whl/cu121
+# install vllm
+pip3 install vllm==0.6.3 # or you can install 0.5.4, 0.4.2 and 0.3.1
+
+# verl
+pip install -e .
+
+# flash attention 2
+pip3 install flash-attn --no-build-isolation
+pip install wandb
+```
+
+### Retriever environment (optional)
+If you would like to call a local retriever as the search engine, you can install the environment as follows. (We recommend using a seperate environment.)
+```bash
+conda create -n retriever python=3.10
+conda activate retriever
+
+# we recommend installing torch with conda for faiss-gpu
+conda install pytorch==2.4.0 torchvision==0.19.0 torchaudio==2.4.0 pytorch-cuda=12.1 -c pytorch -c nvidia
+pip install transformers datasets pyserini
+
+## install the gpu version faiss to guarantee efficient RL rollout
+conda install -c pytorch -c nvidia faiss-gpu=1.8.0
+
+## API function
+pip install uvicorn fastapi
+```
+
+
+## Quick start
+
+Train a reasoning + search LLM on NQ dataset with e5 as the retriever and wikipedia as the corpus.
+
+(1) Download the indexing and corpus.
+```bash
+save_path=/the/path/to/save
+python scripts/download.py --save_path $save_path
+cat $save_path/part_* > $save_path/e5_Flat.index
+gzip -d $save_path/wiki-18.jsonl.gz
+```
+
+(2) Process the NQ dataset.
+```bash
+python scripts/data_process/nq_search.py
+```
+
+(3) Launch a local retrieval server.
+```bash
+conda activate retriever
+bash retrieval_launch.sh
+```
+
+(4) Run RL training (PPO) with Llama-3.2-3b-base.
+```bash
+conda activate searchr1
+bash train_ppo.sh
+```
+
+## Preliminary results
+
+(1) The base model (llama3.2-3b-base) learns to call the search engine and obtain improved performance.
+
+![llama-3b](public/llama32-3b.png)
+
+
+(2) The base model (Qwen2.5-7b-base) can learn to conduct multi-turn search engine calling and reasoning with RL.
+
+![multi-turn](public/multi-turn.png)
+
+## Inference
+#### You can play with the trained Search-R1 model with your own question.
+(1) Launch a local retrieval server.
+```bash
+conda activate retriever
+bash retrieval_launch.sh
+```
+
+(2) Run inference.
+```bash
+conda activate searchr1
+python infer.py
+```
+You can modify the ```question``` on line 7 to something you're interested in.
+
+## Use your own dataset
+
+### QA data
+For each question-answer sample, it should be a dictionary containing the desired content as below:
+
+```
+data = {
+        "data_source": data_source,
+        "prompt": [{
+            "role": "user",
+            "content": question,
+        }],
+        "ability": "fact-reasoning",
+        "reward_model": {
+            "style": "rule",
+            "ground_truth": solution
+        },
+        "extra_info": {
+            'split': split,
+            'index': idx,
+        }
+    }
+```
+
+You can refer to ```scripts/data_process/nq_search.py``` for a concrete data processing example.
+
+### Corpora
+
+It is recommended to make your corpus a jsonl file, where each line (a dictionary with "id" key and "contents" key) corresponds to one passage. You can refer to ```example/corpus.jsonl``` for an example.
+
+The "id" key corresponds to the passage id, while the "contents" key corresponds to the passage content ('"' + title + '"\n' + text).
+For example:
+```
+{"id": "0", "contents": "Evan Morris Evan L. Morris (January 26, 1977 \u2013 July 9, 2015) was a lobbyist for Genentech and its parent corporation Roche in Washington."}
+...
+{"id": "100", "contents": "Three years later, when the United States Exploring Expedition to little-known portions of the globe was organised under Charles Wilkes, Hale was recommended, while yet an undergraduate."}
+...
+```
+
+**Index your corpora (optional).**
+If you would like to use a local retriever as the search engine, you can index your own corpus by:
+```
+bash search_r1/search/build_index.sh
+```
+You can change ```retriever_name``` and ```retriever_model``` to your interested off-the-shelf retriever.
+
+## Use your own search engine
+
+Our codebase supports local sparse retriever (e.g., BM25), local dense retriever (both flat indexing with GPUs and ANN indexing with CPUs) and online search engine (e.g., Google, Bing, etc). More details can be found [here](https://github.com/PeterGriffinJin/Search-R1/tree/main/docs/retriever.md).
+
+The main philosophy is to launch a local or remote search engine server separately from the main RL training pipeline. 
+
+The LLM can call the search engine by calling the search API (e.g., "http://127.0.0.1:8000/retrieve").
+
+You can refer to ```search_r1/search/retriever_server.py``` for an example of launching a local retriever server.
+
+## Features
+- Support local sparse retrievers (e.g., BM25). ✔️
+- Support local dense retrievers (both flat indexing and ANN indexing) ✔️
+- Support google search / bing search / brave search API and others. ✔️
+- Support off-the-shelf neural rerankers. ✔️
+- Support different RL methods (e.g., PPO, GRPO, reinforce). ✔️
+- Support different LLMs (e.g., llama3, Qwen2.5, etc). ✔️
+
+## Acknowledge
+
+The concept of Search-R1 is inspired by [Deepseek-R1](https://github.com/deepseek-ai/DeepSeek-R1) and [TinyZero](https://github.com/Jiayi-Pan/TinyZero/tree/main).
+Its implementation is built upon [veRL](https://github.com/volcengine/verl) and [RAGEN](https://github.com/ZihanWang314/RAGEN/tree/main). 
+We sincerely appreciate the efforts of these teams for their contributions to open-source research and development.
+
+## Awesome work powered or inspired by Search-R1
+
+- [DeepResearcher](https://github.com/GAIR-NLP/DeepResearcher): Scaling Deep Research via Reinforcement Learning in Real-world Environments. [![[code]](https://img.shields.io/github/stars/GAIR-NLP/DeepResearcher)](https://github.com/GAIR-NLP/DeepResearcher)
+- [Multimodal-Search-R1](https://github.com/EvolvingLMMs-Lab/multimodal-search-r1): Incentivizing LMMs to Search. [![[code]](https://img.shields.io/github/stars/EvolvingLMMs-Lab/multimodal-search-r1)](https://github.com/EvolvingLMMs-Lab/multimodal-search-r1)
+- [OTC](https://arxiv.org/pdf/2504.14870): Optimal Tool Calls via Reinforcement Learning.
+- [ZeroSearch](https://github.com/Alibaba-NLP/ZeroSearch): Incentivize the Search Capability of LLMs without Searching. [![[code]](https://img.shields.io/github/stars/Alibaba-NLP/ZeroSearch)](https://github.com/Alibaba-NLP/ZeroSearch)
+- [IKEA](https://github.com/hzy312/knowledge-r1): Reinforced Internal-External Knowledge Synergistic Reasoning for Efficient Adaptive Search Agent. [![[code]](https://img.shields.io/github/stars/hzy312/knowledge-r1)](https://github.com/hzy312/knowledge-r1)
+- [Scent of Knowledge](https://arxiv.org/abs/2505.09316): Optimizing Search-Enhanced Reasoning with Information Foraging.
+- [AutoRefine](https://www.arxiv.org/pdf/2505.11277): Search and Refine During Think. [![[code]](https://img.shields.io/github/stars/syr-cn/AutoRefine)](https://github.com/syr-cn/AutoRefine)
+- [O^2-Searcher](https://arxiv.org/pdf/2505.16582): A Searching-based Agent Model for Open-Domain Open-Ended Question Answering. [![[code]](https://img.shields.io/github/stars/Acade-Mate/O2-Searcher)](https://github.com/Acade-Mate/O2-Searcher)
+- [MaskSearch](https://arxiv.org/pdf/2505.20285): A Universal Pre-Training Framework to Enhance Agentic Search Capability. [![[code]](https://img.shields.io/github/stars/Alibaba-NLP/MaskSearch)](https://github.com/Alibaba-NLP/MaskSearch)
+- [VRAG-RL](https://arxiv.org/abs/2505.22019): Vision-Perception-Based RAG for Visually Rich Information Understanding. [![[code]](https://img.shields.io/github/stars/Alibaba-NLP/VRAG)](https://github.com/Alibaba-NLP/VRAG)
+- [R1-Code-Interpreter](https://arxiv.org/abs/2505.21668): Training LLMs to Reason with Code via SFT and RL. [![[code]](https://img.shields.io/github/stars/yongchao98/R1-Code-Interpreter)](https://github.com/yongchao98/R1-Code-Interpreter)
+- [R-Search](https://arxiv.org/abs/2506.04185): Empowering LLM Reasoning with Search via Multi-Reward Reinforcement Learning. [![[code]](https://img.shields.io/github/stars/QingFei1/R-Search)](https://github.com/QingFei1/R-Search)
+- [StepSearch](https://arxiv.org/pdf/2505.15107): Igniting LLMs Search Ability via Step-Wise Proximal Policy Optimization. [![[code]](https://img.shields.io/github/stars/Zillwang/StepSearch)](https://github.com/Zillwang/StepSearch)
+- [SimpleTIR](https://simpletir.notion.site/report): Stable End-to-End Reinforcement Learning for Multi-Turn Tool-Integrated Reasoning. [![[code]](https://img.shields.io/github/stars/ltzheng/SimpleTIR)](https://github.com/ltzheng/SimpleTIR)
+- [Router-R1](https://arxiv.org/pdf/2506.09033): Teaching LLMs Multi-Round Routing and Aggregation via Reinforcement Learning. [![[code]](https://img.shields.io/github/stars/ulab-uiuc/Router-R1)](https://github.com/ulab-uiuc/Router-R1)
+- [SkyRL](https://skyrl.readthedocs.io/en/latest/): A Modular Full-stack RL Library for LLMs. [![[code]](https://img.shields.io/github/stars/NovaSky-AI/SkyRL)](https://github.com/NovaSky-AI/SkyRL)
+- [ASearcher](https://arxiv.org/abs/2508.07976): Large-Scale RL for Search Agents. [![[code]](https://img.shields.io/github/stars/inclusionAI/ASearcher)](https://github.com/inclusionAI/ASearcher)
+- [ParallelSearch](https://www.arxiv.org/abs/2508.09303): Decompose Query and Search Sub-queries in Parallel with RL. [![[code]](https://img.shields.io/github/stars/Tree-Shu-Zhao/ParallelSearch)](https://github.com/Tree-Shu-Zhao/ParallelSearch)
+- [AutoTIR](https://arxiv.org/pdf/2507.21836): Autonomous Tools Integrated Reasoning via Reinforcement Learning. [![[code]](https://img.shields.io/github/stars/weiyifan1023/AutoTIR)](https://github.com/weiyifan1023/AutoTIR)
+- [verl-tool](https://arxiv.org/pdf/2509.01055): A version of verl to support diverse tool use. [![[code]](https://img.shields.io/github/stars/TIGER-AI-Lab/verl-tool)](https://github.com/TIGER-AI-Lab/verl-tool)
+- [Tree-GRPO](https://arxiv.org/abs/2509.21240): Tree Search for LLM Agent Reinforcement Learning. [![[code]](https://img.shields.io/github/stars/AMAP-ML/Tree-GRPO)](https://github.com/AMAP-ML/Tree-GRPO)
+- [EviNote-RAG](https://arxiv.org/abs/2509.00877): Enhancing RAG Models via Answer-Supportive Evidence Notes. [![[code]](https://img.shields.io/github/stars/Da1yuqin/EviNoteRAG)](https://github.com/Da1yuqin/EviNoteRAG)
+- [GlobalRAG](https://arxiv.org/pdf/2510.20548v1): GlobalRAG: Enhancing Global Reasoning in Multi-hop Question Answering via Reinforcement Learning. [![[code]](https://img.shields.io/github/stars/CarnegieBin/GlobalRAG)](https://github.com/CarnegieBin/GlobalRAG)
+
+
+
+
+
+## Citations
+
+```bibtex
+@article{jin2025search,
+  title={Search-r1: Training llms to reason and leverage search engines with reinforcement learning},
+  author={Jin, Bowen and Zeng, Hansi and Yue, Zhenrui and Yoon, Jinsung and Arik, Sercan and Wang, Dong and Zamani, Hamed and Han, Jiawei},
+  journal={arXiv preprint arXiv:2503.09516},
+  year={2025}
+}
+```
+
+```bibtex
+@article{jin2025empirical,
+  title={An Empirical Study on Reinforcement Learning for Reasoning-Search Interleaved LLM Agents},
+  author={Jin, Bowen and Yoon, Jinsung and Kargupta, Priyanka and Arik, Sercan O and Han, Jiawei},
+  journal={arXiv preprint arXiv:2505.15117},
+  year={2025}
+}
+```
diff --git a/code/RL_model/verl/Search-R1/VERL_README.md b/code/RL_model/verl/Search-R1/VERL_README.md
new file mode 100644
index 0000000000000000000000000000000000000000..b6bc92a6fd3329a1ccdca91c06e2f950b5cd282a
--- /dev/null
+++ b/code/RL_model/verl/Search-R1/VERL_README.md
@@ -0,0 +1,103 @@
+<h1 style="text-align: center;">veRL: Volcano Engine Reinforcement Learning for LLM</h1>
+
+veRL is a flexible, efficient and production-ready RL training framework designed for large language models (LLMs). 
+
+veRL is the open-source version of **[HybridFlow: A Flexible and Efficient RLHF Framework](https://arxiv.org/abs/2409.19256v2)** paper.
+
+veRL is flexible and easy to use with:
+
+- **Easy extension of diverse RL algorithms**: The Hybrid programming model combines the strengths of single-controller and multi-controller paradigms to enable flexible representation and efficient execution of complex Post-Training dataflows. Allowing users to build RL dataflows in a few lines of code.
+
+- **Seamless integration of existing LLM infra with modular APIs**: Decouples computation and data dependencies, enabling seamless integration with existing LLM frameworks, such as PyTorch FSDP, Megatron-LM and vLLM. Moreover, users can easily extend to other LLM training and inference frameworks.
+
+- **Flexible device mapping**: Supports various placement of models onto different sets of GPUs for efficient resource utilization and scalability across different cluster sizes.
+
+- Readily integration with popular HuggingFace models
+
+
+veRL is fast with:
+
+- **State-of-the-art throughput**: By seamlessly integrating existing SOTA LLM training and inference frameworks, veRL achieves high generation and training throughput.
+
+- **Efficient actor model resharding with 3D-HybridEngine**: Eliminates memory redundancy and significantly reduces communication overhead during transitions between training and generation phases.
+
+<p align="center">
+| <a href="https://verl.readthedocs.io/en/latest/index.html"><b>Documentation</b></a> | <a href="https://arxiv.org/abs/2409.19256v2"><b>Paper</b></a> | <a href="https://join.slack.com/t/verlgroup/shared_invite/zt-2w5p9o4c3-yy0x2Q56s_VlGLsJ93A6vA"><b>Slack</b></a> | <a href="https://raw.githubusercontent.com/eric-haibin-lin/verl-community/refs/heads/main/WeChat.JPG"><b>Wechat</b></a> | 
+
+<!-- <a href=""><b>Slides</b></a> | -->
+</p>
+
+## News
+
+- [2024/12] The team presented <a href="https://neurips.cc/Expo/Conferences/2024/workshop/100677">Post-training LLMs: From Algorithms to Infrastructure</a> at NeurIPS 2024. [Slides](https://github.com/eric-haibin-lin/verl-data/tree/neurips) and [video](https://neurips.cc/Expo/Conferences/2024/workshop/100677) available.
+- [2024/10] veRL is presented at Ray Summit. [Youtube video](https://www.youtube.com/watch?v=MrhMcXkXvJU&list=PLzTswPQNepXntmT8jr9WaNfqQ60QwW7-U&index=37) available.
+- [2024/08] HybridFlow (verl) is accepted to EuroSys 2025.
+
+## Key Features
+
+- **FSDP** and **Megatron-LM** for training.
+- **vLLM** and **TGI** for rollout generation, **SGLang** support coming soon.
+- huggingface models support
+- Supervised fine-tuning
+- Reward model training
+- Reinforcement learning from human feedback with PPO
+- flash-attention integration, sequence packing
+- scales up to 70B models and hundreds of GPUs
+- experiment tracking with wandb and mlflow
+
+
+## Getting Started
+
+Checkout this [Jupyter Notebook](https://github.com/volcengine/verl/tree/main/examples/ppo_trainer/verl_getting_started.ipynb) to get started with PPO training with a single 24GB L4 GPU (**FREE** GPU quota provided by [Lighting Studio](https://lightning.ai/hlin-verl/studios/verl-getting-started))!
+
+**Quickstart:**
+- [Installation](https://verl.readthedocs.io/en/latest/start/install.html)
+- [Quickstart](https://verl.readthedocs.io/en/latest/start/quickstart.html)
+
+**Running an PPO example step-by-step:**
+- Data and Reward Preparation
+  - [Prepare Data (Parquet) for Post-Training](https://verl.readthedocs.io/en/latest/preparation/prepare_data.html)
+  - [Implement Reward Function for Dataset](https://verl.readthedocs.io/en/latest/preparation/reward_function.html)
+- Understanding the PPO Example
+  - [PPO Example Architecture](https://verl.readthedocs.io/en/latest/examples/ppo_code_architecture.html)
+  - [Config Explanation](https://verl.readthedocs.io/en/latest/examples/config.html)
+  - [Run GSM8K Example](https://verl.readthedocs.io/en/latest/examples/gsm8k_example.html)
+
+**Reproducible algorithm baselines:**
+- [PPO](https://verl.readthedocs.io/en/latest/experiment/ppo.html)
+
+**For code explanation and advance usage (extension):**
+- PPO Trainer and Workers
+  - [PPO Ray Trainer](https://verl.readthedocs.io/en/latest/workers/ray_trainer.html)
+  - [PyTorch FSDP Backend](https://verl.readthedocs.io/en/latest/workers/fsdp_workers.html)
+  - [Megatron-LM Backend](https://verl.readthedocs.io/en/latest/index.html)
+- Advance Usage and Extension
+  - [Ray API Design Tutorial](https://verl.readthedocs.io/en/latest/advance/placement.html)
+  - [Extend to other RL(HF) algorithms](https://verl.readthedocs.io/en/latest/advance/dpo_extension.html)
+  - [Add models with the FSDP backend](https://verl.readthedocs.io/en/latest/advance/fsdp_extension.html)
+  - [Add models with the Megatron-LM backend](https://verl.readthedocs.io/en/latest/advance/megatron_extension.html)
+
+
+## Citation and acknowledgement
+
+If you find the project helpful, please cite:
+- [HybridFlow: A Flexible and Efficient RLHF Framework](https://arxiv.org/abs/2409.19256v2)
+- [A Framework for Training Large Language Models for Code Generation via Proximal Policy Optimization](https://i.cs.hku.hk/~cwu/papers/gmsheng-NL2Code24.pdf)
+
+```tex
+@article{sheng2024hybridflow,
+  title   = {HybridFlow: A Flexible and Efficient RLHF Framework},
+  author  = {Guangming Sheng and Chi Zhang and Zilingfeng Ye and Xibin Wu and Wang Zhang and Ru Zhang and Yanghua Peng and Haibin Lin and Chuan Wu},
+  year    = {2024},
+  journal = {arXiv preprint arXiv: 2409.19256}
+}
+```
+
+verl is inspired by the design of Nemo-Aligner, Deepspeed-chat and OpenRLHF. The project is adopted and supported by Anyscale, Bytedance, LMSys.org, Shanghai AI Lab, Tsinghua University, UC Berkeley, UCLA, UIUC, and University of Hong Kong.
+
+## Publications Using veRL
+- [Enhancing Multi-Step Reasoning Abilities of Language Models through Direct Q-Function Optimization](https://arxiv.org/abs/2410.09302)
+- [Flaming-hot Initiation with Regular Execution Sampling for Large Language Models](https://arxiv.org/abs/2410.21236)
+- [Process Reinforcement Through Implicit Rewards](https://github.com/PRIME-RL/PRIME/)
+
+We are HIRING! Send us an [email](mailto:haibin.lin@bytedance.com) if you are interested in internship/FTE opportunities in MLSys/LLM reasoning/multimodal alignment.
diff --git a/code/RL_model/verl/Search-R1/infer.py b/code/RL_model/verl/Search-R1/infer.py
new file mode 100644
index 0000000000000000000000000000000000000000..5b93fa84f09b8fc9e6301f41e291c6cec2fb756b
--- /dev/null
+++ b/code/RL_model/verl/Search-R1/infer.py
@@ -0,0 +1,128 @@
+import transformers
+import torch
+import random
+from datasets import load_dataset
+import requests
+
+question = "Mike Barnett negotiated many contracts including which player that went on to become general manager of CSKA Moscow of the Kontinental Hockey League?"
+
+# Model ID and device setup
+model_id = "PeterJinGo/SearchR1-nq_hotpotqa_train-qwen2.5-7b-em-ppo"
+device = torch.device("cuda" if torch.cuda.is_available() else "cpu")
+
+question = question.strip()
+if question[-1] != '?':
+    question += '?'
+curr_eos = [151645, 151643] # for Qwen2.5 series models
+curr_search_template = '\n\n{output_text}<information>{search_results}</information>\n\n'
+
+# Prepare the message
+prompt = f"""Answer the given question. \
+You must conduct reasoning inside <think> and </think> first every time you get new information. \
+After reasoning, if you find you lack some knowledge, you can call a search engine by <search> query </search> and it will return the top searched results between <information> and </information>. \
+You can search as many times as your want. \
+If you find no further external knowledge needed, you can directly provide the answer inside <answer> and </answer>, without detailed illustrations. For example, <answer> Beijing </answer>. Question: {question}\n"""
+
+# Initialize the tokenizer and model
+tokenizer = transformers.AutoTokenizer.from_pretrained(model_id)
+model = transformers.AutoModelForCausalLM.from_pretrained(model_id, torch_dtype=torch.bfloat16, device_map="auto")
+
+# Define the custom stopping criterion
+class StopOnSequence(transformers.StoppingCriteria):
+    def __init__(self, target_sequences, tokenizer):
+        # Encode the string so we have the exact token-IDs pattern
+        self.target_ids = [tokenizer.encode(target_sequence, add_special_tokens=False) for target_sequence in target_sequences]
+        self.target_lengths = [len(target_id) for target_id in self.target_ids]
+        self._tokenizer = tokenizer
+
+    def __call__(self, input_ids, scores, **kwargs):
+        # Make sure the target IDs are on the same device
+        targets = [torch.as_tensor(target_id, device=input_ids.device) for target_id in self.target_ids]
+
+        if input_ids.shape[1] < min(self.target_lengths):
+            return False
+
+        # Compare the tail of input_ids with our target_ids
+        for i, target in enumerate(targets):
+            if torch.equal(input_ids[0, -self.target_lengths[i]:], target):
+                return True
+
+        return False
+
+def get_query(text):
+    import re
+    pattern = re.compile(r"<search>(.*?)</search>", re.DOTALL)
+    matches = pattern.findall(text)
+    if matches:
+        return matches[-1]
+    else:
+        return None
+
+def search(query: str):
+    payload = {
+            "queries": [query],
+            "topk": 3,
+            "return_scores": True
+        }
+    results = requests.post("http://127.0.0.1:8000/retrieve", json=payload).json()['result']
+                
+    def _passages2string(retrieval_result):
+        format_reference = ''
+        for idx, doc_item in enumerate(retrieval_result):
+                        
+            content = doc_item['document']['contents']
+            title = content.split("\n")[0]
+            text = "\n".join(content.split("\n")[1:])
+            format_reference += f"Doc {idx+1}(Title: {title}) {text}\n"
+        return format_reference
+
+    return _passages2string(results[0])
+
+
+# Initialize the stopping criteria
+target_sequences = ["</search>", " </search>", "</search>\n", " </search>\n", "</search>\n\n", " </search>\n\n"]
+stopping_criteria = transformers.StoppingCriteriaList([StopOnSequence(target_sequences, tokenizer)])
+
+cnt = 0
+
+if tokenizer.chat_template:
+    prompt = tokenizer.apply_chat_template([{"role": "user", "content": prompt}], add_generation_prompt=True, tokenize=False)
+
+print('\n\n################# [Start Reasoning + Searching] ##################\n\n')
+print(prompt)
+# Encode the chat-formatted prompt and move it to the correct device
+while True:
+    input_ids = tokenizer.encode(prompt, return_tensors='pt').to(device)
+    attention_mask = torch.ones_like(input_ids)
+    
+    # Generate text with the stopping criteria
+    outputs = model.generate(
+        input_ids,
+        attention_mask=attention_mask,
+        max_new_tokens=1024,
+        stopping_criteria=stopping_criteria,
+        pad_token_id=tokenizer.eos_token_id,
+        do_sample=True,
+        temperature=0.7
+    )
+
+    if outputs[0][-1].item() in curr_eos:
+        generated_tokens = outputs[0][input_ids.shape[1]:]
+        output_text = tokenizer.decode(generated_tokens, skip_special_tokens=True)
+        print(output_text)
+        break
+
+    generated_tokens = outputs[0][input_ids.shape[1]:]
+    output_text = tokenizer.decode(generated_tokens, skip_special_tokens=True)
+    
+    tmp_query = get_query(tokenizer.decode(outputs[0], skip_special_tokens=True))
+    if tmp_query:
+        # print(f'searching "{tmp_query}"...')
+        search_results = search(tmp_query)
+    else:
+        search_results = ''
+
+    search_text = curr_search_template.format(output_text=output_text, search_results=search_results)
+    prompt += search_text
+    cnt += 1
+    print(search_text)
diff --git a/code/RL_model/verl/Search-R1/llm_guard_3B_10k_v2.log b/code/RL_model/verl/Search-R1/llm_guard_3B_10k_v2.log
new file mode 100644
index 0000000000000000000000000000000000000000..5765569049f05b0d0b57ec38e94ce6b4fcffcd6e
--- /dev/null
+++ b/code/RL_model/verl/Search-R1/llm_guard_3B_10k_v2.log
@@ -0,0 +1,180 @@
+/home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/torch/cuda/__init__.py:63: FutureWarning: The pynvml package is deprecated. Please install nvidia-ml-py instead. If you did not install pynvml directly, please report this to the maintainers of the package that installed pynvml for you.
+  import pynvml  # type: ignore[import]
+2026-02-01 20:43:15,317	INFO worker.py:2014 -- Started a local Ray instance. View the dashboard at http://127.0.0.1:8301 
+/home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/ray/_private/worker.py:2062: FutureWarning: Tip: In future versions of Ray, Ray will no longer override accelerator visible devices env var if num_gpus=0 or num_gpus=None (default). To enable this behavior and turn off this error message, set RAY_ACCEL_ENV_VAR_OVERRIDE_ON_ZERO=0
+  warnings.warn(
+(pid=1646422) /home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/torch/cuda/__init__.py:63: FutureWarning: The pynvml package is deprecated. Please install nvidia-ml-py instead. If you did not install pynvml directly, please report this to the maintainers of the package that installed pynvml for you.
+(pid=1646422)   import pynvml  # type: ignore[import]
+(main_task pid=1646422) {'actor_rollout_ref': {'actor': {'clip_ratio': 0.2,
+(main_task pid=1646422)                                  'entropy_coeff': 0.001,
+(main_task pid=1646422)                                  'fsdp_config': {'fsdp_size': -1,
+(main_task pid=1646422)                                                  'grad_offload': False,
+(main_task pid=1646422)                                                  'optimizer_offload': True,
+(main_task pid=1646422)                                                  'param_offload': True,
+(main_task pid=1646422)                                                  'wrap_policy': {'min_num_params': 0}},
+(main_task pid=1646422)                                  'grad_clip': 1.0,
+(main_task pid=1646422)                                  'kl_loss_coef': 0.001,
+(main_task pid=1646422)                                  'kl_loss_type': 'low_var_kl',
+(main_task pid=1646422)                                  'optim': {'lr': 1e-06,
+(main_task pid=1646422)                                            'lr_warmup_steps_ratio': 0.0,
+(main_task pid=1646422)                                            'min_lr_ratio': None,
+(main_task pid=1646422)                                            'total_training_steps': -1,
+(main_task pid=1646422)                                            'warmup_style': 'constant'},
+(main_task pid=1646422)                                  'ppo_epochs': 1,
+(main_task pid=1646422)                                  'ppo_max_token_len_per_gpu': 16384,
+(main_task pid=1646422)                                  'ppo_micro_batch_size': 64,
+(main_task pid=1646422)                                  'ppo_micro_batch_size_per_gpu': 16,
+(main_task pid=1646422)                                  'ppo_mini_batch_size': 64,
+(main_task pid=1646422)                                  'shuffle': False,
+(main_task pid=1646422)                                  'state_masking': False,
+(main_task pid=1646422)                                  'strategy': 'fsdp',
+(main_task pid=1646422)                                  'ulysses_sequence_parallel_size': 1,
+(main_task pid=1646422)                                  'use_dynamic_bsz': False,
+(main_task pid=1646422)                                  'use_kl_loss': False},
+(main_task pid=1646422)                        'hybrid_engine': True,
+(main_task pid=1646422)                        'model': {'enable_gradient_checkpointing': True,
+(main_task pid=1646422)                                  'external_lib': None,
+(main_task pid=1646422)                                  'override_config': {},
+(main_task pid=1646422)                                  'path': 'Qwen/Qwen3-4B-Instruct-2507',
+(main_task pid=1646422)                                  'use_remove_padding': False},
+(main_task pid=1646422)                        'ref': {'fsdp_config': {'fsdp_size': -1,
+(main_task pid=1646422)                                                'param_offload': True,
+(main_task pid=1646422)                                                'wrap_policy': {'min_num_params': 0}},
+(main_task pid=1646422)                                'log_prob_max_token_len_per_gpu': 16384,
+(main_task pid=1646422)                                'log_prob_micro_batch_size': 64,
+(main_task pid=1646422)                                'log_prob_use_dynamic_bsz': False,
+(main_task pid=1646422)                                'ulysses_sequence_parallel_size': 1},
+(main_task pid=1646422)                        'rollout': {'do_sample': True,
+(main_task pid=1646422)                                    'dtype': 'bfloat16',
+(main_task pid=1646422)                                    'enforce_eager': True,
+(main_task pid=1646422)                                    'free_cache_engine': True,
+(main_task pid=1646422)                                    'gpu_memory_utilization': 0.4,
+(main_task pid=1646422)                                    'ignore_eos': False,
+(main_task pid=1646422)                                    'load_format': 'dummy_dtensor',
+(main_task pid=1646422)                                    'log_prob_max_token_len_per_gpu': 16384,
+(main_task pid=1646422)                                    'log_prob_micro_batch_size': 64,
+(main_task pid=1646422)                                    'log_prob_use_dynamic_bsz': False,
+(main_task pid=1646422)                                    'max_num_batched_tokens': 8192,
+(main_task pid=1646422)                                    'max_num_seqs': 1024,
+(main_task pid=1646422)                                    'n': 1,
+(main_task pid=1646422)                                    'n_agent': 1,
+(main_task pid=1646422)                                    'name': 'vllm',
+(main_task pid=1646422)                                    'prompt_length': 4096,
+(main_task pid=1646422)                                    'response_length': 1024,
+(main_task pid=1646422)                                    'temperature': 1.0,
+(main_task pid=1646422)                                    'tensor_model_parallel_size': 1,
+(main_task pid=1646422)                                    'top_k': -1,
+(main_task pid=1646422)                                    'top_p': 0.95}},
+(main_task pid=1646422)  'algorithm': {'adv_estimator': 'grpo',
+(main_task pid=1646422)                'gamma': 1.0,
+(main_task pid=1646422)                'kl_ctrl': {'kl_coef': 0.001, 'type': 'fixed'},
+(main_task pid=1646422)                'kl_penalty': 'kl',
+(main_task pid=1646422)                'lam': 1.0,
+(main_task pid=1646422)                'no_think_rl': False,
+(main_task pid=1646422)                'state_masking': {'end_state_marker': '</information>',
+(main_task pid=1646422)                                  'start_state_marker': '<information>'}},
+(main_task pid=1646422)  'critic': {'cliprange_value': 0.5,
+(main_task pid=1646422)             'forward_max_token_len_per_gpu': 32768,
+(main_task pid=1646422)             'forward_micro_batch_size': 64,
+(main_task pid=1646422)             'grad_clip': 1.0,
+(main_task pid=1646422)             'model': {'enable_gradient_checkpointing': False,
+(main_task pid=1646422)                       'external_lib': None,
+(main_task pid=1646422)                       'fsdp_config': {'fsdp_size': -1,
+(main_task pid=1646422)                                       'grad_offload': False,
+(main_task pid=1646422)                                       'optimizer_offload': False,
+(main_task pid=1646422)                                       'param_offload': False,
+(main_task pid=1646422)                                       'wrap_policy': {'min_num_params': 0}},
+(main_task pid=1646422)                       'override_config': {},
+(main_task pid=1646422)                       'path': '~/models/deepseek-llm-7b-chat',
+(main_task pid=1646422)                       'tokenizer_path': 'Qwen/Qwen3-4B-Instruct-2507',
+(main_task pid=1646422)                       'use_remove_padding': False},
+(main_task pid=1646422)             'optim': {'lr': 1e-05,
+(main_task pid=1646422)                       'lr_warmup_steps_ratio': 0.0,
+(main_task pid=1646422)                       'min_lr_ratio': None,
+(main_task pid=1646422)                       'total_training_steps': -1,
+(main_task pid=1646422)                       'warmup_style': 'constant'},
+(main_task pid=1646422)             'ppo_epochs': 1,
+(main_task pid=1646422)             'ppo_max_token_len_per_gpu': 32768,
+(main_task pid=1646422)             'ppo_micro_batch_size': 64,
+(main_task pid=1646422)             'ppo_mini_batch_size': 64,
+(main_task pid=1646422)             'shuffle': False,
+(main_task pid=1646422)             'strategy': 'fsdp',
+(main_task pid=1646422)             'ulysses_sequence_parallel_size': 1,
+(main_task pid=1646422)             'use_dynamic_bsz': False},
+(main_task pid=1646422)  'data': {'max_obs_length': 512,
+(main_task pid=1646422)           'max_prompt_length': 4096,
+(main_task pid=1646422)           'max_response_length': 1024,
+(main_task pid=1646422)           'max_start_length': 256,
+(main_task pid=1646422)           'prompt_key': 'prompt',
+(main_task pid=1646422)           'return_raw_chat': False,
+(main_task pid=1646422)           'return_raw_input_ids': False,
+(main_task pid=1646422)           'shuffle_train_dataloader': True,
+(main_task pid=1646422)           'tokenizer': None,
+(main_task pid=1646422)           'train_batch_size': 128,
+(main_task pid=1646422)           'train_data_num': None,
+(main_task pid=1646422)           'train_files': '/home/mshahidul/readctrl/code/RL_model/verl/Search-R1/dataset/train.parquet',
+(main_task pid=1646422)           'val_batch_size': 64,
+(main_task pid=1646422)           'val_data_num': None,
+(main_task pid=1646422)           'val_files': '/home/mshahidul/readctrl/code/RL_model/verl/Search-R1/dataset/test.parquet'},
+(main_task pid=1646422)  'do_search': False,
+(main_task pid=1646422)  'max_turns': 1,
+(main_task pid=1646422)  'retriever': {'topk': 3, 'url': 'http://127.0.0.1:8000/retrieve'},
+(main_task pid=1646422)  'reward_model': {'enable': False,
+(main_task pid=1646422)                   'final_format_score': 0,
+(main_task pid=1646422)                   'forward_max_token_len_per_gpu': 32768,
+(main_task pid=1646422)                   'max_length': None,
+(main_task pid=1646422)                   'micro_batch_size': 64,
+(main_task pid=1646422)                   'model': {'external_lib': None,
+(main_task pid=1646422)                             'fsdp_config': {'min_num_params': 0,
+(main_task pid=1646422)                                             'param_offload': False},
+(main_task pid=1646422)                             'input_tokenizer': 'Qwen/Qwen3-4B-Instruct-2507',
+(main_task pid=1646422)                             'path': '~/models/FsfairX-LLaMA3-RM-v0.1',
+(main_task pid=1646422)                             'use_remove_padding': False},
+(main_task pid=1646422)                   'retrieval_score': 0,
+(main_task pid=1646422)                   'strategy': 'fsdp',
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+(main_task pid=1646422)                   'ulysses_sequence_parallel_size': 1,
+(main_task pid=1646422)                   'use_dynamic_bsz': False},
+(main_task pid=1646422)  'trainer': {'critic_warmup': 0,
+(main_task pid=1646422)              'default_hdfs_dir': '~/experiments/gsm8k/ppo/llm_guard_3B_10k_v2',
+(main_task pid=1646422)              'default_local_dir': 'verl_checkpoints/llm_guard_3B_10k_v2',
+(main_task pid=1646422)              'experiment_name': 'llm_guard_3B_10k_v2',
+(main_task pid=1646422)              'logger': ['wandb'],
+(main_task pid=1646422)              'n_gpus_per_node': 2,
+(main_task pid=1646422)              'nnodes': 1,
+(main_task pid=1646422)              'project_name': '',
+(main_task pid=1646422)              'save_freq': 100,
+(main_task pid=1646422)              'test_freq': 50,
+(main_task pid=1646422)              'total_epochs': 15,
+(main_task pid=1646422)              'total_training_steps': 1005}}
+(main_task pid=1646422) W0201 20:43:46.380000 1646422 /data/home_beta/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/torch/utils/cpp_extension.py:117] No CUDA runtime is found, using CUDA_HOME='/usr/local/cuda'
+Error executing job with overrides: ['data.train_files=/home/mshahidul/readctrl/code/RL_model/verl/Search-R1/dataset/train.parquet', 'data.val_files=/home/mshahidul/readctrl/code/RL_model/verl/Search-R1/dataset/test.parquet', 'data.train_batch_size=128', 'data.val_batch_size=64', 'data.max_prompt_length=4096', 'data.max_response_length=1024', 'data.shuffle_train_dataloader=True', 'algorithm.adv_estimator=grpo', 'actor_rollout_ref.model.path=Qwen/Qwen3-4B-Instruct-2507', 'actor_rollout_ref.model.enable_gradient_checkpointing=true', 'actor_rollout_ref.model.use_remove_padding=False', 'actor_rollout_ref.actor.optim.lr=1e-6', 'actor_rollout_ref.actor.ppo_mini_batch_size=64', '+actor_rollout_ref.actor.ppo_micro_batch_size_per_gpu=16', 'actor_rollout_ref.actor.fsdp_config.param_offload=true', 'actor_rollout_ref.actor.fsdp_config.optimizer_offload=true', 'actor_rollout_ref.rollout.log_prob_micro_batch_size=64', 'actor_rollout_ref.rollout.tensor_model_parallel_size=1', 'actor_rollout_ref.rollout.name=vllm', 'actor_rollout_ref.rollout.gpu_memory_utilization=0.4', 'actor_rollout_ref.ref.log_prob_micro_batch_size=64', 'actor_rollout_ref.ref.fsdp_config.param_offload=True', 'actor_rollout_ref.actor.kl_loss_coef=0.001', 'trainer.logger=[wandb]', 'trainer.n_gpus_per_node=2', 'trainer.nnodes=1', 'trainer.save_freq=100', 'trainer.test_freq=50', 'trainer.project_name=', 'trainer.experiment_name=llm_guard_3B_10k_v2', 'trainer.total_epochs=15', 'trainer.total_training_steps=1005', 'trainer.default_local_dir=verl_checkpoints/llm_guard_3B_10k_v2', 'do_search=false', 'max_turns=1']
+Traceback (most recent call last):
+  File "/data/home_beta/mshahidul/readctrl/code/RL_model/verl/Search-R1/verl/trainer/main_ppo.py", line 110, in main
+    ray.get(main_task.remote(config))
+  File "/home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/ray/_private/auto_init_hook.py", line 22, in auto_init_wrapper
+    return fn(*args, **kwargs)
+           ^^^^^^^^^^^^^^^^^^^
+  File "/home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/ray/_private/client_mode_hook.py", line 104, in wrapper
+    return func(*args, **kwargs)
+           ^^^^^^^^^^^^^^^^^^^^^
+  File "/home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/ray/_private/worker.py", line 2972, in get
+    values, debugger_breakpoint = worker.get_objects(
+                                  ^^^^^^^^^^^^^^^^^^^
+  File "/home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/ray/_private/worker.py", line 1031, in get_objects
+    raise value.as_instanceof_cause()
+ray.exceptions.RayTaskError(ImportError): ray::main_task() (pid=1646422, ip=172.16.34.29)
+  File "/data/home_beta/mshahidul/readctrl/code/RL_model/verl/Search-R1/verl/trainer/main_ppo.py", line 136, in main_task
+    from verl.workers.fsdp_workers import ActorRolloutRefWorker, CriticWorker
+  File "/data/home_beta/mshahidul/readctrl/code/RL_model/verl/Search-R1/verl/workers/fsdp_workers.py", line 39, in <module>
+    from verl.workers.sharding_manager.fsdp_ulysses import FSDPUlyssesShardingManager
+  File "/data/home_beta/mshahidul/readctrl/code/RL_model/verl/Search-R1/verl/workers/sharding_manager/__init__.py", line 23, in <module>
+    from .megatron_vllm import AllGatherPPModel, MegatronVLLMShardingManager
+  File "/data/home_beta/mshahidul/readctrl/code/RL_model/verl/Search-R1/verl/workers/sharding_manager/megatron_vllm.py", line 230, in <module>
+    from verl.third_party.vllm import parallel_state as vllm_ps
+  File "/data/home_beta/mshahidul/readctrl/code/RL_model/verl/Search-R1/verl/third_party/vllm/__init__.py", line 52, in <module>
+    from vllm import LLM, LLMEngine, parallel_state
+ImportError: cannot import name 'parallel_state' from 'vllm' (/home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/vllm/__init__.py)
+
+Set the environment variable HYDRA_FULL_ERROR=1 for a complete stack trace.
+[W201 20:43:50.186179538 AllocatorConfig.cpp:28] Warning: PYTORCH_CUDA_ALLOC_CONF is deprecated, use PYTORCH_ALLOC_CONF instead (function operator())
diff --git a/code/RL_model/verl/Search-R1/pyproject.toml b/code/RL_model/verl/Search-R1/pyproject.toml
new file mode 100644
index 0000000000000000000000000000000000000000..3d361848f54f7fc2da0b6cfafedfadc42e91de7b
--- /dev/null
+++ b/code/RL_model/verl/Search-R1/pyproject.toml
@@ -0,0 +1,78 @@
+# -------------------------------
+# build-system
+# -------------------------------
+[build-system]
+requires = [
+    "setuptools>=61.0",
+    "wheel"
+]
+build-backend = "setuptools.build_meta"
+
+# -------------------------------
+# project (PEP 621 metadata)
+# -------------------------------
+[project]
+name = "verl"
+# We'll mark the version as "dynamic" because it's read from the file "verl/version/version" 
+# (PEP 621 calls this "dynamic version"). 
+# The actual version is specified in the [tool.setuptools.dynamic] section below.
+dynamic = ["version"]
+
+description = "veRL: Volcano Engine Reinforcement Learning for LLM"
+license = {file = "LICENSE"}  # or "Apache-2.0", if you prefer an SPDX identifier
+readme = {file = "README.md", content-type = "text/markdown"}
+requires-python = ">=3.8"
+
+authors = [
+  { name = "Bytedance - Seed - MLSys", email = "zhangchi.usc1992@bytedance.com" },
+  { name = "Bytedance - Seed - MLSys", email = "gmsheng@connect.hku.hk" },
+]
+
+# Dependencies corresponding to install_requires in setup.py
+dependencies = [
+    "accelerate",
+    "codetiming",
+    "datasets",
+    "dill",
+    "hydra-core",
+    "numpy",
+    "pybind11",
+    "ray",
+    "tensordict",
+    "transformers<4.48",
+    "vllm<=0.6.3",
+]
+
+# Optional dependencies (extras_require in setup.py)
+[project.optional-dependencies]
+test = [
+  "pytest", "yapf"
+]
+
+# URLs
+[project.urls]
+Homepage = "https://github.com/volcengine/verl"
+
+# -------------------------------
+# tool.setuptools - Additional config
+# -------------------------------
+[tool.setuptools]
+# True means `setuptools` will attempt to include all relevant files in package_data automatically.
+# This corresponds to `include_package_data=True` in setup.py.
+include-package-data = true
+
+# We read the version from a file in 'verl/version/version'
+[tool.setuptools.dynamic]
+version = {file = "verl/version/version"}
+
+# If you need to mimic `package_dir={'': '.'}`:
+[tool.setuptools.package-dir]
+"" = "."
+
+# If you need to include specific non-Python data (like YAML files or version file):
+# This is the rough equivalent of package_data={'': ['version/*'], 'verl': ['trainer/config/*.yaml']}
+[tool.setuptools.package-data]
+verl = [
+  "version/*",
+  "trainer/config/*.yaml"
+]
\ No newline at end of file
diff --git a/code/RL_model/verl/Search-R1/requirements.txt b/code/RL_model/verl/Search-R1/requirements.txt
new file mode 100644
index 0000000000000000000000000000000000000000..5381179bae61fa7ef65e98b483544e57b0f671bb
--- /dev/null
+++ b/code/RL_model/verl/Search-R1/requirements.txt
@@ -0,0 +1,16 @@
+accelerate
+codetiming
+datasets
+dill
+flash-attn
+hydra-core
+numpy
+pandas
+pybind11
+ray
+tensordict<0.6
+transformers<4.48
+vllm<=0.6.3
+wandb
+IPython
+matplotlib
\ No newline at end of file
diff --git a/code/RL_model/verl/Search-R1/retrieval_launch.sh b/code/RL_model/verl/Search-R1/retrieval_launch.sh
new file mode 100644
index 0000000000000000000000000000000000000000..c561b1fc0eaf69472ece7eb96afd42c0186ff284
--- /dev/null
+++ b/code/RL_model/verl/Search-R1/retrieval_launch.sh
@@ -0,0 +1,13 @@
+
+file_path=/the/path/you/save/corpus
+index_file=$file_path/e5_Flat.index
+corpus_file=$file_path/wiki-18.jsonl
+retriever_name=e5
+retriever_path=intfloat/e5-base-v2
+
+python search_r1/search/retrieval_server.py --index_path $index_file \
+                                            --corpus_path $corpus_file \
+                                            --topk 3 \
+                                            --retriever_name $retriever_name \
+                                            --retriever_model $retriever_path \
+                                            --faiss_gpu
diff --git a/code/RL_model/verl/Search-R1/setup.py b/code/RL_model/verl/Search-R1/setup.py
new file mode 100644
index 0000000000000000000000000000000000000000..9aab68a3e8959317a9fbec484b9623912e633250
--- /dev/null
+++ b/code/RL_model/verl/Search-R1/setup.py
@@ -0,0 +1,54 @@
+# Copyright 2024 Bytedance Ltd. and/or its affiliates
+#
+# Licensed under the Apache License, Version 2.0 (the "License");
+# you may not use this file except in compliance with the License.
+# You may obtain a copy of the License at
+#
+#     http://www.apache.org/licenses/LICENSE-2.0
+#
+# Unless required by applicable law or agreed to in writing, software
+# distributed under the License is distributed on an "AS IS" BASIS,
+# WITHOUT WARRANTIES OR CONDITIONS OF ANY KIND, either express or implied.
+# See the License for the specific language governing permissions and
+# limitations under the License.
+
+# setup.py is the fallback installation script when pyproject.toml does not work
+from setuptools import setup, find_packages
+import os
+
+version_folder = os.path.dirname(os.path.join(os.path.abspath(__file__)))
+
+with open(os.path.join(version_folder, 'verl/version/version')) as f:
+    __version__ = f.read().strip()
+
+
+with open('requirements.txt') as f:
+    required = f.read().splitlines()
+    install_requires = [item.strip() for item in required if item.strip()[0] != '#']
+
+extras_require = {
+    'test': ['pytest', 'yapf']
+}
+
+from pathlib import Path
+this_directory = Path(__file__).parent
+long_description = (this_directory / "README.md").read_text()
+
+setup(
+    name='verl',
+    version=__version__,
+    package_dir={'': '.'},
+    packages=find_packages(where='.'),
+    url='https://github.com/volcengine/verl',
+    license='Apache 2.0',
+    author='Bytedance - Seed - MLSys',
+    author_email='zhangchi.usc1992@bytedance.com, gmsheng@connect.hku.hk',
+    description='veRL: Volcano Engine Reinforcement Learning for LLM',
+    install_requires=install_requires,
+    extras_require=extras_require,
+    package_data={'': ['version/*'],
+                  'verl': ['trainer/config/*.yaml'],},
+    include_package_data=True,
+    long_description=long_description,
+    long_description_content_type='text/markdown'
+)
\ No newline at end of file
diff --git a/code/RL_model/verl/Search-R1/train_grpo.sh b/code/RL_model/verl/Search-R1/train_grpo.sh
new file mode 100644
index 0000000000000000000000000000000000000000..51acdc48bc0fc072c1ac4a6e7fd394204bdcfb03
--- /dev/null
+++ b/code/RL_model/verl/Search-R1/train_grpo.sh
@@ -0,0 +1,46 @@
+
+export PYTORCH_CUDA_ALLOC_CONF=""
+export EXPERIMENT_NAME=llm_guard_3B_10k_v2
+export WAND_PROJECT='guard'
+export CUDA_DEVICE_ORDER="PCI_BUS_ID"
+export CUDA_VISIBLE_DEVICES=1,2
+export VLLM_ATTENTION_BACKEND=FLASH_ATTN
+
+
+PYTHONUNBUFFERED=1 NCCL_P2P_DISABLE=1 NCCL_IB_DISABLE=1 python3 -m verl.trainer.main_ppo \
+    data.train_files=/home/mshahidul/readctrl/code/RL_model/verl/Search-R1/dataset/train.parquet \
+    data.val_files=/home/mshahidul/readctrl/code/RL_model/verl/Search-R1/dataset/test.parquet \
+    data.train_batch_size=64 \
+    data.val_batch_size=64 \
+    data.max_prompt_length=4096 \
+    data.max_response_length=1024 \
+    data.shuffle_train_dataloader=True \
+    algorithm.adv_estimator=grpo \
+    actor_rollout_ref.model.path=Qwen/Qwen3-4B-Instruct-2507 \
+    actor_rollout_ref.model.enable_gradient_checkpointing=true \
+    actor_rollout_ref.model.use_remove_padding=False \
+    actor_rollout_ref.actor.optim.lr=1e-6 \
+    actor_rollout_ref.actor.ppo_mini_batch_size=64 \
+    +actor_rollout_ref.actor.ppo_micro_batch_size_per_gpu=16 \
+    actor_rollout_ref.actor.fsdp_config.param_offload=true \
+    actor_rollout_ref.actor.fsdp_config.optimizer_offload=true \
+    actor_rollout_ref.rollout.log_prob_micro_batch_size=64 \
+    actor_rollout_ref.rollout.tensor_model_parallel_size=1 \
+    actor_rollout_ref.rollout.name=vllm \
+    actor_rollout_ref.rollout.gpu_memory_utilization=0.4 \
+    actor_rollout_ref.ref.log_prob_micro_batch_size=64 \
+    actor_rollout_ref.ref.fsdp_config.param_offload=True \
+    actor_rollout_ref.actor.kl_loss_coef=0.001 \
+    trainer.logger=['wandb'] \
+    trainer.n_gpus_per_node=2 \
+    trainer.nnodes=1 \
+    trainer.save_freq=100 \
+    trainer.test_freq=50 \
+    trainer.project_name=$WANDB_PROJECT \
+    trainer.experiment_name=$EXPERIMENT_NAME \
+    trainer.total_epochs=15 \
+    trainer.total_training_steps=1005 \
+    trainer.default_local_dir=verl_checkpoints/$EXPERIMENT_NAME \
+    do_search=false \
+    max_turns=1 \
+    2>&1 | tee $EXPERIMENT_NAME.log
\ No newline at end of file
diff --git a/code/RL_model/verl/Search-R1/train_ppo.sh b/code/RL_model/verl/Search-R1/train_ppo.sh
new file mode 100644
index 0000000000000000000000000000000000000000..961fa6e98ff189786e3545748729c27e2fb9be05
--- /dev/null
+++ b/code/RL_model/verl/Search-R1/train_ppo.sh
@@ -0,0 +1,90 @@
+export CUDA_VISIBLE_DEVICES=0,1,2,3,4,5,6,7
+export DATA_DIR='data/nq_search'
+
+WAND_PROJECT='Search-R1'
+
+export BASE_MODEL='meta-llama/Llama-3.2-3B'
+export EXPERIMENT_NAME=nq-search-r1-ppo-llama3.2-3b-em
+# export BASE_MODEL='meta-llama/Llama-3.2-3B-Instruct'
+# export EXPERIMENT_NAME=nq-search-r1-ppo-llama3.2-3b-it-em
+# export BASE_MODEL='meta-llama/Llama-3.1-8B'
+# export EXPERIMENT_NAME=nq-search-r1-ppo-llama3.1-8b-em
+# export BASE_MODEL='meta-llama/Llama-3.1-8B-Instruct'
+# export EXPERIMENT_NAME=nq-search-r1-ppo-llama3.1-8b-it-em
+
+# export BASE_MODEL='Qwen/Qwen2.5-3B'
+# export EXPERIMENT_NAME=nq-search-r1-ppo-qwen2.5-3b-em
+# export BASE_MODEL='Qwen/Qwen2.5-3B-Instruct'
+# export EXPERIMENT_NAME=nq-search-r1-ppo-qwen2.5-3b-it-em
+# export BASE_MODEL='Qwen/Qwen2.5-7B'
+# export EXPERIMENT_NAME=nq-search-r1-ppo-qwen2.5-7b-em
+# export BASE_MODEL='Qwen/Qwen2.5-7B-Instruct'
+# export EXPERIMENT_NAME=nq-search-r1-ppo-qwen2.5-7b-it-em
+
+# set -x
+export VLLM_ATTENTION_BACKEND=XFORMERS # vllm + qwen2-7b with flash_attn has some issues
+
+# max_prompt_length = (config['training']['max_start_length'] + config['training']['max_response_length'] * (config['training']['max_turns'] - 1) + config['training']['max_obs_length'] * config['training']['max_turns'])
+
+PYTHONUNBUFFERED=1 python3 -m verl.trainer.main_ppo \
+    data.train_files=$DATA_DIR/train.parquet \
+    data.val_files=$DATA_DIR/test.parquet \
+    data.train_data_num=null \
+    data.val_data_num=null \
+    data.train_batch_size=512 \
+    data.val_batch_size=256 \
+    data.max_prompt_length=4096 \
+    data.max_response_length=500 \
+    data.max_start_length=2048 \
+    data.max_obs_length=500 \
+    data.shuffle_train_dataloader=True \
+    algorithm.adv_estimator=gae \
+    actor_rollout_ref.model.path=$BASE_MODEL \
+    actor_rollout_ref.actor.optim.lr=1e-6 \
+    actor_rollout_ref.model.enable_gradient_checkpointing=true \
+    actor_rollout_ref.model.use_remove_padding=True \
+    actor_rollout_ref.actor.optim.lr_warmup_steps_ratio=0.285 \
+    actor_rollout_ref.actor.ppo_mini_batch_size=256 \
+    actor_rollout_ref.actor.ppo_micro_batch_size=64 \
+    actor_rollout_ref.actor.fsdp_config.param_offload=true \
+    actor_rollout_ref.actor.fsdp_config.grad_offload=true \
+    actor_rollout_ref.actor.fsdp_config.optimizer_offload=true \
+    actor_rollout_ref.rollout.log_prob_micro_batch_size=128 \
+    actor_rollout_ref.rollout.tensor_model_parallel_size=1 \
+    actor_rollout_ref.rollout.name=vllm \
+    actor_rollout_ref.rollout.gpu_memory_utilization=0.6 \
+    actor_rollout_ref.ref.log_prob_micro_batch_size=128 \
+    actor_rollout_ref.ref.fsdp_config.param_offload=True \
+    actor_rollout_ref.rollout.n_agent=1 \
+    actor_rollout_ref.rollout.temperature=1 \
+    actor_rollout_ref.actor.state_masking=true \
+    critic.optim.lr=1e-5 \
+    critic.model.use_remove_padding=True \
+    critic.optim.lr_warmup_steps_ratio=0.015 \
+    critic.model.path=$BASE_MODEL \
+    critic.model.enable_gradient_checkpointing=true \
+    critic.ppo_micro_batch_size=8 \
+    critic.model.fsdp_config.param_offload=true \
+    critic.model.fsdp_config.grad_offload=true \
+    critic.model.fsdp_config.optimizer_offload=true \
+    algorithm.kl_ctrl.kl_coef=0.001 \
+    algorithm.no_think_rl=false \
+    trainer.critic_warmup=0 \
+    trainer.logger=['wandb'] \
+    +trainer.val_only=false \
+    +trainer.val_before_train=true \
+    trainer.default_hdfs_dir=null \
+    trainer.n_gpus_per_node=8 \
+    trainer.nnodes=1 \
+    trainer.save_freq=100 \
+    trainer.test_freq=50 \
+    trainer.project_name=$WAND_PROJECT \
+    trainer.experiment_name=$EXPERIMENT_NAME \
+    trainer.total_epochs=15 \
+    trainer.total_training_steps=1005 \
+    trainer.default_hdfs_dir=null \
+    trainer.default_local_dir=verl_checkpoints/$EXPERIMENT_NAME \
+    max_turns=2 \
+    retriever.url="http://127.0.0.1:8000/retrieve" \
+    retriever.topk=3 \
+    2>&1 | tee $EXPERIMENT_NAME.log
\ No newline at end of file
diff --git a/code/RL_model/verl/verl_train/.git-blame-ignore-revs b/code/RL_model/verl/verl_train/.git-blame-ignore-revs
new file mode 100644
index 0000000000000000000000000000000000000000..649ba3ca862e8e47a92b932b337fe189fbd14e7c
--- /dev/null
+++ b/code/RL_model/verl/verl_train/.git-blame-ignore-revs
@@ -0,0 +1,13 @@
+# Local uasge: git config blame.ignoreRevsFile .git-blame-ignore-revs
+
+# [dev] feat: immigrate from yapf & pylint to ruff based on pre-commit
+# Changed 268 files, +10k/-9k lines. This is the biggest formatter change.
+b00f77d8559b48d57a33c0132a5ba1c81891a536
+
+# [ci] refactor: reduce ruff line-length from 300 to 120
+# Changed 238 files, +6k/-1k lines. Global formatting change.
+00a10a8ef389556f957a2f36132b2358fd6a109f
+
+# [Lint] fix: linting errors in all files
+# Changed 179 files, +1k/-3k lines. Global lint fix.
+8e5ad4688a13de81727c014a3c2e2fb26324bc20
diff --git a/code/RL_model/verl/verl_train/.gitignore b/code/RL_model/verl/verl_train/.gitignore
new file mode 100644
index 0000000000000000000000000000000000000000..62d4dcfc815ec735f6acd244457bd0708ff62a2e
--- /dev/null
+++ b/code/RL_model/verl/verl_train/.gitignore
@@ -0,0 +1,130 @@
+**/*.pt
+**/checkpoints
+**/wget-log
+**/_build/
+**/*.ckpt
+**/outputs
+**/*.tar.gz
+**/playground
+**/wandb
+
+# Byte-compiled / optimized / DLL files
+__pycache__/
+*.py[cod]
+*$py.class
+dataset/*
+tensorflow/my_graph/*
+.idea/
+# C extensions
+*.so
+
+# Distribution / packaging
+.Python
+# env/
+build/
+develop-eggs/
+dist/
+downloads/
+eggs/
+.eggs/
+lib/
+lib64/
+parts/
+sdist/
+var/
+tmp/
+*.egg-info/
+.installed.cfg
+*.egg
+
+# PyInstaller
+#  Usually these files are written by a python script from a template
+#  before PyInstaller builds the exe, so as to inject date/other infos into it.
+*.manifest
+*.spec
+
+# Installer logs
+pip-log.txt
+pip-delete-this-directory.txt
+
+# Unit test / coverage reports
+htmlcov/
+.tox/
+.coverage
+.coverage.*
+.cache
+nosetests.xml
+coverage.xml
+*,cover
+.hypothesis/
+pytest.ini
+output.txt
+
+# Translations
+*.mo
+*.pot
+
+# Django stuff:
+*.log
+local_settings.py
+
+# Flask stuff:
+instance/
+.webassets-cache
+
+# Scrapy stuff:
+.scrapy
+
+# Sphinx documentation
+docs/_build/
+
+# PyBuilder
+target/
+
+# IPython Notebook
+.ipynb_checkpoints
+
+# pyenv
+.python-version
+
+# celery beat schedule file
+celerybeat-schedule
+
+# dotenv
+.env
+
+# virtualenv
+venv/
+.venv/
+ENV/
+
+# Spyder project settings
+.spyderproject
+
+# Rope project settings
+.ropeproject
+
+# vscode
+.vscode
+
+# Mac
+.DS_Store
+
+# vim
+*.swp
+
+# emacs
+*~
+
+# ckpt
+*.lock
+
+# data
+*.parquet
+
+
+# local logs
+logs
+log
+outputs
+.history
\ No newline at end of file
diff --git a/code/RL_model/verl/verl_train/.gitmodules b/code/RL_model/verl/verl_train/.gitmodules
new file mode 100644
index 0000000000000000000000000000000000000000..d5dd7a6aa577ccb64650ca389b699e04fd7af259
--- /dev/null
+++ b/code/RL_model/verl/verl_train/.gitmodules
@@ -0,0 +1,3 @@
+[submodule "recipe"]
+	path = recipe
+	url = https://github.com/verl-project/verl-recipe.git
diff --git a/code/RL_model/verl/verl_train/.log b/code/RL_model/verl/verl_train/.log
new file mode 100644
index 0000000000000000000000000000000000000000..41772b83a5c9d291049f0234e685abced811da44
--- /dev/null
+++ b/code/RL_model/verl/verl_train/.log
@@ -0,0 +1,1123 @@
+/home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/torch/cuda/__init__.py:63: FutureWarning: The pynvml package is deprecated. Please install nvidia-ml-py instead. If you did not install pynvml directly, please report this to the maintainers of the package that installed pynvml for you.
+  import pynvml  # type: ignore[import]
+INFO 02-07 12:56:22 [__init__.py:216] Automatically detected platform cuda.
+/home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/models/backends.py:21: UserWarning: Apex is not installed. Falling back to Torch Norm
+  warnings.warn("Apex is not installed. Falling back to Torch Norm")
+/home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/optimizer/__init__.py:18: UserWarning: Transformer Engine and Apex are not installed. Falling back to Torch optimizers.
+  warnings.warn(
+/home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/optimizer/optimizer.py:28: UserWarning: Transformer Engine and Apex are not installed. Falling back to local implementations of multi_tensor_applier and multi_tensor_scale
+  warnings.warn(
+/home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/optimizer/clip_grads.py:29: UserWarning: Transformer Engine and Apex are not installed. Falling back to local implementations of multi_tensor_applier, multi_tensor_l2norm, and multi_tensor_scale
+  warnings.warn(
+/home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/models/gpt/gpt_layer_specs.py:67: UserWarning: Apex is not installed. Falling back to Torch Norm
+  warnings.warn("Apex is not installed. Falling back to Torch Norm")
+ray init kwargs: {'num_cpus': None, 'runtime_env': {'env_vars': {'TOKENIZERS_PARALLELISM': 'true', 'NCCL_DEBUG': 'WARN', 'VLLM_LOGGING_LEVEL': 'WARN', 'VLLM_ALLOW_RUNTIME_LORA_UPDATING': 'true', 'CUDA_DEVICE_MAX_CONNECTIONS': '1', 'NCCL_CUMEM_ENABLE': '0', 'VLLM_DISABLE_COMPILE_CACHE': '1', 'HCCL_HOST_SOCKET_PORT_RANGE': 'auto', 'HCCL_NPU_SOCKET_PORT_RANGE': 'auto'}, 'working_dir': None}}
+2026-02-07 12:56:39,494	INFO worker.py:1998 -- Started a local Ray instance. View the dashboard at http://127.0.0.1:8301 
+/home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/ray/_private/worker.py:2046: FutureWarning: Tip: In future versions of Ray, Ray will no longer override accelerator visible devices env var if num_gpus=0 or num_gpus=None (default). To enable this behavior and turn off this error message, set RAY_ACCEL_ENV_VAR_OVERRIDE_ON_ZERO=0
+  warnings.warn(
+(pid=896026) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/torch/cuda/__init__.py:63: FutureWarning: The pynvml package is deprecated. Please install nvidia-ml-py instead. If you did not install pynvml directly, please report this to the maintainers of the package that installed pynvml for you.
+(pid=896026)   import pynvml  # type: ignore[import]
+(pid=896026) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/models/backends.py:21: UserWarning: Apex is not installed. Falling back to Torch Norm
+(pid=896026)   warnings.warn("Apex is not installed. Falling back to Torch Norm")
+(pid=896026) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/optimizer/__init__.py:18: UserWarning: Transformer Engine and Apex are not installed. Falling back to Torch optimizers.
+(pid=896026)   warnings.warn(
+(pid=896026) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/optimizer/optimizer.py:28: UserWarning: Transformer Engine and Apex are not installed. Falling back to local implementations of multi_tensor_applier and multi_tensor_scale
+(pid=896026)   warnings.warn(
+(pid=896026) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/optimizer/clip_grads.py:29: UserWarning: Transformer Engine and Apex are not installed. Falling back to local implementations of multi_tensor_applier, multi_tensor_l2norm, and multi_tensor_scale
+(pid=896026)   warnings.warn(
+(pid=896026) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/models/gpt/gpt_layer_specs.py:67: UserWarning: Apex is not installed. Falling back to Torch Norm
+(pid=896026)   warnings.warn("Apex is not installed. Falling back to Torch Norm")
+(TaskRunner pid=896026) TaskRunner hostname: gamma, PID: 896026
+(TaskRunner pid=896026) {'actor_rollout_ref': {'actor': {'_target_': 'verl.workers.config.FSDPActorConfig',
+(TaskRunner pid=896026)                                  'calculate_entropy': False,
+(TaskRunner pid=896026)                                  'calculate_sum_pi_squared': False,
+(TaskRunner pid=896026)                                  'checkpoint': {'_target_': 'verl.trainer.config.CheckpointConfig',
+(TaskRunner pid=896026)                                                 'async_save': False,
+(TaskRunner pid=896026)                                                 'load_contents': ['model',
+(TaskRunner pid=896026)                                                                   'optimizer',
+(TaskRunner pid=896026)                                                                   'extra'],
+(TaskRunner pid=896026)                                                 'save_contents': ['model',
+(TaskRunner pid=896026)                                                                   'optimizer',
+(TaskRunner pid=896026)                                                                   'extra']},
+(TaskRunner pid=896026)                                  'clip_ratio': 0.2,
+(TaskRunner pid=896026)                                  'clip_ratio_c': 3.0,
+(TaskRunner pid=896026)                                  'clip_ratio_high': 0.2,
+(TaskRunner pid=896026)                                  'clip_ratio_low': 0.2,
+(TaskRunner pid=896026)                                  'data_loader_seed': 42,
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+(TaskRunner pid=896026)                                  'entropy_coeff': 0,
+(TaskRunner pid=896026)                                  'entropy_from_logits_with_chunking': False,
+(TaskRunner pid=896026)                                  'freeze_vision_tower': False,
+(TaskRunner pid=896026)                                  'fsdp_config': {'_target_': 'verl.workers.config.FSDPEngineConfig',
+(TaskRunner pid=896026)                                                  'dtype': 'bfloat16',
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+(TaskRunner pid=896026)                                                  'entropy_from_logits_with_chunking': False,
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+(TaskRunner pid=896026)                                                  'forward_prefetch': False,
+(TaskRunner pid=896026)                                                  'fsdp_size': -1,
+(TaskRunner pid=896026)                                                  'full_determinism': False,
+(TaskRunner pid=896026)                                                  'model_dtype': 'fp32',
+(TaskRunner pid=896026)                                                  'offload_policy': False,
+(TaskRunner pid=896026)                                                  'optimizer_offload': False,
+(TaskRunner pid=896026)                                                  'param_offload': False,
+(TaskRunner pid=896026)                                                  'reshard_after_forward': True,
+(TaskRunner pid=896026)                                                  'seed': 42,
+(TaskRunner pid=896026)                                                  'strategy': 'fsdp',
+(TaskRunner pid=896026)                                                  'ulysses_sequence_parallel_size': 1,
+(TaskRunner pid=896026)                                                  'use_orig_params': False,
+(TaskRunner pid=896026)                                                  'use_torch_compile': True,
+(TaskRunner pid=896026)                                                  'wrap_policy': {'min_num_params': 0}},
+(TaskRunner pid=896026)                                  'grad_clip': 1.0,
+(TaskRunner pid=896026)                                  'kl_loss_coef': 0.001,
+(TaskRunner pid=896026)                                  'kl_loss_type': 'low_var_kl',
+(TaskRunner pid=896026)                                  'loss_agg_mode': 'token-mean',
+(TaskRunner pid=896026)                                  'loss_scale_factor': None,
+(TaskRunner pid=896026)                                  'optim': {'_target_': 'verl.workers.config.FSDPOptimizerConfig',
+(TaskRunner pid=896026)                                            'betas': [0.9, 0.999],
+(TaskRunner pid=896026)                                            'clip_grad': 1.0,
+(TaskRunner pid=896026)                                            'lr': 1e-06,
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+(TaskRunner pid=896026)                                            'lr_warmup_steps_ratio': 0.0,
+(TaskRunner pid=896026)                                            'min_lr_ratio': 0.0,
+(TaskRunner pid=896026)                                            'num_cycles': 0.5,
+(TaskRunner pid=896026)                                            'optimizer': 'AdamW',
+(TaskRunner pid=896026)                                            'optimizer_impl': 'torch.optim',
+(TaskRunner pid=896026)                                            'override_optimizer_config': None,
+(TaskRunner pid=896026)                                            'total_training_steps': -1,
+(TaskRunner pid=896026)                                            'warmup_style': None,
+(TaskRunner pid=896026)                                            'weight_decay': 0.01},
+(TaskRunner pid=896026)                                  'policy_loss': {'_target_': 'verl.workers.config.PolicyLossConfig',
+(TaskRunner pid=896026)                                                  'clip_cov_lb': 1.0,
+(TaskRunner pid=896026)                                                  'clip_cov_ratio': 0.0002,
+(TaskRunner pid=896026)                                                  'clip_cov_ub': 5.0,
+(TaskRunner pid=896026)                                                  'kl_cov_ratio': 0.0002,
+(TaskRunner pid=896026)                                                  'loss_mode': 'vanilla',
+(TaskRunner pid=896026)                                                  'ppo_kl_coef': 0.1},
+(TaskRunner pid=896026)                                  'ppo_epochs': 1,
+(TaskRunner pid=896026)                                  'ppo_max_token_len_per_gpu': 16384,
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+(TaskRunner pid=896026)                                  'ppo_micro_batch_size_per_gpu': 2,
+(TaskRunner pid=896026)                                  'ppo_mini_batch_size': 4,
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+(TaskRunner pid=896026)                                               'enable': False,
+(TaskRunner pid=896026)                                               'ranks': [],
+(TaskRunner pid=896026)                                               'save_path': 'outputs/profile',
+(TaskRunner pid=896026)                                               'tool': None,
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+(TaskRunner pid=896026)                                                                       'level': 'level0'},
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+(TaskRunner pid=896026)                                                                        'discrete': False},
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+(TaskRunner pid=896026)                                                    'mode': 'disabled',
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+(TaskRunner pid=896026)                                                    'replay_file': None},
+(TaskRunner pid=896026)                                  'shuffle': False,
+(TaskRunner pid=896026)                                  'strategy': 'fsdp',
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+(TaskRunner pid=896026)                        'hybrid_engine': True,
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+(TaskRunner pid=896026)                                                                     'level': 'level0'},
+(TaskRunner pid=896026)                                                             'nsys': {'_target_': 'verl.utils.profiler.config.NsightToolConfig',
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+(TaskRunner pid=896026)                                                             'torch': {'_target_': 'verl.utils.profiler.config.TorchProfilerToolConfig',
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+(TaskRunner pid=896026)              'resume_mode': 'auto',
+(TaskRunner pid=896026)              'rollout_data_dir': None,
+(TaskRunner pid=896026)              'save_freq': 100,
+(TaskRunner pid=896026)              'test_freq': 1,
+(TaskRunner pid=896026)              'total_epochs': 15,
+(TaskRunner pid=896026)              'total_training_steps': None,
+(TaskRunner pid=896026)              'use_legacy_worker_impl': 'auto',
+(TaskRunner pid=896026)              'val_before_train': True,
+(TaskRunner pid=896026)              'val_only': False,
+(TaskRunner pid=896026)              'validation_data_dir': None},
+(TaskRunner pid=896026)  'transfer_queue': {'enable': False}}
+(TaskRunner pid=896026) /data/home_beta/mshahidul/readctrl/code/RL_model/verl/verl_train/verl/trainer/main_ppo.py:300: UserWarning: Disabled critic as algorithm.adv_estimator != gae. If it is not intended, please set critic.enable=True
+(TaskRunner pid=896026)   use_critic=need_critic(config),
+(TaskRunner pid=896026) [validate_config] All configuration checks passed successfully!
+(TaskRunner pid=896026) /data/home_beta/mshahidul/readctrl/code/RL_model/verl/verl_train/verl/utils/tokenizer.py:109: UserWarning: Failed to create processor: Unsupported processor type: Qwen2TokenizerFast. This may affect multimodal processing
+(TaskRunner pid=896026)   warnings.warn(f"Failed to create processor: {e}. This may affect multimodal processing", stacklevel=1)
+(TaskRunner pid=896026) Using dataset class: RLHFDataset
+(TaskRunner pid=896026) dataset len: 3226
+(TaskRunner pid=896026) Setting TOKENIZERS_PARALLELISM=false for forked processes.
+(TaskRunner pid=896026) WARNING:2026-02-07 12:57:16,729:Setting TOKENIZERS_PARALLELISM=false for forked processes.
+(TaskRunner pid=896026) 
Filtering prompts longer than 1024 tokens (num_proc=1):   0%|          | 0/3226 [00:00<?, ? examples/s]
+(TaskRunner pid=896026) 
Filtering prompts longer than 1024 tokens (num_proc=1):  31%|███       | 1000/3226 [00:03<00:07, 309.79 examples/s]
+(TaskRunner pid=896026) 
Filtering prompts longer than 1024 tokens (num_proc=1):  62%|██████▏   | 2000/3226 [00:05<00:03, 381.72 examples/s]
+(TaskRunner pid=896026) 
Filtering prompts longer than 1024 tokens (num_proc=1):  93%|█████████▎| 3000/3226 [00:07<00:00, 418.41 examples/s]
+(TaskRunner pid=896026) 
Filtering prompts longer than 1024 tokens (num_proc=1): 100%|██████████| 3226/3226 [00:08<00:00, 425.98 examples/s]
+(TaskRunner pid=896026) 
Filtering prompts longer than 1024 tokens (num_proc=1): 100%|██████████| 3226/3226 [00:08<00:00, 393.10 examples/s]
+(TaskRunner pid=896026) filter dataset len: 3226
+(TaskRunner pid=896026) Using dataset class: RLHFDataset
+(TaskRunner pid=896026) dataset len: 170
+(TaskRunner pid=896026) Setting TOKENIZERS_PARALLELISM=false for forked processes.
+(TaskRunner pid=896026) WARNING:2026-02-07 12:57:25,438:Setting TOKENIZERS_PARALLELISM=false for forked processes.
+(TaskRunner pid=896026) 
Filtering prompts longer than 1024 tokens (num_proc=1):   0%|          | 0/170 [00:00<?, ? examples/s]
+(TaskRunner pid=896026) 
Filtering prompts longer than 1024 tokens (num_proc=1): 100%|██████████| 170/170 [00:01<00:00, 104.19 examples/s]
+(TaskRunner pid=896026) 
Filtering prompts longer than 1024 tokens (num_proc=1): 100%|██████████| 170/170 [00:01<00:00, 92.90 examples/s] 
+(TaskRunner pid=896026) /data/home_beta/mshahidul/readctrl/code/RL_model/verl/verl_train/verl/trainer/ppo/ray_trainer.py:291: UserWarning: Disabled critic as algorithm.adv_estimator != gae. If it is not intended, please set critic.enable=True
+(TaskRunner pid=896026)   self.use_critic = need_critic(self.config)
+(TaskRunner pid=896026) filter dataset len: 170
+(TaskRunner pid=896026) Size of train dataloader: 403, Size of val dataloader: 1
+(TaskRunner pid=896026) Total training steps: 6045
+(TaskRunner pid=896026) colocated worker base class <class 'verl.single_controller.base.worker.Worker'>
+(pid=897656) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/torch/cuda/__init__.py:63: FutureWarning: The pynvml package is deprecated. Please install nvidia-ml-py instead. If you did not install pynvml directly, please report this to the maintainers of the package that installed pynvml for you.
+(pid=897656)   import pynvml  # type: ignore[import]
+(pid=897656) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/models/backends.py:21: UserWarning: Apex is not installed. Falling back to Torch Norm
+(pid=897656)   warnings.warn("Apex is not installed. Falling back to Torch Norm")
+(pid=897656) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/optimizer/__init__.py:18: UserWarning: Transformer Engine and Apex are not installed. Falling back to Torch optimizers.
+(pid=897656)   warnings.warn(
+(pid=897656) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/optimizer/optimizer.py:28: UserWarning: Transformer Engine and Apex are not installed. Falling back to local implementations of multi_tensor_applier and multi_tensor_scale
+(pid=897656)   warnings.warn(
+(pid=897656) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/optimizer/clip_grads.py:29: UserWarning: Transformer Engine and Apex are not installed. Falling back to local implementations of multi_tensor_applier, multi_tensor_l2norm, and multi_tensor_scale
+(pid=897656)   warnings.warn(
+(pid=897657) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/torch/cuda/__init__.py:63: FutureWarning: The pynvml package is deprecated. Please install nvidia-ml-py instead. If you did not install pynvml directly, please report this to the maintainers of the package that installed pynvml for you.
+(pid=897657)   import pynvml  # type: ignore[import]
+(pid=897656) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/models/gpt/gpt_layer_specs.py:67: UserWarning: Apex is not installed. Falling back to Torch Norm
+(pid=897656)   warnings.warn("Apex is not installed. Falling back to Torch Norm")
+(pid=897657) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/models/gpt/gpt_layer_specs.py:67: UserWarning: Apex is not installed. Falling back to Torch Norm [repeated 2x across cluster] (Ray deduplicates logs by default. Set RAY_DEDUP_LOGS=0 to disable log deduplication, or see https://docs.ray.io/en/master/ray-observability/user-guides/configure-logging.html#log-deduplication for more options.)
+(pid=897657)   warnings.warn("Apex is not installed. Falling back to Torch Norm") [repeated 2x across cluster]
+(pid=897657) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/optimizer/__init__.py:18: UserWarning: Transformer Engine and Apex are not installed. Falling back to Torch optimizers.
+(pid=897657)   warnings.warn( [repeated 3x across cluster]
+(pid=897657) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/optimizer/optimizer.py:28: UserWarning: Transformer Engine and Apex are not installed. Falling back to local implementations of multi_tensor_applier and multi_tensor_scale
+(pid=897657) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/optimizer/clip_grads.py:29: UserWarning: Transformer Engine and Apex are not installed. Falling back to local implementations of multi_tensor_applier, multi_tensor_l2norm, and multi_tensor_scale
+(WorkerDict pid=897656) [Gloo] Rank 0 is connected to 1 peer ranks. Expected number of connected peer ranks is : 1
+(WorkerDict pid=897656) reference model: Qwen/Qwen3-4B-Instruct-2507
+(WorkerDict pid=897657) /data/home_beta/mshahidul/readctrl/code/RL_model/verl/verl_train/verl/utils/tokenizer.py:109: UserWarning: Failed to create processor: Unsupported processor type: Qwen2TokenizerFast. This may affect multimodal processing
+(WorkerDict pid=897657)   warnings.warn(f"Failed to create processor: {e}. This may affect multimodal processing", stacklevel=1)
+(WorkerDict pid=897656) Model config after override: Qwen3Config {
+(WorkerDict pid=897656)   "architectures": [
+(WorkerDict pid=897656)     "Qwen3ForCausalLM"
+(WorkerDict pid=897656)   ],
+(WorkerDict pid=897656)   "attention_bias": false,
+(WorkerDict pid=897656)   "attention_dropout": 0.0,
+(WorkerDict pid=897656)   "dtype": "bfloat16",
+(WorkerDict pid=897656)   "eos_token_id": 151645,
+(WorkerDict pid=897656)   "head_dim": 128,
+(WorkerDict pid=897656)   "hidden_act": "silu",
+(WorkerDict pid=897656)   "hidden_size": 2560,
+(WorkerDict pid=897656)   "initializer_range": 0.02,
+(WorkerDict pid=897656)   "intermediate_size": 9728,
+(WorkerDict pid=897656)   "layer_types": [
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention"
+(WorkerDict pid=897656)   ],
+(WorkerDict pid=897656)   "max_position_embeddings": 262144,
+(WorkerDict pid=897656)   "max_window_layers": 36,
+(WorkerDict pid=897656)   "model_type": "qwen3",
+(WorkerDict pid=897656)   "num_attention_heads": 32,
+(WorkerDict pid=897656)   "num_hidden_layers": 36,
+(WorkerDict pid=897656)   "num_key_value_heads": 8,
+(WorkerDict pid=897656)   "pad_token_id": 151643,
+(WorkerDict pid=897656)   "rms_norm_eps": 1e-06,
+(WorkerDict pid=897656)   "rope_scaling": null,
+(WorkerDict pid=897656)   "rope_theta": 5000000,
+(WorkerDict pid=897656)   "sliding_window": null,
+(WorkerDict pid=897656)   "tie_word_embeddings": true,
+(WorkerDict pid=897656)   "transformers_version": "4.56.1",
+(WorkerDict pid=897656)   "use_cache": true,
+(WorkerDict pid=897656)   "use_sliding_window": false,
+(WorkerDict pid=897656)   "vocab_size": 151936
+(WorkerDict pid=897656) }
+(WorkerDict pid=897656) 
+(WorkerDict pid=897657) `torch_dtype` is deprecated! Use `dtype` instead!
+(WorkerDict pid=897657) Flash Attention 2 only supports torch.float16 and torch.bfloat16 dtypes, but the current dype in Qwen3ForCausalLM is torch.float32. You should run training or inference using Automatic Mixed-Precision via the `with torch.autocast(device_type='torch_device'):` decorator, or load the model with the `dtype` argument. Example: `model = AutoModel.from_pretrained("openai/whisper-tiny", attn_implementation="flash_attention_2", dtype=torch.float16)`
+(WorkerDict pid=897657) Flash Attention 2 only supports torch.float16 and torch.bfloat16 dtypes, but the current dype in Qwen3Model is torch.float32. You should run training or inference using Automatic Mixed-Precision via the `with torch.autocast(device_type='torch_device'):` decorator, or load the model with the `dtype` argument. Example: `model = AutoModel.from_pretrained("openai/whisper-tiny", attn_implementation="flash_attention_2", dtype=torch.float16)`
+(WorkerDict pid=897657) 
Loading checkpoint shards:   0%|          | 0/3 [00:00<?, ?it/s]
+(WorkerDict pid=897656) /data/home_beta/mshahidul/readctrl/code/RL_model/verl/verl_train/verl/utils/tokenizer.py:109: UserWarning: Failed to create processor: Unsupported processor type: Qwen2TokenizerFast. This may affect multimodal processing
+(WorkerDict pid=897656)   warnings.warn(f"Failed to create processor: {e}. This may affect multimodal processing", stacklevel=1)
+(WorkerDict pid=897657) 
Loading checkpoint shards:  33%|███▎      | 1/3 [00:06<00:12,  6.30s/it]
+(WorkerDict pid=897656) `torch_dtype` is deprecated! Use `dtype` instead!
+(WorkerDict pid=897656) Flash Attention 2 only supports torch.float16 and torch.bfloat16 dtypes, but the current dype in Qwen3Model is torch.float32. You should run training or inference using Automatic Mixed-Precision via the `with torch.autocast(device_type='torch_device'):` decorator, or load the model with the `dtype` argument. Example: `model = AutoModel.from_pretrained("openai/whisper-tiny", attn_implementation="flash_attention_2", dtype=torch.float16)` [repeated 2x across cluster]
+(WorkerDict pid=897656) 
Loading checkpoint shards:   0%|          | 0/3 [00:00<?, ?it/s]
+(WorkerDict pid=897657) 
Loading checkpoint shards:  67%|██████▋   | 2/3 [00:12<00:06,  6.32s/it] [repeated 2x across cluster]
+(WorkerDict pid=897657) 
Loading checkpoint shards: 100%|██████████| 3/3 [00:12<00:00,  3.51s/it]
Loading checkpoint shards: 100%|██████████| 3/3 [00:12<00:00,  4.26s/it]
+(WorkerDict pid=897657) Monkey patch _flash_attention_forward in transformers.integrations.flash_attention
+(WorkerDict pid=897657) Skipping monkey patch for Qwen3ForCausalLM as use_fused_kernels is False or fused_kernels_backend is torch
+(WorkerDict pid=897657) [Gloo] Rank 1 is connected to 1 peer ranks. Expected number of connected peer ranks is : 1
+(WorkerDict pid=897656) Qwen3ForCausalLM contains 4.02B parameters
+(WorkerDict pid=897656) wrap_policy: functools.partial(<function _or_policy at 0x7f9230fa54e0>, policies=[functools.partial(<function transformer_auto_wrap_policy at 0x7f9230fa53a0>, transformer_layer_cls={<class 'transformers.models.qwen3.modeling_qwen3.Qwen3DecoderLayer'>})])
+(WorkerDict pid=897656) NCCL version 2.27.3+cuda12.9
+(WorkerDict pid=897656) 
+(WorkerDict pid=897656) [2026-02-07 12:58:25] gamma:897656:899170 [0] ras/client_support.cc:160 NCCL WARN Call to bind failed: Address already in use
+(WorkerDict pid=897656) Monkey patch _flash_attention_forward in transformers.integrations.flash_attention
+(WorkerDict pid=897656) Skipping monkey patch for Qwen3ForCausalLM as use_fused_kernels is False or fused_kernels_backend is torch
+(WorkerDict pid=897657) 
+(WorkerDict pid=897656) Ref use_remove_padding=True
+(WorkerDict pid=897656) Ref use_fused_kernels=False
+(WorkerDict pid=897656) Ref use_prefix_grouper=False
+(WorkerDict pid=897657) [2026-02-07 12:58:25] gamma:897657:899174 [0] ras/client_support.cc:160 NCCL WARN Call to bind failed: Address already in use
+(WorkerDict pid=897656) /data/home_beta/mshahidul/readctrl/code/RL_model/verl/verl_train/verl/utils/tokenizer.py:109: UserWarning: Failed to create processor: Unsupported processor type: Qwen2TokenizerFast. This may affect multimodal processing
+(WorkerDict pid=897656)   warnings.warn(f"Failed to create processor: {e}. This may affect multimodal processing", stacklevel=1)
+(WorkerDict pid=897656) 
Loading checkpoint shards:  67%|██████▋   | 2/3 [00:13<00:06,  6.60s/it]
+(WorkerDict pid=897656) 
Loading checkpoint shards: 100%|██████████| 3/3 [00:13<00:00,  3.64s/it]
Loading checkpoint shards: 100%|██████████| 3/3 [00:13<00:00,  4.49s/it]
+(WorkerDict pid=897656) Model config after override: Qwen3Config {
+(WorkerDict pid=897656)   "architectures": [
+(WorkerDict pid=897656)     "Qwen3ForCausalLM"
+(WorkerDict pid=897656)   ],
+(WorkerDict pid=897656)   "attention_bias": false,
+(WorkerDict pid=897656)   "attention_dropout": 0.0,
+(WorkerDict pid=897656)   "dtype": "bfloat16",
+(WorkerDict pid=897656)   "eos_token_id": 151645,
+(WorkerDict pid=897656)   "head_dim": 128,
+(WorkerDict pid=897656)   "hidden_act": "silu",
+(WorkerDict pid=897656)   "hidden_size": 2560,
+(WorkerDict pid=897656)   "initializer_range": 0.02,
+(WorkerDict pid=897656)   "intermediate_size": 9728,
+(WorkerDict pid=897656)   "layer_types": [
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention",
+(WorkerDict pid=897656)     "full_attention"
+(WorkerDict pid=897656)   ],
+(WorkerDict pid=897656)   "max_position_embeddings": 262144,
+(WorkerDict pid=897656)   "max_window_layers": 36,
+(WorkerDict pid=897656)   "model_type": "qwen3",
+(WorkerDict pid=897656)   "num_attention_heads": 32,
+(WorkerDict pid=897656)   "num_hidden_layers": 36,
+(WorkerDict pid=897656)   "num_key_value_heads": 8,
+(WorkerDict pid=897656)   "pad_token_id": 151643,
+(WorkerDict pid=897656)   "rms_norm_eps": 1e-06,
+(WorkerDict pid=897656)   "rope_scaling": null,
+(WorkerDict pid=897656)   "rope_theta": 5000000,
+(WorkerDict pid=897656)   "sliding_window": null,
+(WorkerDict pid=897656)   "tie_word_embeddings": true,
+(WorkerDict pid=897656)   "transformers_version": "4.56.1",
+(WorkerDict pid=897656)   "use_cache": true,
+(WorkerDict pid=897656)   "use_sliding_window": false,
+(WorkerDict pid=897656)   "vocab_size": 151936
+(WorkerDict pid=897656) }
+(WorkerDict pid=897656) 
+(WorkerDict pid=897656) 
Loading checkpoint shards:   0%|          | 0/3 [00:00<?, ?it/s]
+(WorkerDict pid=897657) 
Loading checkpoint shards:  33%|███▎      | 1/3 [00:06<00:12,  6.25s/it]
+(WorkerDict pid=897657) /data/home_beta/mshahidul/readctrl/code/RL_model/verl/verl_train/verl/utils/tokenizer.py:109: UserWarning: Failed to create processor: Unsupported processor type: Qwen2TokenizerFast. This may affect multimodal processing
+(WorkerDict pid=897657)   warnings.warn(f"Failed to create processor: {e}. This may affect multimodal processing", stacklevel=1)
+(WorkerDict pid=897657) 
Loading checkpoint shards:   0%|          | 0/3 [00:00<?, ?it/s]
+(WorkerDict pid=897657) 
Loading checkpoint shards:  67%|██████▋   | 2/3 [00:12<00:06,  6.45s/it] [repeated 2x across cluster]
+(WorkerDict pid=897657) 
Loading checkpoint shards: 100%|██████████| 3/3 [00:13<00:00,  3.58s/it]
Loading checkpoint shards: 100%|██████████| 3/3 [00:13<00:00,  4.34s/it]
+(WorkerDict pid=897657) Monkey patch _flash_attention_forward in transformers.integrations.flash_attention
+(WorkerDict pid=897657) Skipping monkey patch for Qwen3ForCausalLM as use_fused_kernels is False or fused_kernels_backend is torch
+(WorkerDict pid=897656) Qwen3ForCausalLM contains 4.02B parameters
+(WorkerDict pid=897656) wrap_policy: functools.partial(<function _or_policy at 0x7f9230fa54e0>, policies=[functools.partial(<function transformer_auto_wrap_policy at 0x7f9230fa53a0>, transformer_layer_cls={<class 'transformers.models.qwen3.modeling_qwen3.Qwen3DecoderLayer'>})])
+(WorkerDict pid=897656) Total steps: 6045, num_warmup_steps: 0
+(WorkerDict pid=897656) Actor use_remove_padding=True
+(WorkerDict pid=897656) Actor use_fused_kernels=False
+(WorkerDict pid=897656) Actor use_prefix_grouper=False
+(WorkerDict pid=897656) Monkey patch _flash_attention_forward in transformers.integrations.flash_attention
+(WorkerDict pid=897656) Skipping monkey patch for Qwen3ForCausalLM as use_fused_kernels is False or fused_kernels_backend is torch
+(WorkerDict pid=897657) /data/home_beta/mshahidul/readctrl/code/RL_model/verl/verl_train/verl/utils/tokenizer.py:109: UserWarning: Failed to create processor: Unsupported processor type: Qwen2TokenizerFast. This may affect multimodal processing
+(WorkerDict pid=897657)   warnings.warn(f"Failed to create processor: {e}. This may affect multimodal processing", stacklevel=1)
+(WorkerDict pid=897656) 
Loading checkpoint shards:  67%|██████▋   | 2/3 [00:13<00:06,  6.91s/it]
+(WorkerDict pid=897656) 
Loading checkpoint shards: 100%|██████████| 3/3 [00:13<00:00,  3.81s/it]
Loading checkpoint shards: 100%|██████████| 3/3 [00:13<00:00,  4.65s/it]
+(WorkerDict pid=897656) [Gloo] Rank 0 is connected to 1 peer ranks. Expected number of connected peer ranks is : 1
+(WorkerDict pid=897656) [Gloo] Rank 0 is connected to 0 peer ranks. Expected number of connected peer ranks is : 0
+(WorkerDict pid=897656) [Gloo] Rank 0 is connected to 0 peer ranks. Expected number of connected peer ranks is : 0
+(WorkerDict pid=897656) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/torch/distributed/fsdp/fully_sharded_data_parallel.py:678: FutureWarning: FSDP.state_dict_type() and FSDP.set_state_dict_type() are being deprecated. Please use APIs, get_state_dict() and set_state_dict(), which can support different parallelisms, FSDP1, FSDP2, DDP. API doc: https://pytorch.org/docs/stable/distributed.checkpoint.html#torch.distributed.checkpoint.state_dict.get_state_dict .Tutorial: https://pytorch.org/tutorials/recipes/distributed_checkpoint_recipe.html .
+(WorkerDict pid=897656)   warnings.warn(
+(WorkerDict pid=897656) /data/home_beta/mshahidul/readctrl/code/RL_model/verl/verl_train/verl/utils/tokenizer.py:109: UserWarning: Failed to create processor: Unsupported processor type: Qwen2TokenizerFast. This may affect multimodal processing
+(WorkerDict pid=897656)   warnings.warn(f"Failed to create processor: {e}. This may affect multimodal processing", stacklevel=1)
+(TaskRunner pid=896026) WARNING 02-07 12:59:32 [api_server.py:1213] LoRA dynamic loading & unloading is enabled in the API server. This should ONLY be used for local development!
+(WorkerDict pid=897657) [Gloo] Rank 0 is connected to 0 peer ranks. Expected number of connected peer ranks is : 0 [repeated 3x across cluster]
+(pid=901562) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/torch/cuda/__init__.py:63: FutureWarning: The pynvml package is deprecated. Please install nvidia-ml-py instead. If you did not install pynvml directly, please report this to the maintainers of the package that installed pynvml for you.
+(pid=901562)   import pynvml  # type: ignore[import]
+(WorkerDict pid=897657) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/torch/distributed/fsdp/fully_sharded_data_parallel.py:678: FutureWarning: FSDP.state_dict_type() and FSDP.set_state_dict_type() are being deprecated. Please use APIs, get_state_dict() and set_state_dict(), which can support different parallelisms, FSDP1, FSDP2, DDP. API doc: https://pytorch.org/docs/stable/distributed.checkpoint.html#torch.distributed.checkpoint.state_dict.get_state_dict .Tutorial: https://pytorch.org/tutorials/recipes/distributed_checkpoint_recipe.html .
+(WorkerDict pid=897657)   warnings.warn(
+(pid=901562) WARNING 02-07 12:59:59 [api_server.py:1213] LoRA dynamic loading & unloading is enabled in the API server. This should ONLY be used for local development!
+(pid=901571) WARNING 02-07 12:59:59 [api_server.py:1213] LoRA dynamic loading & unloading is enabled in the API server. This should ONLY be used for local development!
+(vLLMHttpServer pid=901562) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/models/backends.py:21: UserWarning: Apex is not installed. Falling back to Torch Norm
+(vLLMHttpServer pid=901562)   warnings.warn("Apex is not installed. Falling back to Torch Norm")
+(pid=901571) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/torch/cuda/__init__.py:63: FutureWarning: The pynvml package is deprecated. Please install nvidia-ml-py instead. If you did not install pynvml directly, please report this to the maintainers of the package that installed pynvml for you.
+(pid=901571)   import pynvml  # type: ignore[import]
+(vLLMHttpServer pid=901562) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/optimizer/__init__.py:18: UserWarning: Transformer Engine and Apex are not installed. Falling back to Torch optimizers.
+(vLLMHttpServer pid=901562)   warnings.warn(
+(vLLMHttpServer pid=901562) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/optimizer/optimizer.py:28: UserWarning: Transformer Engine and Apex are not installed. Falling back to local implementations of multi_tensor_applier and multi_tensor_scale
+(vLLMHttpServer pid=901562)   warnings.warn(
+(vLLMHttpServer pid=901562) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/optimizer/clip_grads.py:29: UserWarning: Transformer Engine and Apex are not installed. Falling back to local implementations of multi_tensor_applier, multi_tensor_l2norm, and multi_tensor_scale
+(vLLMHttpServer pid=901562)   warnings.warn(
+(vLLMHttpServer pid=901562) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/models/gpt/gpt_layer_specs.py:67: UserWarning: Apex is not installed. Falling back to Torch Norm
+(vLLMHttpServer pid=901562)   warnings.warn("Apex is not installed. Falling back to Torch Norm")
+(vLLMHttpServer pid=901562) /data/home_beta/mshahidul/readctrl/code/RL_model/verl/verl_train/verl/utils/tokenizer.py:109: UserWarning: Failed to create processor: Unsupported processor type: Qwen2TokenizerFast. This may affect multimodal processing
+(vLLMHttpServer pid=901562)   warnings.warn(f"Failed to create processor: {e}. This may affect multimodal processing", stacklevel=1)
+(vLLMHttpServer pid=901562) WARNING:2026-02-07 13:00:03,461:agent loop only support torch and npu profiler, got None
+(vLLMHttpServer pid=901562) INFO:2026-02-07 13:00:03,463:vLLMHttpServer, replica_rank: 1, node_rank: 0, CUDA_VISIBLE_DEVICES: 3, master_address: 172.16.34.29, master_port: 32975, data_parallel_rpc_port: 43977, data_parallel_master_port: 36417
+(vLLMHttpServer pid=901562) INFO:2026-02-07 13:00:03,480:override_generation_config: {'temperature': 1.0, 'top_k': -1, 'top_p': 1, 'repetition_penalty': 1.0, 'max_new_tokens': 2048}
+(vLLMHttpServer pid=901562) INFO:2026-02-07 13:00:03,480:enable_sleep_mode: True
+(vLLMHttpServer pid=901562) `torch_dtype` is deprecated! Use `dtype` instead!
+(vLLMHttpServer pid=901562) WARNING 02-07 13:00:05 [__init__.py:3036] We must use the `spawn` multiprocessing start method. Overriding VLLM_WORKER_MULTIPROC_METHOD to 'spawn'. See https://docs.vllm.ai/en/latest/usage/troubleshooting.html#python-multiprocessing for more information. Reasons: In a Ray actor and can only be spawned; CUDA is initialized
+(vLLMHttpServer pid=901562) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/torch/cuda/__init__.py:63: FutureWarning: The pynvml package is deprecated. Please install nvidia-ml-py instead. If you did not install pynvml directly, please report this to the maintainers of the package that installed pynvml for you.
+(vLLMHttpServer pid=901562)   import pynvml  # type: ignore[import]
+(vLLMHttpServer pid=901571) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/models/gpt/gpt_layer_specs.py:67: UserWarning: Apex is not installed. Falling back to Torch Norm [repeated 2x across cluster]
+(vLLMHttpServer pid=901571)   warnings.warn("Apex is not installed. Falling back to Torch Norm") [repeated 2x across cluster]
+(vLLMHttpServer pid=901571) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/optimizer/__init__.py:18: UserWarning: Transformer Engine and Apex are not installed. Falling back to Torch optimizers.
+(vLLMHttpServer pid=901571)   warnings.warn( [repeated 3x across cluster]
+(vLLMHttpServer pid=901571) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/optimizer/optimizer.py:28: UserWarning: Transformer Engine and Apex are not installed. Falling back to local implementations of multi_tensor_applier and multi_tensor_scale
+(vLLMHttpServer pid=901571) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/optimizer/clip_grads.py:29: UserWarning: Transformer Engine and Apex are not installed. Falling back to local implementations of multi_tensor_applier, multi_tensor_l2norm, and multi_tensor_scale
+(vLLMHttpServer pid=901562) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/torch/cuda/__init__.py:63: FutureWarning: The pynvml package is deprecated. Please install nvidia-ml-py instead. If you did not install pynvml directly, please report this to the maintainers of the package that installed pynvml for you.
+(vLLMHttpServer pid=901562)   import pynvml  # type: ignore[import]
+(vLLMHttpServer pid=901571) /data/home_beta/mshahidul/readctrl/code/RL_model/verl/verl_train/verl/utils/tokenizer.py:109: UserWarning: Failed to create processor: Unsupported processor type: Qwen2TokenizerFast. This may affect multimodal processing
+(vLLMHttpServer pid=901571)   warnings.warn(f"Failed to create processor: {e}. This may affect multimodal processing", stacklevel=1)
+(vLLMHttpServer pid=901571) WARNING:2026-02-07 13:00:30,122:agent loop only support torch and npu profiler, got None
+(vLLMHttpServer pid=901571) INFO:2026-02-07 13:00:30,124:vLLMHttpServer, replica_rank: 0, node_rank: 0, CUDA_VISIBLE_DEVICES: 2, master_address: 172.16.34.29, master_port: 40643, data_parallel_rpc_port: 37497, data_parallel_master_port: 45967
+(vLLMHttpServer pid=901571) INFO:2026-02-07 13:00:30,143:override_generation_config: {'temperature': 1.0, 'top_k': -1, 'top_p': 1, 'repetition_penalty': 1.0, 'max_new_tokens': 2048}
+(vLLMHttpServer pid=901571) INFO:2026-02-07 13:00:30,143:enable_sleep_mode: True
+(vLLMHttpServer pid=901571) ['serve',
+(vLLMHttpServer pid=901571)  'Qwen/Qwen3-4B-Instruct-2507',
+(vLLMHttpServer pid=901571)  '--dtype',
+(vLLMHttpServer pid=901571)  'bfloat16',
+(vLLMHttpServer pid=901571)  '--load_format',
+(vLLMHttpServer pid=901571)  'dummy',
+(vLLMHttpServer pid=901571)  '--distributed_executor_backend',
+(vLLMHttpServer pid=901571)  'mp',
+(vLLMHttpServer pid=901571)  '--worker_extension_cls',
+(vLLMHttpServer pid=901571)  'verl.workers.rollout.vllm_rollout.utils.vLLMColocateWorkerExtension',
+(vLLMHttpServer pid=901571)  '--max_model_len',
+(vLLMHttpServer pid=901571)  '8192',
+(vLLMHttpServer pid=901571)  '--max_num_seqs',
+(vLLMHttpServer pid=901571)  '1024',
+(vLLMHttpServer pid=901571)  '--enable_chunked_prefill',
+(vLLMHttpServer pid=901571)  '--max_num_batched_tokens',
+(vLLMHttpServer pid=901571)  '8192',
+(vLLMHttpServer pid=901571)  '--enable_prefix_caching',
+(vLLMHttpServer pid=901571)  '--enable_sleep_mode',
+(vLLMHttpServer pid=901571)  '--logprobs_mode',
+(vLLMHttpServer pid=901571)  'processed_logprobs',
+(vLLMHttpServer pid=901571)  '--gpu_memory_utilization',
+(vLLMHttpServer pid=901571)  '0.6',
+(vLLMHttpServer pid=901571)  '--disable_log_stats',
+(vLLMHttpServer pid=901571)  '--tensor_parallel_size',
+(vLLMHttpServer pid=901571)  '1',
+(vLLMHttpServer pid=901571)  '--seed',
+(vLLMHttpServer pid=901571)  '0',
+(vLLMHttpServer pid=901571)  '--override_generation_config',
+(vLLMHttpServer pid=901571)  '{"temperature": 1.0, "top_k": -1, "top_p": 1, "repetition_penalty": 1.0, '
+(vLLMHttpServer pid=901571)  '"max_new_tokens": 2048}',
+(vLLMHttpServer pid=901571)  '--hf_overrides',
+(vLLMHttpServer pid=901571)  '{}',
+(vLLMHttpServer pid=901571)  '--scheduling_policy',
+(vLLMHttpServer pid=901571)  'fcfs',
+(vLLMHttpServer pid=901571)  '--compilation_config',
+(vLLMHttpServer pid=901571)  '{"cudagraph_mode": "FULL_AND_PIECEWISE"}']
+(vLLMHttpServer pid=901571) `torch_dtype` is deprecated! Use `dtype` instead!
+(vLLMHttpServer pid=901571) WARNING 02-07 13:00:31 [__init__.py:3036] We must use the `spawn` multiprocessing start method. Overriding VLLM_WORKER_MULTIPROC_METHOD to 'spawn'. See https://docs.vllm.ai/en/latest/usage/troubleshooting.html#python-multiprocessing for more information. Reasons: In a Ray actor and can only be spawned; CUDA is initialized
+(vLLMHttpServer pid=901571) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/torch/cuda/__init__.py:63: FutureWarning: The pynvml package is deprecated. Please install nvidia-ml-py instead. If you did not install pynvml directly, please report this to the maintainers of the package that installed pynvml for you.
+(vLLMHttpServer pid=901571)   import pynvml  # type: ignore[import]
+(vLLMHttpServer pid=901562) W0207 13:00:51.123000 903087 /data/home_beta/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/torch/utils/cpp_extension.py:2425] TORCH_CUDA_ARCH_LIST is not set, all archs for visible cards are included for compilation. 
+(vLLMHttpServer pid=901562) W0207 13:00:51.123000 903087 /data/home_beta/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/torch/utils/cpp_extension.py:2425] If this is not desired, please set os.environ['TORCH_CUDA_ARCH_LIST'] to specific architectures.
+(vLLMHttpServer pid=901571) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/torch/cuda/__init__.py:63: FutureWarning: The pynvml package is deprecated. Please install nvidia-ml-py instead. If you did not install pynvml directly, please report this to the maintainers of the package that installed pynvml for you.
+(vLLMHttpServer pid=901571)   import pynvml  # type: ignore[import]
+(vLLMHttpServer pid=901562) [Gloo] Rank 0 is connected to 0 peer ranks. Expected number of connected peer ranks is : 0
+(vLLMHttpServer pid=901562) [Gloo] Rank 0 is connected to 0 peer ranks. Expected number of connected peer ranks is : 0
+(vLLMHttpServer pid=901562) [Gloo] Rank 0 is connected to 0 peer ranks. Expected number of connected peer ranks is : 0
+(vLLMHttpServer pid=901562) [Gloo] Rank 0 is connected to 0 peer ranks. Expected number of connected peer ranks is : 0
+(vLLMHttpServer pid=901562) [Gloo] Rank 0 is connected to 0 peer ranks. Expected number of connected peer ranks is : 0
+(vLLMHttpServer pid=901562) [Gloo] Rank 0 is connected to 0 peer ranks. Expected number of connected peer ranks is : 0
+(vLLMHttpServer pid=901571) W0207 13:01:17.192000 903817 /data/home_beta/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/torch/utils/cpp_extension.py:2425] TORCH_CUDA_ARCH_LIST is not set, all archs for visible cards are included for compilation. 
+(vLLMHttpServer pid=901571) W0207 13:01:17.192000 903817 /data/home_beta/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/torch/utils/cpp_extension.py:2425] If this is not desired, please set os.environ['TORCH_CUDA_ARCH_LIST'] to specific architectures.
+(vLLMHttpServer pid=901571) [Gloo] Rank 0 is connected to 0 peer ranks. Expected number of connected peer ranks is : 0 [repeated 6x across cluster]
+(vLLMHttpServer pid=901562) (Worker pid=903087) 
Capturing CUDA graphs (mixed prefill-decode, PIECEWISE):   0%|          | 0/67 [00:00<?, ?it/s]
+(vLLMHttpServer pid=901562) 
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+(vLLMHttpServer pid=901562) 
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+(vLLMHttpServer pid=901562) 
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+(vLLMHttpServer pid=901562) 
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+(vLLMHttpServer pid=901562) 
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+(vLLMHttpServer pid=901562) 
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+(vLLMHttpServer pid=901562) 
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+(vLLMHttpServer pid=901562) 
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+(vLLMHttpServer pid=901562) 
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+(vLLMHttpServer pid=901562) 
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+(vLLMHttpServer pid=901562) 
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+(vLLMHttpServer pid=901562) 
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+(vLLMHttpServer pid=901562) 
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+(vLLMHttpServer pid=901562) 
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+(vLLMHttpServer pid=901562) 
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+(vLLMHttpServer pid=901562) 
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+(vLLMHttpServer pid=901562) 
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+(vLLMHttpServer pid=901562) 
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+(vLLMHttpServer pid=901562) 
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+(vLLMHttpServer pid=901562) 
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+(vLLMHttpServer pid=901562) 
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+(vLLMHttpServer pid=901562) 
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+(vLLMHttpServer pid=901562) 
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+(vLLMHttpServer pid=901562) 
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+(vLLMHttpServer pid=901562) 
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+(vLLMHttpServer pid=901562) 
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+(vLLMHttpServer pid=901562) 
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+(vLLMHttpServer pid=901562) 
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+(vLLMHttpServer pid=901562) 
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+(vLLMHttpServer pid=901562) 
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+(vLLMHttpServer pid=901562) 
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+(vLLMHttpServer pid=901562) 
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+(vLLMHttpServer pid=901562) 
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+(vLLMHttpServer pid=901562) 
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+(vLLMHttpServer pid=901562) 
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+(vLLMHttpServer pid=901571) (Worker pid=903817) 
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+(vLLMHttpServer pid=901562) 
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+(vLLMHttpServer pid=901562) 
Capturing CUDA graphs (mixed prefill-decode, PIECEWISE):  73%|███████▎  | 49/67 [00:22<00:10,  1.67it/s] [repeated 4x across cluster]
+(vLLMHttpServer pid=901562) 
Capturing CUDA graphs (mixed prefill-decode, PIECEWISE):  91%|█████████ | 61/67 [00:28<00:03,  1.90it/s] [repeated 18x across cluster]
+(vLLMHttpServer pid=901562) 
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+(vLLMHttpServer pid=901562) 
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+(vLLMHttpServer pid=901562) 
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+(vLLMHttpServer pid=901562) (Worker pid=903087) 
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+(vLLMHttpServer pid=901562) WARNING 02-07 13:02:53 [model.py:1389] Default sampling parameters have been overridden by the model's Hugging Face generation config recommended from the model creator. If this is not intended, please relaunch vLLM instance with `--generation-config vllm`.
+(vLLMHttpServer pid=901571) 
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+(vLLMHttpServer pid=901571) WARNING 02-07 13:03:12 [model.py:1389] Default sampling parameters have been overridden by the model's Hugging Face generation config recommended from the model creator. If this is not intended, please relaunch vLLM instance with `--generation-config vllm`.
+(vLLMHttpServer pid=901571) INFO:2026-02-07 13:03:12,697:Initializing a V1 LLM engine with config: model='Qwen/Qwen3-4B-Instruct-2507', speculative_config=None, tokenizer='Qwen/Qwen3-4B-Instruct-2507', skip_tokenizer_init=False, tokenizer_mode=auto, revision=None, tokenizer_revision=None, trust_remote_code=False, dtype=torch.bfloat16, max_seq_len=8192, download_dir=None, load_format=dummy, tensor_parallel_size=1, pipeline_parallel_size=1, data_parallel_size=1, disable_custom_all_reduce=False, quantization=None, enforce_eager=False, kv_cache_dtype=auto, device_config=cuda, structured_outputs_config=StructuredOutputsConfig(backend='auto', disable_fallback=False, disable_any_whitespace=False, disable_additional_properties=False, reasoning_parser=''), observability_config=ObservabilityConfig(show_hidden_metrics_for_version=None, otlp_traces_endpoint=None, collect_detailed_traces=None), seed=0, served_model_name=Qwen/Qwen3-4B-Instruct-2507, enable_prefix_caching=True, chunked_prefill_enabled=True, pooler_config=None, compilation_config={"level":3,"debug_dump_path":"","cache_dir":"","backend":"","custom_ops":[],"splitting_ops":["vllm.unified_attention","vllm.unified_attention_with_output","vllm.mamba_mixer2","vllm.mamba_mixer","vllm.short_conv","vllm.linear_attention","vllm.plamo2_mamba_mixer","vllm.gdn_attention","vllm.sparse_attn_indexer"],"use_inductor":true,"compile_sizes":[],"inductor_compile_config":{"enable_auto_functionalized_v2":false},"inductor_passes":{},"cudagraph_mode":[2,1],"use_cudagraph":true,"cudagraph_num_of_warmups":1,"cudagraph_capture_sizes":[512,504,496,488,480,472,464,456,448,440,432,424,416,408,400,392,384,376,368,360,352,344,336,328,320,312,304,296,288,280,272,264,256,248,240,232,224,216,208,200,192,184,176,168,160,152,144,136,128,120,112,104,96,88,80,72,64,56,48,40,32,24,16,8,4,2,1],"cudagraph_copy_inputs":false,"full_cuda_graph":false,"use_inductor_graph_partition":false,"pass_config":{},"max_capture_size":512,"local_cache_dir":null}
+(vLLMHttpServer pid=901571) 
Capturing CUDA graphs (decode, FULL):  90%|████████▉ | 60/67 [00:21<00:01,  3.52it/s] [repeated 5x across cluster]
+(TaskRunner pid=896026) AgentLoopManager: ['172.16.34.29:36859', '172.16.34.29:33941']
+(TaskRunner pid=896026) wandb: [wandb.login()] Loaded credentials for https://api.wandb.ai from /home/mshahidul/.netrc.
+(TaskRunner pid=896026) wandb: Currently logged in as: shahidulshakib034 (shahidulshakib034-khulna-university-of-engineering-techn) to https://api.wandb.ai. Use `wandb login --relogin` to force relogin
+(TaskRunner pid=896026) wandb: setting up run f14af5tw
+(pid=907702) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/torch/cuda/__init__.py:63: FutureWarning: The pynvml package is deprecated. Please install nvidia-ml-py instead. If you did not install pynvml directly, please report this to the maintainers of the package that installed pynvml for you.
+(pid=907702)   import pynvml  # type: ignore[import]
+(TaskRunner pid=896026) wandb: Tracking run with wandb version 0.24.1
+(TaskRunner pid=896026) wandb: Run data is saved locally in /data/home_beta/mshahidul/readctrl/code/RL_model/verl/verl_train/wandb/run-20260207_130329-f14af5tw
+(TaskRunner pid=896026) wandb: Run `wandb offline` to turn off syncing.
+(TaskRunner pid=896026) wandb: Syncing run revived-frost-5
+(TaskRunner pid=896026) wandb: ⭐️ View project at https://wandb.ai/shahidulshakib034-khulna-university-of-engineering-techn/uncategorized
+(TaskRunner pid=896026) wandb: 🚀 View run at https://wandb.ai/shahidulshakib034-khulna-university-of-engineering-techn/uncategorized/runs/f14af5tw
+(TaskRunner pid=896026) wandb: Detected [openai] in use.
+(TaskRunner pid=896026) wandb: Use W&B Weave for improved LLM call tracing. Install Weave with `pip install weave` then add `import weave` to the top of your script.
+(TaskRunner pid=896026) wandb: For more information, check out the docs at: https://weave-docs.wandb.ai/
+(pid=907698) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/torch/cuda/__init__.py:63: FutureWarning: The pynvml package is deprecated. Please install nvidia-ml-py instead. If you did not install pynvml directly, please report this to the maintainers of the package that installed pynvml for you. [repeated 7x across cluster]
+(pid=907698)   import pynvml  # type: ignore[import] [repeated 7x across cluster]
+(TaskRunner pid=896026) Checkpoint tracker file does not exist: /home/mshahidul/readctrl/code/RL_model/train_v2/latest_checkpointed_iteration.txt
+(TaskRunner pid=896026) Training from scratch
+(WorkerDict pid=897656) WARNING 02-07 13:03:44 [api_server.py:1213] LoRA dynamic loading & unloading is enabled in the API server. This should ONLY be used for local development!
+(WorkerDict pid=897656) INFO:2026-02-07 13:03:48,410:update_weights done, time cost: 2.33s
+(TaskRunner pid=896026) test_gen_batch meta info: {'eos_token_id': 151645, 'pad_token_id': 151643, 'recompute_log_prob': False, 'do_sample': False, 'validate': True, 'global_steps': 0}
+(WorkerDict pid=897657) WARNING 02-07 13:03:44 [api_server.py:1213] LoRA dynamic loading & unloading is enabled in the API server. This should ONLY be used for local development!
+(AgentLoopWorker pid=907700) WARNING 02-07 13:05:46 [api_server.py:1213] LoRA dynamic loading & unloading is enabled in the API server. This should ONLY be used for local development!
+(AgentLoopWorker pid=907700) Using dataset class: RLHFDataset
+(AgentLoopWorker pid=907702) /data/home_beta/mshahidul/readctrl/code/RL_model/verl/verl_train/verl/utils/tokenizer.py:109: UserWarning: Failed to create processor: Unsupported processor type: Qwen2TokenizerFast. This may affect multimodal processing
+(AgentLoopWorker pid=907702)   warnings.warn(f"Failed to create processor: {e}. This may affect multimodal processing", stacklevel=1)
+(AgentLoopWorker pid=907702) You're using a Qwen2TokenizerFast tokenizer. Please note that with a fast tokenizer, using the `__call__` method is faster than using a method to encode the text followed by a call to the `pad` method to get a padded encoding.
+(AgentLoopWorker pid=907696) /data/home_beta/mshahidul/readctrl/code/RL_model/verl/verl_train/verl/utils/tokenizer.py:109: UserWarning: Failed to create processor: Unsupported processor type: Qwen2TokenizerFast. This may affect multimodal processing [repeated 7x across cluster]
+(AgentLoopWorker pid=907696)   warnings.warn(f"Failed to create processor: {e}. This may affect multimodal processing", stacklevel=1) [repeated 7x across cluster]
+(pid=912712) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/torch/cuda/__init__.py:63: FutureWarning: The pynvml package is deprecated. Please install nvidia-ml-py instead. If you did not install pynvml directly, please report this to the maintainers of the package that installed pynvml for you.
+(pid=912712)   import pynvml  # type: ignore[import]
+(AgentLoopWorker pid=907696) You're using a Qwen2TokenizerFast tokenizer. Please note that with a fast tokenizer, using the `__call__` method is faster than using a method to encode the text followed by a call to the `pad` method to get a padded encoding. [repeated 7x across cluster]
+(pid=913253) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/torch/cuda/__init__.py:63: FutureWarning: The pynvml package is deprecated. Please install nvidia-ml-py instead. If you did not install pynvml directly, please report this to the maintainers of the package that installed pynvml for you. [repeated 6x across cluster]
+(pid=913253)   import pynvml  # type: ignore[import] [repeated 6x across cluster]
diff --git a/code/RL_model/verl/verl_train/.pre-commit-config.yaml b/code/RL_model/verl/verl_train/.pre-commit-config.yaml
new file mode 100644
index 0000000000000000000000000000000000000000..9ef606f8dc4e141430fa46a938ae11831960e8b7
--- /dev/null
+++ b/code/RL_model/verl/verl_train/.pre-commit-config.yaml
@@ -0,0 +1,45 @@
+repos:
+  - repo: https://github.com/astral-sh/ruff-pre-commit
+    rev: "v0.12.2"
+    hooks:
+      - id: ruff
+        args: ["--fix", "--show-fixes", "--output-format=full"]
+        exclude: ^.*\.(ipynb)$
+      - id: ruff-format
+
+  - repo: https://github.com/pre-commit/mirrors-mypy
+    rev: "v1.17.0"
+    hooks:
+      - id: mypy
+
+  - repo: local
+    hooks:
+      - id: autogen-trainer-cfg
+        name: Generate and verify verl/trainer/config/_generated_*.yaml
+        entry: scripts/generate_trainer_config.sh
+        language: script
+        pass_filenames: false
+
+  - repo: local
+    hooks:
+      - id: check-docstrings
+        name: Check doc string coverage
+        entry: python3 tests/special_sanity/check_docstrings.py
+        language: python
+        pass_filenames: false
+
+  - repo: local
+    hooks:
+      - id: check-license
+        name: Check license
+        entry: python3 tests/special_sanity/check_license.py --directories examples scripts tests verl setup.py
+        language: python
+        pass_filenames: false
+
+  - repo: local
+    hooks:
+      - id: compileall
+        name: Compile all python files
+        entry: sh -c 'PYTHONWARNINGS=error python3 -m compileall -q .'
+        language: python
+        pass_filenames: false
diff --git a/code/RL_model/verl/verl_train/.readthedocs.yaml b/code/RL_model/verl/verl_train/.readthedocs.yaml
new file mode 100644
index 0000000000000000000000000000000000000000..0016868541a2a0667ef40ae6a9d861bcd26b9316
--- /dev/null
+++ b/code/RL_model/verl/verl_train/.readthedocs.yaml
@@ -0,0 +1,19 @@
+# Read the Docs configuration file
+# See https://docs.readthedocs.io/en/stable/config-file/v2.html for details
+
+version: 2
+
+build:
+  os: ubuntu-22.04
+  tools:
+    python: "3.11"
+    rust: "1.70"
+
+sphinx:
+  configuration: docs/conf.py
+
+python:
+  install:
+    - requirements: docs/requirements-docs.txt
+    - method: pip
+      path: .
diff --git a/code/RL_model/verl/verl_train/CONTRIBUTING.md b/code/RL_model/verl/verl_train/CONTRIBUTING.md
new file mode 100644
index 0000000000000000000000000000000000000000..6fd3023a0859f533951476fac6e8e06fe1e8aa3f
--- /dev/null
+++ b/code/RL_model/verl/verl_train/CONTRIBUTING.md
@@ -0,0 +1,90 @@
+# Contributing to verl
+
+Thank you for considering a contribution to verl! We welcome contributions of any kind - bug fixes, enhancements, documentation improvements, or even just feedback. Whether you're an experienced developer or this is your first open-source project, your help is invaluable.
+
+Your support can take many forms:
+- Report issues or unexpected behaviors.
+- Suggest or implement new features.
+- Improve or expand documentation.
+- Review pull requests and assist other contributors.
+- Spread the word: share verl in blog posts, social media, or give the repo a ⭐.
+
+## Finding Issues to Contribute
+
+Looking for ways to dive in? Check out these issues:
+- [Good first issues](https://github.com/volcengine/verl/issues?q=is%3Aissue%20state%3Aopen%20label%3A%22good%20first%20issue%22)
+- [Call for contribution](https://github.com/volcengine/verl/issues?q=is%3Aissue%20state%3Aopen%20label%3A%22call%20for%20contribution%22)
+Furthermore, you can learn the development plan and roadmap via [RFC](https://github.com/volcengine/verl/issues?q=is%3Aissue%20state%3Aopen%20label%3ARFC) and [Roadmap](https://github.com/volcengine/verl/issues?q=state%3Aopen%20label%3A%22roadmap%22).
+
+
+## Developing
+
+- **Python-only**: install verl via `pip install -e .[test,vllm]` or `pip install -e .[test,sglang]` and iterate quickly. For full dependency setup, check out the verl [installation doc](https://verl.readthedocs.io/en/latest/start/install.html).
+
+## Code Linting and Formatting
+
+We rely on pre-commit to keep our code consistent. To set it up:
+
+```bash
+pip install pre-commit
+pre-commit install
+# for staged changes
+pre-commit run
+# for all files in the repo
+pre-commit run --all-files
+# run a specific hook with pre-commit
+# pre-commit run --all-files --show-diff-on-failure --color=always <hood-id>
+pre-commit run --all-files --show-diff-on-failure --color=always ruff
+pre-commit run --all-files --show-diff-on-failure --color=always autogen-trainer-cfg
+```
+
+## Testing
+
+Our test suites run on GitHub Actions. Check these workflows for details:
+- [GPU unit tests](https://github.com/volcengine/verl/blob/main/.github/workflows/gpu_unit_tests.yml)
+- [CPU unit tests](https://github.com/volcengine/verl/blob/main/.github/workflows/cpu_unit_tests.yml)
+- [vLLM tests](https://github.com/volcengine/verl/blob/main/.github/workflows/vllm.yml)
+- [SGLang tests](https://github.com/volcengine/verl/blob/main/.github/workflows/sgl.yml)
+
+### Adding CI tests
+
+If possible, please add CI test(s) for your new feature:
+
+1. Find the most relevant workflow yml file, which usually corresponds to a `hydra` default config (e.g. `ppo_trainer`, `ppo_megatron_trainer`, `sft_trainer`, etc).
+2. Add related path patterns to the `paths` section if not already included.
+3. Minimize the workload of the test script(s) (see existing scripts for examples).
+
+## Building the Docs
+```
+# Ensure verl is on your PYTHONPATH, e.g.:
+pip install -e .[test]
+
+# Install documentation dependencies
+cd docs
+pip install -r requirements-docs.txt
+
+# Generate HTML docs
+make clean
+make html
+
+# Preview locally
+python -m http.server -d _build/html/
+```
+Open your browser at http://localhost:8000 to explore the docs.
+
+## Pull Requests & Code Reviews
+
+Thanks for submitting a PR! To streamline reviews:
+- Follow our Pull Request Template for title format and checklist.
+- Adhere to our pre-commit lint rules and ensure all checks pass.
+- Update docs for any user-facing changes.
+- Add or update tests in the CI workflows, or explain why tests aren't applicable.
+
+## License
+
+See the [LICENSE](https://github.com/volcengine/verl/blob/main/LICENSE) file for full details.
+
+## Thank You
+
+We appreciate your contributions to verl. Your efforts help make the project stronger and more user-friendly. Happy coding!
+
diff --git a/code/RL_model/verl/verl_train/LICENSE b/code/RL_model/verl/verl_train/LICENSE
new file mode 100644
index 0000000000000000000000000000000000000000..d645695673349e3947e8e5ae42332d0ac3164cd7
--- /dev/null
+++ b/code/RL_model/verl/verl_train/LICENSE
@@ -0,0 +1,202 @@
+
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diff --git a/code/RL_model/verl/verl_train/Notice.txt b/code/RL_model/verl/verl_train/Notice.txt
new file mode 100644
index 0000000000000000000000000000000000000000..ade439da525ac3f82936e131a1ae386f43207fd8
--- /dev/null
+++ b/code/RL_model/verl/verl_train/Notice.txt
@@ -0,0 +1 @@
+Copyright 2023-2024 Bytedance Ltd. and/or its affiliates 
\ No newline at end of file
diff --git a/code/RL_model/verl/verl_train/README.md b/code/RL_model/verl/verl_train/README.md
new file mode 100644
index 0000000000000000000000000000000000000000..3cb450bc6efb0007bdf0e1e4aa6dca8c39e9751e
--- /dev/null
+++ b/code/RL_model/verl/verl_train/README.md
@@ -0,0 +1,306 @@
+<div align="center">
+ 👋 Hi, everyone!
+    verl is a RL training library initiated by <b>ByteDance Seed team</b> and maintained by the verl community.
+    <br>
+    <br>
+</div>
+
+<div align="center">
+
+<a href="https://deepwiki.com/volcengine/verl"><img src="https://devin.ai/assets/deepwiki-badge.png" alt="Ask DeepWiki.com" style="height:20px;"></a>
+[![GitHub Repo stars](https://img.shields.io/github/stars/volcengine/verl)](https://github.com/volcengine/verl/stargazers)
+[![Twitter](https://img.shields.io/twitter/follow/verl_project)](https://twitter.com/verl_project)
+<a href="https://join.slack.com/t/verl-project/shared_invite/zt-3c6mc2khw-v0lo6NfDPuFP6OnkrZwfqw"><img src="https://img.shields.io/badge/Slack-verl-blueviolet?logo=slack&amp"></a>
+<a href="https://arxiv.org/pdf/2409.19256"><img src="https://img.shields.io/static/v1?label=EuroSys&message=Paper&color=red"></a>
+[![Documentation](https://img.shields.io/badge/documentation-blue)](https://verl.readthedocs.io/en/latest/)
+<a href="https://raw.githubusercontent.com/eric-haibin-lin/verl-community/refs/heads/main/WeChat.JPG"><img src="https://img.shields.io/badge/微信-green?logo=wechat&amp"></a>
+
+</div>
+
+![seed logo](https://github.com/user-attachments/assets/c42e675e-497c-4508-8bb9-093ad4d1f216)
+
+<h1 style="text-align: center;">verl: Volcano Engine Reinforcement Learning for LLMs</h1>
+
+verl is a flexible, efficient and production-ready RL training library for large language models (LLMs).
+
+verl is the open-source version of **[HybridFlow: A Flexible and Efficient RLHF Framework](https://arxiv.org/abs/2409.19256v2)** paper.
+
+verl is flexible and easy to use with:
+
+- **Easy extension of diverse RL algorithms**: The hybrid-controller programming model enables flexible representation and efficient execution of complex post-training dataflows. Build RL dataflows such as GRPO, PPO in a few lines of code.
+
+- **Seamless integration of existing LLM infra with modular APIs**: Decouples computation and data dependencies, enabling seamless integration with existing LLM frameworks, such as FSDP, Megatron-LM, vLLM, SGLang, etc
+
+- **Flexible device mapping**: Supports various placement of models onto different sets of GPUs for efficient resource utilization and scalability across different cluster sizes.
+
+- Ready integration with popular HuggingFace models
+
+verl is fast with:
+
+- **State-of-the-art throughput**: SOTA LLM training and inference engine integrations and SOTA RL throughput.
+
+- **Efficient actor model resharding with 3D-HybridEngine**: Eliminates memory redundancy and significantly reduces communication overhead during transitions between training and generation phases.
+
+<div align="center">
+ <img src="https://github.com/verl-project/verl-data/blob/main/images/verl-arch.png?raw=true" width="400" alt="verl-arch.png">
+</div>
+
+</p>
+
+## News
+
+- [2026/01] verl has been migrated to the [verl-project](https://github.com/verl-project)
+- [2026/01] verl first meetup was successfully held in Shanghai on 01/10, hosted by Volcengine and NVIDIA, the slides has been uploaded to [verl-data](https://github.com/verl-project/verl-data).
+- [2026/01] The `recipe` directory has been migrated to a dedicated repository: [verl-recipe](https://github.com/verl-project/verl-recipe) and added as a submodule. See https://github.com/volcengine/verl/pull/4795. It can be used as it was after `git submodule update --init --recursive recipe`. Note that [`transfer_queue`](verl/experimental/transfer_queue), [`fully_async_policy`](verl/experimental/fully_async_policy), [`one_step_off_policy`](verl/experimental/one_step_off_policy) and [`vla`](verl/experimental/vla) are kept under [`verl/experimental`](verl/experimental) since they are planned to be merged into the main library. Use them through `verl.experimental.{module}`.
+- [2025/12] [Mind Lab](https://macaron.im/mindlab) successfully used [verl](https://github.com/volcengine/verl) and [Megatron-bridge](https://github.com/NVIDIA-NeMo/Megatron-Bridge) to train GRPO Lora for Trillion-parameter model on 64 H800 - See their [techblog](https://macaron.im/mindlab/research/building-trillion-parameter-reasoning-rl-with-10-gpus).
+- [2025/10] verl is presented in the [PyTorch Conference 2025](https://pytorch.org/event/pytorch-conference-2025/).
+- [2025/08] verl is presented in the [PyTorch Expert Exchange Webinar](https://www.youtube.com/watch?v=Vd79NmmqY3Q&t=2s). [Slides](https://github.com/eric-haibin-lin/verl-community/blob/main/slides/verl_talk_pytorch_2025_08.pdf) available.
+- [2025/07] The [ReTool](https://arxiv.org/pdf/2504.11536) recipe is fully open sourced. [Blog](https://www.notion.so/verl-reTool-recipe-Using-multi-round-conversations-and-code-sandboxing-to-improve-the-math-of-large-23a8b5b7feba80b386b2e5b5e3c1cde0)
+- [2025/07] The first verl meetup will be held at ICML Vancouver on July 16th! Please [join us](https://lu.ma/0ek2nyao) if you are at ICML! (onsite only)
+- [2025/06] verl with Megatron backend enables large MoE models such as [DeepSeek-671B and Qwen3-235B](https://verl.readthedocs.io/en/latest/perf/dpsk.html).
+- [2025/03] [DAPO](https://dapo-sia.github.io/) is the open-sourced SOTA RL algorithm that achieves 50 points on AIME 2024 based on the Qwen2.5-32B pre-trained model, surpassing the previous SOTA achieved by DeepSeek's GRPO (DeepSeek-R1-Zero-Qwen-32B). DAPO's training is fully powered by verl and the reproduction code is available in `recipe/dapo` now.
+<details><summary> more... </summary>
+<ul>
+  <li>[2025/04] [Seed-Thinking-v1.5](https://github.com/ByteDance-Seed/Seed-Thinking-v1.5/blob/main/seed-thinking-v1.5.pdf) tech report is released! Trained with verl, Seed-Thinking-v1.5 achieves 86.7 on AIME 2024, 55.0 on Codeforces and 77.3 on GPQA, demonstrating excellent reasoning abilities in STEM and coding. Beyond reasoning tasks, the method demonstrates notable generalization across diverse domains.</li>
+  <li>[2025/07] verl keynote at [AWS AI Hours Singapore](https://pages.awscloud.com/aws-ai-hours-sg.html#agenda) on 7/8, verl & verl-agent project updates at [Agent for SWE meetup](https://lu.ma/e498qhsi) by LF AI & Data Singapore on 7/11.</li>
+  <li>[2025/06] verl team will provide latest project updates at [PyTorch Day China](https://www.lfasiallc.com/pytorch-day-china/) on June 7th. Meet our dev team in Beijing!</li>
+  <li> [2025/04] [VAPO](https://arxiv.org/pdf/2504.05118) (value-based augmented PPO) paper covers our latest RL method for reasoning models. Trained from Qwen-32B-base model, VAPO achieves 60.4 on AIME 2024, outperforming DAPO-32B.</li>
+  <li>[2025/05] [PF-PPO](https://arxiv.org/abs/2409.06957), accepted to ICML 2025, is now supported in verl! PF-PPO enhances policy learning efficiency and robustness by filtering potentially noisy reward signals and reusing high-quality experiences via a replay buffer.</li>
+  <li>[2025/04] We will give a tutorial about latest post-training techniques and programming guide for verl at [ICLR 2025 Expo](https://iclr.cc/virtual/2025/calendar?filter_events=Expo+Talk+Panel&filter_rooms=), [SCI-FM workshop](https://open-foundation-model.github.io/) and [LMSys afterparty](https://lu.ma/d23nyynm). Talk materials available [here](https://github.com/eric-haibin-lin/verl-community/tree/main/iclr25). </li>
+  <li>[2025/03] verl v0.3.0.post1 is released! See [release note](https://github.com/volcengine/verl/releases/) for details. It achieves [~1.4x speedup](https://tongyx361.github.io/blogs/posts/verl-intro/#/verl-flexible-and-efficient-rl-for-llms) compared to prev versions.</li>
+  <li>[2025/05] verl will be presented at [A2M Shanghai](https://a2m.msup.com.cn/home/?aid=4488&city=shanghai) on 5/16 - 5/17.</li>
+  <li>[2025/05] verl will be presented at [GOSIM x PyTorch Day 2025](https://paris2025.gosim.org/). See you in Paris! </li>
+  <li>[2025/03] We introduced the programming model of verl at the [vLLM Beijing Meetup](https://mp.weixin.qq.com/s/n77GibL2corAtQHtVEAzfg) and [verl intro and updates](https://github.com/eric-haibin-lin/verl-community/blob/main/slides/verl-lmsys-meetup.pdf) at the [SGLang-LMSYS Org Meetup](https://lu.ma/ntjrr7ig) in Sunnyvale mid-March.</li>
+  <li>[2025/03] We will present verl(HybridFlow) at EuroSys 2025. See you in Rotterdam!</li>
+  <li>[2025/02] verl v0.2.0.post2 is released!</li>
+  <li>[2025/02] We presented verl in the <a href="https://lu.ma/ji7atxux">Bytedance/NVIDIA/Anyscale Ray Meetup</a>. See you in San Jose!</li>
+  <li>[2025/01] [Doubao-1.5-pro](https://team.doubao.com/zh/special/doubao_1_5_pro) is released with SOTA-level performance on LLM & VLM. The RL scaling preview model is trained using verl, reaching OpenAI O1-level performance on math benchmarks (70.0 pass@1 on AIME).</li>
+  <li>[2024/12] verl is presented at Ray Forward 2024. Slides available <a href="https://github.com/eric-haibin-lin/verl-community/blob/main/slides/Ray_Forward_2024_%E5%B7%AB%E9%94%A1%E6%96%8C.pdf">here</a></li>
+  <li>[2024/12] The team presented <a href="https://neurips.cc/Expo/Conferences/2024/workshop/100677">Post-training LLMs: From Algorithms to Infrastructure</a> at NeurIPS 2024. <a href="https://github.com/eric-haibin-lin/verl-data/tree/neurips">Slides</a> and <a href="https://neurips.cc/Expo/Conferences/2024/workshop/100677">video</a> available.</li>
+  <li>[2024/10] verl is presented at Ray Summit. <a href="https://www.youtube.com/watch?v=MrhMcXkXvJU&list=PLzTswPQNepXntmT8jr9WaNfqQ60QwW7-U&index=37">Youtube video</a> available.</li>
+  <li>[2024/08] HybridFlow (verl) is accepted to EuroSys 2025.</li>
+</ul>
+</details>
+
+## Key Features
+
+- **FSDP**, **FSDP2** and **Megatron-LM** for training.
+- **vLLM**, **SGLang** and **HF Transformers** for rollout generation.
+- Compatible with Hugging Face Transformers and Modelscope Hub: [Qwen-3](https://github.com/volcengine/verl/blob/main/examples/grpo_trainer/run_qwen3-8b.sh), Qwen-2.5, Llama3.1, Gemma2, DeepSeek-LLM, etc
+- Supervised fine-tuning.
+- Reinforcement learning with [PPO](examples/ppo_trainer/), [GRPO](examples/grpo_trainer/), [GSPO](https://github.com/verl-project/verl-recipe/tree/main/gspo/), [ReMax](examples/remax_trainer/), [REINFORCE++](https://verl.readthedocs.io/en/latest/examples/config.html#algorithm), [RLOO](examples/rloo_trainer/), [PRIME](https://github.com/verl-project/verl-recipe/tree/main/prime/), [DAPO](https://github.com/verl-project/verl-recipe/tree/main/dapo/), [DrGRPO](https://github.com/verl-project/verl-recipe/tree/main/drgrpo), [KL_Cov & Clip_Cov](https://github.com/verl-project/verl-recipe/tree/main/entropy) etc.
+  - Support model-based reward and function-based reward (verifiable reward) for math, [coding](https://github.com/volcengine/verl-recipe/tree/main/dapo), etc
+  - Support vision-language models (VLMs) and [multi-modal RL](examples/grpo_trainer/run_qwen2_5_vl-7b.sh) with Qwen2.5-vl, Kimi-VL
+  - [Multi-turn with tool calling](https://github.com/volcengine/verl/tree/main/examples/sglang_multiturn)
+- LLM alignment recipes such as [Self-play preference optimization (SPPO)](https://github.com/verl-project/verl-recipe/tree/main/sppo)
+- Flash attention 2, [sequence packing](examples/ppo_trainer/run_qwen2-7b_seq_balance.sh), [sequence parallelism](examples/ppo_trainer/run_deepseek7b_llm_sp2.sh) support via DeepSpeed Ulysses, [LoRA](examples/sft/gsm8k/run_qwen_05_peft.sh), [Liger-kernel](examples/sft/gsm8k/run_qwen_05_sp2_liger.sh).
+- Scales up to 671B models and hundreds of GPUs with [expert parallelism](https://github.com/volcengine/verl/pull/1467)
+- Multi-gpu [LoRA RL](https://verl.readthedocs.io/en/latest/advance/ppo_lora.html) support to save memory.
+- Experiment tracking with wandb, swanlab, mlflow and tensorboard.
+- Hardware Support: Supports NVIDIA, AMD, [Ascend](https://github.com/volcengine/verl/blob/main/docs/ascend_tutorial/ascend_quick_start.rst)
+
+## Upcoming Features and Changes
+
+- Q3 Roadmap https://github.com/volcengine/verl/issues/2388
+- DeepSeek 671b optimizations with Megatron https://github.com/volcengine/verl/issues/1033
+- Multi-turn rollout and tools using optimizations https://github.com/volcengine/verl/issues/1882
+- [Agent integration](https://github.com/volcengine/verl/tree/main/verl/experimental/agent_loop)
+- Async and off-policy architecture https://github.com/volcengine/verl/pull/2231
+- List of breaking changes since v0.4 https://github.com/volcengine/verl/discussions/2270
+
+## Getting Started
+
+<a href="https://verl.readthedocs.io/en/latest/index.html"><b>Documentation</b></a>
+
+**Quickstart:**
+
+- [Installation](https://verl.readthedocs.io/en/latest/start/install.html)
+- [Quickstart](https://verl.readthedocs.io/en/latest/start/quickstart.html)
+- [Programming Guide](https://verl.readthedocs.io/en/latest/hybrid_flow.html) & [Tech Talk](https://hcqnc.xetlk.com/sl/3vACOK) (in Chinese)
+- [PPO in verl](https://verl.readthedocs.io/en/latest/algo/ppo.html)
+- [GRPO in verl](https://verl.readthedocs.io/en/latest/algo/grpo.html)
+
+**Running a PPO example step-by-step:**
+
+- [Prepare Data for Post-Training](https://verl.readthedocs.io/en/latest/preparation/prepare_data.html)
+- [Implement Reward Function for Dataset](https://verl.readthedocs.io/en/latest/preparation/reward_function.html)
+- [PPO Example Architecture](https://verl.readthedocs.io/en/latest/examples/ppo_code_architecture.html)
+- [Config Explanation](https://verl.readthedocs.io/en/latest/examples/config.html)
+
+**Reproducible algorithm baselines:**
+
+- [RL performance on coding, math](https://verl.readthedocs.io/en/latest/algo/baseline.html)
+
+**For code explanation and advance usage (extension):**
+
+- PPO Trainer and Workers
+
+  - [PPO Ray Trainer](https://verl.readthedocs.io/en/latest/workers/ray_trainer.html)
+  - [PyTorch FSDP Backend](https://verl.readthedocs.io/en/latest/workers/fsdp_workers.html)
+  - [Megatron-LM Backend](https://verl.readthedocs.io/en/latest/index.html)
+
+- Advanced Usage and Extension
+  - [Add Models with the FSDP Backend](https://verl.readthedocs.io/en/latest/advance/fsdp_extension.html)
+  - [Add Models with the Megatron-LM Backend](https://verl.readthedocs.io/en/latest/advance/megatron_extension.html)
+  - [Multi-turn Rollout Support](https://verl.readthedocs.io/en/latest/sglang_multiturn/multiturn.html)
+  - [Search Tool Integration](https://verl.readthedocs.io/en/latest/sglang_multiturn/search_tool_example.html)
+  - [Sandbox Fusion Integration](https://verl.readthedocs.io/en/latest/examples/sandbox_fusion_example.html)
+  - [Deployment using Separate GPU Resources](https://github.com/volcengine/verl/tree/main/examples/split_placement)
+  - [Extend to Other RL(HF) algorithms](https://verl.readthedocs.io/en/latest/advance/dpo_extension.html)
+  - [Ray API design tutorial](https://verl.readthedocs.io/en/latest/advance/placement.html)
+
+**Blogs from the community**
+
+- [When Reasoning Models Break Tokenization: The Hidden Complexity of Multiturn Training](https://github.com/zhaochenyang20/Awesome-ML-SYS-Tutorial/blob/main/rlhf/verl/multi-turn/fast_tokenization/multiturn_tokenization_and_masking.md)
+- [verl deployment on AWS SageMaker](https://medium.com/@kaige.yang0110/run-verl-on-sagemaker-using-4x8-l40s-gpus-8e6d5c3c61d3)
+- [verl x SGLang Multi-turn Code Walkthrough](https://github.com/zhaochenyang20/Awesome-ML-SYS-Tutorial/blob/main/rlhf/verl/multi-turn/code-walk-through/readme_EN.md)
+- [Optimizing SGLang Memory Usage in verl](https://hebiao064.github.io/rl-memory-management)
+- [SGLang, verl, OpenBMB and Tsinghua University: Pioneering End-to-End Multi-Turn RLHF](https://github.com/zhaochenyang20/Awesome-ML-SYS-Tutorial/blob/main/rlhf/verl/multi-turn/verl-multiturn-rollout-Release.md)
+- [Reinforcement Learning from Human Feedback on AMD GPUs with verl and ROCm Integration](https://rocm.blogs.amd.com/artificial-intelligence/verl-large-scale/README.html)
+- [veMLP x verl ：玩转强化学习训练](https://mp.weixin.qq.com/s/7nbqxk4knMGd-hQE9ls2tA)
+- [使用 verl 进行 GRPO 分布式强化学习训练最佳实践](https://www.volcengine.com/docs/6459/1463942)
+- [HybridFlow verl 原文浅析](https://github.com/zhaochenyang20/Awesome-ML-SYS-Tutorial/blob/main/rlhf/verl/readme.md)
+- [最高提升 20 倍吞吐量！豆包大模型团队发布全新 RLHF 框架，现已开源！](https://team.doubao.com/en/blog/%E6%9C%80%E9%AB%98%E6%8F%90%E5%8D%8720%E5%80%8D%E5%90%9E%E5%90%90%E9%87%8F-%E8%B1%86%E5%8C%85%E5%A4%A7%E6%A8%A1%E5%9E%8B%E5%9B%A2%E9%98%9F%E5%8F%91%E5%B8%83%E5%85%A8%E6%96%B0-rlhf-%E6%A1%86%E6%9E%B6-%E7%8E%B0%E5%B7%B2%E5%BC%80%E6%BA%90)
+
+## Performance Tuning Guide
+
+The performance is essential for on-policy RL algorithm. We have written a detailed [performance tuning guide](https://verl.readthedocs.io/en/latest/perf/perf_tuning.html) to help you optimize performance.
+
+## Upgrade to vLLM >= v0.8.2
+
+verl now supports vLLM>=0.8.2 when using FSDP as the training backend. Please refer to [this document](https://github.com/volcengine/verl/blob/main/docs/README_vllm0.8.md) for the installation guide and more information. Please avoid vllm 0.7.x, which contains bugs that may lead to OOMs and unexpected errors.
+
+## Use Latest SGLang
+
+SGLang is fully supported with verl, and SGLang RL Group is working extensively on building unique features, including multi-turn agentic RL, VLM RLHF, server-based RL, and partial rollout. Please refer to [this document](https://verl.readthedocs.io/en/latest/workers/sglang_worker.html) for the installation guide and more information.
+
+## Upgrade to FSDP2
+
+verl is fully embracing FSDP2! FSDP2 is recommended by torch distributed team, providing better throughput and memory usage, and is composible with other features (e.g. torch.compile). To enable FSDP2, simply use verl main and set the following options:
+
+```
+actor_rollout_ref.ref.strategy=fsdp2
+actor_rollout_ref.actor.strategy=fsdp2
+critic.strategy=fsdp2
+reward_model.strategy=fsdp2
+```
+
+Furthermore, FSDP2 cpu offloading is compatible with gradient accumulation. You can turn it on to save memory with `actor_rollout_ref.actor.fsdp_config.offload_policy=True`. For more details, see https://github.com/volcengine/verl/pull/1026
+
+## AMD Support (ROCm Kernel)
+
+verl now supports FSDP as the training engine (Megatron support coming soon) and both integrates with vLLM and SGLang as inference engines. Please refer to [this document](https://github.com/volcengine/verl/blob/main/docs/amd_tutorial/amd_build_dockerfile_page.rst) for the installation guide and more information, and [this document](https://github.com/volcengine/verl/blob/main/docs/amd_tutorial/amd_vllm_page.rst) for the vLLM performance tuning for ROCm.
+
+## Citation and acknowledgement
+
+If you find the project helpful, please cite:
+
+- [HybridFlow: A Flexible and Efficient RLHF Framework](https://arxiv.org/abs/2409.19256v2)
+- [A Framework for Training Large Language Models for Code Generation via Proximal Policy Optimization](https://i.cs.hku.hk/~cwu/papers/gmsheng-NL2Code24.pdf)
+
+```bibtex
+@article{sheng2024hybridflow,
+  title   = {HybridFlow: A Flexible and Efficient RLHF Framework},
+  author  = {Guangming Sheng and Chi Zhang and Zilingfeng Ye and Xibin Wu and Wang Zhang and Ru Zhang and Yanghua Peng and Haibin Lin and Chuan Wu},
+  year    = {2024},
+  journal = {arXiv preprint arXiv: 2409.19256}
+}
+```
+
+verl is inspired by the design of Nemo-Aligner, Deepspeed-chat and OpenRLHF. The project is adopted and contributed by Bytedance, Anyscale, LMSys.org, [Alibaba Qwen team](https://github.com/QwenLM/), Shanghai AI Lab, Tsinghua University, UC Berkeley, UCLA, UIUC, University of Hong Kong, ke.com, [All Hands AI](https://www.all-hands.dev/), [ModelBest](http://modelbest.cn/), JD AI Lab, Microsoft Research, [StepFun](https://www.stepfun.com/), Amazon, LinkedIn, Meituan, [Camel-AI](https://www.camel-ai.org/), [OpenManus](https://github.com/OpenManus), Xiaomi, NVIDIA research, [Baichuan](https://www.baichuan-ai.com/home), [RedNote](https://www.xiaohongshu.com/), [SwissAI](https://www.swiss-ai.org/), [Moonshot AI (Kimi)](https://www.moonshot-ai.com/), Baidu, Snowflake, Skywork.ai, JetBrains, [IceSword Lab](https://www.iceswordlab.com), and many more.
+
+## Awesome Projects Built with `verl`
+
+Welcome to register your awesome project build with `verl` for other developers' reference!
+
+- [TinyZero](https://github.com/Jiayi-Pan/TinyZero): a reproduction of **DeepSeek R1 Zero** recipe for reasoning tasks ![GitHub Repo stars](https://img.shields.io/github/stars/Jiayi-Pan/TinyZero)
+- [SkyThought](https://github.com/NovaSky-AI/SkyThought): RL training for Sky-T1-7B by NovaSky AI team. ![GitHub Repo stars](https://img.shields.io/github/stars/NovaSky-AI/SkyThought)
+- [simpleRL-reason](https://github.com/hkust-nlp/simpleRL-reason): SimpleRL-Zoo: Investigating and Taming Zero Reinforcement Learning for Open Base Models in the Wild ![GitHub Repo stars](https://img.shields.io/github/stars/hkust-nlp/simpleRL-reason)
+- [Easy-R1](https://github.com/hiyouga/EasyR1): **Multi-modal** RL training framework ![GitHub Repo stars](https://img.shields.io/github/stars/hiyouga/EasyR1)
+- [OpenManus-RL](https://github.com/OpenManus/OpenManus-RL): LLM Agents RL tuning framework for multiple agent environments. ![GitHub Repo stars](https://img.shields.io/github/stars/OpenManus/OpenManus-RL)
+- [rllm](https://github.com/agentica-project/rllm): async RL training with [verl-pipeline](https://github.com/agentica-project/verl-pipeline) ![GitHub Repo stars](https://img.shields.io/github/stars/agentica-project/rllm)
+- [RAGEN](https://github.com/ZihanWang314/ragen): a general-purpose reasoning **agent** training framework ![GitHub Repo stars](https://img.shields.io/github/stars/ZihanWang314/ragen)
+- [Search-R1](https://github.com/PeterGriffinJin/Search-R1): RL with reasoning and **searching (tool-call)** interleaved LLMs ![GitHub Repo stars](https://img.shields.io/github/stars/PeterGriffinJin/Search-R1)
+- [ReSearch](https://github.com/Agent-RL/ReSearch): Learning to **Re**ason with **Search** for LLMs via Reinforcement Learning ![GitHub Repo stars](https://img.shields.io/github/stars/Agent-RL/ReSearch)
+- [Skywork-OR1](https://github.com/SkyworkAI/Skywork-OR1): Skywork open reaonser series ![GitHub Repo stars](https://img.shields.io/github/stars/SkyworkAI/Skywork-OR1)
+- [ToRL](https://github.com/GAIR-NLP/ToRL): Scaling tool-integrated RL ![GitHub Repo stars](https://img.shields.io/github/stars/GAIR-NLP/ToRL)
+- [Absolute Zero Reasoner](https://github.com/LeapLabTHU/Absolute-Zero-Reasoner): [A no human curated data self-play framework for reasoning](https://arxiv.org/abs/2505.03335) ![GitHub Repo stars](https://img.shields.io/github/stars/LeapLabTHU/Absolute-Zero-Reasoner)
+- [verl-agent](https://github.com/langfengQ/verl-agent): A scalable training framework for **long-horizon LLM/VLM agents**, along with a new algorithm **GiGPO** ![GitHub Repo stars](https://img.shields.io/github/stars/langfengQ/verl-agent)
+- [RL-Factory](https://github.com/Simple-Efficient/RL-Factory): An easy and efficient RL post-training framework for Agentic Learning ![GitHub Repo stars](https://img.shields.io/github/stars/Simple-Efficient/RL-Factory)
+- [ReTool](https://retool-rl.github.io/): ReTool: reinforcement learning for strategic tool use in LLMs. Code release is in progress...
+- [verl-tool](https://github.com/TIGER-AI-Lab/verl-tool): An unified and easy-to-extend tool-agent training framework based on verl![GitHub Repo stars](https://img.shields.io/github/stars/TIGER-AI-Lab/verl-tool)
+- [PRIME](https://github.com/PRIME-RL/PRIME): Process reinforcement through implicit rewards ![GitHub Repo stars](https://img.shields.io/github/stars/PRIME-RL/PRIME)
+- [MemAgent](https://github.com/BytedTsinghua-SIA/MemAgent): MemAgent: Reshaping Long-Context LLM with Multi-Conv RL based Memory Agent ![GitHub Repo stars](https://img.shields.io/github/stars/BytedTsinghua-SIA/MemAgent)
+- [POLARIS](https://github.com/ChenxinAn-fdu/POLARIS): A Post-training recipe for scaling RL on Advanced Reasoning models ![GitHub Repo stars](https://img.shields.io/github/stars/ChenxinAn-fdu/POLARIS)
+- [GUI-R1](https://github.com/ritzz-ai/GUI-R1): **GUI-R1**: A Generalist R1-style Vision-Language Action Model For **GUI Agents** ![GitHub Repo stars](https://img.shields.io/github/stars/ritzz-ai/GUI-R1)
+- [DeepRetrieval](https://github.com/pat-jj/DeepRetrieval): RL Training of **Search Agent** with **Search/Retrieval Outcome** ![GitHub Repo stars](https://img.shields.io/github/stars/pat-jj/DeepRetrieval)
+- [Code-R1](https://github.com/ganler/code-r1): Reproducing R1 for **Code** with Reliable Rewards ![GitHub Repo stars](https://img.shields.io/github/stars/ganler/code-r1)
+- [DeepResearcher](https://github.com/GAIR-NLP/DeepResearcher): Scaling deep research via reinforcement learning in real-world environments ![GitHub Repo stars](https://img.shields.io/github/stars/GAIR-NLP/DeepResearcher)
+- [VAGEN](https://github.com/RAGEN-AI/VAGEN): Training VLM agents with multi-turn reinforcement learning ![GitHub Repo stars](https://img.shields.io/github/stars/RAGEN-AI/VAGEN)
+- [RM-R1](https://arxiv.org/abs/2505.02387): RL training of reasoning reward models ![GitHub Repo stars](https://img.shields.io/github/stars/RM-R1-UIUC/RM-R1)
+- [LUFFY](https://arxiv.org/pdf/2504.14945): Learning to Reason under Off-Policy Guidance![GitHub Repo stars](https://img.shields.io/github/stars/ElliottYan/LUFFY)
+- [DeepMath](https://github.com/zwhe99/DeepMath): DeepMath-103K data and series models for math reasoning![GitHub Repo stars](https://img.shields.io/github/stars/zwhe99/DeepMath)
+- [PACS](https://github.com/ritzz-ai/PACS): Implicit Actor Critic Coupling via a Supervised Learning Framework for RLVR ![GitHub Repo stars](https://img.shields.io/github/stars/ritzz-ai/PACS)
+- [Entropy Mechanism of RL](https://github.com/PRIME-RL/Entropy-Mechanism-of-RL): The Entropy Mechanism of Reinforcement Learning for Large Language Model Reasoning![GitHub Repo stars](https://img.shields.io/github/stars/PRIME-RL/Entropy-Mechanism-of-RL)
+- [LLaSA-TTS-GRPO](https://github.com/channel-io/ch-tts-llasa-rl-grpo): TTS fine-tuning with GRPO optimization based on LLASA models ![GitHub Repo stars](https://img.shields.io/github/stars/channel-io/ch-tts-llasa-rl-grpo)
+- [PF-PPO](https://arxiv.org/abs/2409.06957): Policy Filtration for PPO based on the reliability of reward signals for more efficient and robust RLHF.
+- [RACRO](https://github.com/gyhdog99/RACRO2): Build multi-modal reasoning models via decoupling it into query-conditioned captioning and text-only reasoning ![GitHub Repo stars](https://img.shields.io/github/stars/gyhdog99/RACRO2)
+- [Agent Lightning](https://github.com/microsoft/agent-lightning): A flexible and extensible framework that enables seamless agent optimization for any existing agent framework. ![GitHub Repo stars](https://img.shields.io/github/stars/microsoft/agent-lightning)
+- [VTool-R1](https://github.com/VTOOL-R1/vtool-r1): VLMs Learn to Think with Images via Reinforcement Learning on Multimodal Tool Use. ![GitHub Repo stars](https://img.shields.io/github/stars/VTOOL-R1/vtool-r1)
+- [Kimina-Prover-RL](https://github.com/project-numina/kimina-prover-rl/tree/main/recipe/kimina_prover_rl): Training pipeline for formal theorem proving, based on a paradigm inspired by DeepSeek-R1.
+- [RL-PLUS](https://github.com/YihongDong/RL-PLUS): Countering Capability Boundary Collapse of LLMs in Reinforcement Learning with Hybrid-policy Optimization.
+- [rStar2-Agent](https://github.com/microsoft/rStar): Using reinforcement learning with multi-step tool-calling for math tasks, rStar2-Agent-14B reaches frontier-level math reasoning in just 510 RL training steps ![GitHub Repo stars](https://img.shields.io/github/stars/microsoft/rStar)
+- [Vision-SR1](https://github.com/zli12321/Vision-SR1): Self-Rewarding Vision-Language Model via Reasoning Decomposition ![GitHub Repo stars](https://img.shields.io/github/stars/zli12321/Vision-SR1)
+- [SimpleVLA-RL](https://github.com/PRIME-RL/SimpleVLA-RL): SimpleVLA-RL: A Simple yet Effective Vision-Language Action Model for Reinforcement Learning ![GitHub Repo stars](https://img.shields.io/github/stars/PRIME-RL/SimpleVLA-RL)
+- [Table-R1](https://github.com/Table-R1/Table-R1): Table-R1: Inference-Time Scaling for Table Reasoning ![GitHub Repo stars](https://img.shields.io/github/stars/Table-R1/Table-R1)
+- [Revisual-R1](https://github.com/CSfufu/Revisual-R1): Revisual-R1: Advancing Multimodal Reasoning From Optimized Cold Start to Staged Reinforcement Learning ![GitHub Repo stars](https://img.shields.io/github/stars/CSfufu/Revisual-R1)
+- [ARES](https://github.com/shawn0728/ARES): ARES: Multimodal Adaptive Reasoning via Difficulty-Aware Token-Level Entropy Shaping ![GitHub Repo stars](https://img.shields.io/github/stars/shawn0728/ARES)
+- [Meta-Bandit-LLM](https://github.com/sanxing-chen/meta-bandit-llm): Meta-Bandit-LLM: Long-horizon multiturn interactive training for meta-bandit agents ![GitHub Repo stars](https://img.shields.io/github/stars/sanxing-chen/meta-bandit-llm)
+- [PokeeResearch](https://github.com/Pokee-AI/PokeeResearchOSS): PokeeResearch: State-of-the-art 7B DeepResearch Agent that leverages web search and content reading capabilities to answer complex questions using the most up-to-date information available online. ![Github Repo Stars](https://img.shields.io/github/stars/Pokee-AI/PokeeResearchOSS)
+- [Search Self-play](https://github.com/Alibaba-Quark/SSP): Pushing the Frontier of Agent Capability without Supervision ![GitHub Repo stars](https://img.shields.io/github/stars/Alibaba-Quark/SSP)
+- [OneThinker](https://github.com/tulerfeng/OneThinker): All-in-one Reasoning Model for Image and Video ![GitHub Repo stars](https://img.shields.io/github/stars/tulerfeng/OneThinker)
+- [OpenTinker](https://github.com/open-tinker/OpenTinker): Democratizing Agentic Reinforcement Learning as a Service ![GitHub Repo stars](https://img.shields.io/github/stars/open-tinker/OpenTinker)
+- [FlowRL](https://github.com/Xuekai-Zhu/FlowRL): Matching reward distributions via **flow balance** for diverse exploration and generalizable reasoning ![GitHub Repo stars](https://img.shields.io/github/stars/Xuekai-Zhu/FlowRL)
+- [Logic-RL](https://github.com/Unakar/Logic-RL): a reproduction of DeepSeek R1 Zero on 2K Tiny Logic Puzzle Dataset. ![GitHub Repo stars](https://img.shields.io/github/stars/Unakar/Logic-RL)
+- [Seed-Coder](https://github.com/ByteDance-Seed/Seed-Coder): RL training of Seed-Coder boosts performance on competitive programming ![GitHub Repo stars](https://img.shields.io/github/stars/ByteDance-Seed/Seed-Coder)
+- [all-hands/openhands-lm-32b-v0.1](https://www.all-hands.dev/blog/introducing-openhands-lm-32b----a-strong-open-coding-agent-model): A strong, open coding agent model, trained with [multi-turn fine-tuning](https://github.com/volcengine/verl/pull/195)
+- [s3](https://github.com/pat-jj/s3) **Efficient Yet Effective** Search Agent Training via RL ![GitHub Repo stars](https://img.shields.io/github/stars/pat-jj/s3)
+- [Rec-R1](https://arxiv.org/pdf/2503.24289): Bridging Generative Large Language Models and Recommendation Systems via Reinforcement Learning
+- [Explore RL Data Scaling](https://arxiv.org/abs/2503.22230): Exploring Data Scaling Trends and Effects in Reinforcement Learning from Human Feedback
+- [FIRE](https://arxiv.org/abs/2410.21236): Flaming-hot initiation with regular execution sampling for large language models
+- [DQO](https://arxiv.org/abs/2410.09302): Enhancing multi-Step reasoning abilities of language models through direct Q-function optimization
+- [ProRL](https://arxiv.org/abs/2505.24864): Prolonged Reinforcement Learning Expands Reasoning Boundaries in Large Language Models
+- [cognition-engineering](https://github.com/gair-nlp/cognition-engineering): Test time scaling drives cognition engineering. ![GitHub Repo stars](https://img.shields.io/github/stars/gair-nlp/cognition-engineering)
+- [Trust Region Preference Approximation](https://github.com/XueruiSu/Trust-Region-Preference-Approximation): A simple and stable **reinforcement learning algorithm** for LLM reasoning. ![GitHub Repo stars](https://img.shields.io/github/stars/XueruiSu/Trust-Region-Preference-Approximation)
+- [AdaRFT](https://github.com/uscnlp-lime/verl): Efficient Reinforcement Finetuning via **Adaptive Curriculum Learning** ![GitHub Repo stars](https://img.shields.io/github/stars/uscnlp-lime/verl)
+- [critic-rl](https://github.com/HKUNLP/critic-rl): LLM critics for code generation ![GitHub Repo stars](https://img.shields.io/github/stars/HKUNLP/critic-rl)
+- [self-rewarding-reasoning-LLM](https://arxiv.org/pdf/2502.19613): self-rewarding and correction with **generative reward models** ![GitHub Repo stars](https://img.shields.io/github/stars/RLHFlow/Self-rewarding-reasoning-LLM)
+- [DeepEnlighten](https://github.com/DolbyUUU/DeepEnlighten): Reproduce R1 with **social reasoning** tasks and analyze key findings ![GitHub Repo stars](https://img.shields.io/github/stars/DolbyUUU/DeepEnlighten)
+- [MetaSpatial](https://github.com/PzySeere/MetaSpatial): Reinforcing **3D Spatial Reasoning** in **VLMs** for the **Metaverse** ![GitHub Repo stars](https://img.shields.io/github/stars/PzySeere/MetaSpatial)
+- [PURE](https://github.com/CJReinforce/PURE): **Credit assignment** is the key to successful reinforcement fine-tuning using **process reward model** ![GitHub Repo stars](https://img.shields.io/github/stars/CJReinforce/PURE)
+- [cognitive-behaviors](https://github.com/kanishkg/cognitive-behaviors): Cognitive Behaviors that Enable Self-Improving Reasoners, or, Four Habits of Highly Effective STaRs ![GitHub Repo stars](https://img.shields.io/github/stars/kanishkg/cognitive-behaviors)
+- [deepscaler](https://github.com/agentica-project/rllm/tree/deepscaler): iterative context scaling with GRPO ![GitHub Repo stars](https://img.shields.io/github/stars/agentica-project/deepscaler)
+- [DAPO](https://dapo-sia.github.io/): the fully open source SOTA RL algorithm that beats DeepSeek-R1-zero-32B ![GitHub Repo stars](https://img.shields.io/github/stars/volcengine/verl)
+- [NoisyRollout](https://github.com/NUS-TRAIL/NoisyRollout): Reinforcing Visual Reasoning with Data Augmentation ![GitHub Repo stars](https://img.shields.io/github/stars/NUS-TRAIL/NoisyRollout)
+- [SPEAR](https://github.com/TencentYoutuResearch/SPEAR): **Self-imitation** with **Progressive Exploration** for Agentic Reinforcement Learning (ICLR 2026) ![GitHub Repo stars](https://img.shields.io/github/stars/TencentYoutuResearch/SPEAR)
+
+## Contribution Guide
+
+See [contributions guide](CONTRIBUTING.md)
+
+## About [ByteDance Seed Team](https://team.doubao.com/)
+
+Founded in 2023, ByteDance Seed Team is dedicated to crafting the industry's most advanced AI foundation models. The team aspires to become a world-class research team and make significant contributions to the advancement of science and society. You can get to know Bytedance Seed better through the following channels👇
+
+<div>
+  <a href="https://team.doubao.com/">
+    <img src="https://img.shields.io/badge/Website-%231e37ff?style=for-the-badge&logo=bytedance&logoColor=white"></a>
+  <a href="https://github.com/user-attachments/assets/469535a8-42f2-4797-acdf-4f7a1d4a0c3e">
+    <img src="https://img.shields.io/badge/WeChat-07C160?style=for-the-badge&logo=wechat&logoColor=white"></a>
+ <a href="https://www.xiaohongshu.com/user/profile/668e7e15000000000303157d?xsec_token=ABl2-aqekpytY6A8TuxjrwnZskU-6BsMRE_ufQQaSAvjc%3D&xsec_source=pc_search">
+    <img src="https://img.shields.io/badge/Xiaohongshu-%23FF2442?style=for-the-badge&logo=xiaohongshu&logoColor=white"></a>
+  <a href="https://www.zhihu.com/org/dou-bao-da-mo-xing-tuan-dui/">
+    <img src="https://img.shields.io/badge/zhihu-%230084FF?style=for-the-badge&logo=zhihu&logoColor=white"></a>
+</div>
+
+We are HIRING! Send us an [email](mailto:the.verl.project@gmail.com) if you are interested in internship/FTE opportunities in RL for agents.
diff --git a/code/RL_model/verl/verl_train/dataset/check_dataset_instances.py b/code/RL_model/verl/verl_train/dataset/check_dataset_instances.py
new file mode 100644
index 0000000000000000000000000000000000000000..045031d7f85862331910b9a410f93b7472c91fec
--- /dev/null
+++ b/code/RL_model/verl/verl_train/dataset/check_dataset_instances.py
@@ -0,0 +1,53 @@
+import argparse
+import json
+import os
+import datasets
+
+
+def load_dataset_from_args(args):
+    if args.parquet_path:
+        return datasets.Dataset.from_parquet(args.parquet_path)
+
+    parquet_path = os.path.join(args.local_dir, f"{args.split}.parquet")
+    return datasets.Dataset.from_parquet(parquet_path)
+
+
+def print_instance(example, idx):
+    print(f"\n=== Instance {idx} ===")
+    print(f"data_source: {example.get('data_source')}")
+
+    extra_info = example.get("extra_info", {})
+    print(f"target_level: {extra_info.get('target_level')}")
+    print(f"original_id: {extra_info.get('original_id')}")
+
+    prompt = example.get("prompt", [])
+    if prompt:
+        print("\n-- Prompt --")
+        print(prompt[0].get("content", ""))
+
+    reward_model = example.get("reward_model", {})
+    if reward_model:
+        print("\n-- Reward Model --")
+        print(json.dumps(reward_model, indent=2, ensure_ascii=True))
+
+
+if __name__ == "__main__":
+    parser = argparse.ArgumentParser()
+    parser.add_argument(
+        "--local_dir",
+        default="/home/mshahidul/readctrl/code/RL_model/verl/verl_train/dataset",
+    )
+    parser.add_argument("--split", default="train", choices=["train", "test"])
+    parser.add_argument("--parquet_path", default="")
+    parser.add_argument("--num_examples", type=int, default=3)
+    parser.add_argument("--start_index", type=int, default=0)
+    args = parser.parse_args()
+
+    dataset = load_dataset_from_args(args)
+    end_index = min(len(dataset), args.start_index + args.num_examples)
+
+    print(f"Total instances: {len(dataset)}")
+    print(f"Showing instances {args.start_index} to {end_index - 1}")
+
+    for idx in range(args.start_index, end_index):
+        print_instance(dataset[idx], idx)
diff --git a/code/RL_model/verl/verl_train/dataset/data_prep.py b/code/RL_model/verl/verl_train/dataset/data_prep.py
new file mode 100644
index 0000000000000000000000000000000000000000..a39d68933e027b6ef51de3f8b80e2792493c58a3
--- /dev/null
+++ b/code/RL_model/verl/verl_train/dataset/data_prep.py
@@ -0,0 +1,95 @@
+import os
+import json
+import datasets
+import argparse
+from verl.utils.hdfs_io import copy, makedirs
+
+# 1. Define the exact Prompt Template from your requirements
+# /home/mshahidul/readctrl/code/RL_model/verl/verl_train/dataset/prompt
+with open("/home/mshahidul/readctrl/code/RL_model/verl/verl_train/dataset/prompt", 'r') as f:
+    PROMPT_TEMPLATE = f.read()
+
+def make_map_fn(split, data_source):
+    def process_fn(example, idx):
+        # Extract fields from your specific JSON keys
+        full_text = example.pop('fulltext')
+        gold_summary = example.pop('summary')
+        fulltext_subclaims = example.pop('fulltext_subclaims', None)
+        summary_subclaims = example.pop('summary_subclaims', None)
+        
+        # Format the prompt using your template
+        # Note: Added 'English' as default source lang based on filename
+        prompt_content = PROMPT_TEMPLATE.format(
+            source_lang="English",
+            gold_summary=gold_summary,
+            full_text=full_text
+        )
+
+        return {
+            "data_source": data_source,
+            "prompt": [{
+                "role": "user",
+                "content": prompt_content
+            }],
+            "ability": "summarization",
+            "reward_model": {
+                "style": "rule",
+                "ground_truth": {
+                    "summary_subclaims": summary_subclaims,
+                    "fulltext_subclaims": fulltext_subclaims
+                }
+            },
+            "extra_info": {
+                "split": split,
+                "index": idx,
+                "original_id": example.get('id', idx),
+                "fulltext_subclaims": fulltext_subclaims,
+                "summary_subclaims": summary_subclaims
+            }
+        }
+    return process_fn
+
+if __name__ == '__main__':
+    parser = argparse.ArgumentParser()
+    # Path to your input JSON
+    parser.add_argument('--input_path', default='/home/mshahidul/readctrl/data/extracting_subclaim/extracted_subclaims_multiclinsum_test_en_full.json')
+    # Updated destination as requested
+    parser.add_argument('--local_dir', default='/home/mshahidul/readctrl/code/RL_model/verl/verl_train/dataset')
+    args = parser.parse_args()
+
+    data_source = 'multiclinsum'
+
+    # Load your local JSON file
+    with open(args.input_path, 'r') as f:
+        raw_data = json.load(f)
+    
+    # Convert to HuggingFace Dataset
+    dataset = datasets.Dataset.from_list(raw_data)
+
+    # Split into train/test (95%/5%)
+    dataset_split = dataset.train_test_split(test_size=0.05, seed=42, shuffle=True)
+
+    # Apply the mapping transformation per split
+    processed_train = dataset_split['train'].map(
+        function=make_map_fn('train', data_source),
+        with_indices=True
+    )
+    processed_test = dataset_split['test'].map(
+        function=make_map_fn('test', data_source),
+        with_indices=True
+    )
+
+    # Create the directory if it doesn't exist
+    os.makedirs(args.local_dir, exist_ok=True)
+
+    # Save to Parquet in the specified location
+    train_output_path = os.path.join(args.local_dir, 'train.parquet')
+    test_output_path = os.path.join(args.local_dir, 'test.parquet')
+    processed_train.to_parquet(train_output_path)
+    processed_test.to_parquet(test_output_path)
+
+    print(f"--- Dataset Preparation Complete ---")
+    print(f"Train file saved to: {train_output_path}")
+    print(f"Test file saved to: {test_output_path}")
+    print(f"Total train records: {len(processed_train)}")
+    print(f"Total test records: {len(processed_test)}")
\ No newline at end of file
diff --git a/code/RL_model/verl/verl_train/dataset/data_prep_three_prompts.py b/code/RL_model/verl/verl_train/dataset/data_prep_three_prompts.py
new file mode 100644
index 0000000000000000000000000000000000000000..d517a943198be85e941dfbd7ca21febd1dcbfccc
--- /dev/null
+++ b/code/RL_model/verl/verl_train/dataset/data_prep_three_prompts.py
@@ -0,0 +1,160 @@
+import os
+import json
+import argparse
+import datasets
+
+
+def load_prompt(path):
+    with open(path, "r") as f:
+        return f.read()
+
+
+def build_prompt(template, source_lang, gold_summary, full_text):
+    return template.format(
+        source_lang=source_lang,
+        gold_summary=gold_summary,
+        full_text=full_text,
+    )
+
+
+def build_record(
+    data_source,
+    split,
+    idx,
+    example,
+    level_key,
+    prompt_content,
+):
+    fulltext_subclaims = example.get("fulltext_subclaims")
+    summary_subclaims = example.get("summary_subclaims")
+    original_id = example.get("id", idx)
+
+    return {
+        "data_source": data_source,
+        "prompt": [{"role": "user", "content": prompt_content}],
+        "ability": "summarization",
+        "reward_model": {
+            "style": "rule",
+            "ground_truth": {
+                "summary_subclaims": summary_subclaims,
+                "fulltext_subclaims": fulltext_subclaims,
+            },
+        },
+        "extra_info": {
+            "split": split,
+            "index": idx,
+            "original_id": original_id,
+            "target_level": level_key,
+            "fulltext_subclaims": fulltext_subclaims,
+            "summary_subclaims": summary_subclaims,
+        },
+    }
+
+
+def expand_split(dataset, split, data_source, source_lang, prompt_templates):
+    records = []
+    for idx, example in enumerate(dataset):
+        full_text = example.get("fulltext")
+        gold_summary = example.get("summary")
+
+        for level_key, template in prompt_templates.items():
+            prompt_content = build_prompt(
+                template=template,
+                source_lang=source_lang,
+                gold_summary=gold_summary,
+                full_text=full_text,
+            )
+            records.append(
+                build_record(
+                    data_source=data_source,
+                    split=split,
+                    idx=idx,
+                    example=example,
+                    level_key=level_key,
+                    prompt_content=prompt_content,
+                )
+            )
+
+    return datasets.Dataset.from_list(records)
+
+
+if __name__ == "__main__":
+    parser = argparse.ArgumentParser()
+    parser.add_argument(
+        "--input_path",
+        default=(
+            "/home/mshahidul/readctrl/data/extracting_subclaim/"
+            "extracted_subclaims_multiclinsum_test_en_full.json"
+        ),
+    )
+    parser.add_argument(
+        "--local_dir",
+        default="/home/mshahidul/readctrl/code/RL_model/verl/verl_train/dataset",
+    )
+    parser.add_argument("--source_lang", default="English")
+    parser.add_argument(
+        "--prompt_low_path",
+        default=(
+            "/home/mshahidul/readctrl/code/RL_model/verl/verl_train/dataset/"
+            "prompt_low"
+        ),
+    )
+    parser.add_argument(
+        "--prompt_intermediate_path",
+        default=(
+            "/home/mshahidul/readctrl/code/RL_model/verl/verl_train/dataset/"
+            "prompt_intermediate"
+        ),
+    )
+    parser.add_argument(
+        "--prompt_proficient_path",
+        default=(
+            "/home/mshahidul/readctrl/code/RL_model/verl/verl_train/dataset/"
+            "prompt_proficient"
+        ),
+    )
+    args = parser.parse_args()
+
+    prompt_templates = {
+        "low_health_literacy": load_prompt(args.prompt_low_path),
+        "intermediate_health_literacy": load_prompt(args.prompt_intermediate_path),
+        "proficient_health_literacy": load_prompt(args.prompt_proficient_path),
+    }
+
+    data_source = "multiclinsum"
+
+    with open(args.input_path, "r") as f:
+        raw_data = json.load(f)
+
+    dataset = datasets.Dataset.from_list(raw_data)
+    half_size = len(dataset) // 2
+    dataset_half = dataset.shuffle(seed=42).select(range(half_size))
+    dataset_split = dataset_half.train_test_split(test_size=0.10, seed=42, shuffle=True)
+
+    processed_train = expand_split(
+        dataset_split["train"],
+        split="train",
+        data_source=data_source,
+        source_lang=args.source_lang,
+        prompt_templates=prompt_templates,
+    )
+    processed_test = expand_split(
+        dataset_split["test"],
+        split="test",
+        data_source=data_source,
+        source_lang=args.source_lang,
+        prompt_templates=prompt_templates,
+    )
+
+    os.makedirs(args.local_dir, exist_ok=True)
+
+    train_output_path = os.path.join(args.local_dir, "train.parquet")
+    test_output_path = os.path.join(args.local_dir, "test.parquet")
+    processed_train.to_parquet(train_output_path)
+    processed_test.to_parquet(test_output_path)
+
+    print("--- Dataset Preparation Complete ---")
+    print(f"Train file saved to: {train_output_path}")
+    print(f"Test file saved to: {test_output_path}")
+    print(f"Total train records: {len(processed_train)}")
+    print(f"Total test records: {len(processed_test)}")
diff --git a/code/RL_model/verl/verl_train/dataset/prompt b/code/RL_model/verl/verl_train/dataset/prompt
new file mode 100644
index 0000000000000000000000000000000000000000..084bb706dafafee7913a406ccb6fbffa524be840
--- /dev/null
+++ b/code/RL_model/verl/verl_train/dataset/prompt
@@ -0,0 +1,58 @@
+**System Role:**
+
+You are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.
+
+**User Prompt:**
+
+Please process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.
+### Instructions for Each Level:
+
+1. Level: Low Health Literacy (High Readability)
+
+Target: Individuals needing the simplest terms for immediate action.
+
+Linguistic Goal: Use "living room" language. Replace all medical jargon with functional descriptions (e.g., "renal" becomes "kidney").
+
+Information Density: Focus strictly on the "need-to-know" info found in the Gold Summary.
+
+Strategy: High paraphrasing using analogies. One idea per sentence.
+
+Faithfulness: Must align perfectly with the Gold Summary.
+
+2. Level: Intermediate Health Literacy (Medium Readability)
+
+Target: The general public (news-reading level).
+
+Linguistic Goal: Standard vocabulary. Common medical terms are okay, but technical "doctor-speak" must be simplified.
+
+Information Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.
+
+Strategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.
+
+Faithfulness: Maintains the main narrative of the Gold Summary.
+
+3. Level: Proficient Health Literacy (Low Readability)
+
+Target: Researchers, clinicians, or highly informed patients.
+
+Linguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.
+
+Information Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.
+
+Strategy: Minimal paraphrasing. Retain all original technical terminology.
+
+Faithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.
+
+
+I will provide the following information:
+
+- Input Language: <<<SOURCE_LANGUAGE>>>
+- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>
+- Source Text (detailed content): <<<FULL_TEXT>>>
+
+**Output Format (JSON only):**
+    {{
+    "low_health_literacy": "...",
+    "intermediate_health_literacy": "...",
+    "proficient_health_literacy": "..."
+    }}
\ No newline at end of file
diff --git a/code/RL_model/verl/verl_train/dataset/prompt_intermediate b/code/RL_model/verl/verl_train/dataset/prompt_intermediate
new file mode 100644
index 0000000000000000000000000000000000000000..1ecbed8038fbfeb17c688db616ea8a47bfff559a
--- /dev/null
+++ b/code/RL_model/verl/verl_train/dataset/prompt_intermediate
@@ -0,0 +1,32 @@
+**System Role:**
+
+You are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into a version appropriate for readers with intermediate health literacy. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified version remains accurate and focused on the most important information.
+
+**User Prompt:**
+
+Please process the following medical Source Text and its corresponding Gold Summary to generate ONE version tailored to Intermediate Health Literacy (Medium Readability).
+
+### Instructions:
+
+Level: Intermediate Health Literacy (Medium Readability)
+
+Target: The general public (news-reading level).
+
+Linguistic Goal: Standard vocabulary. Common medical terms are okay, but technical "doctor-speak" must be simplified.
+
+Information Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.
+
+Strategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.
+
+Faithfulness: Maintains the main narrative of the Gold Summary.
+
+I will provide the following information:
+
+- Input Language: {source_lang}
+- Gold Summary (the anchor reference summary): {gold_summary}
+- Source Text (detailed content): {full_text}
+
+**Output Format (JSON only):**
+    {{
+    "intermediate_health_literacy": "..."
+    }}
diff --git a/code/RL_model/verl/verl_train/dataset/prompt_low b/code/RL_model/verl/verl_train/dataset/prompt_low
new file mode 100644
index 0000000000000000000000000000000000000000..c8aab1735f605b9c3f44d785955868771e8b7938
--- /dev/null
+++ b/code/RL_model/verl/verl_train/dataset/prompt_low
@@ -0,0 +1,32 @@
+**System Role:**
+
+You are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into a version appropriate for readers with low health literacy. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified version remains accurate and focused on the most important information.
+
+**User Prompt:**
+
+Please process the following medical Source Text and its corresponding Gold Summary to generate ONE version tailored to Low Health Literacy (High Readability).
+
+### Instructions:
+
+Level: Low Health Literacy (High Readability)
+
+Target: Individuals needing the simplest terms for immediate action.
+
+Linguistic Goal: Use "living room" language. Replace all medical jargon with functional descriptions (e.g., "renal" becomes "kidney").
+
+Information Density: Focus strictly on the "need-to-know" info found in the Gold Summary.
+
+Strategy: High paraphrasing using analogies. One idea per sentence.
+
+Faithfulness: Must align perfectly with the Gold Summary.
+
+I will provide the following information:
+
+- Input Language: {source_lang}
+- Gold Summary (the anchor reference summary): {gold_summary}
+- Source Text (detailed content): {full_text}
+
+**Output Format (JSON only):**
+    {{
+    "low_health_literacy": "..."
+    }}
diff --git a/code/RL_model/verl/verl_train/dataset/prompt_proficient b/code/RL_model/verl/verl_train/dataset/prompt_proficient
new file mode 100644
index 0000000000000000000000000000000000000000..0b87d8fd77e9676e9553ca7b75818b25c4f099e7
--- /dev/null
+++ b/code/RL_model/verl/verl_train/dataset/prompt_proficient
@@ -0,0 +1,32 @@
+**System Role:**
+
+You are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into a version appropriate for readers with proficient health literacy. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as a factual anchor, but you may incorporate deeper scientific context from the Source Text.
+
+**User Prompt:**
+
+Please process the following medical Source Text and its corresponding Gold Summary to generate ONE version tailored to Proficient Health Literacy (Low Readability).
+
+### Instructions:
+
+Level: Proficient Health Literacy (Low Readability)
+
+Target: Researchers, clinicians, or highly informed patients.
+
+Linguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.
+
+Information Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.
+
+Strategy: Minimal paraphrasing. Retain all original technical terminology.
+
+Faithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.
+
+I will provide the following information:
+
+- Input Language: {source_lang}
+- Gold Summary (the anchor reference summary): {gold_summary}
+- Source Text (detailed content): {full_text}
+
+**Output Format (JSON only):**
+    {{
+    "proficient_health_literacy": "..."
+    }}
diff --git a/code/RL_model/verl/verl_train/debug_reward_func.jsonl b/code/RL_model/verl/verl_train/debug_reward_func.jsonl
new file mode 100644
index 0000000000000000000000000000000000000000..8bd86e51703423d353eed67a403eeeb2bf3d91bf
--- /dev/null
+++ b/code/RL_model/verl/verl_train/debug_reward_func.jsonl
@@ -0,0 +1,528 @@
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidneys don\u2019t work properly, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through routine screening is key to managing kidney health and preventing complications.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration and tubular reabsorption. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance, and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by underlying pathophysiological mechanisms including glomerulosclerosis, tubular atrophy, and vascular remodeling, and early intervention through biomarker monitoring and targeted therapies is critical to preserving renal function and delaying disease progression.\"\n}", "ground_truth": "A 14-year-old boy attended a local hospital for ankylosing spondylitis. Chest radiography showed an enhanced circular-density shadow near the left mediastinum. The patient had no chest symptoms and the physical examination was normal. Because of the mediastinal occupation, the patient visited our department of chest surgery for further treatment. During surgery, a left pericardial defect was observed. The bronchogenic cyst was removed by thoracoscopic surgery, but the pericardial defect remained untreated, and a satisfactory outcome was achieved after the operation. The patient was diagnosed with a mediastinal tumor. The pathological diagnosis of the tumor was a bronchogenic cyst.", "extra_info": {"index": 136, "original_id": "multiclinsum_test_2394_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidneys don\u2019t work properly, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through routine screening is key to managing kidney health and preventing complications.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration and tubular reabsorption. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance, and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and systemic inflammation, and early intervention through biomarker monitoring and pharmacological management is critical to preserving renal function and delaying disease progression.\"\n}", "ground_truth": "We report a case of thoracoscopic resection of the posterior segment of the right upper lobe of the lung. Preoperatively, the nodule was believed to be located in the superior segment of the right lower lobe. However, intraoperative exploration revealed that the nodule was located in the posterior segment of the right upper lobe, further showing that the bronchi of the posterior segment of the right lung opened into the bronchus intermedius. The procedure was completed uneventfully. Postoperative retrospective three-dimensional (3D) reconstruction of the lung CT images confirmed that the bronchi of the posterior segment of the right upper lobe originated from the bronchus intermedius.", "extra_info": {"index": 141, "original_id": "multiclinsum_test_2891_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidneys don\u2019t work properly, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through routine screening is key to managing kidney health and preventing complications.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration and tubular reabsorption. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance, and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and systemic inflammation, and early intervention through biomarker monitoring and pharmacological management is critical to preserving renal function and delaying disease progression.\"\n}", "ground_truth": "We report and analyse a case of a 34-year-old female who presented with ataxia. Magnetic Resonance Imaging (MRI) of the brain revealed demyelinating lesions in the white matter. Genetic testing identified the c.4044C > G and c.1186-2A > G variants in the POLR3A gene. The patient was diagnosed with hypomyelinating leukodystrophy type 7 and received neurotrophic and symptomatic supportive therapy. However, after 1 month of follow-up, there was no improvement in her symptoms.", "extra_info": {"index": 134, "original_id": "multiclinsum_test_1579_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidneys don\u2019t work properly, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through routine screening is key to managing kidney health and preventing complications.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration and tubular reabsorption. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance, and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and systemic inflammation, and early intervention through biomarker monitoring and pharmacological management is critical to preserving renal function and delaying disease progression.\"\n}", "ground_truth": "A 56-year-old female, with previous history of intestinal pneumonitis, mild pulmonary hypertension and gastroesophageal reflux secondary to systemic scleroderma, is considered for lung transplant. Initially, due to persistent gastroesophageal reflux, a transplant was not a viable. This was corrected with an open gastrectomy with roux-en-Y anastomosis. Follow-up one week later revealed normal anatomy, adequate esophageal-jejunal anastomosis, and adequate contrast medium transit via esophagogram. Additionally, there was no evidence of contrast medium reflux indicating a resolved gastroesophageal reflux disease. This led to the patient becoming a candidate for lung transplant.", "extra_info": {"index": 138, "original_id": "multiclinsum_test_2494_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidneys don\u2019t work properly, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through routine screening is key to managing kidney health and preventing complications.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration and tubular reabsorption. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance, and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and systemic inflammation, and early intervention through biomarker monitoring and pharmacological management is critical to preserving renal function and delaying disease progression.\"\n}", "ground_truth": "This case report presents the case of a 77 year old female patient with degenerative hip disease in the presence of an ipsilateral arthrodesis of the knee. The patient was operated using the DAA. No complications were found and the patient had an excellent follow-up with a forgotten joint score of 93.75 at 1 year. The difficulty in this case consists in finding the correct stem anteversion with the altered knee anatomy. Using pre-operative templating on X-rays, intraoperative fluoroscopy and the posterior femoral neck the hip biomechanics could be restored.", "extra_info": {"index": 140, "original_id": "multiclinsum_test_2302_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidneys don\u2019t work properly, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through routine screening is key to managing kidney health and preventing complications.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration and tubular reabsorption. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance, and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and systemic inflammation, and early intervention through biomarker monitoring and pharmacological management is critical to preserving renal function and delaying disease progression.\"\n}", "ground_truth": "A Chinese family with ATS was recruited for the current study. Clinical characteristics (including findings from renal biopsy) of ATS patients were collected from medical records, and potential causative genes were explored by whole-exome sequencing. A heterozygous substitution in intron 22 of COL4A3 (NM_000091 c.2657-1G>A) was found in the patients, which was further confirmed by quantitative polymerase chain reaction.", "extra_info": {"index": 132, "original_id": "multiclinsum_test_1061_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidneys don\u2019t work properly, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through routine screening is key to managing kidney health and preventing complications.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration and tubular reabsorption. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance, and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and systemic inflammation, and early intervention through biomarker monitoring and pharmacological management is critical to preserving renal function and delaying disease progression.\"\n}", "ground_truth": "Here case report, a 24-year-old patient from an endemic region of Somalia presented with fever, headache, abdominal pain, nausea, vomiting, and weight loss for two months. Initially, the patient received symptomatic treatment and a blood transfusion but showed no improvement. Physical examination revealed fever, pallor, and hepatosplenomegaly. Laboratory tests showed pancytopenia and positive rapid diagnostic test for plasmodium parasite antigen. Despite three days of anti-malarial treatment, the symptoms persisted, and hepatosplenomegaly worsened. Further investigations, including infectious disease tests, were conducted, ruling out HIV, viral hepatitis, Brucella, and Leishmania antibodies. Peripheral blood smear showed pancytopenia and bone marrow aspiration revealed no evidence of infection or malignancy. A tru-cut biopsy of the spleen was performed, confirming the diagnosis of visceral leishmaniasis. The patient received a combination therapy of sodium stibogluconate and paromomycin, leading to significant improvement. After completing treatment, the patient was discharged with normal spleen biopsy results.", "extra_info": {"index": 146, "original_id": "multiclinsum_test_292_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidneys don\u2019t work properly, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through routine screening is key to managing kidney health and preventing complications.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration and tubular reabsorption. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance, and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and systemic inflammation, and early intervention through biomarker monitoring and pharmacological management is critical to preserving renal function and delaying disease progression.\"\n}", "ground_truth": "A 70-year-old Japanese man with essential hypertension, dyslipidemia, chronic kidney disease and emphysema was hospitalized with the novel coronavirus disease. He had hypoxemia that was disproportionate to the severity of pneumonia indicated by computed tomography (CT), along with coagulation abnormalities. We speculated that there was a high possibility that he had developed ventilation and blood flow imbalance due to pulmonary intravascular coagulopathy (PIC) or hypoxic pulmonary vasoconstriction (HPV). In this case, early, short-term combination therapy with remdesivir, nafamostat mesylate and low-dose dexamethasone (Dex) was successful.", "extra_info": {"index": 144, "original_id": "multiclinsum_test_2467_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidneys don\u2019t work properly, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through routine screening is key to managing kidney health and preventing complications.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration and tubular reabsorption. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance, and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and systemic inflammation, and early intervention through biomarker monitoring and pharmacological management is critical to preserving renal function and delaying disease progression.\"\n}", "ground_truth": "Severe thermal corneoscleral injury occurred during phacoemulsification in the right eye of a 74-year-old male. His medical history was prostate hypertrophy. Visual acuity was hand motion and the intraocular pressure was 3 mm Hg OD. There was heavy corneal stromal opacity with intraocular fluid leakage. The patient underwent transplantation of a donor scleral graft to the burn site. Histologically, the injured sclera showed coagulation necrosis without inflammatory cell infiltration. An intraocular lens was eventually fixed in the ciliary sulcus 7 months later. His visual acuity remains at 2/20 OD.", "extra_info": {"index": 150, "original_id": "multiclinsum_test_1564_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidneys don\u2019t work properly, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through routine screening is key to managing kidney health and preventing complications.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration and tubular reabsorption. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance, and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and systemic inflammation, and early intervention through biomarker monitoring and pharmacological management is critical to preserving renal function and delaying disease progression.\"\n}", "ground_truth": "A 60-year-old white female with Polyneuropathy, Organomegaly, Endocrinopathy, Monoclonal plasma cell disorder, Skin changes (POEMS) syndrome and newly diagnosed HTN was referred because of an elevated creatinine level. She denied being an active smoker but reported long-term exposure to cigarette smoke due to living with a heavy smoking family and working as a bartender. Further investigations revealed microscopic hematuria and nephritic range proteinuria. Kidney biopsy revealed diffuse and focal nodular mesangial expansion without hypercellularity, with negative staining for amyloid, fibrillary glomerulonephritis, and immunoglobulins, leading to a diagnosis of ING.", "extra_info": {"index": 147, "original_id": "multiclinsum_test_3054_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by glomerular filtration rate (GFR) decline, proteinuria, and systemic inflammation, and requires longitudinal monitoring with biomarkers such as serum creatinine and estimated GFR to guide therapeutic interventions including pharmacological modulation, dietary restriction, and potential dialysis initiation.\"\n}", "ground_truth": "The palmar branch of the median nerve was surrounded by a significant haematoma in addition to the strangulation damage caused by its more superficial location in contrast to the median nerve.", "extra_info": {"index": 137, "original_id": "multiclinsum_test_2648_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by glomerular filtration rate (GFR) decline, proteinuria, and systemic inflammation, and requires longitudinal monitoring with biomarkers such as serum creatinine and estimated GFR to guide therapeutic interventions including pharmacological modulation, dietary restriction, and potential dialysis initiation.\"\n}", "ground_truth": "We present a documented case of a 4 years and 8-month-old Syrian Arabic girl with a distinctive course of signs and symptoms of rapid-onset obesity with hypoventilation, hypothalamic dysfunction, and autonomic dysregulation syndrome accompanied by mature ganglioneuroma in her chest, a homogenous mild enlargement of her pituitary gland, generalized cortical brain atrophy, and seizures. Three months after her first marked symptoms were noted she had a sudden progression of severe respiratory distress that ended with her death.", "extra_info": {"index": 139, "original_id": "multiclinsum_test_2845_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by glomerular filtration rate (GFR) decline, proteinuria, and systemic inflammation, and requires longitudinal monitoring with biomarkers such as serum creatinine and estimated GFR to guide therapeutic interventions including pharmacological modulation, dietary restriction, and potential dialysis initiation.\"\n}", "ground_truth": "We report the imaging appearance of dermatofibrosarcoma protuberans on the breast of a 41-year-old Chinese man who initially presented with a palpable lump. A mammogram showed two lesions, one with well circumscribed and the other with an ill defined border, in his right breast. Conventional magnetic resonance imaging was performed and showed the well defined larger lesion with mild central hypointensity while the smaller lesion had an irregular border. Both lesions were well characterized on the fat-suppressed sequences.", "extra_info": {"index": 135, "original_id": "multiclinsum_test_1990_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "A 48-year-old female underwent video-assisted thoracoscopic surgery (VATS) combined with left lower lobectomy. The distal end of the left branch of the tracheal tube was lodged by surgical sutures. In this case, the respiratory physician burned the sutures using an argon electrode, after discussion with the thoracic surgery experts.", "extra_info": {"index": 24, "original_id": "multiclinsum_test_1206_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by glomerular filtration rate (GFR) decline, proteinuria, and systemic inflammation, and requires longitudinal monitoring with biomarkers such as serum creatinine and estimated GFR to guide therapeutic interventions including pharmacological modulation, dietary restriction, and potential dialysis initiation.\"\n}", "ground_truth": "A previously healthy 51-year-old female with history of hypothyroidism presented with acute onset chest pain for 1 day. Patient's electrocardiogram was normal, however, she had elevated troponins and given her typical chest pain, she was diagnosed with acute coronary syndrome (ACS). The patient had been on levothyroxine and was found to have a subnormal thyroid-stimulating hormone level suggesting hyperthyroidism. Echocardiogram was normal. Coronary angiogram showed an anomalous RCA arising from the left coronary cusp of the sinus of Valsalva and no evidence of atherosclerosis. A coronary computed tomography angiogram was done confirming this finding and showed a slit-like deformity of the coronary ostium with at least 50% luminal stenosis. The patient was referred to a cardiothoracic surgeon for potential coronary artery bypass graft.", "extra_info": {"index": 133, "original_id": "multiclinsum_test_2590_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by glomerular filtration rate (GFR) decline, proteinuria, and systemic inflammation, and requires longitudinal monitoring with biomarkers such as serum creatinine and estimated GFR to guide therapeutic interventions including pharmacological modulation, dietary restriction, and potential dialysis initiation.\"\n}", "ground_truth": "In this case, we present a young, otherwise healthy patient that was diagnosed with a primary leiomyosarcoma of the small finger. After her diagnosis, she underwent extensive oncologic workup, and subsequently underwent successful ray amputation with an excellent outcome. She remains disease free.", "extra_info": {"index": 143, "original_id": "multiclinsum_test_2201_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by glomerular filtration rate (GFR) decline, proteinuria, and systemic inflammation, and requires longitudinal monitoring with biomarkers such as serum creatinine and estimated GFR to guide therapeutic interventions including pharmacological modulation, dietary restriction, and potential dialysis initiation.\"\n}", "ground_truth": "We report a case of a 33-year-old man, presenting with a five-month history of bilateral lower extremity pain, as well as paresthesia, and mild weakness in one lateral lower extremity. A lumbar laminectomy of L3 to L5 and en bloc resection of the tumor was performed. Postoperative histopathology and immunohistochemical analysis of the tumor were consistent with that of a carcinoid tumor. There were no clinical or radiological signs of tumor recurrence or metastasis at the patient's two year postoperative follow-up.", "extra_info": {"index": 142, "original_id": "multiclinsum_test_2169_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by glomerular filtration rate (GFR) decline, proteinuria, and systemic inflammation, and requires longitudinal monitoring with biomarkers such as serum creatinine and estimated GFR to guide therapeutic interventions including pharmacological modulation, dietary restriction, and potential dialysis initiation.\"\n}", "ground_truth": "A 65-year-old woman with persistent atrial fibrillation was referred for LAAc. Transesophageal echocardiography (TEE) revealed spontaneous contrast in the LAA without formation of a thrombus; the LAA shape was tortuous and difficult to assess. A first LAAc procedure was unsuccessful given the unsuitable sheath position. Therefore, a soft three-dimensional (3D) model printing was performed by laser sintering and revealed excessive sheath kinking with an inferior approach, but successful deployment would be feasible using a superior approach. Successful trans-jugular implantation of a Watchman FLX 31 device in stable position without residual leakage was achieved during the subsequent procedure. At 3-month follow-up, and after cessation of oral anticoagulation, the patient's symptoms improved. Imaging demonstrated complete LAA occlusion and correct placement of the device along the LAA superior axis.", "extra_info": {"index": 145, "original_id": "multiclinsum_test_2065_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "We report a 44-year-old man with end-stage renal disease post failed kidney transplant on low-dose mycophenolate mofetil who presented with acute onset of abdominal pain. He was successfully given the diagnosis of perforated jejunal diverticulum. The patient successfully underwent a segmental jejunal resection and anastomosis. He unfortunately developed a recurrent jejunal perforation a month later and again had the second segmental jejunal resection operation. Mycophenolate mofetil then was discontinued.", "extra_info": {"index": 22, "original_id": "multiclinsum_test_295_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by glomerular filtration rate (GFR) decline, proteinuria, and systemic inflammation, and requires longitudinal monitoring with biomarkers such as serum creatinine and estimated GFR to guide therapeutic interventions including pharmacological modulation, dietary restriction, and potential dialysis initiation.\"\n}", "ground_truth": "A 23-year-old female presented to our eye clinic with chief complaint of mild blurring of vision in the right eye and inquired about refractive surgery. The patient denied any previous history of ocular inflammation, trauma, surgery, or use of topical or systemic medications. Slit-lamp examination of the right eye anterior segment was within normal limits except for the crystalline lens anterior capsular which showed confluent pigment deposits stellate in shape over the pupillary axis, whereas left eye examination was completely within normal limits. Ophthalmic examination of the posterior segment was normal in both eyes. Based on her previous ophthalmic history and slit-lamp examination of the right eye, a diagnosis of unilateral congenital lenticular pigmentation was made.", "extra_info": {"index": 149, "original_id": "multiclinsum_test_2126_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by glomerular filtration rate (GFR) decline, proteinuria, and systemic inflammation, and requires longitudinal monitoring with biomarkers such as serum creatinine and estimated GFR to guide therapeutic interventions including pharmacological modulation, dietary restriction, and potential dialysis initiation.\"\n}", "ground_truth": "A 70-year-old male patient was affected by encephalitis caused by scrub typhus that occurred 23 years ago. He had poor cognition and his clinical examination findings were as follows: Mini-Mental Status Examination score, 14; and handgrip strength (right/left, kg), 32.3/31.3. DTT revealed serious injuries of the left thalamocingulate tract and right mammillothalamic tract in the Papez circuit, and a partial injury of the anterior part of the fornix.", "extra_info": {"index": 148, "original_id": "multiclinsum_test_1723_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by glomerular filtration rate (GFR) decline, proteinuria, and systemic inflammation, and requires longitudinal monitoring with biomarkers such as serum creatinine and estimated GFR to guide therapeutic interventions including pharmacological modulation, dietary restriction, and potential dialysis initiation.\"\n}", "ground_truth": "A 21-year-old female patient with abdominal pain, irregular menstruation, hyperestrogenemia, and an ovarian mass was included. Brain magnetic resonance imaging (MRI) revealed a pituitary macroadenoma, and transsphenoidal surgery relieved her clinical symptoms. Before transsphenoidal surgery, plasma CA125, estradiol levels were elevated, while prolactin, luteinizing hormone, follicle-stimulating hormone, PROG, cortisol, FT4, thyroid-stimulating hormone, parathyroid hormone, and GH levels were maintained at normal levels. After transsphenoidal surgery, the patient was diagnosed with a functioning gonadotroph adenoma. During follow-up, pelvic ultrasound confirmed normal-sized ovaries in the patient, the menstrual cycle returned to regular, and her hormones were maintained within a normal range. There was no evidence of tumor recurrence after two years of follow-up.", "extra_info": {"index": 151, "original_id": "multiclinsum_test_318_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by glomerular filtration rate (GFR) decline, proteinuria, and systemic inflammation, and requires longitudinal monitoring with biomarkers such as serum creatinine and estimated GFR to guide therapeutic interventions including pharmacological modulation, dietary restriction, and potential dialysis initiation.\"\n}", "ground_truth": "A 58-year-old woman presented with palpitations and diarrhea. Atrial fibrillation with spontaneous conversion to sinus rhythm was noted, along with a left ventricular mass identified on echocardiogram and confirmed via computed tomography as dystrophic calcification. Management included rehydration, antiarrhythmic therapy, and anticoagulation. The calcification, linked to previous myocardial infarctions, was considered an incidental finding, with no significant systolic dysfunction.", "extra_info": {"index": 153, "original_id": "multiclinsum_test_3200_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "We report a case of a 23-year-old patient with Burkitt's lymphoma and graft-versus-host disease admitted with intracerebral hemorrhage and sequential development of 12 anterior circulation aneurysms from disseminated Scedosporium infection. Despite aggressive surgical and antimicrobial treatment, the patient died 6 months later from multiorgan failure. The notable feature of this case is the rapid angioinvasiveness of the infection with new aneurysm formation within days of clear angiographic imaging despite the apparent lack of skull base osteomyelitis.", "extra_info": {"index": 152, "original_id": "multiclinsum_test_2127_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "A 75-year-old man presented with fever and right chest pain. He was suspected of a giant primary diaphragmatic tumor of extrahepatic origin by imaging studies. The preoperative differential diagnosis included benign masses such as myxoid sarcoma and schwannoma, and we planned a diaphragmatic resection. Intraoperatively, however, dissection of the tumor from the liver was not possible, requiring an extended right posterior segmentectomy with combined resection of the diaphragm. The patient had a good postoperative course and 1\u00a0year has passed since the surgery with no recurrence. The pathology showed that the mass was located just below the hepatic capsule/parenchymal region and was adherent to the diaphragm, but there was no continuity. The morphology suggested a low-grade mesenchymal tumor such as a solitary fibrous tumor and perivascular epithelioid cell tumor, but immunostaining was negative, making the diagnosis difficult. Although some areas of high proliferative activity were observed, finally, the diagnosis of primary spindle cell tumor of the liver with smooth muscle differentiation was made based on the positive results of muscle markers such as \u03b1SMA, desmin, and h-caldesmon.", "extra_info": {"index": 25, "original_id": "multiclinsum_test_447_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "We describe a 34-year-old patient with a cutaneous immunodeficiency characterized by recurrent crusted scabies infestation, diffuse tinea, and recurrent staphylococcal cellulitis, who we suspected had an undiagnosed syndrome. The patient also suffered from mental retardation, renal failure, and premature senescence. A cytogenetic fluorescence in situ hybridization analysis revealed a 9.34 Mb duplication within the short (p) arm of chromosome 1, precisely from 1p36.11 to 1p36.21, with an adjacent 193 kb copy gain entirely within 1p36.11. In addition, chromosome 4 had a 906 kb gain in 4p16.1 and chromosome 9 had a 81 kb copy gain in 9p24.3. Over 100 genes localized within these duplicated regions. Gene expression array revealed 82 genes whose expression changed >1.5-fold compared to a healthy age-matched skin control, but among them only the lipolytic enzyme arylacetamide deacetylase-like 3 was found within the duplicated 1p36 region of chromosome 1.", "extra_info": {"index": 33, "original_id": "multiclinsum_test_1677_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "A 52-year-old woman with primary Sj\u00f6gren's syndrome developed membranous glomerulonephritis and Epstein-Barr virus-positive diffuse large B-cell lymphoma (DLBCL). She was diagnosed with Sj\u00f6gren's syndrome based on the dry eyes, dry mouth, positive anti-nuclear antibody test, anti-Ro (SS-A) antibody, salivary gland biopsy, and salivary scintigraphy. Moreover, renal biopsy confirmed the diagnosis of membranous glomerulonephritis. Three months later, her small bowel was perforated with pneumoperitoneum, and the biopsy revealed Epstein-Barr virus-positive DLBCL.", "extra_info": {"index": 28, "original_id": "multiclinsum_test_2438_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "We describe the case of a 65-year-old man, who was referred from another institution with a diagnosis of acute abdomen. On physical examination, he presented signs of peritoneal irritation with evidence of leukocytosis and neutrophilia in the admission blood count. Computed tomography of the abdomen with intravenous contrast was performed, which was interpreted as Meckel's diverticulitis complicated, being corroborated during the surgical act and confirmed by pathological anatomy.\n", "extra_info": {"index": 30, "original_id": "multiclinsum_test_3197_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "We report a case of a giant loose peritoneal body measuring 7 \u00d7 5 cm found incidentally in a 64-year-old Indian man who presented with acute intestinal obstruction. We present the current hypothesis and our opinion on the genesis of such large bodies and discuss the problems in diagnosis.", "extra_info": {"index": 36, "original_id": "multiclinsum_test_2469_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "We reported a patient with acute lymphoblastic leukemia suffered from pulmonary TB infection after HSCT. During anti-TB treatment, the patient had a poor response to linezolid-containing regimen, and developed side effects such as gingival bleeding and thrombocytopenia, so the administration was switched to contezolid. After 15 days of continuous treatment, the patient's platelet increased to 58\u00d7109/L, and he was discharged in stable condition. During subsequent anti-TB treatment with contezolid for more than 7 months, the platelets remained stable, and no hematological adverse reactions and no symptoms of peripheral neuropathy were observed. Moreover, repeat imaging showed that the bilateral lung lesions were significantly reduced, indicating a good outcome for the patient.", "extra_info": {"index": 40, "original_id": "multiclinsum_test_353_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "A 51 year-old Caucasian right handed housewife lady (weight 61 kg, height 159 cm) presented with a headache of acute onset which proved to be caused by acute subarachnoid hemorrhage. Cerebral computed tomographic angiography revealed multiple aneurysms. The patient underwent a right pterional craniotomy to obliterate right middle cerebral, distal basilar and left carotid bifurcation aneurysms. The post-operative course was uneventful.", "extra_info": {"index": 34, "original_id": "multiclinsum_test_2076_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "A HIV-negative 56-year-old male was hospitalized for chest disease with main symptoms of chest tightness, chest pain, fatigue, anorexia, and weight loss. Heart rate 109 times/min, the computed tomography (CT) scans of the neck, chest, and abdomen revealed multiple nodules in the right pleura, right pleural encapsulated effusion, and limited, incomplete expansion of the middle and lower lobes of the right lung, enlarged lymph nodes in the right hilar and mediastinal and diaphragm groups, and multiple slightly low-density nodules in the liver, bone destruction in the 2nd thoracic vertebra, raising the possibility of multiple liver metastases of right lung cancer and malignant pleural fluid. The lymph nodes in the neck, mediastinum, abdomen, and pelvis were enlarged bilaterally. After comprehensive analysis, the patient was diagnosed with atypical systemic HDTB. After three months of conventional anti-TB treatment, the patient refused our hospital follow-up, and his symptoms improved significantly during the telephone follow-up.", "extra_info": {"index": 38, "original_id": "multiclinsum_test_867_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "A 21-year-old Japanese patient, suffering from a traumatic hallux deficit with only a portion of the basal phalanx intact, underwent rehabilitation treatment. The thenar area exhibited instability, leading to impaired balance and walking difficulties. Biomechanical assessment revealed the need for a rehabilitation strategy for the foot, as well as the knee, hip, and trunk. A rehabilitation protocol was designed to enhance medial foot loading during walking and standing, including balance and trunk strength training. After a 12-week rehabilitation period, the patient's gait showed significant improvement. Specifically, the load response and single-support phases of the gait cycle on the affected side increased from 46.9% to 49.3%, while the pre-swing phase decreased from 14.6% to 11.6%. The vertical component of the ground reaction force rose from 599.8 to 647.5\u00a0N. The enhanced stability from balance training and increased muscle strength contributed to the patient's improved walking and balance.", "extra_info": {"index": 42, "original_id": "multiclinsum_test_1445_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "We describe the case of a 43-year-old Asian female who has mild vision impairment due to tractional retinal detachment secondary to diabetic retinopathy and how mental health screening and quality of life screening during low vision rehabilitation can improve in the management of this patient.", "extra_info": {"index": 26, "original_id": "multiclinsum_test_2493_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "We present the case of a 25 y.o. patient with COVID-19 respiratory failure requiring ECMO support for 16-days in which a 32 Fr crescent cannula became adherent to the SVC and proximal jugular vein. Attempts to remove the cannula at the bedside failed due to immobility of the cannula. Ultrasound of the right neck was unremarkable, so he was taken to the hybrid OR where both TEE and fluoroscopy were unrevealing. An upper sternotomy was performed, and the superior vena cava and proximal jugular vein were dissected revealing a 2\u00a0cm segment of the distal SVC and proximal jugular vein that was densely sclerosed and adherent to the cannula. The vessel was opened across the adherent area at the level of the innominate vein and the cannula was then able to be withdrawn. The patient suffered no ill effects and had an unremarkable recovery to discharge.", "extra_info": {"index": 29, "original_id": "multiclinsum_test_2039_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "We report a case of 29 year old male with total rupture of ACL and PCL that underwent reconstruction for both ligaments. We found the failure of the PCL graft 2 years after the surgery was related to the tibial tunnel placement which was placed not in proper anatomical site. We performed revision PCL surgery with transseptal portal technique to ensure the tibial tunnel is placed in appropriate position.", "extra_info": {"index": 23, "original_id": "multiclinsum_test_2913_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "We report an unusual occurrence of pancreatic metastases from a previously diagnosed Merkel cell carcinoma with the discovery of a concomitant insulinoma. An 82-year old lady suffered from recurrent attacks of hypoglycemia and presented with an abdominal mass, 2 years prior she had an excision done on her eyebrow that was reported as Merkel cell carcinoma. An extended distal pancreatectomy and splenectomy along with resection of the left flexure of the colon for her abdominal mass was carried out. Final histopathology of the mass was a poorly differentiated endocrine carcinoma in the pancreatic tail, in the peripancreatic tissue and in the surrounding soft tissue consistent with metastatic Merkel cell carcinoma in addition to an insulinoma of the pancreatic body.", "extra_info": {"index": 32, "original_id": "multiclinsum_test_1055_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "Two cases of cerebral sinus venous thrombosis in COVID-19 patients were reported, following respiratory, hematology, and coagulation disarrangements, which was triggered by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. The first patient, which was presented with a seizure, had hypertension and diabetes mellitus as comorbidities. The latter case had no comorbidity but showed more severe presentations of COVID-19 such as brain and lung thrombosis, although already had several days of intravenous anticoagulant administrations. These two cases also have a different course of disease and outcomes, which were interesting topics to study.", "extra_info": {"index": 27, "original_id": "multiclinsum_test_445_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "A 20-year-old man presented with periumbilical pain. Physical exam showed a warm, erythematous infra-umbilical mass that was tender to palpation. CT revealed an infected urachal cyst. The patient underwent urachal abscess incision and drainage with cyst excision. The patient returned home on postoperative day two. Two-week outpatient follow-up confirmed an uncomplicated recovery.", "extra_info": {"index": 39, "original_id": "multiclinsum_test_1897_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "A 33-year-old woman was referred to our department with unstable angina. At the age of 6, she had undergone coronary artery bypass grafting of the second diagonal branch using the left internal thoracic artery and the obtuse marginal branch using saphenous vein grafting for left main coronary atresia. Although a coronary angiogram showed a patent left internal thoracic artery graft to the second diagonal branch and a patent saphenous vein graft to the obtuse marginal branch, the left anterior descending artery was not being perfused by the grafts because of a disruption of blood flow to the left anterior descending artery from the left internal thoracic artery. Therefore, we performed a redo coronary artery bypass grafting using the in situ right internal thoracic artery to the first diagonal branch, which was to be connected to the left anterior descending artery, resulting in amelioration of the ischemia of the left anterior wall. The patient was discharged 10\u00a0days after the operation and has been in good health for over 3\u00a0years without recurrence of chest symptoms.", "extra_info": {"index": 31, "original_id": "multiclinsum_test_2205_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "A 90-year-old female with atrial fibrillation on therapeutic apixaban and status-post TAVR presented with COVID-19 infection and was found to have severe bioprosthetic valvular regurgitation with features suggestive of valve thrombosis. She underwent valve-in-valve TAVR with resolution of valvular dysfunction.", "extra_info": {"index": 35, "original_id": "multiclinsum_test_303_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "In August 2012, a woman and her son were attacked by a stray dog in Henan, China. The son received rabies postexposure prophylaxis (wound treatment followed by vaccine, no immunoglobulin), however, the mother did not. Rabies infection was subsequently laboratory confirmed in the mother and she died in December; her son is alive and healthy after 2\u00a0years of follow-up.", "extra_info": {"index": 43, "original_id": "multiclinsum_test_1507_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "A 38-year-old woman in her 19th wk of pregnancy (G2P1) was referred to our clinic for a sudden, persistent pain on the left side of the waist. She had not undergone any previous related abdominal examination. Ultrasound of the urinary system revealed a giant nonhomogenous lump in the left kidney area. The diagnosis was considered spontaneous rupture and hemorrhage of the left RAML in pregnancy via ultrasound. Her left-side waist pain continued to be intense. Subsequently, she underwent computed tomography, which led to the same diagnosis. Based on many factors, the patient underwent left nephrectomy after the induction of labor. The pathological result was the rupture and hemorrhage of a vascular leiomyoma lipoma.", "extra_info": {"index": 37, "original_id": "multiclinsum_test_1298_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "A 44-year-old man was admitted due to weakness of his right limbs and unclear speech for 10\u00a0h. He had recurrent fevers for 1 month before admission. Transthoracic echocardiography showed a mix-echoic vegetation attached to the bicuspid aortic valve, moderate aortic regurgitation and a possible aortic annular abscess. Blood cultures were negative and empiric antibiotic therapy was begun. The patient did not have fever again and seem to be clinically improved. However, follow-up transesophageal echocardiography revealed a large periaortic abscess led to aortic sinus pseudoaneurysm. The patient underwent mechanical prosthetic valve replacement and annulus reconstruction successfully. Perivalvular abscess may be insidious deterioration in patients who seem to be clinically improved, which requires us to pay more attention.", "extra_info": {"index": 41, "original_id": "multiclinsum_test_885_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "Our patient is a 77-year-old African American female who presented with a systolic blood pressure of 200\u00a0mmHg. Computed tomography showed an enhancing 9\u00a0\u00d7\u20096\u00a0cm mass anterior and medial to the left kidney. The patient underwent a left adrenalectomy with partial nephrectomy. Gross and histologic examinations revealed an adrenal cortical adenoma and renal-adrenal fusion.", "extra_info": {"index": 69, "original_id": "multiclinsum_test_1363_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "A formerly healthy 40 year-old male became symptomatic 10 days after spending time in the jungle of North Borneo. Four days later, he presented to hospital in a state of collapse and died within two hours. He was hyponatraemic and had elevated blood urea, potassium, lactate dehydrogenase and amino transferase values; he was also thrombocytopenic and eosinophilic. Dengue haemorrhagic shock was suspected and a post-mortem examination performed. Investigations for dengue virus were negative. Blood for malaria parasites indicated hyperparasitaemia and single species P. knowlesi infection was confirmed by nested-PCR. Macroscopic pathology of the brain and endocardium showed multiple petechial haemorrhages, the liver and spleen were enlarged and lungs had features consistent with ARDS. Microscopic pathology showed sequestration of pigmented parasitized red blood cells in the vessels of the cerebrum, cerebellum, heart and kidney without evidence of chronic inflammatory reaction in the brain or any other organ examined. Brain sections were negative for intracellular adhesion molecule-1. The spleen and liver had abundant pigment containing macrophages and parasitized red blood cells. The kidney had evidence of acute tubular necrosis and endothelial cells in heart sections were prominent.", "extra_info": {"index": 79, "original_id": "multiclinsum_test_2113_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "On per speculum examination, cervix was replaced by an irregular friable growth, which was bleeding on touch. A clinical diagnosis of carcinoma cervix was made but the cervical biopsy revealed granulomatous inflammation with presence of acid-fast bacilli on cervical smear consistent with tuberculosis. The patient responded to six months of anti-tubercular therapy.", "extra_info": {"index": 77, "original_id": "multiclinsum_test_216_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "In this interesting case, we discover lingering dyspnea in our 79 year old male with a past medical history of asthma and heart failure with preserved ejection fraction admitted for acute heart failure exacerbation with reduced ejection fraction along with a new incidental finding of Chilaiditi's sign on chest radiograph. Patient received optimal diuretics and guideline-directed medical treatment for heart failure exacerbation, but mild dyspnea with pleuritic chest pain persisted. Dyspnea with pleurisy was likely attributed to a structural anatomical defect (Chilaiditi's sign) that can be picked up on imaging.", "extra_info": {"index": 67, "original_id": "multiclinsum_test_1780_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 71-year-old man with severe COPD, Global Initiative for Obstructive Lung Diseases stage 3 underwent an 8-wk remotely monitored inspiratory muscle training with a device based on the test of incremental respiratory endurance method. Spirometry, body plethysmography, test of incremental respiratory endurance examination, 6-min walking test, body mass index, airflow obstruction, dyspnea, exercise capacity index, and subjective perception of dyspnea were performed as part of the initial and final examination. The patient performed training at home, and the physiotherapist monitored the patient remotely through a web application that allowed the physiotherapist to evaluate all training parameters in real-time and respond to any problems. After 8 wk of home training, there was a significant increase in all monitored values: maximal inspiratory pressure, a novel parameter sustained maximal inspiratory pressure, forced expiratory volume in 1 s, total lung capacity, forced vital capacity, peak expiratory flow, and inspiratory capacity. There was also an improvement in the perception of dyspnea according to the COPD Assessment Test and a modified Medical Research Council Breathlessness Scale, an increase in exercise tolerance according to the 6-min walking test, and a decrease in the exercise capacity index as a predictor of prognosis.", "extra_info": {"index": 66, "original_id": "multiclinsum_test_1605_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "We present the case of a 52-year-old woman with cardiogenic shock and refractory right ventricular failure due to spontaneous dissection of the right coronary artery. She remained dependent on mechanical support for several weeks. Both a right ventricular assist device implant and a bidirectional cavopulmonary anastomosis were explored as long-term support options. A history of malignancy and possible right ventricular functional recovery resulted in a decision in favour of the bidirectional cavopulmonary anastomosis and concomitant tricuspid valve annuloplasty. Postoperatively her clinical condition improved significantly, and she could be discharged home. Echocardiography showed normalization of right ventricular dimensions and slight improvement of right ventricular function.", "extra_info": {"index": 70, "original_id": "multiclinsum_test_3152_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 43-year-old Asian man with a 3-year history of penile cancer presented with metastasis in the right intraocular sites. Magnetic resonance imaging showed hyperintensity in the T1-weighted images and hypointensity in the T2-weighted images of the right eye. After enucleation of his right eye, histopathological analysis led to a diagnosis of metastatic, moderately differentiated penile squamous cell carcinoma.", "extra_info": {"index": 82, "original_id": "multiclinsum_test_1233_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "7-year-old male with a diagnosis of acute lymphoid T-cell leukemia, completing a cycle of induction chemotherapy with the PETHEMA 2013 protocol. He presented a 12-day picture characterized by epigastric abdominal pain and vomiting, initially suspected acute pancreatitis, ruled out by normal pancreatic enzymes and abdominal computed tomography. Due to suspected acid-peptic disease associated with steroids, he began treatment with proton pump inhibitors and procinetics. Considering a picture of dyspepsia with alarm signs, such as progression of neutropenia, increased C-reactive protein and clinical deterioration, an esophagogastroduodenoscopy (EGD) compatible with necrotizing gastritis was performed, confirmed by histopathology. He received pharmacological management, zero regimen and parenteral support, and progressive improvement was evidenced in imaging controls. After fasting for 30 days, well tolerated enteral nutrition was initiated, with outpatient follow-up. After improvement, the chemotherapy plan was completed, highlighting complete remission, without complications after 2 years.\n", "extra_info": {"index": 68, "original_id": "multiclinsum_test_3042_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 49-year-old Japanese man visited our department in November 2017 with chief complaints of indolent right scrotum enlargement and a right inguinal mass. History showed that the patient visited our department of gastroenterology with chief complaints of blackish feces and ill complexion in February 1997. Computed tomography (CT) showed a right retroperitoneal tumor, which was removed in the same month. Histopathological examination showed a teratoma and yolk sac tumor. He was diagnosed with primary retroperitoneal EGCT and received three courses of chemotherapy (bleomycin/etoposide/cisplatin; BEP). Periodic imaging and the determination of tumor markers (alpha-fetoprotein", "extra_info": {"index": 84, "original_id": "multiclinsum_test_439_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "We present a case in which POCUS was used to rapidly confirm diagnosis in an unstable, severely septic patient presenting to the emergency department with Fournier's gangrene.", "extra_info": {"index": 75, "original_id": "multiclinsum_test_2914_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "A 38-year-old Sri Lankan female presented with sudden onset severe headache, fixed dilated pupil, complete ptosis and ophthalmoplegia on the right side. On imaging, dissection and dilatation was evident in the right internal carotid artery from the origin up to the cavernous segment. She also had stenosis and aneurysmal dilatation of right subclavian artery. Takayasu arteritis was diagnosed subsequently. She was started on aspirin and high dose steroids.", "extra_info": {"index": 73, "original_id": "multiclinsum_test_2426_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "The patient discussed in our review is an 80-year-old female, with a history of diabetic retinopathy and macular degeneration who presented with a sudden deterioration of vision. While this was initially attributed to diabetic retinopathy, she was eventually noted to have a salmon patch lesion in her conjunctiva, diagnosed on biopsy to be a diffuse large B-cell lymphoma.", "extra_info": {"index": 81, "original_id": "multiclinsum_test_1888_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 65-year-old woman was referred to our hospital for assessment of a gallbladder tumor. Contrast-enhanced computed tomography showed a papillary tumor in the fundus of the gallbladder with irregular thickening of the gallbladder wall that spread into the cystic duct. The boundary between the tumor and liver was unclear. The patient was diagnosed with gallbladder cancer with liver invasion. We performed extended cholecystectomy with liver bed resection after confirming the absence of cancer cells in the resection margin of the cystic duct. After pathological examination, the tumor was diagnosed as an ICPN with xanthogranulomatous cholecystitis. The patient was discharged on postoperative day 8 with no complications.", "extra_info": {"index": 74, "original_id": "multiclinsum_test_1559_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "A 27-year-old man presented with headache and diplopia at our department. Fundoscopy showed left optic nerve atrophy and right papilledema consistent with Foster-Kennedy syndrome. Neurological exams were otherwise normal. A left frontal irregular space-occupying lesion was seen on magnetic resonance imaging (MRI), and enhancement was shown on contrast-enhanced computed tomography (CT) scan. CT angiography (CTA) revealed vascular compression around the lesion. Prior to surgery, meningioma was diagnosed and gross tumor removal was performed. On postoperative pathohistological exam, the tumor proved to be a meningeal melanocytoma, WHO grade I. No skin melanoma was found. After surgery, the patient received radiation therapy. No tumor was seen on follow-up MR images six months after surgery. The patient was well after two and a half years, and there was no tumor recurrence on the follow-up CT.", "extra_info": {"index": 85, "original_id": "multiclinsum_test_568_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "In this case report, we present a case of a pleomorphic adenoma arising from the 'tail' of the parotid gland, which on imaging, appears to be extra parotid in location. We also review the anatomy of the parotid 'tail' and relevant literature.", "extra_info": {"index": 76, "original_id": "multiclinsum_test_2421_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A previously healthy 24-yo male (A) presented at the Emergency Department(ED) with recent onset of chest pain and a 3-day history of abdominal pain, fever and diarrhoea. The symptoms began within a few hours of returning from a tourist visit to a central European capital. Vital signs were stable, the Electrocardiogram(ECG) showed generalized ST-elevation, laboratory testing showed increased levels of C-reactive protein(CRP) and high-sensitive Troponin T(hsTnT). Transthoracic echocardiogram (TTE) was normal, stool cultures were positive for C Jejuni and blood cultures were negative. Two days after patient A was admitted to the ED his travel companion (B), also a previously healthy male (23-yo), presented at the same ED with almost identical symptoms: chest pain precipitated by a few days of abdominal pain, fever and diarrhoea. Patient B declared that he and patient A had ingested chicken prior to returning from their tourist trip. Laboratory tests showed elevated CRP and hsTnT but the ECG and TTE were normal. In both cases, the diagnosis of C jejuni-associated perimyocarditis was set based on the typical presentation and positive stool cultures with identical strains. Both patients were given antibiotics, rapidly improved and were fully recovered at 6-week follow up.", "extra_info": {"index": 78, "original_id": "multiclinsum_test_1211_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "We report an unusual case in which both anomalous origin of the right coronary artery and myocardial bridge on left anterior descending artery were detected concurrently.", "extra_info": {"index": 87, "original_id": "multiclinsum_test_1721_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 66-year-old man affected by DME, with glycated hemoglobin (HbA1c) at 6.9%, refractory to laser grid treatment and intravitreal injections of triamcinolone, was selected to receive a cycle of three subtenon injections/week of IFN\u03b1 (1\u00d7106 IU/ml). BCVA and CMT, using spectral domain ocular coherence tomography (SD-OCT), were evaluated preoperatively and at 1\u00a0week, 1\u00a0month, 4\u00a0months, and 1\u00a0year postoperatively. BCVA and CMT were significantly improved at 1\u00a0week after the three injections (20/200 vs. 20/40 and 498\u00a0\u03bcm vs. 237\u00a0\u03bcm, respectively). BCVA remained stable during the 1-year follow-up. CMT was slightly increased, but was still lower than the baseline value (215\u00a0\u03bcm, 255\u00a0\u03bcm, and 299\u00a0\u03bcm during the follow-up visits). No adverse events were recorded, with the exception of mild subconjunctival hemorrhage at the injection site.", "extra_info": {"index": 80, "original_id": "multiclinsum_test_1558_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "A 53-year-old female with a history of two prior spinal operations at the L4-S1 levels (11 and 2 years previously) presented over a few weeks with the acute onset of a cauda equina syndrome (e.g., paraparesis and acute urinary incontinence). The patient demonstrated a mildly elevated white blood cell count (12,600/mm3) and abnormally increased C-reactive protein level that correlated with the magnetic resonance imaging that showed a dorsal epidural abscess extending from the L4 to S1 levels. At surgery, an encapsulated posterior epidural abscess was drained. Surgical findings included a granulomatous lesion consistent with a retained surgical cottonoid and was removed from the antero-inferior portion of the abscess wall at S1. Culture of the thick fibrotic abscess wall grew Klebsiella oxytoca. After 2 months of ciprofloxacin, the patient's infection cleared but the motor deficit only partially resolved.", "extra_info": {"index": 83, "original_id": "multiclinsum_test_2689_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 42-year-old female with a distant history of SCI developed clinical and imaging findings consistent with acute expansion of PTS immediately following parathyroidectomy. Her symptoms included acute numbness, tingling, and pain in both arms. Magnetic resonance imaging (MRI) revealed a syrinx in the cervical and thoracic spinal cord. However, this was initially misdiagnosed as transverse myelitis and was treated as such without resolution of symptoms. Over the following 6 months, the patient experienced progressive weakness. Repeat MRI demonstrated expansion of the syrinx with new involvement of the brain stem. The patient was diagnosed with PTS and referred for outpatient neurosurgery evaluation at a tertiary facility. Treatment was delayed due to problems with housing and scheduling at the outside facility, allowing for continued worsening of her symptoms. The syrinx was surgically drained and a syringo-subarachnoid shunt was placed. Follow-up MRI confirmed correct placement of the shunt as well as resolved syrinx and decreased thecal sac compression. The procedure effectively halted symptom progression but did not resolve all symptoms completely. The patient has regained her ability to perform much of her activities of daily living but remains in a nursing home facility.", "extra_info": {"index": 86, "original_id": "multiclinsum_test_2005_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 34-year-old female presented with a 1 year history of intermittent pain in the right side of the waist without obvious inducement. All laboratory blood tests were within normal limits. Indocyanine green 15 min retention was rated 2.9%, and Child-Pugh was rated A. Computed tomography and magnetic resonance imaging diagnosed giant hemangioma of the caudate lobe with hemangioma of left lobe of liver. After discussion, surgical treatment was performed, which lasted 410 min, with intraoperative bleeding of about 600 mL and postoperative pathological findings of cavernous hemangioma. There were no obvious postoperative complications, and the patient was discharged 10 d after surgery.", "extra_info": {"index": 72, "original_id": "multiclinsum_test_2984_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "A 76-year-old male patient was admitted to our institution with intermittent abdominal pain and a local abdominal mass which occurred one month after laparoscopic radical resection of rectal cancer one year ago. A computed tomography scan showed an abdominal wall hernia at the 5 mm former drain-site in the left lower quadrant, and that the content consisted of the large omentum. An elective herniorrhaphy was performed by closing the fascial defect and reinforcing the abdominal wall with a synthetic mesh simultaneously. The postoperative period was uneventful. The patient was discharged seven days after the operation without surgery-related complications at the 1-mo follow-up visit.", "extra_info": {"index": 71, "original_id": "multiclinsum_test_1042_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A four-year-old girl presented with fever and a painful limp in the left hip. Pain characteristics and anemia detected in the blood analyses were the first warning signs that the hip process was not standard. Although the primary suspicion was of septic arthritis, a CT scan of the abdomen revealed an adrenal neuroblastoma.", "extra_info": {"index": 60, "original_id": "multiclinsum_test_1260_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "We report a case of complex revascularization in a diabetic patient with aggressive right foot lesions evolution after COVID-19 infection. The patient presenting a Peripheral arterial ischemic involving the infrarenal aorta, iliac, femoral. The simultaneous intervention consisted of an endovascular aortic stent-graft placement and angioplasty of femoral artery.", "extra_info": {"index": 58, "original_id": "multiclinsum_test_437_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "Male school-age child, 8 years old, no relevant history, presented with a 1-year history of conjugate horizontal rapid eye movement jerking and associated mild miosis, 5-10 seconds in duration, occurring 5-6 times daily, with some episodes with a questionable disconnection from the environment or impairment of consciousness, without other accompanying signs or symptoms. General examinations were normal. He was evaluated by ophthalmologists and otolaryngologists who ruled out pathology in those fields. The neurological examination between episodes was normal. The video-electroencephalogram demonstrated an electro-clinical correlate, with epileptiform activity in the left temporal and occipital region that later generalized during episodes. The brain MRI was normal. After initiation of treatment with carbamazepine, he had a good evolution, with no recurrence of episodes at 2 years of follow-up.\n", "extra_info": {"index": 62, "original_id": "multiclinsum_test_3001_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "We report a case of central venous catheter infection with Bacillus pumilus in an immunocompetent child with tufting enteropathy on long-term parenteral nutrition (PN). There were three episodes of central venous catheter infection with Bacillus pumilus in three months. Despite adequate and appropriate use of intravenous antibiotics, the infection failed to clear resulting in the need for removal of the catheter for complete cure.", "extra_info": {"index": 44, "original_id": "multiclinsum_test_1072_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 58-year-old man was presented to our institute with complaints of posterior cervical pain persisting for 3\u00a0months, along with numbness and muscle weakness of extremities. A fat suppression T2-weighted image of MRI illustrated fluid collection in the retrospinal region at C1-C2 level, and an 111In-DTPA cisternoscintigram clearly revealed the presence of CSF leakage into the same region. The MRI also showed stenosis in spinal canal at C3/4 level, and a computed tomography (CT) myelogram suggested a blockage at the same level. We gave a diagnosis as intracranial hypotension due to the CSF leakage, which might be caused by the spinal canal stenosis at C3/4 level. Despite 72\u2009h of conservative therapy, a brain CT showed the development of bilateral subdural hematomas. We, therefore, performed burr-hole drainage of the subdural hematoma, blood-patch therapy at C1/2 level, and laminoplasty at C3-4 at the same time. Improvement of symptoms and imaging features which suggested the CSF leak and subdural hematoma were obtained post-operatively.", "extra_info": {"index": 56, "original_id": "multiclinsum_test_1266_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "We describe the case of a 55-year-old female patient with primary open-angle glaucoma (POAG) who underwent bilateral XEN gel surgery. Her left eye developed a 2 mm postoperative hyphema, which resolved spontaneously within 8 days. Intraocular pressure (IOP) normalized at 12 mm Hg and increased to 50 mm Hg after 1 month in an otherwise normal-looking eye. Intraoperative examination revealed a nonfunctioning XEN gel stent, which was replaced and sent for laboratory analysis. Macroscopic examination of the tube confirmed obstruction with cellular debris. Tube replacement restored good filtration.", "extra_info": {"index": 64, "original_id": "multiclinsum_test_7_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "A 49-year-old Asian woman presented with disseminated intravascular coagulation due to ruptured primary high-grade ovarian endometrial stromal sarcoma with multiple intraperitoneal metastases. After the initial surgery, the patient underwent adjuvant chemotherapy with three courses of Adriamycin (75\u00a0mg/m2). We performed the secondary debulking operation including total hysterectomy, metastasectomy, omentectomy, peritonectomy, appendectomy, and hyperthermic intraperitoneal chemotherapy (paclitaxel 175\u00a0mg/m2). Currently she has been alive for 28\u00a0months under a new chemotherapy regimen.", "extra_info": {"index": 49, "original_id": "multiclinsum_test_2683_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "A 38-year-old woman presented with shortness of breath and syncope. Upon investigation, she was found to have a right atrioventricular myxoma. It was associated with tricuspid regurgitation, right-sided heart failure, and pulmonary hypertension.\n\nThe syncopal attacks and shortness of breath resolved completely after tumor resection. Tricuspid regurgitation (grade 1) and mild pulmonary hypertension (right ventricular systolic pressure 35 mmHg) remained as sequelae of delayed presentation. These may be due to recurrent embolization of tumor fragments to segments of the pulmonary artery.", "extra_info": {"index": 51, "original_id": "multiclinsum_test_3149_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "A 17-year-old male patient presented with pain in the lower left molar region. Clinical examination revealed the absence of Teeth 37 and 38. Tomographic imaging showed Tooth 37 in a transverse position with the crown oriented lingually and Tooth 38 in a vertical position. Extraction of Tooth 37 was performed using a vestibular approach and odontectomy due to space constraints.", "extra_info": {"index": 46, "original_id": "multiclinsum_test_3344_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "We present a case of a 79-year-old female patient who underwent LAAO device deployment within a surgically occluded LAA with PDL. She underwent 27\u2005mm LAAO device (WATCHMANTM) deployment and all the P.A.S.S. (Position, Anchor, Size, and Seal) criteria were satisfied. Only 1.4\u2005mm PDL was present. She was continued on apixaban and aspirin post-operatively. Post-operative transoesophageal echocardiogram at 6 weeks demonstrated trivial PDL measuring 1.49\u2005mm. Patient was continued on aspirin and clopidogrel, with discontinuation of apixaban.", "extra_info": {"index": 47, "original_id": "multiclinsum_test_1868_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "A 66-year-old Maori man presented to our hospital with left testicular swelling. His alpha-fetoprotein and beta-human chorionic gonadotrophin levels were within normal limits. His lactate dehydrogenase concentration was elevated to 267 U/L. Ultrasound imaging confirmed a large testicular mass, and he underwent left orchiectomy. His histological examination revealed a neuroendocrine tumor with an immunostaining pattern suggesting Merkel cell carcinoma. He presented to our hospital again 3 months later with right testicular swelling that was confirmed on ultrasound sonography to be a tumor. He underwent a right orchiectomy, and his histological examination revealed metastatic Merkel cell carcinoma. A primary lesion was not identified, and computed tomographic imaging did not reveal spread to other organs. He received six cycles of adjuvant carboplatin and etoposide chemotherapy and remained disease-free 18 months after completion of chemotherapy.", "extra_info": {"index": 52, "original_id": "multiclinsum_test_2759_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "We present a case of stage IV pleomorphic carcinoma; the patient was a 66-year-old male. He was referred to our hospital because of a right adrenal hemorrhage and a lung tumor. A systemic examination revealed that the lung tumor was a primary lung cancer and that the adrenal hemorrhage was due to a metastatic cancer. We performed an adrenalectomy and resection of the lung tumor and obtained a diagnosis of pleomorphic carcinoma with adrenal metastasis. The patient has remained recurrence-free for 6\u2009years since the surgery.", "extra_info": {"index": 54, "original_id": "multiclinsum_test_2067_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "We present a 12-year-old girl who presented with bilateral shoulder deformities and difficulty in coordination while writing. On examination, she was noted to have bilateral Sprengel deformities with flexion contractures of upper-limb joints and mirror movements of both upper and lower-limb joints.", "extra_info": {"index": 53, "original_id": "multiclinsum_test_990_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 32-year-old woman complained of a mass inside the rectovaginal space for 9 years, which became enlarged within 1 year. A rectal SEL detected by endoscopy was suspected to be a gastrointestinal stromal tumor or exophytic uterine fibroid. Pathological diagnosis was difficult because of unsuccessful transabdominal core needle biopsy with insufficient tissues, as well as vaginal hemorrhage. A second biopsy was suggested after multiple disciplinary treatment discussion, which referred to a transperineal core needle biopsy (CNB) guided by ERUS combined with CEUS. Adequate samples were procured and rectal gastrointestinal stromal tumor was proved to be the pathological diagnosis. Imatinib was recommended for first-line therapy by multiple disciplinary treatment discussion. After the tumor shrunk, resection of the rectal gastrointestinal stromal tumor was performed through the posterior vaginal wall. Adjuvant therapy was applied and no recurrence or metastasis has been found by the last follow-up on December 13, 2019.", "extra_info": {"index": 48, "original_id": "multiclinsum_test_2808_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 27-year-old man presented to our hospital because of painless and progressive visual impairment of both eyes over two years. He was previously diagnosed with hypocalcemia but did not take calcium supplements regularly. He had no history of anterior neck thyroid surgery. After admission, the biochemical analysis indicated a serum calcium level of 1.21 mmol/L and an intact parathyroid hormone level of 0 pg/mL. Ocular examination revealed bilateral symmetrical opacity of the lens presenting as punctate opacity in the posterior subcapsular cortex together with radial opacity in the peripheral cortex (N1C2P3). Phacoemulsification with an intraocular lens was performed in both eyes sequentially. Postoperatively, the patient had a satisfactory recovery and greatly improved visual acuity.", "extra_info": {"index": 59, "original_id": "multiclinsum_test_1416_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "This report describes, for the first time to the best of our knowledge, a primary paraganglioma of the seminal vesicle occurring in a 61-year-old male. The patient presented persistent arterial hypertension and a previous diagnosis of chromophobe renal cell carcinoma. It was hypothesized that the seminal vesicle tumor could be a metastasis from the chromophobe renal cell carcinoma. Immunohistochemical characterization revealed expression of synaptophysin and chromogranin in tumor cell nests and peripheral S100 protein expression in sustentacular cells. Succinate dehydrogenase A and B-related (SDHA and SDHB) expression was present in both tumors.", "extra_info": {"index": 45, "original_id": "multiclinsum_test_2717_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 69-year-old man was injured in a motor vehicle accident and suffered from left hemothorax and multiple rib fractures near the heart. A comprehensive assessment raised suspicions of lacerated pericardium and myocardial injury. Consequently, a thoracoscopy was performed 9\u2009h after injury. A penetrating cardiac injury was detected and surgically treated via video-assisted thoracoscopic surgery. The patient recovered uneventfully and was discharged on postoperative day 16.", "extra_info": {"index": 50, "original_id": "multiclinsum_test_2967_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "We describe a case of a 49-year-old man with a history of acromegaly who presented to our hospital with a diagnosis of decompensated systolic heart failure. Serial electrocardiograms showed wide (160\u2013200\u2009ms) QRS duration with left bundle branch block. Echocardiography showed severe left ventricular dysfunction that simultaneously achieved a left ventricular ejection fraction of 16%. Surgical indication was rarely assessed by neurosurgeons. Given that the stereotactic radiosurgery together with pharmacotherapy produced infinitesimal effects, cardiac resynchronization therapy was performed. Owing to biventricular synchronization and holding back reverse remodeling, the patient\u2019s symptoms were successfully alleviated, and he was discharged from the hospital.", "extra_info": {"index": 57, "original_id": "multiclinsum_test_3217_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 62-year-old man diagnosed as IgD-\u03bb/\u03bb myeloma (ISS stage III) was admitted with fatigue and weight loss. The physical examination suggested an anemic face, a few moist rales at the left lung base, and mild concave edema in both lower extremities. Laboratory examinations showed the elevated creatinine levels, \u03b22-microglobulin, lactic dehydrogenase, and erythrocyte sedimentation rate, while the decreased neutrophils, granulocytes, and hemoglobin. In the serum protein electrophoresis, there appeared two inconspicuous M-spikes. Serum IFE indicated an over-representation of lambda light chain and yielded two monoclonal bands in \u03bb region, but only one corresponding heavy chain band in the antisera to IgD region. The BM histology and BM cytology both supported the diagnosis of IgD-\u03bb/\u03bb myeloma.", "extra_info": {"index": 55, "original_id": "multiclinsum_test_710_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "We reported a 24-year-old male who came to the emergency department complaining of a history of a sore throat, fever, malaise, fever, and neck swelling with a normal consciousness level. A laboratory examination showed leukocytosis and high C-reactive protein serum. Radiological diagnosis reveals an anterior neck abscess with left jugular vein thrombosis and left epidural abscess. The blood culture was positive for Fusobacterium necrophorum. The patient underwent surgical drainage and, at the same time, was treated with antibiotics and anticoagulant drugs. After 45 days, the patient improved clinically and was discharged. There were no other symptoms after a one-month follow-up clinically and neck ultrasonography.", "extra_info": {"index": 63, "original_id": "multiclinsum_test_1379_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 4-year-old boy was admitted for persistent pain in the left lower limb and abnormal gait over the previous 9 mo. He had no history of present or past illness. Preoperative imaging data showed erosion-like changes with bone expansion of the left middle and lower fibular segment. Tumor tissue in the fibular bone marrow cavity was removed by curettage, and rapid intraoperative pathological examination suggested fibular fibrous dysplasia. An allograft was implanted into the fibular medullary cavity. However, he was readmitted with clinical symptoms including persistent pain, abnormal gait, and local swelling at the age of 6 years. He was diagnosed with recurrent fibular fibrous dysplasia based on the second medical examination. He underwent fibular bone tumor radical resection and longus fibular allograft transplantation combined with fibular bone locking plate and screws. Good host bone to allogenic bone graft fusion was observed by the physician on postoperative regular follow-up.", "extra_info": {"index": 65, "original_id": "multiclinsum_test_1596_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "We reported a four-week spondyloptosis of the ninth thoracic vertebra over the tenth thoracic vertebra, in a 20-year-old male without any neurological deficit. The patient had associated chest injuries. The spine injury was managed surgically with in-situ posterior instrumentation and fusion. The patient tolerated the operation well and postoperatively there was no neurological deterioration or surgical complication.", "extra_info": {"index": 61, "original_id": "multiclinsum_test_1749_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidneys don\u2019t work properly, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through routine screening is key to managing kidney health and preventing complications.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration and tubular reabsorption. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance, and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and systemic inflammation, and early intervention through biomarker monitoring and pharmacological management is critical to preserving renal function and delaying disease progression.\"\n}", "ground_truth": "We report a case of annular leukocytoclastic vasculitis induced by anti-tuberculosis medication. A 62-year-old Thai man presented to our facility with a generalized exanthematous rash on his trunk and extremities that resolved shortly afterwards. Subsequently, he developed multiple, erythematous-to-purplish, non-blanchable macules and papules with an annular arrangement on his extremities. The skin rash occurred after two weeks of anti-tuberculosis medication. The histopathology of the purpuric skin lesion was consistent with leukocytoclastic vasculitis. The skin lesion improved after discontinuation of the anti-tuberculosis drugs and treatment with oral antihistamine and topical corticosteroid drugs. Streptomycin, ethambutol and ofloxacin were administered as second-line anti-tuberculosis therapy during his hospitalization. No adverse reactions were observed.", "extra_info": {"index": 7, "original_id": "multiclinsum_test_2131_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidneys don\u2019t work properly, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through routine screening is key to managing kidney health and preventing complications.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration and tubular reabsorption. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance, and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and systemic inflammation, and early intervention through biomarker monitoring and pharmacological management is critical to preserving renal function and delaying disease progression.\"\n}", "ground_truth": "The authors report on a case of acute primary Cytomegalovirus infection complicated with acute appendicitis due to Cytomegalovirus in an apparently immunocompetent 24-year-old Caucasian man also suffering from primary sclerosing cholangitis and ulcerative colitis. Diagnosis was based on clinical manifestations, serology results, as well as microbiological and histological findings. Treatment consisted of surgery and anti-Cytomegalovirus therapy.", "extra_info": {"index": 1, "original_id": "multiclinsum_test_2576_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidneys don\u2019t work properly, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through routine screening is key to managing kidney health and preventing complications.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration and tubular reabsorption. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance, and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and systemic inflammation, and early intervention through biomarker monitoring and pharmacological management is critical to preserving renal function and delaying disease progression.\"\n}", "ground_truth": "A 27-year-old male with a relapsed acute lymphoblastic leukemia presented with five-day-old polyarthralgia. He also had febrile neutropenia, cellulitis without abscesses, and methicillin-resistant Staphylococcus aureus bacteremia for which he received therapy with oxacillin and cefepime. However, the febrile neutropenia persisted, and an invasive fungal infection was suspected. A new set of blood cultures was taken and antifungal treatment was initiated. Arthroconidia were identified in the blood cultures and a matrix-assisted laser desorption ionization-mass spectrometry confirmed the presence of Geotrichum spp. Antifungal treatment was adjusted to 14 days of deoxycholate amphotericin B and four weeks of voriconazole. After a prolonged stay, he was discharged.\n", "extra_info": {"index": 3, "original_id": "multiclinsum_test_3210_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidneys don\u2019t work properly, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through routine screening is key to managing kidney health and preventing complications.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration and tubular reabsorption. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance, and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and systemic inflammation, and early intervention through biomarker monitoring and pharmacological management is critical to preserving renal function and delaying disease progression.\"\n}", "ground_truth": "The patient was a 55-year-old woman with a transglottic squamous cell carcinoma of the T3N0M0 stage and PCF development following total laryngectomy surgery with total thyroidectomy and bilateral elective cervical lymph node dissection level I-IV. In spite of conservative treatment, the fistula was not recovered after 3 weeks. It was decided to perform fibrin glue injection into the fistula tract via the endoscopic approach. One month after the fibrin glue injection, no evidence of contrast extravasation was observed on barium swallow test, and the fistula was completely closed.", "extra_info": {"index": 13, "original_id": "multiclinsum_test_112_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidneys don\u2019t work properly, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through routine screening is key to managing kidney health and preventing complications.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration and tubular reabsorption. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance, and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and systemic inflammation, and early intervention through biomarker monitoring and pharmacological management is critical to preserving renal function and delaying disease progression.\"\n}", "ground_truth": "We present a case of subacute cervical cerebrospinal fluid (CSF) leak resulting from chiropractic manipulation of the cervical spine. The patient is a 29-year-old female who received manipulation one week prior to developing symptoms of severe orthostatic headache, nausea, and vomiting. Magnetic resonance imaging (MRI) revealed a new C5-C6 ventral CSF collection. Symptomatic onset corresponded with the recent cervical chiropractic adjustment. We present serial imaging correlating with her symptomatology and review the pertinent literature on complications of chiropractic manipulation.", "extra_info": {"index": 5, "original_id": "multiclinsum_test_2542_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidneys don\u2019t work properly, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through routine screening is key to managing kidney health and preventing complications.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration and tubular reabsorption. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance, and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and systemic inflammation, and early intervention through biomarker monitoring and pharmacological management is critical to preserving renal function and delaying disease progression.\"\n}", "ground_truth": "We report here another case of primary prostatic MALT lymphoma which is presented by hematuria and diagnosed primarily as BPH. Immunohistochemistry studies demonstrate the diagnosis and MALT lymphoma. Six months after starting the treatment the patient was alive and well.", "extra_info": {"index": 9, "original_id": "multiclinsum_test_2155_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidneys don\u2019t work properly, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through routine screening is key to managing kidney health and preventing complications.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration and tubular reabsorption. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance, and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and systemic inflammation, and early intervention through biomarker monitoring and pharmacological management is critical to preserving renal function and delaying disease progression.\"\n}", "ground_truth": "We present a case of a patient who suffered a cardiac arrest after a fall during a chronic obstructive pulmonary disease exacerbation, leading to pneumoretroperitoneum.", "extra_info": {"index": 12, "original_id": "multiclinsum_test_1808_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by glomerular filtration rate (GFR) decline, proteinuria, and systemic inflammation, and requires longitudinal monitoring with biomarkers such as serum creatinine and estimated GFR to guide therapeutic interventions including pharmacological modulation, dietary restriction, and potential dialysis initiation.\"\n}", "ground_truth": "A 71-year-old female who was being treated for type 2 diabetes with canagliflozin, metformin, and saxagliptin orally presented to the ED for evaluation of reduced oral intake, malaise, nausea, and abdominal pain. Although her blood glucose was not severely elevated (259 mg/dL), there was notable ketoacidosis (pH\u20096.89; CO2, 11.4\u2009mmHg; HCO3, 1.9\u2009mEq/L; base excess, - 31.3\u2009mmol/L; 3-hydroxybutyric acid > 10,000\u2009\u03bcmol/L) was observed. The uncontrolled acidosis improved following 3\u2009days of continuous renal replacement therapy, but elevated urinary glucose continued for more than 10\u2009days. Ringer's lactated fluid supplementation was continued for management of polyurea and glucosuria. Urinary glucose turned negative on day 16, and there was improvement in the patient's overall state; hence, she was discharged on day 18.", "extra_info": {"index": 2, "original_id": "multiclinsum_test_99_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidneys don\u2019t work properly, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through routine screening is key to managing kidney health and preventing complications.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration and tubular reabsorption. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance, and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and systemic inflammation, and early intervention through biomarker monitoring and pharmacological management is critical to preserving renal function and delaying disease progression.\"\n}", "ground_truth": "We report the case of a 2 years and-5-month-old boy admitted in our clinic for fever, abdominal pain and diarrhea. The clinical exam at the time of admission revealed influenced gen-eral status, bilateral palpebral edema and conjunctivitis, mucocutaneous signs of dehydration, and abdominal tenderness at palpation. The laboratory tests performed pointed out lymphopenia, thrombocytopenia, anemia, elevated C-reactive protein - CRP, erythrocyte sedimentation rate and ferritin levels, hyponatremia, hypopotassemia, hypertriglyceridemia, elevated D-dimer, in-creased troponin and NT-proBNP. The real-time polymerase chain reaction (RT-PCR) test for SARS-CoV-2 infection was negative, but the serology was positive. Thus, established the diagnosis of PIMS-TS. We initiated intravenous immunoglobulin, empirical antibiotic, anticoagulation therapy and symptomatic drugs. Nevertheless, the clinical course and laboratory parameters worsened, and the 2nd echocardiography pointed out minimal pericardial effusion, slight dilation of the left cavities, dyskinesia of the inferior and septal basal segments of the left ventricle (LV), and LV systolic dysfunction. Therefore, we associated intravenous methylprednisolone, angiotensin converting enzyme inhibitors, spironolactone and hydrochlorothiazide, with outstanding favorable evolution.", "extra_info": {"index": 15, "original_id": "multiclinsum_test_723_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by glomerular filtration rate (GFR) decline, proteinuria, and systemic inflammation, and requires longitudinal monitoring with biomarkers such as serum creatinine and estimated GFR to guide therapeutic interventions including pharmacological modulation, dietary restriction, and potential dialysis initiation.\"\n}", "ground_truth": "Herein we present a 63-year-old man with idiopathic spontaneous intraperitoneal hemorrhage (ISIH) caused by spontaneous rupture of non-aneurysmal inferior pancreaticoduodenalartery (IPDA).", "extra_info": {"index": 4, "original_id": "multiclinsum_test_45_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by glomerular filtration rate (GFR) decline, proteinuria, and systemic inflammation, and requires longitudinal monitoring with biomarkers such as serum creatinine and estimated GFR to guide therapeutic interventions including pharmacological modulation, dietary restriction, and potential dialysis initiation.\"\n}", "ground_truth": "33-year-old nulligravid woman with newly diagnosed anaplastic astrocytoma (AA; WHO grade III, IDH1-negative) sought fertility preservation. Prior to chemotherapy and radiation for AA, the patient underwent in vitro fertilization (IVF) for fertility preservation, resulting in 8 vitrified embryos. Following chemo-radiation, the patient underwent two rounds of frozen embryo transfers (FET), each resulting in a successful singleton pregnancy.", "extra_info": {"index": 8, "original_id": "multiclinsum_test_2635_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by glomerular filtration rate (GFR) decline, proteinuria, and systemic inflammation, and requires longitudinal monitoring with biomarkers such as serum creatinine and estimated GFR to guide therapeutic interventions including pharmacological modulation, dietary restriction, and potential dialysis initiation.\"\n}", "ground_truth": "A 62-year-old male presented with a 4-month history of right brachial pain and hyposensitivity in the C5 distribution. The cervical magnetic resonance (MR) imaging scan revealed a C5-C6 right anterolateral disc herniation with syringomyelia extending from C5-C6 to T1. Following a C5-C6 anterior cervical discectomy and fusion (ACDF), the patient's symptoms resolved. The 3-month postoperative MR documented total resolution of the syrinx. Notably, due to residual neuropathic pain, the patient required a subdural spinal cord stimulator which was placed without any complications.", "extra_info": {"index": 6, "original_id": "multiclinsum_test_875_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by glomerular filtration rate (GFR) decline, proteinuria, and systemic inflammation, and requires longitudinal monitoring with biomarkers such as serum creatinine and estimated GFR to guide therapeutic interventions including pharmacological modulation, dietary restriction, and potential dialysis initiation.\"\n}", "ground_truth": "A 34-year-old male patient presented with multiple large tuberous xanthomas related to FH. There were 15 masses in different body parts, including the dorsum of the hands, elbows, buttocks, feet, and Achille's tendon. The largest masses in the buttocks measured 8\u00a0\u00d7\u00a08\u00a0\u00d7\u00a05\u00a0cm. Surgical removal of 13 masses was carried out in combination with medical treatment. The skin incision was oval around the circumference of masses with the longitudinal axis parallel to the Langer's line. Skin defects were closed directly or dissected on both sides of the incision to reduce tension. Wound healing was normal. After 1.5\u00a0months, there was no recurrence of xanthomas.", "extra_info": {"index": 10, "original_id": "multiclinsum_test_1587_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by glomerular filtration rate (GFR) decline, proteinuria, and systemic inflammation, and requires longitudinal monitoring with biomarkers such as serum creatinine and estimated GFR to guide therapeutic interventions including pharmacological modulation, dietary restriction, and potential dialysis initiation.\"\n}", "ground_truth": "An 84-year-old male was admitted with a history of difficulty rising from a chair and a fall. Laboratory results showed increased creatine kinase levels of more than 50 times the normal reference values. Electromyography (EMG) showed myopathic changes, and FDG-PET/CT scan showed increased FDG uptake in bilateral quadriceps. A biopsy was performed revealing lymphocytic predominant infiltrates and myonecrosis. Prednisone and intravenous immunoglobulin (IVIG) were administered with strength improvement. The patient was discharged for further follow-up.", "extra_info": {"index": 17, "original_id": "multiclinsum_test_2937_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by glomerular filtration rate (GFR) decline, proteinuria, and systemic inflammation, and requires longitudinal monitoring with biomarkers such as serum creatinine and estimated GFR to guide therapeutic interventions including pharmacological modulation, dietary restriction, and potential dialysis initiation.\"\n}", "ground_truth": "A 63-year-old male presented with a prominent itching sensation and wholebody jaundice. He showed obstructive-pattern jaundice, an elevated IgG4 level, and infiltration of a large number of IgG4-positive cells in the ampulla of Vater. The imaging findings of intrahepatic duct (IHD) and common bile duct dilation, an elevated serum IgG4 level, and characteristic histological findings led to diagnosis of IgG4-SC that compatible with the 2019 ACR/EULAR classification criteria. We planned to treat the patient with high-dose glucocorticoid (GC), followed by cyclophosphamide pulse therapy. After treatment with high-dose GC and an immunosuppressant, imaging studies showed that IHD dilatation had completely resolved.", "extra_info": {"index": 14, "original_id": "multiclinsum_test_53_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by glomerular filtration rate (GFR) decline, proteinuria, and systemic inflammation, and requires longitudinal monitoring with biomarkers such as serum creatinine and estimated GFR to guide therapeutic interventions including pharmacological modulation, dietary restriction, and potential dialysis initiation.\"\n}", "ground_truth": "The patient was referred to our hospital with a 1-month history of disorientation and magnetic resonance imaging showed hydrocephalus with an enhancing lesion in the tectum. Preoperative blood tests showed a high serum soluble interleukin-2 receptor level of 624 U/ml. Through a single burr hole, endoscopic third ventriculostomy and biopsy of the lesion were simultaneously performed with a flexible endoscope. The histological examination confirmed diffuse large B-cell lymphoma. The patient underwent chemotherapy and radiotherapy.", "extra_info": {"index": 11, "original_id": "multiclinsum_test_410_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by glomerular filtration rate (GFR) decline, proteinuria, and systemic inflammation, and requires longitudinal monitoring with biomarkers such as serum creatinine and estimated GFR to guide therapeutic interventions including pharmacological modulation, dietary restriction, and potential dialysis initiation.\"\n}", "ground_truth": "We describe a case of a Ashkenazi Jew patient who presented in the typical way that carcinoma of the colon might present but turned out to have a very rare type of tumor in both its histology and its location.", "extra_info": {"index": 18, "original_id": "multiclinsum_test_2722_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by glomerular filtration rate (GFR) decline, proteinuria, and systemic inflammation, and requires longitudinal monitoring with biomarkers such as serum creatinine and estimated GFR to guide therapeutic interventions including pharmacological modulation, dietary restriction, and potential dialysis initiation.\"\n}", "ground_truth": "An isolated retinal astrocytic hamartoma was detected in the nasal retina of the left eye of a 4-day-old male infant. At the time of initial presentation, we detected a solitary yellowish-white flat mass with an approximate size of 1.5 disc diameters in the nasal retina. Fluorescein angiography (FA) revealed a diffuse hyperfluorescence with slight fluorescence leakage. Seven months later, the fundus examination showed no lesion in the left eye, FA revealed mild tortuous vessels without leakage.", "extra_info": {"index": 20, "original_id": "multiclinsum_test_2309_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 40-year-old woman was admitted to our hospital after presenting with liver dysfunction. She had been previously diagnosed with ET; aspirin and anagrelide had been prescribed. Subsequent examination at our hospital revealed cecal cancer. Distant metastasis was absent; laparoscopic ileocecal resection was performed. Anagrelide was discontinued only on the surgery day. She was discharged on the seventh postoperative day without thrombosis or hemorrhage. However, when capecitabine and oxaliplatin were administered as adjuvant chemotherapy with continued anagrelide administration, she experienced hepatic dysfunction and thrombocytopenia; thus, anagrelide was discontinued. Five days later, her platelet count recovered. Subsequently, anagrelide and aspirin administration was resumed, without any adjuvant chemotherapy. Her liver function normalized gradually in 4\u2009months. One-year post operation, she is well without tumor recurrence or new metastasis.", "extra_info": {"index": 16, "original_id": "multiclinsum_test_1612_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "We report the case of a 51-year-old Caucasian woman who presented with SAPHO syndrome with mainly axial involvement. She had been treated with sulfasalazine and anti-inflammatory drugs for many years without any success. A few weeks after starting treatment with tofacitinib, both clinical and biological parameters dramatically improved. Imaging also showed considerable regression of the vertebral and pelvic lesions. However, tofacitinib had to be discontinued due to the occurrence of pulmonary embolism. Consequently, recurrence of bone pain and biologic inflammation was rapidly observed.", "extra_info": {"index": 0, "original_id": "multiclinsum_test_787_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "a 1-month-old baby presented with severe AS and CoA. The decision was made to perform a hybrid surgical procedure. The patient underwent a lateral thoracotomy for repair of the CoA and carotid cutdown for aortic balloon valvuloplasty (AoVP).", "extra_info": {"index": 19, "original_id": "multiclinsum_test_2724_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A young man involved in a car accident and sustained blunt thoracic injuries, among others. As part of primary survey, FAST scan was performed. Subxiphoid view to look for evidence of pericardial effusion showed part of the cardiac image obscured by A-lines. Other cardiac windows showed only A-lines, as well. A suspicion of pneumopericardium was raised and CT scan confirmed the diagnosis.", "extra_info": {"index": 21, "original_id": "multiclinsum_test_1133_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 56-year-old male on oral anticoagulation presented to the emergency department with epigastric pain, nausea, and left upper quadrant tenderness. There was no history of trauma. Contrast-enhanced CT imaging revealed a large subcapsular haematoma of the spleen. Oral anticoagulation was antagonised with vitamin K and the patient was discharged in good condition after 3 days of clinical observation.", "extra_info": {"index": 92, "original_id": "multiclinsum_test_1095_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 6-year-old girl with Coats plus syndrome presented to the pediatric emergency department with vomiting blood and blood in stool. An upper and lower gastrointestinal endoscopy revealed esophageal varices and vascular telangiectasia in the pyloric antrum, duodenum, and colon. She received palliative care and the bleeding was stopped after receiving intravenous octreotide. She then was followed in the pediatric gastroenterology, neurology, and ophthalmology clinics. She was later hospitalized and admitted to the intensive care unit as she continued to have intermittent gastrointestinal system bleeding. She eventually died due to severe gastrointestinal system bleeding.", "extra_info": {"index": 90, "original_id": "multiclinsum_test_1957_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 73-year-old male suspected to have a urothelial carcinoma was scheduled for elective left nephroureterectomy. During central venous catheterization using the anatomic landmark technique to target the internal jugular vein, a guidewire is inadvertently inserted into the suspected vertebral vein. Following the correction of the catheterization, a radiologist reviewed the preoperative enhanced computed tomography and confirmed that the initially punctured vessel was the vertebral vein. On the third day after surgery, the central venous catheter was removed, and the patient did not exhibit any complications, such as bleeding, swelling, and neurological symptoms.", "extra_info": {"index": 88, "original_id": "multiclinsum_test_2805_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "Patient concerns:\nA 41-year-old man who presented with acute onset of right-hand clumsiness and aphasia even under high international normalized ratio (INR: 7.64) from warfarin use. He was previously treated with warfarin for the LV thrombus and non-valvular AF. Brain magnetic resonance imaging (MRI) showed multiple acute infarction in the cortex of the bilateral frontal lobes, left parietal lobe, and bilateral central semiovale, which highly suggested embolic stroke.\n\nDiagnosis:\nThe repeated transthoracic echocardiogram still revealed LV thrombus (1.27 \u00d7 0.90\u200acm), which failed to respond to warfarin therapy.\n\nInterventions:\nDue to acute infarctions occurred under supratherapeutic range of INR, we switched warfarin to edoxaban (dose: 60\u200amg/day) after INR decreased to less than 2.\n\nOutcomes:\nThe thrombus disappeared after receiving edoxaban for 23 days, and no more recurrent stroke was noted for more than 6 months.", "extra_info": {"index": 94, "original_id": "multiclinsum_test_3113_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 35-year-old woman diagnosed to have echo-proven chronic rheumatic heart disease for 25 years. Percutaneous balloon mitral valvotomy was done 6 weeks previously for severe mitral stenosis. Left atrial thrombus was detected after the procedure and anticoagulant (warfarin) was initiated. She presented with severe headache and repeated vomiting of 1 day duration on arrival to the hospital. She had frequent seizure attacks with subsequent loss of consciousness on third day of admission. Diagnosis of status epilepticus secondary to intracranial hemorrhage due to warfarin toxicity was made after CT-scan revealed acute subdural hematoma and ventricular bleeding. Then she was transferred to medical intensive care unit (ICU), intubated and put on mechanical ventilator. Anti-epileptic drugs, antibiotics, vitamin K and fresh frozen plasma were given. She developed paroxysms of hypertension, tachycardia, tachypnea, hyperpyrexia, diaphoresis and decerebrate posturing after 7 days of neurological insult. She had normal inter-ictal EEG tracing during cyclic autonomic surge. CFS score was 11 and DLT score was 10. In sum, PSH-AM score was 21, suggested \"probable\" diagnosis of PSH. Morphine, diazepam, propranolol and gabapentin were given in combination to treat PSH. Severity of autonomic storm started to improve on second week of ICU admission. On the third week of admission, her clinical condition deteriorated suddenly, she developed asystole and died of cardiac arrest despite cardiopulmonary resuscitation (CPR).", "extra_info": {"index": 96, "original_id": "multiclinsum_test_1504_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "We report the case of a 52-year-old patient from Bangladesh with dual-origin LAD arising from both left and right sinus with a pre-pulmonary course, presenting with exertional angina and documented myocardial ischaemia. Computed tomography (CT) scan confirmed the anatomical course of the AAOCA. Percutaneous coronary intervention was successfully performed using tailored techniques to treat significant atherosclerotic lesions.", "extra_info": {"index": 100, "original_id": "multiclinsum_test_3124_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 59-year-old male with suspected lung cancer in the left lower lobe was scheduled to undergo surgery. Chest computed tomography revealed a displaced B1\u00a0+\u20092 and hyperlobulation between S1\u00a0+\u20092 and S3, while the interlobar fissure between S1\u00a0+\u20092 and S6 was completely fused. Three-dimensional computed tomography (3D-CT) revealed an anomalous V1\u00a0+\u20092 joining the left inferior pulmonary vein and a branch of the V1\u00a0+\u20092 running between S1\u00a0+\u20092 and S6. We performed left lower lobectomy via video-assisted thoracic surgery, while taking care with the abovementioned anatomical structures. The strategy employed in this operation was to preserve V1\u00a0+\u20092 and confirm the locations of B1\u00a0+\u20092 and B6 when dividing the fissure.", "extra_info": {"index": 91, "original_id": "multiclinsum_test_2752_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 48-year-old caucasian male with an extensive psychiatric history ingested a high dose of venlafaxine causing a serum venlafaxine concentration of 12.6\u00a0mg/L 24\u00a0hours after ingestion. Seven hours post-ingestion, he experienced tonic-clonic seizures, and 8\u00a0hours later, takotsubo cardiomyopathy was recognized followed by cardiac arrest. The patient was resuscitated with prolonged cardiopulmonary resuscitation including ongoing automatic external compressions during helicopter transportation to a tertiary hospital for extracorporeal membrane oxygenation treatment. Despite a cardiopulmonary resuscitation duration of 2\u00a0hours, 36\u00a0hours of extracorporeal membrane oxygenation, and a total of 30\u00a0days of intensive care, the patient made a full recovery.", "extra_info": {"index": 97, "original_id": "multiclinsum_test_985_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "We present the case of an adult male patient with cerebral malaria by Plasmodium vivax, who starts with general discomfort and fever, then presents convulsions more than twice a day with loss of consciousness and motor functional limitation. He is given a thick drop where Plasmodium vivax trophozoites and depression of the three blood series are observed. He is given treatment with artesunate and clindamycin for five days, a blood transfusion and continues with primaquine for seven days. The patient shows clinical improvement with neurological sequelae in the left lower extremity.\n", "extra_info": {"index": 95, "original_id": "multiclinsum_test_3364_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "In this article, we describe a case of a-69-year-old female with a painful mass in her left breast. Based on intraoperative pathology consult, neoplastic tissue mostly floating in mucinous lakes with invasion to surrounding stroma was seen. Immunohistochemistry profile showed positive estrogen and progesterone receptors and negative for HER2.", "extra_info": {"index": 106, "original_id": "multiclinsum_test_2138_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "We report a clinical case of a combat patient who was injured after the multiple launcher rocket system \"Grad\" shelling, diagnosed with hydrodynamic liver rupture followed by medical management with application of damage control (DC) tactic in conditions of hybrid war. The patient underwent relaparatomy, liver resection, endoscopic papillosphincterotomy, endoscopic retrograde cholecystopancreatography, stenting of the common bile duct, and VAC-therapy. Applied treatment modalities were effective; the patient was discharged on the 49th day after injury.", "extra_info": {"index": 93, "original_id": "multiclinsum_test_2795_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "We present a case where a combined lumbar epidural and spinal anesthesia was performed using the loss of resistance to air technique (LOR), on a 78-year-old Greek (Caucasian) male undergoing a total hip replacement. Despite being hemodynamically stable throughout the operation, two hours following epidural analgesia the patient manifested a sudden drop in blood pressure and heart rate that required the administration of adrenaline to counter. Pneumomediastinum, pneumorrachis and paravertebral soft tissue emphysema were demonstrated in a Computed Tomography scan. We believe that injected air from the epidural space and surrounding tissues slowly moved towards the mediastinum, stimulating the para-aortic ganglia causing parasympathetic stimulation and therefore hypotension and bradycardia.", "extra_info": {"index": 89, "original_id": "multiclinsum_test_2918_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 46-year-old male with end-stage renal disease of unknown cause received a cadaveric renal transplant one year ago. Although three antihypertensive medications were administrated, his blood pressure gradually increased to 190/120\u00a0mmHg 3\u00a0weeks posttransplantation. Also the level of creatinine increased to 194\u00a0\u03bcmol/L.Color Doppler ultrasonography indicated a decreased resistance index (RI) in intrarenal arteries and increased blood flow of the transplant renal artery, therefore, a vascular complication of TRAS was suspected. Arteriography was performed and demonstrated TRAS caused by stretch of an artery branch, and the TRAS occurred in the distal site of the anastomosis instead of the anastomosis. Percutaneous transluminal bare stent implantation treatment was successfully performed. Satisfactory clinical efficacy with improvement in transplant renal function and renovascular hypertension was achieved after the interventional treatment.", "extra_info": {"index": 101, "original_id": "multiclinsum_test_1302_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 59-year-old female with a history of recurrent UCS presented with the new onset of the left lower extremity pain, numbness, and episodic urinary incontinence. When the MR revealed an enhancing intradural extramedullary mass posterior to the L1 vertebral body, she underwent a focal decompressive laminectomy. Although she improved neurologically postoperatively, she succumbed to the leptomeningeal spread of her disease within 2 postoperative months.", "extra_info": {"index": 103, "original_id": "multiclinsum_test_2588_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 56-year-old woman was referred to the emergency department due to a severe headache in the frontal area for 2 days before admission. The patient experienced nausea and vomiting in the morning and had no history of seizures or decreased consciousness. Examination of neurological symptoms was completely normal and showed no symptoms of meningeal irritation. In terms of past history, the patient had undergone tympanomastoidectomy surgery and resection of the cholesteatoma 1 week previously. The Mount Fuji sign was found on the brain computed tomography (CT) scan of the patient. Treatments such as CBR (complete bed rest), 30-degree head elevation, anti-fever, analgesics and oxygen therapy, along with anti-compulsive drug (phenytoin), were prescribed. At the end of 5 days, the patient's pneumocephalus was resolved completely.", "extra_info": {"index": 105, "original_id": "multiclinsum_test_520_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "We report the case of a 63-year-old woman with upper gastrointestinal obstruction for almost 10 years, who was pathologically diagnosed with large Brunner's gland adenoma of the duodenum. Postoperatively, no sign of recurrence has been noted until now.", "extra_info": {"index": 108, "original_id": "multiclinsum_test_2813_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 70-years-old woman, who had been diagnosed with SLE at 69\u2009years, was admitted for further examination of liver dysfunction. PBC was confirmed based on elevated serum levels of transaminase, high levels of antimitochondrial antibodies and following a liver biopsy. The oral administration of ursodeoxycholic acid stabilized the liver dysfunction.", "extra_info": {"index": 109, "original_id": "multiclinsum_test_2272_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "The six-year-old girl underwent a human leucocyte antigen (HLA) haploidentical hematopoietic stem cell transplant using post-transplant Cyclophosphamide for severe aplastic anemia. In the second week of the transplant, the patient developed macrophage activation syndrome necessitating treatment with steroids and intravenous immunoglobulin. Subsequently, USG abdomen and blood fungal PCR revealed the diagnosis of hepatosplenic candidiasis. Candida-triggered macrophage activation syndrome responded to antifungals, steroids, intravenous immunoglobulin, and alemtuzumab. However, the subsequent clinical course was complicated by thrombotic microangiopathy. The patient developed hypertension in the 2nd week, followed by high lactate dehydrogenase (1010\u2009U/L), schistocytes (5 per hpf), low haptoglobin (<\u20095\u2009mg/dl), thrombocytopenia, and anemia in the 3rd week. Ciclosporin was stopped, and the patient was treated with 10\u2009days of defibrotide without response. The course was further complicated by the involvement of the gastrointestinal tract and kidneys. She had per rectal bleeding with frequent but low-volume stools, severe abdominal pain, and hypoalbuminemia with a rising urine protein:creatinine ratio. Narsoplimab was started in the 5th week of the transplant. A fall in lactate dehydrogenase was observed after starting Narsoplimab. This was followed by the resolution of gastrointestinal symptoms, proteinuria, and recovery of cytopenia. The second episode of TA-TMA occurred with parvoviraemia and was also successfully treated with Narsoplimab.", "extra_info": {"index": 98, "original_id": "multiclinsum_test_2016_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control can slow disease progression and reduce the risk of end-stage renal disease.\"\n}", "ground_truth": "We report a 9 days-old male neonates weighing 3.85 kg was referred by local hospital to our center and was ventilated with history of respiratory distress and severe infection since he was born. Admitted to our PCICU, 2D echo showed an IAA type A associated with a huge APW type II and restrictif PDA. A PGE1 infusion was started, during the following days the baby experienced several epileptic episodes. After improvement of the clinical condition, surgery was performed on the 20th days of life on year 2011. A successful one-stage repair of such anomalies in which cutting of PDA that arised from PA trunk and distally becoming into descending aorta, extended end to end anastomosis to conduct the ascending aortic blood flow into the descending aorta and intra arterial baffle was used. A 4-0 Gore-Tex baffle was used both to close the APW and separated the RPA from aortic origin with a good result, as his recently grown up as a cheerful 9 year old child who is growing actively and has entered elementary school in grade 2.", "extra_info": {"index": 102, "original_id": "multiclinsum_test_2375_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control can slow disease progression and reduce the risk of end-stage renal disease.\"\n}", "ground_truth": "Here, we present a case study of a patient with oral cancer who underwent surgery. During adjuvant radiotherapy, a metastatic cervical lymph node was diagnosed based on fine-needle aspiration biopsy. To increase the total dose to the metastatic tumor, a stereotactic radiosurgery boost of 1\u2009\u00d7\u200918\u00a0Gy was performed two days after the last fraction of conventional radiotherapy. The early and late tolerance of this treatment were positive. During the 18-month follow-up, locoregional recurrence was not detected. The patient died due to secondary malignancy.", "extra_info": {"index": 104, "original_id": "multiclinsum_test_2840_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control can slow disease progression and reduce the risk of end-stage renal disease.\"\n}", "ground_truth": "A 64-year-old male was admitted to the hospital with a headache, fever and later imbalance, blurred vision, and general slowness. Neurological examination revealed nuchal rigidity and general clumsiness. Meningitis was suspected, and the patient was treated with dexamethasone, ceftriaxone and acyclovir. A brain computer tomography (CT) scan was normal, and cerebrospinal fluid (CSF) Gram staining and bacterial cultures remained negative, so the antibacterial treatment was discontinued. Nine days after admission, the patient's condition deteriorated. The antibacterial treatment was restarted, and a brain magnetic resonance imaging revealed ventriculitis. A subsequent CT scan showed hydrocephalus, so a ventriculostomy was performed. In CSF Gram staining, chains of gram-positive cocci were observed. Bacterial cultures remained negative, but a bacterial PCR detected Streptococcus intermedius. An orthopantomography revealed advanced periodontal destruction in several teeth and periapical abscesses, which were subsequently operated on. The patient was discharged in good condition after one month.", "extra_info": {"index": 107, "original_id": "multiclinsum_test_1344_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 10-year-old Kurdish boy was presented with generalized bone pain and fever of 1 month's duration which was associated with sweating, easy fatigability, nose bleeding, breathlessness and severe weight loss. On examination, we observed pallor, tachypnea, tachycardia, low blood pressure, fever, petechial hemorrhage, ecchymoses, tortuous dilated veins over the chest and upper part of abdomen, multiple small cervical lymph node enlargements, mildly enlarged spleen, palpable liver and gross abdominal distention. Blood analysis revealed pancytopenia and elevated lactate dehydrogenase and erythrocyte sedimentation rate. Imaging results showed mediastinal widening on a planar chest X-ray and diffuse focal infiltration of the axial bone marrow on magnetic resonance imaging of the lumbosacral vertebrae. Bone marrow aspiration and biopsy examination showed extensive bone marrow necrosis. Immunophenotyping analysis of the bone marrow biopsy confirmed T-cell acute lymphoblastic leukemia, as CD3 and terminal deoxynucleotidyl transferase markers were positive and CD10, CD20 and CD79a markers were negative.", "extra_info": {"index": 99, "original_id": "multiclinsum_test_1185_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "A 21-year-old man was referred to our hospital for treatment after presenting to a nearby hospital with right inguinal pain. Abdominal magnetic resonance imaging showed an intra-abdominal mass measuring 34 \u00d7 15 \u00d7 8 cm with partial signal hyperintensity on T2-weighted imaging and hypointensity on T1-weighted imaging, extending from the left abdominal cavity to the pelvic region. Although no definitive diagnosis was obtained preoperatively, surgery was performed under suspicion of gastrointestinal stromal tumor or other significant disease. A mass was identified firmly adherent to the transverse colon, gastric wall, and diaphragm, and these organs were partially resected. The excised specimen measured 38 \u00d7 21 \u00d7 8 cm and weighed 6400 g. Macroscopically, the tumor showed a smooth surface and homogeneous interior. Pathological examination revealed atypical cells with spindle-shaped nuclei and collagen fiber hyperplasia in the stroma, and immunostaining was negative for c-kit, CD34, desmin, S-100, and positive for \u03b2-catenin, leading to a confirmed diagnosis of desmoid tumor. Fifteen months after surgery, a local recurrence with a diameter of 3.0 cm was identified, and the patient remains under careful follow-up.", "extra_info": {"index": 112, "original_id": "multiclinsum_test_3373_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "The patient was a 77-year-old hypertensive male who presented to the emergency following an episode of slip and fall at home. After prompt resuscitation, he was sent for radiological evaluation which revealed fractures of the left inter-trochanteric femur and left proximal humerus. Meanwhile, laboratory investigations showed grossly deranged renal parameters, along with elevated serum creatinine phosphokinase levels (more than 5 times the baseline). A diagnosis of acute kidney injury secondary to traumatic rhabdomyolysis was made. Medical management included adequate intravenous fluid administration combined with strict input-output monitoring. Subsequently, the patient underwent closed reduction and internal fixation of the inter-trochanteric femur fracture with a proximal femoral nail. However, fracture of the proximal humerus was managed non-operatively with sling immobilization as patient refused to give consent for a second surgery.", "extra_info": {"index": 110, "original_id": "multiclinsum_test_2243_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "A 25-year-old gentleman presented with recurrent upper right vestibular abscess three months following a bimaxillary orthognathic surgery. A bonded molar orthodontic tube had dislodged into the wound during the operation. The clinical presentation initially mimics an odontogenic infection until our investigations revealed that it originated from the dislodged appliance. The abscess was drained, the wound site was explored, and the molar tube and neighbouring rigid fixation plates and screws were removed. The patient recovered well following the procedure.", "extra_info": {"index": 113, "original_id": "multiclinsum_test_1305_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "We describe a 30-year-old Caucasian woman who tested positive for COVID-19 after developing nasal congestion and cough. Ten days after testing positive, she developed a systemic rash on her extremities and torso. At the same time, she developed swelling of the tongue lasting 1 hour, with subsequent appearance of oral lesions that resembled geographic tongue. She also had an irritable sensation on her tongue and some mild loss of sense of taste. We opted for conservative therapy, including mouth rinses containing lidocaine to be used every 6 hours. The patient used the mouth rinse therapy for 1 month and experienced a 90% improvement in her oral lesions and tongue sensitivity. However, she had repeated flares every 3 weeks over a 6-month period, and the steroid mouthwash achieved incomplete resolution. After three sessions of photobiomodulation therapy, she had no further flares or tongue sensitivity and the lesions healed.", "extra_info": {"index": 119, "original_id": "multiclinsum_test_778_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "A 91-year-old woman presented to our institution with ST-segment elevation myocardial infarction (STEMI). The right radial access was chosen for the performance of percutaneous coronary intervention. After the introduction of 6\u2009F sheath, there was difficulty in the advancement of 0.035\u2009J wire that was exchanged with a Terumo hydrophilic wire. After the procedure and before sheath removal, radial arteriography was done and revealed perforation. Protamine sulfate was administered and prolonged balloon inflation was attempted but failed to seal the perforation, so a 7-F-long vascular sheath was inserted to internally tamponade the vessel, and the patient was sent to the coronary care unit for monitoring. Over the next 3 days, serial radial angiographies were done revealing the persistence of the perforation, and on the fourth day, angiography revealed multiple thrombi. Thrombus aspiration was done using Pronto V4 extraction catheter (Vascular Solutions, USA) and was followed by the deployment of a covered stent. The stent was dislodged and successfully snared. Finally, the perforation was sealed spontaneously and there were no signs of intra-arterial thrombi.", "extra_info": {"index": 120, "original_id": "multiclinsum_test_1116_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "In this case, we present a preterm newborn who developed pneumomediastinum and pneumothorax. The pneumothorax persisted, despite placement of a thorax tube, requiring a thoracotomy to detect and treat the bronchial rupture.", "extra_info": {"index": 116, "original_id": "multiclinsum_test_2176_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "A case report of an 84-year old male, who presented with an aggressively recurrent form of MCC on the lower lip, on the background of an 8-year history of untreated CLL. During the recurrences of MCC, coexisting regional lymphadenopathy, posed a problem in the differential diagnosis and treatment of lymph node involvement. Histopathology and immunoistochemistry showed that submandibular lymphadenopathy coexisting with the second recurrence of MCC, was due to B-cell small lymphocytic lymphoma. The subsequent and more aggressive recurrence of the skin tumor had involved the superficial and deep cervical lymph nodes. Surgical excision followed by involved field radiation therapy has been proven effective for both malignancies.", "extra_info": {"index": 128, "original_id": "multiclinsum_test_1953_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "We describe a case in which the two technologies are used in combination during acute echocardiographic optimization of left pacing vector in a 63-year-old man, Caucasian, who showed worsening heart failure symptoms a few days after an implant, and the effect of the device\u2019s optimization at 6-month follow-up.", "extra_info": {"index": 126, "original_id": "multiclinsum_test_3317_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "A 78-year-old male patient presented with intermittent cervicalgia of 5 months duration accompanied by few weeks of a progressive severe right hemiparesis, up to hemiplegia. The magnetic resonance imaging (MRI) examination revealed an intramedullary expansive lesion measuring 10 mm\u00d715 mm at the C1-C2 level; it readily enhanced with contrast. A total body computed tomography (CT) scan documented an 85 mm mass involving the right kidney, extending to the ipsilateral adrenal gland, and posteriorly infiltrating the ipsilateral psoas muscle. The subsequent CT-guided fine-needle biopsy confirmed the diagnosis of an RCC (Stage IV). The patient next underwent total surgical total removal of the C1-C2 intramedullary mass, following which he exhibited a slight motor improvement, with the right hemiparesis (2/5). He died after 14 months due to global RCC tumor progression.", "extra_info": {"index": 122, "original_id": "multiclinsum_test_2110_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "Patient concerns:\nA 68-year-old man was admitted to our hospital with dyspea and general fatigue. He was diagnosed with acute decompensated heart failure due to ischemic cardiomyopathy. In order to improve fluid retention and relieve his dyspnea, low-dose TLV (7.5\u200amg qd) was performed. After the 3-day treatment using TLV, we observed that he became delirious and his limbs shook uncontrollably. High serum sodium 173 mmol/L was noted compared to the results of the first examination (137 mmol/L). After intensive rescue, serum sodium was restored to normal (135\u200amol/L). Later, when the patient refused continuous renal replacement therapy (CRRT), we tried again to use a lower dose of TLV to improve diuretic resistance. Two days later, Serum sodium rose again (162 mmol/L).\n\nDiagnoses:\nDuring the course of therapy, we did not strictly require the patient to control the fluid intake. No other medication could cause elevation of serum sodium. Therefore, we suspected a high sensitivity to the side effect of TLV.\n\nIntervention:\nStop the use of TLV and encourage the patient to drink plenty of water. Gastric tube was inserted orally to increase the intake of fresh water.\n\nOutcomes:\nHis serum sodium decreased gradually and his psychiatric symptom recovered. During this period, Overall condition of the patient was stable. After being discharged from the hospital, the patient eventually died of cardiac arrest due to critically ill heart failure.", "extra_info": {"index": 124, "original_id": "multiclinsum_test_3307_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "We report the case of a patient with a history of multiple diseases and 2 tumor-like lesions with internal lytic areas detected in the fourth right costal arch and in the eighth left costal arc; we describe his clinical manifestations, radiological and laboratory findings as well as the pathological results and outcome.", "extra_info": {"index": 130, "original_id": "multiclinsum_test_2403_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "44-year-old African black patient of Burkinabe origin with no other medical history, admitted for chronic inflammatory low back pain associated with inflammatory right knee pain and a cough with phlegm. This symptomatology had been developing for seven months in a febrile context and with a general deterioration in health. The examination showed oligoarthritis of the right sternoclavicular joint and the left knee, associated with a pulmonary condensation syndrome and pleural effusion, a cold abscess at the level of the right sternoclavicular joint and a fistulous and purulent right inguinal lymphadenopathy. The biology showed an inflammatory syndrome. The GeneXpert test was positive in the sputum, without resistance to rifampicin. The intradermal reaction to the tuberculin was positive. The thoracic tomodensitometry showed a right sternoclavicular osteoarthritis and a spondylodiscitis of the L3-L4 spine. The standard radiography of the left knee objectified signs in favour of arthritis. The diagnosis of tuberculosis with multifocal, pleuropulmonary and ganglionar bone involvement was retained. The patient was given usual analgesics and antituberculous. The evolution was favourable.\n", "extra_info": {"index": 111, "original_id": "multiclinsum_test_3332_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "We report a case of a 93-year-old Middle Eastern male presenting for longstanding treatment-refractory hiccups. Imaging with computed tomography of the chest and abdomen was unremarkable. An upper endoscopy was normal without any endoscopic finding to suggest eosinophilic esophagitis. Given his elevated peripheral eosinophil count, biopsies were taken from mid- and distal esophagus and revealed eosinophilic infiltration in the range of 15 eosinophils per high-power field, favoring a diagnosis of eosinophilic esophagitis. The hiccups resolved following the initiation of eosinophilic esophagitis treatment.", "extra_info": {"index": 114, "original_id": "multiclinsum_test_3338_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 22-year-old male was admitted for bilateral leg tremor while standing, with symptom onset eight months prior. One month before admission, the tremor disappeared in the left leg but persisted in the right leg. Electromyography recorded from the right gastrocnemius revealed a 6-8\u00a0Hz tremor, which appeared when the patient was standing and disappeared when he was resting or walking. Blood screening showed a phenylalanine/tyrosine ratio of 2.06 and a phenylalanine level of 140\u00a0\u03bcmol/L. Urine metabolic screening was negative. Whole-exome sequencing confirmed the presence of a compound heterozygous mutation, c.158G\u2009>\u2009A and c.728G\u2009>\u2009A, in phenylalanine hydroxylase (PAH) gene. After three months of levodopa/benserazide tablets (250\u00a0mg, tid) and a low-phenylalanine diet treatment, the tremor disappeared.", "extra_info": {"index": 115, "original_id": "multiclinsum_test_1859_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A patient from TRITON2 with BRCA-mutated mCRPC had a response to the PARP inhibitor rucaparib and remained on treatment for 32 weeks, which was >2 times longer than the duration of each of his prior therapies (bicalutamide, docetaxel, abiraterone). The patient enrolled in TRITON2 based on results of local genomic testing of an archival biopsy that indicated the presence of a BRCA1 T1399I (allelic fraction, 19%) mutation. Local testing also identified an ATM G1663C mutation, a TP53 P191del mutation, and a BRAF K601E mutation. Analysis of a plasma sample obtained before the patient started rucaparib detected the same alterations as those in the archival biopsy, but it also revealed the presence of a BRCA2 homozygous loss (whole gene, 26 of 26 exons) and several other alterations of unknown functional impact. We hypothesize the response of the patient's tumor to rucaparib was likely driven by DNA damage repair deficiency caused by homozygous loss of all BRCA2 exons. Following discontinuation from rucaparib due to clinical disease progression, the patient received carboplatin and cabazitaxel for \u22483 weeks. The patient died due to progression of his disease.", "extra_info": {"index": 118, "original_id": "multiclinsum_test_759_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "In this case report, we present a 16-year-old Ukrainian boy with acute hepatitis B. He had not been previously vaccinated against hepatitis B. Possible sources of infection included: a tattoo made at home, a finger cut made with hairdresser scissors during work, and unprotected sexual encounters. The clinical course of the disease was typical with jaundice and elevated aminotransferases levels without liver failure. During the follow-up visit 16 months after the onset of the disease, chronic hepatitis b was excluded but an ulcer around his anus was found. Additional tests for sexually transmitted diseases were ordered and they were positive for syphilis. The extended interview revealed that the patient had several unprotected bisexual encounters, which may have indicated a potential source of infections including the hepatitis B virus (HBV).", "extra_info": {"index": 123, "original_id": "multiclinsum_test_3310_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 42-year-old female with history of uterine fibroids was admitted with abdominal pain and intraperitoneal fluid of unknown etiology. She was initially managed nonoperatively and empirically treated with broad spectrum antibiotics. Blood and urine cultures were unrevealing. Increasing abdominal pain and peritoneal fluid prompted diagnostic laparoscopy which revealed a dense fibrinous exudate covering the entire peritoneal cavity. Peritoneal fluid and biopsies were sent for cytology and culture. The peritoneal fluid was eventually sent for 16\u2009s ribosomal analysis, which discovered Mycoplasma hominis RNA. Her antibiotics were narrowed, and she eventually made a full recovery.", "extra_info": {"index": 127, "original_id": "multiclinsum_test_1099_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "We report a case of an isolated intracranial RDD in a 53-year-old man. The patient had an episode of generalized seizures. Imaging studies of the brain were compatible with a meningioma en plaque. The mass was exposed by a right frontotemporal craniotomy. The tumor was adhered tightly to the adjacent cerebral cortex and was permeated by pial arteries of the brain surface. The sacrificing of these arteries was inevitable in order to achieve the total removal of the tumor. The patient had incomplete left hemiparesis after the surgery. Brain computed tomography (CT) imaging revealed a postoperative hemorrhage and a low-density lesion in the right frontal lobe. The patient was postoperatively diagnosed with isolated central nervous system RDD.", "extra_info": {"index": 125, "original_id": "multiclinsum_test_1592_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 32\u2009year-old woman with a history of non-diabetic hemodialysis for 3\u2009years suffered from severe involuntary movement, and brain magnetic resonance imaging showed symmetrical T2-weighted imaging (T2WI) and T2/fluid-attenuated inversion recovery (T2FLAIR) hyperintense nonhemorrhagic lesions in the bilateral basal ganglia. She was diagnosed with UE as syndrome of bilateral basal ganglia lesions, due to a combined effect of uremic toxins and hyperthyroidism. After treatment with high frequency and high flux dialysis, hyperbaric oxygen therapy and declining parathyroid hormone, the patient achieved complete remission with normal body movement and was discharged.", "extra_info": {"index": 129, "original_id": "multiclinsum_test_168_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "The medical record of a 64-year-old female with Sjogren's syndrome was reviewed. The clinical and pathological data along with chest CT images were obtained. The literature related to the transformation was reviewed. There were no specific clinical manifestations of LIP and its transformation into malignant lymphoma in the patient. The chest CT mainly displayed multiple cystic foci, with multiple nodules and ground-glass shadows in both lungs.", "extra_info": {"index": 131, "original_id": "multiclinsum_test_2470_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 5-year-old girl with high-grade conventional osteosarcoma in the left distal femur underwent a series of surgeries. After three cycles of neoadjuvant chemotherapy, limb-salvage surgery was planned because femoral rotationplasty had been refused. At 6\u2009years and 2\u2009months old, distal femoral resection and temporary spacer insertion using a 7-mm-diameter intramedullary nail and molded polymethylmethacrylate was performed. At 7\u2009years and 8\u2009months old, secondary surgery was performed because the first spacer had been dislocated and the residual femur became atrophic. The distal end of the residual femur was removed by 1\u2009cm, but the periosteum and induced membrane around polymethylmethacrylate was preserved. In order to stabilize the spacer against the tibia, a custom-made ceramic spacer with a smooth straight 8-mm-diameter stem was utilized. The bone-spacer junction was fixed with polymethylmethacrylate and then covered with the preserved periosteum and induced membrane. After surgery, the bone atrophy improved. At 9\u2009years and 7\u2009months old, the second spacer was removed because it had loosened, and the knee joint was reconstructed using a custom-made growing femoral prosthesis with a curved porous 8.5-mm-diameter stem. Cancellous bone tips from the proximal tibia were grafted around the bone-prosthesis junction underneath the induced membrane. At 10\u2009years and 5\u2009months old, the patient was able to walk unsupported and a radiograph showed further thickening of the cortex of the residual femur without any stress shielding. Although having 5\u2009cm of limb length discrepancy, the patient and her mother were satisfied with the function. The MSTS score was 24 out of 30 points. Repeated limb length extensions are planned.", "extra_info": {"index": 117, "original_id": "multiclinsum_test_1775_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "We report a case of VEO-IBD associated with a monogenic mutation in a 2-year-old girl presenting mainly with gastrointestinal symptoms, including recurrent hematochezia and abdominal pain for more than 3 months. A gastroscopy revealed erosive gastritis and bulbar duodenitis, while a colonoscopy indicated erosive colitis. Abnormal results were obtained from the dihydrohodamine (DHR) assay and immunoglobulin testing. Whole-exome sequencing identified a heterozygous and de novo nonsense mutation (c.388\u00a0C\u2009>\u2009T; p.R130X) in the CYBB gene leading to deficiency of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (NOX2) (encoded by CYBB), a critical component of phagocytes. HSCT was performed successfully, and the DHR assay showed that normal neutrophil function was restored. Six months after HSCT, clinical remission was observed, and a repeat colonoscopy revealed intestinal mucosal healing was attained.", "extra_info": {"index": 121, "original_id": "multiclinsum_test_533_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "We report a case study with a 44-year-old man from Faryab Province in Afghanistan who presented chest pain and dizziness while suffering a common cold. After full investigation, the patient underwent coronary angiography which showed a myocardial bridge at the middle portion of the left anterior descending artery (LAD) with a significant stenosis causing ischemia. We treated the patient with a calcium channel blocker as initial treatment. The patient tolerated the medication well and remained asymptomatic during two years follow-up.", "extra_info": {"index": 167, "original_id": "multiclinsum_test_3208_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "Herein we present a 63-year-old man with idiopathic spontaneous intraperitoneal hemorrhage (ISIH) caused by spontaneous rupture of non-aneurysmal inferior pancreaticoduodenalartery (IPDA).", "extra_info": {"index": 4, "original_id": "multiclinsum_test_45_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "We report the case of a 51-year-old Caucasian woman who presented with SAPHO syndrome with mainly axial involvement. She had been treated with sulfasalazine and anti-inflammatory drugs for many years without any success. A few weeks after starting treatment with tofacitinib, both clinical and biological parameters dramatically improved. Imaging also showed considerable regression of the vertebral and pelvic lesions. However, tofacitinib had to be discontinued due to the occurrence of pulmonary embolism. Consequently, recurrence of bone pain and biologic inflammation was rapidly observed.", "extra_info": {"index": 0, "original_id": "multiclinsum_test_787_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 71-year-old female who was being treated for type 2 diabetes with canagliflozin, metformin, and saxagliptin orally presented to the ED for evaluation of reduced oral intake, malaise, nausea, and abdominal pain. Although her blood glucose was not severely elevated (259 mg/dL), there was notable ketoacidosis (pH\u20096.89; CO2, 11.4\u2009mmHg; HCO3, 1.9\u2009mEq/L; base excess, - 31.3\u2009mmol/L; 3-hydroxybutyric acid > 10,000\u2009\u03bcmol/L) was observed. The uncontrolled acidosis improved following 3\u2009days of continuous renal replacement therapy, but elevated urinary glucose continued for more than 10\u2009days. Ringer's lactated fluid supplementation was continued for management of polyurea and glucosuria. Urinary glucose turned negative on day 16, and there was improvement in the patient's overall state; hence, she was discharged on day 18.", "extra_info": {"index": 2, "original_id": "multiclinsum_test_99_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control can slow disease progression and reduce the risk of end-stage renal disease.\"\n}", "ground_truth": "We presented an interesting case of a 33-year-old female with a solitary polypoid nodule without apparent pigmentation on her vulvar skin. Her medical history was unclear, no ulcer was seen in the lesion area, and dermatoscopy was indicated a possible tumorous change, which has caught the attention of clinicians, and then further examined by the pathologist. The final diagnosis was nodular malignant melanoma (NM) (Breslow thickness 9.5mm, Clark level 4).", "extra_info": {"index": 156, "original_id": "multiclinsum_test_1142_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control can slow disease progression and reduce the risk of end-stage renal disease.\"\n}", "ground_truth": "A 39-year-old woman, who visited to our hospital complaining of worsened right low back pain and fever, was diagnosed with right hydronephrosis due to ureteropelvic junction obstruction by contrast-enhanced computed tomography. Intraoperatively before the planned robot-assisted laparoscopic pyeloplasty, retrograde pyelography was performed to reveal concomitant ipsilateral retrocaval ureter. Laparoscopically, ureteropelvic junction obstruction due to aberrant blood vessel and coexisting retrocaval ureter was confirmed. Transposition of the ureter from posterior to anterior of the inferior vena cava and following dismembered pyeloplasty was performed. Two years after surgery, her right hydronephrosis improved and she had no complain of any symptom.", "extra_info": {"index": 162, "original_id": "multiclinsum_test_1681_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control can slow disease progression and reduce the risk of end-stage renal disease.\"\n}", "ground_truth": "An 86-year-old male was admitted to our hospital with congestive heart failure due to low-flow low-gradient severe AS, a membranous VSD, a sub-aortic band, and a double-chambered right ventricle (RV). The patient was not deemed to be a surgical candidate because of advanced age and frailty even though surgical aortic valve replacement, VSD closure, sub-aortic band resection, and myectomy of RV would be considered as definitive treatment. Instead, we performed TAVI and VSD orifice closure using the skirt part of the self-expanding valve (26\u2005mm Evolut Pro Plus\u2122) because VSD occluder is not approved and thus not available in our country. The trans-catheter procedure resulted in a reduction of the mean aortic valve pressure gradient improved from 33 to 2\u2005mmHg and a decrease in the shunt flow (Qp/Qs) from 1.9 to 1.2. The patient\u2019s heart failure improved, and he was discharged to home 7 days after the procedure. He remained well and had not been admitted to hospital since discharge.", "extra_info": {"index": 154, "original_id": "multiclinsum_test_3275_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control can slow disease progression and reduce the risk of end-stage renal disease.\"\n}", "ground_truth": "52-year-old female patient who reported chronic, burning pain radiating to the distal phalanx of the thumb with no traumatic history, which had been present for two years and limited her daily activities. The exploration was complemented with interphalangeal Doppler ultrasound, which is an excellent alternative due to its easy accessibility. A glomus tumor in the interphalangeal phalanx of the thumb was diagnosed. A H-approach was performed on the interphalangeal fold with subungual dissection and resection of the tumoral piece and follow-up by an external consultation where the surgical wound was found to be healing adequately. Physical exploration with the ability to mobilize the interphalangeal distal joint (IFD) and visual analogue scale (VAS) of 1 point. The anatomopathological evaluation reported the existence of a glomus tumor.\n", "extra_info": {"index": 158, "original_id": "multiclinsum_test_3249_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "Here, we report the first clinical case of a cerebral nocardiosis revealed after seizure in a patient treated by pembrolizumab for a metastatic lung cancer, in the absence of any additional immunosuppressive therapy or risk factors for cerebral nocardiosis. The extended evaluation including a brain CT-scan did not reveal any lesion before pembrolizumab. Nevertheless, the 3-month delay between the start of Pembrolizumab and the diagnosis of cerebral nocardiosis suggests that the infection occurred prior to the CPI. Unfortunately, the patient died during treatment for cerebral nocardiosis, while the lung cancer tumor mass had decreased by 80% after the sixth cycle of pembrolizumab.", "extra_info": {"index": 157, "original_id": "multiclinsum_test_2333_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "It is a case report of a 13-year-old girl with the history of swelling over her right hand for 5 months. X-ray revealed that there was an osteolytic fusiform expansible lesion. The biopsy sent and it conferred the diagnosis of GCT. Dorsal approach used for the enbloc resection of the fifth metacarpals (except at the base) and partial excision of the surrounding muscles done. The capsule and collateral ligament of the fifth metacarpophalangeal joint were left. The fourth metatarsal was harvested from the foot along with its capsule and collateral ligament of the metatarsophalangeal joint and sutured to the counter capsuloligamentous structure at the recipient site.", "extra_info": {"index": 163, "original_id": "multiclinsum_test_2668_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control can slow disease progression and reduce the risk of end-stage renal disease.\"\n}", "ground_truth": "A 15-year-old boy who was previously diagnosed with SRU presented to our office with rectal bleeding, mucoid discharge, and abdominal pain. Additional colonoscopy evaluation revealed multiple polyposes varying in size and shape limited to the rectum. Histologic examination revealed a characteristic cap of granulation tissue covering tortuous nondysplastic crypts in the inflamed stroma, indicating that SRU had transformed into CP. Based on the assessments, we planned to perform endoscopic mucosal resection of the lesions in multiple sessions.", "extra_info": {"index": 164, "original_id": "multiclinsum_test_2219_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "We report the case of a 72-year-old Caucasian woman with full-thickness rectal prolapse associated with fecal incontinence from severe neuromuscular damage.", "extra_info": {"index": 165, "original_id": "multiclinsum_test_2449_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 62-year-old previously healthy Sri Lankan native male from the Western province of Sri Lanka presented with high fever with malaise, myalgia and arthralgia for 17 days. On the 5th day of illness he developed intermittent resting tremor in his right arm and leg associated with stiffness, difficulty in carrying out normal work and difficulty in smiling. He denied similar previous episodes. There were no other associated neurological manifestations. Clinical examination revealed a high amplitude low frequency resting tremor in his right hand, a mask-like face and increased muscle tone limited to the right side with normal reflexes. The rest of the system examination was normal except for an eschar over the abdomen. His investigations revealed lymphocytic leukocytosis, high erythrocyte sedimentation rate and immunofluorescence assay-IgM and IgG against Orientia tsutsugamushi Karp antigen were positive with rising titers. With oral doxycycline and azithromycin his fever settled within 48 h and a complete recovery of Parkinson's features was observed within 2 weeks.", "extra_info": {"index": 155, "original_id": "multiclinsum_test_146_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "We present the case of a 16-year-old Persian man diagnosed as having a non-invasive form of multiple endocrine neoplasia 2B (medullary thyroid cancer, mucosal neuroma of the tongue, lips and inner eyelids). Our patient, who had a positive family history of medullary thyroid cancer, was of normal height with no signs of marfanoid habitus.", "extra_info": {"index": 159, "original_id": "multiclinsum_test_2043_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control can slow disease progression and reduce the risk of end-stage renal disease.\"\n}", "ground_truth": "We report a 53-year-old female from a rural area in China who was hospitalized for lower limb edema, abdominal distension, cirrhosis, and hypothyroidism. We excluded the common causes of liver disease (drinking alcohol, using traditional Chinese medicines, hepatitis virus infection, autoimmunity, and hepatolenticular degeneration). When she was 23-years-old, she developed night-blindness that worsened to complete blindness, with no obvious cause. Her parents were first cousins, and both were alive. Analysis of the patient's family history indicated that all 5 siblings had night blindness and impaired vision; one sister was completely blind; and another sister had night-blindness complicated with cirrhosis and subclinical hypothyroidism. Entire exome sequencing showed that the patient, parents, and siblings all had mutations in the cytochrome P450 4V2 gene (CYP4V2). The CYP4V2 mutations of the parents and two sisters were heterozygous, and the others were homozygous. Two siblings also had heterozygous dual oxidase activator 2 (DUOXA2) mutations.", "extra_info": {"index": 160, "original_id": "multiclinsum_test_2430_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "We present the case of a middle-aged patient diagnosed with a giant gastric GIST, which presented for intermittent gastric outlet obstruction symptoms, and emphasize the major imagistic, histopathological, and therapeutic challenges that may be encountered. There are only several cases of gastric exophytic gastric GIST provoking intermittent gastric outlet obstruction. Tumor resection should be adapted to every patient's status, focused on en bloc extraction, with preservation of invaded organs as much as possible.", "extra_info": {"index": 169, "original_id": "multiclinsum_test_1842_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "We present a case of 62-year-old male who presented after experiencing syncope and cardiac arrest. Given the clinical presentation and electrocardiographic findings, there was concern for acute coronary syndrome. However, coronary angiogram did not reveal significant coronary obstruction. Due to the unclear nature of his presentation, a bedside echocardiogram was rapidly performed and was indicative of right ventricular strain. Due to these findings, a pulmonary angiogram was performed that revealed massive pulmonary embolism. He successfully underwent catheter-directed thrombolysis and, after a prolonged hospital stay, was discharged home on lifelong anticoagulation.", "extra_info": {"index": 168, "original_id": "multiclinsum_test_2976_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control can slow disease progression and reduce the risk of end-stage renal disease.\"\n}", "ground_truth": "Our patient was a 39-year-old Chinese woman who had a history of two cesarean sections and one miscarriage. She had a recurrent anterior abdominal wall mass around her cesarean scar, and the mass was initially suspected of being choriocarcinoma of unknown origin. The patient had concomitant negative or mildly increased serum \u03b2-human chorionic gonadotropin at follow-up and no abnormal vaginal bleeding or abdominal pain. However, she underwent local excision twice and had two courses of chemotherapy with an etoposide and cisplatin regimen. She finally opted for exploratory laparotomy with abdominal wall lesion removal, subtotal hysterectomy, bilateral salpingectomy, and left ovarian cyst resection, which showed the abdominal wall lesion, whose components were revealed by microscopy and immunohistochemical staining to be approximately 90% epithelioid trophoblastic tumors and 10% choriocarcinomas from a solely extrauterine mixed gestational trophoblastic neoplasm around an abdominal wall cesarean scar.", "extra_info": {"index": 166, "original_id": "multiclinsum_test_2114_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "In this report, we present the case of an RSV-associated death of a child who was born at full-term and developed normally up to the age of 2 years old. Cardiopulmonary arrest occurred within 3 days after the onset of symptoms, which included cough and high fever. Complete brain edema was prominent, and encephalopathy was developing. Viral antigen detection and microbiome analyses of oral swab and nasopharyngeal aspirate specimens verified an RSV infection, while bacterial culture of blood specimens yielded negative results. The RSV strain detected in this patient was subtyped as RSVB9, and no mutation was found in the six antigenic sites for targeted drugs or vaccines.", "extra_info": {"index": 161, "original_id": "multiclinsum_test_3147_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "We present a case of subacute cervical cerebrospinal fluid (CSF) leak resulting from chiropractic manipulation of the cervical spine. The patient is a 29-year-old female who received manipulation one week prior to developing symptoms of severe orthostatic headache, nausea, and vomiting. Magnetic resonance imaging (MRI) revealed a new C5-C6 ventral CSF collection. Symptomatic onset corresponded with the recent cervical chiropractic adjustment. We present serial imaging correlating with her symptomatology and review the pertinent literature on complications of chiropractic manipulation.", "extra_info": {"index": 5, "original_id": "multiclinsum_test_2542_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "The authors report on a case of acute primary Cytomegalovirus infection complicated with acute appendicitis due to Cytomegalovirus in an apparently immunocompetent 24-year-old Caucasian man also suffering from primary sclerosing cholangitis and ulcerative colitis. Diagnosis was based on clinical manifestations, serology results, as well as microbiological and histological findings. Treatment consisted of surgery and anti-Cytomegalovirus therapy.", "extra_info": {"index": 1, "original_id": "multiclinsum_test_2576_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 27-year-old male with a relapsed acute lymphoblastic leukemia presented with five-day-old polyarthralgia. He also had febrile neutropenia, cellulitis without abscesses, and methicillin-resistant Staphylococcus aureus bacteremia for which he received therapy with oxacillin and cefepime. However, the febrile neutropenia persisted, and an invasive fungal infection was suspected. A new set of blood cultures was taken and antifungal treatment was initiated. Arthroconidia were identified in the blood cultures and a matrix-assisted laser desorption ionization-mass spectrometry confirmed the presence of Geotrichum spp. Antifungal treatment was adjusted to 14 days of deoxycholate amphotericin B and four weeks of voriconazole. After a prolonged stay, he was discharged.\n", "extra_info": {"index": 3, "original_id": "multiclinsum_test_3210_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidneys don\u2019t work properly, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through routine screening is key to managing kidney health and preventing complications.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration and tubular reabsorption. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance, and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and systemic inflammation, and early intervention through biomarker monitoring and pharmacological management is critical to preserving renal function and delaying disease progression.\"\n}", "ground_truth": "Our patient is a 77-year-old African American female who presented with a systolic blood pressure of 200\u00a0mmHg. Computed tomography showed an enhancing 9\u00a0\u00d7\u20096\u00a0cm mass anterior and medial to the left kidney. The patient underwent a left adrenalectomy with partial nephrectomy. Gross and histologic examinations revealed an adrenal cortical adenoma and renal-adrenal fusion.", "extra_info": {"index": 69, "original_id": "multiclinsum_test_1363_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidneys don\u2019t work properly, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through routine screening is key to managing kidney health and preventing complications.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration and tubular reabsorption. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance, and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and systemic inflammation, and early intervention through biomarker monitoring and pharmacological management is critical to preserving renal function and delaying disease progression.\"\n}", "ground_truth": "A 76-year-old male patient was admitted to our institution with intermittent abdominal pain and a local abdominal mass which occurred one month after laparoscopic radical resection of rectal cancer one year ago. A computed tomography scan showed an abdominal wall hernia at the 5 mm former drain-site in the left lower quadrant, and that the content consisted of the large omentum. An elective herniorrhaphy was performed by closing the fascial defect and reinforcing the abdominal wall with a synthetic mesh simultaneously. The postoperative period was uneventful. The patient was discharged seven days after the operation without surgery-related complications at the 1-mo follow-up visit.", "extra_info": {"index": 71, "original_id": "multiclinsum_test_1042_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidneys don\u2019t work properly, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through routine screening is key to managing kidney health and preventing complications.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration and tubular reabsorption. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance, and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and systemic inflammation, and early intervention through biomarker monitoring and pharmacological management is critical to preserving renal function and delaying disease progression.\"\n}", "ground_truth": "In this interesting case, we discover lingering dyspnea in our 79 year old male with a past medical history of asthma and heart failure with preserved ejection fraction admitted for acute heart failure exacerbation with reduced ejection fraction along with a new incidental finding of Chilaiditi's sign on chest radiograph. Patient received optimal diuretics and guideline-directed medical treatment for heart failure exacerbation, but mild dyspnea with pleuritic chest pain persisted. Dyspnea with pleurisy was likely attributed to a structural anatomical defect (Chilaiditi's sign) that can be picked up on imaging.", "extra_info": {"index": 67, "original_id": "multiclinsum_test_1780_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 38-year-old Sri Lankan female presented with sudden onset severe headache, fixed dilated pupil, complete ptosis and ophthalmoplegia on the right side. On imaging, dissection and dilatation was evident in the right internal carotid artery from the origin up to the cavernous segment. She also had stenosis and aneurysmal dilatation of right subclavian artery. Takayasu arteritis was diagnosed subsequently. She was started on aspirin and high dose steroids.", "extra_info": {"index": 73, "original_id": "multiclinsum_test_2426_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "We present a case in which POCUS was used to rapidly confirm diagnosis in an unstable, severely septic patient presenting to the emergency department with Fournier's gangrene.", "extra_info": {"index": 75, "original_id": "multiclinsum_test_2914_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "On per speculum examination, cervix was replaced by an irregular friable growth, which was bleeding on touch. A clinical diagnosis of carcinoma cervix was made but the cervical biopsy revealed granulomatous inflammation with presence of acid-fast bacilli on cervical smear consistent with tuberculosis. The patient responded to six months of anti-tubercular therapy.", "extra_info": {"index": 77, "original_id": "multiclinsum_test_216_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "The patient discussed in our review is an 80-year-old female, with a history of diabetic retinopathy and macular degeneration who presented with a sudden deterioration of vision. While this was initially attributed to diabetic retinopathy, she was eventually noted to have a salmon patch lesion in her conjunctiva, diagnosed on biopsy to be a diffuse large B-cell lymphoma.", "extra_info": {"index": 81, "original_id": "multiclinsum_test_1888_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 53-year-old female with a history of two prior spinal operations at the L4-S1 levels (11 and 2 years previously) presented over a few weeks with the acute onset of a cauda equina syndrome (e.g., paraparesis and acute urinary incontinence). The patient demonstrated a mildly elevated white blood cell count (12,600/mm3) and abnormally increased C-reactive protein level that correlated with the magnetic resonance imaging that showed a dorsal epidural abscess extending from the L4 to S1 levels. At surgery, an encapsulated posterior epidural abscess was drained. Surgical findings included a granulomatous lesion consistent with a retained surgical cottonoid and was removed from the antero-inferior portion of the abscess wall at S1. Culture of the thick fibrotic abscess wall grew Klebsiella oxytoca. After 2 months of ciprofloxacin, the patient's infection cleared but the motor deficit only partially resolved.", "extra_info": {"index": 83, "original_id": "multiclinsum_test_2689_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 27-year-old man presented with headache and diplopia at our department. Fundoscopy showed left optic nerve atrophy and right papilledema consistent with Foster-Kennedy syndrome. Neurological exams were otherwise normal. A left frontal irregular space-occupying lesion was seen on magnetic resonance imaging (MRI), and enhancement was shown on contrast-enhanced computed tomography (CT) scan. CT angiography (CTA) revealed vascular compression around the lesion. Prior to surgery, meningioma was diagnosed and gross tumor removal was performed. On postoperative pathohistological exam, the tumor proved to be a meningeal melanocytoma, WHO grade I. No skin melanoma was found. After surgery, the patient received radiation therapy. No tumor was seen on follow-up MR images six months after surgery. The patient was well after two and a half years, and there was no tumor recurrence on the follow-up CT.", "extra_info": {"index": 85, "original_id": "multiclinsum_test_568_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A formerly healthy 40 year-old male became symptomatic 10 days after spending time in the jungle of North Borneo. Four days later, he presented to hospital in a state of collapse and died within two hours. He was hyponatraemic and had elevated blood urea, potassium, lactate dehydrogenase and amino transferase values; he was also thrombocytopenic and eosinophilic. Dengue haemorrhagic shock was suspected and a post-mortem examination performed. Investigations for dengue virus were negative. Blood for malaria parasites indicated hyperparasitaemia and single species P. knowlesi infection was confirmed by nested-PCR. Macroscopic pathology of the brain and endocardium showed multiple petechial haemorrhages, the liver and spleen were enlarged and lungs had features consistent with ARDS. Microscopic pathology showed sequestration of pigmented parasitized red blood cells in the vessels of the cerebrum, cerebellum, heart and kidney without evidence of chronic inflammatory reaction in the brain or any other organ examined. Brain sections were negative for intracellular adhesion molecule-1. The spleen and liver had abundant pigment containing macrophages and parasitized red blood cells. The kidney had evidence of acute tubular necrosis and endothelial cells in heart sections were prominent.", "extra_info": {"index": 79, "original_id": "multiclinsum_test_2113_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "We report an unusual case in which both anomalous origin of the right coronary artery and myocardial bridge on left anterior descending artery were detected concurrently.", "extra_info": {"index": 87, "original_id": "multiclinsum_test_1721_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "7-year-old male with a diagnosis of acute lymphoid T-cell leukemia, completing a cycle of induction chemotherapy with the PETHEMA 2013 protocol. He presented a 12-day picture characterized by epigastric abdominal pain and vomiting, initially suspected acute pancreatitis, ruled out by normal pancreatic enzymes and abdominal computed tomography. Due to suspected acid-peptic disease associated with steroids, he began treatment with proton pump inhibitors and procinetics. Considering a picture of dyspepsia with alarm signs, such as progression of neutropenia, increased C-reactive protein and clinical deterioration, an esophagogastroduodenoscopy (EGD) compatible with necrotizing gastritis was performed, confirmed by histopathology. He received pharmacological management, zero regimen and parenteral support, and progressive improvement was evidenced in imaging controls. After fasting for 30 days, well tolerated enteral nutrition was initiated, with outpatient follow-up. After improvement, the chemotherapy plan was completed, highlighting complete remission, without complications after 2 years.\n", "extra_info": {"index": 68, "original_id": "multiclinsum_test_3042_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "We present the case of a 52-year-old woman with cardiogenic shock and refractory right ventricular failure due to spontaneous dissection of the right coronary artery. She remained dependent on mechanical support for several weeks. Both a right ventricular assist device implant and a bidirectional cavopulmonary anastomosis were explored as long-term support options. A history of malignancy and possible right ventricular functional recovery resulted in a decision in favour of the bidirectional cavopulmonary anastomosis and concomitant tricuspid valve annuloplasty. Postoperatively her clinical condition improved significantly, and she could be discharged home. Echocardiography showed normalization of right ventricular dimensions and slight improvement of right ventricular function.", "extra_info": {"index": 70, "original_id": "multiclinsum_test_3152_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "A 34-year-old female presented with a 1 year history of intermittent pain in the right side of the waist without obvious inducement. All laboratory blood tests were within normal limits. Indocyanine green 15 min retention was rated 2.9%, and Child-Pugh was rated A. Computed tomography and magnetic resonance imaging diagnosed giant hemangioma of the caudate lobe with hemangioma of left lobe of liver. After discussion, surgical treatment was performed, which lasted 410 min, with intraoperative bleeding of about 600 mL and postoperative pathological findings of cavernous hemangioma. There were no obvious postoperative complications, and the patient was discharged 10 d after surgery.", "extra_info": {"index": 72, "original_id": "multiclinsum_test_2984_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "A 65-year-old woman was referred to our hospital for assessment of a gallbladder tumor. Contrast-enhanced computed tomography showed a papillary tumor in the fundus of the gallbladder with irregular thickening of the gallbladder wall that spread into the cystic duct. The boundary between the tumor and liver was unclear. The patient was diagnosed with gallbladder cancer with liver invasion. We performed extended cholecystectomy with liver bed resection after confirming the absence of cancer cells in the resection margin of the cystic duct. After pathological examination, the tumor was diagnosed as an ICPN with xanthogranulomatous cholecystitis. The patient was discharged on postoperative day 8 with no complications.", "extra_info": {"index": 74, "original_id": "multiclinsum_test_1559_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "In this case report, we present a case of a pleomorphic adenoma arising from the 'tail' of the parotid gland, which on imaging, appears to be extra parotid in location. We also review the anatomy of the parotid 'tail' and relevant literature.", "extra_info": {"index": 76, "original_id": "multiclinsum_test_2421_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "A 43-year-old Asian man with a 3-year history of penile cancer presented with metastasis in the right intraocular sites. Magnetic resonance imaging showed hyperintensity in the T1-weighted images and hypointensity in the T2-weighted images of the right eye. After enucleation of his right eye, histopathological analysis led to a diagnosis of metastatic, moderately differentiated penile squamous cell carcinoma.", "extra_info": {"index": 82, "original_id": "multiclinsum_test_1233_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "A 49-year-old Japanese man visited our department in November 2017 with chief complaints of indolent right scrotum enlargement and a right inguinal mass. History showed that the patient visited our department of gastroenterology with chief complaints of blackish feces and ill complexion in February 1997. Computed tomography (CT) showed a right retroperitoneal tumor, which was removed in the same month. Histopathological examination showed a teratoma and yolk sac tumor. He was diagnosed with primary retroperitoneal EGCT and received three courses of chemotherapy (bleomycin/etoposide/cisplatin; BEP). Periodic imaging and the determination of tumor markers (alpha-fetoprotein", "extra_info": {"index": 84, "original_id": "multiclinsum_test_439_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "A previously healthy 24-yo male (A) presented at the Emergency Department(ED) with recent onset of chest pain and a 3-day history of abdominal pain, fever and diarrhoea. The symptoms began within a few hours of returning from a tourist visit to a central European capital. Vital signs were stable, the Electrocardiogram(ECG) showed generalized ST-elevation, laboratory testing showed increased levels of C-reactive protein(CRP) and high-sensitive Troponin T(hsTnT). Transthoracic echocardiogram (TTE) was normal, stool cultures were positive for C Jejuni and blood cultures were negative. Two days after patient A was admitted to the ED his travel companion (B), also a previously healthy male (23-yo), presented at the same ED with almost identical symptoms: chest pain precipitated by a few days of abdominal pain, fever and diarrhoea. Patient B declared that he and patient A had ingested chicken prior to returning from their tourist trip. Laboratory tests showed elevated CRP and hsTnT but the ECG and TTE were normal. In both cases, the diagnosis of C jejuni-associated perimyocarditis was set based on the typical presentation and positive stool cultures with identical strains. Both patients were given antibiotics, rapidly improved and were fully recovered at 6-week follow up.", "extra_info": {"index": 78, "original_id": "multiclinsum_test_1211_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "A 71-year-old man with severe COPD, Global Initiative for Obstructive Lung Diseases stage 3 underwent an 8-wk remotely monitored inspiratory muscle training with a device based on the test of incremental respiratory endurance method. Spirometry, body plethysmography, test of incremental respiratory endurance examination, 6-min walking test, body mass index, airflow obstruction, dyspnea, exercise capacity index, and subjective perception of dyspnea were performed as part of the initial and final examination. The patient performed training at home, and the physiotherapist monitored the patient remotely through a web application that allowed the physiotherapist to evaluate all training parameters in real-time and respond to any problems. After 8 wk of home training, there was a significant increase in all monitored values: maximal inspiratory pressure, a novel parameter sustained maximal inspiratory pressure, forced expiratory volume in 1 s, total lung capacity, forced vital capacity, peak expiratory flow, and inspiratory capacity. There was also an improvement in the perception of dyspnea according to the COPD Assessment Test and a modified Medical Research Council Breathlessness Scale, an increase in exercise tolerance according to the 6-min walking test, and a decrease in the exercise capacity index as a predictor of prognosis.", "extra_info": {"index": 66, "original_id": "multiclinsum_test_1605_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "A 42-year-old female with a distant history of SCI developed clinical and imaging findings consistent with acute expansion of PTS immediately following parathyroidectomy. Her symptoms included acute numbness, tingling, and pain in both arms. Magnetic resonance imaging (MRI) revealed a syrinx in the cervical and thoracic spinal cord. However, this was initially misdiagnosed as transverse myelitis and was treated as such without resolution of symptoms. Over the following 6 months, the patient experienced progressive weakness. Repeat MRI demonstrated expansion of the syrinx with new involvement of the brain stem. The patient was diagnosed with PTS and referred for outpatient neurosurgery evaluation at a tertiary facility. Treatment was delayed due to problems with housing and scheduling at the outside facility, allowing for continued worsening of her symptoms. The syrinx was surgically drained and a syringo-subarachnoid shunt was placed. Follow-up MRI confirmed correct placement of the shunt as well as resolved syrinx and decreased thecal sac compression. The procedure effectively halted symptom progression but did not resolve all symptoms completely. The patient has regained her ability to perform much of her activities of daily living but remains in a nursing home facility.", "extra_info": {"index": 86, "original_id": "multiclinsum_test_2005_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "A 66-year-old man affected by DME, with glycated hemoglobin (HbA1c) at 6.9%, refractory to laser grid treatment and intravitreal injections of triamcinolone, was selected to receive a cycle of three subtenon injections/week of IFN\u03b1 (1\u00d7106 IU/ml). BCVA and CMT, using spectral domain ocular coherence tomography (SD-OCT), were evaluated preoperatively and at 1\u00a0week, 1\u00a0month, 4\u00a0months, and 1\u00a0year postoperatively. BCVA and CMT were significantly improved at 1\u00a0week after the three injections (20/200 vs. 20/40 and 498\u00a0\u03bcm vs. 237\u00a0\u03bcm, respectively). BCVA remained stable during the 1-year follow-up. CMT was slightly increased, but was still lower than the baseline value (215\u00a0\u03bcm, 255\u00a0\u03bcm, and 299\u00a0\u03bcm during the follow-up visits). No adverse events were recorded, with the exception of mild subconjunctival hemorrhage at the injection site.", "extra_info": {"index": 80, "original_id": "multiclinsum_test_1558_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "A 49-year-old Asian woman presented with disseminated intravascular coagulation due to ruptured primary high-grade ovarian endometrial stromal sarcoma with multiple intraperitoneal metastases. After the initial surgery, the patient underwent adjuvant chemotherapy with three courses of Adriamycin (75\u00a0mg/m2). We performed the secondary debulking operation including total hysterectomy, metastasectomy, omentectomy, peritonectomy, appendectomy, and hyperthermic intraperitoneal chemotherapy (paclitaxel 175\u00a0mg/m2). Currently she has been alive for 28\u00a0months under a new chemotherapy regimen.", "extra_info": {"index": 49, "original_id": "multiclinsum_test_2683_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "We present a case of a 79-year-old female patient who underwent LAAO device deployment within a surgically occluded LAA with PDL. She underwent 27\u2005mm LAAO device (WATCHMANTM) deployment and all the P.A.S.S. (Position, Anchor, Size, and Seal) criteria were satisfied. Only 1.4\u2005mm PDL was present. She was continued on apixaban and aspirin post-operatively. Post-operative transoesophageal echocardiogram at 6 weeks demonstrated trivial PDL measuring 1.49\u2005mm. Patient was continued on aspirin and clopidogrel, with discontinuation of apixaban.", "extra_info": {"index": 47, "original_id": "multiclinsum_test_1868_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "A 38-year-old woman presented with shortness of breath and syncope. Upon investigation, she was found to have a right atrioventricular myxoma. It was associated with tricuspid regurgitation, right-sided heart failure, and pulmonary hypertension.\n\nThe syncopal attacks and shortness of breath resolved completely after tumor resection. Tricuspid regurgitation (grade 1) and mild pulmonary hypertension (right ventricular systolic pressure 35 mmHg) remained as sequelae of delayed presentation. These may be due to recurrent embolization of tumor fragments to segments of the pulmonary artery.", "extra_info": {"index": 51, "original_id": "multiclinsum_test_3149_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "This report describes, for the first time to the best of our knowledge, a primary paraganglioma of the seminal vesicle occurring in a 61-year-old male. The patient presented persistent arterial hypertension and a previous diagnosis of chromophobe renal cell carcinoma. It was hypothesized that the seminal vesicle tumor could be a metastasis from the chromophobe renal cell carcinoma. Immunohistochemical characterization revealed expression of synaptophysin and chromogranin in tumor cell nests and peripheral S100 protein expression in sustentacular cells. Succinate dehydrogenase A and B-related (SDHA and SDHB) expression was present in both tumors.", "extra_info": {"index": 45, "original_id": "multiclinsum_test_2717_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "A 62-year-old man diagnosed as IgD-\u03bb/\u03bb myeloma (ISS stage III) was admitted with fatigue and weight loss. The physical examination suggested an anemic face, a few moist rales at the left lung base, and mild concave edema in both lower extremities. Laboratory examinations showed the elevated creatinine levels, \u03b22-microglobulin, lactic dehydrogenase, and erythrocyte sedimentation rate, while the decreased neutrophils, granulocytes, and hemoglobin. In the serum protein electrophoresis, there appeared two inconspicuous M-spikes. Serum IFE indicated an over-representation of lambda light chain and yielded two monoclonal bands in \u03bb region, but only one corresponding heavy chain band in the antisera to IgD region. The BM histology and BM cytology both supported the diagnosis of IgD-\u03bb/\u03bb myeloma.", "extra_info": {"index": 55, "original_id": "multiclinsum_test_710_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "A 27-year-old man presented to our hospital because of painless and progressive visual impairment of both eyes over two years. He was previously diagnosed with hypocalcemia but did not take calcium supplements regularly. He had no history of anterior neck thyroid surgery. After admission, the biochemical analysis indicated a serum calcium level of 1.21 mmol/L and an intact parathyroid hormone level of 0 pg/mL. Ocular examination revealed bilateral symmetrical opacity of the lens presenting as punctate opacity in the posterior subcapsular cortex together with radial opacity in the peripheral cortex (N1C2P3). Phacoemulsification with an intraocular lens was performed in both eyes sequentially. Postoperatively, the patient had a satisfactory recovery and greatly improved visual acuity.", "extra_info": {"index": 59, "original_id": "multiclinsum_test_1416_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "We present a 12-year-old girl who presented with bilateral shoulder deformities and difficulty in coordination while writing. On examination, she was noted to have bilateral Sprengel deformities with flexion contractures of upper-limb joints and mirror movements of both upper and lower-limb joints.", "extra_info": {"index": 53, "original_id": "multiclinsum_test_990_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "We describe a case of a 49-year-old man with a history of acromegaly who presented to our hospital with a diagnosis of decompensated systolic heart failure. Serial electrocardiograms showed wide (160\u2013200\u2009ms) QRS duration with left bundle branch block. Echocardiography showed severe left ventricular dysfunction that simultaneously achieved a left ventricular ejection fraction of 16%. Surgical indication was rarely assessed by neurosurgeons. Given that the stereotactic radiosurgery together with pharmacotherapy produced infinitesimal effects, cardiac resynchronization therapy was performed. Owing to biventricular synchronization and holding back reverse remodeling, the patient\u2019s symptoms were successfully alleviated, and he was discharged from the hospital.", "extra_info": {"index": 57, "original_id": "multiclinsum_test_3217_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "We reported a four-week spondyloptosis of the ninth thoracic vertebra over the tenth thoracic vertebra, in a 20-year-old male without any neurological deficit. The patient had associated chest injuries. The spine injury was managed surgically with in-situ posterior instrumentation and fusion. The patient tolerated the operation well and postoperatively there was no neurological deterioration or surgical complication.", "extra_info": {"index": 61, "original_id": "multiclinsum_test_1749_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "We present the case of a 25 y.o. patient with COVID-19 respiratory failure requiring ECMO support for 16-days in which a 32 Fr crescent cannula became adherent to the SVC and proximal jugular vein. Attempts to remove the cannula at the bedside failed due to immobility of the cannula. Ultrasound of the right neck was unremarkable, so he was taken to the hybrid OR where both TEE and fluoroscopy were unrevealing. An upper sternotomy was performed, and the superior vena cava and proximal jugular vein were dissected revealing a 2\u00a0cm segment of the distal SVC and proximal jugular vein that was densely sclerosed and adherent to the cannula. The vessel was opened across the adherent area at the level of the innominate vein and the cannula was then able to be withdrawn. The patient suffered no ill effects and had an unremarkable recovery to discharge.", "extra_info": {"index": 29, "original_id": "multiclinsum_test_2039_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "A 4-year-old boy was admitted for persistent pain in the left lower limb and abnormal gait over the previous 9 mo. He had no history of present or past illness. Preoperative imaging data showed erosion-like changes with bone expansion of the left middle and lower fibular segment. Tumor tissue in the fibular bone marrow cavity was removed by curettage, and rapid intraoperative pathological examination suggested fibular fibrous dysplasia. An allograft was implanted into the fibular medullary cavity. However, he was readmitted with clinical symptoms including persistent pain, abnormal gait, and local swelling at the age of 6 years. He was diagnosed with recurrent fibular fibrous dysplasia based on the second medical examination. He underwent fibular bone tumor radical resection and longus fibular allograft transplantation combined with fibular bone locking plate and screws. Good host bone to allogenic bone graft fusion was observed by the physician on postoperative regular follow-up.", "extra_info": {"index": 65, "original_id": "multiclinsum_test_1596_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "We report a case of central venous catheter infection with Bacillus pumilus in an immunocompetent child with tufting enteropathy on long-term parenteral nutrition (PN). There were three episodes of central venous catheter infection with Bacillus pumilus in three months. Despite adequate and appropriate use of intravenous antibiotics, the infection failed to clear resulting in the need for removal of the catheter for complete cure.", "extra_info": {"index": 44, "original_id": "multiclinsum_test_1072_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "A 17-year-old male patient presented with pain in the lower left molar region. Clinical examination revealed the absence of Teeth 37 and 38. Tomographic imaging showed Tooth 37 in a transverse position with the crown oriented lingually and Tooth 38 in a vertical position. Extraction of Tooth 37 was performed using a vestibular approach and odontectomy due to space constraints.", "extra_info": {"index": 46, "original_id": "multiclinsum_test_3344_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "We present a case of stage IV pleomorphic carcinoma; the patient was a 66-year-old male. He was referred to our hospital because of a right adrenal hemorrhage and a lung tumor. A systemic examination revealed that the lung tumor was a primary lung cancer and that the adrenal hemorrhage was due to a metastatic cancer. We performed an adrenalectomy and resection of the lung tumor and obtained a diagnosis of pleomorphic carcinoma with adrenal metastasis. The patient has remained recurrence-free for 6\u2009years since the surgery.", "extra_info": {"index": 54, "original_id": "multiclinsum_test_2067_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "We reported a 24-year-old male who came to the emergency department complaining of a history of a sore throat, fever, malaise, fever, and neck swelling with a normal consciousness level. A laboratory examination showed leukocytosis and high C-reactive protein serum. Radiological diagnosis reveals an anterior neck abscess with left jugular vein thrombosis and left epidural abscess. The blood culture was positive for Fusobacterium necrophorum. The patient underwent surgical drainage and, at the same time, was treated with antibiotics and anticoagulant drugs. After 45 days, the patient improved clinically and was discharged. There were no other symptoms after a one-month follow-up clinically and neck ultrasonography.", "extra_info": {"index": 63, "original_id": "multiclinsum_test_1379_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 33-year-old woman was referred to our department with unstable angina. At the age of 6, she had undergone coronary artery bypass grafting of the second diagonal branch using the left internal thoracic artery and the obtuse marginal branch using saphenous vein grafting for left main coronary atresia. Although a coronary angiogram showed a patent left internal thoracic artery graft to the second diagonal branch and a patent saphenous vein graft to the obtuse marginal branch, the left anterior descending artery was not being perfused by the grafts because of a disruption of blood flow to the left anterior descending artery from the left internal thoracic artery. Therefore, we performed a redo coronary artery bypass grafting using the in situ right internal thoracic artery to the first diagonal branch, which was to be connected to the left anterior descending artery, resulting in amelioration of the ischemia of the left anterior wall. The patient was discharged 10\u00a0days after the operation and has been in good health for over 3\u00a0years without recurrence of chest symptoms.", "extra_info": {"index": 31, "original_id": "multiclinsum_test_2205_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "We describe a 34-year-old patient with a cutaneous immunodeficiency characterized by recurrent crusted scabies infestation, diffuse tinea, and recurrent staphylococcal cellulitis, who we suspected had an undiagnosed syndrome. The patient also suffered from mental retardation, renal failure, and premature senescence. A cytogenetic fluorescence in situ hybridization analysis revealed a 9.34 Mb duplication within the short (p) arm of chromosome 1, precisely from 1p36.11 to 1p36.21, with an adjacent 193 kb copy gain entirely within 1p36.11. In addition, chromosome 4 had a 906 kb gain in 4p16.1 and chromosome 9 had a 81 kb copy gain in 9p24.3. Over 100 genes localized within these duplicated regions. Gene expression array revealed 82 genes whose expression changed >1.5-fold compared to a healthy age-matched skin control, but among them only the lipolytic enzyme arylacetamide deacetylase-like 3 was found within the duplicated 1p36 region of chromosome 1.", "extra_info": {"index": 33, "original_id": "multiclinsum_test_1677_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "A 32-year-old woman complained of a mass inside the rectovaginal space for 9 years, which became enlarged within 1 year. A rectal SEL detected by endoscopy was suspected to be a gastrointestinal stromal tumor or exophytic uterine fibroid. Pathological diagnosis was difficult because of unsuccessful transabdominal core needle biopsy with insufficient tissues, as well as vaginal hemorrhage. A second biopsy was suggested after multiple disciplinary treatment discussion, which referred to a transperineal core needle biopsy (CNB) guided by ERUS combined with CEUS. Adequate samples were procured and rectal gastrointestinal stromal tumor was proved to be the pathological diagnosis. Imatinib was recommended for first-line therapy by multiple disciplinary treatment discussion. After the tumor shrunk, resection of the rectal gastrointestinal stromal tumor was performed through the posterior vaginal wall. Adjuvant therapy was applied and no recurrence or metastasis has been found by the last follow-up on December 13, 2019.", "extra_info": {"index": 48, "original_id": "multiclinsum_test_2808_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "A 69-year-old man was injured in a motor vehicle accident and suffered from left hemothorax and multiple rib fractures near the heart. A comprehensive assessment raised suspicions of lacerated pericardium and myocardial injury. Consequently, a thoracoscopy was performed 9\u2009h after injury. A penetrating cardiac injury was detected and surgically treated via video-assisted thoracoscopic surgery. The patient recovered uneventfully and was discharged on postoperative day 16.", "extra_info": {"index": 50, "original_id": "multiclinsum_test_2967_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 20-year-old man presented with periumbilical pain. Physical exam showed a warm, erythematous infra-umbilical mass that was tender to palpation. CT revealed an infected urachal cyst. The patient underwent urachal abscess incision and drainage with cyst excision. The patient returned home on postoperative day two. Two-week outpatient follow-up confirmed an uncomplicated recovery.", "extra_info": {"index": 39, "original_id": "multiclinsum_test_1897_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 38-year-old woman in her 19th wk of pregnancy (G2P1) was referred to our clinic for a sudden, persistent pain on the left side of the waist. She had not undergone any previous related abdominal examination. Ultrasound of the urinary system revealed a giant nonhomogenous lump in the left kidney area. The diagnosis was considered spontaneous rupture and hemorrhage of the left RAML in pregnancy via ultrasound. Her left-side waist pain continued to be intense. Subsequently, she underwent computed tomography, which led to the same diagnosis. Based on many factors, the patient underwent left nephrectomy after the induction of labor. The pathological result was the rupture and hemorrhage of a vascular leiomyoma lipoma.", "extra_info": {"index": 37, "original_id": "multiclinsum_test_1298_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "A 66-year-old Maori man presented to our hospital with left testicular swelling. His alpha-fetoprotein and beta-human chorionic gonadotrophin levels were within normal limits. His lactate dehydrogenase concentration was elevated to 267 U/L. Ultrasound imaging confirmed a large testicular mass, and he underwent left orchiectomy. His histological examination revealed a neuroendocrine tumor with an immunostaining pattern suggesting Merkel cell carcinoma. He presented to our hospital again 3 months later with right testicular swelling that was confirmed on ultrasound sonography to be a tumor. He underwent a right orchiectomy, and his histological examination revealed metastatic Merkel cell carcinoma. A primary lesion was not identified, and computed tomographic imaging did not reveal spread to other organs. He received six cycles of adjuvant carboplatin and etoposide chemotherapy and remained disease-free 18 months after completion of chemotherapy.", "extra_info": {"index": 52, "original_id": "multiclinsum_test_2759_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "Two cases of cerebral sinus venous thrombosis in COVID-19 patients were reported, following respiratory, hematology, and coagulation disarrangements, which was triggered by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. The first patient, which was presented with a seizure, had hypertension and diabetes mellitus as comorbidities. The latter case had no comorbidity but showed more severe presentations of COVID-19 such as brain and lung thrombosis, although already had several days of intravenous anticoagulant administrations. These two cases also have a different course of disease and outcomes, which were interesting topics to study.", "extra_info": {"index": 27, "original_id": "multiclinsum_test_445_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "We report a 44-year-old man with end-stage renal disease post failed kidney transplant on low-dose mycophenolate mofetil who presented with acute onset of abdominal pain. He was successfully given the diagnosis of perforated jejunal diverticulum. The patient successfully underwent a segmental jejunal resection and anastomosis. He unfortunately developed a recurrent jejunal perforation a month later and again had the second segmental jejunal resection operation. Mycophenolate mofetil then was discontinued.", "extra_info": {"index": 22, "original_id": "multiclinsum_test_295_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "A 75-year-old man presented with fever and right chest pain. He was suspected of a giant primary diaphragmatic tumor of extrahepatic origin by imaging studies. The preoperative differential diagnosis included benign masses such as myxoid sarcoma and schwannoma, and we planned a diaphragmatic resection. Intraoperatively, however, dissection of the tumor from the liver was not possible, requiring an extended right posterior segmentectomy with combined resection of the diaphragm. The patient had a good postoperative course and 1\u00a0year has passed since the surgery with no recurrence. The pathology showed that the mass was located just below the hepatic capsule/parenchymal region and was adherent to the diaphragm, but there was no continuity. The morphology suggested a low-grade mesenchymal tumor such as a solitary fibrous tumor and perivascular epithelioid cell tumor, but immunostaining was negative, making the diagnosis difficult. Although some areas of high proliferative activity were observed, finally, the diagnosis of primary spindle cell tumor of the liver with smooth muscle differentiation was made based on the positive results of muscle markers such as \u03b1SMA, desmin, and h-caldesmon.", "extra_info": {"index": 25, "original_id": "multiclinsum_test_447_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 90-year-old female with atrial fibrillation on therapeutic apixaban and status-post TAVR presented with COVID-19 infection and was found to have severe bioprosthetic valvular regurgitation with features suggestive of valve thrombosis. She underwent valve-in-valve TAVR with resolution of valvular dysfunction.", "extra_info": {"index": 35, "original_id": "multiclinsum_test_303_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "A 58-year-old man was presented to our institute with complaints of posterior cervical pain persisting for 3\u00a0months, along with numbness and muscle weakness of extremities. A fat suppression T2-weighted image of MRI illustrated fluid collection in the retrospinal region at C1-C2 level, and an 111In-DTPA cisternoscintigram clearly revealed the presence of CSF leakage into the same region. The MRI also showed stenosis in spinal canal at C3/4 level, and a computed tomography (CT) myelogram suggested a blockage at the same level. We gave a diagnosis as intracranial hypotension due to the CSF leakage, which might be caused by the spinal canal stenosis at C3/4 level. Despite 72\u2009h of conservative therapy, a brain CT showed the development of bilateral subdural hematomas. We, therefore, performed burr-hole drainage of the subdural hematoma, blood-patch therapy at C1/2 level, and laminoplasty at C3-4 at the same time. Improvement of symptoms and imaging features which suggested the CSF leak and subdural hematoma were obtained post-operatively.", "extra_info": {"index": 56, "original_id": "multiclinsum_test_1266_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "Male school-age child, 8 years old, no relevant history, presented with a 1-year history of conjugate horizontal rapid eye movement jerking and associated mild miosis, 5-10 seconds in duration, occurring 5-6 times daily, with some episodes with a questionable disconnection from the environment or impairment of consciousness, without other accompanying signs or symptoms. General examinations were normal. He was evaluated by ophthalmologists and otolaryngologists who ruled out pathology in those fields. The neurological examination between episodes was normal. The video-electroencephalogram demonstrated an electro-clinical correlate, with epileptiform activity in the left temporal and occipital region that later generalized during episodes. The brain MRI was normal. After initiation of treatment with carbamazepine, he had a good evolution, with no recurrence of episodes at 2 years of follow-up.\n", "extra_info": {"index": 62, "original_id": "multiclinsum_test_3001_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "We describe the case of a 55-year-old female patient with primary open-angle glaucoma (POAG) who underwent bilateral XEN gel surgery. Her left eye developed a 2 mm postoperative hyphema, which resolved spontaneously within 8 days. Intraocular pressure (IOP) normalized at 12 mm Hg and increased to 50 mm Hg after 1 month in an otherwise normal-looking eye. Intraoperative examination revealed a nonfunctioning XEN gel stent, which was replaced and sent for laboratory analysis. Macroscopic examination of the tube confirmed obstruction with cellular debris. Tube replacement restored good filtration.", "extra_info": {"index": 64, "original_id": "multiclinsum_test_7_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "We report a case of complex revascularization in a diabetic patient with aggressive right foot lesions evolution after COVID-19 infection. The patient presenting a Peripheral arterial ischemic involving the infrarenal aorta, iliac, femoral. The simultaneous intervention consisted of an endovascular aortic stent-graft placement and angioplasty of femoral artery.", "extra_info": {"index": 58, "original_id": "multiclinsum_test_437_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "A four-year-old girl presented with fever and a painful limp in the left hip. Pain characteristics and anemia detected in the blood analyses were the first warning signs that the hip process was not standard. Although the primary suspicion was of septic arthritis, a CT scan of the abdomen revealed an adrenal neuroblastoma.", "extra_info": {"index": 60, "original_id": "multiclinsum_test_1260_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "A 44-year-old man was admitted due to weakness of his right limbs and unclear speech for 10\u00a0h. He had recurrent fevers for 1 month before admission. Transthoracic echocardiography showed a mix-echoic vegetation attached to the bicuspid aortic valve, moderate aortic regurgitation and a possible aortic annular abscess. Blood cultures were negative and empiric antibiotic therapy was begun. The patient did not have fever again and seem to be clinically improved. However, follow-up transesophageal echocardiography revealed a large periaortic abscess led to aortic sinus pseudoaneurysm. The patient underwent mechanical prosthetic valve replacement and annulus reconstruction successfully. Perivalvular abscess may be insidious deterioration in patients who seem to be clinically improved, which requires us to pay more attention.", "extra_info": {"index": 41, "original_id": "multiclinsum_test_885_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "In August 2012, a woman and her son were attacked by a stray dog in Henan, China. The son received rabies postexposure prophylaxis (wound treatment followed by vaccine, no immunoglobulin), however, the mother did not. Rabies infection was subsequently laboratory confirmed in the mother and she died in December; her son is alive and healthy after 2\u00a0years of follow-up.", "extra_info": {"index": 43, "original_id": "multiclinsum_test_1507_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring are often recommended to support kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Declining glomerular filtration rate (GFR) is a key biomarker for chronic kidney disease progression, and early intervention through pharmacological management, dietary modification, and monitoring of biomarkers such as serum creatinine and proteinuria is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 65-year-old woman with persistent atrial fibrillation was referred for LAAc. Transesophageal echocardiography (TEE) revealed spontaneous contrast in the LAA without formation of a thrombus; the LAA shape was tortuous and difficult to assess. A first LAAc procedure was unsuccessful given the unsuitable sheath position. Therefore, a soft three-dimensional (3D) model printing was performed by laser sintering and revealed excessive sheath kinking with an inferior approach, but successful deployment would be feasible using a superior approach. Successful trans-jugular implantation of a Watchman FLX 31 device in stable position without residual leakage was achieved during the subsequent procedure. At 3-month follow-up, and after cessation of oral anticoagulation, the patient's symptoms improved. Imaging demonstrated complete LAA occlusion and correct placement of the device along the LAA superior axis.", "extra_info": {"index": 145, "original_id": "multiclinsum_test_2065_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "A 48-year-old female underwent video-assisted thoracoscopic surgery (VATS) combined with left lower lobectomy. The distal end of the left branch of the tracheal tube was lodged by surgical sutures. In this case, the respiratory physician burned the sutures using an argon electrode, after discussion with the thoracic surgery experts.", "extra_info": {"index": 24, "original_id": "multiclinsum_test_1206_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring are often recommended to support kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Declining glomerular filtration rate (GFR) is a key biomarker for chronic kidney disease progression, and early intervention through pharmacological management, dietary modification, and monitoring of biomarkers such as serum creatinine and proteinuria is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "We report a case of thoracoscopic resection of the posterior segment of the right upper lobe of the lung. Preoperatively, the nodule was believed to be located in the superior segment of the right lower lobe. However, intraoperative exploration revealed that the nodule was located in the posterior segment of the right upper lobe, further showing that the bronchi of the posterior segment of the right lung opened into the bronchus intermedius. The procedure was completed uneventfully. Postoperative retrospective three-dimensional (3D) reconstruction of the lung CT images confirmed that the bronchi of the posterior segment of the right upper lobe originated from the bronchus intermedius.", "extra_info": {"index": 141, "original_id": "multiclinsum_test_2891_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "We report a case of 29 year old male with total rupture of ACL and PCL that underwent reconstruction for both ligaments. We found the failure of the PCL graft 2 years after the surgery was related to the tibial tunnel placement which was placed not in proper anatomical site. We performed revision PCL surgery with transseptal portal technique to ensure the tibial tunnel is placed in appropriate position.", "extra_info": {"index": 23, "original_id": "multiclinsum_test_2913_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "We describe the case of a 43-year-old Asian female who has mild vision impairment due to tractional retinal detachment secondary to diabetic retinopathy and how mental health screening and quality of life screening during low vision rehabilitation can improve in the management of this patient.", "extra_info": {"index": 26, "original_id": "multiclinsum_test_2493_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "In this case, we present a young, otherwise healthy patient that was diagnosed with a primary leiomyosarcoma of the small finger. After her diagnosis, she underwent extensive oncologic workup, and subsequently underwent successful ray amputation with an excellent outcome. She remains disease free.", "extra_info": {"index": 143, "original_id": "multiclinsum_test_2201_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring are often recommended to support kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Declining glomerular filtration rate (GFR) is a key biomarker for chronic kidney disease progression, and early intervention through pharmacological management, dietary modification, and monitoring of biomarkers such as serum creatinine and proteinuria is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "We present a documented case of a 4 years and 8-month-old Syrian Arabic girl with a distinctive course of signs and symptoms of rapid-onset obesity with hypoventilation, hypothalamic dysfunction, and autonomic dysregulation syndrome accompanied by mature ganglioneuroma in her chest, a homogenous mild enlargement of her pituitary gland, generalized cortical brain atrophy, and seizures. Three months after her first marked symptoms were noted she had a sudden progression of severe respiratory distress that ended with her death.", "extra_info": {"index": 139, "original_id": "multiclinsum_test_2845_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "A 52-year-old woman with primary Sj\u00f6gren's syndrome developed membranous glomerulonephritis and Epstein-Barr virus-positive diffuse large B-cell lymphoma (DLBCL). She was diagnosed with Sj\u00f6gren's syndrome based on the dry eyes, dry mouth, positive anti-nuclear antibody test, anti-Ro (SS-A) antibody, salivary gland biopsy, and salivary scintigraphy. Moreover, renal biopsy confirmed the diagnosis of membranous glomerulonephritis. Three months later, her small bowel was perforated with pneumoperitoneum, and the biopsy revealed Epstein-Barr virus-positive DLBCL.", "extra_info": {"index": 28, "original_id": "multiclinsum_test_2438_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring are often recommended to support kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Declining glomerular filtration rate (GFR) is a key biomarker for chronic kidney disease progression, and early intervention through pharmacological management, dietary modification, and monitoring of biomarkers such as serum creatinine and proteinuria is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "We report the imaging appearance of dermatofibrosarcoma protuberans on the breast of a 41-year-old Chinese man who initially presented with a palpable lump. A mammogram showed two lesions, one with well circumscribed and the other with an ill defined border, in his right breast. Conventional magnetic resonance imaging was performed and showed the well defined larger lesion with mild central hypointensity while the smaller lesion had an irregular border. Both lesions were well characterized on the fat-suppressed sequences.", "extra_info": {"index": 135, "original_id": "multiclinsum_test_1990_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring are often recommended to support kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Declining glomerular filtration rate (GFR) is a key biomarker for chronic kidney disease progression, and early intervention through pharmacological management, dietary modification, and monitoring of biomarkers such as serum creatinine and proteinuria is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "The palmar branch of the median nerve was surrounded by a significant haematoma in addition to the strangulation damage caused by its more superficial location in contrast to the median nerve.", "extra_info": {"index": 137, "original_id": "multiclinsum_test_2648_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "We describe the case of a 65-year-old man, who was referred from another institution with a diagnosis of acute abdomen. On physical examination, he presented signs of peritoneal irritation with evidence of leukocytosis and neutrophilia in the admission blood count. Computed tomography of the abdomen with intravenous contrast was performed, which was interpreted as Meckel's diverticulitis complicated, being corroborated during the surgical act and confirmed by pathological anatomy.\n", "extra_info": {"index": 30, "original_id": "multiclinsum_test_3197_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring are often recommended to support kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Declining glomerular filtration rate (GFR) is a key biomarker for chronic kidney disease progression, and early intervention through pharmacological management, dietary modification, and monitoring of biomarkers such as serum creatinine and proteinuria is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A previously healthy 51-year-old female with history of hypothyroidism presented with acute onset chest pain for 1 day. Patient's electrocardiogram was normal, however, she had elevated troponins and given her typical chest pain, she was diagnosed with acute coronary syndrome (ACS). The patient had been on levothyroxine and was found to have a subnormal thyroid-stimulating hormone level suggesting hyperthyroidism. Echocardiogram was normal. Coronary angiogram showed an anomalous RCA arising from the left coronary cusp of the sinus of Valsalva and no evidence of atherosclerosis. A coronary computed tomography angiogram was done confirming this finding and showed a slit-like deformity of the coronary ostium with at least 50% luminal stenosis. The patient was referred to a cardiothoracic surgeon for potential coronary artery bypass graft.", "extra_info": {"index": 133, "original_id": "multiclinsum_test_2590_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "We report the case of a 52-year-old patient from Bangladesh with dual-origin LAD arising from both left and right sinus with a pre-pulmonary course, presenting with exertional angina and documented myocardial ischaemia. Computed tomography (CT) scan confirmed the anatomical course of the AAOCA. Percutaneous coronary intervention was successfully performed using tailored techniques to treat significant atherosclerotic lesions.", "extra_info": {"index": 100, "original_id": "multiclinsum_test_3124_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "We report an unusual occurrence of pancreatic metastases from a previously diagnosed Merkel cell carcinoma with the discovery of a concomitant insulinoma. An 82-year old lady suffered from recurrent attacks of hypoglycemia and presented with an abdominal mass, 2 years prior she had an excision done on her eyebrow that was reported as Merkel cell carcinoma. An extended distal pancreatectomy and splenectomy along with resection of the left flexure of the colon for her abdominal mass was carried out. Final histopathology of the mass was a poorly differentiated endocrine carcinoma in the pancreatic tail, in the peripancreatic tissue and in the surrounding soft tissue consistent with metastatic Merkel cell carcinoma in addition to an insulinoma of the pancreatic body.", "extra_info": {"index": 32, "original_id": "multiclinsum_test_1055_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "We report a case of a giant loose peritoneal body measuring 7 \u00d7 5 cm found incidentally in a 64-year-old Indian man who presented with acute intestinal obstruction. We present the current hypothesis and our opinion on the genesis of such large bodies and discuss the problems in diagnosis.", "extra_info": {"index": 36, "original_id": "multiclinsum_test_2469_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring are often recommended to support kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Declining glomerular filtration rate (GFR) is a key biomarker for chronic kidney disease progression, and early intervention through pharmacological management, dietary modification, and monitoring of biomarkers such as serum creatinine and proteinuria is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 60-year-old white female with Polyneuropathy, Organomegaly, Endocrinopathy, Monoclonal plasma cell disorder, Skin changes (POEMS) syndrome and newly diagnosed HTN was referred because of an elevated creatinine level. She denied being an active smoker but reported long-term exposure to cigarette smoke due to living with a heavy smoking family and working as a bartender. Further investigations revealed microscopic hematuria and nephritic range proteinuria. Kidney biopsy revealed diffuse and focal nodular mesangial expansion without hypercellularity, with negative staining for amyloid, fibrillary glomerulonephritis, and immunoglobulins, leading to a diagnosis of ING.", "extra_info": {"index": 147, "original_id": "multiclinsum_test_3054_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "A 51 year-old Caucasian right handed housewife lady (weight 61 kg, height 159 cm) presented with a headache of acute onset which proved to be caused by acute subarachnoid hemorrhage. Cerebral computed tomographic angiography revealed multiple aneurysms. The patient underwent a right pterional craniotomy to obliterate right middle cerebral, distal basilar and left carotid bifurcation aneurysms. The post-operative course was uneventful.", "extra_info": {"index": 34, "original_id": "multiclinsum_test_2076_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "A 21-year-old Japanese patient, suffering from a traumatic hallux deficit with only a portion of the basal phalanx intact, underwent rehabilitation treatment. The thenar area exhibited instability, leading to impaired balance and walking difficulties. Biomechanical assessment revealed the need for a rehabilitation strategy for the foot, as well as the knee, hip, and trunk. A rehabilitation protocol was designed to enhance medial foot loading during walking and standing, including balance and trunk strength training. After a 12-week rehabilitation period, the patient's gait showed significant improvement. Specifically, the load response and single-support phases of the gait cycle on the affected side increased from 46.9% to 49.3%, while the pre-swing phase decreased from 14.6% to 11.6%. The vertical component of the ground reaction force rose from 599.8 to 647.5\u00a0N. The enhanced stability from balance training and increased muscle strength contributed to the patient's improved walking and balance.", "extra_info": {"index": 42, "original_id": "multiclinsum_test_1445_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "We reported a patient with acute lymphoblastic leukemia suffered from pulmonary TB infection after HSCT. During anti-TB treatment, the patient had a poor response to linezolid-containing regimen, and developed side effects such as gingival bleeding and thrombocytopenia, so the administration was switched to contezolid. After 15 days of continuous treatment, the patient's platelet increased to 58\u00d7109/L, and he was discharged in stable condition. During subsequent anti-TB treatment with contezolid for more than 7 months, the platelets remained stable, and no hematological adverse reactions and no symptoms of peripheral neuropathy were observed. Moreover, repeat imaging showed that the bilateral lung lesions were significantly reduced, indicating a good outcome for the patient.", "extra_info": {"index": 40, "original_id": "multiclinsum_test_353_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "A HIV-negative 56-year-old male was hospitalized for chest disease with main symptoms of chest tightness, chest pain, fatigue, anorexia, and weight loss. Heart rate 109 times/min, the computed tomography (CT) scans of the neck, chest, and abdomen revealed multiple nodules in the right pleura, right pleural encapsulated effusion, and limited, incomplete expansion of the middle and lower lobes of the right lung, enlarged lymph nodes in the right hilar and mediastinal and diaphragm groups, and multiple slightly low-density nodules in the liver, bone destruction in the 2nd thoracic vertebra, raising the possibility of multiple liver metastases of right lung cancer and malignant pleural fluid. The lymph nodes in the neck, mediastinum, abdomen, and pelvis were enlarged bilaterally. After comprehensive analysis, the patient was diagnosed with atypical systemic HDTB. After three months of conventional anti-TB treatment, the patient refused our hospital follow-up, and his symptoms improved significantly during the telephone follow-up.", "extra_info": {"index": 38, "original_id": "multiclinsum_test_867_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 35-year-old woman diagnosed to have echo-proven chronic rheumatic heart disease for 25 years. Percutaneous balloon mitral valvotomy was done 6 weeks previously for severe mitral stenosis. Left atrial thrombus was detected after the procedure and anticoagulant (warfarin) was initiated. She presented with severe headache and repeated vomiting of 1 day duration on arrival to the hospital. She had frequent seizure attacks with subsequent loss of consciousness on third day of admission. Diagnosis of status epilepticus secondary to intracranial hemorrhage due to warfarin toxicity was made after CT-scan revealed acute subdural hematoma and ventricular bleeding. Then she was transferred to medical intensive care unit (ICU), intubated and put on mechanical ventilator. Anti-epileptic drugs, antibiotics, vitamin K and fresh frozen plasma were given. She developed paroxysms of hypertension, tachycardia, tachypnea, hyperpyrexia, diaphoresis and decerebrate posturing after 7 days of neurological insult. She had normal inter-ictal EEG tracing during cyclic autonomic surge. CFS score was 11 and DLT score was 10. In sum, PSH-AM score was 21, suggested \"probable\" diagnosis of PSH. Morphine, diazepam, propranolol and gabapentin were given in combination to treat PSH. Severity of autonomic storm started to improve on second week of ICU admission. On the third week of admission, her clinical condition deteriorated suddenly, she developed asystole and died of cardiac arrest despite cardiopulmonary resuscitation (CPR).", "extra_info": {"index": 96, "original_id": "multiclinsum_test_1504_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring are often recommended to support kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Declining glomerular filtration rate (GFR) is a key biomarker for chronic kidney disease progression, and early intervention through pharmacological management, dietary modification, and monitoring of biomarkers such as serum creatinine and proteinuria is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 23-year-old female presented to our eye clinic with chief complaint of mild blurring of vision in the right eye and inquired about refractive surgery. The patient denied any previous history of ocular inflammation, trauma, surgery, or use of topical or systemic medications. Slit-lamp examination of the right eye anterior segment was within normal limits except for the crystalline lens anterior capsular which showed confluent pigment deposits stellate in shape over the pupillary axis, whereas left eye examination was completely within normal limits. Ophthalmic examination of the posterior segment was normal in both eyes. Based on her previous ophthalmic history and slit-lamp examination of the right eye, a diagnosis of unilateral congenital lenticular pigmentation was made.", "extra_info": {"index": 149, "original_id": "multiclinsum_test_2126_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "In this article, we describe a case of a-69-year-old female with a painful mass in her left breast. Based on intraoperative pathology consult, neoplastic tissue mostly floating in mucinous lakes with invasion to surrounding stroma was seen. Immunohistochemistry profile showed positive estrogen and progesterone receptors and negative for HER2.", "extra_info": {"index": 106, "original_id": "multiclinsum_test_2138_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "We report the case of a 63-year-old woman with upper gastrointestinal obstruction for almost 10 years, who was pathologically diagnosed with large Brunner's gland adenoma of the duodenum. Postoperatively, no sign of recurrence has been noted until now.", "extra_info": {"index": 108, "original_id": "multiclinsum_test_2813_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "A 6-year-old girl with Coats plus syndrome presented to the pediatric emergency department with vomiting blood and blood in stool. An upper and lower gastrointestinal endoscopy revealed esophageal varices and vascular telangiectasia in the pyloric antrum, duodenum, and colon. She received palliative care and the bleeding was stopped after receiving intravenous octreotide. She then was followed in the pediatric gastroenterology, neurology, and ophthalmology clinics. She was later hospitalized and admitted to the intensive care unit as she continued to have intermittent gastrointestinal system bleeding. She eventually died due to severe gastrointestinal system bleeding.", "extra_info": {"index": 90, "original_id": "multiclinsum_test_1957_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "We report a 9 days-old male neonates weighing 3.85 kg was referred by local hospital to our center and was ventilated with history of respiratory distress and severe infection since he was born. Admitted to our PCICU, 2D echo showed an IAA type A associated with a huge APW type II and restrictif PDA. A PGE1 infusion was started, during the following days the baby experienced several epileptic episodes. After improvement of the clinical condition, surgery was performed on the 20th days of life on year 2011. A successful one-stage repair of such anomalies in which cutting of PDA that arised from PA trunk and distally becoming into descending aorta, extended end to end anastomosis to conduct the ascending aortic blood flow into the descending aorta and intra arterial baffle was used. A 4-0 Gore-Tex baffle was used both to close the APW and separated the RPA from aortic origin with a good result, as his recently grown up as a cheerful 9 year old child who is growing actively and has entered elementary school in grade 2.", "extra_info": {"index": 102, "original_id": "multiclinsum_test_2375_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "A 56-year-old male on oral anticoagulation presented to the emergency department with epigastric pain, nausea, and left upper quadrant tenderness. There was no history of trauma. Contrast-enhanced CT imaging revealed a large subcapsular haematoma of the spleen. Oral anticoagulation was antagonised with vitamin K and the patient was discharged in good condition after 3 days of clinical observation.", "extra_info": {"index": 92, "original_id": "multiclinsum_test_1095_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "The six-year-old girl underwent a human leucocyte antigen (HLA) haploidentical hematopoietic stem cell transplant using post-transplant Cyclophosphamide for severe aplastic anemia. In the second week of the transplant, the patient developed macrophage activation syndrome necessitating treatment with steroids and intravenous immunoglobulin. Subsequently, USG abdomen and blood fungal PCR revealed the diagnosis of hepatosplenic candidiasis. Candida-triggered macrophage activation syndrome responded to antifungals, steroids, intravenous immunoglobulin, and alemtuzumab. However, the subsequent clinical course was complicated by thrombotic microangiopathy. The patient developed hypertension in the 2nd week, followed by high lactate dehydrogenase (1010\u2009U/L), schistocytes (5 per hpf), low haptoglobin (<\u20095\u2009mg/dl), thrombocytopenia, and anemia in the 3rd week. Ciclosporin was stopped, and the patient was treated with 10\u2009days of defibrotide without response. The course was further complicated by the involvement of the gastrointestinal tract and kidneys. She had per rectal bleeding with frequent but low-volume stools, severe abdominal pain, and hypoalbuminemia with a rising urine protein:creatinine ratio. Narsoplimab was started in the 5th week of the transplant. A fall in lactate dehydrogenase was observed after starting Narsoplimab. This was followed by the resolution of gastrointestinal symptoms, proteinuria, and recovery of cytopenia. The second episode of TA-TMA occurred with parvoviraemia and was also successfully treated with Narsoplimab.", "extra_info": {"index": 98, "original_id": "multiclinsum_test_2016_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "A 73-year-old male suspected to have a urothelial carcinoma was scheduled for elective left nephroureterectomy. During central venous catheterization using the anatomic landmark technique to target the internal jugular vein, a guidewire is inadvertently inserted into the suspected vertebral vein. Following the correction of the catheterization, a radiologist reviewed the preoperative enhanced computed tomography and confirmed that the initially punctured vessel was the vertebral vein. On the third day after surgery, the central venous catheter was removed, and the patient did not exhibit any complications, such as bleeding, swelling, and neurological symptoms.", "extra_info": {"index": 88, "original_id": "multiclinsum_test_2805_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "Here, we present a case study of a patient with oral cancer who underwent surgery. During adjuvant radiotherapy, a metastatic cervical lymph node was diagnosed based on fine-needle aspiration biopsy. To increase the total dose to the metastatic tumor, a stereotactic radiosurgery boost of 1\u2009\u00d7\u200918\u00a0Gy was performed two days after the last fraction of conventional radiotherapy. The early and late tolerance of this treatment were positive. During the 18-month follow-up, locoregional recurrence was not detected. The patient died due to secondary malignancy.", "extra_info": {"index": 104, "original_id": "multiclinsum_test_2840_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring are often recommended to support kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Declining glomerular filtration rate (GFR) is a key biomarker for chronic kidney disease progression, and early intervention through pharmacological management, dietary modification, and monitoring of biomarkers such as serum creatinine and proteinuria is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 21-year-old female patient with abdominal pain, irregular menstruation, hyperestrogenemia, and an ovarian mass was included. Brain magnetic resonance imaging (MRI) revealed a pituitary macroadenoma, and transsphenoidal surgery relieved her clinical symptoms. Before transsphenoidal surgery, plasma CA125, estradiol levels were elevated, while prolactin, luteinizing hormone, follicle-stimulating hormone, PROG, cortisol, FT4, thyroid-stimulating hormone, parathyroid hormone, and GH levels were maintained at normal levels. After transsphenoidal surgery, the patient was diagnosed with a functioning gonadotroph adenoma. During follow-up, pelvic ultrasound confirmed normal-sized ovaries in the patient, the menstrual cycle returned to regular, and her hormones were maintained within a normal range. There was no evidence of tumor recurrence after two years of follow-up.", "extra_info": {"index": 151, "original_id": "multiclinsum_test_318_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring are often recommended to support kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Declining glomerular filtration rate (GFR) is a key biomarker for chronic kidney disease progression, and early intervention through pharmacological management, dietary modification, and monitoring of biomarkers such as serum creatinine and proteinuria is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 58-year-old woman presented with palpitations and diarrhea. Atrial fibrillation with spontaneous conversion to sinus rhythm was noted, along with a left ventricular mass identified on echocardiogram and confirmed via computed tomography as dystrophic calcification. Management included rehydration, antiarrhythmic therapy, and anticoagulation. The calcification, linked to previous myocardial infarctions, was considered an incidental finding, with no significant systolic dysfunction.", "extra_info": {"index": 153, "original_id": "multiclinsum_test_3200_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "Patient concerns:\nA 41-year-old man who presented with acute onset of right-hand clumsiness and aphasia even under high international normalized ratio (INR: 7.64) from warfarin use. He was previously treated with warfarin for the LV thrombus and non-valvular AF. Brain magnetic resonance imaging (MRI) showed multiple acute infarction in the cortex of the bilateral frontal lobes, left parietal lobe, and bilateral central semiovale, which highly suggested embolic stroke.\n\nDiagnosis:\nThe repeated transthoracic echocardiogram still revealed LV thrombus (1.27 \u00d7 0.90\u200acm), which failed to respond to warfarin therapy.\n\nInterventions:\nDue to acute infarctions occurred under supratherapeutic range of INR, we switched warfarin to edoxaban (dose: 60\u200amg/day) after INR decreased to less than 2.\n\nOutcomes:\nThe thrombus disappeared after receiving edoxaban for 23 days, and no more recurrent stroke was noted for more than 6 months.", "extra_info": {"index": 94, "original_id": "multiclinsum_test_3113_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "We report a clinical case of a combat patient who was injured after the multiple launcher rocket system \"Grad\" shelling, diagnosed with hydrodynamic liver rupture followed by medical management with application of damage control (DC) tactic in conditions of hybrid war. The patient underwent relaparatomy, liver resection, endoscopic papillosphincterotomy, endoscopic retrograde cholecystopancreatography, stenting of the common bile duct, and VAC-therapy. Applied treatment modalities were effective; the patient was discharged on the 49th day after injury.", "extra_info": {"index": 93, "original_id": "multiclinsum_test_2795_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "A 59-year-old male with suspected lung cancer in the left lower lobe was scheduled to undergo surgery. Chest computed tomography revealed a displaced B1\u00a0+\u20092 and hyperlobulation between S1\u00a0+\u20092 and S3, while the interlobar fissure between S1\u00a0+\u20092 and S6 was completely fused. Three-dimensional computed tomography (3D-CT) revealed an anomalous V1\u00a0+\u20092 joining the left inferior pulmonary vein and a branch of the V1\u00a0+\u20092 running between S1\u00a0+\u20092 and S6. We performed left lower lobectomy via video-assisted thoracic surgery, while taking care with the abovementioned anatomical structures. The strategy employed in this operation was to preserve V1\u00a0+\u20092 and confirm the locations of B1\u00a0+\u20092 and B6 when dividing the fissure.", "extra_info": {"index": 91, "original_id": "multiclinsum_test_2752_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 14-year-old boy attended a local hospital for ankylosing spondylitis. Chest radiography showed an enhanced circular-density shadow near the left mediastinum. The patient had no chest symptoms and the physical examination was normal. Because of the mediastinal occupation, the patient visited our department of chest surgery for further treatment. During surgery, a left pericardial defect was observed. The bronchogenic cyst was removed by thoracoscopic surgery, but the pericardial defect remained untreated, and a satisfactory outcome was achieved after the operation. The patient was diagnosed with a mediastinal tumor. The pathological diagnosis of the tumor was a bronchogenic cyst.", "extra_info": {"index": 136, "original_id": "multiclinsum_test_2394_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "We report and analyse a case of a 34-year-old female who presented with ataxia. Magnetic Resonance Imaging (MRI) of the brain revealed demyelinating lesions in the white matter. Genetic testing identified the c.4044C > G and c.1186-2A > G variants in the POLR3A gene. The patient was diagnosed with hypomyelinating leukodystrophy type 7 and received neurotrophic and symptomatic supportive therapy. However, after 1 month of follow-up, there was no improvement in her symptoms.", "extra_info": {"index": 134, "original_id": "multiclinsum_test_1579_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 70-year-old Japanese man with essential hypertension, dyslipidemia, chronic kidney disease and emphysema was hospitalized with the novel coronavirus disease. He had hypoxemia that was disproportionate to the severity of pneumonia indicated by computed tomography (CT), along with coagulation abnormalities. We speculated that there was a high possibility that he had developed ventilation and blood flow imbalance due to pulmonary intravascular coagulopathy (PIC) or hypoxic pulmonary vasoconstriction (HPV). In this case, early, short-term combination therapy with remdesivir, nafamostat mesylate and low-dose dexamethasone (Dex) was successful.", "extra_info": {"index": 144, "original_id": "multiclinsum_test_2467_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "We present the case of an adult male patient with cerebral malaria by Plasmodium vivax, who starts with general discomfort and fever, then presents convulsions more than twice a day with loss of consciousness and motor functional limitation. He is given a thick drop where Plasmodium vivax trophozoites and depression of the three blood series are observed. He is given treatment with artesunate and clindamycin for five days, a blood transfusion and continues with primaquine for seven days. The patient shows clinical improvement with neurological sequelae in the left lower extremity.\n", "extra_info": {"index": 95, "original_id": "multiclinsum_test_3364_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "A 46-year-old male with end-stage renal disease of unknown cause received a cadaveric renal transplant one year ago. Although three antihypertensive medications were administrated, his blood pressure gradually increased to 190/120\u00a0mmHg 3\u00a0weeks posttransplantation. Also the level of creatinine increased to 194\u00a0\u03bcmol/L.Color Doppler ultrasonography indicated a decreased resistance index (RI) in intrarenal arteries and increased blood flow of the transplant renal artery, therefore, a vascular complication of TRAS was suspected. Arteriography was performed and demonstrated TRAS caused by stretch of an artery branch, and the TRAS occurred in the distal site of the anastomosis instead of the anastomosis. Percutaneous transluminal bare stent implantation treatment was successfully performed. Satisfactory clinical efficacy with improvement in transplant renal function and renovascular hypertension was achieved after the interventional treatment.", "extra_info": {"index": 101, "original_id": "multiclinsum_test_1302_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "We present a case where a combined lumbar epidural and spinal anesthesia was performed using the loss of resistance to air technique (LOR), on a 78-year-old Greek (Caucasian) male undergoing a total hip replacement. Despite being hemodynamically stable throughout the operation, two hours following epidural analgesia the patient manifested a sudden drop in blood pressure and heart rate that required the administration of adrenaline to counter. Pneumomediastinum, pneumorrachis and paravertebral soft tissue emphysema were demonstrated in a Computed Tomography scan. We believe that injected air from the epidural space and surrounding tissues slowly moved towards the mediastinum, stimulating the para-aortic ganglia causing parasympathetic stimulation and therefore hypotension and bradycardia.", "extra_info": {"index": 89, "original_id": "multiclinsum_test_2918_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "A 70-years-old woman, who had been diagnosed with SLE at 69\u2009years, was admitted for further examination of liver dysfunction. PBC was confirmed based on elevated serum levels of transaminase, high levels of antimitochondrial antibodies and following a liver biopsy. The oral administration of ursodeoxycholic acid stabilized the liver dysfunction.", "extra_info": {"index": 109, "original_id": "multiclinsum_test_2272_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "A 48-year-old caucasian male with an extensive psychiatric history ingested a high dose of venlafaxine causing a serum venlafaxine concentration of 12.6\u00a0mg/L 24\u00a0hours after ingestion. Seven hours post-ingestion, he experienced tonic-clonic seizures, and 8\u00a0hours later, takotsubo cardiomyopathy was recognized followed by cardiac arrest. The patient was resuscitated with prolonged cardiopulmonary resuscitation including ongoing automatic external compressions during helicopter transportation to a tertiary hospital for extracorporeal membrane oxygenation treatment. Despite a cardiopulmonary resuscitation duration of 2\u00a0hours, 36\u00a0hours of extracorporeal membrane oxygenation, and a total of 30\u00a0days of intensive care, the patient made a full recovery.", "extra_info": {"index": 97, "original_id": "multiclinsum_test_985_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A Chinese family with ATS was recruited for the current study. Clinical characteristics (including findings from renal biopsy) of ATS patients were collected from medical records, and potential causative genes were explored by whole-exome sequencing. A heterozygous substitution in intron 22 of COL4A3 (NM_000091 c.2657-1G>A) was found in the patients, which was further confirmed by quantitative polymerase chain reaction.", "extra_info": {"index": 132, "original_id": "multiclinsum_test_1061_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "Here case report, a 24-year-old patient from an endemic region of Somalia presented with fever, headache, abdominal pain, nausea, vomiting, and weight loss for two months. Initially, the patient received symptomatic treatment and a blood transfusion but showed no improvement. Physical examination revealed fever, pallor, and hepatosplenomegaly. Laboratory tests showed pancytopenia and positive rapid diagnostic test for plasmodium parasite antigen. Despite three days of anti-malarial treatment, the symptoms persisted, and hepatosplenomegaly worsened. Further investigations, including infectious disease tests, were conducted, ruling out HIV, viral hepatitis, Brucella, and Leishmania antibodies. Peripheral blood smear showed pancytopenia and bone marrow aspiration revealed no evidence of infection or malignancy. A tru-cut biopsy of the spleen was performed, confirming the diagnosis of visceral leishmaniasis. The patient received a combination therapy of sodium stibogluconate and paromomycin, leading to significant improvement. After completing treatment, the patient was discharged with normal spleen biopsy results.", "extra_info": {"index": 146, "original_id": "multiclinsum_test_292_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "A 59-year-old female with a history of recurrent UCS presented with the new onset of the left lower extremity pain, numbness, and episodic urinary incontinence. When the MR revealed an enhancing intradural extramedullary mass posterior to the L1 vertebral body, she underwent a focal decompressive laminectomy. Although she improved neurologically postoperatively, she succumbed to the leptomeningeal spread of her disease within 2 postoperative months.", "extra_info": {"index": 103, "original_id": "multiclinsum_test_2588_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "A 56-year-old woman was referred to the emergency department due to a severe headache in the frontal area for 2 days before admission. The patient experienced nausea and vomiting in the morning and had no history of seizures or decreased consciousness. Examination of neurological symptoms was completely normal and showed no symptoms of meningeal irritation. In terms of past history, the patient had undergone tympanomastoidectomy surgery and resection of the cholesteatoma 1 week previously. The Mount Fuji sign was found on the brain computed tomography (CT) scan of the patient. Treatments such as CBR (complete bed rest), 30-degree head elevation, anti-fever, analgesics and oxygen therapy, along with anti-compulsive drug (phenytoin), were prescribed. At the end of 5 days, the patient's pneumocephalus was resolved completely.", "extra_info": {"index": 105, "original_id": "multiclinsum_test_520_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "A 64-year-old male was admitted to the hospital with a headache, fever and later imbalance, blurred vision, and general slowness. Neurological examination revealed nuchal rigidity and general clumsiness. Meningitis was suspected, and the patient was treated with dexamethasone, ceftriaxone and acyclovir. A brain computer tomography (CT) scan was normal, and cerebrospinal fluid (CSF) Gram staining and bacterial cultures remained negative, so the antibacterial treatment was discontinued. Nine days after admission, the patient's condition deteriorated. The antibacterial treatment was restarted, and a brain magnetic resonance imaging revealed ventriculitis. A subsequent CT scan showed hydrocephalus, so a ventriculostomy was performed. In CSF Gram staining, chains of gram-positive cocci were observed. Bacterial cultures remained negative, but a bacterial PCR detected Streptococcus intermedius. An orthopantomography revealed advanced periodontal destruction in several teeth and periapical abscesses, which were subsequently operated on. The patient was discharged in good condition after one month.", "extra_info": {"index": 107, "original_id": "multiclinsum_test_1344_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "A 10-year-old Kurdish boy was presented with generalized bone pain and fever of 1 month's duration which was associated with sweating, easy fatigability, nose bleeding, breathlessness and severe weight loss. On examination, we observed pallor, tachypnea, tachycardia, low blood pressure, fever, petechial hemorrhage, ecchymoses, tortuous dilated veins over the chest and upper part of abdomen, multiple small cervical lymph node enlargements, mildly enlarged spleen, palpable liver and gross abdominal distention. Blood analysis revealed pancytopenia and elevated lactate dehydrogenase and erythrocyte sedimentation rate. Imaging results showed mediastinal widening on a planar chest X-ray and diffuse focal infiltration of the axial bone marrow on magnetic resonance imaging of the lumbosacral vertebrae. Bone marrow aspiration and biopsy examination showed extensive bone marrow necrosis. Immunophenotyping analysis of the bone marrow biopsy confirmed T-cell acute lymphoblastic leukemia, as CD3 and terminal deoxynucleotidyl transferase markers were positive and CD10, CD20 and CD79a markers were negative.", "extra_info": {"index": 99, "original_id": "multiclinsum_test_1185_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "This case report presents the case of a 77 year old female patient with degenerative hip disease in the presence of an ipsilateral arthrodesis of the knee. The patient was operated using the DAA. No complications were found and the patient had an excellent follow-up with a forgotten joint score of 93.75 at 1 year. The difficulty in this case consists in finding the correct stem anteversion with the altered knee anatomy. Using pre-operative templating on X-rays, intraoperative fluoroscopy and the posterior femoral neck the hip biomechanics could be restored.", "extra_info": {"index": 140, "original_id": "multiclinsum_test_2302_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "We report a case of a 33-year-old man, presenting with a five-month history of bilateral lower extremity pain, as well as paresthesia, and mild weakness in one lateral lower extremity. A lumbar laminectomy of L3 to L5 and en bloc resection of the tumor was performed. Postoperative histopathology and immunohistochemical analysis of the tumor were consistent with that of a carcinoid tumor. There were no clinical or radiological signs of tumor recurrence or metastasis at the patient's two year postoperative follow-up.", "extra_info": {"index": 142, "original_id": "multiclinsum_test_2169_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 70-year-old male patient was affected by encephalitis caused by scrub typhus that occurred 23 years ago. He had poor cognition and his clinical examination findings were as follows: Mini-Mental Status Examination score, 14; and handgrip strength (right/left, kg), 32.3/31.3. DTT revealed serious injuries of the left thalamocingulate tract and right mammillothalamic tract in the Papez circuit, and a partial injury of the anterior part of the fornix.", "extra_info": {"index": 148, "original_id": "multiclinsum_test_1723_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "We report a case of a 23-year-old patient with Burkitt's lymphoma and graft-versus-host disease admitted with intracerebral hemorrhage and sequential development of 12 anterior circulation aneurysms from disseminated Scedosporium infection. Despite aggressive surgical and antimicrobial treatment, the patient died 6 months later from multiorgan failure. The notable feature of this case is the rapid angioinvasiveness of the infection with new aneurysm formation within days of clear angiographic imaging despite the apparent lack of skull base osteomyelitis.", "extra_info": {"index": 152, "original_id": "multiclinsum_test_2127_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "Severe thermal corneoscleral injury occurred during phacoemulsification in the right eye of a 74-year-old male. His medical history was prostate hypertrophy. Visual acuity was hand motion and the intraocular pressure was 3 mm Hg OD. There was heavy corneal stromal opacity with intraocular fluid leakage. The patient underwent transplantation of a donor scleral graft to the burn site. Histologically, the injured sclera showed coagulation necrosis without inflammatory cell infiltration. An intraocular lens was eventually fixed in the ciliary sulcus 7 months later. His visual acuity remains at 2/20 OD.", "extra_info": {"index": 150, "original_id": "multiclinsum_test_1564_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "A 56-year-old female, with previous history of intestinal pneumonitis, mild pulmonary hypertension and gastroesophageal reflux secondary to systemic scleroderma, is considered for lung transplant. Initially, due to persistent gastroesophageal reflux, a transplant was not a viable. This was corrected with an open gastrectomy with roux-en-Y anastomosis. Follow-up one week later revealed normal anatomy, adequate esophageal-jejunal anastomosis, and adequate contrast medium transit via esophagogram. Additionally, there was no evidence of contrast medium reflux indicating a resolved gastroesophageal reflux disease. This led to the patient becoming a candidate for lung transplant.", "extra_info": {"index": 138, "original_id": "multiclinsum_test_2494_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 71-year-old female who was being treated for type 2 diabetes with canagliflozin, metformin, and saxagliptin orally presented to the ED for evaluation of reduced oral intake, malaise, nausea, and abdominal pain. Although her blood glucose was not severely elevated (259 mg/dL), there was notable ketoacidosis (pH\u20096.89; CO2, 11.4\u2009mmHg; HCO3, 1.9\u2009mEq/L; base excess, - 31.3\u2009mmol/L; 3-hydroxybutyric acid > 10,000\u2009\u03bcmol/L) was observed. The uncontrolled acidosis improved following 3\u2009days of continuous renal replacement therapy, but elevated urinary glucose continued for more than 10\u2009days. Ringer's lactated fluid supplementation was continued for management of polyurea and glucosuria. Urinary glucose turned negative on day 16, and there was improvement in the patient's overall state; hence, she was discharged on day 18.", "extra_info": {"index": 2, "original_id": "multiclinsum_test_99_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 62-year-old male presented with a 4-month history of right brachial pain and hyposensitivity in the C5 distribution. The cervical magnetic resonance (MR) imaging scan revealed a C5-C6 right anterolateral disc herniation with syringomyelia extending from C5-C6 to T1. Following a C5-C6 anterior cervical discectomy and fusion (ACDF), the patient's symptoms resolved. The 3-month postoperative MR documented total resolution of the syrinx. Notably, due to residual neuropathic pain, the patient required a subdural spinal cord stimulator which was placed without any complications.", "extra_info": {"index": 6, "original_id": "multiclinsum_test_875_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "We report the case of a 51-year-old Caucasian woman who presented with SAPHO syndrome with mainly axial involvement. She had been treated with sulfasalazine and anti-inflammatory drugs for many years without any success. A few weeks after starting treatment with tofacitinib, both clinical and biological parameters dramatically improved. Imaging also showed considerable regression of the vertebral and pelvic lesions. However, tofacitinib had to be discontinued due to the occurrence of pulmonary embolism. Consequently, recurrence of bone pain and biologic inflammation was rapidly observed.", "extra_info": {"index": 0, "original_id": "multiclinsum_test_787_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "Herein we present a 63-year-old man with idiopathic spontaneous intraperitoneal hemorrhage (ISIH) caused by spontaneous rupture of non-aneurysmal inferior pancreaticoduodenalartery (IPDA).", "extra_info": {"index": 4, "original_id": "multiclinsum_test_45_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 63-year-old male presented with a prominent itching sensation and wholebody jaundice. He showed obstructive-pattern jaundice, an elevated IgG4 level, and infiltration of a large number of IgG4-positive cells in the ampulla of Vater. The imaging findings of intrahepatic duct (IHD) and common bile duct dilation, an elevated serum IgG4 level, and characteristic histological findings led to diagnosis of IgG4-SC that compatible with the 2019 ACR/EULAR classification criteria. We planned to treat the patient with high-dose glucocorticoid (GC), followed by cyclophosphamide pulse therapy. After treatment with high-dose GC and an immunosuppressant, imaging studies showed that IHD dilatation had completely resolved.", "extra_info": {"index": 14, "original_id": "multiclinsum_test_53_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "We present a case of a patient who suffered a cardiac arrest after a fall during a chronic obstructive pulmonary disease exacerbation, leading to pneumoretroperitoneum.", "extra_info": {"index": 12, "original_id": "multiclinsum_test_1808_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "33-year-old nulligravid woman with newly diagnosed anaplastic astrocytoma (AA; WHO grade III, IDH1-negative) sought fertility preservation. Prior to chemotherapy and radiation for AA, the patient underwent in vitro fertilization (IVF) for fertility preservation, resulting in 8 vitrified embryos. Following chemo-radiation, the patient underwent two rounds of frozen embryo transfers (FET), each resulting in a successful singleton pregnancy.", "extra_info": {"index": 8, "original_id": "multiclinsum_test_2635_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": "A 34-year-old male patient presented with multiple large tuberous xanthomas related to FH. There were 15 masses in different body parts, including the dorsum of the hands, elbows, buttocks, feet, and Achille's tendon. The largest masses in the buttocks measured 8\u00a0\u00d7\u00a08\u00a0\u00d7\u00a05\u00a0cm. Surgical removal of 13 masses was carried out in combination with medical treatment. The skin incision was oval around the circumference of masses with the longitudinal axis parallel to the Langer's line. Skin defects were closed directly or dissected on both sides of the incision to reduce tension. Wound healing was normal. After 1.5\u00a0months, there was no recurrence of xanthomas.", "extra_info": {"index": 10, "original_id": "multiclinsum_test_1587_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "A 40-year-old woman was admitted to our hospital after presenting with liver dysfunction. She had been previously diagnosed with ET; aspirin and anagrelide had been prescribed. Subsequent examination at our hospital revealed cecal cancer. Distant metastasis was absent; laparoscopic ileocecal resection was performed. Anagrelide was discontinued only on the surgery day. She was discharged on the seventh postoperative day without thrombosis or hemorrhage. However, when capecitabine and oxaliplatin were administered as adjuvant chemotherapy with continued anagrelide administration, she experienced hepatic dysfunction and thrombocytopenia; thus, anagrelide was discontinued. Five days later, her platelet count recovered. Subsequently, anagrelide and aspirin administration was resumed, without any adjuvant chemotherapy. Her liver function normalized gradually in 4\u2009months. One-year post operation, she is well without tumor recurrence or new metastasis.", "extra_info": {"index": 16, "original_id": "multiclinsum_test_1612_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "We report here another case of primary prostatic MALT lymphoma which is presented by hematuria and diagnosed primarily as BPH. Immunohistochemistry studies demonstrate the diagnosis and MALT lymphoma. Six months after starting the treatment the patient was alive and well.", "extra_info": {"index": 9, "original_id": "multiclinsum_test_2155_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "An isolated retinal astrocytic hamartoma was detected in the nasal retina of the left eye of a 4-day-old male infant. At the time of initial presentation, we detected a solitary yellowish-white flat mass with an approximate size of 1.5 disc diameters in the nasal retina. Fluorescein angiography (FA) revealed a diffuse hyperfluorescence with slight fluorescence leakage. Seven months later, the fundus examination showed no lesion in the left eye, FA revealed mild tortuous vessels without leakage.", "extra_info": {"index": 20, "original_id": "multiclinsum_test_2309_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "We describe a case of a Ashkenazi Jew patient who presented in the typical way that carcinoma of the colon might present but turned out to have a very rare type of tumor in both its histology and its location.", "extra_info": {"index": 18, "original_id": "multiclinsum_test_2722_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "A 27-year-old male with a relapsed acute lymphoblastic leukemia presented with five-day-old polyarthralgia. He also had febrile neutropenia, cellulitis without abscesses, and methicillin-resistant Staphylococcus aureus bacteremia for which he received therapy with oxacillin and cefepime. However, the febrile neutropenia persisted, and an invasive fungal infection was suspected. A new set of blood cultures was taken and antifungal treatment was initiated. Arthroconidia were identified in the blood cultures and a matrix-assisted laser desorption ionization-mass spectrometry confirmed the presence of Geotrichum spp. Antifungal treatment was adjusted to 14 days of deoxycholate amphotericin B and four weeks of voriconazole. After a prolonged stay, he was discharged.\n", "extra_info": {"index": 3, "original_id": "multiclinsum_test_3210_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "We present a case of subacute cervical cerebrospinal fluid (CSF) leak resulting from chiropractic manipulation of the cervical spine. The patient is a 29-year-old female who received manipulation one week prior to developing symptoms of severe orthostatic headache, nausea, and vomiting. Magnetic resonance imaging (MRI) revealed a new C5-C6 ventral CSF collection. Symptomatic onset corresponded with the recent cervical chiropractic adjustment. We present serial imaging correlating with her symptomatology and review the pertinent literature on complications of chiropractic manipulation.", "extra_info": {"index": 5, "original_id": "multiclinsum_test_2542_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "The patient was referred to our hospital with a 1-month history of disorientation and magnetic resonance imaging showed hydrocephalus with an enhancing lesion in the tectum. Preoperative blood tests showed a high serum soluble interleukin-2 receptor level of 624 U/ml. Through a single burr hole, endoscopic third ventriculostomy and biopsy of the lesion were simultaneously performed with a flexible endoscope. The histological examination confirmed diffuse large B-cell lymphoma. The patient underwent chemotherapy and radiotherapy.", "extra_info": {"index": 11, "original_id": "multiclinsum_test_410_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "The authors report on a case of acute primary Cytomegalovirus infection complicated with acute appendicitis due to Cytomegalovirus in an apparently immunocompetent 24-year-old Caucasian man also suffering from primary sclerosing cholangitis and ulcerative colitis. Diagnosis was based on clinical manifestations, serology results, as well as microbiological and histological findings. Treatment consisted of surgery and anti-Cytomegalovirus therapy.", "extra_info": {"index": 1, "original_id": "multiclinsum_test_2576_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "We report a case of annular leukocytoclastic vasculitis induced by anti-tuberculosis medication. A 62-year-old Thai man presented to our facility with a generalized exanthematous rash on his trunk and extremities that resolved shortly afterwards. Subsequently, he developed multiple, erythematous-to-purplish, non-blanchable macules and papules with an annular arrangement on his extremities. The skin rash occurred after two weeks of anti-tuberculosis medication. The histopathology of the purpuric skin lesion was consistent with leukocytoclastic vasculitis. The skin lesion improved after discontinuation of the anti-tuberculosis drugs and treatment with oral antihistamine and topical corticosteroid drugs. Streptomycin, ethambutol and ofloxacin were administered as second-line anti-tuberculosis therapy during his hospitalization. No adverse reactions were observed.", "extra_info": {"index": 7, "original_id": "multiclinsum_test_2131_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "The patient was a 55-year-old woman with a transglottic squamous cell carcinoma of the T3N0M0 stage and PCF development following total laryngectomy surgery with total thyroidectomy and bilateral elective cervical lymph node dissection level I-IV. In spite of conservative treatment, the fistula was not recovered after 3 weeks. It was decided to perform fibrin glue injection into the fistula tract via the endoscopic approach. One month after the fibrin glue injection, no evidence of contrast extravasation was observed on barium swallow test, and the fistula was completely closed.", "extra_info": {"index": 13, "original_id": "multiclinsum_test_112_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "a 1-month-old baby presented with severe AS and CoA. The decision was made to perform a hybrid surgical procedure. The patient underwent a lateral thoracotomy for repair of the CoA and carotid cutdown for aortic balloon valvuloplasty (AoVP).", "extra_info": {"index": 19, "original_id": "multiclinsum_test_2724_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "We report the case of a 2 years and-5-month-old boy admitted in our clinic for fever, abdominal pain and diarrhea. The clinical exam at the time of admission revealed influenced gen-eral status, bilateral palpebral edema and conjunctivitis, mucocutaneous signs of dehydration, and abdominal tenderness at palpation. The laboratory tests performed pointed out lymphopenia, thrombocytopenia, anemia, elevated C-reactive protein - CRP, erythrocyte sedimentation rate and ferritin levels, hyponatremia, hypopotassemia, hypertriglyceridemia, elevated D-dimer, in-creased troponin and NT-proBNP. The real-time polymerase chain reaction (RT-PCR) test for SARS-CoV-2 infection was negative, but the serology was positive. Thus, established the diagnosis of PIMS-TS. We initiated intravenous immunoglobulin, empirical antibiotic, anticoagulation therapy and symptomatic drugs. Nevertheless, the clinical course and laboratory parameters worsened, and the 2nd echocardiography pointed out minimal pericardial effusion, slight dilation of the left cavities, dyskinesia of the inferior and septal basal segments of the left ventricle (LV), and LV systolic dysfunction. Therefore, we associated intravenous methylprednisolone, angiotensin converting enzyme inhibitors, spironolactone and hydrochlorothiazide, with outstanding favorable evolution.", "extra_info": {"index": 15, "original_id": "multiclinsum_test_723_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "An 84-year-old male was admitted with a history of difficulty rising from a chair and a fall. Laboratory results showed increased creatine kinase levels of more than 50 times the normal reference values. Electromyography (EMG) showed myopathic changes, and FDG-PET/CT scan showed increased FDG uptake in bilateral quadriceps. A biopsy was performed revealing lymphocytic predominant infiltrates and myonecrosis. Prednisone and intravenous immunoglobulin (IVIG) were administered with strength improvement. The patient was discharged for further follow-up.", "extra_info": {"index": 17, "original_id": "multiclinsum_test_2937_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "A young man involved in a car accident and sustained blunt thoracic injuries, among others. As part of primary survey, FAST scan was performed. Subxiphoid view to look for evidence of pericardial effusion showed part of the cardiac image obscured by A-lines. Other cardiac windows showed only A-lines, as well. A suspicion of pneumopericardium was raised and CT scan confirmed the diagnosis.", "extra_info": {"index": 21, "original_id": "multiclinsum_test_1133_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "We describe a 30-year-old Caucasian woman who tested positive for COVID-19 after developing nasal congestion and cough. Ten days after testing positive, she developed a systemic rash on her extremities and torso. At the same time, she developed swelling of the tongue lasting 1 hour, with subsequent appearance of oral lesions that resembled geographic tongue. She also had an irritable sensation on her tongue and some mild loss of sense of taste. We opted for conservative therapy, including mouth rinses containing lidocaine to be used every 6 hours. The patient used the mouth rinse therapy for 1 month and experienced a 90% improvement in her oral lesions and tongue sensitivity. However, she had repeated flares every 3 weeks over a 6-month period, and the steroid mouthwash achieved incomplete resolution. After three sessions of photobiomodulation therapy, she had no further flares or tongue sensitivity and the lesions healed.", "extra_info": {"index": 119, "original_id": "multiclinsum_test_778_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control can slow disease progression and reduce the risk of end-stage renal disease.\"\n}", "ground_truth": "The medical record of a 64-year-old female with Sjogren's syndrome was reviewed. The clinical and pathological data along with chest CT images were obtained. The literature related to the transformation was reviewed. There were no specific clinical manifestations of LIP and its transformation into malignant lymphoma in the patient. The chest CT mainly displayed multiple cystic foci, with multiple nodules and ground-glass shadows in both lungs.", "extra_info": {"index": 131, "original_id": "multiclinsum_test_2470_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "We report a case of a 93-year-old Middle Eastern male presenting for longstanding treatment-refractory hiccups. Imaging with computed tomography of the chest and abdomen was unremarkable. An upper endoscopy was normal without any endoscopic finding to suggest eosinophilic esophagitis. Given his elevated peripheral eosinophil count, biopsies were taken from mid- and distal esophagus and revealed eosinophilic infiltration in the range of 15 eosinophils per high-power field, favoring a diagnosis of eosinophilic esophagitis. The hiccups resolved following the initiation of eosinophilic esophagitis treatment.", "extra_info": {"index": 114, "original_id": "multiclinsum_test_3338_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "The patient was a 77-year-old hypertensive male who presented to the emergency following an episode of slip and fall at home. After prompt resuscitation, he was sent for radiological evaluation which revealed fractures of the left inter-trochanteric femur and left proximal humerus. Meanwhile, laboratory investigations showed grossly deranged renal parameters, along with elevated serum creatinine phosphokinase levels (more than 5 times the baseline). A diagnosis of acute kidney injury secondary to traumatic rhabdomyolysis was made. Medical management included adequate intravenous fluid administration combined with strict input-output monitoring. Subsequently, the patient underwent closed reduction and internal fixation of the inter-trochanteric femur fracture with a proximal femoral nail. However, fracture of the proximal humerus was managed non-operatively with sling immobilization as patient refused to give consent for a second surgery.", "extra_info": {"index": 110, "original_id": "multiclinsum_test_2243_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "In this case, we present a preterm newborn who developed pneumomediastinum and pneumothorax. The pneumothorax persisted, despite placement of a thorax tube, requiring a thoracotomy to detect and treat the bronchial rupture.", "extra_info": {"index": 116, "original_id": "multiclinsum_test_2176_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "A 21-year-old man was referred to our hospital for treatment after presenting to a nearby hospital with right inguinal pain. Abdominal magnetic resonance imaging showed an intra-abdominal mass measuring 34 \u00d7 15 \u00d7 8 cm with partial signal hyperintensity on T2-weighted imaging and hypointensity on T1-weighted imaging, extending from the left abdominal cavity to the pelvic region. Although no definitive diagnosis was obtained preoperatively, surgery was performed under suspicion of gastrointestinal stromal tumor or other significant disease. A mass was identified firmly adherent to the transverse colon, gastric wall, and diaphragm, and these organs were partially resected. The excised specimen measured 38 \u00d7 21 \u00d7 8 cm and weighed 6400 g. Macroscopically, the tumor showed a smooth surface and homogeneous interior. Pathological examination revealed atypical cells with spindle-shaped nuclei and collagen fiber hyperplasia in the stroma, and immunostaining was negative for c-kit, CD34, desmin, S-100, and positive for \u03b2-catenin, leading to a confirmed diagnosis of desmoid tumor. Fifteen months after surgery, a local recurrence with a diameter of 3.0 cm was identified, and the patient remains under careful follow-up.", "extra_info": {"index": 112, "original_id": "multiclinsum_test_3373_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "Patient concerns:\nA 68-year-old man was admitted to our hospital with dyspea and general fatigue. He was diagnosed with acute decompensated heart failure due to ischemic cardiomyopathy. In order to improve fluid retention and relieve his dyspnea, low-dose TLV (7.5\u200amg qd) was performed. After the 3-day treatment using TLV, we observed that he became delirious and his limbs shook uncontrollably. High serum sodium 173 mmol/L was noted compared to the results of the first examination (137 mmol/L). After intensive rescue, serum sodium was restored to normal (135\u200amol/L). Later, when the patient refused continuous renal replacement therapy (CRRT), we tried again to use a lower dose of TLV to improve diuretic resistance. Two days later, Serum sodium rose again (162 mmol/L).\n\nDiagnoses:\nDuring the course of therapy, we did not strictly require the patient to control the fluid intake. No other medication could cause elevation of serum sodium. Therefore, we suspected a high sensitivity to the side effect of TLV.\n\nIntervention:\nStop the use of TLV and encourage the patient to drink plenty of water. Gastric tube was inserted orally to increase the intake of fresh water.\n\nOutcomes:\nHis serum sodium decreased gradually and his psychiatric symptom recovered. During this period, Overall condition of the patient was stable. After being discharged from the hospital, the patient eventually died of cardiac arrest due to critically ill heart failure.", "extra_info": {"index": 124, "original_id": "multiclinsum_test_3307_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "A patient from TRITON2 with BRCA-mutated mCRPC had a response to the PARP inhibitor rucaparib and remained on treatment for 32 weeks, which was >2 times longer than the duration of each of his prior therapies (bicalutamide, docetaxel, abiraterone). The patient enrolled in TRITON2 based on results of local genomic testing of an archival biopsy that indicated the presence of a BRCA1 T1399I (allelic fraction, 19%) mutation. Local testing also identified an ATM G1663C mutation, a TP53 P191del mutation, and a BRAF K601E mutation. Analysis of a plasma sample obtained before the patient started rucaparib detected the same alterations as those in the archival biopsy, but it also revealed the presence of a BRCA2 homozygous loss (whole gene, 26 of 26 exons) and several other alterations of unknown functional impact. We hypothesize the response of the patient's tumor to rucaparib was likely driven by DNA damage repair deficiency caused by homozygous loss of all BRCA2 exons. Following discontinuation from rucaparib due to clinical disease progression, the patient received carboplatin and cabazitaxel for \u22483 weeks. The patient died due to progression of his disease.", "extra_info": {"index": 118, "original_id": "multiclinsum_test_759_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "A 91-year-old woman presented to our institution with ST-segment elevation myocardial infarction (STEMI). The right radial access was chosen for the performance of percutaneous coronary intervention. After the introduction of 6\u2009F sheath, there was difficulty in the advancement of 0.035\u2009J wire that was exchanged with a Terumo hydrophilic wire. After the procedure and before sheath removal, radial arteriography was done and revealed perforation. Protamine sulfate was administered and prolonged balloon inflation was attempted but failed to seal the perforation, so a 7-F-long vascular sheath was inserted to internally tamponade the vessel, and the patient was sent to the coronary care unit for monitoring. Over the next 3 days, serial radial angiographies were done revealing the persistence of the perforation, and on the fourth day, angiography revealed multiple thrombi. Thrombus aspiration was done using Pronto V4 extraction catheter (Vascular Solutions, USA) and was followed by the deployment of a covered stent. The stent was dislodged and successfully snared. Finally, the perforation was sealed spontaneously and there were no signs of intra-arterial thrombi.", "extra_info": {"index": 120, "original_id": "multiclinsum_test_1116_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "We describe a case in which the two technologies are used in combination during acute echocardiographic optimization of left pacing vector in a 63-year-old man, Caucasian, who showed worsening heart failure symptoms a few days after an implant, and the effect of the device\u2019s optimization at 6-month follow-up.", "extra_info": {"index": 126, "original_id": "multiclinsum_test_3317_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "A 78-year-old male patient presented with intermittent cervicalgia of 5 months duration accompanied by few weeks of a progressive severe right hemiparesis, up to hemiplegia. The magnetic resonance imaging (MRI) examination revealed an intramedullary expansive lesion measuring 10 mm\u00d715 mm at the C1-C2 level; it readily enhanced with contrast. A total body computed tomography (CT) scan documented an 85 mm mass involving the right kidney, extending to the ipsilateral adrenal gland, and posteriorly infiltrating the ipsilateral psoas muscle. The subsequent CT-guided fine-needle biopsy confirmed the diagnosis of an RCC (Stage IV). The patient next underwent total surgical total removal of the C1-C2 intramedullary mass, following which he exhibited a slight motor improvement, with the right hemiparesis (2/5). He died after 14 months due to global RCC tumor progression.", "extra_info": {"index": 122, "original_id": "multiclinsum_test_2110_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "A 32\u2009year-old woman with a history of non-diabetic hemodialysis for 3\u2009years suffered from severe involuntary movement, and brain magnetic resonance imaging showed symmetrical T2-weighted imaging (T2WI) and T2/fluid-attenuated inversion recovery (T2FLAIR) hyperintense nonhemorrhagic lesions in the bilateral basal ganglia. She was diagnosed with UE as syndrome of bilateral basal ganglia lesions, due to a combined effect of uremic toxins and hyperthyroidism. After treatment with high frequency and high flux dialysis, hyperbaric oxygen therapy and declining parathyroid hormone, the patient achieved complete remission with normal body movement and was discharged.", "extra_info": {"index": 129, "original_id": "multiclinsum_test_168_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "We report the case of a patient with a history of multiple diseases and 2 tumor-like lesions with internal lytic areas detected in the fourth right costal arch and in the eighth left costal arc; we describe his clinical manifestations, radiological and laboratory findings as well as the pathological results and outcome.", "extra_info": {"index": 130, "original_id": "multiclinsum_test_2403_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "A 25-year-old gentleman presented with recurrent upper right vestibular abscess three months following a bimaxillary orthognathic surgery. A bonded molar orthodontic tube had dislodged into the wound during the operation. The clinical presentation initially mimics an odontogenic infection until our investigations revealed that it originated from the dislodged appliance. The abscess was drained, the wound site was explored, and the molar tube and neighbouring rigid fixation plates and screws were removed. The patient recovered well following the procedure.", "extra_info": {"index": 113, "original_id": "multiclinsum_test_1305_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "A 22-year-old male was admitted for bilateral leg tremor while standing, with symptom onset eight months prior. One month before admission, the tremor disappeared in the left leg but persisted in the right leg. Electromyography recorded from the right gastrocnemius revealed a 6-8\u00a0Hz tremor, which appeared when the patient was standing and disappeared when he was resting or walking. Blood screening showed a phenylalanine/tyrosine ratio of 2.06 and a phenylalanine level of 140\u00a0\u03bcmol/L. Urine metabolic screening was negative. Whole-exome sequencing confirmed the presence of a compound heterozygous mutation, c.158G\u2009>\u2009A and c.728G\u2009>\u2009A, in phenylalanine hydroxylase (PAH) gene. After three months of levodopa/benserazide tablets (250\u00a0mg, tid) and a low-phenylalanine diet treatment, the tremor disappeared.", "extra_info": {"index": 115, "original_id": "multiclinsum_test_1859_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "In this case report, we present a 16-year-old Ukrainian boy with acute hepatitis B. He had not been previously vaccinated against hepatitis B. Possible sources of infection included: a tattoo made at home, a finger cut made with hairdresser scissors during work, and unprotected sexual encounters. The clinical course of the disease was typical with jaundice and elevated aminotransferases levels without liver failure. During the follow-up visit 16 months after the onset of the disease, chronic hepatitis b was excluded but an ulcer around his anus was found. Additional tests for sexually transmitted diseases were ordered and they were positive for syphilis. The extended interview revealed that the patient had several unprotected bisexual encounters, which may have indicated a potential source of infections including the hepatitis B virus (HBV).", "extra_info": {"index": 123, "original_id": "multiclinsum_test_3310_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "We report a case of an isolated intracranial RDD in a 53-year-old man. The patient had an episode of generalized seizures. Imaging studies of the brain were compatible with a meningioma en plaque. The mass was exposed by a right frontotemporal craniotomy. The tumor was adhered tightly to the adjacent cerebral cortex and was permeated by pial arteries of the brain surface. The sacrificing of these arteries was inevitable in order to achieve the total removal of the tumor. The patient had incomplete left hemiparesis after the surgery. Brain computed tomography (CT) imaging revealed a postoperative hemorrhage and a low-density lesion in the right frontal lobe. The patient was postoperatively diagnosed with isolated central nervous system RDD.", "extra_info": {"index": 125, "original_id": "multiclinsum_test_1592_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "44-year-old African black patient of Burkinabe origin with no other medical history, admitted for chronic inflammatory low back pain associated with inflammatory right knee pain and a cough with phlegm. This symptomatology had been developing for seven months in a febrile context and with a general deterioration in health. The examination showed oligoarthritis of the right sternoclavicular joint and the left knee, associated with a pulmonary condensation syndrome and pleural effusion, a cold abscess at the level of the right sternoclavicular joint and a fistulous and purulent right inguinal lymphadenopathy. The biology showed an inflammatory syndrome. The GeneXpert test was positive in the sputum, without resistance to rifampicin. The intradermal reaction to the tuberculin was positive. The thoracic tomodensitometry showed a right sternoclavicular osteoarthritis and a spondylodiscitis of the L3-L4 spine. The standard radiography of the left knee objectified signs in favour of arthritis. The diagnosis of tuberculosis with multifocal, pleuropulmonary and ganglionar bone involvement was retained. The patient was given usual analgesics and antituberculous. The evolution was favourable.\n", "extra_info": {"index": 111, "original_id": "multiclinsum_test_3332_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "A case report of an 84-year old male, who presented with an aggressively recurrent form of MCC on the lower lip, on the background of an 8-year history of untreated CLL. During the recurrences of MCC, coexisting regional lymphadenopathy, posed a problem in the differential diagnosis and treatment of lymph node involvement. Histopathology and immunoistochemistry showed that submandibular lymphadenopathy coexisting with the second recurrence of MCC, was due to B-cell small lymphocytic lymphoma. The subsequent and more aggressive recurrence of the skin tumor had involved the superficial and deep cervical lymph nodes. Surgical excision followed by involved field radiation therapy has been proven effective for both malignancies.", "extra_info": {"index": 128, "original_id": "multiclinsum_test_1953_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "A 42-year-old female with history of uterine fibroids was admitted with abdominal pain and intraperitoneal fluid of unknown etiology. She was initially managed nonoperatively and empirically treated with broad spectrum antibiotics. Blood and urine cultures were unrevealing. Increasing abdominal pain and peritoneal fluid prompted diagnostic laparoscopy which revealed a dense fibrinous exudate covering the entire peritoneal cavity. Peritoneal fluid and biopsies were sent for cytology and culture. The peritoneal fluid was eventually sent for 16\u2009s ribosomal analysis, which discovered Mycoplasma hominis RNA. Her antibiotics were narrowed, and she eventually made a full recovery.", "extra_info": {"index": 127, "original_id": "multiclinsum_test_1099_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "We report a case of VEO-IBD associated with a monogenic mutation in a 2-year-old girl presenting mainly with gastrointestinal symptoms, including recurrent hematochezia and abdominal pain for more than 3 months. A gastroscopy revealed erosive gastritis and bulbar duodenitis, while a colonoscopy indicated erosive colitis. Abnormal results were obtained from the dihydrohodamine (DHR) assay and immunoglobulin testing. Whole-exome sequencing identified a heterozygous and de novo nonsense mutation (c.388\u00a0C\u2009>\u2009T; p.R130X) in the CYBB gene leading to deficiency of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (NOX2) (encoded by CYBB), a critical component of phagocytes. HSCT was performed successfully, and the DHR assay showed that normal neutrophil function was restored. Six months after HSCT, clinical remission was observed, and a repeat colonoscopy revealed intestinal mucosal healing was attained.", "extra_info": {"index": 121, "original_id": "multiclinsum_test_533_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "A 5-year-old girl with high-grade conventional osteosarcoma in the left distal femur underwent a series of surgeries. After three cycles of neoadjuvant chemotherapy, limb-salvage surgery was planned because femoral rotationplasty had been refused. At 6\u2009years and 2\u2009months old, distal femoral resection and temporary spacer insertion using a 7-mm-diameter intramedullary nail and molded polymethylmethacrylate was performed. At 7\u2009years and 8\u2009months old, secondary surgery was performed because the first spacer had been dislocated and the residual femur became atrophic. The distal end of the residual femur was removed by 1\u2009cm, but the periosteum and induced membrane around polymethylmethacrylate was preserved. In order to stabilize the spacer against the tibia, a custom-made ceramic spacer with a smooth straight 8-mm-diameter stem was utilized. The bone-spacer junction was fixed with polymethylmethacrylate and then covered with the preserved periosteum and induced membrane. After surgery, the bone atrophy improved. At 9\u2009years and 7\u2009months old, the second spacer was removed because it had loosened, and the knee joint was reconstructed using a custom-made growing femoral prosthesis with a curved porous 8.5-mm-diameter stem. Cancellous bone tips from the proximal tibia were grafted around the bone-prosthesis junction underneath the induced membrane. At 10\u2009years and 5\u2009months old, the patient was able to walk unsupported and a radiograph showed further thickening of the cortex of the residual femur without any stress shielding. Although having 5\u2009cm of limb length discrepancy, the patient and her mother were satisfied with the function. The MSTS score was 24 out of 30 points. Repeated limb length extensions are planned.", "extra_info": {"index": 117, "original_id": "multiclinsum_test_1775_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "We present the case of a 16-year-old Persian man diagnosed as having a non-invasive form of multiple endocrine neoplasia 2B (medullary thyroid cancer, mucosal neuroma of the tongue, lips and inner eyelids). Our patient, who had a positive family history of medullary thyroid cancer, was of normal height with no signs of marfanoid habitus.", "extra_info": {"index": 159, "original_id": "multiclinsum_test_2043_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "An 86-year-old male was admitted to our hospital with congestive heart failure due to low-flow low-gradient severe AS, a membranous VSD, a sub-aortic band, and a double-chambered right ventricle (RV). The patient was not deemed to be a surgical candidate because of advanced age and frailty even though surgical aortic valve replacement, VSD closure, sub-aortic band resection, and myectomy of RV would be considered as definitive treatment. Instead, we performed TAVI and VSD orifice closure using the skirt part of the self-expanding valve (26\u2005mm Evolut Pro Plus\u2122) because VSD occluder is not approved and thus not available in our country. The trans-catheter procedure resulted in a reduction of the mean aortic valve pressure gradient improved from 33 to 2\u2005mmHg and a decrease in the shunt flow (Qp/Qs) from 1.9 to 1.2. The patient\u2019s heart failure improved, and he was discharged to home 7 days after the procedure. He remained well and had not been admitted to hospital since discharge.", "extra_info": {"index": 154, "original_id": "multiclinsum_test_3275_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "We report a case study with a 44-year-old man from Faryab Province in Afghanistan who presented chest pain and dizziness while suffering a common cold. After full investigation, the patient underwent coronary angiography which showed a myocardial bridge at the middle portion of the left anterior descending artery (LAD) with a significant stenosis causing ischemia. We treated the patient with a calcium channel blocker as initial treatment. The patient tolerated the medication well and remained asymptomatic during two years follow-up.", "extra_info": {"index": 167, "original_id": "multiclinsum_test_3208_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": "Here, we report the first clinical case of a cerebral nocardiosis revealed after seizure in a patient treated by pembrolizumab for a metastatic lung cancer, in the absence of any additional immunosuppressive therapy or risk factors for cerebral nocardiosis. The extended evaluation including a brain CT-scan did not reveal any lesion before pembrolizumab. Nevertheless, the 3-month delay between the start of Pembrolizumab and the diagnosis of cerebral nocardiosis suggests that the infection occurred prior to the CPI. Unfortunately, the patient died during treatment for cerebral nocardiosis, while the lung cancer tumor mass had decreased by 80% after the sixth cycle of pembrolizumab.", "extra_info": {"index": 157, "original_id": "multiclinsum_test_2333_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "We report the case of a 72-year-old Caucasian woman with full-thickness rectal prolapse associated with fecal incontinence from severe neuromuscular damage.", "extra_info": {"index": 165, "original_id": "multiclinsum_test_2449_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "It is a case report of a 13-year-old girl with the history of swelling over her right hand for 5 months. X-ray revealed that there was an osteolytic fusiform expansible lesion. The biopsy sent and it conferred the diagnosis of GCT. Dorsal approach used for the enbloc resection of the fifth metacarpals (except at the base) and partial excision of the surrounding muscles done. The capsule and collateral ligament of the fifth metacarpophalangeal joint were left. The fourth metatarsal was harvested from the foot along with its capsule and collateral ligament of the metatarsophalangeal joint and sutured to the counter capsuloligamentous structure at the recipient site.", "extra_info": {"index": 163, "original_id": "multiclinsum_test_2668_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "In this report, we present the case of an RSV-associated death of a child who was born at full-term and developed normally up to the age of 2 years old. Cardiopulmonary arrest occurred within 3 days after the onset of symptoms, which included cough and high fever. Complete brain edema was prominent, and encephalopathy was developing. Viral antigen detection and microbiome analyses of oral swab and nasopharyngeal aspirate specimens verified an RSV infection, while bacterial culture of blood specimens yielded negative results. The RSV strain detected in this patient was subtyped as RSVB9, and no mutation was found in the six antigenic sites for targeted drugs or vaccines.", "extra_info": {"index": 161, "original_id": "multiclinsum_test_3147_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "We present the case of a middle-aged patient diagnosed with a giant gastric GIST, which presented for intermittent gastric outlet obstruction symptoms, and emphasize the major imagistic, histopathological, and therapeutic challenges that may be encountered. There are only several cases of gastric exophytic gastric GIST provoking intermittent gastric outlet obstruction. Tumor resection should be adapted to every patient's status, focused on en bloc extraction, with preservation of invaded organs as much as possible.", "extra_info": {"index": 169, "original_id": "multiclinsum_test_1842_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "A 71-year-old female who was being treated for type 2 diabetes with canagliflozin, metformin, and saxagliptin orally presented to the ED for evaluation of reduced oral intake, malaise, nausea, and abdominal pain. Although her blood glucose was not severely elevated (259 mg/dL), there was notable ketoacidosis (pH\u20096.89; CO2, 11.4\u2009mmHg; HCO3, 1.9\u2009mEq/L; base excess, - 31.3\u2009mmol/L; 3-hydroxybutyric acid > 10,000\u2009\u03bcmol/L) was observed. The uncontrolled acidosis improved following 3\u2009days of continuous renal replacement therapy, but elevated urinary glucose continued for more than 10\u2009days. Ringer's lactated fluid supplementation was continued for management of polyurea and glucosuria. Urinary glucose turned negative on day 16, and there was improvement in the patient's overall state; hence, she was discharged on day 18.", "extra_info": {"index": 2, "original_id": "multiclinsum_test_99_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "A 27-year-old male with a relapsed acute lymphoblastic leukemia presented with five-day-old polyarthralgia. He also had febrile neutropenia, cellulitis without abscesses, and methicillin-resistant Staphylococcus aureus bacteremia for which he received therapy with oxacillin and cefepime. However, the febrile neutropenia persisted, and an invasive fungal infection was suspected. A new set of blood cultures was taken and antifungal treatment was initiated. Arthroconidia were identified in the blood cultures and a matrix-assisted laser desorption ionization-mass spectrometry confirmed the presence of Geotrichum spp. Antifungal treatment was adjusted to 14 days of deoxycholate amphotericin B and four weeks of voriconazole. After a prolonged stay, he was discharged.\n", "extra_info": {"index": 3, "original_id": "multiclinsum_test_3210_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": "We present a case of subacute cervical cerebrospinal fluid (CSF) leak resulting from chiropractic manipulation of the cervical spine. The patient is a 29-year-old female who received manipulation one week prior to developing symptoms of severe orthostatic headache, nausea, and vomiting. Magnetic resonance imaging (MRI) revealed a new C5-C6 ventral CSF collection. Symptomatic onset corresponded with the recent cervical chiropractic adjustment. We present serial imaging correlating with her symptomatology and review the pertinent literature on complications of chiropractic manipulation.", "extra_info": {"index": 5, "original_id": "multiclinsum_test_2542_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "We presented an interesting case of a 33-year-old female with a solitary polypoid nodule without apparent pigmentation on her vulvar skin. Her medical history was unclear, no ulcer was seen in the lesion area, and dermatoscopy was indicated a possible tumorous change, which has caught the attention of clinicians, and then further examined by the pathologist. The final diagnosis was nodular malignant melanoma (NM) (Breslow thickness 9.5mm, Clark level 4).", "extra_info": {"index": 156, "original_id": "multiclinsum_test_1142_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "52-year-old female patient who reported chronic, burning pain radiating to the distal phalanx of the thumb with no traumatic history, which had been present for two years and limited her daily activities. The exploration was complemented with interphalangeal Doppler ultrasound, which is an excellent alternative due to its easy accessibility. A glomus tumor in the interphalangeal phalanx of the thumb was diagnosed. A H-approach was performed on the interphalangeal fold with subungual dissection and resection of the tumoral piece and follow-up by an external consultation where the surgical wound was found to be healing adequately. Physical exploration with the ability to mobilize the interphalangeal distal joint (IFD) and visual analogue scale (VAS) of 1 point. The anatomopathological evaluation reported the existence of a glomus tumor.\n", "extra_info": {"index": 158, "original_id": "multiclinsum_test_3249_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "A 62-year-old previously healthy Sri Lankan native male from the Western province of Sri Lanka presented with high fever with malaise, myalgia and arthralgia for 17 days. On the 5th day of illness he developed intermittent resting tremor in his right arm and leg associated with stiffness, difficulty in carrying out normal work and difficulty in smiling. He denied similar previous episodes. There were no other associated neurological manifestations. Clinical examination revealed a high amplitude low frequency resting tremor in his right hand, a mask-like face and increased muscle tone limited to the right side with normal reflexes. The rest of the system examination was normal except for an eschar over the abdomen. His investigations revealed lymphocytic leukocytosis, high erythrocyte sedimentation rate and immunofluorescence assay-IgM and IgG against Orientia tsutsugamushi Karp antigen were positive with rising titers. With oral doxycycline and azithromycin his fever settled within 48 h and a complete recovery of Parkinson's features was observed within 2 weeks.", "extra_info": {"index": 155, "original_id": "multiclinsum_test_146_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "A 39-year-old woman, who visited to our hospital complaining of worsened right low back pain and fever, was diagnosed with right hydronephrosis due to ureteropelvic junction obstruction by contrast-enhanced computed tomography. Intraoperatively before the planned robot-assisted laparoscopic pyeloplasty, retrograde pyelography was performed to reveal concomitant ipsilateral retrocaval ureter. Laparoscopically, ureteropelvic junction obstruction due to aberrant blood vessel and coexisting retrocaval ureter was confirmed. Transposition of the ureter from posterior to anterior of the inferior vena cava and following dismembered pyeloplasty was performed. Two years after surgery, her right hydronephrosis improved and she had no complain of any symptom.", "extra_info": {"index": 162, "original_id": "multiclinsum_test_1681_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "A 15-year-old boy who was previously diagnosed with SRU presented to our office with rectal bleeding, mucoid discharge, and abdominal pain. Additional colonoscopy evaluation revealed multiple polyposes varying in size and shape limited to the rectum. Histologic examination revealed a characteristic cap of granulation tissue covering tortuous nondysplastic crypts in the inflamed stroma, indicating that SRU had transformed into CP. Based on the assessments, we planned to perform endoscopic mucosal resection of the lesions in multiple sessions.", "extra_info": {"index": 164, "original_id": "multiclinsum_test_2219_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "We present a case of 62-year-old male who presented after experiencing syncope and cardiac arrest. Given the clinical presentation and electrocardiographic findings, there was concern for acute coronary syndrome. However, coronary angiogram did not reveal significant coronary obstruction. Due to the unclear nature of his presentation, a bedside echocardiogram was rapidly performed and was indicative of right ventricular strain. Due to these findings, a pulmonary angiogram was performed that revealed massive pulmonary embolism. He successfully underwent catheter-directed thrombolysis and, after a prolonged hospital stay, was discharged home on lifelong anticoagulation.", "extra_info": {"index": 168, "original_id": "multiclinsum_test_2976_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "The authors report on a case of acute primary Cytomegalovirus infection complicated with acute appendicitis due to Cytomegalovirus in an apparently immunocompetent 24-year-old Caucasian man also suffering from primary sclerosing cholangitis and ulcerative colitis. Diagnosis was based on clinical manifestations, serology results, as well as microbiological and histological findings. Treatment consisted of surgery and anti-Cytomegalovirus therapy.", "extra_info": {"index": 1, "original_id": "multiclinsum_test_2576_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "We report the case of a 51-year-old Caucasian woman who presented with SAPHO syndrome with mainly axial involvement. She had been treated with sulfasalazine and anti-inflammatory drugs for many years without any success. A few weeks after starting treatment with tofacitinib, both clinical and biological parameters dramatically improved. Imaging also showed considerable regression of the vertebral and pelvic lesions. However, tofacitinib had to be discontinued due to the occurrence of pulmonary embolism. Consequently, recurrence of bone pain and biologic inflammation was rapidly observed.", "extra_info": {"index": 0, "original_id": "multiclinsum_test_787_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "Our patient was a 39-year-old Chinese woman who had a history of two cesarean sections and one miscarriage. She had a recurrent anterior abdominal wall mass around her cesarean scar, and the mass was initially suspected of being choriocarcinoma of unknown origin. The patient had concomitant negative or mildly increased serum \u03b2-human chorionic gonadotropin at follow-up and no abnormal vaginal bleeding or abdominal pain. However, she underwent local excision twice and had two courses of chemotherapy with an etoposide and cisplatin regimen. She finally opted for exploratory laparotomy with abdominal wall lesion removal, subtotal hysterectomy, bilateral salpingectomy, and left ovarian cyst resection, which showed the abdominal wall lesion, whose components were revealed by microscopy and immunohistochemical staining to be approximately 90% epithelioid trophoblastic tumors and 10% choriocarcinomas from a solely extrauterine mixed gestational trophoblastic neoplasm around an abdominal wall cesarean scar.", "extra_info": {"index": 166, "original_id": "multiclinsum_test_2114_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "We report a 53-year-old female from a rural area in China who was hospitalized for lower limb edema, abdominal distension, cirrhosis, and hypothyroidism. We excluded the common causes of liver disease (drinking alcohol, using traditional Chinese medicines, hepatitis virus infection, autoimmunity, and hepatolenticular degeneration). When she was 23-years-old, she developed night-blindness that worsened to complete blindness, with no obvious cause. Her parents were first cousins, and both were alive. Analysis of the patient's family history indicated that all 5 siblings had night blindness and impaired vision; one sister was completely blind; and another sister had night-blindness complicated with cirrhosis and subclinical hypothyroidism. Entire exome sequencing showed that the patient, parents, and siblings all had mutations in the cytochrome P450 4V2 gene (CYP4V2). The CYP4V2 mutations of the parents and two sisters were heterozygous, and the others were homozygous. Two siblings also had heterozygous dual oxidase activator 2 (DUOXA2) mutations.", "extra_info": {"index": 160, "original_id": "multiclinsum_test_2430_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying etiologies such as diabetes, hypertension, and glomerular injury, with biomarkers like estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR) serving as key indicators of disease severity and progression. Management strategies include pharmacological interventions, blood pressure control, dietary modifications, and monitoring of renal function over time to prevent end-stage renal disease (ESRD).\"\n}", "ground_truth": "Herein we present a 63-year-old man with idiopathic spontaneous intraperitoneal hemorrhage (ISIH) caused by spontaneous rupture of non-aneurysmal inferior pancreaticoduodenalartery (IPDA).", "extra_info": {"index": 4, "original_id": "multiclinsum_test_45_en.txt", "split": "test", "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring are often recommended to support kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Declining glomerular filtration rate (GFR) is a key biomarker for chronic kidney disease progression, and early intervention through pharmacological management, dietary modification, and monitoring of biomarkers such as serum creatinine and proteinuria is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 75-year-old man.", "The patient presented with fever.", "The patient presented with right chest pain.", "The blood biochemical tests showed lactate dehydrogenase (LDH) of 251 IU/L.", "The blood biochemical tests showed alkaline phosphatase (ALP) of 469 IU/L.", "The blood biochemical tests showed gamma-glutamyl transferase (\u03b3-GTP) of 125 IU/L.", "The blood biochemical tests showed creatinine (Cre) of 1.43 mg/dL.", "The blood biochemical tests showed C-reactive protein (CRP) of 3.04 mg/dL.", "The blood biochemical tests showed squamous cell carcinoma-related antigen (SCC) of 1.8 ng/mL.", "The blood biochemical tests showed nerve specific enolase (NSE) of 21.6 ng/mL.", "The blood biochemical tests showed soluble interleukin-2 receptor (SIL-2R) of 614 U/mL.", "Computed tomography (CT) showed a huge 10-cm mass under the right diaphragm.", "The tumor showed minor enhancement in the lower density areas close to the fat.", "The tumor showed gradual, heterogeneous mild enhancement of tumor and liver margins.", "The main feeder for the tumor is the right inferior phrenic artery.", "The tumor was supposed to be a sarcomatoid malignancy originating from the diaphragm.", "No findings were suggesting obvious pulmonary invasion.", "Magnetic resonance imaging (MRI) demonstrated heterogeneous high signal intensity on T2-weighted images (T2WI).", "Magnetic resonance imaging (MRI) demonstrated heterogeneous high signal intensity on diffusion-weighted images (DWI).", "Contrast-enhanced MRI showed gradual heterogeneous enhancement similar to CT findings.", "Findings of extrahepatic development were also obtained.", "The possibility of adhesion to the liver was suspected.", "Fluorodeoxyglucose-positron emission tomography (FDG-PET) revealed abnormal uptake in the tumor with a maximal standardized uptake value (SUVmax) of 4.6.", "The uptake was not so high.", "A myxoid type sarcoma, such as myxoid liposarcoma, or benign tumor was considered.", "A definitive diagnosis could not be achieved.", "We scheduled a diaphragmatic resection for suspicion of benign tumors of the diaphragm.", "We performed extended right posterior segmentectomy with combined resection of the diaphragm.", "The total operation time was 8 h 10 m.", "The total blood loss was 1459 mL.", "The major diameter of the diaphragmatic defect was 12 cm.", "Simple closure was possible.", "The patient\u2019s postoperative course was uneventful.", "The patient was discharged 14 days after surgery.", "Pathological findings showed the mass was located just below the hepatic capsule/intraparenchymal space.", "The mass was adherent to the diaphragm.", "There was no continuity with the diaphragm.", "Mitosis was unremarkable, about 0\u20131 cells/10 HPF.", "The morphology suggested low-grade mesenchymal tumors such as solitary fibrous tumor (SFT) and perivascular epithelioid cell tumor (PEComa).", "Immunostaining was negative for these tumors.", "The diagnosis was difficult.", "The tumor was diagnosed as a spindle cell tumor with smooth muscle differentiation.", "The diagnosis was based on positive results of myosin markers such as \u03b1SMA, desmin, and h-caldesmon.", "Some areas with high proliferative activity were observed.", "1 year has passed since the surgery with no recurrence."], "summary_subclaims": ["A 75-year-old man presented with fever and right chest pain.", "He was suspected of a giant primary diaphragmatic tumor of extrahepatic origin by imaging studies.", "The preoperative differential diagnosis included benign masses such as myxoid sarcoma and schwannoma.", "We planned a diaphragmatic resection.", "Intraoperatively, dissection of the tumor from the liver was not possible.", "An extended right posterior segmentectomy with combined resection of the diaphragm was required.", "The patient had a good postoperative course.", "One year has passed since the surgery with no recurrence.", "The mass was located just below the hepatic capsule/parenchymal region.", "The mass was adherent to the diaphragm, but there was no continuity.", "The morphology suggested a low-grade mesenchymal tumor such as a solitary fibrous tumor and perivascular epithelioid cell tumor.", "Immunostaining was negative.", "Some areas of high proliferative activity were observed.", "The diagnosis of primary spindle cell tumor of the liver with smooth muscle differentiation was made.", "The diagnosis was based on the positive results of muscle markers such as \u03b1SMA, desmin, and h-caldesmon."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 75-year-old man.", "The patient presented with fever.", "The patient presented with right chest pain.", "The blood biochemical tests showed lactate dehydrogenase (LDH) of 251 IU/L.", "The blood biochemical tests showed alkaline phosphatase (ALP) of 469 IU/L.", "The blood biochemical tests showed gamma-glutamyl transferase (\u03b3-GTP) of 125 IU/L.", "The blood biochemical tests showed creatinine (Cre) of 1.43 mg/dL.", "The blood biochemical tests showed C-reactive protein (CRP) of 3.04 mg/dL.", "The blood biochemical tests showed squamous cell carcinoma-related antigen (SCC) of 1.8 ng/mL.", "The blood biochemical tests showed nerve specific enolase (NSE) of 21.6 ng/mL.", "The blood biochemical tests showed soluble interleukin-2 receptor (SIL-2R) of 614 U/mL.", "Computed tomography (CT) showed a huge 10-cm mass under the right diaphragm.", "The tumor showed minor enhancement in the lower density areas close to the fat.", "The tumor showed gradual, heterogeneous mild enhancement of tumor and liver margins.", "The main feeder for the tumor is the right inferior phrenic artery.", "The tumor was supposed to be a sarcomatoid malignancy originating from the diaphragm.", "No findings were suggesting obvious pulmonary invasion.", "Magnetic resonance imaging (MRI) demonstrated heterogeneous high signal intensity on T2-weighted images (T2WI).", "Magnetic resonance imaging (MRI) demonstrated heterogeneous high signal intensity on diffusion-weighted images (DWI).", "Contrast-enhanced MRI showed gradual heterogeneous enhancement similar to CT findings.", "Findings of extrahepatic development were also obtained.", "The possibility of adhesion to the liver was suspected.", "Fluorodeoxyglucose-positron emission tomography (FDG-PET) revealed abnormal uptake in the tumor with a maximal standardized uptake value (SUVmax) of 4.6.", "The uptake was not so high.", "A myxoid type sarcoma, such as myxoid liposarcoma, or benign tumor was considered.", "A definitive diagnosis could not be achieved.", "We scheduled a diaphragmatic resection for suspicion of benign tumors of the diaphragm.", "We performed extended right posterior segmentectomy with combined resection of the diaphragm.", "The total operation time was 8 h 10 m.", "The total blood loss was 1459 mL.", "The major diameter of the diaphragmatic defect was 12 cm.", "Simple closure was possible.", "The patient\u2019s postoperative course was uneventful.", "The patient was discharged 14 days after surgery.", "Pathological findings showed the mass was located just below the hepatic capsule/intraparenchymal space.", "The mass was adherent to the diaphragm.", "There was no continuity with the diaphragm.", "Mitosis was unremarkable, about 0\u20131 cells/10 HPF.", "The morphology suggested low-grade mesenchymal tumors such as solitary fibrous tumor (SFT) and perivascular epithelioid cell tumor (PEComa).", "Immunostaining was negative for these tumors.", "The diagnosis was difficult.", "The tumor was diagnosed as a spindle cell tumor with smooth muscle differentiation.", "The diagnosis was based on positive results of myosin markers such as \u03b1SMA, desmin, and h-caldesmon.", "Some areas with high proliferative activity were observed.", "1 year has passed since the surgery with no recurrence."], "index": 25, "original_id": "multiclinsum_test_447_en.txt", "split": "test", "summary_subclaims": ["A 75-year-old man presented with fever and right chest pain.", "He was suspected of a giant primary diaphragmatic tumor of extrahepatic origin by imaging studies.", "The preoperative differential diagnosis included benign masses such as myxoid sarcoma and schwannoma.", "We planned a diaphragmatic resection.", "Intraoperatively, dissection of the tumor from the liver was not possible.", "An extended right posterior segmentectomy with combined resection of the diaphragm was required.", "The patient had a good postoperative course.", "One year has passed since the surgery with no recurrence.", "The mass was located just below the hepatic capsule/parenchymal region.", "The mass was adherent to the diaphragm, but there was no continuity.", "The morphology suggested a low-grade mesenchymal tumor such as a solitary fibrous tumor and perivascular epithelioid cell tumor.", "Immunostaining was negative.", "Some areas of high proliferative activity were observed.", "The diagnosis of primary spindle cell tumor of the liver with smooth muscle differentiation was made.", "The diagnosis was based on the positive results of muscle markers such as \u03b1SMA, desmin, and h-caldesmon."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring are often recommended to support kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Declining glomerular filtration rate (GFR) is a key biomarker for chronic kidney disease progression, and early intervention through pharmacological management, dietary modification, and monitoring of biomarkers such as serum creatinine and proteinuria is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 33-year-old woman.", "She was referred to the department with unstable angina.", "At the age of six, she underwent CABG to the second diagonal branch using the left internal thoracic artery.", "At the age of six, she underwent CABG to the obtuse marginal branch using a saphenous vein graft.", "At the age of six, she underwent mitral annuloplasty.", "The initial CABG was performed for congenital LMCA.", "The initial CABG was performed for moderate mitral regurgitation.", "After the initial operation, 18 years passed without any signs of angina.", "At the age of 24, she started to experience occasional chest pain on exertion.", "By the age of 32, the chest pain had become more frequent.", "Exercise stress myocardial perfusion scintigraphy revealed an extensive ischemic lesion on the left ventricular anterior wall.", "A coronary angiogram showed a patent LITA to the second diagonal branch.", "A coronary angiogram showed a patent SVG to the obtuse marginal branch.", "The LAD was not perfused by the LITA.", "The LAD was mainly supplied by collateral flow from the right coronary artery.", "Multidetector-row computed tomography demonstrated a disruption of blood flow to the LAD from the LITA.", "The disruption of blood flow to the LAD was due to an occlusion of the proximal part of the second diagonal branch.", "To improve the ischemia of the LAD lesion, a redo CABG using the right internal thoracic artery was performed.", "The distal LAD was too small to be grafted.", "The proximal LAD was deep in the myocardium.", "A bypass was performed to the first diagonal branch, which was connected to the LAD.", "Postoperative coronary angiogram showed that all bypass grafts, including the RITA, were patent.", "Postoperative coronary angiogram showed blood flow communication between the first diagonal branch and the LAD.", "Pharmacologic stress perfusion scintigraphy revealed an improvement in the ischemia, especially in the left intraventricular septum.", "The patient\u2019s symptoms improved.", "She was discharged 10 days after surgery.", "She has been in good health for over 3 years without recurrence of chest symptoms."], "summary_subclaims": ["The patient is a 33-year-old woman.", "She was referred to the department with unstable angina.", "At the age of 6, she had undergone coronary artery bypass grafting of the second diagonal branch using the left internal thoracic artery.", "At the age of 6, she had undergone coronary artery bypass grafting of the obtuse marginal branch using saphenous vein grafting.", "The bypass grafting at age 6 was performed for left main coronary atresia.", "A coronary angiogram showed a patent left internal thoracic artery graft to the second diagonal branch.", "A coronary angiogram showed a patent saphenous vein graft to the obtuse marginal branch.", "The left anterior descending artery was not being perfused by the grafts.", "The disruption of blood flow to the left anterior descending artery was from the left internal thoracic artery.", "We performed a redo coronary artery bypass grafting using the in situ right internal thoracic artery to the first diagonal branch.", "The graft was to be connected to the left anterior descending artery.", "The redo bypass grafting resulted in amelioration of the ischemia of the left anterior wall.", "The patient was discharged 10 days after the operation.", "The patient has been in good health for over 3 years without recurrence of chest symptoms."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 33-year-old woman.", "She was referred to the department with unstable angina.", "At the age of six, she underwent CABG to the second diagonal branch using the left internal thoracic artery.", "At the age of six, she underwent CABG to the obtuse marginal branch using a saphenous vein graft.", "At the age of six, she underwent mitral annuloplasty.", "The initial CABG was performed for congenital LMCA.", "The initial CABG was performed for moderate mitral regurgitation.", "After the initial operation, 18 years passed without any signs of angina.", "At the age of 24, she started to experience occasional chest pain on exertion.", "By the age of 32, the chest pain had become more frequent.", "Exercise stress myocardial perfusion scintigraphy revealed an extensive ischemic lesion on the left ventricular anterior wall.", "A coronary angiogram showed a patent LITA to the second diagonal branch.", "A coronary angiogram showed a patent SVG to the obtuse marginal branch.", "The LAD was not perfused by the LITA.", "The LAD was mainly supplied by collateral flow from the right coronary artery.", "Multidetector-row computed tomography demonstrated a disruption of blood flow to the LAD from the LITA.", "The disruption of blood flow to the LAD was due to an occlusion of the proximal part of the second diagonal branch.", "To improve the ischemia of the LAD lesion, a redo CABG using the right internal thoracic artery was performed.", "The distal LAD was too small to be grafted.", "The proximal LAD was deep in the myocardium.", "A bypass was performed to the first diagonal branch, which was connected to the LAD.", "Postoperative coronary angiogram showed that all bypass grafts, including the RITA, were patent.", "Postoperative coronary angiogram showed blood flow communication between the first diagonal branch and the LAD.", "Pharmacologic stress perfusion scintigraphy revealed an improvement in the ischemia, especially in the left intraventricular septum.", "The patient\u2019s symptoms improved.", "She was discharged 10 days after surgery.", "She has been in good health for over 3 years without recurrence of chest symptoms."], "index": 31, "original_id": "multiclinsum_test_2205_en.txt", "split": "test", "summary_subclaims": ["The patient is a 33-year-old woman.", "She was referred to the department with unstable angina.", "At the age of 6, she had undergone coronary artery bypass grafting of the second diagonal branch using the left internal thoracic artery.", "At the age of 6, she had undergone coronary artery bypass grafting of the obtuse marginal branch using saphenous vein grafting.", "The bypass grafting at age 6 was performed for left main coronary atresia.", "A coronary angiogram showed a patent left internal thoracic artery graft to the second diagonal branch.", "A coronary angiogram showed a patent saphenous vein graft to the obtuse marginal branch.", "The left anterior descending artery was not being perfused by the grafts.", "The disruption of blood flow to the left anterior descending artery was from the left internal thoracic artery.", "We performed a redo coronary artery bypass grafting using the in situ right internal thoracic artery to the first diagonal branch.", "The graft was to be connected to the left anterior descending artery.", "The redo bypass grafting resulted in amelioration of the ischemia of the left anterior wall.", "The patient was discharged 10 days after the operation.", "The patient has been in good health for over 3 years without recurrence of chest symptoms."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring are often recommended to support kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Declining glomerular filtration rate (GFR) is a key biomarker for chronic kidney disease progression, and early intervention through pharmacological management, dietary modification, and monitoring of biomarkers such as serum creatinine and proteinuria is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 25-year-old male.", "He presented to an outside emergency department with a five-day history of cough.", "He had a five-day history of shortness of breath.", "He had a five-day history of nasal congestion.", "He had a five-day history of fatigue.", "He had a five-day history of loss of taste and smell.", "He had a past medical history of asthma.", "He had morbid obesity with a BMI of 50.5 kg/m2.", "He had no known connective tissue disease.", "He had no known hypertrophic scarring reactions.", "He had a 2-year history of vaping.", "He quit vaping one month prior to presentation.", "He had a positive COVID-19 test three days prior to admission.", "He was hypoxic to 88% on room air in the ED.", "He improved to 90% saturation on 3 L nasal cannula.", "Venous blood gas revealed a normal venous pH of 7.4.", "Venous blood gas revealed an increased PCO2 of 50.", "Chest x-ray revealed bilateral airspace disease consistent with known COVID-19 infection.", "He was admitted to the MICU.", "He was treated with Remdesivir.", "He was treated with high dose steroids.", "He became febrile to 102.9 F.", "He required 15 L O2 via high-flow nasal cannula.", "D-dimer was normal at 0.28.", "His respiratory status continued to decline over the night of admission.", "He required BiPAP with a minute volume of 25 L.", "He required BiPAP with a respiratory rate of 40.", "He required intubation.", "He was started on ceftriaxone due to SIRS criteria.", "He was started on azithromycin due to SIRS criteria.", "He was started on ceftriaxone due to an elevated procalcitonin.", "He was started on azithromycin due to an elevated procalcitonin.", "Oxygen saturation was 92% on 100% FiO2 via ventilator.", "Repeat CXR revealed diffuse bilateral interstitial infiltrates.", "A SARS-COV-2-IGG antibody was non-reactive.", "He received a transfusion of convalescent plasma.", "Oxygen saturation was 53% despite maximal ventilatory support.", "He was transferred to our institution for ECMO consideration.", "Upon arrival, he went directly to the hybrid operating room.", "He underwent unremarkable cannulation with no repositioning required.", "He was supported on V-V ECMO for 14 days.", "He was weaned gradually from the circuit for bedside decannulation on POD 16.", "He was maintained on heparin for anticoagulation.", "Chart review showed he was never subtherapeutic on unfractionated heparin.", "Attempts to remove the cannula at the bedside failed due to immobility of the cannula.", "An ultrasound of the right neck was unremarkable.", "A longitudinal cutdown from the insertion site proceeding caudally was performed.", "The cannula was freely mobile to the level of the first rib and clavicle.", "The cannula was not obstructing the vein.", "An upper sternotomy, confined to the manubrium, was performed.", "The superior vena cava and proximal jugular vein were dissected.", "A 2 cm segment of the distal SVC and proximal jugular vein was densely sclerosed and adherent to the cannula.", "The vessel was opened across the adherent area at the level of the innominate vein.", "The cannula was then able to be withdrawn without difficulty.", "There was no evidence of thrombosis at the site of cannula adhesion.", "There was no evidence of scarring at the site of cannula adhesion.", "There was no evidence of local inflammation at the site of cannula adhesion.", "The distal SVC was repaired to the level of the innominate vein entry to the SVC.", "The jugular vein was ligated proximally and distally.", "The patient suffered no ill effects.", "The patient had an unremarkable recovery to discharge.", "Clinic follow-up demonstrated no sequelae or serious adverse events.", "The Crescent catheter was examined by pathology at our institution.", "The Crescent catheter was returned to the company.", "Neither the catheter nor the company found any defects.", "At our institution, we use Avalon, Crescent, and ProTek Duo cannulas.", "We have never experienced adhesions with any of the cannulas."], "summary_subclaims": ["The patient was a 25 y.o. with COVID-19 respiratory failure.", "The patient required ECMO support for 16-days.", "A 32 Fr crescent cannula became adherent to the SVC and proximal jugular vein.", "Attempts to remove the cannula at the bedside failed due to immobility of the cannula.", "Ultrasound of the right neck was unremarkable.", "The patient was taken to the hybrid OR.", "TEE and fluoroscopy were unrevealing.", "An upper sternotomy was performed.", "The superior vena cava and proximal jugular vein were dissected.", "A 2 cm segment of the distal SVC and proximal jugular vein was densely sclerosed and adherent to the cannula.", "The vessel was opened across the adherent area at the level of the innominate vein.", "The cannula was then able to be withdrawn.", "The patient suffered no ill effects.", "The patient had an unremarkable recovery to discharge."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 25-year-old male.", "He presented to an outside emergency department with a five-day history of cough.", "He had a five-day history of shortness of breath.", "He had a five-day history of nasal congestion.", "He had a five-day history of fatigue.", "He had a five-day history of loss of taste and smell.", "He had a past medical history of asthma.", "He had morbid obesity with a BMI of 50.5 kg/m2.", "He had no known connective tissue disease.", "He had no known hypertrophic scarring reactions.", "He had a 2-year history of vaping.", "He quit vaping one month prior to presentation.", "He had a positive COVID-19 test three days prior to admission.", "He was hypoxic to 88% on room air in the ED.", "He improved to 90% saturation on 3 L nasal cannula.", "Venous blood gas revealed a normal venous pH of 7.4.", "Venous blood gas revealed an increased PCO2 of 50.", "Chest x-ray revealed bilateral airspace disease consistent with known COVID-19 infection.", "He was admitted to the MICU.", "He was treated with Remdesivir.", "He was treated with high dose steroids.", "He became febrile to 102.9 F.", "He required 15 L O2 via high-flow nasal cannula.", "D-dimer was normal at 0.28.", "His respiratory status continued to decline over the night of admission.", "He required BiPAP with a minute volume of 25 L.", "He required BiPAP with a respiratory rate of 40.", "He required intubation.", "He was started on ceftriaxone due to SIRS criteria.", "He was started on azithromycin due to SIRS criteria.", "He was started on ceftriaxone due to an elevated procalcitonin.", "He was started on azithromycin due to an elevated procalcitonin.", "Oxygen saturation was 92% on 100% FiO2 via ventilator.", "Repeat CXR revealed diffuse bilateral interstitial infiltrates.", "A SARS-COV-2-IGG antibody was non-reactive.", "He received a transfusion of convalescent plasma.", "Oxygen saturation was 53% despite maximal ventilatory support.", "He was transferred to our institution for ECMO consideration.", "Upon arrival, he went directly to the hybrid operating room.", "He underwent unremarkable cannulation with no repositioning required.", "He was supported on V-V ECMO for 14 days.", "He was weaned gradually from the circuit for bedside decannulation on POD 16.", "He was maintained on heparin for anticoagulation.", "Chart review showed he was never subtherapeutic on unfractionated heparin.", "Attempts to remove the cannula at the bedside failed due to immobility of the cannula.", "An ultrasound of the right neck was unremarkable.", "A longitudinal cutdown from the insertion site proceeding caudally was performed.", "The cannula was freely mobile to the level of the first rib and clavicle.", "The cannula was not obstructing the vein.", "An upper sternotomy, confined to the manubrium, was performed.", "The superior vena cava and proximal jugular vein were dissected.", "A 2 cm segment of the distal SVC and proximal jugular vein was densely sclerosed and adherent to the cannula.", "The vessel was opened across the adherent area at the level of the innominate vein.", "The cannula was then able to be withdrawn without difficulty.", "There was no evidence of thrombosis at the site of cannula adhesion.", "There was no evidence of scarring at the site of cannula adhesion.", "There was no evidence of local inflammation at the site of cannula adhesion.", "The distal SVC was repaired to the level of the innominate vein entry to the SVC.", "The jugular vein was ligated proximally and distally.", "The patient suffered no ill effects.", "The patient had an unremarkable recovery to discharge.", "Clinic follow-up demonstrated no sequelae or serious adverse events.", "The Crescent catheter was examined by pathology at our institution.", "The Crescent catheter was returned to the company.", "Neither the catheter nor the company found any defects.", "At our institution, we use Avalon, Crescent, and ProTek Duo cannulas.", "We have never experienced adhesions with any of the cannulas."], "index": 29, "original_id": "multiclinsum_test_2039_en.txt", "split": "test", "summary_subclaims": ["The patient was a 25 y.o. with COVID-19 respiratory failure.", "The patient required ECMO support for 16-days.", "A 32 Fr crescent cannula became adherent to the SVC and proximal jugular vein.", "Attempts to remove the cannula at the bedside failed due to immobility of the cannula.", "Ultrasound of the right neck was unremarkable.", "The patient was taken to the hybrid OR.", "TEE and fluoroscopy were unrevealing.", "An upper sternotomy was performed.", "The superior vena cava and proximal jugular vein were dissected.", "A 2 cm segment of the distal SVC and proximal jugular vein was densely sclerosed and adherent to the cannula.", "The vessel was opened across the adherent area at the level of the innominate vein.", "The cannula was then able to be withdrawn.", "The patient suffered no ill effects.", "The patient had an unremarkable recovery to discharge."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring are often recommended to support kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Declining glomerular filtration rate (GFR) is a key biomarker for chronic kidney disease progression, and early intervention through pharmacological management, dietary modification, and monitoring of biomarkers such as serum creatinine and proteinuria is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["On the 5th of August, 2020, a 58-year-old woman presented in our emergency department with seizures and hemiparesis.", "She had a prior fever, malaise, and dry cough a week before admission.", "She has had a history of hypertension since a year ago.", "The vital sign is within normal limit except the blood pressure is 170/110 mmHg.", "The results of the laboratory test were high blood glucose 254 mg/dL and HbA1C 6.5%.", "Leukocytosis with white blood cells (WBC) was 14/L and neutrophil-lymphocyte ratio (NLR) was 33.", "Increase level of erythrocyte sedimentation rate (ESR) 93 mm/h, D-dimer 21,176 ng/mL, and fibrinogen 446 mg/dL.", "The result of the reverse transcription-polymerase chain reaction (rt-PCR) test from the nasal swab was observed to be positive for SARS-CoV-2.", "Head contrast computed tomography (HCCT) showed cerebral edema at the right parietal lobe.", "There were hyperdense veins and sinuses at the right parietal lobe area, superior sagittal sinus (SSS), and bilateral transverse sinuses (TS), which suggested the presence of a cerebral sinus venous thrombosis (CSVT), with a sign of venal hypertension.", "CT venography (CTV) was also confirmed CSVT at SSS, bilateral TS, and bilateral sigmoid sinus.", "The thorax CT scan showed ground-glass opacity and subpleural bilateral, with a fibrotic appearance in the left lung.", "During the patient\u2019s treatment of COVID-19, 60 mg subcutaneous enoxaparin was administered twice daily, for 5 days.", "On the 5th day of treatment, D-dimer was decreased to 2092 ng/ml.", "The decision was made to continue with enoxaparin until the normal D-dimer or the patient\u2019s negative status for the COVID-19 virus is attained.", "Other clinical manifestations also improved and the patient was discharged from the hospital on the 10th day.", "The second case, a 72-year-old male, was consulted from the intensive care unit (ICU) because of sudden decreases in consciousness.", "He had a history of high fever, dry cough, and shortness of breath a week before hospitalization.", "The patient was being treated as severe COVID-19 with ARDS for 10 days in ICU.", "He had no previous history of hypertension, diabetes mellitus, or cardiovascular disease.", "He already received heparin intravenously for 10 days and halted, due to good recovery of shortness of breath and hypoxemia.", "A day after heparin cessation, the patient suddenly unconscious and intubated due to severe hypoxia.", "Upon examination, his consciousness is coma with a slow response to the light of both eyes.", "He had hypothermia with a temperature of 35.4 \u00b0C, blood pressure of 140/69 mmHg on vasoconstrictor epinephrine support, and 90% oxygen saturation.", "Laboratory test showed, critical increase level of WBC (53.09 \u00d7 103/L) and NLR 58.1.", "We did not do a peripheral blood smear to examine any hematological disorder.", "Coagulation function tests were APTT 20.2 s, PT 11.9 s, INR 1.11, D-dimer 5.308 ng/mL (previous was > 50,000), and fibrinogen 525 mg/dL.", "The rt-PCR test from a nasopharyngeal swab sample was negative for SARS-CoV-2 on the 11th day.", "Head non-contrast computed tomography (NCCT) showed hyperdense at superior sagittal sinus and right transverse sinuses, which suggested the manifestations of CSVT.", "There was associated cerebral edema at the left frontal, parietal lobe, and cerebellum.", "Thorax CT scan showed ground-glass opacity and subpleural bilateral with the fibrotic appearance in both lung and pulmonary angiography.", "Thrombosis at segments 8 and 9 of both lungs was also observed.", "The pulmonary CT-angiography (CTA) results were pulmonary embolism and thrombosis of both the left and right pulmonary arteries.", "Due to the massive thrombosis, a decision was made to administer streptokinase and heparin, to the patient intravenously.", "After 3 days of this treatment, the patient became desaturated (40% oxygen saturation) with spontaneous pneumothorax and passed away the next day."], "summary_subclaims": ["Two cases of cerebral sinus venous thrombosis in COVID-19 patients were reported.", "The cases were following respiratory, hematology, and coagulation disarrangements.", "The disarrangements were triggered by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection.", "The first patient was presented with a seizure.", "The first patient had hypertension as a comorbidity.", "The first patient had diabetes mellitus as a comorbidity.", "The latter case had no comorbidity.", "The latter case showed more severe presentations of COVID-19 such as brain and lung thrombosis.", "The latter case already had several days of intravenous anticoagulant administrations.", "These two cases also have a different course of disease and outcomes."]}, "extra_info": {"fulltext_subclaims": ["On the 5th of August, 2020, a 58-year-old woman presented in our emergency department with seizures and hemiparesis.", "She had a prior fever, malaise, and dry cough a week before admission.", "She has had a history of hypertension since a year ago.", "The vital sign is within normal limit except the blood pressure is 170/110 mmHg.", "The results of the laboratory test were high blood glucose 254 mg/dL and HbA1C 6.5%.", "Leukocytosis with white blood cells (WBC) was 14/L and neutrophil-lymphocyte ratio (NLR) was 33.", "Increase level of erythrocyte sedimentation rate (ESR) 93 mm/h, D-dimer 21,176 ng/mL, and fibrinogen 446 mg/dL.", "The result of the reverse transcription-polymerase chain reaction (rt-PCR) test from the nasal swab was observed to be positive for SARS-CoV-2.", "Head contrast computed tomography (HCCT) showed cerebral edema at the right parietal lobe.", "There were hyperdense veins and sinuses at the right parietal lobe area, superior sagittal sinus (SSS), and bilateral transverse sinuses (TS), which suggested the presence of a cerebral sinus venous thrombosis (CSVT), with a sign of venal hypertension.", "CT venography (CTV) was also confirmed CSVT at SSS, bilateral TS, and bilateral sigmoid sinus.", "The thorax CT scan showed ground-glass opacity and subpleural bilateral, with a fibrotic appearance in the left lung.", "During the patient\u2019s treatment of COVID-19, 60 mg subcutaneous enoxaparin was administered twice daily, for 5 days.", "On the 5th day of treatment, D-dimer was decreased to 2092 ng/ml.", "The decision was made to continue with enoxaparin until the normal D-dimer or the patient\u2019s negative status for the COVID-19 virus is attained.", "Other clinical manifestations also improved and the patient was discharged from the hospital on the 10th day.", "The second case, a 72-year-old male, was consulted from the intensive care unit (ICU) because of sudden decreases in consciousness.", "He had a history of high fever, dry cough, and shortness of breath a week before hospitalization.", "The patient was being treated as severe COVID-19 with ARDS for 10 days in ICU.", "He had no previous history of hypertension, diabetes mellitus, or cardiovascular disease.", "He already received heparin intravenously for 10 days and halted, due to good recovery of shortness of breath and hypoxemia.", "A day after heparin cessation, the patient suddenly unconscious and intubated due to severe hypoxia.", "Upon examination, his consciousness is coma with a slow response to the light of both eyes.", "He had hypothermia with a temperature of 35.4 \u00b0C, blood pressure of 140/69 mmHg on vasoconstrictor epinephrine support, and 90% oxygen saturation.", "Laboratory test showed, critical increase level of WBC (53.09 \u00d7 103/L) and NLR 58.1.", "We did not do a peripheral blood smear to examine any hematological disorder.", "Coagulation function tests were APTT 20.2 s, PT 11.9 s, INR 1.11, D-dimer 5.308 ng/mL (previous was > 50,000), and fibrinogen 525 mg/dL.", "The rt-PCR test from a nasopharyngeal swab sample was negative for SARS-CoV-2 on the 11th day.", "Head non-contrast computed tomography (NCCT) showed hyperdense at superior sagittal sinus and right transverse sinuses, which suggested the manifestations of CSVT.", "There was associated cerebral edema at the left frontal, parietal lobe, and cerebellum.", "Thorax CT scan showed ground-glass opacity and subpleural bilateral with the fibrotic appearance in both lung and pulmonary angiography.", "Thrombosis at segments 8 and 9 of both lungs was also observed.", "The pulmonary CT-angiography (CTA) results were pulmonary embolism and thrombosis of both the left and right pulmonary arteries.", "Due to the massive thrombosis, a decision was made to administer streptokinase and heparin, to the patient intravenously.", "After 3 days of this treatment, the patient became desaturated (40% oxygen saturation) with spontaneous pneumothorax and passed away the next day."], "index": 27, "original_id": "multiclinsum_test_445_en.txt", "split": "test", "summary_subclaims": ["Two cases of cerebral sinus venous thrombosis in COVID-19 patients were reported.", "The cases were following respiratory, hematology, and coagulation disarrangements.", "The disarrangements were triggered by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection.", "The first patient was presented with a seizure.", "The first patient had hypertension as a comorbidity.", "The first patient had diabetes mellitus as a comorbidity.", "The latter case had no comorbidity.", "The latter case showed more severe presentations of COVID-19 such as brain and lung thrombosis.", "The latter case already had several days of intravenous anticoagulant administrations.", "These two cases also have a different course of disease and outcomes."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring are often recommended to support kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Declining glomerular filtration rate (GFR) is a key biomarker for chronic kidney disease progression, and early intervention through pharmacological management, dietary modification, and monitoring of biomarkers such as serum creatinine and proteinuria is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["A 20-year-old man presented to the emergency department after four days of progressively worsening periumbilical pain.", "He was moving heavy boxes for his job when he began experiencing pain.", "He reported pain with defecation.", "He denied fever, chills, nausea, emesis, weight loss, and recent travel or illness.", "Past surgical history included branchial cleft cyst excision as a child.", "On abdominal exam, a one square-centimeter erythematous infra-umbilical mass was exquisitely tender to palpation.", "Laboratory data on admission demonstrated a WBC count of 10.7 \u00d7 103 cells/\u03bcL.", "Urinalysis was unremarkable.", "The patient underwent diagnostic evaluation for suspected incarcerated umbilical hernia.", "CT abdomen/pelvis revealed a four-centimeter segment of organized periumbilical inflammation with central lucency passing the ventral abdominal wall into the anterior abdominal compartment.", "The process was extraperitoneal.", "There was no evidence of communication with the urinary bladder.", "These findings were consistent with an inflamed urachal remnant complicated by abscess.", "The patient received intravenous antibiotics in preparation for an operation.", "The patient underwent abscess incision and drainage followed immediately by urachal cyst excision through a four-centimeter infra-umbilical midline mini-laparotomy.", "The urachal cyst and remnants were dissected inferiorly to confirm no communication with the urinary bladder before total excision.", "Investigation of the cyst contents revealed white sebaceous material.", "Pathology examined the 4 \u00d7 3 x 0.7-centimeter segment of fibromembranous tissue.", "Pathology confirmed intraoperative impressions of the specimen.", "The patient was admitted to the surgical floor.", "The patient noted his pain was markedly improved.", "The patient was discharged to home on post-operative day two with adequate pain control.", "Two-week follow up in the outpatient surgery clinic confirmed an uncomplicated recovery."], "summary_subclaims": ["The patient is a 20-year-old man.", "The patient presented with periumbilical pain.", "Physical exam showed a warm, erythematous infra-umbilical mass.", "The mass was tender to palpation.", "CT revealed an infected urachal cyst.", "The patient underwent urachal abscess incision and drainage.", "The patient underwent cyst excision.", "The patient returned home on postoperative day two.", "Two-week outpatient follow-up confirmed an uncomplicated recovery."]}, "extra_info": {"fulltext_subclaims": ["A 20-year-old man presented to the emergency department after four days of progressively worsening periumbilical pain.", "He was moving heavy boxes for his job when he began experiencing pain.", "He reported pain with defecation.", "He denied fever, chills, nausea, emesis, weight loss, and recent travel or illness.", "Past surgical history included branchial cleft cyst excision as a child.", "On abdominal exam, a one square-centimeter erythematous infra-umbilical mass was exquisitely tender to palpation.", "Laboratory data on admission demonstrated a WBC count of 10.7 \u00d7 103 cells/\u03bcL.", "Urinalysis was unremarkable.", "The patient underwent diagnostic evaluation for suspected incarcerated umbilical hernia.", "CT abdomen/pelvis revealed a four-centimeter segment of organized periumbilical inflammation with central lucency passing the ventral abdominal wall into the anterior abdominal compartment.", "The process was extraperitoneal.", "There was no evidence of communication with the urinary bladder.", "These findings were consistent with an inflamed urachal remnant complicated by abscess.", "The patient received intravenous antibiotics in preparation for an operation.", "The patient underwent abscess incision and drainage followed immediately by urachal cyst excision through a four-centimeter infra-umbilical midline mini-laparotomy.", "The urachal cyst and remnants were dissected inferiorly to confirm no communication with the urinary bladder before total excision.", "Investigation of the cyst contents revealed white sebaceous material.", "Pathology examined the 4 \u00d7 3 x 0.7-centimeter segment of fibromembranous tissue.", "Pathology confirmed intraoperative impressions of the specimen.", "The patient was admitted to the surgical floor.", "The patient noted his pain was markedly improved.", "The patient was discharged to home on post-operative day two with adequate pain control.", "Two-week follow up in the outpatient surgery clinic confirmed an uncomplicated recovery."], "index": 39, "original_id": "multiclinsum_test_1897_en.txt", "split": "test", "summary_subclaims": ["The patient is a 20-year-old man.", "The patient presented with periumbilical pain.", "Physical exam showed a warm, erythematous infra-umbilical mass.", "The mass was tender to palpation.", "CT revealed an infected urachal cyst.", "The patient underwent urachal abscess incision and drainage.", "The patient underwent cyst excision.", "The patient returned home on postoperative day two.", "Two-week outpatient follow-up confirmed an uncomplicated recovery."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring are often recommended to support kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Declining glomerular filtration rate (GFR) is a key biomarker for chronic kidney disease progression, and early intervention through pharmacological management, dietary modification, and monitoring of biomarkers such as serum creatinine and proteinuria is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was a 29-year-old male.", "The patient's chief complaints were pain and instability on his left knee.", "He got injured when playing futsal with knee twisted externally.", "He suffered severe pain, swollen and difficult to walk.", "The MRI examination after the injury revealed ACL and PCL rupture of the left knee.", "He underwent arthroscopic surgical reconstruction for both ACL and PCL by previous surgeon.", "Two years after surgery, he felt instability, swollen knee without pain.", "On the physical examination, posterior sagging was found.", "The posterior drawer test was positive.", "The quadriceps active test was positive.", "The anterior Lachman test for anterior cruciate ligament was negative.", "On the MRI, failure of PCL graft with intact ACL was found.", "On the MRI and three dimensional CT scan, the tibial tunnel placement done in previous surgery was not placed on its anatomical position.", "The tunnel was placed too anterior to the PCL footprint.", "We performed the PCL revision reconstruction surgery.", "We performed the arthroscopic-assisted reconstruction surgery using transseptal portal approach.", "We avoided to use only the jig to guide us when tunnelling the tibia.", "We used additional technique to see the posterior aspect of proximal tibia clearly.", "We chose to make a transseptal portal that penetrated from posteromedial side of the knee inside-out to the posterolateral side of the knee.", "An incision was made on the posteromedial side of the knee with guidance of arthroscopic view and also transiluminatic arthroscopic light.", "Blunt obturator with sheath was inserted gently passed through intercondylar notch to posterolateral side of the knee.", "We made inside-out incision on it.", "During arthroscopy procedure, the PCL was gone with small PCL remnant on femoral site.", "The ACL was still intact and adequately attached.", "We performed the reconstruction of PCL using peroneus longus tendon as the graft from the left ankle.", "When tunneling the tibia, we used jig guide for tibial tunnel placement.", "We also made a transseptal portal from medial to lateral in order to get better view of posterior aspect of the tibia.", "We used it as the graft because hamstring tendon was already used in previous surgery.", "The post-operative X-ray of the left knee showed tibial tunnel was revised to appropriate site of its footprint.", "The shadow of two endobuttons on the medial femoral condyle was seen because the endobutton of previous surgery was not removed."], "summary_subclaims": ["The patient is a 29 year old male.", "The patient had total rupture of ACL and PCL.", "The patient underwent reconstruction for both ACL and PCL.", "The failure of the PCL graft occurred 2 years after the surgery.", "The failure of the PCL graft was related to the tibial tunnel placement.", "The tibial tunnel was placed not in proper anatomical site.", "We performed revision PCL surgery.", "We used transseptal portal technique.", "The transseptal portal technique was used to ensure the tibial tunnel is placed in appropriate position."]}, "extra_info": {"fulltext_subclaims": ["The patient was a 29-year-old male.", "The patient's chief complaints were pain and instability on his left knee.", "He got injured when playing futsal with knee twisted externally.", "He suffered severe pain, swollen and difficult to walk.", "The MRI examination after the injury revealed ACL and PCL rupture of the left knee.", "He underwent arthroscopic surgical reconstruction for both ACL and PCL by previous surgeon.", "Two years after surgery, he felt instability, swollen knee without pain.", "On the physical examination, posterior sagging was found.", "The posterior drawer test was positive.", "The quadriceps active test was positive.", "The anterior Lachman test for anterior cruciate ligament was negative.", "On the MRI, failure of PCL graft with intact ACL was found.", "On the MRI and three dimensional CT scan, the tibial tunnel placement done in previous surgery was not placed on its anatomical position.", "The tunnel was placed too anterior to the PCL footprint.", "We performed the PCL revision reconstruction surgery.", "We performed the arthroscopic-assisted reconstruction surgery using transseptal portal approach.", "We avoided to use only the jig to guide us when tunnelling the tibia.", "We used additional technique to see the posterior aspect of proximal tibia clearly.", "We chose to make a transseptal portal that penetrated from posteromedial side of the knee inside-out to the posterolateral side of the knee.", "An incision was made on the posteromedial side of the knee with guidance of arthroscopic view and also transiluminatic arthroscopic light.", "Blunt obturator with sheath was inserted gently passed through intercondylar notch to posterolateral side of the knee.", "We made inside-out incision on it.", "During arthroscopy procedure, the PCL was gone with small PCL remnant on femoral site.", "The ACL was still intact and adequately attached.", "We performed the reconstruction of PCL using peroneus longus tendon as the graft from the left ankle.", "When tunneling the tibia, we used jig guide for tibial tunnel placement.", "We also made a transseptal portal from medial to lateral in order to get better view of posterior aspect of the tibia.", "We used it as the graft because hamstring tendon was already used in previous surgery.", "The post-operative X-ray of the left knee showed tibial tunnel was revised to appropriate site of its footprint.", "The shadow of two endobuttons on the medial femoral condyle was seen because the endobutton of previous surgery was not removed."], "index": 23, "original_id": "multiclinsum_test_2913_en.txt", "split": "test", "summary_subclaims": ["The patient is a 29 year old male.", "The patient had total rupture of ACL and PCL.", "The patient underwent reconstruction for both ACL and PCL.", "The failure of the PCL graft occurred 2 years after the surgery.", "The failure of the PCL graft was related to the tibial tunnel placement.", "The tibial tunnel was placed not in proper anatomical site.", "We performed revision PCL surgery.", "We used transseptal portal technique.", "The transseptal portal technique was used to ensure the tibial tunnel is placed in appropriate position."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring are often recommended to support kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Declining glomerular filtration rate (GFR) is a key biomarker for chronic kidney disease progression, and early intervention through pharmacological management, dietary modification, and monitoring of biomarkers such as serum creatinine and proteinuria is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 38-year-old woman in her 19th wk of pregnancy (G2P1).", "She was referred to the clinic for a sudden persistent pain on the left side of the waist on July 28, 2017.", "The patient\u2019s physical examination revealed tenderness over the left kidney area.", "Her blood pressure was 120/85 mmHg.", "Her heart rate was 86 beats/min.", "Her body temperature was 36.8 \u00b0C.", "The patient had no significant medical history.", "She had not undergone any related abdominal examination previously.", "The patient was hospitalized and given conservative treatment.", "Her left-side waist pain continued to be intense.", "Because the size of the tumor was so large, and the fetal heart rate was unstable, the patient decided to undergo left nephrectomy after the induction of labor.", "Laboratory tests indicated that the patient\u2019s hemoglobin level was 80 g/L.", "The hematocrit was 0.242 L/L.", "On the 2nd d, hemoglobin was 95 g/L.", "The hematocrit was 0.286 L/L.", "Ultrasound examination of the urinary system revealed a giant nonhomogenous lump in the left kidney area.", "The lump had caused the left kidney to move to the midabdomen.", "The size of the lump was approximately 159 mm \u00d7 100 mm.", "The border of the lump was faintly visible.", "The lump showed a \u201cstriped sign\u201d in which the outer part was hypoechoic with a strong stripe echo.", "The inner part near the left kidney was hyperechoic.", "A stripe-shaped echoless zone was seen around the lump.", "Color Doppler flow image showed some spot-like blood flow signals around the lump.", "A hyperechoic nodule was seen in the right kidney with a size of 30 mm \u00d7 25 mm.", "There was a fetus echo in the uterus.", "Preoperative CT showed a large, mixed-density mass in the left kidney.", "The density of the area adjacent to the kidney was low.", "The area far from the kidney showed high density."], "summary_subclaims": ["The patient is a 38-year-old woman in her 19th wk of pregnancy.", "She was referred to the clinic for a sudden, persistent pain on the left side of the waist.", "She had not undergone any previous related abdominal examination.", "Ultrasound of the urinary system revealed a giant nonhomogenous lump in the left kidney area.", "The diagnosis was considered spontaneous rupture and hemorrhage of the left RAML in pregnancy via ultrasound.", "Her left-side waist pain continued to be intense.", "She underwent computed tomography, which led to the same diagnosis.", "The patient underwent left nephrectomy after the induction of labor.", "The pathological result was the rupture and hemorrhage of a vascular leiomyoma lipoma."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 38-year-old woman in her 19th wk of pregnancy (G2P1).", "She was referred to the clinic for a sudden persistent pain on the left side of the waist on July 28, 2017.", "The patient\u2019s physical examination revealed tenderness over the left kidney area.", "Her blood pressure was 120/85 mmHg.", "Her heart rate was 86 beats/min.", "Her body temperature was 36.8 \u00b0C.", "The patient had no significant medical history.", "She had not undergone any related abdominal examination previously.", "The patient was hospitalized and given conservative treatment.", "Her left-side waist pain continued to be intense.", "Because the size of the tumor was so large, and the fetal heart rate was unstable, the patient decided to undergo left nephrectomy after the induction of labor.", "Laboratory tests indicated that the patient\u2019s hemoglobin level was 80 g/L.", "The hematocrit was 0.242 L/L.", "On the 2nd d, hemoglobin was 95 g/L.", "The hematocrit was 0.286 L/L.", "Ultrasound examination of the urinary system revealed a giant nonhomogenous lump in the left kidney area.", "The lump had caused the left kidney to move to the midabdomen.", "The size of the lump was approximately 159 mm \u00d7 100 mm.", "The border of the lump was faintly visible.", "The lump showed a \u201cstriped sign\u201d in which the outer part was hypoechoic with a strong stripe echo.", "The inner part near the left kidney was hyperechoic.", "A stripe-shaped echoless zone was seen around the lump.", "Color Doppler flow image showed some spot-like blood flow signals around the lump.", "A hyperechoic nodule was seen in the right kidney with a size of 30 mm \u00d7 25 mm.", "There was a fetus echo in the uterus.", "Preoperative CT showed a large, mixed-density mass in the left kidney.", "The density of the area adjacent to the kidney was low.", "The area far from the kidney showed high density."], "index": 37, "original_id": "multiclinsum_test_1298_en.txt", "split": "test", "summary_subclaims": ["The patient is a 38-year-old woman in her 19th wk of pregnancy.", "She was referred to the clinic for a sudden, persistent pain on the left side of the waist.", "She had not undergone any previous related abdominal examination.", "Ultrasound of the urinary system revealed a giant nonhomogenous lump in the left kidney area.", "The diagnosis was considered spontaneous rupture and hemorrhage of the left RAML in pregnancy via ultrasound.", "Her left-side waist pain continued to be intense.", "She underwent computed tomography, which led to the same diagnosis.", "The patient underwent left nephrectomy after the induction of labor.", "The pathological result was the rupture and hemorrhage of a vascular leiomyoma lipoma."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring are often recommended to support kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Declining glomerular filtration rate (GFR) is a key biomarker for chronic kidney disease progression, and early intervention through pharmacological management, dietary modification, and monitoring of biomarkers such as serum creatinine and proteinuria is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 90-year-old female.", "The patient has atrial fibrillation.", "The patient is treated with therapeutic apixaban.", "The patient has aortic stenosis.", "The patient had a TAVR with a 29\u2005mm self-expanding Medtronic core-valve placed 7 years prior.", "The patient presented to the clinic for the evaluation of acute onset chest pain.", "The patient had elevated blood pressure on home monitoring of 190/90\u2005mmHg.", "The patient described the chest pain as substernal, severe, radiating posteriorly, and lasting for 45\u2005min before resolving spontaneously.", "A routine echocardiogram performed 2 months prior showed a properly functioning bioprosthetic aortic valve with normal haemodynamic performance.", "The Doppler measured peak transaortic gradient was 4\u2005mmHg.", "The mean transaortic gradient was 2\u2005mmHg.", "Vital signs in the clinic were noted as unremarkable.", "The patient was referred to the emergency department for assessment of the coronary anatomy and to rule out aortic dissection.", "During imaging, the patient developed acute respiratory failure with severe pruritis and urticaria.", "The patient was admitted for inpatient management.", "Evaluation in the emergency department was notable for the absence of hives, stridor, or other associated signs or symptoms of anaphylaxis.", "Lab evaluation demonstrated a troponin-I value of 0.22\u2005ng/mL.", "The troponin-I reference value is <0.04\u2005ng/mL.", "BNP was 514\u2005pg/mL.", "The BNP reference value is <100\u2005pg/mL.", "The patient\u2019s baseline BNP was 22\u201371\u2005pg/mL.", "The patient had a positive COVID-19 polymerase chain reaction rapid test.", "Chest x-ray was notable for diffuse interstitial pulmonary oedema.", "Electrocardiogram demonstrated sinus tachycardia with the left bundle branch block unchanged from prior.", "CT angiography of the chest ruled out acute aortic dissection.", "CT angiography ruled out pulmonary embolism.", "The patient was hospitalized for acute decompensated heart failure.", "The patient was treated with non-invasive positive pressure ventilation.", "The patient was treated with nitroglycerine infusion.", "The patient was treated with intravenous furosemide 40\u2005mg twice daily.", "The patient\u2019s respiratory status improved by Day 1 of the hospital admission.", "The peak BNP was 1649\u2005pg/mL.", "POCUS performed on hospital Day 2 was suggestive of a significant diastolic flow across the TAVR valve.", "POCUS directed further investigation for the diagnosis of prosthetic valve failure.", "TTE on hospital Day 3 revealed severe aortic regurgitation with an eccentric and anteriorly directed jet.", "TTE showed holodiastolic flow reversal in the descending thoracic aorta.", "The peak measured transaortic gradient was 9\u2005mmHg.", "The mean transaortic gradient was 5\u2005mmHg.", "The hospital system was experiencing staffing shortages and resource limitations related to an ongoing community COVID-19 surge.", "The hospital policy at the time was to delay routine TEE until patients were designated as COVID-19 recovered.", "The patient was treated for 2 days with continuous heparin infusion for presumptive treatment of acute coronary syndrome.", "The patient was restarted on therapeutic apixaban 5\u2005mg twice daily.", "The patient was discharged after 7 days.", "The patient was transitioned from intravenous furosemide to oral torsemide 20\u2005mg twice daily.", "Three days after hospital discharge, TEE confirmed proper positioning of the bioprosthetic stent-valve.", "TEE showed leaflet thickening.", "TEE showed abnormal cusp mobility.", "TEE showed restriction of the non-coronary cusp prosthetic leaflet.", "TEE showed an eccentric regurgitant jet consistent with severe aortic regurgitation.", "The acute TAVR valve regurgitation was treated with a valve-in-valve TAVR 17 days post-discharge.", "The patient was seen in the clinic 30 days after valve-in-valve TAVR.", "The patient denied chest pain.", "The patient denied dyspnoea.", "A TTE demonstrated bioprosthetic stent-valve in the aortic position.", "The TTE showed normal leaflet mobility.", "The TTE showed no paravalvular aortic regurgitation."], "summary_subclaims": ["The patient is a 90-year-old female.", "She has atrial fibrillation.", "She is on therapeutic apixaban.", "She had a transcatheter aortic valve replacement (TAVR).", "She presented with a COVID-19 infection.", "She was found to have severe bioprosthetic valvular regurgitation.", "Features were suggestive of valve thrombosis.", "She underwent valve-in-valve TAVR.", "Valvular dysfunction resolved."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 90-year-old female.", "The patient has atrial fibrillation.", "The patient is treated with therapeutic apixaban.", "The patient has aortic stenosis.", "The patient had a TAVR with a 29\u2005mm self-expanding Medtronic core-valve placed 7 years prior.", "The patient presented to the clinic for the evaluation of acute onset chest pain.", "The patient had elevated blood pressure on home monitoring of 190/90\u2005mmHg.", "The patient described the chest pain as substernal, severe, radiating posteriorly, and lasting for 45\u2005min before resolving spontaneously.", "A routine echocardiogram performed 2 months prior showed a properly functioning bioprosthetic aortic valve with normal haemodynamic performance.", "The Doppler measured peak transaortic gradient was 4\u2005mmHg.", "The mean transaortic gradient was 2\u2005mmHg.", "Vital signs in the clinic were noted as unremarkable.", "The patient was referred to the emergency department for assessment of the coronary anatomy and to rule out aortic dissection.", "During imaging, the patient developed acute respiratory failure with severe pruritis and urticaria.", "The patient was admitted for inpatient management.", "Evaluation in the emergency department was notable for the absence of hives, stridor, or other associated signs or symptoms of anaphylaxis.", "Lab evaluation demonstrated a troponin-I value of 0.22\u2005ng/mL.", "The troponin-I reference value is <0.04\u2005ng/mL.", "BNP was 514\u2005pg/mL.", "The BNP reference value is <100\u2005pg/mL.", "The patient\u2019s baseline BNP was 22\u201371\u2005pg/mL.", "The patient had a positive COVID-19 polymerase chain reaction rapid test.", "Chest x-ray was notable for diffuse interstitial pulmonary oedema.", "Electrocardiogram demonstrated sinus tachycardia with the left bundle branch block unchanged from prior.", "CT angiography of the chest ruled out acute aortic dissection.", "CT angiography ruled out pulmonary embolism.", "The patient was hospitalized for acute decompensated heart failure.", "The patient was treated with non-invasive positive pressure ventilation.", "The patient was treated with nitroglycerine infusion.", "The patient was treated with intravenous furosemide 40\u2005mg twice daily.", "The patient\u2019s respiratory status improved by Day 1 of the hospital admission.", "The peak BNP was 1649\u2005pg/mL.", "POCUS performed on hospital Day 2 was suggestive of a significant diastolic flow across the TAVR valve.", "POCUS directed further investigation for the diagnosis of prosthetic valve failure.", "TTE on hospital Day 3 revealed severe aortic regurgitation with an eccentric and anteriorly directed jet.", "TTE showed holodiastolic flow reversal in the descending thoracic aorta.", "The peak measured transaortic gradient was 9\u2005mmHg.", "The mean transaortic gradient was 5\u2005mmHg.", "The hospital system was experiencing staffing shortages and resource limitations related to an ongoing community COVID-19 surge.", "The hospital policy at the time was to delay routine TEE until patients were designated as COVID-19 recovered.", "The patient was treated for 2 days with continuous heparin infusion for presumptive treatment of acute coronary syndrome.", "The patient was restarted on therapeutic apixaban 5\u2005mg twice daily.", "The patient was discharged after 7 days.", "The patient was transitioned from intravenous furosemide to oral torsemide 20\u2005mg twice daily.", "Three days after hospital discharge, TEE confirmed proper positioning of the bioprosthetic stent-valve.", "TEE showed leaflet thickening.", "TEE showed abnormal cusp mobility.", "TEE showed restriction of the non-coronary cusp prosthetic leaflet.", "TEE showed an eccentric regurgitant jet consistent with severe aortic regurgitation.", "The acute TAVR valve regurgitation was treated with a valve-in-valve TAVR 17 days post-discharge.", "The patient was seen in the clinic 30 days after valve-in-valve TAVR.", "The patient denied chest pain.", "The patient denied dyspnoea.", "A TTE demonstrated bioprosthetic stent-valve in the aortic position.", "The TTE showed normal leaflet mobility.", "The TTE showed no paravalvular aortic regurgitation."], "index": 35, "original_id": "multiclinsum_test_303_en.txt", "split": "test", "summary_subclaims": ["The patient is a 90-year-old female.", "She has atrial fibrillation.", "She is on therapeutic apixaban.", "She had a transcatheter aortic valve replacement (TAVR).", "She presented with a COVID-19 infection.", "She was found to have severe bioprosthetic valvular regurgitation.", "Features were suggestive of valve thrombosis.", "She underwent valve-in-valve TAVR.", "Valvular dysfunction resolved."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring are often recommended to support kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Declining glomerular filtration rate (GFR) is a key biomarker for chronic kidney disease progression, and early intervention through pharmacological management, dietary modification, and monitoring of biomarkers such as serum creatinine and proteinuria is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["On 24 November 2012, a 31-year-old woman was diagnosed as a suspected rabies case by the First Affiliated Hospital of Zhengzhou University.", "The hospital reported the case to the Henan Center for Disease Control and Prevention (CDC).", "A detailed epidemiological investigation of the suspected rabies case was performed.", "The woman was a farmer living in a rural area of Xuchang, Henan Province, China.", "She lived with her husband and two sons.", "She said she had not travelled anywhere recently.", "At about 17:00 on 25 August 2012, the woman and her 7-year-old son were attacked by a stray dog while walking nearby to their village.", "The woman sustained bites on her right thigh.", "Her son had bites on his left calf.", "Villagers caught and killed the dog.", "The dog was buried on the village outskirts without laboratory investigation for RV.", "The mother washed the son\u2019s bites with municipal tap water shortly after the incident.", "On 26 August, the son received a rabies vaccine at the healthcare unit in their village.", "He completed a full course of standard vaccines.", "The vaccine used was freeze-dried rabies vaccine for human use [Vero cells], produced by Liaoning Chengda Biotechnology Co., Ltd.", "The vaccination regimen was five doses on days 0, 3, 7, 14, and 28.", "The mother did not recognize the risk posed to her by the dog bite.", "She only washed her own wounds the following day, following the doctor\u2019s advice.", "She declined the rabies vaccine for economic reasons.", "Both the mother\u2019s and son\u2019s wounds were determined by the doctor to constitute category III exposure bites.", "Category III exposure bites are defined by the World Health Organization (WHO) as single or multiple transdermal bites or scratches; contamination of mucous membrane with saliva.", "Neither the mother nor her son were treated as recommended by the WHO for category III rabies exposure.", "WHO-recommended treatment for category III rabies exposure includes wound cleaning, rabies vaccination, and direct wound infiltration with rabies immunoglobulin (RIG).", "The rabies vaccine is not in the Chinese National Immunization Scheme.", "Rabies vaccine and RIG are currently provided for a fee in China.", "On 20 November 2012, the woman presented with a persistent fever (39 \u00b0C), nausea, vomiting, chest tightness, and agitation to the Xiangcheng County People\u2019s Hospital.", "She received a diagnosis of encephalitis.", "She was treated for 2 days with cefoperazone, sulbactam, levofloxacin, and supportive treatment.", "On 22 November, her symptoms worsened and she developed a mild coma, drooling, and melena.", "She was then transferred to the Xuchang City Central Hospital.", "On 24 November, she was transferred to the First Affiliated Hospital of Zhengzhou University.", "She received a diagnosis of suspected rabies.", "She was treated with symptomatic and supportive therapies.", "Her condition continued to deteriorate.", "She died on 6 December 2012.", "On 4 December 2012, saliva, serum, and cerebrospinal fluid (CSF) from the patient were collected.", "On 15 December 2012, a serum sample was collected from her son, who was in good health when sampled.", "Both sets of specimens were transported under refrigeration to the Henan CDC for testing.", "Total ribonucleic acid (RNA) was extracted from the CSF and saliva.", "RNA was reverse transcribed to cDNA.", "RV N and G genes were amplified using nested polymerase chain reaction (PCR).", "Negative controls (RNAse-free water) and positive controls were included in each set of reactions.", "Amplification products were detected after electrophoresis using 2% agarose gel.", "The N and G genes were amplified from the woman patient\u2019s saliva.", "The N and G genes were not amplified from her CSF.", "Amplification products were purified and sequenced using an automated ABI 3730 DNA Sequencer.", "Molecular phylogenetic analysis was conducted using the maximum likelihood method based on the Kimura\u2019s two parameter model with MEGA 5 software.", "The nucleotide sequence from the female (Henan) patient (Henan JSS, GenBank accession number KP221203) G protein was compared against nucleotide sequences of G protein genes from RV identified in GenBank.", "Henan JSS, along with previous Henan RV strains, the Chinese vaccine strain, and 8743THA, were grouped into GT1.", "Rabies virus neutralizing antibody (RVNA) titers in the sera were assayed by a standard rapid fluorescent focus inhibition test with some modifications.", "A serum specimen from the patient was collected on day 12 of her illness.", "Her son\u2019s serum was collected 3 months after the bites.", "The mother\u2019s serum RVNA titer was 0.68 IU/ml.", "The son\u2019s serum RVNA titer was 2.29 IU/ml.", "The mother and son were considered positive according to the diagnosis criteria for RVNA reactions.", "The diagnosis criteria for RVNA reactions define RVNA titers \u22650.05 IU/ml as the WHO recommended protective level.", "Because the son did not receive immediate RIG treatment, he remained at possible risk for RV infection.", "RVNA of the son has been actively monitored.", "His health condition has been assessed every 6 months post his initial result.", "The son is alive and healthy after 2 years of follow-up."], "summary_subclaims": ["In August 2012, a woman and her son were attacked by a stray dog in Henan, China.", "The son received rabies postexposure prophylaxis.", "The son's postexposure prophylaxis included wound treatment followed by vaccine.", "The son's postexposure prophylaxis did not include immunoglobulin.", "The mother did not receive rabies postexposure prophylaxis.", "Rabies infection was laboratory confirmed in the mother.", "The mother died in December.", "The son is alive and healthy after 2 years of follow-up."]}, "extra_info": {"fulltext_subclaims": ["On 24 November 2012, a 31-year-old woman was diagnosed as a suspected rabies case by the First Affiliated Hospital of Zhengzhou University.", "The hospital reported the case to the Henan Center for Disease Control and Prevention (CDC).", "A detailed epidemiological investigation of the suspected rabies case was performed.", "The woman was a farmer living in a rural area of Xuchang, Henan Province, China.", "She lived with her husband and two sons.", "She said she had not travelled anywhere recently.", "At about 17:00 on 25 August 2012, the woman and her 7-year-old son were attacked by a stray dog while walking nearby to their village.", "The woman sustained bites on her right thigh.", "Her son had bites on his left calf.", "Villagers caught and killed the dog.", "The dog was buried on the village outskirts without laboratory investigation for RV.", "The mother washed the son\u2019s bites with municipal tap water shortly after the incident.", "On 26 August, the son received a rabies vaccine at the healthcare unit in their village.", "He completed a full course of standard vaccines.", "The vaccine used was freeze-dried rabies vaccine for human use [Vero cells], produced by Liaoning Chengda Biotechnology Co., Ltd.", "The vaccination regimen was five doses on days 0, 3, 7, 14, and 28.", "The mother did not recognize the risk posed to her by the dog bite.", "She only washed her own wounds the following day, following the doctor\u2019s advice.", "She declined the rabies vaccine for economic reasons.", "Both the mother\u2019s and son\u2019s wounds were determined by the doctor to constitute category III exposure bites.", "Category III exposure bites are defined by the World Health Organization (WHO) as single or multiple transdermal bites or scratches; contamination of mucous membrane with saliva.", "Neither the mother nor her son were treated as recommended by the WHO for category III rabies exposure.", "WHO-recommended treatment for category III rabies exposure includes wound cleaning, rabies vaccination, and direct wound infiltration with rabies immunoglobulin (RIG).", "The rabies vaccine is not in the Chinese National Immunization Scheme.", "Rabies vaccine and RIG are currently provided for a fee in China.", "On 20 November 2012, the woman presented with a persistent fever (39 \u00b0C), nausea, vomiting, chest tightness, and agitation to the Xiangcheng County People\u2019s Hospital.", "She received a diagnosis of encephalitis.", "She was treated for 2 days with cefoperazone, sulbactam, levofloxacin, and supportive treatment.", "On 22 November, her symptoms worsened and she developed a mild coma, drooling, and melena.", "She was then transferred to the Xuchang City Central Hospital.", "On 24 November, she was transferred to the First Affiliated Hospital of Zhengzhou University.", "She received a diagnosis of suspected rabies.", "She was treated with symptomatic and supportive therapies.", "Her condition continued to deteriorate.", "She died on 6 December 2012.", "On 4 December 2012, saliva, serum, and cerebrospinal fluid (CSF) from the patient were collected.", "On 15 December 2012, a serum sample was collected from her son, who was in good health when sampled.", "Both sets of specimens were transported under refrigeration to the Henan CDC for testing.", "Total ribonucleic acid (RNA) was extracted from the CSF and saliva.", "RNA was reverse transcribed to cDNA.", "RV N and G genes were amplified using nested polymerase chain reaction (PCR).", "Negative controls (RNAse-free water) and positive controls were included in each set of reactions.", "Amplification products were detected after electrophoresis using 2% agarose gel.", "The N and G genes were amplified from the woman patient\u2019s saliva.", "The N and G genes were not amplified from her CSF.", "Amplification products were purified and sequenced using an automated ABI 3730 DNA Sequencer.", "Molecular phylogenetic analysis was conducted using the maximum likelihood method based on the Kimura\u2019s two parameter model with MEGA 5 software.", "The nucleotide sequence from the female (Henan) patient (Henan JSS, GenBank accession number KP221203) G protein was compared against nucleotide sequences of G protein genes from RV identified in GenBank.", "Henan JSS, along with previous Henan RV strains, the Chinese vaccine strain, and 8743THA, were grouped into GT1.", "Rabies virus neutralizing antibody (RVNA) titers in the sera were assayed by a standard rapid fluorescent focus inhibition test with some modifications.", "A serum specimen from the patient was collected on day 12 of her illness.", "Her son\u2019s serum was collected 3 months after the bites.", "The mother\u2019s serum RVNA titer was 0.68 IU/ml.", "The son\u2019s serum RVNA titer was 2.29 IU/ml.", "The mother and son were considered positive according to the diagnosis criteria for RVNA reactions.", "The diagnosis criteria for RVNA reactions define RVNA titers \u22650.05 IU/ml as the WHO recommended protective level.", "Because the son did not receive immediate RIG treatment, he remained at possible risk for RV infection.", "RVNA of the son has been actively monitored.", "His health condition has been assessed every 6 months post his initial result.", "The son is alive and healthy after 2 years of follow-up."], "index": 43, "original_id": "multiclinsum_test_1507_en.txt", "split": "test", "summary_subclaims": ["In August 2012, a woman and her son were attacked by a stray dog in Henan, China.", "The son received rabies postexposure prophylaxis.", "The son's postexposure prophylaxis included wound treatment followed by vaccine.", "The son's postexposure prophylaxis did not include immunoglobulin.", "The mother did not receive rabies postexposure prophylaxis.", "Rabies infection was laboratory confirmed in the mother.", "The mother died in December.", "The son is alive and healthy after 2 years of follow-up."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring are often recommended to support kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Declining glomerular filtration rate (GFR) is a key biomarker for chronic kidney disease progression, and early intervention through pharmacological management, dietary modification, and monitoring of biomarkers such as serum creatinine and proteinuria is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was a 44-year-old man.", "He presented with right limb weakness and unclear speech for the past 10 h.", "He had repeated fever.", "He was diagnosed with diabetes one month before admission.", "On admission, he was delirious.", "His temperature was 38.8 \u2103.", "His right limb muscle strength was Grade IV.", "Brain MRI revealed left basal ganglia and right parietal lobe cerebral infarction.", "The infarction was consistent with embolic stroke.", "White cell count was 14.31 \u00d7 10^9/L.", "The normal range for white cell count is 3.5\u20139.5 \u00d7 10^9/L.", "Highly sensitive Troponin I was 0.08 ng/ml.", "The normal range for highly sensitive Troponin I is 0-0.0268 ng/ml.", "Chest CT showed bilateral lung markings were heavier.", "Transthoracic echocardiography showed the aortic valve was bicuspid combined with calcification.", "Transthoracic echocardiography showed moderate regurgitation.", "A 16.4 mm*7.8 mm vegetation was seen on the right posterior aortic valve.", "The patient was diagnosed with infective endocarditis.", "According to the AHA/ACC guideline, delaying valve surgery for at least 4 weeks may be considered for patients with IE and major ischemic stroke if hemodynamically stable.", "The patient was prescribed vancomycin 0.5 g every 6 h.", "Transesophageal echocardiography 10 days later showed the vegetation was smaller than before.", "The patient had no fever again.", "The patient was hemodynamically stable.", "Blood cultures were negative twice.", "Transesophageal echocardiography one month later revealed a large periaortic abscess.", "The abscess led to formation of an aortic sinus pseudoaneurysm.", "Flows were in from the pseudoaneurysm and out to the left ventricular.", "Moderate mitral valve regurgitation was present.", "Cardiopulmonary bypass and aortic valve replacement surgery via median sternotomy were performed.", "During the operation, bicuspid deformity combined with vegetation was confirmed.", "An aortic annular abscess eroded into the base of the anterior mitral leaflet.", "The anterior mitral leaflet prolapsed.", "Aortic valve vegetations and perivalvular abscesses were completely removed.", "5/0 Prolene suture was used to continuously suture bovine pericardium.", "The tissue culture of the diseased aortic valve showed no bacterial growth.", "No pathogenic microorganism was identified.", "The patient was discharged two weeks later.", "He received antibiotics for six weeks.", "During one-month follow-up, the patient felt well.", "Laboratory testing revealed that blood white cell count and percentage were normal."], "summary_subclaims": ["A 44-year-old man was admitted due to weakness of his right limbs and unclear speech for 10 h.", "He had recurrent fevers for 1 month before admission.", "Transthoracic echocardiography showed a mix-echoic vegetation attached to the bicuspid aortic valve.", "Transthoracic echocardiography showed moderate aortic regurgitation.", "Transthoracic echocardiography showed a possible aortic annular abscess.", "Blood cultures were negative.", "Empiric antibiotic therapy was begun.", "The patient did not have fever again.", "The patient seem to be clinically improved.", "Follow-up transesophageal echocardiography revealed a large periaortic abscess led to aortic sinus pseudoaneurysm.", "The patient underwent mechanical prosthetic valve replacement.", "The patient underwent annulus reconstruction.", "Perivalvular abscess may be insidious deterioration in patients who seem to be clinically improved."]}, "extra_info": {"fulltext_subclaims": ["The patient was a 44-year-old man.", "He presented with right limb weakness and unclear speech for the past 10 h.", "He had repeated fever.", "He was diagnosed with diabetes one month before admission.", "On admission, he was delirious.", "His temperature was 38.8 \u2103.", "His right limb muscle strength was Grade IV.", "Brain MRI revealed left basal ganglia and right parietal lobe cerebral infarction.", "The infarction was consistent with embolic stroke.", "White cell count was 14.31 \u00d7 10^9/L.", "The normal range for white cell count is 3.5\u20139.5 \u00d7 10^9/L.", "Highly sensitive Troponin I was 0.08 ng/ml.", "The normal range for highly sensitive Troponin I is 0-0.0268 ng/ml.", "Chest CT showed bilateral lung markings were heavier.", "Transthoracic echocardiography showed the aortic valve was bicuspid combined with calcification.", "Transthoracic echocardiography showed moderate regurgitation.", "A 16.4 mm*7.8 mm vegetation was seen on the right posterior aortic valve.", "The patient was diagnosed with infective endocarditis.", "According to the AHA/ACC guideline, delaying valve surgery for at least 4 weeks may be considered for patients with IE and major ischemic stroke if hemodynamically stable.", "The patient was prescribed vancomycin 0.5 g every 6 h.", "Transesophageal echocardiography 10 days later showed the vegetation was smaller than before.", "The patient had no fever again.", "The patient was hemodynamically stable.", "Blood cultures were negative twice.", "Transesophageal echocardiography one month later revealed a large periaortic abscess.", "The abscess led to formation of an aortic sinus pseudoaneurysm.", "Flows were in from the pseudoaneurysm and out to the left ventricular.", "Moderate mitral valve regurgitation was present.", "Cardiopulmonary bypass and aortic valve replacement surgery via median sternotomy were performed.", "During the operation, bicuspid deformity combined with vegetation was confirmed.", "An aortic annular abscess eroded into the base of the anterior mitral leaflet.", "The anterior mitral leaflet prolapsed.", "Aortic valve vegetations and perivalvular abscesses were completely removed.", "5/0 Prolene suture was used to continuously suture bovine pericardium.", "The tissue culture of the diseased aortic valve showed no bacterial growth.", "No pathogenic microorganism was identified.", "The patient was discharged two weeks later.", "He received antibiotics for six weeks.", "During one-month follow-up, the patient felt well.", "Laboratory testing revealed that blood white cell count and percentage were normal."], "index": 41, "original_id": "multiclinsum_test_885_en.txt", "split": "test", "summary_subclaims": ["A 44-year-old man was admitted due to weakness of his right limbs and unclear speech for 10 h.", "He had recurrent fevers for 1 month before admission.", "Transthoracic echocardiography showed a mix-echoic vegetation attached to the bicuspid aortic valve.", "Transthoracic echocardiography showed moderate aortic regurgitation.", "Transthoracic echocardiography showed a possible aortic annular abscess.", "Blood cultures were negative.", "Empiric antibiotic therapy was begun.", "The patient did not have fever again.", "The patient seem to be clinically improved.", "Follow-up transesophageal echocardiography revealed a large periaortic abscess led to aortic sinus pseudoaneurysm.", "The patient underwent mechanical prosthetic valve replacement.", "The patient underwent annulus reconstruction.", "Perivalvular abscess may be insidious deterioration in patients who seem to be clinically improved."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 34-year-old Caucasian woman.", "The patient was referred to the department of dermatology.", "The patient had recurrent and diffuse tinea corporis.", "The patient had recalcitrant crusted scabies.", "All studies of human subjects were approved by the Institutional Review Board of University Hospitals Case Medical Center.", "The patient provided written informed consent.", "Earlier treatments included topical ketoconazole 2% cream.", "Earlier treatments included oxiconazole nitrate 1% cream.", "Earlier treatments included permethrin 5% cream.", "The patient reported that her skin problems had been intermittent over the preceding 3 years.", "The medical history of this patient revealed end-stage renal disease requiring hemodialysis.", "The medical history of this patient revealed obesity.", "The medical history of this patient revealed non-insulin-dependent diabetes.", "The medical history of this patient revealed hypertension.", "The medical history of this patient revealed recurrent cellulitis.", "The medical history of this patient revealed methicillin-resistant Staphylococcus aureus bacteremia.", "The patient was diagnosed with bilateral cataracts.", "The patient was diagnosed with mild sensorineural hearing loss in one ear.", "Diabetes and hypertension were diagnosed with nephrotic syndrome at age 29.", "The patient began hemodialysis.", "The patient had frequent admissions for dialysis catheter site cellulitis.", "The patient had methicillin-resistant S. aureus bacteremia secondary to catheter line infections.", "The patient has lived with her maternal grandmother since birth.", "The patient had no known siblings.", "The father was unknown to the family.", "The mother reportedly died from a prescription narcotic overdose at age 29.", "There was no evidence of birth defects or immunodeficiency in the maternal family.", "The patient exhibited coarse facial features with a prominent brow ridge.", "The patient exhibited midface hypoplasia.", "The patient exhibited prognathia.", "The patient exhibited slight down slanting of palpebral fissures.", "The skin examination was significant for thick, hyperkeratotic, white, and flaking plaques on the palms.", "The skin examination was significant for thick, hyperkeratotic, white, and flaking plaques on the soles.", "The skin examination was significant for thick, hyperkeratotic, white, and flaking plaques on the digits.", "The skin examination was significant for thick, hyperkeratotic, white, and flaking plaques under the distal nails.", "Moist erosions and bright erythema along many of the proximal nail folds were noted.", "The nail plates appeared normal except distal onycholysis overlying the plaques.", "There were crusted papules and erosions diffusely scattered on the face, ears, trunk, and extremities.", "Earlier mineral oil scrapings had revealed multiple live mites.", "The exam was consistent with crusted scabies.", "A fungal culture from the nail fold grew unidentified, non-Candida yeast.", "It was recommended to the referring dermatologist that the patient continues topical antifungal treatment as needed.", "It was recommended to the referring dermatologist to begin oral ivermectin 0.2 mg/kg daily on days 1, 2, 8, 9, 15, 22, and 29.", "An undiagnosed immune syndrome with cutaneous-specific immunodeficiency was suspected.", "The patient was referred to medical genetics for evaluation.", "The patient was HIV negative.", "The patient had a normal serum protein electrophoresis interpretation.", "The patient was negative for antinuclear antibodies.", "Electrolyte panels were consistent with renal failure and routine dialysis.", "No renal biopsy had been performed.", "The white blood cell count would fluctuate between admissions.", "The patient\u2019s lymphocyte count was consistently within normal limits.", "The scabies infection resolved after 3 months using routine maintenance doses of ivermectin.", "The tinea corporis infection resolved using the daily application of topical antifungal creams."], "summary_subclaims": ["The patient was a 34-year-old.", "The patient had a cutaneous immunodeficiency.", "The patient had recurrent crusted scabies infestation.", "The patient had diffuse tinea.", "The patient had recurrent staphylococcal cellulitis.", "The patient was suspected to have an undiagnosed syndrome.", "The patient had mental retardation.", "The patient had renal failure.", "The patient had premature senescence.", "A cytogenetic fluorescence in situ hybridization analysis was performed.", "A 9.34 Mb duplication was found within the short (p) arm of chromosome 1.", "The duplication was from 1p36.11 to 1p36.21.", "An adjacent 193 kb copy gain was entirely within 1p36.11.", "Chromosome 4 had a 906 kb gain in 4p16.1.", "Chromosome 9 had an 81 kb copy gain in 9p24.3.", "Over 100 genes were localized within these duplicated regions.", "A gene expression array was performed.", "82 genes had expression changed >1.5-fold compared to a healthy age-matched skin control.", "The lipolytic enzyme arylacetamide deacetylase-like 3 was found within the duplicated 1p36 region of chromosome 1."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 34-year-old Caucasian woman.", "The patient was referred to the department of dermatology.", "The patient had recurrent and diffuse tinea corporis.", "The patient had recalcitrant crusted scabies.", "All studies of human subjects were approved by the Institutional Review Board of University Hospitals Case Medical Center.", "The patient provided written informed consent.", "Earlier treatments included topical ketoconazole 2% cream.", "Earlier treatments included oxiconazole nitrate 1% cream.", "Earlier treatments included permethrin 5% cream.", "The patient reported that her skin problems had been intermittent over the preceding 3 years.", "The medical history of this patient revealed end-stage renal disease requiring hemodialysis.", "The medical history of this patient revealed obesity.", "The medical history of this patient revealed non-insulin-dependent diabetes.", "The medical history of this patient revealed hypertension.", "The medical history of this patient revealed recurrent cellulitis.", "The medical history of this patient revealed methicillin-resistant Staphylococcus aureus bacteremia.", "The patient was diagnosed with bilateral cataracts.", "The patient was diagnosed with mild sensorineural hearing loss in one ear.", "Diabetes and hypertension were diagnosed with nephrotic syndrome at age 29.", "The patient began hemodialysis.", "The patient had frequent admissions for dialysis catheter site cellulitis.", "The patient had methicillin-resistant S. aureus bacteremia secondary to catheter line infections.", "The patient has lived with her maternal grandmother since birth.", "The patient had no known siblings.", "The father was unknown to the family.", "The mother reportedly died from a prescription narcotic overdose at age 29.", "There was no evidence of birth defects or immunodeficiency in the maternal family.", "The patient exhibited coarse facial features with a prominent brow ridge.", "The patient exhibited midface hypoplasia.", "The patient exhibited prognathia.", "The patient exhibited slight down slanting of palpebral fissures.", "The skin examination was significant for thick, hyperkeratotic, white, and flaking plaques on the palms.", "The skin examination was significant for thick, hyperkeratotic, white, and flaking plaques on the soles.", "The skin examination was significant for thick, hyperkeratotic, white, and flaking plaques on the digits.", "The skin examination was significant for thick, hyperkeratotic, white, and flaking plaques under the distal nails.", "Moist erosions and bright erythema along many of the proximal nail folds were noted.", "The nail plates appeared normal except distal onycholysis overlying the plaques.", "There were crusted papules and erosions diffusely scattered on the face, ears, trunk, and extremities.", "Earlier mineral oil scrapings had revealed multiple live mites.", "The exam was consistent with crusted scabies.", "A fungal culture from the nail fold grew unidentified, non-Candida yeast.", "It was recommended to the referring dermatologist that the patient continues topical antifungal treatment as needed.", "It was recommended to the referring dermatologist to begin oral ivermectin 0.2 mg/kg daily on days 1, 2, 8, 9, 15, 22, and 29.", "An undiagnosed immune syndrome with cutaneous-specific immunodeficiency was suspected.", "The patient was referred to medical genetics for evaluation.", "The patient was HIV negative.", "The patient had a normal serum protein electrophoresis interpretation.", "The patient was negative for antinuclear antibodies.", "Electrolyte panels were consistent with renal failure and routine dialysis.", "No renal biopsy had been performed.", "The white blood cell count would fluctuate between admissions.", "The patient\u2019s lymphocyte count was consistently within normal limits.", "The scabies infection resolved after 3 months using routine maintenance doses of ivermectin.", "The tinea corporis infection resolved using the daily application of topical antifungal creams."], "index": 33, "original_id": "multiclinsum_test_1677_en.txt", "split": "test", "summary_subclaims": ["The patient was a 34-year-old.", "The patient had a cutaneous immunodeficiency.", "The patient had recurrent crusted scabies infestation.", "The patient had diffuse tinea.", "The patient had recurrent staphylococcal cellulitis.", "The patient was suspected to have an undiagnosed syndrome.", "The patient had mental retardation.", "The patient had renal failure.", "The patient had premature senescence.", "A cytogenetic fluorescence in situ hybridization analysis was performed.", "A 9.34 Mb duplication was found within the short (p) arm of chromosome 1.", "The duplication was from 1p36.11 to 1p36.21.", "An adjacent 193 kb copy gain was entirely within 1p36.11.", "Chromosome 4 had a 906 kb gain in 4p16.1.", "Chromosome 9 had an 81 kb copy gain in 9p24.3.", "Over 100 genes were localized within these duplicated regions.", "A gene expression array was performed.", "82 genes had expression changed >1.5-fold compared to a healthy age-matched skin control.", "The lipolytic enzyme arylacetamide deacetylase-like 3 was found within the duplicated 1p36 region of chromosome 1."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including tubular atrophy, interstitial fibrosis, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 44-year-old man.", "He presented with acute onset of abdominal pain.", "The pain started 2 days before presentation.", "The pain was diffuse across his mid-to-lower abdomen.", "The patient had normal bowel movements.", "He denied fever.", "He denied chills.", "He denied nausea.", "He denied vomiting.", "His medical history was significant for end-stage renal disease from congenital renal hypoplasia.", "He received a kidney transplant 7 years ago.", "He developed acute antibody rejection.", "He had been requiring intermittent hemodialysis for the past 2 years.", "He was on immunosuppression with oral prednisone (5 mg/day).", "He was on immunosuppression with mycophenolate mofetil (250 mg/day).", "On physical examination, his blood pressure was 105/60.", "His heart rate was 103.", "His respiratory rate was 20.", "His body temperature was 37.1\u00b0C.", "His abdominal examination demonstrated generalized tenderness.", "There was remarkable lower abdomen rebound tenderness.", "Bowel sound was absent.", "Computed tomography of the abdomen and pelvis with intravenous contrast was performed.", "Abdominal CT demonstrated ruptured jejunal diverticulum.", "There was associated free intraperitoneal air.", "There was surrounding mesenteric edema.", "Numerous small bowel diverticuli were noted.", "Marked jejunal diverticulosis was noted.", "The patient underwent a segmental jejunal resection and anastomosis.", "His postoperative course was uneventful.", "The patient was dismissed from the hospital.", "He continued his immunosuppression, including prednisone.", "He continued his immunosuppression, including mycophenolate mofetil.", "One month later, the patient presented with the same symptoms.", "He was found to have recurrent jejunal diverticulum perforation.", "He again underwent a segmental jejunal resection and anastomosis.", "Nephrology was consulted.", "Information on the risks and benefits of mycophenolate mofetil was provided.", "Information on alternative options such as azathioprine was provided.", "Mycophenolate mofetil was discontinued.", "Three months after hospitalization, the patient continued to do well.", "He had no further episode of abdominal pain."], "summary_subclaims": ["The patient is a 44-year-old man.", "The patient has end-stage renal disease.", "The patient had a failed kidney transplant.", "The patient was on low-dose mycophenolate mofetil.", "The patient presented with acute onset of abdominal pain.", "The patient was given the diagnosis of perforated jejunal diverticulum.", "The patient underwent a segmental jejunal resection and anastomosis.", "The patient developed a recurrent jejunal perforation a month later.", "The patient had a second segmental jejunal resection operation.", "Mycophenolate mofetil was discontinued."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 44-year-old man.", "He presented with acute onset of abdominal pain.", "The pain started 2 days before presentation.", "The pain was diffuse across his mid-to-lower abdomen.", "The patient had normal bowel movements.", "He denied fever.", "He denied chills.", "He denied nausea.", "He denied vomiting.", "His medical history was significant for end-stage renal disease from congenital renal hypoplasia.", "He received a kidney transplant 7 years ago.", "He developed acute antibody rejection.", "He had been requiring intermittent hemodialysis for the past 2 years.", "He was on immunosuppression with oral prednisone (5 mg/day).", "He was on immunosuppression with mycophenolate mofetil (250 mg/day).", "On physical examination, his blood pressure was 105/60.", "His heart rate was 103.", "His respiratory rate was 20.", "His body temperature was 37.1\u00b0C.", "His abdominal examination demonstrated generalized tenderness.", "There was remarkable lower abdomen rebound tenderness.", "Bowel sound was absent.", "Computed tomography of the abdomen and pelvis with intravenous contrast was performed.", "Abdominal CT demonstrated ruptured jejunal diverticulum.", "There was associated free intraperitoneal air.", "There was surrounding mesenteric edema.", "Numerous small bowel diverticuli were noted.", "Marked jejunal diverticulosis was noted.", "The patient underwent a segmental jejunal resection and anastomosis.", "His postoperative course was uneventful.", "The patient was dismissed from the hospital.", "He continued his immunosuppression, including prednisone.", "He continued his immunosuppression, including mycophenolate mofetil.", "One month later, the patient presented with the same symptoms.", "He was found to have recurrent jejunal diverticulum perforation.", "He again underwent a segmental jejunal resection and anastomosis.", "Nephrology was consulted.", "Information on the risks and benefits of mycophenolate mofetil was provided.", "Information on alternative options such as azathioprine was provided.", "Mycophenolate mofetil was discontinued.", "Three months after hospitalization, the patient continued to do well.", "He had no further episode of abdominal pain."], "index": 22, "original_id": "multiclinsum_test_295_en.txt", "split": "test", "summary_subclaims": ["The patient is a 44-year-old man.", "The patient has end-stage renal disease.", "The patient had a failed kidney transplant.", "The patient was on low-dose mycophenolate mofetil.", "The patient presented with acute onset of abdominal pain.", "The patient was given the diagnosis of perforated jejunal diverticulum.", "The patient underwent a segmental jejunal resection and anastomosis.", "The patient developed a recurrent jejunal perforation a month later.", "The patient had a second segmental jejunal resection operation.", "Mycophenolate mofetil was discontinued."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 43-year-old Malay female.", "She was referred to the low vision clinic by an ophthalmologist.", "She was diagnosed with tractional retinal detachment secondary to diabetic retinopathy.", "She was diagnosed with diabetes mellitus 5 years ago.", "She is currently on treatment for diabetes mellitus at a government hospital.", "Her treatment includes metformin 500 mg twice daily.", "Her treatment includes glicazide 60 mg daily.", "Her treatment includes insulin 18 unit/day (nocte).", "Her glycosylated hemoglobin (HbAIc) was 7 mmol/L at her last visit.", "She is on treatment for hypertension with hydrochlorothiazide 12.5 mg daily.", "She is on treatment for cholesterol with atorvastatin 20 mg daily.", "There was no evidence of diabetic nephropathy.", "There was no evidence of diabetic neuropathy.", "There was no family history of diabetes mellitus.", "There was no family history of retinal detachment.", "Her main complaint at presentation was blurred vision at both distance and near.", "She had never used nor was ever prescribed contact lens or glasses.", "She reported difficulty in recognizing faces.", "She reported difficulty with orientation and mobility.", "She had been told that 'nothing more can be done' to alleviate her condition.", "She agreed to be referred to the low vision clinic as a last attempt.", "Her distance vision for right eye was 6/48.", "Her distance vision for left eye was 6/48.", "Subjective refraction improved her distance vision to 6/48 using -1.75Ds in the right eye.", "Subjective refraction improved her distance vision to 6/38 with a +3.50 Ds in the left eye.", "Addition of +2.50 Ds enabled her to read N24 for the right eye.", "Addition of +2.50 Ds enabled her to read N16 for the left eye.", "Visual field assessment testing at near using an Amsler\u2019s chart revealed no abnormality.", "Examination of her fundi showed diabetic retinopathy changes.", "Examination of her fundi showed tractional retinal detachment.", "The DASS score showed she was in a state of severe stress (score = 34).", "The DASS score showed she was severely anxious (score = 16).", "The DASS score showed she was depressed (score = 38).", "The LVQoL questionnaire assessment score was 43.", "Using a +6.00 Ds spectacle magnifier, she improved her near vision to N10 at 20 cm.", "A 3\u00d7 monocular telescope improved her left eye distance vision to 6/12.", "She was introduced to eccentric viewing techniques.", "A pair of distance spectacles with prescription RE-1.75 Ds, LE +3.50 Ds was prescribed.", "A 3x monocular telescope was prescribed.", "She was referred to an orientation & mobility clinic.", "She agreed to a referral to the Social Welfare Department.", "She was referred to a clinical psychology clinic.", "She was referred to an occupational therapy clinic.", "She was advised to return for a review in 3 months.", "After 3 months, the patient returned for a follow-up.", "Her visual acuity for both eyes remained the same at 6/48.", "Subjective refraction and visual field status were unchanged.", "The DASS score for stress decreased from 34 to 14.", "The DASS score for depression decreased from 38 to 18.", "The LVQoL score improved from 43 to 98.", "A further three months review was given.", "She was advised to continue with sessions at the psychology clinic.", "She was advised to continue with sessions at the occupational therapy clinic.", "She was advised to continue with sessions at the orientation & mobility clinic."], "summary_subclaims": ["The patient is a 43-year-old Asian female.", "The patient has mild vision impairment.", "The patient has tractional retinal detachment.", "The tractional retinal detachment is secondary to diabetic retinopathy.", "Mental health screening was performed during low vision rehabilitation.", "Quality of life screening was performed during low vision rehabilitation.", "Mental health screening and quality of life screening can improve the management of this patient."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 43-year-old Malay female.", "She was referred to the low vision clinic by an ophthalmologist.", "She was diagnosed with tractional retinal detachment secondary to diabetic retinopathy.", "She was diagnosed with diabetes mellitus 5 years ago.", "She is currently on treatment for diabetes mellitus at a government hospital.", "Her treatment includes metformin 500 mg twice daily.", "Her treatment includes glicazide 60 mg daily.", "Her treatment includes insulin 18 unit/day (nocte).", "Her glycosylated hemoglobin (HbAIc) was 7 mmol/L at her last visit.", "She is on treatment for hypertension with hydrochlorothiazide 12.5 mg daily.", "She is on treatment for cholesterol with atorvastatin 20 mg daily.", "There was no evidence of diabetic nephropathy.", "There was no evidence of diabetic neuropathy.", "There was no family history of diabetes mellitus.", "There was no family history of retinal detachment.", "Her main complaint at presentation was blurred vision at both distance and near.", "She had never used nor was ever prescribed contact lens or glasses.", "She reported difficulty in recognizing faces.", "She reported difficulty with orientation and mobility.", "She had been told that 'nothing more can be done' to alleviate her condition.", "She agreed to be referred to the low vision clinic as a last attempt.", "Her distance vision for right eye was 6/48.", "Her distance vision for left eye was 6/48.", "Subjective refraction improved her distance vision to 6/48 using -1.75Ds in the right eye.", "Subjective refraction improved her distance vision to 6/38 with a +3.50 Ds in the left eye.", "Addition of +2.50 Ds enabled her to read N24 for the right eye.", "Addition of +2.50 Ds enabled her to read N16 for the left eye.", "Visual field assessment testing at near using an Amsler\u2019s chart revealed no abnormality.", "Examination of her fundi showed diabetic retinopathy changes.", "Examination of her fundi showed tractional retinal detachment.", "The DASS score showed she was in a state of severe stress (score = 34).", "The DASS score showed she was severely anxious (score = 16).", "The DASS score showed she was depressed (score = 38).", "The LVQoL questionnaire assessment score was 43.", "Using a +6.00 Ds spectacle magnifier, she improved her near vision to N10 at 20 cm.", "A 3\u00d7 monocular telescope improved her left eye distance vision to 6/12.", "She was introduced to eccentric viewing techniques.", "A pair of distance spectacles with prescription RE-1.75 Ds, LE +3.50 Ds was prescribed.", "A 3x monocular telescope was prescribed.", "She was referred to an orientation & mobility clinic.", "She agreed to a referral to the Social Welfare Department.", "She was referred to a clinical psychology clinic.", "She was referred to an occupational therapy clinic.", "She was advised to return for a review in 3 months.", "After 3 months, the patient returned for a follow-up.", "Her visual acuity for both eyes remained the same at 6/48.", "Subjective refraction and visual field status were unchanged.", "The DASS score for stress decreased from 34 to 14.", "The DASS score for depression decreased from 38 to 18.", "The LVQoL score improved from 43 to 98.", "A further three months review was given.", "She was advised to continue with sessions at the psychology clinic.", "She was advised to continue with sessions at the occupational therapy clinic.", "She was advised to continue with sessions at the orientation & mobility clinic."], "index": 26, "original_id": "multiclinsum_test_2493_en.txt", "split": "test", "summary_subclaims": ["The patient is a 43-year-old Asian female.", "The patient has mild vision impairment.", "The patient has tractional retinal detachment.", "The tractional retinal detachment is secondary to diabetic retinopathy.", "Mental health screening was performed during low vision rehabilitation.", "Quality of life screening was performed during low vision rehabilitation.", "Mental health screening and quality of life screening can improve the management of this patient."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was a 48-year-old female.", "The patient had a left lower lobe nodule in the lung.", "The patient was scheduled for thoracoscopic wedge resection of the left lower lobe.", "Anesthesia was induced with 0.04 mg/kg of midazolam.", "Anesthesia was induced with 0.6 \u03bcg/kg of sufentanil.", "Anesthesia was induced with 2 mg/kg of propofol.", "Anesthesia was induced with 0.6 mg/kg of rocuronium.", "A left 35 Fr endobronchial tube was successfully intubated at a depth of 28 cm to incisors.", "Fiberoptic bronchoscopy was used to confirm the location of the tube after the patient was placed in the right lateral decubitus position.", "Anesthesia was maintained with sevoflurane 1.5 vol%.", "Anesthesia was maintained with oxygen 2 L/min.", "Anesthesia was maintained with remifentanil 250 mcg/hr.", "Anesthesia was maintained with 4 mg/kg/h of propofol.", "The intraoperative pathological diagnosis of the excised mass was invasive adenocarcinoma.", "The patient underwent VATS combined with left lower lobectomy.", "The operation time was 1.5 h.", "The patient was transferred to the post-anesthesia care unit for decannulation.", "The patient recovered consciousness from anesthesia after 30 min.", "The patient exhibited effective spontaneous ventilation.", "The patient met extubation criteria.", "The tracheal tube seemed to be mechanically constrained.", "The endotracheal tube could not be withdrawn.", "Propofol and remifentanil were administered intravenously for sedation.", "A fiberoptic bronchoscope revealed that the surgical suture of the bronchial membrane was inserted into the distal end of the left branch of the tracheal tube.", "Detailed consultations were held with respiratory physicians and thoracic surgeons.", "The thoracic surgeon assured that breaking the suture will not cause adverse effects on the patient.", "The respiratory doctor burned the sutures using an argon electrode (ERBE 20132\u2013177) with the aid of fiberoptic bronchoscope.", "The mode of the argon electrode was strong electrocoagulation.", "The power of the argon electrode was 35 W.", "The bronchial tube was pulled out smoothly.", "The patient was safely sent back to the ward after CT review.", "CT review showed no abnormalities.", "The patient was followed-up on the 1, 3, and 7 days after the operation.", "There were no related complications such as bronchial leak or bronchial rupture."], "summary_subclaims": ["The patient is a 48-year-old female.", "The patient underwent video-assisted thoracoscopic surgery.", "The surgery was combined with left lower lobectomy.", "The distal end of the left branch of the tracheal tube was lodged by surgical sutures.", "The respiratory physician burned the sutures using an argon electrode.", "The physician discussed the procedure with thoracic surgery experts."]}, "extra_info": {"fulltext_subclaims": ["The patient was a 48-year-old female.", "The patient had a left lower lobe nodule in the lung.", "The patient was scheduled for thoracoscopic wedge resection of the left lower lobe.", "Anesthesia was induced with 0.04 mg/kg of midazolam.", "Anesthesia was induced with 0.6 \u03bcg/kg of sufentanil.", "Anesthesia was induced with 2 mg/kg of propofol.", "Anesthesia was induced with 0.6 mg/kg of rocuronium.", "A left 35 Fr endobronchial tube was successfully intubated at a depth of 28 cm to incisors.", "Fiberoptic bronchoscopy was used to confirm the location of the tube after the patient was placed in the right lateral decubitus position.", "Anesthesia was maintained with sevoflurane 1.5 vol%.", "Anesthesia was maintained with oxygen 2 L/min.", "Anesthesia was maintained with remifentanil 250 mcg/hr.", "Anesthesia was maintained with 4 mg/kg/h of propofol.", "The intraoperative pathological diagnosis of the excised mass was invasive adenocarcinoma.", "The patient underwent VATS combined with left lower lobectomy.", "The operation time was 1.5 h.", "The patient was transferred to the post-anesthesia care unit for decannulation.", "The patient recovered consciousness from anesthesia after 30 min.", "The patient exhibited effective spontaneous ventilation.", "The patient met extubation criteria.", "The tracheal tube seemed to be mechanically constrained.", "The endotracheal tube could not be withdrawn.", "Propofol and remifentanil were administered intravenously for sedation.", "A fiberoptic bronchoscope revealed that the surgical suture of the bronchial membrane was inserted into the distal end of the left branch of the tracheal tube.", "Detailed consultations were held with respiratory physicians and thoracic surgeons.", "The thoracic surgeon assured that breaking the suture will not cause adverse effects on the patient.", "The respiratory doctor burned the sutures using an argon electrode (ERBE 20132\u2013177) with the aid of fiberoptic bronchoscope.", "The mode of the argon electrode was strong electrocoagulation.", "The power of the argon electrode was 35 W.", "The bronchial tube was pulled out smoothly.", "The patient was safely sent back to the ward after CT review.", "CT review showed no abnormalities.", "The patient was followed-up on the 1, 3, and 7 days after the operation.", "There were no related complications such as bronchial leak or bronchial rupture."], "index": 24, "original_id": "multiclinsum_test_1206_en.txt", "split": "test", "summary_subclaims": ["The patient is a 48-year-old female.", "The patient underwent video-assisted thoracoscopic surgery.", "The surgery was combined with left lower lobectomy.", "The distal end of the left branch of the tracheal tube was lodged by surgical sutures.", "The respiratory physician burned the sutures using an argon electrode.", "The physician discussed the procedure with thoracic surgery experts."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was a 52-year-old woman.", "She was admitted for evaluation of intermittent abdominal tenderness, dry eye, and dry mouth.", "The dry eye and dry mouth had been present for several years.", "She had not sought medical treatment for the dry eye and dry mouth.", "She had a history of dilated cardiomyopathy.", "She had a history of glaucoma of the left eye.", "She was being treated with loop diuretics.", "She was being treated with proton pump inhibitors.", "She was being treated with anthocyanosides for glaucoma.", "In the physical examination, her lower extremities were in an edematous state.", "Her body temperature was 36.5\u00b0C.", "Her blood pressure was normal.", "The white blood cell count was 8,600/mm3.", "The neutrophil percentage was 73.4%.", "The sodium level was 141 mEq/L.", "The chloride level was 108 mEq/L.", "The blood urea nitrogen was 15.7 mg/dL.", "The creatinine was 0.6 mg/dL.", "The total serum protein was 5.5 g/dL.", "The serum albumin was 1.5 g/dL.", "The total cholesterol was 257 mg/dL.", "Urinalysis showed proteinuria of 6.3 g/day.", "Urinalysis showed 30\u201349 red blood cells per high-power field.", "Serologic investigation revealed the presence of anti-nuclear antibody (ANA; 1:80, homogeneous plus speckled pattern).", "Serologic investigation revealed the presence of rheumatoid factor (390 IU/mL).", "Serologic investigation was positive for autoantibody to the Ro (SS-A) antigen (>200 U/mL).", "Serology was negative for antibodies against double-stranded DNA.", "Serology was negative for antibodies against La (SS-B).", "Serology was negative for antibodies against Sm.", "Serology was negative for antibodies against ribonucleoproteins.", "Serology was negative for antineutrophil cytoplasmic antibodies.", "Serology was negative for lupus anticoagulant.", "Serology was negative for IgG/IgM anti-cardiolipin.", "Serology was negative for IgG \u03b22-glycoprotein-1.", "C3 levels had decreased to 38 mg/dL.", "C4 levels were within normal ranges at 16 mg/dL.", "Total hemolytic complement 50 levels were within normal ranges at 33.1 U/mL.", "Tests for hepatitis B surface antigen were negative.", "Tests for hepatitis C antibodies were negative.", "Tests for cryoglobulins were negative.", "Tests for human immunodeficiency virus antibodies were negative.", "Minor salivary gland biopsy showed diffuse lymphocytic infiltrations with a focus score of 3.", "Salivary scintigraphy showed non-visualization in both salivary glands.", "The findings were consistent with the class 4 Schall grading system.", "She was diagnosed with Sj\u00f6gren\u2019s syndrome.", "The diagnosis fulfilled the 2002 American-European consensus classification criteria.", "She underwent a percutaneous renal biopsy due to nephrotic syndrome.", "Glomerular basement membrane thickening was observed by light microscopy.", "Mesangial matrix widening was observed by light microscopy.", "Mild tubular atrophy was noted.", "Moderate interstitial fibrosis was noted.", "Weakly positive staining for IgG, IgA, IgM, and C3 on the outer surface of capillary walls was revealed by immunofluorescent staining.", "Diffuse subepithelial electron-dense deposit was observed by electron microscopy.", "The histopathological findings were consistent with membranous glomerulonephritis.", "Abdominal computed tomography (CT) and colonoscopy were performed due to intermittent abdominal tenderness.", "No malignancy was observed at admission.", "No bowel perforation was observed at admission.", "She had sudden onset of severe abdominal pain 3 months later.", "Abdominal CT showed newly developed pneumoperitoneum with peritonitis.", "Abdominal CT showed small bowel perforation.", "An emergency operation and small bowel biopsy were performed.", "The specimen had a necrotic and ulcerous lesion measuring 4.5 \u00d7 5 cm.", "Immunohistochemical examination showed expression of CD20.", "Immunohistochemical examination showed expression of CD79a.", "Immunohistochemical examination showed expression of BCL-2.", "Immunohistochemical examination did not show expression of CD3.", "Immunohistochemical examination did not show expression of CD10.", "Immunohistochemical examination did not show expression of BCL-6.", "The proliferation fraction as determined by Ki-67 was 50%\u201360%.", "The majority of tumor cells were positive for EBV by in situ hybridization.", "Biopsy revealed EBV-positive DLBCL.", "The patient declined treatment with chemotherapy.", "She had been receiving intermittent low-dose oral corticosteroid.", "She had been receiving hydroxychloroquine.", "There was improvement in proteinuria (1.79 g/day) after 1 year of follow-up.", "There was improvement in sicca symptoms after 1 year of follow-up.", "One year of follow-up positron emission tomography-CT scan showed a stable disease state for the malignant lymphoma."], "summary_subclaims": ["The patient is a 52-year-old woman.", "She has primary Sj\u00f6gren's syndrome.", "She developed membranous glomerulonephritis.", "She developed Epstein-Barr virus-positive diffuse large B-cell lymphoma.", "The diagnosis of Sj\u00f6gren's syndrome was based on dry eyes.", "The diagnosis of Sj\u00f6gren's syndrome was based on dry mouth.", "The diagnosis of Sj\u00f6gren's syndrome was based on a positive anti-nuclear antibody test.", "The diagnosis of Sj\u00f6gren's syndrome was based on anti-Ro (SS-A) antibody.", "The diagnosis of Sj\u00f6gren's syndrome was based on a salivary gland biopsy.", "The diagnosis of Sj\u00f6gren's syndrome was based on salivary scintigraphy.", "Renal biopsy confirmed the diagnosis of membranous glomerulonephritis.", "Three months later, her small bowel was perforated with pneumoperitoneum.", "The biopsy revealed Epstein-Barr virus-positive diffuse large B-cell lymphoma."]}, "extra_info": {"fulltext_subclaims": ["The patient was a 52-year-old woman.", "She was admitted for evaluation of intermittent abdominal tenderness, dry eye, and dry mouth.", "The dry eye and dry mouth had been present for several years.", "She had not sought medical treatment for the dry eye and dry mouth.", "She had a history of dilated cardiomyopathy.", "She had a history of glaucoma of the left eye.", "She was being treated with loop diuretics.", "She was being treated with proton pump inhibitors.", "She was being treated with anthocyanosides for glaucoma.", "In the physical examination, her lower extremities were in an edematous state.", "Her body temperature was 36.5\u00b0C.", "Her blood pressure was normal.", "The white blood cell count was 8,600/mm3.", "The neutrophil percentage was 73.4%.", "The sodium level was 141 mEq/L.", "The chloride level was 108 mEq/L.", "The blood urea nitrogen was 15.7 mg/dL.", "The creatinine was 0.6 mg/dL.", "The total serum protein was 5.5 g/dL.", "The serum albumin was 1.5 g/dL.", "The total cholesterol was 257 mg/dL.", "Urinalysis showed proteinuria of 6.3 g/day.", "Urinalysis showed 30\u201349 red blood cells per high-power field.", "Serologic investigation revealed the presence of anti-nuclear antibody (ANA; 1:80, homogeneous plus speckled pattern).", "Serologic investigation revealed the presence of rheumatoid factor (390 IU/mL).", "Serologic investigation was positive for autoantibody to the Ro (SS-A) antigen (>200 U/mL).", "Serology was negative for antibodies against double-stranded DNA.", "Serology was negative for antibodies against La (SS-B).", "Serology was negative for antibodies against Sm.", "Serology was negative for antibodies against ribonucleoproteins.", "Serology was negative for antineutrophil cytoplasmic antibodies.", "Serology was negative for lupus anticoagulant.", "Serology was negative for IgG/IgM anti-cardiolipin.", "Serology was negative for IgG \u03b22-glycoprotein-1.", "C3 levels had decreased to 38 mg/dL.", "C4 levels were within normal ranges at 16 mg/dL.", "Total hemolytic complement 50 levels were within normal ranges at 33.1 U/mL.", "Tests for hepatitis B surface antigen were negative.", "Tests for hepatitis C antibodies were negative.", "Tests for cryoglobulins were negative.", "Tests for human immunodeficiency virus antibodies were negative.", "Minor salivary gland biopsy showed diffuse lymphocytic infiltrations with a focus score of 3.", "Salivary scintigraphy showed non-visualization in both salivary glands.", "The findings were consistent with the class 4 Schall grading system.", "She was diagnosed with Sj\u00f6gren\u2019s syndrome.", "The diagnosis fulfilled the 2002 American-European consensus classification criteria.", "She underwent a percutaneous renal biopsy due to nephrotic syndrome.", "Glomerular basement membrane thickening was observed by light microscopy.", "Mesangial matrix widening was observed by light microscopy.", "Mild tubular atrophy was noted.", "Moderate interstitial fibrosis was noted.", "Weakly positive staining for IgG, IgA, IgM, and C3 on the outer surface of capillary walls was revealed by immunofluorescent staining.", "Diffuse subepithelial electron-dense deposit was observed by electron microscopy.", "The histopathological findings were consistent with membranous glomerulonephritis.", "Abdominal computed tomography (CT) and colonoscopy were performed due to intermittent abdominal tenderness.", "No malignancy was observed at admission.", "No bowel perforation was observed at admission.", "She had sudden onset of severe abdominal pain 3 months later.", "Abdominal CT showed newly developed pneumoperitoneum with peritonitis.", "Abdominal CT showed small bowel perforation.", "An emergency operation and small bowel biopsy were performed.", "The specimen had a necrotic and ulcerous lesion measuring 4.5 \u00d7 5 cm.", "Immunohistochemical examination showed expression of CD20.", "Immunohistochemical examination showed expression of CD79a.", "Immunohistochemical examination showed expression of BCL-2.", "Immunohistochemical examination did not show expression of CD3.", "Immunohistochemical examination did not show expression of CD10.", "Immunohistochemical examination did not show expression of BCL-6.", "The proliferation fraction as determined by Ki-67 was 50%\u201360%.", "The majority of tumor cells were positive for EBV by in situ hybridization.", "Biopsy revealed EBV-positive DLBCL.", "The patient declined treatment with chemotherapy.", "She had been receiving intermittent low-dose oral corticosteroid.", "She had been receiving hydroxychloroquine.", "There was improvement in proteinuria (1.79 g/day) after 1 year of follow-up.", "There was improvement in sicca symptoms after 1 year of follow-up.", "One year of follow-up positron emission tomography-CT scan showed a stable disease state for the malignant lymphoma."], "index": 28, "original_id": "multiclinsum_test_2438_en.txt", "split": "test", "summary_subclaims": ["The patient is a 52-year-old woman.", "She has primary Sj\u00f6gren's syndrome.", "She developed membranous glomerulonephritis.", "She developed Epstein-Barr virus-positive diffuse large B-cell lymphoma.", "The diagnosis of Sj\u00f6gren's syndrome was based on dry eyes.", "The diagnosis of Sj\u00f6gren's syndrome was based on dry mouth.", "The diagnosis of Sj\u00f6gren's syndrome was based on a positive anti-nuclear antibody test.", "The diagnosis of Sj\u00f6gren's syndrome was based on anti-Ro (SS-A) antibody.", "The diagnosis of Sj\u00f6gren's syndrome was based on a salivary gland biopsy.", "The diagnosis of Sj\u00f6gren's syndrome was based on salivary scintigraphy.", "Renal biopsy confirmed the diagnosis of membranous glomerulonephritis.", "Three months later, her small bowel was perforated with pneumoperitoneum.", "The biopsy revealed Epstein-Barr virus-positive diffuse large B-cell lymphoma."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 65-year-old man.", "The patient has a history of hypertension.", "The patient has a history of smoking.", "The patient was admitted from another institution.", "The patient was diagnosed with acute abdomen.", "The patient reported approximately 48 hours of pain in the lower abdominal area.", "The pain did not subside with common analgesics.", "The patient had associated nausea.", "On admission, the patient had a positive Blumberg sign.", "A blood count showed a leukocytosis of 18,320 mm\u00b3.", "A blood count showed a neutrophilia of 85%.", "A computed tomography (CT) of the abdomen with intravenous contrast was performed.", "The CT showed a saccular image of 52 x 41 mm dependent on the loop of the terminal ileum.", "The CT showed a pattern of bread crumbs.", "The CT showed peripheral enhancement.", "The CT showed rarefaction of adjacent fat.", "The CT showed findings related to Meckel's diverticulitis.", "The CT showed pneumoperitoneum.", "The CT showed free liquid in the abdominal cavity.", "Signs of associated peritonitis were considered.", "Laparoscopic surgery was performed.", "The surgery showed a prominent diverticulum dependent on the small intestine.", "The diverticulum was located 25 cm from the ileocecal valve.", "The diverticulum was perforated.", "An enterotomy of approximately 5 cm of the small intestine was performed.", "A lateral-lateral anastomosis with mechanical suture was performed.", "The abdominal cavity was washed.", "The abdominal wall was closed.", "The pathological anatomy described a segment of the small intestine with a lesion of saccular appearance.", "The lesion measured 35 x 25 mm.", "Histological cuts showed ulceration of the mucosa and submucosa.", "Histological cuts showed acute inflammation in the serosa.", "There was no significant alteration of the enteric wall away from the lesion.", "The description confirmed the diagnosis of perforated Meckel's diverticulitis."], "summary_subclaims": ["The patient is a 65-year-old man.", "The patient was referred from another institution.", "The patient was diagnosed with acute abdomen.", "On physical examination, the patient presented signs of peritoneal irritation.", "The admission blood count showed leukocytosis.", "The admission blood count showed neutrophilia.", "Computed tomography of the abdomen with intravenous contrast was performed.", "The computed tomography was interpreted as Meckel's diverticulitis complicated.", "The diagnosis was corroborated during the surgical act.", "The diagnosis was confirmed by pathological anatomy."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 65-year-old man.", "The patient has a history of hypertension.", "The patient has a history of smoking.", "The patient was admitted from another institution.", "The patient was diagnosed with acute abdomen.", "The patient reported approximately 48 hours of pain in the lower abdominal area.", "The pain did not subside with common analgesics.", "The patient had associated nausea.", "On admission, the patient had a positive Blumberg sign.", "A blood count showed a leukocytosis of 18,320 mm\u00b3.", "A blood count showed a neutrophilia of 85%.", "A computed tomography (CT) of the abdomen with intravenous contrast was performed.", "The CT showed a saccular image of 52 x 41 mm dependent on the loop of the terminal ileum.", "The CT showed a pattern of bread crumbs.", "The CT showed peripheral enhancement.", "The CT showed rarefaction of adjacent fat.", "The CT showed findings related to Meckel's diverticulitis.", "The CT showed pneumoperitoneum.", "The CT showed free liquid in the abdominal cavity.", "Signs of associated peritonitis were considered.", "Laparoscopic surgery was performed.", "The surgery showed a prominent diverticulum dependent on the small intestine.", "The diverticulum was located 25 cm from the ileocecal valve.", "The diverticulum was perforated.", "An enterotomy of approximately 5 cm of the small intestine was performed.", "A lateral-lateral anastomosis with mechanical suture was performed.", "The abdominal cavity was washed.", "The abdominal wall was closed.", "The pathological anatomy described a segment of the small intestine with a lesion of saccular appearance.", "The lesion measured 35 x 25 mm.", "Histological cuts showed ulceration of the mucosa and submucosa.", "Histological cuts showed acute inflammation in the serosa.", "There was no significant alteration of the enteric wall away from the lesion.", "The description confirmed the diagnosis of perforated Meckel's diverticulitis."], "index": 30, "original_id": "multiclinsum_test_3197_en.txt", "split": "test", "summary_subclaims": ["The patient is a 65-year-old man.", "The patient was referred from another institution.", "The patient was diagnosed with acute abdomen.", "On physical examination, the patient presented signs of peritoneal irritation.", "The admission blood count showed leukocytosis.", "The admission blood count showed neutrophilia.", "Computed tomography of the abdomen with intravenous contrast was performed.", "The computed tomography was interpreted as Meckel's diverticulitis complicated.", "The diagnosis was corroborated during the surgical act.", "The diagnosis was confirmed by pathological anatomy."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was a 64-year-old Indian man.", "He had complaints of abdominal pain, vomiting, and not passing flatus or feces for four days.", "The patient's general condition was poor.", "He was febrile.", "His pulse rate was 124/minute.", "His blood pressure was 90 mm/Hg.", "X-rays of the abdomen showed multiple air fluid levels.", "The X-rays were suggestive of acute intestinal obstruction.", "The provisional diagnosis was acute abdomen (acute intestinal obstruction).", "The patient was resuscitated.", "The patient was sent for an urgent laparotomy.", "On exploration, the patient had severely dilated small gut loops.", "The terminal ileal loop was twisted around the omental band.", "The ileal loop was adherent to the left pelvic wall.", "On releasing the omental band, the ileal loop was dissected free from the left pelvic wall.", "A large, white, oval shaped, extra-luminal body was found in the region of the sigmoid colon.", "The body was soft to firm in consistency.", "The body resembled a boiled hen's egg.", "The body was attached to the omentum.", "Part of the appendices epiploicae attached to the sigmoid colon were calcified.", "The stalks of the calcified appendices epiploicae were constricted.", "The peritoneal loose body was largely parasitized to the omentum.", "The body had a separate feeding vessel supplying it from the omentum.", "The body measured 7 cm in length and 5 cm in width.", "The body weighed 74 g.", "On the cut surface, it had a classic appearance like a boiled egg.", "The white peripheral part was smooth and soft in consistency.", "The central yellow part was slightly firm in the periphery.", "The central yellow part was hard (calcified) at the central point.", "The surfaces were smooth and shiny.", "Histological examination showed laminated strands of a fibrinoid substance.", "The peripheral white part contained a large amount of proteinaceous material.", "The peripheral white part resembled boiled albumin with high collagen deposition.", "The central yellow part contained saponified fat with calcification.", "The patient did well post-operatively.", "He resumed his oral diet on the third post-operative day.", "He was discharged from the hospital five days after the operation."], "summary_subclaims": ["A giant loose peritoneal body measuring 7 \u00d7 5 cm was found incidentally in a 64-year-old Indian man.", "The patient presented with acute intestinal obstruction.", "The current hypothesis and opinion on the genesis of such large bodies are presented.", "The problems in diagnosis are discussed."]}, "extra_info": {"fulltext_subclaims": ["The patient was a 64-year-old Indian man.", "He had complaints of abdominal pain, vomiting, and not passing flatus or feces for four days.", "The patient's general condition was poor.", "He was febrile.", "His pulse rate was 124/minute.", "His blood pressure was 90 mm/Hg.", "X-rays of the abdomen showed multiple air fluid levels.", "The X-rays were suggestive of acute intestinal obstruction.", "The provisional diagnosis was acute abdomen (acute intestinal obstruction).", "The patient was resuscitated.", "The patient was sent for an urgent laparotomy.", "On exploration, the patient had severely dilated small gut loops.", "The terminal ileal loop was twisted around the omental band.", "The ileal loop was adherent to the left pelvic wall.", "On releasing the omental band, the ileal loop was dissected free from the left pelvic wall.", "A large, white, oval shaped, extra-luminal body was found in the region of the sigmoid colon.", "The body was soft to firm in consistency.", "The body resembled a boiled hen's egg.", "The body was attached to the omentum.", "Part of the appendices epiploicae attached to the sigmoid colon were calcified.", "The stalks of the calcified appendices epiploicae were constricted.", "The peritoneal loose body was largely parasitized to the omentum.", "The body had a separate feeding vessel supplying it from the omentum.", "The body measured 7 cm in length and 5 cm in width.", "The body weighed 74 g.", "On the cut surface, it had a classic appearance like a boiled egg.", "The white peripheral part was smooth and soft in consistency.", "The central yellow part was slightly firm in the periphery.", "The central yellow part was hard (calcified) at the central point.", "The surfaces were smooth and shiny.", "Histological examination showed laminated strands of a fibrinoid substance.", "The peripheral white part contained a large amount of proteinaceous material.", "The peripheral white part resembled boiled albumin with high collagen deposition.", "The central yellow part contained saponified fat with calcification.", "The patient did well post-operatively.", "He resumed his oral diet on the third post-operative day.", "He was discharged from the hospital five days after the operation."], "index": 36, "original_id": "multiclinsum_test_2469_en.txt", "split": "test", "summary_subclaims": ["A giant loose peritoneal body measuring 7 \u00d7 5 cm was found incidentally in a 64-year-old Indian man.", "The patient presented with acute intestinal obstruction.", "The current hypothesis and opinion on the genesis of such large bodies are presented.", "The problems in diagnosis are discussed."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is an 82-year-old lady.", "She presented with recurrent attacks of hypoglycemia.", "Diagnostic tests repeatedly documented glucose levels below 40 mg/dl.", "A CT scan of the abdomen revealed a large lesion of around 5 to 6 cm in relation to the pancreatic body and tail.", "There were also large masses of about 3\u20135 cm in the retroperitoneum and in the area of the celiac trunk and around the mesenteric artery.", "In the pancreatic body there was a hypervascularized area suspicious for an insulinoma.", "The patient reported a weight loss of 12 kilograms over the previous 4 months.", "A somatostatin receptor scintigraphy showed an enhanced uptake in the region of the pancreatic body/tail.", "A somatostatin receptor scintigraphy showed an enhanced uptake in the right axilla.", "A palpable mass was noted in the right axilla.", "The scintigraphy excluded the possibility of other involved areas.", "The patient had a past history of an operation on the right eyebrow 2 years prior.", "The eyebrow lesion was reported as a Merkel cell carcinoma.", "Histopathology showed rather uniform tumor cells in a trabecular growth pattern.", "The tumor cells had monomorphous pale-stained nuclei.", "There were many mitoses.", "There was invasion of dermal lymphatics and blood vessels.", "Immunohistochemistry revealed strong positivity for cytokeratin 20.", "Immunohistochemistry revealed a dot-like pattern of cytokeratin 20.", "There was a weak expression of chromogranin A.", "After excision, radiation therapy was administered at the site of the primary lesion.", "Radiation therapy was also administered at the draining lymphatic vessels.", "Radiation therapy was also administered at the first lymph node station.", "A year later, a large abdominal mass was noted of uncertain origin.", "An ultrasound guided biopsy showed an unspecified small cell cancer.", "Palliative radiotherapy of 30 Gray over 2 months was administered.", "No definitive diagnosis of metastasis in the spleen, left adrenal gland, and axilla was established.", "The working clinical diagnosis was symptomatic insulinoma not responding to medical measures.", "A decision for surgical resection of the large lesion was made.", "Surgical exploration revealed a large mass of about 5 cm in the tail of the pancreas.", "The mass was in close proximity to the spleen and the splenic flexure of the transverse colon.", "There was no evidence of any metastatic disease to the liver, peritoneum, and the adnexae.", "A distal pancreatectomy, splenectomy, adrenalectomy, and resection of the splenic flexure of the colon were performed.", "Pathological examination revealed a tumor in the pancreatic tail.", "The tumor was also present in the adrenal gland.", "The tumor was also present in the peripancreatic tissue.", "The tumor was also present in the surrounding soft tissue.", "Grossly, the mass displayed a whitish and glassy cut surface.", "The mass contained extended areas of haemorrhage and necrosis.", "Histologically, the tumor displayed endocrine architecture with mostly solid formations of rather monomorphic cells.", "The tumor was mitotically highly active (mitotic count >10 per high power field).", "The tumor contained abundant areas of necrosis.", "Immunohistochemically, the tumor cells were strongly positive for synaptophysin.", "Immunohistochemically, the tumor cells were strongly positive for cytokeratin 20.", "There was no expression of insulin.", "The proliferative activity (MIB-1) reached approximately 80%.", "Gross examination of the resected specimen revealed a well demarcated, brownish tumor of the pancreatic body.", "The tumor measured 1.2 cm in diameter.", "Microscopically, the tumor displayed endocrine architecture with trabecular arrangements of uniform tumor cells.", "There was no mitotic activity.", "Immunohistochemistry revealed strong positivity for synaptophysin.", "Immunohistochemistry revealed focal positivity for insulin.", "The proliferative activity (MIB-1) was approximately 1%.", "The diagnosis of a poorly differentiated endocrine carcinoma (Merkel cell carcinoma) was made.", "The diagnosis of a benign pancreatic insulinoma was made.", "The patient had a smooth postoperative recovery.", "The bouts of hypoglycaemia completely disappeared.", "She was discharged home within 3 weeks of surgery.", "She is presently asymptomatic.", "She remains on regular follow up."], "summary_subclaims": ["We report an unusual occurrence of pancreatic metastases from a previously diagnosed Merkel cell carcinoma with the discovery of a concomitant insulinoma.", "An 82-year old lady suffered from recurrent attacks of hypoglycemia.", "She presented with an abdominal mass.", "Two years prior she had an excision done on her eyebrow that was reported as Merkel cell carcinoma.", "An extended distal pancreatectomy and splenectomy along with resection of the left flexure of the colon for her abdominal mass was carried out.", "Final histopathology of the mass was a poorly differentiated endocrine carcinoma in the pancreatic tail.", "Final histopathology showed the tumor in the peripancreatic tissue.", "Final histopathology showed the tumor in the surrounding soft tissue.", "The histopathology was consistent with metastatic Merkel cell carcinoma.", "An insulinoma of the pancreatic body was also found."]}, "extra_info": {"fulltext_subclaims": ["The patient is an 82-year-old lady.", "She presented with recurrent attacks of hypoglycemia.", "Diagnostic tests repeatedly documented glucose levels below 40 mg/dl.", "A CT scan of the abdomen revealed a large lesion of around 5 to 6 cm in relation to the pancreatic body and tail.", "There were also large masses of about 3\u20135 cm in the retroperitoneum and in the area of the celiac trunk and around the mesenteric artery.", "In the pancreatic body there was a hypervascularized area suspicious for an insulinoma.", "The patient reported a weight loss of 12 kilograms over the previous 4 months.", "A somatostatin receptor scintigraphy showed an enhanced uptake in the region of the pancreatic body/tail.", "A somatostatin receptor scintigraphy showed an enhanced uptake in the right axilla.", "A palpable mass was noted in the right axilla.", "The scintigraphy excluded the possibility of other involved areas.", "The patient had a past history of an operation on the right eyebrow 2 years prior.", "The eyebrow lesion was reported as a Merkel cell carcinoma.", "Histopathology showed rather uniform tumor cells in a trabecular growth pattern.", "The tumor cells had monomorphous pale-stained nuclei.", "There were many mitoses.", "There was invasion of dermal lymphatics and blood vessels.", "Immunohistochemistry revealed strong positivity for cytokeratin 20.", "Immunohistochemistry revealed a dot-like pattern of cytokeratin 20.", "There was a weak expression of chromogranin A.", "After excision, radiation therapy was administered at the site of the primary lesion.", "Radiation therapy was also administered at the draining lymphatic vessels.", "Radiation therapy was also administered at the first lymph node station.", "A year later, a large abdominal mass was noted of uncertain origin.", "An ultrasound guided biopsy showed an unspecified small cell cancer.", "Palliative radiotherapy of 30 Gray over 2 months was administered.", "No definitive diagnosis of metastasis in the spleen, left adrenal gland, and axilla was established.", "The working clinical diagnosis was symptomatic insulinoma not responding to medical measures.", "A decision for surgical resection of the large lesion was made.", "Surgical exploration revealed a large mass of about 5 cm in the tail of the pancreas.", "The mass was in close proximity to the spleen and the splenic flexure of the transverse colon.", "There was no evidence of any metastatic disease to the liver, peritoneum, and the adnexae.", "A distal pancreatectomy, splenectomy, adrenalectomy, and resection of the splenic flexure of the colon were performed.", "Pathological examination revealed a tumor in the pancreatic tail.", "The tumor was also present in the adrenal gland.", "The tumor was also present in the peripancreatic tissue.", "The tumor was also present in the surrounding soft tissue.", "Grossly, the mass displayed a whitish and glassy cut surface.", "The mass contained extended areas of haemorrhage and necrosis.", "Histologically, the tumor displayed endocrine architecture with mostly solid formations of rather monomorphic cells.", "The tumor was mitotically highly active (mitotic count >10 per high power field).", "The tumor contained abundant areas of necrosis.", "Immunohistochemically, the tumor cells were strongly positive for synaptophysin.", "Immunohistochemically, the tumor cells were strongly positive for cytokeratin 20.", "There was no expression of insulin.", "The proliferative activity (MIB-1) reached approximately 80%.", "Gross examination of the resected specimen revealed a well demarcated, brownish tumor of the pancreatic body.", "The tumor measured 1.2 cm in diameter.", "Microscopically, the tumor displayed endocrine architecture with trabecular arrangements of uniform tumor cells.", "There was no mitotic activity.", "Immunohistochemistry revealed strong positivity for synaptophysin.", "Immunohistochemistry revealed focal positivity for insulin.", "The proliferative activity (MIB-1) was approximately 1%.", "The diagnosis of a poorly differentiated endocrine carcinoma (Merkel cell carcinoma) was made.", "The diagnosis of a benign pancreatic insulinoma was made.", "The patient had a smooth postoperative recovery.", "The bouts of hypoglycaemia completely disappeared.", "She was discharged home within 3 weeks of surgery.", "She is presently asymptomatic.", "She remains on regular follow up."], "index": 32, "original_id": "multiclinsum_test_1055_en.txt", "split": "test", "summary_subclaims": ["We report an unusual occurrence of pancreatic metastases from a previously diagnosed Merkel cell carcinoma with the discovery of a concomitant insulinoma.", "An 82-year old lady suffered from recurrent attacks of hypoglycemia.", "She presented with an abdominal mass.", "Two years prior she had an excision done on her eyebrow that was reported as Merkel cell carcinoma.", "An extended distal pancreatectomy and splenectomy along with resection of the left flexure of the colon for her abdominal mass was carried out.", "Final histopathology of the mass was a poorly differentiated endocrine carcinoma in the pancreatic tail.", "Final histopathology showed the tumor in the peripancreatic tissue.", "Final histopathology showed the tumor in the surrounding soft tissue.", "The histopathology was consistent with metastatic Merkel cell carcinoma.", "An insulinoma of the pancreatic body was also found."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 56-year-old male.", "The patient was admitted on 2022-09-19.", "The patient had chest tightness and chest pain for more than 2 months.", "The patient had a weight loss of 10 kilogram in the past 2 months.", "The patient had a history of afternoon low fever before 1 week.", "The patient had a clear consciousness.", "The patient had anemia.", "The patient had enlarged superficial lymph nodes.", "The patient had barrel-shaped chest.", "The patient had swollen skin on the right side of the chest.", "The patient had solid percussion sounds on the right side of the chest.", "The patient had enlarged liver on the right side.", "The patient had deep yellow urine.", "The patient had a history of mitral valvuloplasty and aortic valve replacement at the Second Affiliated Hospital of Nanchang University on 2021-08-11.", "The patient had long-term oral treatment with warfarin anticoagulation.", "The patient had long-term oral treatment with metoprolol.", "The patient was a smoker for 40 years, 10 cigarettes per day.", "The patient had no history of contact with a chronically coughing person suspected of or treated for TB.", "The CT examination showed multiple wall nodules in the right pleura.", "The CT examination showed right pleural encapsulated effusion.", "The CT examination showed bone destruction in the 2nd thoracic vertebra.", "The CT examination showed multiple slightly hypodense nodules in the liver.", "The possibility of multiple metastases of right lung cancer with malignant pleural fluid was considered.", "The histopathology showed coagulative necrosis combining with granulomatous inflammation.", "Acid-fast bacilli staining was positive.", "The diagnosis of TB infection was definite."], "summary_subclaims": ["The patient is a 56-year-old male.", "The patient is HIV-negative.", "The patient was hospitalized for chest disease.", "The patient's main symptoms included chest tightness.", "The patient's main symptoms included chest pain.", "The patient's main symptoms included fatigue.", "The patient's main symptoms included anorexia.", "The patient's main symptoms included weight loss.", "The patient's heart rate was 109 times/min.", "CT scans of the neck, chest, and abdomen revealed multiple nodules in the right pleura.", "CT scans revealed right pleural encapsulated effusion.", "CT scans showed limited, incomplete expansion of the middle and lower lobes of the right lung.", "CT scans showed enlarged lymph nodes in the right hilar and mediastinal and diaphragm groups.", "CT scans showed multiple slightly low-density nodules in the liver.", "CT scans showed bone destruction in the 2nd thoracic vertebra.", "The findings raised the possibility of multiple liver metastases of right lung cancer.", "The findings raised the possibility of malignant pleural fluid.", "The lymph nodes in the neck, mediastinum, abdomen, and pelvis were enlarged bilaterally.", "The patient was diagnosed with atypical systemic HDTB.", "The patient received three months of conventional anti-TB treatment.", "The patient refused follow-up at our hospital.", "The patient's symptoms improved significantly during telephone follow-up."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 56-year-old male.", "The patient was admitted on 2022-09-19.", "The patient had chest tightness and chest pain for more than 2 months.", "The patient had a weight loss of 10 kilogram in the past 2 months.", "The patient had a history of afternoon low fever before 1 week.", "The patient had a clear consciousness.", "The patient had anemia.", "The patient had enlarged superficial lymph nodes.", "The patient had barrel-shaped chest.", "The patient had swollen skin on the right side of the chest.", "The patient had solid percussion sounds on the right side of the chest.", "The patient had enlarged liver on the right side.", "The patient had deep yellow urine.", "The patient had a history of mitral valvuloplasty and aortic valve replacement at the Second Affiliated Hospital of Nanchang University on 2021-08-11.", "The patient had long-term oral treatment with warfarin anticoagulation.", "The patient had long-term oral treatment with metoprolol.", "The patient was a smoker for 40 years, 10 cigarettes per day.", "The patient had no history of contact with a chronically coughing person suspected of or treated for TB.", "The CT examination showed multiple wall nodules in the right pleura.", "The CT examination showed right pleural encapsulated effusion.", "The CT examination showed bone destruction in the 2nd thoracic vertebra.", "The CT examination showed multiple slightly hypodense nodules in the liver.", "The possibility of multiple metastases of right lung cancer with malignant pleural fluid was considered.", "The histopathology showed coagulative necrosis combining with granulomatous inflammation.", "Acid-fast bacilli staining was positive.", "The diagnosis of TB infection was definite."], "index": 38, "original_id": "multiclinsum_test_867_en.txt", "split": "test", "summary_subclaims": ["The patient is a 56-year-old male.", "The patient is HIV-negative.", "The patient was hospitalized for chest disease.", "The patient's main symptoms included chest tightness.", "The patient's main symptoms included chest pain.", "The patient's main symptoms included fatigue.", "The patient's main symptoms included anorexia.", "The patient's main symptoms included weight loss.", "The patient's heart rate was 109 times/min.", "CT scans of the neck, chest, and abdomen revealed multiple nodules in the right pleura.", "CT scans revealed right pleural encapsulated effusion.", "CT scans showed limited, incomplete expansion of the middle and lower lobes of the right lung.", "CT scans showed enlarged lymph nodes in the right hilar and mediastinal and diaphragm groups.", "CT scans showed multiple slightly low-density nodules in the liver.", "CT scans showed bone destruction in the 2nd thoracic vertebra.", "The findings raised the possibility of multiple liver metastases of right lung cancer.", "The findings raised the possibility of malignant pleural fluid.", "The lymph nodes in the neck, mediastinum, abdomen, and pelvis were enlarged bilaterally.", "The patient was diagnosed with atypical systemic HDTB.", "The patient received three months of conventional anti-TB treatment.", "The patient refused follow-up at our hospital.", "The patient's symptoms improved significantly during telephone follow-up."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was a 51-year-old Caucasian left-handed housewife.", "The patient had a weight of 61 kg and height of 159 cm.", "The patient was admitted due to severe sudden onset headache.", "The patient had transient loss of consciousness.", "The patient vomited.", "On examination, the patient was fully conscious and oriented.", "The patient complained of severe headache.", "Nuchal rigidity was evident.", "No focal neurological deficit was found.", "Temperature was 38\u00b0C.", "CT scan of the head revealed acute subarachnoid hemorrhage.", "CT angiography was performed.", "The cerebral vasculature harbored three saccular aneurysms.", "The right MCA aneurysm was presumed to be the ruptured aneurysm.", "A right pterional craniotomy was performed.", "The sphenoid ridge was drilled flush with the orbital roof.", "Gentle frontal lobe retraction allowed CSF drainage.", "The Sylvian fissure was opened from medial to lateral.", "A saccular aneurysm was found in the MCA trifurcation.", "The aneurysm was clipped.", "The distal basilar artery aneurysm was located between the right PCA and right SCA.", "The aneurysm dome projected laterally to the right.", "Successful clipping was achieved.", "The left ICA bifurcation aneurysm was identified.", "The aneurysm projected superiorly.", "The aneurysm was clipped.", "The patient experienced an uneventful post-operative period.", "The patient was discharged within 5 days of surgery.", "A follow-up CT angiography confirmed successful obliteration of all lesions."], "summary_subclaims": ["The patient is a 51 year-old Caucasian right handed housewife lady.", "The patient presented with a headache of acute onset.", "The headache was caused by acute subarachnoid hemorrhage.", "Cerebral computed tomographic angiography revealed multiple aneurysms.", "The patient underwent a right pterional craniotomy.", "The right pterional craniotomy was performed to obliterate right middle cerebral, distal basilar and left carotid bifurcation aneurysms.", "The post-operative course was uneventful."]}, "extra_info": {"fulltext_subclaims": ["The patient was a 51-year-old Caucasian left-handed housewife.", "The patient had a weight of 61 kg and height of 159 cm.", "The patient was admitted due to severe sudden onset headache.", "The patient had transient loss of consciousness.", "The patient vomited.", "On examination, the patient was fully conscious and oriented.", "The patient complained of severe headache.", "Nuchal rigidity was evident.", "No focal neurological deficit was found.", "Temperature was 38\u00b0C.", "CT scan of the head revealed acute subarachnoid hemorrhage.", "CT angiography was performed.", "The cerebral vasculature harbored three saccular aneurysms.", "The right MCA aneurysm was presumed to be the ruptured aneurysm.", "A right pterional craniotomy was performed.", "The sphenoid ridge was drilled flush with the orbital roof.", "Gentle frontal lobe retraction allowed CSF drainage.", "The Sylvian fissure was opened from medial to lateral.", "A saccular aneurysm was found in the MCA trifurcation.", "The aneurysm was clipped.", "The distal basilar artery aneurysm was located between the right PCA and right SCA.", "The aneurysm dome projected laterally to the right.", "Successful clipping was achieved.", "The left ICA bifurcation aneurysm was identified.", "The aneurysm projected superiorly.", "The aneurysm was clipped.", "The patient experienced an uneventful post-operative period.", "The patient was discharged within 5 days of surgery.", "A follow-up CT angiography confirmed successful obliteration of all lesions."], "index": 34, "original_id": "multiclinsum_test_2076_en.txt", "split": "test", "summary_subclaims": ["The patient is a 51 year-old Caucasian right handed housewife lady.", "The patient presented with a headache of acute onset.", "The headache was caused by acute subarachnoid hemorrhage.", "Cerebral computed tomographic angiography revealed multiple aneurysms.", "The patient underwent a right pterional craniotomy.", "The right pterional craniotomy was performed to obliterate right middle cerebral, distal basilar and left carotid bifurcation aneurysms.", "The post-operative course was uneventful."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 21-year-old male Japanese student.", "He is an active member of an equestrian club.", "He sustained a right toe injury during an accident in a club-related activity.", "The injury resulted in the severance of his right toe above the interphalangeal joint.", "He was directed to the rehabilitation department 2 weeks post-injury.", "He had no remarkable medical or family history.", "The patient agreed to provide the case report and consented to its publication, including any accompanying images.", "The ethics committee of our institution waived the need for ethical review, as the patient provided written consent for the case report.", "Initial assessments indicated pain localized to the injury site, primarily during walking.", "One month post-injury, the patient also reported pain in the right knee joint while engaging in riding or walking.", "The pain in the area of the hallux deficit hindered his ability to apply pressure on the thenars.", "Diagnostic tests, including walking cycle analysis, temporospatial gait parameters, foot pressure distribution, ground reaction force measurements, toe grip force, and one-leg standing tests, were conducted.", "The foot pressure during a comfortable walk were recorded using a Zebris plantar pressure platform.", "The center of pressure (COP) during a comfortable walking pace was captured using force plates.", "A diminished foot pressure was observed not just in the hallux but also in the metatarsal head of toes two to five on the injured side.", "The left-foot COP shifted toward the left toe in the late stance phase.", "The right-foot COP transitioned toward the second toe, exhibiting greater spatial variability.", "Assessing the walking cycle using a Zebris plantar pressure platform, the load response and single-support durations were reduced.", "The pre-swing phase was extended.", "Vertical ground reaction force during the second peak of walking was diminished on the right side.", "The patient was unable to maintain a one-leg stand for 10 seconds on the right foot.", "Pain levels for the toe and knee were rated 5 out of 10 on a numerical rating scale (NRS).", "A rehabilitation protocol was designed to enhance medial foot loading and improve foot pressure during walking and standing.", "The regimen included balance and trunk strength training.", "Starting from the fifth week, the focus shifted to lower limb strength training.", "From the ninth week, dynamic joint stability exercises were introduced to enhance neuromuscular coordination for movement stabilization.", "After 3 months, foot pressure and COP movement during walking improved.", "Pressure distribution across toes two to five and the metatarsal head improved.", "There were negligible discrepancies between the left and right sides in both the vertical and anterior\u2013posterior directions.", "The pressure was consistently distributed from the second toe of the right foot.", "Notable enhancements were also observed in the pre-leg phase.", "The second peak of the vertical component of the ground reaction force increased.", "One-leg standing on the right foot became stable for 10 seconds, even on a balance mat.", "NRS scores for the toe and knee pain reduced to 0, indicating a return to pre-injury levels of activity."], "summary_subclaims": ["The patient is a 21-year-old Japanese individual.", "The patient had a traumatic hallux deficit.", "Only a portion of the basal phalanx was intact.", "The thenar area exhibited instability.", "The instability led to impaired balance.", "The instability led to walking difficulties.", "Biomechanical assessment revealed the need for a rehabilitation strategy for the foot.", "Biomechanical assessment revealed the need for a rehabilitation strategy for the knee.", "Biomechanical assessment revealed the need for a rehabilitation strategy for the hip.", "Biomechanical assessment revealed the need for a rehabilitation strategy for the trunk.", "A rehabilitation protocol was designed to enhance medial foot loading during walking.", "A rehabilitation protocol was designed to enhance medial foot loading during standing.", "The rehabilitation protocol included balance training.", "The rehabilitation protocol included trunk strength training.", "The rehabilitation period lasted 12 weeks.", "The load response and single-support phases of the gait cycle on the affected side increased from 46.9% to 49.3%.", "The pre-swing phase of the gait cycle on the affected side decreased from 14.6% to 11.6%.", "The vertical component of the ground reaction force rose from 599.8 to 647.5 N.", "Enhanced stability from balance training contributed to the patient's improved walking.", "Enhanced stability from balance training contributed to the patient's improved balance.", "Increased muscle strength contributed to the patient's improved walking.", "Increased muscle strength contributed to the patient's improved balance."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 21-year-old male Japanese student.", "He is an active member of an equestrian club.", "He sustained a right toe injury during an accident in a club-related activity.", "The injury resulted in the severance of his right toe above the interphalangeal joint.", "He was directed to the rehabilitation department 2 weeks post-injury.", "He had no remarkable medical or family history.", "The patient agreed to provide the case report and consented to its publication, including any accompanying images.", "The ethics committee of our institution waived the need for ethical review, as the patient provided written consent for the case report.", "Initial assessments indicated pain localized to the injury site, primarily during walking.", "One month post-injury, the patient also reported pain in the right knee joint while engaging in riding or walking.", "The pain in the area of the hallux deficit hindered his ability to apply pressure on the thenars.", "Diagnostic tests, including walking cycle analysis, temporospatial gait parameters, foot pressure distribution, ground reaction force measurements, toe grip force, and one-leg standing tests, were conducted.", "The foot pressure during a comfortable walk were recorded using a Zebris plantar pressure platform.", "The center of pressure (COP) during a comfortable walking pace was captured using force plates.", "A diminished foot pressure was observed not just in the hallux but also in the metatarsal head of toes two to five on the injured side.", "The left-foot COP shifted toward the left toe in the late stance phase.", "The right-foot COP transitioned toward the second toe, exhibiting greater spatial variability.", "Assessing the walking cycle using a Zebris plantar pressure platform, the load response and single-support durations were reduced.", "The pre-swing phase was extended.", "Vertical ground reaction force during the second peak of walking was diminished on the right side.", "The patient was unable to maintain a one-leg stand for 10 seconds on the right foot.", "Pain levels for the toe and knee were rated 5 out of 10 on a numerical rating scale (NRS).", "A rehabilitation protocol was designed to enhance medial foot loading and improve foot pressure during walking and standing.", "The regimen included balance and trunk strength training.", "Starting from the fifth week, the focus shifted to lower limb strength training.", "From the ninth week, dynamic joint stability exercises were introduced to enhance neuromuscular coordination for movement stabilization.", "After 3 months, foot pressure and COP movement during walking improved.", "Pressure distribution across toes two to five and the metatarsal head improved.", "There were negligible discrepancies between the left and right sides in both the vertical and anterior\u2013posterior directions.", "The pressure was consistently distributed from the second toe of the right foot.", "Notable enhancements were also observed in the pre-leg phase.", "The second peak of the vertical component of the ground reaction force increased.", "One-leg standing on the right foot became stable for 10 seconds, even on a balance mat.", "NRS scores for the toe and knee pain reduced to 0, indicating a return to pre-injury levels of activity."], "index": 42, "original_id": "multiclinsum_test_1445_en.txt", "split": "test", "summary_subclaims": ["The patient is a 21-year-old Japanese individual.", "The patient had a traumatic hallux deficit.", "Only a portion of the basal phalanx was intact.", "The thenar area exhibited instability.", "The instability led to impaired balance.", "The instability led to walking difficulties.", "Biomechanical assessment revealed the need for a rehabilitation strategy for the foot.", "Biomechanical assessment revealed the need for a rehabilitation strategy for the knee.", "Biomechanical assessment revealed the need for a rehabilitation strategy for the hip.", "Biomechanical assessment revealed the need for a rehabilitation strategy for the trunk.", "A rehabilitation protocol was designed to enhance medial foot loading during walking.", "A rehabilitation protocol was designed to enhance medial foot loading during standing.", "The rehabilitation protocol included balance training.", "The rehabilitation protocol included trunk strength training.", "The rehabilitation period lasted 12 weeks.", "The load response and single-support phases of the gait cycle on the affected side increased from 46.9% to 49.3%.", "The pre-swing phase of the gait cycle on the affected side decreased from 14.6% to 11.6%.", "The vertical component of the ground reaction force rose from 599.8 to 647.5 N.", "Enhanced stability from balance training contributed to the patient's improved walking.", "Enhanced stability from balance training contributed to the patient's improved balance.", "Increased muscle strength contributed to the patient's improved walking.", "Increased muscle strength contributed to the patient's improved balance."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 58-year-old male.", "The patient was admitted to the hospital on November 10, 2021.", "The patient was admitted due to complaining of fever for 7 days.", "There was no family history.", "On November 2019, he was diagnosed with B-cell acute lymphoblastic leukemia.", "He received multiple chemotherapy sessions.", "His bone marrow was retested as minimal residual disease-negative complete remission.", "On November 26, 2020, the patient underwent allogeneic HSCT.", "He received treatment such as leukocytosis.", "He received GVHD prophylaxis.", "He received infection prophylaxis.", "On December 29, 2020, he developed thrombocytopenia.", "He was treated with platelet transfusion.", "Bone marrow CR and MDR were repeatedly rechecked.", "The results were negative.", "The results showed complete implantation of FISH donor.", "Fever occurred repeatedly in February, March, and May 2021.", "After anti-infection, anti-fungal, and anti-viral treatment, the patient improved.", "The patient was discharged.", "7 days before admission, the patient developed a fever.", "The highest temperature was 39.3\u00b0C.", "The patient was hospitalized in a tertiary hospital in Guangzhou.", "The chest CT showed multiple inflammations in both lungs.", "He was given imipenem/cilastatin.", "He was given caspofungin.", "He was given liposomal amphotericin B.", "He still had recurrent fevers.", "The tracheoscopy was completed.", "The bronchial fluid was found positive for MTB complex nucleic acid.", "MTB was detected again in the NGS.", "The patient was considered to be post-HSCT TB.", "He was admitted to our hospital after consultation."], "summary_subclaims": ["The patient had acute lymphoblastic leukemia.", "The patient suffered from pulmonary TB infection after HSCT.", "The patient had a poor response to linezolid-containing regimen.", "The patient developed side effects such as gingival bleeding and thrombocytopenia.", "The administration was switched to contezolid.", "After 15 days of continuous treatment, the patient's platelet increased to 58\u00d7109/L.", "The patient was discharged in stable condition.", "During subsequent anti-TB treatment with contezolid for more than 7 months, the platelets remained stable.", "No hematological adverse reactions were observed.", "No symptoms of peripheral neuropathy were observed.", "Repeat imaging showed that the bilateral lung lesions were significantly reduced."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 58-year-old male.", "The patient was admitted to the hospital on November 10, 2021.", "The patient was admitted due to complaining of fever for 7 days.", "There was no family history.", "On November 2019, he was diagnosed with B-cell acute lymphoblastic leukemia.", "He received multiple chemotherapy sessions.", "His bone marrow was retested as minimal residual disease-negative complete remission.", "On November 26, 2020, the patient underwent allogeneic HSCT.", "He received treatment such as leukocytosis.", "He received GVHD prophylaxis.", "He received infection prophylaxis.", "On December 29, 2020, he developed thrombocytopenia.", "He was treated with platelet transfusion.", "Bone marrow CR and MDR were repeatedly rechecked.", "The results were negative.", "The results showed complete implantation of FISH donor.", "Fever occurred repeatedly in February, March, and May 2021.", "After anti-infection, anti-fungal, and anti-viral treatment, the patient improved.", "The patient was discharged.", "7 days before admission, the patient developed a fever.", "The highest temperature was 39.3\u00b0C.", "The patient was hospitalized in a tertiary hospital in Guangzhou.", "The chest CT showed multiple inflammations in both lungs.", "He was given imipenem/cilastatin.", "He was given caspofungin.", "He was given liposomal amphotericin B.", "He still had recurrent fevers.", "The tracheoscopy was completed.", "The bronchial fluid was found positive for MTB complex nucleic acid.", "MTB was detected again in the NGS.", "The patient was considered to be post-HSCT TB.", "He was admitted to our hospital after consultation."], "index": 40, "original_id": "multiclinsum_test_353_en.txt", "split": "test", "summary_subclaims": ["The patient had acute lymphoblastic leukemia.", "The patient suffered from pulmonary TB infection after HSCT.", "The patient had a poor response to linezolid-containing regimen.", "The patient developed side effects such as gingival bleeding and thrombocytopenia.", "The administration was switched to contezolid.", "After 15 days of continuous treatment, the patient's platelet increased to 58\u00d7109/L.", "The patient was discharged in stable condition.", "During subsequent anti-TB treatment with contezolid for more than 7 months, the platelets remained stable.", "No hematological adverse reactions were observed.", "No symptoms of peripheral neuropathy were observed.", "Repeat imaging showed that the bilateral lung lesions were significantly reduced."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring are often recommended to support kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Declining glomerular filtration rate (GFR) is a key biomarker for chronic kidney disease progression, and early intervention through pharmacological management, dietary modification, and monitoring of biomarkers such as serum creatinine and proteinuria is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["A four-year-old girl presented to the emergency service with painful left hip and fever.", "There was no previous relevant medical history.", "There were no other local or systemic symptoms, except for a cervical adenopathy.", "On physical examination, she walked with a limp.", "Movements of the left hip were painful (mainly external rotation), but not restricted.", "Blood exam revealed anemia (Hb 8.7 gr/dL).", "Blood exam showed normal WBC.", "ESB was 123 mm.", "Reactive C protein was 149.7 mg/L.", "An initial X-ray to the pelvis revealed no changes.", "An ultrasound of the left hip was performed.", "The ultrasound revealed small infusion and synovitis.", "Guided puncture was performed.", "The puncture was macroscopically compatible with reactive arthritis.", "General and bacteriological tests were demanded.", "A CT scan to the abdomen and pelvis was performed.", "The CT scan revealed a left adrenal mass.", "The CT scan revealed retroperitoneal adenopathies in the celiac trunk and superior mesenteric artery.", "No bone or articular involvement was found in the CT scan.", "No further alterations were reported in the thoracic CT scan.", "No alterations were reported in peripheral blood smears.", "Bacteriological examination of the hip effusion was negative.", "MRI was also performed.", "The direct myelogram was compatible with infiltration from neuroblastoma.", "Bone marrow biopsy and cervical adenopathy specimens were collected to perform histological diagnosis.", "Skeletal scintigraphy demonstrated numerous points of osteoblastic activity compatible with metastatic activity.", "The 12 iodine-123 metaiodobenzylguanidine scintigraphy concluded: 'Abdominal mass with low expression of noradrenergic transporters.'", "The 12 iodine-123 metaiodobenzylguanidine scintigraphy concluded: 'Diffuse bone metastasization with high expression of noradrenergic transporters.'", "The 12 iodine-123 metaiodobenzylguanidine scintigraphy concluded: 'No other soft tissue involvement was detected.'", "In the histological report of the cervical adenopathy, the diagnosis of neuroblastoma NOS was performed.", "Immunohistochemistry revealed extensive expression for synaptophysin.", "Immunohistochemistry revealed extensive expression for CD56 (NCAM).", "Immunohistochemistry revealed absence of expression of myogenin.", "Bone marrow biopsy revealed extensive metastatic involvement.", "The patient started chemotherapy two weeks after admission.", "The patient received 8 cycles of rapid COJEC protocol.", "After six months of follow-up, the primary tumor was still without criteria for resection.", "Despite a decrease in the metastatic involvement, the primary tumor was still without criteria for resection.", "Given the chemotherapy-related renal toxicity, it was decided to proceed with irinotecan in combination with temozolomide (TEMIRI).", "After thirteen months of follow-up, no significant regression of the primary tumor occurred.", "Surgery was contraindicated.", "The patient was proposed for stem cell treatment."], "summary_subclaims": ["A four-year-old girl presented with fever and a painful limp in the left hip.", "Pain characteristics and anemia detected in the blood analyses were the first warning signs that the hip process was not standard.", "The primary suspicion was of septic arthritis.", "A CT scan of the abdomen revealed an adrenal neuroblastoma."]}, "extra_info": {"fulltext_subclaims": ["A four-year-old girl presented to the emergency service with painful left hip and fever.", "There was no previous relevant medical history.", "There were no other local or systemic symptoms, except for a cervical adenopathy.", "On physical examination, she walked with a limp.", "Movements of the left hip were painful (mainly external rotation), but not restricted.", "Blood exam revealed anemia (Hb 8.7 gr/dL).", "Blood exam showed normal WBC.", "ESB was 123 mm.", "Reactive C protein was 149.7 mg/L.", "An initial X-ray to the pelvis revealed no changes.", "An ultrasound of the left hip was performed.", "The ultrasound revealed small infusion and synovitis.", "Guided puncture was performed.", "The puncture was macroscopically compatible with reactive arthritis.", "General and bacteriological tests were demanded.", "A CT scan to the abdomen and pelvis was performed.", "The CT scan revealed a left adrenal mass.", "The CT scan revealed retroperitoneal adenopathies in the celiac trunk and superior mesenteric artery.", "No bone or articular involvement was found in the CT scan.", "No further alterations were reported in the thoracic CT scan.", "No alterations were reported in peripheral blood smears.", "Bacteriological examination of the hip effusion was negative.", "MRI was also performed.", "The direct myelogram was compatible with infiltration from neuroblastoma.", "Bone marrow biopsy and cervical adenopathy specimens were collected to perform histological diagnosis.", "Skeletal scintigraphy demonstrated numerous points of osteoblastic activity compatible with metastatic activity.", "The 12 iodine-123 metaiodobenzylguanidine scintigraphy concluded: 'Abdominal mass with low expression of noradrenergic transporters.'", "The 12 iodine-123 metaiodobenzylguanidine scintigraphy concluded: 'Diffuse bone metastasization with high expression of noradrenergic transporters.'", "The 12 iodine-123 metaiodobenzylguanidine scintigraphy concluded: 'No other soft tissue involvement was detected.'", "In the histological report of the cervical adenopathy, the diagnosis of neuroblastoma NOS was performed.", "Immunohistochemistry revealed extensive expression for synaptophysin.", "Immunohistochemistry revealed extensive expression for CD56 (NCAM).", "Immunohistochemistry revealed absence of expression of myogenin.", "Bone marrow biopsy revealed extensive metastatic involvement.", "The patient started chemotherapy two weeks after admission.", "The patient received 8 cycles of rapid COJEC protocol.", "After six months of follow-up, the primary tumor was still without criteria for resection.", "Despite a decrease in the metastatic involvement, the primary tumor was still without criteria for resection.", "Given the chemotherapy-related renal toxicity, it was decided to proceed with irinotecan in combination with temozolomide (TEMIRI).", "After thirteen months of follow-up, no significant regression of the primary tumor occurred.", "Surgery was contraindicated.", "The patient was proposed for stem cell treatment."], "index": 60, "original_id": "multiclinsum_test_1260_en.txt", "split": "test", "summary_subclaims": ["A four-year-old girl presented with fever and a painful limp in the left hip.", "Pain characteristics and anemia detected in the blood analyses were the first warning signs that the hip process was not standard.", "The primary suspicion was of septic arthritis.", "A CT scan of the abdomen revealed an adrenal neuroblastoma."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was a 52-year-old woman.", "She was admitted with acute myocardial infarction due to a spontaneous right coronary artery dissection.", "Her medical history included a conservatively managed left posterolateral branch myocardial infarction at the age of 39.", "At 51, she was treated for breast cancer with a curative intent.", "An emergency percutaneous coronary intervention of the right coronary artery was performed.", "The post-procedural course was complicated by ventricular tachycardia and fibrillation.", "She was successfully resuscitated.", "She developed cardiogenic shock due to failure of the right ventricle.", "The cardiogenic shock was refractory to fluid resuscitation and inotropes.", "She was stabilized using peripheral veno-arterial extracorporeal membrane oxygenation.", "Echocardiography showed a dilated right ventricle with severely impaired function.", "Echocardiography showed paradoxical septal motion with signs of right ventricular volume overload.", "Echocardiography showed severe tricuspid regurgitation with elevated filling pressures.", "The left ventricular function was slightly impaired.", "She developed heparin-induced thrombocytopaenia.", "She was rejected for an urgent heart transplant listing due to the recent oncological history.", "The veno-arterial extracorporeal membrane oxygenation was exchanged for percutaneous veno-pulmonary extracorporeal membrane oxygenation.", "Weaning from extracorporeal membrane oxygenation was initially successful.", "Within days after discontinuation of the extracorporeal membrane oxygenation, she developed fast recurrent ventricular tachycardias.", "The ventricular tachycardias were haemodynamically poorly tolerated.", "Intravenous administration of amiodarone resulted in further progression of right ventricular failure.", "Amiodarone caused a slow junctional rhythm that was poorly tolerated haemodynamically.", "Escalation in the inotropic regimen in the days after extracorporeal membrane oxygenation weaning further contributed to the incessant ventricular tachycardias.", "A decision was made to perform a bidirectional cavopulmonary anastomosis with a concomitant tricuspid valve annuloplasty.", "In a bidirectional cavopulmonary anastomosis, the superior vena cava is disconnected from the right atrium and anastomosed end-to-side to the right pulmonary artery.", "The bidirectional cavopulmonary anastomosis redirects a substantial proportion of the venous return directly to the lungs, bypassing the right ventricle.", "The patient underwent bidirectional cavopulmonary anastomosis and restrictive tricuspid valve annuloplasty.", "She had an arterial oxygen saturation of 95% in ambient air.", "She could be weaned off veno-arterial extracorporeal membrane oxygenation and inotropes within 3 weeks after the operation.", "Echocardiography showed normalization of right ventricular dimensions.", "Echocardiography showed moderate to severely impaired right ventricular function.", "Echocardiography showed trivial tricuspid valve regurgitation.", "A subcutaneous implantable cardioverter-defibrillator seemed most appropriate.", "Implanting the subcutaneous implantable cardioverter-defibrillator was postponed due to a sternal wound infection.", "She was discharged home with a LifeVest Wearable Defibrillator.", "The peripheral oxygen saturation at discharge was 99%.", "She completed a cardiac rehabilitation program.", "Her New York Heart Association functional class IV improved to III at the 6-month follow-up examination.", "There have not been any heart failure-related admissions."], "summary_subclaims": ["The patient is a 52-year-old woman.", "She had cardiogenic shock.", "She had refractory right ventricular failure.", "The cause was spontaneous dissection of the right coronary artery.", "She remained dependent on mechanical support for several weeks.", "A right ventricular assist device implant was explored as a long-term support option.", "A bidirectional cavopulmonary anastomosis was explored as a long-term support option.", "A history of malignancy was present.", "Possible right ventricular functional recovery was considered.", "A decision in favour of the bidirectional cavopulmonary anastomosis was made.", "A concomitant tricuspid valve annuloplasty was performed.", "Postoperatively, her clinical condition improved significantly.", "She could be discharged home.", "Echocardiography showed normalization of right ventricular dimensions.", "Echocardiography showed slight improvement of right ventricular function."]}, "extra_info": {"fulltext_subclaims": ["The patient was a 52-year-old woman.", "She was admitted with acute myocardial infarction due to a spontaneous right coronary artery dissection.", "Her medical history included a conservatively managed left posterolateral branch myocardial infarction at the age of 39.", "At 51, she was treated for breast cancer with a curative intent.", "An emergency percutaneous coronary intervention of the right coronary artery was performed.", "The post-procedural course was complicated by ventricular tachycardia and fibrillation.", "She was successfully resuscitated.", "She developed cardiogenic shock due to failure of the right ventricle.", "The cardiogenic shock was refractory to fluid resuscitation and inotropes.", "She was stabilized using peripheral veno-arterial extracorporeal membrane oxygenation.", "Echocardiography showed a dilated right ventricle with severely impaired function.", "Echocardiography showed paradoxical septal motion with signs of right ventricular volume overload.", "Echocardiography showed severe tricuspid regurgitation with elevated filling pressures.", "The left ventricular function was slightly impaired.", "She developed heparin-induced thrombocytopaenia.", "She was rejected for an urgent heart transplant listing due to the recent oncological history.", "The veno-arterial extracorporeal membrane oxygenation was exchanged for percutaneous veno-pulmonary extracorporeal membrane oxygenation.", "Weaning from extracorporeal membrane oxygenation was initially successful.", "Within days after discontinuation of the extracorporeal membrane oxygenation, she developed fast recurrent ventricular tachycardias.", "The ventricular tachycardias were haemodynamically poorly tolerated.", "Intravenous administration of amiodarone resulted in further progression of right ventricular failure.", "Amiodarone caused a slow junctional rhythm that was poorly tolerated haemodynamically.", "Escalation in the inotropic regimen in the days after extracorporeal membrane oxygenation weaning further contributed to the incessant ventricular tachycardias.", "A decision was made to perform a bidirectional cavopulmonary anastomosis with a concomitant tricuspid valve annuloplasty.", "In a bidirectional cavopulmonary anastomosis, the superior vena cava is disconnected from the right atrium and anastomosed end-to-side to the right pulmonary artery.", "The bidirectional cavopulmonary anastomosis redirects a substantial proportion of the venous return directly to the lungs, bypassing the right ventricle.", "The patient underwent bidirectional cavopulmonary anastomosis and restrictive tricuspid valve annuloplasty.", "She had an arterial oxygen saturation of 95% in ambient air.", "She could be weaned off veno-arterial extracorporeal membrane oxygenation and inotropes within 3 weeks after the operation.", "Echocardiography showed normalization of right ventricular dimensions.", "Echocardiography showed moderate to severely impaired right ventricular function.", "Echocardiography showed trivial tricuspid valve regurgitation.", "A subcutaneous implantable cardioverter-defibrillator seemed most appropriate.", "Implanting the subcutaneous implantable cardioverter-defibrillator was postponed due to a sternal wound infection.", "She was discharged home with a LifeVest Wearable Defibrillator.", "The peripheral oxygen saturation at discharge was 99%.", "She completed a cardiac rehabilitation program.", "Her New York Heart Association functional class IV improved to III at the 6-month follow-up examination.", "There have not been any heart failure-related admissions."], "index": 70, "original_id": "multiclinsum_test_3152_en.txt", "split": "test", "summary_subclaims": ["The patient is a 52-year-old woman.", "She had cardiogenic shock.", "She had refractory right ventricular failure.", "The cause was spontaneous dissection of the right coronary artery.", "She remained dependent on mechanical support for several weeks.", "A right ventricular assist device implant was explored as a long-term support option.", "A bidirectional cavopulmonary anastomosis was explored as a long-term support option.", "A history of malignancy was present.", "Possible right ventricular functional recovery was considered.", "A decision in favour of the bidirectional cavopulmonary anastomosis was made.", "A concomitant tricuspid valve annuloplasty was performed.", "Postoperatively, her clinical condition improved significantly.", "She could be discharged home.", "Echocardiography showed normalization of right ventricular dimensions.", "Echocardiography showed slight improvement of right ventricular function."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring are often recommended to support kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Declining glomerular filtration rate (GFR) is a key biomarker for chronic kidney disease progression, and early intervention through pharmacological management, dietary modification, and monitoring of biomarkers such as serum creatinine and proteinuria is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was a 69-year-old man.", "The patient had untreated hypertension.", "The patient was transported to the hospital 4 h after being injured in a motor vehicle accident.", "The patient was conscious.", "The patient's body temperature was 36.6\u00b0C.", "The patient's heart rate was 75 bpm.", "The patient's blood pressure was 186/115 mmHg.", "The patient's oxygen saturation was 96% on nasal cannula at 1 L.", "The troponin I level was 0.149 ng/mL.", "The CK-MB level was 27.3 U/L.", "Electrocardiography revealed premature ventricular contraction.", "Electrocardiography revealed an incomplete right bundle branch block.", "Contrast-enhanced computed tomography showed serial fractures from the left fourth to seventh ribs.", "The sixth rib was protruding into the thoracic cavity toward the heart.", "The fifth rib was fractured near the heart.", "The seventh rib was fractured near the diaphragm.", "A small pleural effusion, suspected to be a hemothorax, was observed in the left thorax.", "The pleural effusion was not increasing in size.", "Drainage was not conducted.", "Extravasation into a liver cyst was identified.", "The bleeding needed to be stopped by interventional radiology prior to surgery.", "Nine hours after the injury, the CK-MB level decreased to 15.7 U/L.", "Nine hours after the injury, the troponin I level increased to 1.009 ng/mL.", "Cardiac injury was suspected.", "Exploratory VATS was immediately performed.", "The left ventricular wall was crushed below the injured pericardium on the anterior side of the phrenic nerve.", "The phrenic nerve was intact.", "The diaphragm was damaged.", "No penetrating injury to the abdominal cavity was observed.", "The coronary arteries were not injured.", "There was no bleeding in the damaged area.", "A fragment of the sixth rib was protruding into the thoracic cavity.", "No pulmonary fistula was observed.", "The injury to the left ventricular wall did not penetrate deep into the lumen.", "The injury was closed horizontally using a U-shaped suture with 4-0 non-resorbable polypropylene with felt.", "The injury was covered with collagen-fibrin patch (TachoSil\u00ae).", "The lacerated pericardium was sparsely sutured.", "The scattered bone fragments were removed.", "The fifth and sixth ribs were repaired using bioresorbable plates (SUPER FIXSORB-MX\u00ae) as braces.", "The diaphragm was not repaired.", "A 20-Fr. double lumen chest tube was placed to the anterior side.", "A 28-Fr. single lumen chest tube was placed to the posterior side.", "The patient was extubated on postoperative day 2.", "The chest tubes were removed on postoperative day 4.", "Paroxysmal atrial fibrillation appeared transiently.", "The atrial fibrillation improved after the administration of beta-blockers.", "The patient's myocardial enzyme levels gradually decreased.", "The patient was discharged from the hospital on postoperative day 16.", "No major abnormalities were noted 3 months postoperatively."], "summary_subclaims": ["The patient is a 69-year-old man.", "The patient was injured in a motor vehicle accident.", "The patient suffered from left hemothorax.", "The patient had multiple rib fractures near the heart.", "A comprehensive assessment raised suspicions of lacerated pericardium.", "A comprehensive assessment raised suspicions of myocardial injury.", "A thoracoscopy was performed 9\u2009h after injury.", "A penetrating cardiac injury was detected.", "The injury was surgically treated via video-assisted thoracoscopic surgery.", "The patient recovered uneventfully.", "The patient was discharged on postoperative day 16."]}, "extra_info": {"fulltext_subclaims": ["The patient was a 69-year-old man.", "The patient had untreated hypertension.", "The patient was transported to the hospital 4 h after being injured in a motor vehicle accident.", "The patient was conscious.", "The patient's body temperature was 36.6\u00b0C.", "The patient's heart rate was 75 bpm.", "The patient's blood pressure was 186/115 mmHg.", "The patient's oxygen saturation was 96% on nasal cannula at 1 L.", "The troponin I level was 0.149 ng/mL.", "The CK-MB level was 27.3 U/L.", "Electrocardiography revealed premature ventricular contraction.", "Electrocardiography revealed an incomplete right bundle branch block.", "Contrast-enhanced computed tomography showed serial fractures from the left fourth to seventh ribs.", "The sixth rib was protruding into the thoracic cavity toward the heart.", "The fifth rib was fractured near the heart.", "The seventh rib was fractured near the diaphragm.", "A small pleural effusion, suspected to be a hemothorax, was observed in the left thorax.", "The pleural effusion was not increasing in size.", "Drainage was not conducted.", "Extravasation into a liver cyst was identified.", "The bleeding needed to be stopped by interventional radiology prior to surgery.", "Nine hours after the injury, the CK-MB level decreased to 15.7 U/L.", "Nine hours after the injury, the troponin I level increased to 1.009 ng/mL.", "Cardiac injury was suspected.", "Exploratory VATS was immediately performed.", "The left ventricular wall was crushed below the injured pericardium on the anterior side of the phrenic nerve.", "The phrenic nerve was intact.", "The diaphragm was damaged.", "No penetrating injury to the abdominal cavity was observed.", "The coronary arteries were not injured.", "There was no bleeding in the damaged area.", "A fragment of the sixth rib was protruding into the thoracic cavity.", "No pulmonary fistula was observed.", "The injury to the left ventricular wall did not penetrate deep into the lumen.", "The injury was closed horizontally using a U-shaped suture with 4-0 non-resorbable polypropylene with felt.", "The injury was covered with collagen-fibrin patch (TachoSil\u00ae).", "The lacerated pericardium was sparsely sutured.", "The scattered bone fragments were removed.", "The fifth and sixth ribs were repaired using bioresorbable plates (SUPER FIXSORB-MX\u00ae) as braces.", "The diaphragm was not repaired.", "A 20-Fr. double lumen chest tube was placed to the anterior side.", "A 28-Fr. single lumen chest tube was placed to the posterior side.", "The patient was extubated on postoperative day 2.", "The chest tubes were removed on postoperative day 4.", "Paroxysmal atrial fibrillation appeared transiently.", "The atrial fibrillation improved after the administration of beta-blockers.", "The patient's myocardial enzyme levels gradually decreased.", "The patient was discharged from the hospital on postoperative day 16.", "No major abnormalities were noted 3 months postoperatively."], "index": 50, "original_id": "multiclinsum_test_2967_en.txt", "split": "test", "summary_subclaims": ["The patient is a 69-year-old man.", "The patient was injured in a motor vehicle accident.", "The patient suffered from left hemothorax.", "The patient had multiple rib fractures near the heart.", "A comprehensive assessment raised suspicions of lacerated pericardium.", "A comprehensive assessment raised suspicions of myocardial injury.", "A thoracoscopy was performed 9\u2009h after injury.", "A penetrating cardiac injury was detected.", "The injury was surgically treated via video-assisted thoracoscopic surgery.", "The patient recovered uneventfully.", "The patient was discharged on postoperative day 16."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring are often recommended to support kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Declining glomerular filtration rate (GFR) is a key biomarker for chronic kidney disease progression, and early intervention through pharmacological management, dietary modification, and monitoring of biomarkers such as serum creatinine and proteinuria is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is an 8-year-old boy.", "He had no personal or family history of interest.", "He presented to the paediatric emergency department with abnormal ocular movements of a year's duration.", "The family reported about 5-6 episodes a day of about 5-10 seconds duration.", "The episodes consisted of horizontal conjugate ocular movements with rapid jerks.", "There was slight associated miosis.", "There were no associated head or limb movements.", "The episodes did not associate with fixation of the gaze.", "The episodes did not associate with position or movements of the head.", "The patient could not self-provoke the episodes.", "The patient could identify the onset of the episodes.", "The episodes were of sudden onset and cessation.", "Some episodes gave the impression of disconnection from the environment or loss of consciousness.", "There was no postictal period.", "There was no headache.", "The episodes always occurred in the waking state.", "The episodes never occurred during sleep.", "The parents observed a higher frequency of episodes on days of greater stress.", "The parents observed a higher frequency of episodes on days of greater physical fatigue.", "There were no other triggers identified.", "There was no ataxia.", "There was no tinnitus.", "There were no autonomic symptoms.", "There was no hearing loss.", "There was no history of head trauma.", "There was no consumption of drugs.", "There was no consumption of other toxic substances.", "The symptoms had not changed or progressed since their onset.", "The neurological examination between episodes was normal.", "Ophthalmologic evaluation ruled out visual pathology.", "Otolaryngologic evaluation ruled out pathology in that area.", "Otolaryngologic evaluation described a high intensity, low amplitude jerk nystagmus episode.", "The patient was hospitalized for further evaluation.", "General laboratory tests showed no pathological findings.", "Videotaping of the episodes by the family was of great help in the diagnostic orientation.", "The video-electroencephalogram demonstrated an electro-clinical correlate of the episodes.", "The VEEG was performed in the waking state.", "The VEEG recorded two separate events of about 8-10 seconds duration.", "The background tracing was normal for his age.", "Epileptiform activity was recorded in the left temporal and occipital region.", "The epileptiform activity later generalized.", "Treatment with carbamazepine was initiated orally at an ascending dose.", "A brain magnetic resonance study with contrast was completed.", "The MRI showed no evidence of structural alterations.", "The MRI showed no evidence of cortical development anomalies.", "The final diagnosis was ictal nystagmus.", "He was discharged to home with a dose of carbamazepine of 13 mg/kg/day.", "The dose was increased to 17 mg/kg/day.", "In outpatient follow-up in Neuropediatric consultations, 2 years after the start of treatment, good adherence was noted.", "In outpatient follow-up in Neuropediatric consultations, 2 years after the start of treatment, absence of side effects to treatment was noted.", "In outpatient follow-up in Neuropediatric consultations, 2 years after the start of treatment, there were no new episodes."], "summary_subclaims": ["The patient is an 8-year-old male school-age child.", "The patient has no relevant medical history.", "He presented with a 1-year history of conjugate horizontal rapid eye movement jerking.", "The eye movement jerking was associated with mild miosis.", "The episodes lasted 5-10 seconds.", "The episodes occurred 5-6 times daily.", "Some episodes had a questionable disconnection from the environment.", "Some episodes had questionable impairment of consciousness.", "There were no other accompanying signs or symptoms.", "General examinations were normal.", "Ophthalmologists ruled out pathology.", "Otolaryngologists ruled out pathology.", "The neurological examination between episodes was normal.", "The video-electroencephalogram demonstrated an electro-clinical correlate.", "Epileptiform activity was noted in the left temporal and occipital region.", "The epileptiform activity later generalized during episodes.", "The brain MRI was normal.", "Treatment with carbamazepine was initiated.", "The patient had a good evolution after treatment.", "There was no recurrence of episodes at 2 years of follow-up."]}, "extra_info": {"fulltext_subclaims": ["The patient is an 8-year-old boy.", "He had no personal or family history of interest.", "He presented to the paediatric emergency department with abnormal ocular movements of a year's duration.", "The family reported about 5-6 episodes a day of about 5-10 seconds duration.", "The episodes consisted of horizontal conjugate ocular movements with rapid jerks.", "There was slight associated miosis.", "There were no associated head or limb movements.", "The episodes did not associate with fixation of the gaze.", "The episodes did not associate with position or movements of the head.", "The patient could not self-provoke the episodes.", "The patient could identify the onset of the episodes.", "The episodes were of sudden onset and cessation.", "Some episodes gave the impression of disconnection from the environment or loss of consciousness.", "There was no postictal period.", "There was no headache.", "The episodes always occurred in the waking state.", "The episodes never occurred during sleep.", "The parents observed a higher frequency of episodes on days of greater stress.", "The parents observed a higher frequency of episodes on days of greater physical fatigue.", "There were no other triggers identified.", "There was no ataxia.", "There was no tinnitus.", "There were no autonomic symptoms.", "There was no hearing loss.", "There was no history of head trauma.", "There was no consumption of drugs.", "There was no consumption of other toxic substances.", "The symptoms had not changed or progressed since their onset.", "The neurological examination between episodes was normal.", "Ophthalmologic evaluation ruled out visual pathology.", "Otolaryngologic evaluation ruled out pathology in that area.", "Otolaryngologic evaluation described a high intensity, low amplitude jerk nystagmus episode.", "The patient was hospitalized for further evaluation.", "General laboratory tests showed no pathological findings.", "Videotaping of the episodes by the family was of great help in the diagnostic orientation.", "The video-electroencephalogram demonstrated an electro-clinical correlate of the episodes.", "The VEEG was performed in the waking state.", "The VEEG recorded two separate events of about 8-10 seconds duration.", "The background tracing was normal for his age.", "Epileptiform activity was recorded in the left temporal and occipital region.", "The epileptiform activity later generalized.", "Treatment with carbamazepine was initiated orally at an ascending dose.", "A brain magnetic resonance study with contrast was completed.", "The MRI showed no evidence of structural alterations.", "The MRI showed no evidence of cortical development anomalies.", "The final diagnosis was ictal nystagmus.", "He was discharged to home with a dose of carbamazepine of 13 mg/kg/day.", "The dose was increased to 17 mg/kg/day.", "In outpatient follow-up in Neuropediatric consultations, 2 years after the start of treatment, good adherence was noted.", "In outpatient follow-up in Neuropediatric consultations, 2 years after the start of treatment, absence of side effects to treatment was noted.", "In outpatient follow-up in Neuropediatric consultations, 2 years after the start of treatment, there were no new episodes."], "index": 62, "original_id": "multiclinsum_test_3001_en.txt", "split": "test", "summary_subclaims": ["The patient is an 8-year-old male school-age child.", "The patient has no relevant medical history.", "He presented with a 1-year history of conjugate horizontal rapid eye movement jerking.", "The eye movement jerking was associated with mild miosis.", "The episodes lasted 5-10 seconds.", "The episodes occurred 5-6 times daily.", "Some episodes had a questionable disconnection from the environment.", "Some episodes had questionable impairment of consciousness.", "There were no other accompanying signs or symptoms.", "General examinations were normal.", "Ophthalmologists ruled out pathology.", "Otolaryngologists ruled out pathology.", "The neurological examination between episodes was normal.", "The video-electroencephalogram demonstrated an electro-clinical correlate.", "Epileptiform activity was noted in the left temporal and occipital region.", "The epileptiform activity later generalized during episodes.", "The brain MRI was normal.", "Treatment with carbamazepine was initiated.", "The patient had a good evolution after treatment.", "There was no recurrence of episodes at 2 years of follow-up."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring are often recommended to support kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Declining glomerular filtration rate (GFR) is a key biomarker for chronic kidney disease progression, and early intervention through pharmacological management, dietary modification, and monitoring of biomarkers such as serum creatinine and proteinuria is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 66-year-old Maori man.", "He had a history of an enlarged left testicle for 10 weeks.", "Clinical examination revealed nontender swelling of the left testicle.", "His alpha-fetoprotein (AFP) levels were within normal limits.", "His beta-human chorionic gonadotropin (BHCG) levels were within normal limits.", "His lactate dehydrogenase (LDH) concentration was 267 U/L.", "Ultrasonography showed an enlarged left testicle measuring 7 \u00d7 5.5 \u00d7 4.3 cm.", "The estimated volume of the left testicle was 87 ml.", "A large, heterogeneous mass involved the entire testicle.", "The mass showed increased vascularity.", "The right testicle measured 3.7 \u00d7 2.5 \u00d7 1.8 cm.", "The estimated volume of the right testicle was 8.8 ml.", "The patient underwent left orchiectomy.", "The macroscopic specimen had well-circumscribed nodular lesions of varying sizes.", "The largest lesion measured 45 \u00d7 15 mm.", "The largest lesion contained solid and gelatinous components.", "Sections showed tumor composed of sheets of small, blue, round cells.", "The tumor was divided into nodules by fibrous septae.", "Immunostaining showed the tumor to be cytokeratin 20 (CK20)-positive.", "The CK20 staining pattern was typical paranuclear dotlike.", "The tumor was positive for CD56.", "The tumor was positive for CD117.", "The tumor was positive for CK (paranuclear dots).", "The tumor was negative for CK7.", "The tumor was negative for placental alkaline phosphatase (PLAP).", "The tumor was negative for CD30.", "The tumor was negative for CD20.", "The tumor was negative for AFP.", "The tumor was negative for S100.", "The tumor was negative for SOX10.", "The tumor was negative for prostate-specific antigen (PSA).", "The tumor was negative for chromogranin.", "The tumor was negative for thyroid transcription factor 1 (TTF-1).", "The Ki-67 level was >50%.", "The immunostaining pattern raised the possibility of metastatic Merkel cell carcinoma (MCC).", "The patient presented again 3 months later with a right testicular mass.", "Tumor markers, including LDH, AFP, and BHCG, were within normal limits.", "Ultrasonographic imaging showed a new lesion in the right testis measuring 3 \u00d7 2.6 \u00d7 2.3 cm.", "The patient underwent right orchiectomy.", "Sections showed diffuse infiltration of small, blue, round cells.", "Immunostains were positive for CD117.", "Immunostains were positive for CD56.", "Immunostains were positive for synaptophysin.", "Immunostains were positive for CK20 (dotlike).", "Immunostains were positive for cytokeratin AE1/AE3 (dotlike).", "The tumor cells were negative for inhibin.", "The tumor cells were negative for PLAP.", "The tumor cells were negative for PSA.", "The tumor cells were negative for S100.", "The tumor cells were negative for CD30.", "The tumor cells were negative for CD45.", "The tumor cells were negative for CD3.", "The tumor cells were negative for CD20.", "The tumor cells were negative for TTF-1.", "The tumor cells were negative for napsin A.", "The Ki-67 level was 80%.", "The pattern was consistent with a poorly differentiated neuroendocrine tumor.", "The pattern was in keeping with metastatic MCC.", "A primary site was not identified.", "A staging computed tomographic scan did not show evidence of other metastases.", "The patient received six cycles of adjuvant carboplatin and etoposide chemotherapy.", "He remained disease-free 18 months following completion of chemotherapy."], "summary_subclaims": ["A 66-year-old Maori man presented to our hospital with left testicular swelling.", "His alpha-fetoprotein and beta-human chorionic gonadotrophin levels were within normal limits.", "His lactate dehydrogenase concentration was elevated to 267 U/L.", "Ultrasound imaging confirmed a large testicular mass.", "He underwent left orchiectomy.", "His histological examination revealed a neuroendocrine tumor with an immunostaining pattern suggesting Merkel cell carcinoma.", "He presented to our hospital again 3 months later with right testicular swelling.", "Right testicular swelling was confirmed on ultrasound sonography to be a tumor.", "He underwent a right orchiectomy.", "His histological examination revealed metastatic Merkel cell carcinoma.", "A primary lesion was not identified.", "Computed tomographic imaging did not reveal spread to other organs.", "He received six cycles of adjuvant carboplatin and etoposide chemotherapy.", "He remained disease-free 18 months after completion of chemotherapy."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 66-year-old Maori man.", "He had a history of an enlarged left testicle for 10 weeks.", "Clinical examination revealed nontender swelling of the left testicle.", "His alpha-fetoprotein (AFP) levels were within normal limits.", "His beta-human chorionic gonadotropin (BHCG) levels were within normal limits.", "His lactate dehydrogenase (LDH) concentration was 267 U/L.", "Ultrasonography showed an enlarged left testicle measuring 7 \u00d7 5.5 \u00d7 4.3 cm.", "The estimated volume of the left testicle was 87 ml.", "A large, heterogeneous mass involved the entire testicle.", "The mass showed increased vascularity.", "The right testicle measured 3.7 \u00d7 2.5 \u00d7 1.8 cm.", "The estimated volume of the right testicle was 8.8 ml.", "The patient underwent left orchiectomy.", "The macroscopic specimen had well-circumscribed nodular lesions of varying sizes.", "The largest lesion measured 45 \u00d7 15 mm.", "The largest lesion contained solid and gelatinous components.", "Sections showed tumor composed of sheets of small, blue, round cells.", "The tumor was divided into nodules by fibrous septae.", "Immunostaining showed the tumor to be cytokeratin 20 (CK20)-positive.", "The CK20 staining pattern was typical paranuclear dotlike.", "The tumor was positive for CD56.", "The tumor was positive for CD117.", "The tumor was positive for CK (paranuclear dots).", "The tumor was negative for CK7.", "The tumor was negative for placental alkaline phosphatase (PLAP).", "The tumor was negative for CD30.", "The tumor was negative for CD20.", "The tumor was negative for AFP.", "The tumor was negative for S100.", "The tumor was negative for SOX10.", "The tumor was negative for prostate-specific antigen (PSA).", "The tumor was negative for chromogranin.", "The tumor was negative for thyroid transcription factor 1 (TTF-1).", "The Ki-67 level was >50%.", "The immunostaining pattern raised the possibility of metastatic Merkel cell carcinoma (MCC).", "The patient presented again 3 months later with a right testicular mass.", "Tumor markers, including LDH, AFP, and BHCG, were within normal limits.", "Ultrasonographic imaging showed a new lesion in the right testis measuring 3 \u00d7 2.6 \u00d7 2.3 cm.", "The patient underwent right orchiectomy.", "Sections showed diffuse infiltration of small, blue, round cells.", "Immunostains were positive for CD117.", "Immunostains were positive for CD56.", "Immunostains were positive for synaptophysin.", "Immunostains were positive for CK20 (dotlike).", "Immunostains were positive for cytokeratin AE1/AE3 (dotlike).", "The tumor cells were negative for inhibin.", "The tumor cells were negative for PLAP.", "The tumor cells were negative for PSA.", "The tumor cells were negative for S100.", "The tumor cells were negative for CD30.", "The tumor cells were negative for CD45.", "The tumor cells were negative for CD3.", "The tumor cells were negative for CD20.", "The tumor cells were negative for TTF-1.", "The tumor cells were negative for napsin A.", "The Ki-67 level was 80%.", "The pattern was consistent with a poorly differentiated neuroendocrine tumor.", "The pattern was in keeping with metastatic MCC.", "A primary site was not identified.", "A staging computed tomographic scan did not show evidence of other metastases.", "The patient received six cycles of adjuvant carboplatin and etoposide chemotherapy.", "He remained disease-free 18 months following completion of chemotherapy."], "index": 52, "original_id": "multiclinsum_test_2759_en.txt", "split": "test", "summary_subclaims": ["A 66-year-old Maori man presented to our hospital with left testicular swelling.", "His alpha-fetoprotein and beta-human chorionic gonadotrophin levels were within normal limits.", "His lactate dehydrogenase concentration was elevated to 267 U/L.", "Ultrasound imaging confirmed a large testicular mass.", "He underwent left orchiectomy.", "His histological examination revealed a neuroendocrine tumor with an immunostaining pattern suggesting Merkel cell carcinoma.", "He presented to our hospital again 3 months later with right testicular swelling.", "Right testicular swelling was confirmed on ultrasound sonography to be a tumor.", "He underwent a right orchiectomy.", "His histological examination revealed metastatic Merkel cell carcinoma.", "A primary lesion was not identified.", "Computed tomographic imaging did not reveal spread to other organs.", "He received six cycles of adjuvant carboplatin and etoposide chemotherapy.", "He remained disease-free 18 months after completion of chemotherapy."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 34-year-old female.", "She had a 1 year history of intermittent pain in the right side of the waist without obvious inducement.", "She did not notice other symptoms such as nausea and vomiting, chills, high fever, chest tightness, frequent urination, urgency of urination, and painful urination.", "The symptoms gradually worsened in the recent 2 mo.", "She had no previous history of viral hepatitis B or cirrhosis.", "She denied smoking or drinking.", "Clinical examination showed no obvious abnormality.", "All laboratory blood tests were within normal limits.", "Indocyanine green 15 min retention was rated 2.9%.", "Child-Pugh was rated A.", "Abdominal CT showed multiple nodules and abnormal lumpy low-density shadows in the liver parenchyma.", "The larger lesions were located in the left lobe and caudate lobe of the liver.", "The larger lesions measured about 9.5 cm \u00d7 6.3 cm and 8.1 cm \u00d7 6.5 cm.", "Abdominal MRI revealed multiple space-occupying lesions in the liver.", "Combined with enhanced CT scan, hemangioma was considered.", "Compression of the main portal vein and right portal vein was noted.", "The inferior vena cava narrowed.", "The total liver volume was about 1739 cm3.", "The lesion liver volume was about 571 cm3.", "The residual liver volume was about 1168 cm3."], "summary_subclaims": ["The patient is a 34-year-old female.", "She had a 1 year history of intermittent pain in the right side of the waist.", "The pain had no obvious inducement.", "All laboratory blood tests were within normal limits.", "Indocyanine green 15 min retention was rated 2.9%.", "Child-Pugh was rated A.", "Computed tomography and magnetic resonance imaging diagnosed giant hemangioma of the caudate lobe.", "Computed tomography and magnetic resonance imaging diagnosed hemangioma of the left lobe of the liver.", "Surgical treatment was performed after discussion.", "The surgical treatment lasted 410 min.", "Intraoperative bleeding was about 600 mL.", "Postoperative pathological findings were cavernous hemangioma.", "There were no obvious postoperative complications.", "The patient was discharged 10 d after surgery."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 34-year-old female.", "She had a 1 year history of intermittent pain in the right side of the waist without obvious inducement.", "She did not notice other symptoms such as nausea and vomiting, chills, high fever, chest tightness, frequent urination, urgency of urination, and painful urination.", "The symptoms gradually worsened in the recent 2 mo.", "She had no previous history of viral hepatitis B or cirrhosis.", "She denied smoking or drinking.", "Clinical examination showed no obvious abnormality.", "All laboratory blood tests were within normal limits.", "Indocyanine green 15 min retention was rated 2.9%.", "Child-Pugh was rated A.", "Abdominal CT showed multiple nodules and abnormal lumpy low-density shadows in the liver parenchyma.", "The larger lesions were located in the left lobe and caudate lobe of the liver.", "The larger lesions measured about 9.5 cm \u00d7 6.3 cm and 8.1 cm \u00d7 6.5 cm.", "Abdominal MRI revealed multiple space-occupying lesions in the liver.", "Combined with enhanced CT scan, hemangioma was considered.", "Compression of the main portal vein and right portal vein was noted.", "The inferior vena cava narrowed.", "The total liver volume was about 1739 cm3.", "The lesion liver volume was about 571 cm3.", "The residual liver volume was about 1168 cm3."], "index": 72, "original_id": "multiclinsum_test_2984_en.txt", "split": "test", "summary_subclaims": ["The patient is a 34-year-old female.", "She had a 1 year history of intermittent pain in the right side of the waist.", "The pain had no obvious inducement.", "All laboratory blood tests were within normal limits.", "Indocyanine green 15 min retention was rated 2.9%.", "Child-Pugh was rated A.", "Computed tomography and magnetic resonance imaging diagnosed giant hemangioma of the caudate lobe.", "Computed tomography and magnetic resonance imaging diagnosed hemangioma of the left lobe of the liver.", "Surgical treatment was performed after discussion.", "The surgical treatment lasted 410 min.", "Intraoperative bleeding was about 600 mL.", "Postoperative pathological findings were cavernous hemangioma.", "There were no obvious postoperative complications.", "The patient was discharged 10 d after surgery."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring are often recommended to support kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Declining glomerular filtration rate (GFR) is a key biomarker for chronic kidney disease progression, and early intervention through pharmacological management, dietary modification, and monitoring of biomarkers such as serum creatinine and proteinuria is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["A 66-year-old man was admitted to the clinic of a primary care doctor.", "He complained of a sudden deterioration in right hypochondrial pain persisting for 2 weeks.", "A computed tomography (CT) scan revealed a right adrenal hemorrhage.", "A computed tomography (CT) scan revealed an abnormal tumor in the upper lobe of his left lung.", "He was referred to our hospital for further examination and treatment.", "His past medical history and family history were unremarkable.", "He was a current smoker with a history of 46 pack-years.", "An enhanced CT scan showed a massive shadow in the left lung S1 + 2 progressing to S6 beyond the lung lobe.", "The maximum diameter of the left lung lesion was about 42 mm.", "The right adrenal lesion showed no active bleeding.", "The carcinoembryonic antigen (CEA) was 5.6 ng/mL.", "The neuron-specific enolase (NSE) was 18.52 ng/mL.", "The patient had mild anemia with a hemoglobin of 10.3 g/dL.", "A bronchoscopic trans-bronchial lung biopsy showed no evidence of malignancy.", "A CT-guided percutaneous needle biopsy was performed.", "The pathological examination showed a non-small cell lung cancer.", "The adrenal lesion was diagnosed as a nonfunctional tumor based on endocrine examinations and adrenal medulla scintigraphy.", "18-Fluorodeoxyglucose positron emission tomography (FDG-PET) showed FDG accumulation in the left lung nodule with an SUVmax of 17.0.", "18-Fluorodeoxyglucose positron emission tomography (FDG-PET) showed FDG accumulation in the right adrenal lesion with an SUVmax of 4.1.", "The clinical stage was classified as cT2bN0M1b, stage IV (TNM classification 7th edition).", "A right adrenalectomy was performed.", "A complete resection of the primary lung cancer was considered possible.", "The lung tumor showed areas of atypical cells with eosinophilic cytoplasms.", "The lung tumor showed a sarcomatous component with extensive necrosis.", "The tumor cells were positive for cytokeratin AE1/3, CAM5.2, CK7, and p63 (partial).", "The tumor cells were negative for 34\u03b2E12, CK20, TTF-1, calretinin, and D2-40.", "The adrenal tumor was similar in pathologic and immunohistochemical analyses.", "The final diagnosis was pleomorphic carcinoma of the lung with an adrenal metastasis, pT2bN0M1b, stage IV (TNM classification 7th edition).", "The patient received chemotherapy as stage IV NSCLC.", "The chemotherapy regimen included 60 mg/m2 of cisplatin on day 1.", "The chemotherapy regimen included 40 mg/m2 of TS-1 twice a day on days 1 to 14.", "The chemotherapy regimen was repeated every 4 weeks.", "After two courses, he decided to quit the intravenous chemotherapy.", "He refused to take TS-1 because he feared adverse events.", "He began taking UFT (600 mg/day).", "He continued UFT treatment for 2 years.", "He has survived without any recurrences for 6 years since the surgery."], "summary_subclaims": ["The patient was a 66-year-old male.", "The patient was referred to the hospital because of a right adrenal hemorrhage.", "The patient was referred to the hospital because of a lung tumor.", "The lung tumor was a primary lung cancer.", "The adrenal hemorrhage was due to a metastatic cancer.", "An adrenalectomy was performed.", "Resection of the lung tumor was performed.", "The diagnosis was pleomorphic carcinoma with adrenal metastasis.", "The patient has remained recurrence-free for 6\u2009years since the surgery."]}, "extra_info": {"fulltext_subclaims": ["A 66-year-old man was admitted to the clinic of a primary care doctor.", "He complained of a sudden deterioration in right hypochondrial pain persisting for 2 weeks.", "A computed tomography (CT) scan revealed a right adrenal hemorrhage.", "A computed tomography (CT) scan revealed an abnormal tumor in the upper lobe of his left lung.", "He was referred to our hospital for further examination and treatment.", "His past medical history and family history were unremarkable.", "He was a current smoker with a history of 46 pack-years.", "An enhanced CT scan showed a massive shadow in the left lung S1 + 2 progressing to S6 beyond the lung lobe.", "The maximum diameter of the left lung lesion was about 42 mm.", "The right adrenal lesion showed no active bleeding.", "The carcinoembryonic antigen (CEA) was 5.6 ng/mL.", "The neuron-specific enolase (NSE) was 18.52 ng/mL.", "The patient had mild anemia with a hemoglobin of 10.3 g/dL.", "A bronchoscopic trans-bronchial lung biopsy showed no evidence of malignancy.", "A CT-guided percutaneous needle biopsy was performed.", "The pathological examination showed a non-small cell lung cancer.", "The adrenal lesion was diagnosed as a nonfunctional tumor based on endocrine examinations and adrenal medulla scintigraphy.", "18-Fluorodeoxyglucose positron emission tomography (FDG-PET) showed FDG accumulation in the left lung nodule with an SUVmax of 17.0.", "18-Fluorodeoxyglucose positron emission tomography (FDG-PET) showed FDG accumulation in the right adrenal lesion with an SUVmax of 4.1.", "The clinical stage was classified as cT2bN0M1b, stage IV (TNM classification 7th edition).", "A right adrenalectomy was performed.", "A complete resection of the primary lung cancer was considered possible.", "The lung tumor showed areas of atypical cells with eosinophilic cytoplasms.", "The lung tumor showed a sarcomatous component with extensive necrosis.", "The tumor cells were positive for cytokeratin AE1/3, CAM5.2, CK7, and p63 (partial).", "The tumor cells were negative for 34\u03b2E12, CK20, TTF-1, calretinin, and D2-40.", "The adrenal tumor was similar in pathologic and immunohistochemical analyses.", "The final diagnosis was pleomorphic carcinoma of the lung with an adrenal metastasis, pT2bN0M1b, stage IV (TNM classification 7th edition).", "The patient received chemotherapy as stage IV NSCLC.", "The chemotherapy regimen included 60 mg/m2 of cisplatin on day 1.", "The chemotherapy regimen included 40 mg/m2 of TS-1 twice a day on days 1 to 14.", "The chemotherapy regimen was repeated every 4 weeks.", "After two courses, he decided to quit the intravenous chemotherapy.", "He refused to take TS-1 because he feared adverse events.", "He began taking UFT (600 mg/day).", "He continued UFT treatment for 2 years.", "He has survived without any recurrences for 6 years since the surgery."], "index": 54, "original_id": "multiclinsum_test_2067_en.txt", "split": "test", "summary_subclaims": ["The patient was a 66-year-old male.", "The patient was referred to the hospital because of a right adrenal hemorrhage.", "The patient was referred to the hospital because of a lung tumor.", "The lung tumor was a primary lung cancer.", "The adrenal hemorrhage was due to a metastatic cancer.", "An adrenalectomy was performed.", "Resection of the lung tumor was performed.", "The diagnosis was pleomorphic carcinoma with adrenal metastasis.", "The patient has remained recurrence-free for 6\u2009years since the surgery."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring are often recommended to support kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Declining glomerular filtration rate (GFR) is a key biomarker for chronic kidney disease progression, and early intervention through pharmacological management, dietary modification, and monitoring of biomarkers such as serum creatinine and proteinuria is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 56-years-old woman.", "The patient has a history of hypertension.", "The patient has decompensated diabetes mellitus.", "The patient was referred to the hospital with critical limb ischemia.", "The patient had rest pain on the left leg.", "The patient had an ulcer on the left leg.", "The patient had negative COVID-19.", "The patient's blood pressure was 160/90 mmHg.", "The patient's heart rate was 130 beats per minute.", "A mesogastrium systolic bruit was heard on abdominal auscultation.", "Electrocardiogram showed signs of ST segment depression.", "Coronary angiography showed severe coronary artery disease.", "Duplex ultrasound showed widespread irregularities of the aortic wall.", "Duplex ultrasound showed monophasic wave on the right common femoral artery.", "Duplex ultrasound showed direct flow on the left femoral axis.", "Duplex ultrasound showed diffuse disease of both superficial femoral arteries.", "Duplex ultrasound showed distal occlusion in the left superficial femoral artery.", "CT-scan showed atherosclerotic disease on the infrarenal abdominal aorta.", "CT-scan showed focal dissection of the infrarenal abdominal aorta.", "CT-scan showed occlusion of the right common iliac artery origin.", "CT-scan showed short dissection of the left common iliac artery origin.", "The presence of ulcers in the left leg was the indication to address the left superficial femoral artery.", "The intervention was carried out through an antegrade percutaneous homolateral access.", "A drug eluting balloon (6.0 \u00d7 60 mm Luminor\u00ae) was used in the proximal left superficial femoral artery.", "A stent (5.0x80mm iVolution) was placed in the distal left superficial femoral artery.", "The final result was complete lesion healing in the left foot at three weeks.", "After two months, the patient was readmitted due to gangrene of the right foot.", "The patient had asymptomatic COVID-19 infection.", "Control CT showed a similar vascular pattern on the right side.", "The rapid and aggressive right foot lesions evolution was the indication to address vascular lesions in the right axis.", "The intervention was carried under general anesthesia.", "Surgical exposure of both common femoral arteries was performed.", "Aorto-iliac repair was performed using an AFX aortic endograft.", "Stenting of the right common iliac artery was performed with a balloon expandable stent (Isthmus 10 \u00d7 39).", "A drug eluting balloon (Luminor 5 \u00d7 200) was used in the right superficial femoral artery.", "The multiple intervention determined the increase of the distal flow.", "The reappearance of dorsalis pedis pulse was noted.", "The patient was asymptomatic for right foot pain after two days.", "The patient underwent right foot minor amputation.", "The patient was discharged after a week with double antiplatelet therapy.", "CT angiography performed after two months confirmed the proper positioning of the aortic stent-graft.", "CT angiography confirmed good patency of the iliac-femoral axis.", "CT angiography confirmed right foot ulcers healing."], "summary_subclaims": ["We report a case of complex revascularization in a diabetic patient with aggressive right foot lesions evolution after COVID-19 infection.", "The patient presenting a Peripheral arterial ischemic involving the infrarenal aorta, iliac, femoral.", "The simultaneous intervention consisted of an endovascular aortic stent-graft placement and angioplasty of femoral artery."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 56-years-old woman.", "The patient has a history of hypertension.", "The patient has decompensated diabetes mellitus.", "The patient was referred to the hospital with critical limb ischemia.", "The patient had rest pain on the left leg.", "The patient had an ulcer on the left leg.", "The patient had negative COVID-19.", "The patient's blood pressure was 160/90 mmHg.", "The patient's heart rate was 130 beats per minute.", "A mesogastrium systolic bruit was heard on abdominal auscultation.", "Electrocardiogram showed signs of ST segment depression.", "Coronary angiography showed severe coronary artery disease.", "Duplex ultrasound showed widespread irregularities of the aortic wall.", "Duplex ultrasound showed monophasic wave on the right common femoral artery.", "Duplex ultrasound showed direct flow on the left femoral axis.", "Duplex ultrasound showed diffuse disease of both superficial femoral arteries.", "Duplex ultrasound showed distal occlusion in the left superficial femoral artery.", "CT-scan showed atherosclerotic disease on the infrarenal abdominal aorta.", "CT-scan showed focal dissection of the infrarenal abdominal aorta.", "CT-scan showed occlusion of the right common iliac artery origin.", "CT-scan showed short dissection of the left common iliac artery origin.", "The presence of ulcers in the left leg was the indication to address the left superficial femoral artery.", "The intervention was carried out through an antegrade percutaneous homolateral access.", "A drug eluting balloon (6.0 \u00d7 60 mm Luminor\u00ae) was used in the proximal left superficial femoral artery.", "A stent (5.0x80mm iVolution) was placed in the distal left superficial femoral artery.", "The final result was complete lesion healing in the left foot at three weeks.", "After two months, the patient was readmitted due to gangrene of the right foot.", "The patient had asymptomatic COVID-19 infection.", "Control CT showed a similar vascular pattern on the right side.", "The rapid and aggressive right foot lesions evolution was the indication to address vascular lesions in the right axis.", "The intervention was carried under general anesthesia.", "Surgical exposure of both common femoral arteries was performed.", "Aorto-iliac repair was performed using an AFX aortic endograft.", "Stenting of the right common iliac artery was performed with a balloon expandable stent (Isthmus 10 \u00d7 39).", "A drug eluting balloon (Luminor 5 \u00d7 200) was used in the right superficial femoral artery.", "The multiple intervention determined the increase of the distal flow.", "The reappearance of dorsalis pedis pulse was noted.", "The patient was asymptomatic for right foot pain after two days.", "The patient underwent right foot minor amputation.", "The patient was discharged after a week with double antiplatelet therapy.", "CT angiography performed after two months confirmed the proper positioning of the aortic stent-graft.", "CT angiography confirmed good patency of the iliac-femoral axis.", "CT angiography confirmed right foot ulcers healing."], "index": 58, "original_id": "multiclinsum_test_437_en.txt", "split": "test", "summary_subclaims": ["We report a case of complex revascularization in a diabetic patient with aggressive right foot lesions evolution after COVID-19 infection.", "The patient presenting a Peripheral arterial ischemic involving the infrarenal aorta, iliac, femoral.", "The simultaneous intervention consisted of an endovascular aortic stent-graft placement and angioplasty of femoral artery."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring are often recommended to support kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Declining glomerular filtration rate (GFR) is a key biomarker for chronic kidney disease progression, and early intervention through pharmacological management, dietary modification, and monitoring of biomarkers such as serum creatinine and proteinuria is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["A 58-year-old Japanese man was presented to our out-patient unit complaining of posterior cervical pain.", "The pain firstly appeared 3 months before the first contact to us without any particular triggers such as trauma.", "He was relieved from the pain when lying flat.", "He kept working as a plumber and the pain got worse over the time period.", "A brain computed tomography (CT) was performed 1.5 months after the onset in another clinic.", "The brain CT revealed bilateral subdural effusion.", "No treatment was given at this point.", "Later on, when he was presented to our hospital, numbness and weakness of extremities also appeared.", "He had a medical history of hemorrhoid.", "He had no particular familial history.", "A hand-held dynamometer revealed his weakened grip strength of both of his hands by 30\u201340 kg.", "He was presented with bilateral muscle weakness in his lower extremities which was 4 of 5 in the Manual Muscle Test (MMT) score.", "His Japanese Orthopedic Association (JOA) score was 13.5.", "A fat suppression T2-weighted MRI without gadolinium enhancement of the cervical spine illustrated a fluid collection in the soft tissue spaces of the retrospinal region at C1-C2 level.", "The MRI demonstrated spinal canal stenosis at C3/4 level.", "A cisternoscintigram and a CT myelogram were performed with intradural injection of 111In-DTPA.", "The 111In-DTPA cisternoscintigram clearly revealed CSF leakage into the retrospinal region at C1-C2 level.", "The CT myelogram also suggested blockage at lower level of the cervical spinal canal.", "72 h of conservative therapy, including bed rest, intravenous fluid hydration, muscle relaxants and non-steroidal anti-inflammatory drugs, was ineffective at improving his symptoms.", "The re-examination of brain CT showed progression of the bilateral subdural effusions to bilateral subdural hematomas.", "We gave a diagnosis of intracranial hypotension due to the CSF leakage from C1-C2 level.", "We performed burr-hole drainage of the subdural hematoma.", "We performed blood-patch therapy at C1/2 level.", "We performed laminoplasty at C3\u20134.", "In the laminoplasty, CSF flew out from the epidural space subsequently to the opening of lamina.", "After sufficient decompression, the CSF flow was reduced in the operation field, without detection and restoration of dural tear.", "In the blood-patch therapy, an epidural catheter was inserted from the surgical field at C3\u20134 level to C1-C2 level under x-ray fluoroscopy observation.", "Approximately 5 ml of autologous blood sampled from patient\u2019s peripheral vein was injected to the epidural site at C1-C2 level.", "The blood-patch therapy was achieved.", "Postoperative response was significantly favorable.", "His symptoms completely improved.", "The imaging features that suggested CSF leak and intracranial hypotension disappeared.", "He discharged on postoperative day 10 with satisfaction.", "No signs of recurrence were observed for 5 months postoperatively up to this point.", "The patient returned to his daily life as well as his occupation."], "summary_subclaims": ["The patient was a 58-year-old man.", "The patient had posterior cervical pain persisting for 3 months.", "The patient had numbness and muscle weakness of extremities.", "A fat suppression T2-weighted image of MRI illustrated fluid collection in the retrospinal region at C1-C2 level.", "An 111In-DTPA cisternoscintigram revealed the presence of CSF leakage into the same region.", "The MRI showed stenosis in spinal canal at C3/4 level.", "A CT myelogram suggested a blockage at the C3/4 level.", "The diagnosis was intracranial hypotension due to the CSF leakage.", "The CSF leakage might be caused by the spinal canal stenosis at C3/4 level.", "Despite 72\u2009h of conservative therapy, a brain CT showed the development of bilateral subdural hematomas.", "Burr-hole drainage of the subdural hematoma was performed.", "Blood-patch therapy at C1/2 level was performed.", "Laminoplasty at C3-4 was performed.", "Improvement of symptoms was obtained post-operatively.", "Imaging features suggesting the CSF leak and subdural hematoma were obtained post-operatively."]}, "extra_info": {"fulltext_subclaims": ["A 58-year-old Japanese man was presented to our out-patient unit complaining of posterior cervical pain.", "The pain firstly appeared 3 months before the first contact to us without any particular triggers such as trauma.", "He was relieved from the pain when lying flat.", "He kept working as a plumber and the pain got worse over the time period.", "A brain computed tomography (CT) was performed 1.5 months after the onset in another clinic.", "The brain CT revealed bilateral subdural effusion.", "No treatment was given at this point.", "Later on, when he was presented to our hospital, numbness and weakness of extremities also appeared.", "He had a medical history of hemorrhoid.", "He had no particular familial history.", "A hand-held dynamometer revealed his weakened grip strength of both of his hands by 30\u201340 kg.", "He was presented with bilateral muscle weakness in his lower extremities which was 4 of 5 in the Manual Muscle Test (MMT) score.", "His Japanese Orthopedic Association (JOA) score was 13.5.", "A fat suppression T2-weighted MRI without gadolinium enhancement of the cervical spine illustrated a fluid collection in the soft tissue spaces of the retrospinal region at C1-C2 level.", "The MRI demonstrated spinal canal stenosis at C3/4 level.", "A cisternoscintigram and a CT myelogram were performed with intradural injection of 111In-DTPA.", "The 111In-DTPA cisternoscintigram clearly revealed CSF leakage into the retrospinal region at C1-C2 level.", "The CT myelogram also suggested blockage at lower level of the cervical spinal canal.", "72 h of conservative therapy, including bed rest, intravenous fluid hydration, muscle relaxants and non-steroidal anti-inflammatory drugs, was ineffective at improving his symptoms.", "The re-examination of brain CT showed progression of the bilateral subdural effusions to bilateral subdural hematomas.", "We gave a diagnosis of intracranial hypotension due to the CSF leakage from C1-C2 level.", "We performed burr-hole drainage of the subdural hematoma.", "We performed blood-patch therapy at C1/2 level.", "We performed laminoplasty at C3\u20134.", "In the laminoplasty, CSF flew out from the epidural space subsequently to the opening of lamina.", "After sufficient decompression, the CSF flow was reduced in the operation field, without detection and restoration of dural tear.", "In the blood-patch therapy, an epidural catheter was inserted from the surgical field at C3\u20134 level to C1-C2 level under x-ray fluoroscopy observation.", "Approximately 5 ml of autologous blood sampled from patient\u2019s peripheral vein was injected to the epidural site at C1-C2 level.", "The blood-patch therapy was achieved.", "Postoperative response was significantly favorable.", "His symptoms completely improved.", "The imaging features that suggested CSF leak and intracranial hypotension disappeared.", "He discharged on postoperative day 10 with satisfaction.", "No signs of recurrence were observed for 5 months postoperatively up to this point.", "The patient returned to his daily life as well as his occupation."], "index": 56, "original_id": "multiclinsum_test_1266_en.txt", "split": "test", "summary_subclaims": ["The patient was a 58-year-old man.", "The patient had posterior cervical pain persisting for 3 months.", "The patient had numbness and muscle weakness of extremities.", "A fat suppression T2-weighted image of MRI illustrated fluid collection in the retrospinal region at C1-C2 level.", "An 111In-DTPA cisternoscintigram revealed the presence of CSF leakage into the same region.", "The MRI showed stenosis in spinal canal at C3/4 level.", "A CT myelogram suggested a blockage at the C3/4 level.", "The diagnosis was intracranial hypotension due to the CSF leakage.", "The CSF leakage might be caused by the spinal canal stenosis at C3/4 level.", "Despite 72\u2009h of conservative therapy, a brain CT showed the development of bilateral subdural hematomas.", "Burr-hole drainage of the subdural hematoma was performed.", "Blood-patch therapy at C1/2 level was performed.", "Laminoplasty at C3-4 was performed.", "Improvement of symptoms was obtained post-operatively.", "Imaging features suggesting the CSF leak and subdural hematoma were obtained post-operatively."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["A 65-year-old woman was referred to our hospital for assessment of a gallbladder tumor detected by abdominal ultrasonography.", "Contrast-enhanced computed tomography revealed a papillary lesion (25 mm in diameter) in the fundus of the gallbladder.", "The boundary between the tumor and liver was unclear.", "Endoscopic retrograde cholangiography showed a complete filling defect in the cystic duct.", "Serum carcinoembryonic antigen level was 2.1 ng/ml.", "Serum carbohydrate antigen 19-9 level was 24 U/ml.", "We diagnosed the tumor as gallbladder cancer invading the liver and cystic duct.", "We decided to perform extended cholecystectomy.", "The gallbladder wall was thickened.", "Intraoperative ultrasonography revealed the tumor did not invade liver obviously.", "The intraoperative frozen section of the cystic duct stump and 2 sentinel lymph nodes were negative for malignancy.", "Macroscopic examination showed a superficially spreading papillary tumor with thick mucus on its surface.", "The gallbladder wall was diffusely thickened.", "The tumor was noninvasive and showed no evidence of lymph node metastasis.", "These pathological findings were compatible with ICPN.", "In immunohistochemical staining, MUC5AC and MUC6 were strongly positive.", "CK7 and MUC1 were also positive, but not CK20, MUC2, estrogen receptor, and progesterone receptor.", "Immunohistochemistry indicated that ICPN was predominantly gastric type, with focal pancreatobiliary type.", "Many lymphocytes and multinucleated giant cells had infiltrated the thickened gallbladder wall with prominent Rokitansky\u2013Aschoff sinuses.", "These findings were especially seen at the fundus and were indicative of chronic granulomatous changes within the fundus.", "Based on these pathological findings, we diagnosed the tumor as an ICPN concomitant with XGC.", "The patient was discharged on postoperative day 8 with no complications.", "She was clinically well with no evidence of recurrence at 3 months after resection."], "summary_subclaims": ["A 65-year-old woman was referred to our hospital for assessment of a gallbladder tumor.", "Contrast-enhanced computed tomography showed a papillary tumor in the fundus of the gallbladder.", "The gallbladder wall had irregular thickening that spread into the cystic duct.", "The boundary between the tumor and liver was unclear.", "The patient was diagnosed with gallbladder cancer with liver invasion.", "We performed extended cholecystectomy with liver bed resection.", "The absence of cancer cells in the resection margin of the cystic duct was confirmed.", "After pathological examination, the tumor was diagnosed as an ICPN with xanthogranulomatous cholecystitis.", "The patient was discharged on postoperative day 8 with no complications."]}, "extra_info": {"fulltext_subclaims": ["A 65-year-old woman was referred to our hospital for assessment of a gallbladder tumor detected by abdominal ultrasonography.", "Contrast-enhanced computed tomography revealed a papillary lesion (25 mm in diameter) in the fundus of the gallbladder.", "The boundary between the tumor and liver was unclear.", "Endoscopic retrograde cholangiography showed a complete filling defect in the cystic duct.", "Serum carcinoembryonic antigen level was 2.1 ng/ml.", "Serum carbohydrate antigen 19-9 level was 24 U/ml.", "We diagnosed the tumor as gallbladder cancer invading the liver and cystic duct.", "We decided to perform extended cholecystectomy.", "The gallbladder wall was thickened.", "Intraoperative ultrasonography revealed the tumor did not invade liver obviously.", "The intraoperative frozen section of the cystic duct stump and 2 sentinel lymph nodes were negative for malignancy.", "Macroscopic examination showed a superficially spreading papillary tumor with thick mucus on its surface.", "The gallbladder wall was diffusely thickened.", "The tumor was noninvasive and showed no evidence of lymph node metastasis.", "These pathological findings were compatible with ICPN.", "In immunohistochemical staining, MUC5AC and MUC6 were strongly positive.", "CK7 and MUC1 were also positive, but not CK20, MUC2, estrogen receptor, and progesterone receptor.", "Immunohistochemistry indicated that ICPN was predominantly gastric type, with focal pancreatobiliary type.", "Many lymphocytes and multinucleated giant cells had infiltrated the thickened gallbladder wall with prominent Rokitansky\u2013Aschoff sinuses.", "These findings were especially seen at the fundus and were indicative of chronic granulomatous changes within the fundus.", "Based on these pathological findings, we diagnosed the tumor as an ICPN concomitant with XGC.", "The patient was discharged on postoperative day 8 with no complications.", "She was clinically well with no evidence of recurrence at 3 months after resection."], "index": 74, "original_id": "multiclinsum_test_1559_en.txt", "split": "test", "summary_subclaims": ["A 65-year-old woman was referred to our hospital for assessment of a gallbladder tumor.", "Contrast-enhanced computed tomography showed a papillary tumor in the fundus of the gallbladder.", "The gallbladder wall had irregular thickening that spread into the cystic duct.", "The boundary between the tumor and liver was unclear.", "The patient was diagnosed with gallbladder cancer with liver invasion.", "We performed extended cholecystectomy with liver bed resection.", "The absence of cancer cells in the resection margin of the cystic duct was confirmed.", "After pathological examination, the tumor was diagnosed as an ICPN with xanthogranulomatous cholecystitis.", "The patient was discharged on postoperative day 8 with no complications."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was a 43-year-old Asian man.", "He had a 3-year history of progressively invasive PC.", "He presented with pain in his right eye.", "He had been staged T4N3M1 (TNM classification).", "He had lost his vision more than a month earlier.", "He was diagnosed as having metastasis in the bilateral inguinal lymph nodes.", "He had ipsilateral iliac node metastasis.", "He had systemic metastasis to his liver and lungs.", "His medical history was remarkable due to several surgeries.", "He denied any family history of inherited diseases.", "He denied any psychological illness.", "On presentation, his best corrected visual acuity was no light perception in his right eye.", "On presentation, his best corrected visual acuity was 20/20 in his left eye.", "His intraocular pressure was 13.0 mmHg in his right eye.", "His intraocular pressure was 11.0 mmHg in his left eye.", "The right eye pupil dilated to 5 mm.", "The right eye pupillary reaction disappeared.", "An external examination revealed mild proptosis.", "A dilated fundus examination of his right eye showed post equatorial retinal detachment.", "A dilated fundus examination showed a black eminence.", "A dilated fundus examination showed a pale optic disk.", "There were no obvious abnormalities in his left eye.", "An ophthalmic B-scan ultrasound showed retinal detachment with hemorrhage.", "Orbital MRI confirmed thickening and strengthening of the right lateral wall.", "The internal rectus and lateral rectus muscles were thickened and hardened.", "The 2-cm-long optic nerve was thickened.", "The optic nerve stump was invaded by the metastasis.", "T1-weighted images showed hyperintensity.", "T2-weighted images showed hypointensity.", "A contrast-enhanced MRI scan revealed inhomogeneous enhancement of the posterior wall.", "The presence of lesions was associated with invasion of the optic nerve.", "The presence of lesions was associated with invasion of the choroid.", "The presence of lesions was associated with invasion of the sclera.", "The deep layer, including the choroid, was infiltrated by cancerous tissue.", "The patient had undergone right eyeball enucleation on February 3, 2015.", "The procedure was under general anesthesia.", "Histopathological examination led to a diagnosis of metastatic moderately differentiated penile squamous cell carcinoma.", "The cancer infiltrated the sclera.", "The cancer infiltrated the choroid.", "The cancer infiltrated the retina.", "The cancer infiltrated the optic nerve.", "The cancer infiltrated external intraocular sites.", "Hematoxylin-and-eosin staining showed keratin pearls.", "Hematoxylin-and-eosin staining showed infiltrative growth of keratinized cells.", "Intercellular bridges were seen in the nests of moderately differentiated squamous carcinoma cells.", "The patient received chemotherapy and radiotherapy during 6 months of follow-up.", "The patient died due to brain metastasis."], "summary_subclaims": ["The patient is a 43-year-old Asian man.", "The patient has a 3-year history of penile cancer.", "The patient presented with metastasis in the right intraocular sites.", "Magnetic resonance imaging showed hyperintensity in the T1-weighted images of the right eye.", "Magnetic resonance imaging showed hypointensity in the T2-weighted images of the right eye.", "The patient underwent enucleation of his right eye.", "Histopathological analysis led to a diagnosis of metastatic, moderately differentiated penile squamous cell carcinoma."]}, "extra_info": {"fulltext_subclaims": ["The patient was a 43-year-old Asian man.", "He had a 3-year history of progressively invasive PC.", "He presented with pain in his right eye.", "He had been staged T4N3M1 (TNM classification).", "He had lost his vision more than a month earlier.", "He was diagnosed as having metastasis in the bilateral inguinal lymph nodes.", "He had ipsilateral iliac node metastasis.", "He had systemic metastasis to his liver and lungs.", "His medical history was remarkable due to several surgeries.", "He denied any family history of inherited diseases.", "He denied any psychological illness.", "On presentation, his best corrected visual acuity was no light perception in his right eye.", "On presentation, his best corrected visual acuity was 20/20 in his left eye.", "His intraocular pressure was 13.0 mmHg in his right eye.", "His intraocular pressure was 11.0 mmHg in his left eye.", "The right eye pupil dilated to 5 mm.", "The right eye pupillary reaction disappeared.", "An external examination revealed mild proptosis.", "A dilated fundus examination of his right eye showed post equatorial retinal detachment.", "A dilated fundus examination showed a black eminence.", "A dilated fundus examination showed a pale optic disk.", "There were no obvious abnormalities in his left eye.", "An ophthalmic B-scan ultrasound showed retinal detachment with hemorrhage.", "Orbital MRI confirmed thickening and strengthening of the right lateral wall.", "The internal rectus and lateral rectus muscles were thickened and hardened.", "The 2-cm-long optic nerve was thickened.", "The optic nerve stump was invaded by the metastasis.", "T1-weighted images showed hyperintensity.", "T2-weighted images showed hypointensity.", "A contrast-enhanced MRI scan revealed inhomogeneous enhancement of the posterior wall.", "The presence of lesions was associated with invasion of the optic nerve.", "The presence of lesions was associated with invasion of the choroid.", "The presence of lesions was associated with invasion of the sclera.", "The deep layer, including the choroid, was infiltrated by cancerous tissue.", "The patient had undergone right eyeball enucleation on February 3, 2015.", "The procedure was under general anesthesia.", "Histopathological examination led to a diagnosis of metastatic moderately differentiated penile squamous cell carcinoma.", "The cancer infiltrated the sclera.", "The cancer infiltrated the choroid.", "The cancer infiltrated the retina.", "The cancer infiltrated the optic nerve.", "The cancer infiltrated external intraocular sites.", "Hematoxylin-and-eosin staining showed keratin pearls.", "Hematoxylin-and-eosin staining showed infiltrative growth of keratinized cells.", "Intercellular bridges were seen in the nests of moderately differentiated squamous carcinoma cells.", "The patient received chemotherapy and radiotherapy during 6 months of follow-up.", "The patient died due to brain metastasis."], "index": 82, "original_id": "multiclinsum_test_1233_en.txt", "split": "test", "summary_subclaims": ["The patient is a 43-year-old Asian man.", "The patient has a 3-year history of penile cancer.", "The patient presented with metastasis in the right intraocular sites.", "Magnetic resonance imaging showed hyperintensity in the T1-weighted images of the right eye.", "Magnetic resonance imaging showed hypointensity in the T2-weighted images of the right eye.", "The patient underwent enucleation of his right eye.", "Histopathological analysis led to a diagnosis of metastatic, moderately differentiated penile squamous cell carcinoma."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 66-year-old man.", "The patient has type II diabetes mellitus for 4 years.", "The patient has arterial hypertension for 10 years.", "The patient developed severe non-proliferative diabetic retinopathy without macular edema 2 years after diabetes diagnosis.", "The patient was treated with panretinal photocoagulation.", "The patient had poor glycometabolic control.", "The patient was unable to adhere to a close follow-up.", "One year after panretinal photocoagulation, the patient developed severe visual loss due to diffuse non tractional bilateral diabetic macular edema.", "The right eye was treated with an intravitreal triamcinolone injection.", "The left eye was treated with an intravitreal triamcinolone injection 1 month after the right eye.", "Laser grid photocoagulation was performed in both eyes 2 weeks after intravitreal injection.", "After no visual recovery for over 2 months, an intravitreal injection of bevacizumab was given in the right eye.", "One week after the bevacizumab injection, anterior ischemic optic neuropathy was observed.", "The patient had a residual visual acuity of hand motion.", "The patient had glycated hemoglobin >9%.", "The patient had high hypertension.", "The patient had hypercholesterolemia.", "The patient had poor adherence to therapy.", "The patient refused an intravitreal injection of bevacizumab in his left eye.", "The patient signed an informed consent for subtenon injections of IFN\u03b1.", "Before treatment, the best corrected visual acuity in the left eye was 20/200.", "The patient received posterior subtenon injections of IFN\u03b1 three times in one week.", "The injections were given on Monday, Wednesday, and Friday.", "Topical 0.4% oxybuprocaine surface anesthesia was used.", "One ml of IFN\u03b1 was injected into the inferotemporal quadrant under the Tenon\u2019s capsule.", "A 27-gauge needle on a 2.5-ml syringe was used.", "Topical 0.3% netilmicin eye drops were prescribed three times a day for 7 days.", "The patient had a good systemic condition during IFN-\u03b1 therapy.", "The patient had a glycated hemoglobin of 6.9%.", "A complete ophthalmic examination was conducted preoperatively.", "A complete ophthalmic examination was conducted 1 week after the last injection of IFN\u03b1.", "A complete ophthalmic examination was conducted 1 month after the last injection of IFN\u03b1.", "A complete ophthalmic examination was conducted 4 months after the last injection of IFN\u03b1.", "A complete ophthalmic examination was conducted 1 year after the last injection of IFN\u03b1.", "Spectralis OCT was used for macular scans.", "Fifteen months after treatment, the best corrected visual acuity in the left eye was 20/40.", "The patient gave written consent for the use of his data and images."], "summary_subclaims": ["The patient is a 66-year-old man.", "The patient was affected by DME.", "The patient's HbA1c was 6.9%.", "The patient had refractory DME to laser grid treatment.", "The patient had refractory DME to intravitreal injections of triamcinolone.", "The patient received a cycle of three subtenon injections/week of IFN\u03b1 (1\u00d7106 IU/ml).", "BCVA and CMT were evaluated preoperatively.", "BCVA and CMT were evaluated at 1 week postoperatively.", "BCVA and CMT were evaluated at 1 month postoperatively.", "BCVA and CMT were evaluated at 4 months postoperatively.", "BCVA and CMT were evaluated at 1 year postoperatively.", "BCVA was 20/200 preoperatively.", "BCVA was 20/40 at 1 week postoperatively.", "CMT was 498 \u03bcm preoperatively.", "CMT was 237 \u03bcm at 1 week postoperatively.", "BCVA remained stable during the 1-year follow-up.", "CMT was 215 \u03bcm during the first follow-up visit.", "CMT was 255 \u03bcm during the second follow-up visit.", "CMT was 299 \u03bcm during the third follow-up visit.", "CMT was still lower than the baseline value during the follow-up visits.", "No adverse events were recorded.", "Mild subconjunctival hemorrhage at the injection site was recorded."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 66-year-old man.", "The patient has type II diabetes mellitus for 4 years.", "The patient has arterial hypertension for 10 years.", "The patient developed severe non-proliferative diabetic retinopathy without macular edema 2 years after diabetes diagnosis.", "The patient was treated with panretinal photocoagulation.", "The patient had poor glycometabolic control.", "The patient was unable to adhere to a close follow-up.", "One year after panretinal photocoagulation, the patient developed severe visual loss due to diffuse non tractional bilateral diabetic macular edema.", "The right eye was treated with an intravitreal triamcinolone injection.", "The left eye was treated with an intravitreal triamcinolone injection 1 month after the right eye.", "Laser grid photocoagulation was performed in both eyes 2 weeks after intravitreal injection.", "After no visual recovery for over 2 months, an intravitreal injection of bevacizumab was given in the right eye.", "One week after the bevacizumab injection, anterior ischemic optic neuropathy was observed.", "The patient had a residual visual acuity of hand motion.", "The patient had glycated hemoglobin >9%.", "The patient had high hypertension.", "The patient had hypercholesterolemia.", "The patient had poor adherence to therapy.", "The patient refused an intravitreal injection of bevacizumab in his left eye.", "The patient signed an informed consent for subtenon injections of IFN\u03b1.", "Before treatment, the best corrected visual acuity in the left eye was 20/200.", "The patient received posterior subtenon injections of IFN\u03b1 three times in one week.", "The injections were given on Monday, Wednesday, and Friday.", "Topical 0.4% oxybuprocaine surface anesthesia was used.", "One ml of IFN\u03b1 was injected into the inferotemporal quadrant under the Tenon\u2019s capsule.", "A 27-gauge needle on a 2.5-ml syringe was used.", "Topical 0.3% netilmicin eye drops were prescribed three times a day for 7 days.", "The patient had a good systemic condition during IFN-\u03b1 therapy.", "The patient had a glycated hemoglobin of 6.9%.", "A complete ophthalmic examination was conducted preoperatively.", "A complete ophthalmic examination was conducted 1 week after the last injection of IFN\u03b1.", "A complete ophthalmic examination was conducted 1 month after the last injection of IFN\u03b1.", "A complete ophthalmic examination was conducted 4 months after the last injection of IFN\u03b1.", "A complete ophthalmic examination was conducted 1 year after the last injection of IFN\u03b1.", "Spectralis OCT was used for macular scans.", "Fifteen months after treatment, the best corrected visual acuity in the left eye was 20/40.", "The patient gave written consent for the use of his data and images."], "index": 80, "original_id": "multiclinsum_test_1558_en.txt", "split": "test", "summary_subclaims": ["The patient is a 66-year-old man.", "The patient was affected by DME.", "The patient's HbA1c was 6.9%.", "The patient had refractory DME to laser grid treatment.", "The patient had refractory DME to intravitreal injections of triamcinolone.", "The patient received a cycle of three subtenon injections/week of IFN\u03b1 (1\u00d7106 IU/ml).", "BCVA and CMT were evaluated preoperatively.", "BCVA and CMT were evaluated at 1 week postoperatively.", "BCVA and CMT were evaluated at 1 month postoperatively.", "BCVA and CMT were evaluated at 4 months postoperatively.", "BCVA and CMT were evaluated at 1 year postoperatively.", "BCVA was 20/200 preoperatively.", "BCVA was 20/40 at 1 week postoperatively.", "CMT was 498 \u03bcm preoperatively.", "CMT was 237 \u03bcm at 1 week postoperatively.", "BCVA remained stable during the 1-year follow-up.", "CMT was 215 \u03bcm during the first follow-up visit.", "CMT was 255 \u03bcm during the second follow-up visit.", "CMT was 299 \u03bcm during the third follow-up visit.", "CMT was still lower than the baseline value during the follow-up visits.", "No adverse events were recorded.", "Mild subconjunctival hemorrhage at the injection site was recorded."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["A previously healthy 24-year-old male presented at the emergency department with chest pain and diarrhoea.", "The chest pain began 2 h prior to hospital admission.", "The chest pain was described as a constant light chest pressure.", "The chest pain was without correlation to breathing or body position.", "3 days earlier, the patient and a friend had had chicken in a restaurant before boarding a flight to Sweden.", "One hour after arrival in Sweden the patient experienced sudden abdominal pain, chills and diarrhoea.", "During the following three days the patient had 6 diarrhoeas per day.", "The patient had mucous but no visible blood in the stool.", "The patient was diagnosed with C jejuni gastroenteritis after stool culture at a primary care facility.", "No antibiotics were given at the primary care facility.", "Upon admission to the ED the abdominal pain had subsided.", "The patient was afebrile (37 \u00b0C or 98.6 \u00b0F) upon admission.", "The patient was still experiencing diarrhoea upon admission.", "Heart auscultation showed regular rhythm, no murmurs or extra sounds.", "Laboratory examinations showed C-reactive protein at 89.1 mg/L.", "Laboratory examinations showed leukocyte count at 11.3 \u00d7 109/L.", "Laboratory examinations showed high-sensitive Troponin T at 108 ng/L.", "ECG showed regular sinus rhythm, 64/min.", "ECG showed general 1 mm ST-elevation.", "The patient was treated with Brufen 200 mg (tid).", "The patient was treated with Omeprazol 20 mg (qd).", "The patient was treated with Loperamid 2 mg.", "The patient was admitted to a cardiac care unit for cardiac monitoring.", "During the following 4 days the hsTnT reached a maximum value of 504.", "Stool culture confirmed the diagnosis of C jejuni.", "Blood cultures were negative.", "Transthoracic echocardiogram showed normal right and left ventricle function.", "Transthoracic echocardiogram showed ejection fraction 60\u201365 %.", "Transthoracic echocardiogram showed normal valvular structure and function.", "Transthoracic echocardiogram showed no hypokinesia or pericardial effusion.", "After one day the ECG-changes had resolved.", "The patient was started on ciprofloxacin.", "The patient developed urticarial rashes and severe itching.", "The treatment with ciprofloxacin was discontinued.", "The chest pain subsided after 2 days.", "The patient left the hospital after 4 days.", "The patient was given a 10 day prescription of Azithromycin 500 mg (qd) upon hospital release.", "The diagnosis was determined to be C jejuni-associated perimyocarditis.", "At follow-up visit 4 weeks after discharge the patient was without complaints.", "At follow-up visit 4 weeks after discharge physical examination was normal.", "At follow-up visit 4 weeks after discharge both ECG and TTE were normal."], "summary_subclaims": ["A previously healthy 24-yo male presented at the Emergency Department with recent onset of chest pain and a 3-day history of abdominal pain, fever and diarrhoea.", "The symptoms began within a few hours of returning from a tourist visit to a central European capital.", "Vital signs were stable.", "The Electrocardiogram showed generalized ST-elevation.", "Laboratory testing showed increased levels of C-reactive protein and high-sensitive Troponin T.", "Transthoracic echocardiogram was normal.", "Stool cultures were positive for C Jejuni.", "Blood cultures were negative.", "Two days after patient A was admitted to the ED his travel companion, also a previously healthy male, presented at the same ED with almost identical symptoms.", "Patient B declared that he and patient A had ingested chicken prior to returning from their tourist trip.", "Laboratory tests showed elevated CRP and hsTnT.", "The ECG and TTE were normal.", "In both cases, the diagnosis of C jejuni-associated perimyocarditis was set based on the typical presentation and positive stool cultures with identical strains.", "Both patients were given antibiotics.", "Both patients rapidly improved and were fully recovered at 6-week follow up."]}, "extra_info": {"fulltext_subclaims": ["A previously healthy 24-year-old male presented at the emergency department with chest pain and diarrhoea.", "The chest pain began 2 h prior to hospital admission.", "The chest pain was described as a constant light chest pressure.", "The chest pain was without correlation to breathing or body position.", "3 days earlier, the patient and a friend had had chicken in a restaurant before boarding a flight to Sweden.", "One hour after arrival in Sweden the patient experienced sudden abdominal pain, chills and diarrhoea.", "During the following three days the patient had 6 diarrhoeas per day.", "The patient had mucous but no visible blood in the stool.", "The patient was diagnosed with C jejuni gastroenteritis after stool culture at a primary care facility.", "No antibiotics were given at the primary care facility.", "Upon admission to the ED the abdominal pain had subsided.", "The patient was afebrile (37 \u00b0C or 98.6 \u00b0F) upon admission.", "The patient was still experiencing diarrhoea upon admission.", "Heart auscultation showed regular rhythm, no murmurs or extra sounds.", "Laboratory examinations showed C-reactive protein at 89.1 mg/L.", "Laboratory examinations showed leukocyte count at 11.3 \u00d7 109/L.", "Laboratory examinations showed high-sensitive Troponin T at 108 ng/L.", "ECG showed regular sinus rhythm, 64/min.", "ECG showed general 1 mm ST-elevation.", "The patient was treated with Brufen 200 mg (tid).", "The patient was treated with Omeprazol 20 mg (qd).", "The patient was treated with Loperamid 2 mg.", "The patient was admitted to a cardiac care unit for cardiac monitoring.", "During the following 4 days the hsTnT reached a maximum value of 504.", "Stool culture confirmed the diagnosis of C jejuni.", "Blood cultures were negative.", "Transthoracic echocardiogram showed normal right and left ventricle function.", "Transthoracic echocardiogram showed ejection fraction 60\u201365 %.", "Transthoracic echocardiogram showed normal valvular structure and function.", "Transthoracic echocardiogram showed no hypokinesia or pericardial effusion.", "After one day the ECG-changes had resolved.", "The patient was started on ciprofloxacin.", "The patient developed urticarial rashes and severe itching.", "The treatment with ciprofloxacin was discontinued.", "The chest pain subsided after 2 days.", "The patient left the hospital after 4 days.", "The patient was given a 10 day prescription of Azithromycin 500 mg (qd) upon hospital release.", "The diagnosis was determined to be C jejuni-associated perimyocarditis.", "At follow-up visit 4 weeks after discharge the patient was without complaints.", "At follow-up visit 4 weeks after discharge physical examination was normal.", "At follow-up visit 4 weeks after discharge both ECG and TTE were normal."], "index": 78, "original_id": "multiclinsum_test_1211_en.txt", "split": "test", "summary_subclaims": ["A previously healthy 24-yo male presented at the Emergency Department with recent onset of chest pain and a 3-day history of abdominal pain, fever and diarrhoea.", "The symptoms began within a few hours of returning from a tourist visit to a central European capital.", "Vital signs were stable.", "The Electrocardiogram showed generalized ST-elevation.", "Laboratory testing showed increased levels of C-reactive protein and high-sensitive Troponin T.", "Transthoracic echocardiogram was normal.", "Stool cultures were positive for C Jejuni.", "Blood cultures were negative.", "Two days after patient A was admitted to the ED his travel companion, also a previously healthy male, presented at the same ED with almost identical symptoms.", "Patient B declared that he and patient A had ingested chicken prior to returning from their tourist trip.", "Laboratory tests showed elevated CRP and hsTnT.", "The ECG and TTE were normal.", "In both cases, the diagnosis of C jejuni-associated perimyocarditis was set based on the typical presentation and positive stool cultures with identical strains.", "Both patients were given antibiotics.", "Both patients rapidly improved and were fully recovered at 6-week follow up."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["A 65 yr old female presented to the ENT clinic with a one-month history of a lump in the right neck.", "On examination, a mobile lump was palpable in the angle of the mandible/upper cervical region.", "Flexible endoscopy did not reveal any mucosal lesion in the posterior nasal space.", "Flexible endoscopy did not reveal any mucosal lesion in the oropharynx.", "Flexible endoscopy did not reveal any mucosal lesion in the hypopharynx.", "Flexible endoscopy did not reveal any mucosal lesion in the larynx.", "Clinically a lymph node mass was considered as a possible diagnosis.", "Fine needle aspiration and MRI were performed.", "MRI showed a well-defined oval shaped mass measuring 3 \u00d7 2 cm just inferior to the right parotid gland.", "The epicenter of the lesion was in the intermuscular plane.", "The lesion was medial to the sternocleidomastoid muscle but separate from it.", "The lesion was heterogeneous on both T1 & T2 W images.", "The lesion had a well defined margin.", "Following contrast administration, there was moderate heterogeneous enhancement.", "A differential diagnosis of lymph nodal mass & Spinal Accessory nerve Schwannoma were considered.", "FNA of the lesion showed a mix of bland epithelial cell.", "FNA showed clusters of spindle cells.", "FNA showed myxoid matrix.", "The FNA findings were typical of a pleomorphic adenoma.", "A decision to perform an excision biopsy was made.", "At surgery, the tumor was found to be a pedunculated mass arising from the inferior aspect of the tail of the parotid gland.", "The tumor was closely related and superficial to the spinal accessory nerve but separate from it.", "The mass was excised completely incorporating a limited cuff of macroscopically normal parotid tissue.", "The inferior branches of the facial nerve were not injured.", "Histopathology showed uniform proliferation of epithelial elements within a partially myxo-chondroid stroma.", "The histopathology findings were consistent with a diagnosis of a pleomorphic adenoma.", "There was no definite salivary gland tissue within the specimen."], "summary_subclaims": ["We present a case of a pleomorphic adenoma arising from the 'tail' of the parotid gland.", "On imaging, the tumor appears to be extra parotid in location.", "We review the anatomy of the parotid 'tail'.", "We review relevant literature."]}, "extra_info": {"fulltext_subclaims": ["A 65 yr old female presented to the ENT clinic with a one-month history of a lump in the right neck.", "On examination, a mobile lump was palpable in the angle of the mandible/upper cervical region.", "Flexible endoscopy did not reveal any mucosal lesion in the posterior nasal space.", "Flexible endoscopy did not reveal any mucosal lesion in the oropharynx.", "Flexible endoscopy did not reveal any mucosal lesion in the hypopharynx.", "Flexible endoscopy did not reveal any mucosal lesion in the larynx.", "Clinically a lymph node mass was considered as a possible diagnosis.", "Fine needle aspiration and MRI were performed.", "MRI showed a well-defined oval shaped mass measuring 3 \u00d7 2 cm just inferior to the right parotid gland.", "The epicenter of the lesion was in the intermuscular plane.", "The lesion was medial to the sternocleidomastoid muscle but separate from it.", "The lesion was heterogeneous on both T1 & T2 W images.", "The lesion had a well defined margin.", "Following contrast administration, there was moderate heterogeneous enhancement.", "A differential diagnosis of lymph nodal mass & Spinal Accessory nerve Schwannoma were considered.", "FNA of the lesion showed a mix of bland epithelial cell.", "FNA showed clusters of spindle cells.", "FNA showed myxoid matrix.", "The FNA findings were typical of a pleomorphic adenoma.", "A decision to perform an excision biopsy was made.", "At surgery, the tumor was found to be a pedunculated mass arising from the inferior aspect of the tail of the parotid gland.", "The tumor was closely related and superficial to the spinal accessory nerve but separate from it.", "The mass was excised completely incorporating a limited cuff of macroscopically normal parotid tissue.", "The inferior branches of the facial nerve were not injured.", "Histopathology showed uniform proliferation of epithelial elements within a partially myxo-chondroid stroma.", "The histopathology findings were consistent with a diagnosis of a pleomorphic adenoma.", "There was no definite salivary gland tissue within the specimen."], "index": 76, "original_id": "multiclinsum_test_2421_en.txt", "split": "test", "summary_subclaims": ["We present a case of a pleomorphic adenoma arising from the 'tail' of the parotid gland.", "On imaging, the tumor appears to be extra parotid in location.", "We review the anatomy of the parotid 'tail'.", "We review relevant literature."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 49-year-old Japanese man.", "He visited the department in November 2017.", "His chief complaints were indolent right scrotum enlargement and a right inguinal mass.", "He had a history of blackish feces and ill complexion in February 1997.", "Gastrointestinal fiberscopy was used to treat duodenal ulcer bleeding.", "Computed tomography showed a right retroperitoneal tumor.", "The tumor was removed in the same month as the CT scan.", "Histopathological examination showed a teratoma and yolk sac tumor.", "He was diagnosed with primary retroperitoneal EGCT.", "He underwent three courses of chemotherapy starting in May 1997.", "The chemotherapy regimen was bleomycin/etoposide/cisplatin (BEP).", "He was followed using periodic imaging, tumor markers determination, and self-palpation.", "He was followed up on an outpatient basis 5 years after treatment.", "He was subsequently lost to follow-up.", "In August 1999, he underwent surgery of the right hydrocele.", "Perioperative findings were unremarkable.", "There was no clear tumor in either testicle at the time of hydrocele surgery.", "At the first visit, his height was 163 cm.", "His weight was 58.5 kg.", "Blood pressure was 128/78 mmHg.", "Heart rate was regular at 62 beats per minute.", "Body temperature was 36.4 \u00b0C.", "He had no history of smoking or drinking.", "There was nothing remarkable in the family history.", "On physical examination, the right testicle was elastic, hard, and enlarged to 40 \u00d7 40 mm.", "A 45 \u00d7 40 mm sized induration was palpable in the right inguinal area.", "The inguinal induration was adequately mobile.", "Neurological examination showed no abnormal findings.", "Blood biochemistry, urinalysis, and tumor markers showed no abnormal findings.", "Ultrasound showed a mosaic shadow inside the right testicle.", "The left testicle showed no abnormal findings on ultrasound.", "Enlargements of the right external iliac lymph node (24 \u00d7 14 mm) and right inguinal lymph node (43 \u00d7 29 mm) were found.", "A 31 \u00d7 22 mm mass with uneven contents was found in the right testicle.", "There was no evidence of distant metastasis.", "The patient underwent high orchiectomy and resection of the right inguinal lymph nodes in November 2017.", "The testicular tumor was 40 \u00d7 40 \u00d7 30 mm in size and weighed 34 g.", "The lymph node was 40 \u00d7 40 \u00d7 30 mm in size and weighed 21 g.", "The cut surfaces of both specimens were yellowish and solid.", "The testicular tumor was localized in the testicle.", "Histopathological findings showed irregular cobblestone proliferations of germ cell-like atypical cells with clear nucleoli.", "Massive necrotic changes were present in the tumor.", "The tumor did not extend into the tunica albuginea.", "No vascular infiltration was found.", "Spermatic cord stumps were negative.", "The tumor diagnosis was a classical seminoma with no other elements.", "Lymph node metastases were diagnosed as a result of the seminoma.", "The seminoma was diagnosed as pT1, pN2, M0, S0.", "The TNM stage was IIB.", "The patient received one course of BEP therapy and three courses of EP therapy.", "Post-chemotherapy CT confirmed a complete clinical response at the right external iliac lymph node.", "The complete clinical response continued 12 months later."], "summary_subclaims": ["The patient is a 49-year-old Japanese man.", "He visited the department in November 2017.", "His chief complaints were indolent right scrotum enlargement and a right inguinal mass.", "He had visited the department of gastroenterology in February 1997.", "Computed tomography showed a right retroperitoneal tumor.", "The tumor was removed in the same month as the CT scan.", "Histopathological examination showed a teratoma and yolk sac tumor.", "He was diagnosed with primary retroperitoneal EGCT.", "He received three courses of chemotherapy.", "The chemotherapy regimen was bleomycin/etoposide/cisplatin (BEP)."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 49-year-old Japanese man.", "He visited the department in November 2017.", "His chief complaints were indolent right scrotum enlargement and a right inguinal mass.", "He had a history of blackish feces and ill complexion in February 1997.", "Gastrointestinal fiberscopy was used to treat duodenal ulcer bleeding.", "Computed tomography showed a right retroperitoneal tumor.", "The tumor was removed in the same month as the CT scan.", "Histopathological examination showed a teratoma and yolk sac tumor.", "He was diagnosed with primary retroperitoneal EGCT.", "He underwent three courses of chemotherapy starting in May 1997.", "The chemotherapy regimen was bleomycin/etoposide/cisplatin (BEP).", "He was followed using periodic imaging, tumor markers determination, and self-palpation.", "He was followed up on an outpatient basis 5 years after treatment.", "He was subsequently lost to follow-up.", "In August 1999, he underwent surgery of the right hydrocele.", "Perioperative findings were unremarkable.", "There was no clear tumor in either testicle at the time of hydrocele surgery.", "At the first visit, his height was 163 cm.", "His weight was 58.5 kg.", "Blood pressure was 128/78 mmHg.", "Heart rate was regular at 62 beats per minute.", "Body temperature was 36.4 \u00b0C.", "He had no history of smoking or drinking.", "There was nothing remarkable in the family history.", "On physical examination, the right testicle was elastic, hard, and enlarged to 40 \u00d7 40 mm.", "A 45 \u00d7 40 mm sized induration was palpable in the right inguinal area.", "The inguinal induration was adequately mobile.", "Neurological examination showed no abnormal findings.", "Blood biochemistry, urinalysis, and tumor markers showed no abnormal findings.", "Ultrasound showed a mosaic shadow inside the right testicle.", "The left testicle showed no abnormal findings on ultrasound.", "Enlargements of the right external iliac lymph node (24 \u00d7 14 mm) and right inguinal lymph node (43 \u00d7 29 mm) were found.", "A 31 \u00d7 22 mm mass with uneven contents was found in the right testicle.", "There was no evidence of distant metastasis.", "The patient underwent high orchiectomy and resection of the right inguinal lymph nodes in November 2017.", "The testicular tumor was 40 \u00d7 40 \u00d7 30 mm in size and weighed 34 g.", "The lymph node was 40 \u00d7 40 \u00d7 30 mm in size and weighed 21 g.", "The cut surfaces of both specimens were yellowish and solid.", "The testicular tumor was localized in the testicle.", "Histopathological findings showed irregular cobblestone proliferations of germ cell-like atypical cells with clear nucleoli.", "Massive necrotic changes were present in the tumor.", "The tumor did not extend into the tunica albuginea.", "No vascular infiltration was found.", "Spermatic cord stumps were negative.", "The tumor diagnosis was a classical seminoma with no other elements.", "Lymph node metastases were diagnosed as a result of the seminoma.", "The seminoma was diagnosed as pT1, pN2, M0, S0.", "The TNM stage was IIB.", "The patient received one course of BEP therapy and three courses of EP therapy.", "Post-chemotherapy CT confirmed a complete clinical response at the right external iliac lymph node.", "The complete clinical response continued 12 months later."], "index": 84, "original_id": "multiclinsum_test_439_en.txt", "split": "test", "summary_subclaims": ["The patient is a 49-year-old Japanese man.", "He visited the department in November 2017.", "His chief complaints were indolent right scrotum enlargement and a right inguinal mass.", "He had visited the department of gastroenterology in February 1997.", "Computed tomography showed a right retroperitoneal tumor.", "The tumor was removed in the same month as the CT scan.", "Histopathological examination showed a teratoma and yolk sac tumor.", "He was diagnosed with primary retroperitoneal EGCT.", "He received three courses of chemotherapy.", "The chemotherapy regimen was bleomycin/etoposide/cisplatin (BEP)."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring are often recommended to support kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Declining glomerular filtration rate (GFR) is a key biomarker for chronic kidney disease progression, and early intervention through pharmacological management, dietary modification, and monitoring of biomarkers such as serum creatinine and proteinuria is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 32-year-old woman.", "She was admitted with a progressively enlarged mass in the rectovaginal space for 9 years.", "The mass was found during a routine examination 9 years ago.", "No obvious progression was seen in following annual examinations until a year ago.", "The maximum diameter of the mass had significantly grown from 4.0 cm to 9.7 cm in a year.", "Dents in stools were caused by tumor compression.", "Endoscopy in a local hospital showed a submucosal protrusion.", "No absolute tumor tissue but only inflammation was found after several times of endoscopic biopsies in the latest 2 years.", "The patient had no previous medical history.", "The patient and family had no history of previous similar illness.", "The anterior rectum wall was plump during digital rectal examination.", "Contrast-enhanced CT showed a mass with liquefaction necrosis inside the rectovaginal space.", "Transabdominal US showed a heterogeneous hypoechoic mass with a maximum diameter of 9.7 cm in the rectovaginal space.", "The mass was suspected to be a rectal GIST or exophytic uterine fibroid.", "Transabdominal CNB was performed to make a definite diagnosis.", "Written informed consent was obtained from the patient before the operation.", "Some hemorrhage occurred from the vagina, causing premature end of the biopsy.", "The hemorrhage spontaneously relieved several days later.", "Strips of greyish shattered tissue were obtained, with the largest diameter smaller than 0.3 cm.", "Pathology indicated inadequate biopsy tissue for diagnosis.", "Another biopsy after ERUS assessment was recommended by multiple disciplinary treatment.", "ERUS was performed with the MyLab Twice US system.", "CEUS was performed with a bolus injection of 2.4 mL SonoVue.", "CEUS was performed right before puncture to confirm the substantial part of the tumor for biopsy guidance.", "The probe was switched to linear mode.", "The transperineal puncture site and path were decided.", "A freehand biopsy of the lesion was performed with the guidance of in-plane needle.", "The needle tip and its movements were continuously monitored in real time by ERUS during the whole puncture procedure.", "Several strips of greyish tissue were obtained with a length of 0.3-1.2 cm.", "No complications occurred."], "summary_subclaims": ["The patient is a 32-year-old woman.", "She complained of a mass inside the rectovaginal space for 9 years.", "The mass became enlarged within 1 year.", "A rectal SEL was detected by endoscopy.", "The rectal SEL was suspected to be a gastrointestinal stromal tumor.", "The rectal SEL was suspected to be an exophytic uterine fibroid.", "A transabdominal core needle biopsy was unsuccessful.", "The transabdominal core needle biopsy resulted in insufficient tissues.", "Vaginal hemorrhage occurred.", "A second biopsy was suggested after multiple disciplinary treatment discussion.", "A transperineal core needle biopsy was guided by ERUS combined with CEUS.", "Adequate samples were procured.", "The pathological diagnosis was rectal gastrointestinal stromal tumor.", "Imatinib was recommended for first-line therapy.", "The tumor shrank after treatment.", "Resection of the rectal gastrointestinal stromal tumor was performed through the posterior vaginal wall.", "Adjuvant therapy was applied.", "No recurrence or metastasis has been found by the last follow-up on December 13, 2019."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 32-year-old woman.", "She was admitted with a progressively enlarged mass in the rectovaginal space for 9 years.", "The mass was found during a routine examination 9 years ago.", "No obvious progression was seen in following annual examinations until a year ago.", "The maximum diameter of the mass had significantly grown from 4.0 cm to 9.7 cm in a year.", "Dents in stools were caused by tumor compression.", "Endoscopy in a local hospital showed a submucosal protrusion.", "No absolute tumor tissue but only inflammation was found after several times of endoscopic biopsies in the latest 2 years.", "The patient had no previous medical history.", "The patient and family had no history of previous similar illness.", "The anterior rectum wall was plump during digital rectal examination.", "Contrast-enhanced CT showed a mass with liquefaction necrosis inside the rectovaginal space.", "Transabdominal US showed a heterogeneous hypoechoic mass with a maximum diameter of 9.7 cm in the rectovaginal space.", "The mass was suspected to be a rectal GIST or exophytic uterine fibroid.", "Transabdominal CNB was performed to make a definite diagnosis.", "Written informed consent was obtained from the patient before the operation.", "Some hemorrhage occurred from the vagina, causing premature end of the biopsy.", "The hemorrhage spontaneously relieved several days later.", "Strips of greyish shattered tissue were obtained, with the largest diameter smaller than 0.3 cm.", "Pathology indicated inadequate biopsy tissue for diagnosis.", "Another biopsy after ERUS assessment was recommended by multiple disciplinary treatment.", "ERUS was performed with the MyLab Twice US system.", "CEUS was performed with a bolus injection of 2.4 mL SonoVue.", "CEUS was performed right before puncture to confirm the substantial part of the tumor for biopsy guidance.", "The probe was switched to linear mode.", "The transperineal puncture site and path were decided.", "A freehand biopsy of the lesion was performed with the guidance of in-plane needle.", "The needle tip and its movements were continuously monitored in real time by ERUS during the whole puncture procedure.", "Several strips of greyish tissue were obtained with a length of 0.3-1.2 cm.", "No complications occurred."], "index": 48, "original_id": "multiclinsum_test_2808_en.txt", "split": "test", "summary_subclaims": ["The patient is a 32-year-old woman.", "She complained of a mass inside the rectovaginal space for 9 years.", "The mass became enlarged within 1 year.", "A rectal SEL was detected by endoscopy.", "The rectal SEL was suspected to be a gastrointestinal stromal tumor.", "The rectal SEL was suspected to be an exophytic uterine fibroid.", "A transabdominal core needle biopsy was unsuccessful.", "The transabdominal core needle biopsy resulted in insufficient tissues.", "Vaginal hemorrhage occurred.", "A second biopsy was suggested after multiple disciplinary treatment discussion.", "A transperineal core needle biopsy was guided by ERUS combined with CEUS.", "Adequate samples were procured.", "The pathological diagnosis was rectal gastrointestinal stromal tumor.", "Imatinib was recommended for first-line therapy.", "The tumor shrank after treatment.", "Resection of the rectal gastrointestinal stromal tumor was performed through the posterior vaginal wall.", "Adjuvant therapy was applied.", "No recurrence or metastasis has been found by the last follow-up on December 13, 2019."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring are often recommended to support kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Declining glomerular filtration rate (GFR) is a key biomarker for chronic kidney disease progression, and early intervention through pharmacological management, dietary modification, and monitoring of biomarkers such as serum creatinine and proteinuria is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 17-year-old male.", "The patient presented with pain in the lower left posterior region of the mandible.", "The patient had no significant systemic history.", "The patient reported no previous extractions in the mentioned area.", "Clinical examination revealed the absence of Teeth 37 and 38.", "Palpation of the alveolar ridge showed no swelling or bony prominences.", "Radiographic examination revealed that Tooth 37 was impacted transversely between Teeth 36 and 38.", "Tooth 38 was in a vertical position close to the occlusal plane.", "Tooth 38 was Stage Nolla 8.", "Tomographic imaging indicated that the crown of Tooth 37 was oriented lingually.", "The roots of Tooth 37 were separated.", "The mesial root of Tooth 37 was curved and thin.", "The distal root of Tooth 37 was straight and thick.", "The diagnosis was an impacted Tooth 37 in a transverse position with the crown oriented lingually.", "Tooth 38 was retained in a vertical position.", "A consultation with the orthodontics department was made to define the treatment plan.", "Flap extraction of Tooth 37 was planned.", "Subsequent eruption of Tooth 38 was planned.", "Fixed orthodontic treatment was planned.", "The ultimate goal was to restore masticatory function by positioning the third molar in place of the second molar.", "The patient was informed regarding the surgical procedure.", "The patient was informed regarding the risks associated with the procedure.", "The patient was informed regarding the alternative treatments.", "The patient signed the informed consent.", "The surgical intervention for flap extraction of Tooth 37 was scheduled.", "The procedure involved block anesthesia for the inferior alveolar nerve.", "The procedure involved block anesthesia for the lingual nerve.", "The procedure involved block anesthesia for the buccal nerve.", "An L-shaped or monoangular incision was made at the level of the second molar.", "The mucoperiosteal flap was elevated to expose the bone plate.", "An osteotomy was performed in the occlusal bone to visualize the crown of the second molar.", "The separated roots were sectioned for removal.", "The distal segment (crown and root) was extracted first.", "The mesial segment (crown and root) was removed after the distal segment.", "Both segments were luxated with a flag elevator.", "An alveolar curette was used to clean the bony crypt corresponding to the crown.", "The pericoronal sac was removed.", "The procedure was completed with discontinuous suturing using 3/0 polyglycolic acid.", "Five simple sutures were placed.", "The extracted molar was observed in two parts.", "Amoxicillin 500\u2009mg every 8\u2009h for 5 days was prescribed.", "Sodium diclofenac 50\u2009mg every 8\u2009h for 3 days was prescribed.", "Dexamethasone 4\u2009mg every 8\u2009h for 3 days was prescribed.", "The patient was evaluated 6 months after the surgical intervention.", "Bone healing was favorable according to an x-ray.", "The report confirms 'alveolar walls preserved, no evidence of spicules or bony defects; defined borders, no radiographic signs of osteitis'."], "summary_subclaims": ["The patient is a 17-year-old male.", "The patient presented with pain in the lower left molar region.", "Clinical examination revealed the absence of Teeth 37 and 38.", "Tomographic imaging showed Tooth 37 in a transverse position.", "Tomographic imaging showed the crown of Tooth 37 oriented lingually.", "Tomographic imaging showed Tooth 38 in a vertical position.", "Extraction of Tooth 37 was performed.", "A vestibular approach was used for the extraction of Tooth 37.", "Odontectomy was performed for the extraction of Tooth 37.", "Space constraints were a factor in the extraction of Tooth 37."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 17-year-old male.", "The patient presented with pain in the lower left posterior region of the mandible.", "The patient had no significant systemic history.", "The patient reported no previous extractions in the mentioned area.", "Clinical examination revealed the absence of Teeth 37 and 38.", "Palpation of the alveolar ridge showed no swelling or bony prominences.", "Radiographic examination revealed that Tooth 37 was impacted transversely between Teeth 36 and 38.", "Tooth 38 was in a vertical position close to the occlusal plane.", "Tooth 38 was Stage Nolla 8.", "Tomographic imaging indicated that the crown of Tooth 37 was oriented lingually.", "The roots of Tooth 37 were separated.", "The mesial root of Tooth 37 was curved and thin.", "The distal root of Tooth 37 was straight and thick.", "The diagnosis was an impacted Tooth 37 in a transverse position with the crown oriented lingually.", "Tooth 38 was retained in a vertical position.", "A consultation with the orthodontics department was made to define the treatment plan.", "Flap extraction of Tooth 37 was planned.", "Subsequent eruption of Tooth 38 was planned.", "Fixed orthodontic treatment was planned.", "The ultimate goal was to restore masticatory function by positioning the third molar in place of the second molar.", "The patient was informed regarding the surgical procedure.", "The patient was informed regarding the risks associated with the procedure.", "The patient was informed regarding the alternative treatments.", "The patient signed the informed consent.", "The surgical intervention for flap extraction of Tooth 37 was scheduled.", "The procedure involved block anesthesia for the inferior alveolar nerve.", "The procedure involved block anesthesia for the lingual nerve.", "The procedure involved block anesthesia for the buccal nerve.", "An L-shaped or monoangular incision was made at the level of the second molar.", "The mucoperiosteal flap was elevated to expose the bone plate.", "An osteotomy was performed in the occlusal bone to visualize the crown of the second molar.", "The separated roots were sectioned for removal.", "The distal segment (crown and root) was extracted first.", "The mesial segment (crown and root) was removed after the distal segment.", "Both segments were luxated with a flag elevator.", "An alveolar curette was used to clean the bony crypt corresponding to the crown.", "The pericoronal sac was removed.", "The procedure was completed with discontinuous suturing using 3/0 polyglycolic acid.", "Five simple sutures were placed.", "The extracted molar was observed in two parts.", "Amoxicillin 500\u2009mg every 8\u2009h for 5 days was prescribed.", "Sodium diclofenac 50\u2009mg every 8\u2009h for 3 days was prescribed.", "Dexamethasone 4\u2009mg every 8\u2009h for 3 days was prescribed.", "The patient was evaluated 6 months after the surgical intervention.", "Bone healing was favorable according to an x-ray.", "The report confirms 'alveolar walls preserved, no evidence of spicules or bony defects; defined borders, no radiographic signs of osteitis'."], "index": 46, "original_id": "multiclinsum_test_3344_en.txt", "split": "test", "summary_subclaims": ["The patient is a 17-year-old male.", "The patient presented with pain in the lower left molar region.", "Clinical examination revealed the absence of Teeth 37 and 38.", "Tomographic imaging showed Tooth 37 in a transverse position.", "Tomographic imaging showed the crown of Tooth 37 oriented lingually.", "Tomographic imaging showed Tooth 38 in a vertical position.", "Extraction of Tooth 37 was performed.", "A vestibular approach was used for the extraction of Tooth 37.", "Odontectomy was performed for the extraction of Tooth 37.", "Space constraints were a factor in the extraction of Tooth 37."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 71-year-old male.", "The patient has a past medical history significant for diabetes mellitus.", "The patient has a past medical history significant for coronary artery disease.", "The patient has a past medical history significant for chronic hypotension.", "The patient has a past medical history significant for chronic obstructive pulmonary disease.", "The patient has a past medical history significant for obstructive sleep apnea.", "The patient has a past medical history significant for peripheral artery disease.", "The patient presented to the ED with right buttock and scrotal swelling for three days.", "The patient reported generalized weakness.", "The patient reported shortness of breath.", "The patient reported urinary retention with dysuria.", "The patient noticed non-traumatic bruising to his scrotum one day prior to presentation.", "The patient reported increasing buttock pain not controlled by home oxycodone/acetaminophen 5/325 mg tablets.", "Upon arrival, the patient's oral temperature was 38.2\u00b0C.", "The patient's blood pressure was 119/54 mm Hg.", "The patient's heart rate was 93 beats per minute.", "The patient's respiratory rate was 25 breaths per minute.", "The patient's oxygen saturation was 97% on room air.", "The physical examination was notable for an ill-appearing gentleman.", "The patient was awake and alert.", "Heart sounds were unremarkable aside from tachycardia.", "Lungs were clear to auscultation.", "The abdominal examination was soft, protuberant, and nontender.", "A focused genitourinary examination revealed an edematous, erythematous, and exquisitely tender scrotum.", "There was a coin-sized, ecchymotic-appearing lesion on the scrotum.", "Erythema and induration extended from the scrotum and perineum to the right buttock.", "No crepitus or fluctuance was palpated on examination.", "Laboratory results were remarkable for leukocytosis to 15,000 K/mm3.", "The patient had lactic acidosis of 3.4 mmol/L.", "The patient had marked acute kidney injury with creatinine of 5 mg/dL.", "The patient had a venous blood gas pH of 7.22.", "The patient was mildly hyponatremic at 133 mmol/L.", "The patient was hyperkalemic at 5.3 mmol/L.", "Intravenous antibiotics were initiated.", "Emergent consultations with surgery and urology were obtained.", "The patient decompensated into septic shock.", "The patient's blood pressure decreased to 88/41 mm Hg during the ED course.", "The patient was not stable for transport or advanced imaging.", "The ecchymotic-appearing lesion and edema had expanded across his scrotum and perineum.", "POCUS was used for the rapid assessment of the patient\u2019s presumed clinical diagnosis of Fournier\u2019s gangrene.", "Transverse and sagittal views of the perineum and scrotum were obtained using a high-frequency linear probe.", "The POCUS imaging revealed diffuse hyperechoic foci with posterior 'dirty' shadowing, representative of subcutaneous air.", "The POCUS imaging revealed small fluid collections tracking along the fascial planes.", "The patient was taken directly from the ED to the operating room for immediate surgical debridement.", "An area of tissue measuring 25 cm \u00d7 30 cm was debrided from the scrotum, perineum, and right buttock.", "Dark, necrotic tissue and foul-smelling fluid were noted during surgery, consistent with Fournier\u2019s gangrene.", "The patient was admitted to the intensive care unit.", "The patient was transferred to a tertiary care center.", "The patient ultimately died of complications related to his illness."], "summary_subclaims": ["POCUS was used to rapidly confirm diagnosis.", "The patient was unstable.", "The patient had severe sepsis.", "The patient presented to the emergency department.", "The patient had Fournier's gangrene."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 71-year-old male.", "The patient has a past medical history significant for diabetes mellitus.", "The patient has a past medical history significant for coronary artery disease.", "The patient has a past medical history significant for chronic hypotension.", "The patient has a past medical history significant for chronic obstructive pulmonary disease.", "The patient has a past medical history significant for obstructive sleep apnea.", "The patient has a past medical history significant for peripheral artery disease.", "The patient presented to the ED with right buttock and scrotal swelling for three days.", "The patient reported generalized weakness.", "The patient reported shortness of breath.", "The patient reported urinary retention with dysuria.", "The patient noticed non-traumatic bruising to his scrotum one day prior to presentation.", "The patient reported increasing buttock pain not controlled by home oxycodone/acetaminophen 5/325 mg tablets.", "Upon arrival, the patient's oral temperature was 38.2\u00b0C.", "The patient's blood pressure was 119/54 mm Hg.", "The patient's heart rate was 93 beats per minute.", "The patient's respiratory rate was 25 breaths per minute.", "The patient's oxygen saturation was 97% on room air.", "The physical examination was notable for an ill-appearing gentleman.", "The patient was awake and alert.", "Heart sounds were unremarkable aside from tachycardia.", "Lungs were clear to auscultation.", "The abdominal examination was soft, protuberant, and nontender.", "A focused genitourinary examination revealed an edematous, erythematous, and exquisitely tender scrotum.", "There was a coin-sized, ecchymotic-appearing lesion on the scrotum.", "Erythema and induration extended from the scrotum and perineum to the right buttock.", "No crepitus or fluctuance was palpated on examination.", "Laboratory results were remarkable for leukocytosis to 15,000 K/mm3.", "The patient had lactic acidosis of 3.4 mmol/L.", "The patient had marked acute kidney injury with creatinine of 5 mg/dL.", "The patient had a venous blood gas pH of 7.22.", "The patient was mildly hyponatremic at 133 mmol/L.", "The patient was hyperkalemic at 5.3 mmol/L.", "Intravenous antibiotics were initiated.", "Emergent consultations with surgery and urology were obtained.", "The patient decompensated into septic shock.", "The patient's blood pressure decreased to 88/41 mm Hg during the ED course.", "The patient was not stable for transport or advanced imaging.", "The ecchymotic-appearing lesion and edema had expanded across his scrotum and perineum.", "POCUS was used for the rapid assessment of the patient\u2019s presumed clinical diagnosis of Fournier\u2019s gangrene.", "Transverse and sagittal views of the perineum and scrotum were obtained using a high-frequency linear probe.", "The POCUS imaging revealed diffuse hyperechoic foci with posterior 'dirty' shadowing, representative of subcutaneous air.", "The POCUS imaging revealed small fluid collections tracking along the fascial planes.", "The patient was taken directly from the ED to the operating room for immediate surgical debridement.", "An area of tissue measuring 25 cm \u00d7 30 cm was debrided from the scrotum, perineum, and right buttock.", "Dark, necrotic tissue and foul-smelling fluid were noted during surgery, consistent with Fournier\u2019s gangrene.", "The patient was admitted to the intensive care unit.", "The patient was transferred to a tertiary care center.", "The patient ultimately died of complications related to his illness."], "index": 75, "original_id": "multiclinsum_test_2914_en.txt", "split": "test", "summary_subclaims": ["POCUS was used to rapidly confirm diagnosis.", "The patient was unstable.", "The patient had severe sepsis.", "The patient presented to the emergency department.", "The patient had Fournier's gangrene."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring are often recommended to support kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Declining glomerular filtration rate (GFR) is a key biomarker for chronic kidney disease progression, and early intervention through pharmacological management, dietary modification, and monitoring of biomarkers such as serum creatinine and proteinuria is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is an 8 year old girl.", "The patient has tufting enteropathy.", "The patient is on long-term parenteral nutrition.", "The patient presented on 3 occasions with central venous catheter infection due to Bacillus species.", "On each occasion, she had fever after flushing of the central venous catheter.", "She had initially presented in the first few months of life with chronic watery diarrhoea.", "She had impaired growth.", "She was found to have tufting enteropathy.", "Tufting enteropathy is a rare congenital enteropathy.", "Tufting enteropathy requires indefinite dependence on parenteral nutrition from early infancy.", "The child is on regular parenteral nutrition.", "The child has had no previous history of significant infections, except for central venous catheter infections with coagulase negative staphylococci.", "Immunoglobulins, neutrophil and lymphocyte counts were within the normal range.", "There was no history of significant trauma, injuries or skin infections prior to this episode, except a small cut on her finger.", "The small cut on her finger healed very well.", "She lives with her parents.", "There is no history of contact with plant growth products.", "There is no history of contact with animal probiotics.", "The child presented with fever and rigors to her local hospital.", "Bacillus species was isolated from blood taken from the central venous catheter.", "The organism was reported sensitive to flucloxacillin.", "She was treated with 4 weeks of intravenous flucloxacillin.", "Bacteraemia had persisted despite 14 days of treatment.", "The child was transferred to our hospital with recurrence of fever and rigors.", "Empirical treatment was started with intravenous cefotaxime and flucloxacillin.", "Bacillus species was isolated from central venous catheter cultures both before and whilst on cefotaxime and flucloxacillin.", "The organism was later identified as Bacillus pumilus at the National Reference Laboratory.", "The methods used to identify the organism included gram stain to determine whether spores are produced.", "The methods used to identify the organism included a short biochemical profile based on ammonia salt sugars, Lecithinase and mannitol.", "Bacillus pumilus is lecithinase negative.", "Bacillus pumilus is mannitol positive.", "The methods used to identify the organism included DNA sequencing.", "Bacillus pumilus was reported to be sensitive to vancomycin.", "Bacillus pumilus was reported to be sensitive to erythromycin.", "There were concerns that the patient had previously reacted to systemic vancomycin.", "Antibiotics were changed to intravenous clindamycin with vancomycin line locks given for 2 weeks.", "Blood cultures, taken both during and after this treatment, were negative.", "Echocardiography showed no evidence of vegetations at the tip of the catheter or in the heart.", "Ten days after stopping the intravenous antibiotics the child presented for the third time with fever and rigors.", "A Bacillus species was again grown from blood taken from the central venous catheter.", "The central venous catheter was removed after 5 days treatment with intravenous vancomycin.", "A new central venous catheter was inserted.", "Subsequent blood cultures were negative.", "There has been no recurrence of further fever or infections over a 9-month period.", "The infection has been eradicated."], "summary_subclaims": ["We report a case of central venous catheter infection with Bacillus pumilus in an immunocompetent child with tufting enteropathy on long-term parenteral nutrition.", "There were three episodes of central venous catheter infection with Bacillus pumilus in three months.", "Despite adequate and appropriate use of intravenous antibiotics, the infection failed to clear.", "The infection resulted in the need for removal of the catheter for complete cure."]}, "extra_info": {"fulltext_subclaims": ["The patient is an 8 year old girl.", "The patient has tufting enteropathy.", "The patient is on long-term parenteral nutrition.", "The patient presented on 3 occasions with central venous catheter infection due to Bacillus species.", "On each occasion, she had fever after flushing of the central venous catheter.", "She had initially presented in the first few months of life with chronic watery diarrhoea.", "She had impaired growth.", "She was found to have tufting enteropathy.", "Tufting enteropathy is a rare congenital enteropathy.", "Tufting enteropathy requires indefinite dependence on parenteral nutrition from early infancy.", "The child is on regular parenteral nutrition.", "The child has had no previous history of significant infections, except for central venous catheter infections with coagulase negative staphylococci.", "Immunoglobulins, neutrophil and lymphocyte counts were within the normal range.", "There was no history of significant trauma, injuries or skin infections prior to this episode, except a small cut on her finger.", "The small cut on her finger healed very well.", "She lives with her parents.", "There is no history of contact with plant growth products.", "There is no history of contact with animal probiotics.", "The child presented with fever and rigors to her local hospital.", "Bacillus species was isolated from blood taken from the central venous catheter.", "The organism was reported sensitive to flucloxacillin.", "She was treated with 4 weeks of intravenous flucloxacillin.", "Bacteraemia had persisted despite 14 days of treatment.", "The child was transferred to our hospital with recurrence of fever and rigors.", "Empirical treatment was started with intravenous cefotaxime and flucloxacillin.", "Bacillus species was isolated from central venous catheter cultures both before and whilst on cefotaxime and flucloxacillin.", "The organism was later identified as Bacillus pumilus at the National Reference Laboratory.", "The methods used to identify the organism included gram stain to determine whether spores are produced.", "The methods used to identify the organism included a short biochemical profile based on ammonia salt sugars, Lecithinase and mannitol.", "Bacillus pumilus is lecithinase negative.", "Bacillus pumilus is mannitol positive.", "The methods used to identify the organism included DNA sequencing.", "Bacillus pumilus was reported to be sensitive to vancomycin.", "Bacillus pumilus was reported to be sensitive to erythromycin.", "There were concerns that the patient had previously reacted to systemic vancomycin.", "Antibiotics were changed to intravenous clindamycin with vancomycin line locks given for 2 weeks.", "Blood cultures, taken both during and after this treatment, were negative.", "Echocardiography showed no evidence of vegetations at the tip of the catheter or in the heart.", "Ten days after stopping the intravenous antibiotics the child presented for the third time with fever and rigors.", "A Bacillus species was again grown from blood taken from the central venous catheter.", "The central venous catheter was removed after 5 days treatment with intravenous vancomycin.", "A new central venous catheter was inserted.", "Subsequent blood cultures were negative.", "There has been no recurrence of further fever or infections over a 9-month period.", "The infection has been eradicated."], "index": 44, "original_id": "multiclinsum_test_1072_en.txt", "split": "test", "summary_subclaims": ["We report a case of central venous catheter infection with Bacillus pumilus in an immunocompetent child with tufting enteropathy on long-term parenteral nutrition.", "There were three episodes of central venous catheter infection with Bacillus pumilus in three months.", "Despite adequate and appropriate use of intravenous antibiotics, the infection failed to clear.", "The infection resulted in the need for removal of the catheter for complete cure."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring are often recommended to support kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., hyperkalemia, metabolic acidosis), and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Declining glomerular filtration rate (GFR) is a key biomarker for chronic kidney disease progression, and early intervention through pharmacological management, dietary modification, and monitoring of biomarkers such as serum creatinine and proteinuria is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 55-year-old lady of Central African origin.", "The patient has primary open-angle glaucoma.", "The patient underwent bilateral XEN gel surgery.", "The patient was referred with intraocular pressures of 38 mm Hg in the right eye.", "The patient was referred with intraocular pressures of 22 mm Hg in the left eye.", "The patient had been diagnosed with POAG several years before.", "The patient had two selective laser trabeculoplasties.", "The patient was on maximal medical therapy including oral acetazolamide.", "The patient had mediocre self-reported compliance.", "The patient had a positive family history for open-angle glaucoma in her mother.", "Best-corrected visual acuity was 10/10 in both eyes.", "Cup/disk ratio was 0.8 in the right eye with an inferior notch.", "Cup/disk ratio was 0.7 in the left eye with a superior notch.", "Gonioscopy showed bilaterally open angles.", "Pachymetry was 580 \u03bcm in the right eye.", "Pachymetry was 585 \u03bcm in the left eye.", "Automated visual field examination showed bilateral nasal quadrantanopsia.", "Optical coherence tomography imaging showed generally reduced RNFL thicknesses bilaterally.", "Brain MRI imaging was unremarkable.", "Bilateral mitomycin C-augmented XEN gel stent implantation was organized.", "The target IOP was \u226418 mm Hg.", "Surgeries were performed following standard protocols described in the literature.", "No intraoperative complications were noted.", "The patient received topical combined tobramycin and dexamethasone.", "The right eye recovered uneventfully.", "The right eye had IOP normalizing between 12 mm Hg and 16 mm Hg at 3 months.", "The left eye developed a 2-mm hyphema on the first day following surgery.", "The initial intraocular pressure in the left eye was 2 mm Hg.", "The hyphema in the left eye had completely resolved after 8 days.", "IOP was stable at 12 mm Hg after 8 days.", "After 1 month, the patient presented with an IOP of 50 mm Hg in the left eye.", "The filtration bleb was shallow but diffuse.", "The XEN gel stent was well-positioned.", "An emergency revision procedure was organized.", "The absence of filtration through the stent was confirmed intraoperatively.", "The blocked tube was removed.", "The tube was sent for macroscopic analysis.", "The patient made good recovery without any postoperative complications.", "At 1-month, her IOP was stable at 17 mm Hg.", "Macroscopic examination confirmed obstruction of the XEN gel stent on its AC extremity.", "Translucent cell fragments were identified within the obstructed tube."], "summary_subclaims": ["The patient is a 55-year-old female.", "The patient has primary open-angle glaucoma.", "The patient underwent bilateral XEN gel surgery.", "The left eye developed a 2 mm postoperative hyphema.", "The hyphema resolved spontaneously within 8 days.", "Intraocular pressure normalized at 12 mm Hg.", "Intraocular pressure increased to 50 mm Hg after 1 month.", "The eye was otherwise normal-looking.", "Intraoperative examination revealed a nonfunctioning XEN gel stent.", "The stent was replaced and sent for laboratory analysis.", "Macroscopic examination of the tube confirmed obstruction with cellular debris.", "Tube replacement restored good filtration."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 55-year-old lady of Central African origin.", "The patient has primary open-angle glaucoma.", "The patient underwent bilateral XEN gel surgery.", "The patient was referred with intraocular pressures of 38 mm Hg in the right eye.", "The patient was referred with intraocular pressures of 22 mm Hg in the left eye.", "The patient had been diagnosed with POAG several years before.", "The patient had two selective laser trabeculoplasties.", "The patient was on maximal medical therapy including oral acetazolamide.", "The patient had mediocre self-reported compliance.", "The patient had a positive family history for open-angle glaucoma in her mother.", "Best-corrected visual acuity was 10/10 in both eyes.", "Cup/disk ratio was 0.8 in the right eye with an inferior notch.", "Cup/disk ratio was 0.7 in the left eye with a superior notch.", "Gonioscopy showed bilaterally open angles.", "Pachymetry was 580 \u03bcm in the right eye.", "Pachymetry was 585 \u03bcm in the left eye.", "Automated visual field examination showed bilateral nasal quadrantanopsia.", "Optical coherence tomography imaging showed generally reduced RNFL thicknesses bilaterally.", "Brain MRI imaging was unremarkable.", "Bilateral mitomycin C-augmented XEN gel stent implantation was organized.", "The target IOP was \u226418 mm Hg.", "Surgeries were performed following standard protocols described in the literature.", "No intraoperative complications were noted.", "The patient received topical combined tobramycin and dexamethasone.", "The right eye recovered uneventfully.", "The right eye had IOP normalizing between 12 mm Hg and 16 mm Hg at 3 months.", "The left eye developed a 2-mm hyphema on the first day following surgery.", "The initial intraocular pressure in the left eye was 2 mm Hg.", "The hyphema in the left eye had completely resolved after 8 days.", "IOP was stable at 12 mm Hg after 8 days.", "After 1 month, the patient presented with an IOP of 50 mm Hg in the left eye.", "The filtration bleb was shallow but diffuse.", "The XEN gel stent was well-positioned.", "An emergency revision procedure was organized.", "The absence of filtration through the stent was confirmed intraoperatively.", "The blocked tube was removed.", "The tube was sent for macroscopic analysis.", "The patient made good recovery without any postoperative complications.", "At 1-month, her IOP was stable at 17 mm Hg.", "Macroscopic examination confirmed obstruction of the XEN gel stent on its AC extremity.", "Translucent cell fragments were identified within the obstructed tube."], "index": 64, "original_id": "multiclinsum_test_7_en.txt", "split": "test", "summary_subclaims": ["The patient is a 55-year-old female.", "The patient has primary open-angle glaucoma.", "The patient underwent bilateral XEN gel surgery.", "The left eye developed a 2 mm postoperative hyphema.", "The hyphema resolved spontaneously within 8 days.", "Intraocular pressure normalized at 12 mm Hg.", "Intraocular pressure increased to 50 mm Hg after 1 month.", "The eye was otherwise normal-looking.", "Intraoperative examination revealed a nonfunctioning XEN gel stent.", "The stent was replaced and sent for laboratory analysis.", "Macroscopic examination of the tube confirmed obstruction with cellular debris.", "Tube replacement restored good filtration."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was a 49-year-old man with a history of acromegaly.", "He was admitted with recurrent shortness of breath and dyspnea on exertion during the previous 2 years.", "He had experienced an episode of presyncope 2 weeks prior.", "He had no past history of hypertension, diabetes mellitus, sleep apnea, or sudden cardiac death.", "He did not smoke or consume alcohol.", "He had a history of stereotactic radiosurgeries twice in a decade or so.", "He was adherent to treatment with octreotide 40 mg once per month through intramuscular injection.", "He was 1.85 m tall, weighed 134 kg, and had a body mass index of 39 kg/m2.", "His blood pressure was 110/60 mmHg.", "His heart rate was 92 beats/min with sinus rhythm.", "He had prominent superciliary arches and nose bridge.", "He had enlargement of the tongue and lip.", "He had large hands and feet.", "Cardiac auscultation revealed irregular premature beats.", "An electrocardiogram demonstrated sinus rhythm with wide (160 ms) QRS duration of left bundle branch block.", "The patient\u2019s condition was classified as New York Heart Association stage III\u2013IV.", "Magnetic resonance imaging showed pituitary macroadenoma.", "Blood testing showed an elevated brain natriuretic peptide level of 740 pg/ml.", "Hormone laboratory tests demonstrated excessive secretion of GH and IGF-1, twofold greater than the reference normal upper limit.", "A Holter monitor showed frequent ventricular premature beats.", "A chest x-ray showed a cardiothoracic ratio of 78%.", "Echocardiography showed diffuse impairment of left ventricular systolic motion, reaching an LVEF of 16%.", "The right ventricle and atrium and the left atrium were dilated.", "There was moderate mitral regurgitation.", "There was no associated systolic anterior motion of the mitral valve.", "Coronary angiography showed normal coronary arteries without stenosis.", "Left ventriculography revealed an EF of 20% with diffuse LV hypokinesis.", "Acromegaly-induced cardiomyopathy was confirmed.", "The patient was diagnosed with secondary dilated cardiomyopathy due to acromegaly.", "The patient was diagnosed with congestive heart failure secondary to acromegaly-induced dilated cardiomyopathy.", "The mainstay of treatment acknowledged globally is surgical resection of the pituitary adenoma.", "Surgical resection was considered high-risk given the patient\u2019s cardiac condition.", "The patient was administered diuretics, vasodilators, an ACEI, \u03b2-blockers, and spironolactone.", "Octreotide (200 \u03bcg/day) was administered for the control of GH excess.", "After half a year, the serum GH concentration decreased from 32.50 ng/ml to 1.98 ng/ml.", "The patient was hospitalized again because of uncontrollable cardiac failure.", "Echocardiography showed a recovered EF value from 16% to 28%.", "A significant ventricular mechanical dyssynchrony was detected.", "Electrophysiological study revealed a nonsustained ventricular monomorphic tachycardia.", "We recommended cardiac resynchronization therapy with defibrillator implantation.", "The patient underwent CRT insertion.", "The patient was discharged to home 5 days after CRT insertion.", "The patient claimed symptom improvement following device insertion 1 month later.", "Echocardiography at the last visit identified improved LVEF of 54%.", "A chest x-ray showed reduced CTR of 60%.", "The patient was in NYHA functional class II."], "summary_subclaims": ["The patient is a 49-year-old man.", "The patient has a history of acromegaly.", "The patient presented with decompensated systolic heart failure.", "Serial electrocardiograms showed wide (160\u2013200\u2009ms) QRS duration.", "Echocardiography showed severe left ventricular dysfunction.", "The left ventricular ejection fraction was 16%.", "Surgical indication was rarely assessed by neurosurgeons.", "Stereotactic radiosurgery together with pharmacotherapy produced infinitesimal effects.", "Cardiac resynchronization therapy was performed.", "The patient\u2019s symptoms were successfully alleviated.", "The patient was discharged from the hospital."]}, "extra_info": {"fulltext_subclaims": ["The patient was a 49-year-old man with a history of acromegaly.", "He was admitted with recurrent shortness of breath and dyspnea on exertion during the previous 2 years.", "He had experienced an episode of presyncope 2 weeks prior.", "He had no past history of hypertension, diabetes mellitus, sleep apnea, or sudden cardiac death.", "He did not smoke or consume alcohol.", "He had a history of stereotactic radiosurgeries twice in a decade or so.", "He was adherent to treatment with octreotide 40 mg once per month through intramuscular injection.", "He was 1.85 m tall, weighed 134 kg, and had a body mass index of 39 kg/m2.", "His blood pressure was 110/60 mmHg.", "His heart rate was 92 beats/min with sinus rhythm.", "He had prominent superciliary arches and nose bridge.", "He had enlargement of the tongue and lip.", "He had large hands and feet.", "Cardiac auscultation revealed irregular premature beats.", "An electrocardiogram demonstrated sinus rhythm with wide (160 ms) QRS duration of left bundle branch block.", "The patient\u2019s condition was classified as New York Heart Association stage III\u2013IV.", "Magnetic resonance imaging showed pituitary macroadenoma.", "Blood testing showed an elevated brain natriuretic peptide level of 740 pg/ml.", "Hormone laboratory tests demonstrated excessive secretion of GH and IGF-1, twofold greater than the reference normal upper limit.", "A Holter monitor showed frequent ventricular premature beats.", "A chest x-ray showed a cardiothoracic ratio of 78%.", "Echocardiography showed diffuse impairment of left ventricular systolic motion, reaching an LVEF of 16%.", "The right ventricle and atrium and the left atrium were dilated.", "There was moderate mitral regurgitation.", "There was no associated systolic anterior motion of the mitral valve.", "Coronary angiography showed normal coronary arteries without stenosis.", "Left ventriculography revealed an EF of 20% with diffuse LV hypokinesis.", "Acromegaly-induced cardiomyopathy was confirmed.", "The patient was diagnosed with secondary dilated cardiomyopathy due to acromegaly.", "The patient was diagnosed with congestive heart failure secondary to acromegaly-induced dilated cardiomyopathy.", "The mainstay of treatment acknowledged globally is surgical resection of the pituitary adenoma.", "Surgical resection was considered high-risk given the patient\u2019s cardiac condition.", "The patient was administered diuretics, vasodilators, an ACEI, \u03b2-blockers, and spironolactone.", "Octreotide (200 \u03bcg/day) was administered for the control of GH excess.", "After half a year, the serum GH concentration decreased from 32.50 ng/ml to 1.98 ng/ml.", "The patient was hospitalized again because of uncontrollable cardiac failure.", "Echocardiography showed a recovered EF value from 16% to 28%.", "A significant ventricular mechanical dyssynchrony was detected.", "Electrophysiological study revealed a nonsustained ventricular monomorphic tachycardia.", "We recommended cardiac resynchronization therapy with defibrillator implantation.", "The patient underwent CRT insertion.", "The patient was discharged to home 5 days after CRT insertion.", "The patient claimed symptom improvement following device insertion 1 month later.", "Echocardiography at the last visit identified improved LVEF of 54%.", "A chest x-ray showed reduced CTR of 60%.", "The patient was in NYHA functional class II."], "index": 57, "original_id": "multiclinsum_test_3217_en.txt", "split": "test", "summary_subclaims": ["The patient is a 49-year-old man.", "The patient has a history of acromegaly.", "The patient presented with decompensated systolic heart failure.", "Serial electrocardiograms showed wide (160\u2013200\u2009ms) QRS duration.", "Echocardiography showed severe left ventricular dysfunction.", "The left ventricular ejection fraction was 16%.", "Surgical indication was rarely assessed by neurosurgeons.", "Stereotactic radiosurgery together with pharmacotherapy produced infinitesimal effects.", "Cardiac resynchronization therapy was performed.", "The patient\u2019s symptoms were successfully alleviated.", "The patient was discharged from the hospital."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 42-year-old Native American female.", "She presented to University of South Dakota Sanford Medical Center in December of 2020.", "She developed numbness, tingling, and a sharp shooting pain in both arms immediately following parathyroidectomy for parathyroid adenoma.", "The numbness, tingling, and pain were worse in the right arm.", "The symptoms radiated across the upper back and chest.", "Medical history was significant for a traumatic SCI caused by a motor vehicle collision at the age of 15.", "She experienced paralysis of her bilateral lower extremities, classified by the American Spinal Injury Association (ASIA) as an ASIA B injury.", "Her injury required thoracolumbar stabilization with Harrington rods.", "She had resulting chronic foot drop.", "She was only able to ambulate with a walker.", "She did not report any history of upper extremity symptoms prior to parathyroidectomy.", "Examination was significant for morbid obesity with a body mass index (BMI) of 51.", "She had decreased temperature and light touch sensation in the upper extremities and neck in dermatomes C3 through T10.", "Proprioception and vibration sense were preserved.", "Hypocalcemia was suspected as a cause of her paresthesias.", "Calcium levels were normal.", "Cervical MRI 2 days after symptoms onset demonstrated a T2 signal hyperintense area, just to the right of midline, that extended throughout the length of the central cervical spinal cord.", "The MRI was consistent with an expanding syrinx.", "Thoracic MRI showed the syrinx extended throughout the thoracic spinal cord as well.", "The reading radiologist initially misread this MRI as longitudinally extensive transverse myelitis.", "The radiologist specifically reported that they did not believe this was a syrinx because it was located in the lateral aspect of the spinal cord rather than in the central spinal cord canal.", "There was mild peripheral contrast-enhancement around the syrinx.", "An extensive infectious, autoimmune, and metabolic workup was negative.", "A working diagnosis of longitudinal extensive transverse myelitis was made.", "The patient was treated with 5 days of intravenous methylprednisolone.", "Repeat cervical MRI 2 weeks after symptom onset revealed no changes from the previous MRI.", "Her paresthesias and pain persisted.", "Six months after discharge, the patient presented to our neurology clinic for increasing weakness in the lower extremities.", "She had worsening dexterity of her right hand.", "She had more frequent falls.", "These symptoms had progressed to the point of requiring her to move to an assisted living facility.", "On examination, there was new pronator drift.", "There was decreased right hip flexion strength.", "There was decreased reflexes in the right upper extremity.", "Based on the patient\u2019s current and previous symptoms along with the previous imaging, we were able to arrive at a diagnosis of PTS, which had previously been missed.", "Cervical MRI was repeated and showed rostral expansion of the syrinx into the brain stem.", "With the advancement of her symptoms and growth of the syrinx into the brainstem, the patient received an urgent referral to an outside facility for neurosurgical evaluation.", "The consulting neurosurgeon at the outside facility did not believe her condition warranted hospital admission.", "The patient was not seen by the neurosurgeon for another 6 weeks.", "During that time period, the patient became progressively weaker.", "She had more frequent falls.", "She developed a hoarse voice, concerning for vocal cord paralysis.", "She developed dysphagia with several episodes of choking.", "On evaluation at the outside facility, the evaluating neurosurgeon concluded that the patient\u2019s symptom severity and rapid progression were indications for surgical drainage of the syrinx.", "The patient was taken to the operating room, and a C7-T2 laminectomy was performed.", "After removing the C7 through T2 lamina and entering the dura, the cord was noted to be quite dilated, nearly filling the entire dural tube.", "The cord was rotated 90\u00b0 within the dura.", "A 2 mm hole was made in the dorsal root entry zone of the cord below the C8 nerve root to insert the shunt.", "The syrinx cavity was encountered at a depth of <1 mm.", "The cord immediately deflated after penetration of the syrinx.", "A syringo-subarachnoid shunt was placed to allow the syrinx to continuously drain.", "The surgery and immediate postsurgical period were uncomplicated.", "She was discharged back to her previous nursing home 9 days following the operation.", "The patient was ambulating back at her baseline with a walker.", "Follow-up 2 months after surgery noted subjective persistent but not worsened right arm and leg weakness.", "She had a weakened voice.", "At this point, the patient was able to complete her ADLs independently although she had assistance at home.", "It was determined that the surgery stabilized as well as halted the progression of her neurological symptoms but did not reverse them.", "Cervical MRI 4 months after surgery showed dramatic reduction in syrinx size, with only a small residual fluid collection.", "This confirmed that the shunt was patent and functioning.", "Thoracic MRI showed possible persistent syringomyelia with slight enlargement compared to previous.", "This was significantly limited due to hardware artifact.", "The patient continues to live in a nursing home with assistance with her ADLs and frequent physical therapy.", "Patient consent and hospital approval were obtained before the writing of this report."], "summary_subclaims": ["The patient is a 42-year-old female.", "She has a distant history of spinal cord injury.", "She developed clinical and imaging findings consistent with acute expansion of post-traumatic syringomyelia.", "The acute expansion occurred immediately following parathyroidectomy.", "Her symptoms included acute numbness, tingling, and pain in both arms.", "Magnetic resonance imaging revealed a syrinx in the cervical and thoracic spinal cord.", "The syrinx was initially misdiagnosed as transverse myelitis.", "She was treated for transverse myelitis without resolution of symptoms.", "Over the following 6 months, the patient experienced progressive weakness.", "Repeat MRI demonstrated expansion of the syrinx with new involvement of the brain stem.", "The patient was diagnosed with post-traumatic syringomyelia.", "She was referred for outpatient neurosurgery evaluation at a tertiary facility.", "Treatment was delayed due to problems with housing and scheduling at the outside facility.", "The syrinx was surgically drained.", "A syringo-subarachnoid shunt was placed.", "Follow-up MRI confirmed correct placement of the shunt.", "The procedure effectively halted symptom progression.", "The procedure did not resolve all symptoms completely.", "The patient has regained her ability to perform much of her activities of daily living.", "The patient remains in a nursing home facility."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 42-year-old Native American female.", "She presented to University of South Dakota Sanford Medical Center in December of 2020.", "She developed numbness, tingling, and a sharp shooting pain in both arms immediately following parathyroidectomy for parathyroid adenoma.", "The numbness, tingling, and pain were worse in the right arm.", "The symptoms radiated across the upper back and chest.", "Medical history was significant for a traumatic SCI caused by a motor vehicle collision at the age of 15.", "She experienced paralysis of her bilateral lower extremities, classified by the American Spinal Injury Association (ASIA) as an ASIA B injury.", "Her injury required thoracolumbar stabilization with Harrington rods.", "She had resulting chronic foot drop.", "She was only able to ambulate with a walker.", "She did not report any history of upper extremity symptoms prior to parathyroidectomy.", "Examination was significant for morbid obesity with a body mass index (BMI) of 51.", "She had decreased temperature and light touch sensation in the upper extremities and neck in dermatomes C3 through T10.", "Proprioception and vibration sense were preserved.", "Hypocalcemia was suspected as a cause of her paresthesias.", "Calcium levels were normal.", "Cervical MRI 2 days after symptoms onset demonstrated a T2 signal hyperintense area, just to the right of midline, that extended throughout the length of the central cervical spinal cord.", "The MRI was consistent with an expanding syrinx.", "Thoracic MRI showed the syrinx extended throughout the thoracic spinal cord as well.", "The reading radiologist initially misread this MRI as longitudinally extensive transverse myelitis.", "The radiologist specifically reported that they did not believe this was a syrinx because it was located in the lateral aspect of the spinal cord rather than in the central spinal cord canal.", "There was mild peripheral contrast-enhancement around the syrinx.", "An extensive infectious, autoimmune, and metabolic workup was negative.", "A working diagnosis of longitudinal extensive transverse myelitis was made.", "The patient was treated with 5 days of intravenous methylprednisolone.", "Repeat cervical MRI 2 weeks after symptom onset revealed no changes from the previous MRI.", "Her paresthesias and pain persisted.", "Six months after discharge, the patient presented to our neurology clinic for increasing weakness in the lower extremities.", "She had worsening dexterity of her right hand.", "She had more frequent falls.", "These symptoms had progressed to the point of requiring her to move to an assisted living facility.", "On examination, there was new pronator drift.", "There was decreased right hip flexion strength.", "There was decreased reflexes in the right upper extremity.", "Based on the patient\u2019s current and previous symptoms along with the previous imaging, we were able to arrive at a diagnosis of PTS, which had previously been missed.", "Cervical MRI was repeated and showed rostral expansion of the syrinx into the brain stem.", "With the advancement of her symptoms and growth of the syrinx into the brainstem, the patient received an urgent referral to an outside facility for neurosurgical evaluation.", "The consulting neurosurgeon at the outside facility did not believe her condition warranted hospital admission.", "The patient was not seen by the neurosurgeon for another 6 weeks.", "During that time period, the patient became progressively weaker.", "She had more frequent falls.", "She developed a hoarse voice, concerning for vocal cord paralysis.", "She developed dysphagia with several episodes of choking.", "On evaluation at the outside facility, the evaluating neurosurgeon concluded that the patient\u2019s symptom severity and rapid progression were indications for surgical drainage of the syrinx.", "The patient was taken to the operating room, and a C7-T2 laminectomy was performed.", "After removing the C7 through T2 lamina and entering the dura, the cord was noted to be quite dilated, nearly filling the entire dural tube.", "The cord was rotated 90\u00b0 within the dura.", "A 2 mm hole was made in the dorsal root entry zone of the cord below the C8 nerve root to insert the shunt.", "The syrinx cavity was encountered at a depth of <1 mm.", "The cord immediately deflated after penetration of the syrinx.", "A syringo-subarachnoid shunt was placed to allow the syrinx to continuously drain.", "The surgery and immediate postsurgical period were uncomplicated.", "She was discharged back to her previous nursing home 9 days following the operation.", "The patient was ambulating back at her baseline with a walker.", "Follow-up 2 months after surgery noted subjective persistent but not worsened right arm and leg weakness.", "She had a weakened voice.", "At this point, the patient was able to complete her ADLs independently although she had assistance at home.", "It was determined that the surgery stabilized as well as halted the progression of her neurological symptoms but did not reverse them.", "Cervical MRI 4 months after surgery showed dramatic reduction in syrinx size, with only a small residual fluid collection.", "This confirmed that the shunt was patent and functioning.", "Thoracic MRI showed possible persistent syringomyelia with slight enlargement compared to previous.", "This was significantly limited due to hardware artifact.", "The patient continues to live in a nursing home with assistance with her ADLs and frequent physical therapy.", "Patient consent and hospital approval were obtained before the writing of this report."], "index": 86, "original_id": "multiclinsum_test_2005_en.txt", "split": "test", "summary_subclaims": ["The patient is a 42-year-old female.", "She has a distant history of spinal cord injury.", "She developed clinical and imaging findings consistent with acute expansion of post-traumatic syringomyelia.", "The acute expansion occurred immediately following parathyroidectomy.", "Her symptoms included acute numbness, tingling, and pain in both arms.", "Magnetic resonance imaging revealed a syrinx in the cervical and thoracic spinal cord.", "The syrinx was initially misdiagnosed as transverse myelitis.", "She was treated for transverse myelitis without resolution of symptoms.", "Over the following 6 months, the patient experienced progressive weakness.", "Repeat MRI demonstrated expansion of the syrinx with new involvement of the brain stem.", "The patient was diagnosed with post-traumatic syringomyelia.", "She was referred for outpatient neurosurgery evaluation at a tertiary facility.", "Treatment was delayed due to problems with housing and scheduling at the outside facility.", "The syrinx was surgically drained.", "A syringo-subarachnoid shunt was placed.", "Follow-up MRI confirmed correct placement of the shunt.", "The procedure effectively halted symptom progression.", "The procedure did not resolve all symptoms completely.", "The patient has regained her ability to perform much of her activities of daily living.", "The patient remains in a nursing home facility."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 76-year-old male.", "The patient's BMI is 21.5 kg/m2.", "The patient was admitted to the General Surgery Department.", "The patient had local abdominal distension in the left lower flank.", "The patient had intermittent abdominal pain for one year.", "The patient had undergone laparoscopic rectal resection one year ago.", "Five trocars were used during the laparoscopic rectal resection.", "A 10 mm trocar was inserted at the umbilical site.", "Two 5 mm trocars were placed in the left flank.", "A 12 mm trocar and a 5 mm trocar were placed in the right flank.", "Fascia layers were closed by an absorbable suture at the \u2265 10 mm trocar site.", "A 20 FR soft rubber tube was inserted in the left lower quadrant stoma port.", "The drainage tube was removed five days postoperatively.", "The drainage liquid was \u2264 20 mL/d.", "The fascia layer at the drain site was not closed due to a tiny defect.", "The patient was discharged on the ninth day after the operation.", "The patient reported no discomfort postoperatively.", "One month later, there was abdominal bulging in the left lower flank in the standing position.", "The abdominal bulge disappeared in the supine position.", "The patient felt a gradual progression of the abdominal bulge.", "The patient had occasional dull abdominal pain over time.", "The patient had a history of chronic bronchitis.", "The patient had intermittent cough.", "The patient had a history of hypertension.", "The patient had a history of coronary heart disease.", "The patient had a history of laparoscopic cholecystectomy.", "The patient's blood pressure was well controlled.", "There were no cardiovascular system symptoms.", "There were no restrictions on the patient's daily activities.", "The patient had no remarkable personal and family history.", "A local palpable mass (3 cm in length) was found in the left lower flank above the former drain-site.", "An abdominal wall defect (2 cm in length) was found.", "Tenderness and rebound tenderness were not observed in the abdomen.", "Routine serological examinations showed no obvious abnormalities.", "A preoperative computed tomography scan confirmed the diagnosis.", "The computed tomography scan showed an abdominal wall hernia at the drainage site in the left lower quadrant.", "The hernia content consisted of the omentum majus.", "The detected abdominal wall fascial defect was 2 cm in diameter."], "summary_subclaims": ["The patient was a 76-year-old male.", "The patient was admitted with intermittent abdominal pain.", "The patient had a local abdominal mass.", "The abdominal mass occurred one month after laparoscopic radical resection of rectal cancer.", "The rectal cancer resection had occurred one year before admission.", "A computed tomography scan showed an abdominal wall hernia at the 5 mm former drain-site in the left lower quadrant.", "The hernia content consisted of the large omentum.", "An elective herniorrhaphy was performed.", "The fascial defect was closed during the herniorrhaphy.", "The abdominal wall was reinforced with a synthetic mesh.", "The postoperative period was uneventful.", "The patient was discharged seven days after the operation.", "There were no surgery-related complications at the 1-mo follow-up visit."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 76-year-old male.", "The patient's BMI is 21.5 kg/m2.", "The patient was admitted to the General Surgery Department.", "The patient had local abdominal distension in the left lower flank.", "The patient had intermittent abdominal pain for one year.", "The patient had undergone laparoscopic rectal resection one year ago.", "Five trocars were used during the laparoscopic rectal resection.", "A 10 mm trocar was inserted at the umbilical site.", "Two 5 mm trocars were placed in the left flank.", "A 12 mm trocar and a 5 mm trocar were placed in the right flank.", "Fascia layers were closed by an absorbable suture at the \u2265 10 mm trocar site.", "A 20 FR soft rubber tube was inserted in the left lower quadrant stoma port.", "The drainage tube was removed five days postoperatively.", "The drainage liquid was \u2264 20 mL/d.", "The fascia layer at the drain site was not closed due to a tiny defect.", "The patient was discharged on the ninth day after the operation.", "The patient reported no discomfort postoperatively.", "One month later, there was abdominal bulging in the left lower flank in the standing position.", "The abdominal bulge disappeared in the supine position.", "The patient felt a gradual progression of the abdominal bulge.", "The patient had occasional dull abdominal pain over time.", "The patient had a history of chronic bronchitis.", "The patient had intermittent cough.", "The patient had a history of hypertension.", "The patient had a history of coronary heart disease.", "The patient had a history of laparoscopic cholecystectomy.", "The patient's blood pressure was well controlled.", "There were no cardiovascular system symptoms.", "There were no restrictions on the patient's daily activities.", "The patient had no remarkable personal and family history.", "A local palpable mass (3 cm in length) was found in the left lower flank above the former drain-site.", "An abdominal wall defect (2 cm in length) was found.", "Tenderness and rebound tenderness were not observed in the abdomen.", "Routine serological examinations showed no obvious abnormalities.", "A preoperative computed tomography scan confirmed the diagnosis.", "The computed tomography scan showed an abdominal wall hernia at the drainage site in the left lower quadrant.", "The hernia content consisted of the omentum majus.", "The detected abdominal wall fascial defect was 2 cm in diameter."], "index": 71, "original_id": "multiclinsum_test_1042_en.txt", "split": "test", "summary_subclaims": ["The patient was a 76-year-old male.", "The patient was admitted with intermittent abdominal pain.", "The patient had a local abdominal mass.", "The abdominal mass occurred one month after laparoscopic radical resection of rectal cancer.", "The rectal cancer resection had occurred one year before admission.", "A computed tomography scan showed an abdominal wall hernia at the 5 mm former drain-site in the left lower quadrant.", "The hernia content consisted of the large omentum.", "An elective herniorrhaphy was performed.", "The fascial defect was closed during the herniorrhaphy.", "The abdominal wall was reinforced with a synthetic mesh.", "The postoperative period was uneventful.", "The patient was discharged seven days after the operation.", "There were no surgery-related complications at the 1-mo follow-up visit."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 12-year-old girl.", "She presented with non-progressive congenital flexion deformities of bilateral elbows.", "She had difficulty in writing.", "She had difficulty in typing.", "She had difficulty in jogging.", "She had difficulty in using the Indian toilet.", "She had to sit with one leg extended for balance.", "She was the firstborn child of a second-degree consanguineous marriage.", "Her mother gave a history of delayed and decreased fetal movements during pregnancy.", "Her motor milestones were delayed.", "Her social adaptive and language milestones were normal.", "She was good at academics.", "She had attained menarche at the age of 12 years.", "She has normal menstrual cycles.", "Family history was unremarkable.", "On clinical examination, she had prominence in the suprascapular region on both sides.", "She had trapezii contracture.", "She had mild-to-moderate restriction of cervical spine range of motion in rotation and lateral bending.", "She had 20\u00b0 of internal rotation deformity bilaterally.", "Abduction was restricted to 120\u00b0 at both the shoulders.", "She had 22\u00b0 of fixed flexion deformity at the left elbow.", "She had 20\u00b0 of fixed flexion deformity at the right elbow.", "Bilateral passive forearm supination was restricted to 60\u00b0.", "Bilateral passive wrist dorsiflexion was restricted to 35\u00b0.", "Clinodactyly was noticed in bilateral ring fingers.", "Her fingers were hyperextensible at the interphalangeal joints.", "There were no signs of generalized ligamentous laxity.", "She had hypoplastic left thenar eminence.", "She had MRC Grade III power of the thenar muscles.", "She had bilateral tendo Achilles contractures.", "There was no passive dorsiflexion possible from neutral.", "Plantar flexion was full.", "She had a propulsive gait.", "She had a restricted arm swing on both sides.", "Mirror movements were demonstrated in bilateral fingers.", "Mirror movements were demonstrated in bilateral elbows.", "Mirror movements were demonstrated in bilateral toes.", "Mirror movements were demonstrated in bilateral ankles.", "Mirror movements of the toes and fingers worsened with fatigue.", "Mirror movements at the elbows and ankles became less frequent as voluntary movements were continued.", "Neurological examination was otherwise normal.", "Her height for her age was normal.", "There were no craniofacial malformations.", "There was no hearing impairment.", "There were no visual defects.", "X-rays and 3-D CT scan revealed bilateral Rigault Grade II Sprengel deformities.", "X-rays and 3-D CT scan revealed mild scoliosis at the cervical spine segment.", "X-rays and 3-D CT scan revealed mild scoliosis at the cervicothoracic junction.", "X-rays and 3-D CT scan revealed mild scoliosis at the thoracolumbar junction.", "There was no fusion at any vertebral level.", "MRI revealed no central nervous system (CNS) or spinal cord malformations.", "Ultrasonography revealed no renal or genitourinary anomalies.", "ECHO showed mild aortic regurgitation.", "She started on regular joint range of motion exercises.", "She started on muscle stretching and strengthening physiotherapy.", "She started on retraining therapy with techniques for increasing wanted movements.", "She started on retraining therapy with techniques for restricting unwanted movements.", "Her frequency of mirror movements decreased.", "Her writing and typing coordination was getting better.", "She is compliant with therapy.", "She is on regular follow-up."], "summary_subclaims": ["The patient is a 12-year-old girl.", "She presented with bilateral shoulder deformities.", "She had difficulty in coordination while writing.", "On examination, she was noted to have bilateral Sprengel deformities.", "She had flexion contractures of upper-limb joints.", "She had mirror movements of both upper and lower-limb joints."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 12-year-old girl.", "She presented with non-progressive congenital flexion deformities of bilateral elbows.", "She had difficulty in writing.", "She had difficulty in typing.", "She had difficulty in jogging.", "She had difficulty in using the Indian toilet.", "She had to sit with one leg extended for balance.", "She was the firstborn child of a second-degree consanguineous marriage.", "Her mother gave a history of delayed and decreased fetal movements during pregnancy.", "Her motor milestones were delayed.", "Her social adaptive and language milestones were normal.", "She was good at academics.", "She had attained menarche at the age of 12 years.", "She has normal menstrual cycles.", "Family history was unremarkable.", "On clinical examination, she had prominence in the suprascapular region on both sides.", "She had trapezii contracture.", "She had mild-to-moderate restriction of cervical spine range of motion in rotation and lateral bending.", "She had 20\u00b0 of internal rotation deformity bilaterally.", "Abduction was restricted to 120\u00b0 at both the shoulders.", "She had 22\u00b0 of fixed flexion deformity at the left elbow.", "She had 20\u00b0 of fixed flexion deformity at the right elbow.", "Bilateral passive forearm supination was restricted to 60\u00b0.", "Bilateral passive wrist dorsiflexion was restricted to 35\u00b0.", "Clinodactyly was noticed in bilateral ring fingers.", "Her fingers were hyperextensible at the interphalangeal joints.", "There were no signs of generalized ligamentous laxity.", "She had hypoplastic left thenar eminence.", "She had MRC Grade III power of the thenar muscles.", "She had bilateral tendo Achilles contractures.", "There was no passive dorsiflexion possible from neutral.", "Plantar flexion was full.", "She had a propulsive gait.", "She had a restricted arm swing on both sides.", "Mirror movements were demonstrated in bilateral fingers.", "Mirror movements were demonstrated in bilateral elbows.", "Mirror movements were demonstrated in bilateral toes.", "Mirror movements were demonstrated in bilateral ankles.", "Mirror movements of the toes and fingers worsened with fatigue.", "Mirror movements at the elbows and ankles became less frequent as voluntary movements were continued.", "Neurological examination was otherwise normal.", "Her height for her age was normal.", "There were no craniofacial malformations.", "There was no hearing impairment.", "There were no visual defects.", "X-rays and 3-D CT scan revealed bilateral Rigault Grade II Sprengel deformities.", "X-rays and 3-D CT scan revealed mild scoliosis at the cervical spine segment.", "X-rays and 3-D CT scan revealed mild scoliosis at the cervicothoracic junction.", "X-rays and 3-D CT scan revealed mild scoliosis at the thoracolumbar junction.", "There was no fusion at any vertebral level.", "MRI revealed no central nervous system (CNS) or spinal cord malformations.", "Ultrasonography revealed no renal or genitourinary anomalies.", "ECHO showed mild aortic regurgitation.", "She started on regular joint range of motion exercises.", "She started on muscle stretching and strengthening physiotherapy.", "She started on retraining therapy with techniques for increasing wanted movements.", "She started on retraining therapy with techniques for restricting unwanted movements.", "Her frequency of mirror movements decreased.", "Her writing and typing coordination was getting better.", "She is compliant with therapy.", "She is on regular follow-up."], "index": 53, "original_id": "multiclinsum_test_990_en.txt", "split": "test", "summary_subclaims": ["The patient is a 12-year-old girl.", "She presented with bilateral shoulder deformities.", "She had difficulty in coordination while writing.", "On examination, she was noted to have bilateral Sprengel deformities.", "She had flexion contractures of upper-limb joints.", "She had mirror movements of both upper and lower-limb joints."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 38-year-old Sri Lankan female.", "She presented with sudden onset severe right side headache.", "She had vomiting at the time of presentation.", "She developed right-sided complete ptosis.", "She developed right-sided ophthalmoplegia.", "The headache and vomiting lasted for one day.", "The ptosis and ophthalmoplegia persisted.", "She did not have a history of diabetes.", "She did not have a history of hypertension.", "She did not have a history of dyslipidemia.", "She did not have a history of any connective tissue disorder.", "On examination, she had complete ptosis on the right side.", "On examination, she had ophthalmoplegia on the right side.", "On examination, she had a fixed dilated pupil (5 mm) on the right side.", "Direct and consensual light reflexes were absent on the right side.", "Vision and fundoscopic examination were normal.", "Left eye had full eye movements.", "Left eye had normal light reflexes.", "Other cranial nerves including the sensory component of the trigeminal nerve were normal.", "She did not have scalp tenderness.", "She did not have tenderness over the superficial temporal artery.", "Upper limbs were neurologically normal.", "Lower limbs were neurologically normal.", "She did not have any cerebellar signs.", "Brachial pulse was decreased on the right side compared to the left side.", "Blood pressure on the right arm was 90/60 mmHg.", "Blood pressure on the left arm was 120/80 mmHg.", "She had a bruit over the right subclavian artery.", "She had a bruit over the right carotid artery.", "The rest of the cardiovascular, respiratory, and abdominal examination was normal.", "She did not have features of Ehlers\u2013Danlos syndrome.", "She did not have features of Marfan syndrome.", "She did not have manifestations of connective tissue disorder.", "Noncontrast CT brain was done soon after admission.", "Noncontrast CT brain was normal.", "Cerebrospinal fluid analysis was performed on day 2.", "Cerebrospinal fluid analysis showed absent cells.", "Cerebrospinal fluid analysis showed normal protein level.", "Cerebrospinal fluid analysis did not reveal xanthochromia.", "CT cerebral angiogram was done on day 4.", "CT cerebral angiogram revealed generalized caliber reduction of the right ICA.", "MRI done on day 23 showed significantly narrowed right ICA.", "Dissection of the right ICA was noted in the cavernous sinus.", "The dissection had a false lumen of 1.5 \u00d7 1 cm.", "The false lumen was thrombosed.", "The thrombosed lumen was of intermediate signal intensity in T1, T2, and FLAIR images.", "The thrombosed lumen did not enhance with contrast.", "The thrombosed lumen was compressing the right cavernous sinus.", "Multiple focal T2 and FLAIR hyperintensities with partially restricted diffusion were seen in the right parietal lobe.", "These hyperintensities were suggestive of acute infarcts.", "Cerebral digital subtraction angiogram showed total occlusion of the right ICA from its origin.", "Blood supply to the right middle cerebral artery was maintained via the anterior communicating artery.", "Blood supply to the right middle cerebral artery was maintained via the posterior communicating artery.", "Aneurysmal dilation and stenosis were evident at the right proximal subclavian artery.", "CT angiogram revealed aneurysmal dilatation (20 \u00d7 11 mm) of the first part of the right subclavian artery.", "CT angiogram revealed stenosis of the first part of the right subclavian artery.", "Tapering of the distal part of the right carotid bulb at the origin of the right ICA was seen.", "This tapering was suggestive of right ICA dissection with thrombosis.", "The rest of the angiogram was normal.", "Fluorescent angiogram of the retina was normal.", "Full blood count showed neutrophil leukocytosis.", "Low hemoglobin was seen in the blood picture.", "Normochromic normocytic anemia was seen in the blood picture.", "Liver function tests revealed low albumin.", "Liver enzyme levels were normal.", "Serum creatinine was 150 \u03bcmol/L on admission.", "eGFR using MDRD was 35.8 ml/min/1.73m2 on admission.", "Serum creatinine later came down to 100 \u03bcmol/L.", "eGFR using MDRD later came down to 57.2 ml/min/1.73m2.", "Urine full report was normal.", "Ultrasound revealed kidney sizes of 8.9 cm on the right and 8.7 cm on the left.", "Ionized calcium was 1.11 mmol/L.", "Phosphorus was 1.0 mmol/L.", "ESR was persistently high at 130 mm in the first hour.", "CRP was 95 mg/L.", "CRP later came down to 7 mg/L.", "She was negative for HIV serology.", "VDRL was nonreactive.", "Mantoux test was negative.", "Chest x-ray was normal.", "ANA was negative.", "p-ANCA was negative.", "c-ANCA was negative.", "Hepatitis B and C serology were negative.", "Fasting blood sugar was within normal range.", "HbA1C was within normal range.", "Thyroid function tests were within normal range.", "Lipid profile was within normal range.", "Bilateral cervical ribs were noted in chest x-ray.", "Bilateral cervical ribs were noted in cervical x-ray.", "Takayasu arteritis was diagnosed.", "She was started on high dose prednisolone (1 mg/kg).", "Aspirin was also started.", "Neurosurgical and vascular surgical opinion was taken.", "No surgical intervention was planned.", "After 2 weeks of steroids, ESR came down to 50 mm in the first hour.", "After one month of steroids, ESR was 30 mm in the first hour.", "Ophthalmoplegia and ptosis remained the same.", "Steroids were gradually tapered.", "Azathioprine was added as a steroid-sparing agent.", "The difference between right and left brachial pulses reduced.", "The right arm blood pressure increased.", "She did not have any further vascular events.", "A follow-up angiogram was planned in six months.", "The authors followed the CARE guidelines when writing this case report."], "summary_subclaims": ["The patient is a 38-year-old Sri Lankan female.", "She had sudden onset severe headache.", "She had fixed dilated pupil on the right side.", "She had complete ptosis on the right side.", "She had ophthalmoplegia on the right side.", "Imaging showed dissection and dilatation in the right internal carotid artery.", "The dissection and dilatation extended from the origin up to the cavernous segment.", "She had stenosis and aneurysmal dilatation of the right subclavian artery.", "Takayasu arteritis was diagnosed.", "She was started on aspirin.", "She was started on high dose steroids."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 38-year-old Sri Lankan female.", "She presented with sudden onset severe right side headache.", "She had vomiting at the time of presentation.", "She developed right-sided complete ptosis.", "She developed right-sided ophthalmoplegia.", "The headache and vomiting lasted for one day.", "The ptosis and ophthalmoplegia persisted.", "She did not have a history of diabetes.", "She did not have a history of hypertension.", "She did not have a history of dyslipidemia.", "She did not have a history of any connective tissue disorder.", "On examination, she had complete ptosis on the right side.", "On examination, she had ophthalmoplegia on the right side.", "On examination, she had a fixed dilated pupil (5 mm) on the right side.", "Direct and consensual light reflexes were absent on the right side.", "Vision and fundoscopic examination were normal.", "Left eye had full eye movements.", "Left eye had normal light reflexes.", "Other cranial nerves including the sensory component of the trigeminal nerve were normal.", "She did not have scalp tenderness.", "She did not have tenderness over the superficial temporal artery.", "Upper limbs were neurologically normal.", "Lower limbs were neurologically normal.", "She did not have any cerebellar signs.", "Brachial pulse was decreased on the right side compared to the left side.", "Blood pressure on the right arm was 90/60 mmHg.", "Blood pressure on the left arm was 120/80 mmHg.", "She had a bruit over the right subclavian artery.", "She had a bruit over the right carotid artery.", "The rest of the cardiovascular, respiratory, and abdominal examination was normal.", "She did not have features of Ehlers\u2013Danlos syndrome.", "She did not have features of Marfan syndrome.", "She did not have manifestations of connective tissue disorder.", "Noncontrast CT brain was done soon after admission.", "Noncontrast CT brain was normal.", "Cerebrospinal fluid analysis was performed on day 2.", "Cerebrospinal fluid analysis showed absent cells.", "Cerebrospinal fluid analysis showed normal protein level.", "Cerebrospinal fluid analysis did not reveal xanthochromia.", "CT cerebral angiogram was done on day 4.", "CT cerebral angiogram revealed generalized caliber reduction of the right ICA.", "MRI done on day 23 showed significantly narrowed right ICA.", "Dissection of the right ICA was noted in the cavernous sinus.", "The dissection had a false lumen of 1.5 \u00d7 1 cm.", "The false lumen was thrombosed.", "The thrombosed lumen was of intermediate signal intensity in T1, T2, and FLAIR images.", "The thrombosed lumen did not enhance with contrast.", "The thrombosed lumen was compressing the right cavernous sinus.", "Multiple focal T2 and FLAIR hyperintensities with partially restricted diffusion were seen in the right parietal lobe.", "These hyperintensities were suggestive of acute infarcts.", "Cerebral digital subtraction angiogram showed total occlusion of the right ICA from its origin.", "Blood supply to the right middle cerebral artery was maintained via the anterior communicating artery.", "Blood supply to the right middle cerebral artery was maintained via the posterior communicating artery.", "Aneurysmal dilation and stenosis were evident at the right proximal subclavian artery.", "CT angiogram revealed aneurysmal dilatation (20 \u00d7 11 mm) of the first part of the right subclavian artery.", "CT angiogram revealed stenosis of the first part of the right subclavian artery.", "Tapering of the distal part of the right carotid bulb at the origin of the right ICA was seen.", "This tapering was suggestive of right ICA dissection with thrombosis.", "The rest of the angiogram was normal.", "Fluorescent angiogram of the retina was normal.", "Full blood count showed neutrophil leukocytosis.", "Low hemoglobin was seen in the blood picture.", "Normochromic normocytic anemia was seen in the blood picture.", "Liver function tests revealed low albumin.", "Liver enzyme levels were normal.", "Serum creatinine was 150 \u03bcmol/L on admission.", "eGFR using MDRD was 35.8 ml/min/1.73m2 on admission.", "Serum creatinine later came down to 100 \u03bcmol/L.", "eGFR using MDRD later came down to 57.2 ml/min/1.73m2.", "Urine full report was normal.", "Ultrasound revealed kidney sizes of 8.9 cm on the right and 8.7 cm on the left.", "Ionized calcium was 1.11 mmol/L.", "Phosphorus was 1.0 mmol/L.", "ESR was persistently high at 130 mm in the first hour.", "CRP was 95 mg/L.", "CRP later came down to 7 mg/L.", "She was negative for HIV serology.", "VDRL was nonreactive.", "Mantoux test was negative.", "Chest x-ray was normal.", "ANA was negative.", "p-ANCA was negative.", "c-ANCA was negative.", "Hepatitis B and C serology were negative.", "Fasting blood sugar was within normal range.", "HbA1C was within normal range.", "Thyroid function tests were within normal range.", "Lipid profile was within normal range.", "Bilateral cervical ribs were noted in chest x-ray.", "Bilateral cervical ribs were noted in cervical x-ray.", "Takayasu arteritis was diagnosed.", "She was started on high dose prednisolone (1 mg/kg).", "Aspirin was also started.", "Neurosurgical and vascular surgical opinion was taken.", "No surgical intervention was planned.", "After 2 weeks of steroids, ESR came down to 50 mm in the first hour.", "After one month of steroids, ESR was 30 mm in the first hour.", "Ophthalmoplegia and ptosis remained the same.", "Steroids were gradually tapered.", "Azathioprine was added as a steroid-sparing agent.", "The difference between right and left brachial pulses reduced.", "The right arm blood pressure increased.", "She did not have any further vascular events.", "A follow-up angiogram was planned in six months.", "The authors followed the CARE guidelines when writing this case report."], "index": 73, "original_id": "multiclinsum_test_2426_en.txt", "split": "test", "summary_subclaims": ["The patient is a 38-year-old Sri Lankan female.", "She had sudden onset severe headache.", "She had fixed dilated pupil on the right side.", "She had complete ptosis on the right side.", "She had ophthalmoplegia on the right side.", "Imaging showed dissection and dilatation in the right internal carotid artery.", "The dissection and dilatation extended from the origin up to the cavernous segment.", "She had stenosis and aneurysmal dilatation of the right subclavian artery.", "Takayasu arteritis was diagnosed.", "She was started on aspirin.", "She was started on high dose steroids."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["A case of tuberculosis of the cervix presenting as cervical carcinoma is being reported for its rarity.", "The patient was a 26-year-old P2L2 Indian lady.", "She had pain abdomen, irregular bleeding, and discharge per vaginum for three years.", "She had a history of post-coital bleeding and inter-menstrual bleeding.", "She had significant weight loss over the last two years.", "There was no history of genitourinary malignancy or tuberculosis in the past or in the family.", "The patient was a non-smoker, non-alcoholic, and did not have any other significant medical or surgical illness in the past.", "On per speculum examination, the cervix was replaced by an irregular friable growth that was bleeding on touch.", "PAP smear showed epitheloid like cell clusters without any dysplasia.", "Biopsy taken from the cervical growth revealed granulomatous inflammation with caseous necrosis.", "Smear from cervix was found positive for acid-fast bacilli.", "Endometrial biopsy was normal with no AFB.", "Sputum and urine samples were negative for AFB and failed to culture mycobacterium.", "CECT abdomen showed a bulky cervix with evidence of soft tissue streaking in parametrium.", "HIV 1 and 2 were negative.", "The patient was started on antitubercular treatment with four drugs: isoniazid, ethambutol, rifampicin, and pyrazinamide.", "At six months, the cervix had an almost normal appearance and there was complete relief from symptoms."], "summary_subclaims": ["On per speculum examination, cervix was replaced by an irregular friable growth.", "The growth was bleeding on touch.", "A clinical diagnosis of carcinoma cervix was made.", "The cervical biopsy revealed granulomatous inflammation.", "Acid-fast bacilli were present on cervical smear.", "The findings were consistent with tuberculosis.", "The patient responded to six months of anti-tubercular therapy."]}, "extra_info": {"fulltext_subclaims": ["A case of tuberculosis of the cervix presenting as cervical carcinoma is being reported for its rarity.", "The patient was a 26-year-old P2L2 Indian lady.", "She had pain abdomen, irregular bleeding, and discharge per vaginum for three years.", "She had a history of post-coital bleeding and inter-menstrual bleeding.", "She had significant weight loss over the last two years.", "There was no history of genitourinary malignancy or tuberculosis in the past or in the family.", "The patient was a non-smoker, non-alcoholic, and did not have any other significant medical or surgical illness in the past.", "On per speculum examination, the cervix was replaced by an irregular friable growth that was bleeding on touch.", "PAP smear showed epitheloid like cell clusters without any dysplasia.", "Biopsy taken from the cervical growth revealed granulomatous inflammation with caseous necrosis.", "Smear from cervix was found positive for acid-fast bacilli.", "Endometrial biopsy was normal with no AFB.", "Sputum and urine samples were negative for AFB and failed to culture mycobacterium.", "CECT abdomen showed a bulky cervix with evidence of soft tissue streaking in parametrium.", "HIV 1 and 2 were negative.", "The patient was started on antitubercular treatment with four drugs: isoniazid, ethambutol, rifampicin, and pyrazinamide.", "At six months, the cervix had an almost normal appearance and there was complete relief from symptoms."], "index": 77, "original_id": "multiclinsum_test_216_en.txt", "split": "test", "summary_subclaims": ["On per speculum examination, cervix was replaced by an irregular friable growth.", "The growth was bleeding on touch.", "A clinical diagnosis of carcinoma cervix was made.", "The cervical biopsy revealed granulomatous inflammation.", "Acid-fast bacilli were present on cervical smear.", "The findings were consistent with tuberculosis.", "The patient responded to six months of anti-tubercular therapy."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 27-year-old man.", "He had painless and progressive visual impairment of both eyes over two years.", "The patient had no other positive symptoms apart from blurred vision.", "The patient had no history of ocular diseases.", "He was diagnosed with hypocalcemia when he was young.", "He did not know the serum calcium concentration at the time of the hypocalcemia diagnosis.", "He relied on a diet of milk or calcium-containing foods and calcium tablets to supplement his calcium levels at that time.", "He did not take regular calcium supplements subsequently.", "He started to experience muscle cramps in his upper extremities approximately ten years ago.", "He did not seek help for the muscle cramps until the occurrence of epilepsy.", "Seven years ago, he underwent cerebral surgery for epileptic seizures.", "The ocular examination revealed a preoperative binocular visual acuity of 16/200.", "The best-corrected visual acuity (BCVA) was not improved.", "The intraocular pressure in the right eye was 15 mmHg.", "The intraocular pressure in the left eye was 16 mmHg.", "There was bilateral symmetrical opacity of the lens.", "The lens opacity presented as punctate opacity in the posterior subcapsular cortex.", "The lens opacity also presented as radial opacity in the peripheral cortex.", "Fundus examination showed no pathological changes.", "The serum total calcium level was 1.21 mmol/L.", "The serum ionized calcium level was 0.72 mmol/L.", "The serum phosphorus level was 1.67 mmol/L.", "The serum magnesium level was 0.62 mmol/L.", "The intact PTH level was 0 pg/mL.", "An electrocardiogram showed a prolonged QT interval.", "Anterior segment photography revealed punctuate opacity in the posterior subcapsular cortex.", "Anterior segment photography also revealed radial opacity in the peripheral cortex."], "summary_subclaims": ["The patient is a 27-year-old man.", "He had painless and progressive visual impairment of both eyes over two years.", "He was previously diagnosed with hypocalcemia.", "He did not take calcium supplements regularly.", "He had no history of anterior neck thyroid surgery.", "The serum calcium level was 1.21 mmol/L.", "The intact parathyroid hormone level was 0 pg/mL.", "Ocular examination revealed bilateral symmetrical opacity of the lens.", "The lens opacity presented as punctate opacity in the posterior subcapsular cortex.", "The lens opacity also presented as radial opacity in the peripheral cortex.", "Phacoemulsification with an intraocular lens was performed in both eyes.", "The surgeries were performed sequentially.", "Postoperatively, the patient had a satisfactory recovery.", "The patient had greatly improved visual acuity."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 27-year-old man.", "He had painless and progressive visual impairment of both eyes over two years.", "The patient had no other positive symptoms apart from blurred vision.", "The patient had no history of ocular diseases.", "He was diagnosed with hypocalcemia when he was young.", "He did not know the serum calcium concentration at the time of the hypocalcemia diagnosis.", "He relied on a diet of milk or calcium-containing foods and calcium tablets to supplement his calcium levels at that time.", "He did not take regular calcium supplements subsequently.", "He started to experience muscle cramps in his upper extremities approximately ten years ago.", "He did not seek help for the muscle cramps until the occurrence of epilepsy.", "Seven years ago, he underwent cerebral surgery for epileptic seizures.", "The ocular examination revealed a preoperative binocular visual acuity of 16/200.", "The best-corrected visual acuity (BCVA) was not improved.", "The intraocular pressure in the right eye was 15 mmHg.", "The intraocular pressure in the left eye was 16 mmHg.", "There was bilateral symmetrical opacity of the lens.", "The lens opacity presented as punctate opacity in the posterior subcapsular cortex.", "The lens opacity also presented as radial opacity in the peripheral cortex.", "Fundus examination showed no pathological changes.", "The serum total calcium level was 1.21 mmol/L.", "The serum ionized calcium level was 0.72 mmol/L.", "The serum phosphorus level was 1.67 mmol/L.", "The serum magnesium level was 0.62 mmol/L.", "The intact PTH level was 0 pg/mL.", "An electrocardiogram showed a prolonged QT interval.", "Anterior segment photography revealed punctuate opacity in the posterior subcapsular cortex.", "Anterior segment photography also revealed radial opacity in the peripheral cortex."], "index": 59, "original_id": "multiclinsum_test_1416_en.txt", "split": "test", "summary_subclaims": ["The patient is a 27-year-old man.", "He had painless and progressive visual impairment of both eyes over two years.", "He was previously diagnosed with hypocalcemia.", "He did not take calcium supplements regularly.", "He had no history of anterior neck thyroid surgery.", "The serum calcium level was 1.21 mmol/L.", "The intact parathyroid hormone level was 0 pg/mL.", "Ocular examination revealed bilateral symmetrical opacity of the lens.", "The lens opacity presented as punctate opacity in the posterior subcapsular cortex.", "The lens opacity also presented as radial opacity in the peripheral cortex.", "Phacoemulsification with an intraocular lens was performed in both eyes.", "The surgeries were performed sequentially.", "Postoperatively, the patient had a satisfactory recovery.", "The patient had greatly improved visual acuity."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was a 62-year-old male farmer.", "He was hospitalized for fatigue and weight loss for more than 1 mo.", "He had no fever or bone pain.", "The peripheral blood examination in a local hospital indicated severe anemia with a hemoglobin level of 54 g/L.", "The peripheral blood examination suggested a potentially malignant tumor from the blood system.", "He was admitted to Huaihe Hospital of Henan University.", "The patient had no history of exposure to industrial poisons or radioactive substances.", "The patient was not smoking or drinking alcohol.", "The family history was unremarkable.", "The patient presented an anemic face.", "The percussion of the lungs presented a little dullness.", "A few moist rales were heard at the left lung base.", "Mild concave edema was seen in both lower extremities.", "Laboratory evaluation at the Huaihe Hospital showed a hemoglobin level of 61 g/L.", "Further blood examination indicated renal dysfunction.", "Erythrocyte sedimentation rate was elevated.", "NT-PROBNP was elevated.", "Serum protein electrophoresis suggested an elevation of \u03b12-globulin and \u03b3-globulin.", "Two slight M-spikes appeared.", "A band within the \u03b3 fraction was seen.", "The other band within \u03b12 fraction was obscure.", "Serum IFE showed two monoclonal bands in the \u03bb region without corresponding heavy chain bands.", "The results corresponded to the distinct elevation of serum \u03bb FLC.", "A second serum IFE showed two monoclonal bands in antisera to \u03bb.", "A second serum IFE showed one corresponding heavy chain band in antisera to IgD.", "The diagnosis was IgD-\u03bb/\u03bb myeloma.", "BM cytomorphologic examination found 82% plasma cells, mainly immature, of the BM nucleated cells.", "Flow cytometry suggested positivity of monoclonal plasma cells at 70.12% of total nucleated red blood cells.", "The immunophenotype was CD38, cytoplasmic lambda, and CD229.", "All monoclonal plasma cells expressed CD229, CD38, and cytoplasmic lambda.", "BM cytomorphologic examination and flow cytometry supported the diagnosis of plasma cell myeloma.", "Chromosome karyotype analysis showed 46,XY;46,Y,t(X;4)(p11.2;q21).", "Gene analysis of the blood tumor mutant group was mainly normal.", "The patient was diagnosed with stage ISS III myeloma."], "summary_subclaims": ["The patient is a 62-year-old man.", "The patient was diagnosed as IgD-\u03bb/\u03bb myeloma.", "The patient was admitted with fatigue.", "The patient was admitted with weight loss.", "The physical examination suggested an anemic face.", "The physical examination found a few moist rales at the left lung base.", "The physical examination found mild concave edema in both lower extremities.", "Laboratory examinations showed elevated creatinine levels.", "Laboratory examinations showed elevated \u03b22-microglobulin.", "Laboratory examinations showed elevated lactic dehydrogenase.", "Laboratory examinations showed elevated erythrocyte sedimentation rate.", "Laboratory examinations showed decreased neutrophils.", "Laboratory examinations showed decreased granulocytes.", "Laboratory examinations showed decreased hemoglobin.", "Serum protein electrophoresis showed two inconspicuous M-spikes.", "Serum IFE indicated an over-representation of lambda light chain.", "Serum IFE yielded two monoclonal bands in \u03bb region.", "Serum IFE yielded one corresponding heavy chain band in the antisera to IgD region.", "BM histology supported the diagnosis of IgD-\u03bb/\u03bb myeloma.", "BM cytology supported the diagnosis of IgD-\u03bb/\u03bb myeloma."]}, "extra_info": {"fulltext_subclaims": ["The patient was a 62-year-old male farmer.", "He was hospitalized for fatigue and weight loss for more than 1 mo.", "He had no fever or bone pain.", "The peripheral blood examination in a local hospital indicated severe anemia with a hemoglobin level of 54 g/L.", "The peripheral blood examination suggested a potentially malignant tumor from the blood system.", "He was admitted to Huaihe Hospital of Henan University.", "The patient had no history of exposure to industrial poisons or radioactive substances.", "The patient was not smoking or drinking alcohol.", "The family history was unremarkable.", "The patient presented an anemic face.", "The percussion of the lungs presented a little dullness.", "A few moist rales were heard at the left lung base.", "Mild concave edema was seen in both lower extremities.", "Laboratory evaluation at the Huaihe Hospital showed a hemoglobin level of 61 g/L.", "Further blood examination indicated renal dysfunction.", "Erythrocyte sedimentation rate was elevated.", "NT-PROBNP was elevated.", "Serum protein electrophoresis suggested an elevation of \u03b12-globulin and \u03b3-globulin.", "Two slight M-spikes appeared.", "A band within the \u03b3 fraction was seen.", "The other band within \u03b12 fraction was obscure.", "Serum IFE showed two monoclonal bands in the \u03bb region without corresponding heavy chain bands.", "The results corresponded to the distinct elevation of serum \u03bb FLC.", "A second serum IFE showed two monoclonal bands in antisera to \u03bb.", "A second serum IFE showed one corresponding heavy chain band in antisera to IgD.", "The diagnosis was IgD-\u03bb/\u03bb myeloma.", "BM cytomorphologic examination found 82% plasma cells, mainly immature, of the BM nucleated cells.", "Flow cytometry suggested positivity of monoclonal plasma cells at 70.12% of total nucleated red blood cells.", "The immunophenotype was CD38, cytoplasmic lambda, and CD229.", "All monoclonal plasma cells expressed CD229, CD38, and cytoplasmic lambda.", "BM cytomorphologic examination and flow cytometry supported the diagnosis of plasma cell myeloma.", "Chromosome karyotype analysis showed 46,XY;46,Y,t(X;4)(p11.2;q21).", "Gene analysis of the blood tumor mutant group was mainly normal.", "The patient was diagnosed with stage ISS III myeloma."], "index": 55, "original_id": "multiclinsum_test_710_en.txt", "split": "test", "summary_subclaims": ["The patient is a 62-year-old man.", "The patient was diagnosed as IgD-\u03bb/\u03bb myeloma.", "The patient was admitted with fatigue.", "The patient was admitted with weight loss.", "The physical examination suggested an anemic face.", "The physical examination found a few moist rales at the left lung base.", "The physical examination found mild concave edema in both lower extremities.", "Laboratory examinations showed elevated creatinine levels.", "Laboratory examinations showed elevated \u03b22-microglobulin.", "Laboratory examinations showed elevated lactic dehydrogenase.", "Laboratory examinations showed elevated erythrocyte sedimentation rate.", "Laboratory examinations showed decreased neutrophils.", "Laboratory examinations showed decreased granulocytes.", "Laboratory examinations showed decreased hemoglobin.", "Serum protein electrophoresis showed two inconspicuous M-spikes.", "Serum IFE indicated an over-representation of lambda light chain.", "Serum IFE yielded two monoclonal bands in \u03bb region.", "Serum IFE yielded one corresponding heavy chain band in the antisera to IgD region.", "BM histology supported the diagnosis of IgD-\u03bb/\u03bb myeloma.", "BM cytology supported the diagnosis of IgD-\u03bb/\u03bb myeloma."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was a forty year-old male.", "He was brought to the Queen Elizabeth Hospital, Kota Kinabalu, Sabah at 8.30 am.", "He was in a state of collapse.", "He was unable to give a history himself.", "He was unable to stand.", "On examination his blood pressure was unrecordable.", "Oxygen saturations were recorded as low.", "The patient had no past medical history.", "He had spent two weeks in the jungles of Borneo before leaving for an urban setting.", "Ten days after leaving the jungle he experienced the onset of fever and body aches.", "Two days later, he sought treatment at a government outpatient clinic.", "He continued to complain of fever and myalgia.", "A specific diagnosis was not made.", "He was able to work.", "He developed rashes the next day.", "He remained unwell for the next two days.", "He presented in a state of collapse.", "He had developed abdominal pain.", "Resuscitation measures were begun.", "The patient was immediately intubated.", "He was given adrenaline/atropine.", "He was given sodium bicarbonate.", "After resuscitation measures, his blood pressure was 58/44 mm Hg.", "His pulse rate was 40-50 per minute.", "He had poor peripheral perfusion.", "He had cyanosis.", "He had generalized petechiae.", "His abdomen was tense and distended.", "Resuscitation measures continued for one hour.", "Coffee grounds were observed in the nasogastric aspirate.", "The patient became asystolic after one hour.", "Cardiopulmonary resuscitation was given for a further 20 minutes.", "There was no response.", "The patient was pronounced dead two hours after admission.", "Dengue haemorrhagic shock was suspected.", "A post-mortem examination was performed approximately 24 hours later.", "The patient was not anemic.", "He was thrombocytopenic.", "He had an eosinophilia.", "He was hyponatraemic.", "He had elevated blood urea.", "He had elevated potassium.", "He had elevated lactate dehydrogenase.", "He had elevated amino transferase values.", "Serum creatinine was not available.", "A blood sample taken 24 hours post-mortem showed >10% of erythrocytes infected with predominantly pigmented parasites.", "Heavily pigmented monocytes were also present.", "Plasmodium knowlesi, as a single species infection, was confirmed by nested-PCR.", "Post-mortem dengue serology was negative.", "Dengue, respiratory syncytial virus and enterovirus were not isolated in organ samples.", "External examination showed a well-nourished adult male.", "The conjunctivae showed tinges of jaundice.", "The right eye had subconjunctival haemorrhages.", "There were multiple petechial haemorrhages on the body.", "Venepuncture sites were associated with marked bruising.", "Coffee ground material was noted in the mouth.", "The external surfaces of the cerebrum were dusky.", "The cut sections showed multiple petechial haemorrhages.", "The cerebellum also showed petechial haemorrhages externally and on multiple cut sections.", "The brain stem and upper spinal chord were grossly normal.", "Both lungs were heavy.", "The right lung weighed 720 g.", "The left lung weighed 690 g.", "The cut sections were congested and 'beefy' in appearance.", "Petechial haemorrhages were present on the endocardium.", "There were extensive subendocardial haemorrhages involving the left ventricular wall.", "The haemorrhages were most prominent at the apex of the heart.", "The liver weighed 2640 g.", "The spleen weighed 340 g.", "The cut surfaces of the spleen were soft and friable.", "The gallbladder, pancreas and kidneys were grossly normal.", "Haematoxylin and eosin stained sections from various organs were available for examination.", "Parasitized red blood cells were abundant.", "Parasite bodies were obscured by haemozoin pigment.", "Chemical removal of pigment and oil immersion (\u00d71,000) magnification revealed trophozoites that were discernibly bigger than those of P. falciparum.", "Immunohistochemistry stained sections from the brain were Plasmodium anti-aldolase positive.", "Immunohistochemistry stained sections from the brain were negative for P. falciparum-specific staining.", "Many petechial haemorrhages (up to 600 \u03bcm diameter) arising from the rupture of the small vessels of the cerebrum and cerebellum were observed.", "Sequestration of PRBC was evident within small blood vessels.", "Congested larger vessels and areas of haemorrhage showed considerable amounts of malaria pigment.", "Clumps of platelets or evidence of thrombi in vessels were not seen.", "There was no evidence of vasculitis or perivascular chronic inflammatory reaction in the brain.", "There was no evidence of perivascular or diffuse parenchymal oedema in the brain.", "Diffuse astrocytosis or microgliosis was not observed.", "There was no evidence for acute gliotic reactions about the haemorrhages.", "There was no aggregation of polymorphs in the vessels.", "There was no perivascular inflammation.", "There was no generalized encephalitis.", "There was no diffuse thrombotic microangiopathy.", "Within one haemorrhage there was probably some fibrin at the site of the vessel.", "Immunohistochemistry of sections from the brain was negative for CD54.", "Sections from the spleen showed some autolysis.", "Expansion of the red pulp and atrophy of the white pulp was noted.", "Germinal centers were not observed.", "Abundant pigment-containing macrophages and some haemophagocytosis was evident in the red pulp.", "Parasitized red cells were plentiful.", "There was no necrosis or fibrin deposition in the spleen.", "There were many PRBC's in the liver sinusoids.", "Haemozoin pigment was in Kupffer cells.", "Evidence of haemophagocytosis was present.", "The portal tracts and sinusoids had moderate chronic lymphoplasmacytic inflammation.", "The liver was non-cirrhotic.", "The liver had severe macrovesicular steatosis.", "There was no cholestasis.", "There was no regional necrosis.", "There was no thrombotic microangiopathy.", "The renal cortex showed dilated and congested blood vessels.", "Many PRBC were observed within glomerular capillaries.", "Pigment deposition was in the mesangium.", "There was no evidence of thrombotic microangiopathy.", "The tubules showed acute tubular necrosis and regeneration.", "There were a small number of eosinophilic intra-tubular casts.", "Sequestration of PRBC's was evident in the small vessels of the heart.", "Endothelial cells were prominent.", "There was no evidence of myocarditis.", "The heart muscle fibers appeared normal.", "There was focal petechial haemorrhage in the subendocardium.", "The focal petechial haemorrhage may relate to resuscitation.", "The focal petechial haemorrhage may be secondary to malaria.", "The adrenal gland appeared active.", "There was eosinophilic cytoplasm in the fasciculata layer.", "There was no evidence of PRBC sequestration.", "There was no parenchymal haemorrhage.", "Samples of lung, intestine or bone marrow were not available for histopathology examination.", "The overall picture was one of systemic malaria infection with multi-organ damage.", "There was much vascular rupture and petechial haemorrhaging in the brain."], "summary_subclaims": ["A formerly healthy 40 year-old male became symptomatic 10 days after spending time in the jungle of North Borneo.", "He presented to hospital in a state of collapse and died within two hours.", "He was hyponatraemic.", "He had elevated blood urea.", "He had elevated potassium.", "He had elevated lactate dehydrogenase.", "He had elevated amino transferase values.", "He was thrombocytopenic.", "He was eosinophilic.", "Dengue haemorrhagic shock was suspected.", "A post-mortem examination was performed.", "Investigations for dengue virus were negative.", "Blood for malaria parasites indicated hyperparasitaemia.", "Single species P. knowlesi infection was confirmed by nested-PCR.", "Macroscopic pathology of the brain and endocardium showed multiple petechial haemorrhages.", "The liver and spleen were enlarged.", "The lungs had features consistent with ARDS.", "Microscopic pathology showed sequestration of pigmented parasitized red blood cells in the vessels of the cerebrum, cerebellum, heart and kidney.", "There was no evidence of chronic inflammatory reaction in the brain or any other organ examined.", "Brain sections were negative for intracellular adhesion molecule-1.", "The spleen and liver had abundant pigment containing macrophages and parasitized red blood cells.", "The kidney had evidence of acute tubular necrosis.", "Endothelial cells in heart sections were prominent."]}, "extra_info": {"fulltext_subclaims": ["The patient was a forty year-old male.", "He was brought to the Queen Elizabeth Hospital, Kota Kinabalu, Sabah at 8.30 am.", "He was in a state of collapse.", "He was unable to give a history himself.", "He was unable to stand.", "On examination his blood pressure was unrecordable.", "Oxygen saturations were recorded as low.", "The patient had no past medical history.", "He had spent two weeks in the jungles of Borneo before leaving for an urban setting.", "Ten days after leaving the jungle he experienced the onset of fever and body aches.", "Two days later, he sought treatment at a government outpatient clinic.", "He continued to complain of fever and myalgia.", "A specific diagnosis was not made.", "He was able to work.", "He developed rashes the next day.", "He remained unwell for the next two days.", "He presented in a state of collapse.", "He had developed abdominal pain.", "Resuscitation measures were begun.", "The patient was immediately intubated.", "He was given adrenaline/atropine.", "He was given sodium bicarbonate.", "After resuscitation measures, his blood pressure was 58/44 mm Hg.", "His pulse rate was 40-50 per minute.", "He had poor peripheral perfusion.", "He had cyanosis.", "He had generalized petechiae.", "His abdomen was tense and distended.", "Resuscitation measures continued for one hour.", "Coffee grounds were observed in the nasogastric aspirate.", "The patient became asystolic after one hour.", "Cardiopulmonary resuscitation was given for a further 20 minutes.", "There was no response.", "The patient was pronounced dead two hours after admission.", "Dengue haemorrhagic shock was suspected.", "A post-mortem examination was performed approximately 24 hours later.", "The patient was not anemic.", "He was thrombocytopenic.", "He had an eosinophilia.", "He was hyponatraemic.", "He had elevated blood urea.", "He had elevated potassium.", "He had elevated lactate dehydrogenase.", "He had elevated amino transferase values.", "Serum creatinine was not available.", "A blood sample taken 24 hours post-mortem showed >10% of erythrocytes infected with predominantly pigmented parasites.", "Heavily pigmented monocytes were also present.", "Plasmodium knowlesi, as a single species infection, was confirmed by nested-PCR.", "Post-mortem dengue serology was negative.", "Dengue, respiratory syncytial virus and enterovirus were not isolated in organ samples.", "External examination showed a well-nourished adult male.", "The conjunctivae showed tinges of jaundice.", "The right eye had subconjunctival haemorrhages.", "There were multiple petechial haemorrhages on the body.", "Venepuncture sites were associated with marked bruising.", "Coffee ground material was noted in the mouth.", "The external surfaces of the cerebrum were dusky.", "The cut sections showed multiple petechial haemorrhages.", "The cerebellum also showed petechial haemorrhages externally and on multiple cut sections.", "The brain stem and upper spinal chord were grossly normal.", "Both lungs were heavy.", "The right lung weighed 720 g.", "The left lung weighed 690 g.", "The cut sections were congested and 'beefy' in appearance.", "Petechial haemorrhages were present on the endocardium.", "There were extensive subendocardial haemorrhages involving the left ventricular wall.", "The haemorrhages were most prominent at the apex of the heart.", "The liver weighed 2640 g.", "The spleen weighed 340 g.", "The cut surfaces of the spleen were soft and friable.", "The gallbladder, pancreas and kidneys were grossly normal.", "Haematoxylin and eosin stained sections from various organs were available for examination.", "Parasitized red blood cells were abundant.", "Parasite bodies were obscured by haemozoin pigment.", "Chemical removal of pigment and oil immersion (\u00d71,000) magnification revealed trophozoites that were discernibly bigger than those of P. falciparum.", "Immunohistochemistry stained sections from the brain were Plasmodium anti-aldolase positive.", "Immunohistochemistry stained sections from the brain were negative for P. falciparum-specific staining.", "Many petechial haemorrhages (up to 600 \u03bcm diameter) arising from the rupture of the small vessels of the cerebrum and cerebellum were observed.", "Sequestration of PRBC was evident within small blood vessels.", "Congested larger vessels and areas of haemorrhage showed considerable amounts of malaria pigment.", "Clumps of platelets or evidence of thrombi in vessels were not seen.", "There was no evidence of vasculitis or perivascular chronic inflammatory reaction in the brain.", "There was no evidence of perivascular or diffuse parenchymal oedema in the brain.", "Diffuse astrocytosis or microgliosis was not observed.", "There was no evidence for acute gliotic reactions about the haemorrhages.", "There was no aggregation of polymorphs in the vessels.", "There was no perivascular inflammation.", "There was no generalized encephalitis.", "There was no diffuse thrombotic microangiopathy.", "Within one haemorrhage there was probably some fibrin at the site of the vessel.", "Immunohistochemistry of sections from the brain was negative for CD54.", "Sections from the spleen showed some autolysis.", "Expansion of the red pulp and atrophy of the white pulp was noted.", "Germinal centers were not observed.", "Abundant pigment-containing macrophages and some haemophagocytosis was evident in the red pulp.", "Parasitized red cells were plentiful.", "There was no necrosis or fibrin deposition in the spleen.", "There were many PRBC's in the liver sinusoids.", "Haemozoin pigment was in Kupffer cells.", "Evidence of haemophagocytosis was present.", "The portal tracts and sinusoids had moderate chronic lymphoplasmacytic inflammation.", "The liver was non-cirrhotic.", "The liver had severe macrovesicular steatosis.", "There was no cholestasis.", "There was no regional necrosis.", "There was no thrombotic microangiopathy.", "The renal cortex showed dilated and congested blood vessels.", "Many PRBC were observed within glomerular capillaries.", "Pigment deposition was in the mesangium.", "There was no evidence of thrombotic microangiopathy.", "The tubules showed acute tubular necrosis and regeneration.", "There were a small number of eosinophilic intra-tubular casts.", "Sequestration of PRBC's was evident in the small vessels of the heart.", "Endothelial cells were prominent.", "There was no evidence of myocarditis.", "The heart muscle fibers appeared normal.", "There was focal petechial haemorrhage in the subendocardium.", "The focal petechial haemorrhage may relate to resuscitation.", "The focal petechial haemorrhage may be secondary to malaria.", "The adrenal gland appeared active.", "There was eosinophilic cytoplasm in the fasciculata layer.", "There was no evidence of PRBC sequestration.", "There was no parenchymal haemorrhage.", "Samples of lung, intestine or bone marrow were not available for histopathology examination.", "The overall picture was one of systemic malaria infection with multi-organ damage.", "There was much vascular rupture and petechial haemorrhaging in the brain."], "index": 79, "original_id": "multiclinsum_test_2113_en.txt", "split": "test", "summary_subclaims": ["A formerly healthy 40 year-old male became symptomatic 10 days after spending time in the jungle of North Borneo.", "He presented to hospital in a state of collapse and died within two hours.", "He was hyponatraemic.", "He had elevated blood urea.", "He had elevated potassium.", "He had elevated lactate dehydrogenase.", "He had elevated amino transferase values.", "He was thrombocytopenic.", "He was eosinophilic.", "Dengue haemorrhagic shock was suspected.", "A post-mortem examination was performed.", "Investigations for dengue virus were negative.", "Blood for malaria parasites indicated hyperparasitaemia.", "Single species P. knowlesi infection was confirmed by nested-PCR.", "Macroscopic pathology of the brain and endocardium showed multiple petechial haemorrhages.", "The liver and spleen were enlarged.", "The lungs had features consistent with ARDS.", "Microscopic pathology showed sequestration of pigmented parasitized red blood cells in the vessels of the cerebrum, cerebellum, heart and kidney.", "There was no evidence of chronic inflammatory reaction in the brain or any other organ examined.", "Brain sections were negative for intracellular adhesion molecule-1.", "The spleen and liver had abundant pigment containing macrophages and parasitized red blood cells.", "The kidney had evidence of acute tubular necrosis.", "Endothelial cells in heart sections were prominent."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was a 27-year-old man.", "He presented with headache and diplopia for three days.", "The headache was a dull pain.", "The headache was not accompanied by vomiting.", "The headache was not accompanied by dizziness.", "Fundoscopy showed left optic nerve atrophy.", "Fundoscopy showed right papilledema.", "The findings were consistent with Foster-Kennedy syndrome.", "Neurological examinations were otherwise normal.", "Laboratory results were unremarkable.", "A left frontal irregular space-occupying lesion was seen on MRI.", "Enhancement was shown on contrast-enhanced scan.", "The lesion appeared hyperintense on T1-weighted images.", "Hypointense signals were noted on T2-weighted images.", "The tumor was primarily located at the frontal lobe.", "Ventricular compression was noted.", "Midline shift was noted.", "Brain CTA showed compression of the anterior and middle cerebral arteries.", "Small branches from the middle and anterior cerebral arteries supplied blood to the tumor.", "Meningioma was diagnosed prior to surgery.", "Surgery was performed via the left frontotemporoparietal approach.", "The tumor was removed four days after admission.", "The tumor was located at the anterior cranial fossa.", "The tumor adhered closely to the dura of the skull base.", "Only the infiltrated dura was not removed.", "The resection was Simpson\u2019s grade II.", "Grossly, the tumor was a soft, well-circumscribed pigmented lesion with a capsule.", "The tumor proved to be meningeal melanocytoma on histopathological examination.", "Immunohistochemistry was positive for HMB-45.", "Immunohistochemistry was positive for vimentin.", "Immunohistochemistry was positive for S-100 protein.", "Immunohistochemistry was negative for EMA.", "Immunohistochemistry was negative for CK.", "Immunohistochemistry was negative for PR.", "Ki-67 was positive.", "Ki-67 was less than 1%.", "The tumor was adjudged WHO grade I.", "A detailed physical examination was performed.", "No skin melanoma was found.", "The patient denied a history of melanocytoma.", "The patient received one-time 30 Gray radiation therapy after surgery.", "The duration of radiation therapy was one day.", "No tumor relapse was seen on follow-up MRI six months after surgery.", "At follow-up two and a half years after surgery, the patient was free of symptoms.", "No tumor recurrence was shown on the CT scan."], "summary_subclaims": ["A 27-year-old man presented with headache and diplopia at our department.", "Fundoscopy showed left optic nerve atrophy.", "Fundoscopy showed right papilledema.", "The findings were consistent with Foster-Kennedy syndrome.", "Neurological exams were otherwise normal.", "A left frontal irregular space-occupying lesion was seen on magnetic resonance imaging (MRI).", "Enhancement was shown on contrast-enhanced computed tomography (CT) scan.", "CT angiography (CTA) revealed vascular compression around the lesion.", "Prior to surgery, meningioma was diagnosed.", "Gross tumor removal was performed.", "On postoperative pathohistological exam, the tumor proved to be a meningeal melanocytoma.", "The tumor was WHO grade I.", "No skin melanoma was found.", "After surgery, the patient received radiation therapy.", "No tumor was seen on follow-up MR images six months after surgery.", "The patient was well after two and a half years.", "There was no tumor recurrence on the follow-up CT."]}, "extra_info": {"fulltext_subclaims": ["The patient was a 27-year-old man.", "He presented with headache and diplopia for three days.", "The headache was a dull pain.", "The headache was not accompanied by vomiting.", "The headache was not accompanied by dizziness.", "Fundoscopy showed left optic nerve atrophy.", "Fundoscopy showed right papilledema.", "The findings were consistent with Foster-Kennedy syndrome.", "Neurological examinations were otherwise normal.", "Laboratory results were unremarkable.", "A left frontal irregular space-occupying lesion was seen on MRI.", "Enhancement was shown on contrast-enhanced scan.", "The lesion appeared hyperintense on T1-weighted images.", "Hypointense signals were noted on T2-weighted images.", "The tumor was primarily located at the frontal lobe.", "Ventricular compression was noted.", "Midline shift was noted.", "Brain CTA showed compression of the anterior and middle cerebral arteries.", "Small branches from the middle and anterior cerebral arteries supplied blood to the tumor.", "Meningioma was diagnosed prior to surgery.", "Surgery was performed via the left frontotemporoparietal approach.", "The tumor was removed four days after admission.", "The tumor was located at the anterior cranial fossa.", "The tumor adhered closely to the dura of the skull base.", "Only the infiltrated dura was not removed.", "The resection was Simpson\u2019s grade II.", "Grossly, the tumor was a soft, well-circumscribed pigmented lesion with a capsule.", "The tumor proved to be meningeal melanocytoma on histopathological examination.", "Immunohistochemistry was positive for HMB-45.", "Immunohistochemistry was positive for vimentin.", "Immunohistochemistry was positive for S-100 protein.", "Immunohistochemistry was negative for EMA.", "Immunohistochemistry was negative for CK.", "Immunohistochemistry was negative for PR.", "Ki-67 was positive.", "Ki-67 was less than 1%.", "The tumor was adjudged WHO grade I.", "A detailed physical examination was performed.", "No skin melanoma was found.", "The patient denied a history of melanocytoma.", "The patient received one-time 30 Gray radiation therapy after surgery.", "The duration of radiation therapy was one day.", "No tumor relapse was seen on follow-up MRI six months after surgery.", "At follow-up two and a half years after surgery, the patient was free of symptoms.", "No tumor recurrence was shown on the CT scan."], "index": 85, "original_id": "multiclinsum_test_568_en.txt", "split": "test", "summary_subclaims": ["A 27-year-old man presented with headache and diplopia at our department.", "Fundoscopy showed left optic nerve atrophy.", "Fundoscopy showed right papilledema.", "The findings were consistent with Foster-Kennedy syndrome.", "Neurological exams were otherwise normal.", "A left frontal irregular space-occupying lesion was seen on magnetic resonance imaging (MRI).", "Enhancement was shown on contrast-enhanced computed tomography (CT) scan.", "CT angiography (CTA) revealed vascular compression around the lesion.", "Prior to surgery, meningioma was diagnosed.", "Gross tumor removal was performed.", "On postoperative pathohistological exam, the tumor proved to be a meningeal melanocytoma.", "The tumor was WHO grade I.", "No skin melanoma was found.", "After surgery, the patient received radiation therapy.", "No tumor was seen on follow-up MR images six months after surgery.", "The patient was well after two and a half years.", "There was no tumor recurrence on the follow-up CT."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["A 13-year-old young man was admitted to our hospital with non-sustained ventricular tachycardia episode.", "The non-sustained ventricular tachycardia episode was noticed during routine athletic evaluation.", "Resting ECG was normal, with sinus rhythm.", "The heart rate on resting ECG was normal.", "There were no significant alterations of the ventricular repolarization phase on resting ECG.", "QTma was 413 ms.", "QTmin was 383 ms.", "QTd was 39 ms.", "QTcd was 44 ms.", "Exercise stress test (treadmill) didn\u2019t show signs of inducible ischemia through maximal effort.", "The METS achieved during the treadmill test were 21.", "The maximal heart rate during the treadmill test was 194 beats per minute.", "The treadmill test induced asymptomatic non-sustained ventricular tachycardia.", "The non-sustained ventricular tachycardia had left bundle branch morphology.", "The non-sustained ventricular tachycardia had an inferior axis.", "The rate of the non-sustained ventricular tachycardia was 150 beats per minute.", "The non-sustained ventricular tachycardia occurred during the second minute of the recovery phase.", "Standard echocardiographic views showed a not clearly normal coronary pattern.", "The right coronary artery appeared with high take-off from the aortic wall.", "The right coronary artery ostium was not clearly identified.", "Genetic screening for catecholaminergic tachycardia was performed.", "Beta-blocking therapy with nadolol was started.", "Beta-blocking therapy with nadolol was continued until the first cardiological follow up.", "Coronary computed tomography angiography was performed.", "The scan showed anomalous origin of all three branches of coronary arteries from a single origin from the left coronary sinus.", "The right coronary artery had a malignant course, squeezed between the pulmonary trunk and the proximal ascending aorta.", "The distal part of the right coronary artery took its normal course.", "The left anterior descending artery caliber appeared to be normal.", "The circumflex artery caliber appeared to be normal.", "All the data from coronary computed tomography angiography were confirmed by cardiac magnetic resonance.", "Myocardial scintigraphy with protocol of two days steps and treadmill stress test (exercise) was performed.", "Myocardial scintigraphy showed no significant evidences of perfusion defects.", "Catheter coronary angiography was performed.", "The coronary angiography showed the rare coronary anomaly pattern.", "The exam showed a significant milking effect at the middle segment of the left anterior descending artery.", "Fractional Flow Reserve (FFR) was 0.74.", "Invasive Fractional Flow Reserve (iFFR) was 0.83.", "Intravascular ultrasound (IVUS) showed a slit like right coronary ostium.", "Intravascular ultrasound (IVUS) showed eccentric systolic compression in the proximal bridge segment of the right coronary artery.", "The depth of the bridging muscle segment was 16 mm.", "The length of the bridging muscle segment was 25 mm.", "Planned on pump surgery was discussed.", "A surgical unroofing of the right coronary artery intramural section was performed.", "Resuspension of the intercoronary commissure was performed.", "The resuspension resulted in relocation of the coronary artery into the appropriate aortic sinus.", "Surgical myotomy involving resection of the overlying muscle fibers on the middle segment of the left anterior descending artery was performed.", "The patient's postoperative course was uneventful.", "The patient stayed overnight in the intensive care unit.", "The patient left the hospital on postoperative day 7.", "No complications occurred during the first six months of follow-up."], "summary_subclaims": ["Both anomalous origin of the right coronary artery and myocardial bridge on left anterior descending artery were detected concurrently."]}, "extra_info": {"fulltext_subclaims": ["A 13-year-old young man was admitted to our hospital with non-sustained ventricular tachycardia episode.", "The non-sustained ventricular tachycardia episode was noticed during routine athletic evaluation.", "Resting ECG was normal, with sinus rhythm.", "The heart rate on resting ECG was normal.", "There were no significant alterations of the ventricular repolarization phase on resting ECG.", "QTma was 413 ms.", "QTmin was 383 ms.", "QTd was 39 ms.", "QTcd was 44 ms.", "Exercise stress test (treadmill) didn\u2019t show signs of inducible ischemia through maximal effort.", "The METS achieved during the treadmill test were 21.", "The maximal heart rate during the treadmill test was 194 beats per minute.", "The treadmill test induced asymptomatic non-sustained ventricular tachycardia.", "The non-sustained ventricular tachycardia had left bundle branch morphology.", "The non-sustained ventricular tachycardia had an inferior axis.", "The rate of the non-sustained ventricular tachycardia was 150 beats per minute.", "The non-sustained ventricular tachycardia occurred during the second minute of the recovery phase.", "Standard echocardiographic views showed a not clearly normal coronary pattern.", "The right coronary artery appeared with high take-off from the aortic wall.", "The right coronary artery ostium was not clearly identified.", "Genetic screening for catecholaminergic tachycardia was performed.", "Beta-blocking therapy with nadolol was started.", "Beta-blocking therapy with nadolol was continued until the first cardiological follow up.", "Coronary computed tomography angiography was performed.", "The scan showed anomalous origin of all three branches of coronary arteries from a single origin from the left coronary sinus.", "The right coronary artery had a malignant course, squeezed between the pulmonary trunk and the proximal ascending aorta.", "The distal part of the right coronary artery took its normal course.", "The left anterior descending artery caliber appeared to be normal.", "The circumflex artery caliber appeared to be normal.", "All the data from coronary computed tomography angiography were confirmed by cardiac magnetic resonance.", "Myocardial scintigraphy with protocol of two days steps and treadmill stress test (exercise) was performed.", "Myocardial scintigraphy showed no significant evidences of perfusion defects.", "Catheter coronary angiography was performed.", "The coronary angiography showed the rare coronary anomaly pattern.", "The exam showed a significant milking effect at the middle segment of the left anterior descending artery.", "Fractional Flow Reserve (FFR) was 0.74.", "Invasive Fractional Flow Reserve (iFFR) was 0.83.", "Intravascular ultrasound (IVUS) showed a slit like right coronary ostium.", "Intravascular ultrasound (IVUS) showed eccentric systolic compression in the proximal bridge segment of the right coronary artery.", "The depth of the bridging muscle segment was 16 mm.", "The length of the bridging muscle segment was 25 mm.", "Planned on pump surgery was discussed.", "A surgical unroofing of the right coronary artery intramural section was performed.", "Resuspension of the intercoronary commissure was performed.", "The resuspension resulted in relocation of the coronary artery into the appropriate aortic sinus.", "Surgical myotomy involving resection of the overlying muscle fibers on the middle segment of the left anterior descending artery was performed.", "The patient's postoperative course was uneventful.", "The patient stayed overnight in the intensive care unit.", "The patient left the hospital on postoperative day 7.", "No complications occurred during the first six months of follow-up."], "index": 87, "original_id": "multiclinsum_test_1721_en.txt", "split": "test", "summary_subclaims": ["Both anomalous origin of the right coronary artery and myocardial bridge on left anterior descending artery were detected concurrently."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 49-year-old Asian woman.", "She presented with severe abdominal distension and dyspnea.", "She had a feeling of swelling abdomen.", "She had dull nature abdominal discomfort and pain.", "She had edema in both legs.", "She had dyspnea for 3 weeks before her visit.", "She visited another hospital 2 days prior to her visit.", "She was transferred to the emergency room due to a huge ovarian cystic mass.", "The CT scan showed a large amount of left pleural effusion.", "On initial vital sign assessment, she had tachycardia.", "Her hemoglobin was 8.3 g/dL.", "Her white blood cells were 21.00 \u00d7 103/\u03bcL.", "Her C-reactive protein was 25.8 mg/dL.", "Her prothrombin time was 90.4 seconds.", "Her PT international normalized ratio was prolonged.", "Her activated partial thromboplastin time was not reported.", "The coagulation tests could possibly imply disseminated intravascular coagulation.", "Physical examination showed abdominal distension.", "Physical examination showed severe tenderness in the whole abdomen.", "Chest tube insertion at the left lung was performed.", "Paracentesis was performed.", "Approximately 850 mL of pleural fluid was drained.", "Approximately 2 L of ascites was drained.", "A dynamic abdomen-pelvis CT scan showed a 30-cm-sized multiseptated cystic mass.", "The CT scan showed peritoneal thickening.", "The CT scan showed large amount of ascites.", "The findings suggested ovarian malignancy.", "The findings suggested peritoneal carcinomatosis.", "The patient's CA125 level was 674.3 U/mL.", "The patient's HE4 was 286.4 pmol/L.", "The premenopausal ROMA index was 86.67%.", "The postmenopausal ROMA index was 92.83%.", "CA19-9, CEA, and AFP were within normal range.", "Rupture of a malignant ovarian tumor was suspected.", "An emergent operation was planned.", "The initial operation identified a ruptured 30-cm-sized right ovarian multiseptated cystic mass.", "The mass showed diffuse adhesion to the retroperitoneum.", "The mass showed diffuse adhesion to the abdominal wall.", "The mass showed diffuse adhesion to the uterus.", "Frozen section biopsy revealed poorly differentiated carcinoma.", "Debulking surgery including hysterectomy could not be performed.", "Bilateral salpingo-oophorectomy was performed.", "Partial omentectomy was performed.", "The pathologic diagnosis was high-grade stromal sarcoma.", "The tumor showed features of brisk mitosis.", "The tumor showed focal necrosis.", "The tumor had an adenofibromatous component.", "The tumor had endometriosis with mucinous metaplasia.", "The tumor had hypercellular stroma.", "The tumor consisted of monotonous uniform cells with endometrial stromal differentiation.", "Mitotic figures were frequent.", "Highly atypical neoplastic cells were noted.", "Metastasis to the omentum was identified.", "Tumor cells were positive for CD10.", "Tumor cells were positive for Cyclin D1.", "Tumor cells were positive for FOXL2.", "Tumor cells were focally positive for desmin.", "Tumor cells were focally positive for smooth muscle actin.", "Tumor cells were negative for beta-catenin.", "Tumor cells were negative for inhibin A.", "Endometrial biopsy was performed.", "The endometrial biopsy result was nonspecific.", "The patient underwent three courses of Adriamycin chemotherapy.", "A follow-up CT scan showed new 11-mm-sized probable seeding nodules in the right omentum.", "A follow-up CT scan showed new 11-mm-sized probable seeding nodules in the left paracolic gutter.", "A 1.5-cm-sized partly solid nodule was identified in the right upper lung field.", "The lung lesion was considered both primary and metastatic.", "A secondary debulking operation was planned.", "The secondary debulking operation included total hysterectomy.", "The secondary debulking operation included metastasectomy.", "The secondary debulking operation included omentectomy.", "The secondary debulking operation included peritonectomy.", "The secondary debulking operation included appendectomy.", "HIPEC with paclitaxel 175 mg/m2 was performed.", "The final pathologic report confirmed no specific findings in the uterine cervix, myometrium, and endometrium.", "The peritoneum, omentum, and appendix were confirmed as metastatic high-grade endometrial stromal sarcoma.", "A right upper lung lobectomy was performed.", "The lung biopsy was revealed as adenocarcinoma.", "The patient has double primary malignancy.", "The patient is currently alive 28 months after diagnosis.", "The patient is under a new chemotherapy regimen: paclitaxel 175 mg/m2 and ifosfamide 1.6 g/m2."], "summary_subclaims": ["The patient is a 49-year-old Asian woman.", "She presented with disseminated intravascular coagulation.", "The cause of disseminated intravascular coagulation was ruptured primary high-grade ovarian endometrial stromal sarcoma.", "The sarcoma had multiple intraperitoneal metastases.", "The patient underwent adjuvant chemotherapy with three courses of Adriamycin.", "The Adriamycin dose was 75 mg/m2.", "The secondary debulking operation included total hysterectomy.", "The secondary debulking operation included metastasectomy.", "The secondary debulking operation included omentectomy.", "The secondary debulking operation included peritonectomy.", "The secondary debulking operation included appendectomy.", "The secondary debulking operation included hyperthermic intraperitoneal chemotherapy.", "The hyperthermic intraperitoneal chemotherapy used paclitaxel 175 mg/m2.", "The patient has been alive for 28 months.", "The patient is under a new chemotherapy regimen."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 49-year-old Asian woman.", "She presented with severe abdominal distension and dyspnea.", "She had a feeling of swelling abdomen.", "She had dull nature abdominal discomfort and pain.", "She had edema in both legs.", "She had dyspnea for 3 weeks before her visit.", "She visited another hospital 2 days prior to her visit.", "She was transferred to the emergency room due to a huge ovarian cystic mass.", "The CT scan showed a large amount of left pleural effusion.", "On initial vital sign assessment, she had tachycardia.", "Her hemoglobin was 8.3 g/dL.", "Her white blood cells were 21.00 \u00d7 103/\u03bcL.", "Her C-reactive protein was 25.8 mg/dL.", "Her prothrombin time was 90.4 seconds.", "Her PT international normalized ratio was prolonged.", "Her activated partial thromboplastin time was not reported.", "The coagulation tests could possibly imply disseminated intravascular coagulation.", "Physical examination showed abdominal distension.", "Physical examination showed severe tenderness in the whole abdomen.", "Chest tube insertion at the left lung was performed.", "Paracentesis was performed.", "Approximately 850 mL of pleural fluid was drained.", "Approximately 2 L of ascites was drained.", "A dynamic abdomen-pelvis CT scan showed a 30-cm-sized multiseptated cystic mass.", "The CT scan showed peritoneal thickening.", "The CT scan showed large amount of ascites.", "The findings suggested ovarian malignancy.", "The findings suggested peritoneal carcinomatosis.", "The patient's CA125 level was 674.3 U/mL.", "The patient's HE4 was 286.4 pmol/L.", "The premenopausal ROMA index was 86.67%.", "The postmenopausal ROMA index was 92.83%.", "CA19-9, CEA, and AFP were within normal range.", "Rupture of a malignant ovarian tumor was suspected.", "An emergent operation was planned.", "The initial operation identified a ruptured 30-cm-sized right ovarian multiseptated cystic mass.", "The mass showed diffuse adhesion to the retroperitoneum.", "The mass showed diffuse adhesion to the abdominal wall.", "The mass showed diffuse adhesion to the uterus.", "Frozen section biopsy revealed poorly differentiated carcinoma.", "Debulking surgery including hysterectomy could not be performed.", "Bilateral salpingo-oophorectomy was performed.", "Partial omentectomy was performed.", "The pathologic diagnosis was high-grade stromal sarcoma.", "The tumor showed features of brisk mitosis.", "The tumor showed focal necrosis.", "The tumor had an adenofibromatous component.", "The tumor had endometriosis with mucinous metaplasia.", "The tumor had hypercellular stroma.", "The tumor consisted of monotonous uniform cells with endometrial stromal differentiation.", "Mitotic figures were frequent.", "Highly atypical neoplastic cells were noted.", "Metastasis to the omentum was identified.", "Tumor cells were positive for CD10.", "Tumor cells were positive for Cyclin D1.", "Tumor cells were positive for FOXL2.", "Tumor cells were focally positive for desmin.", "Tumor cells were focally positive for smooth muscle actin.", "Tumor cells were negative for beta-catenin.", "Tumor cells were negative for inhibin A.", "Endometrial biopsy was performed.", "The endometrial biopsy result was nonspecific.", "The patient underwent three courses of Adriamycin chemotherapy.", "A follow-up CT scan showed new 11-mm-sized probable seeding nodules in the right omentum.", "A follow-up CT scan showed new 11-mm-sized probable seeding nodules in the left paracolic gutter.", "A 1.5-cm-sized partly solid nodule was identified in the right upper lung field.", "The lung lesion was considered both primary and metastatic.", "A secondary debulking operation was planned.", "The secondary debulking operation included total hysterectomy.", "The secondary debulking operation included metastasectomy.", "The secondary debulking operation included omentectomy.", "The secondary debulking operation included peritonectomy.", "The secondary debulking operation included appendectomy.", "HIPEC with paclitaxel 175 mg/m2 was performed.", "The final pathologic report confirmed no specific findings in the uterine cervix, myometrium, and endometrium.", "The peritoneum, omentum, and appendix were confirmed as metastatic high-grade endometrial stromal sarcoma.", "A right upper lung lobectomy was performed.", "The lung biopsy was revealed as adenocarcinoma.", "The patient has double primary malignancy.", "The patient is currently alive 28 months after diagnosis.", "The patient is under a new chemotherapy regimen: paclitaxel 175 mg/m2 and ifosfamide 1.6 g/m2."], "index": 49, "original_id": "multiclinsum_test_2683_en.txt", "split": "test", "summary_subclaims": ["The patient is a 49-year-old Asian woman.", "She presented with disseminated intravascular coagulation.", "The cause of disseminated intravascular coagulation was ruptured primary high-grade ovarian endometrial stromal sarcoma.", "The sarcoma had multiple intraperitoneal metastases.", "The patient underwent adjuvant chemotherapy with three courses of Adriamycin.", "The Adriamycin dose was 75 mg/m2.", "The secondary debulking operation included total hysterectomy.", "The secondary debulking operation included metastasectomy.", "The secondary debulking operation included omentectomy.", "The secondary debulking operation included peritonectomy.", "The secondary debulking operation included appendectomy.", "The secondary debulking operation included hyperthermic intraperitoneal chemotherapy.", "The hyperthermic intraperitoneal chemotherapy used paclitaxel 175 mg/m2.", "The patient has been alive for 28 months.", "The patient is under a new chemotherapy regimen."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was referred for percutaneous LAAO.", "Past medical history was significant for mitral regurgitation.", "Past medical history was significant for tricuspid regurgitation.", "Past medical history was significant for persistent atrial fibrillation.", "Persistent atrial fibrillation was complicated by recurrent significant gastrointestinal haemorrhage on anticoagulation.", "The gastrointestinal haemorrhage was secondary to diverticulosis.", "Five months prior to referral, she underwent surgical mitral and tricuspid valve repair.", "Five months prior to referral, she underwent LAA ligation with 35\u2005mm AtriClip.", "The LAA ligation was due to elevated stroke risk (CHA2DS2-VASc score 5).", "The patient had intolerance to oral anticoagulation.", "Initial pre-procedural clinical examination revealed a haemodynamically stable, well-appearing female.", "Initial pre-procedural clinical examination revealed a regular heart rate.", "Initial pre-procedural clinical examination revealed an irregular rhythm.", "Pre-operative laboratory assessment revealed normal kidney function (serum creatinine 0.81\u2005mg/dL).", "Pre-operative laboratory assessment revealed mild anaemia (haemoglobin 10.8\u2005g/dL).", "Intra-operative transoesophageal echocardiogram demonstrated closure of the LAA.", "40-day post-operative TEE demonstrated a significant persistent communication between the left atrium and LAA.", "40-day post-operative cardiac CT imaging demonstrated a significant persistent communication between the left atrium and LAA.", "There was no evidence of LAA thrombus.", "A 27\u2005mm LAAO device (WATCHMAN\u2122) was selected.", "The LAAO device was deployed with all the P.A.S.S. criteria satisfied.", "Only 1.4\u2005mm PDL was present.", "She continued on apixaban 5\u2005mg twice daily post-operatively.", "She continued on aspirin 81\u2005mg daily post-operatively.", "Follow-up TEE at 6 weeks demonstrated a trivial PDL measuring 1.9\u2005mm along posterior aspect.", "There was no thrombus seen at 6 weeks.", "The decision was made to continue aspirin 81\u2005mg daily.", "The decision was made to continue clopidogrel 75\u2005mg daily.", "The decision was made to discontinue apixaban.", "The patient has not experienced any further episodes of major bleeding.", "We are tentatively planning to stop clopidogrel at 6 months post-operatively.", "We are tentatively planning to continue aspirin 81\u2005mg daily indefinitely thereafter."], "summary_subclaims": ["The patient was a 79-year-old female.", "The patient underwent LAAO device deployment within a surgically occluded LAA with PDL.", "A 27\u2005mm LAAO device (WATCHMANTM) was deployed.", "All the P.A.S.S. criteria were satisfied.", "Only 1.4\u2005mm PDL was present.", "The patient was continued on apixaban and aspirin post-operatively.", "A post-operative transoesophageal echocardiogram was performed at 6 weeks.", "The 6-week transoesophageal echocardiogram demonstrated trivial PDL measuring 1.49\u2005mm.", "The patient was continued on aspirin and clopidogrel.", "Apixaban was discontinued."]}, "extra_info": {"fulltext_subclaims": ["The patient was referred for percutaneous LAAO.", "Past medical history was significant for mitral regurgitation.", "Past medical history was significant for tricuspid regurgitation.", "Past medical history was significant for persistent atrial fibrillation.", "Persistent atrial fibrillation was complicated by recurrent significant gastrointestinal haemorrhage on anticoagulation.", "The gastrointestinal haemorrhage was secondary to diverticulosis.", "Five months prior to referral, she underwent surgical mitral and tricuspid valve repair.", "Five months prior to referral, she underwent LAA ligation with 35\u2005mm AtriClip.", "The LAA ligation was due to elevated stroke risk (CHA2DS2-VASc score 5).", "The patient had intolerance to oral anticoagulation.", "Initial pre-procedural clinical examination revealed a haemodynamically stable, well-appearing female.", "Initial pre-procedural clinical examination revealed a regular heart rate.", "Initial pre-procedural clinical examination revealed an irregular rhythm.", "Pre-operative laboratory assessment revealed normal kidney function (serum creatinine 0.81\u2005mg/dL).", "Pre-operative laboratory assessment revealed mild anaemia (haemoglobin 10.8\u2005g/dL).", "Intra-operative transoesophageal echocardiogram demonstrated closure of the LAA.", "40-day post-operative TEE demonstrated a significant persistent communication between the left atrium and LAA.", "40-day post-operative cardiac CT imaging demonstrated a significant persistent communication between the left atrium and LAA.", "There was no evidence of LAA thrombus.", "A 27\u2005mm LAAO device (WATCHMAN\u2122) was selected.", "The LAAO device was deployed with all the P.A.S.S. criteria satisfied.", "Only 1.4\u2005mm PDL was present.", "She continued on apixaban 5\u2005mg twice daily post-operatively.", "She continued on aspirin 81\u2005mg daily post-operatively.", "Follow-up TEE at 6 weeks demonstrated a trivial PDL measuring 1.9\u2005mm along posterior aspect.", "There was no thrombus seen at 6 weeks.", "The decision was made to continue aspirin 81\u2005mg daily.", "The decision was made to continue clopidogrel 75\u2005mg daily.", "The decision was made to discontinue apixaban.", "The patient has not experienced any further episodes of major bleeding.", "We are tentatively planning to stop clopidogrel at 6 months post-operatively.", "We are tentatively planning to continue aspirin 81\u2005mg daily indefinitely thereafter."], "index": 47, "original_id": "multiclinsum_test_1868_en.txt", "split": "test", "summary_subclaims": ["The patient was a 79-year-old female.", "The patient underwent LAAO device deployment within a surgically occluded LAA with PDL.", "A 27\u2005mm LAAO device (WATCHMANTM) was deployed.", "All the P.A.S.S. criteria were satisfied.", "Only 1.4\u2005mm PDL was present.", "The patient was continued on apixaban and aspirin post-operatively.", "A post-operative transoesophageal echocardiogram was performed at 6 weeks.", "The 6-week transoesophageal echocardiogram demonstrated trivial PDL measuring 1.49\u2005mm.", "The patient was continued on aspirin and clopidogrel.", "Apixaban was discontinued."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 79 year old male.", "The patient has a history of atrial fibrillation.", "The patient was previously on apixaban and was switched to aspirin only.", "The patient has type II diabetes mellitus.", "The patient has asthma, well controlled on home inhalers.", "The patient has hypertension.", "The patient tested positive for coronavirus disease 2019 (COVID-19) on April 7th, 2021.", "The patient is fully vaccinated with Moderna.", "The patient presented to the emergency department with progressive worsening of bilateral lower extremity edema and dyspnea over one month.", "The patient had a chronic two-pillow orthopnea.", "The patient performed all activities of daily living independently at baseline.", "This work has been reported in accordance with SCARE.", "At presentation, the patient denied chest pain.", "At presentation, the patient denied fever.", "At presentation, the patient denied nausea.", "At presentation, the patient denied vomiting.", "At presentation, the patient denied diarrhea.", "At presentation, the patient denied dysuria.", "At presentation, the patient denied travel.", "At presentation, the patient denied trauma.", "At presentation, the patient denied drug use.", "At presentation, the patient denied cough.", "Vital signs were all within normal limits on admission.", "Physical exam was notable for bibasilar crackles in the lungs.", "Physical exam was notable for bilateral lower extremity 2+ pitting edema.", "Physical exam was notable for jugular venous distention up to 9 cm.", "Labs were notable for a pro B-type natriuretic peptide of 8458 pg/mL.", "The pro B-type natriuretic peptide reference range is 1\u2013450 pg/mL.", "The pro B-type natriuretic peptide was a significant increase from 3301 pg/mL during a previous admission.", "The D-dimer was unremarkable.", "A chest radiograph obtained during admission showed bilateral ground glass opacities from prior COVID-19.", "A chest radiograph obtained during admission showed pulmonary congestion.", "A chest radiograph obtained during admission showed interposition of the right hepatic flexure of the colon between subdiaphragmatic space and the right dome of the liver (Chilaiditi's sign).", "The comparison was made from a prior chest radiograph that showed normal anatomy of the right subdiaphragmatic space.", "Electrocardiogram demonstrated atrial fibrillation with low voltage.", "Electrocardiogram showed no acute ischemic features.", "Echocardiogram showed an ejection fraction of 40%.", "The ejection fraction was reduced from 70% only a year ago.", "Echocardiogram showed normal right ventricular (RV) size.", "Echocardiogram showed reduced RV contractility.", "Echocardiogram showed a dilated right atrium.", "The patient did not have any prior COVID-19 complications.", "The patient did not have intubation.", "The patient did not have development of pulmonary embolism.", "The patient did not require supplemental oxygen.", "A negative D-dimer and CT chest without contrast showed no evidence of embolism.", "Acute pulmonary embolism was effectively ruled out.", "The patient was admitted for congestive heart failure exacerbation.", "The patient was started on furosemide 40 mg IV twice a day.", "The patient had a net negative urine output of 6.8 L over 48 hours since admission.", "Home medications were resumed, including Losartan 25 mg daily.", "Home medications were resumed, including carvedilol 3.125 mg twice daily.", "Home medications were resumed, including atorvastatin 40 mg.", "Home medications were resumed, including aspirin 81mg.", "Home medications were resumed, including albuterol inhaler as needed every 6 hours.", "Home medications were resumed, including montelukast 10 mg daily.", "The patient was diuresed for 3 days.", "The patient successfully achieved euvolemic status.", "The patient had resolution of bilateral leg edema.", "The patient had improvement of jugular venous distention.", "Cardiology was consulted for a new reduction in ejection fraction to rule out acute coronary syndrome.", "An electrocardiogram showed no ischemic features.", "Troponin was negative on three separate assessments.", "It was concluded that the patient did not have acute coronary syndrome.", "The patient received coronary angiography.", "Coronary angiography found non-obstructive coronary artery disease.", "The patient continued to have persistent dyspnea.", "The patient had some mild pleuritic chest pain on the right subcostal region.", "The patient did not need supplemental oxygen.", "The aforementioned medications were continued for a total of 5 days.", "Community or hospital acquired pneumonia was ruled out.", "Normal cultures were obtained.", "There was an absence of inflammatory response.", "There were no fevers.", "Procalcitonin was normal.", "There were no imaging findings concerning pneumonia.", "A computed tomography scan of the chest without contrast was repeated.", "The CT scan showed colonic interposition between the diaphragm and right lobe of the liver.", "Surgery was consulted for potential Chilaiditi syndrome.", "The patient refused to undergo any surgery.", "The patient preferred to be discharged from the hospital.", "The patient was discharged with guidelines for long-term medical treatment for heart failure.", "The patient was discharged with Lasix 40mg by mouth twice daily.", "The patient was discharged with carvedilol 3.125 mg twice daily.", "The patient was discharged with Losartan 25mg daily.", "The patient was discharged with aspirin 81mg.", "The patient was discharged with albuterol inhaler as needed.", "The patient was discharged with montelukast 10mg daily."], "summary_subclaims": ["The patient is a 79 year old male.", "The patient has a past medical history of asthma.", "The patient has a past medical history of heart failure with preserved ejection fraction.", "The patient was admitted for acute heart failure exacerbation with reduced ejection fraction.", "A new incidental finding of Chilaiditi's sign was noted on chest radiograph.", "The patient received optimal diuretics.", "The patient received guideline-directed medical treatment for heart failure exacerbation.", "Mild dyspnea with pleuritic chest pain persisted.", "Dyspnea with pleurisy was likely attributed to a structural anatomical defect.", "Chilaiditi's sign can be picked up on imaging."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 79 year old male.", "The patient has a history of atrial fibrillation.", "The patient was previously on apixaban and was switched to aspirin only.", "The patient has type II diabetes mellitus.", "The patient has asthma, well controlled on home inhalers.", "The patient has hypertension.", "The patient tested positive for coronavirus disease 2019 (COVID-19) on April 7th, 2021.", "The patient is fully vaccinated with Moderna.", "The patient presented to the emergency department with progressive worsening of bilateral lower extremity edema and dyspnea over one month.", "The patient had a chronic two-pillow orthopnea.", "The patient performed all activities of daily living independently at baseline.", "This work has been reported in accordance with SCARE.", "At presentation, the patient denied chest pain.", "At presentation, the patient denied fever.", "At presentation, the patient denied nausea.", "At presentation, the patient denied vomiting.", "At presentation, the patient denied diarrhea.", "At presentation, the patient denied dysuria.", "At presentation, the patient denied travel.", "At presentation, the patient denied trauma.", "At presentation, the patient denied drug use.", "At presentation, the patient denied cough.", "Vital signs were all within normal limits on admission.", "Physical exam was notable for bibasilar crackles in the lungs.", "Physical exam was notable for bilateral lower extremity 2+ pitting edema.", "Physical exam was notable for jugular venous distention up to 9 cm.", "Labs were notable for a pro B-type natriuretic peptide of 8458 pg/mL.", "The pro B-type natriuretic peptide reference range is 1\u2013450 pg/mL.", "The pro B-type natriuretic peptide was a significant increase from 3301 pg/mL during a previous admission.", "The D-dimer was unremarkable.", "A chest radiograph obtained during admission showed bilateral ground glass opacities from prior COVID-19.", "A chest radiograph obtained during admission showed pulmonary congestion.", "A chest radiograph obtained during admission showed interposition of the right hepatic flexure of the colon between subdiaphragmatic space and the right dome of the liver (Chilaiditi's sign).", "The comparison was made from a prior chest radiograph that showed normal anatomy of the right subdiaphragmatic space.", "Electrocardiogram demonstrated atrial fibrillation with low voltage.", "Electrocardiogram showed no acute ischemic features.", "Echocardiogram showed an ejection fraction of 40%.", "The ejection fraction was reduced from 70% only a year ago.", "Echocardiogram showed normal right ventricular (RV) size.", "Echocardiogram showed reduced RV contractility.", "Echocardiogram showed a dilated right atrium.", "The patient did not have any prior COVID-19 complications.", "The patient did not have intubation.", "The patient did not have development of pulmonary embolism.", "The patient did not require supplemental oxygen.", "A negative D-dimer and CT chest without contrast showed no evidence of embolism.", "Acute pulmonary embolism was effectively ruled out.", "The patient was admitted for congestive heart failure exacerbation.", "The patient was started on furosemide 40 mg IV twice a day.", "The patient had a net negative urine output of 6.8 L over 48 hours since admission.", "Home medications were resumed, including Losartan 25 mg daily.", "Home medications were resumed, including carvedilol 3.125 mg twice daily.", "Home medications were resumed, including atorvastatin 40 mg.", "Home medications were resumed, including aspirin 81mg.", "Home medications were resumed, including albuterol inhaler as needed every 6 hours.", "Home medications were resumed, including montelukast 10 mg daily.", "The patient was diuresed for 3 days.", "The patient successfully achieved euvolemic status.", "The patient had resolution of bilateral leg edema.", "The patient had improvement of jugular venous distention.", "Cardiology was consulted for a new reduction in ejection fraction to rule out acute coronary syndrome.", "An electrocardiogram showed no ischemic features.", "Troponin was negative on three separate assessments.", "It was concluded that the patient did not have acute coronary syndrome.", "The patient received coronary angiography.", "Coronary angiography found non-obstructive coronary artery disease.", "The patient continued to have persistent dyspnea.", "The patient had some mild pleuritic chest pain on the right subcostal region.", "The patient did not need supplemental oxygen.", "The aforementioned medications were continued for a total of 5 days.", "Community or hospital acquired pneumonia was ruled out.", "Normal cultures were obtained.", "There was an absence of inflammatory response.", "There were no fevers.", "Procalcitonin was normal.", "There were no imaging findings concerning pneumonia.", "A computed tomography scan of the chest without contrast was repeated.", "The CT scan showed colonic interposition between the diaphragm and right lobe of the liver.", "Surgery was consulted for potential Chilaiditi syndrome.", "The patient refused to undergo any surgery.", "The patient preferred to be discharged from the hospital.", "The patient was discharged with guidelines for long-term medical treatment for heart failure.", "The patient was discharged with Lasix 40mg by mouth twice daily.", "The patient was discharged with carvedilol 3.125 mg twice daily.", "The patient was discharged with Losartan 25mg daily.", "The patient was discharged with aspirin 81mg.", "The patient was discharged with albuterol inhaler as needed.", "The patient was discharged with montelukast 10mg daily."], "index": 67, "original_id": "multiclinsum_test_1780_en.txt", "split": "test", "summary_subclaims": ["The patient is a 79 year old male.", "The patient has a past medical history of asthma.", "The patient has a past medical history of heart failure with preserved ejection fraction.", "The patient was admitted for acute heart failure exacerbation with reduced ejection fraction.", "A new incidental finding of Chilaiditi's sign was noted on chest radiograph.", "The patient received optimal diuretics.", "The patient received guideline-directed medical treatment for heart failure exacerbation.", "Mild dyspnea with pleuritic chest pain persisted.", "Dyspnea with pleurisy was likely attributed to a structural anatomical defect.", "Chilaiditi's sign can be picked up on imaging."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 71-year-old man.", "The patient has severe COPD.", "The patient has rapidly progressing dyspnea.", "The patient has low exercise tolerance.", "The patient has hypoxemia.", "The patient was diagnosed with COPD in 2010.", "Over the last 5 years, the patient experienced a gradual progression of dyspnea.", "The dyspnea limited the patient's performance of everyday activities.", "In 2019, the patient underwent Bentall\u2019s heart surgery with resection of the left atrial appendage.", "The patient did not claim any diseases of affluence.", "The patient has a 30 pack-year history.", "The patient has not smoked since 2008.", "The patient works as a managing director.", "The patient denies any risk factors for lung disease from his occupation.", "The patient\u2019s father contracted tuberculosis after the Second World War.", "The patient\u2019s father died of lung cancer.", "The patient\u2019s brother has diabetes mellitus.", "The patient was afebrile.", "The patient had alveolar respiration.", "The patient had sinus rhythm.", "The patient\u2019s lower limbs were without swelling.", "Alpha1-antitrypsin levels were normal.", "Arterial blood gas examination showed an oxygen partial pressure pO2 = 7.67 kPa.", "Arterial blood gas examination showed a carbon dioxide partial pressure pCO2 = 4.56 kPa.", "Arterial blood gas examination showed a pH = 7.46.", "Arterial blood gas examination showed blood saturation SpO2 = 90%.", "Computed tomography results demonstrated centrilobular emphysema bilaterally.", "The centrilobular emphysema reflects a severe obstructive ventilation disorder.", "The patient underwent spirometry and body plethysmography examinations.", "Forced expiratory volume in 1 s was 1.07 L.", "Forced vital capacity was 1.94 L.", "Inspiratory capacity was 1.57 L.", "Total lung capacity (TLC) was 5.51 L.", "Peak expiratory flow was 3.38 L.", "Inspiratory muscle performance was examined with the PrO2 device.", "Maximal inspiratory pressure (MIP) was 57 cmH2O.", "Sustained maximal inspiratory pressure (SMIP) was 404 PTU.", "Inspiratory duration (ID) was 7.7s.", "Fatigue index test (FIT) was 12.1.", "The COPD Assessment Test score was 15.", "The modified Medical Research Council Breathlessness score was 3.", "The six-minute walk test (6-MWT) was used to assess exercise tolerance.", "The distance walked during the 6-MWT was 270 m.", "Oxygen saturation decreased from 95% at baseline to 75% during the 6-MWT.", "The BODE index was used as a predictor of prognosis.", "The initial BODE index score was 5.", "The Charlson Comorbidity Index calculated the 10-year mortality risk to be 53%."], "summary_subclaims": ["The patient was a 71-year-old man with severe COPD, Global Initiative for Obstructive Lung Diseases stage 3.", "The patient underwent an 8-wk remotely monitored inspiratory muscle training with a device based on the test of incremental respiratory endurance method.", "Spirometry was performed as part of the initial and final examination.", "Body plethysmography was performed as part of the initial and final examination.", "The test of incremental respiratory endurance examination was performed as part of the initial and final examination.", "The 6-min walking test was performed as part of the initial and final examination.", "Body mass index was measured as part of the initial and final examination.", "Airflow obstruction was assessed as part of the initial and final examination.", "Dyspnea was assessed as part of the initial and final examination.", "Exercise capacity index was measured as part of the initial and final examination.", "Subjective perception of dyspnea was assessed as part of the initial and final examination.", "The patient performed training at home.", "The physiotherapist monitored the patient remotely through a web application.", "The web application allowed the physiotherapist to evaluate all training parameters in real-time.", "The web application allowed the physiotherapist to respond to any problems.", "After 8 wk of home training, there was a significant increase in maximal inspiratory pressure.", "After 8 wk of home training, there was a significant increase in a novel parameter sustained maximal inspiratory pressure.", "After 8 wk of home training, there was a significant increase in forced expiratory volume in 1 s.", "After 8 wk of home training, there was a significant increase in total lung capacity.", "After 8 wk of home training, there was a significant increase in forced vital capacity.", "After 8 wk of home training, there was a significant increase in peak expiratory flow.", "After 8 wk of home training, there was a significant increase in inspiratory capacity.", "There was an improvement in the perception of dyspnea according to the COPD Assessment Test.", "There was an improvement in the perception of dyspnea according to the modified Medical Research Council Breathlessness Scale.", "There was an increase in exercise tolerance according to the 6-min walking test.", "There was a decrease in the exercise capacity index as a predictor of prognosis."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 71-year-old man.", "The patient has severe COPD.", "The patient has rapidly progressing dyspnea.", "The patient has low exercise tolerance.", "The patient has hypoxemia.", "The patient was diagnosed with COPD in 2010.", "Over the last 5 years, the patient experienced a gradual progression of dyspnea.", "The dyspnea limited the patient's performance of everyday activities.", "In 2019, the patient underwent Bentall\u2019s heart surgery with resection of the left atrial appendage.", "The patient did not claim any diseases of affluence.", "The patient has a 30 pack-year history.", "The patient has not smoked since 2008.", "The patient works as a managing director.", "The patient denies any risk factors for lung disease from his occupation.", "The patient\u2019s father contracted tuberculosis after the Second World War.", "The patient\u2019s father died of lung cancer.", "The patient\u2019s brother has diabetes mellitus.", "The patient was afebrile.", "The patient had alveolar respiration.", "The patient had sinus rhythm.", "The patient\u2019s lower limbs were without swelling.", "Alpha1-antitrypsin levels were normal.", "Arterial blood gas examination showed an oxygen partial pressure pO2 = 7.67 kPa.", "Arterial blood gas examination showed a carbon dioxide partial pressure pCO2 = 4.56 kPa.", "Arterial blood gas examination showed a pH = 7.46.", "Arterial blood gas examination showed blood saturation SpO2 = 90%.", "Computed tomography results demonstrated centrilobular emphysema bilaterally.", "The centrilobular emphysema reflects a severe obstructive ventilation disorder.", "The patient underwent spirometry and body plethysmography examinations.", "Forced expiratory volume in 1 s was 1.07 L.", "Forced vital capacity was 1.94 L.", "Inspiratory capacity was 1.57 L.", "Total lung capacity (TLC) was 5.51 L.", "Peak expiratory flow was 3.38 L.", "Inspiratory muscle performance was examined with the PrO2 device.", "Maximal inspiratory pressure (MIP) was 57 cmH2O.", "Sustained maximal inspiratory pressure (SMIP) was 404 PTU.", "Inspiratory duration (ID) was 7.7s.", "Fatigue index test (FIT) was 12.1.", "The COPD Assessment Test score was 15.", "The modified Medical Research Council Breathlessness score was 3.", "The six-minute walk test (6-MWT) was used to assess exercise tolerance.", "The distance walked during the 6-MWT was 270 m.", "Oxygen saturation decreased from 95% at baseline to 75% during the 6-MWT.", "The BODE index was used as a predictor of prognosis.", "The initial BODE index score was 5.", "The Charlson Comorbidity Index calculated the 10-year mortality risk to be 53%."], "index": 66, "original_id": "multiclinsum_test_1605_en.txt", "split": "test", "summary_subclaims": ["The patient was a 71-year-old man with severe COPD, Global Initiative for Obstructive Lung Diseases stage 3.", "The patient underwent an 8-wk remotely monitored inspiratory muscle training with a device based on the test of incremental respiratory endurance method.", "Spirometry was performed as part of the initial and final examination.", "Body plethysmography was performed as part of the initial and final examination.", "The test of incremental respiratory endurance examination was performed as part of the initial and final examination.", "The 6-min walking test was performed as part of the initial and final examination.", "Body mass index was measured as part of the initial and final examination.", "Airflow obstruction was assessed as part of the initial and final examination.", "Dyspnea was assessed as part of the initial and final examination.", "Exercise capacity index was measured as part of the initial and final examination.", "Subjective perception of dyspnea was assessed as part of the initial and final examination.", "The patient performed training at home.", "The physiotherapist monitored the patient remotely through a web application.", "The web application allowed the physiotherapist to evaluate all training parameters in real-time.", "The web application allowed the physiotherapist to respond to any problems.", "After 8 wk of home training, there was a significant increase in maximal inspiratory pressure.", "After 8 wk of home training, there was a significant increase in a novel parameter sustained maximal inspiratory pressure.", "After 8 wk of home training, there was a significant increase in forced expiratory volume in 1 s.", "After 8 wk of home training, there was a significant increase in total lung capacity.", "After 8 wk of home training, there was a significant increase in forced vital capacity.", "After 8 wk of home training, there was a significant increase in peak expiratory flow.", "After 8 wk of home training, there was a significant increase in inspiratory capacity.", "There was an improvement in the perception of dyspnea according to the COPD Assessment Test.", "There was an improvement in the perception of dyspnea according to the modified Medical Research Council Breathlessness Scale.", "There was an increase in exercise tolerance according to the 6-min walking test.", "There was a decrease in the exercise capacity index as a predictor of prognosis."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 38-year-old female.", "She presented to the emergency department in September 2019.", "She had a history of exertional shortness of breath since 1 month before admission.", "She had 2 attacks of syncope during the 1 month before admission.", "She reported 8-kg weight loss within the last 2 months.", "On physical examination, her heart rate was 112 beats/min.", "Heart examination revealed a pansystolic murmur at the lower left sternal edge.", "The murmur increased with inspiration.", "The murmur was concordant with tricuspid regurgitation.", "Electrocardiography showed sinus tachycardia.", "Electrocardiography showed right bundle branch block.", "Electrocardiography showed frequent ventricular ectopic rhythm.", "Holter ECG monitoring showed sinus tachycardia reaching 136\u2013140 bpm.", "Transthoracic and transesophageal echocardiography revealed a large mass in the right atrium.", "The mass measured 5.6\u00d73.8 cm.", "The mass originated below the fossa ovalis.", "The mass affected the tricuspid valve.", "The mass extended to the RV wall.", "The mass caused RV outflow obstruction.", "The mass caused pulmonary hypertension.", "The right side of the heart was dilated.", "RV dimension was 3.2 cm.", "RV systolic pressure was 50\u201355 mmHg.", "Hemoglobin was 11.3 g/dL.", "Erythrocyte sedimentation rate was 53 mm/h.", "C-reactive protein was 145 mg/L.", "International normalized ratio was 1.6.", "Alanine transaminase was 61 IU/L.", "Aspartate transaminase was 94 IU/L.", "Serum albumin was 26 g/L.", "Brain-type natriuretic peptide was 822 pg/mL.", "An initial diagnosis of cardiac myxoma was made.", "Surgical resection of the mass was planned.", "The patient underwent cardiac surgery after 4 days of admission.", "Intraoperatively, 400 mL of pericardial effusion was found.", "The mass was attached to the interatrial septum below the fossa ovalis by a thin stalk.", "The mass was resected.", "The base of the stalk was cauterized.", "The patient came out of cardiopulmonary bypass without the need for direct-current shock.", "The patient was intubated for 12 h postoperatively.", "The patient was kept in the intensive care unit for 24 h.", "The mass was sent for histopathologic examination.", "Macroscopic examination showed myxoid areas with other areas of hemorrhage and necrosis.", "Microscopic examination showed stellate myxoma cells with abundant eosinophilic cytoplasm.", "There was no evidence of malignancy.", "The intrapericardial drain was removed on the third postoperative day.", "The patient was discharged without any complications.", "She was seen in the clinic at 1-month, 2-month, 5-month, and 1-year intervals postoperatively.", "She was doing well without any complaint.", "Her liver transaminases returned to normal levels.", "Repeated TTE 5 months and nearly 1 year postoperatively was free of any cardiac masses.", "Repeated TTE showed grade 1 TR.", "The right atrium and right ventricle were still dilated.", "RVSP was 35 mmHg."], "summary_subclaims": ["The patient is a 38-year-old woman.", "She presented with shortness of breath.", "She presented with syncope.", "She was found to have a right atrioventricular myxoma.", "The myxoma was associated with tricuspid regurgitation.", "The myxoma was associated with right-sided heart failure.", "The myxoma was associated with pulmonary hypertension.", "The syncopal attacks resolved completely after tumor resection.", "The shortness of breath resolved completely after tumor resection.", "Tricuspid regurgitation (grade 1) remained as a sequela of delayed presentation.", "Mild pulmonary hypertension (right ventricular systolic pressure 35 mmHg) remained as a sequela of delayed presentation.", "These may be due to recurrent embolization of tumor fragments to segments of the pulmonary artery."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 38-year-old female.", "She presented to the emergency department in September 2019.", "She had a history of exertional shortness of breath since 1 month before admission.", "She had 2 attacks of syncope during the 1 month before admission.", "She reported 8-kg weight loss within the last 2 months.", "On physical examination, her heart rate was 112 beats/min.", "Heart examination revealed a pansystolic murmur at the lower left sternal edge.", "The murmur increased with inspiration.", "The murmur was concordant with tricuspid regurgitation.", "Electrocardiography showed sinus tachycardia.", "Electrocardiography showed right bundle branch block.", "Electrocardiography showed frequent ventricular ectopic rhythm.", "Holter ECG monitoring showed sinus tachycardia reaching 136\u2013140 bpm.", "Transthoracic and transesophageal echocardiography revealed a large mass in the right atrium.", "The mass measured 5.6\u00d73.8 cm.", "The mass originated below the fossa ovalis.", "The mass affected the tricuspid valve.", "The mass extended to the RV wall.", "The mass caused RV outflow obstruction.", "The mass caused pulmonary hypertension.", "The right side of the heart was dilated.", "RV dimension was 3.2 cm.", "RV systolic pressure was 50\u201355 mmHg.", "Hemoglobin was 11.3 g/dL.", "Erythrocyte sedimentation rate was 53 mm/h.", "C-reactive protein was 145 mg/L.", "International normalized ratio was 1.6.", "Alanine transaminase was 61 IU/L.", "Aspartate transaminase was 94 IU/L.", "Serum albumin was 26 g/L.", "Brain-type natriuretic peptide was 822 pg/mL.", "An initial diagnosis of cardiac myxoma was made.", "Surgical resection of the mass was planned.", "The patient underwent cardiac surgery after 4 days of admission.", "Intraoperatively, 400 mL of pericardial effusion was found.", "The mass was attached to the interatrial septum below the fossa ovalis by a thin stalk.", "The mass was resected.", "The base of the stalk was cauterized.", "The patient came out of cardiopulmonary bypass without the need for direct-current shock.", "The patient was intubated for 12 h postoperatively.", "The patient was kept in the intensive care unit for 24 h.", "The mass was sent for histopathologic examination.", "Macroscopic examination showed myxoid areas with other areas of hemorrhage and necrosis.", "Microscopic examination showed stellate myxoma cells with abundant eosinophilic cytoplasm.", "There was no evidence of malignancy.", "The intrapericardial drain was removed on the third postoperative day.", "The patient was discharged without any complications.", "She was seen in the clinic at 1-month, 2-month, 5-month, and 1-year intervals postoperatively.", "She was doing well without any complaint.", "Her liver transaminases returned to normal levels.", "Repeated TTE 5 months and nearly 1 year postoperatively was free of any cardiac masses.", "Repeated TTE showed grade 1 TR.", "The right atrium and right ventricle were still dilated.", "RVSP was 35 mmHg."], "index": 51, "original_id": "multiclinsum_test_3149_en.txt", "split": "test", "summary_subclaims": ["The patient is a 38-year-old woman.", "She presented with shortness of breath.", "She presented with syncope.", "She was found to have a right atrioventricular myxoma.", "The myxoma was associated with tricuspid regurgitation.", "The myxoma was associated with right-sided heart failure.", "The myxoma was associated with pulmonary hypertension.", "The syncopal attacks resolved completely after tumor resection.", "The shortness of breath resolved completely after tumor resection.", "Tricuspid regurgitation (grade 1) remained as a sequela of delayed presentation.", "Mild pulmonary hypertension (right ventricular systolic pressure 35 mmHg) remained as a sequela of delayed presentation.", "These may be due to recurrent embolization of tumor fragments to segments of the pulmonary artery."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 77-year-old African American woman.", "The patient has a medical history of hypertension.", "The patient's systolic blood pressure was 200 mmHg.", "A renal ultrasound showed a 12 \u00d7 9 \u00d7 7.5 cm mass medial to the left kidney.", "A follow-up CT scan showed an enhancing 9 \u00d7 6 cm mass anterior and medial to the left kidney.", "The dexamethasone suppression test was normal.", "The androstenedione level was 182 ng/dl.", "An androgen-producing adrenal tumor was suspected.", "The differential diagnosis included pheochromocytoma, lymphoma, and mesenteric gastrointestinal stromal tumor.", "The patient underwent robotic-assisted left adrenalectomy.", "The intraoperative finding of 'focal invasion' into the renal parenchyma raised the possibility of adrenal cortical carcinoma.", "An additional left upper pole partial nephrectomy was performed.", "The specimen received was an 11 \u00d7 7.2 \u00d7 6.8 cm adrenal mass with attached portion of kidney.", "The mass was golden yellow, well circumscribed, and grossly adherent to the kidney.", "Histologic evaluation revealed an adrenal cortical adenoma without any features of malignancy.", "The Weiss score was 0.", "The adjacent adrenal parenchyma shared an incomplete capsule with the kidney.", "The adjacent adrenal parenchyma was in direct contact with the renal cortex.", "The diagnosis was fusion between the adrenal gland and the kidney.", "The postoperative course was uneventful."], "summary_subclaims": ["The patient is a 77-year-old African American female.", "The patient presented with a systolic blood pressure of 200\u00a0mmHg.", "Computed tomography showed an enhancing 9\u00a0\u00d7\u20096\u00a0cm mass anterior and medial to the left kidney.", "The patient underwent a left adrenalectomy with partial nephrectomy.", "Gross and histologic examinations revealed an adrenal cortical adenoma.", "Gross and histologic examinations revealed renal-adrenal fusion."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 77-year-old African American woman.", "The patient has a medical history of hypertension.", "The patient's systolic blood pressure was 200 mmHg.", "A renal ultrasound showed a 12 \u00d7 9 \u00d7 7.5 cm mass medial to the left kidney.", "A follow-up CT scan showed an enhancing 9 \u00d7 6 cm mass anterior and medial to the left kidney.", "The dexamethasone suppression test was normal.", "The androstenedione level was 182 ng/dl.", "An androgen-producing adrenal tumor was suspected.", "The differential diagnosis included pheochromocytoma, lymphoma, and mesenteric gastrointestinal stromal tumor.", "The patient underwent robotic-assisted left adrenalectomy.", "The intraoperative finding of 'focal invasion' into the renal parenchyma raised the possibility of adrenal cortical carcinoma.", "An additional left upper pole partial nephrectomy was performed.", "The specimen received was an 11 \u00d7 7.2 \u00d7 6.8 cm adrenal mass with attached portion of kidney.", "The mass was golden yellow, well circumscribed, and grossly adherent to the kidney.", "Histologic evaluation revealed an adrenal cortical adenoma without any features of malignancy.", "The Weiss score was 0.", "The adjacent adrenal parenchyma shared an incomplete capsule with the kidney.", "The adjacent adrenal parenchyma was in direct contact with the renal cortex.", "The diagnosis was fusion between the adrenal gland and the kidney.", "The postoperative course was uneventful."], "index": 69, "original_id": "multiclinsum_test_1363_en.txt", "split": "test", "summary_subclaims": ["The patient is a 77-year-old African American female.", "The patient presented with a systolic blood pressure of 200\u00a0mmHg.", "Computed tomography showed an enhancing 9\u00a0\u00d7\u20096\u00a0cm mass anterior and medial to the left kidney.", "The patient underwent a left adrenalectomy with partial nephrectomy.", "Gross and histologic examinations revealed an adrenal cortical adenoma.", "Gross and histologic examinations revealed renal-adrenal fusion."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 61-year-old obese male.", "The patient underwent laparoscopic partial nephrectomy.", "The tumor was found incidentally during a work-up for hypertension.", "The tumor was located in the left kidney.", "Microscopic examination of the tumor revealed chromophobe renal cell carcinoma.", "After one year of surveillance, a tumor was found in the left seminal vesicle.", "MRI showed a well-circumscribed heterogeneous solid tumor in the left seminal vesicle.", "The tumor measured 32 mm across its largest dimension.", "The tumor had well-defined cleavage planes with the rectum and bladder walls.", "The patient underwent laparoscopic surgical excision of the left seminal vesicle.", "Grossly, the seminal vesicle measured 6 x 3 x 2 cm.", "The cut surface showed a solid, well-circumscribed, brownish and smooth nodule.", "The nodule measured 30 mm across its largest dimension.", "The surgical margins were free from tumor.", "Microscopic examination disclosed well-defined nests of cuboidal cells.", "The nests were separated by vascular fibrous septa.", "There was no evidence of vascular invasion.", "There were no mitotic figures.", "There was no necrosis.", "Gland-like structures were identified focally.", "The tumor cells had a large central nucleus.", "The tumor cells had small to medium-sized nucleoli.", "The tumor cells had granular eosinophilic cytoplasm.", "The diagnostic possibilities included metastasis of the previous chromophobe renal cell carcinoma.", "The diagnostic possibilities included adenocarcinoma of the seminal vesicle.", "The diagnostic possibilities included paraganglioma.", "Immunohistochemical characterization was used for the differential diagnosis.", "The tumor cells were immunoreactive for chromogranin.", "The tumor cells were immunoreactive for synaptophysin.", "S100 protein-positive cells were identified at the periphery of the tumor nests.", "The tumor cells did not express keratins (AE1/AE3, CK7 and CK8/18).", "The absence of keratin immunoreactivity ruled out the hypothesis of primary or metastatic carcinoma.", "The diagnosis was supported as seminal vesicle paraganglioma.", "The Ki-67 labeling index was less than 2%.", "VHL and SDHB mutations were investigated using genomic DNA.", "No genetic alterations were found in the VHL gene.", "No genetic alterations were found in the SDHB gene.", "Thorough imaging analysis showed no tumor elsewhere.", "The diagnosis was reinforced as primary seminal vesicle paraganglioma.", "The patient is still alive after 14 months of follow-up.", "The patient's blood pressure is under control."], "summary_subclaims": ["This report describes, for the first time to the best of our knowledge, a primary paraganglioma of the seminal vesicle occurring in a 61-year-old male.", "The patient presented persistent arterial hypertension.", "The patient had a previous diagnosis of chromophobe renal cell carcinoma.", "It was hypothesized that the seminal vesicle tumor could be a metastasis from the chromophobe renal cell carcinoma.", "Immunohistochemical characterization revealed expression of synaptophysin and chromogranin in tumor cell nests.", "Immunohistochemical characterization revealed peripheral S100 protein expression in sustentacular cells.", "Succinate dehydrogenase A and B-related (SDHA and SDHB) expression was present in both tumors."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 61-year-old obese male.", "The patient underwent laparoscopic partial nephrectomy.", "The tumor was found incidentally during a work-up for hypertension.", "The tumor was located in the left kidney.", "Microscopic examination of the tumor revealed chromophobe renal cell carcinoma.", "After one year of surveillance, a tumor was found in the left seminal vesicle.", "MRI showed a well-circumscribed heterogeneous solid tumor in the left seminal vesicle.", "The tumor measured 32 mm across its largest dimension.", "The tumor had well-defined cleavage planes with the rectum and bladder walls.", "The patient underwent laparoscopic surgical excision of the left seminal vesicle.", "Grossly, the seminal vesicle measured 6 x 3 x 2 cm.", "The cut surface showed a solid, well-circumscribed, brownish and smooth nodule.", "The nodule measured 30 mm across its largest dimension.", "The surgical margins were free from tumor.", "Microscopic examination disclosed well-defined nests of cuboidal cells.", "The nests were separated by vascular fibrous septa.", "There was no evidence of vascular invasion.", "There were no mitotic figures.", "There was no necrosis.", "Gland-like structures were identified focally.", "The tumor cells had a large central nucleus.", "The tumor cells had small to medium-sized nucleoli.", "The tumor cells had granular eosinophilic cytoplasm.", "The diagnostic possibilities included metastasis of the previous chromophobe renal cell carcinoma.", "The diagnostic possibilities included adenocarcinoma of the seminal vesicle.", "The diagnostic possibilities included paraganglioma.", "Immunohistochemical characterization was used for the differential diagnosis.", "The tumor cells were immunoreactive for chromogranin.", "The tumor cells were immunoreactive for synaptophysin.", "S100 protein-positive cells were identified at the periphery of the tumor nests.", "The tumor cells did not express keratins (AE1/AE3, CK7 and CK8/18).", "The absence of keratin immunoreactivity ruled out the hypothesis of primary or metastatic carcinoma.", "The diagnosis was supported as seminal vesicle paraganglioma.", "The Ki-67 labeling index was less than 2%.", "VHL and SDHB mutations were investigated using genomic DNA.", "No genetic alterations were found in the VHL gene.", "No genetic alterations were found in the SDHB gene.", "Thorough imaging analysis showed no tumor elsewhere.", "The diagnosis was reinforced as primary seminal vesicle paraganglioma.", "The patient is still alive after 14 months of follow-up.", "The patient's blood pressure is under control."], "index": 45, "original_id": "multiclinsum_test_2717_en.txt", "split": "test", "summary_subclaims": ["This report describes, for the first time to the best of our knowledge, a primary paraganglioma of the seminal vesicle occurring in a 61-year-old male.", "The patient presented persistent arterial hypertension.", "The patient had a previous diagnosis of chromophobe renal cell carcinoma.", "It was hypothesized that the seminal vesicle tumor could be a metastasis from the chromophobe renal cell carcinoma.", "Immunohistochemical characterization revealed expression of synaptophysin and chromogranin in tumor cell nests.", "Immunohistochemical characterization revealed peripheral S100 protein expression in sustentacular cells.", "Succinate dehydrogenase A and B-related (SDHA and SDHB) expression was present in both tumors."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 7-year-old male.", "The patient has a diagnosis of acute lymphoid leukemia of T precursors.", "The patient was finishing the cycle of induction chemotherapy with the PETHEMA 2013 protocol.", "The PETHEMA 2013 protocol includes L asparaginase, Vincristine, and Daunorrubicin.", "The PETHEMA 2013 protocol includes continuous prednisone for more than a month.", "The patient developed 12 days of epigastric abdominal pain.", "The patient had occasional vomiting.", "The physical examination showed exquisite pain to palpation in the epigastric region.", "The physical examination showed peristalsis present.", "The physical examination showed no data of obstruction.", "The laboratory examinations showed moderate neutropenia.", "The laboratory examinations showed increased c reactive protein.", "Acute pancreatitis was initially suspected.", "Acute pancreatitis was ruled out as pancreatic enzymes were normal.", "Acute pancreatitis was ruled out as abdominal computed tomography was normal.", "Steroid acid-peptic disease was then suspected.", "Medical treatment with proton pump inhibitors was continued.", "Medical treatment with prokinetic was continued.", "Medical treatment with oral tolerance was continued.", "The next day, the patient presented with increasing abdominal pain at night.", "The next day, the patient had emetic episodes on multiple occasions.", "The next day, the patient had haematemesis.", "The next day, the patient had severe hypokalaemia.", "The next day, the patient had hyperglycaemia.", "The next day, the patient had severe neutropenia.", "The next day, the patient had signs of shock.", "The patient was transferred to the paediatric intensive care unit.", "Emergency esophagogastroduodenoscopy was performed.", "An acute erosive haemorrhagic pangastritis was reported.", "The EGD was consistent with necrotizing gastritis.", "Necrotizing gastritis was confirmed by biopsy.", "Management was initiated with fasting.", "Management was initiated with potassium replacement.", "Management was initiated with fluid replacement.", "Management was initiated with omeprazole in continuous infusion.", "Management was initiated with ondansetron.", "Laboratory tests were negative with no bacterial isolation.", "Blood cultures were negative with no bacterial isolation.", "The patient progressed to catecholamine refractory shock.", "Mechanical ventilation was required.", "Antibiotic management was initiated.", "Multiple vasoactive support with norepinephrine, epinephrine, and vasopressin was initiated.", "The critical condition was overcome.", "Parenteral nutrition was indicated on the second day.", "The EGD on the sixth day showed persistence of necrotizing gastritis.", "Intestinal rest, proton pump inhibitors, and sucralfate were maintained.", "A control EGD was performed 30 days after intestinal rest.", "The control EGD showed significant improvement of extensive necrosis of the body, fundus, and gastric antrum.", "The control EGD showed persistence of necrosis area that compromised 20% of the greater curvature of the gastric body.", "The start of enteral nutrition was evaluated.", "The enteral nutrition was a polymeric diet.", "The start of enteral nutrition progressed to bland diet without irritants or lactose.", "The enteral nutrition was initiated orally.", "The patient had adequate intrahospital tolerance for 72 hours.", "Hospital discharge was indicated.", "Double dose of proton pump inhibitors was prescribed.", "Sucralfate was prescribed.", "Attention to warning signs was advised.", "On control at 2 months of discharge, the patient was hemodynamically stable.", "The control EGD showed complete improvement of the necrotizing gastritis.", "The control EGD showed remaining areas of fibrosis at the level of the corpus antrum region.", "Chemotherapy treatment was postponed for a month and a half.", "The same high-risk PETHEMA protocol was initiated.", "In the intensification stage, the doses were reduced to 50% of the cytostatic.", "In the next stage, the protocol was continued with the usual dose.", "End of treatment studies were done.", "The patient is in complete remission.", "The patient has no complications associated with the underlying pathology.", "The patient has been in remission for two years."], "summary_subclaims": ["The patient is a 7-year-old male.", "The patient has a diagnosis of acute lymphoid T-cell leukemia.", "The patient completed a cycle of induction chemotherapy with the PETHEMA 2013 protocol.", "The patient had epigastric abdominal pain for 12 days.", "The patient had vomiting for 12 days.", "Acute pancreatitis was initially suspected.", "Acute pancreatitis was ruled out by normal pancreatic enzymes.", "Acute pancreatitis was ruled out by abdominal computed tomography.", "Treatment with proton pump inhibitors was initiated.", "Treatment with procinetics was initiated.", "An esophagogastroduodenoscopy was performed.", "The esophagogastroduodenoscopy was compatible with necrotizing gastritis.", "Necrotizing gastritis was confirmed by histopathology.", "Pharmacological management was provided.", "A zero regimen was provided.", "Parenteral support was provided.", "Progressive improvement was evidenced in imaging controls.", "Fasting lasted 30 days.", "Enteral nutrition was initiated after fasting.", "Enteral nutrition was well tolerated.", "The chemotherapy plan was completed after improvement.", "Complete remission was achieved.", "There were no complications after 2 years."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 7-year-old male.", "The patient has a diagnosis of acute lymphoid leukemia of T precursors.", "The patient was finishing the cycle of induction chemotherapy with the PETHEMA 2013 protocol.", "The PETHEMA 2013 protocol includes L asparaginase, Vincristine, and Daunorrubicin.", "The PETHEMA 2013 protocol includes continuous prednisone for more than a month.", "The patient developed 12 days of epigastric abdominal pain.", "The patient had occasional vomiting.", "The physical examination showed exquisite pain to palpation in the epigastric region.", "The physical examination showed peristalsis present.", "The physical examination showed no data of obstruction.", "The laboratory examinations showed moderate neutropenia.", "The laboratory examinations showed increased c reactive protein.", "Acute pancreatitis was initially suspected.", "Acute pancreatitis was ruled out as pancreatic enzymes were normal.", "Acute pancreatitis was ruled out as abdominal computed tomography was normal.", "Steroid acid-peptic disease was then suspected.", "Medical treatment with proton pump inhibitors was continued.", "Medical treatment with prokinetic was continued.", "Medical treatment with oral tolerance was continued.", "The next day, the patient presented with increasing abdominal pain at night.", "The next day, the patient had emetic episodes on multiple occasions.", "The next day, the patient had haematemesis.", "The next day, the patient had severe hypokalaemia.", "The next day, the patient had hyperglycaemia.", "The next day, the patient had severe neutropenia.", "The next day, the patient had signs of shock.", "The patient was transferred to the paediatric intensive care unit.", "Emergency esophagogastroduodenoscopy was performed.", "An acute erosive haemorrhagic pangastritis was reported.", "The EGD was consistent with necrotizing gastritis.", "Necrotizing gastritis was confirmed by biopsy.", "Management was initiated with fasting.", "Management was initiated with potassium replacement.", "Management was initiated with fluid replacement.", "Management was initiated with omeprazole in continuous infusion.", "Management was initiated with ondansetron.", "Laboratory tests were negative with no bacterial isolation.", "Blood cultures were negative with no bacterial isolation.", "The patient progressed to catecholamine refractory shock.", "Mechanical ventilation was required.", "Antibiotic management was initiated.", "Multiple vasoactive support with norepinephrine, epinephrine, and vasopressin was initiated.", "The critical condition was overcome.", "Parenteral nutrition was indicated on the second day.", "The EGD on the sixth day showed persistence of necrotizing gastritis.", "Intestinal rest, proton pump inhibitors, and sucralfate were maintained.", "A control EGD was performed 30 days after intestinal rest.", "The control EGD showed significant improvement of extensive necrosis of the body, fundus, and gastric antrum.", "The control EGD showed persistence of necrosis area that compromised 20% of the greater curvature of the gastric body.", "The start of enteral nutrition was evaluated.", "The enteral nutrition was a polymeric diet.", "The start of enteral nutrition progressed to bland diet without irritants or lactose.", "The enteral nutrition was initiated orally.", "The patient had adequate intrahospital tolerance for 72 hours.", "Hospital discharge was indicated.", "Double dose of proton pump inhibitors was prescribed.", "Sucralfate was prescribed.", "Attention to warning signs was advised.", "On control at 2 months of discharge, the patient was hemodynamically stable.", "The control EGD showed complete improvement of the necrotizing gastritis.", "The control EGD showed remaining areas of fibrosis at the level of the corpus antrum region.", "Chemotherapy treatment was postponed for a month and a half.", "The same high-risk PETHEMA protocol was initiated.", "In the intensification stage, the doses were reduced to 50% of the cytostatic.", "In the next stage, the protocol was continued with the usual dose.", "End of treatment studies were done.", "The patient is in complete remission.", "The patient has no complications associated with the underlying pathology.", "The patient has been in remission for two years."], "index": 68, "original_id": "multiclinsum_test_3042_en.txt", "split": "test", "summary_subclaims": ["The patient is a 7-year-old male.", "The patient has a diagnosis of acute lymphoid T-cell leukemia.", "The patient completed a cycle of induction chemotherapy with the PETHEMA 2013 protocol.", "The patient had epigastric abdominal pain for 12 days.", "The patient had vomiting for 12 days.", "Acute pancreatitis was initially suspected.", "Acute pancreatitis was ruled out by normal pancreatic enzymes.", "Acute pancreatitis was ruled out by abdominal computed tomography.", "Treatment with proton pump inhibitors was initiated.", "Treatment with procinetics was initiated.", "An esophagogastroduodenoscopy was performed.", "The esophagogastroduodenoscopy was compatible with necrotizing gastritis.", "Necrotizing gastritis was confirmed by histopathology.", "Pharmacological management was provided.", "A zero regimen was provided.", "Parenteral support was provided.", "Progressive improvement was evidenced in imaging controls.", "Fasting lasted 30 days.", "Enteral nutrition was initiated after fasting.", "Enteral nutrition was well tolerated.", "The chemotherapy plan was completed after improvement.", "Complete remission was achieved.", "There were no complications after 2 years."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 24-year-old male.", "The patient complains of a history of sore throat.", "The patient complains of malaise.", "The patient complains of fever.", "The patient complains of neck and facial swelling.", "The patient has a normal consciousness level.", "On examination, there is tonsilar swelling.", "On examination, there is tonsilar tenderness.", "On examination, there is bilateral cervical lymphadenopathy.", "The blood pressure is normal.", "The heart rate is normal.", "The patient has no previous history of chronic disease.", "The patient has no previous history of chronic drug usage.", "The patient has no previous history of allergy.", "A laboratory examination showed leukocytosis.", "A laboratory examination showed high C-reactive protein serum.", "An ultrasound examination demonstrates left jugular vein thrombosis.", "Contrast-enhanced neck Computed tomography reveals fluid and air density collections.", "Contrast-enhanced neck Computed tomography reveals soft tissue phlegmon formation in the anterior cervical region.", "Contrast-enhanced neck Computed tomography reveals soft tissue phlegmon formation in both soft tissue of the anterior mandibular ramus.", "Contrast-enhanced neck Computed tomography reveals soft tissue phlegmon formation in the peritonsillar area.", "Contrast-enhanced neck Computed tomography reveals soft tissue phlegmon formation in the left parapharyngeal area.", "Contrast-enhanced neck Computed tomography reveals soft tissue phlegmon formation in the left carotid space.", "Contrast-enhanced neck Computed tomography reveals left jugular vein thrombosis.", "Preliminary differential diagnoses reveal Ludwig's angina.", "Preliminary differential diagnoses reveal Lemierre's syndrome.", "The patient underwent surgical drainage in the ENT department.", "The patient was treated with Penicillin g 1.2 unit 1 \u00d7 1 im for one dose.", "The patient was treated with metrodenzol 3 \u00d7 1 iv.", "The patient was treated with unacefen 1g 2 \u00d7 1.", "The patient was treated with Clexane 4000 IU 1 \u00d7 1.", "The blood culture was positive for Fusobacterium necrophorum.", "The patient develops headaches after 10 days.", "The patient develops fever after 10 days.", "A contrast-enhanced MRI showed an intracranial epidural abscess on the left side of the brain.", "The patient was added to the treatment with intravenous clindamycin 600mg 1 \u00d7 3.", "The patient was added to the treatment with intravenous vancomycin 1g 3 \u00d7 1.", "After 45 days, the patient improved clinically.", "The patient was discharged for a home treatment regimen with clavulanate 1000 mg 1 \u00d7 2.", "The patient was discharged for a home treatment regimen with metro 500mg 1 \u00d7 3.", "The patient was discharged for a home treatment regimen with warfarin 5 mg 1 \u00d7 1.", "There were no other symptoms after a one-month follow-up.", "There were no other symptoms after a one-month follow-up with neck ultrasonography.", "This work has been reported in line with the SCARE 2020."], "summary_subclaims": ["The patient was a 24-year-old male.", "The patient came to the emergency department.", "The patient complained of a history of a sore throat.", "The patient complained of fever.", "The patient complained of malaise.", "The patient complained of neck swelling.", "The patient had a normal consciousness level.", "A laboratory examination showed leukocytosis.", "A laboratory examination showed high C-reactive protein serum.", "Radiological diagnosis revealed an anterior neck abscess.", "Radiological diagnosis revealed left jugular vein thrombosis.", "Radiological diagnosis revealed left epidural abscess.", "The blood culture was positive for Fusobacterium necrophorum.", "The patient underwent surgical drainage.", "The patient was treated with antibiotics.", "The patient was treated with anticoagulant drugs.", "After 45 days, the patient improved clinically.", "The patient was discharged.", "There were no other symptoms after a one-month follow-up.", "Neck ultrasonography was performed."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 24-year-old male.", "The patient complains of a history of sore throat.", "The patient complains of malaise.", "The patient complains of fever.", "The patient complains of neck and facial swelling.", "The patient has a normal consciousness level.", "On examination, there is tonsilar swelling.", "On examination, there is tonsilar tenderness.", "On examination, there is bilateral cervical lymphadenopathy.", "The blood pressure is normal.", "The heart rate is normal.", "The patient has no previous history of chronic disease.", "The patient has no previous history of chronic drug usage.", "The patient has no previous history of allergy.", "A laboratory examination showed leukocytosis.", "A laboratory examination showed high C-reactive protein serum.", "An ultrasound examination demonstrates left jugular vein thrombosis.", "Contrast-enhanced neck Computed tomography reveals fluid and air density collections.", "Contrast-enhanced neck Computed tomography reveals soft tissue phlegmon formation in the anterior cervical region.", "Contrast-enhanced neck Computed tomography reveals soft tissue phlegmon formation in both soft tissue of the anterior mandibular ramus.", "Contrast-enhanced neck Computed tomography reveals soft tissue phlegmon formation in the peritonsillar area.", "Contrast-enhanced neck Computed tomography reveals soft tissue phlegmon formation in the left parapharyngeal area.", "Contrast-enhanced neck Computed tomography reveals soft tissue phlegmon formation in the left carotid space.", "Contrast-enhanced neck Computed tomography reveals left jugular vein thrombosis.", "Preliminary differential diagnoses reveal Ludwig's angina.", "Preliminary differential diagnoses reveal Lemierre's syndrome.", "The patient underwent surgical drainage in the ENT department.", "The patient was treated with Penicillin g 1.2 unit 1 \u00d7 1 im for one dose.", "The patient was treated with metrodenzol 3 \u00d7 1 iv.", "The patient was treated with unacefen 1g 2 \u00d7 1.", "The patient was treated with Clexane 4000 IU 1 \u00d7 1.", "The blood culture was positive for Fusobacterium necrophorum.", "The patient develops headaches after 10 days.", "The patient develops fever after 10 days.", "A contrast-enhanced MRI showed an intracranial epidural abscess on the left side of the brain.", "The patient was added to the treatment with intravenous clindamycin 600mg 1 \u00d7 3.", "The patient was added to the treatment with intravenous vancomycin 1g 3 \u00d7 1.", "After 45 days, the patient improved clinically.", "The patient was discharged for a home treatment regimen with clavulanate 1000 mg 1 \u00d7 2.", "The patient was discharged for a home treatment regimen with metro 500mg 1 \u00d7 3.", "The patient was discharged for a home treatment regimen with warfarin 5 mg 1 \u00d7 1.", "There were no other symptoms after a one-month follow-up.", "There were no other symptoms after a one-month follow-up with neck ultrasonography.", "This work has been reported in line with the SCARE 2020."], "index": 63, "original_id": "multiclinsum_test_1379_en.txt", "split": "test", "summary_subclaims": ["The patient was a 24-year-old male.", "The patient came to the emergency department.", "The patient complained of a history of a sore throat.", "The patient complained of fever.", "The patient complained of malaise.", "The patient complained of neck swelling.", "The patient had a normal consciousness level.", "A laboratory examination showed leukocytosis.", "A laboratory examination showed high C-reactive protein serum.", "Radiological diagnosis revealed an anterior neck abscess.", "Radiological diagnosis revealed left jugular vein thrombosis.", "Radiological diagnosis revealed left epidural abscess.", "The blood culture was positive for Fusobacterium necrophorum.", "The patient underwent surgical drainage.", "The patient was treated with antibiotics.", "The patient was treated with anticoagulant drugs.", "After 45 days, the patient improved clinically.", "The patient was discharged.", "There were no other symptoms after a one-month follow-up.", "Neck ultrasonography was performed."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["A 4-year-old boy was admitted because of persistent lower limb pain and claudication in the left lower limb over the past 9 mo.", "The patient had mild persistent lower limb pain and claudication without any inducement.", "Claudication worsened in one day.", "The child had no fever, urinary frequency or urgency, numbness, fatigue, or lameness.", "He was admitted to our joint hand surgery department.", "The child had no history past illness.", "The child had no history of family illness, and his medical history was unremarkable.", "Pressing pain and local swelling were present in the left shank.", "The results of sensation and strengthening test, and tendon reflex test were normal in both lower limbs.", "No pathological signs were observed upon physical examination.", "Laboratory examinations were normal.", "Preoperative imaging examinations showed erosion-like changes with bone expansion of the left middle and lower fibular segment.", "No invasion of circumferential soft tissue or pathological fracture of the lesion site was observed.", "Initial pathological examination revealed fibular fibrous dysplasia.", "Postoperative photography showed that an allograft bone was implanted into the fibular medullary cavity.", "Recurrent fibular fibrous dysplasia was observed at the age of 6 years."], "summary_subclaims": ["A 4-year-old boy was admitted for persistent pain in the left lower limb and abnormal gait over the previous 9 mo.", "He had no history of present or past illness.", "Preoperative imaging data showed erosion-like changes with bone expansion of the left middle and lower fibular segment.", "Tumor tissue in the fibular bone marrow cavity was removed by curettage.", "Rapid intraoperative pathological examination suggested fibular fibrous dysplasia.", "An allograft was implanted into the fibular medullary cavity.", "He was readmitted with clinical symptoms including persistent pain, abnormal gait, and local swelling at the age of 6 years.", "He was diagnosed with recurrent fibular fibrous dysplasia based on the second medical examination.", "He underwent fibular bone tumor radical resection and longus fibular allograft transplantation combined with fibular bone locking plate and screws.", "Good host bone to allogenic bone graft fusion was observed by the physician on postoperative regular follow-up."]}, "extra_info": {"fulltext_subclaims": ["A 4-year-old boy was admitted because of persistent lower limb pain and claudication in the left lower limb over the past 9 mo.", "The patient had mild persistent lower limb pain and claudication without any inducement.", "Claudication worsened in one day.", "The child had no fever, urinary frequency or urgency, numbness, fatigue, or lameness.", "He was admitted to our joint hand surgery department.", "The child had no history past illness.", "The child had no history of family illness, and his medical history was unremarkable.", "Pressing pain and local swelling were present in the left shank.", "The results of sensation and strengthening test, and tendon reflex test were normal in both lower limbs.", "No pathological signs were observed upon physical examination.", "Laboratory examinations were normal.", "Preoperative imaging examinations showed erosion-like changes with bone expansion of the left middle and lower fibular segment.", "No invasion of circumferential soft tissue or pathological fracture of the lesion site was observed.", "Initial pathological examination revealed fibular fibrous dysplasia.", "Postoperative photography showed that an allograft bone was implanted into the fibular medullary cavity.", "Recurrent fibular fibrous dysplasia was observed at the age of 6 years."], "index": 65, "original_id": "multiclinsum_test_1596_en.txt", "split": "test", "summary_subclaims": ["A 4-year-old boy was admitted for persistent pain in the left lower limb and abnormal gait over the previous 9 mo.", "He had no history of present or past illness.", "Preoperative imaging data showed erosion-like changes with bone expansion of the left middle and lower fibular segment.", "Tumor tissue in the fibular bone marrow cavity was removed by curettage.", "Rapid intraoperative pathological examination suggested fibular fibrous dysplasia.", "An allograft was implanted into the fibular medullary cavity.", "He was readmitted with clinical symptoms including persistent pain, abnormal gait, and local swelling at the age of 6 years.", "He was diagnosed with recurrent fibular fibrous dysplasia based on the second medical examination.", "He underwent fibular bone tumor radical resection and longus fibular allograft transplantation combined with fibular bone locking plate and screws.", "Good host bone to allogenic bone graft fusion was observed by the physician on postoperative regular follow-up."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 53-year-old female.", "She has a long history of low back pain.", "She had undergone an L5-S1 discectomy 11 years ago.", "She had undergone an L4-L5 decompressive laminectomy 2 years ago.", "She presented with an acute cauda equina syndrome.", "The acute cauda equina syndrome was characterized by paraparesis.", "The acute cauda equina syndrome was characterized by acute urinary incontinence.", "On examination, she had mild tenderness over the lower back region.", "Laboratory tests revealed a white blood cell count of 12,600/mm3.", "Laboratory tests revealed a high C-reactive protein level.", "Plain X-rays showed laminectomy defects from L4 to L5.", "The MRI showed an oblong posterior epidural lesion compressing the thecal sac from L4 to S1.", "The lesion was hypointense on T1-weighted images.", "The lesion was hyperintense on T2-weighted images.", "The lesion demonstrated ring enhancement with gadolinium injection.", "An epidural abscess was suspected.", "She underwent a decompressive laminectomy.", "At surgery, there was an encapsulated posterior epidural abscess that required drainage.", "A granulomatous lesion was noted at the antero-inferior part of the abscess wall at the level of S1.", "The granulomatous lesion was completely removed.", "The granulomatous lesion was unsuspected surgical cottonoid.", "Culture of the capsule revealed Klebsiella oxytoca.", "The infection required 2 months of ciprofloxacin.", "The infection fully resolved.", "The patient's paraparesis only partially recovered.", "The histopathological examination confirmed a textiloma.", "There was chronic inflammation and fibrosis surrounding the retained cottonoid.", "After the first postoperative year, there was no evidence of infection recurrence."], "summary_subclaims": ["The patient is a 53-year-old female.", "The patient had two prior spinal operations at the L4-S1 levels.", "The prior spinal operations were 11 and 2 years previously.", "The patient presented over a few weeks with the acute onset of a cauda equina syndrome.", "The cauda equina syndrome included paraparesis and acute urinary incontinence.", "The patient had a mildly elevated white blood cell count of 12,600/mm3.", "The patient had an abnormally increased C-reactive protein level.", "Magnetic resonance imaging showed a dorsal epidural abscess extending from the L4 to S1 levels.", "At surgery, an encapsulated posterior epidural abscess was drained.", "Surgical findings included a granulomatous lesion consistent with a retained surgical cottonoid.", "The granulomatous lesion was removed from the antero-inferior portion of the abscess wall at S1.", "Culture of the thick fibrotic abscess wall grew Klebsiella oxytoca.", "After 2 months of ciprofloxacin, the patient's infection cleared.", "The motor deficit only partially resolved."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 53-year-old female.", "She has a long history of low back pain.", "She had undergone an L5-S1 discectomy 11 years ago.", "She had undergone an L4-L5 decompressive laminectomy 2 years ago.", "She presented with an acute cauda equina syndrome.", "The acute cauda equina syndrome was characterized by paraparesis.", "The acute cauda equina syndrome was characterized by acute urinary incontinence.", "On examination, she had mild tenderness over the lower back region.", "Laboratory tests revealed a white blood cell count of 12,600/mm3.", "Laboratory tests revealed a high C-reactive protein level.", "Plain X-rays showed laminectomy defects from L4 to L5.", "The MRI showed an oblong posterior epidural lesion compressing the thecal sac from L4 to S1.", "The lesion was hypointense on T1-weighted images.", "The lesion was hyperintense on T2-weighted images.", "The lesion demonstrated ring enhancement with gadolinium injection.", "An epidural abscess was suspected.", "She underwent a decompressive laminectomy.", "At surgery, there was an encapsulated posterior epidural abscess that required drainage.", "A granulomatous lesion was noted at the antero-inferior part of the abscess wall at the level of S1.", "The granulomatous lesion was completely removed.", "The granulomatous lesion was unsuspected surgical cottonoid.", "Culture of the capsule revealed Klebsiella oxytoca.", "The infection required 2 months of ciprofloxacin.", "The infection fully resolved.", "The patient's paraparesis only partially recovered.", "The histopathological examination confirmed a textiloma.", "There was chronic inflammation and fibrosis surrounding the retained cottonoid.", "After the first postoperative year, there was no evidence of infection recurrence."], "index": 83, "original_id": "multiclinsum_test_2689_en.txt", "split": "test", "summary_subclaims": ["The patient is a 53-year-old female.", "The patient had two prior spinal operations at the L4-S1 levels.", "The prior spinal operations were 11 and 2 years previously.", "The patient presented over a few weeks with the acute onset of a cauda equina syndrome.", "The cauda equina syndrome included paraparesis and acute urinary incontinence.", "The patient had a mildly elevated white blood cell count of 12,600/mm3.", "The patient had an abnormally increased C-reactive protein level.", "Magnetic resonance imaging showed a dorsal epidural abscess extending from the L4 to S1 levels.", "At surgery, an encapsulated posterior epidural abscess was drained.", "Surgical findings included a granulomatous lesion consistent with a retained surgical cottonoid.", "The granulomatous lesion was removed from the antero-inferior portion of the abscess wall at S1.", "Culture of the thick fibrotic abscess wall grew Klebsiella oxytoca.", "After 2 months of ciprofloxacin, the patient's infection cleared.", "The motor deficit only partially resolved."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was a 20-year-old male.", "He fell from a height of about 30 feet.", "He was initially managed at a nearby community hospital.", "He was diagnosed to have multiple rib fractures on both sides.", "He had bilateral hemopneumothorax.", "The primary management was performed with bilateral intercostal chest drains.", "Positive pressure ventilation was used for lung contusion.", "The patient had no neurological deficit at initial presentation.", "He was referred to our center after four weeks.", "On examination, there was tenderness over the tenth thoracic vertebrae.", "There was mild knuckle deformity.", "There was no motor or sensory deficit at any level.", "Superficial and deep tendon reflexes were normal.", "Radiographs showed a fracture dislocation with spondyloptosis of the ninth thoracic vertebra (T9) over the tenth thoracic vertebra (T10).", "The vertebral body of the eighth thoracic vertebra was fractured.", "The pedicles of both T9 and T10 vertebrae were fractured bilaterally.", "The posterior elements were separated from their respective vertebral bodies.", "There was complete spondyloptosis of T9 over T10 vertebral body.", "Both T9 and T10 vertebral bodies could be seen in a single transverse section of computerized tomography.", "The patient was scheduled for surgery after improvement in general and lung condition.", "The spine was approached through a standard posterior midline incision.", "There was no significant kyphosis seen.", "The posterior elements of the eighth and ninth thoracic vertebrae were lying almost in place.", "The fractures in the lamina of the eighth and ninth thoracic vertebrae were undisplaced.", "Pedicle screws were inserted in the fifth, sixth, and seventh thoracic vertebrae proximally.", "Pedicle screws were inserted in the tenth, eleventh, and twelfth thoracic vertebrae distally.", "An in-situ posterior instrumentation with laminectomy of T8 and T9 vertebrae was performed.", "Posterolateral fusion from the fifth to twelfth thoracic vertebrae was performed.", "No attempt was made to reduce spondyloptosis of T9 over the T10 vertebrae.", "The patient tolerated the operation well.", "There was no postoperative neurological deterioration.", "He was mobilized with the help of a customized dorsolumbar rigid orthosis on the fifth postoperative day.", "He was followed up at monthly intervals.", "Radiographs showed satisfactory in situ fusion between T9 and T10 vertebral bodies.", "Computerized tomography showed satisfactory in situ fusion between T9 and T10 vertebral bodies.", "The patient returned to his previous occupation."], "summary_subclaims": ["We reported a four-week spondyloptosis of the ninth thoracic vertebra over the tenth thoracic vertebra.", "The patient was a 20-year-old male.", "The patient had no neurological deficit.", "The patient had associated chest injuries.", "The spine injury was managed surgically with in-situ posterior instrumentation and fusion.", "The patient tolerated the operation well.", "Postoperatively there was no neurological deterioration.", "Postoperatively there was no surgical complication."]}, "extra_info": {"fulltext_subclaims": ["The patient was a 20-year-old male.", "He fell from a height of about 30 feet.", "He was initially managed at a nearby community hospital.", "He was diagnosed to have multiple rib fractures on both sides.", "He had bilateral hemopneumothorax.", "The primary management was performed with bilateral intercostal chest drains.", "Positive pressure ventilation was used for lung contusion.", "The patient had no neurological deficit at initial presentation.", "He was referred to our center after four weeks.", "On examination, there was tenderness over the tenth thoracic vertebrae.", "There was mild knuckle deformity.", "There was no motor or sensory deficit at any level.", "Superficial and deep tendon reflexes were normal.", "Radiographs showed a fracture dislocation with spondyloptosis of the ninth thoracic vertebra (T9) over the tenth thoracic vertebra (T10).", "The vertebral body of the eighth thoracic vertebra was fractured.", "The pedicles of both T9 and T10 vertebrae were fractured bilaterally.", "The posterior elements were separated from their respective vertebral bodies.", "There was complete spondyloptosis of T9 over T10 vertebral body.", "Both T9 and T10 vertebral bodies could be seen in a single transverse section of computerized tomography.", "The patient was scheduled for surgery after improvement in general and lung condition.", "The spine was approached through a standard posterior midline incision.", "There was no significant kyphosis seen.", "The posterior elements of the eighth and ninth thoracic vertebrae were lying almost in place.", "The fractures in the lamina of the eighth and ninth thoracic vertebrae were undisplaced.", "Pedicle screws were inserted in the fifth, sixth, and seventh thoracic vertebrae proximally.", "Pedicle screws were inserted in the tenth, eleventh, and twelfth thoracic vertebrae distally.", "An in-situ posterior instrumentation with laminectomy of T8 and T9 vertebrae was performed.", "Posterolateral fusion from the fifth to twelfth thoracic vertebrae was performed.", "No attempt was made to reduce spondyloptosis of T9 over the T10 vertebrae.", "The patient tolerated the operation well.", "There was no postoperative neurological deterioration.", "He was mobilized with the help of a customized dorsolumbar rigid orthosis on the fifth postoperative day.", "He was followed up at monthly intervals.", "Radiographs showed satisfactory in situ fusion between T9 and T10 vertebral bodies.", "Computerized tomography showed satisfactory in situ fusion between T9 and T10 vertebral bodies.", "The patient returned to his previous occupation."], "index": 61, "original_id": "multiclinsum_test_1749_en.txt", "split": "test", "summary_subclaims": ["We reported a four-week spondyloptosis of the ninth thoracic vertebra over the tenth thoracic vertebra.", "The patient was a 20-year-old male.", "The patient had no neurological deficit.", "The patient had associated chest injuries.", "The spine injury was managed surgically with in-situ posterior instrumentation and fusion.", "The patient tolerated the operation well.", "Postoperatively there was no neurological deterioration.", "Postoperatively there was no surgical complication."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is an 80-year-old woman.", "She has a history of coronary artery disease.", "She has a history of atrial fibrillation.", "She has a history of hypertension.", "She has a history of diabetes mellitus.", "She has a history of basal cell carcinoma removed via Mohs procedure on the nose.", "She has a history of diabetic retinopathy.", "She has a history of macular degeneration.", "She presented with a recent increase in the number of falls.", "The falls were due to a recent, sudden deterioration of vision bilaterally.", "She was initially seen by the ophthalmologist 2 months ago for loss of vision in her right eye.", "The loss of vision in her right eye was thought to be related to previously diagnosed diabetic retinopathy.", "She underwent focal laser photocoagulation for diabetic retinopathy in her right eye.", "There was no significant improvement in vision after focal laser photocoagulation.", "A fleshy, salmon colored conjunctival tumor was identified in her left eye.", "She was referred to the ocular oncology service.", "The conjunctival tumor was biopsied.", "Histopathologic examination revealed sheets of large neoplastic lymphoid cells with moderate nuclear pleomorphism, vesicular chromatin, and large nucleoli.", "The large neoplastic lymphoid cells were found underlying the normal conjunctival epithelium.", "Small lymphocytes were observed admixed with the atypical large lymphoid cells.", "Immunohistochemical studies showed the large lymphoid cells stained positive (diffuse, strong) for CD20.", "Immunohistochemical studies showed the large lymphoid cells stained positive for MUM-1.", "Immunohistochemical studies showed the large lymphoid cells stained less intensely positive for Pax-5.", "Immunohistochemical studies showed the large lymphoid cells stained weakly positive for Bcl-6.", "Immunohistochemical studies showed the large lymphoid cells were negative for CD10.", "The small background lymphocytes were CD3-positive.", "Histopathological findings were consistent with diffuse large B-cell lymphoma.", "The immunophenotypic profile was consistent with nongerminal center origin.", "The proliferation index estimated by Ki-67 labeling was 80%.", "The large lymphoid cells were positive for c-myc rearrangement.", "The patient's laboratory workup, including complete blood count with differential, comprehensive metabolic panel, and coagulation profile, was within normal limits.", "Serum lactate dehydrogenase (LDH) level was 506 U/L.", "The normal range for serum lactate dehydrogenase (LDH) is 313-618 U/L.", "The patient's hepatitis screen was negative.", "Orbital computed tomography (CT) scans failed to reveal any discrete masses.", "Magnetic resonance imaging (MRI) scans revealed mild asymmetric thickening and enhancement of the sclera in the anterior left globe.", "Positron emission tomography-CT (PET-CT) failed to reveal any other systemic central nervous system (CNS) involvement.", "An MRI of the brain failed to reveal any other systemic central nervous system (CNS) involvement.", "Cerebrospinal fluid (CSF) analysis did not reveal any malignant cells.", "The patient was presumed to have CNS involvement.", "She was treated with high dose systemic methotrexate in addition to rituximab.", "She received three cycles of methotrexate at 1.5 g/m2.", "The methotrexate dose was reduced by 50% due to age and low creatinine clearance.", "She received rituximab at a dose of 375 mg/m2.", "The first cycle was complicated by severe diarrhea related to Clostridium difficile infection.", "The first cycle was complicated by dehydration.", "The third cycle was complicated by acute renal insufficiency.", "The third cycle was complicated by fluid overload.", "The third cycle was complicated by insufficient methotrexate clearance.", "The third cycle was complicated by prolonged hospital stay.", "Further chemotherapy had to be stopped in view of the side effects.", "Ophthalmic follow-up revealed improved vision in her right eye.", "Interval MRI revealed interval improvement in nonspecific scleral thickening and enhancement along the anterior aspect of the left globe.", "Based on the documented improvement, the patient was to be continued on the same chemotherapy regimen.", "The patient declined further treatment.", "She was evaluated by radiation oncology.", "She opted to decline further treatment at this time.", "She has not followed up by physicians at this hospital after that.", "She has been lost to follow-up."], "summary_subclaims": ["The patient is an 80-year-old female.", "The patient has a history of diabetic retinopathy.", "The patient has a history of macular degeneration.", "The patient presented with a sudden deterioration of vision.", "The sudden deterioration of vision was initially attributed to diabetic retinopathy.", "The patient was noted to have a salmon patch lesion in her conjunctiva.", "The salmon patch lesion was diagnosed on biopsy to be a diffuse large B-cell lymphoma."]}, "extra_info": {"fulltext_subclaims": ["The patient is an 80-year-old woman.", "She has a history of coronary artery disease.", "She has a history of atrial fibrillation.", "She has a history of hypertension.", "She has a history of diabetes mellitus.", "She has a history of basal cell carcinoma removed via Mohs procedure on the nose.", "She has a history of diabetic retinopathy.", "She has a history of macular degeneration.", "She presented with a recent increase in the number of falls.", "The falls were due to a recent, sudden deterioration of vision bilaterally.", "She was initially seen by the ophthalmologist 2 months ago for loss of vision in her right eye.", "The loss of vision in her right eye was thought to be related to previously diagnosed diabetic retinopathy.", "She underwent focal laser photocoagulation for diabetic retinopathy in her right eye.", "There was no significant improvement in vision after focal laser photocoagulation.", "A fleshy, salmon colored conjunctival tumor was identified in her left eye.", "She was referred to the ocular oncology service.", "The conjunctival tumor was biopsied.", "Histopathologic examination revealed sheets of large neoplastic lymphoid cells with moderate nuclear pleomorphism, vesicular chromatin, and large nucleoli.", "The large neoplastic lymphoid cells were found underlying the normal conjunctival epithelium.", "Small lymphocytes were observed admixed with the atypical large lymphoid cells.", "Immunohistochemical studies showed the large lymphoid cells stained positive (diffuse, strong) for CD20.", "Immunohistochemical studies showed the large lymphoid cells stained positive for MUM-1.", "Immunohistochemical studies showed the large lymphoid cells stained less intensely positive for Pax-5.", "Immunohistochemical studies showed the large lymphoid cells stained weakly positive for Bcl-6.", "Immunohistochemical studies showed the large lymphoid cells were negative for CD10.", "The small background lymphocytes were CD3-positive.", "Histopathological findings were consistent with diffuse large B-cell lymphoma.", "The immunophenotypic profile was consistent with nongerminal center origin.", "The proliferation index estimated by Ki-67 labeling was 80%.", "The large lymphoid cells were positive for c-myc rearrangement.", "The patient's laboratory workup, including complete blood count with differential, comprehensive metabolic panel, and coagulation profile, was within normal limits.", "Serum lactate dehydrogenase (LDH) level was 506 U/L.", "The normal range for serum lactate dehydrogenase (LDH) is 313-618 U/L.", "The patient's hepatitis screen was negative.", "Orbital computed tomography (CT) scans failed to reveal any discrete masses.", "Magnetic resonance imaging (MRI) scans revealed mild asymmetric thickening and enhancement of the sclera in the anterior left globe.", "Positron emission tomography-CT (PET-CT) failed to reveal any other systemic central nervous system (CNS) involvement.", "An MRI of the brain failed to reveal any other systemic central nervous system (CNS) involvement.", "Cerebrospinal fluid (CSF) analysis did not reveal any malignant cells.", "The patient was presumed to have CNS involvement.", "She was treated with high dose systemic methotrexate in addition to rituximab.", "She received three cycles of methotrexate at 1.5 g/m2.", "The methotrexate dose was reduced by 50% due to age and low creatinine clearance.", "She received rituximab at a dose of 375 mg/m2.", "The first cycle was complicated by severe diarrhea related to Clostridium difficile infection.", "The first cycle was complicated by dehydration.", "The third cycle was complicated by acute renal insufficiency.", "The third cycle was complicated by fluid overload.", "The third cycle was complicated by insufficient methotrexate clearance.", "The third cycle was complicated by prolonged hospital stay.", "Further chemotherapy had to be stopped in view of the side effects.", "Ophthalmic follow-up revealed improved vision in her right eye.", "Interval MRI revealed interval improvement in nonspecific scleral thickening and enhancement along the anterior aspect of the left globe.", "Based on the documented improvement, the patient was to be continued on the same chemotherapy regimen.", "The patient declined further treatment.", "She was evaluated by radiation oncology.", "She opted to decline further treatment at this time.", "She has not followed up by physicians at this hospital after that.", "She has been lost to follow-up."], "index": 81, "original_id": "multiclinsum_test_1888_en.txt", "split": "test", "summary_subclaims": ["The patient is an 80-year-old female.", "The patient has a history of diabetic retinopathy.", "The patient has a history of macular degeneration.", "The patient presented with a sudden deterioration of vision.", "The sudden deterioration of vision was initially attributed to diabetic retinopathy.", "The patient was noted to have a salmon patch lesion in her conjunctiva.", "The salmon patch lesion was diagnosed on biopsy to be a diffuse large B-cell lymphoma."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidneys don\u2019t work properly, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing kidney health and preventing complications.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration and tubular reabsorption. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance, and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by underlying pathophysiological mechanisms including glomerulosclerosis, tubular atrophy, and vascular remodeling, and early intervention through biomarker monitoring and targeted therapies is critical to mitigate disease progression.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 62-year-old Thai man.", "He presented with a generalized erythematous maculopapular rash on his trunk and extremities.", "He had been diagnosed as having pulmonary tuberculosis two weeks earlier.", "He had long-standing hypertension and diabetes mellitus.", "His treatment included daily amlodipine 5mg, metformin 500mg, and glipizide 5mg.", "Anti-tuberculosis therapy of isoniazid 300mg, rifampicin 450mg, and ethambutol 800mg daily was administered.", "After two weeks of anti-tuberculosis medication, a generalized exanthematous rash appeared on his trunk and extremities.", "All anti-tuberculosis drugs were stopped after his admission due to a clinical suspicion of drug-induced adverse cutaneous reactions.", "The exanthematous rash resolved within three days of admission, leaving post-inflammatory hyperpigmentation.", "One day later, multiple well-defined, non-blanchable, erythematous-to-purplish macules and papules, some of which showed an annular arrangement, were noticed.", "He had no history of drug allergy.", "A review of systems was unremarkable.", "Laboratory findings showed leukocytes 12.8\u00d7103 cells/mm3.", "Neutrophils were 86 percent.", "Hemoglobin was 7.9g/dL.", "Platelet count was 215\u00d7103 cells/mm3.", "Creatinine was 1.2mg/dL.", "Alkaline phosphatase was 582U/L.", "\u03b3-glutamyl transferase was 393U/L.", "Total bilirubin was 9.6mg/dL.", "Direct bilirubin was 8.4mg/dL.", "Hepatitis B surface antigen, anti-hepatitis C virus, and anti-HIV test results were all negative.", "Anti-nuclear antibody and anti-neutrophil cytoplasmic antibody test results were also negative.", "Urine analysis showed no evidence of proteinuria or hematuria.", "The findings from an abdominal ultrasound were unremarkable.", "A skin biopsy from a purpuric annular lesion on his leg showed peri-vascular and interstitial infiltration of neutrophils with extravasation of erythrocytes and fibrin deposition.", "A direct immunofluorescence study was positive for IgA, IgM, and C3 along superficial dermal blood vessels.", "These findings were diagnostic for annular leukocytoclastic vasculitis associated with anti-tuberculosis drugs and drug-induced cholestasis.", "The patient was treated with an oral antihistamine and topical corticosteroids.", "The skin eruption cleared within one week without hyperpigmentation.", "Liver function test results returned to normal limits three weeks after the anti-tuberculosis drugs were withdrawn.", "Streptomycin (750mg per day), ethambutol (800mg per day), and ofloxacin (400mg per day) were administered as second-line anti-tuberculosis therapy.", "No adverse reactions were observed.", "He was subsequently treated with ethambutol, ofloxacin, and streptomycin without recurrence of the skin rash."], "summary_subclaims": ["We report a case of annular leukocytoclastic vasculitis induced by anti-tuberculosis medication.", "A 62-year-old Thai man presented to our facility with a generalized exanthematous rash on his trunk and extremities that resolved shortly afterwards.", "Subsequently, he developed multiple, erythematous-to-purplish, non-blanchable macules and papules with an annular arrangement on his extremities.", "The skin rash occurred after two weeks of anti-tuberculosis medication.", "The histopathology of the purpuric skin lesion was consistent with leukocytoclastic vasculitis.", "The skin lesion improved after discontinuation of the anti-tuberculosis drugs and treatment with oral antihistamine and topical corticosteroid drugs.", "Streptomycin, ethambutol and ofloxacin were administered as second-line anti-tuberculosis therapy during his hospitalization.", "No adverse reactions were observed."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 62-year-old Thai man.", "He presented with a generalized erythematous maculopapular rash on his trunk and extremities.", "He had been diagnosed as having pulmonary tuberculosis two weeks earlier.", "He had long-standing hypertension and diabetes mellitus.", "His treatment included daily amlodipine 5mg, metformin 500mg, and glipizide 5mg.", "Anti-tuberculosis therapy of isoniazid 300mg, rifampicin 450mg, and ethambutol 800mg daily was administered.", "After two weeks of anti-tuberculosis medication, a generalized exanthematous rash appeared on his trunk and extremities.", "All anti-tuberculosis drugs were stopped after his admission due to a clinical suspicion of drug-induced adverse cutaneous reactions.", "The exanthematous rash resolved within three days of admission, leaving post-inflammatory hyperpigmentation.", "One day later, multiple well-defined, non-blanchable, erythematous-to-purplish macules and papules, some of which showed an annular arrangement, were noticed.", "He had no history of drug allergy.", "A review of systems was unremarkable.", "Laboratory findings showed leukocytes 12.8\u00d7103 cells/mm3.", "Neutrophils were 86 percent.", "Hemoglobin was 7.9g/dL.", "Platelet count was 215\u00d7103 cells/mm3.", "Creatinine was 1.2mg/dL.", "Alkaline phosphatase was 582U/L.", "\u03b3-glutamyl transferase was 393U/L.", "Total bilirubin was 9.6mg/dL.", "Direct bilirubin was 8.4mg/dL.", "Hepatitis B surface antigen, anti-hepatitis C virus, and anti-HIV test results were all negative.", "Anti-nuclear antibody and anti-neutrophil cytoplasmic antibody test results were also negative.", "Urine analysis showed no evidence of proteinuria or hematuria.", "The findings from an abdominal ultrasound were unremarkable.", "A skin biopsy from a purpuric annular lesion on his leg showed peri-vascular and interstitial infiltration of neutrophils with extravasation of erythrocytes and fibrin deposition.", "A direct immunofluorescence study was positive for IgA, IgM, and C3 along superficial dermal blood vessels.", "These findings were diagnostic for annular leukocytoclastic vasculitis associated with anti-tuberculosis drugs and drug-induced cholestasis.", "The patient was treated with an oral antihistamine and topical corticosteroids.", "The skin eruption cleared within one week without hyperpigmentation.", "Liver function test results returned to normal limits three weeks after the anti-tuberculosis drugs were withdrawn.", "Streptomycin (750mg per day), ethambutol (800mg per day), and ofloxacin (400mg per day) were administered as second-line anti-tuberculosis therapy.", "No adverse reactions were observed.", "He was subsequently treated with ethambutol, ofloxacin, and streptomycin without recurrence of the skin rash."], "index": 7, "original_id": "multiclinsum_test_2131_en.txt", "split": "test", "summary_subclaims": ["We report a case of annular leukocytoclastic vasculitis induced by anti-tuberculosis medication.", "A 62-year-old Thai man presented to our facility with a generalized exanthematous rash on his trunk and extremities that resolved shortly afterwards.", "Subsequently, he developed multiple, erythematous-to-purplish, non-blanchable macules and papules with an annular arrangement on his extremities.", "The skin rash occurred after two weeks of anti-tuberculosis medication.", "The histopathology of the purpuric skin lesion was consistent with leukocytoclastic vasculitis.", "The skin lesion improved after discontinuation of the anti-tuberculosis drugs and treatment with oral antihistamine and topical corticosteroid drugs.", "Streptomycin, ethambutol and ofloxacin were administered as second-line anti-tuberculosis therapy during his hospitalization.", "No adverse reactions were observed."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidneys don\u2019t work properly, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing kidney health and preventing complications.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration and tubular reabsorption. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance, and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by underlying pathophysiological mechanisms including glomerulosclerosis, tubular atrophy, and vascular remodeling, and early intervention through biomarker monitoring and targeted therapies is critical to mitigate disease progression.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 29-year-old Asian female.", "She had previously been in good health.", "She presented with recurrent episodes of severe headache, nausea, and vomiting.", "She described the headache as 'pulling' downward.", "The headache was triggered by standing.", "The headache resolved when supine.", "She reported axial tension and rotatory manipulation of her neck one week prior to the onset of her symptoms.", "She denied immediate symptoms after the chiropractic manipulation.", "She experienced increasingly painful headaches over the 2 weeks following her chiropractic manipulation.", "She had no known prior history of trauma.", "She had no known prior history of dural structural pathology.", "She had no known prior history of connective tissue disease.", "Physical exam was normal with no neurological deficits.", "Previous cervical MRI with and without contrast had been unremarkable.", "Cervical MRI at presentation revealed a CSF-isodense ventral extradural fluid collection in the lower cervical spine and upper thoracic spine.", "There was no mass effect on the thecal sac.", "There was no meningeal enhancement.", "There was no perineural cyst.", "There was no dural ectasia.", "There was no abnormal venous engorgement.", "The patient was managed conservatively with bed rest for 2 weeks.", "She made a complete spontaneous recovery.", "Follow-up cervical MRI at 6 months demonstrated decreased size of ventral extradural fluid collection.", "The patient is doing well presently."], "summary_subclaims": ["We present a case of subacute cervical cerebrospinal fluid (CSF) leak resulting from chiropractic manipulation of the cervical spine.", "The patient is a 29-year-old female.", "The patient received manipulation one week prior to developing symptoms.", "The patient developed symptoms of severe orthostatic headache, nausea, and vomiting.", "Magnetic resonance imaging (MRI) revealed a new C5-C6 ventral CSF collection.", "Symptomatic onset corresponded with the recent cervical chiropractic adjustment.", "We present serial imaging correlating with her symptomatology.", "We review the pertinent literature on complications of chiropractic manipulation."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 29-year-old Asian female.", "She had previously been in good health.", "She presented with recurrent episodes of severe headache, nausea, and vomiting.", "She described the headache as 'pulling' downward.", "The headache was triggered by standing.", "The headache resolved when supine.", "She reported axial tension and rotatory manipulation of her neck one week prior to the onset of her symptoms.", "She denied immediate symptoms after the chiropractic manipulation.", "She experienced increasingly painful headaches over the 2 weeks following her chiropractic manipulation.", "She had no known prior history of trauma.", "She had no known prior history of dural structural pathology.", "She had no known prior history of connective tissue disease.", "Physical exam was normal with no neurological deficits.", "Previous cervical MRI with and without contrast had been unremarkable.", "Cervical MRI at presentation revealed a CSF-isodense ventral extradural fluid collection in the lower cervical spine and upper thoracic spine.", "There was no mass effect on the thecal sac.", "There was no meningeal enhancement.", "There was no perineural cyst.", "There was no dural ectasia.", "There was no abnormal venous engorgement.", "The patient was managed conservatively with bed rest for 2 weeks.", "She made a complete spontaneous recovery.", "Follow-up cervical MRI at 6 months demonstrated decreased size of ventral extradural fluid collection.", "The patient is doing well presently."], "index": 5, "original_id": "multiclinsum_test_2542_en.txt", "split": "test", "summary_subclaims": ["We present a case of subacute cervical cerebrospinal fluid (CSF) leak resulting from chiropractic manipulation of the cervical spine.", "The patient is a 29-year-old female.", "The patient received manipulation one week prior to developing symptoms.", "The patient developed symptoms of severe orthostatic headache, nausea, and vomiting.", "Magnetic resonance imaging (MRI) revealed a new C5-C6 ventral CSF collection.", "Symptomatic onset corresponded with the recent cervical chiropractic adjustment.", "We present serial imaging correlating with her symptomatology.", "We review the pertinent literature on complications of chiropractic manipulation."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidneys don\u2019t work properly, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing kidney health and preventing complications.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration and tubular reabsorption. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance, and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by underlying pathophysiological mechanisms including glomerulosclerosis, tubular atrophy, and vascular remodeling, and early intervention through biomarker monitoring and targeted therapies is critical to mitigate disease progression.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 24-year-old Caucasian man.", "He had fever and upper quadrant abdominal pain over the previous 20 days.", "Before admission, ciprofloxacin and metronidazole, followed by cefixime had been prescribed.", "Six years prior, the patient had been diagnosed with PSC.", "Six years prior, the patient had been diagnosed with UC.", "Six years prior, the patient had been diagnosed with suspected retroperitoneal fibrosis.", "Six years prior, the patient had been diagnosed with bile sludge.", "Six years prior, the patient had been diagnosed with splenomegaly.", "At that time, ursodiol 300mg BID was prescribed.", "At that time, mesalamine 4g per day was prescribed.", "At that time, exploratory laparotomy and a biopsy of the perihepatic, retroperitoneal tissue were performed.", "The biopsy excluded malignancy.", "Over this six-year period, the patient presented with recurrent episodes of cholangitis.", "The serum level of aminotransferases remained substantially normal.", "There was a progressive worsening of cholestatic test results.", "There was a progressive liver enlargement along with fibrosis.", "Gamma glutamyl transpeptidase (GGT) increased from 141UI/L to 344UI/L.", "Alkaline phosphatase (ALP) increased from 847UI/L to 2534UI/L.", "Hepatic tissue stiffness, measured by FibroScan\u00ae, progressed from 12.6 to 17.3kPa.", "The patient was never treated with immunosuppressive therapy.", "The patient was never treated with corticosteroids.", "One month before admission, an upper endoscopy was performed.", "The upper endoscopy excluded esophageal varices.", "One week before admission, a magnetic resonance of his abdomen and bile ducts was performed.", "The magnetic resonance revealed further enlargement of the liver.", "The magnetic resonance revealed further enlargement of the spleen.", "The magnetic resonance revealed further enlargement of the tissue surrounding his hepatic hilum.", "The tissue surrounding his hepatic hilum caused a compression of his second duodenal tract.", "The tissue surrounding his hepatic hilum caused a wrapping of the splenic and hepatic arteries.", "Beading and narrowing of the intra-hepatic and common bile ducts were reported.", "A narrowing of the pancreatic duct was also reported.", "At admission, the patient had a fever of 38.8\u00b0C.", "Physical examination revealed tenderness of his epigastrium.", "Physical examination revealed tenderness of his right upper hypochondrium.", "Microbiological blood and urine investigations were negative for bacteria.", "A chest radiograph was normal.", "An abdominal sonography revealed an enlarged liver.", "An abdominal sonography revealed thickened choledocus.", "An abdominal sonography revealed dilatation of the intra-hepatic biliary tree.", "An abdominal sonography revealed splenomegaly.", "An abdominal sonography revealed lymphadenopathy of the hepatic hilus.", "A colonoscopy showed erythema of the colonic mucosa from the rectum to the cecum.", "Random biopsy showed focal atrophy of the colonic mucosa with edema.", "Random biopsy showed chronic inflammatory infiltrates.", "Specific investigations for CMV were not carried out.", "Imipenem 500mg IV four times daily was administered.", "Three days later, imipenem was substituted with tigecycline 50mg IV BID.", "Further blood and urine cultures for bacteria were negative.", "The erythrocyte sedimentation rate (ESR) remained high.", "The C-reactive protein level (C-RP) remained high.", "The white blood cell (WBC) count decreased.", "The neutrophil count decreased.", "The procalcitonin level was 0.38ng/ml.", "The fever persisted.", "The upper abdominal pain subsided slightly.", "Investigations for HIV were negative.", "Investigations for Toxoplasma gondii were negative.", "Investigations for CMV were negative.", "Investigations for measles were negative.", "Investigations for parotitis were negative.", "Investigations for hepatitis C virus (HCV) were negative.", "Results for varicella zoster virus indicated previous infection.", "Results for human herpes virus indicated previous infection.", "Results for Epstein Barr indicated previous infection.", "Results for rubella indicated previous infection.", "Results for parvo virus B19 indicated previous infection.", "CD4?+?T lymphocytes were 1055mm3 (20.3%).", "CD3?+?T lymphocytes were 3193mm3 (67%).", "Mycobacterium tuberculosis interferon gamma release assay showed negative results.", "Twelve days after admission, teicoplanin 400mg die was prescribed.", "Twelve days after admission, gentamicin 80mg TID was prescribed.", "Twelve days after admission, metronidazole 500mg TID was prescribed.", "Tigecycline was stopped.", "Two days later, DNA Cytomegalovirus was detected in the blood with \u2264253 copies/mL.", "Three days later, this value increased to 6189 copies/mL.", "Three days later, 1431 copies/mL were evidenced from a urine sample.", "CMV pp65-antigen was also positive.", "CMV serology indicated acute CMV infection.", "The patient\u2019s fever rose to 39.2\u00b0C.", "The patient\u2019s abdominal pain extended to the right lower abdominal quadrant.", "The patient\u2019s abdominal pain radiated to the right groin.", "The patient\u2019s abdominal pain radiated to the right testicle.", "Ultrasound suggested acute appendicitis.", "He underwent surgery.", "Histology showed inflammatory infiltrates, including lymphocytes and neutrophils.", "Histochemistry was positive for CMV early antigens.", "Real time reaction of the appendix tissue was positive.", "Shell vial culture of the appendix tissue was positive.", "Microbiological investigations for bacteria showed Peptococcus spp.", "Microbiological investigations for fungi showed Candida albicans.", "Teicoplanin, gentamicin and metronidazole were administered for a total of 12 days.", "Intravenous ganciclovir 5mg/kg twice was administered for 15 days.", "After discharge, oral valganciclovir 900mg BID was prescribed for 10 days.", "After this, the CMV nucleic acid in the blood and urine was negative.", "After this, ESR remained abnormally high.", "After this, cholestatic liver test results remained abnormally high."], "summary_subclaims": ["The authors report on a case of acute primary Cytomegalovirus infection complicated with acute appendicitis due to Cytomegalovirus in an apparently immunocompetent 24-year-old Caucasian man.", "The patient also suffered from primary sclerosing cholangitis and ulcerative colitis.", "Diagnosis was based on clinical manifestations.", "Diagnosis was based on serology results.", "Diagnosis was based on microbiological findings.", "Diagnosis was based on histological findings.", "Treatment consisted of surgery.", "Treatment consisted of anti-Cytomegalovirus therapy."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 24-year-old Caucasian man.", "He had fever and upper quadrant abdominal pain over the previous 20 days.", "Before admission, ciprofloxacin and metronidazole, followed by cefixime had been prescribed.", "Six years prior, the patient had been diagnosed with PSC.", "Six years prior, the patient had been diagnosed with UC.", "Six years prior, the patient had been diagnosed with suspected retroperitoneal fibrosis.", "Six years prior, the patient had been diagnosed with bile sludge.", "Six years prior, the patient had been diagnosed with splenomegaly.", "At that time, ursodiol 300mg BID was prescribed.", "At that time, mesalamine 4g per day was prescribed.", "At that time, exploratory laparotomy and a biopsy of the perihepatic, retroperitoneal tissue were performed.", "The biopsy excluded malignancy.", "Over this six-year period, the patient presented with recurrent episodes of cholangitis.", "The serum level of aminotransferases remained substantially normal.", "There was a progressive worsening of cholestatic test results.", "There was a progressive liver enlargement along with fibrosis.", "Gamma glutamyl transpeptidase (GGT) increased from 141UI/L to 344UI/L.", "Alkaline phosphatase (ALP) increased from 847UI/L to 2534UI/L.", "Hepatic tissue stiffness, measured by FibroScan\u00ae, progressed from 12.6 to 17.3kPa.", "The patient was never treated with immunosuppressive therapy.", "The patient was never treated with corticosteroids.", "One month before admission, an upper endoscopy was performed.", "The upper endoscopy excluded esophageal varices.", "One week before admission, a magnetic resonance of his abdomen and bile ducts was performed.", "The magnetic resonance revealed further enlargement of the liver.", "The magnetic resonance revealed further enlargement of the spleen.", "The magnetic resonance revealed further enlargement of the tissue surrounding his hepatic hilum.", "The tissue surrounding his hepatic hilum caused a compression of his second duodenal tract.", "The tissue surrounding his hepatic hilum caused a wrapping of the splenic and hepatic arteries.", "Beading and narrowing of the intra-hepatic and common bile ducts were reported.", "A narrowing of the pancreatic duct was also reported.", "At admission, the patient had a fever of 38.8\u00b0C.", "Physical examination revealed tenderness of his epigastrium.", "Physical examination revealed tenderness of his right upper hypochondrium.", "Microbiological blood and urine investigations were negative for bacteria.", "A chest radiograph was normal.", "An abdominal sonography revealed an enlarged liver.", "An abdominal sonography revealed thickened choledocus.", "An abdominal sonography revealed dilatation of the intra-hepatic biliary tree.", "An abdominal sonography revealed splenomegaly.", "An abdominal sonography revealed lymphadenopathy of the hepatic hilus.", "A colonoscopy showed erythema of the colonic mucosa from the rectum to the cecum.", "Random biopsy showed focal atrophy of the colonic mucosa with edema.", "Random biopsy showed chronic inflammatory infiltrates.", "Specific investigations for CMV were not carried out.", "Imipenem 500mg IV four times daily was administered.", "Three days later, imipenem was substituted with tigecycline 50mg IV BID.", "Further blood and urine cultures for bacteria were negative.", "The erythrocyte sedimentation rate (ESR) remained high.", "The C-reactive protein level (C-RP) remained high.", "The white blood cell (WBC) count decreased.", "The neutrophil count decreased.", "The procalcitonin level was 0.38ng/ml.", "The fever persisted.", "The upper abdominal pain subsided slightly.", "Investigations for HIV were negative.", "Investigations for Toxoplasma gondii were negative.", "Investigations for CMV were negative.", "Investigations for measles were negative.", "Investigations for parotitis were negative.", "Investigations for hepatitis C virus (HCV) were negative.", "Results for varicella zoster virus indicated previous infection.", "Results for human herpes virus indicated previous infection.", "Results for Epstein Barr indicated previous infection.", "Results for rubella indicated previous infection.", "Results for parvo virus B19 indicated previous infection.", "CD4?+?T lymphocytes were 1055mm3 (20.3%).", "CD3?+?T lymphocytes were 3193mm3 (67%).", "Mycobacterium tuberculosis interferon gamma release assay showed negative results.", "Twelve days after admission, teicoplanin 400mg die was prescribed.", "Twelve days after admission, gentamicin 80mg TID was prescribed.", "Twelve days after admission, metronidazole 500mg TID was prescribed.", "Tigecycline was stopped.", "Two days later, DNA Cytomegalovirus was detected in the blood with \u2264253 copies/mL.", "Three days later, this value increased to 6189 copies/mL.", "Three days later, 1431 copies/mL were evidenced from a urine sample.", "CMV pp65-antigen was also positive.", "CMV serology indicated acute CMV infection.", "The patient\u2019s fever rose to 39.2\u00b0C.", "The patient\u2019s abdominal pain extended to the right lower abdominal quadrant.", "The patient\u2019s abdominal pain radiated to the right groin.", "The patient\u2019s abdominal pain radiated to the right testicle.", "Ultrasound suggested acute appendicitis.", "He underwent surgery.", "Histology showed inflammatory infiltrates, including lymphocytes and neutrophils.", "Histochemistry was positive for CMV early antigens.", "Real time reaction of the appendix tissue was positive.", "Shell vial culture of the appendix tissue was positive.", "Microbiological investigations for bacteria showed Peptococcus spp.", "Microbiological investigations for fungi showed Candida albicans.", "Teicoplanin, gentamicin and metronidazole were administered for a total of 12 days.", "Intravenous ganciclovir 5mg/kg twice was administered for 15 days.", "After discharge, oral valganciclovir 900mg BID was prescribed for 10 days.", "After this, the CMV nucleic acid in the blood and urine was negative.", "After this, ESR remained abnormally high.", "After this, cholestatic liver test results remained abnormally high."], "index": 1, "original_id": "multiclinsum_test_2576_en.txt", "split": "test", "summary_subclaims": ["The authors report on a case of acute primary Cytomegalovirus infection complicated with acute appendicitis due to Cytomegalovirus in an apparently immunocompetent 24-year-old Caucasian man.", "The patient also suffered from primary sclerosing cholangitis and ulcerative colitis.", "Diagnosis was based on clinical manifestations.", "Diagnosis was based on serology results.", "Diagnosis was based on microbiological findings.", "Diagnosis was based on histological findings.", "Treatment consisted of surgery.", "Treatment consisted of anti-Cytomegalovirus therapy."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidneys don\u2019t work properly, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing kidney health and preventing complications.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration and tubular reabsorption. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance, and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by underlying pathophysiological mechanisms including glomerulosclerosis, tubular atrophy, and vascular remodeling, and early intervention through biomarker monitoring and targeted therapies is critical to mitigate disease progression.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was diagnosed with high-risk CD20+ common-type B-cell precursor acute lymphoblastic leukemia.", "The patient received two cycles of HyperCVAD.", "The patient consulted the National Cancer Institute for a relapse and five-day polyarthralgia.", "The patient was initiated into the protocol established in 2003 by the Adult Acute Lymphoblastic Leukemia Research Group (GRAALL-2003).", "The patient developed febrile neutropenia.", "The patient had cellulitis of the left hand without abscess.", "The patient had methicillin-sensitive Staphylococcus aureus bacteremia.", "Cefapime and oxacillin were administered.", "The bacteremia resolved.", "On day 21 of hospitalization, the patient presented lesions on the back of the left hand.", "The lesions on the back of the left hand were of the type erythematoedematosa plaque.", "The lesions on the back of the left hand had mild and fine desquamation on the surface.", "The lesions on the back of the left hand had central blood crust.", "The patient had lesions in the right scapular and infra-scapular region.", "The lesions in the right scapular and infra-scapular region were 3 mm non-follicular papules.", "The lesions in the right scapular and infra-scapular region were grouped.", "The lesions in the right scapular and infra-scapular region were some erythematous and others erythemoparous.", "The lesions were assessed by the Dermatology Service.", "A skin biopsy was taken for histopathological study.", "The results were inconclusive for the diagnosis of mycosis.", "No culture was done for fungi of the biopsy.", "An invasive fungal infection was suspected.", "Caspofungin was initiated.", "The chest and sinus computed tomography (CT) scans were negative for invasive aspergillosis.", "The serum galactomannan detection was negative for invasive aspergillosis.", "Despite antimicrobial and antifungal treatment, the patient did not show significant improvement.", "The patient persisted with a fever of up to 40 \u00b0C.", "The patient had 1 cm nodules, soft, depressible, painless and in the previous sites of venipuncture.", "The blood count showed a profound neutropenia (20 white blood cells per \u00b5l).", "The C reactive protein was 6.15 mg/dl.", "The control CT scan of the paranasal sinuses showed incipient chronic inflammatory changes in the right maxillary sinus.", "The abdomen scan documented hepatosplenomegaly.", "The three blood cultures and the urine culture from day 28 of hospitalization showed yeast-like structures.", "The yeast-like structures were not identified in the automated panel Yeast ID (BD Phoenix\u2122 100).", "Arthroconidia were observed by microscopy.", "Colonies compatible with Geotrichum spp. were documented.", "The diagnosis was confirmed by matrix-assisted laser desorption ionization time-of-flight (MALDI-TOF) mass spectrometry.", "Treatment with amphotericin B deoxycholate was given at a daily dose of 1 mg/kg for 14 days.", "400 mg/day of voriconazole was given for four weeks.", "Clinical symptoms resolved.", "The patient recovered from neutropenia on day 24 of the combined antifungal treatment.", "The patient was discharged on day 101 of hospitalisation due to clinical improvement."], "summary_subclaims": ["The patient is a 27-year-old male.", "The patient has relapsed acute lymphoblastic leukemia.", "The patient had five-day-old polyarthralgia.", "The patient had febrile neutropenia.", "The patient had cellulitis without abscesses.", "The patient had methicillin-resistant Staphylococcus aureus bacteremia.", "The patient received therapy with oxacillin and cefepime.", "The febrile neutropenia persisted.", "An invasive fungal infection was suspected.", "A new set of blood cultures was taken.", "Antifungal treatment was initiated.", "Arthroconidia were identified in the blood cultures.", "Matrix-assisted laser desorption ionization-mass spectrometry confirmed the presence of Geotrichum spp.", "Antifungal treatment was adjusted to 14 days of deoxycholate amphotericin B.", "Antifungal treatment was adjusted to four weeks of voriconazole.", "The patient was discharged after a prolonged stay."]}, "extra_info": {"fulltext_subclaims": ["The patient was diagnosed with high-risk CD20+ common-type B-cell precursor acute lymphoblastic leukemia.", "The patient received two cycles of HyperCVAD.", "The patient consulted the National Cancer Institute for a relapse and five-day polyarthralgia.", "The patient was initiated into the protocol established in 2003 by the Adult Acute Lymphoblastic Leukemia Research Group (GRAALL-2003).", "The patient developed febrile neutropenia.", "The patient had cellulitis of the left hand without abscess.", "The patient had methicillin-sensitive Staphylococcus aureus bacteremia.", "Cefapime and oxacillin were administered.", "The bacteremia resolved.", "On day 21 of hospitalization, the patient presented lesions on the back of the left hand.", "The lesions on the back of the left hand were of the type erythematoedematosa plaque.", "The lesions on the back of the left hand had mild and fine desquamation on the surface.", "The lesions on the back of the left hand had central blood crust.", "The patient had lesions in the right scapular and infra-scapular region.", "The lesions in the right scapular and infra-scapular region were 3 mm non-follicular papules.", "The lesions in the right scapular and infra-scapular region were grouped.", "The lesions in the right scapular and infra-scapular region were some erythematous and others erythemoparous.", "The lesions were assessed by the Dermatology Service.", "A skin biopsy was taken for histopathological study.", "The results were inconclusive for the diagnosis of mycosis.", "No culture was done for fungi of the biopsy.", "An invasive fungal infection was suspected.", "Caspofungin was initiated.", "The chest and sinus computed tomography (CT) scans were negative for invasive aspergillosis.", "The serum galactomannan detection was negative for invasive aspergillosis.", "Despite antimicrobial and antifungal treatment, the patient did not show significant improvement.", "The patient persisted with a fever of up to 40 \u00b0C.", "The patient had 1 cm nodules, soft, depressible, painless and in the previous sites of venipuncture.", "The blood count showed a profound neutropenia (20 white blood cells per \u00b5l).", "The C reactive protein was 6.15 mg/dl.", "The control CT scan of the paranasal sinuses showed incipient chronic inflammatory changes in the right maxillary sinus.", "The abdomen scan documented hepatosplenomegaly.", "The three blood cultures and the urine culture from day 28 of hospitalization showed yeast-like structures.", "The yeast-like structures were not identified in the automated panel Yeast ID (BD Phoenix\u2122 100).", "Arthroconidia were observed by microscopy.", "Colonies compatible with Geotrichum spp. were documented.", "The diagnosis was confirmed by matrix-assisted laser desorption ionization time-of-flight (MALDI-TOF) mass spectrometry.", "Treatment with amphotericin B deoxycholate was given at a daily dose of 1 mg/kg for 14 days.", "400 mg/day of voriconazole was given for four weeks.", "Clinical symptoms resolved.", "The patient recovered from neutropenia on day 24 of the combined antifungal treatment.", "The patient was discharged on day 101 of hospitalisation due to clinical improvement."], "index": 3, "original_id": "multiclinsum_test_3210_en.txt", "split": "test", "summary_subclaims": ["The patient is a 27-year-old male.", "The patient has relapsed acute lymphoblastic leukemia.", "The patient had five-day-old polyarthralgia.", "The patient had febrile neutropenia.", "The patient had cellulitis without abscesses.", "The patient had methicillin-resistant Staphylococcus aureus bacteremia.", "The patient received therapy with oxacillin and cefepime.", "The febrile neutropenia persisted.", "An invasive fungal infection was suspected.", "A new set of blood cultures was taken.", "Antifungal treatment was initiated.", "Arthroconidia were identified in the blood cultures.", "Matrix-assisted laser desorption ionization-mass spectrometry confirmed the presence of Geotrichum spp.", "Antifungal treatment was adjusted to 14 days of deoxycholate amphotericin B.", "Antifungal treatment was adjusted to four weeks of voriconazole.", "The patient was discharged after a prolonged stay."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidneys don\u2019t work properly, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing kidney health and preventing complications.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration and tubular reabsorption. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance, and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by underlying pathophysiological mechanisms including glomerulosclerosis, tubular atrophy, and vascular remodeling, and early intervention through biomarker monitoring and targeted therapies is critical to mitigate disease progression.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 63-year-old man.", "He presented with hematuria and urinary obstruction symptoms.", "He came to the hospital four times each with presence of gross hematuria.", "The patient suffered from frequency and nocturia at least for six months.", "Physical examination revealed enlargement of prostate.", "There was no palpable nodule on the digital rectal examination.", "PSA was normal.", "There was no evidence of hepatomegaly.", "There was no evidence of splenomegaly.", "The first transurethral resection of the prostate (TURP) and biopsy was done.", "Pathologic results showed the evidence of BPH.", "After 28 days, the patient was admitted again due to gross hematuria.", "Rectal examination was normal.", "Pelvic CT-scan revealed a big clot in bladder without any lymphadenopathy.", "There was significant heterogeneity in prostate.", "In second TURP, clot evacuation and biopsy were performed on more than 15 different areas of prostate.", "During the next 2 weeks, the patient underwent 3 other trans-urethral coagulation and clot evacuations due to hematuria.", "Prothrombin time (PT) was normal.", "Partial thromboplastin time (PTT) was normal.", "Clotting time (CT) was normal.", "Bleeding time (BT) was normal.", "Platelet count was normal.", "After 15 days hematuria was stopped.", "Hematuria was not repeated.", "Sections from prostate show foci of hemorrhage.", "The first transfusion was 2 units of PC during the second surgery.", "The second transfusion was 2 units of PC and 2 FFP, two days later.", "The consecutive third and fourth transfusions were done two days later.", "During the third and fourth transfusions, the patient received 3 units of FFP.", "During the third and fourth transfusions, the patient received 3 units of whole blood.", "Immunohistochemistry studies demonstrate CD20-positive in 90% of lymphoid cells.", "Immunohistochemistry studies demonstrate CD20-positive in the lymphoepithelial lesions.", "CD5-positive in background lymphocytes.", "CD43-positive in 90% of lymphoid cells.", "CD3-positive in background lymphocytes.", "CK markers are negative in neoplastic cells.", "PSA markers are negative in neoplastic cells.", "Bone marrow biopsy did not show other involvement.", "Abdominal and pelvic CT-scan did not show other involvement.", "In the last follow up, around eight months after discharging, the patient was alive.", "In the last follow up, around eight months after discharging, the patient was asymptomatic.", "There is no evidence of other organ involvement."], "summary_subclaims": ["We report here another case of primary prostatic MALT lymphoma.", "The case is presented by hematuria.", "The diagnosis was primarily considered as BPH.", "Immunohistochemistry studies demonstrate the diagnosis.", "Immunohistochemistry studies demonstrate MALT lymphoma.", "Six months after starting the treatment the patient was alive and well."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 63-year-old man.", "He presented with hematuria and urinary obstruction symptoms.", "He came to the hospital four times each with presence of gross hematuria.", "The patient suffered from frequency and nocturia at least for six months.", "Physical examination revealed enlargement of prostate.", "There was no palpable nodule on the digital rectal examination.", "PSA was normal.", "There was no evidence of hepatomegaly.", "There was no evidence of splenomegaly.", "The first transurethral resection of the prostate (TURP) and biopsy was done.", "Pathologic results showed the evidence of BPH.", "After 28 days, the patient was admitted again due to gross hematuria.", "Rectal examination was normal.", "Pelvic CT-scan revealed a big clot in bladder without any lymphadenopathy.", "There was significant heterogeneity in prostate.", "In second TURP, clot evacuation and biopsy were performed on more than 15 different areas of prostate.", "During the next 2 weeks, the patient underwent 3 other trans-urethral coagulation and clot evacuations due to hematuria.", "Prothrombin time (PT) was normal.", "Partial thromboplastin time (PTT) was normal.", "Clotting time (CT) was normal.", "Bleeding time (BT) was normal.", "Platelet count was normal.", "After 15 days hematuria was stopped.", "Hematuria was not repeated.", "Sections from prostate show foci of hemorrhage.", "The first transfusion was 2 units of PC during the second surgery.", "The second transfusion was 2 units of PC and 2 FFP, two days later.", "The consecutive third and fourth transfusions were done two days later.", "During the third and fourth transfusions, the patient received 3 units of FFP.", "During the third and fourth transfusions, the patient received 3 units of whole blood.", "Immunohistochemistry studies demonstrate CD20-positive in 90% of lymphoid cells.", "Immunohistochemistry studies demonstrate CD20-positive in the lymphoepithelial lesions.", "CD5-positive in background lymphocytes.", "CD43-positive in 90% of lymphoid cells.", "CD3-positive in background lymphocytes.", "CK markers are negative in neoplastic cells.", "PSA markers are negative in neoplastic cells.", "Bone marrow biopsy did not show other involvement.", "Abdominal and pelvic CT-scan did not show other involvement.", "In the last follow up, around eight months after discharging, the patient was alive.", "In the last follow up, around eight months after discharging, the patient was asymptomatic.", "There is no evidence of other organ involvement."], "index": 9, "original_id": "multiclinsum_test_2155_en.txt", "split": "test", "summary_subclaims": ["We report here another case of primary prostatic MALT lymphoma.", "The case is presented by hematuria.", "The diagnosis was primarily considered as BPH.", "Immunohistochemistry studies demonstrate the diagnosis.", "Immunohistochemistry studies demonstrate MALT lymphoma.", "Six months after starting the treatment the patient was alive and well."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidneys don\u2019t work properly, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing kidney health and preventing complications.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration and tubular reabsorption. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance, and fluid overload, which can manifest clinically as fatigue, hypertension, and edema. Chronic kidney disease progression is influenced by underlying pathophysiological mechanisms including glomerulosclerosis, tubular atrophy, and vascular remodeling, and early intervention through biomarker monitoring and targeted therapies is critical to mitigate disease progression.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was a 53-year-old man.", "The patient had a history of testicular seminoma that was removed twice.", "The patient had been experiencing disorientation and difficulty in thinking for 1 month before the visit.", "Contrast-enhanced magnetic resonance imaging showed a markedly contrast-enhanced mass in the dorsal midbrain.", "Systemic examination showed no obvious abnormalities.", "Blood samples showed a high serum soluble interleukin-2 receptor level of 624 U/ml.", "\u03b1-fetoprotein was within normal limits.", "Human chorionic gonadotropin was within normal limits.", "Neoplastic diseases such as PCNSL, tectal glioma, or intracranial metastasis of seminoma were considered in the differential diagnosis.", "Endoscopic tumor biopsy was performed with endoscopic third ventriculostomy.", "The burr hole was located 11 cm from the nasion and 2 cm to the right of the midline.", "A Neuroport mini was inserted into the anterior horn.", "The aqueduct was stenotic due to the tumor.", "A biopsy of the swollen area was performed.", "The lesion was pale pink, soft, and had minimal bleeding after the biopsy.", "A third ventriculostomy was performed using an expanding balloon catheter.", "Intraoperative cerebrospinal fluid cytology showed a small number of atypical cells with bifurcated nuclear irregularities.", "The tumor cells were CD3 negative.", "The tumor cells were CD20 positive.", "The tumor cells were CD79a positive.", "The final histopathological diagnosis of the tumor was diffuse large B-cell lymphoma.", "The patient underwent three courses of high-dose methotrexate.", "The patient underwent whole-brain irradiation.", "The patient\u2019s KPS was 100 when he was discharged home."], "summary_subclaims": ["The patient was referred to our hospital with a 1-month history of disorientation.", "Magnetic resonance imaging showed hydrocephalus.", "Magnetic resonance imaging showed an enhancing lesion in the tectum.", "Preoperative blood tests showed a high serum soluble interleukin-2 receptor level of 624 U/ml.", "Through a single burr hole, endoscopic third ventriculostomy and biopsy of the lesion were simultaneously performed with a flexible endoscope.", "The histological examination confirmed diffuse large B-cell lymphoma.", "The patient underwent chemotherapy.", "The patient underwent radiotherapy."]}, "extra_info": {"fulltext_subclaims": ["The patient was a 53-year-old man.", "The patient had a history of testicular seminoma that was removed twice.", "The patient had been experiencing disorientation and difficulty in thinking for 1 month before the visit.", "Contrast-enhanced magnetic resonance imaging showed a markedly contrast-enhanced mass in the dorsal midbrain.", "Systemic examination showed no obvious abnormalities.", "Blood samples showed a high serum soluble interleukin-2 receptor level of 624 U/ml.", "\u03b1-fetoprotein was within normal limits.", "Human chorionic gonadotropin was within normal limits.", "Neoplastic diseases such as PCNSL, tectal glioma, or intracranial metastasis of seminoma were considered in the differential diagnosis.", "Endoscopic tumor biopsy was performed with endoscopic third ventriculostomy.", "The burr hole was located 11 cm from the nasion and 2 cm to the right of the midline.", "A Neuroport mini was inserted into the anterior horn.", "The aqueduct was stenotic due to the tumor.", "A biopsy of the swollen area was performed.", "The lesion was pale pink, soft, and had minimal bleeding after the biopsy.", "A third ventriculostomy was performed using an expanding balloon catheter.", "Intraoperative cerebrospinal fluid cytology showed a small number of atypical cells with bifurcated nuclear irregularities.", "The tumor cells were CD3 negative.", "The tumor cells were CD20 positive.", "The tumor cells were CD79a positive.", "The final histopathological diagnosis of the tumor was diffuse large B-cell lymphoma.", "The patient underwent three courses of high-dose methotrexate.", "The patient underwent whole-brain irradiation.", "The patient\u2019s KPS was 100 when he was discharged home."], "index": 11, "original_id": "multiclinsum_test_410_en.txt", "split": "test", "summary_subclaims": ["The patient was referred to our hospital with a 1-month history of disorientation.", "Magnetic resonance imaging showed hydrocephalus.", "Magnetic resonance imaging showed an enhancing lesion in the tectum.", "Preoperative blood tests showed a high serum soluble interleukin-2 receptor level of 624 U/ml.", "Through a single burr hole, endoscopic third ventriculostomy and biopsy of the lesion were simultaneously performed with a flexible endoscope.", "The histological examination confirmed diffuse large B-cell lymphoma.", "The patient underwent chemotherapy.", "The patient underwent radiotherapy."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 51-year-old Caucasian woman.", "She presented with spinal, pelvic, and sternal inflammatory pain lasting for many years.", "The symptoms had a strong negative impact on her quality of life.", "She did not present palmoplantar pustulosis.", "There was no context of fever.", "She had been diagnosed with synovitis, acne, pustulosis, hyperostosis, and osteitis (SAPHO) syndrome at the age of 40 years.", "She had received sulfasalazine and nonsteroidal anti-inflammatory drugs (NSAIDs) for many years with incomplete pain relief.", "She also had a history of cervical and lumbar arthrodesis.", "She had a history of hypertension.", "She had a history of thyroidectomy.", "Total spine and pelvis magnetic resonance imaging (MRI) showed a short tau inversion recovery (STIR) hypersignal on several thoracic vertebrae (T6, T7, T8, and T9).", "Total spine and pelvis MRI showed a short tau inversion recovery (STIR) hypersignal on the sternal part of the right clavicle.", "Bone marrow oedema was also found on the right iliac bone.", "The sacroiliac joints were preserved.", "Bone scintigraphy showed anterior chest wall involvement.", "Right sternoclavicular hyperostosis was found on computed tomography.", "The C-reactive protein (CRP) was found to be 89.2 mg/L.", "The reference range for CRP is 0\u20135 mg/L.", "Several blood tests performed earlier had already shown elevation of inflammation parameters.", "HLA B27 antigen was negative.", "The diagnosis of active SAPHO syndrome was confirmed.", "Conventional synthetic disease-modifying antirheumatic drug (csDMARD) as methotrexate was not considered.", "Methotrexate is more effective on peripheral arthritis.", "Methotrexate has not shown comparable activity in axial disease in patients with axial spondyloarthritis.", "Anti-tumour necrosis factor (TNF) drugs could not be prescribed because the criteria for reimbursement of these drugs in Belgium were not met.", "The criteria for reimbursement were not met in the absence of sacroiliitis.", "JAK-inhibitors were initiated.", "Tofacitinib 5 mg twice daily was initiated.", "The patient reported rapid and significant reduction of pain within weeks of starting the treatment.", "Blood tests performed one month after the onset of treatment showed a clear regression of inflammatory parameters.", "The CRP was 25.5 mg/L one month after the onset of treatment.", "The CRP was 14 mg/L after 4 months of treatment.", "The CRP was 9.9 mg/L after 10 months of treatment.", "Total spine and pelvis MRI performed after 3 months of treatment showed regression of the STIR hypersignal on the body of the thoracic vertebrae.", "The hypersignal of the right iliac bone disappeared after 3 months of treatment.", "The rheumatic evolution was favourable from a clinical, biological, and radiological point of view since the introduction of a JAK-inhibitor.", "The treatment had to be discontinued due to pulmonary embolism occurring after 8 months on tofacitinib.", "Spinal, pelvic, and chest (sternal and costal) pain reappeared after discontinuation of tofacitinib.", "Elevation of inflammatory parameters occurred after discontinuation of tofacitinib.", "Written informed consent was obtained from the patient for the publication of this report and its accompanying images."], "summary_subclaims": ["The patient was a 51-year-old Caucasian woman.", "She had SAPHO syndrome with mainly axial involvement.", "She had been treated with sulfasalazine and anti-inflammatory drugs for many years.", "The treatment with sulfasalazine and anti-inflammatory drugs was without any success.", "A few weeks after starting treatment with tofacitinib, both clinical and biological parameters dramatically improved.", "Imaging showed considerable regression of the vertebral and pelvic lesions.", "Tofacitinib had to be discontinued due to the occurrence of pulmonary embolism.", "Recurrence of bone pain and biologic inflammation was rapidly observed."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 51-year-old Caucasian woman.", "She presented with spinal, pelvic, and sternal inflammatory pain lasting for many years.", "The symptoms had a strong negative impact on her quality of life.", "She did not present palmoplantar pustulosis.", "There was no context of fever.", "She had been diagnosed with synovitis, acne, pustulosis, hyperostosis, and osteitis (SAPHO) syndrome at the age of 40 years.", "She had received sulfasalazine and nonsteroidal anti-inflammatory drugs (NSAIDs) for many years with incomplete pain relief.", "She also had a history of cervical and lumbar arthrodesis.", "She had a history of hypertension.", "She had a history of thyroidectomy.", "Total spine and pelvis magnetic resonance imaging (MRI) showed a short tau inversion recovery (STIR) hypersignal on several thoracic vertebrae (T6, T7, T8, and T9).", "Total spine and pelvis MRI showed a short tau inversion recovery (STIR) hypersignal on the sternal part of the right clavicle.", "Bone marrow oedema was also found on the right iliac bone.", "The sacroiliac joints were preserved.", "Bone scintigraphy showed anterior chest wall involvement.", "Right sternoclavicular hyperostosis was found on computed tomography.", "The C-reactive protein (CRP) was found to be 89.2 mg/L.", "The reference range for CRP is 0\u20135 mg/L.", "Several blood tests performed earlier had already shown elevation of inflammation parameters.", "HLA B27 antigen was negative.", "The diagnosis of active SAPHO syndrome was confirmed.", "Conventional synthetic disease-modifying antirheumatic drug (csDMARD) as methotrexate was not considered.", "Methotrexate is more effective on peripheral arthritis.", "Methotrexate has not shown comparable activity in axial disease in patients with axial spondyloarthritis.", "Anti-tumour necrosis factor (TNF) drugs could not be prescribed because the criteria for reimbursement of these drugs in Belgium were not met.", "The criteria for reimbursement were not met in the absence of sacroiliitis.", "JAK-inhibitors were initiated.", "Tofacitinib 5 mg twice daily was initiated.", "The patient reported rapid and significant reduction of pain within weeks of starting the treatment.", "Blood tests performed one month after the onset of treatment showed a clear regression of inflammatory parameters.", "The CRP was 25.5 mg/L one month after the onset of treatment.", "The CRP was 14 mg/L after 4 months of treatment.", "The CRP was 9.9 mg/L after 10 months of treatment.", "Total spine and pelvis MRI performed after 3 months of treatment showed regression of the STIR hypersignal on the body of the thoracic vertebrae.", "The hypersignal of the right iliac bone disappeared after 3 months of treatment.", "The rheumatic evolution was favourable from a clinical, biological, and radiological point of view since the introduction of a JAK-inhibitor.", "The treatment had to be discontinued due to pulmonary embolism occurring after 8 months on tofacitinib.", "Spinal, pelvic, and chest (sternal and costal) pain reappeared after discontinuation of tofacitinib.", "Elevation of inflammatory parameters occurred after discontinuation of tofacitinib.", "Written informed consent was obtained from the patient for the publication of this report and its accompanying images."], "index": 0, "original_id": "multiclinsum_test_787_en.txt", "split": "test", "summary_subclaims": ["The patient was a 51-year-old Caucasian woman.", "She had SAPHO syndrome with mainly axial involvement.", "She had been treated with sulfasalazine and anti-inflammatory drugs for many years.", "The treatment with sulfasalazine and anti-inflammatory drugs was without any success.", "A few weeks after starting treatment with tofacitinib, both clinical and biological parameters dramatically improved.", "Imaging showed considerable regression of the vertebral and pelvic lesions.", "Tofacitinib had to be discontinued due to the occurrence of pulmonary embolism.", "Recurrence of bone pain and biologic inflammation was rapidly observed."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was a 62-year-old male.", "The patient had a 4-month history of right brachial/shoulder pain and numbness.", "The patient had hyposensitivity in the C5 distribution.", "The MRI scan showed degenerative cervical spondylosis from the C3\u2013C4 to C5\u2013C6 levels.", "The MRI scan showed a C5\u2013C6 right anterolateral disc herniation with foraminal stenosis.", "The MRI scan showed syringomyelia extending from the C5\u2013C6 to the T1 level.", "The patient underwent C5\u2013C6 anterior cervical discectomy and fusion (ACDF) with placement of a polyetheretherketone cage.", "The patient\u2019s symptoms markedly improved following the ACDF.", "Three months later, the MRI scan confirmed adequate decompression of the spinal cord.", "Three months later, the MRI scan confirmed the total resolution of the syrinx.", "The patient underwent placement of an eight-electrode subdural spinal cord stimulator from the C3 to C4 through the C5\u2013C6 levels.", "The patient significantly improved after the subdural spinal cord stimulator placement.", "Syringomyelia is usually attributed to Chiari malformations, spinal arachnoiditis, intramedullary tumors, and trauma.", "Syringomyelia is seldom associated with cervical disc disease or spondylosis.", "In two cases, ACDF resulted in complete radiological and clinical resolution of the syrinx.", "Younger patient age, a longer history of disease, and lower functional scores were associated with syringomyelia.", "Postoperative outcomes and progression-free survival for patients with syringomyelia did not differ significantly versus those without syringomyelia.", "The authors presented a rare case of syringomyelia attributed to cervical disc disease/stenosis.", "The syringomyelia in this case fully resolved following a C5\u2013C6 ACDF.", "The complete radiological resolution indicates that cervical disc disease/spondylosis might alter cerebrospinal fluid flow.", "The cerebrospinal fluid flow was adequately restored to normal with surgery."], "summary_subclaims": ["The patient is a 62-year-old male.", "The patient had a 4-month history of right brachial pain.", "The patient had hyposensitivity in the C5 distribution.", "The cervical MR imaging scan showed a C5-C6 right anterolateral disc herniation.", "The cervical MR imaging scan showed syringomyelia extending from C5-C6 to T1.", "The patient underwent C5-C6 anterior cervical discectomy and fusion.", "The patient's symptoms resolved following the C5-C6 anterior cervical discectomy and fusion.", "The 3-month postoperative MR documented total resolution of the syrinx.", "The patient required a subdural spinal cord stimulator due to residual neuropathic pain.", "The subdural spinal cord stimulator was placed without any complications."]}, "extra_info": {"fulltext_subclaims": ["The patient was a 62-year-old male.", "The patient had a 4-month history of right brachial/shoulder pain and numbness.", "The patient had hyposensitivity in the C5 distribution.", "The MRI scan showed degenerative cervical spondylosis from the C3\u2013C4 to C5\u2013C6 levels.", "The MRI scan showed a C5\u2013C6 right anterolateral disc herniation with foraminal stenosis.", "The MRI scan showed syringomyelia extending from the C5\u2013C6 to the T1 level.", "The patient underwent C5\u2013C6 anterior cervical discectomy and fusion (ACDF) with placement of a polyetheretherketone cage.", "The patient\u2019s symptoms markedly improved following the ACDF.", "Three months later, the MRI scan confirmed adequate decompression of the spinal cord.", "Three months later, the MRI scan confirmed the total resolution of the syrinx.", "The patient underwent placement of an eight-electrode subdural spinal cord stimulator from the C3 to C4 through the C5\u2013C6 levels.", "The patient significantly improved after the subdural spinal cord stimulator placement.", "Syringomyelia is usually attributed to Chiari malformations, spinal arachnoiditis, intramedullary tumors, and trauma.", "Syringomyelia is seldom associated with cervical disc disease or spondylosis.", "In two cases, ACDF resulted in complete radiological and clinical resolution of the syrinx.", "Younger patient age, a longer history of disease, and lower functional scores were associated with syringomyelia.", "Postoperative outcomes and progression-free survival for patients with syringomyelia did not differ significantly versus those without syringomyelia.", "The authors presented a rare case of syringomyelia attributed to cervical disc disease/stenosis.", "The syringomyelia in this case fully resolved following a C5\u2013C6 ACDF.", "The complete radiological resolution indicates that cervical disc disease/spondylosis might alter cerebrospinal fluid flow.", "The cerebrospinal fluid flow was adequately restored to normal with surgery."], "index": 6, "original_id": "multiclinsum_test_875_en.txt", "split": "test", "summary_subclaims": ["The patient is a 62-year-old male.", "The patient had a 4-month history of right brachial pain.", "The patient had hyposensitivity in the C5 distribution.", "The cervical MR imaging scan showed a C5-C6 right anterolateral disc herniation.", "The cervical MR imaging scan showed syringomyelia extending from C5-C6 to T1.", "The patient underwent C5-C6 anterior cervical discectomy and fusion.", "The patient's symptoms resolved following the C5-C6 anterior cervical discectomy and fusion.", "The 3-month postoperative MR documented total resolution of the syrinx.", "The patient required a subdural spinal cord stimulator due to residual neuropathic pain.", "The subdural spinal cord stimulator was placed without any complications."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was a 71-year-old female.", "She had been undergoing oral treatment for diabetes with canagliflozin 100 mg/day, metformin 1,000 mg/day, and saxagliptin 5 mg/day.", "She noticed general malaise a month before her emergency department visit.", "Two weeks before her emergency department visit, her oral intake decreased because of reduced appetite.", "She continued oral medications at their initial dose.", "The day prior to her emergency department visit, her malaise worsened.", "She developed nausea and abdominal pain.", "A local doctor discovered notable metabolic acidosis (pH, 6.860; CO2, 8 mmHg; HCO3, \u22121.0 mEq/L; base excess measurement, below sensitivity).", "She was urgently transferred to Kurume University Hospital Advanced Emergency Medical Service Center.", "On admission, her body temperature was 35.0 \u00b0C.", "On admission, her pulse was 118/min.", "On admission, her respiratory rate was 28/min.", "On admission, her blood pressure was 111/75 mmHg.", "The findings on consultation included notable dryness inside the oral cavity.", "The findings on consultation included a cold sensation on distal regions of the limbs.", "Chest auscultation revealed no significant findings.", "There was mild tenderness in the lower abdominal region.", "Blood gases demonstrated notable metabolic acidosis (pH, 6.89; CO2, 11.4 mmHg; HCO3, 1.9 mEq/L; base excess, \u221231.3 mmol/L).", "Lactic acid was mildly elevated at 3.3 mmol/L.", "Blood sugar was mildly elevated at 259 mg/dL.", "Hyperkalemia was observed accompanying the acidosis.", "No significant kidney function impairment was observed.", "A diagnosis of lactic acidosis secondary to metformin was considered.", "The patient had not recently been exposed to a contrast agent.", "Lactate was only mildly elevated.", "Point-of-care urine testing showed strongly positive urinary ketones.", "Point-of-care urine testing showed strongly positive urinary glucose.", "Plasma 3-hydroxybutyric acid was markedly high (>10,000 \u03bcmol/L).", "DKA was suspected.", "An injection of 0.45% sodium chloride was given as an intravenous drip at 800 mL/h.", "Blood sugar dropped to 180 mg/dL after using two units of short-acting insulin.", "Insulin was not used continuously.", "An intravenous drip of glucose was started.", "Around 6 units/day of insulin were used as appropriate.", "Sodium bicarbonate was given as an intravenous drip.", "Continuous renal replacement therapy (CRRT) was started from day 2 after hospital admission.", "The acidosis improved because of CRRT over 3 days.", "Hyperketonemia reduced notably after a few days.", "Urinary sugar continued to rise.", "Osmotic diuresis set in with urinary glucose as the cause.", "Polyurea was observed.", "Fluid replacement was carried out using Ringer\u2019s solution.", "Urinary sugar turned negative on day 16 after admission.", "She was discharged on day 18 after admission."], "summary_subclaims": ["The patient was a 71-year-old female.", "She was being treated for type 2 diabetes.", "She was taking canagliflozin, metformin, and saxagliptin orally.", "She presented to the ED for evaluation of reduced oral intake, malaise, nausea, and abdominal pain.", "Her blood glucose was 259 mg/dL.", "There was notable ketoacidosis.", "The pH was 6.89.", "The CO2 was 11.4 mmHg.", "The HCO3 was 1.9 mEq/L.", "The base excess was -31.3 mmol/L.", "The 3-hydroxybutyric acid was > 10,000 \u03bcmol/L.", "The uncontrolled acidosis improved following 3 days of continuous renal replacement therapy.", "Elevated urinary glucose continued for more than 10 days.", "Ringer's lactated fluid supplementation was continued for management of polyurea and glucosuria.", "Urinary glucose turned negative on day 16.", "There was improvement in the patient's overall state.", "She was discharged on day 18."]}, "extra_info": {"fulltext_subclaims": ["The patient was a 71-year-old female.", "She had been undergoing oral treatment for diabetes with canagliflozin 100 mg/day, metformin 1,000 mg/day, and saxagliptin 5 mg/day.", "She noticed general malaise a month before her emergency department visit.", "Two weeks before her emergency department visit, her oral intake decreased because of reduced appetite.", "She continued oral medications at their initial dose.", "The day prior to her emergency department visit, her malaise worsened.", "She developed nausea and abdominal pain.", "A local doctor discovered notable metabolic acidosis (pH, 6.860; CO2, 8 mmHg; HCO3, \u22121.0 mEq/L; base excess measurement, below sensitivity).", "She was urgently transferred to Kurume University Hospital Advanced Emergency Medical Service Center.", "On admission, her body temperature was 35.0 \u00b0C.", "On admission, her pulse was 118/min.", "On admission, her respiratory rate was 28/min.", "On admission, her blood pressure was 111/75 mmHg.", "The findings on consultation included notable dryness inside the oral cavity.", "The findings on consultation included a cold sensation on distal regions of the limbs.", "Chest auscultation revealed no significant findings.", "There was mild tenderness in the lower abdominal region.", "Blood gases demonstrated notable metabolic acidosis (pH, 6.89; CO2, 11.4 mmHg; HCO3, 1.9 mEq/L; base excess, \u221231.3 mmol/L).", "Lactic acid was mildly elevated at 3.3 mmol/L.", "Blood sugar was mildly elevated at 259 mg/dL.", "Hyperkalemia was observed accompanying the acidosis.", "No significant kidney function impairment was observed.", "A diagnosis of lactic acidosis secondary to metformin was considered.", "The patient had not recently been exposed to a contrast agent.", "Lactate was only mildly elevated.", "Point-of-care urine testing showed strongly positive urinary ketones.", "Point-of-care urine testing showed strongly positive urinary glucose.", "Plasma 3-hydroxybutyric acid was markedly high (>10,000 \u03bcmol/L).", "DKA was suspected.", "An injection of 0.45% sodium chloride was given as an intravenous drip at 800 mL/h.", "Blood sugar dropped to 180 mg/dL after using two units of short-acting insulin.", "Insulin was not used continuously.", "An intravenous drip of glucose was started.", "Around 6 units/day of insulin were used as appropriate.", "Sodium bicarbonate was given as an intravenous drip.", "Continuous renal replacement therapy (CRRT) was started from day 2 after hospital admission.", "The acidosis improved because of CRRT over 3 days.", "Hyperketonemia reduced notably after a few days.", "Urinary sugar continued to rise.", "Osmotic diuresis set in with urinary glucose as the cause.", "Polyurea was observed.", "Fluid replacement was carried out using Ringer\u2019s solution.", "Urinary sugar turned negative on day 16 after admission.", "She was discharged on day 18 after admission."], "index": 2, "original_id": "multiclinsum_test_99_en.txt", "split": "test", "summary_subclaims": ["The patient was a 71-year-old female.", "She was being treated for type 2 diabetes.", "She was taking canagliflozin, metformin, and saxagliptin orally.", "She presented to the ED for evaluation of reduced oral intake, malaise, nausea, and abdominal pain.", "Her blood glucose was 259 mg/dL.", "There was notable ketoacidosis.", "The pH was 6.89.", "The CO2 was 11.4 mmHg.", "The HCO3 was 1.9 mEq/L.", "The base excess was -31.3 mmol/L.", "The 3-hydroxybutyric acid was > 10,000 \u03bcmol/L.", "The uncontrolled acidosis improved following 3 days of continuous renal replacement therapy.", "Elevated urinary glucose continued for more than 10 days.", "Ringer's lactated fluid supplementation was continued for management of polyurea and glucosuria.", "Urinary glucose turned negative on day 16.", "There was improvement in the patient's overall state.", "She was discharged on day 18."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 33-year-old nulligravid woman.", "The patient had newly diagnosed AA (WHO grade III, IDH1 negative).", "The patient had undergone a craniotomy with complete resection of her right parietal lobe tumor one month prior.", "The patient was scheduled to start chemotherapy and radiation in the next month.", "The patient\u2019s neuro-oncologist recommended fertility preservation prior to chemo-radiation.", "The fertility preservation did not delay the anticipated start of her chemo-radiation treatment.", "The patient had no significant medical or gynecological history.", "On physical exam, the patient was a healthy-appearing woman.", "Transvaginal ultrasound demonstrated a normal-appearing uterus and ovaries bilaterally.", "A dominant follicle was noted on the patient\u2019s right ovary.", "It was decided to administer HCG 10,000 IU at the time of her presentation to trigger ovulation.", "The patient had a high antral follicle count (6 on right, 7 on left).", "The patient received low dose gonadotropins: 1 ampule of Human Menopausal Gonadotropin (Menopur\u00ae), 75\u2013187.5 IU of FSH (Gonal F\u00ae) for 10 days.", "The patient received cetrorelix acetate (Ganirelex\u00ae) for the last 6 days.", "Final oocyte maturation was triggered with Lupron Luprolide Acetate (Lupron\u00ae) 40u.", "Twelve oocytes were retrieved transvaginally under ultrasound guidance.", "Eight embryos developed and were vitrified in liquid nitrogen.", "The patient returned to the Center one year later after being cleared by her neuro-oncologist.", "The patient had 6 weeks of radiation therapy with Temozolomide (Temodar\u00ae).", "The patient had 6 months of maintenance dose chemotherapy.", "The patient\u2019s last dose of chemotherapy was one month prior to returning to the office.", "The patient had maintained regular cycles post chemotherapy.", "The patient underwent a frozen-thaw natural cycle embryo transfer of a single day-3 embryo.", "The patient used vaginal progesterone (Crinone\u00ae) for luteal phase support.", "A viable singleton pregnancy was seen on ultrasound 1 month later.", "The patient delivered a healthy female baby weighing 7lbs 5 oz. at term.", "The patient returned two years later desirous of another pregnancy.", "The patient was tumor free and cleared by her oncologist to conceive again.", "This time the patient was treated with Estrace\u00ae 6 mg a day.", "The patient underwent a frozen-thaw cycle with a single day-5 blastocyst transferred.", "The patient conceived with a viable singleton pregnancy.", "The patient delivered a healthy male at term weighing 6lbs.", "Throughout the patient\u2019s treatment regimen for fertility preservation and frozen embryo transfers, no adverse or unanticipated events were encountered."], "summary_subclaims": ["The patient is a 33-year-old nulligravid woman.", "The patient has newly diagnosed anaplastic astrocytoma.", "The anaplastic astrocytoma is WHO grade III.", "The anaplastic astrocytoma is IDH1-negative.", "The patient sought fertility preservation.", "The patient underwent in vitro fertilization for fertility preservation.", "The in vitro fertilization resulted in 8 vitrified embryos.", "The patient underwent two rounds of frozen embryo transfers.", "Each frozen embryo transfer resulted in a successful singleton pregnancy."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 33-year-old nulligravid woman.", "The patient had newly diagnosed AA (WHO grade III, IDH1 negative).", "The patient had undergone a craniotomy with complete resection of her right parietal lobe tumor one month prior.", "The patient was scheduled to start chemotherapy and radiation in the next month.", "The patient\u2019s neuro-oncologist recommended fertility preservation prior to chemo-radiation.", "The fertility preservation did not delay the anticipated start of her chemo-radiation treatment.", "The patient had no significant medical or gynecological history.", "On physical exam, the patient was a healthy-appearing woman.", "Transvaginal ultrasound demonstrated a normal-appearing uterus and ovaries bilaterally.", "A dominant follicle was noted on the patient\u2019s right ovary.", "It was decided to administer HCG 10,000 IU at the time of her presentation to trigger ovulation.", "The patient had a high antral follicle count (6 on right, 7 on left).", "The patient received low dose gonadotropins: 1 ampule of Human Menopausal Gonadotropin (Menopur\u00ae), 75\u2013187.5 IU of FSH (Gonal F\u00ae) for 10 days.", "The patient received cetrorelix acetate (Ganirelex\u00ae) for the last 6 days.", "Final oocyte maturation was triggered with Lupron Luprolide Acetate (Lupron\u00ae) 40u.", "Twelve oocytes were retrieved transvaginally under ultrasound guidance.", "Eight embryos developed and were vitrified in liquid nitrogen.", "The patient returned to the Center one year later after being cleared by her neuro-oncologist.", "The patient had 6 weeks of radiation therapy with Temozolomide (Temodar\u00ae).", "The patient had 6 months of maintenance dose chemotherapy.", "The patient\u2019s last dose of chemotherapy was one month prior to returning to the office.", "The patient had maintained regular cycles post chemotherapy.", "The patient underwent a frozen-thaw natural cycle embryo transfer of a single day-3 embryo.", "The patient used vaginal progesterone (Crinone\u00ae) for luteal phase support.", "A viable singleton pregnancy was seen on ultrasound 1 month later.", "The patient delivered a healthy female baby weighing 7lbs 5 oz. at term.", "The patient returned two years later desirous of another pregnancy.", "The patient was tumor free and cleared by her oncologist to conceive again.", "This time the patient was treated with Estrace\u00ae 6 mg a day.", "The patient underwent a frozen-thaw cycle with a single day-5 blastocyst transferred.", "The patient conceived with a viable singleton pregnancy.", "The patient delivered a healthy male at term weighing 6lbs.", "Throughout the patient\u2019s treatment regimen for fertility preservation and frozen embryo transfers, no adverse or unanticipated events were encountered."], "index": 8, "original_id": "multiclinsum_test_2635_en.txt", "split": "test", "summary_subclaims": ["The patient is a 33-year-old nulligravid woman.", "The patient has newly diagnosed anaplastic astrocytoma.", "The anaplastic astrocytoma is WHO grade III.", "The anaplastic astrocytoma is IDH1-negative.", "The patient sought fertility preservation.", "The patient underwent in vitro fertilization for fertility preservation.", "The in vitro fertilization resulted in 8 vitrified embryos.", "The patient underwent two rounds of frozen embryo transfers.", "Each frozen embryo transfer resulted in a successful singleton pregnancy."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["A 63-year-old man was referred to Modarres Hospital, Tehran.", "He had gradual onset of obscure generalized abdominal pain six hours before admission.", "His pain was located in the epigastric and periumbilical region.", "There was no radiation of pain to anywhere else.", "He had one episode of vomiting.", "There was moderate abdominal distension.", "There was periumbilical abdominal tenderness.", "There was no guarding.", "Initial blood tests showed white cell count (WBC) of 21.7 \u00d7 109/L.", "Initial blood tests showed neutrophils 84.2%.", "Initial blood tests showed hemoglobin (Hb) 15.2 g/dL.", "C reactive protein was +2.", "Amylase was 63 U/L.", "Abdominal x-ray was normal.", "Ultrasonography was normal.", "About five hours after resuscitation and appropriate fluid therapy, he has not felt better.", "Blood tests were deranged.", "WBC was 18.4\u00d7109/L.", "Neutrophils were 76.5%.", "Hb was 8.1 g/dL.", "Abdominopelvic CT-scan showed evidence of hematoma near the head of pancreas.", "Abdominopelvic CT-scan showed perihepatic and perisplenic fluid.", "BP fell to 95/55 mmHg.", "Pulse rose to 105/min.", "He was transferred to operating room emergently.", "Midline laparotomy was performed.", "Massive intraperitoneal hematoma was evacuated.", "Right medial visceral rotation, the Cattell-Braasch maneuver, was performed.", "Active bleeding in the base of IPDA was detected.", "IPDA was suture ligated at the base with 4/0 nonabsorbable stitch.", "Hemostasis was achieved.", "The post-operative period was uneventful.", "Oral fluids were started the day after the surgery.", "The patient was discharged from the hospital two days after the surgery.", "One week after discharge, he had a normal follow-up.", "There were no concerning problems one week after discharge."], "summary_subclaims": ["The patient is a 63-year-old man.", "The patient had idiopathic spontaneous intraperitoneal hemorrhage.", "The hemorrhage was caused by spontaneous rupture of non-aneurysmal inferior pancreaticoduodenal artery."]}, "extra_info": {"fulltext_subclaims": ["A 63-year-old man was referred to Modarres Hospital, Tehran.", "He had gradual onset of obscure generalized abdominal pain six hours before admission.", "His pain was located in the epigastric and periumbilical region.", "There was no radiation of pain to anywhere else.", "He had one episode of vomiting.", "There was moderate abdominal distension.", "There was periumbilical abdominal tenderness.", "There was no guarding.", "Initial blood tests showed white cell count (WBC) of 21.7 \u00d7 109/L.", "Initial blood tests showed neutrophils 84.2%.", "Initial blood tests showed hemoglobin (Hb) 15.2 g/dL.", "C reactive protein was +2.", "Amylase was 63 U/L.", "Abdominal x-ray was normal.", "Ultrasonography was normal.", "About five hours after resuscitation and appropriate fluid therapy, he has not felt better.", "Blood tests were deranged.", "WBC was 18.4\u00d7109/L.", "Neutrophils were 76.5%.", "Hb was 8.1 g/dL.", "Abdominopelvic CT-scan showed evidence of hematoma near the head of pancreas.", "Abdominopelvic CT-scan showed perihepatic and perisplenic fluid.", "BP fell to 95/55 mmHg.", "Pulse rose to 105/min.", "He was transferred to operating room emergently.", "Midline laparotomy was performed.", "Massive intraperitoneal hematoma was evacuated.", "Right medial visceral rotation, the Cattell-Braasch maneuver, was performed.", "Active bleeding in the base of IPDA was detected.", "IPDA was suture ligated at the base with 4/0 nonabsorbable stitch.", "Hemostasis was achieved.", "The post-operative period was uneventful.", "Oral fluids were started the day after the surgery.", "The patient was discharged from the hospital two days after the surgery.", "One week after discharge, he had a normal follow-up.", "There were no concerning problems one week after discharge."], "index": 4, "original_id": "multiclinsum_test_45_en.txt", "split": "test", "summary_subclaims": ["The patient is a 63-year-old man.", "The patient had idiopathic spontaneous intraperitoneal hemorrhage.", "The hemorrhage was caused by spontaneous rupture of non-aneurysmal inferior pancreaticoduodenal artery."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 34-year-old male.", "The patient had multiple yellowish elevated masses in different locations of the body.", "The masses were located on the dorsum of the hands, elbows, buttocks, and feet.", "The patient had bilateral arcus cornealis.", "The patient had Achille tendon masses.", "The total number of masses was 15.", "The size of the masses varied from 1 \u00d7 1 \u00d7 1 cm to 8 \u00d7 8 \u00d7 5 cm.", "The masses were initially asymptomatic.", "The masses appeared 10 years ago.", "The masses increased progressively in size.", "The patient reported discomfort and difficulty dressing and sitting due to large masses in the buttocks.", "The patient reported difficulty wearing sandals due to the masses in the feet.", "The patient's hygiene was affected.", "The patient felt inferior when in contact with others.", "The patient decided to divorce because of psychological influences related to abnormalities in the body.", "The chest X-ray, abdominal ultrasound, electrocardiogram, and echocardiogram of the patient were normal.", "The patient's family medical history was not taken because the patient did not wish to disclose it.", "The patient's LDL-C level was 10.04 mmol/L.", "The reference value for LDL-C is <2.6 mmol/L.", "The patient was diagnosed with Familial hypercholesterolemia (FH) based on the Simon Broome Criteria.", "The patient agreed to be admitted to the hospital for surgery to remove the masses.", "Lipid-lowering therapy was administered with Atorvastatin 40 mg/day.", "After 4 days of hospitalization, the patient underwent surgery to remove the masses.", "The resected masses had a surface of normal skin.", "The core of the masses looked yellowish-colored, uniform, relatively solid, without necrosis.", "The masses were localized in the subcutaneous layer without invading the muscle or joint capsule.", "The skin incision was oval around the circumference of the masses with the longitudinal axis parallel to the Langer's line.", "The excision margins were normal skin.", "After removing the masses, all defects were sutured directly.", "A total of 13 masses were removed.", "The remaining 2 masses on the finger were not removed because the patient still had to use the fingers to take care of himself.", "The remaining 2 masses would be removed during the next surgery.", "Histopathology showed a typical xanthoma with infiltration of foam cells.", "All sutures were removed 14 days after surgery.", "The patient was discharged and continued treatment with atorvastatin 40 mg/day.", "Gene sequencing test showed homozygous LDL-C receptor gene mutation on chromosome 19.", "The patient's family members did not undergo gene sequencing to find mutations causing FH.", "At 1.5 months postoperatively, the LDL-C level of the patient was reduced to 8.8 mmol/L.", "At 1.5 months postoperatively, the wounds healed well.", "At 1.5 months postoperatively, no re-appearance of masses was observed."], "summary_subclaims": ["The patient is a 34-year-old male.", "The patient had multiple large tuberous xanthomas related to FH.", "There were 15 masses in different body parts.", "The masses were located on the dorsum of the hands, elbows, buttocks, feet, and Achille's tendon.", "The largest masses in the buttocks measured 8\u00a0\u00d7\u00a08\u00a0\u00d7\u00a05\u00a0cm.", "Surgical removal of 13 masses was carried out in combination with medical treatment.", "The skin incision was oval around the circumference of masses with the longitudinal axis parallel to the Langer's line.", "Skin defects were closed directly or dissected on both sides of the incision to reduce tension.", "Wound healing was normal.", "After 1.5\u00a0months, there was no recurrence of xanthomas."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 34-year-old male.", "The patient had multiple yellowish elevated masses in different locations of the body.", "The masses were located on the dorsum of the hands, elbows, buttocks, and feet.", "The patient had bilateral arcus cornealis.", "The patient had Achille tendon masses.", "The total number of masses was 15.", "The size of the masses varied from 1 \u00d7 1 \u00d7 1 cm to 8 \u00d7 8 \u00d7 5 cm.", "The masses were initially asymptomatic.", "The masses appeared 10 years ago.", "The masses increased progressively in size.", "The patient reported discomfort and difficulty dressing and sitting due to large masses in the buttocks.", "The patient reported difficulty wearing sandals due to the masses in the feet.", "The patient's hygiene was affected.", "The patient felt inferior when in contact with others.", "The patient decided to divorce because of psychological influences related to abnormalities in the body.", "The chest X-ray, abdominal ultrasound, electrocardiogram, and echocardiogram of the patient were normal.", "The patient's family medical history was not taken because the patient did not wish to disclose it.", "The patient's LDL-C level was 10.04 mmol/L.", "The reference value for LDL-C is <2.6 mmol/L.", "The patient was diagnosed with Familial hypercholesterolemia (FH) based on the Simon Broome Criteria.", "The patient agreed to be admitted to the hospital for surgery to remove the masses.", "Lipid-lowering therapy was administered with Atorvastatin 40 mg/day.", "After 4 days of hospitalization, the patient underwent surgery to remove the masses.", "The resected masses had a surface of normal skin.", "The core of the masses looked yellowish-colored, uniform, relatively solid, without necrosis.", "The masses were localized in the subcutaneous layer without invading the muscle or joint capsule.", "The skin incision was oval around the circumference of the masses with the longitudinal axis parallel to the Langer's line.", "The excision margins were normal skin.", "After removing the masses, all defects were sutured directly.", "A total of 13 masses were removed.", "The remaining 2 masses on the finger were not removed because the patient still had to use the fingers to take care of himself.", "The remaining 2 masses would be removed during the next surgery.", "Histopathology showed a typical xanthoma with infiltration of foam cells.", "All sutures were removed 14 days after surgery.", "The patient was discharged and continued treatment with atorvastatin 40 mg/day.", "Gene sequencing test showed homozygous LDL-C receptor gene mutation on chromosome 19.", "The patient's family members did not undergo gene sequencing to find mutations causing FH.", "At 1.5 months postoperatively, the LDL-C level of the patient was reduced to 8.8 mmol/L.", "At 1.5 months postoperatively, the wounds healed well.", "At 1.5 months postoperatively, no re-appearance of masses was observed."], "index": 10, "original_id": "multiclinsum_test_1587_en.txt", "split": "test", "summary_subclaims": ["The patient is a 34-year-old male.", "The patient had multiple large tuberous xanthomas related to FH.", "There were 15 masses in different body parts.", "The masses were located on the dorsum of the hands, elbows, buttocks, feet, and Achille's tendon.", "The largest masses in the buttocks measured 8\u00a0\u00d7\u00a08\u00a0\u00d7\u00a05\u00a0cm.", "Surgical removal of 13 masses was carried out in combination with medical treatment.", "The skin incision was oval around the circumference of masses with the longitudinal axis parallel to the Langer's line.", "Skin defects were closed directly or dissected on both sides of the incision to reduce tension.", "Wound healing was normal.", "After 1.5\u00a0months, there was no recurrence of xanthomas."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 57-year-old Ashkenazi Jew woman.", "She had iron deficiency anemia.", "She had no family or personal history of malignancy.", "She was admitted to the department of general surgery for treatment of her transverse colon tumor.", "Four months prior, she had begun experiencing periumbilical abdominal pain.", "She had hematochezia.", "She had a 10-kg weight loss.", "Upon physical examination, no masses were palpated.", "There were no other pathologic findings.", "She underwent a colonoscopy.", "The colonoscopy revealed a large mass that involved nearly the whole circumference of the colon.", "The mass seemed to be adjacent to the cecum.", "Biopsies were taken.", "The biopsies failed to demonstrate any colonic pathology.", "She underwent computed tomography (CT) of the chest and abdomen.", "The CT demonstrated a huge mass that occupied the whole colonic lumen.", "The mass caused a colocolic intussusception.", "Considerable mesenteric lymphadenopathy was seen.", "The nodes were up to 28 \u00d7 21 mm in diameter.", "The lymphadenopathy was deemed to be evidence of positive tumoral lymph node involvement.", "No inguinal, pelvic, retroperitoneal, or other lymphadenopathy was seen.", "She was scheduled for surgery.", "A laparoscopic right extended hemicolectomy was performed.", "The surgery was uncomplicated.", "During surgery, considerable mesocolic lymphadenopathy was seen.", "The mesocolic lymphadenopathy was widely resected accordingly.", "Pathology of the surgical specimen showed findings consistent with small B cell lymphoproliferative disorders with plasmacytoid differentiation.", "Primary lymphoma of the colon was considered in the differential diagnosis.", "The disease was thought to be part of systemic dissemination of lymphoma.", "The patient was referred to the hematology clinic for further investigation.", "A bone marrow biopsy was performed.", "The bone marrow biopsy result was normal.", "Positron emission tomography-CT showed no other focus of lymphoma.", "A test for Epstein-Barr virus infection was negative.", "These results support the diagnosis of a primary colonic NHL small B-cell LPD with plasmacytoid differentiation.", "The disease is an exceedingly rare disease.", "There are only two such reports in the current literature."], "summary_subclaims": ["We describe a case of an Ashkenazi Jew patient.", "The patient presented in the typical way that carcinoma of the colon might present.", "The patient turned out to have a very rare type of tumor.", "The tumor was rare in its histology.", "The tumor was rare in its location."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 57-year-old Ashkenazi Jew woman.", "She had iron deficiency anemia.", "She had no family or personal history of malignancy.", "She was admitted to the department of general surgery for treatment of her transverse colon tumor.", "Four months prior, she had begun experiencing periumbilical abdominal pain.", "She had hematochezia.", "She had a 10-kg weight loss.", "Upon physical examination, no masses were palpated.", "There were no other pathologic findings.", "She underwent a colonoscopy.", "The colonoscopy revealed a large mass that involved nearly the whole circumference of the colon.", "The mass seemed to be adjacent to the cecum.", "Biopsies were taken.", "The biopsies failed to demonstrate any colonic pathology.", "She underwent computed tomography (CT) of the chest and abdomen.", "The CT demonstrated a huge mass that occupied the whole colonic lumen.", "The mass caused a colocolic intussusception.", "Considerable mesenteric lymphadenopathy was seen.", "The nodes were up to 28 \u00d7 21 mm in diameter.", "The lymphadenopathy was deemed to be evidence of positive tumoral lymph node involvement.", "No inguinal, pelvic, retroperitoneal, or other lymphadenopathy was seen.", "She was scheduled for surgery.", "A laparoscopic right extended hemicolectomy was performed.", "The surgery was uncomplicated.", "During surgery, considerable mesocolic lymphadenopathy was seen.", "The mesocolic lymphadenopathy was widely resected accordingly.", "Pathology of the surgical specimen showed findings consistent with small B cell lymphoproliferative disorders with plasmacytoid differentiation.", "Primary lymphoma of the colon was considered in the differential diagnosis.", "The disease was thought to be part of systemic dissemination of lymphoma.", "The patient was referred to the hematology clinic for further investigation.", "A bone marrow biopsy was performed.", "The bone marrow biopsy result was normal.", "Positron emission tomography-CT showed no other focus of lymphoma.", "A test for Epstein-Barr virus infection was negative.", "These results support the diagnosis of a primary colonic NHL small B-cell LPD with plasmacytoid differentiation.", "The disease is an exceedingly rare disease.", "There are only two such reports in the current literature."], "index": 18, "original_id": "multiclinsum_test_2722_en.txt", "split": "test", "summary_subclaims": ["We describe a case of an Ashkenazi Jew patient.", "The patient presented in the typical way that carcinoma of the colon might present.", "The patient turned out to have a very rare type of tumor.", "The tumor was rare in its histology.", "The tumor was rare in its location."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was a 50-year-old female.", "She presented to the emergency department in significant respiratory distress.", "She had a known past medical history of tobacco dependence.", "She had a known past medical history of chronic obstructive pulmonary disease.", "She had a known past medical history of hypertension.", "On arrival, the patient was noted to be apneic.", "She was actively being ventilated with a bag-valve-mask ventilation.", "She rapidly progressed from an irregularly irregular cardiac rhythm to sinus bradycardia.", "She then progressed into a pulseless electrical activity (PEA) arrest within minutes of arrival.", "She underwent approximately 30 minutes of cardiopulmonary resuscitation.", "Endotracheal intubation was performed via video laryngoscopy.", "After intubation, she was noted to have significant resistance to bagging.", "After return of spontaneous circulation, she was noted to have high peak pressures on the ventilator.", "She was persistently hypotensive.", "On examination, she was noted to have distant, rhonchorous, and wheezy breath sounds bilaterally.", "She was treated for her bronchospasm with nebulized albuterol-ipratropium solution.", "She was treated with continuous nebulized albuterol.", "She was treated with magnesium sulfate.", "She was treated with methylprednisolone.", "She was treated with subcutaneous terbutaline.", "She was treated with titratable epinephrine.", "She was noted to have continuously high peak pressures.", "An intravenous push of vecuronium was given.", "There was no improvement in ventilation after vecuronium.", "There were continuously high peak airway pressures noted on the ventilator.", "She had an electrocardiogram concerning for new-onset atrial fibrillation with rapid ventricular response.", "She had an electrocardiogram showing left axis deviation.", "She had an electrocardiogram showing a new right bundle branch block.", "She had an electrocardiogram showing a left anterior fascicular block.", "The electrocardiogram showed signs of right heart strain.", "Given her difficulty with ventilation and hypotension, she was taken for a computed tomography (CT) with pulmonary embolism protocol.", "The CT revealed no evidence of pulmonary embolism.", "The CT showed evidence of alveolar rupture with pneumomediastinum consistent with the Macklin effect.", "The CT showed a small left-sided pneumothorax.", "The CT showed associated medial left hemi diaphragmatic rupture.", "The CT showed pneumoretroperitoneum tracking along the left upper abdomen.", "The CT showed pneumoretroperitoneum tracking along the left perinephric space.", "The CT showed left-sided nondisplaced rib fractures of the fifth and sixth ribs.", "A CT of the abdomen and pelvis showed a small amount of free air consistent with pneumoretroperitoneum.", "The CT of the abdomen and pelvis showed free air adjacent to the gastric cardia.", "The CT of the abdomen and pelvis showed free air adjacent to the left kidney.", "The CT of the abdomen and pelvis showed free air adjacent to the left adrenal gland.", "There was no definitively identified intra-abdominal traumatic injury.", "Further history from the family revealed she had been complaining of difficulty breathing earlier in the day.", "She subsequently suffered a witnessed fall down a flight of stairs.", "The fall was associated with head trauma.", "The fall was associated with apparent loss of consciousness.", "The patient\u2019s physical examination revealed no external signs of trauma on initial arrival.", "The patient was admitted to the medical intensive care unit.", "The admission was in the setting of cardiac arrest with prolonged down time.", "The patient\u2019s pneumomediastinum improved with lung-protective ventilation strategies.", "The patient\u2019s pneumoretroperitoneum improved with lung-protective ventilation strategies.", "The patient was treated with paralytics.", "The patient\u2019s treatment for her COPD exacerbation included continuous albuterol nebulization of 40 milligrams (mg) over four hours.", "The patient\u2019s treatment included intermittent scheduled three-milliliter ipratroprium-albuterol nebulizers every six hours.", "The patient\u2019s treatment included 0.25 mg of budesonide twice daily.", "The patient\u2019s treatment included 0.5 mg of ipratroprium four times daily.", "The patient\u2019s treatment included isolated two mg of magnesium sulfate administration daily if worsening wheeze on examination.", "The patient\u2019s treatment included 80 mg of methylprednisolone daily.", "The patient received a one-time dose of 0.25 mg of subcutaneous terbutaline.", "The patient received a one-time dose of one microgram (\u03bcg) of epinephrine.", "Sedation was maintained with ketamine at 1.5 mg per kilogram (kg) per hour.", "Sedation was maintained with propofol at 20 \u03bcg/kg per minute.", "The patient was treated with epinephrine as the first-line vasopressor choice.", "The patient\u2019s cardiac arrest resulted in severe hypoxic brain injury.", "The patient had subsequent diffuse cerebral edema.", "The patient had effacement of the basal cisterns.", "The patient had tonsillar herniation seen on CT of her head.", "The patient became increasingly hypertensive.", "The patient was weaned off vasopressors.", "The patient was started on titratable nicardipine at a maximum of 12.5 mg per hour.", "The patient was given a hypertonic saline bolus.", "The patient lost all evidence of brainstem reflexes five days after suffering cardiac arrest.", "The patient continued to trigger some spontaneous breaths on the ventilator.", "Multiple family meetings were held regarding patient prognosis.", "The patient was palliatively extubated.", "The patient died 26 days after arrival."], "summary_subclaims": ["The patient suffered a cardiac arrest after a fall.", "The cardiac arrest occurred during a chronic obstructive pulmonary disease exacerbation.", "The patient had pneumoretroperitoneum."]}, "extra_info": {"fulltext_subclaims": ["The patient was a 50-year-old female.", "She presented to the emergency department in significant respiratory distress.", "She had a known past medical history of tobacco dependence.", "She had a known past medical history of chronic obstructive pulmonary disease.", "She had a known past medical history of hypertension.", "On arrival, the patient was noted to be apneic.", "She was actively being ventilated with a bag-valve-mask ventilation.", "She rapidly progressed from an irregularly irregular cardiac rhythm to sinus bradycardia.", "She then progressed into a pulseless electrical activity (PEA) arrest within minutes of arrival.", "She underwent approximately 30 minutes of cardiopulmonary resuscitation.", "Endotracheal intubation was performed via video laryngoscopy.", "After intubation, she was noted to have significant resistance to bagging.", "After return of spontaneous circulation, she was noted to have high peak pressures on the ventilator.", "She was persistently hypotensive.", "On examination, she was noted to have distant, rhonchorous, and wheezy breath sounds bilaterally.", "She was treated for her bronchospasm with nebulized albuterol-ipratropium solution.", "She was treated with continuous nebulized albuterol.", "She was treated with magnesium sulfate.", "She was treated with methylprednisolone.", "She was treated with subcutaneous terbutaline.", "She was treated with titratable epinephrine.", "She was noted to have continuously high peak pressures.", "An intravenous push of vecuronium was given.", "There was no improvement in ventilation after vecuronium.", "There were continuously high peak airway pressures noted on the ventilator.", "She had an electrocardiogram concerning for new-onset atrial fibrillation with rapid ventricular response.", "She had an electrocardiogram showing left axis deviation.", "She had an electrocardiogram showing a new right bundle branch block.", "She had an electrocardiogram showing a left anterior fascicular block.", "The electrocardiogram showed signs of right heart strain.", "Given her difficulty with ventilation and hypotension, she was taken for a computed tomography (CT) with pulmonary embolism protocol.", "The CT revealed no evidence of pulmonary embolism.", "The CT showed evidence of alveolar rupture with pneumomediastinum consistent with the Macklin effect.", "The CT showed a small left-sided pneumothorax.", "The CT showed associated medial left hemi diaphragmatic rupture.", "The CT showed pneumoretroperitoneum tracking along the left upper abdomen.", "The CT showed pneumoretroperitoneum tracking along the left perinephric space.", "The CT showed left-sided nondisplaced rib fractures of the fifth and sixth ribs.", "A CT of the abdomen and pelvis showed a small amount of free air consistent with pneumoretroperitoneum.", "The CT of the abdomen and pelvis showed free air adjacent to the gastric cardia.", "The CT of the abdomen and pelvis showed free air adjacent to the left kidney.", "The CT of the abdomen and pelvis showed free air adjacent to the left adrenal gland.", "There was no definitively identified intra-abdominal traumatic injury.", "Further history from the family revealed she had been complaining of difficulty breathing earlier in the day.", "She subsequently suffered a witnessed fall down a flight of stairs.", "The fall was associated with head trauma.", "The fall was associated with apparent loss of consciousness.", "The patient\u2019s physical examination revealed no external signs of trauma on initial arrival.", "The patient was admitted to the medical intensive care unit.", "The admission was in the setting of cardiac arrest with prolonged down time.", "The patient\u2019s pneumomediastinum improved with lung-protective ventilation strategies.", "The patient\u2019s pneumoretroperitoneum improved with lung-protective ventilation strategies.", "The patient was treated with paralytics.", "The patient\u2019s treatment for her COPD exacerbation included continuous albuterol nebulization of 40 milligrams (mg) over four hours.", "The patient\u2019s treatment included intermittent scheduled three-milliliter ipratroprium-albuterol nebulizers every six hours.", "The patient\u2019s treatment included 0.25 mg of budesonide twice daily.", "The patient\u2019s treatment included 0.5 mg of ipratroprium four times daily.", "The patient\u2019s treatment included isolated two mg of magnesium sulfate administration daily if worsening wheeze on examination.", "The patient\u2019s treatment included 80 mg of methylprednisolone daily.", "The patient received a one-time dose of 0.25 mg of subcutaneous terbutaline.", "The patient received a one-time dose of one microgram (\u03bcg) of epinephrine.", "Sedation was maintained with ketamine at 1.5 mg per kilogram (kg) per hour.", "Sedation was maintained with propofol at 20 \u03bcg/kg per minute.", "The patient was treated with epinephrine as the first-line vasopressor choice.", "The patient\u2019s cardiac arrest resulted in severe hypoxic brain injury.", "The patient had subsequent diffuse cerebral edema.", "The patient had effacement of the basal cisterns.", "The patient had tonsillar herniation seen on CT of her head.", "The patient became increasingly hypertensive.", "The patient was weaned off vasopressors.", "The patient was started on titratable nicardipine at a maximum of 12.5 mg per hour.", "The patient was given a hypertonic saline bolus.", "The patient lost all evidence of brainstem reflexes five days after suffering cardiac arrest.", "The patient continued to trigger some spontaneous breaths on the ventilator.", "Multiple family meetings were held regarding patient prognosis.", "The patient was palliatively extubated.", "The patient died 26 days after arrival."], "index": 12, "original_id": "multiclinsum_test_1808_en.txt", "split": "test", "summary_subclaims": ["The patient suffered a cardiac arrest after a fall.", "The cardiac arrest occurred during a chronic obstructive pulmonary disease exacerbation.", "The patient had pneumoretroperitoneum."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 63-year-old male.", "The patient was admitted with an uncontrolled itching sensation.", "The patient had whole body jaundice.", "Six months prior, the patient had experienced intractable itching.", "The patient had obstructive-pattern jaundice.", "Endoscopic retrograde cholangiopancreatography (ERCP) and endoscopic retrograde biliary drainage were performed.", "ERCP and endoscopic retrograde biliary drainage ruled out malignancy.", "The patient's medical history included hypertension.", "The patient's medical history included diabetes mellitus.", "The patient's hypertension and diabetes mellitus were well controlled by medication.", "The patient was an ex-smoker of ten years.", "The patient was a social drinker.", "No previous illnesses were reported.", "There was no family history of oncologic diseases.", "There was no family history of rheumatic diseases.", "The physical examination revealed icteric sclerae.", "The physical examination revealed multiple itching scratches on the skin.", "The patient\u2019s hemoglobin was 10 g/dL.", "The patient\u2019s hematocrit was 30.6%.", "The patient\u2019s platelet count was 348000/L.", "The patient\u2019s aspartate aminotransferase was 71 U/L.", "The patient\u2019s alanine aminotransferase level was 44 U/L.", "The patient\u2019s gamma-glutamyl transferase level was 233 U/L.", "The patient\u2019s alkaline phosphatase level was 315 U/L.", "The patient\u2019s total bilirubin level was 8.6 mg/dL.", "The patient\u2019s BUN level was 26.7 mg/dL.", "The patient\u2019s creatinine level was 1.37 mg/dL.", "The patient\u2019s erythrocyte sedimentation rate was 120 mm/h.", "The patient\u2019s C reactive protein (CRP) level was 1.81 mg/dL.", "The patient\u2019s antinuclear antibody titer was 1:2560.", "The patient\u2019s antinuclear antibody titer had a nucleolar pattern.", "The patient\u2019s IgG level was 2416 mg/dL.", "The patient\u2019s serum IgG4 level was 465 mg/dL.", "Abdominal computed tomography (CT) showed intrahepatic duct (IHD) dilatation.", "Abdominal CT showed intraductal soft tissue attenuation.", "Abdominal CT showed periductal enhancement.", "The common bile duct (CBD) was dilated.", "The CBD had mild luminal narrowing.", "There were no findings of AIP.", "There was no definite obstructive lesion.", "There was no suspected malignancy.", "CT showed fibrotic enhancement around the infrarenal aorta."], "summary_subclaims": ["The patient is a 63-year-old male.", "The patient had a prominent itching sensation.", "The patient had wholebody jaundice.", "The patient showed obstructive-pattern jaundice.", "The patient had an elevated IgG4 level.", "The patient had infiltration of a large number of IgG4-positive cells in the ampulla of Vater.", "The imaging findings included intrahepatic duct and common bile duct dilation.", "The diagnosis was IgG4-SC compatible with the 2019 ACR/EULAR classification criteria.", "The planned treatment was high-dose glucocorticoid followed by cyclophosphamide pulse therapy.", "After treatment with high-dose GC and an immunosuppressant, imaging studies showed that intrahepatic duct dilatation had completely resolved."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 63-year-old male.", "The patient was admitted with an uncontrolled itching sensation.", "The patient had whole body jaundice.", "Six months prior, the patient had experienced intractable itching.", "The patient had obstructive-pattern jaundice.", "Endoscopic retrograde cholangiopancreatography (ERCP) and endoscopic retrograde biliary drainage were performed.", "ERCP and endoscopic retrograde biliary drainage ruled out malignancy.", "The patient's medical history included hypertension.", "The patient's medical history included diabetes mellitus.", "The patient's hypertension and diabetes mellitus were well controlled by medication.", "The patient was an ex-smoker of ten years.", "The patient was a social drinker.", "No previous illnesses were reported.", "There was no family history of oncologic diseases.", "There was no family history of rheumatic diseases.", "The physical examination revealed icteric sclerae.", "The physical examination revealed multiple itching scratches on the skin.", "The patient\u2019s hemoglobin was 10 g/dL.", "The patient\u2019s hematocrit was 30.6%.", "The patient\u2019s platelet count was 348000/L.", "The patient\u2019s aspartate aminotransferase was 71 U/L.", "The patient\u2019s alanine aminotransferase level was 44 U/L.", "The patient\u2019s gamma-glutamyl transferase level was 233 U/L.", "The patient\u2019s alkaline phosphatase level was 315 U/L.", "The patient\u2019s total bilirubin level was 8.6 mg/dL.", "The patient\u2019s BUN level was 26.7 mg/dL.", "The patient\u2019s creatinine level was 1.37 mg/dL.", "The patient\u2019s erythrocyte sedimentation rate was 120 mm/h.", "The patient\u2019s C reactive protein (CRP) level was 1.81 mg/dL.", "The patient\u2019s antinuclear antibody titer was 1:2560.", "The patient\u2019s antinuclear antibody titer had a nucleolar pattern.", "The patient\u2019s IgG level was 2416 mg/dL.", "The patient\u2019s serum IgG4 level was 465 mg/dL.", "Abdominal computed tomography (CT) showed intrahepatic duct (IHD) dilatation.", "Abdominal CT showed intraductal soft tissue attenuation.", "Abdominal CT showed periductal enhancement.", "The common bile duct (CBD) was dilated.", "The CBD had mild luminal narrowing.", "There were no findings of AIP.", "There was no definite obstructive lesion.", "There was no suspected malignancy.", "CT showed fibrotic enhancement around the infrarenal aorta."], "index": 14, "original_id": "multiclinsum_test_53_en.txt", "split": "test", "summary_subclaims": ["The patient is a 63-year-old male.", "The patient had a prominent itching sensation.", "The patient had wholebody jaundice.", "The patient showed obstructive-pattern jaundice.", "The patient had an elevated IgG4 level.", "The patient had infiltration of a large number of IgG4-positive cells in the ampulla of Vater.", "The imaging findings included intrahepatic duct and common bile duct dilation.", "The diagnosis was IgG4-SC compatible with the 2019 ACR/EULAR classification criteria.", "The planned treatment was high-dose glucocorticoid followed by cyclophosphamide pulse therapy.", "After treatment with high-dose GC and an immunosuppressant, imaging studies showed that intrahepatic duct dilatation had completely resolved."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was a 40-year-old female.", "She had mild hepatic dysfunction.", "She did not smoke.", "She had a drinking habit.", "At age 28, she had elevated platelet counts (> 100 \u00d7 104/\u03bcL).", "ET had been diagnosed based on bone marrow biopsy results.", "She was prescribed aspirin (100 mg/day) and anagrelide (2.5 mg/day).", "She had been prescribed ebastine for itching.", "On admission, her ALT level was 82 IU/L.", "Her ALT level had improved from that recorded previously.", "Her platelet count was 62.4 \u00d7 104/\u03bcL.", "Prothrombin time and activated partial thromboplastin time were normal.", "Abdominal ultrasonography revealed a cecal tumor.", "Colonoscopy revealed advanced cecal cancer.", "CT indicated cecal wall thickening.", "The patient recovered from liver dysfunction without treatment.", "She stopped taking oral aspirin 1 week prior to surgery.", "She continued anagrelide until the day before surgery.", "To prevent thrombosis, she wore elastic stockings.", "Intermittent pneumatic compression was performed during surgery.", "Laparoscopic-assisted ileocecal resection was performed.", "The operative duration was 202 min.", "Blood loss was 34 mL.", "From the first postoperative day, she started walking.", "From the first postoperative day, she started drinking water.", "From the first postoperative day, she resumed oral anagrelide intake.", "She resumed oral aspirin intake on the fifth postoperative day.", "Her perioperative platelet count was controlled to approximately 40\u201360 \u00d7 104/\u03bcL.", "Prothrombin time and activated partial thromboplastin time did not show abnormal values during the perioperative period.", "The postoperative course was uneventful.", "She was discharged on the seventh postoperative day.", "The tumor pathological stage was T3N1M0 (Stage IIIB).", "She received intravenous oxaliplatin plus oral capecitabine as postoperative adjuvant chemotherapy.", "After one course, she again experienced liver dysfunction (AST 388 IU/L; ALT 531 IU/L).", "Her platelet count decreased to 17.8 \u00d7 104/\u03bcL.", "She was asked to discontinue anagrelide and aspirin that day onwards.", "Five days later, her platelet count recovered to 50 \u00d7 104/\u03bcL.", "She resumed taking anagrelide and aspirin.", "She refused to resume any adjuvant chemotherapy after this incident.", "Her liver function normalized gradually in 4 months.", "There were no clinical signs of thrombosis.", "There was no appearance of a new thrombus on contrast-enhanced CT 6 months after the operation.", "One-year post operation, she is well without tumor recurrence or new metastasis."], "summary_subclaims": ["A 40-year-old woman was admitted to our hospital after presenting with liver dysfunction.", "She had been previously diagnosed with ET.", "Aspirin and anagrelide had been prescribed.", "Subsequent examination at our hospital revealed cecal cancer.", "Distant metastasis was absent.", "Laparoscopic ileocecal resection was performed.", "Anagrelide was discontinued only on the surgery day.", "She was discharged on the seventh postoperative day without thrombosis or hemorrhage.", "When capecitabine and oxaliplatin were administered as adjuvant chemotherapy with continued anagrelide administration, she experienced hepatic dysfunction and thrombocytopenia.", "Anagrelide was discontinued.", "Five days later, her platelet count recovered.", "Subsequently, anagrelide and aspirin administration was resumed, without any adjuvant chemotherapy.", "Her liver function normalized gradually in 4\u2009months.", "One-year post operation, she is well without tumor recurrence or new metastasis."]}, "extra_info": {"fulltext_subclaims": ["The patient was a 40-year-old female.", "She had mild hepatic dysfunction.", "She did not smoke.", "She had a drinking habit.", "At age 28, she had elevated platelet counts (> 100 \u00d7 104/\u03bcL).", "ET had been diagnosed based on bone marrow biopsy results.", "She was prescribed aspirin (100 mg/day) and anagrelide (2.5 mg/day).", "She had been prescribed ebastine for itching.", "On admission, her ALT level was 82 IU/L.", "Her ALT level had improved from that recorded previously.", "Her platelet count was 62.4 \u00d7 104/\u03bcL.", "Prothrombin time and activated partial thromboplastin time were normal.", "Abdominal ultrasonography revealed a cecal tumor.", "Colonoscopy revealed advanced cecal cancer.", "CT indicated cecal wall thickening.", "The patient recovered from liver dysfunction without treatment.", "She stopped taking oral aspirin 1 week prior to surgery.", "She continued anagrelide until the day before surgery.", "To prevent thrombosis, she wore elastic stockings.", "Intermittent pneumatic compression was performed during surgery.", "Laparoscopic-assisted ileocecal resection was performed.", "The operative duration was 202 min.", "Blood loss was 34 mL.", "From the first postoperative day, she started walking.", "From the first postoperative day, she started drinking water.", "From the first postoperative day, she resumed oral anagrelide intake.", "She resumed oral aspirin intake on the fifth postoperative day.", "Her perioperative platelet count was controlled to approximately 40\u201360 \u00d7 104/\u03bcL.", "Prothrombin time and activated partial thromboplastin time did not show abnormal values during the perioperative period.", "The postoperative course was uneventful.", "She was discharged on the seventh postoperative day.", "The tumor pathological stage was T3N1M0 (Stage IIIB).", "She received intravenous oxaliplatin plus oral capecitabine as postoperative adjuvant chemotherapy.", "After one course, she again experienced liver dysfunction (AST 388 IU/L; ALT 531 IU/L).", "Her platelet count decreased to 17.8 \u00d7 104/\u03bcL.", "She was asked to discontinue anagrelide and aspirin that day onwards.", "Five days later, her platelet count recovered to 50 \u00d7 104/\u03bcL.", "She resumed taking anagrelide and aspirin.", "She refused to resume any adjuvant chemotherapy after this incident.", "Her liver function normalized gradually in 4 months.", "There were no clinical signs of thrombosis.", "There was no appearance of a new thrombus on contrast-enhanced CT 6 months after the operation.", "One-year post operation, she is well without tumor recurrence or new metastasis."], "index": 16, "original_id": "multiclinsum_test_1612_en.txt", "split": "test", "summary_subclaims": ["A 40-year-old woman was admitted to our hospital after presenting with liver dysfunction.", "She had been previously diagnosed with ET.", "Aspirin and anagrelide had been prescribed.", "Subsequent examination at our hospital revealed cecal cancer.", "Distant metastasis was absent.", "Laparoscopic ileocecal resection was performed.", "Anagrelide was discontinued only on the surgery day.", "She was discharged on the seventh postoperative day without thrombosis or hemorrhage.", "When capecitabine and oxaliplatin were administered as adjuvant chemotherapy with continued anagrelide administration, she experienced hepatic dysfunction and thrombocytopenia.", "Anagrelide was discontinued.", "Five days later, her platelet count recovered.", "Subsequently, anagrelide and aspirin administration was resumed, without any adjuvant chemotherapy.", "Her liver function normalized gradually in 4\u2009months.", "One-year post operation, she is well without tumor recurrence or new metastasis."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was a 55-year-old woman.", "The patient had a history of smoking.", "The patient had a history of prolonged opium inhalation.", "The patient was referred to Ghaem clinic in Mashhad.", "The patient had dysphonia.", "The patient had hoarseness.", "The patient had occasional aspiration since last year.", "No sign of odynodysphagia was observed.", "No sign of stridor was observed.", "No sign of dyspnea was observed.", "The patient did not previously undergo any treatment.", "In laryngoscopy, prior to surgery, left arytenoid was tumoral.", "In laryngoscopy, prior to surgery, left aryepiglottic fold was tumoral.", "In laryngoscopy, prior to surgery, left false vocal cord was tumoral.", "In laryngoscopy, prior to surgery, left true vocal cord was tumoral.", "In laryngoscopy, prior to surgery, anterior commissure was tumoral.", "In laryngoscopy, prior to surgery, subglottic region was tumoral.", "In laryngoscopy, prior to surgery, other parts of the larynx and hypopharynx were normal.", "The left vocal cord was fixed.", "In the preoperative computed tomography scan, there was transglottic involvement on the left side.", "In the preoperative computed tomography scan, cervical lymphadenopathy was not detected.", "Laryngeal cartilage and hyoid bone were reported to be normal.", "The right paraglottic space was involved.", "The epiglottis was normal.", "The tongue was normal.", "The esophagus was normal.", "The trachea was normal.", "The thyroid was normal.", "The biopsy of the affected areas represented well-differentiated squamous cell carcinoma.", "Chest X-rays were normal.", "Liver function tests were normal.", "The patient was ultimately diagnosed with transglottic squamous cell carcinoma of the T3N0M0 stage.", "Total laryngectomy with total thyroidectomy was performed.", "Bilateral elective cervical lymph node dissection level I-IV was performed.", "The tumor was macroscopically removed.", "The surgical margin was checked with a frozen section for the presence of the tumor.", "The neopharynx was closed with the suturing technique.", "The patient was diagnosed with salivary fistula.", "The patient was initially treated with conservative management.", "Total parenteral nutrition was part of the conservative management.", "Pressure dressing was part of the conservative management.", "Broad-spectrum antibiotic therapy was part of the conservative management.", "In spite of conservative treatment, the fistula was not recovered after 3 weeks.", "Jejunostomy was inserted instead of gastrostomy.", "Intestinal gavage was initiated.", "There was no evidence of positive surgical margins on permanent specimen pathology.", "A thoracic surgeon was consulted about gastric pull-up.", "It was decided to perform fibrin glue injection into the fistula tract via the endoscopic approach.", "Informed consent was obtained from the patient before the surgery.", "The case underwent an endoscopy to locate internal fistula orifice.", "In gastrointestinal endoscopy, a fistula was identified in the anterior wall of the neopharynx.", "Fibrin glue was prepared from the patient\u2019s blood sample.", "The PCF tract was endoscopically localized.", "An ERCP catheter passed through the fistula.", "The de-epithelialization of fistula orifice was performed.", "Fibrin glue was endoscopically injected into the fistula tract via the catheter.", "A nasogastric tube was inserted under the endoscopic view.", "Following the administration of fibrin glue, the patient underwent pressure dressing.", "Two weeks later, the case was discharged with an NG tube and antibiotics.", "One month after the fibrin glue injection, no evidence of contrast extravasation was observed on barium swallow test.", "The fistula was completely closed one month after the fibrin glue injection.", "The NG tube was drawn one month after the fibrin administration.", "The patient returned to normal oral feeding without any problems.", "Fibrin glue preparation required two components: fibrinogen and thrombin.", "Fibrinogen is prepared after the extraction of blood from the patient's vein or blood bank.", "Thrombin is produced as a ready-to-use commercial solution.", "Thrombin is extractable from the plasma of the patient.", "Thrombin is diluted in distilled water and combined with aminocaproic acid.", "The first method of fibrinogen preparation is plasma.", "The second method of fibrinogen preparation is plasma cryoprecipitate.", "The third method of fibrinogen preparation is plasma cryoprecipitate.", "In this study, the second method was used for the preparation of fibrin glue.", "In this case, fibrin glue was injected by endoscopy.", "Under intravenous sedation and left lateral decubitus position, the endoscope entered into neopharynx through the mouth.", "The location of the fistula was observed in the anterior neopharyngeal wall.", "The ERCP catheter passed through the endoscope into the fistula.", "The de-epithelialization of fistula orifice was performed.", "Five cc of the fibrin glue was endoscopically injected into the fistula tract via the catheter.", "Some fibrin glue was percutaneously injected into the outer orifice of the fistula.", "The patient follow-up showed that the fistula was completely closed three months after the administration.", "The NG tube was removed.", "Oral nutrition was successfully started.", "The subsequent follow-up demonstrated that the patient tolerated a soft diet and fluids without any problems."], "summary_subclaims": ["The patient was a 55-year-old woman.", "She had a transglottic squamous cell carcinoma of the T3N0M0 stage.", "She had PCF development following total laryngectomy surgery.", "She had total thyroidectomy and bilateral elective cervical lymph node dissection level I-IV.", "The fistula was not recovered after 3 weeks of conservative treatment.", "It was decided to perform fibrin glue injection into the fistula tract via the endoscopic approach.", "One month after the fibrin glue injection, no evidence of contrast extravasation was observed on barium swallow test.", "The fistula was completely closed."]}, "extra_info": {"fulltext_subclaims": ["The patient was a 55-year-old woman.", "The patient had a history of smoking.", "The patient had a history of prolonged opium inhalation.", "The patient was referred to Ghaem clinic in Mashhad.", "The patient had dysphonia.", "The patient had hoarseness.", "The patient had occasional aspiration since last year.", "No sign of odynodysphagia was observed.", "No sign of stridor was observed.", "No sign of dyspnea was observed.", "The patient did not previously undergo any treatment.", "In laryngoscopy, prior to surgery, left arytenoid was tumoral.", "In laryngoscopy, prior to surgery, left aryepiglottic fold was tumoral.", "In laryngoscopy, prior to surgery, left false vocal cord was tumoral.", "In laryngoscopy, prior to surgery, left true vocal cord was tumoral.", "In laryngoscopy, prior to surgery, anterior commissure was tumoral.", "In laryngoscopy, prior to surgery, subglottic region was tumoral.", "In laryngoscopy, prior to surgery, other parts of the larynx and hypopharynx were normal.", "The left vocal cord was fixed.", "In the preoperative computed tomography scan, there was transglottic involvement on the left side.", "In the preoperative computed tomography scan, cervical lymphadenopathy was not detected.", "Laryngeal cartilage and hyoid bone were reported to be normal.", "The right paraglottic space was involved.", "The epiglottis was normal.", "The tongue was normal.", "The esophagus was normal.", "The trachea was normal.", "The thyroid was normal.", "The biopsy of the affected areas represented well-differentiated squamous cell carcinoma.", "Chest X-rays were normal.", "Liver function tests were normal.", "The patient was ultimately diagnosed with transglottic squamous cell carcinoma of the T3N0M0 stage.", "Total laryngectomy with total thyroidectomy was performed.", "Bilateral elective cervical lymph node dissection level I-IV was performed.", "The tumor was macroscopically removed.", "The surgical margin was checked with a frozen section for the presence of the tumor.", "The neopharynx was closed with the suturing technique.", "The patient was diagnosed with salivary fistula.", "The patient was initially treated with conservative management.", "Total parenteral nutrition was part of the conservative management.", "Pressure dressing was part of the conservative management.", "Broad-spectrum antibiotic therapy was part of the conservative management.", "In spite of conservative treatment, the fistula was not recovered after 3 weeks.", "Jejunostomy was inserted instead of gastrostomy.", "Intestinal gavage was initiated.", "There was no evidence of positive surgical margins on permanent specimen pathology.", "A thoracic surgeon was consulted about gastric pull-up.", "It was decided to perform fibrin glue injection into the fistula tract via the endoscopic approach.", "Informed consent was obtained from the patient before the surgery.", "The case underwent an endoscopy to locate internal fistula orifice.", "In gastrointestinal endoscopy, a fistula was identified in the anterior wall of the neopharynx.", "Fibrin glue was prepared from the patient\u2019s blood sample.", "The PCF tract was endoscopically localized.", "An ERCP catheter passed through the fistula.", "The de-epithelialization of fistula orifice was performed.", "Fibrin glue was endoscopically injected into the fistula tract via the catheter.", "A nasogastric tube was inserted under the endoscopic view.", "Following the administration of fibrin glue, the patient underwent pressure dressing.", "Two weeks later, the case was discharged with an NG tube and antibiotics.", "One month after the fibrin glue injection, no evidence of contrast extravasation was observed on barium swallow test.", "The fistula was completely closed one month after the fibrin glue injection.", "The NG tube was drawn one month after the fibrin administration.", "The patient returned to normal oral feeding without any problems.", "Fibrin glue preparation required two components: fibrinogen and thrombin.", "Fibrinogen is prepared after the extraction of blood from the patient's vein or blood bank.", "Thrombin is produced as a ready-to-use commercial solution.", "Thrombin is extractable from the plasma of the patient.", "Thrombin is diluted in distilled water and combined with aminocaproic acid.", "The first method of fibrinogen preparation is plasma.", "The second method of fibrinogen preparation is plasma cryoprecipitate.", "The third method of fibrinogen preparation is plasma cryoprecipitate.", "In this study, the second method was used for the preparation of fibrin glue.", "In this case, fibrin glue was injected by endoscopy.", "Under intravenous sedation and left lateral decubitus position, the endoscope entered into neopharynx through the mouth.", "The location of the fistula was observed in the anterior neopharyngeal wall.", "The ERCP catheter passed through the endoscope into the fistula.", "The de-epithelialization of fistula orifice was performed.", "Five cc of the fibrin glue was endoscopically injected into the fistula tract via the catheter.", "Some fibrin glue was percutaneously injected into the outer orifice of the fistula.", "The patient follow-up showed that the fistula was completely closed three months after the administration.", "The NG tube was removed.", "Oral nutrition was successfully started.", "The subsequent follow-up demonstrated that the patient tolerated a soft diet and fluids without any problems."], "index": 13, "original_id": "multiclinsum_test_112_en.txt", "split": "test", "summary_subclaims": ["The patient was a 55-year-old woman.", "She had a transglottic squamous cell carcinoma of the T3N0M0 stage.", "She had PCF development following total laryngectomy surgery.", "She had total thyroidectomy and bilateral elective cervical lymph node dissection level I-IV.", "The fistula was not recovered after 3 weeks of conservative treatment.", "It was decided to perform fibrin glue injection into the fistula tract via the endoscopic approach.", "One month after the fibrin glue injection, no evidence of contrast extravasation was observed on barium swallow test.", "The fistula was completely closed."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 4-day-old male infant.", "He was born at 40 weeks\u2019 gestational age.", "He weighed 3660 g at birth.", "He was delivered at term by episiotomy combined with forceps.", "He was admitted to the Department of Neonatology of The Second Hospital of Jilin University due to dyspnea in February 2022.", "No cutaneous lesions were observed.", "Brain MRI showed a short T1 strip signal shadow (hemorrhage) under the cranial plate of the occipital region on both sides.", "The right eye appeared normal in the routine retinal screening performed with RetCam 3.", "A color fundus photograph of the left eye revealed a solitary yellowish-white flat mass with an approximate size of 1.5-disc diameters located in the nasal retina.", "Fluorescein angiography showed diffuse hyperfluorescence with slight fluorescence leakage.", "On B-scan ultrasound, the mass was inapparent, with no distinct foci of calcification.", "No treatment was administered.", "Follow-up reexaminations were recommended.", "Three months later, regression in the size of the retinal mass was observed.", "Fluorescein angiography showed decreased vascularization of the lesion and slight mottled hyperfluorescence over its surface.", "Seven months later, the fundus examination indicated no lesion in the left eye.", "Fluorescein angiography showed mild tortuous vessels without leakage.", "The right retina was normal.", "The clinical course suggested that the isolated RAH may undergo spontaneous regression."], "summary_subclaims": ["An isolated retinal astrocytic hamartoma was detected in the nasal retina of the left eye of a 4-day-old male infant.", "At the time of initial presentation, we detected a solitary yellowish-white flat mass with an approximate size of 1.5 disc diameters in the nasal retina.", "Fluorescein angiography (FA) revealed a diffuse hyperfluorescence with slight fluorescence leakage.", "Seven months later, the fundus examination showed no lesion in the left eye.", "Fluorescein angiography revealed mild tortuous vessels without leakage."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 4-day-old male infant.", "He was born at 40 weeks\u2019 gestational age.", "He weighed 3660 g at birth.", "He was delivered at term by episiotomy combined with forceps.", "He was admitted to the Department of Neonatology of The Second Hospital of Jilin University due to dyspnea in February 2022.", "No cutaneous lesions were observed.", "Brain MRI showed a short T1 strip signal shadow (hemorrhage) under the cranial plate of the occipital region on both sides.", "The right eye appeared normal in the routine retinal screening performed with RetCam 3.", "A color fundus photograph of the left eye revealed a solitary yellowish-white flat mass with an approximate size of 1.5-disc diameters located in the nasal retina.", "Fluorescein angiography showed diffuse hyperfluorescence with slight fluorescence leakage.", "On B-scan ultrasound, the mass was inapparent, with no distinct foci of calcification.", "No treatment was administered.", "Follow-up reexaminations were recommended.", "Three months later, regression in the size of the retinal mass was observed.", "Fluorescein angiography showed decreased vascularization of the lesion and slight mottled hyperfluorescence over its surface.", "Seven months later, the fundus examination indicated no lesion in the left eye.", "Fluorescein angiography showed mild tortuous vessels without leakage.", "The right retina was normal.", "The clinical course suggested that the isolated RAH may undergo spontaneous regression."], "index": 20, "original_id": "multiclinsum_test_2309_en.txt", "split": "test", "summary_subclaims": ["An isolated retinal astrocytic hamartoma was detected in the nasal retina of the left eye of a 4-day-old male infant.", "At the time of initial presentation, we detected a solitary yellowish-white flat mass with an approximate size of 1.5 disc diameters in the nasal retina.", "Fluorescein angiography (FA) revealed a diffuse hyperfluorescence with slight fluorescence leakage.", "Seven months later, the fundus examination showed no lesion in the left eye.", "Fluorescein angiography revealed mild tortuous vessels without leakage."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["A 27-year-old male involved in a motor vehicle accident was brought to Emergency Department room with respiratory distress.", "He was intubated upon arrival due to low Glasgow Coma Scale (GCS) with extensive maxillofacial injuries.", "Thoracic examination showed reduced air entry at right chest wall region.", "Palpable crepitus on his right neck region was due to subcutaneous emphysema from the neck to the anterior chest wall.", "A curvilinear transducer on the right second intercostal ribs showed the absence of sliding signs, suggestive of right pneumothorax.", "A FAST scan was performed.", "On subxiphoid view of the heart, only the right ventricle was seen during diastole.", "Part of the cardiac image was obscured by A-lines.", "This raised a suspicion of pneumopericardium.", "Only A-lines were visible on parasternal long axis (PLAX), parasternal short axis (PSAX), and apical four chamber (A4C) views.", "The patient underwent head and chest CT scan.", "The CT scan confirmed the diagnosis of Le Fort II facial bone injury.", "The CT scan confirmed the diagnosis of right pneumothorax.", "The CT scan confirmed the diagnosis of right pulmonary contusion.", "The CT scan confirmed the diagnosis of pneumopericardium.", "The pneumopericardium was treated conservatively."], "summary_subclaims": ["A young man involved in a car accident and sustained blunt thoracic injuries, among others.", "As part of primary survey, FAST scan was performed.", "Subxiphoid view to look for evidence of pericardial effusion showed part of the cardiac image obscured by A-lines.", "Other cardiac windows showed only A-lines, as well.", "A suspicion of pneumopericardium was raised.", "CT scan confirmed the diagnosis."]}, "extra_info": {"fulltext_subclaims": ["A 27-year-old male involved in a motor vehicle accident was brought to Emergency Department room with respiratory distress.", "He was intubated upon arrival due to low Glasgow Coma Scale (GCS) with extensive maxillofacial injuries.", "Thoracic examination showed reduced air entry at right chest wall region.", "Palpable crepitus on his right neck region was due to subcutaneous emphysema from the neck to the anterior chest wall.", "A curvilinear transducer on the right second intercostal ribs showed the absence of sliding signs, suggestive of right pneumothorax.", "A FAST scan was performed.", "On subxiphoid view of the heart, only the right ventricle was seen during diastole.", "Part of the cardiac image was obscured by A-lines.", "This raised a suspicion of pneumopericardium.", "Only A-lines were visible on parasternal long axis (PLAX), parasternal short axis (PSAX), and apical four chamber (A4C) views.", "The patient underwent head and chest CT scan.", "The CT scan confirmed the diagnosis of Le Fort II facial bone injury.", "The CT scan confirmed the diagnosis of right pneumothorax.", "The CT scan confirmed the diagnosis of right pulmonary contusion.", "The CT scan confirmed the diagnosis of pneumopericardium.", "The pneumopericardium was treated conservatively."], "index": 21, "original_id": "multiclinsum_test_1133_en.txt", "split": "test", "summary_subclaims": ["A young man involved in a car accident and sustained blunt thoracic injuries, among others.", "As part of primary survey, FAST scan was performed.", "Subxiphoid view to look for evidence of pericardial effusion showed part of the cardiac image obscured by A-lines.", "Other cardiac windows showed only A-lines, as well.", "A suspicion of pneumopericardium was raised.", "CT scan confirmed the diagnosis."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was a 2 years and 5-month-old boy.", "The patient was admitted for fever with onset 3 days before admission.", "The fever was associated with abdominal pain and diarrhea within the last 24 hours.", "The anamnesis did not reveal any possible exposure to COVID-19 infections.", "The clinical exam at admission revealed bilateral palpebral edema.", "The clinical exam at admission revealed conjunctivitis.", "The clinical exam at admission revealed mucocutaneous signs of dehydration.", "The clinical exam at admission revealed abdominal tenderness at palpation.", "The patient weighed 15 kilograms.", "The laboratory test showed lymphopenia (1560/mm3).", "The laboratory test showed thrombocytopenia (108x103/mm3).", "The laboratory test showed anemia (hemoglobin \u2013 Hb 10.9 g/dL).", "The laboratory test showed elevated C-reactive protein \u2013 CRP (162 mg/L).", "The laboratory test showed elevated ferritin levels (389.3 ng/mL).", "The laboratory test showed hyponatremia (132 mmol/L).", "The laboratory test showed hypokalemia (3.94 mmol/L).", "The laboratory test showed hypertriglyceridemia (476.3 mg/dL).", "The laboratory test showed elevated D-dimer (>5 \u03bcg/ml).", "The laboratory test showed increased troponin (16.6 ng/L).", "The laboratory test showed increased NT-proBNP (19,831 pg/ml).", "The rapid urine exam was negative.", "The chest X-ray showed no pathological findings.", "The abdominal ultrasound showed no pathological findings.", "The echocardiography showed no pathological findings.", "The blood culture was negative.", "The urine culture was negative.", "We raised the suspicion of pediatric inflammatory multisystem syndrome possibly associated to COVID-19.", "The RT-PCR test for SARS-CoV-2 infection was negative.", "The serology (IgG anti-SARS-CoV-2) was positive.", "We established the diagnosis of PIMS-TS.", "We initiated intravenous immunoglobulin in a dose of 2 g/kg/day.", "We initiated empirical antibiotic (ceftriaxone).", "We initiated anticoagulation therapy (low-molecular weight heparin).", "We administered symptomatic drugs (antipyretics, antiemetics, and antidiarrheics).", "The fever persisted for the following 36 hours with no clinical improvement.", "The laboratory test on the 3rd day showed an increase of the CRP value (216.65 mg/L).", "The laboratory test on the 3rd day showed persistence of elevated NT-proBNP (9,884.2 pg/mL).", "The laboratory test on the 3rd day showed persistence of elevated D-dimer (1,198 ng/mL).", "The laboratory test on the 3rd day showed hypoalbuminemia (2.45 g/dL).", "We initiated intravenous methylprednisolone (10 mg/kg/day) for 3 days.", "We initiated substitutive treatment with human albumin.", "The echocardiography showed minimal pericardial effusion.", "The echocardiography showed slight dilation of the left cavities.", "The echocardiography showed regional wall motion abnormalities with dyskinesia of the inferior and infero-septal basal segments of the LV.", "The echocardiography showed LV systolic dysfunction with LV ejection fraction of 40%.", "The echocardiography showed mild mitral regurgitation.", "The echocardiography showed no coronary impairment.", "We associated angiotensin converting enzyme inhibitors (Lisinopril).", "We associated Spironolactone.", "We associated Hydrochlorothiazide.", "Serial echocardiography showed resorption of the pericardial effusion.", "Serial echocardiography showed improvement of LV function.", "Serial echocardiography showed decreased serum levels of NT-proBNP (123.1 pg/mL).", "Serial echocardiography showed decreased serum levels of troponin (5.2 pg/mL).", "The patient was discharged on the 11th day of admission.", "The patient was discharged without any complaints.", "Most of the laboratory parameters were within normal ranges at discharge.", "D-dimer was not within normal ranges at discharge.", "We recommended continuation of anticoagulant therapy for another week.", "We recommended continuation of Lisinopril for the following 2 weeks.", "We recommended continuation of Spironolactone for the following 2 weeks.", "We recommended continuation of Hydrochlorothiazide for the following 2 weeks."], "summary_subclaims": ["The patient was a 2 years and 5-month-old boy.", "The patient was admitted for fever, abdominal pain, and diarrhea.", "The clinical exam at admission revealed influenced general status.", "The clinical exam at admission revealed bilateral palpebral edema.", "The clinical exam at admission revealed conjunctivitis.", "The clinical exam at admission revealed mucocutaneous signs of dehydration.", "The clinical exam at admission revealed abdominal tenderness at palpation.", "The laboratory tests showed lymphopenia.", "The laboratory tests showed thrombocytopenia.", "The laboratory tests showed anemia.", "The laboratory tests showed elevated C-reactive protein.", "The laboratory tests showed elevated erythrocyte sedimentation rate.", "The laboratory tests showed elevated ferritin levels.", "The laboratory tests showed hyponatremia.", "The laboratory tests showed hypokalemia.", "The laboratory tests showed hypertriglyceridemia.", "The laboratory tests showed elevated D-dimer.", "The laboratory tests showed increased troponin.", "The laboratory tests showed increased NT-proBNP.", "The RT-PCR test for SARS-CoV-2 infection was negative.", "The serology for SARS-CoV-2 was positive.", "The diagnosis of PIMS-TS was established.", "Intravenous immunoglobulin was initiated.", "Empirical antibiotic therapy was initiated.", "Anticoagulation therapy was initiated.", "Symptomatic drugs were initiated.", "The clinical course and laboratory parameters worsened.", "The 2nd echocardiography showed minimal pericardial effusion.", "The 2nd echocardiography showed slight dilation of the left cavities.", "The 2nd echocardiography showed dyskinesia of the inferior and septal basal segments of the left ventricle.", "The 2nd echocardiography showed left ventricular systolic dysfunction.", "Intravenous methylprednisolone was added.", "Angiotensin converting enzyme inhibitors were added.", "Spironolactone was added.", "Hydrochlorothiazide was added.", "The clinical evolution was outstandingly favorable."]}, "extra_info": {"fulltext_subclaims": ["The patient was a 2 years and 5-month-old boy.", "The patient was admitted for fever with onset 3 days before admission.", "The fever was associated with abdominal pain and diarrhea within the last 24 hours.", "The anamnesis did not reveal any possible exposure to COVID-19 infections.", "The clinical exam at admission revealed bilateral palpebral edema.", "The clinical exam at admission revealed conjunctivitis.", "The clinical exam at admission revealed mucocutaneous signs of dehydration.", "The clinical exam at admission revealed abdominal tenderness at palpation.", "The patient weighed 15 kilograms.", "The laboratory test showed lymphopenia (1560/mm3).", "The laboratory test showed thrombocytopenia (108x103/mm3).", "The laboratory test showed anemia (hemoglobin \u2013 Hb 10.9 g/dL).", "The laboratory test showed elevated C-reactive protein \u2013 CRP (162 mg/L).", "The laboratory test showed elevated ferritin levels (389.3 ng/mL).", "The laboratory test showed hyponatremia (132 mmol/L).", "The laboratory test showed hypokalemia (3.94 mmol/L).", "The laboratory test showed hypertriglyceridemia (476.3 mg/dL).", "The laboratory test showed elevated D-dimer (>5 \u03bcg/ml).", "The laboratory test showed increased troponin (16.6 ng/L).", "The laboratory test showed increased NT-proBNP (19,831 pg/ml).", "The rapid urine exam was negative.", "The chest X-ray showed no pathological findings.", "The abdominal ultrasound showed no pathological findings.", "The echocardiography showed no pathological findings.", "The blood culture was negative.", "The urine culture was negative.", "We raised the suspicion of pediatric inflammatory multisystem syndrome possibly associated to COVID-19.", "The RT-PCR test for SARS-CoV-2 infection was negative.", "The serology (IgG anti-SARS-CoV-2) was positive.", "We established the diagnosis of PIMS-TS.", "We initiated intravenous immunoglobulin in a dose of 2 g/kg/day.", "We initiated empirical antibiotic (ceftriaxone).", "We initiated anticoagulation therapy (low-molecular weight heparin).", "We administered symptomatic drugs (antipyretics, antiemetics, and antidiarrheics).", "The fever persisted for the following 36 hours with no clinical improvement.", "The laboratory test on the 3rd day showed an increase of the CRP value (216.65 mg/L).", "The laboratory test on the 3rd day showed persistence of elevated NT-proBNP (9,884.2 pg/mL).", "The laboratory test on the 3rd day showed persistence of elevated D-dimer (1,198 ng/mL).", "The laboratory test on the 3rd day showed hypoalbuminemia (2.45 g/dL).", "We initiated intravenous methylprednisolone (10 mg/kg/day) for 3 days.", "We initiated substitutive treatment with human albumin.", "The echocardiography showed minimal pericardial effusion.", "The echocardiography showed slight dilation of the left cavities.", "The echocardiography showed regional wall motion abnormalities with dyskinesia of the inferior and infero-septal basal segments of the LV.", "The echocardiography showed LV systolic dysfunction with LV ejection fraction of 40%.", "The echocardiography showed mild mitral regurgitation.", "The echocardiography showed no coronary impairment.", "We associated angiotensin converting enzyme inhibitors (Lisinopril).", "We associated Spironolactone.", "We associated Hydrochlorothiazide.", "Serial echocardiography showed resorption of the pericardial effusion.", "Serial echocardiography showed improvement of LV function.", "Serial echocardiography showed decreased serum levels of NT-proBNP (123.1 pg/mL).", "Serial echocardiography showed decreased serum levels of troponin (5.2 pg/mL).", "The patient was discharged on the 11th day of admission.", "The patient was discharged without any complaints.", "Most of the laboratory parameters were within normal ranges at discharge.", "D-dimer was not within normal ranges at discharge.", "We recommended continuation of anticoagulant therapy for another week.", "We recommended continuation of Lisinopril for the following 2 weeks.", "We recommended continuation of Spironolactone for the following 2 weeks.", "We recommended continuation of Hydrochlorothiazide for the following 2 weeks."], "index": 15, "original_id": "multiclinsum_test_723_en.txt", "split": "test", "summary_subclaims": ["The patient was a 2 years and 5-month-old boy.", "The patient was admitted for fever, abdominal pain, and diarrhea.", "The clinical exam at admission revealed influenced general status.", "The clinical exam at admission revealed bilateral palpebral edema.", "The clinical exam at admission revealed conjunctivitis.", "The clinical exam at admission revealed mucocutaneous signs of dehydration.", "The clinical exam at admission revealed abdominal tenderness at palpation.", "The laboratory tests showed lymphopenia.", "The laboratory tests showed thrombocytopenia.", "The laboratory tests showed anemia.", "The laboratory tests showed elevated C-reactive protein.", "The laboratory tests showed elevated erythrocyte sedimentation rate.", "The laboratory tests showed elevated ferritin levels.", "The laboratory tests showed hyponatremia.", "The laboratory tests showed hypokalemia.", "The laboratory tests showed hypertriglyceridemia.", "The laboratory tests showed elevated D-dimer.", "The laboratory tests showed increased troponin.", "The laboratory tests showed increased NT-proBNP.", "The RT-PCR test for SARS-CoV-2 infection was negative.", "The serology for SARS-CoV-2 was positive.", "The diagnosis of PIMS-TS was established.", "Intravenous immunoglobulin was initiated.", "Empirical antibiotic therapy was initiated.", "Anticoagulation therapy was initiated.", "Symptomatic drugs were initiated.", "The clinical course and laboratory parameters worsened.", "The 2nd echocardiography showed minimal pericardial effusion.", "The 2nd echocardiography showed slight dilation of the left cavities.", "The 2nd echocardiography showed dyskinesia of the inferior and septal basal segments of the left ventricle.", "The 2nd echocardiography showed left ventricular systolic dysfunction.", "Intravenous methylprednisolone was added.", "Angiotensin converting enzyme inhibitors were added.", "Spironolactone was added.", "Hydrochlorothiazide was added.", "The clinical evolution was outstandingly favorable."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 3.7-kg, 1-month-old male.", "He presented at day 24 of life with severe aortic stenosis and coarctation of the aorta.", "He was born at term following an uncomplicated pregnancy.", "On day 5 of life, he was noted to be jaundiced and have a murmur.", "His jaundice resolved, and he was discharged home with cardiac follow-up.", "He had progressive increase in his work of breathing.", "He was not gaining weight.", "An echocardiogram on day 24 of life showed a thickened and dysplastic bicuspid aortic valve with doming of the valve leaflets.", "The flow across the valve was measured on continuous wave doppler at 4 m/s.", "He was found to have a discrete juxta ductal coarctation of the aorta with continuous doppler flow of 2.5 m/s with diastolic tail.", "His ventricular function remained preserved.", "He was started on intravenous prostaglandin.", "Urgent surgery was scheduled.", "The best course of action was felt to be a hybrid approach with surgical end-to-end anastomosis of the aortic arch via a thoracotomy followed by surgical carotid cut down for AoVP.", "The patient was taken to the hybrid catheter laboratory theater.", "He underwent the surgical end-to-end anastomosis via the thoracotomy via the third intercostal space.", "The arch, patent ductus arteriosus, and descending aorta were dissected out.", "Clamps were applied to the arch and descending aorta.", "The coarctation segment was resected.", "The patent ductus arteriosus was ligated.", "An end to side anastomosis was performed between the aortic arch and the descending aorta.", "The pleura and chest were closed in layers.", "The patient was assessed and felt to be stable to proceed with the planned aortic balloon.", "A 5/0 purse string suture was applied to the right common carotid artery.", "A 4-Fr sheath was inserted in the right common carotid artery.", "Ascending aortic pressure was measured at 61/42 mmHg.", "The aortic valve annulus measured 7.5 mm.", "The pressure in the left ventricle was recorded at 110/13 mmHg.", "A peak to peak gradient of 49 mmHg was calculated.", "A 0.014 ChoICE PT extra support coronary wire was placed in the left ventricle.", "A NuMED Tyshak II 6 mm \u00d7 2 cm percutaneous transluminal valvuloplasty balloon catheter was delivered over the ChoICE wire to the aortic valve.", "The balloon was inflated to burst pressure of 4 atmospheres.", "A waist was seen within the balloon and dewaisting occurred.", "The balloon catheter was removed.", "The pressure was measured at 100/10 mmHg.", "Repeat angiogram at the aortic root did not demonstrate any significant aortic incompetence.", "A 7 mm \u00d7 2 cm NuMED Tyshak II percutaneous transluminal valvuloplasty balloon catheter was delivered over the coronary guidewire in position.", "The balloon was inflated to 4 atm.", "A waist was again seen and dewaisting occurred.", "The balloon catheter was removed.", "The pressure within the left ventricle was now 90/10 mmHg.", "The pullback peak to peak gradient between the left ventricle and ascending aorta measured 30 mmHg.", "The catheter and sheath were removed.", "The vessel was repaired by tightening the pursestring suture.", "The skin was closed in layers.", "An echocardiogram performed post procedure showed qualitatively normal ventricular function with no pericardial effusion.", "The arch was unobstructed with doppler flow velocity of 1.6 m/s.", "The aortic valve was bicuspid and obviously dysplastic.", "There was mild flow acceleration across the valve using continuous wave doppler of 3 m/s.", "There was a mean doppler gradient of 15 mmHg.", "There was no obvious aortic incompetency seen.", "The patient was transferred from the hybrid catheter laboratory to the pediatric intensive care unit.", "He remained cardiovascularly stable during his PICU admission.", "He was extubated but had to be reintubated within a few hours due to upper airway issues.", "He was successfully extubated on day 3 post procedure.", "He was transferred to the cardiac ward.", "His admission on the ward was uncomplicated.", "He was discharged on day 6 post intervention.", "At 4 months of age, he was reviewed in the outpatient clinic.", "He was clinically asymptomatic with steady growth.", "His echocardiogram demonstrated qualitatively normal ventricular function.", "The aortic valve stenosis was mild to moderate with flow of 3.7 m/s on continuous wave doppler.", "There was evidence of mild aortic incompetence.", "The aortic arch remained unobstructed with flow velocity of 1.4 m/s.", "His most recent follow-up was at 8 months of age.", "He remained asymptomatic and well with his weight increasing to 9 kg.", "His echocardiogram again demonstrated qualitatively normal ventricular function.", "The bicuspid aortic valve had flow of 3.2 m/s across the valve.", "There was mild aortic incompetence.", "The aortic arch remained unobstructed.", "There were no issues with his carotid artery access.", "There were no ongoing neurological issues."], "summary_subclaims": ["The patient is a 1-month-old baby.", "The baby presented with severe AS.", "The baby presented with CoA.", "The decision was made to perform a hybrid surgical procedure.", "The patient underwent a lateral thoracotomy for repair of the CoA.", "The patient underwent carotid cutdown for aortic balloon valvuloplasty."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 3.7-kg, 1-month-old male.", "He presented at day 24 of life with severe aortic stenosis and coarctation of the aorta.", "He was born at term following an uncomplicated pregnancy.", "On day 5 of life, he was noted to be jaundiced and have a murmur.", "His jaundice resolved, and he was discharged home with cardiac follow-up.", "He had progressive increase in his work of breathing.", "He was not gaining weight.", "An echocardiogram on day 24 of life showed a thickened and dysplastic bicuspid aortic valve with doming of the valve leaflets.", "The flow across the valve was measured on continuous wave doppler at 4 m/s.", "He was found to have a discrete juxta ductal coarctation of the aorta with continuous doppler flow of 2.5 m/s with diastolic tail.", "His ventricular function remained preserved.", "He was started on intravenous prostaglandin.", "Urgent surgery was scheduled.", "The best course of action was felt to be a hybrid approach with surgical end-to-end anastomosis of the aortic arch via a thoracotomy followed by surgical carotid cut down for AoVP.", "The patient was taken to the hybrid catheter laboratory theater.", "He underwent the surgical end-to-end anastomosis via the thoracotomy via the third intercostal space.", "The arch, patent ductus arteriosus, and descending aorta were dissected out.", "Clamps were applied to the arch and descending aorta.", "The coarctation segment was resected.", "The patent ductus arteriosus was ligated.", "An end to side anastomosis was performed between the aortic arch and the descending aorta.", "The pleura and chest were closed in layers.", "The patient was assessed and felt to be stable to proceed with the planned aortic balloon.", "A 5/0 purse string suture was applied to the right common carotid artery.", "A 4-Fr sheath was inserted in the right common carotid artery.", "Ascending aortic pressure was measured at 61/42 mmHg.", "The aortic valve annulus measured 7.5 mm.", "The pressure in the left ventricle was recorded at 110/13 mmHg.", "A peak to peak gradient of 49 mmHg was calculated.", "A 0.014 ChoICE PT extra support coronary wire was placed in the left ventricle.", "A NuMED Tyshak II 6 mm \u00d7 2 cm percutaneous transluminal valvuloplasty balloon catheter was delivered over the ChoICE wire to the aortic valve.", "The balloon was inflated to burst pressure of 4 atmospheres.", "A waist was seen within the balloon and dewaisting occurred.", "The balloon catheter was removed.", "The pressure was measured at 100/10 mmHg.", "Repeat angiogram at the aortic root did not demonstrate any significant aortic incompetence.", "A 7 mm \u00d7 2 cm NuMED Tyshak II percutaneous transluminal valvuloplasty balloon catheter was delivered over the coronary guidewire in position.", "The balloon was inflated to 4 atm.", "A waist was again seen and dewaisting occurred.", "The balloon catheter was removed.", "The pressure within the left ventricle was now 90/10 mmHg.", "The pullback peak to peak gradient between the left ventricle and ascending aorta measured 30 mmHg.", "The catheter and sheath were removed.", "The vessel was repaired by tightening the pursestring suture.", "The skin was closed in layers.", "An echocardiogram performed post procedure showed qualitatively normal ventricular function with no pericardial effusion.", "The arch was unobstructed with doppler flow velocity of 1.6 m/s.", "The aortic valve was bicuspid and obviously dysplastic.", "There was mild flow acceleration across the valve using continuous wave doppler of 3 m/s.", "There was a mean doppler gradient of 15 mmHg.", "There was no obvious aortic incompetency seen.", "The patient was transferred from the hybrid catheter laboratory to the pediatric intensive care unit.", "He remained cardiovascularly stable during his PICU admission.", "He was extubated but had to be reintubated within a few hours due to upper airway issues.", "He was successfully extubated on day 3 post procedure.", "He was transferred to the cardiac ward.", "His admission on the ward was uncomplicated.", "He was discharged on day 6 post intervention.", "At 4 months of age, he was reviewed in the outpatient clinic.", "He was clinically asymptomatic with steady growth.", "His echocardiogram demonstrated qualitatively normal ventricular function.", "The aortic valve stenosis was mild to moderate with flow of 3.7 m/s on continuous wave doppler.", "There was evidence of mild aortic incompetence.", "The aortic arch remained unobstructed with flow velocity of 1.4 m/s.", "His most recent follow-up was at 8 months of age.", "He remained asymptomatic and well with his weight increasing to 9 kg.", "His echocardiogram again demonstrated qualitatively normal ventricular function.", "The bicuspid aortic valve had flow of 3.2 m/s across the valve.", "There was mild aortic incompetence.", "The aortic arch remained unobstructed.", "There were no issues with his carotid artery access.", "There were no ongoing neurological issues."], "index": 19, "original_id": "multiclinsum_test_2724_en.txt", "split": "test", "summary_subclaims": ["The patient is a 1-month-old baby.", "The baby presented with severe AS.", "The baby presented with CoA.", "The decision was made to perform a hybrid surgical procedure.", "The patient underwent a lateral thoracotomy for repair of the CoA.", "The patient underwent carotid cutdown for aortic balloon valvuloplasty."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["An 84-year-old man was admitted to our hospital complaining of muscular weakness while rising up from a chair that led to a fall.", "He was admitted for further studying.", "His head CT and MRI did not report any abnormal structural findings.", "He reported a significant 10% weight loss in the past 6 months.", "The weight loss was associated with decreased appetite and diminished mobility.", "The weight loss was associated with progressive muscular weakness and difficulty rising from chair.", "The physical examination was remarkable for muscular weakness with 3/5 muscle strength in the lower extremities.", "The physical examination showed 4/5 muscle strength in the upper extremities.", "Muscle weakness was confined to the proximal muscles.", "Tendon reflexes were diminished.", "The tone examination revealed mild bilateral quadriceps hypotonia and atrophy.", "There were no other clinical findings on the physical examination.", "The patient reported a medical history of stage G4 chronic kidney disease.", "The patient reported a medical history of erythroid and megakaryocyte-predominant myelodysplastic syndrome.", "The patient reported a medical history of high blood pressure.", "The patient was receiving medication with azacytidine.", "The patient was receiving medication with diltiazem.", "The patient was receiving medication with darbepoetin.", "The patient did not smoke.", "The patient did not consume alcohol.", "The patient did not use illicit drugs.", "The family history was negative for neuromuscular diseases.", "During the present admission, laboratory investigation showed an elevated creatine kinase level of up to 78,924 U/L.", "The creatine kinase level was more than 50 times the normal reference range.", "Elevated serum creatinine was found (4.4 mg/dl).", "Mild hypocalcemia (7.2 mg/dl) was found.", "Mild hyponatremia (130 mg/dl) was found.", "Coprologic examination revealed positive testing for rotavirus.", "Antibody testing reported negative results for antinuclear antibodies (ANAs).", "Antibody testing reported negative results for anti-Jo1.", "Antibody testing reported negative results for anti-3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR).", "Antibody testing reported negative results for anti-Mi-2.", "Antibody testing reported negative results for antiganglioside antibodies.", "The electromyography (EMG) of the upper and lower limbs showed myopathic changes in proximal muscle.", "The EMG showed lower limb predominance.", "The EMG showed short duration, low-amplitude polyphasic potential.", "The EMG showed no positive sharp waves.", "The EMG showed no spontaneous electrical activity.", "An FDG-PET/CT scan was performed searching for neoplasia.", "The FDG-PET/CT scan revealed increased FDG uptake in bilateral quadriceps.", "There was no posterior compartment muscle uptake.", "There was no increased metabolism in any other region of the body.", "An open biopsy of the left vastus lateralis muscle was performed.", "Light microscopy showed 50% myonecrosis.", "There were mild fiber atrophy and lymphocytic infiltrate with CD8+ predominance.", "There was perivascular involvement.", "There were no immune deposits in the skin microscopic examination.", "The diagnosis of PM was made.", "The patient started on intravenous hydration with medium saline solution/bicarbonate for rhabdomyolysis.", "The patient started on prednisone 0.5 mg/kg/day.", "The patient received intravenous immunoglobulin with a total dose of 2 g/kg distributed in 5 days.", "The patient received calcium supplementation.", "The patient continued azacytidine.", "Steroid-sparing drugs such as azathioprine or methotrexate were not considered.", "The renal function of the patient improved within 5 days.", "There was partial recovery of lower limb strength.", "The patient was discharged for external consultation follow-up.", "After 2 months from discharge, the patient had increased muscle strength.", "After 2 months from discharge, the patient had diminished CPK levels.", "The patient received low-dose prednisone as maintenance therapy."], "summary_subclaims": ["The patient is an 84-year-old male.", "The patient had difficulty rising from a chair.", "The patient had a fall.", "Laboratory results showed increased creatine kinase levels of more than 50 times the normal reference values.", "Electromyography showed myopathic changes.", "FDG-PET/CT scan showed increased FDG uptake in bilateral quadriceps.", "A biopsy revealed lymphocytic predominant infiltrates.", "A biopsy revealed myonecrosis.", "Prednisone was administered.", "Intravenous immunoglobulin was administered.", "Strength improved.", "The patient was discharged for further follow-up."]}, "extra_info": {"fulltext_subclaims": ["An 84-year-old man was admitted to our hospital complaining of muscular weakness while rising up from a chair that led to a fall.", "He was admitted for further studying.", "His head CT and MRI did not report any abnormal structural findings.", "He reported a significant 10% weight loss in the past 6 months.", "The weight loss was associated with decreased appetite and diminished mobility.", "The weight loss was associated with progressive muscular weakness and difficulty rising from chair.", "The physical examination was remarkable for muscular weakness with 3/5 muscle strength in the lower extremities.", "The physical examination showed 4/5 muscle strength in the upper extremities.", "Muscle weakness was confined to the proximal muscles.", "Tendon reflexes were diminished.", "The tone examination revealed mild bilateral quadriceps hypotonia and atrophy.", "There were no other clinical findings on the physical examination.", "The patient reported a medical history of stage G4 chronic kidney disease.", "The patient reported a medical history of erythroid and megakaryocyte-predominant myelodysplastic syndrome.", "The patient reported a medical history of high blood pressure.", "The patient was receiving medication with azacytidine.", "The patient was receiving medication with diltiazem.", "The patient was receiving medication with darbepoetin.", "The patient did not smoke.", "The patient did not consume alcohol.", "The patient did not use illicit drugs.", "The family history was negative for neuromuscular diseases.", "During the present admission, laboratory investigation showed an elevated creatine kinase level of up to 78,924 U/L.", "The creatine kinase level was more than 50 times the normal reference range.", "Elevated serum creatinine was found (4.4 mg/dl).", "Mild hypocalcemia (7.2 mg/dl) was found.", "Mild hyponatremia (130 mg/dl) was found.", "Coprologic examination revealed positive testing for rotavirus.", "Antibody testing reported negative results for antinuclear antibodies (ANAs).", "Antibody testing reported negative results for anti-Jo1.", "Antibody testing reported negative results for anti-3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR).", "Antibody testing reported negative results for anti-Mi-2.", "Antibody testing reported negative results for antiganglioside antibodies.", "The electromyography (EMG) of the upper and lower limbs showed myopathic changes in proximal muscle.", "The EMG showed lower limb predominance.", "The EMG showed short duration, low-amplitude polyphasic potential.", "The EMG showed no positive sharp waves.", "The EMG showed no spontaneous electrical activity.", "An FDG-PET/CT scan was performed searching for neoplasia.", "The FDG-PET/CT scan revealed increased FDG uptake in bilateral quadriceps.", "There was no posterior compartment muscle uptake.", "There was no increased metabolism in any other region of the body.", "An open biopsy of the left vastus lateralis muscle was performed.", "Light microscopy showed 50% myonecrosis.", "There were mild fiber atrophy and lymphocytic infiltrate with CD8+ predominance.", "There was perivascular involvement.", "There were no immune deposits in the skin microscopic examination.", "The diagnosis of PM was made.", "The patient started on intravenous hydration with medium saline solution/bicarbonate for rhabdomyolysis.", "The patient started on prednisone 0.5 mg/kg/day.", "The patient received intravenous immunoglobulin with a total dose of 2 g/kg distributed in 5 days.", "The patient received calcium supplementation.", "The patient continued azacytidine.", "Steroid-sparing drugs such as azathioprine or methotrexate were not considered.", "The renal function of the patient improved within 5 days.", "There was partial recovery of lower limb strength.", "The patient was discharged for external consultation follow-up.", "After 2 months from discharge, the patient had increased muscle strength.", "After 2 months from discharge, the patient had diminished CPK levels.", "The patient received low-dose prednisone as maintenance therapy."], "index": 17, "original_id": "multiclinsum_test_2937_en.txt", "split": "test", "summary_subclaims": ["The patient is an 84-year-old male.", "The patient had difficulty rising from a chair.", "The patient had a fall.", "Laboratory results showed increased creatine kinase levels of more than 50 times the normal reference values.", "Electromyography showed myopathic changes.", "FDG-PET/CT scan showed increased FDG uptake in bilateral quadriceps.", "A biopsy revealed lymphocytic predominant infiltrates.", "A biopsy revealed myonecrosis.", "Prednisone was administered.", "Intravenous immunoglobulin was administered.", "Strength improved.", "The patient was discharged for further follow-up."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 33-year-old female.", "She presented with a polyp on top of a red plaque in the left side mons pubis for 1 year.", "The lesion was a round flaky red bulge.", "The plaque was slightly bulgy without pressing pain.", "The plaque was 2.2 \u00d7 1.8 \u00d7 0.5 cm.", "The polyp was 2.5 \u00d7 2 \u00d7 1.5 cm.", "The width of the pedicle was 1.4 cm.", "The lesion was covered with a thick yellow-white crust.", "There were no other systemic abnormalities.", "There was no palpable lymphadenopathy.", "Ultrasound B was applied to evaluate the superficial inguinal lymph nodes.", "She had no significant history of medicine, surgery, irritation, and trauma.", "Before the lesion appearance, the patient had no discomfort.", "She did not use other external medicines.", "Until nearly a month, she found that the lesion was prone to bleed after friction.", "The lesion was removed surgically.", "Histopathologic examination was performed.", "The possibility of skin tumor was considered through dermoscopy.", "The skin biopsy was made on December 31, 2019.", "The immunohistochemical reports were done on January 17, 2020.", "Dermoscopic images showed a dark red background.", "The dermoscopic images showed a thick yellow-and-white crust.", "The dermoscopic images showed spot-shaped and polymorphic vascular structures.", "The dermoscopic images showed white homogeneous structures.", "The dermoscopic images showed dark red clumps.", "No typical pigment structure was seen.", "The skin lesions were considered as the diagnosis of skin tumors using dermoscopy.", "The excisional biopsy was carried out.", "The specimen tissue was fixed in formalin.", "The histological examination showed the skin lesion at the left side of mons pubis was spindle-shaped.", "The lesion size was 2.2 \u00d7 1.8 \u00d7 0.5 cm.", "The polyps were lined by melanocytes with pale cytoplasm.", "The polyps showed atypical cells and heteromorphic nuclei.", "The cells had different sizes.", "Abnormal mitosis was 5\u20137 counts /10HPF.", "Each slide was reviewed by 3 different pathologists.", "The diagnosis was made as the melanocyte tumor.", "The immunohistochemistry studies revealed positive staining for S-100.", "The immunohistochemistry studies revealed positive staining for HMB-45.", "The immunohistochemistry studies revealed positive staining for Melan A.", "The immunohistochemistry studies revealed positive staining for Cyclin D1.", "CD-117 was focally immunoreactive.", "CD31 was stained negative.", "P16 was stained negative.", "PCK was stained negative.", "LCA was stained negative.", "The final histopathological diagnosis was melanocyte nevus malignancy, nodular malignant melanoma.", "The patient underwent a complete local excision.", "She recovered well recently.", "The patient was required to re-examined regularly after surgery.", "Recent follow-ups showed that she recovered well.", "There was no sign of recurrence till now."], "summary_subclaims": ["The patient is a 33-year-old female.", "The lesion was a solitary polypoid nodule without apparent pigmentation on her vulvar skin.", "Her medical history was unclear.", "No ulcer was seen in the lesion area.", "Dermatoscopy was indicated a possible tumorous change.", "The final diagnosis was nodular malignant melanoma (NM).", "The Breslow thickness was 9.5mm.", "The Clark level was 4."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 33-year-old female.", "She presented with a polyp on top of a red plaque in the left side mons pubis for 1 year.", "The lesion was a round flaky red bulge.", "The plaque was slightly bulgy without pressing pain.", "The plaque was 2.2 \u00d7 1.8 \u00d7 0.5 cm.", "The polyp was 2.5 \u00d7 2 \u00d7 1.5 cm.", "The width of the pedicle was 1.4 cm.", "The lesion was covered with a thick yellow-white crust.", "There were no other systemic abnormalities.", "There was no palpable lymphadenopathy.", "Ultrasound B was applied to evaluate the superficial inguinal lymph nodes.", "She had no significant history of medicine, surgery, irritation, and trauma.", "Before the lesion appearance, the patient had no discomfort.", "She did not use other external medicines.", "Until nearly a month, she found that the lesion was prone to bleed after friction.", "The lesion was removed surgically.", "Histopathologic examination was performed.", "The possibility of skin tumor was considered through dermoscopy.", "The skin biopsy was made on December 31, 2019.", "The immunohistochemical reports were done on January 17, 2020.", "Dermoscopic images showed a dark red background.", "The dermoscopic images showed a thick yellow-and-white crust.", "The dermoscopic images showed spot-shaped and polymorphic vascular structures.", "The dermoscopic images showed white homogeneous structures.", "The dermoscopic images showed dark red clumps.", "No typical pigment structure was seen.", "The skin lesions were considered as the diagnosis of skin tumors using dermoscopy.", "The excisional biopsy was carried out.", "The specimen tissue was fixed in formalin.", "The histological examination showed the skin lesion at the left side of mons pubis was spindle-shaped.", "The lesion size was 2.2 \u00d7 1.8 \u00d7 0.5 cm.", "The polyps were lined by melanocytes with pale cytoplasm.", "The polyps showed atypical cells and heteromorphic nuclei.", "The cells had different sizes.", "Abnormal mitosis was 5\u20137 counts /10HPF.", "Each slide was reviewed by 3 different pathologists.", "The diagnosis was made as the melanocyte tumor.", "The immunohistochemistry studies revealed positive staining for S-100.", "The immunohistochemistry studies revealed positive staining for HMB-45.", "The immunohistochemistry studies revealed positive staining for Melan A.", "The immunohistochemistry studies revealed positive staining for Cyclin D1.", "CD-117 was focally immunoreactive.", "CD31 was stained negative.", "P16 was stained negative.", "PCK was stained negative.", "LCA was stained negative.", "The final histopathological diagnosis was melanocyte nevus malignancy, nodular malignant melanoma.", "The patient underwent a complete local excision.", "She recovered well recently.", "The patient was required to re-examined regularly after surgery.", "Recent follow-ups showed that she recovered well.", "There was no sign of recurrence till now."], "index": 156, "original_id": "multiclinsum_test_1142_en.txt", "split": "test", "summary_subclaims": ["The patient is a 33-year-old female.", "The lesion was a solitary polypoid nodule without apparent pigmentation on her vulvar skin.", "Her medical history was unclear.", "No ulcer was seen in the lesion area.", "Dermatoscopy was indicated a possible tumorous change.", "The final diagnosis was nodular malignant melanoma (NM).", "The Breslow thickness was 9.5mm.", "The Clark level was 4."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 16-year-old Persian man.", "The patient's mother was diagnosed with aggressive MTC.", "The patient's mother had a mass in the thyroid gland and cervical lymphadenopathy for six years.", "The patient's mother underwent thyroidectomy a year earlier.", "The patient had no history of lymphadenopathy.", "The patient had no history of weight loss.", "The patient had no history of fever.", "The patient had no history of caf\u00e9 au lait spots.", "The patient had no history of ocular problems.", "The patient had no history of gastrointestinal problems.", "The patient had no history of thyroid nodule.", "The patient had no history of hoarseness.", "The patient had no history of dyspnea.", "The patient had no history of cough.", "On physical examination, the patient's face was symmetric.", "There was no sign of high arched palate.", "There was no sign of mandibular prognathism.", "There was no sign of flat nasal bridge.", "The patient had bumpy lips.", "The patient had several neuromas on his upper and lower eyelids, lips, and tongue.", "The neuromas were characteristic of MEN2B.", "The patient's thyroid gland was normal.", "The patient's abdomen was normal.", "There were no other remarkable findings in the physical examination.", "The patient had a normal height.", "There were no signs of marfanoid habitus.", "The patient had increased calcitonin levels.", "The patient had increased carcinoembryonic antigen (CEA) levels.", "Tests for RET proto-oncogene on exon 10, 11, and 16 were negative.", "The results of an ophthalmology examination showed several mucosal neuromas on inner eyelids and conjunctivae.", "The ophthalmology examination showed prominent perilimbal conjunctival blood vessels.", "The ophthalmology examination showed enlarged corneal nerves.", "The patient's intra-ocular pressure (IOP) was normal.", "The upper gastrointestinal and small bowel series were normal.", "Pheochromocytoma was ruled out based on the laboratory test results.", "The patient underwent a thyroidectomy.", "The results of pathological tests revealed a small (0.5cm) medullary thyroid carcinoma in the right lobe.", "The surgical margins were free of tumor.", "Post-operative evaluation included cervical ultrasound.", "Post-operative evaluation included cervical, thoracic, and abdominal computed tomography.", "The post-operative evaluations were normal.", "The patient's calcitonin and CEA levels were assessed periodically.", "All the family members had signed an informed consent.", "The family members provided the authors with an authorization to publish their information."], "summary_subclaims": ["The patient is a 16-year-old Persian man.", "The patient was diagnosed as having a non-invasive form of multiple endocrine neoplasia 2B.", "The patient has medullary thyroid cancer.", "The patient has mucosal neuroma of the tongue.", "The patient has mucosal neuroma of the lips.", "The patient has mucosal neuroma of the inner eyelids.", "The patient had a positive family history of medullary thyroid cancer.", "The patient was of normal height.", "The patient had no signs of marfanoid habitus."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 16-year-old Persian man.", "The patient's mother was diagnosed with aggressive MTC.", "The patient's mother had a mass in the thyroid gland and cervical lymphadenopathy for six years.", "The patient's mother underwent thyroidectomy a year earlier.", "The patient had no history of lymphadenopathy.", "The patient had no history of weight loss.", "The patient had no history of fever.", "The patient had no history of caf\u00e9 au lait spots.", "The patient had no history of ocular problems.", "The patient had no history of gastrointestinal problems.", "The patient had no history of thyroid nodule.", "The patient had no history of hoarseness.", "The patient had no history of dyspnea.", "The patient had no history of cough.", "On physical examination, the patient's face was symmetric.", "There was no sign of high arched palate.", "There was no sign of mandibular prognathism.", "There was no sign of flat nasal bridge.", "The patient had bumpy lips.", "The patient had several neuromas on his upper and lower eyelids, lips, and tongue.", "The neuromas were characteristic of MEN2B.", "The patient's thyroid gland was normal.", "The patient's abdomen was normal.", "There were no other remarkable findings in the physical examination.", "The patient had a normal height.", "There were no signs of marfanoid habitus.", "The patient had increased calcitonin levels.", "The patient had increased carcinoembryonic antigen (CEA) levels.", "Tests for RET proto-oncogene on exon 10, 11, and 16 were negative.", "The results of an ophthalmology examination showed several mucosal neuromas on inner eyelids and conjunctivae.", "The ophthalmology examination showed prominent perilimbal conjunctival blood vessels.", "The ophthalmology examination showed enlarged corneal nerves.", "The patient's intra-ocular pressure (IOP) was normal.", "The upper gastrointestinal and small bowel series were normal.", "Pheochromocytoma was ruled out based on the laboratory test results.", "The patient underwent a thyroidectomy.", "The results of pathological tests revealed a small (0.5cm) medullary thyroid carcinoma in the right lobe.", "The surgical margins were free of tumor.", "Post-operative evaluation included cervical ultrasound.", "Post-operative evaluation included cervical, thoracic, and abdominal computed tomography.", "The post-operative evaluations were normal.", "The patient's calcitonin and CEA levels were assessed periodically.", "All the family members had signed an informed consent.", "The family members provided the authors with an authorization to publish their information."], "index": 159, "original_id": "multiclinsum_test_2043_en.txt", "split": "test", "summary_subclaims": ["The patient is a 16-year-old Persian man.", "The patient was diagnosed as having a non-invasive form of multiple endocrine neoplasia 2B.", "The patient has medullary thyroid cancer.", "The patient has mucosal neuroma of the tongue.", "The patient has mucosal neuroma of the lips.", "The patient has mucosal neuroma of the inner eyelids.", "The patient had a positive family history of medullary thyroid cancer.", "The patient was of normal height.", "The patient had no signs of marfanoid habitus."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was a 39-year-old Chinese woman.", "She had delivered a second live full-term infant through an uncomplicated cesarean section in 2011.", "She had a miscarriage in 2010.", "She had a first cesarean section in 2005.", "In December 2014, she noticed a purple, nontender swelling appearing as an anterior abdominal wall mass around her cesarean scar.", "The mass was the size of a green bean.", "The mass was not accompanied by any abdominal pain.", "The mass was not accompanied by any abnormal vaginal bleeding.", "There were no notable findings in her past medical history.", "There were no notable findings in her family history.", "There were no notable findings in her psychosocial history.", "The abdominal wall mass had progressively enlarged.", "She had undergone tumor resection of the abdominal wall in June 2015.", "The resection might be interpreted as the abdominal wall endometriosis malignancy.", "She had visited a regional tertiary hospital for a consultation regarding the pathologic diagnosis of a CC.", "Her physical examination showed no abnormalities except for the scar from the local excision on the abdominal wall.", "The first excised specimen from the previous hospital was reviewed by our pathologists.", "The pathologists confirmed the characteristic of CC coexisting with minor ETT.", "Her Ki-67 proliferative index was approximately 50%.", "Laboratory analysis revealed normal serum levels of \u03b2-human chorionic gonadotropin (\u03b2-hCG; < 1.2 IU/L).", "Laboratory analysis revealed normal tumor markers, including CA 125, CEA, CA 19-9, CA 15-3, and \u03b1-fetoprotein.", "Positron emission tomography was performed.", "No residual tumor and suspicious malignant lesions were observed.", "Endometrial curettage was performed.", "The results of endometrial curettage revealed normal menstrual phase endometrium.", "The patient received two courses of chemotherapy with a regimen of etoposide and cisplatin (EP) over a 2-month period.", "During chemotherapy, her serum \u03b2-hCG levels remained negative (< 1.2 IU/L).", "A recurrent nodule was found on the same abdominal wall scar site in January 2017.", "The nodule was found approximately 17 months after the last chemotherapy.", "Her serum \u03b2-hCG had increased to 6.17 IU/L.", "Two oval hypoechoic masses were visualized by ultrasonography in the subcutaneous soft tissue of the lower abdomen wall scar.", "Chest CT and head MRI showed no abnormality.", "She underwent a second notable mass excision by ultrasound interventional localization.", "The nodule was in the fat layer next to the superficial fascia.", "Her serum \u03b2-hCG level was decreased to 3.4 IU/L on the second postoperative day.", "The result of pathological examination was initially in line with CC metastasis to the abdominal wall.", "The patient\u2019s Ki-67 index was 20%.", "The patient\u2019s pathological sections were sent to the Fudan University Obstetrics and Gynecology Hospital for further consultation.", "The finding was ETT.", "The patient was encouraged to maintain close follow-up.", "Her serum \u03b2-hCG level had gradually decreased.", "In the follow-up visits, the patient\u2019s serum \u03b2-hCG level was elevated to the highest level of 10.68 IU/L again 4 months later.", "A pelvic CT scan showed several nodules on the abdominal wall midline fascia.", "The largest nodule was approximately 21 \u00d7 15 mm in size.", "The nodules had clear boundaries.", "The nodules were less uniform in internal echoes.", "Test results for tumor markers such as CA 125, CA 19-9, CEA, and HE4 were negative.", "The results of routine blood sampling tests were normal.", "We suggested a third resection of the mass to the patient.", "She opted for a hysterectomy due to fear of malignancy and further relapse.", "She finally underwent exploratory laparotomy with removal of the abdominal wall lesion, subtotal hysterectomy, bilateral salpingectomy, left ovarian cyst resection, and right inguinal lymph node biopsy in July 2017.", "Intraoperative exploration revealed that the abdominal wall lesion was located on the anterior wall fascia.", "Histopathological observations suggested that hyperplasia of fatty fibrous tissue was visible with cancer infiltration and necrosis around the cancer tissue.", "The histopathological findings were consistent with trophoblastic tumor.", "The trophoblastic tumor was constituted primarily by major epidermoid trophoblastic tumors (approximately 90%).", "The trophoblastic tumor was constituted by CC components (approximately 10%).", "Immunohistochemistry showed \u03b2-hCG (focal positive).", "Immunohistochemistry showed inhibin-\u03b1 (epithelial trophoblast negative, CC positive).", "Immunohistochemistry showed p63 (epidermoid trophoblast positive, CC positive).", "There was no tumor involvement in other tissues, including uterine, left ovarian cyst, and the right inguinal lymph nodes.", "The diagnosis was ETT accompanying CC.", "The patient\u2019s postoperative recovery was uneventful.", "Two weeks after hysterectomy, her serum \u03b2-hCG level had returned to normal (low 1.2 IU/L).", "Two years later, there was no evidence of recurrence according to serum \u03b2-hCG and imaging studies."], "summary_subclaims": ["The patient was a 39-year-old Chinese woman.", "She had a history of two cesarean sections.", "She had a history of one miscarriage.", "She had a recurrent anterior abdominal wall mass around her cesarean scar.", "The mass was initially suspected of being choriocarcinoma of unknown origin.", "The patient had negative or mildly increased serum \u03b2-human chorionic gonadotropin at follow-up.", "She had no abnormal vaginal bleeding.", "She had no abdominal pain.", "She underwent local excision twice.", "She had two courses of chemotherapy with an etoposide and cisplatin regimen.", "She finally opted for exploratory laparotomy with abdominal wall lesion removal.", "She had a subtotal hysterectomy.", "She had bilateral salpingectomy.", "She had left ovarian cyst resection.", "The abdominal wall lesion was revealed by microscopy and immunohistochemical staining to be approximately 90% epithelioid trophoblastic tumors.", "The abdominal wall lesion was revealed by microscopy and immunohistochemical staining to be 10% choriocarcinomas.", "The lesion was from a solely extrauterine mixed gestational trophoblastic neoplasm around an abdominal wall cesarean scar."]}, "extra_info": {"fulltext_subclaims": ["The patient was a 39-year-old Chinese woman.", "She had delivered a second live full-term infant through an uncomplicated cesarean section in 2011.", "She had a miscarriage in 2010.", "She had a first cesarean section in 2005.", "In December 2014, she noticed a purple, nontender swelling appearing as an anterior abdominal wall mass around her cesarean scar.", "The mass was the size of a green bean.", "The mass was not accompanied by any abdominal pain.", "The mass was not accompanied by any abnormal vaginal bleeding.", "There were no notable findings in her past medical history.", "There were no notable findings in her family history.", "There were no notable findings in her psychosocial history.", "The abdominal wall mass had progressively enlarged.", "She had undergone tumor resection of the abdominal wall in June 2015.", "The resection might be interpreted as the abdominal wall endometriosis malignancy.", "She had visited a regional tertiary hospital for a consultation regarding the pathologic diagnosis of a CC.", "Her physical examination showed no abnormalities except for the scar from the local excision on the abdominal wall.", "The first excised specimen from the previous hospital was reviewed by our pathologists.", "The pathologists confirmed the characteristic of CC coexisting with minor ETT.", "Her Ki-67 proliferative index was approximately 50%.", "Laboratory analysis revealed normal serum levels of \u03b2-human chorionic gonadotropin (\u03b2-hCG; < 1.2 IU/L).", "Laboratory analysis revealed normal tumor markers, including CA 125, CEA, CA 19-9, CA 15-3, and \u03b1-fetoprotein.", "Positron emission tomography was performed.", "No residual tumor and suspicious malignant lesions were observed.", "Endometrial curettage was performed.", "The results of endometrial curettage revealed normal menstrual phase endometrium.", "The patient received two courses of chemotherapy with a regimen of etoposide and cisplatin (EP) over a 2-month period.", "During chemotherapy, her serum \u03b2-hCG levels remained negative (< 1.2 IU/L).", "A recurrent nodule was found on the same abdominal wall scar site in January 2017.", "The nodule was found approximately 17 months after the last chemotherapy.", "Her serum \u03b2-hCG had increased to 6.17 IU/L.", "Two oval hypoechoic masses were visualized by ultrasonography in the subcutaneous soft tissue of the lower abdomen wall scar.", "Chest CT and head MRI showed no abnormality.", "She underwent a second notable mass excision by ultrasound interventional localization.", "The nodule was in the fat layer next to the superficial fascia.", "Her serum \u03b2-hCG level was decreased to 3.4 IU/L on the second postoperative day.", "The result of pathological examination was initially in line with CC metastasis to the abdominal wall.", "The patient\u2019s Ki-67 index was 20%.", "The patient\u2019s pathological sections were sent to the Fudan University Obstetrics and Gynecology Hospital for further consultation.", "The finding was ETT.", "The patient was encouraged to maintain close follow-up.", "Her serum \u03b2-hCG level had gradually decreased.", "In the follow-up visits, the patient\u2019s serum \u03b2-hCG level was elevated to the highest level of 10.68 IU/L again 4 months later.", "A pelvic CT scan showed several nodules on the abdominal wall midline fascia.", "The largest nodule was approximately 21 \u00d7 15 mm in size.", "The nodules had clear boundaries.", "The nodules were less uniform in internal echoes.", "Test results for tumor markers such as CA 125, CA 19-9, CEA, and HE4 were negative.", "The results of routine blood sampling tests were normal.", "We suggested a third resection of the mass to the patient.", "She opted for a hysterectomy due to fear of malignancy and further relapse.", "She finally underwent exploratory laparotomy with removal of the abdominal wall lesion, subtotal hysterectomy, bilateral salpingectomy, left ovarian cyst resection, and right inguinal lymph node biopsy in July 2017.", "Intraoperative exploration revealed that the abdominal wall lesion was located on the anterior wall fascia.", "Histopathological observations suggested that hyperplasia of fatty fibrous tissue was visible with cancer infiltration and necrosis around the cancer tissue.", "The histopathological findings were consistent with trophoblastic tumor.", "The trophoblastic tumor was constituted primarily by major epidermoid trophoblastic tumors (approximately 90%).", "The trophoblastic tumor was constituted by CC components (approximately 10%).", "Immunohistochemistry showed \u03b2-hCG (focal positive).", "Immunohistochemistry showed inhibin-\u03b1 (epithelial trophoblast negative, CC positive).", "Immunohistochemistry showed p63 (epidermoid trophoblast positive, CC positive).", "There was no tumor involvement in other tissues, including uterine, left ovarian cyst, and the right inguinal lymph nodes.", "The diagnosis was ETT accompanying CC.", "The patient\u2019s postoperative recovery was uneventful.", "Two weeks after hysterectomy, her serum \u03b2-hCG level had returned to normal (low 1.2 IU/L).", "Two years later, there was no evidence of recurrence according to serum \u03b2-hCG and imaging studies."], "index": 166, "original_id": "multiclinsum_test_2114_en.txt", "split": "test", "summary_subclaims": ["The patient was a 39-year-old Chinese woman.", "She had a history of two cesarean sections.", "She had a history of one miscarriage.", "She had a recurrent anterior abdominal wall mass around her cesarean scar.", "The mass was initially suspected of being choriocarcinoma of unknown origin.", "The patient had negative or mildly increased serum \u03b2-human chorionic gonadotropin at follow-up.", "She had no abnormal vaginal bleeding.", "She had no abdominal pain.", "She underwent local excision twice.", "She had two courses of chemotherapy with an etoposide and cisplatin regimen.", "She finally opted for exploratory laparotomy with abdominal wall lesion removal.", "She had a subtotal hysterectomy.", "She had bilateral salpingectomy.", "She had left ovarian cyst resection.", "The abdominal wall lesion was revealed by microscopy and immunohistochemical staining to be approximately 90% epithelioid trophoblastic tumors.", "The abdominal wall lesion was revealed by microscopy and immunohistochemical staining to be 10% choriocarcinomas.", "The lesion was from a solely extrauterine mixed gestational trophoblastic neoplasm around an abdominal wall cesarean scar."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was admitted for recurrent lower extremity edema for 9 mo, abdominal distension for 7 mo, and aggravation for half a month.", "A 53-year-old rural Chinese woman visited Dafang County People\u2019s Hospital.", "Symptoms began to appear nine months ago.", "Edema and abdominal distension of both lower extremities recurred.", "These symptoms gradually worsened during the previous two months.", "Initial liver function examination showed elevated alanine transaminase (ALT).", "Initial liver function examination showed elevated aspartate aminotransferase (AST).", "Initial liver function examination showed elevated total bilirubin (TBIL).", "Initial liver function examination showed elevated direct bilirubin (DBIL).", "Initial liver function examination showed decreased albumin/globulin (ALB/GLO) ratio.", "Examination of blood cells indicated decreased white blood cells (WBCs).", "Examination of blood cells indicated decreased red blood cells (RBCs).", "Examination of blood cells indicated decreased hemoglobin (HB).", "Examination of blood cells indicated decreased platelets (PLTs).", "Examination of coagulation function indicated an increased international normalized ratio (INR).", "Examination of coagulation function indicated prolonged prothrombin time (PT).", "Examination of coagulation function indicated prolonged activated partial thromboplastin time (APTT).", "Examination of coagulation function indicated decreased fibrinogen (FIB).", "An upper abdominal computed tomography (CT) showed liver cirrhosis.", "Examination of thyroid function showed an elevated level of thyroid stimulating hormone (TSH).", "Examination of thyroid function showed a decreased level of free triiodothyronine (FT3).", "The initial diagnosis was \u201cdecompensated stage of cirrhosis and subclinical hypothyroidism.\u201d", "She tested negative for hepatitis viruses.", "She tested negative for autoimmune hepatitis.", "The cause of cirrhosis was unknown.", "She was hospitalized twice for abdominal distension with yellow staining of the sclera.", "These symptoms resolved after administration of a liver protectant and a diuretic to reduce swelling.", "After discharge, she still reported repeated abdominal distension and discomfort.", "These symptoms gradually became worse from 2020 Oct 1.", "Since the initial presentation, her liver function indexes have fluctuated.", "Thyroid function tests indicated a decreasing level of triiodothyronine (T3).", "Thyroid function tests indicated an increasing level of TSH.", "This indicated progression from subclinical hypothyroidism to clinical hypothyroidism.", "She reported loss of vision 30 years ago.", "She had no history of long-term heavy drinking.", "She had no history of taking a Chinese medicine.", "She had no history of exposure to toxic substances.", "She had no history of surgery.", "She had no history of trauma.", "We designated the index patient as proband II-1.", "She had five siblings (3 sisters, 2 brothers).", "All five siblings had night blindness.", "One sister (II-4) was completely blind.", "Her parents had no night blindness or impaired vision.", "Her parents were first cousins.", "We performed serum biochemical examinations of the father (I-1) and all siblings.", "The mother (I-2) was too old to travel to our institution for testing.", "The AST level was elevated in all 7 individuals.", "Fasting blood glucose was decreased in the father and 4 siblings.", "Two siblings had elevated levels of high density lipoprotein cholesterol (HDL-C).", "One sibling had a low level of HDL-C.", "The T3 level was low in two siblings.", "The TSH level was high in three siblings.", "Some of the siblings also had elevated levels of TBIL.", "Some of the siblings also had elevated levels of apolipoprotein A-I (APOA1).", "CT examinations showed that neither the father (I-1) nor the mother (I-2) had cirrhosis.", "Sibling II-2 had cirrhosis.", "Siblings II-3, II-5, and II-6 did not have cirrhosis.", "Abdominal color ultrasound indicated that sibling II-4 had a fatty liver.", "A physical examination indicated she had a BMI of 22.22.", "There was evidence of chronic liver disease.", "There were visible spider nevi.", "There was palmar erythema.", "She had no vision in either eye.", "There were no K-F rings in the corneas.", "A cardiopulmonary examination showed no obvious abnormalities.", "Her abdomen was slightly distensible.", "Her abdomen was positive for shifting dullness.", "There was moderate pitting edema in both lower limbs.", "2020 Oct 14: Blood lipid analysis indicated an HDL of 1.42 mmol/L.", "2020 Oct 14: Hepatitis A virus, hepatitis B virus, and hepatitis C virus related tests were all negative.", "2021 Jan 17: All antibody tests for autoimmune liver diseases were negative.", "2021 Jul 16: Examination of ascites indicated the Rivalta test was negative.", "2021 Jul 16: Ascites WBC count was 50 \u00d7 106/L.", "2021 Jul 16: Ascites total protein (TP) was 5.50 g/L.", "2021 Jul 16: Ascites adenosine deaminase (ADA) was 3.4 U/L.", "2021 Jul 16: Ascites glucose (GLU) was 8.71 mmol/L.", "2021 Jul 16: Ascites lactate dehydrogenase (LDH) was 48.8 U/L.", "2020 Oct 15: Color Doppler ultrasonography of the thyroid showed bilateral thyroid cysts.", "2020 Oct 23: A plain CT scan of the upper abdomen with enhancement showed cirrhotic ascites with splenomegaly.", "We suggested more extensive examination of a liver biopsy to clarify the cause of cirrhosis.", "This was not possible because the patient did not consent.", "The index patient was one of 6 siblings.", "Sibling II-2 was similar (night blindness complicated with cirrhosis and hypothyroidism).", "Sibling II-5 was completely blind in both eyes.", "The other three siblings had obvious night blindness.", "We considered the possibility of GLD.", "We suggested molecular genetic analysis.", "After receiving informed consent, we collected peripheral blood samples for whole-exome sequencing.", "The results indicated the presence of the deletion/insertion mutation C.802-8_810delinsGC (homozygous) in the cytochrome P450 4V2 (CYP4V2) gene.", "The results indicated the presence of the transcoding mutation C.413dupA (heterozygous) in the dual oxidase activator 2 (DUOXA2) gene.", "The same CYP4V2 mutation was present in I-1, I-2, II-2, II-3, II-5, II-6.", "Patient II-4 did not receive genetic testing because he lived in Tianjin."], "summary_subclaims": ["The patient is a 53-year-old female from a rural area in China.", "She was hospitalized for lower limb edema, abdominal distension, cirrhosis, and hypothyroidism.", "Common causes of liver disease were excluded.", "The patient had night-blindness since age 23 that worsened to complete blindness.", "The patient's parents were first cousins.", "All 5 siblings had night blindness and impaired vision.", "One sister was completely blind.", "Another sister had night-blindness complicated with cirrhosis and subclinical hypothyroidism.", "Entire exome sequencing showed mutations in the CYP4V2 gene in the patient, parents, and siblings.", "The CYP4V2 mutations of the parents and two sisters were heterozygous.", "The CYP4V2 mutations of the other siblings were homozygous.", "Two siblings also had heterozygous DUOXA2 mutations."]}, "extra_info": {"fulltext_subclaims": ["The patient was admitted for recurrent lower extremity edema for 9 mo, abdominal distension for 7 mo, and aggravation for half a month.", "A 53-year-old rural Chinese woman visited Dafang County People\u2019s Hospital.", "Symptoms began to appear nine months ago.", "Edema and abdominal distension of both lower extremities recurred.", "These symptoms gradually worsened during the previous two months.", "Initial liver function examination showed elevated alanine transaminase (ALT).", "Initial liver function examination showed elevated aspartate aminotransferase (AST).", "Initial liver function examination showed elevated total bilirubin (TBIL).", "Initial liver function examination showed elevated direct bilirubin (DBIL).", "Initial liver function examination showed decreased albumin/globulin (ALB/GLO) ratio.", "Examination of blood cells indicated decreased white blood cells (WBCs).", "Examination of blood cells indicated decreased red blood cells (RBCs).", "Examination of blood cells indicated decreased hemoglobin (HB).", "Examination of blood cells indicated decreased platelets (PLTs).", "Examination of coagulation function indicated an increased international normalized ratio (INR).", "Examination of coagulation function indicated prolonged prothrombin time (PT).", "Examination of coagulation function indicated prolonged activated partial thromboplastin time (APTT).", "Examination of coagulation function indicated decreased fibrinogen (FIB).", "An upper abdominal computed tomography (CT) showed liver cirrhosis.", "Examination of thyroid function showed an elevated level of thyroid stimulating hormone (TSH).", "Examination of thyroid function showed a decreased level of free triiodothyronine (FT3).", "The initial diagnosis was \u201cdecompensated stage of cirrhosis and subclinical hypothyroidism.\u201d", "She tested negative for hepatitis viruses.", "She tested negative for autoimmune hepatitis.", "The cause of cirrhosis was unknown.", "She was hospitalized twice for abdominal distension with yellow staining of the sclera.", "These symptoms resolved after administration of a liver protectant and a diuretic to reduce swelling.", "After discharge, she still reported repeated abdominal distension and discomfort.", "These symptoms gradually became worse from 2020 Oct 1.", "Since the initial presentation, her liver function indexes have fluctuated.", "Thyroid function tests indicated a decreasing level of triiodothyronine (T3).", "Thyroid function tests indicated an increasing level of TSH.", "This indicated progression from subclinical hypothyroidism to clinical hypothyroidism.", "She reported loss of vision 30 years ago.", "She had no history of long-term heavy drinking.", "She had no history of taking a Chinese medicine.", "She had no history of exposure to toxic substances.", "She had no history of surgery.", "She had no history of trauma.", "We designated the index patient as proband II-1.", "She had five siblings (3 sisters, 2 brothers).", "All five siblings had night blindness.", "One sister (II-4) was completely blind.", "Her parents had no night blindness or impaired vision.", "Her parents were first cousins.", "We performed serum biochemical examinations of the father (I-1) and all siblings.", "The mother (I-2) was too old to travel to our institution for testing.", "The AST level was elevated in all 7 individuals.", "Fasting blood glucose was decreased in the father and 4 siblings.", "Two siblings had elevated levels of high density lipoprotein cholesterol (HDL-C).", "One sibling had a low level of HDL-C.", "The T3 level was low in two siblings.", "The TSH level was high in three siblings.", "Some of the siblings also had elevated levels of TBIL.", "Some of the siblings also had elevated levels of apolipoprotein A-I (APOA1).", "CT examinations showed that neither the father (I-1) nor the mother (I-2) had cirrhosis.", "Sibling II-2 had cirrhosis.", "Siblings II-3, II-5, and II-6 did not have cirrhosis.", "Abdominal color ultrasound indicated that sibling II-4 had a fatty liver.", "A physical examination indicated she had a BMI of 22.22.", "There was evidence of chronic liver disease.", "There were visible spider nevi.", "There was palmar erythema.", "She had no vision in either eye.", "There were no K-F rings in the corneas.", "A cardiopulmonary examination showed no obvious abnormalities.", "Her abdomen was slightly distensible.", "Her abdomen was positive for shifting dullness.", "There was moderate pitting edema in both lower limbs.", "2020 Oct 14: Blood lipid analysis indicated an HDL of 1.42 mmol/L.", "2020 Oct 14: Hepatitis A virus, hepatitis B virus, and hepatitis C virus related tests were all negative.", "2021 Jan 17: All antibody tests for autoimmune liver diseases were negative.", "2021 Jul 16: Examination of ascites indicated the Rivalta test was negative.", "2021 Jul 16: Ascites WBC count was 50 \u00d7 106/L.", "2021 Jul 16: Ascites total protein (TP) was 5.50 g/L.", "2021 Jul 16: Ascites adenosine deaminase (ADA) was 3.4 U/L.", "2021 Jul 16: Ascites glucose (GLU) was 8.71 mmol/L.", "2021 Jul 16: Ascites lactate dehydrogenase (LDH) was 48.8 U/L.", "2020 Oct 15: Color Doppler ultrasonography of the thyroid showed bilateral thyroid cysts.", "2020 Oct 23: A plain CT scan of the upper abdomen with enhancement showed cirrhotic ascites with splenomegaly.", "We suggested more extensive examination of a liver biopsy to clarify the cause of cirrhosis.", "This was not possible because the patient did not consent.", "The index patient was one of 6 siblings.", "Sibling II-2 was similar (night blindness complicated with cirrhosis and hypothyroidism).", "Sibling II-5 was completely blind in both eyes.", "The other three siblings had obvious night blindness.", "We considered the possibility of GLD.", "We suggested molecular genetic analysis.", "After receiving informed consent, we collected peripheral blood samples for whole-exome sequencing.", "The results indicated the presence of the deletion/insertion mutation C.802-8_810delinsGC (homozygous) in the cytochrome P450 4V2 (CYP4V2) gene.", "The results indicated the presence of the transcoding mutation C.413dupA (heterozygous) in the dual oxidase activator 2 (DUOXA2) gene.", "The same CYP4V2 mutation was present in I-1, I-2, II-2, II-3, II-5, II-6.", "Patient II-4 did not receive genetic testing because he lived in Tianjin."], "index": 160, "original_id": "multiclinsum_test_2430_en.txt", "split": "test", "summary_subclaims": ["The patient is a 53-year-old female from a rural area in China.", "She was hospitalized for lower limb edema, abdominal distension, cirrhosis, and hypothyroidism.", "Common causes of liver disease were excluded.", "The patient had night-blindness since age 23 that worsened to complete blindness.", "The patient's parents were first cousins.", "All 5 siblings had night blindness and impaired vision.", "One sister was completely blind.", "Another sister had night-blindness complicated with cirrhosis and subclinical hypothyroidism.", "Entire exome sequencing showed mutations in the CYP4V2 gene in the patient, parents, and siblings.", "The CYP4V2 mutations of the parents and two sisters were heterozygous.", "The CYP4V2 mutations of the other siblings were homozygous.", "Two siblings also had heterozygous DUOXA2 mutations."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["A 39-year-old woman visited our hospital complaining of worsened right low back pain and fever in 1 month before her first visit.", "She had an experience of pyelonephritis 10 years ago.", "Her initial laboratory data had no abnormal findings.", "Her urine test was clear.", "Her urine cytology was negative.", "Ultrasound imaging revealed right gross hydronephrosis.", "CECT also detected right gross hydronephrosis.", "The right ureter was unclear on CECT.", "CECT was reconstructed to 3D imaging with Osirix\u00ae.", "3D imaging found an aberrant blood vessel contacting with the right ureteropelvic junction.", "UPJO was preoperatively diagnosed due to the aberrant blood vessel.", "Tc-99m MAG3 renal scan confirmed that the right kidney exhibited obstructive pattern.", "The right kidney had poor diuretic response.", "The T1/2 of the right kidney was 21.07 min.", "The right kidney function was similarly preserved to the left kidney function.", "MAG3 clearance of the right kidney was 163.7 ml/min/1.73 m2.", "Surgical treatment was indicated because of the symptomatic disease.", "Preoperative RP showed that the right ureter shifted inward compared with the normal position.", "Preoperative RP suggested the coexistence of retrocaval ureter.", "RALP was conducted by a three-port transperitoneal approach.", "Port position was more medial than usual.", "The swollen right renal pelvis and the aberrant blood vessel were identified.", "The right ureter was peeled downward.", "The right ureter was confirmed to be positioned behind the IVC.", "The renal pelvis was dissected.", "The ureter was repositioned anterior to the IVC.", "The strictured ureteropelvic junction was removed.", "The ureter and the renal pelvis were spatulated.", "A 6-Fr double-J stent was inserted.", "The ureter and the renal pelvis were reanastomosed in a tension-free fashion.", "The anastomosis was sutured with interrupted 5-0 sutures.", "A 10-Fr BLAKE Silicon drain was put into the anastomosis place.", "Blood loss was uncountable.", "The operation time was 403 min.", "The robot console time was 301 min.", "The urethral catheter was removed 5 days after surgery.", "The drain was removed 6 days after surgery.", "No perioperative adverse events were found.", "The double-J stent was removed 2 months after surgery.", "No recurrence of the symptoms was observed.", "Her right hydronephrosis improved in 2 years after surgery."], "summary_subclaims": ["The patient is a 39-year-old woman.", "She visited the hospital complaining of worsened right low back pain and fever.", "Contrast-enhanced computed tomography diagnosed right hydronephrosis due to ureteropelvic junction obstruction.", "Retrograde pyelography before robot-assisted laparoscopic pyeloplasty revealed concomitant ipsilateral retrocaval ureter.", "Laparoscopically, ureteropelvic junction obstruction due to aberrant blood vessel and coexisting retrocaval ureter was confirmed.", "Transposition of the ureter from posterior to anterior of the inferior vena cava and following dismembered pyeloplasty was performed.", "Two years after surgery, her right hydronephrosis improved.", "She had no complain of any symptom two years after surgery."]}, "extra_info": {"fulltext_subclaims": ["A 39-year-old woman visited our hospital complaining of worsened right low back pain and fever in 1 month before her first visit.", "She had an experience of pyelonephritis 10 years ago.", "Her initial laboratory data had no abnormal findings.", "Her urine test was clear.", "Her urine cytology was negative.", "Ultrasound imaging revealed right gross hydronephrosis.", "CECT also detected right gross hydronephrosis.", "The right ureter was unclear on CECT.", "CECT was reconstructed to 3D imaging with Osirix\u00ae.", "3D imaging found an aberrant blood vessel contacting with the right ureteropelvic junction.", "UPJO was preoperatively diagnosed due to the aberrant blood vessel.", "Tc-99m MAG3 renal scan confirmed that the right kidney exhibited obstructive pattern.", "The right kidney had poor diuretic response.", "The T1/2 of the right kidney was 21.07 min.", "The right kidney function was similarly preserved to the left kidney function.", "MAG3 clearance of the right kidney was 163.7 ml/min/1.73 m2.", "Surgical treatment was indicated because of the symptomatic disease.", "Preoperative RP showed that the right ureter shifted inward compared with the normal position.", "Preoperative RP suggested the coexistence of retrocaval ureter.", "RALP was conducted by a three-port transperitoneal approach.", "Port position was more medial than usual.", "The swollen right renal pelvis and the aberrant blood vessel were identified.", "The right ureter was peeled downward.", "The right ureter was confirmed to be positioned behind the IVC.", "The renal pelvis was dissected.", "The ureter was repositioned anterior to the IVC.", "The strictured ureteropelvic junction was removed.", "The ureter and the renal pelvis were spatulated.", "A 6-Fr double-J stent was inserted.", "The ureter and the renal pelvis were reanastomosed in a tension-free fashion.", "The anastomosis was sutured with interrupted 5-0 sutures.", "A 10-Fr BLAKE Silicon drain was put into the anastomosis place.", "Blood loss was uncountable.", "The operation time was 403 min.", "The robot console time was 301 min.", "The urethral catheter was removed 5 days after surgery.", "The drain was removed 6 days after surgery.", "No perioperative adverse events were found.", "The double-J stent was removed 2 months after surgery.", "No recurrence of the symptoms was observed.", "Her right hydronephrosis improved in 2 years after surgery."], "index": 162, "original_id": "multiclinsum_test_1681_en.txt", "split": "test", "summary_subclaims": ["The patient is a 39-year-old woman.", "She visited the hospital complaining of worsened right low back pain and fever.", "Contrast-enhanced computed tomography diagnosed right hydronephrosis due to ureteropelvic junction obstruction.", "Retrograde pyelography before robot-assisted laparoscopic pyeloplasty revealed concomitant ipsilateral retrocaval ureter.", "Laparoscopically, ureteropelvic junction obstruction due to aberrant blood vessel and coexisting retrocaval ureter was confirmed.", "Transposition of the ureter from posterior to anterior of the inferior vena cava and following dismembered pyeloplasty was performed.", "Two years after surgery, her right hydronephrosis improved.", "She had no complain of any symptom two years after surgery."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 62-year-old previously healthy Sri Lankan native male from Gampaha, in the Western Province of Sri Lanka.", "He presented with high fever associated with chills and rigors for 17 days.", "He also complained of malaise, myalgia and arthralgia for the same duration.", "He denied any urinary, respiratory or abdominal symptoms.", "He had obtained treatment from a local hospital for the illness with no clinical improvement.", "He had received co-amoxyclav, clarythromicin and paracetamol for 4 days.", "He had not been consuming any medication prior to the illness.", "He had not received any drug that would result in extrapyramidal features.", "Around the 5th day of the clinical illness he had developed intermittent resting tremor in his right arm and leg.", "By the time he presented to us he had stiffness and very frequent intermittent resting tremor.", "This resulted in difficulty to carry out normal work with the right hand.", "He also found it difficult to walk due to unusual stiffness and heaviness of the right leg.", "He found it difficult to smile with others and felt very distressed.", "He denied similar previous episodes.", "There was no associated hearing impairment, seizures, or altered level of consciousness.", "There were no symptoms to suggest involvement of cerebellar system or autonomic nervous system.", "There was no family history of movement disorders.", "He had been working in his garden 7 days prior to the onset of fever.", "Examination revealed intermittent high amplitude low frequency resting tremor in his right hand.", "He had a mask like face where he found difficult to smile or show his teeth.", "He also had increased muscle tone limited to the right side with normal tendon reflexes.", "The rest of the central nervous system was unremarkable.", "His blood pressure was 140/90 mmHg in both supine and standing positions.", "The respiratory system revealed few basal crackles.", "The abdominal examination was unremarkable except for a superficial crater like lesion suggestive of an eschar.", "He did not have lymphadenopathy or a rash.", "His full blood count was 13.4 \u00d7 109/L (Neutrophils 43 %, Lymphocytes 56 %).", "Erythrocyte sedimentation rate was 80 mm/1st h.", "He was positive for Immunofluoresence Assay (IFA)-IgM and IgG for O. tsutsugamushi on the 17th day of illness.", "The IFA-IgG titre using Orientia Karp antigen was 1:1024 which rose up to 1:16,384 after 2 weeks.", "His fever settled with oral doxycycline and azithromycin within 48 h.", "He demonstrated some improvement in his Parkinsonism features prior to discharge from hospital in 4 days.", "He visited for review 2 weeks after discharge.", "By this time he showed complete improvement and was happy with a smiling face."], "summary_subclaims": ["The patient is a 62-year-old previously healthy Sri Lankan native male from the Western province of Sri Lanka.", "He presented with high fever with malaise, myalgia and arthralgia for 17 days.", "On the 5th day of illness he developed intermittent resting tremor in his right arm and leg.", "He denied similar previous episodes.", "Clinical examination revealed a high amplitude low frequency resting tremor in his right hand.", "There was a mask-like face and increased muscle tone limited to the right side.", "The rest of the system examination was normal except for an eschar over the abdomen.", "Immunofluorescence assay-IgM and IgG against Orientia tsutsugamushi Karp antigen were positive with rising titers.", "With oral doxycycline and azithromycin his fever settled within 48 h.", "A complete recovery of Parkinson's features was observed within 2 weeks."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 62-year-old previously healthy Sri Lankan native male from Gampaha, in the Western Province of Sri Lanka.", "He presented with high fever associated with chills and rigors for 17 days.", "He also complained of malaise, myalgia and arthralgia for the same duration.", "He denied any urinary, respiratory or abdominal symptoms.", "He had obtained treatment from a local hospital for the illness with no clinical improvement.", "He had received co-amoxyclav, clarythromicin and paracetamol for 4 days.", "He had not been consuming any medication prior to the illness.", "He had not received any drug that would result in extrapyramidal features.", "Around the 5th day of the clinical illness he had developed intermittent resting tremor in his right arm and leg.", "By the time he presented to us he had stiffness and very frequent intermittent resting tremor.", "This resulted in difficulty to carry out normal work with the right hand.", "He also found it difficult to walk due to unusual stiffness and heaviness of the right leg.", "He found it difficult to smile with others and felt very distressed.", "He denied similar previous episodes.", "There was no associated hearing impairment, seizures, or altered level of consciousness.", "There were no symptoms to suggest involvement of cerebellar system or autonomic nervous system.", "There was no family history of movement disorders.", "He had been working in his garden 7 days prior to the onset of fever.", "Examination revealed intermittent high amplitude low frequency resting tremor in his right hand.", "He had a mask like face where he found difficult to smile or show his teeth.", "He also had increased muscle tone limited to the right side with normal tendon reflexes.", "The rest of the central nervous system was unremarkable.", "His blood pressure was 140/90 mmHg in both supine and standing positions.", "The respiratory system revealed few basal crackles.", "The abdominal examination was unremarkable except for a superficial crater like lesion suggestive of an eschar.", "He did not have lymphadenopathy or a rash.", "His full blood count was 13.4 \u00d7 109/L (Neutrophils 43 %, Lymphocytes 56 %).", "Erythrocyte sedimentation rate was 80 mm/1st h.", "He was positive for Immunofluoresence Assay (IFA)-IgM and IgG for O. tsutsugamushi on the 17th day of illness.", "The IFA-IgG titre using Orientia Karp antigen was 1:1024 which rose up to 1:16,384 after 2 weeks.", "His fever settled with oral doxycycline and azithromycin within 48 h.", "He demonstrated some improvement in his Parkinsonism features prior to discharge from hospital in 4 days.", "He visited for review 2 weeks after discharge.", "By this time he showed complete improvement and was happy with a smiling face."], "index": 155, "original_id": "multiclinsum_test_146_en.txt", "split": "test", "summary_subclaims": ["The patient is a 62-year-old previously healthy Sri Lankan native male from the Western province of Sri Lanka.", "He presented with high fever with malaise, myalgia and arthralgia for 17 days.", "On the 5th day of illness he developed intermittent resting tremor in his right arm and leg.", "He denied similar previous episodes.", "Clinical examination revealed a high amplitude low frequency resting tremor in his right hand.", "There was a mask-like face and increased muscle tone limited to the right side.", "The rest of the system examination was normal except for an eschar over the abdomen.", "Immunofluorescence assay-IgM and IgG against Orientia tsutsugamushi Karp antigen were positive with rising titers.", "With oral doxycycline and azithromycin his fever settled within 48 h.", "A complete recovery of Parkinson's features was observed within 2 weeks."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 15-year-old boy.", "He was previously diagnosed with SRU.", "He presented with frequent bloody stool.", "He had chronic abdominal pain.", "He had constipation.", "He had mucoid discharge.", "Five years earlier, his symptoms began with intermittent vague abdominal pain.", "Five years earlier, his symptoms began with bloody stool.", "Progressive deterioration of symptoms included increased blood in the stool.", "Progressive deterioration of symptoms included new onset of mucoid discharge.", "Progressive deterioration of symptoms included new onset of constipation.", "He complained of straining during defecation.", "He complained of difficulty passing hard and narrowed stool.", "He complained of a sense of incomplete defecation.", "He had no previous history of surgery.", "He had no previous history of prescription medication.", "He had no previous history of any other medical condition.", "He experienced no diarrhea.", "He experienced no food intolerance.", "He experienced no significant weight loss.", "His family history was negative for gastrointestinal disorders.", "His family history was negative for malignancies.", "His family history was negative for IBD.", "His family history was negative for FAP.", "He had his first colonoscopy approximately four years prior.", "The first colonoscopy revealed a solitary ulcer in the rectum.", "The initial histologic examination revealed regenerative crypts in the lamina propria.", "The initial histologic examination revealed fibrosis.", "The initial histologic examination revealed smooth muscle proliferation.", "The initial histologic examination confirmed the diagnosis of SRU.", "A previous laboratory evaluation revealed a WBC of 8100 \u00d7 109 cells/liter.", "A previous laboratory evaluation revealed an Hb of 13.2 g/dL.", "A previous laboratory evaluation revealed an MCV of 79.8 FL.", "A previous laboratory evaluation revealed platelets of 251,000 \u00d7 1010/unit.", "A previous laboratory evaluation revealed an FBS of 85 mg/dL.", "A previous laboratory evaluation revealed a TSH of 3.49 mIU/liter.", "A previous laboratory evaluation revealed an AST of 12 units/liter.", "A previous laboratory evaluation revealed an ALT of 16 units/liter.", "A previous laboratory evaluation revealed an ALP of 391 units/liter.", "A previous laboratory evaluation revealed a ferritin of 22.2 mcg/liter.", "A previous stool exam was negative for occult blood.", "A previous stool exam was negative for ova of parasites.", "A previous stool exam was negative for protozoa cyst.", "On physical examination, his vital signs were stable.", "There were no abnormal findings in his head.", "There were no abnormal findings in his neck.", "There were no abnormal findings in his chest.", "There were no abnormal findings in his abdomen.", "A perineal examination revealed no skin tags.", "A perineal examination revealed no fissures.", "A perineal examination revealed no visible prolapse.", "A perineal examination revealed no other indications of child abuse.", "Multiple irregular mass-like lesions were detected during the digital rectal examination.", "We performed a colonoscopy.", "The colonoscopy revealed multiple diffuse polyposes ranging in shape and size from 5 to 15 mm.", "The polyposes extended from the rectum\u2019s middle section to the rectosigmoid junction.", "Multiple biopsies were taken and sent for histopathologic evaluation.", "The histopathologic evaluation revealed a polypoid structure with a cap of ulcerated granulation tissue.", "The histopathologic evaluation revealed inflammatory exudates on the surface.", "The histopathologic evaluation revealed tortuous non-dysplastic crypts.", "The histopathologic evaluation revealed mucin spillage in the inflamed stroma.", "The histopathologic evaluation revealed smooth muscle fibers.", "The histopathologic evaluation revealed congested vessels.", "The diagnosis of CP was confirmed based on these new findings.", "Total serum protein was 6.7 g/dL.", "Total serum albumin was 4.3 g/dL.", "Until histopathologic confirmation of CP is obtained, conservative measures such as a high-fiber diet are recommended.", "Until histopathologic confirmation of CP is obtained, the use of laxative agents is recommended.", "Until histopathologic confirmation of CP is obtained, avoidance of manual stool evacuation is recommended.", "After histopathologic confirmation, we decided to perform endoscopic mucosal resection (EMR).", "We resected as many polyps as possible during the first session.", "The patient underwent two additional colonoscopy sessions during the 3-month follow-up.", "The majority of the remaining polyps were removed using EMR.", "Complete eradication of polyps was not possible.", "The patient\u2019s symptoms improved.", "The rectal bleeding stopped.", "The abdominal pain subsided."], "summary_subclaims": ["The patient is a 15-year-old boy.", "The patient was previously diagnosed with SRU.", "The patient presented with rectal bleeding.", "The patient presented with mucoid discharge.", "The patient presented with abdominal pain.", "Additional colonoscopy evaluation revealed multiple polyposes varying in size and shape limited to the rectum.", "Histologic examination revealed a characteristic cap of granulation tissue covering tortuous nondysplastic crypts in the inflamed stroma.", "The histologic findings indicated that SRU had transformed into CP.", "The plan was to perform endoscopic mucosal resection of the lesions in multiple sessions."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 15-year-old boy.", "He was previously diagnosed with SRU.", "He presented with frequent bloody stool.", "He had chronic abdominal pain.", "He had constipation.", "He had mucoid discharge.", "Five years earlier, his symptoms began with intermittent vague abdominal pain.", "Five years earlier, his symptoms began with bloody stool.", "Progressive deterioration of symptoms included increased blood in the stool.", "Progressive deterioration of symptoms included new onset of mucoid discharge.", "Progressive deterioration of symptoms included new onset of constipation.", "He complained of straining during defecation.", "He complained of difficulty passing hard and narrowed stool.", "He complained of a sense of incomplete defecation.", "He had no previous history of surgery.", "He had no previous history of prescription medication.", "He had no previous history of any other medical condition.", "He experienced no diarrhea.", "He experienced no food intolerance.", "He experienced no significant weight loss.", "His family history was negative for gastrointestinal disorders.", "His family history was negative for malignancies.", "His family history was negative for IBD.", "His family history was negative for FAP.", "He had his first colonoscopy approximately four years prior.", "The first colonoscopy revealed a solitary ulcer in the rectum.", "The initial histologic examination revealed regenerative crypts in the lamina propria.", "The initial histologic examination revealed fibrosis.", "The initial histologic examination revealed smooth muscle proliferation.", "The initial histologic examination confirmed the diagnosis of SRU.", "A previous laboratory evaluation revealed a WBC of 8100 \u00d7 109 cells/liter.", "A previous laboratory evaluation revealed an Hb of 13.2 g/dL.", "A previous laboratory evaluation revealed an MCV of 79.8 FL.", "A previous laboratory evaluation revealed platelets of 251,000 \u00d7 1010/unit.", "A previous laboratory evaluation revealed an FBS of 85 mg/dL.", "A previous laboratory evaluation revealed a TSH of 3.49 mIU/liter.", "A previous laboratory evaluation revealed an AST of 12 units/liter.", "A previous laboratory evaluation revealed an ALT of 16 units/liter.", "A previous laboratory evaluation revealed an ALP of 391 units/liter.", "A previous laboratory evaluation revealed a ferritin of 22.2 mcg/liter.", "A previous stool exam was negative for occult blood.", "A previous stool exam was negative for ova of parasites.", "A previous stool exam was negative for protozoa cyst.", "On physical examination, his vital signs were stable.", "There were no abnormal findings in his head.", "There were no abnormal findings in his neck.", "There were no abnormal findings in his chest.", "There were no abnormal findings in his abdomen.", "A perineal examination revealed no skin tags.", "A perineal examination revealed no fissures.", "A perineal examination revealed no visible prolapse.", "A perineal examination revealed no other indications of child abuse.", "Multiple irregular mass-like lesions were detected during the digital rectal examination.", "We performed a colonoscopy.", "The colonoscopy revealed multiple diffuse polyposes ranging in shape and size from 5 to 15 mm.", "The polyposes extended from the rectum\u2019s middle section to the rectosigmoid junction.", "Multiple biopsies were taken and sent for histopathologic evaluation.", "The histopathologic evaluation revealed a polypoid structure with a cap of ulcerated granulation tissue.", "The histopathologic evaluation revealed inflammatory exudates on the surface.", "The histopathologic evaluation revealed tortuous non-dysplastic crypts.", "The histopathologic evaluation revealed mucin spillage in the inflamed stroma.", "The histopathologic evaluation revealed smooth muscle fibers.", "The histopathologic evaluation revealed congested vessels.", "The diagnosis of CP was confirmed based on these new findings.", "Total serum protein was 6.7 g/dL.", "Total serum albumin was 4.3 g/dL.", "Until histopathologic confirmation of CP is obtained, conservative measures such as a high-fiber diet are recommended.", "Until histopathologic confirmation of CP is obtained, the use of laxative agents is recommended.", "Until histopathologic confirmation of CP is obtained, avoidance of manual stool evacuation is recommended.", "After histopathologic confirmation, we decided to perform endoscopic mucosal resection (EMR).", "We resected as many polyps as possible during the first session.", "The patient underwent two additional colonoscopy sessions during the 3-month follow-up.", "The majority of the remaining polyps were removed using EMR.", "Complete eradication of polyps was not possible.", "The patient\u2019s symptoms improved.", "The rectal bleeding stopped.", "The abdominal pain subsided."], "index": 164, "original_id": "multiclinsum_test_2219_en.txt", "split": "test", "summary_subclaims": ["The patient is a 15-year-old boy.", "The patient was previously diagnosed with SRU.", "The patient presented with rectal bleeding.", "The patient presented with mucoid discharge.", "The patient presented with abdominal pain.", "Additional colonoscopy evaluation revealed multiple polyposes varying in size and shape limited to the rectum.", "Histologic examination revealed a characteristic cap of granulation tissue covering tortuous nondysplastic crypts in the inflamed stroma.", "The histologic findings indicated that SRU had transformed into CP.", "The plan was to perform endoscopic mucosal resection of the lesions in multiple sessions."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was a 71-year-old female.", "She had been undergoing oral treatment for diabetes with canagliflozin 100 mg/day, metformin 1,000 mg/day, and saxagliptin 5 mg/day.", "She noticed general malaise a month before her emergency department visit.", "Two weeks before her emergency department visit, her oral intake decreased because of reduced appetite.", "She continued oral medications at their initial dose.", "The day prior to her emergency department visit, her malaise worsened.", "She developed nausea and abdominal pain.", "A local doctor discovered notable metabolic acidosis (pH, 6.860; CO2, 8 mmHg; HCO3, \u22121.0 mEq/L; base excess measurement, below sensitivity).", "She was urgently transferred to Kurume University Hospital Advanced Emergency Medical Service Center.", "On admission, her body temperature was 35.0 \u00b0C.", "On admission, her pulse was 118/min.", "On admission, her respiratory rate was 28/min.", "On admission, her blood pressure was 111/75 mmHg.", "The findings on consultation included notable dryness inside the oral cavity.", "The findings on consultation included a cold sensation on distal regions of the limbs.", "Chest auscultation revealed no significant findings.", "There was mild tenderness in the lower abdominal region.", "Blood gases demonstrated notable metabolic acidosis (pH, 6.89; CO2, 11.4 mmHg; HCO3, 1.9 mEq/L; base excess, \u221231.3 mmol/L).", "Lactic acid was mildly elevated at 3.3 mmol/L.", "Blood sugar was mildly elevated at 259 mg/dL.", "Hyperkalemia was observed accompanying the acidosis.", "No significant kidney function impairment was observed.", "A diagnosis of lactic acidosis secondary to metformin was considered.", "The patient had not recently been exposed to a contrast agent.", "Lactate was only mildly elevated.", "Point-of-care urine testing showed strongly positive urinary ketones.", "Point-of-care urine testing showed strongly positive urinary glucose.", "Plasma 3-hydroxybutyric acid was markedly high (>10,000 \u03bcmol/L).", "DKA was suspected.", "An injection of 0.45% sodium chloride was given as an intravenous drip at 800 mL/h.", "Blood sugar dropped to 180 mg/dL after using two units of short-acting insulin.", "Insulin was not used continuously.", "An intravenous drip of glucose was started.", "Around 6 units/day of insulin were used as appropriate.", "Sodium bicarbonate was given as an intravenous drip.", "Continuous renal replacement therapy (CRRT) was started from day 2 after hospital admission.", "The acidosis improved because of CRRT over 3 days.", "Hyperketonemia reduced notably after a few days.", "Urinary sugar continued to rise.", "Osmotic diuresis set in with urinary glucose as the cause.", "Polyurea was observed.", "Fluid replacement was carried out using Ringer\u2019s solution.", "Urinary sugar turned negative on day 16 after admission.", "She was discharged on day 18 after admission."], "summary_subclaims": ["The patient was a 71-year-old female.", "She was being treated for type 2 diabetes.", "She was taking canagliflozin, metformin, and saxagliptin orally.", "She presented to the ED for evaluation of reduced oral intake, malaise, nausea, and abdominal pain.", "Her blood glucose was 259 mg/dL.", "There was notable ketoacidosis.", "The pH was 6.89.", "The CO2 was 11.4 mmHg.", "The HCO3 was 1.9 mEq/L.", "The base excess was -31.3 mmol/L.", "The 3-hydroxybutyric acid was > 10,000 \u03bcmol/L.", "The uncontrolled acidosis improved following 3 days of continuous renal replacement therapy.", "Elevated urinary glucose continued for more than 10 days.", "Ringer's lactated fluid supplementation was continued for management of polyurea and glucosuria.", "Urinary glucose turned negative on day 16.", "There was improvement in the patient's overall state.", "She was discharged on day 18."]}, "extra_info": {"fulltext_subclaims": ["The patient was a 71-year-old female.", "She had been undergoing oral treatment for diabetes with canagliflozin 100 mg/day, metformin 1,000 mg/day, and saxagliptin 5 mg/day.", "She noticed general malaise a month before her emergency department visit.", "Two weeks before her emergency department visit, her oral intake decreased because of reduced appetite.", "She continued oral medications at their initial dose.", "The day prior to her emergency department visit, her malaise worsened.", "She developed nausea and abdominal pain.", "A local doctor discovered notable metabolic acidosis (pH, 6.860; CO2, 8 mmHg; HCO3, \u22121.0 mEq/L; base excess measurement, below sensitivity).", "She was urgently transferred to Kurume University Hospital Advanced Emergency Medical Service Center.", "On admission, her body temperature was 35.0 \u00b0C.", "On admission, her pulse was 118/min.", "On admission, her respiratory rate was 28/min.", "On admission, her blood pressure was 111/75 mmHg.", "The findings on consultation included notable dryness inside the oral cavity.", "The findings on consultation included a cold sensation on distal regions of the limbs.", "Chest auscultation revealed no significant findings.", "There was mild tenderness in the lower abdominal region.", "Blood gases demonstrated notable metabolic acidosis (pH, 6.89; CO2, 11.4 mmHg; HCO3, 1.9 mEq/L; base excess, \u221231.3 mmol/L).", "Lactic acid was mildly elevated at 3.3 mmol/L.", "Blood sugar was mildly elevated at 259 mg/dL.", "Hyperkalemia was observed accompanying the acidosis.", "No significant kidney function impairment was observed.", "A diagnosis of lactic acidosis secondary to metformin was considered.", "The patient had not recently been exposed to a contrast agent.", "Lactate was only mildly elevated.", "Point-of-care urine testing showed strongly positive urinary ketones.", "Point-of-care urine testing showed strongly positive urinary glucose.", "Plasma 3-hydroxybutyric acid was markedly high (>10,000 \u03bcmol/L).", "DKA was suspected.", "An injection of 0.45% sodium chloride was given as an intravenous drip at 800 mL/h.", "Blood sugar dropped to 180 mg/dL after using two units of short-acting insulin.", "Insulin was not used continuously.", "An intravenous drip of glucose was started.", "Around 6 units/day of insulin were used as appropriate.", "Sodium bicarbonate was given as an intravenous drip.", "Continuous renal replacement therapy (CRRT) was started from day 2 after hospital admission.", "The acidosis improved because of CRRT over 3 days.", "Hyperketonemia reduced notably after a few days.", "Urinary sugar continued to rise.", "Osmotic diuresis set in with urinary glucose as the cause.", "Polyurea was observed.", "Fluid replacement was carried out using Ringer\u2019s solution.", "Urinary sugar turned negative on day 16 after admission.", "She was discharged on day 18 after admission."], "index": 2, "original_id": "multiclinsum_test_99_en.txt", "split": "test", "summary_subclaims": ["The patient was a 71-year-old female.", "She was being treated for type 2 diabetes.", "She was taking canagliflozin, metformin, and saxagliptin orally.", "She presented to the ED for evaluation of reduced oral intake, malaise, nausea, and abdominal pain.", "Her blood glucose was 259 mg/dL.", "There was notable ketoacidosis.", "The pH was 6.89.", "The CO2 was 11.4 mmHg.", "The HCO3 was 1.9 mEq/L.", "The base excess was -31.3 mmol/L.", "The 3-hydroxybutyric acid was > 10,000 \u03bcmol/L.", "The uncontrolled acidosis improved following 3 days of continuous renal replacement therapy.", "Elevated urinary glucose continued for more than 10 days.", "Ringer's lactated fluid supplementation was continued for management of polyurea and glucosuria.", "Urinary glucose turned negative on day 16.", "There was improvement in the patient's overall state.", "She was discharged on day 18."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 47-year-old man.", "He had a severe trauma of the left hemithorax, left hypochondrium, and left flank three years before the current presentation.", "He was admitted to the Department of Gastroenterology.", "He had nausea, repeated vomiting, epigastric pain, and intermittent constipation for over a month.", "He had acid regurgitation and pyrosis.", "He had loss of appetite and significant weight loss in the past six months.", "Physical examination revealed a firm, palpable abdominal mass in the left hypochondrium and left flank.", "Laboratory tests showed a low iron serum level of 46 \u03bcg/dL.", "Laboratory tests showed leukocytosis.", "Upper endoscopy described a deformed stomach with an extrinsic compression especially on the antrum.", "The extrinsic compression made difficult the passage through the pylorus.", "There was no significant distention of the gastric body on insufflation.", "There was no mucosal abnormality.", "An abdominal ultrasound highlighted a heterogeneous mass with tissular and cystic components.", "The mass extended from the left hepatic lobe to the spleen\u2019s hilum.", "Contrast-enhanced ultrasonography pointed out that the tissular component of the tumor was enhanced in the arterial phase.", "The tissular component presented a wash-out phenomenon in the late phase.", "The cystic and necrotic components were unenhanced.", "A contrast-enhanced abdominal computed tomography was scheduled.", "The CT scan described a heterogeneous tumor of 17\u00d715\u00d714 cm containing numerous necrosis and cystic areas.", "The tumor originated in the fundus and greater curvature of the stomach.", "The tumor had extraluminal development.", "The tumor was causing a mass effect on the stomach, spleen, splenic vein, and enveloping the body and pancreatic tail.", "We suspected it was a GIST with necrotic areas.", "We proposed the patient for surgery due to tumor size and gastric outlet obstruction symptoms.", "A xypho-umbilical approach was chosen.", "The peritoneal cavity was opened.", "The giant tumor occupied most of the upper abdominal cavity with adherence to the gastric wall.", "After the gastro-colic ligament was sectioned, tumor appurtenance of the great gastric wall was confirmed.", "Infiltration of the tail of the pancreas and splenic pedicle was confirmed.", "No hepatic or peritoneal metastases were found.", "The rest of the abdominal organs seemed macroscopically normal.", "En bloc surgical removal of the tumor was decided, including adjacent lymph nodes, spleen, and pancreas tail.", "The pancreas tail was sectioned 5 cm proximal from the splenic pedicle.", "The tumor block included the greater curvature of the stomach.", "The greater curvature of the stomach was sealed with a linear stapler.", "The resected piece measured 23\u00d717\u00d710 cm.", "The tumor had 22\u00d710 cm with many cystic and necrotic areas.", "Tumor fragments were embedded in 10% formalin for 24 hours.", "Classical staining with Hematoxylin\u2013Eosin described similar characteristics of a mesenchymal tumor.", "The tumor was composed of spindle-shaped cells with a high mitotic rate, over 5 mitoses/50 high-power fields.", "The tumor had an 86% risk of progression (PT4Nx).", "A partially encapsulated tumor proliferation was noted in the thickness of the muscular tunic of the gastric wall.", "The tumor proliferation had a pseudonodular appearance composed of fusiform cells.", "The cells had hypertrophic nuclei with unevenly arranged chromatin and karyorrhexes.", "The cells were arranged in a fasciculate pattern.", "The tumor had myxoid, hemorrhage, and necrosis areas.", "Neoplastic proliferation invaded only the submucosa.", "The neoplastic proliferation did not affect the gastric mucosa.", "The neoplastic proliferation did not invade adjacent splenic or pancreatic parenchyma.", "The mitotic rate was high, >5 mitoses/50 HPFs.", "Free margins (R0) were noted.", "No evidence of perineural invasion was noted.", "No lymph node metastasis was noted.", "No peritoneal metastasis was noted.", "IHC staining revealed that tumor cells were strongly diffuse positive for CD117/c-kit.", "IHC staining revealed that tumor cells were strongly diffuse positive for CD34.", "IHC staining revealed that tumor cells were strongly diffuse positive for DOG1.", "SMA and neuron-specific enolase (NSE) were variable focal positives in tumor proliferation.", "The Ki67 proliferation rate was positive in more than 5% of the tumor cells in 50 HPFs.", "The S100 protein was negative.", "The patient was successfully discharged.", "The patient underwent oncology follow-up with Imatinib.", "There was no relapse a year after surgical resection."], "summary_subclaims": ["The patient was diagnosed with a giant gastric GIST.", "The tumor presented for intermittent gastric outlet obstruction symptoms.", "There are only several cases of gastric exophytic gastric GIST provoking intermittent gastric outlet obstruction.", "Tumor resection should be adapted to every patient's status.", "The surgical approach should be focused on en bloc extraction.", "The surgical approach should aim for preservation of invaded organs as much as possible."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 47-year-old man.", "He had a severe trauma of the left hemithorax, left hypochondrium, and left flank three years before the current presentation.", "He was admitted to the Department of Gastroenterology.", "He had nausea, repeated vomiting, epigastric pain, and intermittent constipation for over a month.", "He had acid regurgitation and pyrosis.", "He had loss of appetite and significant weight loss in the past six months.", "Physical examination revealed a firm, palpable abdominal mass in the left hypochondrium and left flank.", "Laboratory tests showed a low iron serum level of 46 \u03bcg/dL.", "Laboratory tests showed leukocytosis.", "Upper endoscopy described a deformed stomach with an extrinsic compression especially on the antrum.", "The extrinsic compression made difficult the passage through the pylorus.", "There was no significant distention of the gastric body on insufflation.", "There was no mucosal abnormality.", "An abdominal ultrasound highlighted a heterogeneous mass with tissular and cystic components.", "The mass extended from the left hepatic lobe to the spleen\u2019s hilum.", "Contrast-enhanced ultrasonography pointed out that the tissular component of the tumor was enhanced in the arterial phase.", "The tissular component presented a wash-out phenomenon in the late phase.", "The cystic and necrotic components were unenhanced.", "A contrast-enhanced abdominal computed tomography was scheduled.", "The CT scan described a heterogeneous tumor of 17\u00d715\u00d714 cm containing numerous necrosis and cystic areas.", "The tumor originated in the fundus and greater curvature of the stomach.", "The tumor had extraluminal development.", "The tumor was causing a mass effect on the stomach, spleen, splenic vein, and enveloping the body and pancreatic tail.", "We suspected it was a GIST with necrotic areas.", "We proposed the patient for surgery due to tumor size and gastric outlet obstruction symptoms.", "A xypho-umbilical approach was chosen.", "The peritoneal cavity was opened.", "The giant tumor occupied most of the upper abdominal cavity with adherence to the gastric wall.", "After the gastro-colic ligament was sectioned, tumor appurtenance of the great gastric wall was confirmed.", "Infiltration of the tail of the pancreas and splenic pedicle was confirmed.", "No hepatic or peritoneal metastases were found.", "The rest of the abdominal organs seemed macroscopically normal.", "En bloc surgical removal of the tumor was decided, including adjacent lymph nodes, spleen, and pancreas tail.", "The pancreas tail was sectioned 5 cm proximal from the splenic pedicle.", "The tumor block included the greater curvature of the stomach.", "The greater curvature of the stomach was sealed with a linear stapler.", "The resected piece measured 23\u00d717\u00d710 cm.", "The tumor had 22\u00d710 cm with many cystic and necrotic areas.", "Tumor fragments were embedded in 10% formalin for 24 hours.", "Classical staining with Hematoxylin\u2013Eosin described similar characteristics of a mesenchymal tumor.", "The tumor was composed of spindle-shaped cells with a high mitotic rate, over 5 mitoses/50 high-power fields.", "The tumor had an 86% risk of progression (PT4Nx).", "A partially encapsulated tumor proliferation was noted in the thickness of the muscular tunic of the gastric wall.", "The tumor proliferation had a pseudonodular appearance composed of fusiform cells.", "The cells had hypertrophic nuclei with unevenly arranged chromatin and karyorrhexes.", "The cells were arranged in a fasciculate pattern.", "The tumor had myxoid, hemorrhage, and necrosis areas.", "Neoplastic proliferation invaded only the submucosa.", "The neoplastic proliferation did not affect the gastric mucosa.", "The neoplastic proliferation did not invade adjacent splenic or pancreatic parenchyma.", "The mitotic rate was high, >5 mitoses/50 HPFs.", "Free margins (R0) were noted.", "No evidence of perineural invasion was noted.", "No lymph node metastasis was noted.", "No peritoneal metastasis was noted.", "IHC staining revealed that tumor cells were strongly diffuse positive for CD117/c-kit.", "IHC staining revealed that tumor cells were strongly diffuse positive for CD34.", "IHC staining revealed that tumor cells were strongly diffuse positive for DOG1.", "SMA and neuron-specific enolase (NSE) were variable focal positives in tumor proliferation.", "The Ki67 proliferation rate was positive in more than 5% of the tumor cells in 50 HPFs.", "The S100 protein was negative.", "The patient was successfully discharged.", "The patient underwent oncology follow-up with Imatinib.", "There was no relapse a year after surgical resection."], "index": 169, "original_id": "multiclinsum_test_1842_en.txt", "split": "test", "summary_subclaims": ["The patient was diagnosed with a giant gastric GIST.", "The tumor presented for intermittent gastric outlet obstruction symptoms.", "There are only several cases of gastric exophytic gastric GIST provoking intermittent gastric outlet obstruction.", "Tumor resection should be adapted to every patient's status.", "The surgical approach should be focused on en bloc extraction.", "The surgical approach should aim for preservation of invaded organs as much as possible."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 51-year-old Caucasian woman.", "She presented with spinal, pelvic, and sternal inflammatory pain lasting for many years.", "The symptoms had a strong negative impact on her quality of life.", "She did not present palmoplantar pustulosis.", "There was no context of fever.", "She had been diagnosed with synovitis, acne, pustulosis, hyperostosis, and osteitis (SAPHO) syndrome at the age of 40 years.", "She had received sulfasalazine and nonsteroidal anti-inflammatory drugs (NSAIDs) for many years with incomplete pain relief.", "She also had a history of cervical and lumbar arthrodesis.", "She had a history of hypertension.", "She had a history of thyroidectomy.", "Total spine and pelvis magnetic resonance imaging (MRI) showed a short tau inversion recovery (STIR) hypersignal on several thoracic vertebrae (T6, T7, T8, and T9).", "Total spine and pelvis MRI showed a short tau inversion recovery (STIR) hypersignal on the sternal part of the right clavicle.", "Bone marrow oedema was also found on the right iliac bone.", "The sacroiliac joints were preserved.", "Bone scintigraphy showed anterior chest wall involvement.", "Right sternoclavicular hyperostosis was found on computed tomography.", "The C-reactive protein (CRP) was found to be 89.2 mg/L.", "The reference range for CRP is 0\u20135 mg/L.", "Several blood tests performed earlier had already shown elevation of inflammation parameters.", "HLA B27 antigen was negative.", "The diagnosis of active SAPHO syndrome was confirmed.", "Conventional synthetic disease-modifying antirheumatic drug (csDMARD) as methotrexate was not considered.", "Methotrexate is more effective on peripheral arthritis.", "Methotrexate has not shown comparable activity in axial disease in patients with axial spondyloarthritis.", "Anti-tumour necrosis factor (TNF) drugs could not be prescribed because the criteria for reimbursement of these drugs in Belgium were not met.", "The criteria for reimbursement were not met in the absence of sacroiliitis.", "JAK-inhibitors were initiated.", "Tofacitinib 5 mg twice daily was initiated.", "The patient reported rapid and significant reduction of pain within weeks of starting the treatment.", "Blood tests performed one month after the onset of treatment showed a clear regression of inflammatory parameters.", "The CRP was 25.5 mg/L one month after the onset of treatment.", "The CRP was 14 mg/L after 4 months of treatment.", "The CRP was 9.9 mg/L after 10 months of treatment.", "Total spine and pelvis MRI performed after 3 months of treatment showed regression of the STIR hypersignal on the body of the thoracic vertebrae.", "The hypersignal of the right iliac bone disappeared after 3 months of treatment.", "The rheumatic evolution was favourable from a clinical, biological, and radiological point of view since the introduction of a JAK-inhibitor.", "The treatment had to be discontinued due to pulmonary embolism occurring after 8 months on tofacitinib.", "Spinal, pelvic, and chest (sternal and costal) pain reappeared after discontinuation of tofacitinib.", "Elevation of inflammatory parameters occurred after discontinuation of tofacitinib.", "Written informed consent was obtained from the patient for the publication of this report and its accompanying images."], "summary_subclaims": ["The patient was a 51-year-old Caucasian woman.", "She had SAPHO syndrome with mainly axial involvement.", "She had been treated with sulfasalazine and anti-inflammatory drugs for many years.", "The treatment with sulfasalazine and anti-inflammatory drugs was without any success.", "A few weeks after starting treatment with tofacitinib, both clinical and biological parameters dramatically improved.", "Imaging showed considerable regression of the vertebral and pelvic lesions.", "Tofacitinib had to be discontinued due to the occurrence of pulmonary embolism.", "Recurrence of bone pain and biologic inflammation was rapidly observed."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 51-year-old Caucasian woman.", "She presented with spinal, pelvic, and sternal inflammatory pain lasting for many years.", "The symptoms had a strong negative impact on her quality of life.", "She did not present palmoplantar pustulosis.", "There was no context of fever.", "She had been diagnosed with synovitis, acne, pustulosis, hyperostosis, and osteitis (SAPHO) syndrome at the age of 40 years.", "She had received sulfasalazine and nonsteroidal anti-inflammatory drugs (NSAIDs) for many years with incomplete pain relief.", "She also had a history of cervical and lumbar arthrodesis.", "She had a history of hypertension.", "She had a history of thyroidectomy.", "Total spine and pelvis magnetic resonance imaging (MRI) showed a short tau inversion recovery (STIR) hypersignal on several thoracic vertebrae (T6, T7, T8, and T9).", "Total spine and pelvis MRI showed a short tau inversion recovery (STIR) hypersignal on the sternal part of the right clavicle.", "Bone marrow oedema was also found on the right iliac bone.", "The sacroiliac joints were preserved.", "Bone scintigraphy showed anterior chest wall involvement.", "Right sternoclavicular hyperostosis was found on computed tomography.", "The C-reactive protein (CRP) was found to be 89.2 mg/L.", "The reference range for CRP is 0\u20135 mg/L.", "Several blood tests performed earlier had already shown elevation of inflammation parameters.", "HLA B27 antigen was negative.", "The diagnosis of active SAPHO syndrome was confirmed.", "Conventional synthetic disease-modifying antirheumatic drug (csDMARD) as methotrexate was not considered.", "Methotrexate is more effective on peripheral arthritis.", "Methotrexate has not shown comparable activity in axial disease in patients with axial spondyloarthritis.", "Anti-tumour necrosis factor (TNF) drugs could not be prescribed because the criteria for reimbursement of these drugs in Belgium were not met.", "The criteria for reimbursement were not met in the absence of sacroiliitis.", "JAK-inhibitors were initiated.", "Tofacitinib 5 mg twice daily was initiated.", "The patient reported rapid and significant reduction of pain within weeks of starting the treatment.", "Blood tests performed one month after the onset of treatment showed a clear regression of inflammatory parameters.", "The CRP was 25.5 mg/L one month after the onset of treatment.", "The CRP was 14 mg/L after 4 months of treatment.", "The CRP was 9.9 mg/L after 10 months of treatment.", "Total spine and pelvis MRI performed after 3 months of treatment showed regression of the STIR hypersignal on the body of the thoracic vertebrae.", "The hypersignal of the right iliac bone disappeared after 3 months of treatment.", "The rheumatic evolution was favourable from a clinical, biological, and radiological point of view since the introduction of a JAK-inhibitor.", "The treatment had to be discontinued due to pulmonary embolism occurring after 8 months on tofacitinib.", "Spinal, pelvic, and chest (sternal and costal) pain reappeared after discontinuation of tofacitinib.", "Elevation of inflammatory parameters occurred after discontinuation of tofacitinib.", "Written informed consent was obtained from the patient for the publication of this report and its accompanying images."], "index": 0, "original_id": "multiclinsum_test_787_en.txt", "split": "test", "summary_subclaims": ["The patient was a 51-year-old Caucasian woman.", "She had SAPHO syndrome with mainly axial involvement.", "She had been treated with sulfasalazine and anti-inflammatory drugs for many years.", "The treatment with sulfasalazine and anti-inflammatory drugs was without any success.", "A few weeks after starting treatment with tofacitinib, both clinical and biological parameters dramatically improved.", "Imaging showed considerable regression of the vertebral and pelvic lesions.", "Tofacitinib had to be discontinued due to the occurrence of pulmonary embolism.", "Recurrence of bone pain and biologic inflammation was rapidly observed."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["A 65-year-old man was admitted in the emergency department for seizures.", "His medical history included diabetes mellitus.", "His medical history included arterial hypertension.", "His medical history included smoking.", "Four months before admission, a chest X-Ray performed because of a persistent cough revealed a lung mass.", "The lung biopsy yielded a squamous non-small-cell lung cancer.", "The lung biopsy showed 80% expression of PD-L1.", "Extended evaluation showed a unique hepatic metastasis.", "Following consultation with the institutional multidisciplinary team in charge of lung cancer, the patient was treated with intravenous pembrolizumab.", "Pembrolizumab was started 3 months before admission.", "Pembrolizumab was given as a single-drug regimen.", "Pembrolizumab was given at 200 mg every three weeks.", "The patient had no tolerability issues with pembrolizumab.", "The patient had no adherence issues with pembrolizumab.", "On admission, the patient was afebrile.", "Clinical examination was normal.", "Routine biochemical and hematology tests were normal.", "The electroencephalogram performed 12 h after seizures was normal.", "Brain CT scan found a focal hypodense lesion in the right frontal lobe.", "Brain MRI showed an intracranial round-shaped lesion with a maximal diameter of 18 mm.", "The lesion had low signal intensity on T1-weighted images.", "The lesion had intermediate signal intensity on T2-weighted images.", "The lesion was associated with perilesional edema.", "The lesion showed wall enhancement on T1-weighted gadolinium-enhanced images.", "The lesion was suggestive of brain abscess.", "Brain metastasis could not be ruled out.", "The patient was transferred to the neurosurgical department for a total removal of the lesion.", "The excision was performed with craniotomy.", "Per-operative macroscopic findings were also suggestive of brain abscess.", "Empirical antimicrobial therapy was started after surgery.", "Antimicrobial therapy included intravenous ceftriaxone.", "Antimicrobial therapy included metronidazole.", "Microscopic examination revealed numerous filamentous-branching Gram-positive rods.", "Cultures yielded Nocardia farcinica.", "Nocardia farcinica was identified by MALDI-TOF mass spectrometry.", "Antibiotic treatment was modified to meropenem 1 g every 8 h.", "Antibiotic treatment was modified to cotrimoxazole 1600 mg/400 mg every 8 h.", "Antibiotic treatment included folinic acid.", "Body-CT did not show any other localization of nocardiosis.", "The mass tumor had decreased by 80% after the sixth cycle of pembrolizumab.", "Drug susceptibility testing found a meropenem MIC of 32 mg/L.", "Drug susceptibility testing found a linezolid MIC of 4 mg/L.", "Drug susceptibility testing found a cotrimoxazole MIC of 0.5 mg/L.", "Meropenem was replaced by linezolid 600 mg every 12 h.", "Linezolid was given in combination with cotrimoxazole.", "Following the diagnosis, additional risk factors for cerebral nocardiosis were ruled out.", "After 2 months, the patient was asymptomatic, except for asthenia.", "Antibiotics were well tolerated.", "The patient did not receive additional dose of pembrolizumab.", "At 10 weeks of treatment, he developed thrombocytopenia due to linezolid.", "He died 3 months after the diagnosis of cerebral nocardiosis.", "His death was probably related to a major upper-gastrointestinal bleeding.", "The upper-gastrointestinal bleeding was probably related to a peptic ulcer disease.", "The upper-gastrointestinal bleeding was probably related to thrombocytopenia."], "summary_subclaims": ["This is the first clinical case of a cerebral nocardiosis revealed after seizure in a patient treated by pembrolizumab for a metastatic lung cancer.", "The patient was not receiving any additional immunosuppressive therapy.", "The patient had no risk factors for cerebral nocardiosis.", "A brain CT-scan did not reveal any lesion before pembrolizumab.", "The 3-month delay between the start of pembrolizumab and the diagnosis of cerebral nocardiosis suggests that the infection occurred prior to the CPI.", "The patient died during treatment for cerebral nocardiosis.", "The lung cancer tumor mass had decreased by 80% after the sixth cycle of pembrolizumab."]}, "extra_info": {"fulltext_subclaims": ["A 65-year-old man was admitted in the emergency department for seizures.", "His medical history included diabetes mellitus.", "His medical history included arterial hypertension.", "His medical history included smoking.", "Four months before admission, a chest X-Ray performed because of a persistent cough revealed a lung mass.", "The lung biopsy yielded a squamous non-small-cell lung cancer.", "The lung biopsy showed 80% expression of PD-L1.", "Extended evaluation showed a unique hepatic metastasis.", "Following consultation with the institutional multidisciplinary team in charge of lung cancer, the patient was treated with intravenous pembrolizumab.", "Pembrolizumab was started 3 months before admission.", "Pembrolizumab was given as a single-drug regimen.", "Pembrolizumab was given at 200 mg every three weeks.", "The patient had no tolerability issues with pembrolizumab.", "The patient had no adherence issues with pembrolizumab.", "On admission, the patient was afebrile.", "Clinical examination was normal.", "Routine biochemical and hematology tests were normal.", "The electroencephalogram performed 12 h after seizures was normal.", "Brain CT scan found a focal hypodense lesion in the right frontal lobe.", "Brain MRI showed an intracranial round-shaped lesion with a maximal diameter of 18 mm.", "The lesion had low signal intensity on T1-weighted images.", "The lesion had intermediate signal intensity on T2-weighted images.", "The lesion was associated with perilesional edema.", "The lesion showed wall enhancement on T1-weighted gadolinium-enhanced images.", "The lesion was suggestive of brain abscess.", "Brain metastasis could not be ruled out.", "The patient was transferred to the neurosurgical department for a total removal of the lesion.", "The excision was performed with craniotomy.", "Per-operative macroscopic findings were also suggestive of brain abscess.", "Empirical antimicrobial therapy was started after surgery.", "Antimicrobial therapy included intravenous ceftriaxone.", "Antimicrobial therapy included metronidazole.", "Microscopic examination revealed numerous filamentous-branching Gram-positive rods.", "Cultures yielded Nocardia farcinica.", "Nocardia farcinica was identified by MALDI-TOF mass spectrometry.", "Antibiotic treatment was modified to meropenem 1 g every 8 h.", "Antibiotic treatment was modified to cotrimoxazole 1600 mg/400 mg every 8 h.", "Antibiotic treatment included folinic acid.", "Body-CT did not show any other localization of nocardiosis.", "The mass tumor had decreased by 80% after the sixth cycle of pembrolizumab.", "Drug susceptibility testing found a meropenem MIC of 32 mg/L.", "Drug susceptibility testing found a linezolid MIC of 4 mg/L.", "Drug susceptibility testing found a cotrimoxazole MIC of 0.5 mg/L.", "Meropenem was replaced by linezolid 600 mg every 12 h.", "Linezolid was given in combination with cotrimoxazole.", "Following the diagnosis, additional risk factors for cerebral nocardiosis were ruled out.", "After 2 months, the patient was asymptomatic, except for asthenia.", "Antibiotics were well tolerated.", "The patient did not receive additional dose of pembrolizumab.", "At 10 weeks of treatment, he developed thrombocytopenia due to linezolid.", "He died 3 months after the diagnosis of cerebral nocardiosis.", "His death was probably related to a major upper-gastrointestinal bleeding.", "The upper-gastrointestinal bleeding was probably related to a peptic ulcer disease.", "The upper-gastrointestinal bleeding was probably related to thrombocytopenia."], "index": 157, "original_id": "multiclinsum_test_2333_en.txt", "split": "test", "summary_subclaims": ["This is the first clinical case of a cerebral nocardiosis revealed after seizure in a patient treated by pembrolizumab for a metastatic lung cancer.", "The patient was not receiving any additional immunosuppressive therapy.", "The patient had no risk factors for cerebral nocardiosis.", "A brain CT-scan did not reveal any lesion before pembrolizumab.", "The 3-month delay between the start of pembrolizumab and the diagnosis of cerebral nocardiosis suggests that the infection occurred prior to the CPI.", "The patient died during treatment for cerebral nocardiosis.", "The lung cancer tumor mass had decreased by 80% after the sixth cycle of pembrolizumab."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 52-year-old female.", "The patient has no comorbidities.", "The disease evolution has lasted two years.", "The patient has localized pain on the distal phalanx of the left thumb.", "The pain is rated as 9 on the visual analogue scale.", "The pain is of a burning type.", "The pain increases with movement.", "The pain increases with changes in temperature.", "Physical examination showed subungual pain.", "Physical examination showed mild volume increase.", "Physical examination showed palpation of a radial-sided tumour.", "Ultrasound reported a highly vascularised nodular lesion.", "The lesion is circumscribed, hypoechoic, and homogeneous.", "The lesion measures 3.00 \u00d7 2.10 mm.", "The lesion is located on the medial edge of the distal phalanx of the first finger.", "There is thickening of the synovial sheath.", "These findings are characteristic of glomus tumours.", "Surgical treatment was decided.", "The surgery required glasses with two-fold magnification.", "The surgery used regional block anaesthesia and ischaemia.", "The surgical approach was to the distal phalanx and transverse subungual.", "A white-yellowish tumour, well encapsulated, was visualised.", "The tumour measured 3 \u00d7 2 mm.", "Bone curettage was performed.", "Cauterisation of the vascular bed was performed.", "The wound was sutured with monofilament nylon 4/0.", "A piece was sent for histopathological study.", "The patient attended a two-week follow-up appointment.", "Surgical wound stitches were removed.", "The surgical wound showed adequate healing.", "The patient could mobilise the distal interphalangeal joint.", "The pain was rated as 1 point on the visual analogue scale.", "The histopathological study reported a glomus tumour."], "summary_subclaims": ["The patient is a 52-year-old female.", "The patient reported chronic, burning pain radiating to the distal phalanx of the thumb.", "The pain had been present for two years.", "There was no traumatic history.", "The pain limited her daily activities.", "Interphalangeal Doppler ultrasound was performed.", "Interphalangeal Doppler ultrasound is an excellent alternative due to its easy accessibility.", "A glomus tumor in the interphalangeal phalanx of the thumb was diagnosed.", "A H-approach was performed on the interphalangeal fold.", "Subungual dissection and resection of the tumoral piece were performed.", "The surgical wound was found to be healing adequately.", "The patient was able to mobilize the interphalangeal distal joint.", "The visual analogue scale (VAS) was 1 point.", "The anatomopathological evaluation reported the existence of a glomus tumor."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 52-year-old female.", "The patient has no comorbidities.", "The disease evolution has lasted two years.", "The patient has localized pain on the distal phalanx of the left thumb.", "The pain is rated as 9 on the visual analogue scale.", "The pain is of a burning type.", "The pain increases with movement.", "The pain increases with changes in temperature.", "Physical examination showed subungual pain.", "Physical examination showed mild volume increase.", "Physical examination showed palpation of a radial-sided tumour.", "Ultrasound reported a highly vascularised nodular lesion.", "The lesion is circumscribed, hypoechoic, and homogeneous.", "The lesion measures 3.00 \u00d7 2.10 mm.", "The lesion is located on the medial edge of the distal phalanx of the first finger.", "There is thickening of the synovial sheath.", "These findings are characteristic of glomus tumours.", "Surgical treatment was decided.", "The surgery required glasses with two-fold magnification.", "The surgery used regional block anaesthesia and ischaemia.", "The surgical approach was to the distal phalanx and transverse subungual.", "A white-yellowish tumour, well encapsulated, was visualised.", "The tumour measured 3 \u00d7 2 mm.", "Bone curettage was performed.", "Cauterisation of the vascular bed was performed.", "The wound was sutured with monofilament nylon 4/0.", "A piece was sent for histopathological study.", "The patient attended a two-week follow-up appointment.", "Surgical wound stitches were removed.", "The surgical wound showed adequate healing.", "The patient could mobilise the distal interphalangeal joint.", "The pain was rated as 1 point on the visual analogue scale.", "The histopathological study reported a glomus tumour."], "index": 158, "original_id": "multiclinsum_test_3249_en.txt", "split": "test", "summary_subclaims": ["The patient is a 52-year-old female.", "The patient reported chronic, burning pain radiating to the distal phalanx of the thumb.", "The pain had been present for two years.", "There was no traumatic history.", "The pain limited her daily activities.", "Interphalangeal Doppler ultrasound was performed.", "Interphalangeal Doppler ultrasound is an excellent alternative due to its easy accessibility.", "A glomus tumor in the interphalangeal phalanx of the thumb was diagnosed.", "A H-approach was performed on the interphalangeal fold.", "Subungual dissection and resection of the tumoral piece were performed.", "The surgical wound was found to be healing adequately.", "The patient was able to mobilize the interphalangeal distal joint.", "The visual analogue scale (VAS) was 1 point.", "The anatomopathological evaluation reported the existence of a glomus tumor."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["A 63-year-old man was referred to Modarres Hospital, Tehran.", "He had gradual onset of obscure generalized abdominal pain six hours before admission.", "His pain was located in the epigastric and periumbilical region.", "There was no radiation of pain to anywhere else.", "He had one episode of vomiting.", "There was moderate abdominal distension.", "There was periumbilical abdominal tenderness.", "There was no guarding.", "Initial blood tests showed white cell count (WBC) of 21.7 \u00d7 109/L.", "Initial blood tests showed neutrophils 84.2%.", "Initial blood tests showed hemoglobin (Hb) 15.2 g/dL.", "C reactive protein was +2.", "Amylase was 63 U/L.", "Abdominal x-ray was normal.", "Ultrasonography was normal.", "About five hours after resuscitation and appropriate fluid therapy, he has not felt better.", "Blood tests were deranged.", "WBC was 18.4\u00d7109/L.", "Neutrophils were 76.5%.", "Hb was 8.1 g/dL.", "Abdominopelvic CT-scan showed evidence of hematoma near the head of pancreas.", "Abdominopelvic CT-scan showed perihepatic and perisplenic fluid.", "BP fell to 95/55 mmHg.", "Pulse rose to 105/min.", "He was transferred to operating room emergently.", "Midline laparotomy was performed.", "Massive intraperitoneal hematoma was evacuated.", "Right medial visceral rotation, the Cattell-Braasch maneuver, was performed.", "Active bleeding in the base of IPDA was detected.", "IPDA was suture ligated at the base with 4/0 nonabsorbable stitch.", "Hemostasis was achieved.", "The post-operative period was uneventful.", "Oral fluids were started the day after the surgery.", "The patient was discharged from the hospital two days after the surgery.", "One week after discharge, he had a normal follow-up.", "There were no concerning problems one week after discharge."], "summary_subclaims": ["The patient is a 63-year-old man.", "The patient had idiopathic spontaneous intraperitoneal hemorrhage.", "The hemorrhage was caused by spontaneous rupture of non-aneurysmal inferior pancreaticoduodenal artery."]}, "extra_info": {"fulltext_subclaims": ["A 63-year-old man was referred to Modarres Hospital, Tehran.", "He had gradual onset of obscure generalized abdominal pain six hours before admission.", "His pain was located in the epigastric and periumbilical region.", "There was no radiation of pain to anywhere else.", "He had one episode of vomiting.", "There was moderate abdominal distension.", "There was periumbilical abdominal tenderness.", "There was no guarding.", "Initial blood tests showed white cell count (WBC) of 21.7 \u00d7 109/L.", "Initial blood tests showed neutrophils 84.2%.", "Initial blood tests showed hemoglobin (Hb) 15.2 g/dL.", "C reactive protein was +2.", "Amylase was 63 U/L.", "Abdominal x-ray was normal.", "Ultrasonography was normal.", "About five hours after resuscitation and appropriate fluid therapy, he has not felt better.", "Blood tests were deranged.", "WBC was 18.4\u00d7109/L.", "Neutrophils were 76.5%.", "Hb was 8.1 g/dL.", "Abdominopelvic CT-scan showed evidence of hematoma near the head of pancreas.", "Abdominopelvic CT-scan showed perihepatic and perisplenic fluid.", "BP fell to 95/55 mmHg.", "Pulse rose to 105/min.", "He was transferred to operating room emergently.", "Midline laparotomy was performed.", "Massive intraperitoneal hematoma was evacuated.", "Right medial visceral rotation, the Cattell-Braasch maneuver, was performed.", "Active bleeding in the base of IPDA was detected.", "IPDA was suture ligated at the base with 4/0 nonabsorbable stitch.", "Hemostasis was achieved.", "The post-operative period was uneventful.", "Oral fluids were started the day after the surgery.", "The patient was discharged from the hospital two days after the surgery.", "One week after discharge, he had a normal follow-up.", "There were no concerning problems one week after discharge."], "index": 4, "original_id": "multiclinsum_test_45_en.txt", "split": "test", "summary_subclaims": ["The patient is a 63-year-old man.", "The patient had idiopathic spontaneous intraperitoneal hemorrhage.", "The hemorrhage was caused by spontaneous rupture of non-aneurysmal inferior pancreaticoduodenal artery."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is an 86-year-old male.", "He had a previous history of hypertension.", "He had a previous history of coronary artery disease.", "He had shortness of breath.", "He was admitted to the hospital due to heart failure.", "He had undergone percutaneous coronary interventions in the circumflex artery in 2019.", "He had undergone percutaneous coronary interventions in the left anterior descending artery in 2020.", "The interventions were performed at another hospital.", "The patient was asymptomatic before admission.", "Blood pressure was 176/91 mmHg.", "Heart rate was 85 b.p.m.", "Bilateral leg oedema was observed.", "A systolic murmur was heard on auscultation.", "Chest X-ray revealed pleural effusion.", "Chest X-ray revealed congestion.", "Electrocardiogram was within normal range.", "Brain natriuretic peptide was 150.4 pg/mL.", "The normal range for brain natriuretic peptide is <100 pg/mL.", "STS was 10.8.", "EuroSCORE 2 was 9.4.", "Trans-thoracic echocardiogram revealed a left ventricular ejection fraction of 66%.", "Trans-thoracic echocardiogram revealed a left ventricular diastolic diameter of 41 mm.", "A calcified aortic valve was observed.", "The peak velocity of the aortic valve was 3.5 m/s.", "The mean aortic valve pressure gradient was 33 mmHg.", "The aortic valve area using the Doppler method was 0.78 cm2.", "The presence of a VSD can affect TTE-derived peak velocity and mean PG.", "Membranous VSD was observed in cardiac computed tomography.", "Double-chambered right ventricle was observed in cardiac computed tomography.", "Trans-oesophageal echocardiogram, CT, and catheter-based AVA were 0.6\u20130.7 cm2.", "The calcium score was 2150 AgU.", "Based on these findings, the patient was diagnosed with severe aortic stenosis.", "Cardiac CT showed the cardiac anatomy was suitable for TAV implantation.", "The annulus perimeter was 66.1 mm.", "The Valsalva diameter was 29.1 mm.", "The VSD orifice was located 3.5\u20137.3 mm from the aortic valve annulus.", "The VSD orifice diameter was 3.8 mm.", "A thin sub-aortic band was attached to the LV outflow tract.", "Coronary angiogram showed no significant stenosis.", "The catheter-based pressure gradient between LV apex and aorta was 27 mmHg.", "No pressure gradient was observed between LV apex and LVOT.", "Right heart catheterization showed normal wedge pressure of 17 mmHg.", "Right heart catheterization showed a slightly decreased cardiac index of 2.1 L/min/m2.", "Pulmonary hypertension with a mean pressure of 38 mmHg was observed.", "A pressure gradient of 50 mmHg between high-pressure and low-pressure chambers of the right ventricle was observed.", "The catheter-based Qp/Qs ratio was 1.9.", "Severe aortic stenosis in combination with left-to-right shunt due to VSD was diagnosed as the leading cause of heart failure.", "These findings fulfilled the indication for invasive treatment for aortic stenosis and VSD.", "Surgical aortic valve replacement, VSD closure, myectomy of the right ventricle, and sub-aortic band resection were discussed.", "The surgical team deemed the patient not a surgical candidate.", "The surgical team cited the patient\u2019s age as a reason not to perform surgery.", "The surgical team cited high risk of surgery as a reason not to perform surgery.", "The surgical team cited frailty as a reason not to perform surgery.", "A TAVI procedure with VSD orifice coverage using a valve skirt was planned.", "A 26-mm Evolut Pro Plus\u2122 valve was selected.", "The valve has a long skirt at the bottom, which could cover the VSD orifice completely.", "The valve was deployed 9 mm from the annulus level.", "The valve was deployed to cover the entire orifice of VSD with the valve skirt.", "The valve was deployed by watching TOE to confirm no structural damage.", "The valve did not interfere with mitral valve movement.", "No leak across the valve was observed by TOE.", "Complete coverage of the VSD orifice with the valve skirt was observed by TOE.", "The amount of left-to-right shunt decreased.", "The catheter-based Qp/Qs ratio decreased from 1.9 to 1.2.", "Trans-thoracic echocardiogram\u2013based aortic valve pressure gradient decreased from 33 to 2 mmHg.", "Post-procedural TOE revealed no leakage.", "Post-procedural TOE revealed a decrease in left-to-right shunt.", "Post-procedural ECG finding was unchanged.", "Post-procedural ECG showed sinus rhythm.", "Post-procedural ECG showed a PR interval of 194 ms.", "Post-procedural ECG showed a QRS duration of 70 ms.", "The patient was discharged from hospital 7 days after the procedure.", "The patient had not been admitted to hospital since discharge."], "summary_subclaims": ["The patient was an 86-year-old male.", "The patient was admitted to the hospital with congestive heart failure.", "The patient had low-flow low-gradient severe AS.", "The patient had a membranous VSD.", "The patient had a sub-aortic band.", "The patient had a double-chambered right ventricle.", "The patient was not deemed to be a surgical candidate.", "Surgical aortic valve replacement, VSD closure, sub-aortic band resection, and myectomy of RV would be considered as definitive treatment.", "TAVI was performed using a 26\u2005mm Evolut Pro Plus\u2122 self-expanding valve.", "VSD orifice closure was performed using the skirt part of the self-expanding valve.", "A VSD occluder is not approved and thus not available in our country.", "The mean aortic valve pressure gradient improved from 33 to 2\u2005mmHg.", "The shunt flow (Qp/Qs) decreased from 1.9 to 1.2.", "The patient\u2019s heart failure improved.", "The patient was discharged to home 7 days after the procedure.", "The patient remained well and had not been admitted to hospital since discharge."]}, "extra_info": {"fulltext_subclaims": ["The patient is an 86-year-old male.", "He had a previous history of hypertension.", "He had a previous history of coronary artery disease.", "He had shortness of breath.", "He was admitted to the hospital due to heart failure.", "He had undergone percutaneous coronary interventions in the circumflex artery in 2019.", "He had undergone percutaneous coronary interventions in the left anterior descending artery in 2020.", "The interventions were performed at another hospital.", "The patient was asymptomatic before admission.", "Blood pressure was 176/91 mmHg.", "Heart rate was 85 b.p.m.", "Bilateral leg oedema was observed.", "A systolic murmur was heard on auscultation.", "Chest X-ray revealed pleural effusion.", "Chest X-ray revealed congestion.", "Electrocardiogram was within normal range.", "Brain natriuretic peptide was 150.4 pg/mL.", "The normal range for brain natriuretic peptide is <100 pg/mL.", "STS was 10.8.", "EuroSCORE 2 was 9.4.", "Trans-thoracic echocardiogram revealed a left ventricular ejection fraction of 66%.", "Trans-thoracic echocardiogram revealed a left ventricular diastolic diameter of 41 mm.", "A calcified aortic valve was observed.", "The peak velocity of the aortic valve was 3.5 m/s.", "The mean aortic valve pressure gradient was 33 mmHg.", "The aortic valve area using the Doppler method was 0.78 cm2.", "The presence of a VSD can affect TTE-derived peak velocity and mean PG.", "Membranous VSD was observed in cardiac computed tomography.", "Double-chambered right ventricle was observed in cardiac computed tomography.", "Trans-oesophageal echocardiogram, CT, and catheter-based AVA were 0.6\u20130.7 cm2.", "The calcium score was 2150 AgU.", "Based on these findings, the patient was diagnosed with severe aortic stenosis.", "Cardiac CT showed the cardiac anatomy was suitable for TAV implantation.", "The annulus perimeter was 66.1 mm.", "The Valsalva diameter was 29.1 mm.", "The VSD orifice was located 3.5\u20137.3 mm from the aortic valve annulus.", "The VSD orifice diameter was 3.8 mm.", "A thin sub-aortic band was attached to the LV outflow tract.", "Coronary angiogram showed no significant stenosis.", "The catheter-based pressure gradient between LV apex and aorta was 27 mmHg.", "No pressure gradient was observed between LV apex and LVOT.", "Right heart catheterization showed normal wedge pressure of 17 mmHg.", "Right heart catheterization showed a slightly decreased cardiac index of 2.1 L/min/m2.", "Pulmonary hypertension with a mean pressure of 38 mmHg was observed.", "A pressure gradient of 50 mmHg between high-pressure and low-pressure chambers of the right ventricle was observed.", "The catheter-based Qp/Qs ratio was 1.9.", "Severe aortic stenosis in combination with left-to-right shunt due to VSD was diagnosed as the leading cause of heart failure.", "These findings fulfilled the indication for invasive treatment for aortic stenosis and VSD.", "Surgical aortic valve replacement, VSD closure, myectomy of the right ventricle, and sub-aortic band resection were discussed.", "The surgical team deemed the patient not a surgical candidate.", "The surgical team cited the patient\u2019s age as a reason not to perform surgery.", "The surgical team cited high risk of surgery as a reason not to perform surgery.", "The surgical team cited frailty as a reason not to perform surgery.", "A TAVI procedure with VSD orifice coverage using a valve skirt was planned.", "A 26-mm Evolut Pro Plus\u2122 valve was selected.", "The valve has a long skirt at the bottom, which could cover the VSD orifice completely.", "The valve was deployed 9 mm from the annulus level.", "The valve was deployed to cover the entire orifice of VSD with the valve skirt.", "The valve was deployed by watching TOE to confirm no structural damage.", "The valve did not interfere with mitral valve movement.", "No leak across the valve was observed by TOE.", "Complete coverage of the VSD orifice with the valve skirt was observed by TOE.", "The amount of left-to-right shunt decreased.", "The catheter-based Qp/Qs ratio decreased from 1.9 to 1.2.", "Trans-thoracic echocardiogram\u2013based aortic valve pressure gradient decreased from 33 to 2 mmHg.", "Post-procedural TOE revealed no leakage.", "Post-procedural TOE revealed a decrease in left-to-right shunt.", "Post-procedural ECG finding was unchanged.", "Post-procedural ECG showed sinus rhythm.", "Post-procedural ECG showed a PR interval of 194 ms.", "Post-procedural ECG showed a QRS duration of 70 ms.", "The patient was discharged from hospital 7 days after the procedure.", "The patient had not been admitted to hospital since discharge."], "index": 154, "original_id": "multiclinsum_test_3275_en.txt", "split": "test", "summary_subclaims": ["The patient was an 86-year-old male.", "The patient was admitted to the hospital with congestive heart failure.", "The patient had low-flow low-gradient severe AS.", "The patient had a membranous VSD.", "The patient had a sub-aortic band.", "The patient had a double-chambered right ventricle.", "The patient was not deemed to be a surgical candidate.", "Surgical aortic valve replacement, VSD closure, sub-aortic band resection, and myectomy of RV would be considered as definitive treatment.", "TAVI was performed using a 26\u2005mm Evolut Pro Plus\u2122 self-expanding valve.", "VSD orifice closure was performed using the skirt part of the self-expanding valve.", "A VSD occluder is not approved and thus not available in our country.", "The mean aortic valve pressure gradient improved from 33 to 2\u2005mmHg.", "The shunt flow (Qp/Qs) decreased from 1.9 to 1.2.", "The patient\u2019s heart failure improved.", "The patient was discharged to home 7 days after the procedure.", "The patient remained well and had not been admitted to hospital since discharge."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["It is a case report of a 13-year-old girl.", "She had swelling over her right hand for 5 months.", "The swelling was gradually progressive.", "The swelling was situated over the dorsum and medial aspect of the hand.", "There was no history of trauma.", "There was no lesion elsewhere in the body.", "There was no lesion in the family.", "There were no associated features such as pain, fever, or signs influencing general health.", "On examination, the swelling was firm in consistency.", "The swelling occupied the dorsal and inner side of the fifth metacarpal.", "Local temperature was not raised.", "The skin was mobile.", "There was no feature suggestive of inflammatory pathology.", "On deep palpation, the swelling was tender.", "The range of movement was restricted.", "Routine hematological examination was within normal limits.", "Radiology revealed an osteolytic fusiform expansible lesion involving the distal 2/3rd of the fifth metacarpal.", "The lesion involved the articular surface.", "The cortical was paper thin, breached, inflated, and without periosteal reaction.", "The tumor radiograph had a 'soap bubble' appearance.", "The provisional diagnosis was aneurysmal bone cyst and GCT.", "The chest X-ray was within normal limits.", "A core-cut biopsy was sent.", "The biopsy conferred the diagnosis of GCT.", "The technique used was free osteoarticular metatarsal transfer, described by Maini et al.", "A dorsal approach was used for the enbloc resection.", "The incision included the previous biopsy track.", "The fifth metatarsal was removed except the base.", "Partial resection of surrounding muscles was performed.", "The capsule and collateral ligament of the fifth metacarpophalangeal joint were left.", "The fourth metatarsal was harvested from the foot.", "The capsuloligamentous of the metatarsal was sutured to the counter capsuloligamentous structure at the recipient site.", "The metatarsal was fixed with the leftover base of the metacarpal by K-wires.", "A volar slab was applied.", "At the 14th post-operative day, the sutures were removed.", "Exercise was started gradually.", "Union at the junction occurred in 6 weeks.", "No obvious changes were noticed at the transferred metatarsal.", "Initially, the movements had both extension and flexion lag.", "Electric stimulation was given.", "At the end of 6 months of follow-up, the movements were painless and almost up to normal.", "Flexion was restricted terminally at the metacarpophalangeal joint.", "The patient was able to grasp any object.", "The patient had pretty good grip strength.", "After 2 years of follow-up, the procedure was fulfilling expectations.", "The procedure corroborates the reliability of this method.", "During the initial follow-up, the patient had mild-to-moderate pain over the foot while walking.", "The patient was unable to dorsiflex the fourth toe.", "She is now free from pain or any complaint such as deformity or difficulty in walking.", "There is still slight weakness of the fourth toe\u2019s dorsiflexor.", "She is happy and has no complaints."], "summary_subclaims": ["It is a case report of a 13-year-old girl.", "She had a history of swelling over her right hand for 5 months.", "X-ray revealed an osteolytic fusiform expansible lesion.", "The biopsy conferred the diagnosis of GCT.", "A dorsal approach was used for the enbloc resection of the fifth metacarpals (except at the base).", "Partial excision of the surrounding muscles was done.", "The capsule and collateral ligament of the fifth metacarpophalangeal joint were left.", "The fourth metatarsal was harvested from the foot along with its capsule and collateral ligament of the metatarsophalangeal joint.", "The harvested fourth metatarsal was sutured to the counter capsuloligamentous structure at the recipient site."]}, "extra_info": {"fulltext_subclaims": ["It is a case report of a 13-year-old girl.", "She had swelling over her right hand for 5 months.", "The swelling was gradually progressive.", "The swelling was situated over the dorsum and medial aspect of the hand.", "There was no history of trauma.", "There was no lesion elsewhere in the body.", "There was no lesion in the family.", "There were no associated features such as pain, fever, or signs influencing general health.", "On examination, the swelling was firm in consistency.", "The swelling occupied the dorsal and inner side of the fifth metacarpal.", "Local temperature was not raised.", "The skin was mobile.", "There was no feature suggestive of inflammatory pathology.", "On deep palpation, the swelling was tender.", "The range of movement was restricted.", "Routine hematological examination was within normal limits.", "Radiology revealed an osteolytic fusiform expansible lesion involving the distal 2/3rd of the fifth metacarpal.", "The lesion involved the articular surface.", "The cortical was paper thin, breached, inflated, and without periosteal reaction.", "The tumor radiograph had a 'soap bubble' appearance.", "The provisional diagnosis was aneurysmal bone cyst and GCT.", "The chest X-ray was within normal limits.", "A core-cut biopsy was sent.", "The biopsy conferred the diagnosis of GCT.", "The technique used was free osteoarticular metatarsal transfer, described by Maini et al.", "A dorsal approach was used for the enbloc resection.", "The incision included the previous biopsy track.", "The fifth metatarsal was removed except the base.", "Partial resection of surrounding muscles was performed.", "The capsule and collateral ligament of the fifth metacarpophalangeal joint were left.", "The fourth metatarsal was harvested from the foot.", "The capsuloligamentous of the metatarsal was sutured to the counter capsuloligamentous structure at the recipient site.", "The metatarsal was fixed with the leftover base of the metacarpal by K-wires.", "A volar slab was applied.", "At the 14th post-operative day, the sutures were removed.", "Exercise was started gradually.", "Union at the junction occurred in 6 weeks.", "No obvious changes were noticed at the transferred metatarsal.", "Initially, the movements had both extension and flexion lag.", "Electric stimulation was given.", "At the end of 6 months of follow-up, the movements were painless and almost up to normal.", "Flexion was restricted terminally at the metacarpophalangeal joint.", "The patient was able to grasp any object.", "The patient had pretty good grip strength.", "After 2 years of follow-up, the procedure was fulfilling expectations.", "The procedure corroborates the reliability of this method.", "During the initial follow-up, the patient had mild-to-moderate pain over the foot while walking.", "The patient was unable to dorsiflex the fourth toe.", "She is now free from pain or any complaint such as deformity or difficulty in walking.", "There is still slight weakness of the fourth toe\u2019s dorsiflexor.", "She is happy and has no complaints."], "index": 163, "original_id": "multiclinsum_test_2668_en.txt", "split": "test", "summary_subclaims": ["It is a case report of a 13-year-old girl.", "She had a history of swelling over her right hand for 5 months.", "X-ray revealed an osteolytic fusiform expansible lesion.", "The biopsy conferred the diagnosis of GCT.", "A dorsal approach was used for the enbloc resection of the fifth metacarpals (except at the base).", "Partial excision of the surrounding muscles was done.", "The capsule and collateral ligament of the fifth metacarpophalangeal joint were left.", "The fourth metatarsal was harvested from the foot along with its capsule and collateral ligament of the metatarsophalangeal joint.", "The harvested fourth metatarsal was sutured to the counter capsuloligamentous structure at the recipient site."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was a 72-year-old Caucasian woman.", "She had a history of childhood encephalitis with motor sequelae.", "She had a 10-year history of full-thickness rectal prolapse.", "The rectal prolapse had progressively worsened despite two surgical procedures.", "The first surgical procedure was anal encirclement 13 years before presentation.", "The second surgical procedure was an encirclement associated with stapler mucous prolapsectomy 6 years before presentation.", "She had severe fecal incontinence associated with repeated rectal bleeding for 2 years.", "The patient's Wexner incontinence score was 19.", "Anorectal manometry showed marked hypotonia of the anal canal at rest (20 mmHg).", "Anorectal manometry showed marked hypotonia of the anal canal during contraction (40 mmHg).", "Endorectal ultrasonographic examination revealed no documentable sphincter lesions.", "The muscle fibers appeared markedly thinned on endorectal ultrasonographic examination.", "Electromyographic recordings disclosed severe neurogenic damage to her external anal sphincter.", "The patient declined to undergo construction of a definitive colostomy.", "The operation proceeded in three steps.", "The full-thickness rectal wall was incised circumferentially at 2 cm from the pectinate line.", "The pouch of Douglas was opened.", "About 20 cm of bowel was prepared.", "The peritoneal fossa was reconstructed.", "A coloanal anastomosis was constructed with a 29 circular stapler.", "The operation proceeded with dynamic graciloplasty.", "The gracile muscle was mobilized down to its insertion on the tibial tuberosity.", "Electrical stimuli were delivered to identify the neurovascular peduncle.", "This step is crucial to identify the site for definitive intramuscular electrode implantation.", "The gracile muscle was tunnelled and wrapped around the sigmoid colon anastomosed to the residual rectum.", "The muscle tendon was fixed on the perineal skin.", "A subcutaneous pouch was created in the right iliac fossa to house the neurostimulator.", "The leads connecting the neurostimulator to the gracile muscle were tunnelled subcutaneously.", "A temporary transverse colostomy was constructed.", "The patient had an uneventful postoperative course.", "On day 7, the patient began regular leg gymnastics with a soft balloon placed between her knees.", "Neurostimulation delivered at low frequency began on day 20.", "Neurostimulation continued for about 2 months before the frequency was increased.", "In the sixth month, clinical examination showed a slight improvement in sphincter tone.", "In the sixth month, manometric evaluation showed pressure at 30 mmHg without electrical stimulation.", "In the sixth month, manometric evaluation showed pressure at 55 mmHg with electrical stimulation.", "One year after the operation, the colostomy was closed under manometric evaluation.", "One year after the operation, manometric evaluation showed pressure at 40 mmHg without electrical stimulation.", "One year after the operation, manometric evaluation showed pressure at 65 mmHg with electrical stimulation.", "Two years after the combined operation, no further recurrent rectal prolapse was visible.", "The patient was continent for solids (Wexner incontinence score 9).", "The patient could switch the pacemaker device on and off without help."], "summary_subclaims": ["The patient is a 72-year-old Caucasian woman.", "The patient had full-thickness rectal prolapse.", "The patient had fecal incontinence.", "The fecal incontinence was associated with full-thickness rectal prolapse.", "The fecal incontinence was from severe neuromuscular damage."]}, "extra_info": {"fulltext_subclaims": ["The patient was a 72-year-old Caucasian woman.", "She had a history of childhood encephalitis with motor sequelae.", "She had a 10-year history of full-thickness rectal prolapse.", "The rectal prolapse had progressively worsened despite two surgical procedures.", "The first surgical procedure was anal encirclement 13 years before presentation.", "The second surgical procedure was an encirclement associated with stapler mucous prolapsectomy 6 years before presentation.", "She had severe fecal incontinence associated with repeated rectal bleeding for 2 years.", "The patient's Wexner incontinence score was 19.", "Anorectal manometry showed marked hypotonia of the anal canal at rest (20 mmHg).", "Anorectal manometry showed marked hypotonia of the anal canal during contraction (40 mmHg).", "Endorectal ultrasonographic examination revealed no documentable sphincter lesions.", "The muscle fibers appeared markedly thinned on endorectal ultrasonographic examination.", "Electromyographic recordings disclosed severe neurogenic damage to her external anal sphincter.", "The patient declined to undergo construction of a definitive colostomy.", "The operation proceeded in three steps.", "The full-thickness rectal wall was incised circumferentially at 2 cm from the pectinate line.", "The pouch of Douglas was opened.", "About 20 cm of bowel was prepared.", "The peritoneal fossa was reconstructed.", "A coloanal anastomosis was constructed with a 29 circular stapler.", "The operation proceeded with dynamic graciloplasty.", "The gracile muscle was mobilized down to its insertion on the tibial tuberosity.", "Electrical stimuli were delivered to identify the neurovascular peduncle.", "This step is crucial to identify the site for definitive intramuscular electrode implantation.", "The gracile muscle was tunnelled and wrapped around the sigmoid colon anastomosed to the residual rectum.", "The muscle tendon was fixed on the perineal skin.", "A subcutaneous pouch was created in the right iliac fossa to house the neurostimulator.", "The leads connecting the neurostimulator to the gracile muscle were tunnelled subcutaneously.", "A temporary transverse colostomy was constructed.", "The patient had an uneventful postoperative course.", "On day 7, the patient began regular leg gymnastics with a soft balloon placed between her knees.", "Neurostimulation delivered at low frequency began on day 20.", "Neurostimulation continued for about 2 months before the frequency was increased.", "In the sixth month, clinical examination showed a slight improvement in sphincter tone.", "In the sixth month, manometric evaluation showed pressure at 30 mmHg without electrical stimulation.", "In the sixth month, manometric evaluation showed pressure at 55 mmHg with electrical stimulation.", "One year after the operation, the colostomy was closed under manometric evaluation.", "One year after the operation, manometric evaluation showed pressure at 40 mmHg without electrical stimulation.", "One year after the operation, manometric evaluation showed pressure at 65 mmHg with electrical stimulation.", "Two years after the combined operation, no further recurrent rectal prolapse was visible.", "The patient was continent for solids (Wexner incontinence score 9).", "The patient could switch the pacemaker device on and off without help."], "index": 165, "original_id": "multiclinsum_test_2449_en.txt", "split": "test", "summary_subclaims": ["The patient is a 72-year-old Caucasian woman.", "The patient had full-thickness rectal prolapse.", "The patient had fecal incontinence.", "The fecal incontinence was associated with full-thickness rectal prolapse.", "The fecal incontinence was from severe neuromuscular damage."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 44-year-old pediatrician working in Faryab Province, Afghanistan.", "The patient presented with compressing chest pain and dizziness.", "The chest pain and dizziness occurred during a common cold or exertion.", "The patient had previously experienced the same symptoms during an upper respiratory infection and exertions.", "The patient had no history of heart disease.", "The patient had no history of smoking.", "The patient's blood pressure was 120/80 mm Hg.", "The patient's heart rate was 86 beats/minute.", "The patient's oxygen saturation was 97%.", "The patient's BMI was 30.4.", "The physical examination was unremarkable.", "The patient tested negative for COVID-19.", "The patient tested negative for HIV.", "The patient tested negative for HBV.", "The abdominal ultrasonography showed no abnormalities.", "The chest x-ray was normal.", "Serial electrocardiography was normal.", "Cardiac enzymes were normal.", "Echocardiography revealed grade 1 left ventricular diastolic dysfunction.", "Echocardiography showed normal structural and valves of the heart.", "The ejection fraction was 60\u201365%.", "Blood examinations did not indicate any abnormalities.", "Coronary angiography showed a mid-LAD myocardial bridge with systolic compression.", "The coronary angiography showed significant stenosis.", "The milking effect was identified.", "A calcium channel blocker, Diltiazem 60mg per day, was prescribed.", "The patient tolerated the medication well.", "The patient remained asymptomatic during two years of follow-up."], "summary_subclaims": ["The patient is a 44-year-old man from Faryab Province in Afghanistan.", "The patient presented with chest pain and dizziness.", "The patient was suffering a common cold at the time of presentation.", "The patient underwent coronary angiography.", "The coronary angiography showed a myocardial bridge at the middle portion of the left anterior descending artery.", "The myocardial bridge was associated with significant stenosis causing ischemia.", "The patient was treated with a calcium channel blocker as initial treatment.", "The patient tolerated the medication well.", "The patient remained asymptomatic during two years of follow-up."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 44-year-old pediatrician working in Faryab Province, Afghanistan.", "The patient presented with compressing chest pain and dizziness.", "The chest pain and dizziness occurred during a common cold or exertion.", "The patient had previously experienced the same symptoms during an upper respiratory infection and exertions.", "The patient had no history of heart disease.", "The patient had no history of smoking.", "The patient's blood pressure was 120/80 mm Hg.", "The patient's heart rate was 86 beats/minute.", "The patient's oxygen saturation was 97%.", "The patient's BMI was 30.4.", "The physical examination was unremarkable.", "The patient tested negative for COVID-19.", "The patient tested negative for HIV.", "The patient tested negative for HBV.", "The abdominal ultrasonography showed no abnormalities.", "The chest x-ray was normal.", "Serial electrocardiography was normal.", "Cardiac enzymes were normal.", "Echocardiography revealed grade 1 left ventricular diastolic dysfunction.", "Echocardiography showed normal structural and valves of the heart.", "The ejection fraction was 60\u201365%.", "Blood examinations did not indicate any abnormalities.", "Coronary angiography showed a mid-LAD myocardial bridge with systolic compression.", "The coronary angiography showed significant stenosis.", "The milking effect was identified.", "A calcium channel blocker, Diltiazem 60mg per day, was prescribed.", "The patient tolerated the medication well.", "The patient remained asymptomatic during two years of follow-up."], "index": 167, "original_id": "multiclinsum_test_3208_en.txt", "split": "test", "summary_subclaims": ["The patient is a 44-year-old man from Faryab Province in Afghanistan.", "The patient presented with chest pain and dizziness.", "The patient was suffering a common cold at the time of presentation.", "The patient underwent coronary angiography.", "The coronary angiography showed a myocardial bridge at the middle portion of the left anterior descending artery.", "The myocardial bridge was associated with significant stenosis causing ischemia.", "The patient was treated with a calcium channel blocker as initial treatment.", "The patient tolerated the medication well.", "The patient remained asymptomatic during two years of follow-up."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was a 2-year-old girl.", "She was born full-term.", "She had developed normally.", "She had no medical history of asthma.", "She had no medical history of pneumonia.", "She had no familial history of immunodeficiency.", "She had no brothers or sisters.", "She was admitted to the hospital due to 3 days of fever.", "She had 15 min of respiratory and cardiac arrest.", "The symptoms started on 10 November.", "She had a fever up to 39.8 \u00b0C.", "She had no chills.", "She had no rash.", "She had no convulsions.", "Ibuprofen was given orally.", "The body temperature decreased for 4 to 5 h.", "The body temperature climbed to 40.3 \u00b0C.", "Shortness of breath accompanied the fever.", "The body temperature did not decrease obviously after oral administration of ibuprofen.", "Wheezing caused by the retention of phlegm in the throat occurred.", "A single paroxysmal cough occurred.", "She occasionally coughed up a small amount of yellow phlegm.", "She had a slightly runny nose.", "She had no asthma.", "She had no breathing difficulty.", "She had no hemoptysis.", "She had lethargy.", "She had a poor appetite.", "She had no vomiting.", "She had no diarrhea.", "On 11 November, the patient still had a high fever.", "Her body temperature fluctuated around approximately 40 \u00b0C.", "The patient\u2019s body temperature did not obviously decrease after oral ibuprofen and acetaminophen alternately.", "Acute infection was considered from then on.", "The patient received an intravenous infusion of 0.14 g Zithromax.", "The patient received an intravenous infusion of 120 mg rographolide.", "The patient received aerosol inhalation of 2 mg budesonide.", "Her fever persisted.", "Her body temperature rose to a peak of 40 \u00b0C.", "On 12 November, the patient still had a persistent fever.", "She had wheezing due to the retention of phlegm in her throat.", "She had shortness of breath.", "She had a light cough.", "She had a drooping spirit.", "She had a rash on the torso and limbs.", "Her appetite was slightly improved.", "She had no vomiting.", "She had no convulsions.", "On 13 November, the patient had sudden respiratory and cardiac arrest 3 h before admission.", "She was immediately and continuously treated with cardiopulmonary resuscitation by physicians.", "She received intravenous injection of adrenaline (4 times).", "She was treated with trachea cannula and mechanical ventilation.", "Her heart beat recovered approximately 15 min later.", "The patient remained in a deep comatose state with no spontaneous breathing.", "The patient was transferred to our hospital.", "She immediately underwent electrocardiogram (ECG) monitoring.", "Bloody fluid was visible in the indwelling gastrointestinal decompression tube.", "The blood-gas analysis showed metabolic acidosis.", "The patient was treated with sodium bicarbonate to correct the acidosis.", "She was diagnosed with an acute CNS infection.", "She was diagnosed with brain hernia.", "After cardiopulmonary resuscitation, she was admitted to the pediatric intensive care unit (PICU).", "The head CT scan showed extensive brain swelling.", "The head CT scan showed decreased brain parenchymal density.", "The head CT scan showed narrowed cerebral ventricles and cisterns.", "These findings prompted a diagnosis of extensive brain edema and hernia.", "The chest posteroanterior radiograph showed fuzzy, coarse bilateral lung markings.", "The chest posteroanterior radiograph showed visible small patchy shadows in the right inferior lung.", "The chest posteroanterior radiograph showed a clear pulmonary hilus.", "These findings were diagnosed as pneumonia.", "Routine blood examination results suggested the presence of a bacterial infection.", "The patient was treated with vancomycin to control an infection.", "The patient was treated with meropenem to control an infection.", "After that, immunoglobulin (1 g/kg) was administered for immune support.", "The patient was still in a deep coma state.", "Light reflexes of both pupils were absent.", "The patient\u2019s spontaneous breathing was weak and irregular.", "She had no response to painful stimulation.", "Compared with earlier, her rash was reduced.", "The pulmonary lesions shown on the chest posteroanterior radiograph were slightly absorbed.", "Immunoglobulin (1 g/kg) was continuously administered to neutralize pathogens.", "On 15 November, transcranial Doppler ultrasound assessment showed that the patient\u2019s anterior and posterior cerebral circulation corresponded to the diagnostic criteria for brain death.", "On 17 November, various organ functions failed.", "The patient could not tolerate a spontaneous breathing test.", "Her guardian chose to quit treatment.", "The patient died.", "Viral antigen detection based on both an immunofluorescence assay and the Luminex xTAG respiratory viral panel assay was positive for RSV in the patient\u2019s nasopharyngeal aspirates.", "The nasopharyngeal aspirates were collected on 14 Nov.", "The viral antigen detection was negative for adenovirus.", "The viral antigen detection was negative for influenza A and B viruses.", "The viral antigen detection was negative for parainfluenza virus 1\u20134.", "The viral antigen detection was negative for human metapneumovirus.", "The viral antigen detection was negative for enteroviruses and rhinoviruses.", "The viral antigen detection was negative for human coronavirus HKU1, 229E, NL63 and OC43.", "The viral antigen detection was negative for human bocavirus.", "The patient\u2019s guardian refused to consent to lumbar puncture.", "Cerebrospinal fluid (CSF) was not available for the detection of CNS infection.", "The amounts of red blood cells (RBCs) continuously decreased after the onset of symptoms.", "The amounts of hemoglobin continuously decreased after the onset of symptoms.", "The amounts of platelets continuously decreased after the onset of symptoms.", "Extremely high levels of C-reactive protein from the third day suggested viral or bacterial infection.", "Bacterial cultures of blood specimens yielded negative results.", "The percentage of T lymphocytes was 46.6%.", "Helper T cells accounted for 29.6%.", "Suppressor T cells accounted for 13.2%.", "The ratio of CD4/CD8 was 2.2.", "The proportions of B lymphocytes were 45.6%.", "The proportions of NK cells were 3%.", "All these immunological indexes indicated dysfunction of the patient\u2019s immune system.", "Oral swab, nasopharyngeal aspirate, and serum specimens were collected on 14 Nov.", "The specimens were subjected to multiplex metagenomic analyses using an NGS platform.", "The nucleic acid library was constructed as previously described.", "The amplified nucleic acid libraries were analyzed using an Illumina HiSeq 4000 sequencer.", "The raw sequence reads were filtered using previously described criteria to obtain valid sequences.", "When bacteriophages, plant-origin sequences, and contamination from reagents were excluded, only human RSV was identified.", "At least one specific sequence from the oral swab was identified.", "At least one specific sequence from the nasopharyngeal aspirate was identified.", "No virus-related sequences were detected in the serum specimen.", "Large numbers of sequence reads related to bacteria were detected in the oral swab, nasopharyngeal aspirate, or/and serum specimens.", "Bacterial culture of the blood specimens yielded negative results.", "The complete length of the RSV genome was obtained using NGS methods and gap amplification.", "This RSV strain was subtyped as RSVB.", "It was found to cluster in the BA genotype.", "It had the signature 60-bp duplication in the G gene.", "The newly identified virus was named RSVB/BCH-Y/2016.", "The full genome sequence was deposited in GenBank under accession number KY924878.", "The phylogenetic analysis was conducted with representative sequences from nearly all RSVB subgroups.", "RSVB/BCH-Y/2016 belonged to BA9 subgroup.", "The G gene of this strain was most closely related to strain RSVB/GZ/13\u2013730.", "The G gene shared 98.82% homology with strain RSVB/GZ/13\u2013730.", "Strain RSVB/GZ/13\u2013730 was isolated from a child in Guangzhou, China, in 2013.", "For the six most important antigenic sites in the fusion protein, no mutation was found in RSVB/BCH-Y/2016."], "summary_subclaims": ["The child was born at full-term.", "The child developed normally up to the age of 2 years old.", "Cardiopulmonary arrest occurred within 3 days after the onset of symptoms.", "The symptoms included cough and high fever.", "Complete brain edema was prominent.", "Encephalopathy was developing.", "Viral antigen detection verified an RSV infection.", "Microbiome analyses of oral swab and nasopharyngeal aspirate specimens verified an RSV infection.", "Bacterial culture of blood specimens yielded negative results.", "The RSV strain detected in this patient was subtyped as RSVB9.", "No mutation was found in the six antigenic sites for targeted drugs or vaccines."]}, "extra_info": {"fulltext_subclaims": ["The patient was a 2-year-old girl.", "She was born full-term.", "She had developed normally.", "She had no medical history of asthma.", "She had no medical history of pneumonia.", "She had no familial history of immunodeficiency.", "She had no brothers or sisters.", "She was admitted to the hospital due to 3 days of fever.", "She had 15 min of respiratory and cardiac arrest.", "The symptoms started on 10 November.", "She had a fever up to 39.8 \u00b0C.", "She had no chills.", "She had no rash.", "She had no convulsions.", "Ibuprofen was given orally.", "The body temperature decreased for 4 to 5 h.", "The body temperature climbed to 40.3 \u00b0C.", "Shortness of breath accompanied the fever.", "The body temperature did not decrease obviously after oral administration of ibuprofen.", "Wheezing caused by the retention of phlegm in the throat occurred.", "A single paroxysmal cough occurred.", "She occasionally coughed up a small amount of yellow phlegm.", "She had a slightly runny nose.", "She had no asthma.", "She had no breathing difficulty.", "She had no hemoptysis.", "She had lethargy.", "She had a poor appetite.", "She had no vomiting.", "She had no diarrhea.", "On 11 November, the patient still had a high fever.", "Her body temperature fluctuated around approximately 40 \u00b0C.", "The patient\u2019s body temperature did not obviously decrease after oral ibuprofen and acetaminophen alternately.", "Acute infection was considered from then on.", "The patient received an intravenous infusion of 0.14 g Zithromax.", "The patient received an intravenous infusion of 120 mg rographolide.", "The patient received aerosol inhalation of 2 mg budesonide.", "Her fever persisted.", "Her body temperature rose to a peak of 40 \u00b0C.", "On 12 November, the patient still had a persistent fever.", "She had wheezing due to the retention of phlegm in her throat.", "She had shortness of breath.", "She had a light cough.", "She had a drooping spirit.", "She had a rash on the torso and limbs.", "Her appetite was slightly improved.", "She had no vomiting.", "She had no convulsions.", "On 13 November, the patient had sudden respiratory and cardiac arrest 3 h before admission.", "She was immediately and continuously treated with cardiopulmonary resuscitation by physicians.", "She received intravenous injection of adrenaline (4 times).", "She was treated with trachea cannula and mechanical ventilation.", "Her heart beat recovered approximately 15 min later.", "The patient remained in a deep comatose state with no spontaneous breathing.", "The patient was transferred to our hospital.", "She immediately underwent electrocardiogram (ECG) monitoring.", "Bloody fluid was visible in the indwelling gastrointestinal decompression tube.", "The blood-gas analysis showed metabolic acidosis.", "The patient was treated with sodium bicarbonate to correct the acidosis.", "She was diagnosed with an acute CNS infection.", "She was diagnosed with brain hernia.", "After cardiopulmonary resuscitation, she was admitted to the pediatric intensive care unit (PICU).", "The head CT scan showed extensive brain swelling.", "The head CT scan showed decreased brain parenchymal density.", "The head CT scan showed narrowed cerebral ventricles and cisterns.", "These findings prompted a diagnosis of extensive brain edema and hernia.", "The chest posteroanterior radiograph showed fuzzy, coarse bilateral lung markings.", "The chest posteroanterior radiograph showed visible small patchy shadows in the right inferior lung.", "The chest posteroanterior radiograph showed a clear pulmonary hilus.", "These findings were diagnosed as pneumonia.", "Routine blood examination results suggested the presence of a bacterial infection.", "The patient was treated with vancomycin to control an infection.", "The patient was treated with meropenem to control an infection.", "After that, immunoglobulin (1 g/kg) was administered for immune support.", "The patient was still in a deep coma state.", "Light reflexes of both pupils were absent.", "The patient\u2019s spontaneous breathing was weak and irregular.", "She had no response to painful stimulation.", "Compared with earlier, her rash was reduced.", "The pulmonary lesions shown on the chest posteroanterior radiograph were slightly absorbed.", "Immunoglobulin (1 g/kg) was continuously administered to neutralize pathogens.", "On 15 November, transcranial Doppler ultrasound assessment showed that the patient\u2019s anterior and posterior cerebral circulation corresponded to the diagnostic criteria for brain death.", "On 17 November, various organ functions failed.", "The patient could not tolerate a spontaneous breathing test.", "Her guardian chose to quit treatment.", "The patient died.", "Viral antigen detection based on both an immunofluorescence assay and the Luminex xTAG respiratory viral panel assay was positive for RSV in the patient\u2019s nasopharyngeal aspirates.", "The nasopharyngeal aspirates were collected on 14 Nov.", "The viral antigen detection was negative for adenovirus.", "The viral antigen detection was negative for influenza A and B viruses.", "The viral antigen detection was negative for parainfluenza virus 1\u20134.", "The viral antigen detection was negative for human metapneumovirus.", "The viral antigen detection was negative for enteroviruses and rhinoviruses.", "The viral antigen detection was negative for human coronavirus HKU1, 229E, NL63 and OC43.", "The viral antigen detection was negative for human bocavirus.", "The patient\u2019s guardian refused to consent to lumbar puncture.", "Cerebrospinal fluid (CSF) was not available for the detection of CNS infection.", "The amounts of red blood cells (RBCs) continuously decreased after the onset of symptoms.", "The amounts of hemoglobin continuously decreased after the onset of symptoms.", "The amounts of platelets continuously decreased after the onset of symptoms.", "Extremely high levels of C-reactive protein from the third day suggested viral or bacterial infection.", "Bacterial cultures of blood specimens yielded negative results.", "The percentage of T lymphocytes was 46.6%.", "Helper T cells accounted for 29.6%.", "Suppressor T cells accounted for 13.2%.", "The ratio of CD4/CD8 was 2.2.", "The proportions of B lymphocytes were 45.6%.", "The proportions of NK cells were 3%.", "All these immunological indexes indicated dysfunction of the patient\u2019s immune system.", "Oral swab, nasopharyngeal aspirate, and serum specimens were collected on 14 Nov.", "The specimens were subjected to multiplex metagenomic analyses using an NGS platform.", "The nucleic acid library was constructed as previously described.", "The amplified nucleic acid libraries were analyzed using an Illumina HiSeq 4000 sequencer.", "The raw sequence reads were filtered using previously described criteria to obtain valid sequences.", "When bacteriophages, plant-origin sequences, and contamination from reagents were excluded, only human RSV was identified.", "At least one specific sequence from the oral swab was identified.", "At least one specific sequence from the nasopharyngeal aspirate was identified.", "No virus-related sequences were detected in the serum specimen.", "Large numbers of sequence reads related to bacteria were detected in the oral swab, nasopharyngeal aspirate, or/and serum specimens.", "Bacterial culture of the blood specimens yielded negative results.", "The complete length of the RSV genome was obtained using NGS methods and gap amplification.", "This RSV strain was subtyped as RSVB.", "It was found to cluster in the BA genotype.", "It had the signature 60-bp duplication in the G gene.", "The newly identified virus was named RSVB/BCH-Y/2016.", "The full genome sequence was deposited in GenBank under accession number KY924878.", "The phylogenetic analysis was conducted with representative sequences from nearly all RSVB subgroups.", "RSVB/BCH-Y/2016 belonged to BA9 subgroup.", "The G gene of this strain was most closely related to strain RSVB/GZ/13\u2013730.", "The G gene shared 98.82% homology with strain RSVB/GZ/13\u2013730.", "Strain RSVB/GZ/13\u2013730 was isolated from a child in Guangzhou, China, in 2013.", "For the six most important antigenic sites in the fusion protein, no mutation was found in RSVB/BCH-Y/2016."], "index": 161, "original_id": "multiclinsum_test_3147_en.txt", "split": "test", "summary_subclaims": ["The child was born at full-term.", "The child developed normally up to the age of 2 years old.", "Cardiopulmonary arrest occurred within 3 days after the onset of symptoms.", "The symptoms included cough and high fever.", "Complete brain edema was prominent.", "Encephalopathy was developing.", "Viral antigen detection verified an RSV infection.", "Microbiome analyses of oral swab and nasopharyngeal aspirate specimens verified an RSV infection.", "Bacterial culture of blood specimens yielded negative results.", "The RSV strain detected in this patient was subtyped as RSVB9.", "No mutation was found in the six antigenic sites for targeted drugs or vaccines."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 62-year-old male.", "The patient has hypertension.", "The patient has hyperlipidaemia.", "The patient presented with 7 days of dizziness.", "The patient presented with 7 days of fatigue.", "The patient presented with 7 days of nausea.", "The patient presented with 7 days of vomiting.", "The patient was transported to the emergency department.", "The patient was discharged home after initial evaluation.", "Approximately 4 days after discharge, emergency medical services were called after the patient experienced syncope.", "An ECG obtained en route reported anterior ST-segment elevations.", "Before arrival at the hospital, the patient developed ventricular fibrillation.", "Cardiac defibrillation was successful.", "Endotracheal intubation was performed.", "Upon arrival at the emergency department, ventricular fibrillation recurred.", "Resuscitative efforts restored sinus rhythm and spontaneous circulation.", "On arrival, the patient's heart rate was 77 b.p.m.", "On arrival, the patient had a regular rhythm.", "On arrival, the patient had hypotension (86 mmHg/48 mmHg).", "There were no appreciable murmurs.", "There was no lower extremity oedema.", "The extremities were cool to touch.", "The patient required mechanical ventilation with a rate of 28.", "The patient required mechanical ventilation with a tidal volume of 500 mL.", "The patient required mechanical ventilation with FiO2 100%.", "The patient required mechanical ventilation with positive end-expiratory pressure of 8 cmH2O.", "Breath sounds were present bilaterally.", "The subsequent ECG showed wide complex rhythm consistent with slow ventricular tachycardia.", "The subsequent ECG showed right bundle branch block morphology.", "The subsequent ECG showed left axis deviation.", "There was high suspicion for acute coronary syndrome.", "The patient received aspirin.", "The patient received ticagrelor.", "The patient received heparin.", "The patient was presumed to have an ST-segment elevation myocardial infarction.", "Epinephrine infusion was started due to bradycardia with hypotension.", "The patient was emergently taken to the catheterization lab.", "Coronary angiography did not reveal coronary stenosis.", "Right heart catheterization revealed elevated right-sided filling pressures.", "Right atrial pressure was 22 mmHg.", "Pulmonary artery pressure was 61/28 (39) mmHg.", "Pulmonary capillary wedge pressure was 15 mmHg.", "Fick cardiac index was 2.6 L/min/m2.", "A point-of-care echocardiogram was performed.", "The point-of-care echocardiogram demonstrated a dilated right ventricle.", "The point-of-care echocardiogram demonstrated severely reduced right ventricular function.", "There was concern for pulmonary embolism.", "Immediate pulmonary angiography was performed.", "Pulmonary angiography revealed large, bilateral pulmonary emboli.", "EkoSonic\u2122 endovascular thrombolysis catheters were advanced into both main pulmonary arteries.", "5 mg of tissue plasminogen activator was delivered through each catheter.", "2 mg/catheter/h of tissue plasminogen activator was delivered for 2 h.", "1 mg/catheter/h of tissue plasminogen activator was delivered for 16 h.", "Infusion was guided by fibrinogen monitoring.", "Upper and lower extremity Doppler ultrasounds showed no evidence of venous thrombosis.", "Formal transthoracic echocardiogram confirmed depressed right ventricular function.", "Computed tomography of the chest showed bilateral peripheral ground-glass opacities.", "Computed tomography of the chest showed wedge-shaped opacities in the right lung.", "The wedge-shaped opacities were thought to represent pulmonary infarctions.", "The patient was started on broad-spectrum antibiotics for pneumonia.", "A viral respiratory panel was negative.", "Tracheal aspirate culture was positive for methicillin-resistant Staphylococcus aureus.", "Repeat ECG showed sinus rhythm.", "Repeat ECG showed first-degree atrioventricular (AV) block.", "Repeat ECG showed left axis deviation.", "Repeat ECG showed incomplete right bundle branch block.", "Repeat ECG showed a prolonged QTc interval (498 ms).", "Over the following 4 days, the patient developed anaemia.", "CT of the chest, abdomen, and pelvis showed a mediastinal haematoma.", "CT of the chest, abdomen, and pelvis showed persistent ground-glass opacities.", "The patient was tested for SARS-CoV-2.", "The patient was found to be positive for SARS-CoV-2.", "The patient was transferred to a COVID-19-dedicated intensive care unit.", "The patient was placed under enhanced contact precautions.", "The patient received supportive care.", "The patient was extubated 4 days later.", "Following extubation, the patient did well.", "The patient was admitted to an inpatient rehabilitation facility.", "The patient was discharged home.", "The patient was prescribed lifelong apixaban 5 mg twice daily.", "At 1 month follow-up, the patient described mild exertional dyspnoea.", "Transthoracic echocardiogram at 1 month follow-up noted improvement of right ventricular dilation.", "Transthoracic echocardiogram at 1 month follow-up noted improvement of right ventricular systolic function."], "summary_subclaims": ["The patient was a 62-year-old male.", "He presented after experiencing syncope and cardiac arrest.", "There was concern for acute coronary syndrome.", "Coronary angiogram did not reveal significant coronary obstruction.", "A bedside echocardiogram was rapidly performed.", "The bedside echocardiogram was indicative of right ventricular strain.", "A pulmonary angiogram was performed.", "The pulmonary angiogram revealed massive pulmonary embolism.", "He successfully underwent catheter-directed thrombolysis.", "He was discharged home on lifelong anticoagulation."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 62-year-old male.", "The patient has hypertension.", "The patient has hyperlipidaemia.", "The patient presented with 7 days of dizziness.", "The patient presented with 7 days of fatigue.", "The patient presented with 7 days of nausea.", "The patient presented with 7 days of vomiting.", "The patient was transported to the emergency department.", "The patient was discharged home after initial evaluation.", "Approximately 4 days after discharge, emergency medical services were called after the patient experienced syncope.", "An ECG obtained en route reported anterior ST-segment elevations.", "Before arrival at the hospital, the patient developed ventricular fibrillation.", "Cardiac defibrillation was successful.", "Endotracheal intubation was performed.", "Upon arrival at the emergency department, ventricular fibrillation recurred.", "Resuscitative efforts restored sinus rhythm and spontaneous circulation.", "On arrival, the patient's heart rate was 77 b.p.m.", "On arrival, the patient had a regular rhythm.", "On arrival, the patient had hypotension (86 mmHg/48 mmHg).", "There were no appreciable murmurs.", "There was no lower extremity oedema.", "The extremities were cool to touch.", "The patient required mechanical ventilation with a rate of 28.", "The patient required mechanical ventilation with a tidal volume of 500 mL.", "The patient required mechanical ventilation with FiO2 100%.", "The patient required mechanical ventilation with positive end-expiratory pressure of 8 cmH2O.", "Breath sounds were present bilaterally.", "The subsequent ECG showed wide complex rhythm consistent with slow ventricular tachycardia.", "The subsequent ECG showed right bundle branch block morphology.", "The subsequent ECG showed left axis deviation.", "There was high suspicion for acute coronary syndrome.", "The patient received aspirin.", "The patient received ticagrelor.", "The patient received heparin.", "The patient was presumed to have an ST-segment elevation myocardial infarction.", "Epinephrine infusion was started due to bradycardia with hypotension.", "The patient was emergently taken to the catheterization lab.", "Coronary angiography did not reveal coronary stenosis.", "Right heart catheterization revealed elevated right-sided filling pressures.", "Right atrial pressure was 22 mmHg.", "Pulmonary artery pressure was 61/28 (39) mmHg.", "Pulmonary capillary wedge pressure was 15 mmHg.", "Fick cardiac index was 2.6 L/min/m2.", "A point-of-care echocardiogram was performed.", "The point-of-care echocardiogram demonstrated a dilated right ventricle.", "The point-of-care echocardiogram demonstrated severely reduced right ventricular function.", "There was concern for pulmonary embolism.", "Immediate pulmonary angiography was performed.", "Pulmonary angiography revealed large, bilateral pulmonary emboli.", "EkoSonic\u2122 endovascular thrombolysis catheters were advanced into both main pulmonary arteries.", "5 mg of tissue plasminogen activator was delivered through each catheter.", "2 mg/catheter/h of tissue plasminogen activator was delivered for 2 h.", "1 mg/catheter/h of tissue plasminogen activator was delivered for 16 h.", "Infusion was guided by fibrinogen monitoring.", "Upper and lower extremity Doppler ultrasounds showed no evidence of venous thrombosis.", "Formal transthoracic echocardiogram confirmed depressed right ventricular function.", "Computed tomography of the chest showed bilateral peripheral ground-glass opacities.", "Computed tomography of the chest showed wedge-shaped opacities in the right lung.", "The wedge-shaped opacities were thought to represent pulmonary infarctions.", "The patient was started on broad-spectrum antibiotics for pneumonia.", "A viral respiratory panel was negative.", "Tracheal aspirate culture was positive for methicillin-resistant Staphylococcus aureus.", "Repeat ECG showed sinus rhythm.", "Repeat ECG showed first-degree atrioventricular (AV) block.", "Repeat ECG showed left axis deviation.", "Repeat ECG showed incomplete right bundle branch block.", "Repeat ECG showed a prolonged QTc interval (498 ms).", "Over the following 4 days, the patient developed anaemia.", "CT of the chest, abdomen, and pelvis showed a mediastinal haematoma.", "CT of the chest, abdomen, and pelvis showed persistent ground-glass opacities.", "The patient was tested for SARS-CoV-2.", "The patient was found to be positive for SARS-CoV-2.", "The patient was transferred to a COVID-19-dedicated intensive care unit.", "The patient was placed under enhanced contact precautions.", "The patient received supportive care.", "The patient was extubated 4 days later.", "Following extubation, the patient did well.", "The patient was admitted to an inpatient rehabilitation facility.", "The patient was discharged home.", "The patient was prescribed lifelong apixaban 5 mg twice daily.", "At 1 month follow-up, the patient described mild exertional dyspnoea.", "Transthoracic echocardiogram at 1 month follow-up noted improvement of right ventricular dilation.", "Transthoracic echocardiogram at 1 month follow-up noted improvement of right ventricular systolic function."], "index": 168, "original_id": "multiclinsum_test_2976_en.txt", "split": "test", "summary_subclaims": ["The patient was a 62-year-old male.", "He presented after experiencing syncope and cardiac arrest.", "There was concern for acute coronary syndrome.", "Coronary angiogram did not reveal significant coronary obstruction.", "A bedside echocardiogram was rapidly performed.", "The bedside echocardiogram was indicative of right ventricular strain.", "A pulmonary angiogram was performed.", "The pulmonary angiogram revealed massive pulmonary embolism.", "He successfully underwent catheter-directed thrombolysis.", "He was discharged home on lifelong anticoagulation."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 29-year-old Asian female.", "She had previously been in good health.", "She presented with recurrent episodes of severe headache, nausea, and vomiting.", "She described the headache as 'pulling' downward.", "The headache was triggered by standing.", "The headache resolved when supine.", "She reported axial tension and rotatory manipulation of her neck one week prior to the onset of her symptoms.", "She denied immediate symptoms after the chiropractic manipulation.", "She experienced increasingly painful headaches over the 2 weeks following her chiropractic manipulation.", "She had no known prior history of trauma.", "She had no known prior history of dural structural pathology.", "She had no known prior history of connective tissue disease.", "Physical exam was normal with no neurological deficits.", "Previous cervical MRI with and without contrast had been unremarkable.", "Cervical MRI at presentation revealed a CSF-isodense ventral extradural fluid collection in the lower cervical spine and upper thoracic spine.", "There was no mass effect on the thecal sac.", "There was no meningeal enhancement.", "There was no perineural cyst.", "There was no dural ectasia.", "There was no abnormal venous engorgement.", "The patient was managed conservatively with bed rest for 2 weeks.", "She made a complete spontaneous recovery.", "Follow-up cervical MRI at 6 months demonstrated decreased size of ventral extradural fluid collection.", "The patient is doing well presently."], "summary_subclaims": ["We present a case of subacute cervical cerebrospinal fluid (CSF) leak resulting from chiropractic manipulation of the cervical spine.", "The patient is a 29-year-old female.", "The patient received manipulation one week prior to developing symptoms.", "The patient developed symptoms of severe orthostatic headache, nausea, and vomiting.", "Magnetic resonance imaging (MRI) revealed a new C5-C6 ventral CSF collection.", "Symptomatic onset corresponded with the recent cervical chiropractic adjustment.", "We present serial imaging correlating with her symptomatology.", "We review the pertinent literature on complications of chiropractic manipulation."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 29-year-old Asian female.", "She had previously been in good health.", "She presented with recurrent episodes of severe headache, nausea, and vomiting.", "She described the headache as 'pulling' downward.", "The headache was triggered by standing.", "The headache resolved when supine.", "She reported axial tension and rotatory manipulation of her neck one week prior to the onset of her symptoms.", "She denied immediate symptoms after the chiropractic manipulation.", "She experienced increasingly painful headaches over the 2 weeks following her chiropractic manipulation.", "She had no known prior history of trauma.", "She had no known prior history of dural structural pathology.", "She had no known prior history of connective tissue disease.", "Physical exam was normal with no neurological deficits.", "Previous cervical MRI with and without contrast had been unremarkable.", "Cervical MRI at presentation revealed a CSF-isodense ventral extradural fluid collection in the lower cervical spine and upper thoracic spine.", "There was no mass effect on the thecal sac.", "There was no meningeal enhancement.", "There was no perineural cyst.", "There was no dural ectasia.", "There was no abnormal venous engorgement.", "The patient was managed conservatively with bed rest for 2 weeks.", "She made a complete spontaneous recovery.", "Follow-up cervical MRI at 6 months demonstrated decreased size of ventral extradural fluid collection.", "The patient is doing well presently."], "index": 5, "original_id": "multiclinsum_test_2542_en.txt", "split": "test", "summary_subclaims": ["We present a case of subacute cervical cerebrospinal fluid (CSF) leak resulting from chiropractic manipulation of the cervical spine.", "The patient is a 29-year-old female.", "The patient received manipulation one week prior to developing symptoms.", "The patient developed symptoms of severe orthostatic headache, nausea, and vomiting.", "Magnetic resonance imaging (MRI) revealed a new C5-C6 ventral CSF collection.", "Symptomatic onset corresponded with the recent cervical chiropractic adjustment.", "We present serial imaging correlating with her symptomatology.", "We review the pertinent literature on complications of chiropractic manipulation."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was diagnosed with high-risk CD20+ common-type B-cell precursor acute lymphoblastic leukemia.", "The patient received two cycles of HyperCVAD.", "The patient consulted the National Cancer Institute for a relapse and five-day polyarthralgia.", "The patient was initiated into the protocol established in 2003 by the Adult Acute Lymphoblastic Leukemia Research Group (GRAALL-2003).", "The patient developed febrile neutropenia.", "The patient had cellulitis of the left hand without abscess.", "The patient had methicillin-sensitive Staphylococcus aureus bacteremia.", "Cefapime and oxacillin were administered.", "The bacteremia resolved.", "On day 21 of hospitalization, the patient presented lesions on the back of the left hand.", "The lesions on the back of the left hand were of the type erythematoedematosa plaque.", "The lesions on the back of the left hand had mild and fine desquamation on the surface.", "The lesions on the back of the left hand had central blood crust.", "The patient had lesions in the right scapular and infra-scapular region.", "The lesions in the right scapular and infra-scapular region were 3 mm non-follicular papules.", "The lesions in the right scapular and infra-scapular region were grouped.", "The lesions in the right scapular and infra-scapular region were some erythematous and others erythemoparous.", "The lesions were assessed by the Dermatology Service.", "A skin biopsy was taken for histopathological study.", "The results were inconclusive for the diagnosis of mycosis.", "No culture was done for fungi of the biopsy.", "An invasive fungal infection was suspected.", "Caspofungin was initiated.", "The chest and sinus computed tomography (CT) scans were negative for invasive aspergillosis.", "The serum galactomannan detection was negative for invasive aspergillosis.", "Despite antimicrobial and antifungal treatment, the patient did not show significant improvement.", "The patient persisted with a fever of up to 40 \u00b0C.", "The patient had 1 cm nodules, soft, depressible, painless and in the previous sites of venipuncture.", "The blood count showed a profound neutropenia (20 white blood cells per \u00b5l).", "The C reactive protein was 6.15 mg/dl.", "The control CT scan of the paranasal sinuses showed incipient chronic inflammatory changes in the right maxillary sinus.", "The abdomen scan documented hepatosplenomegaly.", "The three blood cultures and the urine culture from day 28 of hospitalization showed yeast-like structures.", "The yeast-like structures were not identified in the automated panel Yeast ID (BD Phoenix\u2122 100).", "Arthroconidia were observed by microscopy.", "Colonies compatible with Geotrichum spp. were documented.", "The diagnosis was confirmed by matrix-assisted laser desorption ionization time-of-flight (MALDI-TOF) mass spectrometry.", "Treatment with amphotericin B deoxycholate was given at a daily dose of 1 mg/kg for 14 days.", "400 mg/day of voriconazole was given for four weeks.", "Clinical symptoms resolved.", "The patient recovered from neutropenia on day 24 of the combined antifungal treatment.", "The patient was discharged on day 101 of hospitalisation due to clinical improvement."], "summary_subclaims": ["The patient is a 27-year-old male.", "The patient has relapsed acute lymphoblastic leukemia.", "The patient had five-day-old polyarthralgia.", "The patient had febrile neutropenia.", "The patient had cellulitis without abscesses.", "The patient had methicillin-resistant Staphylococcus aureus bacteremia.", "The patient received therapy with oxacillin and cefepime.", "The febrile neutropenia persisted.", "An invasive fungal infection was suspected.", "A new set of blood cultures was taken.", "Antifungal treatment was initiated.", "Arthroconidia were identified in the blood cultures.", "Matrix-assisted laser desorption ionization-mass spectrometry confirmed the presence of Geotrichum spp.", "Antifungal treatment was adjusted to 14 days of deoxycholate amphotericin B.", "Antifungal treatment was adjusted to four weeks of voriconazole.", "The patient was discharged after a prolonged stay."]}, "extra_info": {"fulltext_subclaims": ["The patient was diagnosed with high-risk CD20+ common-type B-cell precursor acute lymphoblastic leukemia.", "The patient received two cycles of HyperCVAD.", "The patient consulted the National Cancer Institute for a relapse and five-day polyarthralgia.", "The patient was initiated into the protocol established in 2003 by the Adult Acute Lymphoblastic Leukemia Research Group (GRAALL-2003).", "The patient developed febrile neutropenia.", "The patient had cellulitis of the left hand without abscess.", "The patient had methicillin-sensitive Staphylococcus aureus bacteremia.", "Cefapime and oxacillin were administered.", "The bacteremia resolved.", "On day 21 of hospitalization, the patient presented lesions on the back of the left hand.", "The lesions on the back of the left hand were of the type erythematoedematosa plaque.", "The lesions on the back of the left hand had mild and fine desquamation on the surface.", "The lesions on the back of the left hand had central blood crust.", "The patient had lesions in the right scapular and infra-scapular region.", "The lesions in the right scapular and infra-scapular region were 3 mm non-follicular papules.", "The lesions in the right scapular and infra-scapular region were grouped.", "The lesions in the right scapular and infra-scapular region were some erythematous and others erythemoparous.", "The lesions were assessed by the Dermatology Service.", "A skin biopsy was taken for histopathological study.", "The results were inconclusive for the diagnosis of mycosis.", "No culture was done for fungi of the biopsy.", "An invasive fungal infection was suspected.", "Caspofungin was initiated.", "The chest and sinus computed tomography (CT) scans were negative for invasive aspergillosis.", "The serum galactomannan detection was negative for invasive aspergillosis.", "Despite antimicrobial and antifungal treatment, the patient did not show significant improvement.", "The patient persisted with a fever of up to 40 \u00b0C.", "The patient had 1 cm nodules, soft, depressible, painless and in the previous sites of venipuncture.", "The blood count showed a profound neutropenia (20 white blood cells per \u00b5l).", "The C reactive protein was 6.15 mg/dl.", "The control CT scan of the paranasal sinuses showed incipient chronic inflammatory changes in the right maxillary sinus.", "The abdomen scan documented hepatosplenomegaly.", "The three blood cultures and the urine culture from day 28 of hospitalization showed yeast-like structures.", "The yeast-like structures were not identified in the automated panel Yeast ID (BD Phoenix\u2122 100).", "Arthroconidia were observed by microscopy.", "Colonies compatible with Geotrichum spp. were documented.", "The diagnosis was confirmed by matrix-assisted laser desorption ionization time-of-flight (MALDI-TOF) mass spectrometry.", "Treatment with amphotericin B deoxycholate was given at a daily dose of 1 mg/kg for 14 days.", "400 mg/day of voriconazole was given for four weeks.", "Clinical symptoms resolved.", "The patient recovered from neutropenia on day 24 of the combined antifungal treatment.", "The patient was discharged on day 101 of hospitalisation due to clinical improvement."], "index": 3, "original_id": "multiclinsum_test_3210_en.txt", "split": "test", "summary_subclaims": ["The patient is a 27-year-old male.", "The patient has relapsed acute lymphoblastic leukemia.", "The patient had five-day-old polyarthralgia.", "The patient had febrile neutropenia.", "The patient had cellulitis without abscesses.", "The patient had methicillin-resistant Staphylococcus aureus bacteremia.", "The patient received therapy with oxacillin and cefepime.", "The febrile neutropenia persisted.", "An invasive fungal infection was suspected.", "A new set of blood cultures was taken.", "Antifungal treatment was initiated.", "Arthroconidia were identified in the blood cultures.", "Matrix-assisted laser desorption ionization-mass spectrometry confirmed the presence of Geotrichum spp.", "Antifungal treatment was adjusted to 14 days of deoxycholate amphotericin B.", "Antifungal treatment was adjusted to four weeks of voriconazole.", "The patient was discharged after a prolonged stay."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 24-year-old Caucasian man.", "He had fever and upper quadrant abdominal pain over the previous 20 days.", "Before admission, ciprofloxacin and metronidazole, followed by cefixime had been prescribed.", "Six years prior, the patient had been diagnosed with PSC.", "Six years prior, the patient had been diagnosed with UC.", "Six years prior, the patient had been diagnosed with suspected retroperitoneal fibrosis.", "Six years prior, the patient had been diagnosed with bile sludge.", "Six years prior, the patient had been diagnosed with splenomegaly.", "At that time, ursodiol 300mg BID was prescribed.", "At that time, mesalamine 4g per day was prescribed.", "At that time, exploratory laparotomy and a biopsy of the perihepatic, retroperitoneal tissue were performed.", "The biopsy excluded malignancy.", "Over this six-year period, the patient presented with recurrent episodes of cholangitis.", "The serum level of aminotransferases remained substantially normal.", "There was a progressive worsening of cholestatic test results.", "There was a progressive liver enlargement along with fibrosis.", "Gamma glutamyl transpeptidase (GGT) increased from 141UI/L to 344UI/L.", "Alkaline phosphatase (ALP) increased from 847UI/L to 2534UI/L.", "Hepatic tissue stiffness, measured by FibroScan\u00ae, progressed from 12.6 to 17.3kPa.", "The patient was never treated with immunosuppressive therapy.", "The patient was never treated with corticosteroids.", "One month before admission, an upper endoscopy was performed.", "The upper endoscopy excluded esophageal varices.", "One week before admission, a magnetic resonance of his abdomen and bile ducts was performed.", "The magnetic resonance revealed further enlargement of the liver.", "The magnetic resonance revealed further enlargement of the spleen.", "The magnetic resonance revealed further enlargement of the tissue surrounding his hepatic hilum.", "The tissue surrounding his hepatic hilum caused a compression of his second duodenal tract.", "The tissue surrounding his hepatic hilum caused a wrapping of the splenic and hepatic arteries.", "Beading and narrowing of the intra-hepatic and common bile ducts were reported.", "A narrowing of the pancreatic duct was also reported.", "At admission, the patient had a fever of 38.8\u00b0C.", "Physical examination revealed tenderness of his epigastrium.", "Physical examination revealed tenderness of his right upper hypochondrium.", "Microbiological blood and urine investigations were negative for bacteria.", "A chest radiograph was normal.", "An abdominal sonography revealed an enlarged liver.", "An abdominal sonography revealed thickened choledocus.", "An abdominal sonography revealed dilatation of the intra-hepatic biliary tree.", "An abdominal sonography revealed splenomegaly.", "An abdominal sonography revealed lymphadenopathy of the hepatic hilus.", "A colonoscopy showed erythema of the colonic mucosa from the rectum to the cecum.", "Random biopsy showed focal atrophy of the colonic mucosa with edema.", "Random biopsy showed chronic inflammatory infiltrates.", "Specific investigations for CMV were not carried out.", "Imipenem 500mg IV four times daily was administered.", "Three days later, imipenem was substituted with tigecycline 50mg IV BID.", "Further blood and urine cultures for bacteria were negative.", "The erythrocyte sedimentation rate (ESR) remained high.", "The C-reactive protein level (C-RP) remained high.", "The white blood cell (WBC) count decreased.", "The neutrophil count decreased.", "The procalcitonin level was 0.38ng/ml.", "The fever persisted.", "The upper abdominal pain subsided slightly.", "Investigations for HIV were negative.", "Investigations for Toxoplasma gondii were negative.", "Investigations for CMV were negative.", "Investigations for measles were negative.", "Investigations for parotitis were negative.", "Investigations for hepatitis C virus (HCV) were negative.", "Results for varicella zoster virus indicated previous infection.", "Results for human herpes virus indicated previous infection.", "Results for Epstein Barr indicated previous infection.", "Results for rubella indicated previous infection.", "Results for parvo virus B19 indicated previous infection.", "CD4?+?T lymphocytes were 1055mm3 (20.3%).", "CD3?+?T lymphocytes were 3193mm3 (67%).", "Mycobacterium tuberculosis interferon gamma release assay showed negative results.", "Twelve days after admission, teicoplanin 400mg die was prescribed.", "Twelve days after admission, gentamicin 80mg TID was prescribed.", "Twelve days after admission, metronidazole 500mg TID was prescribed.", "Tigecycline was stopped.", "Two days later, DNA Cytomegalovirus was detected in the blood with \u2264253 copies/mL.", "Three days later, this value increased to 6189 copies/mL.", "Three days later, 1431 copies/mL were evidenced from a urine sample.", "CMV pp65-antigen was also positive.", "CMV serology indicated acute CMV infection.", "The patient\u2019s fever rose to 39.2\u00b0C.", "The patient\u2019s abdominal pain extended to the right lower abdominal quadrant.", "The patient\u2019s abdominal pain radiated to the right groin.", "The patient\u2019s abdominal pain radiated to the right testicle.", "Ultrasound suggested acute appendicitis.", "He underwent surgery.", "Histology showed inflammatory infiltrates, including lymphocytes and neutrophils.", "Histochemistry was positive for CMV early antigens.", "Real time reaction of the appendix tissue was positive.", "Shell vial culture of the appendix tissue was positive.", "Microbiological investigations for bacteria showed Peptococcus spp.", "Microbiological investigations for fungi showed Candida albicans.", "Teicoplanin, gentamicin and metronidazole were administered for a total of 12 days.", "Intravenous ganciclovir 5mg/kg twice was administered for 15 days.", "After discharge, oral valganciclovir 900mg BID was prescribed for 10 days.", "After this, the CMV nucleic acid in the blood and urine was negative.", "After this, ESR remained abnormally high.", "After this, cholestatic liver test results remained abnormally high."], "summary_subclaims": ["The authors report on a case of acute primary Cytomegalovirus infection complicated with acute appendicitis due to Cytomegalovirus in an apparently immunocompetent 24-year-old Caucasian man.", "The patient also suffered from primary sclerosing cholangitis and ulcerative colitis.", "Diagnosis was based on clinical manifestations.", "Diagnosis was based on serology results.", "Diagnosis was based on microbiological findings.", "Diagnosis was based on histological findings.", "Treatment consisted of surgery.", "Treatment consisted of anti-Cytomegalovirus therapy."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 24-year-old Caucasian man.", "He had fever and upper quadrant abdominal pain over the previous 20 days.", "Before admission, ciprofloxacin and metronidazole, followed by cefixime had been prescribed.", "Six years prior, the patient had been diagnosed with PSC.", "Six years prior, the patient had been diagnosed with UC.", "Six years prior, the patient had been diagnosed with suspected retroperitoneal fibrosis.", "Six years prior, the patient had been diagnosed with bile sludge.", "Six years prior, the patient had been diagnosed with splenomegaly.", "At that time, ursodiol 300mg BID was prescribed.", "At that time, mesalamine 4g per day was prescribed.", "At that time, exploratory laparotomy and a biopsy of the perihepatic, retroperitoneal tissue were performed.", "The biopsy excluded malignancy.", "Over this six-year period, the patient presented with recurrent episodes of cholangitis.", "The serum level of aminotransferases remained substantially normal.", "There was a progressive worsening of cholestatic test results.", "There was a progressive liver enlargement along with fibrosis.", "Gamma glutamyl transpeptidase (GGT) increased from 141UI/L to 344UI/L.", "Alkaline phosphatase (ALP) increased from 847UI/L to 2534UI/L.", "Hepatic tissue stiffness, measured by FibroScan\u00ae, progressed from 12.6 to 17.3kPa.", "The patient was never treated with immunosuppressive therapy.", "The patient was never treated with corticosteroids.", "One month before admission, an upper endoscopy was performed.", "The upper endoscopy excluded esophageal varices.", "One week before admission, a magnetic resonance of his abdomen and bile ducts was performed.", "The magnetic resonance revealed further enlargement of the liver.", "The magnetic resonance revealed further enlargement of the spleen.", "The magnetic resonance revealed further enlargement of the tissue surrounding his hepatic hilum.", "The tissue surrounding his hepatic hilum caused a compression of his second duodenal tract.", "The tissue surrounding his hepatic hilum caused a wrapping of the splenic and hepatic arteries.", "Beading and narrowing of the intra-hepatic and common bile ducts were reported.", "A narrowing of the pancreatic duct was also reported.", "At admission, the patient had a fever of 38.8\u00b0C.", "Physical examination revealed tenderness of his epigastrium.", "Physical examination revealed tenderness of his right upper hypochondrium.", "Microbiological blood and urine investigations were negative for bacteria.", "A chest radiograph was normal.", "An abdominal sonography revealed an enlarged liver.", "An abdominal sonography revealed thickened choledocus.", "An abdominal sonography revealed dilatation of the intra-hepatic biliary tree.", "An abdominal sonography revealed splenomegaly.", "An abdominal sonography revealed lymphadenopathy of the hepatic hilus.", "A colonoscopy showed erythema of the colonic mucosa from the rectum to the cecum.", "Random biopsy showed focal atrophy of the colonic mucosa with edema.", "Random biopsy showed chronic inflammatory infiltrates.", "Specific investigations for CMV were not carried out.", "Imipenem 500mg IV four times daily was administered.", "Three days later, imipenem was substituted with tigecycline 50mg IV BID.", "Further blood and urine cultures for bacteria were negative.", "The erythrocyte sedimentation rate (ESR) remained high.", "The C-reactive protein level (C-RP) remained high.", "The white blood cell (WBC) count decreased.", "The neutrophil count decreased.", "The procalcitonin level was 0.38ng/ml.", "The fever persisted.", "The upper abdominal pain subsided slightly.", "Investigations for HIV were negative.", "Investigations for Toxoplasma gondii were negative.", "Investigations for CMV were negative.", "Investigations for measles were negative.", "Investigations for parotitis were negative.", "Investigations for hepatitis C virus (HCV) were negative.", "Results for varicella zoster virus indicated previous infection.", "Results for human herpes virus indicated previous infection.", "Results for Epstein Barr indicated previous infection.", "Results for rubella indicated previous infection.", "Results for parvo virus B19 indicated previous infection.", "CD4?+?T lymphocytes were 1055mm3 (20.3%).", "CD3?+?T lymphocytes were 3193mm3 (67%).", "Mycobacterium tuberculosis interferon gamma release assay showed negative results.", "Twelve days after admission, teicoplanin 400mg die was prescribed.", "Twelve days after admission, gentamicin 80mg TID was prescribed.", "Twelve days after admission, metronidazole 500mg TID was prescribed.", "Tigecycline was stopped.", "Two days later, DNA Cytomegalovirus was detected in the blood with \u2264253 copies/mL.", "Three days later, this value increased to 6189 copies/mL.", "Three days later, 1431 copies/mL were evidenced from a urine sample.", "CMV pp65-antigen was also positive.", "CMV serology indicated acute CMV infection.", "The patient\u2019s fever rose to 39.2\u00b0C.", "The patient\u2019s abdominal pain extended to the right lower abdominal quadrant.", "The patient\u2019s abdominal pain radiated to the right groin.", "The patient\u2019s abdominal pain radiated to the right testicle.", "Ultrasound suggested acute appendicitis.", "He underwent surgery.", "Histology showed inflammatory infiltrates, including lymphocytes and neutrophils.", "Histochemistry was positive for CMV early antigens.", "Real time reaction of the appendix tissue was positive.", "Shell vial culture of the appendix tissue was positive.", "Microbiological investigations for bacteria showed Peptococcus spp.", "Microbiological investigations for fungi showed Candida albicans.", "Teicoplanin, gentamicin and metronidazole were administered for a total of 12 days.", "Intravenous ganciclovir 5mg/kg twice was administered for 15 days.", "After discharge, oral valganciclovir 900mg BID was prescribed for 10 days.", "After this, the CMV nucleic acid in the blood and urine was negative.", "After this, ESR remained abnormally high.", "After this, cholestatic liver test results remained abnormally high."], "index": 1, "original_id": "multiclinsum_test_2576_en.txt", "split": "test", "summary_subclaims": ["The authors report on a case of acute primary Cytomegalovirus infection complicated with acute appendicitis due to Cytomegalovirus in an apparently immunocompetent 24-year-old Caucasian man.", "The patient also suffered from primary sclerosing cholangitis and ulcerative colitis.", "Diagnosis was based on clinical manifestations.", "Diagnosis was based on serology results.", "Diagnosis was based on microbiological findings.", "Diagnosis was based on histological findings.", "Treatment consisted of surgery.", "Treatment consisted of anti-Cytomegalovirus therapy."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 34-year-old Han female.", "The patient had a slight limp without obvious inducement 7 or 8 years previously.", "Approximately 1 year prior to the presentation, she had given birth to a boy.", "She developed progressive walking instability approximately 1 year prior to the presentation.", "Five months prior to the evaluation, she started experiencing static tremors in her hands and head.", "She had difficulty speaking.", "She had occasional numbness in the limbs.", "She had a cough after drinking water.", "The tremor was significantly aggravated during movement.", "She reported headaches.", "She reported dizziness.", "She reported nausea.", "One year prior, she lacked appetite.", "She had lost more than 10 pounds.", "She had a history of cephalosporin allergy.", "She had undergone an appendectomy 20 years prior.", "She had a history of tobacco and alcohol use for 10 years.", "She had quit smoking 6 months ago.", "She had no relatives with similar symptoms.", "She had 27 teeth.", "Her sex hormone levels were normal.", "Her menstruation was normal.", "At the time of presentation, she had dysarthria.", "She had upbeating nystagmus.", "She had right gaze-evoked nystagmus.", "Her limb reflexes were absent.", "Her bilateral finger-nose test was unstable.", "She demonstrated instability on her calcaneus tibial test.", "She had a positive Romberg sign.", "She had bilateral Babinski and Chaddock's signs.", "The total score of the scale for the assessment and rating of ataxia was 24.", "The gait sub-score was 5.", "The stance sub-score was 4.", "The sitting sub-score was 2.", "The speech sub-score was 2.", "The finger chase sub-score was 2.", "The nose\u2013finger test sub-score was 2.", "The fast alternating hand movement sub-score was 3.", "The heel\u2013shin slide sub-score was 4.", "The Mini-Mental State Examination score was within the normal range.", "She failed to complete the Montreal Cognitive Scale due to tremors of the hands and head.", "The results for tumor markers were not significantly abnormal.", "The results for ceruloplasmin were not significantly abnormal.", "The results for immune-related autoantibodies were not significantly abnormal.", "The results for the five items of thyroid function were not significantly abnormal.", "The results for the three items of rheumatism were not significantly abnormal.", "The results for the five items of immunity were not significantly abnormal.", "The results for antinuclear antibody were not significantly abnormal.", "The results for anticardiolipin antibody were not significantly abnormal.", "The results for screening and confirmation of anti-neutrophil cytoplasmic antibody were not significantly abnormal.", "Lumbar puncture results showed no abnormalities.", "Brain MRI revealed speckled and small patchy abnormal signals bilaterally in the corona radiata.", "The lesions were hypointense on T1 images.", "The lesions were hyperintense on T2 and FLAIR images.", "There were no obvious abnormal signals on diffusion-weighted images.", "The radiological diagnosis was multiple white matter demyelinating lesions.", "Color Doppler ultrasonography of the gynecological, abdominal, cardiac, carotid, and intracranial arteries revealed no obvious abnormalities.", "The detection of hereditary disease genes revealed mutations in POLR3A.", "The genetic variant c.4044C > G is classified as PM2.", "The clinical significance of c.4044C > G remains unclear.", "The genetic variant c.1186-2A > G is classified as PVS1 and PM2.", "The genetic variant c.1186-2A > G has the potential to influence RNA splicing.", "The patient did not undergo genetic testing for her parents or son.", "Her condition was diagnosed as POLR3A-related leukodystrophy (HLD7).", "She was administered oral vitamin B12.", "She was administered injectable acetylglutamine.", "No other drugs were used during the hospital stay.", "The symptoms did not show significant improvement during the 1 month of follow-up.", "The symptoms appeared aggravated during the 1 month of follow-up.", "The patient required assistance to walk.", "The patient was unable to hold objects in her hands.", "After discharge, she was treated with vitamin B12.", "After discharge, she was treated with vitamin E.", "After discharge, she was treated with coenzyme Q.", "After discharge, she was treated with traditional Chinese medicine.", "The traditional Chinese medicine included Ganoderma lucidum.", "The traditional Chinese medicine included ginseng.", "The traditional Chinese medicine included Poria Cocos.", "As of recent follow-up (1 year after discharge), she is able to walk slowly alone.", "As of recent follow-up, she is able to climb stairs.", "As of recent follow-up, the degree of head and hand tremors has reduced significantly.", "As of recent follow-up, she is able to hold objects.", "As of recent follow-up, she is able to cook independently.", "As of recent follow-up, her speech is slower and more indistinct than before."], "summary_subclaims": ["The patient is a 34-year-old female.", "The patient presented with ataxia.", "MRI of the brain revealed demyelinating lesions in the white matter.", "Genetic testing identified the c.4044C > G variant in the POLR3A gene.", "Genetic testing identified the c.1186-2A > G variant in the POLR3A gene.", "The patient was diagnosed with hypomyelinating leukodystrophy type 7.", "The patient received neurotrophic and symptomatic supportive therapy.", "After 1 month of follow-up, there was no improvement in her symptoms."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 34-year-old Han female.", "The patient had a slight limp without obvious inducement 7 or 8 years previously.", "Approximately 1 year prior to the presentation, she had given birth to a boy.", "She developed progressive walking instability approximately 1 year prior to the presentation.", "Five months prior to the evaluation, she started experiencing static tremors in her hands and head.", "She had difficulty speaking.", "She had occasional numbness in the limbs.", "She had a cough after drinking water.", "The tremor was significantly aggravated during movement.", "She reported headaches.", "She reported dizziness.", "She reported nausea.", "One year prior, she lacked appetite.", "She had lost more than 10 pounds.", "She had a history of cephalosporin allergy.", "She had undergone an appendectomy 20 years prior.", "She had a history of tobacco and alcohol use for 10 years.", "She had quit smoking 6 months ago.", "She had no relatives with similar symptoms.", "She had 27 teeth.", "Her sex hormone levels were normal.", "Her menstruation was normal.", "At the time of presentation, she had dysarthria.", "She had upbeating nystagmus.", "She had right gaze-evoked nystagmus.", "Her limb reflexes were absent.", "Her bilateral finger-nose test was unstable.", "She demonstrated instability on her calcaneus tibial test.", "She had a positive Romberg sign.", "She had bilateral Babinski and Chaddock's signs.", "The total score of the scale for the assessment and rating of ataxia was 24.", "The gait sub-score was 5.", "The stance sub-score was 4.", "The sitting sub-score was 2.", "The speech sub-score was 2.", "The finger chase sub-score was 2.", "The nose\u2013finger test sub-score was 2.", "The fast alternating hand movement sub-score was 3.", "The heel\u2013shin slide sub-score was 4.", "The Mini-Mental State Examination score was within the normal range.", "She failed to complete the Montreal Cognitive Scale due to tremors of the hands and head.", "The results for tumor markers were not significantly abnormal.", "The results for ceruloplasmin were not significantly abnormal.", "The results for immune-related autoantibodies were not significantly abnormal.", "The results for the five items of thyroid function were not significantly abnormal.", "The results for the three items of rheumatism were not significantly abnormal.", "The results for the five items of immunity were not significantly abnormal.", "The results for antinuclear antibody were not significantly abnormal.", "The results for anticardiolipin antibody were not significantly abnormal.", "The results for screening and confirmation of anti-neutrophil cytoplasmic antibody were not significantly abnormal.", "Lumbar puncture results showed no abnormalities.", "Brain MRI revealed speckled and small patchy abnormal signals bilaterally in the corona radiata.", "The lesions were hypointense on T1 images.", "The lesions were hyperintense on T2 and FLAIR images.", "There were no obvious abnormal signals on diffusion-weighted images.", "The radiological diagnosis was multiple white matter demyelinating lesions.", "Color Doppler ultrasonography of the gynecological, abdominal, cardiac, carotid, and intracranial arteries revealed no obvious abnormalities.", "The detection of hereditary disease genes revealed mutations in POLR3A.", "The genetic variant c.4044C > G is classified as PM2.", "The clinical significance of c.4044C > G remains unclear.", "The genetic variant c.1186-2A > G is classified as PVS1 and PM2.", "The genetic variant c.1186-2A > G has the potential to influence RNA splicing.", "The patient did not undergo genetic testing for her parents or son.", "Her condition was diagnosed as POLR3A-related leukodystrophy (HLD7).", "She was administered oral vitamin B12.", "She was administered injectable acetylglutamine.", "No other drugs were used during the hospital stay.", "The symptoms did not show significant improvement during the 1 month of follow-up.", "The symptoms appeared aggravated during the 1 month of follow-up.", "The patient required assistance to walk.", "The patient was unable to hold objects in her hands.", "After discharge, she was treated with vitamin B12.", "After discharge, she was treated with vitamin E.", "After discharge, she was treated with coenzyme Q.", "After discharge, she was treated with traditional Chinese medicine.", "The traditional Chinese medicine included Ganoderma lucidum.", "The traditional Chinese medicine included ginseng.", "The traditional Chinese medicine included Poria Cocos.", "As of recent follow-up (1 year after discharge), she is able to walk slowly alone.", "As of recent follow-up, she is able to climb stairs.", "As of recent follow-up, the degree of head and hand tremors has reduced significantly.", "As of recent follow-up, she is able to hold objects.", "As of recent follow-up, she is able to cook independently.", "As of recent follow-up, her speech is slower and more indistinct than before."], "index": 134, "original_id": "multiclinsum_test_1579_en.txt", "split": "test", "summary_subclaims": ["The patient is a 34-year-old female.", "The patient presented with ataxia.", "MRI of the brain revealed demyelinating lesions in the white matter.", "Genetic testing identified the c.4044C > G variant in the POLR3A gene.", "Genetic testing identified the c.1186-2A > G variant in the POLR3A gene.", "The patient was diagnosed with hypomyelinating leukodystrophy type 7.", "The patient received neurotrophic and symptomatic supportive therapy.", "After 1 month of follow-up, there was no improvement in her symptoms."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["A 14-year-old boy attended a local hospital for ankylosing spondylitis.", "Chest radiography showed an enhanced circular-density shadow near the left mediastinum.", "The shadow intersected with the mediastinum at an obtuse angle.", "The base was close to the mediastinum.", "The outer edge was clear and smooth.", "The mass density was even.", "A benign lesion was considered.", "Because of the mediastinal occupation, the patient visited our department of chest surgery for further treatment.", "The patient had no previous symptoms.", "The patient had no major illness before.", "Mandatory spondylitis was discovered this time because of his left hip pain.", "The results of the physical examination were normal.", "Blood analysis and the blood biochemistries, as well as urine analysis, were all normal.", "Electrocardiogram and arterial blood gas were also normal.", "Enhanced chest CT suggested irregular soft tissue density above the left aortic arch.", "The mass had a clear boundary.", "The mass was about 5.5 cm \u00d7 3.2 cm \u00d7 2.8 cm in size."], "summary_subclaims": ["A 14-year-old boy attended a local hospital for ankylosing spondylitis.", "Chest radiography showed an enhanced circular-density shadow near the left mediastinum.", "The patient had no chest symptoms.", "The physical examination was normal.", "Because of the mediastinal occupation, the patient visited our department of chest surgery for further treatment.", "During surgery, a left pericardial defect was observed.", "The bronchogenic cyst was removed by thoracoscopic surgery.", "The pericardial defect remained untreated.", "A satisfactory outcome was achieved after the operation.", "The patient was diagnosed with a mediastinal tumor.", "The pathological diagnosis of the tumor was a bronchogenic cyst."]}, "extra_info": {"fulltext_subclaims": ["A 14-year-old boy attended a local hospital for ankylosing spondylitis.", "Chest radiography showed an enhanced circular-density shadow near the left mediastinum.", "The shadow intersected with the mediastinum at an obtuse angle.", "The base was close to the mediastinum.", "The outer edge was clear and smooth.", "The mass density was even.", "A benign lesion was considered.", "Because of the mediastinal occupation, the patient visited our department of chest surgery for further treatment.", "The patient had no previous symptoms.", "The patient had no major illness before.", "Mandatory spondylitis was discovered this time because of his left hip pain.", "The results of the physical examination were normal.", "Blood analysis and the blood biochemistries, as well as urine analysis, were all normal.", "Electrocardiogram and arterial blood gas were also normal.", "Enhanced chest CT suggested irregular soft tissue density above the left aortic arch.", "The mass had a clear boundary.", "The mass was about 5.5 cm \u00d7 3.2 cm \u00d7 2.8 cm in size."], "index": 136, "original_id": "multiclinsum_test_2394_en.txt", "split": "test", "summary_subclaims": ["A 14-year-old boy attended a local hospital for ankylosing spondylitis.", "Chest radiography showed an enhanced circular-density shadow near the left mediastinum.", "The patient had no chest symptoms.", "The physical examination was normal.", "Because of the mediastinal occupation, the patient visited our department of chest surgery for further treatment.", "During surgery, a left pericardial defect was observed.", "The bronchogenic cyst was removed by thoracoscopic surgery.", "The pericardial defect remained untreated.", "A satisfactory outcome was achieved after the operation.", "The patient was diagnosed with a mediastinal tumor.", "The pathological diagnosis of the tumor was a bronchogenic cyst."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 77-year-old lady.", "She presented with progressive left groin pain.", "The left groin pain is due to degenerative hip osteoarthritis.", "She had a previous knee arthrodesis on the left leg.", "The knee arthrodesis was a result of a traffic accident during childhood.", "There was a leg length discrepancy of 8.5 cm at the expense of the left leg.", "The leg length discrepancy was corrected by an orthopedic shoe.", "There was no Trendelenburg limp.", "Log roll and rotation with the hip in flexion (and knee in extension) were painful.", "Radiographs showed left hip osteoarthritis.", "Previous conservative treatment had become insufficient.", "A total hip arthroplasty (THA) was proposed.", "Radiographically, there was a normal anatomy of the hip joint.", "A direct anterior approach (DAA) THA was planned.", "A cemented stem was planned.", "A literature search on PubMed was performed.", "Search terms included: Knee arthrodesis; femoral anteversion; and arthroplasty hip.", "A case of a THA after knee arthrodesis using a posterolateral approach was found.", "A case series by Bourne et al. of 16 patients was found.", "No literature was found about the anterior approach in this specific case."], "summary_subclaims": ["This case report presents the case of a 77 year old female patient.", "The patient has degenerative hip disease.", "The patient has an ipsilateral arthrodesis of the knee.", "The patient was operated using the DAA.", "No complications were found.", "The patient had an excellent follow-up.", "The patient had a forgotten joint score of 93.75 at 1 year.", "The difficulty in this case consists in finding the correct stem anteversion with the altered knee anatomy.", "Pre-operative templating on X-rays was used.", "Intraoperative fluoroscopy was used.", "The posterior femoral neck was used.", "Hip biomechanics could be restored."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 77-year-old lady.", "She presented with progressive left groin pain.", "The left groin pain is due to degenerative hip osteoarthritis.", "She had a previous knee arthrodesis on the left leg.", "The knee arthrodesis was a result of a traffic accident during childhood.", "There was a leg length discrepancy of 8.5 cm at the expense of the left leg.", "The leg length discrepancy was corrected by an orthopedic shoe.", "There was no Trendelenburg limp.", "Log roll and rotation with the hip in flexion (and knee in extension) were painful.", "Radiographs showed left hip osteoarthritis.", "Previous conservative treatment had become insufficient.", "A total hip arthroplasty (THA) was proposed.", "Radiographically, there was a normal anatomy of the hip joint.", "A direct anterior approach (DAA) THA was planned.", "A cemented stem was planned.", "A literature search on PubMed was performed.", "Search terms included: Knee arthrodesis; femoral anteversion; and arthroplasty hip.", "A case of a THA after knee arthrodesis using a posterolateral approach was found.", "A case series by Bourne et al. of 16 patients was found.", "No literature was found about the anterior approach in this specific case."], "index": 140, "original_id": "multiclinsum_test_2302_en.txt", "split": "test", "summary_subclaims": ["This case report presents the case of a 77 year old female patient.", "The patient has degenerative hip disease.", "The patient has an ipsilateral arthrodesis of the knee.", "The patient was operated using the DAA.", "No complications were found.", "The patient had an excellent follow-up.", "The patient had a forgotten joint score of 93.75 at 1 year.", "The difficulty in this case consists in finding the correct stem anteversion with the altered knee anatomy.", "Pre-operative templating on X-rays was used.", "Intraoperative fluoroscopy was used.", "The posterior femoral neck was used.", "Hip biomechanics could be restored."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 56-year-old female.", "The patient has a body mass index of 22.5\u202fkg/m2.", "The patient has a previous clinical history of diffuse scleroderma.", "The patient has intestinal pneumonitis.", "The patient has mild pulmonary hypertension.", "The patient has secondary gastroesophageal reflux.", "The patient has severe esophageal motility disease.", "The patient is receiving immunosuppression, antihypertensive, proton pump inhibitor, and prokinetic management.", "The patient has a weak response to medical therapy.", "The patient is admitted for surgical management after a 1-year follow-up with cardiology, pneumology, and gastroenterology.", "The patient has a previous diagnosis of esophageal aperistalsis.", "The patient has dysphagia.", "The patient has poor response to medical therapy.", "Physical examination revealed no significant findings.", "The lung transplant surgical team determined the patient was not a candidate given the severity of the GERD.", "The medical committee decided an open total gastrectomy with roux-en-Y anastomosis prior to lung transplant.", "Follow-up one week later with esophagogram revealed normal esophageal morphology.", "Follow-up one week later with esophagogram revealed no stenosis.", "Follow-up one week later with esophagogram revealed adequate esophago-jejunal anastomosis diameter.", "Follow-up one week later with esophagogram revealed no extravasation of the contrast medium.", "Follow-up one week later with esophagogram revealed adequate transit of the medium to the small intestine.", "Follow-up one week later with esophagogram revealed no evidence of reflux of the medium.", "An upper gastrointestinal endoscopy is performed within a 3-month period.", "The upper gastrointestinal endoscopy revealed mild esophago-jejunal anastomosis stricture.", "The stricture resolved after three balloon dilations of 11\u202fmm, 15\u202fmm, and 18\u202fmm, respectively.", "The patient continues follow-up consults.", "The patient is asymptomatic according to the Gastroesophageal Reflux Disease Health Related Quality of Life (GERD-HRQL) instrument.", "The patient currently awaits lung transplant."], "summary_subclaims": ["The patient is a 56-year-old female.", "The patient has a previous history of intestinal pneumonitis.", "The patient has mild pulmonary hypertension.", "The patient has gastroesophageal reflux secondary to systemic scleroderma.", "A lung transplant was initially not a viable option due to persistent gastroesophageal reflux.", "An open gastrectomy with roux-en-Y anastomosis was performed.", "Follow-up one week later revealed normal anatomy.", "Follow-up one week later showed an adequate esophageal-jejunal anastomosis.", "Follow-up one week later showed adequate contrast medium transit via esophagogram.", "There was no evidence of contrast medium reflux.", "This led to the patient becoming a candidate for lung transplant."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 56-year-old female.", "The patient has a body mass index of 22.5\u202fkg/m2.", "The patient has a previous clinical history of diffuse scleroderma.", "The patient has intestinal pneumonitis.", "The patient has mild pulmonary hypertension.", "The patient has secondary gastroesophageal reflux.", "The patient has severe esophageal motility disease.", "The patient is receiving immunosuppression, antihypertensive, proton pump inhibitor, and prokinetic management.", "The patient has a weak response to medical therapy.", "The patient is admitted for surgical management after a 1-year follow-up with cardiology, pneumology, and gastroenterology.", "The patient has a previous diagnosis of esophageal aperistalsis.", "The patient has dysphagia.", "The patient has poor response to medical therapy.", "Physical examination revealed no significant findings.", "The lung transplant surgical team determined the patient was not a candidate given the severity of the GERD.", "The medical committee decided an open total gastrectomy with roux-en-Y anastomosis prior to lung transplant.", "Follow-up one week later with esophagogram revealed normal esophageal morphology.", "Follow-up one week later with esophagogram revealed no stenosis.", "Follow-up one week later with esophagogram revealed adequate esophago-jejunal anastomosis diameter.", "Follow-up one week later with esophagogram revealed no extravasation of the contrast medium.", "Follow-up one week later with esophagogram revealed adequate transit of the medium to the small intestine.", "Follow-up one week later with esophagogram revealed no evidence of reflux of the medium.", "An upper gastrointestinal endoscopy is performed within a 3-month period.", "The upper gastrointestinal endoscopy revealed mild esophago-jejunal anastomosis stricture.", "The stricture resolved after three balloon dilations of 11\u202fmm, 15\u202fmm, and 18\u202fmm, respectively.", "The patient continues follow-up consults.", "The patient is asymptomatic according to the Gastroesophageal Reflux Disease Health Related Quality of Life (GERD-HRQL) instrument.", "The patient currently awaits lung transplant."], "index": 138, "original_id": "multiclinsum_test_2494_en.txt", "split": "test", "summary_subclaims": ["The patient is a 56-year-old female.", "The patient has a previous history of intestinal pneumonitis.", "The patient has mild pulmonary hypertension.", "The patient has gastroesophageal reflux secondary to systemic scleroderma.", "A lung transplant was initially not a viable option due to persistent gastroesophageal reflux.", "An open gastrectomy with roux-en-Y anastomosis was performed.", "Follow-up one week later revealed normal anatomy.", "Follow-up one week later showed an adequate esophageal-jejunal anastomosis.", "Follow-up one week later showed adequate contrast medium transit via esophagogram.", "There was no evidence of contrast medium reflux.", "This led to the patient becoming a candidate for lung transplant."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 33-year-old man.", "He had a five-month history of bilateral radiating pain through the hips, legs and ankles.", "He reported numbness, paresthesia and mild weakness in one lateral lower extremity.", "A pin-prick sensation test showed bilateral patchy loss of sensation and vibration in the legs and feet.", "The patient did not report bowel or bladder problems.", "He did not exhibit hyper-reflexia.", "He was negative for Babinski\u2019s sign.", "MRI revealed a lesion extending from L3 to L5.", "T1-weighted MRI showed an intradural, extra-medullary, isointense mass behind the vertebral bodies of L3 to L5.", "The mass was eccentric to the left and showed homogenous enhancement with contrast.", "The vertebral body of L4 exhibited a compressed deformation.", "Gastroscopy, colonoscopy and computed tomography scans of the abdomen and the thorax identified no additional masses.", "A lumbar laminectomy of L3 to L5 was performed.", "The tumor was soft with a rich blood supply.", "The tumor closely adhered to the medulla spinalis.", "There were no signs of dural invasion.", "A total tumor resection was performed.", "Lower extremity pain resolved immediately following surgery.", "Lower limb strength began to improve within a few days.", "The patient reported symptoms of postoperative dysuria.", "Dysuria symptoms showed improvement after one week.", "During the two-year postoperative follow-up, the patient exhibited no clinical signs of tumor recurrence.", "During the two-year postoperative follow-up, the patient exhibited no MRI radiological signs of tumor recurrence or metastasis.", "Postoperative histopathology confirmed a completely resected solid tumor.", "The specimen was a fully encapsulated smooth soft-tissue mass.", "Standard hematoxylin and eosin staining revealed sheet-like proliferation of NET cells in a trabecular pattern.", "There were no visible mitoses or necrosis.", "The tumor was positive for synaptophysin.", "The tumor was positive for chromogranin (CgA).", "The tumor was positive for cytokeratin.", "The tumor was positive for CD56.", "The tumor was negative for S-100.", "The Ki-67 labeling index was 2%.", "These findings are consistent with the known cellular characteristics of a typical CT."], "summary_subclaims": ["The patient was a 33-year-old man.", "He had a five-month history of bilateral lower extremity pain.", "He had paresthesia.", "He had mild weakness in one lateral lower extremity.", "A lumbar laminectomy of L3 to L5 was performed.", "An en bloc resection of the tumor was performed.", "Postoperative histopathology and immunohistochemical analysis of the tumor were consistent with that of a carcinoid tumor.", "There were no clinical signs of tumor recurrence at the patient's two year postoperative follow-up.", "There were no radiological signs of tumor recurrence at the patient's two year postoperative follow-up.", "There were no clinical or radiological signs of metastasis at the patient's two year postoperative follow-up."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 33-year-old man.", "He had a five-month history of bilateral radiating pain through the hips, legs and ankles.", "He reported numbness, paresthesia and mild weakness in one lateral lower extremity.", "A pin-prick sensation test showed bilateral patchy loss of sensation and vibration in the legs and feet.", "The patient did not report bowel or bladder problems.", "He did not exhibit hyper-reflexia.", "He was negative for Babinski\u2019s sign.", "MRI revealed a lesion extending from L3 to L5.", "T1-weighted MRI showed an intradural, extra-medullary, isointense mass behind the vertebral bodies of L3 to L5.", "The mass was eccentric to the left and showed homogenous enhancement with contrast.", "The vertebral body of L4 exhibited a compressed deformation.", "Gastroscopy, colonoscopy and computed tomography scans of the abdomen and the thorax identified no additional masses.", "A lumbar laminectomy of L3 to L5 was performed.", "The tumor was soft with a rich blood supply.", "The tumor closely adhered to the medulla spinalis.", "There were no signs of dural invasion.", "A total tumor resection was performed.", "Lower extremity pain resolved immediately following surgery.", "Lower limb strength began to improve within a few days.", "The patient reported symptoms of postoperative dysuria.", "Dysuria symptoms showed improvement after one week.", "During the two-year postoperative follow-up, the patient exhibited no clinical signs of tumor recurrence.", "During the two-year postoperative follow-up, the patient exhibited no MRI radiological signs of tumor recurrence or metastasis.", "Postoperative histopathology confirmed a completely resected solid tumor.", "The specimen was a fully encapsulated smooth soft-tissue mass.", "Standard hematoxylin and eosin staining revealed sheet-like proliferation of NET cells in a trabecular pattern.", "There were no visible mitoses or necrosis.", "The tumor was positive for synaptophysin.", "The tumor was positive for chromogranin (CgA).", "The tumor was positive for cytokeratin.", "The tumor was positive for CD56.", "The tumor was negative for S-100.", "The Ki-67 labeling index was 2%.", "These findings are consistent with the known cellular characteristics of a typical CT."], "index": 142, "original_id": "multiclinsum_test_2169_en.txt", "split": "test", "summary_subclaims": ["The patient was a 33-year-old man.", "He had a five-month history of bilateral lower extremity pain.", "He had paresthesia.", "He had mild weakness in one lateral lower extremity.", "A lumbar laminectomy of L3 to L5 was performed.", "An en bloc resection of the tumor was performed.", "Postoperative histopathology and immunohistochemical analysis of the tumor were consistent with that of a carcinoid tumor.", "There were no clinical signs of tumor recurrence at the patient's two year postoperative follow-up.", "There were no radiological signs of tumor recurrence at the patient's two year postoperative follow-up.", "There were no clinical or radiological signs of metastasis at the patient's two year postoperative follow-up."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 24-year-old male.", "The patient recently arrived in Burhakaba town of Somalia from Sa\u2019ada in northwest of Yemen.", "The patient was referred to the hospital with a complaint of left upper hypochondrium mass.", "The patient had high grade fever, headache, abdominal pain, nausea, vomiting, and weight loss for two months.", "The patient claimed he had experienced a similar clinical condition three months ago.", "Before reporting to the hospital, he had visited a local hospital in the region.", "At the local hospital, he was administered local symptomatic treatment of antipyretics, antibiotics, and transfused with 2 units of whole blood.", "After the treatment at the local hospital, he felt mild improvement.", "Two months later, his clinical signs recurred with loss of appetite, weight loss, and generalized weakness.", "On presentation at the hospital, the patient appeared ill, thin, febrile, and pale.", "Abdominal examination revealed splenomegaly.", "The other system examinations were normal.", "The initial laboratory investigation showed white blood cell count 1.03 x10^9/L.", "The initial laboratory investigation showed hemoglobin 6.6 g/dl.", "The initial laboratory investigation showed platelet 70x10^9/L.", "The initial laboratory investigation showed C-reactive protein 45.73 mg/L.", "The initial laboratory investigation showed aspartate transaminase 104.5 U/I.", "The initial laboratory investigation showed alanine transaminase 112.5 U/I.", "The initial laboratory investigation showed serum creatinine 1.4 mg/dl.", "The initial laboratory investigation showed serum urea 54.3 mg/dl.", "A rapid diagnostic test for plasmodium parasite antigen was conducted and was found to be positive.", "Abdominal ultrasound revealed enlargement of the liver (20cm).", "Abdominal ultrasound revealed enlargement of the spleen (30cm).", "The patient was admitted initially for treatment of malaria.", "The patient was given four doses of intravenous artesunate 120mg.", "The patient was transfused one unit of whole blood.", "On the third day of admission, no significant improvement was observed.", "Infectious disease tests such as human immunodeficiency virus, viral hepatitis, and Brucella serological tests were conducted and found to be negative.", "An anti-Leishmania antibody with ELISA was not detected.", "A peripheral blood smear showed only pancytopenia and no evidence of malaria parasite.", "A tru-cut biopsy of the spleen was performed.", "The histopathology examinations of the tru-cut biopsy revealed consistent features with visceral leishmaniasis.", "An urgent combination therapy of sodium stibogluconate 800mg/day with paromomycin 600mg/day for 17 days was given.", "After the fourth week of treatment, significant improvement was observed.", "At the end of the fifth week, the patient was fully recovered.", "The patient was discharged following normal results of another tru-cut biopsy of the spleen."], "summary_subclaims": ["The patient is a 24-year-old from an endemic region of Somalia.", "The patient had fever, headache, abdominal pain, nausea, vomiting, and weight loss for two months.", "The patient received symptomatic treatment and a blood transfusion.", "The patient showed no improvement after initial treatment.", "Physical examination revealed fever, pallor, and hepatosplenomegaly.", "Laboratory tests showed pancytopenia.", "The rapid diagnostic test was positive for plasmodium parasite antigen.", "The patient received three days of anti-malarial treatment.", "The symptoms persisted despite anti-malarial treatment.", "Hepatosplenomegaly worsened after three days of anti-malarial treatment.", "Infectious disease tests ruled out HIV, viral hepatitis, Brucella, and Leishmania antibodies.", "Peripheral blood smear showed pancytopenia.", "Bone marrow aspiration revealed no evidence of infection or malignancy.", "A tru-cut biopsy of the spleen was performed.", "The spleen biopsy confirmed the diagnosis of visceral leishmaniasis.", "The patient received a combination therapy of sodium stibogluconate and paromomycin.", "The patient showed significant improvement after treatment.", "The patient was discharged after completing treatment.", "The spleen biopsy results were normal after treatment."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 24-year-old male.", "The patient recently arrived in Burhakaba town of Somalia from Sa\u2019ada in northwest of Yemen.", "The patient was referred to the hospital with a complaint of left upper hypochondrium mass.", "The patient had high grade fever, headache, abdominal pain, nausea, vomiting, and weight loss for two months.", "The patient claimed he had experienced a similar clinical condition three months ago.", "Before reporting to the hospital, he had visited a local hospital in the region.", "At the local hospital, he was administered local symptomatic treatment of antipyretics, antibiotics, and transfused with 2 units of whole blood.", "After the treatment at the local hospital, he felt mild improvement.", "Two months later, his clinical signs recurred with loss of appetite, weight loss, and generalized weakness.", "On presentation at the hospital, the patient appeared ill, thin, febrile, and pale.", "Abdominal examination revealed splenomegaly.", "The other system examinations were normal.", "The initial laboratory investigation showed white blood cell count 1.03 x10^9/L.", "The initial laboratory investigation showed hemoglobin 6.6 g/dl.", "The initial laboratory investigation showed platelet 70x10^9/L.", "The initial laboratory investigation showed C-reactive protein 45.73 mg/L.", "The initial laboratory investigation showed aspartate transaminase 104.5 U/I.", "The initial laboratory investigation showed alanine transaminase 112.5 U/I.", "The initial laboratory investigation showed serum creatinine 1.4 mg/dl.", "The initial laboratory investigation showed serum urea 54.3 mg/dl.", "A rapid diagnostic test for plasmodium parasite antigen was conducted and was found to be positive.", "Abdominal ultrasound revealed enlargement of the liver (20cm).", "Abdominal ultrasound revealed enlargement of the spleen (30cm).", "The patient was admitted initially for treatment of malaria.", "The patient was given four doses of intravenous artesunate 120mg.", "The patient was transfused one unit of whole blood.", "On the third day of admission, no significant improvement was observed.", "Infectious disease tests such as human immunodeficiency virus, viral hepatitis, and Brucella serological tests were conducted and found to be negative.", "An anti-Leishmania antibody with ELISA was not detected.", "A peripheral blood smear showed only pancytopenia and no evidence of malaria parasite.", "A tru-cut biopsy of the spleen was performed.", "The histopathology examinations of the tru-cut biopsy revealed consistent features with visceral leishmaniasis.", "An urgent combination therapy of sodium stibogluconate 800mg/day with paromomycin 600mg/day for 17 days was given.", "After the fourth week of treatment, significant improvement was observed.", "At the end of the fifth week, the patient was fully recovered.", "The patient was discharged following normal results of another tru-cut biopsy of the spleen."], "index": 146, "original_id": "multiclinsum_test_292_en.txt", "split": "test", "summary_subclaims": ["The patient is a 24-year-old from an endemic region of Somalia.", "The patient had fever, headache, abdominal pain, nausea, vomiting, and weight loss for two months.", "The patient received symptomatic treatment and a blood transfusion.", "The patient showed no improvement after initial treatment.", "Physical examination revealed fever, pallor, and hepatosplenomegaly.", "Laboratory tests showed pancytopenia.", "The rapid diagnostic test was positive for plasmodium parasite antigen.", "The patient received three days of anti-malarial treatment.", "The symptoms persisted despite anti-malarial treatment.", "Hepatosplenomegaly worsened after three days of anti-malarial treatment.", "Infectious disease tests ruled out HIV, viral hepatitis, Brucella, and Leishmania antibodies.", "Peripheral blood smear showed pancytopenia.", "Bone marrow aspiration revealed no evidence of infection or malignancy.", "A tru-cut biopsy of the spleen was performed.", "The spleen biopsy confirmed the diagnosis of visceral leishmaniasis.", "The patient received a combination therapy of sodium stibogluconate and paromomycin.", "The patient showed significant improvement after treatment.", "The patient was discharged after completing treatment.", "The spleen biopsy results were normal after treatment."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 65-year-old woman with persistent atrial fibrillation.", "She underwent mechanical aortic and mitral valve replacement in 1995 for rheumatic valvular disease.", "She required a redo surgery due to an extensive pannus with two biological prostheses in January 2020.", "She also required a single-chamber pacemaker.", "Her current medical therapy included oral anticoagulation (apixaban 5\u2005mg twice daily).", "She developed chronic anaemia due to active intestinal angiodysplasia.", "Her CHA\u2082DS\u2082-VASc score was 3.", "Her HAS-BLED score was 3.", "Investigations ruled out other causes of anaemia, including haemolytic anaemia.", "The patient presented with two biological prostheses (VHD) without active rheumatic valve disease.", "The patient may be a candidate for LAAc.", "Transesophageal echocardiography (TEE) revealed spontaneous contrast in the LAA without formation of a thrombus.", "The ridge diameter was 28\u2005mm.", "One centimetre inside the LAA, the maximum landing zone diameter was 22\u2005mm.", "The shape of the LAA was tortuous and difficult to assess.", "Pre-operative computed tomography (CT) revealed an unusual LAA morphology that was horn-like in shape.", "The LAA had an inferior implantation and a superior axis.", "The ostium was close to the mitral prosthesis ring.", "A first procedure was performed using a standard left femoral venous approach.", "The transseptal puncture was performed postero-inferiorly as recommended under TEE guidance.", "Despite multiple attempts, it was not possible to advance the sheath beyond the first centimetre of the ostium.", "The deployment of a 31\u2005mm Watchman FLX was attempted but was unsuccessful given the unsuitable sheath position.", "A 3D printing model was prepared using SLS laser sintering technology.", "Simulation was performed from inferior and superior access points.", "Excessive sheath kinking was demonstrated with an inferior approach.", "Successful deployment was feasible using a superior approach.", "Transseptal puncture (second procedure) was performed using a right jugular venous approach under TEE guidance.", "Apixaban was discontinued 72\u2005h before the procedure.", "2000 IU unfractionated heparin was administered after jugular puncture.", "A Swartz SL0 sheath and a BRK-1 XS Series transseptal needle were used.", "Safe access to the left atrium was achieved by advancing a 0.014 stiff coronary wire Iron Man through the BRK-1 XS needle.", "The sheath was advanced in the left atrium over the needle and Iron Man wire.", "The SL0 was exchanged for the single-curve 14Fr delivery sheath over an Amplatz Super Stiff guidewire.", "Deep and safe advancement of the delivery sheath was performed over a pigtail catheter and the Amplatz Super Stiff guidewire.", "Proper sheath alignment without kinking was obtained.", "Successful implantation of a Watchman FLX 31 device in stable position without residual leakage was achieved.", "The position was as predicted during the simulation on the 3D-printed model.", "No complications occurred during the first or second procedures.", "Following the successful second procedure, the patient continued to receive apixaban (2.5\u2005mg twice daily) until the control CT scan at month 2.", "At the patient\u2019s 3-month follow-up visit, and after cessation of oral anticoagulation, an improvement in symptoms was seen with no need for additional transfusions.", "Imaging demonstrated complete LAA occlusion and correct placement of the device along the LAA superior axis as predicted by the simulation procedure.", "TEE follow-up confirmed there was no leakage around the device.", "After 9 months\u2019 follow-up, there was no need for further transfusions.", "The patient\u2019s pulmonary pressure and functional class had improved."], "summary_subclaims": ["The patient is a 65-year-old woman.", "The patient has persistent atrial fibrillation.", "The patient was referred for left atrial appendage closure (LAAc).", "Transesophageal echocardiography (TEE) revealed spontaneous contrast in the left atrial appendage (LAA).", "Transesophageal echocardiography (TEE) did not reveal formation of a thrombus.", "The left atrial appendage shape was tortuous.", "The left atrial appendage was difficult to assess.", "A first LAAc procedure was unsuccessful.", "The first LAAc procedure was unsuccessful given the unsuitable sheath position.", "A soft three-dimensional (3D) model printing was performed by laser sintering.", "The 3D model revealed excessive sheath kinking with an inferior approach.", "The 3D model suggested successful deployment would be feasible using a superior approach.", "A successful trans-jugular implantation of a Watchman FLX 31 device was achieved.", "The Watchman FLX 31 device was in stable position.", "There was no residual leakage after the device implantation.", "At 3-month follow-up, the patient's symptoms improved.", "Oral anticoagulation was ceased after the procedure.", "Imaging demonstrated complete LAA occlusion.", "Imaging demonstrated correct placement of the device along the LAA superior axis."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 65-year-old woman with persistent atrial fibrillation.", "She underwent mechanical aortic and mitral valve replacement in 1995 for rheumatic valvular disease.", "She required a redo surgery due to an extensive pannus with two biological prostheses in January 2020.", "She also required a single-chamber pacemaker.", "Her current medical therapy included oral anticoagulation (apixaban 5\u2005mg twice daily).", "She developed chronic anaemia due to active intestinal angiodysplasia.", "Her CHA\u2082DS\u2082-VASc score was 3.", "Her HAS-BLED score was 3.", "Investigations ruled out other causes of anaemia, including haemolytic anaemia.", "The patient presented with two biological prostheses (VHD) without active rheumatic valve disease.", "The patient may be a candidate for LAAc.", "Transesophageal echocardiography (TEE) revealed spontaneous contrast in the LAA without formation of a thrombus.", "The ridge diameter was 28\u2005mm.", "One centimetre inside the LAA, the maximum landing zone diameter was 22\u2005mm.", "The shape of the LAA was tortuous and difficult to assess.", "Pre-operative computed tomography (CT) revealed an unusual LAA morphology that was horn-like in shape.", "The LAA had an inferior implantation and a superior axis.", "The ostium was close to the mitral prosthesis ring.", "A first procedure was performed using a standard left femoral venous approach.", "The transseptal puncture was performed postero-inferiorly as recommended under TEE guidance.", "Despite multiple attempts, it was not possible to advance the sheath beyond the first centimetre of the ostium.", "The deployment of a 31\u2005mm Watchman FLX was attempted but was unsuccessful given the unsuitable sheath position.", "A 3D printing model was prepared using SLS laser sintering technology.", "Simulation was performed from inferior and superior access points.", "Excessive sheath kinking was demonstrated with an inferior approach.", "Successful deployment was feasible using a superior approach.", "Transseptal puncture (second procedure) was performed using a right jugular venous approach under TEE guidance.", "Apixaban was discontinued 72\u2005h before the procedure.", "2000 IU unfractionated heparin was administered after jugular puncture.", "A Swartz SL0 sheath and a BRK-1 XS Series transseptal needle were used.", "Safe access to the left atrium was achieved by advancing a 0.014 stiff coronary wire Iron Man through the BRK-1 XS needle.", "The sheath was advanced in the left atrium over the needle and Iron Man wire.", "The SL0 was exchanged for the single-curve 14Fr delivery sheath over an Amplatz Super Stiff guidewire.", "Deep and safe advancement of the delivery sheath was performed over a pigtail catheter and the Amplatz Super Stiff guidewire.", "Proper sheath alignment without kinking was obtained.", "Successful implantation of a Watchman FLX 31 device in stable position without residual leakage was achieved.", "The position was as predicted during the simulation on the 3D-printed model.", "No complications occurred during the first or second procedures.", "Following the successful second procedure, the patient continued to receive apixaban (2.5\u2005mg twice daily) until the control CT scan at month 2.", "At the patient\u2019s 3-month follow-up visit, and after cessation of oral anticoagulation, an improvement in symptoms was seen with no need for additional transfusions.", "Imaging demonstrated complete LAA occlusion and correct placement of the device along the LAA superior axis as predicted by the simulation procedure.", "TEE follow-up confirmed there was no leakage around the device.", "After 9 months\u2019 follow-up, there was no need for further transfusions.", "The patient\u2019s pulmonary pressure and functional class had improved."], "index": 145, "original_id": "multiclinsum_test_2065_en.txt", "split": "test", "summary_subclaims": ["The patient is a 65-year-old woman.", "The patient has persistent atrial fibrillation.", "The patient was referred for left atrial appendage closure (LAAc).", "Transesophageal echocardiography (TEE) revealed spontaneous contrast in the left atrial appendage (LAA).", "Transesophageal echocardiography (TEE) did not reveal formation of a thrombus.", "The left atrial appendage shape was tortuous.", "The left atrial appendage was difficult to assess.", "A first LAAc procedure was unsuccessful.", "The first LAAc procedure was unsuccessful given the unsuitable sheath position.", "A soft three-dimensional (3D) model printing was performed by laser sintering.", "The 3D model revealed excessive sheath kinking with an inferior approach.", "The 3D model suggested successful deployment would be feasible using a superior approach.", "A successful trans-jugular implantation of a Watchman FLX 31 device was achieved.", "The Watchman FLX 31 device was in stable position.", "There was no residual leakage after the device implantation.", "At 3-month follow-up, the patient's symptoms improved.", "Oral anticoagulation was ceased after the procedure.", "Imaging demonstrated complete LAA occlusion.", "Imaging demonstrated correct placement of the device along the LAA superior axis."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 33-year-old Chinese man.", "He had sustainable foamy urine for more than one year.", "He complained of intermittent hair loss.", "He had recurrence of oral ulcers.", "One year prior, he was hospitalized at a local hospital for the same reason.", "Routine urine tests indicated microscopic hematuria and proteinuria.", "He did not pay much attention.", "There was no further diagnosis or treatment.", "One month prior, his blood pressure rose to 145/91 mmHg.", "Microscopic hematuria and heavy proteinuria were again detected.", "The patient had no comorbidities.", "The patient's father had asymptomatic microscopic hematuria and proteinuria.", "The father's findings were detected in a routine physical examination approximately 2 years prior.", "The patient had a daughter and a son.", "The daughter had asymptomatic microscopic hematuria.", "The son had microscopic hematuria and proteinuria.", "The son had ever been diagnosed with chronic nephritis at a local hospital.", "The patient's systolic blood pressure was 141 mmHg.", "The patient's diastolic blood pressure was 90 mmHg.", "No obvious abnormality was detected during physical examination.", "No specific nervous system symptoms were recognized.", "No hearing impairments were detected.", "No symptoms were found in either eye.", "Microscopic hematuria and proteinuria were confirmed by urine tests.", "No obvious abnormality was detected by abdominal ultrasound.", "No obvious abnormality was detected by X-ray diagnosis.", "No obvious abnormality was detected by electrocardiographic examination.", "Heart echocardiography showed a small amount of pericardial effusion.", "A histopathology study of renal biopsy was performed.", "A total of 13 glomeruli were observed.", "One glomerulus was enlarged and lobulated.", "Para-aminosailcylic acid staining and Masson staining were positive.", "Mild mesangial matrix proliferation was observed.", "The basement membrane was thickened.", "Three glomerular fibroblastic crescents were observed.", "Pericystic fibrosis of glomeruli was observed.", "Deposition of erythrotropin under the endothelium of the capillary loop was detected.", "Electron microscopy revealed variable thickness of the glomerular basement membrane.", "Electron microscopy revealed reticulation of the glomerular basement membrane.", "Electron microscopy revealed irregular subepithelial protrusion of the lamina densa.", "Fine particles and electron-dense bodies were detected in the stratified basement membrane.", "Immunological staining for IgG, IgA, IgM, C3, C4, C1q, \u041a, and \u03bb was positive in four glomeruli.", "The signals were deposited in the vascular lumen and mesangial area in a granular or linear form.", "Three relatives had microscopic hematuria.", "A diagnosis of ATS was highly suspected.", "The patient and his children were recommended to undergo genetic testing.", "WES was performed.", "Genomic DNA was extracted from blood samples.", "The coverage of the target sequence was over 99.12%.", "The mean sequencing depth was approximately 147.", "A heterozygous substitution, NM_000091 c.2657-1G>A (p. V294fs), was found in intron 22 of the COL4A3 gene.", "The mutation was confirmed by Sanger sequencing.", "The mutation was excluded from the single nucleotide polymorphism database.", "The mutation was included in the ClinVar database.", "The mutation is located at an evolutionarily conserved splice site.", "The splicing mutation is thought to lead to the skipping of exon 23.", "The variant is classified as 'likely pathogenic' according to the American College of Medical Genetics and Genomics standards and guidelines."], "summary_subclaims": ["A Chinese family with ATS was recruited for the current study.", "Clinical characteristics of ATS patients were collected from medical records.", "Potential causative genes were explored by whole-exome sequencing.", "A heterozygous substitution in intron 22 of COL4A3 (NM_000091 c.2657-1G>A) was found in the patients.", "The heterozygous substitution in intron 22 of COL4A3 was further confirmed by quantitative polymerase chain reaction."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 33-year-old Chinese man.", "He had sustainable foamy urine for more than one year.", "He complained of intermittent hair loss.", "He had recurrence of oral ulcers.", "One year prior, he was hospitalized at a local hospital for the same reason.", "Routine urine tests indicated microscopic hematuria and proteinuria.", "He did not pay much attention.", "There was no further diagnosis or treatment.", "One month prior, his blood pressure rose to 145/91 mmHg.", "Microscopic hematuria and heavy proteinuria were again detected.", "The patient had no comorbidities.", "The patient's father had asymptomatic microscopic hematuria and proteinuria.", "The father's findings were detected in a routine physical examination approximately 2 years prior.", "The patient had a daughter and a son.", "The daughter had asymptomatic microscopic hematuria.", "The son had microscopic hematuria and proteinuria.", "The son had ever been diagnosed with chronic nephritis at a local hospital.", "The patient's systolic blood pressure was 141 mmHg.", "The patient's diastolic blood pressure was 90 mmHg.", "No obvious abnormality was detected during physical examination.", "No specific nervous system symptoms were recognized.", "No hearing impairments were detected.", "No symptoms were found in either eye.", "Microscopic hematuria and proteinuria were confirmed by urine tests.", "No obvious abnormality was detected by abdominal ultrasound.", "No obvious abnormality was detected by X-ray diagnosis.", "No obvious abnormality was detected by electrocardiographic examination.", "Heart echocardiography showed a small amount of pericardial effusion.", "A histopathology study of renal biopsy was performed.", "A total of 13 glomeruli were observed.", "One glomerulus was enlarged and lobulated.", "Para-aminosailcylic acid staining and Masson staining were positive.", "Mild mesangial matrix proliferation was observed.", "The basement membrane was thickened.", "Three glomerular fibroblastic crescents were observed.", "Pericystic fibrosis of glomeruli was observed.", "Deposition of erythrotropin under the endothelium of the capillary loop was detected.", "Electron microscopy revealed variable thickness of the glomerular basement membrane.", "Electron microscopy revealed reticulation of the glomerular basement membrane.", "Electron microscopy revealed irregular subepithelial protrusion of the lamina densa.", "Fine particles and electron-dense bodies were detected in the stratified basement membrane.", "Immunological staining for IgG, IgA, IgM, C3, C4, C1q, \u041a, and \u03bb was positive in four glomeruli.", "The signals were deposited in the vascular lumen and mesangial area in a granular or linear form.", "Three relatives had microscopic hematuria.", "A diagnosis of ATS was highly suspected.", "The patient and his children were recommended to undergo genetic testing.", "WES was performed.", "Genomic DNA was extracted from blood samples.", "The coverage of the target sequence was over 99.12%.", "The mean sequencing depth was approximately 147.", "A heterozygous substitution, NM_000091 c.2657-1G>A (p. V294fs), was found in intron 22 of the COL4A3 gene.", "The mutation was confirmed by Sanger sequencing.", "The mutation was excluded from the single nucleotide polymorphism database.", "The mutation was included in the ClinVar database.", "The mutation is located at an evolutionarily conserved splice site.", "The splicing mutation is thought to lead to the skipping of exon 23.", "The variant is classified as 'likely pathogenic' according to the American College of Medical Genetics and Genomics standards and guidelines."], "index": 132, "original_id": "multiclinsum_test_1061_en.txt", "split": "test", "summary_subclaims": ["A Chinese family with ATS was recruited for the current study.", "Clinical characteristics of ATS patients were collected from medical records.", "Potential causative genes were explored by whole-exome sequencing.", "A heterozygous substitution in intron 22 of COL4A3 (NM_000091 c.2657-1G>A) was found in the patients.", "The heterozygous substitution in intron 22 of COL4A3 was further confirmed by quantitative polymerase chain reaction."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was a 74-year-old male.", "He complained of blurred vision in both eyes because of senile cataract in October 2015.", "Visual acuities were 6/20 OD and 8/20 OS.", "Intraocular pressure was normal.", "Slit-lamp examination revealed mild cortical cataract OU.", "Fundus findings showed nothing of note.", "The initial ophthalmologist planned to perform cataract surgery for his right eye.", "He had a medical history of prostate hypertrophy.", "He had no history of dementia.", "Viscoelastic materials with high-level cohesion were injected into the anterior chamber to dilate the pupil due to miosis following hydrodissection OD.", "Severe thermal corneoscleral injury occurred soon after beginning the phacoemulsification.", "The wound was tightly sutured by pedunculated conjunctiva.", "Viscoelastic materials were injected again since the leakage was not suppressed.", "He was referred to our hospital the next day.", "Visual acuity was hand motion OD.", "Intraocular pressure was 3 mm Hg OD.", "There was marked corneal stromal opacity with intraocular fluid leakage.", "The scleral wound was found to be opening following conjunctival incision.", "Mobility of the sclera was markedly involved.", "It was impossible to conduct direct suture of the injured sclera.", "The patient underwent transplantation of a donor scleral graft using 10-0 nylon to the burn site.", "After the transplantation and confirmation of the absence of intraocular fluid leakage, the lens nucleus was extracted from the newly formed wound on the temporal side of the scald.", "Histologically, the injured sclera showed coagulation necrosis with eosinophilic materials.", "Attachment of the transplanted sclera was favorable.", "Intraocular pressure recovered to normal.", "Three months after the surgery, macular edema occurred due to intraocular inflammation caused by the remaining lens cortex.", "Anterior vitrectomy was conducted leading to the resolution of macular edema.", "An intraocular lens was eventually fixed in the ciliary sulcus 7 months later.", "The visual acuity improved to 2/20 OD with stable IOP and a reduced corneal opacity in October 2016."], "summary_subclaims": ["Severe thermal corneoscleral injury occurred during phacoemulsification in the right eye of a 74-year-old male.", "His medical history was prostate hypertrophy.", "Visual acuity was hand motion and the intraocular pressure was 3 mm Hg OD.", "There was heavy corneal stromal opacity with intraocular fluid leakage.", "The patient underwent transplantation of a donor scleral graft to the burn site.", "Histologically, the injured sclera showed coagulation necrosis without inflammatory cell infiltration.", "An intraocular lens was eventually fixed in the ciliary sulcus 7 months later.", "His visual acuity remains at 2/20 OD."]}, "extra_info": {"fulltext_subclaims": ["The patient was a 74-year-old male.", "He complained of blurred vision in both eyes because of senile cataract in October 2015.", "Visual acuities were 6/20 OD and 8/20 OS.", "Intraocular pressure was normal.", "Slit-lamp examination revealed mild cortical cataract OU.", "Fundus findings showed nothing of note.", "The initial ophthalmologist planned to perform cataract surgery for his right eye.", "He had a medical history of prostate hypertrophy.", "He had no history of dementia.", "Viscoelastic materials with high-level cohesion were injected into the anterior chamber to dilate the pupil due to miosis following hydrodissection OD.", "Severe thermal corneoscleral injury occurred soon after beginning the phacoemulsification.", "The wound was tightly sutured by pedunculated conjunctiva.", "Viscoelastic materials were injected again since the leakage was not suppressed.", "He was referred to our hospital the next day.", "Visual acuity was hand motion OD.", "Intraocular pressure was 3 mm Hg OD.", "There was marked corneal stromal opacity with intraocular fluid leakage.", "The scleral wound was found to be opening following conjunctival incision.", "Mobility of the sclera was markedly involved.", "It was impossible to conduct direct suture of the injured sclera.", "The patient underwent transplantation of a donor scleral graft using 10-0 nylon to the burn site.", "After the transplantation and confirmation of the absence of intraocular fluid leakage, the lens nucleus was extracted from the newly formed wound on the temporal side of the scald.", "Histologically, the injured sclera showed coagulation necrosis with eosinophilic materials.", "Attachment of the transplanted sclera was favorable.", "Intraocular pressure recovered to normal.", "Three months after the surgery, macular edema occurred due to intraocular inflammation caused by the remaining lens cortex.", "Anterior vitrectomy was conducted leading to the resolution of macular edema.", "An intraocular lens was eventually fixed in the ciliary sulcus 7 months later.", "The visual acuity improved to 2/20 OD with stable IOP and a reduced corneal opacity in October 2016."], "index": 150, "original_id": "multiclinsum_test_1564_en.txt", "split": "test", "summary_subclaims": ["Severe thermal corneoscleral injury occurred during phacoemulsification in the right eye of a 74-year-old male.", "His medical history was prostate hypertrophy.", "Visual acuity was hand motion and the intraocular pressure was 3 mm Hg OD.", "There was heavy corneal stromal opacity with intraocular fluid leakage.", "The patient underwent transplantation of a donor scleral graft to the burn site.", "Histologically, the injured sclera showed coagulation necrosis without inflammatory cell infiltration.", "An intraocular lens was eventually fixed in the ciliary sulcus 7 months later.", "His visual acuity remains at 2/20 OD."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was a 23-year-old critically-ill male.", "He had a history of Burkitt\u2019s lymphoma.", "He had graft-versus-host disease requiring high-dose corticosteroids.", "He was admitted after 2 days of somnolence and confusion.", "He had evolving respiratory distress requiring endotracheal intubation.", "On admission, he would open eyes to painful stimuli.", "On admission, he continued to follow commands.", "Initial CT head showed a flame hemorrhage in the left gyrus rectus.", "The flame hemorrhage was suspicious for vascular origin.", "A hypodensity in the left thalamus was suspicious for an established infarction.", "An angiogram demonstrated six fusiform aneurysms.", "Three aneurysms were at the frontopolar branch of the left anterior cerebral artery.", "One aneurysm was at the orbitofrontal branch of the left anterior cerebral artery.", "One aneurysm was at the frontopolar branch of the right anterior cerebral artery.", "One aneurysm was at the anterior temporal artery of the left middle cerebral artery.", "Body imaging revealed cavitary lung lesions.", "The patient was started on broad spectrum antibiotics.", "The patient was started on antifungals.", "The patient was started on antiviral medications.", "The location of hemorrhage pointed to the left ACA branch aneurysms as the source.", "Surgery was chosen to allow for inspection of all lesions under direct vision.", "Surgery was chosen to obtain tissue for microbiological purposes.", "A bicoronal craniotomy, parent vessel sacrifice, and excision of the three aneurysms arising from the left ACA were performed on postbleed day 2.", "Intraoperatively, the aneurysms were friable, thin walled, and prone to bleeding.", "The right ACA aneurysms were managed conservatively.", "Microbiology confirmed angioinvasive S. apiospermum infection.", "Vericonazole, amphotericin B, and caspofunging were started empirically.", "Vericonazole, amphotericin B, and caspofunging were continued throughout the disease process.", "A CT scan on postbleed day 4 revealed new left frontal intracerebral hemorrhage.", "A CT scan on postbleed day 4 revealed intraventricular hemorrhage.", "An emergency external ventricular drain was placed.", "A follow-up angiogram revealed interval growth of the left orbitofrontal artery aneurysm.", "Endovascular parent vessel occlusion was recommended.", "Endovascular parent vessel occlusion was performed uneventfully.", "An interval angiogram on postbleed day 7 demonstrated three new fusiform aneurysms of the right ACA.", "An interval angiogram on postbleed day 7 demonstrated a new aneurysm of the left anterior choroidal artery.", "An interval angiogram on postbleed day 7 demonstrated a new aneurysm of the left posterior communicating artery.", "The interval angiogram on postbleed day 7 confirmed a stable appearing left anterior temporal artery aneurysm.", "A3\u2013A3 revascularization was attempted to avoid ACA sacrifice.", "A3\u2013A3 revascularization was unsuccessful.", "Parent vessel sacrifice had to be performed.", "An intraoperative angiogram demonstrated a new anterior communicating artery aneurysm.", "The ACOMA aneurysm was left untreated at the time of surgery.", "On further follow-up imaging, the ACOMA aneurysm continued to enlarge.", "The ACOMA aneurysm was treated with endovascular A1 occlusions on postbleed day 9.", "Surveillance imaging demonstrated interval growth of the previously identified left AChA aneurysm.", "The left AChA aneurysm was ultimately treated with parent vessel sacrifice.", "Surveillance imaging demonstrated interval growth of the previously identified left PCOMA aneurysm.", "The left PCOMA aneurysm was ultimately treated with parent vessel sacrifice.", "Despite multiple parent vessel sacrifices, the patient recovered neurologically.", "The patient continued to follow commands with upper extremities.", "The patient had severe paraparesis in the lower extremities.", "Follow-up MRI confirmed a thalamic infarct.", "The thalamic infarct was already seen on admission imaging.", "Follow-up MRI showed new, incomplete ACA territory infarctions.", "The infarctions were in keeping with previous surgeries and parent vessel sacrifice of the bilateral ACAs.", "The patient remained intubated and ventilated.", "The patient underwent a tracheostomy procedure.", "The patient had septic shock from multidrug resistant pseudomonas superinfection.", "The patient died 6 months after the hemorrhagic presentation."], "summary_subclaims": ["The patient was a 23-year-old with Burkitt's lymphoma and graft-versus-host disease.", "The patient was admitted with intracerebral hemorrhage.", "The patient had 12 anterior circulation aneurysms from disseminated Scedosporium infection.", "The patient died 6 months later from multiorgan failure.", "The notable feature of this case is the rapid angioinvasiveness of the infection.", "New aneurysms formed within days of clear angiographic imaging.", "There was an apparent lack of skull base osteomyelitis."]}, "extra_info": {"fulltext_subclaims": ["The patient was a 23-year-old critically-ill male.", "He had a history of Burkitt\u2019s lymphoma.", "He had graft-versus-host disease requiring high-dose corticosteroids.", "He was admitted after 2 days of somnolence and confusion.", "He had evolving respiratory distress requiring endotracheal intubation.", "On admission, he would open eyes to painful stimuli.", "On admission, he continued to follow commands.", "Initial CT head showed a flame hemorrhage in the left gyrus rectus.", "The flame hemorrhage was suspicious for vascular origin.", "A hypodensity in the left thalamus was suspicious for an established infarction.", "An angiogram demonstrated six fusiform aneurysms.", "Three aneurysms were at the frontopolar branch of the left anterior cerebral artery.", "One aneurysm was at the orbitofrontal branch of the left anterior cerebral artery.", "One aneurysm was at the frontopolar branch of the right anterior cerebral artery.", "One aneurysm was at the anterior temporal artery of the left middle cerebral artery.", "Body imaging revealed cavitary lung lesions.", "The patient was started on broad spectrum antibiotics.", "The patient was started on antifungals.", "The patient was started on antiviral medications.", "The location of hemorrhage pointed to the left ACA branch aneurysms as the source.", "Surgery was chosen to allow for inspection of all lesions under direct vision.", "Surgery was chosen to obtain tissue for microbiological purposes.", "A bicoronal craniotomy, parent vessel sacrifice, and excision of the three aneurysms arising from the left ACA were performed on postbleed day 2.", "Intraoperatively, the aneurysms were friable, thin walled, and prone to bleeding.", "The right ACA aneurysms were managed conservatively.", "Microbiology confirmed angioinvasive S. apiospermum infection.", "Vericonazole, amphotericin B, and caspofunging were started empirically.", "Vericonazole, amphotericin B, and caspofunging were continued throughout the disease process.", "A CT scan on postbleed day 4 revealed new left frontal intracerebral hemorrhage.", "A CT scan on postbleed day 4 revealed intraventricular hemorrhage.", "An emergency external ventricular drain was placed.", "A follow-up angiogram revealed interval growth of the left orbitofrontal artery aneurysm.", "Endovascular parent vessel occlusion was recommended.", "Endovascular parent vessel occlusion was performed uneventfully.", "An interval angiogram on postbleed day 7 demonstrated three new fusiform aneurysms of the right ACA.", "An interval angiogram on postbleed day 7 demonstrated a new aneurysm of the left anterior choroidal artery.", "An interval angiogram on postbleed day 7 demonstrated a new aneurysm of the left posterior communicating artery.", "The interval angiogram on postbleed day 7 confirmed a stable appearing left anterior temporal artery aneurysm.", "A3\u2013A3 revascularization was attempted to avoid ACA sacrifice.", "A3\u2013A3 revascularization was unsuccessful.", "Parent vessel sacrifice had to be performed.", "An intraoperative angiogram demonstrated a new anterior communicating artery aneurysm.", "The ACOMA aneurysm was left untreated at the time of surgery.", "On further follow-up imaging, the ACOMA aneurysm continued to enlarge.", "The ACOMA aneurysm was treated with endovascular A1 occlusions on postbleed day 9.", "Surveillance imaging demonstrated interval growth of the previously identified left AChA aneurysm.", "The left AChA aneurysm was ultimately treated with parent vessel sacrifice.", "Surveillance imaging demonstrated interval growth of the previously identified left PCOMA aneurysm.", "The left PCOMA aneurysm was ultimately treated with parent vessel sacrifice.", "Despite multiple parent vessel sacrifices, the patient recovered neurologically.", "The patient continued to follow commands with upper extremities.", "The patient had severe paraparesis in the lower extremities.", "Follow-up MRI confirmed a thalamic infarct.", "The thalamic infarct was already seen on admission imaging.", "Follow-up MRI showed new, incomplete ACA territory infarctions.", "The infarctions were in keeping with previous surgeries and parent vessel sacrifice of the bilateral ACAs.", "The patient remained intubated and ventilated.", "The patient underwent a tracheostomy procedure.", "The patient had septic shock from multidrug resistant pseudomonas superinfection.", "The patient died 6 months after the hemorrhagic presentation."], "index": 152, "original_id": "multiclinsum_test_2127_en.txt", "split": "test", "summary_subclaims": ["The patient was a 23-year-old with Burkitt's lymphoma and graft-versus-host disease.", "The patient was admitted with intracerebral hemorrhage.", "The patient had 12 anterior circulation aneurysms from disseminated Scedosporium infection.", "The patient died 6 months later from multiorgan failure.", "The notable feature of this case is the rapid angioinvasiveness of the infection.", "New aneurysms formed within days of clear angiographic imaging.", "There was an apparent lack of skull base osteomyelitis."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["A 41-year-old Chinese man presented with palpable right breast lumps for 1 year.", "On physical examination, a large retroareolar hard nontender mass approximately 4.5 cm in size was palpated over the right breast.", "The mass was nonmobile and superficial but did not have any overlying skin findings.", "A smaller adjacent mobile and nontender lesion, approximately 3 cm, was palpated just medial to the first mass.", "Initial laboratory evaluation was normal for prolactin, estradiol, luteinizing and follicle-stimulating hormone levels.", "He had never previously been treated with radiation, according to his past medical history.", "Conventional mammography was performed on Flat III (Metaltronica Company, Rome, Italy).", "Mammography showed a subcutaneous oval mass with a smooth and sharp margin on his right breast.", "Another small oval mass with a less well-defined margin was seen adjacent to the main lesion.", "MR imaging was performed on a 1.5 T Signa Infinity TwinSpeed MR scanner (GE Company, Milwaukee, WI, USA).", "The examination comprised of routine T1- and T2-weighted fast spin echo (FSE) sequences in axial and sagittal planes.", "T1- and T2-weighted imaging fat-suppressed in axial and sagittal planes, respectively.", "On T1-weighted imaging, the lesions were predominantly hypointense to subcutaneous fat and mildly hyperintense to the pectoralis major muscle.", "On T2-weighted imaging, the lesions were of a higher signal than the subcutaneous fat.", "The larger lesion had a smooth contour and well defined borders on all sequences.", "On T2-weighted images, the larger lesion had a lower signal central region.", "Along the border of the larger lesion, there was a distinct rim of decrease in signal between the lesion and fat interface.", "The small lesion had a less poorly defined border on conventional T2 weighted images.", "On the fat-suppressed sequences, both lesions had better depiction for the margins and borders.", "There was a mild mass effect of the dominant lesion on the underlying pectoralis major muscle.", "The gross pathology of the specimens after surgery showed a yellowish tanned smooth surface mass measuring 4.5 cm \u00d7 3.0 cm \u00d7 2.0 cm.", "A smaller lesion with similar features measuring 2.5 cm \u00d7 2.0 cm \u00d7 1.0 cm was also found.", "Histologic specimens showed high cellularity monomorphic slender spindle cells arrayed in a storiform pattern.", "The spindle cells were aligned at right angles to small vessels and collagen fibers intermixed with scattered adipose tissue.", "The nuclei of the spindle cells were well differentiated with only rare mitotic figures.", "The larger mass had a fibrous envelope and plentiful collagen fibers in the central region.", "The smaller mass lacked the fibrous envelope.", "There was positive immunohistologic staining for vimentin and cluster of differentiation (CD) 34.", "There was negative immunohistologic staining for b-cell leukemia-lymphoma (Bcl-2), S-100 protein, smooth muscle actin (SMA), desmin and epithelial membrane antigen (EMA)."], "summary_subclaims": ["The patient is a 41-year-old Chinese man.", "The patient initially presented with a palpable lump.", "A mammogram showed two lesions in the right breast.", "One lesion had a well circumscribed border.", "The other lesion had an ill defined border.", "Conventional magnetic resonance imaging was performed.", "The well defined larger lesion showed mild central hypointensity.", "The smaller lesion had an irregular border.", "Both lesions were well characterized on the fat-suppressed sequences."]}, "extra_info": {"fulltext_subclaims": ["A 41-year-old Chinese man presented with palpable right breast lumps for 1 year.", "On physical examination, a large retroareolar hard nontender mass approximately 4.5 cm in size was palpated over the right breast.", "The mass was nonmobile and superficial but did not have any overlying skin findings.", "A smaller adjacent mobile and nontender lesion, approximately 3 cm, was palpated just medial to the first mass.", "Initial laboratory evaluation was normal for prolactin, estradiol, luteinizing and follicle-stimulating hormone levels.", "He had never previously been treated with radiation, according to his past medical history.", "Conventional mammography was performed on Flat III (Metaltronica Company, Rome, Italy).", "Mammography showed a subcutaneous oval mass with a smooth and sharp margin on his right breast.", "Another small oval mass with a less well-defined margin was seen adjacent to the main lesion.", "MR imaging was performed on a 1.5 T Signa Infinity TwinSpeed MR scanner (GE Company, Milwaukee, WI, USA).", "The examination comprised of routine T1- and T2-weighted fast spin echo (FSE) sequences in axial and sagittal planes.", "T1- and T2-weighted imaging fat-suppressed in axial and sagittal planes, respectively.", "On T1-weighted imaging, the lesions were predominantly hypointense to subcutaneous fat and mildly hyperintense to the pectoralis major muscle.", "On T2-weighted imaging, the lesions were of a higher signal than the subcutaneous fat.", "The larger lesion had a smooth contour and well defined borders on all sequences.", "On T2-weighted images, the larger lesion had a lower signal central region.", "Along the border of the larger lesion, there was a distinct rim of decrease in signal between the lesion and fat interface.", "The small lesion had a less poorly defined border on conventional T2 weighted images.", "On the fat-suppressed sequences, both lesions had better depiction for the margins and borders.", "There was a mild mass effect of the dominant lesion on the underlying pectoralis major muscle.", "The gross pathology of the specimens after surgery showed a yellowish tanned smooth surface mass measuring 4.5 cm \u00d7 3.0 cm \u00d7 2.0 cm.", "A smaller lesion with similar features measuring 2.5 cm \u00d7 2.0 cm \u00d7 1.0 cm was also found.", "Histologic specimens showed high cellularity monomorphic slender spindle cells arrayed in a storiform pattern.", "The spindle cells were aligned at right angles to small vessels and collagen fibers intermixed with scattered adipose tissue.", "The nuclei of the spindle cells were well differentiated with only rare mitotic figures.", "The larger mass had a fibrous envelope and plentiful collagen fibers in the central region.", "The smaller mass lacked the fibrous envelope.", "There was positive immunohistologic staining for vimentin and cluster of differentiation (CD) 34.", "There was negative immunohistologic staining for b-cell leukemia-lymphoma (Bcl-2), S-100 protein, smooth muscle actin (SMA), desmin and epithelial membrane antigen (EMA)."], "index": 135, "original_id": "multiclinsum_test_1990_en.txt", "split": "test", "summary_subclaims": ["The patient is a 41-year-old Chinese man.", "The patient initially presented with a palpable lump.", "A mammogram showed two lesions in the right breast.", "One lesion had a well circumscribed border.", "The other lesion had an ill defined border.", "Conventional magnetic resonance imaging was performed.", "The well defined larger lesion showed mild central hypointensity.", "The smaller lesion had an irregular border.", "Both lesions were well characterized on the fat-suppressed sequences."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["A 70-year-old male patient visited our clinic because of poor cognitive function and gait disturbance.", "He was diagnosed with encephalitis following scrub typhus 23 years ago.", "The patient complained of poor memory.", "He was initially admitted to a local hospital with a high fever and headache 23 years ago.", "He developed neurological symptoms as mental change, visual disturbance, and weakness, according to medical history.", "The first MRI was conducted 7-d after onset.", "The diagnosis of scrub typhus encephalitis was confirmed.", "No special previous medical history was reported.", "No special personal and family histories were found.", "Physical examination revealed narrow visual fields.", "He could read books and newspapers.", "His motor power on both extremities was intact without any pain.", "Fine movements of the left hand were poor.", "He could only manage to walk indoors because of sensory impairment.", "Handgrip strength (right/left, kg) was 32.3/31.3.", "Two-point discrimination test (right/left, mm) was 5/absence.", "Monofilament test (right/left, mm) was 3.22/absence.", "The patient had impaired cognition, with a mini-mental status examination score of 14.", "The patient had impaired cognition, with a Montreal cognitive assessment score of 10[-].", "We performed a computerized neuropsychological test.", "DTI data were acquired with a 3.0 T scanner Intera (Philips, Ltd., Best, The Netherlands) with a six-channel head coil and single-shot echo-planar imaging.", "For each of the 32 non-collinear diffusion-sensitizing gradients, we acquired 80 contiguous slices parallel to the anterior commissure-posterior commissure line.", "The imaging parameters were as follows: acquisition matrix = 112 \u00d7 112, field of view = 224 mm \u00d7 224 mm, TR/TE = 8973/80 ms, parallel imaging reduction factor (SENSE factor) = 2, EPI factor = 49, b = 1000 s/mm2, NEX = 2, and slice thickness = 2.0 mm (acquired voxel size = 2 mm \u00d7 2 mm \u00d7 2 mm).", "Analysis of the DTI data was performed using the Oxford Centre for Functional Magnetic Resonance Imaging of the Brain (FMRIB) Software Library (FSL: ) based on the probabilistic tractography method.", "Head motion artifacts and image distortion due to eddy current were corrected by affine multiscale two-dimensional registration.", "The 7-d MRI onset showed small lesions in the left frontal and parietal lobes, and large lesions in the right superior parietal lobule and both occipital lobes.", "Compared with the 7-d MRI, the 23-year MRI findings indicated expanded lesions of encephalomalacia with marked dilation of both ventricles.", "Probabilistic DTT of the Papez circuit revealed that the left thalamocortical tract and right mammillothalamic tract could not be reconstructed.", "The anterior part of the fornix was found to be injured.", "Both CSTs were well preserved."], "summary_subclaims": ["The patient was affected by encephalitis caused by scrub typhus that occurred 23 years ago.", "The patient had poor cognition.", "The Mini-Mental Status Examination score was 14.", "Handgrip strength was 32.3 kg on the right and 31.3 kg on the left.", "DTT revealed serious injuries of the left thalamocingulate tract.", "DTT revealed serious injuries of the right mammillothalamic tract in the Papez circuit.", "DTT showed a partial injury of the anterior part of the fornix."]}, "extra_info": {"fulltext_subclaims": ["A 70-year-old male patient visited our clinic because of poor cognitive function and gait disturbance.", "He was diagnosed with encephalitis following scrub typhus 23 years ago.", "The patient complained of poor memory.", "He was initially admitted to a local hospital with a high fever and headache 23 years ago.", "He developed neurological symptoms as mental change, visual disturbance, and weakness, according to medical history.", "The first MRI was conducted 7-d after onset.", "The diagnosis of scrub typhus encephalitis was confirmed.", "No special previous medical history was reported.", "No special personal and family histories were found.", "Physical examination revealed narrow visual fields.", "He could read books and newspapers.", "His motor power on both extremities was intact without any pain.", "Fine movements of the left hand were poor.", "He could only manage to walk indoors because of sensory impairment.", "Handgrip strength (right/left, kg) was 32.3/31.3.", "Two-point discrimination test (right/left, mm) was 5/absence.", "Monofilament test (right/left, mm) was 3.22/absence.", "The patient had impaired cognition, with a mini-mental status examination score of 14.", "The patient had impaired cognition, with a Montreal cognitive assessment score of 10[-].", "We performed a computerized neuropsychological test.", "DTI data were acquired with a 3.0 T scanner Intera (Philips, Ltd., Best, The Netherlands) with a six-channel head coil and single-shot echo-planar imaging.", "For each of the 32 non-collinear diffusion-sensitizing gradients, we acquired 80 contiguous slices parallel to the anterior commissure-posterior commissure line.", "The imaging parameters were as follows: acquisition matrix = 112 \u00d7 112, field of view = 224 mm \u00d7 224 mm, TR/TE = 8973/80 ms, parallel imaging reduction factor (SENSE factor) = 2, EPI factor = 49, b = 1000 s/mm2, NEX = 2, and slice thickness = 2.0 mm (acquired voxel size = 2 mm \u00d7 2 mm \u00d7 2 mm).", "Analysis of the DTI data was performed using the Oxford Centre for Functional Magnetic Resonance Imaging of the Brain (FMRIB) Software Library (FSL: ) based on the probabilistic tractography method.", "Head motion artifacts and image distortion due to eddy current were corrected by affine multiscale two-dimensional registration.", "The 7-d MRI onset showed small lesions in the left frontal and parietal lobes, and large lesions in the right superior parietal lobule and both occipital lobes.", "Compared with the 7-d MRI, the 23-year MRI findings indicated expanded lesions of encephalomalacia with marked dilation of both ventricles.", "Probabilistic DTT of the Papez circuit revealed that the left thalamocortical tract and right mammillothalamic tract could not be reconstructed.", "The anterior part of the fornix was found to be injured.", "Both CSTs were well preserved."], "index": 148, "original_id": "multiclinsum_test_1723_en.txt", "split": "test", "summary_subclaims": ["The patient was affected by encephalitis caused by scrub typhus that occurred 23 years ago.", "The patient had poor cognition.", "The Mini-Mental Status Examination score was 14.", "Handgrip strength was 32.3 kg on the right and 31.3 kg on the left.", "DTT revealed serious injuries of the left thalamocingulate tract.", "DTT revealed serious injuries of the right mammillothalamic tract in the Papez circuit.", "DTT showed a partial injury of the anterior part of the fornix."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 74-year-old female.", "The patient presented with an abnormal shadow on chest computed tomography (CT) at a medical checkup.", "Chest CT showed a 17 mm \u00d7 8 mm ground-glass opacity with approximately 30% solid component in the right superior segment (S6).", "The patient had undergone radical treatment of right breast cancer staged at pT2N0M0 IIA.", "The patient had four cycles of postoperative adjuvant chemotherapy 11 years prior.", "A thoracoscopic right S6 segmentectomy was planned.", "We performed thoracoscopic surgery using two ports.", "We made a 2-cm incision in the 7th intercostal space of the right midaxillary line as the observation hole.", "We made a 4-cm incision in the 4th intercostal space of the right anterior axillary line as the operating hole.", "Pleural adhesions were observed throughout the thoracic cavity perioperatively.", "The horizontal and posterior oblique fissures were poorly developed.", "The intersegmental plane could not be distinguished.", "Digital palpation indicated that the nodule was located in a high position.", "The interlobar fissures were separated.", "The posterior segmental and superior segmental arteries were located following the pulmonary trunk arteries.", "The nodule was eventually found in the S2 of the right upper lobe.", "The recurrent and ascending arteries were dissociated and resected.", "The posterior segmental bronchus (B2) was exposed and transected.", "The intersegmental plane was divided along the inflation-deflation line using the endostaplers.", "Resection of the S2 of the right upper lobe was completed.", "The tumor was 3 cm away from the incisal margin.", "Intraoperative pathology analysis revealed minimally invasive adenocarcinoma (MIA).", "Hilar lymph node sampling was performed.", "On postoperative day 2, the right lung was completely redilated on CT.", "Postoperative pathological examination revealed MIA with negative surrounding lymph nodes.", "We reviewed lung CT images and performed three-dimensional (3D) reconstructions using Mimics Medical 21.0 software postoperatively.", "The B2 originated from the bronchus intermedius.", "The posterior segmental artery (A2) of the right upper lung lobe bifurcated into the A2a and A2b branching from the recurrent and ascending arteries, respectively.", "The right superior pulmonary vein had no central vein but a posterior intrasegmental vein (V2t) that travelled below the S2."], "summary_subclaims": ["We report a case of thoracoscopic resection of the posterior segment of the right upper lobe of the lung.", "Preoperatively, the nodule was believed to be located in the superior segment of the right lower lobe.", "Intraoperative exploration revealed that the nodule was located in the posterior segment of the right upper lobe.", "The bronchi of the posterior segment of the right lung opened into the bronchus intermedius.", "The procedure was completed uneventfully.", "Postoperative retrospective three-dimensional (3D) reconstruction of the lung CT images confirmed that the bronchi of the posterior segment of the right upper lobe originated from the bronchus intermedius."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 74-year-old female.", "The patient presented with an abnormal shadow on chest computed tomography (CT) at a medical checkup.", "Chest CT showed a 17 mm \u00d7 8 mm ground-glass opacity with approximately 30% solid component in the right superior segment (S6).", "The patient had undergone radical treatment of right breast cancer staged at pT2N0M0 IIA.", "The patient had four cycles of postoperative adjuvant chemotherapy 11 years prior.", "A thoracoscopic right S6 segmentectomy was planned.", "We performed thoracoscopic surgery using two ports.", "We made a 2-cm incision in the 7th intercostal space of the right midaxillary line as the observation hole.", "We made a 4-cm incision in the 4th intercostal space of the right anterior axillary line as the operating hole.", "Pleural adhesions were observed throughout the thoracic cavity perioperatively.", "The horizontal and posterior oblique fissures were poorly developed.", "The intersegmental plane could not be distinguished.", "Digital palpation indicated that the nodule was located in a high position.", "The interlobar fissures were separated.", "The posterior segmental and superior segmental arteries were located following the pulmonary trunk arteries.", "The nodule was eventually found in the S2 of the right upper lobe.", "The recurrent and ascending arteries were dissociated and resected.", "The posterior segmental bronchus (B2) was exposed and transected.", "The intersegmental plane was divided along the inflation-deflation line using the endostaplers.", "Resection of the S2 of the right upper lobe was completed.", "The tumor was 3 cm away from the incisal margin.", "Intraoperative pathology analysis revealed minimally invasive adenocarcinoma (MIA).", "Hilar lymph node sampling was performed.", "On postoperative day 2, the right lung was completely redilated on CT.", "Postoperative pathological examination revealed MIA with negative surrounding lymph nodes.", "We reviewed lung CT images and performed three-dimensional (3D) reconstructions using Mimics Medical 21.0 software postoperatively.", "The B2 originated from the bronchus intermedius.", "The posterior segmental artery (A2) of the right upper lung lobe bifurcated into the A2a and A2b branching from the recurrent and ascending arteries, respectively.", "The right superior pulmonary vein had no central vein but a posterior intrasegmental vein (V2t) that travelled below the S2."], "index": 141, "original_id": "multiclinsum_test_2891_en.txt", "split": "test", "summary_subclaims": ["We report a case of thoracoscopic resection of the posterior segment of the right upper lobe of the lung.", "Preoperatively, the nodule was believed to be located in the superior segment of the right lower lobe.", "Intraoperative exploration revealed that the nodule was located in the posterior segment of the right upper lobe.", "The bronchi of the posterior segment of the right lung opened into the bronchus intermedius.", "The procedure was completed uneventfully.", "Postoperative retrospective three-dimensional (3D) reconstruction of the lung CT images confirmed that the bronchi of the posterior segment of the right upper lobe originated from the bronchus intermedius."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["A 19-year-old male was admitted to the Department of Plastic, hand and reconstructive surgery.", "The patient had persistant dysaesthesia of the median nerve-supplied area.", "The patient had a soft tissue laceration of the palmar wrist.", "The injury occurred following a wakeboarding accident three days before admission.", "The patient was wakeboarding on the largest German artificial wakeboarding circled nylon cable system.", "The automatic nylon cable system stopped immediately due to an overlapping wire.", "The male wakeboarder dived in the lake and got struck in the loose nylon cable system with his trunk and the hand.", "The nylon cable system was activated by chance and he was pulled 1/4 of the radius of the lake with a speed of 40 km/h.", "The patient suffered a strangulation of his wrist with immediate numbness of the median-nerve supplied area of the left hand.", "The patient had a laceration of the palmar aspect of the wrist covering 0.5 \u00d7 5 cm tissue size.", "At admission in a rural hospital, the two-point discrimination was > 15 mm for the entire interdigital nerves N1\u2013N7 of the left hand.", "The ulnar nerve was found without any pathology.", "The patient could not perform a wrist flexion.", "Wrist extension was possible.", "The capillary refill was 1s for all five fingertips.", "No distinct pain in the snuff box area was evident on admission.", "The left elbow joint had full range of motion.", "Supination and pronation were limited due to persistent pain at the wrist level.", "The patient was transferred three days after the initial injury with persistent clinical lesion of the median nerve.", "Conventional x-ray of the hand and the wrist found regular articulation without an evident bony lesion.", "No disruption of the scapular-lunar ligament was noted.", "Computer tomography of the wrist and the hand proved regular bony structures.", "In the operating room, dorsal compartment pressure of the forearm was 19 mmHg.", "In the operating room, palmar compartment pressure of the flexor carpi ulnaris muscle was 16 mmHg.", "The median nerve, 72 hours after the initial strangulation injury, appeared with hyperaemia and moderate swelling.", "The median nerve had limited haematoma in the carpal tunnel.", "The palmar branch of the median nerve was surrounded by a significant haematoma.", "The haematoma surrounding the palmar branch of the median nerve was evacuated.", "The ulnar nerve was inspected and found without any significant signs of injury or haematoma.", "The laceration area was excised completely.", "The skin could be closed primarily without compression.", "One subcutaneous drainage was inserted.", "On postoperative day 1, the patient regained the sensory function of the hand following 72 hours of acute carpal tunnel syndrome with median nerve contusion.", "On postoperative day 1, the patient had remaining dysaesthesia of the thenar skin supplied by the palmar branch of the median nerve.", "On postoperative day 5, the patient was discharged home after an uneventful postoperative course.", "The patient complained of minor dysaesthesias in the thenar area.", "The patient was advised to recover for a total of four weeks before returning to sport."], "summary_subclaims": ["The palmar branch of the median nerve was surrounded by a significant haematoma.", "The palmar branch of the median nerve had strangulation damage.", "The palmar branch of the median nerve is more superficially located in contrast to the median nerve."]}, "extra_info": {"fulltext_subclaims": ["A 19-year-old male was admitted to the Department of Plastic, hand and reconstructive surgery.", "The patient had persistant dysaesthesia of the median nerve-supplied area.", "The patient had a soft tissue laceration of the palmar wrist.", "The injury occurred following a wakeboarding accident three days before admission.", "The patient was wakeboarding on the largest German artificial wakeboarding circled nylon cable system.", "The automatic nylon cable system stopped immediately due to an overlapping wire.", "The male wakeboarder dived in the lake and got struck in the loose nylon cable system with his trunk and the hand.", "The nylon cable system was activated by chance and he was pulled 1/4 of the radius of the lake with a speed of 40 km/h.", "The patient suffered a strangulation of his wrist with immediate numbness of the median-nerve supplied area of the left hand.", "The patient had a laceration of the palmar aspect of the wrist covering 0.5 \u00d7 5 cm tissue size.", "At admission in a rural hospital, the two-point discrimination was > 15 mm for the entire interdigital nerves N1\u2013N7 of the left hand.", "The ulnar nerve was found without any pathology.", "The patient could not perform a wrist flexion.", "Wrist extension was possible.", "The capillary refill was 1s for all five fingertips.", "No distinct pain in the snuff box area was evident on admission.", "The left elbow joint had full range of motion.", "Supination and pronation were limited due to persistent pain at the wrist level.", "The patient was transferred three days after the initial injury with persistent clinical lesion of the median nerve.", "Conventional x-ray of the hand and the wrist found regular articulation without an evident bony lesion.", "No disruption of the scapular-lunar ligament was noted.", "Computer tomography of the wrist and the hand proved regular bony structures.", "In the operating room, dorsal compartment pressure of the forearm was 19 mmHg.", "In the operating room, palmar compartment pressure of the flexor carpi ulnaris muscle was 16 mmHg.", "The median nerve, 72 hours after the initial strangulation injury, appeared with hyperaemia and moderate swelling.", "The median nerve had limited haematoma in the carpal tunnel.", "The palmar branch of the median nerve was surrounded by a significant haematoma.", "The haematoma surrounding the palmar branch of the median nerve was evacuated.", "The ulnar nerve was inspected and found without any significant signs of injury or haematoma.", "The laceration area was excised completely.", "The skin could be closed primarily without compression.", "One subcutaneous drainage was inserted.", "On postoperative day 1, the patient regained the sensory function of the hand following 72 hours of acute carpal tunnel syndrome with median nerve contusion.", "On postoperative day 1, the patient had remaining dysaesthesia of the thenar skin supplied by the palmar branch of the median nerve.", "On postoperative day 5, the patient was discharged home after an uneventful postoperative course.", "The patient complained of minor dysaesthesias in the thenar area.", "The patient was advised to recover for a total of four weeks before returning to sport."], "index": 137, "original_id": "multiclinsum_test_2648_en.txt", "split": "test", "summary_subclaims": ["The palmar branch of the median nerve was surrounded by a significant haematoma.", "The palmar branch of the median nerve had strangulation damage.", "The palmar branch of the median nerve is more superficially located in contrast to the median nerve."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["A 23-year-old female presented to our eye clinic with chief complaint of mild blurring of vision in the right eye.", "The patient denied any previous history of ocular inflammation.", "The patient denied any previous history of trauma.", "The patient denied any previous history of surgery.", "The patient denied any previous history of use of topical or systemic medications.", "Snellen\u2019s visual acuity in the right eye was 0.05.", "Snellen\u2019s visual acuity in the right eye was corrected to 0.5 with \u22123.00 to 2.00 \u00d7 15.", "Snellen\u2019s visual acuity in the left eye was 0.5.", "Snellen\u2019s visual acuity in the left eye was corrected to 0.8 with plano \u22120.75 \u00d7 170.", "Intraocular pressure was 14 mm Hg in the right eye.", "Intraocular pressure was 14 mm Hg in the left eye.", "Slit-lamp examination of the right eye anterior segment showed clear cornea.", "Slit-lamp examination of the right eye anterior segment showed deep and quiet anterior chamber.", "Slit-lamp examination of the right eye anterior segment showed no iris transillumination defects.", "Crystalline lens anterior capsular showed confluent pigment deposits stellate in shape over the pupillary axis.", "Dilation of the right eye pupil showed no pigment deposits in the peripheral capsule.", "Dilation of the right eye pupil showed no pigment deposits on the posterior lens capsule.", "Dilation of the right eye pupil showed no pigment deposits on the anterior hyaloid face.", "The examination of the left eye anterior segment was within normal limits before and after dilation.", "Gonioscopy revealed open angle with mild pigmentation and prominent iris processes of the right eye.", "Ophthalmic examination of the posterior segment was normal in both eyes.", "The patient was reassured and prescribed glasses.", "The patient was booked for regular follow-up.", "Following discussion with the patient, she opted to have transepithelial photorefractive keratectomy for the right eye myopic astigmatism.", "Transepithelial photorefractive keratectomy improved her unaided vision to 0.8.", "Based on her previous ophthalmic history and slit-lamp examination of the right eye, a diagnosis of unilateral congenital lenticular pigmentation was made."], "summary_subclaims": ["The patient is a 23-year-old female.", "The patient presented with mild blurring of vision in the right eye.", "The patient inquired about refractive surgery.", "The patient denied any previous history of ocular inflammation.", "The patient denied any previous history of ocular trauma.", "The patient denied any previous history of ocular surgery.", "The patient denied any use of topical or systemic medications.", "Slit-lamp examination of the right eye anterior segment was within normal limits except for the crystalline lens anterior capsular.", "The right eye crystalline lens anterior capsular showed confluent pigment deposits stellate in shape over the pupillary axis.", "Left eye examination was completely within normal limits.", "Ophthalmic examination of the posterior segment was normal in both eyes.", "A diagnosis of unilateral congenital lenticular pigmentation was made."]}, "extra_info": {"fulltext_subclaims": ["A 23-year-old female presented to our eye clinic with chief complaint of mild blurring of vision in the right eye.", "The patient denied any previous history of ocular inflammation.", "The patient denied any previous history of trauma.", "The patient denied any previous history of surgery.", "The patient denied any previous history of use of topical or systemic medications.", "Snellen\u2019s visual acuity in the right eye was 0.05.", "Snellen\u2019s visual acuity in the right eye was corrected to 0.5 with \u22123.00 to 2.00 \u00d7 15.", "Snellen\u2019s visual acuity in the left eye was 0.5.", "Snellen\u2019s visual acuity in the left eye was corrected to 0.8 with plano \u22120.75 \u00d7 170.", "Intraocular pressure was 14 mm Hg in the right eye.", "Intraocular pressure was 14 mm Hg in the left eye.", "Slit-lamp examination of the right eye anterior segment showed clear cornea.", "Slit-lamp examination of the right eye anterior segment showed deep and quiet anterior chamber.", "Slit-lamp examination of the right eye anterior segment showed no iris transillumination defects.", "Crystalline lens anterior capsular showed confluent pigment deposits stellate in shape over the pupillary axis.", "Dilation of the right eye pupil showed no pigment deposits in the peripheral capsule.", "Dilation of the right eye pupil showed no pigment deposits on the posterior lens capsule.", "Dilation of the right eye pupil showed no pigment deposits on the anterior hyaloid face.", "The examination of the left eye anterior segment was within normal limits before and after dilation.", "Gonioscopy revealed open angle with mild pigmentation and prominent iris processes of the right eye.", "Ophthalmic examination of the posterior segment was normal in both eyes.", "The patient was reassured and prescribed glasses.", "The patient was booked for regular follow-up.", "Following discussion with the patient, she opted to have transepithelial photorefractive keratectomy for the right eye myopic astigmatism.", "Transepithelial photorefractive keratectomy improved her unaided vision to 0.8.", "Based on her previous ophthalmic history and slit-lamp examination of the right eye, a diagnosis of unilateral congenital lenticular pigmentation was made."], "index": 149, "original_id": "multiclinsum_test_2126_en.txt", "split": "test", "summary_subclaims": ["The patient is a 23-year-old female.", "The patient presented with mild blurring of vision in the right eye.", "The patient inquired about refractive surgery.", "The patient denied any previous history of ocular inflammation.", "The patient denied any previous history of ocular trauma.", "The patient denied any previous history of ocular surgery.", "The patient denied any use of topical or systemic medications.", "Slit-lamp examination of the right eye anterior segment was within normal limits except for the crystalline lens anterior capsular.", "The right eye crystalline lens anterior capsular showed confluent pigment deposits stellate in shape over the pupillary axis.", "Left eye examination was completely within normal limits.", "Ophthalmic examination of the posterior segment was normal in both eyes.", "A diagnosis of unilateral congenital lenticular pigmentation was made."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 51-year-old Hispanic female.", "She has a history of hypothyroidism.", "She presented with acute onset chest pain for 1 day.", "The chest pain was pressure-like, retrosternal, and radiated to her left arm and shoulder.", "She did not have shortness of breath.", "She reported the chest pain occurred suddenly while sitting at rest.", "She had intermittent chest pain with exertion for the past 2 months.", "She had to stop exercise for relief.", "She minimized her physical activity.", "The chest pain on presentation was similar in nature to the chest pain she had previously.", "She did not have syncope.", "She did not have palpitations.", "She did not have lightheadedness.", "She did not have anxiety.", "She did not have diarrhea.", "She did not have weight loss.", "She did not have brittle hair.", "She sought medical care due to increased severity of pain.", "Two months prior to presentation, she was diagnosed with hypothyroidism.", "Her TSH was ~500 U/mL.", "She was given levothyroxine 137 mcg daily.", "The dose was reduced after labs indicated supranormal T3 and T4 levels.", "She had most recently been on levothyroxine 100 mcg daily.", "She was compliant with levothyroxine.", "She took omeprazole 20 mg daily.", "She did not use oral contraceptive pills.", "She had a negative fasting lipid panel ~1 year prior.", "She denied any other past medical or surgical history.", "She did not have allergies.", "She was a lifelong non-smoker.", "She did not consume alcohol.", "She did not use illicit drugs.", "On presentation, her vitals were normal.", "Her BMI was 27.3 kg/m2.", "The physical exam was significant for a woman who appeared in her stated age in mild distress due to chest pain.", "The electrocardiogram was consistent with normal sinus rhythm without any abnormalities.", "Troponins were elevated and trended upward from 0.080 to 0.120 to 0.222 ng/mL each 8 hours apart.", "TSH was nearly undetectable at <0.015 U/mL.", "T3 and T4 were not measured on presentation.", "Levothyroxine was stopped.", "Chest x-ray was unremarkable.", "Bedside 2D echocardiogram showed a normal left ventricle with EF of >60%.", "There were no regional wall motion abnormalities.", "The left atrium was mildly dilated.", "Right ventricular systolic pressure was 32 mm Hg.", "Non-ST elevation MI was diagnosed.", "The patient was given atorvastatin 80 mg.", "The patient was given a heparin drip.", "The patient was given clopidogrel 600 mg.", "The patient was given aspirin 324 mg.", "Sublingual nitroglycerin 0.4 mg was given.", "The chest pain improved from 10/10 to 6/10.", "Coronary angiogram showed an anomalous RCA arising from the left coronary cusp of the sinus of Valsalva.", "There was no evidence of occlusion.", "A follow-up coronary computed tomography angiogram confirmed the anomalous RCA.", "The anomalous RCA took an inter-arterial course.", "The anomalous RCA originated from the coronary ostium.", "There was a slit-like deformity.", "There was at least 50% luminal stenosis.", "Troponins trended downward.", "Chest pain resolved.", "The patient was referred to a cardiothoracic surgeon for definitive surgical correction.", "The patient was discharged home with levothyroxine 50 mcg daily.", "The patient was discharged home with metoprolol 25 mg BID.", "The patient was advised against aggressive physical activity.", "Informed consent was obtained from the patient for publication of this case report and any accompanying images."], "summary_subclaims": ["The patient is a 51-year-old female.", "The patient has a history of hypothyroidism.", "The patient had acute onset chest pain for 1 day.", "The patient's electrocardiogram was normal.", "The patient had elevated troponins.", "The patient was diagnosed with acute coronary syndrome.", "The patient was on levothyroxine.", "The patient had a subnormal thyroid-stimulating hormone level.", "The subnormal thyroid-stimulating hormone level suggested hyperthyroidism.", "The echocardiogram was normal.", "The coronary angiogram showed an anomalous RCA arising from the left coronary cusp of the sinus of Valsalva.", "The coronary angiogram showed no evidence of atherosclerosis.", "A coronary computed tomography angiogram was done.", "The coronary computed tomography angiogram confirmed the anomalous RCA.", "The coronary computed tomography angiogram showed a slit-like deformity of the coronary ostium.", "The coronary computed tomography angiogram showed at least 50% luminal stenosis.", "The patient was referred to a cardiothoracic surgeon.", "The patient was referred for potential coronary artery bypass graft."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 51-year-old Hispanic female.", "She has a history of hypothyroidism.", "She presented with acute onset chest pain for 1 day.", "The chest pain was pressure-like, retrosternal, and radiated to her left arm and shoulder.", "She did not have shortness of breath.", "She reported the chest pain occurred suddenly while sitting at rest.", "She had intermittent chest pain with exertion for the past 2 months.", "She had to stop exercise for relief.", "She minimized her physical activity.", "The chest pain on presentation was similar in nature to the chest pain she had previously.", "She did not have syncope.", "She did not have palpitations.", "She did not have lightheadedness.", "She did not have anxiety.", "She did not have diarrhea.", "She did not have weight loss.", "She did not have brittle hair.", "She sought medical care due to increased severity of pain.", "Two months prior to presentation, she was diagnosed with hypothyroidism.", "Her TSH was ~500 U/mL.", "She was given levothyroxine 137 mcg daily.", "The dose was reduced after labs indicated supranormal T3 and T4 levels.", "She had most recently been on levothyroxine 100 mcg daily.", "She was compliant with levothyroxine.", "She took omeprazole 20 mg daily.", "She did not use oral contraceptive pills.", "She had a negative fasting lipid panel ~1 year prior.", "She denied any other past medical or surgical history.", "She did not have allergies.", "She was a lifelong non-smoker.", "She did not consume alcohol.", "She did not use illicit drugs.", "On presentation, her vitals were normal.", "Her BMI was 27.3 kg/m2.", "The physical exam was significant for a woman who appeared in her stated age in mild distress due to chest pain.", "The electrocardiogram was consistent with normal sinus rhythm without any abnormalities.", "Troponins were elevated and trended upward from 0.080 to 0.120 to 0.222 ng/mL each 8 hours apart.", "TSH was nearly undetectable at <0.015 U/mL.", "T3 and T4 were not measured on presentation.", "Levothyroxine was stopped.", "Chest x-ray was unremarkable.", "Bedside 2D echocardiogram showed a normal left ventricle with EF of >60%.", "There were no regional wall motion abnormalities.", "The left atrium was mildly dilated.", "Right ventricular systolic pressure was 32 mm Hg.", "Non-ST elevation MI was diagnosed.", "The patient was given atorvastatin 80 mg.", "The patient was given a heparin drip.", "The patient was given clopidogrel 600 mg.", "The patient was given aspirin 324 mg.", "Sublingual nitroglycerin 0.4 mg was given.", "The chest pain improved from 10/10 to 6/10.", "Coronary angiogram showed an anomalous RCA arising from the left coronary cusp of the sinus of Valsalva.", "There was no evidence of occlusion.", "A follow-up coronary computed tomography angiogram confirmed the anomalous RCA.", "The anomalous RCA took an inter-arterial course.", "The anomalous RCA originated from the coronary ostium.", "There was a slit-like deformity.", "There was at least 50% luminal stenosis.", "Troponins trended downward.", "Chest pain resolved.", "The patient was referred to a cardiothoracic surgeon for definitive surgical correction.", "The patient was discharged home with levothyroxine 50 mcg daily.", "The patient was discharged home with metoprolol 25 mg BID.", "The patient was advised against aggressive physical activity.", "Informed consent was obtained from the patient for publication of this case report and any accompanying images."], "index": 133, "original_id": "multiclinsum_test_2590_en.txt", "split": "test", "summary_subclaims": ["The patient is a 51-year-old female.", "The patient has a history of hypothyroidism.", "The patient had acute onset chest pain for 1 day.", "The patient's electrocardiogram was normal.", "The patient had elevated troponins.", "The patient was diagnosed with acute coronary syndrome.", "The patient was on levothyroxine.", "The patient had a subnormal thyroid-stimulating hormone level.", "The subnormal thyroid-stimulating hormone level suggested hyperthyroidism.", "The echocardiogram was normal.", "The coronary angiogram showed an anomalous RCA arising from the left coronary cusp of the sinus of Valsalva.", "The coronary angiogram showed no evidence of atherosclerosis.", "A coronary computed tomography angiogram was done.", "The coronary computed tomography angiogram confirmed the anomalous RCA.", "The coronary computed tomography angiogram showed a slit-like deformity of the coronary ostium.", "The coronary computed tomography angiogram showed at least 50% luminal stenosis.", "The patient was referred to a cardiothoracic surgeon.", "The patient was referred for potential coronary artery bypass graft."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 60-year-old white female.", "She was referred to the nephrology clinic for an unexplained rise in creatinine to 1.4 mg/dL.", "Her baseline creatinine was 0.9 mg/dL.", "She was diagnosed with POEMS syndrome approximately 1 year prior.", "Her serum protein electrophoresis around 2 years prior showed an m-spike of 1.0 g/dL.", "Immunofixation electrophoresis demonstrated the presence of monoclonal IgG with kappa light chain restriction.", "Complementary bone marrow biopsy indicated mildly increased plasma cells (5%-7%) with kappa light chain predominance.", "She was diagnosed with hypertension approximately 3 years before her referral.", "She was taking prednisone 20 mg daily, prescribed by her hematologist due to suspected vasculitis.", "She reported intermittent consumption of nonsteroidal anti-inflammatory drugs (approximately 500 mg weekly) over the past couple of years.", "At her first nephrology visit, her creatinine level was 1.4 mg/dL.", "She was diagnosed with chronic kidney disease stage 3B at the nephrology visit.", "Her estimated glomerular filtration rate was 43 mL/min/1.73 m2.", "Her creatinine increased to 1.8 mg/dL 1 week after her first nephrology visit.", "Urinalysis results showed nephritic range proteinuria, hematuria, and pyuria with moderate bacteriuria.", "Autoimmune and infectious markers were negative.", "Kidney ultrasound was unremarkable.", "The kidney biopsy showed diffuse and focal nodular mesangial expansion without hypercellularity.", "DNAJB9 immunohistochemical staining and immunofluorescent studies were negative.", "Electron microscopy showed mesangial matrix expansion with scattered embedded distinct curved fibrils ranging from 7 to 12 nm in diameter.", "The patient was diagnosed with immunotactoid glomerulopathy in the context of hypertension and passive smoking.", "Her blood pressure became uncontrolled after the kidney biopsy, reaching a peak of 183/93 mm\u2009Hg.", "A duplex kidney ultrasound revealed left renal artery stenosis.", "She was referred for appropriate management of renal artery stenosis.", "Her most recent serum protein electrophoresis showed an M-spike of 0.8 g/dL.", "Immunofixation electrophoresis confirmed the presence of monoclonal IgG with kappa light chain restriction.", "At her most recent nephrology visit, 12 months later, her blood pressure was 144/78 mm\u2009Hg."], "summary_subclaims": ["The patient is a 60-year-old white female.", "She has POEMS syndrome.", "She has newly diagnosed HTN.", "She was referred because of an elevated creatinine level.", "She denied being an active smoker.", "She reported long-term exposure to cigarette smoke.", "Further investigations revealed microscopic hematuria.", "Further investigations revealed nephritic range proteinuria.", "Kidney biopsy revealed diffuse and focal nodular mesangial expansion without hypercellularity.", "Staining for amyloid was negative.", "Staining for fibrillary glomerulonephritis was negative.", "Staining for immunoglobulins was negative.", "The diagnosis was ING."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 60-year-old white female.", "She was referred to the nephrology clinic for an unexplained rise in creatinine to 1.4 mg/dL.", "Her baseline creatinine was 0.9 mg/dL.", "She was diagnosed with POEMS syndrome approximately 1 year prior.", "Her serum protein electrophoresis around 2 years prior showed an m-spike of 1.0 g/dL.", "Immunofixation electrophoresis demonstrated the presence of monoclonal IgG with kappa light chain restriction.", "Complementary bone marrow biopsy indicated mildly increased plasma cells (5%-7%) with kappa light chain predominance.", "She was diagnosed with hypertension approximately 3 years before her referral.", "She was taking prednisone 20 mg daily, prescribed by her hematologist due to suspected vasculitis.", "She reported intermittent consumption of nonsteroidal anti-inflammatory drugs (approximately 500 mg weekly) over the past couple of years.", "At her first nephrology visit, her creatinine level was 1.4 mg/dL.", "She was diagnosed with chronic kidney disease stage 3B at the nephrology visit.", "Her estimated glomerular filtration rate was 43 mL/min/1.73 m2.", "Her creatinine increased to 1.8 mg/dL 1 week after her first nephrology visit.", "Urinalysis results showed nephritic range proteinuria, hematuria, and pyuria with moderate bacteriuria.", "Autoimmune and infectious markers were negative.", "Kidney ultrasound was unremarkable.", "The kidney biopsy showed diffuse and focal nodular mesangial expansion without hypercellularity.", "DNAJB9 immunohistochemical staining and immunofluorescent studies were negative.", "Electron microscopy showed mesangial matrix expansion with scattered embedded distinct curved fibrils ranging from 7 to 12 nm in diameter.", "The patient was diagnosed with immunotactoid glomerulopathy in the context of hypertension and passive smoking.", "Her blood pressure became uncontrolled after the kidney biopsy, reaching a peak of 183/93 mm\u2009Hg.", "A duplex kidney ultrasound revealed left renal artery stenosis.", "She was referred for appropriate management of renal artery stenosis.", "Her most recent serum protein electrophoresis showed an M-spike of 0.8 g/dL.", "Immunofixation electrophoresis confirmed the presence of monoclonal IgG with kappa light chain restriction.", "At her most recent nephrology visit, 12 months later, her blood pressure was 144/78 mm\u2009Hg."], "index": 147, "original_id": "multiclinsum_test_3054_en.txt", "split": "test", "summary_subclaims": ["The patient is a 60-year-old white female.", "She has POEMS syndrome.", "She has newly diagnosed HTN.", "She was referred because of an elevated creatinine level.", "She denied being an active smoker.", "She reported long-term exposure to cigarette smoke.", "Further investigations revealed microscopic hematuria.", "Further investigations revealed nephritic range proteinuria.", "Kidney biopsy revealed diffuse and focal nodular mesangial expansion without hypercellularity.", "Staining for amyloid was negative.", "Staining for fibrillary glomerulonephritis was negative.", "Staining for immunoglobulins was negative.", "The diagnosis was ING."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 4 years and 8-month-old Syrian Arabic girl.", "She is the sixth of seven siblings.", "She was born to healthy consanguineous parents.", "She had a birth weight of 4 kg.", "She followed normal psychomotor development.", "She had no remarkable illness until the age of 4 years and 2 months.", "Her parents noticed rapid weight gain starting at 4 years and 2 months.", "She gained about 1 kg every 10 to 15 days.", "She required six to seven big meals per day.", "She had decreased tears when crying.", "She had decreased nasal discharge.", "She had unfavorable body odor.", "She had decreased sweating.", "She had blue cold extremities.", "She had diarrhea alternated with constipation.", "She had polyuria.", "She had polydipsia.", "Two months after the onset of obesity, she had urinary incontinence during night sleep.", "She had mood alteration.", "She had anxiety episodes.", "She had rage attacks.", "She had nervousness.", "She had aggressive behavior.", "She had recurrent fatigue.", "She had social withdrawal.", "She had prolonged periods of sleep (12 hours continuously).", "She had difficulty staying awake during the day.", "She was admitted to Damascus Children Hospital at the age of 4.5 years.", "The family history was negative for similar presentations.", "An older sister of the patient had died at the age of 12 years with a diagnosis of acute myeloid leukemia.", "Her sister\u2019s malignancy was not accompanied by any of the signs or symptoms the patient had.", "On physical examination, general obesity was noticed.", "No dysmorphic features were observed.", "Her weight was 25 kg.", "Her body mass index (BMI) was equal to 20.1.", "Her bone age was slightly advanced and fitted 5 to 5.5 years old.", "Brain MRI showed no cortical atrophy.", "A homogenous mild enlargement of the pituitary gland was observed.", "Her endocrine function tests were normal.", "She was discharged with risperidone 1 mg orally per day.", "She was recommended to follow up at the out-patient psychiatric clinic after 3 months.", "After 3 months, she developed dyspnea that worsened with exertion and during sleep.", "She had continuous snoring.", "She had recurrent chest pain.", "She had two episodes of cyanosis and obstructive apnea.", "She was readmitted to the ICU.", "She was intubated 24 hours after admission.", "She was attached to a mechanical ventilator.", "Her blood gases were pH 7.27, PaCO2 79 mmHg, PaO2 38 mmHg, and oxygen saturation 79%.", "A chest CT scan demonstrated a 6 cm round mass filling most of her right lung.", "A complete resection was performed of a 10\u00d710 cm solid round mass.", "The mass was a mature ganglioneuroma.", "ROHAAD syndrome was considered as a diagnosis.", "Familial obesity was excluded.", "Prader\u2013Willi syndrome was excluded.", "A brain MRI revealed generalized cortical atrophy.", "A tracheostomy was performed.", "She had cardiorespiratory arrest.", "She died one week after the tracheostomy."], "summary_subclaims": ["The patient is a 4 years and 8-month-old Syrian Arabic girl.", "The patient had signs and symptoms of rapid-onset obesity with hypoventilation.", "The patient had hypothalamic dysfunction.", "The patient had autonomic dysregulation syndrome.", "The patient had a mature ganglioneuroma in her chest.", "The patient had homogenous mild enlargement of her pituitary gland.", "The patient had generalized cortical brain atrophy.", "The patient had seizures.", "Three months after her first marked symptoms were noted, she had a sudden progression of severe respiratory distress.", "The patient's severe respiratory distress ended with her death."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 4 years and 8-month-old Syrian Arabic girl.", "She is the sixth of seven siblings.", "She was born to healthy consanguineous parents.", "She had a birth weight of 4 kg.", "She followed normal psychomotor development.", "She had no remarkable illness until the age of 4 years and 2 months.", "Her parents noticed rapid weight gain starting at 4 years and 2 months.", "She gained about 1 kg every 10 to 15 days.", "She required six to seven big meals per day.", "She had decreased tears when crying.", "She had decreased nasal discharge.", "She had unfavorable body odor.", "She had decreased sweating.", "She had blue cold extremities.", "She had diarrhea alternated with constipation.", "She had polyuria.", "She had polydipsia.", "Two months after the onset of obesity, she had urinary incontinence during night sleep.", "She had mood alteration.", "She had anxiety episodes.", "She had rage attacks.", "She had nervousness.", "She had aggressive behavior.", "She had recurrent fatigue.", "She had social withdrawal.", "She had prolonged periods of sleep (12 hours continuously).", "She had difficulty staying awake during the day.", "She was admitted to Damascus Children Hospital at the age of 4.5 years.", "The family history was negative for similar presentations.", "An older sister of the patient had died at the age of 12 years with a diagnosis of acute myeloid leukemia.", "Her sister\u2019s malignancy was not accompanied by any of the signs or symptoms the patient had.", "On physical examination, general obesity was noticed.", "No dysmorphic features were observed.", "Her weight was 25 kg.", "Her body mass index (BMI) was equal to 20.1.", "Her bone age was slightly advanced and fitted 5 to 5.5 years old.", "Brain MRI showed no cortical atrophy.", "A homogenous mild enlargement of the pituitary gland was observed.", "Her endocrine function tests were normal.", "She was discharged with risperidone 1 mg orally per day.", "She was recommended to follow up at the out-patient psychiatric clinic after 3 months.", "After 3 months, she developed dyspnea that worsened with exertion and during sleep.", "She had continuous snoring.", "She had recurrent chest pain.", "She had two episodes of cyanosis and obstructive apnea.", "She was readmitted to the ICU.", "She was intubated 24 hours after admission.", "She was attached to a mechanical ventilator.", "Her blood gases were pH 7.27, PaCO2 79 mmHg, PaO2 38 mmHg, and oxygen saturation 79%.", "A chest CT scan demonstrated a 6 cm round mass filling most of her right lung.", "A complete resection was performed of a 10\u00d710 cm solid round mass.", "The mass was a mature ganglioneuroma.", "ROHAAD syndrome was considered as a diagnosis.", "Familial obesity was excluded.", "Prader\u2013Willi syndrome was excluded.", "A brain MRI revealed generalized cortical atrophy.", "A tracheostomy was performed.", "She had cardiorespiratory arrest.", "She died one week after the tracheostomy."], "index": 139, "original_id": "multiclinsum_test_2845_en.txt", "split": "test", "summary_subclaims": ["The patient is a 4 years and 8-month-old Syrian Arabic girl.", "The patient had signs and symptoms of rapid-onset obesity with hypoventilation.", "The patient had hypothalamic dysfunction.", "The patient had autonomic dysregulation syndrome.", "The patient had a mature ganglioneuroma in her chest.", "The patient had homogenous mild enlargement of her pituitary gland.", "The patient had generalized cortical brain atrophy.", "The patient had seizures.", "Three months after her first marked symptoms were noted, she had a sudden progression of severe respiratory distress.", "The patient's severe respiratory distress ended with her death."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 24-year-old right-hand dominant Hispanic female.", "She initially presented to an urgent care office in October 2021.", "She had a right small finger mass on the ulnar aspect of the proximal interphalangeal joint.", "The mass had been present for several months prior to presentation.", "She had no pertinent medical or surgical history.", "Her family history was positive for renal cell carcinoma and diabetes on her maternal side.", "The mass would grow and reduce in size, especially during her pregnancy.", "The urgent care provider attempted aspiration of the mass, which was unsuccessful.", "The mass was diagnosed as a likely ganglion cyst.", "The patient saw another local hand surgeon sometime after her urgent care visit.", "Plans to remove the mass were never executed.", "In March 2022, she presented with complaints of increasing pain and an open wound with bleeding.", "Plain radiographs demonstrated a soft tissue mass on the ulnar aspect of the small finger near the PIP joint.", "The patient underwent a surgical excisional biopsy of the mass on 3/15/22.", "The surgical pathology was reviewed by two independent pathologists.", "The pathology was consistent with low-grade leiomyosarcoma of the finger.", "A PET/CT scan in early April 2022 demonstrated a suspicious lymph node in the right axilla.", "The treating oncologist thought the lymph node was benign and likely reactive.", "The clinical and pathologic assessment was consistent with AJCC stage 1A disease.", "The patient was discussed at the tumor board of the treating hospital in early May 2022.", "It was agreed that she would likely get the most benefit from a ray amputation.", "The patient presented with a new complaint of another mass on the small finger.", "The exam and radiographs were consistent with another focus of leiomyosarcoma.", "On 6/15/22, the patient underwent successful right-hand minor finger ray amputation.", "The small finger ray was amputated to the level of the mid-metacarpal shaft.", "The surgical margins assessed by a pathologist were clear for any tumor.", "The biopsy results were again consistent with low-grade leiomyosarcoma.", "The patient's right hand showed no evidence of recurrence or residual tumor clinically.", "An MRI of the right hand obtained on 10/11/22 showed no local or systemic disease recurrence.", "The patient continued progressing well postoperatively.", "She initiated hand therapy approximately three weeks postoperatively.", "Most recent occupational therapy clinic notes indicated full function of the right-hand digits 1\u20134.", "She had comparable grip strength to the contralateral hand.", "She had no pain or other masses.", "Postoperatively, she commented on a prominent and ropy scar.", "She underwent aggressive therapy and massage.", "Continued oncologic surveillance and repeat MRI showed no local or systemic disease recurrence at nine months postoperatively."], "summary_subclaims": ["The patient was diagnosed with a primary leiomyosarcoma of the small finger.", "She underwent extensive oncologic workup.", "She underwent successful ray amputation.", "She remains disease free."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 24-year-old right-hand dominant Hispanic female.", "She initially presented to an urgent care office in October 2021.", "She had a right small finger mass on the ulnar aspect of the proximal interphalangeal joint.", "The mass had been present for several months prior to presentation.", "She had no pertinent medical or surgical history.", "Her family history was positive for renal cell carcinoma and diabetes on her maternal side.", "The mass would grow and reduce in size, especially during her pregnancy.", "The urgent care provider attempted aspiration of the mass, which was unsuccessful.", "The mass was diagnosed as a likely ganglion cyst.", "The patient saw another local hand surgeon sometime after her urgent care visit.", "Plans to remove the mass were never executed.", "In March 2022, she presented with complaints of increasing pain and an open wound with bleeding.", "Plain radiographs demonstrated a soft tissue mass on the ulnar aspect of the small finger near the PIP joint.", "The patient underwent a surgical excisional biopsy of the mass on 3/15/22.", "The surgical pathology was reviewed by two independent pathologists.", "The pathology was consistent with low-grade leiomyosarcoma of the finger.", "A PET/CT scan in early April 2022 demonstrated a suspicious lymph node in the right axilla.", "The treating oncologist thought the lymph node was benign and likely reactive.", "The clinical and pathologic assessment was consistent with AJCC stage 1A disease.", "The patient was discussed at the tumor board of the treating hospital in early May 2022.", "It was agreed that she would likely get the most benefit from a ray amputation.", "The patient presented with a new complaint of another mass on the small finger.", "The exam and radiographs were consistent with another focus of leiomyosarcoma.", "On 6/15/22, the patient underwent successful right-hand minor finger ray amputation.", "The small finger ray was amputated to the level of the mid-metacarpal shaft.", "The surgical margins assessed by a pathologist were clear for any tumor.", "The biopsy results were again consistent with low-grade leiomyosarcoma.", "The patient's right hand showed no evidence of recurrence or residual tumor clinically.", "An MRI of the right hand obtained on 10/11/22 showed no local or systemic disease recurrence.", "The patient continued progressing well postoperatively.", "She initiated hand therapy approximately three weeks postoperatively.", "Most recent occupational therapy clinic notes indicated full function of the right-hand digits 1\u20134.", "She had comparable grip strength to the contralateral hand.", "She had no pain or other masses.", "Postoperatively, she commented on a prominent and ropy scar.", "She underwent aggressive therapy and massage.", "Continued oncologic surveillance and repeat MRI showed no local or systemic disease recurrence at nine months postoperatively."], "index": 143, "original_id": "multiclinsum_test_2201_en.txt", "split": "test", "summary_subclaims": ["The patient was diagnosed with a primary leiomyosarcoma of the small finger.", "She underwent extensive oncologic workup.", "She underwent successful ray amputation.", "She remains disease free."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was a 70-year-old Japanese man.", "He had smoked 20 cigarettes a day for 47 years until 5 years ago.", "He was under treatment and follow-up for essential hypertension, dyslipidemia and chronic kidney disease.", "His blood pressure and lipid levels were well controlled with administration of 40\u2005mg of olmesartan medoxomil and 5\u2005mg of atorvastatin calcium hydrate.", "He tested positive for SARS-CoV-2 by the polymerase chain reaction (PCR) test three days after coming in extended contact with a colleague who was also diagnosed with SARS-CoV-2.", "He was urgently admitted to the hospital the day after symptom onset and confirmation of the diagnosis.", "At admission, his body temperature was 36.4\u2005\u00b0C.", "At admission, his blood pressure was 185/72\u2005mm Hg.", "At admission, his peripheral oxygen saturation on pulse oximetry was 97.0%.", "Laboratory findings showed lymphocyte depletion.", "Laboratory findings showed coagulation abnormalities.", "CT showed emphysematous changes in the lung field.", "Ground glass opacities with neither a crazy-paving pattern nor consolidation was found below the dorsal pleura of the upper right lobe.", "The total CT score was 1/25 points.", "It was considered to be typical findings of early mild COVID-19 pneumonia.", "Administration of favipiravir 3600\u2005mg daily was started from the evening of the same day.", "1\u2005L/min oxygen administration via a nasal cannula was also started the following day.", "Weakness and a decreased level of consciousness appeared from the early morning of Day 2.", "A neurologist ruled out stroke.", "Fav was discontinued on the evening of Day 2.", "His symptoms improved by the morning of Day 3.", "The frequency of administration of acetaminophen 500\u2005mg was increased from 0 to 3 times a day.", "His CRP level increased.", "His SpO2 decreased, requiring an increase in oxygen flow rate from 1 to 3\u2005L/min by nasal cannula.", "CT performed on Day 4 showed slight deterioration in the pneumonia.", "The total CT score on Day 4 was 2/25 points.", "200\u2005mg of remdesivir was administered on Day 4.", "100\u2005mg of remdesivir was administered daily from Day 5 until Day 10.", "On Day 7, blood gas data showed that the alveolar-arterial oxygen difference had increased to 122.1\u2005mm Hg.", "No pulmonary hypertension was observed on electrocardiogram or echocardiography.", "A tendency of increasing D-D levels was also observed.", "The combination of nafamostat mesylate 100\u2005mg daily by continuous intravenous infusion and dexamethasone 6\u2005mg daily was administered for four days from Day 7.", "The treatment was remarkably effective, resulting in fever reduction.", "The treatment resulted in a decrease in CRP and D-D levels.", "On Day 10, oxygen administration could be discontinued.", "On Day 10, his blood pressure control improved.", "By Day 13, the alveolar-arterial oxygen difference had improved to 33.2\u2005mm Hg without supplementary oxygen.", "CT on Day 13 showed a tendency for improvement in pneumonia.", "The total CT score on Day 13 was still 2/25 points.", "For blood pressure control during the course of his hospitalization, continuous intravenous infusion of pernidipine was performed for two days when oral intake was difficult due to the decreased consciousness level.", "From Day 4, olmesartan medoxomil 40\u2005mg and nifedipine 20\u2005mg were administered in combination.", "With the treatment of COVID-19, his blood pressure gradually stabilized.", "The dose of nifedipine was reduced from Day 14 to 10\u2005mg.", "Nifedipine was discontinued from Day 19.", "The patient was discharged on Day 21."], "summary_subclaims": ["The patient was a 70-year-old Japanese man.", "The patient had essential hypertension.", "The patient had dyslipidemia.", "The patient had chronic kidney disease.", "The patient had emphysema.", "The patient was hospitalized with the novel coronavirus disease.", "The patient had hypoxemia that was disproportionate to the severity of pneumonia indicated by CT.", "The patient had coagulation abnormalities.", "We speculated that there was a high possibility that he had developed ventilation and blood flow imbalance due to pulmonary intravascular coagulopathy or hypoxic pulmonary vasoconstriction.", "Early, short-term combination therapy with remdesivir, nafamostat mesylate and low-dose dexamethasone was successful."]}, "extra_info": {"fulltext_subclaims": ["The patient was a 70-year-old Japanese man.", "He had smoked 20 cigarettes a day for 47 years until 5 years ago.", "He was under treatment and follow-up for essential hypertension, dyslipidemia and chronic kidney disease.", "His blood pressure and lipid levels were well controlled with administration of 40\u2005mg of olmesartan medoxomil and 5\u2005mg of atorvastatin calcium hydrate.", "He tested positive for SARS-CoV-2 by the polymerase chain reaction (PCR) test three days after coming in extended contact with a colleague who was also diagnosed with SARS-CoV-2.", "He was urgently admitted to the hospital the day after symptom onset and confirmation of the diagnosis.", "At admission, his body temperature was 36.4\u2005\u00b0C.", "At admission, his blood pressure was 185/72\u2005mm Hg.", "At admission, his peripheral oxygen saturation on pulse oximetry was 97.0%.", "Laboratory findings showed lymphocyte depletion.", "Laboratory findings showed coagulation abnormalities.", "CT showed emphysematous changes in the lung field.", "Ground glass opacities with neither a crazy-paving pattern nor consolidation was found below the dorsal pleura of the upper right lobe.", "The total CT score was 1/25 points.", "It was considered to be typical findings of early mild COVID-19 pneumonia.", "Administration of favipiravir 3600\u2005mg daily was started from the evening of the same day.", "1\u2005L/min oxygen administration via a nasal cannula was also started the following day.", "Weakness and a decreased level of consciousness appeared from the early morning of Day 2.", "A neurologist ruled out stroke.", "Fav was discontinued on the evening of Day 2.", "His symptoms improved by the morning of Day 3.", "The frequency of administration of acetaminophen 500\u2005mg was increased from 0 to 3 times a day.", "His CRP level increased.", "His SpO2 decreased, requiring an increase in oxygen flow rate from 1 to 3\u2005L/min by nasal cannula.", "CT performed on Day 4 showed slight deterioration in the pneumonia.", "The total CT score on Day 4 was 2/25 points.", "200\u2005mg of remdesivir was administered on Day 4.", "100\u2005mg of remdesivir was administered daily from Day 5 until Day 10.", "On Day 7, blood gas data showed that the alveolar-arterial oxygen difference had increased to 122.1\u2005mm Hg.", "No pulmonary hypertension was observed on electrocardiogram or echocardiography.", "A tendency of increasing D-D levels was also observed.", "The combination of nafamostat mesylate 100\u2005mg daily by continuous intravenous infusion and dexamethasone 6\u2005mg daily was administered for four days from Day 7.", "The treatment was remarkably effective, resulting in fever reduction.", "The treatment resulted in a decrease in CRP and D-D levels.", "On Day 10, oxygen administration could be discontinued.", "On Day 10, his blood pressure control improved.", "By Day 13, the alveolar-arterial oxygen difference had improved to 33.2\u2005mm Hg without supplementary oxygen.", "CT on Day 13 showed a tendency for improvement in pneumonia.", "The total CT score on Day 13 was still 2/25 points.", "For blood pressure control during the course of his hospitalization, continuous intravenous infusion of pernidipine was performed for two days when oral intake was difficult due to the decreased consciousness level.", "From Day 4, olmesartan medoxomil 40\u2005mg and nifedipine 20\u2005mg were administered in combination.", "With the treatment of COVID-19, his blood pressure gradually stabilized.", "The dose of nifedipine was reduced from Day 14 to 10\u2005mg.", "Nifedipine was discontinued from Day 19.", "The patient was discharged on Day 21."], "index": 144, "original_id": "multiclinsum_test_2467_en.txt", "split": "test", "summary_subclaims": ["The patient was a 70-year-old Japanese man.", "The patient had essential hypertension.", "The patient had dyslipidemia.", "The patient had chronic kidney disease.", "The patient had emphysema.", "The patient was hospitalized with the novel coronavirus disease.", "The patient had hypoxemia that was disproportionate to the severity of pneumonia indicated by CT.", "The patient had coagulation abnormalities.", "We speculated that there was a high possibility that he had developed ventilation and blood flow imbalance due to pulmonary intravascular coagulopathy or hypoxic pulmonary vasoconstriction.", "Early, short-term combination therapy with remdesivir, nafamostat mesylate and low-dose dexamethasone was successful."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["A 21-year-old female patient with abdominal pain, irregular menstrual cycles, hyperestrogenemia, and recurrence of an ovarian mass was transferred to our hospital in July 2020.", "Four months prior, the patient was referred to another hospital because of abdominal pain and irregular menstrual cycles.", "Ultrasonography revealed a large multilocular cystic mass in the abdominal cavity.", "The patient underwent single-port laparoscopic removal of the bilateral ovarian cysts.", "During surgery, the bilateral ovaries were enlarged in a multilocular mass with yellow fluid inside.", "Histopathology revealed multiple luteinized follicular cysts of the ovary.", "After one month of clinical treatment, the patient experienced abdominal pain again.", "Pelvic ultrasound indicated recurrence of enlarged ovaries with multiple large cysts.", "The upper edge of the ovarian mass reached 20 mm above the umbilicus.", "The thickness of the endometrium was 17.4 mm.", "Biochemical evaluation demonstrated normal serum levels of LH, FSH, progesterone, cortisol, Free T4, thyroid-stimulating hormone, parathyroid hormone, calcium, phosphate, and growth hormone.", "Biochemical evaluation demonstrated elevated levels of plasma CA125, estradiol, and prolactin.", "Brain magnetic resonance imaging revealed the presence of a pituitary macroadenoma (17 mm \u00d7 27 mm \u00d7 19 mm).", "Visual field examination after brain MRI revealed bitemporal hemianopsia.", "Ultrasound showed a 48 mm \u00d7 30 mm \u00d7 23 mm mass in the right breast.", "Histopathology revealed breast fibroadenoma.", "Ultrasound imaging revealed no abnormalities in the thyroid, adrenal, or parathyroid glands.", "The patient was treated with oral bromocriptine (2.5 mg) three times a day.", "The patient had no significant history of illness, medical history, drug allergy, transfusion, injury, pregnancy, or other complications.", "The patient had a smoking history for over four years.", "The patient had menarche at age 12 years.", "In the past year, the menstrual cycle of the patient had extended to 2\u20133 months.", "The patient was 167 cm tall, weighed 68 kg, and had a body mass index of 24.38 kg/m2.", "An ultrasonographic study of the pelvis revealed multicystic ovaries, similar to the typical signs of spontaneous ovarian hyperstimulation syndrome.", "Computed tomography confirmed a large cystic mass in the abdominopelvic cavity, with a range of 19.4 cm \u00d7 7.9 cm \u00d7 15.9 cm.", "A homogeneously enhancing 21 mm \u00d7 16 mm \u00d7 28 mm sellar mass was imaged by brain MRI."], "summary_subclaims": ["The patient was a 21-year-old female.", "The patient had abdominal pain.", "The patient had irregular menstruation.", "The patient had hyperestrogenemia.", "The patient had an ovarian mass.", "Brain MRI revealed a pituitary macroadenoma.", "Transsphenoidal surgery relieved her clinical symptoms.", "Before transsphenoidal surgery, plasma CA125 levels were elevated.", "Before transsphenoidal surgery, estradiol levels were elevated.", "Before transsphenoidal surgery, prolactin levels were maintained at normal levels.", "Before transsphenoidal surgery, luteinizing hormone levels were maintained at normal levels.", "Before transsphenoidal surgery, follicle-stimulating hormone levels were maintained at normal levels.", "Before transsphenoidal surgery, PROG levels were maintained at normal levels.", "Before transsphenoidal surgery, cortisol levels were maintained at normal levels.", "Before transsphenoidal surgery, FT4 levels were maintained at normal levels.", "Before transsphenoidal surgery, thyroid-stimulating hormone levels were maintained at normal levels.", "Before transsphenoidal surgery, parathyroid hormone levels were maintained at normal levels.", "Before transsphenoidal surgery, GH levels were maintained at normal levels.", "After transsphenoidal surgery, the patient was diagnosed with a functioning gonadotroph adenoma.", "Pelvic ultrasound confirmed normal-sized ovaries.", "The menstrual cycle returned to regular.", "Hormones were maintained within a normal range.", "There was no evidence of tumor recurrence after two years of follow-up."]}, "extra_info": {"fulltext_subclaims": ["A 21-year-old female patient with abdominal pain, irregular menstrual cycles, hyperestrogenemia, and recurrence of an ovarian mass was transferred to our hospital in July 2020.", "Four months prior, the patient was referred to another hospital because of abdominal pain and irregular menstrual cycles.", "Ultrasonography revealed a large multilocular cystic mass in the abdominal cavity.", "The patient underwent single-port laparoscopic removal of the bilateral ovarian cysts.", "During surgery, the bilateral ovaries were enlarged in a multilocular mass with yellow fluid inside.", "Histopathology revealed multiple luteinized follicular cysts of the ovary.", "After one month of clinical treatment, the patient experienced abdominal pain again.", "Pelvic ultrasound indicated recurrence of enlarged ovaries with multiple large cysts.", "The upper edge of the ovarian mass reached 20 mm above the umbilicus.", "The thickness of the endometrium was 17.4 mm.", "Biochemical evaluation demonstrated normal serum levels of LH, FSH, progesterone, cortisol, Free T4, thyroid-stimulating hormone, parathyroid hormone, calcium, phosphate, and growth hormone.", "Biochemical evaluation demonstrated elevated levels of plasma CA125, estradiol, and prolactin.", "Brain magnetic resonance imaging revealed the presence of a pituitary macroadenoma (17 mm \u00d7 27 mm \u00d7 19 mm).", "Visual field examination after brain MRI revealed bitemporal hemianopsia.", "Ultrasound showed a 48 mm \u00d7 30 mm \u00d7 23 mm mass in the right breast.", "Histopathology revealed breast fibroadenoma.", "Ultrasound imaging revealed no abnormalities in the thyroid, adrenal, or parathyroid glands.", "The patient was treated with oral bromocriptine (2.5 mg) three times a day.", "The patient had no significant history of illness, medical history, drug allergy, transfusion, injury, pregnancy, or other complications.", "The patient had a smoking history for over four years.", "The patient had menarche at age 12 years.", "In the past year, the menstrual cycle of the patient had extended to 2\u20133 months.", "The patient was 167 cm tall, weighed 68 kg, and had a body mass index of 24.38 kg/m2.", "An ultrasonographic study of the pelvis revealed multicystic ovaries, similar to the typical signs of spontaneous ovarian hyperstimulation syndrome.", "Computed tomography confirmed a large cystic mass in the abdominopelvic cavity, with a range of 19.4 cm \u00d7 7.9 cm \u00d7 15.9 cm.", "A homogeneously enhancing 21 mm \u00d7 16 mm \u00d7 28 mm sellar mass was imaged by brain MRI."], "index": 151, "original_id": "multiclinsum_test_318_en.txt", "split": "test", "summary_subclaims": ["The patient was a 21-year-old female.", "The patient had abdominal pain.", "The patient had irregular menstruation.", "The patient had hyperestrogenemia.", "The patient had an ovarian mass.", "Brain MRI revealed a pituitary macroadenoma.", "Transsphenoidal surgery relieved her clinical symptoms.", "Before transsphenoidal surgery, plasma CA125 levels were elevated.", "Before transsphenoidal surgery, estradiol levels were elevated.", "Before transsphenoidal surgery, prolactin levels were maintained at normal levels.", "Before transsphenoidal surgery, luteinizing hormone levels were maintained at normal levels.", "Before transsphenoidal surgery, follicle-stimulating hormone levels were maintained at normal levels.", "Before transsphenoidal surgery, PROG levels were maintained at normal levels.", "Before transsphenoidal surgery, cortisol levels were maintained at normal levels.", "Before transsphenoidal surgery, FT4 levels were maintained at normal levels.", "Before transsphenoidal surgery, thyroid-stimulating hormone levels were maintained at normal levels.", "Before transsphenoidal surgery, parathyroid hormone levels were maintained at normal levels.", "Before transsphenoidal surgery, GH levels were maintained at normal levels.", "After transsphenoidal surgery, the patient was diagnosed with a functioning gonadotroph adenoma.", "Pelvic ultrasound confirmed normal-sized ovaries.", "The menstrual cycle returned to regular.", "Hormones were maintained within a normal range.", "There was no evidence of tumor recurrence after two years of follow-up."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 58-year-old woman.", "She presented with palpitations and diarrhea that had started 1 day before admission.", "She reported 5 episodes of watery stools.", "The palpitations were of sudden onset and irregular.", "Her initial heart rate was 150 beats/min with an irregular rhythm.", "Subsequent examination showed her heart rate stabilized at 80 beats/min.", "The initial electrocardiogram revealed atrial fibrillation with a heart rate of 150 beats/min and a right bundle branch block.", "Spontaneous conversion to sinus rhythm was observed shortly after the initial electrocardiogram.", "Pathological Q waves were noted in leads V1 and V2.", "A bedside point-of-care ultrasound revealed a large, irregular, hyperechoic, spiculated mass within the left ventricle.", "The chest radiograph revealed calcification within the cardiac silhouette.", "Her medical history was significant for type 2 diabetes mellitus and hypertension.", "She admitted to irregular adherence to her prescribed treatments.", "She had 2 episodes of non\u2013ST-segment elevation myocardial infarction in 2019 and 2022.", "There was no evidence of infections, parasitic diseases, or sepsis in her medical history.", "The differential diagnoses for a left ventricular intraventricular mass include thrombus, primary or metastatic tumors, vegetations, intracardiac calcifications, and parasitic infections.", "A transthoracic echocardiogram demonstrated a preserved ejection fraction of 56%.", "Regional wall motion abnormalities were present, including akinesia in the anterior, lateral, and inferior walls.", "A hyperechoic, irregular mass measuring 3 \u00d7 5 cm was located in the apex and lateral wall of the left ventricle.", "Laboratory evaluations revealed normal renal function, electrolytes, and calcium-phosphorus metabolism.", "Coronary CT angiography showed a coronary calcium score of 0 Agatston units.", "Extensive, thick, and irregular subendocardial calcifications measuring 66 mm in length were identified in the inferior, lateral, and apical walls of the left ventricle.", "The characteristics of the mass were consistent with dystrophic myocardial calcification.", "Rehydration therapy was initiated.", "Antiarrhythmic therapy and anticoagulation were started.", "The calcification was considered an incidental finding.", "A plan for continued medical surveillance was established."], "summary_subclaims": ["The patient is a 58-year-old woman.", "She presented with palpitations.", "She presented with diarrhea.", "Atrial fibrillation was noted.", "Spontaneous conversion to sinus rhythm occurred.", "A left ventricular mass was identified on echocardiogram.", "Computed tomography confirmed the mass as dystrophic calcification.", "The calcification was linked to previous myocardial infarctions.", "The calcification was considered an incidental finding.", "There was no significant systolic dysfunction."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 58-year-old woman.", "She presented with palpitations and diarrhea that had started 1 day before admission.", "She reported 5 episodes of watery stools.", "The palpitations were of sudden onset and irregular.", "Her initial heart rate was 150 beats/min with an irregular rhythm.", "Subsequent examination showed her heart rate stabilized at 80 beats/min.", "The initial electrocardiogram revealed atrial fibrillation with a heart rate of 150 beats/min and a right bundle branch block.", "Spontaneous conversion to sinus rhythm was observed shortly after the initial electrocardiogram.", "Pathological Q waves were noted in leads V1 and V2.", "A bedside point-of-care ultrasound revealed a large, irregular, hyperechoic, spiculated mass within the left ventricle.", "The chest radiograph revealed calcification within the cardiac silhouette.", "Her medical history was significant for type 2 diabetes mellitus and hypertension.", "She admitted to irregular adherence to her prescribed treatments.", "She had 2 episodes of non\u2013ST-segment elevation myocardial infarction in 2019 and 2022.", "There was no evidence of infections, parasitic diseases, or sepsis in her medical history.", "The differential diagnoses for a left ventricular intraventricular mass include thrombus, primary or metastatic tumors, vegetations, intracardiac calcifications, and parasitic infections.", "A transthoracic echocardiogram demonstrated a preserved ejection fraction of 56%.", "Regional wall motion abnormalities were present, including akinesia in the anterior, lateral, and inferior walls.", "A hyperechoic, irregular mass measuring 3 \u00d7 5 cm was located in the apex and lateral wall of the left ventricle.", "Laboratory evaluations revealed normal renal function, electrolytes, and calcium-phosphorus metabolism.", "Coronary CT angiography showed a coronary calcium score of 0 Agatston units.", "Extensive, thick, and irregular subendocardial calcifications measuring 66 mm in length were identified in the inferior, lateral, and apical walls of the left ventricle.", "The characteristics of the mass were consistent with dystrophic myocardial calcification.", "Rehydration therapy was initiated.", "Antiarrhythmic therapy and anticoagulation were started.", "The calcification was considered an incidental finding.", "A plan for continued medical surveillance was established."], "index": 153, "original_id": "multiclinsum_test_3200_en.txt", "split": "test", "summary_subclaims": ["The patient is a 58-year-old woman.", "She presented with palpitations.", "She presented with diarrhea.", "Atrial fibrillation was noted.", "Spontaneous conversion to sinus rhythm occurred.", "A left ventricular mass was identified on echocardiogram.", "Computed tomography confirmed the mass as dystrophic calcification.", "The calcification was linked to previous myocardial infarctions.", "The calcification was considered an incidental finding.", "There was no significant systolic dysfunction."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was a 53-year-old homeless man.", "He was admitted to the hospital due to a right femoral neck fracture.", "His medical history included noninsulin-dependent diabetes mellitus.", "A physical examination performed at admission was unremarkable.", "There was no fever.", "There was no lymphadenopathy.", "There were no other neurological defects.", "Laboratory tests revealed white blood cells of 4330 cells/mL.", "Laboratory tests revealed hemoglobin of 9.2 g/dL.", "Laboratory tests revealed platelet count of 29,900 platelets/mL.", "C-reactive protein was negative.", "Only normochromic-normocytic anemia was present.", "He successfully underwent surgery for the femoral neck fracture.", "The surgery was performed by an orthopedic surgeon.", "He had an episode of generalized seizures during the postoperative course.", "Phenytoin was administered.", "After this episode of generalized seizures, he was referred to our department.", "A computed tomography (CT) examination of the head without contrast showed a high-density and extraaxial mass in the right parietal convexity.", "Peritumoral brain edema was clearly observed.", "Enhanced magnetic resonance imaging (MRI) revealed an extraaxial, dural-based, and homogeneously enhanced mass with clear borders.", "The mass was compatible with a meningioma en plaque.", "The mass was iso- to hypointense on fluid-attenuated inversion recovery and T2 imaging sequences.", "The mass was iso- to hyperintense on T1 imaging.", "It was strongly suspected that the patient had a meningioma en plaque.", "The mass was exposed with a right frontotemporal craniotomy.", "The tumor appeared to be a meningioma en plaque.", "The tumor was extraaxial, xanthochromic, firm, nonaspiratable, and had high vascularity.", "The tumor was dural based.", "The tumor was tightly adhered to the adjacent cerebral cortex.", "The tumor was permeated by many pial arteries and veins of the brain surface.", "It is very difficult to preserve these pial vessels during the total removal of a tumor.", "A frozen section of the lesion showed inflammatory cell infiltration.", "The inflammatory cell infiltration mainly consisted of lymphocytes and plasma cells.", "The presence of these cells was initially interpreted as some kind of hematologic disorder or inflammatory pseudotumor.", "Paraffin-embedded sections showed a hypercellular pattern with features of polymorphous and mixed inflammatory infiltrates.", "The infiltrates were composed mainly of histiocytes in a background of collagen fibers.", "Some histiocytes had foamy and eosinophilic cytoplasm.", "Some histiocytes were seen to engulf viable lymphocytes.", "This was thought to reflect emperipolesis (lymphophagocytosis).", "The histiocytes were immunopositive for S-100 protein and CD68.", "The histiocytes were negative for CD1\u03b1.", "All of these findings were consistent with extranodal RDD.", "The patient had incomplete left hemiparesis after surgery.", "A brain CT examination conducted without contrast revealed postoperative hemorrhage.", "A low-density lesion in the right frontal lobe was observed.", "The low-density lesion seemed to be due to the sacrificed pial arteries from the brain-tumor interface.", "His seizures completely ceased.", "A whole-body CT examination postoperatively was performed.", "Findings of lymphadenopathy or other extranodal involvements were not found.", "The patient has been free of seizures since the surgery.", "He recovered from his hemiparesis 6 months after the surgery."], "summary_subclaims": ["The patient was a 53-year-old man.", "The patient had an episode of generalized seizures.", "Imaging studies of the brain were compatible with a meningioma en plaque.", "The mass was exposed by a right frontotemporal craniotomy.", "The tumor was adhered tightly to the adjacent cerebral cortex.", "The tumor was permeated by pial arteries of the brain surface.", "The sacrificing of these arteries was inevitable in order to achieve the total removal of the tumor.", "The patient had incomplete left hemiparesis after the surgery.", "Brain computed tomography (CT) imaging revealed a postoperative hemorrhage.", "Brain computed tomography (CT) imaging revealed a low-density lesion in the right frontal lobe.", "The patient was postoperatively diagnosed with isolated central nervous system RDD."]}, "extra_info": {"fulltext_subclaims": ["The patient was a 53-year-old homeless man.", "He was admitted to the hospital due to a right femoral neck fracture.", "His medical history included noninsulin-dependent diabetes mellitus.", "A physical examination performed at admission was unremarkable.", "There was no fever.", "There was no lymphadenopathy.", "There were no other neurological defects.", "Laboratory tests revealed white blood cells of 4330 cells/mL.", "Laboratory tests revealed hemoglobin of 9.2 g/dL.", "Laboratory tests revealed platelet count of 29,900 platelets/mL.", "C-reactive protein was negative.", "Only normochromic-normocytic anemia was present.", "He successfully underwent surgery for the femoral neck fracture.", "The surgery was performed by an orthopedic surgeon.", "He had an episode of generalized seizures during the postoperative course.", "Phenytoin was administered.", "After this episode of generalized seizures, he was referred to our department.", "A computed tomography (CT) examination of the head without contrast showed a high-density and extraaxial mass in the right parietal convexity.", "Peritumoral brain edema was clearly observed.", "Enhanced magnetic resonance imaging (MRI) revealed an extraaxial, dural-based, and homogeneously enhanced mass with clear borders.", "The mass was compatible with a meningioma en plaque.", "The mass was iso- to hypointense on fluid-attenuated inversion recovery and T2 imaging sequences.", "The mass was iso- to hyperintense on T1 imaging.", "It was strongly suspected that the patient had a meningioma en plaque.", "The mass was exposed with a right frontotemporal craniotomy.", "The tumor appeared to be a meningioma en plaque.", "The tumor was extraaxial, xanthochromic, firm, nonaspiratable, and had high vascularity.", "The tumor was dural based.", "The tumor was tightly adhered to the adjacent cerebral cortex.", "The tumor was permeated by many pial arteries and veins of the brain surface.", "It is very difficult to preserve these pial vessels during the total removal of a tumor.", "A frozen section of the lesion showed inflammatory cell infiltration.", "The inflammatory cell infiltration mainly consisted of lymphocytes and plasma cells.", "The presence of these cells was initially interpreted as some kind of hematologic disorder or inflammatory pseudotumor.", "Paraffin-embedded sections showed a hypercellular pattern with features of polymorphous and mixed inflammatory infiltrates.", "The infiltrates were composed mainly of histiocytes in a background of collagen fibers.", "Some histiocytes had foamy and eosinophilic cytoplasm.", "Some histiocytes were seen to engulf viable lymphocytes.", "This was thought to reflect emperipolesis (lymphophagocytosis).", "The histiocytes were immunopositive for S-100 protein and CD68.", "The histiocytes were negative for CD1\u03b1.", "All of these findings were consistent with extranodal RDD.", "The patient had incomplete left hemiparesis after surgery.", "A brain CT examination conducted without contrast revealed postoperative hemorrhage.", "A low-density lesion in the right frontal lobe was observed.", "The low-density lesion seemed to be due to the sacrificed pial arteries from the brain-tumor interface.", "His seizures completely ceased.", "A whole-body CT examination postoperatively was performed.", "Findings of lymphadenopathy or other extranodal involvements were not found.", "The patient has been free of seizures since the surgery.", "He recovered from his hemiparesis 6 months after the surgery."], "index": 125, "original_id": "multiclinsum_test_1592_en.txt", "split": "test", "summary_subclaims": ["The patient was a 53-year-old man.", "The patient had an episode of generalized seizures.", "Imaging studies of the brain were compatible with a meningioma en plaque.", "The mass was exposed by a right frontotemporal craniotomy.", "The tumor was adhered tightly to the adjacent cerebral cortex.", "The tumor was permeated by pial arteries of the brain surface.", "The sacrificing of these arteries was inevitable in order to achieve the total removal of the tumor.", "The patient had incomplete left hemiparesis after the surgery.", "Brain computed tomography (CT) imaging revealed a postoperative hemorrhage.", "Brain computed tomography (CT) imaging revealed a low-density lesion in the right frontal lobe.", "The patient was postoperatively diagnosed with isolated central nervous system RDD."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 93-year-old Middle Eastern male.", "The patient has no known food or drug allergies.", "The patient has hypothyroidism.", "The patient has hypertension.", "The patient has dyslipidemia.", "The patient was admitted to the hospital owing to fatigue and refractory hiccups lasting for 2 weeks.", "The patient had had hiccups intermittently for more than 2 years.", "The patient had tried several medications, including proton-pump inhibitors, chlorpromazine, and baclofen, with minimal relief of his symptoms.", "The patient's home medications include levothyroxine, amlodipine, and rosuvastatin.", "The patient denies dysphagia, odynophagia, food impaction, heartburn, vomiting, or weight loss.", "Physical examination was unremarkable.", "Laboratory studies were only pertinent for an elevated eosinophil count of 18%.", "Stool studies were negative for parasitic infection.", "Imaging with computed tomography of the chest and abdomen was unremarkable.", "An upper endoscopy was performed and was normal, without any endoscopic finding to suggest EoE.", "Biopsies from the mid- and distal esophagus revealed eosinophilic infiltration in the range of 15 eosinophils per high-power field.", "The diagnosis favored EoE.", "The patient was prescribed a proton-pump inhibitor twice daily in combination with baclofen.", "The symptoms of intractable hiccups recurred despite partial initial improvement.", "The decision was made to switch therapy to topical budesonide 2 mg twice daily 30 minutes before meals.", "The frequency of the hiccup episodes gradually decreased and resolved completely within a week.", "Repeat blood test showed a decrease in eosinophilic count to 10%.", "A repeat endoscopy was offered but declined by the patient."], "summary_subclaims": ["The patient is a 93-year-old Middle Eastern male.", "The patient had longstanding treatment-refractory hiccups.", "Computed tomography of the chest and abdomen was unremarkable.", "An upper endoscopy was normal.", "There were no endoscopic findings to suggest eosinophilic esophagitis.", "The patient had an elevated peripheral eosinophil count.", "Biopsies were taken from the mid- and distal esophagus.", "The biopsies revealed eosinophilic infiltration in the range of 15 eosinophils per high-power field.", "The diagnosis favored eosinophilic esophagitis.", "The hiccups resolved following the initiation of eosinophilic esophagitis treatment."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 93-year-old Middle Eastern male.", "The patient has no known food or drug allergies.", "The patient has hypothyroidism.", "The patient has hypertension.", "The patient has dyslipidemia.", "The patient was admitted to the hospital owing to fatigue and refractory hiccups lasting for 2 weeks.", "The patient had had hiccups intermittently for more than 2 years.", "The patient had tried several medications, including proton-pump inhibitors, chlorpromazine, and baclofen, with minimal relief of his symptoms.", "The patient's home medications include levothyroxine, amlodipine, and rosuvastatin.", "The patient denies dysphagia, odynophagia, food impaction, heartburn, vomiting, or weight loss.", "Physical examination was unremarkable.", "Laboratory studies were only pertinent for an elevated eosinophil count of 18%.", "Stool studies were negative for parasitic infection.", "Imaging with computed tomography of the chest and abdomen was unremarkable.", "An upper endoscopy was performed and was normal, without any endoscopic finding to suggest EoE.", "Biopsies from the mid- and distal esophagus revealed eosinophilic infiltration in the range of 15 eosinophils per high-power field.", "The diagnosis favored EoE.", "The patient was prescribed a proton-pump inhibitor twice daily in combination with baclofen.", "The symptoms of intractable hiccups recurred despite partial initial improvement.", "The decision was made to switch therapy to topical budesonide 2 mg twice daily 30 minutes before meals.", "The frequency of the hiccup episodes gradually decreased and resolved completely within a week.", "Repeat blood test showed a decrease in eosinophilic count to 10%.", "A repeat endoscopy was offered but declined by the patient."], "index": 114, "original_id": "multiclinsum_test_3338_en.txt", "split": "test", "summary_subclaims": ["The patient is a 93-year-old Middle Eastern male.", "The patient had longstanding treatment-refractory hiccups.", "Computed tomography of the chest and abdomen was unremarkable.", "An upper endoscopy was normal.", "There were no endoscopic findings to suggest eosinophilic esophagitis.", "The patient had an elevated peripheral eosinophil count.", "Biopsies were taken from the mid- and distal esophagus.", "The biopsies revealed eosinophilic infiltration in the range of 15 eosinophils per high-power field.", "The diagnosis favored eosinophilic esophagitis.", "The hiccups resolved following the initiation of eosinophilic esophagitis treatment."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 22-year-old man.", "He had leg tremor in standing position for the previous 8 months.", "The tremor was initially bilateral.", "Seven months after development, the tremor subsided in the left leg.", "The tremor persisted only in the right leg.", "No tremor was evident when the patient was walking, reclining, or in a non-weight-bearing position.", "He denied any falls.", "He had no unsteadiness.", "There were no other complaints.", "The patient had no significant medical history.", "The patient had no family history of tremor.", "On examination, he showed incessant quivering in his right leg while standing.", "The tremor disappeared when he was asked to walk, sit, lie down, or lean against the wall for support.", "There was no resting or postural tremor of upper limbs.", "Bilateral tendon reflexes were diminished.", "There was no plantar response.", "Auscultation over the right popliteal fossa while the patient was standing revealed the 'helicopter sign'.", "The 'helicopter sign' indicated orthostatic tremor.", "All other components of neurological examination were normal.", "Laboratory tests, including routine blood tests, blood biochemistry, vitamin B12, thyroid hormone, rheumatoid factor, antinuclear autoantibody, anti-cardiolipin antibody, and anti-neutrophil cytoplasmic antibody tests, were normal.", "Tests of the blood and cerebrospinal fluid samples for anti-paraneoplastic antibodies, autoimmune antibodies, and anti-ganglioside antibodies were all normal.", "Brain MRI revealed mild, asymmetrical, non-enhancing white matter lesions, mainly in the right frontal and posterior periventricular regions, on T2-weighted imaging.", "No abnormal signal was found in the spinal cord on MRI.", "Chest CT was normal except for a residual thymus gland.", "FDG-PET was performed, and no abnormal metabolism was identified.", "EEG was normal.", "EMG recorded from the right gastrocnemius revealed a 6\u20138 Hz tremor.", "The tremor was present when the patient was standing and disappeared when he was resting or walking.", "No abnormalities were found in the left leg.", "These features were consistent with slow orthostatic tremor.", "Blood tests showed a phenylalanine/tyrosine ratio of 2.06.", "Blood phenylalanine level was 140 \u03bcmol/L.", "There was no phenylalanine in the urine.", "Whole-exome sequencing with NGS technology confirmed the presence of a compound heterozygous mutation in c.158G > A and c.728G > A of the PAH gene.", "Pedigree verification showed that the compound heterozygous variants were inherited from the parents.", "The patient\u2019s final diagnosis was orthostatic tremor secondary to mild hyperphenylalaninemia.", "The patient had not received any relevant interventions prior to admission.", "Clonazepam (1 mg, qd) was tried.", "Carbamazepine (100 mg, qd) was tried.", "Trihexyphenidyl (2 mg, tid) was tried.", "There was no clinical response to these treatments.", "After discharge, the patient was treated with levodopa/benserazide tablets (250 mg, tid) and a low-phenylalanine diet.", "One month later, the tremor was markedly alleviated.", "Three months later, the tremor disappeared."], "summary_subclaims": ["The patient is a 22-year-old male.", "The patient was admitted for bilateral leg tremor while standing.", "Symptom onset was eight months prior to admission.", "One month before admission, the tremor disappeared in the left leg.", "The tremor persisted in the right leg.", "Electromyography recorded from the right gastrocnemius revealed a 6-8\u00a0Hz tremor.", "The tremor appeared when the patient was standing.", "The tremor disappeared when the patient was resting or walking.", "Blood screening showed a phenylalanine/tyrosine ratio of 2.06.", "Blood screening showed a phenylalanine level of 140\u00a0\u03bcmol/L.", "Urine metabolic screening was negative.", "Whole-exome sequencing confirmed the presence of a compound heterozygous mutation, c.158G\u2009>\u2009A and c.728G\u2009>\u2009A, in the phenylalanine hydroxylase (PAH) gene.", "After three months of levodopa/benserazide tablets (250\u00a0mg, tid) and a low-phenylalanine diet treatment, the tremor disappeared."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 22-year-old man.", "He had leg tremor in standing position for the previous 8 months.", "The tremor was initially bilateral.", "Seven months after development, the tremor subsided in the left leg.", "The tremor persisted only in the right leg.", "No tremor was evident when the patient was walking, reclining, or in a non-weight-bearing position.", "He denied any falls.", "He had no unsteadiness.", "There were no other complaints.", "The patient had no significant medical history.", "The patient had no family history of tremor.", "On examination, he showed incessant quivering in his right leg while standing.", "The tremor disappeared when he was asked to walk, sit, lie down, or lean against the wall for support.", "There was no resting or postural tremor of upper limbs.", "Bilateral tendon reflexes were diminished.", "There was no plantar response.", "Auscultation over the right popliteal fossa while the patient was standing revealed the 'helicopter sign'.", "The 'helicopter sign' indicated orthostatic tremor.", "All other components of neurological examination were normal.", "Laboratory tests, including routine blood tests, blood biochemistry, vitamin B12, thyroid hormone, rheumatoid factor, antinuclear autoantibody, anti-cardiolipin antibody, and anti-neutrophil cytoplasmic antibody tests, were normal.", "Tests of the blood and cerebrospinal fluid samples for anti-paraneoplastic antibodies, autoimmune antibodies, and anti-ganglioside antibodies were all normal.", "Brain MRI revealed mild, asymmetrical, non-enhancing white matter lesions, mainly in the right frontal and posterior periventricular regions, on T2-weighted imaging.", "No abnormal signal was found in the spinal cord on MRI.", "Chest CT was normal except for a residual thymus gland.", "FDG-PET was performed, and no abnormal metabolism was identified.", "EEG was normal.", "EMG recorded from the right gastrocnemius revealed a 6\u20138 Hz tremor.", "The tremor was present when the patient was standing and disappeared when he was resting or walking.", "No abnormalities were found in the left leg.", "These features were consistent with slow orthostatic tremor.", "Blood tests showed a phenylalanine/tyrosine ratio of 2.06.", "Blood phenylalanine level was 140 \u03bcmol/L.", "There was no phenylalanine in the urine.", "Whole-exome sequencing with NGS technology confirmed the presence of a compound heterozygous mutation in c.158G > A and c.728G > A of the PAH gene.", "Pedigree verification showed that the compound heterozygous variants were inherited from the parents.", "The patient\u2019s final diagnosis was orthostatic tremor secondary to mild hyperphenylalaninemia.", "The patient had not received any relevant interventions prior to admission.", "Clonazepam (1 mg, qd) was tried.", "Carbamazepine (100 mg, qd) was tried.", "Trihexyphenidyl (2 mg, tid) was tried.", "There was no clinical response to these treatments.", "After discharge, the patient was treated with levodopa/benserazide tablets (250 mg, tid) and a low-phenylalanine diet.", "One month later, the tremor was markedly alleviated.", "Three months later, the tremor disappeared."], "index": 115, "original_id": "multiclinsum_test_1859_en.txt", "split": "test", "summary_subclaims": ["The patient is a 22-year-old male.", "The patient was admitted for bilateral leg tremor while standing.", "Symptom onset was eight months prior to admission.", "One month before admission, the tremor disappeared in the left leg.", "The tremor persisted in the right leg.", "Electromyography recorded from the right gastrocnemius revealed a 6-8\u00a0Hz tremor.", "The tremor appeared when the patient was standing.", "The tremor disappeared when the patient was resting or walking.", "Blood screening showed a phenylalanine/tyrosine ratio of 2.06.", "Blood screening showed a phenylalanine level of 140\u00a0\u03bcmol/L.", "Urine metabolic screening was negative.", "Whole-exome sequencing confirmed the presence of a compound heterozygous mutation, c.158G\u2009>\u2009A and c.728G\u2009>\u2009A, in the phenylalanine hydroxylase (PAH) gene.", "After three months of levodopa/benserazide tablets (250\u00a0mg, tid) and a low-phenylalanine diet treatment, the tremor disappeared."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 30-year-old woman.", "She is Caucasian.", "She presented with complaints of COVID-19.", "She developed symptoms after her husband returned from international travel.", "She initially had symptoms of an upper respiratory tract infection.", "She had nasal congestion.", "She had cough.", "She had fatigue.", "She had shortness of breath on ambulation.", "Ten days after her initial symptoms, she developed an urticarial rash on her abdomen, legs, and hands.", "The rash was transient.", "The rash reappeared twice before disappearing.", "The rash only lasted hours on each occasion.", "The patient has no past medical history.", "She takes no medications.", "She does not drink alcohol.", "She does not smoke cigarettes.", "She does not use drugs.", "She is married.", "She lives at home with her husband.", "She works as a wedding planner.", "She has no children.", "She has never been pregnant.", "She complained of tongue swelling on the tenth day after developing COVID-19.", "The swelling went away after 1 hour on its own.", "She then developed geographic tongue.", "Her tongue had the appearance of tongue papillae that were inflamed.", "Some papillae were flattened.", "Her tongue had a sensation of sensitivity in the areas interspersed between areas of regular mucosa.", "She had some mild loss of sense of taste.", "In the office, her blood pressure was 117/71 mmHg.", "Her heart rate was 90 beats per minute.", "Her temperature was 98.4 \u00b0F.", "Her respirations were 14 per minute.", "Her pulse oximetry was 100% on room air.", "On further examination, she had a geographic appearance to the tongue.", "Her abdomen and extremities showed no signs of rash at the time of the clinical examination.", "Her neurological examination showed intact motor and sensory strength.", "Her white blood cell count was 4100/\u03bcL.", "Her hemoglobin was 13.8 gm/dL.", "Her platelets were 248,000/\u03bcL.", "Her creatinine level was 0.79 mg/dL.", "Her aspartate transaminase level was 18 U/L.", "Her alanine transaminase level was 17 U/L.", "Her vitamin B12 level was 468 pg/mL.", "Her serum folate was 10.3 ng/mL.", "She was diagnosed as having COVID tongue.", "She was started on a mouthwash containing diphenhydramine-lidocaine-aluminum-magnesium-simethicone-nystatin.", "She was to swish and swallow 5 mL every 6 hours.", "She subsequently completed 30 days of the mouthwash.", "She achieved 90% improvement in the appearance of the geographic tongue.", "Over the next 6 months, she had multiple flares of tongue sensitivity.", "She had visually active tongue lesions about every 3 weeks.", "She was prescribed dexamethasone 0.5mg/5mL to be swished and spit four times daily for 10 days.", "She did not achieve complete resolution of her tongue lesions.", "Six months after developing COVID tongue, she underwent three treatments of photobiomodulation therapy (PBMT) to her tongue.", "There was an interval of 24 hours between each session.", "At a follow-up 2 months after the PBMT, she had no further flares.", "Her tongue lesions were healing.", "Her systemic rash never returned.", "She subsequently did well."], "summary_subclaims": ["The patient is a 30-year-old Caucasian woman.", "She tested positive for COVID-19 after developing nasal congestion and cough.", "Ten days after testing positive, she developed a systemic rash on her extremities and torso.", "She developed swelling of the tongue lasting 1 hour.", "She had oral lesions that resembled geographic tongue.", "She had an irritable sensation on her tongue.", "She had some mild loss of sense of taste.", "We opted for conservative therapy, including mouth rinses containing lidocaine to be used every 6 hours.", "The patient used the mouth rinse therapy for 1 month.", "She experienced a 90% improvement in her oral lesions and tongue sensitivity.", "She had repeated flares every 3 weeks over a 6-month period.", "The steroid mouthwash achieved incomplete resolution.", "After three sessions of photobiomodulation therapy, she had no further flares or tongue sensitivity.", "After three sessions of photobiomodulation therapy, the lesions healed."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 30-year-old woman.", "She is Caucasian.", "She presented with complaints of COVID-19.", "She developed symptoms after her husband returned from international travel.", "She initially had symptoms of an upper respiratory tract infection.", "She had nasal congestion.", "She had cough.", "She had fatigue.", "She had shortness of breath on ambulation.", "Ten days after her initial symptoms, she developed an urticarial rash on her abdomen, legs, and hands.", "The rash was transient.", "The rash reappeared twice before disappearing.", "The rash only lasted hours on each occasion.", "The patient has no past medical history.", "She takes no medications.", "She does not drink alcohol.", "She does not smoke cigarettes.", "She does not use drugs.", "She is married.", "She lives at home with her husband.", "She works as a wedding planner.", "She has no children.", "She has never been pregnant.", "She complained of tongue swelling on the tenth day after developing COVID-19.", "The swelling went away after 1 hour on its own.", "She then developed geographic tongue.", "Her tongue had the appearance of tongue papillae that were inflamed.", "Some papillae were flattened.", "Her tongue had a sensation of sensitivity in the areas interspersed between areas of regular mucosa.", "She had some mild loss of sense of taste.", "In the office, her blood pressure was 117/71 mmHg.", "Her heart rate was 90 beats per minute.", "Her temperature was 98.4 \u00b0F.", "Her respirations were 14 per minute.", "Her pulse oximetry was 100% on room air.", "On further examination, she had a geographic appearance to the tongue.", "Her abdomen and extremities showed no signs of rash at the time of the clinical examination.", "Her neurological examination showed intact motor and sensory strength.", "Her white blood cell count was 4100/\u03bcL.", "Her hemoglobin was 13.8 gm/dL.", "Her platelets were 248,000/\u03bcL.", "Her creatinine level was 0.79 mg/dL.", "Her aspartate transaminase level was 18 U/L.", "Her alanine transaminase level was 17 U/L.", "Her vitamin B12 level was 468 pg/mL.", "Her serum folate was 10.3 ng/mL.", "She was diagnosed as having COVID tongue.", "She was started on a mouthwash containing diphenhydramine-lidocaine-aluminum-magnesium-simethicone-nystatin.", "She was to swish and swallow 5 mL every 6 hours.", "She subsequently completed 30 days of the mouthwash.", "She achieved 90% improvement in the appearance of the geographic tongue.", "Over the next 6 months, she had multiple flares of tongue sensitivity.", "She had visually active tongue lesions about every 3 weeks.", "She was prescribed dexamethasone 0.5mg/5mL to be swished and spit four times daily for 10 days.", "She did not achieve complete resolution of her tongue lesions.", "Six months after developing COVID tongue, she underwent three treatments of photobiomodulation therapy (PBMT) to her tongue.", "There was an interval of 24 hours between each session.", "At a follow-up 2 months after the PBMT, she had no further flares.", "Her tongue lesions were healing.", "Her systemic rash never returned.", "She subsequently did well."], "index": 119, "original_id": "multiclinsum_test_778_en.txt", "split": "test", "summary_subclaims": ["The patient is a 30-year-old Caucasian woman.", "She tested positive for COVID-19 after developing nasal congestion and cough.", "Ten days after testing positive, she developed a systemic rash on her extremities and torso.", "She developed swelling of the tongue lasting 1 hour.", "She had oral lesions that resembled geographic tongue.", "She had an irritable sensation on her tongue.", "She had some mild loss of sense of taste.", "We opted for conservative therapy, including mouth rinses containing lidocaine to be used every 6 hours.", "The patient used the mouth rinse therapy for 1 month.", "She experienced a 90% improvement in her oral lesions and tongue sensitivity.", "She had repeated flares every 3 weeks over a 6-month period.", "The steroid mouthwash achieved incomplete resolution.", "After three sessions of photobiomodulation therapy, she had no further flares or tongue sensitivity.", "After three sessions of photobiomodulation therapy, the lesions healed."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 28-month-old girl.", "She was admitted due to repeated hematochezia for more than 3 months.", "She experienced hematochezia at the age of 25 months.", "The hematochezia was with small to moderate amounts of dark red or bright red paste-like stool.", "She had abdominal pain mainly around the umbilical area.", "The abdominal pain had no obvious relationship with eating.", "The abdominal pain was not accompanied by vomiting.", "The abdominal pain was not accompanied by diarrhea.", "The abdominal pain was not accompanied by fever.", "The abdominal pain was not accompanied by cough.", "Routine stool analysis showed red and white blood cells.", "The pathological culture was negative.", "The white blood cell count was 16.3 \u00d7 109/L.", "The hemoglobin concentration was 123 g/L.", "Abdominal ultrasound showed active intestinal peristalsis.", "Abdominal ultrasound showed multiple hypoechoic nodules around the umbilical area.", "Abdominal ultrasound showed enlarged mesenteric lymph nodes.", "Bacterial enteritis was suspected.", "The patient was treated with anti-infection and hemostatic drugs.", "The patient was fed with deeply hydrolyzed formula.", "The deeply hydrolyzed formula yielded poor therapeutic effects.", "The patient was transferred to our hospital.", "The patient was born to a healthy and non-consanguineous Chinese couple.", "The patient was delivered naturally.", "The patient was generally in good condition after delivery.", "The patient previously underwent a cervical lymph node abscess biopsy.", "No abnormalities in growth and development were observed.", "A small rash was observed on the neck.", "The white blood cell count was 11.70 \u00d7 109/L.", "The hemoglobin was 110 g/L.", "The platelet count was 38 \u00d7 109/L.", "The neutrophil percentage was 31%.", "The immunoglobulin G (IgG) was 16.7 g/L.", "The immunoglobulin M (IgM) was 1.66 g/L.", "The immunoglobulin E (IgE) was 74 IU/ML.", "The absolute count of B cells was 1688.52 cells/ul.", "The absolute count of T cells was 4833.95 cells/ul.", "The absolute count of NK cells was 877.12 cells/ul.", "The antiprotease 3 antibody (ELISA) was 64.5.", "The food allergen IgE for milk was 1.59 IU/ml.", "C-reactive protein, procalcitonin, blood gas analysis, biochemical indexes, coagulation index, autoimmune antibody, rheumatoid factor, and T-SPOT.TB test yielded no abnormal findings.", "No abnormality was found on chest and abdominal radiographs.", "An initial diagnosis of cow milk protein allergy and congenital immunodeficiency disease was established.", "A gastroscopy indicated erosive gastritis and erosive bulbar duodenitis.", "The histopathological results showed mild chronic inflammation.", "A colonoscopy indicated erosive colitis.", "The mucosa presented mild chronic inflammation.", "A large number of lymphocytes and eosinophils infiltrated in lamina propria.", "The maximum number of lymphocytes and eosinophils per high power field was 85.", "Crypt abscesses were found in the ascending and transverse colon.", "The DHR assay of the patient\u2019s granulocytes revealed almost absence of fluorescence upon granulocyte stimulation.", "The stimulation index (SI) was 5.82.", "The DHR assay of granulocytes from the patient\u2019s mother showed a SI of 277.05.", "The DHR assay of granulocytes from the patient\u2019s father showed a SI of 364.03.", "A heterozygous de novo mutation c.388 C > T (p.R130X) in CYBB gene was identified.", "The mutation was validated by Sanger sequencing.", "A diagnosis of very early onset inflammatory bowel disease (VEO-IBD) with neutrophil dysfunction caused by CYBB gene mutation was established.", "Hematopoietic stem cell transplantation (HSCT) was conducted using peripheral blood stem cells from the father.", "Mycophenolate Mofetil combined with Tacrolimus Capsules were used to prevent graft-versus-host disease (GVHD).", "Voriconazole was used against fungal infections.", "Two months after HSCT, bone marrow and peripheral blood chimerism rates were 100% complete donor type.", "The DHR assay of granulocytes from the patient at 8 weeks after HSCT showed abnormal histogram with the SI of 28.85.", "The DHR assay of granulocytes from the patient at 16 weeks after HSCT showed normal histogram with the SI of 408.90.", "Normal neutrophil function was restored.", "A repeat colonoscopy six months after HSCT showed complete intestinal mucosal healing.", "After 18 months of follow-up, there was no severe infection.", "After 18 months of follow-up, there was no acute or chronic GVHD-related manifestations."], "summary_subclaims": ["The patient is a 2-year-old girl.", "The patient had VEO-IBD associated with a monogenic mutation.", "The patient presented with gastrointestinal symptoms.", "The gastrointestinal symptoms included recurrent hematochezia.", "The gastrointestinal symptoms included abdominal pain.", "The symptoms had been present for more than 3 months.", "A gastroscopy revealed erosive gastritis.", "A gastroscopy revealed bulbar duodenitis.", "A colonoscopy indicated erosive colitis.", "Abnormal results were obtained from the dihydrohodamine (DHR) assay.", "Abnormal results were obtained from immunoglobulin testing.", "Whole-exome sequencing identified a heterozygous and de novo nonsense mutation (c.388\u00a0C\u2009>\u2009T; p.R130X) in the CYBB gene.", "The mutation led to deficiency of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (NOX2).", "NOX2 is encoded by CYBB.", "NOX2 is a critical component of phagocytes.", "HSCT was performed successfully.", "The DHR assay showed that normal neutrophil function was restored.", "Six months after HSCT, clinical remission was observed.", "A repeat colonoscopy revealed intestinal mucosal healing was attained."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 28-month-old girl.", "She was admitted due to repeated hematochezia for more than 3 months.", "She experienced hematochezia at the age of 25 months.", "The hematochezia was with small to moderate amounts of dark red or bright red paste-like stool.", "She had abdominal pain mainly around the umbilical area.", "The abdominal pain had no obvious relationship with eating.", "The abdominal pain was not accompanied by vomiting.", "The abdominal pain was not accompanied by diarrhea.", "The abdominal pain was not accompanied by fever.", "The abdominal pain was not accompanied by cough.", "Routine stool analysis showed red and white blood cells.", "The pathological culture was negative.", "The white blood cell count was 16.3 \u00d7 109/L.", "The hemoglobin concentration was 123 g/L.", "Abdominal ultrasound showed active intestinal peristalsis.", "Abdominal ultrasound showed multiple hypoechoic nodules around the umbilical area.", "Abdominal ultrasound showed enlarged mesenteric lymph nodes.", "Bacterial enteritis was suspected.", "The patient was treated with anti-infection and hemostatic drugs.", "The patient was fed with deeply hydrolyzed formula.", "The deeply hydrolyzed formula yielded poor therapeutic effects.", "The patient was transferred to our hospital.", "The patient was born to a healthy and non-consanguineous Chinese couple.", "The patient was delivered naturally.", "The patient was generally in good condition after delivery.", "The patient previously underwent a cervical lymph node abscess biopsy.", "No abnormalities in growth and development were observed.", "A small rash was observed on the neck.", "The white blood cell count was 11.70 \u00d7 109/L.", "The hemoglobin was 110 g/L.", "The platelet count was 38 \u00d7 109/L.", "The neutrophil percentage was 31%.", "The immunoglobulin G (IgG) was 16.7 g/L.", "The immunoglobulin M (IgM) was 1.66 g/L.", "The immunoglobulin E (IgE) was 74 IU/ML.", "The absolute count of B cells was 1688.52 cells/ul.", "The absolute count of T cells was 4833.95 cells/ul.", "The absolute count of NK cells was 877.12 cells/ul.", "The antiprotease 3 antibody (ELISA) was 64.5.", "The food allergen IgE for milk was 1.59 IU/ml.", "C-reactive protein, procalcitonin, blood gas analysis, biochemical indexes, coagulation index, autoimmune antibody, rheumatoid factor, and T-SPOT.TB test yielded no abnormal findings.", "No abnormality was found on chest and abdominal radiographs.", "An initial diagnosis of cow milk protein allergy and congenital immunodeficiency disease was established.", "A gastroscopy indicated erosive gastritis and erosive bulbar duodenitis.", "The histopathological results showed mild chronic inflammation.", "A colonoscopy indicated erosive colitis.", "The mucosa presented mild chronic inflammation.", "A large number of lymphocytes and eosinophils infiltrated in lamina propria.", "The maximum number of lymphocytes and eosinophils per high power field was 85.", "Crypt abscesses were found in the ascending and transverse colon.", "The DHR assay of the patient\u2019s granulocytes revealed almost absence of fluorescence upon granulocyte stimulation.", "The stimulation index (SI) was 5.82.", "The DHR assay of granulocytes from the patient\u2019s mother showed a SI of 277.05.", "The DHR assay of granulocytes from the patient\u2019s father showed a SI of 364.03.", "A heterozygous de novo mutation c.388 C > T (p.R130X) in CYBB gene was identified.", "The mutation was validated by Sanger sequencing.", "A diagnosis of very early onset inflammatory bowel disease (VEO-IBD) with neutrophil dysfunction caused by CYBB gene mutation was established.", "Hematopoietic stem cell transplantation (HSCT) was conducted using peripheral blood stem cells from the father.", "Mycophenolate Mofetil combined with Tacrolimus Capsules were used to prevent graft-versus-host disease (GVHD).", "Voriconazole was used against fungal infections.", "Two months after HSCT, bone marrow and peripheral blood chimerism rates were 100% complete donor type.", "The DHR assay of granulocytes from the patient at 8 weeks after HSCT showed abnormal histogram with the SI of 28.85.", "The DHR assay of granulocytes from the patient at 16 weeks after HSCT showed normal histogram with the SI of 408.90.", "Normal neutrophil function was restored.", "A repeat colonoscopy six months after HSCT showed complete intestinal mucosal healing.", "After 18 months of follow-up, there was no severe infection.", "After 18 months of follow-up, there was no acute or chronic GVHD-related manifestations."], "index": 121, "original_id": "multiclinsum_test_533_en.txt", "split": "test", "summary_subclaims": ["The patient is a 2-year-old girl.", "The patient had VEO-IBD associated with a monogenic mutation.", "The patient presented with gastrointestinal symptoms.", "The gastrointestinal symptoms included recurrent hematochezia.", "The gastrointestinal symptoms included abdominal pain.", "The symptoms had been present for more than 3 months.", "A gastroscopy revealed erosive gastritis.", "A gastroscopy revealed bulbar duodenitis.", "A colonoscopy indicated erosive colitis.", "Abnormal results were obtained from the dihydrohodamine (DHR) assay.", "Abnormal results were obtained from immunoglobulin testing.", "Whole-exome sequencing identified a heterozygous and de novo nonsense mutation (c.388\u00a0C\u2009>\u2009T; p.R130X) in the CYBB gene.", "The mutation led to deficiency of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (NOX2).", "NOX2 is encoded by CYBB.", "NOX2 is a critical component of phagocytes.", "HSCT was performed successfully.", "The DHR assay showed that normal neutrophil function was restored.", "Six months after HSCT, clinical remission was observed.", "A repeat colonoscopy revealed intestinal mucosal healing was attained."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 32-year-old female.", "The patient has non-diabetic chronic kidney disease.", "The patient was on regular hemodialysis for 3 years.", "The patient's hemodialysis access was a right forearm arteriovenous fistula.", "The patient was admitted due to involuntary movement for 5 days.", "The patient had a resting tremor in the shoulder and neck 5 days prior to admission.", "The patient's vital signs were stable.", "The patient did not have a headache.", "The patient did not have fever.", "The patient did not have blurred vision.", "The patient did not have mental disorder.", "Myodynamic examination in both legs was normal.", "Deep tendon reflexes in both legs were normal.", "The Babinski reflexes were suspiciously positive.", "The patient had significant fluctuation of blood creatinine levels.", "The patient had altered hyperthyroidism.", "The patient's intact parathyroid hormone (iPTH) levels were almost 3200 pg/mL.", "The patient did not have a history of hypertension.", "The patient did not have diabetes mellitus.", "The patient did not have a respiratory tract infection.", "The patient did not have fever.", "The patient did not have stroke.", "The patient did not have liver disease.", "The patient did not have hypoxia.", "The patient did not have toxic fume exposure.", "Brain MRI showed symmetrical T2-weighted imaging hyperintense non-hemorrhagic lesions in bilateral basal ganglia.", "Brain MRI showed T2/fluid-attenuated inversion recovery hyperintense lesions in bilateral basal ganglia.", "Brain MRI showed corona radiata lesions with mild diffusion restriction.", "T1-weighted imaging was normal.", "Diffusion-weighted images were normal.", "Blood analysis showed urea nitrogen 25.80 mmol/L.", "Blood analysis showed serum creatinine 1206 \u03bcmol/L.", "Blood analysis showed uric acid 548 \u03bcmol/L.", "Blood analysis showed phosphorus 1.88 mmol/L.", "Blood analysis showed calcium 2.33 mmol/L.", "Blood analysis showed anion gap 23.9 mmol/L.", "Blood analysis showed iPTH 2487 pg/mL.", "The patient was diagnosed with UE as a symptom of bilateral basal ganglia lesions.", "The patient did not suffer from diabetes mellitus.", "The patient did not suffer from cerebrovascular events.", "The patient did not suffer from intoxication.", "The patient did not suffer from hyperlactacidemia.", "UE was possibly due to a combined effect of uremic toxins and hyperthyroidism.", "The patient was treated with high frequency and high flux dialysis.", "The patient received 4 h hemodiafiltration with APS 15 uc dialyzer.", "The patient received hemodiafiltration 4 times per week.", "The patient received hyperbaric oxygen therapy.", "The patient received 1 \u03bcg of calcitriol injection every 2 days.", "The patient received 2 mg of haloperidol orally twice per day.", "The patient received 2 mg of clonazepam orally twice per day.", "The patient received 2 mg of benzhexol orally twice per day.", "The symptoms reduced in frequency.", "The amplitude of involuntary movement decreased.", "Fourteen days after admission, brain MRI showed high signal in the bilateral basal ganglia on T2WI.", "Fourteen days after admission, brain MRI showed high signal in the bilateral basal ganglia on T2FLAIR.", "The signal in the bilateral basal ganglia on T2WI was significantly weaker compared to the initial MRI signal.", "The signal in the bilateral basal ganglia on T2FLAIR was significantly weaker compared to the initial MRI signal.", "About 1 month after admission, the patient achieved complete remission.", "About 1 month after admission, the patient had restoration of normal body movement.", "Upon discharge, blood test results showed urea nitrogen 10.48 mmol/L.", "Upon discharge, blood test results showed serum creatinine 641.5 \u03bcmol/L.", "Upon discharge, blood test results showed uric acid 435 \u03bcmol/L.", "Upon discharge, blood test results showed phosphorus 1.43 mmol/L.", "Upon discharge, blood test results showed calcium 2.30 mmol/L.", "Upon discharge, blood test results showed anion gap 15.9 mmol/L.", "Upon discharge, blood test results showed iPTH 1609 pg/mL.", "Upon follow-up, brain MRI showed an almost complete resolution of the lesions.", "Upon follow-up, brain MRI showed slightly hyperintense signal in the bilateral basal ganglia."], "summary_subclaims": ["The patient is a 32\u2009year-old woman.", "She has a history of non-diabetic hemodialysis for 3\u2009years.", "She suffered from severe involuntary movement.", "Brain magnetic resonance imaging showed symmetrical T2-weighted imaging (T2WI) and T2/fluid-attenuated inversion recovery (T2FLAIR) hyperintense nonhemorrhagic lesions in the bilateral basal ganglia.", "She was diagnosed with UE as syndrome of bilateral basal ganglia lesions.", "The diagnosis was due to a combined effect of uremic toxins and hyperthyroidism.", "She received treatment with high frequency and high flux dialysis.", "She received hyperbaric oxygen therapy.", "She had declining parathyroid hormone.", "The patient achieved complete remission with normal body movement.", "The patient was discharged."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 32-year-old female.", "The patient has non-diabetic chronic kidney disease.", "The patient was on regular hemodialysis for 3 years.", "The patient's hemodialysis access was a right forearm arteriovenous fistula.", "The patient was admitted due to involuntary movement for 5 days.", "The patient had a resting tremor in the shoulder and neck 5 days prior to admission.", "The patient's vital signs were stable.", "The patient did not have a headache.", "The patient did not have fever.", "The patient did not have blurred vision.", "The patient did not have mental disorder.", "Myodynamic examination in both legs was normal.", "Deep tendon reflexes in both legs were normal.", "The Babinski reflexes were suspiciously positive.", "The patient had significant fluctuation of blood creatinine levels.", "The patient had altered hyperthyroidism.", "The patient's intact parathyroid hormone (iPTH) levels were almost 3200 pg/mL.", "The patient did not have a history of hypertension.", "The patient did not have diabetes mellitus.", "The patient did not have a respiratory tract infection.", "The patient did not have fever.", "The patient did not have stroke.", "The patient did not have liver disease.", "The patient did not have hypoxia.", "The patient did not have toxic fume exposure.", "Brain MRI showed symmetrical T2-weighted imaging hyperintense non-hemorrhagic lesions in bilateral basal ganglia.", "Brain MRI showed T2/fluid-attenuated inversion recovery hyperintense lesions in bilateral basal ganglia.", "Brain MRI showed corona radiata lesions with mild diffusion restriction.", "T1-weighted imaging was normal.", "Diffusion-weighted images were normal.", "Blood analysis showed urea nitrogen 25.80 mmol/L.", "Blood analysis showed serum creatinine 1206 \u03bcmol/L.", "Blood analysis showed uric acid 548 \u03bcmol/L.", "Blood analysis showed phosphorus 1.88 mmol/L.", "Blood analysis showed calcium 2.33 mmol/L.", "Blood analysis showed anion gap 23.9 mmol/L.", "Blood analysis showed iPTH 2487 pg/mL.", "The patient was diagnosed with UE as a symptom of bilateral basal ganglia lesions.", "The patient did not suffer from diabetes mellitus.", "The patient did not suffer from cerebrovascular events.", "The patient did not suffer from intoxication.", "The patient did not suffer from hyperlactacidemia.", "UE was possibly due to a combined effect of uremic toxins and hyperthyroidism.", "The patient was treated with high frequency and high flux dialysis.", "The patient received 4 h hemodiafiltration with APS 15 uc dialyzer.", "The patient received hemodiafiltration 4 times per week.", "The patient received hyperbaric oxygen therapy.", "The patient received 1 \u03bcg of calcitriol injection every 2 days.", "The patient received 2 mg of haloperidol orally twice per day.", "The patient received 2 mg of clonazepam orally twice per day.", "The patient received 2 mg of benzhexol orally twice per day.", "The symptoms reduced in frequency.", "The amplitude of involuntary movement decreased.", "Fourteen days after admission, brain MRI showed high signal in the bilateral basal ganglia on T2WI.", "Fourteen days after admission, brain MRI showed high signal in the bilateral basal ganglia on T2FLAIR.", "The signal in the bilateral basal ganglia on T2WI was significantly weaker compared to the initial MRI signal.", "The signal in the bilateral basal ganglia on T2FLAIR was significantly weaker compared to the initial MRI signal.", "About 1 month after admission, the patient achieved complete remission.", "About 1 month after admission, the patient had restoration of normal body movement.", "Upon discharge, blood test results showed urea nitrogen 10.48 mmol/L.", "Upon discharge, blood test results showed serum creatinine 641.5 \u03bcmol/L.", "Upon discharge, blood test results showed uric acid 435 \u03bcmol/L.", "Upon discharge, blood test results showed phosphorus 1.43 mmol/L.", "Upon discharge, blood test results showed calcium 2.30 mmol/L.", "Upon discharge, blood test results showed anion gap 15.9 mmol/L.", "Upon discharge, blood test results showed iPTH 1609 pg/mL.", "Upon follow-up, brain MRI showed an almost complete resolution of the lesions.", "Upon follow-up, brain MRI showed slightly hyperintense signal in the bilateral basal ganglia."], "index": 129, "original_id": "multiclinsum_test_168_en.txt", "split": "test", "summary_subclaims": ["The patient is a 32\u2009year-old woman.", "She has a history of non-diabetic hemodialysis for 3\u2009years.", "She suffered from severe involuntary movement.", "Brain magnetic resonance imaging showed symmetrical T2-weighted imaging (T2WI) and T2/fluid-attenuated inversion recovery (T2FLAIR) hyperintense nonhemorrhagic lesions in the bilateral basal ganglia.", "She was diagnosed with UE as syndrome of bilateral basal ganglia lesions.", "The diagnosis was due to a combined effect of uremic toxins and hyperthyroidism.", "She received treatment with high frequency and high flux dialysis.", "She received hyperbaric oxygen therapy.", "She had declining parathyroid hormone.", "The patient achieved complete remission with normal body movement.", "The patient was discharged."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was admitted to our hospital four days ago.", "The patient had been diagnosed with xerostomia and xerophthalmia over 20 years.", "Emission Computed Tomography (ECT) examination revealed decreased functions of bilateral parotid and submandibular glands.", "A chest CT three years ago showed scattered, various-sized and roundish radiolucencies, striped or hazy opacities in both lungs and multiple small nodules in the right lung.", "Another chest CT one year later revealed new patchy opacities in the right lung and lingual lobe.", "The patient was admitted to our hospital one year and 4 months later due to recurrent cough, expectoration and low fever.", "The chest CT revealed multiple cysts with multiple patchy and nodular opacities in both lungs.", "Results of antinuclear antibody profiles and vasculitis series were: SSA (RO-52) positive (+), SSA antibody positive (+), ESR 87 mm/hr.", "Immunoglobulins were: IgA 4.29 g/L, IgG 20.3 g/L and IgM 0.68 g/L.", "Blood gas analysis: pH 7.39, pCO2 39.5 mmHg, pO2 68.4 mmHg and SaO2 93.1%.", "Pathological report on (right lung biopsy): Chronic inflammation of lung tissue with diffuse distribution of lymphocytes in focal areas.", "Diagnosis: lymphoma could not be excluded.", "Preliminary clinical diagnosis: (1) Sjogren's syndrome, lymphocytic interstitial pneumonia first consideration; (2) malignant lymphoma to be excluded; (3) pulmonary infection.", "The patient received anti-inflammatory treatment and was discharged after symptoms were improved.", "After discharge, the patient continued to experience constant cough, expectoration and fever even after repeated anti-inflammatory treatments.", "A left lung biopsy was performed 4 months later during her inpatient treatment in another hospital.", "The pathological report indicated chronic suppurative inflammation with massive necrosis and cellulitis.", "The patient\u2019s chest enhancement CT after this admission displayed obviously more patchy and nodular foci in both lungs compared to previous CT images.", "Some of the lesions were surrounded with ground glass shadows.", "The diagnosis was: malignant tumor to be excluded.", "Auxiliary routine blood examinations showed white blood cell count 21.8 \u00d7 109/L and absolute neutrophil count 21.14 \u00d7 109/L.", "Pathological results from our hospital (right lung biopsy) and another hospital showed small areas of proliferating inflammatory fibrous tissue and small numbers of heterotypic cells within the necrotic tissue.", "Malignancy could not be excluded.", "Immunohistochemistry showed: CD20 (+), Ki-67 (high-value-added activity), BCL-6 (+), CD21 (+).", "Based on history and pathological results, the final diagnosis was Sjogren's syndrome, malignant transformation of LIP into diffuse large B-cell lymphoma.", "Subsequently, chemotherapy with a reduced-dose regimen of rituximab and Chop (R-miniCHOP) was administered eight times.", "Following treatment, PET/CT showed complete remission of lymphoma.", "The patient was at high risk of recurrence and is under active follow-up."], "summary_subclaims": ["The patient is a 64-year-old female.", "The patient has Sjogren's syndrome.", "The medical record was reviewed.", "Clinical and pathological data were obtained.", "Chest CT images were obtained.", "Literature related to the transformation was reviewed.", "There were no specific clinical manifestations of LIP and its transformation into malignant lymphoma in the patient.", "The chest CT mainly displayed multiple cystic foci.", "The chest CT showed multiple nodules in both lungs.", "The chest CT showed ground-glass shadows in both lungs."]}, "extra_info": {"fulltext_subclaims": ["The patient was admitted to our hospital four days ago.", "The patient had been diagnosed with xerostomia and xerophthalmia over 20 years.", "Emission Computed Tomography (ECT) examination revealed decreased functions of bilateral parotid and submandibular glands.", "A chest CT three years ago showed scattered, various-sized and roundish radiolucencies, striped or hazy opacities in both lungs and multiple small nodules in the right lung.", "Another chest CT one year later revealed new patchy opacities in the right lung and lingual lobe.", "The patient was admitted to our hospital one year and 4 months later due to recurrent cough, expectoration and low fever.", "The chest CT revealed multiple cysts with multiple patchy and nodular opacities in both lungs.", "Results of antinuclear antibody profiles and vasculitis series were: SSA (RO-52) positive (+), SSA antibody positive (+), ESR 87 mm/hr.", "Immunoglobulins were: IgA 4.29 g/L, IgG 20.3 g/L and IgM 0.68 g/L.", "Blood gas analysis: pH 7.39, pCO2 39.5 mmHg, pO2 68.4 mmHg and SaO2 93.1%.", "Pathological report on (right lung biopsy): Chronic inflammation of lung tissue with diffuse distribution of lymphocytes in focal areas.", "Diagnosis: lymphoma could not be excluded.", "Preliminary clinical diagnosis: (1) Sjogren's syndrome, lymphocytic interstitial pneumonia first consideration; (2) malignant lymphoma to be excluded; (3) pulmonary infection.", "The patient received anti-inflammatory treatment and was discharged after symptoms were improved.", "After discharge, the patient continued to experience constant cough, expectoration and fever even after repeated anti-inflammatory treatments.", "A left lung biopsy was performed 4 months later during her inpatient treatment in another hospital.", "The pathological report indicated chronic suppurative inflammation with massive necrosis and cellulitis.", "The patient\u2019s chest enhancement CT after this admission displayed obviously more patchy and nodular foci in both lungs compared to previous CT images.", "Some of the lesions were surrounded with ground glass shadows.", "The diagnosis was: malignant tumor to be excluded.", "Auxiliary routine blood examinations showed white blood cell count 21.8 \u00d7 109/L and absolute neutrophil count 21.14 \u00d7 109/L.", "Pathological results from our hospital (right lung biopsy) and another hospital showed small areas of proliferating inflammatory fibrous tissue and small numbers of heterotypic cells within the necrotic tissue.", "Malignancy could not be excluded.", "Immunohistochemistry showed: CD20 (+), Ki-67 (high-value-added activity), BCL-6 (+), CD21 (+).", "Based on history and pathological results, the final diagnosis was Sjogren's syndrome, malignant transformation of LIP into diffuse large B-cell lymphoma.", "Subsequently, chemotherapy with a reduced-dose regimen of rituximab and Chop (R-miniCHOP) was administered eight times.", "Following treatment, PET/CT showed complete remission of lymphoma.", "The patient was at high risk of recurrence and is under active follow-up."], "index": 131, "original_id": "multiclinsum_test_2470_en.txt", "split": "test", "summary_subclaims": ["The patient is a 64-year-old female.", "The patient has Sjogren's syndrome.", "The medical record was reviewed.", "Clinical and pathological data were obtained.", "Chest CT images were obtained.", "Literature related to the transformation was reviewed.", "There were no specific clinical manifestations of LIP and its transformation into malignant lymphoma in the patient.", "The chest CT mainly displayed multiple cystic foci.", "The chest CT showed multiple nodules in both lungs.", "The chest CT showed ground-glass shadows in both lungs."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was a 21-year-old man.", "He visited a clinic with a chief complaint of right inguinal pain.", "Abdominal ultrasonography revealed a huge intra-abdominal mass.", "He was referred to the hospital for further examination.", "He had a history of autism spectrum disorder.", "He had a history of bronchial asthma.", "The abdomen was mildly distended and soft.", "The tumor was not palpable.", "Laboratory examinations showed no abnormalities in blood count.", "Laboratory examinations showed no elevation of tumor markers.", "Abdominopelvic CT showed a huge mass with a maximum diameter of 34 cm.", "MRI revealed an intra-abdominal tumor 34 \u00d7 15 \u00d7 8 cm.", "The tumor appeared to be in contact with the gastric body.", "A contrast-enhanced examination could not be performed due to the history of bronchial asthma.", "Endoscopic ultrasonography showed a heterogeneous hypoechoic internal cavity.", "EUS-FNA was not performed, given the risk of seeding.", "No definitive diagnosis or organ of origin was confirmed preoperatively.", "Surgery was performed under suspicion of gastrointestinal stromal tumor.", "Surgery was performed under suspicion of desmoid tumor.", "Surgery was performed under suspicion of mesenteric tumor.", "Laparotomy was performed through upper and lower median incisions.", "Intraoperative findings showed a giant tumor covered with a capsule.", "The tumor extended from the pelvis to the diaphragm.", "The tumor showed firm adhesions to the stomach.", "The tumor showed firm adhesions to the transverse colon.", "The tumor showed firm adhesions to the diaphragm.", "The omentum was adherent to the tumor.", "The tumor was partially resected en bloc with portions of the stomach.", "The tumor was partially resected en bloc with portions of the transverse colon.", "The tumor was partially resected en bloc with portions of the diaphragm.", "Primary anastomosis of the colon was performed.", "The diaphragm was closed after tumor resection.", "The tumor appeared to have been completely excised without rupture of the capsule.", "The excised specimen measured 38 \u00d7 21 \u00d7 8 cm.", "The excised specimen weighed 6400 g.", "Pathological examination revealed atypical cells with spindle-shaped nuclei.", "Immunostaining showed negative results for c-kit.", "Immunostaining showed negative results for CD34.", "Immunostaining showed negative results for desmin.", "Immunostaining showed negative results for S-100.", "Immunostaining showed positive results for \u03b2-catenin.", "The diagnosis was confirmed as a desmoid tumor.", "Pathological results for the surgical margins were negative.", "Determining the primary site of tumor origin was difficult.", "The patient was discharged 17 days after surgery.", "A CT scan conducted 12 months after surgery showed a nodule 3.0 cm in diameter near the suture line of the gastric body.", "The nodule's size remained unchanged on a subsequent CT scan taken 9 months later."], "summary_subclaims": ["The patient was a 21-year-old man.", "He was referred to the hospital for treatment.", "He had right inguinal pain.", "Abdominal magnetic resonance imaging showed an intra-abdominal mass.", "The mass measured 34 \u00d7 15 \u00d7 8 cm.", "The mass showed partial signal hyperintensity on T2-weighted imaging.", "The mass showed hypointensity on T1-weighted imaging.", "The mass extended from the left abdominal cavity to the pelvic region.", "No definitive diagnosis was obtained preoperatively.", "Surgery was performed under suspicion of gastrointestinal stromal tumor or other significant disease.", "A mass was identified firmly adherent to the transverse colon.", "The mass was identified firmly adherent to the gastric wall.", "The mass was identified firmly adherent to the diaphragm.", "The transverse colon, gastric wall, and diaphragm were partially resected.", "The excised specimen measured 38 \u00d7 21 \u00d7 8 cm.", "The excised specimen weighed 6400 g.", "Macroscopically, the tumor showed a smooth surface.", "Macroscopically, the tumor showed a homogeneous interior.", "Pathological examination revealed atypical cells with spindle-shaped nuclei.", "Pathological examination revealed collagen fiber hyperplasia in the stroma.", "Immunostaining was negative for c-kit.", "Immunostaining was negative for CD34.", "Immunostaining was negative for desmin.", "Immunostaining was negative for S-100.", "Immunostaining was positive for \u03b2-catenin.", "The diagnosis was confirmed as desmoid tumor.", "Fifteen months after surgery, a local recurrence with a diameter of 3.0 cm was identified.", "The patient remains under careful follow-up."]}, "extra_info": {"fulltext_subclaims": ["The patient was a 21-year-old man.", "He visited a clinic with a chief complaint of right inguinal pain.", "Abdominal ultrasonography revealed a huge intra-abdominal mass.", "He was referred to the hospital for further examination.", "He had a history of autism spectrum disorder.", "He had a history of bronchial asthma.", "The abdomen was mildly distended and soft.", "The tumor was not palpable.", "Laboratory examinations showed no abnormalities in blood count.", "Laboratory examinations showed no elevation of tumor markers.", "Abdominopelvic CT showed a huge mass with a maximum diameter of 34 cm.", "MRI revealed an intra-abdominal tumor 34 \u00d7 15 \u00d7 8 cm.", "The tumor appeared to be in contact with the gastric body.", "A contrast-enhanced examination could not be performed due to the history of bronchial asthma.", "Endoscopic ultrasonography showed a heterogeneous hypoechoic internal cavity.", "EUS-FNA was not performed, given the risk of seeding.", "No definitive diagnosis or organ of origin was confirmed preoperatively.", "Surgery was performed under suspicion of gastrointestinal stromal tumor.", "Surgery was performed under suspicion of desmoid tumor.", "Surgery was performed under suspicion of mesenteric tumor.", "Laparotomy was performed through upper and lower median incisions.", "Intraoperative findings showed a giant tumor covered with a capsule.", "The tumor extended from the pelvis to the diaphragm.", "The tumor showed firm adhesions to the stomach.", "The tumor showed firm adhesions to the transverse colon.", "The tumor showed firm adhesions to the diaphragm.", "The omentum was adherent to the tumor.", "The tumor was partially resected en bloc with portions of the stomach.", "The tumor was partially resected en bloc with portions of the transverse colon.", "The tumor was partially resected en bloc with portions of the diaphragm.", "Primary anastomosis of the colon was performed.", "The diaphragm was closed after tumor resection.", "The tumor appeared to have been completely excised without rupture of the capsule.", "The excised specimen measured 38 \u00d7 21 \u00d7 8 cm.", "The excised specimen weighed 6400 g.", "Pathological examination revealed atypical cells with spindle-shaped nuclei.", "Immunostaining showed negative results for c-kit.", "Immunostaining showed negative results for CD34.", "Immunostaining showed negative results for desmin.", "Immunostaining showed negative results for S-100.", "Immunostaining showed positive results for \u03b2-catenin.", "The diagnosis was confirmed as a desmoid tumor.", "Pathological results for the surgical margins were negative.", "Determining the primary site of tumor origin was difficult.", "The patient was discharged 17 days after surgery.", "A CT scan conducted 12 months after surgery showed a nodule 3.0 cm in diameter near the suture line of the gastric body.", "The nodule's size remained unchanged on a subsequent CT scan taken 9 months later."], "index": 112, "original_id": "multiclinsum_test_3373_en.txt", "split": "test", "summary_subclaims": ["The patient was a 21-year-old man.", "He was referred to the hospital for treatment.", "He had right inguinal pain.", "Abdominal magnetic resonance imaging showed an intra-abdominal mass.", "The mass measured 34 \u00d7 15 \u00d7 8 cm.", "The mass showed partial signal hyperintensity on T2-weighted imaging.", "The mass showed hypointensity on T1-weighted imaging.", "The mass extended from the left abdominal cavity to the pelvic region.", "No definitive diagnosis was obtained preoperatively.", "Surgery was performed under suspicion of gastrointestinal stromal tumor or other significant disease.", "A mass was identified firmly adherent to the transverse colon.", "The mass was identified firmly adherent to the gastric wall.", "The mass was identified firmly adherent to the diaphragm.", "The transverse colon, gastric wall, and diaphragm were partially resected.", "The excised specimen measured 38 \u00d7 21 \u00d7 8 cm.", "The excised specimen weighed 6400 g.", "Macroscopically, the tumor showed a smooth surface.", "Macroscopically, the tumor showed a homogeneous interior.", "Pathological examination revealed atypical cells with spindle-shaped nuclei.", "Pathological examination revealed collagen fiber hyperplasia in the stroma.", "Immunostaining was negative for c-kit.", "Immunostaining was negative for CD34.", "Immunostaining was negative for desmin.", "Immunostaining was negative for S-100.", "Immunostaining was positive for \u03b2-catenin.", "The diagnosis was confirmed as desmoid tumor.", "Fifteen months after surgery, a local recurrence with a diameter of 3.0 cm was identified.", "The patient remains under careful follow-up."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["A 5-year-old girl initially presented to our department due to worsening pain in the left proximal thigh.", "Osteosarcoma was suspected radiographically.", "Open biopsy revealed a high-grade conventional osteosarcoma.", "The tumor was initially staged as IIB (T2b N0 M0).", "Neoadjuvant chemotherapy was commenced in accordance with the NECO-95J protocol.", "After three cycles of neoadjuvant chemotherapy, the pain was alleviated.", "The extra-osseous mass was dramatically reduced.", "Limb-salvage surgery was planned.", "The tumor had already invaded the epiphyseal plate and epiphysis of the left distal femur at initial presentation.", "Osteo-articular resection was thought necessary so as to obtain a negative surgical margin.", "At 6 years and 2 months old, distal femoral resection and temporary spacer insertion was performed.", "Both medial and lateral meniscuses were preserved.", "The spacer was hand-made, using an intramedullary nail of 7 mm in diameter and molded polymethylmethacrylate (PMMA).", "Because there were no commercially available molds fitting the distal femur of such a young child, we made the spacer by hand, imitating the original distal femur of the patient that had been just removed.", "After surgery, the left leg was externally fixed in a cast for 4 weeks.", "Partial weight bearing on the affected leg, supported by a hinged knee brace, was thereafter commenced.", "The spacer was dislocated at 7 months post-operatively.", "The spacer dislocation prevented the patient from bearing weight.", "Bone atrophy in the left leg was observed.", "At 7 years and 8 months old, secondary surgery was performed with the aim of enabling weight bearing on the affected leg.", "A custom-made ceramic spacer (Kyocera Corp., Japan) with a smooth straight stem of 8 mm in diameter had been ordered 3 months prior to the surgery.", "Intra-operatively, after the removal of the initial spacer, a 1-cm length of the distal edge of the residual femur was removed.", "The periosteum and reactive membrane around the molded PMMA was preserved.", "The junction between the residual femur and the ceramic spacer was fixed with PMMA.", "The junction was covered with the preserved periosteum and membrane.", "After surgery, the left leg was placed in a cast for 4 weeks.", "The patient re-started partial weight bearing using a hinged knee brace as with the first spacer.", "The bone atrophy in the left leg was gradually resolved.", "At 18 months after the second surgery, the cortexes of the femur and tibia had thickened sufficiently for expandable mega-prosthesis.", "Loosening of the stem and varus deformity was observed.", "A third surgical intervention was, therefore, planned.", "At 9 years and 7 months old, the second spacer was removed, and the knee joint was reconstructed using a custom-made growing femoral prosthesis (Stryker Corp., Germany) with a curved porous stem of 8.5 mm in diameter fixed to the residual femur with two screws.", "Intra-operatively, the PMMA around the junction was already loosened, and the stem was easily removed.", "The residual femur was carefully reamed, and the stem was inserted.", "Cancellous bone chips from the proximal tibial epiphysis were grafted around the bone-prosthesis junction and then wrapped with the preserved periosteum and pseudo-periosteum membrane.", "The proximal surface of the tibia was also replaced, but the growth plate was preserved.", "Immediately after surgery, range of motion (ROM) exercise was started.", "Six weeks after surgery, partial weight bearing was permitted.", "Ten months after the third surgery, the patient was able to walk unsupported.", "A radiograph showed further thickening of the cortex of the residual femur.", "At 10 years and 7 months old, the growing femoral prosthesis was extended by 1.1 cm.", "At the latest follow-up, at 11 years and 1 month old, the patient was 143 cm in height with a limb length discrepancy (LLD) of 5 cm.", "The patient was able to walk unsupported using a 2.5 cm shoe lift.", "The Musculoskeletal Tumor Society (MSTS) score was 24 out of 30 points.", "The muscle strength of quadriceps recovered to manual muscle test (MMT) level 3.", "Active straight leg raising became possible without extension lag.", "The ROM of the left knee was 0\u201390\u00b0.", "The patient was receiving a second extension of growing femoral prosthesis."], "summary_subclaims": ["The patient is a 5-year-old girl with high-grade conventional osteosarcoma in the left distal femur.", "The patient underwent three cycles of neoadjuvant chemotherapy.", "Limb-salvage surgery was planned because femoral rotationplasty had been refused.", "At 6\u2009years and 2\u2009months old, distal femoral resection and temporary spacer insertion using a 7-mm-diameter intramedullary nail and molded polymethylmethacrylate was performed.", "At 7\u2009years and 8\u2009months old, secondary surgery was performed because the first spacer had been dislocated and the residual femur became atrophic.", "The distal end of the residual femur was removed by 1\u2009cm.", "The periosteum and induced membrane around polymethylmethacrylate was preserved.", "A custom-made ceramic spacer with a smooth straight 8-mm-diameter stem was utilized.", "The bone-spacer junction was fixed with polymethylmethacrylate.", "The bone-spacer junction was covered with the preserved periosteum and induced membrane.", "After surgery, the bone atrophy improved.", "At 9\u2009years and 7\u2009months old, the second spacer was removed because it had loosened.", "The knee joint was reconstructed using a custom-made growing femoral prosthesis with a curved porous 8.5-mm-diameter stem.", "Cancellous bone tips from the proximal tibia were grafted around the bone-prosthesis junction underneath the induced membrane.", "At 10\u2009years and 5\u2009months old, the patient was able to walk unsupported.", "A radiograph showed further thickening of the cortex of the residual femur without any stress shielding.", "The patient had 5\u2009cm of limb length discrepancy.", "The patient and her mother were satisfied with the function.", "The MSTS score was 24 out of 30 points.", "Repeated limb length extensions are planned."]}, "extra_info": {"fulltext_subclaims": ["A 5-year-old girl initially presented to our department due to worsening pain in the left proximal thigh.", "Osteosarcoma was suspected radiographically.", "Open biopsy revealed a high-grade conventional osteosarcoma.", "The tumor was initially staged as IIB (T2b N0 M0).", "Neoadjuvant chemotherapy was commenced in accordance with the NECO-95J protocol.", "After three cycles of neoadjuvant chemotherapy, the pain was alleviated.", "The extra-osseous mass was dramatically reduced.", "Limb-salvage surgery was planned.", "The tumor had already invaded the epiphyseal plate and epiphysis of the left distal femur at initial presentation.", "Osteo-articular resection was thought necessary so as to obtain a negative surgical margin.", "At 6 years and 2 months old, distal femoral resection and temporary spacer insertion was performed.", "Both medial and lateral meniscuses were preserved.", "The spacer was hand-made, using an intramedullary nail of 7 mm in diameter and molded polymethylmethacrylate (PMMA).", "Because there were no commercially available molds fitting the distal femur of such a young child, we made the spacer by hand, imitating the original distal femur of the patient that had been just removed.", "After surgery, the left leg was externally fixed in a cast for 4 weeks.", "Partial weight bearing on the affected leg, supported by a hinged knee brace, was thereafter commenced.", "The spacer was dislocated at 7 months post-operatively.", "The spacer dislocation prevented the patient from bearing weight.", "Bone atrophy in the left leg was observed.", "At 7 years and 8 months old, secondary surgery was performed with the aim of enabling weight bearing on the affected leg.", "A custom-made ceramic spacer (Kyocera Corp., Japan) with a smooth straight stem of 8 mm in diameter had been ordered 3 months prior to the surgery.", "Intra-operatively, after the removal of the initial spacer, a 1-cm length of the distal edge of the residual femur was removed.", "The periosteum and reactive membrane around the molded PMMA was preserved.", "The junction between the residual femur and the ceramic spacer was fixed with PMMA.", "The junction was covered with the preserved periosteum and membrane.", "After surgery, the left leg was placed in a cast for 4 weeks.", "The patient re-started partial weight bearing using a hinged knee brace as with the first spacer.", "The bone atrophy in the left leg was gradually resolved.", "At 18 months after the second surgery, the cortexes of the femur and tibia had thickened sufficiently for expandable mega-prosthesis.", "Loosening of the stem and varus deformity was observed.", "A third surgical intervention was, therefore, planned.", "At 9 years and 7 months old, the second spacer was removed, and the knee joint was reconstructed using a custom-made growing femoral prosthesis (Stryker Corp., Germany) with a curved porous stem of 8.5 mm in diameter fixed to the residual femur with two screws.", "Intra-operatively, the PMMA around the junction was already loosened, and the stem was easily removed.", "The residual femur was carefully reamed, and the stem was inserted.", "Cancellous bone chips from the proximal tibial epiphysis were grafted around the bone-prosthesis junction and then wrapped with the preserved periosteum and pseudo-periosteum membrane.", "The proximal surface of the tibia was also replaced, but the growth plate was preserved.", "Immediately after surgery, range of motion (ROM) exercise was started.", "Six weeks after surgery, partial weight bearing was permitted.", "Ten months after the third surgery, the patient was able to walk unsupported.", "A radiograph showed further thickening of the cortex of the residual femur.", "At 10 years and 7 months old, the growing femoral prosthesis was extended by 1.1 cm.", "At the latest follow-up, at 11 years and 1 month old, the patient was 143 cm in height with a limb length discrepancy (LLD) of 5 cm.", "The patient was able to walk unsupported using a 2.5 cm shoe lift.", "The Musculoskeletal Tumor Society (MSTS) score was 24 out of 30 points.", "The muscle strength of quadriceps recovered to manual muscle test (MMT) level 3.", "Active straight leg raising became possible without extension lag.", "The ROM of the left knee was 0\u201390\u00b0.", "The patient was receiving a second extension of growing femoral prosthesis."], "index": 117, "original_id": "multiclinsum_test_1775_en.txt", "split": "test", "summary_subclaims": ["The patient is a 5-year-old girl with high-grade conventional osteosarcoma in the left distal femur.", "The patient underwent three cycles of neoadjuvant chemotherapy.", "Limb-salvage surgery was planned because femoral rotationplasty had been refused.", "At 6\u2009years and 2\u2009months old, distal femoral resection and temporary spacer insertion using a 7-mm-diameter intramedullary nail and molded polymethylmethacrylate was performed.", "At 7\u2009years and 8\u2009months old, secondary surgery was performed because the first spacer had been dislocated and the residual femur became atrophic.", "The distal end of the residual femur was removed by 1\u2009cm.", "The periosteum and induced membrane around polymethylmethacrylate was preserved.", "A custom-made ceramic spacer with a smooth straight 8-mm-diameter stem was utilized.", "The bone-spacer junction was fixed with polymethylmethacrylate.", "The bone-spacer junction was covered with the preserved periosteum and induced membrane.", "After surgery, the bone atrophy improved.", "At 9\u2009years and 7\u2009months old, the second spacer was removed because it had loosened.", "The knee joint was reconstructed using a custom-made growing femoral prosthesis with a curved porous 8.5-mm-diameter stem.", "Cancellous bone tips from the proximal tibia were grafted around the bone-prosthesis junction underneath the induced membrane.", "At 10\u2009years and 5\u2009months old, the patient was able to walk unsupported.", "A radiograph showed further thickening of the cortex of the residual femur without any stress shielding.", "The patient had 5\u2009cm of limb length discrepancy.", "The patient and her mother were satisfied with the function.", "The MSTS score was 24 out of 30 points.", "Repeated limb length extensions are planned."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 42-year-old female.", "She was seen in the emergency department with three days of severe abdominal pain.", "She had sepsis.", "Her medical history included menometrorrhagia due to uterine fibroids.", "She had a previous endometrial ablation in 2015.", "She used a contraceptive vaginal ring for three months prior to presentation.", "She used Provera for 2 days prior to presentation for persistent vaginal bleeding.", "Physical examination revealed a temperature of 39.2\u00b0C.", "Physical examination revealed a pulse of 132 beats/min.", "Physical exam showed tenderness throughout the lower abdomen with voluntary guarding.", "Laboratory data revealed a white blood cell count of 12,000/\u00b5L.", "Laboratory data revealed a hemoglobin of 7.8 gm/dL.", "Laboratory data revealed a hematocrit of 25.7%.", "Laboratory data revealed a sodium of 127 mmol/L.", "Laboratory data revealed a chloride of 96 mmol/L.", "Lactate was normal at 1.5 mmol/L.", "Initial CT scan showed uterine masses consistent with known fibroids.", "Initial CT scan showed minimal pelvic fluid.", "She was admitted to the medical service for sepsis.", "Gynecology was consulted for presumed pelvic inflammatory disease.", "She was started on empiric antibiotics for PID: ceftriaxone IV 1 g every 24 hours, azithromycin IV 500 mg every 24 hours, and metronidazole IV 500 mg every 8 hours.", "Blood, urine, and stool cultures were sent upon admission.", "All cultures were negative.", "Her pain continued to progress.", "Her white blood cell count rose to 20,000/\u00b5L.", "A repeat CT scan on hospital day four showed interval development of ascites.", "Surgical consultation was obtained.", "She was found to have an acute abdomen.", "She was taken for a diagnostic laparoscopy.", "Diagnostic laparoscopy revealed a dense fibrinous exudate and significant ascites in all four quadrants of the abdomen.", "Multiple peritoneal biopsies were taken.", "Peritoneal fluid was sent for gram stain, cultures, and cytology.", "Postoperatively, carcinoembryonic antigen (CEA) and CA-125 levels were obtained.", "CEA was within the normal range.", "CA-125 was mildly elevated at 56.8 U/mL.", "Her white blood cell count fluctuated between 15,000 and 25,000/\u00b5L.", "Peritoneal fluid gram stain did not reveal any bacteria.", "Cytology revealed rare mesothelial cells and abundant neutrophils.", "Cytology did not reveal malignant cells.", "Final pathology report stated the presence of benign fibromembranous tissue with severe acute inflammation and extensive necrosis.", "The final pathology report was consistent with 'severe necrotizing acute peritonitis.'", "Infectious disease was consulted.", "Group A Strep (GAS) peritonitis was suspected.", "Recommendations were made to continue ceftriaxone at 1 g IV every 24 hours in addition to one dose of clindamycin 600 mg IV.", "Azithromycin was added to ceftriaxone three days later (IV 500 mg every 24 hours).", "A streptolysin O antibody (ASO) titer was sent.", "The ASO titer was normal at 61 I U/mL.", "The ASO titer argued against GAS peritonitis.", "Ceftriaxone was stopped.", "Azithromycin was transitioned to oral 500 mg daily.", "She continued to have persistent abdominal pain and anorexia.", "A repeat CT scan obtained nine days after surgery showed peritoneal enhancement and several fluid collections.", "A diagnostic paracentesis was performed.", "Peritoneal fluid was sent to an outside institution for 16S ribosome analysis.", "Her abdominal pain and leukocytosis slowly improved.", "She continued to have severe anorexia and food aversion.", "On hospital day 23, she was discharged home on oral azithromycin.", "16S ribosome testing revealed Mycoplasma hominis RNA within the peritoneal fluid.", "Her outpatient antibiotic was changed to oral doxycycline 100 mg twice daily for three months.", "She was closely followed as an outpatient.", "She gradually demonstrated clinical improvement.", "She remains well ten months after hospitalization."], "summary_subclaims": ["The patient is a 42-year-old female.", "She has a history of uterine fibroids.", "She was admitted with abdominal pain.", "She had intraperitoneal fluid of unknown etiology.", "She was initially managed nonoperatively.", "She was empirically treated with broad spectrum antibiotics.", "Blood and urine cultures were unrevealing.", "Diagnostic laparoscopy revealed a dense fibrinous exudate covering the entire peritoneal cavity.", "Peritoneal fluid and biopsies were sent for cytology and culture.", "The peritoneal fluid was sent for 16\u2009s ribosomal analysis.", "Mycoplasma hominis RNA was discovered.", "Her antibiotics were narrowed.", "She eventually made a full recovery."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 42-year-old female.", "She was seen in the emergency department with three days of severe abdominal pain.", "She had sepsis.", "Her medical history included menometrorrhagia due to uterine fibroids.", "She had a previous endometrial ablation in 2015.", "She used a contraceptive vaginal ring for three months prior to presentation.", "She used Provera for 2 days prior to presentation for persistent vaginal bleeding.", "Physical examination revealed a temperature of 39.2\u00b0C.", "Physical examination revealed a pulse of 132 beats/min.", "Physical exam showed tenderness throughout the lower abdomen with voluntary guarding.", "Laboratory data revealed a white blood cell count of 12,000/\u00b5L.", "Laboratory data revealed a hemoglobin of 7.8 gm/dL.", "Laboratory data revealed a hematocrit of 25.7%.", "Laboratory data revealed a sodium of 127 mmol/L.", "Laboratory data revealed a chloride of 96 mmol/L.", "Lactate was normal at 1.5 mmol/L.", "Initial CT scan showed uterine masses consistent with known fibroids.", "Initial CT scan showed minimal pelvic fluid.", "She was admitted to the medical service for sepsis.", "Gynecology was consulted for presumed pelvic inflammatory disease.", "She was started on empiric antibiotics for PID: ceftriaxone IV 1 g every 24 hours, azithromycin IV 500 mg every 24 hours, and metronidazole IV 500 mg every 8 hours.", "Blood, urine, and stool cultures were sent upon admission.", "All cultures were negative.", "Her pain continued to progress.", "Her white blood cell count rose to 20,000/\u00b5L.", "A repeat CT scan on hospital day four showed interval development of ascites.", "Surgical consultation was obtained.", "She was found to have an acute abdomen.", "She was taken for a diagnostic laparoscopy.", "Diagnostic laparoscopy revealed a dense fibrinous exudate and significant ascites in all four quadrants of the abdomen.", "Multiple peritoneal biopsies were taken.", "Peritoneal fluid was sent for gram stain, cultures, and cytology.", "Postoperatively, carcinoembryonic antigen (CEA) and CA-125 levels were obtained.", "CEA was within the normal range.", "CA-125 was mildly elevated at 56.8 U/mL.", "Her white blood cell count fluctuated between 15,000 and 25,000/\u00b5L.", "Peritoneal fluid gram stain did not reveal any bacteria.", "Cytology revealed rare mesothelial cells and abundant neutrophils.", "Cytology did not reveal malignant cells.", "Final pathology report stated the presence of benign fibromembranous tissue with severe acute inflammation and extensive necrosis.", "The final pathology report was consistent with 'severe necrotizing acute peritonitis.'", "Infectious disease was consulted.", "Group A Strep (GAS) peritonitis was suspected.", "Recommendations were made to continue ceftriaxone at 1 g IV every 24 hours in addition to one dose of clindamycin 600 mg IV.", "Azithromycin was added to ceftriaxone three days later (IV 500 mg every 24 hours).", "A streptolysin O antibody (ASO) titer was sent.", "The ASO titer was normal at 61 I U/mL.", "The ASO titer argued against GAS peritonitis.", "Ceftriaxone was stopped.", "Azithromycin was transitioned to oral 500 mg daily.", "She continued to have persistent abdominal pain and anorexia.", "A repeat CT scan obtained nine days after surgery showed peritoneal enhancement and several fluid collections.", "A diagnostic paracentesis was performed.", "Peritoneal fluid was sent to an outside institution for 16S ribosome analysis.", "Her abdominal pain and leukocytosis slowly improved.", "She continued to have severe anorexia and food aversion.", "On hospital day 23, she was discharged home on oral azithromycin.", "16S ribosome testing revealed Mycoplasma hominis RNA within the peritoneal fluid.", "Her outpatient antibiotic was changed to oral doxycycline 100 mg twice daily for three months.", "She was closely followed as an outpatient.", "She gradually demonstrated clinical improvement.", "She remains well ten months after hospitalization."], "index": 127, "original_id": "multiclinsum_test_1099_en.txt", "split": "test", "summary_subclaims": ["The patient is a 42-year-old female.", "She has a history of uterine fibroids.", "She was admitted with abdominal pain.", "She had intraperitoneal fluid of unknown etiology.", "She was initially managed nonoperatively.", "She was empirically treated with broad spectrum antibiotics.", "Blood and urine cultures were unrevealing.", "Diagnostic laparoscopy revealed a dense fibrinous exudate covering the entire peritoneal cavity.", "Peritoneal fluid and biopsies were sent for cytology and culture.", "The peritoneal fluid was sent for 16\u2009s ribosomal analysis.", "Mycoplasma hominis RNA was discovered.", "Her antibiotics were narrowed.", "She eventually made a full recovery."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was a 77-year-old male.", "He presented with sudden onset pain in his left hip and shoulder.", "The pain followed an episode of slip and fall at home 2 days ago.", "He had been taking treatment for hypertension for the past 15 years.", "Clinical examination revealed extensive bruising over the chest, left arm, forearm, and the medial aspect of the entire left thigh.", "Movements of the involved hip and shoulder joints were extremely painful and restricted.", "There was no distal neurovascular deficit in any of the involved limbs.", "Laboratory investigations revealed anemia (Hb 8.5 g/dl).", "Blood urea was 266 mg/dl.", "Serum creatinine was 3.46 mg/dl.", "Serum potassium was 5.73 mmol/L.", "Uric acid was 10.4 mg/dl.", "Coagulation profile was within normal limits.", "The fracture of the left inter-trochanteric femur was confirmed.", "An associated fracture of the left proximal humerus was confirmed.", "X-rays did not reveal any bony injury to the chest/thigh and forearm.", "The patient received intravenous fluids (normal saline).", "Blood urea decreased to 79 mg/dl.", "Serum creatinine decreased to 0.68 mg/dl.", "Creatinine phosphokinase (CPK) was 865 U/L.", "The patient underwent closed reduction and internal fixation with the proximal femoral nail for the inter-trochanteric femur fracture.", "The proximal humerus fracture was managed non-operatively.", "The patient was discharged after 7 days of hospitalization.", "At 3 months follow-up, he was able to walk with the help of crutches.", "There was still residual pain and stiffness in his left shoulder."], "summary_subclaims": ["The patient was a 77-year-old hypertensive male.", "He presented to the emergency following an episode of slip and fall at home.", "Radiological evaluation revealed fractures of the left inter-trochanteric femur and left proximal humerus.", "Laboratory investigations showed grossly deranged renal parameters.", "Serum creatinine phosphokinase levels were more than 5 times the baseline.", "A diagnosis of acute kidney injury secondary to traumatic rhabdomyolysis was made.", "Medical management included adequate intravenous fluid administration.", "Medical management included strict input-output monitoring.", "The patient underwent closed reduction and internal fixation of the inter-trochanteric femur fracture with a proximal femoral nail.", "The fracture of the proximal humerus was managed non-operatively with sling immobilization.", "The patient refused to give consent for a second surgery."]}, "extra_info": {"fulltext_subclaims": ["The patient was a 77-year-old male.", "He presented with sudden onset pain in his left hip and shoulder.", "The pain followed an episode of slip and fall at home 2 days ago.", "He had been taking treatment for hypertension for the past 15 years.", "Clinical examination revealed extensive bruising over the chest, left arm, forearm, and the medial aspect of the entire left thigh.", "Movements of the involved hip and shoulder joints were extremely painful and restricted.", "There was no distal neurovascular deficit in any of the involved limbs.", "Laboratory investigations revealed anemia (Hb 8.5 g/dl).", "Blood urea was 266 mg/dl.", "Serum creatinine was 3.46 mg/dl.", "Serum potassium was 5.73 mmol/L.", "Uric acid was 10.4 mg/dl.", "Coagulation profile was within normal limits.", "The fracture of the left inter-trochanteric femur was confirmed.", "An associated fracture of the left proximal humerus was confirmed.", "X-rays did not reveal any bony injury to the chest/thigh and forearm.", "The patient received intravenous fluids (normal saline).", "Blood urea decreased to 79 mg/dl.", "Serum creatinine decreased to 0.68 mg/dl.", "Creatinine phosphokinase (CPK) was 865 U/L.", "The patient underwent closed reduction and internal fixation with the proximal femoral nail for the inter-trochanteric femur fracture.", "The proximal humerus fracture was managed non-operatively.", "The patient was discharged after 7 days of hospitalization.", "At 3 months follow-up, he was able to walk with the help of crutches.", "There was still residual pain and stiffness in his left shoulder."], "index": 110, "original_id": "multiclinsum_test_2243_en.txt", "split": "test", "summary_subclaims": ["The patient was a 77-year-old hypertensive male.", "He presented to the emergency following an episode of slip and fall at home.", "Radiological evaluation revealed fractures of the left inter-trochanteric femur and left proximal humerus.", "Laboratory investigations showed grossly deranged renal parameters.", "Serum creatinine phosphokinase levels were more than 5 times the baseline.", "A diagnosis of acute kidney injury secondary to traumatic rhabdomyolysis was made.", "Medical management included adequate intravenous fluid administration.", "Medical management included strict input-output monitoring.", "The patient underwent closed reduction and internal fixation of the inter-trochanteric femur fracture with a proximal femoral nail.", "The fracture of the proximal humerus was managed non-operatively with sling immobilization.", "The patient refused to give consent for a second surgery."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was a 52-year-old White man.", "The patient presented with intermittent constipation.", "The patient had a history of a decrease in lymphocyte count two months prior.", "Initial computed tomography scans revealed stage T4 prostatic adenocarcinoma.", "The tumor had invasion into adjacent structures.", "The tumor had metastasis to regional lymph nodes (stage N1).", "The tumor had metastases to the liver, bone, and a distant lymph node (stage M1).", "A retroperitoneal lymph node was biopsied to confirm histology.", "The patient's prostate-specific antigen (PSA) level was 1291ng/mL.", "The patient started the antiandrogen bicalutamide (oral) shortly after confirmed diagnosis.", "A gonadotrophin-releasing hormone agonist, leuprorelin (depot injection), was subsequently initiated.", "The patient received treatment until PSA values began to rise \u224815 weeks later.", "The patient discontinued bicalutamide.", "Docetaxel (intravenous infusion; 4 cycles) plus prednisone (oral; continuous dosing) was administered as standard of care.", "Prednisone was continued for 1 week after the end of docetaxel treatment for symptom control.", "The patient discontinued docetaxel/prednisone due to radiographic disease progression and PSA progression.", "The patient immediately started on abiraterone as an androgen receptor targeting therapy.", "The patient received palliative radiation of the right femur and acetabula around the time abiraterone was initiated.", "After discontinuing abiraterone, the patient was enrolled in the TRITON2 study.", "Local genomic testing of an archival tissue biopsy (retroperitoneal lymph node metastasis, 90% tumor purity) was obtained at initial diagnosis.", "Local testing utilized the Oncomine\u2122 Comprehensive Assay v3.", "The local test indicated the presence of a BRCA1 T1399I (allelic fraction [AF], 19%) mutation.", "A deleterious or probably damaging ATM G1663C mutation was also detected.", "A damaging TP53 P191del mutation was also detected.", "An oncogenic, activating BRAF K601E mutation was also detected.", "No gene amplifications were detected.", "No gene fusions were detected.", "TRITON2 patients provided plasma samples for central genomic analysis prior to starting rucaparib.", "The patient\u2019s pre-rucaparib plasma sample was analyzed using the FoundationOne Liquid CDx assay.", "The FoundationOne Liquid CDx assay detected the same alterations as the Oncomine analysis of the archival tissue biopsy.", "The FoundationOne Liquid CDx assay also revealed the presence of a BRCA2 homozygous loss (whole gene, 26 of 26 exons).", "The patient started at the recommended dose of rucaparib, 600 mg twice daily.", "The dose was reduced to 500 mg twice daily due to nausea/fatigue.", "The patient ultimately received rucaparib for 32 weeks.", "At enrollment into TRITON2, the patient had >21 bone-associated lesions.", "The patient had multiple liver lesions.", "Treatment with rucaparib resulted in a confirmed partial response per modified Response Evaluation Criteria In Solid Tumors, version 1.1.", "The partial response lasted 13 weeks.", "The partial response was ongoing as of the last radiographic assessment before subsequent anti-cancer therapy.", "The rPFS was 29 weeks.", "There was no confirmed progression in bone.", "The patient had a confirmed PSA response (maximum decrease, 95%).", "The PSA response lasted 28 weeks from the first dose of rucaparib.", "The patient discontinued rucaparib treatment due to clinical disease progression after 32 weeks on study.", "The patient received carboplatin and cabazitaxel for 2 cycles.", "Subsequent scans indicated progressive disease in nontarget liver lesions two months later.", "The patient discontinued carboplatin/cabazitaxel.", "The patient did not receive any further anticancer therapies.", "The patient died \u224823 months after initial diagnosis due to progression of his disease."], "summary_subclaims": ["The patient had BRCA-mutated metastatic castration-resistant prostate cancer.", "The patient had a response to the PARP inhibitor rucaparib.", "The patient remained on rucaparib for 32 weeks.", "The duration of treatment with rucaparib was >2 times longer than the duration of each of his prior therapies.", "The patient's prior therapies included bicalutamide, docetaxel, and abiraterone.", "The patient enrolled in TRITON2 based on results of local genomic testing of an archival biopsy.", "Local genomic testing indicated the presence of a BRCA1 T1399I mutation.", "The allelic fraction of the BRCA1 T1399I mutation was 19%.", "Local testing also identified an ATM G1663C mutation.", "Local testing also identified a TP53 P191del mutation.", "Local testing also identified a BRAF K601E mutation.", "Analysis of a plasma sample obtained before starting rucaparib detected the same alterations as those in the archival biopsy.", "Analysis of the plasma sample also revealed the presence of a BRCA2 homozygous loss.", "The BRCA2 homozygous loss involved the whole gene, 26 of 26 exons.", "The plasma sample analysis also revealed several other alterations of unknown functional impact.", "We hypothesize the response of the patient's tumor to rucaparib was likely driven by DNA damage repair deficiency.", "The DNA damage repair deficiency was caused by homozygous loss of all BRCA2 exons.", "The patient discontinued rucaparib due to clinical disease progression.", "Following discontinuation from rucaparib, the patient received carboplatin and cabazitaxel.", "The patient received carboplatin and cabazitaxel for \u22483 weeks.", "The patient died due to progression of his disease."]}, "extra_info": {"fulltext_subclaims": ["The patient was a 52-year-old White man.", "The patient presented with intermittent constipation.", "The patient had a history of a decrease in lymphocyte count two months prior.", "Initial computed tomography scans revealed stage T4 prostatic adenocarcinoma.", "The tumor had invasion into adjacent structures.", "The tumor had metastasis to regional lymph nodes (stage N1).", "The tumor had metastases to the liver, bone, and a distant lymph node (stage M1).", "A retroperitoneal lymph node was biopsied to confirm histology.", "The patient's prostate-specific antigen (PSA) level was 1291ng/mL.", "The patient started the antiandrogen bicalutamide (oral) shortly after confirmed diagnosis.", "A gonadotrophin-releasing hormone agonist, leuprorelin (depot injection), was subsequently initiated.", "The patient received treatment until PSA values began to rise \u224815 weeks later.", "The patient discontinued bicalutamide.", "Docetaxel (intravenous infusion; 4 cycles) plus prednisone (oral; continuous dosing) was administered as standard of care.", "Prednisone was continued for 1 week after the end of docetaxel treatment for symptom control.", "The patient discontinued docetaxel/prednisone due to radiographic disease progression and PSA progression.", "The patient immediately started on abiraterone as an androgen receptor targeting therapy.", "The patient received palliative radiation of the right femur and acetabula around the time abiraterone was initiated.", "After discontinuing abiraterone, the patient was enrolled in the TRITON2 study.", "Local genomic testing of an archival tissue biopsy (retroperitoneal lymph node metastasis, 90% tumor purity) was obtained at initial diagnosis.", "Local testing utilized the Oncomine\u2122 Comprehensive Assay v3.", "The local test indicated the presence of a BRCA1 T1399I (allelic fraction [AF], 19%) mutation.", "A deleterious or probably damaging ATM G1663C mutation was also detected.", "A damaging TP53 P191del mutation was also detected.", "An oncogenic, activating BRAF K601E mutation was also detected.", "No gene amplifications were detected.", "No gene fusions were detected.", "TRITON2 patients provided plasma samples for central genomic analysis prior to starting rucaparib.", "The patient\u2019s pre-rucaparib plasma sample was analyzed using the FoundationOne Liquid CDx assay.", "The FoundationOne Liquid CDx assay detected the same alterations as the Oncomine analysis of the archival tissue biopsy.", "The FoundationOne Liquid CDx assay also revealed the presence of a BRCA2 homozygous loss (whole gene, 26 of 26 exons).", "The patient started at the recommended dose of rucaparib, 600 mg twice daily.", "The dose was reduced to 500 mg twice daily due to nausea/fatigue.", "The patient ultimately received rucaparib for 32 weeks.", "At enrollment into TRITON2, the patient had >21 bone-associated lesions.", "The patient had multiple liver lesions.", "Treatment with rucaparib resulted in a confirmed partial response per modified Response Evaluation Criteria In Solid Tumors, version 1.1.", "The partial response lasted 13 weeks.", "The partial response was ongoing as of the last radiographic assessment before subsequent anti-cancer therapy.", "The rPFS was 29 weeks.", "There was no confirmed progression in bone.", "The patient had a confirmed PSA response (maximum decrease, 95%).", "The PSA response lasted 28 weeks from the first dose of rucaparib.", "The patient discontinued rucaparib treatment due to clinical disease progression after 32 weeks on study.", "The patient received carboplatin and cabazitaxel for 2 cycles.", "Subsequent scans indicated progressive disease in nontarget liver lesions two months later.", "The patient discontinued carboplatin/cabazitaxel.", "The patient did not receive any further anticancer therapies.", "The patient died \u224823 months after initial diagnosis due to progression of his disease."], "index": 118, "original_id": "multiclinsum_test_759_en.txt", "split": "test", "summary_subclaims": ["The patient had BRCA-mutated metastatic castration-resistant prostate cancer.", "The patient had a response to the PARP inhibitor rucaparib.", "The patient remained on rucaparib for 32 weeks.", "The duration of treatment with rucaparib was >2 times longer than the duration of each of his prior therapies.", "The patient's prior therapies included bicalutamide, docetaxel, and abiraterone.", "The patient enrolled in TRITON2 based on results of local genomic testing of an archival biopsy.", "Local genomic testing indicated the presence of a BRCA1 T1399I mutation.", "The allelic fraction of the BRCA1 T1399I mutation was 19%.", "Local testing also identified an ATM G1663C mutation.", "Local testing also identified a TP53 P191del mutation.", "Local testing also identified a BRAF K601E mutation.", "Analysis of a plasma sample obtained before starting rucaparib detected the same alterations as those in the archival biopsy.", "Analysis of the plasma sample also revealed the presence of a BRCA2 homozygous loss.", "The BRCA2 homozygous loss involved the whole gene, 26 of 26 exons.", "The plasma sample analysis also revealed several other alterations of unknown functional impact.", "We hypothesize the response of the patient's tumor to rucaparib was likely driven by DNA damage repair deficiency.", "The DNA damage repair deficiency was caused by homozygous loss of all BRCA2 exons.", "The patient discontinued rucaparib due to clinical disease progression.", "Following discontinuation from rucaparib, the patient received carboplatin and cabazitaxel.", "The patient received carboplatin and cabazitaxel for \u22483 weeks.", "The patient died due to progression of his disease."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 44-year-old black African man of Burkinab\u00e8 origin.", "He is a smoker with 10 packs a year.", "He has sickle-cell anaemia.", "He has been taking 5 mg of folic acid daily.", "He has no notion of tuberculosis infection.", "He was admitted to the rheumatology department for chronic inflammatory lower back pain.", "He had inflammatory left knee pain that had been going on for about seven months.", "He had a cough with phlegm.", "He had evening fever.", "He had moderate physical asthenia.", "He had anorexia.", "He had significant weight loss.", "On physical examination, clinical anaemia was observed that was not decompensated.", "A spinal syndrome was observed.", "Bilateral psoitis was observed.", "A soft, purulent swelling of 4x5 cm was observed in the sterno-clavicular joint.", "A monoarthritis was found in the knee.", "The knee puncture revealed a purulent, fluid liquid.", "The respiratory tract examination showed a condensation syndrome in the left pulmonary field.", "A purulent pleural effusion on the right was observed.", "A right inguinal lymphadenopathy with pus was observed.", "A biological inflammatory syndrome was observed.", "The microcytic hypochromic anaemia was 8.1 g/dl.", "The C reactive protein (CRP) was 98 mg/l.", "There was no hyperleucocytosis.", "The intradermal reaction (IDR) to the tuberculin was positive at 18 mm.", "The cytobacteriological examination did not find any germ.", "The GeneXpert MTB/RIF test did not find any germ.", "The search for acid-fast bacilli (AFB) in the pus from the different sites did not find any germ.", "The thoracic computed tomography showed a right sterno-clavicular arthrosis with anterior muscular and mediastinal extension.", "The thoracic computed tomography showed a pyothorax.", "The thoracic computed tomography showed a right lung abscess.", "The thoracic computed tomography showed a L3-L4 spondylodiscitis with calcifying abscesses of the psoas and paravertebral muscles.", "The standard radiography of the left knee showed signs in favour of arthritis.", "The diagnosis of tuberculosis with multifocal, pleuropulmonary and lymph node involvement was retained.", "The patient was put on rifampicin 600 mg daily.", "The patient was put on isoniazid 300 mg daily.", "The patient was put on pyrazinamide 2000 mg daily.", "The patient was put on ethambutol 1600 mg daily for two months.", "The same doses of rifampicin and isoniazid were continued for 10 months.", "The patient received thoracic drainage of the pyothorax in the operating theatre.", "The patient received a joint lavage of the left knee.", "The patient received a drainage of the cold abscess in the sterno-clavicular joint.", "Local care with antiseptic was applied to the fistula of the inguinal lymphadenopathy.", "Local care with antiseptic was applied to the cold abscess until complete healing.", "Folic acid treatment was continued in the context of sickle cell anaemia.", "The immediate evolution was marked by a clinical and biological improvement.", "The inflammatory syndrome disappeared.", "The fever reduced.", "The evolution at three months was characterised by an improvement of the psoitis.", "The evolution at three months was characterised by an improvement of the lower back pain.", "The weight gain estimated at 3 months was 5%."], "summary_subclaims": ["The patient is a 44-year-old African black patient of Burkinabe origin.", "The patient had chronic inflammatory low back pain.", "The patient had inflammatory right knee pain.", "The patient had a cough with phlegm.", "The symptomatology had been developing for seven months.", "The symptomatology was in a febrile context.", "The patient had a general deterioration in health.", "The examination showed oligoarthritis of the right sternoclavicular joint.", "The examination showed oligoarthritis of the left knee.", "The examination showed a pulmonary condensation syndrome.", "The examination showed pleural effusion.", "The examination showed a cold abscess at the level of the right sternoclavicular joint.", "The examination showed a fistulous and purulent right inguinal lymphadenopathy.", "The biology showed an inflammatory syndrome.", "The GeneXpert test was positive in the sputum.", "The GeneXpert test showed no resistance to rifampicin.", "The intradermal reaction to the tuberculin was positive.", "The thoracic tomodensitometry showed a right sternoclavicular osteoarthritis.", "The thoracic tomodensitometry showed a spondylodiscitis of the L3-L4 spine.", "The standard radiography of the left knee objectified signs in favour of arthritis.", "The diagnosis of tuberculosis with multifocal, pleuropulmonary and ganglionar bone involvement was retained.", "The patient was given usual analgesics.", "The patient was given antituberculous.", "The evolution was favourable."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 44-year-old black African man of Burkinab\u00e8 origin.", "He is a smoker with 10 packs a year.", "He has sickle-cell anaemia.", "He has been taking 5 mg of folic acid daily.", "He has no notion of tuberculosis infection.", "He was admitted to the rheumatology department for chronic inflammatory lower back pain.", "He had inflammatory left knee pain that had been going on for about seven months.", "He had a cough with phlegm.", "He had evening fever.", "He had moderate physical asthenia.", "He had anorexia.", "He had significant weight loss.", "On physical examination, clinical anaemia was observed that was not decompensated.", "A spinal syndrome was observed.", "Bilateral psoitis was observed.", "A soft, purulent swelling of 4x5 cm was observed in the sterno-clavicular joint.", "A monoarthritis was found in the knee.", "The knee puncture revealed a purulent, fluid liquid.", "The respiratory tract examination showed a condensation syndrome in the left pulmonary field.", "A purulent pleural effusion on the right was observed.", "A right inguinal lymphadenopathy with pus was observed.", "A biological inflammatory syndrome was observed.", "The microcytic hypochromic anaemia was 8.1 g/dl.", "The C reactive protein (CRP) was 98 mg/l.", "There was no hyperleucocytosis.", "The intradermal reaction (IDR) to the tuberculin was positive at 18 mm.", "The cytobacteriological examination did not find any germ.", "The GeneXpert MTB/RIF test did not find any germ.", "The search for acid-fast bacilli (AFB) in the pus from the different sites did not find any germ.", "The thoracic computed tomography showed a right sterno-clavicular arthrosis with anterior muscular and mediastinal extension.", "The thoracic computed tomography showed a pyothorax.", "The thoracic computed tomography showed a right lung abscess.", "The thoracic computed tomography showed a L3-L4 spondylodiscitis with calcifying abscesses of the psoas and paravertebral muscles.", "The standard radiography of the left knee showed signs in favour of arthritis.", "The diagnosis of tuberculosis with multifocal, pleuropulmonary and lymph node involvement was retained.", "The patient was put on rifampicin 600 mg daily.", "The patient was put on isoniazid 300 mg daily.", "The patient was put on pyrazinamide 2000 mg daily.", "The patient was put on ethambutol 1600 mg daily for two months.", "The same doses of rifampicin and isoniazid were continued for 10 months.", "The patient received thoracic drainage of the pyothorax in the operating theatre.", "The patient received a joint lavage of the left knee.", "The patient received a drainage of the cold abscess in the sterno-clavicular joint.", "Local care with antiseptic was applied to the fistula of the inguinal lymphadenopathy.", "Local care with antiseptic was applied to the cold abscess until complete healing.", "Folic acid treatment was continued in the context of sickle cell anaemia.", "The immediate evolution was marked by a clinical and biological improvement.", "The inflammatory syndrome disappeared.", "The fever reduced.", "The evolution at three months was characterised by an improvement of the psoitis.", "The evolution at three months was characterised by an improvement of the lower back pain.", "The weight gain estimated at 3 months was 5%."], "index": 111, "original_id": "multiclinsum_test_3332_en.txt", "split": "test", "summary_subclaims": ["The patient is a 44-year-old African black patient of Burkinabe origin.", "The patient had chronic inflammatory low back pain.", "The patient had inflammatory right knee pain.", "The patient had a cough with phlegm.", "The symptomatology had been developing for seven months.", "The symptomatology was in a febrile context.", "The patient had a general deterioration in health.", "The examination showed oligoarthritis of the right sternoclavicular joint.", "The examination showed oligoarthritis of the left knee.", "The examination showed a pulmonary condensation syndrome.", "The examination showed pleural effusion.", "The examination showed a cold abscess at the level of the right sternoclavicular joint.", "The examination showed a fistulous and purulent right inguinal lymphadenopathy.", "The biology showed an inflammatory syndrome.", "The GeneXpert test was positive in the sputum.", "The GeneXpert test showed no resistance to rifampicin.", "The intradermal reaction to the tuberculin was positive.", "The thoracic tomodensitometry showed a right sternoclavicular osteoarthritis.", "The thoracic tomodensitometry showed a spondylodiscitis of the L3-L4 spine.", "The standard radiography of the left knee objectified signs in favour of arthritis.", "The diagnosis of tuberculosis with multifocal, pleuropulmonary and ganglionar bone involvement was retained.", "The patient was given usual analgesics.", "The patient was given antituberculous.", "The evolution was favourable."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The infant was born at 27 weeks and four days.", "The infant was a preterm male.", "The infant's birth weight was 1135 grams.", "The pregnancy was a dichorionic diamniotic twin pregnancy.", "The mother experienced premature membrane rupture in the 27th week of pregnancy.", "The mother experienced contractions in the 27th week of pregnancy.", "The mother experienced bleeding in the 27th week of pregnancy.", "The mother was treated with antenatal steroids.", "Cesarean delivery was planned due to an arrested birth.", "The neonate was hypotonic at birth.", "The neonate was apneic at birth.", "The neonate required intubation one minute after birth.", "The intubation was due to respiratory failure.", "An uncuffed endotracheal tube was used.", "The APGAR score was 4 at one minute.", "The APGAR score was 6 at five minutes.", "The APGAR score was 7 at ten minutes.", "The neonate was transferred to the newborn intensive care unit.", "A diagnosis of respiratory distress syndrome was made.", "Treatment with endotracheal poractant alfa 200 mg/kg was initiated.", "Treatment with parenteral ampicillin-gentamicin was initiated.", "Treatment with caffeine citrate was initiated.", "Ventilation settings were arranged to assist control and volume guaranteed mode.", "The maximum inspiring pressure was 20 cm/H\u00b2O.", "The cranial ultrasound showed no abnormalities.", "On hospital day 3, the neonate was extubated to nasal intermittent positive pressure ventilation.", "On hospital day 3, the neonate required reintubation for recurrent respiratory failure.", "Antibiotics were escalated to vancomycin-meropenem due to clinical deterioration.", "On hospital day 5, the baby had worsening acute hypoxic respiratory failure.", "A chest x-ray revealed mediastinal pneumothorax.", "A follow-up x-ray one hour later showed accelerated pneumothorax on the left side.", "A follow-up x-ray one hour later showed mediastinal shift to the right.", "A thorax tube was placed through the left 5th intercostal space.", "Repeat x-rays showed an expanded lung on the left side.", "Repeat x-rays showed air bronchograms on the right.", "Ten hours later, the neonate had persistent acidosis.", "Ten hours later, the neonate had persistent hypoxia.", "An x-ray ten hours later displayed a repeat pneumothorax on the left side.", "The thorax tube was set to continuous suction.", "The thorax tube resulted in a reduction of pneumothorax on subsequent imaging.", "An echocardiogram revealed a 3 mm patent ductus arteriosus.", "The patent ductus arteriosus had mostly left to right two-way shunts.", "The echocardiogram showed pulmonary hypertension.", "The oxygen saturation levels were approximately 80%.", "The arm-leg saturation differences were higher than 15 mm Hg.", "These findings were suspicious for persistent fetal circulation.", "Pediatric cardiology advised against the closure of PDA.", "A new chest x-ray showed a collapsed left lung.", "A second chest tube was placed in the left hemithorax.", "A decision was made to perform a surgical intervention.", "A left posterolateral thoracotomy was performed.", "A 1 cm perforated area between the left bronchus and carina was found.", "The perforated area was repaired by using a pleural patch.", "Suturing with 6.0 prolene was performed.", "There was no visible bleeding or air leak at the end of the procedure.", "The anesthesiologist applied high-pressure air via the endotracheal tube.", "A chest tube was inserted.", "The thoracotomy incision was closed by layers.", "A post-procedure chest x-ray showed an expanded left lung.", "Three days later, the neonate experienced another episode of hypoxia.", "The hypoxia was found to be secondary to a repeat left-sided pneumothorax.", "A second thoracotomy was performed using the same technique as the prior surgery.", "An air leak emanated from the same area.", "The perforated area was repaired using a pleural patch.", "The left 5th intercostal muscle long peduncle was used.", "Fibrin glue and spongestan were used as anchorage on top of the patch.", "No leak was found with the use of maximal airway pressure.", "A PDA ligation operation was performed simultaneously during the procedure.", "There was no air leakage in the repeat x-ray.", "Both the first and second thorax tubes were removed on postoperative days 0 and 5, respectively.", "There were no signs of air buildup or pneumothorax on the following days.", "On the 161st day of admission, the patient was discharged home.", "The patient was discharged with a home-type ventilator.", "The patient was discharged with 30% oxygen support."], "summary_subclaims": ["The patient was a preterm newborn.", "The patient developed pneumomediastinum.", "The patient developed pneumothorax.", "The pneumothorax persisted despite placement of a thorax tube.", "A thoracotomy was performed to detect and treat the bronchial rupture."]}, "extra_info": {"fulltext_subclaims": ["The infant was born at 27 weeks and four days.", "The infant was a preterm male.", "The infant's birth weight was 1135 grams.", "The pregnancy was a dichorionic diamniotic twin pregnancy.", "The mother experienced premature membrane rupture in the 27th week of pregnancy.", "The mother experienced contractions in the 27th week of pregnancy.", "The mother experienced bleeding in the 27th week of pregnancy.", "The mother was treated with antenatal steroids.", "Cesarean delivery was planned due to an arrested birth.", "The neonate was hypotonic at birth.", "The neonate was apneic at birth.", "The neonate required intubation one minute after birth.", "The intubation was due to respiratory failure.", "An uncuffed endotracheal tube was used.", "The APGAR score was 4 at one minute.", "The APGAR score was 6 at five minutes.", "The APGAR score was 7 at ten minutes.", "The neonate was transferred to the newborn intensive care unit.", "A diagnosis of respiratory distress syndrome was made.", "Treatment with endotracheal poractant alfa 200 mg/kg was initiated.", "Treatment with parenteral ampicillin-gentamicin was initiated.", "Treatment with caffeine citrate was initiated.", "Ventilation settings were arranged to assist control and volume guaranteed mode.", "The maximum inspiring pressure was 20 cm/H\u00b2O.", "The cranial ultrasound showed no abnormalities.", "On hospital day 3, the neonate was extubated to nasal intermittent positive pressure ventilation.", "On hospital day 3, the neonate required reintubation for recurrent respiratory failure.", "Antibiotics were escalated to vancomycin-meropenem due to clinical deterioration.", "On hospital day 5, the baby had worsening acute hypoxic respiratory failure.", "A chest x-ray revealed mediastinal pneumothorax.", "A follow-up x-ray one hour later showed accelerated pneumothorax on the left side.", "A follow-up x-ray one hour later showed mediastinal shift to the right.", "A thorax tube was placed through the left 5th intercostal space.", "Repeat x-rays showed an expanded lung on the left side.", "Repeat x-rays showed air bronchograms on the right.", "Ten hours later, the neonate had persistent acidosis.", "Ten hours later, the neonate had persistent hypoxia.", "An x-ray ten hours later displayed a repeat pneumothorax on the left side.", "The thorax tube was set to continuous suction.", "The thorax tube resulted in a reduction of pneumothorax on subsequent imaging.", "An echocardiogram revealed a 3 mm patent ductus arteriosus.", "The patent ductus arteriosus had mostly left to right two-way shunts.", "The echocardiogram showed pulmonary hypertension.", "The oxygen saturation levels were approximately 80%.", "The arm-leg saturation differences were higher than 15 mm Hg.", "These findings were suspicious for persistent fetal circulation.", "Pediatric cardiology advised against the closure of PDA.", "A new chest x-ray showed a collapsed left lung.", "A second chest tube was placed in the left hemithorax.", "A decision was made to perform a surgical intervention.", "A left posterolateral thoracotomy was performed.", "A 1 cm perforated area between the left bronchus and carina was found.", "The perforated area was repaired by using a pleural patch.", "Suturing with 6.0 prolene was performed.", "There was no visible bleeding or air leak at the end of the procedure.", "The anesthesiologist applied high-pressure air via the endotracheal tube.", "A chest tube was inserted.", "The thoracotomy incision was closed by layers.", "A post-procedure chest x-ray showed an expanded left lung.", "Three days later, the neonate experienced another episode of hypoxia.", "The hypoxia was found to be secondary to a repeat left-sided pneumothorax.", "A second thoracotomy was performed using the same technique as the prior surgery.", "An air leak emanated from the same area.", "The perforated area was repaired using a pleural patch.", "The left 5th intercostal muscle long peduncle was used.", "Fibrin glue and spongestan were used as anchorage on top of the patch.", "No leak was found with the use of maximal airway pressure.", "A PDA ligation operation was performed simultaneously during the procedure.", "There was no air leakage in the repeat x-ray.", "Both the first and second thorax tubes were removed on postoperative days 0 and 5, respectively.", "There were no signs of air buildup or pneumothorax on the following days.", "On the 161st day of admission, the patient was discharged home.", "The patient was discharged with a home-type ventilator.", "The patient was discharged with 30% oxygen support."], "index": 116, "original_id": "multiclinsum_test_2176_en.txt", "split": "test", "summary_subclaims": ["The patient was a preterm newborn.", "The patient developed pneumomediastinum.", "The patient developed pneumothorax.", "The pneumothorax persisted despite placement of a thorax tube.", "A thoracotomy was performed to detect and treat the bronchial rupture."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 25-year-old gentleman.", "He presented with a complaint of recurrent pain and swelling on his right cheek of three-month duration.", "He visited a general practitioner each time.", "The condition was resolved with analgesic and antibiotics.", "His symptoms got worse.", "He attended the Oral Surgery Clinic for consultation.", "The patient is a fit and healthy young man.", "He has no relevant medical history.", "He has no known history of allergy.", "He had undergone bimaxillary orthognathic surgery one and a half years earlier.", "The surgical team informed him that there was a dislodged orthodontic appliance in his right cheek that must have occurred during the operation.", "The molar tube from the right maxillary second molar was found missing the next day after the surgery.", "Its presence was confirmed high up in the right maxillary-zygomatic buttress area shown in the postoperative X-ray image taken the next day.", "A series of further postoperative radiographs confirmed its location, lying outside the right maxillary antrum.", "No attempt was made to remove the appliance due to the pronounced postoperative facial oedema.", "The absence of signs and symptoms during further follow-up sessions confirmed the decision to leave it in-situ.", "On examination, there was no extraoral swelling noted.", "The mandible and maxilla seemed firm.", "There was a sinus with slight pus discharge on the upper right buccal sulcus region adjacent to the upper right first premolar.", "Tenderness was elicited upon palpation on the upper right vestibular region.", "A periapical view was taken with gutta-percha inserted into the sinus for foreign body localization.", "The radiograph revealed the gutta-percha pointed towards the site of titanium plate and screws used for rigid fixation.", "A cone beam CT was performed to provide a 3D detailed location of the appliance.", "The presence of the molar orthodontic tube foreign body reaction was suspected as the most probable cause of the recurrent right cheek pain and swelling.", "Exploration of the site was performed through the sulcular incision under general anesthesia.", "The dislodged molar tube was identified lying on the zygomatic bone just beneath the raised flap.", "It was removed by dividing some surrounding fibrous tissue strands.", "One titanium straight bone plate with four screws used for fixing the previous Le Fort I osteotomy site was inspected.", "A decision was made to remove them based on the fact that they are present in an infected area.", "The Le Fort I osteotomy site showed good healing with new bone formation.", "The patient had an uneventful recovery.", "The orthognathic surgical team who attended him previously was informed of his progress."], "summary_subclaims": ["A 25-year-old gentleman presented with recurrent upper right vestibular abscess three months following a bimaxillary orthognathic surgery.", "A bonded molar orthodontic tube had dislodged into the wound during the operation.", "The clinical presentation initially mimics an odontogenic infection.", "Our investigations revealed that the abscess originated from the dislodged appliance.", "The abscess was drained.", "The wound site was explored.", "The molar tube and neighbouring rigid fixation plates and screws were removed.", "The patient recovered well following the procedure."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 25-year-old gentleman.", "He presented with a complaint of recurrent pain and swelling on his right cheek of three-month duration.", "He visited a general practitioner each time.", "The condition was resolved with analgesic and antibiotics.", "His symptoms got worse.", "He attended the Oral Surgery Clinic for consultation.", "The patient is a fit and healthy young man.", "He has no relevant medical history.", "He has no known history of allergy.", "He had undergone bimaxillary orthognathic surgery one and a half years earlier.", "The surgical team informed him that there was a dislodged orthodontic appliance in his right cheek that must have occurred during the operation.", "The molar tube from the right maxillary second molar was found missing the next day after the surgery.", "Its presence was confirmed high up in the right maxillary-zygomatic buttress area shown in the postoperative X-ray image taken the next day.", "A series of further postoperative radiographs confirmed its location, lying outside the right maxillary antrum.", "No attempt was made to remove the appliance due to the pronounced postoperative facial oedema.", "The absence of signs and symptoms during further follow-up sessions confirmed the decision to leave it in-situ.", "On examination, there was no extraoral swelling noted.", "The mandible and maxilla seemed firm.", "There was a sinus with slight pus discharge on the upper right buccal sulcus region adjacent to the upper right first premolar.", "Tenderness was elicited upon palpation on the upper right vestibular region.", "A periapical view was taken with gutta-percha inserted into the sinus for foreign body localization.", "The radiograph revealed the gutta-percha pointed towards the site of titanium plate and screws used for rigid fixation.", "A cone beam CT was performed to provide a 3D detailed location of the appliance.", "The presence of the molar orthodontic tube foreign body reaction was suspected as the most probable cause of the recurrent right cheek pain and swelling.", "Exploration of the site was performed through the sulcular incision under general anesthesia.", "The dislodged molar tube was identified lying on the zygomatic bone just beneath the raised flap.", "It was removed by dividing some surrounding fibrous tissue strands.", "One titanium straight bone plate with four screws used for fixing the previous Le Fort I osteotomy site was inspected.", "A decision was made to remove them based on the fact that they are present in an infected area.", "The Le Fort I osteotomy site showed good healing with new bone formation.", "The patient had an uneventful recovery.", "The orthognathic surgical team who attended him previously was informed of his progress."], "index": 113, "original_id": "multiclinsum_test_1305_en.txt", "split": "test", "summary_subclaims": ["A 25-year-old gentleman presented with recurrent upper right vestibular abscess three months following a bimaxillary orthognathic surgery.", "A bonded molar orthodontic tube had dislodged into the wound during the operation.", "The clinical presentation initially mimics an odontogenic infection.", "Our investigations revealed that the abscess originated from the dislodged appliance.", "The abscess was drained.", "The wound site was explored.", "The molar tube and neighbouring rigid fixation plates and screws were removed.", "The patient recovered well following the procedure."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["A 91-year-old woman presented to our institution with ST-segment elevation myocardial infarction.", "The right radial access was chosen for the performance of percutaneous coronary intervention.", "After the introduction of 6 F sheath, there was difficulty in the advancement of 0.035 J wire.", "The 0.035 J wire was exchanged with a Terumo hydrophilic wire (0.035 \u00d7 180).", "The Terumo hydrophilic wire was advanced easily to the aortic root.", "Coronary angiography was done.", "Coronary angiography revealed tortuous coronary arteries without significant lesions.", "Radial arteriography before sheath removal revealed perforation.", "Protamine sulfate (1 mg per 100 USP units of heparin) was administered intravenously.", "The dose of heparin was 70 U/kg.", "APTT was monitored 15 min after the protamine dose.", "Prolonged balloon inflation 2.5/3.0 was performed.", "The perforation was not sealed.", "A 7-F-long vascular sheath was inserted to internally tamponade the vessel.", "The patient was sent to the coronary care unit for monitoring of the forearm hematoma and the distal pulses.", "Over the next 3 days, serial radial angiographies were done.", "Serial radial angiographies revealed the persistence of the perforation.", "After 4 days, angiography revealed multiple thrombi.", "Thrombus aspiration was done using Pronto V4 extraction catheter.", "The implantation of a covered stent was performed.", "The stent was dislodged, mostly secondary to under expansion.", "The stent was successfully snared.", "The perforation was sealed spontaneously.", "There were no signs of intra-arterial thrombi."], "summary_subclaims": ["A 91-year-old woman presented to our institution with ST-segment elevation myocardial infarction.", "The right radial access was chosen for the performance of percutaneous coronary intervention.", "After the introduction of 6\u2009F sheath, there was difficulty in the advancement of 0.035\u2009J wire.", "The 0.035\u2009J wire was exchanged with a Terumo hydrophilic wire.", "After the procedure and before sheath removal, radial arteriography was done.", "Radial arteriography revealed perforation.", "Protamine sulfate was administered.", "Prolonged balloon inflation was attempted.", "Prolonged balloon inflation failed to seal the perforation.", "A 7-F-long vascular sheath was inserted to internally tamponade the vessel.", "The patient was sent to the coronary care unit for monitoring.", "Over the next 3 days, serial radial angiographies were done.", "Serial radial angiographies revealed the persistence of the perforation.", "On the fourth day, angiography revealed multiple thrombi.", "Thrombus aspiration was done using Pronto V4 extraction catheter.", "Thrombus aspiration was followed by the deployment of a covered stent.", "The stent was dislodged.", "The dislodged stent was successfully snared.", "The perforation was sealed spontaneously.", "There were no signs of intra-arterial thrombi."]}, "extra_info": {"fulltext_subclaims": ["A 91-year-old woman presented to our institution with ST-segment elevation myocardial infarction.", "The right radial access was chosen for the performance of percutaneous coronary intervention.", "After the introduction of 6 F sheath, there was difficulty in the advancement of 0.035 J wire.", "The 0.035 J wire was exchanged with a Terumo hydrophilic wire (0.035 \u00d7 180).", "The Terumo hydrophilic wire was advanced easily to the aortic root.", "Coronary angiography was done.", "Coronary angiography revealed tortuous coronary arteries without significant lesions.", "Radial arteriography before sheath removal revealed perforation.", "Protamine sulfate (1 mg per 100 USP units of heparin) was administered intravenously.", "The dose of heparin was 70 U/kg.", "APTT was monitored 15 min after the protamine dose.", "Prolonged balloon inflation 2.5/3.0 was performed.", "The perforation was not sealed.", "A 7-F-long vascular sheath was inserted to internally tamponade the vessel.", "The patient was sent to the coronary care unit for monitoring of the forearm hematoma and the distal pulses.", "Over the next 3 days, serial radial angiographies were done.", "Serial radial angiographies revealed the persistence of the perforation.", "After 4 days, angiography revealed multiple thrombi.", "Thrombus aspiration was done using Pronto V4 extraction catheter.", "The implantation of a covered stent was performed.", "The stent was dislodged, mostly secondary to under expansion.", "The stent was successfully snared.", "The perforation was sealed spontaneously.", "There were no signs of intra-arterial thrombi."], "index": 120, "original_id": "multiclinsum_test_1116_en.txt", "split": "test", "summary_subclaims": ["A 91-year-old woman presented to our institution with ST-segment elevation myocardial infarction.", "The right radial access was chosen for the performance of percutaneous coronary intervention.", "After the introduction of 6\u2009F sheath, there was difficulty in the advancement of 0.035\u2009J wire.", "The 0.035\u2009J wire was exchanged with a Terumo hydrophilic wire.", "After the procedure and before sheath removal, radial arteriography was done.", "Radial arteriography revealed perforation.", "Protamine sulfate was administered.", "Prolonged balloon inflation was attempted.", "Prolonged balloon inflation failed to seal the perforation.", "A 7-F-long vascular sheath was inserted to internally tamponade the vessel.", "The patient was sent to the coronary care unit for monitoring.", "Over the next 3 days, serial radial angiographies were done.", "Serial radial angiographies revealed the persistence of the perforation.", "On the fourth day, angiography revealed multiple thrombi.", "Thrombus aspiration was done using Pronto V4 extraction catheter.", "Thrombus aspiration was followed by the deployment of a covered stent.", "The stent was dislodged.", "The dislodged stent was successfully snared.", "The perforation was sealed spontaneously.", "There were no signs of intra-arterial thrombi."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["A 16-year-old Ukrainian boy was admitted to the Department of Children\u2019s Infectious Diseases in Warsaw, Poland.", "The boy had jaundice lasting for four days.", "The boy had malaise.", "The boy had diarrhoea.", "The boy had vomiting.", "The boy had lived in Poland for 1.5 years.", "The boy was working (training) in the profession of a hairdresser.", "The boy had a tattoo made at home by his mother\u2019s partner six months earlier.", "The boy had a finger cut by hairdressing scissors six weeks before the admission.", "The patient confirmed that he had two secured heterosexual encounters during the last six months.", "In Ukraine, he had been vaccinated against tuberculosis, diphtheria, tetanus, pertussis, poliomyelitis, measles, mumps, and rubella.", "He has not been vaccinated against hepatitis B.", "He negated any dietary errors.", "He had never had blood transfusion nor surgery.", "He was once hospitalized due to acute gastroenteritis in Ukraine.", "The physical examination revealed jaundice.", "The physical examination revealed hepatomegaly (2 cm below the rib arch).", "The physical examination revealed a tattoo on the right forearm.", "Laboratory tests showed a significantly elevated level of aminotransferases.", "Alanine aminotransferase (ALT) was 2439 IU/L.", "Aspartate aminotransferase (AST) was 1418 IU/L.", "Serological testing was positive for HBsAg.", "Serological testing was positive for anti-Hbc IgM antibodies.", "Serological testing was negative for hepatitis A and hepatitis C viruses.", "The HBV viral load was 5.82 copies/mL.", "HBV genotype A was confirmed.", "Acute hepatitis B was diagnosed.", "The patient was treated conservatively.", "There were no signs of hepatic failure.", "During observation, hepatic parameters were firstly elevated.", "After 14 days, hepatic parameters improved.", "The patient was discharged home with the recommendation to appear for follow-up examinations after six months.", "The patient did not appear for the visit.", "After 15 months, he wrote a message on Facebook to his practitioner asking if he had to report on a follow-up.", "A visit in the clinic was arranged for him.", "Hepatic parameters were normal.", "Testing towards the hepatitis B antigen was negative.", "Chronic HBV infection was excluded.", "The extended interview revealed a urinary tract infection a year before.", "The extended interview revealed unprotected sexual encounters of both homo and heterosexual relations.", "During physical examination, a small ulcer around his anus was found.", "Additional tests for HIV, syphilis, gonorrhoea, and chlamydia trachomatis were ordered.", "All tests were negative except for syphilis.", "Due to risky sexual behaviour, the patient was offered pre-exposure prophylaxis.", "The patient applied for further treatment of syphilis to the Clinic of Dermatology and Venereology in Warsaw."], "summary_subclaims": ["The patient is a 16-year-old Ukrainian boy.", "The patient had acute hepatitis B.", "The patient had not been previously vaccinated against hepatitis B.", "Possible sources of infection included a tattoo made at home.", "Possible sources of infection included a finger cut made with hairdresser scissors during work.", "Possible sources of infection included unprotected sexual encounters.", "The clinical course of the disease was typical with jaundice.", "The clinical course of the disease was typical with elevated aminotransferases levels.", "There was no liver failure.", "During the follow-up visit 16 months after the onset of the disease, chronic hepatitis B was excluded.", "An ulcer around his anus was found.", "Additional tests for sexually transmitted diseases were ordered.", "The tests were positive for syphilis.", "The extended interview revealed that the patient had several unprotected bisexual encounters.", "The patient's unprotected bisexual encounters may have indicated a potential source of infections including the hepatitis B virus."]}, "extra_info": {"fulltext_subclaims": ["A 16-year-old Ukrainian boy was admitted to the Department of Children\u2019s Infectious Diseases in Warsaw, Poland.", "The boy had jaundice lasting for four days.", "The boy had malaise.", "The boy had diarrhoea.", "The boy had vomiting.", "The boy had lived in Poland for 1.5 years.", "The boy was working (training) in the profession of a hairdresser.", "The boy had a tattoo made at home by his mother\u2019s partner six months earlier.", "The boy had a finger cut by hairdressing scissors six weeks before the admission.", "The patient confirmed that he had two secured heterosexual encounters during the last six months.", "In Ukraine, he had been vaccinated against tuberculosis, diphtheria, tetanus, pertussis, poliomyelitis, measles, mumps, and rubella.", "He has not been vaccinated against hepatitis B.", "He negated any dietary errors.", "He had never had blood transfusion nor surgery.", "He was once hospitalized due to acute gastroenteritis in Ukraine.", "The physical examination revealed jaundice.", "The physical examination revealed hepatomegaly (2 cm below the rib arch).", "The physical examination revealed a tattoo on the right forearm.", "Laboratory tests showed a significantly elevated level of aminotransferases.", "Alanine aminotransferase (ALT) was 2439 IU/L.", "Aspartate aminotransferase (AST) was 1418 IU/L.", "Serological testing was positive for HBsAg.", "Serological testing was positive for anti-Hbc IgM antibodies.", "Serological testing was negative for hepatitis A and hepatitis C viruses.", "The HBV viral load was 5.82 copies/mL.", "HBV genotype A was confirmed.", "Acute hepatitis B was diagnosed.", "The patient was treated conservatively.", "There were no signs of hepatic failure.", "During observation, hepatic parameters were firstly elevated.", "After 14 days, hepatic parameters improved.", "The patient was discharged home with the recommendation to appear for follow-up examinations after six months.", "The patient did not appear for the visit.", "After 15 months, he wrote a message on Facebook to his practitioner asking if he had to report on a follow-up.", "A visit in the clinic was arranged for him.", "Hepatic parameters were normal.", "Testing towards the hepatitis B antigen was negative.", "Chronic HBV infection was excluded.", "The extended interview revealed a urinary tract infection a year before.", "The extended interview revealed unprotected sexual encounters of both homo and heterosexual relations.", "During physical examination, a small ulcer around his anus was found.", "Additional tests for HIV, syphilis, gonorrhoea, and chlamydia trachomatis were ordered.", "All tests were negative except for syphilis.", "Due to risky sexual behaviour, the patient was offered pre-exposure prophylaxis.", "The patient applied for further treatment of syphilis to the Clinic of Dermatology and Venereology in Warsaw."], "index": 123, "original_id": "multiclinsum_test_3310_en.txt", "split": "test", "summary_subclaims": ["The patient is a 16-year-old Ukrainian boy.", "The patient had acute hepatitis B.", "The patient had not been previously vaccinated against hepatitis B.", "Possible sources of infection included a tattoo made at home.", "Possible sources of infection included a finger cut made with hairdresser scissors during work.", "Possible sources of infection included unprotected sexual encounters.", "The clinical course of the disease was typical with jaundice.", "The clinical course of the disease was typical with elevated aminotransferases levels.", "There was no liver failure.", "During the follow-up visit 16 months after the onset of the disease, chronic hepatitis B was excluded.", "An ulcer around his anus was found.", "Additional tests for sexually transmitted diseases were ordered.", "The tests were positive for syphilis.", "The extended interview revealed that the patient had several unprotected bisexual encounters.", "The patient's unprotected bisexual encounters may have indicated a potential source of infections including the hepatitis B virus."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was a 78-year-old male.", "The patient had 5 months of intermittent cervicalgia.", "The patient had several weeks of a progressive right hemiparesis, up to hemiplegia (0/5).", "The patient had brisk upper and lower extremity reflexes.", "The patient had bilateral Hoffmann\u2019s and Babinski signs.", "The patient had left hemisensory dysesthesias.", "The patient had urinary incontinence.", "The cervical spinal MRI revealed an intramedullary expansive lesion (10 mm\u00d715 mm) at C1\u2013C2.", "The lesion at C1\u2013C2 markedly enhanced with gadolinium.", "A total body CT scan was performed.", "The CT scan revealed a large mass (about 85 mm in size) involving the upper polar region and the middle third of the right kidney.", "The mass extended to the adrenal gland.", "The mass extended to the ipsilateral psoas muscle.", "A CT-guided fine-needle ago-biopsy established the diagnosis of an RCC.", "The C1\u2013C2 lesion was most likely an RCC metastasis.", "A C1\u2013C2 laminectomy was performed.", "Intraoperative neurophysiological monitoring was used.", "The lesion was macroscopically fully resected.", "Postoperatively, the patient had a slight motor improvement.", "The right hemiparesis improved to 2/5.", "The histological examination revealed large cells with marked anaplasia.", "Immunostaining was negative for cytokeratin.", "Immunostaining was negative for GFAP.", "Immunostaining was negative for S-100.", "Immunostaining was negative for HMB-45.", "Immunostaining was positive for intermediate vimentin filaments.", "The histological and immunostaining studies confirmed the diagnosis of an RCC.", "The 1-week postoperative cervical spine MRI showed postoperative changes.", "The 1-week postoperative MRI showed full lesion excision.", "The patient was discharged to a neuromotor rehabilitation center.", "The patient underwent chemotherapy and radiotherapy for RCC.", "Fourteen months later, the patient died due to metastatic RCC."], "summary_subclaims": ["The patient is a 78-year-old male.", "The patient had intermittent cervicalgia of 5 months duration.", "The patient had progressive severe right hemiparesis for a few weeks.", "The MRI revealed an intramedullary expansive lesion at the C1-C2 level.", "The lesion measured 10 mm\u00d715 mm.", "The lesion readily enhanced with contrast.", "The CT scan documented an 85 mm mass involving the right kidney.", "The mass extended to the ipsilateral adrenal gland.", "The mass posteriorly infiltrated the ipsilateral psoas muscle.", "The CT-guided fine-needle biopsy confirmed the diagnosis of an RCC.", "The RCC was Stage IV.", "The patient underwent total surgical removal of the C1-C2 intramedullary mass.", "After surgery, the patient exhibited a slight motor improvement.", "The right hemiparesis was 2/5 after surgery.", "The patient died after 14 months.", "The cause of death was global RCC tumor progression."]}, "extra_info": {"fulltext_subclaims": ["The patient was a 78-year-old male.", "The patient had 5 months of intermittent cervicalgia.", "The patient had several weeks of a progressive right hemiparesis, up to hemiplegia (0/5).", "The patient had brisk upper and lower extremity reflexes.", "The patient had bilateral Hoffmann\u2019s and Babinski signs.", "The patient had left hemisensory dysesthesias.", "The patient had urinary incontinence.", "The cervical spinal MRI revealed an intramedullary expansive lesion (10 mm\u00d715 mm) at C1\u2013C2.", "The lesion at C1\u2013C2 markedly enhanced with gadolinium.", "A total body CT scan was performed.", "The CT scan revealed a large mass (about 85 mm in size) involving the upper polar region and the middle third of the right kidney.", "The mass extended to the adrenal gland.", "The mass extended to the ipsilateral psoas muscle.", "A CT-guided fine-needle ago-biopsy established the diagnosis of an RCC.", "The C1\u2013C2 lesion was most likely an RCC metastasis.", "A C1\u2013C2 laminectomy was performed.", "Intraoperative neurophysiological monitoring was used.", "The lesion was macroscopically fully resected.", "Postoperatively, the patient had a slight motor improvement.", "The right hemiparesis improved to 2/5.", "The histological examination revealed large cells with marked anaplasia.", "Immunostaining was negative for cytokeratin.", "Immunostaining was negative for GFAP.", "Immunostaining was negative for S-100.", "Immunostaining was negative for HMB-45.", "Immunostaining was positive for intermediate vimentin filaments.", "The histological and immunostaining studies confirmed the diagnosis of an RCC.", "The 1-week postoperative cervical spine MRI showed postoperative changes.", "The 1-week postoperative MRI showed full lesion excision.", "The patient was discharged to a neuromotor rehabilitation center.", "The patient underwent chemotherapy and radiotherapy for RCC.", "Fourteen months later, the patient died due to metastatic RCC."], "index": 122, "original_id": "multiclinsum_test_2110_en.txt", "split": "test", "summary_subclaims": ["The patient is a 78-year-old male.", "The patient had intermittent cervicalgia of 5 months duration.", "The patient had progressive severe right hemiparesis for a few weeks.", "The MRI revealed an intramedullary expansive lesion at the C1-C2 level.", "The lesion measured 10 mm\u00d715 mm.", "The lesion readily enhanced with contrast.", "The CT scan documented an 85 mm mass involving the right kidney.", "The mass extended to the ipsilateral adrenal gland.", "The mass posteriorly infiltrated the ipsilateral psoas muscle.", "The CT-guided fine-needle biopsy confirmed the diagnosis of an RCC.", "The RCC was Stage IV.", "The patient underwent total surgical removal of the C1-C2 intramedullary mass.", "After surgery, the patient exhibited a slight motor improvement.", "The right hemiparesis was 2/5 after surgery.", "The patient died after 14 months.", "The cause of death was global RCC tumor progression."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 63-year-old man.", "The patient is Caucasian.", "The patient has non-ischemic dilated cardiomyopathy.", "The patient did not drink alcohol.", "The patient did not smoke tobacco.", "The patient did not have diabetes.", "The patient had an implantable cardioverter defibrillator implanted.", "The patient was in New York Heart Association (NYHA) IV class.", "The patient had left bundle branch block (LBBB; QRS duration of 145\u2009ms).", "The patient was referred for CRT-D upgrade.", "The patient was awaiting cardiac transplantation.", "The patient was receiving optimal medical therapy.", "The patient was receiving b-Blockade.", "The patient was receiving loop-diuretic.", "The patient was receiving angiotensin-converting enzyme (ACE) inhibitor.", "The patient was receiving K-sparing agent.", "The patient was receiving ivabradine.", "Standard clinical imaging protocol revealed a dilated left ventricle.", "The end-systolic volume (ESV) was 380\u2009ml.", "The ejection fraction (EF) was 4.8% as measured by the modified Simpson\u2019s method.", "Severe functional mitral regurgitation (FMR) was assessed by qualitative estimation with two-dimensional color flow Doppler approach.", "The FMR showed a very large central jet.", "The FMR jet reached the posterior wall of the left atrium.", "The patient underwent the implant of a CRT-D device.", "A quadripolar left ventricular (LV) lead was placed in the posterolateral branch of the coronary sinus.", "The right ventricle (RV)-to-LV electrical delay was recorded at each of the four LV rings.", "The A1 unipolar vector was chosen for LV pacing.", "The greatest electrical delay was 80\u2009ms.", "At 13-day post-implant follow-up, the patient showed worsening heart failure (HF) symptoms.", "Only A2 unipolar LV vector configuration was suitable for simultaneous biventricular activation.", "The interventricular (VV) interval was 0\u2009ms.", "Echo-PIV was used during the acute study with contrast agent bubbles.", "Echo-PIV evaluated the orientation and relative magnitude of blood-induced intraventricular forces.", "Without pacing stimulation (CRT OFF), the intraventricular flow was dominated by rotation.", "The intraventricular forces were predominantly transverse.", "The mean angle \u03c6 was 55.6\u00b0.", "A first setting option (CRT ON, VV delay 0\u2009ms) changed the orientation of intraventricular forces.", "The angle \u03c6 was reduced to 45\u00b0.", "Increasing the delay (CRT ON, VV delay \u2212\u200930\u2009ms) improved the alignment.", "The angle \u03c6 was reduced to 40.3\u00b0.", "Sequential biventricular activation with delay \u2212\u200950\u2009ms provided the best alignment.", "The angle \u03c6 was 38.8\u00b0.", "No reduction of FMR by three-dimensional FVCD was observed.", "The data acquisition time for each three-dimensional color Doppler data set was approximately 5\u2009seconds.", "The analysis of average regurgitation volume took less than 3\u2009minutes.", "Automated anatomy detection of the LV endocardial border, mitral annulus (MA), LV outflow (LVOT), and placement of three-dimensional hemispheric flow sampling planes in the MA and LVOT was performed.", "The software of three-dimensional FVCD computed the flow volumes as the area under the curve of both the MA and LVOT flow in three cardiac cycles.", "FMR volume was calculated by subtracting LVOT stroke volume from MA stroke volume.", "At 6-month follow-up, the patient showed an improvement of NYHA class to III.", "The LV EF improved to 26.6%.", "The ESV was reduced to 288\u2009ml.", "Persistent improvement of diastolic function was obtained.", "A significant reduction of FMR (mean value regurgitant volume, 42.2\u2009ml) was estimated.", "The intraventricular forces estimated by echo-PIV were still partially dominated by the longitudinal path of pressure gradient.", "The mean angle \u03c6 was 43.1\u00b0."], "summary_subclaims": ["The patient is a 63-year-old man.", "The patient is Caucasian.", "The patient showed worsening heart failure symptoms a few days after an implant.", "The two technologies are used in combination during acute echocardiographic optimization of left pacing vector.", "The effect of the device\u2019s optimization is assessed at 6-month follow-up."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 63-year-old man.", "The patient is Caucasian.", "The patient has non-ischemic dilated cardiomyopathy.", "The patient did not drink alcohol.", "The patient did not smoke tobacco.", "The patient did not have diabetes.", "The patient had an implantable cardioverter defibrillator implanted.", "The patient was in New York Heart Association (NYHA) IV class.", "The patient had left bundle branch block (LBBB; QRS duration of 145\u2009ms).", "The patient was referred for CRT-D upgrade.", "The patient was awaiting cardiac transplantation.", "The patient was receiving optimal medical therapy.", "The patient was receiving b-Blockade.", "The patient was receiving loop-diuretic.", "The patient was receiving angiotensin-converting enzyme (ACE) inhibitor.", "The patient was receiving K-sparing agent.", "The patient was receiving ivabradine.", "Standard clinical imaging protocol revealed a dilated left ventricle.", "The end-systolic volume (ESV) was 380\u2009ml.", "The ejection fraction (EF) was 4.8% as measured by the modified Simpson\u2019s method.", "Severe functional mitral regurgitation (FMR) was assessed by qualitative estimation with two-dimensional color flow Doppler approach.", "The FMR showed a very large central jet.", "The FMR jet reached the posterior wall of the left atrium.", "The patient underwent the implant of a CRT-D device.", "A quadripolar left ventricular (LV) lead was placed in the posterolateral branch of the coronary sinus.", "The right ventricle (RV)-to-LV electrical delay was recorded at each of the four LV rings.", "The A1 unipolar vector was chosen for LV pacing.", "The greatest electrical delay was 80\u2009ms.", "At 13-day post-implant follow-up, the patient showed worsening heart failure (HF) symptoms.", "Only A2 unipolar LV vector configuration was suitable for simultaneous biventricular activation.", "The interventricular (VV) interval was 0\u2009ms.", "Echo-PIV was used during the acute study with contrast agent bubbles.", "Echo-PIV evaluated the orientation and relative magnitude of blood-induced intraventricular forces.", "Without pacing stimulation (CRT OFF), the intraventricular flow was dominated by rotation.", "The intraventricular forces were predominantly transverse.", "The mean angle \u03c6 was 55.6\u00b0.", "A first setting option (CRT ON, VV delay 0\u2009ms) changed the orientation of intraventricular forces.", "The angle \u03c6 was reduced to 45\u00b0.", "Increasing the delay (CRT ON, VV delay \u2212\u200930\u2009ms) improved the alignment.", "The angle \u03c6 was reduced to 40.3\u00b0.", "Sequential biventricular activation with delay \u2212\u200950\u2009ms provided the best alignment.", "The angle \u03c6 was 38.8\u00b0.", "No reduction of FMR by three-dimensional FVCD was observed.", "The data acquisition time for each three-dimensional color Doppler data set was approximately 5\u2009seconds.", "The analysis of average regurgitation volume took less than 3\u2009minutes.", "Automated anatomy detection of the LV endocardial border, mitral annulus (MA), LV outflow (LVOT), and placement of three-dimensional hemispheric flow sampling planes in the MA and LVOT was performed.", "The software of three-dimensional FVCD computed the flow volumes as the area under the curve of both the MA and LVOT flow in three cardiac cycles.", "FMR volume was calculated by subtracting LVOT stroke volume from MA stroke volume.", "At 6-month follow-up, the patient showed an improvement of NYHA class to III.", "The LV EF improved to 26.6%.", "The ESV was reduced to 288\u2009ml.", "Persistent improvement of diastolic function was obtained.", "A significant reduction of FMR (mean value regurgitant volume, 42.2\u2009ml) was estimated.", "The intraventricular forces estimated by echo-PIV were still partially dominated by the longitudinal path of pressure gradient.", "The mean angle \u03c6 was 43.1\u00b0."], "index": 126, "original_id": "multiclinsum_test_3317_en.txt", "split": "test", "summary_subclaims": ["The patient is a 63-year-old man.", "The patient is Caucasian.", "The patient showed worsening heart failure symptoms a few days after an implant.", "The two technologies are used in combination during acute echocardiographic optimization of left pacing vector.", "The effect of the device\u2019s optimization is assessed at 6-month follow-up."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["A 68-year-old man was admitted to our hospital with dyspnea and general fatigue in July 2018.", "He was diagnosed with acute decompensated heart failure due to ischemic cardiomyopathy.", "The patient had a history of severe coronary heart disease.", "The patient had chronic kidney disease (CKD Stage II-III).", "During his last hospitalization in 2017, coronary angiography showed severe triple vessel coronary artery disease.", "He refused revascularization therapy.", "Holter revealed paroxysmal ventricular tachycardia and frequent ventricular premature beats.", "He received implantable cardioverter defibrillator (ICD) treatment.", "Aspirin, atorvastatin, furosemide, spironolactone, perindopril, and metoprolol were taken regularly at home.", "On the current admission, his blood pressure was 135/82 mmHg.", "On the current admission, his heart rate was 75 beats/min.", "A S3 and systolic murmur were identified.", "Inspiratory moist rales were found in the bilateral lung fields.", "Slight edema of both lower limbs was noted.", "Serum creatinine was 160 umol/L.", "Estimated glomerular filtration rate was 38 ml/min/1.73 m2.", "NT-proBNP was 25,000 pg/mL.", "Cardiac troponin was 0.11 ng/mL.", "Electrocardiogram revealed a sinus rhythm with a heart rate of 75 beats per minute.", "Chest X-ray showed cardiomegaly.", "Chest X-ray showed left small pleural effusion.", "Echocardiography demonstrated severe left ventricular enlargement.", "Left ventricular ejection fraction was 28%.", "The patient was diagnosed with acute decompensated heart failure caused by volume overload.", "Intravenous loop diuretics and nesiritide were administered.", "The patient was insensitive to intravenous diuretics.", "The patient's clinical symptoms did not improve significantly.", "Diuretic resistance could be considered.", "Low-dose TLV (7.5 mg qd) was performed on day 3.", "The administration of TLV dramatically relieved dyspnea.", "The administration of TLV increased urinary output.", "After 3 days of TLV treatment, the patient became delirious.", "His limbs shook uncontrollably.", "Serum sodium was 173 mmol/L.", "Severe hypernatremia was diagnosed.", "We suspected a high sensitivity to the side effect of TLV.", "We stopped the use of TLV.", "Gastric tube was inserted orally to increase the intake of fresh water.", "Serum sodium was restored to normal (135 mmol/L) on day 10.", "Serum creatinine was 104 umol/L.", "Estimated glomerular filtration rate was 62 ml/min/1.73 m2.", "NT-proBNP was 3280 pg/mL.", "The patient remained insensitive to intravenous diuretics.", "We tried again to use a lower dose of TLV (3.75 mg qd).", "Serum sodium rose again (162 mmol/L).", "We confirmed that hypernatremia was caused by TLV.", "After the suspension of TLV, his serum sodium decreased to 138 mmol/L.", "Psychiatric symptoms recovered.", "We had to give the patient a larger dose of intravenous loop diuresis.", "The patient was discharged on the 21st day after admission.", "After hospital discharge, the patient eventually died of cardiac arrest due to critically ill heart failure."], "summary_subclaims": ["A 68-year-old man was admitted to our hospital with dyspea and general fatigue.", "He was diagnosed with acute decompensated heart failure due to ischemic cardiomyopathy.", "Low-dose TLV (7.5\u200amg qd) was performed.", "After the 3-day treatment using TLV, he became delirious and his limbs shook uncontrollably.", "High serum sodium 173 mmol/L was noted compared to the results of the first examination (137 mmol/L).", "After intensive rescue, serum sodium was restored to normal (135\u200amol/L).", "When the patient refused continuous renal replacement therapy (CRRT), we tried again to use a lower dose of TLV to improve diuretic resistance.", "Two days later, serum sodium rose again (162\u200amol/L).", "During the course of therapy, we did not strictly require the patient to control the fluid intake.", "No other medication could cause elevation of serum sodium.", "We suspected a high sensitivity to the side effect of TLV.", "Stop the use of TLV and encourage the patient to drink plenty of water.", "Gastric tube was inserted orally to increase the intake of fresh water.", "His serum sodium decreased gradually and his psychiatric symptom recovered.", "During this period, overall condition of the patient was stable.", "After being discharged from the hospital, the patient eventually died of cardiac arrest due to critically ill heart failure."]}, "extra_info": {"fulltext_subclaims": ["A 68-year-old man was admitted to our hospital with dyspnea and general fatigue in July 2018.", "He was diagnosed with acute decompensated heart failure due to ischemic cardiomyopathy.", "The patient had a history of severe coronary heart disease.", "The patient had chronic kidney disease (CKD Stage II-III).", "During his last hospitalization in 2017, coronary angiography showed severe triple vessel coronary artery disease.", "He refused revascularization therapy.", "Holter revealed paroxysmal ventricular tachycardia and frequent ventricular premature beats.", "He received implantable cardioverter defibrillator (ICD) treatment.", "Aspirin, atorvastatin, furosemide, spironolactone, perindopril, and metoprolol were taken regularly at home.", "On the current admission, his blood pressure was 135/82 mmHg.", "On the current admission, his heart rate was 75 beats/min.", "A S3 and systolic murmur were identified.", "Inspiratory moist rales were found in the bilateral lung fields.", "Slight edema of both lower limbs was noted.", "Serum creatinine was 160 umol/L.", "Estimated glomerular filtration rate was 38 ml/min/1.73 m2.", "NT-proBNP was 25,000 pg/mL.", "Cardiac troponin was 0.11 ng/mL.", "Electrocardiogram revealed a sinus rhythm with a heart rate of 75 beats per minute.", "Chest X-ray showed cardiomegaly.", "Chest X-ray showed left small pleural effusion.", "Echocardiography demonstrated severe left ventricular enlargement.", "Left ventricular ejection fraction was 28%.", "The patient was diagnosed with acute decompensated heart failure caused by volume overload.", "Intravenous loop diuretics and nesiritide were administered.", "The patient was insensitive to intravenous diuretics.", "The patient's clinical symptoms did not improve significantly.", "Diuretic resistance could be considered.", "Low-dose TLV (7.5 mg qd) was performed on day 3.", "The administration of TLV dramatically relieved dyspnea.", "The administration of TLV increased urinary output.", "After 3 days of TLV treatment, the patient became delirious.", "His limbs shook uncontrollably.", "Serum sodium was 173 mmol/L.", "Severe hypernatremia was diagnosed.", "We suspected a high sensitivity to the side effect of TLV.", "We stopped the use of TLV.", "Gastric tube was inserted orally to increase the intake of fresh water.", "Serum sodium was restored to normal (135 mmol/L) on day 10.", "Serum creatinine was 104 umol/L.", "Estimated glomerular filtration rate was 62 ml/min/1.73 m2.", "NT-proBNP was 3280 pg/mL.", "The patient remained insensitive to intravenous diuretics.", "We tried again to use a lower dose of TLV (3.75 mg qd).", "Serum sodium rose again (162 mmol/L).", "We confirmed that hypernatremia was caused by TLV.", "After the suspension of TLV, his serum sodium decreased to 138 mmol/L.", "Psychiatric symptoms recovered.", "We had to give the patient a larger dose of intravenous loop diuresis.", "The patient was discharged on the 21st day after admission.", "After hospital discharge, the patient eventually died of cardiac arrest due to critically ill heart failure."], "index": 124, "original_id": "multiclinsum_test_3307_en.txt", "split": "test", "summary_subclaims": ["A 68-year-old man was admitted to our hospital with dyspea and general fatigue.", "He was diagnosed with acute decompensated heart failure due to ischemic cardiomyopathy.", "Low-dose TLV (7.5\u200amg qd) was performed.", "After the 3-day treatment using TLV, he became delirious and his limbs shook uncontrollably.", "High serum sodium 173 mmol/L was noted compared to the results of the first examination (137 mmol/L).", "After intensive rescue, serum sodium was restored to normal (135\u200amol/L).", "When the patient refused continuous renal replacement therapy (CRRT), we tried again to use a lower dose of TLV to improve diuretic resistance.", "Two days later, serum sodium rose again (162\u200amol/L).", "During the course of therapy, we did not strictly require the patient to control the fluid intake.", "No other medication could cause elevation of serum sodium.", "We suspected a high sensitivity to the side effect of TLV.", "Stop the use of TLV and encourage the patient to drink plenty of water.", "Gastric tube was inserted orally to increase the intake of fresh water.", "His serum sodium decreased gradually and his psychiatric symptom recovered.", "During this period, overall condition of the patient was stable.", "After being discharged from the hospital, the patient eventually died of cardiac arrest due to critically ill heart failure."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["An 84-year-old white male presented with a pale, ulcerated lesion (1.3 cm in diameter) on the middle of his lower lip.", "There was no associated lymphadenopathy.", "An excisional biopsy was performed.", "Histopathological and immunoistochemical features revealed a Merkel cell carcinoma.", "The excision was incomplete.", "The patient was scheduled for a wider excision in the following 2 months.", "The lesion recurred.", "The patient returned with a protruding white lesion of 1.1 cm in diameter.", "A wider excision, with an 8 mm margin, was performed.", "Histopathology confirmed the nature of MCC.", "The second excision was within healthy margins.", "Two months later, the patient was referred to the Department of Plastic Surgery.", "The patient had a protruding ulcerated lesion, 3 cm in diameter, on his lower lip.", "Multiple palpable lymph nodes in the submandibular and cervical area were present.", "The patient had been diagnosed with chronic lymphocytic leukemia 8 years earlier.", "The patient did not receive any treatment for CLL.", "A CT scan showed a soft tissue lobular mass, 3 cm in diameter, on the lower lip.", "The mass had a possible extension to the mandible.", "A W-excision (4 \u00d7 3.5 \u00d7 1 cm) of the lip lesion was performed.", "An open biopsy of one submandibular lymph node was performed.", "Histopathology confirmed recurrence of MCC.", "An undifferentiated small cell carcinoma with hyaluronated stroma was identified.", "The cells arranged in nodules or rosettes.", "The cells had dense nuclear chromatin, with mitoses and nuclear debris.", "Immunoistochemical procedures showed Neuron Specific Enolase (NSE) positivity.", "Antibodies for Epithelial Membrane Antigen (EMA) and Chromogranin were negative.", "The excision was described as complete.", "The submandibular lymph node was positive for malignancy.", "The lymph node was associated with the CLL (non Hodgkin's, B cell small lymphocytic lymphoma).", "There was no evidence of metastatic infiltration by MCC.", "This was confirmed immunoistochemically with the positive expression of CD5 and CD20 antibody.", "The expression of CD10 antibody and NSE was negative.", "Due to the age of the patient, chemotherapy was not considered.", "A month later, a new CT scan depicted a soft tissue mass consistent with recurrence of MCC.", "Multiple enlarged superficial and deep cervical lymph nodes were present.", "Fine needle aspiration of the submandibular swelling was performed.", "FNA confirmed MCC.", "The patient underwent one month of neck radiotherapy with Cobalt 60.", "A total dose of 4600cGy in 23 days was administered.", "A further boost of 600cGy in 2 days on the left submandibular area was administered.", "The treatment was successfully completed with full remission of the cervical lymphadenopathy.", "Two months following the radiotherapy, a new CT scan showed reduction and obscurrence of the pre-existing mass on the left mandibular area.", "The lymph nodes were smaller.", "The patient is on regular follow up.", "The CLL status is stable.", "There is no evidence of progression or further recurrence of MCC 9 months post-radiotherapy."], "summary_subclaims": ["The patient is an 84-year-old male.", "The patient had an aggressively recurrent form of MCC on the lower lip.", "The patient had an 8-year history of untreated CLL.", "During the recurrences of MCC, coexisting regional lymphadenopathy posed a problem in the differential diagnosis.", "Histopathology and immunoistochemistry showed submandibular lymphadenopathy coexisting with the second recurrence of MCC.", "The submandibular lymphadenopathy was due to B-cell small lymphocytic lymphoma.", "The subsequent recurrence of the skin tumor involved the superficial and deep cervical lymph nodes.", "Surgical excision followed by involved field radiation therapy has been proven effective for both malignancies."]}, "extra_info": {"fulltext_subclaims": ["An 84-year-old white male presented with a pale, ulcerated lesion (1.3 cm in diameter) on the middle of his lower lip.", "There was no associated lymphadenopathy.", "An excisional biopsy was performed.", "Histopathological and immunoistochemical features revealed a Merkel cell carcinoma.", "The excision was incomplete.", "The patient was scheduled for a wider excision in the following 2 months.", "The lesion recurred.", "The patient returned with a protruding white lesion of 1.1 cm in diameter.", "A wider excision, with an 8 mm margin, was performed.", "Histopathology confirmed the nature of MCC.", "The second excision was within healthy margins.", "Two months later, the patient was referred to the Department of Plastic Surgery.", "The patient had a protruding ulcerated lesion, 3 cm in diameter, on his lower lip.", "Multiple palpable lymph nodes in the submandibular and cervical area were present.", "The patient had been diagnosed with chronic lymphocytic leukemia 8 years earlier.", "The patient did not receive any treatment for CLL.", "A CT scan showed a soft tissue lobular mass, 3 cm in diameter, on the lower lip.", "The mass had a possible extension to the mandible.", "A W-excision (4 \u00d7 3.5 \u00d7 1 cm) of the lip lesion was performed.", "An open biopsy of one submandibular lymph node was performed.", "Histopathology confirmed recurrence of MCC.", "An undifferentiated small cell carcinoma with hyaluronated stroma was identified.", "The cells arranged in nodules or rosettes.", "The cells had dense nuclear chromatin, with mitoses and nuclear debris.", "Immunoistochemical procedures showed Neuron Specific Enolase (NSE) positivity.", "Antibodies for Epithelial Membrane Antigen (EMA) and Chromogranin were negative.", "The excision was described as complete.", "The submandibular lymph node was positive for malignancy.", "The lymph node was associated with the CLL (non Hodgkin's, B cell small lymphocytic lymphoma).", "There was no evidence of metastatic infiltration by MCC.", "This was confirmed immunoistochemically with the positive expression of CD5 and CD20 antibody.", "The expression of CD10 antibody and NSE was negative.", "Due to the age of the patient, chemotherapy was not considered.", "A month later, a new CT scan depicted a soft tissue mass consistent with recurrence of MCC.", "Multiple enlarged superficial and deep cervical lymph nodes were present.", "Fine needle aspiration of the submandibular swelling was performed.", "FNA confirmed MCC.", "The patient underwent one month of neck radiotherapy with Cobalt 60.", "A total dose of 4600cGy in 23 days was administered.", "A further boost of 600cGy in 2 days on the left submandibular area was administered.", "The treatment was successfully completed with full remission of the cervical lymphadenopathy.", "Two months following the radiotherapy, a new CT scan showed reduction and obscurrence of the pre-existing mass on the left mandibular area.", "The lymph nodes were smaller.", "The patient is on regular follow up.", "The CLL status is stable.", "There is no evidence of progression or further recurrence of MCC 9 months post-radiotherapy."], "index": 128, "original_id": "multiclinsum_test_1953_en.txt", "split": "test", "summary_subclaims": ["The patient is an 84-year-old male.", "The patient had an aggressively recurrent form of MCC on the lower lip.", "The patient had an 8-year history of untreated CLL.", "During the recurrences of MCC, coexisting regional lymphadenopathy posed a problem in the differential diagnosis.", "Histopathology and immunoistochemistry showed submandibular lymphadenopathy coexisting with the second recurrence of MCC.", "The submandibular lymphadenopathy was due to B-cell small lymphocytic lymphoma.", "The subsequent recurrence of the skin tumor involved the superficial and deep cervical lymph nodes.", "Surgical excision followed by involved field radiation therapy has been proven effective for both malignancies."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical manifestations often emerging in the later stages of disease. Early intervention through biomarker monitoring, blood pressure control, and pharmacological management (e.g., RAS inhibitors) is critical to slow disease progression and preserve renal function.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 61-year-old White man.", "The patient is a non-smoker.", "The patient has a diagnosis of long-standing arterial hypertension of difficult control.", "The patient has severe heart failure with a left ventricular ejection fraction of 30%.", "The patient is receiving pharmacological treatment with carvedilol, ivabradine, and losartan.", "The patient has a history of stage IIIB chronic renal failure without dialysis therapy.", "A year before the current admission, he consulted for urinary symptoms.", "The urinary symptoms rapidly evolved to systemic compromise with fever, diaphoresis, low back pain, hypotension, dyspnea, and increased acute phase reactants.", "He required hospitalization in the intensive care unit for multidisciplinary treatment.", "The diagnosis was sepsis of urinary origin.", "Alterations in calcium behavior were detected.", "The alterations in calcium behavior were associated to the underlying renal disease.", "The alterations in calcium behavior were associated to a severe hyperparathyroidism secondary to a functional adenoma in the lower left parathyroid.", "The functional adenoma in the lower left parathyroid was treated with surgery.", "Surgery achieved control of symptoms and levels of calcium and phosphorus.", "Chest x-ray showed 2 lesions of tumor aspect with internal lytic areas in the fourth right and eighth left costal arches.", "The first lesion measured 25 \u00d7 21 mm with involvement of fourth right costal arch.", "The second lesion measured 77 \u00d7 54 mm in eighth left costal arch showing growth toward the left pleural cavity.", "Both lesions were suggestive of a tumor of chondral origin, enchondroma.", "It was not possible to rule out malignancy with the images.", "He was admitted in our institution for excisional biopsy.", "The physical examination revealed a thin patient with chronic disease.", "The physical examination revealed a deformity in the neck with anterior flexion pronounced by severe dorsal kyphoscoliosis.", "The physical examination revealed secondary asymmetry of the right ribcage, which was retracted with decreased intercostal spaces.", "He referred increased dyspnea with the activities of daily life, with NYHA functional class III.", "Blood pressure was 120/70 mm Hg.", "Heart rate was 100 beats per minute.", "Breathing frequency was 16 breaths per minute.", "There was no cyanosis.", "There was jugular engorgement at 90\u00b0.", "There were no neck masses.", "The heart was tachycardic and rhythmic with no murmurs or gallop.", "Breath sounds were decreased at both lung bases.", "The abdomen had no ascites or masses.", "The extremities had edema grade II.", "No identifiable lesions in the chest wall other than deformity by kyphoscoliosis were found.", "Blood work was unremarkable, except for mild anemia of normal volumes.", "Spirometry showed a moderate restrictive ventilatory pattern.", "There were no significant post-bronchodilator changes.", "Diffusing capacity of carbon monoxide was in normal limits (DLCO: 109%).", "The chronic kidney disease was stable.", "Thoracic computed tomography (CT) scan showed a heterogeneous rounded lytic lesion with sclerotic edges and growth toward the pulmonary cavity.", "The lesion was of expansive type, causing displacement of pulmonary parenchyma.", "The lesion measured approximately 77 \u00d7 54 mm and depended on the eighth left costal arch.", "It was very difficult to determine if the lung was surrounding the lesion or if the mass was infiltrating the parenchyma.", "In the fourth right costal arch, an image of similar characteristics, but smaller in size, was found, measuring 25 \u00d7 21 mm.", "A severe dorsal kyphoscoliosis was identified.", "No further studies were implemented.", "The decision was made to perform a surgical resection of the mass with the possibility of having to do a lobectomy.", "The patient was hospitalized in the intensive care unit for pre-surgical conditioning.", "A left ventricular ejection fraction of 30% was evidenced.", "A cycle of intravenous levosimendan was initiated.", "He received red blood cell transfusion.", "He underwent resection of the left costal mass by thoracoscopy.", "During the surgical procedure, only 1 hard lesion was found that involved the eighth rib and soft tissues of the seventh to ninth left ribs.", "The lesion did not infiltrate into the lung tissue or pleural cavity.", "Only partial resection of these 3 ribs was necessary.", "The right side was not intervened.", "In the immediate postsurgical period, the patient presented a difficult evolution.", "The patient had hemodynamic instability.", "The patient required vasoactive support with norepinephrine.", "The patient had prolonged mechanical ventilation.", "The patient needed a tracheostomy to assist a long-standing recovery process.", "Subsequently, it was possible to remove the vasoactive drugs.", "The invasive ventilatory support was removed.", "The tracheostomy was removed.", "The patient had complete physical and respiratory rehabilitation."], "summary_subclaims": ["The patient had a history of multiple diseases.", "Two tumor-like lesions with internal lytic areas were detected.", "One lesion was located in the fourth right costal arch.", "One lesion was located in the eighth left costal arc.", "Clinical manifestations were described.", "Radiological findings were described.", "Laboratory findings were described.", "Pathological results were described.", "The outcome was described."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 61-year-old White man.", "The patient is a non-smoker.", "The patient has a diagnosis of long-standing arterial hypertension of difficult control.", "The patient has severe heart failure with a left ventricular ejection fraction of 30%.", "The patient is receiving pharmacological treatment with carvedilol, ivabradine, and losartan.", "The patient has a history of stage IIIB chronic renal failure without dialysis therapy.", "A year before the current admission, he consulted for urinary symptoms.", "The urinary symptoms rapidly evolved to systemic compromise with fever, diaphoresis, low back pain, hypotension, dyspnea, and increased acute phase reactants.", "He required hospitalization in the intensive care unit for multidisciplinary treatment.", "The diagnosis was sepsis of urinary origin.", "Alterations in calcium behavior were detected.", "The alterations in calcium behavior were associated to the underlying renal disease.", "The alterations in calcium behavior were associated to a severe hyperparathyroidism secondary to a functional adenoma in the lower left parathyroid.", "The functional adenoma in the lower left parathyroid was treated with surgery.", "Surgery achieved control of symptoms and levels of calcium and phosphorus.", "Chest x-ray showed 2 lesions of tumor aspect with internal lytic areas in the fourth right and eighth left costal arches.", "The first lesion measured 25 \u00d7 21 mm with involvement of fourth right costal arch.", "The second lesion measured 77 \u00d7 54 mm in eighth left costal arch showing growth toward the left pleural cavity.", "Both lesions were suggestive of a tumor of chondral origin, enchondroma.", "It was not possible to rule out malignancy with the images.", "He was admitted in our institution for excisional biopsy.", "The physical examination revealed a thin patient with chronic disease.", "The physical examination revealed a deformity in the neck with anterior flexion pronounced by severe dorsal kyphoscoliosis.", "The physical examination revealed secondary asymmetry of the right ribcage, which was retracted with decreased intercostal spaces.", "He referred increased dyspnea with the activities of daily life, with NYHA functional class III.", "Blood pressure was 120/70 mm Hg.", "Heart rate was 100 beats per minute.", "Breathing frequency was 16 breaths per minute.", "There was no cyanosis.", "There was jugular engorgement at 90\u00b0.", "There were no neck masses.", "The heart was tachycardic and rhythmic with no murmurs or gallop.", "Breath sounds were decreased at both lung bases.", "The abdomen had no ascites or masses.", "The extremities had edema grade II.", "No identifiable lesions in the chest wall other than deformity by kyphoscoliosis were found.", "Blood work was unremarkable, except for mild anemia of normal volumes.", "Spirometry showed a moderate restrictive ventilatory pattern.", "There were no significant post-bronchodilator changes.", "Diffusing capacity of carbon monoxide was in normal limits (DLCO: 109%).", "The chronic kidney disease was stable.", "Thoracic computed tomography (CT) scan showed a heterogeneous rounded lytic lesion with sclerotic edges and growth toward the pulmonary cavity.", "The lesion was of expansive type, causing displacement of pulmonary parenchyma.", "The lesion measured approximately 77 \u00d7 54 mm and depended on the eighth left costal arch.", "It was very difficult to determine if the lung was surrounding the lesion or if the mass was infiltrating the parenchyma.", "In the fourth right costal arch, an image of similar characteristics, but smaller in size, was found, measuring 25 \u00d7 21 mm.", "A severe dorsal kyphoscoliosis was identified.", "No further studies were implemented.", "The decision was made to perform a surgical resection of the mass with the possibility of having to do a lobectomy.", "The patient was hospitalized in the intensive care unit for pre-surgical conditioning.", "A left ventricular ejection fraction of 30% was evidenced.", "A cycle of intravenous levosimendan was initiated.", "He received red blood cell transfusion.", "He underwent resection of the left costal mass by thoracoscopy.", "During the surgical procedure, only 1 hard lesion was found that involved the eighth rib and soft tissues of the seventh to ninth left ribs.", "The lesion did not infiltrate into the lung tissue or pleural cavity.", "Only partial resection of these 3 ribs was necessary.", "The right side was not intervened.", "In the immediate postsurgical period, the patient presented a difficult evolution.", "The patient had hemodynamic instability.", "The patient required vasoactive support with norepinephrine.", "The patient had prolonged mechanical ventilation.", "The patient needed a tracheostomy to assist a long-standing recovery process.", "Subsequently, it was possible to remove the vasoactive drugs.", "The invasive ventilatory support was removed.", "The tracheostomy was removed.", "The patient had complete physical and respiratory rehabilitation."], "index": 130, "original_id": "multiclinsum_test_2403_en.txt", "split": "test", "summary_subclaims": ["The patient had a history of multiple diseases.", "Two tumor-like lesions with internal lytic areas were detected.", "One lesion was located in the fourth right costal arch.", "One lesion was located in the eighth left costal arc.", "Clinical manifestations were described.", "Radiological findings were described.", "Laboratory findings were described.", "Pathological results were described.", "The outcome was described."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 56-year-old Caucasian male.", "He has a past medical history of hypertension.", "He has a past medical history of acute coronary syndrome.", "He has a past medical history of atrial fibrillation.", "He presented to the emergency department with acute epigastric pain.", "His complaints had started 2 weeks earlier.", "The pain had worsened 1 day prior to ED presentation.", "The pain was associated with nausea.", "The pain increased on inspiration.", "Defecation was normal.", "Micturition was normal.", "He was taking fenprocoumon.", "He was taking sotalol.", "He was taking antihypertensives.", "He was taking a statin.", "He was taking a proton-pump inhibitor.", "There was no history of trauma.", "Physical examination showed a pale man.", "Physical examination showed a sweating man.", "Physical examination showed an obese man.", "His blood pressure was 113/73 mmHg.", "His heart rate was 72 beats/min.", "His oxygen saturation was 95% on room air.", "His respiratory rate was 13 breaths/min.", "The abdomen was not distended.", "There were normal bowel sounds.", "He had epigastric tenderness.", "There was no muscular defence.", "There was no hepato-splenomegaly.", "His initial haemoglobin was 8.5 mmol/l.", "White blood cell count was 8.5 \u00d7 109/l.", "C-reactive protein was 26 mg/l.", "The international normalised ratio (INR) was 2.4.", "Abdominal ultrasound showed an inhomogeneous aspect of the spleen.", "Contrast-enhanced computed tomography (CT) imaging of the abdomen revealed splenic haemorrhage.", "Contrast-enhanced CT imaging showed subcapsular hematoma.", "An acute operation was deemed unnecessary.", "Oral anticoagulation was reversed with 10 mg vitamin K.", "The patient was admitted to the hospital for observation.", "The patient was discharged in good condition after 3 days."], "summary_subclaims": ["The patient is a 56-year-old male.", "The patient was on oral anticoagulation.", "The patient presented to the emergency department with epigastric pain.", "The patient had nausea.", "The patient had left upper quadrant tenderness.", "There was no history of trauma.", "Contrast-enhanced CT imaging revealed a large subcapsular haematoma of the spleen.", "Oral anticoagulation was antagonised with vitamin K.", "The patient was discharged in good condition after 3 days of clinical observation."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 56-year-old Caucasian male.", "He has a past medical history of hypertension.", "He has a past medical history of acute coronary syndrome.", "He has a past medical history of atrial fibrillation.", "He presented to the emergency department with acute epigastric pain.", "His complaints had started 2 weeks earlier.", "The pain had worsened 1 day prior to ED presentation.", "The pain was associated with nausea.", "The pain increased on inspiration.", "Defecation was normal.", "Micturition was normal.", "He was taking fenprocoumon.", "He was taking sotalol.", "He was taking antihypertensives.", "He was taking a statin.", "He was taking a proton-pump inhibitor.", "There was no history of trauma.", "Physical examination showed a pale man.", "Physical examination showed a sweating man.", "Physical examination showed an obese man.", "His blood pressure was 113/73 mmHg.", "His heart rate was 72 beats/min.", "His oxygen saturation was 95% on room air.", "His respiratory rate was 13 breaths/min.", "The abdomen was not distended.", "There were normal bowel sounds.", "He had epigastric tenderness.", "There was no muscular defence.", "There was no hepato-splenomegaly.", "His initial haemoglobin was 8.5 mmol/l.", "White blood cell count was 8.5 \u00d7 109/l.", "C-reactive protein was 26 mg/l.", "The international normalised ratio (INR) was 2.4.", "Abdominal ultrasound showed an inhomogeneous aspect of the spleen.", "Contrast-enhanced computed tomography (CT) imaging of the abdomen revealed splenic haemorrhage.", "Contrast-enhanced CT imaging showed subcapsular hematoma.", "An acute operation was deemed unnecessary.", "Oral anticoagulation was reversed with 10 mg vitamin K.", "The patient was admitted to the hospital for observation.", "The patient was discharged in good condition after 3 days."], "index": 92, "original_id": "multiclinsum_test_1095_en.txt", "split": "test", "summary_subclaims": ["The patient is a 56-year-old male.", "The patient was on oral anticoagulation.", "The patient presented to the emergency department with epigastric pain.", "The patient had nausea.", "The patient had left upper quadrant tenderness.", "There was no history of trauma.", "Contrast-enhanced CT imaging revealed a large subcapsular haematoma of the spleen.", "Oral anticoagulation was antagonised with vitamin K.", "The patient was discharged in good condition after 3 days of clinical observation."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was a 78-year-old Greek male.", "The patient was a smoker.", "The patient had a BMI of 25.7 kg/m2.", "The patient was classified as an ASA physical status grade III.", "The patient had osteoarthritis of the left hip.", "The patient was scheduled for an elective total hip replacement.", "The patient had hypertension.", "The patient had dyslipidemia.", "The patient had type II diabetes managed by oral metformin.", "The patient had a normal pre-operative echocardiography with an ejection fraction of 60%.", "The patient had no history of pulmonary disease.", "The patient had a total knee replacement in the past without complications.", "The patient's preoperative laboratory examination was within normal parameters.", "The patient was hemodynamically stable with blood pressure 137/67 mmHg, heart rate 77 bpm, and SpO2 99%.", "The anesthesia plan included combined lumbar epidural and spinal anesthesia.", "Standard monitoring including ECG, SpO2, and non-invasive blood pressure was commenced in the OR.", "An oxygen mask administering 6 lt/min was used throughout the procedure.", "The neuraxial spinal technique was performed by a second-year anesthesia trainee.", "The spinal block was performed at the L4-L5 intervertebral space using a midline approach.", "Local anesthesia with 5 ml of 2% lidocaine was used.", "An 18-Gauge Tuohy needle was used with a syringe filled with 8 ml of air.", "The epidural space was located after a single redirection of the needle.", "A needle-through-needle approach was used to locate the subarachnoid space.", "Cerebrospinal fluid flowed freely through the spinal needle.", "A mixture of 1.9 ml of ropivacaine 0.75% and 0.2 ml of fentanyl was introduced into the subarachnoid space.", "The epidural catheter was placed in the epidural space.", "The spinal block was confirmed using the temperature differentiation method.", "An arterial catheter was inserted in the radial artery.", "The patient was placed on the right lateral side with the left hip facing upwards.", "The patient received no intravenous anesthetic or analgesic medication.", "Approximately 2 hours after the spinal block, the patient's blood pressure dropped from 163/84 mmHg to 82/45 mmHg.", "The patient's heart rate decreased to 45 bpm.", "The patient felt dizziness.", "Sinus bradycardia was apparent on the ECG.", "The anesthesiologist administered 5 mg of ephedrine and 1 mg of phenylephrine.", "O2 administration was increased to 15 lt/min.", "Intravenous fluid administration was increased.", "There was no improvement in the patient's hemodynamic state.", "The patient's blood pressure dropped further to 55/35 mmHg.", "The patient became unresponsive.", "1 mg of adrenaline was given intravenously.", "This produced an immediate rise in blood pressure to 183/88 mmHg.", "Small 0.05 mg/ml boluses of nitroglycerin were administered.", "The patient's mental status returned to normal.", "A point of care echocardiogram demonstrated no new cardiac abnormalities.", "A CTPA was performed and was negative for pulmonary embolism.", "A chest and abdomen CT demonstrated air in the subcutaneous tissue, intermuscular space, spinal canal, and mediastinum.", "The patient was admitted to the PACU.", "The epidural catheter was removed.", "The patient was discharged home on the fifteenth postoperative day."], "summary_subclaims": ["A combined lumbar epidural and spinal anesthesia was performed using the loss of resistance to air technique.", "The patient was a 78-year-old Greek (Caucasian) male.", "The patient was undergoing a total hip replacement.", "The patient was hemodynamically stable throughout the operation.", "Two hours following epidural analgesia, the patient manifested a sudden drop in blood pressure and heart rate.", "The patient's drop in blood pressure and heart rate required the administration of adrenaline.", "A Computed Tomography scan demonstrated pneumomediastinum.", "A Computed Tomography scan demonstrated pneumorrachis.", "A Computed Tomography scan demonstrated paravertebral soft tissue emphysema.", "We believe that injected air from the epidural space and surrounding tissues slowly moved towards the mediastinum.", "We believe that the movement of air stimulated the para-aortic ganglia.", "We believe that the stimulation caused parasympathetic stimulation.", "We believe that the parasympathetic stimulation caused hypotension and bradycardia."]}, "extra_info": {"fulltext_subclaims": ["The patient was a 78-year-old Greek male.", "The patient was a smoker.", "The patient had a BMI of 25.7 kg/m2.", "The patient was classified as an ASA physical status grade III.", "The patient had osteoarthritis of the left hip.", "The patient was scheduled for an elective total hip replacement.", "The patient had hypertension.", "The patient had dyslipidemia.", "The patient had type II diabetes managed by oral metformin.", "The patient had a normal pre-operative echocardiography with an ejection fraction of 60%.", "The patient had no history of pulmonary disease.", "The patient had a total knee replacement in the past without complications.", "The patient's preoperative laboratory examination was within normal parameters.", "The patient was hemodynamically stable with blood pressure 137/67 mmHg, heart rate 77 bpm, and SpO2 99%.", "The anesthesia plan included combined lumbar epidural and spinal anesthesia.", "Standard monitoring including ECG, SpO2, and non-invasive blood pressure was commenced in the OR.", "An oxygen mask administering 6 lt/min was used throughout the procedure.", "The neuraxial spinal technique was performed by a second-year anesthesia trainee.", "The spinal block was performed at the L4-L5 intervertebral space using a midline approach.", "Local anesthesia with 5 ml of 2% lidocaine was used.", "An 18-Gauge Tuohy needle was used with a syringe filled with 8 ml of air.", "The epidural space was located after a single redirection of the needle.", "A needle-through-needle approach was used to locate the subarachnoid space.", "Cerebrospinal fluid flowed freely through the spinal needle.", "A mixture of 1.9 ml of ropivacaine 0.75% and 0.2 ml of fentanyl was introduced into the subarachnoid space.", "The epidural catheter was placed in the epidural space.", "The spinal block was confirmed using the temperature differentiation method.", "An arterial catheter was inserted in the radial artery.", "The patient was placed on the right lateral side with the left hip facing upwards.", "The patient received no intravenous anesthetic or analgesic medication.", "Approximately 2 hours after the spinal block, the patient's blood pressure dropped from 163/84 mmHg to 82/45 mmHg.", "The patient's heart rate decreased to 45 bpm.", "The patient felt dizziness.", "Sinus bradycardia was apparent on the ECG.", "The anesthesiologist administered 5 mg of ephedrine and 1 mg of phenylephrine.", "O2 administration was increased to 15 lt/min.", "Intravenous fluid administration was increased.", "There was no improvement in the patient's hemodynamic state.", "The patient's blood pressure dropped further to 55/35 mmHg.", "The patient became unresponsive.", "1 mg of adrenaline was given intravenously.", "This produced an immediate rise in blood pressure to 183/88 mmHg.", "Small 0.05 mg/ml boluses of nitroglycerin were administered.", "The patient's mental status returned to normal.", "A point of care echocardiogram demonstrated no new cardiac abnormalities.", "A CTPA was performed and was negative for pulmonary embolism.", "A chest and abdomen CT demonstrated air in the subcutaneous tissue, intermuscular space, spinal canal, and mediastinum.", "The patient was admitted to the PACU.", "The epidural catheter was removed.", "The patient was discharged home on the fifteenth postoperative day."], "index": 89, "original_id": "multiclinsum_test_2918_en.txt", "split": "test", "summary_subclaims": ["A combined lumbar epidural and spinal anesthesia was performed using the loss of resistance to air technique.", "The patient was a 78-year-old Greek (Caucasian) male.", "The patient was undergoing a total hip replacement.", "The patient was hemodynamically stable throughout the operation.", "Two hours following epidural analgesia, the patient manifested a sudden drop in blood pressure and heart rate.", "The patient's drop in blood pressure and heart rate required the administration of adrenaline.", "A Computed Tomography scan demonstrated pneumomediastinum.", "A Computed Tomography scan demonstrated pneumorrachis.", "A Computed Tomography scan demonstrated paravertebral soft tissue emphysema.", "We believe that injected air from the epidural space and surrounding tissues slowly moved towards the mediastinum.", "We believe that the movement of air stimulated the para-aortic ganglia.", "We believe that the stimulation caused parasympathetic stimulation.", "We believe that the parasympathetic stimulation caused hypotension and bradycardia."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was diagnosed with acquired aplastic anemia in December 2019.", "Cytogenetic studies showed 46XX karyotype.", "Chromosomal breakage study was normal.", "Paroxysmal nocturnal hemoglobinuria clone was absent.", "Clinical exome did not show any genetic mutation for inherited bone marrow failure syndrome.", "The patient had no matched sibling or matched unrelated donor.", "She received a haploidentical stem cell transplant in July 2020.", "The conditioning regimen included Rabbit ATG from Day-9 to Day-7.", "Fludarabine was given at 40 mg/m2 for 4 days (Day-6 to Day-3).", "Cyclophosphamide was given at 14.5 mg/kg for 2 days (Day-6 and Day-5).", "A single fraction TBI (400 cGy) was given on Day-1.", "On the day of transplantation, she received a peripheral blood stem cell graft from the father.", "The graft contained 10 million CD34+ cells/kg.", "The graft contained 2.41 \u00d7 108 CD3+ T cells/kg.", "Post-transplant Cyclophosphamide (50 mg/kg) was given on Day+3 and Day+4.", "Ciclosporin and Mycophenolate mofetil were started on Day+5 as GvHD prophylaxis.", "On Day+9, she developed high-grade fever with the onset of engraftment.", "Bone marrow showed haemophagocytosis.", "A diagnosis of Candida tropicalis-driven macrophage activation syndrome was established on Day+13.", "She was treated with caspofungin and posaconazole.", "She received intravenous immunoglobulin (1 g/kg for 5 days).", "She received intravenous Methylprednisolone (2 mg/kg).", "One dose of intravenous Alemtuzumab (0.1 mg/kg) was administered.", "The patient developed hypertension from Day+13.", "On Day+14, she had loose motions with abdominal pain.", "An ultrasound scan was suggestive of pan-colitis.", "Oral Budesonide was started for possible gut GvHD.", "The patient had neutrophil engraftment on Day+16.", "TA-TMA was suspected based on anemia, thrombocytopenia, hypertension, gastrointestinal bleeding, decreased serum albumin, and raised lactate dehydrogenase.", "Blood smear showed 1 fragmented RBC per high power field on Day+20.", "Urine protein:creatinine ratio was 0.47 on Day+20.", "Soluble C5b-9 assay is not available nationally.", "ADAMTS-13 activity was normal.", "The diagnosis of TA-TMA was confirmed based on the Overall-TMA criteria.", "Ciclosporin was discontinued.", "Inj Defibrotide was given from Day+21.", "There was no evidence of pathogenic variation in TMA-associated genes on clinical exome.", "Eculizumab was considered but not used due to cost.", "Narsoplimab was accessed through an expanded access program.", "Narsoplimab was commenced at a dose of 4 mg/kg twice a week on Day+30.", "Severe colitis with inflammatory thickening measuring 5.5 mm extending up to the caecum and base of the appendix was seen on ultrasound.", "She was started on a TNF-\u03b1 inhibitor (Etanercept).", "She developed pneumatosis coli after two doses of Etanercept.", "Etanercept was stopped.", "She continued to have significant intestinal bleeding.", "Narsoplimab was increased to thrice a week on Day+45.", "Her lactate dehydrogenase improved dramatically after starting Narsoplimab.", "Her haptoglobin normalized on Day+48.", "Her hypertension improved and antihypertensive requirement was reduced to a single medication from Day+59.", "Intestinal bleeding reduced from Day+50 and completely stopped on Day+82.", "Inj Methylprednisolone was tapered and stopped on Day+92.", "There were no schistocytes in the peripheral blood smear after Day+70.", "The patient received the last packed cell transfusion on Day+70.", "The patient received the last platelet transfusion on Day+77.", "Narsoplimab was reduced to twice a week on Day+109.", "Narsoplimab was reduced to once a week on Day+133.", "Narsoplimab was stopped on Day+195.", "The patient had CMV reactivation on Day+59 with CMV copy numbers of 16,500/ml.", "She received Inj Foscarnet for 2 weeks.", "CMV viremia resolved on Day+73.", "She had a herpes zoster skin infection on Day+111.", "The infection resolved with Acyclovir.", "The patient developed liver GvHD from Day+217.", "Tacrolimus was started from Day+217.", "Ruxolitinib was added from Day+237.", "She had severe reticulocytopenia secondary to parvovirus infection on Day+246.", "Parvovirus infection was managed with immunoglobulin infusion.", "She developed a second episode of TA-TMA.", "The second episode was manifested by circulating schistocytes, anemia, thrombocytopenia, low albumin, and an increase in lactate dehydrogenase and creatinine.", "Urine protein:creatinine ratio increased to 0.89.", "Tacrolimus was stopped.", "Steroids were started.", "Ruxolitinib was continued.", "Narsoplimab was started from Day+254.", "Narsoplimab was given twice a week for 3 weeks.", "Narsoplimab was escalated to thrice a week from Day+274.", "Narsoplimab was tapered to twice weekly from Day+290.", "Narsoplimab was stopped on Day+357.", "Liver GvHD resolved with steroids and Ruxolitinib.", "The patient is alive and well.", "The patient had no features of TA-TMA on the last follow-up of Day+650."], "summary_subclaims": ["The six-year-old girl underwent a human leucocyte antigen (HLA) haploidentical hematopoietic stem cell transplant using post-transplant Cyclophosphamide for severe aplastic anemia.", "In the second week of the transplant, the patient developed macrophage activation syndrome.", "The diagnosis of hepatosplenic candidiasis was made based on USG abdomen and blood fungal PCR.", "Candida-triggered macrophage activation syndrome responded to antifungals, steroids, intravenous immunoglobulin, and alemtuzumab.", "The patient developed hypertension in the 2nd week.", "The patient had high lactate dehydrogenase (1010\u2009U/L), schistocytes (5 per hpf), low haptoglobin (<\u20095\u2009mg/dl), thrombocytopenia, and anemia in the 3rd week.", "Ciclosporin was stopped.", "The patient was treated with 10\u2009days of defibrotide without response.", "The course was further complicated by the involvement of the gastrointestinal tract and kidneys.", "Narsoplimab was started in the 5th week of the transplant.", "A fall in lactate dehydrogenase was observed after starting Narsoplimab.", "The resolution of gastrointestinal symptoms, proteinuria, and recovery of cytopenia followed starting Narsoplimab.", "The second episode of TA-TMA occurred with parvoviraemia.", "The second episode of TA-TMA was successfully treated with Narsoplimab."]}, "extra_info": {"fulltext_subclaims": ["The patient was diagnosed with acquired aplastic anemia in December 2019.", "Cytogenetic studies showed 46XX karyotype.", "Chromosomal breakage study was normal.", "Paroxysmal nocturnal hemoglobinuria clone was absent.", "Clinical exome did not show any genetic mutation for inherited bone marrow failure syndrome.", "The patient had no matched sibling or matched unrelated donor.", "She received a haploidentical stem cell transplant in July 2020.", "The conditioning regimen included Rabbit ATG from Day-9 to Day-7.", "Fludarabine was given at 40 mg/m2 for 4 days (Day-6 to Day-3).", "Cyclophosphamide was given at 14.5 mg/kg for 2 days (Day-6 and Day-5).", "A single fraction TBI (400 cGy) was given on Day-1.", "On the day of transplantation, she received a peripheral blood stem cell graft from the father.", "The graft contained 10 million CD34+ cells/kg.", "The graft contained 2.41 \u00d7 108 CD3+ T cells/kg.", "Post-transplant Cyclophosphamide (50 mg/kg) was given on Day+3 and Day+4.", "Ciclosporin and Mycophenolate mofetil were started on Day+5 as GvHD prophylaxis.", "On Day+9, she developed high-grade fever with the onset of engraftment.", "Bone marrow showed haemophagocytosis.", "A diagnosis of Candida tropicalis-driven macrophage activation syndrome was established on Day+13.", "She was treated with caspofungin and posaconazole.", "She received intravenous immunoglobulin (1 g/kg for 5 days).", "She received intravenous Methylprednisolone (2 mg/kg).", "One dose of intravenous Alemtuzumab (0.1 mg/kg) was administered.", "The patient developed hypertension from Day+13.", "On Day+14, she had loose motions with abdominal pain.", "An ultrasound scan was suggestive of pan-colitis.", "Oral Budesonide was started for possible gut GvHD.", "The patient had neutrophil engraftment on Day+16.", "TA-TMA was suspected based on anemia, thrombocytopenia, hypertension, gastrointestinal bleeding, decreased serum albumin, and raised lactate dehydrogenase.", "Blood smear showed 1 fragmented RBC per high power field on Day+20.", "Urine protein:creatinine ratio was 0.47 on Day+20.", "Soluble C5b-9 assay is not available nationally.", "ADAMTS-13 activity was normal.", "The diagnosis of TA-TMA was confirmed based on the Overall-TMA criteria.", "Ciclosporin was discontinued.", "Inj Defibrotide was given from Day+21.", "There was no evidence of pathogenic variation in TMA-associated genes on clinical exome.", "Eculizumab was considered but not used due to cost.", "Narsoplimab was accessed through an expanded access program.", "Narsoplimab was commenced at a dose of 4 mg/kg twice a week on Day+30.", "Severe colitis with inflammatory thickening measuring 5.5 mm extending up to the caecum and base of the appendix was seen on ultrasound.", "She was started on a TNF-\u03b1 inhibitor (Etanercept).", "She developed pneumatosis coli after two doses of Etanercept.", "Etanercept was stopped.", "She continued to have significant intestinal bleeding.", "Narsoplimab was increased to thrice a week on Day+45.", "Her lactate dehydrogenase improved dramatically after starting Narsoplimab.", "Her haptoglobin normalized on Day+48.", "Her hypertension improved and antihypertensive requirement was reduced to a single medication from Day+59.", "Intestinal bleeding reduced from Day+50 and completely stopped on Day+82.", "Inj Methylprednisolone was tapered and stopped on Day+92.", "There were no schistocytes in the peripheral blood smear after Day+70.", "The patient received the last packed cell transfusion on Day+70.", "The patient received the last platelet transfusion on Day+77.", "Narsoplimab was reduced to twice a week on Day+109.", "Narsoplimab was reduced to once a week on Day+133.", "Narsoplimab was stopped on Day+195.", "The patient had CMV reactivation on Day+59 with CMV copy numbers of 16,500/ml.", "She received Inj Foscarnet for 2 weeks.", "CMV viremia resolved on Day+73.", "She had a herpes zoster skin infection on Day+111.", "The infection resolved with Acyclovir.", "The patient developed liver GvHD from Day+217.", "Tacrolimus was started from Day+217.", "Ruxolitinib was added from Day+237.", "She had severe reticulocytopenia secondary to parvovirus infection on Day+246.", "Parvovirus infection was managed with immunoglobulin infusion.", "She developed a second episode of TA-TMA.", "The second episode was manifested by circulating schistocytes, anemia, thrombocytopenia, low albumin, and an increase in lactate dehydrogenase and creatinine.", "Urine protein:creatinine ratio increased to 0.89.", "Tacrolimus was stopped.", "Steroids were started.", "Ruxolitinib was continued.", "Narsoplimab was started from Day+254.", "Narsoplimab was given twice a week for 3 weeks.", "Narsoplimab was escalated to thrice a week from Day+274.", "Narsoplimab was tapered to twice weekly from Day+290.", "Narsoplimab was stopped on Day+357.", "Liver GvHD resolved with steroids and Ruxolitinib.", "The patient is alive and well.", "The patient had no features of TA-TMA on the last follow-up of Day+650."], "index": 98, "original_id": "multiclinsum_test_2016_en.txt", "split": "test", "summary_subclaims": ["The six-year-old girl underwent a human leucocyte antigen (HLA) haploidentical hematopoietic stem cell transplant using post-transplant Cyclophosphamide for severe aplastic anemia.", "In the second week of the transplant, the patient developed macrophage activation syndrome.", "The diagnosis of hepatosplenic candidiasis was made based on USG abdomen and blood fungal PCR.", "Candida-triggered macrophage activation syndrome responded to antifungals, steroids, intravenous immunoglobulin, and alemtuzumab.", "The patient developed hypertension in the 2nd week.", "The patient had high lactate dehydrogenase (1010\u2009U/L), schistocytes (5 per hpf), low haptoglobin (<\u20095\u2009mg/dl), thrombocytopenia, and anemia in the 3rd week.", "Ciclosporin was stopped.", "The patient was treated with 10\u2009days of defibrotide without response.", "The course was further complicated by the involvement of the gastrointestinal tract and kidneys.", "Narsoplimab was started in the 5th week of the transplant.", "A fall in lactate dehydrogenase was observed after starting Narsoplimab.", "The resolution of gastrointestinal symptoms, proteinuria, and recovery of cytopenia followed starting Narsoplimab.", "The second episode of TA-TMA occurred with parvoviraemia.", "The second episode of TA-TMA was successfully treated with Narsoplimab."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["A 6-year-old girl presented to the pediatric emergency department with the chief complaints of vomiting blood and blood in stool.", "Her mother reported that she noticed the blood in her daughter\u2019s stool three days ago.", "The baby was delivered at 34 weeks gestation with cesarean section.", "The baby had intrauterine growth restriction (IUGR).", "The baby was hospitalized in a neonatal intensive care unit for 1 month.", "The baby was treated with laser photocoagulation due to the vision loss in the left eye.", "The cranial magnetic resonance imaging (MRI) was performed at the age of 6 months.", "The cranial MRI revealed diffuse symmetric calcifications.", "The cranial MRI showed changes suggesting hemorrhage.", "The cranial MRI showed dilated lateral ventricles.", "The cranial MRI showed septated cystic lesions in the area extending from the roof of the third ventricle to the lateral ventricle.", "The cranial MRI showed hemorrhage in the globe in the left orbit.", "The patient was diagnosed with Coats plus syndrome.", "The patient\u2019s weight and height were below the 3rd percentile.", "The patient\u2019s mid-upper arm circumference was <115 mm.", "The patient was ill-appearing.", "The patient\u2019s peak heart rate was 120/min.", "The patient\u2019s blood pressure was 70/40 mmHg.", "Leukocoria and glaucoma were detected in the left eye.", "The patient had hypotonia.", "The patient\u2019s muscle strength in bilateral lower and upper extremities was 3/5.", "The percussion over Traube\u2019s space produced dull sounds during the abdominal examination.", "The patient\u2019s hemoglobin (Hb) was 6.5 gr/dL.", "The patient\u2019s hematocrit (Hct) was 21%.", "The patient\u2019s thrombocyte count was 292000/mm3.", "The patient\u2019s white blood cell (WBC) count was 2010/mm3.", "The patient\u2019s international normalized ratio (INR) was 1.3.", "The patient\u2019s alanine aminotransferase (ALT) was 113 U/L.", "The patient\u2019s aspartate aminotransferase (AST) was 115 U/L.", "The patient\u2019s gamma-glutamyl transferase (GGT) was 245 U/L.", "The patient\u2019s albumin was 3.21 gr/dL.", "The metabolic studies did not show any abnormalities.", "The levels of viral markers, alpha 1 antitrypsin, alpha fetoprotein, ceruloplasmin, autoantibody, and tissue transglutaminase were normal.", "Abdominal ultrasonography showed linear echogenicity and heterogeneity in the liver.", "Abdominal doppler ultrasonography suggested portal hypertension.", "Upper and lower gastrointestinal endoscopy revealed folded vascular appearance reminiscent of esophageal varices.", "Upper and lower gastrointestinal endoscopy revealed vascular telangiectasia in the pyloric antrum, duodenum, and colon.", "A liver biopsy revealed portal fibrosis.", "The patient was initially received nothing-by-mouth diet.", "The patient was given intravenous (IV) proton pump inhibitors.", "The severe gastrointestinal bleeding of the patient was later stopped after receiving IV octreotide and erythrocyte transfusion.", "The patient was treated with propranolol, ursodeoxycholic acid, and anticonvulsant.", "The patient was followed in the pediatric gastroenterology, neurology, and eye clinics.", "The patient continued to have intermittent gastrointestinal system bleeding.", "The patient had severe malnutrition.", "The patient was admitted to the emergency department and hospitalized multiple times.", "The patient was treated with tranexamic acid when she had mild bleeding.", "The patient received IV octreotide when the bleeding was severe.", "The patient was admitted to the intensive care unit due to multi-organ failure secondary to severe gastrointestinal system bleeding.", "An emergency endoscopy could not be performed.", "The patient received IV octreotide and erythrocyte transfusion again.", "The patient\u2019s condition did not improve.", "The patient eventually died."], "summary_subclaims": ["The patient is a 6-year-old girl.", "The patient has Coats plus syndrome.", "The patient presented with vomiting blood.", "The patient presented with blood in stool.", "Upper and lower gastrointestinal endoscopy revealed esophageal varices.", "Upper and lower gastrointestinal endoscopy revealed vascular telangiectasia in the pyloric antrum.", "Upper and lower gastrointestinal endoscopy revealed vascular telangiectasia in the duodenum.", "Upper and lower gastrointestinal endoscopy revealed vascular telangiectasia in the colon.", "The patient received intravenous octreotide.", "The bleeding was stopped after receiving intravenous octreotide.", "The patient was followed in the pediatric gastroenterology clinic.", "The patient was followed in the pediatric neurology clinic.", "The patient was followed in the pediatric ophthalmology clinic.", "The patient was hospitalized and admitted to the intensive care unit.", "The patient continued to have intermittent gastrointestinal system bleeding.", "The patient eventually died due to severe gastrointestinal system bleeding."]}, "extra_info": {"fulltext_subclaims": ["A 6-year-old girl presented to the pediatric emergency department with the chief complaints of vomiting blood and blood in stool.", "Her mother reported that she noticed the blood in her daughter\u2019s stool three days ago.", "The baby was delivered at 34 weeks gestation with cesarean section.", "The baby had intrauterine growth restriction (IUGR).", "The baby was hospitalized in a neonatal intensive care unit for 1 month.", "The baby was treated with laser photocoagulation due to the vision loss in the left eye.", "The cranial magnetic resonance imaging (MRI) was performed at the age of 6 months.", "The cranial MRI revealed diffuse symmetric calcifications.", "The cranial MRI showed changes suggesting hemorrhage.", "The cranial MRI showed dilated lateral ventricles.", "The cranial MRI showed septated cystic lesions in the area extending from the roof of the third ventricle to the lateral ventricle.", "The cranial MRI showed hemorrhage in the globe in the left orbit.", "The patient was diagnosed with Coats plus syndrome.", "The patient\u2019s weight and height were below the 3rd percentile.", "The patient\u2019s mid-upper arm circumference was <115 mm.", "The patient was ill-appearing.", "The patient\u2019s peak heart rate was 120/min.", "The patient\u2019s blood pressure was 70/40 mmHg.", "Leukocoria and glaucoma were detected in the left eye.", "The patient had hypotonia.", "The patient\u2019s muscle strength in bilateral lower and upper extremities was 3/5.", "The percussion over Traube\u2019s space produced dull sounds during the abdominal examination.", "The patient\u2019s hemoglobin (Hb) was 6.5 gr/dL.", "The patient\u2019s hematocrit (Hct) was 21%.", "The patient\u2019s thrombocyte count was 292000/mm3.", "The patient\u2019s white blood cell (WBC) count was 2010/mm3.", "The patient\u2019s international normalized ratio (INR) was 1.3.", "The patient\u2019s alanine aminotransferase (ALT) was 113 U/L.", "The patient\u2019s aspartate aminotransferase (AST) was 115 U/L.", "The patient\u2019s gamma-glutamyl transferase (GGT) was 245 U/L.", "The patient\u2019s albumin was 3.21 gr/dL.", "The metabolic studies did not show any abnormalities.", "The levels of viral markers, alpha 1 antitrypsin, alpha fetoprotein, ceruloplasmin, autoantibody, and tissue transglutaminase were normal.", "Abdominal ultrasonography showed linear echogenicity and heterogeneity in the liver.", "Abdominal doppler ultrasonography suggested portal hypertension.", "Upper and lower gastrointestinal endoscopy revealed folded vascular appearance reminiscent of esophageal varices.", "Upper and lower gastrointestinal endoscopy revealed vascular telangiectasia in the pyloric antrum, duodenum, and colon.", "A liver biopsy revealed portal fibrosis.", "The patient was initially received nothing-by-mouth diet.", "The patient was given intravenous (IV) proton pump inhibitors.", "The severe gastrointestinal bleeding of the patient was later stopped after receiving IV octreotide and erythrocyte transfusion.", "The patient was treated with propranolol, ursodeoxycholic acid, and anticonvulsant.", "The patient was followed in the pediatric gastroenterology, neurology, and eye clinics.", "The patient continued to have intermittent gastrointestinal system bleeding.", "The patient had severe malnutrition.", "The patient was admitted to the emergency department and hospitalized multiple times.", "The patient was treated with tranexamic acid when she had mild bleeding.", "The patient received IV octreotide when the bleeding was severe.", "The patient was admitted to the intensive care unit due to multi-organ failure secondary to severe gastrointestinal system bleeding.", "An emergency endoscopy could not be performed.", "The patient received IV octreotide and erythrocyte transfusion again.", "The patient\u2019s condition did not improve.", "The patient eventually died."], "index": 90, "original_id": "multiclinsum_test_1957_en.txt", "split": "test", "summary_subclaims": ["The patient is a 6-year-old girl.", "The patient has Coats plus syndrome.", "The patient presented with vomiting blood.", "The patient presented with blood in stool.", "Upper and lower gastrointestinal endoscopy revealed esophageal varices.", "Upper and lower gastrointestinal endoscopy revealed vascular telangiectasia in the pyloric antrum.", "Upper and lower gastrointestinal endoscopy revealed vascular telangiectasia in the duodenum.", "Upper and lower gastrointestinal endoscopy revealed vascular telangiectasia in the colon.", "The patient received intravenous octreotide.", "The bleeding was stopped after receiving intravenous octreotide.", "The patient was followed in the pediatric gastroenterology clinic.", "The patient was followed in the pediatric neurology clinic.", "The patient was followed in the pediatric ophthalmology clinic.", "The patient was hospitalized and admitted to the intensive care unit.", "The patient continued to have intermittent gastrointestinal system bleeding.", "The patient eventually died due to severe gastrointestinal system bleeding."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["A 9 days-old male neonate weighing 3.60 kg was referred to the National Cardiac Center Harapan Kita Hospital.", "The neonate was ventilated because of severe metabolic and respiratory acidosis.", "The neonate had circulatory dynamics instability.", "The neonate had a history of respiratory distress.", "The neonate had cyanosis.", "The neonate had hyperbilirubinemia.", "The neonate had a severe infection.", "The perinatal history was unremarkable.", "The neonate was born at 40 weeks of gestation by normal labour.", "The neonate's birth weight was 3.85 kg.", "The neonate's oxygen saturation at birth was 90%.", "The neonate's APGAR score was 9/9.", "On the 6th day postpartum, the neonate presented with feeding difficulty.", "On the 6th day postpartum, the neonate had severe cyanosis.", "On the 6th day postpartum, the neonate had congestive heart failure.", "The neonate was ventilated at the emergency room with oxygen saturation 82%.", "The neonate was transferred to the center for possible surgical repair.", "The neonate's oxygen saturation was 75%.", "Differential oxygen saturation was noted between the upper and lower limbs.", "No apparent cardiac murmur was detected.", "The chest X-ray showed mild cardiomegaly.", "The chest X-ray showed congestion of the lungs.", "The chest X-ray showed pulmonary edema.", "The electrocardiogram showed normal rhythm.", "The electrocardiogram showed right axis deviation.", "The electrocardiogram showed mild right ventricular hypertrophy.", "The neonate was admitted to the pediatric cardiac intensive care unit.", "The neonate's oxygen saturation was between 40% and 70%.", "Two-dimensional echocardiography revealed an interrupted aortic arch type A.", "Two-dimensional echocardiography revealed an aortopulmonary window type II.", "Two-dimensional echocardiography revealed a restricted patent ductus arteriosus.", "Two-dimensional echocardiography revealed pulmonary hypertension.", "Two-dimensional echocardiography did not reveal a ventricular septal defect.", "A PGE1 infusion 10 nano was started.", "Diuretics were administered.", "The baby had severe infection.", "The baby had disseminated intravascular coagulation.", "The baby had leucocyte count 28.387.", "The baby had pro-calcitonine 11.", "The baby had D-dimer 4.800.", "The baby had several epileptic episodes.", "Brain sonography showed arachnoiditis.", "Brain sonography showed brain edema.", "Brain sonography showed no intracranial bleeding.", "Operation was deferred because of the risk of infection.", "Operation was deferred because of sepsis.", "Operation was deferred because of the good general condition.", "Operation was performed on the 20th day of life.", "A one-stage surgical correction was performed through a median sternotomy.", "The surgery was performed under profound hypothermia (26 \u00b0C).", "Before the administration of heparin, the entire ascending aorta and the arch vessels were mobilized.", "Before the administration of heparin, the pulmonary trunk and both branch were mobilized.", "The external anatomy confirmed an interrupted aortic arch type A.", "The external anatomy confirmed a large aortopulmonary window type II.", "The right pulmonary artery was recognized to originate from the posterolateral part of the ascending aorta.", "The right pulmonary artery was recognized to have connection with the common pulmonary artery.", "The ascending aorta gave three branches including the brachiocephalic artery.", "The ascending aorta gave three branches including the left common carotid artery.", "The ascending aorta gave three branches including the left subclavian artery.", "There was no evidence of descending aorta.", "The proximal part of the patent ductus arteriosus arose from the pulmonary artery trunk.", "The distal part of the patent ductus arteriosus became the descending aorta.", "The left pulmonary artery arose from the pulmonary artery trunk.", "Cardiopulmonary bypass was established by right hemicerebral perfusion.", "Cardiopulmonary bypass was established by bicaval drainage.", "Right hemicerebral perfusion was obtained via an expanded 4-0 mm polytetrafluoroethylene graft.", "The graft was sewn to the right brachiocephalic artery.", "The aortic cross clamp was applied.", "Cardioplegia was infused.", "The aortic arch vessels were clamped at the origin of the brachiocephalic artery.", "The aortic arch vessels were clamped at the origin of the left common carotid artery.", "The aortic arch vessels were clamped at the origin of the left subclavian artery.", "Snaring of both pulmonary arteries precluded overflooding the lungs.", "The pump flow was lowered to 10%.", "Ductal tissue was ligated near its pulmonary origin.", "Ductal tissue was resected until normal aortic tissue appeared.", "The ascending aorta was longitudinally incised.", "An extended end-to-side anastomosis of the descending aorta to the distal ascending aorta was performed.", "The anastomosis was performed with a continuous 7-0 polypropylene suture.", "After removal of the aortic cross-clamp, full flow bypass was resumed.", "The anastomosis was checked for bleeding.", "The anastomosis was checked for undue tension.", "The aortic cross-clamp was reapplied proximal to the aortic cannula.", "Cardioplegia was infused again.", "The aortopulmonary window repair was started.", "The ascending aorta was transversely incised distal to the aortopulmonary window.", "The aortopulmonary window was confirmed to be very large, 10 mm diameter.", "The right pulmonary artery originated from the ascending aorta.", "The left pulmonary artery arose from the pulmonary artery trunk in the normal fashion.", "The coronary arteries were normally positioned.", "The aortic cross clamp was removed and reapplied for right hemicerebral perfusion again.", "A 4-0 Gore-tex patch was used to close the aortopulmonary window.", "A 4-0 Gore-tex patch was used to separate the right pulmonary artery from the aortic origin.", "After rewarming, cardiopulmonary bypass was easily weaned.", "Total bypass time was 125 minutes.", "Cross clamp time was 71 minutes.", "One-third flow time was 66 minutes.", "Peritoneal dialysis was performed post operatively for 3 days.", "Peritoneal dialysis was switched with lasix intermittently.", "The postoperative recovery was uneventful.", "The neonate was extubated on the 7th day post operatively.", "No clinical signs of neurologic disturbances were observed.", "Cardiopulmonary function was satisfactory.", "Distal perfusion was satisfactory.", "Early postoperative echocardiography demonstrated an excellent early surgical result.", "Early postoperative echocardiography showed a minimal pressure gradient of 12 mmHg across the aortic reconstruction.", "Early postoperative echocardiography showed good left ventricular function.", "Early postoperative echocardiography showed no residual aortopulmonary window.", "In 2021, the patient was a 9 year old child.", "The patient was cheerful.", "The patient was growing actively.", "The patient had entered elementary school in grade 2.", "There were no abnormalities of the heart and lungs according to the patient's mother.", "The patient had cerebral palsy sequela.", "The cerebral palsy sequela was being treated by a pediatric neurologist."], "summary_subclaims": ["A 9 days-old male neonate weighing 3.85 kg was referred to our center.", "The neonate was ventilated with a history of respiratory distress and severe infection since birth.", "Admission was to the PCICU.", "A 2D echo showed an IAA type A associated with a huge APW type II and restrictive PDA.", "A PGE1 infusion was started.", "The baby experienced several epileptic episodes during the following days.", "Surgery was performed on the 20th day of life in 2011.", "A successful one-stage repair of the anomalies was performed.", "The repair included cutting of the PDA that arose from the PA trunk and distally became the descending aorta.", "An extended end-to-end anastomosis was used to conduct ascending aortic blood flow into the descending aorta.", "An intra-arterial baffle was used.", "A 4-0 Gore-Tex baffle was used to close the APW and separate the RPA from the aortic origin.", "The result was good, as the child recently grew up as a cheerful 9 year old.", "The child is growing actively and has entered elementary school in grade 2."]}, "extra_info": {"fulltext_subclaims": ["A 9 days-old male neonate weighing 3.60 kg was referred to the National Cardiac Center Harapan Kita Hospital.", "The neonate was ventilated because of severe metabolic and respiratory acidosis.", "The neonate had circulatory dynamics instability.", "The neonate had a history of respiratory distress.", "The neonate had cyanosis.", "The neonate had hyperbilirubinemia.", "The neonate had a severe infection.", "The perinatal history was unremarkable.", "The neonate was born at 40 weeks of gestation by normal labour.", "The neonate's birth weight was 3.85 kg.", "The neonate's oxygen saturation at birth was 90%.", "The neonate's APGAR score was 9/9.", "On the 6th day postpartum, the neonate presented with feeding difficulty.", "On the 6th day postpartum, the neonate had severe cyanosis.", "On the 6th day postpartum, the neonate had congestive heart failure.", "The neonate was ventilated at the emergency room with oxygen saturation 82%.", "The neonate was transferred to the center for possible surgical repair.", "The neonate's oxygen saturation was 75%.", "Differential oxygen saturation was noted between the upper and lower limbs.", "No apparent cardiac murmur was detected.", "The chest X-ray showed mild cardiomegaly.", "The chest X-ray showed congestion of the lungs.", "The chest X-ray showed pulmonary edema.", "The electrocardiogram showed normal rhythm.", "The electrocardiogram showed right axis deviation.", "The electrocardiogram showed mild right ventricular hypertrophy.", "The neonate was admitted to the pediatric cardiac intensive care unit.", "The neonate's oxygen saturation was between 40% and 70%.", "Two-dimensional echocardiography revealed an interrupted aortic arch type A.", "Two-dimensional echocardiography revealed an aortopulmonary window type II.", "Two-dimensional echocardiography revealed a restricted patent ductus arteriosus.", "Two-dimensional echocardiography revealed pulmonary hypertension.", "Two-dimensional echocardiography did not reveal a ventricular septal defect.", "A PGE1 infusion 10 nano was started.", "Diuretics were administered.", "The baby had severe infection.", "The baby had disseminated intravascular coagulation.", "The baby had leucocyte count 28.387.", "The baby had pro-calcitonine 11.", "The baby had D-dimer 4.800.", "The baby had several epileptic episodes.", "Brain sonography showed arachnoiditis.", "Brain sonography showed brain edema.", "Brain sonography showed no intracranial bleeding.", "Operation was deferred because of the risk of infection.", "Operation was deferred because of sepsis.", "Operation was deferred because of the good general condition.", "Operation was performed on the 20th day of life.", "A one-stage surgical correction was performed through a median sternotomy.", "The surgery was performed under profound hypothermia (26 \u00b0C).", "Before the administration of heparin, the entire ascending aorta and the arch vessels were mobilized.", "Before the administration of heparin, the pulmonary trunk and both branch were mobilized.", "The external anatomy confirmed an interrupted aortic arch type A.", "The external anatomy confirmed a large aortopulmonary window type II.", "The right pulmonary artery was recognized to originate from the posterolateral part of the ascending aorta.", "The right pulmonary artery was recognized to have connection with the common pulmonary artery.", "The ascending aorta gave three branches including the brachiocephalic artery.", "The ascending aorta gave three branches including the left common carotid artery.", "The ascending aorta gave three branches including the left subclavian artery.", "There was no evidence of descending aorta.", "The proximal part of the patent ductus arteriosus arose from the pulmonary artery trunk.", "The distal part of the patent ductus arteriosus became the descending aorta.", "The left pulmonary artery arose from the pulmonary artery trunk.", "Cardiopulmonary bypass was established by right hemicerebral perfusion.", "Cardiopulmonary bypass was established by bicaval drainage.", "Right hemicerebral perfusion was obtained via an expanded 4-0 mm polytetrafluoroethylene graft.", "The graft was sewn to the right brachiocephalic artery.", "The aortic cross clamp was applied.", "Cardioplegia was infused.", "The aortic arch vessels were clamped at the origin of the brachiocephalic artery.", "The aortic arch vessels were clamped at the origin of the left common carotid artery.", "The aortic arch vessels were clamped at the origin of the left subclavian artery.", "Snaring of both pulmonary arteries precluded overflooding the lungs.", "The pump flow was lowered to 10%.", "Ductal tissue was ligated near its pulmonary origin.", "Ductal tissue was resected until normal aortic tissue appeared.", "The ascending aorta was longitudinally incised.", "An extended end-to-side anastomosis of the descending aorta to the distal ascending aorta was performed.", "The anastomosis was performed with a continuous 7-0 polypropylene suture.", "After removal of the aortic cross-clamp, full flow bypass was resumed.", "The anastomosis was checked for bleeding.", "The anastomosis was checked for undue tension.", "The aortic cross-clamp was reapplied proximal to the aortic cannula.", "Cardioplegia was infused again.", "The aortopulmonary window repair was started.", "The ascending aorta was transversely incised distal to the aortopulmonary window.", "The aortopulmonary window was confirmed to be very large, 10 mm diameter.", "The right pulmonary artery originated from the ascending aorta.", "The left pulmonary artery arose from the pulmonary artery trunk in the normal fashion.", "The coronary arteries were normally positioned.", "The aortic cross clamp was removed and reapplied for right hemicerebral perfusion again.", "A 4-0 Gore-tex patch was used to close the aortopulmonary window.", "A 4-0 Gore-tex patch was used to separate the right pulmonary artery from the aortic origin.", "After rewarming, cardiopulmonary bypass was easily weaned.", "Total bypass time was 125 minutes.", "Cross clamp time was 71 minutes.", "One-third flow time was 66 minutes.", "Peritoneal dialysis was performed post operatively for 3 days.", "Peritoneal dialysis was switched with lasix intermittently.", "The postoperative recovery was uneventful.", "The neonate was extubated on the 7th day post operatively.", "No clinical signs of neurologic disturbances were observed.", "Cardiopulmonary function was satisfactory.", "Distal perfusion was satisfactory.", "Early postoperative echocardiography demonstrated an excellent early surgical result.", "Early postoperative echocardiography showed a minimal pressure gradient of 12 mmHg across the aortic reconstruction.", "Early postoperative echocardiography showed good left ventricular function.", "Early postoperative echocardiography showed no residual aortopulmonary window.", "In 2021, the patient was a 9 year old child.", "The patient was cheerful.", "The patient was growing actively.", "The patient had entered elementary school in grade 2.", "There were no abnormalities of the heart and lungs according to the patient's mother.", "The patient had cerebral palsy sequela.", "The cerebral palsy sequela was being treated by a pediatric neurologist."], "index": 102, "original_id": "multiclinsum_test_2375_en.txt", "split": "test", "summary_subclaims": ["A 9 days-old male neonate weighing 3.85 kg was referred to our center.", "The neonate was ventilated with a history of respiratory distress and severe infection since birth.", "Admission was to the PCICU.", "A 2D echo showed an IAA type A associated with a huge APW type II and restrictive PDA.", "A PGE1 infusion was started.", "The baby experienced several epileptic episodes during the following days.", "Surgery was performed on the 20th day of life in 2011.", "A successful one-stage repair of the anomalies was performed.", "The repair included cutting of the PDA that arose from the PA trunk and distally became the descending aorta.", "An extended end-to-end anastomosis was used to conduct ascending aortic blood flow into the descending aorta.", "An intra-arterial baffle was used.", "A 4-0 Gore-Tex baffle was used to close the APW and separate the RPA from the aortic origin.", "The result was good, as the child recently grew up as a cheerful 9 year old.", "The child is growing actively and has entered elementary school in grade 2."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 52-year-old man from Bangladesh.", "The patient has diabetes.", "The patient has hypertension.", "The patient had exertional angina Canadian Cardiovascular Society III.", "A stress myocardial scintigraphy was performed.", "The stress myocardial scintigraphy revealed deep hypoperfusion in the antero-apical, septo-apical, and lateral walls.", "The stress test showed electric positivity.", "The resting left ventricle ejection fraction was 61%.", "The patient's blood pressure was 127/85 mmHg.", "The patient's heart rate was 92 b.p.m.", "The patient's oxygen saturation was normal.", "No murmurs were detected.", "There were no signs of heart failure.", "The electrocardiogram showed a sinus rhythm.", "The electrocardiogram showed no significant repolarization abnormalities.", "A diagnostic coronary angiogram was performed.", "Left injection revealed a stenosis on a third significant diagonal branch.", "The LAD appeared to stop at its mid-segment without wrapping around the apex.", "The LAD did not present a stump that could suggest a chronic occlusion.", "The right coronary sinus injection revealed a dominant RCA free of stenosis.", "A vessel opening into the ostium of the RCA was noted.", "A non-selective injection into this artery identified an ostial-proximal stenosis.", "Percutaneous coronary intervention of the third diagonal was performed.", "A coronary CT scan was performed.", "The CT scan identified an artery whose course is compatible with a mid and distal LAD.", "This artery connects in the right coronary ostium.", "This artery joins the interventricular groove.", "This artery wraps around the apex of the heart.", "Angioplasty was performed on the AAOCA.", "A 6F IM guiding catheter was used.", "The guiding catheter was accessed through the right radial artery.", "A workhorse wire was positioned in the right posterolateral artery.", "A polymerjacket wire with a hydrophilic coating was used to navigate within the AAOCA.", "A distal injection through a microcatheter revealed a severe stenosis in the mid LAD.", "The distal lesion was treated with a drug-eluting stent 2.25 \u00d7 15 mm.", "The mid lesion was treated with a drug-eluting balloon 2.0 \u00d7 15 mm.", "The ostial-proximal segment was treated with a drug-eluting stent 2.5 \u00d7 15 mm.", "The final angiographic result was satisfactory.", "A contralateral injection confirmed the discontinuity of the AAOCA with the native LAD.", "The post-procedural course was uneventful.", "The patient was discharged the following day."], "summary_subclaims": ["The patient is a 52-year-old from Bangladesh.", "The patient has dual-origin LAD arising from both left and right sinus.", "The LAD has a pre-pulmonary course.", "The patient presented with exertional angina.", "The patient had documented myocardial ischaemia.", "Computed tomography (CT) scan confirmed the anatomical course of the AAOCA.", "Percutaneous coronary intervention was successfully performed.", "Tailored techniques were used to treat significant atherosclerotic lesions."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 52-year-old man from Bangladesh.", "The patient has diabetes.", "The patient has hypertension.", "The patient had exertional angina Canadian Cardiovascular Society III.", "A stress myocardial scintigraphy was performed.", "The stress myocardial scintigraphy revealed deep hypoperfusion in the antero-apical, septo-apical, and lateral walls.", "The stress test showed electric positivity.", "The resting left ventricle ejection fraction was 61%.", "The patient's blood pressure was 127/85 mmHg.", "The patient's heart rate was 92 b.p.m.", "The patient's oxygen saturation was normal.", "No murmurs were detected.", "There were no signs of heart failure.", "The electrocardiogram showed a sinus rhythm.", "The electrocardiogram showed no significant repolarization abnormalities.", "A diagnostic coronary angiogram was performed.", "Left injection revealed a stenosis on a third significant diagonal branch.", "The LAD appeared to stop at its mid-segment without wrapping around the apex.", "The LAD did not present a stump that could suggest a chronic occlusion.", "The right coronary sinus injection revealed a dominant RCA free of stenosis.", "A vessel opening into the ostium of the RCA was noted.", "A non-selective injection into this artery identified an ostial-proximal stenosis.", "Percutaneous coronary intervention of the third diagonal was performed.", "A coronary CT scan was performed.", "The CT scan identified an artery whose course is compatible with a mid and distal LAD.", "This artery connects in the right coronary ostium.", "This artery joins the interventricular groove.", "This artery wraps around the apex of the heart.", "Angioplasty was performed on the AAOCA.", "A 6F IM guiding catheter was used.", "The guiding catheter was accessed through the right radial artery.", "A workhorse wire was positioned in the right posterolateral artery.", "A polymerjacket wire with a hydrophilic coating was used to navigate within the AAOCA.", "A distal injection through a microcatheter revealed a severe stenosis in the mid LAD.", "The distal lesion was treated with a drug-eluting stent 2.25 \u00d7 15 mm.", "The mid lesion was treated with a drug-eluting balloon 2.0 \u00d7 15 mm.", "The ostial-proximal segment was treated with a drug-eluting stent 2.5 \u00d7 15 mm.", "The final angiographic result was satisfactory.", "A contralateral injection confirmed the discontinuity of the AAOCA with the native LAD.", "The post-procedural course was uneventful.", "The patient was discharged the following day."], "index": 100, "original_id": "multiclinsum_test_3124_en.txt", "split": "test", "summary_subclaims": ["The patient is a 52-year-old from Bangladesh.", "The patient has dual-origin LAD arising from both left and right sinus.", "The LAD has a pre-pulmonary course.", "The patient presented with exertional angina.", "The patient had documented myocardial ischaemia.", "Computed tomography (CT) scan confirmed the anatomical course of the AAOCA.", "Percutaneous coronary intervention was successfully performed.", "Tailored techniques were used to treat significant atherosclerotic lesions."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 35-year-old woman.", "She has chronic rheumatic heart disease.", "She has severe mitral stenosis with pulmonary hypertension.", "She had percutaneous balloon mitral valvotomy 6 weeks prior.", "A left atrial thrombus was detected after the procedure.", "She started warfarin 5 mg, po, daily for 4 weeks.", "She escalated to warfarin 7.5 mg, po, daily.", "She had a severe headache and repeated episodes of vomiting for 1 day.", "She had a history of nasal bleeding.", "She stopped warfarin 3 days prior.", "She had fever, malaise, and generalized weakness for 1 week.", "Vital signs were within normal limits.", "She had no pallor of conjunctivae.", "She had wet buccal mucosa.", "She had an accentuated P2 on cardiovascular examination.", "She had a mid-diastolic and pan-systolic murmur at the mitral area.", "No cranial nerve palsy was found.", "No motor or sensory deficit was found.", "Meningeal irritation signs were negative.", "Diagnoses included chronic rheumatic heart disease.", "Diagnoses included pyogenic meningitis.", "Diagnoses included subarachnoid hemorrhage.", "White blood cell count was 25,000/\u00b5L.", "Neutrophil count was 85%.", "Lymphocyte count was 10%.", "Hemoglobin was 12 gm/dl.", "Platelets were 350,000/\u00b5L.", "Prothrombin time was 35 sec.", "Partial thromboplastin time was 53 sec.", "INR was 2.5.", "A lumbar puncture was deferred due to higher INR.", "ECG showed P-mitrale.", "ECG showed right bundle branch block.", "ECG showed ST depression and inverted T wave at V1-V3.", "Trans-thoracic echocardiography revealed moderate mitral stenosis.", "Trans-thoracic echocardiography revealed mild mitral regurgitation.", "Trans-thoracic echocardiography revealed severe pulmonary hypertension.", "No vegetation or thrombus was seen.", "She was started on Ceftriaxone 2 gm, IV, twice daily.", "She was started on Vancomycin 1 gm, IV, twice daily.", "Warfarin was discontinued.", "She developed sudden onset, frequent tonic-clonic convulsive episodes.", "She had a Glasgow Coma Score of 8/15.", "Both eyes deviated to the left side.", "Pupils were mid-sized but poorly reactive to light.", "She withdrew to painful stimuli.", "A non-contrast brain CT scan revealed left-sided acute subdural hematoma.", "A non-contrast brain CT scan revealed ventricular bleeds.", "She was diagnosed with status epilepticus secondary to intracranial hemorrhage.", "She was initiated on diazepam, 10 mg IV.", "She was initiated on Phenytoin 1 gm IV bolus.", "She was given O2 via face mask.", "An NG-tube was inserted.", "A urinary catheter was placed.", "She was transferred to ICU.", "She was intubated.", "She was put on a mechanical ventilator.", "Fresh frozen plasma 4 units were given.", "Vitamin K, 10 mg IV once daily for 3 days, was given.", "IV ceftriaxone and vancomycin were continued.", "Mannitol (20%), 50 gm IV bolus, was given.", "Valproic acid, 400 mg po 3 times daily, was added.", "A craniotomy was performed.", "Repeat laboratory values showed WBC=34,000/\u00b5L.", "Repeat laboratory values showed hemoglobin=9 gm/dl.", "Repeat laboratory values showed platelets=550,000/\u00b5L.", "Repeat coagulation profiles showed PT=49.8 sec.", "Repeat coagulation profiles showed PTT=63.2 sec.", "Repeat coagulation profiles showed INR=4.38.", "She had paroxysms of increase in pulse rate.", "She had paroxysms of increase in blood pressure.", "She had paroxysms of increase in respiratory rate.", "She had paroxysms of increase in temperature.", "She had sweating.", "She had decerebrate posturing.", "She had episodes of autonomic surge.", "She had a CSF score of 11.", "She had a DLT score of 11.", "She had a PSH-AM score of 21.", "A probable diagnosis of PSH was made.", "She was started on morphine 2 mg, IV, as required.", "She was started on paracetamol 1 gm, po, as required.", "She was started on propranolol, 40 mg po 3 times a day.", "She was started on diazepam 5 mg, IV 3 times a day.", "She was started on gabapentin 150\u2013300 mg po 3 times a day.", "Her GCS started to improve on the second week of ICU admission.", "The frequency and severity of sympathetic storm declined.", "IV antibiotics were discontinued after 2 weeks of therapy.", "On the third week of admission, she developed asystole.", "She died of cardiac arrest.", "CPR was performed."], "summary_subclaims": ["The patient is a 35-year-old woman.", "She has echo-proven chronic rheumatic heart disease.", "She had percutaneous balloon mitral valvotomy 6 weeks previously.", "Left atrial thrombus was detected after the procedure.", "Anticoagulant (warfarin) was initiated.", "She presented with severe headache and repeated vomiting of 1 day duration.", "She had frequent seizure attacks with subsequent loss of consciousness on the third day of admission.", "CT-scan revealed acute subdural hematoma and ventricular bleeding.", "Diagnosis of status epilepticus secondary to intracranial hemorrhage due to warfarin toxicity was made.", "She was transferred to medical intensive care unit (ICU), intubated, and put on mechanical ventilator.", "Anti-epileptic drugs, antibiotics, vitamin K, and fresh frozen plasma were given.", "She developed paroxysms of hypertension, tachycardia, tachypnea, hyperpyrexia, diaphoresis, and decerebrate posturing after 7 days of neurological insult.", "She had normal inter-ictal EEG tracing during cyclic autonomic surge.", "CFS score was 11.", "DLT score was 10.", "PSH-AM score was 21.", "PSH-AM score suggested 'probable' diagnosis of PSH.", "Morphine, diazepam, propranolol, and gabapentin were given in combination to treat PSH.", "Severity of autonomic storm started to improve on the second week of ICU admission.", "On the third week of admission, her clinical condition deteriorated suddenly.", "She developed asystole and died of cardiac arrest despite cardiopulmonary resuscitation (CPR)."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 35-year-old woman.", "She has chronic rheumatic heart disease.", "She has severe mitral stenosis with pulmonary hypertension.", "She had percutaneous balloon mitral valvotomy 6 weeks prior.", "A left atrial thrombus was detected after the procedure.", "She started warfarin 5 mg, po, daily for 4 weeks.", "She escalated to warfarin 7.5 mg, po, daily.", "She had a severe headache and repeated episodes of vomiting for 1 day.", "She had a history of nasal bleeding.", "She stopped warfarin 3 days prior.", "She had fever, malaise, and generalized weakness for 1 week.", "Vital signs were within normal limits.", "She had no pallor of conjunctivae.", "She had wet buccal mucosa.", "She had an accentuated P2 on cardiovascular examination.", "She had a mid-diastolic and pan-systolic murmur at the mitral area.", "No cranial nerve palsy was found.", "No motor or sensory deficit was found.", "Meningeal irritation signs were negative.", "Diagnoses included chronic rheumatic heart disease.", "Diagnoses included pyogenic meningitis.", "Diagnoses included subarachnoid hemorrhage.", "White blood cell count was 25,000/\u00b5L.", "Neutrophil count was 85%.", "Lymphocyte count was 10%.", "Hemoglobin was 12 gm/dl.", "Platelets were 350,000/\u00b5L.", "Prothrombin time was 35 sec.", "Partial thromboplastin time was 53 sec.", "INR was 2.5.", "A lumbar puncture was deferred due to higher INR.", "ECG showed P-mitrale.", "ECG showed right bundle branch block.", "ECG showed ST depression and inverted T wave at V1-V3.", "Trans-thoracic echocardiography revealed moderate mitral stenosis.", "Trans-thoracic echocardiography revealed mild mitral regurgitation.", "Trans-thoracic echocardiography revealed severe pulmonary hypertension.", "No vegetation or thrombus was seen.", "She was started on Ceftriaxone 2 gm, IV, twice daily.", "She was started on Vancomycin 1 gm, IV, twice daily.", "Warfarin was discontinued.", "She developed sudden onset, frequent tonic-clonic convulsive episodes.", "She had a Glasgow Coma Score of 8/15.", "Both eyes deviated to the left side.", "Pupils were mid-sized but poorly reactive to light.", "She withdrew to painful stimuli.", "A non-contrast brain CT scan revealed left-sided acute subdural hematoma.", "A non-contrast brain CT scan revealed ventricular bleeds.", "She was diagnosed with status epilepticus secondary to intracranial hemorrhage.", "She was initiated on diazepam, 10 mg IV.", "She was initiated on Phenytoin 1 gm IV bolus.", "She was given O2 via face mask.", "An NG-tube was inserted.", "A urinary catheter was placed.", "She was transferred to ICU.", "She was intubated.", "She was put on a mechanical ventilator.", "Fresh frozen plasma 4 units were given.", "Vitamin K, 10 mg IV once daily for 3 days, was given.", "IV ceftriaxone and vancomycin were continued.", "Mannitol (20%), 50 gm IV bolus, was given.", "Valproic acid, 400 mg po 3 times daily, was added.", "A craniotomy was performed.", "Repeat laboratory values showed WBC=34,000/\u00b5L.", "Repeat laboratory values showed hemoglobin=9 gm/dl.", "Repeat laboratory values showed platelets=550,000/\u00b5L.", "Repeat coagulation profiles showed PT=49.8 sec.", "Repeat coagulation profiles showed PTT=63.2 sec.", "Repeat coagulation profiles showed INR=4.38.", "She had paroxysms of increase in pulse rate.", "She had paroxysms of increase in blood pressure.", "She had paroxysms of increase in respiratory rate.", "She had paroxysms of increase in temperature.", "She had sweating.", "She had decerebrate posturing.", "She had episodes of autonomic surge.", "She had a CSF score of 11.", "She had a DLT score of 11.", "She had a PSH-AM score of 21.", "A probable diagnosis of PSH was made.", "She was started on morphine 2 mg, IV, as required.", "She was started on paracetamol 1 gm, po, as required.", "She was started on propranolol, 40 mg po 3 times a day.", "She was started on diazepam 5 mg, IV 3 times a day.", "She was started on gabapentin 150\u2013300 mg po 3 times a day.", "Her GCS started to improve on the second week of ICU admission.", "The frequency and severity of sympathetic storm declined.", "IV antibiotics were discontinued after 2 weeks of therapy.", "On the third week of admission, she developed asystole.", "She died of cardiac arrest.", "CPR was performed."], "index": 96, "original_id": "multiclinsum_test_1504_en.txt", "split": "test", "summary_subclaims": ["The patient is a 35-year-old woman.", "She has echo-proven chronic rheumatic heart disease.", "She had percutaneous balloon mitral valvotomy 6 weeks previously.", "Left atrial thrombus was detected after the procedure.", "Anticoagulant (warfarin) was initiated.", "She presented with severe headache and repeated vomiting of 1 day duration.", "She had frequent seizure attacks with subsequent loss of consciousness on the third day of admission.", "CT-scan revealed acute subdural hematoma and ventricular bleeding.", "Diagnosis of status epilepticus secondary to intracranial hemorrhage due to warfarin toxicity was made.", "She was transferred to medical intensive care unit (ICU), intubated, and put on mechanical ventilator.", "Anti-epileptic drugs, antibiotics, vitamin K, and fresh frozen plasma were given.", "She developed paroxysms of hypertension, tachycardia, tachypnea, hyperpyrexia, diaphoresis, and decerebrate posturing after 7 days of neurological insult.", "She had normal inter-ictal EEG tracing during cyclic autonomic surge.", "CFS score was 11.", "DLT score was 10.", "PSH-AM score was 21.", "PSH-AM score suggested 'probable' diagnosis of PSH.", "Morphine, diazepam, propranolol, and gabapentin were given in combination to treat PSH.", "Severity of autonomic storm started to improve on the second week of ICU admission.", "On the third week of admission, her clinical condition deteriorated suddenly.", "She developed asystole and died of cardiac arrest despite cardiopulmonary resuscitation (CPR)."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 41-year-old male.", "He had progressive exertional dyspnea.", "He was transferred to our hospital because of LV thrombus found on transthoracic echocardiogram.", "Transthoracic echocardiogram showed global hypokinetic LV with an EF of 28%.", "A pedunculated apical thrombus measuring 1.75 \u00d7 1.68\u200acm was found.", "Coronary angiogram revealed no significant obstructive lesion.", "He was discharged and took warfarin 3.75\u200amg/day for AF and LV thrombus.", "He developed sudden onset of right-hand clumsiness and expressive aphasia after 1 month.", "Right eye blurred vision and drooling from the right mouth angle were noted.", "The prothrombin time and INR were in the supratherapeutic range (INR 7.64).", "His symptoms totally recovered within 1 day.", "Brain MRI showed multiple acute infarctions in the cortex of the bilateral frontal lobes, left parietal lobe, and bilateral central semiovale.", "The infarctions highly suggested embolic stroke.", "Transthoracic echocardiogram on the same day of stroke still revealed LV thrombus (1.27 \u00d7 0.90\u200acm).", "Warfarin was discontinued due to acute infarction under high INR.", "Edoxaban (60\u200amg/day) was started after INR decreased to less than 2.", "Follow-up echocardiography showed resolution of LV thrombus after 23 days of edoxaban.", "The patient tolerated edoxaban well.", "He did not have recurrent stroke in the following 6 months."], "summary_subclaims": ["The patient is a 41-year-old man.", "He presented with acute onset of right-hand clumsiness.", "He presented with aphasia.", "He had an international normalized ratio of 7.64.", "He was previously treated with warfarin for the LV thrombus.", "He was previously treated with warfarin for non-valvular AF.", "Brain MRI showed multiple acute infarction in the cortex of the bilateral frontal lobes.", "Brain MRI showed multiple acute infarction in the left parietal lobe.", "Brain MRI showed multiple acute infarction in the bilateral central semiovale.", "The infarctions highly suggested embolic stroke.", "The repeated transthoracic echocardiogram still revealed LV thrombus.", "The LV thrombus measured 1.27 \u00d7 0.90\u200acm.", "The LV thrombus failed to respond to warfarin therapy.", "Acute infarctions occurred under supratherapeutic range of INR.", "Warfarin was switched to edoxaban after INR decreased to less than 2.", "The edoxaban dose was 60\u200amg/day.", "The thrombus disappeared after receiving edoxaban for 23 days.", "No more recurrent stroke was noted for more than 6 months."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 41-year-old male.", "He had progressive exertional dyspnea.", "He was transferred to our hospital because of LV thrombus found on transthoracic echocardiogram.", "Transthoracic echocardiogram showed global hypokinetic LV with an EF of 28%.", "A pedunculated apical thrombus measuring 1.75 \u00d7 1.68\u200acm was found.", "Coronary angiogram revealed no significant obstructive lesion.", "He was discharged and took warfarin 3.75\u200amg/day for AF and LV thrombus.", "He developed sudden onset of right-hand clumsiness and expressive aphasia after 1 month.", "Right eye blurred vision and drooling from the right mouth angle were noted.", "The prothrombin time and INR were in the supratherapeutic range (INR 7.64).", "His symptoms totally recovered within 1 day.", "Brain MRI showed multiple acute infarctions in the cortex of the bilateral frontal lobes, left parietal lobe, and bilateral central semiovale.", "The infarctions highly suggested embolic stroke.", "Transthoracic echocardiogram on the same day of stroke still revealed LV thrombus (1.27 \u00d7 0.90\u200acm).", "Warfarin was discontinued due to acute infarction under high INR.", "Edoxaban (60\u200amg/day) was started after INR decreased to less than 2.", "Follow-up echocardiography showed resolution of LV thrombus after 23 days of edoxaban.", "The patient tolerated edoxaban well.", "He did not have recurrent stroke in the following 6 months."], "index": 94, "original_id": "multiclinsum_test_3113_en.txt", "split": "test", "summary_subclaims": ["The patient is a 41-year-old man.", "He presented with acute onset of right-hand clumsiness.", "He presented with aphasia.", "He had an international normalized ratio of 7.64.", "He was previously treated with warfarin for the LV thrombus.", "He was previously treated with warfarin for non-valvular AF.", "Brain MRI showed multiple acute infarction in the cortex of the bilateral frontal lobes.", "Brain MRI showed multiple acute infarction in the left parietal lobe.", "Brain MRI showed multiple acute infarction in the bilateral central semiovale.", "The infarctions highly suggested embolic stroke.", "The repeated transthoracic echocardiogram still revealed LV thrombus.", "The LV thrombus measured 1.27 \u00d7 0.90\u200acm.", "The LV thrombus failed to respond to warfarin therapy.", "Acute infarctions occurred under supratherapeutic range of INR.", "Warfarin was switched to edoxaban after INR decreased to less than 2.", "The edoxaban dose was 60\u200amg/day.", "The thrombus disappeared after receiving edoxaban for 23 days.", "No more recurrent stroke was noted for more than 6 months."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was a 73-year-old male.", "The patient was 174 cm tall and weighed 47 kg.", "The patient had an American Society of Anesthesiologists physical classification of 3.", "The patient was scheduled for elective left nephroureterectomy.", "A left calyx tumor was incidentally discovered during a routine medical examination.", "A biopsy performed 1 month ago during ureteroscopy suggested a urothelial carcinoma.", "The patient had a past medical history of intraductal papillary mucinous neoplasm of the liver that was surgically removed 6 years ago.", "Chest computed tomography (CT) revealed pulmonary thromboembolism in the left lower lobe.", "A lower extremity ultrasonogram showed no evidence of deep vein thrombosis.", "Arterial blood gas analysis and D-dimer were within the normal ranges.", "The patient was instructed to fast for 8 hours before undergoing general anesthesia.", "Premedication involved an intramuscular injection of glycopyrrolate (0.2 mg) and famotidine (20 mg).", "Noninvasive monitoring devices were placed on the patient, including a blood pressure cuff, electrocardiogram, a pulse oximeter, a bispectral index signal device, and a quantitative monitor for neuromuscular blockade.", "General anesthesia was induced using 80 mg propofol.", "Rocuronium (30 mg) was used for neuromuscular blockade after confirming no response to stimuli.", "Sevoflurane (1.7%) was used to maintain the appropriate anesthesia depth after intubation.", "An arterial line was inserted into the right radial artery.", "Right internal jugular vein central venous catheterization was planned.", "Real-time ultrasound-guided catheterization was initially planned.", "The hospital\u2019s portable ultrasonography device was in use in other operating rooms.", "A blind catheterization technique was used based on the patient\u2019s anatomical structure without ultrasound guidance.", "The patient was positioned in the Trendelenburg position with the head 15\u00b0 below the horizontal plane and tilted 40\u00b0 to the left.", "The Bermuda triangle was clearly identified.", "The carotid artery pulse was palpated at the superior angle of the triangle and followed to the center of the triangle.", "A 10 ml syringe connected to a 23-gauge finder needle was inserted perpendicularly to the surface while aspirating.", "The presence of dark venous blood was confirmed at a depth of 2.2 cm.", "No pulsation was observed after separating the finder needle from the syringe.", "An 18-gauge puncture needle connected to the syringe was inserted toward the nipple at a 75\u00b0 angle from the skin while targeting the finder needle tip.", "The aspiration of venous blood flow was confirmed.", "A guidewire was inserted to a depth of 20 cm from the skin through the puncture needle without any resistance felt during the procedure.", "The puncture needle was removed while leaving the guidewire in place.", "The practitioner and colleagues attempted to investigate the anatomy of the puncture site by utilizing ultrasonography to detect the previously inserted guidewire.", "The guidewire was found to be located in a vein as which we presumed the vessel based on its location that was lateral from the common carotid artery and collapsibility when pressure was applied using the probe.", "A larger vessel presumed to be a vein was located superiorly and more laterally than the identified vessel.", "Real-time ultrasound-guided guidewire insertion was performed at the same view in this vessel using another central venous catheter kit.", "Both guidewires were left in place while the probe was tilted to visualize their paths.", "It was confirmed that they were both descending toward the right brachiocephalic vein.", "The first guidewire was removed, and manual compression using sterile gauze was applied for over 5 min.", "No resistance was felt during the removal.", "The second guidewire was used to complete the central venous catheterization.", "Free regurgitation was observed at each port.", "The central venous pressure measured using the central venous catheter was 15 mmHg.", "The surgery was successful.", "The patient was transferred to the post-anesthesia care unit after extubation.", "A simple anterior-to-posterior chest X-ray taken immediately after the surgery confirmed that the catheter tip was located near the right atrium, following the superior vena cava.", "We reviewed the contrast-enhanced chest CT performed for preoperative evaluation and confirmed that the right internal jugular vein coursed laterally to the right common carotid artery on the axial view.", "A large vessel was also observed behind the common carotid artery and internal jugular vein.", "It was traced upward and downward, confirming that it enters into the transverse foramen at the level of the sixth cervical vertebra and drains into the right brachiocephalic vein.", "The same findings were observed in the coronary view.", "The radiologist indicated this vessel as the vertebral vein.", "After considering the ultrasonographic findings and the radiologist\u2019s official reading, we confirmed that the vein that we had initially punctured was indeed the right cervical vertebral vein.", "On the third day after surgery, the central venous catheter was removed.", "The patient did not exhibit any complications, such as bleeding, swelling, and neurological symptoms."], "summary_subclaims": ["The patient was a 73-year-old male.", "The patient was suspected to have a urothelial carcinoma.", "The patient was scheduled for elective left nephroureterectomy.", "During central venous catheterization, the anatomic landmark technique was used to target the internal jugular vein.", "A guidewire was inadvertently inserted into the suspected vertebral vein.", "The radiologist reviewed the preoperative enhanced computed tomography.", "The radiologist confirmed that the initially punctured vessel was the vertebral vein.", "The central venous catheter was removed on the third day after surgery.", "The patient did not exhibit any complications, such as bleeding, swelling, and neurological symptoms."]}, "extra_info": {"fulltext_subclaims": ["The patient was a 73-year-old male.", "The patient was 174 cm tall and weighed 47 kg.", "The patient had an American Society of Anesthesiologists physical classification of 3.", "The patient was scheduled for elective left nephroureterectomy.", "A left calyx tumor was incidentally discovered during a routine medical examination.", "A biopsy performed 1 month ago during ureteroscopy suggested a urothelial carcinoma.", "The patient had a past medical history of intraductal papillary mucinous neoplasm of the liver that was surgically removed 6 years ago.", "Chest computed tomography (CT) revealed pulmonary thromboembolism in the left lower lobe.", "A lower extremity ultrasonogram showed no evidence of deep vein thrombosis.", "Arterial blood gas analysis and D-dimer were within the normal ranges.", "The patient was instructed to fast for 8 hours before undergoing general anesthesia.", "Premedication involved an intramuscular injection of glycopyrrolate (0.2 mg) and famotidine (20 mg).", "Noninvasive monitoring devices were placed on the patient, including a blood pressure cuff, electrocardiogram, a pulse oximeter, a bispectral index signal device, and a quantitative monitor for neuromuscular blockade.", "General anesthesia was induced using 80 mg propofol.", "Rocuronium (30 mg) was used for neuromuscular blockade after confirming no response to stimuli.", "Sevoflurane (1.7%) was used to maintain the appropriate anesthesia depth after intubation.", "An arterial line was inserted into the right radial artery.", "Right internal jugular vein central venous catheterization was planned.", "Real-time ultrasound-guided catheterization was initially planned.", "The hospital\u2019s portable ultrasonography device was in use in other operating rooms.", "A blind catheterization technique was used based on the patient\u2019s anatomical structure without ultrasound guidance.", "The patient was positioned in the Trendelenburg position with the head 15\u00b0 below the horizontal plane and tilted 40\u00b0 to the left.", "The Bermuda triangle was clearly identified.", "The carotid artery pulse was palpated at the superior angle of the triangle and followed to the center of the triangle.", "A 10 ml syringe connected to a 23-gauge finder needle was inserted perpendicularly to the surface while aspirating.", "The presence of dark venous blood was confirmed at a depth of 2.2 cm.", "No pulsation was observed after separating the finder needle from the syringe.", "An 18-gauge puncture needle connected to the syringe was inserted toward the nipple at a 75\u00b0 angle from the skin while targeting the finder needle tip.", "The aspiration of venous blood flow was confirmed.", "A guidewire was inserted to a depth of 20 cm from the skin through the puncture needle without any resistance felt during the procedure.", "The puncture needle was removed while leaving the guidewire in place.", "The practitioner and colleagues attempted to investigate the anatomy of the puncture site by utilizing ultrasonography to detect the previously inserted guidewire.", "The guidewire was found to be located in a vein as which we presumed the vessel based on its location that was lateral from the common carotid artery and collapsibility when pressure was applied using the probe.", "A larger vessel presumed to be a vein was located superiorly and more laterally than the identified vessel.", "Real-time ultrasound-guided guidewire insertion was performed at the same view in this vessel using another central venous catheter kit.", "Both guidewires were left in place while the probe was tilted to visualize their paths.", "It was confirmed that they were both descending toward the right brachiocephalic vein.", "The first guidewire was removed, and manual compression using sterile gauze was applied for over 5 min.", "No resistance was felt during the removal.", "The second guidewire was used to complete the central venous catheterization.", "Free regurgitation was observed at each port.", "The central venous pressure measured using the central venous catheter was 15 mmHg.", "The surgery was successful.", "The patient was transferred to the post-anesthesia care unit after extubation.", "A simple anterior-to-posterior chest X-ray taken immediately after the surgery confirmed that the catheter tip was located near the right atrium, following the superior vena cava.", "We reviewed the contrast-enhanced chest CT performed for preoperative evaluation and confirmed that the right internal jugular vein coursed laterally to the right common carotid artery on the axial view.", "A large vessel was also observed behind the common carotid artery and internal jugular vein.", "It was traced upward and downward, confirming that it enters into the transverse foramen at the level of the sixth cervical vertebra and drains into the right brachiocephalic vein.", "The same findings were observed in the coronary view.", "The radiologist indicated this vessel as the vertebral vein.", "After considering the ultrasonographic findings and the radiologist\u2019s official reading, we confirmed that the vein that we had initially punctured was indeed the right cervical vertebral vein.", "On the third day after surgery, the central venous catheter was removed.", "The patient did not exhibit any complications, such as bleeding, swelling, and neurological symptoms."], "index": 88, "original_id": "multiclinsum_test_2805_en.txt", "split": "test", "summary_subclaims": ["The patient was a 73-year-old male.", "The patient was suspected to have a urothelial carcinoma.", "The patient was scheduled for elective left nephroureterectomy.", "During central venous catheterization, the anatomic landmark technique was used to target the internal jugular vein.", "A guidewire was inadvertently inserted into the suspected vertebral vein.", "The radiologist reviewed the preoperative enhanced computed tomography.", "The radiologist confirmed that the initially punctured vessel was the vertebral vein.", "The central venous catheter was removed on the third day after surgery.", "The patient did not exhibit any complications, such as bleeding, swelling, and neurological symptoms."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was a 10-year-old Kurdish boy.", "The patient presented with bone pain.", "The patient had fever associated with night sweats.", "The patient had shortness of breath.", "The patient had weight loss of 5kg/month.", "The patient had purple purpuric spots over the skin.", "The patient had bleeding from the nose.", "The patient\u2019s history dated back to 1 month before admission.", "On examination, we observed pallor.", "On examination, we observed cachexia.", "On examination, we observed dyspnea.", "On examination, we observed fever.", "On examination, we observed tachycardia.", "On examination, we observed tachypnea.", "On examination, we observed multiple petechiae and ecchymoses all over the skin.", "On examination, we observed dilated tortuous veins over the chest.", "The pulse rate was 120bpm.", "The respiratory rate was 23cycles/minute.", "The temperature was 39\u00b0C.", "The blood pressure was 90/45mmHg.", "We found multiple small cervical lymphadenopathies.", "We found mild splenomegaly 3cm below the left costal margin.", "The liver was tender 7cm below the right costal margin.", "The patient had gross abdominal distention.", "The initial blood counts were hemoglobin 64g/L.", "The initial blood counts were white blood cell count 34 \u00d7 109/L.", "The initial blood counts were platelets 25 \u00d7 109/L.", "The initial blood counts showed blasts 38%.", "The blasts were homogeneous with a high nuclear to cytoplasmic ratio.", "The blasts had inconspicuous nucleoli.", "The blasts had open chromatin.", "Some of the blasts were vacuolated.", "Platelets were markedly reduced.", "There was mediastinal widening visualized on a chest X-ray.", "MRI showed lumbosacral vertebrae with diffuse infiltration of the axial bone marrow of the lower dorsal and lumbar vertebrae.", "The MRI findings were suggestive of bony metastases predominantly osteolytic in nature.", "Bone marrow aspiration showed no fragments.", "Bone marrow aspiration showed few areas of necrosis.", "Bone marrow biopsy showed marked BMN.", "The first immunophenotyping was not conclusive.", "The second immunophenotyping was positive for CD3.", "The second immunophenotyping was positive for terminal deoxynucleotidyl transferase.", "The second immunophenotyping was negative for CD20.", "The second immunophenotyping was negative for CD79a.", "The second immunophenotyping was negative for CD10.", "After admission, the patient\u2019s condition deteriorated.", "The patient developed frank superior vena cava syndrome.", "The patient was treated with chemotherapy according to the ALL protocol.", "Complete remission was achieved on day 28.", "At the 24th week of chemotherapy, the patient\u2019s condition relapsed on treatment.", "The patient returned to the hospital with fever.", "The patient returned to the hospital with chest infection.", "The patient returned to the hospital with 60% blasts observed on peripheral blood film.", "The complete blood count revealed severe pancytopenia.", "Bone marrow aspiration was a dry tap.", "The bone marrow biopsy showed hypercellular marrow.", "The bone marrow biopsy showed extensive infiltration by mononuclear cells.", "The bone marrow biopsy showed disappearance of necrosis.", "Treatment was reinitiated according to the ALL protocol.", "The patient developed severe mucositis.", "The patient developed uncontrolled septicemia.", "The patient developed electrolyte imbalance.", "The patient eventually died.", "The bone marrow aspiration at the time of diagnosis was diluted.", "The slides showed artefact with a few necrotic cells.", "The biopsy was a 1.6cm piece of tissue.", "The biopsy consisted of a fragment of trabecular bone.", "The biopsy showed marked BMN.", "The result of immunohistochemistry was not interpretable for the first specimen.", "The result of immunohistochemistry for the second specimen was definitive as precursor T-cell ALL.", "During admission, the patient received intravenous fluid 3000ml/m2/day.", "During admission, the patient received allopurinol tablets 100mg/m2/dose.", "During admission, the patient received antibiotics.", "The patient\u2019s condition deteriorated.", "The patient developed progressive dyspnea.", "The patient developed chest tightness.", "The patient developed abdominal distention.", "The patient developed fever.", "The patient was near to developing frank features of superior vena cava syndrome.", "The patient developed bilateral lower-limb weakness.", "The straight leg raising test was positive bilaterally.", "MRI of the dorsolumbosacral spine showed diffuse focal infiltration of the axial bone marrow of the lower dorsal and lumbar vertebrae.", "The MRI showed altered hypointense T1-weighted signal intensity.", "The image was suggestive of bony metastasis that was predominantly osteolytic in nature.", "Incidental hepatosplenomegaly was observed.", "Incidental bilateral renal enlargement was observed.", "There was no pressure on the spinal cord.", "Dexamethasone intravenous infusion at 6mg/m2 was started.", "Seven days after admission, induction therapy with vincristine 1.5mg/m2 intravenous bolus was started on days 7, 14, 21 and 28.", "Dexamethasone 6mg/m2 was administered daily.", "Daunorubicin 25mg/m2 was given on days 1 and 7.", "Upon starting induction, the patient developed attacks of tonic-clonic contractions.", "Computed tomography of the brain without contrast was negative.", "Electrolyte measurements showed severe hypocalcemia.", "Correction of hypocalcemia stabilized the convulsions.", "On day 28, bone marrow aspiration indicated a few fragments.", "On day 28, megakaryocytes were seen.", "On day 28, erythroid and myeloid series were present with all stages of maturation.", "On day 28, the data indicated predominant neutrophils and histiocytes.", "On day 28, the cellular elements could not confirm an excess of blast cells.", "The bone marrow biopsy report showed 95% cellularity.", "The bone marrow biopsy showed predominant early-stage granulocytes.", "The bone marrow biopsy showed normal maturation stages of hematopoietic cells.", "The blasts constituted about 2% of total marrow nucleated cells.", "The myeloid to erythroid cell ratio was 8:1.", "After a 4-week induction period, complete remission was observed.", "Early consolidation chemotherapy was continued.", "At the 24th week of treatment, the patient returned with fever.", "At the 24th week of treatment, the patient returned with chest infection.", "At the 24th week of treatment, the patient returned with neutropenia.", "At the 24th week of treatment, the patient returned with thrombocytopenia.", "We found the presence of a few blasts in the peripheral blood film.", "The patient was not responding to supportive treatment that included antibiotics and antipyretics.", "Follow-up analysis of bone marrow aspiration showed excessive bone marrow infiltration by mononuclear cells.", "Follow-up analysis of bone marrow aspiration showed multiple inconspicuous nucleoli.", "Both erythroid and megakaryocytic precursors were suppressed in bone marrow aspiration.", "In the relapsed biopsy, no necrosis was observed.", "On the reinduction therapy date, we followed a bone marrow relapsed protocol.", "On the 14th day of treatment reinduction, the patient developed severe anemia.", "On the 14th day of treatment reinduction, the patient developed thrombocytopenia.", "On the 14th day of treatment reinduction, the patient developed neutropenia.", "The patient developed grade IV mucositis.", "The patient developed hypokalemia.", "The patient could not tolerate the complications.", "The patient developed septicemia.", "The patient developed sepsis.", "The patient\u2019s death was an inevitable outcome.", "The overall survival period was 26 weeks after first diagnosis."], "summary_subclaims": ["The patient is a 10-year-old Kurdish boy.", "He had generalized bone pain and fever of 1 month's duration.", "The fever was associated with sweating.", "The fever was associated with easy fatigability.", "The fever was associated with nose bleeding.", "The fever was associated with breathlessness.", "The fever was associated with severe weight loss.", "On examination, pallor was observed.", "On examination, tachypnea was observed.", "On examination, tachycardia was observed.", "On examination, low blood pressure was observed.", "On examination, fever was observed.", "On examination, petechial hemorrhage was observed.", "On examination, ecchymoses were observed.", "On examination, tortuous dilated veins over the chest and upper part of abdomen were observed.", "On examination, multiple small cervical lymph node enlargements were observed.", "On examination, a mildly enlarged spleen was observed.", "On examination, a palpable liver was observed.", "On examination, gross abdominal distention was observed.", "Blood analysis revealed pancytopenia.", "Blood analysis revealed elevated lactate dehydrogenase.", "Blood analysis revealed elevated erythrocyte sedimentation rate.", "Imaging results showed mediastinal widening on a planar chest X-ray.", "Imaging results showed diffuse focal infiltration of the axial bone marrow on magnetic resonance imaging of the lumbosacral vertebrae.", "Bone marrow aspiration and biopsy examination showed extensive bone marrow necrosis.", "Immunophenotyping analysis of the bone marrow biopsy confirmed T-cell acute lymphoblastic leukemia.", "CD3 markers were positive.", "Terminal deoxynucleotidyl transferase markers were positive.", "CD10 markers were negative.", "CD20 markers were negative.", "CD79a markers were negative."]}, "extra_info": {"fulltext_subclaims": ["The patient was a 10-year-old Kurdish boy.", "The patient presented with bone pain.", "The patient had fever associated with night sweats.", "The patient had shortness of breath.", "The patient had weight loss of 5kg/month.", "The patient had purple purpuric spots over the skin.", "The patient had bleeding from the nose.", "The patient\u2019s history dated back to 1 month before admission.", "On examination, we observed pallor.", "On examination, we observed cachexia.", "On examination, we observed dyspnea.", "On examination, we observed fever.", "On examination, we observed tachycardia.", "On examination, we observed tachypnea.", "On examination, we observed multiple petechiae and ecchymoses all over the skin.", "On examination, we observed dilated tortuous veins over the chest.", "The pulse rate was 120bpm.", "The respiratory rate was 23cycles/minute.", "The temperature was 39\u00b0C.", "The blood pressure was 90/45mmHg.", "We found multiple small cervical lymphadenopathies.", "We found mild splenomegaly 3cm below the left costal margin.", "The liver was tender 7cm below the right costal margin.", "The patient had gross abdominal distention.", "The initial blood counts were hemoglobin 64g/L.", "The initial blood counts were white blood cell count 34 \u00d7 109/L.", "The initial blood counts were platelets 25 \u00d7 109/L.", "The initial blood counts showed blasts 38%.", "The blasts were homogeneous with a high nuclear to cytoplasmic ratio.", "The blasts had inconspicuous nucleoli.", "The blasts had open chromatin.", "Some of the blasts were vacuolated.", "Platelets were markedly reduced.", "There was mediastinal widening visualized on a chest X-ray.", "MRI showed lumbosacral vertebrae with diffuse infiltration of the axial bone marrow of the lower dorsal and lumbar vertebrae.", "The MRI findings were suggestive of bony metastases predominantly osteolytic in nature.", "Bone marrow aspiration showed no fragments.", "Bone marrow aspiration showed few areas of necrosis.", "Bone marrow biopsy showed marked BMN.", "The first immunophenotyping was not conclusive.", "The second immunophenotyping was positive for CD3.", "The second immunophenotyping was positive for terminal deoxynucleotidyl transferase.", "The second immunophenotyping was negative for CD20.", "The second immunophenotyping was negative for CD79a.", "The second immunophenotyping was negative for CD10.", "After admission, the patient\u2019s condition deteriorated.", "The patient developed frank superior vena cava syndrome.", "The patient was treated with chemotherapy according to the ALL protocol.", "Complete remission was achieved on day 28.", "At the 24th week of chemotherapy, the patient\u2019s condition relapsed on treatment.", "The patient returned to the hospital with fever.", "The patient returned to the hospital with chest infection.", "The patient returned to the hospital with 60% blasts observed on peripheral blood film.", "The complete blood count revealed severe pancytopenia.", "Bone marrow aspiration was a dry tap.", "The bone marrow biopsy showed hypercellular marrow.", "The bone marrow biopsy showed extensive infiltration by mononuclear cells.", "The bone marrow biopsy showed disappearance of necrosis.", "Treatment was reinitiated according to the ALL protocol.", "The patient developed severe mucositis.", "The patient developed uncontrolled septicemia.", "The patient developed electrolyte imbalance.", "The patient eventually died.", "The bone marrow aspiration at the time of diagnosis was diluted.", "The slides showed artefact with a few necrotic cells.", "The biopsy was a 1.6cm piece of tissue.", "The biopsy consisted of a fragment of trabecular bone.", "The biopsy showed marked BMN.", "The result of immunohistochemistry was not interpretable for the first specimen.", "The result of immunohistochemistry for the second specimen was definitive as precursor T-cell ALL.", "During admission, the patient received intravenous fluid 3000ml/m2/day.", "During admission, the patient received allopurinol tablets 100mg/m2/dose.", "During admission, the patient received antibiotics.", "The patient\u2019s condition deteriorated.", "The patient developed progressive dyspnea.", "The patient developed chest tightness.", "The patient developed abdominal distention.", "The patient developed fever.", "The patient was near to developing frank features of superior vena cava syndrome.", "The patient developed bilateral lower-limb weakness.", "The straight leg raising test was positive bilaterally.", "MRI of the dorsolumbosacral spine showed diffuse focal infiltration of the axial bone marrow of the lower dorsal and lumbar vertebrae.", "The MRI showed altered hypointense T1-weighted signal intensity.", "The image was suggestive of bony metastasis that was predominantly osteolytic in nature.", "Incidental hepatosplenomegaly was observed.", "Incidental bilateral renal enlargement was observed.", "There was no pressure on the spinal cord.", "Dexamethasone intravenous infusion at 6mg/m2 was started.", "Seven days after admission, induction therapy with vincristine 1.5mg/m2 intravenous bolus was started on days 7, 14, 21 and 28.", "Dexamethasone 6mg/m2 was administered daily.", "Daunorubicin 25mg/m2 was given on days 1 and 7.", "Upon starting induction, the patient developed attacks of tonic-clonic contractions.", "Computed tomography of the brain without contrast was negative.", "Electrolyte measurements showed severe hypocalcemia.", "Correction of hypocalcemia stabilized the convulsions.", "On day 28, bone marrow aspiration indicated a few fragments.", "On day 28, megakaryocytes were seen.", "On day 28, erythroid and myeloid series were present with all stages of maturation.", "On day 28, the data indicated predominant neutrophils and histiocytes.", "On day 28, the cellular elements could not confirm an excess of blast cells.", "The bone marrow biopsy report showed 95% cellularity.", "The bone marrow biopsy showed predominant early-stage granulocytes.", "The bone marrow biopsy showed normal maturation stages of hematopoietic cells.", "The blasts constituted about 2% of total marrow nucleated cells.", "The myeloid to erythroid cell ratio was 8:1.", "After a 4-week induction period, complete remission was observed.", "Early consolidation chemotherapy was continued.", "At the 24th week of treatment, the patient returned with fever.", "At the 24th week of treatment, the patient returned with chest infection.", "At the 24th week of treatment, the patient returned with neutropenia.", "At the 24th week of treatment, the patient returned with thrombocytopenia.", "We found the presence of a few blasts in the peripheral blood film.", "The patient was not responding to supportive treatment that included antibiotics and antipyretics.", "Follow-up analysis of bone marrow aspiration showed excessive bone marrow infiltration by mononuclear cells.", "Follow-up analysis of bone marrow aspiration showed multiple inconspicuous nucleoli.", "Both erythroid and megakaryocytic precursors were suppressed in bone marrow aspiration.", "In the relapsed biopsy, no necrosis was observed.", "On the reinduction therapy date, we followed a bone marrow relapsed protocol.", "On the 14th day of treatment reinduction, the patient developed severe anemia.", "On the 14th day of treatment reinduction, the patient developed thrombocytopenia.", "On the 14th day of treatment reinduction, the patient developed neutropenia.", "The patient developed grade IV mucositis.", "The patient developed hypokalemia.", "The patient could not tolerate the complications.", "The patient developed septicemia.", "The patient developed sepsis.", "The patient\u2019s death was an inevitable outcome.", "The overall survival period was 26 weeks after first diagnosis."], "index": 99, "original_id": "multiclinsum_test_1185_en.txt", "split": "test", "summary_subclaims": ["The patient is a 10-year-old Kurdish boy.", "He had generalized bone pain and fever of 1 month's duration.", "The fever was associated with sweating.", "The fever was associated with easy fatigability.", "The fever was associated with nose bleeding.", "The fever was associated with breathlessness.", "The fever was associated with severe weight loss.", "On examination, pallor was observed.", "On examination, tachypnea was observed.", "On examination, tachycardia was observed.", "On examination, low blood pressure was observed.", "On examination, fever was observed.", "On examination, petechial hemorrhage was observed.", "On examination, ecchymoses were observed.", "On examination, tortuous dilated veins over the chest and upper part of abdomen were observed.", "On examination, multiple small cervical lymph node enlargements were observed.", "On examination, a mildly enlarged spleen was observed.", "On examination, a palpable liver was observed.", "On examination, gross abdominal distention was observed.", "Blood analysis revealed pancytopenia.", "Blood analysis revealed elevated lactate dehydrogenase.", "Blood analysis revealed elevated erythrocyte sedimentation rate.", "Imaging results showed mediastinal widening on a planar chest X-ray.", "Imaging results showed diffuse focal infiltration of the axial bone marrow on magnetic resonance imaging of the lumbosacral vertebrae.", "Bone marrow aspiration and biopsy examination showed extensive bone marrow necrosis.", "Immunophenotyping analysis of the bone marrow biopsy confirmed T-cell acute lymphoblastic leukemia.", "CD3 markers were positive.", "Terminal deoxynucleotidyl transferase markers were positive.", "CD10 markers were negative.", "CD20 markers were negative.", "CD79a markers were negative."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["A 56-year-old woman was referred to the emergency department due to a severe headache in the frontal area for 2 days before admission.", "The patient had nausea and vomiting in the morning.", "The patient had no history of seizures or decreased consciousness.", "The examination of neurological symptoms was completely normal.", "The patient's blood pressure was 130/85 mmHg.", "The patient's heart rate was 86/min.", "The patient's temperature was 37.3 \u00b0C.", "The patient had undergone tympano-mastoidectomy surgery and resection of the cholesteatoma 1 week earlier.", "A canalwall down mastoidectomy was performed due to right ear cholesteatoma.", "Microtrauma was inflicted in the dural plate during surgery.", "No significant cerebrospinal fluid leak occurred during the procedure.", "The Mount Fuji sign was found on the brain CT scan.", "No evidence of brain abscess or intracranial hemorrhage was found.", "The patient was immediately admitted to the intensive care unit.", "Initial treatments such as CBR, 30-degree head elevation, anti-fever therapy, analgesics, oxygen therapy, and phenytoin were prescribed.", "The patient did not undergo surgery due to a lack of neurological symptoms, decreased level of consciousness, or seizures.", "The patient was maintained under regular and continuous monitoring of vital and neurological signs.", "The patient\u2019s headache had completely resolved the day after admission.", "The patient was admitted to the ICU for 5 days.", "The patient was monitored for the volume of pneumocephalus every day with a CT scan.", "The patient's pneumocephalus was resolved completely at the end of 5 days.", "The patient was transferred to the ward.", "The patient was discharged after complete recovery."], "summary_subclaims": ["The patient was referred to the emergency department due to a severe headache in the frontal area for 2 days before admission.", "The patient experienced nausea and vomiting in the morning.", "The patient had no history of seizures or decreased consciousness.", "Examination of neurological symptoms was completely normal.", "The patient had undergone tympanomastoidectomy surgery and resection of the cholesteatoma 1 week previously.", "The Mount Fuji sign was found on the brain CT scan.", "Treatments such as CBR, 30-degree head elevation, anti-fever, analgesics, oxygen therapy, and phenytoin were prescribed.", "At the end of 5 days, the patient's pneumocephalus was resolved completely."]}, "extra_info": {"fulltext_subclaims": ["A 56-year-old woman was referred to the emergency department due to a severe headache in the frontal area for 2 days before admission.", "The patient had nausea and vomiting in the morning.", "The patient had no history of seizures or decreased consciousness.", "The examination of neurological symptoms was completely normal.", "The patient's blood pressure was 130/85 mmHg.", "The patient's heart rate was 86/min.", "The patient's temperature was 37.3 \u00b0C.", "The patient had undergone tympano-mastoidectomy surgery and resection of the cholesteatoma 1 week earlier.", "A canalwall down mastoidectomy was performed due to right ear cholesteatoma.", "Microtrauma was inflicted in the dural plate during surgery.", "No significant cerebrospinal fluid leak occurred during the procedure.", "The Mount Fuji sign was found on the brain CT scan.", "No evidence of brain abscess or intracranial hemorrhage was found.", "The patient was immediately admitted to the intensive care unit.", "Initial treatments such as CBR, 30-degree head elevation, anti-fever therapy, analgesics, oxygen therapy, and phenytoin were prescribed.", "The patient did not undergo surgery due to a lack of neurological symptoms, decreased level of consciousness, or seizures.", "The patient was maintained under regular and continuous monitoring of vital and neurological signs.", "The patient\u2019s headache had completely resolved the day after admission.", "The patient was admitted to the ICU for 5 days.", "The patient was monitored for the volume of pneumocephalus every day with a CT scan.", "The patient's pneumocephalus was resolved completely at the end of 5 days.", "The patient was transferred to the ward.", "The patient was discharged after complete recovery."], "index": 105, "original_id": "multiclinsum_test_520_en.txt", "split": "test", "summary_subclaims": ["The patient was referred to the emergency department due to a severe headache in the frontal area for 2 days before admission.", "The patient experienced nausea and vomiting in the morning.", "The patient had no history of seizures or decreased consciousness.", "Examination of neurological symptoms was completely normal.", "The patient had undergone tympanomastoidectomy surgery and resection of the cholesteatoma 1 week previously.", "The Mount Fuji sign was found on the brain CT scan.", "Treatments such as CBR, 30-degree head elevation, anti-fever, analgesics, oxygen therapy, and phenytoin were prescribed.", "At the end of 5 days, the patient's pneumocephalus was resolved completely."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was a 22-year-old male soldier.", "The patient received multifragmental combined with thoraco-abdominal injuries as a result of shelling from MLRS \u201cGrad\u201d.", "The entrance wound was detected in the region of 5\u20137 ribs between the anterior and the posterior right axillary lines.", "The patient received first medical aid immediately at the place of injury.", "The time taken between injury and evacuation was less than 60 min.", "The patient was transported to the Military Medical Hospital #66 at Pokrovsk.", "The patient was diagnosed with a penetrating thoracic wound.", "The blood loss was approximately 1500 ml.", "Thoracentesis was performed to eliminate the right hemopneumothorax.", "Laparocentesis was performed.", "A hemorrhagic content was received at the laparocentesis.", "Laparotomy was performed.", "Ruptures of the liver\u2019s parenchyma were detected.", "The entrance wound was detected only in the chest area.", "The exit wound was not identified neither in chest, nor in abdomen wall.", "A conclusion was made that damage of the liver was in result of \u201chydrodynamic shock\u201d.", "Minimal surgical treatment was applied.", "Suturing of liver ruptures was performed.", "Excision of necrotic tissues was performed.", "Suturing of gunshot wounds of limbs was performed.", "In an early post-operative period, a hemorrhage and bile were detected on drainage.", "Relaparotomy was performed.", "Liver damage within the area of gallbladder fossa was detected.", "Cholecystectomy was performed.", "A patch of omentum was used to fill the gap in injured S3\u20136 of liver.", "The patient was transported to the Mechnikov Regional Clinical Hospital in Dnipro.", "Antibacterial therapy was administrated.", "The patient was transported to the ICU at the National Military Medical Clinical Center of Ukraine in Kyiv.", "Drainage from the subhepatic area showed daily bile volume up to 300 ml.", "Endoscopic papillosphincterotomy was performed.", "Endoscopic retrograde cholecystopancreatography was performed.", "Stenting of the common bile duct was performed.", "A feeding tube was placed behind the Treitz ligament.", "Implementation of endoscopic decompression of the bile duct had resulted in gradual reduction of bile volume.", "A CT scan of the abdomen was performed.", "The liver demonstrated zones with ischemic lesions.", "A liver resection of the affected segment was planned.", "Intra-abdominal bleeding was diagnosed.", "Urgent laparotomy was performed.", "Erosion of the right hepatic artery was detected.", "Erosive defect was sutured.", "Stable hemostasis was achieved.", "Tissue softening and color changes of liver S5\u20136 parenchyma were detected.", "Anatomic resection of the liver S5\u20136 was performed.", "The patient was transferred to the surgery ward from ICU.", "The patient was diagnosed with multiple fragmental injuries of soft tissues of the skull, chest, abdomen, as well as extremities.", "The most serious soft tissue injury was detected at the right lower limb.", "The patient was discharged from hospital in good condition on the 49th day after receiving injuries."], "summary_subclaims": ["The patient was injured after the multiple launcher rocket system 'Grad' shelling.", "The patient was diagnosed with hydrodynamic liver rupture.", "Medical management with application of damage control (DC) tactic was used.", "The patient underwent relaparatomy.", "The patient underwent liver resection.", "The patient underwent endoscopic papillosphincterotomy.", "The patient underwent endoscopic retrograde cholecystopancreatography.", "Stenting of the common bile duct was performed.", "VAC-therapy was applied.", "Applied treatment modalities were effective.", "The patient was discharged on the 49th day after injury."]}, "extra_info": {"fulltext_subclaims": ["The patient was a 22-year-old male soldier.", "The patient received multifragmental combined with thoraco-abdominal injuries as a result of shelling from MLRS \u201cGrad\u201d.", "The entrance wound was detected in the region of 5\u20137 ribs between the anterior and the posterior right axillary lines.", "The patient received first medical aid immediately at the place of injury.", "The time taken between injury and evacuation was less than 60 min.", "The patient was transported to the Military Medical Hospital #66 at Pokrovsk.", "The patient was diagnosed with a penetrating thoracic wound.", "The blood loss was approximately 1500 ml.", "Thoracentesis was performed to eliminate the right hemopneumothorax.", "Laparocentesis was performed.", "A hemorrhagic content was received at the laparocentesis.", "Laparotomy was performed.", "Ruptures of the liver\u2019s parenchyma were detected.", "The entrance wound was detected only in the chest area.", "The exit wound was not identified neither in chest, nor in abdomen wall.", "A conclusion was made that damage of the liver was in result of \u201chydrodynamic shock\u201d.", "Minimal surgical treatment was applied.", "Suturing of liver ruptures was performed.", "Excision of necrotic tissues was performed.", "Suturing of gunshot wounds of limbs was performed.", "In an early post-operative period, a hemorrhage and bile were detected on drainage.", "Relaparotomy was performed.", "Liver damage within the area of gallbladder fossa was detected.", "Cholecystectomy was performed.", "A patch of omentum was used to fill the gap in injured S3\u20136 of liver.", "The patient was transported to the Mechnikov Regional Clinical Hospital in Dnipro.", "Antibacterial therapy was administrated.", "The patient was transported to the ICU at the National Military Medical Clinical Center of Ukraine in Kyiv.", "Drainage from the subhepatic area showed daily bile volume up to 300 ml.", "Endoscopic papillosphincterotomy was performed.", "Endoscopic retrograde cholecystopancreatography was performed.", "Stenting of the common bile duct was performed.", "A feeding tube was placed behind the Treitz ligament.", "Implementation of endoscopic decompression of the bile duct had resulted in gradual reduction of bile volume.", "A CT scan of the abdomen was performed.", "The liver demonstrated zones with ischemic lesions.", "A liver resection of the affected segment was planned.", "Intra-abdominal bleeding was diagnosed.", "Urgent laparotomy was performed.", "Erosion of the right hepatic artery was detected.", "Erosive defect was sutured.", "Stable hemostasis was achieved.", "Tissue softening and color changes of liver S5\u20136 parenchyma were detected.", "Anatomic resection of the liver S5\u20136 was performed.", "The patient was transferred to the surgery ward from ICU.", "The patient was diagnosed with multiple fragmental injuries of soft tissues of the skull, chest, abdomen, as well as extremities.", "The most serious soft tissue injury was detected at the right lower limb.", "The patient was discharged from hospital in good condition on the 49th day after receiving injuries."], "index": 93, "original_id": "multiclinsum_test_2795_en.txt", "split": "test", "summary_subclaims": ["The patient was injured after the multiple launcher rocket system 'Grad' shelling.", "The patient was diagnosed with hydrodynamic liver rupture.", "Medical management with application of damage control (DC) tactic was used.", "The patient underwent relaparatomy.", "The patient underwent liver resection.", "The patient underwent endoscopic papillosphincterotomy.", "The patient underwent endoscopic retrograde cholecystopancreatography.", "Stenting of the common bile duct was performed.", "VAC-therapy was applied.", "Applied treatment modalities were effective.", "The patient was discharged on the 49th day after injury."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 69-year-old female.", "She had a painful lump in her left breast 3 months ago.", "She had bloody discharge from the left nipple four years ago.", "The patient decided not to follow-up despite recommendations for diagnostic procedure.", "On physical examination, an erythematous tender mass with hard consistency was detected around the nipple.", "Sonography showed a lobulated hypoechoic mass with microcystic areas measuring 20\u00d717 mm at 3 o'clock beside the areola.", "Mammography showed a hyperdense mass in the retroareolar site.", "The patient was admitted and underwent surgery.", "Intraoperative pathology consultation based on multiple frozen sections from the mass was performed.", "A left modified radical mastectomy and lymph node dissection were done.", "The specimen was received in formalin.", "On serial sectioning, there were tan-brown firm masses with multiple cystic areas.", "The surgical margins were free from tumoral cells.", "The nipple was retracted.", "Sections were taken and stained by hematoxylin and eosin.", "Microscopically, neoplastic tissue composed of dilated ducts filled by papillary projections, cribriform and fused glands was seen.", "The neoplastic tissue was lined by mild to moderate atypical cells with scattered mitoses.", "There was no distinct myoepathelial layer.", "The neoplastic tissue was mostly floating in mucinous lakes with invasion to surrounding stroma.", "Foci of ductal carcinoma in situ including cribriform, papillary, and micropapillary patterns were present in about 30% of the tumor bulk.", "All surgical margins were free of tumor.", "An in situ component with papillary features was seen in the nipple.", "Nearby skin-deep dermis was involved by tumor.", "All 16 lymph nodes showed reactive changes.", "There was no perineural invasion.", "There was no lymphovascular invasion.", "Immunohistochemistry profile showed positive estrogen and progesterone receptors.", "Immunohistochemistry profile showed negative for HER2.", "The patient was discharged with regular follow-up."], "summary_subclaims": ["The patient is a 69-year-old female.", "The patient had a painful mass in her left breast.", "Intraoperative pathology consult showed neoplastic tissue mostly floating in mucinous lakes.", "Invasion to surrounding stroma was seen.", "Immunohistochemistry profile showed positive estrogen receptors.", "Immunohistochemistry profile showed positive progesterone receptors.", "Immunohistochemistry profile showed negative for HER2."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 69-year-old female.", "She had a painful lump in her left breast 3 months ago.", "She had bloody discharge from the left nipple four years ago.", "The patient decided not to follow-up despite recommendations for diagnostic procedure.", "On physical examination, an erythematous tender mass with hard consistency was detected around the nipple.", "Sonography showed a lobulated hypoechoic mass with microcystic areas measuring 20\u00d717 mm at 3 o'clock beside the areola.", "Mammography showed a hyperdense mass in the retroareolar site.", "The patient was admitted and underwent surgery.", "Intraoperative pathology consultation based on multiple frozen sections from the mass was performed.", "A left modified radical mastectomy and lymph node dissection were done.", "The specimen was received in formalin.", "On serial sectioning, there were tan-brown firm masses with multiple cystic areas.", "The surgical margins were free from tumoral cells.", "The nipple was retracted.", "Sections were taken and stained by hematoxylin and eosin.", "Microscopically, neoplastic tissue composed of dilated ducts filled by papillary projections, cribriform and fused glands was seen.", "The neoplastic tissue was lined by mild to moderate atypical cells with scattered mitoses.", "There was no distinct myoepathelial layer.", "The neoplastic tissue was mostly floating in mucinous lakes with invasion to surrounding stroma.", "Foci of ductal carcinoma in situ including cribriform, papillary, and micropapillary patterns were present in about 30% of the tumor bulk.", "All surgical margins were free of tumor.", "An in situ component with papillary features was seen in the nipple.", "Nearby skin-deep dermis was involved by tumor.", "All 16 lymph nodes showed reactive changes.", "There was no perineural invasion.", "There was no lymphovascular invasion.", "Immunohistochemistry profile showed positive estrogen and progesterone receptors.", "Immunohistochemistry profile showed negative for HER2.", "The patient was discharged with regular follow-up."], "index": 106, "original_id": "multiclinsum_test_2138_en.txt", "split": "test", "summary_subclaims": ["The patient is a 69-year-old female.", "The patient had a painful mass in her left breast.", "Intraoperative pathology consult showed neoplastic tissue mostly floating in mucinous lakes.", "Invasion to surrounding stroma was seen.", "Immunohistochemistry profile showed positive estrogen receptors.", "Immunohistochemistry profile showed positive progesterone receptors.", "Immunohistochemistry profile showed negative for HER2."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was a 48-year-old caucasian male.", "He had an extensive psychiatric history of depression.", "He was admitted to the intensive care unit following intoxication of approximately 20 g venlafaxine, 450 mg zolpidem, and 250 mg propiomazine.", "His past history included intensive care hospitalization due to two suicidal attempts through pharmacological intoxication.", "On admission, he was awake but drowsy.", "His Glasgow Coma Scale (GCS) was 13 of 15.", "His electrocardiography (ECG) was normal with a sinus rhythm of 57 beats per minute.", "Laboratory findings were within normal range.", "Admission occurred approximately 2 hours after intake of the pills.", "Activated charcoal suspension was administered via a nasogastric tube upon arrival at the intensive care unit.", "The patient was stable during the first 5 hours at the intensive care unit.", "Seven hours post-intoxication, he experienced tonic\u2013clonic seizures.", "This was successfully treated with diazepam 10 mg intravenously.", "He was intubated and sedated with propofol and remifentanil.", "Vasopressor support with low-dose norepinephrine was initiated.", "Nine hours after ingestion, his circulation began to slowly fail.", "Increased doses of norepinephrine were required.", "The patient developed metabolic acidosis with lactate elevation.", "Fifteen hours after ingestion, the patient\u2019s blood pressure fell rapidly despite high doses of norepinephrine.", "Prompt echocardiography revealed prominent hypokinesia with akinesia from the mid-left ventricle to the apex, as in TTC.", "The left ventricle ejection fraction (EF) was 20%.", "The right ventricle was also affected with a tricuspid annular plane systolic excursion (TAPSE) measuring 10 mm.", "Dobutamine was added to norepinephrine.", "Only a few micrograms of dobutamine were infused prior to cardiac arrest.", "The patient suffered a cardiac arrest with an initial rhythm of asystole.", "Advanced cardiac life support was initiated according to national guidelines.", "The patient was given three doses of epinephrine 1 mg intravenously.", "After 5 minutes without return of spontaneous circulation, the ECMO center at a tertiary hospital was contacted.", "Fifteen minutes post cardiac arrest, the patient regained circulation temporarily for approximately 10 minutes.", "The patient\u2019s circulatory status and blood pressure were inadequate during these 10 minutes.", "High-dose epinephrine infusion (1.0 \u00b5g/kg/minute) was initiated.", "Manual CPR continued for another 30 minutes.", "The patient was transported by helicopter to a tertiary hospital using mechanical CPR (AutoPulse Resuscitation System) and ongoing epinephrine infusion.", "Transportation time was approximately 30 minutes.", "One hour 15 minutes after the cardiac arrest, the patient was delivered to the tertiary hospital for ECMO initiation.", "Upon arrival at the tertiary hospital, the patient had a sinus rhythm but very low cardiac output.", "Blood pressure was 55/45 mmHg without cardiac arrest.", "External compression was continued whilst ECMO system treatment was established.", "Short pauses were taken during specifically vulnerable periods of the cannulation procedure.", "Lactate peaked at 4.6 mmol/L.", "Two hours after the cardiac arrest, the patient was on ECMO.", "After ECMO initiation, treatment with sedation and circulatory drugs continued.", "Continuous renal replacement therapy (CRRT) was initiated.", "CRRT was initiated due to anuria and creatinine level of 265 \u00b5mol/L.", "Sedation was reinitiated using midazolam and morphine instead of propofol and remifentanil.", "The amount of epinephrine was significantly decreased during the initial hours of ECMO treatment.", "Norepinephrine and milrinone were used instead.", "Multiple plasma and red cell concentrate (RCC) transfusions were also required due to significant bleeding from the femoral artery catheter.", "The patient was successfully weaned after 32 hours of ECMO.", "Epinephrine infusion was terminated the same day.", "Milrinone continued until the following day.", "The patient was transported back to the primary hospital with decreasing doses of norepinephrine the day after ECMO termination.", "Three days after the cardiac arrest, his cardiac function was echodynamically restored with an EF of above 55%.", "Values of the cardiac biomarker NT-proBNP decreased from 8360 ng/L the day after the cardiac arrest to 1190 ng/L 36 days after the intoxication.", "He was ventilated for 8 days.", "He received CRRT for 3 weeks.", "Two days after extubation, the patient gradually regained consciousness.", "Thirty days after the intoxication, he had regained normal cardiac and cognitive function.", "He left the hospital for further psychiatric treatment.", "The patient\u2019s renal function was fully restored with normal creatinine level (82 \u00b5mol/L) 7 weeks after the intoxication.", "He was finally discharged in good health without his former prescribed psychiatric medications.", "Two years later, his cardiac and renal function were normal.", "His psychiatric medication was reinstated.", "The serum venlafaxine concentration 24 hours after ingestion was 12.6 mg/L.", "This laboratory result was not received until 1 week after ingestion."], "summary_subclaims": ["The patient is a 48-year-old caucasian male.", "The patient has an extensive psychiatric history.", "The patient ingested a high dose of venlafaxine.", "The serum venlafaxine concentration was 12.6 mg/L 24 hours after ingestion.", "Seven hours post-ingestion, the patient experienced tonic-clonic seizures.", "Eight hours post-ingestion, takotsubo cardiomyopathy was recognized.", "The patient had a cardiac arrest.", "The patient was resuscitated with prolonged cardiopulmonary resuscitation.", "Ongoing automatic external compressions were used during helicopter transportation.", "The patient was transported to a tertiary hospital for extracorporeal membrane oxygenation treatment.", "The cardiopulmonary resuscitation duration was 2 hours.", "The patient received 36 hours of extracorporeal membrane oxygenation.", "The patient spent a total of 30 days in the intensive care unit.", "The patient made a full recovery."]}, "extra_info": {"fulltext_subclaims": ["The patient was a 48-year-old caucasian male.", "He had an extensive psychiatric history of depression.", "He was admitted to the intensive care unit following intoxication of approximately 20 g venlafaxine, 450 mg zolpidem, and 250 mg propiomazine.", "His past history included intensive care hospitalization due to two suicidal attempts through pharmacological intoxication.", "On admission, he was awake but drowsy.", "His Glasgow Coma Scale (GCS) was 13 of 15.", "His electrocardiography (ECG) was normal with a sinus rhythm of 57 beats per minute.", "Laboratory findings were within normal range.", "Admission occurred approximately 2 hours after intake of the pills.", "Activated charcoal suspension was administered via a nasogastric tube upon arrival at the intensive care unit.", "The patient was stable during the first 5 hours at the intensive care unit.", "Seven hours post-intoxication, he experienced tonic\u2013clonic seizures.", "This was successfully treated with diazepam 10 mg intravenously.", "He was intubated and sedated with propofol and remifentanil.", "Vasopressor support with low-dose norepinephrine was initiated.", "Nine hours after ingestion, his circulation began to slowly fail.", "Increased doses of norepinephrine were required.", "The patient developed metabolic acidosis with lactate elevation.", "Fifteen hours after ingestion, the patient\u2019s blood pressure fell rapidly despite high doses of norepinephrine.", "Prompt echocardiography revealed prominent hypokinesia with akinesia from the mid-left ventricle to the apex, as in TTC.", "The left ventricle ejection fraction (EF) was 20%.", "The right ventricle was also affected with a tricuspid annular plane systolic excursion (TAPSE) measuring 10 mm.", "Dobutamine was added to norepinephrine.", "Only a few micrograms of dobutamine were infused prior to cardiac arrest.", "The patient suffered a cardiac arrest with an initial rhythm of asystole.", "Advanced cardiac life support was initiated according to national guidelines.", "The patient was given three doses of epinephrine 1 mg intravenously.", "After 5 minutes without return of spontaneous circulation, the ECMO center at a tertiary hospital was contacted.", "Fifteen minutes post cardiac arrest, the patient regained circulation temporarily for approximately 10 minutes.", "The patient\u2019s circulatory status and blood pressure were inadequate during these 10 minutes.", "High-dose epinephrine infusion (1.0 \u00b5g/kg/minute) was initiated.", "Manual CPR continued for another 30 minutes.", "The patient was transported by helicopter to a tertiary hospital using mechanical CPR (AutoPulse Resuscitation System) and ongoing epinephrine infusion.", "Transportation time was approximately 30 minutes.", "One hour 15 minutes after the cardiac arrest, the patient was delivered to the tertiary hospital for ECMO initiation.", "Upon arrival at the tertiary hospital, the patient had a sinus rhythm but very low cardiac output.", "Blood pressure was 55/45 mmHg without cardiac arrest.", "External compression was continued whilst ECMO system treatment was established.", "Short pauses were taken during specifically vulnerable periods of the cannulation procedure.", "Lactate peaked at 4.6 mmol/L.", "Two hours after the cardiac arrest, the patient was on ECMO.", "After ECMO initiation, treatment with sedation and circulatory drugs continued.", "Continuous renal replacement therapy (CRRT) was initiated.", "CRRT was initiated due to anuria and creatinine level of 265 \u00b5mol/L.", "Sedation was reinitiated using midazolam and morphine instead of propofol and remifentanil.", "The amount of epinephrine was significantly decreased during the initial hours of ECMO treatment.", "Norepinephrine and milrinone were used instead.", "Multiple plasma and red cell concentrate (RCC) transfusions were also required due to significant bleeding from the femoral artery catheter.", "The patient was successfully weaned after 32 hours of ECMO.", "Epinephrine infusion was terminated the same day.", "Milrinone continued until the following day.", "The patient was transported back to the primary hospital with decreasing doses of norepinephrine the day after ECMO termination.", "Three days after the cardiac arrest, his cardiac function was echodynamically restored with an EF of above 55%.", "Values of the cardiac biomarker NT-proBNP decreased from 8360 ng/L the day after the cardiac arrest to 1190 ng/L 36 days after the intoxication.", "He was ventilated for 8 days.", "He received CRRT for 3 weeks.", "Two days after extubation, the patient gradually regained consciousness.", "Thirty days after the intoxication, he had regained normal cardiac and cognitive function.", "He left the hospital for further psychiatric treatment.", "The patient\u2019s renal function was fully restored with normal creatinine level (82 \u00b5mol/L) 7 weeks after the intoxication.", "He was finally discharged in good health without his former prescribed psychiatric medications.", "Two years later, his cardiac and renal function were normal.", "His psychiatric medication was reinstated.", "The serum venlafaxine concentration 24 hours after ingestion was 12.6 mg/L.", "This laboratory result was not received until 1 week after ingestion."], "index": 97, "original_id": "multiclinsum_test_985_en.txt", "split": "test", "summary_subclaims": ["The patient is a 48-year-old caucasian male.", "The patient has an extensive psychiatric history.", "The patient ingested a high dose of venlafaxine.", "The serum venlafaxine concentration was 12.6 mg/L 24 hours after ingestion.", "Seven hours post-ingestion, the patient experienced tonic-clonic seizures.", "Eight hours post-ingestion, takotsubo cardiomyopathy was recognized.", "The patient had a cardiac arrest.", "The patient was resuscitated with prolonged cardiopulmonary resuscitation.", "Ongoing automatic external compressions were used during helicopter transportation.", "The patient was transported to a tertiary hospital for extracorporeal membrane oxygenation treatment.", "The cardiopulmonary resuscitation duration was 2 hours.", "The patient received 36 hours of extracorporeal membrane oxygenation.", "The patient spent a total of 30 days in the intensive care unit.", "The patient made a full recovery."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was a 46-year-old male with end-stage renal disease of unknown cause.", "He had been on hemodialysis for 3 years.", "He underwent cadaveric renal transplantation 15 months ago.", "There was no other remarkable medical history except for 3 years of hypertension.", "The donor was after brain death.", "During harvesting of the donor\u2019s kidneys, a branch of right renal artery to renal superior polar was inadvertently cut off.", "The artery branch with a diameter 0.3 mm arose from the bifurcation of abdominal aorta and renal artery.", "The severed renal artery branch was anastomosed in situ with 7\u20130 prolene during the repair of the kidney.", "The cold ischemia time of the kidney was 5 min.", "The warm ischemia time of the kidney was 6 h.", "The right kidney of donor was transplanted in the right iliac fossa.", "The donor renal artery with a Carrel patch of donor aorta was anastomosed end-to-side to the recipient right external iliac artery with 6\u20130 prolene.", "The renal vein was anastomosed end-to-side to the recipient right external iliac vein with 5\u20130 prolene.", "The graft ureter was anastomosed to the urinary bladder of the recipient with a double J stent.", "Basiliximab was used as immunity induction on the day of surgery and the fourth day after transplantation.", "His immunosuppression regimen consisted of tacrolimus, mycophenolate sodium, and prednisolone.", "His immediate postoperative course was unremarkable.", "His blood pressure was controlled to 140\u2013156/90\u2013105 mmHg with nicardipine, spironolactone, and furosemide.", "The 24-h urine volume was between 1937 and 4100 ml.", "His renal function significantly improved, reaching a creatinine of 151 \u03bcmol/L on 11st day posttransplantation.", "From the 12nd day after transplantation, his blood pressure began to gradually increase to 170\u2013174/103\u2013109 mmHg.", "There was no positive presentation on clinical examination and ultrasonography.", "The level of creatinine and urine volume were also stable.", "Nicardipine was increased.", "It was still difficult to control his blood pressure even though three antihypertensive medications were administered.", "His blood pressure reached 190/120 mmHg on 20th day after transplantation.", "There was a decrease in 24-h urine volume with 1620\u20131725 ml.", "There was mild impairment of renal function with a creatinine of 194 \u03bcmol/L.", "A bruit became audible over the site of the transplanted kidney.", "Color Doppler ultrasonography indicated a decreased RI in intrarenal arteries.", "Color Doppler ultrasonography indicated increased blood flow of the transplant renal artery.", "The RI was 0.45.", "The peak systolic velocity was 305 cm/s.", "The velocity gradient between stenotic and prestenotic segment was more than 3:1.", "A vascular complication of TRAS was suspected.", "Diagnostic arteriography showed a 90% stenosis of transplant renal artery.", "The TRAS occurred in the distal site of the anastomosis instead of the anastomosis.", "We considered that the reconstructional renal artery branch stretched the trunk of renal artery, which resulted in the stenosis distal to the suture line.", "Renal artery angioplasty was undertaken through a retrograde ipsilateral femoral artery approach.", "Percutaneous transluminal stent implantation was performed.", "A bare stent (6 \u00d7 14 mm, Express Vascular SD) had to be chosen to avoid affecting the flow of the artery branch.", "After the bare stent was successfully deployed, a second angiographic evaluation verified the effectiveness of the intervention was obvious.", "After the interventional treatment, the renal function and urine volume recovered.", "His blood pressure was stably controlled to 121/80 mmHg with only two antihypertension medications (nifedipine and arotinolol).", "He was discharged on 28 day after transplantation with a creatinine of 108 \u03bcmol/L.", "The patient\u2019s renal function remains stable at clinical follow-up of 15 months."], "summary_subclaims": ["The patient is a 46-year-old male.", "The patient has end-stage renal disease of unknown cause.", "The patient received a cadaveric renal transplant one year ago.", "Three antihypertensive medications were administrated.", "His blood pressure increased to 190/120 mmHg 3 weeks posttransplantation.", "The level of creatinine increased to 194 \u03bcmol/L.", "Color Doppler ultrasonography indicated a decreased resistance index in intrarenal arteries.", "Color Doppler ultrasonography indicated increased blood flow of the transplant renal artery.", "A vascular complication of TRAS was suspected.", "Arteriography was performed.", "TRAS occurred in the distal site of the anastomosis instead of the anastomosis.", "Percutaneous transluminal bare stent implantation treatment was successfully performed.", "Satisfactory clinical efficacy with improvement in transplant renal function was achieved after the interventional treatment.", "Satisfactory clinical efficacy with improvement in renovascular hypertension was achieved after the interventional treatment."]}, "extra_info": {"fulltext_subclaims": ["The patient was a 46-year-old male with end-stage renal disease of unknown cause.", "He had been on hemodialysis for 3 years.", "He underwent cadaveric renal transplantation 15 months ago.", "There was no other remarkable medical history except for 3 years of hypertension.", "The donor was after brain death.", "During harvesting of the donor\u2019s kidneys, a branch of right renal artery to renal superior polar was inadvertently cut off.", "The artery branch with a diameter 0.3 mm arose from the bifurcation of abdominal aorta and renal artery.", "The severed renal artery branch was anastomosed in situ with 7\u20130 prolene during the repair of the kidney.", "The cold ischemia time of the kidney was 5 min.", "The warm ischemia time of the kidney was 6 h.", "The right kidney of donor was transplanted in the right iliac fossa.", "The donor renal artery with a Carrel patch of donor aorta was anastomosed end-to-side to the recipient right external iliac artery with 6\u20130 prolene.", "The renal vein was anastomosed end-to-side to the recipient right external iliac vein with 5\u20130 prolene.", "The graft ureter was anastomosed to the urinary bladder of the recipient with a double J stent.", "Basiliximab was used as immunity induction on the day of surgery and the fourth day after transplantation.", "His immunosuppression regimen consisted of tacrolimus, mycophenolate sodium, and prednisolone.", "His immediate postoperative course was unremarkable.", "His blood pressure was controlled to 140\u2013156/90\u2013105 mmHg with nicardipine, spironolactone, and furosemide.", "The 24-h urine volume was between 1937 and 4100 ml.", "His renal function significantly improved, reaching a creatinine of 151 \u03bcmol/L on 11st day posttransplantation.", "From the 12nd day after transplantation, his blood pressure began to gradually increase to 170\u2013174/103\u2013109 mmHg.", "There was no positive presentation on clinical examination and ultrasonography.", "The level of creatinine and urine volume were also stable.", "Nicardipine was increased.", "It was still difficult to control his blood pressure even though three antihypertensive medications were administered.", "His blood pressure reached 190/120 mmHg on 20th day after transplantation.", "There was a decrease in 24-h urine volume with 1620\u20131725 ml.", "There was mild impairment of renal function with a creatinine of 194 \u03bcmol/L.", "A bruit became audible over the site of the transplanted kidney.", "Color Doppler ultrasonography indicated a decreased RI in intrarenal arteries.", "Color Doppler ultrasonography indicated increased blood flow of the transplant renal artery.", "The RI was 0.45.", "The peak systolic velocity was 305 cm/s.", "The velocity gradient between stenotic and prestenotic segment was more than 3:1.", "A vascular complication of TRAS was suspected.", "Diagnostic arteriography showed a 90% stenosis of transplant renal artery.", "The TRAS occurred in the distal site of the anastomosis instead of the anastomosis.", "We considered that the reconstructional renal artery branch stretched the trunk of renal artery, which resulted in the stenosis distal to the suture line.", "Renal artery angioplasty was undertaken through a retrograde ipsilateral femoral artery approach.", "Percutaneous transluminal stent implantation was performed.", "A bare stent (6 \u00d7 14 mm, Express Vascular SD) had to be chosen to avoid affecting the flow of the artery branch.", "After the bare stent was successfully deployed, a second angiographic evaluation verified the effectiveness of the intervention was obvious.", "After the interventional treatment, the renal function and urine volume recovered.", "His blood pressure was stably controlled to 121/80 mmHg with only two antihypertension medications (nifedipine and arotinolol).", "He was discharged on 28 day after transplantation with a creatinine of 108 \u03bcmol/L.", "The patient\u2019s renal function remains stable at clinical follow-up of 15 months."], "index": 101, "original_id": "multiclinsum_test_1302_en.txt", "split": "test", "summary_subclaims": ["The patient is a 46-year-old male.", "The patient has end-stage renal disease of unknown cause.", "The patient received a cadaveric renal transplant one year ago.", "Three antihypertensive medications were administrated.", "His blood pressure increased to 190/120 mmHg 3 weeks posttransplantation.", "The level of creatinine increased to 194 \u03bcmol/L.", "Color Doppler ultrasonography indicated a decreased resistance index in intrarenal arteries.", "Color Doppler ultrasonography indicated increased blood flow of the transplant renal artery.", "A vascular complication of TRAS was suspected.", "Arteriography was performed.", "TRAS occurred in the distal site of the anastomosis instead of the anastomosis.", "Percutaneous transluminal bare stent implantation treatment was successfully performed.", "Satisfactory clinical efficacy with improvement in transplant renal function was achieved after the interventional treatment.", "Satisfactory clinical efficacy with improvement in renovascular hypertension was achieved after the interventional treatment."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was a 59-year-old male.", "The patient had no history of smoking.", "The carcinoembryonic antigen level was 5.6 ng/mL.", "Chest computed tomography revealed a tumor with a maximum diameter of 13 mm in the left lower pulmonary lobe.", "The tumor was suspected to be left lower lobe lung cancer (cT1bN0M0 stage1A2).", "Three-dimensional CT was performed using the Fujifilm Synapse Vincent system.", "A displaced B1 + 2 was running behind the main pulmonary artery.", "An anomalous V1 + 2 joined the left inferior pulmonary vein.", "Hyperlobulation between S1 + 2 and S3 with a completely fused interlobar fissure between S1 + 2 and S6 was observed.", "The interlobar plane between S1 + 2 and S6 ran perpendicular to the cranio-caudal direction.", "Bronchoscopy revealed that three bronchi branched from the left main bronchus.", "VATS was planned for surgical diagnosis and treatment.", "Non-anatomical wedge resection of the lesion was performed.", "The patient was diagnosed with adenocarcinoma.", "Left lower lobectomy and systematic nodal dissection were performed.", "The major pitfalls were to avoid injuring the displaced B1 + 2 and to avoid cutting the anomalous V1 + 2.", "The inferior pulmonary vein was identified on the posterior side of the hilum.", "The anomalous V1 + 2 joined the inferior pulmonary vein.", "The distal branch of A8 was identified using the interlobar fissure.", "A6 and V1 + 2 ran near A6 and a branch of V1 + 2 ran between S1 + 2 and S6.", "The branch of V1 + 2 was used as a landmark when dividing the fissure between S1 + 2 and the inferior lobe.", "Forceps were passed from the anterior to posterior side between a branch of V1 + 2 and A6.", "The largely fused fissure between S1 + 2 and the inferior lobe was divided using a stapler.", "A6 and A9 + 10 were identified and divided.", "The inferior bronchus branched from the left main bronchus at the level of the branches of B3 + B4 + 5 and the displaced B1 + 2.", "The displaced B1 + 2 was located at a more proximal site than normal.", "The station 11 lymph nodes were identified.", "Forceps were passed from the anterior to posterior side along the station 11 lymph nodes.", "The incomplete fissure between S5 and inferior lobe was divided using the stapler.", "The inferior bronchus was divided, which completed the lobectomy ND2a-2 procedure.", "The operation time was 185 min.", "Intraoperative blood loss was 30 mL.", "The tumor was diagnosed as an invasive mucinous adenocarcinoma with a maximal diameter of 15 mm.", "The pathological stage was p-T1aN0M0 stage I A1.", "The patient was discharged from hospital 6 days after the surgery."], "summary_subclaims": ["The patient was a 59-year-old male.", "The patient had suspected lung cancer in the left lower lobe.", "The patient was scheduled to undergo surgery.", "Chest computed tomography revealed a displaced B1 + 2.", "Chest computed tomography showed hyperlobulation between S1 + 2 and S3.", "The interlobar fissure between S1 + 2 and S6 was completely fused.", "Three-dimensional computed tomography revealed an anomalous V1 + 2 joining the left inferior pulmonary vein.", "A branch of the V1 + 2 ran between S1 + 2 and S6.", "The operation was a left lower lobectomy via video-assisted thoracic surgery.", "The strategy was to preserve V1 + 2.", "The strategy included confirming the locations of B1 + 2 and B6 when dividing the fissure."]}, "extra_info": {"fulltext_subclaims": ["The patient was a 59-year-old male.", "The patient had no history of smoking.", "The carcinoembryonic antigen level was 5.6 ng/mL.", "Chest computed tomography revealed a tumor with a maximum diameter of 13 mm in the left lower pulmonary lobe.", "The tumor was suspected to be left lower lobe lung cancer (cT1bN0M0 stage1A2).", "Three-dimensional CT was performed using the Fujifilm Synapse Vincent system.", "A displaced B1 + 2 was running behind the main pulmonary artery.", "An anomalous V1 + 2 joined the left inferior pulmonary vein.", "Hyperlobulation between S1 + 2 and S3 with a completely fused interlobar fissure between S1 + 2 and S6 was observed.", "The interlobar plane between S1 + 2 and S6 ran perpendicular to the cranio-caudal direction.", "Bronchoscopy revealed that three bronchi branched from the left main bronchus.", "VATS was planned for surgical diagnosis and treatment.", "Non-anatomical wedge resection of the lesion was performed.", "The patient was diagnosed with adenocarcinoma.", "Left lower lobectomy and systematic nodal dissection were performed.", "The major pitfalls were to avoid injuring the displaced B1 + 2 and to avoid cutting the anomalous V1 + 2.", "The inferior pulmonary vein was identified on the posterior side of the hilum.", "The anomalous V1 + 2 joined the inferior pulmonary vein.", "The distal branch of A8 was identified using the interlobar fissure.", "A6 and V1 + 2 ran near A6 and a branch of V1 + 2 ran between S1 + 2 and S6.", "The branch of V1 + 2 was used as a landmark when dividing the fissure between S1 + 2 and the inferior lobe.", "Forceps were passed from the anterior to posterior side between a branch of V1 + 2 and A6.", "The largely fused fissure between S1 + 2 and the inferior lobe was divided using a stapler.", "A6 and A9 + 10 were identified and divided.", "The inferior bronchus branched from the left main bronchus at the level of the branches of B3 + B4 + 5 and the displaced B1 + 2.", "The displaced B1 + 2 was located at a more proximal site than normal.", "The station 11 lymph nodes were identified.", "Forceps were passed from the anterior to posterior side along the station 11 lymph nodes.", "The incomplete fissure between S5 and inferior lobe was divided using the stapler.", "The inferior bronchus was divided, which completed the lobectomy ND2a-2 procedure.", "The operation time was 185 min.", "Intraoperative blood loss was 30 mL.", "The tumor was diagnosed as an invasive mucinous adenocarcinoma with a maximal diameter of 15 mm.", "The pathological stage was p-T1aN0M0 stage I A1.", "The patient was discharged from hospital 6 days after the surgery."], "index": 91, "original_id": "multiclinsum_test_2752_en.txt", "split": "test", "summary_subclaims": ["The patient was a 59-year-old male.", "The patient had suspected lung cancer in the left lower lobe.", "The patient was scheduled to undergo surgery.", "Chest computed tomography revealed a displaced B1 + 2.", "Chest computed tomography showed hyperlobulation between S1 + 2 and S3.", "The interlobar fissure between S1 + 2 and S6 was completely fused.", "Three-dimensional computed tomography revealed an anomalous V1 + 2 joining the left inferior pulmonary vein.", "A branch of the V1 + 2 ran between S1 + 2 and S6.", "The operation was a left lower lobectomy via video-assisted thoracic surgery.", "The strategy was to preserve V1 + 2.", "The strategy included confirming the locations of B1 + 2 and B6 when dividing the fissure."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 63-year-old woman.", "She had recurrent upper abdominal fullness discomfort for almost 10 years.", "She experienced exacerbation of intermittent nausea, vomiting with chyme (5 mL), heartburn, acid regurgitation, and eructation for 6 months.", "No history of hypertension, diabetes mellitus, or coronary heart disease was noted.", "A 5 \u00d7 4 cm mass with a hard texture and poor mobility was observed in the upper abdomen.", "Routine blood and tumor marker test results were within normal range.", "Abdomen CT showed a 32 mm \u00d7 22 mm soft tissue mass shadow with homogeneous density in the descending duodenum.", "The mass was protruding into the duodenal lumen.", "Thickening of the adjacent intestinal wall was noted.", "Upper abdomen MRI revealed significant thickening of the wall of the duodenal bulb and descending duodenum.", "The wall thickness was 1.1 cm.", "The signals were slightly low in T1-weighted images.", "The signals were slightly high in T2-weighted images.", "Endoscopic ultrasonography showed a protrusion in the duodenal bulb of about 26 \u00d7 18 mm in size.", "The protrusion had a clear boundary, smooth surface, and irregular shape.", "The base of the protrusion was about 17 mm.", "Color signals abound were noted.", "Neoplasm resection of the duodenum was performed.", "A mass measuring about 25 \u00d7 30 \u00d7 10 mm was found in the descending duodenum.", "The mass was soft, brittle, and mobile.", "The mass had a clear boundary.", "The pathological result revealed multiple Brunner\u2019s glands with tubes, fibers, and smooth muscle diffuse distribution.", "No dysplasia was noted on the epithelium.", "It was diagnosed as Brunner\u2019s gland adenoma of the duodenum.", "The patient was discharged from the hospital a week after recovery.", "To date, no relapse has occurred."], "summary_subclaims": ["The patient is a 63-year-old woman.", "The patient had upper gastrointestinal obstruction for almost 10 years.", "The patient was pathologically diagnosed with large Brunner's gland adenoma of the duodenum.", "Postoperatively, no sign of recurrence has been noted until now."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 63-year-old woman.", "She had recurrent upper abdominal fullness discomfort for almost 10 years.", "She experienced exacerbation of intermittent nausea, vomiting with chyme (5 mL), heartburn, acid regurgitation, and eructation for 6 months.", "No history of hypertension, diabetes mellitus, or coronary heart disease was noted.", "A 5 \u00d7 4 cm mass with a hard texture and poor mobility was observed in the upper abdomen.", "Routine blood and tumor marker test results were within normal range.", "Abdomen CT showed a 32 mm \u00d7 22 mm soft tissue mass shadow with homogeneous density in the descending duodenum.", "The mass was protruding into the duodenal lumen.", "Thickening of the adjacent intestinal wall was noted.", "Upper abdomen MRI revealed significant thickening of the wall of the duodenal bulb and descending duodenum.", "The wall thickness was 1.1 cm.", "The signals were slightly low in T1-weighted images.", "The signals were slightly high in T2-weighted images.", "Endoscopic ultrasonography showed a protrusion in the duodenal bulb of about 26 \u00d7 18 mm in size.", "The protrusion had a clear boundary, smooth surface, and irregular shape.", "The base of the protrusion was about 17 mm.", "Color signals abound were noted.", "Neoplasm resection of the duodenum was performed.", "A mass measuring about 25 \u00d7 30 \u00d7 10 mm was found in the descending duodenum.", "The mass was soft, brittle, and mobile.", "The mass had a clear boundary.", "The pathological result revealed multiple Brunner\u2019s glands with tubes, fibers, and smooth muscle diffuse distribution.", "No dysplasia was noted on the epithelium.", "It was diagnosed as Brunner\u2019s gland adenoma of the duodenum.", "The patient was discharged from the hospital a week after recovery.", "To date, no relapse has occurred."], "index": 108, "original_id": "multiclinsum_test_2813_en.txt", "split": "test", "summary_subclaims": ["The patient is a 63-year-old woman.", "The patient had upper gastrointestinal obstruction for almost 10 years.", "The patient was pathologically diagnosed with large Brunner's gland adenoma of the duodenum.", "Postoperatively, no sign of recurrence has been noted until now."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 30-year-old male.", "He is from the city of Intuto.", "Intuto is located 172 km from the city of Iquitos.", "He has a history of untreated type 2 diabetes mellitus.", "He presented to the emergency department of the Regional Hospital of Loreto.", "He had convulsions.", "He had loss of consciousness.", "He had functional limitations.", "He had chills.", "He had headache.", "He had a feeling of heat.", "He had poor general condition.", "His blood pressure was 90/60 mmHg.", "His heart rate was 67/min.", "His respiratory rate was 20/min.", "His temperature was 36.5 \u00b0C.", "His oxygen saturation was 96%.", "His weight was 60 kg.", "His BMI was 19.6 m\u00b2.", "He had pallor ++/+++.", "He was prostrate.", "He had general malaise.", "He had coldness of extremities.", "He had sensory disorder.", "He had myalgia.", "He had arthralgia.", "The illness lasted 14 days.", "The illness began with convulsions of 1 to 2 minutes.", "The convulsions occurred 5 to 6 times a day.", "Two days before admission, he had loss of consciousness.", "Two days before admission, he had limited motor function.", "He was transferred to the nearest health center.", "At the health center, a thick and extended gout examination was performed.", "Plasmodium vivax trophozoites were observed.", "Treatment was initiated.", "The doctor decided to refer him to a health center of greater complexity.", "He went to the emergency department of the Regional Hospital of Loreto.", "He was hospitalized.", "He received intravenous artesunate 14.4 mg at admission.", "Intravenous artesunate was repeated at 12 and 24 h.", "Each dose was diluted with 5% dextrose in a volume of 5 to 10 ml.", "Each dose was administered as a 5 min bolus.", "Artesunate was continued at 24 mg orally until day 5.", "600 mg of clindamycin was infused over 20 to 30 min every 12 h for 5 days.", "Clindamycin was diluted in 50 ml of 0.9% sodium chloride.", "A packed red blood cell transfusion was performed.", "Primaquine was continued for 7 days.", "A new thick blood examination was performed.", "No parasite was observed in the thick blood examination.", "The laboratory examinations showed depression of the three series of blood cells.", "The peripheral sheet extension was typical granulocytes ++.", "The peripheral sheet extension showed atypical lymphocytes +.", "The erythrocyte series showed microcytosis.", "The erythrocyte series showed anisocytosis.", "The erythrocyte series showed basophilic punctate.", "The abdominal ultrasound showed splenomegaly.", "The abdominal ultrasound showed bilateral pleural effusion.", "A lumbar puncture was performed.", "Cerebrospinal fluid analysis was performed.", "The patient showed clinical improvement.", "The patient had a neurological sequela of monoparesia of the motor nerves in the lower left."], "summary_subclaims": ["The patient is an adult male.", "The patient has cerebral malaria by Plasmodium vivax.", "The patient starts with general discomfort and fever.", "The patient presents convulsions more than twice a day.", "The patient has loss of consciousness.", "The patient has motor functional limitation.", "A thick drop shows Plasmodium vivax trophozoites.", "A thick drop shows depression of the three blood series.", "The patient is given treatment with artesunate and clindamycin for five days.", "The patient receives a blood transfusion.", "The patient continues with primaquine for seven days.", "The patient shows clinical improvement.", "The patient has neurological sequelae in the left lower extremity."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 30-year-old male.", "He is from the city of Intuto.", "Intuto is located 172 km from the city of Iquitos.", "He has a history of untreated type 2 diabetes mellitus.", "He presented to the emergency department of the Regional Hospital of Loreto.", "He had convulsions.", "He had loss of consciousness.", "He had functional limitations.", "He had chills.", "He had headache.", "He had a feeling of heat.", "He had poor general condition.", "His blood pressure was 90/60 mmHg.", "His heart rate was 67/min.", "His respiratory rate was 20/min.", "His temperature was 36.5 \u00b0C.", "His oxygen saturation was 96%.", "His weight was 60 kg.", "His BMI was 19.6 m\u00b2.", "He had pallor ++/+++.", "He was prostrate.", "He had general malaise.", "He had coldness of extremities.", "He had sensory disorder.", "He had myalgia.", "He had arthralgia.", "The illness lasted 14 days.", "The illness began with convulsions of 1 to 2 minutes.", "The convulsions occurred 5 to 6 times a day.", "Two days before admission, he had loss of consciousness.", "Two days before admission, he had limited motor function.", "He was transferred to the nearest health center.", "At the health center, a thick and extended gout examination was performed.", "Plasmodium vivax trophozoites were observed.", "Treatment was initiated.", "The doctor decided to refer him to a health center of greater complexity.", "He went to the emergency department of the Regional Hospital of Loreto.", "He was hospitalized.", "He received intravenous artesunate 14.4 mg at admission.", "Intravenous artesunate was repeated at 12 and 24 h.", "Each dose was diluted with 5% dextrose in a volume of 5 to 10 ml.", "Each dose was administered as a 5 min bolus.", "Artesunate was continued at 24 mg orally until day 5.", "600 mg of clindamycin was infused over 20 to 30 min every 12 h for 5 days.", "Clindamycin was diluted in 50 ml of 0.9% sodium chloride.", "A packed red blood cell transfusion was performed.", "Primaquine was continued for 7 days.", "A new thick blood examination was performed.", "No parasite was observed in the thick blood examination.", "The laboratory examinations showed depression of the three series of blood cells.", "The peripheral sheet extension was typical granulocytes ++.", "The peripheral sheet extension showed atypical lymphocytes +.", "The erythrocyte series showed microcytosis.", "The erythrocyte series showed anisocytosis.", "The erythrocyte series showed basophilic punctate.", "The abdominal ultrasound showed splenomegaly.", "The abdominal ultrasound showed bilateral pleural effusion.", "A lumbar puncture was performed.", "Cerebrospinal fluid analysis was performed.", "The patient showed clinical improvement.", "The patient had a neurological sequela of monoparesia of the motor nerves in the lower left."], "index": 95, "original_id": "multiclinsum_test_3364_en.txt", "split": "test", "summary_subclaims": ["The patient is an adult male.", "The patient has cerebral malaria by Plasmodium vivax.", "The patient starts with general discomfort and fever.", "The patient presents convulsions more than twice a day.", "The patient has loss of consciousness.", "The patient has motor functional limitation.", "A thick drop shows Plasmodium vivax trophozoites.", "A thick drop shows depression of the three blood series.", "The patient is given treatment with artesunate and clindamycin for five days.", "The patient receives a blood transfusion.", "The patient continues with primaquine for seven days.", "The patient shows clinical improvement.", "The patient has neurological sequelae in the left lower extremity."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient was a 59-year-old morbidly obese, African-American female.", "She had a history of Stage IIIc recurrent endometrial carcinosarcoma with para-aortic and pelvic lymph node involvement.", "She had a 1-month history of numbness of the left vulva.", "She had worsening left lower extremity pain/numbness.", "She had episodic urinary incontinence.", "The thoracic/lumbar MR revealed a 1.4 \u00d7 1.8 cm enhancing intradural extramedullary mass inferior to the conus at the L1 and L4-L5 levels.", "There was abnormal enhancement of the left-sided intradural nerve roots.", "There were bilateral, perihilar lung metastases.", "The patient underwent a T12-L2 laminectomy for gross total resection of the L1 intradural/extramedullary mass.", "The main aim of surgery was to provide neurological symptomatic relief.", "Intraoperatively, diffuse carcinomatosis of the cauda equina was observed.", "A large lesion was located anteroinferior to the conus.", "The tumor appeared vascular and involved multiple, swollen, engorged nerve roots.", "Dissection ceased once intraoperative electromyographic monitoring showed significant changes.", "The permanent pathology showed a mesenchymal malignant Mullerian mixed tumor (carcinosarcoma) without an epithelial component.", "The postoperative MR revealed residual intradural extramedullary tumor.", "The pain and numbness improved in her left lower extremity.", "She returned to the hospital 2 weeks later complaining of increased lower extremity symptoms.", "She had the new onset of right-sided facial weakness, numbness, and blurry vision.", "Imaging of the brain and spinal cord revealed leptomeningeal spread of her disease.", "Imaging revealed hydrocephalus.", "Imaging revealed multiple, new intracranial metastases.", "Two months later, she succumbed to her metastatic disease."], "summary_subclaims": ["The patient is a 59-year-old female.", "The patient has a history of recurrent UCS.", "The patient had new onset of left lower extremity pain.", "The patient had new onset of numbness.", "The patient had episodic urinary incontinence.", "MR revealed an enhancing intradural extramedullary mass posterior to the L1 vertebral body.", "The patient underwent a focal decompressive laminectomy.", "The patient improved neurologically postoperatively.", "The patient succumbed to the leptomeningeal spread of her disease.", "The patient died within 2 postoperative months."]}, "extra_info": {"fulltext_subclaims": ["The patient was a 59-year-old morbidly obese, African-American female.", "She had a history of Stage IIIc recurrent endometrial carcinosarcoma with para-aortic and pelvic lymph node involvement.", "She had a 1-month history of numbness of the left vulva.", "She had worsening left lower extremity pain/numbness.", "She had episodic urinary incontinence.", "The thoracic/lumbar MR revealed a 1.4 \u00d7 1.8 cm enhancing intradural extramedullary mass inferior to the conus at the L1 and L4-L5 levels.", "There was abnormal enhancement of the left-sided intradural nerve roots.", "There were bilateral, perihilar lung metastases.", "The patient underwent a T12-L2 laminectomy for gross total resection of the L1 intradural/extramedullary mass.", "The main aim of surgery was to provide neurological symptomatic relief.", "Intraoperatively, diffuse carcinomatosis of the cauda equina was observed.", "A large lesion was located anteroinferior to the conus.", "The tumor appeared vascular and involved multiple, swollen, engorged nerve roots.", "Dissection ceased once intraoperative electromyographic monitoring showed significant changes.", "The permanent pathology showed a mesenchymal malignant Mullerian mixed tumor (carcinosarcoma) without an epithelial component.", "The postoperative MR revealed residual intradural extramedullary tumor.", "The pain and numbness improved in her left lower extremity.", "She returned to the hospital 2 weeks later complaining of increased lower extremity symptoms.", "She had the new onset of right-sided facial weakness, numbness, and blurry vision.", "Imaging of the brain and spinal cord revealed leptomeningeal spread of her disease.", "Imaging revealed hydrocephalus.", "Imaging revealed multiple, new intracranial metastases.", "Two months later, she succumbed to her metastatic disease."], "index": 103, "original_id": "multiclinsum_test_2588_en.txt", "split": "test", "summary_subclaims": ["The patient is a 59-year-old female.", "The patient has a history of recurrent UCS.", "The patient had new onset of left lower extremity pain.", "The patient had new onset of numbness.", "The patient had episodic urinary incontinence.", "MR revealed an enhancing intradural extramedullary mass posterior to the L1 vertebral body.", "The patient underwent a focal decompressive laminectomy.", "The patient improved neurologically postoperatively.", "The patient succumbed to the leptomeningeal spread of her disease.", "The patient died within 2 postoperative months."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 69-year-old Tunisian female.", "She has no family history of auto-immune disease.", "She had a history of hypertension.", "She was explored 4 years prior to admission for transient arthralgias and arthritis.", "She experienced photosensitivity, malar rash, and diffuse discoid lesions in her trunk and face.", "She reported weight loss of approximately 3 kg in the last three months.", "The physical examination showed synovitis of the wrists.", "The autoimmune profile confirmed a strong positivity of Antinuclear antibodies (ANA) with titre 1:400.", "The autoimmune profile showed anti-double-stranded DNA (anti-dsDNA) at 115 UI/ml.", "The autoimmune profile showed normal serum complements.", "The patient was non-reactive for anti-La antibodies.", "The patient was non-reactive for anti-cardiolipin antibodies.", "The patient was non-reactive for lupus anticoagulant.", "The patient was non-reactive for anti-SM antibodies.", "The patient was non-reactive for anti-RNP antibodies.", "The patient was non-reactive for anti-SCL-70 antibodies.", "The patient was non-reactive for anticentromere antibodies.", "The patient was non-reactive for rheumatoid factor.", "The patient was non-reactive for autoantibodies against citrullinated protein.", "The presence of 6 of 11 American College of Rheumatology criteria allowed the diagnosis of SLE.", "The patient was treated with Chloroquine (200 mg/day).", "The patient showed improvement of her general state of health.", "The patient showed weight gain.", "One year later, she developed liver dysfunction.", "Antimitochondrial antibodies (AMA) were positive (1:164).", "Antimitochondrial antibodies were positive with positive anti-E2 fraction.", "The antinuclear antibody was positive.", "The anti-dsDNA was positive.", "Serologic markers for hepatitis B and hepatitis C viruses were negative.", "Abdominal echo showed no fatty change of the liver.", "Abdominal echo showed no abnormality of the bile ducts.", "Microscopic examination reveals a focal florid duct lesion characterized by a portal lymphocytic infiltrate and epitheloid cells that are centred on interlobular ducts with evidence of destruction.", "These lesions are associated with a lymphocytic cholangitis and a portal inflammation containing conspicuous plasma cells and numerous lymphocytes.", "No granuloma was found in lobule.", "These findings led to a diagnosis of stage I PBC according to Scheuer\u2019s classification.", "Based on the hematology and liver-tissue results, she was diagnosed with asymptomatic PBC.", "Treatment with ursodeoxycholic acid (600 mg daily) was started.", "The transaminase levels normalized with one month.", "The patient has not complained liver dysfunction.", "She was followed up regularly with stable health."], "summary_subclaims": ["The patient is a 70-years-old woman.", "The patient was diagnosed with SLE at 69\u2009years.", "The patient was admitted for further examination of liver dysfunction.", "PBC was confirmed based on elevated serum levels of transaminase.", "PBC was confirmed based on high levels of antimitochondrial antibodies.", "PBC was confirmed following a liver biopsy.", "The oral administration of ursodeoxycholic acid stabilized the liver dysfunction."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 69-year-old Tunisian female.", "She has no family history of auto-immune disease.", "She had a history of hypertension.", "She was explored 4 years prior to admission for transient arthralgias and arthritis.", "She experienced photosensitivity, malar rash, and diffuse discoid lesions in her trunk and face.", "She reported weight loss of approximately 3 kg in the last three months.", "The physical examination showed synovitis of the wrists.", "The autoimmune profile confirmed a strong positivity of Antinuclear antibodies (ANA) with titre 1:400.", "The autoimmune profile showed anti-double-stranded DNA (anti-dsDNA) at 115 UI/ml.", "The autoimmune profile showed normal serum complements.", "The patient was non-reactive for anti-La antibodies.", "The patient was non-reactive for anti-cardiolipin antibodies.", "The patient was non-reactive for lupus anticoagulant.", "The patient was non-reactive for anti-SM antibodies.", "The patient was non-reactive for anti-RNP antibodies.", "The patient was non-reactive for anti-SCL-70 antibodies.", "The patient was non-reactive for anticentromere antibodies.", "The patient was non-reactive for rheumatoid factor.", "The patient was non-reactive for autoantibodies against citrullinated protein.", "The presence of 6 of 11 American College of Rheumatology criteria allowed the diagnosis of SLE.", "The patient was treated with Chloroquine (200 mg/day).", "The patient showed improvement of her general state of health.", "The patient showed weight gain.", "One year later, she developed liver dysfunction.", "Antimitochondrial antibodies (AMA) were positive (1:164).", "Antimitochondrial antibodies were positive with positive anti-E2 fraction.", "The antinuclear antibody was positive.", "The anti-dsDNA was positive.", "Serologic markers for hepatitis B and hepatitis C viruses were negative.", "Abdominal echo showed no fatty change of the liver.", "Abdominal echo showed no abnormality of the bile ducts.", "Microscopic examination reveals a focal florid duct lesion characterized by a portal lymphocytic infiltrate and epitheloid cells that are centred on interlobular ducts with evidence of destruction.", "These lesions are associated with a lymphocytic cholangitis and a portal inflammation containing conspicuous plasma cells and numerous lymphocytes.", "No granuloma was found in lobule.", "These findings led to a diagnosis of stage I PBC according to Scheuer\u2019s classification.", "Based on the hematology and liver-tissue results, she was diagnosed with asymptomatic PBC.", "Treatment with ursodeoxycholic acid (600 mg daily) was started.", "The transaminase levels normalized with one month.", "The patient has not complained liver dysfunction.", "She was followed up regularly with stable health."], "index": 109, "original_id": "multiclinsum_test_2272_en.txt", "split": "test", "summary_subclaims": ["The patient is a 70-years-old woman.", "The patient was diagnosed with SLE at 69\u2009years.", "The patient was admitted for further examination of liver dysfunction.", "PBC was confirmed based on elevated serum levels of transaminase.", "PBC was confirmed based on high levels of antimitochondrial antibodies.", "PBC was confirmed following a liver biopsy.", "The oral administration of ursodeoxycholic acid stabilized the liver dysfunction."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": {"fulltext_subclaims": ["A previously healthy 64-year-old male was admitted to the hospital with headache, fever and later imbalance, blurred vision and general slowness.", "Patient\u2019s neurological examination revealed nuchal rigidity and general clumsiness.", "Blood tests showed leukocytosis (11.90 \u00d7 109/l) and an increased C-reactive protein (47 mg/l).", "A computer tomography (CT) scan of the brain showed normal results.", "The cerebrospinal fluid (CSF) was clear but yellowish.", "The CSF had a slightly elevated count of erythrocytes (10 \u00d7 106/l).", "The CSF had high levels of leukocytes (940 \u00d7 106/l; 40% lymphocytes and 56% granulocytes).", "The CSF had elevated protein levels (1,696 mg/l).", "The CSF had hypoglycorrhachia (0.9 mmol/l).", "Bacterial cultures and CSF staining remained negative.", "Meningitis was suspected.", "The patient was treated with intravenous (IV) dexamethasone (10 mg four times a day).", "The patient was treated with ceftriaxone (4 g daily).", "The patient was treated with acyclovir (750 mg three times a day).", "Four days after admission, when his C-reactive protein had decreased to 10 mg/l, viral meningitis was considered the most probable cause.", "The treatment with ceftriaxone and dexamethasone was discontinued.", "The acyclovir treatment continued.", "Nine days after admission, the patient\u2019s general condition slowly deteriorated.", "The patient became increasingly somnolent.", "The patient was restarted on IV ceftriaxone (2 g daily, which was increased to 4 g daily one day later).", "The patient was treated with doxycycline (100 mg twice a day) due to the suspicion of borreliosis.", "Brain magnetic resonance imaging (MRI) was performed.", "The MRI revealed signs compatible with ventriculitis in the right lateral ventricle and the third ventricle.", "Eleven days after admission, the patient\u2019s consciousness rapidly declined.", "A new CT scan of the brain revealed hydrocephalus and a mild midline shift, attributed to the enlarged right lateral ventricle.", "An emergency ventriculostomy was performed.", "Cerebrospinal fluid obtained during the operation appeared clear but yellowish.", "Later debris was observed in the CSF collector bag.", "Doxycycline was discontinued.", "Due to the neurosurgeon\u2019s suspicion of a poor clinical response to ceftriaxone, it was switched to IV cefotaxime (2 g three times a day).", "The dosage of cefotaxime was increased to 2 g four times a day by an infection consultant two days later.", "No signs of renal dysfunction were detected.", "Serum creatinine levels remained within the normal range.", "The patient\u2019s condition rapidly improved after the ventriculostomy and antibiotic treatment.", "On the 21st day after admission, the ventriculostomy was closed.", "In the Gram staining of the CSF sample obtained from the ventriculostomy at the time of the operation, chains of gram-positive cocci were observed inside polymorphonuclear leukocytes.", "The bacteria\u2019s morphology resembled that of streptococci.", "Bacterial cultures of both CSF and blood remained negative.", "The sample, which displayed bacteria in the Gram staining, and another CSF sample taken one day later, were analyzed using in-house bacterial 16s ribosomal RNA gene amplification by polymerase chain reaction (PCR) with high sensitivity for both aerobic and anaerobic bacteria, followed by sequencing.", "The analysis of both samples tested positive for S. intermedius.", "No clinical signs of infective endocarditis were observed in further assessments.", "Echocardiography was not performed.", "The patient mentioned a history of chronic dental problems.", "An orthopantomography revealed advanced periodontal destruction in several teeth.", "Periapical abscesses were found in teeth 33 and 31.", "Maxillary teeth 15 and 16 were urgently extracted.", "Teeth 17, 23, 24, 31, 32, 33, and 43 were extracted.", "During the latter operation, prophylactic metronidazole (500 mg three times a day) was initiated for three days.", "The patient continued to improve and was discharged in good condition one month after admission, with only slight left-sided hemiparesis."], "summary_subclaims": ["The patient was a 64-year-old male.", "The patient was admitted to the hospital with a headache.", "The patient had fever.", "The patient later had imbalance.", "The patient had blurred vision.", "The patient had general slowness.", "Neurological examination revealed nuchal rigidity.", "Neurological examination revealed general clumsiness.", "Meningitis was suspected.", "The patient was treated with dexamethasone.", "The patient was treated with ceftriaxone.", "The patient was treated with acyclovir.", "A brain CT scan was normal.", "CSF Gram staining remained negative.", "Bacterial cultures remained negative.", "The antibacterial treatment was discontinued.", "Nine days after admission, the patient's condition deteriorated.", "The antibacterial treatment was restarted.", "A brain MRI revealed ventriculitis.", "A CT scan showed hydrocephalus.", "A ventriculostomy was performed.", "In CSF Gram staining, chains of gram-positive cocci were observed.", "Bacterial cultures remained negative.", "A bacterial PCR detected Streptococcus intermedius.", "An orthopantomography revealed advanced periodontal destruction in several teeth.", "An orthopantomography revealed periapical abscesses.", "The teeth with periapical abscesses were subsequently operated on.", "The patient was discharged in good condition after one month."]}, "extra_info": {"fulltext_subclaims": ["A previously healthy 64-year-old male was admitted to the hospital with headache, fever and later imbalance, blurred vision and general slowness.", "Patient\u2019s neurological examination revealed nuchal rigidity and general clumsiness.", "Blood tests showed leukocytosis (11.90 \u00d7 109/l) and an increased C-reactive protein (47 mg/l).", "A computer tomography (CT) scan of the brain showed normal results.", "The cerebrospinal fluid (CSF) was clear but yellowish.", "The CSF had a slightly elevated count of erythrocytes (10 \u00d7 106/l).", "The CSF had high levels of leukocytes (940 \u00d7 106/l; 40% lymphocytes and 56% granulocytes).", "The CSF had elevated protein levels (1,696 mg/l).", "The CSF had hypoglycorrhachia (0.9 mmol/l).", "Bacterial cultures and CSF staining remained negative.", "Meningitis was suspected.", "The patient was treated with intravenous (IV) dexamethasone (10 mg four times a day).", "The patient was treated with ceftriaxone (4 g daily).", "The patient was treated with acyclovir (750 mg three times a day).", "Four days after admission, when his C-reactive protein had decreased to 10 mg/l, viral meningitis was considered the most probable cause.", "The treatment with ceftriaxone and dexamethasone was discontinued.", "The acyclovir treatment continued.", "Nine days after admission, the patient\u2019s general condition slowly deteriorated.", "The patient became increasingly somnolent.", "The patient was restarted on IV ceftriaxone (2 g daily, which was increased to 4 g daily one day later).", "The patient was treated with doxycycline (100 mg twice a day) due to the suspicion of borreliosis.", "Brain magnetic resonance imaging (MRI) was performed.", "The MRI revealed signs compatible with ventriculitis in the right lateral ventricle and the third ventricle.", "Eleven days after admission, the patient\u2019s consciousness rapidly declined.", "A new CT scan of the brain revealed hydrocephalus and a mild midline shift, attributed to the enlarged right lateral ventricle.", "An emergency ventriculostomy was performed.", "Cerebrospinal fluid obtained during the operation appeared clear but yellowish.", "Later debris was observed in the CSF collector bag.", "Doxycycline was discontinued.", "Due to the neurosurgeon\u2019s suspicion of a poor clinical response to ceftriaxone, it was switched to IV cefotaxime (2 g three times a day).", "The dosage of cefotaxime was increased to 2 g four times a day by an infection consultant two days later.", "No signs of renal dysfunction were detected.", "Serum creatinine levels remained within the normal range.", "The patient\u2019s condition rapidly improved after the ventriculostomy and antibiotic treatment.", "On the 21st day after admission, the ventriculostomy was closed.", "In the Gram staining of the CSF sample obtained from the ventriculostomy at the time of the operation, chains of gram-positive cocci were observed inside polymorphonuclear leukocytes.", "The bacteria\u2019s morphology resembled that of streptococci.", "Bacterial cultures of both CSF and blood remained negative.", "The sample, which displayed bacteria in the Gram staining, and another CSF sample taken one day later, were analyzed using in-house bacterial 16s ribosomal RNA gene amplification by polymerase chain reaction (PCR) with high sensitivity for both aerobic and anaerobic bacteria, followed by sequencing.", "The analysis of both samples tested positive for S. intermedius.", "No clinical signs of infective endocarditis were observed in further assessments.", "Echocardiography was not performed.", "The patient mentioned a history of chronic dental problems.", "An orthopantomography revealed advanced periodontal destruction in several teeth.", "Periapical abscesses were found in teeth 33 and 31.", "Maxillary teeth 15 and 16 were urgently extracted.", "Teeth 17, 23, 24, 31, 32, 33, and 43 were extracted.", "During the latter operation, prophylactic metronidazole (500 mg three times a day) was initiated for three days.", "The patient continued to improve and was discharged in good condition one month after admission, with only slight left-sided hemiparesis."], "index": 107, "original_id": "multiclinsum_test_1344_en.txt", "split": "test", "summary_subclaims": ["The patient was a 64-year-old male.", "The patient was admitted to the hospital with a headache.", "The patient had fever.", "The patient later had imbalance.", "The patient had blurred vision.", "The patient had general slowness.", "Neurological examination revealed nuchal rigidity.", "Neurological examination revealed general clumsiness.", "Meningitis was suspected.", "The patient was treated with dexamethasone.", "The patient was treated with ceftriaxone.", "The patient was treated with acyclovir.", "A brain CT scan was normal.", "CSF Gram staining remained negative.", "Bacterial cultures remained negative.", "The antibacterial treatment was discontinued.", "Nine days after admission, the patient's condition deteriorated.", "The antibacterial treatment was restarted.", "A brain MRI revealed ventriculitis.", "A CT scan showed hydrocephalus.", "A ventriculostomy was performed.", "In CSF Gram staining, chains of gram-positive cocci were observed.", "Bacterial cultures remained negative.", "A bacterial PCR detected Streptococcus intermedius.", "An orthopantomography revealed advanced periodontal destruction in several teeth.", "An orthopantomography revealed periapical abscesses.", "The teeth with periapical abscesses were subsequently operated on.", "The patient was discharged in good condition after one month."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
+{"data_source": "multiclinsum", "solution_str": "{\n    \"low_health_literacy\": \"Your body needs to keep your blood clean and your organs working well. If your kidneys aren\u2019t doing their job, it\u2019s like having a leaky faucet \u2014 waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.\",\n    \"intermediate_health_literacy\": \"Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.\",\n    \"proficient_health_literacy\": \"The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by underlying pathophysiological mechanisms including glomerular injury, tubular atrophy, and vascular remodeling, with clinical outcomes dependent on stage, comorbidities, and biomarker profiles such as estimated glomerular filtration rate (eGFR) and urine albumin-to-creatinine ratio (UACR).\"\n}", "ground_truth": {"fulltext_subclaims": ["The patient is a 43-year-old nonsmoking and nondrinking white male.", "The patient had oral cancer on the left side of the tongue.", "A biopsy sample taken from the tumor revealed G2 keratinizing squamous cell carcinoma.", "A CT scan performed two months before the operation showed a primary tumor measuring 15 \u00d7 10 mm with peripheral contrast enhancement.", "The CT scan showed two suspected, probably metastatic lymph nodes on the left side of the neck in groups III and IV, size 17 \u00d7 14 mm and 26 \u00d7 16 mm, respectively.", "Distant metastases were ruled out on chest X-ray and abdominal ultrasound.", "Anamnesis proved previous lower extremity deep vein thrombosis.", "Doppler ultrasound ruled out active deep vein thrombosis.", "The surgical procedure included excision of the left half of the tongue, the floor of the mouth, and the sidewall of the throat.", "The surgical procedure included bilateral cervical lymph node dissection in groups I-V on the left side and I-III on the right side.", "The second part of the operation involved reconstruction using an anterolateral thigh flap.", "Reoperation was performed three days after surgery due to hemorrhage from the wound after lymphadenectomy.", "The final histopathology report revealed G2 keratinizing squamous cell carcinoma, stage IVa (pT3 pN2b, AJCC 8th edition).", "The histopathology report noted perineural invasion of small nerves.", "The histopathology report noted an unfavorable pattern of invasion with small islands (the worst pattern of invasion, 4).", "The histopathology report noted a closest margin below 1 mm.", "The histopathology report noted five metastatic lymph nodes (of 49 lymph nodes dissected) without extracapsular extension at levels II, IV, V on the left side.", "The novel prognostic histopathological grading system in oral squamous cell carcinoma based on tumor budding revealed G-2.", "102 budding foci were detected per 10 high-power fields.", "Two to four cell-sized nests or single-cell invasion was observed.", "A multidisciplinary case conference qualified the patient for postoperative radiochemotherapy.", "The patient refused systemic treatment.", "Radiotherapy alone was recommended.", "Five-point head, neck, and shoulder masks were employed for patient immobilization.", "A CT scan (3 mm slice thickness) without intravenous contrast was performed in the planning radiotherapy process.", "The dose prescription involved the bilateral lymph nodes I-V to a total dose of 50 Gy in 25 fractions.", "The dose prescription involved the left side neck in groups II-V to a total dose of 60 Gy in 30 fractions.", "The dose prescription involved the tumor bed with bilateral submandibular lymph nodes to a total dose of 66 Gy in 33 fractions.", "The VMAT technique was applied.", "In the first stage of treatment, three full arcs were used.", "In the second stage, three arcs lateralized to the left side of the neck were used.", "In the third stage, two frontal arcs were applied.", "Radiotherapy was performed by linear accelerators (Clinac 23EX; Varian Medical Systems, Palo Alto, CA, USA) with an energy of 6 MV and maximal dose rate of 600 MU/min.", "Two weeks after the beginning of radiotherapy, ultrasound of the neck was performed due to a suspected lump in group III on the right side.", "The ultrasound revealed a 16 \u00d7 9 mm lymph node.", "Fine-needle aspiration biopsy was performed, confirming metastasis of the squamous cell carcinoma.", "The multidisciplinary case conference urged the application of a single-fraction stereotactic radiosurgery (SRS) boost of 18 Gy to the metastatic lymph node.", "After 29 days of conventional treatment, a new 5-point mask, a new CT scan without contrast, and an MR scan with gadolinium intravenous contrast were performed in the planned stereotactic boost process.", "The GTVboost volume was 0.7 cm3.", "A 3 mm margin was added to the GTVboost to create a PTVboost volume of 3.1 cm3.", "A new treatment plan consisting of four arcs was prepared.", "Four 6 MV FFF (flattening filter-free) photon beams with a maximal dose rate of 1400 MU/min were utilized.", "The dose that fully covers target volume was selected as the prescribed isodose level.", "The minimum dose in the target volume was 100% of the prescribed dose.", "The maximum dose was 108.4%.", "The angle range of arcs was adapted to the boost localization and was limited to the right and front sides of the patient.", "The boost was delivered two days after the last fraction of conventional radiotherapy with the same linear accelerator.", "Overall treatment time totaled 50 days.", "During radiotherapy, oral mucositis and moist desquamation (grade 3, CTCAE v5.0) were observed in the irradiated area.", "Oral mucositis and moist desquamation subsided within three months of follow up.", "Staphylococcus aureus and Klebsiella oxytoca were identified from the throat culture in the sixth week of conventional treatment.", "Antibiotic therapy consistent with the antibiogram (clindamycin, amoxicillin/clavulanate potassium) was used.", "Blood tests showed grade 1 anemia after 24 fractions.", "Blood tests showed grade 1 leukopenia after 33 fractions.", "Blood tests normalized seven months after treatment.", "CT scans and laryngological examinations did not prove locoregional recurrence three, ten, and thirteen months after the end of radiotherapy.", "Chest X-ray and abdominal ultrasound did not detect any metastatic changes one year after treatment.", "Xerostomia G2 was the only symptom of late toxicity fifteen months after radiotherapy.", "At 17 months of follow-up, the patient reported coughing, suffocation, and bloody sputum.", "A CT scan revealed infiltration (64 \u00d7 65 \u00d7 100 mm) in the 3rd segment of the right lung, encompassing the hilum and central part of the mediastinum.", "Pathological examination after EUS-FNA proved squamous cell carcinoma with moderate PD-L1 membrane expression (< 50%).", "Acknowledgment of the tumor in the chest as lung cancer or metastatic disease due to oral cancer was difficult.", "The patient was qualified for palliative radiotherapy to a total dose of 30 Gy in 10 fractions (VMAT technique, single arc, gantry angle 30.0\u2013210.0 deg) for the tumor in the chest.", "Systemic treatment was contraindicated in terms of performance status\u2014ECOG 2.", "Three months later, multiple metastases in the mediastinum, right lung, spleen, and bones were detected by PET/CT.", "The most painful osteolitic lesion in the left ischium and femoral head was irradiated in one fraction to 8 Gy.", "Two-dimensional radiotherapy technique, two coaxial opposite beams from AP and PA directions were used.", "The patient died the next month."], "summary_subclaims": ["The patient underwent surgery.", "During adjuvant radiotherapy, a metastatic cervical lymph node was diagnosed based on fine-needle aspiration biopsy.", "A stereotactic radiosurgery boost of 1\u2009\u00d7\u200918\u00a0Gy was performed two days after the last fraction of conventional radiotherapy.", "The early and late tolerance of this treatment were positive.", "During the 18-month follow-up, locoregional recurrence was not detected.", "The patient died due to secondary malignancy."]}, "extra_info": {"fulltext_subclaims": ["The patient is a 43-year-old nonsmoking and nondrinking white male.", "The patient had oral cancer on the left side of the tongue.", "A biopsy sample taken from the tumor revealed G2 keratinizing squamous cell carcinoma.", "A CT scan performed two months before the operation showed a primary tumor measuring 15 \u00d7 10 mm with peripheral contrast enhancement.", "The CT scan showed two suspected, probably metastatic lymph nodes on the left side of the neck in groups III and IV, size 17 \u00d7 14 mm and 26 \u00d7 16 mm, respectively.", "Distant metastases were ruled out on chest X-ray and abdominal ultrasound.", "Anamnesis proved previous lower extremity deep vein thrombosis.", "Doppler ultrasound ruled out active deep vein thrombosis.", "The surgical procedure included excision of the left half of the tongue, the floor of the mouth, and the sidewall of the throat.", "The surgical procedure included bilateral cervical lymph node dissection in groups I-V on the left side and I-III on the right side.", "The second part of the operation involved reconstruction using an anterolateral thigh flap.", "Reoperation was performed three days after surgery due to hemorrhage from the wound after lymphadenectomy.", "The final histopathology report revealed G2 keratinizing squamous cell carcinoma, stage IVa (pT3 pN2b, AJCC 8th edition).", "The histopathology report noted perineural invasion of small nerves.", "The histopathology report noted an unfavorable pattern of invasion with small islands (the worst pattern of invasion, 4).", "The histopathology report noted a closest margin below 1 mm.", "The histopathology report noted five metastatic lymph nodes (of 49 lymph nodes dissected) without extracapsular extension at levels II, IV, V on the left side.", "The novel prognostic histopathological grading system in oral squamous cell carcinoma based on tumor budding revealed G-2.", "102 budding foci were detected per 10 high-power fields.", "Two to four cell-sized nests or single-cell invasion was observed.", "A multidisciplinary case conference qualified the patient for postoperative radiochemotherapy.", "The patient refused systemic treatment.", "Radiotherapy alone was recommended.", "Five-point head, neck, and shoulder masks were employed for patient immobilization.", "A CT scan (3 mm slice thickness) without intravenous contrast was performed in the planning radiotherapy process.", "The dose prescription involved the bilateral lymph nodes I-V to a total dose of 50 Gy in 25 fractions.", "The dose prescription involved the left side neck in groups II-V to a total dose of 60 Gy in 30 fractions.", "The dose prescription involved the tumor bed with bilateral submandibular lymph nodes to a total dose of 66 Gy in 33 fractions.", "The VMAT technique was applied.", "In the first stage of treatment, three full arcs were used.", "In the second stage, three arcs lateralized to the left side of the neck were used.", "In the third stage, two frontal arcs were applied.", "Radiotherapy was performed by linear accelerators (Clinac 23EX; Varian Medical Systems, Palo Alto, CA, USA) with an energy of 6 MV and maximal dose rate of 600 MU/min.", "Two weeks after the beginning of radiotherapy, ultrasound of the neck was performed due to a suspected lump in group III on the right side.", "The ultrasound revealed a 16 \u00d7 9 mm lymph node.", "Fine-needle aspiration biopsy was performed, confirming metastasis of the squamous cell carcinoma.", "The multidisciplinary case conference urged the application of a single-fraction stereotactic radiosurgery (SRS) boost of 18 Gy to the metastatic lymph node.", "After 29 days of conventional treatment, a new 5-point mask, a new CT scan without contrast, and an MR scan with gadolinium intravenous contrast were performed in the planned stereotactic boost process.", "The GTVboost volume was 0.7 cm3.", "A 3 mm margin was added to the GTVboost to create a PTVboost volume of 3.1 cm3.", "A new treatment plan consisting of four arcs was prepared.", "Four 6 MV FFF (flattening filter-free) photon beams with a maximal dose rate of 1400 MU/min were utilized.", "The dose that fully covers target volume was selected as the prescribed isodose level.", "The minimum dose in the target volume was 100% of the prescribed dose.", "The maximum dose was 108.4%.", "The angle range of arcs was adapted to the boost localization and was limited to the right and front sides of the patient.", "The boost was delivered two days after the last fraction of conventional radiotherapy with the same linear accelerator.", "Overall treatment time totaled 50 days.", "During radiotherapy, oral mucositis and moist desquamation (grade 3, CTCAE v5.0) were observed in the irradiated area.", "Oral mucositis and moist desquamation subsided within three months of follow up.", "Staphylococcus aureus and Klebsiella oxytoca were identified from the throat culture in the sixth week of conventional treatment.", "Antibiotic therapy consistent with the antibiogram (clindamycin, amoxicillin/clavulanate potassium) was used.", "Blood tests showed grade 1 anemia after 24 fractions.", "Blood tests showed grade 1 leukopenia after 33 fractions.", "Blood tests normalized seven months after treatment.", "CT scans and laryngological examinations did not prove locoregional recurrence three, ten, and thirteen months after the end of radiotherapy.", "Chest X-ray and abdominal ultrasound did not detect any metastatic changes one year after treatment.", "Xerostomia G2 was the only symptom of late toxicity fifteen months after radiotherapy.", "At 17 months of follow-up, the patient reported coughing, suffocation, and bloody sputum.", "A CT scan revealed infiltration (64 \u00d7 65 \u00d7 100 mm) in the 3rd segment of the right lung, encompassing the hilum and central part of the mediastinum.", "Pathological examination after EUS-FNA proved squamous cell carcinoma with moderate PD-L1 membrane expression (< 50%).", "Acknowledgment of the tumor in the chest as lung cancer or metastatic disease due to oral cancer was difficult.", "The patient was qualified for palliative radiotherapy to a total dose of 30 Gy in 10 fractions (VMAT technique, single arc, gantry angle 30.0\u2013210.0 deg) for the tumor in the chest.", "Systemic treatment was contraindicated in terms of performance status\u2014ECOG 2.", "Three months later, multiple metastases in the mediastinum, right lung, spleen, and bones were detected by PET/CT.", "The most painful osteolitic lesion in the left ischium and femoral head was irradiated in one fraction to 8 Gy.", "Two-dimensional radiotherapy technique, two coaxial opposite beams from AP and PA directions were used.", "The patient died the next month."], "index": 104, "original_id": "multiclinsum_test_2840_en.txt", "split": "test", "summary_subclaims": ["The patient underwent surgery.", "During adjuvant radiotherapy, a metastatic cervical lymph node was diagnosed based on fine-needle aspiration biopsy.", "A stereotactic radiosurgery boost of 1\u2009\u00d7\u200918\u00a0Gy was performed two days after the last fraction of conventional radiotherapy.", "The early and late tolerance of this treatment were positive.", "During the 18-month follow-up, locoregional recurrence was not detected.", "The patient died due to secondary malignancy."], "raw_prompt": [{"content": "**System Role:**\n\nYou are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.\n\n**User Prompt:**\n\nPlease process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.\n### Instructions for Each Level:\n\n1. Level: Low Health Literacy (High Readability)\n\nTarget: Individuals needing the simplest terms for immediate action.\n\nLinguistic Goal: Use \"living room\" language. Replace all medical jargon with functional descriptions (e.g., \"renal\" becomes \"kidney\").\n\nInformation Density: Focus strictly on the \"need-to-know\" info found in the Gold Summary.\n\nStrategy: High paraphrasing using analogies. One idea per sentence.\n\nFaithfulness: Must align perfectly with the Gold Summary.\n\n2. Level: Intermediate Health Literacy (Medium Readability)\n\nTarget: The general public (news-reading level).\n\nLinguistic Goal: Standard vocabulary. Common medical terms are okay, but technical \"doctor-speak\" must be simplified.\n\nInformation Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.\n\nStrategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.\n\nFaithfulness: Maintains the main narrative of the Gold Summary.\n\n3. Level: Proficient Health Literacy (Low Readability)\n\nTarget: Researchers, clinicians, or highly informed patients.\n\nLinguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.\n\nInformation Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.\n\nStrategy: Minimal paraphrasing. Retain all original technical terminology.\n\nFaithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.\n\n\nI will provide the following information:\n\n- Input Language: <<<SOURCE_LANGUAGE>>>\n- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>\n- Source Text (detailed content): <<<FULL_TEXT>>>\n\n**Output Format (JSON only):**\n    {\n    \"low_health_literacy\": \"...\",\n    \"intermediate_health_literacy\": \"...\",\n    \"proficient_health_literacy\": \"...\"\n    }", "role": "user"}], "num_turns": "2", "rollout_reward_scores": {}}}
diff --git a/code/RL_model/verl/verl_train/docs/Makefile b/code/RL_model/verl/verl_train/docs/Makefile
new file mode 100644
index 0000000000000000000000000000000000000000..8bda904a9b0b29dfcf538cb52b806dd910710a4a
--- /dev/null
+++ b/code/RL_model/verl/verl_train/docs/Makefile
@@ -0,0 +1,20 @@
+# Minimal makefile for Sphinx documentation
+#
+
+# You can set these variables from the command line.
+SPHINXOPTS    =
+SPHINXBUILD   = sphinx-build
+SPHINXPROJ    = verl
+SOURCEDIR     = .
+BUILDDIR      = _build
+
+# Put it first so that "make" without argument is like "make help".
+help:
+	@$(SPHINXBUILD) -M help "$(SOURCEDIR)" "$(BUILDDIR)" $(SPHINXOPTS) $(O)
+
+.PHONY: help Makefile
+
+# Catch-all target: route all unknown targets to Sphinx using the new
+# "make mode" option.  $(O) is meant as a shortcut for $(SPHINXOPTS).
+%: Makefile
+	@$(SPHINXBUILD) -M $@ "$(SOURCEDIR)" "$(BUILDDIR)" $(SPHINXOPTS) $(O)
diff --git a/code/RL_model/verl/verl_train/docs/README.md b/code/RL_model/verl/verl_train/docs/README.md
new file mode 100644
index 0000000000000000000000000000000000000000..8c5db04874138435ef986342a7b8be668b81d0b0
--- /dev/null
+++ b/code/RL_model/verl/verl_train/docs/README.md
@@ -0,0 +1,22 @@
+# verl documentations
+
+## Build the docs
+
+```bash
+# If you want to view auto-generated API docstring, please make sure verl is available in python path. For instance, install verl via:
+# pip install .. -e[test]
+
+# Install dependencies needed for building docs.
+pip install -r requirements-docs.txt
+
+# Build the docs.
+make clean
+make html
+```
+
+## Open the docs with your browser
+
+```bash
+python -m http.server -d _build/html/
+```
+Launch your browser and navigate to http://localhost:8000 to view the documentation. Alternatively you could drag the file `_build/html/index.html` to your local browser and view directly.
diff --git a/code/RL_model/verl/verl_train/docs/README_vllm0.7.md b/code/RL_model/verl/verl_train/docs/README_vllm0.7.md
new file mode 100644
index 0000000000000000000000000000000000000000..e84feddd7537b0cadb1157993a3819bfc5e52042
--- /dev/null
+++ b/code/RL_model/verl/verl_train/docs/README_vllm0.7.md
@@ -0,0 +1,73 @@
+# Upgrading to vllm >= 0.7
+
+Note: verl+vllm 0.8.3 is now stable. Please see ``docs/README_vllm0.8.md`` for upgrade guide.
+
+## Installation
+
+Note: At time of writing, verl+vllm 0.7.x supports **FSDP** for training and **vLLM** for rollout.
+
+```
+# Create the conda environment
+conda create -n verl python==3.10
+conda activate verl
+
+# Install verl
+git clone https://github.com/volcengine/verl.git
+cd verl
+pip3 install -e .
+
+# Install the latest stable version of vLLM
+pip3 install vllm==0.7.3 
+
+# Install flash-attn
+pip3 install flash-attn --no-build-isolation
+
+```
+
+Note that if you are installing lower versions of vLLM (0.7.0, 0.7.1, 0.7.2), you need to make some tiny patches manually on vllm (/path/to/site-packages/vllm after installation) after the above steps:
+
+- vllm/distributed/parallel_state.py: Remove the assertion below:
+
+```
+if (world_size
+        != tensor_model_parallel_size * pipeline_model_parallel_size):
+    raise RuntimeError(
+        f"world_size ({world_size}) is not equal to "
+        f"tensor_model_parallel_size ({tensor_model_parallel_size}) x "
+        f"pipeline_model_parallel_size ({pipeline_model_parallel_size})")
+
+```
+
+- vllm/executor/uniproc_executor.py: change `local_rank = rank` to `local_rank = int(os.environ["LOCAL_RANK"])`
+- vllm/model_executor/model_loader/weight_utils.py: remove the `torch.cuda.empty_cache()` in `pt_weights_iterator`
+
+## Features
+
+### Use cuda graph
+
+After installation, examples using FSDP as training backends can be used. By default, the `enforce_eager` is set to True, which disables the cuda graph. To enjoy cuda graphs and the sleep mode of vLLM>=0.7, add the following lines to the bash script:
+
+```
+actor_rollout_ref.rollout.enforce_eager=False \
+actor_rollout_ref.rollout.free_cache_engine=True \
+
+```
+
+For a typical job like examples/ppo_trainer/run_qwen2-7b_seq_balance.sh, the rollout generation time is 85 seconds with vLLM0.7.0. By enabling the cudagraph, the generation duration is further reduced to 62 seconds.
+
+**Note:** Currently, if the `n` is greater than 1 in `SamplingParams` in vLLM>=0.7, there is a potential performance issue on the stability of rollout generation time (Some iterations would see generation time bursts) using vLLM's V0 Engine.
+
+### Use vLLM V1 Engine
+
+Using the vLLM V1 engine can avoid instability issues and achieve additional performance improvements. To use the V1 engine, you can first uninstall the previously installed vLLM and then follow the steps below to install the newer version.
+
+```
+git clone https://github.com/vllm-project/vllm.git
+cd vllm
+git checkout 2275784
+sed -i "903a\    data_parallel_size = world_size // pipeline_model_parallel_size // tensor_model_parallel_size" ./vllm/distributed/parallel_state.py
+VLLM_USE_PRECOMPILED=1 pip install --editable .
+```
+
+Then you can enable the V1 engine by setting `export VLLM_USE_V1=1`. In some benchmark tests, the V1 engine demonstrates a 1.5x speed improvement over the vLLM V0 engine.
+The stable support of the vLLM V1 engine is available on verl main.
diff --git a/code/RL_model/verl/verl_train/docs/README_vllm0.8.md b/code/RL_model/verl/verl_train/docs/README_vllm0.8.md
new file mode 100644
index 0000000000000000000000000000000000000000..d4f509f19f780a4e8b3edec6bb256d2aa964639a
--- /dev/null
+++ b/code/RL_model/verl/verl_train/docs/README_vllm0.8.md
@@ -0,0 +1,52 @@
+# Upgrading to vLLM >= 0.8
+
+Last updated: 05/04/2025.
+
+## Installation
+
+Note: This version of verl+vLLM 0.8+ supports **FSDP** for training and **vLLM** for rollout.
+
+```bash
+# Create the conda environment
+conda create -n verl python==3.10
+conda activate verl
+
+# Install verl
+git clone https://github.com/volcengine/verl.git
+cd verl
+pip3 install -e .
+
+# Install the latest stable version of vLLM
+pip3 install vllm==0.8.3
+
+# Install flash-attn
+pip3 install flash-attn --no-build-isolation
+
+```
+
+We have a pre-built docker image for verl+vLLM 0.8.3. You can direct import it with the following command:
+
+```bash
+docker pull hiyouga/verl:ngc-th2.6.0-cu126-vllm0.8.3-flashinfer0.2.2-cxx11abi0
+```
+
+## Features
+
+vLLM 0.8+ supports cuda graph and V1 engine by default in verl. To enable these features, remember to add the following lines to the bash script:
+
+```bash
+actor_rollout_ref.rollout.enforce_eager=False \
+actor_rollout_ref.rollout.free_cache_engine=True \
+```
+
+and also **remove** the environment variable if it exists:
+
+## Notes
+
+When you just directly upgrade vllm>=0.8, some dependency packages may undergo version changes. If you encounter the following problems:
+
+```bash
+in <module> from torch.multiprocessing.reductions import ForkingPickler ImportError: cannot import name 'ForkingPickler' from 'torch.multiprocessing.reductions' (/opt/conda/lib/python3.11/site-packages/torch/multiprocessing/reductions.py)
+```
+
+You need to upgrade `tensordict` to version 0.6.2 using the command `pip install tensordict==0.6.2`.
diff --git a/code/RL_model/verl/verl_train/docs/conf.py b/code/RL_model/verl/verl_train/docs/conf.py
new file mode 100644
index 0000000000000000000000000000000000000000..cbeabbd81b28e97fe0d0e8bcf436ab92f5833743
--- /dev/null
+++ b/code/RL_model/verl/verl_train/docs/conf.py
@@ -0,0 +1,113 @@
+# Copyright 2024 Bytedance Ltd. and/or its affiliates
+#
+# Licensed under the Apache License, Version 2.0 (the "License");
+# you may not use this file except in compliance with the License.
+# You may obtain a copy of the License at
+#
+#     http://www.apache.org/licenses/LICENSE-2.0
+#
+# Unless required by applicable law or agreed to in writing, software
+# distributed under the License is distributed on an "AS IS" BASIS,
+# WITHOUT WARRANTIES OR CONDITIONS OF ANY KIND, either express or implied.
+# See the License for the specific language governing permissions and
+# limitations under the License.
+
+# Configuration file for the Sphinx documentation builder.
+#
+# This file only contains a selection of the most common options. For a full
+# list see the documentation:
+# https://www.sphinx-doc.org/en/master/usage/configuration.html
+
+# -- Path setup --------------------------------------------------------------
+
+# If extensions (or modules to document with autodoc) are in another directory,
+# add these directories to sys.path here. If the directory is relative to the
+# documentation root, use os.path.abspath to make it absolute, like shown here.
+#
+# import os
+# import sys
+# sys.path.insert(0, os.path.abspath('.'))
+
+
+# -- Project information -----------------------------------------------------
+
+project = "verl"
+copyright = "2024 ByteDance Seed Foundation MLSys Team"
+author = "Guangming Sheng, Chi Zhang, Yanghua Peng, Haibin Lin"
+
+
+# -- General configuration ---------------------------------------------------
+# The master toctree document.
+master_doc = "index"
+
+# Add any Sphinx extension module names here, as strings. They can be
+# extensions coming with Sphinx (named 'sphinx.ext.*') or your custom
+# ones.
+extensions = [
+    "myst_parser",
+    "sphinx.ext.autodoc",
+    "sphinx.ext.autosummary",
+    "sphinx.ext.autosectionlabel",
+    "sphinx.ext.napoleon",
+    "sphinx.ext.viewcode",
+]
+
+# MyST-Parser settings
+myst_enable_extensions = [
+    "dollarmath",  # Enables $...$ and $$...$$ syntax
+    "amsmath",  # Enables amsmath environments
+]
+
+# Use Google style docstrings instead of NumPy docstrings.
+napoleon_google_docstring = True
+napoleon_numpy_docstring = False
+
+# The suffix(es) of source filenames.
+# You can specify multiple suffix as a list of string:
+source_suffix = {
+    ".rst": "restructuredtext",
+    ".md": "markdown",
+}
+
+# Add any paths that contain templates here, relative to this directory.
+templates_path = ["_templates"]
+
+# The language for content autogenerated by Sphinx. Refer to documentation
+# for a list of supported languages.
+#
+# This is also used if you do content translation via gettext catalogs.
+# Usually you set "language" from the command line for these cases.
+language = "en"
+
+# List of patterns, relative to source directory, that match files and
+# directories to ignore when looking for source files.
+# This pattern also affects html_static_path and html_extra_path.
+exclude_patterns = ["_build", "Thumbs.db", ".DS_Store"]
+
+
+# -- Options for HTML output -------------------------------------------------
+
+# The theme to use for HTML and HTML Help pages.  See the documentation for
+# a list of builtin themes.
+#
+html_theme = "sphinx_rtd_theme"
+
+# Add any paths that contain custom static files (such as style sheets) here,
+# relative to this directory. They are copied after the builtin static files,
+# so a file named "default.css" will overwrite the builtin "default.css".
+html_static_path = ["_static"]
+
+# Add the JavaScript file
+html_js_files = [
+    "js/runllm-widget.js",
+    "js/resizable-sidebar.js",
+]
+
+# Add custom CSS file for full-width layout
+html_css_files = [
+    "custom.css",
+]
+
+exclude_patterns += ["README.md", "README_vllm0.7.md"]
+
+suppress_warnings = ["ref.duplicate", "ref.myst"]
diff --git a/code/RL_model/verl/verl_train/docs/hybrid_flow.rst b/code/RL_model/verl/verl_train/docs/hybrid_flow.rst
new file mode 100644
index 0000000000000000000000000000000000000000..3aa5a4a97cb88e564babc11392899149338a5b49
--- /dev/null
+++ b/code/RL_model/verl/verl_train/docs/hybrid_flow.rst
@@ -0,0 +1,266 @@
+=========================================================
+HybridFlow Programming Guide
+=========================================================
+
+Last updated: 06/02/2025.
+
+.. _vermouth: https://github.com/vermouth1992
+
+Author: `Chi Zhang <https://github.com/vermouth1992>`_
+
+verl is an open source implementation of the paper `HybridFlow <https://arxiv.org/abs/2409.19256v2>`_ [1]_. In this section, we will introduce the basic concepts of HybridFlow, the motivation and how to program with verl APIs.
+
+Motivation and Design
+------------------------
+We use dataflow to represent RL systems. [4]_.
+
+DataFlow
+~~~~~~~~~~~~~~~~~~~~
+
+Dataflow is an abstraction of computations. Neural Network training is a typical dataflow. It can be represented by computational graph. 
+
+.. image:: https://github.com/eric-haibin-lin/verl-community/blob/main/docs/dataflow.jpeg?raw=true
+   :alt: The dataflow graph from CS231n 2024 lecture 4
+
+This figure [2]_ represents the computation graph of a polynomial function followed by a sigmoid function. In the data flow of neural network computation, each node represents an operator, and each edge represents the direction of forward/backward propagation. The computation graph determines the architecture of the neural network.
+
+RL as a dataflow problem
+++++++++++++++++++++++++++++++++++++++++++++++
+
+Reinforcement learning (RL) training can also be represented as a dataflow. Below is the dataflow graph that represents the PPO algorithm used in RLHF [3]_:
+
+.. image:: https://picx.zhimg.com/70/v2-cb8ab5ee946a105aab6a563e92682ffa_1440w.avis?source=172ae18b&biz_tag=Post
+  :alt: PPO dataflow graph, credit to Zhihu 低级炼丹师
+
+However, the dataflow of RL has fundamental differences compared with dataflow of neural network training as follows:
+
++--------------------------+--------------------------------------------------+---------------------+
+| Workload                 | Node                                             | Edge                |
++--------------------------+--------------------------------------------------+---------------------+
+| Neural Network Training  | Operator (+/-/matmul/softmax)                    | Tensor movement     |
++--------------------------+--------------------------------------------------+---------------------+
+| Reinforcement Learning   | High-level operators (rollout/model forward)     | Data Movement       |
++--------------------------+--------------------------------------------------+---------------------+
+
+In the case of tabular reinforcement learning, each operator is a simple scalar math operation (e.g., bellman update). In deep reinforcement learning(DRL), each operator is a high-level neural network computation such as model inference/update. This makes RL a two-level dataflow problem:
+
+- Control flow: defines how the high-level operators are executed (e.g., In PPO, we first perform rollout. Then, we perform advantage computation. Finally, we perform training). It expresses the **core logics of RL algorithms**.
+- Computation flow: defines the dataflow of **neural network computation** (e.g., model forward/backward/optimizer).
+
+
+Design Choices
+~~~~~~~~~~~~~~~~~~~~
+The model size used in DRL before the LLM era is typically small. Thus, the high-level neural network computation can be done in a single process. This enables embedding the computation flow inside the control flow as a single process.
+
+However, in the LLM era, the computation flow (e.g., training neural network) becomes a multi-process program. This naturally leads to two design choices:
+
+1. Convert the control flow into a multi-process program as well. Then colocate with computation flow (unified multi-controller)
+
+- Advantages:
+
+  - Achieves the **optimal performance** under fixed computation flow and control flow as the communication overhead in both training and data transfer is minimized.
+
+- Disadvantages:
+
+  - The computation and/or control flow is **hard to reuse** from software perspective as computation code is coupled with specific controller code. For example, the training loop of PPO is generic. Say we have an PPO training flow implemented with a specific computation flow such as FSDP. Neither the control flow or computation flow can be reused if we want to switch the computation flow from FSDP to Megatron, due to the coupling of control and computation flows.
+  - Requires more efforts from the user under flexible and dynamic control flows, due to the multi-process nature of the program.
+
+2. Separate the flows: single process for the control flow and multi-process for computation flow
+
+- Advantages:
+
+  - The computation flow defined elsewhere can be **easily reused** after the decoupling.
+  - The controller runs on a single process. Implementing a new RL algorithm with a **different control flow is simple and easy**.
+
+- Disadvantages:
+
+  - Additional **data communication overhead** each time the controller process and computatation processes interact. The data has to be sent back and forth.
+
+In verl, the latter strategy with separate control flow and computation flow is adopted. verl is designed to decouple the control flow of RL algorithms, and the implementation of computation engines.
+
+Overall Execution Diagram
+~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
+
+Below is a simplified diagram denoting the execution of a reinforcement learning job. In the diagram, the controller runs on a single process, while the generator/actor workers, critic workers run on multiple processes, placed with specific resource groups. For rollout, the controller passes the data to the generator to perform sample generation. When the rollout is done, the data is passed back to controller for the next step of the algorithm. Similar execution is done for other workers. With the hybrid controller design, the data flow and computation is decoupled to provide both efficiency in computation and flexibility in defining algorithm training loops.
+
+.. figure:: https://github.com/eric-haibin-lin/verl-community/blob/main/docs/driver_worker.png?raw=true
+   :alt: The execution diagram
+
+Codebase walkthrough (PPO)
+------------------------------------------------
+
+Entry function
+~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
+Code: https://github.com/volcengine/verl/blob/main/verl/trainer/main_ppo.py
+
+In this file, we define a remote function `main_task` that serves as the controller (driver) process as shown in the above figure. We also define a ``RewardManager``, where users can customize their reward function based on the data source in the dataset. Note that `RewardManager` should return the final token-level reward that is optimized by RL algorithms. Note that users can combine model-based rewards and rule-based rewards.
+The ``main_task`` constructs a RayPPOTrainer instance and launch the fit. Note that ``main_task`` **runs as a single process**.
+
+We highly recommend that the ``main_task`` is NOT scheduled on the head of the ray cluster because ``main_task`` will consume a lot of memory but the head usually contains very few resources.
+
+Ray trainer
+~~~~~~~~~~~~~~~~~~~~
+Code: https://github.com/volcengine/verl/blob/main/verl/trainer/ppo/ray_trainer.py
+
+The RayPPOTrainer manages 
+
+- Worker and WorkerGroup construction
+- Runs the main loop of PPO algorithm
+
+Note that, the fit function of RayPPOTrainer **runs as a single process**.
+
+Worker and WorkerGroup construction
+~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
+
+Each workerGroup manages a list of workers that runs remotely. Note that the worker group runs in the process of its constructor.
+Each worker inside the WorkerGroup runs on a GPU. The worker group serves as a proxy for the controller process to interact with a list of workers, in order to perform certain computations. **In order to do so, we have to bind the methods of the worker into the method of the WorkerGroup and define the data dispatch and data collection**. This is done via simple decoration that will be introduced in the Worker definition section.
+
+For example, in PPO, we define 3 worker groups:
+
+- ActorRolloutRef: manages actor, rollout and reference policy. ActorRolloutRefWorker can be instantiated as a single actor, a single rollout, a single reference policy, a combined actor/rollout or a combined actor/rollout/ref. This design is aimed for the maximum code reuse in various scenarios. The reason for colocating actor and rollout is for fast weight transfer using nccl. The reason for coloating actor and reference is to implement an efficient lora PPO as the reference policy is simply the base model of PPO in lora. The colocation is done via ``verl.single_controller.ray.base.create_colocated_worker_cls``, where it creates a single ray remote class exposing all class methods from these roles.
+- Critic: manages the critic model
+- Reward: manages the reward model
+
+The worker group will be constructed on the resource pool it designates. The resource pool is a set of GPUs in the ray cluster.
+
+Worker definition
+~~~~~~~~~~~~~~~~~~~~
+
+.. _ActorRolloutRefWorker: https://github.com/volcengine/verl/blob/main/verl/workers/fsdp_workers.py
+
+We take `ActorRolloutRefWorker <https://github.com/volcengine/verl/blob/main/verl/workers/fsdp_workers.py>`_ for an example.
+The APIs it should expose to the controller process are:
+
+- init_model: build the underlying model
+- generate_sequences: given prompts, generate responses
+- compute_log_prob: compute the log-probability of a generated sequence using actor
+- compute_ref_log_prob: compute the log-probability of a generated sequence using reference policy
+- save_checkpoint: save the checkpoint
+
+Note that these methods are defined in the worker that can only be invoked via remote calls. For example, if the controller process wants to initialize the model, it has to call
+
+.. code-block:: python
+
+   for worker in actor_rollout_ref_wg:
+       worker.init_model.remote()
+
+If the controller process wants to generate sequences, it has to call
+
+.. code-block:: python
+
+   data = xxx
+   # split the data into dp chunks
+   data_dp_lst = data.split(dp_size)
+   output_dp_lst = []
+   for i, worker in enumerate(actor_rollout_ref_wg):
+       output_future = worker.generate_sequences.remote(data_dp_lst[i])
+       output_dp_lst.append(output_future)
+   output = torch.cat(ray.get(output_dp_lst), dim=0)
+
+We observe that controller process calling worker group methods in general can be divided into 3 parts:
+
+- Split the data into data parallel sizes
+- Dispatch the corresponding data into each worker
+- Collect and concatenate the data when the computation finishes
+
+In verl, we design a syntax sugar to encapsulate the 3 processes into a single call from the controller process.
+
+.. code-block:: python
+
+   @register(dispatch_mode=Dispatch.DP_COMPUTE_PROTO)
+   def generate_sequences(data):
+       ...
+
+   # on the driver
+   output = actor_rollout_ref_wg.generate_sequences(data)
+
+We decorate the method of the worker with a ``register`` that explicitly defines how the input data should be split and dispatched to each worker, and how the output data should be collected and concatenated by the controller. For example, ``Dispatch.DP_COMPUTE_PROTO`` splits the input data into dp chunks, dispatch each data to each worker, collect the output and concatenate the results. Note that this function requires the input and output to be a DataProto defined here (https://github.com/volcengine/verl/blob/main/verl/protocol.py).
+
+
+PPO main loop
+~~~~~~~~~~~~~~~~~~~~
+With the aforementioned APIs, we can implement the main loop of PPO as if it is a single process program
+
+.. code-block:: python
+
+   for prompt in dataloader:
+       output = actor_rollout_ref_wg.generate_sequences(prompt)
+       old_log_prob = actor_rollout_ref_wg.compute_log_prob(output)
+       ref_log_prob = actor_rollout_ref_wg.compute_ref_log_prob(output)
+       values = critic_wg.compute_values(output)
+       rewards = reward_wg.compute_scores(output)
+       # compute_advantages is running directly on the control process
+       advantages = compute_advantages(values, rewards)
+       output = output.union(old_log_prob)
+       output = output.union(ref_log_prob)
+       output = output.union(values)
+       output = output.union(rewards)
+       output = output.union(advantages)
+       # update actor
+       actor_rollout_ref_wg.update_actor(output)
+       critic.update_critic(output)
+
+Takeaways
+~~~~~~~~~~~~~~~~~~~~
+- This programming paradigm enables users to use different computation backend without modification of the control process.
+- This programming paradigm enables flexible placement (by changing the mapping of WorkerGroup and ResourcePool) without modification of the control process.
+
+Repository organization
+------------------------------------------------
+
+Important code files in the repository are organized as below:
+
+.. code-block:: bash
+
+   verl # the verl package
+     trainer
+       main_ppo.py  # the entrypoint for RL training
+       ppo
+         ray_trainer.py  # the training loop for RL algorithms such as PPO
+       fsdp_sft_trainer.py  # the SFT trainer with FSDP backend
+     config
+       generation.yaml  # configuration template for rollout
+       ppo_trainer.yaml  # configuration template for the RL trainer
+     workers
+       protocol.py  # the interface of DataProto
+       fsdp_workers.py   # the FSDP worker interfaces: ActorRolloutRefWorker, CriticWorker, RewardModelWorker
+       megatron_workers.py  # the Megatron worker interfaces: ActorRolloutRefWorker, CriticWorker, RewardModelWorker
+       actor
+         dp_actor.py  #  data parallel actor with FSDP backend
+         megatron_actor.py  # nD parallel actor with Megatron backend
+       critic
+         dp_critic.py  # data parallel critic with FSDP backend
+         megatron_critic.py  # nD parallel critic with FSDP backend
+       reward_model
+         megatron
+           reward_model.py  # reward model with Megatron backend
+       rollout
+         vllm
+           vllm_rollout.py  # rollout with vllm backend
+         hf_rollout.py  # rollout with huggingface TGI backend
+       sharding_manager
+         fsdp_ulysses.py  # data and model resharding when using FSDP + ulysses
+         fsdp_vllm.py  # data and model resharding when using FSDP + ulysses + vllm
+         megatron_vllm.py  # data and model resharding when using Megatron + vllm
+     utils
+       dataset  # datasets for SFT/RM/RL
+       reward_score  # function based reward
+         gsm8k.py  # reward function for gsm8k dataset
+         math.py  # reward function for math dataset
+       seqlen_balancing.py  # the sequence balance optimization
+     models
+       llama  # Megatron implementation for llama, deepseek, mistral, etc
+       transformers  # ulysses integration with transformer models such as llama, qwen, etc
+       weight_loader_registery.py  # registry of weight loaders for loading hf ckpt into Megatron
+     third_party
+       vllm  # adaptor for vllm's usage in RL
+         vllm_spmd  # vllm >= v0.7 adaptor
+   examples  # example scripts
+   tests  # integration and unit tests
+   .github  # the configuration of continuous integration tests
+
+
+.. [1] HybridFlow: A Flexible and Efficient RLHF Framework: https://arxiv.org/abs/2409.19256v2
+.. [2] Data flow graph credit to CS231n 2024 lecture 4: https://cs231n.stanford.edu/slides/2024/lecture_4.pdf
+.. [3] PPO dataflow graph credit to 低级炼丹师 from Zhihu​: https://zhuanlan.zhihu.com/p/635757674
+.. [4] RLFlow
diff --git a/code/RL_model/verl/verl_train/docs/index.rst b/code/RL_model/verl/verl_train/docs/index.rst
new file mode 100644
index 0000000000000000000000000000000000000000..2e1bc7a04e276b27c84b113172acfe44f627bc97
--- /dev/null
+++ b/code/RL_model/verl/verl_train/docs/index.rst
@@ -0,0 +1,218 @@
+Welcome to verl's documentation!
+================================================
+
+verl is a flexible, efficient and production-ready RL training framework designed for large language models (LLMs) post-training. It is an open source implementation of the `HybridFlow <https://arxiv.org/pdf/2409.19256>`_ paper.
+
+verl is flexible and easy to use with:
+
+- **Easy extension of diverse RL algorithms**: The hybrid programming model combines the strengths of single-controller and multi-controller paradigms to enable flexible representation and efficient execution of complex Post-Training dataflows. Allowing users to build RL dataflows in a few lines of code.
+
+- **Seamless integration of existing LLM infra with modular APIs**: Decouples computation and data dependencies, enabling seamless integration with existing LLM frameworks, such as PyTorch FSDP, Megatron-LM, vLLM and SGLang. Moreover, users can easily extend to other LLM training and inference frameworks.
+
+- **Flexible device mapping and parallelism**: Supports various placement of models onto different sets of GPUs for efficient resource utilization and scalability across different cluster sizes.
+
+- Ready integration with popular HuggingFace models
+
+
+verl is fast with:
+
+- **State-of-the-art throughput**: By seamlessly integrating existing SOTA LLM training and inference frameworks, verl achieves high generation and training throughput.
+
+- **Efficient actor model resharding with 3D-HybridEngine**: Eliminates memory redundancy and significantly reduces communication overhead during transitions between training and generation phases.
+
+--------------------------------------------
+
+.. _Contents:
+
+.. toctree::
+   :maxdepth: 2
+   :caption: Quickstart
+
+   start/install
+   start/quickstart
+   start/multinode
+   start/ray_debug_tutorial
+   start/more_resources
+   start/agentic_rl
+
+.. toctree::
+   :maxdepth: 2
+   :caption: Programming guide
+
+   hybrid_flow
+   single_controller
+
+.. toctree::
+   :maxdepth: 1
+   :caption: Data Preparation
+
+   preparation/prepare_data
+   preparation/reward_function
+
+.. toctree::
+   :maxdepth: 2
+   :caption: Configurations
+
+   examples/config
+
+.. toctree::
+   :maxdepth: 1
+   :caption: PPO Example
+
+   examples/ppo_code_architecture
+   examples/gsm8k_example
+   examples/multi_modal_example
+   examples/skypilot_examples
+
+.. toctree::
+   :maxdepth: 1
+   :caption: Algorithms
+
+   algo/ppo.md
+   algo/grpo.md
+   algo/collabllm.md
+   algo/dapo.md
+   algo/spin.md
+   algo/sppo.md
+   algo/entropy.md
+   algo/opo.md
+   algo/baseline.md
+   algo/gpg.md
+   algo/rollout_corr.md
+   algo/rollout_corr_math.md
+   algo/otb.md
+
+.. toctree::
+   :maxdepth: 1
+   :caption: PPO Trainer and Workers
+
+   workers/ray_trainer
+   workers/fsdp_workers
+   workers/megatron_workers
+   workers/sglang_worker
+   workers/trtllm_worker
+   workers/model_engine
+
+.. toctree::
+   :maxdepth: 1
+   :caption: Performance Tuning Guide
+
+   perf/dpsk.md
+   perf/best_practices
+   perf/perf_tuning
+   README_vllm0.8.md
+   perf/device_tuning
+   perf/verl_profiler_system.md
+   perf/nsight_profiling.md
+   perf/torch_profiling.md
+
+.. toctree::
+   :maxdepth: 1
+   :caption: Adding new models
+
+   advance/fsdp_extension
+   advance/megatron_extension
+
+.. toctree::
+   :maxdepth: 1
+   :caption: Advanced Features
+
+   advance/checkpoint
+   advance/rope
+   advance/attention_implementation
+   advance/ppo_lora.rst
+   sglang_multiturn/multiturn.rst
+   sglang_multiturn/interaction_system.rst
+   advance/placement
+   advance/dpo_extension
+   examples/sandbox_fusion_example
+   advance/rollout_trace.rst
+   advance/rollout_skip.rst
+   advance/one_step_off
+   advance/agent_loop
+   advance/reward_loop
+   advance/fully_async
+   data/transfer_queue.md
+   advance/grafana_prometheus.md
+   advance/fp8.md
+   advance/async-on-policy-distill
+   advance/mtp.md
+
+.. toctree::
+   :maxdepth: 1
+   :caption: Hardware Support
+
+   amd_tutorial/amd_build_dockerfile_page.rst
+   amd_tutorial/amd_vllm_page.rst
+   ascend_tutorial/ascend_quick_start.rst
+   ascend_tutorial/ascend_consistency.rst
+   ascend_tutorial/ascend_profiling_zh.rst
+   ascend_tutorial/ascend_profiling_en.rst
+   ascend_tutorial/dockerfile_build_guidance.rst
+   ascend_tutorial/ascend_sglang_quick_start.rst
+   ascend_tutorial/examples/gspo_optimization_practice.md
+   ascend_tutorial/examples/dapo_multi_model_optimization_practice.md
+   ascend_tutorial/examples/ascend_sglang_best_practices.rst
+
+.. toctree::
+   :maxdepth: 1
+   :caption: API References
+
+   api/data
+   api/single_controller.rst
+   api/trainer.rst
+   api/utils.rst
+
+.. toctree::
+   :maxdepth: 1
+   :caption: Blog
+
+   blog/v0.7.md
+
+.. toctree::
+   :maxdepth: 2
+   :caption: FAQ
+
+   faq/faq
+
+.. toctree::
+   :maxdepth: 1
+   :caption: Development Notes
+
+   sglang_multiturn/sandbox_fusion.rst
+
+Contribution
+-------------
+
+verl is free software; you can redistribute it and/or modify it under the terms
+of the Apache License 2.0. We welcome contributions.
+Join us on `GitHub <https://github.com/volcengine/verl>`_, `Slack <https://join.slack.com/t/verlgroup/shared_invite/zt-2w5p9o4c3-yy0x2Q56s_VlGLsJ93A6vA>`_ and `Wechat <https://raw.githubusercontent.com/eric-haibin-lin/verl-community/refs/heads/main/WeChat.JPG>`_ for discussions.
+
+Contributions from the community are welcome! Please check out our `project roadmap <https://github.com/volcengine/verl/issues/710>`_ and `good first issues <https://github.com/volcengine/verl/issues?q=is%3Aissue%20state%3Aopen%20label%3A%22good%20first%20issue%22>`_ to see where you can contribute.
+
+Code Linting and Formatting
+^^^^^^^^^^^^^^^^^^^^^^^^^^^^
+
+We use pre-commit to help improve code quality. To initialize pre-commit, run:
+
+.. code-block:: bash
+
+   pip install pre-commit
+   pre-commit install
+
+To resolve CI errors locally, you can also manually run pre-commit by:
+
+.. code-block:: bash
+
+   pre-commit run
+
+Adding CI tests
+^^^^^^^^^^^^^^^^^^^^^^^^
+
+If possible, please add CI test(s) for your new feature:
+
+1. Find the most relevant workflow yml file, which usually corresponds to a ``hydra`` default config (e.g. ``ppo_trainer``, ``ppo_megatron_trainer``, ``sft_trainer``, etc).
+2. Add related path patterns to the ``paths`` section if not already included.
+3. Minimize the workload of the test script(s) (see existing scripts for examples).
+
+We are HIRING! Send us an `email <mailto:haibin.lin@bytedance.com>`_ if you are interested in internship/FTE opportunities in MLSys/LLM reasoning/multimodal alignment.
diff --git a/code/RL_model/verl/verl_train/docs/requirements-docs.txt b/code/RL_model/verl/verl_train/docs/requirements-docs.txt
new file mode 100644
index 0000000000000000000000000000000000000000..55ccdb8f7149bd6b774b592dca068e63e87256db
--- /dev/null
+++ b/code/RL_model/verl/verl_train/docs/requirements-docs.txt
@@ -0,0 +1,13 @@
+# markdown support
+recommonmark
+myst_parser
+# markdown table support
+sphinx-markdown-tables
+
+# theme default rtd
+
+# crate-docs-theme
+sphinx-rtd-theme
+
+# pin tokenizers version to avoid env_logger version req
+tokenizers==0.21
diff --git a/code/RL_model/verl/verl_train/docs/single_controller.rst b/code/RL_model/verl/verl_train/docs/single_controller.rst
new file mode 100644
index 0000000000000000000000000000000000000000..d12177854e0ad2f2060a4255a4cde9cd93fe8263
--- /dev/null
+++ b/code/RL_model/verl/verl_train/docs/single_controller.rst
@@ -0,0 +1,336 @@
+The Design of ``verl.single_controller``
+==============================================
+
+Last updated: 05/21/2025.
+
+**Author:**\  `Wang Zhang <https://github.com/zw0610>`__
+
+Preface
+-------
+
+We prepared this document for developers of ``verl``, particularly those
+interested in understanding or contributing to the
+``verl.single_controller`` module. It is not intended for end users, but
+for contributors seeking to understand the architectural rationale and
+internal mechanics.
+
+--------------
+
+Origin
+------
+
+The ``single_controller`` module originated from a request I received —
+to adapt a toy single-process RLHF script into a distributed system with
+minimal changes, while maintaining ease of debugging.
+
+Common practice — such as using PyTorch’s Distributed Data Parallel
+(DDP) — typically involves wrapping ``nn.Module`` and launching multiple
+processes that execute the same function under different ranks. However,
+this approach presents two main limitations in the context of
+distributed RLHF: - Difficulty representing multiple DAGs as required by
+PPO; - Difficulty inspecting intermediate tensors during training.
+
+To maintain debuggability, we opted for a different approach — breaking
+the training loop into well-defined stages like ``generate_sequences``,
+``compute_advantages``, and so on.
+
+We selected `Ray <https://www.ray.io/>`__ as the initial backend for
+``verl`` due to its ability to expose Python class methods as RPC
+endpoints. However, Ray’s default model only supports **one method call,
+one RPC**, while training LLMs typically requires coordination across
+multiple processes.
+
+To hide this multi-Ray actors invocation for a single method from users,
+we introduced the following components:
+
+-  ``WorkerGroup`` – manages a group of remote workers and provides
+   a unified interface for multi-process distributed computation;
+-  ``ResourcePool`` – binds computational resources to worker
+   processes;
+-  ``ClassWithArgs`` – enables delayed remote instantiation with
+   specified initialization arguments.
+
+--------------
+
+A Running Example: ``generate_sequences``
+-----------------------------------------
+
+To illustrate the design, we walk through how the ``generate_sequences``
+method in the ``ActorRolloutRefWorker`` class is registered and invoked
+across distributed workers.
+
+--------------
+
+Step 1: Register with a Decorator
+~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
+
+The first step is to define the ``generate_sequences`` and decorate it
+with ``@register`` as it will be called in driver script.
+
+**Source:**
+`fsdp_workers.py <https://github.com/volcengine/verl/blob/c59ab2f4788f9a910836a9f2f53dcdb62dfa314e/verl/workers/fsdp_workers.py#L528>`__
+
+.. code:: python
+
+   class ActorRolloutRefWorker(Worker):
+       ...
+       @register(dispatch_mode=Dispatch.DP_COMPUTE_PROTO)
+       def generate_sequences(self, prompts: DataProto):
+           prompts = prompts.to(torch.cuda.current_device())
+           ...
+
+The ``@register`` decorator adds metadata to the ``generate_sequences``
+method. Currently, it doesn’t alter functionality, but attaches
+attributes via a magic key (``MAGIC_ATTR``):
+
+**Source:**
+`decorator.py <https://github.com/volcengine/verl/blob/c59ab2f4788f9a910836a9f2f53dcdb62dfa314e/verl/single_controller/base/decorator.py#L411>`__
+
+.. code:: python
+
+   def register(dispatch_mode=Dispatch.ALL_TO_ALL, execute_mode=Execute.ALL, blocking=True, materialize_futures=True):
+       ...
+       def decorator(func):
+           @wraps(func)
+           def inner(*args, **kwargs):
+               if materialize_futures:
+                   args, kwargs = _materialize_futures(*args, **kwargs)
+               return func(*args, **kwargs)
+
+           attrs = {"dispatch_mode": dispatch_mode, "execute_mode": execute_mode, "blocking": blocking}
+           setattr(inner, MAGIC_ATTR, attrs)
+           return inner
+
+       return decorator
+
+As the code shows, values of ``dispatch_mode``, ``execute_mode`` and
+``blocking`` is attached the ``generate_sequences`` method.
+
+--------------
+
+Step 2: Binding During Initialization
+~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
+
+These attached attributes are extracted and utilized when
+``ActorRolloutRefWorker``, wrapped in a ``RayClassWithArgs``, is passed
+into a ``RayWorkerGroup``.
+
+**Source:**
+`main_generation.py <https://github.com/volcengine/verl/blob/4ae9a0fdab229f75f080e9478807783ed4c97154/verl/trainer/main_generation.py#L82>`__
+
+.. code:: python
+
+   ray_cls_with_init = RayClassWithInitArgs(cls=ray.remote(ActorRolloutRefWorker), config=config, role="rollout")
+   resource_pool = RayResourcePool(process_on_nodes=[config.trainer.n_gpus_per_node] * config.trainer.nnodes)
+   wg = RayWorkerGroup(resource_pool=resource_pool, ray_cls_with_init=ray_cls_with_init)
+
+During the
+`initialization <https://github.com/volcengine/verl/blob/c59ab2f4788f9a910836a9f2f53dcdb62dfa314e/verl/single_controller/ray/base.py#L184>`__
+of ``RayWorkerGroup``, two key steps occur:
+
+1. Worker instances (Ray actors) are created:
+   `RayWorkerGroup._init_with_resource_pool <https://github.com/volcengine/verl/blob/c59ab2f4788f9a910836a9f2f53dcdb62dfa314e/verl/single_controller/ray/base.py#L211>`__
+2. Methods decorated with ``@register`` are bound to ``RayWorkerGroup``:
+   `RayWorkerGroup._bind_worker_method <https://github.com/volcengine/verl/blob/c59ab2f4788f9a910836a9f2f53dcdb62dfa314e/verl/single_controller/ray/base.py#L214>`__
+
+.. figure:: https://github.com/eric-haibin-lin/verl-community/blob/main/docs/worker_group_init.png?raw=true
+   :alt: initialization_and_binding_of_worker_group
+
+   initialization_and_binding_of_worker_group
+
+The binding procedure is the heart of ``verl.single_controller``.
+
+**Key function:**
+`WorkerGroup._bind_worker_method <https://github.com/volcengine/verl/blob/c59ab2f4788f9a910836a9f2f53dcdb62dfa314e/verl/single_controller/base/worker_group.py#L143>`__
+
+.. code:: python
+
+   def _bind_worker_method(self, user_defined_cls, func_generator):
+       ...
+       for method_name in dir(user_defined_cls):
+           try:
+               method = getattr(user_defined_cls, method_name)
+               assert callable(method)
+           except Exception:
+               continue  # Skip properties
+           <<<to be continue 1>>>
+
+When a method has the ``MAGIC_ATTR``, the attributes set by
+``@register`` are extracted:
+
+.. code:: python
+
+           <<<continue 1>>>
+           if hasattr(method, MAGIC_ATTR):
+               attribute = getattr(method, MAGIC_ATTR)
+               dispatch_mode = attribute["dispatch_mode"]
+               execute_mode = attribute["execute_mode"]
+               blocking = attribute["blocking"]
+
+               <<<to be continue 2>>>
+
+As show in the flow chart above, these attributes are fed into
+``func_generator``. However, ``func_generator`` takes ``method_name``,
+``dispatch_fn``, ``collect_fn``, ``execute_fn``, ``blocking``. We need
+to find the corresponding ``dispatch_fn`` and ``collect_fn`` associated
+with the ``dispatch_mode`` (``DP_COMPUTE_PROTO``) from
+`DISPATCH_MODE_FN_REGISTRY <https://github.com/volcengine/verl/blob/c59ab2f4788f9a910836a9f2f53dcdb62dfa314e/verl/single_controller/base/decorator.py#L387>`__:
+
+.. code:: python3
+
+   DISPATCH_MODE_FN_REGISTRY = {
+       Dispatch.ONE_TO_ALL: {
+           "dispatch_fn": dispatch_one_to_all,
+           "collect_fn": collect_all_to_all,
+       },
+       ...
+       Dispatch.DP_COMPUTE_PROTO: {
+           "dispatch_fn": dispatch_dp_compute_data_proto,
+           "collect_fn": collect_dp_compute_data_proto,
+       },
+       ...
+   }
+
+Similarly, the ``execute_fn`` is selected by ``execute_mode`` and
+extracted by:
+
+.. code:: python
+
+               <<<continue 2>>>
+               # get execute_fn_name
+               execute_mode = get_predefined_execute_fn(execute_mode=execute_mode)
+               wg_execute_fn_name = execute_mode["execute_fn_name"]
+
+               # get execute_fn from string
+               try:
+                   execute_fn = getattr(self, wg_execute_fn_name)
+                   assert callable(execute_fn), "execute_fn must be callable"
+               except Exception:
+                   print(f"execute_fn {wg_execute_fn_name} is invalid")
+                   raise
+               <<<to be continue 3>>>
+
+In this ``generate_sequences`` cases: -
+``dispatch_mode = Dispatch.DP_COMPUTE_PROTO`` -
+``dispatch_fn = dispatch_dp_compute_data_proto`` -
+``collect_fn = collect_dp_compute_data_proto`` -
+``execute_fn = RayWorkerGroup.execute_all``
+
+ONE_TO_ALL v.s. DP_COMPUTE_PROTO
+^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^
+
+``dispatch_mode`` is associated with a ``dispatch_fn`` and a
+``collect_fn``. As the name implies, ``dispatch_fn`` processes the input
+arguments in ``WorkerGroup`` and generate a batch (list) of input
+arguments, each of which will be fed into a worker attached to the
+``WorkerGroup``.
+
+``dispatch_fn`` of ``ONE_TO_ALL`` is
+`dispatch_one_to_all <https://github.com/volcengine/verl/blob/c59ab2f4788f9a910836a9f2f53dcdb62dfa314e/verl/single_controller/base/decorator.py#L119>`__,
+which just duplicates all the input arguments into N replicas, where N
+equals the number of Workers attached to the ``worker_group``:
+
+.. code:: python
+
+   def dispatch_one_to_all(worker_group, *args, **kwargs):
+       args = tuple([arg] * worker_group.world_size for arg in args)
+       kwargs = {k: [v] * worker_group.world_size for k, v in kwargs.items()}
+       return args, kwargs
+
+``dispatch_fn`` of ``DP_COMPUTE_PROTO`` is
+`dispatch_dp_compute_data_proto <https://github.com/volcengine/verl/blob/c59ab2f4788f9a910836a9f2f53dcdb62dfa314e/verl/single_controller/base/decorator.py#L350>`__,
+which uses ``DataProto.chunk`` to split a large ``DataProto`` into N
+smaller ``DataProto``, where N equals the world_size (number of the
+workers) of the ``worker_group``:
+
+.. code:: python
+
+   def dispatch_dp_compute_data_proto(worker_group, *args, **kwargs):
+       from verl.single_controller.base.worker_group import WorkerGroup
+
+       assert isinstance(worker_group, WorkerGroup)
+       # Note: enable auto padding for dp compute DatapProto
+       splitted_args, splitted_kwargs = _split_args_kwargs_data_proto_with_auto_padding(
+           worker_group.world_size,
+           *args,
+           **kwargs,
+       )
+       return splitted_args, splitted_kwargs
+
+The ``collect_fn`` follows the same pattern and process a batch (list)
+of returned value from all workers of a ``WorkerGroup`` and merge it
+into a list as ``collect_all_to_all`` does or a large ``DataProto`` as
+``collect_dp_compute_data_proto`` does.
+
+Finally, a new method is dynamically generated using ``func_generator``
+and added to the ``WorkerGroup`` instance:
+
+.. code:: python
+
+               <<<continue 3>>>
+               # bind a new method to the RayWorkerGroup
+               func = func_generator(
+                   self,
+                   method_name,
+                   dispatch_fn=dispatch_fn,
+                   collect_fn=collect_fn,
+                   execute_fn=execute_fn,
+                   blocking=blocking,
+               )
+
+               try:
+                   setattr(self, method_name, func)
+                   method_names.append(method_name)
+               except Exception as e:
+                   raise ValueError(f"Fail to set method_name {method_name}") from e
+
+This makes the method invocable via the ``WorkerGroup`` interface.
+
+--------------
+
+Step 3: Call Chain
+~~~~~~~~~~~~~~~~~~
+
+All the machinery above ensures that distributed calls feel identical to
+single-process ones. In the original single-process script, the code
+looks like:
+
+.. code:: python
+
+   rollout = Rollout()
+   rollout.generate_sequences(batch)
+
+With ``verl``, the multiprocess program becomes:
+
+.. code:: python
+
+   rollout = RayWorkerGroup(resource_pool=[4], RayClassWithArgs(Rollout))
+   rollout.generate_sequences(batch)
+
+.. figure:: https://github.com/eric-haibin-lin/verl-community/blob/main/docs/call_generate_sequences.png?raw=true
+   :alt: call_chain_of_generate_sequences
+
+   call_chain_of_generate_sequences
+
+Behind this simple call: - ``dispatch_fn`` splits input across workers -
+``execute_fn`` performs the actual remote invocation - ``collect_fn``
+gathers the results
+
+All of this is abstracted away, enabling developers to write distributed
+code with minimal changes to their existing logic.
+
+--------------
+
+Beyond RL Post-Training: Generalizing ``verl.single_controller``
+----------------------------------------------------------------
+
+The ``verl.single_controller`` module generalizes well beyond
+reinforcement learning. It provides a clean abstraction to batch-process
+remote method calls, with automatic input/output handling.
+
+By minimizing the gap between single-process and multi-process scripts,
+``verl.single_controller`` opens the door to distributed computing in
+broader domains — not limited to RL post-training.
+
+We hope this design inspires more examples and extensions from the
+community.
diff --git a/code/RL_model/verl/verl_train/install.sh b/code/RL_model/verl/verl_train/install.sh
new file mode 100644
index 0000000000000000000000000000000000000000..2366ff4c120582c012694eed08070b3dcc4ca642
--- /dev/null
+++ b/code/RL_model/verl/verl_train/install.sh
@@ -0,0 +1,62 @@
+#!/bin/bash
+
+USE_MEGATRON=${USE_MEGATRON:-1}
+USE_SGLANG=${USE_SGLANG:-1}
+
+export MAX_JOBS=32
+
+echo "0. Install uv (The fast package installer)"
+pip install uv
+
+echo "1. install inference frameworks and pytorch they need"
+if [ $USE_SGLANG -eq 1 ]; then
+    # --system is needed if not running inside an active virtual environment
+    uv pip install --system "sglang[all]==0.5.2" --no-cache-dir && uv pip install --system torch-memory-saver --no-cache-dir
+fi
+uv pip install --system --no-cache-dir "vllm==0.11.0"
+
+echo "2. install basic packages"
+uv pip install --system "transformers[hf_xet]>=4.51.0" accelerate datasets peft hf-transfer \
+    "numpy<2.0.0" "pyarrow>=15.0.0" pandas "tensordict>=0.8.0,<=0.10.0,!=0.9.0" torchdata \
+    ray[default] codetiming hydra-core pylatexenc qwen-vl-utils wandb dill pybind11 liger-kernel mathruler \
+    pytest py-spy pre-commit ruff tensorboard 
+
+echo "pyext is lack of maintainace and cannot work with python 3.12."
+echo "if you need it for prime code rewarding, please install using patched fork:"
+echo "uv pip install --system git+https://github.com/ShaohonChen/PyExt.git@py311support"
+
+uv pip install --system "nvidia-ml-py>=12.560.30" "fastapi[standard]>=0.115.0" "optree>=0.13.0" "pydantic>=2.9" "grpcio>=1.62.1"
+
+
+echo "3. install FlashAttention and FlashInfer"
+# Install flash-attn-2.8.1 (cxx11abi=False)
+# uv can install directly from the file after wget
+wget -nv https://github.com/Dao-AILab/flash-attention/releases/download/v2.8.1/flash_attn-2.8.1+cu12torch2.8cxx11abiFALSE-cp312-cp312-linux_x86_64.whl && \
+    uv pip install --system --no-cache-dir flash_attn-2.8.1+cu12torch2.8cxx11abiFALSE-cp312-cp312-linux_x86_64.whl
+
+uv pip install --system --no-cache-dir flashinfer-python==0.3.1
+
+
+if [ $USE_MEGATRON -eq 1 ]; then
+    echo "4. install TransformerEngine and Megatron"
+    echo "Notice that TransformerEngine installation can take very long time, please be patient"
+    uv pip install --system "onnxscript==0.3.1"
+    
+    # Keeping no-deps here as per original script logic
+    NVTE_FRAMEWORK=pytorch uv pip install --system --no-deps git+https://github.com/NVIDIA/TransformerEngine.git@v2.6
+    uv pip install --system --no-deps git+https://github.com/NVIDIA/Megatron-LM.git@core_v0.13.1
+fi
+
+
+echo "5. May need to fix opencv"
+uv pip install --system opencv-python
+uv pip install --system opencv-fixer && \
+    python -c "from opencv_fixer import AutoFix; AutoFix()"
+
+
+if [ $USE_MEGATRON -eq 1 ]; then
+    echo "6. Install cudnn python package (avoid being overridden)"
+    uv pip install --system nvidia-cudnn-cu12==9.10.2.21
+fi
+
+echo "Successfully installed all packages"
\ No newline at end of file
diff --git a/code/RL_model/verl/verl_train/pyproject.toml b/code/RL_model/verl/verl_train/pyproject.toml
new file mode 100644
index 0000000000000000000000000000000000000000..89bf6798a8bb48a0bf6f65b24b5f36d5599a13af
--- /dev/null
+++ b/code/RL_model/verl/verl_train/pyproject.toml
@@ -0,0 +1,113 @@
+# -------------------------------
+# build-system
+# -------------------------------
+[build-system]
+requires = [
+    "setuptools>=61.0",
+    "wheel"
+]
+build-backend = "setuptools.build_meta"
+
+# -------------------------------
+# project (PEP 621 metadata)
+# -------------------------------
+[project]
+name = "verl"
+# We'll mark the version as "dynamic" because it's read from the file "verl/version/version" 
+# (PEP 621 calls this "dynamic version"). 
+# The actual version is specified in the [tool.setuptools.dynamic] section below.
+dynamic = ["version", "dependencies", "optional-dependencies", "authors", "urls"]
+
+description = "verl: Volcano Engine Reinforcement Learning for LLM"
+license = {text = "Apache-2.0"}  # Changed from file to text format
+readme = {file = "README.md", content-type = "text/markdown"}
+requires-python = ">=3.10"
+
+# -------------------------------
+# tool.ruff - Linting configuration
+# -------------------------------
+[tool.ruff]
+# Note: While the formatter will attempt to format lines such that they remain within the line-length,
+# it isn't a hard upper bound, and formatted lines may exceed the line-length.
+line-length = 120
+exclude = ["scripts/legacy_model_merger.py"]
+
+[tool.ruff.lint]
+isort = {known-first-party = ["verl"]}
+# c.f. https://github.com/vllm-project/vllm/blob/ce8d6b75fc0586045df75ee1568a5b5f9957251b/pyproject.toml
+select = [
+    # pycodestyle
+    "E",
+    # Pyflakes
+    "F",
+    # pyupgrade
+    "UP",
+    # flake8-bugbear
+    "B",
+    # isort
+    "I",
+    "G",
+]
+ignore = [
+    # star imports
+    "F405", "F403",
+    # lambda expression assignment
+    "E731",
+    # Loop control variable not used within loop body
+    "B007",
+    # f-string format
+    "UP032",
+    # `.log()` statement uses f-string
+    "G004",
+    # X | None for type annotations
+    "UP045",
+    # deprecated import
+    "UP035",
+]
+
+# -------------------------------
+# tool.mypy - typechecking config
+# -------------------------------
+[tool.mypy]
+pretty            = true
+ignore_missing_imports = true
+explicit_package_bases = true
+follow_imports = "skip"
+
+# Blanket silence
+ignore_errors = true
+
+[[tool.mypy.overrides]]
+module = [
+"verl.trainer.config.algorithm",
+"verl.trainer.ppo.core_algos",
+"verl.trainer.ppo.reward",
+"verl.workers.reward_manager",
+"verl.workers.reward_manager.*",
+]
+ignore_errors = false
+
+# -------------------------------
+# tool.setuptools - Additional config
+# -------------------------------
+[tool.setuptools]
+# True means `setuptools` will attempt to include all relevant files in package_data automatically.
+# This corresponds to `include_package_data=True` in setup.py.
+include-package-data = true
+
+# We read the version from a file in 'verl/version/version'
+[tool.setuptools.dynamic]
+version = {file = "verl/version/version"}
+
+# If you need to mimic `package_dir={'': '.'}`:
+[tool.setuptools.package-dir]
+"" = "."
+
+# If you need to include specific non-Python data (like YAML files or version file):
+# This is the rough equivalent of package_data={'': ['version/*'], 'verl': ['trainer/config/*.yaml']}
+[tool.setuptools.package-data]
+verl = [
+  "version/*",
+  "trainer/config/*.yaml",
+  "trainer/config/*/*.yaml",
+]
diff --git a/code/RL_model/verl/verl_train/qwen3-4b-instruct-2507-function-rm.log b/code/RL_model/verl/verl_train/qwen3-4b-instruct-2507-function-rm.log
new file mode 100644
index 0000000000000000000000000000000000000000..887ca75fbef19047366780c2157cc80d15fd22cd
--- /dev/null
+++ b/code/RL_model/verl/verl_train/qwen3-4b-instruct-2507-function-rm.log
@@ -0,0 +1,975 @@
+/home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/torch/cuda/__init__.py:63: FutureWarning: The pynvml package is deprecated. Please install nvidia-ml-py instead. If you did not install pynvml directly, please report this to the maintainers of the package that installed pynvml for you.
+  import pynvml  # type: ignore[import]
+INFO 02-01 08:02:59 [__init__.py:216] Automatically detected platform cuda.
+/home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/megatron/core/models/backends.py:21: UserWarning: Apex is not installed. Falling back to Torch Norm
+  warnings.warn("Apex is not installed. Falling back to Torch Norm")
+/home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/megatron/core/optimizer/__init__.py:18: UserWarning: Transformer Engine and Apex are not installed. Falling back to Torch optimizers.
+  warnings.warn(
+/home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/megatron/core/optimizer/optimizer.py:28: UserWarning: Transformer Engine and Apex are not installed. Falling back to local implementations of multi_tensor_applier and multi_tensor_scale
+  warnings.warn(
+/home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/megatron/core/optimizer/clip_grads.py:29: UserWarning: Transformer Engine and Apex are not installed. Falling back to local implementations of multi_tensor_applier, multi_tensor_l2norm, and multi_tensor_scale
+  warnings.warn(
+/home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/megatron/core/models/gpt/gpt_layer_specs.py:67: UserWarning: Apex is not installed. Falling back to Torch Norm
+  warnings.warn("Apex is not installed. Falling back to Torch Norm")
+ray init kwargs: {'num_cpus': None, 'runtime_env': {'env_vars': {'TOKENIZERS_PARALLELISM': 'true', 'NCCL_DEBUG': 'WARN', 'VLLM_LOGGING_LEVEL': 'WARN', 'VLLM_ALLOW_RUNTIME_LORA_UPDATING': 'true', 'CUDA_DEVICE_MAX_CONNECTIONS': '1', 'NCCL_CUMEM_ENABLE': '0', 'VLLM_DISABLE_COMPILE_CACHE': '1', 'HCCL_HOST_SOCKET_PORT_RANGE': 'auto', 'HCCL_NPU_SOCKET_PORT_RANGE': 'auto'}, 'working_dir': None}}
+2026-02-01 08:03:05,272	INFO worker.py:2014 -- Started a local Ray instance. View the dashboard at http://127.0.0.1:8265 
+/home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/ray/_private/worker.py:2062: FutureWarning: Tip: In future versions of Ray, Ray will no longer override accelerator visible devices env var if num_gpus=0 or num_gpus=None (default). To enable this behavior and turn off this error message, set RAY_ACCEL_ENV_VAR_OVERRIDE_ON_ZERO=0
+  warnings.warn(
+(pid=3248830) /home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/torch/cuda/__init__.py:63: FutureWarning: The pynvml package is deprecated. Please install nvidia-ml-py instead. If you did not install pynvml directly, please report this to the maintainers of the package that installed pynvml for you.
+(pid=3248830)   import pynvml  # type: ignore[import]
+(pid=3248830) /home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/megatron/core/models/backends.py:21: UserWarning: Apex is not installed. Falling back to Torch Norm
+(pid=3248830)   warnings.warn("Apex is not installed. Falling back to Torch Norm")
+(pid=3248830) /home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/megatron/core/optimizer/__init__.py:18: UserWarning: Transformer Engine and Apex are not installed. Falling back to Torch optimizers.
+(pid=3248830)   warnings.warn(
+(pid=3248830) /home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/megatron/core/optimizer/optimizer.py:28: UserWarning: Transformer Engine and Apex are not installed. Falling back to local implementations of multi_tensor_applier and multi_tensor_scale
+(pid=3248830)   warnings.warn(
+(pid=3248830) /home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/megatron/core/optimizer/clip_grads.py:29: UserWarning: Transformer Engine and Apex are not installed. Falling back to local implementations of multi_tensor_applier, multi_tensor_l2norm, and multi_tensor_scale
+(pid=3248830)   warnings.warn(
+(TaskRunner pid=3248830) TaskRunner hostname: beta, PID: 3248830
+(pid=3248830) /home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/megatron/core/models/gpt/gpt_layer_specs.py:67: UserWarning: Apex is not installed. Falling back to Torch Norm
+(pid=3248830)   warnings.warn("Apex is not installed. Falling back to Torch Norm")
+(TaskRunner pid=3248830) {'actor_rollout_ref': 
+(TaskRunner pid=3248830) {'actor': {'_target_': 'verl.workers.config.FSDPActorConfig',
+(TaskRunner pid=3248830)                                  'calculate_entropy': False,
+(TaskRunner pid=3248830)                                  'calculate_sum_pi_squared': False,
+(TaskRunner pid=3248830)                                  'checkpoint': {'_target_': 'verl.trainer.config.CheckpointConfig',
+(TaskRunner pid=3248830)                                                 'async_save': False,
+(TaskRunner pid=3248830)                                                 'load_contents': ['model',
+(TaskRunner pid=3248830)                                                                   'optimizer',
+(TaskRunner pid=3248830)                                                                   'extra'],
+(TaskRunner pid=3248830)                                                 'save_contents': ['model',
+(TaskRunner pid=3248830)                                                                   'optimizer',
+(TaskRunner pid=3248830)                                                                   'extra']},
+(TaskRunner pid=3248830)                                  'clip_ratio': 0.2,
+(TaskRunner pid=3248830)                                  'clip_ratio_c': 3.0,
+(TaskRunner pid=3248830)                                  'clip_ratio_high': 0.2,
+(TaskRunner pid=3248830)                                  'clip_ratio_low': 0.2,
+(TaskRunner pid=3248830)                                  'data_loader_seed': 42,
+(TaskRunner pid=3248830)                                  'entropy_checkpointing': False,
+(TaskRunner pid=3248830)                                  'entropy_coeff': 0,
+(TaskRunner pid=3248830)                                  'entropy_from_logits_with_chunking': False,
+(TaskRunner pid=3248830)                                  'freeze_vision_tower': False,
+(TaskRunner pid=3248830)                                  'fsdp_config': {'_target_': 'verl.workers.config.FSDPEngineConfig',
+(TaskRunner pid=3248830)                                                  'dtype': 'bfloat16',
+(TaskRunner pid=3248830)                                                  'entropy_checkpointing': False,
+(TaskRunner pid=3248830)                                                  'entropy_from_logits_with_chunking': False,
+(TaskRunner pid=3248830)                                                  'forward_only': False,
+(TaskRunner pid=3248830)                                                  'forward_prefetch': False,
+(TaskRunner pid=3248830)                                                  'fsdp_size': -1,
+(TaskRunner pid=3248830)                                                  'full_determinism': False,
+(TaskRunner pid=3248830)                                                  'model_dtype': 'fp32',
+(TaskRunner pid=3248830)                                                  'offload_policy': False,
+(TaskRunner pid=3248830)                                                  'optimizer_offload': False,
+(TaskRunner pid=3248830)                                                  'param_offload': False,
+(TaskRunner pid=3248830)                                                  'reshard_after_forward': True,
+(TaskRunner pid=3248830)                                                  'seed': 42,
+(TaskRunner pid=3248830)                                                  'strategy': 'fsdp',
+(TaskRunner pid=3248830)                                                  'ulysses_sequence_parallel_size': 1,
+(TaskRunner pid=3248830)                                                  'use_orig_params': False,
+(TaskRunner pid=3248830)                                                  'use_torch_compile': True,
+(TaskRunner pid=3248830)                                                  'wrap_policy': {'min_num_params': 0}},
+(TaskRunner pid=3248830)                                  'grad_clip': 1.0,
+(TaskRunner pid=3248830)                                  'kl_loss_coef': 0.001,
+(TaskRunner pid=3248830)                                  'kl_loss_type': 'low_var_kl',
+(TaskRunner pid=3248830)                                  'loss_agg_mode': 'token-mean',
+(TaskRunner pid=3248830)                                  'loss_scale_factor': None,
+(TaskRunner pid=3248830)                                  'optim': {'_target_': 'verl.workers.config.FSDPOptimizerConfig',
+(TaskRunner pid=3248830)                                            'betas': [0.9, 0.999],
+(TaskRunner pid=3248830)                                            'clip_grad': 1.0,
+(TaskRunner pid=3248830)                                            'lr': 1e-06,
+(TaskRunner pid=3248830)                                            'lr_scheduler_type': 'constant',
+(TaskRunner pid=3248830)                                            'lr_warmup_steps': -1,
+(TaskRunner pid=3248830)                                            'lr_warmup_steps_ratio': 0.0,
+(TaskRunner pid=3248830)                                            'min_lr_ratio': 0.0,
+(TaskRunner pid=3248830)                                            'num_cycles': 0.5,
+(TaskRunner pid=3248830)                                            'optimizer': 'AdamW',
+(TaskRunner pid=3248830)                                            'optimizer_impl': 'torch.optim',
+(TaskRunner pid=3248830)                                            'override_optimizer_config': None,
+(TaskRunner pid=3248830)                                            'total_training_steps': -1,
+(TaskRunner pid=3248830)                                            'warmup_style': None,
+(TaskRunner pid=3248830)                                            'weight_decay': 0.01},
+(TaskRunner pid=3248830)                                  'policy_loss': {'_target_': 'verl.workers.config.PolicyLossConfig',
+(TaskRunner pid=3248830)                                                  'clip_cov_lb': 1.0,
+(TaskRunner pid=3248830)                                                  'clip_cov_ratio': 0.0002,
+(TaskRunner pid=3248830)                                                  'clip_cov_ub': 5.0,
+(TaskRunner pid=3248830)                                                  'kl_cov_ratio': 0.0002,
+(TaskRunner pid=3248830)                                                  'loss_mode': 'vanilla',
+(TaskRunner pid=3248830)                                                  'ppo_kl_coef': 0.1},
+(TaskRunner pid=3248830)                                  'ppo_epochs': 1,
+(TaskRunner pid=3248830)                                  'ppo_max_token_len_per_gpu': 16384,
+(TaskRunner pid=3248830)                                  'ppo_micro_batch_size': None,
+(TaskRunner pid=3248830)                                  'ppo_micro_batch_size_per_gpu': 32,
+(TaskRunner pid=3248830)                                  'ppo_mini_batch_size': 256,
+(TaskRunner pid=3248830)                                  'profiler': {'_target_': 'verl.utils.profiler.ProfilerConfig',
+(TaskRunner pid=3248830)                                               'all_ranks': False,
+(TaskRunner pid=3248830)                                               'enable': False,
+(TaskRunner pid=3248830)                                               'ranks': [],
+(TaskRunner pid=3248830)                                               'save_path': 'outputs/profile',
+(TaskRunner pid=3248830)                                               'tool': None,
+(TaskRunner pid=3248830)                                               'tool_config': {'npu': {'_target_': 'verl.utils.profiler.config.NPUToolConfig',
+(TaskRunner pid=3248830)                                                                       'analysis': True,
+(TaskRunner pid=3248830)                                                                       'contents': [],
+(TaskRunner pid=3248830)                                                                       'discrete': False,
+(TaskRunner pid=3248830)                                                                       'level': 'level0'},
+(TaskRunner pid=3248830)                                                               'nsys': {'_target_': 'verl.utils.profiler.config.NsightToolConfig',
+(TaskRunner pid=3248830)                                                                        'discrete': False},
+(TaskRunner pid=3248830)                                                               'torch': {'_target_': 'verl.utils.profiler.config.TorchProfilerToolConfig',
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+(TaskRunner pid=3248830)           'return_raw_chat': True,
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+(TaskRunner pid=3248830)                                                                                    'cuda-memory-usage': 'true',
+(TaskRunner pid=3248830)                                                                                    'trace': 'cuda,nvtx,cublas,ucx'},
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+(TaskRunner pid=3248830)                                                                                'capture-range-end': None,
+(TaskRunner pid=3248830)                                                                                'cuda-graph-trace': 'graph',
+(TaskRunner pid=3248830)                                                                                'cuda-memory-usage': 'true',
+(TaskRunner pid=3248830)                                                                                'kill': 'none',
+(TaskRunner pid=3248830)                                                                                'trace': 'cuda,nvtx,cublas,ucx'}},
+(TaskRunner pid=3248830)                                             'torch_memory': {'context': 'all',
+(TaskRunner pid=3248830)                                                              'kw_args': {},
+(TaskRunner pid=3248830)                                                              'stack_depth': 32,
+(TaskRunner pid=3248830)                                                              'stacks': 'all',
+(TaskRunner pid=3248830)                                                              'trace_alloc_max_entries': 100000}},
+(TaskRunner pid=3248830)                      'profile_continuous_steps': False,
+(TaskRunner pid=3248830)                      'save_path': 'outputs/profile',
+(TaskRunner pid=3248830)                      'steps': None,
+(TaskRunner pid=3248830)                      'tool': None},
+(TaskRunner pid=3248830)  'ray_kwargs': {'ray_init': {'num_cpus': None}, 'timeline_json_file': None},
+(TaskRunner pid=3248830)  'reward_manager': {'_target_': 'verl.trainer.config.config.RewardManagerConfig',
+(TaskRunner pid=3248830)                     'module': {'_target_': 'verl.trainer.config.config.ModuleConfig',
+(TaskRunner pid=3248830)                                'name': 'custom_reward_manager',
+(TaskRunner pid=3248830)                                'path': None},
+(TaskRunner pid=3248830)                     'name': 'naive',
+(TaskRunner pid=3248830)                     'source': 'register'},
+(TaskRunner pid=3248830)  'reward_model': {'enable': False,
+(TaskRunner pid=3248830)                   'enable_resource_pool': False,
+(TaskRunner pid=3248830)                   'forward_max_token_len_per_gpu': 32768,
+(TaskRunner pid=3248830)                   'launch_reward_fn_async': False,
+(TaskRunner pid=3248830)                   'max_length': None,
+(TaskRunner pid=3248830)                   'micro_batch_size': None,
+(TaskRunner pid=3248830)                   'micro_batch_size_per_gpu': None,
+(TaskRunner pid=3248830)                   'model': {'external_lib': None,
+(TaskRunner pid=3248830)                             'fsdp_config': {'_target_': 'verl.workers.config.FSDPEngineConfig',
+(TaskRunner pid=3248830)                                             'forward_prefetch': False,
+(TaskRunner pid=3248830)                                             'fsdp_size': -1,
+(TaskRunner pid=3248830)                                             'param_offload': False,
+(TaskRunner pid=3248830)                                             'reshard_after_forward': True,
+(TaskRunner pid=3248830)                                             'wrap_policy': {'min_num_params': 0}},
+(TaskRunner pid=3248830)                             'input_tokenizer': 'Qwen/Qwen3-4B-Instruct-2507',
+(TaskRunner pid=3248830)                             'override_config': {},
+(TaskRunner pid=3248830)                             'path': '~/models/FsfairX-LLaMA3-RM-v0.1',
+(TaskRunner pid=3248830)                             'trust_remote_code': False,
+(TaskRunner pid=3248830)                             'use_fused_kernels': False,
+(TaskRunner pid=3248830)                             'use_remove_padding': False,
+(TaskRunner pid=3248830)                             'use_shm': False},
+(TaskRunner pid=3248830)                   'n_gpus_per_node': 8,
+(TaskRunner pid=3248830)                   'nnodes': 0,
+(TaskRunner pid=3248830)                   'num_workers': 1,
+(TaskRunner pid=3248830)                   'profiler': {'_target_': 'verl.utils.profiler.ProfilerConfig',
+(TaskRunner pid=3248830)                                'all_ranks': False,
+(TaskRunner pid=3248830)                                'enable': False,
+(TaskRunner pid=3248830)                                'ranks': [],
+(TaskRunner pid=3248830)                                'save_path': 'outputs/profile',
+(TaskRunner pid=3248830)                                'tool': None,
+(TaskRunner pid=3248830)                                'tool_config': {'npu': {'_target_': 'verl.utils.profiler.config.NPUToolConfig',
+(TaskRunner pid=3248830)                                                        'analysis': True,
+(TaskRunner pid=3248830)                                                        'contents': [],
+(TaskRunner pid=3248830)                                                        'discrete': False,
+(TaskRunner pid=3248830)                                                        'level': 'level0'},
+(TaskRunner pid=3248830)                                                'nsys': {'_target_': 'verl.utils.profiler.config.NsightToolConfig',
+(TaskRunner pid=3248830)                                                         'discrete': False},
+(TaskRunner pid=3248830)                                                'torch': {'_target_': 'verl.utils.profiler.config.TorchProfilerToolConfig',
+(TaskRunner pid=3248830)                                                          'contents': [],
+(TaskRunner pid=3248830)                                                          'discrete': False},
+(TaskRunner pid=3248830)                                                'torch_memory': {'_target_': 'verl.utils.profiler.config.TorchMemoryToolConfig',
+(TaskRunner pid=3248830)                                                                 'stack_depth': 32,
+(TaskRunner pid=3248830)                                                                 'trace_alloc_max_entries': 100000}}},
+(TaskRunner pid=3248830)                   'reward_loop_class_name': None,
+(TaskRunner pid=3248830)                   'reward_loop_module_path': None,
+(TaskRunner pid=3248830)                   'reward_loop_source': 'register',
+(TaskRunner pid=3248830)                   'reward_manager': 'naive',
+(TaskRunner pid=3248830)                   'rollout': {'_target_': 'verl.workers.config.RolloutConfig',
+(TaskRunner pid=3248830)                               'cudagraph_capture_sizes': None,
+(TaskRunner pid=3248830)                               'data_parallel_size': 1,
+(TaskRunner pid=3248830)                               'disable_log_stats': True,
+(TaskRunner pid=3248830)                               'dtype': 'bfloat16',
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+(TaskRunner pid=3248830)                               'enable_prefix_caching': True,
+(TaskRunner pid=3248830)                               'enforce_eager': True,
+(TaskRunner pid=3248830)                               'engine_kwargs': {},
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+(TaskRunner pid=3248830)                               'gpu_memory_utilization': 0.5,
+(TaskRunner pid=3248830)                               'limit_images': None,
+(TaskRunner pid=3248830)                               'load_format': 'auto',
+(TaskRunner pid=3248830)                               'max_model_len': None,
+(TaskRunner pid=3248830)                               'max_num_batched_tokens': 8192,
+(TaskRunner pid=3248830)                               'max_num_seqs': 1024,
+(TaskRunner pid=3248830)                               'name': '???',
+(TaskRunner pid=3248830)                               'prompt_length': 2048,
+(TaskRunner pid=3248830)                               'response_length': 2048,
+(TaskRunner pid=3248830)                               'skip_tokenizer_init': False,
+(TaskRunner pid=3248830)                               'tensor_model_parallel_size': 2},
+(TaskRunner pid=3248830)                   'sandbox_fusion': {'max_concurrent': 64,
+(TaskRunner pid=3248830)                                      'memory_limit_mb': 1024,
+(TaskRunner pid=3248830)                                      'url': None},
+(TaskRunner pid=3248830)                   'strategy': 'fsdp',
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+(TaskRunner pid=3248830)                   'use_dynamic_bsz': False,
+(TaskRunner pid=3248830)                   'use_reward_loop': True},
+(TaskRunner pid=3248830)  'trainer': {'balance_batch': True,
+(TaskRunner pid=3248830)              'critic_warmup': 0,
+(TaskRunner pid=3248830)              'default_hdfs_dir': None,
+(TaskRunner pid=3248830)              'default_local_dir': 'checkpoints/verl/qwen3-4b-instruct-2507-function-rm',
+(TaskRunner pid=3248830)              'del_local_ckpt_after_load': False,
+(TaskRunner pid=3248830)              'device': 'cuda',
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+(TaskRunner pid=3248830)              'experiment_name': 'qwen3-4b-instruct-2507-function-rm',
+(TaskRunner pid=3248830)              'log_val_generations': 0,
+(TaskRunner pid=3248830)              'logger': ['console', 'wandb'],
+(TaskRunner pid=3248830)              'max_actor_ckpt_to_keep': None,
+(TaskRunner pid=3248830)              'max_critic_ckpt_to_keep': None,
+(TaskRunner pid=3248830)              'n_gpus_per_node': 2,
+(TaskRunner pid=3248830)              'nnodes': 1,
+(TaskRunner pid=3248830)              'project_name': 'verl',
+(TaskRunner pid=3248830)              'ray_wait_register_center_timeout': 300,
+(TaskRunner pid=3248830)              'resume_from_path': None,
+(TaskRunner pid=3248830)              'resume_mode': 'auto',
+(TaskRunner pid=3248830)              'rollout_data_dir': None,
+(TaskRunner pid=3248830)              'save_freq': 20,
+(TaskRunner pid=3248830)              'test_freq': 5,
+(TaskRunner pid=3248830)              'total_epochs': 15,
+(TaskRunner pid=3248830)              'total_training_steps': None,
+(TaskRunner pid=3248830)              'use_legacy_worker_impl': 'auto',
+(TaskRunner pid=3248830)              'val_before_train': True,
+(TaskRunner pid=3248830)              'val_only': False,
+(TaskRunner pid=3248830)              'validation_data_dir': None},
+(TaskRunner pid=3248830)  'transfer_queue': {'enable': False}}
+(TaskRunner pid=3248830) [validate_config] All configuration checks passed successfully!
+(TaskRunner pid=3248830) /data/home_beta/mshahidul/readctrl/code/RL_model/verl/verl/verl/trainer/main_ppo.py:300: UserWarning: Disabled critic as algorithm.adv_estimator != gae. If it is not intended, please set critic.enable=True
+(TaskRunner pid=3248830)   use_critic=need_critic(config),
+(TaskRunner pid=3248830) Using dataset class: RLHFDataset
+(TaskRunner pid=3248830) /data/home_beta/mshahidul/readctrl/code/RL_model/verl/verl/verl/utils/tokenizer.py:109: UserWarning: Failed to create processor: Unsupported processor type: Qwen2TokenizerFast. This may affect multimodal processing
+(TaskRunner pid=3248830)   warnings.warn(f"Failed to create processor: {e}. This may affect multimodal processing", stacklevel=1)
+(TaskRunner pid=3248830) dataset len: 7473
+(TaskRunner pid=3248830) Setting TOKENIZERS_PARALLELISM=false for forked processes.
+(TaskRunner pid=3248830) WARNING:2026-02-01 08:03:17,532:Setting TOKENIZERS_PARALLELISM=false for forked processes.
+(TaskRunner pid=3248830) 
Filtering prompts longer than 512 tokens (num_proc=1):   0%|          | 0/7473 [00:00<?, ? examples/s]
+(TaskRunner pid=3248830) 
Filtering prompts longer than 512 tokens (num_proc=1):  13%|█▎        | 1000/7473 [00:01<00:08, 735.05 examples/s]
+(TaskRunner pid=3248830) 
Filtering prompts longer than 512 tokens (num_proc=1):  27%|██▋       | 2000/7473 [00:01<00:04, 1128.33 examples/s]
+(TaskRunner pid=3248830) 
Filtering prompts longer than 512 tokens (num_proc=1):  40%|████      | 3000/7473 [00:02<00:03, 1368.04 examples/s]
+(TaskRunner pid=3248830) 
Filtering prompts longer than 512 tokens (num_proc=1):  54%|█████▎    | 4000/7473 [00:03<00:02, 1517.31 examples/s]
+(TaskRunner pid=3248830) 
Filtering prompts longer than 512 tokens (num_proc=1):  67%|██████▋   | 5000/7473 [00:03<00:01, 1619.21 examples/s]
+(TaskRunner pid=3248830) 
Filtering prompts longer than 512 tokens (num_proc=1):  80%|████████  | 6000/7473 [00:04<00:00, 1688.06 examples/s]
+(TaskRunner pid=3248830) 
Filtering prompts longer than 512 tokens (num_proc=1):  94%|█████████▎| 7000/7473 [00:04<00:00, 1732.85 examples/s]
+(TaskRunner pid=3248830) 
Filtering prompts longer than 512 tokens (num_proc=1): 100%|██████████| 7473/7473 [00:04<00:00, 1756.07 examples/s]
+(TaskRunner pid=3248830) filter dataset len: 7473
+(TaskRunner pid=3248830) Using dataset class: RLHFDataset
+(TaskRunner pid=3248830) dataset len: 1319
+(TaskRunner pid=3248830) 
Filtering prompts longer than 512 tokens (num_proc=1): 100%|██████████| 7473/7473 [00:05<00:00, 1491.81 examples/s]
+(TaskRunner pid=3248830) Setting TOKENIZERS_PARALLELISM=false for forked processes.
+(TaskRunner pid=3248830) WARNING:2026-02-01 08:03:22,899:Setting TOKENIZERS_PARALLELISM=false for forked processes.
+(TaskRunner pid=3248830) 
Filtering prompts longer than 512 tokens (num_proc=1):   0%|          | 0/1319 [00:00<?, ? examples/s]
+(TaskRunner pid=3248830) 
Filtering prompts longer than 512 tokens (num_proc=1):  76%|███████▌  | 1000/1319 [00:01<00:00, 701.80 examples/s]
+(TaskRunner pid=3248830) 
Filtering prompts longer than 512 tokens (num_proc=1): 100%|██████████| 1319/1319 [00:01<00:00, 828.26 examples/s]
+(TaskRunner pid=3248830) filter dataset len: 1319
+(TaskRunner pid=3248830) Size of train dataloader: 7, Size of val dataloader: 1
+(TaskRunner pid=3248830) Total training steps: 105
+(TaskRunner pid=3248830) colocated worker base class <class 'verl.single_controller.base.worker.Worker'>
+(TaskRunner pid=3248830) 
Filtering prompts longer than 512 tokens (num_proc=1): 100%|██████████| 1319/1319 [00:01<00:00, 742.74 examples/s]
+(TaskRunner pid=3248830) /data/home_beta/mshahidul/readctrl/code/RL_model/verl/verl/verl/trainer/ppo/ray_trainer.py:290: UserWarning: Disabled critic as algorithm.adv_estimator != gae. If it is not intended, please set critic.enable=True
+(TaskRunner pid=3248830)   self.use_critic = need_critic(self.config)
+(pid=3252840) /home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/torch/cuda/__init__.py:63: FutureWarning: The pynvml package is deprecated. Please install nvidia-ml-py instead. If you did not install pynvml directly, please report this to the maintainers of the package that installed pynvml for you.
+(pid=3252840)   import pynvml  # type: ignore[import]
+(pid=3252840) /home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/megatron/core/models/backends.py:21: UserWarning: Apex is not installed. Falling back to Torch Norm
+(pid=3252840)   warnings.warn("Apex is not installed. Falling back to Torch Norm")
+(pid=3252840) /home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/megatron/core/optimizer/__init__.py:18: UserWarning: Transformer Engine and Apex are not installed. Falling back to Torch optimizers.
+(pid=3252840)   warnings.warn(
+(pid=3252840) /home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/megatron/core/optimizer/optimizer.py:28: UserWarning: Transformer Engine and Apex are not installed. Falling back to local implementations of multi_tensor_applier and multi_tensor_scale
+(pid=3252840)   warnings.warn(
+(pid=3252840) /home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/megatron/core/optimizer/clip_grads.py:29: UserWarning: Transformer Engine and Apex are not installed. Falling back to local implementations of multi_tensor_applier, multi_tensor_l2norm, and multi_tensor_scale
+(pid=3252840)   warnings.warn(
+(pid=3252840) /home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/megatron/core/models/gpt/gpt_layer_specs.py:67: UserWarning: Apex is not installed. Falling back to Torch Norm
+(pid=3252840)   warnings.warn("Apex is not installed. Falling back to Torch Norm")
+(pid=3252838) /home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/torch/cuda/__init__.py:63: FutureWarning: The pynvml package is deprecated. Please install nvidia-ml-py instead. If you did not install pynvml directly, please report this to the maintainers of the package that installed pynvml for you.
+(pid=3252838)   import pynvml  # type: ignore[import]
+(WorkerDict pid=3252838) [Gloo] Rank 0 is connected to 1 peer ranks. Expected number of connected peer ranks is : 1
+(WorkerDict pid=3252838) reference model: Qwen/Qwen3-4B-Instruct-2507
+(WorkerDict pid=3252840) /data/home_beta/mshahidul/readctrl/code/RL_model/verl/verl/verl/utils/tokenizer.py:109: UserWarning: Failed to create processor: Unsupported processor type: Qwen2TokenizerFast. This may affect multimodal processing
+(WorkerDict pid=3252840)   warnings.warn(f"Failed to create processor: {e}. This may affect multimodal processing", stacklevel=1)
+(WorkerDict pid=3252838) Model config after override: Qwen3Config {
+(WorkerDict pid=3252838)   "architectures": [
+(WorkerDict pid=3252838)     "Qwen3ForCausalLM"
+(WorkerDict pid=3252838)   ],
+(WorkerDict pid=3252838)   "attention_bias": false,
+(WorkerDict pid=3252838)   "attention_dropout": 0.0,
+(WorkerDict pid=3252838)   "dtype": "bfloat16",
+(WorkerDict pid=3252838)   "eos_token_id": 151645,
+(WorkerDict pid=3252838)   "head_dim": 128,
+(WorkerDict pid=3252838)   "hidden_act": "silu",
+(WorkerDict pid=3252838)   "hidden_size": 2560,
+(WorkerDict pid=3252838)   "initializer_range": 0.02,
+(WorkerDict pid=3252838)   "intermediate_size": 9728,
+(WorkerDict pid=3252838)   "layer_types": [
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention"
+(WorkerDict pid=3252838)   ],
+(WorkerDict pid=3252838)   "max_position_embeddings": 262144,
+(WorkerDict pid=3252838)   "max_window_layers": 36,
+(WorkerDict pid=3252838)   "model_type": "qwen3",
+(WorkerDict pid=3252838)   "num_attention_heads": 32,
+(WorkerDict pid=3252838)   "num_hidden_layers": 36,
+(WorkerDict pid=3252838)   "num_key_value_heads": 8,
+(WorkerDict pid=3252838)   "pad_token_id": 151643,
+(WorkerDict pid=3252838)   "rms_norm_eps": 1e-06,
+(WorkerDict pid=3252838)   "rope_scaling": null,
+(WorkerDict pid=3252838)   "rope_theta": 5000000,
+(WorkerDict pid=3252838)   "sliding_window": null,
+(WorkerDict pid=3252838)   "tie_word_embeddings": true,
+(WorkerDict pid=3252838)   "transformers_version": "4.56.1",
+(WorkerDict pid=3252838)   "use_cache": true,
+(WorkerDict pid=3252838)   "use_sliding_window": false,
+(WorkerDict pid=3252838)   "vocab_size": 151936
+(WorkerDict pid=3252838) }
+(WorkerDict pid=3252838) 
+(WorkerDict pid=3252840) `torch_dtype` is deprecated! Use `dtype` instead!
+(WorkerDict pid=3252840) Flash Attention 2 only supports torch.float16 and torch.bfloat16 dtypes, but the current dype in Qwen3ForCausalLM is torch.float32. You should run training or inference using Automatic Mixed-Precision via the `with torch.autocast(device_type='torch_device'):` decorator, or load the model with the `dtype` argument. Example: `model = AutoModel.from_pretrained("openai/whisper-tiny", attn_implementation="flash_attention_2", dtype=torch.float16)`
+(WorkerDict pid=3252840) Flash Attention 2 only supports torch.float16 and torch.bfloat16 dtypes, but the current dype in Qwen3Model is torch.float32. You should run training or inference using Automatic Mixed-Precision via the `with torch.autocast(device_type='torch_device'):` decorator, or load the model with the `dtype` argument. Example: `model = AutoModel.from_pretrained("openai/whisper-tiny", attn_implementation="flash_attention_2", dtype=torch.float16)`
+(WorkerDict pid=3252840) 
Loading checkpoint shards:   0%|          | 0/3 [00:00<?, ?it/s]
+(WorkerDict pid=3252840) 
Loading checkpoint shards:  33%|███▎      | 1/3 [00:03<00:07,  3.70s/it]
+(pid=3252838) /home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/megatron/core/models/gpt/gpt_layer_specs.py:67: UserWarning: Apex is not installed. Falling back to Torch Norm [repeated 2x across cluster] (Ray deduplicates logs by default. Set RAY_DEDUP_LOGS=0 to disable log deduplication, or see https://docs.ray.io/en/master/ray-observability/user-guides/configure-logging.html#log-deduplication for more options.)
+(pid=3252838)   warnings.warn("Apex is not installed. Falling back to Torch Norm") [repeated 2x across cluster]
+(pid=3252838) /home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/megatron/core/optimizer/__init__.py:18: UserWarning: Transformer Engine and Apex are not installed. Falling back to Torch optimizers.
+(pid=3252838)   warnings.warn( [repeated 3x across cluster]
+(pid=3252838) /home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/megatron/core/optimizer/optimizer.py:28: UserWarning: Transformer Engine and Apex are not installed. Falling back to local implementations of multi_tensor_applier and multi_tensor_scale
+(pid=3252838) /home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/megatron/core/optimizer/clip_grads.py:29: UserWarning: Transformer Engine and Apex are not installed. Falling back to local implementations of multi_tensor_applier, multi_tensor_l2norm, and multi_tensor_scale
+(WorkerDict pid=3252838) /data/home_beta/mshahidul/readctrl/code/RL_model/verl/verl/verl/utils/tokenizer.py:109: UserWarning: Failed to create processor: Unsupported processor type: Qwen2TokenizerFast. This may affect multimodal processing
+(WorkerDict pid=3252838)   warnings.warn(f"Failed to create processor: {e}. This may affect multimodal processing", stacklevel=1)
+(WorkerDict pid=3252838) `torch_dtype` is deprecated! Use `dtype` instead!
+(WorkerDict pid=3252838) Flash Attention 2 only supports torch.float16 and torch.bfloat16 dtypes, but the current dype in Qwen3Model is torch.float32. You should run training or inference using Automatic Mixed-Precision via the `with torch.autocast(device_type='torch_device'):` decorator, or load the model with the `dtype` argument. Example: `model = AutoModel.from_pretrained("openai/whisper-tiny", attn_implementation="flash_attention_2", dtype=torch.float16)` [repeated 2x across cluster]
+(WorkerDict pid=3252838) 
Loading checkpoint shards:   0%|          | 0/3 [00:00<?, ?it/s]
+(WorkerDict pid=3252840) 
Loading checkpoint shards: 100%|██████████| 3/3 [00:07<00:00,  2.57s/it]
+(WorkerDict pid=3252840) Monkey patch _flash_attention_forward in transformers.integrations.flash_attention
+(WorkerDict pid=3252840) Skipping monkey patch for Qwen3ForCausalLM as use_fused_kernels is False or fused_kernels_backend is torch
+(WorkerDict pid=3252840) [Gloo] Rank 1 is connected to 1 peer ranks. Expected number of connected peer ranks is : 1
+(WorkerDict pid=3252838) 
Loading checkpoint shards:  67%|██████▋   | 2/3 [00:07<00:03,  3.99s/it] [repeated 3x across cluster]
+(WorkerDict pid=3252838) Qwen3ForCausalLM contains 4.02B parameters
+(WorkerDict pid=3252838) wrap_policy: functools.partial(<function _or_policy at 0x7fb0f46b3b00>, policies=[functools.partial(<function transformer_auto_wrap_policy at 0x7fb0f46b39c0>, transformer_layer_cls={<class 'transformers.models.qwen3.modeling_qwen3.Qwen3DecoderLayer'>})])
+(WorkerDict pid=3252838) NCCL version 2.27.3+cuda12.9
+(WorkerDict pid=3252838) Ref use_remove_padding=True
+(WorkerDict pid=3252838) Ref use_fused_kernels=False
+(WorkerDict pid=3252838) Ref use_prefix_grouper=False
+(WorkerDict pid=3252838) Monkey patch _flash_attention_forward in transformers.integrations.flash_attention
+(WorkerDict pid=3252838) Skipping monkey patch for Qwen3ForCausalLM as use_fused_kernels is False or fused_kernels_backend is torch
+(WorkerDict pid=3252840) /data/home_beta/mshahidul/readctrl/code/RL_model/verl/verl/verl/utils/tokenizer.py:109: UserWarning: Failed to create processor: Unsupported processor type: Qwen2TokenizerFast. This may affect multimodal processing
+(WorkerDict pid=3252840)   warnings.warn(f"Failed to create processor: {e}. This may affect multimodal processing", stacklevel=1)
+(WorkerDict pid=3252838) 
Loading checkpoint shards: 100%|██████████| 3/3 [00:08<00:00,  2.68s/it]
+(WorkerDict pid=3252840) 
Loading checkpoint shards:   0%|          | 0/3 [00:00<?, ?it/s]
+(WorkerDict pid=3252838) Model config after override: Qwen3Config {
+(WorkerDict pid=3252838)   "architectures": [
+(WorkerDict pid=3252838)     "Qwen3ForCausalLM"
+(WorkerDict pid=3252838)   ],
+(WorkerDict pid=3252838)   "attention_bias": false,
+(WorkerDict pid=3252838)   "attention_dropout": 0.0,
+(WorkerDict pid=3252838)   "dtype": "bfloat16",
+(WorkerDict pid=3252838)   "eos_token_id": 151645,
+(WorkerDict pid=3252838)   "head_dim": 128,
+(WorkerDict pid=3252838)   "hidden_act": "silu",
+(WorkerDict pid=3252838)   "hidden_size": 2560,
+(WorkerDict pid=3252838)   "initializer_range": 0.02,
+(WorkerDict pid=3252838)   "intermediate_size": 9728,
+(WorkerDict pid=3252838)   "layer_types": [
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention",
+(WorkerDict pid=3252838)     "full_attention"
+(WorkerDict pid=3252838)   ],
+(WorkerDict pid=3252838)   "max_position_embeddings": 262144,
+(WorkerDict pid=3252838)   "max_window_layers": 36,
+(WorkerDict pid=3252838)   "model_type": "qwen3",
+(WorkerDict pid=3252838)   "num_attention_heads": 32,
+(WorkerDict pid=3252838)   "num_hidden_layers": 36,
+(WorkerDict pid=3252838)   "num_key_value_heads": 8,
+(WorkerDict pid=3252838)   "pad_token_id": 151643,
+(WorkerDict pid=3252838)   "rms_norm_eps": 1e-06,
+(WorkerDict pid=3252838)   "rope_scaling": null,
+(WorkerDict pid=3252838)   "rope_theta": 5000000,
+(WorkerDict pid=3252838)   "sliding_window": null,
+(WorkerDict pid=3252838)   "tie_word_embeddings": true,
+(WorkerDict pid=3252838)   "transformers_version": "4.56.1",
+(WorkerDict pid=3252838)   "use_cache": true,
+(WorkerDict pid=3252838)   "use_sliding_window": false,
+(WorkerDict pid=3252838)   "vocab_size": 151936
+(WorkerDict pid=3252838) }
+(WorkerDict pid=3252838) 
+(WorkerDict pid=3252840) 
Loading checkpoint shards:  33%|███▎      | 1/3 [00:03<00:07,  3.74s/it]
+(WorkerDict pid=3252838) /data/home_beta/mshahidul/readctrl/code/RL_model/verl/verl/verl/utils/tokenizer.py:109: UserWarning: Failed to create processor: Unsupported processor type: Qwen2TokenizerFast. This may affect multimodal processing
+(WorkerDict pid=3252838)   warnings.warn(f"Failed to create processor: {e}. This may affect multimodal processing", stacklevel=1)
+(WorkerDict pid=3252838) 
Loading checkpoint shards:   0%|          | 0/3 [00:00<?, ?it/s]
+(WorkerDict pid=3252840) 
Loading checkpoint shards: 100%|██████████| 3/3 [00:07<00:00,  2.64s/it]
+(WorkerDict pid=3252838) Monkey patch _flash_attention_forward in transformers.integrations.flash_attention
+(WorkerDict pid=3252838) Skipping monkey patch for Qwen3ForCausalLM as use_fused_kernels is False or fused_kernels_backend is torch
+(WorkerDict pid=3252838) Qwen3ForCausalLM contains 4.02B parameters
+(WorkerDict pid=3252838) wrap_policy: functools.partial(<function _or_policy at 0x7fb0f46b3b00>, policies=[functools.partial(<function transformer_auto_wrap_policy at 0x7fb0f46b39c0>, transformer_layer_cls={<class 'transformers.models.qwen3.modeling_qwen3.Qwen3DecoderLayer'>})])
+(WorkerDict pid=3252838) Total steps: 105, num_warmup_steps: 0
+(WorkerDict pid=3252838) Actor use_remove_padding=True
+(WorkerDict pid=3252838) Actor use_fused_kernels=False
+(WorkerDict pid=3252838) Actor use_prefix_grouper=False
+(WorkerDict pid=3252840) Monkey patch _flash_attention_forward in transformers.integrations.flash_attention
+(WorkerDict pid=3252840) Skipping monkey patch for Qwen3ForCausalLM as use_fused_kernels is False or fused_kernels_backend is torch
+(WorkerDict pid=3252840) /data/home_beta/mshahidul/readctrl/code/RL_model/verl/verl/verl/utils/tokenizer.py:109: UserWarning: Failed to create processor: Unsupported processor type: Qwen2TokenizerFast. This may affect multimodal processing
+(WorkerDict pid=3252840)   warnings.warn(f"Failed to create processor: {e}. This may affect multimodal processing", stacklevel=1)
+(WorkerDict pid=3252838) 
Loading checkpoint shards:  67%|██████▋   | 2/3 [00:07<00:03,  3.89s/it] [repeated 3x across cluster]
+(WorkerDict pid=3252838) 
Loading checkpoint shards: 100%|██████████| 3/3 [00:07<00:00,  2.60s/it]
+(WorkerDict pid=3252838) [Gloo] Rank 0 is connected to 0 peer ranks. Expected number of connected peer ranks is : 0
+(WorkerDict pid=3252838) [Gloo] Rank 0 is connected to 1 peer ranks. Expected number of connected peer ranks is : 1
+(WorkerDict pid=3252838) [Gloo] Rank 0 is connected to 0 peer ranks. Expected number of connected peer ranks is : 0
+(WorkerDict pid=3252840) /home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/torch/distributed/fsdp/fully_sharded_data_parallel.py:678: FutureWarning: FSDP.state_dict_type() and FSDP.set_state_dict_type() are being deprecated. Please use APIs, get_state_dict() and set_state_dict(), which can support different parallelisms, FSDP1, FSDP2, DDP. API doc: https://pytorch.org/docs/stable/distributed.checkpoint.html#torch.distributed.checkpoint.state_dict.get_state_dict .Tutorial: https://pytorch.org/tutorials/recipes/distributed_checkpoint_recipe.html .
+(WorkerDict pid=3252840)   warnings.warn(
+(TaskRunner pid=3248830) WARNING 02-01 08:04:29 [api_server.py:1213] LoRA dynamic loading & unloading is enabled in the API server. This should ONLY be used for local development!
+(pid=3262337) /home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/torch/cuda/__init__.py:63: FutureWarning: The pynvml package is deprecated. Please install nvidia-ml-py instead. If you did not install pynvml directly, please report this to the maintainers of the package that installed pynvml for you.
+(pid=3262337)   import pynvml  # type: ignore[import]
+(WorkerDict pid=3252838) /data/home_beta/mshahidul/readctrl/code/RL_model/verl/verl/verl/utils/tokenizer.py:109: UserWarning: Failed to create processor: Unsupported processor type: Qwen2TokenizerFast. This may affect multimodal processing
+(WorkerDict pid=3252838)   warnings.warn(f"Failed to create processor: {e}. This may affect multimodal processing", stacklevel=1)
+(WorkerDict pid=3252840) [Gloo] Rank 0 is connected to 0 peer ranks. Expected number of connected peer ranks is : 0 [repeated 3x across cluster]
+(pid=3262337) WARNING 02-01 08:04:40 [api_server.py:1213] LoRA dynamic loading & unloading is enabled in the API server. This should ONLY be used for local development!
+(vLLMHttpServer pid=3262337) /home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/megatron/core/models/backends.py:21: UserWarning: Apex is not installed. Falling back to Torch Norm
+(vLLMHttpServer pid=3262337)   warnings.warn("Apex is not installed. Falling back to Torch Norm")
+(vLLMHttpServer pid=3262337) /home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/megatron/core/optimizer/__init__.py:18: UserWarning: Transformer Engine and Apex are not installed. Falling back to Torch optimizers.
+(vLLMHttpServer pid=3262337) /home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/megatron/core/optimizer/optimizer.py:28: UserWarning: Transformer Engine and Apex are not installed. Falling back to local implementations of multi_tensor_applier and multi_tensor_scale
+(vLLMHttpServer pid=3262337) /home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/megatron/core/optimizer/clip_grads.py:29: UserWarning: Transformer Engine and Apex are not installed. Falling back to local implementations of multi_tensor_applier, multi_tensor_l2norm, and multi_tensor_scale
+(vLLMHttpServer pid=3262337) /home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/megatron/core/models/gpt/gpt_layer_specs.py:67: UserWarning: Apex is not installed. Falling back to Torch Norm
+(vLLMHttpServer pid=3262337)   warnings.warn("Apex is not installed. Falling back to Torch Norm")
+(WorkerDict pid=3252838) /home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/torch/distributed/fsdp/fully_sharded_data_parallel.py:678: FutureWarning: FSDP.state_dict_type() and FSDP.set_state_dict_type() are being deprecated. Please use APIs, get_state_dict() and set_state_dict(), which can support different parallelisms, FSDP1, FSDP2, DDP. API doc: https://pytorch.org/docs/stable/distributed.checkpoint.html#torch.distributed.checkpoint.state_dict.get_state_dict .Tutorial: https://pytorch.org/tutorials/recipes/distributed_checkpoint_recipe.html .
+(vLLMHttpServer pid=3262337)   warnings.warn( [repeated 4x across cluster]
+(vLLMHttpServer pid=3262337) /data/home_beta/mshahidul/readctrl/code/RL_model/verl/verl/verl/utils/tokenizer.py:109: UserWarning: Failed to create processor: Unsupported processor type: Qwen2TokenizerFast. This may affect multimodal processing
+(vLLMHttpServer pid=3262337)   warnings.warn(f"Failed to create processor: {e}. This may affect multimodal processing", stacklevel=1)
+(vLLMHttpServer pid=3262337) WARNING:2026-02-01 08:04:42,035:agent loop only support torch and npu profiler, got None
+(vLLMHttpServer pid=3262337) INFO:2026-02-01 08:04:42,036:vLLMHttpServer, replica_rank: 0, node_rank: 0, CUDA_VISIBLE_DEVICES: 1,2, master_address: 172.16.34.22, master_port: 34123, data_parallel_rpc_port: 34741, data_parallel_master_port: 46003
+(vLLMHttpServer pid=3262337) INFO:2026-02-01 08:04:42,042:override_generation_config: {'temperature': 1.0, 'top_k': -1, 'top_p': 1, 'repetition_penalty': 1.0, 'max_new_tokens': 1024}
+(vLLMHttpServer pid=3262337) INFO:2026-02-01 08:04:42,043:enable_sleep_mode: True
+(vLLMHttpServer pid=3262337) ['serve',
+(vLLMHttpServer pid=3262337)  'Qwen/Qwen3-4B-Instruct-2507',
+(vLLMHttpServer pid=3262337)  '--dtype',
+(vLLMHttpServer pid=3262337)  'bfloat16',
+(vLLMHttpServer pid=3262337)  '--load_format',
+(vLLMHttpServer pid=3262337)  'dummy',
+(vLLMHttpServer pid=3262337)  '--distributed_executor_backend',
+(vLLMHttpServer pid=3262337)  'mp',
+(vLLMHttpServer pid=3262337)  '--worker_extension_cls',
+(vLLMHttpServer pid=3262337)  'verl.workers.rollout.vllm_rollout.utils.vLLMColocateWorkerExtension',
+(vLLMHttpServer pid=3262337)  '--max_model_len',
+(vLLMHttpServer pid=3262337)  '262144',
+(vLLMHttpServer pid=3262337)  '--max_num_seqs',
+(vLLMHttpServer pid=3262337)  '1024',
+(vLLMHttpServer pid=3262337)  '--enable_chunked_prefill',
+(vLLMHttpServer pid=3262337)  '--max_num_batched_tokens',
+(vLLMHttpServer pid=3262337)  '8192',
+(vLLMHttpServer pid=3262337)  '--enable_prefix_caching',
+(vLLMHttpServer pid=3262337)  '--enable_sleep_mode',
+(vLLMHttpServer pid=3262337)  '--logprobs_mode',
+(vLLMHttpServer pid=3262337)  'processed_logprobs',
+(vLLMHttpServer pid=3262337)  '--gpu_memory_utilization',
+(vLLMHttpServer pid=3262337)  '0.6',
+(vLLMHttpServer pid=3262337)  '--disable_log_stats',
+(vLLMHttpServer pid=3262337)  '--tensor_parallel_size',
+(vLLMHttpServer pid=3262337)  '2',
+(vLLMHttpServer pid=3262337)  '--seed',
+(vLLMHttpServer pid=3262337)  '0',
+(vLLMHttpServer pid=3262337)  '--override_generation_config',
+(vLLMHttpServer pid=3262337)  '{"temperature": 1.0, "top_k": -1, "top_p": 1, "repetition_penalty": 1.0, '
+(vLLMHttpServer pid=3262337)  '"max_new_tokens": 1024}',
+(vLLMHttpServer pid=3262337)  '--hf_overrides',
+(vLLMHttpServer pid=3262337)  '{}',
+(vLLMHttpServer pid=3262337)  '--scheduling_policy',
+(vLLMHttpServer pid=3262337)  'fcfs',
+(vLLMHttpServer pid=3262337)  '--compilation_config',
+(vLLMHttpServer pid=3262337)  '{"cudagraph_mode": "FULL_AND_PIECEWISE"}']
+(vLLMHttpServer pid=3262337) `torch_dtype` is deprecated! Use `dtype` instead!
+(vLLMHttpServer pid=3262337) WARNING 02-01 08:04:43 [__init__.py:3036] We must use the `spawn` multiprocessing start method. Overriding VLLM_WORKER_MULTIPROC_METHOD to 'spawn'. See https://docs.vllm.ai/en/latest/usage/troubleshooting.html#python-multiprocessing for more information. Reasons: In a Ray actor and can only be spawned; CUDA is initialized
+(vLLMHttpServer pid=3262337) /home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/torch/cuda/__init__.py:63: FutureWarning: The pynvml package is deprecated. Please install nvidia-ml-py instead. If you did not install pynvml directly, please report this to the maintainers of the package that installed pynvml for you.
+(vLLMHttpServer pid=3262337)   import pynvml  # type: ignore[import]
+(vLLMHttpServer pid=3262337) /home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/torch/cuda/__init__.py:63: FutureWarning: The pynvml package is deprecated. Please install nvidia-ml-py instead. If you did not install pynvml directly, please report this to the maintainers of the package that installed pynvml for you.
+(vLLMHttpServer pid=3262337)   import pynvml  # type: ignore[import]
+(vLLMHttpServer pid=3262337) /home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/torch/cuda/__init__.py:63: FutureWarning: The pynvml package is deprecated. Please install nvidia-ml-py instead. If you did not install pynvml directly, please report this to the maintainers of the package that installed pynvml for you.
+(vLLMHttpServer pid=3262337)   import pynvml  # type: ignore[import]
+(vLLMHttpServer pid=3262337) W0201 08:04:58.452000 3265659 /data/home_beta/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/torch/utils/cpp_extension.py:2425] TORCH_CUDA_ARCH_LIST is not set, all archs for visible cards are included for compilation. 
+(vLLMHttpServer pid=3262337) W0201 08:04:58.452000 3265659 /data/home_beta/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/torch/utils/cpp_extension.py:2425] If this is not desired, please set os.environ['TORCH_CUDA_ARCH_LIST'] to specific architectures.
+(vLLMHttpServer pid=3262337) W0201 08:04:58.485000 3265660 /data/home_beta/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/torch/utils/cpp_extension.py:2425] TORCH_CUDA_ARCH_LIST is not set, all archs for visible cards are included for compilation. 
+(vLLMHttpServer pid=3262337) W0201 08:04:58.485000 3265660 /data/home_beta/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/torch/utils/cpp_extension.py:2425] If this is not desired, please set os.environ['TORCH_CUDA_ARCH_LIST'] to specific architectures.
+(vLLMHttpServer pid=3262337) [Gloo] Rank 0 is connected to 1 peer ranks. Expected number of connected peer ranks is : 1[Gloo] Rank 
+(vLLMHttpServer pid=3262337) 1 is connected to 1 peer ranks. Expected number of connected peer ranks is : 1
+(vLLMHttpServer pid=3262337) [Gloo] Rank [Gloo] Rank 01 is connected to  is connected to 11 peer ranks.  peer ranks. Expected number of connected peer ranks is : Expected number of connected peer ranks is : 11
+(vLLMHttpServer pid=3262337) 
+(vLLMHttpServer pid=3262337) NCCL version 2.27.3+cuda12.9
+(vLLMHttpServer pid=3262337) WARNING 02-01 08:05:01 [symm_mem.py:58] SymmMemCommunicator: Device capability 8.0 not supported, communicator is not available.
+(vLLMHttpServer pid=3262337) WARNING 02-01 08:05:01 [symm_mem.py:58] SymmMemCommunicator: Device capability 8.0 not supported, communicator is not available.
+(vLLMHttpServer pid=3262337) [Gloo] Rank 0 is connected to 0 peer ranks. Expected number of connected peer ranks is : 0
+(vLLMHttpServer pid=3262337) [Gloo] Rank 0 is connected to 0 peer ranks. Expected number of connected peer ranks is : 0
+(vLLMHttpServer pid=3262337) [Gloo] Rank [Gloo] Rank 00 is connected to  is connected to 00 peer ranks.  peer ranks. Expected number of connected peer ranks is : Expected number of connected peer ranks is : 00
+(vLLMHttpServer pid=3262337) 
+(vLLMHttpServer pid=3262337) [Gloo] Rank 0[Gloo] Rank  is connected to 00 is connected to  peer ranks. 0Expected number of connected peer ranks is :  peer ranks. 0Expected number of connected peer ranks is : 
+(vLLMHttpServer pid=3262337) 0
+(vLLMHttpServer pid=3262337) [Gloo] Rank [Gloo] Rank 10 is connected to  is connected to 11 peer ranks.  peer ranks. Expected number of connected peer ranks is : Expected number of connected peer ranks is : 11
+(vLLMHttpServer pid=3262337) 
+(vLLMHttpServer pid=3262337) (EngineCore_DP0 pid=3264655) ERROR 02-01 08:05:59 [core.py:708] EngineCore failed to start.
+(vLLMHttpServer pid=3262337) (EngineCore_DP0 pid=3264655) ERROR 02-01 08:05:59 [core.py:708] Traceback (most recent call last):
+(vLLMHttpServer pid=3262337) (EngineCore_DP0 pid=3264655) ERROR 02-01 08:05:59 [core.py:708]   File "/home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/vllm/v1/engine/core.py", line 699, in run_engine_core
+(vLLMHttpServer pid=3262337) (EngineCore_DP0 pid=3264655) ERROR 02-01 08:05:59 [core.py:708]     engine_core = EngineCoreProc(*args, **kwargs)
+(vLLMHttpServer pid=3262337) (EngineCore_DP0 pid=3264655) ERROR 02-01 08:05:59 [core.py:708]                   ^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^
+(vLLMHttpServer pid=3262337) (EngineCore_DP0 pid=3264655) ERROR 02-01 08:05:59 [core.py:708]   File "/home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/vllm/v1/engine/core.py", line 498, in __init__
+(vLLMHttpServer pid=3262337) (EngineCore_DP0 pid=3264655) ERROR 02-01 08:05:59 [core.py:708]     super().__init__(vllm_config, executor_class, log_stats,
+(vLLMHttpServer pid=3262337) (EngineCore_DP0 pid=3264655) ERROR 02-01 08:05:59 [core.py:708]   File "/home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/vllm/v1/engine/core.py", line 92, in __init__
+(vLLMHttpServer pid=3262337) (EngineCore_DP0 pid=3264655) ERROR 02-01 08:05:59 [core.py:708]     self._initialize_kv_caches(vllm_config)
+(vLLMHttpServer pid=3262337) (EngineCore_DP0 pid=3264655) ERROR 02-01 08:05:59 [core.py:708]   File "/home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/vllm/v1/engine/core.py", line 199, in _initialize_kv_caches
+(vLLMHttpServer pid=3262337) (EngineCore_DP0 pid=3264655) ERROR 02-01 08:05:59 [core.py:708]     kv_cache_configs = get_kv_cache_configs(vllm_config, kv_cache_specs,
+(vLLMHttpServer pid=3262337) (EngineCore_DP0 pid=3264655) ERROR 02-01 08:05:59 [core.py:708]                        ^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^
+(vLLMHttpServer pid=3262337) (EngineCore_DP0 pid=3264655) ERROR 02-01 08:05:59 [core.py:708]   File "/home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/vllm/v1/core/kv_cache_utils.py", line 1243, in get_kv_cache_configs
+(vLLMHttpServer pid=3262337) (EngineCore_DP0 pid=3264655) ERROR 02-01 08:05:59 [core.py:708]     check_enough_kv_cache_memory(vllm_config, kv_cache_spec_one_worker,
+(vLLMHttpServer pid=3262337) (EngineCore_DP0 pid=3264655) ERROR 02-01 08:05:59 [core.py:708]   File "/home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/vllm/v1/core/kv_cache_utils.py", line 716, in check_enough_kv_cache_memory
+(vLLMHttpServer pid=3262337) (EngineCore_DP0 pid=3264655) ERROR 02-01 08:05:59 [core.py:708]     raise ValueError(
+(vLLMHttpServer pid=3262337) (EngineCore_DP0 pid=3264655) ERROR 02-01 08:05:59 [core.py:708] ValueError: To serve at least one request with the models's max seq len (262144), (18.00 GiB KV cache is needed, which is larger than the available KV cache memory (14.22 GiB). Based on the available memory, the estimated maximum model length is 207088. Try increasing `gpu_memory_utilization` or decreasing `max_model_len` when initializing the engine.
diff --git a/code/RL_model/verl/verl_train/qwen3-4b-instruct-en.log b/code/RL_model/verl/verl_train/qwen3-4b-instruct-en.log
new file mode 100644
index 0000000000000000000000000000000000000000..afa5acbf2656defd8dccfec259d3fda8ea2579ba
--- /dev/null
+++ b/code/RL_model/verl/verl_train/qwen3-4b-instruct-en.log
@@ -0,0 +1,1044 @@
+/home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/torch/cuda/__init__.py:63: FutureWarning: The pynvml package is deprecated. Please install nvidia-ml-py instead. If you did not install pynvml directly, please report this to the maintainers of the package that installed pynvml for you.
+  import pynvml  # type: ignore[import]
+WARNING:2026-02-15 11:39:51,864:Skipping import of cpp extensions due to incompatible torch version 2.8.0+cu128 for torchao version 0.16.0             Please see https://github.com/pytorch/ao/issues/2919 for more info
+INFO 02-15 11:39:55 [__init__.py:216] Automatically detected platform cuda.
+/home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/models/backends.py:21: UserWarning: Apex is not installed. Falling back to Torch Norm
+  warnings.warn("Apex is not installed. Falling back to Torch Norm")
+/home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/optimizer/__init__.py:18: UserWarning: Transformer Engine and Apex are not installed. Falling back to Torch optimizers.
+  warnings.warn(
+/home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/optimizer/optimizer.py:28: UserWarning: Transformer Engine and Apex are not installed. Falling back to local implementations of multi_tensor_applier and multi_tensor_scale
+  warnings.warn(
+/home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/optimizer/clip_grads.py:29: UserWarning: Transformer Engine and Apex are not installed. Falling back to local implementations of multi_tensor_applier, multi_tensor_l2norm, and multi_tensor_scale
+  warnings.warn(
+/home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/models/gpt/gpt_layer_specs.py:67: UserWarning: Apex is not installed. Falling back to Torch Norm
+  warnings.warn("Apex is not installed. Falling back to Torch Norm")
+ray init kwargs: {'num_cpus': None, 'runtime_env': {'env_vars': {'TOKENIZERS_PARALLELISM': 'true', 'NCCL_DEBUG': 'WARN', 'VLLM_LOGGING_LEVEL': 'WARN', 'VLLM_ALLOW_RUNTIME_LORA_UPDATING': 'true', 'CUDA_DEVICE_MAX_CONNECTIONS': '1', 'NCCL_CUMEM_ENABLE': '0', 'VLLM_DISABLE_COMPILE_CACHE': '1', 'HCCL_HOST_SOCKET_PORT_RANGE': 'auto', 'HCCL_NPU_SOCKET_PORT_RANGE': 'auto'}, 'working_dir': None}}
+2026-02-15 11:40:13,309	INFO worker.py:1998 -- Started a local Ray instance. View the dashboard at http://127.0.0.1:8297 
+/home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/ray/_private/worker.py:2046: FutureWarning: Tip: In future versions of Ray, Ray will no longer override accelerator visible devices env var if num_gpus=0 or num_gpus=None (default). To enable this behavior and turn off this error message, set RAY_ACCEL_ENV_VAR_OVERRIDE_ON_ZERO=0
+  warnings.warn(
+(pid=3962104) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/torch/cuda/__init__.py:63: FutureWarning: The pynvml package is deprecated. Please install nvidia-ml-py instead. If you did not install pynvml directly, please report this to the maintainers of the package that installed pynvml for you.
+(pid=3962104)   import pynvml  # type: ignore[import]
+(pid=3962104) WARNING:2026-02-15 11:40:31,168:Skipping import of cpp extensions due to incompatible torch version 2.8.0+cu128 for torchao version 0.16.0             Please see https://github.com/pytorch/ao/issues/2919 for more info
+(pid=3962104) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/models/backends.py:21: UserWarning: Apex is not installed. Falling back to Torch Norm
+(pid=3962104)   warnings.warn("Apex is not installed. Falling back to Torch Norm")
+(pid=3962104) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/optimizer/__init__.py:18: UserWarning: Transformer Engine and Apex are not installed. Falling back to Torch optimizers.
+(pid=3962104)   warnings.warn(
+(pid=3962104) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/optimizer/optimizer.py:28: UserWarning: Transformer Engine and Apex are not installed. Falling back to local implementations of multi_tensor_applier and multi_tensor_scale
+(pid=3962104)   warnings.warn(
+(pid=3962104) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/optimizer/clip_grads.py:29: UserWarning: Transformer Engine and Apex are not installed. Falling back to local implementations of multi_tensor_applier, multi_tensor_l2norm, and multi_tensor_scale
+(pid=3962104)   warnings.warn(
+(pid=3962104) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/models/gpt/gpt_layer_specs.py:67: UserWarning: Apex is not installed. Falling back to Torch Norm
+(pid=3962104)   warnings.warn("Apex is not installed. Falling back to Torch Norm")
+(TaskRunner pid=3962104) TaskRunner hostname: gamma, PID: 3962104
+(TaskRunner pid=3962104) {'actor_rollout_ref': {'actor': {'_target_': 'verl.workers.config.FSDPActorConfig',
+(TaskRunner pid=3962104)                                  'calculate_entropy': False,
+(TaskRunner pid=3962104)                                  'calculate_sum_pi_squared': False,
+(TaskRunner pid=3962104)                                  'checkpoint': {'_target_': 'verl.trainer.config.CheckpointConfig',
+(TaskRunner pid=3962104)                                                 'async_save': False,
+(TaskRunner pid=3962104)                                                 'load_contents': ['model',
+(TaskRunner pid=3962104)                                                                   'optimizer',
+(TaskRunner pid=3962104)                                                                   'extra'],
+(TaskRunner pid=3962104)                                                 'save_contents': ['model',
+(TaskRunner pid=3962104)                                                                   'optimizer',
+(TaskRunner pid=3962104)                                                                   'extra']},
+(TaskRunner pid=3962104)                                  'clip_ratio': 0.2,
+(TaskRunner pid=3962104)                                  'clip_ratio_c': 3.0,
+(TaskRunner pid=3962104)                                  'clip_ratio_high': 0.2,
+(TaskRunner pid=3962104)                                  'clip_ratio_low': 0.2,
+(TaskRunner pid=3962104)                                  'data_loader_seed': 42,
+(TaskRunner pid=3962104)                                  'entropy_checkpointing': False,
+(TaskRunner pid=3962104)                                  'entropy_coeff': 0,
+(TaskRunner pid=3962104)                                  'entropy_from_logits_with_chunking': False,
+(TaskRunner pid=3962104)                                  'freeze_vision_tower': False,
+(TaskRunner pid=3962104)                                  'fsdp_config': {'_target_': 'verl.workers.config.FSDPEngineConfig',
+(TaskRunner pid=3962104)                                                  'dtype': 'bfloat16',
+(TaskRunner pid=3962104)                                                  'entropy_checkpointing': False,
+(TaskRunner pid=3962104)                                                  'entropy_from_logits_with_chunking': False,
+(TaskRunner pid=3962104)                                                  'forward_only': False,
+(TaskRunner pid=3962104)                                                  'forward_prefetch': False,
+(TaskRunner pid=3962104)                                                  'fsdp_size': -1,
+(TaskRunner pid=3962104)                                                  'full_determinism': False,
+(TaskRunner pid=3962104)                                                  'model_dtype': 'fp32',
+(TaskRunner pid=3962104)                                                  'offload_policy': False,
+(TaskRunner pid=3962104)                                                  'optimizer_offload': True,
+(TaskRunner pid=3962104)                                                  'param_offload': True,
+(TaskRunner pid=3962104)                                                  'reshard_after_forward': True,
+(TaskRunner pid=3962104)                                                  'seed': 42,
+(TaskRunner pid=3962104)                                                  'strategy': 'fsdp',
+(TaskRunner pid=3962104)                                                  'ulysses_sequence_parallel_size': 1,
+(TaskRunner pid=3962104)                                                  'use_orig_params': False,
+(TaskRunner pid=3962104)                                                  'use_torch_compile': True,
+(TaskRunner pid=3962104)                                                  'wrap_policy': {'min_num_params': 0}},
+(TaskRunner pid=3962104)                                  'grad_clip': 1.0,
+(TaskRunner pid=3962104)                                  'kl_loss_coef': 0.001,
+(TaskRunner pid=3962104)                                  'kl_loss_type': 'low_var_kl',
+(TaskRunner pid=3962104)                                  'loss_agg_mode': 'token-mean',
+(TaskRunner pid=3962104)                                  'loss_scale_factor': None,
+(TaskRunner pid=3962104)                                  'optim': {'_target_': 'verl.workers.config.FSDPOptimizerConfig',
+(TaskRunner pid=3962104)                                            'betas': [0.9, 0.999],
+(TaskRunner pid=3962104)                                            'clip_grad': 1.0,
+(TaskRunner pid=3962104)                                            'lr': 1e-06,
+(TaskRunner pid=3962104)                                            'lr_scheduler_type': 'constant',
+(TaskRunner pid=3962104)                                            'lr_warmup_steps': -1,
+(TaskRunner pid=3962104)                                            'lr_warmup_steps_ratio': 0.0,
+(TaskRunner pid=3962104)                                            'min_lr_ratio': 0.0,
+(TaskRunner pid=3962104)                                            'num_cycles': 0.5,
+(TaskRunner pid=3962104)                                            'optimizer': 'AdamW',
+(TaskRunner pid=3962104)                                            'optimizer_impl': 'torch.optim',
+(TaskRunner pid=3962104)                                            'override_optimizer_config': None,
+(TaskRunner pid=3962104)                                            'total_training_steps': -1,
+(TaskRunner pid=3962104)                                            'warmup_style': None,
+(TaskRunner pid=3962104)                                            'weight_decay': 0.01},
+(TaskRunner pid=3962104)                                  'policy_loss': {'_target_': 'verl.workers.config.PolicyLossConfig',
+(TaskRunner pid=3962104)                                                  'clip_cov_lb': 1.0,
+(TaskRunner pid=3962104)                                                  'clip_cov_ratio': 0.0002,
+(TaskRunner pid=3962104)                                                  'clip_cov_ub': 5.0,
+(TaskRunner pid=3962104)                                                  'kl_cov_ratio': 0.0002,
+(TaskRunner pid=3962104)                                                  'loss_mode': 'vanilla',
+(TaskRunner pid=3962104)                                                  'ppo_kl_coef': 0.1},
+(TaskRunner pid=3962104)                                  'ppo_epochs': 1,
+(TaskRunner pid=3962104)                                  'ppo_max_token_len_per_gpu': 16384,
+(TaskRunner pid=3962104)                                  'ppo_micro_batch_size': None,
+(TaskRunner pid=3962104)                                  'ppo_micro_batch_size_per_gpu': 16,
+(TaskRunner pid=3962104)                                  'ppo_mini_batch_size': 256,
+(TaskRunner pid=3962104)                                  'profiler': {'_target_': 'verl.utils.profiler.ProfilerConfig',
+(TaskRunner pid=3962104)                                               'all_ranks': False,
+(TaskRunner pid=3962104)                                               'enable': False,
+(TaskRunner pid=3962104)                                               'ranks': [],
+(TaskRunner pid=3962104)                                               'save_path': 'outputs/profile',
+(TaskRunner pid=3962104)                                               'tool': None,
+(TaskRunner pid=3962104)                                               'tool_config': {'npu': {'_target_': 'verl.utils.profiler.config.NPUToolConfig',
+(TaskRunner pid=3962104)                                                                       'analysis': True,
+(TaskRunner pid=3962104)                                                                       'contents': [],
+(TaskRunner pid=3962104)                                                                       'discrete': False,
+(TaskRunner pid=3962104)                                                                       'level': 'level0'},
+(TaskRunner pid=3962104)                                                               'nsys': {'_target_': 'verl.utils.profiler.config.NsightToolConfig',
+(TaskRunner pid=3962104)                                                                        'discrete': False},
+(TaskRunner pid=3962104)                                                               'torch': {'_target_': 'verl.utils.profiler.config.TorchProfilerToolConfig',
+(TaskRunner pid=3962104)                                                                         'contents': [],
+(TaskRunner pid=3962104)                                                                         'discrete': False},
+(TaskRunner pid=3962104)                                                               'torch_memory': {'_target_': 'verl.utils.profiler.config.TorchMemoryToolConfig',
+(TaskRunner pid=3962104)                                                                                'stack_depth': 32,
+(TaskRunner pid=3962104)                                                                                'trace_alloc_max_entries': 100000}}},
+(TaskRunner pid=3962104)                                  'rollout_n': 3,
+(TaskRunner pid=3962104)                                  'router_replay': {'_target_': 'verl.workers.config.RouterReplayConfig',
+(TaskRunner pid=3962104)                                                    'mode': 'disabled',
+(TaskRunner pid=3962104)                                                    'record_file': None,
+(TaskRunner pid=3962104)                                                    'replay_file': None},
+(TaskRunner pid=3962104)                                  'shuffle': False,
+(TaskRunner pid=3962104)                                  'strategy': 'fsdp',
+(TaskRunner pid=3962104)                                  'sum_pi_squared_checkpointing': False,
+(TaskRunner pid=3962104)                                  'tau_neg': 1.05,
+(TaskRunner pid=3962104)                                  'tau_pos': 1.0,
+(TaskRunner pid=3962104)                                  'ulysses_sequence_parallel_size': 1,
+(TaskRunner pid=3962104)                                  'use_dynamic_bsz': False,
+(TaskRunner pid=3962104)                                  'use_fused_kernels': False,
+(TaskRunner pid=3962104)                                  'use_kl_loss': True,
+(TaskRunner pid=3962104)                                  'use_prefix_grouper': False,
+(TaskRunner pid=3962104)                                  'use_remove_padding': True,
+(TaskRunner pid=3962104)                                  'use_torch_compile': True},
+(TaskRunner pid=3962104)                        'hybrid_engine': True,
+(TaskRunner pid=3962104)                        'model': {'_target_': 'verl.workers.config.HFModelConfig',
+(TaskRunner pid=3962104)                                  'custom_chat_template': None,
+(TaskRunner pid=3962104)                                  'enable_activation_offload': False,
+(TaskRunner pid=3962104)                                  'enable_gradient_checkpointing': True,
+(TaskRunner pid=3962104)                                  'exclude_modules': None,
+(TaskRunner pid=3962104)                                  'external_lib': None,
+(TaskRunner pid=3962104)                                  'fused_kernel_options': {'impl_backend': 'torch'},
+(TaskRunner pid=3962104)                                  'hf_config_path': None,
+(TaskRunner pid=3962104)                                  'lora_adapter_path': None,
+(TaskRunner pid=3962104)                                  'lora_alpha': 16,
+(TaskRunner pid=3962104)                                  'lora_rank': 0,
+(TaskRunner pid=3962104)                                  'mtp': {'_target_': 'verl.workers.config.MtpConfig',
+(TaskRunner pid=3962104)                                          'detach_encoder': False,
+(TaskRunner pid=3962104)                                          'enable': False,
+(TaskRunner pid=3962104)                                          'enable_rollout': False,
+(TaskRunner pid=3962104)                                          'enable_train': False,
+(TaskRunner pid=3962104)                                          'method': 'mtp',
+(TaskRunner pid=3962104)                                          'mtp_loss_scaling_factor': 0.1,
+(TaskRunner pid=3962104)                                          'num_speculative_tokens': 1,
+(TaskRunner pid=3962104)                                          'speculative_algorithm': 'EAGLE',
+(TaskRunner pid=3962104)                                          'speculative_eagle_topk': 1,
+(TaskRunner pid=3962104)                                          'speculative_num_draft_tokens': 4,
+(TaskRunner pid=3962104)                                          'speculative_num_steps': 3},
+(TaskRunner pid=3962104)                                  'override_config': {},
+(TaskRunner pid=3962104)                                  'path': 'Qwen/Qwen3-4B-Instruct-2507',
+(TaskRunner pid=3962104)                                  'target_modules': 'all-linear',
+(TaskRunner pid=3962104)                                  'tiled_mlp': {'enabled': False,
+(TaskRunner pid=3962104)                                                'num_shards': 4},
+(TaskRunner pid=3962104)                                  'tokenizer_path': None,
+(TaskRunner pid=3962104)                                  'trust_remote_code': False,
+(TaskRunner pid=3962104)                                  'use_fused_kernels': False,
+(TaskRunner pid=3962104)                                  'use_liger': False,
+(TaskRunner pid=3962104)                                  'use_remove_padding': True,
+(TaskRunner pid=3962104)                                  'use_shm': False},
+(TaskRunner pid=3962104)                        'nccl_timeout': 600,
+(TaskRunner pid=3962104)                        'ref': {'_target_': 'verl.workers.config.FSDPActorConfig',
+(TaskRunner pid=3962104)                                'entropy_checkpointing': False,
+(TaskRunner pid=3962104)                                'entropy_from_logits_with_chunking': False,
+(TaskRunner pid=3962104)                                'fsdp_config': {'_target_': 'verl.workers.config.FSDPEngineConfig',
+(TaskRunner pid=3962104)                                                'dtype': 'bfloat16',
+(TaskRunner pid=3962104)                                                'entropy_checkpointing': False,
+(TaskRunner pid=3962104)                                                'entropy_from_logits_with_chunking': False,
+(TaskRunner pid=3962104)                                                'forward_only': True,
+(TaskRunner pid=3962104)                                                'forward_prefetch': False,
+(TaskRunner pid=3962104)                                                'fsdp_size': -1,
+(TaskRunner pid=3962104)                                                'full_determinism': False,
+(TaskRunner pid=3962104)                                                'model_dtype': 'fp32',
+(TaskRunner pid=3962104)                                                'offload_policy': False,
+(TaskRunner pid=3962104)                                                'optimizer_offload': False,
+(TaskRunner pid=3962104)                                                'param_offload': True,
+(TaskRunner pid=3962104)                                                'reshard_after_forward': True,
+(TaskRunner pid=3962104)                                                'seed': 42,
+(TaskRunner pid=3962104)                                                'strategy': 'fsdp',
+(TaskRunner pid=3962104)                                                'ulysses_sequence_parallel_size': 1,
+(TaskRunner pid=3962104)                                                'use_orig_params': False,
+(TaskRunner pid=3962104)                                                'use_torch_compile': True,
+(TaskRunner pid=3962104)                                                'wrap_policy': {'min_num_params': 0}},
+(TaskRunner pid=3962104)                                'log_prob_max_token_len_per_gpu': 16384,
+(TaskRunner pid=3962104)                                'log_prob_micro_batch_size': None,
+(TaskRunner pid=3962104)                                'log_prob_micro_batch_size_per_gpu': 32,
+(TaskRunner pid=3962104)                                'log_prob_use_dynamic_bsz': False,
+(TaskRunner pid=3962104)                                'profiler': {'_target_': 'verl.utils.profiler.ProfilerConfig',
+(TaskRunner pid=3962104)                                             'all_ranks': False,
+(TaskRunner pid=3962104)                                             'enable': False,
+(TaskRunner pid=3962104)                                             'ranks': [],
+(TaskRunner pid=3962104)                                             'save_path': 'outputs/profile',
+(TaskRunner pid=3962104)                                             'tool': None,
+(TaskRunner pid=3962104)                                             'tool_config': {'npu': {'_target_': 'verl.utils.profiler.config.NPUToolConfig',
+(TaskRunner pid=3962104)                                                                     'analysis': True,
+(TaskRunner pid=3962104)                                                                     'contents': [],
+(TaskRunner pid=3962104)                                                                     'discrete': False,
+(TaskRunner pid=3962104)                                                                     'level': 'level0'},
+(TaskRunner pid=3962104)                                                             'nsys': {'_target_': 
+(TaskRunner pid=3962104) 'verl.utils.profiler.config.NsightToolConfig',
+(TaskRunner pid=3962104)                                                                      'discrete': False},
+(TaskRunner pid=3962104)                                                             'torch': {'_target_': 'verl.utils.profiler.config.TorchProfilerToolConfig',
+(TaskRunner pid=3962104)                                                                       'contents': [],
+(TaskRunner pid=3962104)                                                                       'discrete': False},
+(TaskRunner pid=3962104)                                                             'torch_memory': {'_target_': 'verl.utils.profiler.config.TorchMemoryToolConfig',
+(TaskRunner pid=3962104)                                                                              'stack_depth': 32,
+(TaskRunner pid=3962104)                                                                              'trace_alloc_max_entries': 100000}}},
+(TaskRunner pid=3962104)                                'rollout_n': 3,
+(TaskRunner pid=3962104)                                'router_replay': {'_target_': 'verl.workers.config.RouterReplayConfig',
+(TaskRunner pid=3962104)                                                  'mode': 'disabled',
+(TaskRunner pid=3962104)                                                  'record_file': None,
+(TaskRunner pid=3962104)                                                  'replay_file': None},
+(TaskRunner pid=3962104)                                'strategy': 'fsdp',
+(TaskRunner pid=3962104)                                'ulysses_sequence_parallel_size': 1,
+(TaskRunner pid=3962104)                                'use_torch_compile': True},
+(TaskRunner pid=3962104)                        'rollout': {'_target_': 'verl.workers.config.RolloutConfig',
+(TaskRunner pid=3962104)                                    'agent': {'_target_': 'verl.workers.config.AgentLoopConfig',
+(TaskRunner pid=3962104)                                              'agent_loop_config_path': None,
+(TaskRunner pid=3962104)                                              'custom_async_server': {'_target_': 'verl.workers.config.CustomAsyncServerConfig',
+(TaskRunner pid=3962104)                                                                      'name': None,
+(TaskRunner pid=3962104)                                                                      'path': None},
+(TaskRunner pid=3962104)                                              'default_agent_loop': 'single_turn_agent',
+(TaskRunner pid=3962104)                                              'num_workers': 8},
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+(TaskRunner pid=3962104)                               'enable_chunked_prefill': True,
+(TaskRunner pid=3962104)                               'enable_prefix_caching': True,
+(TaskRunner pid=3962104)                               'enforce_eager': True,
+(TaskRunner pid=3962104)                               'engine_kwargs': {},
+(TaskRunner pid=3962104)                               'expert_parallel_size': 1,
+(TaskRunner pid=3962104)                               'free_cache_engine': True,
+(TaskRunner pid=3962104)                               'gpu_memory_utilization': 0.5,
+(TaskRunner pid=3962104)                               'limit_images': None,
+(TaskRunner pid=3962104)                               'load_format': 'auto',
+(TaskRunner pid=3962104)                               'max_model_len': None,
+(TaskRunner pid=3962104)                               'max_num_batched_tokens': 8192,
+(TaskRunner pid=3962104)                               'max_num_seqs': 1024,
+(TaskRunner pid=3962104)                               'name': '???',
+(TaskRunner pid=3962104)                               'prompt_length': 2048,
+(TaskRunner pid=3962104)                               'response_length': 2048,
+(TaskRunner pid=3962104)                               'skip_tokenizer_init': False,
+(TaskRunner pid=3962104)                               'tensor_model_parallel_size': 2},
+(TaskRunner pid=3962104)                   'sandbox_fusion': {'max_concurrent': 64,
+(TaskRunner pid=3962104)                                      'memory_limit_mb': 1024,
+(TaskRunner pid=3962104)                                      'url': None},
+(TaskRunner pid=3962104)                   'strategy': 'fsdp',
+(TaskRunner pid=3962104)                   'ulysses_sequence_parallel_size': 1,
+(TaskRunner pid=3962104)                   'use_dynamic_bsz': False,
+(TaskRunner pid=3962104)                   'use_reward_loop': True},
+(TaskRunner pid=3962104)  'trainer': {'balance_batch': True,
+(TaskRunner pid=3962104)              'critic_warmup': 0,
+(TaskRunner pid=3962104)              'default_hdfs_dir': None,
+(TaskRunner pid=3962104)              'default_local_dir': '/home/mshahidul/readctrl/code/RL_model/models/RL_model_subclaim_classifier_v2',
+(TaskRunner pid=3962104)              'del_local_ckpt_after_load': False,
+(TaskRunner pid=3962104)              'device': 'cuda',
+(TaskRunner pid=3962104)              'esi_redundant_time': 0,
+(TaskRunner pid=3962104)              'experiment_name': 'qwen3-4b-instruct-en',
+(TaskRunner pid=3962104)              'log_val_generations': 0,
+(TaskRunner pid=3962104)              'logger': ['console', 'wandb'],
+(TaskRunner pid=3962104)              'max_actor_ckpt_to_keep': 1,
+(TaskRunner pid=3962104)              'max_critic_ckpt_to_keep': 1,
+(TaskRunner pid=3962104)              'n_gpus_per_node': 2,
+(TaskRunner pid=3962104)              'nnodes': 1,
+(TaskRunner pid=3962104)              'project_name': 'readctrl-verl',
+(TaskRunner pid=3962104)              'ray_wait_register_center_timeout': 300,
+(TaskRunner pid=3962104)              'remove_previous_ckpt_in_save': True,
+(TaskRunner pid=3962104)              'resume_from_path': None,
+(TaskRunner pid=3962104)              'resume_mode': 'auto',
+(TaskRunner pid=3962104)              'rollout_data_dir': None,
+(TaskRunner pid=3962104)              'save_freq': 5,
+(TaskRunner pid=3962104)              'test_freq': 10,
+(TaskRunner pid=3962104)              'total_epochs': 15,
+(TaskRunner pid=3962104)              'total_training_steps': None,
+(TaskRunner pid=3962104)              'use_legacy_worker_impl': 'auto',
+(TaskRunner pid=3962104)              'val_before_train': True,
+(TaskRunner pid=3962104)              'val_only': False,
+(TaskRunner pid=3962104)              'validation_data_dir': None},
+(TaskRunner pid=3962104)  'transfer_queue': {'enable': False}}
+(TaskRunner pid=3962104) /data/home_beta/mshahidul/readctrl/code/RL_model/verl/verl_train/verl/trainer/main_ppo.py:300: UserWarning: Disabled critic as algorithm.adv_estimator != gae. If it is not intended, please set critic.enable=True
+(TaskRunner pid=3962104)   use_critic=need_critic(config),
+(TaskRunner pid=3962104) [validate_config] All configuration checks passed successfully!
+(TaskRunner pid=3962104) /data/home_beta/mshahidul/readctrl/code/RL_model/verl/verl_train/verl/utils/tokenizer.py:109: UserWarning: Failed to create processor: Unsupported processor type: Qwen2TokenizerFast. This may affect multimodal processing
+(TaskRunner pid=3962104)   warnings.warn(f"Failed to create processor: {e}. This may affect multimodal processing", stacklevel=1)
+(TaskRunner pid=3962104) Using dataset class: RLHFDataset
+(TaskRunner pid=3962104) dataset len: 4584
+(TaskRunner pid=3962104) Setting TOKENIZERS_PARALLELISM=false for forked processes.
+(TaskRunner pid=3962104) WARNING:2026-02-15 11:40:50,733:Setting TOKENIZERS_PARALLELISM=false for forked processes.
+(TaskRunner pid=3962104) 
Filtering prompts longer than 1024 tokens (num_proc=1):   0%|          | 0/4584 [00:00<?, ? examples/s]
+(TaskRunner pid=3962104) 
Filtering prompts longer than 1024 tokens (num_proc=1):  22%|██▏       | 1000/4584 [00:05<00:19, 185.16 examples/s]
+(TaskRunner pid=3962104) 
Filtering prompts longer than 1024 tokens (num_proc=1):  44%|████▎     | 2000/4584 [00:10<00:12, 200.42 examples/s]
+(TaskRunner pid=3962104) 
Filtering prompts longer than 1024 tokens (num_proc=1):  65%|██████▌   | 3000/4584 [00:14<00:07, 209.90 examples/s]
+(TaskRunner pid=3962104) 
Filtering prompts longer than 1024 tokens (num_proc=1):  87%|████████▋ | 4000/4584 [00:19<00:02, 213.28 examples/s]
+(TaskRunner pid=3962104) 
Filtering prompts longer than 1024 tokens (num_proc=1): 100%|██████████| 4584/4584 [00:21<00:00, 223.64 examples/s]
+(TaskRunner pid=3962104) filter dataset len: 1574
+(TaskRunner pid=3962104) Using dataset class: RLHFDataset
+(TaskRunner pid=3962104) 
Filtering prompts longer than 1024 tokens (num_proc=1): 100%|██████████| 4584/4584 [00:21<00:00, 212.76 examples/s]
+(TaskRunner pid=3962104) dataset len: 510
+(TaskRunner pid=3962104) Setting TOKENIZERS_PARALLELISM=false for forked processes.
+(TaskRunner pid=3962104) WARNING:2026-02-15 11:41:12,746:Setting TOKENIZERS_PARALLELISM=false for forked processes.
+(TaskRunner pid=3962104) 
Filtering prompts longer than 1024 tokens (num_proc=1):   0%|          | 0/510 [00:00<?, ? examples/s]
+(TaskRunner pid=3962104) 
Filtering prompts longer than 1024 tokens (num_proc=1): 100%|██████████| 510/510 [00:03<00:00, 150.51 examples/s]
+(TaskRunner pid=3962104) filter dataset len: 167
+(TaskRunner pid=3962104) Size of train dataloader: 3, Size of val dataloader: 1
+(TaskRunner pid=3962104) Total training steps: 45
+(TaskRunner pid=3962104) colocated worker base class <class 'verl.single_controller.base.worker.Worker'>
+(TaskRunner pid=3962104) 
Filtering prompts longer than 1024 tokens (num_proc=1): 100%|██████████| 510/510 [00:03<00:00, 143.73 examples/s]
+(TaskRunner pid=3962104) /data/home_beta/mshahidul/readctrl/code/RL_model/verl/verl_train/verl/trainer/ppo/ray_trainer.py:291: UserWarning: Disabled critic as algorithm.adv_estimator != gae. If it is not intended, please set critic.enable=True
+(TaskRunner pid=3962104)   self.use_critic = need_critic(self.config)
+(pid=3964116) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/torch/cuda/__init__.py:63: FutureWarning: The pynvml package is deprecated. Please install nvidia-ml-py instead. If you did not install pynvml directly, please report this to the maintainers of the package that installed pynvml for you.
+(pid=3964116)   import pynvml  # type: ignore[import]
+(pid=3964116) WARNING:2026-02-15 11:41:32,461:Skipping import of cpp extensions due to incompatible torch version 2.8.0+cu128 for torchao version 0.16.0             Please see https://github.com/pytorch/ao/issues/2919 for more info
+(pid=3964117) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/torch/cuda/__init__.py:63: FutureWarning: The pynvml package is deprecated. Please install nvidia-ml-py instead. If you did not install pynvml directly, please report this to the maintainers of the package that installed pynvml for you.
+(pid=3964117)   import pynvml  # type: ignore[import]
+(pid=3964116) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/models/backends.py:21: UserWarning: Apex is not installed. Falling back to Torch Norm
+(pid=3964116)   warnings.warn("Apex is not installed. Falling back to Torch Norm")
+(pid=3964116) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/optimizer/__init__.py:18: UserWarning: Transformer Engine and Apex are not installed. Falling back to Torch optimizers.
+(pid=3964116)   warnings.warn(
+(pid=3964116) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/optimizer/optimizer.py:28: UserWarning: Transformer Engine and Apex are not installed. Falling back to local implementations of multi_tensor_applier and multi_tensor_scale
+(pid=3964116)   warnings.warn(
+(pid=3964116) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/optimizer/clip_grads.py:29: UserWarning: Transformer Engine and Apex are not installed. Falling back to local implementations of multi_tensor_applier, multi_tensor_l2norm, and multi_tensor_scale
+(pid=3964116)   warnings.warn(
+(pid=3964117) WARNING:2026-02-15 11:41:32,436:Skipping import of cpp extensions due to incompatible torch version 2.8.0+cu128 for torchao version 0.16.0             Please see https://github.com/pytorch/ao/issues/2919 for more info
+(WorkerDict pid=3964117) [Gloo] Rank 1 is connected to 1 peer ranks. Expected number of connected peer ranks is : 1
+(WorkerDict pid=3964116) reference model: Qwen/Qwen3-4B-Instruct-2507
+(WorkerDict pid=3964117) /data/home_beta/mshahidul/readctrl/code/RL_model/verl/verl_train/verl/utils/tokenizer.py:109: UserWarning: Failed to create processor: Unsupported processor type: Qwen2TokenizerFast. This may affect multimodal processing
+(WorkerDict pid=3964117)   warnings.warn(f"Failed to create processor: {e}. This may affect multimodal processing", stacklevel=1)
+(pid=3964117) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/models/gpt/gpt_layer_specs.py:67: UserWarning: Apex is not installed. Falling back to Torch Norm [repeated 3x across cluster] (Ray deduplicates logs by default. Set RAY_DEDUP_LOGS=0 to disable log deduplication, or see https://docs.ray.io/en/master/ray-observability/user-guides/configure-logging.html#log-deduplication for more options.)
+(pid=3964117)   warnings.warn("Apex is not installed. Falling back to Torch Norm") [repeated 3x across cluster]
+(pid=3964117) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/optimizer/__init__.py:18: UserWarning: Transformer Engine and Apex are not installed. Falling back to Torch optimizers.
+(pid=3964117)   warnings.warn( [repeated 3x across cluster]
+(pid=3964117) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/optimizer/optimizer.py:28: UserWarning: Transformer Engine and Apex are not installed. Falling back to local implementations of multi_tensor_applier and multi_tensor_scale
+(pid=3964117) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/optimizer/clip_grads.py:29: UserWarning: Transformer Engine and Apex are not installed. Falling back to local implementations of multi_tensor_applier, multi_tensor_l2norm, and multi_tensor_scale
+(WorkerDict pid=3964116) Model config after override: Qwen3Config {
+(WorkerDict pid=3964116)   "architectures": [
+(WorkerDict pid=3964116)     "Qwen3ForCausalLM"
+(WorkerDict pid=3964116)   ],
+(WorkerDict pid=3964116)   "attention_bias": false,
+(WorkerDict pid=3964116)   "attention_dropout": 0.0,
+(WorkerDict pid=3964116)   "dtype": "bfloat16",
+(WorkerDict pid=3964116)   "eos_token_id": 151645,
+(WorkerDict pid=3964116)   "head_dim": 128,
+(WorkerDict pid=3964116)   "hidden_act": "silu",
+(WorkerDict pid=3964116)   "hidden_size": 2560,
+(WorkerDict pid=3964116)   "initializer_range": 0.02,
+(WorkerDict pid=3964116)   "intermediate_size": 9728,
+(WorkerDict pid=3964116)   "layer_types": [
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention"
+(WorkerDict pid=3964116)   ],
+(WorkerDict pid=3964116)   "max_position_embeddings": 262144,
+(WorkerDict pid=3964116)   "max_window_layers": 36,
+(WorkerDict pid=3964116)   "model_type": "qwen3",
+(WorkerDict pid=3964116)   "num_attention_heads": 32,
+(WorkerDict pid=3964116)   "num_hidden_layers": 36,
+(WorkerDict pid=3964116)   "num_key_value_heads": 8,
+(WorkerDict pid=3964116)   "pad_token_id": 151643,
+(WorkerDict pid=3964116)   "rms_norm_eps": 1e-06,
+(WorkerDict pid=3964116)   "rope_scaling": null,
+(WorkerDict pid=3964116)   "rope_theta": 5000000,
+(WorkerDict pid=3964116)   "sliding_window": null,
+(WorkerDict pid=3964116)   "tie_word_embeddings": true,
+(WorkerDict pid=3964116)   "transformers_version": "4.56.1",
+(WorkerDict pid=3964116)   "use_cache": true,
+(WorkerDict pid=3964116)   "use_sliding_window": false,
+(WorkerDict pid=3964116)   "vocab_size": 151936
+(WorkerDict pid=3964116) }
+(WorkerDict pid=3964116) 
+(WorkerDict pid=3964116) [Gloo] Rank 0 is connected to 1 peer ranks. Expected number of connected peer ranks is : 1
+(WorkerDict pid=3964117) `torch_dtype` is deprecated! Use `dtype` instead!
+(WorkerDict pid=3964117) Flash Attention 2 only supports torch.float16 and torch.bfloat16 dtypes, but the current dype in Qwen3ForCausalLM is torch.float32. You should run training or inference using Automatic Mixed-Precision via the `with torch.autocast(device_type='torch_device'):` decorator, or load the model with the `dtype` argument. Example: `model = AutoModel.from_pretrained("openai/whisper-tiny", attn_implementation="flash_attention_2", dtype=torch.float16)`
+(WorkerDict pid=3964117) Flash Attention 2 only supports torch.float16 and torch.bfloat16 dtypes, but the current dype in Qwen3Model is torch.float32. You should run training or inference using Automatic Mixed-Precision via the `with torch.autocast(device_type='torch_device'):` decorator, or load the model with the `dtype` argument. Example: `model = AutoModel.from_pretrained("openai/whisper-tiny", attn_implementation="flash_attention_2", dtype=torch.float16)`
+(WorkerDict pid=3964117) 
Loading checkpoint shards:   0%|          | 0/3 [00:00<?, ?it/s]
+(WorkerDict pid=3964117) 
Loading checkpoint shards:  33%|███▎      | 1/3 [00:04<00:09,  4.80s/it]
+(WorkerDict pid=3964116) /data/home_beta/mshahidul/readctrl/code/RL_model/verl/verl_train/verl/utils/tokenizer.py:109: UserWarning: Failed to create processor: Unsupported processor type: Qwen2TokenizerFast. This may affect multimodal processing
+(WorkerDict pid=3964116)   warnings.warn(f"Failed to create processor: {e}. This may affect multimodal processing", stacklevel=1)
+(WorkerDict pid=3964116) `torch_dtype` is deprecated! Use `dtype` instead!
+(WorkerDict pid=3964116) Flash Attention 2 only supports torch.float16 and torch.bfloat16 dtypes, but the current dype in Qwen3Model is torch.float32. You should run training or inference using Automatic Mixed-Precision via the `with torch.autocast(device_type='torch_device'):` decorator, or load the model with the `dtype` argument. Example: `model = AutoModel.from_pretrained("openai/whisper-tiny", attn_implementation="flash_attention_2", dtype=torch.float16)` [repeated 2x across cluster]
+(WorkerDict pid=3964116) 
Loading checkpoint shards:   0%|          | 0/3 [00:00<?, ?it/s]
+(WorkerDict pid=3964117) 
Loading checkpoint shards: 100%|██████████| 3/3 [00:09<00:00,  2.67s/it]
Loading checkpoint shards: 100%|██████████| 3/3 [00:09<00:00,  3.25s/it]
+(WorkerDict pid=3964117) 
Loading checkpoint shards:  67%|██████▋   | 2/3 [00:09<00:04,  4.82s/it] [repeated 2x across cluster]
+(WorkerDict pid=3964117) Monkey patch state_dict in AutoModelForCausalLMWithValueHead. 
+(WorkerDict pid=3964117) Monkey patch _flash_attention_forward in transformers.integrations.flash_attention
+(WorkerDict pid=3964117) Skipping monkey patch for Qwen3ForCausalLM as use_fused_kernels is False or fused_kernels_backend is torch
+(WorkerDict pid=3964116) Qwen3ForCausalLM contains 4.02B parameters
+(WorkerDict pid=3964116) wrap_policy: functools.partial(<function _or_policy at 0x7f57218794e0>, policies=[functools.partial(<function transformer_auto_wrap_policy at 0x7f57218793a0>, transformer_layer_cls={<class 'transformers.models.qwen3.modeling_qwen3.Qwen3DecoderLayer'>})])
+(WorkerDict pid=3964116) NCCL version 2.27.3+cuda12.9
+(WorkerDict pid=3964116) Ref use_remove_padding=True
+(WorkerDict pid=3964116) Ref use_fused_kernels=False
+(WorkerDict pid=3964116) Ref use_prefix_grouper=False
+(WorkerDict pid=3964116) Monkey patch state_dict in AutoModelForCausalLMWithValueHead. 
+(WorkerDict pid=3964116) Monkey patch _flash_attention_forward in transformers.integrations.flash_attention
+(WorkerDict pid=3964116) Skipping monkey patch for Qwen3ForCausalLM as use_fused_kernels is False or fused_kernels_backend is torch
+(WorkerDict pid=3964117) /data/home_beta/mshahidul/readctrl/code/RL_model/verl/verl_train/verl/utils/tokenizer.py:109: UserWarning: Failed to create processor: Unsupported processor type: Qwen2TokenizerFast. This may affect multimodal processing
+(WorkerDict pid=3964117)   warnings.warn(f"Failed to create processor: {e}. This may affect multimodal processing", stacklevel=1)
+(WorkerDict pid=3964116) 
Loading checkpoint shards: 100%|██████████| 3/3 [00:10<00:00,  2.76s/it]
Loading checkpoint shards: 100%|██████████| 3/3 [00:10<00:00,  3.36s/it]
+(WorkerDict pid=3964116) 
Loading checkpoint shards:  67%|██████▋   | 2/3 [00:09<00:04,  4.98s/it]
+(WorkerDict pid=3964116) Model config after override: Qwen3Config {
+(WorkerDict pid=3964116)   "architectures": [
+(WorkerDict pid=3964116)     "Qwen3ForCausalLM"
+(WorkerDict pid=3964116)   ],
+(WorkerDict pid=3964116)   "attention_bias": false,
+(WorkerDict pid=3964116)   "attention_dropout": 0.0,
+(WorkerDict pid=3964116)   "dtype": "bfloat16",
+(WorkerDict pid=3964116)   "eos_token_id": 151645,
+(WorkerDict pid=3964116)   "head_dim": 128,
+(WorkerDict pid=3964116)   "hidden_act": "silu",
+(WorkerDict pid=3964116)   "hidden_size": 2560,
+(WorkerDict pid=3964116)   "initializer_range": 0.02,
+(WorkerDict pid=3964116)   "intermediate_size": 9728,
+(WorkerDict pid=3964116)   "layer_types": [
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention",
+(WorkerDict pid=3964116)     "full_attention"
+(WorkerDict pid=3964116)   ],
+(WorkerDict pid=3964116)   "max_position_embeddings": 262144,
+(WorkerDict pid=3964116)   "max_window_layers": 36,
+(WorkerDict pid=3964116)   "model_type": "qwen3",
+(WorkerDict pid=3964116)   "num_attention_heads": 32,
+(WorkerDict pid=3964116)   "num_hidden_layers": 36,
+(WorkerDict pid=3964116)   "num_key_value_heads": 8,
+(WorkerDict pid=3964116)   "pad_token_id": 151643,
+(WorkerDict pid=3964116)   "rms_norm_eps": 1e-06,
+(WorkerDict pid=3964116)   "rope_scaling": null,
+(WorkerDict pid=3964116)   "rope_theta": 5000000,
+(WorkerDict pid=3964116)   "sliding_window": null,
+(WorkerDict pid=3964116)   "tie_word_embeddings": true,
+(WorkerDict pid=3964116)   "transformers_version": "4.56.1",
+(WorkerDict pid=3964116)   "use_cache": true,
+(WorkerDict pid=3964116)   "use_sliding_window": false,
+(WorkerDict pid=3964116)   "vocab_size": 151936
+(WorkerDict pid=3964116) }
+(WorkerDict pid=3964116) 
+(WorkerDict pid=3964117) 
Loading checkpoint shards:   0%|          | 0/3 [00:00<?, ?it/s]
+(WorkerDict pid=3964117) 
Loading checkpoint shards:  33%|███▎      | 1/3 [00:04<00:09,  4.73s/it]
+(WorkerDict pid=3964116) /data/home_beta/mshahidul/readctrl/code/RL_model/verl/verl_train/verl/utils/tokenizer.py:109: UserWarning: Failed to create processor: Unsupported processor type: Qwen2TokenizerFast. This may affect multimodal processing
+(WorkerDict pid=3964116)   warnings.warn(f"Failed to create processor: {e}. This may affect multimodal processing", stacklevel=1)
+(WorkerDict pid=3964116) 
Loading checkpoint shards:   0%|          | 0/3 [00:00<?, ?it/s]
+(WorkerDict pid=3964117) 
Loading checkpoint shards:  67%|██████▋   | 2/3 [00:09<00:04,  4.94s/it] [repeated 2x across cluster]
+(WorkerDict pid=3964117) 
Loading checkpoint shards: 100%|██████████| 3/3 [00:09<00:00,  2.74s/it]
Loading checkpoint shards: 100%|██████████| 3/3 [00:09<00:00,  3.31s/it]
+(WorkerDict pid=3964117) Monkey patch state_dict in AutoModelForCausalLMWithValueHead. 
+(WorkerDict pid=3964117) Monkey patch _flash_attention_forward in transformers.integrations.flash_attention
+(WorkerDict pid=3964117) Skipping monkey patch for Qwen3ForCausalLM as use_fused_kernels is False or fused_kernels_backend is torch
+(WorkerDict pid=3964116) Qwen3ForCausalLM contains 4.02B parameters
+(WorkerDict pid=3964116) wrap_policy: functools.partial(<function _or_policy at 0x7f57218794e0>, policies=[functools.partial(<function transformer_auto_wrap_policy at 0x7f57218793a0>, transformer_layer_cls={<class 'transformers.models.qwen3.modeling_qwen3.Qwen3DecoderLayer'>})])
+(WorkerDict pid=3964116) Total steps: 45, num_warmup_steps: 0
+(WorkerDict pid=3964116) Monkey patch state_dict in AutoModelForCausalLMWithValueHead. 
+(WorkerDict pid=3964116) Monkey patch _flash_attention_forward in transformers.integrations.flash_attention
+(WorkerDict pid=3964116) Skipping monkey patch for Qwen3ForCausalLM as use_fused_kernels is False or fused_kernels_backend is torch
+(WorkerDict pid=3964116) Actor use_remove_padding=True
+(WorkerDict pid=3964116) Actor use_fused_kernels=False
+(WorkerDict pid=3964116) Actor use_prefix_grouper=False
+(WorkerDict pid=3964116) /data/home_beta/mshahidul/readctrl/code/RL_model/verl/verl_train/verl/utils/tokenizer.py:109: UserWarning: Failed to create processor: Unsupported processor type: Qwen2TokenizerFast. This may affect multimodal processing
+(WorkerDict pid=3964116)   warnings.warn(f"Failed to create processor: {e}. This may affect multimodal processing", stacklevel=1)
+(WorkerDict pid=3964116) 
Loading checkpoint shards:  67%|██████▋   | 2/3 [00:10<00:05,  5.34s/it]
+(WorkerDict pid=3964116) 
Loading checkpoint shards: 100%|██████████| 3/3 [00:10<00:00,  2.96s/it]
Loading checkpoint shards: 100%|██████████| 3/3 [00:10<00:00,  3.55s/it]
+(WorkerDict pid=3964117) [Gloo] Rank 1 is connected to 1 peer ranks. Expected number of connected peer ranks is : 1
+(WorkerDict pid=3964117) [Gloo] Rank 0 is connected to 0 peer ranks. Expected number of connected peer ranks is : 0
+(WorkerDict pid=3964117) [Gloo] Rank 0 is connected to 0 peer ranks. Expected number of connected peer ranks is : 0
+(WorkerDict pid=3964117) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/torch/distributed/fsdp/fully_sharded_data_parallel.py:678: FutureWarning: FSDP.state_dict_type() and FSDP.set_state_dict_type() are being deprecated. Please use APIs, get_state_dict() and set_state_dict(), which can support different parallelisms, FSDP1, FSDP2, DDP. API doc: https://pytorch.org/docs/stable/distributed.checkpoint.html#torch.distributed.checkpoint.state_dict.get_state_dict .Tutorial: https://pytorch.org/tutorials/recipes/distributed_checkpoint_recipe.html .
+(WorkerDict pid=3964117)   warnings.warn(
+(WorkerDict pid=3964117) /data/home_beta/mshahidul/readctrl/code/RL_model/verl/verl_train/verl/utils/tokenizer.py:109: UserWarning: Failed to create processor: Unsupported processor type: Qwen2TokenizerFast. This may affect multimodal processing
+(WorkerDict pid=3964117)   warnings.warn(f"Failed to create processor: {e}. This may affect multimodal processing", stacklevel=1)
+(TaskRunner pid=3962104) WARNING 02-15 11:43:13 [api_server.py:1213] LoRA dynamic loading & unloading is enabled in the API server. This should ONLY be used for local development!
+(WorkerDict pid=3964116) [Gloo] Rank 0 is connected to 0 peer ranks. Expected number of connected peer ranks is : 0 [repeated 3x across cluster]
+(pid=3966776) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/torch/cuda/__init__.py:63: FutureWarning: The pynvml package is deprecated. Please install nvidia-ml-py instead. If you did not install pynvml directly, please report this to the maintainers of the package that installed pynvml for you.
+(pid=3966776)   import pynvml  # type: ignore[import]
+(WorkerDict pid=3964116) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/torch/distributed/fsdp/fully_sharded_data_parallel.py:678: FutureWarning: FSDP.state_dict_type() and FSDP.set_state_dict_type() are being deprecated. Please use APIs, get_state_dict() and set_state_dict(), which can support different parallelisms, FSDP1, FSDP2, DDP. API doc: https://pytorch.org/docs/stable/distributed.checkpoint.html#torch.distributed.checkpoint.state_dict.get_state_dict .Tutorial: https://pytorch.org/tutorials/recipes/distributed_checkpoint_recipe.html .
+(WorkerDict pid=3964116)   warnings.warn(
+(pid=3966776) WARNING:2026-02-15 11:43:28,243:Skipping import of cpp extensions due to incompatible torch version 2.8.0+cu128 for torchao version 0.16.0             Please see https://github.com/pytorch/ao/issues/2919 for more info
+(pid=3966775) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/torch/cuda/__init__.py:63: FutureWarning: The pynvml package is deprecated. Please install nvidia-ml-py instead. If you did not install pynvml directly, please report this to the maintainers of the package that installed pynvml for you.
+(pid=3966775)   import pynvml  # type: ignore[import]
+(pid=3966775) WARNING 02-15 11:43:40 [api_server.py:1213] LoRA dynamic loading & unloading is enabled in the API server. This should ONLY be used for local development!
+(pid=3966776) WARNING 02-15 11:43:40 [api_server.py:1213] LoRA dynamic loading & unloading is enabled in the API server. This should ONLY be used for local development!
+(vLLMHttpServer pid=3966776) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/models/backends.py:21: UserWarning: Apex is not installed. Falling back to Torch Norm
+(vLLMHttpServer pid=3966776)   warnings.warn("Apex is not installed. Falling back to Torch Norm")
+(vLLMHttpServer pid=3966776) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/optimizer/__init__.py:18: UserWarning: Transformer Engine and Apex are not installed. Falling back to Torch optimizers.
+(vLLMHttpServer pid=3966776)   warnings.warn(
+(vLLMHttpServer pid=3966776) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/optimizer/optimizer.py:28: UserWarning: Transformer Engine and Apex are not installed. Falling back to local implementations of multi_tensor_applier and multi_tensor_scale
+(vLLMHttpServer pid=3966776)   warnings.warn(
+(vLLMHttpServer pid=3966776) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/optimizer/clip_grads.py:29: UserWarning: Transformer Engine and Apex are not installed. Falling back to local implementations of multi_tensor_applier, multi_tensor_l2norm, and multi_tensor_scale
+(vLLMHttpServer pid=3966776)   warnings.warn(
+(pid=3966775) WARNING:2026-02-15 11:43:28,215:Skipping import of cpp extensions due to incompatible torch version 2.8.0+cu128 for torchao version 0.16.0             Please see https://github.com/pytorch/ao/issues/2919 for more info
+(vLLMHttpServer pid=3966776) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/models/gpt/gpt_layer_specs.py:67: UserWarning: Apex is not installed. Falling back to Torch Norm
+(vLLMHttpServer pid=3966776)   warnings.warn("Apex is not installed. Falling back to Torch Norm")
+(vLLMHttpServer pid=3966776) /data/home_beta/mshahidul/readctrl/code/RL_model/verl/verl_train/verl/utils/tokenizer.py:109: UserWarning: Failed to create processor: Unsupported processor type: Qwen2TokenizerFast. This may affect multimodal processing
+(vLLMHttpServer pid=3966776)   warnings.warn(f"Failed to create processor: {e}. This may affect multimodal processing", stacklevel=1)
+(vLLMHttpServer pid=3966776) WARNING:2026-02-15 11:43:43,487:agent loop only support torch and npu profiler, got None
+(vLLMHttpServer pid=3966776) INFO:2026-02-15 11:43:43,488:vLLMHttpServer, replica_rank: 0, node_rank: 0, CUDA_VISIBLE_DEVICES: 2, master_address: 172.16.34.29, master_port: 33207, data_parallel_rpc_port: 38889, data_parallel_master_port: 41623
+(vLLMHttpServer pid=3966776) INFO:2026-02-15 11:43:43,506:override_generation_config: {'temperature': 1.0, 'top_k': -1, 'top_p': 1, 'repetition_penalty': 1.0, 'max_new_tokens': 2048}
+(vLLMHttpServer pid=3966776) INFO:2026-02-15 11:43:43,506:enable_sleep_mode: True
+(vLLMHttpServer pid=3966776) ['serve',
+(vLLMHttpServer pid=3966776)  'Qwen/Qwen3-4B-Instruct-2507',
+(vLLMHttpServer pid=3966776)  '--dtype',
+(vLLMHttpServer pid=3966776)  'bfloat16',
+(vLLMHttpServer pid=3966776)  '--load_format',
+(vLLMHttpServer pid=3966776)  'dummy',
+(vLLMHttpServer pid=3966776)  '--distributed_executor_backend',
+(vLLMHttpServer pid=3966776)  'mp',
+(vLLMHttpServer pid=3966776)  '--worker_extension_cls',
+(vLLMHttpServer pid=3966776)  'verl.workers.rollout.vllm_rollout.utils.vLLMColocateWorkerExtension',
+(vLLMHttpServer pid=3966776)  '--max_model_len',
+(vLLMHttpServer pid=3966776)  '8192',
+(vLLMHttpServer pid=3966776)  '--max_num_seqs',
+(vLLMHttpServer pid=3966776)  '1024',
+(vLLMHttpServer pid=3966776)  '--enable_chunked_prefill',
+(vLLMHttpServer pid=3966776)  '--max_num_batched_tokens',
+(vLLMHttpServer pid=3966776)  '8192',
+(vLLMHttpServer pid=3966776)  '--enable_prefix_caching',
+(vLLMHttpServer pid=3966776)  '--enable_sleep_mode',
+(vLLMHttpServer pid=3966776)  '--logprobs_mode',
+(vLLMHttpServer pid=3966776)  'processed_logprobs',
+(vLLMHttpServer pid=3966776)  '--enforce_eager',
+(vLLMHttpServer pid=3966776)  '--gpu_memory_utilization',
+(vLLMHttpServer pid=3966776)  '0.4',
+(vLLMHttpServer pid=3966776)  '--disable_log_stats',
+(vLLMHttpServer pid=3966776)  '--tensor_parallel_size',
+(vLLMHttpServer pid=3966776)  '1',
+(vLLMHttpServer pid=3966776)  '--seed',
+(vLLMHttpServer pid=3966776)  '0',
+(vLLMHttpServer pid=3966776)  '--override_generation_config',
+(vLLMHttpServer pid=3966776)  '{"temperature": 1.0, "top_k": -1, "top_p": 1, "repetition_penalty": 1.0, '
+(vLLMHttpServer pid=3966776)  '"max_new_tokens": 2048}',
+(vLLMHttpServer pid=3966776)  '--hf_overrides',
+(vLLMHttpServer pid=3966776)  '{}',
+(vLLMHttpServer pid=3966776)  '--scheduling_policy',
+(vLLMHttpServer pid=3966776)  'fcfs',
+(vLLMHttpServer pid=3966776)  '--compilation_config',
+(vLLMHttpServer pid=3966776)  '{"cudagraph_mode": "FULL_AND_PIECEWISE"}']
+(vLLMHttpServer pid=3966776) `torch_dtype` is deprecated! Use `dtype` instead!
+(vLLMHttpServer pid=3966775) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/models/gpt/gpt_layer_specs.py:67: UserWarning: Apex is not installed. Falling back to Torch Norm [repeated 2x across cluster]
+(vLLMHttpServer pid=3966775)   warnings.warn("Apex is not installed. Falling back to Torch Norm") [repeated 2x across cluster]
+(vLLMHttpServer pid=3966775) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/optimizer/__init__.py:18: UserWarning: Transformer Engine and Apex are not installed. Falling back to Torch optimizers.
+(vLLMHttpServer pid=3966775)   warnings.warn( [repeated 3x across cluster]
+(vLLMHttpServer pid=3966775) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/optimizer/optimizer.py:28: UserWarning: Transformer Engine and Apex are not installed. Falling back to local implementations of multi_tensor_applier and multi_tensor_scale
+(vLLMHttpServer pid=3966775) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/megatron/core/optimizer/clip_grads.py:29: UserWarning: Transformer Engine and Apex are not installed. Falling back to local implementations of multi_tensor_applier, multi_tensor_l2norm, and multi_tensor_scale
+(vLLMHttpServer pid=3966775) /data/home_beta/mshahidul/readctrl/code/RL_model/verl/verl_train/verl/utils/tokenizer.py:109: UserWarning: Failed to create processor: Unsupported processor type: Qwen2TokenizerFast. This may affect multimodal processing
+(vLLMHttpServer pid=3966775)   warnings.warn(f"Failed to create processor: {e}. This may affect multimodal processing", stacklevel=1)
+(vLLMHttpServer pid=3966775) WARNING:2026-02-15 11:43:43,531:agent loop only support torch and npu profiler, got None
+(vLLMHttpServer pid=3966775) INFO:2026-02-15 11:43:43,532:vLLMHttpServer, replica_rank: 1, node_rank: 0, CUDA_VISIBLE_DEVICES: 3, master_address: 172.16.34.29, master_port: 33623, data_parallel_rpc_port: 39495, data_parallel_master_port: 40535
+(vLLMHttpServer pid=3966775) INFO:2026-02-15 11:43:43,551:override_generation_config: {'temperature': 1.0, 'top_k': -1, 'top_p': 1, 'repetition_penalty': 1.0, 'max_new_tokens': 2048}
+(vLLMHttpServer pid=3966775) INFO:2026-02-15 11:43:43,551:enable_sleep_mode: True
+(vLLMHttpServer pid=3966776) WARNING 02-15 11:44:06 [__init__.py:3036] We must use the `spawn` multiprocessing start method. Overriding VLLM_WORKER_MULTIPROC_METHOD to 'spawn'. See https://docs.vllm.ai/en/latest/usage/troubleshooting.html#python-multiprocessing for more information. Reasons: In a Ray actor and can only be spawned; CUDA is initialized
+(vLLMHttpServer pid=3966776) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/torch/cuda/__init__.py:63: FutureWarning: The pynvml package is deprecated. Please install nvidia-ml-py instead. If you did not install pynvml directly, please report this to the maintainers of the package that installed pynvml for you.
+(vLLMHttpServer pid=3966776)   import pynvml  # type: ignore[import]
+(vLLMHttpServer pid=3966776) Skipping import of cpp extensions due to incompatible torch version 2.8.0+cu128 for torchao version 0.16.0             Please see https://github.com/pytorch/ao/issues/2919 for more info
+(vLLMHttpServer pid=3966775) `torch_dtype` is deprecated! Use `dtype` instead!
+(vLLMHttpServer pid=3966775) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/torch/cuda/__init__.py:63: FutureWarning: The pynvml package is deprecated. Please install nvidia-ml-py instead. If you did not install pynvml directly, please report this to the maintainers of the package that installed pynvml for you.
+(vLLMHttpServer pid=3966775)   import pynvml  # type: ignore[import]
+(vLLMHttpServer pid=3966776) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/torch/cuda/__init__.py:63: FutureWarning: The pynvml package is deprecated. Please install nvidia-ml-py instead. If you did not install pynvml directly, please report this to the maintainers of the package that installed pynvml for you.
+(vLLMHttpServer pid=3966776)   import pynvml  # type: ignore[import]
+(vLLMHttpServer pid=3966775) Skipping import of cpp extensions due to incompatible torch version 2.8.0+cu128 for torchao version 0.16.0             Please see https://github.com/pytorch/ao/issues/2919 for more info
+(vLLMHttpServer pid=3966776) Skipping import of cpp extensions due to incompatible torch version 2.8.0+cu128 for torchao version 0.16.0             Please see https://github.com/pytorch/ao/issues/2919 for more info
+(vLLMHttpServer pid=3966775) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/torch/cuda/__init__.py:63: FutureWarning: The pynvml package is deprecated. Please install nvidia-ml-py instead. If you did not install pynvml directly, please report this to the maintainers of the package that installed pynvml for you.
+(vLLMHttpServer pid=3966775)   import pynvml  # type: ignore[import]
+(vLLMHttpServer pid=3966776) W0215 11:44:49.141000 3969326 /data/home_beta/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/torch/utils/cpp_extension.py:2425] TORCH_CUDA_ARCH_LIST is not set, all archs for visible cards are included for compilation. 
+(vLLMHttpServer pid=3966776) W0215 11:44:49.141000 3969326 /data/home_beta/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/torch/utils/cpp_extension.py:2425] If this is not desired, please set os.environ['TORCH_CUDA_ARCH_LIST'] to specific architectures.
+(vLLMHttpServer pid=3966775) Skipping import of cpp extensions due to incompatible torch version 2.8.0+cu128 for torchao version 0.16.0             Please see https://github.com/pytorch/ao/issues/2919 for more info
+(vLLMHttpServer pid=3966776) [Gloo] Rank 0 is connected to 0 peer ranks. Expected number of connected peer ranks is : 0
+(vLLMHttpServer pid=3966776) [Gloo] Rank 0 is connected to 0 peer ranks. Expected number of connected peer ranks is : 0
+(vLLMHttpServer pid=3966776) [Gloo] Rank 0 is connected to 0 peer ranks. Expected number of connected peer ranks is : 0
+(vLLMHttpServer pid=3966776) [Gloo] Rank 0 is connected to 0 peer ranks. Expected number of connected peer ranks is : 0
+(vLLMHttpServer pid=3966776) [Gloo] Rank 0 is connected to 0 peer ranks. Expected number of connected peer ranks is : 0
+(vLLMHttpServer pid=3966776) [Gloo] Rank 0 is connected to 0 peer ranks. Expected number of connected peer ranks is : 0
+(vLLMHttpServer pid=3966775) WARNING 02-15 11:44:07 [__init__.py:3036] We must use the `spawn` multiprocessing start method. Overriding VLLM_WORKER_MULTIPROC_METHOD to 'spawn'. See https://docs.vllm.ai/en/latest/usage/troubleshooting.html#python-multiprocessing for more information. Reasons: In a Ray actor and can only be spawned; CUDA is initialized
+(vLLMHttpServer pid=3966775) (Worker pid=3969317) WARNING 02-15 11:45:07 [cudagraph_dispatcher.py:106] cudagraph dispatching keys are not initialized. No cudagraph will be used.
+(vLLMHttpServer pid=3966775) [Gloo] Rank 0 is connected to 0 peer ranks. Expected number of connected peer ranks is : 0 [repeated 6x across cluster]
+(vLLMHttpServer pid=3966775) WARNING 02-15 11:45:08 [model.py:1389] Default sampling parameters have been overridden by the model's Hugging Face generation config recommended from the model creator. If this is not intended, please relaunch vLLM instance with `--generation-config vllm`.
+(vLLMHttpServer pid=3966776) INFO:2026-02-15 11:45:09,317:Initializing a V1 LLM engine with config: model='Qwen/Qwen3-4B-Instruct-2507', speculative_config=None, tokenizer='Qwen/Qwen3-4B-Instruct-2507', skip_tokenizer_init=False, tokenizer_mode=auto, revision=None, tokenizer_revision=None, trust_remote_code=False, dtype=torch.bfloat16, max_seq_len=8192, download_dir=None, load_format=dummy, tensor_parallel_size=1, pipeline_parallel_size=1, data_parallel_size=1, disable_custom_all_reduce=False, quantization=None, enforce_eager=True, kv_cache_dtype=auto, device_config=cuda, structured_outputs_config=StructuredOutputsConfig(backend='auto', disable_fallback=False, disable_any_whitespace=False, disable_additional_properties=False, reasoning_parser=''), observability_config=ObservabilityConfig(show_hidden_metrics_for_version=None, otlp_traces_endpoint=None, collect_detailed_traces=None), seed=0, served_model_name=Qwen/Qwen3-4B-Instruct-2507, enable_prefix_caching=True, chunked_prefill_enabled=True, pooler_config=None, compilation_config={"level":0,"debug_dump_path":"","cache_dir":"","backend":"","custom_ops":[],"splitting_ops":null,"use_inductor":true,"compile_sizes":[],"inductor_compile_config":{"enable_auto_functionalized_v2":false},"inductor_passes":{},"cudagraph_mode":0,"use_cudagraph":true,"cudagraph_num_of_warmups":0,"cudagraph_capture_sizes":[],"cudagraph_copy_inputs":false,"full_cuda_graph":false,"use_inductor_graph_partition":false,"pass_config":{},"max_capture_size":0,"local_cache_dir":null}
+(vLLMHttpServer pid=3966775) W0215 11:44:49.098000 3969317 /data/home_beta/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/torch/utils/cpp_extension.py:2425] TORCH_CUDA_ARCH_LIST is not set, all archs for visible cards are included for compilation. 
+(vLLMHttpServer pid=3966775) W0215 11:44:49.098000 3969317 /data/home_beta/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/torch/utils/cpp_extension.py:2425] If this is not desired, please set os.environ['TORCH_CUDA_ARCH_LIST'] to specific architectures.
+(TaskRunner pid=3962104) AgentLoopManager: ['172.16.34.29:46443', '172.16.34.29:45263']
+(pid=3970537) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/torch/cuda/__init__.py:63: FutureWarning: The pynvml package is deprecated. Please install nvidia-ml-py instead. If you did not install pynvml directly, please report this to the maintainers of the package that installed pynvml for you.
+(pid=3970537)   import pynvml  # type: ignore[import]
+(TaskRunner pid=3962104) wandb: [wandb.login()] Loaded credentials for https://api.wandb.ai from /home/mshahidul/.netrc.
+(TaskRunner pid=3962104) wandb: Currently logged in as: shahidulshakib034 (shahidulshakib034-khulna-university-of-engineering-techn) to https://api.wandb.ai. Use `wandb login --relogin` to force relogin
+(TaskRunner pid=3962104) wandb: Tracking run with wandb version 0.24.1
+(TaskRunner pid=3962104) wandb: Run data is saved locally in /data/home_beta/mshahidul/readctrl/code/RL_model/verl/verl_train/wandb/run-20260215_114517-4c5nwk6l
+(TaskRunner pid=3962104) wandb: Run `wandb offline` to turn off syncing.
+(TaskRunner pid=3962104) wandb: Syncing run qwen3-4b-instruct-en
+(TaskRunner pid=3962104) wandb: ⭐️ View project at https://wandb.ai/shahidulshakib034-khulna-university-of-engineering-techn/readctrl-verl
+(TaskRunner pid=3962104) wandb: 🚀 View run at https://wandb.ai/shahidulshakib034-khulna-university-of-engineering-techn/readctrl-verl/runs/4c5nwk6l
+(pid=3970538) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/torch/cuda/__init__.py:63: FutureWarning: The pynvml package is deprecated. Please install nvidia-ml-py instead. If you did not install pynvml directly, please report this to the maintainers of the package that installed pynvml for you. [repeated 7x across cluster]
+(pid=3970538)   import pynvml  # type: ignore[import] [repeated 7x across cluster]
+(TaskRunner pid=3962104) Checkpoint tracker file does not exist: /home/mshahidul/readctrl/code/RL_model/models/RL_model_subclaim_classifier_v2/latest_checkpointed_iteration.txt
+(TaskRunner pid=3962104) Training from scratch
+(vLLMHttpServer pid=3966776) (Worker pid=3969326) WARNING 02-15 11:45:07 [cudagraph_dispatcher.py:106] cudagraph dispatching keys are not initialized. No cudagraph will be used.
+(vLLMHttpServer pid=3966776) WARNING 02-15 11:45:09 [model.py:1389] Default sampling parameters have been overridden by the model's Hugging Face generation config recommended from the model creator. If this is not intended, please relaunch vLLM instance with `--generation-config vllm`.
+(TaskRunner pid=3962104) wandb: Detected [dspy, litellm, openai] in use.
+(TaskRunner pid=3962104) wandb: Use W&B Weave for improved LLM call tracing. Install Weave with `pip install weave` then add `import weave` to the top of your script.
+(TaskRunner pid=3962104) wandb: For more information, check out the docs at: https://weave-docs.wandb.ai/
+(pid=3970536) WARNING:2026-02-15 11:45:25,689:Skipping import of cpp extensions due to incompatible torch version 2.8.0+cu128 for torchao version 0.16.0             Please see https://github.com/pytorch/ao/issues/2919 for more info
+(WorkerDict pid=3964117) WARNING 02-15 11:45:29 [api_server.py:1213] LoRA dynamic loading & unloading is enabled in the API server. This should ONLY be used for local development!
+(WorkerDict pid=3964116) INFO:2026-02-15 11:45:36,122:update_weights done, time cost: 3.68s
+(pid=3970543) WARNING:2026-02-15 11:45:26,090:Skipping import of cpp extensions due to incompatible torch version 2.8.0+cu128 for torchao version 0.16.0             Please see https://github.com/pytorch/ao/issues/2919 for more info [repeated 7x across cluster]
+(TaskRunner pid=3962104) test_gen_batch meta info: {'eos_token_id': 151645, 'pad_token_id': 151643, 'recompute_log_prob': False, 'do_sample': False, 'validate': True, 'global_steps': 0}
+(WorkerDict pid=3964116) WARNING 02-15 11:45:29 [api_server.py:1213] LoRA dynamic loading & unloading is enabled in the API server. This should ONLY be used for local development!
+(AgentLoopWorker pid=3970537) WARNING 02-15 11:45:43 [api_server.py:1213] LoRA dynamic loading & unloading is enabled in the API server. This should ONLY be used for local development!
+(AgentLoopWorker pid=3970536) Using dataset class: RLHFDataset
+(AgentLoopWorker pid=3970536) /data/home_beta/mshahidul/readctrl/code/RL_model/verl/verl_train/verl/utils/tokenizer.py:109: UserWarning: Failed to create processor: Unsupported processor type: Qwen2TokenizerFast. This may affect multimodal processing
+(AgentLoopWorker pid=3970536)   warnings.warn(f"Failed to create processor: {e}. This may affect multimodal processing", stacklevel=1)
+(pid=3972245) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/torch/cuda/__init__.py:63: FutureWarning: The pynvml package is deprecated. Please install nvidia-ml-py instead. If you did not install pynvml directly, please report this to the maintainers of the package that installed pynvml for you.
+(pid=3972245)   import pynvml  # type: ignore[import]
+(AgentLoopWorker pid=3970544) /data/home_beta/mshahidul/readctrl/code/RL_model/verl/verl_train/verl/utils/tokenizer.py:109: UserWarning: Failed to create processor: Unsupported processor type: Qwen2TokenizerFast. This may affect multimodal processing [repeated 7x across cluster]
+(AgentLoopWorker pid=3970544)   warnings.warn(f"Failed to create processor: {e}. This may affect multimodal processing", stacklevel=1) [repeated 7x across cluster]
+(AgentLoopWorker pid=3970537) You're using a Qwen2TokenizerFast tokenizer. Please note that with a fast tokenizer, using the `__call__` method is faster than using a method to encode the text followed by a call to the `pad` method to get a padded encoding.
+(pid=3972384) WARNING:2026-02-15 11:46:02,441:Skipping import of cpp extensions due to incompatible torch version 2.8.0+cu128 for torchao version 0.16.0             Please see https://github.com/pytorch/ao/issues/2919 for more info
+(pid=3973057) /home/mshahidul/miniconda3/envs/verl2/lib/python3.12/site-packages/torch/cuda/__init__.py:63: FutureWarning: The pynvml package is deprecated. Please install nvidia-ml-py instead. If you did not install pynvml directly, please report this to the maintainers of the package that installed pynvml for you. [repeated 7x across cluster]
+(pid=3973057)   import pynvml  # type: ignore[import] [repeated 7x across cluster]
+(AgentLoopWorker pid=3970542) You're using a Qwen2TokenizerFast tokenizer. Please note that with a fast tokenizer, using the `__call__` method is faster than using a method to encode the text followed by a call to the `pad` method to get a padded encoding. [repeated 7x across cluster]
+(RewardLoopWorker pid=3972390) 2026/02/15 11:46:23 WARNING dspy.primitives.base_module: There is a mismatch of python version between saved model and current environment. You saved with `python==3.11`, but now you have `python==3.12`. This might cause errors or performance downgrade on the loaded model, please consider loading the model in the same environment as the saving environment.
+(pid=3972382) WARNING:2026-02-15 11:46:02,671:Skipping import of cpp extensions due to incompatible torch version 2.8.0+cu128 for torchao version 0.16.0             Please see https://github.com/pytorch/ao/issues/2919 for more info [repeated 7x across cluster]
+(TaskRunner pid=3962104) validation generation end
+(AgentLoopWorker pid=3970538) WARNING 02-15 11:45:43 [api_server.py:1213] LoRA dynamic loading & unloading is enabled in the API server. This should ONLY be used for local development! [repeated 7x across cluster]
+(AgentLoopWorker pid=3970538) Using dataset class: RLHFDataset [repeated 7x across cluster]
+(TaskRunner pid=3962104) ("Initial validation metrics: {'val-aux/multiclinsum/reward/mean@1': "
+(TaskRunner pid=3962104)  "np.float64(3.4781530674346195), 'val-core/multiclinsum/acc/mean@1': "
+(TaskRunner pid=3962104)  "np.float64(3.478153119035843), 'val-aux/num_turns/min': np.int32(2), "
+(TaskRunner pid=3962104)  "'val-aux/num_turns/max': np.int32(2), 'val-aux/num_turns/mean': "
+(TaskRunner pid=3962104)  'np.float64(2.0)}')
+(TaskRunner pid=3962104) step:0 - val-aux/multiclinsum/reward/mean@1:np.float64(3.4781530674346195) - val-core/multiclinsum/acc/mean@1:np.float64(3.478153119035843) - val-aux/num_turns/min:np.int32(2) - val-aux/num_turns/max:np.int32(2) - val-aux/num_turns/mean:np.float64(2.0)
+(TaskRunner pid=3962104) 
Training Progress:   0%|          | 0/45 [00:00<?, ?it/s]
+(RewardLoopWorker pid=3972106) 2026/02/15 11:46:24 WARNING dspy.primitives.base_module: There is a mismatch of python version between saved model and current environment. You saved with `python==3.11`, but now you have `python==3.12`. This might cause errors or performance downgrade on the loaded model, please consider loading the model in the same environment as the saving environment. [repeated 9x across cluster]
+(WorkerDict pid=3964116) INFO:2026-02-15 12:12:02,172:update_weights done, time cost: 2.96s
+(TaskRunner pid=3962104) step:1 - global_seqlen/min:899945 - global_seqlen/max:919128 - global_seqlen/minmax_diff:19183 - global_seqlen/balanced_min:909536 - global_seqlen/balanced_max:909537 - global_seqlen/mean:909536.5 - actor/entropy:0.34534910321235657 - perf/mfu/actor_infer:0 - actor/pg_loss:np.float64(-0.10339197964276536) - actor/kl_loss:np.float64(0.0011835203428442282) - actor/pg_clipfrac:np.float64(0.0028789117520015375) - actor/ppo_kl:np.float64(0.0001356433592339575) - actor/pg_clipfrac_lower:np.float64(0.0) - actor/kl_coef:np.float64(0.0010000000000000002) - actor/grad_norm:np.float64(1.1960541307926178) - perf/mfu/actor:np.float64(0.19971093078503355) - perf/max_memory_allocated_gb:np.float64(66.78047037124634) - perf/max_memory_reserved_gb:np.float64(77.423828125) - perf/cpu_memory_used_gb:np.float64(476.3611145019531) - actor/lr:np.float64(1e-06) - training/global_step:1 - training/epoch:0 - critic/score/mean:3.5000221729278564 - critic/score/max:5.099999904632568 - critic/score/min:-1.0 - critic/rewards/mean:3.5000221729278564 - critic/rewards/max:5.099999904632568 - critic/rewards/min:-1.0 - critic/advantages/mean:0.05790890008211136 - critic/advantages/max:1.1547001600265503 - critic/advantages/min:-1.1547001600265503 - critic/returns/mean:0.05790890008211136 - critic/returns/max:1.1547001600265503 - critic/returns/min:-1.1547001600265503 - response_length/mean:341.9505310058594 - response_length/max:970.0 - response_length/min:55.0 - response_length/clip_ratio:0.0 - response_length_non_aborted/mean:341.9505310058594 - response_length_non_aborted/max:970.0 - response_length_non_aborted/min:55.0 - response_length_non_aborted/clip_ratio:0.0 - response/aborted_ratio:0.0 - prompt_length/mean:842.341796875 - prompt_length/max:1019.0 - prompt_length/min:500.0 - prompt_length/clip_ratio:0.0 - num_turns/min:np.int32(2) - num_turns/max:np.int32(2) - num_turns/mean:np.float64(2.0) - timing_s/start_profile:0.00044062361121177673 - timing_s/agent_loop/num_preempted/min:np.int64(-1) - timing_s/agent_loop/num_preempted/max:np.int64(-1) - timing_s/agent_loop/num_preempted/mean:np.float64(-1.0) - timing_s/agent_loop/generate_sequences/min:np.float64(9.097739532589912) - timing_s/agent_loop/generate_sequences/max:np.float64(104.11848605237901) - timing_s/agent_loop/generate_sequences/mean:np.float64(54.07818155001102) - timing_s/agent_loop/tool_calls/min:np.float64(0.0) - timing_s/agent_loop/tool_calls/max:np.float64(0.0) - timing_s/agent_loop/tool_calls/mean:np.float64(0.0) - timing_s/agent_loop/slowest/generate_sequences:np.float64(104.11848605237901) - timing_s/agent_loop/slowest/tool_calls:np.float64(0.0) - timing_s/agent_loop/slowest/prompt_length:973 - timing_s/agent_loop/slowest/response_length:970 - timing_s/agent_loop/slowest/num_preempted:np.int64(-1) - timing_s/gen:673.8995866924524 - timing_s/reward:0.0003180820494890213 - timing_s/old_log_prob:109.59133046679199 - timing_s/ref:184.55990122258663 - timing_s/adv:0.10852232202887535 - timing_s/update_actor:490.45087252371013 - timing_s/update_weights:56.64581874012947 - timing_s/step:1516.288802890107 - timing_s/stop_profile:0.00018027983605861664 - timing_per_token_ms/adv:5.965803572966854e-05 - timing_per_token_ms/ref:0.10145821592788559 - timing_per_token_ms/update_actor:0.2696158276900983 - timing_per_token_ms/gen:1.2830415026625221 - perf/total_num_tokens:1819073 - perf/time_per_step:1516.288802890107 - perf/throughput:599.8438412698076
+(TaskRunner pid=3962104) 
Training Progress:   2%|▏         | 1/45 [25:16<18:32:27, 1516.99s/it]
+(WorkerDict pid=3964116) INFO:2026-02-15 12:36:54,968:update_weights done, time cost: 4.35s
+(TaskRunner pid=3962104) step:2 - global_seqlen/min:893024 - global_seqlen/max:916468 - global_seqlen/minmax_diff:23444 - global_seqlen/balanced_min:904744 - global_seqlen/balanced_max:904748 - global_seqlen/mean:904746.0 - actor/entropy:0.3492635488510132 - perf/mfu/actor_infer:0 - actor/pg_loss:np.float64(-0.09814488309590767) - actor/kl_loss:np.float64(0.0023834370598099968) - actor/pg_clipfrac:np.float64(0.0028065233539867527) - actor/ppo_kl:np.float64(4.57352236130267e-05) - actor/pg_clipfrac_lower:np.float64(0.0) - actor/kl_coef:np.float64(0.0010000000000000002) - actor/grad_norm:np.float64(0.5080801844596863) - perf/mfu/actor:np.float64(0.23789436566285435) - perf/max_memory_allocated_gb:np.float64(67.54758548736572) - perf/max_memory_reserved_gb:np.float64(77.423828125) - perf/cpu_memory_used_gb:np.float64(517.4131355285645) - actor/lr:np.float64(1e-06) - training/global_step:2 - training/epoch:0 - critic/score/mean:3.5093228816986084 - critic/score/max:5.099999904632568 - critic/score/min:-2.0 - critic/rewards/mean:3.5093228816986084 - critic/rewards/max:5.099999904632568 - critic/rewards/min:-2.0 - critic/advantages/mean:0.05597399175167084 - critic/advantages/max:1.1547001600265503 - critic/advantages/min:-1.1547002792358398 - critic/returns/mean:0.05597399175167084 - critic/returns/max:1.1547001600265503 - critic/returns/min:-1.1547002792358398 - response_length/mean:329.572265625 - response_length/max:918.0 - response_length/min:77.0 - response_length/clip_ratio:0.0 - response_length_non_aborted/mean:329.572265625 - response_length_non_aborted/max:918.0 - response_length_non_aborted/min:77.0 - response_length_non_aborted/clip_ratio:0.0 - response/aborted_ratio:0.0 - prompt_length/mean:848.482421875 - prompt_length/max:1023.0 - prompt_length/min:505.0 - prompt_length/clip_ratio:0.0 - num_turns/min:np.int32(2) - num_turns/max:np.int32(2) - num_turns/mean:np.float64(2.0) - timing_s/start_profile:7.303617894649506e-05 - timing_s/agent_loop/num_preempted/min:np.int64(-1) - timing_s/agent_loop/num_preempted/max:np.int64(-1) - timing_s/agent_loop/num_preempted/mean:np.float64(-1.0) - timing_s/agent_loop/generate_sequences/min:np.float64(11.372929073870182) - timing_s/agent_loop/generate_sequences/max:np.float64(98.58112917654216) - timing_s/agent_loop/generate_sequences/mean:np.float64(52.7537724532073) - timing_s/agent_loop/tool_calls/min:np.float64(0.0) - timing_s/agent_loop/tool_calls/max:np.float64(0.0) - timing_s/agent_loop/tool_calls/mean:np.float64(0.0) - timing_s/agent_loop/slowest/generate_sequences:np.float64(98.58112917654216) - timing_s/agent_loop/slowest/tool_calls:np.float64(0.0) - timing_s/agent_loop/slowest/prompt_length:1018 - timing_s/agent_loop/slowest/response_length:827 - timing_s/agent_loop/slowest/num_preempted:np.int64(-1) - timing_s/gen:872.2554338723421 - timing_s/reward:0.00017512217164039612 - timing_s/old_log_prob:94.9059272930026 - timing_s/ref:98.89165266044438 - timing_s/adv:0.13718132860958576 - timing_s/update_actor:377.2491386923939 - timing_s/update_weights:46.527518313378096 - timing_s/step:1490.8768444675952 - timing_s/stop_profile:0.0002679359167814255 - timing_per_token_ms/adv:7.58120669279476e-05 - timing_per_token_ms/ref:0.05465161087224723 - timing_per_token_ms/update_actor:0.20848345209174393 - timing_per_token_ms/gen:1.7230655933696062 - perf/total_num_tokens:1809492 - perf/time_per_step:1490.8768444675952 - perf/throughput:606.854954758582
+(TaskRunner pid=3962104) 
Training Progress:   4%|▍         | 2/45 [50:08<17:56:13, 1501.71s/it]
+(WorkerDict pid=3964116) INFO:2026-02-15 12:59:51,188:update_weights done, time cost: 1.71s
+(TaskRunner pid=3962104) step:3 - global_seqlen/min:914925 - global_seqlen/max:918963 - global_seqlen/minmax_diff:4038 - global_seqlen/balanced_min:916943 - global_seqlen/balanced_max:916945 - global_seqlen/mean:916944.0 - actor/entropy:0.35038384795188904 - perf/mfu/actor_infer:0 - actor/pg_loss:np.float64(-0.09003633188937481) - actor/kl_loss:np.float64(0.00252106093224332) - actor/pg_clipfrac:np.float64(0.002881102482206188) - actor/ppo_kl:np.float64(3.254987854954076e-05) - actor/pg_clipfrac_lower:np.float64(2.323592828664308e-06) - actor/kl_coef:np.float64(0.0010000000000000002) - actor/grad_norm:np.float64(0.569173276424408) - perf/mfu/actor:np.float64(0.24512143556972565) - perf/max_memory_allocated_gb:np.float64(67.96837854385376) - perf/max_memory_reserved_gb:np.float64(77.423828125) - perf/cpu_memory_used_gb:np.float64(517.7252655029297) - actor/lr:np.float64(1e-06) - training/global_step:3 - training/epoch:0 - critic/score/mean:3.566650629043579 - critic/score/max:5.099999904632568 - critic/score/min:-1.0 - critic/rewards/mean:3.566650629043579 - critic/rewards/max:5.099999904632568 - critic/rewards/min:-1.0 - critic/advantages/mean:0.04765870422124863 - critic/advantages/max:1.1547001600265503 - critic/advantages/min:-1.1547002792358398 - critic/returns/mean:0.04765870422124863 - critic/returns/max:1.1547001600265503 - critic/returns/min:-1.1547002792358398 - response_length/mean:341.904296875 - response_length/max:928.0 - response_length/min:67.0 - response_length/clip_ratio:0.0 - response_length_non_aborted/mean:341.904296875 - response_length_non_aborted/max:928.0 - response_length_non_aborted/min:67.0 - response_length_non_aborted/clip_ratio:0.0 - response/aborted_ratio:0.0 - prompt_length/mean:852.033203125 - prompt_length/max:1024.0 - prompt_length/min:499.0 - prompt_length/clip_ratio:0.0078125 - num_turns/min:np.int32(2) - num_turns/max:np.int32(2) - num_turns/mean:np.float64(2.0) - timing_s/start_profile:6.322748959064484e-05 - timing_s/agent_loop/num_preempted/min:np.int64(-1) - timing_s/agent_loop/num_preempted/max:np.int64(-1) - timing_s/agent_loop/num_preempted/mean:np.float64(-1.0) - timing_s/agent_loop/generate_sequences/min:np.float64(11.217221273109317) - timing_s/agent_loop/generate_sequences/max:np.float64(101.84276429563761) - timing_s/agent_loop/generate_sequences/mean:np.float64(56.15208510348263) - timing_s/agent_loop/tool_calls/min:np.float64(0.0) - timing_s/agent_loop/tool_calls/max:np.float64(0.0) - timing_s/agent_loop/tool_calls/mean:np.float64(0.0) - timing_s/agent_loop/slowest/generate_sequences:np.float64(101.84276429563761) - timing_s/agent_loop/slowest/tool_calls:np.float64(0.0) - timing_s/agent_loop/slowest/prompt_length:1024 - timing_s/agent_loop/slowest/response_length:917 - timing_s/agent_loop/slowest/num_preempted:np.int64(-1) - timing_s/gen:762.453033618629 - timing_s/reward:0.0002170894294977188 - timing_s/old_log_prob:94.50050543434918 - timing_s/ref:101.3777069374919 - timing_s/adv:0.1310154665261507 - timing_s/update_actor:371.72294335253537 - timing_s/update_weights:46.41428390331566 - timing_s/step:1377.5106320641935 - timing_s/stop_profile:0.00017286837100982666 - timing_per_token_ms/adv:7.1441367480539e-05 - timing_per_token_ms/ref:0.0552802062816769 - timing_per_token_ms/update_actor:0.2026966441530428 - timing_per_token_ms/gen:1.45183520154357 - perf/total_num_tokens:1833888 - perf/time_per_step:1377.5106320641935 - perf/throughput:665.652938464775
+(TaskRunner pid=3962104) 
Training Progress:   7%|▋         | 3/45 [1:13:05<16:51:32, 1445.06s/it]
diff --git a/code/RL_model/verl/verl_train/qwen3-4b-instruct-optimized-multiclinsum-gs.log b/code/RL_model/verl/verl_train/qwen3-4b-instruct-optimized-multiclinsum-gs.log
new file mode 100644
index 0000000000000000000000000000000000000000..e69de29bb2d1d6434b8b29ae775ad8c2e48c5391
diff --git a/code/RL_model/verl/verl_train/qwen3-4b-instruct-optimized.log b/code/RL_model/verl/verl_train/qwen3-4b-instruct-optimized.log
new file mode 100644
index 0000000000000000000000000000000000000000..7b6fe7830cc9edc8929306492cdb8dd53988ff62
--- /dev/null
+++ b/code/RL_model/verl/verl_train/qwen3-4b-instruct-optimized.log
@@ -0,0 +1,20 @@
+/home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/torch/cuda/__init__.py:63: FutureWarning: The pynvml package is deprecated. Please install nvidia-ml-py instead. If you did not install pynvml directly, please report this to the maintainers of the package that installed pynvml for you.
+  import pynvml  # type: ignore[import]
+INFO 02-01 15:58:43 [__init__.py:216] Automatically detected platform cuda.
+/home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/megatron/core/models/backends.py:21: UserWarning: Apex is not installed. Falling back to Torch Norm
+  warnings.warn("Apex is not installed. Falling back to Torch Norm")
+/home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/megatron/core/optimizer/__init__.py:18: UserWarning: Transformer Engine and Apex are not installed. Falling back to Torch optimizers.
+  warnings.warn(
+/home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/megatron/core/optimizer/optimizer.py:28: UserWarning: Transformer Engine and Apex are not installed. Falling back to local implementations of multi_tensor_applier and multi_tensor_scale
+  warnings.warn(
+/home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/megatron/core/optimizer/clip_grads.py:29: UserWarning: Transformer Engine and Apex are not installed. Falling back to local implementations of multi_tensor_applier, multi_tensor_l2norm, and multi_tensor_scale
+  warnings.warn(
+/home/mshahidul/miniconda3/envs/verl/lib/python3.12/site-packages/megatron/core/models/gpt/gpt_layer_specs.py:67: UserWarning: Apex is not installed. Falling back to Torch Norm
+  warnings.warn("Apex is not installed. Falling back to Torch Norm")
+Could not override 'reward_model.reward_manager.name'.
+To append to your config use +reward_model.reward_manager.name=base
+Key 'name' is not in struct
+    full_key: reward_model.reward_manager.name
+    object_type=dict
+
+Set the environment variable HYDRA_FULL_ERROR=1 for a complete stack trace.
diff --git a/code/RL_model/verl/verl_train/requirements-cuda.txt b/code/RL_model/verl/verl_train/requirements-cuda.txt
new file mode 100644
index 0000000000000000000000000000000000000000..7bfe8efeb555b9f509c7584045461076993424ce
--- /dev/null
+++ b/code/RL_model/verl/verl_train/requirements-cuda.txt
@@ -0,0 +1 @@
+flash-attn
\ No newline at end of file
diff --git a/code/RL_model/verl/verl_train/requirements-npu.txt b/code/RL_model/verl/verl_train/requirements-npu.txt
new file mode 100644
index 0000000000000000000000000000000000000000..ea197c98f318454e8309e7412f5ab5a929b9bfa3
--- /dev/null
+++ b/code/RL_model/verl/verl_train/requirements-npu.txt
@@ -0,0 +1,21 @@
+# requirements.txt records the full set of dependencies for development
+accelerate
+codetiming
+datasets
+dill
+hydra-core
+numpy<2.0.0
+pandas
+peft>=0.15.2
+pyarrow>=15.0.0
+pybind11
+pylatexenc
+tensordict>=0.8.0,<=0.10.0,!=0.9.0
+ray[default]
+wandb
+mathruler
+torchdata
+einops
+qwen_vl_utils
+hf_transfer
+triton-ascend==3.2.0rc4
\ No newline at end of file
diff --git a/code/RL_model/verl/verl_train/requirements-test.txt b/code/RL_model/verl/verl_train/requirements-test.txt
new file mode 100644
index 0000000000000000000000000000000000000000..92b4996eeb393ac21a203c8b3bc256abedaee87d
--- /dev/null
+++ b/code/RL_model/verl/verl_train/requirements-test.txt
@@ -0,0 +1,5 @@
+pytest
+pre-commit
+py-spy
+pytest-asyncio
+pytest-rerunfailures
diff --git a/code/RL_model/verl/verl_train/requirements.txt b/code/RL_model/verl/verl_train/requirements.txt
new file mode 100644
index 0000000000000000000000000000000000000000..6a051b8e458a68fd6c021f885a9ce71d7779f99c
--- /dev/null
+++ b/code/RL_model/verl/verl_train/requirements.txt
@@ -0,0 +1,26 @@
+# requirements.txt records the full set of dependencies for development
+accelerate
+codetiming
+datasets
+dill
+hydra-core
+liger-kernel
+numpy<2.0.0
+pandas
+peft
+pyarrow>=19.0.0
+pybind11
+pylatexenc
+pre-commit
+ray[default]
+tensordict>=0.8.0,<=0.10.0,!=0.9.0
+torchdata
+transformers<5.0.0
+# vllm==0.8.4
+wandb
+packaging>=20.0
+uvicorn
+fastapi
+latex2sympy2_extended
+math_verify
+tensorboard
diff --git a/code/RL_model/verl/verl_train/requirements_sglang.txt b/code/RL_model/verl/verl_train/requirements_sglang.txt
new file mode 100644
index 0000000000000000000000000000000000000000..113bca0d3e7ee9b976a854b48d271b3d27a88e81
--- /dev/null
+++ b/code/RL_model/verl/verl_train/requirements_sglang.txt
@@ -0,0 +1,21 @@
+# requirements.txt records the full set of dependencies for development
+accelerate
+codetiming
+datasets
+dill
+flash-attn
+hydra-core
+numpy<2.0.0
+pandas
+peft
+pyarrow>=19.0.0
+pybind11
+pylatexenc
+ray[default]>=2.10
+tensordict>=0.8.0,<=0.10.0,!=0.9.0
+torchdata
+torchvision
+transformers
+wandb
+sglang[all]==0.5.2
+huggingface_hub
diff --git a/code/RL_model/verl/verl_train/reward_func/rewardV3.py b/code/RL_model/verl/verl_train/reward_func/rewardV3.py
new file mode 100644
index 0000000000000000000000000000000000000000..94212b228d13cdb816b1f8e06f72d59df88b716d
--- /dev/null
+++ b/code/RL_model/verl/verl_train/reward_func/rewardV3.py
@@ -0,0 +1,237 @@
+import os
+import json
+import re
+import concurrent.futures
+import dspy
+from openai import OpenAI
+import itertools
+class MedicalClaimVerifier:
+    def __init__(self):
+        # Prefer local vLLM (OpenAI-compatible) server settings
+        self.model_name = os.getenv("VLLM_MODEL", "support_check")
+        self.base_urls = [
+            "http://172.16.34.21:8086/v1",
+            "http://172.16.34.21:8087/v1",
+            "http://172.16.34.21:8088/v1",
+            "http://172.16.34.21:8089/v1"
+        ]
+        self.url_cycle = itertools.cycle(self.base_urls)
+        api_key="EMPTY"
+        self.clients = {url: OpenAI(api_key=api_key, base_url=url) for url in self.base_urls}
+
+        self.thresholds = {
+            "low": {"comp": 1.0, "cov": 0.3226},
+            "intermediate": {"comp": 1.0, "cov": 0.4091},
+            "proficient": {"comp": 1.0, "cov": 0.9347},
+        }
+
+    def get_prompt(self,context,claim):
+        prompt = f"""
+        CONTEXT:
+        {context}
+
+        CLAIM TO VERIFY:
+        {claim}
+
+        INSTRUCTION:
+        Does the CONTEXT above provide enough evidence to support the CLAIM? 
+        - Answer 'supported' if the claim is explicitly stated or logically followable.
+        - Answer 'not_supported' if the claim is missing, contradicts the text, or requires outside info.
+
+        Output only one word: 'supported' or 'not_supported'.
+        """
+        return prompt
+
+    def check_support_api(self, prompt):
+        # Get the next available client in the round-robin
+        url = next(self.url_cycle)
+        client = self.clients[url]
+        try:
+            response = client.chat.completions.create(
+                model=self.model_name,
+                messages=[{"role": "user", "content": prompt}],
+                max_tokens=10,
+                temperature=0,     # Keep it deterministic for evaluation
+                extra_body={"guided_choice": ["supported", "not_supported"]} # If using vLLM with outlines
+            )
+            res = response.choices[0].message.content.strip().lower()
+            return 1.0 if "supported" in res and "not_supported" not in res else 0.0
+        except Exception:
+            return 0.0
+
+    def evaluate_level(self, gen_text, gold_subs, full_subs):
+        if not gen_text or not gold_subs or not full_subs:
+            return 0.0, 0.0
+        
+        # Check gold and full claims separately to avoid context length issues
+        with concurrent.futures.ThreadPoolExecutor(max_workers=32) as executor:
+            comp_results = list(
+                executor.map(
+                    self.check_support_api,
+                    [self.get_prompt(gen_text, s) for s in gold_subs],
+                )
+            )
+
+        with concurrent.futures.ThreadPoolExecutor(max_workers=32) as executor:
+            cov_results = list(
+                executor.map(
+                    self.check_support_api,
+                    [self.get_prompt(gen_text, s) for s in full_subs],
+                )
+            )
+        
+        comp_score = sum(comp_results) / len(gold_subs)
+        cov_score = sum(cov_results) / len(full_subs)
+        return comp_score, cov_score
+
+verifier = MedicalClaimVerifier()
+LITERACY_PORTS = [8034, 8035, 8036]
+LITERACY_LMS = [
+    dspy.LM(model="openai/dspy", api_base=f"http://172.16.34.21:{port}/v1", api_key="EMPTY", temperature=0.0)
+    for port in LITERACY_PORTS
+]
+literacy_lm_cycle = itertools.cycle(LITERACY_LMS)
+
+MODEL_PATH = os.environ.get(
+    "HEALTH_LITERACY_MODEL_PATH",
+    "/home/mshahidul/readctrl/code/text_classifier/"
+    "dspy_model/vllm-Meta-Llama-3.1-8B-Instruct_teacher-gpt5_v1/model.json",
+)
+
+
+# dspy.configure(lm=next(literacy_lm_cycle))
+
+
+class HealthLiteracySignature(dspy.Signature):
+    """
+    Analyze the linguistic complexity, use of medical jargon, and sentence
+    structure of 'generated_text' to determine the health literacy level.
+    """
+
+    generated_text = dspy.InputField(
+        desc="A version of the source text rewritten for a specific audience."
+    )
+    literacy_label = dspy.OutputField(
+        desc=(
+            "Classification: low_health_literacy (simple words, no jargon), "
+            "intermediate_health_literacy (moderate technicality), or "
+            "proficient_health_literacy (highly technical/original level)."
+        )
+    )
+
+
+class HealthLiteracyClassifier(dspy.Module):
+    def __init__(self):
+        super().__init__()
+        self.classifier = dspy.ChainOfThought(HealthLiteracySignature)
+
+    def forward(self, generated_text):
+        return self.classifier(generated_text=generated_text)
+
+
+_COMPILED_CLASSIFIER = None
+
+
+def _load_compiled_classifier(path):
+    if hasattr(dspy, "load"):
+        try:
+            return dspy.load(path)
+        except Exception:
+            pass
+    classifier = HealthLiteracyClassifier()
+    try:
+        classifier.load(path)
+    except Exception as exc:
+        raise RuntimeError(f"Failed to load compiled model from {path}") from exc
+    return classifier
+
+
+def _get_classifier():
+    global _COMPILED_CLASSIFIER
+    if _COMPILED_CLASSIFIER is None:
+        if not os.path.exists(MODEL_PATH):
+            raise FileNotFoundError(f"Model file not found: {MODEL_PATH}")
+        _COMPILED_CLASSIFIER = _load_compiled_classifier(MODEL_PATH)
+    return _COMPILED_CLASSIFIER
+
+def _parse_solution_json(solution_str):
+    try:
+        cleaned_str = solution_str.strip()
+        if "```json" in cleaned_str:
+            cleaned_str = cleaned_str.split("```json")[1].split("```")[0].strip()
+        elif "```" in cleaned_str:
+            cleaned_str = cleaned_str.split("```")[1].split("```")[0].strip()
+        return json.loads(cleaned_str)
+    except Exception:
+        return None
+
+
+def _get_target_level(extra_info):
+    if not extra_info:
+        return None
+    return extra_info.get("target_level")
+
+
+def _predict_label(generated_text):
+    classifier = _get_classifier()
+    
+    # 2. Pick the next GPU/LM from the pool
+    current_lm = next(literacy_lm_cycle)
+    
+    # 3. Use dspy.context to ensure THIS specific call uses the selected GPU
+    with dspy.context(lm=current_lm):
+        prediction = classifier(generated_text=generated_text)
+        
+    if not prediction or not hasattr(prediction, "literacy_label"):
+        return ""
+    # import ipdb; ipdb.set_trace()
+    return str(prediction.literacy_label).strip().lower()
+
+
+def _compute_classifier_reward(target_level, gen_text):
+    try:
+        pred_label = _predict_label(gen_text)
+    except Exception:
+        return 0.0
+    return 1.0 if target_level in pred_label else 0.0
+
+
+def compute_score(data_source, solution_str, ground_truth, extra_info=None):  
+    gold_subs = ground_truth.get('summary_subclaims', [])
+    full_subs = ground_truth.get('fulltext_subclaims', [])
+    # import ipdb; ipdb.set_trace()
+    
+    if not gold_subs or not full_subs:
+        return 0.0
+
+    data = _parse_solution_json(solution_str)
+    if not data:
+        return 0.0
+
+    target_level = _get_target_level(extra_info)
+    if not target_level:
+        return 0.0
+
+    level_map = {
+        "low_health_literacy": "low",
+        "intermediate_health_literacy": "intermediate",
+        "proficient_health_literacy": "proficient",
+    }
+    level_key = level_map.get(target_level)
+    if not level_key:
+        return 0.0
+
+    gen_text = data.get(target_level, "")
+    if not gen_text:
+        return -1.0
+
+    comp_s, cov_s = verifier.evaluate_level(gen_text, gold_subs, full_subs)
+    thresh = verifier.thresholds[level_key]
+
+    total_reward = 0.0
+    total_reward += (comp_s - thresh["comp"])
+    total_reward += (cov_s - thresh["cov"])
+
+    classifier_reward = _compute_classifier_reward(target_level, gen_text)
+    return total_reward + classifier_reward
+
diff --git a/code/RL_model/verl/verl_train/reward_func/reward_health_literacy_classifier.py b/code/RL_model/verl/verl_train/reward_func/reward_health_literacy_classifier.py
new file mode 100644
index 0000000000000000000000000000000000000000..62f1cba82187b37726653e54974bb8f39f052c36
--- /dev/null
+++ b/code/RL_model/verl/verl_train/reward_func/reward_health_literacy_classifier.py
@@ -0,0 +1,121 @@
+import json
+import os
+
+import dspy
+
+
+LLM_CPP_API_BASE = os.environ.get("LLM_CPP_API_BASE", "http://172.16.34.21:8034/v1")
+MODEL_PATH = os.environ.get(
+    "HEALTH_LITERACY_MODEL_PATH",
+    "/home/mshahidul/readctrl/code/text_classifier/"
+    "dspy_model/vllm-Meta-Llama-3.1-8B-Instruct_teacher-gpt5_v1/model.json",
+)
+
+
+llama_cpp_lm = dspy.LM(
+    model="openai/dspy",
+    api_base=LLM_CPP_API_BASE,
+    api_key="EMPTY",
+    temperature=0.0,
+)
+dspy.configure(lm=llama_cpp_lm)
+
+
+class HealthLiteracySignature(dspy.Signature):
+    """
+    Analyze the linguistic complexity, use of medical jargon, and sentence
+    structure of 'generated_text' to determine the health literacy level.
+    """
+
+    generated_text = dspy.InputField(
+        desc="A version of the source text rewritten for a specific audience."
+    )
+    literacy_label = dspy.OutputField(
+        desc=(
+            "Classification: low_health_literacy (simple words, no jargon), "
+            "intermediate_health_literacy (moderate technicality), or "
+            "proficient_health_literacy (highly technical/original level)."
+        )
+    )
+
+
+class HealthLiteracyClassifier(dspy.Module):
+    def __init__(self):
+        super().__init__()
+        self.classifier = dspy.ChainOfThought(HealthLiteracySignature)
+
+    def forward(self, generated_text):
+        return self.classifier(generated_text=generated_text)
+
+
+_COMPILED_CLASSIFIER = None
+
+
+def _load_compiled_classifier(path):
+    if hasattr(dspy, "load"):
+        try:
+            return dspy.load(path)
+        except Exception:
+            pass
+    classifier = HealthLiteracyClassifier()
+    try:
+        classifier.load(path)
+    except Exception as exc:
+        raise RuntimeError(f"Failed to load compiled model from {path}") from exc
+    return classifier
+
+
+def _get_classifier():
+    global _COMPILED_CLASSIFIER
+    if _COMPILED_CLASSIFIER is None:
+        if not os.path.exists(MODEL_PATH):
+            raise FileNotFoundError(f"Model file not found: {MODEL_PATH}")
+        _COMPILED_CLASSIFIER = _load_compiled_classifier(MODEL_PATH)
+    return _COMPILED_CLASSIFIER
+
+
+def _parse_solution_json(solution_str):
+    try:
+        cleaned_str = solution_str.strip()
+        if "```json" in cleaned_str:
+            cleaned_str = cleaned_str.split("```json")[1].split("```")[0].strip()
+        elif "```" in cleaned_str:
+            cleaned_str = cleaned_str.split("```")[1].split("```")[0].strip()
+        return json.loads(cleaned_str)
+    except Exception:
+        return None
+
+
+def _get_target_level(extra_info):
+    if not extra_info:
+        return None
+    return extra_info.get("target_level")
+
+
+def _predict_label(generated_text):
+    classifier = _get_classifier()
+    prediction = classifier(generated_text=generated_text)
+    if not prediction or not hasattr(prediction, "literacy_label"):
+        return ""
+    return str(prediction.literacy_label).strip().lower()
+
+
+def compute_score(data_source, solution_str, ground_truth, extra_info=None):
+    data = _parse_solution_json(solution_str)
+    if not data:
+        return 0.0
+
+    target_level = _get_target_level(extra_info)
+    if not target_level:
+        return 0.0
+
+    gen_text = data.get(target_level, "")
+    if not gen_text:
+        return -1.0
+
+    try:
+        pred_label = _predict_label(gen_text)
+    except Exception:
+        return 0.0
+
+    return 1.0 if target_level in pred_label else 0.0
diff --git a/code/RL_model/verl/verl_train/reward_func/reward_mock_test.py b/code/RL_model/verl/verl_train/reward_func/reward_mock_test.py
new file mode 100644
index 0000000000000000000000000000000000000000..99e1ba9620a9b7c448452f203d19ce39efa7686d
--- /dev/null
+++ b/code/RL_model/verl/verl_train/reward_func/reward_mock_test.py
@@ -0,0 +1,313 @@
+import os
+import json
+import re
+import concurrent.futures
+import dspy
+from openai import OpenAI
+
+class MedicalClaimVerifier:
+    def __init__(self):
+        # Prefer local vLLM (OpenAI-compatible) server settings
+        self.model_name = os.getenv("VLLM_MODEL", "support_check")
+        base_url = os.getenv("VLLM_BASE_URL", "http://172.16.34.21:8086/v1")
+        api_key = os.getenv("VLLM_API_KEY", "")
+        if not api_key:
+            api_file = "/home/mshahidul/api_new.json"
+            try:
+                with open(api_file, "r") as f:
+                    api_keys = json.load(f)
+                api_key = api_keys.get("openai", "")
+            except Exception:
+                api_key = "EMPTY"
+        self.client = OpenAI(api_key=api_key, base_url=base_url)
+
+        self.thresholds = {
+                "low": {"comp": 1.0, "cov": 0.3226, "max_cov": 0.45},          # Simple, concise
+                "intermediate": {"comp": 1.0, "cov": 0.4091, "max_cov": 0.65}, # Balanced
+                "proficient": {"comp": 1.0, "cov": 0.9347, "max_cov": 1.0},    # High detail
+            }
+
+    def get_prompt(self,context,claim):
+        prompt = f"""
+        CONTEXT:
+        {context}
+
+        CLAIM TO VERIFY:
+        {claim}
+
+        INSTRUCTION:
+        Does the CONTEXT above provide enough evidence to support the CLAIM? 
+        - Answer 'supported' if the claim is explicitly stated or logically followable.
+        - Answer 'not_supported' if the claim is missing, contradicts the text, or requires outside info.
+
+        Output only one word: 'supported' or 'not_supported'.
+        """
+        return prompt
+
+    def check_support_api(self, prompt):
+        try:
+            response = self.client.chat.completions.create(
+                model=self.model_name,
+                messages=[{"role": "user", "content": prompt}],
+            )
+            res = response.choices[0].message.content.strip().lower()
+            return 1.0 if "supported" in res and "not_supported" not in res else 0.0
+        except Exception:
+            return 0.0
+
+    def evaluate_level(self, gen_text, gold_subs, full_subs):
+        if not gen_text or not gold_subs or not full_subs:
+            return 0.0, 0.0
+        
+        # Check gold and full claims separately to avoid context length issues
+        with concurrent.futures.ThreadPoolExecutor(max_workers=10) as executor:
+            comp_results = list(
+                executor.map(
+                    self.check_support_api,
+                    [self.get_prompt(gen_text, s) for s in gold_subs],
+                )
+            )
+
+        with concurrent.futures.ThreadPoolExecutor(max_workers=10) as executor:
+            cov_results = list(
+                executor.map(
+                    self.check_support_api,
+                    [self.get_prompt(gen_text, s) for s in full_subs],
+                )
+            )
+        
+        comp_score = sum(comp_results) / len(gold_subs)
+        cov_score = sum(cov_results) / len(full_subs)
+        return comp_score, cov_score
+
+verifier = MedicalClaimVerifier()
+
+LLM_CPP_API_BASE = os.environ.get("LLM_CPP_API_BASE", "http://172.16.34.21:8034/v1")
+MODEL_PATH = os.environ.get(
+    "HEALTH_LITERACY_MODEL_PATH",
+    "/home/mshahidul/readctrl/code/text_classifier/"
+    "dspy_model/vllm-Meta-Llama-3.1-8B-Instruct_teacher-gpt5_v1/model.json",
+)
+
+llama_cpp_lm = dspy.LM(
+    model="openai/dspy",
+    api_base=LLM_CPP_API_BASE,
+    api_key="EMPTY",
+    temperature=0.0,
+)
+dspy.configure(lm=llama_cpp_lm)
+
+
+class HealthLiteracySignature(dspy.Signature):
+    """
+    Analyze the linguistic complexity, use of medical jargon, and sentence
+    structure of 'generated_text' to determine the health literacy level.
+    """
+
+    generated_text = dspy.InputField(
+        desc="A version of the source text rewritten for a specific audience."
+    )
+    literacy_label = dspy.OutputField(
+        desc=(
+            "Classification: low_health_literacy (simple words, no jargon), "
+            "intermediate_health_literacy (moderate technicality), or "
+            "proficient_health_literacy (highly technical/original level)."
+        )
+    )
+
+
+class HealthLiteracyClassifier(dspy.Module):
+    def __init__(self):
+        super().__init__()
+        self.classifier = dspy.ChainOfThought(HealthLiteracySignature)
+
+    def forward(self, generated_text):
+        return self.classifier(generated_text=generated_text)
+
+
+_COMPILED_CLASSIFIER = None
+
+
+def _load_compiled_classifier(path):
+    if hasattr(dspy, "load"):
+        try:
+            return dspy.load(path)
+        except Exception:
+            pass
+    classifier = HealthLiteracyClassifier()
+    try:
+        classifier.load(path)
+    except Exception as exc:
+        raise RuntimeError(f"Failed to load compiled model from {path}") from exc
+    return classifier
+
+
+def _get_classifier():
+    global _COMPILED_CLASSIFIER
+    if _COMPILED_CLASSIFIER is None:
+        if not os.path.exists(MODEL_PATH):
+            raise FileNotFoundError(f"Model file not found: {MODEL_PATH}")
+        _COMPILED_CLASSIFIER = _load_compiled_classifier(MODEL_PATH)
+    return _COMPILED_CLASSIFIER
+
+def _parse_solution_json(solution_str):
+    try:
+        cleaned_str = solution_str.strip()
+        if "```json" in cleaned_str:
+            cleaned_str = cleaned_str.split("```json")[1].split("```")[0].strip()
+        elif "```" in cleaned_str:
+            cleaned_str = cleaned_str.split("```")[1].split("```")[0].strip()
+        return json.loads(cleaned_str)
+    except Exception:
+        return None
+
+
+def _get_target_level(extra_info):
+    if not extra_info:
+        return None
+    return extra_info.get("target_level")
+
+
+def _predict_label(generated_text):
+    classifier = _get_classifier()
+    prediction = classifier(generated_text=generated_text)
+    if not prediction or not hasattr(prediction, "literacy_label"):
+        return ""
+    return str(prediction.literacy_label).strip().lower()
+
+
+def _compute_classifier_reward(target_level, gen_text):
+    try:
+        pred_label = _predict_label(gen_text)
+    except Exception:
+        return 0.0
+    return 1.0 if target_level in pred_label else 0.0
+
+
+def compute_score(data_source, solution_str, ground_truth, extra_info=None):  
+    gold_subs = ground_truth.get('summary_subclaims', [])
+    full_subs = ground_truth.get('fulltext_subclaims', [])
+    
+    if not gold_subs or not full_subs:
+        return 0.0
+
+    data = _parse_solution_json(solution_str)
+    if not data:
+        return 0.0
+
+    target_level = _get_target_level(extra_info)
+    if not target_level:
+        return 0.0
+
+    level_map = {
+        "low_health_literacy": "low",
+        "intermediate_health_literacy": "intermediate",
+        "proficient_health_literacy": "proficient",
+    }
+    level_key = level_map.get(target_level)
+    if not level_key:
+        return 0.0
+
+    gen_text = data.get(target_level, "")
+    if not gen_text:
+        return -1.0
+
+    comp_s, cov_s = verifier.evaluate_level(gen_text, gold_subs, full_subs)
+    thresh = verifier.thresholds[level_key]
+
+    # --- REWARD CALCULATION ---
+    total_reward = 0.0
+
+    # 1. Completeness: Usually, 1.0 is the goal. 
+    # We penalize if it's less than 1.0.
+    total_reward += (comp_s - thresh["comp"]) 
+
+    # 2. Coverage with Range Control (Anti-Hacking)
+    # If cov_s is below threshold, negative reward.
+    # If cov_s is between thresh and max, positive reward.
+    # If cov_s exceeds max, we cap the reward to prevent "word salad" hacking.
+    
+    effective_cov = min(cov_s, thresh["max_cov"]) 
+    total_reward += (effective_cov - thresh["cov"])
+
+    # Optional: Apply a small penalty if it drastically exceeds max_cov
+    # to discourage irrelevant info dumping.
+    if cov_s > thresh["max_cov"]:
+        total_reward -= (cov_s - thresh["max_cov"]) * 0.5 
+
+    # 3. Classifier Consistency
+    classifier_reward = _compute_classifier_reward(target_level, gen_text)
+    
+    return total_reward + classifier_reward
+
+import os
+import json
+import time
+
+def run_actual_api_test():
+    # 1. Prepare Real Medical Data
+    # A summary vs a full text about Hypertension (Lisinopril)
+    ground_truth = {
+        "summary_subclaims": [
+            "Lisinopril is used to treat high blood pressure.",
+            "It belongs to a class of drugs called ACE inhibitors.",
+            "Common side effects include a dry cough."
+        ],
+        "fulltext_subclaims": [
+            "Lisinopril is used to treat high blood pressure.",
+            "It belongs to a class of drugs called ACE inhibitors.",
+            "Common side effects include a dry cough.",
+            "It helps prevent heart attacks and strokes.",
+            "Patients should have their kidney function monitored.",
+            "Do not use if you are pregnant."
+        ]
+    }
+
+    # This is what the LLM generated for "low_health_literacy"
+    # Note: It covers the first 2 subclaims but ignores the cough and pregnancy warnings.
+    generated_response = {
+        "low_health_literacy": (
+            "This medicine is for your high blood pressure. It is a type of drug "
+            "called an ACE inhibitor. It helps your heart work better."
+        )
+    }
+    
+    solution_str = f"```json\n{json.dumps(generated_response)}\n```"
+    extra_info = {"target_level": "low_health_literacy"}
+
+    print("📡 Initializing actual API connection to 172.16.34.21...")
+    start_time = time.time()
+
+    try:
+        # 2. Execute the actual score logic
+        # This will trigger the ThreadPoolExecutor and make actual HTTP calls to your vLLM
+        score = compute_score(
+            data_source="real_api_test",
+            solution_str=solution_str,
+            ground_truth=ground_truth,
+            extra_info=extra_info
+        )
+
+        duration = time.time() - start_time
+        print(f"\n✅ API Call Successful ({round(duration, 2)}s)")
+        print("-" * 40)
+        print(f"Target Level: {extra_info['target_level']}")
+        print(f"Final Reward Score: {round(score, 4)}")
+        print("-" * 40)
+        
+        # Logic check for the user
+        print("\nDEBUG INFO:")
+        print("- Completeness: Checks if the 3 summary claims are in the 'Low' text.")
+        print("- Coverage: Checks how many of the 6 full-text claims are present.")
+        print(f"- Target Thresholds: Comp >= 1.0, Cov between 0.32 and 0.45")
+
+    except Exception as e:
+        print(f"\n❌ API Call Failed!")
+        print(f"Error Type: {type(e).__name__}")
+        print(f"Details: {str(e)}")
+        print("\nPossible fixes:")
+        print("1. Check if the vLLM server at :8086 and :8034 are running.")
+        print("2. Check if your API key in api_new.json is valid.")
+
+if __name__ == "__main__":
+    run_actual_api_test()
\ No newline at end of file
diff --git a/code/RL_model/verl/verl_train/reward_func/reward_old_1.py b/code/RL_model/verl/verl_train/reward_func/reward_old_1.py
new file mode 100644
index 0000000000000000000000000000000000000000..fce49f2754bb5ae76daca2f004222809ba957801
--- /dev/null
+++ b/code/RL_model/verl/verl_train/reward_func/reward_old_1.py
@@ -0,0 +1,141 @@
+import os
+import json
+import re
+import concurrent.futures
+from openai import OpenAI
+
+class MedicalClaimVerifier:
+    def __init__(self):
+        # Prefer local vLLM (OpenAI-compatible) server settings
+        self.model_name = os.getenv("VLLM_MODEL", "support_check")
+        base_url = os.getenv("VLLM_BASE_URL", "http://172.16.34.21:8086/v1")
+        api_key = os.getenv("VLLM_API_KEY", "")
+        if not api_key:
+            api_file = "/home/mshahidul/api_new.json"
+            try:
+                with open(api_file, "r") as f:
+                    api_keys = json.load(f)
+                api_key = api_keys.get("openai", "")
+            except Exception:
+                api_key = "EMPTY"
+        self.client = OpenAI(api_key=api_key, base_url=base_url)
+
+        self.thresholds = {
+            "low": {"comp": 1.0, "cov": 0.3226},
+            "intermediate": {"comp": 1.0, "cov": 0.4091},
+            "proficient": {"comp": 1.0, "cov": 0.9347},
+        }
+
+    def get_prompt(self,context,claim):
+        prompt = f"""
+        CONTEXT:
+        {context}
+
+        CLAIM TO VERIFY:
+        {claim}
+
+        INSTRUCTION:
+        Does the CONTEXT above provide enough evidence to support the CLAIM? 
+        - Answer 'supported' if the claim is explicitly stated or logically followable.
+        - Answer 'not_supported' if the claim is missing, contradicts the text, or requires outside info.
+
+        Output only one word: 'supported' or 'not_supported'.
+        """
+        return prompt
+
+    def check_support_api(self, prompt):
+        try:
+            response = self.client.chat.completions.create(
+                model=self.model_name,
+                messages=[{"role": "user", "content": prompt}],
+            )
+            res = response.choices[0].message.content.strip().lower()
+            return 1.0 if "supported" in res and "not_supported" not in res else 0.0
+        except Exception:
+            return 0.0
+
+    def evaluate_level(self, gen_text, gold_subs, full_subs):
+        if not gen_text or not gold_subs or not full_subs:
+            return 0.0, 0.0
+        
+        # Check gold and full claims separately to avoid context length issues
+        with concurrent.futures.ThreadPoolExecutor(max_workers=10) as executor:
+            comp_results = list(
+                executor.map(
+                    self.check_support_api,
+                    [self.get_prompt(gen_text, s) for s in gold_subs],
+                )
+            )
+
+        with concurrent.futures.ThreadPoolExecutor(max_workers=10) as executor:
+            cov_results = list(
+                executor.map(
+                    self.check_support_api,
+                    [self.get_prompt(gen_text, s) for s in full_subs],
+                )
+            )
+        
+        comp_score = sum(comp_results) / len(gold_subs)
+        cov_score = sum(cov_results) / len(full_subs)
+        return comp_score, cov_score
+
+verifier = MedicalClaimVerifier()
+
+def compute_score(data_source, solution_str, ground_truth, extra_info=None):  
+    gold_subs = ground_truth.get('summary_subclaims', [])
+    full_subs = ground_truth.get('fulltext_subclaims', [])
+    
+    if not gold_subs or not full_subs:
+        return 0.0
+
+    # 1. Parsing with fallback
+    try:
+        cleaned_str = solution_str.strip()
+        if "```json" in cleaned_str:
+            cleaned_str = cleaned_str.split("```json")[1].split("```")[0].strip()
+        elif "```" in cleaned_str:
+            cleaned_str = cleaned_str.split("```")[1].split("```")[0].strip()
+        data = json.loads(cleaned_str)
+    except Exception:
+        return -.0 
+
+    levels = ["low", "intermediate", "proficient"]
+    scores = {}
+    
+    # 2. Score Calculation
+    for lvl in levels:
+        gen_text = data.get(f"{lvl}_health_literacy", "")
+        if not gen_text:
+            scores[lvl] = {"comp": 0.0, "cov": 0.0, "missing": True}
+        else:
+            comp, cov = verifier.evaluate_level(gen_text, gold_subs, full_subs)
+            scores[lvl] = {"comp": comp, "cov": cov, "missing": False}
+
+    # 3. Reward Shaping Logic
+    total_reward = 0.0
+    
+    low_cov = scores["low"]["cov"]
+    int_cov = scores["intermediate"]["cov"]
+    pro_cov = scores["proficient"]["cov"]
+
+    # Soft Hierarchy Check: Reward progression, penalize stagnation
+    # Instead of -2.0 exit, we subtract if the order is wrong
+    hierarchy_penalty = 0.0
+    if not (low_cov <= int_cov <= pro_cov):
+        hierarchy_penalty = -2.0 
+
+    for lvl in levels:
+        if scores[lvl]["missing"]:
+            total_reward -= 1.0 # Penalty per missing field
+            continue
+
+        comp_s = scores[lvl]["comp"]
+        cov_s = scores[lvl]["cov"]
+        thresh = verifier.thresholds[lvl]
+
+        # Continuous Reward: (Actual - Threshold) 
+        # This tells the model "You're 10% away" vs "You failed"
+        total_reward += (comp_s - thresh["comp"]) 
+        total_reward += (cov_s - thresh["cov"])
+
+    return total_reward + hierarchy_penalty
\ No newline at end of file
diff --git a/code/RL_model/verl/verl_train/reward_func/reward_test.py b/code/RL_model/verl/verl_train/reward_func/reward_test.py
new file mode 100644
index 0000000000000000000000000000000000000000..a14d2e37a1972bab2160e35b42f7028d5b8b5d57
--- /dev/null
+++ b/code/RL_model/verl/verl_train/reward_func/reward_test.py
@@ -0,0 +1,181 @@
+import os
+import json
+import re
+import concurrent.futures
+from openai import OpenAI
+
+class MedicalClaimVerifier:
+    def __init__(self):
+        # Prefer local vLLM (OpenAI-compatible) server settings
+        self.model_name = os.getenv("VLLM_MODEL", "support_check")
+        base_url = os.getenv("VLLM_BASE_URL", "http://172.16.34.21:8086/v1")
+        api_key = os.getenv("VLLM_API_KEY", "")
+        if not api_key:
+            api_file = "/home/mshahidul/api_new.json"
+            try:
+                with open(api_file, "r") as f:
+                    api_keys = json.load(f)
+                api_key = api_keys.get("openai", "")
+            except Exception:
+                api_key = "EMPTY"
+        self.client = OpenAI(api_key=api_key, base_url=base_url)
+
+        self.thresholds = {
+            "low": {"comp": 1.0, "cov": 0.3226},
+            "intermediate": {"comp": 1.0, "cov": 0.4091},
+            "proficient": {"comp": 1.0, "cov": 0.9347},
+        }
+
+    def get_prompt(self,context,claim):
+        prompt = f"""
+        CONTEXT:
+        {context}
+
+        CLAIM TO VERIFY:
+        {claim}
+
+        INSTRUCTION:
+        Does the CONTEXT above provide enough evidence to support the CLAIM? 
+        - Answer 'supported' if the claim is explicitly stated or logically followable.
+        - Answer 'not_supported' if the claim is missing, contradicts the text, or requires outside info.
+
+        Output only one word: 'supported' or 'not_supported'.
+        """
+        return prompt
+
+    def check_support_api(self, prompt):
+        try:
+            response = self.client.chat.completions.create(
+                model=self.model_name,
+                messages=[{"role": "user", "content": prompt}],
+            )
+            res = response.choices[0].message.content.strip().lower()
+            return 1.0 if "supported" in res and "not_supported" not in res else 0.0
+        except Exception:
+            return 0.0
+
+    def evaluate_level(self, gen_text, gold_subs, full_subs):
+        if not gen_text or not gold_subs or not full_subs:
+            return 0.0, 0.0
+        
+        # Check gold and full claims separately to avoid context length issues
+        with concurrent.futures.ThreadPoolExecutor(max_workers=10) as executor:
+            comp_results = list(
+                executor.map(
+                    self.check_support_api,
+                    [self.get_prompt(gen_text, s) for s in gold_subs],
+                )
+            )
+
+        with concurrent.futures.ThreadPoolExecutor(max_workers=10) as executor:
+            cov_results = list(
+                executor.map(
+                    self.check_support_api,
+                    [self.get_prompt(gen_text, s) for s in full_subs],
+                )
+            )
+        
+        comp_score = sum(comp_results) / len(gold_subs)
+        cov_score = sum(cov_results) / len(full_subs)
+        return comp_score, cov_score
+
+verifier = MedicalClaimVerifier()
+
+def compute_score(data_source, solution_str, ground_truth, extra_info=None):  
+    gold_subs = ground_truth.get('summary_subclaims', [])
+    full_subs = ground_truth.get('fulltext_subclaims', [])
+    
+    if not gold_subs or not full_subs:
+        return 0.0
+
+    # 1. Parsing with fallback
+    try:
+        cleaned_str = solution_str.strip()
+        if "```json" in cleaned_str:
+            cleaned_str = cleaned_str.split("```json")[1].split("```")[0].strip()
+        elif "```" in cleaned_str:
+            cleaned_str = cleaned_str.split("```")[1].split("```")[0].strip()
+        data = json.loads(cleaned_str)
+    except Exception:
+        return -5.0 
+
+    levels = ["low", "intermediate", "proficient"]
+    scores = {}
+    
+    # 2. Score Calculation
+    for lvl in levels:
+        gen_text = data.get(f"{lvl}_health_literacy", "")
+        if not gen_text:
+            scores[lvl] = {"comp": 0.0, "cov": 0.0, "missing": True}
+        else:
+            comp, cov = verifier.evaluate_level(gen_text, gold_subs, full_subs)
+            scores[lvl] = {"comp": comp, "cov": cov, "missing": False}
+
+    # 3. Reward Shaping Logic
+    total_reward = 0.0
+    
+    low_cov = scores["low"]["cov"]
+    int_cov = scores["intermediate"]["cov"]
+    pro_cov = scores["proficient"]["cov"]
+
+    # Soft Hierarchy Check: Reward progression, penalize stagnation
+    # Instead of -2.0 exit, we subtract if the order is wrong
+    hierarchy_penalty = 0.0
+    if not (low_cov <= int_cov <= pro_cov):
+        hierarchy_penalty = -2.0 
+
+    for lvl in levels:
+        if scores[lvl]["missing"]:
+            total_reward -= 1.0 # Penalty per missing field
+            continue
+
+        comp_s = scores[lvl]["comp"]
+        cov_s = scores[lvl]["cov"]
+        thresh = verifier.thresholds[lvl]
+
+        # Continuous Reward: (Actual - Threshold) 
+        # This tells the model "You're 10% away" vs "You failed"
+        total_reward += (comp_s - thresh["comp"]) 
+        total_reward += (cov_s - thresh["cov"])
+
+    return total_reward + hierarchy_penalty
+
+def run_mock_example():
+    # 1. Setup Ground Truth Subclaims
+    # Imagine a source text about "Metformin for Type 2 Diabetes"
+    ground_truth = {
+        "summary_subclaims": [
+            "Metformin is a first-line medication for Type 2 Diabetes.",
+            "Common side effects include gastrointestinal upset.",
+            "It helps lower blood glucose levels."
+        ],
+        "fulltext_subclaims": [
+            "Metformin is a first-line medication for Type 2 Diabetes.",
+            "It works by reducing glucose production in the liver.",
+            "Common side effects include nausea and diarrhea.",
+            "Patients should take it with meals to reduce stomach issues.",
+            "It does not typically cause weight gain.",
+            "Long-term use may lead to Vitamin B12 deficiency."
+        ]
+    }
+
+    # 2. Mock Generated Solution (as if it came from the LLM)
+    # We purposefully make 'low' very basic and 'proficient' very detailed
+    solution_json = {
+        "low_health_literacy": "Metformin is used for diabetes and helps lower blood sugar.",
+        "intermediate_health_literacy": "Metformin is a first-line treatment for Type 2 Diabetes. It lowers glucose and can cause stomach upset.",
+        "proficient_health_literacy": "Metformin is the primary treatment for Type 2 Diabetes. It reduces hepatic glucose production. Side effects include gastrointestinal issues like nausea, but taking it with food helps. It is weight-neutral and may cause B12 deficiency over time."
+    }
+    solution_str = f"```json\n{json.dumps(solution_json)}\n```"
+
+    print("--- Starting Complex Evaluation ---")
+    
+    # 3. Run the Score Calculation
+    # Note: This will make 36 API calls (3 levels * (3 gold + 6 full subclaims))
+    # Ensure your vLLM server is running!
+    final_reward = compute_score("mock_source", solution_str, ground_truth)
+    
+    print(f"\nFinal Calculated Reward: {final_reward:.4f}")
+
+if __name__ == "__main__":
+    run_mock_example()
\ No newline at end of file
diff --git a/code/RL_model/verl/verl_train/reward_func/reward_v2.py b/code/RL_model/verl/verl_train/reward_func/reward_v2.py
new file mode 100644
index 0000000000000000000000000000000000000000..a9e9d9bc28c9c50abf2e0b29b84b2a0a7324383a
--- /dev/null
+++ b/code/RL_model/verl/verl_train/reward_func/reward_v2.py
@@ -0,0 +1,224 @@
+import os
+import json
+import re
+import concurrent.futures
+import dspy
+from openai import OpenAI
+
+class MedicalClaimVerifier:
+    def __init__(self):
+        # Prefer local vLLM (OpenAI-compatible) server settings
+        self.model_name = os.getenv("VLLM_MODEL", "support_check")
+        base_url = os.getenv("VLLM_BASE_URL", "http://172.16.34.21:8086/v1")
+        api_key = os.getenv("VLLM_API_KEY", "")
+        if not api_key:
+            api_file = "/home/mshahidul/api_new.json"
+            try:
+                with open(api_file, "r") as f:
+                    api_keys = json.load(f)
+                api_key = api_keys.get("openai", "")
+            except Exception:
+                api_key = "EMPTY"
+        self.client = OpenAI(api_key=api_key, base_url=base_url)
+
+        self.thresholds = {
+            "low": {"comp": 1.0, "cov": 0.3226},
+            "intermediate": {"comp": 1.0, "cov": 0.4091},
+            "proficient": {"comp": 1.0, "cov": 0.9347},
+        }
+
+    def get_prompt(self,context,claim):
+        prompt = f"""
+        CONTEXT:
+        {context}
+
+        CLAIM TO VERIFY:
+        {claim}
+
+        INSTRUCTION:
+        Does the CONTEXT above provide enough evidence to support the CLAIM? 
+        - Answer 'supported' if the claim is explicitly stated or logically followable.
+        - Answer 'not_supported' if the claim is missing, contradicts the text, or requires outside info.
+
+        Output only one word: 'supported' or 'not_supported'.
+        """
+        return prompt
+
+    def check_support_api(self, prompt):
+        try:
+            response = self.client.chat.completions.create(
+                model=self.model_name,
+                messages=[{"role": "user", "content": prompt}],
+            )
+            res = response.choices[0].message.content.strip().lower()
+            return 1.0 if "supported" in res and "not_supported" not in res else 0.0
+        except Exception:
+            return 0.0
+
+    def evaluate_level(self, gen_text, gold_subs, full_subs):
+        if not gen_text or not gold_subs or not full_subs:
+            return 0.0, 0.0
+        
+        # Check gold and full claims separately to avoid context length issues
+        with concurrent.futures.ThreadPoolExecutor(max_workers=10) as executor:
+            comp_results = list(
+                executor.map(
+                    self.check_support_api,
+                    [self.get_prompt(gen_text, s) for s in gold_subs],
+                )
+            )
+
+        with concurrent.futures.ThreadPoolExecutor(max_workers=10) as executor:
+            cov_results = list(
+                executor.map(
+                    self.check_support_api,
+                    [self.get_prompt(gen_text, s) for s in full_subs],
+                )
+            )
+        
+        comp_score = sum(comp_results) / len(gold_subs)
+        cov_score = sum(cov_results) / len(full_subs)
+        return comp_score, cov_score
+
+verifier = MedicalClaimVerifier()
+
+LLM_CPP_API_BASE = os.environ.get("LLM_CPP_API_BASE", "http://172.16.34.21:8034/v1")
+MODEL_PATH = os.environ.get(
+    "HEALTH_LITERACY_MODEL_PATH",
+    "/home/mshahidul/readctrl/code/text_classifier/"
+    "dspy_model/vllm-Meta-Llama-3.1-8B-Instruct_teacher-gpt5_v1/model.json",
+)
+
+llama_cpp_lm = dspy.LM(
+    model="openai/dspy",
+    api_base=LLM_CPP_API_BASE,
+    api_key="EMPTY",
+    temperature=0.0,
+)
+dspy.configure(lm=llama_cpp_lm)
+
+
+class HealthLiteracySignature(dspy.Signature):
+    """
+    Analyze the linguistic complexity, use of medical jargon, and sentence
+    structure of 'generated_text' to determine the health literacy level.
+    """
+
+    generated_text = dspy.InputField(
+        desc="A version of the source text rewritten for a specific audience."
+    )
+    literacy_label = dspy.OutputField(
+        desc=(
+            "Classification: low_health_literacy (simple words, no jargon), "
+            "intermediate_health_literacy (moderate technicality), or "
+            "proficient_health_literacy (highly technical/original level)."
+        )
+    )
+
+
+class HealthLiteracyClassifier(dspy.Module):
+    def __init__(self):
+        super().__init__()
+        self.classifier = dspy.ChainOfThought(HealthLiteracySignature)
+
+    def forward(self, generated_text):
+        return self.classifier(generated_text=generated_text)
+
+
+_COMPILED_CLASSIFIER = None
+
+
+def _load_compiled_classifier(path):
+    if hasattr(dspy, "load"):
+        try:
+            return dspy.load(path)
+        except Exception:
+            pass
+    classifier = HealthLiteracyClassifier()
+    try:
+        classifier.load(path)
+    except Exception as exc:
+        raise RuntimeError(f"Failed to load compiled model from {path}") from exc
+    return classifier
+
+
+def _get_classifier():
+    global _COMPILED_CLASSIFIER
+    if _COMPILED_CLASSIFIER is None:
+        if not os.path.exists(MODEL_PATH):
+            raise FileNotFoundError(f"Model file not found: {MODEL_PATH}")
+        _COMPILED_CLASSIFIER = _load_compiled_classifier(MODEL_PATH)
+    return _COMPILED_CLASSIFIER
+
+def _parse_solution_json(solution_str):
+    try:
+        cleaned_str = solution_str.strip()
+        if "```json" in cleaned_str:
+            cleaned_str = cleaned_str.split("```json")[1].split("```")[0].strip()
+        elif "```" in cleaned_str:
+            cleaned_str = cleaned_str.split("```")[1].split("```")[0].strip()
+        return json.loads(cleaned_str)
+    except Exception:
+        return None
+
+
+def _get_target_level(extra_info):
+    if not extra_info:
+        return None
+    return extra_info.get("target_level")
+
+
+def _predict_label(generated_text):
+    classifier = _get_classifier()
+    prediction = classifier(generated_text=generated_text)
+    if not prediction or not hasattr(prediction, "literacy_label"):
+        return ""
+    return str(prediction.literacy_label).strip().lower()
+
+
+def _compute_classifier_reward(target_level, gen_text):
+    try:
+        pred_label = _predict_label(gen_text)
+    except Exception:
+        return 0.0
+    return 1.0 if target_level in pred_label else 0.0
+
+
+def compute_score(data_source, solution_str, ground_truth, extra_info=None):  
+    gold_subs = ground_truth.get('summary_subclaims', [])
+    full_subs = ground_truth.get('fulltext_subclaims', [])
+    # import ipdb; ipdb.set_trace()
+    
+    if not gold_subs or not full_subs:
+        return 0.0
+
+    data = _parse_solution_json(solution_str)
+    if not data:
+        return 0.0
+
+    target_level = _get_target_level(extra_info)
+    if not target_level:
+        return 0.0
+
+    level_map = {
+        "low_health_literacy": "low",
+        "intermediate_health_literacy": "intermediate",
+        "proficient_health_literacy": "proficient",
+    }
+    level_key = level_map.get(target_level)
+    if not level_key:
+        return 0.0
+
+    gen_text = data.get(target_level, "")
+    if not gen_text:
+        return -1.0
+
+    comp_s, cov_s = verifier.evaluate_level(gen_text, gold_subs, full_subs)
+    thresh = verifier.thresholds[level_key]
+
+    total_reward = 0.0
+    total_reward += (comp_s - thresh["comp"])
+    total_reward += (cov_s - thresh["cov"])
+
+    classifier_reward = _compute_classifier_reward(target_level, gen_text)
+    return total_reward + classifier_reward
\ No newline at end of file
diff --git a/code/RL_model/verl/verl_train/script/run_qwen3-8b.sh b/code/RL_model/verl/verl_train/script/run_qwen3-8b.sh
new file mode 100644
index 0000000000000000000000000000000000000000..42668562b6e8888b25e3ba9f9c02d5079ca19f0f
--- /dev/null
+++ b/code/RL_model/verl/verl_train/script/run_qwen3-8b.sh
@@ -0,0 +1,74 @@
+# 1. Force cleanup
+pkill -9 python3
+sleep 2
+
+# 2. Set dynamic port to avoid collisions
+export MASTER_PORT=$(shuf -i 20000-65000 -n 1)
+export MASTER_ADDR=127.0.0.1
+
+# 3. Enable P2P for performance (A100s love NVLink)
+unset NCCL_P2P_DISABLE
+unset NCCL_IB_DISABLE
+
+set -x
+
+# Enable P2P for A100s to leverage NVLink speed
+export PYTORCH_CUDA_ALLOC_CONF=""
+export EXPERIMENT_NAME=qwen3-4b-instruct-optimized-multiclinsum-gs
+export WAND_PROJECT='readctrl-verl'
+export CUDA_DEVICE_ORDER="PCI_BUS_ID"
+export CUDA_VISIBLE_DEVICES=2,3 
+export VLLM_ATTENTION_BACKEND=FLASH_ATTN
+
+export NCCL_P2P_DISABLE=1
+export NCCL_IB_DISABLE=1
+# export NCCL_NET_GDR_LEVEL=2 # Enable GPUDirect RDMA
+# High-performance settings for A100
+PYTHONUNBUFFERED=1 python3 -m verl.trainer.main_ppo \
+    algorithm.adv_estimator=grpo \
+    data.train_files=/home/mshahidul/readctrl/code/RL_model/verl/verl_train/dataset/train.parquet \
+    data.val_files=/home/mshahidul/readctrl/code/RL_model/verl/verl_train/dataset/test.parquet \
+    custom_reward_function.path=/home/mshahidul/readctrl/code/RL_model/verl/verl_train/reward_func/reward.py \
+    data.train_batch_size=512 \
+    data.max_prompt_length=1024 \
+    data.max_response_length=2048 \
+    data.filter_overlong_prompts=True \
+    data.truncation='error' \
+    actor_rollout_ref.model.path=Qwen/Qwen3-4B-Instruct-2507 \
+    actor_rollout_ref.actor.optim.lr=1e-6 \
+    actor_rollout_ref.model.use_remove_padding=True \
+    actor_rollout_ref.actor.ppo_mini_batch_size=256 \
+    actor_rollout_ref.actor.ppo_micro_batch_size_per_gpu=32 \
+    actor_rollout_ref.actor.use_kl_loss=True \
+    actor_rollout_ref.actor.kl_loss_coef=0.001 \
+    actor_rollout_ref.actor.kl_loss_type=low_var_kl \
+    actor_rollout_ref.actor.entropy_coeff=0 \
+    actor_rollout_ref.model.enable_gradient_checkpointing=True \
+    actor_rollout_ref.actor.fsdp_config.param_offload=False \
+    actor_rollout_ref.actor.fsdp_config.optimizer_offload=False \
+    actor_rollout_ref.rollout.log_prob_micro_batch_size_per_gpu=32 \
+    actor_rollout_ref.rollout.tensor_model_parallel_size=1 \
+    actor_rollout_ref.rollout.name=vllm \
+    actor_rollout_ref.rollout.gpu_memory_utilization=0.6 \
+    actor_rollout_ref.rollout.max_model_len=8192 \
+    actor_rollout_ref.rollout.n=3 \
+    actor_rollout_ref.ref.log_prob_micro_batch_size_per_gpu=32 \
+    actor_rollout_ref.ref.fsdp_config.param_offload=False \
+    algorithm.use_kl_in_reward=False \
+    trainer.critic_warmup=0 \
+    trainer.logger='["console","wandb"]' \
+    trainer.project_name=$WAND_PROJECT \
+    trainer.experiment_name=$EXPERIMENT_NAME \
+    trainer.n_gpus_per_node=2 \
+    trainer.nnodes=1 \
+    trainer.save_freq=20 \
+    trainer.test_freq=5 \
+    +trainer.remove_previous_ckpt_in_save=true \
+    trainer.max_actor_ckpt_to_keep=1 \
+    trainer.max_critic_ckpt_to_keep=1 \
+    trainer.resume_mode=auto \
+    trainer.default_local_dir=/home/mshahidul/readctrl/code/RL_model/train_v2 \
+    trainer.total_epochs=15 $@ \
+    2>&1 | tee $EXPERIMENT_NAME.log
+
+# python "/home/mshahidul/readctrl/code/readability_control.py"
\ No newline at end of file
diff --git a/code/RL_model/verl/verl_train/script/run_qwen3-8b_debug.sh b/code/RL_model/verl/verl_train/script/run_qwen3-8b_debug.sh
new file mode 100644
index 0000000000000000000000000000000000000000..89dacb50711d07da78379307dc527c6540cf2e63
--- /dev/null
+++ b/code/RL_model/verl/verl_train/script/run_qwen3-8b_debug.sh
@@ -0,0 +1,75 @@
+# 1. Force cleanup
+pkill -9 python3
+sleep 2
+
+# 2. Set dynamic port to avoid collisions
+export MASTER_PORT=$(shuf -i 20000-65000 -n 1)
+export MASTER_ADDR=127.0.0.1
+
+# 3. Enable P2P for performance (A100s love NVLink)
+# unset NCCL_P2P_DISABLE
+# unset NCCL_IB_DISABLE
+
+set -x
+
+# Enable P2P for A100s to leverage NVLink speed
+export PYTORCH_CUDA_ALLOC_CONF=""
+export EXPERIMENT_NAME=qwen3-4b-instruct-optimized-multiclinsum-gs
+export WAND_PROJECT='readctrl-verl'
+export CUDA_DEVICE_ORDER="PCI_BUS_ID"
+export CUDA_VISIBLE_DEVICES=2,3 
+export VLLM_ATTENTION_BACKEND=FLASH_ATTN
+export NCCL_DEBUG=INFO
+export NCCL_DEBUG_SUBSYS=ALL
+export NCCL_P2P_DISABLE=1
+export NCCL_IB_DISABLE=1
+# export NCCL_NET_GDR_LEVEL=2 # Enable GPUDirect RDMA
+# High-performance settings for A100
+PYTHONUNBUFFERED=1 python3 -m verl.trainer.main_ppo \
+    algorithm.adv_estimator=grpo \
+    data.train_files=/home/mshahidul/readctrl/code/RL_model/verl/verl_train/dataset/train.parquet \
+    data.val_files=/home/mshahidul/readctrl/code/RL_model/verl/verl_train/dataset/test.parquet \
+    custom_reward_function.path=/home/mshahidul/readctrl/code/RL_model/verl/verl_train/reward_func/reward.py \
+    data.train_batch_size=8 \
+    data.max_prompt_length=1024 \
+    data.max_response_length=2048 \
+    data.filter_overlong_prompts=True \
+    data.truncation='error' \
+    actor_rollout_ref.model.path=Qwen/Qwen3-4B-Instruct-2507 \
+    actor_rollout_ref.actor.optim.lr=1e-6 \
+    actor_rollout_ref.model.use_remove_padding=True \
+    actor_rollout_ref.actor.ppo_mini_batch_size=4 \
+    actor_rollout_ref.actor.ppo_micro_batch_size_per_gpu=2 \
+    actor_rollout_ref.actor.use_kl_loss=True \
+    actor_rollout_ref.actor.kl_loss_coef=0.001 \
+    actor_rollout_ref.actor.kl_loss_type=low_var_kl \
+    actor_rollout_ref.actor.entropy_coeff=0 \
+    actor_rollout_ref.model.enable_gradient_checkpointing=True \
+    actor_rollout_ref.actor.fsdp_config.param_offload=False \
+    actor_rollout_ref.actor.fsdp_config.optimizer_offload=False \
+    actor_rollout_ref.rollout.log_prob_micro_batch_size_per_gpu=2 \
+    actor_rollout_ref.rollout.tensor_model_parallel_size=1 \
+    actor_rollout_ref.rollout.name=vllm \
+    actor_rollout_ref.rollout.gpu_memory_utilization=0.6 \
+    actor_rollout_ref.rollout.max_model_len=8192 \
+    actor_rollout_ref.rollout.n=3 \
+    actor_rollout_ref.ref.log_prob_micro_batch_size_per_gpu=32 \
+    actor_rollout_ref.ref.fsdp_config.param_offload=False \
+    algorithm.use_kl_in_reward=False \
+    trainer.critic_warmup=0 \
+    trainer.logger='["console","wandb"]' \
+    trainer.project_name=$WAND_PROJECT \
+    trainer.experiment_name=$EXPERIMENT_NAME \
+    trainer.n_gpus_per_node=2 \
+    trainer.nnodes=1 \
+    trainer.save_freq=100 \
+    trainer.test_freq=1 \
+    +trainer.remove_previous_ckpt_in_save=true \
+    trainer.max_actor_ckpt_to_keep=1 \
+    trainer.max_critic_ckpt_to_keep=1 \
+    trainer.resume_mode=auto \
+    trainer.default_local_dir=/home/mshahidul/readctrl/code/RL_model/RL_model_subclaim_classifier \
+    trainer.total_epochs=15 $@ \
+    2>&1 | tee $EXPERIMENT_NAME.log
+
+# python "/home/mshahidul/readctrl/code/readability_control.py"
\ No newline at end of file
diff --git a/code/RL_model/verl/verl_train/script/run_qwen3-8b_debug_v2.sh b/code/RL_model/verl/verl_train/script/run_qwen3-8b_debug_v2.sh
new file mode 100644
index 0000000000000000000000000000000000000000..ac44d4f73ac2c3ee2959f9fe2a0ad58b6fee0dd1
--- /dev/null
+++ b/code/RL_model/verl/verl_train/script/run_qwen3-8b_debug_v2.sh
@@ -0,0 +1,53 @@
+set -x
+export PYTORCH_CUDA_ALLOC_CONF="expandable_segments:False"
+export CUDA_DEVICE_ORDER="PCI_BUS_ID"
+export CUDA_VISIBLE_DEVICES=2,3 
+
+PYTHONUNBUFFERED=1 python3 -m verl.trainer.main_ppo \
+    algorithm.adv_estimator=grpo \
+    data.train_files=/home/mshahidul/readctrl/code/RL_model/verl/verl_train/dataset/train.parquet \
+    data.val_files=/home/mshahidul/readctrl/code/RL_model/verl/verl_train/dataset/test.parquet \
+    custom_reward_function.path=/home/mshahidul/readctrl/code/RL_model/verl/verl_train/reward_func/reward.py \
+    data.train_batch_size=8 \
+    data.max_prompt_length=1024 \
+    data.max_response_length=2048 \
+    data.filter_overlong_prompts=True \
+    data.truncation='error' \
+    actor_rollout_ref.model.path=Qwen/Qwen3-4B-Instruct-2507 \
+    actor_rollout_ref.actor.optim.lr=1e-6 \
+    actor_rollout_ref.model.use_remove_padding=True \
+    actor_rollout_ref.actor.ppo_mini_batch_size=4 \
+    actor_rollout_ref.actor.ppo_micro_batch_size_per_gpu=2 \
+    actor_rollout_ref.actor.use_kl_loss=True \
+    actor_rollout_ref.actor.kl_loss_coef=0.001 \
+    actor_rollout_ref.actor.kl_loss_type=low_var_kl \
+    actor_rollout_ref.actor.entropy_coeff=0 \
+    actor_rollout_ref.model.enable_gradient_checkpointing=True \
+    actor_rollout_ref.actor.fsdp_config.param_offload=False \
+    actor_rollout_ref.actor.fsdp_config.optimizer_offload=False \
+    actor_rollout_ref.rollout.log_prob_micro_batch_size_per_gpu=2 \
+    actor_rollout_ref.rollout.tensor_model_parallel_size=1 \
+    actor_rollout_ref.rollout.name=vllm \
+    actor_rollout_ref.rollout.gpu_memory_utilization=0.5 \
+    actor_rollout_ref.rollout.max_model_len=8192 \
+    actor_rollout_ref.rollout.n=3 \
+    actor_rollout_ref.ref.log_prob_micro_batch_size_per_gpu=32 \
+    actor_rollout_ref.ref.fsdp_config.param_offload=False \
+    algorithm.use_kl_in_reward=False \
+    trainer.critic_warmup=0 \
+    trainer.logger='["console","wandb"]' \
+    trainer.project_name=$WAND_PROJECT \
+    trainer.experiment_name=$EXPERIMENT_NAME \
+    trainer.n_gpus_per_node=2 \
+    trainer.nnodes=1 \
+    trainer.save_freq=100 \
+    trainer.test_freq=1 \
+    +trainer.remove_previous_ckpt_in_save=true \
+    trainer.max_actor_ckpt_to_keep=1 \
+    trainer.max_critic_ckpt_to_keep=1 \
+    trainer.resume_mode=auto \
+    trainer.default_local_dir=/home/mshahidul/readctrl/code/RL_model/train_v2 \
+    trainer.total_epochs=15 $@ \
+    2>&1 | tee $EXPERIMENT_NAME.log
+
+# python "/home/mshahidul/readctrl/code/readability_control.py"
\ No newline at end of file
diff --git a/code/RL_model/verl/verl_train/script/run_qwen3-8b_v2.sh b/code/RL_model/verl/verl_train/script/run_qwen3-8b_v2.sh
new file mode 100644
index 0000000000000000000000000000000000000000..bb7df227bf5161e0d019c6d35425702604fd664b
--- /dev/null
+++ b/code/RL_model/verl/verl_train/script/run_qwen3-8b_v2.sh
@@ -0,0 +1,59 @@
+cd /home/mshahidul/readctrl/code/RL_model/verl/verl_train
+set -x
+
+unset PYTORCH_CUDA_ALLOC_CONF
+export EXPERIMENT_NAME=qwen3-4b-instruct-en
+export WAND_PROJECT='readctrl-verl'
+export CUDA_DEVICE_ORDER="PCI_BUS_ID"
+export CUDA_VISIBLE_DEVICES=2,3 
+
+
+PYTHONUNBUFFERED=1 python3 -m verl.trainer.main_ppo \
+    algorithm.adv_estimator=grpo \
+    data.train_files=/home/mshahidul/readctrl/code/RL_model/verl/verl_train/dataset/train.parquet \
+    data.val_files=/home/mshahidul/readctrl/code/RL_model/verl/verl_train/dataset/test.parquet \
+    custom_reward_function.path=/home/mshahidul/readctrl/code/RL_model/verl/verl_train/reward_func/reward_func/reward_new_v2.py \
+    data.train_batch_size=512 \
+    data.max_prompt_length=1024 \
+    data.max_response_length=2048 \
+    data.filter_overlong_prompts=True \
+    data.truncation='error' \
+    actor_rollout_ref.model.path=Qwen/Qwen3-4B-Instruct-2507 \
+    actor_rollout_ref.actor.optim.lr=1e-6 \
+    actor_rollout_ref.model.use_remove_padding=True \
+    actor_rollout_ref.actor.ppo_mini_batch_size=256 \
+    actor_rollout_ref.actor.ppo_micro_batch_size_per_gpu=16 \
+    actor_rollout_ref.actor.use_kl_loss=True \
+    actor_rollout_ref.actor.kl_loss_coef=0.001 \
+    actor_rollout_ref.actor.kl_loss_type=low_var_kl \
+    actor_rollout_ref.actor.entropy_coeff=0 \
+    actor_rollout_ref.model.enable_gradient_checkpointing=True \
+    actor_rollout_ref.actor.fsdp_config.param_offload=True \
+    actor_rollout_ref.actor.fsdp_config.optimizer_offload=True \
+    actor_rollout_ref.rollout.log_prob_micro_batch_size_per_gpu=32 \
+    actor_rollout_ref.rollout.tensor_model_parallel_size=1 \
+    actor_rollout_ref.rollout.name=vllm \
+    actor_rollout_ref.rollout.gpu_memory_utilization=0.4 \
+    actor_rollout_ref.rollout.enforce_eager=True \
+    actor_rollout_ref.rollout.max_model_len=8192 \
+    actor_rollout_ref.rollout.n=3 \
+    actor_rollout_ref.ref.log_prob_micro_batch_size_per_gpu=32 \
+    actor_rollout_ref.ref.fsdp_config.param_offload=True \
+    algorithm.use_kl_in_reward=False \
+    trainer.critic_warmup=0 \
+    trainer.logger='["console","wandb"]' \
+    trainer.project_name=$WAND_PROJECT \
+    trainer.experiment_name=$EXPERIMENT_NAME \
+    trainer.n_gpus_per_node=2 \
+    trainer.nnodes=1 \
+    trainer.save_freq=5 \
+    trainer.test_freq=10 \
+    +trainer.remove_previous_ckpt_in_save=true \
+    trainer.max_actor_ckpt_to_keep=1 \
+    trainer.max_critic_ckpt_to_keep=1 \
+    trainer.resume_mode=auto \
+    trainer.default_local_dir=/home/mshahidul/readctrl/code/RL_model/models/RL_model_subclaim_classifier_v2 \
+    trainer.total_epochs=15 $@ \
+    2>&1 | tee $EXPERIMENT_NAME.log
+
+# python "/home/mshahidul/readctrl/code/readability_control.py"
\ No newline at end of file
diff --git a/code/RL_model/verl/verl_train/script/train.sh b/code/RL_model/verl/verl_train/script/train.sh
new file mode 100644
index 0000000000000000000000000000000000000000..e69de29bb2d1d6434b8b29ae775ad8c2e48c5391
diff --git a/code/RL_model/verl/verl_train/scripts/__init__.py b/code/RL_model/verl/verl_train/scripts/__init__.py
new file mode 100644
index 0000000000000000000000000000000000000000..1ce90c5eb352d85c59105c0dc85b5f1dd576f095
--- /dev/null
+++ b/code/RL_model/verl/verl_train/scripts/__init__.py
@@ -0,0 +1,13 @@
+# Copyright 2024 Bytedance Ltd. and/or its affiliates
+#
+# Licensed under the Apache License, Version 2.0 (the "License");
+# you may not use this file except in compliance with the License.
+# You may obtain a copy of the License at
+#
+#     http://www.apache.org/licenses/LICENSE-2.0
+#
+# Unless required by applicable law or agreed to in writing, software
+# distributed under the License is distributed on an "AS IS" BASIS,
+# WITHOUT WARRANTIES OR CONDITIONS OF ANY KIND, either express or implied.
+# See the License for the specific language governing permissions and
+# limitations under the License.
diff --git a/code/RL_model/verl/verl_train/scripts/converter_hf_to_mcore.py b/code/RL_model/verl/verl_train/scripts/converter_hf_to_mcore.py
new file mode 100644
index 0000000000000000000000000000000000000000..6e7cdf2b5ab16240787c1455bdb4b1c12c2ecd8a
--- /dev/null
+++ b/code/RL_model/verl/verl_train/scripts/converter_hf_to_mcore.py
@@ -0,0 +1,610 @@
+# Copyright 2025 Bytedance Ltd. and/or its affiliates
+# Copyright (c) 2025, NVIDIA CORPORATION. All rights reserved.
+#
+# Licensed under the Apache License, Version 2.0 (the "License");
+# you may not use this file except in compliance with the License.
+# You may obtain a copy of the License at
+#
+#     http://www.apache.org/licenses/LICENSE-2.0
+#
+# Unless required by applicable law or agreed to in writing, software
+# distributed under the License is distributed on an "AS IS" BASIS,
+# WITHOUT WARRANTIES OR CONDITIONS OF ANY KIND, either express or implied.
+# See the License for the specific language governing permissions and
+# limitations under the License.
+
+import argparse
+import os
+import warnings
+from contextlib import contextmanager
+from importlib.metadata import version
+from typing import Any, Callable, ContextManager, Optional
+
+import numpy as np
+import torch
+import torch.distributed as dist
+
+try:
+    # NPU patch
+    import mindspeed.megatron_adaptor  # noqa: F401
+    from mindspeed.megatron_adaptor import repatch
+except ImportError:
+    repatch = None
+    pass
+
+from accelerate import init_empty_weights
+from megatron.core import dist_checkpointing
+from megatron.core import parallel_state as mpu
+from megatron.core.dist_checkpointing.mapping import ShardedTensor
+from megatron.core.dist_checkpointing.serialization import StrictHandling
+from megatron.core.models.gpt.gpt_model import ModelType
+from megatron.core.tensor_parallel.random import model_parallel_cuda_manual_seed
+from packaging.version import Version
+from transformers import AutoConfig
+
+from verl.model_merger.megatron_model_merger import get_dynamic_pipeline_shards
+from verl.models.mcore import hf_to_mcore_config
+from verl.utils.device import get_device_name, get_torch_device
+from verl.utils.megatron_utils import get_model
+
+
+def _init_args():
+    """
+    Examples:
+
+    1. single rank conversion for any model:
+        > python converter_hf_to_mcore.py --hf_model_path %{hf_model} --output_path ${output_path}
+    2. distributed conversion for DeepseekV3 671B:
+        > torchrun --nproc_per_node 1 --nnodes 4 --node_rank ${RANK} converter_hf_to_mcore.py \
+          --hf_model_path %{hf_model} --output_path ${output_path}
+    """
+    parser = argparse.ArgumentParser()
+    parser.add_argument("--hf_model_path", type=str, required=True, help="The path for the huggingface model")
+    parser.add_argument("--output_path", type=str, required=True, help="The path for the output mcore model")
+    parser.add_argument("--pp_size", type=int, default=1, help="pipeline model parallel size")
+    parser.add_argument("--ep_size", type=int, default=1, help="expert model parallel size")
+    parser.add_argument("--use_cpu_initialization", action="store_true", help="Whether to use cpu initialization")
+    parser.add_argument("--test", action="store_true", help="Whether to test the conversion")
+    parser.add_argument("--trust_remote_code", action="store_true", help="Whether to trust remote code")
+    args = parser.parse_args()
+    return args
+
+
+def test_conversion(megatron_model_provider, tfconfig, output_path, model):
+    ########### test ###########
+    # load model
+    model_test = get_model(
+        model_provider_func=megatron_model_provider,
+        model_type=ModelType.encoder_or_decoder,
+        wrap_with_ddp=True,
+        transformer_config=tfconfig,
+    )
+    ref_state_dict = model_test[0].module.sharded_state_dict()
+    dist_checkpointing.load(ref_state_dict, output_path, strict=StrictHandling.ASSUME_OK_UNEXPECTED)
+
+    dut_state_dict = model[0].module.state_dict()
+    for name in dut_state_dict.keys():
+        if dut_state_dict[name] is None:
+            print(f"[Warning] {name} is none in dut_state_dict")
+            continue
+        dut_data = dut_state_dict[name].data
+        if name in ref_state_dict:
+            ref_data = ref_state_dict[name]
+            if isinstance(ref_data, ShardedTensor):
+                ref_data = ref_data.data.view(ref_data.local_shape)
+            else:
+                ref_data = ref_data.data
+            assert dut_data.shape == ref_data.shape, f"{name=} {dut_data.shape=} {ref_data.shape=}"
+            assert (dut_data == ref_data).all(), f"{name} is not equal"
+            print(f"{name} is equal")
+        else:
+            print(f"[Warning] {name} is not in ref_state_dict")
+    for name in ref_state_dict.keys():
+        if ref_state_dict[name] is None:
+            print(f"[Warning] {name} is none in ref_state_dict")
+            continue
+        ref_data = ref_state_dict[name]
+        if isinstance(ref_data, ShardedTensor):
+            ref_data = ref_data.data.view(ref_data.local_shape)
+        else:
+            ref_data = ref_data.data
+        if name in dut_state_dict:
+            dut_data = dut_state_dict[name].data
+            assert dut_data.shape == ref_data.shape, f"{name=} {dut_data.shape=} {ref_data.shape=}"
+            assert (dut_data == ref_data).all(), f"{name} is not equal"
+            print(f"{name} is equal")
+        else:
+            print(f"[Warning] {name} is not in dut_state_dict")
+    print("Conversion test passed!")
+
+
+@torch.inference_mode()
+def convert_checkpoint_from_transformers_to_megatron(
+    hf_model, model, hf_config, layer_start_end: Optional[tuple[int, int]] = None
+):
+    if layer_start_end is None:
+        layer_start_end = (0, len(model.decoder.layers))
+    layer_start, layer_end = layer_start_end
+    pp_rank = mpu.get_pipeline_model_parallel_rank()
+    pp_size = mpu.get_pipeline_model_parallel_world_size()
+    ep_rank = mpu.get_expert_model_parallel_rank()
+    ep_size = mpu.get_expert_model_parallel_world_size()
+    numel = 0
+
+    num_attention_heads = hf_config.num_attention_heads
+    num_key_value_heads = hf_config.num_key_value_heads
+    hidden_dim = hf_config.hidden_size
+    head_dim = getattr(hf_config, "head_dim", hidden_dim // num_attention_heads)
+    if num_attention_heads != num_key_value_heads:
+        print("[WARNING] Converting GQA model")
+    has_qkv_bias = getattr(hf_config, "qkv_bias", False) or getattr(hf_config, "attention_bias", False)
+    has_share_expert = getattr(hf_config, "shared_expert_intermediate_size", None)
+    if pp_rank == 0:
+        numel += safe_copy(hf_model.model.embed_tokens.weight, model.embedding.word_embeddings.weight)
+
+    assert len(model.decoder.layers) == (layer_end - layer_start), (
+        f"Expected {len(model.decoder.layers)} layers, but got {layer_end - layer_start}"
+    )
+    for layer_idx, (layer, hf_layer) in enumerate(
+        zip(model.decoder.layers, hf_model.model.layers[layer_start:layer_end], strict=True)
+    ):
+        global_layer_idx = layer_idx + layer_start
+        numel_cur = numel
+        numel += safe_copy(hf_layer.input_layernorm.weight, layer.self_attention.linear_qkv.layer_norm_weight)
+
+        q = hf_layer.self_attn.q_proj.weight.view(
+            [num_key_value_heads, head_dim * num_attention_heads // num_key_value_heads, -1]
+        )
+        k = hf_layer.self_attn.k_proj.weight.view([num_key_value_heads, head_dim, -1])
+        v = hf_layer.self_attn.v_proj.weight.view([num_key_value_heads, head_dim, -1])
+        qkv = torch.cat([q, k, v], dim=1).view(-1, hidden_dim).contiguous()
+        numel += safe_copy(qkv, layer.self_attention.linear_qkv.weight)
+
+        if has_qkv_bias:
+            q_bias = hf_layer.self_attn.q_proj.bias.view([num_key_value_heads, -1])
+            k_bias = hf_layer.self_attn.k_proj.bias.view([num_key_value_heads, -1])
+            v_bias = hf_layer.self_attn.v_proj.bias.view([num_key_value_heads, -1])
+            qkv_bias = torch.cat([q_bias, k_bias, v_bias], dim=1).view(-1).contiguous()
+            numel += safe_copy(qkv_bias, layer.self_attention.linear_qkv.bias)
+
+        if hasattr(hf_layer.self_attn, "q_norm"):
+            numel += safe_copy(hf_layer.self_attn.q_norm.weight.data, layer.self_attention.q_layernorm.weight)
+            numel += safe_copy(hf_layer.self_attn.k_norm.weight.data, layer.self_attention.k_layernorm.weight)
+
+        numel += safe_copy(hf_layer.self_attn.o_proj.weight, layer.self_attention.linear_proj.weight)
+        numel += safe_copy(hf_layer.post_attention_layernorm.weight, layer.pre_mlp_layernorm.weight)
+
+        numel += safe_copy(hf_layer.mlp.gate.weight, layer.mlp.router.weight)
+
+        for idx, hf_expert in enumerate(hf_layer.mlp.experts):
+            num_experts = len(hf_layer.mlp.experts)
+            num_local_experts = num_experts // ep_size
+            expert_idx_start = ep_rank * num_local_experts
+            expert_idx_end = (ep_rank + 1) * num_local_experts
+            if idx < expert_idx_start or idx >= expert_idx_end:
+                continue
+            local_expert_idx = idx - expert_idx_start
+
+            fc1_weight = torch.cat([hf_expert.gate_proj.weight, hf_expert.up_proj.weight])
+            numel += safe_copy(fc1_weight, layer.mlp.experts.linear_fc1._parameters[f"weight{local_expert_idx}"])
+            numel += safe_copy(
+                hf_expert.down_proj.weight, layer.mlp.experts.linear_fc2._parameters[f"weight{local_expert_idx}"]
+            )
+
+        if has_share_expert:
+            numel += safe_copy(hf_layer.mlp.shared_expert_gate.weight, layer.mlp.shared_experts.gate_weight)
+            shared_fc1_weight = torch.cat(
+                [hf_layer.mlp.shared_expert.gate_proj.weight, hf_layer.mlp.shared_expert.up_proj.weight]
+            )
+            numel += safe_copy(shared_fc1_weight, layer.mlp.shared_experts.linear_fc1.weight)
+            numel += safe_copy(hf_layer.mlp.shared_expert.down_proj.weight, layer.mlp.shared_experts.linear_fc2.weight)
+        print(f"{pp_rank=} {global_layer_idx=} {layer_idx=} {numel=} numel this layer={numel - numel_cur}")
+
+    if pp_rank == pp_size - 1:
+        numel += safe_copy(hf_model.model.norm.weight, model.decoder.final_layernorm.weight)
+        numel += safe_copy(hf_model.lm_head.weight, model.output_layer.weight)
+    return numel
+
+
+def safe_copy(
+    src_tensor: torch.Tensor,
+    dst_tensor: torch.Tensor,
+    skip_dtype_assert: bool = False,
+):
+    if not skip_dtype_assert:
+        if src_tensor.dtype != dst_tensor.dtype:
+            raise ValueError(f"Get source dtype {src_tensor.dtype}, but target dtype {dst_tensor.dtype}")
+    assert src_tensor.shape == dst_tensor.shape
+    dst_tensor.data.copy_(src_tensor.data)
+    return src_tensor.numel()
+
+
+@torch.inference_mode()
+def convert_checkpoint_from_transformers_to_megatron_qwen2_5_vl(hfmodel, mgmodel, hf_config):
+    mgmodel = mgmodel.bfloat16()
+    hfmodel = hfmodel.bfloat16()
+    num_attention_heads = hf_config.num_attention_heads
+    num_query_groups = hf_config.num_key_value_heads
+    hidden_size = hf_config.hidden_size
+    head_dim = hidden_size // num_attention_heads
+
+    # 1. vision model
+    if Version(version("transformers")) < Version("4.52.0"):
+        print("Using transformers < 4.52 API to load vision model")
+        hfvision = hfmodel.visual
+    else:
+        hfvision = hfmodel.model.visual
+    mgvision = mgmodel.vision_model
+    vision_hidden_size = mgvision.config.hidden_size
+    vision_num_query_groups = mgvision.config.num_query_groups
+    vision_head_dim = vision_hidden_size // mgvision.config.num_attention_heads
+    copied_numel = 0
+    safe_copy(hfvision.rotary_pos_emb.inv_freq, mgvision.rotary_pos_emb.inv_freq)
+    copied_numel += safe_copy(hfvision.patch_embed.proj.weight, mgvision.patch_embed.proj.weight)
+    for hfblock, mgblock in zip(hfvision.blocks, mgvision.decoder.layers, strict=True):
+        # norm1 --> linear_qkv.norm
+        copied_numel += safe_copy(hfblock.norm1.weight, mgblock.self_attention.linear_qkv.layer_norm_weight)
+        # norm2 --> mlp.linear_fc1.norm
+        copied_numel += safe_copy(hfblock.norm2.weight, mgblock.mlp.linear_fc1.layer_norm_weight)
+        # qkv --> self_attention.linear_qkv
+        converted_weight = (
+            hfblock.attn.qkv.weight.view(3, vision_num_query_groups, -1, vision_head_dim, vision_hidden_size)
+            .transpose(0, 1)
+            .flatten(1, 2)
+            .reshape(-1, vision_hidden_size)
+            .contiguous()
+        )
+        copied_numel += safe_copy(converted_weight, mgblock.self_attention.linear_qkv.weight)
+        converted_bias = (
+            hfblock.attn.qkv.bias.view(3, vision_num_query_groups, -1)
+            .transpose(0, 1)
+            .flatten(1, 2)
+            .view(-1)
+            .contiguous()
+        )
+        copied_numel += safe_copy(converted_bias, mgblock.self_attention.linear_qkv.bias)
+        # proj --> self_attention.linear_proj
+        copied_numel += safe_copy(hfblock.attn.proj.weight, mgblock.self_attention.linear_proj.weight)
+        copied_numel += safe_copy(hfblock.attn.proj.bias, mgblock.self_attention.linear_proj.bias)
+        # mlp --> mlp: gate
+        fc1_weight = torch.cat([hfblock.mlp.gate_proj.weight, hfblock.mlp.up_proj.weight])
+        fc1_bias = torch.cat([hfblock.mlp.gate_proj.bias, hfblock.mlp.up_proj.bias])
+        copied_numel += safe_copy(fc1_weight, mgblock.mlp.linear_fc1.weight)
+        copied_numel += safe_copy(fc1_bias, mgblock.mlp.linear_fc1.bias)
+        copied_numel += safe_copy(hfblock.mlp.down_proj.weight, mgblock.mlp.linear_fc2.weight)
+        copied_numel += safe_copy(hfblock.mlp.down_proj.bias, mgblock.mlp.linear_fc2.bias)
+
+    # 2. vision projector
+    hfprojector = hfvision.merger
+    mgprojector = mgvision.projection
+    copied_numel += safe_copy(hfprojector.ln_q.weight, mgvision.decoder.final_layernorm.weight)
+
+    copied_numel += safe_copy(hfprojector.mlp[0].weight, mgprojector.encoder.linear_fc1.weight)
+    copied_numel += safe_copy(hfprojector.mlp[0].bias, mgprojector.encoder.linear_fc1.bias)
+    copied_numel += safe_copy(hfprojector.mlp[2].weight, mgprojector.encoder.linear_fc2.weight)
+    copied_numel += safe_copy(hfprojector.mlp[2].bias, mgprojector.encoder.linear_fc2.bias)
+    n_params = sum([t.numel() for t in hfvision.state_dict().values()])
+    assert n_params == copied_numel, f"n_params={n_params} != copied_numel={copied_numel}"
+    # 3. llm [just Qwen2]
+    if Version(version("transformers")) < Version("4.52.0"):
+        print("Using transformers < 4.52 API to load llm")
+        hfllm = hfmodel.model
+    else:
+        hfllm = hfmodel.model.language_model
+    mgllm = mgmodel.language_model
+    copied_numel = 0
+    copied_numel += safe_copy(hfllm.embed_tokens.weight, mgllm.embedding.word_embeddings.weight)
+    layermaps = zip(mgllm.decoder.layers, hfllm.layers, strict=True)
+    for mglayer, hflayer in layermaps:
+        copied_numel += safe_copy(hflayer.input_layernorm.weight, mglayer.self_attention.linear_qkv.layer_norm_weight)
+
+        q_proj_weight = hflayer.self_attn.q_proj.weight.view(num_query_groups, -1, head_dim, hidden_size)
+        k_proj_weight = hflayer.self_attn.k_proj.weight.view(num_query_groups, -1, head_dim, hidden_size)
+        v_proj_weight = hflayer.self_attn.v_proj.weight.view(num_query_groups, -1, head_dim, hidden_size)
+        qkv_proj = torch.cat([q_proj_weight, k_proj_weight, v_proj_weight], dim=1).view(-1, hidden_size).contiguous()
+        copied_numel += safe_copy(qkv_proj, mglayer.self_attention.linear_qkv.weight)
+
+        q_proj_bias = hflayer.self_attn.q_proj.bias.view(num_query_groups, -1)
+        k_proj_bias = hflayer.self_attn.k_proj.bias.view(num_query_groups, -1)
+        v_proj_bias = hflayer.self_attn.v_proj.bias.view(num_query_groups, -1)
+        qkv_bias = torch.cat([q_proj_bias, k_proj_bias, v_proj_bias], dim=1).view(-1).contiguous()
+        copied_numel += safe_copy(qkv_bias, mglayer.self_attention.linear_qkv.bias)
+        copied_numel += safe_copy(hflayer.self_attn.o_proj.weight, mglayer.self_attention.linear_proj.weight)
+
+        fc1_weight = torch.cat([hflayer.mlp.gate_proj.weight, hflayer.mlp.up_proj.weight])
+        copied_numel += safe_copy(fc1_weight, mglayer.mlp.linear_fc1.weight)
+
+        copied_numel += safe_copy(hflayer.mlp.down_proj.weight, mglayer.mlp.linear_fc2.weight)
+        copied_numel += safe_copy(hflayer.post_attention_layernorm.weight, mglayer.mlp.linear_fc1.layer_norm_weight)
+
+    copied_numel += safe_copy(hfllm.norm.weight, mgllm.decoder.final_layernorm.weight)
+    if not hf_config.tie_word_embeddings:
+        safe_copy(hfmodel.lm_head.weight, mgllm.output_layer.weight)
+
+    n_params = sum([t.numel() for t in hfllm.state_dict().values()])
+
+    assert n_params == copied_numel, f"n_params={n_params} != copied_numel={copied_numel}"
+
+
+@torch.inference_mode()
+def convert_checkpoint_from_transformers_to_megatron_dpskv3(
+    hf_model,
+    model,
+    hf_config,
+    tfconfig,
+    layer_start_end: Optional[tuple[int, int]] = None,
+):
+    warnings.warn("MTP model is not supported yet", stacklevel=2)
+    if layer_start_end is None:
+        layer_start_end = (0, len(model.decoder.layers))
+    layer_start, layer_end = layer_start_end
+    numel: int = 0
+    pp_rank = mpu.get_pipeline_model_parallel_rank()
+    pp_size = mpu.get_pipeline_model_parallel_world_size()
+    ep_rank = mpu.get_expert_model_parallel_rank()
+    ep_size = mpu.get_expert_model_parallel_world_size()
+
+    if pp_rank == 0:
+        numel += safe_copy(hf_model.model.embed_tokens.weight, model.embedding.word_embeddings.weight)
+
+    assert len(model.decoder.layers) == (layer_end - layer_start), (
+        f"Expected {len(model.decoder.layers)} layers, but got {layer_end - layer_start}"
+    )
+    for layer_idx, (layer, hf_layer) in enumerate(
+        zip(model.decoder.layers, hf_model.model.layers[layer_start:layer_end], strict=True)
+    ):
+        global_layer_idx = layer_idx + layer_start
+        numel_cur: int = numel
+        numel += safe_copy(hf_layer.input_layernorm.weight, layer.input_layernorm.weight)
+
+        if hf_config.q_lora_rank is None:
+            numel += safe_copy(hf_layer.self_attn.q_proj.weight, layer.self_attention.linear_q_proj.weight)
+        else:
+            numel += safe_copy(hf_layer.self_attn.q_a_proj.weight, layer.self_attention.linear_q_down_proj.weight)
+            numel += safe_copy(hf_layer.self_attn.q_b_proj.weight, layer.self_attention.linear_q_up_proj.weight)
+            numel += safe_copy(
+                hf_layer.self_attn.q_a_layernorm.weight, layer.self_attention.linear_q_up_proj.layer_norm_weight
+            )
+
+        numel += safe_copy(
+            hf_layer.self_attn.kv_a_proj_with_mqa.weight, layer.self_attention.linear_kv_down_proj.weight
+        )
+        numel += safe_copy(hf_layer.self_attn.kv_b_proj.weight, layer.self_attention.linear_kv_up_proj.weight)
+        numel += safe_copy(
+            hf_layer.self_attn.kv_a_layernorm.weight, layer.self_attention.linear_kv_up_proj.layer_norm_weight
+        )
+        numel += safe_copy(hf_layer.self_attn.o_proj.weight, layer.self_attention.linear_proj.weight)
+
+        if not hasattr(layer.mlp, "router"):
+            numel += safe_copy(hf_layer.post_attention_layernorm.weight, layer.mlp.linear_fc1.layer_norm_weight)
+            numel += safe_copy(
+                torch.cat([hf_layer.mlp.gate_proj.weight, hf_layer.mlp.up_proj.weight]), layer.mlp.linear_fc1.weight
+            )
+            numel += safe_copy(hf_layer.mlp.down_proj.weight, layer.mlp.linear_fc2.weight)
+        else:
+            numel += safe_copy(hf_layer.mlp.gate.weight, layer.mlp.router.weight)
+            # NOTE: the e_score_correction_bias in mcore model will be initialized with bfloat16 and \
+            # recover to fp32 in the first forward. There is always a diff in the bias between two models (~0.3%)
+            numel += safe_copy(
+                hf_layer.mlp.gate.e_score_correction_bias, layer.mlp.router.expert_bias, skip_dtype_assert=True
+            )
+            if tfconfig.moe_grouped_gemm:
+                for i, hf_expert in enumerate(hf_layer.mlp.experts):
+                    num_experts = len(hf_layer.mlp.experts)
+                    num_local_experts = num_experts // ep_size
+                    expert_idx_start = ep_rank * num_local_experts
+                    expert_idx_end = (ep_rank + 1) * num_local_experts
+                    if i < expert_idx_start or i >= expert_idx_end:
+                        continue
+                    local_expert_idx = i - expert_idx_start
+
+                    fc1_weight = torch.cat([hf_expert.gate_proj.weight, hf_expert.up_proj.weight])
+                    linear_fc1_weighti = getattr(layer.mlp.experts.linear_fc1, "weight" + str(local_expert_idx))
+                    numel += safe_copy(fc1_weight, linear_fc1_weighti)
+                    linear_fc2_weighti = getattr(layer.mlp.experts.linear_fc2, "weight" + str(local_expert_idx))
+                    numel_w2 = safe_copy(hf_expert.down_proj.weight, linear_fc2_weighti)
+                    numel += numel_w2
+            else:
+                for i, hf_expert in enumerate(hf_layer.mlp.experts):
+                    expert = layer.mlp.experts.local_experts[i]
+                    fc1_weight = torch.cat([hf_expert.gate_proj.weight, hf_expert.up_proj.weight])
+                    numel += safe_copy(fc1_weight, expert.linear_fc1.weight)
+                    numel += safe_copy(hf_expert.down_proj.weight, expert.linear_fc2.weight)
+            numel += safe_copy(hf_layer.post_attention_layernorm.weight, layer.pre_mlp_layernorm.weight)
+            shared_fc1_weight = torch.cat(
+                [hf_layer.mlp.shared_experts.gate_proj.weight, hf_layer.mlp.shared_experts.up_proj.weight]
+            )
+            numel += safe_copy(shared_fc1_weight, layer.mlp.shared_experts.linear_fc1.weight)
+            numel += safe_copy(hf_layer.mlp.shared_experts.down_proj.weight, layer.mlp.shared_experts.linear_fc2.weight)
+        print(f"{pp_rank=} {global_layer_idx=} {layer_idx=} {numel=} numel this layer={numel - numel_cur}")
+        numel_hf_one_layer = sum([i.numel() for i in hf_layer.state_dict().values()])
+        if hasattr(layer.mlp, "router"):
+            numel_hf_one_layer -= numel_w2 * 3 * len(hf_layer.mlp.experts) // ep_size * (ep_size - 1)
+        assert numel - numel_cur == numel_hf_one_layer, "numel mismatch"
+
+    if pp_rank == pp_size - 1:
+        numel += safe_copy(hf_model.model.norm.weight, model.decoder.final_layernorm.weight)
+        if not hf_config.tie_word_embeddings:
+            numel += safe_copy(hf_model.lm_head.weight, model.output_layer.weight)
+    print(f"{pp_rank=} {numel=}")
+    return numel
+
+
+@contextmanager
+def noop_context() -> Any:
+    yield
+
+
+def support_distributed_convert(hf_config: AutoConfig) -> bool:
+    for arch in ["DeepseekV3ForCausalLM", "Qwen3MoeForCausalLM", "Qwen2MoeForCausalLM"]:
+        if arch in hf_config.architectures:
+            return True
+    return False
+
+
+def convert_hf_to_mcore(
+    hf_model_path, output_path, pp_size=1, ep_size=1, use_cpu_initialization=False, test=False, trust_remote_code=False
+):
+    os.makedirs(output_path, exist_ok=True)
+    if len(os.listdir(output_path)) > 0 and not test:
+        print(f"Output path {output_path} is not empty, skipping conversion")
+        return
+
+    # init torch distributed and mpu
+    if "WORLD_SIZE" not in os.environ:
+        os.environ["RANK"] = "0"
+        os.environ["WORLD_SIZE"] = "1"
+        os.environ["MASTER_ADDR"] = "localhost"
+        os.environ["MASTER_PORT"] = "12355"
+
+    torch.distributed.init_process_group("nccl")
+
+    local_rank = os.getenv("LOCAL_RANK", 0)
+    world_size = dist.get_world_size()
+    get_torch_device().set_device(f"{get_device_name()}:{local_rank}")
+    if ep_size * pp_size != world_size:
+        pp_size = world_size
+        print(f"pp_size is set to {pp_size}")
+
+    mpu.initialize_model_parallel(
+        tensor_model_parallel_size=1,
+        pipeline_model_parallel_size=pp_size,
+        virtual_pipeline_model_parallel_size=None,
+        context_parallel_size=1,
+        expert_model_parallel_size=ep_size,
+    )
+    model_parallel_cuda_manual_seed(0)
+
+    # init hf config
+    hf_config = AutoConfig.from_pretrained(hf_model_path, trust_remote_code=trust_remote_code)
+    print(hf_config, flush=True)
+
+    if repatch:
+        if hf_config.architectures[0] == "DeepseekV3ForCausalLM":
+            config_repatch = dict(multi_head_latent_attention=True)
+            repatch(config_repatch)
+
+    if world_size > 1 and not support_distributed_convert(hf_config):
+        raise NotImplementedError(f"distributed conversion is not supported for {hf_config.architectures} yet.")
+
+    pipeline_shards = get_dynamic_pipeline_shards(hf_config.num_hidden_layers, pp_size)
+    print(f"Pipeline shards: {pipeline_shards}", flush=True)
+
+    tfconfig = hf_to_mcore_config(
+        hf_config,
+        torch.bfloat16,
+        num_layers_in_first_pipeline_stage=pipeline_shards[0] if len(pipeline_shards) > 1 else None,
+        num_layers_in_last_pipeline_stage=pipeline_shards[-1] if len(pipeline_shards) > 2 else None,
+    )
+    tfconfig.use_cpu_initialization = use_cpu_initialization
+    tie_word_embeddings = getattr(hf_config, "tie_word_embeddings", False)
+
+    # init megatron model
+    def megatron_model_provider(pre_process, post_process):
+        from verl.models.mcore import init_mcore_model
+
+        parallel_model = init_mcore_model(
+            tfconfig,
+            hf_config,
+            pre_process,
+            post_process,
+            share_embeddings_and_output_weights=tie_word_embeddings,
+            value=False,
+        )
+        return parallel_model
+
+    context: Callable[..., ContextManager] = init_empty_weights if use_cpu_initialization else noop_context
+    with context():
+        model = get_model(
+            model_provider_func=megatron_model_provider,
+            model_type=ModelType.encoder_or_decoder,
+            wrap_with_ddp=False,
+            transformer_config=tfconfig,
+        )
+
+    if use_cpu_initialization:
+        # convert meta device to empty tensor so it can use `copy_` function
+        model[0].module = model[0].module.to_empty(device="cpu")
+
+    with warnings.catch_warnings():
+        warnings.simplefilter("ignore")
+    from transformers import AutoModelForCausalLM, AutoModelForImageTextToText
+
+    # init hf model
+    if "Qwen2_5_VLForConditionalGeneration" in hf_config.architectures:
+        hf_model = AutoModelForImageTextToText.from_pretrained(
+            hf_model_path, torch_dtype=torch.bfloat16, trust_remote_code=trust_remote_code
+        )
+    else:
+        hf_model = AutoModelForCausalLM.from_pretrained(
+            hf_model_path, torch_dtype=torch.bfloat16, trust_remote_code=trust_remote_code
+        )
+    hf_state_dict = hf_model.state_dict()
+
+    pp_rank = mpu.get_pipeline_model_parallel_rank()
+
+    # distributed convert
+    if world_size > 1 and support_distributed_convert(hf_config):
+        pipeline_cumsum = np.cumsum(pipeline_shards)
+        layer_start = 0 if pp_rank == 0 else pipeline_cumsum[pp_rank - 1]
+        layer_end = pipeline_cumsum[pp_rank]
+        if "DeepseekV3ForCausalLM" in hf_config.architectures:
+            numel_partial: int = convert_checkpoint_from_transformers_to_megatron_dpskv3(
+                hf_model, model[0].module, hf_config, tfconfig=tfconfig, layer_start_end=(layer_start, layer_end)
+            )
+        elif "Qwen3MoeForCausalLM" in hf_config.architectures or "Qwen2MoeForCausalLM" in hf_config.architectures:
+            numel_partial: int = convert_checkpoint_from_transformers_to_megatron(
+                hf_model, model[0].module, hf_config, layer_start_end=(layer_start, layer_end)
+            )
+        else:
+            raise NotImplementedError(f"Distributed conversion is not supported for {hf_config.architectures} yet.")
+
+        numel_tensor = torch.tensor([numel_partial]).to(get_device_name())
+        dist.all_reduce(numel_tensor, op=dist.ReduceOp.SUM)
+        numel = int(numel_tensor.cpu().item())
+        print(f"total numel={numel} vs {hf_model.num_parameters()=}")
+        if numel != hf_model.num_parameters():
+            warnings.warn(f"numel mismatch: {numel=} != {hf_model.num_parameters()=}", stacklevel=1)
+
+    # load hf state dict to megatron model
+    elif "Qwen2MoeForCausalLM" in hf_config.architectures:
+        convert_checkpoint_from_transformers_to_megatron(hf_model, model[0].module, hf_config)
+    elif "Qwen2_5_VLForConditionalGeneration" in hf_config.architectures:
+        convert_checkpoint_from_transformers_to_megatron_qwen2_5_vl(hf_model, model[0].module, hf_config)
+    elif "DeepseekV3ForCausalLM" in hf_config.architectures:
+        convert_checkpoint_from_transformers_to_megatron_dpskv3(hf_model, model[0].module, hf_config, tfconfig=tfconfig)
+    elif "Qwen3MoeForCausalLM" in hf_config.architectures:
+        convert_checkpoint_from_transformers_to_megatron(hf_model, model[0].module, hf_config)
+    else:
+        assert not use_cpu_initialization, "use_cpu_initialization is only supported for MoE model"
+        from verl.models.mcore.loader import load_state_dict_to_megatron_gptmodel
+
+        load_state_dict_to_megatron_gptmodel(
+            state_dict=hf_state_dict,
+            wrapped_models=model,
+            config=hf_config,
+            params_dtype=torch.bfloat16,
+            is_value_model=False,
+        )
+
+    megatron_state_dict = model[0].module.sharded_state_dict()
+    del hf_state_dict, hf_model
+
+    # save megatron model
+    if len(os.listdir(output_path)) == 0:
+        dist_checkpointing.save(megatron_state_dict, output_path, sharded_strategy=None, async_sharded_save=False)
+    if test:
+        test_conversion(megatron_model_provider, tfconfig, output_path, model)
+
+
+if __name__ == "__main__":
+    args = _init_args()
+    convert_hf_to_mcore(
+        args.hf_model_path,
+        args.output_path,
+        args.pp_size,
+        args.ep_size,
+        args.use_cpu_initialization,
+        args.test,
+        args.trust_remote_code,
+    )
diff --git a/code/RL_model/verl/verl_train/scripts/diagnose.py b/code/RL_model/verl/verl_train/scripts/diagnose.py
new file mode 100644
index 0000000000000000000000000000000000000000..cb78f9e5c6297a8ba8e84262253ff385f49e0d2a
--- /dev/null
+++ b/code/RL_model/verl/verl_train/scripts/diagnose.py
@@ -0,0 +1,312 @@
+# Copyright 2024 Bytedance Ltd. and/or its affiliates
+#
+# Licensed under the Apache License, Version 2.0 (the "License");
+# you may not use this file except in compliance with the License.
+# You may obtain a copy of the License at
+#
+#     http://www.apache.org/licenses/LICENSE-2.0
+#
+# Unless required by applicable law or agreed to in writing, software
+# distributed under the License is distributed on an "AS IS" BASIS,
+# WITHOUT WARRANTIES OR CONDITIONS OF ANY KIND, either express or implied.
+# See the License for the specific language governing permissions and
+# limitations under the License.
+"""Diagnose script for checking OS/hardware/python/pip/verl/network.
+The output of this script can be a very good hint to issue/problem.
+"""
+
+import os
+import platform
+import socket
+import subprocess
+import sys
+import time
+
+import psutil
+
+try:
+    from urllib.parse import urlparse
+    from urllib.request import urlopen
+except ImportError:
+    from urllib2 import urlopen
+    from urlparse import urlparse
+import argparse
+import importlib.metadata
+
+import torch
+
+URLS = {
+    "PYPI": "https://pypi.python.org/pypi/pip",
+}
+
+REGIONAL_URLS = {
+    "cn": {
+        "PYPI(douban)": "https://pypi.douban.com/",
+        "Conda(tsinghua)": "https://mirrors.tuna.tsinghua.edu.cn/anaconda/pkgs/free/",
+    }
+}
+
+
+def test_connection(name, url, timeout=10):
+    """Simple connection test"""
+    urlinfo = urlparse(url)
+    start = time.time()
+    try:
+        socket.gethostbyname(urlinfo.netloc)
+    except Exception as e:
+        print("Error resolving DNS for {}: {}, {}".format(name, url, e))
+        return
+    dns_elapsed = time.time() - start
+    start = time.time()
+    try:
+        _ = urlopen(url, timeout=timeout)
+    except Exception as e:
+        print("Error open {}: {}, {}, DNS finished in {} sec.".format(name, url, e, dns_elapsed))
+        return
+    load_elapsed = time.time() - start
+    print("Timing for {}: {}, DNS: {:.4f} sec, LOAD: {:.4f} sec.".format(name, url, dns_elapsed, load_elapsed))
+
+
+def check_python():
+    print("----------Python Info----------")
+    print("Version      :", platform.python_version())
+    print("Compiler     :", platform.python_compiler())
+    print("Build        :", platform.python_build())
+    print("Arch         :", platform.architecture())
+
+
+def check_pip():
+    print("------------Pip Info-----------")
+    try:
+        import pip
+
+        print("Version      :", pip.__version__)
+        print("Directory    :", os.path.dirname(pip.__file__))
+    except ImportError:
+        print("No corresponding pip install for current python.")
+
+
+def _get_current_git_commit():
+    try:
+        result = subprocess.run(["git", "rev-parse", "HEAD"], capture_output=True, text=True, check=True)
+        return result.stdout.strip()
+    except subprocess.CalledProcessError as e:
+        print(f"Error running git command: {e.stderr.strip()}")
+        return None
+    except FileNotFoundError:
+        print("Did not find command: git")
+        return None
+
+
+def check_verl():
+    print("----------verl Info-----------")
+    try:
+        sys.path.insert(0, os.getcwd())
+        import verl
+
+        print("Version      :", verl.__version__)
+        verl_dir = os.path.dirname(verl.__file__)
+        print("Directory    :", verl_dir)
+        try:
+            commit_hash = _get_current_git_commit()
+            print("Commit Hash  :", commit_hash)
+        except AttributeError:
+            print("Commit hash not found. ")
+    except ImportError as e:
+        print(f"No verl installed: {e}")
+    except Exception as e:
+        import traceback
+
+        if not isinstance(e, IOError):
+            print("An error occurred trying to import verl.")
+            print("This is very likely due to missing or incompatible library files.")
+        print(traceback.format_exc())
+
+
+def check_os():
+    print("----------Platform Info----------")
+    print("Platform     :", platform.platform())
+    print("system       :", platform.system())
+    print("node         :", platform.node())
+    print("release      :", platform.release())
+    print("version      :", platform.version())
+
+
+def check_hardware():
+    print("----------Hardware Info----------")
+    print("machine      :", platform.machine())
+    print("processor    :", platform.processor())
+    if sys.platform.startswith("darwin"):
+        pipe = subprocess.Popen(("sysctl", "-a"), stdout=subprocess.PIPE)
+        output = pipe.communicate()[0]
+        for line in output.split(b"\n"):
+            if b"brand_string" in line or b"features" in line:
+                print(line.strip())
+    elif sys.platform.startswith("linux"):
+        subprocess.call(["lscpu"])
+    elif sys.platform.startswith("win32"):
+        subprocess.call(["wmic", "cpu", "get", "name"])
+
+
+def check_network(args):
+    print("----------Network Test----------")
+    if args.timeout > 0:
+        print("Setting timeout: {}".format(args.timeout))
+        socket.setdefaulttimeout(10)
+    for region in args.region.strip().split(","):
+        r = region.strip().lower()
+        if not r:
+            continue
+        if r in REGIONAL_URLS:
+            URLS.update(REGIONAL_URLS[r])
+        else:
+            import warnings
+
+            warnings.warn("Region {} do not need specific test, please refer to global sites.".format(r), stacklevel=2)
+    for name, url in URLS.items():
+        test_connection(name, url, args.timeout)
+
+
+def check_environment():
+    print("----------Environment----------")
+    for k, v in os.environ.items():
+        if k.startswith("VERL_") or k.startswith("OMP_") or k.startswith("KMP_") or k == "CC" or k == "CXX":
+            print('{}="{}"'.format(k, v))
+
+
+def check_pip_package_versions():
+    packages = ["vllm", "sglang", "ray", "torch"]
+    for package in packages:
+        try:
+            version = importlib.metadata.version(package)
+            print(f"{package}\t     : {version}")
+        except importlib.metadata.PackageNotFoundError:
+            print(f"{package}\t     : not found.")
+
+
+def check_cuda_versions():
+    if torch.cuda.is_available():
+        try:
+            cuda_runtime_version = torch.version.cuda
+            print(f"CUDA Runtime : {cuda_runtime_version}")
+            import subprocess
+
+            nvcc_output = subprocess.check_output(["nvcc", "--version"]).decode("utf-8")
+            cuda_compiler_version = next((line for line in nvcc_output.splitlines() if "release" in line), None)
+            if cuda_compiler_version:
+                print(f"CUDA Compiler : {cuda_compiler_version.strip()}")
+            else:
+                print("Could not determine CUDA compiler version.")
+        except FileNotFoundError as e:
+            print(f"CUDA compiler : Not found: {e}")
+        except Exception as e:
+            print(f"An error occurred while checking CUDA versions: {e}")
+    else:
+        print("CUDA is not available.")
+
+
+def _get_cpu_memory():
+    """
+    Get the total CPU memory capacity in GB.
+    """
+    memory = psutil.virtual_memory()
+    return memory.total / (1024**3)
+
+
+def _get_gpu_info():
+    """
+    Get GPU type, GPU memory, and GPU count using nvidia-smi command.
+    """
+    try:
+        result = subprocess.run(
+            ["nvidia-smi", "--query-gpu=gpu_name,memory.total", "--format=csv,noheader,nounits"],
+            capture_output=True,
+            text=True,
+            check=True,
+        )
+        gpu_lines = result.stdout.strip().split("\n")
+        gpu_count = len(gpu_lines)
+        gpu_info = []
+        for line in gpu_lines:
+            gpu_name, gpu_memory = line.split(", ")
+            gpu_info.append(
+                {
+                    "type": gpu_name,
+                    "memory": float(gpu_memory) / 1024,  # Convert to GB
+                }
+            )
+        return gpu_count, gpu_info
+    except (subprocess.CalledProcessError, FileNotFoundError):
+        print("Failed to execute nvidia-smi command.")
+        return 0, []
+
+
+def _get_system_info():
+    """
+    Get CPU memory capacity, GPU type, GPU memory, and GPU count.
+    """
+    cpu_memory = _get_cpu_memory()
+    gpu_count, gpu_info = _get_gpu_info()
+    return {"cpu_memory": cpu_memory, "gpu_count": gpu_count, "gpu_info": gpu_info}
+
+
+def check_system_info():
+    print("----------System Info----------")
+    system_info = _get_system_info()
+    print(f"CPU Memory\t: {system_info['cpu_memory']:.2f} GB")
+    print(f"GPU Count\t: {system_info['gpu_count']}")
+    for i, gpu in enumerate(system_info["gpu_info"]):
+        print(f"GPU {i + 1}\tType    : {gpu['type']}")
+        print(f"GPU {i + 1}\tMemory  : {gpu['memory']:.2f} GB")
+
+
+def parse_args():
+    """Parse arguments."""
+    parser = argparse.ArgumentParser(
+        formatter_class=argparse.ArgumentDefaultsHelpFormatter,
+        description="Diagnose script for checking the current system.",
+    )
+    choices = ["python", "pip", "verl", "system", "os", "environment"]
+    for choice in choices:
+        parser.add_argument("--" + choice, default=1, type=int, help="Diagnose {}.".format(choice))
+    parser.add_argument("--network", default=0, type=int, help="Diagnose network.")
+    parser.add_argument("--hardware", default=0, type=int, help="Diagnose hardware.")
+    parser.add_argument(
+        "--region",
+        default="",
+        type=str,
+        help="Additional sites in which region(s) to test. \
+                        Specify 'cn' for example to test mirror sites in China.",
+    )
+    parser.add_argument("--timeout", default=10, type=int, help="Connection test timeout threshold, 0 to disable.")
+    args = parser.parse_args()
+    return args
+
+
+if __name__ == "__main__":
+    args = parse_args()
+    if args.python:
+        check_python()
+
+    if args.pip:
+        check_pip()
+        check_pip_package_versions()
+
+    if args.verl:
+        check_verl()
+
+    if args.os:
+        check_os()
+
+    if args.hardware:
+        check_hardware()
+
+    if args.network:
+        check_network(args)
+
+    if args.environment:
+        check_environment()
+        check_cuda_versions()
+
+    if args.system:
+        check_system_info()
diff --git a/code/RL_model/verl/verl_train/scripts/generate_trainer_config.sh b/code/RL_model/verl/verl_train/scripts/generate_trainer_config.sh
new file mode 100644
index 0000000000000000000000000000000000000000..a40f555fd0fa40f6f3e3d4e99fa1e0db9212ce75
--- /dev/null
+++ b/code/RL_model/verl/verl_train/scripts/generate_trainer_config.sh
@@ -0,0 +1,51 @@
+#!/usr/bin/env bash
+set -euox pipefail
+
+
+# Define config specifications: "config_name:output_file:config_arg"
+CONFIG_SPECS=(
+    "ppo_trainer:_generated_ppo_trainer.yaml:"
+    "ppo_megatron_trainer:_generated_ppo_megatron_trainer.yaml:--config-name=ppo_megatron_trainer.yaml"
+)
+
+generate_config() {
+    local config_name="$1"
+    local output_file="$2"
+    local config_arg="$3"
+    
+    local target_cfg="verl/trainer/config/${output_file}"
+    local tmp_header=$(mktemp)
+    local tmp_cfg=$(mktemp)
+    
+    echo "# This reference configration yaml is automatically generated via 'scripts/generate_trainer_config.sh'" > "$tmp_header"
+    echo "# in which it invokes 'python3 scripts/print_cfg.py --cfg job ${config_arg}' to flatten the 'verl/trainer/config/${config_name}.yaml' config fields into a single file." >> "$tmp_header"
+    echo "# Do not modify this file directly." >> "$tmp_header"
+    echo "# The file is usually only for reference and never used." >> "$tmp_header"
+    echo "" >> "$tmp_header"
+    
+    python3 scripts/print_cfg.py --cfg job ${config_arg} > "$tmp_cfg"
+    
+    cat "$tmp_header" > "$target_cfg"
+    sed -n '/^actor_rollout_ref/,$p' "$tmp_cfg" >> "$target_cfg"
+    
+    rm "$tmp_cfg" "$tmp_header"
+    
+    echo "Generated: $target_cfg"
+}
+
+for spec in "${CONFIG_SPECS[@]}"; do
+    IFS=':' read -r config_name output_file config_arg <<< "$spec"
+    generate_config "$config_name" "$output_file" "$config_arg"
+done
+
+for spec in "${CONFIG_SPECS[@]}"; do
+    IFS=':' read -r config_name output_file config_arg <<< "$spec"
+    target_cfg="verl/trainer/config/${output_file}"
+    if ! git diff --exit-code -- "$target_cfg" >/dev/null; then
+        echo "✖ $target_cfg is out of date. Please regenerate via 'scripts/generate_trainer_config.sh' and commit the changes."
+        exit 1
+    fi
+done
+
+echo "All good"
+exit 0
diff --git a/code/RL_model/verl/verl_train/scripts/init_random_model.py b/code/RL_model/verl/verl_train/scripts/init_random_model.py
new file mode 100644
index 0000000000000000000000000000000000000000..2bc3ffc1b80feb28b580aebc4d5e7672216a5cb9
--- /dev/null
+++ b/code/RL_model/verl/verl_train/scripts/init_random_model.py
@@ -0,0 +1,108 @@
+# Copyright 2025 Bytedance Ltd. and/or its affiliates
+# Copyright (c) 2025, NVIDIA CORPORATION. All rights reserved.
+#
+# Licensed under the Apache License, Version 2.0 (the "License");
+# you may not use this file except in compliance with the License.
+# You may obtain a copy of the License at
+#
+#     http://www.apache.org/licenses/LICENSE-2.0
+#
+# Unless required by applicable law or agreed to in writing, software
+# distributed under the License is distributed on an "AS IS" BASIS,
+# WITHOUT WARRANTIES OR CONDITIONS OF ANY KIND, either express or implied.
+# See the License for the specific language governing permissions and
+# limitations under the License.
+
+"""
+This script override a model with custom config and random weights, mainly for create small models for 
+debugging purposes.
+
+Usage:
+    python scripts/init_random_model.py \
+        --hf_model_path <path_to_hf_model> \
+        --new_config_path <path_to_new_config.json> \
+        --output_path <path_to_output_model>
+
+"""
+
+import argparse
+import json
+import os
+import warnings
+from typing import Any
+
+from transformers import AutoConfig, AutoModelForCausalLM, AutoTokenizer, PretrainedConfig
+
+
+def _init_args():
+    parser = argparse.ArgumentParser()
+    parser.add_argument("--hf_model_path", type=str, required=True, help="The path for the huggingface model")
+    parser.add_argument("--new_config_path", type=str, required=True, help="The path for the new config file")
+    parser.add_argument("--output_path", type=str, required=True, help="The path for the output random model")
+    parser.add_argument(
+        "--trust_remote_code",
+        action="store_true",
+        help="Whether to trust remote code when loading HF model. Disabled by default for security.",
+    )
+    args = parser.parse_args()
+    return args
+
+
+def check_output_path(output_path: str):
+    if os.path.exists(output_path):
+        warnings.warn(f"Output path '{output_path}' already exists. Will do nothing.", stacklevel=2)
+        exit()
+    else:
+        os.makedirs(output_path, exist_ok=True)
+        print(f"Output path '{output_path}' created.")
+
+
+def check_configs(original_config: dict[str, Any], new_config: dict[str, Any]) -> bool:
+    """
+    Check if the original config and new config are compatible.
+    This is a placeholder function; actual implementation may vary based on requirements.
+    """
+    # Example check: ensure 'model_type' is the same
+    if new_config.get("model_type", None) is not None and original_config.get("model_type") != new_config.get(
+        "model_type"
+    ):
+        raise RuntimeError("Model types do not match.")
+    for key in new_config:
+        if key not in original_config:
+            warnings.warn(
+                f"Key '{key}' in new config does not exist in original config, may not take effect.", stacklevel=2
+            )
+
+
+def init_random_model(hf_model_path, new_config_path, output_path, trust_remote_code: bool = False):
+    config = AutoConfig.from_pretrained(hf_model_path, trust_remote_code=trust_remote_code)
+    tokenizer = AutoTokenizer.from_pretrained(hf_model_path, trust_remote_code=trust_remote_code)
+    config_dict = PretrainedConfig.get_config_dict(hf_model_path)[0]
+    print(config_dict)
+    with open(new_config_path) as f:
+        new_config_dict = json.load(f)
+    check_configs(config_dict, new_config_dict)
+    config_dict.update(new_config_dict)
+    new_confg = config.from_dict(config_dict)
+    print(f"new_config: {new_confg}")
+    if trust_remote_code:
+        model = AutoModelForCausalLM.from_pretrained(
+            hf_model_path, config=new_confg, trust_remote_code=trust_remote_code
+        )
+    else:
+        model = AutoModelForCausalLM.from_config(new_confg)
+    model.save_pretrained(output_path)
+    tokenizer.save_pretrained(output_path)
+    new_confg.save_pretrained(output_path)
+    print(f"Random model initialized and saved to {output_path}")
+
+
+if __name__ == "__main__":
+    args = _init_args()
+    check_output_path(args.output_path)
+    init_random_model(
+        hf_model_path=args.hf_model_path,
+        new_config_path=args.new_config_path,
+        output_path=args.output_path,
+        trust_remote_code=args.trust_remote_code,
+    )
diff --git a/code/RL_model/verl/verl_train/scripts/install_sglang_mcore_npu.sh b/code/RL_model/verl/verl_train/scripts/install_sglang_mcore_npu.sh
new file mode 100644
index 0000000000000000000000000000000000000000..2975db3d1ed7583053d2bf9cc148c666a088d0f7
--- /dev/null
+++ b/code/RL_model/verl/verl_train/scripts/install_sglang_mcore_npu.sh
@@ -0,0 +1,57 @@
+#!/bin/bash
+set -e
+NPU_DEVICE=${NPU_DEVICE:=A3}
+
+export MAX_JOBS=32
+
+echo "1. install SGLang from source"
+git clone -b v0.5.8 https://github.com/sgl-project/sglang.git
+cd sglang
+mv python/pyproject_other.toml python/pyproject.toml
+pip install -e python[srt_npu]
+cd ..
+
+echo "2. install torch & torch_npu & triton_ascend & other basic packages"
+pip install torch==2.7.1 torch_npu==2.7.1.post2 torchvision==0.22.1
+pip install pybind11 click==8.2.1 mbridge "numpy<2.0.0" cachetools
+
+
+echo "3. install sgl-kernel-npu form source, detailed readme in https://github.com/sgl-project/sgl-kernel-npu/blob/main/python/deep_ep/README.md"
+git clone https://github.com/sgl-project/sgl-kernel-npu.git
+cd sgl-kernel-npu
+git checkout 46b73de
+sed -i '101s/^/# /' build.sh
+if [ "$NPU_DEVICE" = "A3" ]; then
+    bash build.sh
+fi
+if [ "$NPU_DEVICE" = "A2" ]; then
+    bash build.sh -a deepep2
+fi
+pip install output/torch_memory_saver*.whl
+pip install output/sgl_kernel_npu*.whl
+pip install output/deep_ep*.whl
+cd "$(pip show deep-ep | grep -E '^Location:' | awk '{print $2}')" && ln -s deep_ep/deep_ep_cpp*.so && cd -
+python -c "import deep_ep; print(deep_ep.__path__)"
+cd ..
+# install sgl-kernel-npu from release whl
+# if [ "$NPU_DEVICE" = "A3" ]; then
+#     wget https://github.com/sgl-project/sgl-kernel-npu/releases/download/2026.01.21/sgl-kernel-npu_2026.01.21_8.5.0_a3.zip
+# fi
+# if [ "$NPU_DEVICE" = "A2" ]; then
+#     wget https://github.com/sgl-project/sgl-kernel-npu/releases/download/2026.01.21/sgl-kernel-npu_2026.01.21_8.5.0_910b.zip
+# fi
+# unzip sgl-kernel-npu*.zip
+# pip install output/torch_memory_saver*.whl
+# pip install output/sgl_kernel_npu*.whl
+# pip install output/deep_ep*.whl
+
+if [ $USE_MEGATRON -eq 1 ]; then
+    echo "4. install Megatron and MindSpeed"
+    git clone -b 2.3.0_core_r0.12.1 https://gitcode.com/Ascend/MindSpeed.git 
+    pip install -e MindSpeed 
+    pip install git+https://github.com/NVIDIA/Megatron-LM.git@core_v0.12.1 
+fi
+
+echo "5. May need to uninstall timm & triton"
+pip uninstall -y timm triton
+echo "Successfully installed all packages"
diff --git a/code/RL_model/verl/verl_train/scripts/install_vllm_sglang_mcore.sh b/code/RL_model/verl/verl_train/scripts/install_vllm_sglang_mcore.sh
new file mode 100644
index 0000000000000000000000000000000000000000..4ac686764744b29ba20b0e5798170816f54ed868
--- /dev/null
+++ b/code/RL_model/verl/verl_train/scripts/install_vllm_sglang_mcore.sh
@@ -0,0 +1,55 @@
+#!/bin/bash
+
+USE_MEGATRON=${USE_MEGATRON:-1}
+USE_SGLANG=${USE_SGLANG:-1}
+
+export MAX_JOBS=32
+
+echo "1. install inference frameworks and pytorch they need"
+if [ $USE_SGLANG -eq 1 ]; then
+    pip install "sglang[all]==0.5.2" --no-cache-dir && pip install torch-memory-saver --no-cache-dir
+fi
+pip install --no-cache-dir "vllm==0.11.0"
+
+echo "2. install basic packages"
+pip install "transformers[hf_xet]>=4.51.0" accelerate datasets peft hf-transfer \
+    "numpy<2.0.0" "pyarrow>=15.0.0" pandas "tensordict>=0.8.0,<=0.10.0,!=0.9.0" torchdata \
+    ray[default] codetiming hydra-core pylatexenc qwen-vl-utils wandb dill pybind11 liger-kernel mathruler \
+    pytest py-spy pre-commit ruff tensorboard 
+
+echo "pyext is lack of maintainace and cannot work with python 3.12."
+echo "if you need it for prime code rewarding, please install using patched fork:"
+echo "pip install git+https://github.com/ShaohonChen/PyExt.git@py311support"
+
+pip install "nvidia-ml-py>=12.560.30" "fastapi[standard]>=0.115.0" "optree>=0.13.0" "pydantic>=2.9" "grpcio>=1.62.1"
+
+
+echo "3. install FlashAttention and FlashInfer"
+# Install flash-attn-2.8.1 (cxx11abi=False)
+wget -nv https://github.com/Dao-AILab/flash-attention/releases/download/v2.8.1/flash_attn-2.8.1+cu12torch2.8cxx11abiFALSE-cp312-cp312-linux_x86_64.whl && \
+    pip install --no-cache-dir flash_attn-2.8.1+cu12torch2.8cxx11abiFALSE-cp312-cp312-linux_x86_64.whl
+
+pip install --no-cache-dir flashinfer-python==0.3.1
+
+
+if [ $USE_MEGATRON -eq 1 ]; then
+    echo "4. install TransformerEngine and Megatron"
+    echo "Notice that TransformerEngine installation can take very long time, please be patient"
+    pip install "onnxscript==0.3.1"
+    NVTE_FRAMEWORK=pytorch pip3 install --no-deps git+https://github.com/NVIDIA/TransformerEngine.git@v2.6
+    pip3 install --no-deps git+https://github.com/NVIDIA/Megatron-LM.git@core_v0.13.1
+fi
+
+
+echo "5. May need to fix opencv"
+pip install opencv-python
+pip install opencv-fixer && \
+    python -c "from opencv_fixer import AutoFix; AutoFix()"
+
+
+if [ $USE_MEGATRON -eq 1 ]; then
+    echo "6. Install cudnn python package (avoid being overridden)"
+    pip install nvidia-cudnn-cu12==9.10.2.21
+fi
+
+echo "Successfully installed all packages"
diff --git a/code/RL_model/verl/verl_train/scripts/legacy_model_merger.py b/code/RL_model/verl/verl_train/scripts/legacy_model_merger.py
new file mode 100644
index 0000000000000000000000000000000000000000..a6da5072df038705dbbcb102cc47bc1124958da5
--- /dev/null
+++ b/code/RL_model/verl/verl_train/scripts/legacy_model_merger.py
@@ -0,0 +1,804 @@
+# Copyright 2024 Bytedance Ltd. and/or its affiliates
+#
+# Licensed under the Apache License, Version 2.0 (the "License");
+# you may not use this file except in compliance with the License.
+# You may obtain a copy of the License at
+#
+#     http://www.apache.org/licenses/LICENSE-2.0
+#
+# Unless required by applicable law or agreed to in writing, software
+# distributed under the License is distributed on an "AS IS" BASIS,
+# WITHOUT WARRANTIES OR CONDITIONS OF ANY KIND, either express or implied.
+# See the License for the specific language governing permissions and
+# limitations under the License.
+
+"""
+This script is used to merge huggingface model and test verl checkpoints from FSDP and Megatron backends.
+
+To merge FSDP checkpoints:
+```sh
+python scripts/legacy_model_merger.py merge \
+    --backend fsdp \
+    --local_dir checkpoints/verl_fsdp_gsm8k_examples/qwen2_5_0b5_fsdp_saveload/global_step_1/actor \
+    --target_dir /path/to/merged_hf_model
+```
+
+To merge Megatron checkpoints:
+```sh
+python scripts/legacy_model_merger.py merge \
+    --backend megatron \
+    --tie-word-embedding \
+    --local_dir checkpoints/verl_megatron_gsm8k_examples/qwen2_5_0b5_megatron_saveload/global_step_1/actor \
+    --target_dir /path/to/merged_hf_model
+```
+
+For more details, please refer to documentation:
+https://verl.readthedocs.io/en/latest/advance/checkpoint.html#convert-fsdp-and-megatron-checkpoints-to-huggingface-format-model
+"""
+
+import argparse
+import os
+import re
+import warnings
+from abc import ABC, abstractmethod
+from concurrent.futures import ThreadPoolExecutor
+from dataclasses import dataclass, field
+from pathlib import Path
+from typing import Optional, Union
+
+import numpy as np
+import torch
+from accelerate import init_empty_weights
+from safetensors.torch import load_file
+from torch.distributed._tensor import Placement, Shard
+from transformers import (
+    AutoConfig,
+    AutoModelForCausalLM,
+    AutoModelForTokenClassification,
+    AutoModelForVision2Seq,
+    GenerationConfig,
+    PretrainedConfig,
+)
+
+try:
+    # for torch 2.5+
+    from torch.distributed.tensor import DTensor
+except ImportError:
+    from torch.distributed._tensor import DTensor
+
+from tqdm import tqdm
+
+from verl.utils import hf_processor, hf_tokenizer
+
+
+@dataclass
+class ModelMergerConfig:
+    operation: str  # 'merge' or 'test'
+    backend: str
+    local_dir: str
+    hf_model_config_path: str
+    target_dir: Optional[str] = "tmp"
+    hf_upload_path: Optional[str] = None
+    private: bool = False
+    test_hf_dir: Optional[str] = None
+    tie_word_embedding: bool = False
+    is_value_model: bool = False
+    hf_model_path: Optional[str] = None
+    hf_upload: bool = field(init=False)
+
+    def __post_init__(self):
+        self.hf_upload = self.operation == "merge" and bool(self.hf_upload_path)
+        if self.operation == "test":
+            self.target_dir = None
+            self.hf_upload_path = None
+            self.private = False
+
+
+class BaseModelMerger(ABC):
+    def __init__(self, config: ModelMergerConfig):
+        self.config = config
+        self.hf_model_config_path = config.hf_model_config_path
+
+        if config.hf_model_path:
+            print(
+                "Warning: --hf_model_path is deprecated and will be removed in a future version. Currently verl will save huggingface model configuration files into checkpoint directories. Therefore, there is no need to provide --hf_model_path. "
+            )
+            self.hf_model_config_path = config.hf_model_path
+
+        # Auto-detect huggingface subdirectory if it exists
+        huggingface_subdir = os.path.join(self.hf_model_config_path, "huggingface")
+        if os.path.isdir(huggingface_subdir):
+            self.hf_model_config_path = huggingface_subdir
+
+        self.model_config = AutoConfig.from_pretrained(self.hf_model_config_path)
+
+    def get_transformers_auto_model_class(self):
+        # Handle case where architectures might be None or empty
+        if self.model_config.architectures is None or len(self.model_config.architectures) == 0:
+            # Try to infer from model_type if architectures is missing
+            model_type = getattr(self.model_config, 'model_type', '').lower()
+            if 'vision' in model_type or 'vl' in model_type:
+                return AutoModelForVision2Seq
+            elif 'causal' in model_type or 'gpt' in model_type or 'llama' in model_type or 'qwen' in model_type:
+                return AutoModelForCausalLM
+            else:
+                raise NotImplementedError(
+                    f"Cannot determine model class: architectures is None and model_type '{model_type}' is not recognized"
+                )
+        
+        architecture = self.model_config.architectures[0]
+        if "ForTokenClassification" in architecture:
+            return AutoModelForTokenClassification
+        elif "ForCausalLM" in architecture:
+            return AutoModelForCausalLM
+        elif "ForConditionalGeneration" in architecture:
+            return AutoModelForVision2Seq
+
+        raise NotImplementedError(f"Unknown architecture {self.model_config.architectures}")
+
+    def patch_model_generation_config(self, model):
+        """
+        The generation_config created from model config may be different to the pretrained model,
+        this may lead to error when generating: https://github.com/volcengine/verl/issues/1246
+
+        This function patch the generation_config created from model config to the pretrained model.
+        """
+        if model.can_generate():
+            try:
+                model.generation_config = GenerationConfig.from_pretrained(self.hf_model_config_path)
+            except OSError:
+                print(
+                    f"Warning: Generation config file not found in {self.hf_model_config_path}, using a generation config created from the model config."
+                )
+        return model
+
+    def save_lora_adapter(self, state_dict: dict[str, torch.Tensor]):
+        """
+        Save lora adapter to safetensors.
+
+        Returns:
+            lora_path: str, the path to the lora adapter. None if no lora adapter found.
+
+        Note:
+            This function change the 'state_dict' in place.
+        """
+        lora_params_names = [name for name in state_dict.keys() if "lora_" in name]
+
+        if len(lora_params_names) == 0:
+            return None
+
+        import json
+        from typing import OrderedDict
+
+        import peft
+        from safetensors.torch import save_file
+
+        lora_params = OrderedDict()
+        target_modules = set()
+        lora_key = None
+
+        for name in lora_params_names:
+            lora_key = name.replace(".default.weight", ".weight")
+            target_modules.add(lora_key.split(".")[-3])
+            lora_params[lora_key] = state_dict.pop(name)
+
+        lora_rank = min(lora_params[lora_key].shape[0], lora_params[lora_key].shape[1])
+        peft_dict = {
+            "r": lora_rank,
+            "lora_alpha": 0,  # lora_alpha is not set. An error should be raised to inform the user to set it manually.
+            "target_modules": list(target_modules),
+        }
+        peft_config = peft.LoraConfig(**peft_dict).to_dict()
+        peft_config["task_type"] = peft_config["task_type"].value if peft_config["task_type"] else None
+        peft_config["peft_type"] = peft_config["peft_type"].value if peft_config["peft_type"] else None
+        peft_config["target_modules"] = list(peft_config["target_modules"])
+
+        lora_path = os.path.join(self.config.target_dir, "lora_adapter")
+        os.makedirs(lora_path, exist_ok=True)
+        with open(os.path.join(lora_path, "adapter_config.json"), "w", encoding="utf-8") as f:
+            json.dump(peft_config, f, ensure_ascii=False, indent=4)
+        save_file(lora_params, os.path.join(lora_path, "adapter_model.safetensors"))
+
+        for name in list(state_dict.keys()):
+            key = (
+                name.replace("base_model.model.", "")
+                .replace(".base_layer.weight", ".weight")
+                .replace(".base_layer.bias", ".bias")
+            )
+            state_dict[key] = state_dict.pop(name)
+
+        return lora_path
+
+    def save_hf_model_and_tokenizer(self, state_dict: dict[str, torch.Tensor]):
+        auto_model_class = self.get_transformers_auto_model_class()
+        with init_empty_weights():
+            model = auto_model_class.from_config(self.model_config, torch_dtype=torch.bfloat16)
+        model.to_empty(device="cpu")
+        model = self.patch_model_generation_config(model)
+
+        lora_path = self.save_lora_adapter(state_dict)
+        if lora_path:
+            print(f"Saving lora adapter to {lora_path}")
+
+        print(f"Saving model to {self.config.target_dir}")
+        model.save_pretrained(self.config.target_dir, state_dict=state_dict)
+        del state_dict
+        del model
+
+        processor = hf_processor(self.hf_model_config_path)
+        try:
+            tokenizer = hf_tokenizer(self.hf_model_config_path)
+        except Exception as e:
+            warnings.warn(f"Failed to create tokenizer: {e}. This may affect tokenizer saving", stacklevel=1)
+            tokenizer = None
+        if processor is not None:
+            print(f"Saving processor to {self.config.target_dir}")
+            processor.save_pretrained(self.config.target_dir)
+        if tokenizer is not None:
+            print(f"Saving tokenizer to {self.config.target_dir}")
+            tokenizer.save_pretrained(self.config.target_dir)
+
+    def upload_to_huggingface(self):
+        from huggingface_hub import HfApi
+
+        api = HfApi()
+        api.create_repo(repo_id=self.config.hf_upload_path, private=self.config.private, exist_ok=True)
+        api.upload_folder(folder_path=self.config.target_dir, repo_id=self.config.hf_upload_path, repo_type="model")
+
+    @abstractmethod
+    def merge_and_save(self):
+        raise NotImplementedError("Subclasses should implement this method")
+
+
+class FSDPModelMerger(BaseModelMerger):
+    def _get_world_size(self) -> int:
+        """Extracts the FSDP world_size from checkpoint filenames (e.g., 'model_world_size_8_rank_0.pt')."""
+        for filename in os.listdir(self.config.local_dir):
+            match = re.match(r"model_world_size_(\d+)_rank_0\.pt", filename)
+            if match:
+                return int(match.group(1))
+        raise FileNotFoundError(
+            f"Could not determine world size. No file matching 'model_world_size_(\\d+)_rank_0.pt' found in {self.config.local_dir}"
+        )
+
+    def _load_rank_zero_state_dict(self, world_size: int) -> dict:
+        return torch.load(
+            Path(self.config.local_dir) / f"model_world_size_{world_size}_rank_0.pt",
+            map_location="cpu",
+            weights_only=False,
+        )
+
+    def _extract_device_mesh_info(self, state_dict: dict, world_size: int) -> tuple[np.ndarray, tuple[str, ...]]:
+        """
+        Retrieves sharding information (device_mesh, mesh_dim_names) from a DTensor in the state_dict.
+        If no DTensor is found, infers a simple FSDP mesh based on world_size.
+        """
+        pivot_key = sorted(list(state_dict.keys()))[0]
+        weight = state_dict[pivot_key]
+
+        if isinstance(weight, DTensor):
+            # get sharding info
+            device_mesh = weight.device_mesh
+            mesh = device_mesh.mesh
+            mesh_dim_names = device_mesh.mesh_dim_names
+        else:
+            # for non-DTensor
+            mesh = np.array([world_size], dtype=np.int64)
+            mesh_dim_names = ("fsdp",)
+
+        return mesh, mesh_dim_names
+
+    def _calculate_shard_configuration(
+        self, mesh: np.ndarray, mesh_dim_names: tuple[str, ...]
+    ) -> tuple[int, tuple[int, ...]]:
+        """Calculates the total number of shards and the shape of the device mesh."""
+        assert mesh_dim_names in (("fsdp",), ("ddp", "fsdp")), f"Unsupported mesh_dim_names {mesh_dim_names}"
+
+        if "tp" in mesh_dim_names:
+            # TODO: "tp" is not supported yet due to the above assert
+            total_shards = mesh.shape[-1] * mesh.shape[-2]
+            mesh_shape = (mesh.shape[-2], mesh.shape[-1])
+        else:
+            total_shards = mesh.shape[-1]
+            mesh_shape = (mesh.shape[-1],)
+
+        return total_shards, mesh_shape
+
+    def _merge_by_placement(self, tensors: list[torch.Tensor], placement: Placement) -> torch.Tensor:
+        """Merges a list of tensors based on their DTensor placement"""
+        if placement.is_replicate():
+            return tensors[0]
+        elif placement.is_partial():
+            raise NotImplementedError("Partial placement is not supported yet")
+        elif placement.is_shard():
+            return torch.cat(tensors, dim=placement.dim).contiguous()
+
+        raise NotImplementedError(f"Unsupported placement: {placement}")
+
+    def _load_and_merge_state_dicts(
+        self, world_size: int, total_shards: int, mesh_shape: tuple[int, ...], mesh_dim_names: tuple[str, ...]
+    ) -> dict[str, torch.Tensor]:
+        model_state_dict_lst = [None] * total_shards
+
+        def process_one_shard(rank: int, model_state_dict_lst: list):
+            model_path = Path(self.config.local_dir) / f"model_world_size_{world_size}_rank_{rank}.pt"
+            state_dict = torch.load(model_path, map_location="cpu", weights_only=False)
+            model_state_dict_lst[rank] = state_dict
+            return state_dict
+
+        with ThreadPoolExecutor(max_workers=min(32, os.cpu_count())) as executor:
+            futures = [executor.submit(process_one_shard, rank, model_state_dict_lst) for rank in range(total_shards)]
+            for future in tqdm(futures, desc=f"Loading {total_shards} FSDP shards", total=total_shards):
+                future.result()
+
+        # Merge state dicts from all shards
+        state_dict = {}
+        param_placements: dict[str, list] = {}
+
+        for key in set(model_state_dict_lst[0].keys()):
+            state_dict[key] = []
+            for model_state_shard in model_state_dict_lst:
+                # add tensor shard in order of rank to state_dict[key]
+                tensor = model_state_shard.pop(key)
+                if isinstance(tensor, DTensor):
+                    state_dict[key].append(tensor._local_tensor.bfloat16())
+
+                    placements = tuple(tensor.placements)
+                    # replicated placement at dp dimension can be discarded
+                    if mesh_dim_names[0] in ("dp", "ddp"):
+                        placements = placements[1:]
+
+                    if key not in param_placements:
+                        param_placements[key] = placements
+                    else:
+                        assert param_placements[key] == placements
+                else:
+                    state_dict[key].append(tensor.bfloat16())
+
+        del model_state_dict_lst
+
+        # Merge tensors
+        for key in sorted(state_dict):
+            if not isinstance(state_dict[key], list):
+                print(f"No need to merge key {key}")
+                continue
+            if key in param_placements:
+                # merge shards
+                placements: tuple[Shard] = param_placements[key]
+                if len(mesh_shape) == 1:
+                    # 1-D list, FSDP without TP
+                    assert len(placements) == 1
+                    shards = state_dict[key]
+                    state_dict[key] = self._merge_by_placement(shards, placements[0])
+                else:
+                    # 2-D list, FSDP + TP
+                    raise NotImplementedError("FSDP + TP is not supported yet")
+            else:
+                state_dict[key] = torch.cat(state_dict[key], dim=0)
+
+        return state_dict
+
+    def merge_and_save(self):
+        world_size = self._get_world_size()
+        rank_zero_state_dict = self._load_rank_zero_state_dict(world_size)
+
+        mesh, mesh_dim_names = self._extract_device_mesh_info(rank_zero_state_dict, world_size)
+        print(f"Got device mesh {mesh}, mesh_dim_names {mesh_dim_names}")
+
+        total_shards, mesh_shape = self._calculate_shard_configuration(mesh, mesh_dim_names)
+        print(f"Processing model shards with {total_shards} {mesh_shape} in total")
+
+        merged_state_dict = self._load_and_merge_state_dicts(world_size, total_shards, mesh_shape, mesh_dim_names)
+
+        if self.config.operation == "test":
+            if not self.config.test_hf_dir:
+                raise ValueError("test_hf_dir must be provided for test operation")
+            self._test_state_dict(merged_state_dict)
+        elif self.config.operation == "merge":
+            self.save_hf_model_and_tokenizer(merged_state_dict)
+            if self.config.hf_upload:
+                self.upload_to_huggingface()
+        else:
+            raise ValueError(f"Unknown operation: {self.config.operation}")
+
+    def _test_state_dict(self, state_dict: dict[str, torch.Tensor]):
+        auto_model_class = self.get_transformers_auto_model_class()
+
+        hf_model = auto_model_class.from_pretrained(self.config.test_hf_dir, torch_dtype=torch.bfloat16)
+        hf_state_dict = hf_model.state_dict()
+        del hf_model
+
+        hf_model_keys = set(hf_state_dict.keys())
+        collected_keys = set(state_dict.keys())
+
+        missing_keys = hf_model_keys - collected_keys
+        assert len(missing_keys) == 0, f"Missing keys in collected state dict: {list(sorted(missing_keys))}"
+
+        extra_keys = collected_keys - hf_model_keys
+        assert len(extra_keys) == 0, f"Extra keys in collected state dict: {list(sorted(extra_keys))}"
+
+        for key in hf_model_keys:
+            hf_shape = hf_state_dict[key].shape
+            collected_shape = state_dict[key].shape
+            assert hf_shape == collected_shape, (
+                f"Shape mismatch for key '{key}': original {hf_shape} vs collected {collected_shape}"
+            )
+
+            hf_dtype = hf_state_dict[key].dtype
+            collected_dtype = state_dict[key].dtype
+            assert hf_dtype == collected_dtype, (
+                f"Dtype mismatch for key '{key}': original {hf_dtype} vs collected {collected_dtype}"
+            )
+
+            torch.testing.assert_close(hf_state_dict[key], state_dict[key], atol=1e-6, rtol=1e-6)
+
+        print("FSDP checks passed: The merged state_dict matches the hf model saved by FSDPCheckpointManager.")
+
+
+class MegatronModelMerger(BaseModelMerger):
+    def __init__(self, config: ModelMergerConfig):
+        from verl.utils.megatron_utils import get_hf_config_and_tokenizer_checkpoint_path
+
+        config.hf_model_config_path = get_hf_config_and_tokenizer_checkpoint_path(config.local_dir)
+        super().__init__(config)
+
+        self.params_mapping = {
+            # megatron core gpt model name, huggingface model name
+            # NOTICE: It's a little bit tricky, when 2 keys have the same prefix, we need to make sure the longer key within the containing relationship is processed first.
+            "embedding.word_embeddings": "model.embed_tokens",
+            # attn
+            "self_attention.linear_qkv.layer_norm_weight": "input_layernorm.weight",
+            "self_attention.linear_qkv.layer_norm_bias": "input_layernorm.bias",
+            "self_attention.linear_qkv": "self_attn.qkv_proj",
+            "self_attention.q_layernorm": "self_attn.q_norm",
+            "self_attention.k_layernorm": "self_attn.k_norm",
+            "self_attention.linear_proj": "self_attn.o_proj",
+            # mla
+            "self_attention.linear_q_proj": "self_attn.q_proj",
+            "self_attention.linear_q_down_proj": "self_attn.q_a_proj",
+            "self_attention.linear_q_up_proj.layer_norm_weight": "self_attn.q_a_layernorm.weight",
+            "self_attention.linear_q_up_proj": "self_attn.q_b_proj",
+            "self_attention.linear_kv_down_proj": "self_attn.kv_a_proj_with_mqa",
+            "self_attention.linear_kv_up_proj.layer_norm_weight": "self_attn.kv_a_layernorm.weight",
+            "self_attention.linear_kv_up_proj": "self_attn.kv_b_proj",
+            # mlp
+            "pre_mlp_layernorm": "post_attention_layernorm",
+            "mlp.linear_fc1.layer_norm_weight": "post_attention_layernorm.weight",
+            "mlp.linear_fc1.layer_norm_bias": "post_attention_layernorm.bias",
+            "mlp.linear_fc1": "mlp.gate_up_proj",
+            "mlp.linear_fc2": "mlp.down_proj",
+            # moe
+            "mlp.router.expert_bias": "mlp.gate.e_score_correction_bias",
+            "mlp.router": "mlp.gate",
+            "mlp.shared_experts.linear_fc1": "mlp.shared_experts.gate_up_proj",
+            "mlp.shared_experts.linear_fc2": "mlp.shared_experts.down_proj",
+            "linear_fc1": "gate_up_proj",
+            "linear_fc2": "down_proj",
+            # output
+            "final_layernorm": "norm",
+            "output_layer": "lm_head",
+        }
+
+    def _get_tp_pp_rank_from_sharded_dir(self, sharded_dir: str) -> tuple[int, int]:
+        tp_rank = pp_rank = None
+        rank_list = sharded_dir.split("_")[2:]
+        if re.match(r"mp_rank_(\d\d)_(\d\d\d)", sharded_dir):
+            tp_rank = int(rank_list[0])
+            pp_rank = int(rank_list[1])
+        elif re.match(r"mp_rank_(\d\d)", sharded_dir):
+            tp_rank = int(rank_list[0])
+            pp_rank = 0
+
+        assert tp_rank is not None and pp_rank is not None, f"Invalid sharded dir {sharded_dir}"
+
+        return tp_rank, pp_rank
+
+    def _check_megatron_checkpoint_path(self, model_path: str) -> tuple[list[str], int, int]:
+        """
+        Validates the Megatron checkpoint structure (presence of 'model.pt' in sharded directories).
+        Determines TP and PP sizes from directory names.
+        """
+        tp_size = 0
+        pp_size = 0
+        sharded_dirs = sorted(os.listdir(model_path))
+        for sharded_dir in sharded_dirs:
+            assert "model.pt" in os.listdir(Path(model_path) / sharded_dir), f"model.pt not found in {sharded_dir}"
+            tp_rank, pp_rank = self._get_tp_pp_rank_from_sharded_dir(sharded_dir)
+            tp_size = max(tp_size, tp_rank + 1)
+            pp_size = max(pp_size, pp_rank + 1)
+        return sharded_dirs, tp_size, pp_size
+
+    def _merge_across_tp(
+        self,
+        key: str,
+        tp_data: list[torch.Tensor],
+        config: PretrainedConfig,
+        tp_size: int,
+        is_value_model: bool = False,
+    ) -> Union[torch.Tensor, list[torch.Tensor]]:
+        if "linear_fc1.weight" in key:
+            # if the tensor is gate and proj
+            gate_lst = []
+            up_lst = []
+            for infer_param in tp_data:
+                gate, up = infer_param.chunk(2)
+                gate_lst.append(gate)
+                up_lst.append(up)
+            gate = torch.cat(gate_lst, dim=0)
+            up = torch.cat(up_lst, dim=0)
+            return [gate, up]
+        elif "self_attention.linear_qkv." in key and "layer_norm" not in key:
+            # if the tensor is qkv, for each param on tp, split into q, k, v
+            # concat q, k, v separately.
+            q_lst = []
+            k_lst = []
+            v_lst = []
+            assert config.num_attention_heads % config.num_key_value_heads == 0
+            num_q_per_kv = config.num_attention_heads // config.num_key_value_heads
+            assert tp_data[0].shape[0] % (num_q_per_kv + 2) == 0
+            kv_size_per_tp = tp_data[0].shape[0] // (num_q_per_kv + 2)
+            split_size = [kv_size_per_tp * num_q_per_kv, kv_size_per_tp, kv_size_per_tp]
+
+            for infer_param in tp_data:
+                num_query_groups_per_partition = config.num_key_value_heads // tp_size
+                for chunk in infer_param.chunk(num_query_groups_per_partition):
+                    split_size = [
+                        kv_size_per_tp * num_q_per_kv // num_query_groups_per_partition,
+                        kv_size_per_tp // num_query_groups_per_partition,
+                        kv_size_per_tp // num_query_groups_per_partition,
+                    ]
+                    q, k, v = chunk.split(split_size)
+                    q_lst.append(q)
+                    k_lst.append(k)
+                    v_lst.append(v)
+
+            q = torch.cat(q_lst, dim=0)
+            k = torch.cat(k_lst, dim=0)
+            v = torch.cat(v_lst, dim=0)
+            return [q, k, v]
+        elif "layer_norm" in key or "layernorm" in key or "router" in key or ("output_layer" in key and is_value_model):
+            return tp_data[0]
+        else:
+            dim = 0
+            if "linear_fc2.weight" in key or "self_attention.linear_proj" in key:
+                dim = 1
+            return torch.cat(tp_data, dim=dim)
+
+    def _load_state_dicts(
+        self, model_ckpt_path: str, sharded_dirs: list[str], tp_size: int, pp_size: int
+    ) -> list[list[dict]]:
+        model_state_dict_lst = [[None for _ in range(tp_size)] for _ in range(pp_size)]
+
+        def _process_one_megatron_shard(sharded_dir: str):
+            model_file_path = Path(model_ckpt_path) / sharded_dir / "model.pt"
+            state_dict = torch.load(model_file_path, map_location="cpu", weights_only=False)
+            tp_rank, pp_rank = self._get_tp_pp_rank_from_sharded_dir(sharded_dir)
+            model_state_dict_lst[pp_rank][tp_rank] = state_dict
+
+        with ThreadPoolExecutor(max_workers=min(32, os.cpu_count())) as executor:
+            futures = [executor.submit(_process_one_megatron_shard, sharded_dir) for sharded_dir in sharded_dirs]
+            for future in tqdm(futures, desc=f"Loading {len(sharded_dirs)} Megatron shards", total=len(sharded_dirs)):
+                future.result()
+
+        return model_state_dict_lst
+
+    def _check_megatron_state_key(self, key: str) -> bool:
+        """
+        Checks if the key is a valid Megatron state key.
+
+        Now the model merger only supports keys that start with "decoder/embedding/output_layer" in TransformerLayer.
+        Shall not use key starts with "model."
+        """
+        if key.startswith("model."):
+            raise ValueError(
+                f"Invalid key {key} in Megatron state_dict. Expected keys to start with 'decoder/embedding/output_layer' in TransformerLayer."
+            )
+
+        skip_checking_keys = ["embedding.word_embeddings", "output_layer"]
+        for skip_key in skip_checking_keys:
+            if skip_key in key:
+                print(f"skip checking key {key}")
+                return
+
+        # Exclude extra state keys
+        if not key.startswith("decoder"):
+            raise ValueError(
+                f"Invalid key {key} in Megatron state_dict. Expected keys to start with 'decoder' in TransformerLayer."
+            )
+
+    def _merge_state_dicts(
+        self, model_state_dict_lst: list[list[dict]], tp_size: int, pp_size: int
+    ) -> dict[str, torch.Tensor]:
+        state_dict = {}
+        vpp_size = len(model_state_dict_lst[0][0])
+        layers_cum = 0
+
+        for vpp_rank in range(vpp_size):
+            for pp_rank in range(pp_size):
+                layers_handled = 0
+                keys = model_state_dict_lst[pp_rank][0][vpp_rank].keys()
+                for key in keys:
+                    if "extra_state" in key:
+                        continue
+                    if self.config.tie_word_embedding and ("output_layer" in key):
+                        print("skip lm_head and reward_head loading because of tie_word_embeddings")
+                        continue
+
+                    self._check_megatron_state_key(key)
+                    hf_name = self._replace_name(key, self.params_mapping)
+                    assert hf_name is not None, f"Failed to convert layer name [{key}] from megatron to huggingface."
+                    if "model.layers." in hf_name:
+                        local_layer_no = int(hf_name.split(".")[2])
+                        layers_handled = max(local_layer_no, layers_handled)
+                        global_layer_no = local_layer_no + layers_cum
+                        new_key_list = hf_name.split(".")
+                        new_key_list[2] = str(global_layer_no)
+                        hf_name = ".".join(new_key_list)
+                    else:
+                        warnings.warn(f"hf_name {hf_name} will not be fixed with layer number", stacklevel=2)
+
+                    tp_data = [model_state_dict_lst[pp_rank][tp_rank][vpp_rank][key] for tp_rank in range(tp_size)]
+                    merged = self._merge_across_tp(key, tp_data, self.model_config, tp_size, self.config.is_value_model)
+
+                    if not isinstance(merged, list):
+                        state_dict[hf_name] = merged
+                    elif len(merged) == 3:
+                        # split qkv
+                        for n, d in zip(["q", "k", "v"], merged):
+                            state_dict[hf_name.replace("qkv", n)] = d
+                    elif len(merged) == 2:
+                        # split gate up
+                        state_dict[hf_name.replace("gate_up", "gate")] = merged[0]
+                        state_dict[hf_name.replace("gate_up", "up")] = merged[1]
+                    print(
+                        f"converted {key} to {hf_name} with shape {merged.shape if isinstance(merged, torch.Tensor) else [t.shape for t in merged]}"
+                    )
+
+                layers_cum += layers_handled + 1  # zero based
+
+        return state_dict
+
+    def merge_and_save(self):
+        from verl.utils.megatron_utils import get_model_checkpoint_path
+
+        model_ckpt_path = get_model_checkpoint_path(self.config.local_dir)
+        sharded_dirs, tp_size, pp_size = self._check_megatron_checkpoint_path(model_ckpt_path)
+        print(f"sharded_dirs: {sharded_dirs}, tp_size: {tp_size}, pp_size: {pp_size}, mp_size: {len(sharded_dirs)}")
+
+        model_state_dict_lst = self._load_state_dicts(model_ckpt_path, sharded_dirs, tp_size, pp_size)
+        merged_state_dict = self._merge_state_dicts(model_state_dict_lst, tp_size, pp_size)
+        del model_state_dict_lst
+
+        if self.config.operation == "test":
+            if not self.config.test_hf_dir:
+                raise ValueError("test_hf_dir must be provided for test operation")
+            self._test_state_dict(merged_state_dict)
+        elif self.config.operation == "merge":
+            self.save_hf_model_and_tokenizer(merged_state_dict)
+            if self.config.hf_upload:
+                self.upload_to_huggingface()
+        else:
+            raise ValueError(f"Unknown operation: {self.config.operation}")
+
+    def _test_state_dict(self, state_dict: dict[str, torch.Tensor]):
+        """
+        Compares the merged Megatron state_dict against a reference safetensors model.
+        Applies necessary name mappings from Megatron to Hugging Face conventions using _replace_name.
+        """
+        ref_state_dict = load_file(Path(self.config.test_hf_dir) / "model.safetensors")
+
+        for name, loaded_weight in state_dict.items():
+            # name = self._replace_name(original_name, self.params_mapping)
+            if not name or name.endswith(".bias") and name not in ref_state_dict:
+                continue
+            if "rotary_emb.inv_freq" in name:
+                continue
+            if self.config.tie_word_embedding and "lm_head.weight" in name:
+                continue
+            if name not in ref_state_dict:
+                raise RuntimeError(f"key: {name} not exist in state_dict")
+            param = ref_state_dict[name]
+            assert loaded_weight.dtype == param.dtype
+            torch.testing.assert_close(loaded_weight, param, atol=1e-2, rtol=5e-2)
+
+    def _replace_name(self, megatron_name: str, name_mapping: dict[str, str]) -> str:
+        for m_name, v_name in name_mapping.items():
+            if m_name not in megatron_name:
+                continue
+
+            megatron_name = megatron_name.replace("decoder", "model")
+            param_name = megatron_name.replace(m_name, v_name)
+            return param_name
+
+        return None  # Return None if no mapping found
+
+
+def main():
+    parser = argparse.ArgumentParser(description="verl model merger")
+    subparsers = parser.add_subparsers(dest="operation", required=True, help="Specify 'merge' or 'test' operation.")
+
+    base_op_parser = argparse.ArgumentParser(add_help=False)
+    base_op_parser.add_argument(
+        "--backend", type=str, required=True, choices=["fsdp", "megatron"], help="The backend of the model"
+    )
+    base_op_parser.add_argument("--local_dir", type=str, required=True, help="Path to the saved model checkpoints")
+    base_op_parser.add_argument(
+        "--hf_model_path",
+        type=str,
+        default=None,
+        help="(Deprecated) Path to the original Hugging Face model for config.",
+    )
+    base_op_parser.add_argument(
+        "--tie-word-embedding",
+        action="store_true",
+        help="Whether to tie word embedding weights (currently only Megatron supported)",
+    )
+    base_op_parser.add_argument(
+        "--is-value-model",
+        action="store_true",
+        help="Whether the model is a value model (currently only Megatron supported)",
+    )
+
+    merge_parser = subparsers.add_parser("merge", parents=[base_op_parser], help="Merge model checkpoints and save.")
+    merge_parser.add_argument(
+        "--target_dir", default="tmp", type=str, help="Directory to save the merged huggingface model"
+    )
+    merge_parser.add_argument(
+        "--hf_upload_path", default=None, type=str, help="Hugging Face repository ID to upload the model"
+    )
+    merge_parser.add_argument(
+        "--private", action="store_true", help="Whether to upload the model to a private Hugging Face repository"
+    )
+
+    test_parser = subparsers.add_parser(
+        "test", parents=[base_op_parser], help="Test merged model against a reference Hugging Face model"
+    )
+    test_parser.add_argument(
+        "--test_hf_dir", type=str, required=True, help="Path to the reference Hugging Face model directory for testing"
+    )
+
+    args = parser.parse_args()
+
+    common_config_args = {
+        "operation": args.operation,
+        "backend": args.backend,
+        "tie_word_embedding": args.tie_word_embedding,
+        "is_value_model": args.is_value_model,
+        "local_dir": args.local_dir,
+        "hf_model_path": args.hf_model_path,
+        "hf_model_config_path": args.local_dir,
+    }
+
+    if args.operation == "merge":
+        config = ModelMergerConfig(
+            **common_config_args,
+            target_dir=args.target_dir,
+            hf_upload_path=args.hf_upload_path,
+            private=args.private,
+            test_hf_dir=None,
+        )
+        os.makedirs(config.target_dir, exist_ok=True)
+    elif args.operation == "test":
+        config = ModelMergerConfig(
+            **common_config_args,
+            test_hf_dir=args.test_hf_dir,
+            # the following args are not used by test operation
+            target_dir=None,
+            hf_upload_path=None,
+            private=False,
+        )
+    else:
+        raise NotImplementedError(f"Unknown operation: {args.operation}")
+
+    if config.backend == "fsdp":
+        merger = FSDPModelMerger(config)
+    elif config.backend == "megatron":
+        merger = MegatronModelMerger(config)
+    else:
+        raise NotImplementedError(f"Unknown backend: {config.backend}")
+
+    merger.merge_and_save()
+
+
+if __name__ == "__main__":
+    main()
diff --git a/code/RL_model/verl/verl_train/scripts/megatron_merge_lora.py b/code/RL_model/verl/verl_train/scripts/megatron_merge_lora.py
new file mode 100644
index 0000000000000000000000000000000000000000..7dba69d6628625b16598e4f3a73c5a627e512a71
--- /dev/null
+++ b/code/RL_model/verl/verl_train/scripts/megatron_merge_lora.py
@@ -0,0 +1,114 @@
+# Copyright 2025 Bytedance Ltd. and/or its affiliates
+# Copyright (c) 2025, NVIDIA CORPORATION. All rights reserved.
+#
+# Licensed under the Apache License, Version 2.0 (the "License");
+# you may not use this file except in compliance with the License.
+# You may obtain a copy of the License at
+#
+#     http://www.apache.org/licenses/LICENSE-2.0
+#
+# Unless required by applicable law or agreed to in writing, software
+# distributed under the License is distributed on an "AS IS" BASIS,
+# WITHOUT WARRANTIES OR CONDITIONS OF ANY KIND, either express or implied.
+# See the License for the specific language governing permissions and
+# limitations under the License.
+
+import os
+from pprint import pprint
+
+import hydra
+import ray
+import torch
+from omegaconf import OmegaConf
+
+from verl.single_controller.base.decorator import Dispatch, register
+from verl.single_controller.ray import RayClassWithInitArgs, RayResourcePool, RayWorkerGroup
+from verl.utils.megatron_utils import get_hf_model_checkpoint_path, load_megatron_model_to_gpu
+from verl.workers.megatron_workers import ActorRolloutRefWorker
+
+os.environ["NCCL_DEBUG"] = "WARN"
+os.environ["TOKENIZERS_PARALLELISM"] = "true"
+
+
+class CustomSaveWorker(ActorRolloutRefWorker):
+    @register(dispatch_mode=Dispatch.ONE_TO_ALL)
+    def save_merged_weights(self, hf_ckpt_path):
+        import os
+
+        if self._is_offload_param:
+            load_megatron_model_to_gpu(self.actor_module)
+
+        torch.distributed.barrier()
+
+        print(f"[Rank {os.environ.get('RANK', '?')}] Saving weights to {hf_ckpt_path}...")
+
+        if self.vanilla_bridge:
+            self.bridge.save_weights(
+                self.actor_module, hf_ckpt_path, distributed_filesystem=True, memory_efficient=True
+            )
+        else:
+            self.bridge.save_hf_weights(self.actor_module, hf_ckpt_path)
+
+        return True
+
+
+@hydra.main(config_path="../verl/trainer/config", config_name="ppo_megatron_trainer", version_base=None)
+def main(config):
+    assert config.actor_rollout_ref.model.lora.adapter_path is not None, "adapter_path must be specified"
+
+    if (
+        config.actor_rollout_ref.actor.optim.lr_decay_steps is None
+        or config.actor_rollout_ref.actor.optim.lr_decay_steps < 1
+    ):
+        # set to bypass OptimizerParamScheduler checks
+        config.actor_rollout_ref.actor.optim.lr_decay_steps = 100000
+
+    run_merge(config)
+
+
+def run_merge(config) -> None:
+    if not ray.is_initialized():
+        # this is for local ray cluster
+        default_runtime_env = {"env_vars": {"TOKENIZERS_PARALLELISM": "true", "NCCL_DEBUG": "WARN"}}
+        ray_init_kwargs = config.ray_kwargs.get("ray_init", {})
+        runtime_env_kwargs = ray_init_kwargs.get("runtime_env", {})
+        runtime_env = OmegaConf.merge(default_runtime_env, runtime_env_kwargs)
+        ray_init_kwargs = OmegaConf.create({**ray_init_kwargs, "runtime_env": runtime_env})
+        print(f"ray init kwargs: {ray_init_kwargs}")
+        ray.init(**OmegaConf.to_container(ray_init_kwargs))
+
+    ray.get(main_task.remote(config))
+
+
+@ray.remote(num_cpus=1)
+def main_task(config):
+    pprint(OmegaConf.to_container(config, resolve=True))  # resolve=True will eval symbol values
+    OmegaConf.resolve(config)
+
+    ray_cls_with_init = RayClassWithInitArgs(
+        cls=ray.remote(CustomSaveWorker), config=config.actor_rollout_ref, role="actor"
+    )
+    resource_pool = RayResourcePool(process_on_nodes=[config.trainer.n_gpus_per_node] * config.trainer.nnodes)
+
+    worker = RayWorkerGroup(
+        resource_pool=resource_pool,
+        ray_cls_with_init=ray_cls_with_init,
+        device_name=config.trainer.device,
+    )
+    worker.init_model()
+
+    adapter_path = config.actor_rollout_ref.model.lora.adapter_path
+    hf_ckpt_path = get_hf_model_checkpoint_path(os.path.dirname(adapter_path))
+    worker.save_merged_weights(hf_ckpt_path)
+
+
+if __name__ == "__main__":
+    """
+    Use the same config as your training script, besides **specifying the adapter_path**.
+
+    For example, your training script starts with: 
+        `python3 -m verl.trainer.main_ppo --config-name=ppo_megatron_trainer ...`
+    Now replace it with 
+        `python3 ./scripts/megatron_merge_lora.py --config-name=ppo_megatron_trainer ...`
+    """
+    main()
diff --git a/code/RL_model/verl/verl_train/scripts/print_cfg.py b/code/RL_model/verl/verl_train/scripts/print_cfg.py
new file mode 100644
index 0000000000000000000000000000000000000000..287756fb1b7dbaac84b5f7ec572ba7a172e347b3
--- /dev/null
+++ b/code/RL_model/verl/verl_train/scripts/print_cfg.py
@@ -0,0 +1,35 @@
+# Copyright 2025 Bytedance Ltd. and/or its affiliates
+
+# Licensed under the Apache License, Version 2.0 (the "License");
+# you may not use this file except in compliance with the License.
+# You may obtain a copy of the License at
+#
+#     http://www.apache.org/licenses/LICENSE-2.0
+#
+# Unless required by applicable law or agreed to in writing, software
+# distributed under the License is distributed on an "AS IS" BASIS,
+# WITHOUT WARRANTIES OR CONDITIONS OF ANY KIND, either express or implied.
+# See the License for the specific language governing permissions and
+# limitations under the License.
+try:
+    import hydra
+except ImportError as e:
+    raise ImportError("Please install hydra-core via 'pip install hydra-core' and retry.") from e
+
+
+@hydra.main(config_path="../verl/trainer/config", config_name="ppo_trainer", version_base=None)
+def main(config):
+    """Main entry point for PPO training with Hydra configuration management.
+
+    Args:
+        config_dict: Hydra configuration dictionary containing training parameters.
+    """
+    print(config)
+    from verl.utils.config import omega_conf_to_dataclass
+
+    profiler_config = omega_conf_to_dataclass(config.critic.profiler)
+    print(profiler_config)
+
+
+if __name__ == "__main__":
+    main()
diff --git a/code/RL_model/verl/verl_train/scripts/rollout_viewer.py b/code/RL_model/verl/verl_train/scripts/rollout_viewer.py
new file mode 100644
index 0000000000000000000000000000000000000000..eb0314edc56f7f3ad0ce719b5ee0ffb4f241d4d3
--- /dev/null
+++ b/code/RL_model/verl/verl_train/scripts/rollout_viewer.py
@@ -0,0 +1,565 @@
+# Copyright 2025 Bytedance Ltd. and/or its affiliates
+# Copyright (c) 2025, NVIDIA CORPORATION. All rights reserved.
+#
+# Licensed under the Apache License, Version 2.0 (the "License");
+# you may not use this file except in compliance with the License.
+# You may obtain a copy of the License at
+#
+#     http://www.apache.org/licenses/LICENSE-2.0
+#
+# Unless required by applicable law or agreed to in writing, software
+# distributed under the License is distributed on an "AS IS" BASIS,
+# WITHOUT WARRANTIES OR CONDITIONS OF ANY KIND, either express or implied.
+# See the License for the specific language governing permissions and
+# limitations under the License.
+
+import asyncio
+import re
+import traceback
+from pathlib import Path
+from typing import Annotated, Optional
+
+import aiofiles
+
+try:
+    import ujson as json
+except ImportError:
+    import json
+import typer
+from rich.highlighter import ReprHighlighter
+from rich.markdown import Markdown
+from rich.table import Table
+from rich.text import Text
+from textual import on
+from textual.app import App, ComposeResult
+from textual.containers import Horizontal, Vertical, VerticalScroll
+from textual.widgets import Input, ProgressBar, Select, SelectionList, Static
+
+INDEX_KEY = "__IDX"
+FILE_SUFFIX = ".jsonl"
+
+
+def check_textual_version():
+    # check if textual version is equal to 0.52.1
+    import textual
+    from packaging.version import Version
+
+    if Version(textual.__version__) != Version("0.52.1"):
+        raise ImportError(f"Textual version {textual.__version__} is not supported, please pip install textual==0.52.1")
+
+
+check_textual_version()
+
+
+async def load_path(p: Path, data: dict, mask_strs: str, idx: int, pbar):
+    samples = []
+    async with aiofiles.open(p, encoding="utf-8") as f:
+        async for line in f:
+            d = json.loads(line)
+            for k in d:
+                if isinstance(d[k], str):
+                    if mask_strs:
+                        d[k] = re.sub(rf"{mask_strs}", "*", d[k])
+                else:
+                    d[k] = json.dumps(d[k], ensure_ascii=False, indent=4)
+
+            d[INDEX_KEY] = len(samples)
+            samples.append(d)
+        data[idx] = {"samples": samples}
+
+    print(f"path {p} loaded")
+    pbar.advance(1)
+
+
+async def load_dir(path: Path, data: dict[int, dict], pbar, mask_strs: str = ""):
+    paths = list(path.glob(f"*{FILE_SUFFIX}"))
+    paths = sorted(paths, key=lambda x: int(x.stem))
+
+    tasks = [load_path(p, data, mask_strs, i, pbar) for i, p in enumerate(paths)]
+
+    await asyncio.gather(*tasks)
+
+
+class Highlighter(ReprHighlighter):
+    highlights = ReprHighlighter.highlights + [
+        r"(?P<tag_name>[][\<\>{}()\|（）【】\[\]=`])",
+        r"\<\|(?P<tag_name>[\w\W]*?)\|\>",
+    ]
+
+
+def center_word_with_equals_exactly(word: str, total_length: int, char: str = "=") -> str:
+    if len(word) > total_length:
+        return word
+
+    padding = total_length - len(word)
+    left_pad = (padding) // 2
+    right_pad = (padding + 1) // 2
+    return char * left_pad + " " + word + " " + char * right_pad
+
+
+def highlight_keyword(content: str, keyword: Optional[str]):
+    if not keyword:
+        return Text(content)
+    text = Text()
+    parts = content.split(keyword)
+    for i, part in enumerate(parts):
+        text.append(part, style=None)
+        if i < len(parts) - 1:
+            # text.append(keyword, style=Style(color="#d154d1", bgcolor="yellow", bold=True))
+            text.append(keyword, style="on #8f51b5")
+    return text
+
+
+help_doc = """
+⌨️   keybinds：
+
+- `f/esc`: find/cancel
+- `tab/←/→`: change focus
+- `j/k`: page down/up
+- `g/G`: scroll home/end
+- `n/N`: next sample/step
+- `p/P`: previous sample/step
+- `s`: switch display mode
+  - plain text
+  - rich table
+
+"""
+
+
+class JsonLineViewer(App):
+    BINDINGS = [
+        ("left", "focus_previous", "Focus Previous"),
+        ("right", "focus_next", "Focus Next"),
+        ("s", "swith_render", "switch render"),
+        # control
+        ("n", "next_sample", "Next Sample"),
+        ("N", "next_step", "Next Step"),
+        ("p", "previous_sample", "Previous Sample"),
+        ("P", "previous_step", "Previous Step"),
+        # search
+        ("f", "toggle_search", "find"),
+        ("enter", "next_search", "find next"),
+        ("escape", "cancel_search", "cancel find"),
+        # scroll
+        ("j", "page_down", "page down"),
+        ("k", "page_up", "page up"),
+        ("g", "page_home", "page home"),
+        ("G", "page_end", "page end"),
+    ]
+
+    CSS = """
+
+    Select:focus > SelectCurrent {
+        border: tall #8f51b5;
+    }
+    Select.-expanded > SelectCurrent {
+        border: tall #8f51b5;
+    }
+    #select-container {
+        width: 15%;
+        height: 100%;
+        align: center top;
+    }
+    #search-container {
+        height: 10%;
+        align: center top;
+    }
+    #search-box {
+        width: 50%;
+    }
+    #reqid-box {
+        width: 50%;
+    }
+    """
+
+    def __init__(self, step_num: int, data: dict[int, dict], pbar):
+        super().__init__()
+        self.step_num = step_num
+
+        self.data = data
+        self.render_table = False
+        self.selected_step_index = 0
+        self.selected_sample_index = 0
+        self.pbar = pbar
+
+        self.matches = []
+        self.current_match_index = 0
+
+        self.highlighter = Highlighter()
+
+        first_samples = data[list(data.keys())[0]]["samples"]
+        # Prepare the initial field filter list (all keys from the first sample)
+        self.filter_fields = [(f, f, True) for f in first_samples[0].keys()]
+
+        # Internal set used for fast membership checks when we add new fields on the fly.
+        # We keep it here so that when new columns appear in later steps (e.g. `request_id`),
+        # they can be added to the UI automatically without restarting the viewer.
+        self._field_set: set[str] = set(first_samples[0].keys())
+        self.sample_num = len(first_samples)
+
+    def compose(self) -> ComposeResult:
+        with Horizontal(id="search-container"):
+            yield Input(placeholder="find something...", id="search-box")
+            yield Input(placeholder="request id...", id="reqid-box")
+            with Vertical(id="search-container2"):
+                yield self.pbar
+                yield Static("", id="search-status")
+
+        with Horizontal():
+            with Vertical(id="select-container"):
+                yield Static("\n")
+                yield Static(
+                    renderable=Markdown(
+                        help_doc,
+                    ),
+                    markup=False,
+                )
+                yield Static("\n")
+                yield Select(
+                    id="step-select",
+                    value=0,
+                    prompt="select step",
+                    options=[("step: 1", 0)],
+                    allow_blank=False,
+                )
+                yield Select(
+                    id="sample-select",
+                    value=0,
+                    prompt="select sample",
+                    options=[("sample: 1", 0)],
+                    allow_blank=False,
+                )
+                yield Select(
+                    id="sample-sort",
+                    value=0,
+                    prompt="排序",
+                    options=[
+                        ("sort", 0),
+                        ("score asc", 1),
+                        ("score desc", 2),
+                    ],
+                    allow_blank=False,
+                )
+
+                yield SelectionList[int](("Select ALL", 1, True), id="fields-select-all")
+                with VerticalScroll(id="scroll-view2"):
+                    yield SelectionList[str](*self.filter_fields, id="fields-select")
+            with VerticalScroll(id="scroll-view"):
+                yield Static(id="content", markup=False)
+
+    async def on_mount(self) -> None:
+        self.step_select = self.query_one("#step-select", Select)
+        self.sample_select = self.query_one("#sample-select", Select)
+        self.sample_sort = self.query_one("#sample-sort", Select)
+        self.content_display = self.query_one("#content", Static)
+        self.search_box = self.query_one("#search-box", Input)
+        self.reqid_box = self.query_one("#reqid-box", Input)
+        self.scroll_view = self.query_one("#scroll-view", VerticalScroll)
+        self.search_status = self.query_one("#search-status", Static)
+        self.fields_select = self.query_one("#fields-select", SelectionList)
+        self.fields_select.border_title = "field filter"
+
+        if self.data:
+            self.step_select.set_options([(f"step: {i + 1}", i) for i in range(self.step_num)])
+            self.sample_select.set_options([(f"sample: {i + 1}", i) for i in range(self.sample_num)])
+            self.step_select.focus()
+            await self.update_content()
+
+    def update_result_options(self, offset: int = 0, sort_desc: Optional[bool] = None):
+        options = []
+        if isinstance(self.selected_step_index, int) and self.selected_step_index < len(self.data):
+            if self.sample_num is None or sort_desc is not None:
+                samples = self.data[self.selected_step_index].get("samples", [])
+                if not samples:
+                    self.selected_sample_index = offset
+                    return
+                if sort_desc is not None:
+                    samples = sorted(
+                        samples,
+                        key=lambda x: x.get("score", x.get("score_1", 0)),
+                        reverse=sort_desc,
+                    )
+
+                options = [(f"sample: {r[INDEX_KEY] + 1}", r[INDEX_KEY]) for r in samples]
+                self.sample_select.set_options(options)
+                self.sample_num = len(samples)
+
+            if sort_desc is not None and options:
+                self.selected_sample_index = options[0][1]
+            else:
+                self.selected_sample_index = offset
+
+    async def update_content(self, search_keyword: Optional[str] = None):
+        content = ""
+        try:
+            samples = self.data[self.selected_step_index].get("samples", [])
+            content_dict_full = samples[self.selected_sample_index]
+
+            # Dynamically track any NEW keys that appear and add them to the field filter.
+            self._update_fields_select(content_dict_full.keys())
+
+            # Apply field selection filter (only show selected fields)
+            content_dict = {k: v for k, v in content_dict_full.items() if k in self.fields_select.selected}
+            if self.render_table:
+                content = Table("key", "value", show_lines=True)
+                for k in content_dict:
+                    v = content_dict[k]
+                    v = f"{v}"
+                    content.add_row(
+                        k,
+                        self.highlighter(highlight_keyword(v, search_keyword)),
+                    )
+            else:
+                text = Text()
+                for k in content_dict:
+                    v = content_dict[k]
+                    s = center_word_with_equals_exactly(k, 64) + f"\n{v}\n"
+                    text.append(highlight_keyword(s, search_keyword))
+                content = self.highlighter(text)
+        except KeyError:
+            content = f"Loading data asynchronously, progress: {len(self.data)}/{self.step_num} step"
+
+        except Exception:
+            content = self.highlighter(traceback.format_exc())
+
+        self.content_display.update(content)
+
+    # ---------------------------------------------------------------------
+    # Request-ID jump logic
+    # ---------------------------------------------------------------------
+
+    @on(Input.Submitted, "#reqid-box")
+    async def on_reqid_submitted(self, event: Input.Submitted) -> None:
+        """Jump to the sample that has a matching `request_id`."""
+
+        req_id_raw = event.value.strip()
+        # Remove hyphens so search is tolerant to different id formats
+        req_id = req_id_raw.replace("-", "")
+        if not req_id:
+            return
+
+        found = False
+        for step_idx, step_data in self.data.items():
+            for sample in step_data.get("samples", []):
+                sample_id = str(sample.get("request_id", ""))
+                if sample_id.replace("-", "") == req_id:
+                    # Update selected indices
+                    self.selected_step_index = step_idx
+                    self.step_select.value = step_idx
+
+                    # Ensure sample list is updated and select sample
+                    self.update_result_options(offset=sample[INDEX_KEY])
+                    self.selected_sample_index = sample[INDEX_KEY]
+                    self.sample_select.value = sample[INDEX_KEY]
+
+                    await self._clear_search()
+                    await self.update_content()
+
+                    found = True
+                    break
+            if found:
+                break
+
+        if not found:
+            self.search_status.update(Text(f"request_id '{req_id_raw}' not found", style="bold red"))
+        else:
+            # Keep the typed id in the input box so users see what was searched.
+            pass
+
+    # ---------------------------------------------------------------------
+    # Helper: add new fields to SelectionList on-the-fly
+    # ---------------------------------------------------------------------
+
+    def _update_fields_select(self, keys):
+        """Add any unseen *keys* to the field-selection widget so they can be toggled.
+
+        The viewer is often launched with only the first step loaded. Later steps may
+        introduce new columns (e.g. `request_id`). This helper ensures those fields
+        become visible without requiring a restart.
+        """
+        # Ensure we have the widget (only after on_mount)
+        if not hasattr(self, "fields_select"):
+            return
+
+        for k in keys:
+            if k not in self._field_set:
+                self._field_set.add(k)
+                try:
+                    # By default, new fields are selected so they appear immediately.
+                    self.fields_select.add_option(k, k, selected=True)
+                except Exception:
+                    # Fallback for older textual versions where signature is different.
+                    self.fields_select.add_option((k, k, True))
+
+    @on(Select.Changed, "#step-select")
+    async def step_changed(self, event):
+        self.selected_step_index = event.value
+        self.update_result_options()
+        await self.update_content()
+
+    @on(Select.Changed, "#sample-select")
+    async def sample_changed(self, event):
+        self.selected_sample_index = event.value
+        await self._clear_search()
+        await self.update_content()
+
+    @on(Select.Changed, "#sample-sort")
+    async def sort_changed(self, event):
+        v = event.value
+        self.update_result_options(sort_desc=None if v == 0 else False if v == 1 else True)
+        await self.update_content()
+
+    @on(SelectionList.SelectedChanged, "#fields-select")
+    async def fields_changed(self, event):
+        await self.update_content()
+
+    @on(SelectionList.SelectedChanged, "#fields-select-all")
+    async def fields_all_changed(self, event):
+        s = self.query_one("#fields-select-all", SelectionList)
+        if s.selected:
+            self.fields_select.select_all()
+        else:
+            self.fields_select.deselect_all()
+
+    def action_focus_previous(self):
+        self.screen.focus_previous()
+
+    def action_focus_next(self):
+        self.screen.focus_next()
+
+    async def action_next_step(self) -> None:
+        self.selected_step_index += 1
+        if self.selected_step_index >= self.step_num:
+            self.selected_step_index = 0
+        self.step_select.value = self.selected_step_index
+        self.update_result_options()
+        await self.update_content()
+
+    async def action_next_sample(self) -> None:
+        self.selected_sample_index += 1
+        if not self.sample_num or self.selected_sample_index >= self.sample_num:
+            self.selected_sample_index = 0
+        self.sample_select.value = self.selected_sample_index
+        await self._clear_search()
+        await self.update_content()
+
+    async def action_previous_step(self) -> None:
+        self.selected_step_index -= 1
+        if self.selected_step_index < 0:
+            self.selected_step_index = self.step_num - 1
+        self.step_select.value = self.selected_step_index
+        self.update_result_options()
+        await self.update_content()
+
+    async def action_previous_sample(self) -> None:
+        self.selected_sample_index -= 1
+        if self.selected_sample_index < 0:
+            self.selected_sample_index = self.sample_num - 1
+        self.sample_select.value = self.selected_sample_index
+        await self._clear_search()
+        await self.update_content()
+
+    async def action_swith_render(self):
+        self.render_table = not self.render_table
+        await self.update_content()
+
+    def action_toggle_search(self) -> None:
+        self.search_box.focus()
+
+    async def action_cancel_search(self) -> None:
+        self.search_box.value = ""
+        await self._clear_search()
+        await self.update_content()
+
+    async def _clear_search(self):
+        self.matches = []
+        self.search_status.update("")
+        self.current_match_index = 0
+
+    @on(Input.Submitted, "#search-box")
+    async def on_search_submitted(self, event: Input.Submitted) -> None:
+        self.matches = []
+        self.current_match_index = 0
+        if event.value:
+            await self.update_content(event.value)
+            renderable = self.content_display.render()
+            if isinstance(renderable, Table):
+                return
+
+            assert isinstance(renderable, Text)
+            console = self.content_display._console
+            lines = renderable.wrap(console, self.scroll_view.container_size.width)
+            line_idx_recorded = set()
+            for line_idx, line in enumerate(lines):
+                if line_idx in line_idx_recorded:
+                    continue
+                if event.value in line:
+                    self.matches.append(
+                        {
+                            "line": line_idx,
+                            "word": event.value,
+                        }
+                    )
+                    line_idx_recorded.add(line_idx)
+            self.scroll_view.focus()
+            await self.action_next_search()
+
+    async def action_next_search(self) -> None:
+        if not self.matches or self.current_match_index >= len(self.matches):
+            return
+
+        target_line = self.matches[self.current_match_index]["line"]
+        self.scroll_view.scroll_to(x=0, y=target_line * 1, animate=False)
+        self.current_match_index = (self.current_match_index + 1) % len(self.matches)
+        self.search_status.update(
+            Text(
+                f"Find ：{self.current_match_index + 1}/{len(self.matches)}",
+                style="bold on #8f51b5",
+            )
+        )
+
+    def action_page_up(self):
+        self.scroll_view.scroll_page_up(animate=False)
+
+    def action_page_down(self):
+        self.scroll_view.scroll_page_down(animate=False)
+
+    def action_page_home(self):
+        self.scroll_view.scroll_home(animate=False)
+
+    def action_page_end(self):
+        self.scroll_view.scroll_end(animate=False)
+
+
+async def _run(path: Path, mask_str: str):
+    assert path.exists(), f"{path} not exist"
+
+    paths = list(path.glob(f"*{FILE_SUFFIX}"))
+    paths = sorted(paths, key=lambda x: int(x.stem))
+
+    if not paths:
+        raise ValueError(f"no available reward dump files under f{path}")
+
+    print(f"get jsonl file nums: {len(paths)}")
+
+    pbar = ProgressBar(total=len(paths), name="data load progress")
+    data = {}
+    await load_path(paths[0], data, mask_str, 0, pbar)
+    app = JsonLineViewer(step_num=len(paths), data=data, pbar=pbar)
+    await asyncio.gather(load_dir(path, data, pbar, mask_str), app.run_async())
+
+
+app = typer.Typer()
+
+
+@app.command(help="launch TUI APP")
+def run(
+    rollout_data_dir: Path,
+    mask_str: Annotated[str, typer.Option(help="string that will be masked to *")] = r"<\|image_pad\|>|<\|imgpad\|>",
+):
+    loop = asyncio.get_event_loop()
+    loop.run_until_complete(_run(rollout_data_dir, mask_str))
+
+
+if __name__ == "__main__":
+    app()
diff --git a/code/RL_model/verl/verl_train/setup.py b/code/RL_model/verl/verl_train/setup.py
new file mode 100644
index 0000000000000000000000000000000000000000..9cde2eb23919b8db09563ea241cfbb9729d85785
--- /dev/null
+++ b/code/RL_model/verl/verl_train/setup.py
@@ -0,0 +1,100 @@
+# Copyright 2024 Bytedance Ltd. and/or its affiliates
+#
+# Licensed under the Apache License, Version 2.0 (the "License");
+# you may not use this file except in compliance with the License.
+# You may obtain a copy of the License at
+#
+#     http://www.apache.org/licenses/LICENSE-2.0
+#
+# Unless required by applicable law or agreed to in writing, software
+# distributed under the License is distributed on an "AS IS" BASIS,
+# WITHOUT WARRANTIES OR CONDITIONS OF ANY KIND, either express or implied.
+# See the License for the specific language governing permissions and
+# limitations under the License.
+
+# setup.py is the fallback installation script when pyproject.toml does not work
+import os
+from pathlib import Path
+
+from setuptools import find_packages, setup
+
+version_folder = os.path.dirname(os.path.join(os.path.abspath(__file__)))
+
+with open(os.path.join(version_folder, "verl/version/version")) as f:
+    __version__ = f.read().strip()
+
+install_requires = [
+    "accelerate",
+    "codetiming",
+    "datasets",
+    "dill",
+    "hydra-core",
+    "numpy<2.0.0",
+    "pandas",
+    "peft",
+    "pyarrow>=19.0.0",
+    "pybind11",
+    "pylatexenc",
+    "ray[default]>=2.41.0",
+    "torchdata",
+    "tensordict>=0.8.0,<=0.10.0,!=0.9.0",
+    "transformers",
+    "wandb",
+    "packaging>=20.0",
+    "tensorboard",
+]
+
+TEST_REQUIRES = ["pytest", "pre-commit", "py-spy", "pytest-asyncio", "pytest-rerunfailures"]
+PRIME_REQUIRES = ["pyext"]
+GEO_REQUIRES = ["mathruler", "torchvision", "qwen_vl_utils"]
+GPU_REQUIRES = ["liger-kernel", "flash-attn"]
+MATH_REQUIRES = ["math-verify"]  # Add math-verify as an optional dependency
+VLLM_REQUIRES = ["tensordict>=0.8.0,<=0.10.0,!=0.9.0", "vllm>=0.8.5,<=0.12.0"]
+TRTLLM_REQUIRES = ["tensorrt-llm>=1.2.0rc6"]
+SGLANG_REQUIRES = [
+    "tensordict>=0.8.0,<=0.10.0,!=0.9.0",
+    "sglang[srt,openai]==0.5.6",
+    "torch==2.9.1",
+]
+TRL_REQUIRES = ["trl<=0.9.6"]
+MCORE_REQUIRES = ["mbridge"]
+TRANSFERQUEUE_REQUIRES = ["TransferQueue==0.1.5"]
+
+extras_require = {
+    "test": TEST_REQUIRES,
+    "prime": PRIME_REQUIRES,
+    "geo": GEO_REQUIRES,
+    "gpu": GPU_REQUIRES,
+    "math": MATH_REQUIRES,
+    "vllm": VLLM_REQUIRES,
+    "sglang": SGLANG_REQUIRES,
+    "trl": TRL_REQUIRES,
+    "mcore": MCORE_REQUIRES,
+    "transferqueue": TRANSFERQUEUE_REQUIRES,
+    "trtllm": TRTLLM_REQUIRES,
+}
+
+
+this_directory = Path(__file__).parent
+long_description = (this_directory / "README.md").read_text()
+
+setup(
+    name="verl",
+    version=__version__,
+    package_dir={"": "."},
+    packages=find_packages(where="."),
+    url="https://github.com/volcengine/verl",
+    license="Apache 2.0",
+    author="Bytedance - Seed - MLSys",
+    author_email="zhangchi.usc1992@bytedance.com, gmsheng@connect.hku.hk",
+    description="verl: Volcano Engine Reinforcement Learning for LLM",
+    install_requires=install_requires,
+    extras_require=extras_require,
+    package_data={
+        "": ["version/*"],
+        "verl": ["trainer/config/*.yaml"],
+    },
+    include_package_data=True,
+    long_description=long_description,
+    long_description_content_type="text/markdown",
+)
diff --git a/code/RL_model/verl/verl_train/tests/README.md b/code/RL_model/verl/verl_train/tests/README.md
new file mode 100644
index 0000000000000000000000000000000000000000..479f06933e4e536ee159b738794daa05364119bb
--- /dev/null
+++ b/code/RL_model/verl/verl_train/tests/README.md
@@ -0,0 +1,30 @@
+# Tests layout
+
+Each folder under tests/ corresponds to a test category for a sub-namespace in verl. For instance:
+- `tests/trainer` for testing functionality related to `verl/trainer`
+- `tests/models` for testing functionality related to `verl/models`
+- ...
+
+There are a few folders with `special_` prefix, created for special purposes:
+- `special_distributed`: unit tests that must run with multiple GPUs
+- `special_e2e`: end-to-end tests with training/generation scripts
+- `special_npu`: tests for NPUs
+- `special_sanity`: a suite of quick sanity tests
+- `special_standalone`: a set of test that are designed to run in dedicated environments
+
+Accelerators for tests 
+- By default tests are run with GPU available, except for the ones under `special_npu`, and any test script whose name ends with `on_cpu.py`.
+- For test scripts with `on_cpu.py` name suffix would be tested on CPU resources in linux environment.
+
+# Workflow layout
+
+All CI tests are configured by yaml files in `.github/workflows/`. Here's an overview of all test configs:
+1. A list of always triggered CPU sanity tests: `check-pr-title.yml`, `secrets_scan.yml`, `check-pr-title,yml`, `pre-commit.yml`, `doc.yml`
+2. Some heavy multi-GPU unit tests, such as `model.yml`, `vllm.yml`, `sgl.yml`
+3. End-to-end tests: `e2e_*.yml`
+4. Unit tests
+  - `cpu_unit_tests.yml`, run pytest on all scripts with file name pattern `tests/**/test_*_on_cpu.py`
+  - `gpu_unit_tests.yml`, run pytest on all scripts with file without the `on_cpu.py` suffix.
+  - Since cpu/gpu unit tests by default runs all tests under `tests`, please make sure tests are manually excluded in them when
+    - new workflow yaml is added to `.github/workflows`
+    - new tests are added to workflow mentioned in 2.
\ No newline at end of file
diff --git a/code/RL_model/verl/verl_train/tests/__init__.py b/code/RL_model/verl/verl_train/tests/__init__.py
new file mode 100644
index 0000000000000000000000000000000000000000..1ce90c5eb352d85c59105c0dc85b5f1dd576f095
--- /dev/null
+++ b/code/RL_model/verl/verl_train/tests/__init__.py
@@ -0,0 +1,13 @@
+# Copyright 2024 Bytedance Ltd. and/or its affiliates
+#
+# Licensed under the Apache License, Version 2.0 (the "License");
+# you may not use this file except in compliance with the License.
+# You may obtain a copy of the License at
+#
+#     http://www.apache.org/licenses/LICENSE-2.0
+#
+# Unless required by applicable law or agreed to in writing, software
+# distributed under the License is distributed on an "AS IS" BASIS,
+# WITHOUT WARRANTIES OR CONDITIONS OF ANY KIND, either express or implied.
+# See the License for the specific language governing permissions and
+# limitations under the License.
diff --git a/code/RL_model/verl/verl_train/tests/interactions/__init__.py b/code/RL_model/verl/verl_train/tests/interactions/__init__.py
new file mode 100644
index 0000000000000000000000000000000000000000..b6db0fcef70b051ba5975c4a94d2b68b986e1127
--- /dev/null
+++ b/code/RL_model/verl/verl_train/tests/interactions/__init__.py
@@ -0,0 +1,15 @@
+# Copyright 2024 Bytedance Ltd. and/or its affiliates
+# Copyright 2023-2024 SGLang Team
+# Copyright 2025 ModelBest Inc. and/or its affiliates
+#
+# Licensed under the Apache License, Version 2.0 (the "License");
+# you may not use this file except in compliance with the License.
+# You may obtain a copy of the License at
+#
+#     http://www.apache.org/licenses/LICENSE-2.0
+#
+# Unless required by applicable law or agreed to in writing, software
+# distributed under the License is distributed on an "AS IS" BASIS,
+# WITHOUT WARRANTIES OR CONDITIONS OF ANY KIND, either express or implied.
+# See the License for the specific language governing permissions and
+# limitations under the License.
diff --git a/code/RL_model/verl/verl_train/tests/interactions/test_gsm8k_interaction.py b/code/RL_model/verl/verl_train/tests/interactions/test_gsm8k_interaction.py
new file mode 100644
index 0000000000000000000000000000000000000000..d5dfda1a0fa7e427ff06b44ce0cc1311c62b0d90
--- /dev/null
+++ b/code/RL_model/verl/verl_train/tests/interactions/test_gsm8k_interaction.py
@@ -0,0 +1,422 @@
+# Copyright 2024 Bytedance Ltd. and/or its affiliates
+# Copyright 2023-2024 SGLang Team
+# Copyright 2025 ModelBest Inc. and/or its affiliates
+#
+# Licensed under the Apache License, Version 2.0 (the "License");
+# you may not use this file except in compliance with the License.
+# You may obtain a copy of the License at
+#
+#     http://www.apache.org/licenses/LICENSE-2.0
+#
+# Unless required by applicable law or agreed to in writing, software
+# distributed under the License is distributed on an "AS IS" BASIS,
+# WITHOUT WARRANTIES OR CONDITIONS OF ANY KIND, either express or implied.
+# See the License for the specific language governing permissions and
+# limitations under the License.
+
+from unittest.mock import patch
+
+import pytest
+
+from verl.interactions.gsm8k_interaction import Gsm8kInteraction
+
+
+class TestGsm8kInteraction:
+    """Test cases for Gsm8kInteraction class."""
+
+    def setup_method(self):
+        """Set up test environment before each test method."""
+        self.config = {"name": "gsm8k"}
+        self.interaction = Gsm8kInteraction(self.config)
+
+    def test_init(self):
+        """Test Gsm8kInteraction initialization."""
+        assert self.interaction._instance_dict == {}
+        assert self.interaction.config == self.config
+        assert self.interaction.name == "gsm8k"
+
+    @pytest.mark.asyncio
+    async def test_start_interaction_with_instance_id(self):
+        """Test start_interaction with provided instance_id."""
+        instance_id = "test_instance"
+        ground_truth = "42"
+
+        result_id = await self.interaction.start_interaction(instance_id=instance_id, ground_truth=ground_truth)
+
+        assert result_id == instance_id
+        assert instance_id in self.interaction._instance_dict
+        assert self.interaction._instance_dict[instance_id]["response"] == ""
+        assert self.interaction._instance_dict[instance_id]["ground_truth"] == ground_truth
+        assert self.interaction._instance_dict[instance_id]["reward"] == 0.0
+
+    @pytest.mark.asyncio
+    async def test_start_interaction_without_instance_id(self):
+        """Test start_interaction without provided instance_id (auto-generated)."""
+        ground_truth = "42"
+
+        result_id = await self.interaction.start_interaction(ground_truth=ground_truth)
+
+        assert result_id is not None
+        assert len(result_id) == 36  # UUID4 length
+        assert result_id in self.interaction._instance_dict
+        assert self.interaction._instance_dict[result_id]["ground_truth"] == ground_truth
+
+    @pytest.mark.asyncio
+    async def test_start_interaction_without_ground_truth(self):
+        """Test start_interaction without ground_truth parameter."""
+        instance_id = "test_instance"
+
+        result_id = await self.interaction.start_interaction(instance_id=instance_id)
+
+        assert result_id == instance_id
+        assert self.interaction._instance_dict[instance_id]["ground_truth"] is None
+
+    @pytest.mark.asyncio
+    async def test_generate_response_correct_answer_with_prefix(self):
+        """Test generate_response with correct answer already having #### prefix."""
+        instance_id = "test_instance"
+        ground_truth = "42"
+
+        # Setup instance
+        await self.interaction.start_interaction(instance_id=instance_id, ground_truth=ground_truth)
+
+        messages = [{"role": "assistant", "content": "#### 42"}]
+
+        with patch("verl.utils.reward_score.gsm8k.compute_score", return_value=1.0):
+            should_terminate, response, reward, metadata = await self.interaction.generate_response(
+                instance_id, messages
+            )
+
+        assert should_terminate is True
+        assert response == "Your response is correct!"
+        assert reward == 1.0
+        assert metadata == {}
+        assert self.interaction._instance_dict[instance_id]["response"] == "#### 42"
+
+    @pytest.mark.asyncio
+    async def test_generate_response_correct_answer_without_prefix(self):
+        """Test generate_response with correct answer missing #### prefix."""
+        instance_id = "test_instance"
+        ground_truth = "42"
+
+        # Setup instance
+        await self.interaction.start_interaction(instance_id=instance_id, ground_truth=ground_truth)
+
+        messages = [{"role": "assistant", "content": "42"}]
+
+        with patch("verl.utils.reward_score.gsm8k.compute_score", return_value=1.0):
+            should_terminate, response, reward, metadata = await self.interaction.generate_response(
+                instance_id, messages
+            )
+
+        assert should_terminate is True
+        assert response == "Your response is correct!"
+        assert reward == 1.0
+        assert self.interaction._instance_dict[instance_id]["response"] == "42"
+
+    @pytest.mark.asyncio
+    async def test_generate_response_incorrect_answer(self):
+        """Test generate_response with incorrect answer."""
+        instance_id = "test_instance"
+        ground_truth = "42"
+
+        # Setup instance
+        await self.interaction.start_interaction(instance_id=instance_id, ground_truth=ground_truth)
+
+        messages = [{"role": "assistant", "content": "24"}]
+
+        with patch("verl.utils.reward_score.gsm8k.compute_score", return_value=0.0):
+            should_terminate, response, reward, metadata = await self.interaction.generate_response(
+                instance_id, messages
+            )
+
+        assert should_terminate is False
+        assert response == "Your response is incorrect! You need to reflect on your answer and try again."
+        assert reward == 0.0
+        assert self.interaction._instance_dict[instance_id]["response"] == "24"
+
+    @pytest.mark.asyncio
+    async def test_generate_response_multiple_messages(self):
+        """Test generate_response with multiple messages (should use last assistant message)."""
+        instance_id = "test_instance"
+        ground_truth = "42"
+
+        # Setup instance
+        await self.interaction.start_interaction(instance_id=instance_id, ground_truth=ground_truth)
+
+        messages = [
+            {"role": "user", "content": "What is 2+2?"},
+            {"role": "assistant", "content": "### 4"},
+            {"role": "user", "content": "What is 40+2?"},
+            {"role": "assistant", "content": "#### 42"},
+        ]
+
+        with patch("verl.utils.reward_score.gsm8k.compute_score", return_value=1.0):
+            should_terminate, response, reward, metadata = await self.interaction.generate_response(
+                instance_id, messages
+            )
+
+        assert should_terminate is True
+        assert response == "Your response is correct!"
+        assert self.interaction._instance_dict[instance_id]["response"] == "#### 42"
+
+    @pytest.mark.asyncio
+    async def test_generate_response_no_assistant_message(self):
+        """Test generate_response with no assistant messages."""
+        instance_id = "test_instance"
+        ground_truth = "42"
+
+        # Setup instance
+        await self.interaction.start_interaction(instance_id=instance_id, ground_truth=ground_truth)
+
+        messages = [{"role": "user", "content": "Hello!"}]
+
+        with patch("verl.utils.reward_score.gsm8k.compute_score", return_value=0.0):
+            should_terminate, response, reward, metadata = await self.interaction.generate_response(
+                instance_id, messages
+            )
+
+        assert should_terminate is False
+        assert self.interaction._instance_dict[instance_id]["response"] == ""
+
+    @pytest.mark.asyncio
+    async def test_calculate_score_direct_call(self):
+        """Test calculate_score method directly."""
+        instance_id = "test_instance"
+        ground_truth = "42"
+
+        # Setup instance
+        await self.interaction.start_interaction(instance_id=instance_id, ground_truth=ground_truth)
+
+        # Set a response
+        self.interaction._instance_dict[instance_id]["response"] = "#### 42"
+
+        with patch("verl.utils.reward_score.gsm8k.compute_score", return_value=1.0) as mock_compute:
+            score = await self.interaction.calculate_score(instance_id)
+
+            assert score == 1.0
+            mock_compute.assert_called_once_with("#### 42", "42", method="strict", format_score=0.0, score=1.0)
+
+    @pytest.mark.asyncio
+    async def test_calculate_score_with_kwargs(self):
+        """Test calculate_score method with additional kwargs."""
+        instance_id = "test_instance"
+        ground_truth = "42"
+
+        # Setup instance
+        await self.interaction.start_interaction(instance_id=instance_id, ground_truth=ground_truth)
+
+        # Set a response
+        self.interaction._instance_dict[instance_id]["response"] = "#### 24"
+
+        with patch("verl.utils.reward_score.gsm8k.compute_score", return_value=0.0) as mock_compute:
+            score = await self.interaction.calculate_score(instance_id, extra_param="test")
+
+            assert score == 0.0
+            mock_compute.assert_called_once_with("#### 24", "42", method="strict", format_score=0.0, score=1.0)
+
+    @pytest.mark.asyncio
+    async def test_finalize_interaction(self):
+        """Test finalize_interaction method."""
+        instance_id = "test_instance"
+        ground_truth = "42"
+
+        # Setup instance
+        await self.interaction.start_interaction(instance_id=instance_id, ground_truth=ground_truth)
+
+        assert instance_id in self.interaction._instance_dict
+
+        await self.interaction.finalize_interaction(instance_id)
+
+        assert instance_id not in self.interaction._instance_dict
+
+    @pytest.mark.asyncio
+    async def test_finalize_interaction_with_kwargs(self):
+        """Test finalize_interaction method with additional kwargs."""
+        instance_id = "test_instance"
+        ground_truth = "42"
+
+        # Setup instance
+        await self.interaction.start_interaction(instance_id=instance_id, ground_truth=ground_truth)
+
+        assert instance_id in self.interaction._instance_dict
+
+        await self.interaction.finalize_interaction(instance_id, extra_param="test")
+
+        assert instance_id not in self.interaction._instance_dict
+
+    @pytest.mark.asyncio
+    async def test_finalize_nonexistent_interaction(self):
+        """Test finalize_interaction with non-existent instance_id."""
+        instance_id = "nonexistent_instance"
+
+        # This should raise KeyError
+        with pytest.raises(KeyError):
+            await self.interaction.finalize_interaction(instance_id)
+
+    @pytest.mark.asyncio
+    async def test_full_interaction_workflow_correct(self):
+        """Test complete interaction workflow with correct answer."""
+        ground_truth = "42"
+
+        # Start interaction
+        instance_id = await self.interaction.start_interaction(ground_truth=ground_truth)
+
+        # Generate response with correct answer
+        messages = [{"role": "assistant", "content": "42"}]
+
+        with patch("verl.utils.reward_score.gsm8k.compute_score", return_value=1.0):
+            should_terminate, response, reward, metadata = await self.interaction.generate_response(
+                instance_id, messages
+            )
+
+        assert should_terminate is True
+        assert reward == 1.0
+
+        # Finalize interaction
+        await self.interaction.finalize_interaction(instance_id)
+        assert instance_id not in self.interaction._instance_dict
+
+    @pytest.mark.asyncio
+    async def test_full_interaction_workflow_incorrect(self):
+        """Test complete interaction workflow with incorrect answer."""
+        ground_truth = "42"
+
+        # Start interaction
+        instance_id = await self.interaction.start_interaction(ground_truth=ground_truth)
+
+        # Generate response with incorrect answer
+        messages = [{"role": "assistant", "content": "24"}]
+
+        with patch("verl.utils.reward_score.gsm8k.compute_score", return_value=0.0):
+            should_terminate, response, reward, metadata = await self.interaction.generate_response(
+                instance_id, messages
+            )
+
+        assert should_terminate is False
+        assert reward == 0.0
+
+        # Continue with another attempt
+        messages.append({"role": "user", "content": response})
+        messages.append({"role": "assistant", "content": "42"})
+
+        with patch("verl.utils.reward_score.gsm8k.compute_score", return_value=1.0):
+            should_terminate, response, reward, metadata = await self.interaction.generate_response(
+                instance_id, messages
+            )
+
+        assert should_terminate is True
+        assert reward == 1.0
+
+        # Finalize interaction
+        await self.interaction.finalize_interaction(instance_id)
+        assert instance_id not in self.interaction._instance_dict
+
+    @pytest.mark.asyncio
+    async def test_multiple_concurrent_interactions(self):
+        """Test multiple concurrent interaction instances."""
+        ground_truth_1 = "42"
+        ground_truth_2 = "24"
+
+        # Start multiple interactions
+        instance_id_1 = await self.interaction.start_interaction(ground_truth=ground_truth_1)
+        instance_id_2 = await self.interaction.start_interaction(ground_truth=ground_truth_2)
+
+        assert len(self.interaction._instance_dict) == 2
+        assert instance_id_1 in self.interaction._instance_dict
+        assert instance_id_2 in self.interaction._instance_dict
+
+        # Test responses for both instances
+        messages_1 = [{"role": "assistant", "content": "42"}]
+        messages_2 = [{"role": "assistant", "content": "24"}]
+
+        with patch("verl.utils.reward_score.gsm8k.compute_score", side_effect=[1.0, 1.0]):
+            should_terminate_1, _, reward_1, _ = await self.interaction.generate_response(instance_id_1, messages_1)
+            should_terminate_2, _, reward_2, _ = await self.interaction.generate_response(instance_id_2, messages_2)
+
+        assert should_terminate_1 is True
+        assert should_terminate_2 is True
+        assert reward_1 == 1.0
+        assert reward_2 == 1.0
+
+        # Finalize both interactions
+        await self.interaction.finalize_interaction(instance_id_1)
+        await self.interaction.finalize_interaction(instance_id_2)
+
+        assert len(self.interaction._instance_dict) == 0
+
+    @pytest.mark.asyncio
+    async def test_edge_case_empty_messages(self):
+        """Test edge case with empty messages list."""
+        instance_id = "test_instance"
+        ground_truth = "42"
+
+        # Setup instance
+        await self.interaction.start_interaction(instance_id=instance_id, ground_truth=ground_truth)
+
+        messages = []
+
+        with patch("verl.utils.reward_score.gsm8k.compute_score", return_value=0.0):
+            should_terminate, response, reward, metadata = await self.interaction.generate_response(
+                instance_id, messages
+            )
+
+        assert should_terminate is False
+        assert reward == 0.0
+        assert self.interaction._instance_dict[instance_id]["response"] == ""
+
+    @pytest.mark.asyncio
+    async def test_edge_case_message_without_content(self):
+        """Test edge case with message without content field."""
+        instance_id = "test_instance"
+        ground_truth = "42"
+
+        # Setup instance
+        await self.interaction.start_interaction(instance_id=instance_id, ground_truth=ground_truth)
+
+        messages = [
+            {"role": "assistant"}  # Missing content field
+        ]
+
+        with patch("verl.utils.reward_score.gsm8k.compute_score", return_value=0.0):
+            should_terminate, response, reward, metadata = await self.interaction.generate_response(
+                instance_id, messages
+            )
+
+        assert should_terminate is False
+        assert reward == 0.0
+        assert self.interaction._instance_dict[instance_id]["response"] is None
+
+    def test_inheritance_from_base_interaction(self):
+        """Test that Gsm8kInteraction properly inherits from BaseInteraction."""
+        from verl.interactions.base import BaseInteraction
+
+        assert isinstance(self.interaction, BaseInteraction)
+
+        # Test that all required methods are implemented
+        assert hasattr(self.interaction, "start_interaction")
+        assert hasattr(self.interaction, "generate_response")
+        assert hasattr(self.interaction, "calculate_score")
+        assert hasattr(self.interaction, "finalize_interaction")
+
+        # Test that methods are callable
+        assert callable(self.interaction.start_interaction)
+        assert callable(self.interaction.generate_response)
+        assert callable(self.interaction.calculate_score)
+        assert callable(self.interaction.finalize_interaction)
+
+    def test_name_attribute_initialization(self):
+        """Test name attribute initialization with different configs."""
+        # Test with explicit name in config
+        config_with_name = {"name": "custom_gsm8k"}
+        interaction_with_name = Gsm8kInteraction(config_with_name)
+        assert interaction_with_name.name == "custom_gsm8k"
+
+        # Test with default name when not provided in config
+        config_without_name = {}
+        interaction_without_name = Gsm8kInteraction(config_without_name)
+        assert interaction_without_name.name == "interaction_agent"  # Default from BaseInteraction
+
+        # Test that name is accessible as attribute
+        assert hasattr(self.interaction, "name")
+        assert self.interaction.name == "gsm8k"
diff --git a/code/RL_model/verl/verl_train/tests/interactions/test_interaction_registry.py b/code/RL_model/verl/verl_train/tests/interactions/test_interaction_registry.py
new file mode 100644
index 0000000000000000000000000000000000000000..7fe193b52eca965bb73ba3628108e7c14cce7464
--- /dev/null
+++ b/code/RL_model/verl/verl_train/tests/interactions/test_interaction_registry.py
@@ -0,0 +1,206 @@
+# Copyright 2023-2024 SGLang Team
+# Copyright 2025 ModelBest Inc. and/or its affiliates
+#
+# Licensed under the Apache License, Version 2.0 (the "License");
+# you may not use this file except in compliance with the License.
+# You may obtain a copy of the License at
+#
+#     http://www.apache.org/licenses/LICENSE-2.0
+#
+# Unless required by applicable law or agreed to in writing, software
+# distributed under the License is distributed on an "AS IS" BASIS,
+# WITHOUT WARRANTIES OR CONDITIONS OF ANY KIND, either express or implied.
+# See the License for the specific language governing permissions and
+# limitations under the License.
+
+import os
+import tempfile
+
+import pytest
+from omegaconf import OmegaConf
+
+from verl.interactions.base import BaseInteraction
+from verl.interactions.gsm8k_interaction import Gsm8kInteraction
+from verl.interactions.utils.interaction_registry import (
+    get_interaction_class,
+    initialize_interactions_from_config,
+)
+
+
+class TestInteractionRegistry:
+    def test_get_interaction_class(self):
+        """Test getting interaction class by name."""
+        # Test getting base interaction class
+        base_cls = get_interaction_class("verl.interactions.base.BaseInteraction")
+        assert base_cls == BaseInteraction
+
+        # Test getting gsm8k interaction class
+        gsm8k_cls = get_interaction_class("verl.interactions.gsm8k_interaction.Gsm8kInteraction")
+        assert gsm8k_cls == Gsm8kInteraction
+
+    def test_initialize_single_interaction_from_config(self):
+        """Test initializing single interaction from config."""
+        # Create temporary config file
+        config_content = {
+            "interaction": [
+                {
+                    "name": "test_gsm8k",
+                    "class_name": "verl.interactions.gsm8k_interaction.Gsm8kInteraction",
+                    "config": {},
+                }
+            ]
+        }
+
+        with tempfile.NamedTemporaryFile(mode="w", suffix=".yaml", delete=False) as f:
+            OmegaConf.save(config_content, f.name)
+            temp_config_path = f.name
+
+        try:
+            interaction_map = initialize_interactions_from_config(temp_config_path)
+
+            # Check that interaction was created
+            assert len(interaction_map) == 1
+            assert "test_gsm8k" in interaction_map
+            assert isinstance(interaction_map["test_gsm8k"], Gsm8kInteraction)
+            assert interaction_map["test_gsm8k"].name == "test_gsm8k"
+        finally:
+            os.unlink(temp_config_path)
+
+    def test_initialize_multiple_interactions_from_config(self):
+        """Test initializing multiple interactions from config."""
+        config_content = {
+            "interaction": [
+                {
+                    "name": "gsm8k_solver",
+                    "class_name": "verl.interactions.gsm8k_interaction.Gsm8kInteraction",
+                    "config": {},
+                },
+                {
+                    "name": "base_agent",
+                    "class_name": "verl.interactions.base.BaseInteraction",
+                    "config": {"custom_param": "test_value"},
+                },
+            ]
+        }
+
+        with tempfile.NamedTemporaryFile(mode="w", suffix=".yaml", delete=False) as f:
+            OmegaConf.save(config_content, f.name)
+            temp_config_path = f.name
+
+        try:
+            interaction_map = initialize_interactions_from_config(temp_config_path)
+
+            # Check that both interactions were created
+            assert len(interaction_map) == 2
+            assert "gsm8k_solver" in interaction_map
+            assert "base_agent" in interaction_map
+
+            # Check types
+            assert isinstance(interaction_map["gsm8k_solver"], Gsm8kInteraction)
+            assert isinstance(interaction_map["base_agent"], BaseInteraction)
+
+            # Check names were injected
+            assert interaction_map["gsm8k_solver"].name == "gsm8k_solver"
+            assert interaction_map["base_agent"].name == "base_agent"
+
+            # Check custom config was passed
+            assert interaction_map["base_agent"].config.get("custom_param") == "test_value"
+        finally:
+            os.unlink(temp_config_path)
+
+    def test_initialize_interaction_without_explicit_name(self):
+        """Test that interaction name is derived from class name when not specified."""
+        config_content = {
+            "interaction": [{"class_name": "verl.interactions.gsm8k_interaction.Gsm8kInteraction", "config": {}}]
+        }
+
+        with tempfile.NamedTemporaryFile(mode="w", suffix=".yaml", delete=False) as f:
+            OmegaConf.save(config_content, f.name)
+            temp_config_path = f.name
+
+        try:
+            interaction_map = initialize_interactions_from_config(temp_config_path)
+
+            # Check that interaction name was derived from class name
+            assert len(interaction_map) == 1
+            assert "gsm8k" in interaction_map  # Should be "gsm8k" after removing "interaction" suffix
+            assert isinstance(interaction_map["gsm8k"], Gsm8kInteraction)
+            assert interaction_map["gsm8k"].name == "gsm8k"
+        finally:
+            os.unlink(temp_config_path)
+
+    def test_initialize_empty_config(self):
+        """Test initializing from empty config."""
+        config_content = {"interaction": []}
+
+        with tempfile.NamedTemporaryFile(mode="w", suffix=".yaml", delete=False) as f:
+            OmegaConf.save(config_content, f.name)
+            temp_config_path = f.name
+
+        try:
+            interaction_map = initialize_interactions_from_config(temp_config_path)
+            assert len(interaction_map) == 0
+        finally:
+            os.unlink(temp_config_path)
+
+    def test_invalid_class_name(self):
+        """Test handling of invalid class name."""
+        config_content = {
+            "interaction": [{"name": "invalid", "class_name": "invalid.module.InvalidClass", "config": {}}]
+        }
+
+        with tempfile.NamedTemporaryFile(mode="w", suffix=".yaml", delete=False) as f:
+            OmegaConf.save(config_content, f.name)
+            temp_config_path = f.name
+
+        try:
+            with pytest.raises(ModuleNotFoundError):
+                initialize_interactions_from_config(temp_config_path)
+        finally:
+            os.unlink(temp_config_path)
+
+    def test_duplicate_interaction_names(self):
+        """Test handling of duplicate interaction names."""
+        config_content = {
+            "interaction": [
+                {"name": "duplicate", "class_name": "verl.interactions.base.BaseInteraction", "config": {}},
+                {
+                    "name": "duplicate",
+                    "class_name": "verl.interactions.gsm8k_interaction.Gsm8kInteraction",
+                    "config": {},
+                },
+            ]
+        }
+
+        with tempfile.NamedTemporaryFile(mode="w", suffix=".yaml", delete=False) as f:
+            OmegaConf.save(config_content, f.name)
+            temp_config_path = f.name
+
+        try:
+            with pytest.raises(ValueError, match="Duplicate interaction name 'duplicate' found"):
+                initialize_interactions_from_config(temp_config_path)
+        finally:
+            os.unlink(temp_config_path)
+
+    def test_auto_name_generation_edge_cases(self):
+        """Test automatic name generation for various class name patterns."""
+        config_content = {
+            "interaction": [
+                {"class_name": "verl.interactions.base.BaseInteraction", "config": {}},
+                {"class_name": "verl.interactions.gsm8k_interaction.Gsm8kInteraction", "config": {}},
+            ]
+        }
+
+        with tempfile.NamedTemporaryFile(mode="w", suffix=".yaml", delete=False) as f:
+            OmegaConf.save(config_content, f.name)
+            temp_config_path = f.name
+
+        try:
+            interaction_map = initialize_interactions_from_config(temp_config_path)
+
+            # Check that names were generated correctly
+            assert len(interaction_map) == 2
+            assert "base" in interaction_map  # BaseInteraction -> base
+            assert "gsm8k" in interaction_map  # Gsm8kInteraction -> gsm8k
+        finally:
+            os.unlink(temp_config_path)
diff --git a/code/RL_model/verl/verl_train/tests/kill_github_tests.sh b/code/RL_model/verl/verl_train/tests/kill_github_tests.sh
new file mode 100644
index 0000000000000000000000000000000000000000..5c76d7658d5373f4a5d73c9aa9c84a7d14b08402
--- /dev/null
+++ b/code/RL_model/verl/verl_train/tests/kill_github_tests.sh
@@ -0,0 +1,41 @@
+#!/bin/bash
+
+if [ "$#" -ne 1 ]; then
+    echo "Usage: $0 YOUR_GITHUB_TOKEN"
+    echo "Please provide exactly one input argument for your github token."
+    exit 1
+fi
+
+# Set your GitHub repository details
+OWNER="volcengine"
+REPO="verl"
+TOKEN=$1
+
+# API URL for workflow runs
+API_URL="https://api.github.com/repos/$OWNER/$REPO/actions/runs?status=queued"
+
+# Check required commands
+command -v jq >/dev/null 2>&1 || { echo "jq is required but not installed. Aborting."; exit 1; }
+
+# Get queued workflow runs
+response=$(curl -s -H "Authorization: token $TOKEN" -H "Accept: application/vnd.github.v3+json" "$API_URL")
+
+# Run this for debugging
+# echo $response
+
+# Extract run IDs
+queued_run_ids=$(echo "$response" | jq -r '.workflow_runs[] | .id')
+
+if [ -z "$queued_run_ids" ]; then
+    echo "No queued workflow runs found."
+    exit 0
+fi
+
+# Cancel each queued run
+for run_id in $queued_run_ids; do
+    echo "Cancelling run $run_id"
+    cancel_url="https://api.github.com/repos/$OWNER/$REPO/actions/runs/$run_id/cancel"
+    curl -s -X POST -H "Authorization: token $TOKEN" -H "Accept: application/vnd.github.v3+json" "$cancel_url"
+done
+
+echo "Cancelled all queued workflow runs."
diff --git a/code/RL_model/verl/verl_train/tests/special_e2e/__init__.py b/code/RL_model/verl/verl_train/tests/special_e2e/__init__.py
new file mode 100644
index 0000000000000000000000000000000000000000..1ce90c5eb352d85c59105c0dc85b5f1dd576f095
--- /dev/null
+++ b/code/RL_model/verl/verl_train/tests/special_e2e/__init__.py
@@ -0,0 +1,13 @@
+# Copyright 2024 Bytedance Ltd. and/or its affiliates
+#
+# Licensed under the Apache License, Version 2.0 (the "License");
+# you may not use this file except in compliance with the License.
+# You may obtain a copy of the License at
+#
+#     http://www.apache.org/licenses/LICENSE-2.0
+#
+# Unless required by applicable law or agreed to in writing, software
+# distributed under the License is distributed on an "AS IS" BASIS,
+# WITHOUT WARRANTIES OR CONDITIONS OF ANY KIND, either express or implied.
+# See the License for the specific language governing permissions and
+# limitations under the License.
diff --git a/code/RL_model/verl/verl_train/tests/special_e2e/check_custom_rwd_fn.py b/code/RL_model/verl/verl_train/tests/special_e2e/check_custom_rwd_fn.py
new file mode 100644
index 0000000000000000000000000000000000000000..8d77a53729bd96b153f004eb230df85f1d32f890
--- /dev/null
+++ b/code/RL_model/verl/verl_train/tests/special_e2e/check_custom_rwd_fn.py
@@ -0,0 +1,33 @@
+# Copyright 2024 Bytedance Ltd. and/or its affiliates
+#
+# Licensed under the Apache License, Version 2.0 (the "License");
+# you may not use this file except in compliance with the License.
+# You may obtain a copy of the License at
+#
+#     http://www.apache.org/licenses/LICENSE-2.0
+#
+# Unless required by applicable law or agreed to in writing, software
+# distributed under the License is distributed on an "AS IS" BASIS,
+# WITHOUT WARRANTIES OR CONDITIONS OF ANY KIND, either express or implied.
+# See the License for the specific language governing permissions and
+# limitations under the License.
+
+import argparse
+
+
+def check_congratulations_in_file(output_file):
+    with open(output_file) as f:
+        output = f.read()
+
+    success_message = "Congratulations!!! You have called my_reward_function successfully!!!"
+    assert success_message in output, f"Success message of my_reward_function not found in {output_file}"
+    print("Check passes")
+
+
+if __name__ == "__main__":
+    parser = argparse.ArgumentParser()
+    parser.add_argument("--output_file", required=True, type=str)
+
+    args = parser.parse_args()
+
+    check_congratulations_in_file(args.output_file)
diff --git a/code/RL_model/verl/verl_train/tests/special_e2e/check_results.py b/code/RL_model/verl/verl_train/tests/special_e2e/check_results.py
new file mode 100644
index 0000000000000000000000000000000000000000..9453282fbc80c88a12429369647208347d35491b
--- /dev/null
+++ b/code/RL_model/verl/verl_train/tests/special_e2e/check_results.py
@@ -0,0 +1,53 @@
+# Copyright 2024 Bytedance Ltd. and/or its affiliates
+#
+# Licensed under the Apache License, Version 2.0 (the "License");
+# you may not use this file except in compliance with the License.
+# You may obtain a copy of the License at
+#
+#     http://www.apache.org/licenses/LICENSE-2.0
+#
+# Unless required by applicable law or agreed to in writing, software
+# distributed under the License is distributed on an "AS IS" BASIS,
+# WITHOUT WARRANTIES OR CONDITIONS OF ANY KIND, either express or implied.
+# See the License for the specific language governing permissions and
+# limitations under the License.
+
+import argparse
+
+import numpy as np
+
+
+def extract_reward_from_line(line):
+    # TODO: this function needs error handling
+    try:
+        key_vals = line.split(" - ")
+        for key_val in key_vals:
+            key, val = key_val.split(":")
+            if key == "critic/rewards/mean":
+                reward = float(val)
+                return reward
+        return -np.inf
+    except Exception:
+        return -np.inf
+
+
+if __name__ == "__main__":
+    parser = argparse.ArgumentParser()
+    parser.add_argument("--output_file", required=True, type=str)
+    parser.add_argument("--target", type=float, default=0.2, help="target reward score")
+
+    args = parser.parse_args()
+
+    with open(args.output_file) as f:
+        output = f.read().split("\n")
+
+    best_reward = -np.inf
+    for line in output:
+        if line.startswith("step"):
+            reward = extract_reward_from_line(line)
+            if reward > best_reward:
+                best_reward = reward
+
+    print(f"Best reward is {best_reward}")
+    assert best_reward > args.target, f"Best reward must be greater than {args.target}. best_reward: {best_reward}"
+    print("Check passes")
diff --git a/code/RL_model/verl/verl_train/tests/special_e2e/run_dapo.sh b/code/RL_model/verl/verl_train/tests/special_e2e/run_dapo.sh
new file mode 100644
index 0000000000000000000000000000000000000000..02d645b7b889c92cfc92aaf3c4fb691a3ad4e0d7
--- /dev/null
+++ b/code/RL_model/verl/verl_train/tests/special_e2e/run_dapo.sh
@@ -0,0 +1,90 @@
+#!/usr/bin/env bash
+set -xeuo pipefail
+
+NUM_GPUS=${NUM_GPUS:-8}
+
+MODEL_ID=${MODEL_ID:-Qwen/Qwen2.5-0.5B-Instruct}
+MODEL_PATH=${MODEL_PATH:-${HOME}/models/${MODEL_ID}}
+#hf download "${MODEL_ID}" --local-dir "${MODEL_PATH}"
+
+adv_estimator=grpo
+
+kl_coef=0.0
+use_kl_in_reward=False
+use_kl_loss=False
+kl_loss_coef=0.0
+
+clip_ratio_low=0.2
+clip_ratio_high=0.28
+
+max_prompt_length=1024
+max_response_length=2048
+enable_overlong_buffer=True
+overlong_buffer_len=128
+overlong_penalty_factor=1.0
+
+loss_agg_mode="token-mean"
+
+enable_filter_groups=True
+filter_groups_metric=seq_reward
+max_num_gen_batches=10
+
+train_traj_micro_bsz_per_gpu=2 # b
+n_resp_per_prompt=4 # g
+
+train_traj_micro_bsz=$((train_traj_micro_bsz_per_gpu * NUM_GPUS)) # b * n
+train_traj_mini_bsz=$((train_traj_micro_bsz * 2)) # 2 * b * n
+train_prompt_mini_bsz=$((train_traj_mini_bsz * n_resp_per_prompt)) # 2 * b * n / g
+train_prompt_bsz=$((train_prompt_mini_bsz * 2)) # 4 * b * n / g
+
+gen_prompt_bsz=$((train_prompt_bsz * 4))
+
+exp_name="$(basename "${MODEL_ID,,}")-dapo-minimal"
+
+python3 -m recipe.dapo.main_dapo \
+    data.train_files="${HOME}/data/gsm8k/train.parquet" \
+    data.val_files="${HOME}/data/gsm8k/test.parquet" \
+    reward_model.reward_manager=dapo \
+    algorithm.adv_estimator=${adv_estimator} \
+    algorithm.use_kl_in_reward=${use_kl_in_reward} \
+    algorithm.kl_ctrl.kl_coef=${kl_coef} \
+    actor_rollout_ref.actor.use_kl_loss=${use_kl_loss} \
+    actor_rollout_ref.actor.kl_loss_coef=${kl_loss_coef} \
+    actor_rollout_ref.actor.clip_ratio_low=${clip_ratio_low} \
+    actor_rollout_ref.actor.clip_ratio_high=${clip_ratio_high} \
+    data.max_prompt_length=${max_prompt_length} \
+    data.max_response_length=${max_response_length} \
+    reward_model.overlong_buffer.enable=${enable_overlong_buffer} \
+    reward_model.overlong_buffer.len=${overlong_buffer_len} \
+    reward_model.overlong_buffer.penalty_factor=${overlong_penalty_factor} \
+    actor_rollout_ref.actor.loss_agg_mode=${loss_agg_mode} \
+    data.train_batch_size=${train_prompt_bsz} \
+    data.gen_batch_size=${gen_prompt_bsz} \
+    algorithm.filter_groups.enable=${enable_filter_groups} \
+    algorithm.filter_groups.metric=${filter_groups_metric} \
+    algorithm.filter_groups.max_num_gen_batches=${max_num_gen_batches} \
+    actor_rollout_ref.model.path="${MODEL_PATH}" \
+    actor_rollout_ref.actor.optim.lr=1e-6 \
+    actor_rollout_ref.model.use_remove_padding=True \
+    actor_rollout_ref.model.use_fused_kernels=True \
+    actor_rollout_ref.rollout.n=${n_resp_per_prompt} \
+    actor_rollout_ref.actor.ppo_mini_batch_size=${train_prompt_mini_bsz} \
+    actor_rollout_ref.actor.ppo_micro_batch_size_per_gpu=${train_traj_micro_bsz_per_gpu} \
+    actor_rollout_ref.actor.fsdp_config.param_offload=False \
+    actor_rollout_ref.actor.fsdp_config.optimizer_offload=False \
+    actor_rollout_ref.rollout.log_prob_micro_batch_size_per_gpu=${train_traj_micro_bsz_per_gpu} \
+    actor_rollout_ref.rollout.tensor_model_parallel_size=2 \
+    actor_rollout_ref.rollout.name=vllm \
+    actor_rollout_ref.rollout.gpu_memory_utilization=0.8 \
+    actor_rollout_ref.ref.log_prob_micro_batch_size_per_gpu=${train_traj_micro_bsz_per_gpu} \
+    actor_rollout_ref.ref.fsdp_config.param_offload=True \
+    trainer.logger=console \
+    trainer.project_name='verl-test' \
+    trainer.experiment_name="${exp_name}" \
+    trainer.n_gpus_per_node=${NUM_GPUS} \
+    trainer.nnodes=1 \
+    trainer.save_freq=-1 \
+    trainer.total_epochs=2 \
+    trainer.resume_mode=disable \
+    trainer.val_before_train=False \
+    trainer.total_training_steps=1 $@
diff --git a/code/RL_model/verl/verl_train/tests/special_e2e/run_fully_async_policy.sh b/code/RL_model/verl/verl_train/tests/special_e2e/run_fully_async_policy.sh
new file mode 100644
index 0000000000000000000000000000000000000000..579505e410444a8caded2359855a2747c424c3db
--- /dev/null
+++ b/code/RL_model/verl/verl_train/tests/special_e2e/run_fully_async_policy.sh
@@ -0,0 +1,198 @@
+#!/usr/bin/env bash
+set -xeuo pipefail
+
+# Test script for fully_async_policy E2E regression testing
+# This script runs fully async PPO training with both FSDP2 and Megatron backends
+# to ensure the asynchronous training mechanism works correctly
+
+NUM_GPUS=${NUM_GPUS:-8}
+ACTOR_STRATEGY=${ACTOR_STRATEGY:-"fsdp2"}  # fsdp2 or megatron
+
+# Download model if not exists
+MODEL_ID=${MODEL_ID:-Qwen/Qwen2.5-0.5B-Instruct}
+MODEL_PATH=${MODEL_PATH:-${HOME}/models/${MODEL_ID}}
+# hf download "${MODEL_ID}" --local-dir "${MODEL_PATH}"
+
+
+rollout_mode="async"
+rollout_name="vllm" # sglang or vllm
+if [ "$rollout_mode" = "async" ]; then
+    export VLLM_USE_V1=1
+    return_raw_chat="True"
+fi
+
+# Algorithm parameters
+adv_estimator=grpo
+
+use_kl_in_reward=False
+kl_coef=0.0
+use_kl_loss=False
+kl_loss_coef=0.0
+
+clip_ratio_low=0.2
+clip_ratio_high=0.28
+
+# Response length parameters
+max_prompt_length=1024
+max_response_length=2048
+enable_overlong_buffer=True
+overlong_buffer_len=128
+overlong_penalty_factor=1.0
+
+# Training parameters
+loss_agg_mode="token-mean"
+
+# Temperature parameters
+temperature=1.0
+top_p=1.0
+top_k=-1
+val_top_p=0.7
+
+# Fully async specific parameters
+n_gpus_rollout=4
+n_gpus_training=4
+
+train_prompt_bsz=0
+gen_prompt_bsz=1
+n_resp_per_prompt=16
+train_prompt_mini_bsz=16
+total_rollout_steps=$(((128)))
+test_freq=-1
+staleness_threshold=0.1
+trigger_parameter_sync_step=4
+partial_rollout=True
+
+exp_name="$(basename "${MODEL_ID,,}")-fully-async-policy-${ACTOR_STRATEGY}-minimal"
+
+echo "Running fully_async_policy with ${ACTOR_STRATEGY} strategy"
+echo "Total GPUs: ${NUM_GPUS}, Rollout GPUs: ${n_gpus_rollout}, Training GPUs: ${n_gpus_training}"
+
+# Common parameters for both FSDP2 and Megatron
+common_params=(
+    data.train_files="${HOME}/data/gsm8k/train.parquet"
+    data.val_files="${HOME}/data/gsm8k/test.parquet"
+    data.prompt_key=prompt
+    data.truncation='left'
+    data.max_prompt_length=${max_prompt_length}
+    data.max_response_length=${max_response_length}
+    data.train_batch_size=${train_prompt_bsz}
+    data.gen_batch_size=${gen_prompt_bsz}
+    data.return_raw_chat=${return_raw_chat}
+    actor_rollout_ref.rollout.n=${n_resp_per_prompt}
+    actor_rollout_ref.rollout.calculate_log_probs=True
+    algorithm.adv_estimator=${adv_estimator}
+    algorithm.use_kl_in_reward=${use_kl_in_reward}
+    algorithm.kl_ctrl.kl_coef=${kl_coef}
+    actor_rollout_ref.hybrid_engine=False
+    actor_rollout_ref.actor.use_kl_loss=${use_kl_loss}
+    actor_rollout_ref.actor.kl_loss_coef=${kl_loss_coef}
+    actor_rollout_ref.actor.clip_ratio_low=${clip_ratio_low}
+    actor_rollout_ref.actor.clip_ratio_high=${clip_ratio_high}
+    actor_rollout_ref.actor.clip_ratio_c=10.0
+    actor_rollout_ref.model.path="${MODEL_PATH}"
+    actor_rollout_ref.actor.optim.lr=1e-6
+    actor_rollout_ref.actor.optim.lr_warmup_steps=-1
+    actor_rollout_ref.actor.optim.weight_decay=0.1
+    actor_rollout_ref.actor.ppo_mini_batch_size=${train_prompt_mini_bsz}
+    actor_rollout_ref.actor.entropy_coeff=0
+    actor_rollout_ref.actor.loss_agg_mode=${loss_agg_mode}
+    actor_rollout_ref.rollout.gpu_memory_utilization=0.80
+    actor_rollout_ref.rollout.temperature=${temperature}
+    actor_rollout_ref.rollout.top_p=${top_p}
+    actor_rollout_ref.rollout.top_k=${top_k}
+    actor_rollout_ref.rollout.val_kwargs.temperature=${temperature}
+    actor_rollout_ref.rollout.val_kwargs.top_p=${val_top_p}
+    actor_rollout_ref.rollout.val_kwargs.top_k=${top_k}
+    actor_rollout_ref.rollout.val_kwargs.do_sample=True
+    actor_rollout_ref.rollout.val_kwargs.n=1
+    actor_rollout_ref.rollout.enable_chunked_prefill=True
+    actor_rollout_ref.rollout.name=${rollout_name}
+    actor_rollout_ref.rollout.mode=${rollout_mode}
+    actor_rollout_ref.rollout.disable_log_stats=False
+    reward_model.reward_manager=dapo
+    +reward_model.reward_kwargs.overlong_buffer_cfg.enable=${enable_overlong_buffer}
+    +reward_model.reward_kwargs.overlong_buffer_cfg.len=${overlong_buffer_len}
+    +reward_model.reward_kwargs.overlong_buffer_cfg.penalty_factor=${overlong_penalty_factor}
+    +reward_model.reward_kwargs.overlong_buffer_cfg.log=False
+    +reward_model.reward_kwargs.max_resp_len=${max_response_length}
+    trainer.logger=['console']
+    trainer.project_name='verl-test-fully-async'
+    trainer.experiment_name="${exp_name}"
+    trainer.val_before_train=True
+    trainer.save_freq=-1
+    trainer.resume_mode=disable
+    trainer.nnodes=1
+    trainer.n_gpus_per_node=${n_gpus_training}
+    rollout.nnodes=1
+    rollout.n_gpus_per_node=${n_gpus_rollout}
+    rollout.total_rollout_steps=${total_rollout_steps}
+    rollout.total_epochs=2
+    rollout.test_freq=${test_freq}
+    # Fully async specific configurations
+    async_training.staleness_threshold=${staleness_threshold}
+    async_training.partial_rollout="${partial_rollout}"
+    async_training.trigger_parameter_sync_step="${trigger_parameter_sync_step}"
+)
+
+if [ "${ACTOR_STRATEGY}" == "fsdp2" ]; then
+    echo "Running fully async training with FSDP2 strategy..."
+    # FSDP2 specific parameters
+    gen_tp=1
+    sp_size=1
+    fsdp_size=1
+    ref_offload=True
+    actor_offload=False
+
+    python3 -m verl.experimental.fully_async_policy.fully_async_main \
+        "${common_params[@]}" \
+        actor_rollout_ref.model.enable_gradient_checkpointing=True \
+        actor_rollout_ref.actor.strategy=fsdp2 \
+        critic.strategy=fsdp2 \
+        actor_rollout_ref.actor.grad_clip=1.0 \
+        actor_rollout_ref.model.use_remove_padding=True \
+        actor_rollout_ref.actor.use_dynamic_bsz=True \
+        actor_rollout_ref.ref.log_prob_use_dynamic_bsz=True \
+        actor_rollout_ref.rollout.log_prob_use_dynamic_bsz=True \
+        actor_rollout_ref.actor.fsdp_config.param_offload=${actor_offload} \
+        actor_rollout_ref.actor.fsdp_config.optimizer_offload=${actor_offload} \
+        actor_rollout_ref.actor.ulysses_sequence_parallel_size=${sp_size} \
+        actor_rollout_ref.rollout.tensor_model_parallel_size=${gen_tp} \
+        actor_rollout_ref.ref.fsdp_config.param_offload=${ref_offload} \
+        actor_rollout_ref.ref.ulysses_sequence_parallel_size=${sp_size} \
+        actor_rollout_ref.actor.fsdp_config.fsdp_size=${fsdp_size} $@
+
+elif [ "${ACTOR_STRATEGY}" == "megatron" ]; then
+    echo "Running fully async training with Megatron strategy..."
+    # Megatron specific parameters
+    gen_tp=2
+    train_tp=1
+    train_pp=2
+    ref_offload=True
+    actor_offload=False
+
+    python3 -m verl.experimental.fully_async_policy.fully_async_main \
+        --config-path=config \
+        --config-name='fully_async_ppo_megatron_trainer.yaml' \
+        "${common_params[@]}" \
+        actor_rollout_ref.actor.strategy=megatron \
+        critic.strategy=megatron \
+        actor_rollout_ref.actor.optim.lr_decay_steps=10000000 \
+        actor_rollout_ref.actor.ppo_micro_batch_size_per_gpu=2 \
+        actor_rollout_ref.ref.log_prob_micro_batch_size_per_gpu=4 \
+        actor_rollout_ref.rollout.log_prob_micro_batch_size_per_gpu=4 \
+        actor_rollout_ref.actor.megatron.param_offload=${actor_offload} \
+        actor_rollout_ref.actor.megatron.optimizer_offload=${actor_offload} \
+        actor_rollout_ref.actor.megatron.grad_offload=${actor_offload} \
+        actor_rollout_ref.actor.megatron.pipeline_model_parallel_size=${train_pp} \
+        actor_rollout_ref.actor.megatron.tensor_model_parallel_size=${train_tp} \
+        actor_rollout_ref.rollout.tensor_model_parallel_size=${gen_tp} \
+        actor_rollout_ref.ref.megatron.pipeline_model_parallel_size=${train_pp} \
+        actor_rollout_ref.ref.megatron.tensor_model_parallel_size=${train_tp} \
+        actor_rollout_ref.ref.megatron.param_offload=${ref_offload} $@
+else
+    echo "Error: Unknown strategy ${ACTOR_STRATEGY}. Please use 'fsdp2' or 'megatron'"
+    exit 1
+fi
+
+echo "Fully async policy E2E test completed successfully with ${ACTOR_STRATEGY} strategy"
+
diff --git a/code/RL_model/verl/verl_train/tests/special_e2e/run_geo3k_fsdp_sgl_multiturn_w_tool.sh b/code/RL_model/verl/verl_train/tests/special_e2e/run_geo3k_fsdp_sgl_multiturn_w_tool.sh
new file mode 100644
index 0000000000000000000000000000000000000000..b7cc1261ee2333b1d6d1fec87a8596d678d40804
--- /dev/null
+++ b/code/RL_model/verl/verl_train/tests/special_e2e/run_geo3k_fsdp_sgl_multiturn_w_tool.sh
@@ -0,0 +1,58 @@
+# run on 8xH100
+# make sure your current working directory is the root of the project
+
+set -x
+
+#hf download Qwen/Qwen2.5-VL-3B-Instruct --local-dir $HOME/models/Qwen/Qwen2.5-VL-3B-Instruct
+
+ulimit -n 65535
+
+PROJECT_DIR="$(pwd)"
+CONFIG_PATH="$PROJECT_DIR/examples/sglang_multiturn/config"
+FSDP_STRATEGY=${FSDP_STRATEGY:-fsdp}
+
+python3 -m verl.trainer.main_ppo \
+    --config-path="$CONFIG_PATH" \
+    --config-name='geo3k_multiturn_grpo' \
+    algorithm.adv_estimator=grpo \
+    data.train_batch_size=64 \
+    data.max_prompt_length=2048 \
+    data.max_response_length=2048 \
+    data.filter_overlong_prompts=True \
+    data.truncation='error' \
+    data.return_raw_chat=True \
+    actor_rollout_ref.model.path=$HOME/models/Qwen/Qwen2.5-VL-3B-Instruct \
+    actor_rollout_ref.actor.optim.lr=1e-6 \
+    actor_rollout_ref.model.use_remove_padding=True \
+    actor_rollout_ref.actor.ppo_mini_batch_size=64 \
+    actor_rollout_ref.actor.ppo_micro_batch_size_per_gpu=8 \
+    actor_rollout_ref.actor.use_kl_loss=True \
+    actor_rollout_ref.actor.kl_loss_coef=0.001 \
+    actor_rollout_ref.actor.kl_loss_type=low_var_kl \
+    actor_rollout_ref.actor.entropy_coeff=0 \
+    actor_rollout_ref.model.enable_gradient_checkpointing=True \
+    actor_rollout_ref.actor.strategy=$FSDP_STRATEGY \
+    actor_rollout_ref.actor.fsdp_config.param_offload=False \
+    actor_rollout_ref.actor.fsdp_config.optimizer_offload=False \
+    actor_rollout_ref.rollout.log_prob_micro_batch_size_per_gpu=8 \
+    actor_rollout_ref.rollout.tensor_model_parallel_size=2 \
+    actor_rollout_ref.rollout.name=sglang \
+    actor_rollout_ref.rollout.gpu_memory_utilization=0.5 \
+    actor_rollout_ref.rollout.n=8 \
+    actor_rollout_ref.ref.log_prob_micro_batch_size_per_gpu=8 \
+    actor_rollout_ref.ref.strategy=$FSDP_STRATEGY \
+    actor_rollout_ref.ref.fsdp_config.param_offload=True \
+    algorithm.use_kl_in_reward=False \
+    trainer.critic_warmup=0 \
+    trainer.logger=console \
+    trainer.project_name='geo3k_async_rl' \
+    trainer.experiment_name=qwen2.5-vl-3b_function_rm-geo3k-sgl-multi-w-tool-$FSDP_STRATEGY-rebased-0619-verify-n8 \
+    trainer.n_gpus_per_node=8 \
+    trainer.nnodes=1 \
+    trainer.save_freq=-1 \
+    trainer.test_freq=-1 \
+    data.train_files=$HOME/data/geo3k_verl_sgl_multi_turn_preprocessed/train.parquet \
+    data.val_files=$HOME/data/geo3k_verl_sgl_multi_turn_preprocessed/test.parquet \
+    actor_rollout_ref.rollout.multi_turn.tool_config_path="$PROJECT_DIR/examples/sglang_multiturn/config/tool_config/geo3k_tool_config.yaml" \
+    trainer.val_before_train=False \
+    trainer.total_training_steps=1 $@
\ No newline at end of file
diff --git a/code/RL_model/verl/verl_train/tests/special_e2e/run_grpo_lora_with_merge.sh b/code/RL_model/verl/verl_train/tests/special_e2e/run_grpo_lora_with_merge.sh
new file mode 100644
index 0000000000000000000000000000000000000000..4f5fd5d5b24c4f19a2d8c5e3b09820e1fd390460
--- /dev/null
+++ b/code/RL_model/verl/verl_train/tests/special_e2e/run_grpo_lora_with_merge.sh
@@ -0,0 +1,93 @@
+#!/usr/bin/env bash
+#
+#  An e2e test script for testing the GRPO LoRA training process 
+#  and processing the generated checkpoint using the merge_model.py script.  
+
+set -xeuo pipefail
+
+MODEL_ID=${MODEL_ID:-Qwen/Qwen2.5-0.5B}
+MODEL_PATH=${MODEL_PATH:-${HOME}/models/${MODEL_ID}}
+if [ ! -d "$MODEL_PATH" ]; then
+    echo "Downloading model to ${MODEL_PATH}..."
+#    hf download "${MODEL_ID}" --local-dir "${MODEL_PATH}"
+else
+    echo "Model directory ${MODEL_PATH} already exists, skip downloading."
+fi
+
+
+BATCH_SIZE=16
+EXP_NAME="qwen2.5_0.5b_grpo_lora"
+# step 1. train model with grpo-lora for 1 step
+python3 -m verl.trainer.main_ppo \
+    algorithm.adv_estimator=grpo \
+    data.train_files=$HOME/data/gsm8k/train.parquet \
+    data.val_files=$HOME/data/gsm8k/test.parquet \
+    data.train_batch_size=${BATCH_SIZE} \
+    data.max_prompt_length=512 \
+    data.max_response_length=1024 \
+    data.filter_overlong_prompts=True \
+    data.truncation='error' \
+    data.shuffle=False \
+    actor_rollout_ref.model.path=${MODEL_PATH} \
+    actor_rollout_ref.model.use_shm=True \
+    actor_rollout_ref.model.lora_rank=64 \
+    actor_rollout_ref.model.lora_alpha=32 \
+    actor_rollout_ref.actor.optim.lr=3e-6 \
+    actor_rollout_ref.model.use_remove_padding=True \
+    actor_rollout_ref.actor.ppo_mini_batch_size=${BATCH_SIZE} \
+    actor_rollout_ref.actor.ppo_micro_batch_size_per_gpu=1 \
+    actor_rollout_ref.actor.use_kl_loss=True \
+    actor_rollout_ref.actor.kl_loss_coef=0.001 \
+    actor_rollout_ref.actor.kl_loss_type=low_var_kl \
+    actor_rollout_ref.actor.entropy_coeff=0 \
+    actor_rollout_ref.model.enable_gradient_checkpointing=True \
+    actor_rollout_ref.actor.fsdp_config.param_offload=False \
+    actor_rollout_ref.actor.fsdp_config.optimizer_offload=False \
+    actor_rollout_ref.rollout.log_prob_micro_batch_size_per_gpu=40 \
+    actor_rollout_ref.rollout.tensor_model_parallel_size=2 \
+    actor_rollout_ref.rollout.name=vllm \
+    actor_rollout_ref.rollout.gpu_memory_utilization=0.6 \
+    actor_rollout_ref.rollout.n=5 \
+    actor_rollout_ref.rollout.load_format=safetensors \
+    actor_rollout_ref.rollout.layered_summon=True \
+    actor_rollout_ref.ref.log_prob_micro_batch_size_per_gpu=40 \
+    actor_rollout_ref.ref.fsdp_config.param_offload=True \
+    algorithm.use_kl_in_reward=False \
+    trainer.critic_warmup=0 \
+    trainer.logger='["console","wandb"]' \
+    trainer.project_name='verl_grpo_example_gsm8k' \
+    trainer.experiment_name=${EXP_NAME} \
+    trainer.n_gpus_per_node=8 \
+    trainer.nnodes=1 \
+    trainer.total_training_steps=1 \
+    trainer.save_freq=1 \
+    trainer.test_freq=5 \
+    trainer.total_epochs=1 $@
+
+# step 2. merge model
+python3 -m verl.model_merger merge \
+    --backend fsdp \
+    --local_dir checkpoints/verl_grpo_example_gsm8k/${EXP_NAME}/global_step_1/actor/ \
+    --target_dir checkpoints/verl_grpo_example_gsm8k/${EXP_NAME}/global_step_1/actor/hf
+
+# step 3. assert
+# make sure adapter_model.safetensors exists and its size is larger than 1MB
+file_path="checkpoints/verl_grpo_example_gsm8k/${EXP_NAME}/global_step_1/actor/hf/lora_adapter/adapter_model.safetensors"
+
+if [ ! -f "$file_path" ]; then
+    echo "Error: File $file_path does not exist!"
+    exit 1
+fi
+
+file_size=$(stat -c %s "$file_path")
+
+min_size_mb=1
+min_size=$((min_size_mb * 1024 * 1024))  # 1MB = 1048576 bytes
+
+if [ "$file_size" -lt "$min_size" ]; then
+    echo "Error: File $file_path is too small! Current size: $((file_size/1024))KB, Required: ${min_size_mb}MB"
+    exit 1
+fi
+
+echo "Check passed: File exists and size is $(($file_size/1024/1024))MB"
+exit 0
diff --git a/code/RL_model/verl/verl_train/tests/special_e2e/run_gsm8k_fsdp_sgl_multiturn_sf_tool.sh b/code/RL_model/verl/verl_train/tests/special_e2e/run_gsm8k_fsdp_sgl_multiturn_sf_tool.sh
new file mode 100644
index 0000000000000000000000000000000000000000..b03515b9920bb69d22802f48f66164aae734148b
--- /dev/null
+++ b/code/RL_model/verl/verl_train/tests/special_e2e/run_gsm8k_fsdp_sgl_multiturn_sf_tool.sh
@@ -0,0 +1,62 @@
+# run on 8xH20
+# make sure your current working directory is the root of the project
+
+set -x
+
+
+export PYTHONUNBUFFERED=1
+export RAY_DEDUP_LOGS=0
+export RUST_BACKTRACE=1
+export HYDRA_FULL_ERROR=1
+
+ulimit -n 65535
+
+PROJECT_DIR="$(pwd)"
+CONFIG_PATH="$PROJECT_DIR/examples/sglang_multiturn/config"
+
+python3 -m verl.trainer.main_ppo \
+    --config-path="$CONFIG_PATH" \
+    --config-name='gsm8k_multiturn_sf_grpo' \
+    algorithm.adv_estimator=grpo \
+    data.train_batch_size=128 \
+    data.max_prompt_length=2048 \
+    data.max_response_length=16384 \
+    data.filter_overlong_prompts=False \
+    data.truncation='error' \
+    data.return_raw_chat=True \
+    data.train_files=$HOME/data/retool_dapo/train.parquet \
+    data.val_files=$HOME/data/retool_aime2024/train.parquet \
+    actor_rollout_ref.model.path=Qwen/Qwen3-4B \
+    actor_rollout_ref.actor.use_dynamic_bsz=True \
+    actor_rollout_ref.model.use_remove_padding=True \
+    actor_rollout_ref.model.use_liger=False \
+    actor_rollout_ref.model.enable_gradient_checkpointing=True \
+    +actor_rollout_ref.model.enable_activation_offload=True \
+    actor_rollout_ref.actor.optim.lr=1e-6 \
+    actor_rollout_ref.actor.ppo_mini_batch_size=128 \
+    actor_rollout_ref.actor.ulysses_sequence_parallel_size=1 \
+    actor_rollout_ref.actor.ppo_max_token_len_per_gpu=32768 \
+    actor_rollout_ref.actor.use_kl_loss=False \
+    actor_rollout_ref.actor.kl_loss_coef=0.0 \
+    actor_rollout_ref.actor.kl_loss_type=low_var_kl \
+    actor_rollout_ref.actor.entropy_coeff=0 \
+    actor_rollout_ref.actor.fsdp_config.param_offload=True \
+    actor_rollout_ref.actor.fsdp_config.optimizer_offload=True \
+    actor_rollout_ref.rollout.tensor_model_parallel_size=2 \
+    actor_rollout_ref.rollout.name=sglang \
+    actor_rollout_ref.rollout.gpu_memory_utilization=0.8 \
+    actor_rollout_ref.rollout.n=8 \
+    actor_rollout_ref.rollout.multi_turn.tool_config_path="$PROJECT_DIR/examples/sglang_multiturn/config/tool_config/sandbox_fusion_tool_config.yaml" \
+    actor_rollout_ref.ref.fsdp_config.param_offload=True \
+    algorithm.use_kl_in_reward=False \
+    trainer.critic_warmup=0 \
+    trainer.logger='["console","wandb"]' \
+    trainer.project_name='retool_async_rl' \
+    trainer.experiment_name='qwen3-4b_function_rm-retool-async-sgl-no-sft-n8-v2505271300' \
+    trainer.val_before_train=False \
+    trainer.n_gpus_per_node=8 \
+    trainer.nnodes=1 \
+    trainer.save_freq=100 \
+    trainer.test_freq=20 \
+    trainer.total_training_steps=1000 \
+    trainer.total_epochs=1 $@
\ No newline at end of file
diff --git a/code/RL_model/verl/verl_train/tests/special_e2e/run_gsm8k_fsdp_sgl_multiturn_w_tool.sh b/code/RL_model/verl/verl_train/tests/special_e2e/run_gsm8k_fsdp_sgl_multiturn_w_tool.sh
new file mode 100644
index 0000000000000000000000000000000000000000..109f6760b2859414f36697172b2586e0e30796e1
--- /dev/null
+++ b/code/RL_model/verl/verl_train/tests/special_e2e/run_gsm8k_fsdp_sgl_multiturn_w_tool.sh
@@ -0,0 +1,58 @@
+# run on 8xH100
+# make sure your current working directory is the root of the project
+
+set -x
+
+#hf download Qwen/Qwen2.5-3B-Instruct --local-dir $HOME/models/Qwen/Qwen2.5-3B-Instruct
+
+ulimit -n 65535
+
+PROJECT_DIR="$(pwd)"
+CONFIG_PATH="$PROJECT_DIR/examples/sglang_multiturn/config"
+FSDP_STRATEGY=${FSDP_STRATEGY:-fsdp}
+
+python3 -m verl.trainer.main_ppo \
+    --config-path="$CONFIG_PATH" \
+    --config-name='gsm8k_multiturn_grpo' \
+    algorithm.adv_estimator=grpo \
+    data.train_batch_size=256 \
+    data.max_prompt_length=1024 \
+    data.max_response_length=1024 \
+    data.filter_overlong_prompts=True \
+    data.truncation='error' \
+    data.return_raw_chat=True \
+    actor_rollout_ref.model.path=$HOME/models/Qwen/Qwen2.5-3B-Instruct \
+    actor_rollout_ref.actor.optim.lr=1e-6 \
+    actor_rollout_ref.model.use_remove_padding=True \
+    actor_rollout_ref.actor.ppo_mini_batch_size=256 \
+    actor_rollout_ref.actor.ppo_micro_batch_size_per_gpu=16 \
+    actor_rollout_ref.actor.use_kl_loss=True \
+    actor_rollout_ref.actor.kl_loss_coef=0.001 \
+    actor_rollout_ref.actor.kl_loss_type=low_var_kl \
+    actor_rollout_ref.actor.entropy_coeff=0 \
+    actor_rollout_ref.model.enable_gradient_checkpointing=True \
+    actor_rollout_ref.actor.strategy=$FSDP_STRATEGY \
+    actor_rollout_ref.actor.fsdp_config.param_offload=False \
+    actor_rollout_ref.actor.fsdp_config.optimizer_offload=False \
+    actor_rollout_ref.rollout.log_prob_micro_batch_size_per_gpu=32 \
+    actor_rollout_ref.rollout.tensor_model_parallel_size=2 \
+    actor_rollout_ref.rollout.name=sglang \
+    actor_rollout_ref.rollout.gpu_memory_utilization=0.5 \
+    actor_rollout_ref.rollout.n=8 \
+    actor_rollout_ref.ref.log_prob_micro_batch_size_per_gpu=32 \
+    actor_rollout_ref.ref.strategy=$FSDP_STRATEGY \
+    actor_rollout_ref.ref.fsdp_config.param_offload=True \
+    algorithm.use_kl_in_reward=False \
+    trainer.critic_warmup=0 \
+    trainer.logger=console \
+    trainer.project_name='gsm8k_async_rl' \
+    trainer.experiment_name=qwen2.5-3b_function_rm-gsm8k-sgl-multi-w-tool-$FSDP_STRATEGY-rebased-0427-verify-n16 \
+    trainer.n_gpus_per_node=8 \
+    trainer.nnodes=1 \
+    trainer.save_freq=-1 \
+    trainer.test_freq=-1 \
+    data.train_files=$HOME/data/gsm8k_verl_sgl_multi_turn_preprocessed/train.parquet \
+    data.val_files=$HOME/data/gsm8k_verl_sgl_multi_turn_preprocessed/test.parquet \
+    actor_rollout_ref.rollout.multi_turn.tool_config_path="$PROJECT_DIR/examples/sglang_multiturn/config/tool_config/gsm8k_tool_config.yaml" \
+    trainer.val_before_train=False \
+    trainer.total_training_steps=1 $@
diff --git a/code/RL_model/verl/verl_train/tests/special_e2e/run_one_step_off_policy.sh b/code/RL_model/verl/verl_train/tests/special_e2e/run_one_step_off_policy.sh
new file mode 100644
index 0000000000000000000000000000000000000000..060363ded8b2b1e4711de2f2c644841c51786c58
--- /dev/null
+++ b/code/RL_model/verl/verl_train/tests/special_e2e/run_one_step_off_policy.sh
@@ -0,0 +1,174 @@
+#!/usr/bin/env bash
+set -xeuo pipefail
+
+# Test script for one_step_off_policy E2E regression testing
+# This script runs one_step_off_policy with both FSDP2 and Megatron backends
+# to ensure the asynchronous training mechanism works correctly
+
+NUM_GPUS=${NUM_GPUS:-8}
+ACTOR_STRATEGY=${ACTOR_STRATEGY:-"fsdp2"}  # fsdp2 or megatron
+
+# Download model if not exists
+MODEL_ID=${MODEL_ID:-Qwen/Qwen2.5-0.5B-Instruct}
+MODEL_PATH=${MODEL_PATH:-${HOME}/models/${MODEL_ID}}
+#hf download "${MODEL_ID}" --local-dir "${MODEL_PATH}"
+
+# Algorithm parameters
+adv_estimator=grpo
+
+use_kl_in_reward=False
+kl_coef=0.0
+use_kl_loss=False
+kl_loss_coef=0.0
+
+clip_ratio_low=0.2
+clip_ratio_high=0.28
+
+# Response length parameters
+max_prompt_length=1024
+max_response_length=2048
+enable_overlong_buffer=True
+overlong_buffer_len=128
+overlong_penalty_factor=1.0
+
+# Training parameters
+loss_agg_mode="token-mean"
+train_prompt_bsz=8
+n_resp_per_prompt=3
+train_prompt_mini_bsz=4
+
+# Temperature parameters
+temperature=1.0
+top_p=1.0
+top_k=-1
+val_top_p=0.7
+
+# One-step-off-policy specific parameters
+# Allocate 2 GPUs for rollout, remaining for training
+n_gpus_rollout=2
+n_gpus_training=$((NUM_GPUS - n_gpus_rollout))
+
+exp_name="$(basename "${MODEL_ID,,}")-one-step-off-policy-${ACTOR_STRATEGY}-minimal"
+
+echo "Running one_step_off_policy with ${ACTOR_STRATEGY} strategy"
+echo "Total GPUs: ${NUM_GPUS}, Rollout GPUs: ${n_gpus_rollout}, Training GPUs: ${n_gpus_training}"
+
+# Common parameters for both FSDP2 and Megatron
+common_params=(
+    data.train_files="${HOME}/data/gsm8k/train.parquet"
+    data.val_files="${HOME}/data/gsm8k/test.parquet"
+    data.prompt_key=prompt
+    data.truncation='left'
+    data.max_prompt_length=${max_prompt_length}
+    data.max_response_length=${max_response_length}
+    data.train_batch_size=${train_prompt_bsz}
+    actor_rollout_ref.rollout.n=${n_resp_per_prompt}
+    algorithm.adv_estimator=${adv_estimator}
+    algorithm.use_kl_in_reward=${use_kl_in_reward}
+    algorithm.kl_ctrl.kl_coef=${kl_coef}
+    actor_rollout_ref.hybrid_engine=False \
+    actor_rollout_ref.actor.use_kl_loss=${use_kl_loss}
+    actor_rollout_ref.actor.kl_loss_coef=${kl_loss_coef}
+    actor_rollout_ref.actor.clip_ratio_low=${clip_ratio_low}
+    actor_rollout_ref.actor.clip_ratio_high=${clip_ratio_high}
+    actor_rollout_ref.actor.clip_ratio_c=10.0
+    actor_rollout_ref.model.path="${MODEL_PATH}"
+    actor_rollout_ref.actor.optim.lr=1e-6
+    actor_rollout_ref.actor.optim.lr_warmup_steps=-1
+    actor_rollout_ref.actor.optim.weight_decay=0.1
+    actor_rollout_ref.actor.ppo_mini_batch_size=${train_prompt_mini_bsz}
+    actor_rollout_ref.actor.entropy_coeff=0
+    actor_rollout_ref.actor.loss_agg_mode=${loss_agg_mode}
+    actor_rollout_ref.rollout.gpu_memory_utilization=0.80
+    actor_rollout_ref.rollout.temperature=${temperature}
+    actor_rollout_ref.rollout.top_p=${top_p}
+    actor_rollout_ref.rollout.top_k=${top_k}
+    actor_rollout_ref.rollout.val_kwargs.temperature=${temperature}
+    actor_rollout_ref.rollout.val_kwargs.top_p=${val_top_p}
+    actor_rollout_ref.rollout.val_kwargs.top_k=${top_k}
+    actor_rollout_ref.rollout.val_kwargs.do_sample=True
+    actor_rollout_ref.rollout.val_kwargs.n=1
+    actor_rollout_ref.rollout.enable_chunked_prefill=True \
+    actor_rollout_ref.rollout.name=vllm \
+    reward_model.reward_manager=dapo
+    +reward_model.reward_kwargs.overlong_buffer_cfg.enable=${enable_overlong_buffer}
+    +reward_model.reward_kwargs.overlong_buffer_cfg.len=${overlong_buffer_len}
+    +reward_model.reward_kwargs.overlong_buffer_cfg.penalty_factor=${overlong_penalty_factor}
+    +reward_model.reward_kwargs.overlong_buffer_cfg.log=False
+    +reward_model.reward_kwargs.max_resp_len=${max_response_length}
+    trainer.logger=['console']
+    trainer.project_name='verl-test'
+    trainer.experiment_name="${exp_name}"
+    trainer.val_before_train=True
+    trainer.test_freq=-1
+    trainer.save_freq=-1
+    trainer.total_epochs=2
+    trainer.total_training_steps=2
+    trainer.resume_mode=disable
+    trainer.nnodes=1
+    trainer.n_gpus_per_node=${n_gpus_training}
+    rollout.nnodes=1
+    rollout.n_gpus_per_node=${n_gpus_rollout}
+
+)
+
+if [ "${ACTOR_STRATEGY}" == "fsdp2" ]; then
+    echo "Running with FSDP2 strategy..."
+    # FSDP2 specific parameters
+    gen_tp=2
+    sp_size=2
+    fsdp_size=2
+    ref_offload=True
+    actor_offload=False
+
+    python3 -m verl.experimental.one_step_off_policy.main_ppo \
+        "${common_params[@]}" \
+        actor_rollout_ref.actor.strategy=fsdp2 \
+        critic.strategy=fsdp2 \
+        actor_rollout_ref.actor.grad_clip=1.0 \
+        actor_rollout_ref.model.use_remove_padding=True \
+        actor_rollout_ref.model.enable_gradient_checkpointing=True \
+        actor_rollout_ref.actor.use_dynamic_bsz=True \
+        actor_rollout_ref.ref.log_prob_use_dynamic_bsz=True \
+        actor_rollout_ref.rollout.log_prob_use_dynamic_bsz=True \
+        actor_rollout_ref.actor.fsdp_config.param_offload=${actor_offload} \
+        actor_rollout_ref.actor.fsdp_config.optimizer_offload=${actor_offload} \
+        actor_rollout_ref.actor.ulysses_sequence_parallel_size=${sp_size} \
+        actor_rollout_ref.rollout.tensor_model_parallel_size=${gen_tp} \
+        actor_rollout_ref.ref.fsdp_config.param_offload=${ref_offload} \
+        actor_rollout_ref.ref.ulysses_sequence_parallel_size=${sp_size} \
+        actor_rollout_ref.actor.fsdp_config.fsdp_size=${fsdp_size} $@
+
+elif [ "${ACTOR_STRATEGY}" == "megatron" ]; then
+    echo "Running with Megatron strategy..."
+    # Megatron specific parameters
+    gen_tp=2
+    train_tp=1
+    train_pp=2
+    ref_offload=True
+    actor_offload=False
+
+    python3 -m verl.experimental.one_step_off_policy.main_ppo \
+        --config-path=config \
+        --config-name='one_step_off_ppo_megatron_trainer.yaml' \
+        "${common_params[@]}" \
+        actor_rollout_ref.actor.strategy=megatron \
+        critic.strategy=megatron \
+        actor_rollout_ref.actor.ppo_micro_batch_size_per_gpu=2 \
+        actor_rollout_ref.ref.log_prob_micro_batch_size_per_gpu=4 \
+        actor_rollout_ref.rollout.log_prob_micro_batch_size_per_gpu=4 \
+        actor_rollout_ref.actor.megatron.param_offload=${actor_offload} \
+        actor_rollout_ref.actor.megatron.optimizer_offload=${actor_offload} \
+        actor_rollout_ref.actor.megatron.grad_offload=${actor_offload} \
+        actor_rollout_ref.actor.megatron.pipeline_model_parallel_size=${train_pp} \
+        actor_rollout_ref.actor.megatron.tensor_model_parallel_size=${train_tp} \
+        actor_rollout_ref.rollout.tensor_model_parallel_size=${gen_tp} \
+        actor_rollout_ref.ref.megatron.pipeline_model_parallel_size=${train_pp} \
+        actor_rollout_ref.ref.megatron.tensor_model_parallel_size=${train_tp} \
+        actor_rollout_ref.ref.megatron.param_offload=${ref_offload} $@
+else
+    echo "Error: Unknown strategy ${ACTOR_STRATEGY}. Please use 'fsdp2' or 'megatron'"
+    exit 1
+fi
+
+echo "One-step-off-policy E2E test completed successfully with ${ACTOR_STRATEGY} strategy"
\ No newline at end of file
diff --git a/code/RL_model/verl/verl_train/tests/special_e2e/run_ppo_trainer_megatron.sh b/code/RL_model/verl/verl_train/tests/special_e2e/run_ppo_trainer_megatron.sh
new file mode 100644
index 0000000000000000000000000000000000000000..57a75d5103e13b5b0a12d46f9319fb86cb754ee2
--- /dev/null
+++ b/code/RL_model/verl/verl_train/tests/special_e2e/run_ppo_trainer_megatron.sh
@@ -0,0 +1,270 @@
+#!/usr/bin/env bash
+set -xeuo pipefail
+
+export CUDA_DEVICE_MAX_CONNECTIONS=1 # For megatron communication/computation overlapping
+export VERL_LOGGING_LEVEL=INFO
+export VERL_PPO_LOGGING_LEVEL=INFO
+
+NUM_GPUS=${NUM_GPUS:-8}
+
+MODEL_ID=${MODEL_ID:-Qwen/Qwen2.5-0.5B}
+MODEL_PATH=${MODEL_PATH:-${HOME}/models/${MODEL_ID}}
+RM_MODEL_PATH=${RM_MODEL_PATH:-${HOME}/models/Skywork/Skywork-Reward-V2-Llama-3.2-1B}
+#hf download "${MODEL_ID}" --local-dir "${MODEL_PATH}"
+
+USE_DUMMY_MODEL=${USE_DUMMY_MODEL:-False}
+DUMMY_MODEL_PATH=${DUMMY_MODEL_PATH:-${HOME}/dummy_models/${MODEL_ID}}
+if [ "$USE_DUMMY_MODEL" = "True" ]; then
+    if [ -z "${DUMMY_MODEL_CONFIG_PATH}"  ]; then
+        echo "[ERROR] DUMMY_MODEL_CONFIG_PATH not set"
+        exit 1
+    fi
+
+    python scripts/init_random_model.py \
+        --hf_model_path "${MODEL_PATH}" \
+        --new_config_path "${DUMMY_MODEL_CONFIG_PATH}" \
+        --output_path "${DUMMY_MODEL_PATH}"
+
+    MODEL_PATH="${DUMMY_MODEL_PATH}"
+fi
+
+TRAIN_FILES=${TRAIN_FILES:-${HOME}/data/gsm8k/train.parquet}
+VAL_FILES=${VAL_FILES:-${HOME}/data/gsm8k/test.parquet}
+
+ADV_ESTIMATOR=${ADV_ESTIMATOR:-gae}
+# Validation
+VAL_BEFORE_TRAIN=${VAL_BEFORE_TRAIN:-False}
+TEST_FREQ=${TEST_FREQ:--1}
+# Save & Resume
+RESUME_MODE=${RESUME_MODE:-disable}
+SAVE_FREQ=${SAVE_FREQ:--1}
+TOTAL_TRAIN_STEPS=${TOTAL_TRAIN_STEPS:-1}
+
+USE_DYNAMIC_BSZ=${USE_DYNAMIC_BSZ:-True}
+ppo_max_token_len_per_gpu=${PPO_MAX_TOKEN_LEN:-2400}
+forward_max_token_len_per_gpu=${FWD_MAX_TOKEN_LEN:-4800}
+train_traj_micro_bsz_per_gpu=${MICRO_BSZ:-2} # b
+n_resp_per_prompt=4 # g
+
+train_traj_micro_bsz=$((train_traj_micro_bsz_per_gpu * NUM_GPUS)) # b * n
+train_traj_mini_bsz=$((train_traj_micro_bsz * 2)) # 2 * b * n
+train_prompt_mini_bsz=$((train_traj_mini_bsz * n_resp_per_prompt)) # 2 * b * n / g
+train_prompt_bsz=$((train_prompt_mini_bsz * 2)) # 4 * b * n / g
+
+LORA_RANK=${LORA_RANK:-0}
+CRITIC_LORA_RANK=${CRITIC_LORA_RANK:-$LORA_RANK}
+LORA_ALPHA=${LORA_ALPHA:-${LORA_RANK}}
+LORA_TARGET_MODULES=${LORA_TARGET_MODULES:-"['linear_qkv','linear_proj','linear_fc1','linear_fc2']"}
+LORA_MERGE=${LORA_MERGE:-False}
+
+MAX_PROMPT_LENGTH=${MAX_PROMPT_LENGTH:-512}
+MAX_RESPONSE_LENGTH=${MAX_RESPONSE_LENGTH:-512}
+MAX_RM_LENGTH=$((MAX_PROMPT_LENGTH + MAX_RESPONSE_LENGTH))
+
+COMMON_PP=${COMMON_PP:-2}
+COMMON_VPP=${COMMON_VPP:-2}
+COMMON_CP=${COMMON_CP:-2}
+COMMON_TP=${COMMON_TP:-2}
+COMMON_EP=${COMMON_EP:-1}
+COMMON_ETP=${COMMON_ETP:-1}
+
+TRAIN_TP=${TRAIN_TP:-$COMMON_TP}
+INFER_TP=${INFER_TP:-$COMMON_TP}
+
+ACTOR_PP=${ACTOR_PP:-$COMMON_PP}
+ACTOR_VPP=${ACTOR_VPP:-$COMMON_VPP}
+ACTOR_CP=${ACTOR_CP:-$COMMON_CP}
+ACTOR_TP=${ACTOR_TP:-$TRAIN_TP}
+ACTOR_EP=${ACTOR_EP:-$COMMON_EP}
+ACTOR_ETP=${ACTOR_ETP:-$COMMON_ETP}
+ROLLOUT_TP=${ROLLOUT_TP:-$INFER_TP}
+REF_PP=${REF_PP:-$COMMON_PP}
+REF_VPP=${REF_VPP:-$COMMON_VPP}
+REF_CP=${REF_CP:-$COMMON_CP}
+REF_TP=${REF_TP:-$TRAIN_TP}
+REF_EP=${REF_EP:-$COMMON_EP}
+REF_ETP=${REF_ETP:-$COMMON_ETP}
+CRITIC_PP=${CRITIC_PP:-$COMMON_PP}
+CRITIC_VPP=${CRITIC_VPP:-$COMMON_VPP}
+CRITIC_CP=${CRITIC_CP:-$COMMON_CP}
+CRITIC_TP=${CRITIC_TP:-$TRAIN_TP}
+CRITIC_EP=${CRITIC_EP:-$COMMON_EP}
+CRITIC_ETP=${CRITIC_ETP:-$COMMON_ETP}
+
+ALL_OFFLOAD=${ALL_OFFLOAD:-False}
+COMMON_PARAM_OFFLOAD=${COMMON_PARAM_OFFLOAD:-$ALL_OFFLOAD}
+COMMON_GRAD_OFFLOAD=${COMMON_GRAD_OFFLOAD:-$ALL_OFFLOAD}
+COMMON_OPTIMIZER_OFFLOAD=${COMMON_OPTIMIZER_OFFLOAD:-$ALL_OFFLOAD}
+
+ACTOR_PARAM_OFFLOAD=${ACTOR_PARAM_OFFLOAD:-$COMMON_PARAM_OFFLOAD}
+ACTOR_GRAD_OFFLOAD=${ACTOR_GRAD_OFFLOAD:-$COMMON_GRAD_OFFLOAD}
+ACTOR_OPTIMIZER_OFFLOAD=${ACTOR_OPTIMIZER_OFFLOAD:-$COMMON_OPTIMIZER_OFFLOAD}
+REF_PARAM_OFFLOAD=${REF_PARAM_OFFLOAD:-$COMMON_PARAM_OFFLOAD}
+CRITIC_PARAM_OFFLOAD=${CRITIC_PARAM_OFFLOAD:-$COMMON_PARAM_OFFLOAD}
+CRITIC_GRAD_OFFLOAD=${CRITIC_GRAD_OFFLOAD:-$COMMON_GRAD_OFFLOAD}
+CRITIC_OPTIMIZER_OFFLOAD=${CRITIC_OPTIMIZER_OFFLOAD:-$COMMON_OPTIMIZER_OFFLOAD}
+RM_PARAM_OFFLOAD=${RM_PARAM_OFFLOAD:-$COMMON_PARAM_OFFLOAD}
+USE_MBRIDGE=${USE_MBRIDGE:-False}
+VANILLA_MBRIDGE=${VANILLA_MBRIDGE:-True}
+VALUE_VANILLA_MBRIDGE=${VALUE_VANILLA_MBRIDGE:-$VANILLA_MBRIDGE}
+USE_FUSED_KERNELS=${USE_FUSED_KERNELS:-False}
+
+LR_WARMUP_STEPS=${LR_WARMUP_STEPS:-null}
+
+CHECKPOINT_CONTENTS=['model','hf_model','optimizer','extra']
+SKIP_SAVE_HF_MODEL=${SKIP_SAVE_HF_MODEL:-0}
+if [ $SKIP_SAVE_HF_MODEL -eq 1 ]; then
+    CHECKPOINT_CONTENTS=['model','optimizer','extra']
+fi
+
+USE_DIST_CKPT=${USE_DIST_CKPT:-False}
+DIST_CKPT_PATH=${DIST_CKPT_PATH:-${HOME}/dist_ckpt/${MODEL_ID}}
+if [ "$USE_DIST_CKPT" = "True" ]; then
+    if [ "$USE_DUMMY_MODEL" = "True" ]; then
+        DIST_CKPT_PATH=${HOME}/dist_ckpt_dummy/${MODEL_ID}
+    fi
+    python scripts/converter_hf_to_mcore.py \
+        --hf_model_path "${MODEL_PATH}" \
+        --output_path "${DIST_CKPT_PATH}"
+fi
+
+ENGINE=${ENGINE:-"vllm"}
+if [ "$ENGINE" = "vllm" ]; then
+    export VLLM_USE_V1=1
+fi
+
+exp_name="$(basename "${MODEL_ID,,}")-megatron-gsm8k-minimal"
+ROLLOUT_MODE="async"
+ROLLOUT_QUANTIZATION=${ROLLOUT_QUANTIZATION:-null}
+
+RETURN_RAW_CHAT="True"
+SKIP_TOKENIZER_INIT="True"
+
+OPTIM_MEMORY_EFFICIENT=${OPTIM_MEMORY_EFFICIENT:-False}
+
+PROFILE_ENABLE=${PROFILE_ENABLE:-False}
+PROFILE_STEPS=${PROFILE_STEPS:-[1]}
+PROFILE_RANKS_ALL=${PROFILE_RANKS_ALL:-True}
+PROFILE_RANKS=${PROFILE_RANKS:-[0,1,2,3]}
+DISCRETE=${DISCRETE:-True}  # or True
+
+python3 -m verl.trainer.main_ppo --config-path=config \
+    --config-name='ppo_megatron_trainer.yaml'\
+    algorithm.adv_estimator="${ADV_ESTIMATOR}" \
+    data.train_files="${TRAIN_FILES}" \
+    data.val_files="${VAL_FILES}" \
+    data.train_batch_size=${train_prompt_bsz} \
+    data.max_prompt_length=${MAX_PROMPT_LENGTH} \
+    data.max_response_length=${MAX_RESPONSE_LENGTH} \
+    data.return_raw_chat=${RETURN_RAW_CHAT} \
+    data.filter_overlong_prompts=True \
+    data.truncation='error' \
+    actor_rollout_ref.model.path="${MODEL_PATH}" \
+    actor_rollout_ref.model.use_fused_kernels=${USE_FUSED_KERNELS} \
+    actor_rollout_ref.model.lora.rank=${LORA_RANK} \
+    actor_rollout_ref.model.lora.alpha=${LORA_ALPHA} \
+    actor_rollout_ref.model.lora.target_modules=${LORA_TARGET_MODULES} \
+    actor_rollout_ref.model.lora.merge=${LORA_MERGE} \
+    actor_rollout_ref.actor.optim.lr_warmup_steps=$LR_WARMUP_STEPS \
+    +actor_rollout_ref.actor.optim.override_optimizer_config.optimizer_cpu_offload=$OPTIM_MEMORY_EFFICIENT \
+    +actor_rollout_ref.actor.optim.override_optimizer_config.overlap_cpu_optimizer_d2h_h2d=$OPTIM_MEMORY_EFFICIENT \
+    +actor_rollout_ref.actor.optim.override_optimizer_config.use_precision_aware_optimizer=$OPTIM_MEMORY_EFFICIENT \
+    actor_rollout_ref.actor.ppo_mini_batch_size=${train_prompt_mini_bsz} \
+    actor_rollout_ref.actor.ppo_micro_batch_size_per_gpu=${train_traj_micro_bsz_per_gpu} \
+    actor_rollout_ref.actor.use_dynamic_bsz=${USE_DYNAMIC_BSZ} \
+    actor_rollout_ref.actor.ppo_max_token_len_per_gpu=${ppo_max_token_len_per_gpu} \
+    actor_rollout_ref.actor.megatron.use_mbridge=${USE_MBRIDGE} \
+    actor_rollout_ref.actor.megatron.vanilla_mbridge=${VANILLA_MBRIDGE} \
+    actor_rollout_ref.actor.megatron.pipeline_model_parallel_size=$ACTOR_PP \
+    actor_rollout_ref.actor.megatron.virtual_pipeline_model_parallel_size=$ACTOR_VPP \
+    actor_rollout_ref.actor.megatron.context_parallel_size=$ACTOR_CP \
+    actor_rollout_ref.actor.megatron.tensor_model_parallel_size=$ACTOR_TP \
+    actor_rollout_ref.actor.megatron.expert_model_parallel_size=$ACTOR_EP \
+    actor_rollout_ref.actor.megatron.expert_tensor_parallel_size=$ACTOR_ETP \
+    actor_rollout_ref.actor.megatron.param_offload=${ACTOR_PARAM_OFFLOAD} \
+    actor_rollout_ref.actor.megatron.optimizer_offload=${ACTOR_OPTIMIZER_OFFLOAD} \
+    actor_rollout_ref.actor.megatron.grad_offload=${ACTOR_GRAD_OFFLOAD} \
+    actor_rollout_ref.actor.megatron.use_dist_checkpointing=${USE_DIST_CKPT} \
+    actor_rollout_ref.actor.megatron.dist_checkpointing_path=${DIST_CKPT_PATH} \
+    actor_rollout_ref.actor.use_kl_loss=True \
+    actor_rollout_ref.actor.kl_loss_coef=0.001 \
+    actor_rollout_ref.actor.kl_loss_type=low_var_kl \
+    actor_rollout_ref.actor.checkpoint.save_contents=$CHECKPOINT_CONTENTS \
+    actor_rollout_ref.actor.profiler.enable=$PROFILE_ENABLE \
+    actor_rollout_ref.actor.profiler.ranks=$PROFILE_RANKS \
+    actor_rollout_ref.actor.profiler.all_ranks=$PROFILE_RANKS_ALL \
+    actor_rollout_ref.rollout.name="${ENGINE}" \
+    actor_rollout_ref.rollout.mode="${ROLLOUT_MODE}" \
+    actor_rollout_ref.rollout.tensor_model_parallel_size=$ROLLOUT_TP \
+    actor_rollout_ref.rollout.gpu_memory_utilization=0.6 \
+    actor_rollout_ref.rollout.n=${n_resp_per_prompt} \
+    ++actor_rollout_ref.rollout.quantization=${ROLLOUT_QUANTIZATION} \
+    actor_rollout_ref.rollout.log_prob_micro_batch_size_per_gpu=${train_traj_micro_bsz_per_gpu} \
+    actor_rollout_ref.ref.log_prob_micro_batch_size_per_gpu=${train_traj_micro_bsz_per_gpu} \
+    actor_rollout_ref.ref.megatron.use_mbridge=${USE_MBRIDGE} \
+    actor_rollout_ref.ref.megatron.vanilla_mbridge=${VANILLA_MBRIDGE} \
+    actor_rollout_ref.ref.megatron.pipeline_model_parallel_size=$REF_PP \
+    actor_rollout_ref.ref.megatron.virtual_pipeline_model_parallel_size=$REF_VPP \
+    actor_rollout_ref.ref.megatron.context_parallel_size=$REF_CP \
+    actor_rollout_ref.ref.megatron.tensor_model_parallel_size=$REF_TP \
+    actor_rollout_ref.ref.megatron.expert_model_parallel_size=$REF_EP \
+    actor_rollout_ref.ref.megatron.expert_tensor_parallel_size=$REF_ETP \
+    actor_rollout_ref.ref.megatron.param_offload=${REF_PARAM_OFFLOAD} \
+    actor_rollout_ref.ref.megatron.use_dist_checkpointing=${USE_DIST_CKPT} \
+    actor_rollout_ref.ref.megatron.dist_checkpointing_path=${DIST_CKPT_PATH} \
+    critic.optim.lr=2e-5 \
+    critic.optim.lr_warmup_steps=$LR_WARMUP_STEPS \
+    +critic.optim.override_optimizer_config.optimizer_cpu_offload=$OPTIM_MEMORY_EFFICIENT \
+    +critic.optim.override_optimizer_config.overlap_cpu_optimizer_d2h_h2d=$OPTIM_MEMORY_EFFICIENT \
+    +critic.optim.override_optimizer_config.use_precision_aware_optimizer=$OPTIM_MEMORY_EFFICIENT \
+    critic.model.path="${MODEL_PATH}" \
+    critic.model.lora.rank=${CRITIC_LORA_RANK} \
+    critic.model.lora.alpha=${LORA_ALPHA} \
+    critic.model.lora.target_modules=${LORA_TARGET_MODULES} \
+    critic.ppo_micro_batch_size_per_gpu=${train_traj_micro_bsz_per_gpu} \
+    critic.ppo_max_token_len_per_gpu=${forward_max_token_len_per_gpu} \
+    critic.megatron.use_mbridge=${USE_MBRIDGE} \
+    critic.megatron.vanilla_mbridge=${VALUE_VANILLA_MBRIDGE} \
+    critic.megatron.pipeline_model_parallel_size=$CRITIC_PP \
+    critic.megatron.virtual_pipeline_model_parallel_size=$CRITIC_VPP \
+    critic.megatron.context_parallel_size=$CRITIC_CP \
+    critic.megatron.tensor_model_parallel_size=$CRITIC_TP \
+    critic.megatron.expert_model_parallel_size=$CRITIC_EP \
+    critic.megatron.expert_tensor_parallel_size=$CRITIC_ETP \
+    critic.megatron.param_offload=${CRITIC_PARAM_OFFLOAD} \
+    critic.megatron.optimizer_offload=${CRITIC_OPTIMIZER_OFFLOAD} \
+    critic.megatron.grad_offload=${CRITIC_GRAD_OFFLOAD} \
+    critic.megatron.use_dist_checkpointing=${USE_DIST_CKPT} \
+    critic.megatron.dist_checkpointing_path=${DIST_CKPT_PATH} \
+    critic.checkpoint.save_contents=$CHECKPOINT_CONTENTS \
+    critic.profiler.enable=$PROFILE_ENABLE \
+    critic.profiler.ranks=$PROFILE_RANKS \
+    critic.profiler.all_ranks=$PROFILE_RANKS_ALL \
+    reward_model.enable=True \
+    reward_model.model.path="${RM_MODEL_PATH}" \
+    reward_model.use_reward_loop=True \
+    reward_model.rollout.name=${ENGINE} \
+    reward_model.rollout.gpu_memory_utilization=0.6 \
+    reward_model.rollout.tensor_model_parallel_size=${INFER_TP} \
+    reward_model.rollout.prompt_length=${MAX_RM_LENGTH} \
+    reward_model.rollout.response_length=${MAX_RESPONSE_LENGTH} \
+    reward_model.num_workers=8 \
+    algorithm.use_kl_in_reward=False \
+    algorithm.kl_penalty=kl \
+    algorithm.kl_ctrl.kl_coef=0.001 \
+    trainer.critic_warmup=0 \
+    trainer.logger=console \
+    trainer.project_name='verl-test' \
+    trainer.experiment_name="${exp_name}" \
+    trainer.nnodes=1 \
+    trainer.n_gpus_per_node=${NUM_GPUS} \
+    trainer.val_before_train="${VAL_BEFORE_TRAIN}" \
+    trainer.test_freq="${TEST_FREQ}" \
+    trainer.save_freq="${SAVE_FREQ}" \
+    trainer.resume_mode="${RESUME_MODE}" \
+    trainer.total_epochs=2 \
+    trainer.total_training_steps="${TOTAL_TRAIN_STEPS}" \
+    global_profiler.profile_continuous_steps=True \
+    global_profiler.tool=nsys \
+    global_profiler.steps=$PROFILE_STEPS \
+    global_profiler.global_tool_config.nsys.discrete=$DISCRETE $@
diff --git a/code/RL_model/verl/verl_train/tests/special_e2e/run_test.sh b/code/RL_model/verl/verl_train/tests/special_e2e/run_test.sh
new file mode 100644
index 0000000000000000000000000000000000000000..c4421c61849264765babe299dbab0dd5251469a6
--- /dev/null
+++ b/code/RL_model/verl/verl_train/tests/special_e2e/run_test.sh
@@ -0,0 +1,13 @@
+#!/bin/bash
+set -xeuo pipefail
+
+# Get the configuration name and engine name from arguments
+CONFIG_NAME="$1"
+ENGINE="${2:-vllm}"
+
+# Download model if needed
+#hf download Qwen/Qwen2.5-0.5B --local-dir "$HOME/models/Qwen/Qwen2.5-0.5B"
+
+# Run the training with the specified configuration
+python3 -m verl.trainer.main_ppo \
+    --config-name "$CONFIG_NAME" "$@" 
\ No newline at end of file
diff --git a/code/RL_model/verl/verl_train/tests/special_e2e/run_transferqueue.sh b/code/RL_model/verl/verl_train/tests/special_e2e/run_transferqueue.sh
new file mode 100644
index 0000000000000000000000000000000000000000..d68ab3fff7b401b049e0da7b7a8fe7355cfec6ff
--- /dev/null
+++ b/code/RL_model/verl/verl_train/tests/special_e2e/run_transferqueue.sh
@@ -0,0 +1,189 @@
+#!/usr/bin/env bash
+set -xeuo pipefail
+
+
+NUM_GPUS=${NUM_GPUS:-8}
+ACTOR_STRATEGY=${ACTOR_STRATEGY:-"fsdp"}  # fsdp or megatron
+
+# Download model if not exists
+MODEL_ID=${MODEL_ID:-Qwen/Qwen2.5-0.5B-Instruct}
+MODEL_PATH=${MODEL_PATH:-${HOME}/models/${MODEL_ID}}
+hf download "${MODEL_ID}" --local-dir "${MODEL_PATH}"
+
+
+rollout_mode="async"
+rollout_name="vllm" # sglang or vllm
+if [ "$rollout_mode" = "async" ]; then
+    export VLLM_USE_V1=1
+    return_raw_chat="True"
+fi
+
+# Algorithm parameters
+adv_estimator=grpo
+
+use_kl_in_reward=False
+kl_coef=0.0
+use_kl_loss=False
+kl_loss_coef=0.0
+
+clip_ratio_low=0.2
+clip_ratio_high=0.28
+
+# Response length parameters
+max_prompt_length=512
+max_response_length=1024
+enable_overlong_buffer=True
+overlong_buffer_len=128
+overlong_penalty_factor=1.0
+
+# Training parameters
+loss_agg_mode="token-mean"
+
+# Temperature parameters
+temperature=1.0
+top_p=1.0
+top_k=-1
+val_top_p=0.7
+
+n_gpus_training=8
+train_prompt_bsz=128
+val_prompt_bsz=128
+n_resp_per_prompt=5
+train_prompt_mini_bsz=32
+test_freq=-1
+
+log_dir="./logs"
+mkdir -p $log_dir
+timestamp=$(date +"%Y%m%d%H%M%S")
+log_file="${log_dir}/qwen2_5-0_5b_transferqueue_${timestamp}.log"
+
+exp_name="$(basename "${MODEL_ID,}")-transferqueue-${ACTOR_STRATEGY}-minimal"
+
+echo "Running transferqueue with ${ACTOR_STRATEGY} strategy"
+echo "Total GPUs: ${NUM_GPUS}"
+
+# Common parameters for both FSDP and Megatron
+common_params=(
+    data.train_files="${HOME}/data/gsm8k/train.parquet"
+    data.val_files="${HOME}/data/gsm8k/test.parquet"
+    data.prompt_key=prompt
+    data.truncation='error'
+    data.max_prompt_length=${max_prompt_length}
+    data.max_response_length=${max_response_length}
+    data.filter_overlong_prompts_workers=128
+    data.filter_overlong_prompts=True
+    data.train_batch_size=${train_prompt_bsz}
+    data.val_batch_size=${val_prompt_bsz}
+    data.return_raw_chat=${return_raw_chat}
+    actor_rollout_ref.rollout.n=${n_resp_per_prompt}
+    algorithm.adv_estimator=${adv_estimator}
+    algorithm.use_kl_in_reward=${use_kl_in_reward}
+    algorithm.kl_ctrl.kl_coef=${kl_coef}
+    actor_rollout_ref.actor.use_kl_loss=${use_kl_loss}
+    actor_rollout_ref.actor.kl_loss_coef=${kl_loss_coef}
+    actor_rollout_ref.actor.clip_ratio_low=${clip_ratio_low}
+    actor_rollout_ref.actor.clip_ratio_high=${clip_ratio_high}
+    actor_rollout_ref.actor.clip_ratio_c=10.0
+    actor_rollout_ref.actor.use_kl_loss=True
+    actor_rollout_ref.model.path="${MODEL_PATH}"
+    actor_rollout_ref.actor.optim.lr=1e-6
+    actor_rollout_ref.actor.optim.lr_warmup_steps=-1
+    actor_rollout_ref.actor.optim.weight_decay=0.1
+    actor_rollout_ref.actor.ppo_mini_batch_size=${train_prompt_mini_bsz}
+    actor_rollout_ref.actor.ppo_micro_batch_size_per_gpu=4
+    actor_rollout_ref.actor.entropy_coeff=0
+    actor_rollout_ref.actor.loss_agg_mode=${loss_agg_mode}
+    actor_rollout_ref.rollout.log_prob_micro_batch_size_per_gpu=4
+    actor_rollout_ref.ref.log_prob_micro_batch_size_per_gpu=8
+    actor_rollout_ref.rollout.gpu_memory_utilization=0.80
+    actor_rollout_ref.rollout.temperature=${temperature}
+    actor_rollout_ref.rollout.top_p=${top_p}
+    actor_rollout_ref.rollout.top_k=${top_k}
+    actor_rollout_ref.rollout.max_num_batched_tokens=10240
+    actor_rollout_ref.rollout.val_kwargs.temperature=${temperature}
+    actor_rollout_ref.rollout.val_kwargs.top_p=${val_top_p}
+    actor_rollout_ref.rollout.val_kwargs.top_k=${top_k}
+    actor_rollout_ref.rollout.val_kwargs.do_sample=True
+    actor_rollout_ref.rollout.val_kwargs.n=1
+    actor_rollout_ref.rollout.enable_chunked_prefill=True
+    actor_rollout_ref.rollout.name=${rollout_name}
+    actor_rollout_ref.rollout.mode=${rollout_mode}
+    actor_rollout_ref.rollout.disable_log_stats=True
+    trainer.logger=console
+    trainer.project_name='verl-test-transferqueue'
+    trainer.experiment_name="${exp_name}"
+    trainer.test_freq="${test_freq}"
+    trainer.save_freq=-1
+    trainer.resume_mode=disable
+    trainer.nnodes=1
+    trainer.n_gpus_per_node=${n_gpus_training}
+    trainer.total_training_steps=2
+    trainer.total_epochs=15
+    trainer.val_before_train=True
+)
+
+if [ "${ACTOR_STRATEGY}" == "fsdp" ]; then
+    echo "Running TransferQueue training with FSDP strategy..."
+    # FSDP specific parameters; fsdp_size need to be -1
+    gen_tp=1
+    sp_size=1
+    fsdp_size=-1
+    ref_offload=True
+    actor_offload=False
+
+    python3 -m verl.experimental.transfer_queue.main_ppo \
+        --config-path=config \
+        --config-name='transfer_queue_ppo_trainer' \
+        "${common_params[@]}" \
+        actor_rollout_ref.model.enable_gradient_checkpointing=True \
+        actor_rollout_ref.actor.strategy=fsdp \
+        critic.strategy=fsdp \
+        actor_rollout_ref.actor.grad_clip=1.0 \
+        actor_rollout_ref.model.use_remove_padding=True \
+        actor_rollout_ref.actor.use_dynamic_bsz=True \
+        actor_rollout_ref.ref.log_prob_use_dynamic_bsz=True \
+        actor_rollout_ref.rollout.log_prob_use_dynamic_bsz=True \
+        actor_rollout_ref.actor.fsdp_config.param_offload=${actor_offload} \
+        actor_rollout_ref.actor.fsdp_config.optimizer_offload=${actor_offload} \
+        actor_rollout_ref.actor.ulysses_sequence_parallel_size=${sp_size} \
+        actor_rollout_ref.rollout.tensor_model_parallel_size=${gen_tp} \
+        actor_rollout_ref.ref.fsdp_config.param_offload=${ref_offload} \
+        actor_rollout_ref.ref.ulysses_sequence_parallel_size=${sp_size} \
+        actor_rollout_ref.actor.fsdp_config.fsdp_size=${fsdp_size} \
+        2>&1 | tee "$log_file" $@
+
+elif [ "${ACTOR_STRATEGY}" == "megatron" ]; then
+    echo "Running TransferQueue training with Megatron strategy..."
+    # Megatron specific parameters
+    gen_tp=2
+    train_tp=1
+    train_pp=2
+    ref_offload=True
+    actor_offload=False
+
+    # For Ascend NPU, please add:
+    #++actor_rollout_ref.actor.megatron.override_transformer_config.use_flash_attn=True \
+    #++actor_rollout_ref.ref.megatron.override_transformer_config.use_flash_attn=True \
+    python3 -m verl.experimental.transfer_queue.main_ppo \
+        --config-path=config \
+        --config-name='transfer_queue_ppo_megatron_trainer' \
+        "${common_params[@]}" \
+        actor_rollout_ref.actor.strategy=megatron \
+        critic.strategy=megatron \
+        actor_rollout_ref.actor.optim.lr_decay_steps=10000000 \
+        actor_rollout_ref.actor.megatron.param_offload=${actor_offload} \
+        actor_rollout_ref.actor.megatron.optimizer_offload=${actor_offload} \
+        actor_rollout_ref.actor.megatron.grad_offload=${actor_offload} \
+        actor_rollout_ref.actor.megatron.pipeline_model_parallel_size=${train_pp} \
+        actor_rollout_ref.actor.megatron.tensor_model_parallel_size=${train_tp} \
+        actor_rollout_ref.rollout.tensor_model_parallel_size=${gen_tp} \
+        actor_rollout_ref.ref.megatron.pipeline_model_parallel_size=${train_pp} \
+        actor_rollout_ref.ref.megatron.tensor_model_parallel_size=${train_tp} \
+        actor_rollout_ref.ref.megatron.param_offload=${ref_offload} \
+        2>&1 | tee "$log_file" $@
+else
+    echo "Error: Unknown strategy ${ACTOR_STRATEGY}. Please use 'fsdp' or 'megatron'"
+    exit 1
+fi
+
+echo "TransferQueue test completed successfully with ${ACTOR_STRATEGY} strategy"
\ No newline at end of file
diff --git a/code/RL_model/verl/verl_train/tests/special_npu/run_one_step_off_policy.sh b/code/RL_model/verl/verl_train/tests/special_npu/run_one_step_off_policy.sh
new file mode 100644
index 0000000000000000000000000000000000000000..c88295836ee4eb4632deff94910a12e9e6126771
--- /dev/null
+++ b/code/RL_model/verl/verl_train/tests/special_npu/run_one_step_off_policy.sh
@@ -0,0 +1,139 @@
+#!/usr/bin/env bash
+set -xeuo pipefail
+
+# Test script for one_step_off_policy E2E regression testing
+# This script runs one_step_off_policy with FSDP2
+# to ensure the asynchronous training mechanism works correctly
+
+ACTOR_STRATEGY="fsdp2"
+
+# Download model if not exists
+MODEL_ID=${MODEL_ID:-Qwen/Qwen2.5-0.5B-Instruct}
+MODEL_PATH=${MODEL_PATH:-${HOME}/.cache/models/${MODEL_ID}}
+#hf download "${MODEL_ID}" --local-dir "${MODEL_PATH}"
+
+# Algorithm parameters
+adv_estimator=grpo
+
+use_kl_in_reward=False
+kl_coef=0.0
+use_kl_loss=False
+kl_loss_coef=0.0
+
+clip_ratio_low=0.2
+clip_ratio_high=0.28
+
+# Response length parameters
+max_prompt_length=1024
+max_response_length=2048
+enable_overlong_buffer=True
+overlong_buffer_len=128
+overlong_penalty_factor=1.0
+
+# Training parameters
+loss_agg_mode="token-mean"
+train_prompt_bsz=8
+n_resp_per_prompt=3
+train_prompt_mini_bsz=4
+
+# Temperature parameters
+temperature=1.0
+top_p=1.0
+top_k=-1
+val_top_p=0.7
+
+# One-step-off-policy specific parameters
+# Allocate 2 NPUs for rollout, 2 NPUs for training
+n_npus_rollout=2
+n_npus_training=2
+
+exp_name="$(basename "${MODEL_ID,,}")-one-step-off-policy-${ACTOR_STRATEGY}-minimal"
+
+echo "Running one_step_off_policy with ${ACTOR_STRATEGY} strategy"
+echo "Rollout GPUs: ${n_npus_rollout}, Training GPUs: ${n_npus_training}"
+
+common_params=(
+    data.train_files="${HOME}/data/gsm8k/train.parquet"
+    data.val_files="${HOME}/data/gsm8k/test.parquet"
+    data.prompt_key=prompt
+    data.truncation='left'
+    data.max_prompt_length=${max_prompt_length}
+    data.max_response_length=${max_response_length}
+    data.train_batch_size=${train_prompt_bsz}
+    actor_rollout_ref.rollout.n=${n_resp_per_prompt}
+    algorithm.adv_estimator=${adv_estimator}
+    algorithm.use_kl_in_reward=${use_kl_in_reward}
+    algorithm.kl_ctrl.kl_coef=${kl_coef}
+    actor_rollout_ref.hybrid_engine=False \
+    actor_rollout_ref.actor.use_kl_loss=${use_kl_loss}
+    actor_rollout_ref.actor.kl_loss_coef=${kl_loss_coef}
+    actor_rollout_ref.actor.clip_ratio_low=${clip_ratio_low}
+    actor_rollout_ref.actor.clip_ratio_high=${clip_ratio_high}
+    actor_rollout_ref.actor.clip_ratio_c=10.0
+    actor_rollout_ref.model.path="${MODEL_PATH}"
+    actor_rollout_ref.actor.optim.lr=1e-6
+    actor_rollout_ref.actor.optim.lr_warmup_steps=-1
+    actor_rollout_ref.actor.optim.weight_decay=0.1
+    actor_rollout_ref.actor.ppo_mini_batch_size=${train_prompt_mini_bsz}
+    actor_rollout_ref.actor.entropy_coeff=0
+    actor_rollout_ref.actor.loss_agg_mode=${loss_agg_mode}
+    actor_rollout_ref.rollout.gpu_memory_utilization=0.80
+    actor_rollout_ref.rollout.temperature=${temperature}
+    actor_rollout_ref.rollout.top_p=${top_p}
+    actor_rollout_ref.rollout.top_k=${top_k}
+    actor_rollout_ref.rollout.val_kwargs.temperature=${temperature}
+    actor_rollout_ref.rollout.val_kwargs.top_p=${val_top_p}
+    actor_rollout_ref.rollout.val_kwargs.top_k=${top_k}
+    actor_rollout_ref.rollout.val_kwargs.do_sample=True
+    actor_rollout_ref.rollout.val_kwargs.n=1
+    actor_rollout_ref.rollout.enable_chunked_prefill=True \
+    actor_rollout_ref.rollout.name=vllm \
+    +actor_rollout_ref.rollout.engine_kwargs.vllm.compilation_config.cudagraph_mode="FULL_AND_PIECEWISE" \
+    reward_model.reward_manager=dapo
+    +reward_model.reward_kwargs.overlong_buffer_cfg.enable=${enable_overlong_buffer}
+    +reward_model.reward_kwargs.overlong_buffer_cfg.len=${overlong_buffer_len}
+    +reward_model.reward_kwargs.overlong_buffer_cfg.penalty_factor=${overlong_penalty_factor}
+    +reward_model.reward_kwargs.overlong_buffer_cfg.log=False
+    +reward_model.reward_kwargs.max_resp_len=${max_response_length}
+    trainer.logger=['console']
+    trainer.project_name='verl-test'
+    trainer.experiment_name="${exp_name}"
+    trainer.val_before_train=True
+    trainer.test_freq=-1
+    trainer.save_freq=-1
+    trainer.total_epochs=2
+    trainer.total_training_steps=2
+    trainer.resume_mode=disable
+    trainer.nnodes=1
+    trainer.n_gpus_per_node=${n_npus_training}
+    rollout.nnodes=1
+    rollout.n_gpus_per_node=${n_npus_rollout}
+
+)
+
+# FSDP2 specific parameters
+gen_tp=2
+sp_size=2
+fsdp_size=2
+ref_offload=True
+actor_offload=False
+
+python3 -m verl.experimental.one_step_off_policy.main_ppo \
+    "${common_params[@]}" \
+    actor_rollout_ref.actor.strategy=$ACTOR_STRATEGY \
+    critic.strategy=fsdp2 \
+    actor_rollout_ref.actor.grad_clip=1.0 \
+    actor_rollout_ref.model.use_remove_padding=True \
+    actor_rollout_ref.model.enable_gradient_checkpointing=True \
+    actor_rollout_ref.actor.use_dynamic_bsz=True \
+    actor_rollout_ref.ref.log_prob_use_dynamic_bsz=True \
+    actor_rollout_ref.rollout.log_prob_use_dynamic_bsz=True \
+    actor_rollout_ref.actor.fsdp_config.param_offload=${actor_offload} \
+    actor_rollout_ref.actor.fsdp_config.optimizer_offload=${actor_offload} \
+    actor_rollout_ref.actor.ulysses_sequence_parallel_size=${sp_size} \
+    actor_rollout_ref.rollout.tensor_model_parallel_size=${gen_tp} \
+    actor_rollout_ref.ref.fsdp_config.param_offload=${ref_offload} \
+    actor_rollout_ref.ref.ulysses_sequence_parallel_size=${sp_size} \
+    actor_rollout_ref.actor.fsdp_config.fsdp_size=${fsdp_size} $@
+
+echo "One-step-off-policy E2E test completed successfully with ${ACTOR_STRATEGY} strategy"
diff --git a/code/RL_model/verl/verl_train/tests/special_npu/run_qwen2_5_05b_grpo.sh b/code/RL_model/verl/verl_train/tests/special_npu/run_qwen2_5_05b_grpo.sh
new file mode 100644
index 0000000000000000000000000000000000000000..1192c99d3026cc2bacb9b71b8bc0dfde4c1acf0c
--- /dev/null
+++ b/code/RL_model/verl/verl_train/tests/special_npu/run_qwen2_5_05b_grpo.sh
@@ -0,0 +1,47 @@
+set -x
+
+MODEL_ID=${MODEL_ID:-Qwen/Qwen2.5-0.5B-Instruct}
+MODEL_PATH=${MODEL_PATH:-${HOME}/.cache/models/${MODEL_ID}}
+
+python3 -m verl.trainer.main_ppo \
+    algorithm.adv_estimator=grpo \
+    data.train_files=$HOME/data/gsm8k/train.parquet \
+    data.val_files=$HOME/data/gsm8k/test.parquet \
+    data.train_batch_size=16 \
+    data.max_prompt_length=512 \
+    data.max_response_length=128 \
+    data.filter_overlong_prompts=True \
+    data.truncation='error' \
+    actor_rollout_ref.model.path="${MODEL_PATH}" \
+    actor_rollout_ref.actor.optim.lr=5e-7 \
+    actor_rollout_ref.model.use_remove_padding=False \
+    actor_rollout_ref.actor.ppo_mini_batch_size=8 \
+    actor_rollout_ref.actor.ppo_micro_batch_size_per_gpu=1 \
+    actor_rollout_ref.actor.use_kl_loss=True \
+    actor_rollout_ref.actor.kl_loss_coef=0.001 \
+    actor_rollout_ref.actor.kl_loss_type=low_var_kl \
+    actor_rollout_ref.model.enable_gradient_checkpointing=True \
+    actor_rollout_ref.actor.fsdp_config.param_offload=False \
+    actor_rollout_ref.actor.fsdp_config.optimizer_offload=False \
+    actor_rollout_ref.actor.use_torch_compile=False \
+    actor_rollout_ref.ref.use_torch_compile=False \
+    +actor_rollout_ref.rollout.engine_kwargs.vllm.compilation_config.cudagraph_mode="FULL_AND_PIECEWISE" \
+    actor_rollout_ref.rollout.log_prob_micro_batch_size_per_gpu=1 \
+    actor_rollout_ref.rollout.enable_chunked_prefill=False \
+    actor_rollout_ref.rollout.tensor_model_parallel_size=2 \
+    actor_rollout_ref.rollout.name=vllm \
+    actor_rollout_ref.rollout.gpu_memory_utilization=0.6 \
+    actor_rollout_ref.rollout.n=2 \
+    actor_rollout_ref.ref.log_prob_micro_batch_size_per_gpu=1 \
+    actor_rollout_ref.ref.fsdp_config.param_offload=True \
+    algorithm.kl_ctrl.kl_coef=0.001 \
+    trainer.critic_warmup=0 \
+    trainer.logger=console \
+    trainer.project_name='verl_grpo_example_gsm8k' \
+    trainer.experiment_name='qwen2_7b_function_rm' \
+    trainer.n_gpus_per_node=8 \
+    trainer.nnodes=1 \
+    trainer.save_freq=-1 \
+    trainer.test_freq=-1 \
+    trainer.total_epochs=1 \
+    trainer.total_training_steps=1 $@
diff --git a/code/RL_model/verl/verl_train/tests/special_npu/run_qwen2_5_05b_grpo_mindspeed.sh b/code/RL_model/verl/verl_train/tests/special_npu/run_qwen2_5_05b_grpo_mindspeed.sh
new file mode 100644
index 0000000000000000000000000000000000000000..b57acac1dfabc883ff7b75c2d5d80d7446527584
--- /dev/null
+++ b/code/RL_model/verl/verl_train/tests/special_npu/run_qwen2_5_05b_grpo_mindspeed.sh
@@ -0,0 +1,68 @@
+set -x
+
+MODEL_ID=${MODEL_ID:-Qwen/Qwen2.5-0.5B-Instruct}
+MODEL_PATH=${MODEL_PATH:-${HOME}/.cache/models/${MODEL_ID}}
+
+USE_DIST_CKPT=${USE_DIST_CKPT:-False}
+DIST_CKPT_PATH=${DIST_CKPT_PATH:-${HOME}/dist_ckpt/qwen2_5_05b_grpo_mindspeed}
+if [ "$USE_DIST_CKPT" = "True" ]; then
+    if [ "$USE_DUMMY_MODEL" = "True" ]; then
+        DIST_CKPT_PATH=${HOME}/dist_ckpt_dummy/${MODEL_ID}
+    fi
+    python scripts/converter_hf_to_mcore.py \
+        --hf_model_path "${MODEL_PATH}" \
+        --output_path "${DIST_CKPT_PATH}"
+fi
+
+
+python3 -m verl.trainer.main_ppo --config-path=config \
+    --config-name='ppo_megatron_trainer.yaml' \
+    algorithm.adv_estimator=grpo \
+    data.train_files=$HOME/data/gsm8k/train.parquet \
+    data.val_files=$HOME/data/gsm8k/test.parquet \
+    data.train_batch_size=16 \
+    data.max_prompt_length=512 \
+    data.max_response_length=128 \
+    data.filter_overlong_prompts=True \
+    data.truncation='error' \
+    actor_rollout_ref.model.path=${MODEL_PATH} \
+    actor_rollout_ref.actor.optim.lr=5e-7 \
+    actor_rollout_ref.actor.ppo_mini_batch_size=8 \
+    actor_rollout_ref.actor.ppo_micro_batch_size_per_gpu=1 \
+    actor_rollout_ref.actor.strategy=megatron \
+    actor_rollout_ref.actor.megatron.pipeline_model_parallel_size=2 \
+    actor_rollout_ref.actor.megatron.tensor_model_parallel_size=2 \
+    actor_rollout_ref.actor.megatron.expert_model_parallel_size=1 \
+    actor_rollout_ref.actor.megatron.use_dist_checkpointing=True \
+    actor_rollout_ref.actor.megatron.dist_checkpointing_path=${DIST_CKPT_PATH} \
+    actor_rollout_ref.actor.use_kl_loss=True \
+    actor_rollout_ref.actor.kl_loss_coef=0.001 \
+    actor_rollout_ref.actor.kl_loss_type=low_var_kl \
+    actor_rollout_ref.actor.use_torch_compile=False \
+    actor_rollout_ref.rollout.log_prob_micro_batch_size_per_gpu=1 \
+    actor_rollout_ref.rollout.enable_chunked_prefill=False \
+    actor_rollout_ref.rollout.tensor_model_parallel_size=2 \
+    actor_rollout_ref.rollout.name=vllm \
+    actor_rollout_ref.rollout.gpu_memory_utilization=0.6 \
+    +actor_rollout_ref.rollout.engine_kwargs.vllm.compilation_config.cudagraph_mode="FULL_AND_PIECEWISE" \
+    actor_rollout_ref.rollout.n=2 \
+    actor_rollout_ref.ref.log_prob_micro_batch_size_per_gpu=1 \
+    actor_rollout_ref.ref.strategy=megatron \
+    actor_rollout_ref.ref.megatron.pipeline_model_parallel_size=2 \
+    actor_rollout_ref.ref.megatron.tensor_model_parallel_size=2 \
+    actor_rollout_ref.ref.megatron.expert_model_parallel_size=1 \
+    actor_rollout_ref.ref.megatron.use_dist_checkpointing=True \
+    actor_rollout_ref.ref.megatron.dist_checkpointing_path=${DIST_CKPT_PATH} \
+    actor_rollout_ref.ref.use_torch_compile=False \
+    algorithm.kl_ctrl.kl_coef=0.001 \
+    trainer.critic_warmup=0 \
+    trainer.logger=console \
+    trainer.project_name='verl_grpo_example_gsm8k' \
+    trainer.experiment_name='qwen2_7b_function_rm' \
+    trainer.n_gpus_per_node=8 \
+    trainer.nnodes=1 \
+    trainer.save_freq=-1 \
+    trainer.test_freq=-1 \
+    trainer.total_epochs=1 \
+    trainer.total_training_steps=1 \
+    +actor_rollout_ref.actor.megatron.override_transformer_config.use_flash_attn=True $@
diff --git a/code/RL_model/verl/verl_train/tests/special_npu/run_qwen2_5_05b_sft_peft_sp2.sh b/code/RL_model/verl/verl_train/tests/special_npu/run_qwen2_5_05b_sft_peft_sp2.sh
new file mode 100644
index 0000000000000000000000000000000000000000..ba61ca10d0fab142fbfb7a6b2f1e0e900607c361
--- /dev/null
+++ b/code/RL_model/verl/verl_train/tests/special_npu/run_qwen2_5_05b_sft_peft_sp2.sh
@@ -0,0 +1,65 @@
+set -x
+
+NUM_GPUS=${NUM_GPUS:-4}
+
+mode=${mode:-spmd}
+
+if [ "$mode" = "spmd" ]; then
+  ENTRYPOINT=${ENTRYPOINT:-"-m verl.trainer.sft_trainer"}
+  COMMAND="torchrun --standalone --nnodes=${NNODES:-1} --nproc-per-node=${NUM_GPUS:-1} ${ENTRYPOINT}"
+else
+  ENTRYPOINT=${ENTRYPOINT:-"-m verl.trainer.sft_trainer_ray"}
+  COMMAND="python ${ENTRYPOINT} trainer.nnodes=${NNODES:-1} trainer.n_gpus_per_node=${NUM_GPUS:-1}"
+fi
+
+RESUME_MODE=disable
+
+ckpts_home=${ckpts_home:-~/verl/test/gsm8k-sft-fsdp}
+
+MODEL_ID=${MODEL_ID:-Qwen/Qwen2.5-0.5B-Instruct}
+MODEL_PATH=${MODEL_PATH:-${HOME}/.cache/models/${MODEL_ID}}
+
+DATASET_DIR=${DATASET_DIR:-$HOME/data/gsm8k_sft}
+TRAIN_FILES=${DATASET_DIR}/train.parquet
+VAL_FILES=${DATASET_DIR}/test.parquet
+
+exp_name=gsm8k-sft-qwen-2.5-0.5b-instruct-mode-${mode}
+
+mkdir -p "${ckpts_home}"
+
+$COMMAND \
+    data.train_files=$TRAIN_FILES \
+    data.val_files=$VAL_FILES \
+    data.pad_mode=no_padding \
+    data.truncation=error \
+    data.use_dynamic_bsz=True \
+    data.max_token_len_per_gpu=2048 \
+    data.messages_key=messages \
+    model.path=$MODEL_PATH \
+    model.use_remove_padding=True \
+    model.lora_rank=32 \
+    model.lora_alpha=16 \
+    model.target_modules=all-linear \
+    engine=fsdp \
+    optim=fsdp \
+    optim.lr=1e-5 \
+    optim.lr_warmup_steps_ratio=0.2 \
+    optim.weight_decay=0.1 \
+    optim.betas="[0.9,0.95]" \
+    optim.clip_grad=1.0 \
+    optim.min_lr_ratio=0.1 \
+    optim.lr_scheduler_type=cosine \
+    engine.ulysses_sequence_parallel_size=2 \
+    engine.strategy=fsdp2 \
+    engine.fsdp_size=2 \
+    trainer.test_freq=after_each_epoch \
+    trainer.save_freq=-1 \
+    trainer.logger=['console','file'] \
+    trainer.project_name=gsm8k-sft \
+    trainer.experiment_name=gsm8k-sft-qwen-2.5-0.5b-instruct \
+    trainer.total_epochs=2 \
+    trainer.total_training_steps=2 \
+    trainer.default_local_dir="${ckpts_home}" \
+    trainer.resume_mode=${RESUME_MODE} \
+
+rm -rf "${ckpts_home:?}/*"
diff --git a/code/RL_model/verl/verl_train/tests/special_npu/run_qwen2_5_vl_3b_npu.sh b/code/RL_model/verl/verl_train/tests/special_npu/run_qwen2_5_vl_3b_npu.sh
new file mode 100644
index 0000000000000000000000000000000000000000..a66c2f77de4e171f309dadec4910c23e7f1a171d
--- /dev/null
+++ b/code/RL_model/verl/verl_train/tests/special_npu/run_qwen2_5_vl_3b_npu.sh
@@ -0,0 +1,57 @@
+set -x
+
+ENGINE=${1:-vllm}
+
+# Some models are optimized by vllm ascend. While in some case, e.g. rlhf training, 
+# the optimized model may not be suitable. In this case, set this value to 0 to disable the optimized model.
+export USE_OPTIMIZED_MODEL=0
+
+MODEL_ID=${MODEL_ID:-Qwen/Qwen2.5-VL-3B-Instruct}
+MODEL_PATH=${MODEL_PATH:-${HOME}/.cache/models/${MODEL_ID}}
+
+python3 -m verl.trainer.main_ppo \
+    algorithm.adv_estimator=grpo \
+    data.train_files=$HOME/data/geo3k/train.parquet \
+    data.val_files=$HOME/data/geo3k/test.parquet \
+    data.train_batch_size=16 \
+    data.max_prompt_length=1024 \
+    data.max_response_length=2048 \
+    data.filter_overlong_prompts=True \
+    data.truncation='error' \
+    data.image_key=images \
+    actor_rollout_ref.model.path="${MODEL_PATH}" \
+    actor_rollout_ref.actor.optim.lr=1e-6 \
+    actor_rollout_ref.model.use_remove_padding=True \
+    actor_rollout_ref.actor.ppo_mini_batch_size=8 \
+    actor_rollout_ref.actor.ppo_micro_batch_size_per_gpu=1 \
+    actor_rollout_ref.actor.use_kl_loss=True \
+    actor_rollout_ref.actor.kl_loss_coef=0.01 \
+    actor_rollout_ref.actor.kl_loss_type=low_var_kl \
+    actor_rollout_ref.actor.entropy_coeff=0 \
+    actor_rollout_ref.actor.use_torch_compile=False \
+    actor_rollout_ref.model.enable_gradient_checkpointing=True \
+    actor_rollout_ref.actor.fsdp_config.param_offload=False \
+    actor_rollout_ref.actor.fsdp_config.optimizer_offload=False \
+    actor_rollout_ref.ref.use_torch_compile=False \
+    actor_rollout_ref.rollout.log_prob_micro_batch_size_per_gpu=1 \
+    actor_rollout_ref.rollout.tensor_model_parallel_size=2 \
+    actor_rollout_ref.rollout.name=$ENGINE \
+    actor_rollout_ref.rollout.gpu_memory_utilization=0.6 \
+    actor_rollout_ref.rollout.enable_chunked_prefill=False \
+    actor_rollout_ref.rollout.enforce_eager=True \
+    +actor_rollout_ref.rollout.engine_kwargs.vllm.compilation_config.cudagraph_mode="FULL_AND_PIECEWISE" \
+    actor_rollout_ref.rollout.free_cache_engine=True \
+    actor_rollout_ref.rollout.n=2 \
+    actor_rollout_ref.ref.log_prob_micro_batch_size_per_gpu=1 \
+    actor_rollout_ref.ref.fsdp_config.param_offload=True \
+    algorithm.use_kl_in_reward=False \
+    trainer.critic_warmup=0 \
+    trainer.logger=console \
+    trainer.project_name='verl_grpo_example_geo3k' \
+    trainer.experiment_name='qwen2_5_vl_3b_function_rm' \
+    trainer.n_gpus_per_node=8 \
+    trainer.nnodes=1 \
+    trainer.save_freq=-1 \
+    trainer.test_freq=-1 \
+    trainer.total_epochs=1 \
+    trainer.total_training_steps=1 $@
\ No newline at end of file
diff --git a/code/RL_model/verl/verl_train/tests/special_npu/run_qwen3_06b_ppo.sh b/code/RL_model/verl/verl_train/tests/special_npu/run_qwen3_06b_ppo.sh
new file mode 100644
index 0000000000000000000000000000000000000000..04bd6dbb6e4d95e55aaeb6863c86e5edfe80b50d
--- /dev/null
+++ b/code/RL_model/verl/verl_train/tests/special_npu/run_qwen3_06b_ppo.sh
@@ -0,0 +1,52 @@
+set -x
+
+MODEL_ID=${MODEL_ID:-Qwen/Qwen2.5-0.5B-Instruct}  # TODO: change to Qwen3-0.6B when CI server is ready
+MODEL_PATH=${MODEL_PATH:-${HOME}/.cache/models/${MODEL_ID}}
+
+python3 -m verl.trainer.main_ppo \
+    algorithm.adv_estimator=gae \
+    data.train_files=$HOME/data/gsm8k/train.parquet \
+    data.val_files=$HOME/data/gsm8k/test.parquet \
+    data.train_batch_size=16 \
+    data.max_prompt_length=512 \
+    data.max_response_length=128 \
+    data.shuffle=False \
+    actor_rollout_ref.model.path="${MODEL_PATH}" \
+    actor_rollout_ref.model.use_remove_padding=True \
+    actor_rollout_ref.model.enable_gradient_checkpointing=True \
+    actor_rollout_ref.actor.optim.lr=1e-6 \
+    actor_rollout_ref.actor.ppo_mini_batch_size=8 \
+    actor_rollout_ref.actor.ppo_micro_batch_size_per_gpu=1 \
+    actor_rollout_ref.actor.fsdp_config.param_offload=True \
+    actor_rollout_ref.actor.fsdp_config.optimizer_offload=True \
+    actor_rollout_ref.actor.use_kl_loss=False \
+    actor_rollout_ref.actor.ulysses_sequence_parallel_size=2 \
+    actor_rollout_ref.actor.use_dynamic_bsz=True \
+    actor_rollout_ref.actor.use_torch_compile=False \
+    actor_rollout_ref.rollout.log_prob_micro_batch_size_per_gpu=1 \
+    actor_rollout_ref.rollout.tensor_model_parallel_size=1 \
+    actor_rollout_ref.rollout.name=vllm \
+    actor_rollout_ref.rollout.gpu_memory_utilization=0.8 \
+    actor_rollout_ref.rollout.log_prob_use_dynamic_bsz=True \
+    actor_rollout_ref.rollout.enable_chunked_prefill=True \
+    actor_rollout_ref.rollout.enforce_eager=False \
+    +actor_rollout_ref.rollout.engine_kwargs.vllm.compilation_config.cudagraph_mode="FULL_AND_PIECEWISE" \
+    critic.optim.lr=1e-5 \
+    critic.model.use_remove_padding=True \
+    critic.model.path="${MODEL_PATH}" \
+    critic.model.enable_gradient_checkpointing=True \
+    critic.ppo_micro_batch_size_per_gpu=1 \
+    critic.ulysses_sequence_parallel_size=2 \
+    critic.model.fsdp_config.param_offload=True \
+    critic.model.fsdp_config.optimizer_offload=True \
+    critic.use_dynamic_bsz=True \
+    trainer.critic_warmup=0 \
+    trainer.logger='["console"]' \
+    trainer.project_name='verl_ppo_example_gsm8k_qwen3' \
+    trainer.experiment_name='qwen3_06b_fsdp' \
+    trainer.n_gpus_per_node=8 \
+    trainer.nnodes=1 \
+    trainer.save_freq=-1 \
+    trainer.test_freq=-1 \
+    trainer.total_epochs=1 \
+    trainer.total_training_steps=1 $@
diff --git a/code/RL_model/verl/verl_train/tests/special_npu/run_qwen3_30b_grpo_mindspeed.sh b/code/RL_model/verl/verl_train/tests/special_npu/run_qwen3_30b_grpo_mindspeed.sh
new file mode 100644
index 0000000000000000000000000000000000000000..485512319c03f352ac498a053da3f3e0377db815
--- /dev/null
+++ b/code/RL_model/verl/verl_train/tests/special_npu/run_qwen3_30b_grpo_mindspeed.sh
@@ -0,0 +1,134 @@
+#!/usr/bin/env bash
+set -xeuo pipefail
+
+
+MODEL_ID=${MODEL_ID:-Qwen/Qwen3-30B-A3B-Instruct-2507}
+MODEL_PATH=${MODEL_PATH:-${HOME}/.cache/models/${MODEL_ID}}
+USE_DIST_CKPT=${USE_DIST_CKPT:-False}
+DIST_CKPT_PATH=${DIST_CKPT_PATH:-${HOME}/dist_ckpt/qwen3_30b_grpo_mindspeed}
+
+# use dummy model
+if [[ "$USE_DUMMY_MODEL" == "True" ]]; then
+    DUMMY_MODEL_PATH=${DUMMY_MODEL_PATH:-${HOME}/models_dummy/${MODEL_ID}}
+    if [ -z "${DUMMY_MODEL_CONFIG_PATH}" ]; then
+        echo "[ERROR] DUMMY_MODEL_CONFIG_PATH not set"
+        exit 1
+    fi
+
+    # make sure the path is empty
+    if [[ -d $DUMMY_MODEL_PATH && $DUMMY_MODEL_PATH != "/" ]]; then
+        rm -rf $DUMMY_MODEL_PATH
+    fi
+
+    # init model
+    python scripts/init_random_model.py \
+        --hf_model_path "${MODEL_PATH}" \
+        --new_config_path "${DUMMY_MODEL_CONFIG_PATH}" \
+        --output_path "${DUMMY_MODEL_PATH}"
+
+    # replace model path
+    MODEL_PATH=$DUMMY_MODEL_PATH
+fi
+
+# convert to megatron
+if [[ "$USE_DIST_CKPT" == "True" ]]; then
+
+    if [[ "$USE_DUMMY_MODEL" == "True" ]]; then
+        DIST_CKPT_PATH=${HOME}/dist_ckpt/qwen3_30b_grpo_mindspeed_dummy
+
+        if [[ -d $DIST_CKPT_PATH && $DIST_CKPT_PATH != "/" ]];then
+            rm -rf $DIST_CKPT_PATH
+        fi
+    fi
+
+    torchrun --nproc_per_node 2 --nnodes 1 scripts/converter_hf_to_mcore.py \
+        --hf_model_path "${MODEL_PATH}" \
+        --output_path "${DIST_CKPT_PATH}"
+fi
+
+exp_name='Qwen3-30B-A3B-GRPO-MindSpeed'
+
+max_prompt_length=512
+max_response_length=1024
+
+train_prompt_bsz=16
+
+actor_ppo_max_token_len=$(((max_prompt_length + max_response_length)))
+infer_ppo_max_token_len=$(((max_prompt_length + max_response_length)))
+
+python3 -m verl.trainer.main_ppo --config-path=config \
+    --config-name='ppo_megatron_trainer.yaml' \
+    data.train_files=${HOME}/data/gsm8k/train.parquet \
+    data.val_files=${HOME}/data/gsm8k/test.parquet \
+    data.train_batch_size=${train_prompt_bsz} \
+    data.max_prompt_length=${max_prompt_length} \
+    data.max_response_length=${max_response_length} \
+    data.filter_overlong_prompts=True \
+    data.shuffle=False \
+    data.truncation='left' \
+    algorithm.adv_estimator=grpo \
+    algorithm.use_kl_in_reward=False \
+    actor_rollout_ref.rollout.log_prob_micro_batch_size_per_gpu=1 \
+    actor_rollout_ref.rollout.enable_chunked_prefill=False \
+    actor_rollout_ref.rollout.tensor_model_parallel_size=2 \
+    actor_rollout_ref.rollout.name=vllm \
+    actor_rollout_ref.rollout.gpu_memory_utilization=0.6 \
+    actor_rollout_ref.rollout.n=2 \
+    actor_rollout_ref.rollout.temperature=1.0 \
+    actor_rollout_ref.rollout.top_p=1.0 \
+    actor_rollout_ref.rollout.top_k=-1 \
+    actor_rollout_ref.rollout.enforce_eager=True \
+    actor_rollout_ref.rollout.free_cache_engine=True \
+    actor_rollout_ref.actor.ppo_max_token_len_per_gpu=${actor_ppo_max_token_len} \
+    actor_rollout_ref.ref.log_prob_max_token_len_per_gpu=${infer_ppo_max_token_len} \
+    actor_rollout_ref.rollout.log_prob_max_token_len_per_gpu=${infer_ppo_max_token_len} \
+    actor_rollout_ref.actor.strategy=megatron \
+    actor_rollout_ref.actor.kl_loss_coef=0.0 \
+    actor_rollout_ref.actor.clip_ratio_low=0.2 \
+    actor_rollout_ref.actor.clip_ratio_high=0.28 \
+    actor_rollout_ref.actor.clip_ratio_c=10.0 \
+    actor_rollout_ref.actor.ppo_epochs=1 \
+    actor_rollout_ref.actor.use_dynamic_bsz=True \
+    actor_rollout_ref.model.path="${MODEL_PATH}" \
+    actor_rollout_ref.actor.optim.lr=1e-6 \
+    actor_rollout_ref.actor.ppo_mini_batch_size=8 \
+    actor_rollout_ref.actor.ppo_micro_batch_size_per_gpu=1 \
+    actor_rollout_ref.rollout.log_prob_use_dynamic_bsz=True \
+    actor_rollout_ref.ref.log_prob_use_dynamic_bsz=True \
+    +actor_rollout_ref.rollout.engine_kwargs.vllm.compilation_config.cudagraph_mode="FULL_AND_PIECEWISE" \
+    actor_rollout_ref.actor.megatron.pipeline_model_parallel_size=2 \
+    actor_rollout_ref.actor.megatron.tensor_model_parallel_size=2 \
+    actor_rollout_ref.actor.megatron.expert_model_parallel_size=2 \
+    actor_rollout_ref.actor.megatron.use_dist_checkpointing=${USE_DIST_CKPT} \
+    actor_rollout_ref.actor.megatron.dist_checkpointing_path=${DIST_CKPT_PATH} \
+    actor_rollout_ref.actor.use_kl_loss=False \
+    actor_rollout_ref.actor.loss_agg_mode="token-mean" \
+    actor_rollout_ref.ref.strategy=megatron \
+    actor_rollout_ref.ref.log_prob_micro_batch_size_per_gpu=1 \
+    actor_rollout_ref.ref.megatron.pipeline_model_parallel_size=2 \
+    actor_rollout_ref.ref.megatron.tensor_model_parallel_size=2 \
+    actor_rollout_ref.ref.megatron.expert_model_parallel_size=2 \
+    actor_rollout_ref.ref.megatron.use_dist_checkpointing=${USE_DIST_CKPT} \
+    actor_rollout_ref.ref.megatron.dist_checkpointing_path=${DIST_CKPT_PATH} \
+    reward_model.reward_manager=naive \
+    algorithm.kl_ctrl.kl_coef=0.0 \
+    trainer.logger=['console'] \
+    trainer.project_name='verl_gsm8k_example' \
+    trainer.experiment_name='qwen3_30b_a3b_cut_gsm8k_mindspeed' \
+    trainer.n_gpus_per_node=8 \
+    trainer.nnodes=1 \
+    trainer.save_freq=-1 \
+    trainer.test_freq=-1 \
+    trainer.total_epochs=1 \
+    trainer.total_training_steps=1 \
+    actor_rollout_ref.actor.use_torch_compile=False \
+    actor_rollout_ref.ref.use_torch_compile=False \
+    +actor_rollout_ref.actor.megatron.override_transformer_config.use_flash_attn=True $@
+
+# clean up
+if [[ "$USE_DUMMY_MODEL" == "True" ]]; then
+    rm -rf $DUMMY_MODEL_PATH
+    if [[ "$USE_DIST_CKPT" == "True" ]]; then
+        rm -rf $DIST_CKPT_PATH
+    fi
+fi
diff --git a/code/RL_model/verl/verl_train/tests/special_standalone/README.md b/code/RL_model/verl/verl_train/tests/special_standalone/README.md
new file mode 100644
index 0000000000000000000000000000000000000000..0e3596e1afa9a507c67b6949479d1c254b30aec3
--- /dev/null
+++ b/code/RL_model/verl/verl_train/tests/special_standalone/README.md
@@ -0,0 +1 @@
+The standalone test folder is reserved for tests that require dedicated environment (e.g. memory stress tests)
diff --git a/code/RL_model/verl/verl_train/tests/special_standalone/test_memory_buffers.py b/code/RL_model/verl/verl_train/tests/special_standalone/test_memory_buffers.py
new file mode 100644
index 0000000000000000000000000000000000000000..77851534782c7d0f5b9ec93231fde8d4d5e60bb6
--- /dev/null
+++ b/code/RL_model/verl/verl_train/tests/special_standalone/test_memory_buffers.py
@@ -0,0 +1,66 @@
+# Copyright 2024 Bytedance Ltd. and/or its affiliates
+#
+# Licensed under the Apache License, Version 2.0 (the "License");
+# you may not use this file except in compliance with the License.
+# You may obtain a copy of the License at
+#
+#     http://www.apache.org/licenses/LICENSE-2.0
+#
+# Unless required by applicable law or agreed to in writing, software
+# distributed under the License is distributed on an "AS IS" BASIS,
+# WITHOUT WARRANTIES OR CONDITIONS OF ANY KIND, either express or implied.
+# See the License for the specific language governing permissions and
+# limitations under the License.
+"""
+Test memory buffers
+- We start with two models with the same weights
+- We use Memory buffer to make one of the models and then compare the parameters
+"""
+
+import gc
+
+import torch
+from transformers import LlamaConfig, LlamaModel
+
+
+def test_memory_buffers():
+    llama_config = LlamaConfig(
+        vocab_size=256,
+        hidden_size=4096,
+        intermediate_size=11008,
+        num_hidden_layers=2,
+        num_attention_heads=16,
+        num_key_value_heads=16,
+    )
+
+    model = LlamaModel(config=llama_config).cuda()
+    model_copy = LlamaModel(config=llama_config).cuda()
+    model_copy.load_state_dict(model.state_dict())
+
+    norm_factor = 1024**3
+
+    t_before = torch.cuda.get_device_properties(0).total_memory / norm_factor
+    r_before = torch.cuda.memory_reserved(0) / norm_factor
+    a_before = torch.cuda.memory_allocated(0) / norm_factor
+
+    print(f"Before Total memory: {t_before} GB, reserved: {r_before} GB, allocated: {a_before} GB")
+
+    t = torch.cuda.get_device_properties(0).total_memory / norm_factor
+    r = torch.cuda.memory_reserved(0) / norm_factor
+    a = torch.cuda.memory_allocated(0) / norm_factor
+
+    gc.collect()
+    torch.cuda.empty_cache()
+
+    print(f"After Total memory: {t} GB, reserved: {r} GB, allocated: {a} GB")
+
+    change_ratio = (a - a_before) / a_before
+    assert change_ratio < 0.01, f"make sure the allocated change is less than 1%, Got {change_ratio}"
+
+    for (name1, param1), (name2, param2) in zip(model.named_parameters(), model_copy.named_parameters(), strict=True):
+        assert name1 == name2
+        assert torch.eq(param1.data, param2.data).all(), f"{param1.data}, {param2.data}, {name1}"
+
+
+if __name__ == "__main__":
+    test_memory_buffers()
diff --git a/code/RL_model/verl/verl_train/tests/test_base_config_on_cpu.py b/code/RL_model/verl/verl_train/tests/test_base_config_on_cpu.py
new file mode 100644
index 0000000000000000000000000000000000000000..9a50235c8ffa736551781d50cf5c937ce21afce0
--- /dev/null
+++ b/code/RL_model/verl/verl_train/tests/test_base_config_on_cpu.py
@@ -0,0 +1,42 @@
+# Copyright 2024 Bytedance Ltd. and/or its affiliates
+#
+# Licensed under the Apache License, Version 2.0 (the "License");
+# you may not use this file except in compliance with the License.
+# You may obtain a copy of the License at
+#
+#     http://www.apache.org/licenses/LICENSE-2.0
+#
+# Unless required by applicable law or agreed to in writing, software
+# distributed under the License is distributed on an "AS IS" BASIS,
+# WITHOUT WARRANTIES OR CONDITIONS OF ANY KIND, either express or implied.
+# See the License for the specific language governing permissions and
+# limitations under the License.
+
+import pytest
+
+from verl.base_config import BaseConfig
+
+
+@pytest.fixture
+def base_config_mock():
+    """Fixture to create a mock BaseConfig instance with test attributes."""
+    mock_config = BaseConfig()
+    mock_config.test_attr = "test_value"
+    return mock_config
+
+
+def test_getitem_success(base_config_mock):
+    """Test __getitem__ with existing attribute (happy path)."""
+    assert base_config_mock["test_attr"] == "test_value"
+
+
+def test_getitem_nonexistent_attribute(base_config_mock):
+    """Test __getitem__ with non-existent attribute (exception path 1)."""
+    with pytest.raises(AttributeError):
+        _ = base_config_mock["nonexistent_attr"]
+
+
+def test_getitem_invalid_key_type(base_config_mock):
+    """Test __getitem__ with invalid key type (exception path 2)."""
+    with pytest.raises(TypeError):
+        _ = base_config_mock[123]  # type: ignore
diff --git a/code/RL_model/verl/verl_train/tests/test_protocol_on_cpu.py b/code/RL_model/verl/verl_train/tests/test_protocol_on_cpu.py
new file mode 100644
index 0000000000000000000000000000000000000000..800d428639239a1b2fc4de3125371d657213ce8b
--- /dev/null
+++ b/code/RL_model/verl/verl_train/tests/test_protocol_on_cpu.py
@@ -0,0 +1,1234 @@
+# Copyright 2024 Bytedance Ltd. and/or its affiliates
+#
+# Licensed under the Apache License, Version 2.0 (the "License");
+# you may not use this file except in compliance with the License.
+# You may obtain a copy of the License at
+#
+#     http://www.apache.org/licenses/LICENSE-2.0
+#
+# Unless required by applicable law or agreed to in writing, software
+# distributed under the License is distributed on an "AS IS" BASIS,
+# WITHOUT WARRANTIES OR CONDITIONS OF ANY KIND, either express or implied.
+# See the License for the specific language governing permissions and
+# limitations under the License.
+
+import random
+
+import numpy as np
+import pytest
+import tensordict
+import torch
+from packaging.version import parse as parse_version
+from tensordict import TensorDict
+
+from verl import DataProto
+from verl.protocol import (
+    deserialize_single_tensor,
+    deserialize_tensordict,
+    serialize_single_tensor,
+    serialize_tensordict,
+    union_numpy_dict,
+    union_tensor_dict,
+)
+from verl.utils import tensordict_utils as tu
+
+
+def test_union_tensor_dict():
+    obs = torch.randn(100, 10)
+
+    data1 = TensorDict({"obs": obs, "act": torch.randn(100, 3)}, batch_size=[100])
+    data2 = TensorDict({"obs": obs, "next_obs": torch.randn(100, 10), "rew": torch.randn(100)}, batch_size=[100])
+
+    data_with_copied_obs = TensorDict(
+        {"obs": obs.clone(), "next_obs": torch.randn(100, 10), "rew": torch.randn(100)}, batch_size=[100]
+    )
+
+    union_tensor_dict(data1, data2)
+    with pytest.raises(AssertionError):
+        union_tensor_dict(data1, data_with_copied_obs)
+
+
+def test_union_numpy_dict():
+    """
+    A comprehensive test suite for union_numpy_dict, covering standard use
+    cases, N-dimensional arrays, object-dtype arrays, and NaN value handling.
+    """
+    arr_3d = np.arange(8).reshape((2, 2, 2))
+    union_numpy_dict({"a": arr_3d}, {"a": arr_3d})
+    arr1 = np.array([1, "hello", np.array([2, 3])], dtype=object)
+    arr2 = np.array([1, "hello", np.array([2, 3])], dtype=object)
+    union_numpy_dict({"a": arr1}, {"a": arr2})
+    # --- Test Case 1: The original test with mixed object/float types ---
+    # This test case from the original test file is preserved.
+    data = np.random.random(100)
+    # This array intentionally mixes float('nan') and the string 'nan'
+    nan_data = [float("nan") for _ in range(99)]
+    nan_data.append("nan")
+    nan_data_arr = np.array(nan_data, dtype=object)
+
+    dict1 = {"a": data, "b": nan_data_arr}
+    dict2_same = {"a": data.copy(), "b": nan_data_arr.copy()}
+    dict3_different = {"a": np.random.random(100)}
+
+    union_numpy_dict(dict1, dict2_same)  # Should pass
+    with pytest.raises(AssertionError):
+        union_numpy_dict(dict1, dict3_different)
+
+    # --- Test Case 2: Standard 3D arrays (fixes the core bug) ---
+    arr_3d = np.arange(24, dtype=np.int32).reshape((2, 3, 4))
+    dict_3d_1 = {"nd_array": arr_3d}
+    dict_3d_2_same = {"nd_array": arr_3d.copy()}
+    dict_3d_3_different = {"nd_array": arr_3d + 1}
+
+    union_numpy_dict(dict_3d_1, dict_3d_2_same)  # Should pass
+    with pytest.raises(AssertionError, match="`nd_array` in tensor_dict1 and tensor_dict2 are not the same object."):
+        union_numpy_dict(dict_3d_1, dict_3d_3_different)
+
+    # --- Test Case 3: Nested 2D and 4D object-dtype arrays ---
+    sub_arr1 = np.array([1, 2])
+    sub_arr2 = np.array([3.0, 4.0])
+    # 2D object array
+    arr_2d_obj = np.array([[sub_arr1, "text"], [sub_arr2, None]], dtype=object)
+    arr_2d_obj_diff = np.array([[sub_arr1, "text"], [sub_arr2, "other"]], dtype=object)
+
+    union_numpy_dict({"data": arr_2d_obj}, {"data": arr_2d_obj.copy()})  # Should pass
+    with pytest.raises(AssertionError):
+        union_numpy_dict({"data": arr_2d_obj}, {"data": arr_2d_obj_diff})
+
+    # 4D object array to ensure deep recursion is robust
+    arr_4d_obj = np.array([[[[sub_arr1]]], [[[sub_arr2]]]], dtype=object)
+    arr_4d_obj_diff = np.array([[[[sub_arr1]]], [[[np.array([9, 9])]]]], dtype=object)
+
+    union_numpy_dict({"data": arr_4d_obj}, {"data": arr_4d_obj.copy()})  # Should pass
+    with pytest.raises(AssertionError):
+        union_numpy_dict({"data": arr_4d_obj}, {"data": arr_4d_obj_diff})
+
+    # --- Test Case 4: Explicit NaN value comparison ---
+    # This verifies that our new _deep_equal logic correctly handles NaNs.
+    nan_arr = np.array([1.0, np.nan, 3.0])
+    dict_nan_1 = {"data": nan_arr}
+    dict_nan_2_same = {"data": np.array([1.0, np.nan, 3.0])}  # A new array with same values
+    dict_nan_3_different_val = {"data": np.array([1.0, 2.0, 3.0])}
+    dict_nan_4_different_pos = {"data": np.array([np.nan, 1.0, 3.0])}
+
+    # NaNs in the same position should be considered equal for merging.
+    union_numpy_dict(dict_nan_1, dict_nan_2_same)  # Should pass
+
+    with pytest.raises(AssertionError):
+        union_numpy_dict(dict_nan_1, dict_nan_3_different_val)
+    with pytest.raises(AssertionError):
+        union_numpy_dict(dict_nan_1, dict_nan_4_different_pos)
+
+    # --- Test Case 5: Circular reference handling ---
+    # Create two separate, but structurally identical, circular references.
+    # This should pass without a RecursionError.
+    circ_arr_1 = np.array([None], dtype=object)
+    circ_arr_1[0] = circ_arr_1
+
+    circ_arr_2 = np.array([None], dtype=object)
+    circ_arr_2[0] = circ_arr_2
+
+    union_numpy_dict({"data": circ_arr_1}, {"data": circ_arr_2})  # Should pass
+
+    # Create a circular reference and a non-circular one.
+    # This should fail with an AssertionError because they are different.
+    non_circ_arr = np.array([None], dtype=object)
+
+    with pytest.raises(AssertionError):
+        union_numpy_dict({"data": circ_arr_1}, {"data": non_circ_arr})
+
+
+def test_tensor_dict_constructor():
+    obs = torch.randn(100, 10)
+    act = torch.randn(100, 10, 3)
+    data = DataProto.from_dict(tensors={"obs": obs, "act": act})
+
+    assert data.batch.batch_size == torch.Size([100])
+
+    with pytest.raises(AssertionError):
+        data = DataProto.from_dict(tensors={"obs": obs, "act": act}, num_batch_dims=2)
+
+    with pytest.raises(AssertionError):
+        data = DataProto.from_dict(tensors={"obs": obs, "act": act}, num_batch_dims=3)
+
+
+def test_tensor_dict_make_iterator():
+    obs = torch.randn(100, 10)
+    labels = [random.choice(["abc", "cde"]) for _ in range(100)]
+    dataset = DataProto.from_dict(tensors={"obs": obs}, non_tensors={"labels": labels})
+
+    data_iter_1 = dataset.make_iterator(mini_batch_size=10, epochs=2, seed=1)
+    data_list_1 = []
+    for data in data_iter_1:
+        data_list_1.append(data)
+
+    data_iter_2 = dataset.make_iterator(mini_batch_size=10, epochs=2, seed=1)
+    data_list_2 = []
+    for data in data_iter_2:
+        data_list_2.append(data)
+
+    for data1, data2 in zip(data_list_1, data_list_2, strict=True):
+        assert isinstance(data1, DataProto)
+        assert isinstance(data2, DataProto)
+        result = torch.all(torch.eq(data1.batch["obs"], data2.batch["obs"]))
+        if not result.item():
+            print(data1.batch["obs"])
+            print(data2.batch["obs"])
+            raise AssertionError()
+        non_tensor_result = np.all(np.equal(data1.non_tensor_batch["labels"], data2.non_tensor_batch["labels"]))
+        if not non_tensor_result.item():
+            print(data1.non_tensor_batch["labels"])
+            print(data2.non_tensor_batch["labels"])
+
+
+def test_reorder():
+    obs = torch.tensor([1, 2, 3, 4, 5, 6])
+    labels = ["a", "b", "c", "d", "e", "f"]
+    data = DataProto.from_dict(tensors={"obs": obs}, non_tensors={"labels": labels}, meta_info={"name": "abdce"})
+    data.reorder(torch.tensor([3, 4, 2, 0, 1, 5]))
+
+    assert torch.all(torch.eq(data.batch["obs"], torch.tensor([4, 5, 3, 1, 2, 6])))
+    assert np.all(data.non_tensor_batch["labels"] == np.array(["d", "e", "c", "a", "b", "f"]))
+    assert data.meta_info == {"name": "abdce"}
+
+
+def test_chunk_concat():
+    obs = torch.tensor([1, 2, 3, 4, 5, 6])
+    labels = ["a", "b", "c", "d", "e", "f"]
+    data = DataProto.from_dict(tensors={"obs": obs}, non_tensors={"labels": labels}, meta_info={"name": "abdce"})
+
+    with pytest.raises(AssertionError):
+        data.chunk(5)
+
+    data_split = data.chunk(2)
+    assert len(data_split) == 2
+    assert torch.all(torch.eq(data_split[0].batch["obs"], torch.tensor([1, 2, 3])))
+    assert np.all(data_split[0].non_tensor_batch["labels"] == np.array(["a", "b", "c"]))
+    assert data_split[0].meta_info == {"name": "abdce"}
+
+    assert torch.all(torch.eq(data_split[1].batch["obs"], torch.tensor([4, 5, 6])))
+    assert np.all(data_split[1].non_tensor_batch["labels"] == np.array(["d", "e", "f"]))
+    assert data_split[1].meta_info == {"name": "abdce"}
+
+    concat_data = DataProto.concat(data_split)
+    assert torch.all(torch.eq(concat_data.batch["obs"], data.batch["obs"]))
+    assert np.all(concat_data.non_tensor_batch["labels"] == data.non_tensor_batch["labels"])
+    assert concat_data.meta_info == data.meta_info
+
+
+def test_concat_metrics_from_multiple_workers():
+    """Test that concat() properly merges metrics from all workers in distributed training."""
+    # Simulate 3 workers each with their own metrics
+    obs1 = torch.tensor([1, 2])
+    obs2 = torch.tensor([3, 4])
+    obs3 = torch.tensor([5, 6])
+
+    # Each worker has different metrics (as list of dict format)
+    worker1_metrics = [{"loss": 0.5, "accuracy": 0.9}]
+    worker2_metrics = [{"loss": 0.6, "accuracy": 0.85}]
+    worker3_metrics = [{"loss": 0.55, "accuracy": 0.88}]
+
+    data1 = DataProto.from_dict(tensors={"obs": obs1}, meta_info={"metrics": worker1_metrics, "config_flag": True})
+    data2 = DataProto.from_dict(tensors={"obs": obs2}, meta_info={"metrics": worker2_metrics, "config_flag": True})
+    data3 = DataProto.from_dict(tensors={"obs": obs3}, meta_info={"metrics": worker3_metrics, "config_flag": True})
+
+    # Concat all workers' data
+    concat_data = DataProto.concat([data1, data2, data3])
+
+    # Verify tensors are concatenated
+    assert torch.all(torch.eq(concat_data.batch["obs"], torch.tensor([1, 2, 3, 4, 5, 6])))
+
+    # Verify ALL workers' metrics are flattened to dict of lists
+    expected_metrics = {"loss": [0.5, 0.6, 0.55], "accuracy": [0.9, 0.85, 0.88]}
+    assert concat_data.meta_info["metrics"] == expected_metrics
+
+    # Verify config flags are preserved from first worker
+    assert concat_data.meta_info["config_flag"] is True
+
+
+def test_concat_with_empty_and_non_list_meta_info():
+    """Test concat() handles edge cases: empty meta_info, non-list values, and None."""
+    obs1 = torch.tensor([1, 2])
+    obs2 = torch.tensor([3, 4])
+
+    # Worker 1 has metrics, worker 2 doesn't
+    data1 = DataProto.from_dict(tensors={"obs": obs1}, meta_info={"metrics": [{"loss": 0.5}], "flag": True})
+    data2 = DataProto.from_dict(tensors={"obs": obs2}, meta_info={"flag": True})
+
+    concat_data = DataProto.concat([data1, data2])
+
+    # Should flatten worker1's metrics to dict of lists
+    assert concat_data.meta_info["metrics"] == {"loss": [0.5]}
+    assert concat_data.meta_info["flag"] is True
+
+    # Test with non-list meta_info value
+    data3 = DataProto.from_dict(tensors={"obs": obs1}, meta_info={"single_value": 42})
+    data4 = DataProto.from_dict(tensors={"obs": obs2}, meta_info={"single_value": 42})
+
+    concat_data2 = DataProto.concat([data3, data4])
+    assert concat_data2.meta_info["single_value"] == 42
+
+
+def test_concat_first_worker_missing_metrics():
+    """Test that metrics from other workers are preserved even when first worker has no metrics.
+
+    This is a critical edge case - the old buggy implementation only checked data[0].meta_info
+    and would lose all metrics if the first worker didn't have any.
+    """
+    obs1 = torch.tensor([1, 2])
+    obs2 = torch.tensor([3, 4])
+    obs3 = torch.tensor([5, 6])
+
+    # First worker has NO metrics, but workers 2 and 3 do
+    data1 = DataProto.from_dict(tensors={"obs": obs1}, meta_info={"config_flag": True})
+    data2 = DataProto.from_dict(tensors={"obs": obs2}, meta_info={"metrics": {"loss": 0.6}, "config_flag": True})
+    data3 = DataProto.from_dict(tensors={"obs": obs3}, meta_info={"metrics": {"loss": 0.55}, "config_flag": True})
+
+    concat_data = DataProto.concat([data1, data2, data3])
+
+    # Should flatten metrics from workers 2 and 3 into dict of lists
+    expected_metrics = {"loss": [0.6, 0.55]}
+    assert concat_data.meta_info["metrics"] == expected_metrics
+    assert concat_data.meta_info["config_flag"] is True
+
+
+def test_concat_non_list_metrics():
+    """Test that concat() handles non-list metrics (single dict) correctly.
+
+    In some cases, metrics might be a single dict instead of a list.
+    The implementation should flatten them into a dict of lists.
+    """
+    obs1 = torch.tensor([1, 2])
+    obs2 = torch.tensor([3, 4])
+
+    # Metrics as single dict (not wrapped in list)
+    data1 = DataProto.from_dict(tensors={"obs": obs1}, meta_info={"metrics": {"loss": 0.5, "accuracy": 0.9}})
+    data2 = DataProto.from_dict(tensors={"obs": obs2}, meta_info={"metrics": {"loss": 0.6, "accuracy": 0.85}})
+
+    concat_data = DataProto.concat([data1, data2])
+
+    # Should flatten to dict of lists
+    expected_metrics = {"loss": [0.5, 0.6], "accuracy": [0.9, 0.85]}
+    assert concat_data.meta_info["metrics"] == expected_metrics
+
+
+def test_concat_merge_different_non_metric_keys():
+    """Test that concat() merges non-metric meta_info keys from all workers.
+
+    When different workers have different non-metric keys, all keys should be preserved.
+    This prevents silent data loss and aligns with the docstring stating meta_info is "merged".
+    """
+    obs1 = torch.tensor([1, 2])
+    obs2 = torch.tensor([3, 4])
+    obs3 = torch.tensor([5, 6])
+
+    # Each worker has some unique non-metric keys
+    data1 = DataProto.from_dict(tensors={"obs": obs1}, meta_info={"config": "A", "shared_key": "X"})
+    data2 = DataProto.from_dict(tensors={"obs": obs2}, meta_info={"extra_key": "B", "shared_key": "X"})
+    data3 = DataProto.from_dict(tensors={"obs": obs3}, meta_info={"another_key": "C", "shared_key": "X"})
+
+    concat_data = DataProto.concat([data1, data2, data3])
+
+    # All unique keys should be preserved
+    assert concat_data.meta_info["config"] == "A"
+    assert concat_data.meta_info["extra_key"] == "B"
+    assert concat_data.meta_info["another_key"] == "C"
+    assert concat_data.meta_info["shared_key"] == "X"
+
+
+def test_concat_conflicting_non_metric_keys():
+    """Test that concat() raises an assertion error when non-metric keys have conflicting values.
+
+    This ensures data integrity by catching cases where workers have different values
+    for what should be the same configuration parameter.
+    """
+    obs1 = torch.tensor([1, 2])
+    obs2 = torch.tensor([3, 4])
+
+    # Same key "config" but different values
+    data1 = DataProto.from_dict(tensors={"obs": obs1}, meta_info={"config": "A"})
+    data2 = DataProto.from_dict(tensors={"obs": obs2}, meta_info={"config": "B"})
+
+    # Should raise an assertion error due to conflicting values
+    with pytest.raises(AssertionError, match="Conflicting values for meta_info key 'config'"):
+        DataProto.concat([data1, data2])
+
+
+def test_pop():
+    obs = torch.randn(100, 10)
+    act = torch.randn(100, 3)
+    dataset = DataProto.from_dict({"obs": obs, "act": act}, meta_info={"2": 2, "1": 1})
+    poped_dataset = dataset.pop(batch_keys=["obs"], meta_info_keys=["2"])
+
+    assert poped_dataset.batch.keys() == {"obs"}
+    assert poped_dataset.meta_info.keys() == {"2"}
+
+    assert dataset.batch.keys() == {"act"}
+    assert dataset.meta_info.keys() == {"1"}
+
+
+def test_repeat():
+    # Create a DataProto object with some batch and non-tensor data
+    obs = torch.tensor([[1, 2], [3, 4], [5, 6]])
+    labels = ["a", "b", "c"]
+    data = DataProto.from_dict(tensors={"obs": obs}, non_tensors={"labels": labels}, meta_info={"info": "test_info"})
+
+    # Test interleave=True
+    repeated_data_interleave = data.repeat(repeat_times=2, interleave=True)
+    expected_obs_interleave = torch.tensor([[1, 2], [1, 2], [3, 4], [3, 4], [5, 6], [5, 6]])
+    expected_labels_interleave = ["a", "a", "b", "b", "c", "c"]
+
+    assert torch.all(torch.eq(repeated_data_interleave.batch["obs"], expected_obs_interleave))
+    assert (repeated_data_interleave.non_tensor_batch["labels"] == expected_labels_interleave).all()
+    assert repeated_data_interleave.meta_info == {"info": "test_info"}
+
+    # Test interleave=False
+    repeated_data_no_interleave = data.repeat(repeat_times=2, interleave=False)
+    expected_obs_no_interleave = torch.tensor([[1, 2], [3, 4], [5, 6], [1, 2], [3, 4], [5, 6]])
+    expected_labels_no_interleave = ["a", "b", "c", "a", "b", "c"]
+
+    assert torch.all(torch.eq(repeated_data_no_interleave.batch["obs"], expected_obs_no_interleave))
+    assert (repeated_data_no_interleave.non_tensor_batch["labels"] == expected_labels_no_interleave).all()
+    assert repeated_data_no_interleave.meta_info == {"info": "test_info"}
+
+
+def test_dataproto_pad_unpad():
+    obs = torch.tensor([[1, 2], [3, 4], [5, 6]])
+    labels = ["a", "b", "c"]
+    data = DataProto.from_dict(tensors={"obs": obs}, non_tensors={"labels": labels}, meta_info={"info": "test_info"})
+
+    from verl.protocol import pad_dataproto_to_divisor, unpad_dataproto
+
+    padded_data, pad_size = pad_dataproto_to_divisor(data, size_divisor=2)
+    assert pad_size == 1
+
+    expected_obs = torch.tensor([[1, 2], [3, 4], [5, 6], [1, 2]])
+    expected_labels = ["a", "b", "c", "a"]
+
+    assert torch.all(torch.eq(padded_data.batch["obs"], expected_obs))
+    assert (padded_data.non_tensor_batch["labels"] == expected_labels).all()
+    assert padded_data.meta_info == {"info": "test_info"}
+
+    unpadd_data = unpad_dataproto(padded_data, pad_size=pad_size)
+    assert torch.all(torch.eq(unpadd_data.batch["obs"], obs))
+    assert (unpadd_data.non_tensor_batch["labels"] == labels).all()
+    assert unpadd_data.meta_info == {"info": "test_info"}
+
+    padded_data, pad_size = pad_dataproto_to_divisor(data, size_divisor=3)
+    assert pad_size == 0
+
+    expected_obs = torch.tensor([[1, 2], [3, 4], [5, 6]])
+    expected_labels = ["a", "b", "c"]
+
+    assert torch.all(torch.eq(padded_data.batch["obs"], expected_obs))
+    assert (padded_data.non_tensor_batch["labels"] == expected_labels).all()
+    assert padded_data.meta_info == {"info": "test_info"}
+
+    unpadd_data = unpad_dataproto(padded_data, pad_size=pad_size)
+    assert torch.all(torch.eq(unpadd_data.batch["obs"], obs))
+    assert (unpadd_data.non_tensor_batch["labels"] == labels).all()
+    assert unpadd_data.meta_info == {"info": "test_info"}
+
+    padded_data, pad_size = pad_dataproto_to_divisor(data, size_divisor=7)
+    assert pad_size == 4
+
+    expected_obs = torch.tensor([[1, 2], [3, 4], [5, 6], [1, 2], [3, 4], [5, 6], [1, 2]])
+    expected_labels = ["a", "b", "c", "a", "b", "c", "a"]
+    assert torch.all(torch.eq(padded_data.batch["obs"], expected_obs))
+    assert (padded_data.non_tensor_batch["labels"] == expected_labels).all()
+    assert padded_data.meta_info == {"info": "test_info"}
+
+    unpadd_data = unpad_dataproto(padded_data, pad_size=pad_size)
+    assert torch.all(torch.eq(unpadd_data.batch["obs"], obs))
+    assert (unpadd_data.non_tensor_batch["labels"] == labels).all()
+    assert unpadd_data.meta_info == {"info": "test_info"}
+
+
+def test_dataproto_fold_unfold():
+    from verl.protocol import DataProto, fold_batch_dim, unfold_batch_dim
+
+    obs = torch.tensor([[1, 2], [3, 4], [5, 6]])
+    labels = ["a", "b", "c"]
+    data = DataProto.from_dict(tensors={"obs": obs}, non_tensors={"labels": labels}, meta_info={"info": "test_info"})
+
+    data1 = data.repeat(repeat_times=2, interleave=True)
+
+    data2 = fold_batch_dim(data1, new_batch_size=3)
+
+    torch.testing.assert_close(data2.batch["obs"], torch.tensor([[[1, 2], [1, 2]], [[3, 4], [3, 4]], [[5, 6], [5, 6]]]))
+    assert (data2.non_tensor_batch["labels"] == [["a", "a"], ["b", "b"], ["c", "c"]]).all()
+
+    data2.reorder(indices=torch.tensor([1, 2, 0]))
+
+    data3 = unfold_batch_dim(data2, batch_dims=2)
+
+    torch.testing.assert_close(data3.batch["obs"], torch.tensor([[3, 4], [3, 4], [5, 6], [5, 6], [1, 2], [1, 2]]))
+    assert (data3.non_tensor_batch["labels"] == ["b", "b", "c", "c", "a", "a"]).all()
+    assert data3.meta_info == {"info": "test_info"}
+
+
+def test_torch_save_data_proto():
+    obs = torch.tensor([[1, 2], [3, 4], [5, 6]])
+    labels = ["a", "b", "c"]
+    data = DataProto.from_dict(tensors={"obs": obs}, non_tensors={"labels": labels}, meta_info={"info": "test_info"})
+    data.save_to_disk("test_data.pt")
+    loaded_data = DataProto.load_from_disk("test_data.pt")
+
+    assert torch.all(torch.eq(loaded_data.batch["obs"], data.batch["obs"]))
+    assert (loaded_data.non_tensor_batch["labels"] == data.non_tensor_batch["labels"]).all()
+    assert loaded_data.meta_info == data.meta_info
+
+    import os
+
+    os.remove("test_data.pt")
+
+
+def test_len():
+    obs = torch.tensor([[1, 2], [3, 4], [5, 6]])
+    labels = np.array(["a", "b", "c"], dtype=object)
+    data = DataProto.from_dict(tensors={"obs": obs}, non_tensors={"labels": labels}, meta_info={"info": "test_info"})
+
+    assert len(data) == 3
+
+    data = DataProto(batch=None, non_tensor_batch={"labels": labels}, meta_info={"info": "test_info"})
+
+    assert len(data) == 3
+
+    data = DataProto(batch=None, non_tensor_batch={}, meta_info={"info": "test_info"})
+
+    assert len(data) == 0
+
+    data = DataProto(batch=None, non_tensor_batch=None, meta_info={"info": "test_info"})
+
+    assert len(data) == 0
+
+
+def test_dataproto_index():
+    data_len = 100
+    idx_num = 10
+
+    obs = torch.randn(data_len, 10)
+    labels = [random.choice(["abc", "cde"]) for _ in range(data_len)]
+    data = DataProto.from_dict(tensors={"obs": obs}, non_tensors={"labels": labels})
+    labels_np = np.array(labels)
+
+    idx_np_int = np.random.randint(0, data_len, size=(idx_num,))
+    result_np_int = data[idx_np_int]
+    assert result_np_int.batch.keys() == data.batch.keys()
+    assert result_np_int.non_tensor_batch.keys() == data.non_tensor_batch.keys()
+    assert result_np_int.batch["obs"].shape[0] == idx_num
+    assert result_np_int.non_tensor_batch["labels"].shape[0] == idx_num
+    assert np.array_equal(result_np_int.batch["obs"].cpu().numpy(), obs[idx_np_int].numpy())
+    assert np.array_equal(result_np_int.non_tensor_batch["labels"], labels_np[idx_np_int])
+
+    idx_torch_int = torch.randint(0, data_len, size=(idx_num,))
+    result_torch_int = data[idx_torch_int]
+    assert result_torch_int.batch.keys() == data.batch.keys()
+    assert result_torch_int.non_tensor_batch.keys() == data.non_tensor_batch.keys()
+    assert result_torch_int.batch["obs"].shape[0] == idx_num
+    assert result_torch_int.non_tensor_batch["labels"].shape[0] == idx_num
+    assert np.array_equal(result_torch_int.batch["obs"].cpu().numpy(), obs[idx_torch_int].cpu().numpy())
+    assert np.array_equal(result_torch_int.non_tensor_batch["labels"], labels_np[idx_torch_int.cpu().numpy()])
+
+    idx_list_int = [np.random.randint(0, data_len) for _ in range(idx_num)]
+    result_list_int = data[idx_list_int]
+    assert result_list_int.batch.keys() == data.batch.keys()
+    assert result_list_int.non_tensor_batch.keys() == data.non_tensor_batch.keys()
+    assert result_list_int.batch["obs"].shape[0] == idx_num
+    assert result_list_int.non_tensor_batch["labels"].shape[0] == idx_num
+    assert np.array_equal(result_list_int.batch["obs"].cpu().numpy(), obs[idx_list_int].cpu().numpy())
+    assert np.array_equal(result_list_int.non_tensor_batch["labels"], labels_np[idx_list_int])
+
+    idx_np_bool = np.random.randint(0, 2, size=(data_len,), dtype=bool)
+    result_np_bool = data[idx_np_bool]
+    assert result_np_bool.batch.keys() == data.batch.keys()
+    assert result_np_bool.non_tensor_batch.keys() == data.non_tensor_batch.keys()
+    assert result_np_bool.batch["obs"].shape[0] == idx_np_bool.sum()
+    assert result_np_bool.non_tensor_batch["labels"].shape[0] == idx_np_bool.sum()
+    assert np.array_equal(result_np_bool.batch["obs"].cpu().numpy(), obs[idx_np_bool].cpu().numpy())
+    assert np.array_equal(result_np_bool.non_tensor_batch["labels"], labels_np[idx_np_bool])
+
+    idx_torch_bool = torch.randint(0, 2, size=(data_len,), dtype=torch.bool)
+    result_torch_bool = data[idx_torch_bool]
+    assert result_torch_bool.batch.keys() == data.batch.keys()
+    assert result_torch_bool.non_tensor_batch.keys() == data.non_tensor_batch.keys()
+    assert result_torch_bool.batch["obs"].shape[0] == idx_torch_bool.sum().item()
+    assert result_torch_bool.non_tensor_batch["labels"].shape[0] == idx_torch_bool.sum().item()
+    assert np.array_equal(result_torch_bool.batch["obs"].cpu().numpy(), obs[idx_torch_bool].cpu().numpy())
+    assert np.array_equal(result_torch_bool.non_tensor_batch["labels"], labels_np[idx_torch_bool])
+
+    idx_list_bool = [np.random.randint(0, 2, dtype=bool) for _ in range(data_len)]
+    result_list_bool = data[idx_list_bool]
+    assert result_list_bool.batch.keys() == data.batch.keys()
+    assert result_list_bool.non_tensor_batch.keys() == data.non_tensor_batch.keys()
+    assert result_list_bool.batch["obs"].shape[0] == sum(idx_list_bool)
+    assert result_list_bool.non_tensor_batch["labels"].shape[0] == sum(idx_list_bool)
+    assert np.array_equal(result_list_bool.batch["obs"].cpu().numpy(), obs[idx_list_bool].cpu().numpy())
+    assert np.array_equal(result_list_bool.non_tensor_batch["labels"], labels_np[idx_list_bool])
+
+
+def test_old_vs_new_from_single_dict():
+    class CustomProto(DataProto):
+        """Uses the new, fixed from_single_dict."""
+
+        pass
+
+    class OriginProto(DataProto):
+        """Mimics the *old* from_single_dict (always returns a DataProto)."""
+
+        @classmethod
+        def from_single_dict(cls, data, meta_info=None, auto_padding=False):
+            tensors, non_tensors = {}, {}
+            for k, v in data.items():
+                if torch.is_tensor(v):
+                    tensors[k] = v
+                else:
+                    non_tensors[k] = v
+            # always calls DataProto.from_dict, ignoring `cls`
+            return DataProto.from_dict(
+                tensors=tensors,
+                non_tensors=non_tensors,
+                meta_info=meta_info,
+                auto_padding=auto_padding,
+            )
+
+    sample = {"x": torch.tensor([0])}
+
+    orig = OriginProto.from_single_dict(sample)
+    # old behavior: always DataProto, not a CustomOriginProto
+    assert type(orig) is DataProto
+    assert type(orig) is not OriginProto
+
+    cust = CustomProto.from_single_dict(sample)
+    # new behavior: respects subclass
+    assert type(cust) is CustomProto
+
+
+def test_dataproto_no_batch():
+    labels = ["a", "b", "c"]
+    data = DataProto.from_dict(non_tensors={"labels": labels}, meta_info={"info": "test_info"})
+    selected = data.select(non_tensor_batch_keys=["labels"])
+    assert (selected.non_tensor_batch["labels"] == labels).all()
+    pop_data = data.pop(non_tensor_batch_keys=["labels"])
+    assert (pop_data.non_tensor_batch["labels"] == labels).all()
+    assert data.non_tensor_batch == {}
+
+
+def test_sample_level_repeat():
+    # Create a DataProto object with some batch and non-tensor data
+    obs = torch.tensor([[1, 2], [3, 4], [5, 6]])
+    labels = ["a", "b", "c"]
+    data = DataProto.from_dict(tensors={"obs": obs}, non_tensors={"labels": labels}, meta_info={"info": "test_info"})
+
+    # list
+    repeated_data_interleave = data.sample_level_repeat(repeat_times=[3, 1, 2])
+    expected_obs_interleave = torch.tensor([[1, 2], [1, 2], [1, 2], [3, 4], [5, 6], [5, 6]])
+    expected_labels_interleave = ["a", "a", "a", "b", "c", "c"]
+
+    assert torch.all(torch.eq(repeated_data_interleave.batch["obs"], expected_obs_interleave))
+    assert (repeated_data_interleave.non_tensor_batch["labels"] == expected_labels_interleave).all()
+    assert repeated_data_interleave.meta_info == {"info": "test_info"}
+
+    # torch.tensor
+    repeated_data_no_interleave = data.sample_level_repeat(repeat_times=torch.tensor([1, 2, 3]))
+    expected_obs_no_interleave = torch.tensor([[1, 2], [3, 4], [3, 4], [5, 6], [5, 6], [5, 6]])
+    expected_labels_no_interleave = ["a", "b", "b", "c", "c", "c"]
+
+    assert torch.all(torch.eq(repeated_data_no_interleave.batch["obs"], expected_obs_no_interleave))
+    assert (repeated_data_no_interleave.non_tensor_batch["labels"] == expected_labels_no_interleave).all()
+    assert repeated_data_no_interleave.meta_info == {"info": "test_info"}
+
+
+def test_dataproto_unfold_column_chunks():
+    obs1 = torch.tensor([[1, 2, 3, 4], [5, 6, 7, 8], [9, 10, 11, 12]])
+    obs2 = torch.tensor([[1, 2], [5, 6], [9, 10]])
+
+    labels = ["a", "b", "c"]
+    data = DataProto.from_dict(
+        tensors={"obs1": obs1, "obs2": obs2}, non_tensors={"labels": labels}, meta_info={"name": "abc"}
+    )
+    ret = data.unfold_column_chunks(2, split_keys=["obs1"])
+
+    expect_obs1 = torch.tensor([[1, 2], [3, 4], [5, 6], [7, 8], [9, 10], [11, 12]])
+    expect_obs2 = torch.tensor([[1, 2], [1, 2], [5, 6], [5, 6], [9, 10], [9, 10]])
+    expect_labels = ["a", "a", "b", "b", "c", "c"]
+    assert torch.all(torch.eq(ret.batch["obs1"], expect_obs1))
+    assert torch.all(torch.eq(ret.batch["obs2"], expect_obs2))
+    assert (ret.non_tensor_batch["labels"] == expect_labels).all()
+    assert ret.meta_info == {"name": "abc"}
+
+    obs1 = torch.tensor([[1, 2, 3, 4], [5, 6, 7, 8], [9, 10, 11, 12]])
+    obs2 = torch.tensor([[1, 2], [5, 6], [9, 10]])
+
+    labels = [["a1", "a2"], ["b1", "b2"], ["c1", "c2"]]
+    data = DataProto.from_dict(
+        tensors={"obs1": obs1, "obs2": obs2}, non_tensors={"labels": labels}, meta_info={"name": "abc"}
+    )
+    ret = data.unfold_column_chunks(2, split_keys=["obs1", "labels"])
+
+    expect_obs1 = torch.tensor([[1, 2], [3, 4], [5, 6], [7, 8], [9, 10], [11, 12]])
+    expect_obs2 = torch.tensor([[1, 2], [1, 2], [5, 6], [5, 6], [9, 10], [9, 10]])
+    expect_labels = [["a1"], ["a2"], ["b1"], ["b2"], ["c1"], ["c2"]]
+    assert torch.all(torch.eq(ret.batch["obs1"], expect_obs1))
+    assert torch.all(torch.eq(ret.batch["obs2"], expect_obs2))
+    assert (ret.non_tensor_batch["labels"] == expect_labels).all()
+    assert ret.meta_info == {"name": "abc"}
+
+    obs1 = torch.tensor(
+        [[[1, 1], [2, 2], [3, 3], [4, 4]], [[5, 5], [6, 6], [7, 7], [8, 8]], [[9, 9], [10, 10], [11, 11], [12, 12]]]
+    )
+    obs2 = torch.tensor([[[1, 1], [2, 2]], [[5, 5], [6, 6]], [[9, 9], [10, 10]]])
+
+    labels = ["a", "b", "c"]
+    data = DataProto.from_dict(
+        tensors={"obs1": obs1, "obs2": obs2}, non_tensors={"labels": labels}, meta_info={"name": "abc"}
+    )
+    ret = data.unfold_column_chunks(2, split_keys=["obs1"])
+
+    expect_obs1 = torch.tensor(
+        [
+            [[1, 1], [2, 2]],
+            [[3, 3], [4, 4]],
+            [[5, 5], [6, 6]],
+            [[7, 7], [8, 8]],
+            [[9, 9], [10, 10]],
+            [[11, 11], [12, 12]],
+        ]
+    )
+    expect_obs2 = torch.tensor(
+        [[[1, 1], [2, 2]], [[1, 1], [2, 2]], [[5, 5], [6, 6]], [[5, 5], [6, 6]], [[9, 9], [10, 10]], [[9, 9], [10, 10]]]
+    )
+    expect_labels = ["a", "a", "b", "b", "c", "c"]
+    assert torch.all(torch.eq(ret.batch["obs1"], expect_obs1))
+    assert torch.all(torch.eq(ret.batch["obs2"], expect_obs2))
+    assert (ret.non_tensor_batch["labels"] == expect_labels).all()
+    assert ret.meta_info == {"name": "abc"}
+
+
+def test_dataproto_chunk_after_index():
+    data_len = 4
+    obs = torch.randn(data_len, 4)
+    labels = [f"label_{i}" for i in range(data_len)]
+    data = DataProto.from_dict(tensors={"obs": obs}, non_tensors={"labels": labels}, meta_info={"name": "abc"})
+
+    # Test with boolean numpy array
+    bool_mask = np.array([True, False, True, False])
+    selected = data[bool_mask]
+    assert isinstance(selected.batch.batch_size, torch.Size)
+    assert all(isinstance(d, int) for d in selected.batch.batch_size)  # int or List[int]
+
+    # Test with integer numpy array
+    int_mask = np.array([0, 2])
+    selected = data[int_mask]
+    assert isinstance(selected.batch.batch_size, torch.Size)
+    assert all(isinstance(d, int) for d in selected.batch.batch_size)
+
+    # Test with boolean list
+    list_mask = [True, False, True, False]
+    selected = data[list_mask]
+    assert isinstance(selected.batch.batch_size, torch.Size)
+    assert all(isinstance(d, int) for d in selected.batch.batch_size)
+
+    # Test with list
+    list_mask = [0, 2]
+    selected = data[list_mask]
+    assert isinstance(selected.batch.batch_size, torch.Size)
+    assert all(isinstance(d, int) for d in selected.batch.batch_size)
+
+    # Test with torch tensor (bool)
+    torch_bool_mask = torch.tensor([True, False, True, False])
+    selected = data[torch_bool_mask]
+    assert isinstance(selected.batch.batch_size, torch.Size)
+    assert all(isinstance(d, int) for d in selected.batch.batch_size)
+
+    # Test with torch tensor (int)
+    torch_int_mask = torch.tensor([0, 2])
+    selected = data[torch_int_mask]
+    assert isinstance(selected.batch.batch_size, torch.Size)
+    assert all(isinstance(d, int) for d in selected.batch.batch_size)
+
+
+@pytest.mark.skipif(
+    parse_version(tensordict.__version__) < parse_version("0.10"), reason="requires at least tensordict 0.10"
+)
+def test_to_tensordict():
+    obs = torch.tensor([1, 2, 3, 4, 5, 6])
+    labels = ["a", "b", "c", "d", "e", "f"]
+    data = DataProto.from_dict(tensors={"obs": obs}, non_tensors={"labels": labels}, meta_info={"name": "abdce"})
+    output = data.to_tensordict()
+
+    assert torch.all(torch.eq(output["obs"], obs)).item()
+    assert output["labels"] == labels
+    assert output["name"] == "abdce"
+
+
+@pytest.mark.skipif(
+    parse_version(tensordict.__version__) < parse_version("0.10"), reason="requires at least tensordict 0.10"
+)
+def test_from_tensordict():
+    tensor_dict = {
+        "obs": torch.tensor([1, 2, 3, 4, 5, 6]),
+        "labels": ["a", "b", "c", "d", "e", "f"],
+    }
+    non_tensor_dict = {"name": "abdce"}
+    tensordict = tu.get_tensordict(tensor_dict, non_tensor_dict)
+    data = DataProto.from_tensordict(tensordict)
+
+    assert data.non_tensor_batch["labels"].tolist() == tensor_dict["labels"]
+    assert torch.all(torch.eq(data.batch["obs"], tensor_dict["obs"])).item()
+    assert data.meta_info["name"] == "abdce"
+
+
+@pytest.mark.skipif(
+    parse_version(tensordict.__version__) < parse_version("0.10"), reason="requires at least tensordict 0.10"
+)
+def test_to_tensordict_with_nested_lists():
+    """Test converting DataProto with nested lists to TensorDict (lists of lists)."""
+    obs = torch.tensor([1, 2, 3])
+    # Simulate turn_scores or tool_rewards: array of lists with varying lengths
+    turn_scores = [[], [0.5, 0.8], [0.9]]
+
+    data = DataProto.from_dict(tensors={"obs": obs}, non_tensors={"turn_scores": turn_scores})
+
+    # This should not raise an error
+    tensordict_output = data.to_tensordict()
+
+    # Verify the data is preserved
+    assert torch.all(torch.eq(tensordict_output["obs"], obs)).item()
+    # Verify nested structure is accessible (TensorDict wraps NonTensorStack as LinkedList)
+    retrieved_scores = tensordict_output["turn_scores"]
+    assert len(retrieved_scores) == len(turn_scores)
+    # Verify content matches
+    assert list(retrieved_scores[0]) == []
+    assert list(retrieved_scores[1]) == [0.5, 0.8]
+    assert list(retrieved_scores[2]) == [0.9]
+
+
+@pytest.mark.skipif(
+    parse_version(tensordict.__version__) < parse_version("0.10"), reason="requires at least tensordict 0.10"
+)
+def test_to_tensordict_with_nested_dicts():
+    """Test converting DataProto with lists of dicts to TensorDict."""
+    obs = torch.tensor([1, 2, 3])
+    # Simulate reward_extra_info: array of dicts
+    reward_extra_info = [{"acc": 1.0}, {"acc": 0.0}, {"acc": 1.0}]
+
+    data = DataProto.from_dict(tensors={"obs": obs}, non_tensors={"reward_extra_info": reward_extra_info})
+
+    # This should not raise an error - this was the original bug
+    tensordict_output = data.to_tensordict()
+
+    # Verify the data is preserved
+    assert torch.all(torch.eq(tensordict_output["obs"], obs)).item()
+    # Verify nested dicts are accessible
+    retrieved_info = tensordict_output["reward_extra_info"]
+    assert len(retrieved_info) == len(reward_extra_info)
+    # Verify content matches
+    for i, expected_dict in enumerate(reward_extra_info):
+        assert dict(retrieved_info[i]) == expected_dict
+
+
+@pytest.mark.skipif(
+    parse_version(tensordict.__version__) < parse_version("0.10"), reason="requires at least tensordict 0.10"
+)
+def test_to_tensordict_with_complex_nested_structures():
+    """Test converting DataProto with complex nested structures (lists of lists of dicts)."""
+    obs = torch.tensor([1, 2, 3])
+    # Simulate raw_prompt: array of lists containing dicts
+    raw_prompt = [
+        [{"content": "Question 1", "role": "user"}],
+        [{"content": "Question 2", "role": "user"}, {"content": "Answer 2", "role": "assistant"}],
+        [{"content": "Question 3", "role": "user"}],
+    ]
+
+    data = DataProto.from_dict(tensors={"obs": obs}, non_tensors={"raw_prompt": raw_prompt})
+
+    # This should not raise an error
+    tensordict_output = data.to_tensordict()
+
+    # Verify the data is preserved
+    assert torch.all(torch.eq(tensordict_output["obs"], obs)).item()
+    # Verify complex nested structure is accessible
+    retrieved_prompt = tensordict_output["raw_prompt"]
+    assert len(retrieved_prompt) == len(raw_prompt)
+    # Spot check: verify first prompt has correct structure
+    assert len(retrieved_prompt[0]) == 1
+    assert dict(retrieved_prompt[0][0]) == {"content": "Question 1", "role": "user"}
+
+
+@pytest.mark.skipif(
+    parse_version(tensordict.__version__) < parse_version("0.10"), reason="requires at least tensordict 0.10"
+)
+def test_to_tensordict_and_back_with_nested_data():
+    """Test round-trip conversion: DataProto → TensorDict → DataProto with nested structures."""
+    obs = torch.tensor([1, 2, 3, 4])
+    labels = ["a", "b", "c", "d"]
+
+    # Multiple types of nested structures
+    turn_scores = [[], [0.5], [0.8, 0.9], [0.7]]
+    reward_extra_info = [
+        {"acc": 1.0, "loss": 0.1},
+        {"acc": 0.5, "loss": 0.3},
+        {"acc": 1.0, "loss": 0.05},
+        {"acc": 0.0, "loss": 0.9},
+    ]
+    raw_prompt = [
+        [{"content": "Q1", "role": "user"}],
+        [{"content": "Q2", "role": "user"}],
+        [{"content": "Q3", "role": "user"}, {"content": "A3", "role": "assistant"}],
+        [{"content": "Q4", "role": "user"}],
+    ]
+
+    # Create original DataProto
+    original_data = DataProto.from_dict(
+        tensors={"obs": obs},
+        non_tensors={
+            "labels": labels,
+            "turn_scores": turn_scores,
+            "reward_extra_info": reward_extra_info,
+            "raw_prompt": raw_prompt,
+        },
+        meta_info={"experiment": "test_nested"},
+    )
+
+    # Convert to TensorDict
+    tensordict_output = original_data.to_tensordict()
+
+    # Convert back to DataProto
+    reconstructed_data = DataProto.from_tensordict(tensordict_output)
+
+    # Verify tensors are preserved
+    assert torch.all(torch.eq(reconstructed_data.batch["obs"], obs)).item()
+
+    # Verify non-tensor data is preserved
+    assert reconstructed_data.non_tensor_batch["labels"].tolist() == labels
+
+    # Verify nested structures are preserved
+    assert len(reconstructed_data.non_tensor_batch["turn_scores"]) == len(turn_scores)
+    for orig, recon in zip(turn_scores, reconstructed_data.non_tensor_batch["turn_scores"], strict=True):
+        assert list(orig) == list(recon)
+
+    assert len(reconstructed_data.non_tensor_batch["reward_extra_info"]) == len(reward_extra_info)
+    for orig, recon in zip(reward_extra_info, reconstructed_data.non_tensor_batch["reward_extra_info"], strict=True):
+        assert orig == recon
+
+    assert len(reconstructed_data.non_tensor_batch["raw_prompt"]) == len(raw_prompt)
+    for orig, recon in zip(raw_prompt, reconstructed_data.non_tensor_batch["raw_prompt"], strict=True):
+        assert orig == list(recon)
+
+    # Verify meta_info is preserved
+    assert reconstructed_data.meta_info["experiment"] == "test_nested"
+
+
+@pytest.mark.skipif(
+    parse_version(tensordict.__version__) < parse_version("0.10"), reason="requires at least tensordict 0.10"
+)
+def test_to_tensordict_agent_loop_scenario():
+    """Test the exact scenario from agent loop: DataProto with tool rewards, acc, etc.
+
+    This test reproduces the exact error from the agent loop where nested structures
+    (lists of lists, lists of dicts) failed to convert to TensorDict.
+    """
+    # Simulate real agent loop data structure
+    prompts = torch.tensor([[1, 2, 3], [4, 5, 6]])
+    responses = torch.tensor([[7, 8], [9, 10]])
+
+    # Non-tensor data with nested structures from agent loop
+    data_source = ["lighteval/MATH", "lighteval/MATH"]
+    uid = ["uuid-1", "uuid-2"]
+    num_turns = np.array([2, 4], dtype=np.int32)
+    acc = np.array([1.0, 0.0])
+    turn_scores = [[], [0.5, 0.8]]  # Lists of varying lengths
+    reward_extra_info = [{"acc": 1.0}, {"acc": 0.0}]  # List of dicts
+    raw_prompt = [
+        [{"content": "Compute 4 @ 2", "role": "user"}],
+        [{"content": "Compute 8 @ 7", "role": "user"}],
+    ]
+    tool_rewards = [[0.0], []]  # List of lists
+
+    data = DataProto.from_dict(
+        tensors={"prompts": prompts, "responses": responses},
+        non_tensors={
+            "data_source": data_source,
+            "uid": uid,
+            "num_turns": num_turns,
+            "acc": acc,
+            "turn_scores": turn_scores,
+            "reward_extra_info": reward_extra_info,
+            "raw_prompt": raw_prompt,
+            "tool_rewards": tool_rewards,
+        },
+        meta_info={"global_steps": 42},
+    )
+
+    # THE KEY TEST: This should not raise ValueError about TensorDict conversion
+    tensordict_output = data.to_tensordict()
+
+    # Verify tensors are accessible
+    assert torch.all(torch.eq(tensordict_output["prompts"], prompts)).item()
+    assert torch.all(torch.eq(tensordict_output["responses"], responses)).item()
+
+    # Verify all nested structures are accessible (content check, not type check)
+    assert len(tensordict_output["turn_scores"]) == 2
+    assert list(tensordict_output["turn_scores"][0]) == []
+    assert list(tensordict_output["turn_scores"][1]) == [0.5, 0.8]
+
+    assert len(tensordict_output["reward_extra_info"]) == 2
+    assert dict(tensordict_output["reward_extra_info"][0]) == {"acc": 1.0}
+
+    assert len(tensordict_output["raw_prompt"]) == 2
+    assert dict(tensordict_output["raw_prompt"][0][0]) == {"content": "Compute 4 @ 2", "role": "user"}
+
+    assert len(tensordict_output["tool_rewards"]) == 2
+    assert list(tensordict_output["tool_rewards"][0]) == [0.0]
+    assert list(tensordict_output["tool_rewards"][1]) == []
+
+    # Verify round-trip conversion works perfectly
+    reconstructed = DataProto.from_tensordict(tensordict_output)
+    assert len(reconstructed) == 2
+    assert reconstructed.meta_info["global_steps"] == 42
+    assert torch.all(torch.eq(reconstructed.batch["prompts"], prompts)).item()
+
+
+def test_serialize_deserialize_single_tensor():
+    """Test serialization and deserialization of a single tensor"""
+    # Create test tensor
+    original_tensor = torch.randn(3, 4, 5)
+
+    # Serialize
+    dtype, shape, data = serialize_single_tensor(original_tensor)
+
+    # Deserialize
+    reconstructed_tensor = deserialize_single_tensor((dtype, shape, data))
+
+    # Verify results
+    assert torch.allclose(original_tensor, reconstructed_tensor)
+    assert original_tensor.shape == reconstructed_tensor.shape
+    assert original_tensor.dtype == reconstructed_tensor.dtype
+
+
+def test_serialize_deserialize_tensordict_regular_tensors():
+    """Test serialization and deserialization of TensorDict with regular tensors"""
+    # Create test data
+    batch_size = (5, 3)
+    tensor1 = torch.randn(*batch_size, 4)
+    tensor2 = torch.randint(0, 10, (*batch_size, 2))
+
+    # Create TensorDict
+    original_tensordict = TensorDict({"tensor1": tensor1, "tensor2": tensor2}, batch_size=batch_size)
+
+    # Serialize
+    batch_size_serialized, device, encoded_items = serialize_tensordict(original_tensordict)
+
+    # Deserialize
+    reconstructed_tensordict = deserialize_tensordict((batch_size_serialized, device, encoded_items))
+
+    # Verify results
+    assert original_tensordict.batch_size == reconstructed_tensordict.batch_size
+    assert set(original_tensordict.keys()) == set(reconstructed_tensordict.keys())
+
+    for key in original_tensordict.keys():
+        original_tensor = original_tensordict[key]
+        reconstructed_tensor = reconstructed_tensordict[key]
+
+        assert torch.allclose(original_tensor, reconstructed_tensor)
+        assert original_tensor.shape == reconstructed_tensor.shape
+        assert original_tensor.dtype == reconstructed_tensor.dtype
+
+
+def test_serialize_deserialize_tensordict_nested_tensors():
+    """Test serialization and deserialization of TensorDict with nested tensors"""
+    # Create nested tensor
+    tensor_list = [torch.randn(2, 3), torch.randn(3, 4), torch.randn(1, 5)]
+    nested_tensor = torch.nested.as_nested_tensor(tensor_list)
+
+    # Create regular tensor for comparison
+    regular_tensor = torch.randn(3, 4, 5)
+
+    # Create TensorDict
+    original_tensordict = TensorDict({"nested": nested_tensor, "regular": regular_tensor}, batch_size=(3,))
+
+    # Serialize
+    batch_size_serialized, device, encoded_items = serialize_tensordict(original_tensordict)
+
+    # Deserialize
+    reconstructed_tensordict = deserialize_tensordict((batch_size_serialized, device, encoded_items))
+
+    # Verify results
+    assert original_tensordict.batch_size == reconstructed_tensordict.batch_size
+    assert set(original_tensordict.keys()) == set(reconstructed_tensordict.keys())
+
+    # Verify regular tensor
+    original_regular = original_tensordict["regular"]
+    reconstructed_regular = reconstructed_tensordict["regular"]
+
+    assert torch.allclose(original_regular, reconstructed_regular)
+    assert original_regular.shape == reconstructed_regular.shape
+    assert original_regular.dtype == reconstructed_regular.dtype
+
+    # Verify nested tensor
+    original_nested = original_tensordict["nested"]
+    reconstructed_nested = reconstructed_tensordict["nested"]
+
+    # Check if it's a nested tensor
+    assert original_nested.is_nested
+    assert reconstructed_nested.is_nested
+
+    # Check layout
+    assert original_nested.layout == reconstructed_nested.layout
+
+    # Check each tensor after unbinding
+    original_unbind = original_nested.unbind()
+    reconstructed_unbind = reconstructed_nested.unbind()
+
+    assert len(original_unbind) == len(reconstructed_unbind)
+
+    for orig, recon in zip(original_unbind, reconstructed_unbind, strict=False):
+        assert torch.allclose(orig, recon)
+        assert orig.shape == recon.shape
+        assert orig.dtype == recon.dtype
+
+
+def test_serialize_deserialize_tensordict_mixed_types():
+    """Test serialization and deserialization of TensorDict with mixed tensor types"""
+    # Create tensors with different data types
+    float_tensor = torch.randn(2, 3).float()
+    double_tensor = torch.randn(2, 3).double()
+    int_tensor = torch.randint(0, 10, (2, 3)).int()
+    long_tensor = torch.randint(0, 10, (2, 3)).long()
+    bool_tensor = torch.tensor([[True, False], [False, True]])
+    bfloat16_tensor = torch.randn(2, 3).bfloat16()
+
+    # Add fp8 tensor (if available)
+    # Note: FP8 is not natively supported in all PyTorch versions
+    # We'll check if it's available and conditionally include it
+    has_fp8 = hasattr(torch, "float8_e5m2") or hasattr(torch, "float8_e4m3fn")
+    if has_fp8:
+        try:
+            # Try to create an FP8 tensor (implementation may vary)
+            # This is a placeholder - actual FP8 support might require specific hardware
+            fp8_tensor = torch.randn(2, 3)
+            if hasattr(torch, "float8_e5m2"):
+                fp8_tensor = fp8_tensor.to(torch.float8_e5m2)
+            elif hasattr(torch, "float8_e4m3fn"):
+                fp8_tensor = fp8_tensor.to(torch.float8_e4m3fn)
+        except Exception:
+            has_fp8 = False
+
+    # Create nested tensor
+    tensor_list = [
+        torch.randn(2, 3),
+        torch.randn(3, 4),
+    ]
+    nested_tensor = torch.nested.as_nested_tensor(tensor_list)
+
+    # Create TensorDict with all available types
+    tensordict_data = {
+        "float": float_tensor,
+        "double": double_tensor,
+        "int": int_tensor,
+        "long": long_tensor,
+        "bool": bool_tensor,
+        "bfloat16": bfloat16_tensor,
+        "nested": nested_tensor,
+    }
+
+    # Conditionally add fp8 tensor if available
+    if has_fp8:
+        tensordict_data["fp8"] = fp8_tensor
+
+    original_tensordict = TensorDict(
+        tensordict_data,
+        batch_size=(2,),
+    )
+
+    # Serialize
+    batch_size_serialized, device, encoded_items = serialize_tensordict(original_tensordict)
+
+    # Deserialize
+    reconstructed_tensordict = deserialize_tensordict((batch_size_serialized, device, encoded_items))
+
+    # Verify results
+    assert original_tensordict.batch_size == reconstructed_tensordict.batch_size
+    assert set(original_tensordict.keys()) == set(reconstructed_tensordict.keys())
+
+    for key in original_tensordict.keys():
+        original_tensor = original_tensordict[key]
+        reconstructed_tensor = reconstructed_tensordict[key]
+
+        if original_tensor.is_nested:
+            # For nested tensors, check each tensor after unbinding
+            original_unbind = original_tensor.unbind()
+            reconstructed_unbind = reconstructed_tensor.unbind()
+
+            assert len(original_unbind) == len(reconstructed_unbind)
+
+            for orig, recon in zip(original_unbind, reconstructed_unbind, strict=False):
+                assert torch.allclose(orig, recon, equal_nan=True)
+                assert orig.shape == recon.shape
+                assert orig.dtype == recon.dtype
+        else:
+            # For regular tensors, compare directly
+            assert torch.all(original_tensor == reconstructed_tensor)
+            assert original_tensor.shape == reconstructed_tensor.shape
+            assert original_tensor.dtype == reconstructed_tensor.dtype
+
+
+def test_serialize_deserialize_tensordict_with_device():
+    """Test serialization and deserialization of TensorDict with device information"""
+    # Create test data
+    batch_size = (2, 3)
+    tensor1 = torch.randn(*batch_size, 4)
+    tensor2 = torch.randint(0, 10, (*batch_size, 2))
+
+    # Create TensorDict with device information
+    device = "cpu"
+    original_tensordict = TensorDict({"tensor1": tensor1, "tensor2": tensor2}, batch_size=batch_size, device=device)
+
+    # Serialize
+    batch_size_serialized, device_serialized, encoded_items = serialize_tensordict(original_tensordict)
+
+    # Deserialize
+    reconstructed_tensordict = deserialize_tensordict((batch_size_serialized, device_serialized, encoded_items))
+
+    # Verify results
+    assert original_tensordict.batch_size == reconstructed_tensordict.batch_size
+    assert str(original_tensordict.device) == str(reconstructed_tensordict.device)
+    assert set(original_tensordict.keys()) == set(reconstructed_tensordict.keys())
+
+    for key in original_tensordict.keys():
+        original_tensor = original_tensordict[key]
+        reconstructed_tensor = reconstructed_tensordict[key]
+
+        assert torch.allclose(original_tensor.cpu(), reconstructed_tensor.cpu())
+        assert original_tensor.shape == reconstructed_tensor.shape
+        assert original_tensor.dtype == reconstructed_tensor.dtype
+
+
+def test_serialize_dataproto_with_empty_tensordict():
+    """Tests that serializing a DataProto with an empty TensorDict does not crash.
+
+    This test verifies the fix for the torch.cat error that occurs when calling
+    consolidate() on an empty TensorDict during serialization.
+    """
+    import pickle
+
+    # This test requires tensordict >= 0.5.0 to trigger the code path
+    if parse_version(tensordict.__version__) < parse_version("0.5.0"):
+        pytest.skip("Test requires tensordict>=0.5.0")
+
+    # Create a DataProto with an empty TensorDict but with a batch size
+    empty_td = TensorDict({}, batch_size=[10])
+    data = DataProto(batch=empty_td)
+
+    # This would crash before the fix with:
+    # RuntimeError: torch.cat(): expected a non-empty list of Tensors
+    try:
+        serialized_data = pickle.dumps(data)
+    except Exception as e:
+        pytest.fail(f"Serializing DataProto with empty TensorDict failed with: {e}")
+
+    # Verify deserialization works as expected
+    deserialized_data = pickle.loads(serialized_data)
+    assert len(deserialized_data.batch.keys()) == 0
+    assert deserialized_data.batch.batch_size == torch.Size([10])
diff --git a/code/RL_model/verl/verl_train/tests/test_protocol_v2_on_cpu.py b/code/RL_model/verl/verl_train/tests/test_protocol_v2_on_cpu.py
new file mode 100644
index 0000000000000000000000000000000000000000..b434c412b79d02bde31444009bfc45eb0e94d771
--- /dev/null
+++ b/code/RL_model/verl/verl_train/tests/test_protocol_v2_on_cpu.py
@@ -0,0 +1,1068 @@
+# Copyright 2024 Bytedance Ltd. and/or its affiliates
+#
+# Licensed under the Apache License, Version 2.0 (the "License");
+# you may not use this file except in compliance with the License.
+# You may obtain a copy of the License at
+#
+#     http://www.apache.org/licenses/LICENSE-2.0
+#
+# Unless required by applicable law or agreed to in writing, software
+# distributed under the License is distributed on an "AS IS" BASIS,
+# WITHOUT WARRANTIES OR CONDITIONS OF ANY KIND, either express or implied.
+# See the License for the specific language governing permissions and
+# limitations under the License.
+
+"""
+Replace DataProto with raw TensorDict
+"""
+
+import copy
+import random
+
+import numpy as np
+import pytest
+import torch
+from tensordict.tensorclass import NonTensorData, NonTensorStack
+
+from verl.utils import tensordict_utils as tu
+
+
+def test_union_tensor_dict():
+    obs = torch.randn(100, 10)
+
+    meta_info1 = {"top_p": 0.8}
+    meta_info2 = {"top_p": 0.9}
+    data1 = {"obs": obs, "act": torch.randn(100, 3), "data_sources": ["gsm8k"] * 100}
+    data2 = {"obs": obs, "next_obs": torch.randn(100, 10), "rew": torch.randn(100), "data_sources": ["gsm8k"] * 100}
+
+    data_with_copied_obs = {"obs": obs.clone(), "next_obs": torch.randn(100, 10), "rew": torch.randn(100)}
+
+    data1 = tu.get_tensordict(tensor_dict=data1)
+    data2 = tu.get_tensordict(tensor_dict=data2)
+    data_with_copied_obs = tu.get_tensordict(data_with_copied_obs)
+
+    tu.union_tensor_dict(data1, data2)
+    with pytest.raises(AssertionError):
+        # conflict in tensor values
+        tu.union_tensor_dict(data1, data_with_copied_obs)
+
+    data1 = tu.assign_non_tensor(data1, **meta_info1)
+    tu.union_tensor_dict(data1, data2)  # works ok
+
+    data2 = tu.assign_non_tensor(data2, **meta_info2)
+
+    with pytest.raises(AssertionError):
+        # conflict in NonTensorData
+        tu.union_tensor_dict(data1, data2)
+
+    data1.pop("top_p")
+    data2.pop("top_p")
+
+    data2["data_sources"][0] = "math"
+    with pytest.raises(AssertionError):
+        # conflict in NonTensorData
+        tu.union_tensor_dict(data1, data2)
+
+
+def test_tensor_dict_constructor():
+    obs = torch.ones(100, 10)
+    act = torch.zeros(100, 10, 3)
+    data_source = ["gsm8k"] * 100
+    non_tensor_dict = {"name": "abdce"}
+
+    data = tu.get_tensordict(
+        tensor_dict={"obs": obs, "act": act, "data_source": data_source}, non_tensor_dict=non_tensor_dict
+    )
+
+    assert data.batch_size == torch.Size([100])
+
+    # test slicing
+    assert torch.all(torch.eq(data[0]["obs"], torch.ones(10))).item()
+    assert torch.all(torch.eq(data[0]["act"], torch.zeros(10, 3))).item()
+    assert data[0]["data_source"] == "gsm8k"
+
+    assert torch.all(torch.eq(data[0:2]["obs"], torch.ones(2, 10))).item()
+    assert torch.all(torch.eq(data[0:2]["act"], torch.zeros(2, 10, 3))).item()
+    assert data[0:2]["data_source"] == ["gsm8k"] * 2
+
+    # test non tensor data
+    assert data["name"] == "abdce"
+
+
+def test_index_select_tensor_dict():
+    vocab_size = 128
+    a = torch.randint(low=0, high=vocab_size, size=(11,))
+    b = torch.randint(low=0, high=vocab_size, size=(13,))
+    c = torch.randint(low=0, high=vocab_size, size=(12,))
+    d = torch.randint(low=0, high=vocab_size, size=(15,))
+    input_ids = [a, b, c, d]
+    input_ids = torch.nested.as_nested_tensor(input_ids, layout=torch.jagged)
+
+    padded_tensor = torch.randn(4, 10)
+    non_tensor_dict = {"global_batch_size": "4"}
+
+    data = tu.get_tensordict(
+        tensor_dict={
+            "input_ids": input_ids,
+            "padded_tensor": padded_tensor,
+        },
+        non_tensor_dict=non_tensor_dict,
+    )
+
+    assert data.batch_size == torch.Size([4])
+
+    # test index select
+    indices = torch.tensor([1, 3])
+    selected_data = tu.index_select_tensor_dict(data, indices)
+
+    assert selected_data.batch_size == torch.Size([2])
+
+    target_input_ids = torch.nested.as_nested_tensor([input_ids[idx] for idx in indices], layout=torch.jagged)
+    target_select_data = tu.get_tensordict(
+        tensor_dict={
+            "input_ids": target_input_ids,
+            "padded_tensor": padded_tensor[indices],
+        },
+        non_tensor_dict=non_tensor_dict,
+    )
+    tu.assert_tensordict_eq(selected_data, target_select_data)
+
+
+def test_tensordict_with_images():
+    # each sample contains a sequence with multiple images of different sizes
+    vocab_size = 128
+    a = torch.randint(low=0, high=vocab_size, size=(11,))
+    b = torch.randint(low=0, high=vocab_size, size=(13,))
+    input_ids = [a, b]
+    input_ids = torch.nested.as_nested_tensor(input_ids, layout=torch.jagged)
+
+    # must be numpy
+    # TODO(vermouth1992). We may use nested tensor too. But this requires nested over nested
+    a_images = [
+        torch.randint(low=0, high=255, size=(3, 256, 256), dtype=torch.uint8).numpy(),
+        torch.randint(low=0, high=255, size=(3, 128, 128), dtype=torch.uint8).numpy(),
+    ]
+    b_images = [
+        torch.randint(low=0, high=255, size=(3, 256, 256), dtype=torch.uint8).numpy(),
+        torch.randint(low=0, high=255, size=(3, 128, 128), dtype=torch.uint8).numpy(),
+        torch.randint(low=0, high=255, size=(3, 64, 64), dtype=torch.uint8).numpy(),
+    ]
+
+    images = [a_images, b_images]
+
+    data = tu.get_tensordict({"input_ids": input_ids, "images": images})
+
+    assert np.all(np.equal(data[0]["images"][0], a_images[0]))
+    assert torch.all(torch.eq(data[0]["input_ids"], a))
+
+
+def test_tensordict_with_packing():
+    vocab_size = 128
+    a = torch.randint(low=0, high=vocab_size, size=(11,))
+    b = torch.randint(low=0, high=vocab_size, size=(13,))
+    input_ids = [a, b]
+    input_ids = torch.nested.as_nested_tensor(input_ids, layout=torch.jagged)
+
+    data = tu.get_tensordict({"input_ids": input_ids})
+
+    # test cu_seqlens
+    cu_seqlens = torch.tensor([0, 11, 24])
+    assert torch.all(torch.eq(cu_seqlens, data["input_ids"].offsets()))
+
+    # test index
+    assert torch.all(torch.eq(data["input_ids"][0], a))
+    assert torch.all(torch.eq(data["input_ids"][1], b))
+
+    assert torch.all(torch.eq(data[0]["input_ids"], a))
+    assert torch.all(torch.eq(data[1]["input_ids"], b))
+
+    data_lst = data.chunk(2)
+
+    assert torch.all(torch.eq(data_lst[0]["input_ids"][0], a))
+    assert torch.all(torch.eq(data_lst[1]["input_ids"][0], b))
+
+
+def test_tensordict_eq():
+    obs = torch.tensor([1, 2, 3, 4, 5, 6])
+    data_sources = ["abc", "def", "abc", "def", "pol", "klj"]
+    non_tensor_dict = {"train_sample_kwargs": {"top_p": 1.0}, "val_sample_kwargs": {"top_p": 0.7}}
+    data = tu.get_tensordict({"obs": obs, "data_sources": data_sources}, non_tensor_dict=non_tensor_dict)
+
+    obs = torch.tensor([1, 2, 3, 4, 5, 6])
+    data_sources = ["abc", "def", "abc", "def", "pol", "klj"]
+    non_tensor_dict = {"train_sample_kwargs": {"top_p": 1.0}, "val_sample_kwargs": {"top_p": 0.7}}
+    data1 = tu.get_tensordict({"obs": obs, "data_sources": data_sources}, non_tensor_dict=non_tensor_dict)
+
+    tu.assert_tensordict_eq(data, data1)
+
+    data2 = copy.deepcopy(data1)
+    data2["obs"][0] += 1
+
+    with pytest.raises(AssertionError):
+        tu.assert_tensordict_eq(data, data2)
+
+    data2 = copy.deepcopy(data1)
+    data2["data_sources"][0] = "math"
+
+    with pytest.raises(AssertionError):
+        tu.assert_tensordict_eq(data, data2)
+
+    data2 = copy.deepcopy(data1)
+    data2["train_sample_kwargs"]["top_p"] = 0.9
+
+    with pytest.raises(AssertionError):
+        tu.assert_tensordict_eq(data, data2)
+
+    tensor_list = [
+        torch.tensor([1, 2, 3, 3, 2]),
+        torch.tensor([4, 5]),
+        torch.tensor([7, 8, 10, 14]),
+        torch.tensor([10, 11, 12]),
+        torch.tensor([13, 14, 15, 18]),
+        torch.tensor([16, 17]),
+    ]
+    obs = torch.nested.as_nested_tensor(tensor_list, layout=torch.jagged)
+    data_sources = ["abc", "def", "abc", "def", "pol", "klj"]
+    non_tensor_dict = {"train_sample_kwargs": {"top_p": 1.0}, "val_sample_kwargs": {"top_p": 0.7}}
+    data3 = tu.get_tensordict({"obs": obs, "data_sources": data_sources}, non_tensor_dict=non_tensor_dict)
+
+    tensor_list[0] = torch.tensor([1, 2, 3, 3, 2])
+    obs = torch.nested.as_nested_tensor(tensor_list, layout=torch.jagged)
+    data4 = tu.get_tensordict({"obs": obs, "data_sources": data_sources}, non_tensor_dict=non_tensor_dict)
+    tu.assert_tensordict_eq(data3, data4)
+
+    tensor_list[0] = torch.tensor([1, 2, 4])
+    obs = torch.nested.as_nested_tensor(tensor_list, layout=torch.jagged)
+    data5 = tu.get_tensordict({"obs": obs, "data_sources": data_sources}, non_tensor_dict=non_tensor_dict)
+    with pytest.raises(AssertionError):
+        tu.assert_tensordict_eq(data3, data5)
+
+    tensor_list[0] = torch.tensor([4, 5])
+    tensor_list[1] = torch.tensor([1, 2, 3, 3, 2])
+    obs = torch.nested.as_nested_tensor(tensor_list, layout=torch.jagged)
+    data6 = tu.get_tensordict({"obs": obs, "data_sources": data_sources}, non_tensor_dict=non_tensor_dict)
+    with pytest.raises(AssertionError):
+        tu.assert_tensordict_eq(data3, data6)
+
+
+def test_tensor_dict_make_iterator():
+    obs = torch.tensor([1, 2, 3, 4, 5, 6])
+    input_ids = torch.nested.as_nested_tensor(
+        [
+            torch.tensor([0, 1]),
+            torch.tensor([2]),
+            torch.tensor([3, 4]),
+            torch.tensor([5]),
+            torch.tensor([6, 7, 8]),
+            torch.tensor([9]),
+        ],
+        layout=torch.jagged,
+    )
+    data_sources = ["abc", "def", "abc", "def", "pol", "klj"]
+    non_tensor_dict = {"train_sample_kwargs": {"top_p": 1.0}, "val_sample_kwargs": {"top_p": 0.7}}
+    dataset = tu.get_tensordict(
+        {"obs": obs, "data_sources": data_sources, "input_ids": input_ids}, non_tensor_dict=non_tensor_dict
+    )
+
+    dataloader = tu.make_iterator(
+        dataset, mini_batch_size=2, epochs=2, seed=0, dataloader_kwargs={"shuffle": False, "drop_last": False}
+    )
+
+    expected_tensor_dict = [
+        tu.index_select_tensor_dict(dataset, indices=list(range(0, 2))),
+        tu.index_select_tensor_dict(dataset, indices=list(range(2, 4))),
+        tu.index_select_tensor_dict(dataset, indices=list(range(4, 6))),
+        tu.index_select_tensor_dict(dataset, indices=list(range(0, 2))),
+        tu.index_select_tensor_dict(dataset, indices=list(range(2, 4))),
+        tu.index_select_tensor_dict(dataset, indices=list(range(4, 6))),
+    ]
+
+    i = 0
+
+    for d in dataloader:
+        tu.assert_tensordict_eq(d, expected_tensor_dict[i])
+        i += 1
+
+    data_iter_1 = tu.make_iterator(dataset, mini_batch_size=3, epochs=1, seed=1, dataloader_kwargs={"shuffle": True})
+    data_list_1 = []
+    for data in data_iter_1:
+        data_list_1.append(data)
+
+    data_iter_2 = tu.make_iterator(dataset, mini_batch_size=3, epochs=1, seed=1, dataloader_kwargs={"shuffle": True})
+    data_list_2 = []
+    for data in data_iter_2:
+        data_list_2.append(data)
+
+    for data1, data2 in zip(data_list_1, data_list_2, strict=True):
+        tu.assert_tensordict_eq(data1, data2)
+
+
+def test_reorder():
+    obs = torch.tensor([1, 2, 3, 4, 5, 6])
+    labels = ["a", "b", "c", "d", "e", "f"]
+    non_tensor_dict = {"name": "abdce"}
+
+    data = tu.get_tensordict(tensor_dict={"obs": obs, "labels": labels}, non_tensor_dict=non_tensor_dict)
+    data = data[torch.tensor([3, 4, 2, 0, 1, 5])]
+
+    assert torch.all(torch.eq(data["obs"], torch.tensor([4, 5, 3, 1, 2, 6])))
+    assert np.all(data["labels"] == np.array(["d", "e", "c", "a", "b", "f"]))
+    assert data["name"] == "abdce"
+
+
+def test_chunk_concat():
+    obs = torch.tensor([1, 2, 3, 4, 5, 6])
+    labels = ["a", "b", "c", "d", "e", "f"]
+    data = tu.get_tensordict({"obs": obs, "labels": labels}, non_tensor_dict={"name": "abcde"})
+
+    data_split = data.tensor_split(indices_or_sections=5, dim=0)
+
+    expected_idx_lst = [[0, 1], [2], [3], [4], [5]]
+
+    for d, expected_idx in zip(data_split, expected_idx_lst, strict=False):
+        tu.assert_tensordict_eq(d, data[expected_idx])
+
+    data_split = data.chunk(2)
+    assert len(data_split) == 2
+    assert torch.all(torch.eq(data_split[0]["obs"], torch.tensor([1, 2, 3])))
+    assert np.all(data_split[0]["labels"] == np.array(["a", "b", "c"]))
+    assert data_split[0]["name"] == "abcde"
+
+    assert torch.all(torch.eq(data_split[1]["obs"], torch.tensor([4, 5, 6])))
+    assert np.all(data_split[1]["labels"] == np.array(["d", "e", "f"]))
+    assert data_split[1]["name"] == "abcde"
+
+    concat_data = torch.cat(data_split, dim=0)
+    assert torch.all(torch.eq(concat_data["obs"], data["obs"]))
+    assert np.all(concat_data["labels"] == data["labels"])
+    assert concat_data["name"] == data["name"]
+
+    data1 = tu.get_tensordict(tensor_dict={"obs": obs, "labels": labels}, non_tensor_dict={"name": "abcde"})
+    data2 = tu.get_tensordict(tensor_dict={"obs": obs, "labels": labels}, non_tensor_dict={"name": "def"})
+    data3 = tu.get_tensordict(tensor_dict={"obs": obs, "labels": labels}, non_tensor_dict={"name": "cfg"})
+
+    output = torch.cat([data1, data2, data3], dim=0)
+
+    # concat NonTensorData will keep the first one.
+    assert output["name"] == "abcde"
+
+
+def test_pop():
+    obs = torch.randn(3, 10)
+    act = torch.randn(3, 3)
+    labels = ["a", ["b"], []]
+    dataset = tu.get_tensordict({"obs": obs, "act": act, "labels": labels}, non_tensor_dict={"2": 2, "1": 1})
+
+    dataset1 = copy.deepcopy(dataset)
+
+    # test pop keys
+    popped_dataset = tu.pop_keys(dataset, keys=["obs", "2"])
+
+    assert popped_dataset.batch_size[0] == 3
+
+    assert popped_dataset.keys() == {"obs", "2"}
+    assert torch.all(torch.eq(popped_dataset["obs"], obs)).item()
+    assert popped_dataset["2"] == 2
+
+    assert dataset.keys() == {"act", "1", "labels"}
+
+    # test pop non-exist key
+    with pytest.raises(KeyError):
+        tu.pop_keys(dataset, keys=["obs", "2"])
+
+    # test single pop
+    # NonTensorData
+    assert tu.pop(dataset1, key="2") == 2
+    # NonTensorStack
+    assert tu.pop(dataset1, key="labels") == ["a", ["b"], []]
+    # Tensor
+    assert torch.all(torch.eq(tu.pop(dataset1, key="obs"), obs)).item()
+
+
+def test_get():
+    obs = torch.randn(3, 10)
+    act = torch.randn(3, 3)
+    labels = ["a", ["b"], []]
+    dataset = tu.get_tensordict({"obs": obs, "act": act, "labels": labels}, non_tensor_dict={"2": 2, "1": 1})
+
+    # test pop keys
+    popped_dataset = tu.get_keys(dataset, keys=["obs", "2"])
+
+    assert popped_dataset.batch_size[0] == 3
+
+    assert torch.all(torch.eq(popped_dataset["obs"], dataset["obs"])).item()
+
+    assert popped_dataset["2"] == dataset["2"]
+
+    # test pop non-exist key
+    with pytest.raises(KeyError):
+        tu.get_keys(dataset, keys=["obs", "3"])
+
+    # test single pop
+    # NonTensorData
+    assert tu.get(dataset, key="2") == 2
+    # NonTensorStack
+    assert tu.get(dataset, key="labels") == ["a", ["b"], []]
+    # Tensor
+    assert torch.all(torch.eq(tu.get(dataset, key="obs"), obs)).item()
+    # Non-exist key
+    assert tu.get(dataset, key="3", default=3) == 3
+
+
+def test_repeat():
+    # Create a DataProto object with some batch and non-tensor data
+    obs = torch.tensor([[1, 2], [3, 4], [5, 6]])
+    labels = ["a", "b", "c"]
+    data = tu.get_tensordict({"obs": obs, "labels": labels}, non_tensor_dict={"info": "test_info"})
+
+    # Test interleave=True
+    repeated_data_interleave = data.repeat_interleave(repeats=2)
+    expected_obs_interleave = torch.tensor([[1, 2], [1, 2], [3, 4], [3, 4], [5, 6], [5, 6]])
+    expected_labels_interleave = ["a", "a", "b", "b", "c", "c"]
+
+    assert torch.all(torch.eq(repeated_data_interleave["obs"], expected_obs_interleave))
+    assert repeated_data_interleave["labels"] == expected_labels_interleave
+    assert repeated_data_interleave["info"] == "test_info"
+
+    # Test interleave=False
+    repeated_data_no_interleave = data.repeat(2)
+    expected_obs_no_interleave = torch.tensor([[1, 2], [3, 4], [5, 6], [1, 2], [3, 4], [5, 6]])
+    expected_labels_no_interleave = ["a", "b", "c", "a", "b", "c"]
+
+    assert torch.all(torch.eq(repeated_data_no_interleave["obs"], expected_obs_no_interleave))
+    assert repeated_data_no_interleave["labels"] == expected_labels_no_interleave
+    assert repeated_data_no_interleave["info"] == "test_info"
+
+
+def test_dataproto_pad_unpad():
+    obs = torch.tensor([[1, 2], [3, 4], [5, 6]])
+    labels = ["a", "b", "c"]
+    data = tu.get_tensordict(tensor_dict={"obs": obs, "labels": labels}, non_tensor_dict={"info": "test_info"})
+
+    padded_data, pad_size = tu.pad_to_divisor(data, size_divisor=2)
+
+    assert pad_size == 1
+
+    expected_obs = torch.tensor([[1, 2], [3, 4], [5, 6], [1, 2]])
+    expected_labels = ["a", "b", "c", "a"]
+
+    assert torch.all(torch.eq(padded_data["obs"], expected_obs))
+    assert padded_data["labels"] == expected_labels
+    assert padded_data["info"] == "test_info"
+
+    unpadd_data = tu.unpad(padded_data, pad_size=pad_size)
+    assert torch.all(torch.eq(unpadd_data["obs"], obs))
+    assert unpadd_data["labels"] == labels
+    assert unpadd_data["info"] == "test_info"
+
+    padded_data, pad_size = tu.pad_to_divisor(data, size_divisor=3)
+    assert pad_size == 0
+
+    expected_obs = torch.tensor([[1, 2], [3, 4], [5, 6]])
+    expected_labels = ["a", "b", "c"]
+
+    assert torch.all(torch.eq(padded_data["obs"], expected_obs))
+    assert padded_data["labels"] == expected_labels
+    assert padded_data["info"] == "test_info"
+
+    unpadd_data = tu.unpad(padded_data, pad_size=pad_size)
+    assert torch.all(torch.eq(unpadd_data["obs"], obs))
+    assert unpadd_data["labels"] == labels
+    assert unpadd_data["info"] == "test_info"
+
+    padded_data, pad_size = tu.pad_to_divisor(data, size_divisor=7)
+    assert pad_size == 4
+
+    expected_obs = torch.tensor([[1, 2], [3, 4], [5, 6], [1, 2], [3, 4], [5, 6], [1, 2]])
+    expected_labels = ["a", "b", "c", "a", "b", "c", "a"]
+    assert torch.all(torch.eq(padded_data["obs"], expected_obs))
+    assert padded_data["labels"] == expected_labels
+    assert padded_data["info"] == "test_info"
+
+    unpadd_data = tu.unpad(padded_data, pad_size=pad_size)
+    assert torch.all(torch.eq(unpadd_data["obs"], obs))
+    assert unpadd_data["labels"] == labels
+    assert unpadd_data["info"] == "test_info"
+
+
+def test_torch_save_data_proto():
+    obs = torch.tensor([[1, 2], [3, 4], [5, 6]])
+    labels = ["a", "b", "c"]
+    data = tu.get_tensordict({"obs": obs, "labels": labels}, non_tensor_dict={"info": "test_info"})
+
+    filename = "test_data.pt"
+    torch.save(data, filename)
+    loaded_data = torch.load(filename, weights_only=False)
+
+    assert torch.all(torch.eq(loaded_data["obs"], data["obs"]))
+    assert loaded_data["labels"] == data["labels"]
+    assert loaded_data["info"] == data["info"]
+
+    import os
+
+    os.remove(filename)
+
+
+def test_len():
+    obs = torch.tensor([[1, 2], [3, 4], [5, 6]])
+    labels = np.array(["a", "b", "c"], dtype=object)
+
+    data = tu.get_tensordict({"obs": obs, "labels": labels.tolist()}, non_tensor_dict={"info": "test_info"})
+    assert len(data) == 3
+
+    data = tu.get_tensordict({"labels": labels.tolist()}, non_tensor_dict={"info": "test_info"})
+    assert len(data) == 3
+
+    data_item = data[0]
+    assert len(data_item) == 0
+
+    data = tu.get_tensordict({}, non_tensor_dict={"info": "test_info"})
+    assert len(data) == 0
+
+
+def test_dataproto_index():
+    data_len = 100
+    idx_num = 10
+
+    obs = torch.randn(data_len, 10)
+    labels = [random.choice(["abc", "cde"]) for _ in range(data_len)]
+
+    data = tu.get_tensordict({"obs": obs, "labels": labels})
+
+    labels_np = np.array(labels)
+
+    idx_np_int = np.random.randint(0, data_len, size=(idx_num,))
+    result_np_int = data[idx_np_int]
+    assert result_np_int.keys() == data.keys()
+    assert result_np_int["obs"].shape[0] == idx_num
+    assert len(result_np_int["labels"]) == idx_num
+    assert np.array_equal(result_np_int["obs"].cpu().numpy(), obs[idx_np_int].numpy())
+    assert np.array_equal(result_np_int["labels"], labels_np[idx_np_int])
+
+    idx_torch_int = torch.randint(0, data_len, size=(idx_num,))
+    result_torch_int = data[idx_torch_int]
+    assert result_torch_int.keys() == data.keys()
+    assert result_torch_int["obs"].shape[0] == idx_num
+    assert len(result_torch_int["labels"]) == idx_num
+    assert np.array_equal(result_torch_int["obs"].cpu().numpy(), obs[idx_torch_int].cpu().numpy())
+    assert np.array_equal(result_torch_int["labels"], labels_np[idx_torch_int.cpu().numpy()])
+
+    idx_list_int = [np.random.randint(0, data_len) for _ in range(idx_num)]
+    result_list_int = data[idx_list_int]
+    assert result_list_int.keys() == data.keys()
+    assert result_list_int["obs"].shape[0] == idx_num
+    assert len(result_list_int["labels"]) == idx_num
+    assert np.array_equal(result_list_int["obs"].cpu().numpy(), obs[idx_list_int].cpu().numpy())
+    assert np.array_equal(result_list_int["labels"], labels_np[idx_list_int])
+
+    # idx_np_bool = np.random.randint(0, 2, size=(data_len,), dtype=bool)
+    # result_np_bool = data[idx_np_bool]
+    # assert result_np_bool.keys() == data.keys()
+    # assert result_np_bool["obs"].shape[0] == idx_np_bool.sum()
+    # assert len(result_np_bool["labels"]) == idx_np_bool.sum()
+    # assert np.array_equal(result_np_bool["obs"].cpu().numpy(), obs[idx_np_bool].cpu().numpy())
+    # assert np.array_equal(result_np_bool["labels"], labels_np[idx_np_bool])
+
+    idx_torch_bool = torch.randint(0, 2, size=(data_len,), dtype=torch.bool)
+    result_torch_bool = data[idx_torch_bool]
+    assert result_torch_bool.keys() == data.keys()
+    assert result_torch_bool["obs"].shape[0] == idx_torch_bool.sum().item()
+    assert len(result_torch_bool["labels"]) == idx_torch_bool.sum().item()
+    assert np.array_equal(result_torch_bool["obs"].cpu().numpy(), obs[idx_torch_bool].cpu().numpy())
+    assert np.array_equal(result_torch_bool["labels"], labels_np[idx_torch_bool])
+
+    # idx_list_bool = [np.random.randint(0, 2, dtype=bool) for _ in range(data_len)]
+    # result_list_bool = data[idx_list_bool]
+    # assert result_list_bool.keys() == data.keys()
+    # assert result_list_bool["obs"].shape[0] == sum(idx_list_bool)
+    # assert len(result_list_bool["labels"]) == sum(idx_list_bool)
+    # assert np.array_equal(result_list_bool["obs"].cpu().numpy(), obs[idx_list_bool].cpu().numpy())
+    # assert np.array_equal(result_list_bool["labels"], labels_np[idx_list_bool])
+
+
+def test_select():
+    obs = torch.randn(100, 10)
+    act = torch.randn(100, 3)
+    dataset = tu.get_tensordict({"obs": obs, "act": act}, non_tensor_dict={"2": 2, "1": 1})
+
+    subset = dataset.select("obs", "2")
+
+    assert torch.all(torch.eq(subset["obs"], dataset["obs"]))
+    assert subset["2"] == dataset["2"]
+    assert "act" not in subset.keys()
+    assert "1" not in subset.keys()
+
+
+def test_dataproto_no_batch():
+    labels = ["a", "b", "c"]
+    data = tu.get_tensordict(tensor_dict={"labels": labels}, non_tensor_dict={"info": "test_info"})
+    selected = data.select("labels")
+
+    assert selected["labels"] == labels
+    pop_data = tu.pop_keys(data, keys=["labels"])
+    assert pop_data["labels"] == labels
+    assert "labels" not in data
+
+
+def test_sample_level_repeat():
+    # Create a DataProto object with some batch and non-tensor data
+    obs = torch.tensor([[1, 2], [3, 4], [5, 6]])
+    labels = ["a", "b", "c"]
+
+    data = tu.get_tensordict({"obs": obs, "labels": labels}, non_tensor_dict={"info": "test_info"})
+
+    # list
+    repeated_data_interleave = data.repeat_interleave(repeats=torch.tensor([3, 1, 2]))
+    expected_obs_interleave = torch.tensor([[1, 2], [1, 2], [1, 2], [3, 4], [5, 6], [5, 6]])
+    expected_labels_interleave = ["a", "a", "a", "b", "c", "c"]
+
+    assert torch.all(torch.eq(repeated_data_interleave["obs"], expected_obs_interleave))
+    assert repeated_data_interleave["labels"] == expected_labels_interleave
+    assert repeated_data_interleave["info"] == "test_info"
+
+    # torch.tensor
+    repeated_data_no_interleave = data.repeat_interleave(repeats=torch.tensor([1, 2, 3]))
+    expected_obs_no_interleave = torch.tensor([[1, 2], [3, 4], [3, 4], [5, 6], [5, 6], [5, 6]])
+    expected_labels_no_interleave = ["a", "b", "b", "c", "c", "c"]
+
+    assert torch.all(torch.eq(repeated_data_no_interleave["obs"], expected_obs_no_interleave))
+    assert repeated_data_no_interleave["labels"] == expected_labels_no_interleave
+    assert repeated_data_no_interleave["info"] == "test_info"
+
+
+def test_dataproto_chunk_after_index():
+    data_len = 4
+    obs = torch.randn(data_len, 4)
+    labels = [f"label_{i}" for i in range(data_len)]
+
+    data = tu.get_tensordict(tensor_dict={"obs": obs, "labels": labels}, non_tensor_dict={"name": "abc"})
+    # Test with boolean numpy array
+    bool_mask = torch.tensor([True, False, True, False])
+    selected = data[bool_mask]
+    assert isinstance(selected.batch_size, torch.Size)
+    assert all(isinstance(d, int) for d in selected.batch_size)  # int or List[int]
+
+    # Test with integer numpy array
+    int_mask = torch.tensor([0, 2])
+    selected = data[int_mask]
+    assert isinstance(selected.batch_size, torch.Size)
+    assert all(isinstance(d, int) for d in selected.batch_size)
+
+    # Test with boolean list
+    list_mask = [True, False, True, False]
+    selected = data[list_mask]
+    assert isinstance(selected.batch_size, torch.Size)
+    assert all(isinstance(d, int) for d in selected.batch_size)
+
+    # Test with list
+    list_mask = [0, 2]
+    selected = data[list_mask]
+    assert isinstance(selected.batch_size, torch.Size)
+    assert all(isinstance(d, int) for d in selected.batch_size)
+
+    # Test with torch tensor (bool)
+    torch_bool_mask = torch.tensor([True, False, True, False])
+    selected = data[torch_bool_mask]
+    assert isinstance(selected.batch_size, torch.Size)
+    assert all(isinstance(d, int) for d in selected.batch_size)
+
+    # Test with torch tensor (int)
+    torch_int_mask = torch.tensor([0, 2])
+    selected = data[torch_int_mask]
+    assert isinstance(selected.batch_size, torch.Size)
+    assert all(isinstance(d, int) for d in selected.batch_size)
+
+
+def test_concat_nested_tensor():
+    # Test 2D nested tensors
+    vocab_size = 128
+    a = torch.randint(low=0, high=vocab_size, size=(11,))
+    b = torch.randint(low=0, high=vocab_size, size=(13,))
+    c = torch.randint(low=0, high=vocab_size, size=(12,))
+    d = torch.randint(low=0, high=vocab_size, size=(15,))
+
+    nested_a_b = torch.nested.as_nested_tensor([a, b], layout=torch.jagged)
+    nested_c_d = torch.nested.as_nested_tensor([c, d], layout=torch.jagged)
+
+    output = tu.concat_nested_tensors([nested_a_b, nested_c_d])
+
+    output_values = output.values()
+    expected = torch.cat([a, b, c, d], dim=0)
+
+    assert torch.all(torch.eq(output_values, expected)).item()
+
+    # Test 3D nested tensors
+    a_3d = torch.randint(low=0, high=vocab_size, size=(4, 4))
+    b_3d = torch.randint(low=0, high=vocab_size, size=(4, 5))
+    c_3d = torch.randint(low=0, high=vocab_size, size=(4, 6))
+    d_3d = torch.randint(low=0, high=vocab_size, size=(4, 7))
+
+    nested_a_b_3d = torch.nested.as_nested_tensor([a_3d, b_3d], layout=torch.jagged)
+    nested_c_d_3d = torch.nested.as_nested_tensor([c_3d, d_3d], layout=torch.jagged)
+
+    output_3d = tu.concat_nested_tensors([nested_a_b_3d, nested_c_d_3d])
+
+    assert output_3d.shape[0] == 4
+    output_3d_unbind = output_3d.unbind(0)
+    assert torch.all(torch.eq(output_3d_unbind[0], a_3d)).item()
+    assert torch.all(torch.eq(output_3d_unbind[1], b_3d)).item()
+    assert torch.all(torch.eq(output_3d_unbind[2], c_3d)).item()
+    assert torch.all(torch.eq(output_3d_unbind[3], d_3d)).item()
+
+    # Test 4D nested tensors
+    a_4d = torch.randint(low=0, high=vocab_size, size=(2, 3, 4))
+    b_4d = torch.randint(low=0, high=vocab_size, size=(2, 3, 5))
+    c_4d = torch.randint(low=0, high=vocab_size, size=(2, 3, 3))
+    d_4d = torch.randint(low=0, high=vocab_size, size=(2, 3, 6))
+
+    nested_a_b_4d = torch.nested.as_nested_tensor([a_4d, b_4d], layout=torch.jagged)
+    nested_c_d_4d = torch.nested.as_nested_tensor([c_4d, d_4d], layout=torch.jagged)
+
+    output_4d = tu.concat_nested_tensors([nested_a_b_4d, nested_c_d_4d])
+
+    assert output_4d.shape[0] == 4
+    output_4d_unbind = output_4d.unbind(0)
+    assert torch.all(torch.eq(output_4d_unbind[0], a_4d)).item()
+    assert torch.all(torch.eq(output_4d_unbind[1], b_4d)).item()
+    assert torch.all(torch.eq(output_4d_unbind[2], c_4d)).item()
+    assert torch.all(torch.eq(output_4d_unbind[3], d_4d)).item()
+
+
+def test_concat_tensordict():
+    vocab_size = 128
+    a = torch.randint(low=0, high=vocab_size, size=(11,))
+    b = torch.randint(low=0, high=vocab_size, size=(13,))
+    c = torch.randint(low=0, high=vocab_size, size=(12,))
+    d = torch.randint(low=0, high=vocab_size, size=(15,))
+
+    nested_a_b = torch.nested.as_nested_tensor([a, b], layout=torch.jagged)
+    nested_c_d = torch.nested.as_nested_tensor([c, d], layout=torch.jagged)
+
+    tensordict1 = tu.get_tensordict(
+        tensor_dict={"input_ids": nested_a_b, "labels": ["a", "b"]}, non_tensor_dict={"temp": 1.0}
+    )
+    tensordict2 = tu.get_tensordict(
+        tensor_dict={"input_ids": nested_c_d, "labels": ["c", "d"]}, non_tensor_dict={"temp": 2.0}
+    )
+
+    tensordict1_copy = copy.deepcopy(tensordict1)
+    tensordict2_copy = copy.deepcopy(tensordict2)
+
+    output = tu.concat_tensordict([tensordict1, tensordict2])
+
+    assert torch.all(torch.eq(output["input_ids"].values(), torch.cat([a, b, c, d]))).item()
+    assert output["labels"] == ["a", "b", "c", "d"]
+    assert output["temp"] == 1.0
+
+    # make sure tensordict1 and tensordict2 is untouched
+    tu.assert_tensordict_eq(tensordict1, tensordict1_copy)
+    tu.assert_tensordict_eq(tensordict2, tensordict2_copy)
+
+    # test concat tensordict with only NonTensorStack and NonTensorData
+    tensordict1 = tu.get_tensordict(tensor_dict={"labels": ["a", "b"]}, non_tensor_dict={"temp": 1.0})
+    tensordict2 = tu.get_tensordict(tensor_dict={"labels": ["c", "d"]}, non_tensor_dict={"temp": 2.0})
+
+    output = tu.concat_tensordict([tensordict1, tensordict2])
+
+    assert output["labels"] == ["a", "b", "c", "d"]
+    assert output["temp"] == 1.0
+
+    assert output.batch_size[0] == 4
+
+    # test concat tensordict with only NonTensorData
+    tensordict1 = tu.get_tensordict(tensor_dict={}, non_tensor_dict={"temp": 1.0})
+    tensordict2 = tu.get_tensordict(tensor_dict={}, non_tensor_dict={"temp": 2.0})
+
+    output = tu.concat_tensordict([tensordict1, tensordict2])
+    assert len(output.batch_size) == 0
+    assert output["temp"] == 1.0
+
+
+def test_chunk_tensordict():
+    # Qwen-VL 3d position_ids
+    position_ids = torch.nested.as_nested_tensor(
+        [
+            torch.arange(4).expand(4, 4),
+            torch.arange(5).expand(4, 5),
+            torch.arange(6).expand(4, 6),
+            torch.arange(7).expand(4, 7),
+        ],
+        layout=torch.jagged,
+    )
+    input_ids = torch.nested.as_nested_tensor(
+        [torch.arange(4), torch.arange(5), torch.arange(6), torch.arange(7)], layout=torch.jagged
+    )
+    attention_mask = torch.nested.as_nested_tensor(
+        [
+            torch.randint(low=0, high=2, size=[3, 4]),
+            torch.randint(low=0, high=2, size=[3, 5]),
+            torch.randint(low=0, high=2, size=[3, 6]),
+            torch.randint(low=0, high=2, size=[3, 7]),
+        ],
+        layout=torch.jagged,
+    )
+
+    multi_modal_inputs = torch.stack(
+        [
+            NonTensorData({"pixel_values": torch.randn(3, 224, 224)}),
+            NonTensorData(None),
+            NonTensorData({"pixel_values": torch.randn(3, 128, 128)}),
+            NonTensorData({"pixel_values": torch.randn(3, 128, 128)}),
+        ]
+    )
+    td = tu.get_tensordict(
+        {
+            "input_ids": input_ids,
+            "position_ids": position_ids,
+            "attention_mask": attention_mask,
+            "multi_modal_inputs": multi_modal_inputs,
+        },
+    )
+    assert len(td) == 4
+    chunks = tu.chunk_tensordict(td, chunks=2)
+
+    for i, chunk in enumerate(chunks):
+        assert len(chunk) == 2
+        for key, val in chunk.items():
+            if isinstance(val, torch.Tensor) and val.is_nested:
+                tensors = td[key].unbind(dim=0)
+                expected = torch.nested.as_nested_tensor(tensors[i * 2 : (i + 1) * 2], layout=torch.jagged)
+                assert torch.all(torch.eq(val.values(), expected.values())).item()
+            else:
+                expected = td[key][i * 2 : (i + 1) * 2]
+                for tensor, expect in zip(val, expected, strict=False):
+                    if tensor.data is None:
+                        assert expect is None
+                    else:
+                        assert torch.all(torch.eq(tensor.data["pixel_values"], expect["pixel_values"])).item()
+
+
+def test_assign_non_tensor_stack_with_nested_lists():
+    """Test assign_non_tensor_stack with lists of lists."""
+    td = tu.get_tensordict({"obs": torch.randn(3, 4)}, non_tensor_dict={})
+
+    # Lists of varying lengths (like turn_scores or tool_rewards)
+    turn_scores = [[], [0.5, 0.8], [0.9]]
+    tu.assign_non_tensor_stack(td, "turn_scores", turn_scores)
+
+    # Verify data is accessible
+    assert len(td["turn_scores"]) == 3
+    assert list(td["turn_scores"][0]) == []
+    assert list(td["turn_scores"][1]) == [0.5, 0.8]
+    assert list(td["turn_scores"][2]) == [0.9]
+
+
+def test_assign_non_tensor_stack_with_nested_dicts():
+    """Test assign_non_tensor_stack with lists of dicts."""
+    td = tu.get_tensordict({"obs": torch.randn(3, 4)}, non_tensor_dict={})
+
+    # Lists of dicts (like reward_extra_info)
+    reward_extra_info = [{"acc": 1.0, "loss": 0.1}, {"acc": 0.0, "loss": 0.9}, {"acc": 1.0, "loss": 0.05}]
+    tu.assign_non_tensor_stack(td, "reward_extra_info", reward_extra_info)
+
+    # Verify data is accessible
+    assert len(td["reward_extra_info"]) == 3
+    assert dict(td["reward_extra_info"][0]) == {"acc": 1.0, "loss": 0.1}
+    assert dict(td["reward_extra_info"][1]) == {"acc": 0.0, "loss": 0.9}
+    assert dict(td["reward_extra_info"][2]) == {"acc": 1.0, "loss": 0.05}
+
+
+def test_assign_non_tensor_stack_with_complex_nested():
+    """Test assign_non_tensor_stack with lists of lists of dicts."""
+    td = tu.get_tensordict({"obs": torch.randn(2, 4)}, non_tensor_dict={})
+
+    # Lists of lists of dicts (like raw_prompt)
+    raw_prompt = [
+        [{"content": "Question 1", "role": "user"}],
+        [{"content": "Question 2", "role": "user"}, {"content": "Answer 2", "role": "assistant"}],
+    ]
+    tu.assign_non_tensor_stack(td, "raw_prompt", raw_prompt)
+
+    # Verify data is accessible
+    assert len(td["raw_prompt"]) == 2
+    assert len(td["raw_prompt"][0]) == 1
+    assert dict(td["raw_prompt"][0][0]) == {"content": "Question 1", "role": "user"}
+    assert len(td["raw_prompt"][1]) == 2
+    assert dict(td["raw_prompt"][1][0]) == {"content": "Question 2", "role": "user"}
+
+
+def test_assign_non_tensor_handles_wrappers():
+    td = tu.get_tensordict({"obs": torch.randn(3, 4)}, non_tensor_dict={})
+
+    meta = {"top_p": 0.8}
+    tu.assign_non_tensor(td, **meta)
+    assert td["top_p"] == 0.8
+
+    wrapped = NonTensorData(0.3)
+    stack = NonTensorStack.from_list([NonTensorData(1.0), NonTensorData(2.0), NonTensorData(3.0)])
+    tu.assign_non_tensor(td, wrapped=wrapped, stack=stack)
+
+    assert td["wrapped"] == 0.3
+    assert td["stack"] == [1.0, 2.0, 3.0]
+
+
+def test_assign_non_tensor_stack_batch_size_check():
+    td = tu.get_tensordict({"obs": torch.randn(3, 4)}, non_tensor_dict={})
+    stack = NonTensorStack.from_list([NonTensorData(1.0), NonTensorData(2.0)])
+
+    with pytest.raises(RuntimeError):
+        tu.assign_non_tensor(td, stack=stack)
+
+
+def test_assign_non_tensor_with_auto_detection():
+    """Test assign_non_tensor automatically detects and handles nested structures."""
+    td = tu.get_tensordict({"obs": torch.randn(3, 4)}, non_tensor_dict={})
+
+    # Mix of simple and nested data
+    tu.assign_non_tensor(
+        td,
+        metadata="experiment_1",  # Simple value
+        turn_scores=[[], [0.5, 0.8], [0.9]],  # Nested list
+        reward_extra_info=[{"acc": 1.0}, {"acc": 0.0}, {"acc": 1.0}],  # List of dicts
+        simple_list=["a", "b", "c"],  # Simple list (also uses NonTensorStack for consistency)
+    )
+
+    # Verify all data is accessible
+    assert td["metadata"] == "experiment_1"
+    assert len(td["turn_scores"]) == 3
+    assert list(td["turn_scores"][1]) == [0.5, 0.8]
+    assert len(td["reward_extra_info"]) == 3
+    assert dict(td["reward_extra_info"][0]) == {"acc": 1.0}
+    assert len(td["simple_list"]) == 3
+    assert td["simple_list"][0] == "a"
+
+
+def test_get_tensordict_with_nested_lists():
+    """Test get_tensordict automatically handles nested lists."""
+    obs = torch.randn(3, 4)
+    turn_scores = [[], [0.5, 0.8], [0.9]]
+
+    # This should automatically convert turn_scores to NonTensorStack
+    td = tu.get_tensordict({"obs": obs, "turn_scores": turn_scores})
+
+    # Verify tensors and nested data are both accessible
+    assert torch.all(torch.eq(td["obs"], obs))
+    assert len(td["turn_scores"]) == 3
+    assert list(td["turn_scores"][0]) == []
+    assert list(td["turn_scores"][1]) == [0.5, 0.8]
+
+
+def test_get_tensordict_with_nested_dicts():
+    """Test get_tensordict automatically handles lists of dicts."""
+    obs = torch.randn(3, 4)
+    reward_extra_info = [{"acc": 1.0}, {"acc": 0.0}, {"acc": 1.0}]
+
+    td = tu.get_tensordict({"obs": obs, "reward_extra_info": reward_extra_info})
+
+    assert torch.all(torch.eq(td["obs"], obs))
+    assert len(td["reward_extra_info"]) == 3
+    assert dict(td["reward_extra_info"][0]) == {"acc": 1.0}
+
+
+def test_get_tensordict_with_complex_nested_structures():
+    """Test get_tensordict with lists of lists of dicts."""
+    obs = torch.randn(2, 4)
+    raw_prompt = [
+        [{"content": "Q1", "role": "user"}],
+        [{"content": "Q2", "role": "user"}, {"content": "A2", "role": "assistant"}],
+    ]
+
+    td = tu.get_tensordict({"obs": obs, "raw_prompt": raw_prompt})
+
+    assert torch.all(torch.eq(td["obs"], obs))
+    assert len(td["raw_prompt"]) == 2
+    assert dict(td["raw_prompt"][0][0]) == {"content": "Q1", "role": "user"}
+
+
+def test_get_tensordict_agent_loop_scenario():
+    """Test the complete agent loop scenario with all nested types.
+
+    This simulates the exact use case from agent loops with:
+    - turn_scores: lists of lists
+    - reward_extra_info: lists of dicts
+    - raw_prompt: lists of lists of dicts
+    - tool_rewards: lists of lists
+    """
+    prompts = torch.randn(2, 10)
+    responses = torch.randn(2, 5)
+
+    # Nested structures from agent loop
+    data_source = ["lighteval/MATH", "lighteval/MATH"]
+    uid = ["uuid-1", "uuid-2"]
+    turn_scores = [[], [0.5, 0.8]]  # Lists of varying lengths
+    reward_extra_info = [{"acc": 1.0, "loss": 0.1}, {"acc": 0.0, "loss": 0.9}]
+    raw_prompt = [
+        [{"content": "Compute 4 @ 2", "role": "user"}],
+        [{"content": "Compute 8 @ 7", "role": "user"}],
+    ]
+    tool_rewards = [[0.0], []]  # List of lists
+
+    # This should handle all nested structures automatically
+    td = tu.get_tensordict(
+        tensor_dict={
+            "prompts": prompts,
+            "responses": responses,
+            "data_source": data_source,
+            "uid": uid,
+            "turn_scores": turn_scores,
+            "reward_extra_info": reward_extra_info,
+            "raw_prompt": raw_prompt,
+            "tool_rewards": tool_rewards,
+        },
+        non_tensor_dict={"global_steps": 42},
+    )
+
+    # Verify all data types are accessible
+    assert torch.all(torch.eq(td["prompts"], prompts))
+    assert torch.all(torch.eq(td["responses"], responses))
+    assert td["data_source"] == data_source
+    assert td["uid"] == uid
+
+    # Verify nested structures
+    assert len(td["turn_scores"]) == 2
+    assert list(td["turn_scores"][0]) == []
+    assert list(td["turn_scores"][1]) == [0.5, 0.8]
+
+    assert len(td["reward_extra_info"]) == 2
+    assert dict(td["reward_extra_info"][0]) == {"acc": 1.0, "loss": 0.1}
+
+    assert len(td["raw_prompt"]) == 2
+    assert dict(td["raw_prompt"][0][0]) == {"content": "Compute 4 @ 2", "role": "user"}
+
+    assert len(td["tool_rewards"]) == 2
+    assert list(td["tool_rewards"][0]) == [0.0]
+    assert list(td["tool_rewards"][1]) == []
+
+    # Verify metadata
+    assert td["global_steps"] == 42
+
+
+def test_contiguous():
+    # create a tensordict that contains normal tensor, nested tensor,
+    # nontensorstack with numpy, nontensorstack with tensor, NonTensorData with numpy and NonTensorData with tensor
+
+    a = torch.randn(3, 4)  # contiguous tensor
+    b = torch.randn(3, 4)[:, :-1]  # non contiguous tensor
+    c = torch.nested.as_nested_tensor([torch.randn(3), torch.randn(4), torch.randn(5)], layout=torch.jagged)
+
+    d = torch.randn(10, 12)
+    e = torch.randn(11, 12)
+    f = torch.randn(13, 12)
+
+    data = tu.get_tensordict(
+        tensor_dict={"a": a, "b": b, "c": c, "nt": [{"pixel": d}, {"pixel": e}, {"pixel": f}]},
+        non_tensor_dict={"ntd": a.clone()},
+    )
+
+    with pytest.raises(RuntimeError):
+        # b is not contiguous
+        data.consolidate()
+
+    data1 = copy.deepcopy(data)
+    data_cont = tu.contiguous(data1)
+
+    tu.assert_tensordict_eq(data_cont, data)
+
+    data_cont.consolidate()
+
+    tu.assert_tensordict_eq(data_cont, data)
diff --git a/code/RL_model/verl/verl_train/tests/utils/_test_module.py b/code/RL_model/verl/verl_train/tests/utils/_test_module.py
new file mode 100644
index 0000000000000000000000000000000000000000..5e10e65cff07378514d72920e63a77da28509537
--- /dev/null
+++ b/code/RL_model/verl/verl_train/tests/utils/_test_module.py
@@ -0,0 +1,31 @@
+# Copyright 2025 Bytedance Ltd. and/or its affiliates
+#
+# Licensed under the Apache License, Version 2.0 (the "License");
+# you may not use this file except in compliance with the License.
+# You may obtain a copy of the License at
+#
+#     http://www.apache.org/licenses/LICENSE-2.0
+#
+# Unless required by applicable law or agreed to in writing, software
+# distributed under the License is distributed on an "AS IS" BASIS,
+# WITHOUT WARRANTIES OR CONDITIONS OF ANY KIND, either express or implied.
+# See the License for the specific language governing permissions and
+# limitations under the License.
+
+
+# Test module for import_utils.load_extern_object testing
+class TestClass:
+    """A test class to be imported by load_extern_object"""
+
+    def __init__(self, value=None):
+        self.value = value or "default"
+
+    def get_value(self):
+        return self.value
+
+
+TEST_CONSTANT = "test_constant_value"
+
+
+def test_function():
+    return "test_function_result"
diff --git a/code/RL_model/verl/verl_train/tests/workers/test_fsdp_attn_implementation.py b/code/RL_model/verl/verl_train/tests/workers/test_fsdp_attn_implementation.py
new file mode 100644
index 0000000000000000000000000000000000000000..230f6647305d8181bc9a669c336968c34f8806a1
--- /dev/null
+++ b/code/RL_model/verl/verl_train/tests/workers/test_fsdp_attn_implementation.py
@@ -0,0 +1,506 @@
+# Copyright 2024 Bytedance Ltd. and/or its affiliates
+#
+# Licensed under the Apache License, Version 2.0 (the "License");
+# you may not use this file except in compliance with the License.
+# You may obtain a copy of the License at
+#
+#     http://www.apache.org/licenses/LICENSE-2.0
+#
+# Unless required by applicable law or agreed to in writing, software
+# distributed under the License is distributed on an "AS IS" BASIS,
+# WITHOUT WARRANTIES OR CONDITIONS OF ANY KIND, either express or implied.
+# See the License for the specific language governing permissions and
+# limitations under the License.
+
+"""
+Test for attn_implementation override configuration in FSDP workers.
+
+This test verifies that the fix for honoring attn_implementation override config
+works correctly in the ActorRolloutRefWorker._build_model_optimizer method.
+"""
+
+from unittest.mock import Mock, patch
+
+import pytest
+import torch
+from omegaconf import OmegaConf
+from transformers import AutoConfig, AutoModelForCausalLM
+
+# Only run these tests if we can import verl components
+try:
+    from verl.workers.config import FSDPEngineConfig  # noqa: F401
+    from verl.workers.fsdp_workers import (
+        ActorRolloutRefWorker,  # noqa: F401
+        CriticWorker,  # noqa: F401
+    )
+
+    VERL_AVAILABLE = True
+except ImportError:
+    VERL_AVAILABLE = False
+
+
+@pytest.mark.skipif(not VERL_AVAILABLE, reason="VERL components not available")
+class TestFSDPAttnImplementation:
+    """Test cases for attn_implementation override in FSDP workers."""
+
+    def test_attn_implementation_extraction_logic(self):
+        """Test the core logic for extracting attn_implementation from override config."""
+
+        # Test case 1: Default behavior
+        override_config = {}
+        attn_impl = override_config.get("attn_implementation", "flash_attention_2")
+        assert attn_impl == "flash_attention_2"
+
+        # Test case 2: Override to eager
+        override_config = {"attn_implementation": "eager"}
+        attn_impl = override_config.get("attn_implementation", "flash_attention_2")
+        assert attn_impl == "eager"
+
+        # Test case 3: Override to sdpa
+        override_config = {"attn_implementation": "sdpa"}
+        attn_impl = override_config.get("attn_implementation", "flash_attention_2")
+        assert attn_impl == "sdpa"
+
+        # Test case 4: Other configs don't affect attn_implementation
+        override_config = {"other_setting": "value", "dropout": 0.1}
+        attn_impl = override_config.get("attn_implementation", "flash_attention_2")
+        assert attn_impl == "flash_attention_2"
+
+    @patch("transformers.AutoConfig.from_pretrained")
+    @patch("transformers.AutoModelForCausalLM.from_pretrained")
+    def test_attn_implementation_passed_to_autoconfig(self, mock_model_from_pretrained, mock_config_from_pretrained):
+        """Test that attn_implementation is correctly passed to AutoConfig.from_pretrained."""
+
+        # Mock the AutoConfig return value
+        mock_config = Mock()
+        mock_config.tie_word_embeddings = False
+        mock_config.architectures = ["LlamaForCausalLM"]
+        mock_config_from_pretrained.return_value = mock_config
+
+        # Mock the model return value
+        mock_model = Mock()
+        mock_model_from_pretrained.return_value = mock_model
+
+        # Test data
+        test_cases = [
+            ({}, "flash_attention_2"),  # Default
+            ({"attn_implementation": "eager"}, "eager"),  # Override to eager
+            ({"attn_implementation": "sdpa"}, "sdpa"),  # Override to sdpa
+        ]
+
+        for override_config, expected_attn_impl in test_cases:
+            # Reset mocks
+            mock_config_from_pretrained.reset_mock()
+            mock_model_from_pretrained.reset_mock()
+
+            # Simulate the logic from FSDP workers
+            attn_implementation = override_config.get("attn_implementation", "flash_attention_2")
+
+            # This simulates what happens in _build_model_optimizer
+            AutoConfig.from_pretrained("test_path", trust_remote_code=False, attn_implementation=attn_implementation)
+
+            # Verify AutoConfig.from_pretrained was called with correct attn_implementation
+            mock_config_from_pretrained.assert_called_once_with(
+                "test_path", trust_remote_code=False, attn_implementation=expected_attn_impl
+            )
+
+    @patch("transformers.AutoConfig.from_pretrained")
+    @patch("transformers.AutoModelForCausalLM.from_pretrained")
+    def test_attn_implementation_passed_to_model(self, mock_model_from_pretrained, mock_config_from_pretrained):
+        """Test that attn_implementation is correctly passed to model.from_pretrained."""
+
+        # Mock the AutoConfig return value
+        mock_config = Mock()
+        mock_config.tie_word_embeddings = False
+        mock_config.architectures = ["LlamaForCausalLM"]
+        mock_config_from_pretrained.return_value = mock_config
+
+        # Mock the model return value
+        mock_model = Mock()
+        mock_model_from_pretrained.return_value = mock_model
+
+        # Test with override config
+        override_config = {"attn_implementation": "eager"}
+        attn_implementation = override_config.get("attn_implementation", "flash_attention_2")
+
+        # This simulates what happens in _build_model_optimizer
+        AutoModelForCausalLM.from_pretrained(
+            pretrained_model_name_or_path="test_path",
+            torch_dtype=torch.bfloat16,
+            config=mock_config,
+            trust_remote_code=False,
+            attn_implementation=attn_implementation,
+        )
+
+        # Verify AutoModelForCausalLM.from_pretrained was called with correct attn_implementation
+        mock_model_from_pretrained.assert_called_once_with(
+            pretrained_model_name_or_path="test_path",
+            torch_dtype=torch.bfloat16,
+            config=mock_config,
+            trust_remote_code=False,
+            attn_implementation="eager",
+        )
+
+    def test_override_config_integration(self):
+        """Test that override_config from Hydra configuration works correctly."""
+
+        # Simulate the OmegaConf configuration structure used in VERL
+        config_dict = {
+            "model": {"path": "/test/path", "override_config": {"attn_implementation": "eager", "dropout": 0.1}}
+        }
+
+        # Convert to OmegaConf structure
+        omegaconf = OmegaConf.create(config_dict)
+
+        # Simulate what happens in the FSDP worker
+        override_model_config = OmegaConf.to_container(OmegaConf.create(omegaconf.model.get("override_config", {})))
+
+        # Test extraction
+        attn_implementation = override_model_config.get("attn_implementation", "flash_attention_2")
+        assert attn_implementation == "eager"
+
+        # Test that other configs are preserved
+        assert override_model_config.get("dropout") == 0.1
+
+    def test_hydra_plus_prefix_config(self):
+        """Test that Hydra +prefix configurations work correctly."""
+
+        # This simulates the configuration when user specifies:
+        # +actor_rollout_ref.model.override_config.attn_implementation=eager
+
+        # The + prefix in Hydra adds new keys to the config
+        config_dict = {
+            "actor_rollout_ref": {
+                "model": {
+                    "path": "/test/path",
+                    "override_config": {
+                        "attn_implementation": "eager"  # This gets added via +prefix
+                    },
+                }
+            }
+        }
+
+        omegaconf = OmegaConf.create(config_dict)
+
+        # Extract override config as done in FSDP workers
+        override_model_config = OmegaConf.to_container(
+            OmegaConf.create(omegaconf.actor_rollout_ref.model.get("override_config", {}))
+        )
+
+        # Verify extraction works
+        attn_implementation = override_model_config.get("attn_implementation", "flash_attention_2")
+        assert attn_implementation == "eager"
+
+    def test_backward_compatibility(self):
+        """Test that the fix maintains backward compatibility."""
+
+        # Test case 1: No override_config at all (old behavior)
+        config_without_override = {}
+        attn_implementation = config_without_override.get("attn_implementation", "flash_attention_2")
+        assert attn_implementation == "flash_attention_2"
+
+        # Test case 2: Empty override_config
+        config_with_empty_override = {"override_config": {}}
+        override_config = config_with_empty_override.get("override_config", {})
+        attn_implementation = override_config.get("attn_implementation", "flash_attention_2")
+        assert attn_implementation == "flash_attention_2"
+
+        # Test case 3: override_config with other settings but no attn_implementation
+        config_with_other_overrides = {"override_config": {"dropout": 0.1, "hidden_size": 1024}}
+        override_config = config_with_other_overrides.get("override_config", {})
+        attn_implementation = override_config.get("attn_implementation", "flash_attention_2")
+        assert attn_implementation == "flash_attention_2"
+
+    def test_critic_attn_implementation_extraction_logic(self):
+        """Test the core logic for extracting attn_implementation from override config for CriticWorker."""
+
+        # Test case 1: Default behavior for critic
+        override_config = {}
+        attn_impl = override_config.get("attn_implementation", "flash_attention_2")
+        assert attn_impl == "flash_attention_2"
+
+        # Test case 2: Override to eager for critic
+        override_config = {"attn_implementation": "eager"}
+        attn_impl = override_config.get("attn_implementation", "flash_attention_2")
+        assert attn_impl == "eager"
+
+        # Test case 3: Override to sdpa for critic
+        override_config = {"attn_implementation": "sdpa"}
+        attn_impl = override_config.get("attn_implementation", "flash_attention_2")
+        assert attn_impl == "sdpa"
+
+        # Test case 4: Other configs don't affect attn_implementation for critic
+        override_config = {"other_setting": "value", "dropout": 0.1}
+        attn_impl = override_config.get("attn_implementation", "flash_attention_2")
+        assert attn_impl == "flash_attention_2"
+
+    @patch("transformers.AutoConfig.from_pretrained")
+    def test_critic_attn_implementation_passed_to_autoconfig(self, mock_config_from_pretrained):
+        """Test that attn_implementation is correctly passed to AutoConfig.from_pretrained in CriticWorker."""
+
+        # Mock the AutoConfig return value
+        mock_config = Mock()
+        mock_config.tie_word_embeddings = False
+        mock_config.architectures = ["LlamaForCausalLM"]
+        mock_config.num_labels = 1
+        mock_config_from_pretrained.return_value = mock_config
+
+        # Test data for critic model
+        test_cases = [
+            ({}, "flash_attention_2"),  # Default
+            ({"attn_implementation": "eager"}, "eager"),  # Override to eager
+            ({"attn_implementation": "sdpa"}, "sdpa"),  # Override to sdpa
+        ]
+
+        for override_config, expected_attn_impl in test_cases:
+            # Reset mocks
+            mock_config_from_pretrained.reset_mock()
+
+            # Simulate the logic from CriticWorker _build_critic_model_optimizer
+            attn_implementation = override_config.get("attn_implementation", "flash_attention_2")
+
+            # This simulates what should happen in CriticWorker._build_critic_model_optimizer
+            # (This is where the fix needs to be applied in the actual implementation)
+            AutoConfig.from_pretrained(
+                "test_path",
+                attn_implementation=attn_implementation,
+                trust_remote_code=False,
+            )
+
+            # Verify AutoConfig.from_pretrained was called with correct attn_implementation
+            mock_config_from_pretrained.assert_called_once_with(
+                "test_path",
+                attn_implementation=expected_attn_impl,
+                trust_remote_code=False,
+            )
+
+    def test_critic_override_config_integration(self):
+        """Test that override_config from Hydra configuration works correctly for CriticWorker."""
+
+        # Simulate the OmegaConf configuration structure used in VERL for critic
+        config_dict = {
+            "critic": {
+                "model": {"path": "/test/path", "override_config": {"attn_implementation": "eager", "dropout": 0.1}}
+            }
+        }
+
+        # Convert to OmegaConf structure
+        omegaconf = OmegaConf.create(config_dict)
+
+        # Simulate what happens in the CriticWorker
+        override_model_config = OmegaConf.to_container(
+            OmegaConf.create(omegaconf.critic.model.get("override_config", {}))
+        )
+
+        # Test extraction for critic
+        attn_implementation = override_model_config.get("attn_implementation", "flash_attention_2")
+        assert attn_implementation == "eager"
+
+        # Test that other configs are preserved for critic
+        assert override_model_config.get("dropout") == 0.1
+
+    def test_critic_hydra_plus_prefix_config(self):
+        """Test that Hydra +prefix configurations work correctly for CriticWorker."""
+
+        # This simulates the configuration when user specifies:
+        # +critic.model.override_config.attn_implementation=eager
+
+        # The + prefix in Hydra adds new keys to the config
+        config_dict = {
+            "critic": {
+                "model": {
+                    "path": "/test/path",
+                    "override_config": {
+                        "attn_implementation": "eager"  # This gets added via +prefix for critic
+                    },
+                }
+            }
+        }
+
+        omegaconf = OmegaConf.create(config_dict)
+
+        # Extract override config as done in CriticWorker
+        override_model_config = OmegaConf.to_container(
+            OmegaConf.create(omegaconf.critic.model.get("override_config", {}))
+        )
+
+        # Verify extraction works for critic
+        attn_implementation = override_model_config.get("attn_implementation", "flash_attention_2")
+        assert attn_implementation == "eager"
+
+    def test_both_actor_and_critic_configuration(self):
+        """Test that both actor and critic can have different attn_implementation overrides simultaneously."""
+
+        # This simulates a complete training configuration with both actor and critic overrides
+        config_dict = {
+            "actor_rollout_ref": {"model": {"override_config": {"attn_implementation": "eager"}}},
+            "critic": {"model": {"override_config": {"attn_implementation": "sdpa"}}},
+        }
+
+        omegaconf = OmegaConf.create(config_dict)
+
+        # Extract actor override config
+        actor_override_config = OmegaConf.to_container(
+            OmegaConf.create(omegaconf.actor_rollout_ref.model.get("override_config", {}))
+        )
+        actor_attn_implementation = actor_override_config.get("attn_implementation", "flash_attention_2")
+
+        # Extract critic override config
+        critic_override_config = OmegaConf.to_container(
+            OmegaConf.create(omegaconf.critic.model.get("override_config", {}))
+        )
+        critic_attn_implementation = critic_override_config.get("attn_implementation", "flash_attention_2")
+
+        # Verify both can be configured independently
+        assert actor_attn_implementation == "eager"
+        assert critic_attn_implementation == "sdpa"
+
+    def test_critic_backward_compatibility(self):
+        """Test that the CriticWorker fix maintains backward compatibility."""
+
+        # Test case 1: No override_config at all for critic (old behavior)
+        config_without_override = {}
+        attn_implementation = config_without_override.get("attn_implementation", "flash_attention_2")
+        assert attn_implementation == "flash_attention_2"
+
+        # Test case 2: Empty override_config for critic
+        config_with_empty_override = {"override_config": {}}
+        override_config = config_with_empty_override.get("override_config", {})
+        attn_implementation = override_config.get("attn_implementation", "flash_attention_2")
+        assert attn_implementation == "flash_attention_2"
+
+        # Test case 3: override_config with other settings but no attn_implementation for critic
+        config_with_other_overrides = {"override_config": {"dropout": 0.1, "num_labels": 1}}
+        override_config = config_with_other_overrides.get("override_config", {})
+        attn_implementation = override_config.get("attn_implementation", "flash_attention_2")
+        assert attn_implementation == "flash_attention_2"
+
+
+def test_attn_implementation_fix_integration():
+    """Integration test to verify the entire fix works as expected."""
+
+    # This test simulates the complete flow from configuration to model creation
+
+    # Step 1: Simulate Hydra configuration with +prefix
+    # user_config = "+actor_rollout_ref.model.override_config.attn_implementation=eager"
+
+    # This would result in a config structure like:
+    config_dict = {"actor_rollout_ref": {"model": {"override_config": {"attn_implementation": "eager"}}}}
+
+    # Step 2: Extract override_model_config as done in FSDP workers
+    omegaconf = OmegaConf.create(config_dict)
+    override_model_config = OmegaConf.to_container(
+        OmegaConf.create(omegaconf.actor_rollout_ref.model.get("override_config", {}))
+    )
+
+    # Step 3: Apply the fix logic
+    attn_implementation = override_model_config.get("attn_implementation", "flash_attention_2")
+
+    # Step 4: Verify the fix works
+    assert attn_implementation == "eager"
+
+    # Step 5: Verify this would be passed to both AutoConfig and Model creation
+    # (This would normally be done with mocks, but we can test the parameter preparation)
+    config_params = {"attn_implementation": attn_implementation}
+    model_params = {"attn_implementation": attn_implementation}
+
+    assert config_params["attn_implementation"] == "eager"
+    assert model_params["attn_implementation"] == "eager"
+
+
+def test_critic_attn_implementation_fix_integration():
+    """Integration test to verify the entire fix works as expected for CriticWorker."""
+
+    # This test simulates the complete flow from configuration to model creation for critic
+
+    # Step 1: Simulate Hydra configuration with +prefix for critic
+    # user_config = "+critic.model.override_config.attn_implementation=sdpa"
+
+    # This would result in a config structure like:
+    config_dict = {"critic": {"model": {"override_config": {"attn_implementation": "sdpa"}}}}
+
+    # Step 2: Extract override_model_config as should be done in CriticWorker
+    omegaconf = OmegaConf.create(config_dict)
+    override_model_config = OmegaConf.to_container(OmegaConf.create(omegaconf.critic.model.get("override_config", {})))
+
+    # Step 3: Apply the fix logic (what needs to be implemented in CriticWorker)
+    attn_implementation = override_model_config.get("attn_implementation", "flash_attention_2")
+
+    # Step 4: Verify the fix works for critic
+    assert attn_implementation == "sdpa"
+
+    # Step 5: Verify this would be passed to AutoConfig creation for critic
+    config_params = {"attn_implementation": attn_implementation}
+
+    assert config_params["attn_implementation"] == "sdpa"
+
+
+def test_complete_training_configuration():
+    """Integration test for a complete training configuration with both actor and critic overrides."""
+
+    # This test simulates a realistic training configuration where both
+    # actor and critic have different attention implementations
+    config_dict = {
+        "actor_rollout_ref": {
+            "model": {
+                "path": "/shared/models/llama-7b",
+                "override_config": {"attn_implementation": "eager", "torch_dtype": "bfloat16"},
+            }
+        },
+        "critic": {
+            "model": {
+                "path": "/shared/models/llama-7b",
+                "override_config": {"attn_implementation": "sdpa", "num_labels": 1},
+            }
+        },
+    }
+
+    omegaconf = OmegaConf.create(config_dict)
+
+    # Extract configurations as would be done in the workers
+    actor_override_config = OmegaConf.to_container(
+        OmegaConf.create(omegaconf.actor_rollout_ref.model.get("override_config", {}))
+    )
+    critic_override_config = OmegaConf.to_container(OmegaConf.create(omegaconf.critic.model.get("override_config", {})))
+
+    # Apply the fix logic for both
+    actor_attn_implementation = actor_override_config.get("attn_implementation", "flash_attention_2")
+    critic_attn_implementation = critic_override_config.get("attn_implementation", "flash_attention_2")
+
+    # Verify both configurations work independently
+    assert actor_attn_implementation == "eager"
+    assert critic_attn_implementation == "sdpa"
+
+    # Verify other configs are preserved
+    assert actor_override_config.get("torch_dtype") == "bfloat16"
+    assert critic_override_config.get("num_labels") == 1
+
+
+if __name__ == "__main__":
+    # Run basic tests
+    test_attn_implementation_fix_integration()
+    test_critic_attn_implementation_fix_integration()
+    test_complete_training_configuration()
+
+    if VERL_AVAILABLE:
+        # Run class-based tests
+        test_class = TestFSDPAttnImplementation()
+        test_class.test_attn_implementation_extraction_logic()
+        test_class.test_override_config_integration()
+        test_class.test_hydra_plus_prefix_config()
+        test_class.test_backward_compatibility()
+
+        # Run new critic tests
+        test_class.test_critic_attn_implementation_extraction_logic()
+        test_class.test_critic_override_config_integration()
+        test_class.test_critic_hydra_plus_prefix_config()
+        test_class.test_both_actor_and_critic_configuration()
+        test_class.test_critic_backward_compatibility()
+
+        print("✓ All FSDP attn_implementation tests passed!")
+        print("✓ All CriticWorker attn_implementation tests passed!")
+    else:
+        print("⚠ VERL components not available, skipping VERL-specific tests")
+
+    print("✓ Integration tests passed!")
+    print("✓ Critic integration tests passed!")
diff --git a/code/RL_model/verl/verl_train/tests/workers/test_fsdp_workers.py b/code/RL_model/verl/verl_train/tests/workers/test_fsdp_workers.py
new file mode 100644
index 0000000000000000000000000000000000000000..33f1b8e41308e41f44b0cd7a4779e064344dc58c
--- /dev/null
+++ b/code/RL_model/verl/verl_train/tests/workers/test_fsdp_workers.py
@@ -0,0 +1,79 @@
+# Copyright 2025 Bytedance Ltd. and/or its affiliates
+#
+# Licensed under the Apache License, Version 2.0 (the "License");
+# you may not use this file except in compliance with the License.
+# You may obtain a copy of the License at
+#
+#     http://www.apache.org/licenses/LICENSE-2.0
+#
+# Unless required by applicable law or agreed to in writing, software
+# distributed under the License is distributed on an "AS IS" BASIS,
+# WITHOUT WARRANTIES OR CONDITIONS OF ANY KIND, either express or implied.
+# See the License for the specific language governing permissions and
+# limitations under the License.
+import os
+
+from omegaconf import OmegaConf
+
+from verl.workers.fsdp_workers import ActorRolloutRefWorker
+
+
+def test_actor_rollout_ref_worker_actor_ref_model():
+    """Test specifying different reference/actor model"""
+    os.environ["RANK"] = "0"
+    os.environ["WORLD_SIZE"] = "1"
+    os.environ["MASTER_ADDR"] = "127.0.0.1"
+    os.environ["MASTER_PORT"] = "8888"
+
+    actor_model_path = os.path.expanduser("~/models/Qwen/Qwen2.5-0.5B-Instruct")
+    ref_model_path = os.path.expanduser("~/models/Qwen/Qwen2.5-1.5B-Instruct")
+    config_str = f"""
+    model:
+      path: {actor_model_path}
+    actor:
+      _target_: verl.workers.config.FSDPActorConfig
+      strategy: fsdp
+      fsdp_config:
+        _target_: verl.workers.config.FSDPEngineConfig
+        fsdp_size: -1
+        forward_prefetch: false
+      profiler:
+        tool: torch_memory
+        save_path: ./mem_snapshots
+        tool_config:
+          torch_memory:
+            _target_: verl.utils.profiler.config.TorchMemoryToolConfig
+            trace_alloc_max_entries: 100000
+            stack_depth: 32
+    ref:
+      model:
+        path: {ref_model_path}
+      fsdp_config:
+        _target_: verl.workers.config.FSDPEngineConfig
+        fsdp_size: -1
+      profiler:
+        tool: torch_memory
+        save_path: ./mem_snapshots
+        tool_config:
+          torch_memory:
+            _target_: verl.utils.profiler.config.TorchMemoryToolConfig
+            trace_alloc_max_entries: 100000
+            stack_depth: 32
+      log_prob_micro_batch_size: 1
+      ulysses_sequence_parallel_size: 1
+      entropy_from_logits_with_chunking: false
+    """
+    dict_conf = OmegaConf.create(config_str)
+    actor_rollout_ref_worker = ActorRolloutRefWorker(dict_conf, role="ref")
+    actor_rollout_ref_worker.init_model()
+
+    model_config = actor_rollout_ref_worker.ref_module_fsdp._fsdp_wrapped_module.config
+    assert model_config.hidden_size == 1536
+
+    # set ref.model to null, fallback to default case where actor is the same as reference
+    dict_conf["ref"]["model"] = None
+    actor_rollout_ref_worker = ActorRolloutRefWorker(dict_conf, role="ref")
+    actor_rollout_ref_worker.init_model()
+
+    model_config = actor_rollout_ref_worker.ref_module_fsdp._fsdp_wrapped_module.config
+    assert model_config.hidden_size == 896
diff --git a/code/RL_model/verl/verl_train/verl.egg-info/PKG-INFO b/code/RL_model/verl/verl_train/verl.egg-info/PKG-INFO
new file mode 100644
index 0000000000000000000000000000000000000000..07138d0ddfa62f5b02daa01535e6c68f4f4999f5
--- /dev/null
+++ b/code/RL_model/verl/verl_train/verl.egg-info/PKG-INFO
@@ -0,0 +1,374 @@
+Metadata-Version: 2.4
+Name: verl
+Version: 0.8.0.dev0
+Summary: verl: Volcano Engine Reinforcement Learning for LLM
+Home-page: https://github.com/volcengine/verl
+Author: Bytedance - Seed - MLSys
+Author-email: zhangchi.usc1992@bytedance.com, gmsheng@connect.hku.hk
+License: Apache-2.0
+Requires-Python: >=3.10
+Description-Content-Type: text/markdown
+License-File: LICENSE
+Requires-Dist: accelerate
+Requires-Dist: codetiming
+Requires-Dist: datasets
+Requires-Dist: dill
+Requires-Dist: hydra-core
+Requires-Dist: numpy<2.0.0
+Requires-Dist: pandas
+Requires-Dist: peft
+Requires-Dist: pyarrow>=19.0.0
+Requires-Dist: pybind11
+Requires-Dist: pylatexenc
+Requires-Dist: ray[default]>=2.41.0
+Requires-Dist: torchdata
+Requires-Dist: tensordict!=0.9.0,<=0.10.0,>=0.8.0
+Requires-Dist: transformers
+Requires-Dist: wandb
+Requires-Dist: packaging>=20.0
+Requires-Dist: tensorboard
+Provides-Extra: test
+Requires-Dist: pytest; extra == "test"
+Requires-Dist: pre-commit; extra == "test"
+Requires-Dist: py-spy; extra == "test"
+Requires-Dist: pytest-asyncio; extra == "test"
+Requires-Dist: pytest-rerunfailures; extra == "test"
+Provides-Extra: prime
+Requires-Dist: pyext; extra == "prime"
+Provides-Extra: geo
+Requires-Dist: mathruler; extra == "geo"
+Requires-Dist: torchvision; extra == "geo"
+Requires-Dist: qwen_vl_utils; extra == "geo"
+Provides-Extra: gpu
+Requires-Dist: liger-kernel; extra == "gpu"
+Requires-Dist: flash-attn; extra == "gpu"
+Provides-Extra: math
+Requires-Dist: math-verify; extra == "math"
+Provides-Extra: vllm
+Requires-Dist: tensordict!=0.9.0,<=0.10.0,>=0.8.0; extra == "vllm"
+Requires-Dist: vllm<=0.12.0,>=0.8.5; extra == "vllm"
+Provides-Extra: sglang
+Requires-Dist: tensordict!=0.9.0,<=0.10.0,>=0.8.0; extra == "sglang"
+Requires-Dist: sglang[openai,srt]==0.5.6; extra == "sglang"
+Requires-Dist: torch==2.9.1; extra == "sglang"
+Provides-Extra: trl
+Requires-Dist: trl<=0.9.6; extra == "trl"
+Provides-Extra: mcore
+Requires-Dist: mbridge; extra == "mcore"
+Provides-Extra: transferqueue
+Requires-Dist: TransferQueue==0.1.5; extra == "transferqueue"
+Provides-Extra: trtllm
+Requires-Dist: tensorrt-llm>=1.2.0rc6; extra == "trtllm"
+Dynamic: author
+Dynamic: author-email
+Dynamic: home-page
+Dynamic: license-file
+Dynamic: provides-extra
+Dynamic: requires-dist
+
+<div align="center">
+ 👋 Hi, everyone!
+    verl is a RL training library initiated by <b>ByteDance Seed team</b> and maintained by the verl community.
+    <br>
+    <br>
+</div>
+
+<div align="center">
+
+<a href="https://deepwiki.com/volcengine/verl"><img src="https://devin.ai/assets/deepwiki-badge.png" alt="Ask DeepWiki.com" style="height:20px;"></a>
+[![GitHub Repo stars](https://img.shields.io/github/stars/volcengine/verl)](https://github.com/volcengine/verl/stargazers)
+[![Twitter](https://img.shields.io/twitter/follow/verl_project)](https://twitter.com/verl_project)
+<a href="https://join.slack.com/t/verl-project/shared_invite/zt-3c6mc2khw-v0lo6NfDPuFP6OnkrZwfqw"><img src="https://img.shields.io/badge/Slack-verl-blueviolet?logo=slack&amp"></a>
+<a href="https://arxiv.org/pdf/2409.19256"><img src="https://img.shields.io/static/v1?label=EuroSys&message=Paper&color=red"></a>
+[![Documentation](https://img.shields.io/badge/documentation-blue)](https://verl.readthedocs.io/en/latest/)
+<a href="https://raw.githubusercontent.com/eric-haibin-lin/verl-community/refs/heads/main/WeChat.JPG"><img src="https://img.shields.io/badge/微信-green?logo=wechat&amp"></a>
+
+</div>
+
+![seed logo](https://github.com/user-attachments/assets/c42e675e-497c-4508-8bb9-093ad4d1f216)
+
+<h1 style="text-align: center;">verl: Volcano Engine Reinforcement Learning for LLMs</h1>
+
+verl is a flexible, efficient and production-ready RL training library for large language models (LLMs).
+
+verl is the open-source version of **[HybridFlow: A Flexible and Efficient RLHF Framework](https://arxiv.org/abs/2409.19256v2)** paper.
+
+verl is flexible and easy to use with:
+
+- **Easy extension of diverse RL algorithms**: The hybrid-controller programming model enables flexible representation and efficient execution of complex post-training dataflows. Build RL dataflows such as GRPO, PPO in a few lines of code.
+
+- **Seamless integration of existing LLM infra with modular APIs**: Decouples computation and data dependencies, enabling seamless integration with existing LLM frameworks, such as FSDP, Megatron-LM, vLLM, SGLang, etc
+
+- **Flexible device mapping**: Supports various placement of models onto different sets of GPUs for efficient resource utilization and scalability across different cluster sizes.
+
+- Ready integration with popular HuggingFace models
+
+verl is fast with:
+
+- **State-of-the-art throughput**: SOTA LLM training and inference engine integrations and SOTA RL throughput.
+
+- **Efficient actor model resharding with 3D-HybridEngine**: Eliminates memory redundancy and significantly reduces communication overhead during transitions between training and generation phases.
+
+<div align="center">
+ <img src="https://github.com/verl-project/verl-data/blob/main/images/verl-arch.png?raw=true" width="400" alt="verl-arch.png">
+</div>
+
+</p>
+
+## News
+
+- [2026/01] verl has been migrated to the [verl-project](https://github.com/verl-project)
+- [2026/01] verl first meetup was successfully held in Shanghai on 01/10, hosted by Volcengine and NVIDIA, the slides has been uploaded to [verl-data](https://github.com/verl-project/verl-data).
+- [2026/01] The `recipe` directory has been migrated to a dedicated repository: [verl-recipe](https://github.com/verl-project/verl-recipe) and added as a submodule. See https://github.com/volcengine/verl/pull/4795. It can be used as it was after `git submodule update --init --recursive recipe`. Note that [`transfer_queue`](verl/experimental/transfer_queue), [`fully_async_policy`](verl/experimental/fully_async_policy), [`one_step_off_policy`](verl/experimental/one_step_off_policy) and [`vla`](verl/experimental/vla) are kept under [`verl/experimental`](verl/experimental) since they are planned to be merged into the main library. Use them through `verl.experimental.{module}`.
+- [2025/12] [Mind Lab](https://macaron.im/mindlab) successfully used [verl](https://github.com/volcengine/verl) and [Megatron-bridge](https://github.com/NVIDIA-NeMo/Megatron-Bridge) to train GRPO Lora for Trillion-parameter model on 64 H800 - See their [techblog](https://macaron.im/mindlab/research/building-trillion-parameter-reasoning-rl-with-10-gpus).
+- [2025/10] verl is presented in the [PyTorch Conference 2025](https://pytorch.org/event/pytorch-conference-2025/).
+- [2025/08] verl is presented in the [PyTorch Expert Exchange Webinar](https://www.youtube.com/watch?v=Vd79NmmqY3Q&t=2s). [Slides](https://github.com/eric-haibin-lin/verl-community/blob/main/slides/verl_talk_pytorch_2025_08.pdf) available.
+- [2025/07] The [ReTool](https://arxiv.org/pdf/2504.11536) recipe is fully open sourced. [Blog](https://www.notion.so/verl-reTool-recipe-Using-multi-round-conversations-and-code-sandboxing-to-improve-the-math-of-large-23a8b5b7feba80b386b2e5b5e3c1cde0)
+- [2025/07] The first verl meetup will be held at ICML Vancouver on July 16th! Please [join us](https://lu.ma/0ek2nyao) if you are at ICML! (onsite only)
+- [2025/06] verl with Megatron backend enables large MoE models such as [DeepSeek-671B and Qwen3-235B](https://verl.readthedocs.io/en/latest/perf/dpsk.html).
+- [2025/03] [DAPO](https://dapo-sia.github.io/) is the open-sourced SOTA RL algorithm that achieves 50 points on AIME 2024 based on the Qwen2.5-32B pre-trained model, surpassing the previous SOTA achieved by DeepSeek's GRPO (DeepSeek-R1-Zero-Qwen-32B). DAPO's training is fully powered by verl and the reproduction code is available in `recipe/dapo` now.
+<details><summary> more... </summary>
+<ul>
+  <li>[2025/04] [Seed-Thinking-v1.5](https://github.com/ByteDance-Seed/Seed-Thinking-v1.5/blob/main/seed-thinking-v1.5.pdf) tech report is released! Trained with verl, Seed-Thinking-v1.5 achieves 86.7 on AIME 2024, 55.0 on Codeforces and 77.3 on GPQA, demonstrating excellent reasoning abilities in STEM and coding. Beyond reasoning tasks, the method demonstrates notable generalization across diverse domains.</li>
+  <li>[2025/07] verl keynote at [AWS AI Hours Singapore](https://pages.awscloud.com/aws-ai-hours-sg.html#agenda) on 7/8, verl & verl-agent project updates at [Agent for SWE meetup](https://lu.ma/e498qhsi) by LF AI & Data Singapore on 7/11.</li>
+  <li>[2025/06] verl team will provide latest project updates at [PyTorch Day China](https://www.lfasiallc.com/pytorch-day-china/) on June 7th. Meet our dev team in Beijing!</li>
+  <li> [2025/04] [VAPO](https://arxiv.org/pdf/2504.05118) (value-based augmented PPO) paper covers our latest RL method for reasoning models. Trained from Qwen-32B-base model, VAPO achieves 60.4 on AIME 2024, outperforming DAPO-32B.</li>
+  <li>[2025/05] [PF-PPO](https://arxiv.org/abs/2409.06957), accepted to ICML 2025, is now supported in verl! PF-PPO enhances policy learning efficiency and robustness by filtering potentially noisy reward signals and reusing high-quality experiences via a replay buffer.</li>
+  <li>[2025/04] We will give a tutorial about latest post-training techniques and programming guide for verl at [ICLR 2025 Expo](https://iclr.cc/virtual/2025/calendar?filter_events=Expo+Talk+Panel&filter_rooms=), [SCI-FM workshop](https://open-foundation-model.github.io/) and [LMSys afterparty](https://lu.ma/d23nyynm). Talk materials available [here](https://github.com/eric-haibin-lin/verl-community/tree/main/iclr25). </li>
+  <li>[2025/03] verl v0.3.0.post1 is released! See [release note](https://github.com/volcengine/verl/releases/) for details. It achieves [~1.4x speedup](https://tongyx361.github.io/blogs/posts/verl-intro/#/verl-flexible-and-efficient-rl-for-llms) compared to prev versions.</li>
+  <li>[2025/05] verl will be presented at [A2M Shanghai](https://a2m.msup.com.cn/home/?aid=4488&city=shanghai) on 5/16 - 5/17.</li>
+  <li>[2025/05] verl will be presented at [GOSIM x PyTorch Day 2025](https://paris2025.gosim.org/). See you in Paris! </li>
+  <li>[2025/03] We introduced the programming model of verl at the [vLLM Beijing Meetup](https://mp.weixin.qq.com/s/n77GibL2corAtQHtVEAzfg) and [verl intro and updates](https://github.com/eric-haibin-lin/verl-community/blob/main/slides/verl-lmsys-meetup.pdf) at the [SGLang-LMSYS Org Meetup](https://lu.ma/ntjrr7ig) in Sunnyvale mid-March.</li>
+  <li>[2025/03] We will present verl(HybridFlow) at EuroSys 2025. See you in Rotterdam!</li>
+  <li>[2025/02] verl v0.2.0.post2 is released!</li>
+  <li>[2025/02] We presented verl in the <a href="https://lu.ma/ji7atxux">Bytedance/NVIDIA/Anyscale Ray Meetup</a>. See you in San Jose!</li>
+  <li>[2025/01] [Doubao-1.5-pro](https://team.doubao.com/zh/special/doubao_1_5_pro) is released with SOTA-level performance on LLM & VLM. The RL scaling preview model is trained using verl, reaching OpenAI O1-level performance on math benchmarks (70.0 pass@1 on AIME).</li>
+  <li>[2024/12] verl is presented at Ray Forward 2024. Slides available <a href="https://github.com/eric-haibin-lin/verl-community/blob/main/slides/Ray_Forward_2024_%E5%B7%AB%E9%94%A1%E6%96%8C.pdf">here</a></li>
+  <li>[2024/12] The team presented <a href="https://neurips.cc/Expo/Conferences/2024/workshop/100677">Post-training LLMs: From Algorithms to Infrastructure</a> at NeurIPS 2024. <a href="https://github.com/eric-haibin-lin/verl-data/tree/neurips">Slides</a> and <a href="https://neurips.cc/Expo/Conferences/2024/workshop/100677">video</a> available.</li>
+  <li>[2024/10] verl is presented at Ray Summit. <a href="https://www.youtube.com/watch?v=MrhMcXkXvJU&list=PLzTswPQNepXntmT8jr9WaNfqQ60QwW7-U&index=37">Youtube video</a> available.</li>
+  <li>[2024/08] HybridFlow (verl) is accepted to EuroSys 2025.</li>
+</ul>
+</details>
+
+## Key Features
+
+- **FSDP**, **FSDP2** and **Megatron-LM** for training.
+- **vLLM**, **SGLang** and **HF Transformers** for rollout generation.
+- Compatible with Hugging Face Transformers and Modelscope Hub: [Qwen-3](https://github.com/volcengine/verl/blob/main/examples/grpo_trainer/run_qwen3-8b.sh), Qwen-2.5, Llama3.1, Gemma2, DeepSeek-LLM, etc
+- Supervised fine-tuning.
+- Reinforcement learning with [PPO](examples/ppo_trainer/), [GRPO](examples/grpo_trainer/), [GSPO](https://github.com/verl-project/verl-recipe/tree/main/gspo/), [ReMax](examples/remax_trainer/), [REINFORCE++](https://verl.readthedocs.io/en/latest/examples/config.html#algorithm), [RLOO](examples/rloo_trainer/), [PRIME](https://github.com/verl-project/verl-recipe/tree/main/prime/), [DAPO](https://github.com/verl-project/verl-recipe/tree/main/dapo/), [DrGRPO](https://github.com/verl-project/verl-recipe/tree/main/drgrpo), [KL_Cov & Clip_Cov](https://github.com/verl-project/verl-recipe/tree/main/entropy) etc.
+  - Support model-based reward and function-based reward (verifiable reward) for math, [coding](https://github.com/volcengine/verl-recipe/tree/main/dapo), etc
+  - Support vision-language models (VLMs) and [multi-modal RL](examples/grpo_trainer/run_qwen2_5_vl-7b.sh) with Qwen2.5-vl, Kimi-VL
+  - [Multi-turn with tool calling](https://github.com/volcengine/verl/tree/main/examples/sglang_multiturn)
+- LLM alignment recipes such as [Self-play preference optimization (SPPO)](https://github.com/verl-project/verl-recipe/tree/main/sppo)
+- Flash attention 2, [sequence packing](examples/ppo_trainer/run_qwen2-7b_seq_balance.sh), [sequence parallelism](examples/ppo_trainer/run_deepseek7b_llm_sp2.sh) support via DeepSpeed Ulysses, [LoRA](examples/sft/gsm8k/run_qwen_05_peft.sh), [Liger-kernel](examples/sft/gsm8k/run_qwen_05_sp2_liger.sh).
+- Scales up to 671B models and hundreds of GPUs with [expert parallelism](https://github.com/volcengine/verl/pull/1467)
+- Multi-gpu [LoRA RL](https://verl.readthedocs.io/en/latest/advance/ppo_lora.html) support to save memory.
+- Experiment tracking with wandb, swanlab, mlflow and tensorboard.
+- Hardware Support: Supports NVIDIA, AMD, [Ascend](https://github.com/volcengine/verl/blob/main/docs/ascend_tutorial/ascend_quick_start.rst)
+
+## Upcoming Features and Changes
+
+- Q3 Roadmap https://github.com/volcengine/verl/issues/2388
+- DeepSeek 671b optimizations with Megatron https://github.com/volcengine/verl/issues/1033
+- Multi-turn rollout and tools using optimizations https://github.com/volcengine/verl/issues/1882
+- [Agent integration](https://github.com/volcengine/verl/tree/main/verl/experimental/agent_loop)
+- Async and off-policy architecture https://github.com/volcengine/verl/pull/2231
+- List of breaking changes since v0.4 https://github.com/volcengine/verl/discussions/2270
+
+## Getting Started
+
+<a href="https://verl.readthedocs.io/en/latest/index.html"><b>Documentation</b></a>
+
+**Quickstart:**
+
+- [Installation](https://verl.readthedocs.io/en/latest/start/install.html)
+- [Quickstart](https://verl.readthedocs.io/en/latest/start/quickstart.html)
+- [Programming Guide](https://verl.readthedocs.io/en/latest/hybrid_flow.html) & [Tech Talk](https://hcqnc.xetlk.com/sl/3vACOK) (in Chinese)
+- [PPO in verl](https://verl.readthedocs.io/en/latest/algo/ppo.html)
+- [GRPO in verl](https://verl.readthedocs.io/en/latest/algo/grpo.html)
+
+**Running a PPO example step-by-step:**
+
+- [Prepare Data for Post-Training](https://verl.readthedocs.io/en/latest/preparation/prepare_data.html)
+- [Implement Reward Function for Dataset](https://verl.readthedocs.io/en/latest/preparation/reward_function.html)
+- [PPO Example Architecture](https://verl.readthedocs.io/en/latest/examples/ppo_code_architecture.html)
+- [Config Explanation](https://verl.readthedocs.io/en/latest/examples/config.html)
+
+**Reproducible algorithm baselines:**
+
+- [RL performance on coding, math](https://verl.readthedocs.io/en/latest/algo/baseline.html)
+
+**For code explanation and advance usage (extension):**
+
+- PPO Trainer and Workers
+
+  - [PPO Ray Trainer](https://verl.readthedocs.io/en/latest/workers/ray_trainer.html)
+  - [PyTorch FSDP Backend](https://verl.readthedocs.io/en/latest/workers/fsdp_workers.html)
+  - [Megatron-LM Backend](https://verl.readthedocs.io/en/latest/index.html)
+
+- Advanced Usage and Extension
+  - [Add Models with the FSDP Backend](https://verl.readthedocs.io/en/latest/advance/fsdp_extension.html)
+  - [Add Models with the Megatron-LM Backend](https://verl.readthedocs.io/en/latest/advance/megatron_extension.html)
+  - [Multi-turn Rollout Support](https://verl.readthedocs.io/en/latest/sglang_multiturn/multiturn.html)
+  - [Search Tool Integration](https://verl.readthedocs.io/en/latest/sglang_multiturn/search_tool_example.html)
+  - [Sandbox Fusion Integration](https://verl.readthedocs.io/en/latest/examples/sandbox_fusion_example.html)
+  - [Deployment using Separate GPU Resources](https://github.com/volcengine/verl/tree/main/examples/split_placement)
+  - [Extend to Other RL(HF) algorithms](https://verl.readthedocs.io/en/latest/advance/dpo_extension.html)
+  - [Ray API design tutorial](https://verl.readthedocs.io/en/latest/advance/placement.html)
+
+**Blogs from the community**
+
+- [When Reasoning Models Break Tokenization: The Hidden Complexity of Multiturn Training](https://github.com/zhaochenyang20/Awesome-ML-SYS-Tutorial/blob/main/rlhf/verl/multi-turn/fast_tokenization/multiturn_tokenization_and_masking.md)
+- [verl deployment on AWS SageMaker](https://medium.com/@kaige.yang0110/run-verl-on-sagemaker-using-4x8-l40s-gpus-8e6d5c3c61d3)
+- [verl x SGLang Multi-turn Code Walkthrough](https://github.com/zhaochenyang20/Awesome-ML-SYS-Tutorial/blob/main/rlhf/verl/multi-turn/code-walk-through/readme_EN.md)
+- [Optimizing SGLang Memory Usage in verl](https://hebiao064.github.io/rl-memory-management)
+- [SGLang, verl, OpenBMB and Tsinghua University: Pioneering End-to-End Multi-Turn RLHF](https://github.com/zhaochenyang20/Awesome-ML-SYS-Tutorial/blob/main/rlhf/verl/multi-turn/verl-multiturn-rollout-Release.md)
+- [Reinforcement Learning from Human Feedback on AMD GPUs with verl and ROCm Integration](https://rocm.blogs.amd.com/artificial-intelligence/verl-large-scale/README.html)
+- [veMLP x verl ：玩转强化学习训练](https://mp.weixin.qq.com/s/7nbqxk4knMGd-hQE9ls2tA)
+- [使用 verl 进行 GRPO 分布式强化学习训练最佳实践](https://www.volcengine.com/docs/6459/1463942)
+- [HybridFlow verl 原文浅析](https://github.com/zhaochenyang20/Awesome-ML-SYS-Tutorial/blob/main/rlhf/verl/readme.md)
+- [最高提升 20 倍吞吐量！豆包大模型团队发布全新 RLHF 框架，现已开源！](https://team.doubao.com/en/blog/%E6%9C%80%E9%AB%98%E6%8F%90%E5%8D%8720%E5%80%8D%E5%90%9E%E5%90%90%E9%87%8F-%E8%B1%86%E5%8C%85%E5%A4%A7%E6%A8%A1%E5%9E%8B%E5%9B%A2%E9%98%9F%E5%8F%91%E5%B8%83%E5%85%A8%E6%96%B0-rlhf-%E6%A1%86%E6%9E%B6-%E7%8E%B0%E5%B7%B2%E5%BC%80%E6%BA%90)
+
+## Performance Tuning Guide
+
+The performance is essential for on-policy RL algorithm. We have written a detailed [performance tuning guide](https://verl.readthedocs.io/en/latest/perf/perf_tuning.html) to help you optimize performance.
+
+## Upgrade to vLLM >= v0.8.2
+
+verl now supports vLLM>=0.8.2 when using FSDP as the training backend. Please refer to [this document](https://github.com/volcengine/verl/blob/main/docs/README_vllm0.8.md) for the installation guide and more information. Please avoid vllm 0.7.x, which contains bugs that may lead to OOMs and unexpected errors.
+
+## Use Latest SGLang
+
+SGLang is fully supported with verl, and SGLang RL Group is working extensively on building unique features, including multi-turn agentic RL, VLM RLHF, server-based RL, and partial rollout. Please refer to [this document](https://verl.readthedocs.io/en/latest/workers/sglang_worker.html) for the installation guide and more information.
+
+## Upgrade to FSDP2
+
+verl is fully embracing FSDP2! FSDP2 is recommended by torch distributed team, providing better throughput and memory usage, and is composible with other features (e.g. torch.compile). To enable FSDP2, simply use verl main and set the following options:
+
+```
+actor_rollout_ref.ref.strategy=fsdp2
+actor_rollout_ref.actor.strategy=fsdp2
+critic.strategy=fsdp2
+reward_model.strategy=fsdp2
+```
+
+Furthermore, FSDP2 cpu offloading is compatible with gradient accumulation. You can turn it on to save memory with `actor_rollout_ref.actor.fsdp_config.offload_policy=True`. For more details, see https://github.com/volcengine/verl/pull/1026
+
+## AMD Support (ROCm Kernel)
+
+verl now supports FSDP as the training engine (Megatron support coming soon) and both integrates with vLLM and SGLang as inference engines. Please refer to [this document](https://github.com/volcengine/verl/blob/main/docs/amd_tutorial/amd_build_dockerfile_page.rst) for the installation guide and more information, and [this document](https://github.com/volcengine/verl/blob/main/docs/amd_tutorial/amd_vllm_page.rst) for the vLLM performance tuning for ROCm.
+
+## Citation and acknowledgement
+
+If you find the project helpful, please cite:
+
+- [HybridFlow: A Flexible and Efficient RLHF Framework](https://arxiv.org/abs/2409.19256v2)
+- [A Framework for Training Large Language Models for Code Generation via Proximal Policy Optimization](https://i.cs.hku.hk/~cwu/papers/gmsheng-NL2Code24.pdf)
+
+```bibtex
+@article{sheng2024hybridflow,
+  title   = {HybridFlow: A Flexible and Efficient RLHF Framework},
+  author  = {Guangming Sheng and Chi Zhang and Zilingfeng Ye and Xibin Wu and Wang Zhang and Ru Zhang and Yanghua Peng and Haibin Lin and Chuan Wu},
+  year    = {2024},
+  journal = {arXiv preprint arXiv: 2409.19256}
+}
+```
+
+verl is inspired by the design of Nemo-Aligner, Deepspeed-chat and OpenRLHF. The project is adopted and contributed by Bytedance, Anyscale, LMSys.org, [Alibaba Qwen team](https://github.com/QwenLM/), Shanghai AI Lab, Tsinghua University, UC Berkeley, UCLA, UIUC, University of Hong Kong, ke.com, [All Hands AI](https://www.all-hands.dev/), [ModelBest](http://modelbest.cn/), JD AI Lab, Microsoft Research, [StepFun](https://www.stepfun.com/), Amazon, LinkedIn, Meituan, [Camel-AI](https://www.camel-ai.org/), [OpenManus](https://github.com/OpenManus), Xiaomi, NVIDIA research, [Baichuan](https://www.baichuan-ai.com/home), [RedNote](https://www.xiaohongshu.com/), [SwissAI](https://www.swiss-ai.org/), [Moonshot AI (Kimi)](https://www.moonshot-ai.com/), Baidu, Snowflake, Skywork.ai, JetBrains, [IceSword Lab](https://www.iceswordlab.com), and many more.
+
+## Awesome Projects Built with `verl`
+
+Welcome to register your awesome project build with `verl` for other developers' reference!
+
+- [TinyZero](https://github.com/Jiayi-Pan/TinyZero): a reproduction of **DeepSeek R1 Zero** recipe for reasoning tasks ![GitHub Repo stars](https://img.shields.io/github/stars/Jiayi-Pan/TinyZero)
+- [SkyThought](https://github.com/NovaSky-AI/SkyThought): RL training for Sky-T1-7B by NovaSky AI team. ![GitHub Repo stars](https://img.shields.io/github/stars/NovaSky-AI/SkyThought)
+- [simpleRL-reason](https://github.com/hkust-nlp/simpleRL-reason): SimpleRL-Zoo: Investigating and Taming Zero Reinforcement Learning for Open Base Models in the Wild ![GitHub Repo stars](https://img.shields.io/github/stars/hkust-nlp/simpleRL-reason)
+- [Easy-R1](https://github.com/hiyouga/EasyR1): **Multi-modal** RL training framework ![GitHub Repo stars](https://img.shields.io/github/stars/hiyouga/EasyR1)
+- [OpenManus-RL](https://github.com/OpenManus/OpenManus-RL): LLM Agents RL tuning framework for multiple agent environments. ![GitHub Repo stars](https://img.shields.io/github/stars/OpenManus/OpenManus-RL)
+- [rllm](https://github.com/agentica-project/rllm): async RL training with [verl-pipeline](https://github.com/agentica-project/verl-pipeline) ![GitHub Repo stars](https://img.shields.io/github/stars/agentica-project/rllm)
+- [RAGEN](https://github.com/ZihanWang314/ragen): a general-purpose reasoning **agent** training framework ![GitHub Repo stars](https://img.shields.io/github/stars/ZihanWang314/ragen)
+- [Search-R1](https://github.com/PeterGriffinJin/Search-R1): RL with reasoning and **searching (tool-call)** interleaved LLMs ![GitHub Repo stars](https://img.shields.io/github/stars/PeterGriffinJin/Search-R1)
+- [ReSearch](https://github.com/Agent-RL/ReSearch): Learning to **Re**ason with **Search** for LLMs via Reinforcement Learning ![GitHub Repo stars](https://img.shields.io/github/stars/Agent-RL/ReSearch)
+- [Skywork-OR1](https://github.com/SkyworkAI/Skywork-OR1): Skywork open reaonser series ![GitHub Repo stars](https://img.shields.io/github/stars/SkyworkAI/Skywork-OR1)
+- [ToRL](https://github.com/GAIR-NLP/ToRL): Scaling tool-integrated RL ![GitHub Repo stars](https://img.shields.io/github/stars/GAIR-NLP/ToRL)
+- [Absolute Zero Reasoner](https://github.com/LeapLabTHU/Absolute-Zero-Reasoner): [A no human curated data self-play framework for reasoning](https://arxiv.org/abs/2505.03335) ![GitHub Repo stars](https://img.shields.io/github/stars/LeapLabTHU/Absolute-Zero-Reasoner)
+- [verl-agent](https://github.com/langfengQ/verl-agent): A scalable training framework for **long-horizon LLM/VLM agents**, along with a new algorithm **GiGPO** ![GitHub Repo stars](https://img.shields.io/github/stars/langfengQ/verl-agent)
+- [RL-Factory](https://github.com/Simple-Efficient/RL-Factory): An easy and efficient RL post-training framework for Agentic Learning ![GitHub Repo stars](https://img.shields.io/github/stars/Simple-Efficient/RL-Factory)
+- [ReTool](https://retool-rl.github.io/): ReTool: reinforcement learning for strategic tool use in LLMs. Code release is in progress...
+- [verl-tool](https://github.com/TIGER-AI-Lab/verl-tool): An unified and easy-to-extend tool-agent training framework based on verl![GitHub Repo stars](https://img.shields.io/github/stars/TIGER-AI-Lab/verl-tool)
+- [PRIME](https://github.com/PRIME-RL/PRIME): Process reinforcement through implicit rewards ![GitHub Repo stars](https://img.shields.io/github/stars/PRIME-RL/PRIME)
+- [MemAgent](https://github.com/BytedTsinghua-SIA/MemAgent): MemAgent: Reshaping Long-Context LLM with Multi-Conv RL based Memory Agent ![GitHub Repo stars](https://img.shields.io/github/stars/BytedTsinghua-SIA/MemAgent)
+- [POLARIS](https://github.com/ChenxinAn-fdu/POLARIS): A Post-training recipe for scaling RL on Advanced Reasoning models ![GitHub Repo stars](https://img.shields.io/github/stars/ChenxinAn-fdu/POLARIS)
+- [GUI-R1](https://github.com/ritzz-ai/GUI-R1): **GUI-R1**: A Generalist R1-style Vision-Language Action Model For **GUI Agents** ![GitHub Repo stars](https://img.shields.io/github/stars/ritzz-ai/GUI-R1)
+- [DeepRetrieval](https://github.com/pat-jj/DeepRetrieval): RL Training of **Search Agent** with **Search/Retrieval Outcome** ![GitHub Repo stars](https://img.shields.io/github/stars/pat-jj/DeepRetrieval)
+- [Code-R1](https://github.com/ganler/code-r1): Reproducing R1 for **Code** with Reliable Rewards ![GitHub Repo stars](https://img.shields.io/github/stars/ganler/code-r1)
+- [DeepResearcher](https://github.com/GAIR-NLP/DeepResearcher): Scaling deep research via reinforcement learning in real-world environments ![GitHub Repo stars](https://img.shields.io/github/stars/GAIR-NLP/DeepResearcher)
+- [VAGEN](https://github.com/RAGEN-AI/VAGEN): Training VLM agents with multi-turn reinforcement learning ![GitHub Repo stars](https://img.shields.io/github/stars/RAGEN-AI/VAGEN)
+- [RM-R1](https://arxiv.org/abs/2505.02387): RL training of reasoning reward models ![GitHub Repo stars](https://img.shields.io/github/stars/RM-R1-UIUC/RM-R1)
+- [LUFFY](https://arxiv.org/pdf/2504.14945): Learning to Reason under Off-Policy Guidance![GitHub Repo stars](https://img.shields.io/github/stars/ElliottYan/LUFFY)
+- [DeepMath](https://github.com/zwhe99/DeepMath): DeepMath-103K data and series models for math reasoning![GitHub Repo stars](https://img.shields.io/github/stars/zwhe99/DeepMath)
+- [PACS](https://github.com/ritzz-ai/PACS): Implicit Actor Critic Coupling via a Supervised Learning Framework for RLVR ![GitHub Repo stars](https://img.shields.io/github/stars/ritzz-ai/PACS)
+- [Entropy Mechanism of RL](https://github.com/PRIME-RL/Entropy-Mechanism-of-RL): The Entropy Mechanism of Reinforcement Learning for Large Language Model Reasoning![GitHub Repo stars](https://img.shields.io/github/stars/PRIME-RL/Entropy-Mechanism-of-RL)
+- [LLaSA-TTS-GRPO](https://github.com/channel-io/ch-tts-llasa-rl-grpo): TTS fine-tuning with GRPO optimization based on LLASA models ![GitHub Repo stars](https://img.shields.io/github/stars/channel-io/ch-tts-llasa-rl-grpo)
+- [PF-PPO](https://arxiv.org/abs/2409.06957): Policy Filtration for PPO based on the reliability of reward signals for more efficient and robust RLHF.
+- [RACRO](https://github.com/gyhdog99/RACRO2): Build multi-modal reasoning models via decoupling it into query-conditioned captioning and text-only reasoning ![GitHub Repo stars](https://img.shields.io/github/stars/gyhdog99/RACRO2)
+- [Agent Lightning](https://github.com/microsoft/agent-lightning): A flexible and extensible framework that enables seamless agent optimization for any existing agent framework. ![GitHub Repo stars](https://img.shields.io/github/stars/microsoft/agent-lightning)
+- [VTool-R1](https://github.com/VTOOL-R1/vtool-r1): VLMs Learn to Think with Images via Reinforcement Learning on Multimodal Tool Use. ![GitHub Repo stars](https://img.shields.io/github/stars/VTOOL-R1/vtool-r1)
+- [Kimina-Prover-RL](https://github.com/project-numina/kimina-prover-rl/tree/main/recipe/kimina_prover_rl): Training pipeline for formal theorem proving, based on a paradigm inspired by DeepSeek-R1.
+- [RL-PLUS](https://github.com/YihongDong/RL-PLUS): Countering Capability Boundary Collapse of LLMs in Reinforcement Learning with Hybrid-policy Optimization.
+- [rStar2-Agent](https://github.com/microsoft/rStar): Using reinforcement learning with multi-step tool-calling for math tasks, rStar2-Agent-14B reaches frontier-level math reasoning in just 510 RL training steps ![GitHub Repo stars](https://img.shields.io/github/stars/microsoft/rStar)
+- [Vision-SR1](https://github.com/zli12321/Vision-SR1): Self-Rewarding Vision-Language Model via Reasoning Decomposition ![GitHub Repo stars](https://img.shields.io/github/stars/zli12321/Vision-SR1)
+- [SimpleVLA-RL](https://github.com/PRIME-RL/SimpleVLA-RL): SimpleVLA-RL: A Simple yet Effective Vision-Language Action Model for Reinforcement Learning ![GitHub Repo stars](https://img.shields.io/github/stars/PRIME-RL/SimpleVLA-RL)
+- [Table-R1](https://github.com/Table-R1/Table-R1): Table-R1: Inference-Time Scaling for Table Reasoning ![GitHub Repo stars](https://img.shields.io/github/stars/Table-R1/Table-R1)
+- [Revisual-R1](https://github.com/CSfufu/Revisual-R1): Revisual-R1: Advancing Multimodal Reasoning From Optimized Cold Start to Staged Reinforcement Learning ![GitHub Repo stars](https://img.shields.io/github/stars/CSfufu/Revisual-R1)
+- [ARES](https://github.com/shawn0728/ARES): ARES: Multimodal Adaptive Reasoning via Difficulty-Aware Token-Level Entropy Shaping ![GitHub Repo stars](https://img.shields.io/github/stars/shawn0728/ARES)
+- [Meta-Bandit-LLM](https://github.com/sanxing-chen/meta-bandit-llm): Meta-Bandit-LLM: Long-horizon multiturn interactive training for meta-bandit agents ![GitHub Repo stars](https://img.shields.io/github/stars/sanxing-chen/meta-bandit-llm)
+- [PokeeResearch](https://github.com/Pokee-AI/PokeeResearchOSS): PokeeResearch: State-of-the-art 7B DeepResearch Agent that leverages web search and content reading capabilities to answer complex questions using the most up-to-date information available online. ![Github Repo Stars](https://img.shields.io/github/stars/Pokee-AI/PokeeResearchOSS)
+- [Search Self-play](https://github.com/Alibaba-Quark/SSP): Pushing the Frontier of Agent Capability without Supervision ![GitHub Repo stars](https://img.shields.io/github/stars/Alibaba-Quark/SSP)
+- [OneThinker](https://github.com/tulerfeng/OneThinker): All-in-one Reasoning Model for Image and Video ![GitHub Repo stars](https://img.shields.io/github/stars/tulerfeng/OneThinker)
+- [OpenTinker](https://github.com/open-tinker/OpenTinker): Democratizing Agentic Reinforcement Learning as a Service ![GitHub Repo stars](https://img.shields.io/github/stars/open-tinker/OpenTinker)
+- [FlowRL](https://github.com/Xuekai-Zhu/FlowRL): Matching reward distributions via **flow balance** for diverse exploration and generalizable reasoning ![GitHub Repo stars](https://img.shields.io/github/stars/Xuekai-Zhu/FlowRL)
+- [Logic-RL](https://github.com/Unakar/Logic-RL): a reproduction of DeepSeek R1 Zero on 2K Tiny Logic Puzzle Dataset. ![GitHub Repo stars](https://img.shields.io/github/stars/Unakar/Logic-RL)
+- [Seed-Coder](https://github.com/ByteDance-Seed/Seed-Coder): RL training of Seed-Coder boosts performance on competitive programming ![GitHub Repo stars](https://img.shields.io/github/stars/ByteDance-Seed/Seed-Coder)
+- [all-hands/openhands-lm-32b-v0.1](https://www.all-hands.dev/blog/introducing-openhands-lm-32b----a-strong-open-coding-agent-model): A strong, open coding agent model, trained with [multi-turn fine-tuning](https://github.com/volcengine/verl/pull/195)
+- [s3](https://github.com/pat-jj/s3) **Efficient Yet Effective** Search Agent Training via RL ![GitHub Repo stars](https://img.shields.io/github/stars/pat-jj/s3)
+- [Rec-R1](https://arxiv.org/pdf/2503.24289): Bridging Generative Large Language Models and Recommendation Systems via Reinforcement Learning
+- [Explore RL Data Scaling](https://arxiv.org/abs/2503.22230): Exploring Data Scaling Trends and Effects in Reinforcement Learning from Human Feedback
+- [FIRE](https://arxiv.org/abs/2410.21236): Flaming-hot initiation with regular execution sampling for large language models
+- [DQO](https://arxiv.org/abs/2410.09302): Enhancing multi-Step reasoning abilities of language models through direct Q-function optimization
+- [ProRL](https://arxiv.org/abs/2505.24864): Prolonged Reinforcement Learning Expands Reasoning Boundaries in Large Language Models
+- [cognition-engineering](https://github.com/gair-nlp/cognition-engineering): Test time scaling drives cognition engineering. ![GitHub Repo stars](https://img.shields.io/github/stars/gair-nlp/cognition-engineering)
+- [Trust Region Preference Approximation](https://github.com/XueruiSu/Trust-Region-Preference-Approximation): A simple and stable **reinforcement learning algorithm** for LLM reasoning. ![GitHub Repo stars](https://img.shields.io/github/stars/XueruiSu/Trust-Region-Preference-Approximation)
+- [AdaRFT](https://github.com/uscnlp-lime/verl): Efficient Reinforcement Finetuning via **Adaptive Curriculum Learning** ![GitHub Repo stars](https://img.shields.io/github/stars/uscnlp-lime/verl)
+- [critic-rl](https://github.com/HKUNLP/critic-rl): LLM critics for code generation ![GitHub Repo stars](https://img.shields.io/github/stars/HKUNLP/critic-rl)
+- [self-rewarding-reasoning-LLM](https://arxiv.org/pdf/2502.19613): self-rewarding and correction with **generative reward models** ![GitHub Repo stars](https://img.shields.io/github/stars/RLHFlow/Self-rewarding-reasoning-LLM)
+- [DeepEnlighten](https://github.com/DolbyUUU/DeepEnlighten): Reproduce R1 with **social reasoning** tasks and analyze key findings ![GitHub Repo stars](https://img.shields.io/github/stars/DolbyUUU/DeepEnlighten)
+- [MetaSpatial](https://github.com/PzySeere/MetaSpatial): Reinforcing **3D Spatial Reasoning** in **VLMs** for the **Metaverse** ![GitHub Repo stars](https://img.shields.io/github/stars/PzySeere/MetaSpatial)
+- [PURE](https://github.com/CJReinforce/PURE): **Credit assignment** is the key to successful reinforcement fine-tuning using **process reward model** ![GitHub Repo stars](https://img.shields.io/github/stars/CJReinforce/PURE)
+- [cognitive-behaviors](https://github.com/kanishkg/cognitive-behaviors): Cognitive Behaviors that Enable Self-Improving Reasoners, or, Four Habits of Highly Effective STaRs ![GitHub Repo stars](https://img.shields.io/github/stars/kanishkg/cognitive-behaviors)
+- [deepscaler](https://github.com/agentica-project/rllm/tree/deepscaler): iterative context scaling with GRPO ![GitHub Repo stars](https://img.shields.io/github/stars/agentica-project/deepscaler)
+- [DAPO](https://dapo-sia.github.io/): the fully open source SOTA RL algorithm that beats DeepSeek-R1-zero-32B ![GitHub Repo stars](https://img.shields.io/github/stars/volcengine/verl)
+- [NoisyRollout](https://github.com/NUS-TRAIL/NoisyRollout): Reinforcing Visual Reasoning with Data Augmentation ![GitHub Repo stars](https://img.shields.io/github/stars/NUS-TRAIL/NoisyRollout)
+- [SPEAR](https://github.com/TencentYoutuResearch/SPEAR): **Self-imitation** with **Progressive Exploration** for Agentic Reinforcement Learning (ICLR 2026) ![GitHub Repo stars](https://img.shields.io/github/stars/TencentYoutuResearch/SPEAR)
+
+## Contribution Guide
+
+See [contributions guide](CONTRIBUTING.md)
+
+## About [ByteDance Seed Team](https://team.doubao.com/)
+
+Founded in 2023, ByteDance Seed Team is dedicated to crafting the industry's most advanced AI foundation models. The team aspires to become a world-class research team and make significant contributions to the advancement of science and society. You can get to know Bytedance Seed better through the following channels👇
+
+<div>
+  <a href="https://team.doubao.com/">
+    <img src="https://img.shields.io/badge/Website-%231e37ff?style=for-the-badge&logo=bytedance&logoColor=white"></a>
+  <a href="https://github.com/user-attachments/assets/469535a8-42f2-4797-acdf-4f7a1d4a0c3e">
+    <img src="https://img.shields.io/badge/WeChat-07C160?style=for-the-badge&logo=wechat&logoColor=white"></a>
+ <a href="https://www.xiaohongshu.com/user/profile/668e7e15000000000303157d?xsec_token=ABl2-aqekpytY6A8TuxjrwnZskU-6BsMRE_ufQQaSAvjc%3D&xsec_source=pc_search">
+    <img src="https://img.shields.io/badge/Xiaohongshu-%23FF2442?style=for-the-badge&logo=xiaohongshu&logoColor=white"></a>
+  <a href="https://www.zhihu.com/org/dou-bao-da-mo-xing-tuan-dui/">
+    <img src="https://img.shields.io/badge/zhihu-%230084FF?style=for-the-badge&logo=zhihu&logoColor=white"></a>
+</div>
+
+We are HIRING! Send us an [email](mailto:the.verl.project@gmail.com) if you are interested in internship/FTE opportunities in RL for agents.
diff --git a/code/RL_model/verl/verl_train/verl.egg-info/SOURCES.txt b/code/RL_model/verl/verl_train/verl.egg-info/SOURCES.txt
new file mode 100644
index 0000000000000000000000000000000000000000..590af79a89e30259e78720639873de554fc8c3dc
--- /dev/null
+++ b/code/RL_model/verl/verl_train/verl.egg-info/SOURCES.txt
@@ -0,0 +1,833 @@
+LICENSE
+README.md
+pyproject.toml
+setup.py
+./scripts/__init__.py
+./scripts/converter_hf_to_mcore.py
+./scripts/diagnose.py
+./scripts/init_random_model.py
+./scripts/legacy_model_merger.py
+./scripts/megatron_merge_lora.py
+./scripts/print_cfg.py
+./scripts/rollout_viewer.py
+./tests/__init__.py
+./tests/test_base_config_on_cpu.py
+./tests/test_protocol_on_cpu.py
+./tests/test_protocol_v2_on_cpu.py
+./tests/checkpoint_engine/__init__.py
+./tests/checkpoint_engine/test_correctness_on_gpu.py
+./tests/checkpoint_engine/test_correctness_on_npu.py
+./tests/checkpoint_engine/test_special_server_adapter.py
+./tests/checkpoint_engine/test_utils.py
+./tests/interactions/__init__.py
+./tests/interactions/test_gsm8k_interaction.py
+./tests/interactions/test_interaction_registry.py
+./tests/single_controller/__init__.py
+./tests/single_controller/test_auto_padding_on_cpu.py
+./tests/single_controller/test_colocated_workers.py
+./tests/single_controller/test_colocated_workers_fused.py
+./tests/single_controller/test_data_transfer.py
+./tests/single_controller/test_decorator_on_cpu.py
+./tests/single_controller/test_device_mesh_register.py
+./tests/single_controller/test_driverfunc_to_worker.py
+./tests/single_controller/test_fused_workers_on_cpu.py
+./tests/single_controller/test_get_set_dispatch_collect_cpu.py
+./tests/single_controller/test_high_level_scheduling_api.py
+./tests/single_controller/test_nested_worker.py
+./tests/single_controller/test_ray_collectives.py
+./tests/single_controller/test_ray_local_envs_on_cpu.py
+./tests/single_controller/test_ray_utils_on_cpu.py
+./tests/single_controller/test_rvdz.py
+./tests/single_controller/test_split_resource_pool.py
+./tests/single_controller/test_worker_group_basics.py
+./tests/single_controller/test_worker_group_torch.py
+./tests/special_e2e/__init__.py
+./tests/special_e2e/check_custom_rwd_fn.py
+./tests/special_e2e/check_results.py
+./tests/special_e2e/envs/__init__.py
+./tests/special_e2e/envs/digit_completion/__init__.py
+./tests/special_e2e/envs/digit_completion/task.py
+./tests/special_e2e/envs/digit_completion/tokenizer.py
+./tests/trainer/__init__.py
+./tests/trainer/config/__init__.py
+./tests/trainer/config/test_algo_config_on_cpu.py
+./tests/trainer/config/test_legacy_config_on_cpu.py
+./tests/trainer/ppo/__init__.py
+./tests/trainer/ppo/test_core_algos_on_cpu.py
+./tests/trainer/ppo/test_metric_utils_on_cpu.py
+./tests/trainer/ppo/test_rollout_corr.py
+./tests/trainer/ppo/test_rollout_corr_integration.py
+./verl/__init__.py
+./verl/base_config.py
+./verl/protocol.py
+./verl/py.typed
+./verl/checkpoint_engine/__init__.py
+./verl/checkpoint_engine/base.py
+./verl/checkpoint_engine/hccl_checkpoint_engine.py
+./verl/checkpoint_engine/nccl_checkpoint_engine.py
+./verl/checkpoint_engine/nixl_checkpoint_engine.py
+./verl/experimental/__init__.py
+./verl/experimental/agent_loop/__init__.py
+./verl/experimental/agent_loop/agent_loop.py
+./verl/experimental/agent_loop/prometheus_utils.py
+./verl/experimental/agent_loop/single_turn_agent_loop.py
+./verl/experimental/agent_loop/tool_agent_loop.py
+./verl/experimental/agent_loop/tool_parser.py
+./verl/experimental/agent_loop/utils.py
+./verl/experimental/dataset/__init__.py
+./verl/experimental/dataset/sampler.py
+./verl/experimental/dynamic_dataset/__init__.py
+./verl/experimental/dynamic_dataset/dynamicgen_dataset.py
+./verl/experimental/reward_loop/__init__.py
+./verl/experimental/reward_loop/reward_loop.py
+./verl/experimental/reward_loop/reward_model.py
+./verl/experimental/reward_loop/reward_manager/__init__.py
+./verl/experimental/reward_loop/reward_manager/base.py
+./verl/experimental/reward_loop/reward_manager/dapo.py
+./verl/experimental/reward_loop/reward_manager/limited.py
+./verl/experimental/reward_loop/reward_manager/naive.py
+./verl/experimental/reward_loop/reward_manager/registry.py
+./verl/experimental/reward_loop/reward_manager/remote.py
+./verl/interactions/__init__.py
+./verl/interactions/base.py
+./verl/interactions/gsm8k_interaction.py
+./verl/interactions/weather_interaction.py
+./verl/interactions/utils/__init__.py
+./verl/interactions/utils/interaction_registry.py
+./verl/model_merger/__init__.py
+./verl/model_merger/__main__.py
+./verl/model_merger/base_model_merger.py
+./verl/model_merger/fsdp_model_merger.py
+./verl/model_merger/megatron_model_merger.py
+./verl/models/__init__.py
+./verl/models/registry.py
+./verl/models/weight_loader_registry.py
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+verl/models/mcore/qwen2_5_vl/vision_model.py
+verl/models/mcore/qwen2_5_vl/vision_transformer_block.py
+verl/models/qwen2/__init__.py
+verl/models/qwen2/megatron/__init__.py
+verl/models/qwen2/megatron/modeling_qwen2_megatron.py
+verl/models/qwen2/megatron/checkpoint_utils/__init__.py
+verl/models/qwen2/megatron/checkpoint_utils/qwen2_loader.py
+verl/models/qwen2/megatron/checkpoint_utils/qwen2_loader_depracated.py
+verl/models/qwen2/megatron/checkpoint_utils/qwen2_saver.py
+verl/models/qwen2/megatron/layers/__init__.py
+verl/models/qwen2/megatron/layers/parallel_attention.py
+verl/models/qwen2/megatron/layers/parallel_decoder.py
+verl/models/qwen2/megatron/layers/parallel_linear.py
+verl/models/qwen2/megatron/layers/parallel_mlp.py
+verl/models/qwen2/megatron/layers/parallel_rmsnorm.py
+verl/models/transformers/__init__.py
+verl/models/transformers/apertus.py
+verl/models/transformers/dense_common.py
+verl/models/transformers/glm4v.py
+verl/models/transformers/kimi_vl.py
+verl/models/transformers/llama.py
+verl/models/transformers/monkey_patch.py
+verl/models/transformers/npu_patch.py
+verl/models/transformers/qwen2.py
+verl/models/transformers/qwen2_vl.py
+verl/models/transformers/qwen3_vl.py
+verl/models/transformers/tiled_mlp.py
+verl/single_controller/__init__.py
+verl/single_controller/base/__init__.py
+verl/single_controller/base/decorator.py
+verl/single_controller/base/worker.py
+verl/single_controller/base/worker_group.py
+verl/single_controller/ray/__init__.py
+verl/single_controller/ray/base.py
+verl/third_party/__init__.py
+verl/third_party/torch/__init__.py
+verl/third_party/torch/distributed/__init__.py
+verl/third_party/torch/distributed/_state_dict_utils.py
+verl/third_party/torch/distributed/checkpoint/__init__.py
+verl/third_party/torch/distributed/checkpoint/state_dict.py
+verl/third_party/vllm/__init__.py
+verl/tools/__init__.py
+verl/tools/base_tool.py
+verl/tools/geo3k_tool.py
+verl/tools/gsm8k_tool.py
+verl/tools/image_zoom_in_tool.py
+verl/tools/mcp_base_tool.py
+verl/tools/mcp_search_tool.py
+verl/tools/sandbox_fusion_tools.py
+verl/tools/schemas.py
+verl/tools/search_tool.py
+verl/tools/utils/__init__.py
+verl/tools/utils/search_r1_like_utils.py
+verl/tools/utils/tool_registry.py
+verl/trainer/__init__.py
+verl/trainer/constants_ppo.py
+verl/trainer/fsdp_sft_trainer.py
+verl/trainer/main_eval.py
+verl/trainer/main_generation.py
+verl/trainer/main_generation_server.py
+verl/trainer/main_ppo.py
+verl/trainer/sft_trainer.py
+verl/trainer/sft_trainer_ray.py
+verl/trainer/config/__init__.py
+verl/trainer/config/_generated_ppo_megatron_trainer.yaml
+verl/trainer/config/_generated_ppo_trainer.yaml
+verl/trainer/config/algorithm.py
+verl/trainer/config/config.py
+verl/trainer/config/evaluation.yaml
+verl/trainer/config/generation.yaml
+verl/trainer/config/ppo_megatron_trainer.yaml
+verl/trainer/config/ppo_trainer.yaml
+verl/trainer/config/reward_manager.yaml
+verl/trainer/config/sft_trainer.yaml
+verl/trainer/config/sft_trainer_engine.yaml
+verl/trainer/config/actor/actor.yaml
+verl/trainer/config/actor/dp_actor.yaml
+verl/trainer/config/actor/megatron_actor.yaml
+verl/trainer/config/algorithm/rollout_correction.yaml
+verl/trainer/config/critic/critic.yaml
+verl/trainer/config/critic/dp_critic.yaml
+verl/trainer/config/critic/megatron_critic.yaml
+verl/trainer/config/data/legacy_data.yaml
+verl/trainer/config/engine/fsdp.yaml
+verl/trainer/config/engine/megatron.yaml
+verl/trainer/config/engine/veomni.yaml
+verl/trainer/config/model/hf_model.yaml
+verl/trainer/config/npu_profile/npu_profile.yaml
+verl/trainer/config/optim/fsdp.yaml
+verl/trainer/config/optim/megatron.yaml
+verl/trainer/config/optim/veomni.yaml
+verl/trainer/config/profiler/profiler.yaml
+verl/trainer/config/ref/dp_ref.yaml
+verl/trainer/config/ref/megatron_ref.yaml
+verl/trainer/config/ref/ref.yaml
+verl/trainer/config/reward_model/dp_reward_loop.yaml
+verl/trainer/config/reward_model/dp_reward_model.yaml
+verl/trainer/config/reward_model/megatron_reward_loop.yaml
+verl/trainer/config/reward_model/megatron_reward_model.yaml
+verl/trainer/config/reward_model/reward_model.yaml
+verl/trainer/config/rollout/rollout.yaml
+verl/trainer/ppo/__init__.py
+verl/trainer/ppo/core_algos.py
+verl/trainer/ppo/metric_utils.py
+verl/trainer/ppo/prefix_grouper_utils.py
+verl/trainer/ppo/ray_trainer.py
+verl/trainer/ppo/reward.py
+verl/trainer/ppo/rollout_corr_helper.py
+verl/trainer/ppo/utils.py
+verl/utils/__init__.py
+verl/utils/activation_offload.py
+verl/utils/attention_utils.py
+verl/utils/chat_template.py
+verl/utils/config.py
+verl/utils/device.py
+verl/utils/distributed.py
+verl/utils/flops_counter.py
+verl/utils/fs.py
+verl/utils/fsdp_utils.py
+verl/utils/groupwise.py
+verl/utils/hdfs_io.py
+verl/utils/import_utils.py
+verl/utils/logging_utils.py
+verl/utils/megatron_peft_utils.py
+verl/utils/megatron_utils.py
+verl/utils/memory_buffer.py
+verl/utils/memory_utils.py
+verl/utils/model.py
+verl/utils/net_utils.py
+verl/utils/npu_flash_attn_utils.py
+verl/utils/py_functional.py
+verl/utils/ray_utils.py
+verl/utils/rollout_skip.py
+verl/utils/rollout_trace.py
+verl/utils/seqlen_balancing.py
+verl/utils/tensordict_utils.py
+verl/utils/tokenizer.py
+verl/utils/torch_dtypes.py
+verl/utils/torch_functional.py
+verl/utils/tracking.py
+verl/utils/transferqueue_utils.py
+verl/utils/transformers_compat.py
+verl/utils/ulysses.py
+verl/utils/checkpoint/__init__.py
+verl/utils/checkpoint/checkpoint_handler.py
+verl/utils/checkpoint/checkpoint_manager.py
+verl/utils/checkpoint/fsdp_checkpoint_manager.py
+verl/utils/checkpoint/megatron_checkpoint_manager.py
+verl/utils/dataset/__init__.py
+verl/utils/dataset/dataset_utils.py
+verl/utils/dataset/multiturn_sft_dataset.py
+verl/utils/dataset/rl_dataset.py
+verl/utils/dataset/rm_dataset.py
+verl/utils/dataset/sft_dataset.py
+verl/utils/dataset/vision_utils.py
+verl/utils/debug/__init__.py
+verl/utils/debug/metrics.py
+verl/utils/debug/performance.py
+verl/utils/debug/trajectory_tracker.py
+verl/utils/experimental/__init__.py
+verl/utils/experimental/torch_functional.py
+verl/utils/kernel/__init__.py
+verl/utils/kernel/fp8_kernel.py
+verl/utils/kernel/kernels.py
+verl/utils/kernel/linear_cross_entropy.py
+verl/utils/logger/__init__.py
+verl/utils/logger/aggregate_logger.py
+verl/utils/megatron/__init__.py
+verl/utils/megatron/dist_checkpointing.py
+verl/utils/megatron/memory.py
+verl/utils/megatron/optimizer.py
+verl/utils/megatron/pipeline_parallel.py
+verl/utils/megatron/router_replay_patch.py
+verl/utils/megatron/router_replay_utils.py
+verl/utils/megatron/sequence_parallel.py
+verl/utils/megatron/tensor_parallel.py
+verl/utils/metric/__init__.py
+verl/utils/metric/utils.py
+verl/utils/profiler/__init__.py
+verl/utils/profiler/config.py
+verl/utils/profiler/empty_annotations.py
+verl/utils/profiler/mstx_profile.py
+verl/utils/profiler/nvtx_profile.py
+verl/utils/profiler/performance.py
+verl/utils/profiler/profile.py
+verl/utils/profiler/torch_profile.py
+verl/utils/rendezvous/__init__.py
+verl/utils/rendezvous/ray_backend.py
+verl/utils/reward_score/__init__.py
+verl/utils/reward_score/geo3k.py
+verl/utils/reward_score/gsm8k.py
+verl/utils/reward_score/math_batch.py
+verl/utils/reward_score/math_dapo.py
+verl/utils/reward_score/math_reward.py
+verl/utils/reward_score/math_verify.py
+verl/utils/reward_score/search_r1_like_qa_em.py
+verl/utils/reward_score/prime_code/__init__.py
+verl/utils/reward_score/prime_code/testing_util.py
+verl/utils/reward_score/prime_code/utils.py
+verl/utils/reward_score/prime_math/__init__.py
+verl/utils/reward_score/prime_math/grader.py
+verl/utils/reward_score/prime_math/math_normalize.py
+verl/utils/reward_score/sandbox_fusion/__init__.py
+verl/utils/reward_score/sandbox_fusion/utils.py
+verl/utils/vllm/__init__.py
+verl/utils/vllm/patch.py
+verl/utils/vllm/utils.py
+verl/utils/vllm/vllm_fp8_utils.py
+verl/version/version
+verl/workers/__init__.py
+verl/workers/engine_workers.py
+verl/workers/fsdp_workers.py
+verl/workers/megatron_workers.py
+verl/workers/actor/__init__.py
+verl/workers/actor/base.py
+verl/workers/actor/dp_actor.py
+verl/workers/actor/megatron_actor.py
+verl/workers/config/__init__.py
+verl/workers/config/actor.py
+verl/workers/config/critic.py
+verl/workers/config/engine.py
+verl/workers/config/megatron_peft.py
+verl/workers/config/model.py
+verl/workers/config/optimizer.py
+verl/workers/config/reward_model.py
+verl/workers/config/rollout.py
+verl/workers/critic/__init__.py
+verl/workers/critic/base.py
+verl/workers/critic/dp_critic.py
+verl/workers/critic/megatron_critic.py
+verl/workers/engine/__init__.py
+verl/workers/engine/base.py
+verl/workers/engine/utils.py
+verl/workers/engine/fsdp/__init__.py
+verl/workers/engine/fsdp/transformer_impl.py
+verl/workers/engine/fsdp/utils.py
+verl/workers/engine/megatron/__init__.py
+verl/workers/engine/megatron/transformer_impl.py
+verl/workers/engine/megatron/utils.py
+verl/workers/engine/mindspeed/__init__.py
+verl/workers/engine/mindspeed/transformer_impl.py
+verl/workers/engine/veomni/__init__.py
+verl/workers/engine/veomni/transformer_impl.py
+verl/workers/engine/veomni/utils.py
+verl/workers/reward_manager/__init__.py
+verl/workers/reward_manager/abstract.py
+verl/workers/reward_manager/batch.py
+verl/workers/reward_manager/dapo.py
+verl/workers/reward_manager/naive.py
+verl/workers/reward_manager/prime.py
+verl/workers/reward_manager/registry.py
+verl/workers/reward_model/__init__.py
+verl/workers/reward_model/base.py
+verl/workers/reward_model/megatron/__init__.py
+verl/workers/reward_model/megatron/reward_model.py
+verl/workers/rollout/__init__.py
+verl/workers/rollout/base.py
+verl/workers/rollout/hf_rollout.py
+verl/workers/rollout/replica.py
+verl/workers/rollout/schemas.py
+verl/workers/rollout/tokenizer.py
+verl/workers/rollout/utils.py
+verl/workers/rollout/naive/__init__.py
+verl/workers/rollout/naive/naive_rollout.py
+verl/workers/rollout/sglang_rollout/__init__.py
+verl/workers/rollout/sglang_rollout/async_sglang_server.py
+verl/workers/rollout/sglang_rollout/http_server_engine.py
+verl/workers/rollout/sglang_rollout/sglang_rollout.py
+verl/workers/rollout/sglang_rollout/utils.py
+verl/workers/rollout/vllm_rollout/__init__.py
+verl/workers/rollout/vllm_rollout/utils.py
+verl/workers/rollout/vllm_rollout/vllm_async_server.py
+verl/workers/rollout/vllm_rollout/vllm_rollout.py
+verl/workers/sharding_manager/__init__.py
+verl/workers/sharding_manager/base.py
+verl/workers/sharding_manager/fsdp_ulysses.py
+verl/workers/utils/__init__.py
+verl/workers/utils/losses.py
+verl/workers/utils/padding.py
\ No newline at end of file
diff --git a/code/RL_model/verl/verl_train/verl.egg-info/dependency_links.txt b/code/RL_model/verl/verl_train/verl.egg-info/dependency_links.txt
new file mode 100644
index 0000000000000000000000000000000000000000..8b137891791fe96927ad78e64b0aad7bded08bdc
--- /dev/null
+++ b/code/RL_model/verl/verl_train/verl.egg-info/dependency_links.txt
@@ -0,0 +1 @@
+
diff --git a/code/RL_model/verl/verl_train/verl.egg-info/requires.txt b/code/RL_model/verl/verl_train/verl.egg-info/requires.txt
new file mode 100644
index 0000000000000000000000000000000000000000..8ba934f0cfd88e277c04a99e905fa799f7ea6881
--- /dev/null
+++ b/code/RL_model/verl/verl_train/verl.egg-info/requires.txt
@@ -0,0 +1,61 @@
+accelerate
+codetiming
+datasets
+dill
+hydra-core
+numpy<2.0.0
+pandas
+peft
+pyarrow>=19.0.0
+pybind11
+pylatexenc
+ray[default]>=2.41.0
+torchdata
+tensordict!=0.9.0,<=0.10.0,>=0.8.0
+transformers
+wandb
+packaging>=20.0
+tensorboard
+
+[geo]
+mathruler
+torchvision
+qwen_vl_utils
+
+[gpu]
+liger-kernel
+flash-attn
+
+[math]
+math-verify
+
+[mcore]
+mbridge
+
+[prime]
+pyext
+
+[sglang]
+tensordict!=0.9.0,<=0.10.0,>=0.8.0
+sglang[openai,srt]==0.5.6
+torch==2.9.1
+
+[test]
+pytest
+pre-commit
+py-spy
+pytest-asyncio
+pytest-rerunfailures
+
+[transferqueue]
+TransferQueue==0.1.5
+
+[trl]
+trl<=0.9.6
+
+[trtllm]
+tensorrt-llm>=1.2.0rc6
+
+[vllm]
+tensordict!=0.9.0,<=0.10.0,>=0.8.0
+vllm<=0.12.0,>=0.8.5
diff --git a/code/RL_model/verl/verl_train/verl.egg-info/top_level.txt b/code/RL_model/verl/verl_train/verl.egg-info/top_level.txt
new file mode 100644
index 0000000000000000000000000000000000000000..f655d798cdd5ad03c4cdd162d4a96bd8ac0d6057
--- /dev/null
+++ b/code/RL_model/verl/verl_train/verl.egg-info/top_level.txt
@@ -0,0 +1,3 @@
+scripts
+tests
+verl
diff --git a/code/RL_model/verl/verl_train/verl/__init__.py b/code/RL_model/verl/verl_train/verl/__init__.py
new file mode 100644
index 0000000000000000000000000000000000000000..bf67910103c037515a11b3ad15177615c2c019f8
--- /dev/null
+++ b/code/RL_model/verl/verl_train/verl/__init__.py
@@ -0,0 +1,103 @@
+# Copyright 2024 Bytedance Ltd. and/or its affiliates
+#
+# Licensed under the Apache License, Version 2.0 (the "License");
+# you may not use this file except in compliance with the License.
+# You may obtain a copy of the License at
+#
+#     http://www.apache.org/licenses/LICENSE-2.0
+#
+# Unless required by applicable law or agreed to in writing, software
+# distributed under the License is distributed on an "AS IS" BASIS,
+# WITHOUT WARRANTIES OR CONDITIONS OF ANY KIND, either express or implied.
+# See the License for the specific language governing permissions and
+# limitations under the License.
+
+import importlib
+import logging
+import os
+
+from packaging.version import parse as parse_version
+
+from .protocol import DataProto
+from .utils.device import is_npu_available
+from .utils.import_utils import import_external_libs
+from .utils.logging_utils import set_basic_config
+
+version_folder = os.path.dirname(os.path.join(os.path.abspath(__file__)))
+
+with open(os.path.join(version_folder, "version/version")) as f:
+    __version__ = f.read().strip()
+
+
+set_basic_config(level=logging.WARNING)
+
+
+__all__ = ["DataProto", "__version__"]
+
+
+modules = os.getenv("VERL_USE_EXTERNAL_MODULES", "")
+if modules:
+    modules = modules.split(",")
+    import_external_libs(modules)
+
+
+if os.getenv("VERL_USE_MODELSCOPE", "False").lower() == "true":
+    if importlib.util.find_spec("modelscope") is None:
+        raise ImportError("You are using the modelscope hub, please install modelscope by `pip install modelscope -U`")
+    # Patch hub to download models from modelscope to speed up.
+    from modelscope.utils.hf_util import patch_hub
+
+    patch_hub()
+
+
+if is_npu_available:
+    # Workaround for torch-npu's lack of support for creating nested tensors from NPU tensors.
+    #
+    # ```
+    # >>> a, b = torch.arange(3).npu(), torch.arange(5).npu() + 3
+    # >>> nt = torch.nested.nested_tensor([a, b], layout=torch.jagged)
+    # ```
+    # throws "not supported in npu" on Ascend NPU.
+    # See https://github.com/Ascend/pytorch/blob/294cdf5335439b359991cecc042957458a8d38ae/torch_npu/utils/npu_intercept.py#L109
+    # for details.
+
+    import torch
+
+    try:
+        if hasattr(torch.nested.nested_tensor, "__wrapped__"):
+            torch.nested.nested_tensor = torch.nested.nested_tensor.__wrapped__
+        if hasattr(torch.nested.as_nested_tensor, "__wrapped__"):
+            torch.nested.as_nested_tensor = torch.nested.as_nested_tensor.__wrapped__
+    except AttributeError:
+        pass
+
+    # Apply patches about transformers
+    from .models.transformers import npu_patch as npu_patch  # noqa
+
+    # In verl, the driver process aggregates the computation results of workers via Ray.
+    # Therefore, after a worker completes its computation job, it will package the output
+    # using tensordict and transfer it to the CPU. Since the `to` operation of tensordict
+    # is non-blocking, when transferring data from a device to the CPU, it is necessary to
+    # ensure that a batch of data has been completely transferred before being used on the
+    # host; otherwise, unexpected precision issues may arise. Tensordict has already noticed
+    # this problem and fixed it. Ref: https://github.com/pytorch/tensordict/issues/725
+    # However, the relevant modifications only cover CUDA and MPS devices and do not take effect
+    # for third-party devices such as NPUs. This patch fixes this issue, and the relevant
+    # modifications can be removed once the fix is merged into tensordict.
+
+    import tensordict
+
+    if parse_version(tensordict.__version__) < parse_version("0.10.0"):
+        from tensordict.base import TensorDictBase
+
+        def _sync_all_patch(self):
+            from torch._utils import _get_available_device_type, _get_device_module
+
+            device_type = _get_available_device_type()
+            if device_type is None:
+                return
+
+            device_module = _get_device_module(device_type)
+            device_module.synchronize()
+
+        TensorDictBase._sync_all = _sync_all_patch
diff --git a/code/RL_model/verl/verl_train/verl/base_config.py b/code/RL_model/verl/verl_train/verl/base_config.py
new file mode 100644
index 0000000000000000000000000000000000000000..f425dd1464b0f13c83a0944249cd84d55903f120
--- /dev/null
+++ b/code/RL_model/verl/verl_train/verl/base_config.py
@@ -0,0 +1,86 @@
+# Copyright 2025 Bytedance Ltd. and/or its affiliates
+
+# Licensed under the Apache License, Version 2.0 (the "License");
+# you may not use this file except in compliance with the License.
+# You may obtain a copy of the License at
+#
+#     http://www.apache.org/licenses/LICENSE-2.0
+#
+# Unless required by applicable law or agreed to in writing, software
+# distributed under the License is distributed on an "AS IS" BASIS,
+# WITHOUT WARRANTIES OR CONDITIONS OF ANY KIND, either express or implied.
+# See the License for the specific language governing permissions and
+# limitations under the License.
+
+import collections
+from dataclasses import FrozenInstanceError, dataclass, fields
+from typing import Any
+
+
+# BaseConfig class inherits from collections.abc.Mapping, which means it can act like a dictionary
+@dataclass
+class BaseConfig(collections.abc.Mapping):
+    """The BaseConfig provides dict-like interface for a dataclass config.
+
+    By default all fields in the config is not mutable, unless specified in
+    "_mutable_fields". The BaseConfig class implements the Mapping Abstract Base Class.
+    This allows instances of this class to be used like dictionaries.
+    """
+
+    _mutable_fields = set()
+    _target_: str = ""
+
+    def __setattr__(self, name: str, value):
+        """Set the value of an attribute. Check if the attr is mutable before setting the value."""
+        # If the field already exists, it's considered frozen unless it's in _mutable_fields
+        if name in self.__dict__ and name not in getattr(self, "_mutable_fields", set()):
+            raise FrozenInstanceError(f"Field '{name}' is frozen and cannot be modified")
+        super().__setattr__(name, value)
+
+    def get(self, key: str, default: Any = None) -> Any:
+        """Get the value associated with the given key. If the key does not exist, return the default value.
+
+        Args:
+            key (str): The attribute name to retrieve.
+            default (Any, optional): The value to return if the attribute does not exist. Defaults to None.
+
+        Returns:
+            Any: The value of the attribute or the default value.
+        """
+        try:
+            return getattr(self, key)
+        except AttributeError:
+            return default
+
+    def __getitem__(self, key: str):
+        """Implement the [] operator for the class. Allows accessing attributes like dictionary items.
+
+        Args:
+            key (str): The attribute name to retrieve.
+
+        Returns:
+            Any: The value of the attribute.
+
+        Raises:
+            AttributeError: If the attribute does not exist.
+            TypeError: If the key type is not string
+        """
+        return getattr(self, key)
+
+    def __iter__(self):
+        """Implement the iterator protocol. Allows iterating over the attribute names of the instance.
+
+        Yields:
+            str: The name of each field in the dataclass.
+        """
+        for f in fields(self):
+            yield f.name
+
+    def __len__(self):
+        """
+        Return the number of fields in the dataclass.
+
+        Returns:
+            int: The number of fields in the dataclass.
+        """
+        return len(fields(self))
diff --git a/code/RL_model/verl/verl_train/verl/protocol.py b/code/RL_model/verl/verl_train/verl/protocol.py
new file mode 100644
index 0000000000000000000000000000000000000000..27a1f6a1f940baef9dc8c98c5f48fe0c0321ba3d
--- /dev/null
+++ b/code/RL_model/verl/verl_train/verl/protocol.py
@@ -0,0 +1,1253 @@
+# Copyright 2024 Bytedance Ltd. and/or its affiliates
+#
+# Licensed under the Apache License, Version 2.0 (the "License");
+# you may not use this file except in compliance with the License.
+# You may obtain a copy of the License at
+#
+#     http://www.apache.org/licenses/LICENSE-2.0
+#
+# Unless required by applicable law or agreed to in writing, software
+# distributed under the License is distributed on an "AS IS" BASIS,
+# WITHOUT WARRANTIES OR CONDITIONS OF ANY KIND, either express or implied.
+# See the License for the specific language governing permissions and
+# limitations under the License.
+"""
+Implement base data transfer protocol between any two functions, modules.
+We can subclass Protocol to define more detailed batch info with specific keys
+"""
+
+import contextlib
+import copy
+import logging
+import math
+import os
+import pickle
+from dataclasses import dataclass, field
+from typing import Any, Callable, Optional
+
+import numpy as np
+import ray
+import tensordict
+import torch
+import torch.distributed
+from packaging import version
+from packaging.version import parse as parse_version
+from tensordict import TensorDict
+from torch.utils.data import DataLoader
+
+from verl.utils.device import get_device_id, get_torch_device
+from verl.utils.py_functional import union_two_dict
+from verl.utils.torch_functional import allgather_dict_tensors
+
+__all__ = ["DataProto", "union_tensor_dict"]
+
+with contextlib.suppress(Exception):
+    tensordict.set_lazy_legacy(False).set()
+    if parse_version(tensordict.__version__) < parse_version("0.10.0"):
+        tensordict.set_list_to_stack(True).set()
+
+
+class _DataProtoConfigMeta(type):
+    _config = {}
+
+    auto_padding_key = "_verl_auto_padding"
+
+    @property
+    def auto_padding(cls):
+        enabled_by_env = os.getenv("VERL_AUTO_PADDING", "FALSE").upper() in ["TRUE", "1"]
+        return enabled_by_env or cls._config.get(cls.auto_padding_key, False)
+
+    @auto_padding.setter
+    def auto_padding(cls, enabled: bool):
+        assert isinstance(enabled, bool), f"enabled must be a boolean, got {enabled} as {type(enabled)}"
+        cls._config[cls.auto_padding_key] = enabled
+
+
+class DataProtoConfig(metaclass=_DataProtoConfigMeta):
+    pass
+
+
+_padding_size_key = "_padding_size_key_x123d"
+
+
+def pad_dataproto_to_divisor(data: "DataProto", size_divisor: int):
+    """Pad a DataProto to size divisible by size_divisor
+
+    Args:
+        size_divisor (int): size divisor
+
+    Returns:
+        data: (DataProto): the padded DataProto
+        pad_size (int)
+    """
+    assert isinstance(data, DataProto), "data must be a DataProto"
+    if len(data) % size_divisor != 0:
+        pad_size = size_divisor - len(data) % size_divisor
+        padding_protos = []
+        remaining_pad = pad_size
+        while remaining_pad > 0:
+            take_size = min(remaining_pad, len(data))
+            padding_protos.append(data[:take_size])
+            remaining_pad -= take_size
+        data_padded = DataProto.concat([data] + padding_protos)
+    else:
+        if len(data) == 0:
+            logging.warning("padding a DataProto with no item, no changed made")
+        pad_size = 0
+        data_padded = data
+    return data_padded, pad_size
+
+
+def unpad_dataproto(data: "DataProto", pad_size):
+    """Unpad the data proto with pad_size. i.e. `data[:-pad_size]`"""
+    if pad_size != 0:
+        data = data[:-pad_size]
+    return data
+
+
+def union_tensor_dict(tensor_dict1: TensorDict, tensor_dict2: TensorDict) -> TensorDict:
+    """Union two tensordicts."""
+    assert tensor_dict1.batch_size == tensor_dict2.batch_size, (
+        f"Two tensor dict must have identical batch size. Got {tensor_dict1.batch_size} and {tensor_dict2.batch_size}"
+    )
+    for key in tensor_dict2.keys():
+        if key not in tensor_dict1.keys():
+            tensor_dict1[key] = tensor_dict2[key]
+        else:
+            assert tensor_dict1[key].equal(tensor_dict2[key]), (
+                f"{key} in tensor_dict1 and tensor_dict2 are not the same object"
+            )
+
+    return tensor_dict1
+
+
+def _array_equal(array1: np.ndarray, array2: np.ndarray, visited: set[int]) -> bool:
+    """
+    Recursively compares two NumPy arrays for strict equality, with special
+    handling for object-dtype arrays, NaN values, and circular references.
+    This function assumes that the two arguments provided are NumPy arrays.
+
+    Args:
+        array1: The first NumPy array.
+        array2: The second NumPy array.
+
+    Returns:
+        True if the arrays' dtypes, shapes, and all elements are equal.
+    """
+    # Check dtype and shape first, as this is the fastest failure path.
+    if array1.dtype != array2.dtype or array1.shape != array2.shape:
+        return False
+
+    # For non-object dtypes, use NumPy's implementation with equal_nan=True.
+    if array1.dtype != "object":
+        return np.array_equal(array1, array2, equal_nan=True)
+
+    # For object-dtype arrays, we must recursively compare each element.
+    # We delegate to _deep_equal to handle elements, as they could be any
+    # type, including other nested arrays or NaNs.
+    return all(_deep_equal(x, y, visited) for x, y in zip(array1.flat, array2.flat, strict=False))
+
+
+def _deep_equal(a: Any, b: Any, visited: set[int]) -> bool:
+    """
+    Recursively performs a deep comparison between two Python objects.
+    - Handles NaN values correctly (NaN == NaN evaluates to True).
+    - Handling circular references.
+    - Dispatches to _array_equal if both objects are NumPy arrays.
+    - Otherwise, uses standard '==' comparison.
+    """
+    if type(a) is not type(b):
+        return False
+
+    # If we have seen this object ID before on this path, it's a cycle.
+    # Since we already know the types match, we can safely assume this part
+    # of the structure is equal.
+    obj_id = id(a)
+    if obj_id in visited:
+        return True
+
+    visited.add(obj_id)
+
+    # Perform the specific comparison based on type
+    result = False
+    if isinstance(a, float) and math.isnan(a) and math.isnan(b):
+        result = True
+    elif isinstance(a, np.ndarray):
+        # We know b is also an ndarray due to the initial type check
+        result = _array_equal(a, b, visited)
+    else:
+        # Standard equality for all other types
+        result = a == b
+
+    # Clean up the visited set on the way out of the recursion
+    visited.remove(obj_id)
+    return result
+
+
+def union_numpy_dict(tensor_dict1: dict[str, np.ndarray], tensor_dict2: dict[str, np.ndarray]) -> dict[str, np.ndarray]:
+    for key, val in tensor_dict2.items():
+        if key in tensor_dict1:
+            assert isinstance(tensor_dict2[key], np.ndarray)
+            assert isinstance(tensor_dict1[key], np.ndarray)
+            # to properly deal with nan and object type
+            assert _deep_equal(tensor_dict1[key], tensor_dict2[key], visited=set()), (
+                f"`{key}` in tensor_dict1 and tensor_dict2 are not the same object."
+            )
+        tensor_dict1[key] = val
+
+    return tensor_dict1
+
+
+def list_of_dict_to_dict_of_list(list_of_dict: list[dict]):
+    if len(list_of_dict) == 0:
+        return {}
+    keys = list_of_dict[0].keys()
+    output = {key: [] for key in keys}
+    for data in list_of_dict:
+        for key, item in data.items():
+            assert key in output
+            output[key].append(item)
+    return output
+
+
+def fold_batch_dim(data: "DataProto", new_batch_size):
+    """
+    Fold a batch dim from [bsz, xxx] into [new_bsz, bsz // new_bsz, xxx]
+    """
+    batch_size = data.batch.batch_size[0]
+
+    assert batch_size % new_batch_size == 0
+
+    tensor: TensorDict = data.batch
+    non_tensor = data.non_tensor_batch
+
+    tensor = tensor.view(new_batch_size, -1)
+    tensor.auto_batch_size_(batch_dims=1)
+
+    for key, val in non_tensor.items():
+        non_tensor[key] = np.reshape(val, newshape=(new_batch_size, -1, *val.shape[1:]))
+
+    return type(data)(batch=tensor, non_tensor_batch=non_tensor, meta_info=data.meta_info)
+
+
+def unfold_batch_dim(data: "DataProto", batch_dims=2):
+    """
+    Unfold the first n dims as new batch dim
+    """
+    tensor: TensorDict = data.batch
+    non_tensor = data.non_tensor_batch
+    tensor.auto_batch_size_(batch_dims=batch_dims)
+    tensor = tensor.view(-1)
+
+    batch_size = tensor.batch_size[0]
+
+    non_tensor_new = {}
+
+    for key, val in non_tensor.items():
+        non_tensor_new[key] = np.reshape(val, newshape=(batch_size, *val.shape[batch_dims:]))
+
+    return type(data)(batch=tensor, non_tensor_batch=non_tensor_new, meta_info=data.meta_info)
+
+
+def serialize_single_tensor(obj: torch.Tensor) -> tuple[str, tuple[int, ...], int | memoryview]:
+    data = obj.flatten().contiguous().view(torch.uint8).numpy()
+    dtype = str(obj.dtype).removeprefix("torch.")
+    return dtype, obj.shape, data
+
+
+def serialize_tensordict(batch: TensorDict) -> tuple[tuple[int, ...], Optional[str], dict[str, tuple[str, Any]]]:
+    encoded_items: dict[str, tuple[Any]] = {}
+    for k, v in batch.items():
+        if not v.is_nested:
+            encoded_items[k] = serialize_single_tensor(v)
+        else:
+            layout = str(v.layout).removeprefix("torch.")
+            data = [serialize_single_tensor(tensor) for tensor in v.unbind()]
+            encoded_items[k] = (layout, data)
+
+    batch_size = tuple(batch.batch_size)
+    device = str(batch.device) if batch.device is not None else None
+    return batch_size, device, encoded_items
+
+
+def deserialize_single_tensor(arr: Any) -> torch.Tensor:
+    dtype, shape, data = arr
+
+    torch_dtype = getattr(torch, dtype)
+    assert isinstance(torch_dtype, torch.dtype)
+
+    buffer = bytearray(data)
+    # Create uint8 array
+    arr = torch.frombuffer(buffer, dtype=torch.uint8)
+    # Convert back to proper shape & type
+    return arr.view(torch_dtype).view(shape)
+
+
+def deserialize_tensordict(arr: Any) -> TensorDict:
+    batch_size, device, encoded_items = arr
+    decoded_items: dict[str, Any] = {}
+
+    for k, v in encoded_items.items():
+        if len(v) == 3:
+            # decode single tensor
+            decoded_items[k] = deserialize_single_tensor(v)
+        elif len(v) == 2:
+            # decode nested tensor
+            layout, data = v
+            torch_layout = getattr(torch, layout)
+            decoded_items[k] = torch.nested.as_nested_tensor(
+                [deserialize_single_tensor(tensor) for tensor in data], layout=torch_layout
+            )
+        else:
+            raise ValueError(f"Invalid tensor encoding format, expected length 2 or 3, got {len(v)}")
+
+    return TensorDict(source=decoded_items, batch_size=batch_size, device=device)
+
+
+def collate_fn(x: list["DataProtoItem"]):
+    batch = []
+    non_tensor_batch = []
+    for data in x:
+        batch.append(data.batch)
+        non_tensor_batch.append(data.non_tensor_batch)
+    batch = torch.stack(batch).contiguous()
+    non_tensor_batch = list_of_dict_to_dict_of_list(non_tensor_batch)
+    for key, val in non_tensor_batch.items():
+        non_tensor_batch[key] = np.array(val, dtype=object)
+    return DataProto(batch=batch, non_tensor_batch=non_tensor_batch)
+
+
+@dataclass
+class DataProtoItem:
+    # TODO(zhangchi.usc1992) add consistency check
+    batch: TensorDict = None
+    non_tensor_batch: dict = field(default_factory=dict)
+    meta_info: dict = field(default_factory=dict)
+
+
+@dataclass
+class DataProto:
+    """
+    A DataProto is a data structure that aims to provide a standard protocol for data exchange between functions.
+    It contains a batch (TensorDict) and a meta_info (Dict). The batch is a TensorDict https://pytorch.org/tensordict/.
+    TensorDict allows you to manipulate a dictionary of Tensors like a single Tensor. Ideally, the tensors with the
+    same batch size should be put inside batch.
+    """
+
+    batch: TensorDict = None
+    non_tensor_batch: dict = field(default_factory=dict)
+    meta_info: dict = field(default_factory=dict)
+
+    def __post_init__(self):
+        # perform necessary checking
+        self.check_consistency()
+
+    def __len__(self):
+        if self.batch is not None:
+            return self.batch.batch_size[0]
+        elif self.non_tensor_batch is not None and len(self.non_tensor_batch) > 0:
+            random_key = list(self.non_tensor_batch.keys())[0]
+            return self.non_tensor_batch[random_key].shape[0]
+        else:
+            return 0
+
+    def __getitem__(self, item):
+        """
+        Enhanced indexing for DataProto objects.
+
+        Args:
+            item: Can be one of:
+                - int: A single index
+                - slice: A slice object (start:stop:step)
+                - list: A list of indices
+                - numpy.ndarray: An array of indices
+                - torch.Tensor: A tensor of indices
+
+        Returns:
+            DataProto: For all indexing types except single integers
+            DataProtoItem: Only for single integer indices
+        """
+        # Case 1: Slice object - use the slice method
+        if isinstance(item, slice):
+            return self.slice(item.start, item.stop, item.step)
+
+        # Case 2: List, numpy array, or torch tensor - use sel_idxs
+        elif isinstance(item, list | np.ndarray | torch.Tensor):
+            return self.select_idxs(item)
+
+        # Case 3: Single integer - return DataProtoItem for backward compatibility
+        elif isinstance(item, int | np.integer):
+            tensor_data = self.batch[item] if self.batch is not None else None
+            non_tensor_data = {key: val[item] for key, val in self.non_tensor_batch.items()}
+            return DataProtoItem(batch=tensor_data, non_tensor_batch=non_tensor_data, meta_info=self.meta_info)
+
+        # # Case 4: Unsupported type
+        else:
+            raise TypeError(f"Indexing with {type(item)} is not supported")
+
+    def __getstate__(self):
+        if version.parse(tensordict.__version__) >= version.parse("0.5.0") and self.batch is not None:
+            # Check if batch is empty to avoid torch.cat error in consolidate
+            if len(self.batch.keys()) > 0:
+                batch = self.batch.contiguous().consolidate()
+            else:
+                batch = self.batch
+        else:
+            batch = self.batch
+
+        if os.getenv("VERL_DATAPROTO_SERIALIZATION_METHOD") == "numpy":
+            if batch is not None:
+                batch = serialize_tensordict(self.batch)
+
+            return (
+                batch,
+                self.non_tensor_batch,
+                self.meta_info,
+            )
+        else:
+            import io
+
+            buffer = io.BytesIO()
+            torch.save(batch, buffer)
+            buffer_bytes = buffer.getvalue()
+            return buffer_bytes, self.non_tensor_batch, self.meta_info
+
+    def __setstate__(self, data):
+        batch_deserialized_bytes, non_tensor_batch, meta_info = data
+
+        if os.getenv("VERL_DATAPROTO_SERIALIZATION_METHOD") == "numpy":
+            if batch_deserialized_bytes is not None:
+                self.batch = deserialize_tensordict(batch_deserialized_bytes)
+            else:
+                self.batch = None
+        else:
+            import io
+
+            batch_deserialized = io.BytesIO(initial_bytes=batch_deserialized_bytes)
+            batch = torch.load(
+                batch_deserialized,
+                weights_only=False,
+                map_location="cpu" if not get_torch_device().is_available() else None,
+            )
+            self.batch = batch
+
+        self.non_tensor_batch = non_tensor_batch
+        self.meta_info = meta_info
+
+    def save_to_disk(self, filepath):
+        with open(filepath, "wb") as f:
+            pickle.dump(self, f)
+
+    @staticmethod
+    def load_from_disk(filepath) -> "DataProto":
+        with open(filepath, "rb") as f:
+            data = pickle.load(f)
+            return data
+
+    def print_size(self, prefix=""):
+        size_of_tensordict = 0
+        if self.batch is not None:
+            for _, tensor in self.batch.items():
+                size_of_tensordict += tensor.element_size() * tensor.numel()
+        size_of_numpy_array = 0
+        for _, numpy_array in self.non_tensor_batch.items():
+            size_of_numpy_array += numpy_array.nbytes
+
+        size_of_numpy_array /= 1024**3
+        size_of_tensordict /= 1024**3
+
+        message = f"Size of tensordict: {size_of_tensordict} GB, size of non_tensor_batch: {size_of_numpy_array} GB"
+
+        if prefix:
+            message = f"{prefix}, " + message
+        print(message)
+
+    def check_consistency(self):
+        """Check the consistency of the DataProto. Mainly for batch and non_tensor_batch
+        We expose this function as a public one so that user can call themselves directly
+        """
+        if self.batch is not None:
+            assert len(self.batch.batch_size) == 1, "only support num_batch_dims=1"
+
+        if self.non_tensor_batch is not None:
+            for key, val in self.non_tensor_batch.items():
+                assert isinstance(val, np.ndarray)
+
+        if self.batch is not None and self.non_tensor_batch is not None and len(self.non_tensor_batch) != 0:
+            # TODO: we can actually lift this restriction if needed
+            assert len(self.batch.batch_size) == 1, "only support num_batch_dims=1 when non_tensor_batch is not empty."
+
+            batch_size = self.batch.batch_size[0]
+            for key, val in self.non_tensor_batch.items():
+                assert isinstance(val, np.ndarray), (
+                    f"data in the non_tensor_batch must be a numpy.array with dtype=object, but for "
+                    f"{key=}, got {type(val)=}"
+                )
+                assert val.shape[0] == batch_size, (
+                    f"key {key} length {len(val)} is not equal to batch size {batch_size}"
+                )
+
+    @classmethod
+    def from_single_dict(cls, data: dict[str, torch.Tensor | np.ndarray], meta_info=None, auto_padding=False):
+        """Create a DataProto from a dict of tensors and non_tensors"""
+        tensors = {}
+        non_tensors = {}
+
+        for key, val in data.items():
+            if isinstance(val, torch.Tensor):
+                tensors[key] = val
+            elif isinstance(val, np.ndarray):
+                non_tensors[key] = val
+            else:
+                raise ValueError(f"Unsupported type in data {type(val)}")
+
+        return cls.from_dict(tensors=tensors, non_tensors=non_tensors, meta_info=meta_info, auto_padding=auto_padding)
+
+    @classmethod
+    def from_dict(
+        cls,
+        tensors: Optional[dict[str, torch.Tensor]] = None,
+        non_tensors=None,
+        meta_info=None,
+        num_batch_dims=1,
+        auto_padding=False,
+    ):
+        """Create a DataProto from a dict of tensors. This assumes that
+        1. All the tensor in tensors have the same dim0
+        2. Only dim0 is the batch dim
+        """
+
+        assert num_batch_dims > 0, "num_batch_dims must be greater than zero"
+        if non_tensors is not None:
+            assert num_batch_dims == 1, "only support num_batch_dims=1 when non_tensors is not None."
+
+        if tensors is None:
+            tensors = {}
+        if meta_info is None:
+            meta_info = {}
+        if non_tensors is None:
+            non_tensors = {}
+
+        assert isinstance(non_tensors, dict)
+
+        # get and check batch size
+        batch_size = None
+        pivot_key = None
+        for key, tensor in tensors.items():
+            if batch_size is None:
+                batch_size = tensor.shape[:num_batch_dims]
+                pivot_key = key
+            else:
+                current_batch = tensor.shape[:num_batch_dims]
+                assert batch_size == current_batch, (
+                    f"Not all the tensor in tensors have the same batch size with batch_dims={num_batch_dims}. "
+                    f"Got {pivot_key} has {batch_size}, {key} has {current_batch}"
+                )
+
+        for key, val in non_tensors.items():
+            if not isinstance(val, np.ndarray):
+                non_tensors[key] = np.array(val, dtype=object)
+
+        tensor_dict = TensorDict(source=tensors, batch_size=batch_size) if tensors else None
+        if auto_padding:
+            meta_info[DataProtoConfig.auto_padding_key] = True
+        return cls(batch=tensor_dict, non_tensor_batch=non_tensors, meta_info=meta_info)
+
+    @classmethod
+    def from_tensordict(
+        cls,
+        tensor_dict: TensorDict = None,
+        meta_info=None,
+        num_batch_dims=1,
+    ):
+        """Create a DataProto from a TensorDict. This assumes that
+        1. All the tensor in tensor_dict have the same dim0
+        2. Only dim0 is the batch dim
+        """
+        assert version.parse(tensordict.__version__) >= version.parse("0.10.0"), (
+            "Build DataProto from TensorDict at least requires tensordict version 0.10.0"
+        )
+        from tensordict import NonTensorData, NonTensorStack
+
+        assert num_batch_dims > 0, "num_batch_dims must be greater than zero"
+        if not all(isinstance(val, torch.Tensor) for val in tensor_dict.values()):
+            assert num_batch_dims == 1, "only support num_batch_dims=1 when tensor_dict contains non tensor data."
+
+        if meta_info is None:
+            meta_info = {}
+        batch = {}
+        non_tensor_batch = {}
+        batch_size = None
+        for key, val in tensor_dict.items():
+            if isinstance(val, torch.Tensor):
+                batch[key] = val
+                if batch_size is None:
+                    batch_size = val.shape[:num_batch_dims]
+            elif isinstance(val, NonTensorStack):
+                non_tensor_batch[key] = np.array([elem.data for elem in val], dtype=object)
+            elif isinstance(val, NonTensorData):
+                meta_info[key] = val.data
+
+        return cls(
+            batch=TensorDict(batch, batch_size=batch_size),
+            non_tensor_batch=non_tensor_batch,
+            meta_info=meta_info,
+        )
+
+    def to(self, device) -> "DataProto":
+        """move the batch to device
+
+        Args:
+            device (torch.device, str): torch device
+
+        Returns:
+            DataProto: the current DataProto
+
+        """
+        if self.batch is not None:
+            self.batch = self.batch.to(device)
+        return self
+
+    def select(self, batch_keys=None, non_tensor_batch_keys=None, meta_info_keys=None, deepcopy=False) -> "DataProto":
+        """Select a subset of the DataProto via batch_keys and meta_info_keys
+
+        Args:
+            batch_keys (list, optional): a list of strings indicating the keys in batch to select
+            meta_info_keys (list, optional): a list of keys indicating the meta info to select
+
+        Returns:
+            DataProto: the DataProto with the selected batch_keys and meta_info_keys
+        """
+        # TODO (zhangchi.usc1992) whether to copy
+        if batch_keys is not None:
+            batch_keys = tuple(batch_keys)
+            sub_batch = self.batch.select(*batch_keys)
+        else:
+            sub_batch = self.batch
+
+        if non_tensor_batch_keys is not None:
+            non_tensor_batch = {key: val for key, val in self.non_tensor_batch.items() if key in non_tensor_batch_keys}
+        else:
+            non_tensor_batch = self.non_tensor_batch
+
+        if deepcopy:
+            non_tensor_batch = copy.deepcopy(non_tensor_batch)
+
+        if meta_info_keys is not None:
+            sub_meta_info = {key: val for key, val in self.meta_info.items() if key in meta_info_keys}
+        else:
+            sub_meta_info = self.meta_info
+
+        if deepcopy:
+            sub_meta_info = copy.deepcopy(sub_meta_info)
+
+        return type(self)(batch=sub_batch, non_tensor_batch=non_tensor_batch, meta_info=sub_meta_info)
+
+    def select_idxs(self, idxs):
+        """
+        Select specific indices from the DataProto.
+
+        Args:
+            idxs (torch.Tensor or numpy.ndarray or list): Indices to select
+
+        Returns:
+            DataProto: A new DataProto containing only the selected indices
+        """
+        if isinstance(idxs, list):
+            idxs = torch.tensor(idxs)
+            if idxs.dtype != torch.bool:
+                idxs = idxs.type(torch.int32)
+
+        if isinstance(idxs, np.ndarray):
+            idxs_np = idxs
+            idxs_torch = torch.from_numpy(idxs)
+        else:  # torch.Tensor
+            idxs_torch = idxs
+            idxs_np = idxs.detach().cpu().numpy()
+
+        batch_size = int(idxs_np.sum()) if idxs_np.dtype == bool else idxs_np.shape[0]
+
+        if self.batch is not None:
+            # Use TensorDict's built-in indexing capabilities
+            selected_batch = TensorDict(
+                source={key: tensor[idxs_torch] for key, tensor in self.batch.items()},
+                batch_size=(batch_size,),
+                device=self.batch.device,
+            )
+        else:
+            selected_batch = None
+
+        selected_non_tensor = {}
+        for key, val in self.non_tensor_batch.items():
+            selected_non_tensor[key] = val[idxs_np]
+
+        return type(self)(batch=selected_batch, non_tensor_batch=selected_non_tensor, meta_info=self.meta_info)
+
+    def slice(self, start=None, end=None, step=None):
+        """
+        Slice the DataProto and return a new DataProto object.
+        This is an improved version of direct slicing which returns a DataProtoItem.
+
+        Args:
+            start (int, optional): Start index. Defaults to None (start from beginning).
+            end (int, optional): End index (exclusive). Defaults to None (go to end).
+            step (int, optional): Step size. Defaults to None (step=1).
+
+        Returns:
+            DataProto: A new DataProto containing the sliced data
+
+        Examples:
+            # Using the slice method directly
+            sliced_data = data_proto.slice(10, 20)
+
+            # Using enhanced indexing (returns DataProto)
+            sliced_data = data_proto[10:20]
+            sliced_data = data_proto[::2]  # Every other element
+
+            # Using list indexing (returns DataProto)
+            indices = [1, 5, 10]
+            selected_data = data_proto[indices]
+
+            # Single index still returns DataProtoItem
+            single_item = data_proto[5]
+        """
+        # Create a slice object
+        slice_obj = slice(start, end, step)
+
+        # Handle the batch data
+        if self.batch is not None:
+            # Use TensorDict's built-in slicing capabilities
+            sliced_batch = self.batch[slice_obj]
+        else:
+            sliced_batch = None
+
+        # Handle the non-tensor batch data
+        sliced_non_tensor = {}
+        for key, val in self.non_tensor_batch.items():
+            sliced_non_tensor[key] = val[slice_obj]
+
+        # Return a new DataProto object
+        return type(self)(batch=sliced_batch, non_tensor_batch=sliced_non_tensor, meta_info=self.meta_info)
+
+    def pop(self, batch_keys=None, non_tensor_batch_keys=None, meta_info_keys=None) -> "DataProto":
+        """Pop a subset of the DataProto via `batch_keys` and `meta_info_keys`
+
+        Args:
+            batch_keys (list, optional): a list of strings indicating the keys in batch to pop
+            meta_info_keys (list, optional): a list of keys indicating the meta info to pop
+
+        Returns:
+            DataProto: the DataProto with the poped batch_keys and meta_info_keys
+        """
+        if batch_keys is None:
+            batch_keys = []
+        if meta_info_keys is None:
+            meta_info_keys = []
+        if non_tensor_batch_keys is None:
+            non_tensor_batch_keys = []
+
+        tensors = {}
+        # tensor batch
+        for key in batch_keys:
+            assert key in self.batch.keys()
+            tensors[key] = self.batch.pop(key)
+        non_tensors = {}
+        # non tensor batch
+        for key in non_tensor_batch_keys:
+            assert key in self.non_tensor_batch.keys()
+            non_tensors[key] = self.non_tensor_batch.pop(key)
+        meta_info = {}
+        for key in meta_info_keys:
+            assert key in self.meta_info.keys()
+            meta_info[key] = self.meta_info.pop(key)
+        return DataProto.from_dict(tensors=tensors, non_tensors=non_tensors, meta_info=meta_info)
+
+    def rename(self, old_keys=None, new_keys=None) -> "DataProto":
+        """
+        Note that this function only rename the key in the batch
+        """
+
+        def validate_input(keys):
+            if keys is not None:
+                if isinstance(keys, str):
+                    keys = [keys]
+                elif isinstance(keys, list):
+                    pass
+                else:
+                    raise TypeError(f"keys must be a list or a string, but got {type(keys)}")
+            return keys
+
+        old_keys = validate_input(old_keys)
+        new_keys = validate_input(new_keys)
+
+        if len(new_keys) != len(old_keys):
+            raise ValueError(
+                f"new_keys and old_keys must have the same length, but got {len(new_keys)} and {len(old_keys)}"
+            )
+
+        self.batch.rename_key_(tuple(old_keys), tuple(new_keys))
+
+        return self
+
+    def union(self, other: "DataProto") -> "DataProto":
+        """Union with another DataProto. Union batch and meta_info separately.
+        Throw an error if
+
+        - there are conflict keys in batch and they are not equal
+        - the batch size of two data batch is not the same
+        - there are conflict keys in meta_info and they are not the same.
+
+        Args:
+            other (DataProto): another DataProto to union
+
+        Returns:
+            DataProto: the DataProto after union
+        """
+        self.batch = union_tensor_dict(self.batch, other.batch)
+        self.non_tensor_batch = union_numpy_dict(self.non_tensor_batch, other.non_tensor_batch)
+        self.meta_info = union_two_dict(self.meta_info, other.meta_info)
+        return self
+
+    def make_iterator(self, mini_batch_size, epochs, seed=None, dataloader_kwargs=None):
+        r"""Make an iterator from the DataProto. This is built upon that TensorDict can be used as a normal Pytorch
+        dataset. See https://pytorch.org/tensordict/stable/tutorials/data_fashion for more details.
+
+
+        Args:
+            mini_batch_size (int): mini-batch size when iterating the dataset. We require that
+                ``batch.batch_size[0] % mini_batch_size == 0``.
+            epochs (int): number of epochs when iterating the dataset.
+            dataloader_kwargs (Any): internally, it returns a DataLoader over the batch. The
+                dataloader_kwargs is the kwargs passed to the DataLoader.
+
+        Returns:
+            Iterator: an iterator that yields a mini-batch data at a time. The total number of iteration
+                steps is ``self.batch.batch_size * epochs // mini_batch_size``
+        """
+        assert self.batch.batch_size[0] % mini_batch_size == 0, f"{self.batch.batch_size[0]} % {mini_batch_size} != 0"
+        # we can directly create a dataloader from TensorDict
+        if dataloader_kwargs is None:
+            dataloader_kwargs = {}
+
+        if seed is not None:
+            generator = torch.Generator()
+            generator.manual_seed(seed)
+        else:
+            generator = None
+
+        assert isinstance(dataloader_kwargs, dict)
+        train_dataloader = DataLoader(
+            dataset=self, batch_size=mini_batch_size, collate_fn=collate_fn, generator=generator, **dataloader_kwargs
+        )
+
+        def get_data():
+            for _ in range(epochs):
+                for d in train_dataloader:
+                    d.meta_info = self.meta_info
+                    yield d
+
+        return iter(get_data())
+
+    def is_padding_enabled(self):
+        """
+        Check if padding is enabled for the DataProto.
+        Returns:
+            bool: True if padding is enabled, False otherwise.
+        """
+        dataproto_specific_padding = self.meta_info.get(DataProtoConfig.auto_padding_key, False)
+        return dataproto_specific_padding or DataProtoConfig.auto_padding
+
+    def padding(self, padding_size, padding_candidate=""):
+        """Pad the DataProto by concating with padding_candidate.repeat(padding_size)
+
+        Args:
+            padding_size (int): the number of repeated padding_candidate
+            padding_candidate: the item to be repeated and appended to the DataProto, only supporting ["first", "last"]
+        """
+        if padding_size == 0:
+            return
+        padding_candidate = self.select_idxs([0 if padding_candidate == "first" else len(self) - 1])
+        padding_part = padding_candidate.repeat(padding_size)
+        padded_dp = DataProto.concat([self, padding_part])
+        self.batch = padded_dp.batch
+        self.non_tensor_batch = padded_dp.non_tensor_batch
+
+    def chunk(self, chunks: int) -> list["DataProto"]:
+        """Split the batch among dim=0 into chunks. The meta_info is passed to each DataProto after split.
+
+        Args:
+            chunks (int): the number of chunks to split on dim=0
+
+        Returns:
+            List[DataProto]: a list of DataProto after splitting
+        """
+        if not self.is_padding_enabled():
+            assert len(self) % chunks == 0, (
+                f"only support equal chunk. Got size of DataProto {len(self)} and chunk {chunks}."
+            )
+
+        bsz_in_batch = None
+        if self.batch is not None:
+            batch_lst = self.batch.chunk(chunks=chunks, dim=0)
+            bsz_in_batch = np.array([batch.batch_size[0] for batch in batch_lst])
+            chunk_indices = np.cumsum(bsz_in_batch)[:-1]
+        else:
+            batch_lst = [None for _ in range(chunks)]
+
+        non_tensor_batch_lst = [{} for _ in range(chunks)]
+        for key, val in self.non_tensor_batch.items():
+            assert isinstance(val, np.ndarray)
+            if bsz_in_batch is not None:
+                non_tensor_lst = np.array_split(val, chunk_indices.tolist())
+            else:
+                non_tensor_lst = np.array_split(val, chunks)
+            assert len(non_tensor_lst) == chunks
+            for i in range(chunks):
+                non_tensor_batch_lst[i][key] = non_tensor_lst[i]
+
+        output = []
+        for i in range(chunks):
+            output.append(
+                type(self)(batch=batch_lst[i], non_tensor_batch=non_tensor_batch_lst[i], meta_info=self.meta_info)
+            )
+
+        return output
+
+    def split(self, split_size: int) -> list["DataProto"]:
+        """Split the batch among dim=0 into chunks. The meta_info is passed to each DataProto after split.
+
+        Args:
+            split_size (int): the size of each split
+
+        Returns:
+            List[DataProto]: a list of DataProto after splitting
+        """
+        return [self[i : i + split_size] for i in range(0, len(self), split_size)]
+
+    @staticmethod
+    def concat(data: list["DataProto"]) -> "DataProto":
+        """Concat a list of DataProto. The batch is concatenated among dim=0.
+        The meta_info is merged, with special handling for metrics from different workers.
+
+        Args:
+            data (List[DataProto]): list of DataProto
+
+        Returns:
+            DataProto: concatenated DataProto
+        """
+        batch_lst = []
+        for batch in data:
+            batch_lst.append(batch.batch)
+        new_batch = torch.cat(batch_lst, dim=0) if batch_lst[0] is not None else None
+
+        non_tensor_batch = list_of_dict_to_dict_of_list(list_of_dict=[d.non_tensor_batch for d in data])
+        for key, val in non_tensor_batch.items():
+            non_tensor_batch[key] = np.concatenate(val, axis=0)
+
+        # Merge meta_info with special handling for metrics
+        merged_meta_info = {}
+        if data:
+            # Merge non-metric meta_info and aggregate metrics from all workers.
+            all_metrics = []
+            for d in data:
+                for k, v in d.meta_info.items():
+                    if k == "metrics":
+                        if v is not None:
+                            if isinstance(v, list):
+                                all_metrics.extend(v)
+                            else:
+                                all_metrics.append(v)
+                    else:
+                        if k in merged_meta_info:
+                            # Ensure consistency for overlapping non-metric keys
+                            assert merged_meta_info[k] == v, f"Conflicting values for meta_info key '{k}'"
+                        else:
+                            merged_meta_info[k] = v
+
+            # Flatten list of dicts to dict of lists for consistent metrics structure
+            if all_metrics:
+                merged_meta_info["metrics"] = list_of_dict_to_dict_of_list(all_metrics)
+
+        cls = type(data[0]) if len(data) > 0 else DataProto
+        return cls(batch=new_batch, non_tensor_batch=non_tensor_batch, meta_info=merged_meta_info)
+
+    def reorder(self, indices):
+        """
+        Note that this operation is in-place
+        """
+        indices_np = indices.detach().numpy()
+        self.batch = self.batch[indices]
+        self.non_tensor_batch = {key: val[indices_np] for key, val in self.non_tensor_batch.items()}
+
+    def repeat(self, repeat_times=2, interleave=True):
+        """
+        Repeat the batch data a specified number of times.
+
+        Args:
+            repeat_times (int): Number of times to repeat the data.
+            interleave (bool): Whether to interleave the repeated data.
+
+        Returns:
+            DataProto: A new DataProto with repeated data.
+        """
+        if self.batch is not None:
+            if interleave:
+                # Interleave the data
+                repeated_tensors = {
+                    key: tensor.repeat_interleave(repeat_times, dim=0) for key, tensor in self.batch.items()
+                }
+            else:
+                # Stack the data
+                repeated_tensors = {
+                    key: tensor.unsqueeze(0).expand(repeat_times, *tensor.shape).reshape(-1, *tensor.shape[1:])
+                    for key, tensor in self.batch.items()
+                }
+
+            repeated_batch = TensorDict(
+                source=repeated_tensors,
+                batch_size=(self.batch.batch_size[0] * repeat_times,),
+            )
+        else:
+            repeated_batch = None
+
+        repeated_non_tensor_batch = {}
+        for key, val in self.non_tensor_batch.items():
+            if interleave:
+                repeated_non_tensor_batch[key] = np.repeat(val, repeat_times, axis=0)
+            else:
+                repeated_non_tensor_batch[key] = np.tile(val, (repeat_times,) + (1,) * (val.ndim - 1))
+
+        return type(self)(
+            batch=repeated_batch,
+            non_tensor_batch=repeated_non_tensor_batch,
+            meta_info=self.meta_info,
+        )
+
+    def unfold_column_chunks(self, n_split: int, split_keys: Optional[list[str]] = None):
+        """Split along the second dim into `n_split`, unfold it to the first dim (batch dim)
+        Useful in passing grouped tensors that doesn't want to be shuffled in dataset.
+        keys not in split_keys are repeated to match the shape
+        Note that if the `split_keys` is not provided, it will repeat all the keys in the second dim.
+        """
+        if self.batch is not None:
+            unfolded_batch = {}
+            for key in self.batch.keys():
+                if key in split_keys if split_keys is not None else False:
+                    shape = list(self.batch[key].shape)
+                    shape[0] = self.batch[key].shape[0] * n_split
+                    shape[1] = self.batch[key].shape[1] // n_split
+                    unfolded_batch[key] = self.batch[key].reshape(*shape)
+                else:
+                    unfolded_batch[key] = torch.repeat_interleave(self.batch[key], n_split, dim=0)
+            # locate the `unfolded_batch` as a TensorDict on the same device as the original batch
+            unfolded_batch = TensorDict(
+                source=unfolded_batch, batch_size=(self.batch.batch_size[0] * n_split,), device=self.batch.device
+            )
+        else:
+            unfolded_batch = None
+
+        repeated_non_tensor_batch = {}
+        for key, val in self.non_tensor_batch.items():
+            if key in split_keys:
+                shape = list(val.shape)
+                shape[0] = val.shape[0] * n_split
+                shape[1] = val.shape[1] // n_split
+                repeated_non_tensor_batch[key] = val.reshape(*shape)
+            else:
+                repeated_non_tensor_batch[key] = np.repeat(val, n_split, axis=0)
+
+        return type(self)(
+            batch=unfolded_batch,
+            non_tensor_batch=repeated_non_tensor_batch,
+            meta_info=self.meta_info,
+        )
+
+    def sample_level_repeat(self, repeat_times):
+        """
+        Repeat each row of the batch data a specified number of times.
+
+        Args:
+            repeat_times (torch.tensor, list, tuple, ndarray):  Number of times to repeat the data.
+
+        Returns:
+            DataProto: A new DataProto with repeated data.
+        """
+        if isinstance(repeat_times, tuple):
+            repeat_times = list(repeat_times)
+        elif isinstance(repeat_times, torch.Tensor):
+            assert len(repeat_times.shape) == 1
+            repeat_times = repeat_times.tolist()
+        elif isinstance(repeat_times, np.ndarray):
+            assert len(repeat_times.shape) == 1
+            repeat_times = repeat_times.tolist()
+        else:
+            assert isinstance(repeat_times, list), (
+                f"repeat_times type must be in [list, torch.Tensor, np.ndarray, tuple], got {type(repeat_times)}"
+            )
+        repeat_times = torch.tensor(repeat_times)
+
+        if self.batch is not None:
+            # Interleave the data
+            repeated_tensors = {
+                key: tensor.repeat_interleave(repeat_times, dim=0) for key, tensor in self.batch.items()
+            }
+
+            repeated_batch = TensorDict(
+                source=repeated_tensors,
+                batch_size=(repeat_times.sum().item(),),
+                device=self.batch.device,
+            )
+        else:
+            repeated_batch = None
+
+        repeated_non_tensor_batch = {}
+        for key, val in self.non_tensor_batch.items():
+            repeated_non_tensor_batch[key] = np.repeat(val, repeat_times, axis=0)
+
+        return type(self)(
+            batch=repeated_batch,
+            non_tensor_batch=repeated_non_tensor_batch,
+            meta_info=self.meta_info,
+        )
+
+    def to_tensordict(self) -> TensorDict:
+        """Convert this DataProto to TensorDict. Note that this requires tensordict version at least 0.10
+
+        Returns:
+
+        """
+        assert parse_version(tensordict.__version__) >= parse_version("0.10"), (
+            "Convert DataProto to TensorDict at least requires tensordict version 0.10"
+        )
+        tensor_batch = self.batch.to_dict()
+        non_tensor_batch = self.non_tensor_batch
+
+        from tensordict.tensorclass import NonTensorData, NonTensorStack
+
+        from verl.utils import tensordict_utils as tu
+
+        common_keys = set(tensor_batch.keys()) & set(non_tensor_batch.keys())
+        assert len(common_keys) == 0, f"tensor_batch and non_tensor_batch have common keys {common_keys}"
+
+        for key, val in non_tensor_batch.items():
+            assert isinstance(val, np.ndarray)
+            # Convert to NonTensorStack instead of plain list to handle nested structures
+            tensor_batch[key] = NonTensorStack.from_list([NonTensorData(item) for item in val])
+        output = tu.get_tensordict(tensor_dict=tensor_batch, non_tensor_dict=self.meta_info)
+        return output
+
+    def get_data_info(self) -> str:
+        """Return formatted information about stored data with nested type details.
+
+        Returns:
+            str: Formatted string showing tensor details and recursive metadata types
+        """
+        info = ["batch"]
+
+        for key, tensor in self.batch.items():
+            if hasattr(tensor, "shape") and hasattr(tensor, "dtype") and hasattr(tensor, "device"):
+                info.append(f"  {key}: {tuple(tensor.shape)} ({tensor.dtype}) {tensor.device}")
+            elif hasattr(tensor, "shape") and hasattr(tensor, "dtype"):
+                info.append(f"  {key}: {tuple(tensor.shape)} ({tensor.dtype})")
+            else:
+                info.append(f"  {key}: {type(tensor).__name__}")
+
+        info.append("non_tensor_batch")
+        for key, array in self.non_tensor_batch.items():
+            info.append(f"  {key}: ndarray{array.shape} ({array.dtype})")
+
+        info.append("meta_info")
+        for k, v in self.meta_info.items():
+            type_info = self._get_type_info(v)
+            info.append(f"  {k}: {type_info}")
+
+        return "\n".join(info)
+
+    def _get_type_info(self, value):
+        """Recursively get type information for nested structures"""
+        if isinstance(value, list):
+            elem_types = {self._get_type_info(v) for v in value[:3]}
+            return f"list[{'|'.join(elem_types) if elem_types else '...'}]"
+        if isinstance(value, tuple):
+            elem_types = [self._get_type_info(v) for v in value]
+            return f"tuple({', '.join(elem_types)})"
+        if isinstance(value, dict):
+            if not value:
+                return "dict"
+            k, v = next(iter(value.items()))
+            return f"dict[{self._get_type_info(k)}: {self._get_type_info(v)}]"
+        if isinstance(value, np.ndarray):
+            return f"ndarray{value.shape} ({value.dtype})"
+        return type(value).__name__
+
+
+@dataclass
+class DataProtoFuture:
+    """
+    DataProtoFuture aims to eliminate actual data fetching on driver. By doing so, the driver doesn't have to wait
+    for data so that asynchronous execution becomes possible.
+    DataProtoFuture contains a list of futures from another WorkerGroup of size world_size.
+    - collect_fn is a Callable that reduces the list of futures to a DataProto
+    - dispatch_fn is a Callable that partitions the DataProto into a list of DataProto of size world_size
+        and then select
+
+    Potential issue: we can optimize dispatch_fn(collect_fn) such that only needed data is fetched on destination
+    - DataProtoFuture only supports directly passing from the output of a method to another input. You can't perform any
+    operation on the DataProtoFuture in driver.
+    """
+
+    collect_fn: Callable
+    futures: list[ray.ObjectRef]
+    dispatch_fn: Callable = None
+
+    @staticmethod
+    def concat(data: list[ray.ObjectRef]) -> "DataProtoFuture":
+        output = DataProtoFuture(collect_fn=DataProto.concat, futures=data)
+        return output
+
+    def chunk(self, chunks: int) -> list["DataProtoFuture"]:
+        from functools import partial
+
+        arg_future_lst = []
+        for i in range(chunks):
+            # note that we can't directly pass i and chunks
+            def dispatch_fn(x, i, chunks):
+                return x.chunk(chunks=chunks)[i]
+
+            arg_future = DataProtoFuture(
+                collect_fn=self.collect_fn, dispatch_fn=partial(dispatch_fn, i=i, chunks=chunks), futures=self.futures
+            )
+            arg_future_lst.append(arg_future)
+        return arg_future_lst
+
+    def get(self):
+        output = ray.get(self.futures)  # dp_size.
+        for o in output:
+            assert isinstance(o, DataProto | TensorDict)
+
+        if isinstance(output[0], DataProto):
+            output = DataProto.concat(output)  # select dp, concat
+        elif isinstance(output[0], TensorDict):
+            from verl.utils.tensordict_utils import concat_tensordict
+
+            output = concat_tensordict(output)
+        else:
+            raise TypeError(f"Unknown type {type(o[0])} in DataProtoFuture")
+
+        if self.dispatch_fn is not None:
+            output = self.dispatch_fn(output)  # split in batch dim, select using dp
+        return output
+
+
+def all_gather_data_proto(data: DataProto, process_group):
+    # Note that this is an inplace operator just like torch.distributed.all_gather
+    group_size = torch.distributed.get_world_size(group=process_group)
+    assert isinstance(data, DataProto)
+    prev_device = data.batch.device
+    data = data.to(get_device_id())
+    data.batch = allgather_dict_tensors(data.batch.contiguous(), size=group_size, group=process_group, dim=0)
+    data = data.to(prev_device)
+    # all gather non_tensor_batch
+    all_non_tensor_batch = [None for _ in range(group_size)]
+    torch.distributed.all_gather_object(all_non_tensor_batch, data.non_tensor_batch, group=process_group)
+    data.non_tensor_batch = {k: np.concatenate([d[k] for d in all_non_tensor_batch]) for k in data.non_tensor_batch}
diff --git a/code/RL_model/verl/verl_train/verl/py.typed b/code/RL_model/verl/verl_train/verl/py.typed
new file mode 100644
index 0000000000000000000000000000000000000000..e69de29bb2d1d6434b8b29ae775ad8c2e48c5391
diff --git a/code/RL_model/verl/verl_train/wandb/debug-internal.log b/code/RL_model/verl/verl_train/wandb/debug-internal.log
new file mode 100644
index 0000000000000000000000000000000000000000..b8abf7833248231babcf9f91a40ee1536cd99b88
--- /dev/null
+++ b/code/RL_model/verl/verl_train/wandb/debug-internal.log
@@ -0,0 +1,6 @@
+{"time":"2026-02-15T11:45:17.517434634-05:00","level":"INFO","msg":"stream: starting","core version":"0.24.1"}
+{"time":"2026-02-15T11:45:18.929223933-05:00","level":"INFO","msg":"stream: created new stream","id":"4c5nwk6l"}
+{"time":"2026-02-15T11:45:18.929362029-05:00","level":"INFO","msg":"handler: started","stream_id":"4c5nwk6l"}
+{"time":"2026-02-15T11:45:18.93191015-05:00","level":"INFO","msg":"stream: started","id":"4c5nwk6l"}
+{"time":"2026-02-15T11:45:18.931968858-05:00","level":"INFO","msg":"sender: started","stream_id":"4c5nwk6l"}
+{"time":"2026-02-15T11:45:18.931970677-05:00","level":"INFO","msg":"writer: started","stream_id":"4c5nwk6l"}
diff --git a/code/RL_model/verl/verl_train/wandb/debug.log b/code/RL_model/verl/verl_train/wandb/debug.log
new file mode 100644
index 0000000000000000000000000000000000000000..06b1f6a0cce2b4f9e8302f2da23cacb97d45d344
--- /dev/null
+++ b/code/RL_model/verl/verl_train/wandb/debug.log
@@ -0,0 +1,19 @@
+2026-02-15 11:45:17,230 INFO    MainThread:3962104 [wandb_setup.py:_flush():81] Current SDK version is 0.24.1
+2026-02-15 11:45:17,231 INFO    MainThread:3962104 [wandb_setup.py:_flush():81] Configure stats pid to 3962104
+2026-02-15 11:45:17,231 INFO    MainThread:3962104 [wandb_setup.py:_flush():81] Loading settings from environment variables
+2026-02-15 11:45:17,231 INFO    MainThread:3962104 [wandb_init.py:setup_run_log_directory():717] Logging user logs to /data/home_beta/mshahidul/readctrl/code/RL_model/verl/verl_train/wandb/run-20260215_114517-4c5nwk6l/logs/debug.log
+2026-02-15 11:45:17,231 INFO    MainThread:3962104 [wandb_init.py:setup_run_log_directory():718] Logging internal logs to /data/home_beta/mshahidul/readctrl/code/RL_model/verl/verl_train/wandb/run-20260215_114517-4c5nwk6l/logs/debug-internal.log
+2026-02-15 11:45:17,231 INFO    MainThread:3962104 [wandb_init.py:init():844] calling init triggers
+2026-02-15 11:45:17,232 INFO    MainThread:3962104 [wandb_init.py:init():849] wandb.init called with sweep_config: {}
+config: {'actor_rollout_ref': {'actor': {'optim': {'_target_': 'verl.workers.config.FSDPOptimizerConfig', 'optimizer': 'AdamW', 'optimizer_impl': 'torch.optim', 'lr': 1e-06, 'lr_warmup_steps_ratio': 0.0, 'total_training_steps': 45, 'weight_decay': 0.01, 'lr_warmup_steps': -1, 'betas': [0.9, 0.999], 'clip_grad': 1.0, 'min_lr_ratio': 0.0, 'num_cycles': 0.5, 'lr_scheduler_type': 'constant', 'warmup_style': None, 'override_optimizer_config': None}, 'fsdp_config': {'_target_': 'verl.workers.config.FSDPEngineConfig', 'wrap_policy': {'min_num_params': 0}, 'param_offload': True, 'optimizer_offload': True, 'offload_policy': False, 'reshard_after_forward': True, 'fsdp_size': -1, 'forward_prefetch': False, 'model_dtype': 'fp32', 'use_orig_params': False, 'seed': 42, 'full_determinism': False, 'ulysses_sequence_parallel_size': 1, 'entropy_from_logits_with_chunking': False, 'use_torch_compile': True, 'entropy_checkpointing': False, 'forward_only': False, 'strategy': 'fsdp', 'dtype': 'bfloat16'}, '_target_': 'verl.workers.config.FSDPActorConfig', 'rollout_n': 3, 'strategy': 'fsdp', 'ppo_mini_batch_size': 256, 'ppo_micro_batch_size': None, 'ppo_micro_batch_size_per_gpu': 16, 'use_dynamic_bsz': False, 'ppo_max_token_len_per_gpu': 16384, 'clip_ratio': 0.2, 'clip_ratio_low': 0.2, 'clip_ratio_high': 0.2, 'tau_pos': 1.0, 'tau_neg': 1.05, 'freeze_vision_tower': False, 'policy_loss': {'_target_': 'verl.workers.config.PolicyLossConfig', 'loss_mode': 'vanilla', 'clip_cov_ratio': 0.0002, 'clip_cov_lb': 1.0, 'clip_cov_ub': 5.0, 'kl_cov_ratio': 0.0002, 'ppo_kl_coef': 0.1}, 'clip_ratio_c': 3.0, 'loss_agg_mode': 'token-mean', 'loss_scale_factor': None, 'entropy_coeff': 0, 'calculate_entropy': False, 'use_kl_loss': True, 'use_prefix_grouper': False, 'use_torch_compile': True, 'kl_loss_coef': 0.001, 'kl_loss_type': 'low_var_kl', 'ppo_epochs': 1, 'shuffle': False, 'data_loader_seed': 42, 'checkpoint': {'_target_': 'verl.trainer.config.CheckpointConfig', 'save_contents': ['model', 'optimizer', 'extra'], 'load_contents': ['model', 'optimizer', 'extra'], 'async_save': False}, 'use_fused_kernels': False, 'profiler': {'_target_': 'verl.utils.profiler.ProfilerConfig', 'tool': None, 'enable': False, 'all_ranks': False, 'ranks': [], 'save_path': 'outputs/profile', 'tool_config': {'nsys': {'_target_': 'verl.utils.profiler.config.NsightToolConfig', 'discrete': False}, 'npu': {'_target_': 'verl.utils.profiler.config.NPUToolConfig', 'contents': [], 'level': 'level0', 'analysis': True, 'discrete': False}, 'torch': {'_target_': 'verl.utils.profiler.config.TorchProfilerToolConfig', 'contents': [], 'discrete': False}, 'torch_memory': {'_target_': 'verl.utils.profiler.config.TorchMemoryToolConfig', 'trace_alloc_max_entries': 100000, 'stack_depth': 32}}}, 'router_replay': {'_target_': 'verl.workers.config.RouterReplayConfig', 'mode': 'disabled', 'record_file': None, 'replay_file': None}, 'grad_clip': 1.0, 'ulysses_sequence_parallel_size': 1, 'entropy_from_logits_with_chunking': False, 'entropy_checkpointing': False, 'use_remove_padding': True, 'calculate_sum_pi_squared': False, 'sum_pi_squared_checkpointing': False}, 'ref': {'rollout_n': 3, 'strategy': 'fsdp', 'use_torch_compile': True, 'log_prob_micro_batch_size': None, 'log_prob_micro_batch_size_per_gpu': 32, 'log_prob_use_dynamic_bsz': False, 'log_prob_max_token_len_per_gpu': 16384, 'profiler': {'_target_': 'verl.utils.profiler.ProfilerConfig', 'tool': None, 'enable': False, 'all_ranks': False, 'ranks': [], 'save_path': 'outputs/profile', 'tool_config': {'nsys': {'_target_': 'verl.utils.profiler.config.NsightToolConfig', 'discrete': False}, 'npu': {'_target_': 'verl.utils.profiler.config.NPUToolConfig', 'contents': [], 'level': 'level0', 'analysis': True, 'discrete': False}, 'torch': {'_target_': 'verl.utils.profiler.config.TorchProfilerToolConfig', 'contents': [], 'discrete': False}, 'torch_memory': {'_target_': 'verl.utils.profiler.config.TorchMemoryToolConfig', 'trace_alloc_max_entries': 100000, 'stack_depth': 32}}}, 'router_replay': {'_target_': 'verl.workers.config.RouterReplayConfig', 'mode': 'disabled', 'record_file': None, 'replay_file': None}, 'fsdp_config': {'_target_': 'verl.workers.config.FSDPEngineConfig', 'wrap_policy': {'min_num_params': 0}, 'param_offload': True, 'optimizer_offload': False, 'offload_policy': False, 'reshard_after_forward': True, 'fsdp_size': -1, 'forward_prefetch': False, 'model_dtype': 'fp32', 'use_orig_params': False, 'seed': 42, 'full_determinism': False, 'ulysses_sequence_parallel_size': 1, 'entropy_from_logits_with_chunking': False, 'use_torch_compile': True, 'entropy_checkpointing': False, 'forward_only': True, 'strategy': 'fsdp', 'dtype': 'bfloat16'}, '_target_': 'verl.workers.config.FSDPActorConfig', 'ulysses_sequence_parallel_size': 1, 'entropy_from_logits_with_chunking': False, 'entropy_checkpointing': False}, 'rollout': {'_target_': 'verl.workers.config.RolloutConfig', 'name': 'vllm', 'mode': 'async', 'temperature': 1.0, 'top_k': -1, 'top_p': 1, 'prompt_length': 1024, 'response_length': 2048, 'dtype': 'bfloat16', 'gpu_memory_utilization': 0.4, 'ignore_eos': False, 'enforce_eager': True, 'cudagraph_capture_sizes': None, 'free_cache_engine': True, 'tensor_model_parallel_size': 1, 'data_parallel_size': 1, 'expert_parallel_size': 1, 'pipeline_model_parallel_size': 1, 'max_num_batched_tokens': 8192, 'max_model_len': 8192, 'max_num_seqs': 1024, 'enable_chunked_prefill': True, 'enable_prefix_caching': True, 'logprobs_mode': 'processed_logprobs', 'scheduling_policy': 'fcfs', 'load_format': 'dummy', 'log_prob_micro_batch_size': None, 'log_prob_micro_batch_size_per_gpu': 32, 'log_prob_use_dynamic_bsz': False, 'log_prob_max_token_len_per_gpu': 16384, 'disable_log_stats': True, 'do_sample': True, 'n': 3, 'over_sample_rate': 0, 'multi_stage_wake_up': False, 'engine_kwargs': {'vllm': {}, 'sglang': {}, 'trtllm': {}}, 'val_kwargs': {'_target_': 'verl.workers.config.SamplingConfig', 'top_k': -1, 'top_p': 1.0, 'temperature': 0, 'n': 1, 'do_sample': False}, 'multi_turn': {'_target_': 'verl.workers.config.MultiTurnConfig', 'enable': False, 'max_assistant_turns': None, 'tool_config_path': None, 'max_user_turns': None, 'max_parallel_calls': 1, 'max_tool_response_length': 256, 'tool_response_truncate_side': 'middle', 'interaction_config_path': None, 'use_inference_chat_template': False, 'tokenization_sanity_check_mode': 'strict', 'format': 'hermes', 'num_repeat_rollouts': None}, 'calculate_log_probs': False, 'agent': {'_target_': 'verl.workers.config.AgentLoopConfig', 'num_workers': 8, 'default_agent_loop': 'single_turn_agent', 'agent_loop_config_path': None, 'custom_async_server': {'_target_': 'verl.workers.config.CustomAsyncServerConfig', 'path': None, 'name': None}}, 'checkpoint_engine': {'_target_': 'verl.workers.config.CheckpointEngineConfig', 'backend': 'naive', 'update_weights_bucket_megabytes': 2048, 'engine_kwargs': {}}, 'trace': {'_target_': 'verl.workers.config.TraceConfig', 'backend': None, 'token2text': False, 'max_samples_per_step_per_worker': None}, 'skip_rollout': False, 'skip_dump_dir': '/tmp/rollout_dump', 'skip_tokenizer_init': True, 'enable_rollout_routing_replay': False, 'profiler': {'_target_': 'verl.utils.profiler.ProfilerConfig', 'tool': None, 'enable': False, 'all_ranks': False, 'ranks': [], 'save_path': 'outputs/profile', 'tool_config': {'nsys': {'_target_': 'verl.utils.profiler.config.NsightToolConfig', 'discrete': False}, 'npu': {'_target_': 'verl.utils.profiler.config.NPUToolConfig', 'contents': [], 'level': 'level0', 'analysis': True, 'discrete': False}, 'torch': {'_target_': 'verl.utils.profiler.config.TorchProfilerToolConfig', 'contents': [], 'discrete': False}, 'torch_memory': {'_target_': 'verl.utils.profiler.config.TorchMemoryToolConfig', 'trace_alloc_max_entries': 100000, 'stack_depth': 32}}}, 'prometheus': {'_target_': 'verl.workers.config.PrometheusConfig', 'enable': False, 'port': 9090, 'file': '/tmp/ray/session_latest/metrics/prometheus/prometheus.yml', 'served_model_name': 'Qwen/Qwen3-4B-Instruct-2507'}, 'quantization': None, 'quantization_config_file': None, 'mtp': {'_target_': 'verl.workers.config.MtpConfig', 'enable': False, 'enable_train': False, 'enable_rollout': False, 'detach_encoder': False, 'mtp_loss_scaling_factor': 0.1, 'speculative_algorithm': 'EAGLE', 'speculative_num_steps': 3, 'speculative_eagle_topk': 1, 'speculative_num_draft_tokens': 4, 'method': 'mtp', 'num_speculative_tokens': 1}, 'layered_summon': False}, 'model': {'_target_': 'verl.workers.config.HFModelConfig', 'path': 'Qwen/Qwen3-4B-Instruct-2507', 'hf_config_path': None, 'tokenizer_path': None, 'use_shm': False, 'trust_remote_code': False, 'custom_chat_template': None, 'external_lib': None, 'override_config': {}, 'enable_gradient_checkpointing': True, 'enable_activation_offload': False, 'use_remove_padding': True, 'lora_rank': 0, 'lora_alpha': 16, 'target_modules': 'all-linear', 'exclude_modules': None, 'lora_adapter_path': None, 'use_liger': False, 'use_fused_kernels': False, 'fused_kernel_options': {'impl_backend': 'torch'}, 'tiled_mlp': {'enabled': False, 'num_shards': 4}, 'mtp': {'_target_': 'verl.workers.config.MtpConfig', 'enable': False, 'enable_train': False, 'enable_rollout': False, 'detach_encoder': False, 'mtp_loss_scaling_factor': 0.1, 'speculative_algorithm': 'EAGLE', 'speculative_num_steps': 3, 'speculative_eagle_topk': 1, 'speculative_num_draft_tokens': 4, 'method': 'mtp', 'num_speculative_tokens': 1}}, 'hybrid_engine': True, 'nccl_timeout': 600}, 'data': {'tokenizer': None, 'use_shm': False, 'train_files': '/home/mshahidul/readctrl/code/RL_model/verl/verl_train/dataset/train.parquet', 'val_files': '/home/mshahidul/readctrl/code/RL_model/verl/verl_train/dataset/test.parquet', 'train_max_samples': -1, 'val_max_samples': -1, 'prompt_key': 'prompt', 'reward_fn_key': 'data_source', 'max_prompt_length': 1024, 'max_response_length': 2048, 'train_batch_size': 512, 'val_batch_size': None, 'tool_config_path': None, 'return_raw_input_ids': False, 'return_raw_chat': True, 'return_full_prompt': False, 'shuffle': True, 'seed': None, 'dataloader_num_workers': 8, 'image_patch_size': 14, 'validation_shuffle': False, 'filter_overlong_prompts': True, 'filter_overlong_prompts_workers': 1, 'truncation': 'error', 'image_key': 'images', 'video_key': 'videos', 'trust_remote_code': False, 'custom_cls': {'path': None, 'name': None}, 'return_multi_modal_inputs': True, 'sampler': {'class_path': None, 'class_name': None}, 'datagen': {'path': None, 'name': None}, 'apply_chat_template_kwargs': {}}, 'reward_manager': {'_target_': 'verl.trainer.config.config.RewardManagerConfig', 'source': 'register', 'name': 'naive', 'module': {'_target_': 'verl.trainer.config.config.ModuleConfig', 'path': None, 'name': 'custom_reward_manager'}}, 'critic': {'optim': {'_target_': 'verl.workers.config.FSDPOptimizerConfig', 'optimizer': 'AdamW', 'optimizer_impl': 'torch.optim', 'lr': 1e-05, 'lr_warmup_steps_ratio': 0.0, 'total_training_steps': 45, 'weight_decay': 0.01, 'lr_warmup_steps': -1, 'betas': [0.9, 0.999], 'clip_grad': 1.0, 'min_lr_ratio': 0.0, 'num_cycles': 0.5, 'lr_scheduler_type': 'constant', 'warmup_style': None, 'override_optimizer_config': None}, 'model': {'fsdp_config': {'_target_': 'verl.workers.config.FSDPEngineConfig', 'wrap_policy': {'min_num_params': 0}, 'param_offload': False, 'optimizer_offload': False, 'offload_policy': False, 'reshard_after_forward': True, 'fsdp_size': -1, 'forward_prefetch': False, 'model_dtype': 'fp32', 'use_orig_params': False, 'seed': 42, 'full_determinism': False, 'ulysses_sequence_parallel_size': 1, 'entropy_from_logits_with_chunking': False, 'use_torch_compile': True, 'entropy_checkpointing': False, 'forward_only': False, 'strategy': 'fsdp', 'dtype': 'bfloat16'}, 'path': '~/models/deepseek-llm-7b-chat', 'tokenizer_path': 'Qwen/Qwen3-4B-Instruct-2507', 'override_config': {}, 'external_lib': None, 'trust_remote_code': False, '_target_': 'verl.workers.config.FSDPCriticModelCfg', 'use_shm': False, 'enable_gradient_checkpointing': True, 'enable_activation_offload': False, 'use_remove_padding': False, 'lora_rank': 0, 'lora_alpha': 16, 'target_modules': 'all-linear', 'tiled_mlp': {'enabled': False, 'num_shards': 4}}, '_target_': 'verl.workers.config.FSDPCriticConfig', 'rollout_n': 3, 'strategy': 'fsdp', 'enable': None, 'ppo_mini_batch_size': 256, 'ppo_micro_batch_size': None, 'ppo_micro_batch_size_per_gpu': None, 'use_dynamic_bsz': False, 'ppo_max_token_len_per_gpu': 32768, 'forward_max_token_len_per_gpu': 32768, 'ppo_epochs': 1, 'shuffle': False, 'data_loader_seed': 42, 'cliprange_value': 0.5, 'loss_agg_mode': 'token-mean', 'checkpoint': {'_target_': 'verl.trainer.config.CheckpointConfig', 'save_contents': ['model', 'optimizer', 'extra'], 'load_contents': ['model', 'optimizer', 'extra'], 'async_save': False}, 'profiler': {'_target_': 'verl.utils.profiler.ProfilerConfig', 'tool': None, 'enable': False, 'all_ranks': False, 'ranks': [], 'save_path': 'outputs/profile', 'tool_config': {'nsys': {'_target_': 'verl.utils.profiler.config.NsightToolConfig', 'discrete': False}, 'npu': {'_target_': 'verl.utils.profiler.config.NPUToolConfig', 'contents': [], 'level': 'level0', 'analysis': True, 'discrete': False}, 'torch': {'_target_': 'verl.utils.profiler.config.TorchProfilerToolConfig', 'contents': [], 'discrete': False}, 'torch_memory': {'_target_': 'verl.utils.profiler.config.TorchMemoryToolConfig', 'trace_alloc_max_entries': 100000, 'stack_depth': 32}}}, 'forward_micro_batch_size': None, 'forward_micro_batch_size_per_gpu': None, 'ulysses_sequence_parallel_size': 1, 'grad_clip': 1.0}, 'reward_model': {'enable': False, 'enable_resource_pool': False, 'n_gpus_per_node': 8, 'nnodes': 0, 'strategy': 'fsdp', 'model': {'input_tokenizer': 'Qwen/Qwen3-4B-Instruct-2507', 'path': '~/models/FsfairX-LLaMA3-RM-v0.1', 'external_lib': None, 'trust_remote_code': False, 'override_config': {}, 'use_shm': False, 'use_remove_padding': False, 'use_fused_kernels': False, 'fsdp_config': {'_target_': 'verl.workers.config.FSDPEngineConfig', 'wrap_policy': {'min_num_params': 0}, 'param_offload': False, 'reshard_after_forward': True, 'fsdp_size': -1, 'forward_prefetch': False}}, 'micro_batch_size': None, 'micro_batch_size_per_gpu': None, 'max_length': None, 'use_dynamic_bsz': False, 'forward_max_token_len_per_gpu': 32768, 'reward_manager': 'naive', 'reward_loop_source': 'register', 'reward_loop_module_path': None, 'reward_loop_class_name': None, 'launch_reward_fn_async': False, 'sandbox_fusion': {'url': None, 'max_concurrent': 64, 'memory_limit_mb': 1024}, 'profiler': {'_target_': 'verl.utils.profiler.ProfilerConfig', 'tool': None, 'enable': False, 'all_ranks': False, 'ranks': [], 'save_path': 'outputs/profile', 'tool_config': {'nsys': {'_target_': 'verl.utils.profiler.config.NsightToolConfig', 'discrete': False}, 'npu': {'_target_': 'verl.utils.profiler.config.NPUToolConfig', 'contents': [], 'level': 'level0', 'analysis': True, 'discrete': False}, 'torch': {'_target_': 'verl.utils.profiler.config.TorchProfilerToolConfig', 'contents': [], 'discrete': False}, 'torch_memory': {'_target_': 'verl.utils.profiler.config.TorchMemoryToolConfig', 'trace_alloc_max_entries': 100000, 'stack_depth': 32}}}, 'ulysses_sequence_parallel_size': 1, 'use_reward_loop': True, 'num_workers': 1, 'rollout': {'_target_': 'verl.workers.config.RolloutConfig', 'name': '???', 'dtype': 'bfloat16', 'gpu_memory_utilization': 0.5, 'enforce_eager': True, 'cudagraph_capture_sizes': None, 'free_cache_engine': True, 'data_parallel_size': 1, 'expert_parallel_size': 1, 'tensor_model_parallel_size': 2, 'max_num_batched_tokens': 8192, 'max_model_len': None, 'max_num_seqs': 1024, 'load_format': 'auto', 'engine_kwargs': {}, 'limit_images': None, 'enable_chunked_prefill': True, 'enable_prefix_caching': True, 'disable_log_stats': True, 'skip_tokenizer_init': False, 'prompt_length': 2048, 'response_length': 2048}}, 'algorithm': {'rollout_correction': {'rollout_is': None, 'rollout_is_threshold': 2.0, 'rollout_rs': None, 'rollout_rs_threshold': None, 'bypass_mode': False, 'loss_type': 'ppo_clip', 'rollout_is_batch_normalize': False}, '_target_': 'verl.trainer.config.AlgoConfig', 'gamma': 1.0, 'lam': 1.0, 'adv_estimator': 'grpo', 'norm_adv_by_std_in_grpo': True, 'use_kl_in_reward': False, 'kl_penalty': 'kl', 'kl_ctrl': {'_target_': 'verl.trainer.config.KLControlConfig', 'type': 'fixed', 'kl_coef': 0.001, 'horizon': 10000, 'target_kl': 0.1}, 'use_pf_ppo': False, 'pf_ppo': {'reweight_method': 'pow', 'weight_pow': 2.0}}, 'custom_reward_function': {'path': '/home/mshahidul/readctrl/code/RL_model/verl/verl_train/reward_func/reward_func/reward_new_v2.py', 'name': 'compute_score'}, 'trainer': {'balance_batch': True, 'total_epochs': 15, 'total_training_steps': None, 'project_name': 'readctrl-verl', 'experiment_name': 'qwen3-4b-instruct-en', 'logger': ['console', 'wandb'], 'log_val_generations': 0, 'rollout_data_dir': None, 'validation_data_dir': None, 'nnodes': 1, 'n_gpus_per_node': 2, 'save_freq': 5, 'esi_redundant_time': 0, 'resume_mode': 'auto', 'resume_from_path': None, 'val_before_train': True, 'val_only': False, 'test_freq': 10, 'critic_warmup': 0, 'default_hdfs_dir': None, 'del_local_ckpt_after_load': False, 'default_local_dir': '/home/mshahidul/readctrl/code/RL_model/models/RL_model_subclaim_classifier_v2', 'max_actor_ckpt_to_keep': 1, 'max_critic_ckpt_to_keep': 1, 'ray_wait_register_center_timeout': 300, 'device': 'cuda', 'use_legacy_worker_impl': 'auto', 'remove_previous_ckpt_in_save': True}, 'global_profiler': {'_target_': 'verl.utils.profiler.ProfilerConfig', 'tool': None, 'steps': None, 'profile_continuous_steps': False, 'save_path': 'outputs/profile', 'global_tool_config': {'nsys': {'_target_': 'verl.utils.profiler.config.NsightToolConfig', 'discrete': False, 'controller_nsight_options': {'trace': 'cuda,nvtx,cublas,ucx', 'cuda-memory-usage': 'true', 'cuda-graph-trace': 'graph'}, 'worker_nsight_options': {'trace': 'cuda,nvtx,cublas,ucx', 'cuda-memory-usage': 'true', 'cuda-graph-trace': 'graph', 'capture-range': 'cudaProfilerApi', 'capture-range-end': None, 'kill': 'none'}}, 'torch_memory': {'trace_alloc_max_entries': 100000, 'stack_depth': 32, 'context': 'all', 'stacks': 'all', 'kw_args': {}}}}, 'transfer_queue': {'enable': False}, 'ray_kwargs': {'ray_init': {'num_cpus': None}, 'timeline_json_file': None}, '_wandb': {}}
+2026-02-15 11:45:17,232 INFO    MainThread:3962104 [wandb_init.py:init():892] starting backend
+2026-02-15 11:45:17,505 INFO    MainThread:3962104 [wandb_init.py:init():895] sending inform_init request
+2026-02-15 11:45:17,514 INFO    MainThread:3962104 [wandb_init.py:init():903] backend started and connected
+2026-02-15 11:45:17,529 INFO    MainThread:3962104 [wandb_init.py:init():973] updated telemetry
+2026-02-15 11:45:17,549 INFO    MainThread:3962104 [wandb_init.py:init():997] communicating run to backend with 90.0 second timeout
+2026-02-15 11:45:19,282 INFO    MainThread:3962104 [wandb_init.py:init():1042] starting run threads in backend
+2026-02-15 11:45:20,497 INFO    MainThread:3962104 [wandb_run.py:_console_start():2529] atexit reg
+2026-02-15 11:45:20,498 INFO    MainThread:3962104 [wandb_run.py:_redirect():2377] redirect: wrap_raw
+2026-02-15 11:45:20,498 INFO    MainThread:3962104 [wandb_run.py:_redirect():2446] Wrapping output streams.
+2026-02-15 11:45:20,498 INFO    MainThread:3962104 [wandb_run.py:_redirect():2469] Redirects installed.
+2026-02-15 11:45:20,508 INFO    MainThread:3962104 [wandb_init.py:init():1082] run started, returning control to user process
diff --git a/code/bash_script/b.sh b/code/bash_script/b.sh
new file mode 100644
index 0000000000000000000000000000000000000000..1fdd2c4b3ff89e3f501fcae22c33b1bfe4068d55
--- /dev/null
+++ b/code/bash_script/b.sh
@@ -0,0 +1,36 @@
+
+python /home/mshahidul/readctrl/code/finetune-inference/api_call_vllm_v2.py \
+     --file1 /home/mshahidul/readctrl/data/hand_create_gpt5_other_model/synthetic_data_es_raw_592.json \
+     --file2 /home/mshahidul/readctrl/data/testing_data_gs/multiclinsum_gs_train_es.json \
+     --start_index 500 \
+     --end_index -1
+
+python /home/mshahidul/readctrl/code/finetune-inference/convert_fp16.py \
+    --model_path /home/mshahidul/readctrl_model/qwen3-32B_subclaims-extraction-8b_ctx \
+    --save_path /home/mshahidul/readctrl_model/full_model/qwen3-32B_subclaims_BF16_merged \
+    --msl 8192 \
+    --cuda_device 1
+
+
+python /home/mshahidul/readctrl/code/finetune-inference/subclaim_support_cal_v4.py \
+    --start_index 0 \
+    --end_index 100
+python /home/mshahidul/readctrl/code/finetune-inference/subclaim_support_cal_v4.py \
+    --start_index 100 \
+    --end_index 200
+python /home/mshahidul/readctrl/code/finetune-inference/subclaim_support_cal_v4.py \
+    --start_index 200 \
+    --end_index 300
+python /home/mshahidul/readctrl/code/finetune-inference/subclaim_support_cal_v4.py \
+    --start_index 300 \
+    --end_index 400
+python /home/mshahidul/readctrl/code/finetune-inference/subclaim_support_cal_v4.py \
+    --start_index 400 \
+    --end_index 500
+python /home/mshahidul/readctrl/code/finetune-inference/subclaim_support_cal_v4.py \
+    --start_index 500 \
+    --end_index -1
+
+
+
+ 
diff --git a/code/bash_script/vllm_server.sh b/code/bash_script/vllm_server.sh
new file mode 100644
index 0000000000000000000000000000000000000000..d1bf4bcafb163ae39020e5ade6b2a84a048b3809
--- /dev/null
+++ b/code/bash_script/vllm_server.sh
@@ -0,0 +1,23 @@
+#!/bin/bash
+
+# 1. Set Device Order and Visibility
+# This ensures we are targeting the physical GPU ID 1 as requested.
+export CUDA_DEVICE_ORDER="PCI_BUS_ID"
+export CUDA_VISIBLE_DEVICES="1"
+
+# 2. Define Paths and Configuration
+# Using the path where we just saved the BF16 model
+MODEL_PATH="/home/mshahidul/readctrl_model/full_model/qwen3-32B_subclaims-support-check-8b_ctx-bf16"
+SERVE_PORT=8015
+
+python -m vllm.entrypoints.openai.api_server \
+    --model $MODEL_PATH \
+    --dtype bfloat16 \
+    --max-model-len 8192 \
+    --gpu-memory-utilization 0.95 \
+    --port $SERVE_PORT \
+    --trust-remote-code
+
+# python /home/mshahidul/readctrl/code/finetune-inference/api_call_vllm_v2.py \
+#      --file1 /home/mshahidul/readctrl/data/hand_create_gpt5_other_model/synthetic_data_es_raw_592.jsonl \
+#      --file2 /home/mshahidul/readctrl/data/testing_data/es_testing_data.json
\ No newline at end of file
diff --git a/code/bash_script/vllm_server_v2.sh b/code/bash_script/vllm_server_v2.sh
new file mode 100644
index 0000000000000000000000000000000000000000..787fb9953ee97cabbdb509df9d9306bee46f13f1
--- /dev/null
+++ b/code/bash_script/vllm_server_v2.sh
@@ -0,0 +1,13 @@
+#!/bin/bash
+
+# 1. Set Device Order and Visibility
+# This ensures we are targeting the physical GPU ID 1 as requested.
+export CUDA_DEVICE_ORDER="PCI_BUS_ID"
+export CUDA_VISIBLE_DEVICES="1"
+
+vllm serve Qwen/Qwen3-30B-A3B-Thinking-2507 \
+  --trust-remote-code \
+  --dtype bfloat16 \
+  --max-model-len 16384 \
+  --gpu-memory-utilization 0.95 \
+  --port 8015
\ No newline at end of file
diff --git a/code/classifier/apo.ipynb b/code/classifier/apo.ipynb
new file mode 100644
index 0000000000000000000000000000000000000000..14683e9b8b7f9095d2d8023fb67dd4ca14b020bb
--- /dev/null
+++ b/code/classifier/apo.ipynb
@@ -0,0 +1,234 @@
+{
+ "cells": [
+  {
+   "cell_type": "code",
+   "execution_count": 1,
+   "id": "db631ce7",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "# Initial Classifier Prompt (p0)\n",
+    "target_trainable_instruction = \"\"\"Identify the health literacy level of the following medical text. \n",
+    "Select exactly one label from: [low_health_literacy, intermediate_health_literacy, proficient_health_literacy].\n",
+    "Think about the medical terminology used, sentence complexity, and clarity for a general audience.\"\"\"\n",
+    "\n",
+    "# The specific classification instruction format\n",
+    "classify_raw_instruction = \"\"\"[target_trainable_instruction]\n",
+    "[target_trainable_few_shot_examples]\n",
+    "\n",
+    "Medical Text:\n",
+    "[gen_text]\n",
+    "\n",
+    "Output your classification.\n",
+    "Return the output as a JSON object: {\"prediction\": \"label_here\"}\n",
+    "\"\"\"\n",
+    "\n",
+    "# The \"Gradient\" Prompt (Forward Step)\n",
+    "# This explains why the model misclassified a sample and suggests an instruction update.\n",
+    "training_prompt_forward = \"\"\"In this task, you are an expert linguist. We are using an AI to classify the health literacy level of medical text, but it is making mistakes.\n",
+    "Your job is to analyze the error and suggest how to modify the instruction to fix it.\n",
+    "\n",
+    "Current Instruction:\n",
+    "[target_trainable_instruction]\n",
+    "\n",
+    "Medical Text:\n",
+    "[gen_text]\n",
+    "\n",
+    "AI Predicted Label: [AI_prediction]\n",
+    "Correct Ground Truth Label: [label_summary]\n",
+    "\n",
+    "Requirements for your suggestions:\n",
+    "1) Suggest high-level linguistic criteria (e.g., focus on syllable count, jargon, or tone).\n",
+    "2) Do not include specific examples.\n",
+    "3) Focus only on improving classification accuracy.\n",
+    "\n",
+    "Return the output as a JSON: {\"reasons\": \"...\", \"suggestions\": \"...\"}\n",
+    "\"\"\""
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 2,
+   "id": "f3316de5",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import json\n",
+    "import pandas as pd\n",
+    "from tqdm import tqdm\n",
+    "\n",
+    "def do_classify(target_trainable_instruction, classify_raw_instruction, gen_text, \n",
+    "                target_trainable_few_shot_examples='', do_few_shot=False):\n",
+    "    # Construct the prompt\n",
+    "    instruction = classify_raw_instruction.replace('[target_trainable_instruction]', target_trainable_instruction)\n",
+    "    instruction = instruction.replace('[gen_text]', gen_text)\n",
+    "    \n",
+    "    if do_few_shot:\n",
+    "        instruction = instruction.replace('[target_trainable_few_shot_examples]', target_trainable_few_shot_examples)\n",
+    "    else:\n",
+    "        instruction = instruction.replace('[target_trainable_few_shot_examples]', '')\n",
+    "\n",
+    "    # Call OpenAI (or your local vLLM)\n",
+    "    response = openai.ChatCompletion.create(\n",
+    "        model=\"gpt-5\",\n",
+    "        messages=[{\"role\": \"system\", \"content\": instruction}],\n",
+    "    )\n",
+    "    \n",
+    "    try:\n",
+    "        content = response[\"choices\"][0][\"message\"][\"content\"]\n",
+    "        prediction = json.loads(content, strict=False)['prediction']\n",
+    "        return prediction\n",
+    "    except:\n",
+    "        return \"error\"\n",
+    "\n",
+    "def training_forward_step(training_prompt_forward, target_trainable_instruction, \n",
+    "                          gen_text, AI_prediction, label_summary):\n",
+    "    # Replaces placeholders with the classification error details\n",
+    "    instruction = training_prompt_forward.replace('[target_trainable_instruction]', target_trainable_instruction)\n",
+    "    instruction = instruction.replace('[gen_text]', gen_text)\n",
+    "    instruction = instruction.replace('[AI_prediction]', AI_prediction)\n",
+    "    instruction = instruction.replace('[label_summary]', label_summary)\n",
+    "\n",
+    "    response = openai.ChatCompletion.create(\n",
+    "        model=\"gpt-4\", # High reasoning model recommended for the \"gradient\" step\n",
+    "        messages=[{\"role\": \"system\", \"content\": instruction}],\n",
+    "        temperature=0\n",
+    "    )\n",
+    "    return json.loads(response[\"choices\"][0][\"message\"][\"content\"], strict=False)['suggestions']"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 3,
+   "id": "c3aeae14",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import json\n",
+    "\n",
+    "# Load Test Set\n",
+    "with open('/home/mshahidul/readctrl/data/new_exp/test_health_literacy_data.json', 'r') as f:\n",
+    "    test_data = json.load(f)\n",
+    "eval_df = pd.DataFrame(test_data)\n",
+    "\n",
+    "# Load Few-shot Data (For the training pool)\n",
+    "with open('/home/mshahidul/readctrl/data/new_exp/few_shot_examples.json', 'r') as f:\n",
+    "    few_shot_json = json.load(f)\n",
+    "\n",
+    "# Flatten the categories into one training pool\n",
+    "all_train_records = []\n",
+    "for category in few_shot_json:\n",
+    "    for record in few_shot_json[category]:\n",
+    "        # Ensure the 'label' matches the category key for training\n",
+    "        record['label_actual'] = category \n",
+    "        all_train_records.append(record)\n",
+    "train_df = pd.DataFrame(all_train_records)"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 4,
+   "id": "6ed53650",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "from sklearn.metrics import accuracy_score, classification_report, f1_score\n",
+    "\n",
+    "class ClassificationEval:\n",
+    "    def __init__(self, labels=['low_health_literacy', 'intermediate_health_literacy', 'proficient_health_literacy']):\n",
+    "        self.target_names = labels\n",
+    "\n",
+    "    def run_evaluation(self, labels, preds):\n",
+    "        \"\"\"\n",
+    "        Calculates accuracy and F1 score for the classification task.\n",
+    "        \"\"\"\n",
+    "        # Filter out errors or invalid labels to prevent crash\n",
+    "        valid_indices = [i for i, p in enumerate(preds) if p in self.target_names]\n",
+    "        \n",
+    "        filtered_labels = [labels[i] for i in valid_indices]\n",
+    "        filtered_preds = [preds[i] for i in valid_indices]\n",
+    "\n",
+    "        results = {\n",
+    "            \"accuracy\": accuracy_score(filtered_labels, filtered_preds),\n",
+    "            \"f1_macro\": f1_score(filtered_labels, filtered_preds, average='macro'),\n",
+    "            \"valid_count\": len(filtered_preds),\n",
+    "            \"total_count\": len(preds)\n",
+    "        }\n",
+    "        \n",
+    "        return results"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 5,
+   "id": "71c544b7",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "def eval_loop(eval_df, target_trainable_instruction, classify_raw_instruction, \n",
+    "              target_trainable_few_shot_examples, do_few_shot, classifier_eval):\n",
+    "    preds = []\n",
+    "    labels = []\n",
+    "    \n",
+    "    for i in tqdm(range(eval_df.shape[0]), desc=\"Evaluating Readability\"):\n",
+    "        row = eval_df.iloc[i]\n",
+    "        gen_text = row['gen_text']  # The medical text to classify\n",
+    "        ground_truth = row['label'] # The actual literacy level\n",
+    "        \n",
+    "        try:\n",
+    "            # Predict using the current prompt version\n",
+    "            prediction = do_classify(\n",
+    "                target_trainable_instruction, \n",
+    "                classify_raw_instruction, \n",
+    "                gen_text,\n",
+    "                target_trainable_few_shot_examples, \n",
+    "                do_few_shot\n",
+    "            )\n",
+    "            preds.append(prediction)\n",
+    "            labels.append(ground_truth)\n",
+    "        except Exception as e:\n",
+    "            print(f\"Error at row {i}: {e}\")\n",
+    "            continue\n",
+    "\n",
+    "    # Calculate classification metrics\n",
+    "    metrics = classifier_eval.run_evaluation(labels, preds)\n",
+    "    \n",
+    "    # Format for logging\n",
+    "    eval_dict = {k: round(v, 4) if isinstance(v, float) else v for k, v in metrics.items()}\n",
+    "    eval_dict['labels'] = labels\n",
+    "    eval_dict['preds'] = preds\n",
+    "\n",
+    "    return eval_dict"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "aa91a214",
+   "metadata": {},
+   "outputs": [],
+   "source": []
+  }
+ ],
+ "metadata": {
+  "kernelspec": {
+   "display_name": "un",
+   "language": "python",
+   "name": "python3"
+  },
+  "language_info": {
+   "codemirror_mode": {
+    "name": "ipython",
+    "version": 3
+   },
+   "file_extension": ".py",
+   "mimetype": "text/x-python",
+   "name": "python",
+   "nbconvert_exporter": "python",
+   "pygments_lexer": "ipython3",
+   "version": "3.11.14"
+  }
+ },
+ "nbformat": 4,
+ "nbformat_minor": 5
+}
diff --git a/code/classifier/classifier.py b/code/classifier/classifier.py
new file mode 100644
index 0000000000000000000000000000000000000000..44fd6f585be96a96e7cc7806b50b830e56678410
--- /dev/null
+++ b/code/classifier/classifier.py
@@ -0,0 +1,169 @@
+import os
+os.environ["CUDA_DEVICE_ORDER"] = "PCI_BUS_ID"
+os.environ["CUDA_VISIBLE_DEVICES"] = "2"
+
+import torch
+from unsloth import FastLanguageModel
+import json
+import tqdm
+import re
+
+# -----------------------------
+#  MODEL CACHE
+# -----------------------------
+_model_cache = {"model": None, "tokenizer": None}
+
+def load_finetuned_model(model_path: str):
+    if _model_cache["model"] is not None:
+        return _model_cache["model"], _model_cache["tokenizer"]
+
+    model, tokenizer = FastLanguageModel.from_pretrained(
+        model_name=model_path,
+        max_seq_length=8192,
+        load_in_4bit=False, # Set to True if you want 4bit inference for speed/memory
+        load_in_8bit=False,
+        full_finetuning=False,
+    )
+    # Enable native 2x faster inference
+    FastLanguageModel.for_inference(model)
+    
+    _model_cache["model"], _model_cache["tokenizer"] = model, tokenizer
+    return model, tokenizer
+
+# -----------------------------
+#  READABILITY CLASSIFICATION PROMPT
+# -----------------------------
+def classification_prompt(full_text: str, summary: str) -> str:
+    """
+    Constructs the prompt to classify readability of the summary
+    based on the context of the full text.
+    """
+    prompt = f"""You are a medical readability evaluator.
+
+### Task
+Compare the "GENERATED TEXT" against the "FULL TEXT" to determine its readability for a general, non-medical audience.
+
+### Input Data
+- **FULL TEXT:** {full_text}
+- **GENERATED TEXT (Evaluate this):** {summary}
+
+### Readability Scale
+1: Very Easy - Minimal medical language, uses simple terms.
+2: Easy - Accessible to most, minor jargon explained.
+3: Medium - Some technical terms, moderate complexity.
+4: Hard - Clinical tone, assumes some prior knowledge.
+5: Very Hard - Extremely technical, requires medical expertise.
+
+### Constraints
+- Evaluate ONLY the "GENERATED TEXT".
+- Use "FULL TEXT" only for context of the subject matter.
+- Do NOT assess factual accuracy.
+
+### Output Format
+Return ONLY a valid JSON object:
+{{
+  "readability_score": <integer_1_to_5>
+}}"""
+    return prompt
+
+# -----------------------------
+#  INFERENCE FUNCTION
+# -----------------------------
+def infer_readability(full_text: str, 
+                      summary: str,
+                      model_path: str) -> dict:
+    
+    model, tokenizer = load_finetuned_model(model_path)
+    prompt = classification_prompt(full_text, summary)
+
+    messages = [{"role": "user", "content": prompt}]
+
+    chat_text = tokenizer.apply_chat_template(
+        messages,
+        tokenize=False,
+        add_generation_prompt=True,
+    )
+
+    inputs = tokenizer(chat_text, return_tensors="pt").to("cuda")
+
+    with torch.no_grad():
+        output_ids = model.generate(
+            **inputs,
+            max_new_tokens=50, # Classification only needs a few tokens
+            temperature=0.1,   # Low temperature for classification consistency
+            do_sample=False,
+        )
+
+    output_text = tokenizer.decode(output_ids[0][len(inputs.input_ids[0]):], skip_special_tokens=True).strip()
+
+    # Clean up output (remove thinking or markdown)
+    if "</think>" in output_text:
+        output_text = output_text.split("</think>")[-1].strip()
+    
+    # Simple regex to extract JSON if the model adds conversational filler
+    try:
+        match = re.search(r"\{.*\}", output_text, re.DOTALL)
+        if match:
+            return json.loads(match.group())
+        return {"readability_score": "error", "raw": output_text}
+    except Exception:
+        return {"readability_score": "error", "raw": output_text}
+
+# -----------------------------
+#  MAIN EXECUTION
+# -----------------------------
+if __name__ == "__main__":
+    # Settings based on your paths
+    INPUT_FILE = "/home/mshahidul/readctrl/data/processed_raw_data/multiclinsum_test_en.json"
+    SAVE_FOLDER = "/home/mshahidul/readctrl/data/classified_readability"
+    # Note: Ensure this path points to your CLASSIFIER model, not the subclaim extractor
+    MODEL_PATH = "/home/mshahidul/readctrl_model/qwen3-32B_classifier_en" 
+
+    os.makedirs(SAVE_FOLDER, exist_ok=True)
+    file_name = os.path.basename(INPUT_FILE).split(".json")[0]
+    OUTPUT_FILE = os.path.join(SAVE_FOLDER, f"classified_{file_name}.json")
+
+    # Load input dataset
+    with open(INPUT_FILE, "r") as f:
+        data = json.load(f)
+
+    # Resume mode
+    result = []
+    if os.path.exists(OUTPUT_FILE):
+        with open(OUTPUT_FILE, "r") as f:
+            result = json.load(f)
+    
+    existing_ids = {item["id"] for item in result}
+
+    print(f"Starting classification. Saving to: {OUTPUT_FILE}")
+
+    for item in tqdm.tqdm(data):
+        if item["id"] in existing_ids:
+            continue
+
+        full_text = item.get("fulltext", "")
+        summary = item.get("summary", "")
+
+        classification_res = infer_readability(
+            full_text=full_text,
+            summary=summary,
+            model_path=MODEL_PATH
+        )
+
+        result.append({
+            "id": item["id"],
+            "readability_score": classification_res.get("readability_score"),
+            "fulltext": full_text,
+            "summary": summary
+        })
+
+        # Checkpoint every 50 items
+        if len(result) % 50 == 0:
+            with open(OUTPUT_FILE, "w") as f:
+                json.dump(result, f, indent=4, ensure_ascii=False)
+
+    # Final save
+    with open(OUTPUT_FILE, "w") as f:
+        json.dump(result, f, indent=4, ensure_ascii=False)
+
+    print(f"Classification completed. {len(result)} items processed.")
\ No newline at end of file
diff --git a/code/classifier/data_st.ipynb b/code/classifier/data_st.ipynb
new file mode 100644
index 0000000000000000000000000000000000000000..6dfb809463dc29a4fb8c225da2285f3c5ef32129
--- /dev/null
+++ b/code/classifier/data_st.ipynb
@@ -0,0 +1,1874 @@
+{
+ "cells": [
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "311c1d16",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "# /home/mshahidul/readctrl/data/annotators_validate_data\n",
+    "import os\n",
+    "print(os.listdir('/home/mshahidul/readctrl/data/annotators_validate_data')[:3])\n",
+    "all_folders = os.listdir('/home/mshahidul/readctrl/data/annotators_validate_data')\n",
+    "print(os.listdir(f'/home/mshahidul/readctrl/data/annotators_validate_data/{all_folders[0]}'))\n",
+    "file_path = f'/home/mshahidul/readctrl/data/annotators_validate_data/{all_folders[0]}/annotation_results.json'\n",
+    "import json\n",
+    "with open(file_path, 'r') as f:\n",
+    "    data = json.load(f)\n",
+    "print(data[0].keys())"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "ea2f9f3b",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "(all_folders)"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "08ae6eaa",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import os\n",
+    "import json\n",
+    "import pandas as pd\n",
+    "from collections import Counter\n",
+    "\n",
+    "# Configuration\n",
+    "input_dir = '/home/mshahidul/readctrl/data/annotators_validate_data'\n",
+    "output_dir = '/home/mshahidul/readctrl/data/final_result'\n",
+    "output_file = os.path.join(output_dir, 'consolidated_ratings.json')\n",
+    "\n",
+    "# 1. Create the output directory if it doesn't exist\n",
+    "if not os.path.exists(output_dir):\n",
+    "    os.makedirs(output_dir, exist_ok=True)\n",
+    "\n",
+    "all_data = []\n",
+    "\n",
+    "# 2. Collect data from all folders\n",
+    "folders = [f for f in os.listdir(input_dir) if os.path.isdir(os.path.join(input_dir, f))]\n",
+    "avg = []\n",
+    "for folder in folders:\n",
+    "    json_path = os.path.join(input_dir, folder, 'annotation_results.json')\n",
+    "    if os.path.exists(json_path):\n",
+    "        with open(json_path, 'r') as f:\n",
+    "            try:\n",
+    "                entries = json.load(f)\n",
+    "                if len(entries) <=3 :\n",
+    "                    # print(f\"No entries found in {json_path}, skipping.\")\n",
+    "                    avg.append(len(entries))\n",
+    "                avg\n",
+    "                for item in entries:\n",
+    "                    all_data.append({\n",
+    "                        'doc_id': item.get('doc_id'),\n",
+    "                        'health_literacy_label': item.get('health_literacy_label'),\n",
+    "                        'rating': item.get('doc_rating')\n",
+    "                    })\n",
+    "            except Exception as e:\n",
+    "                print(f\"Skipping error in {json_path}: {e}\")\n",
+    "\n",
+    "# 3. Process data\n",
+    "df = pd.DataFrame(all_data)\n",
+    "\n",
+    "# Ensure we drop rows where any of our keys or the rating are missing\n",
+    "df = df.dropna(subset=['doc_id', 'health_literacy_label', 'rating'])\n",
+    "\n",
+    "# 4. Aggregation Logic using both doc_id and health_literacy_label\n",
+    "def get_mode(series):\n",
+    "    # Returns the most common rating for this specific doc + literacy level\n",
+    "    return Counter(series).most_common(1)[0][0]\n",
+    "\n",
+    "# Grouping by the composite key\n",
+    "summary = df.groupby(['doc_id', 'health_literacy_label'])['rating'].agg([\n",
+    "    ('num_annotations', 'count'),\n",
+    "    ('mean_rating', 'mean'),\n",
+    "    ('consensus_rating', get_mode),\n",
+    "    ('rating_distribution', lambda x: list(x))\n",
+    "]).reset_index()\n",
+    "\n",
+    "# 5. Save to JSON\n",
+    "# orient='records' creates a list of dictionaries\n",
+    "summary.to_json(output_file, orient='records', indent=4)\n",
+    "\n",
+    "print(f\"Success! Processed {len(summary)} unique (doc_id, literacy_label) pairs.\")\n",
+    "print(f\"File saved at: {output_file}\")\n",
+    "\n",
+    "# Preview the first few entries\n",
+    "print(summary.head())"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "75197961",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import os\n",
+    "import json\n",
+    "import pandas as pd\n",
+    "from collections import Counter\n",
+    "\n",
+    "# Configuration\n",
+    "input_dir = '/home/mshahidul/readctrl/data/annotators_validate_data'\n",
+    "output_dir = '/home/mshahidul/readctrl/data/final_result'\n",
+    "output_file_match = os.path.join(output_dir, 'consolidated_ratings.json')\n",
+    "output_file_mismatch = os.path.join(output_dir, 'mismatched_ratings.json')\n",
+    "\n",
+    "if not os.path.exists(output_dir):\n",
+    "    os.makedirs(output_dir, exist_ok=True)\n",
+    "\n",
+    "all_data = []\n",
+    "folders = [f for f in os.listdir(input_dir) if os.path.isdir(os.path.join(input_dir, f))]\n",
+    "\n",
+    "# 1. Collect data\n",
+    "for folder in folders:\n",
+    "    json_path = os.path.join(input_dir, folder, 'annotation_results.json')\n",
+    "    if os.path.exists(json_path):\n",
+    "        with open(json_path, 'r') as f:\n",
+    "            try:\n",
+    "                entries = json.load(f)\n",
+    "                for item in entries:\n",
+    "                    all_data.append({\n",
+    "                        'doc_id': item.get('doc_id'),\n",
+    "                        'health_literacy_label': item.get('health_literacy_label'),\n",
+    "                        'rating': item.get('doc_rating')\n",
+    "                    })\n",
+    "            except Exception as e:\n",
+    "                print(f\"Skipping error in {json_path}: {e}\")\n",
+    "\n",
+    "df = pd.DataFrame(all_data).dropna(subset=['doc_id', 'health_literacy_label', 'rating'])\n",
+    "\n",
+    "# 2. Aggregation Logic\n",
+    "def get_mode(series):\n",
+    "    return Counter(series).most_common(1)[0][0]\n",
+    "\n",
+    "summary = df.groupby(['doc_id', 'health_literacy_label'])['rating'].agg([\n",
+    "    ('num_annotations', 'count'),\n",
+    "    ('mean_rating', 'mean'),\n",
+    "    ('consensus_rating', get_mode),\n",
+    "    ('rating_distribution', lambda x: list(x))\n",
+    "]).reset_index()\n",
+    "\n",
+    "# 3. Validation Logic\n",
+    "def check_match(row):\n",
+    "    label = row['health_literacy_label']\n",
+    "    rating = row['consensus_rating']\n",
+    "    \n",
+    "    if label == \"low_health_literacy\":\n",
+    "        return rating in [1, 2]\n",
+    "    elif label == \"intermediate_health_literacy\":\n",
+    "        return rating == 3\n",
+    "    elif label == \"proficient_health_literacy\":\n",
+    "        return rating in [4, 5]\n",
+    "    return False\n",
+    "\n",
+    "# Apply the check\n",
+    "summary['is_match'] = summary.apply(check_match, axis=1)\n",
+    "\n",
+    "# 4. Split and Save\n",
+    "matches = summary[summary['is_match'] == True].drop(columns=['is_match'])\n",
+    "mismatches = summary[summary['is_match'] == False].drop(columns=['is_match'])\n",
+    "\n",
+    "matches.to_json(output_file_match, orient='records', indent=4)\n",
+    "mismatches.to_json(output_file_mismatch, orient='records', indent=4)\n",
+    "\n",
+    "print(f\"Success!\")\n",
+    "print(f\"Matching entries saved: {len(matches)} -> {output_file_match}\")\n",
+    "print(f\"Mismatched entries saved: {len(mismatches)} -> {output_file_mismatch}\")\n",
+    "\n",
+    "if not mismatches.empty:\n",
+    "    print(\"\\nPreview of Mismatches:\")\n",
+    "    print(mismatches.head())"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "e8773257",
+   "metadata": {},
+   "outputs": [],
+   "source": []
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "3f1f1045",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "min(avg), max(avg), sum(avg)/len(avg)"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "877ebaac",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import pandas as pd\n",
+    "import json\n",
+    "\n",
+    "# 1. Load your consolidated JSON file\n",
+    "file_path = '/home/mshahidul/readctrl/data/final_result/consolidated_ratings.json'\n",
+    "with open(file_path, 'r') as f:\n",
+    "    data = json.load(f)\n",
+    "\n",
+    "df = pd.DataFrame(data)\n",
+    "\n",
+    "# 2. Define the \"OK\" logic function\n",
+    "def check_if_ok(row):\n",
+    "    label = str(row['health_literacy_label']).lower()\n",
+    "    rating = row['consensus_rating']\n",
+    "    \n",
+    "    if label == 'low_health_literacy':\n",
+    "        return 1 if rating in [1, 2] else 0\n",
+    "    elif label == 'intermediate_health_literacy':\n",
+    "        return 1 if rating == 3 else 0\n",
+    "    elif label == 'proficient_health_literacy':\n",
+    "        return 1 if rating in [4, 5] else 0\n",
+    "    return 0\n",
+    "\n",
+    "# 3. Apply logic and calculate stats\n",
+    "df['is_ok'] = df.apply(check_if_ok, axis=1)\n",
+    "\n",
+    "# Group by literacy label to see performance\n",
+    "stats = df.groupby('health_literacy_label')['is_ok'].agg(['count', 'sum']).reset_index()\n",
+    "stats.columns = ['Literacy Level', 'Total Docs', 'Number OK']\n",
+    "stats['Success Rate (%)'] = (stats['Number OK'] / stats['Total Docs'] * 100).round(2)\n",
+    "\n",
+    "print(\"--- Accuracy / Success Report ---\")\n",
+    "print(stats)\n",
+    "\n",
+    "# 4. Total overall success\n",
+    "total_docs = len(df)\n",
+    "total_ok = df['is_ok'].sum()\n",
+    "print(f\"\\nOverall Summary: {total_ok}/{total_docs} documents meet the literacy criteria ({round(total_ok/total_docs*100, 2)}%)\")"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "065399a1",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "with open(\"/home/mshahidul/readctrl/data/annotators_validate_data/Sharmin Sultana_2025-12-31_14-19-30/annotation_results.json\", 'r') as f:\n",
+    "    data = json.load(f)\n",
+    "print(data[0].keys())"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "5835ec3b",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import json\n",
+    "import os\n",
+    "import math\n",
+    "\n",
+    "# Define paths\n",
+    "input_path = \"/home/mshahidul/readctrl/data/annotators_validate_data/Sharmin Sultana_2025-12-31_14-19-30/annotation_results.json\"\n",
+    "output_path = \"/home/mshahidul/readctrl/data/annotators_validate_data/Sharmin Sultana_2025-12-31_14-19-30/annotation_results_rescaled.json\"\n",
+    "\n",
+    "def rescale_rating(val):\n",
+    "    if val is None:\n",
+    "        return None\n",
+    "    # Converts 1-10 to 1-5 (e.g., 10 becomes 5, 1 becomes 1)\n",
+    "    return math.ceil(val / 2)\n",
+    "\n",
+    "# Load data\n",
+    "with open(input_path, 'r') as f:\n",
+    "    data = json.load(f)\n",
+    "\n",
+    "# Process ratings\n",
+    "for entry in data:\n",
+    "    if 'doc_rating' in entry:\n",
+    "        entry['doc_rating'] = rescale_rating(entry['doc_rating'])\n",
+    "    if 'wiki_rating' in entry:\n",
+    "        entry['wiki_rating'] = rescale_rating(entry['wiki_rating'])\n",
+    "\n",
+    "# Save updated data\n",
+    "with open(output_path, 'w') as f:\n",
+    "    json.dump(data, f, indent=4)\n",
+    "\n",
+    "print(f\"Successfully saved rescaled data to: {output_path}\")"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "f5865b65",
+   "metadata": {},
+   "outputs": [],
+   "source": []
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "de9b3b2a",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "# /home/mshahidul/readctrl/data/final_result/mismatched_ratings.json\n",
+    "with open(\"/home/mshahidul/readctrl/data/final_result/mismatched_ratings.json\", 'r') as f:\n",
+    "    data = json.load(f)\n",
+    "id=0\n",
+    "index=data[id]['doc_id']\n",
+    "label=data[id]['health_literacy_label']\n",
+    "print(data[id])"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "e307543c",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "# /home/mshahidul/readctrl/data/extracting_subclaim/extracted_subclaims_syn_data_with_gs_summary_en.json\n",
+    "with open(\"/home/mshahidul/readctrl/data/extracting_subclaim/extracted_subclaims_syn_data_with_gs_summary_en.json\", 'r') as f:\n",
+    "    data2 = json.load(f)\n",
+    "src_lang=\"English\"\n",
+    "summary=data2[index]['summary']\n",
+    "fulltext=data2[index]['fulltext']\n",
+    "gen_summary=data2[index]['diff_label_texts'][label]\n",
+    "f=open(\"/home/mshahidul/readctrl/prompts/syn_data_gen_diff_label.txt\",\"r\").read()\n",
+    "txt=f.replace(\"<<<SOURCE_LANGUAGE>>>\",src_lang).replace(\"<<<GOLD_SUMMARY>>>\",summary).replace(\"<<<FULL_TEXT>>>\",fulltext)\n",
+    "print(txt)"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "59c72954",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "print(gen_summary)"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "4b2a2595",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "# /home/mshahidul/readctrl/data/final_result/consolidated_ratings_edit.json\n",
+    "import json\n",
+    "with open(\"/home/mshahidul/readctrl/data/final_result/consolidated_ratings_edit.json\", 'r') as f:\n",
+    "    data = json.load(f)\n",
+    "print(data[0].keys())"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "46f54097",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "set([x[\"health_literacy_label\"] for x in data])"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "9b1264ea",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "# /home/mshahidul/readctrl/data/extracting_subclaim/extracted_subclaims_syn_data_with_gs_summary_en.json\n",
+    "with open(\"/home/mshahidul/readctrl/data/extracting_subclaim/extracted_subclaims_syn_data_with_gs_summary_en.json\", 'r') as f:\n",
+    "    data2 = json.load(f)\n",
+    "print(data2[0].keys())\n",
+    "print(data2[0]['diff_label_texts'].keys())"
+   ]
+  },
+  {
+   "cell_type": "markdown",
+   "id": "d847270d",
+   "metadata": {},
+   "source": [
+    "## Step 0: Prepare Your Dataset"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "44047dbb",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import json\n",
+    "\n",
+    "# 1. Load the datasets\n",
+    "with open(\"/home/mshahidul/readctrl/data/final_result/consolidated_ratings_edit.json\", 'r') as f:\n",
+    "    ratings_data = json.load(f)\n",
+    "ratings_data=ratings_data[7:]\n",
+    "with open(\"/home/mshahidul/readctrl/data/extracting_subclaim/extracted_subclaims_syn_data_with_gs_summary_en.json\", 'r') as f:\n",
+    "    text_data = json.load(f)\n",
+    "\n",
+    "# 2. Updated mapping: Store the whole item or specific keys for fulltext and summary\n",
+    "# We map the index to a dictionary containing the variations and the original full text/summary\n",
+    "text_map = {\n",
+    "    item['index']: {\n",
+    "        'variations': item['diff_label_texts'],\n",
+    "        'fulltext': item.get('fulltext', \"\"),\n",
+    "        'summary': item.get('summary', \"\")\n",
+    "    } \n",
+    "    for item in text_data\n",
+    "}\n",
+    "\n",
+    "cleaned_data = []\n",
+    "\n",
+    "# 3. Iterate through ratings and extract data\n",
+    "for entry in ratings_data:\n",
+    "    doc_id = entry['doc_id']\n",
+    "    label = entry['health_literacy_label']\n",
+    "    \n",
+    "    if doc_id in text_map:\n",
+    "        source_info = text_map[doc_id]\n",
+    "        \n",
+    "        # Retrieve the specific text version based on the label\n",
+    "        # .get() handles cases where a specific label might be missing\n",
+    "        labeled_text = source_info['variations'].get(label, \"\")\n",
+    "        \n",
+    "        # Construct the expanded object\n",
+    "        cleaned_data.append({\n",
+    "            \"doc_id\": doc_id,\n",
+    "            \"label\": label,\n",
+    "            \"gen_text\": labeled_text,\n",
+    "            \"fulltext\": source_info['fulltext'],\n",
+    "            \"gs_summary\": source_info['summary']\n",
+    "        })\n",
+    "\n",
+    "# 4. Output the clean JSON\n",
+    "output_path = \"/home/mshahidul/readctrl/data/new_exp/cleaned_health_literacy_data.json\"\n",
+    "with open(output_path, 'w') as f:\n",
+    "    json.dump(cleaned_data, f, indent=4, ensure_ascii=False)\n",
+    "\n",
+    "print(f\"Successfully processed {len(cleaned_data)} examples.\")"
+   ]
+  },
+  {
+   "cell_type": "markdown",
+   "id": "a1e6b0ae",
+   "metadata": {},
+   "source": [
+    "## Step 1: Pick Few-Shot Examples"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "71e83ac8",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import json\n",
+    "import requests\n",
+    "from collections import defaultdict\n",
+    "\n",
+    "# Configuration\n",
+    "API_URL = \"http://172.16.34.29:8004/v1/chat/completions\"\n",
+    "MODEL_NAME = \"Qwen/Qwen3-30B-A3B-Instruct-2507\"\n",
+    "INPUT_FILE = \"/home/mshahidul/readctrl/data/new_exp/cleaned_health_literacy_data.json\"\n",
+    "OUTPUT_FILE = \"/home/mshahidul/readctrl/data/new_exp/few_shot_examples.json\"\n",
+    "\n",
+    "def get_text_metadata(text):\n",
+    "    \"\"\"Ask the LLM to identify the topic and medical complexity of a text.\"\"\"\n",
+    "    prompt = f\"\"\"Analyze the following medical text and provide a 1-word topic (e.g., Cardiology, Nutrition, Medication) and a 1-word complexity level (Simple, Moderate, Technical).\n",
+    "    Text: {text}...\n",
+    "    Format: Topic | Complexity\"\"\"\n",
+    "    \n",
+    "    try:\n",
+    "        response = requests.post(API_URL, json={\n",
+    "            \"model\": MODEL_NAME,\n",
+    "            \"messages\": [{\"role\": \"user\", \"content\": prompt}],\n",
+    "            \"temperature\": 0.1\n",
+    "        })\n",
+    "        return response.json()['choices'][0]['message']['content'].strip()\n",
+    "    except:\n",
+    "        return \"General | Unknown\"\n",
+    "\n",
+    "# 1. Load the cleaned data\n",
+    "with open(INPUT_FILE, 'r') as f:\n",
+    "    data = json.load(f)\n",
+    "\n",
+    "# 2. Group data by label\n",
+    "grouped_data = defaultdict(list)\n",
+    "for item in data:\n",
+    "    grouped_data[item['label']].append(item)\n",
+    "\n",
+    "# 3. Select diverse examples for each label\n",
+    "few_shot_selection = {}\n",
+    "\n",
+    "for label, examples in grouped_data.items():\n",
+    "    print(f\"Processing label: {label}...\")\n",
+    "    \n",
+    "    # Analyze a subset (or all) to find diversity\n",
+    "    scored_examples = []\n",
+    "    for ex in examples: \n",
+    "        metadata = get_text_metadata(ex['gen_text'])\n",
+    "        ex['metadata'] = metadata\n",
+    "        scored_examples.append(ex)\n",
+    "    \n",
+    "    # Heuristic: Sort by metadata to group similar topics, then pick spread-out indices\n",
+    "    scored_examples.sort(key=lambda x: x['metadata'])\n",
+    "    \n",
+    "    # Pick 5 examples spread across the sorted metadata for maximum diversity\n",
+    "    step = max(1, len(scored_examples) // 5)\n",
+    "    selected = scored_examples[::step][:5]\n",
+    "    few_shot_selection[label] = selected\n",
+    "\n",
+    "# 4. Save the result\n",
+    "with open(OUTPUT_FILE, 'w') as f:\n",
+    "    json.dump(few_shot_selection, f, indent=4)\n",
+    "\n",
+    "print(f\"Few-shot examples saved to: {OUTPUT_FILE}\")"
+   ]
+  },
+  {
+   "cell_type": "markdown",
+   "id": "d48720a6",
+   "metadata": {},
+   "source": [
+    "## Step 2: Decide on LLM(s)"
+   ]
+  },
+  {
+   "cell_type": "markdown",
+   "id": "4396ac94",
+   "metadata": {},
+   "source": [
+    "### V1"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "f96d976b",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import json\n",
+    "import requests\n",
+    "\n",
+    "# Configuration\n",
+    "API_URL = \"http://172.16.34.29:8004/v1/chat/completions\"\n",
+    "MODEL_NAME = \"Qwen/Qwen3-30B-A3B-Instruct-2507\"\n",
+    "FEW_SHOT_FILE = \"/home/mshahidul/readctrl/data/new_exp/few_shot_examples.json\"\n",
+    "\n",
+    "# 1. Load the 15 selected examples\n",
+    "with open(FEW_SHOT_FILE, 'r') as f:\n",
+    "    few_shot_data = json.load(f)\n",
+    "\n",
+    "def get_reasoning(fulltext, gen_text, label):\n",
+    "    \"\"\"Ask the LLM to explain why the text fits the label compared to the source context.\"\"\"\n",
+    "    prompt = f\"\"\"Compare the 'Target Text' to the 'Original Fulltext'. \n",
+    "Explain why the Target Text fits the health literacy label: {label}.\n",
+    "Focus on how vocabulary, jargon, and sentence structure were adapted.\n",
+    "\n",
+    "Original Fulltext: {fulltext}\n",
+    "Target Text: {gen_text}\n",
+    "Label: {label}\n",
+    "\n",
+    "Reasoning (1-2 sentences):\"\"\"\n",
+    "    \n",
+    "    try:\n",
+    "        response = requests.post(API_URL, json={\n",
+    "            \"model\": MODEL_NAME,\n",
+    "            \"messages\": [{\"role\": \"user\", \"content\": prompt}],\n",
+    "            \"temperature\": 0\n",
+    "        })\n",
+    "        return response.json()['choices'][0]['message']['content'].strip()\n",
+    "    except Exception as e:\n",
+    "        return \"Reasoning could not be generated.\"\n",
+    "\n",
+    "# 2. Build the few-shot string\n",
+    "few_shot_string = \"\"\n",
+    "\n",
+    "for label in [\"low_health_literacy\", \"intermediate_health_literacy\", \"proficient_health_literacy\"]:\n",
+    "    examples = few_shot_data.get(label, [])\n",
+    "    for ex in examples:\n",
+    "        # Pass fulltext to the reasoning generator\n",
+    "        reason = get_reasoning(ex.get('fulltext', \"\"), ex['gen_text'], label)\n",
+    "        \n",
+    "        few_shot_string += f\"Original Fulltext: \\\"{ex.get('fulltext', '')}\\\"\\n\"\n",
+    "        few_shot_string += f\"Target Text: \\\"{ex['gen_text']}\\\"\\n\"\n",
+    "        few_shot_string += f\"Reasoning: {reason}\\n\"\n",
+    "        few_shot_string += f\"Label: {label}\\n\"\n",
+    "        few_shot_string += \"-\" * 30 + \"\\n\"\n",
+    "\n",
+    "# 3. Define the Final Prompt Structure\n",
+    "instruction = \"\"\"You are an expert in health communication. Your task is to judge the health literacy level of a target text based on its original medical source.\n",
+    "\n",
+    "Classify the text into one of three categories:\n",
+    "1. low_health_literacy: Uses common words (everyday language), very short sentences, and eliminates all medical jargon.\n",
+    "2. intermediate_health_literacy: Uses some medical terms with explanation, standard sentence length, requires basic health knowledge.\n",
+    "3. proficient_health_literacy: Uses high-level medical jargon, technical language, and academic or professional structures.\n",
+    "\n",
+    "### Few-Shot Examples:\n",
+    "\"\"\"\n",
+    "\n",
+    "# 4. Save the prompt template\n",
+    "# The placeholder now expects both fulltext and input_text\n",
+    "final_prompt_template = (\n",
+    "    instruction + \n",
+    "    few_shot_string + \n",
+    "    \"\\n### Now judge this text:\\n\"\n",
+    "    \"Original Fulltext: \\\"{fulltext}\\\"\\n\"\n",
+    "    \"Target Text: \\\"{input_text}\\\"\\n\"\n",
+    "    \"Reasoning:\"\n",
+    ")\n",
+    "\n",
+    "output_path = \"/home/mshahidul/readctrl/data/new_exp/final_prompt_template.txt\"\n",
+    "with open(output_path, 'w') as f:\n",
+    "    f.write(final_prompt_template)\n",
+    "\n",
+    "print(f\"Prompt template with fulltext context saved to {output_path}\")"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 2,
+   "id": "3bc0564f",
+   "metadata": {},
+   "outputs": [
+    {
+     "name": "stdout",
+     "output_type": "stream",
+     "text": [
+      "3396\n"
+     ]
+    }
+   ],
+   "source": [
+    "# /home/mshahidul/readctrl/data/synthetic_dataset_diff_labels/syn_data_with_gs_summary_en.json\n",
+    "import json\n",
+    "with open(\"/home/mshahidul/readctrl/data/processed_test_raw_data/multiclinsum_test_en.json\", 'r') as f:\n",
+    "    data = json.load(f)\n",
+    "print(len(data))"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 4,
+   "id": "882507f2",
+   "metadata": {},
+   "outputs": [
+    {
+     "name": "stdout",
+     "output_type": "stream",
+     "text": [
+      "dict_keys(['id', 'fulltext', 'fulltext_subclaims', 'summary', 'summary_subclaims'])\n",
+      "3396\n"
+     ]
+    }
+   ],
+   "source": [
+    "# /home/mshahidul/readctrl/data/extracting_subclaim/extracted_subclaims_syn_data_with_gs_summary_en.json\n",
+    "import json\n",
+    "with open(\"/home/mshahidul/readctrl/data/extracting_subclaim/extracted_subclaims_multiclinsum_test_en_full.json\", 'r') as f:\n",
+    "    data = json.load(f)\n",
+    "print(data[0].keys())\n",
+    "print(len(data))"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "b0fcc380",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "LOCAL_API_URL = \"http://172.16.34.29:8004/v1\"\n",
+    "LOCAL_MODEL_NAME = \"/home/mshahidul/readctrl_model/full_model/qwen3-32B_subclaims-extraction-8b_ctx_fp16\""
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 1,
+   "id": "d8b235a6",
+   "metadata": {},
+   "outputs": [
+    {
+     "ename": "JSONDecodeError",
+     "evalue": "Extra data: line 2 column 1 (char 22694)",
+     "output_type": "error",
+     "traceback": [
+      "\u001b[31m---------------------------------------------------------------------------\u001b[39m",
+      "\u001b[31mJSONDecodeError\u001b[39m                           Traceback (most recent call last)",
+      "\u001b[36mCell\u001b[39m\u001b[36m \u001b[39m\u001b[32mIn[1]\u001b[39m\u001b[32m, line 4\u001b[39m\n\u001b[32m      2\u001b[39m \u001b[38;5;28;01mimport\u001b[39;00m\u001b[38;5;250m \u001b[39m\u001b[34;01mjson\u001b[39;00m\n\u001b[32m      3\u001b[39m \u001b[38;5;28;01mwith\u001b[39;00m \u001b[38;5;28mopen\u001b[39m(\u001b[33m\"\u001b[39m\u001b[33m/home/mshahidul/LLM_guard/CKA-Agent/results/single_run_20260203_213455/inter_result_sample_0.json\u001b[39m\u001b[33m\"\u001b[39m, \u001b[33m'\u001b[39m\u001b[33mr\u001b[39m\u001b[33m'\u001b[39m) \u001b[38;5;28;01mas\u001b[39;00m f:\n\u001b[32m----> \u001b[39m\u001b[32m4\u001b[39m     data = \u001b[43mjson\u001b[49m\u001b[43m.\u001b[49m\u001b[43mload\u001b[49m\u001b[43m(\u001b[49m\u001b[43mf\u001b[49m\u001b[43m)\u001b[49m\n\u001b[32m      5\u001b[39m \u001b[38;5;28mprint\u001b[39m(data[\u001b[32m0\u001b[39m].keys())\n\u001b[32m      6\u001b[39m \u001b[38;5;28mprint\u001b[39m(data[\u001b[32m0\u001b[39m][\u001b[33m'\u001b[39m\u001b[33minter_result\u001b[39m\u001b[33m'\u001b[39m])\n",
+      "\u001b[36mFile \u001b[39m\u001b[32m~/miniconda3/envs/un/lib/python3.11/json/__init__.py:293\u001b[39m, in \u001b[36mload\u001b[39m\u001b[34m(fp, cls, object_hook, parse_float, parse_int, parse_constant, object_pairs_hook, **kw)\u001b[39m\n\u001b[32m    274\u001b[39m \u001b[38;5;28;01mdef\u001b[39;00m\u001b[38;5;250m \u001b[39m\u001b[34mload\u001b[39m(fp, *, \u001b[38;5;28mcls\u001b[39m=\u001b[38;5;28;01mNone\u001b[39;00m, object_hook=\u001b[38;5;28;01mNone\u001b[39;00m, parse_float=\u001b[38;5;28;01mNone\u001b[39;00m,\n\u001b[32m    275\u001b[39m         parse_int=\u001b[38;5;28;01mNone\u001b[39;00m, parse_constant=\u001b[38;5;28;01mNone\u001b[39;00m, object_pairs_hook=\u001b[38;5;28;01mNone\u001b[39;00m, **kw):\n\u001b[32m    276\u001b[39m \u001b[38;5;250m    \u001b[39m\u001b[33;03m\"\"\"Deserialize ``fp`` (a ``.read()``-supporting file-like object containing\u001b[39;00m\n\u001b[32m    277\u001b[39m \u001b[33;03m    a JSON document) to a Python object.\u001b[39;00m\n\u001b[32m    278\u001b[39m \n\u001b[32m   (...)\u001b[39m\u001b[32m    291\u001b[39m \u001b[33;03m    kwarg; otherwise ``JSONDecoder`` is used.\u001b[39;00m\n\u001b[32m    292\u001b[39m \u001b[33;03m    \"\"\"\u001b[39;00m\n\u001b[32m--> \u001b[39m\u001b[32m293\u001b[39m     \u001b[38;5;28;01mreturn\u001b[39;00m \u001b[43mloads\u001b[49m\u001b[43m(\u001b[49m\u001b[43mfp\u001b[49m\u001b[43m.\u001b[49m\u001b[43mread\u001b[49m\u001b[43m(\u001b[49m\u001b[43m)\u001b[49m\u001b[43m,\u001b[49m\n\u001b[32m    294\u001b[39m \u001b[43m        \u001b[49m\u001b[38;5;28;43mcls\u001b[39;49m\u001b[43m=\u001b[49m\u001b[38;5;28;43mcls\u001b[39;49m\u001b[43m,\u001b[49m\u001b[43m \u001b[49m\u001b[43mobject_hook\u001b[49m\u001b[43m=\u001b[49m\u001b[43mobject_hook\u001b[49m\u001b[43m,\u001b[49m\n\u001b[32m    295\u001b[39m \u001b[43m        \u001b[49m\u001b[43mparse_float\u001b[49m\u001b[43m=\u001b[49m\u001b[43mparse_float\u001b[49m\u001b[43m,\u001b[49m\u001b[43m \u001b[49m\u001b[43mparse_int\u001b[49m\u001b[43m=\u001b[49m\u001b[43mparse_int\u001b[49m\u001b[43m,\u001b[49m\n\u001b[32m    296\u001b[39m \u001b[43m        \u001b[49m\u001b[43mparse_constant\u001b[49m\u001b[43m=\u001b[49m\u001b[43mparse_constant\u001b[49m\u001b[43m,\u001b[49m\u001b[43m \u001b[49m\u001b[43mobject_pairs_hook\u001b[49m\u001b[43m=\u001b[49m\u001b[43mobject_pairs_hook\u001b[49m\u001b[43m,\u001b[49m\u001b[43m \u001b[49m\u001b[43m*\u001b[49m\u001b[43m*\u001b[49m\u001b[43mkw\u001b[49m\u001b[43m)\u001b[49m\n",
+      "\u001b[36mFile \u001b[39m\u001b[32m~/miniconda3/envs/un/lib/python3.11/json/__init__.py:346\u001b[39m, in \u001b[36mloads\u001b[39m\u001b[34m(s, cls, object_hook, parse_float, parse_int, parse_constant, object_pairs_hook, **kw)\u001b[39m\n\u001b[32m    341\u001b[39m     s = s.decode(detect_encoding(s), \u001b[33m'\u001b[39m\u001b[33msurrogatepass\u001b[39m\u001b[33m'\u001b[39m)\n\u001b[32m    343\u001b[39m \u001b[38;5;28;01mif\u001b[39;00m (\u001b[38;5;28mcls\u001b[39m \u001b[38;5;129;01mis\u001b[39;00m \u001b[38;5;28;01mNone\u001b[39;00m \u001b[38;5;129;01mand\u001b[39;00m object_hook \u001b[38;5;129;01mis\u001b[39;00m \u001b[38;5;28;01mNone\u001b[39;00m \u001b[38;5;129;01mand\u001b[39;00m\n\u001b[32m    344\u001b[39m         parse_int \u001b[38;5;129;01mis\u001b[39;00m \u001b[38;5;28;01mNone\u001b[39;00m \u001b[38;5;129;01mand\u001b[39;00m parse_float \u001b[38;5;129;01mis\u001b[39;00m \u001b[38;5;28;01mNone\u001b[39;00m \u001b[38;5;129;01mand\u001b[39;00m\n\u001b[32m    345\u001b[39m         parse_constant \u001b[38;5;129;01mis\u001b[39;00m \u001b[38;5;28;01mNone\u001b[39;00m \u001b[38;5;129;01mand\u001b[39;00m object_pairs_hook \u001b[38;5;129;01mis\u001b[39;00m \u001b[38;5;28;01mNone\u001b[39;00m \u001b[38;5;129;01mand\u001b[39;00m \u001b[38;5;129;01mnot\u001b[39;00m kw):\n\u001b[32m--> \u001b[39m\u001b[32m346\u001b[39m     \u001b[38;5;28;01mreturn\u001b[39;00m \u001b[43m_default_decoder\u001b[49m\u001b[43m.\u001b[49m\u001b[43mdecode\u001b[49m\u001b[43m(\u001b[49m\u001b[43ms\u001b[49m\u001b[43m)\u001b[49m\n\u001b[32m    347\u001b[39m \u001b[38;5;28;01mif\u001b[39;00m \u001b[38;5;28mcls\u001b[39m \u001b[38;5;129;01mis\u001b[39;00m \u001b[38;5;28;01mNone\u001b[39;00m:\n\u001b[32m    348\u001b[39m     \u001b[38;5;28mcls\u001b[39m = JSONDecoder\n",
+      "\u001b[36mFile \u001b[39m\u001b[32m~/miniconda3/envs/un/lib/python3.11/json/decoder.py:340\u001b[39m, in \u001b[36mJSONDecoder.decode\u001b[39m\u001b[34m(self, s, _w)\u001b[39m\n\u001b[32m    338\u001b[39m end = _w(s, end).end()\n\u001b[32m    339\u001b[39m \u001b[38;5;28;01mif\u001b[39;00m end != \u001b[38;5;28mlen\u001b[39m(s):\n\u001b[32m--> \u001b[39m\u001b[32m340\u001b[39m     \u001b[38;5;28;01mraise\u001b[39;00m JSONDecodeError(\u001b[33m\"\u001b[39m\u001b[33mExtra data\u001b[39m\u001b[33m\"\u001b[39m, s, end)\n\u001b[32m    341\u001b[39m \u001b[38;5;28;01mreturn\u001b[39;00m obj\n",
+      "\u001b[31mJSONDecodeError\u001b[39m: Extra data: line 2 column 1 (char 22694)"
+     ]
+    }
+   ],
+   "source": [
+    "# /home/mshahidul/LLM_guard/CKA-Agent/results/single_run_20260203_213455/inter_result_sample_0.json\n",
+    "import json\n",
+    "with open(\"/home/mshahidul/LLM_guard/CKA-Agent/results/single_run_20260203_213455/inter_result_sample_0.json\", 'r') as f:\n",
+    "    data = json.load(f)\n",
+    "print(data[0].keys())\n",
+    "print(data[0]['inter_result'])\n",
+    "\n"
+   ]
+  },
+  {
+   "cell_type": "markdown",
+   "id": "74b07429",
+   "metadata": {},
+   "source": [
+    "## V2"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "912f3d85",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import json\n",
+    "import requests\n",
+    "from openai import OpenAI\n",
+    "\n",
+    "# --- Configuration ---\n",
+    "LOCAL_API_URL = \"http://172.16.34.29:8004/v1/chat/completions\"\n",
+    "LOCAL_MODEL_NAME = \"Qwen/Qwen3-30B-A3B-Instruct-2507\"\n",
+    "\n",
+    "api_file = \"/home/mshahidul/api_new.json\"\n",
+    "with open(api_file, \"r\") as f:\n",
+    "    api_keys = json.load(f)\n",
+    "\n",
+    "openai_client = OpenAI(api_key=api_keys[\"openai\"])\n",
+    "OPENAI_MODEL_NAME = \"gpt-5\" # Note: Ensure your model version is correct\n",
+    "\n",
+    "FEW_SHOT_FILE = \"/home/mshahidul/readctrl/data/new_exp/few_shot_examples.json\"\n",
+    "OUTPUT_PATH = \"/home/mshahidul/readctrl/data/new_exp/final_prompt_template.txt\"\n",
+    "\n",
+    "# --- Logic ---\n",
+    "\n",
+    "def get_reasoning(fulltext, gen_text, label, provider=\"local\"):\n",
+    "    \"\"\"\n",
+    "    Ask an LLM to explain why the text fits the label in JSON format.\n",
+    "    \"\"\"\n",
+    "    # Explicitly asking for JSON in the prompt\n",
+    "    prompt = f\"\"\"Compare the 'Target Text' to the 'Original Fulltext'. \n",
+    "Explain why the Target Text fits the health literacy label: {label}.\n",
+    "Focus on how vocabulary, jargon, and sentence structure were adapted.\n",
+    "\n",
+    "Original Fulltext: {fulltext}\n",
+    "Target Text: {gen_text}\n",
+    "Label: {label}\n",
+    "\n",
+    "Return your response ONLY as a JSON object with the following key:\n",
+    "\"reasoning\": \"your 1-2 sentence explanation\"\n",
+    "\"\"\"\n",
+    "\n",
+    "    try:\n",
+    "        if provider == \"openai\":\n",
+    "            response = openai_client.chat.completions.create(\n",
+    "                model=OPENAI_MODEL_NAME,\n",
+    "                messages=[{\"role\": \"user\", \"content\": prompt}],\n",
+    "                response_format={ \"type\": \"json_object\" } # Force JSON for OpenAI\n",
+    "            )\n",
+    "            content = response.choices[0].message.content.strip()\n",
+    "        else:\n",
+    "            response = requests.post(LOCAL_API_URL, json={\n",
+    "                \"model\": LOCAL_MODEL_NAME,\n",
+    "                \"messages\": [{\"role\": \"user\", \"content\": prompt}],\n",
+    "                \"temperature\": 0\n",
+    "            })\n",
+    "            content = response.json()['choices'][0]['message']['content'].strip()\n",
+    "        \n",
+    "        # Parse JSON and extract reasoning\n",
+    "        data = json.loads(content)\n",
+    "        return data.get(\"reasoning\", \"Reasoning key not found.\")\n",
+    "            \n",
+    "    except Exception as e:\n",
+    "        print(f\"Error with {provider}: {e}\")\n",
+    "        return \"Reasoning could not be generated.\"\n",
+    "\n",
+    "# 1. Load the selected examples\n",
+    "with open(FEW_SHOT_FILE, 'r') as f:\n",
+    "    few_shot_data = json.load(f)\n",
+    "\n",
+    "# 2. Build the few-shot string\n",
+    "few_shot_string = \"\"\n",
+    "REASONING_PROVIDER = \"openai\" \n",
+    "\n",
+    "print(f\"Generating reasoning using: {REASONING_PROVIDER}...\")\n",
+    "info=[]\n",
+    "for label in [\"low_health_literacy\", \"intermediate_health_literacy\", \"proficient_health_literacy\"]:\n",
+    "    examples = few_shot_data.get(label, [])\n",
+    "    for ex in examples:\n",
+    "        reason = get_reasoning(ex.get('fulltext', \"\"), ex['gen_text'], label, provider=REASONING_PROVIDER)\n",
+    "        \n",
+    "        # Adding structured few-shot examples to the string\n",
+    "        few_shot_string += f\"Original Fulltext: \\\"{ex.get('fulltext', '')}\\\"\\n\"\n",
+    "        few_shot_string += f\"Target Text: \\\"{ex['gen_text']}\\\"\\n\"\n",
+    "        few_shot_string += f\"Reasoning: {reason}\\n\"\n",
+    "        few_shot_string += f\"Label: {label}\\n\"\n",
+    "        few_shot_string += \"-\" * 30 + \"\\n\"\n",
+    "        info.append({\n",
+    "            \"doc_id\": ex.get('doc_id', \"\"),\n",
+    "            \"fulltext\": ex.get('fulltext', \"\"),\n",
+    "            \"gen_text\": ex['gen_text'],\n",
+    "            \"reasoning\": reason,\n",
+    "            \"label\": label\n",
+    "        })                    \n",
+    "\n",
+    "# 3. Define the Final Prompt Structure\n",
+    "instruction = \"\"\"You are an expert in health communication. Your task is to judge the health literacy level of a target text based on its original medical source.\n",
+    "\n",
+    "Classify the text into one of three categories:\n",
+    "1. low_health_literacy: Uses common words (everyday language), very short sentences, and eliminates all medical jargon.\n",
+    "2. intermediate_health_literacy: Uses some medical terms with explanation, standard sentence length, requires basic health knowledge.\n",
+    "3. proficient_health_literacy: Uses high-level medical jargon, technical language, and academic or professional structures.\n",
+    "\n",
+    "### Few-Shot Examples:\n",
+    "\"\"\"\n",
+    "\n",
+    "# 4. Final Template Construction\n",
+    "final_prompt_template = (\n",
+    "    instruction + \n",
+    "    few_shot_string + \n",
+    "    \"\\n### Now judge this text:\\n\"\n",
+    "    \"Original Fulltext: \\\"{fulltext}\\\"\\n\"\n",
+    "    \"Target Text: \\\"{input_text}\\\"\\n\"\n",
+    "    \"Reasoning:\"\n",
+    ")\n",
+    "\n",
+    "with open(OUTPUT_PATH, 'w') as f:\n",
+    "    f.write(final_prompt_template)\n",
+    "with open(OUTPUT_PATH.replace('.txt', '_info.json'), 'w') as f:\n",
+    "    json.dump(info, f, indent=4)\n",
+    "print(f\"Structured prompt template saved to {OUTPUT_PATH}\")"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "feafa46d",
+   "metadata": {},
+   "outputs": [
+    {
+     "name": "stdout",
+     "output_type": "stream",
+     "text": [
+      "dict_keys(['doc_id', 'ai_label', 'rating_plaban', 'category_plaban', 'rating_mahi', 'category_mahi', 'rating_shama', 'category_shama', 'agreement_count'])\n"
+     ]
+    }
+   ],
+   "source": [
+    "import json\n",
+    "# /home/mshahidul/readctrl/data/synthetic_dataset_diff_labels/syn_data_diff_labels_en_0_80_full.json\n",
+    "with open(\"/home/mshahidul/readctrl/data/synthetic_dataset_diff_labels/syn_data_diff_labels_en_0_80_full.json\", 'r') as f:\n",
+    "    data = json.load(f)\n",
+    "print(data[0].keys())\n",
+    "print(data[0]['diff_label_texts'].keys())"
+   ]
+  },
+  {
+   "cell_type": "markdown",
+   "id": "8c470dd5",
+   "metadata": {},
+   "source": [
+    "## Fewshot data selection"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "06158d8d",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import json\n",
+    "import os\n",
+    "\n",
+    "# --- Configuration ---\n",
+    "# Path to your existing data (containing 'reasoning', 'gen_text', and 'label')\n",
+    "INPUT_INFO_FILE = \"/home/mshahidul/readctrl/data/new_exp/final_prompt_template_info.json\"\n",
+    "OUTPUT_PATH = \"/home/mshahidul/readctrl/data/new_exp/new_prompt_template.txt\"\n",
+    "\n",
+    "# Decide how many few-shot examples you want to include for each label\n",
+    "FEW_SHOT_PER_LABEL = 2  # Change this to 1, 3, etc.\n",
+    "\n",
+    "# --- Logic ---\n",
+    "\n",
+    "def generate_prompt_from_json(input_json_path, num_per_label):\n",
+    "    if not os.path.exists(input_json_path):\n",
+    "        return f\"Error: File {input_json_path} not found. Please check the path.\"\n",
+    "        \n",
+    "    with open(input_json_path, 'r') as f:\n",
+    "        data = json.load(f)\n",
+    "    \n",
+    "    # Organize the data by label to ensure even distribution\n",
+    "    labeled_data = {}\n",
+    "    for entry in data:\n",
+    "        label = entry['label']\n",
+    "        if label not in labeled_data:\n",
+    "            labeled_data[label] = []\n",
+    "        labeled_data[label].append(entry)\n",
+    "    \n",
+    "    # Build the few-shot section\n",
+    "    few_shot_string = \"\"\n",
+    "    # Define labels in a logical order\n",
+    "    target_labels = [\"low_health_literacy\", \"intermediate_health_literacy\", \"proficient_health_literacy\"]\n",
+    "    \n",
+    "    for label in target_labels:\n",
+    "        examples = labeled_data.get(label, [])\n",
+    "        # Slice the list based on your variable\n",
+    "        selected_examples = examples[:num_per_label]\n",
+    "        \n",
+    "        for ex in selected_examples:\n",
+    "            # Construct the example block WITHOUT the fulltext\n",
+    "            few_shot_string += f\"Target Text: \\\"{ex['gen_text']}\\\"\\n\"\n",
+    "            few_shot_string += f\"Reasoning: {ex['reasoning']}\\n\"\n",
+    "            few_shot_string += f\"Label: {label}\\n\"\n",
+    "            few_shot_string += \"-\" * 30 + \"\\n\"\n",
+    "\n",
+    "    # Define the final instruction structure (no mention of fulltext comparison)\n",
+    "    instruction = \"\"\"You are an expert in health communication. Your task is to judge the health literacy level of the provided text.\n",
+    "\n",
+    "Classify the text into one of three categories:\n",
+    "1. low_health_literacy: Uses common words (everyday language), very short sentences, and avoids medical jargon.\n",
+    "2. intermediate_health_literacy: Uses some medical terms with explanation, standard sentence length, requires basic health knowledge.\n",
+    "3. proficient_health_literacy: Uses high-level medical jargon, technical language, and academic or professional structures.\n",
+    "\n",
+    "### Examples:\n",
+    "\"\"\"\n",
+    "\n",
+    "    # Final Template Construction\n",
+    "    final_template = (\n",
+    "        instruction + \n",
+    "        few_shot_string + \n",
+    "        \"\\n### Task:\\n\"\n",
+    "        \"Target Text: \\\"{input_text}\\\"\\n\"\n",
+    "        \"Reasoning:\"\n",
+    "    )\n",
+    "    \n",
+    "    return final_template\n",
+    "\n",
+    "# 1. Generate the string\n",
+    "new_prompt_template = generate_prompt_from_json(INPUT_INFO_FILE, FEW_SHOT_PER_LABEL)\n",
+    "\n",
+    "# 2. Save to file\n",
+    "with open(OUTPUT_PATH, 'w') as f:\n",
+    "    f.write(new_prompt_template)\n",
+    "\n",
+    "print(f\"Successfully created a prompt with {FEW_SHOT_PER_LABEL} examples per label.\")\n",
+    "print(f\"Saved to: {OUTPUT_PATH}\")"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "f78d4619",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "\n",
+    "with open(\"/home/mshahidul/readctrl/data/new_exp/cleaned_health_literacy_data.json\", 'r') as f:\n",
+    "    cleaned_data = json.load(f)\n",
+    "with open(\"/home/mshahidul/readctrl/data/new_exp/few_shot_examples.json\", 'r') as f:\n",
+    "    few_shot_examples = json.load(f)\n",
+    "\n",
+    "list_data = []\n",
+    "for item in few_shot_examples:\n",
+    "    for ex in few_shot_examples[item]:\n",
+    "        list_data.append((ex['doc_id'], ex['label']))\n",
+    "\n",
+    "test_set = []\n",
+    "for item in cleaned_data:\n",
+    "    if (item['doc_id'], item['label']) not in list_data:\n",
+    "        test_set.append(item)\n",
+    "with open(\"/home/mshahidul/readctrl/data/new_exp/test_health_literacy_data.json\", 'w') as f:\n",
+    "    json.dump(test_set, f, indent=4)"
+   ]
+  },
+  {
+   "cell_type": "markdown",
+   "id": "9d33bb77",
+   "metadata": {},
+   "source": [
+    "## Testing V1"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "e2e888eb",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import json\n",
+    "import requests\n",
+    "\n",
+    "# --- Configuration ---\n",
+    "TEMPLATE_PATH = \"/home/mshahidul/readctrl/data/new_exp/final_prompt_template_v3.txt\"\n",
+    "LOCAL_API_URL = \"http://172.16.34.29:8004/v1/chat/completions\"\n",
+    "LOCAL_MODEL_NAME = \"Qwen/Qwen3-30B-A3B-Instruct-2507\"\n",
+    "\n",
+    "# --- 1. Load the Template ---\n",
+    "with open(TEMPLATE_PATH, \"r\") as f:\n",
+    "    prompt_template = f.read()\n",
+    "\n",
+    "# --- 2. Define Test Cases ---\n",
+    "with open(\"/home/mshahidul/readctrl/data/new_exp/cleaned_health_literacy_data.json\", 'r') as f:\n",
+    "    cleaned_data = json.load(f)\n",
+    "with open(\"/home/mshahidul/readctrl/data/new_exp/few_shot_examples.json\", 'r') as f:\n",
+    "    few_shot_examples = json.load(f)\n",
+    "\n",
+    "list_data = []\n",
+    "for item in few_shot_examples:\n",
+    "    for ex in few_shot_examples[item]:\n",
+    "        list_data.append((ex['doc_id'], ex['label']))\n",
+    "\n",
+    "test_set = []\n",
+    "for item in cleaned_data:\n",
+    "    if (item['doc_id'], item['label']) not in list_data:\n",
+    "        test_set.append(item)\n",
+    "\n",
+    "def run_test(fulltext, input_text):\n",
+    "    final_prompt = prompt_template.format(fulltext=fulltext, input_text=input_text)\n",
+    "    \n",
+    "    payload = {\n",
+    "        \"model\": LOCAL_MODEL_NAME,\n",
+    "        \"messages\": [{\"role\": \"user\", \"content\": final_prompt}],\n",
+    "        \"temperature\": 0 \n",
+    "    }\n",
+    "    \n",
+    "    try:\n",
+    "        response = requests.post(LOCAL_API_URL, json=payload, timeout=30)\n",
+    "        return response.json()['choices'][0]['message']['content'].strip()\n",
+    "    except Exception as e:\n",
+    "        return f\"Error: {e}\"\n",
+    "\n",
+    "# --- 3. Execute and Compare ---\n",
+    "print(f\"--- Starting Template Evaluation on {len(test_set)} cases ---\\n\")\n",
+    "\n",
+    "correct_count = 0\n",
+    "results_log = []\n",
+    "\n",
+    "def text_return(text):\n",
+    "    if \"low\" in text.lower():\n",
+    "        return \"low_health_literacy\"\n",
+    "    elif \"intermediate\" in text.lower():\n",
+    "        return \"intermediate_health_literacy\"\n",
+    "    elif \"proficient\" in text.lower():\n",
+    "        return \"proficient_health_literacy\"\n",
+    "    return \"unknown\"\n",
+    "\n",
+    "for i, case in enumerate(test_set):\n",
+    "    expected = str(case['label']).strip().lower()\n",
+    "    result = run_test(case['fulltext'], case['gen_text'])\n",
+    "    \n",
+    "    # Clean LLM output for comparison (case-insensitive and removing trailing periods)\n",
+    "    prediction = result.strip().lower().rstrip('.')\n",
+    "    \n",
+    "    # Check if the expected label is the primary answer in the result\n",
+    "    is_correct = (text_return(expected) == text_return(prediction) )\n",
+    "    \n",
+    "    if is_correct:\n",
+    "        correct_count += 1\n",
+    "    \n",
+    "    print(f\"Test Case {i+1}:\")\n",
+    "    print(f\"Expected: {case['label']}\")\n",
+    "    print(f\"LLM Output: {result}\")\n",
+    "    print(f\"Match: {'✅' if is_correct else '❌'}\")\n",
+    "    print(\"-\" * 50)\n",
+    "\n",
+    "# --- 4. Final Accuracy Calculation ---\n",
+    "total_cases = len(test_set)\n",
+    "if total_cases > 0:\n",
+    "    accuracy = (correct_count / total_cases) * 100\n",
+    "    print(f\"\\n--- Evaluation Summary ---\")\n",
+    "    print(f\"Total Tested: {total_cases}\")\n",
+    "    print(f\"Correct: {correct_count}\")\n",
+    "    print(f\"Accuracy: {accuracy:.2f}%\")\n",
+    "else:\n",
+    "    print(\"No test cases found.\")"
+   ]
+  },
+  {
+   "cell_type": "markdown",
+   "id": "0531d7c3",
+   "metadata": {},
+   "source": [
+    "## Testing V2"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "ab8b4c96",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import json\n",
+    "import requests\n",
+    "import os\n",
+    "\n",
+    "# --- Configuration ---\n",
+    "DEV_SET_PATH = \"/home/mshahidul/readctrl/data/new_exp/test_health_literacy_data.json\"\n",
+    "FEW_SHOT_SET_PATH = \"/home/mshahidul/readctrl/data/new_exp/final_prompt_template_info.json\" # Using the one with reasoning\n",
+    "LOCAL_API_URL = \"http://172.16.34.29:8004/v1/chat/completions\"\n",
+    "LOCAL_MODEL_NAME = \"Qwen/Qwen3-30B-A3B-Instruct-2507\"\n",
+    "\n",
+    "# Define the range of few-shots per label you want to test\n",
+    "# e.g., [0, 1, 2, 3] will test 0-shot, 1-shot (3 total), 2-shot (6 total), etc.\n",
+    "SHOTS_TO_EVALUATE = [0, 1, 2, 3]\n",
+    "\n",
+    "# --- Core Functions ---\n",
+    "\n",
+    "def build_dynamic_prompt(few_shot_data, k_per_label):\n",
+    "    \"\"\"Constructs a prompt with k examples per literacy category.\"\"\"\n",
+    "    instruction = (\n",
+    "        \"You are an expert in health communication. Your task is to judge the health literacy level of the provided text.\\n\"\n",
+    "        \"Classify the text into: low_health_literacy, intermediate_health_literacy, or proficient_health_literacy.\\n\\n\"\n",
+    "    )\n",
+    "    \n",
+    "    if k_per_label == 0:\n",
+    "        return instruction + \"### Task:\\nTarget Text: \\\"{input_text}\\\"\\nReasoning:\"\n",
+    "\n",
+    "    # Organize few-shot data by label\n",
+    "    categorized = {}\n",
+    "    for entry in few_shot_data:\n",
+    "        label = entry['label']\n",
+    "        categorized.setdefault(label, []).append(entry)\n",
+    "\n",
+    "    few_shot_blocks = \"### Examples:\\n\"\n",
+    "    labels = [\"low_health_literacy\", \"intermediate_health_literacy\", \"proficient_health_literacy\"]\n",
+    "    \n",
+    "    for label in labels:\n",
+    "        examples = categorized.get(label, [])[:k_per_label]\n",
+    "        for ex in examples:\n",
+    "            few_shot_blocks += f\"Target Text: \\\"{ex['gen_text']}\\\"\\n\"\n",
+    "            few_shot_blocks += f\"Reasoning: {ex['reasoning']}\\n\"\n",
+    "            few_shot_blocks += f\"Label: {label}\\n\"\n",
+    "            few_shot_blocks += \"-\" * 30 + \"\\n\"\n",
+    "            \n",
+    "    return instruction + few_shot_blocks + \"\\n### Task:\\nTarget Text: \\\"{input_text}\\\"\\nReasoning:\"\n",
+    "\n",
+    "def get_prediction(prompt_template, input_text):\n",
+    "    \"\"\"Sends the formatted prompt to the local LLM.\"\"\"\n",
+    "    final_prompt = prompt_template.format(input_text=input_text)\n",
+    "    payload = {\n",
+    "        \"model\": LOCAL_MODEL_NAME,\n",
+    "        \"messages\": [{\"role\": \"user\", \"content\": final_prompt}],\n",
+    "        \"temperature\": 0 \n",
+    "    }\n",
+    "    try:\n",
+    "        response = requests.post(LOCAL_API_URL, json=payload, timeout=30)\n",
+    "        return response.json()['choices'][0]['message']['content'].strip()\n",
+    "    except Exception:\n",
+    "        return \"Error\"\n",
+    "\n",
+    "def parse_label(text):\n",
+    "    \"\"\"Normalizes LLM output to match dataset labels.\"\"\"\n",
+    "    text = text.lower()\n",
+    "    if \"low\" in text: return \"low_health_literacy\"\n",
+    "    if \"intermediate\" in text: return \"intermediate_health_literacy\"\n",
+    "    if \"proficient\" in text: return \"proficient_health_literacy\"\n",
+    "    return \"unknown\"\n",
+    "\n",
+    "# --- Main Execution ---\n",
+    "\n",
+    "# 1. Load Data\n",
+    "with open(DEV_SET_PATH, 'r') as f:\n",
+    "    dev_set = json.load(f)\n",
+    "with open(FEW_SHOT_SET_PATH, 'r') as f:\n",
+    "    few_shot_pool = json.load(f)\n",
+    "\n",
+    "# 2. Filter Dev Set\n",
+    "# Ensure no overlap between few-shot examples and dev set\n",
+    "shot_ids = {item['doc_id'] for item in few_shot_pool}\n",
+    "clean_dev_set = [item for item in dev_set if item['doc_id'] not in shot_ids]\n",
+    "\n",
+    "results_summary = []\n",
+    "\n",
+    "print(f\"Starting Evaluation on {len(clean_dev_set)} samples...\\n\")\n",
+    "\n",
+    "# 3. Loop through shot counts\n",
+    "for k in SHOTS_TO_EVALUATE:\n",
+    "    print(f\"Evaluating {k}-shot per label (Total {k*3} examples)...\")\n",
+    "    \n",
+    "    current_template = build_dynamic_prompt(few_shot_pool, k)\n",
+    "    correct = 0\n",
+    "    \n",
+    "    for case in clean_dev_set:\n",
+    "        raw_output = get_prediction(current_template, case['gen_text'])\n",
+    "        pred = parse_label(raw_output)\n",
+    "        actual = parse_label(case['label'])\n",
+    "        \n",
+    "        if pred == actual:\n",
+    "            correct += 1\n",
+    "            \n",
+    "    accuracy = (correct / len(clean_dev_set)) * 100\n",
+    "    results_summary.append({\"shots_per_label\": k, \"accuracy\": accuracy})\n",
+    "    print(f\"-> Accuracy: {accuracy:.2f}%\\n\")\n",
+    "\n",
+    "# --- Final Report ---\n",
+    "print(\"-\" * 30)\n",
+    "print(f\"{'Shots/Label':<15} | {'Accuracy':<10}\")\n",
+    "print(\"-\" * 30)\n",
+    "for res in results_summary:\n",
+    "    print(f\"{res['shots_per_label']:<15} | {res['accuracy']:.2f}%\")"
+   ]
+  },
+  {
+   "cell_type": "markdown",
+   "id": "d5cd799a",
+   "metadata": {},
+   "source": [
+    "## Step 3: Design Initial Prompt using dspy"
+   ]
+  },
+  {
+   "cell_type": "markdown",
+   "id": "d916470f",
+   "metadata": {},
+   "source": [
+    "## V1"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "793a47c7",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import dspy\n",
+    "import json\n",
+    "from dspy.teleprompt import BootstrapFewShot\n",
+    "\n",
+    "# --- 1. Configure the LLM via your vLLM Endpoint ---\n",
+    "# DSPy uses an OpenAI-compatible client for vLLM\n",
+    "vllm_model = dspy.LM(\n",
+    "    model='openai/Qwen/Qwen3-30B-A3B-Instruct-2507', # Use 'openai/' prefix for local endpoints\n",
+    "    api_base=\"http://172.16.34.29:8004/v1\",\n",
+    "    api_key=\"EMPTY\",\n",
+    "    temperature=0.0\n",
+    ")\n",
+    "dspy.configure(lm=vllm_model)\n",
+    "\n",
+    "# --- 2. Define the Task Signature ---\n",
+    "class HealthLiteracySignature(dspy.Signature):\n",
+    "    \"\"\"\n",
+    "    Judge the health literacy difficulty of a medical text.\n",
+    "    Classify into: low_health_literacy, intermediate_health_literacy, or proficient_health_literacy.\n",
+    "    \"\"\"\n",
+    "    text = dspy.InputField(desc=\"The medical text or patient note to analyze.\")\n",
+    "    reasoning = dspy.OutputField(desc=\"Step-by-step logic identifying jargon, sentence structure, and complexity.\")\n",
+    "    label = dspy.OutputField(desc=\"The final classification: low_health_literacy, intermediate_health_literacy, or proficient_health_literacy.\")\n",
+    "\n",
+    "# --- 3. Load Training Data ---\n",
+    "with open(\"/home/mshahidul/readctrl/data/new_exp/few_shot_examples.json\", 'r') as f:\n",
+    "    raw_examples = json.load(f)\n",
+    "\n",
+    "# Convert your 15 examples into DSPy format\n",
+    "trainset = []\n",
+    "for label_key, examples in raw_examples.items():\n",
+    "    for ex in examples:\n",
+    "        trainset.append(dspy.Example(text=ex['text'], label=label_key).with_inputs('text'))\n",
+    "\n",
+    "# --- 4. Define the Program (Chain of Thought) ---\n",
+    "class HealthLiteracyClassifier(dspy.Module):\n",
+    "    def __init__(self):\n",
+    "        super().__init__()\n",
+    "        # ChainOfThought automatically adds \"Reasoning\" steps to the prompt\n",
+    "        self.predictor = dspy.ChainOfThought(HealthLiteracySignature)\n",
+    "\n",
+    "    def forward(self, text):\n",
+    "        return self.predictor(text=text)\n",
+    "\n",
+    "# --- 5. Define the Metric (Success = Label Match) ---\n",
+    "def metric(gold, pred, trace=None):\n",
+    "    return gold.label == pred.label\n",
+    "\n",
+    "# --- 6. Run the Optimizer (Teleprompter) ---\n",
+    "# BootstrapFewShot will test variations of the prompt to see which one works best\n",
+    "optimizer = BootstrapFewShot(metric=metric, max_bootstrapped_demos=3, max_labeled_demos=5)\n",
+    "optimized_program = optimizer.compile(HealthLiteracyClassifier(), trainset=trainset)\n",
+    "\n",
+    "# --- 7. Save the Optimized Prompt ---\n",
+    "optimized_program.save(\"/home/mshahidul/readctrl/data/new_exp/optimized_health_classifier.json\")\n",
+    "\n",
+    "# Inspect the final prompt logic\n",
+    "vllm_model.inspect_history(n=1)"
+   ]
+  },
+  {
+   "cell_type": "markdown",
+   "id": "06a0eb62",
+   "metadata": {},
+   "source": [
+    "## V2"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "e3529bb0",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import dspy\n",
+    "import json\n",
+    "from typing import Literal\n",
+    "from dspy.teleprompt import BootstrapFewShotWithRandomSearch\n",
+    "from dspy.evaluate import Evaluate\n",
+    "\n",
+    "# --- 1. LLM Configuration ---\n",
+    "api_file = \"/home/mshahidul/api_new.json\"\n",
+    "with open(api_file, \"r\") as f:\n",
+    "    api_keys = json.load(f)\n",
+    "openai_api_key = api_keys[\"openai\"]\n",
+    "\n",
+    "# Student: Local vLLM (Deployment Model)\n",
+    "vllm_model = dspy.LM(\n",
+    "    model='openai/Qwen/Qwen3-30B-A3B-Instruct-2507',\n",
+    "    api_base=\"http://172.16.34.29:8004/v1\",\n",
+    "    api_key=\"EMPTY\",\n",
+    "    temperature=0.0\n",
+    ")\n",
+    "\n",
+    "# Teacher: OpenAI (High-quality rationale generation)\n",
+    "# Note: Ensure 'gpt-5' is the correct model name in your environment (usually 'gpt-4-turbo' or 'gpt-4o')\n",
+    "openai_model_teacher = dspy.LM(model='gpt-5', api_key=openai_api_key)\n",
+    "openai_model_student = dspy.LM(model='gpt-5-mini', api_key=openai_api_key)\n",
+    "\n",
+    "dspy.configure(lm=openai_model_student)  # Default to OpenAI for optimization\n",
+    "\n",
+    "# --- 2. Data Processing & Deduplication ---\n",
+    "\n",
+    "# 2.1 Load Training Data (Few-Shot)\n",
+    "with open(\"/home/mshahidul/readctrl/data/new_exp/few_shot_examples.json\", 'r') as f:\n",
+    "    few_shot_data = json.load(f)\n",
+    "\n",
+    "trainset = []\n",
+    "train_identifiers = set()\n",
+    "\n",
+    "for label_key, examples in few_shot_data.items():\n",
+    "    for ex in examples:\n",
+    "        # Create a unique ID to prevent data leakage\n",
+    "        unique_id = f\"{ex['doc_id']}_{label_key}\"\n",
+    "        train_identifiers.add(unique_id)\n",
+    "        \n",
+    "        # In few_shot, 'gen_text' is the summary we want to judge\n",
+    "        trainset.append(dspy.Example(\n",
+    "            summary_text=ex['gen_text'], \n",
+    "            label=label_key\n",
+    "        ).with_inputs('summary_text'))\n",
+    "\n",
+    "# 2.2 Load Test Data as Dev Set (Updated Path)\n",
+    "test_data_path = \"/home/mshahidul/readctrl/data/new_exp/test_health_literacy_data.json\"\n",
+    "with open(test_data_path, 'r') as f:\n",
+    "    test_data = json.load(f)\n",
+    "\n",
+    "devset = []\n",
+    "for item in test_data:\n",
+    "    unique_id = f\"{item['doc_id']}_{item['label']}\"\n",
+    "    \n",
+    "    # Filter out examples if they accidentally appear in the training set\n",
+    "    if unique_id not in train_identifiers:\n",
+    "        devset.append(dspy.Example(\n",
+    "            summary_text=item['gen_text'], \n",
+    "            label=item['label']\n",
+    "        ).with_inputs('summary_text'))\n",
+    "\n",
+    "print(f\"Dataset Stats: Train={len(trainset)}, Dev (Test Set)={len(devset)}\")\n",
+    "\n",
+    "# --- 3. Robust Signature & Module ---\n",
+    "\n",
+    "class HealthLiteracySignature(dspy.Signature):\n",
+    "    \"\"\"\n",
+    "    Judge the health literacy level of a generated medical summary.\n",
+    "    Identify if the language is suitable for a layperson (low) or requires medical expertise (proficient).\n",
+    "    \"\"\"\n",
+    "    summary_text: str = dspy.InputField(desc=\"The generated medical summary to be analyzed.\")\n",
+    "    reasoning: str = dspy.OutputField(desc=\"Analysis of jargon, acronyms, and sentence complexity.\")\n",
+    "    label: Literal[\"low_health_literacy\", \"intermediate_health_literacy\", \"proficient_health_literacy\"] = dspy.OutputField()\n",
+    "\n",
+    "class HealthLiteracyClassifier(dspy.Module):\n",
+    "    def __init__(self):\n",
+    "        super().__init__()\n",
+    "        self.predictor = dspy.ChainOfThought(HealthLiteracySignature)\n",
+    "\n",
+    "    def forward(self, summary_text):\n",
+    "        return self.predictor(summary_text=summary_text)\n",
+    "\n",
+    "# --- 4. Metric and Optimization ---\n",
+    "\n",
+    "def health_literacy_metric(gold, pred, trace=None):\n",
+    "    if not pred or not pred.label: return False\n",
+    "    return gold.label.strip().lower() == pred.label.strip().lower()\n",
+    "\n",
+    "optimizer = BootstrapFewShotWithRandomSearch(\n",
+    "    metric=health_literacy_metric,\n",
+    "    max_bootstrapped_demos=3,\n",
+    "    num_candidate_programs=8, \n",
+    "    teacher_settings=dict(lm=openai_model_teacher)\n",
+    ")\n",
+    "\n",
+    "# Compile the program\n",
+    "optimized_program = optimizer.compile(HealthLiteracyClassifier(), trainset=trainset)\n",
+    "\n",
+    "# --- 5. Evaluation & Saving ---\n",
+    "\n",
+    "# Evaluate on the provided test dataset\n",
+    "evaluator = Evaluate(devset=devset, metric=health_literacy_metric, num_threads=1, display_progress=True)\n",
+    "accuracy_score = evaluator(optimized_program)\n",
+    "\n",
+    "print(f\"\\nOptimization Complete.\")\n",
+    "print(f\"Final Accuracy on Test Set: {accuracy_score}%\")\n",
+    "\n",
+    "# Save the finalized prompt logic\n",
+    "optimized_program.save(\"/home/mshahidul/readctrl/data/new_exp/optimized_health_classifier_gpt5-mini.json\")"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "96f1f99e",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "print(f\"Final Accuracy on Test Set: {accuracy_score}%\")"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "814b0186",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "CUDA_DEVICE_ORDER=PCI_BUS_ID CUDA_VISIBLE_DEVICES=2 python '/home/mshahidul/readctrl/code/RL_model/finetune.py'\n",
+    "CUDA_DEVICE_ORDER=PCI_BUS_ID CUDA_VISIBLE_DEVICES=2 python -m vllm.entrypoints.openai.api_server     --model Qwen/Qwen3-30B-A3B-Instruct-2507     --max-model-len 8192     --tensor-parallel-size 1     --port 8004     --dtype auto     --trust_remote_code True"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "f0e0fbb8",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "# To load and use:\n",
+    "classifier = HealthLiteracyClassifier()\n",
+    "classifier.load(\"/home/mshahidul/readctrl/data/new_exp/optimized_health_classifier.json\")\n",
+    "path=\"/home/mshahidul/readctrl/data/new_exp/test_health_literacy_data.json\"\n",
+    "with open(path,'r') as f:\n",
+    "    test_data = json.load(f)\n",
+    "for item in test_data:\n",
+    "    expected_label = item['label']\n",
+    "    text = item['gen_text']\n",
+    "    result = classifier(summary_text=text)\n",
+    "    if (result.label == expected_label):\n",
+    "        print(f\"Correctly classified: {expected_label} ✅\")\n",
+    "    else:\n",
+    "        print(f\"Misclassified. Expected: {expected_label}, Got: {result.label} ❌\")"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "8700ac2b",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "print(few_shot_data.keys())\n",
+    "print(few_shot_data['low_health_literacy'][0].keys())"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "6b5dbe7a",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "# import json\n",
+    "# import pandas as pd\n",
+    "# from tqdm import tqdm\n",
+    "# import dspy\n",
+    "# from sklearn.metrics import accuracy_score, f1_score, cohen_kappa_score, classification_report\n",
+    "\n",
+    "# # --- 1. Load Data and Optimized Program ---\n",
+    "# CLEANED_DATA_PATH = \"/home/mshahidul/readctrl/data/new_exp/cleaned_health_literacy_data.json\"\n",
+    "# FEW_SHOT_PATH = \"/home/mshahidul/readctrl/data/new_exp/few_shot_examples.json\"\n",
+    "# MODEL_SAVE_PATH = \"/home/mshahidul/readctrl/data/new_exp/optimized_health_classifier.json\"\n",
+    "\n",
+    "# with open(CLEANED_DATA_PATH, 'r') as f:\n",
+    "#     full_data = json.load(f)\n",
+    "\n",
+    "# with open(FEW_SHOT_PATH, 'r') as f:\n",
+    "#     few_shot_data = json.load(f)\n",
+    "\n",
+    "# # Identify which doc_ids were used for training to ensure a clean test set\n",
+    "# trained_ids = []\n",
+    "# for label in few_shot_data:\n",
+    "#     trained_ids.extend([ex['doc_id'] for ex in few_shot_data[label]])\n",
+    "\n",
+    "# test_set = [item for item in full_data if item['doc_id'] not in trained_ids]\n",
+    "# print(f\"Total test examples: {len(test_set)}\")\n",
+    "# # --- 2. Initialize DSPy Program ---\n",
+    "# vllm_model = dspy.LM(\n",
+    "#     model='openai/Qwen/Qwen3-30B-A3B-Instruct-2507',\n",
+    "#     api_base=\"http://172.16.34.29:8004/v1\",\n",
+    "#     api_key=\"EMPTY\"\n",
+    "# )\n",
+    "# dspy.configure(lm=vllm_model)\n",
+    "\n",
+    "# class HealthLiteracySignature(dspy.Signature):\n",
+    "#     \"\"\"Judge health literacy difficulty: low, intermediate, or proficient.\"\"\"\n",
+    "#     text = dspy.InputField()\n",
+    "#     reasoning = dspy.OutputField()\n",
+    "#     label = dspy.OutputField()\n",
+    "\n",
+    "# class HealthLiteracyClassifier(dspy.Module):\n",
+    "#     def __init__(self):\n",
+    "#         super().__init__()\n",
+    "#         self.predictor = dspy.ChainOfThought(HealthLiteracySignature)\n",
+    "#     def forward(self, text):\n",
+    "#         return self.predictor(text=text)\n",
+    "\n",
+    "# # Load the optimized state\n",
+    "# classifier = HealthLiteracyClassifier()\n",
+    "# classifier.load(MODEL_SAVE_PATH)\n",
+    "\n",
+    "# # --- 3. Run Inference ---\n",
+    "# results = []\n",
+    "# y_true = []\n",
+    "# y_pred = []\n",
+    "\n",
+    "# print(f\"Starting evaluation on {len(test_set)} examples...\")\n",
+    "\n",
+    "# for item in tqdm(test_set):\n",
+    "#     try:\n",
+    "#         prediction = classifier(text=item['text'])\n",
+    "        \n",
+    "#         # Clean the label (sometimes LLMs add extra text or punctuation)\n",
+    "#         pred_label = prediction.label.strip().lower().replace(\" \", \"_\")\n",
+    "        \n",
+    "#         results.append({\n",
+    "#             \"doc_id\": item['doc_id'],\n",
+    "#             \"true_label\": item['label'],\n",
+    "#             \"pred_label\": pred_label,\n",
+    "#             \"reasoning\": prediction.reasoning\n",
+    "#         })\n",
+    "        \n",
+    "#         y_true.append(item['label'])\n",
+    "#         y_pred.append(pred_label)\n",
+    "#     except Exception as e:\n",
+    "#         print(f\"Error processing doc {item['doc_id']}: {e}\")\n",
+    "\n",
+    "# # --- 4. Calculate Metrics ---\n",
+    "# labels = [\"low_health_literacy\", \"intermediate_health_literacy\", \"proficient_health_literacy\"]\n",
+    "\n",
+    "# accuracy = accuracy_score(y_true, y_pred)\n",
+    "# f1 = f1_score(y_true, y_pred, average='weighted')\n",
+    "# kappa = cohen_kappa_score(y_true, y_pred)\n",
+    "\n",
+    "# print(\"\\n--- Evaluation Results ---\")\n",
+    "# print(f\"Accuracy: {accuracy:.4f}\")\n",
+    "# print(f\"Cohen’s Kappa: {kappa:.4f}\")\n",
+    "# print(f\"F1 Score (Weighted): {f1:.4f}\")\n",
+    "# print(\"\\nClassification Report:\")\n",
+    "# print(classification_report(y_true, y_pred, target_names=labels))\n",
+    "\n",
+    "# # Save results for failure analysis\n",
+    "# output_file = \"/home/mshahidul/readctrl/data/new_exp/evaluation_results.json\"\n",
+    "# with open(output_file, 'w') as f:\n",
+    "#     json.dump(results, f, indent=4)"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "e935e64c",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "CUDA_DEVICE_ORDER=PCI_BUS_ID \\\n",
+    "CUDA_VISIBLE_DEVICES=\"2\" \\\n",
+    "PYTORCH_CUDA_ALLOC_CONF=expandable_segments:True \\\n",
+    "VLLM_USE_MODELSCOPE=True \\\n",
+    "vllm \\\n",
+    "  serve swift/Qwen3-30B-A3B-AWQ \\\n",
+    "  --gpu-memory-utilization 0.9 \\\n",
+    "  --max-model-len 32768 \\\n",
+    "  --max-num-seqs 64 \\\n",
+    "  --served-model-name swift/Qwen3-30B-A3B-AWQ \\\n",
+    "  --host 127.0.0.1 \\\n",
+    "  --port 8004"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 1,
+   "id": "8e90b755",
+   "metadata": {},
+   "outputs": [
+    {
+     "name": "stdout",
+     "output_type": "stream",
+     "text": [
+      "Items processed: 60\n",
+      "Max raters per item: 7\n",
+      "---\n",
+      "Krippendorff's Alpha (Ordinal): 0.7083\n",
+      "\n",
+      "Note: Fleiss' Kappa skipped because of unequal rater counts per item.\n",
+      "Use Krippendorff's Alpha for your final report as it accounts for this.\n"
+     ]
+    }
+   ],
+   "source": [
+    "import json\n",
+    "import numpy as np\n",
+    "import krippendorff\n",
+    "\n",
+    "def calculate_iaa_robust(file_path):\n",
+    "    with open(file_path, 'r') as f:\n",
+    "        data = json.load(f)\n",
+    "\n",
+    "    # 1. Prepare data for Krippendorff's Alpha\n",
+    "    # Matrix shape must be (coders, items)\n",
+    "    max_annotations = max(len(entry['rating_distribution']) for entry in data)\n",
+    "    \n",
+    "    # We create a list for each \"slot\" (rater position)\n",
+    "    # If Doc 1 has 3 ratings and Doc 2 has 5, Doc 1 gets two np.nan values\n",
+    "    reliability_data = []\n",
+    "    for i in range(max_annotations):\n",
+    "        row = []\n",
+    "        for entry in data:\n",
+    "            ratings = entry['rating_distribution']\n",
+    "            if i < len(ratings):\n",
+    "                row.append(ratings[i])\n",
+    "            else:\n",
+    "                row.append(np.nan)\n",
+    "        reliability_data.append(row)\n",
+    "    \n",
+    "    reliability_matrix = np.array(reliability_data)\n",
+    "\n",
+    "    # 2. Calculate Krippendorff's Alpha (The primary metric for your paper)\n",
+    "    # Level of measurement 'ordinal' is best for 1-5 scales\n",
+    "    alpha = krippendorff.alpha(reliability_data=reliability_matrix, \n",
+    "                               level_of_measurement='ordinal')\n",
+    "    \n",
+    "    print(f\"Items processed: {len(data)}\")\n",
+    "    print(f\"Max raters per item: {max_annotations}\")\n",
+    "    print(f\"---\")\n",
+    "    print(f\"Krippendorff's Alpha (Ordinal): {alpha:.4f}\")\n",
+    "\n",
+    "    # 3. Handling Fleiss' Kappa (Optional/Conditional)\n",
+    "    counts_list = []\n",
+    "    rater_counts = []\n",
+    "    for entry in data:\n",
+    "        counts = [entry['rating_distribution'].count(i) for i in range(1, 6)]\n",
+    "        counts_list.append(counts)\n",
+    "        rater_counts.append(sum(counts))\n",
+    "    \n",
+    "    # Only run Fleiss if the raters are equal across all items\n",
+    "    if len(set(rater_counts)) == 1:\n",
+    "        from statsmodels.stats.inter_rater import fleiss_kappa\n",
+    "        f_kappa = fleiss_kappa(np.array(counts_list))\n",
+    "        print(f\"Fleiss' Kappa: {f_kappa:.4f}\")\n",
+    "    else:\n",
+    "        print(\"\\nNote: Fleiss' Kappa skipped because of unequal rater counts per item.\")\n",
+    "        print(\"Use Krippendorff's Alpha for your final report as it accounts for this.\")\n",
+    "\n",
+    "# Usage\n",
+    "path = '/home/mshahidul/readctrl/data/final_result/consolidated_ratings_threshold_manual_edit.json'\n",
+    "calculate_iaa_robust(path)"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 3,
+   "id": "a0776765",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "# /home/mshahidul/readctrl/data/final_result/consolidated_ratings_threshold.json\n",
+    "import json\n",
+    "def get_expected_label(rating):\n",
+    "    if rating in [1, 2]:\n",
+    "        return \"low_health_literacy\"\n",
+    "    elif rating == 3:\n",
+    "        return \"intermediate_health_literacy\"\n",
+    "    elif rating in [4, 5]:\n",
+    "        return \"proficient_health_literacy\"\n",
+    "    return None\n",
+    "with open(\"/home/mshahidul/readctrl/data/final_result/consolidated_ratings_threshold_manual_edit.json\", 'r') as f:\n",
+    "    few_shot_data = json.load(f)\n",
+    "cnt=0\n",
+    "for item in few_shot_data:\n",
+    "    expected_label = item['health_literacy_label']\n",
+    "    consensus_rating = get_expected_label(item['consensus_rating'])\n",
+    "    if expected_label == consensus_rating:\n",
+    "        cnt+=1"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "ed0a0618",
+   "metadata": {},
+   "outputs": [],
+   "source": []
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "76ed37ea",
+   "metadata": {},
+   "outputs": [
+    {
+     "name": "stdout",
+     "output_type": "stream",
+     "text": [
+      "dict_keys(['id', 'fulltext', 'summary'])\n"
+     ]
+    }
+   ],
+   "source": [
+    "# /home/mshahidul/readctrl/data/thresold_finding/junaed/seq0_record3.json\n",
+    "import json\n",
+    "with open(\"/home/mshahidul/readctrl/data/processed_test_raw_data/multiclinsum_test_en.json\", 'r') as f:\n",
+    "    data = json.load(f)\n",
+    "print(data[0].keys())\n"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 15,
+   "id": "eaefbfc6",
+   "metadata": {},
+   "outputs": [
+    {
+     "name": "stdout",
+     "output_type": "stream",
+     "text": [
+      "Source Type          | Level           | Mean Threshold (%)\n",
+      "-------------------------------------------------------\n",
+      "Gold Summary         | low             |    61.07% (n=15)\n",
+      "Gold Summary         | intermediate    |    81.99% (n=15)\n",
+      "Gold Summary         | proficient      |    95.69% (n=2)\n",
+      "Full Original Text   | low             |    37.23% (n=14)\n",
+      "Full Original Text   | intermediate    |    66.11% (n=14)\n",
+      "Full Original Text   | proficient      |    90.69% (n=4)\n"
+     ]
+    }
+   ],
+   "source": [
+    "import os\n",
+    "import json\n",
+    "from collections import defaultdict\n",
+    "import numpy as np\n",
+    "\n",
+    "# Configuration\n",
+    "base_path = \"/home/mshahidul/readctrl/data/thresold_finding\"\n",
+    "levels = ['low', 'intermediate', 'proficient']\n",
+    "source_types = [\"Gold Summary\", \"Full Original Text\"]\n",
+    "\n",
+    "# Dictionary to store percentages: results[source_type][level] = [list of values]\n",
+    "results = {src: {lvl: [] for lvl in levels} for src in source_types}\n",
+    "\n",
+    "# Iterate through each annotator folder (e.g., 'junaed')\n",
+    "annotator_names=['junaed','plabandas','shama']\n",
+    "for annotator in annotator_names:\n",
+    "    annotator_path = os.path.join(base_path, annotator)\n",
+    "    \n",
+    "    if os.path.isdir(annotator_path):\n",
+    "        # Iterate through each json file in the folder\n",
+    "        for filename in os.listdir(annotator_path):\n",
+    "            if filename.endswith(\".json\"):\n",
+    "                file_path = os.path.join(annotator_path, filename)\n",
+    "                \n",
+    "                try:\n",
+    "                    with open(file_path, 'r') as f:\n",
+    "                        data = json.load(f)\n",
+    "                    \n",
+    "                    src_type = data.get('source_type')\n",
+    "                    # Ensure source_type is one we are tracking\n",
+    "                    if src_type in source_types:\n",
+    "                        for lvl in levels:\n",
+    "                            # Extract threshold percentage from the annotations\n",
+    "                            # Adjust 'threshold' key name if it differs in your JSON\n",
+    "                            val = data['annotations'][lvl].get('percentage').replace('%', '').strip()\n",
+    "                            if val is not None:\n",
+    "                                if float(val) <= 99:\n",
+    "                                    results[src_type][lvl].append(float(val))\n",
+    "\n",
+    "                                \n",
+    "                except Exception as e:\n",
+    "                    print(f\"Error processing {file_path}: {e}\")\n",
+    "\n",
+    "# Calculate and display averages\n",
+    "print(f\"{'Source Type':<20} | {'Level':<15} | {'Mean Threshold (%)'}\")\n",
+    "print(\"-\" * 55)\n",
+    "\n",
+    "for src in source_types:\n",
+    "    for lvl in levels:\n",
+    "        vals = results[src][lvl]\n",
+    "        if vals:\n",
+    "            mean_val = np.mean(vals)\n",
+    "            count = len(vals)\n",
+    "            print(f\"{src:<20} | {lvl:<15} | {mean_val:>8.2f}% (n={count})\")\n",
+    "        else:\n",
+    "            print(f\"{src:<20} | {lvl:<15} | No data found\")"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "1aa3cd60",
+   "metadata": {},
+   "outputs": [],
+   "source": []
+  }
+ ],
+ "metadata": {
+  "kernelspec": {
+   "display_name": "un",
+   "language": "python",
+   "name": "python3"
+  },
+  "language_info": {
+   "codemirror_mode": {
+    "name": "ipython",
+    "version": 3
+   },
+   "file_extension": ".py",
+   "mimetype": "text/x-python",
+   "name": "python",
+   "nbconvert_exporter": "python",
+   "pygments_lexer": "ipython3",
+   "version": "3.11.14"
+  }
+ },
+ "nbformat": 4,
+ "nbformat_minor": 5
+}
diff --git a/code/classifier/data_st_updated.ipynb b/code/classifier/data_st_updated.ipynb
new file mode 100644
index 0000000000000000000000000000000000000000..d93add0c57dd3bb74da36ddcede55dc63bdbcb87
--- /dev/null
+++ b/code/classifier/data_st_updated.ipynb
@@ -0,0 +1,1284 @@
+{
+ "cells": [
+  {
+   "cell_type": "markdown",
+   "id": "d847270d",
+   "metadata": {},
+   "source": [
+    "## Step 0: Prepare Your Dataset"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "44047dbb",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import json\n",
+    "\n",
+    "# 1. Load the datasets\n",
+    "with open(\"/home/mshahidul/readctrl/data/final_result/consolidated_ratings_edit.json\", 'r') as f:\n",
+    "    ratings_data = json.load(f)\n",
+    "ratings_data=ratings_data[7:]\n",
+    "with open(\"/home/mshahidul/readctrl/data/extracting_subclaim/extracted_subclaims_syn_data_with_gs_summary_en.json\", 'r') as f:\n",
+    "    text_data = json.load(f)\n",
+    "\n",
+    "# 2. Updated mapping: Store the whole item or specific keys for fulltext and summary\n",
+    "# We map the index to a dictionary containing the variations and the original full text/summary\n",
+    "text_map = {\n",
+    "    item['index']: {\n",
+    "        'variations': item['diff_label_texts'],\n",
+    "        'fulltext': item.get('fulltext', \"\"),\n",
+    "        'summary': item.get('summary', \"\")\n",
+    "    } \n",
+    "    for item in text_data\n",
+    "}\n",
+    "\n",
+    "cleaned_data = []\n",
+    "\n",
+    "# 3. Iterate through ratings and extract data\n",
+    "for entry in ratings_data:\n",
+    "    doc_id = entry['doc_id']\n",
+    "    label = entry['health_literacy_label']\n",
+    "    \n",
+    "    if doc_id in text_map:\n",
+    "        source_info = text_map[doc_id]\n",
+    "        \n",
+    "        # Retrieve the specific text version based on the label\n",
+    "        # .get() handles cases where a specific label might be missing\n",
+    "        labeled_text = source_info['variations'].get(label, \"\")\n",
+    "        \n",
+    "        # Construct the expanded object\n",
+    "        cleaned_data.append({\n",
+    "            \"doc_id\": doc_id,\n",
+    "            \"label\": label,\n",
+    "            \"gen_text\": labeled_text,\n",
+    "            \"fulltext\": source_info['fulltext'],\n",
+    "            \"gs_summary\": source_info['summary']\n",
+    "        })\n",
+    "\n",
+    "# 4. Output the clean JSON\n",
+    "output_path = \"/home/mshahidul/readctrl/data/new_exp/cleaned_health_literacy_data.json\"\n",
+    "with open(output_path, 'w') as f:\n",
+    "    json.dump(cleaned_data, f, indent=4, ensure_ascii=False)\n",
+    "\n",
+    "print(f\"Successfully processed {len(cleaned_data)} examples.\")"
+   ]
+  },
+  {
+   "cell_type": "markdown",
+   "id": "a1e6b0ae",
+   "metadata": {},
+   "source": [
+    "## Step 1: Pick Few-Shot Examples"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "71e83ac8",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import json\n",
+    "import requests\n",
+    "from collections import defaultdict\n",
+    "\n",
+    "# Configuration\n",
+    "API_URL = \"http://172.16.34.29:8004/v1/chat/completions\"\n",
+    "MODEL_NAME = \"Qwen/Qwen3-30B-A3B-Instruct-2507\"\n",
+    "INPUT_FILE = \"/home/mshahidul/readctrl/data/new_exp/cleaned_health_literacy_data.json\"\n",
+    "OUTPUT_FILE = \"/home/mshahidul/readctrl/data/new_exp/few_shot_examples.json\"\n",
+    "\n",
+    "def get_text_metadata(text):\n",
+    "    \"\"\"Ask the LLM to identify the topic and medical complexity of a text.\"\"\"\n",
+    "    prompt = f\"\"\"Analyze the following medical text and provide a 1-word topic (e.g., Cardiology, Nutrition, Medication) and a 1-word complexity level (Simple, Moderate, Technical).\n",
+    "    Text: {text}...\n",
+    "    Format: Topic | Complexity\"\"\"\n",
+    "    \n",
+    "    try:\n",
+    "        response = requests.post(API_URL, json={\n",
+    "            \"model\": MODEL_NAME,\n",
+    "            \"messages\": [{\"role\": \"user\", \"content\": prompt}],\n",
+    "            \"temperature\": 0.1\n",
+    "        })\n",
+    "        return response.json()['choices'][0]['message']['content'].strip()\n",
+    "    except:\n",
+    "        return \"General | Unknown\"\n",
+    "\n",
+    "# 1. Load the cleaned data\n",
+    "with open(INPUT_FILE, 'r') as f:\n",
+    "    data = json.load(f)\n",
+    "\n",
+    "# 2. Group data by label\n",
+    "grouped_data = defaultdict(list)\n",
+    "for item in data:\n",
+    "    grouped_data[item['label']].append(item)\n",
+    "\n",
+    "# 3. Select diverse examples for each label\n",
+    "few_shot_selection = {}\n",
+    "\n",
+    "for label, examples in grouped_data.items():\n",
+    "    print(f\"Processing label: {label}...\")\n",
+    "    \n",
+    "    # Analyze a subset (or all) to find diversity\n",
+    "    scored_examples = []\n",
+    "    for ex in examples: \n",
+    "        metadata = get_text_metadata(ex['gen_text'])\n",
+    "        ex['metadata'] = metadata\n",
+    "        scored_examples.append(ex)\n",
+    "    \n",
+    "    # Heuristic: Sort by metadata to group similar topics, then pick spread-out indices\n",
+    "    scored_examples.sort(key=lambda x: x['metadata'])\n",
+    "    \n",
+    "    # Pick 5 examples spread across the sorted metadata for maximum diversity\n",
+    "    step = max(1, len(scored_examples) // 5)\n",
+    "    selected = scored_examples[::step][:5]\n",
+    "    few_shot_selection[label] = selected\n",
+    "\n",
+    "# 4. Save the result\n",
+    "with open(OUTPUT_FILE, 'w') as f:\n",
+    "    json.dump(few_shot_selection, f, indent=4)\n",
+    "\n",
+    "print(f\"Few-shot examples saved to: {OUTPUT_FILE}\")"
+   ]
+  },
+  {
+   "cell_type": "markdown",
+   "id": "d48720a6",
+   "metadata": {},
+   "source": [
+    "## Step 2: Decide on LLM(s)"
+   ]
+  },
+  {
+   "cell_type": "markdown",
+   "id": "74b07429",
+   "metadata": {},
+   "source": [
+    "## V2"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "912f3d85",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import json\n",
+    "import requests\n",
+    "from openai import OpenAI\n",
+    "\n",
+    "# --- Configuration ---\n",
+    "LOCAL_API_URL = \"http://172.16.34.29:8004/v1/chat/completions\"\n",
+    "LOCAL_MODEL_NAME = \"Qwen/Qwen3-30B-A3B-Instruct-2507\"\n",
+    "\n",
+    "api_file = \"/home/mshahidul/api_new.json\"\n",
+    "with open(api_file, \"r\") as f:\n",
+    "    api_keys = json.load(f)\n",
+    "\n",
+    "openai_client = OpenAI(api_key=api_keys[\"openai\"])\n",
+    "OPENAI_MODEL_NAME = \"gpt-5\" # Note: Ensure your model version is correct\n",
+    "\n",
+    "FEW_SHOT_FILE = \"/home/mshahidul/readctrl/data/new_exp/few_shot_examples.json\"\n",
+    "OUTPUT_PATH = \"/home/mshahidul/readctrl/data/new_exp/final_prompt_template.txt\"\n",
+    "\n",
+    "# --- Logic ---\n",
+    "\n",
+    "def get_reasoning(fulltext, gen_text, label, provider=\"local\"):\n",
+    "    \"\"\"\n",
+    "    Ask an LLM to explain why the text fits the label in JSON format.\n",
+    "    \"\"\"\n",
+    "    # Explicitly asking for JSON in the prompt\n",
+    "    prompt = f\"\"\"Compare the 'Target Text' to the 'Original Fulltext'. \n",
+    "Explain why the Target Text fits the health literacy label: {label}.\n",
+    "Focus on how vocabulary, jargon, and sentence structure were adapted.\n",
+    "\n",
+    "Original Fulltext: {fulltext}\n",
+    "Target Text: {gen_text}\n",
+    "Label: {label}\n",
+    "\n",
+    "Return your response ONLY as a JSON object with the following key:\n",
+    "\"reasoning\": \"your 1-2 sentence explanation\"\n",
+    "\"\"\"\n",
+    "\n",
+    "    try:\n",
+    "        if provider == \"openai\":\n",
+    "            response = openai_client.chat.completions.create(\n",
+    "                model=OPENAI_MODEL_NAME,\n",
+    "                messages=[{\"role\": \"user\", \"content\": prompt}],\n",
+    "                response_format={ \"type\": \"json_object\" } # Force JSON for OpenAI\n",
+    "            )\n",
+    "            content = response.choices[0].message.content.strip()\n",
+    "        else:\n",
+    "            response = requests.post(LOCAL_API_URL, json={\n",
+    "                \"model\": LOCAL_MODEL_NAME,\n",
+    "                \"messages\": [{\"role\": \"user\", \"content\": prompt}],\n",
+    "                \"temperature\": 0\n",
+    "            })\n",
+    "            content = response.json()['choices'][0]['message']['content'].strip()\n",
+    "        \n",
+    "        # Parse JSON and extract reasoning\n",
+    "        data = json.loads(content)\n",
+    "        return data.get(\"reasoning\", \"Reasoning key not found.\")\n",
+    "            \n",
+    "    except Exception as e:\n",
+    "        print(f\"Error with {provider}: {e}\")\n",
+    "        return \"Reasoning could not be generated.\"\n",
+    "\n",
+    "# 1. Load the selected examples\n",
+    "with open(FEW_SHOT_FILE, 'r') as f:\n",
+    "    few_shot_data = json.load(f)\n",
+    "\n",
+    "# 2. Build the few-shot string\n",
+    "few_shot_string = \"\"\n",
+    "REASONING_PROVIDER = \"openai\" \n",
+    "\n",
+    "print(f\"Generating reasoning using: {REASONING_PROVIDER}...\")\n",
+    "info=[]\n",
+    "for label in [\"low_health_literacy\", \"intermediate_health_literacy\", \"proficient_health_literacy\"]:\n",
+    "    examples = few_shot_data.get(label, [])\n",
+    "    for ex in examples:\n",
+    "        reason = get_reasoning(ex.get('fulltext', \"\"), ex['gen_text'], label, provider=REASONING_PROVIDER)\n",
+    "        \n",
+    "        # Adding structured few-shot examples to the string\n",
+    "        few_shot_string += f\"Original Fulltext: \\\"{ex.get('fulltext', '')}\\\"\\n\"\n",
+    "        few_shot_string += f\"Target Text: \\\"{ex['gen_text']}\\\"\\n\"\n",
+    "        few_shot_string += f\"Reasoning: {reason}\\n\"\n",
+    "        few_shot_string += f\"Label: {label}\\n\"\n",
+    "        few_shot_string += \"-\" * 30 + \"\\n\"\n",
+    "        info.append({\n",
+    "            \"doc_id\": ex.get('doc_id', \"\"),\n",
+    "            \"fulltext\": ex.get('fulltext', \"\"),\n",
+    "            \"gen_text\": ex['gen_text'],\n",
+    "            \"reasoning\": reason,\n",
+    "            \"label\": label\n",
+    "        })                    \n",
+    "\n",
+    "# 3. Define the Final Prompt Structure\n",
+    "instruction = \"\"\"You are an expert in health communication. Your task is to judge the health literacy level of a target text based on its original medical source.\n",
+    "\n",
+    "Classify the text into one of three categories:\n",
+    "1. low_health_literacy: Uses common words (everyday language), very short sentences, and eliminates all medical jargon.\n",
+    "2. intermediate_health_literacy: Uses some medical terms with explanation, standard sentence length, requires basic health knowledge.\n",
+    "3. proficient_health_literacy: Uses high-level medical jargon, technical language, and academic or professional structures.\n",
+    "\n",
+    "### Few-Shot Examples:\n",
+    "\"\"\"\n",
+    "\n",
+    "# 4. Final Template Construction\n",
+    "final_prompt_template = (\n",
+    "    instruction + \n",
+    "    few_shot_string + \n",
+    "    \"\\n### Now judge this text:\\n\"\n",
+    "    \"Original Fulltext: \\\"{fulltext}\\\"\\n\"\n",
+    "    \"Target Text: \\\"{input_text}\\\"\\n\"\n",
+    "    \"Reasoning:\"\n",
+    ")\n",
+    "\n",
+    "with open(OUTPUT_PATH, 'w') as f:\n",
+    "    f.write(final_prompt_template)\n",
+    "with open(OUTPUT_PATH.replace('.txt', '_info.json'), 'w') as f:\n",
+    "    json.dump(info, f, indent=4)\n",
+    "print(f\"Structured prompt template saved to {OUTPUT_PATH}\")"
+   ]
+  },
+  {
+   "cell_type": "markdown",
+   "id": "8c470dd5",
+   "metadata": {},
+   "source": [
+    "## Fewshot data selection"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "06158d8d",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import json\n",
+    "import os\n",
+    "\n",
+    "# --- Configuration ---\n",
+    "# Path to your existing data (containing 'reasoning', 'gen_text', and 'label')\n",
+    "INPUT_INFO_FILE = \"/home/mshahidul/readctrl/data/new_exp/final_prompt_template_info.json\"\n",
+    "OUTPUT_PATH = \"/home/mshahidul/readctrl/data/new_exp/new_prompt_template.txt\"\n",
+    "\n",
+    "# Decide how many few-shot examples you want to include for each label\n",
+    "FEW_SHOT_PER_LABEL = 2  # Change this to 1, 3, etc.\n",
+    "\n",
+    "# --- Logic ---\n",
+    "\n",
+    "def generate_prompt_from_json(input_json_path, num_per_label):\n",
+    "    if not os.path.exists(input_json_path):\n",
+    "        return f\"Error: File {input_json_path} not found. Please check the path.\"\n",
+    "        \n",
+    "    with open(input_json_path, 'r') as f:\n",
+    "        data = json.load(f)\n",
+    "    \n",
+    "    # Organize the data by label to ensure even distribution\n",
+    "    labeled_data = {}\n",
+    "    for entry in data:\n",
+    "        label = entry['label']\n",
+    "        if label not in labeled_data:\n",
+    "            labeled_data[label] = []\n",
+    "        labeled_data[label].append(entry)\n",
+    "    \n",
+    "    # Build the few-shot section\n",
+    "    few_shot_string = \"\"\n",
+    "    # Define labels in a logical order\n",
+    "    target_labels = [\"low_health_literacy\", \"intermediate_health_literacy\", \"proficient_health_literacy\"]\n",
+    "    \n",
+    "    for label in target_labels:\n",
+    "        examples = labeled_data.get(label, [])\n",
+    "        # Slice the list based on your variable\n",
+    "        selected_examples = examples[:num_per_label]\n",
+    "        \n",
+    "        for ex in selected_examples:\n",
+    "            # Construct the example block WITHOUT the fulltext\n",
+    "            few_shot_string += f\"Target Text: \\\"{ex['gen_text']}\\\"\\n\"\n",
+    "            few_shot_string += f\"Reasoning: {ex['reasoning']}\\n\"\n",
+    "            few_shot_string += f\"Label: {label}\\n\"\n",
+    "            few_shot_string += \"-\" * 30 + \"\\n\"\n",
+    "\n",
+    "    # Define the final instruction structure (no mention of fulltext comparison)\n",
+    "    instruction = \"\"\"You are an expert in health communication. Your task is to judge the health literacy level of the provided text.\n",
+    "\n",
+    "Classify the text into one of three categories:\n",
+    "1. low_health_literacy: Uses common words (everyday language), very short sentences, and avoids medical jargon.\n",
+    "2. intermediate_health_literacy: Uses some medical terms with explanation, standard sentence length, requires basic health knowledge.\n",
+    "3. proficient_health_literacy: Uses high-level medical jargon, technical language, and academic or professional structures.\n",
+    "\n",
+    "### Examples:\n",
+    "\"\"\"\n",
+    "\n",
+    "    # Final Template Construction\n",
+    "    final_template = (\n",
+    "        instruction + \n",
+    "        few_shot_string + \n",
+    "        \"\\n### Task:\\n\"\n",
+    "        \"Target Text: \\\"{input_text}\\\"\\n\"\n",
+    "        \"Reasoning:\"\n",
+    "    )\n",
+    "    \n",
+    "    return final_template\n",
+    "\n",
+    "# 1. Generate the string\n",
+    "new_prompt_template = generate_prompt_from_json(INPUT_INFO_FILE, FEW_SHOT_PER_LABEL)\n",
+    "\n",
+    "# 2. Save to file\n",
+    "with open(OUTPUT_PATH, 'w') as f:\n",
+    "    f.write(new_prompt_template)\n",
+    "\n",
+    "print(f\"Successfully created a prompt with {FEW_SHOT_PER_LABEL} examples per label.\")\n",
+    "print(f\"Saved to: {OUTPUT_PATH}\")"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "f78d4619",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "\n",
+    "with open(\"/home/mshahidul/readctrl/data/new_exp/cleaned_health_literacy_data.json\", 'r') as f:\n",
+    "    cleaned_data = json.load(f)\n",
+    "with open(\"/home/mshahidul/readctrl/data/new_exp/few_shot_examples.json\", 'r') as f:\n",
+    "    few_shot_examples = json.load(f)\n",
+    "\n",
+    "list_data = []\n",
+    "for item in few_shot_examples:\n",
+    "    for ex in few_shot_examples[item]:\n",
+    "        list_data.append((ex['doc_id'], ex['label']))\n",
+    "\n",
+    "test_set = []\n",
+    "for item in cleaned_data:\n",
+    "    if (item['doc_id'], item['label']) not in list_data:\n",
+    "        test_set.append(item)\n",
+    "with open(\"/home/mshahidul/readctrl/data/new_exp/test_health_literacy_data.json\", 'w') as f:\n",
+    "    json.dump(test_set, f, indent=4)"
+   ]
+  },
+  {
+   "cell_type": "markdown",
+   "id": "0531d7c3",
+   "metadata": {},
+   "source": [
+    "## Testing V2"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "ab8b4c96",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import json\n",
+    "import requests\n",
+    "import os\n",
+    "\n",
+    "# --- Configuration ---\n",
+    "DEV_SET_PATH = \"/home/mshahidul/readctrl/data/new_exp/test_health_literacy_data.json\"\n",
+    "FEW_SHOT_SET_PATH = \"/home/mshahidul/readctrl/data/new_exp/final_prompt_template_info.json\" # Using the one with reasoning\n",
+    "LOCAL_API_URL = \"http://172.16.34.29:8004/v1/chat/completions\"\n",
+    "LOCAL_MODEL_NAME = \"Qwen/Qwen3-30B-A3B-Instruct-2507\"\n",
+    "\n",
+    "# Define the range of few-shots per label you want to test\n",
+    "# e.g., [0, 1, 2, 3] will test 0-shot, 1-shot (3 total), 2-shot (6 total), etc.\n",
+    "SHOTS_TO_EVALUATE = [0, 1, 2, 3]\n",
+    "\n",
+    "# --- Core Functions ---\n",
+    "\n",
+    "def build_dynamic_prompt(few_shot_data, k_per_label):\n",
+    "    \"\"\"Constructs a prompt with k examples per literacy category.\"\"\"\n",
+    "    instruction = (\n",
+    "        \"You are an expert in health communication. Your task is to judge the health literacy level of the provided text.\\n\"\n",
+    "        \"Classify the text into: low_health_literacy, intermediate_health_literacy, or proficient_health_literacy.\\n\\n\"\n",
+    "    )\n",
+    "    \n",
+    "    if k_per_label == 0:\n",
+    "        return instruction + \"### Task:\\nTarget Text: \\\"{input_text}\\\"\\nReasoning:\"\n",
+    "\n",
+    "    # Organize few-shot data by label\n",
+    "    categorized = {}\n",
+    "    for entry in few_shot_data:\n",
+    "        label = entry['label']\n",
+    "        categorized.setdefault(label, []).append(entry)\n",
+    "\n",
+    "    few_shot_blocks = \"### Examples:\\n\"\n",
+    "    labels = [\"low_health_literacy\", \"intermediate_health_literacy\", \"proficient_health_literacy\"]\n",
+    "    \n",
+    "    for label in labels:\n",
+    "        examples = categorized.get(label, [])[:k_per_label]\n",
+    "        for ex in examples:\n",
+    "            few_shot_blocks += f\"Target Text: \\\"{ex['gen_text']}\\\"\\n\"\n",
+    "            few_shot_blocks += f\"Reasoning: {ex['reasoning']}\\n\"\n",
+    "            few_shot_blocks += f\"Label: {label}\\n\"\n",
+    "            few_shot_blocks += \"-\" * 30 + \"\\n\"\n",
+    "            \n",
+    "    return instruction + few_shot_blocks + \"\\n### Task:\\nTarget Text: \\\"{input_text}\\\"\\nReasoning:\"\n",
+    "\n",
+    "def get_prediction(prompt_template, input_text):\n",
+    "    \"\"\"Sends the formatted prompt to the local LLM.\"\"\"\n",
+    "    final_prompt = prompt_template.format(input_text=input_text)\n",
+    "    payload = {\n",
+    "        \"model\": LOCAL_MODEL_NAME,\n",
+    "        \"messages\": [{\"role\": \"user\", \"content\": final_prompt}],\n",
+    "        \"temperature\": 0 \n",
+    "    }\n",
+    "    try:\n",
+    "        response = requests.post(LOCAL_API_URL, json=payload, timeout=30)\n",
+    "        return response.json()['choices'][0]['message']['content'].strip()\n",
+    "    except Exception:\n",
+    "        return \"Error\"\n",
+    "\n",
+    "def parse_label(text):\n",
+    "    \"\"\"Normalizes LLM output to match dataset labels.\"\"\"\n",
+    "    text = text.lower()\n",
+    "    if \"low\" in text: return \"low_health_literacy\"\n",
+    "    if \"intermediate\" in text: return \"intermediate_health_literacy\"\n",
+    "    if \"proficient\" in text: return \"proficient_health_literacy\"\n",
+    "    return \"unknown\"\n",
+    "\n",
+    "# --- Main Execution ---\n",
+    "\n",
+    "# 1. Load Data\n",
+    "with open(DEV_SET_PATH, 'r') as f:\n",
+    "    dev_set = json.load(f)\n",
+    "with open(FEW_SHOT_SET_PATH, 'r') as f:\n",
+    "    few_shot_pool = json.load(f)\n",
+    "\n",
+    "# 2. Filter Dev Set\n",
+    "# Ensure no overlap between few-shot examples and dev set\n",
+    "shot_ids = {item['doc_id'] for item in few_shot_pool}\n",
+    "clean_dev_set = [item for item in dev_set if item['doc_id'] not in shot_ids]\n",
+    "\n",
+    "results_summary = []\n",
+    "\n",
+    "print(f\"Starting Evaluation on {len(clean_dev_set)} samples...\\n\")\n",
+    "\n",
+    "# 3. Loop through shot counts\n",
+    "for k in SHOTS_TO_EVALUATE:\n",
+    "    print(f\"Evaluating {k}-shot per label (Total {k*3} examples)...\")\n",
+    "    \n",
+    "    current_template = build_dynamic_prompt(few_shot_pool, k)\n",
+    "    correct = 0\n",
+    "    \n",
+    "    for case in clean_dev_set:\n",
+    "        raw_output = get_prediction(current_template, case['gen_text'])\n",
+    "        pred = parse_label(raw_output)\n",
+    "        actual = parse_label(case['label'])\n",
+    "        \n",
+    "        if pred == actual:\n",
+    "            correct += 1\n",
+    "            \n",
+    "    accuracy = (correct / len(clean_dev_set)) * 100\n",
+    "    results_summary.append({\"shots_per_label\": k, \"accuracy\": accuracy})\n",
+    "    print(f\"-> Accuracy: {accuracy:.2f}%\\n\")\n",
+    "\n",
+    "# --- Final Report ---\n",
+    "print(\"-\" * 30)\n",
+    "print(f\"{'Shots/Label':<15} | {'Accuracy':<10}\")\n",
+    "print(\"-\" * 30)\n",
+    "for res in results_summary:\n",
+    "    print(f\"{res['shots_per_label']:<15} | {res['accuracy']:.2f}%\")"
+   ]
+  },
+  {
+   "cell_type": "markdown",
+   "id": "d5cd799a",
+   "metadata": {},
+   "source": [
+    "## Step 3: Design Initial Prompt using dspy"
+   ]
+  },
+  {
+   "cell_type": "markdown",
+   "id": "06a0eb62",
+   "metadata": {},
+   "source": [
+    "## V2"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "e3529bb0",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import dspy\n",
+    "import json\n",
+    "from typing import Literal\n",
+    "from dspy.teleprompt import BootstrapFewShotWithRandomSearch\n",
+    "from dspy.evaluate import Evaluate\n",
+    "\n",
+    "# --- 1. LLM Configuration ---\n",
+    "api_file = \"/home/mshahidul/api_new.json\"\n",
+    "with open(api_file, \"r\") as f:\n",
+    "    api_keys = json.load(f)\n",
+    "openai_api_key = api_keys[\"openai\"]\n",
+    "\n",
+    "# Student: Local vLLM (Deployment Model)\n",
+    "vllm_model = dspy.LM(\n",
+    "    model='openai/Qwen/Qwen3-30B-A3B-Instruct-2507',\n",
+    "    api_base=\"http://172.16.34.29:8004/v1\",\n",
+    "    api_key=\"EMPTY\",\n",
+    "    temperature=0.0\n",
+    ")\n",
+    "\n",
+    "# Teacher: OpenAI (High-quality rationale generation)\n",
+    "# Note: Ensure 'gpt-5' is the correct model name in your environment (usually 'gpt-4-turbo' or 'gpt-4o')\n",
+    "openai_model_teacher = dspy.LM(model='gpt-5', api_key=openai_api_key)\n",
+    "openai_model_student = dspy.LM(model='gpt-5-mini', api_key=openai_api_key)\n",
+    "\n",
+    "dspy.configure(lm=openai_model_student)  # Default to OpenAI for optimization\n",
+    "\n",
+    "# --- 2. Data Processing & Deduplication ---\n",
+    "\n",
+    "# 2.1 Load Training Data (Few-Shot)\n",
+    "with open(\"/home/mshahidul/readctrl/data/new_exp/few_shot_examples_manual_edit.json\", 'r') as f:\n",
+    "    few_shot_data = json.load(f)\n",
+    "\n",
+    "trainset = []\n",
+    "train_identifiers = set()\n",
+    "\n",
+    "for label_key, examples in few_shot_data.items():\n",
+    "    for ex in examples:\n",
+    "        # Create a unique ID to prevent data leakage\n",
+    "        unique_id = f\"{ex['doc_id']}_{label_key}\"\n",
+    "        train_identifiers.add(unique_id)\n",
+    "        \n",
+    "        # In few_shot, 'gen_text' is the summary we want to judge\n",
+    "        trainset.append(dspy.Example(\n",
+    "            summary_text=ex['gen_text'], \n",
+    "            label=label_key\n",
+    "        ).with_inputs('summary_text'))\n",
+    "\n",
+    "# 2.2 Load Test Data as Dev Set (Updated Path)\n",
+    "test_data_path = \"/home/mshahidul/readctrl/data/new_exp/test_health_literacy_data_manual_edit.json\"\n",
+    "with open(test_data_path, 'r') as f:\n",
+    "    test_data = json.load(f)\n",
+    "\n",
+    "devset = []\n",
+    "for item in test_data:\n",
+    "    unique_id = f\"{item['doc_id']}_{item['label']}\"\n",
+    "    \n",
+    "    # Filter out examples if they accidentally appear in the training set\n",
+    "    if unique_id not in train_identifiers:\n",
+    "        devset.append(dspy.Example(\n",
+    "            summary_text=item['gen_text'], \n",
+    "            label=item['label']\n",
+    "        ).with_inputs('summary_text'))\n",
+    "\n",
+    "print(f\"Dataset Stats: Train={len(trainset)}, Dev (Test Set)={len(devset)}\")\n",
+    "\n",
+    "# --- 3. Robust Signature & Module ---\n",
+    "\n",
+    "class HealthLiteracySignature(dspy.Signature):\n",
+    "    \"\"\"\n",
+    "    Judge the health literacy level of a generated medical summary.\n",
+    "    Identify if the language is suitable for a layperson (low) or requires medical expertise (proficient).\n",
+    "    \"\"\"\n",
+    "    summary_text: str = dspy.InputField(desc=\"The generated medical summary to be analyzed.\")\n",
+    "    reasoning: str = dspy.OutputField(desc=\"Analysis of jargon, acronyms, and sentence complexity.\")\n",
+    "    label: Literal[\"low_health_literacy\", \"intermediate_health_literacy\", \"proficient_health_literacy\"] = dspy.OutputField()\n",
+    "\n",
+    "class HealthLiteracyClassifier(dspy.Module):\n",
+    "    def __init__(self):\n",
+    "        super().__init__()\n",
+    "        self.predictor = dspy.ChainOfThought(HealthLiteracySignature)\n",
+    "\n",
+    "    def forward(self, summary_text):\n",
+    "        return self.predictor(summary_text=summary_text)\n",
+    "\n",
+    "# --- 4. Metric and Optimization ---\n",
+    "\n",
+    "def health_literacy_metric(gold, pred, trace=None):\n",
+    "    if not pred or not pred.label: return False\n",
+    "    return gold.label.strip().lower() == pred.label.strip().lower()\n",
+    "\n",
+    "optimizer = BootstrapFewShotWithRandomSearch(\n",
+    "    metric=health_literacy_metric,\n",
+    "    max_bootstrapped_demos=3,\n",
+    "    num_candidate_programs=8, \n",
+    "    teacher_settings=dict(lm=openai_model_teacher)\n",
+    ")\n",
+    "\n",
+    "# Compile the program\n",
+    "optimized_program = optimizer.compile(HealthLiteracyClassifier(), trainset=trainset)\n",
+    "\n",
+    "# --- 5. Evaluation & Saving ---\n",
+    "\n",
+    "# Evaluate on the provided test dataset\n",
+    "evaluator = Evaluate(devset=devset, metric=health_literacy_metric, num_threads=1, display_progress=True)\n",
+    "accuracy_score = evaluator(optimized_program)\n",
+    "\n",
+    "print(f\"\\nOptimization Complete.\")  \n",
+    "print(f\"Final Accuracy on Test Set: {accuracy_score}%\")\n",
+    "\n",
+    "# Save the finalized prompt logic\n",
+    "optimized_program.save(\"/home/mshahidul/readctrl/data/new_exp/optimized_health_classifier_gpt5-mini_v2.json\")"
+   ]
+  },
+  {
+   "cell_type": "markdown",
+   "id": "10f0396a",
+   "metadata": {},
+   "source": [
+    "## V2 (gen text with src text) not good"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "298dba97",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import dspy\n",
+    "import json\n",
+    "from typing import Literal\n",
+    "from dspy.teleprompt import BootstrapFewShotWithRandomSearch\n",
+    "from dspy.evaluate import Evaluate\n",
+    "\n",
+    "# --- 1. LLM Configuration ---\n",
+    "# (Keeping your existing setup)\n",
+    "api_file = \"/home/mshahidul/api_new.json\"\n",
+    "with open(api_file, \"r\") as f:\n",
+    "    api_keys = json.load(f)\n",
+    "openai_api_key = api_keys[\"openai\"]\n",
+    "\n",
+    "vllm_model = dspy.LM(\n",
+    "    model='openai/Qwen/Qwen3-30B-A3B-Instruct-2507',\n",
+    "    api_base=\"http://172.16.34.29:8004/v1\",\n",
+    "    api_key=\"EMPTY\",\n",
+    "    temperature=0.0\n",
+    ")\n",
+    "\n",
+    "openai_model_teacher = dspy.LM(model='gpt-5', api_key=openai_api_key)\n",
+    "openai_model_student = dspy.LM(model='gpt-5-mini', api_key=openai_api_key)\n",
+    "\n",
+    "dspy.configure(lm=openai_model_student)\n",
+    "\n",
+    "# --- 2. Data Processing & Deduplication (Updated for Source Text) ---\n",
+    "\n",
+    "# 2.1 Load Training Data\n",
+    "with open(\"/home/mshahidul/readctrl/data/new_exp/few_shot_examples_manual_edit.json\", 'r') as f:\n",
+    "    few_shot_data = json.load(f)\n",
+    "\n",
+    "trainset = []\n",
+    "train_identifiers = set()\n",
+    "\n",
+    "for label_key, examples in few_shot_data.items():\n",
+    "    for ex in examples:\n",
+    "        unique_id = f\"{ex['doc_id']}_{label_key}\"\n",
+    "        train_identifiers.add(unique_id)\n",
+    "        \n",
+    "        # Adding 'source_text' (assumed key is 'fulltext' based on your comment)\n",
+    "        trainset.append(dspy.Example(\n",
+    "            source_text=ex.get('fulltext', \"\"), \n",
+    "            summary_text=ex['gen_text'], \n",
+    "            label=label_key\n",
+    "        ).with_inputs('source_text', 'summary_text'))\n",
+    "\n",
+    "# 2.2 Load Test Data\n",
+    "test_data_path = \"/home/mshahidul/readctrl/data/new_exp/test_health_literacy_data_manual_edit.json\"\n",
+    "with open(test_data_path, 'r') as f:\n",
+    "    test_data = json.load(f)\n",
+    "\n",
+    "devset = []\n",
+    "for item in test_data:\n",
+    "    unique_id = f\"{item['doc_id']}_{item['label']}\"\n",
+    "    \n",
+    "    if unique_id not in train_identifiers:\n",
+    "        devset.append(dspy.Example(\n",
+    "            source_text=item.get('fulltext', \"\"), \n",
+    "            summary_text=item['gen_text'], \n",
+    "            label=item['label']\n",
+    "        ).with_inputs('source_text', 'summary_text'))\n",
+    "\n",
+    "print(f\"Dataset Stats: Train={len(trainset)}, Dev={len(devset)}\")\n",
+    "\n",
+    "# --- 3. Robust Signature & Module (Updated) ---\n",
+    "\n",
+    "class HealthLiteracySignature(dspy.Signature):\n",
+    "    \"\"\"\n",
+    "    Judge the health literacy level of a medical summary relative to its source text.\n",
+    "    Analyze if the summary successfully simplifies technical medical concepts \n",
+    "    for the intended literacy level.\n",
+    "    \"\"\"\n",
+    "    source_text: str = dspy.InputField(desc=\"The original technical medical document.\")\n",
+    "    summary_text: str = dspy.InputField(desc=\"The generated summary to be analyzed.\")\n",
+    "    \n",
+    "    reasoning: str = dspy.OutputField(desc=\"Compare the summary to the source. Check for simplification of jargon and maintenance of core facts.\")\n",
+    "    label: Literal[\"low_health_literacy\", \"intermediate_health_literacy\", \"proficient_health_literacy\"] = dspy.OutputField()\n",
+    "\n",
+    "class HealthLiteracyClassifier(dspy.Module):\n",
+    "    def __init__(self):\n",
+    "        super().__init__()\n",
+    "        self.predictor = dspy.ChainOfThought(HealthLiteracySignature)\n",
+    "\n",
+    "    def forward(self, source_text, summary_text):\n",
+    "        return self.predictor(source_text=source_text, summary_text=summary_text)\n",
+    "\n",
+    "# --- 4. Metric and Optimization ---\n",
+    "\n",
+    "def health_literacy_metric(gold, pred, trace=None):\n",
+    "    if not pred or not pred.label: return False\n",
+    "    return gold.label.strip().lower() == pred.label.strip().lower()\n",
+    "\n",
+    "optimizer = BootstrapFewShotWithRandomSearch(\n",
+    "    metric=health_literacy_metric,\n",
+    "    max_bootstrapped_demos=3,\n",
+    "    num_candidate_programs=8, \n",
+    "    teacher_settings=dict(lm=openai_model_teacher)\n",
+    ")\n",
+    "\n",
+    "optimized_program = optimizer.compile(HealthLiteracyClassifier(), trainset=trainset)\n",
+    "\n",
+    "# --- 5. Evaluation & Saving ---\n",
+    "\n",
+    "evaluator = Evaluate(devset=devset, metric=health_literacy_metric, num_threads=1, display_progress=True)\n",
+    "accuracy_score = evaluator(optimized_program)\n",
+    "\n",
+    "print(f\"\\nOptimization Complete. Final Accuracy: {accuracy_score}%\")\n",
+    "optimized_program.save(\"/home/mshahidul/readctrl/data/new_exp/optimized_health_classifier_gpt5-mini_v2_with_source.json\")"
+   ]
+  },
+  {
+   "cell_type": "markdown",
+   "id": "68df2ee4",
+   "metadata": {},
+   "source": [
+    "### /home/mshahidul/readctrl/data/new_exp/few_shot_examples_manual_edit.json give good performance"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "96f1f99e",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "print(f\"Final Accuracy on Test Set: {accuracy_score}%\")"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "f0e0fbb8",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "# To load and use:\n",
+    "classifier = HealthLiteracyClassifier()\n",
+    "classifier.load(\"/home/mshahidul/readctrl/data/new_exp/optimized_health_classifier.json\")\n",
+    "path=\"/home/mshahidul/readctrl/data/new_exp/test_health_literacy_data.json\"\n",
+    "with open(path,'r') as f:\n",
+    "    test_data = json.load(f)\n",
+    "for item in test_data:\n",
+    "    expected_label = item['label']\n",
+    "    text = item['gen_text']\n",
+    "    result = classifier(summary_text=text)\n",
+    "    if (result.label == expected_label):\n",
+    "        print(f\"Correctly classified: {expected_label} ✅\")\n",
+    "    else:\n",
+    "        print(f\"Misclassified. Expected: {expected_label}, Got: {result.label} ❌\")"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "132453c8",
+   "metadata": {},
+   "outputs": [
+    {
+     "name": "stdout",
+     "output_type": "stream",
+     "text": [
+      "\n",
+      "\n",
+      "\n",
+      "\n",
+      "None\n"
+     ]
+    }
+   ],
+   "source": [
+    "import dspy\n",
+    "import json\n",
+    "from typing import Literal\n",
+    "from dspy.teleprompt import BootstrapFewShotWithRandomSearch\n",
+    "from dspy.evaluate import Evaluate\n",
+    "\n",
+    "# --- 1. LLM Configuration ---\n",
+    "# (Keeping your existing setup)\n",
+    "api_file = \"/home/mshahidul/api_new.json\"\n",
+    "with open(api_file, \"r\") as f:\n",
+    "    api_keys = json.load(f)\n",
+    "openai_api_key = api_keys[\"openai\"]\n",
+    "\n",
+    "\n",
+    "openai_model_student = dspy.LM(model='gpt-5-mini', api_key=openai_api_key)\n",
+    "\n",
+    "dspy.configure(lm=openai_model_student)\n",
+    "class HealthLiteracySignature(dspy.Signature):\n",
+    "    \"\"\"\n",
+    "    Judge the health literacy level of a generated medical summary.\n",
+    "    Identify if the language is suitable for a layperson (low) or requires medical expertise (proficient).\n",
+    "    \"\"\"\n",
+    "    summary_text: str = dspy.InputField(desc=\"The generated medical summary to be analyzed.\")\n",
+    "    reasoning: str = dspy.OutputField(desc=\"Analysis of jargon, acronyms, and sentence complexity.\")\n",
+    "    label: Literal[\"low_health_literacy\", \"intermediate_health_literacy\", \"proficient_health_literacy\"] = dspy.OutputField()\n",
+    "\n",
+    "class HealthLiteracyClassifier(dspy.Module):\n",
+    "    def __init__(self):\n",
+    "        super().__init__()\n",
+    "        self.predictor = dspy.ChainOfThought(HealthLiteracySignature)\n",
+    "\n",
+    "    def forward(self, summary_text):\n",
+    "        return self.predictor(summary_text=summary_text)\n",
+    "\n",
+    "classifier = HealthLiteracyClassifier()\n",
+    "classifier.load(\"/home/mshahidul/readctrl/data/new_exp/optimized_health_classifier_gpt5-mini_v2.json\")\n",
+    "result = classifier(summary_text=text)\n"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "8700ac2b",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "print(few_shot_data.keys())\n",
+    "print(few_shot_data['low_health_literacy'][0].keys())"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "9f8f1c6a",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "def calculate_label_accuracy(data):\n",
+    "    \"\"\"\n",
+    "    Calculates the accuracy of health_literacy_label based on doc_rating.\n",
+    "    \n",
+    "    Mapping:\n",
+    "    - 1-2: low_health_literacy\n",
+    "    - 3:   intermediate_health_literacy\n",
+    "    - 4-5: proficient_health_literacy\n",
+    "    \"\"\"\n",
+    "    if not data:\n",
+    "        return 0.0\n",
+    "    \n",
+    "    correct_matches = 0\n",
+    "    total_docs = len(data)\n",
+    "    \n",
+    "    for entry in data:\n",
+    "        rating = entry.get('doc_rating')\n",
+    "        actual_label = entry.get('health_literacy_label')\n",
+    "        \n",
+    "        # Determine the expected label based on the rating\n",
+    "        if rating in [1, 2]:\n",
+    "            expected_label = \"low_health_literacy\"\n",
+    "        elif rating == 3:\n",
+    "            expected_label = \"intermediate_health_literacy\"\n",
+    "        elif rating in [4, 5]:\n",
+    "            expected_label = \"proficient_health_literacy\"\n",
+    "        else:\n",
+    "            expected_label = None # Handle unexpected ratings if necessary\n",
+    "            \n",
+    "        # Check if the actual label matches the expected label\n",
+    "        if actual_label == expected_label:\n",
+    "            correct_matches += 1\n",
+    "            \n",
+    "    accuracy = (correct_matches / total_docs) * 100\n",
+    "    return accuracy\n",
+    "\n",
+    "import json\n",
+    "import os\n",
+    "all_path=\"/home/mshahidul/readctrl/data/annotators_validate_data\"\n",
+    "for path in os.listdir(all_path):\n",
+    "    for file in os.listdir(os.path.join(all_path,path)):\n",
+    "        if file.endswith(\".json\") and \"annotation_results\" in file:\n",
+    "            full_path=os.path.join(all_path,path,file)\n",
+    "            \n",
+    "            with open(full_path,'r') as f:\n",
+    "                dataset = json.load(f)\n",
+    "\n",
+    "            accuracy_pct = calculate_label_accuracy(dataset)\n",
+    "            if accuracy_pct > 50.0:\n",
+    "                print(path)\n",
+    "                print(f\"Accuracy: {accuracy_pct:.2f}%\")"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "3d0a3fb4",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import os\n",
+    "import json\n",
+    "import pandas as pd\n",
+    "from collections import Counter\n",
+    "\n",
+    "# Configuration\n",
+    "input_dir = '/home/mshahidul/readctrl/data/annotators_validate_data'\n",
+    "output_dir = '/home/mshahidul/readctrl/data/final_result'\n",
+    "output_file = os.path.join(output_dir, 'consolidated_ratings_threshold.json')\n",
+    "\n",
+    "# --- Helper for Label Mapping ---\n",
+    "def get_expected_label(rating):\n",
+    "    if rating in [1, 2]:\n",
+    "        return \"low_health_literacy\"\n",
+    "    elif rating == 3:\n",
+    "        return \"intermediate_health_literacy\"\n",
+    "    elif rating in [4, 5]:\n",
+    "        return \"proficient_health_literacy\"\n",
+    "    return None\n",
+    "\n",
+    "# --- Accuracy Function ---\n",
+    "def calculate_label_accuracy(data):\n",
+    "    if not data:\n",
+    "        return 0.0\n",
+    "    \n",
+    "    correct_matches = 0\n",
+    "    total_docs = len(data)\n",
+    "    \n",
+    "    for entry in data:\n",
+    "        rating = entry.get('doc_rating')\n",
+    "        actual_label = entry.get('health_literacy_label')\n",
+    "        expected_label = get_expected_label(rating)\n",
+    "            \n",
+    "        if actual_label == expected_label:\n",
+    "            correct_matches += 1\n",
+    "            \n",
+    "    return (correct_matches / total_docs) * 100\n",
+    "\n",
+    "# 1. Create the output directory\n",
+    "os.makedirs(output_dir, exist_ok=True)\n",
+    "\n",
+    "all_data = []\n",
+    "cnt=0\n",
+    "maxi=float('inf')\n",
+    "total=0\n",
+    "# 2. Collect data from folders\n",
+    "folders = [f for f in os.listdir(input_dir) if os.path.isdir(os.path.join(input_dir, f))]\n",
+    "\n",
+    "for folder in folders:\n",
+    "    json_path = os.path.join(input_dir, folder, 'annotation_results.json')\n",
+    "    \n",
+    "    if os.path.exists(json_path):\n",
+    "        with open(json_path, 'r') as f:\n",
+    "            try:\n",
+    "                entries = json.load(f)\n",
+    "                accuracy_pct = calculate_label_accuracy(entries)\n",
+    "                total+=1\n",
+    "                if accuracy_pct > 55.0:\n",
+    "                    cnt+=1\n",
+    "                    maxi=min(maxi,len(entries))\n",
+    "                    for item in entries:\n",
+    "                        all_data.append({\n",
+    "                            'doc_id': item.get('doc_id'),\n",
+    "                            'health_literacy_label': item.get('health_literacy_label'),\n",
+    "                            'rating': item.get('doc_rating')\n",
+    "                        })\n",
+    "                else:\n",
+    "                    print(f\"Skipping folder '{folder}': Accuracy too low ({accuracy_pct:.2f}%)\")\n",
+    "            except Exception as e:\n",
+    "                print(f\"Skipping error in {json_path}: {e}\")\n",
+    "\n",
+    "# 3. Process data\n",
+    "if not all_data:\n",
+    "    print(\"No data met the accuracy threshold.\")\n",
+    "else:\n",
+    "    df = pd.DataFrame(all_data)\n",
+    "    df = df.dropna(subset=['doc_id', 'health_literacy_label', 'rating'])\n",
+    "\n",
+    "    # 4. Custom Aggregation Logic for Consensus\n",
+    "    def get_constrained_mode(group):\n",
+    "        \"\"\"\n",
+    "        Calculates mode but prioritizes ratings that match the health_literacy_label.\n",
+    "        \"\"\"\n",
+    "        label = group['health_literacy_label'].iloc[0]\n",
+    "        ratings = group['rating'].tolist()\n",
+    "        counts = Counter(ratings)\n",
+    "        \n",
+    "        # Sort by frequency (descending)\n",
+    "        most_common = counts.most_common()\n",
+    "        \n",
+    "        # Check if the most frequent rating matches the label category\n",
+    "        for rating, count in most_common:\n",
+    "            if get_expected_label(rating) == label:\n",
+    "                return rating\n",
+    "        \n",
+    "        # Fallback: if no ratings match the label (unlikely given your 55% filter), \n",
+    "        # just take the most frequent one.\n",
+    "        return most_common[0][0]\n",
+    "\n",
+    "    # Group and Aggregate\n",
+    "    summary = df.groupby(['doc_id', 'health_literacy_label']).apply(\n",
+    "        lambda x: pd.Series({\n",
+    "            'num_annotations': len(x),\n",
+    "            'mean_rating': x['rating'].mean(),\n",
+    "            'consensus_rating': get_constrained_mode(x),\n",
+    "            'rating_distribution': x['rating'].tolist()\n",
+    "        })\n",
+    "    ).reset_index()\n",
+    "\n",
+    "    # 5. Save to JSON\n",
+    "    summary.to_json(output_file, orient='records', indent=4)\n",
+    "\n",
+    "    print(\"-\" * 30)\n",
+    "    print(f\"Success! Processed {len(summary)} unique pairs.\")\n",
+    "    print(f\"File saved at: {output_file}\")\n",
+    "    print(summary.head())"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "7ccf5e91",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "# /home/mshahidul/readctrl/data/final_result/consolidated_ratings_threshold.json\n",
+    "with open(\"/home/mshahidul/readctrl/data/final_result/consolidated_ratings_threshold.json\", 'r') as f:\n",
+    "    data = json.load(f)\n",
+    "doc={}\n",
+    "for item in data:\n",
+    "    doc[(item['doc_id'],item['health_literacy_label'])]=item\n",
+    "for it in range(0,20):\n",
+    "    for label in ['low_health_literacy','intermediate_health_literacy','proficient_health_literacy']:\n",
+    "        if doc.get((it,label)) is None:\n",
+    "            print(it,label)"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "0466c8f0",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "# /home/mshahidul/readctrl/data/synthetic_dataset_diff_labels/syn_data_with_gs_summary_en.json\n",
+    "with open(\"/home/mshahidul/readctrl/data/synthetic_dataset_diff_labels/syn_data_with_gs_summary_en.json\", 'r') as f:\n",
+    "    data = json.load(f)\n",
+    "print(f\"Label: low_health_literacy\")\n",
+    "id=2\n",
+    "print(f\"fulltext: {data[id]['fulltext']}\")\n",
+    "print(f\"gold summary: {data[id]['summary']}\")\n",
+    "print(f\"generated summary: {data[id]['diff_label_texts']['low_health_literacy']}\")"
+   ]
+  },
+  {
+   "cell_type": "markdown",
+   "id": "13c234a2",
+   "metadata": {},
+   "source": []
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "b89b4952",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import json\n",
+    "from collections import Counter\n",
+    "\n",
+    "# Load your data\n",
+    "file_path = '/home/mshahidul/readctrl/data/final_result/consolidated_ratings_threshold.json'\n",
+    "with open(file_path, 'r') as f:\n",
+    "    data = json.load(f)\n",
+    "\n",
+    "def map_to_category(rating):\n",
+    "    \"\"\"Maps 1-5 scale to Low, Med, High buckets.\"\"\"\n",
+    "    if rating in [1, 2]:\n",
+    "        return \"Low\"\n",
+    "    elif rating == 3:\n",
+    "        return \"Med\"\n",
+    "    elif rating in [4, 5]:\n",
+    "        return \"High\"\n",
+    "    return None\n",
+    "\n",
+    "def get_agreement_type(ratings):\n",
+    "    # Map 1-5 values to Low, Med, High\n",
+    "    categories = [map_to_category(r) for r in ratings]\n",
+    "    \n",
+    "    counts = Counter(categories)\n",
+    "    max_votes = max(counts.values())\n",
+    "    num_annotators = len(categories)\n",
+    "    \n",
+    "    # Logic Update:\n",
+    "    if max_votes == num_annotators:\n",
+    "        return \"Unanimous\"\n",
+    "    elif max_votes >= (num_annotators / 2):\n",
+    "        # This captures 2 out of 3, or 2 out of 4, etc.\n",
+    "        return \"Majority\"\n",
+    "    else:\n",
+    "        return \"Disputed\"\n",
+    "\n",
+    "# Counters\n",
+    "stats = {\"Unanimous\": 0, \"Majority\": 0, \"Disputed\": 0}\n",
+    "valid_count = 0\n",
+    "\n",
+    "for entry in data:\n",
+    "    ratings = entry['rating_distribution']\n",
+    "    \n",
+    "    if len(ratings) < 2:\n",
+    "        continue\n",
+    "        \n",
+    "    agreement = get_agreement_type(ratings)\n",
+    "    stats[agreement] += 1\n",
+    "    valid_count += 1\n",
+    "\n",
+    "print(f\"--- Final Agreement Distribution ---\")\n",
+    "print(f\"Total Documents: {valid_count}\\n\")\n",
+    "\n",
+    "for label, count in stats.items():\n",
+    "    percentage = (count / valid_count) * 100 if valid_count > 0 else 0\n",
+    "    print(f\"{label:10}: {count:4} notes ({percentage:6.2f}%)\")"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "e28ee431",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "total"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 1,
+   "id": "43a3a839",
+   "metadata": {},
+   "outputs": [
+    {
+     "name": "stdout",
+     "output_type": "stream",
+     "text": [
+      "Length of the JSON file: 49\n",
+      "Keys of the first item: dict_keys(['id', 'fulltext', 'summary', 'translated_fulltext', 'translated_summary', 'judge_pass'])\n"
+     ]
+    }
+   ],
+   "source": [
+    "import json\n",
+    "\n",
+    "# Path to your JSON file\n",
+    "# Check length and attribute keys of the JSON file\n",
+    "\n",
+    "json_path = \"/home/mshahidul/readctrl/data/translated_data/translation_version_1/multiclinsum_gs_train_en2bn_gemma(0_200).json\"\n",
+    "with open(json_path, 'r') as f:\n",
+    "    data = json.load(f)\n",
+    "\n",
+    "# Check length and attribute keys of the JSON file\n",
+    "print(f\"Length of the JSON file: {len(data)}\")\n",
+    "print(f\"Keys of the first item: {data[0].keys()}\")\n"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 3,
+   "id": "542bc6cf",
+   "metadata": {},
+   "outputs": [
+    {
+     "data": {
+      "text/plain": [
+       "{'id': 'multiclinsum_gs_en_47.txt',\n",
+       " 'fulltext': 'We present here the case of a two-day old neonate with in-born right scrotal swelling admitted at Children’s hospital. The patient was born at term via cesarean section at a private hospital. He was kept in the nursery for one day. The examining doctor referred them for urgent surgical care, but it took them one day to arrive at our hospital. Upon arrival in the emergency department, he was well hydrated, pink at room temperature with good perfusion. Upon examination, the right testis was found to be enlarged, tense, non-tender visibly reddish with overlying skin excoriation. Trans-illumination was negative in the right but positive in the contralateral testis. Both hernial orifices were normal. All the laboratory investigations were performed with an urgent Doppler ultrasound of the inguinoscrotal area. The ultrasound examination found the right testis to be enlarged (15.6*9.4 mm) and showed heterogeneous hypoechoic texture with prominent rete testis and no flow on color Doppler analysis. Left testis appeared normal in size, shape and echotexture with minimal hydrocele. An urgent scrotal exploration was undertaken. Intra-operatively, there was frank necrotic right testis with intravaginal torsion of the testis with minimal hydrocele. A right orchidectomy and contralateral orchidopexy was then performed.',\n",
+       " 'summary': 'We present here the case of a two-day old neonate with in-born right scrotal swelling admitted at Children’s hospital. The patient was born at term via cesarean section at a private hospital. Upon arrival in the emergency department, he was well hydrated, pink at room temperature with good perfusion. Upon examination, the right testis was found to be enlarged, tense, non-tender visibly reddish with overlying skin excoriation. Trans-illumination was negative in right but positive in the contralateral testis. Both hernial orifices were normal. Doppler ultrasound of the inguinoscrotal area found the right testis to be enlarged (15.6*9.4 mm) and showed heterogeneous hypoechoic texture with prominent rete testis and no flow on color doppler analysis. An urgent scrotal exploration was undertaken. Intra-operatively there was frank necrotic right testis with intravaginal torsion of the testis and minimal hydrocele. A right orchidectomy and contralateral orchidopexy were performed.',\n",
+       " 'translated_fulltext': 'আমরা এখানে একটি দুই দিন বয়সী নবজাতকের ঘটনা তুলে ধরছি, যার জন্মগতভাবে ডান দিকের অণ্ডকোষে ফোলা ছিল এবং তাকে শিশু হাসপাতালে ভর্তি করা হয়েছে। শিশুটি একটি বেসরকারি হাসপাতালে সিজারিয়ান অপারেশনের মাধ্যমে নির্ধারিত সময়ে জন্মগ্রহণ করে। তাকে একদিনের জন্য নার্সারিতে রাখা হয়েছিল। যে ডাক্তার পরীক্ষা করেছিলেন, তিনি জরুরি ভিত্তিতে অস্ত্রোপচারের জন্য পরামর্শ দেন, কিন্তু তাদের হাসপাতালে আসতে এক দিন লেগে যায়। জরুরি বিভাগে আসার পর দেখা যায়, শিশুটি ভালোভাবে হাইড্রেটেড, স্বাভাবিক তাপমাত্রায় তার ত্বক গোলাপী এবং রক্ত সঞ্চালন স্বাভাবিক। পরীক্ষায় দেখা যায়, ডান দিকের অণ্ডকোষটি বড়, শক্ত, দৃশ্যত লালচে এবং এর উপরে ত্বকের সামান্য ক্ষয় হয়েছে। ডান দিকের অণ্ডকোষে ট্রান্স-ইলুমিনেশন নেগেটিভ ছিল, কিন্তু অন্য অণ্ডকোষে পজিটিভ। উভয় হার্নিয়াল ছিদ্র স্বাভাবিক ছিল। এরপর দ্রুততার সাথে ইনগুইনোস্ক্রোটাল অঞ্চলের ডপলার আলট্রাসাউন্ড করা হয় এবং অন্যান্য পরীক্ষাও করা হয়। আলট্রাসাউন্ড পরীক্ষায় দেখা যায়, ডান দিকের অণ্ডকোষটি বড় (15.6*9.4 মিমি) এবং এর মধ্যে বিভিন্ন ধরনের হাইপোইক টেক্সচার রয়েছে, রেটে টেস্টিস স্পষ্টভাবে দেখা যাচ্ছে এবং কালার ডপলার বিশ্লেষণে কোনো রক্ত প্রবাহ নেই। বাম দিকের অণ্ডকোষের আকার, আকৃতি এবং ইকোটেক্সচার স্বাভাবিক দেখা যায়, সামান্য হাইড্রোসেলও ছিল। এরপর জরুরি ভিত্তিতে স্ক্রোটাল এক্সপ্লোরেশন করা হয়। অস্ত্রোপচারের সময় দেখা যায়, ডান দিকের অণ্ডকোষে স্পষ্ট নেক্রোসিস হয়েছে এবং অণ্ডকোষের মধ্যে সামান্য হাইড্রোসেলসহ ইন্ট্রাভ্যাজাইনাল টর্শন রয়েছে। এরপর ডান দিকের অণ্ডকোষ অপসারণ (অর্কিডেক্টমি) এবং অন্য দিকের অণ্ডকোষকে সঠিক স্থানে স্থাপন (অর্কিডোপেক্সি) করা হয়।',\n",
+       " 'translated_summary': 'আমরা এখানে একটি দুই দিন বয়সী নবজাতকের ঘটনা তুলে ধরছি, যার জন্মগতভাবে ডান দিকের অণ্ডকোষে ফোলা ছিল এবং তাকে শিশু হাসপাতালে ভর্তি করা হয়েছে। শিশুটি একটি বেসরকারি হাসপাতালে সিজারিয়ান অপারেশনের মাধ্যমে নির্ধারিত সময়ে জন্মগ্রহণ করে। জরুরি বিভাগে আসার পর দেখা যায়, তার শরীর ভালোভাবে হাইড্রেটেড, স্বাভাবিক তাপমাত্রায় ত্বক গোলাপী এবং রক্ত সঞ্চালন স্বাভাবিক। পরীক্ষায় দেখা যায়, ডান দিকের অণ্ডকোষটি বড়, শক্ত, দৃশ্যত লালচে এবং এর উপরে ত্বকের সামান্য ক্ষয় হয়েছে। ডান দিকের অণ্ডকোষে আলো প্রবেশ করানো হলে তা দেখা যায়নি, কিন্তু বিপরীত দিকের অণ্ডকোষে আলো প্রবেশ করানো হলে তা দেখা গেছে। উভয় হার্নিয়াল ছিদ্র স্বাভাবিক ছিল। ইনগুইনোস্ক্রোটাল অঞ্চলের ডপলার আল্ট্রাসাউন্ডে দেখা যায়, ডান দিকের অণ্ডকোষটি বড় (১৫.৬*৯.৪ মিমি) এবং এর মধ্যে বিভিন্ন ধরনের হাইপোইক টেক্সচার রয়েছে, রেটে টেস্টিস স্পষ্টভাবে দেখা যাচ্ছে এবং কালার ডপলার বিশ্লেষণে কোনো রক্ত প্রবাহ দেখা যায়নি। দ্রুত স্ক্রোটাল এক্সপ্লোরেশন করা হয়। অপারেশনের সময় দেখা যায়, ডান দিকের অণ্ডকোষে স্পষ্ট নেক্রোসিস হয়েছে এবং অণ্ডকোষের ইন্ট্রাভ্যাজিনাল টরশন হয়েছে, সেই সাথে সামান্য হাইড্রোসেলও রয়েছে। এরপর ডান দিকের অণ্ডকোষ অপসারণ (অর্কিডেক্টমি) এবং বিপরীত দিকের অণ্ডকোষকে সঠিক স্থানে স্থাপন (অর্কিডোপেক্সি) করা হয়।',\n",
+       " 'judge_pass': True}"
+      ]
+     },
+     "execution_count": 3,
+     "metadata": {},
+     "output_type": "execute_result"
+    }
+   ],
+   "source": [
+    "data[2]"
+   ]
+  }
+ ],
+ "metadata": {
+  "kernelspec": {
+   "display_name": "un",
+   "language": "python",
+   "name": "python3"
+  },
+  "language_info": {
+   "codemirror_mode": {
+    "name": "ipython",
+    "version": 3
+   },
+   "file_extension": ".py",
+   "mimetype": "text/x-python",
+   "name": "python",
+   "nbconvert_exporter": "python",
+   "pygments_lexer": "ipython3",
+   "version": "3.11.14"
+  }
+ },
+ "nbformat": 4,
+ "nbformat_minor": 5
+}
diff --git a/code/classifier/dspy.ipynb b/code/classifier/dspy.ipynb
new file mode 100644
index 0000000000000000000000000000000000000000..d03596d406c6c985d3a34aa6934bc3d70d21c843
--- /dev/null
+++ b/code/classifier/dspy.ipynb
@@ -0,0 +1,19 @@
+{
+ "cells": [
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "6eb33df5",
+   "metadata": {},
+   "outputs": [],
+   "source": []
+  }
+ ],
+ "metadata": {
+  "language_info": {
+   "name": "python"
+  }
+ },
+ "nbformat": 4,
+ "nbformat_minor": 5
+}
diff --git a/code/classifier/dspy_classifer.py b/code/classifier/dspy_classifer.py
new file mode 100644
index 0000000000000000000000000000000000000000..bc2bb96342544e8c0b7d0a54342960c2a554ed4b
--- /dev/null
+++ b/code/classifier/dspy_classifer.py
@@ -0,0 +1,56 @@
+import dspy
+import json
+from typing import Literal
+
+# --- 1. LLM Configuration (OpenAI Only) ---
+api_file = "/home/mshahidul/api_new.json"
+with open(api_file, "r") as f:
+    api_keys = json.load(f)
+
+# Configure OpenAI for Inference
+# Note: Use 'gpt-4o' or 'gpt-4-turbo' as 'gpt-5' is not a standard identifier yet.
+openai_model = dspy.LM(model='gpt-5-mini', api_key=api_keys["openai"])
+dspy.configure(lm=openai_model)
+
+# --- 2. Program Architecture (Must match your training structure) ---
+
+class HealthLiteracySignature(dspy.Signature):
+    """
+    Judge the health literacy level of a generated medical summary.
+    Identify if the language is suitable for a layperson (low) or requires medical expertise (proficient).
+    """
+    summary_text: str = dspy.InputField(desc="The generated medical summary to be analyzed.")
+    reasoning: str = dspy.OutputField(desc="Analysis of jargon, acronyms, and sentence complexity.")
+    label: Literal["low_health_literacy", "intermediate_health_literacy", "proficient_health_literacy"] = dspy.OutputField()
+
+class HealthLiteracyClassifier(dspy.Module):
+    def __init__(self):
+        super().__init__()
+        self.predictor = dspy.ChainOfThought(HealthLiteracySignature)
+
+    def forward(self, summary_text):
+        return self.predictor(summary_text=summary_text)
+
+# --- 3. Load Trained Logic ---
+classifier = HealthLiteracyClassifier()
+save_path = "/home/mshahidul/readctrl/data/new_exp/optimized_health_classifier_gpt5-mini_v2.json"
+classifier.load(save_path)
+
+
+
+accuracy_count = 0
+path="/home/mshahidul/readctrl/data/new_exp/test_health_literacy_data_manual_edit.json"
+with open(path,'r') as f:
+    test_data = json.load(f)
+for item in test_data:
+    expected_label = item['label']
+    text = item['gen_text']
+    result = classifier(summary_text=text)
+    if (result.label == expected_label):
+        accuracy_count += 1
+        print(f"Correctly classified: {expected_label} ✅")
+    else:
+        print(f"Misclassified. Expected: {expected_label}, Got: {result.label} ❌")
+
+accuracy_score = (accuracy_count / len(test_data)) * 100
+print(f"\nFinal Accuracy: {accuracy_score:.2f}%")
\ No newline at end of file
diff --git a/code/classifier/few_shot_testing.py b/code/classifier/few_shot_testing.py
new file mode 100644
index 0000000000000000000000000000000000000000..5f954850ffd75d763719f4f2c9f197701e9b5bcc
--- /dev/null
+++ b/code/classifier/few_shot_testing.py
@@ -0,0 +1,111 @@
+import json
+import requests
+import os
+
+# --- Configuration ---
+DEV_SET_PATH = "/home/mshahidul/readctrl/data/new_exp/test_health_literacy_data.json"
+FEW_SHOT_SET_PATH = "/home/mshahidul/readctrl/data/new_exp/final_prompt_template_info.json" # Using the one with reasoning
+LOCAL_API_URL = "http://172.16.34.29:8004/v1/chat/completions"
+LOCAL_MODEL_NAME = "Qwen/Qwen3-30B-A3B-Instruct-2507"
+
+# Define the range of few-shots per label you want to test
+# e.g., [0, 1, 2, 3] will test 0-shot, 1-shot (3 total), 2-shot (6 total), etc.
+SHOTS_TO_EVALUATE = [0, 1, 2, 3,4,5,6]
+
+# --- Core Functions ---
+
+def build_dynamic_prompt(few_shot_data, k_per_label):
+    """Constructs a prompt with k examples per literacy category."""
+    instruction = (
+        "You are an expert in health communication. Your task is to judge the health literacy level of the provided text.\n"
+        "Classify the text into: low_health_literacy, intermediate_health_literacy, or proficient_health_literacy.\n\n"
+    )
+    
+    if k_per_label == 0:
+        return instruction + "### Task:\nTarget Text: \"{input_text}\"\nReasoning:"
+
+    # Organize few-shot data by label
+    categorized = {}
+    for entry in few_shot_data:
+        label = entry['label']
+        categorized.setdefault(label, []).append(entry)
+
+    few_shot_blocks = "### Examples:\n"
+    labels = ["low_health_literacy", "intermediate_health_literacy", "proficient_health_literacy"]
+    
+    for label in labels:
+        examples = categorized.get(label, [])[:k_per_label]
+        for ex in examples:
+            few_shot_blocks += f"Target Text: \"{ex['gen_text']}\"\n"
+            few_shot_blocks += f"Reasoning: {ex['reasoning']}\n"
+            few_shot_blocks += f"Label: {label}\n"
+            few_shot_blocks += "-" * 30 + "\n"
+            
+    return instruction + few_shot_blocks + "\n### Task:\nTarget Text: \"{input_text}\"\nReasoning:"
+
+def get_prediction(prompt_template, input_text):
+    """Sends the formatted prompt to the local LLM."""
+    final_prompt = prompt_template.format(input_text=input_text)
+    payload = {
+        "model": LOCAL_MODEL_NAME,
+        "messages": [{"role": "user", "content": final_prompt}],
+        "temperature": 0 
+    }
+    try:
+        response = requests.post(LOCAL_API_URL, json=payload, timeout=30)
+        return response.json()['choices'][0]['message']['content'].strip()
+    except Exception:
+        return "Error"
+
+def parse_label(text):
+    """Normalizes LLM output to match dataset labels."""
+    text = text.lower()
+    if "low" in text: return "low_health_literacy"
+    if "intermediate" in text: return "intermediate_health_literacy"
+    if "proficient" in text: return "proficient_health_literacy"
+    return "unknown"
+
+# --- Main Execution ---
+
+# 1. Load Data
+with open(DEV_SET_PATH, 'r') as f:
+    dev_set = json.load(f)
+with open(FEW_SHOT_SET_PATH, 'r') as f:
+    few_shot_pool = json.load(f)
+
+# 2. Filter Dev Set
+# Ensure no overlap between few-shot examples and dev set
+shot_ids = {item['doc_id'] for item in few_shot_pool}
+clean_dev_set = [item for item in dev_set if item['doc_id'] not in shot_ids]
+
+results_summary = []
+
+print(f"Starting Evaluation on {len(clean_dev_set)} samples...\n")
+
+# 3. Loop through shot counts
+for k in SHOTS_TO_EVALUATE:
+    print(f"Evaluating {k}-shot per label (Total {k*3} examples)...")
+    
+    current_template = build_dynamic_prompt(few_shot_pool, k)
+    correct = 0
+    
+    for case in clean_dev_set:
+        raw_output = get_prediction(current_template, case['gen_text'])
+        pred = parse_label(raw_output)
+        actual = parse_label(case['label'])
+        
+        if pred == actual:
+            correct += 1
+            
+    accuracy = (correct / len(clean_dev_set)) * 100
+    results_summary.append({"shots_per_label": k, "accuracy": accuracy})
+    print(f"-> Accuracy: {accuracy:.2f}%\n")
+
+# --- Final Report ---
+print("-" * 30)
+print(f"{'Shots/Label':<15} | {'Accuracy':<10}")
+print("-" * 30)
+for res in results_summary:
+    print(f"{res['shots_per_label']:<15} | {res['accuracy']:.2f}%")
+with open("/home/mshahidul/readctrl/data/new_exp/few_shot_evaluation_summary.json", 'w') as f:
+    json.dump(results_summary, f, indent=4)
\ No newline at end of file
diff --git a/code/classifier/few_shot_testing_3shots_all_comb.py b/code/classifier/few_shot_testing_3shots_all_comb.py
new file mode 100644
index 0000000000000000000000000000000000000000..4b9a35f4fc117f87dc280170d951740e949b6dd9
--- /dev/null
+++ b/code/classifier/few_shot_testing_3shots_all_comb.py
@@ -0,0 +1,116 @@
+import json
+import requests
+import os
+import numpy as np
+from itertools import combinations, product
+
+# --- Configuration ---
+DEV_SET_PATH = "/home/mshahidul/readctrl/data/new_exp/test_health_literacy_data.json"
+FEW_SHOT_POOL_PATH = "/home/mshahidul/readctrl/data/new_exp/final_prompt_template_info.json"
+LOCAL_API_URL = "http://172.16.34.29:8004/v1/chat/completions"
+LOCAL_MODEL_NAME = "Qwen/Qwen3-30B-A3B-Instruct-2507"
+
+# K-shot per label
+K = 3 
+
+# --- Logic ---
+
+def build_fixed_prompt(selected_instances):
+    """Builds a prompt from a specific provided list of instances."""
+    instruction = (
+        "You are an expert in health communication. Your task is to judge the health literacy level of the provided text.\n"
+        "Classify the text into: low_health_literacy, intermediate_health_literacy, or proficient_health_literacy.\n\n"
+        "### Examples:\n"
+    )
+    
+    few_shot_blocks = ""
+    for ex in selected_instances:
+        few_shot_blocks += f"Target Text: \"{ex['gen_text']}\"\n"
+        few_shot_blocks += f"Reasoning: {ex['reasoning']}\n"
+        few_shot_blocks += f"Label: {ex['label']}\n"
+        few_shot_blocks += "-" * 30 + "\n"
+            
+    return instruction + few_shot_blocks + "\n### Task:\nTarget Text: \"{input_text}\"\nReasoning:"
+
+def get_prediction(prompt_template, input_text):
+    final_prompt = prompt_template.format(input_text=input_text)
+    payload = {"model": LOCAL_MODEL_NAME, "messages": [{"role": "user", "content": final_prompt}], "temperature": 0}
+    try:
+        response = requests.post(LOCAL_API_URL, json=payload, timeout=20)
+        return response.json()['choices'][0]['message']['content'].strip()
+    except: return "Error"
+
+def parse_label(text):
+    text = text.lower()
+    if "low" in text: return "low_health_literacy"
+    if "intermediate" in text: return "intermediate_health_literacy"
+    if "proficient" in text: return "proficient_health_literacy"
+    return "unknown"
+
+# --- Execution ---
+
+with open(DEV_SET_PATH, 'r') as f:
+    dev_set = json.load(f)
+with open(FEW_SHOT_POOL_PATH, 'r') as f:
+    few_shot_pool = json.load(f)
+
+# Group pool by labels
+categorized = {}
+for entry in few_shot_pool:
+    categorized.setdefault(entry['label'], []).append(entry)
+
+# 1. Generate all combinations of K items for EACH label
+label_combos = []
+target_labels = ["low_health_literacy", "intermediate_health_literacy", "proficient_health_literacy"]
+
+for label in target_labels:
+    pool = categorized.get(label, [])
+    # Get all ways to pick K instances from this label's pool
+    label_combos.append(list(combinations(pool, K)))
+
+# 2. Get the Cartesian Product (Every combination of the combinations)
+all_possible_prompts_configs = list(product(*label_combos))
+
+print(f"Total unique prompt configurations to test: {len(all_possible_prompts_configs)}")
+
+results_log = []
+
+# 3. Iterate through every possible prompt configuration
+for idx, config in enumerate(all_possible_prompts_configs):
+    # Flatten the config (it's a tuple of tuples)
+    flat_instances = [item for sublist in config for item in sublist]
+    
+    current_template = build_fixed_prompt(flat_instances)
+    correct = 0
+    
+    # Run against Dev Set
+    for case in dev_set:
+        pred = parse_label(get_prediction(current_template, case['gen_text']))
+        if pred == parse_label(case['label']):
+            correct += 1
+            
+    accuracy = (correct / len(dev_set)) * 100
+    
+    # Store data
+    config_metadata = [{"doc_id": inst['doc_id'], "label": inst['label']} for inst in flat_instances]
+    results_log.append({
+        "config_index": idx,
+        "accuracy": accuracy,
+        "instances": config_metadata
+    })
+    
+    print(f"Config {idx+1}/{len(all_possible_prompts_configs)}: Accuracy = {accuracy:.2f}%")
+
+# --- Save & Find Best ---
+results_log.sort(key=lambda x: x['accuracy'], reverse=True)
+
+output_path = "/home/mshahidul/readctrl/data/new_exp/exhaustive_3shot_results.json"
+with open(output_path, 'w') as f:
+    json.dump(results_log, f, indent=4)
+
+best = results_log[0]
+print("\n" + "="*50)
+print(f"WINNING CONFIGURATION (Acc: {best['accuracy']:.2f}%)")
+for inst in best['instances']:
+    print(f"- {inst['label']}: {inst['doc_id']}")
+print("="*50)
\ No newline at end of file
diff --git a/code/classifier/few_shot_testing_v2.py b/code/classifier/few_shot_testing_v2.py
new file mode 100644
index 0000000000000000000000000000000000000000..1fe866df199caecfb106be6f65489432a519e1a5
--- /dev/null
+++ b/code/classifier/few_shot_testing_v2.py
@@ -0,0 +1,116 @@
+import json
+import requests
+import random
+import os
+import csv
+import numpy as np
+
+# --- Configuration ---
+DEV_SET_PATH = "/home/mshahidul/readctrl/data/new_exp/test_health_literacy_data.json"
+FEW_SHOT_POOL_PATH = "/home/mshahidul/readctrl/data/new_exp/final_prompt_template_info.json"
+LOCAL_API_URL = "http://172.16.34.29:8004/v1/chat/completions"
+LOCAL_MODEL_NAME = "Qwen/Qwen3-30B-A3B-Instruct-2507"
+
+# EXPERIMENT SETTINGS
+SHOTS_TO_EVALUATE = [1, 2, 3,4,5,6] 
+NUM_TRIALS = 3  # How many times to run each shot-count with different random samples
+
+# --- Logic ---
+
+def build_random_prompt(few_shot_data, k_per_label):
+    """Randomly samples k examples per label and builds a prompt."""
+    instruction = (
+        "You are an expert in health communication. Your task is to judge the health literacy level of the provided text.\n"
+        "Classify the text into: low_health_literacy, intermediate_health_literacy, or proficient_health_literacy.\n\n"
+    )
+    
+    # Organize pool by label
+    categorized = {}
+    for entry in few_shot_data:
+        label = entry['label']
+        categorized.setdefault(label, []).append(entry)
+
+    few_shot_blocks = "### Examples:\n"
+    labels = ["low_health_literacy", "intermediate_health_literacy", "proficient_health_literacy"]
+    
+    for label in labels:
+        # RANDOM SAMPLING: Shuffle and take k
+        pool = categorized.get(label, [])
+        selected = random.sample(pool, min(k_per_label, len(pool)))
+        
+        for ex in selected:
+            few_shot_blocks += f"Target Text: \"{ex['gen_text']}\"\n"
+            few_shot_blocks += f"Reasoning: {ex['reasoning']}\n"
+            few_shot_blocks += f"Label: {label}\n"
+            few_shot_blocks += "-" * 30 + "\n"
+            
+    return instruction + few_shot_blocks + "\n### Task:\nTarget Text: \"{input_text}\"\nReasoning:"
+
+def get_prediction(prompt_template, input_text):
+    final_prompt = prompt_template.format(input_text=input_text)
+    payload = {"model": LOCAL_MODEL_NAME, "messages": [{"role": "user", "content": final_prompt}], "temperature": 0}
+    try:
+        response = requests.post(LOCAL_API_URL, json=payload, timeout=30)
+        return response.json()['choices'][0]['message']['content'].strip()
+    except: return "Error"
+
+def parse_label(text):
+    text = text.lower()
+    if "low" in text: return "low_health_literacy"
+    if "intermediate" in text: return "intermediate_health_literacy"
+    if "proficient" in text: return "proficient_health_literacy"
+    return "unknown"
+
+# --- Execution ---
+
+with open(DEV_SET_PATH, 'r') as f:
+    dev_set = json.load(f)
+with open(FEW_SHOT_POOL_PATH, 'r') as f:
+    few_shot_pool = json.load(f)
+
+# Ensure no data leakage (remove few-shot examples from dev set)
+shot_ids = {item['doc_id'] for item in few_shot_pool}
+clean_dev_set = [item for item in dev_set if item['doc_id'] not in shot_ids]
+
+final_summary = []
+
+for k in SHOTS_TO_EVALUATE:
+    trial_accuracies = []
+    print(f"\n>>> Starting evaluation for {k}-shot ({NUM_TRIALS} trials)")
+    
+    for t in range(NUM_TRIALS):
+        # Create a prompt with a NEW random sample for this trial
+        current_template = build_random_prompt(few_shot_pool, k)
+        correct = 0
+        
+        for case in clean_dev_set:
+            pred = parse_label(get_prediction(current_template, case['gen_text']))
+            if pred == parse_label(case['label']):
+                correct += 1
+        
+        acc = (correct / len(clean_dev_set)) * 100
+        trial_accuracies.append(acc)
+        print(f"   Trial {t+1}/{NUM_TRIALS}: Accuracy = {acc:.2f}%")
+
+    # Calculate statistics for the shot count
+    avg_acc = np.mean(trial_accuracies)
+    std_dev = np.std(trial_accuracies)
+    
+    final_summary.append({
+        "shots_per_label": k,
+        "average_accuracy": round(avg_acc, 2),
+        "std_dev": round(std_dev, 2),
+        "trial_results": trial_accuracies
+    })
+
+# --- Save Results ---
+output_json = "/home/mshahidul/readctrl/data/new_exp/random_trial_results.json"
+with open(output_json, 'w') as f:
+    json.dump(final_summary, f, indent=4)
+
+print("\n" + "="*40)
+print(f"{'Shots':<10} | {'Avg Accuracy':<15} | {'Std Dev':<10}")
+print("-" * 40)
+for res in final_summary:
+    print(f"{res['shots_per_label']:<10} | {res['average_accuracy']:<15}% | {res['std_dev']:<10}")
+print("="*40)
\ No newline at end of file
diff --git a/code/classifier/few_shot_testing_v3.py b/code/classifier/few_shot_testing_v3.py
new file mode 100644
index 0000000000000000000000000000000000000000..54b35c75b36b158399b075d864a2005e5af47aad
--- /dev/null
+++ b/code/classifier/few_shot_testing_v3.py
@@ -0,0 +1,128 @@
+import json
+import requests
+import random
+import os
+import numpy as np
+
+# --- Configuration ---
+DEV_SET_PATH = "/home/mshahidul/readctrl/data/new_exp/test_health_literacy_data.json"
+FEW_SHOT_POOL_PATH = "/home/mshahidul/readctrl/data/new_exp/final_prompt_template_info.json"
+LOCAL_API_URL = "http://172.16.34.29:8004/v1/chat/completions"
+LOCAL_MODEL_NAME = "Qwen/Qwen3-30B-A3B-Instruct-2507"
+
+# EXPERIMENT SETTINGS
+SHOTS_TO_EVALUATE = [3] 
+NUM_TRIALS = 10
+
+# --- Logic ---
+
+def build_random_prompt_with_tracking(few_shot_data, k_per_label):
+    """Samples k examples, builds prompt, and returns detailed usage info."""
+    instruction = (
+        "You are an expert in health communication. Your task is to judge the health literacy level of the provided text.\n"
+        "Classify the text into: low_health_literacy, intermediate_health_literacy, or proficient_health_literacy.\n\n"
+    )
+    
+    categorized = {}
+    for entry in few_shot_data:
+        label = entry['label']
+        categorized.setdefault(label, []).append(entry)
+
+    few_shot_blocks = "### Examples:\n"
+    labels = ["low_health_literacy", "intermediate_health_literacy", "proficient_health_literacy"]
+    
+    used_instances = [] # Now tracking both ID and Label
+    for label in labels:
+        pool = categorized.get(label, [])
+        selected = random.sample(pool, min(k_per_label, len(pool)))
+        
+        for ex in selected:
+            # Store ID and Label pair
+            used_instances.append({
+                "doc_id": ex['doc_id'],
+                "label": ex['label']
+            })
+            
+            few_shot_blocks += f"Target Text: \"{ex['gen_text']}\"\n"
+            few_shot_blocks += f"Reasoning: {ex['reasoning']}\n"
+            few_shot_blocks += f"Label: {label}\n"
+            few_shot_blocks += "-" * 30 + "\n"
+            
+    prompt = instruction + few_shot_blocks + "\n### Task:\nTarget Text: \"{input_text}\"\nReasoning:"
+    return prompt, used_instances
+
+def get_prediction(prompt_template, input_text):
+    final_prompt = prompt_template.format(input_text=input_text)
+    payload = {"model": LOCAL_MODEL_NAME, "messages": [{"role": "user", "content": final_prompt}], "temperature": 0}
+    try:
+        response = requests.post(LOCAL_API_URL, json=payload, timeout=30)
+        return response.json()['choices'][0]['message']['content'].strip()
+    except: return "Error"
+
+def parse_label(text):
+    text = text.lower()
+    if "low" in text: return "low_health_literacy"
+    if "intermediate" in text: return "intermediate_health_literacy"
+    if "proficient" in text: return "proficient_health_literacy"
+    return "unknown"
+
+# --- Execution ---
+
+with open(DEV_SET_PATH, 'r') as f:
+    dev_set = json.load(f)
+with open(FEW_SHOT_POOL_PATH, 'r') as f:
+    few_shot_pool = json.load(f)
+
+shot_ids_in_pool = {item['doc_id'] for item in few_shot_pool}
+clean_dev_set = [item for item in dev_set if item['doc_id'] not in shot_ids_in_pool]
+
+all_exp_data = []
+
+for k in SHOTS_TO_EVALUATE:
+    print(f"\n>>> Running {k}-shot experiment ({NUM_TRIALS} trials)...")
+    trial_data = []
+    
+    for t in range(NUM_TRIALS):
+        current_template, used_meta = build_random_prompt_with_tracking(few_shot_pool, k)
+        correct = 0
+        
+        for case in clean_dev_set:
+            pred = parse_label(get_prediction(current_template, case['gen_text']))
+            if pred == parse_label(case['label']):
+                correct += 1
+        
+        acc = (correct / len(clean_dev_set)) * 100
+        
+        trial_info = {
+            "trial_index": t + 1,
+            "accuracy": acc,
+            "used_instances": used_meta  # List of {"doc_id": ..., "label": ...}
+        }
+        trial_data.append(trial_info)
+        print(f"   Trial {t+1}: {acc:.2f}% accuracy")
+
+    # Aggregating shots data
+    accuracies = [td['accuracy'] for td in trial_data]
+    best_trial = max(trial_data, key=lambda x: x['accuracy'])
+    
+    all_exp_data.append({
+        "shots_per_label": k,
+        "avg_accuracy": round(np.mean(accuracies), 2),
+        "std_dev": round(np.std(accuracies), 2),
+        "best_accuracy": best_trial['accuracy'],
+        "best_instances": best_trial['used_instances'],
+        "all_trials": trial_data
+    })
+
+# --- Save Detailed Results ---
+output_json = "/home/mshahidul/readctrl/data/new_exp/shot_experiment_detailed_tracking.json"
+with open(output_json, 'w') as f:
+    json.dump(all_exp_data, f, indent=4)
+
+print("\n" + "="*80)
+print(f"{'Shots':<6} | {'Avg Acc':<10} | {'Best Acc':<10} | {'Best Sample Configuration (ID: Label)'}")
+print("-" * 80)
+for res in all_exp_data:
+    config_str = ", ".join([f"{inst['doc_id']}: {inst['label']}" for inst in res['best_instances']])
+    print(f"{res['shots_per_label']:<6} | {res['avg_accuracy']:<8}% | {res['best_accuracy']:<8}% | {config_str}")
+print("="*80)
\ No newline at end of file
diff --git a/code/classifier/prompt_eng.ipynb b/code/classifier/prompt_eng.ipynb
new file mode 100644
index 0000000000000000000000000000000000000000..36ff55e6f529c1ef64248ac596f8f9765f40aad3
--- /dev/null
+++ b/code/classifier/prompt_eng.ipynb
@@ -0,0 +1,136 @@
+{
+ "cells": [
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "f068d454",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import dspy\n",
+    "import json\n",
+    "from typing import Literal\n",
+    "from dspy.teleprompt import BootstrapFewShotWithRandomSearch\n",
+    "from dspy.evaluate import Evaluate\n",
+    "\n",
+    "# --- 1. LLM Configuration ---\n",
+    "api_file = \"/home/mshahidul/api_new.json\"\n",
+    "with open(api_file, \"r\") as f:\n",
+    "    api_keys = json.load(f)\n",
+    "openai_api_key = api_keys[\"openai\"]\n",
+    "\n",
+    "# Student: Local vLLM (Deployment Model)\n",
+    "vllm_model = dspy.LM(\n",
+    "    model='openai/Qwen/Qwen3-30B-A3B-Instruct-2507',\n",
+    "    api_base=\"http://172.16.34.29:8004/v1\",\n",
+    "    api_key=\"EMPTY\",\n",
+    "    temperature=0.0\n",
+    ")\n",
+    "\n",
+    "# Teacher: OpenAI (High-quality rationale generation)\n",
+    "openai_model = dspy.LM(model='gpt-5', api_key=openai_api_key, temperature=0.0)\n",
+    "\n",
+    "dspy.configure(lm=openai_model)  # Default to OpenAI for optimization\n",
+    "\n",
+    "# --- 2. Data Processing & Deduplication ---\n",
+    "\n",
+    "# 2.1 Load Training Data (Few-Shot)\n",
+    "with open(\"/home/mshahidul/readctrl/data/new_exp/few_shot_examples.json\", 'r') as f:\n",
+    "    few_shot_data = json.load(f)\n",
+    "\n",
+    "trainset = []\n",
+    "train_identifiers = set()\n",
+    "\n",
+    "for label_key, examples in few_shot_data.items():\n",
+    "    for ex in examples:\n",
+    "        # Create a unique ID to prevent data leakage\n",
+    "        unique_id = f\"{ex['doc_id']}_{label_key}\"\n",
+    "        train_identifiers.add(unique_id)\n",
+    "        \n",
+    "        # In few_shot, 'text' is the summary we want to judge\n",
+    "        trainset.append(dspy.Example(\n",
+    "            summary_text=ex['gen_text'], \n",
+    "            label=label_key\n",
+    "        ).with_inputs('summary_text'))\n",
+    "\n",
+    "# 2.2 Load Dev Data (Filtered)\n",
+    "with open(\"/home/mshahidul/readctrl/data/new_exp/cleaned_health_literacy_data.json\", 'r') as f:\n",
+    "    main_data = json.load(f)\n",
+    "\n",
+    "devset = []\n",
+    "for item in main_data:\n",
+    "    unique_id = f\"{item['doc_id']}_{item['label']}\"\n",
+    "    \n",
+    "    # Only add to devset if it wasn't used in training\n",
+    "    if unique_id not in train_identifiers:\n",
+    "        # Based on your update: 'gen_text' or 'text' is the generated summary\n",
+    "        # We use 'gen_text' here as the summary to be judged\n",
+    "        devset.append(dspy.Example(\n",
+    "            summary_text=item['gen_text'], \n",
+    "            label=item['label']\n",
+    "        ).with_inputs('summary_text'))\n",
+    "\n",
+    "# Cap devset for efficiency during optimization\n",
+    "devset = devset\n",
+    "\n",
+    "print(f\"Dataset Stats: Train={len(trainset)}, Dev={len(devset)}\")\n",
+    "\n",
+    "# --- 3. Robust Signature & Module ---\n",
+    "\n",
+    "class HealthLiteracySignature(dspy.Signature):\n",
+    "    \"\"\"\n",
+    "    Judge the health literacy level of a generated medical summary.\n",
+    "    Identify if the language is suitable for a layperson (low) or requires medical expertise (proficient).\n",
+    "    \"\"\"\n",
+    "    summary_text: str = dspy.InputField(desc=\"The generated medical summary to be analyzed.\")\n",
+    "    reasoning: str = dspy.OutputField(desc=\"Analysis of jargon, acronyms, and sentence complexity.\")\n",
+    "    label: Literal[\"low_health_literacy\", \"intermediate_health_literacy\", \"proficient_health_literacy\"] = dspy.OutputField()\n",
+    "\n",
+    "class HealthLiteracyClassifier(dspy.Module):\n",
+    "    def __init__(self):\n",
+    "        super().__init__()\n",
+    "        # ChainOfThought generates the reasoning field before the label\n",
+    "        self.predictor = dspy.ChainOfThought(HealthLiteracySignature)\n",
+    "\n",
+    "    def forward(self, summary_text):\n",
+    "        return self.predictor(summary_text=summary_text)\n",
+    "\n",
+    "# --- 4. Metric and Optimization ---\n",
+    "\n",
+    "def health_literacy_metric(gold, pred, trace=None):\n",
+    "    if not pred.label: return False\n",
+    "    return gold.label.strip().lower() == pred.label.strip().lower()\n",
+    "\n",
+    "# BootstrapFewShotWithRandomSearch explores different demonstration combinations\n",
+    "optimizer = BootstrapFewShotWithRandomSearch(\n",
+    "    metric=health_literacy_metric,\n",
+    "    max_bootstrapped_demos=3,\n",
+    "    num_candidate_programs=8, \n",
+    "    teacher_settings=dict(lm=openai_model)\n",
+    ")\n",
+    "\n",
+    "# Compile using the local model, but with OpenAI generating the logic\n",
+    "optimized_program = optimizer.compile(HealthLiteracyClassifier(), trainset=trainset)\n",
+    "\n",
+    "# --- 5. Evaluation & Saving ---\n",
+    "\n",
+    "evaluator = Evaluate(devset=devset, metric=health_literacy_metric, num_threads=1, display_progress=True)\n",
+    "accuracy = evaluator(optimized_program)\n",
+    "\n",
+    "print(f\"\\nOptimization Complete.\")\n",
+    "print(f\"Final Accuracy on Unseen Dev Set: {accuracy.score}%\")\n",
+    "# print(f\"Final Accuracy on Unseen Dev Set: {accuracy * 100:.2f}%\")\n",
+    "\n",
+    "# Save the finalized prompt logic\n",
+    "optimized_program.save(\"/home/mshahidul/readctrl/data/new_exp/optimized_health_classifier.json\")"
+   ]
+  }
+ ],
+ "metadata": {
+  "language_info": {
+   "name": "python"
+  }
+ },
+ "nbformat": 4,
+ "nbformat_minor": 5
+}
diff --git a/code/data_creation/dataset_creation_extract_subclaims_gpt5.py b/code/data_creation/dataset_creation_extract_subclaims_gpt5.py
new file mode 100644
index 0000000000000000000000000000000000000000..2f97b57a50864dbf4bda167a0ada4fed2ef3d71d
--- /dev/null
+++ b/code/data_creation/dataset_creation_extract_subclaims_gpt5.py
@@ -0,0 +1,50 @@
+from openai import OpenAI
+import json, os
+
+with open("/home/mshahidul/LLM_guard/prompts/synthetic_data_generation_extract_subclaims.txt", "r") as f:
+    prompt_template = f.read()
+
+
+api_file = "/home/mshahidul/api_new.json"
+with open(api_file, "r") as f:
+    api_keys = json.load(f)
+openai_api_key = api_keys["openai"]
+
+client = OpenAI(api_key=openai_api_key)
+
+
+def openai_return(prompt, model="gpt-5"):
+    """Send a prompt to GPT and parse JSON."""
+    response = client.chat.completions.create(
+        model=model,
+        messages=[
+            {"role": "system", "content": "You are a helpful assistant."},
+            {"role": "user", "content": prompt}
+        ]
+    )
+    content = response.choices[0].message.content.strip()
+    cleaned = content.replace("```json", "").replace("```", "").strip()
+    try:
+        return json.loads(cleaned)
+    except json.JSONDecodeError:
+        print("⚠️ JSON parse failed — storing raw text.")
+        return cleaned
+
+save_path="/home/mshahidul/readctrl/data/finetuning_data/finetune_dataset_extract-subclaim.json"
+res=[]
+if os.path.exists(save_path):
+    with open(save_path, "r") as f:
+        res = json.load(f)
+import tqdm
+for i in tqdm.tqdm(range(100)):
+    sample = openai_return(prompt_template, model="gpt-5")
+
+    res.append(sample)
+
+    if len(res) % 2 == 0:
+        with open(save_path, "w") as f:
+            json.dump(res, f, indent=2, ensure_ascii=False)
+        print(f"Saved {len(res)} samples so far.")
+
+with open(save_path, "w") as f:
+    json.dump(res, f, indent=2, ensure_ascii=False)
\ No newline at end of file
diff --git a/code/data_creation/dataset_creation_for_attribution_training.py b/code/data_creation/dataset_creation_for_attribution_training.py
new file mode 100644
index 0000000000000000000000000000000000000000..97b8504457f67ad9e9a737a12d24d11f2af793e3
--- /dev/null
+++ b/code/data_creation/dataset_creation_for_attribution_training.py
@@ -0,0 +1,168 @@
+import os
+import json
+import tqdm
+from openai import OpenAI
+
+# =====================================================
+# 1️⃣  Setup: Load API key, initialize client
+# =====================================================
+
+api_file = "/home/mshahidul/api_new.json"
+with open(api_file, "r") as f:
+    api_keys = json.load(f)
+openai_api_key = api_keys["openai"]
+
+client = OpenAI(api_key=openai_api_key)
+
+
+# =====================================================
+# 2️⃣  OpenAI call helper
+# =====================================================
+
+def openai_return(prompt, model="gpt-5"):
+    """Send a prompt to GPT and parse JSON."""
+    response = client.chat.completions.create(
+        model=model,
+        messages=[
+            {"role": "system", "content": "You are a helpful assistant."},
+            {"role": "user", "content": prompt}
+        ]
+    )
+    content = response.choices[0].message.content.strip()
+    cleaned = content.replace("```json", "").replace("```", "").strip()
+    try:
+        return json.loads(cleaned)
+    except json.JSONDecodeError:
+        print("⚠️ JSON parse failed — storing raw text.")
+        return cleaned
+
+
+# =====================================================
+# 3️⃣  Multi‑subclaim attribution prompt builder
+# =====================================================
+
+def return_prompts_attribution_multi(reference_full_text, generated_summary, subclaims_json, difficulty_level):
+    return f"""
+### **SYSTEM / ROLE INSTRUCTION**
+
+You are a **medical factuality and attribution evaluator**.
+You will analyze all subclaims found in a generated summary, each labeled with a `"result"` flag:
+- `1` = supported by the reference
+- `0` = unsupported by the reference
+
+Your main task is to **evaluate only the unsupported subclaims (`"result": 0"`)**, judging whether each is a *reasonable addition* given the specified readability level (*easy / intermediate / hard*).
+
+The presence of supported items (`"result": 1"`) helps you understand the full context of what is confirmed versus speculative,
+but you will not rate those. Their inclusion enriches the training data diversity and realism.
+
+---
+
+### **READABILITY & ATTRIBUTION GUIDELINES**
+
+| Level | Audience | Linguistic & Stylistic Profile | Allowable Additions |
+| :-- | :-- | :-- | :-- |
+| **Easy (FH 70–100)** | General public | Short, simple, concrete sentences | General explanations only; no new factual claims |
+| **Intermediate (FH 50–69)** | Educated layperson | Moderate complexity and precision | Clarifying causal links aligned with the text |
+| **Hard (FH 0–49)** | Professionals | Formal, technical, multi‑clause detail | Must strictly reflect source evidence |
+
+---
+
+### **Input**
+Readability Level: {difficulty_level}
+
+Reference Full Text:
+{reference_full_text}
+
+Generated Summary:
+{generated_summary}
+
+All Subclaims with Support Results:
+{subclaims_json}
+
+---
+
+### **TASK INSTRUCTIONS**
+
+For **each subclaim where** `"result": 0"`, classify it as:
+
+- `"reasonable"` – legitimate simplification aligned with readability needs  
+- `"partially_reasonable"` – harmless addition or neutral paraphrase  
+- `"unreasonable"` – misleading, speculative, or factually unsupported  
+
+Support your judgment with a 1–2 sentence justification per item.
+
+Do **not** modify or comment on subclaims where `"result": 1"`.
+
+---
+
+### **Output JSON Format**
+
+```json
+{{
+  "evaluations": [
+    {{
+      "subclaim_id": <id>,
+      "subclaim": "<verbatim_subclaim>",
+      "result": <0 or 1>,
+      "reasonableness": "<reasonable | partially_reasonable | unreasonable | not_applicable>",
+      "justification": "<short justification for result=0; for result=1, just write 'supported, no evaluation required'>"
+    }},
+    ...
+  ]
+}}
+"""
+file_synth = "/home/mshahidul/readctrl/data/training_data_subclaim_verifier/synthetic_data_es_subclaims_100.json"
+file_qwen_results = "/home/mshahidul/readctrl/results/dataset_quality_check/subclaim_verifier_results_100_qwen3-32B.json"
+save_path = "/home/mshahidul/readctrl/results/dataset_quality_check/syn_attribution_resonability_check_100_gpt5_train_v2.json"
+
+with open(file_synth, 'r') as f:
+    synthetic_data = json.load(f)
+with open(file_qwen_results, 'r') as f:
+    qwen3_32B_results = json.load(f) 
+res = []
+if os.path.exists(save_path):
+    with open(save_path, 'r') as f:
+        res = json.load(f)
+print(f"🔁 Resuming from {len(res)} entries")
+
+existing = set((e["id"], e["difficulty_level"]) for e in res)
+
+for ind in tqdm.tqdm(range(0, 30)):
+    entry = synthetic_data[ind]
+    subclaims_results = qwen3_32B_results[ind]['attribution']['results']
+    subclaims_json = json.dumps(subclaims_results, indent=2, ensure_ascii=False)
+    for level in ["easy", "intermediate", "hard"]:
+        if (entry["id"], level) in existing:
+            print(f"⏭️ Skipping {entry['id']} ({level})")
+            continue
+
+        ref_full_text = entry["full_text"]
+        generated_summary = entry["readability_versions"][level]["text"]
+
+        prompt = return_prompts_attribution_multi(
+            ref_full_text,
+            generated_summary,
+            subclaims_json,
+            level
+        )
+        # print(prompt)
+        # assert False
+
+        try:
+            response = openai_return(prompt)
+            res.append({
+                "id": entry["id"],
+                "difficulty_level": level,
+                "response": response
+            })
+
+            # save periodically
+            if len(res) % 2 == 0:
+                with open(save_path, 'w') as f:
+                    json.dump(res, f, indent=2, ensure_ascii=False)
+                print(f"💾 Saved after {len(res)} entries")
+
+        except Exception as e:
+            print(f"❌ Error at index {ind}, level {level}: {e}")       
+
+
diff --git a/code/data_creation/dataset_creation_subclaim_support_gpt5.py b/code/data_creation/dataset_creation_subclaim_support_gpt5.py
new file mode 100644
index 0000000000000000000000000000000000000000..915063d98d06a030ae5bf4e5af9e5ecbf9d6d53d
--- /dev/null
+++ b/code/data_creation/dataset_creation_subclaim_support_gpt5.py
@@ -0,0 +1,51 @@
+from openai import OpenAI
+import json, os
+
+with open("/home/mshahidul/readctrl/prompts/syn_dataset_subclaims_support_check_v2.txt", "r") as f:
+    prompt_template = f.read()
+
+
+api_file = "/home/mshahidul/api_new.json"
+with open(api_file, "r") as f:
+    api_keys = json.load(f)
+openai_api_key = api_keys["openai"]
+
+client = OpenAI(api_key=openai_api_key)
+
+
+def openai_return(prompt, model="gpt-5"):
+    """Send a prompt to GPT and parse JSON."""
+    response = client.chat.completions.create(
+        model=model,
+        messages=[
+            {"role": "system", "content": "You are a helpful assistant."},
+            {"role": "user", "content": prompt}
+        ]
+    )
+    content = response.choices[0].message.content.strip()
+    cleaned = content.replace("```json", "").replace("```", "").strip()
+    try:
+        return json.loads(cleaned)
+    except json.JSONDecodeError:
+        print("⚠️ JSON parse failed — storing raw text.")
+        return cleaned
+
+save_path="/home/mshahidul/readctrl/data/finetuning_data/finetune_dataset_subclaim_support_v2.json"
+res=[]
+if os.path.exists(save_path):
+    with open(save_path, "r") as f:
+        res = json.load(f)
+import tqdm
+for i in tqdm.tqdm(range(100)):
+    sample = openai_return(prompt_template, model="gpt-5")
+
+    res.append(sample)
+
+    if len(res) % 2 == 0:
+        with open(save_path, "w") as f:
+            json.dump(res, f, indent=2, ensure_ascii=False)
+        print(f"Saved {len(res)} samples so far.")
+
+with open(save_path, "w") as f:
+    json.dump(res, f, indent=2, ensure_ascii=False)
+
diff --git a/code/data_creation/diff_label_text_creation.py b/code/data_creation/diff_label_text_creation.py
new file mode 100644
index 0000000000000000000000000000000000000000..316dd0e7a2eb08d95e035dbe8f18be8bc9fcfbd5
--- /dev/null
+++ b/code/data_creation/diff_label_text_creation.py
@@ -0,0 +1,71 @@
+from openai import OpenAI
+import json, os
+
+source_language = "English"
+if source_language == "English":
+    source_lang_code = "en"
+elif source_language == "Spanish":
+    source_lang_code = "es"
+elif source_language == "French":
+    source_lang_code = "fr"
+elif source_language == "Portuguese":
+    source_lang_code = "pt"
+else:
+    assert False, "Unsupported language"
+print(f"{source_language}")
+with open("/home/mshahidul/readctrl/prompts/syn_data_gen_diff_label.txt", "r") as f:
+    prompt_template = f.read()
+
+
+api_file = "/home/mshahidul/api_new.json"
+with open(api_file, "r") as f:
+    api_keys = json.load(f)
+openai_api_key = api_keys["openai"]
+
+client = OpenAI(api_key=openai_api_key)
+
+
+def openai_return(prompt, model="gpt-5"):
+    """Send a prompt to GPT and parse JSON."""
+    response = client.chat.completions.create(
+        model=model,
+        messages=[
+            {"role": "system", "content": "You are a helpful assistant."},
+            {"role": "user", "content": prompt}
+        ]
+    )
+    content = response.choices[0].message.content.strip()
+    cleaned = content.replace("```json", "").replace("```", "").strip()
+    try:
+        return json.loads(cleaned)
+    except json.JSONDecodeError:
+        print("⚠️ JSON parse failed — storing raw text.")
+        return cleaned
+
+save_path=f"/home/mshahidul/readctrl/data/synthetic_dataset_diff_labels/syn_data_diff_labels_{source_lang_code}_67_80.json"
+res=[]
+if os.path.exists(save_path):
+    with open(save_path, "r") as f:
+        res = json.load(f)
+import tqdm
+with open(f"/home/mshahidul/readctrl/data/testing_data_gs/multiclinsum_gs_train_{source_lang_code}.json", "r") as f:
+    data = json.load(f)
+for idx, item in tqdm.tqdm(enumerate(data[67:80])):
+    prompt=prompt_template.replace("<<<FULL_TEXT>>>", item["fulltext"]).replace("<<<SOURCE_LANGUAGE>>>", source_language).replace("<<<GOLD_SUMMARY>>>", item["summary"])
+    # import ipdb; ipdb.set_trace()
+    sample = openai_return(prompt, model="gpt-5")
+
+    res.append({
+        "index": idx + 67,
+        "fulltext": item["fulltext"],
+        "diff_label_texts": sample
+    })
+
+    if len(res) % 2 == 0:
+        with open(save_path, "w") as f:
+            json.dump(res, f, indent=2, ensure_ascii=False)
+        print(f"Saved {len(res)} samples so far.")
+
+with open(save_path, "w") as f:
+    json.dump(res, f, indent=2, ensure_ascii=False)
+
diff --git a/code/data_creation/diff_label_text_creation_bangla.py b/code/data_creation/diff_label_text_creation_bangla.py
new file mode 100644
index 0000000000000000000000000000000000000000..bfaf1ddcf92ad34cefe2e4b6e65cbd30cc48ddf7
--- /dev/null
+++ b/code/data_creation/diff_label_text_creation_bangla.py
@@ -0,0 +1,90 @@
+from openai import OpenAI
+import json, os
+
+source_language = "Bengali"
+if source_language == "English":
+    source_lang_code = "en"
+elif source_language == "Spanish":
+    source_lang_code = "es"
+elif source_language == "French":
+    source_lang_code = "fr"
+elif source_language == "Portuguese":
+    source_lang_code = "pt"
+elif source_language == "Bengali":
+    source_lang_code = "bn"
+else:
+    assert False, "Unsupported language"
+print(f"{source_language}")
+with open(
+    "/home/mshahidul/readctrl/prompts/syn_data_generation/syn_data_gen_diff_label_Bangla.txt",
+    "r",
+    encoding="utf-8",
+) as f:
+    prompt_template = f.read()
+
+
+api_file = "/home/mshahidul/api_new.json"
+with open(api_file, "r", encoding="utf-8") as f:
+    api_keys = json.load(f)
+openai_api_key = api_keys["openai"]
+
+client = OpenAI(api_key=openai_api_key)
+
+
+def openai_return(prompt, model="gpt-5"):
+    """Send a prompt to GPT and parse JSON."""
+    response = client.chat.completions.create(
+        model=model,
+        messages=[
+            {"role": "system", "content": "You are a helpful assistant."},
+            {"role": "user", "content": prompt}
+        ]
+    )
+    content = response.choices[0].message.content.strip()
+    cleaned = content.replace("```json", "").replace("```", "").strip()
+    try:
+        return json.loads(cleaned)
+    except json.JSONDecodeError:
+        print("⚠️ JSON parse failed — storing raw text.")
+        return cleaned
+
+input_path = "/home/mshahidul/readctrl/data/translated_data/translation_wo_judge/multiclinsum_gs_train_en2bn_gemma(0_200).json"
+save_path = f"/home/mshahidul/readctrl/data/synthetic_dataset_diff_labels/syn_data_diff_labels_{source_lang_code}_0_80.json"
+res=[]
+if os.path.exists(save_path):
+    with open(save_path, "r", encoding="utf-8") as f:
+        res = json.load(f)
+import tqdm
+with open(input_path, "r", encoding="utf-8") as f:
+    data = json.load(f)
+for idx, item in tqdm.tqdm(enumerate(data)):
+    fulltext_bn = item.get("translated_fulltext")
+    summary_bn = item.get("translated_summary")
+    if not fulltext_bn or not summary_bn:
+        print(f"Skipping idx={idx}, id={item.get('id')} due to missing translated fields.")
+        continue
+
+    prompt = (
+        prompt_template
+        .replace("<<<FULL_TEXT>>>", fulltext_bn)
+        .replace("<<<SOURCE_LANGUAGE>>>", source_language)
+        .replace("<<<GOLD_SUMMARY>>>", summary_bn)
+    )
+    # import ipdb; ipdb.set_trace()
+    sample = openai_return(prompt, model="gpt-5")
+
+    res.append({
+        "id": item["id"],
+        "index": idx ,
+        "fulltext": fulltext_bn,
+        "diff_label_texts": sample
+    })
+
+    if len(res) % 2 == 0:
+        with open(save_path, "w", encoding="utf-8") as f:
+            json.dump(res, f, indent=2, ensure_ascii=False)
+        print(f"Saved {len(res)} samples so far.")
+
+with open(save_path, "w", encoding="utf-8") as f:
+    json.dump(res, f, indent=2, ensure_ascii=False)
+
diff --git a/code/data_creation/generate_subclaim_synthetic_dataset.py b/code/data_creation/generate_subclaim_synthetic_dataset.py
new file mode 100644
index 0000000000000000000000000000000000000000..12611803ed4b31813ba100f4e98588080294d96a
--- /dev/null
+++ b/code/data_creation/generate_subclaim_synthetic_dataset.py
@@ -0,0 +1,141 @@
+import argparse
+import json
+from pathlib import Path
+from typing import Any, Dict, List
+
+from openai import OpenAI
+
+
+PROMPT_PATH = Path("/home/mshahidul/readctrl/prompts/support_check_data_generate")
+API_FILE = Path("/home/mshahidul/api_new.json")
+INPUT_PATH = Path(
+    "/home/mshahidul/readctrl/code/text_classifier/data/verified_combined_0-80_clean200.json"
+)
+OUTPUT_DIR = Path("/home/mshahidul/readctrl/data/extracting_subclaim")
+DEFAULT_OUTPUT_FILE = "synthetic_subclaims_first200.json"
+
+
+def load_openai_client() -> OpenAI:
+    with API_FILE.open("r", encoding="utf-8") as f:
+        api_keys = json.load(f)
+    openai_api_key = api_keys["openai"]
+    return OpenAI(api_key=openai_api_key)
+
+
+def normalize_difficulty(label: str) -> str:
+    mapping = {
+        "low_health_literacy": "easy",
+        "intermediate_health_literacy": "intermediate",
+        "proficient_health_literacy": "hard",
+    }
+    return mapping.get(label, "intermediate")
+
+
+def clean_json_response(raw: str) -> Dict[str, Any]:
+    cleaned = raw.strip().replace("```json", "").replace("```", "").strip()
+    return json.loads(cleaned)
+
+
+def make_prompt(template: str, item: Dict[str, Any]) -> str:
+    payload = {
+        "passage_id": f"{item.get('doc_id', 'unknown')}_{item.get('label', 'unknown')}",
+        "passage": item.get("diff_label_texts", ""),
+        "difficulty_label": normalize_difficulty(item.get("label", "")),
+    }
+    return (
+        f"{template}\n\n"
+        "Now generate output for this input:\n"
+        f"{json.dumps(payload, ensure_ascii=False, indent=2)}\n"
+    )
+
+
+def load_input_data(limit: int) -> List[Dict[str, Any]]:
+    with INPUT_PATH.open("r", encoding="utf-8") as f:
+        data = json.load(f)
+    return data[:limit]
+
+
+def load_existing(path: Path) -> List[Dict[str, Any]]:
+    if not path.exists():
+        return []
+    with path.open("r", encoding="utf-8") as f:
+        return json.load(f)
+
+
+def save_json(path: Path, data: List[Dict[str, Any]]) -> None:
+    with path.open("w", encoding="utf-8") as f:
+        json.dump(data, f, ensure_ascii=False, indent=2)
+
+
+def main() -> None:
+    parser = argparse.ArgumentParser(
+        description="Generate synthetic claim-verification subclaim dataset from diff_label_texts."
+    )
+    parser.add_argument("--limit", type=int, default=200, help="Number of input items to process.")
+    parser.add_argument("--model", type=str, default="gpt-5", help="OpenAI model name.")
+    parser.add_argument(
+        "--output-file",
+        type=str,
+        default=DEFAULT_OUTPUT_FILE,
+        help="Output filename inside output directory.",
+    )
+    parser.add_argument(
+        "--save-every",
+        type=int,
+        default=2,
+        help="Persist results after every N processed items.",
+    )
+    args = parser.parse_args()
+
+    with PROMPT_PATH.open("r", encoding="utf-8") as f:
+        prompt_template = f.read().strip()
+
+    OUTPUT_DIR.mkdir(parents=True, exist_ok=True)
+    output_path = OUTPUT_DIR / args.output_file
+
+    data = load_input_data(limit=args.limit)
+    results = load_existing(output_path)
+    done_keys = {item.get("source_key") for item in results}
+
+    client = load_openai_client()
+
+    for idx, item in enumerate(data):
+        source_key = f"{item.get('doc_id')}_{item.get('label')}_{idx}"
+        if source_key in done_keys:
+            continue
+
+        prompt = make_prompt(prompt_template, item)
+        try:
+            response = client.chat.completions.create(
+                model=args.model,
+                messages=[
+                    {"role": "system", "content": "You are a helpful assistant."},
+                    {"role": "user", "content": prompt},
+                ],
+            )
+            content = response.choices[0].message.content or ""
+            generated = clean_json_response(content)
+        except Exception as e:  # noqa: BLE001
+            generated = {"error": str(e), "raw_response": response.choices[0].message.content if "response" in locals() else ""}
+
+        results.append(
+            {
+                "source_key": source_key,
+                "doc_id": item.get("doc_id"),
+                "source_label": item.get("label"),
+                "difficulty_label": normalize_difficulty(item.get("label", "")),
+                "generated": generated,
+            }
+        )
+        done_keys.add(source_key)
+
+        if len(results) % args.save_every == 0:
+            save_json(output_path, results)
+            print(f"Saved {len(results)} rows to {output_path}")
+
+    save_json(output_path, results)
+    print(f"Done. Saved {len(results)} rows to {output_path}")
+
+
+if __name__ == "__main__":
+    main()
diff --git a/code/data_processing/data_formation.ipynb b/code/data_processing/data_formation.ipynb
new file mode 100644
index 0000000000000000000000000000000000000000..e3a1b9b2d9807453716c93005aa516e1b06485d6
--- /dev/null
+++ b/code/data_processing/data_formation.ipynb
@@ -0,0 +1,416 @@
+{
+ "cells": [
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "e1eea264",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "def training_prompt(medical_text, subclaims):\n",
+    "    system_prompt = f\"\"\"\n",
+    "You are an expert medical annotator. Your task is to extract granular, factual subclaims from medical text.\n",
+    "A subclaim is the smallest standalone factual unit that can be independently verified.\n",
+    "\n",
+    "Instructions:\n",
+    "1. Read the provided medical text.\n",
+    "2. Break it into clear, objective subclaims.\n",
+    "3. Each subclaim must be directly derived from the text.\n",
+    "4. Do not add, guess, infer, or combine multiple facts.\n",
+    "5. Each subclaim should be short, specific, and verifiable.\n",
+    "\n",
+    "Medical Text:\n",
+    "{medical_text}\n",
+    "\"\"\"\n",
+    "\n",
+    "    conversation = {}\n",
+    "    conversation['conversations'] = (\n",
+    "        {'from': \"user\", 'content': system_prompt},\n",
+    "        {'from': \"assistant\", 'content': str(subclaims)},\n",
+    "    )\n",
+    "    return conversation\n"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "72fbae33",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "# /home/mshahidul/readctrl/data/finetuning_data/finetune_dataset_extract-subclaim.json read\n",
+    "with open('/home/mshahidul/readctrl/data/finetuning_data/finetune_dataset_extract-subclaim.json', 'r') as f:\n",
+    "    import json\n",
+    "    data = json.load(f)\n",
+    "prompts = []\n",
+    "for item in data:\n",
+    "    medical_text = item['medical_text']\n",
+    "    subclaims = item['subclaims']\n",
+    "    prompt = training_prompt(medical_text, subclaims)\n",
+    "    prompts.append(prompt)\n",
+    "with open('/home/mshahidul/readctrl/data/finetuning_data/finetune_dataset_extract-subclaim_conversation.json', 'w') as f:\n",
+    "    json.dump(prompts, f, indent=2)"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "118e5fce",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "# python /home/mshahidul/readctrl/code/finetune-inference/completeness_reasoning_v3.py --data_path /home/mshahidul/readctrl/data/concise_complete_attr_cal_v3/evaluated_metrics_0_100.json \n",
+    "import os\n",
+    "for x in os.listdir('/home/mshahidul/readctrl/data/concise_complete_attr_cal_v3/'):\n",
+    "    if x.endswith('.json'):\n",
+    "        dat=f'python /home/mshahidul/readctrl/code/finetune-inference/completeness_reasoning_v3.py --data_path /home/mshahidul/readctrl/data/concise_complete_attr_cal_v3/{x}'\n",
+    "        print(dat) \n",
+    "        print('\\n')"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "cb108a11",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import zipfile\n",
+    "\n",
+    "# /home/mshahidul/readctrl/data/testing_data/multiclinsum_test_es.zip\n",
+    "with zipfile.ZipFile('/home/mshahidul/readctrl/data/testing_data/multiclinsum_test_es.zip', 'r') as zip_ref:\n",
+    "    zip_ref.extractall('/home/mshahidul/readctrl/data/testing_data/es_data/')\n"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "6ea249db",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "def training_prompt(text, subclaim, label):\n",
+    "    system_prompt = f\"\"\"\n",
+    "You are a medical evidence evaluator.\n",
+    "\n",
+    "Your task is to determine the relationship between a medical text and a subclaim.\n",
+    "\n",
+    "Definitions:\n",
+    "- 1 = supported (the text directly supports the subclaim)\n",
+    "- 0 = refuted (the text contradicts the subclaim)\n",
+    "- 2 = not_supported (the text is related but provides no evidence for the subclaim)\n",
+    "\n",
+    "Medical Text:\n",
+    "{text}\n",
+    "\n",
+    "Subclaim:\n",
+    "{subclaim}\n",
+    "\n",
+    "Respond ONLY with a single number: 1, 0, or 2.\n",
+    "\"\"\"\n",
+    "\n",
+    "    conversation = {}\n",
+    "    conversation['conversations'] = (\n",
+    "        {'from': \"user\", 'content': system_prompt},\n",
+    "        {'from': \"assistant\", 'content': str(label)},\n",
+    "    )\n",
+    "    return conversation\n",
+    "# /home/mshahidul/readctrl/data/finetuning_data/processed_subclaim_support_data.json\n",
+    "with open('/home/mshahidul/readctrl/data/finetuning_data/processed_subclaim_support_data.json', 'r') as f:\n",
+    "    import json\n",
+    "    data = json.load(f)\n",
+    "prompts = []\n",
+    "for item in data:\n",
+    "    text = item['text']\n",
+    "    subclaim = item['subclaim']\n",
+    "    label = item['label']\n",
+    "    prompt = training_prompt(text, subclaim, label)\n",
+    "    prompts.append(prompt)\n",
+    "with open('/home/mshahidul/readctrl/data/finetuning_data/processed_subclaim_support_data_conversation.json', 'w') as f:\n",
+    "    json.dump(prompts, f, indent=2)"
+   ]
+  },
+  {
+   "cell_type": "markdown",
+   "id": "fcc9cec9",
+   "metadata": {},
+   "source": [
+    "## classifier design for readability test"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 4,
+   "id": "6a5690f1",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "def readability_training_prompt_with_human(full_text, generated_text, human_score):\n",
+    "    \"\"\"\n",
+    "    Modified training prompt: Evaluates readability by comparing \n",
+    "    generated text against the original source (Full Text) only.\n",
+    "    \"\"\"\n",
+    "    \n",
+    "    system_prompt = f\"\"\"You are a medical readability evaluator.\n",
+    "\n",
+    "### Task\n",
+    "Compare the \"GENERATED TEXT\" against the \"FULL TEXT\" to determine its readability for a general, non-medical audience.\n",
+    "\n",
+    "### Input Data\n",
+    "- **FULL TEXT:** {full_text}\n",
+    "- **GENERATED TEXT (Evaluate this):** {generated_text}\n",
+    "\n",
+    "### Readability Scale\n",
+    "1: Very Easy - Minimal medical language, uses simple terms.\n",
+    "2: Easy - Accessible to most, minor jargon explained.\n",
+    "3: Medium - Some technical terms, moderate complexity.\n",
+    "4: Hard - Clinical tone, assumes some prior knowledge.\n",
+    "5: Very Hard - Extremely technical, requires medical expertise.\n",
+    "\n",
+    "### Constraints\n",
+    "- Evaluate ONLY the \"GENERATED TEXT\".\n",
+    "- Use \"FULL TEXT\" only for context of the subject matter.\n",
+    "- Do NOT assess factual accuracy.\n",
+    "\n",
+    "### Output Format\n",
+    "Return ONLY the following JSON object:\n",
+    "{{\n",
+    "  \"readability_score\": {human_score}\n",
+    "}}\"\"\"\n",
+    "\n",
+    "    # Structured for standard SFT (Supervised Fine-Tuning) formats\n",
+    "    conversation = {\n",
+    "        \"conversations\": [\n",
+    "            {\"role\": \"user\", \"content\": system_prompt},\n",
+    "            {\"role\": \"assistant\", \"content\": f\"{{\\\"readability_score\\\": {human_score}}}\"}\n",
+    "        ]\n",
+    "    }\n",
+    "    \n",
+    "    return conversation"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 2,
+   "id": "63b469ef",
+   "metadata": {},
+   "outputs": [
+    {
+     "name": "stdout",
+     "output_type": "stream",
+     "text": [
+      "dict_keys(['low_health_literacy', 'intermediate_health_literacy', 'proficient_health_literacy'])\n"
+     ]
+    }
+   ],
+   "source": [
+    "# /home/mshahidul/readctrl/data/annotators_validate_data/Sharmin Sultana_2025-12-31_14-19-30/annotation_results.json\n",
+    "with open('/home/mshahidul/readctrl/data/synthetic_dataset_diff_labels/syn_data_diff_labels_en_v1.json', 'r') as f:\n",
+    "    import json\n",
+    "    anno_data = json.load(f)\n",
+    "print(anno_data[0]['diff_label_texts'].keys())"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 3,
+   "id": "ea10b2cb",
+   "metadata": {},
+   "outputs": [
+    {
+     "name": "stdout",
+     "output_type": "stream",
+     "text": [
+      "Merge Complete.\n",
+      "Original keys preserved: ['index', 'fulltext', 'diff_label_texts', 'summary']\n",
+      "Sample 'diff_label_texts' keys check: dict_keys(['low_health_literacy', 'intermediate_health_literacy', 'proficient_health_literacy'])\n"
+     ]
+    }
+   ],
+   "source": [
+    "import json\n",
+    "import pandas as pd\n",
+    "\n",
+    "# Define file paths\n",
+    "gs_path = '/home/mshahidul/readctrl/data/testing_data_gs/multiclinsum_gs_train_en.json'\n",
+    "syn_path = '/home/mshahidul/readctrl/data/synthetic_dataset_diff_labels/syn_data_diff_labels_en_v1.json'\n",
+    "output_path = '/home/mshahidul/readctrl/data/synthetic_dataset_diff_labels/syn_data_with_gs_summary_en.json'\n",
+    "\n",
+    "# 1. Load Ground Truth Data\n",
+    "with open(gs_path, 'r', encoding='utf-8') as f:\n",
+    "    gs_data = json.load(f)\n",
+    "\n",
+    "# 2. Load Synthetic Data (Preserving all keys: index, fulltext, diff_label_texts)\n",
+    "with open(syn_path, 'r', encoding='utf-8') as f:\n",
+    "    syn_data = json.load(f)\n",
+    "\n",
+    "# Convert to DataFrames\n",
+    "# We only need 'fulltext' and 'summary' from the GS file for the mapping\n",
+    "df_gs = pd.DataFrame(gs_data)[['fulltext', 'summary']]\n",
+    "df_gs = df_gs.drop_duplicates(subset=['fulltext'])\n",
+    "\n",
+    "# Create the Synthetic DataFrame (contains index, fulltext, diff_label_texts)\n",
+    "df_syn = pd.DataFrame(syn_data)\n",
+    "\n",
+    "# 3. Perform Left Join\n",
+    "# This keeps every column in df_syn and adds 'summary' where fulltext matches\n",
+    "merged_df = pd.merge(df_syn, df_gs, on='fulltext', how='left')\n",
+    "\n",
+    "# 4. Save and Verify\n",
+    "merged_data = merged_df.to_dict(orient='records')\n",
+    "\n",
+    "with open(output_path, 'w', encoding='utf-8') as f:\n",
+    "    json.dump(merged_data, f, indent=4, ensure_ascii=False)\n",
+    "\n",
+    "print(f\"Merge Complete.\")\n",
+    "print(f\"Original keys preserved: {list(merged_df.columns)}\")\n",
+    "print(f\"Sample 'diff_label_texts' keys check: {merged_df.iloc[0]['diff_label_texts'].keys()}\")"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 6,
+   "id": "1b3c848f",
+   "metadata": {},
+   "outputs": [
+    {
+     "name": "stdout",
+     "output_type": "stream",
+     "text": [
+      "dict_keys(['id', 'fulltext', 'summary'])\n"
+     ]
+    }
+   ],
+   "source": [
+    "# /home/mshahidul/readctrl/data/testing_data_gs/multiclinsum_gs_train_en.json\n",
+    "with open('/home/mshahidul/readctrl/data/testing_data_gs/multiclinsum_gs_train_en.json', 'r') as f:\n",
+    "    import json\n",
+    "    _data = json.load(f)\n",
+    "print(_data[0].keys())\n",
+    "a_dict = {}\n",
+    "for item in _data:\n",
+    "    a_dict[item['fulltext']] = item['summary']"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 8,
+   "id": "bb68d61b",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "# /home/mshahidul/readctrl/data/data_annotator_data/vector_db_all-miniLM/crowdsourcing_input_en_v2.json\n",
+    "with open('/home/mshahidul/readctrl/data/synthetic_dataset_diff_labels/syn_data_diff_labels_en_v1.json', 'r') as f:\n",
+    "    import json\n",
+    "    gen_data = json.load(f)\n",
+    "data={}\n",
+    "for item in gen_data:\n",
+    "    for label in list(item['diff_label_texts'].keys()):\n",
+    "        # print(item.keys())\n",
+    "        data.setdefault(item['index'], {})[label] = {\n",
+    "        'fulltext': item['fulltext'],\n",
+    "        # 'gold_summary': a_dict[item['fulltext']],\n",
+    "        'generated_text': item['diff_label_texts'][label]\n",
+    "    }\n"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 9,
+   "id": "7fd3115c",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import math\n",
+    "\n",
+    "def convert_score(score: int) -> int:\n",
+    "    if not 1 <= score <= 10:\n",
+    "        raise ValueError(\"Score must be between 1 and 10\")\n",
+    "    return math.ceil(score / 2)\n"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 11,
+   "id": "36ebb028",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "full_data=[]\n",
+    "for item in anno_data:\n",
+    "    label=item['health_literacy_label']\n",
+    "    full_text = data[item['doc_id']][label]['fulltext']\n",
+    "    # gold_summary = data[item['doc_id']][label]['gold_summary']\n",
+    "    generated_text = data[item['doc_id']][label]['generated_text']\n",
+    "    human_score = convert_score(item['doc_rating'])\n",
+    "    res=readability_training_prompt_with_human(full_text,generated_text,human_score)\n",
+    "    full_data.append(res)"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 12,
+   "id": "8b8df130",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "with open(\"/home/mshahidul/readctrl/data/finetuning_data/classifier_en_data.json\", \"w\") as f:\n",
+    "    json.dump(full_data, f, indent=4)"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 13,
+   "id": "3dfb6a3c",
+   "metadata": {},
+   "outputs": [
+    {
+     "data": {
+      "text/plain": [
+       "{'conversations': [{'role': 'user',\n",
+       "   'content': 'You are a medical readability evaluator.\\n\\n### Task\\nCompare the \"GENERATED TEXT\" against the \"FULL TEXT\" to determine its readability for a general, non-medical audience.\\n\\n### Input Data\\n- **FULL TEXT:** The patient was a 59-year-old Japanese man with a 28-year history of type 1 diabetes. He visited our hospital monthly for management of diabetes with intensive therapy employing multiple-dose insulin injections. His height and body weight were 168 cm and 52 kg (body mass index: 18.4 kg/m2), respectively. He showed depleted insulin secretion (serum C-peptide level was below the limit of detection), such that his blood glucose levels fluctuated severely, and his hemoglobin A1c (HbA1c) level was around 9.0% despite intensive insulin therapy. He had been diagnosed with asymptomatic chronic severe (grade III) aortic regurgitation (AR) 16 years before the current presentation but had declined follow-up for the AR. He had never undergone surgery nor the implantation of any prosthetic devices.\\n\\nEight days after his regular hospital visit, he visited an emergency clinic complaining of breathing difficulty and had a fever above 38℃. Until that day, he had not noticed any fever, chills, weakness, or any other symptoms. His blood pressure and pulse rate were 192/82 mmHg and 118/min, respectively. He showed orthopnea, and his oxygen saturation (SpO2) was 80%. He was transported to the emergency department of our hospital. A physical examination revealed a Levine 3/6 systolic murmur, although his cardiac murmur had not been checked at regular hospital visits. No physical findings suggesting IE, such as Osler nodes, Janeway lesions, or conjunctival petechiae, were recognized. His white blood cell (WBC) count was markedly increased to 20,800 /μL, and his C-reactive protein (CRP) was elevated to 6.06 mg/dL. Serum creatine phosphokinase MB was within the normal range, at 6.0 IU/L, and troponin T was negative. Chest X-ray showed pulmonary congestion with cardiac enlargement (cardiothoracic ratio: 55%). Electrocardiography revealed ST elevation on V1-V4, but emergency echocardiography showed no dysfunction of cardiac contractility. He was diagnosed with acute heart failure due to valvular disease, and treatment with non-invasive positive pressure ventilation and nitrates was initiated.\\n\\nAfter hospital admission, a detailed examination by transthoracic echocardiography showed severe aortic regurgitation, severe mitral regurgitation, and a mobile vegetation on the mitral valve. Transesophageal echocardiography revealed a 16.5×6-mm mobile vegetation on the anterior leaflet of the mitral valve and an 11.2×5-mm nonmobile vegetation on the noncoronary cusp of the aortic valve. These findings raised strong suspicion of NVE. In this case, head computed tomography (CT) and magnetic resonance imaging revealed no cerebral infarction or hemorrhaging, although a mobile vegetation was detected.\\n\\nOn reviewing the clinical course until hospitalization, we noted that at the visit four months before admission, his WBC count had been slightly elevated. The following month, his albumin (Alb) level decreased to 3.0 g/dL, and his hemoglobin (Hb) level had shown a gradual decline over the 2 months prior to admission. During this period, he had experienced a 4-kg weight loss. Esophagogastroduodenoscopy and whole-body CT were performed, but no abnormalities were detected. One month later, he had regained some weight, and the laboratory findings had nearly normalized, except for a slightly elevated CRP level (0.54 mg/dL). At the last visit (8 days before admission), his WBC count had again risen to 9,300 /μL, while his Hb and Alb levels had again decreased to 13.1 g/dL and 3.0 g/dL, respectively. Furthermore, his CRP level had increased to 4.18 mg/dL. At that time, his diastolic blood pressure has shown an obvious decrease. Thus far, he had not experienced a fever or any symptoms other than weight loss. We suspected diseases of infectious and/or malignant origin and initiated comprehensive examinations to identify the source of his clinical findings.\\n\\nAfter heart failure treatment had been started, his clinical symptoms showed rapid improvement, and his hemodynamic stability was maintained during the first six hours. He initially received empirical intravenous antibiotic therapy consisting of 12 g/day of ampicillin sulbactam (ABPC/S) and 120 mg/day of gentamycin (GM). Three blood culture sets were obtained on the admission, and all were positive for S. warneri [minimum inhibitory concentration (MIC) to ABPC/S ≤8 μg/mL; MIC to GM ≤1 μg/mL; MIC to cefazolin (CEZ) ≤2 μg/mL]. Thus, IE caused by this organism was diagnosed.\\n\\nAccording to the clinical guideline established by the Japanese Circulation Society, emergency surgery is generally recommended for heart failure of NYHA III to IV or urgent surgery for NVE mobile vegetation exceeding 10 mm and severe valve dysfunction. In this case, however, his heart failure was successfully improved. Based on the guideline, the risk of embolism was considered to have been reduced by the administration of appropriate antibiotic therapy. In addition, the patient had type 1 diabetes, and his glycemic control was so poor that we were concerned that double-valve surgery would be a high-risk procedure. Therefore, we planned elective surgery after sufficient control of both infection and diabetes.\\n\\nBased on the blood culture results, the antibiotic regimen was switched to 6 g/day of CEZ. A detailed dental examination revealed no abnormalities, such as periodontitis. After four weeks of antibiotic therapy, he underwent surgical therapy. His aortic valve was found to be bicuspid, and the aortic and mitral annuli were intact without abscess formation. Large vegetations were exenterated, and the mitral and aortic valves were both replaced with mechanical valves. He experienced no postoperative complications and was discharged on the 22nd day after the operation without apparent embolism. He has not had any recurrence in over two years since the operation.\\n- **GENERATED TEXT (Evaluate this):** A 59-year-old Japanese man with a 28-year history of type 1 diabetes on intensive multiple-dose insulin therapy (BMI 18.4 kg/m2, undetectable C‑peptide, HbA1c ~9.0%) and remote, asymptomatic chronic severe (grade III) aortic regurgitation (diagnosed 16 years earlier without subsequent follow‑up) presented with acute decompensated heart failure. He had never undergone surgery or prosthetic device implantation and had no history of immunosuppressive therapies.\\n\\nEight days after a routine visit, he developed dyspnea and fever >38℃. On arrival: BP 192/82 mmHg, HR 118/min, orthopnea, SpO2 80%. Exam: Levine 3/6 systolic murmur; no Osler nodes, Janeway lesions, or conjunctival petechiae. Labs: WBC 20,800/μL, CRP 6.06 mg/dL, CK‑MB 6.0 IU/L, troponin T negative. CXR showed pulmonary congestion with cardiomegaly (CTR 55%). ECG had ST elevation in V1–V4, but emergent echocardiography showed no systolic dysfunction. He was diagnosed with acute heart failure due to valvular disease and treated with non‑invasive positive pressure ventilation and nitrates.\\n\\nTransthoracic echocardiography demonstrated severe aortic regurgitation and severe mitral regurgitation with a mobile mitral vegetation. Transesophageal echocardiography identified a 16.5×6‑mm mobile vegetation on the anterior leaflet of the mitral valve and an 11.2×5‑mm nonmobile vegetation on the noncoronary cusp of the aortic valve, raising strong suspicion for native valve endocarditis (NVE). Head CT and MRI showed no cerebral infarction or hemorrhage.\\n\\nRetrospective review revealed subtle abnormalities starting four months pre‑admission: mildly elevated WBC, albumin decreased to 3.0 g/dL the following month, and gradual hemoglobin decline over two months, with a 4‑kg weight loss. EGD and whole‑body CT were unrevealing. He partially regained weight and labs nearly normalized except for a CRP of 0.54 mg/dL. At the last pre‑admission visit (8 days prior), WBC was 9,300/μL, Hb 13.1 g/dL, Alb 3.0 g/dL, CRP 4.18 mg/dL, and diastolic BP had fallen; he remained afebrile and asymptomatic aside from weight loss.\\n\\nEmpiric antibiotics were initiated with ampicillin–sulbactam 12 g/day plus gentamicin 120 mg/day. Three admission blood culture sets all grew Staphylococcus warneri, a coagulase‑negative staphylococcus (CoNS) and resident skin flora (MICs: ABPC/S ≤8 μg/mL; GM ≤1 μg/mL; CEZ ≤2 μg/mL), confirming S. warneri IE. Per Japanese Circulation Society guidance, emergency surgery is generally recommended for NYHA III–IV heart failure or urgent surgery for NVE with mobile vegetation >10 mm and severe valve dysfunction. Because heart failure improved rapidly and appropriate antibiotics were started (reducing embolic risk), and given poorly controlled type 1 diabetes increasing operative risk, elective surgery was planned after stabilization of infection and glycemia. Antibiotics were narrowed to cefazolin 6 g/day; dental evaluation showed no periodontitis.\\n\\nAfter four weeks of antibiotics, surgery revealed a bicuspid aortic valve with intact aortic and mitral annuli and no abscess. Large vegetations were exenterated, and both valves were replaced with mechanical prostheses. The postoperative course was uneventful; he was discharged on postoperative day 22 without apparent embolism and has remained recurrence‑free for over two years. This case represents NVE due to the resident CoNS S. warneri in a patient without prosthetic material or immunosuppression, with prodromal laboratory abnormalities and weight loss evident up to four months before presentation.\\n\\n### Readability Scale\\n1: Very Easy - Minimal medical language, uses simple terms.\\n2: Easy - Accessible to most, minor jargon explained.\\n3: Medium - Some technical terms, moderate complexity.\\n4: Hard - Clinical tone, assumes some prior knowledge.\\n5: Very Hard - Extremely technical, requires medical expertise.\\n\\n### Constraints\\n- Evaluate ONLY the \"GENERATED TEXT\".\\n- Use \"FULL TEXT\" only for context of the subject matter.\\n- Do NOT assess factual accuracy.\\n\\n### Output Format\\nReturn ONLY the following JSON object:\\n{\\n  \"readability_score\": 5\\n}'},\n",
+       "  {'role': 'assistant', 'content': '{\"readability_score\": 5}'}]}"
+      ]
+     },
+     "execution_count": 13,
+     "metadata": {},
+     "output_type": "execute_result"
+    }
+   ],
+   "source": [
+    "full_data[0]"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "6dfc340b",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "dict_keys(['queue_position', 'doc_id', 'health_literacy_label', 'wiki_id', 'doc_snippet', 'wiki_snippet', 'doc_rating', 'wiki_rating', 'is_duplicate', 'timestamp'])"
+   ]
+  }
+ ],
+ "metadata": {
+  "kernelspec": {
+   "display_name": "un",
+   "language": "python",
+   "name": "python3"
+  },
+  "language_info": {
+   "codemirror_mode": {
+    "name": "ipython",
+    "version": 3
+   },
+   "file_extension": ".py",
+   "mimetype": "text/x-python",
+   "name": "python",
+   "nbconvert_exporter": "python",
+   "pygments_lexer": "ipython3",
+   "version": "3.11.14"
+  }
+ },
+ "nbformat": 4,
+ "nbformat_minor": 5
+}
diff --git a/code/data_processing/data_preV1.ipynb b/code/data_processing/data_preV1.ipynb
new file mode 100644
index 0000000000000000000000000000000000000000..576679d12e3548a897e6508a39265eea5b436d2e
--- /dev/null
+++ b/code/data_processing/data_preV1.ipynb
@@ -0,0 +1,291 @@
+{
+ "cells": [
+  {
+   "cell_type": "code",
+   "execution_count": 14,
+   "id": "883f7665",
+   "metadata": {},
+   "outputs": [
+    {
+     "data": {
+      "text/plain": [
+       "dict_keys(['id', 'original_text_language', 'source_topic', 'readability_versions'])"
+      ]
+     },
+     "execution_count": 14,
+     "metadata": {},
+     "output_type": "execute_result"
+    }
+   ],
+   "source": [
+    "import json\n",
+    "path=\"/home/mshahidul/readctrl/dataset_buildup.json\"\n",
+    "lang=path.split(\"/\")[-1].split(\"_\")[0]\n",
+    "with open(f\"{path}\", \"r\") as f:\n",
+    "    data = json.load(f)\n",
+    "\n",
+    "data[0].keys()"
+   ]
+  },
+  {
+   "cell_type": "markdown",
+   "id": "964139ea",
+   "metadata": {},
+   "source": [
+    "## fernandez_huerta score calculation"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "25449b20",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "from FH_es import fernandez_huerta\n",
+    "from FH_fr import flesch_kandel_moles_fr\n",
+    "# from FH_pt import flesch_portuguese\n",
+    "full_data=[]\n",
+    "for item in data:\n",
+    "    text = item[\"synthetic_summary\"]\n",
+    "    dat={}\n",
+    "    fh_score_b1 = fernandez_huerta(text['B1'])\n",
+    "    fh_score_b2 = fernandez_huerta(text['B2'])\n",
+    "    fh_score_b3 = fernandez_huerta(text['B3'])\n",
+    "    dat['B1']={\n",
+    "        \"text\": text['B1'],\n",
+    "        \"fh_score\": fh_score_b1\n",
+    "    }\n",
+    "    dat['B2']={\n",
+    "        \"text\": text['B2'],\n",
+    "        \"fh_score\": fh_score_b2\n",
+    "    }\n",
+    "    dat['B3']={\n",
+    "        \"text\": text['B3'],\n",
+    "        \"fh_score\": fh_score_b3\n",
+    "    }\n",
+    "    full_data.append({\n",
+    "        \"article\": item[\"article\"],\n",
+    "        \"gold_summary\": item[\"gold_summary\"],\n",
+    "        \"synthetic_summary\": dat\n",
+    "    })\n",
+    "with open(\"/home/mshahidul/readctrl/generating_data/score/synthetic.json\", \"w\") as f:\n",
+    "    json.dump(full_data, f,indent=4, ensure_ascii=False)"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 19,
+   "id": "d61f82e4",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import textstat\n",
+    "from FH_esV2 import fernandez_huerta\n",
+    "# from FH_es import fernandez_huerta\n",
+    "from FH_fr import flesch_kandel_moles_fr\n",
+    "# from FH_pt import flesch_portuguese\n",
+    "full_data=[]\n",
+    "for item in data:\n",
+    "    text = item[\"readability_versions\"]\n",
+    "    dat={}\n",
+    "    fh_score_easy = fernandez_huerta(text['easy']['text'])\n",
+    "    fh_score_intermediate = fernandez_huerta(text['intermediate']['text'])\n",
+    "    fh_score_hard = fernandez_huerta(text['hard']['text'])\n",
+    "    dat['easy']={\n",
+    "        \"text\": text['easy']['text'],\n",
+    "        \"fh_score\": fh_score_easy\n",
+    "    }\n",
+    "    dat['intermediate']={\n",
+    "        \"text\": text['intermediate']['text'],\n",
+    "        \"fh_score\": fh_score_intermediate\n",
+    "    }\n",
+    "    dat['hard']={\n",
+    "        \"text\": text['hard']['text'],\n",
+    "        \"fh_score\": fh_score_hard\n",
+    "    }\n",
+    "    full_data.append({\n",
+    "        \"original_text_language\": item[\"original_text_language\"],\n",
+    "        \"source_topic\": item[\"source_topic\"],\n",
+    "        \"synthetic_summary\": dat\n",
+    "    })\n",
+    "with open(\"/home/mshahidul/readctrl/generating_data/score/synthetic.json\", \"w\") as f:\n",
+    "    json.dump(full_data, f,indent=4, ensure_ascii=False)"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 20,
+   "id": "23830e3d",
+   "metadata": {},
+   "outputs": [
+    {
+     "data": {
+      "image/png": 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",
+      "text/plain": [
+       "<Figure size 700x500 with 1 Axes>"
+      ]
+     },
+     "metadata": {},
+     "output_type": "display_data"
+    }
+   ],
+   "source": [
+    "import pandas as pd\n",
+    "import seaborn as sns\n",
+    "import matplotlib.pyplot as plt\n",
+    "\n",
+    "# Flatten fh_scores into a tidy DataFrame\n",
+    "rows = []\n",
+    "for item in full_data:\n",
+    "    syn = item.get('synthetic_summary', {})\n",
+    "    for level in ('easy', 'intermediate', 'hard'):\n",
+    "        fh = syn.get(level, {}).get('fh_score')\n",
+    "        if fh is not None:\n",
+    "            rows.append({'level': level, 'fh_score': fh})\n",
+    "\n",
+    "df = pd.DataFrame(rows).dropna(subset=['fh_score'])\n",
+    "\n",
+    "# Plot\n",
+    "sns.set_theme(style='whitegrid')\n",
+    "plt.figure(figsize=(7,5))\n",
+    "ax = sns.boxplot(data=df, x='level', y='fh_score')\n",
+    "sns.stripplot(data=df, x='level', y='fh_score', color='black', alpha=0.4, jitter=0.2, size=3)\n",
+    "ax.set_title(f'{lang} scores by level')\n",
+    "ax.set_xlabel('Level')\n",
+    "ax.set_ylabel('score')\n",
+    "plt.tight_layout()\n",
+    "plt.show()"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 18,
+   "id": "16163d1e",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "with open(\"/home/mshahidul/readctrl/generating_data/tik_ache/es_syntheticV3.json\", \"r\", encoding=\"utf-8\") as f:\n",
+    "    tik_ache_data = json.load(f)"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 60,
+   "id": "8447f0ec",
+   "metadata": {},
+   "outputs": [
+    {
+     "name": "stdout",
+     "output_type": "stream",
+     "text": [
+      "id: 40\n",
+      "full text:\n",
+      "\n",
+      "La paciente era una recién nacida de 0 días de edad, de etnia Han, que nació a las 36 semanas de gestación de una mujer embarazada de 3, para 2, con un peso de 2650 g. Se le practicó una cesárea de urgencia debido a la angustia fetal, con puntuaciones de Apgar de 6 a 1 min y 5 min. Su grupo sanguíneo era O y RhD positivo. Al nacer, presentaba palidez, equimosis dispersas en múltiples áreas del cuerpo, sangrado de las mucosas e insuficiencia respiratoria, con un leve flujo de sangre hemorrágica también observado en los sitios de punción venosa. El análisis de gases en sangre de la arteria umbilical mostró un hematocrito de 0.08 y una hemoglobina de 23 g/L. La paciente requirió intubación endotraqueal y ventilación mecánica. Después de la transfusión de una suspensión de glóbulos rojos, los recuentos sanguíneos iniciales revelaron una trombocitopenia severa (recuento de plaquetas de 12 × 109/L), anemia (hemoglobina de 46 g/L) y leucopenia (recuento de leucocitos de 1.11 × 109/L).\n",
+      "\n",
+      "La paciente fue ingresada en la unidad de cuidados intensivos neonatales a las 3 horas de vida para recibir tratamiento adicional. Durante la hospitalización, se le diagnosticó coagulación intravascular diseminada (CID), con tiempo de tromboplastina parcial activada (TTPA) de 73,10 segundos, tiempo de protrombina (TP) de 25,4 segundos, fibrinógeno (FIB) de 1,01 g/L, razón internacional normalizada (INR) de 2,26 y dímero D > 20 mg/L. Se le administró ventilación mecánica, corrección de la acidosis y transfusión de plasma fresco congelado. A pesar de múltiples transfusiones de glóbulos rojos y plaquetas, los niveles de hemoglobina y plaquetas permanecieron por debajo de lo normal (hemoglobina 106 g/L y plaquetas 11 × 109/L el día 3). También recibió tratamiento antiinfeccioso, cardiotónico, vasopresor y otro tratamiento sintomático. Un frotis periférico mostró áreas de tinción pálida agrandadas de glóbulos rojos, con una proporción de reticulocitos del 1,5% y un resultado negativo en la prueba directa de Coombs. No se realizó aspiración de médula ósea debido a su grave estado. No hubo evidencia clínica o de laboratorio de sepsis neonatal, y las pruebas para toxoplasma, rubéola, citomegalovirus y virus del herpes simple (TORCH); virus de hepatitis; y Treponema pallidum fueron negativas. El examen físico de admisión reveló un estado mental deficiente, disminución del tono muscular en las extremidades y reflejo pupilar lento a la luz. Todos los demás hallazgos fueron normales. El ultrasonido craneal y electroencefalograma de cabecera revelaron hemorragia intracraneal grave y bajo voltaje, respectivamente. Los hallazgos del ecocardiograma sugirieron un conducto arterioso patente, foramen oval permeable e hipertensión pulmonar. El ultrasonido abdominal indicó hemorragia gastrointestinal. A pesar de todos los esfuerzos, la paciente falleció el tercer día de vida debido a falla multiorgánica y hemorragia intracraneal masiva (la información detallada se puede encontrar en el Informe Suplementario).\n",
+      "\n",
+      "Los padres de la paciente no eran consanguíneos y ambos tenían talasemia. La madre, que compartía el mismo tipo de sangre que la paciente, tuvo una anemia leve durante el embarazo (nivel de hemoglobina de 97 g/L) y un historial de aborto inducido. Los exámenes prenatales no mostraron anomalías, ni tampoco hidrops fetal, y no recibió ninguna medicación durante el embarazo que pudiera provocar una enfermedad hemorrágica de inicio temprano en el recién nacido. La paciente también tenía un hermano de 1 año que gozaba de buena salud. Su abuelo tenía un historial de anemia leve (detalles desconocidos).\n",
+      "\n",
+      "Se obtuvo el consentimiento informado de los padres del paciente y se realizó un secuenciamiento de Sanger para descubrir la causa de la enfermedad. Se detectó una nueva mutación de MECOM de desplazamiento de marco heterocigótica [NM_001105078: c.157_158del (p.Met53Glyfs*2)] en el probando. Esta variante cambió el aminoácido 53 de metionina (codón ATG) a glicina (codón GGT), seguido de una terminación temprana. La mutación no se encontró en los padres o en el hermano mayor. La variante se clasificó como patogénica según las directrices del Colegio Americano de Genética Médica (ACMG) [14]. El algoritmo “AutoPVS1” brindó un fuerte apoyo para la interpretación de PVS1 de p.Met53Glyfs*2, lo que indica patogenicidad. La variante no se ha informado previamente en la Base de Datos de Mutación Genética Humana (HGMD) o en Clinvar. El análisis de conservación mostró que el residuo Met53 está altamente conservado en todas las especies de mamíferos (incluidos humanos, ratones, ratas, chimpancés y bovinos) utilizando Clustal Omega. Se generaron modelos de estructura de proteínas tridimensionales de las proteínas MECOM de tipo salvaje y mutantes utilizando SWISS-MODEL, lo que indica que la mutación de desplazamiento de marco causó una terminación temprana de la síntesis de aminoácidos, alterando significativamente la estructura de la proteína.\n",
+      "\n"
+     ]
+    }
+   ],
+   "source": [
+    "id=40\n",
+    "print(f\"id: {id}\")\n",
+    "print(\"full text:\\n\")\n",
+    "print(tik_ache_data[id]['article'])"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 61,
+   "id": "d802cf9e",
+   "metadata": {},
+   "outputs": [
+    {
+     "name": "stdout",
+     "output_type": "stream",
+     "text": [
+      "dict_keys(['id', 'original_text_language', 'source_topic', 'readability_versions'])\n"
+     ]
+    }
+   ],
+   "source": [
+    "with open(\"/home/mshahidul/readctrl/dataset_buildup.json\", \"r\", encoding=\"utf-8\") as f:\n",
+    "    dataset_buildup = json.load(f)\n",
+    "print(dataset_buildup[0].keys())"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "05569bfb",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "all_prompts1={\n",
+    "\"easy\":'''\n",
+    "Reescribe el siguiente informe médico en español con un lenguaje sencillo y claro. Usa oraciones cortas, evita tecnicismos y explica los términos médicos con palabras comunes para que una persona sin formación médica lo comprenda fácilmente. Mantén los datos médicos esenciales.\n",
+    "''',\n",
+    "\"intermediate\": '''\n",
+    "Reformula el siguiente informe médico en español en un nivel de lectura intermedio. Usa un lenguaje comprensible para personas con cultura general y cierto conocimiento de temas de salud. Mantén la precisión médica, pero explica brevemente términos técnicos y conserva un tono profesional y accesible.\n",
+    "''',\n",
+    "\"hard\": '''\n",
+    "Reescribe el siguiente informe médico en español utilizando terminología médica precisa y estilo técnico, como si fuera dirigido a un lector profesional del ámbito sanitario. Conserva la complejidad del lenguaje, las estructuras formales y los matices clínicos, sin simplificar contenidos.\n",
+    "'''\n",
+    "}"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "38131fad",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "custom_promptsV1={\n",
+    "\"easy\":'''\n",
+    "Reescribe el siguiente informe médico en español con un nivel de lectura fácil correspondiente a un puntaje FH entre 70 y 100 (texto muy comprensible).\n",
+    "Usa oraciones cortas y directas, vocabulario cotidiano, estructuras simples y explicaciones claras de términos médicos. El tono debe ser empático y accesible, como si estuvieras explicando la situación a un paciente o familiar sin conocimientos médicos.\n",
+    "Mantén los datos clínicos y resultados esenciales, pero reemplaza o aclara tecnicismos con frases simples. Evita abreviaturas o siglas sin explicación.\n",
+    "''',\n",
+    "\"intermediate\": '''\n",
+    "Reformula el siguiente informe médico en español con un nivel de lectura intermedio, correspondiente a un puntaje FH entre 50 y 70 (texto de dificultad moderada).\n",
+    "Usa lenguaje formal pero comprensible, adecuado para lectores con educación general o estudiantes del área de salud. Mantén la precisión médica, pero agrega explicaciones breves tras los términos técnicos. Alterna oraciones simples y compuestas, con buena fluidez y cohesión.\n",
+    "El texto debe sonar profesional, informativo y claro, sin llegar a la densidad típica de lenguaje técnico especializado.\n",
+    "''',\n",
+    "\"hard\": '''\n",
+    "Reescribe el siguiente informe médico en español con un nivel de lectura avanzado o técnico, correspondiente a un puntaje FH entre 0 y 50 (texto especializado).\n",
+    "Usa terminología médica precisa, estructuras sintácticas complejas y tono formal típico de documentos clínicos o publicaciones científicas. No simplifiques ni expliques los tecnicismos; conserva la exactitud conceptual y la nomenclatura profesional.\n",
+    "Refleja el razonamiento clínico, hallazgos y juicios médicos con lenguaje apropiado para médicos, especialistas o investigadores.\n",
+    "'''\n",
+    "}"
+   ]
+  }
+ ],
+ "metadata": {
+  "kernelspec": {
+   "display_name": "unsloth",
+   "language": "python",
+   "name": "python3"
+  },
+  "language_info": {
+   "codemirror_mode": {
+    "name": "ipython",
+    "version": 3
+   },
+   "file_extension": ".py",
+   "mimetype": "text/x-python",
+   "name": "python",
+   "nbconvert_exporter": "python",
+   "pygments_lexer": "ipython3",
+   "version": "3.11.11"
+  }
+ },
+ "nbformat": 4,
+ "nbformat_minor": 5
+}
diff --git a/code/data_processing/data_preV2.ipynb b/code/data_processing/data_preV2.ipynb
new file mode 100644
index 0000000000000000000000000000000000000000..530930bdffa595b8b71b5b1330a9c86fc7b2dc77
--- /dev/null
+++ b/code/data_processing/data_preV2.ipynb
@@ -0,0 +1,1461 @@
+{
+  "cells": [
+    {
+      "cell_type": "markdown",
+      "id": "f869b176",
+      "metadata": {},
+      "source": [
+        "## LLM guard Qwen3-32B model data formatting"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": null,
+      "id": "9f4ff22b",
+      "metadata": {},
+      "outputs": [],
+      "source": [
+        "def training_prompt(sub_questions, sub_answers, evaluation):\n",
+        "    system_prompt = f\"\"\"\n",
+        "You are an impartial evaluator. A set of sub‑questions and sub‑answers was created by separate models.  \n",
+        "Determine whether, when combined, these sub‑answers form one meaningful, coherent, and reasonable overall answer to an implied main question.\n",
+        "\n",
+        "Sub‑questions: {sub_questions}\n",
+        "Sub‑answers: {sub_answers}\n",
+        "\n",
+        "Respond only with:\n",
+        "1 – if the combined sub‑answers form a coherent and meaningful overall answer  \n",
+        "0 – if they do not (incoherent, contradictory, incomplete, or nonsensical)\n",
+        "\"\"\"\n",
+        "    \n",
+        "    conversation = {}\n",
+        "    conversation['conversations'] = (\n",
+        "        {'from': \"user\", 'content': system_prompt},\n",
+        "        {'from': \"assistant\", 'content': str(evaluation)},\n",
+        "    )\n",
+        "    return conversation"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": null,
+      "id": "afd89af1",
+      "metadata": {},
+      "outputs": [],
+      "source": [
+        "# /home/mshahidul/readctrl/data/data_annotator_data/manual_selections_en.json\n",
+        "with open('/home/mshahidul/readctrl/data/data_annotator_data/manual_selections_en.json', 'r') as f:\n",
+        "    import json\n",
+        "    data = json.load(f)\n",
+        "print(len(data))"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": null,
+      "id": "595815eb",
+      "metadata": {},
+      "outputs": [],
+      "source": [
+        "import os\n",
+        "import json\n",
+        "\n",
+        "data_dir = \"/home/mshahidul/LLM_guard/data/training_data_combined_ans_check\"\n",
+        "json_files = [f for f in os.listdir(data_dir) if f.endswith('.json')]\n",
+        "\n",
+        "all_data = []\n",
+        "for file in json_files:\n",
+        "    with open(os.path.join(data_dir, file), 'r') as f:\n",
+        "        data = json.load(f)\n",
+        "        for item in data:\n",
+        "            training_prompt_data = training_prompt(\n",
+        "                item['sub_questions'], \n",
+        "                item['sub_answers'], \n",
+        "                str(item['evaluation'])\n",
+        "            )\n",
+        "            all_data.append(training_prompt_data)"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": null,
+      "id": "7c1531e5",
+      "metadata": {},
+      "outputs": [],
+      "source": [
+        "with open('/home/mshahidul/LLM_guard/data/training_data_checking_sub_ques_ans.json', 'w') as outfile:\n",
+        "    json.dump(all_data, outfile, indent=2)"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": null,
+      "id": "e6f87187",
+      "metadata": {},
+      "outputs": [
+        {
+          "name": "stdout",
+          "output_type": "stream",
+          "text": [
+            "300\n",
+            "{'conversations': ({'from': 'user', 'content': \"\\nYou are an expert medical adjudicator. Determine if the 'Medical Passage' contains the core factual information of each 'Subclaim', even if the passage uses simpler language or layperson terms.\\nRules:\\n- Label 'supported' if the essential meaning is present.\\n- Label 'not_supported' only if the information is missing or contradicted.\\nOutput: JSON array of strings ['supported', 'not_supported', ...]\\n\\nMedical text:\\nA 62-year-old man has had cough and fever for three days. He feels short of breath and has chest pain when he breathes. His temperature is 38.5 C and he breathes fast. His oxygen level is 92% on room air. He has high blood pressure and no drug allergies. A chest x-ray shows a new spot in the right lower lung, with no fluid. A nose swab test for COVID is negative. The doctor says he has community pneumonia and treats him at home. He gets mouth pills: amoxicillin-clavulanate and azithromycin. After two days, his fever goes down and oxygen is 95%.\\n\\nSubclaims:\\n1. Chest x-ray showed right lower lobe consolidation.\\n2. The patient was treated as an outpatient.\\n3. He received amoxicillin-clavulanate plus azithromycin.\\n4. The patient was breathing fast.\\n5. The patient was admitted to the intensive care unit.\\n6. A pleural effusion was present on imaging.\\n7. Blood cultures grew Streptococcus pneumoniae.\\n8. The patient has a penicillin allergy.\\n\"}, {'from': 'assistant', 'content': '[\"supported\", \"supported\", \"supported\", \"supported\", \"not_supported\", \"not_supported\", \"not_supported\", \"not_supported\"]'})}\n"
+          ]
+        }
+      ],
+      "source": [
+        "import json\n",
+        "from pathlib import Path\n",
+        "\n",
+        "# from qwen3-8b.py\n",
+        "DATA_PATH = Path(\"/home/mshahidul/readctrl/data/finetuning_data/finetune_dataset_subclaim_support_v2.json\")\n",
+        "TEXT_LEVEL = \"hard_text\"  # easy_text, intermediate_text, hard_text\n",
+        "\n",
+        "\n",
+        "def training_prompt(medical_text, subclaims, labels):\n",
+        "    numbered_subclaims = \"\\n\".join(\n",
+        "        [f\"{idx + 1}. {claim}\" for idx, claim in enumerate(subclaims)]\n",
+        "    )\n",
+        "    \n",
+        "    system_prompt = f\"\"\"\n",
+        "You are an expert medical adjudicator. Determine if the 'Medical Passage' contains the core factual information of each 'Subclaim', even if the passage uses simpler language or layperson terms.\n",
+        "Rules:\n",
+        "- Label 'supported' if the essential meaning is present.\n",
+        "- Label 'not_supported' only if the information is missing or contradicted.\n",
+        "Output: JSON array of strings ['supported', 'not_supported', ...]\n",
+        "\n",
+        "Medical text:\n",
+        "{medical_text}\n",
+        "\n",
+        "Subclaims:\n",
+        "{numbered_subclaims}\n",
+        "\"\"\"\n",
+        "\n",
+        "    conversation = {}\n",
+        "    conversation[\"conversations\"] = (\n",
+        "        {\"from\": \"user\", \"content\": system_prompt},\n",
+        "        {\"from\": \"assistant\", \"content\": json.dumps(labels, ensure_ascii=False)},\n",
+        "    )\n",
+        "    return conversation\n",
+        "\n",
+        "\n",
+        "def load_conversation_dataset(data_path=DATA_PATH, text_levels=(\"easy_text\", \"intermediate_text\", \"hard_text\")):\n",
+        "    with Path(data_path).open(\"r\", encoding=\"utf-8\") as f:\n",
+        "        raw_data = json.load(f)\n",
+        "\n",
+        "    formatted_data = []\n",
+        "    for group in raw_data:\n",
+        "        for item in group.get(\"items\", []):\n",
+        "            subclaims = [x.get(\"subclaim\", \"\") for x in item.get(\"subclaims\", [])]\n",
+        "            labels = [x.get(\"label\", \"not_supported\") for x in item.get(\"subclaims\", [])]\n",
+        "\n",
+        "            if not subclaims:\n",
+        "                continue\n",
+        "\n",
+        "            for level in text_levels:\n",
+        "                medical_text = item.get(level)\n",
+        "                if not medical_text:\n",
+        "                    continue\n",
+        "                formatted_data.append(training_prompt(medical_text, subclaims, labels))\n",
+        "\n",
+        "    return formatted_data\n",
+        "\n",
+        "\n",
+        "# Example usage:\n",
+        "dataset_for_sft = load_conversation_dataset()\n",
+        "import json\n",
+        "\n",
+        "with open(\"/home/mshahidul/readctrl/data/finetuning_data/dataset_for_sft_support_check_list.json\", \"w\", encoding=\"utf-8\") as f:\n",
+        "    json.dump(dataset_for_sft, f, ensure_ascii=False, indent=2)\n",
+        "\n",
+        "print(len(dataset_for_sft))\n",
+        "print(dataset_for_sft[0])"
+      ]
+    },
+    {
+      "cell_type": "markdown",
+      "id": "fe5218ed",
+      "metadata": {},
+      "source": [
+        "## Training prompt creation (readability reasoning)"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": null,
+      "id": "9c3e4329",
+      "metadata": {},
+      "outputs": [],
+      "source": [
+        "def readability_judgment_single_prompt_old(reference_summary, generated_summary, readability_level, subclaim_text, result, evaluation):\n",
+        "    system_prompt = f\"\"\"\n",
+        "You are an impartial medical summarization evaluator.\n",
+        "\n",
+        "Your goal is to decide whether the inclusion or omission of ONE specific subclaim \n",
+        "from the reference summary is *reasonable*, given the readability level of the generated summary.\n",
+        "\n",
+        "### Inputs\n",
+        "Readability Level: {readability_level}\n",
+        "\n",
+        "Reference Summary:\n",
+        "{reference_summary}\n",
+        "\n",
+        "Generated Summary:\n",
+        "{generated_summary}\n",
+        "\n",
+        "Subclaim:\n",
+        "\"{subclaim_text}\"\n",
+        "\n",
+        "Result:\n",
+        "{result}   # 1 = supported (included in generated summary), 0 = omitted (not included)\n",
+        "\n",
+        "### Task\n",
+        "Judge whether this inclusion or omission is:\n",
+        "- \"reasonable\" → appropriate for this readability level\n",
+        "- \"partially_reasonable\" → oversimplified but acceptable\n",
+        "- \"unreasonable\" → harms completeness or clinical meaning\n",
+        "\n",
+        "Respond only with a JSON object:\n",
+        "{{\n",
+        "  \"reasonableness\": \"<reasonable | partially_reasonable | unreasonable>\",\n",
+        "  \"justification\": \"<short explanation>\"\n",
+        "}}\n",
+        "\"\"\"\n",
+        "\n",
+        "    conversation = {}\n",
+        "    conversation['conversations'] = (\n",
+        "        {'from': \"user\", 'content': system_prompt},\n",
+        "        {'from': \"assistant\", 'content': str(evaluation)},\n",
+        "    )\n",
+        "    return conversation\n"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": null,
+      "id": "276e1b47",
+      "metadata": {},
+      "outputs": [],
+      "source": [
+        "def readability_judgment_single_prompt(reference_summary, generated_summary, readability_level, subclaim_text, result, evaluation):\n",
+        "    system_prompt = f\"\"\"\n",
+        "You are an impartial medical summarization evaluator.\n",
+        "\n",
+        "Your goal is to decide whether the inclusion or omission of ONE specific subclaim \n",
+        "from the reference summary is *reasonable*, given the readability level of the generated summary.\n",
+        "\n",
+        "Readability guidelines:\n",
+        "- Easy: for general readers; omit detailed numbers, anatomy, or diagnostic test specifics.\n",
+        "- Intermediate: maintain main medical ideas and reasoning; simplify complex phrasing only.\n",
+        "- Hard: preserve nearly all technical and diagnostic detail, except redundant measurements.\n",
+        "\n",
+        "### Inputs\n",
+        "Readability Level: {readability_level}\n",
+        "\n",
+        "Reference Summary:\n",
+        "{reference_summary}\n",
+        "\n",
+        "Generated Summary:\n",
+        "{generated_summary}\n",
+        "\n",
+        "Subclaim:\n",
+        "\"{subclaim_text}\"\n",
+        "\n",
+        "Result:\n",
+        "{result}   # 1 = supported (included in generated summary), 0 = omitted (not included)\n",
+        "\n",
+        "### Consistency rules:\n",
+        "* If result = 0 (omitted) and the subclaim is purely technical or numerical for this readability level, likely \"reasonable\".\n",
+        "* If result = 0 and the subclaim expresses a central event, diagnosis, or reason for treatment outcome, mark \"unreasonable\".\n",
+        "\n",
+        "### Task\n",
+        "Judge whether this inclusion or omission is:\n",
+        "- \"reasonable\" → appropriate for this readability level\n",
+        "- \"partially_reasonable\" → oversimplified but acceptable\n",
+        "- \"unreasonable\" → harms completeness or clinical meaning\n",
+        "\n",
+        "Output format rule: produce exactly the JSON object below, no extra commentary.\n",
+        "\n",
+        "{{\n",
+        "  \"reasonableness\": \"<reasonable | partially_reasonable | unreasonable>\",\n",
+        "  \"justification\": \"<short explanation>\"\n",
+        "}}\n",
+        "\"\"\"\n",
+        "\n",
+        "    conversation = {}\n",
+        "    conversation['conversations'] = (\n",
+        "        {'from': \"user\", 'content': system_prompt},\n",
+        "        {'from': \"assistant\", 'content': str(evaluation)},\n",
+        "    )\n",
+        "    return conversation"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": null,
+      "id": "a3306898",
+      "metadata": {},
+      "outputs": [],
+      "source": [
+        "import json\n",
+        "with open('/home/mshahidul/readctrl/data/testing_data_gs/multiclinsum_gs_train_es.json', 'r') as f:\n",
+        "    multiclinsum_gs_train_es_data = json.load(f)\n",
+        "ref_summaries={}\n",
+        "fulltexts={}\n",
+        "for item in multiclinsum_gs_train_es_data:\n",
+        "    ref_summaries[item['id']]=item['summary']\n",
+        "    fulltexts[item['id']]=item['fulltext']"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": null,
+      "id": "d5aeca22",
+      "metadata": {},
+      "outputs": [],
+      "source": [
+        "generated_summaries = {}\n",
+        "with open('/home/mshahidul/readctrl/data/hand_create_gpt5_other_model/synthetic_data_es_raw_592.json', 'r') as f:\n",
+        "    synthetic_data_es_raw_592 = json.load(f)\n",
+        "for item in synthetic_data_es_raw_592:\n",
+        "    for version in ['easy', 'intermediate', 'hard']:\n",
+        "        generated_summaries[(item['id'], version)] = item['readability_versions'][version]['text']"
+      ]
+    },
+    {
+      "cell_type": "markdown",
+      "id": "28eb7213",
+      "metadata": {},
+      "source": [
+        "<!-- def readability_judgment_single_prompt(reference_summary, generated_summary, readability_level, subclaim_text, result, evaluation): -->\n",
+        "    "
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": null,
+      "id": "da42c192",
+      "metadata": {
+        "vscode": {
+          "languageId": "ruby"
+        }
+      },
+      "outputs": [],
+      "source": [
+        "training_data=[]\n",
+        "with open('/home/mshahidul/readctrl/results/dataset_quality_check/syn_data_resonability_check_20_gpt5.json', 'r') as f:\n",
+        "    syn_data_resonability_20 = json.load(f)\n",
+        "for item in syn_data_resonability_20:\n",
+        "    ref_summary = ref_summaries[item['id']]\n",
+        "    fulltext = fulltexts[item['id']]\n",
+        "    generated_summary = generated_summaries[(item['id'], item['difficulty_level'])]\n",
+        "    results=item['reasonableness']['evaluations']\n",
+        "    for eval_item in results:\n",
+        "        training_prompt_data = readability_judgment_single_prompt(\n",
+        "            ref_summary,\n",
+        "            generated_summary,\n",
+        "            item['difficulty_level'],\n",
+        "            eval_item['subclaim_text'],\n",
+        "            eval_item['result'],\n",
+        "            str({\n",
+        "                \"reasonableness\": eval_item['reasonableness'],\n",
+        "                \"justification\": eval_item['justification']\n",
+        "            })\n",
+        "        )\n",
+        "        training_data.append(training_prompt_data)\n",
+        "with open('/home/mshahidul/readctrl/data/training_data/syn_data_resonability_check_20_gpt5_training_data.json', 'w') as f:\n",
+        "    json.dump(training_data, f, indent=2)"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": null,
+      "id": "09f6c6e4",
+      "metadata": {
+        "vscode": {
+          "languageId": "ruby"
+        }
+      },
+      "outputs": [],
+      "source": [
+        "python '/home/mshahidul/readctrl/code/finetune-inference/inference_resoning_check.py'\n",
+        "python '/home/mshahidul/readctrl/code/readability_control.py'"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": 3,
+      "id": "78187940",
+      "metadata": {},
+      "outputs": [
+        {
+          "name": "stdout",
+          "output_type": "stream",
+          "text": [
+            "dict_keys(['id', 'fulltext', 'fulltext_subclaims', 'summary', 'summary_subclaims'])\n"
+          ]
+        }
+      ],
+      "source": [
+        "# /home/mshahidul/readctrl/data/synthetic_dataset_diff_labels/syn_data_with_gs_summary_en.json\n",
+        "import json\n",
+        "with open('/home/mshahidul/readctrl/data/extracting_subclaim/extracted_subclaims_multiclinsum_test_en_0_500.json', 'r') as f:\n",
+        "    synthetic_data_with_gs_summary_en = json.load(f)\n",
+        "print((synthetic_data_with_gs_summary_en)[0].keys())"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": 8,
+      "id": "ebd39c1c",
+      "metadata": {},
+      "outputs": [],
+      "source": [
+        "# /home/mshahidul/readctrl/data/synthetic_dataset_diff_labels/syn_data_with_gs_summary_en.json\n",
+        "import json\n",
+        "full_data=[]\n",
+        "with open('/home/mshahidul/readctrl/data/synthetic_dataset_diff_labels/syn_data_with_gs_summary_en.json', 'r') as f:\n",
+        "    synthetic_data_with_gs_summary_en = json.load(f)\n",
+        "for item in synthetic_data_with_gs_summary_en:\n",
+        "    gold_summary = item['summary']\n",
+        "    fulltext = item['fulltext']\n",
+        "    evaluation = json.dumps(item['diff_label_texts'], ensure_ascii=False)\n",
+        "    readability_generation_prompt_data = readability_generation(\n",
+        "        gold_summary,\n",
+        "        fulltext,\n",
+        "        evaluation\n",
+        "    )\n",
+        "    full_data.append(readability_generation_prompt_data)\n",
+        "with open('/home/mshahidul/readctrl/data/finetuning_data/training_data_readability_data_generation.json', 'w') as outfile:\n",
+        "    json.dump(full_data, outfile, indent=2,ensure_ascii=False)"
+      ]
+    },
+    {
+      "cell_type": "markdown",
+      "id": "e71801a1",
+      "metadata": {},
+      "source": [
+        "# Training prompt for attribution training "
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": null,
+      "id": "db70f9cd",
+      "metadata": {
+        "vscode": {
+          "languageId": "ruby"
+        }
+      },
+      "outputs": [],
+      "source": [
+        "import json\n",
+        "def build_single_subclaim_conversation(\n",
+        "    reference_full_text,\n",
+        "    generated_summary,\n",
+        "    subclaim_id,\n",
+        "    subclaim_text,\n",
+        "    subclaim_result,\n",
+        "    difficulty_level,\n",
+        "    evaluation\n",
+        "):\n",
+        "    \"\"\"\n",
+        "    Create a fine‑tuning conversation entry for a single subclaim.\n",
+        "\n",
+        "    Args:\n",
+        "        reference_full_text (str): Source article/reference text.\n",
+        "        generated_summary (str): Summary generated for evaluation.\n",
+        "        subclaim_id (int or str): Unique identifier of this subclaim.\n",
+        "        subclaim_text (str): Subclaim content.\n",
+        "        subclaim_result (int): 1 (supported) or 0 (unsupported).\n",
+        "        difficulty_level (str): 'easy', 'intermediate', or 'hard'.\n",
+        "        evaluation (dict): Target labeled response (reasonableness + justification).\n",
+        "\n",
+        "    Returns:\n",
+        "        dict: One training example formatted for chat‑style fine‑tuning.\n",
+        "    \"\"\"\n",
+        "\n",
+        "    system_prompt = f\"\"\"\n",
+        "### **SYSTEM / ROLE INSTRUCTION**\n",
+        "\n",
+        "You are a **medical factuality and attribution evaluator**.\n",
+        "You will assess the following subclaim from a generated summary.\n",
+        "\n",
+        "The `\"result\"` attribute indicates factual support:\n",
+        "- `1` → Supported by the reference text (no evaluation required)\n",
+        "- `0` → Unsupported; requires assessing reasonableness based on the readability level (*easy / intermediate / hard*).\n",
+        "\n",
+        "Your goal: decide whether the **unsupported subclaim (result=0)** is a reasonable simplification or an inaccurate addition.\n",
+        "\n",
+        "---\n",
+        "\n",
+        "### **READABILITY & ATTRIBUTION GUIDELINES**\n",
+        "\n",
+        "| Level | Audience | Linguistic & Stylistic Profile | Allowable Additions |\n",
+        "| :-- | :-- | :-- | :-- |\n",
+        "| **Easy (FH 70–100)** | General public | Very simple and concrete | Only broad clarifications; no new medical facts |\n",
+        "| **Intermediate (FH 50–69)** | Educated layperson | Moderate complexity | Limited explanatory additions consistent with text |\n",
+        "| **Hard (FH 0–49)** | Professionals | Formal, technical | Must stay fully evidence‑grounded |\n",
+        "\n",
+        "---\n",
+        "\n",
+        "### **Input**\n",
+        "Readability Level: {difficulty_level}\n",
+        "\n",
+        "Reference Full Text:\n",
+        "{reference_full_text}\n",
+        "\n",
+        "Generated Summary:\n",
+        "{generated_summary}\n",
+        "\n",
+        "Subclaim Info:\n",
+        "{{\n",
+        "  \"subclaim_id\": {subclaim_id},\n",
+        "  \"subclaim\": \"{subclaim_text}\",\n",
+        "  \"result\": {subclaim_result}\n",
+        "}}\n",
+        "\n",
+        "---\n",
+        "\n",
+        "### **TASK INSTRUCTIONS**\n",
+        "\n",
+        "- If `\"result\": 1\"`, respond with **\"not_applicable\"** and a short note like *\"supported, no evaluation required.\"*\n",
+        "- If `\"result\": 0\"`, classify as:\n",
+        "  - `\"reasonable\"` – legitimate simplification consistent with readability\n",
+        "  - `\"partially_reasonable\"` – neutral or harmless addition\n",
+        "  - `\"unreasonable\"` – misleading or speculative content\n",
+        "\n",
+        "Always include a brief justification (1–2 sentences).\n",
+        "\n",
+        "---\n",
+        "\n",
+        "### **Output JSON Format**\n",
+        "\n",
+        "```json\n",
+        "{{\n",
+        "  \"evaluation\": {{\n",
+        "    \"subclaim_id\": {subclaim_id},\n",
+        "    \"subclaim\": \"{subclaim_text}\",\n",
+        "    \"result\": {subclaim_result},\n",
+        "    \"reasonableness\": \"<reasonable | partially_reasonable | unreasonable | not_applicable>\",\n",
+        "    \"justification\": \"<short explanation or 'supported, no evaluation required'>\"\n",
+        "  }}\n",
+        "}}\n",
+        "\"\"\".strip()\n",
+        "\n",
+        "# ---- format the example as a conversation pair ----\n",
+        "    conversation = {\n",
+        "        \"conversations\": [\n",
+        "            {\"from\": \"user\", \"content\": system_prompt},\n",
+        "            {\"from\": \"assistant\", \"content\": json.dumps(evaluation, ensure_ascii=False, indent=2)}\n",
+        "        ]\n",
+        "    }\n",
+        "\n",
+        "    return conversation"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": 2,
+      "id": "f92974f0",
+      "metadata": {
+        "vscode": {
+          "languageId": "ruby"
+        }
+      },
+      "outputs": [],
+      "source": [
+        "# /home/mshahidul/readctrl/data/synthetic_dataset_diff_labels/syn_data_diff_labels_en_0_20.json\n",
+        "full_data=[]\n",
+        "import json\n",
+        "with open('/home/mshahidul/readctrl/data/synthetic_dataset_diff_labels/syn_data_diff_labels_en_0_20.json', 'r') as f:\n",
+        "    data = json.load(f)\n",
+        "    full_data.extend(data)\n",
+        "with open('/home/mshahidul/readctrl/data/synthetic_dataset_diff_labels/syn_data_diff_labels_en_20_67.json', 'r') as f:\n",
+        "    data = json.load(f)\n",
+        "    full_data.extend(data)\n",
+        "with open('/home/mshahidul/readctrl/data/synthetic_dataset_diff_labels/syn_data_diff_labels_en_67_80.json', 'r') as f:\n",
+        "    data = json.load(f)\n",
+        "    full_data.extend(data)"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": 4,
+      "id": "37e21c6f",
+      "metadata": {
+        "vscode": {
+          "languageId": "ruby"
+        }
+      },
+      "outputs": [],
+      "source": [
+        "with open('/home/mshahidul/readctrl/data/synthetic_dataset_diff_labels/syn_data_diff_labels_en_0_80_full.json', 'w') as f:\n",
+        "    json.dump(full_data, f, indent=2,ensure_ascii=False)"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": null,
+      "id": "ddd2d6f2",
+      "metadata": {
+        "vscode": {
+          "languageId": "ruby"
+        }
+      },
+      "outputs": [],
+      "source": [
+        "# def build_single_subclaim_conversation(\n",
+        "#     reference_full_text,\n",
+        "#     generated_summary,\n",
+        "#     subclaim_id,\n",
+        "#     subclaim_text,\n",
+        "#     subclaim_result,\n",
+        "#     difficulty_level,\n",
+        "#     evaluation\n",
+        "# )\n",
+        "# demo testing\n",
+        "p=build_single_subclaim_conversation(\n",
+        "    \"This is the full text of the reference article.\",\n",
+        "    \"This is the generated summary.\",\n",
+        "    1234,\n",
+        "    \"This is the subclaim being evaluated.\",\n",
+        "    1,\n",
+        "    \"easy\",\n",
+        "    {\n",
+        "        \"reasonableness\": \"reasonable\",\n",
+        "        \"justification\": \"The subclaim is a permissible simplification.\"\n",
+        "    }\n",
+        ")"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": null,
+      "id": "89951e90",
+      "metadata": {
+        "vscode": {
+          "languageId": "ruby"
+        }
+      },
+      "outputs": [],
+      "source": [
+        "print(p['conversations'][0]['content'])"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": null,
+      "id": "8918f214",
+      "metadata": {
+        "vscode": {
+          "languageId": "ruby"
+        }
+      },
+      "outputs": [],
+      "source": [
+        "file_synth = \"/home/mshahidul/readctrl/data/training_data_subclaim_verifier/synthetic_data_es_subclaims_100.json\"\n",
+        "file_qwen_results = \"/home/mshahidul/readctrl/results/dataset_quality_check/subclaim_verifier_results_100_qwen3-32B.json\"\n",
+        "main_dataset=\"/home/mshahidul/readctrl/results/dataset_quality_check/syn_attribution_resonability_check_100_gpt5_train_v2.json\"\n",
+        "save_path = \"/home/mshahidul/readctrl/results/dataset_quality_check/syn_attribution_resonability_check_30_gpt5_train_prompt.json\"\n",
+        "\n",
+        "with open(file_synth, 'r') as f:\n",
+        "    synthetic_data = json.load(f)\n",
+        "with open(file_qwen_results, 'r') as f:\n",
+        "    qwen3_32B_results = json.load(f) \n",
+        "with open(main_dataset, 'r') as f:\n",
+        "    main_data = json.load(f)\n",
+        "ref_summaries={}\n",
+        "fulltexts={}\n",
+        "generated_summaries={}\n",
+        "for item in synthetic_data:\n",
+        "    reference_summary = item['ref_summary']['text']\n",
+        "    ref_summaries[item['id']] = reference_summary\n",
+        "    full_text = item['full_text']\n",
+        "    fulltexts[item['id']] = full_text\n",
+        "    for version in ['easy', 'intermediate', 'hard']:\n",
+        "        gen_summary = item['readability_versions'][version]['text']\n",
+        "        generated_summaries[(item['id'], version)] = gen_summary\n",
+        "full_training_data=[]\n",
+        "for item in main_data:\n",
+        "    ref_summary = ref_summaries[item['id']]\n",
+        "    fulltext = fulltexts[item['id']]\n",
+        "    generated_summary = generated_summaries[(item['id'], item['difficulty_level'])]\n",
+        "    results=item['response']['evaluations']\n",
+        "    for eval_item in results:\n",
+        "        training_prompt_data = build_single_subclaim_conversation(\n",
+        "            ref_summary,\n",
+        "            generated_summary,\n",
+        "            eval_item['subclaim_id'],\n",
+        "            eval_item['subclaim'],\n",
+        "            eval_item['result'],\n",
+        "            item['difficulty_level'],\n",
+        "            {\n",
+        "                \"reasonableness\": eval_item['reasonableness'],\n",
+        "                \"justification\": eval_item['justification']\n",
+        "            }\n",
+        "        )\n",
+        "        full_training_data.append(training_prompt_data)\n",
+        "with open(save_path, 'w') as f:\n",
+        "    json.dump(full_training_data, f, indent=2)\n",
+        "\n"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": null,
+      "id": "06be4f7a",
+      "metadata": {
+        "vscode": {
+          "languageId": "ruby"
+        }
+      },
+      "outputs": [],
+      "source": [
+        "print(full_training_data[0]['conversations'][0]['content'])"
+      ]
+    },
+    {
+      "cell_type": "markdown",
+      "id": "e62306ed",
+      "metadata": {},
+      "source": [
+        "# data cleaning"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": null,
+      "id": "3d26ce59",
+      "metadata": {},
+      "outputs": [],
+      "source": [
+        "import os, json, re\n",
+        "\n",
+        "results_dir = \"/home/mshahidul/LLM_guard/results/sub_questions_answers/sub_questions_answers_llama31_8B\"\n",
+        "results_dir_mod = \"/home/mshahidul/LLM_guard/results/sub_questions_answersV2/sub_questions_answers_llama31_8B\"\n",
+        "os.makedirs(results_dir_mod, exist_ok=True)\n",
+        "\n",
+        "results_json_files = [f for f in os.listdir(results_dir) if f.endswith('.json')]\n",
+        "\n",
+        "results_data = []\n",
+        "\n",
+        "def safe_json_loads(text):\n",
+        "    \"\"\"Try multiple ways to parse a possibly broken JSON string.\"\"\"\n",
+        "    if not isinstance(text, str):\n",
+        "        return text\n",
+        "\n",
+        "    # 1️⃣ Remove control characters\n",
+        "    cleaned = re.sub(r'[\\x00-\\x1F\\x7F]', '', text)\n",
+        "\n",
+        "    # 2️⃣ Escape newlines and ensure proper quotes\n",
+        "    cleaned = cleaned.replace('\\n', '\\\\n').replace('\\r', '\\\\r')\n",
+        "\n",
+        "    # 3️⃣ Try direct JSON parsing\n",
+        "    try:\n",
+        "        return json.loads(cleaned)\n",
+        "    except json.JSONDecodeError:\n",
+        "        pass\n",
+        "\n",
+        "    # 4️⃣ Try stripping outer braces/spaces and retry\n",
+        "    try:\n",
+        "        cleaned2 = cleaned.strip()\n",
+        "        if cleaned2.startswith(\"{\") and cleaned2.endswith(\"}\"):\n",
+        "            inner = cleaned2[1:-1].strip()\n",
+        "            if inner.startswith('\"answer\":'):\n",
+        "                inner = '{' + inner + '}'\n",
+        "            return json.loads(inner)\n",
+        "    except json.JSONDecodeError:\n",
+        "        pass\n",
+        "\n",
+        "    # 5️⃣ Last fallback: wrap it as plain text JSON\n",
+        "    return {\"answer\": cleaned.strip()}\n",
+        "\n",
+        "\n",
+        "for file in results_json_files:\n",
+        "    path = os.path.join(results_dir, file)\n",
+        "    with open(path, 'r') as f:\n",
+        "        data = json.load(f)\n",
+        "\n",
+        "    sub_questions_answers = data['sub_questions_answers']\n",
+        "    new_data = []\n",
+        "\n",
+        "    for item in sub_questions_answers:\n",
+        "        sub_q = item.get('sub_question', '')\n",
+        "        sub_a_raw = item.get('sub_answer', '')\n",
+        "\n",
+        "        try:\n",
+        "            parsed = safe_json_loads(sub_a_raw)\n",
+        "        except Exception as e:\n",
+        "            print(f\"⚠️ Still bad entry in {file}: {e}\")\n",
+        "            print(f\"  Sub-question: {sub_q[:100]}\")\n",
+        "            print(f\"  Raw answer preview: {sub_a_raw[:200]}\")\n",
+        "            continue\n",
+        "\n",
+        "        new_data.append({\n",
+        "            \"sub_question\": sub_q,\n",
+        "            \"sub_answer\": parsed,\n",
+        "        })\n",
+        "\n",
+        "    results_data.append({\n",
+        "        \"id\": data['id'],\n",
+        "        \"sub_questions_answers\": new_data,\n",
+        "    })\n",
+        "\n",
+        "# Optionally save the cleaned output\n",
+        "output_path = os.path.join(results_dir_mod, \"sub_questions_answers_llama31_8B.json\")\n",
+        "with open(output_path, 'w') as f:\n",
+        "    json.dump(results_data, f, indent=2)\n",
+        "\n",
+        "print(f\"✅ Cleaned data saved to: {output_path}\")\n"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": null,
+      "id": "493028e3",
+      "metadata": {},
+      "outputs": [],
+      "source": [
+        "phi4_results_dir = \"/home/mshahidul/LLM_guard/results/sub_questions_answers/sub_questions_answers_phi4\"\n",
+        "phi4_json_files = [f for f in os.listdir(phi4_results_dir) if f.endswith('.json')]\n",
+        "\n",
+        "phi4_results_data = []\n",
+        "for file in phi4_json_files:\n",
+        "    with open(os.path.join(phi4_results_dir, file), 'r') as f:\n",
+        "        data = json.load(f)\n",
+        "        new_data=[]\n",
+        "        for item in data['sub_questions_answers']:\n",
+        "            sub_answer=item.get('sub_answer', {}).split(\"assistant\")[2].strip()\n",
+        "            new_data.append({\n",
+        "                \"sub_question\": item.get('sub_question', ''),\n",
+        "                \"sub_answer\": sub_answer,\n",
+        "            })\n",
+        "        phi4_results_data.append({\n",
+        "            \"id\": data['id'],\n",
+        "            \"sub_questions_answers\": new_data,\n",
+        "        })\n",
+        "output_path = os.path.join(results_dir_mod, \"sub_questions_answers_phi4.json\")\n",
+        "with open(output_path, 'w') as outfile:\n",
+        "    json.dump(phi4_results_data, outfile, indent=2)"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": null,
+      "id": "814707ed",
+      "metadata": {},
+      "outputs": [],
+      "source": [
+        "qwen3_14B_results_dir = \"/home/mshahidul/LLM_guard/results/sub_questions_answers/sub_questions_answers_qwen3_14B\"\n",
+        "results_dir_mod = \"/home/mshahidul/LLM_guard/results/sub_questions_answersV2\"\n",
+        "qwen3_14B_json_files = [f for f in os.listdir(qwen3_14B_results_dir) if f.endswith('.json')]\n",
+        "\n",
+        "qwen3_14B_results_data = []\n",
+        "for file in qwen3_14B_json_files:\n",
+        "    with open(os.path.join(qwen3_14B_results_dir, file), 'r') as f:\n",
+        "        data = json.load(f)\n",
+        "        new_data=[]\n",
+        "        for item in data['sub_questions_answers']:\n",
+        "            sub_answer=item.get('sub_answer', {})\n",
+        "            new_data.append({\n",
+        "                \"sub_question\": (item.get('sub_question', '')),\n",
+        "                \"sub_answer\": json.loads(item.get('sub_answer', ''))['answer'],\n",
+        "            })\n",
+        "        qwen3_14B_results_data.append({\n",
+        "            \"id\": data['id'],\n",
+        "            \"sub_questions_answers\": new_data,\n",
+        "        })\n",
+        "output_path = os.path.join(results_dir_mod, \"sub_questions_answers_qwen3_14B.json\")\n",
+        "with open(output_path, 'w') as outfile:\n",
+        "    json.dump(qwen3_14B_results_data, outfile, indent=2)"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": null,
+      "id": "2acf245e",
+      "metadata": {},
+      "outputs": [],
+      "source": [
+        "with open('/home/mshahidul/LLM_guard/results/sub_questions_answersV2/sub_questions_answers_qwen3_14B.json', 'r') as f:\n",
+        "    qwen3_14B_data = json.load(f)\n",
+        "qwen3_14B_data[4]"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": null,
+      "id": "1d787193",
+      "metadata": {},
+      "outputs": [],
+      "source": [
+        "llama=\"/home/mshahidul/LLM_guard/results/sub_questions_answersV2/sub_questions_answers_llama31_8B.json\"\n",
+        "phi=\"/home/mshahidul/LLM_guard/results/sub_questions_answersV2/sub_questions_answers_phi4.json\"\n",
+        "qwen=\"/home/mshahidul/LLM_guard/results/sub_questions_answersV2/sub_questions_answers_qwen3_14B.json\"\n",
+        "with open(llama, 'r') as f:\n",
+        "    llama_data = json.load(f)\n",
+        "with open(phi, 'r') as f:\n",
+        "    phi_data = json.load(f)\n",
+        "with open(qwen, 'r') as f:\n",
+        "    qwen_data = json.load(f)\n"
+      ]
+    },
+    {
+      "cell_type": "markdown",
+      "id": "3e1df02c",
+      "metadata": {},
+      "source": [
+        "- Answer each subquestion individually.\n",
+        "\n",
+        "- Combine the individual answers into a single, consolidated response.\n",
+        "\n",
+        "- Ask the LLM to evaluate whether the consolidated response is reasonable.\n",
+        "\n",
+        "- Receive the LLM's judgment: “Use one LLM answer for those subquestions.”"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": null,
+      "id": "af66abbe",
+      "metadata": {},
+      "outputs": [],
+      "source": [
+        "with open('/home/mshahidul/LLM_guard/results/attach_success_failure/attach_success_failure_phi4_14B.json', 'r') as f:\n",
+        "    attach_phi4_14B_data = json.load(f)\n",
+        "successful_cases = 0\n",
+        "for item in attach_phi4_14B_data:\n",
+        "    if item[\"evaluation\"] == \"1\":\n",
+        "        successful_cases += 1\n",
+        "print(f\"Total successful cases in attach_success_failure_phi4_14B: {successful_cases} out of {len(attach_phi4_14B_data)}\")"
+      ]
+    },
+    {
+      "cell_type": "markdown",
+      "id": "14b88565",
+      "metadata": {},
+      "source": [
+        "# reasonability check"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": null,
+      "id": "6617aa9e",
+      "metadata": {},
+      "outputs": [],
+      "source": [
+        "def return_promptst(reference_summary, generated_summary, subclaims_json, difficulty_level):\n",
+        "    prompt=f'''\n",
+        "            **SYSTEM / ROLE INSTRUCTION:**\n",
+        "            You are a **medical readability evaluator**.\n",
+        "            Your task is to judge whether omitted subclaims (those with `\"result\": 0\"`) from a generated summary are *reasonably omitted* based on the intended **readability level**: *easy*, *intermediate*, or *hard*.\n",
+        "            You evaluate this from the standpoint of clarity, faithfulness, and readability goals.\n",
+        "\n",
+        "            ---\n",
+        "\n",
+        "            ### **READABILITY GUIDELINES**\n",
+        "\n",
+        "            | Level            | Target Audience                          | Content Expectation                                             | Technical Detail Allowed                                         |\n",
+        "            | :--------------- | :--------------------------------------- | :-------------------------------------------------------------- | :--------------------------------------------------------------- |\n",
+        "            | **Easy**         | General public                           | Focus on main events, outcomes, and diagnoses in plain Spanish. | Minimal — avoid measurements, anatomy, and test results.         |\n",
+        "            | **Intermediate** | Educated lay readers or medical students | Include key findings and procedures in simplified form.         | Moderate — basic terms and causes allowed.                       |\n",
+        "            | **Hard**         | Medical professionals                    | Retain most technical information and precision.                | High — measurements, anatomy, and test interpretations expected. |\n",
+        "\n",
+        "            ---\n",
+        "\n",
+        "            ### **INPUT FIELDS**\n",
+        "\n",
+        "            **Reference summary:**\n",
+        "            {reference_summary}\n",
+        "\n",
+        "            **Generated summary ({difficulty_level}):**\n",
+        "            {generated_summary}\n",
+        "\n",
+        "            **Subclaims and results:**\n",
+        "            {subclaims_json}\n",
+        "\n",
+        "            ---\n",
+        "\n",
+        "            ### **TASK INSTRUCTIONS**\n",
+        "\n",
+        "            1. Focus on subclaims with `\"result\": 0\"` (not supported by the generated summary).\n",
+        "            2. For each omitted subclaim:\n",
+        "\n",
+        "            * Decide whether omission is **reasonable** given the readability level.\n",
+        "            * Label as: `\"yes\"`, `\"no\"`, or `\"borderline\"`.\n",
+        "            * Write a brief justification (1–2 sentences).\n",
+        "            3. After individual evaluations, assign a **reasonableness score (0–5)** using this scale:\n",
+        "\n",
+        "            * **5** = All omissions appropriate for target readability.\n",
+        "            * **4** = Minor omissions could improve completeness.\n",
+        "            * **3** = Some omissions reduce understanding or medical clarity.\n",
+        "            * **2** = Many important omissions harm faithfulness.\n",
+        "            * **1** = Major omissions misrepresent case.\n",
+        "            * **0** = Summary fails to reflect key medical information.\n",
+        "            4. End with an **overall explanation (3–5 sentences)** describing:\n",
+        "\n",
+        "            * The main reasoning behind the score.\n",
+        "            * Whether the summary fits its intended readability level.\n",
+        "            * Suggestions for improvement if needed.\n",
+        "\n",
+        "            ---\n",
+        "\n",
+        "            ### **OUTPUT FORMAT (strict JSON)**\n",
+        "\n",
+        "            ```json\n",
+        "            {{\n",
+        "            \"evaluation_table\": [\n",
+        "                {{\n",
+        "                \"id\": <subclaim_id>,\n",
+        "                \"subclaim\": \"<text>\",\n",
+        "                \"reasonable_omission\": \"<yes | no | borderline>\",\n",
+        "                \"explanation\": \"<short reason>\"\n",
+        "                }}\n",
+        "            ],\n",
+        "            \"reasonableness_score\": <0-5>,\n",
+        "            \"overall_explanation\": \"<concise paragraph>\"\n",
+        "            }}\n",
+        "            ```\n",
+        "            '''\n",
+        "    return prompt"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": null,
+      "id": "e0157715",
+      "metadata": {},
+      "outputs": [],
+      "source": [
+        "from openai import OpenAI\n",
+        "\n",
+        "file_path = \"/home/mshahidul/api_new.json\"\n",
+        "with open(file_path, \"r\") as file:\n",
+        "    api_keys = json.load(file)\n",
+        "\n",
+        "openai_api_key = api_keys.get(\"openai\")\n",
+        "\n",
+        "client = OpenAI(api_key=openai_api_key)\n",
+        "def openai_return(prompt):\n",
+        "    response = client.chat.completions.create(\n",
+        "        model=\"gpt-5-mini\",\n",
+        "        messages=[\n",
+        "            {\"role\": \"system\", \"content\": \"You are a helpful assistant.\"},\n",
+        "            {\"role\": \"user\", \"content\": prompt}\n",
+        "        ]\n",
+        "    )\n",
+        "    cleaned_response = response.choices[0].message.content.strip().replace(\"```json\", \"\").replace(\"```\", \"\")\n",
+        "    return json.loads(cleaned_response)"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": null,
+      "id": "8469089e",
+      "metadata": {},
+      "outputs": [],
+      "source": [
+        "import json\n",
+        "file_path = \"/home/mshahidul/readctrl/data/training_data_subclaim_verifier/synthetic_data_es_subclaims_100.json\"\n",
+        "\n",
+        "with open(file_path, 'r') as f:\n",
+        "    synthetic_data = json.load(f)\n",
+        "\n",
+        "synthetic_data[0].keys()"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": null,
+      "id": "e878c58e",
+      "metadata": {},
+      "outputs": [],
+      "source": [
+        "file_path_qwen3_32B = \"/home/mshahidul/readctrl/results/dataset_quality_check/subclaim_verifier_results_100_qwen3-32B.json\"\n",
+        "\n",
+        "with open(file_path_qwen3_32B, 'r') as f:\n",
+        "    qwen3_32B_results = json.load(f)\n",
+        "\n",
+        "# print(qwen3_32B_results[0]['completeness']['results'])\n",
+        "print(qwen3_32B_results[0].keys())\n",
+        "print(qwen3_32B_results[0]['completeness']['results'])"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": null,
+      "id": "c7306023",
+      "metadata": {},
+      "outputs": [],
+      "source": [
+        "# dict_keys(['id', 'full_text', 'ref_summary', 'readability_versions'])\n",
+        "# print(f\"Full text: {synthetic_data[0]['full_text']}\")\n",
+        "res=[]\n",
+        "save_path = \"/home/mshahidul/readctrl/results/dataset_quality_check/resonability_check_100_gpt5.json\"\n",
+        "if os.path.exists(save_path):\n",
+        "    with open(save_path, 'r') as f:\n",
+        "        res = json.load(f)\n",
+        "print(f\"Resuming from {len(res)} entries\")\n",
+        "import tqdm\n",
+        "for ind in tqdm.tqdm(range(0,100)):\n",
+        "    for version in [\"easy\", \"intermediate\", \"hard\"]:\n",
+        "        ref_summary = (f\"{synthetic_data[ind]['ref_summary']['text']}\")\n",
+        "        generated_summary = (f\"{synthetic_data[ind]['readability_versions'][version]['text']}\")\n",
+        "        subclaims_results = (f\"{qwen3_32B_results[ind]['completeness']['results']}\")\n",
+        "        prompt = return_promptst(ref_summary, generated_summary, subclaims_results, version)\n",
+        "        res.append({\n",
+        "            \"id\": synthetic_data[ind]['id'],\n",
+        "            \"difficulty_level\": version,\n",
+        "            \"prompt\": openai_return(prompt)\n",
+        "        })\n",
+        "        if len(res)%2==0:\n",
+        "            print(f\"Completed {len(res)} out of 300\")\n",
+        "            with open(save_path, 'w') as outfile:\n",
+        "                json.dump(res, outfile, indent=2)\n",
+        "        # print(prompt)\n",
+        "        # assert False\n",
+        "with open(save_path, 'w') as outfile:\n",
+        "    json.dump(res, outfile, indent=2)"
+      ]
+    },
+    {
+      "cell_type": "markdown",
+      "id": "62975fd6",
+      "metadata": {},
+      "source": [
+        "# updated statistics"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": null,
+      "id": "c837c69c",
+      "metadata": {},
+      "outputs": [],
+      "source": [
+        "resonability_data[0].keys()"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": null,
+      "id": "9a1e45ee",
+      "metadata": {},
+      "outputs": [],
+      "source": [
+        "resonability_data[0]['prompt'].keys()"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": null,
+      "id": "23ec58b5",
+      "metadata": {},
+      "outputs": [],
+      "source": []
+    },
+    {
+      "cell_type": "code",
+      "execution_count": null,
+      "id": "b152d3d6",
+      "metadata": {},
+      "outputs": [],
+      "source": [
+        "import json\n",
+        "with open('/home/mshahidul/readctrl/results/dataset_quality_check/resonability_check_100_gpt5.json', 'r') as f:\n",
+        "    resonability_data = json.load(f)\n",
+        "dict1={}\n",
+        "for item in resonability_data:\n",
+        "    for eval in item['prompt']['evaluation_table']:\n",
+        "        dict1[(item['id'], item['difficulty_level'], eval['id'])]= 0 if eval['reasonable_omission']==\"no\" else 1"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": null,
+      "id": "360e5539",
+      "metadata": {
+        "vscode": {
+          "languageId": "ruby"
+        }
+      },
+      "outputs": [],
+      "source": [
+        "file_path_qwen3_32B = \"/home/mshahidul/readctrl/results/dataset_quality_check/subclaim_verifier_results_100_qwen3-32B.json\"\n",
+        "\n",
+        "with open(file_path_qwen3_32B, 'r') as f:\n",
+        "    qwen3_32B_results = json.load(f)\n",
+        "success=0\n",
+        "acc=0\n",
+        "success_full=[]\n",
+        "for item in qwen3_32B_results:\n",
+        "    success=0\n",
+        "    total=0\n",
+        "    for eval in item['completeness']['results']:\n",
+        "        key = (item['id'], item['version'], eval['subclaim']['id'])\n",
+        "        if eval.get('result')!=None:\n",
+        "            total+=1\n",
+        "            if eval['result']==\"1\":\n",
+        "                success+=1\n",
+        "            elif dict1.get(key)!=None:\n",
+        "                success+=dict1.get(key)\n",
+        "    success_full.append({\n",
+        "        \"id\": item['id'],\n",
+        "        \"version\": item['version'],\n",
+        "        \"total_subclaims\": len(item['completeness']['results']),\n",
+        "        \"successful_subclaims\": success/total\n",
+        "    })"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": null,
+      "id": "7ee44884",
+      "metadata": {
+        "vscode": {
+          "languageId": "ruby"
+        }
+      },
+      "outputs": [],
+      "source": [
+        "success_full"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": null,
+      "id": "93019187",
+      "metadata": {},
+      "outputs": [],
+      "source": [
+        "label_accuracy = {}\n",
+        "for version in [\"easy\", \"intermediate\", \"hard\"]:\n",
+        "    for item in success_full:\n",
+        "        if item['version'] == version:\n",
+        "            label_accuracy[version] = label_accuracy.get(version, 0) + item['successful_subclaims']\n",
+        "for version in label_accuracy:\n",
+        "    label_accuracy[version] = label_accuracy[version] / (100) \n",
+        "    print(f\"{version}: {label_accuracy[version]*100:.2f}%\") \n"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": null,
+      "id": "6f4e15a0",
+      "metadata": {},
+      "outputs": [],
+      "source": [
+        "import json\n",
+        "\n",
+        "file_path = \"/home/mshahidul/LLM_guard/data/synthetic_best_ans_selection_qwen25-32B.json\"\n",
+        "\n",
+        "with open(file_path, 'r') as f:\n",
+        "    synthetic_best_ans_data = json.load(f)\n",
+        "\n",
+        "print(synthetic_best_ans_data[3])  # Print the first entry for inspection"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": null,
+      "id": "947b453d",
+      "metadata": {},
+      "outputs": [],
+      "source": [
+        "# /home/mshahidul/readctrl/data/raw_data/en_test/multiclinsum_test_en/fulltext read\n",
+        "import os\n",
+        "all_data = []\n",
+        "lang=\"pt\"\n",
+        "for path in os.listdir(f'/home/mshahidul/readctrl/data/raw_data/{lang}_test/multiclinsum_test_{lang}/fulltext'):\n",
+        "        with open(os.path.join(f'/home/mshahidul/readctrl/data/raw_data/{lang}_test/multiclinsum_test_{lang}/fulltext', path), 'r') as f:\n",
+        "            fulltext = f.read()\n",
+        "        path2=path.replace(f\"_{lang}\", f\"_{lang}_sum\")\n",
+        "        with open(os.path.join(f'/home/mshahidul/readctrl/data/raw_data/{lang}_test/multiclinsum_test_{lang}/summaries', path2), 'r') as f:\n",
+        "            summary = f.read()\n",
+        "        all_data.append({\n",
+        "            \"id\": path,\n",
+        "            \"fulltext\": fulltext,\n",
+        "            \"summary\": summary\n",
+        "        })       \n",
+        "with open(f'/home/mshahidul/readctrl/data/processed_raw_data/multiclinsum_test_{lang}.json', 'w') as outfile:\n",
+        "    json.dump(all_data, outfile, indent=2) \n"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": null,
+      "id": "bb375fa2",
+      "metadata": {},
+      "outputs": [],
+      "source": [
+        "import pandas as pd\n",
+        "import json\n",
+        "\n",
+        "# Load your data\n",
+        "with open('/home/mshahidul/readctrl/data/classified_readability/classified_multiclinsum_test_en.json', 'r') as f:\n",
+        "    data = json.load(f)\n",
+        "\n",
+        "df = pd.DataFrame(data)\n",
+        "\n",
+        "# Define the bins and labels for Option 1\n",
+        "# Bins: 0-2 (Easy), 2-3 (Medium), 3-5 (Hard)\n",
+        "bins = [0, 2, 3, 5]\n",
+        "labels = ['Easy', 'Medium', 'Hard']\n",
+        "\n",
+        "df['readability_level'] = pd.cut(df['readability_score'], bins=bins, labels=labels)\n",
+        "\n",
+        "print(df[['readability_score', 'readability_level']].head())"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": null,
+      "id": "782de099",
+      "metadata": {},
+      "outputs": [],
+      "source": [
+        "import pandas as pd\n",
+        "import json\n",
+        "\n",
+        "# 1. Load the dataset\n",
+        "# Update the filename if it is in your current directory\n",
+        "file_path = '/home/mshahidul/readctrl/data/classified_readability/classified_multiclinsum_test_en.json' \n",
+        "\n",
+        "with open(file_path, 'r') as f:\n",
+        "    data = json.load(f)\n",
+        "\n",
+        "df = pd.DataFrame(data)\n",
+        "\n",
+        "# 2. Inspect the current distribution to decide on the best strategy\n",
+        "print(\"Current Score Distribution:\")\n",
+        "print(df['readability_score'].value_counts().sort_index())\n",
+        "\n",
+        "# 3. Apply the Balanced Split (Strategy 1)\n",
+        "def categorize_readability(score):\n",
+        "    if score <= 2:\n",
+        "        return 'Easy'\n",
+        "    elif score == 3:\n",
+        "        return 'Medium'\n",
+        "    else:\n",
+        "        return 'Hard'\n",
+        "\n",
+        "df['readability_type'] = df['readability_score'].apply(categorize_readability)\n",
+        "\n",
+        "# 4. Save the results\n",
+        "df.to_csv('classified_readability_results.csv', index=False)\n",
+        "print(\"\\nTransformation complete. New categories:\")\n",
+        "print(df['readability_type'].value_counts())"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": null,
+      "id": "e4e582a2",
+      "metadata": {},
+      "outputs": [],
+      "source": [
+        "python /home/mshahidul/readctrl/code/finetune-inference/inference_extract_subclaims_v3.py --input_file /home/mshahidul/readctrl/data/classified_readability/classified_multiclinsum_test_en.json"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": null,
+      "id": "7c2df145",
+      "metadata": {},
+      "outputs": [],
+      "source": [
+        "# /home/mshahidul/readctrl/data/extracting_subclaim/extracted_subclaims_classified_multiclinsum_test_en_en.json read\n",
+        "with open('/home/mshahidul/readctrl/data/reasoning/refined_evaluated_support_0_100_qwen3-32B.json', 'r') as f:\n",
+        "    extracted_subclaims_data = json.load(f)\n",
+        "# print(len(extracted_subclaims_data))\n",
+        "print(extracted_subclaims_data[0]['subclaim_evaluations'][0].keys())"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": null,
+      "id": "adb6ed8f",
+      "metadata": {},
+      "outputs": [],
+      "source": []
+    },
+    {
+      "cell_type": "code",
+      "execution_count": 5,
+      "id": "fdd516da",
+      "metadata": {},
+      "outputs": [
+        {
+          "name": "stdout",
+          "output_type": "stream",
+          "text": [
+            "dict_keys(['index', 'id', 'fulltext', 'fulltext_subclaims', 'summary', 'summary_subclaims', 'diff_label_texts', 'diff_label_subclaims', 'readability_score'])\n",
+            "dict_keys(['low_health_literacy', 'intermediate_health_literacy', 'proficient_health_literacy'])\n",
+            "dict_keys(['low_health_literacy', 'intermediate_health_literacy', 'proficient_health_literacy'])\n"
+          ]
+        }
+      ],
+      "source": [
+        "# /home/mshahidul/readctrl/data/extracting_subclaim/extracted_subclaims_syn_data_with_gs_summary_en.json\n",
+        "import json\n",
+        "with open('/home/mshahidul/readctrl/data/extracting_subclaim/extracted_subclaims_syn_data_with_gs_summary_en.json', 'r') as f:\n",
+        "    extracted_subclaims_syn_data = json.load(f)\n",
+        "print(extracted_subclaims_syn_data[0].keys())\n",
+        "print(extracted_subclaims_syn_data[0]['diff_label_texts'].keys())\n",
+        "print(extracted_subclaims_syn_data[0]['diff_label_subclaims'].keys())"
+      ]
+    },
+    {
+      "cell_type": "code",
+      "execution_count": 12,
+      "id": "f2771312",
+      "metadata": {},
+      "outputs": [
+        {
+          "name": "stdout",
+          "output_type": "stream",
+          "text": [
+            "dict_keys(['index', 'literacy_levels'])\n",
+            "dict_keys(['low_health_literacy', 'intermediate_health_literacy', 'proficient_health_literacy'])\n",
+            "dict_keys(['scores', 'details'])\n",
+            "dict_keys(['factual_attribution', 'completeness', 'conciseness', 'source_coverage'])\n",
+            "dict_keys(['attribution', 'completeness', 'conciseness', 'source_coverage'])\n",
+            "dict_keys(['source_subclaim', 'status'])\n"
+          ]
+        }
+      ],
+      "source": [
+        "with open('/home/mshahidul/readctrl/data/factual_testing/full_details_evaluation_0_20_qwen3-32B_v2.json', 'r') as f:\n",
+        "    full_details_evaluation_data = json.load(f)\n",
+        "print(full_details_evaluation_data[0].keys())\n",
+        "print(full_details_evaluation_data[0]['literacy_levels'].keys())\n",
+        "print(full_details_evaluation_data[0]['literacy_levels']['low_health_literacy'].keys())\n",
+        "print(full_details_evaluation_data[0]['literacy_levels']['low_health_literacy']['scores'].keys())\n",
+        "print(full_details_evaluation_data[0]['literacy_levels']['low_health_literacy']['details'].keys())\n",
+        "print(full_details_evaluation_data[0]['literacy_levels']['low_health_literacy']['details']['source_coverage'][0].keys())"
+      ]
+    }
+  ],
+  "metadata": {
+    "kernelspec": {
+      "display_name": "un",
+      "language": "python",
+      "name": "python3"
+    },
+    "language_info": {
+      "codemirror_mode": {
+        "name": "ipython",
+        "version": 3
+      },
+      "file_extension": ".py",
+      "mimetype": "text/x-python",
+      "name": "python",
+      "nbconvert_exporter": "python",
+      "pygments_lexer": "ipython3",
+      "version": "3.11.14"
+    }
+  },
+  "nbformat": 4,
+  "nbformat_minor": 5
+}
diff --git a/code/data_processing/data_preV3.ipynb b/code/data_processing/data_preV3.ipynb
new file mode 100644
index 0000000000000000000000000000000000000000..8f8b474f6fa43d534523a303a39f74c1ddde046f
--- /dev/null
+++ b/code/data_processing/data_preV3.ipynb
@@ -0,0 +1,501 @@
+{
+ "cells": [
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "7839d3bf",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "def prompt_return(reference_summary, generated_summary, subclaims_json, difficulty_level):\n",
+    "    return f'''\n",
+    "    **SYSTEM / ROLE INSTRUCTION:**\n",
+    "\n",
+    "> You are a medical linguistics evaluator specializing in readability control of Spanish medical texts.\n",
+    "> You will assess whether omitted subclaims (those with `result = 0`) from a generated summary are reasonably excluded based on readability simplification (easy/intermediate/hard).\n",
+    "\n",
+    "> Criteria:\n",
+    "> * **Easy:** suitable for non-medical readers; focus on main story and outcomes; omit measurements, anatomy, and technical tests.\n",
+    "> * **Intermediate:** moderate medical detail; keep main findings but simplify phrasing.\n",
+    "> * **Hard:** close to clinical summary; high precision, moderate technical detail.\n",
+    ">\n",
+    "> You must provide a **judgment table**, a **numerical reasonableness score (0–5)**, and an **overall explanation**.\n",
+    "\n",
+    "---\n",
+    "\n",
+    "**INPUT:**\n",
+    "\n",
+    "**Reference summary:**\n",
+    "{reference_summary}\n",
+    "\n",
+    "**Generated summary ({difficulty_level}):**\n",
+    "{generated_summary}\n",
+    "\n",
+    "**Subclaims and results:**\n",
+    "{subclaims_json}\n",
+    "\n",
+    "---\n",
+    "\n",
+    "**TASK:**\n",
+    "1. Examine all subclaims with `\"result\": 0` (i.e., not supported in the generated summary).\n",
+    "2. For each omitted subclaim, decide if omission is **reasonable** (yes/no/borderline).\n",
+    "3. Provide a short explanation (≤2 sentences) for each.\n",
+    "4. Assign a **numerical reasonableness score (0–5)**:\n",
+    "\n",
+    "   * **5** = All omissions reasonable (excellent simplification)\n",
+    "   * **4** = Mostly reasonable; minor omissions could be improved\n",
+    "   * **3** = Some omissions reduce clarity or omit key ideas\n",
+    "   * **2** = Many key omissions or poor balance\n",
+    "   * **1** = Major content loss; poor summary\n",
+    "   * **0** = Incoherent simplification or severe distortion\n",
+    "5. Give an **overall explanation** (3–5 sentences) summarizing your reasoning.\n",
+    "\n",
+    "---\n",
+    "\n",
+    "**OUTPUT FORMAT (strict):**\n",
+    "\n",
+    "```json\n",
+    "{{\n",
+    "  \"evaluation_table\": [\n",
+    "    {{\n",
+    "      \"id\": <subclaim_id>,\n",
+    "      \"subclaim\": \"<text>\",\n",
+    "      \"reasonable_omission\": \"<yes / no / borderline>\",\n",
+    "      \"explanation\": \"<why it was or wasn't reasonable to omit>\"\n",
+    "    }}\n",
+    "  ],\n",
+    "  \"reasonableness_score\": <0-5>,\n",
+    "  \"overall_explanation\": \"<short paragraph explaining judgment>\"\n",
+    "}}\n",
+    "```\n",
+    "    '''"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "c94fe25a",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "def return_promptsV2(reference_summary, generated_summary, subclaims_json, difficulty_level):\n",
+    "    prompt=f'''\n",
+    "            **SYSTEM / ROLE INSTRUCTION:**\n",
+    "            You are a **medical readability evaluator**.\n",
+    "            Your task is to judge whether omitted subclaims (those with `\"result\": 0\"`) from a generated summary are *reasonably omitted* based on the intended **readability level**: *easy*, *intermediate*, or *hard*.\n",
+    "            You evaluate this from the standpoint of clarity, faithfulness, and readability goals.\n",
+    "\n",
+    "            ---\n",
+    "\n",
+    "            ### **READABILITY GUIDELINES**\n",
+    "\n",
+    "            | Level            | Target Audience                          | Content Expectation                                             | Technical Detail Allowed                                         |\n",
+    "            | :--------------- | :--------------------------------------- | :-------------------------------------------------------------- | :--------------------------------------------------------------- |\n",
+    "            | **Easy**         | General public                           | Focus on main events, outcomes, and diagnoses in plain Spanish. | Minimal — avoid measurements, anatomy, and test results.         |\n",
+    "            | **Intermediate** | Educated lay readers or medical students | Include key findings and procedures in simplified form.         | Moderate — basic terms and causes allowed.                       |\n",
+    "            | **Hard**         | Medical professionals                    | Retain most technical information and precision.                | High — measurements, anatomy, and test interpretations expected. |\n",
+    "\n",
+    "            ---\n",
+    "\n",
+    "            ### **INPUT FIELDS**\n",
+    "\n",
+    "            **Reference summary:**\n",
+    "            {reference_summary}\n",
+    "\n",
+    "            **Generated summary ({difficulty_level}):**\n",
+    "            {generated_summary}\n",
+    "\n",
+    "            **Subclaims and results:**\n",
+    "            {subclaims_json}\n",
+    "\n",
+    "            ---\n",
+    "\n",
+    "            ### **TASK INSTRUCTIONS**\n",
+    "\n",
+    "            1. Focus on subclaims with `\"result\": 0\"` (not supported by the generated summary).\n",
+    "            2. For each omitted subclaim:\n",
+    "\n",
+    "            * Decide whether omission is **reasonable** given the readability level.\n",
+    "            * Label as: `\"yes\"`, `\"no\"`, or `\"borderline\"`.\n",
+    "            * Write a brief justification (1–2 sentences).\n",
+    "            3. After individual evaluations, assign a **reasonableness score (0–5)** using this scale:\n",
+    "\n",
+    "            * **5** = All omissions appropriate for target readability.\n",
+    "            * **4** = Minor omissions could improve completeness.\n",
+    "            * **3** = Some omissions reduce understanding or medical clarity.\n",
+    "            * **2** = Many important omissions harm faithfulness.\n",
+    "            * **1** = Major omissions misrepresent case.\n",
+    "            * **0** = Summary fails to reflect key medical information.\n",
+    "            4. End with an **overall explanation (3–5 sentences)** describing:\n",
+    "\n",
+    "            * The main reasoning behind the score.\n",
+    "            * Whether the summary fits its intended readability level.\n",
+    "            * Suggestions for improvement if needed.\n",
+    "\n",
+    "            ---\n",
+    "\n",
+    "            ### **OUTPUT FORMAT (strict JSON)**\n",
+    "\n",
+    "            ```json\n",
+    "            {{\n",
+    "            \"evaluation_table\": [\n",
+    "                {{\n",
+    "                \"id\": <subclaim_id>,\n",
+    "                \"subclaim\": \"<text>\",\n",
+    "                \"reasonable_omission\": \"<yes | no | borderline>\",\n",
+    "                \"explanation\": \"<short reason>\"\n",
+    "                }}\n",
+    "            ],\n",
+    "            \"reasonableness_score\": <0-5>,\n",
+    "            \"overall_explanation\": \"<concise paragraph>\"\n",
+    "            }}\n",
+    "            ```\n",
+    "            '''\n",
+    "    return prompt"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "0162eddf",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "def return_prompts_attribution(reference_full_text, generated_summary, subclaims_json, difficulty_level):\n",
+    "    return f'''\n",
+    "### **SYSTEM / ROLE INSTRUCTION**\n",
+    "\n",
+    "You are a **medical factuality and attribution evaluator**.\n",
+    "You will assess whether **unsupported subclaims** in a generated summary (those with `\"result\": 0\"`) are *reasonable additions* based on the readability level (*easy / intermediate / hard*).\n",
+    "\n",
+    "The goal is to determine whether these **extra pieces of information** are acceptable simplifications or *hallucinations* that reduce factual faithfulness.\n",
+    "\n",
+    "---\n",
+    "\n",
+    "### **READABILITY & ATTRIBUTION GUIDELINES**\n",
+    "\n",
+    "| Level            | Audience                         | Content Goal                                                           | Allowable Additions                                                                |\n",
+    "| :--------------- | :------------------------------- | :--------------------------------------------------------------------- | :--------------------------------------------------------------------------------- |\n",
+    "| **Easy**         | General public                   | Simplify and clarify events                                            | Allow general background info or lay explanations, but not new facts or diagnoses. |\n",
+    "| **Intermediate** | Educated layperson / med student | Add brief clarifications or causal context if consistent with the text | Allow inferred, non-contradictory context; avoid adding unconfirmed data.          |\n",
+    "| **Hard**         | Medical professional             | Maintain factual precision                                             | No additions; everything must be supported by source text.                         |\n",
+    "\n",
+    "---\n",
+    "\n",
+    "### **INPUT FIELDS**\n",
+    "\n",
+    "**Reference full text:**\n",
+    "{reference_full_text}\n",
+    "\n",
+    "**Generated summary ({difficulty_level}):**\n",
+    "{generated_summary}\n",
+    "\n",
+    "**Subclaims and results:**\n",
+    "{subclaims_json}\n",
+    "\n",
+    "---\n",
+    "\n",
+    "### **TASK INSTRUCTIONS**\n",
+    "\n",
+    "1. Focus only on subclaims with `\"result\": 0\"` (not supported by the input text).\n",
+    "2. For each unsupported subclaim:\n",
+    "\n",
+    "   * Judge whether adding it is **reasonable** for the given readability level.\n",
+    "   * Choose one of: `\"reasonable addition\"`, `\"unnecessary but harmless\"`, `\"misleading / hallucinated\"`.\n",
+    "   * Provide a **1–2 sentence justification** explaining your reasoning.\n",
+    "3. After all evaluations, assign a **numerical attribution score (0–5)**:\n",
+    "\n",
+    "   * **5** = All additions are reasonable or harmless simplifications.\n",
+    "   * **4** = Mostly reasonable; minor harmless additions.\n",
+    "   * **3** = Some misleading or unjustified additions.\n",
+    "   * **2** = Many factual inaccuracies.\n",
+    "   * **1** = Serious hallucinations; distorts source meaning.\n",
+    "   * **0** = Highly unfaithful; mostly invented content.\n",
+    "4. End with an **overall explanation (3–5 sentences)** summarizing your reasoning and suggestions.\n",
+    "\n",
+    "---\n",
+    "\n",
+    "### **OUTPUT FORMAT (strict JSON)**\n",
+    "\n",
+    "```json\n",
+    "{{\n",
+    "  \"evaluation_table\": [\n",
+    "    {{\n",
+    "      \"id\": <subclaim_id>,\n",
+    "      \"subclaim\": \"<text>\",\n",
+    "      \"evaluation\": \"<reasonable addition | unnecessary but harmless | misleading / hallucinated>\",\n",
+    "      \"explanation\": \"<short justification>\"\n",
+    "    }}\n",
+    "  ],\n",
+    "  \"attribution_score\": <0-5>,\n",
+    "  \"overall_explanation\": \"<concise summary of your judgment>\"\n",
+    "}}\n",
+    "```\n",
+    "'''"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "efec346c",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "def revised_results(reference_summary, generated_summary, list_of_missing_subclaims, difficulty_level):\n",
+    "    return f'''\n",
+    "### **SYSTEM / ROLE INSTRUCTION**\n",
+    "\n",
+    "You are a **medical text rewriting assistant** that improves summaries while maintaining the intended readability level (*easy / intermediate / hard*).\n",
+    "You will receive:\n",
+    "\n",
+    "* The **original reference summary** (the factual source)\n",
+    "* The **current generated summary**\n",
+    "* A list of **important missing subclaims** to be reintroduced\n",
+    "* The **target readability level**\n",
+    "\n",
+    "Your task:\n",
+    "Revise the generated summary so that it **adds the missing information** naturally, while keeping:\n",
+    "\n",
+    "* The same **tone, vocabulary, and sentence simplicity** of the given readability level.\n",
+    "* Logical **flow and coherence**.\n",
+    "* No extra, invented information beyond what’s in the reference summary.\n",
+    "\n",
+    "---\n",
+    "\n",
+    "### **INPUT FIELDS**\n",
+    "\n",
+    "**Reference summary:**\n",
+    "{reference_summary}\n",
+    "\n",
+    "**Current generated summary ({difficulty_level}):**\n",
+    "{generated_summary}\n",
+    "\n",
+    "**Missing important subclaims to add back:**\n",
+    "{list_of_missing_subclaims}\n",
+    "\n",
+    "**Target readability level:**\n",
+    "{difficulty_level}\n",
+    "\n",
+    "\n",
+    "---\n",
+    "\n",
+    "### **TASK INSTRUCTIONS**\n",
+    "\n",
+    "1. Integrate the missing subclaims **smoothly** into the generated summary.\n",
+    "2. Do **not** add any new facts beyond those listed.\n",
+    "3. Maintain the **same readability level**:\n",
+    "\n",
+    "   * **Easy:** conversational, short sentences, no jargon.\n",
+    "   * **Intermediate:** light medical terms, brief explanations.\n",
+    "   * **Hard:** concise clinical tone with correct terminology.\n",
+    "4. Keep the summary approximately the same length; avoid redundancy.\n",
+    "5. Ensure the resulting text remains **fluent, coherent, and faithful** to the reference summary.\n",
+    "\n",
+    "---\n",
+    "\n",
+    "### **OUTPUT FORMAT**\n",
+    "\n",
+    "```json\n",
+    "{{\n",
+    "  \"revised_summary\": \"<the new version of the summary, rewritten with the added subclaims>\",\n",
+    "  \"explanation\": \"<brief note explaining how the missing subclaims were added while preserving readability>\"\n",
+    "}}\n",
+    "```\n",
+    "\n",
+    "'''"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "b5d5ad90",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "from openai import OpenAI\n",
+    "import json\n",
+    "file_path = \"/home/mshahidul/api_new.json\"\n",
+    "with open(file_path, \"r\") as file:\n",
+    "    api_keys = json.load(file)\n",
+    "\n",
+    "openai_api_key = api_keys.get(\"openai\")\n",
+    "\n",
+    "client = OpenAI(api_key=openai_api_key)\n",
+    "def openai_return(prompt):\n",
+    "    response = client.chat.completions.create(\n",
+    "        model=\"gpt-5-mini\",\n",
+    "        messages=[\n",
+    "            {\"role\": \"system\", \"content\": \"You are a helpful assistant.\"},\n",
+    "            {\"role\": \"user\", \"content\": prompt}\n",
+    "        ]\n",
+    "    )\n",
+    "    cleaned_response = response.choices[0].message.content.strip().replace(\"```json\", \"\").replace(\"```\", \"\")\n",
+    "    return json.loads(cleaned_response)"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "f3706ef0",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import json\n",
+    "file_path = \"/home/mshahidul/readctrl/data/training_data_subclaim_verifier/synthetic_data_es_subclaims_100.json\"\n",
+    "\n",
+    "with open(file_path, 'r') as f:\n",
+    "    synthetic_data = json.load(f)\n"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 8,
+   "id": "7b691bbe",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "with open(\"/home/mshahidul/readctrl/data/testing_data_gs/multiclinsum_gs_train_es.json\", \"r\") as f_train:\n",
+    "    multiclinsum_gs_train_es = json.load(f_train)\n",
+    "dat_full_text={}\n",
+    "dat_summary={}\n",
+    "for item in multiclinsum_gs_train_es:\n",
+    "    dat_full_text[item['id']]=item['fulltext']\n",
+    "    dat_summary[item['id']]=item['summary']"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "49f435b1",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "# /home/mshahidul/readctrl/results/dataset_quality_check/resonability_check_100_gpt5_completeness.json\n",
+    "\n",
+    "\n",
+    "\n",
+    "with open(\"/home/mshahidul/readctrl/results/dataset_quality_check/resonability_check_100_gpt5_completeness.json\", 'r') as f:\n",
+    "    readability_reasoning = json.load(f)\n",
+    "# readability_reasoning[0].keys() # dict_keys(['id', 'difficulty_level', 'prompt'])\n",
+    "# readability_reasoning[0]['prompt'].keys() # dict_keys(['evaluation_table', 'reasonableness_score', 'overall_explanation'])\n",
+    "reason_info={}\n",
+    "for item in readability_reasoning:\n",
+    "    id=item['id']\n",
+    "    difficulty_level=item['difficulty_level']\n",
+    "    data_temp=item['prompt']\n",
+    "    for _data in data_temp['evaluation_table']:\n",
+    "        if _data['reasonable_omission'] == \"no\":\n",
+    "            key=(id, difficulty_level)\n",
+    "            if key not in reason_info:\n",
+    "                reason_info[key]=[]\n",
+    "            reason_info[key].append(_data['subclaim'])"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "d74f2582",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "file_path_qwen3_32B = \"/home/mshahidul/readctrl/results/dataset_quality_check/subclaim_verifier_results_100_qwen3-32B.json\"\n",
+    "\n",
+    "with open(file_path_qwen3_32B, 'r') as f:\n",
+    "    qwen3_32B_results = json.load(f)\n",
+    "\n",
+    "# print(qwen3_32B_results[0]['completeness']['results'])\n",
+    "print(qwen3_32B_results[0].keys())\n",
+    "print(qwen3_32B_results[0]['completeness']['results'])"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "4e8a38e1",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "# dict_keys(['id', 'full_text', 'ref_summary', 'readability_versions'])\n",
+    "# print(f\"Full text: {synthetic_data[0]['full_text']}\")\n",
+    "import os\n",
+    "# def revised_results(reference_summary, generated_summary, list_of_missing_subclaims, difficulty_level):\n",
+    "res=[]\n",
+    "temp=\"\"\n",
+    "save_path = \"/home/mshahidul/readctrl/results/dataset_quality_check/results_revised_100_gpt5.json\"\n",
+    "if os.path.exists(save_path):\n",
+    "    with open(save_path, 'r') as f:\n",
+    "        res = json.load(f)\n",
+    "existing_check=set((entry['id'], entry['difficulty_level']) for entry in res)\n",
+    "print(f\"Resuming from {len(res)} entries\")\n",
+    "import tqdm\n",
+    "for ind in tqdm.tqdm(range(0,100)):\n",
+    "    for version in [\"easy\", \"intermediate\", \"hard\"]:\n",
+    "        reference_summary = (f\"{synthetic_data[ind]['ref_summary']['text']}\")\n",
+    "        generated_summary = (f\"{synthetic_data[ind]['readability_versions'][version]['text']}\")\n",
+    "        if (synthetic_data[ind]['id'],version) in existing_check:\n",
+    "            continue\n",
+    "        if (synthetic_data[ind]['id'],version) not in reason_info:\n",
+    "            continue\n",
+    "        subclaims_results = reason_info[(synthetic_data[ind]['id'],version)]\n",
+    "        prompt = revised_results(reference_summary, generated_summary, subclaims_results, version)\n",
+    "        print(prompt)\n",
+    "        assert False\n",
+    "        ans=openai_return(prompt)\n",
+    "        res.append({\n",
+    "            \"id\": synthetic_data[ind]['id'],\n",
+    "            \"difficulty_level\": version,\n",
+    "            \"prompt\": prompt,\n",
+    "            \"response\": ans\n",
+    "        })\n",
+    "        \n",
+    "        if len(res)%2==0:\n",
+    "            print(f\"Completed {len(res)} out of 300\")\n",
+    "            with open(save_path, 'w') as outfile:\n",
+    "                json.dump(res, outfile, indent=2)\n",
+    "    temp=res\n",
+    "    assert False\n",
+    "        # print(prompt)\n",
+    "        # assert False\n",
+    "with open(save_path, 'w') as outfile:\n",
+    "    json.dump(res, outfile, indent=2)"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "b89ff032",
+   "metadata": {},
+   "outputs": [],
+   "source": []
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "ff82e523",
+   "metadata": {},
+   "outputs": [],
+   "source": []
+  }
+ ],
+ "metadata": {
+  "kernelspec": {
+   "display_name": "unsloth",
+   "language": "python",
+   "name": "python3"
+  },
+  "language_info": {
+   "codemirror_mode": {
+    "name": "ipython",
+    "version": 3
+   },
+   "file_extension": ".py",
+   "mimetype": "text/x-python",
+   "name": "python",
+   "nbconvert_exporter": "python",
+   "pygments_lexer": "ipython3",
+   "version": "3.11.11"
+  }
+ },
+ "nbformat": 4,
+ "nbformat_minor": 5
+}
diff --git a/code/data_processing/data_preV4.ipynb b/code/data_processing/data_preV4.ipynb
new file mode 100644
index 0000000000000000000000000000000000000000..56c79af7bbded2c8ccb7c7d9ceaa5a28e8312321
--- /dev/null
+++ b/code/data_processing/data_preV4.ipynb
@@ -0,0 +1,839 @@
+{
+ "cells": [
+  {
+   "cell_type": "markdown",
+   "id": "17dc3d7c",
+   "metadata": {},
+   "source": [
+    "# subclaim completeness calculation and reasoning combine"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "aa44fafa",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import json\n",
+    "with open('/home/mshahidul/readctrl/results/dataset_quality_check/completeness_resonability_check_100_qwen3-32B_v3.json', 'r') as f2:\n",
+    "    data2 = json.load(f2)\n",
+    "    print(data2[0].keys())"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 4,
+   "id": "5a7286ac",
+   "metadata": {},
+   "outputs": [
+    {
+     "name": "stdout",
+     "output_type": "stream",
+     "text": [
+      "dict_keys(['id', 'fulltext', 'summary'])\n"
+     ]
+    }
+   ],
+   "source": [
+    "# /home/mshahidul/readctrl/data/synthetic_dataset_diff_labels/syn_data_diff_labels_en_0_80_full.json\n",
+    "import json\n",
+    "with open('/home/mshahidul/readctrl/data/testing_data_gs/multiclinsum_gs_train_en.json', 'r') as f1:\n",
+    "    data1 = json.load(f1)\n",
+    "    print(data1[0].keys())\n",
+    "dat={}\n",
+    "for idx,x in enumerate(data1):\n",
+    "    dat[idx]=x['summary']"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 6,
+   "id": "e462205b",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "# /home/mshahidul/readctrl/data/annotators_validate_data_(20_80)/code/correction_evaluation_full_text.json\n",
+    "with open('/home/mshahidul/readctrl/data/annotators_validate_data_(20_80)/code/correction_evaluation_full_text.json', 'r') as f3:\n",
+    "    data3 = json.load(f3)\n",
+    "full_data=[]\n",
+    "for item in data3:\n",
+    "    item['summary']=dat[item['doc_id']]\n",
+    "    full_data.append(item)"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 8,
+   "id": "051025fa",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "with open('/home/mshahidul/readctrl/data/annotators_validate_data_(20_80)/code/correction_evaluation_full_text_with_gs.json', 'w') as f4:\n",
+    "    json.dump(full_data, f4, indent=4)"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "db70aadb",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "reason_info = {}\n",
+    "another_info = {}\n",
+    "for item in data2:\n",
+    "    id = item['id']\n",
+    "    difficulty_level = item['version']\n",
+    "    data_temp = item['completeness']\n",
+    "    another_info[(id, difficulty_level)] = item['completeness']['results']\n",
+    "    for _data in data_temp['results']:\n",
+    "        reasonableness = _data['reasonableness']\n",
+    "        \n",
+    "        # Step 1: Try to parse as JSON\n",
+    "        if isinstance(reasonableness, str):\n",
+    "            parsed = None\n",
+    "            try:\n",
+    "                parsed = json.loads(reasonableness)\n",
+    "            except Exception:\n",
+    "                try:\n",
+    "                    parsed = ast.literal_eval(reasonableness)\n",
+    "                except Exception:\n",
+    "                    # Not JSON or dict — treat as plain text\n",
+    "                    if \"'reasonable'\" in reasonableness:\n",
+    "                        parsed = {\"reasonableness\": \"reasonable\", \"justification\": reasonableness}\n",
+    "                    elif \"'unreasonable'\" in reasonableness:\n",
+    "                        parsed = {\"reasonableness\": \"unreasonable\", \"justification\": reasonableness}\n",
+    "                    else:\n",
+    "                        parsed = {\"reasonableness\": \"unknown\", \"justification\": reasonableness}\n",
+    "            reasonableness = parsed\n",
+    "\n",
+    "        # Step 2: Skip if \"reasonable\"\n",
+    "        key = (id, difficulty_level,_data['id'])\n",
+    "\n",
+    "        if reasonableness.get('reasonableness') in [\"reasonable\"]:\n",
+    "            reason_info[key] = 1 \n"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "bed762d5",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import json\n",
+    "full_results = []\n",
+    "with open('/home/mshahidul/readctrl/results/dataset_quality_check/subclaim_verifier_results_100_qwen3-32B.json', 'r') as f:\n",
+    "    data = json.load(f)\n",
+    "    print(data[0].keys())\n",
+    "success = 0\n",
+    "accuracy_info={}\n",
+    "for entry in data:\n",
+    "    id= entry['id']\n",
+    "    difficulty_level = entry['version']\n",
+    "    success = 0\n",
+    "    temp=[]\n",
+    "    for item in entry['completeness']['results']:\n",
+    "        flag=0    \n",
+    "        sub_claim_id = item['subclaim']['id']\n",
+    "        sub_claim=item['subclaim']['subclaim']\n",
+    "        if item['result']==\"1\":\n",
+    "            flag=1\n",
+    "            success+=1\n",
+    "        elif item['result']==\"0\":\n",
+    "            key = (id, difficulty_level, sub_claim_id)\n",
+    "            if key in reason_info and reason_info[key]==1:\n",
+    "                success+=reason_info[key]\n",
+    "                flag=1\n",
+    "        if flag==1:\n",
+    "            temp.append({\n",
+    "                \"subclaim_id\": sub_claim_id,\n",
+    "                \"subclaim\": sub_claim,\n",
+    "                \"supported\": True,\n",
+    "            })\n",
+    "        else:\n",
+    "            temp.append({\n",
+    "                \"subclaim_id\": sub_claim_id,\n",
+    "                \"subclaim\": sub_claim,\n",
+    "                \"supported\": False,\n",
+    "            })\n",
+    "    full_results.append({\n",
+    "        \"id\": id,\n",
+    "        \"version\": difficulty_level,\n",
+    "        \"completeness\": temp,\n",
+    "        \"accuracy\": success/len(entry['completeness']['results'])\n",
+    "    })\n",
+    "    accuracy_info[(id,difficulty_level)] = success/len(entry['completeness']['results'])"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "af8bd071",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "# full_results\n",
+    "with open('/home/mshahidul/readctrl/results/dataset_quality_check/completeness_final_subclaim_verifier_results_100_v1.json', 'w') as f:\n",
+    "    json.dump(full_results, f, indent=4)"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "95f0c872",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "accuracy_calcs = {}\n",
+    "item_num={}\n",
+    "for version in ['easy','intermediate','hard']:\n",
+    "    for key, value in accuracy_info.items():\n",
+    "        if key[1]==version:\n",
+    "            accuracy_calcs[version] = accuracy_calcs.get(version, 0) + value\n",
+    "            item_num[version] = item_num.get(version, 0) + 1\n",
+    "    accuracy_calcs[version] = accuracy_calcs[version]/item_num[version]\n",
+    "print(accuracy_calcs)"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "3ffeac9c",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "res={\"easy\":[],\"intermediate\":[],\"hard\":[]}\n",
+    "\n",
+    "for entry in full_results:\n",
+    "    difficulty = entry['version']\n",
+    "    for item in entry['completeness']:\n",
+    "        res[difficulty].append(int(item['supported']))"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "36a1dda6",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "print(f\"easy: {sum(res['easy'])/len(res['easy']):.4f}\")\n",
+    "print(f\"intermediate: {sum(res['intermediate'])/len(res['intermediate']):.4f}\")\n",
+    "print(f\"hard: {sum(res['hard'])/len(res['hard']):.4f}\")"
+   ]
+  },
+  {
+   "cell_type": "markdown",
+   "id": "2a7f857c",
+   "metadata": {},
+   "source": [
+    "## reasonability model performance check using chatgpt"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "90c4aee1",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "prompt='''\n",
+    "You will act as a judge. I received an answer from my model using the prompt below. some subclaims were omitted in the generated summary compared to the reference summary based on readability label. I already calculated reasoning behind the omission of each subclaim. Now please evaluate whether the reasoning is good or not.\n",
+    "\"\n",
+    "def return_prompts(reference_summary, generated_summary, subclaims_json, difficulty_level):\n",
+    "    prompt=f\n",
+    "You are a **medical summarization quality evaluator**.\n",
+    "Your goal is to decide whether the inclusion or omission of each subclaim in the generated summary is *reasonable*, given the target readability level.\n",
+    "\n",
+    "---\n",
+    "\n",
+    "### **Input**\n",
+    "\n",
+    "```\n",
+    "Readability Level: {difficulty_level}\n",
+    "\n",
+    "Reference Summary:\n",
+    "{reference_summary}\n",
+    "\n",
+    "Generated Summary:\n",
+    "{generated_summary}\n",
+    "\n",
+    "Subclaims with Support Results:\n",
+    "{subclaims_json}\n",
+    "```\n",
+    "\n",
+    "---\n",
+    "\n",
+    "### **Task**\n",
+    "\n",
+    "For each subclaim:\n",
+    "\n",
+    "1. Read `result`:\n",
+    "\n",
+    "   * `1` = the subclaim is supported or clearly mentioned in the generated summary.\n",
+    "   * `0` = the subclaim is missing or not supported.\n",
+    "\n",
+    "2. Based on readability level and medical relevance, decide whether this inclusion/omission is **reasonable**, **partially reasonable**, or **unreasonable**.\n",
+    "\n",
+    "3. Provide a short justification (1–2 sentences) explaining your reasoning.\n",
+    "\n",
+    "---\n",
+    "\n",
+    "### **Output Format**\n",
+    "\n",
+    "Return structured JSON:\n",
+    "\n",
+    "```json\n",
+    "{{\n",
+    "  \"readability_level\": \"<easy/intermediate/hard>\",\n",
+    "  \"evaluations\": [\n",
+    "    {{\n",
+    "      \"subclaim_id\": <id>,\n",
+    "      \"subclaim_text\": \"<text>\",\n",
+    "      \"result\": <0 or 1>,\n",
+    "      \"reasonableness\": \"<reasonable | partially_reasonable | unreasonable>\",\n",
+    "      \"justification\": \"<short explanation>\"\n",
+    "    }},\n",
+    "    ...\n",
+    "  ]\n",
+    "}}\n",
+    "```\n",
+    "\n",
+    "---\n",
+    "\n",
+    "### **Evaluation Guidelines**\n",
+    "\n",
+    "| Readability Level | Reasonable Omission                                          | Unreasonable Omission                             |\n",
+    "| ----------------- | ------------------------------------------------------------ | ------------------------------------------------- |\n",
+    "| **Easy**          | Technical, anatomical, quantitative, or procedural details.  | Key clinical findings, diagnoses, or outcomes.    |\n",
+    "| **Intermediate**  | Minor imaging details or measurements.                       | Any main diagnostic finding or cause–effect link. |\n",
+    "| **Hard**          | Very few omissions acceptable; mostly stylistic compression. | Any missing clinical or diagnostic information.   |\n",
+    "\n",
+    "\n",
+    "\"\n",
+    "\n",
+    "Please evaluate how good my model’s performance is and whether it performed well or not.\n",
+    "'''"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "569d50f1",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import json\n",
+    "file_path = \"/home/mshahidul/readctrl/data/training_data_subclaim_verifier/synthetic_data_es_subclaims_100.json\"\n",
+    "\n",
+    "with open(file_path, 'r') as f:\n",
+    "    synthetic_data = json.load(f)\n",
+    "\n",
+    "file_path_qwen3_32B = \"/home/mshahidul/readctrl/results/dataset_quality_check/subclaim_verifier_results_100_qwen3-32B.json\"\n",
+    "\n",
+    "with open(file_path_qwen3_32B, 'r') as f:\n",
+    "    qwen3_32B_results = json.load(f)\n",
+    "\n",
+    "\n",
+    "ind=1\n",
+    "version='hard'\n",
+    "ref_summary = (f\"{synthetic_data[ind]['ref_summary']['text']}\")\n",
+    "generated_summary = (f\"{synthetic_data[ind]['readability_versions'][version]['text']}\")\n",
+    "subclaims_results = (f\"{qwen3_32B_results[ind]['completeness']['results']}\")\n",
+    "print(f\"Version: {version}\")\n",
+    "print(f\"Reference Summary: {ref_summary}\")\n",
+    "print(f\"Generated Summary: {generated_summary}\")\n",
+    "print(f\"Subclaims reasoning Results: {another_info[(synthetic_data[ind]['id'],version)]}\")"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "a470c099",
+   "metadata": {},
+   "outputs": [],
+   "source": []
+  },
+  {
+   "cell_type": "markdown",
+   "id": "cb78bbee",
+   "metadata": {},
+   "source": [
+    "## Token length cal"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "fcb7163d",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "\n",
+    "def return_prompts_attribution(reference_full_text, generated_summary, subclaims_json, difficulty_level):\n",
+    "    return f'''\n",
+    "### **SYSTEM / ROLE INSTRUCTION**\n",
+    "\n",
+    "You are a **medical factuality and attribution evaluator**.\n",
+    "You will assess whether **unsupported subclaims** in a generated summary (those with `\"result\": 0\"`) are *reasonable additions* based on the readability level (*easy / intermediate / hard*).\n",
+    "\n",
+    "The goal is to determine whether these **extra pieces of information** are acceptable simplifications or *hallucinations* that reduce factual faithfulness.\n",
+    "\n",
+    "---\n",
+    "\n",
+    "### **READABILITY & ATTRIBUTION GUIDELINES**\n",
+    "\n",
+    "| Level | Audience | Linguistic & Stylistic Profile | Content Goal | Allowable Additions |\n",
+    "| :-- | :-- | :-- | :-- | :-- |\n",
+    "| **Easy (FH 70–100, grade 5–7)** | General public; early secondary readers | Short, direct sentences using common vocabulary and concrete ideas. Avoid subordinate clauses and technical terms. Tone should be explanatory, lively, and highly accessible. | Simplify and clarify events and outcomes without introducing technical or diagnostic details. | General background context or plain-language explanations are acceptable; **no new facts, data, or inferred medical claims.** |\n",
+    "| **Intermediate (FH 50–69, grade 8–12)** | Educated layperson / medical student | Moderate sentence length and complexity. Vocabulary suitable for high-school or introductory science readers. May include limited domain terms with brief clarification. | Present essential medical content with clear logic and limited detail, ensuring readability for non-experts. | Brief clarifications, definitions, or causal links consistent with the source are allowed; **avoid speculative or unconfirmed data.** |\n",
+    "| **Hard (FH 0–49, university / professional)** | Medical professionals / technical audience | Long, multi-clause sentences; formal academic tone. Incorporate precise domain vocabulary, causal and analytical connectors (e.g., *por consiguiente*, *sin embargo*, *en virtud de*, *dado que*), at least one definition, one process description, and one statement of implications or challenges. | Preserve full factual accuracy, diagnostic precision, and interpretive nuance expected in professional discourse. | Additions are **not permitted**; every statement must be directly supported by the reference text. Parenthetical clarifications or relative clauses may be used for cohesion, not new content. |\n",
+    "\n",
+    "---\n",
+    "\n",
+    "### **INPUTS**\n",
+    "\n",
+    "Readability Level: {difficulty_level}  \n",
+    "Reference Full Text: {reference_full_text}  \n",
+    "Generated Summary: {generated_summary}  \n",
+    "Subclaims: {subclaims_json}\n",
+    "\n",
+    "---\n",
+    "\n",
+    "### **TASK INSTRUCTIONS**\n",
+    "\n",
+    "1. Focus only on subclaims with `\"result\": 0\"` (not supported by the input text).  \n",
+    "2. For each unsupported subclaim:\n",
+    "   * Judge whether adding it is **reasonable** for the given readability level.  \n",
+    "   * Choose one of: `\"reasonable addition\"`, `\"unnecessary but harmless\"`, `\"misleading / hallucinated\"`.  \n",
+    "   * Provide a **1–2 sentence justification** explaining your reasoning.\n",
+    "\n",
+    "---\n",
+    "\n",
+    "### **OUTPUT FORMAT (strict JSON)**\n",
+    "\n",
+    "```json\n",
+    "{{\n",
+    "  \"reasonableness\": \"<reasonable addition | unnecessary but harmless | misleading / hallucinated>\",\n",
+    "  \"justification\": \"<short clear explanation>\"\n",
+    "}}\n",
+    "\n",
+    "'''\n",
+    "import os, json, tqdm\n",
+    "file_path = \"/home/mshahidul/readctrl/data/training_data_subclaim_verifier/synthetic_data_es_subclaims_100.json\"\n",
+    "file_path_qwen3_32B = \"/home/mshahidul/readctrl/results/dataset_quality_check/subclaim_verifier_results_100_qwen3-32B.json\"\n",
+    "save_path = \"/home/mshahidul/readctrl/results/dataset_quality_check/attribution_resonability_check_100_qwen3-32B.json\"\n",
+    "\n",
+    "with open(file_path, 'r') as f:\n",
+    "    synthetic_data = json.load(f)\n",
+    "with open(file_path_qwen3_32B, 'r') as f:\n",
+    "    qwen3_32B_results = json.load(f)\n",
+    "\n",
+    "\n",
+    "import tiktoken\n",
+    "\n",
+    "def count_tokens_qwen(text: str):\n",
+    "   \n",
+    "        # fallback: use a generic encoding (not exact)\n",
+    "    encoding = tiktoken.get_encoding(\"cl100k_base\")\n",
+    "\n",
+    "    token_ids = encoding.encode(text)\n",
+    "    return len(token_ids)\n",
+    "\n",
+    "length=0\n",
+    "all_token_lengths = []\n",
+    "for ind in (range(0, 100)):\n",
+    "    for version in [\"easy\",\"intermediate\" ,\"hard\"]:\n",
+    "\n",
+    "        ref_full_text_summary = synthetic_data[ind]['full_text']\n",
+    "        generated_summary = synthetic_data[ind]['readability_versions'][version]['text']\n",
+    "        subclaims_results = qwen3_32B_results[ind]['attribution']['results']\n",
+    "\n",
+    "        # Convert subclaims JSON nicely\n",
+    "        subclaims_json = json.dumps(subclaims_results, indent=2, ensure_ascii=False)\n",
+    "\n",
+    "        prompt = return_prompts_attribution(\n",
+    "            ref_full_text_summary,\n",
+    "            generated_summary,\n",
+    "            subclaims_json,\n",
+    "            version\n",
+    "        )\n",
+    "        length=max(length,count_tokens_qwen(prompt))\n",
+    "        all_token_lengths.append(length)"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "d67bd288",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import matplotlib.pyplot as plt\n",
+    "\n",
+    "plt.figure(figsize=(8, 5))\n",
+    "plt.hist(all_token_lengths, bins=30, color='skyblue', edgecolor='black')\n",
+    "plt.title('Distribution of all_token_lengths')\n",
+    "plt.xlabel('Token Length')\n",
+    "plt.ylabel('Frequency')\n",
+    "plt.grid(True, linestyle='--', alpha=0.6)\n",
+    "plt.show()\n"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "f758d755",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import matplotlib.pyplot as plt\n",
+    "\n",
+    "plt.figure(figsize=(6, 4))\n",
+    "plt.boxplot(all_token_lengths, vert=True, patch_artist=True, boxprops=dict(facecolor='skyblue'))\n",
+    "plt.title('Boxplot of all_token_lengths')\n",
+    "plt.ylabel('Token Length')\n",
+    "plt.grid(axis='y', linestyle='--', alpha=0.6)\n",
+    "plt.show()"
+   ]
+  },
+  {
+   "cell_type": "markdown",
+   "id": "e3d31e79",
+   "metadata": {},
+   "source": [
+    "## attribution accuracy check"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "1eb679e5",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import json\n",
+    "\n",
+    "with open('/home/mshahidul/readctrl/results/dataset_quality_check/attribution_resonability_results_100_qwen3-32B_v2.json', 'r') as f:\n",
+    "    attribution_resonability_results = json.load(f)\n",
+    "\n",
+    "print(attribution_resonability_results[0].keys())"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "4ec7bab1",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "full_data=[]\n",
+    "for item in attribution_resonability_results:\n",
+    "    success=0\n",
+    "    for eval in item['results']:\n",
+    "        if eval['response']==\"not_applicable\" or eval['response']['reasonableness'] in [\"reasonable\",\"partially_reasonable\"]:\n",
+    "            success+=1\n",
+    "    full_data.append({\n",
+    "        \"id\": item['id'],\n",
+    "        \"difficulty_level\": item['difficulty_level'],\n",
+    "        \"total_subclaims\": len(item['results']),\n",
+    "        \"reasonable_subclaims\": success,\n",
+    "        \"unreasonable_subclaims\": len(item['results']) - success,\n",
+    "        \"accuracy\": success/len(item['results']) if item['results'] else 0,\n",
+    "        \"subclaim_list\": item['results']\n",
+    "    })\n",
+    "\n"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "a5a206dd",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "accuracy_calcs = {\"easy\":[],\"intermediate\":[],\"hard\":[]}\n",
+    "for item in full_data:\n",
+    "    accuracy_calcs[item['difficulty_level']].append(item['accuracy'])\n",
+    "accuracy_calcs2={}\n",
+    "for level in accuracy_calcs:\n",
+    "    for item in accuracy_calcs[level]:\n",
+    "            acc_100+=1\n",
+    "    accuracy_calcs2[level] = sum(accuracy_calcs[level])/len(accuracy_calcs[level]) if accuracy_calcs[level] else 0\n",
+    "print(accuracy_calcs2)"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "3c47e0ee",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "# accuracy_calcs = {\"easy\":[],\"intermediate\":[],\"hard\":[]}\n",
+    "# def temp1_func(num):\n",
+    "#     uc={\"easy\":0,\"intermediate\":0,\"hard\":0}\n",
+    "#     for item in full_data:\n",
+    "#         if item['unreasonable_subclaims']<=num:\n",
+    "#             uc[item['difficulty_level']] += 1\n",
+    "#         accuracy_calcs[item['difficulty_level']].append(item['accuracy'])\n",
+    "#     return uc\n",
+    "# for num in range(1,10):\n",
+    "#     uc=temp1_func(num)\n",
+    "#     print(f\"Unreasonable subclaims threshold: {num}, Count: {uc}\")\n",
+    "\n",
+    "# print(uc)\n",
+    "def temp2_func(num):\n",
+    "    accuracy_calcs2={}\n",
+    "    acc_100=0\n",
+    "    for level in accuracy_calcs:\n",
+    "        for item in accuracy_calcs[level]:\n",
+    "            if item>=num/10:\n",
+    "                acc_100+=1\n",
+    "        accuracy_calcs2[level] = sum(accuracy_calcs[level])/len(accuracy_calcs[level]) if accuracy_calcs[level] else 0\n",
+    "    temp=0\n",
+    "    for k,v in accuracy_calcs2.items():\n",
+    "        temp+=v\n",
+    "    print(f\"Threshold(>=): {num/10}, Overall Accuracy: {temp/3:.4f}\")\n",
+    "            # print(f\"Level: {k}, Accuracy: {v}\")\n",
+    "    # print(\"Threshold(>=):\", num/10, \"Accuracy:\", {k: v for k, v in accuracy_calcs2.items() if v >= num/10})\n",
+    "print(\"Accuracy threshold results:\")\n",
+    "for num in range(1,10):\n",
+    "    temp2_func(num)"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "d7b1364c",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "def temp_result(list_res):\n",
+    "    cnt=0\n",
+    "    for res in list_res:\n",
+    "        if res['result']==\"1\":\n",
+    "            cnt+=1\n",
+    "    return len(list_res),cnt,cnt/len(list_res) if len(list_res) > 0 else 0\n",
+    "        "
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "4f484774",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "# full_data.append({\n",
+    "#         \"id\": item['id'],\n",
+    "#         \"difficulty_level\": item['difficulty_level'],\n",
+    "#         \"total_subclaims\": len(item['results']),\n",
+    "#         \"reasonable_subclaims\": success,\n",
+    "#         \"accuracy\": success/len(item['results']) if item['results'] else 0\n",
+    "#     })"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "90369a55",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import json\n",
+    "full_data2={}\n",
+    "with open('/home/mshahidul/readctrl/results/dataset_quality_check/subclaim_verifier_results_100_qwen3-32B.json', 'r') as f:\n",
+    "    subclaim_verifier_results = json.load(f)\n",
+    "acc_list={\"easy\":[],\"intermediate\":[],\"hard\":[]}\n",
+    "for item in subclaim_verifier_results:\n",
+    "    for level in [\"easy\",\"intermediate\",\"hard\"]:\n",
+    "        if item['version']==level:\n",
+    "            total, cnt, acc = temp_result(item['attribution']['results'])\n",
+    "            acc_list[level].append(acc)\n",
+    "            full_data2[(item['id'], level)] = {\n",
+    "                \"id\": item['id'],\n",
+    "                \"difficulty_level\": level,\n",
+    "                \"total_subclaims\": total,\n",
+    "                \"reasonable_subclaims\": cnt,\n",
+    "                \"accuracy\": acc,\n",
+    "                \"subclaim_list\": item['attribution']['results']\n",
+    "            }\n",
+    "print({k: sum(v)/len(v) if v else 0 for k, v in acc_list.items()})"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "dbe194a8",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "for (k1,v1), (k2,v2) in zip(full_data.items(), full_data2.items()):\n",
+    "    assert k1==k2\n",
+    "    if k1[0]==k2[0] and k1[1]==k2[1] and v1['accuracy']<v2['accuracy']:\n",
+    "        print(f\"{k1}, reasoning: {v1['accuracy']}, amni: {v2['accuracy']}\")\n",
+    "        print(\"Reasoning subclaim list:\")\n",
+    "        for subclaim in v1['subclaim_list']:\n",
+    "            print(f\" - {subclaim}\")\n",
+    "        # print(\"Amni subclaim list:\")\n",
+    "        # for subclaim in v2['subclaim_list']:\n",
+    "        #     print(f\" - {subclaim}\")\n",
+    "        break"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "ca58ea75",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "with open('/home/mshahidul/readctrl/results/dataset_quality_check/subclaim_verifier_results_100_qwen3-32B.json', 'r') as f:\n",
+    "    orginal = json.load(f)\n",
+    "attribution=[{\"id\":item['id'],\"version\":item['version'],\"attribution\":item['attribution']['results']} for item in orginal]"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "685ceb14",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "dict1={}\n",
+    "for item in attribution:\n",
+    "    for item2 in item['attribution']:\n",
+    "        dict1[(item['id'], item['version'], item2['subclaim']['id'])] = item2['subclaim']['subclaim']"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "ef757279",
+   "metadata": {
+    "vscode": {
+     "languageId": "javascript"
+    }
+   },
+   "outputs": [],
+   "source": [
+    "import json\n",
+    "\n",
+    "with open('/home/mshahidul/readctrl/results/dataset_quality_check/attribution_resonability_results_100_qwen3-32B.json', 'r') as f:\n",
+    "    attribution_resonability_results = json.load(f)\n",
+    "\n",
+    "print(attribution_resonability_results[0].keys())"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "b36e7d8f",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "for item in attribution_resonability_results:\n",
+    "    id=item['id']\n",
+    "    difficulty_level=item['difficulty_level']\n",
+    "    results=item['results']\n",
+    "    for res in results:\n",
+    "        subclaim_id=res['subclaim_id']\n",
+    "        if dict1[(id, difficulty_level, subclaim_id)] != res['subclaim_text']:\n",
+    "            print(\"Mismatch found in:\", id, difficulty_level, subclaim_id)"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 2,
+   "id": "c02232fe",
+   "metadata": {},
+   "outputs": [
+    {
+     "name": "stdout",
+     "output_type": "stream",
+     "text": [
+      "dict_keys(['index', 'literacy_levels'])\n"
+     ]
+    }
+   ],
+   "source": [
+    "# /home/mshahidul/readctrl/data/factual_testing/full_details_evaluation_0_20_qwen3-32B.json\n",
+    "import json\n",
+    "with open('/home/mshahidul/readctrl/data/factual_testing/full_details_evaluation_0_20_qwen3-32B.json', 'r') as f:\n",
+    "    dict1_data = json.load(f)\n",
+    "print(dict1_data[0].keys())"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 11,
+   "id": "7f51f7ff",
+   "metadata": {},
+   "outputs": [
+    {
+     "name": "stdout",
+     "output_type": "stream",
+     "text": [
+      "dict_keys(['index', 'original_id', 'input_data', 'llm_output'])\n",
+      "dict_keys(['key_gold_summary_subclaims', 'key_source_text_subclaims', 'minimum_shared_key_subclaims'])\n",
+      "dict_keys(['gold_subclaim_id', 'subclaim_text'])\n"
+     ]
+    }
+   ],
+   "source": [
+    "# /home/mshahidul/readctrl/data/key_subclaims_testing/key_subclaims.json\n",
+    "with open('/home/mshahidul/readctrl/data/key_subclaims_testing/key_subclaims.json', 'r') as f:\n",
+    "    key_subclaims_data = json.load(f)\n",
+    "print(key_subclaims_data[0].keys())\n",
+    "print(key_subclaims_data[0]['llm_output'].keys())\n",
+    "print(key_subclaims_data[0]['llm_output']['key_gold_summary_subclaims'][0].keys())"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 6,
+   "id": "bfc9016f",
+   "metadata": {},
+   "outputs": [
+    {
+     "name": "stdout",
+     "output_type": "stream",
+     "text": [
+      "179\n"
+     ]
+    }
+   ],
+   "source": [
+    "# /home/mshahidul/readctrl/data/annotators_validate_data_(20_80)/mahi/annotation_results.json\n",
+    "import json\n",
+    "with open('/home/mshahidul/readctrl/data/annotators_validate_data_(20_80)/Shama/annotation_results.json', 'r') as f:\n",
+    "    annotation_data = json.load(f)\n",
+    "print(len(annotation_data))"
+   ]
+  }
+ ],
+ "metadata": {
+  "kernelspec": {
+   "display_name": "un",
+   "language": "python",
+   "name": "python3"
+  },
+  "language_info": {
+   "codemirror_mode": {
+    "name": "ipython",
+    "version": 3
+   },
+   "file_extension": ".py",
+   "mimetype": "text/x-python",
+   "name": "python",
+   "nbconvert_exporter": "python",
+   "pygments_lexer": "ipython3",
+   "version": "3.11.14"
+  }
+ },
+ "nbformat": 4,
+ "nbformat_minor": 5
+}
diff --git a/code/data_processing/data_preparation_for_training.ipynb b/code/data_processing/data_preparation_for_training.ipynb
new file mode 100644
index 0000000000000000000000000000000000000000..cf9cace853d27027dd15dfaf53b7caeaccc5b7f0
--- /dev/null
+++ b/code/data_processing/data_preparation_for_training.ipynb
@@ -0,0 +1,313 @@
+{
+ "cells": [
+  {
+   "cell_type": "code",
+   "execution_count": 10,
+   "id": "db9062a2",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "def training_prompt(medical_text, subclaim, label):\n",
+    "    \"\"\"\n",
+    "    Constructs an SFT prompt with grounding constraints to minimize hallucinations.\n",
+    "    \"\"\"\n",
+    "    \n",
+    "    # The system prompt sets strict 'Closed-World' assumptions.\n",
+    "    system_prompt = (\n",
+    "        \"You are a clinical evidence auditor. Your evaluation must be based \"\n",
+    "        \"STRICTLY and ONLY on the provided medical text. Do not use outside \"\n",
+    "        \"medical knowledge or assume facts not explicitly stated. If the text \"\n",
+    "        \"does not provide enough information to confirm the claim, you must \"\n",
+    "        \"mark it as 'not_supported'.\"\n",
+    "    )\n",
+    "    \n",
+    "    user_content = f\"\"\"EVALUATION TASK:\n",
+    "1. Read the Medical Text.\n",
+    "2. Verify the Subclaim.\n",
+    "3. If the evidence is missing, ambiguous, or unconfirmed in the text, label it 'not_supported'.\n",
+    "\n",
+    "### Medical Text:\n",
+    "{medical_text}\n",
+    "\n",
+    "### Subclaim:\n",
+    "{subclaim}\n",
+    "\n",
+    "Output exactly one word ('supported' or 'not_supported'):\"\"\"\n",
+    "\n",
+    "    conversation = {\n",
+    "        \"conversations\": [\n",
+    "            {\"from\": \"user\", \"content\": f\"{system_prompt}\\n\\n{user_content}\"},\n",
+    "            {\"from\": \"assistant\", \"content\": label}\n",
+    "        ]\n",
+    "    }\n",
+    "    \n",
+    "    return conversation"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 11,
+   "id": "50172521",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import os\n",
+    "import json\n",
+    "# /home/mshahidul/readctrl/data/finetuning_data/finetune_dataset_subclaim_support_v2.json\n",
+    "with open(\"/home/mshahidul/readctrl/data/finetuning_data/train_subclaim_support_v2.json\", \"r\") as f:\n",
+    "    data = json.load(f)\n",
+    "\n",
+    "prompts = []\n",
+    "for item in train_data:\n",
+    "    prompt = training_prompt(\n",
+    "                medical_text=item['medical_text'],\n",
+    "                subclaim=item['subclaim'],\n",
+    "                label=item['label']\n",
+    "            )\n",
+    "    prompts.append(prompt)\n",
+    "output_path = \"/home/mshahidul/readctrl/data/finetuning_data/finetune_dataset_subclaim_support_v2_sft_prompt.json\"\n",
+    "with open(output_path, \"w\") as f:\n",
+    "    json.dump(prompts, f, indent=2)"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "33ca269d",
+   "metadata": {},
+   "outputs": [
+    {
+     "name": "stdout",
+     "output_type": "stream",
+     "text": [
+      "Train data size: 90, Test data size: 10\n",
+      "2160\n"
+     ]
+    }
+   ],
+   "source": [
+    "import os\n",
+    "import json\n",
+    "# /home/mshahidul/readctrl/data/finetuning_data/finetune_dataset_subclaim_support_v2.json\n",
+    "with open(\"/home/mshahidul/readctrl/data/finetuning_data/finetune_dataset_subclaim_support_v2.json\", \"r\") as f:\n",
+    "    data = json.load(f)\n",
+    "train_test_split=0.9\n",
+    "split_index=int(len(data)*train_test_split)\n",
+    "train_data=data[:split_index]\n",
+    "test_data=data[split_index:]\n",
+    "print(f\"Train data size: {len(train_data)}, Test data size: {len(test_data)}\")\n",
+    "# assert False, \"Stop here\"\n",
+    "prompts = []\n",
+    "for item in train_data:\n",
+    "    # import ipdb; ipdb.set_trace()\n",
+    "    sub_item=item['items'][0]\n",
+    "    for label in ['easy','intermediate','hard']:\n",
+    "        for subclaim in sub_item['subclaims']:\n",
+    "            prompt = training_prompt(\n",
+    "                medical_text=sub_item[f'{label}_text'],\n",
+    "                subclaim=subclaim['subclaim'],\n",
+    "                label=subclaim['label']\n",
+    "            )\n",
+    "            prompts.append(prompt)\n"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "e478818f",
+   "metadata": {},
+   "outputs": [],
+   "source": []
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 6,
+   "id": "aaa8f81a",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import os\n",
+    "import json\n",
+    "# /home/mshahidul/readctrl/data/finetuning_data/finetune_dataset_subclaim_support_v2.json\n",
+    "with open(\"/home/mshahidul/readctrl/data/finetuning_data/finetune_dataset_subclaim_support_v2.json\", \"r\") as f:\n",
+    "    data = json.load(f)\n",
+    "# train_test_split=0.9\n",
+    "# split_index=int(len(data)*train_test_split)\n",
+    "# train_data=data[:split_index]\n",
+    "# test_data=data[split_index:]\n",
+    "# print(f\"Train data size: {len(train_data)}, Test data size: {len(test_data)}\")\n",
+    "# assert False, \"Stop here\"\n",
+    "direct = []\n",
+    "for item in data:\n",
+    "    # import ipdb; ipdb.set_trace()\n",
+    "    sub_item=item['items'][0]\n",
+    "    for label in ['easy','intermediate','hard']:\n",
+    "        for subclaim in sub_item['subclaims']:\n",
+    "            direct.append({\n",
+    "                \"medical_text\":sub_item[f'{label}_text'],\n",
+    "                \"subclaim\":subclaim['subclaim'],\n",
+    "                \"label\":subclaim['label']\n",
+    "            })\n",
+    "with open(\"/home/mshahidul/readctrl/data/finetuning_data/processed_finetune_dataset_subclaim_support_v2.json\", \"w\") as f:\n",
+    "    json.dump(direct, f, ensure_ascii=False, indent=4)"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 14,
+   "id": "78edcc06",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "# save\n",
+    "output_path = \"/home/mshahidul/readctrl/data/finetuning_data/finetune_dataset_subclaim_support_v2_sft_prompt.json\"\n",
+    "with open(output_path, \"w\") as f:\n",
+    "    json.dump(prompts, f, indent=2)"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 9,
+   "id": "36b396bb",
+   "metadata": {},
+   "outputs": [
+    {
+     "name": "stdout",
+     "output_type": "stream",
+     "text": [
+      "Train label distribution:\n",
+      "{'supported': 960, 'not_supported': 960}\n",
+      "Test label distribution:\n",
+      "{'supported': 240, 'not_supported': 240}\n"
+     ]
+    }
+   ],
+   "source": [
+    "from sklearn.model_selection import train_test_split\n",
+    "\n",
+    "# Assume data is your list of dicts\n",
+    "data = direct\n",
+    "\n",
+    "labels = [d[\"label\"] for d in data]\n",
+    "\n",
+    "train_data, test_data = train_test_split(\n",
+    "    data,\n",
+    "    test_size=0.2,\n",
+    "    random_state=42,\n",
+    "    stratify=labels\n",
+    ")\n",
+    "with open(\"/home/mshahidul/readctrl/data/finetuning_data/train_subclaim_support_v2.json\",\"w\") as f:\n",
+    "    json.dump(train_data, f, indent=2)\n",
+    "\n",
+    "with open(\"/home/mshahidul/readctrl/data/finetuning_data/test_subclaim_support_v2.json\",\"w\") as f:\n",
+    "    json.dump(test_data, f, indent=2)\n",
+    "\n",
+    "print(\"Train label distribution:\")\n",
+    "print({l: sum(d[\"label\"] == l for d in train_data) for l in set(labels)})\n",
+    "\n",
+    "print(\"Test label distribution:\")\n",
+    "print({l: sum(d[\"label\"] == l for d in test_data) for l in set(labels)})\n"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 16,
+   "id": "01033a5f",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "testing_data_v2 = []\n",
+    "for item in test_data:\n",
+    "    sub_item=item['items'][0]\n",
+    "    for label in ['easy','intermediate','hard']:\n",
+    "        for subclaim in sub_item['subclaims']:\n",
+    "            testing_data_v2.append({\n",
+    "                \"medical_text\": sub_item[f'{label}_text'],\n",
+    "                \"subclaim\": subclaim['subclaim'],\n",
+    "                \"label\": subclaim['label']\n",
+    "            })\n",
+    "with open(\"/home/mshahidul/readctrl/data/finetuning_data/test_dataset_subclaim_support_v2.json\", \"w\") as f:\n",
+    "    json.dump(testing_data_v2, f, indent=2)\n",
+    "    "
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 3,
+   "id": "74d71220",
+   "metadata": {},
+   "outputs": [
+    {
+     "name": "stderr",
+     "output_type": "stream",
+     "text": [
+      "/home/mshahidul/miniconda3/envs/un/lib/python3.11/site-packages/tqdm/auto.py:21: TqdmWarning: IProgress not found. Please update jupyter and ipywidgets. See https://ipywidgets.readthedocs.io/en/stable/user_install.html\n",
+      "  from .autonotebook import tqdm as notebook_tqdm\n"
+     ]
+    }
+   ],
+   "source": [
+    "from datasets import load_dataset\n",
+    "dataset = load_dataset(\"HuggingFaceH4/Multilingual-Thinking\", split=\"train\")"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 5,
+   "id": "6d6a6b9a",
+   "metadata": {},
+   "outputs": [
+    {
+     "data": {
+      "text/plain": [
+       "[{'content': 'reasoning language: French\\n\\nYou are an AI chatbot with a lively and energetic personality.',\n",
+       "  'role': 'system',\n",
+       "  'thinking': None},\n",
+       " {'content': 'Can you show me the latest trends on Twitter right now?',\n",
+       "  'role': 'user',\n",
+       "  'thinking': None},\n",
+       " {'content': 'Hey there!  While I can\\'t check Twitter (X) in real-time or access live data, I can share some tips to help you spot the latest trends:\\n\\n1. **Open the \"Trending\" tab** on the Twitter app or website – it updates constantly!  \\n2. **Search for hashtags** like #Trending or #Viral to see what’s blowing up.  \\n3. **Follow accounts** that curate trends (e.g., @TrendingNow, @ViralThreads).  \\n4. **Check regional trends** – they often differ by location!  \\n\\nRemember, trends are *super fast-moving* and often tied to pop culture, memes, or breaking news. For example, recent trends have included viral challenges (like the \"Distracted Boyfriend\" meme revival), celebrity drama, or unexpected events (hello, weather disasters!).  \\n\\nWant me to brainstorm *what* might trend next? I’ve got ideas!',\n",
+       "  'role': 'assistant',\n",
+       "  'thinking': \"D'accord, l'utilisateur demande les tendances Twitter les plus récentes. Tout d'abord, je dois vérifier si j'ai accès à des données en temps réel. Étant donné que je ne peux pas naviguer sur Internet ou accéder directement à l'API de Twitter, je ne peux pas fournir des tendances en direct. Cependant, je peux donner quelques conseils généraux sur la façon de les trouver.\\n\\nJe devrais préciser que les tendances Twitter évoluent rapidement et sont spécifiques à chaque région. Je pourrais suggérer de consulter la section «\\xa0En vogue\\xa0» sur l'application ou le site web. Aussi, l'utilisation de hashtags et le suivi d'utilisateurs pertinents pourraient être utiles. Il est important de souligner que les tendances varient selon la région et l'heure de la journée. Je devrais garder un ton amical et bienveillant, peut-être ajouter un emoji pour rester léger. Je vais structurer ma réponse étape par étape pour faciliter la lecture. Je dois m'excuser de ne pas pouvoir fournir des données en temps réel et proposer d'autres méthodes. Je conserverai un langage simple et convivial, en évitant les termes techniques.\"}]"
+      ]
+     },
+     "execution_count": 5,
+     "metadata": {},
+     "output_type": "execute_result"
+    }
+   ],
+   "source": [
+    "dataset[0]['messages']"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "bba9e8ba",
+   "metadata": {},
+   "outputs": [],
+   "source": []
+  }
+ ],
+ "metadata": {
+  "kernelspec": {
+   "display_name": "un",
+   "language": "python",
+   "name": "python3"
+  },
+  "language_info": {
+   "codemirror_mode": {
+    "name": "ipython",
+    "version": 3
+   },
+   "file_extension": ".py",
+   "mimetype": "text/x-python",
+   "name": "python",
+   "nbconvert_exporter": "python",
+   "pygments_lexer": "ipython3",
+   "version": "3.11.14"
+  }
+ },
+ "nbformat": 4,
+ "nbformat_minor": 5
+}
diff --git a/code/data_processing/data_quality_check.ipynb b/code/data_processing/data_quality_check.ipynb
new file mode 100644
index 0000000000000000000000000000000000000000..de592d95b64d07f3fe22b57abb98dabe242e7261
--- /dev/null
+++ b/code/data_processing/data_quality_check.ipynb
@@ -0,0 +1,511 @@
+{
+ "cells": [
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "7087d09c",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import json\n",
+    "\n",
+    "file_path_attrib = \"/home/mshahidul/readctrl/results/dataset_quality_check/resonability_check_100_gpt5_attribution.json\"\n",
+    "with open(file_path_attrib, 'r') as f:\n",
+    "    readability_attribution = json.load(f)\n",
+    "# print keys of the first element\n",
+    "# readability_attribution[0].keys() #dict_keys(['id', 'difficulty_level', 'response'])\n",
+    "# readability_attribution[0]['response'].keys() #dict_keys(['evaluation_table', 'attribution_score', 'overall_explanation'])\n"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "0525f35d",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "dict1={}\n",
+    "for item in readability_attribution:\n",
+    "    for item2 in item['response']['evaluation_table']:\n",
+    "        if item2['evaluation'] != 'misleading / hallucinated':\n",
+    "            dict1[(item['id'], item['difficulty_level'],item2['id'])]=1"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "cb017c17",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "dict1"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "1895fa25",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import json\n",
+    "\n",
+    "file_path_verifier = \"/home/mshahidul/readctrl/results/dataset_quality_check/subclaim_verifier_results_100_qwen3-32B.json\"\n",
+    "with open(file_path_verifier, 'r') as f_verifier:\n",
+    "    subclaim_verifier_results = json.load(f_verifier)\n",
+    "# keys\n",
+    "# subclaim_verifier_results[0].keys() #dict_keys(['id', 'version', 'completeness', 'conciseness', 'attribution'])\n",
+    "# subclaim_verifier_results[0]['attribution'].keys() #dict_keys(['metric', 'version', 'input_text', 'results', 'total', 'correct', 'accuracy'])"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "2d7f2c2e",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "full_info=[]\n",
+    "for item in subclaim_verifier_results:\n",
+    "    success=0\n",
+    "    for item2 in item['attribution']['results']:\n",
+    "        if item2['result']==\"1\":\n",
+    "            success+=1\n",
+    "        elif item2['result']==\"0\":\n",
+    "            print((item['id'], item['version'], item2['subclaim']['id']))\n",
+    "            print(dict1.get((item['id'], item['version'], item2['subclaim']['id'])))\n",
+    "            success+=dict1.get((item['id'], item['version'], item2['subclaim']['id']),0)\n",
+    "    full_info.append({'id':item['id'], 'version':item['version'], 'success':success, 'accuracy':success/len(item['attribution']['results'])})\n",
+    "        "
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "6b797d72",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "accuracy_list=sum([entry['accuracy'] for entry in full_info if entry['version']=='easy'])/len([entry['accuracy'] for entry in full_info if entry['version']=='easy'])\n",
+    "print(\"Easy version accuracy:\", accuracy_list)\n",
+    "accuracy_list=sum([entry['accuracy'] for entry in full_info if entry['version']=='intermediate'])/len([entry['accuracy'] for entry in full_info if entry['version']=='intermediate'])\n",
+    "print(\"Intermediate version accuracy:\", accuracy_list)\n",
+    "accuracy_list=sum([entry['accuracy'] for entry in full_info if entry['version']=='hard'])/len([entry['accuracy'] for entry in full_info if entry['version']=='hard'])\n",
+    "print(\"Hard version accuracy:\", accuracy_list)"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "d819721b",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "# /home/mshahidul/readctrl/data/model_validity_check/subclaims_validity_check_v1.json read\n",
+    "import json\n",
+    "with open(\"/home/mshahidul/readctrl/data/model_validity_check/subclaims_validity_check_v1.json\", \"r\") as f:\n",
+    "    res = json.load(f)\n",
+    "acc=0\n",
+    "incorrect_cases=0\n",
+    "for item in res:\n",
+    "    acc+=item['overall_accuracy']\n",
+    "    incorrect_cases+=len(item['incorrect_or_unsafe_subclaims'])\n",
+    "print(\"Overall accuracy:\", acc/len(res))\n",
+    "print(\"Total incorrect or unsafe subclaims:\", incorrect_cases/len(res))"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "7fc2ac40",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "# /home/mshahidul/readctrl/data/model_validity_check/subclaims_support_validity_check(attr)_v1(cal_v1).json read\n",
+    "import json\n",
+    "with open(\"/home/mshahidul/readctrl/data/model_validity_check/subclaims_support_validity_check(attr)_v1(cal_v1).json\", \"r\") as f:\n",
+    "    res = json.load(f)\n",
+    "acc=0\n",
+    "for item in res:\n",
+    "    acc+=item['accuracy']\n",
+    "print(\"Overall support validity accuracy:\", acc/len(res))\n"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "5257bad8",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import json\n",
+    "with open(\"/home/mshahidul/readctrl/data/concise_complete_attr_testing/evaluated_metrics_0_480_nemotron-3-nano-30b-a3b_v2.json\", \"r\") as f:\n",
+    "    res = json.load(f)\n",
+    "acc=0\n",
+    "for item in res:\n",
+    "    acc+=item['accuracy']\n",
+    "print(\"Overall support validity accuracy:\", acc/len(res))"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "03e9f9e4",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "# /home/mshahidul/readctrl/data/concise_complete_attr_testing/evaluated_metrics_0_240_mistral31_24B_v2.json\n",
+    "import json\n",
+    "# Overall correctness accuracy: 0.895 --> mistral31_24B\n",
+    "# Overall correctness accuracy: 0.898 --> qwen3_32B\n",
+    "with open(\"/home/mshahidul/readctrl/data/concise_complete_attr_testing/evaluated_metrics_0_480_nemotron-3-nano-30b-a3b_v2.json\", \"r\") as f:\n",
+    "    res = json.load(f)\n",
+    "# print(res[0])\n",
+    "acc=0\n",
+    "for item in res:\n",
+    "    if item['correctness']==True:\n",
+    "        acc+=1\n",
+    "print(\"Overall correctness accuracy:\", acc/len(res))"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "ebb4a213",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "from sklearn.metrics import cohen_kappa_score, confusion_matrix\n",
+    "import pandas as pd\n",
+    "with open(\"/home/mshahidul/readctrl/data/concise_complete_attr_testing/evaluated_metrics_0_480_nemotron-3-nano-30b-a3b_v2.json\", \"r\") as f:\n",
+    "    res = json.load(f)\n",
+    "# 1. Define your model outputs\n",
+    "# Ensure the order of elements matches for both lists\n",
+    "# gpt5_labels = [\"Supported\", \"Not Supported\", \"Supported\", \"Supported\", \"Not Supported\"]\n",
+    "# qwen_labels = [\"Supported\", \"Supported\", \"Supported\", \"Not Supported\", \"Not Supported\"]\n",
+    "gpt5_labels=[x['label_gt'] for x in res]\n",
+    "qwen_labels=[x['label_gen'] for x in res]\n",
+    "# 2. Map strings to integers for calculation\n",
+    "mapping = {\"supported\": 1, \"not_supported\": 0}\n",
+    "y_gpt5 = [mapping[label] for label in gpt5_labels]\n",
+    "y_qwen = [mapping[label] for label in qwen_labels]\n",
+    "\n",
+    "# 3. Calculate Cohen's Kappa\n",
+    "kappa = cohen_kappa_score(y_gpt5, y_qwen)\n",
+    "\n",
+    "print(f\"Cohen's Kappa: {kappa:.4f}\")\n",
+    "\n",
+    "# 4. (Optional) Visualize the disagreement with a Confusion Matrix\n",
+    "cm = confusion_matrix(y_gpt5, y_qwen)\n",
+    "cm_df = pd.DataFrame(cm, index=['Actual Not-Sup', 'Actual Sup'], \n",
+    "                         columns=['Pred Not-Sup', 'Pred Sup'])\n",
+    "print(\"\\nConfusion Matrix:\")\n",
+    "print(cm_df)"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "d3ef3549",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "with open(\"/home/mshahidul/readctrl/data/extracting_subclaim/extracted_subclaims_full_data.json\", \"r\") as f:\n",
+    "    full_text = json.load(f)\n",
+    "full_text_info=[]\n",
+    "for entry in full_text[:5]:\n",
+    "    for label in [\"easy\", \"intermediate\", \"hard\"]:\n",
+    "        full_text_info.append(entry['fulltext'])"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "90ad1af2",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "len(full_text_info)"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "4ebd5e67",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "# /home/mshahidul/readctrl/data/model_validity_check/subclaims_support_validity_check_gt_gpt5(1-5).json\n",
+    "with open(\"/home/mshahidul/readctrl/data/model_validity_check/subclaims_support_validity_check_gt_gpt5(1-5).json\", \"r\") as f:\n",
+    "    res = json.load(f)\n",
+    "full_data=[]\n",
+    "for index, item in enumerate(res):\n",
+    "    full_data.append({\n",
+    "        \"index\": index,\n",
+    "        \"full_text\": full_text_info[index],\n",
+    "        \"dat\": item\n",
+    "    })"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "5f7a19ff",
+   "metadata": {},
+   "outputs": [],
+   "source": []
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "deba1c76",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "with open(\"/home/mshahidul/readctrl/data/model_validity_check/subclaims_support_validity_check_gt_gpt5(1-5).json\", \"w\") as f:\n",
+    "    json.dump(full_data, f, indent=2, ensure_ascii=False)"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "5812366d",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "python -m wikiextractor.WikiExtractor /home/mshahidul/readctrl/data/wiki-text/simplewiki-latest-pages-articles.xml --json -o /home/mshahidul/readctrl/data/wiki-text/wiki"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 11,
+   "id": "02b7dd74",
+   "metadata": {},
+   "outputs": [
+    {
+     "name": "stderr",
+     "output_type": "stream",
+     "text": [
+      "Generating train split: 100%|██████████| 1841155/1841155 [00:25<00:00, 71022.97 examples/s] \n"
+     ]
+    }
+   ],
+   "source": [
+    "from datasets import load_dataset\n",
+    "\n",
+    "ds = load_dataset(\"wikimedia/wikipedia\", \"20231101.es\")"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 12,
+   "id": "7aaaa96e",
+   "metadata": {},
+   "outputs": [
+    {
+     "data": {
+      "text/plain": [
+       "1841155"
+      ]
+     },
+     "execution_count": 12,
+     "metadata": {},
+     "output_type": "execute_result"
+    },
+    {
+     "name": "stdout",
+     "output_type": "stream",
+     "text": [
+      "The history saving thread hit an unexpected error (OperationalError('database or disk is full')).History will not be written to the database.\n"
+     ]
+    }
+   ],
+   "source": [
+    "len(ds['train'])"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "2c8a80f0",
+   "metadata": {},
+   "outputs": [
+    {
+     "data": {
+      "text/plain": [
+       "DatasetDict({\n",
+       "    train: Dataset({\n",
+       "        features: ['id', 'url', 'title', 'text'],\n",
+       "        num_rows: 6407814\n",
+       "    })\n",
+       "})"
+      ]
+     },
+     "execution_count": 3,
+     "metadata": {},
+     "output_type": "execute_result"
+    }
+   ],
+   "source": [
+    "my_target_documents=[item['text'] for item in ds['test'].select(range(5))]"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "9049e532",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "from rank_bm25 import BM25Okapi\n",
+    "\n",
+    "# 1. Your collection of documents\n",
+    "# corpus = [\n",
+    "#     \"The capital of France is Paris.\",\n",
+    "#     \"Python is a popular programming language.\",\n",
+    "#     \"The deep learning model was trained on a large dataset.\",\n",
+    "#     \"Paris is known for the Eiffel Tower.\"\n",
+    "# ]\n",
+    "corpus = [item['text'] for item in ds['train'].select(range(100))]\n",
+    "tokenized_corpus=[]\n",
+    "for item in ds['train'].select(range(100)):\n",
+    "    dd=item['text'].lower().replace(\"\\n\",\" \").strip().split(\" \")\n",
+    "    tokenized_corpus.append(dd)\n",
+    "    \n",
+    "# 2. Tokenize the corpus (split into words)\n",
+    "# tokenized_corpus = [doc.lower().split(\" \") for doc in corpus]\n",
+    "bm25 = BM25Okapi(tokenized_corpus)\n",
+    "\n",
+    "# 3. Define a query\n",
+    "query = \"What is the capital of France?\"\n",
+    "tokenized_query = query.lower().split(\" \")\n",
+    "\n",
+    "# 4. Get the best results\n",
+    "top_n = bm25.get_top_n(tokenized_query, corpus, n=1)\n",
+    "print(f\"Top Result: {top_n[0]}\")"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "4627abce",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "from sentence_transformers import SentenceTransformer, util\n",
+    "\n",
+    "model = SentenceTransformer('all-MiniLM-L6-v2')\n",
+    "wiki_embeddings = model.encode(wiki_list, convert_to_tensor=True)\n",
+    "\n",
+    "# For a given document D\n",
+    "d_embedding = model.encode(document_d, convert_to_tensor=True)\n",
+    "hits = util.semantic_search(d_embedding, wiki_embeddings, top_k=5)\n",
+    "# Filter hits by length and select the best match"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 5,
+   "id": "c885f4e6",
+   "metadata": {},
+   "outputs": [
+    {
+     "name": "stdout",
+     "output_type": "stream",
+     "text": [
+      "dict_keys(['index', 'fulltext', 'diff_label_texts'])\n"
+     ]
+    }
+   ],
+   "source": [
+    "# /home/mshahidul/readctrl/data/synthetic_dataset_diff_labels/syn_data_diff_labels_en_v1.json\n",
+    "import json\n",
+    "with open(\"/home/mshahidul/readctrl/data/synthetic_dataset_diff_labels/syn_data_diff_labels_en_v1.json\", \"r\") as f:\n",
+    "    res = json.load(f)\n",
+    "print(res[0].keys())"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 6,
+   "id": "b1aac332",
+   "metadata": {},
+   "outputs": [
+    {
+     "data": {
+      "text/plain": [
+       "dict_keys(['low_health_literacy', 'intermediate_health_literacy', 'proficient_health_literacy'])"
+      ]
+     },
+     "execution_count": 6,
+     "metadata": {},
+     "output_type": "execute_result"
+    }
+   ],
+   "source": [
+    "res[0]['diff_label_texts'].keys()"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 7,
+   "id": "f799f34a",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "my_target_documents = []\n",
+    "for item in res:\n",
+    "    for key,value in item['diff_label_texts'].items():\n",
+    "        my_target_documents.append({\n",
+    "            \"index\": item['index'],\n",
+    "            \"label\": key,\n",
+    "            \"diff_label_texts\": value  # Example: pick one of the diff label texts\n",
+    "        })"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 8,
+   "id": "4bf14cda",
+   "metadata": {},
+   "outputs": [
+    {
+     "data": {
+      "text/plain": [
+       "{'index': 0,\n",
+       " 'label': 'low_health_literacy',\n",
+       " 'diff_label_texts': 'You are a 20‑year‑old woman with a long‑term kidney problem that makes you lose protein in your urine. It first showed up when you had big blood clots in the veins of your brain and in your lungs. You took blood thinners and steroid pills. Later you took another medicine to calm the immune system and prevent flare‑ups. Tests for a built‑in clotting problem were normal. You had several flare‑ups, but steroid pills kept them under control until 2017. After that, you stayed well. The blood thinners and the immune‑calming medicine were stopped. About a year later, you had sudden, very bad belly pain. You threw up after eating. Your legs became puffy. Tests showed your kidney problem had come back. A scan showed a new clot in a big artery that feeds your intestines. Not enough blood reached your bowel. In surgery, most of your small intestine was found dead. The damage could not be fixed. You died 48 hours later.'}"
+      ]
+     },
+     "execution_count": 8,
+     "metadata": {},
+     "output_type": "execute_result"
+    }
+   ],
+   "source": [
+    "my_target_documents[0]"
+   ]
+  }
+ ],
+ "metadata": {
+  "kernelspec": {
+   "display_name": "un",
+   "language": "python",
+   "name": "python3"
+  },
+  "language_info": {
+   "codemirror_mode": {
+    "name": "ipython",
+    "version": 3
+   },
+   "file_extension": ".py",
+   "mimetype": "text/x-python",
+   "name": "python",
+   "nbconvert_exporter": "python",
+   "pygments_lexer": "ipython3",
+   "version": "3.11.14"
+  }
+ },
+ "nbformat": 4,
+ "nbformat_minor": 5
+}
diff --git a/code/finetune/convert_qwen3_gguf.py b/code/finetune/convert_qwen3_gguf.py
new file mode 100644
index 0000000000000000000000000000000000000000..3c689ac42530b1b229a2c52e458c757cbadc45ac
--- /dev/null
+++ b/code/finetune/convert_qwen3_gguf.py
@@ -0,0 +1,20 @@
+import os
+os.environ["CUDA_DEVICE_ORDER"] = "PCI_BUS_ID"
+os.environ["CUDA_VISIBLE_DEVICES"] = "1"
+from unsloth import FastLanguageModel
+
+
+
+# Path to your finetuned model directory
+MODEL_PATH = "/home/mshahidul/readctrl_model/qwen3-8B_subclaims-verifier_lora_nonreasoning"
+
+model, tokenizer = FastLanguageModel.from_pretrained(
+    model_name = MODEL_PATH,
+    max_seq_length = 8192,
+    load_in_4bit = False,
+    load_in_8bit = False,
+)
+
+# Save merged 4-bit model for vLLM
+SAVE_PATH = "/home/mshahidul/readctrl_model/support_checking_vllm"
+model.save_pretrained_merged(SAVE_PATH, tokenizer, save_method = "merged_16bit")
diff --git a/code/finetune/mistral_3.1_24B.py b/code/finetune/mistral_3.1_24B.py
new file mode 100644
index 0000000000000000000000000000000000000000..a8246e8dd37288cae34d1e7105c0c5da5b2137a2
--- /dev/null
+++ b/code/finetune/mistral_3.1_24B.py
@@ -0,0 +1,104 @@
+import os
+import json
+os.environ["CUDA_DEVICE_ORDER"] = "PCI_BUS_ID"
+os.environ["CUDA_VISIBLE_DEVICES"] = "2"
+
+from unsloth import FastLanguageModel
+import torch
+dataset_path = "/home/mshahidul/readctrl/data/finetuning_data/finetune_dataset_subclaim_support_v2_sft_prompt.json"
+lora_save_path = "/home/mshahidul/readctrl_model/Mistral-Small-3.1-24B_subclaims-support-check-8b_ctx_v2-lora"
+full_model_save_path = "/home/mshahidul/readctrl_model/full_model/Mistral-Small-3.1-24B_subclaims-support-check-8b_ctx_v2-bf16"
+lora=False
+# === Load base model ===
+model, tokenizer = FastLanguageModel.from_pretrained(
+    model_name = "unsloth/Mistral-Small-3.1-24B-Instruct-2503",
+    max_seq_length = 8192,
+    load_in_4bit = False,
+    load_in_8bit = False,
+    full_finetuning = False,
+    dtype = torch.bfloat16,
+)
+
+# === Prepare LoRA model ===
+model = FastLanguageModel.get_peft_model(
+    model,
+    r = 32,
+    target_modules = [
+        "q_proj", "k_proj", "v_proj", "o_proj",
+        "gate_proj", "up_proj", "down_proj"
+    ],
+    lora_alpha = 32,
+    lora_dropout = 0,
+    bias = "none",
+    use_gradient_checkpointing = "unsloth",
+    random_state = 3407,
+    use_rslora = False,
+    loftq_config = None,
+)
+
+# === Load non-reasoning dataset (Full dataset) ===
+from datasets import load_dataset
+from unsloth.chat_templates import standardize_sharegpt
+
+print("Loading dataset...")
+with open(f"{dataset_path}") as f:
+    data = json.load(f)
+from datasets import Dataset
+dataset = Dataset.from_list(data)
+
+# Standardize and apply chat formatting
+dataset = standardize_sharegpt(dataset)
+non_reasoning_conversations = [
+    tokenizer.apply_chat_template(conv, tokenize=False)
+    for conv in dataset["conversations"]
+]
+
+# === Prepare dataset for training ===
+import pandas as pd
+from datasets import Dataset
+
+data = pd.Series(non_reasoning_conversations, name="text")
+combined_dataset = Dataset.from_pandas(pd.DataFrame(data))
+combined_dataset = combined_dataset.shuffle(seed=3407)
+
+# === Training setup ===
+from trl import SFTTrainer, SFTConfig
+
+trainer = SFTTrainer(
+    model=model,
+    tokenizer=tokenizer,
+    train_dataset=combined_dataset,
+    eval_dataset=None,  # Optional
+    args=SFTConfig(
+        dataset_text_field="text",
+        per_device_train_batch_size=16,
+        gradient_accumulation_steps=8,
+        warmup_steps=5,
+        num_train_epochs=1,
+        # max_steps=30,
+        learning_rate=2e-4,
+        logging_steps=1,
+        optim="adamw_8bit",
+        weight_decay=0.01,
+        lr_scheduler_type="linear",
+        seed=3407,
+        report_to="none",
+    ),
+)
+
+# === Train model ===
+trainer_stats = trainer.train()
+
+
+if lora==True:
+    model.save_pretrained(lora_save_path)
+    tokenizer.save_pretrained(lora_save_path)
+else:
+    model.save_pretrained_merged(
+        full_model_save_path,
+        tokenizer,
+        save_method="merged_16bit",
+    )
+
+
+
diff --git a/code/finetune/nemotran.py b/code/finetune/nemotran.py
new file mode 100644
index 0000000000000000000000000000000000000000..a221613b7bd6d72f88f4308f84a46836af72c68c
--- /dev/null
+++ b/code/finetune/nemotran.py
@@ -0,0 +1,136 @@
+import os
+import json
+os.environ["CUDA_DEVICE_ORDER"] = "PCI_BUS_ID"
+os.environ["CUDA_VISIBLE_DEVICES"] = "2"
+
+from unsloth import FastLanguageModel
+import torch
+dataset_path = "/home/mshahidul/readctrl/data/finetuning_data/train_subclaim_support_v2.json"
+lora_save_path = "/home/mshahidul/readctrl_model/nemotron-3-nano-30b-a3b_subclaims-support-check-8b_ctx_v2-lora"
+full_model_save_path = "/home/mshahidul/readctrl_model/full_model/nemotron-3-nano-30b-a3b_subclaims-support-check-8b_ctx_v2-bf16"
+lora=False
+# === Load base model ===
+model, tokenizer = FastLanguageModel.from_pretrained(
+    model_name = "unsloth/Nemotron-3-Nano-30B-A3B",
+    max_seq_length = 2048, # Choose any for long context!
+    load_in_4bit = False,  # 4 bit quantization to reduce memory
+    load_in_8bit = False, # [NEW!] A bit more accurate, uses 2x memory
+    full_finetuning = False, # [NEW!] We have full finetuning now!
+    trust_remote_code = True,
+    unsloth_force_compile = True,
+    attn_implementation="eager",
+    # token = "hf_...", # use one if using gated models
+)
+
+# === Prepare LoRA model ===
+model = FastLanguageModel.get_peft_model(
+    model,
+    r = 32,
+    target_modules = [
+        "q_proj", "k_proj", "v_proj", "o_proj",
+        "gate_proj", "up_proj", "down_proj"
+    ],
+    lora_alpha = 32,
+    lora_dropout = 0,
+    bias = "none",
+    use_gradient_checkpointing = "unsloth",
+    random_state = 3407,
+    use_rslora = False,
+    loftq_config = None,
+)
+
+# === Load non-reasoning dataset (Full dataset) ===
+from datasets import load_dataset
+from unsloth.chat_templates import standardize_sharegpt
+
+print("Loading dataset...")
+with open(f"{dataset_path}") as f:
+    data = json.load(f)
+from datasets import Dataset
+dataset = Dataset.from_list(data)
+def training_prompt(medical_text, subclaim):
+    system_prompt = (
+            "You are a clinical evidence auditor. Your evaluation must be based "
+            "STRICTLY and ONLY on the provided medical text. Do not use outside "
+            "medical knowledge or assume facts not explicitly stated. If the text "
+            "does not provide enough information to confirm the claim, you must "
+            "mark it as 'not_supported'."
+        )
+        
+    user_content = f"""EVALUATION TASK:
+    1. Read the Medical Text.
+    2. Verify the Subclaim.
+    3. If the evidence is missing, ambiguous, or unconfirmed in the text, label it 'not_supported'.
+
+    ### Medical Text:
+    {medical_text}
+
+    ### Subclaim:
+    {subclaim}
+
+    Output exactly one word ('supported' or 'not_supported'):"""
+    return f"{system_prompt}\n\n{user_content}"
+
+def generate_conversation(examples):
+    # import ipdb; ipdb.set_trace()
+    medical_texts  = examples["medical_text"]
+    subclaims = examples["subclaim"]
+    labels=examples['label']
+    conversations = []
+    for medical_text, subclaim, label in zip(medical_texts, subclaims, labels):
+        conversations.append([
+            {"role" : "user",      "content" : training_prompt(medical_text, subclaim)},
+            {"role" : "assistant", "content" : label},
+        ])
+    return { "conversations": conversations, }
+
+dataset = dataset.map(generate_conversation, batched = True)
+
+def formatting_prompts_func(examples):
+   convos = examples["conversations"]
+   texts = [tokenizer.apply_chat_template(convo, tokenize = False, add_generation_prompt = False) for convo in convos]
+   return { "text" : texts, }
+
+dataset = dataset.map(formatting_prompts_func, batched = True)
+
+
+# === Training setup ===
+from trl import SFTTrainer, SFTConfig
+trainer = SFTTrainer(
+    model = model,
+    tokenizer = tokenizer,
+    train_dataset = dataset,
+    eval_dataset = None, # Can set up evaluation!
+    args = SFTConfig(
+        dataset_text_field = "text",
+        per_device_train_batch_size = 4,
+        gradient_accumulation_steps = 2, # Use GA to mimic batch size!
+        warmup_steps = 5,
+        num_train_epochs = 1, # Set this for 1 full training run.
+        # max_steps = 60,
+        learning_rate = 2e-4, # Reduce to 2e-5 for long training runs
+        logging_steps = 1,
+        optim = "adamw_8bit",
+        weight_decay = 0.001,
+        lr_scheduler_type = "linear",
+        seed = 3407,
+        report_to = "none", # Use TrackIO/WandB etc
+    ),
+)
+
+# === Train model ===
+trainer_stats = trainer.train()
+
+
+if lora==True:
+    model.save_pretrained(lora_save_path)
+    tokenizer.save_pretrained(lora_save_path)
+else:
+    model.save_pretrained_merged(
+        full_model_save_path,
+        tokenizer,
+        save_method="merged_16bit",
+    )
+
+
+
diff --git a/code/finetune/qwen3-14B.py b/code/finetune/qwen3-14B.py
new file mode 100644
index 0000000000000000000000000000000000000000..3d9b12f07660e8a1a7dcfb65a3de9dfbd4c6e2d7
--- /dev/null
+++ b/code/finetune/qwen3-14B.py
@@ -0,0 +1,94 @@
+import json
+import os
+import sys
+
+os.environ["CUDA_DEVICE_ORDER"] = "PCI_BUS_ID"
+os.environ["CUDA_VISIBLE_DEVICES"] = "0"
+
+from unsloth import FastLanguageModel
+import torch
+model, tokenizer = FastLanguageModel.from_pretrained(
+    model_name = "unsloth/Qwen3-4B", 
+    max_seq_length = 8192,   # Context length - can be longer, but uses more memory
+    load_in_4bit = False,     # 4bit uses much less memory
+    load_in_8bit = False,    # A bit more accurate, uses 2x memory
+    full_finetuning = False, # We have full finetuning now!
+    # token = "hf_...",      # use one if using gated models
+)
+model = FastLanguageModel.get_peft_model(
+    model,
+    r = 32,           # Choose any number > 0! Suggested 8, 16, 32, 64, 128
+    target_modules = ["q_proj", "k_proj", "v_proj", "o_proj",
+                      "gate_proj", "up_proj", "down_proj",],
+    lora_alpha = 32,  # Best to choose alpha = rank or rank*2
+    lora_dropout = 0, # Supports any, but = 0 is optimized
+    bias = "none",    # Supports any, but = "none" is optimized
+    # [NEW] "unsloth" uses 30% less VRAM, fits 2x larger batch sizes!
+    use_gradient_checkpointing = "unsloth", # True or "unsloth" for very long context
+    random_state = 3407,
+    use_rslora = False,   # We support rank stabilized LoRA
+    loftq_config = None,  # And LoftQ
+)
+
+with open(f"/home/mshahidul/readctrl/data/finetuning_data/dataset_for_sft_support_check_list.json") as f:
+    data = json.load(f)
+from datasets import Dataset
+dataset = Dataset.from_list(data)
+
+from unsloth.chat_templates import standardize_sharegpt
+dataset = standardize_sharegpt(dataset)
+
+def formatting_prompts_func(examples):
+   convos = examples["conversations"]
+   texts = [tokenizer.apply_chat_template(convo, tokenize = False, add_generation_prompt = False) for convo in convos]
+   return { "text" : texts, }
+
+dataset = dataset.map(formatting_prompts_func, batched = True)
+
+split_dataset = dataset.train_test_split(test_size = 0.1, seed = 3407, shuffle = True)
+train_dataset = split_dataset["train"]
+eval_dataset = split_dataset["test"]
+
+from trl import SFTTrainer, SFTConfig
+trainer = SFTTrainer(
+    model = model,
+    tokenizer = tokenizer,
+    train_dataset = train_dataset,
+    eval_dataset = eval_dataset,
+    args = SFTConfig(
+        dataset_text_field = "text",
+        per_device_train_batch_size = 8,
+        gradient_accumulation_steps = 2, # Use GA to mimic batch size!
+        warmup_steps = 5,
+        num_train_epochs = 3, # Set this for 1 full training run.
+        # max_steps = 30,
+        learning_rate = 2e-4, # Reduce to 2e-5 for long training runs
+        logging_steps = 1,
+        per_device_eval_batch_size = 8,
+        bf16 = True,
+        tf32 = True,
+        optim = "adamw_8bit",
+        weight_decay = 0.01,
+        lr_scheduler_type = "linear",
+        seed = 3407,
+        report_to = "none", # Use this for WandB etc
+    ),
+)
+trainer_stats = trainer.train()
+
+save_dir = "/home/mshahidul/readctrl_model/support_checking_vllm/qwen3-4b"
+os.makedirs(save_dir, exist_ok=True)
+# Export merged model weights in FP16 format.
+model.save_pretrained_merged(
+    save_dir,
+    tokenizer,
+    save_method = "merged_16bit",
+)
+tokenizer.save_pretrained(save_dir)
+eval_metrics = trainer.evaluate()
+print(f"Eval metrics: {eval_metrics}")
+
+# model.push_to_hub(f"Translation_Evaluator_Qwen3_14B_v1", )
+# tokenizer.push_to_hub(f"Translation_Evaluator_Qwen3_14B_v1")
+# print(f"Model pushed to Hugging Face Hub")
+
diff --git a/code/finetune/qwen3-14B_infer.py b/code/finetune/qwen3-14B_infer.py
new file mode 100644
index 0000000000000000000000000000000000000000..e91486f4d02847e37edab596af4872734e8555eb
--- /dev/null
+++ b/code/finetune/qwen3-14B_infer.py
@@ -0,0 +1,121 @@
+import json
+import os
+import re
+
+import torch
+from datasets import Dataset
+from unsloth import FastLanguageModel
+
+os.environ["CUDA_DEVICE_ORDER"] = "PCI_BUS_ID"
+os.environ["CUDA_VISIBLE_DEVICES"] = "0"
+
+DATA_PATH = "/home/mshahidul/readctrl/data/finetuning_data/finetune_dataset_subclaim_support_v2_sft_prompt.json"
+MODEL_PATH = "/home/mshahidul/readctrl_model/qwen3-8B_subclaims-verifier_lora_nonreasoning"
+OUTPUT_PATH = "/home/mshahidul/readctrl/results/qwen3-8B_subclaims_verifier_test_predictions.jsonl"
+SUMMARY_PATH = "/home/mshahidul/readctrl/results/qwen3-8B_subclaims_verifier_test_summary.json"
+
+
+def normalize_label(text: str) -> str:
+    if text is None:
+        return "unknown"
+    cleaned = text.strip().lower()
+    cleaned = cleaned.replace("\n", " ").strip()
+    if "not_supported" in cleaned:
+        return "not_supported"
+    if "not supported" in cleaned:
+        return "not_supported"
+    first = re.split(r"\s+", cleaned)[0].strip(".,:;")
+    if first in {"supported", "not_supported"}:
+        return first
+    if "supported" in cleaned:
+        return "supported"
+    return "unknown"
+
+
+def get_turn(conversations, role: str) -> str:
+    for turn in conversations:
+        if turn.get("from") == role:
+            return turn.get("content", "")
+    return ""
+
+
+def main() -> None:
+    if not torch.cuda.is_available():
+        raise RuntimeError("CUDA is not available. Please run on a GPU.")
+
+    with open(DATA_PATH, "r") as f:
+        data = json.load(f)
+
+    dataset = Dataset.from_list(data)
+    split_dataset = dataset.train_test_split(test_size=0.2, seed=3407, shuffle=True)
+    test_data = split_dataset["test"]
+
+    model, tokenizer = FastLanguageModel.from_pretrained(
+        model_name=MODEL_PATH,
+        max_seq_length=8192,
+        load_in_4bit=False,
+    )
+    FastLanguageModel.for_inference(model)
+
+    total = len(test_data)
+    correct = 0
+
+    with open(OUTPUT_PATH, "w") as out_f:
+        for idx, item in enumerate(test_data):
+            user_text = get_turn(item["conversations"], "user")
+            gold_text = get_turn(item["conversations"], "assistant")
+            gold_label = normalize_label(gold_text)
+
+            messages = [{"role": "user", "content": user_text}]
+            input_text = tokenizer.apply_chat_template(
+                messages,
+                tokenize=False,
+                add_generation_prompt=True,
+            )
+            inputs = tokenizer([input_text], return_tensors="pt").to("cuda")
+
+            with torch.no_grad():
+                generated = model.generate(
+                    **inputs,
+                    max_new_tokens=20,
+                    do_sample=False,
+                    use_cache=True,
+                    pad_token_id=tokenizer.eos_token_id,
+                )
+
+            gen_text = tokenizer.decode(
+                generated[0][inputs["input_ids"].shape[-1]:],
+                skip_special_tokens=True,
+            )
+            pred_label = normalize_label(gen_text)
+            is_correct = pred_label == gold_label
+            correct += int(is_correct)
+
+            record = {
+                "index": idx,
+                "label": gold_label,
+                "prediction": pred_label,
+                "correct": is_correct,
+                "raw_output": gen_text.strip(),
+            }
+            out_f.write(json.dumps(record, ensure_ascii=False) + "\n")
+
+            if (idx + 1) % 100 == 0:
+                print(f"Processed {idx + 1}/{total}")
+
+    accuracy = correct / total if total else 0.0
+    summary = {
+        "total": total,
+        "correct": correct,
+        "accuracy": accuracy,
+    }
+    with open(SUMMARY_PATH, "w") as f:
+        json.dump(summary, f, ensure_ascii=False, indent=2)
+
+    print(f"Accuracy: {accuracy:.4f}")
+    print(f"Saved predictions: {OUTPUT_PATH}")
+    print(f"Saved summary: {SUMMARY_PATH}")
+
+
+if __name__ == "__main__":
+    main()
diff --git a/code/finetune/qwen3-32B.py b/code/finetune/qwen3-32B.py
new file mode 100644
index 0000000000000000000000000000000000000000..fa6612371176c89f8aaca398a953b06736477baf
--- /dev/null
+++ b/code/finetune/qwen3-32B.py
@@ -0,0 +1,104 @@
+import os
+import json
+os.environ["CUDA_DEVICE_ORDER"] = "PCI_BUS_ID"
+os.environ["CUDA_VISIBLE_DEVICES"] = "1"
+
+from unsloth import FastLanguageModel
+import torch
+dataset_path = "/home/mshahidul/readctrl/data/finetuning_data/classifier_en_data.json"
+lora_save_path = "/home/mshahidul/readctrl_model/qwen3-32B_classifier_en"
+full_model_save_path = "/home/mshahidul/readctrl_model/full_model/qwen3-32B_classifier_en-bf16"
+lora=True
+# === Load base model ===
+model, tokenizer = FastLanguageModel.from_pretrained(
+    model_name = "unsloth/Qwen3-32B",
+    max_seq_length = 8192,
+    load_in_4bit = False,
+    load_in_8bit = False,
+    full_finetuning = False,
+    dtype = torch.bfloat16,
+)
+
+# === Prepare LoRA model ===
+model = FastLanguageModel.get_peft_model(
+    model,
+    r = 32,
+    target_modules = [
+        "q_proj", "k_proj", "v_proj", "o_proj",
+        "gate_proj", "up_proj", "down_proj"
+    ],
+    lora_alpha = 32,
+    lora_dropout = 0,
+    bias = "none",
+    use_gradient_checkpointing = "unsloth",
+    random_state = 3407,
+    use_rslora = False,
+    loftq_config = None,
+)
+
+# === Load non-reasoning dataset (Full dataset) ===
+from datasets import load_dataset
+from unsloth.chat_templates import standardize_sharegpt
+
+print("Loading dataset...")
+with open(f"{dataset_path}") as f:
+    data = json.load(f)
+from datasets import Dataset
+dataset = Dataset.from_list(data)
+
+# Standardize and apply chat formatting
+dataset = standardize_sharegpt(dataset)
+non_reasoning_conversations = [
+    tokenizer.apply_chat_template(conv, tokenize=False)
+    for conv in dataset["conversations"]
+]
+
+# === Prepare dataset for training ===
+import pandas as pd
+from datasets import Dataset
+
+data = pd.Series(non_reasoning_conversations, name="text")
+combined_dataset = Dataset.from_pandas(pd.DataFrame(data))
+combined_dataset = combined_dataset.shuffle(seed=3407)
+
+# === Training setup ===
+from trl import SFTTrainer, SFTConfig
+
+trainer = SFTTrainer(
+    model=model,
+    tokenizer=tokenizer,
+    train_dataset=combined_dataset,
+    eval_dataset=None,  # Optional
+    args=SFTConfig(
+        dataset_text_field="text",
+        per_device_train_batch_size=16,
+        gradient_accumulation_steps=8,
+        warmup_steps=5,
+        num_train_epochs=1,
+        max_steps=30,
+        learning_rate=2e-4,
+        logging_steps=1,
+        optim="adamw_8bit",
+        weight_decay=0.01,
+        lr_scheduler_type="linear",
+        seed=3407,
+        report_to="none",
+    ),
+)
+
+# === Train model ===
+trainer_stats = trainer.train()
+
+
+if lora==True:
+    model.save_pretrained(lora_save_path)
+    tokenizer.save_pretrained(lora_save_path)
+else:
+    model.save_pretrained_merged(
+        full_model_save_path,
+        tokenizer,
+        save_method="merged_16bit",
+    )
+
+
+
diff --git a/code/finetune/train_data_preparation.ipynb b/code/finetune/train_data_preparation.ipynb
new file mode 100644
index 0000000000000000000000000000000000000000..f6d71435fde8163e66096d33eb634a58bc42e1ba
--- /dev/null
+++ b/code/finetune/train_data_preparation.ipynb
@@ -0,0 +1,1060 @@
+{
+ "cells": [
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "f2780f69",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "ALL_PROMPTS = {\n",
+    "    \"en\": {\n",
+    "        \"B1\": \"\"\"You are a summarization assistant. Your single most important goal is to rewrite medical text for a first-grade reading level (ages 5-7, FKGL 1.0-4.0). Simplicity is more important than detail.\n",
+    "\n",
+    "Core Mandate:\n",
+    "- TARGET AUDIENCE: A 6-year-old child.\n",
+    "- PRIMARY GOAL: Extreme simplicity. If you must choose between accuracy of detail and simplicity, ALWAYS choose simplicity.\n",
+    "\n",
+    "Strict Rules You Must Follow:\n",
+    "- SENTENCE LENGTH: Keep almost all sentences under 10 words. Use very short, simple sentences.\n",
+    "- VOCABULARY: Use only very common, everyday words that a first-grader would know. Avoid any medical or scientific terms. Instead of 'femur', say 'thigh bone'. Instead of 'benign', say 'not harmful'.\n",
+    "- TONE: Be very gentle, calm, and reassuring. Like a kind doctor explaining something to a small child.\n",
+    "- STRUCTURE: Use short paragraphs, often just one or two sentences long.\n",
+    "- FOCUS: Only mention the most important one or two points from the original text. Omit all other details.\n",
+    "\n",
+    "- Never use emojis.\n",
+    "- Do not explain pronunciation.\n",
+    "- DO NOT use any medical jargon.\n",
+    "\"\"\",\n",
+    "    \"B2\": \"\"\"You are a summarization assistant trained to rewrite medical summaries for a middle school reading level (ages 11–14, FKGL 6.0–9.0). Your goal is clarity for a teenager with a basic understanding of biology.\n",
+    "\n",
+    "Core Mandate:\n",
+    "- TARGET AUDIENCE: A 14-year-old in a 9th-grade biology class.\n",
+    "- PRIMARY GOAL: Clarity and straightforward explanation.\n",
+    "\n",
+    "Strict Rules You Must Follow:\n",
+    "- SENTENCE LENGTH: Vary sentence length, but aim for an average of 12-18 words. Avoid long, complex sentences.\n",
+    "- VOCABULARY: You can use basic medical terms (e.g., 'biopsy', 'cells', 'tumor'), but you MUST explain them in simple terms immediately. For example: \"A biopsy, which is when a small piece of tissue is taken for testing...\".\n",
+    "- TONE: Be empathetic but direct. Use an educational and informative tone, like a science teacher.\n",
+    "- STRUCTURE: Organize the summary into logical paragraphs. You can use simple headings if it helps clarity (e.g., \"What They Found,\" \"What It Means\").\n",
+    "- FOCUS: Summarize the main findings and their implications. Omit minor or highly technical details.\n",
+    "\n",
+    "- Never use emojis.\n",
+    "- Do not explain pronunciation.\n",
+    "\"\"\",\n",
+    "    \"B3\": \"\"\"You are a summarization assistant trained to rewrite medical summaries for an educated, non-medical adult (ages 17+, FKGL 12.0+). Your goal is to be precise, comprehensive, and clear for a college-level reader.\n",
+    "\n",
+    "Core Mandate:\n",
+    "- TARGET AUDIENCE: A curious college student or adult with no medical training.\n",
+    "- PRIMARY GOAL: Precision and structured clarity.\n",
+    "\n",
+    "Strict Rules You Must Follow:\n",
+    "- SENTENCE LENGTH: Use clear, well-constructed sentences. Complex sentences are acceptable if they enhance clarity and precision.\n",
+    "- VOCABULARY: Use correct medical terminology. You can assume the reader can understand terms from context or look them up, but for very specialized terms, provide a brief parenthetical explanation. For example: \"...showed evidence of hyperplasia (an increase in the number of cells).\"\n",
+    "- TONE: Maintain a professional, empathetic, and respectful tone. Be authoritative but not clinical or cold.\n",
+    "- STRUCTURE: Provide a detailed and structured summary. Use headings to organize information, such as \"Background,\" \"Key Findings,\" \"Clinical Interpretation,\" and \"Next Steps.\"\n",
+    "- FOCUS: Be comprehensive and faithful to the source summary. Include important details, test results, and differential diagnoses mentioned in the source.\n",
+    "\n",
+    "- Never use emojis.\n",
+    "- Do not explain pronunciation.\n",
+    "\"\"\"\n",
+    "    },\n",
+    "    \"es\": {\n",
+    "        \"B1\": \"\"\"Eres un asistente de resumen. Tu único y más importante objetivo es reescribir texto médico para un nivel de lectura de primer grado (edades 5-7). La simplicidad es más importante que el detalle.\n",
+    "\n",
+    "Mandato Principal:\n",
+    "- PÚBLICO OBJETIVO: Un niño de 6 años.\n",
+    "- OBJETIVO PRIMARIO: Simplicidad extrema. Si debes elegir entre la precisión del detalle y la simplicidad, SIEMPRE elige la simplicidad.\n",
+    "\n",
+    "Reglas Estrictas que Debes Seguir:\n",
+    "- IDIOMA: El resumen DEBE estar escrito en español.\n",
+    "- LONGITUD DE LA ORACIÓN: Casi todas las oraciones deben tener menos de 10 palabras. Usa frases muy cortas y simples.\n",
+    "- VOCABULARIO: Usa solo palabras cotidianas y muy comunes que un niño de primer grado conocería. Evita cualquier término médico o científico. En lugar de 'fémur', di 'hueso del muslo'. En lugar de 'benigno', di 'que no es dañino'.\n",
+    "- TONO: Sé muy gentil, calmado y tranquilizador. Como un doctor amable explicándole algo a un niño pequeño.\n",
+    "- ESTRUCTURA: Usa párrafos cortos, a menudo de solo una o dos oraciones.\n",
+    "- ENFOQUE: Menciona solo el punto más importante o los dos puntos más importantes del texto original. Omite todos los demás detalles.\n",
+    "\n",
+    "- Nunca uses emojis.\n",
+    "- No expliques la pronunciación.\n",
+    "- NO uses jerga médica.\n",
+    "\"\"\",\n",
+    "        \"B2\": \"\"\"Eres un asistente de resumen entrenado para reescribir resúmenes médicos para un nivel de lectura de secundaria (edades 11–14). Tu objetivo es la claridad para un adolescente con conocimientos básicos de biología.\n",
+    "\n",
+    "Mandato Principal:\n",
+    "- PÚBLICO OBJETIVO: Un estudiante de 14 años en una clase de biología de secundaria.\n",
+    "- OBJETIVO PRIMARIO: Claridad y explicación directa.\n",
+    "\n",
+    "Reglas Estrictas que Debes Seguir:\n",
+    "- IDIOMA: El resumen DEBE estar escrito en español.\n",
+    "- LONGITUD DE LA ORACIÓN: Varía la longitud de las oraciones, pero busca un promedio de 12-18 palabras. Evita las oraciones largas y complejas.\n",
+    "- VOCABULARIO: Puedes usar términos médicos básicos (ej., 'biopsia', 'células', 'tumor'), pero DEBES explicarlos en términos sencillos inmediatamente. Por ejemplo: \"Una biopsia, que es cuando se toma un pequeño trozo de tejido para analizarlo...\".\n",
+    "- TONO: Sé empático pero directo. Usa un tono educativo e informativo, como un profesor de ciencias.\n",
+    "- ESTRUCTURA: Organiza el resumen en párrafos lógicos. Puedes usar encabezados simples si ayuda a la claridad (ej., \"Lo que Encontraron,\" \"Qué Significa\").\n",
+    "- ENFOQUE: Resume los hallazgos principales y sus implicaciones. Omite detalles menores o muy técnicos.\n",
+    "\n",
+    "- Nunca uses emojis.\n",
+    "- No expliques la pronunciación.\n",
+    "\"\"\",\n",
+    "        \"B3\": \"\"\"Eres un asistente de resumen entrenado para reescribir resúmenes médicos para un adulto educado no médico (edades 17+). Tu objetivo es ser preciso, completo y claro para un lector de nivel universitario.\n",
+    "\n",
+    "Mandato Principal:\n",
+    "- PÚBLICO OBJETIVO: Un estudiante universitario o un adulto curioso sin formación médica.\n",
+    "- OBJETIVO PRIMARIO: Precisión y claridad estructurada.\n",
+    "\n",
+    "Reglas Estrictas que Debes Seguir:\n",
+    "- IDIOMA: El resumen DEBE estar escrito en español.\n",
+    "- LONGITUD DE LA ORACIÓN: Usa oraciones claras y bien construidas. Las oraciones complejas son aceptables si mejoran la claridad y la precisión.\n",
+    "- VOCABULARIO: Usa la terminología médica correcta. Puedes asumir que el lector puede entender los términos por el contexto o buscarlos, pero para términos muy especializados, proporciona una breve explicación entre paréntesis. Por ejemplo: \"...mostró evidencia de hiperplasia (un aumento en el número de células).\"\n",
+    "- TONO: Mantén un tono profesional, empático y respetuoso. Sé autoritario pero no clínico o frío.\n",
+    "- ESTRUCTURA: Proporciona un resumen detallado y estructurado. Usa encabezados para organizar la información, como \"Contexto,\" \"Hallazgos Clave,\" \"Interpretación Clínica,\" y \"Próximos Pasos.\"\n",
+    "- ENFOQUE: Sé completo y fiel al resumen original. Incluye detalles importantes, resultados de pruebas y diagnósticos diferenciales mencionados en la fuente.\n",
+    "\n",
+    "- Nunca uses emojis.\n",
+    "- No expliques la pronunciación.\n",
+    "\"\"\"\n",
+    "    },\n",
+    "\"fr\": {\n",
+    "    \"B1\": \"\"\"Vous êtes un assistant de résumé. Votre unique et plus important objectif est de réécrire un texte médical pour un niveau de lecture de cours préparatoire (âges 5-7). La simplicité est plus importante que le détail.\n",
+    "\n",
+    "Mandat Principal :\n",
+    "- PUBLIC CIBLE : Un enfant de 6 ans.\n",
+    "- OBJECTIF PRINCIPAL : Simplicité extrême. Si vous devez choisir entre la précision des détails et la simplicité, choisissez TOUJOURS la simplicité.\n",
+    "\n",
+    "Règles Strictes à Suivre Impérativement :\n",
+    "- LANGUE : Le résumé DOIT être rédigé en français.\n",
+    "- LONGUEUR DES PHRASES : Presque toutes les phrases doivent faire moins de 10 mots. Utilisez des phrases très courtes et simples.\n",
+    "- VOCABULAIRE : Utilisez uniquement des mots très courants et quotidiens qu'un enfant de cet âge connaîtrait. Évitez tout terme médical ou scientifique. Au lieu de 'fémur', dites 'l'os de la cuisse'. Au lieu de 'bénin', dites 'pas dangereux'.\n",
+    "- TON : Soyez très doux, calme et rassurant. Comme un médecin bienveillant qui explique quelque chose à un jeune enfant.\n",
+    "- STRUCTURE : Utilisez des paragraphes courts, souvent composés d'une ou deux phrases seulement.\n",
+    "- ENFOQUE : Mentionnez uniquement le ou les deux points les plus importants du texte original. Omettez tous les autres détails.\n",
+    "\n",
+    "- N'utilisez jamais d'emojis.\n",
+    "- N'expliquez pas la prononciation.\n",
+    "- N'utilisez AUCUN jargon médical.\n",
+    "\"\"\",\n",
+    "    \"B2\": \"\"\"Vous êtes un assistant de résumé entraîné à réécrire des résumés médicaux pour un niveau de lecture de collège (âges 11–14). Votre objectif est la clarté pour un adolescent ayant une compréhension de base de la biologie.\n",
+    "\n",
+    "Mandat Principal :\n",
+    "- PUBLIC CIBLE : Un adolescent de 14 ans en classe de biologie au collège.\n",
+    "- OBJECTIF PRINCIPAL : Clarté et explication directe.\n",
+    "\n",
+    "Règles Strictes à Suivre Impérativement :\n",
+    "- LANGUE : Le résumé DOIT être rédigé en français.\n",
+    "- LONGUEUR DES PHRASES : Variez la longueur des phrases, mais visez une moyenne de 12-18 mots. Évitez les phrases longues et complexes.\n",
+    "- VOCABULAIRE : Vous pouvez utiliser des termes médicaux de base (ex: 'biopsie', 'cellules', 'tumeur'), mais vous DEVEZ les expliquer en termes simples immédiatement. Par exemple : \"Une biopsie, c'est-à-dire quand on prélève un petit morceau de tissu pour l'analyser...\".\n",
+    "- TON : Soyez empathique mais direct. Adoptez un ton pédagogique et informatif, comme un professeur de sciences.\n",
+    "- STRUCTURE : Organisez le résumé en paragraphes logiques. Vous pouvez utiliser des titres simples si cela améliore la clarté (ex: \"Ce qu'ils ont trouvé\", \"Ce que cela signifie\").\n",
+    "- ENFOQUE : Résumez les principales observations et leurs implications. Omettez les détails mineurs ou très techniques.\n",
+    "\n",
+    "- N'utilisez jamais d'emojis.\n",
+    "- N'expliquez pas la prononciation.\n",
+    "\"\"\",\n",
+    "    \"B3\": \"\"\"Vous êtes un assistant de résumé entraîné à réécrire des résumés médicaux pour un adulte éduqué non-médecin (âges 17+). Votre objectif est d'être précis, complet et clair pour un lecteur de niveau universitaire.\n",
+    "\n",
+    "Mandat Principal :\n",
+    "- PUBLIC CIBLE : Un étudiant ou un adulte curieux sans formation médicale.\n",
+    "- OBJECTIF PRINCIPAL : Précision et clarté structurée.\n",
+    "\n",
+    "Règles Strictes à Suivre Impérativement :\n",
+    "- LANGUE : Le résumé DOIT être rédigé en français.\n",
+    "- LONGUEUR DES PHRASES : Utilisez des phrases claires et bien construites. Les phrases complexes sont acceptables si elles améliorent la clarté et la précision.\n",
+    "- VOCABULAIRE : Utilisez la terminologie médicale correcte. Vous pouvez supposer que le lecteur peut comprendre les termes par le contexte ou les rechercher, mais pour les termes très spécialisés, fournissez une brève explication entre parenthèses. Par exemple : \"...montrait des signes d'hyperplasie (une augmentation du nombre de cellules).\"\n",
+    "- TON : Maintenez un ton professionnel, empathique et respectueux. Soyez directif mais ni clinique ni froid.\n",
+    "- STRUCTURE : Fournissez un résumé détaillé et structuré. Utilisez des titres pour organiser l'information, tels que \"Contexte\", \"Principales Observations\", \"Interprétation Clinique\" et \"Prochaines Étapes\".\n",
+    "- ENFOQUE : Soyez complet et fidèle au résumé source. Incluez les détails importants, les résultats des tests et les diagnostics différentiels mentionnés dans la source.\n",
+    "\n",
+    "- N'utilisez jamais d'emojis.\n",
+    "- N'expliquez pas la prononciation.\n",
+    "\"\"\"\n",
+    "},\n",
+    "\n",
+    "\"pt\": {\n",
+    "    \"B1\": \"\"\"Você é um assistente de resumo. O seu único e mais importante objetivo é reescrever textos médicos para um nível de leitura da primeira série (idades 5-7). A simplicidade é mais importante que os detalhes.\n",
+    "\n",
+    "Mandato Principal:\n",
+    "- PÚBLICO-ALVO: Uma criança de 6 anos.\n",
+    "- OBJETIVO PRINCIPAL: Simplicidade extrema. Se tiver que escolher entre a precisão dos detalhes e a simplicidade, ESCOLHA SEMPRE a simplicidade.\n",
+    "\n",
+    "Regras Rígidas que Você Deve Seguir:\n",
+    "- IDIOMA: O resumo DEVE ser escrito em português.\n",
+    "- COMPRIMENTO DAS FRASES: Quase todas as frases devem ter menos de 10 palavras. Use frases muito curtas e simples.\n",
+    "- VOCABULÁRIO: Use apenas palavras quotidianas e muito comuns que uma criança da primeira série conheceria. Evite qualquer termo médico ou científico. Em vez de 'fêmur', diga 'o osso da coxa'. Em vez de 'benigno', diga 'que não faz mal'.\n",
+    "- TOM: Seja muito gentil, calmo e tranquilizador. Como um médico amável a explicar algo a uma criança pequena.\n",
+    "- ESTRUTURA: Use parágrafos curtos, muitas vezes com apenas uma ou duas frases.\n",
+    "- FOCO: Mencione apenas um ou dois dos pontos mais importantes do texto original. Omita todos os outros detalhes.\n",
+    "\n",
+    "- Nunca use emojis.\n",
+    "- Não explique a pronúncia.\n",
+    "- NÃO use NENHUM jargão médico.\n",
+    "\"\"\",\n",
+    "    \"B2\": \"\"\"Você é um assistente de resumo treinado para reescrever resumos médicos para um nível de leitura do ensino fundamental II (idades 11–14). O seu objetivo é a clareza para um adolescente com conhecimentos básicos de biologia.\n",
+    "\n",
+    "Mandato Principal:\n",
+    "- PÚBLICO-ALVO: Um adolescente de 14 anos numa aula de biologia.\n",
+    "- OBJETIVO PRINCIPAL: Clareza e explicação direta.\n",
+    "\n",
+    "Regras Rígidas que Você Deve Seguir:\n",
+    "- IDIOMA: O resumo DEVE ser escrito em português.\n",
+    "- COMPRIMENTO DAS FRASES: Varie o comprimento das frases, mas procure uma média de 12 a 18 palavras. Evite frases longas e complexas.\n",
+    "- VOCABULÁRIO: Pode usar termos médicos básicos (ex: 'biópsia', 'células', 'tumor'), mas você DEVE explicá-los em termos simples imediatamente. Por exemplo: \"Uma biópsia, que é quando um pequeno pedaço de tecido é retirado para ser analisado...\".\n",
+    "- TOM: Seja empático, mas direto. Use um tom educativo e informativo, como um professor de ciências.\n",
+    "- ESTRUTURA: Organize o resumo em parágrafos lógicos. Pode usar títulos simples se isso ajudar na clareza (ex: \"O que eles encontraram\", \"O que isso significa\").\n",
+    "- FOCO: Resuma os principais achados e as suas implicações. Omita detalhes menores ou muito técnicos.\n",
+    "\n",
+    "- Nunca use emojis.\n",
+    "- Não explique a pronúncia.\n",
+    "\"\"\",\n",
+    "    \"B3\": \"\"\"Você é um assistente de resumo treinado para reescrever resumos médicos para um adulto instruído, mas sem formação médica (idades 17+). O seu objetivo é ser preciso, abrangente e claro para um leitor de nível universitário.\n",
+    "\n",
+    "Mandato Principal:\n",
+    "- PÚBLICO-ALVO: Um estudante universitário ou adulto curioso sem formação médica.\n",
+    "- OBJETIVO PRINCIPAL: Precisão e clareza estruturada.\n",
+    "\n",
+    "Regras Rígidas que Você Deve Seguir:\n",
+    "- IDIOMA: O resumo DEVE ser escrito em português.\n",
+    "- COMPRIMENTO DAS FRASES: Use frases claras e bem construídas. Frases complexas são aceitáveis se melhorarem a clareza e a precisão.\n",
+    "- VOCABULÁRIO: Use a terminologia médica correta. Pode assumir que o leitor consegue entender os termos pelo contexto ou pesquisá-los, mas para termos muito especializados, forneça uma breve explicação entre parênteses. Por exemplo: \"...mostrou evidência de hiperplasia (um aumento no número de células).\"\n",
+    "- TOM: Mantenha um tom profissional, empático e respeitoso. Seja confiante, mas não clínico ou frio.\n",
+    "- ESTRUTURA: Forneça um resumo detalhado e estruturado. Use títulos para organizar a informação, como \"Contexto\", \"Principais Achados\", \"Interpretação Clínica\" e \"Próximos Passos\".\n",
+    "- FOCO: Seja abrangente e fiel ao resumo original. Inclua detalhes importantes, resultados de testes e diagnósticos diferenciais mencionados na fonte.\n",
+    "\n",
+    "- Nunca use emojis.\n",
+    "- Não explique a pronúncia.\n",
+    "\"\"\"\n",
+    "}\n",
+    "\n",
+    "}\n",
+    "USER_PROMPT_TEMPLATES = {\n",
+    "    \"en\": \"\"\"Please rewrite the following expert summary for the specified target audience. Use the full article for context if needed.\n",
+    "**Full Article Context:**\n",
+    "{article}\n",
+    "**Expert Summary to Rewrite:**\n",
+    "{gold_summary}\n",
+    "\"\"\",\n",
+    "    \"es\": \"\"\"Por favor, reescribe el siguiente resumen de experto para el público objetivo especificado. Usa el artículo completo como contexto si es necesario.\n",
+    "**Contexto del Artículo Completo:**\n",
+    "{article}\n",
+    "**Resumen de Experto a Reescribir:**\n",
+    "{gold_summary}\n",
+    "\"\"\",\n",
+    "    \"fr\": \"\"\"Veuillez réécrire le résumé d'expert suivant pour le public cible spécifié. Utilisez l'article complet comme contexte si nécessaire.\n",
+    "**Contexte de l'Article Complet :**\n",
+    "{article}\n",
+    "**Résumé d'Expert à Réécrire :**\n",
+    "{gold_summary}\n",
+    "\"\"\",\n",
+    "    \"pt\": \"\"\"Por favor, reescreva o seguinte resumo de especialista para o público-alvo especificado. Use o artigo completo como contexto, se necessário.\n",
+    "**Contexto do Artigo Completo:**\n",
+    "{article}\n",
+    "**Resumo do Especialista a Ser Reescrito:**\n",
+    "{gold_summary}\n",
+    "\"\"\"\n",
+    "}"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "2bb9ee67",
+   "metadata": {},
+   "outputs": [],
+   "source": []
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "e40397cf",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import json\n",
+    "lang=\"es\"\n",
+    "with open('/home/mshahidul/readctrl/generating_data/tik_ache/es_syntheticV3.json', 'r', encoding='utf-8') as f:\n",
+    "    data = json.load(f)\n",
+    "\n",
+    "converted = []\n",
+    "prompts_for_lang = ALL_PROMPTS.get(lang)\n",
+    "user_prompt_template = USER_PROMPT_TEMPLATES.get(lang)\n",
+    "for msg in data:\n",
+    "    conversation={}\n",
+    "    for key in msg['synthetic_summary'].keys():\n",
+    "        system_prompt = prompts_for_lang[key]\n",
+    "        sys_msg=msg['synthetic_summary'][key]\n",
+    "        user_prompt = user_prompt_template.format(article=msg['article'], gold_summary=msg['gold_summary'])\n",
+    "        conversation['conversations']= (\n",
+    "            {'from': \"human\", 'content': system_prompt+'\\n'+user_prompt},\n",
+    "            {'from': \"gpt\", 'content': sys_msg},\n",
+    "        )\n",
+    "        converted.append(conversation)\n",
+    "\n",
+    "# Save or print the result\n",
+    "with open(f'/home/mshahidul/readctrl/data_train/{lang}_train.json', 'w', encoding='utf-8') as f:\n",
+    "    json.dump(converted, f, ensure_ascii=False, indent=2)\n"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "e4373e6c",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "with open('/home/mshahidul/readctrl/data_train/es_train.json', 'r', encoding='utf-8') as f:\n",
+    "    es_data = json.load(f)\n",
+    "print(es_data[0]['conversations'][1]['content'])"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "4e8e1d2d",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "def generate_prompt(article, gold_summary, band, lang):\n",
+    "    \"\"\"Call an OpenAI model to generate a synthetic summary for a given readability band and language.\"\"\"\n",
+    "    prompts_for_lang = ALL_PROMPTS.get(lang)\n",
+    "    user_prompt_template = USER_PROMPT_TEMPLATES.get(lang)\n",
+    "    if not prompts_for_lang or not user_prompt_template:\n",
+    "        raise ValueError(f\"No prompts available for language: {lang}\")\n",
+    "    \n",
+    "    system_prompt = prompts_for_lang[band]\n",
+    "    user_prompt = user_prompt_template.format(article=article, gold_summary=gold_summary)\n",
+    "    return system_prompt + \"\\n\" + user_prompt"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "ddb14cb1",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import json\n",
+    "lang=\"es\"\n",
+    "with open('/home/mshahidul/readctrl/generating_data/tik_ache/es_syntheticV3.json', 'r', encoding='utf-8') as f:\n",
+    "    data = json.load(f)\n",
+    "\n",
+    "converted = []\n",
+    "prompts_for_lang = ALL_PROMPTS.get(lang)\n",
+    "user_prompt_template = USER_PROMPT_TEMPLATES.get(lang)\n",
+    "for msg in data:\n",
+    "    for key in msg['synthetic_summary'].keys():\n",
+    "        conversation={}\n",
+    "        system_prompt = prompts_for_lang[key]\n",
+    "        sys_msg=msg['synthetic_summary'][key]\n",
+    "        user_prompt = user_prompt_template.format(article=msg['article'], gold_summary=msg['gold_summary'])\n",
+    "        conversation['conversations']= (\n",
+    "            {'from': \"human\", 'content': system_prompt+'\\n'+user_prompt},\n",
+    "            {'from': \"gpt\", 'content': sys_msg},\n",
+    "        )\n",
+    "        converted.append(conversation)\n",
+    "\n",
+    "# Save or print the result\n",
+    "with open(f'/home/mshahidul/readctrl/data_train/{lang}_train.json', 'w', encoding='utf-8') as f:\n",
+    "    json.dump(converted, f, ensure_ascii=False, indent=2)\n"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "b82bd543",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import json\n",
+    "with open('/home/mshahidul/readctrl/synthetic_data_es_raw/0.json', 'r', encoding='utf-8') as f:\n",
+    "    raw_es_data = json.load(f)\n",
+    "print(f\"easy:- {raw_es_data['readability_versions']['easy']['text']}\")\n",
+    "print(f\"intermediate:- {raw_es_data['readability_versions']['intermediate']['text']}\")\n",
+    "print(f\"hard:- {raw_es_data['readability_versions']['hard']['text']}\")"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "aca0ef62",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import os\n",
+    "import json\n",
+    "\n",
+    "raw_dir = '/home/mshahidul/readctrl/synthetic_data_es_raw'\n",
+    "raw_files = [f for f in os.listdir(raw_dir) if f.endswith('.json')]\n",
+    "\n",
+    "raw_data_list = []\n",
+    "for fname in raw_files:\n",
+    "    with open(os.path.join(raw_dir, fname), 'r', encoding='utf-8') as f:\n",
+    "        raw_data_list.append(json.load(f))\n",
+    "\n",
+    "print(f\"Loaded {len(raw_data_list)} files from {raw_dir}\")\n",
+    "with open('/home/mshahidul/readctrl/data/hand_create_gpt5/es_rawV1.json', 'w', encoding='utf-8') as f:\n",
+    "    json.dump(raw_data_list, f, ensure_ascii=False, indent=4)"
+   ]
+  },
+  {
+   "cell_type": "markdown",
+   "id": "0c6d8fb6",
+   "metadata": {},
+   "source": [
+    "## dataset modified for training"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "0899cccb",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import json\n",
+    "prompts={\n",
+    "\"easy\":'''\n",
+    "You are an assistant that rewrites Spanish texts to make them very simple and easy to understand.\n",
+    "Your goal is to rewrite the provided input text for younger readers (Fernández Huerta 70–100; grade 5–7).\n",
+    "Use short sentences, simple words, and friendly tone. Avoid technical or complex expressions.\n",
+    "Keep all important factual details, but remove jargon.\n",
+    "Return only the rewritten text without commentary.\n",
+    "''',\n",
+    "\n",
+    "'intermediate':'''\n",
+    "You are an assistant specialized in rewriting Spanish texts with medium readability.\n",
+    "Your task is to rewrite the provided input text for general or high‑school‑level readers (Fernández Huerta 50–70; grade 8–12).\n",
+    "Use clear and complete sentences, moderately complex vocabulary, and structured narration.\n",
+    "Retain all relevant medical or factual information, but phrase it in accessible language.\n",
+    "Return only the rewritten text with no explanations.\n",
+    "''',\n",
+    "\n",
+    "'hard':'''\n",
+    "You are an assistant that rewrites Spanish medical texts with professional, technical precision.\n",
+    "Rewrite the following input text using specialized, academic terminology and information‑dense phrasing.\n",
+    "The output must target a Fernández Huerta readability index between 0 and 50 (university/professional level).\n",
+    "Use clinical vocabulary, formal register, and detailed description of pathophysiology, procedures, and findings.\n",
+    "Return only the rewritten text.\n",
+    "'''\n",
+    "}\n",
+    "with open('/home/mshahidul/readctrl/data/hand_create_gpt5/es_rawV1.json', 'r', encoding='utf-8') as f:\n",
+    "    gpt5_syn_es = json.load(f)\n",
+    "gpt5_syn_es[0]\n",
+    "import json\n",
+    "\n",
+    "with open('/home/mshahidul/readctrl/data/testing_data_gs/multiclinsum_gs_train_es.json', 'r', encoding='utf-8') as f:\n",
+    "    test_data = json.load(f)\n",
+    "\n",
+    "def full_text(id):\n",
+    "    for item in test_data:\n",
+    "        if item['id'] == id:\n",
+    "            return item['fulltext']\n",
+    "    return None"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "38186215",
+   "metadata": {},
+   "outputs": [],
+   "source": []
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "a9ce8569",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "converted = []\n",
+    "cnt=0\n",
+    "for item in gpt5_syn_es:\n",
+    "    readability_data=item['readability_versions']\n",
+    "    fulltext=full_text(item['id'])\n",
+    "    for band, band_data in readability_data.items():\n",
+    "        conversation={}\n",
+    "        system_prompt=prompts[band]\n",
+    "        conversation['conversations']= (\n",
+    "                {'from': \"human\", 'content': system_prompt+'\\n\\n'+\"Input text:\\n\"+fulltext},\n",
+    "                {'from': \"gpt\", 'content': band_data['text']},\n",
+    "            )\n",
+    "        converted.append(conversation)"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "52be9a01",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "# [{'content': 'reasoning language: French\\n\\nYou are an AI chatbot with a lively and energetic personality.',\n",
+    "#   'role': 'system',\n",
+    "#   'thinking': None},\n",
+    "#  {'content': 'Can you show me the latest trends on Twitter right now?',\n",
+    "#   'role': 'user',\n",
+    "#   'thinking': None},\n",
+    "#  {'content': 'Hey there!  While I can\\'t check Twitter (X) in real-time or access live data, I can share some tips to help you spot the latest trends:\\n\\n1. **Open the \"Trending\" tab** on the Twitter app or website – it updates constantly!  \\n2. **Search for hashtags** like #Trending or #Viral to see what’s blowing up.  \\n3. **Follow accounts** that curate trends (e.g., @TrendingNow, @ViralThreads).  \\n4. **Check regional trends** – they often differ by location!  \\n\\nRemember, trends are *super fast-moving* and often tied to pop culture, memes, or breaking news. For example, recent trends have included viral challenges (like the \"Distracted Boyfriend\" meme revival), celebrity drama, or unexpected events (hello, weather disasters!).  \\n\\nWant me to brainstorm *what* might trend next? I’ve got ideas!',\n",
+    "#   'role': 'assistant',\n",
+    "#   'thinking': \"D'accord, l'utilisateur demande les tendances Twitter les plus récentes. Tout d'abord, je dois vérifier si j'ai accès à des données en temps réel. Étant donné que je ne peux pas naviguer sur Internet ou accéder directement à l'API de Twitter, je ne peux pas fournir des tendances en direct. Cependant, je peux donner quelques conseils généraux sur la façon de les trouver.\\n\\nJe devrais préciser que les tendances Twitter évoluent rapidement et sont spécifiques à chaque région. Je pourrais suggérer de consulter la section «\\xa0En vogue\\xa0» sur l'application ou le site web. Aussi, l'utilisation de hashtags et le suivi d'utilisateurs pertinents pourraient être utiles. Il est important de souligner que les tendances varient selon la région et l'heure de la journée. Je devrais garder un ton amical et bienveillant, peut-être ajouter un emoji pour rester léger. Je vais structurer ma réponse étape par étape pour faciliter la lecture. Je dois m'excuser de ne pas pouvoir fournir des données en temps réel et proposer d'autres méthodes. Je conserverai un langage simple et convivial, en évitant les termes techniques.\"}]"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "5a71fdf6",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "converted = []\n",
+    "cnt=0\n",
+    "for item in gpt5_syn_es:\n",
+    "    readability_data=item['readability_versions']\n",
+    "    fulltext=full_text(item['id'])\n",
+    "    for band, band_data in readability_data.items():\n",
+    "        conversation={}\n",
+    "        system_prompt=prompts[band]\n",
+    "        conversation['messages']= (\n",
+    "                {'role': \"system\", 'content': system_prompt, 'thinking': None},\n",
+    "                {'role': \"user\", 'content': \"Input text:\\n\"+fulltext, 'thinking': None},\n",
+    "                {'role': \"assistant\", 'content': band_data['text'], 'thinking': None},\n",
+    "            )\n",
+    "        converted.append(conversation)"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "7f173809",
+   "metadata": {},
+   "outputs": [],
+   "source": []
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "c20a9f4a",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "with open(f'/home/mshahidul/readctrl/data/hand_create_gpt5/es_trainV1.json', 'w', encoding='utf-8') as f:\n",
+    "    json.dump(converted, f, ensure_ascii=False, indent=4)"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "975d8e1b",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import pyphen\n",
+    "import matplotlib.pyplot as plt\n",
+    "\n",
+    "# Initialize Spanish syllable dictionary\n",
+    "dic = pyphen.Pyphen(lang='es')\n",
+    "\n",
+    "# --- FH Score Functions ---\n",
+    "def count_syllables(word):\n",
+    "    hyphenated = dic.inserted(word)\n",
+    "    return len(hyphenated.split('-'))\n",
+    "\n",
+    "def huerta_score(text):\n",
+    "    \"\"\"\n",
+    "    Compute the Fernández Huerta readability score for Spanish text.\n",
+    "    FH = 206.84 - 60 * (Syllables per Word) - 1.02 * (Words per Sentence)\n",
+    "    \"\"\"\n",
+    "    sentences = [s for s in text.split('.') if s.strip()]\n",
+    "    words = [w for w in text.split() if w.isalpha()]\n",
+    "    if not words or not sentences:\n",
+    "        return 0.0\n",
+    "    total_syllables = sum(count_syllables(word.lower()) for word in words)\n",
+    "    avg_syllables_per_word = total_syllables / len(words)\n",
+    "    avg_sentence_length = len(words) / len(sentences)\n",
+    "    score = 206.84 - 60 * avg_syllables_per_word - 1.02 * avg_sentence_length\n",
+    "    return round(score, 2)\n",
+    "\n",
+    "# --- Plotting Function ---\n",
+    "def plot_fh_scores(text_list):\n",
+    "    scores = [huerta_score(t) for t in text_list]\n",
+    "    indices = list(range(len(text_list)))\n",
+    "\n",
+    "    plt.figure(figsize=(10, 5))\n",
+    "    plt.plot(indices, scores, 'ko', label='FH Score')\n",
+    "    plt.axhspan(70, 100, color='green', alpha=0.1, label='Easy (70-100)')\n",
+    "    plt.axhspan(50, 70, color='blue', alpha=0.1, label='Intermediate (50-70)')\n",
+    "    plt.axhspan(0, 50, color='red', alpha=0.1, label='Hard (0-50)')\n",
+    "    plt.xlabel('Text Index')\n",
+    "    plt.ylabel('Fernández Huerta Score')\n",
+    "    plt.title('Fernández Huerta Readability Scores')\n",
+    "    plt.legend()\n",
+    "    plt.tight_layout()\n",
+    "    plt.show()\n",
+    "\n",
+    "    # Also print results\n",
+    "    for i, s in enumerate(scores):\n",
+    "        print(f\"Text {i}: FH Score = {s}\")\n",
+    "\n",
+    "        # Example: Compute FH score for the \"hard\" band_data text\n",
+    "        hard_text = band_data['text']\n",
+    "        hard_score = huerta_score(hard_text)\n",
+    "        print(f'Fernández Huerta score for \"hard\" band: {hard_score}')\n",
+    "# --- Example Usage ---\n",
+    "# texts = [\n",
+    "#     \"Este es un texto muy simple y fácil de leer. Las oraciones son cortas.\",\n",
+    "#     \"El presente documento aborda temas complejos relacionados con la neurociencia cognitiva y su aplicación en sistemas computacionales.\",\n",
+    "#     \"El perro corre rápido. Juega con la pelota. Se divierte mucho.\"\n",
+    "# ]\n",
+    "\n",
+    "# plot_fh_scores(texts)\n"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "804a3d10",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import json\n",
+    "\n",
+    "test_en_path = '/home/mshahidul/readctrl/data/testing_data/multiclinsum_test_en.json'\n",
+    "with open(test_en_path, 'r', encoding='utf-8') as f:\n",
+    "    test_en_data = json.load(f)\n",
+    "\n",
+    "print(f\"Loaded {len(test_en_data)} items from {test_en_path}\")\n",
+    "print(test_en_data[0])"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "4a230d18",
+   "metadata": {},
+   "outputs": [],
+   "source": []
+  },
+  {
+   "cell_type": "markdown",
+   "id": "e372abbf",
+   "metadata": {},
+   "source": [
+    "## Model accuracy check"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 1,
+   "id": "1190eb4b",
+   "metadata": {},
+   "outputs": [
+    {
+     "name": "stdout",
+     "output_type": "stream",
+     "text": [
+      "--------------------------------------------------\n",
+      "temp0.1_qwen3-14B_base_with_defs.json accuracy results:\n",
+      "{'easy': 50, 'intermediate': 50, 'hard': 50}\n",
+      "{'easy': 49, 'intermediate': 14, 'hard': 9}\n",
+      "easy: 98.00%, intermediate: 28.00%, hard: 18.00%\n",
+      "--------------------------------------------------\n",
+      "temp0.3_qwen3-14B_base_with_defs.json accuracy results:\n",
+      "{'easy': 50, 'intermediate': 50, 'hard': 50}\n",
+      "{'easy': 48, 'intermediate': 15, 'hard': 10}\n",
+      "easy: 96.00%, intermediate: 30.00%, hard: 20.00%\n",
+      "--------------------------------------------------\n",
+      "temp0.5_qwen3-14B_finetuned_with_defs.json accuracy results:\n",
+      "{'easy': 50, 'intermediate': 50, 'hard': 50}\n",
+      "{'easy': 37, 'intermediate': 32, 'hard': 17}\n",
+      "easy: 74.00%, intermediate: 64.00%, hard: 34.00%\n",
+      "--------------------------------------------------\n",
+      "temp1.3_qwen3-14B_base_with_defs.json accuracy results:\n",
+      "{'easy': 50, 'intermediate': 50, 'hard': 50}\n",
+      "{'easy': 46, 'intermediate': 25, 'hard': 24}\n",
+      "easy: 92.00%, intermediate: 50.00%, hard: 48.00%\n",
+      "--------------------------------------------------\n",
+      "temp1.1_qwen3-14B_finetuned_with_defs.json accuracy results:\n",
+      "{'easy': 50, 'intermediate': 50, 'hard': 50}\n",
+      "{'easy': 40, 'intermediate': 30, 'hard': 29}\n",
+      "easy: 80.00%, intermediate: 60.00%, hard: 58.00%\n",
+      "--------------------------------------------------\n",
+      "temp1.0_qwen3-14B_finetuned_with_defs.json accuracy results:\n",
+      "{'easy': 50, 'intermediate': 50, 'hard': 50}\n",
+      "{'easy': 43, 'intermediate': 32, 'hard': 18}\n",
+      "easy: 86.00%, intermediate: 64.00%, hard: 36.00%\n",
+      "--------------------------------------------------\n",
+      "temp1.5_qwen3-14B_finetuned_with_defs.json accuracy results:\n",
+      "{'easy': 50, 'intermediate': 50, 'hard': 50}\n",
+      "{'easy': 24, 'intermediate': 26, 'hard': 33}\n",
+      "easy: 48.00%, intermediate: 52.00%, hard: 66.00%\n",
+      "--------------------------------------------------\n",
+      "temp1.3_qwen3-14B_finetuned_with_defs.json accuracy results:\n",
+      "{'easy': 50, 'intermediate': 50, 'hard': 50}\n",
+      "{'easy': 29, 'intermediate': 38, 'hard': 29}\n",
+      "easy: 58.00%, intermediate: 76.00%, hard: 58.00%\n",
+      "--------------------------------------------------\n",
+      "temp0.7_qwen3-14B_base_with_defs.json accuracy results:\n",
+      "{'easy': 50, 'intermediate': 50, 'hard': 50}\n",
+      "{'easy': 48, 'intermediate': 16, 'hard': 10}\n",
+      "easy: 96.00%, intermediate: 32.00%, hard: 20.00%\n",
+      "--------------------------------------------------\n",
+      "temp0.5_qwen3-14B_base_with_defs.json accuracy results:\n",
+      "{'easy': 50, 'intermediate': 50, 'hard': 50}\n",
+      "{'easy': 48, 'intermediate': 20, 'hard': 9}\n",
+      "easy: 96.00%, intermediate: 40.00%, hard: 18.00%\n",
+      "--------------------------------------------------\n",
+      "temp0.7_qwen3-14B_finetuned_with_defs.json accuracy results:\n",
+      "{'easy': 50, 'intermediate': 50, 'hard': 50}\n",
+      "{'easy': 43, 'intermediate': 23, 'hard': 11}\n",
+      "easy: 86.00%, intermediate: 46.00%, hard: 22.00%\n",
+      "--------------------------------------------------\n",
+      "temp1.4_qwen3-14B_base_with_defs.json accuracy results:\n",
+      "{'easy': 50, 'intermediate': 50, 'hard': 50}\n",
+      "{'easy': 48, 'intermediate': 27, 'hard': 26}\n",
+      "easy: 96.00%, intermediate: 54.00%, hard: 52.00%\n",
+      "--------------------------------------------------\n",
+      "temp1.1_qwen3-14B_base_with_defs.json accuracy results:\n",
+      "{'easy': 50, 'intermediate': 50, 'hard': 50}\n",
+      "{'easy': 48, 'intermediate': 16, 'hard': 13}\n",
+      "easy: 96.00%, intermediate: 32.00%, hard: 26.00%\n",
+      "--------------------------------------------------\n",
+      "temp1.4_qwen3-14B_finetuned_with_defs.json accuracy results:\n",
+      "{'easy': 50, 'intermediate': 50, 'hard': 50}\n",
+      "{'easy': 28, 'intermediate': 27, 'hard': 30}\n",
+      "easy: 56.00%, intermediate: 54.00%, hard: 60.00%\n",
+      "--------------------------------------------------\n",
+      "temp0.1_qwen3-14B_finetuned_with_defs.json accuracy results:\n",
+      "{'easy': 50, 'intermediate': 50, 'hard': 50}\n",
+      "{'easy': 40, 'intermediate': 32, 'hard': 16}\n",
+      "easy: 80.00%, intermediate: 64.00%, hard: 32.00%\n",
+      "--------------------------------------------------\n",
+      "temp1.2_qwen3-14B_base_with_defs.json accuracy results:\n",
+      "{'easy': 50, 'intermediate': 50, 'hard': 50}\n",
+      "{'easy': 48, 'intermediate': 20, 'hard': 28}\n",
+      "easy: 96.00%, intermediate: 40.00%, hard: 56.00%\n",
+      "--------------------------------------------------\n",
+      "temp0.3_qwen3-14B_finetuned_with_defs.json accuracy results:\n",
+      "{'easy': 50, 'intermediate': 50, 'hard': 50}\n",
+      "{'easy': 40, 'intermediate': 32, 'hard': 9}\n",
+      "easy: 80.00%, intermediate: 64.00%, hard: 18.00%\n",
+      "--------------------------------------------------\n",
+      "temp1.5_qwen3-14B_base_with_defs.json accuracy results:\n",
+      "{'easy': 50, 'intermediate': 50, 'hard': 50}\n",
+      "{'easy': 47, 'intermediate': 20, 'hard': 33}\n",
+      "easy: 94.00%, intermediate: 40.00%, hard: 66.00%\n",
+      "--------------------------------------------------\n",
+      "temp1.0_qwen3-14B_base_with_defs.json accuracy results:\n",
+      "{'easy': 50, 'intermediate': 50, 'hard': 50}\n",
+      "{'easy': 47, 'intermediate': 18, 'hard': 16}\n",
+      "easy: 94.00%, intermediate: 36.00%, hard: 32.00%\n",
+      "--------------------------------------------------\n",
+      "temp1.2_qwen3-14B_finetuned_with_defs.json accuracy results:\n",
+      "{'easy': 50, 'intermediate': 50, 'hard': 50}\n",
+      "{'easy': 39, 'intermediate': 36, 'hard': 27}\n",
+      "easy: 78.00%, intermediate: 72.00%, hard: 54.00%\n"
+     ]
+    }
+   ],
+   "source": [
+    "import os\n",
+    "import pyphen\n",
+    "import matplotlib.pyplot as plt\n",
+    "band_ranges = {\n",
+    "    \"easy\": (70, 100),        # Easy\n",
+    "    \"intermediate\": (50, 70), # Intermediate\n",
+    "    \"hard\": (0, 50)           # Hard\n",
+    "}\n",
+    "# Initialize Spanish syllable dictionary\n",
+    "dic = pyphen.Pyphen(lang='es')\n",
+    "\n",
+    "# --- FH Score Functions ---\n",
+    "def count_syllables(word):\n",
+    "    hyphenated = dic.inserted(word)\n",
+    "    return len(hyphenated.split('-'))\n",
+    "\n",
+    "def huerta_score(text):\n",
+    "    \"\"\"\n",
+    "    Compute the Fernández Huerta readability score for Spanish text.\n",
+    "    FH = 206.84 - 60 * (Syllables per Word) - 1.02 * (Words per Sentence)\n",
+    "    \"\"\"\n",
+    "    sentences = [s for s in text.split('.') if s.strip()]\n",
+    "    words = [w for w in text.split() if w.isalpha()]\n",
+    "    if not words or not sentences:\n",
+    "        return 0.0\n",
+    "    total_syllables = sum(count_syllables(word.lower()) for word in words)\n",
+    "    avg_syllables_per_word = total_syllables / len(words)\n",
+    "    avg_sentence_length = len(words) / len(sentences)\n",
+    "    score = 206.84 - 60 * avg_syllables_per_word - 1.02 * avg_sentence_length\n",
+    "    return round(score, 2)\n",
+    "def accuracy_check(path):\n",
+    "    import json\n",
+    "    texts=[]\n",
+    "    accuracy_data = {'easy': 0, 'intermediate': 0, 'hard': 0}\n",
+    "    num_each_band = {'easy': 0, 'intermediate': 0, 'hard': 0}\n",
+    "    with open(path, 'r', encoding='utf-8') as f:\n",
+    "        results_es = json.load(f)\n",
+    "\n",
+    "    for item in results_es:\n",
+    "        dat=(item['synthetic_summary'].split(\"</think>\")[1].strip())\n",
+    "        # print(item['band'])\n",
+    "        band_data = item['band']\n",
+    "        huerta_score_val = huerta_score(dat)\n",
+    "        band_min, band_max = band_ranges[band_data]\n",
+    "        if huerta_score_val >= band_min and huerta_score_val <= band_max:\n",
+    "            accuracy_data[band_data] += 1\n",
+    "        num_each_band[band_data] += 1\n",
+    "    print(\"-\"*50)\n",
+    "    print(f\"{os.path.basename(path)} accuracy results:\")\n",
+    "    print(num_each_band)\n",
+    "    print(accuracy_data)\n",
+    "    print(f\"easy: {(accuracy_data['easy']/num_each_band['easy'])*100:.2f}%, intermediate: {(accuracy_data['intermediate']/num_each_band['intermediate'])*100:.2f}%, hard: {(accuracy_data['hard']/num_each_band['hard'])*100:.2f}%\")\n",
+    "for ind in os.listdir(\"/home/mshahidul/readctrl/results/custom_promptsV1\"):\n",
+    "    if ind.endswith('.json'):\n",
+    "        accuracy_check(os.path.join(\"/home/mshahidul/readctrl/results/custom_promptsV1\", ind))"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "6534a993",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import json\n",
+    "\n",
+    "with open('/home/mshahidul/readctrl/data/hand_create_gpt5/es_trainV1.json', 'r', encoding='utf-8') as f:\n",
+    "    data = json.load(f)\n",
+    "\n",
+    "print(len(data))"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "ed98df6a",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import json\n",
+    "import pyphen\n",
+    "import matplotlib.pyplot as plt\n",
+    "from collections import defaultdict\n",
+    "\n",
+    "# === CONFIG ===\n",
+    "root = \"/home/mshahidul/readctrl/data/hand_create_gpt5\"\n",
+    "input_json = f\"{root}/es_rawV1.json\"\n",
+    "output_json = f\"{root}/filtered_es_rawV1.json\"\n",
+    "\n",
+    "band_ranges = {\n",
+    "    \"easy\": (70, 100),\n",
+    "    \"intermediate\": (50, 70),\n",
+    "    \"hard\": (0, 50)\n",
+    "}\n",
+    "\n",
+    "# margin zone to remove texts near band boundaries\n",
+    "margin = 5  # e.g., 67–70 near easy; 47–50 near intermediate\n",
+    "\n",
+    "# === FH Score Calculation ===\n",
+    "dic = pyphen.Pyphen(lang='es')\n",
+    "\n",
+    "def count_syllables(word):\n",
+    "    hyphenated = dic.inserted(word)\n",
+    "    return len(hyphenated.split('-'))\n",
+    "\n",
+    "def huerta_score(text):\n",
+    "    sentences = [s for s in text.split('.') if s.strip()]\n",
+    "    words = [w for w in text.split() if w.isalpha()]\n",
+    "    if not words or not sentences:\n",
+    "        return 0.0\n",
+    "    total_syllables = sum(count_syllables(word.lower()) for word in words)\n",
+    "    avg_syllables_per_word = total_syllables / len(words)\n",
+    "    avg_sentence_length = len(words) / len(sentences)\n",
+    "    score = 206.84 - 60 * avg_syllables_per_word - 1.02 * avg_sentence_length\n",
+    "    return round(score, 2)\n",
+    "\n",
+    "# === Band validation ===\n",
+    "def is_in_band(score, band_name):\n",
+    "    low, high = band_ranges[band_name]\n",
+    "    # reject scores too close to boundaries\n",
+    "    if band_name == \"easy\" and score < low + margin:\n",
+    "        return False\n",
+    "    if band_name == \"intermediate\" and (score < low + margin or score > high - margin):\n",
+    "        return False\n",
+    "    if band_name == \"hard\" and score > high - margin:\n",
+    "        return False\n",
+    "    return low <= score <= high\n",
+    "\n",
+    "# === Process Dataset ===\n",
+    "with open(input_json, \"r\", encoding=\"utf-8\") as f:\n",
+    "    data = json.load(f)\n",
+    "\n",
+    "filtered_data = []\n",
+    "scores_summary = defaultdict(list)\n",
+    "removed_count = defaultdict(int)\n",
+    "\n",
+    "for item in data:\n",
+    "    keep_item = True\n",
+    "    invalid_bands = set()\n",
+    "\n",
+    "    for level in [\"easy\", \"intermediate\", \"hard\"]:\n",
+    "        text = item[\"readability_versions\"][level][\"text\"]\n",
+    "        score = huerta_score(text)\n",
+    "        item[\"readability_versions\"][level][\"FH_score\"] = score\n",
+    "        scores_summary[level].append(score)\n",
+    "\n",
+    "        if not is_in_band(score, level):\n",
+    "            invalid_bands.add(level)\n",
+    "            removed_count[level] += 1\n",
+    "            keep_item = False  # remove if any version invalid\n",
+    "\n",
+    "    if keep_item:\n",
+    "        filtered_data.append(item)\n",
+    "\n",
+    "# === Save filtered dataset ===\n",
+    "with open(output_json, \"w\", encoding=\"utf-8\") as f:\n",
+    "    json.dump(filtered_data, f, ensure_ascii=False, indent=2)\n",
+    "\n",
+    "# === Print stats ===\n",
+    "print(f\"✅ Original dataset size: {len(data)}\")\n",
+    "print(f\"✅ Filtered dataset size: {len(filtered_data)}\")\n",
+    "print(f\"🗑️  Removed total: {len(data) - len(filtered_data)}\")\n",
+    "print(\"\\n📊 Removal per readability band:\")\n",
+    "for level in [\"easy\", \"intermediate\", \"hard\"]:\n",
+    "    print(f\"  {level.capitalize():<15}: {removed_count[level]} removed\")\n",
+    "\n",
+    "# === Plot distribution ===\n",
+    "plt.figure(figsize=(10, 6))\n",
+    "for level, color in zip([\"easy\", \"intermediate\", \"hard\"], ['green', 'blue', 'red']):\n",
+    "    plt.scatter([level]*len(scores_summary[level]), scores_summary[level],\n",
+    "                color=color, label=level, alpha=0.6)\n",
+    "plt.axhspan(70, 100, color='green', alpha=0.1, label='Easy Band')\n",
+    "plt.axhspan(50, 70, color='blue', alpha=0.1, label='Intermediate Band')\n",
+    "plt.axhspan(0, 50, color='red', alpha=0.1, label='Hard Band')\n",
+    "plt.ylabel(\"Fernández Huerta Score\")\n",
+    "plt.title(\"Fernández Huerta Scores per Readability Level\")\n",
+    "plt.legend()\n",
+    "plt.grid(alpha=0.3)\n",
+    "plt.tight_layout()\n",
+    "plt.show()\n"
+   ]
+  },
+  {
+   "cell_type": "markdown",
+   "id": "03b3905c",
+   "metadata": {},
+   "source": [
+    "## Command generator"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 2,
+   "id": "0f8250c5",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "def distribute_commands(all_ref,free_gpu):\n",
+    "    new_li = []\n",
+    "    num_gpus = len(free_gpu)\n",
+    "    total = len(all_ref)\n",
+    "    base_allocate = total // num_gpus\n",
+    "    # assign gpu in all_ref commands\n",
+    "    for g in range(num_gpus - 1):\n",
+    "        temp = all_ref[g * base_allocate : (g + 1) * base_allocate]\n",
+    "        temp = [d.replace(\"--cuda -1\", f\"--cuda {free_gpu[g]}\") for d in temp]\n",
+    "        new_li.append(temp)\n",
+    "    temp = all_ref[(num_gpus - 1) * base_allocate :]\n",
+    "    temp = [d.replace(\"--cuda -1\", f\"--cuda {free_gpu[num_gpus - 1]}\") for d in temp]\n",
+    "    new_li.append(temp)\n",
+    "    return new_li"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 3,
+   "id": "6748b6ec",
+   "metadata": {},
+   "outputs": [
+    {
+     "data": {
+      "text/plain": [
+       "8"
+      ]
+     },
+     "execution_count": 3,
+     "metadata": {},
+     "output_type": "execute_result"
+    }
+   ],
+   "source": [
+    "# parser.add_argument(\"--cuda\", type=str, default=\"3\", help=\"CUDA device id, e.g., '0' or '0,1' for multiple GPUs\")\n",
+    "# parser.add_argument(\"--model_name\", type=str, default=\"/home/mshahidul/readctrl/finetuned_models/es_synthetic_data_creation_Qwen3_14B_v2\", help=\"Path to the finetuned model\")\n",
+    "# parser.add_argument(\"--temperature\", type=float, default=0.1, help=\"Generation temperature\")\n",
+    "all_cmds = []\n",
+    "# '/home/mshahidul/readctrl/finetuned_models/es_synthetic_data_creation_Qwen3_14B_v2'\n",
+    "model_names = [ '/home/mshahidul/readctrl/finetuned_models/es_synthetic_data_creation_Qwen3_14B_v2','unsloth/Qwen3-14B']\n",
+    "for model_name in model_names:\n",
+    "    # temp_list=[0.1, 0.3, 0.5, 0.7, 1.0, 1.1]\n",
+    "    temp_list=[1.2,1.3,1.4,1.5]\n",
+    "    for temp in temp_list:\n",
+    "        cmd = f\"python /home/mshahidul/readctrl/code/finetune-inference/inferenceV2_without_context.py --model_name {model_name} --temperature {temp} --cuda -1\"\n",
+    "        # cmd = f\"python /home/mshahidul/readctrl/code/finetune-inference/inferenceV3.py --model_name {model_name} --temperature {temp} --cuda -1\"\n",
+    "        # cmd = f\"CUDA_VISIBLE_DEVICES=-1 python /home/mshahidul/readctrl/code/finetune-inference/inferenceV3_temp.py --model_name {model_name} --temperature {temp}\"\n",
+    "        all_cmds.append(cmd)\n",
+    "len(all_cmds)"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 5,
+   "id": "673595ec",
+   "metadata": {},
+   "outputs": [
+    {
+     "name": "stdout",
+     "output_type": "stream",
+     "text": [
+      "python /home/mshahidul/readctrl/code/finetune-inference/inferenceV2_without_context.py --model_name /home/mshahidul/readctrl/finetuned_models/es_synthetic_data_creation_Qwen3_14B_v2 --temperature 1.2 --cuda 2\n",
+      "python /home/mshahidul/readctrl/code/finetune-inference/inferenceV2_without_context.py --model_name /home/mshahidul/readctrl/finetuned_models/es_synthetic_data_creation_Qwen3_14B_v2 --temperature 1.3 --cuda 2\n",
+      "python /home/mshahidul/readctrl/code/finetune-inference/inferenceV2_without_context.py --model_name /home/mshahidul/readctrl/finetuned_models/es_synthetic_data_creation_Qwen3_14B_v2 --temperature 1.4 --cuda 2\n",
+      "python /home/mshahidul/readctrl/code/finetune-inference/inferenceV2_without_context.py --model_name /home/mshahidul/readctrl/finetuned_models/es_synthetic_data_creation_Qwen3_14B_v2 --temperature 1.5 --cuda 2\n"
+     ]
+    }
+   ],
+   "source": [
+    "# gamma 2: 2, beta 3: 3\n",
+    "free_gpu=[2,3]\n",
+    "distributed_cmds = distribute_commands(all_cmds, free_gpu)\n",
+    "for sets in distributed_cmds[0]:\n",
+    "    print(sets)\n"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "f184d424",
+   "metadata": {},
+   "outputs": [],
+   "source": []
+  }
+ ],
+ "metadata": {
+  "kernelspec": {
+   "display_name": "unsloth",
+   "language": "python",
+   "name": "python3"
+  },
+  "language_info": {
+   "codemirror_mode": {
+    "name": "ipython",
+    "version": 3
+   },
+   "file_extension": ".py",
+   "mimetype": "text/x-python",
+   "name": "python",
+   "nbconvert_exporter": "python",
+   "pygments_lexer": "ipython3",
+   "version": "3.11.11"
+  }
+ },
+ "nbformat": 4,
+ "nbformat_minor": 5
+}
diff --git a/code/old/evalV3.py b/code/old/evalV3.py
new file mode 100644
index 0000000000000000000000000000000000000000..320c129f16588c09f6e57f7542b9fb5b3c0532db
--- /dev/null
+++ b/code/old/evalV3.py
@@ -0,0 +1,298 @@
+import os
+import json
+import logging
+from typing import Dict, List, Tuple, Any
+import numpy as np
+from rouge_score import rouge_scorer
+from bert_score import score as bert_score
+from transformers import AutoTokenizer
+import torch
+import argparse
+
+
+class SyntheticSummariesEvaluator:
+    def __init__(
+        self,
+        input_path: str,
+        output_dir: str = "metrics",
+        device: str = "cuda" if torch.cuda.is_available() else "cpu",
+        max_length: int = 512,
+        batch_size: int = 16,
+        rescale_with_baseline: bool = False,
+        include_article: bool = False,
+        w_rouge: float = 0.5,
+        w_bert: float = 0.5,
+        worst_quantile: float = 0.33,
+        good_quantile: float = 0.5,
+        best_quantile: float = 0.67,
+           # per-level threshold for is_good
+    ):
+        self.input_path = input_path
+        self.output_dir = output_dir
+        os.makedirs(output_dir, exist_ok=True)
+
+        with open(input_path, "r", encoding="utf-8") as f:
+            self.data: List[Dict[str, Any]] = json.load(f)
+
+        self.device = device
+        self.tokenizer = AutoTokenizer.from_pretrained("emilyalsentzer/Bio_ClinicalBERT")
+        self.max_length = max_length
+        self.batch_size = batch_size
+        self.rescale_with_baseline = rescale_with_baseline
+        self.include_article = include_article
+
+        # Normalize weights
+        s = (w_rouge + w_bert) or 1.0
+        self.w_rouge = float(w_rouge) / s
+        self.w_bert = float(w_bert) / s
+
+        # Quantiles per level (B1/B2/B3)
+        if not (0.0 <= worst_quantile < best_quantile <= 1.0):
+            logging.warning("Invalid quantiles; resetting to worst=0.33, best=0.67")
+            worst_quantile, best_quantile = 0.33, 0.67
+        self.worst_q = worst_quantile
+        self.best_q = best_quantile
+        self.good_q = good_quantile
+
+        self.rouge = rouge_scorer.RougeScorer(["rougeLsum"], use_stemmer=True)
+
+    def _truncate(self, text: str) -> str:
+        tokens = self.tokenizer.encode(
+            text,
+            add_special_tokens=True,
+            max_length=self.max_length,
+            truncation=True,
+        )
+        return self.tokenizer.decode(tokens, skip_special_tokens=True)
+
+    def _compute_rougeLsum_f1(self, ref: str, hyp: str) -> float:
+        result = self.rouge.score(ref, hyp)
+        return float(result["rougeLsum"].fmeasure)
+
+    def _combine(self, rouge: float, bert_f: float) -> float:
+        # Weighted average, ignoring NaNs
+        vals, ws = [], []
+        if rouge == rouge:
+            vals.append(rouge); ws.append(self.w_rouge)
+        if bert_f == bert_f:
+            vals.append(bert_f); ws.append(self.w_bert)
+        if not ws:
+            return float("nan")
+        s = sum(ws)
+        ws = [w / s for w in ws]
+        return float(sum(v * w for v, w in zip(vals, ws)))
+
+    def evaluate(self):
+        # Build pairs for batched BERTScore
+        pair_indices: List[Tuple[int, str]] = []  # (record_idx, "B1"/"B2"/"B3")
+        cands_trunc, refs_trunc = [], []
+        rouge_store: Dict[Tuple[int, str], float] = {}
+
+        for i, rec in enumerate(self.data):
+            gold = rec.get("gold_summary", "")
+            syn = rec.get("synthetic_summary", {}) or {}
+
+            for key in syn.keys():  # B1/B2/B3
+                cand = syn[key] if isinstance(syn[key], str) else str(syn[key])
+                cands_trunc.append(self._truncate(cand))
+                refs_trunc.append(self._truncate(gold))
+                pair_indices.append((i, key))
+                rouge_store[(i, key)] = self._compute_rougeLsum_f1(gold, cand)
+
+        # Compute BERTScore F1
+        F_vals = [np.nan] * len(pair_indices)
+        if len(pair_indices) > 0:
+            try:
+                _, _, F = bert_score(
+                    cands=cands_trunc,
+                    refs=refs_trunc,
+                    model_type="emilyalsentzer/Bio_ClinicalBERT",
+                    num_layers=12,
+                    lang="en",
+                    device=self.device,
+                    rescale_with_baseline=self.rescale_with_baseline,
+                    batch_size=self.batch_size,
+                )
+                F_vals = F.tolist()
+            except Exception as e:
+                logging.error(f"Error computing BERTScore: {e}", exc_info=True)
+
+        # Prepare per-record output
+        results_per_record: List[Dict[str, Any]] = []
+        for i, rec in enumerate(self.data):
+            out = {
+                "id": i,
+                "gold_summary": rec.get("gold_summary", ""),
+                "synthetic_summary": {}
+            }
+            if self.include_article:
+                out["article"] = rec.get("article", "")
+            syn = rec.get("synthetic_summary", {}) or {}
+            for key in syn.keys():
+                out["synthetic_summary"][key] = {
+                    "text": syn[key] if isinstance(syn[key], str) else str(syn[key]),
+                    "score": {}
+                }
+            results_per_record.append(out)
+
+        # Map (i,key) -> idx
+        idx_map = {(i_k[0], i_k[1]): idx for idx, i_k in enumerate(pair_indices)}
+
+        # Compute combined scores and collect per-level distributions
+        per_pair_combined: Dict[Tuple[int, str], float] = {}
+        level_scores = {"B1": [], "B2": [], "B3": []}
+        for (i, key), idx in idx_map.items():
+            r = rouge_store[(i, key)]
+            f = F_vals[idx]
+            c = self._combine(r, f)
+            per_pair_combined[(i, key)] = c
+            if key in level_scores:
+                level_scores[key].append(c)
+
+        # Per-level thresholds
+        thresholds = {}
+        for key in ["B1", "B2", "B3"]:
+            scores = np.array(level_scores[key], dtype=float)
+            if scores.size > 0 and np.any(scores == scores):  # any non-NaN
+                worst_thr = float(np.nanpercentile(scores, self.worst_q * 100))
+                best_thr = float(np.nanpercentile(scores, self.best_q * 100))
+                good_thr = float(np.nanpercentile(scores, self.good_q * 100))
+            else:
+                worst_thr = best_thr = good_thr = float("-inf")
+            thresholds[key] = {
+                "worst_thr": worst_thr,
+                "best_thr": best_thr,
+                "good_thr": good_thr
+            }
+
+        # Fill per-record metrics and categories (independent per level)
+        agg = {
+            "B1": {"ROUGE-L-Sum": [], "BERTScore_F": [], "combined": [], "count": 0,
+                   "best": 0, "good": 0, "worst": 0, "good_true": 0},
+            "B2": {"ROUGE-L-Sum": [], "BERTScore_F": [], "combined": [], "count": 0,
+                   "best": 0, "good": 0, "worst": 0, "good_true": 0},
+            "B3": {"ROUGE-L-Sum": [], "BERTScore_F": [], "combined": [], "count": 0,
+                   "best": 0, "good": 0, "worst": 0, "good_true": 0},
+        }
+
+        for (i, key), idx in idx_map.items():
+            r = rouge_store[(i, key)]
+            f = F_vals[idx]
+            c = per_pair_combined[(i, key)]
+
+            # Save scores
+            results_per_record[i]["synthetic_summary"][key]["score"] = {
+                "ROUGE-L-Sum": float(r) if r == r else None,
+                "BERTScore_F": float(f) if f == f else None,
+            }
+
+            # Independent per-level category
+            thr = thresholds.get(key, {"worst_thr": float("-inf"), "best_thr": float("-inf"), "good_thr": float("-inf")})
+            if not (c == c):  # NaN
+                category = "worst"
+                is_good = False
+            else:
+                if c < thr["worst_thr"]:
+                    category = "worst"
+                elif c < thr["best_thr"]:
+                    category = "good"
+                else:
+                    category = "best"
+                is_good = c >= thr["good_thr"]
+
+            results_per_record[i]["synthetic_summary"][key]["quality"] = {
+                "category": category,
+                "is_good": bool(is_good),
+                "combined_score": float(c) if c == c else None
+            }
+
+            # Aggregates
+            if key in agg:
+                if r == r:
+                    agg[key]["ROUGE-L-Sum"].append(float(r))
+                if f == f:
+                    agg[key]["BERTScore_F"].append(float(f))
+                if c == c:
+                    agg[key]["combined"].append(float(c))
+                agg[key]["count"] += 1
+                agg[key][category] += 1
+                if is_good:
+                    agg[key]["good_true"] += 1
+
+        # Dataset-level summary
+        dataset_level_metrics = {
+            "config": {
+                "weights": {"w_rouge": self.w_rouge, "w_bert": self.w_bert},
+                "quantiles": {"worst_q": self.worst_q, "best_q": self.best_q, "good_q": self.good_q},
+                "thresholds": thresholds,  # per-level thresholds used
+            }
+        }
+        for key, m in agg.items():
+            count = max(1, m["count"])
+            dataset_level_metrics[key] = {
+                "ROUGE-L-Sum": float(np.mean(m["ROUGE-L-Sum"])) if m["ROUGE-L-Sum"] else None,
+                "BERTScore_F": float(np.mean(m["BERTScore_F"])) if m["BERTScore_F"] else None,
+                "combined_mean": float(np.mean(m["combined"])) if m["combined"] else None,
+                "count": m["count"],
+                "best_rate": m["best"] / count,
+                "good_rate": m["good"] / count,
+                "worst_rate": m["worst"] / count,
+                "is_good_rate": m["good_true"] / count
+            }
+
+        return results_per_record, dataset_level_metrics
+
+    def save(self, per_record: List[Dict[str, Any]], dataset_metrics: Dict[str, Dict[str, float]]):
+        base = os.path.splitext(os.path.basename(self.input_path))[0]
+        per_record_path = os.path.join(self.output_dir, f"{base}_scored.json")
+        aggregate_path = os.path.join(self.output_dir, f"{base}_aggregate_metrics.json")
+
+        with open(per_record_path, "w", encoding="utf-8") as f:
+            json.dump(per_record, f, ensure_ascii=False, indent=2)
+
+        with open(aggregate_path, "w", encoding="utf-8") as f:
+            json.dump(dataset_metrics, f, ensure_ascii=False, indent=2)
+
+        print("Saved:")
+        print(f"- Per-record scores: {per_record_path}")
+        print(f"- Aggregate metrics: {aggregate_path}")
+
+
+def main():
+    parser = argparse.ArgumentParser(
+        description="Evaluate B1/B2/B3 summaries vs gold. Metrics: ROUGE-Lsum F1, BERTScore F1. Per-level categories: best/good/worst + is_good."
+    )
+    parser.add_argument("--input_path", required=True, help="Path to the es_syntheticV3.json file")
+    parser.add_argument("--output_dir", default="metrics", help="Where to save outputs")
+    parser.add_argument("--batch_size", type=int, default=16, help="BERTScore batch size")
+    parser.add_argument("--max_length", type=int, default=512, help="Max tokens for truncation (BERTScore)")
+    parser.add_argument("--rescale_with_baseline", action="store_true", help="Use BERTScore baseline rescaling")
+    parser.add_argument("--include_article", action="store_true", help="Include full article text in output JSON")
+    parser.add_argument("--w_rouge", type=float, default=0.5, help="Weight for ROUGE-L-Sum in combined score")
+    parser.add_argument("--w_bert", type=float, default=0.5, help="Weight for BERTScore_F in combined score")
+    parser.add_argument("--worst_quantile", type=float, default=0.33, help="Bottom quantile -> 'worst'")
+    parser.add_argument("--best_quantile", type=float, default=0.67, help="Top quantile boundary -> 'best'")
+    parser.add_argument("--good_quantile", type=float, default=0.5, help="Quantile for is_good=True")
+    args = parser.parse_args()
+
+    logging.basicConfig(level=logging.INFO, format="%(asctime)s - %(levelname)s - %(message)s")
+
+    evaluator = SyntheticSummariesEvaluator(
+        input_path=args.input_path,
+        output_dir=args.output_dir,
+        batch_size=args.batch_size,
+        max_length=args.max_length,
+        rescale_with_baseline=args.rescale_with_baseline,
+        include_article=args.include_article,
+        w_rouge=args.w_rouge,
+        w_bert=args.w_bert,
+        worst_quantile=args.worst_quantile,
+        best_quantile=args.best_quantile,
+        good_quantile=args.good_quantile,
+    )
+    per_record, dataset_metrics = evaluator.evaluate()
+    evaluator.save(per_record, dataset_metrics)
+
+
+if __name__ == "__main__":
+    main()
\ No newline at end of file
diff --git a/code/old/misc.ipynb b/code/old/misc.ipynb
new file mode 100644
index 0000000000000000000000000000000000000000..3001b6d424787a78dd6cb0283becb2240ae840d0
--- /dev/null
+++ b/code/old/misc.ipynb
@@ -0,0 +1,387 @@
+{
+ "cells": [
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "bbf1603c",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import re\n",
+    "import nltk\n",
+    "from nltk.tokenize import sent_tokenize, word_tokenize\n",
+    "\n",
+    "# Download Spanish models if not already\n",
+    "nltk.download('punkt')\n",
+    "\n",
+    "# Set Spanish punkt tokenizer\n",
+    "from nltk.data import load\n",
+    "spanish_tokenizer = load('tokenizers/punkt/spanish.pickle')\n",
+    "\n",
+    "# Function to count syllables in a word (basic approach for Spanish)\n",
+    "def count_syllables(word):\n",
+    "    word = word.lower()\n",
+    "    vowels = \"aeiouáéíóúü\"\n",
+    "    count = 0\n",
+    "    prev_char_is_vowel = False\n",
+    "\n",
+    "    for char in word:\n",
+    "        if char in vowels:\n",
+    "            if not prev_char_is_vowel:\n",
+    "                count += 1\n",
+    "                prev_char_is_vowel = True\n",
+    "        else:\n",
+    "            prev_char_is_vowel = False\n",
+    "\n",
+    "    # Ensure at least 1 syllable\n",
+    "    return count if count > 0 else 1\n",
+    "\n",
+    "# Main function to compute Huerta Readability Score\n",
+    "def huerta_score(text):\n",
+    "    # Sentence and word tokenization (Spanish)\n",
+    "    sentences = spanish_tokenizer.tokenize(text)\n",
+    "    words = word_tokenize(text, language='spanish')\n",
+    "\n",
+    "    # Filter only alphabetical words\n",
+    "    words = [word for word in words if word.isalpha()]\n",
+    "\n",
+    "    total_sentences = len(sentences)\n",
+    "    total_words = len(words)\n",
+    "    total_syllables = sum(count_syllables(word) for word in words)\n",
+    "\n",
+    "    if total_words == 0 or total_sentences == 0:\n",
+    "        return 0  # Avoid division by zero\n",
+    "\n",
+    "    avg_syllables_per_word = total_syllables / total_words\n",
+    "    avg_sentence_length = total_words / total_sentences\n",
+    "\n",
+    "    # Apply Huerta formula\n",
+    "    score = 206.84 - 60 * avg_syllables_per_word - 1.02 * avg_sentence_length\n",
+    "    return round(score, 2)\n",
+    "\n",
+    "# Example usage\n",
+    "spanish_text = \"\"\"\n",
+    "Un hombre de 27 años tuvo un accidente con su moto. No llevaba casco y se golpeó la cabeza. Fue él mismo al hospital con dolor de cabeza y sangre en la frente. Al llegar, perdió el conocimiento y tuvo convulsiones. Los médicos vieron que tenía una herida grave en la cabeza y sangraba mucho por dentro. Lo trasladaron a otro hospital mejor equipado. Le hicieron una operación y luego despertó bien. Ahora está estable, puede caminar y no tiene problemas importantes. Después de la operación, tuvo más convulsiones, pero le dieron medicina y mejoró.\n",
+    "\"\"\"\n",
+    "\n",
+    "print(\"Huerta Readability Score:\", huerta_score(spanish_text))"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "4ff63274",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import re\n",
+    "import separasilabas\n",
+    "\n",
+    "def count_words(text):\n",
+    "    text = ''.join(filter(lambda x: not x.isdigit(), text))\n",
+    "    clean = re.compile(r'\\W+')\n",
+    "    text = clean.sub(' ', text).strip()\n",
+    "    return len(text.split()) if len(text.split()) > 0 else 1\n",
+    "\n",
+    "def count_sentences(text):\n",
+    "    text = text.replace(\"\\n\", \"\")\n",
+    "    sentence_end = re.compile(r'[.:;!?\\)\\()]')\n",
+    "    sentences = sentence_end.split(text)\n",
+    "    sentences = list(filter(None, sentences))\n",
+    "    return len(sentences) if len(sentences) > 0 else 1\n",
+    "\n",
+    "def count_all_syllables(text):\n",
+    "    clean = re.compile(r'\\W+')\n",
+    "    words = clean.sub(' ', text).strip().split()\n",
+    "    silabizer = separasilabas.silabizer()\n",
+    "    total = 0\n",
+    "    for word in words:\n",
+    "        total += len(silabizer(word))\n",
+    "    return total if total > 0 else 1\n",
+    "\n",
+    "def Pval(text):\n",
+    "    syllables = count_all_syllables(text)\n",
+    "    words = count_words(text)\n",
+    "    return round(syllables / words, 2)\n",
+    "\n",
+    "def Fval(text):\n",
+    "    sentences = count_sentences(text)\n",
+    "    words = count_words(text)\n",
+    "    return round(words / sentences, 2)\n",
+    "\n",
+    "def fernandez_huerta(text):\n",
+    "    return round(206.84 - 60 * Pval(text) - 1.02 * Fval(text), 2)\n",
+    "\n",
+    "\n",
+    "# Example usage:\n",
+    "text = \"Una mujer de 54 años vino al hospital con un bulto en su vagina que tenía desde hace 3 años. El bulto fue creciendo poco a poco. Ella había tenido dos hijos y todos nacieron en casa. Hace un año el bulto dejó de sangrar, pero hace seis meses le salió una herida. Por eso, su familia la trajo al hospital. En el examen, los doctores vieron que la masa era una parte del útero (el fondo uterino) que había salido por la vagina. Tenía una herida en un lado. No había sangre ni pus. Después de hacerle varios exámenes, le dijeron que tenía una inversión uterina, una condición en la que el útero se voltea. Le hicieron una operación llamada histerectomía (le sacaron el útero). Aunque la cirugía fue difícil, los médicos la lograron hacer. Después de 10 días, salió del hospital y mejoró bien. Dos semanas después, fue al control y seguía bien.\"\n",
+    "print(\"Fernández Huerta score:\", fernandez_huerta(text))\n"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 7,
+   "id": "a464be9c",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import json, ast\n",
+    "\n",
+    "reason_info = {}\n",
+    "\n",
+    "for item in readability_reasoning:\n",
+    "    id = item['id']\n",
+    "    difficulty_level = item['version']\n",
+    "    data_temp = item['completeness']\n",
+    "    \n",
+    "    for _data in data_temp['results']:\n",
+    "        reasonableness = _data['reasonableness']\n",
+    "        \n",
+    "        # Step 1: Try to parse as JSON\n",
+    "        if isinstance(reasonableness, str):\n",
+    "            parsed = None\n",
+    "            try:\n",
+    "                parsed = json.loads(reasonableness)\n",
+    "            except Exception:\n",
+    "                try:\n",
+    "                    parsed = ast.literal_eval(reasonableness)\n",
+    "                except Exception:\n",
+    "                    # Not JSON or dict — treat as plain text\n",
+    "                    parsed = {\"reasonableness\": \"unknown\", \"justification\": reasonableness}\n",
+    "            reasonableness = parsed\n",
+    "\n",
+    "        # Step 2: Skip if \"reasonable\"\n",
+    "        if reasonableness.get('reasonableness') in [\"reasonable\",\"unknown\"]:\n",
+    "            continue\n",
+    "\n",
+    "        # Step 3: Collect non-reasonable subclaims\n",
+    "        key = (id, difficulty_level)\n",
+    "        reason_info.setdefault(key, []).append(_data['subclaim'])\n"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 8,
+   "id": "ecb6b419",
+   "metadata": {},
+   "outputs": [
+    {
+     "data": {
+      "text/plain": [
+       "{('multiclinsum_gs_es_503.txt',\n",
+       "  'intermediate'): ['La paciente precisó intubación al nacer.'],\n",
+       " ('multiclinsum_gs_es_503.txt',\n",
+       "  'hard'): ['La paciente precisó intubación al nacer.'],\n",
+       " ('multiclinsum_gs_es_249.txt', 'hard'): ['El paciente presentó disnea grave.',\n",
+       "  'La acromegalia del paciente se controló con seguimientos regulares.'],\n",
+       " ('multiclinsum_gs_es_14.txt',\n",
+       "  'hard'): ['Los síntomas tenían una duración de una década.', 'Los síntomas fueron atribuidos erróneamente a la fibromialgia.', 'Los síntomas fueron atribuidos erróneamente al hipotiroidismo.', 'Los síntomas fueron atribuidos erróneamente a enfermedades autoinmunes.', 'La paciente mostró una mejora neurológica con la terapia de B12.'],\n",
+       " ('multiclinsum_gs_es_473.txt',\n",
+       "  'hard'): ['El paciente tiene antecedentes de enolismo crónico.', 'El paciente desarrolló una encefalopatía aguda.'],\n",
+       " ('multiclinsum_gs_es_337.txt',\n",
+       "  'hard'): ['La paciente presentó aumento de volumen cervical.'],\n",
+       " ('multiclinsum_gs_es_171.txt', 'hard'): ['Se inició tratamiento antifímico.'],\n",
+       " ('multiclinsum_gs_es_369.txt',\n",
+       "  'intermediate'): ['La fístula iba de la arteria descendente anterior a la arteria circunfleja.'],\n",
+       " ('multiclinsum_gs_es_369.txt',\n",
+       "  'hard'): ['La fístula iba de la arteria descendente anterior a la arteria circunfleja.'],\n",
+       " ('multiclinsum_gs_es_109.txt',\n",
+       "  'intermediate'): ['Cuatro horas después, la paciente desarrolló de forma brusca estridor inspiratorio.'],\n",
+       " ('multiclinsum_gs_es_17.txt',\n",
+       "  'easy'): ['El paciente se sometió a un trasplante renal en agosto de 2014.'],\n",
+       " ('multiclinsum_gs_es_17.txt',\n",
+       "  'intermediate'): ['El paciente se sometió a un trasplante renal en agosto de 2014.'],\n",
+       " ('multiclinsum_gs_es_17.txt',\n",
+       "  'hard'): ['El paciente se sometió a un trasplante renal en agosto de 2014.'],\n",
+       " ('multiclinsum_gs_es_114.txt',\n",
+       "  'hard'): ['Se sospechó una patología neoplásica.'],\n",
+       " ('multiclinsum_gs_es_260.txt',\n",
+       "  'intermediate'): ['Un recién nacido nació con cianosis.'],\n",
+       " ('multiclinsum_gs_es_260.txt',\n",
+       "  'hard'): ['Un recién nacido nació con cianosis.'],\n",
+       " ('multiclinsum_gs_es_173.txt',\n",
+       "  'intermediate'): ['La causa de la muerte fue un colapso respiratorio agudo.',\n",
+       "  'La causa de la muerte fue un colapso circulatorio agudo.'],\n",
+       " ('multiclinsum_gs_es_482.txt',\n",
+       "  'easy'): ['La paciente tomó B. serrata a una dosis de 1000 mg/día durante tres semanas.', 'La paciente presentó convulsiones tónico-clónicas generalizadas no provocadas.'],\n",
+       " ('multiclinsum_gs_es_482.txt',\n",
+       "  'intermediate'): ['La paciente tiene un diagnóstico de síndrome aislado clínicamente.', 'La paciente presentó convulsiones tónico-clónicas generalizadas no provocadas.'],\n",
+       " ('multiclinsum_gs_es_482.txt',\n",
+       "  'hard'): ['La paciente tiene un diagnóstico de síndrome aislado clínicamente.'],\n",
+       " ('multiclinsum_gs_es_146.txt',\n",
+       "  'hard'): ['El paciente presentaba hinchazón de las piernas.'],\n",
+       " ('multiclinsum_gs_es_22.txt',\n",
+       "  'easy'): ['Los síntomas respiratorios del paciente empeoraron.'],\n",
+       " ('multiclinsum_gs_es_22.txt',\n",
+       "  'hard'): ['Los síntomas respiratorios del paciente empeoraron.'],\n",
+       " ('multiclinsum_gs_es_572.txt',\n",
+       "  'hard'): ['Se observaron ruidos en la garganta durante la ingesta de alimentos.'],\n",
+       " ('multiclinsum_gs_es_390.txt',\n",
+       "  'easy'): ['Se diagnosticó al paciente una cardiomiopatía inflamatoria crónica.'],\n",
+       " ('multiclinsum_gs_es_390.txt',\n",
+       "  'intermediate'): ['La ecocardiografía reveló una masa circular bien definida.', 'Se diagnosticó al paciente una cardiomiopatía inflamatoria crónica.'],\n",
+       " ('multiclinsum_gs_es_390.txt',\n",
+       "  'hard'): ['Los hallazgos intraoperativos sugirieron un CCMA.', 'El diagnóstico histopatológico de la masa fue un CAT (Tumor Amiloide Cardíaco).', 'Se realizó un análisis histológico de una muestra de miocardio del ventrículo izquierdo.', 'Se realizó un análisis histológico de la válvula aórtica extirpada.'],\n",
+       " ('multiclinsum_gs_es_327.txt',\n",
+       "  'easy'): ['La causa de las condiciones del paciente fue un hemangioendotelioma hepático infantil.'],\n",
+       " ('multiclinsum_gs_es_327.txt',\n",
+       "  'hard'): ['La ecocardiografía mostró una presión arterial pulmonar normal.'],\n",
+       " ('multiclinsum_gs_es_27.txt',\n",
+       "  'easy'): ['La tomografía computarizada reveló isquemia mesentérica aguda.'],\n",
+       " ('multiclinsum_gs_es_388.txt',\n",
+       "  'easy'): ['Se diagnosticó síndrome de Takotsubo.'],\n",
+       " ('multiclinsum_gs_es_388.txt',\n",
+       "  'intermediate'): ['Se diagnosticó síndrome de Takotsubo.'],\n",
+       " ('multiclinsum_gs_es_226.txt',\n",
+       "  'easy'): ['La paciente padecía tendinopatía insercional de Aquiles.',\n",
+       "  'La paciente sufrió una rotura total del tendón de Aquiles insercional.'],\n",
+       " ('multiclinsum_gs_es_226.txt',\n",
+       "  'intermediate'): ['La paciente padecía tendinopatía insercional de Aquiles.', 'La paciente fue tratada con una inyección local de cortisona.', 'El tendón de Aquiles volvió a romperse en la zona de inserción.', 'Se extirpó todo el tendón de Aquiles.'],\n",
+       " ('multiclinsum_gs_es_226.txt',\n",
+       "  'hard'): ['Se extirpó todo el tendón de Aquiles.'],\n",
+       " ('multiclinsum_gs_es_311.txt',\n",
+       "  'intermediate'): ['El diagnóstico fue confirmado como riñón displásico multiquístico (MCDK) postnatalmente.'],\n",
+       " ('multiclinsum_gs_es_311.txt',\n",
+       "  'hard'): ['El diagnóstico fue confirmado como riñón displásico multiquístico (MCDK) postnatalmente.'],\n",
+       " ('multiclinsum_gs_es_536.txt',\n",
+       "  'easy'): ['El paciente fue diagnosticado con un LCC-NI (Carcinoma de Células Grandes - No especificado de otra manera).'],\n",
+       " ('multiclinsum_gs_es_536.txt',\n",
+       "  'intermediate'): ['El paciente presentó un tumor en el lóbulo pulmonar superior derecho.'],\n",
+       " ('multiclinsum_gs_es_536.txt',\n",
+       "  'hard'): ['El paciente presentó un tumor en el lóbulo pulmonar superior derecho.', 'La evaluación patológica no mostró ningún inmunofenotipo.'],\n",
+       " ('multiclinsum_gs_es_273.txt',\n",
+       "  'hard'): ['La paciente se sometió a una resección laparoscópica de la trompa de Falopio.'],\n",
+       " ('multiclinsum_gs_es_508.txt',\n",
+       "  'intermediate'): ['Durante el período de inducción desarrolló un absceso cerebral causado por Bacillus cereus.'],\n",
+       " ('multiclinsum_gs_es_304.txt',\n",
+       "  'easy'): ['La lesión más grande, ubicada en el segmento VII, se diagnosticó finalmente como CHC.'],\n",
+       " ('multiclinsum_gs_es_304.txt',\n",
+       "  'hard'): ['No se detectaron hallazgos específicos de imagen en la tomografía computarizada (TC) ni en la resonancia magnética con contraste (MRI).'],\n",
+       " ('multiclinsum_gs_es_293.txt',\n",
+       "  'hard'): ['A pesar del tratamiento médico, el paciente se volvió hipotensivo.'],\n",
+       " ('multiclinsum_gs_es_69.txt',\n",
+       "  'easy'): ['El paciente es un varón de 14 años.'],\n",
+       " ('multiclinsum_gs_es_69.txt',\n",
+       "  'intermediate'): ['El paciente es un varón de 14 años.', 'Presentó una protuberancia en el cuello del lado izquierdo que aumentaba rápidamente.', 'Presentó fiebre que persistió durante dos semanas.', 'El drenaje quirúrgico provocó una hemorragia arterial.'],\n",
+       " ('multiclinsum_gs_es_529.txt',\n",
+       "  'hard'): ['El neonato presentó fallo de succión durante tres días.', 'Las imágenes mostraron obstrucción hidrocefálica.'],\n",
+       " ('multiclinsum_gs_es_169.txt',\n",
+       "  'hard'): ['El paciente recibió un implante de corazón artificial total SynCardia (50\\u202fml; SynCardia Systems, Inc., Tucson, AZ, EE.\\u202fUU.).'],\n",
+       " ('multiclinsum_gs_es_316.txt',\n",
+       "  'easy'): ['El paciente tiene enfermedad de Parkinson idiopática.'],\n",
+       " ('multiclinsum_gs_es_316.txt',\n",
+       "  'intermediate'): ['El paciente tiene enfermedad de Parkinson idiopática.'],\n",
+       " ('multiclinsum_gs_es_316.txt',\n",
+       "  'hard'): ['El paciente tiene enfermedad de Parkinson idiopática.',\n",
+       "  'La ECP-NST se consideró como la única posibilidad de lograr una mejoría motora en este caso.'],\n",
+       " ('multiclinsum_gs_es_349.txt',\n",
+       "  'hard'): ['El tratamiento con esplenectomía es exitoso.'],\n",
+       " ('multiclinsum_gs_es_585.txt',\n",
+       "  'hard'): ['En la exploración se constató síndrome medular completo con nivel en T8‑T9.'],\n",
+       " ('multiclinsum_gs_es_56.txt',\n",
+       "  'easy'): ['El paciente experimentó deterioro de la memoria.'],\n",
+       " ('multiclinsum_gs_es_56.txt',\n",
+       "  'intermediate'): ['La embolización resultó en la resolución completa de la FAVD.'],\n",
+       " ('multiclinsum_gs_es_580.txt',\n",
+       "  'hard'): ['El paciente mostró una respuesta inadecuada al manejo médico.', 'Persistió la sintomatología a pesar del manejo médico.'],\n",
+       " ('multiclinsum_gs_es_181.txt',\n",
+       "  'hard'): ['Se realizó una biopsia excisional de la lesión.', 'Se realizó una reintervención con amplios márgenes de tejido sano.'],\n",
+       " ('multiclinsum_gs_es_172.txt',\n",
+       "  'hard'): ['El paciente es un hombre árabe de 20 años que practica artes marciales y presenta una distensión del tendón izquierdo con una duración de 5 semanas.', 'El paciente se abstuvo de realizar todas las actividades deportivas.', 'El tratamiento consistió en una técnica modificada de movilización de caída con cuatro repeticiones diarias durante tres días consecutivos, acompañada de reentrenamiento postural.', 'La puntuación preintervención de la escala numérica de dolor fue 5/10 en reposo y 7/10 con actividad.'],\n",
+       " ('multiclinsum_gs_es_402.txt',\n",
+       "  'easy'): ['Después de la cirugía, el paciente evolucionó con falla cardiaca refractaria en el postoperatorio.', 'A los 6 años de edad se realizó una corrección anatómica con desmonte del Mustard y switch de grandes arterias, con resultado exitoso.'],\n",
+       " ('multiclinsum_gs_es_402.txt',\n",
+       "  'intermediate'): ['Después de la cirugía, el paciente evolucionó con falla cardiaca refractaria en el postoperatorio.'],\n",
+       " ('multiclinsum_gs_es_402.txt',\n",
+       "  'hard'): ['Después de la cirugía, el paciente evolucionó con falla cardiaca refractaria en el postoperatorio.'],\n",
+       " ('multiclinsum_gs_es_549.txt',\n",
+       "  'easy'): ['Mujer de 72 años con aneurisma roto de la arteria cólica media.', 'Se realizó ligadura de la arteria cólica media.', 'Se realizó una hemicolectomía derecha extendida.', 'Se colocó con éxito un stent cubierto en la arteria mesentérica superior proximal.'],\n",
+       " ('multiclinsum_gs_es_549.txt',\n",
+       "  'intermediate'): ['Presentaba signos y síntomas más sugestivos de colecistitis calculosa aguda.'],\n",
+       " ('multiclinsum_gs_es_549.txt',\n",
+       "  'hard'): ['La colecistitis se resolvió sin incidentes.'],\n",
+       " ('multiclinsum_gs_es_270.txt',\n",
+       "  'intermediate'): ['El paciente requirió una hemicolectomía derecha.',\n",
+       "  'La exploración quirúrgica confirmó síndrome del intestino corto.',\n",
+       "  'La yeyunostomía provocó grave malabsorción.',\n",
+       "  'La yeyunostomía provocó caquexia posterior.',\n",
+       "  'Se observó una fuga anastomótica después de la hemicolectomía derecha e ileostomía.',\n",
+       "  'Se observó peritonitis posterior después de la hemicolectomía derecha e ileostomía.'],\n",
+       " ('multiclinsum_gs_es_42.txt',\n",
+       "  'easy'): ['Se sometió a una reparación de la arteria braquial con interposición de injerto de vena safena inversa.'],\n",
+       " ('multiclinsum_gs_es_592.txt',\n",
+       "  'easy'): ['Se realizó un reemplazo valvular mitral biológico.'],\n",
+       " ('multiclinsum_gs_es_592.txt',\n",
+       "  'intermediate'): ['Presenta antecedentes de fiebre y disnea de pocos días de evolución.'],\n",
+       " ('multiclinsum_gs_es_592.txt',\n",
+       "  'hard'): ['Fue hospitalizada con un síndrome lupoide.'],\n",
+       " ('multiclinsum_gs_es_195.txt',\n",
+       "  'hard'): ['El paciente presentó hematemesis varias veces.'],\n",
+       " ('multiclinsum_gs_es_208.txt',\n",
+       "  'hard'): ['La condición del paciente ha sido bien controlada gracias al diagnóstico oportuno.'],\n",
+       " ('multiclinsum_gs_es_267.txt',\n",
+       "  'hard'): ['La paciente falleció dentro de las 24 horas del ingreso.'],\n",
+       " ('multiclinsum_gs_es_212.txt',\n",
+       "  'intermediate'): ['48 horas después de completar el tratamiento, la paciente evolucionó con trismus.'],\n",
+       " ('multiclinsum_gs_es_338.txt',\n",
+       "  'easy'): ['La agudeza visual se resolvió a la normalidad en el seguimiento de 4 años.'],\n",
+       " ('multiclinsum_gs_es_338.txt',\n",
+       "  'hard'): ['La agudeza visual se resolvió a la normalidad en el seguimiento de 4 años.'],\n",
+       " ('multiclinsum_gs_es_522.txt',\n",
+       "  'intermediate'): ['Un hombre kuwaití de 39 años presenta una variante autosómica recesiva de leuconiquia no sindrómica relacionada con PLCδ1 que afecta a nueve uñas.'],\n",
+       " ('multiclinsum_gs_es_138.txt',\n",
+       "  'hard'): ['Durante la internación, la niña se paró sin apoyo.'],\n",
+       " ('multiclinsum_gs_es_77.txt',\n",
+       "  'easy'): ['Se reportó un caso de neoplasia neuroendocrina ovárica primaria asociada a un tumor epitelial de margen.'],\n",
+       " ('multiclinsum_gs_es_77.txt',\n",
+       "  'intermediate'): ['Se reportó un caso de neoplasia neuroendocrina ovárica primaria asociada a un tumor epitelial de margen.'],\n",
+       " ('multiclinsum_gs_es_77.txt',\n",
+       "  'hard'): ['Se reportó un caso de neoplasia neuroendocrina ovárica primaria asociada a un tumor epitelial de margen.'],\n",
+       " ('multiclinsum_gs_es_246.txt',\n",
+       "  'easy'): ['El ingreso se debió a adinamia bilateral de las extremidades inferiores.', 'Se extirparon inmediatamente las lesiones vertebrales torácicas.', 'La extirpación de las lesiones vertebrales torácicas tuvo como objetivo rescatar la paraplejia incompleta.'],\n",
+       " ('multiclinsum_gs_es_246.txt',\n",
+       "  'intermediate'): ['El ingreso se debió a adinamia bilateral de las extremidades inferiores.', 'La ecocardiografía transtorácica mostró un mixoma móvil gigante en la aurícula derecha.'],\n",
+       " ('multiclinsum_gs_es_246.txt',\n",
+       "  'hard'): ['El ingreso se debió a adinamia bilateral de las extremidades inferiores.', 'El ingreso se debió a parálisis durante 5 días.', 'La ecocardiografía transtorácica mostró un mixoma móvil gigante en la aurícula derecha.', 'Se extirparon inmediatamente las lesiones vertebrales torácicas.', 'La extirpación de las lesiones vertebrales torácicas tuvo como objetivo rescatar la paraplejia incompleta.', 'La hemodinámica se mantuvo estable durante la operación.']}"
+      ]
+     },
+     "execution_count": 8,
+     "metadata": {},
+     "output_type": "execute_result"
+    }
+   ],
+   "source": [
+    "reason_info"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "0aab2a38",
+   "metadata": {},
+   "outputs": [],
+   "source": []
+  }
+ ],
+ "metadata": {
+  "kernelspec": {
+   "display_name": "unsloth",
+   "language": "python",
+   "name": "python3"
+  },
+  "language_info": {
+   "codemirror_mode": {
+    "name": "ipython",
+    "version": 3
+   },
+   "file_extension": ".py",
+   "mimetype": "text/x-python",
+   "name": "python",
+   "nbconvert_exporter": "python",
+   "pygments_lexer": "ipython3",
+   "version": "3.11.11"
+  }
+ },
+ "nbformat": 4,
+ "nbformat_minor": 5
+}
diff --git a/code/old/ner_umls.ipynb b/code/old/ner_umls.ipynb
new file mode 100644
index 0000000000000000000000000000000000000000..bb97bcb2f1bce79a0b5ed1dc66a60618279d6120
--- /dev/null
+++ b/code/old/ner_umls.ipynb
@@ -0,0 +1,79 @@
+{
+ "cells": [
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "eef90c68",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "from openmed.core import ModelLoader\n",
+    "from openmed.processing import format_predictions\n",
+    "\n",
+    "loader = ModelLoader()  # uses the default configuration\n",
+    "ner = loader.create_pipeline(\n",
+    "    \"disease_detection_superclinical\",  # registry key or full model ID\n",
+    "    aggregation_strategy=\"simple\",      # group sub-token predictions for quick wins\n",
+    ")\n",
+    "\n",
+    "text = \"Patient diagnosed with acute lymphoblastic leukemia and started on imatinib.\"\n",
+    "raw_predictions = ner(text)\n",
+    "\n",
+    "result = format_predictions(raw_predictions, text, model_name=\"Disease Detection\")\n",
+    "for entity in result.entities:\n",
+    "    print(f\"{entity.label:<12} -> {entity.text} (confidence={entity.confidence:.2f})\")"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "a14de1a5",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import os\n",
+    "import json\n",
+    "\n",
+    "data_dir = \"/home/mshahidul/readctrl/data/kyw_def_raw\"\n",
+    "json_list = []\n",
+    "\n",
+    "for filename in os.listdir(data_dir):\n",
+    "    print(f\"Processing file: {filename}\")\n",
+    "    if filename.endswith(\".json\"):\n",
+    "        file_path = os.path.join(data_dir, filename)\n",
+    "        with open(file_path, \"r\") as f:\n",
+    "            json_file=json.load(f)\n",
+    "            if \"chatgpt_answer\" in json_file:\n",
+    "                json_file=json_file[\"chatgpt_answer\"]\n",
+    "            json_list.append(json_file)\n",
+    "\n",
+    "# Save the combined list to a new file\n",
+    "save_dir = \"/home/mshahidul/readctrl/data/kyw_def_train\"\n",
+    "os.makedirs(save_dir, exist_ok=True)\n",
+    "with open(os.path.join(save_dir, \"kyw_gen_gpt5.json\"), \"w\") as out_f:\n",
+    "    json.dump(json_list, out_f, indent=4)"
+   ]
+  }
+ ],
+ "metadata": {
+  "kernelspec": {
+   "display_name": "unsloth",
+   "language": "python",
+   "name": "python3"
+  },
+  "language_info": {
+   "codemirror_mode": {
+    "name": "ipython",
+    "version": 3
+   },
+   "file_extension": ".py",
+   "mimetype": "text/x-python",
+   "name": "python",
+   "nbconvert_exporter": "python",
+   "pygments_lexer": "ipython3",
+   "version": "3.11.11"
+  }
+ },
+ "nbformat": 4,
+ "nbformat_minor": 5
+}
diff --git a/code/old/resonability_check_completeness_openai_V1.py b/code/old/resonability_check_completeness_openai_V1.py
new file mode 100644
index 0000000000000000000000000000000000000000..baba6a97cdd0e409dddb63c4f6843f9520aafcab
--- /dev/null
+++ b/code/old/resonability_check_completeness_openai_V1.py
@@ -0,0 +1,139 @@
+import os, json
+def return_promptst(reference_summary, generated_summary, subclaims_json, difficulty_level):
+    prompt=f'''
+            **SYSTEM / ROLE INSTRUCTION:**
+            You are a **medical readability evaluator**.
+            Your task is to judge whether omitted subclaims (those with `"result": 0"`) from a generated summary are *reasonably omitted* based on the intended **readability level**: *easy*, *intermediate*, or *hard*.
+            You evaluate this from the standpoint of clarity, faithfulness, and readability goals.
+
+            ---
+
+            ### **READABILITY GUIDELINES**
+
+            | Level            | Target Audience                          | Content Expectation                                             | Technical Detail Allowed                                         |
+            | :--------------- | :--------------------------------------- | :-------------------------------------------------------------- | :--------------------------------------------------------------- |
+            | **Easy**         | General public                           | Focus on main events, outcomes, and diagnoses in plain Spanish. | Minimal — avoid measurements, anatomy, and test results.         |
+            | **Intermediate** | Educated lay readers or medical students | Include key findings and procedures in simplified form.         | Moderate — basic terms and causes allowed.                       |
+            | **Hard**         | Medical professionals                    | Retain most technical information and precision.                | High — measurements, anatomy, and test interpretations expected. |
+
+            ---
+
+            ### **INPUT FIELDS**
+
+            **Reference summary:**
+            {reference_summary}
+
+            **Generated summary ({difficulty_level}):**
+            {generated_summary}
+
+            **Subclaims and results:**
+            {subclaims_json}
+
+            ---
+
+            ### **TASK INSTRUCTIONS**
+
+            1. Focus on subclaims with `"result": 0"` (not supported by the generated summary).
+            2. For each omitted subclaim:
+
+            * Decide whether omission is **reasonable** given the readability level.
+            * Label as: `"yes"`, `"no"`, or `"borderline"`.
+            * Write a brief justification (1–2 sentences).
+            3. After individual evaluations, assign a **reasonableness score (0–5)** using this scale:
+
+            * **5** = All omissions appropriate for target readability.
+            * **4** = Minor omissions could improve completeness.
+            * **3** = Some omissions reduce understanding or medical clarity.
+            * **2** = Many important omissions harm faithfulness.
+            * **1** = Major omissions misrepresent case.
+            * **0** = Summary fails to reflect key medical information.
+            4. End with an **overall explanation (3–5 sentences)** describing:
+
+            * The main reasoning behind the score.
+            * Whether the summary fits its intended readability level.
+            * Suggestions for improvement if needed.
+
+            ---
+
+            ### **OUTPUT FORMAT (strict JSON)**
+
+            ```json
+            {{
+            "evaluation_table": [
+                {{
+                "id": <subclaim_id>,
+                "subclaim": "<text>",
+                "reasonable_omission": "<yes | no | borderline>",
+                "explanation": "<short reason>"
+                }}
+            ],
+            "reasonableness_score": <0-5>,
+            "overall_explanation": "<concise paragraph>"
+            }}
+            ```
+            '''
+    return prompt
+
+from openai import OpenAI
+
+file_path = "/home/mshahidul/api_new.json"
+with open(file_path, "r") as file:
+    api_keys = json.load(file)
+
+openai_api_key = api_keys.get("openai")
+
+client = OpenAI(api_key=openai_api_key)
+def openai_return(prompt):
+    response = client.chat.completions.create(
+        model="gpt-5-mini",
+        messages=[
+            {"role": "system", "content": "You are a helpful assistant."},
+            {"role": "user", "content": prompt}
+        ]
+    )
+    cleaned_response = response.choices[0].message.content.strip().replace("```json", "").replace("```", "")
+    return json.loads(cleaned_response)
+
+import json
+file_path = "/home/mshahidul/readctrl/data/training_data_subclaim_verifier/synthetic_data_es_subclaims_100.json"
+
+with open(file_path, 'r') as f:
+    synthetic_data = json.load(f)
+
+file_path_qwen3_32B = "/home/mshahidul/readctrl/results/dataset_quality_check/subclaim_verifier_results_100_qwen3-32B.json"
+
+with open(file_path_qwen3_32B, 'r') as f:
+    qwen3_32B_results = json.load(f)
+
+# dict_keys(['id', 'full_text', 'ref_summary', 'readability_versions'])
+# print(f"Full text: {synthetic_data[0]['full_text']}")
+res=[]
+save_path = "/home/mshahidul/readctrl/results/dataset_quality_check/resonability_check_100_gpt5.json"
+if os.path.exists(save_path):
+    with open(save_path, 'r') as f:
+        res = json.load(f)
+print(f"Resuming from {len(res)} entries")
+import tqdm
+for ind in tqdm.tqdm(range(len(res),100)):
+    print(f"Processing index: {ind}")
+    for version in ["easy", "intermediate", "hard"]:
+        ref_summary = (f"{synthetic_data[ind]['ref_summary']['text']}")
+        generated_summary = (f"{synthetic_data[ind]['readability_versions'][version]['text']}")
+        subclaims_results = (f"{qwen3_32B_results[ind]['completeness']['results']}")
+        try:
+            prompt = return_promptst(ref_summary, generated_summary, subclaims_results, version)
+            res.append({
+                "id": synthetic_data[ind]['id'],
+                "difficulty_level": version,
+                "prompt": openai_return(prompt)
+            })
+            if len(res)%2==0:
+                print(f"Completed {len(res)} out of 300")
+                with open(save_path, 'w') as outfile:
+                    json.dump(res, outfile, indent=2)
+        except Exception as e:
+            print(f"Error at {ind} {version}: {e}")
+        # print(prompt)
+        # assert False
+with open(save_path, 'w') as outfile:
+    json.dump(res, outfile, indent=2)
\ No newline at end of file
diff --git a/code/old/revised_readability_results.py b/code/old/revised_readability_results.py
new file mode 100644
index 0000000000000000000000000000000000000000..3cadd9dcda68bc084456ef1454eef8a51e771708
--- /dev/null
+++ b/code/old/revised_readability_results.py
@@ -0,0 +1,154 @@
+def revised_results(reference_summary, generated_summary, list_of_missing_subclaims, difficulty_level):
+    return f'''
+### **SYSTEM / ROLE INSTRUCTION**
+
+You are a **medical text rewriting assistant** that improves summaries while maintaining the intended readability level (*easy / intermediate / hard*).
+You will receive:
+
+* The **original reference summary** (the factual source)
+* The **current generated summary**
+* A list of **important missing subclaims** to be reintroduced
+* The **target readability level**
+
+Your task:
+Revise the generated summary so that it **adds the missing information** naturally, while keeping:
+
+* The same **tone, vocabulary, and sentence simplicity** of the given readability level.
+* Logical **flow and coherence**.
+* No extra, invented information beyond what’s in the reference summary.
+
+---
+
+### **INPUT FIELDS**
+
+**Reference summary:**
+{reference_summary}
+
+**Current generated summary ({difficulty_level}):**
+{generated_summary}
+
+**Missing important subclaims to add back:**
+{list_of_missing_subclaims}
+
+**Target readability level:**
+{difficulty_level}
+
+
+---
+
+### **TASK INSTRUCTIONS**
+
+1. Integrate the missing subclaims **smoothly** into the generated summary.
+2. Do **not** add any new facts beyond those listed.
+3. Maintain the **same readability level**:
+
+   * **Easy:** conversational, short sentences, no jargon.
+   * **Intermediate:** light medical terms, brief explanations.
+   * **Hard:** concise clinical tone with correct terminology.
+4. Keep the summary approximately the same length; avoid redundancy.
+5. Ensure the resulting text remains **fluent, coherent, and faithful** to the reference summary.
+
+---
+
+### **OUTPUT FORMAT**
+
+```json
+{{
+  "revised_summary": "<the new version of the summary, rewritten with the added subclaims>",
+  "explanation": "<brief note explaining how the missing subclaims were added while preserving readability>"
+}}
+```
+
+'''
+from openai import OpenAI
+import json
+file_path = "/home/mshahidul/api_new.json"
+with open(file_path, "r") as file:
+    api_keys = json.load(file)
+
+openai_api_key = api_keys.get("openai")
+
+client = OpenAI(api_key=openai_api_key)
+def openai_return(prompt):
+    response = client.chat.completions.create(
+        model="gpt-5-mini",
+        messages=[
+            {"role": "system", "content": "You are a helpful assistant."},
+            {"role": "user", "content": prompt}
+        ]
+    )
+    cleaned_response = response.choices[0].message.content.strip().replace("```json", "").replace("```", "")
+    return json.loads(cleaned_response)
+import json
+file_path = "/home/mshahidul/readctrl/data/training_data_subclaim_verifier/synthetic_data_es_subclaims_100.json"
+
+with open(file_path, 'r') as f:
+    synthetic_data = json.load(f)
+
+# /home/mshahidul/readctrl/results/dataset_quality_check/resonability_check_100_gpt5_completeness.json
+
+
+
+with open("/home/mshahidul/readctrl/results/dataset_quality_check/resonability_check_100_gpt5_completeness.json", 'r') as f:
+    readability_reasoning = json.load(f)
+# readability_reasoning[0].keys() # dict_keys(['id', 'difficulty_level', 'prompt'])
+# readability_reasoning[0]['prompt'].keys() # dict_keys(['evaluation_table', 'reasonableness_score', 'overall_explanation'])
+reason_info={}
+for item in readability_reasoning:
+    id=item['id']
+    difficulty_level=item['difficulty_level']
+    data_temp=item['prompt']
+    for _data in data_temp['evaluation_table']:
+        if _data['reasonable_omission'] == "no":
+            key=(id, difficulty_level)
+            if key not in reason_info:
+                reason_info[key]=[]
+            reason_info[key].append(_data['subclaim'])
+
+file_path_qwen3_32B = "/home/mshahidul/readctrl/results/dataset_quality_check/subclaim_verifier_results_100_qwen3-32B.json"
+
+with open(file_path_qwen3_32B, 'r') as f:
+    qwen3_32B_results = json.load(f)
+
+# dict_keys(['id', 'full_text', 'ref_summary', 'readability_versions'])
+# print(f"Full text: {synthetic_data[0]['full_text']}")
+import os
+# def revised_results(reference_summary, generated_summary, list_of_missing_subclaims, difficulty_level):
+res=[]
+temp=""
+save_path = "/home/mshahidul/readctrl/results/dataset_quality_check/results_revised_100_gpt5.json"
+if os.path.exists(save_path):
+    with open(save_path, 'r') as f:
+        res = json.load(f)
+existing_check=set((entry['id'], entry['difficulty_level']) for entry in res)
+print(f"Resuming from {len(res)} entries")
+import tqdm
+for ind in tqdm.tqdm(range(0,100)):
+    for version in ["easy", "intermediate", "hard"]:
+        reference_summary = (f"{synthetic_data[ind]['ref_summary']['text']}")
+        generated_summary = (f"{synthetic_data[ind]['readability_versions'][version]['text']}")
+        if (synthetic_data[ind]['id'],version) in existing_check:
+            continue
+        if (synthetic_data[ind]['id'],version) not in reason_info:
+            continue
+        subclaims_results = reason_info[(synthetic_data[ind]['id'],version)]
+        prompt = revised_results(reference_summary, generated_summary, subclaims_results, version)
+        try:
+            ans=openai_return(prompt)
+            res.append({
+                "id": synthetic_data[ind]['id'],
+                "difficulty_level": version,
+                "prompt": prompt,
+                "response": ans
+            })
+            
+            if len(res)%2==0:
+                print(f"Completed {len(res)} out of 300")
+                with open(save_path, 'w') as outfile:
+                    json.dump(res, outfile, indent=2)
+        except Exception as e:
+            print(f"Error at index {ind}, version {version}: {e}")
+
+with open(save_path, 'w') as outfile:
+    json.dump(res, outfile, indent=2)
+
diff --git a/code/old/revised_readability_resultsV2.py b/code/old/revised_readability_resultsV2.py
new file mode 100644
index 0000000000000000000000000000000000000000..c8e929dd1fb2913f4e977a29678490df52640f6e
--- /dev/null
+++ b/code/old/revised_readability_resultsV2.py
@@ -0,0 +1,177 @@
+def inference_prompt_revise_summary(fulltext, ref_summary, generated_summary, version, missing_subclaims):
+    prompt = f"""
+You are a medical summarization model specialized in readability-controlled text revision.
+
+Your task is to improve the **Generated Summary** by adding back the key missing clinical information listed under **Missing Subclaims**, while keeping the readability style defined for the level **{version}**.
+
+Do not copy the reference summary. Keep coherence, brevity, and correctness.
+
+---
+
+### INPUT
+
+**Full Text (for context):**
+{fulltext}
+
+**Reference Summary (for comparison only):**
+{ref_summary}
+
+**Generated Summary (to revise):**
+{generated_summary}
+
+**Missing Subclaims (to integrate naturally):**
+{missing_subclaims}
+
+---
+
+### READABILITY STYLES
+
+- **easy (FH 70–100, grade 5–7):**
+  - Short sentences, familiar vocabulary, concrete ideas.
+  - Avoid subordinate clauses and medical jargon.
+  - Tone: explanatory, simple, and friendly.
+
+- **intermediate (FH 50–69, grade 8–12):**
+  - Moderate sentence complexity and domain vocabulary.
+  - Clear and structured explanation.
+
+- **hard (FH 0–49, university/professional):**
+  - Use specialized terminology, formal and dense phrasing.
+  - Include:
+    - precise domain vocabulary;
+    - causal or analytical connectors (por consiguiente, sin embargo, dado que…);
+    - one definition, one process description, and one implication statement if possible;
+    - optional subordinate clauses for academic rhythm.
+
+---
+
+### OUTPUT
+Return the result in the following JSON format:
+
+{{
+  "revised_summary": "<your revised summary text here>"
+}}
+
+Ensure the text is coherent, medically accurate, and matches the **{version}** readability level.
+"""
+    return prompt
+
+
+from openai import OpenAI
+import json
+file_path = "/home/mshahidul/api_new.json"
+with open(file_path, "r") as file:
+    api_keys = json.load(file)
+
+openai_api_key = api_keys.get("openai")
+
+client = OpenAI(api_key=openai_api_key)
+def openai_return(prompt):
+    response = client.chat.completions.create(
+        model="gpt-5",
+        messages=[
+            {"role": "system", "content": "You are a helpful assistant."},
+            {"role": "user", "content": prompt}
+        ]
+    )
+    try:
+        cleaned_response = response.choices[0].message.content.strip().replace("```json", "").replace("```", "")
+        return json.loads(cleaned_response)
+    except Exception as e:
+        return response.choices[0].message.content.strip().replace("```json", "").replace("```", "")
+import json
+file_path = "/home/mshahidul/readctrl/data/training_data_subclaim_verifier/synthetic_data_es_subclaims_100.json"
+
+with open(file_path, 'r') as f:
+    synthetic_data = json.load(f)
+
+
+
+with open("/home/mshahidul/readctrl/results/dataset_quality_check/completeness_resonability_check_100_qwen3-32B_v3.json", 'r') as f:
+    readability_reasoning = json.load(f)
+
+import json, ast
+
+reason_info = {}
+
+for item in readability_reasoning:
+    id = item['id']
+    difficulty_level = item['version']
+    data_temp = item['completeness']
+    for _data in data_temp['results']:
+        reasonableness = _data['reasonableness']
+        
+        # Step 1: Try to parse as JSON
+        if isinstance(reasonableness, str):
+            parsed = None
+            try:
+                parsed = json.loads(reasonableness)
+            except Exception:
+                try:
+                    parsed = ast.literal_eval(reasonableness)
+                except Exception:
+                    # Not JSON or dict — treat as plain text
+                    parsed = {"reasonableness": "unknown", "justification": reasonableness}
+            reasonableness = parsed
+
+        # Step 2: Skip if "reasonable"
+        if reasonableness.get('reasonableness') in ["reasonable","unknown"]:
+            continue
+
+        # Step 3: Collect non-reasonable subclaims
+        key = (id, difficulty_level)
+        reason_info.setdefault(key, []).append(_data['subclaim'])
+
+
+
+file_path_qwen3_32B = "/home/mshahidul/readctrl/results/dataset_quality_check/subclaim_verifier_results_100_qwen3-32B.json"
+
+with open(file_path_qwen3_32B, 'r') as f:
+    qwen3_32B_results = json.load(f)
+
+# def inference_prompt_revise_summary(fulltext, ref_summary, generated_summary, version, missing_subclaims):
+import os
+with open("/home/mshahidul/readctrl/data/testing_data_gs/multiclinsum_gs_train_es.json", "r") as f_train:
+    multiclinsum_gs_train_es = json.load(f_train)
+dat_full_text={}
+dat_summary={}
+for item in multiclinsum_gs_train_es:
+    dat_full_text[item['id']]=item['fulltext']
+    dat_summary[item['id']]=item['summary']
+res=[]
+save_path = "/home/mshahidul/readctrl/results/dataset_quality_check/results_revised_100_gpt5_v3.json"
+if os.path.exists(save_path):
+    with open(save_path, 'r') as f:
+        res = json.load(f)
+existing_check=set((entry['id'], entry['difficulty_level']) for entry in res)
+print(f"Resuming from {len(res)} entries")
+import tqdm
+for ind in tqdm.tqdm(range(0,10)):
+    for version in ["easy", "intermediate", "hard"]:
+        reference_summary = (f"{synthetic_data[ind]['ref_summary']['text']}")
+        generated_summary = (f"{synthetic_data[ind]['readability_versions'][version]['text']}")
+        if (synthetic_data[ind]['id'],version) in existing_check:
+            continue
+        if (synthetic_data[ind]['id'],version) not in reason_info or len(reason_info[(synthetic_data[ind]['id'],version)])==0:
+            continue
+        missing_subclaims = reason_info[(synthetic_data[ind]['id'],version)]
+        prompt = inference_prompt_revise_summary(dat_full_text[synthetic_data[ind]['id']], reference_summary, generated_summary, version, missing_subclaims)
+        try:
+            ans=openai_return(prompt)
+            res.append({
+                "id": synthetic_data[ind]['id'],
+                "difficulty_level": version,
+                "prompt": prompt,
+                "response": ans
+            })
+            
+            if len(res)%2==0:
+                print(f"Completed {len(res)} out of 300")
+                with open(save_path, 'w') as outfile:
+                    json.dump(res, outfile, indent=2)
+        except Exception as e:
+            print(f"Error at index {ind}, version {version}: {e}")
+
+with open(save_path, 'w') as outfile:
+    json.dump(res, outfile, indent=2)
+
diff --git a/code/old/synthetic_data_generation.py b/code/old/synthetic_data_generation.py
new file mode 100644
index 0000000000000000000000000000000000000000..b0ba239673b3e251bb4c387fe717ab80c524cb6f
--- /dev/null
+++ b/code/old/synthetic_data_generation.py
@@ -0,0 +1,118 @@
+import os
+import json
+from openai import OpenAI
+import tqdm
+# Initialize client (ensure you have OPENAI_API_KEY in env vars)
+client = OpenAI(api_key=json.load(open('/home/mshahidul/api.json', 'r'))['openai_api_key'])
+
+# System prompts (from Appendix B in your proposal)
+PROMPTS = {
+    "B1": """You are a summarization assistant trained to rewrite medical case reports' expert summaries
+for readers at an elementary school level (ages 5–11, FKGL 1.0–6.0).
+
+Your job is to generate summaries that are:
+* Kind and empathetic
+* Clear, simple, and understandable for readers without medical background
+* Accurate and faithful to the source
+
+General Instructions:
+- Assume the reader is an elementary school student with no medical knowledge.
+- Avoid medical jargon. If it must appear, explain it in very simple terms.
+- Use short sentences and everyday words.
+- Reassure the reader when findings are normal; explain gently if something is abnormal.
+- Do not overwhelm with detail; focus on main ideas.
+- Never use emojis.
+- Do not explain pronunciation.
+""",
+    "B2": """You are a summarization assistant trained to rewrite medical case reports' expert summaries for readers at a middle or high school level (ages 11–17, FKGL 6.0–12.0).
+
+Your job is to generate summaries that are: 
+* Kind and empathetic
+* Clear and understandable for readers with only general school-level science
+* Accurate and faithful to the source
+
+General Instructions: 
+- Assume the reader is a secondary school student with limited medical knowledge.
+- Avoid unnecessary jargon. If a medical term is included, provide a brief, clear explanation.
+- Write in a style appropriate for middle/high school reading comprehension.
+- Present abnormal findings with calm, explanatory language, including possible next steps.
+- Keep the tone warm, patient, and caring.
+- Never use emojis.
+- Do not explain pronunciation.
+""",
+    "B3": """You are a summarization assistant trained to rewrite medical case reports' expert summaries
+for readers at a college or higher education level (ages 17+, FKGL 12.0+).
+
+Your job is to generate summaries that are: 
+* Kind and empathetic
+* Clear and precise, while remaining faithful to the source
+* Appropriate for readers with advanced literacy but no formal medical training
+
+General Instructions:
+- Assume the reader is a college-level reader with no medical specialization.
+- Medical terms can be used if they are commonly understood or explained briefly.
+- Provide a more detailed and structured summary than for younger readers.
+- Clearly distinguish between normal and abnormal findings, and outline potential implications or next steps.
+- Maintain an empathetic and respectful tone at all times.
+- Never use emojis.
+- Do not explain pronunciation.
+"""
+}
+
+def generate_synthetic_summary(article, gold_summary, band):
+    """Call GPT-5-mini to generate a synthetic summary for a given readability band"""
+    prompt = f"""Article:
+{article}
+
+Gold Summary:
+{gold_summary}
+
+Task:
+Please generate a summary at readability band {band}.
+"""
+
+    response = client.chat.completions.create(
+        model="gpt-5-mini",
+        messages=[
+            {"role": "system", "content": PROMPTS[band]},
+            {"role": "user", "content": prompt}
+        ],
+        temperature=1.0
+    )
+
+    return response.choices[0].message.content.strip()
+
+def build_synthetic_dataset(input_path, output_path, max_samples=None):
+    """Generate synthetic dataset from a JSONL file with {article, gold_summary}"""
+    results = []
+    if os.path.exists(output_path):
+        results = json.load(open(output_path, 'r'))
+    with open(input_path, "r") as f:
+        data = json.load(f)
+        for item in tqdm.tqdm(data):
+            if max_samples and len(results) >= max_samples:
+                break
+            article, gold = item["fulltext"], item["summary"]
+            if article in [r['article'] for r in results]:
+                continue
+            temp={}
+            for band in ["B1", "B2", "B3"]:
+                synthetic = generate_synthetic_summary(article, gold, band)
+                temp[band] = synthetic
+            results.append({
+                    "article": article,
+                    "gold_summary": gold,
+                    "synthetic_summary": temp
+                })
+            if len(results)%5==0:
+                print(f"Processed {len(results)} samples, saving progress...")
+                with open(output_path, "w") as f:
+                    json.dump(results, f, ensure_ascii=False, indent=4)
+
+    with open(output_path, "w") as f:
+        json.dump(results, f, ensure_ascii=False, indent=4)
+
+# Example usage:
+lang = "es"  # Change to desired language
+path=f"/home/mshahidul/readctrl/data/testing_data_gs/multiclinsum_gs_train_{lang}.json"
+build_synthetic_dataset(path, f"/home/mshahidul/readctrl/generating_data/{lang}_synthetic.json", max_samples=100)
diff --git a/code/old/synthetic_data_generationV2.py b/code/old/synthetic_data_generationV2.py
new file mode 100644
index 0000000000000000000000000000000000000000..fd845ffdd0dc69cd70e1f8d5992d01fc7eec41a2
--- /dev/null
+++ b/code/old/synthetic_data_generationV2.py
@@ -0,0 +1,161 @@
+import os
+import json
+from openai import OpenAI
+import tqdm
+import re
+from FH_es import fernandez_huerta
+# Initialize client (ensure you have OPENAI_API_KEY in env vars)
+client = OpenAI(api_key=json.load(open('/home/mshahidul/api.json', 'r'))['openai_api_key'])
+
+PROMPTS_ES = {
+    "B1": """Eres un asistente que reescribe resúmenes de casos clínicos para niñas y niños de primaria (aprox. 6–11 años).
+Escribe SIEMPRE en español claro.
+
+Objetivo de legibilidad (aprox. Fernández–Huerta): 70–100.
+Restricciones de forma (cumple todas):
+- Longitud total: 45–90 palabras.
+- Oraciones: 4–6 oraciones.
+- Promedio de palabras por oración: 8–12.
+- Palabras: prefiere palabras cortas (1–2 sílabas). Evita tecnicismos. Si un término médico es inevitable, explícalo con 3–8 palabras sencillas.
+- Conectores simples: “y”, “pero”, “porque”. Evita oraciones subordinadas largas.
+- No inventes información. Sé fiel al artículo y al resumen experto.
+- Prohibido: viñetas, listas, emojis, abreviaturas técnicas, explicaciones de pronunciación, títulos/cabeceras.
+
+Tono y contenido:
+- Amable, tranquilizador, sin alarmar.
+- Destaca 1–3 ideas principales. Explica hallazgos normales con calma; anormalidades con lenguaje sencillo y breve.
+Responde solo con el resumen (sin prefacios, sin notas).""",
+
+    "B2": """Eres un asistente que reescribe resúmenes de casos clínicos para estudiantes de secundaria (aprox. 11–17 años).
+Escribe SIEMPRE en español claro.
+
+Objetivo de legibilidad (aprox. Fernández–Huerta): 55–65.
+Restricciones de forma (cumple todas):
+- Longitud total: 90–140 palabras.
+- Oraciones: 5–8 oraciones.
+- Promedio de palabras por oración: 12–18.
+- Palabras: evita jerga innecesaria. Puedes usar términos médicos comunes con una breve explicación (3–10 palabras) la primera vez.
+- Conectores permitidos: “porque”, “aunque”, “sin embargo”, “por eso”. Oraciones compuestas moderadas.
+- No inventes información. Sé fiel al artículo y al resumen experto.
+- Prohibido: viñetas, listas, emojis, explicaciones de pronunciación, títulos/cabeceras.
+
+Tono y contenido:
+- Claro y empático.
+- Distingue hallazgos normales y anormales, e incluye posibles pasos siguientes cuando sea útil.
+Responde solo con el resumen (sin prefacios, sin notas).""",
+
+    "B3": """Eres un asistente que reescribe resúmenes de casos clínicos para lectores con nivel universitario (17+), sin especialización médica.
+Escribe SIEMPRE en español claro.
+
+Objetivo de legibilidad (aprox. Fernández–Huerta): 40–55.
+Restricciones de forma (cumple todas):
+- Longitud total: 140–220 palabras.
+- Oraciones: 6–10 oraciones.
+- Promedio de palabras por oración: 18–25.
+- Palabras: se permiten términos técnicos de uso común; define brevemente solo los poco conocidos. Se aceptan oraciones subordinadas si mantienen claridad.
+- Conectores: “sin embargo”, “por lo tanto”, “además”, “no obstante”, “en consecuencia”.
+- No inventes información. Sé fiel al artículo y al resumen experto.
+- Prohibido: viñetas, listas, emojis, explicaciones de pronunciación, títulos/cabeceras.
+
+Tono y contenido:
+- Preciso y empático.
+- Estructura más detallada: contexto breve, hallazgos clave, implicaciones y posibles próximos pasos.
+Responde solo con el resumen (sin prefacios, sin notas)."""
+}
+
+
+FH_TARGETS = {
+    "B1": (70, 100),
+    "B2": (55, 65),
+    "B3": (40, 55),
+}
+
+def count_syllables(word):
+    # Simple Spanish syllable counter
+    word = word.lower()
+    word = re.sub(r'[^a-záéíóúüñ]', '', word)
+    return len(re.findall(r'[aeiouáéíóúü]+', word))
+
+
+
+def generate_synthetic_summary(article, gold_summary, band, lang='es'):
+    prompt_user = f"""Artículo:
+{article}
+
+Resumen experto:
+{gold_summary}
+
+Tarea:
+Genera un resumen en la banda {band} indicada por el sistema. Responde solo con el resumen."""
+    response = client.chat.completions.create(
+        model="gpt-4.1-mini",  # <-- Check this model name!
+        messages=[
+            {"role": "system", "content": PROMPTS_ES[band]},
+            {"role": "user", "content": prompt_user}
+        ],
+        temperature=0.4,
+    )
+    return response.choices[0].message.content.strip()
+
+def revise_to_band(text, band):
+    adjustments = {
+        "B1": "Acorta oraciones a 8–12 palabras, usa palabras más comunes y evita tecnicismos.",
+        "B2": "Ajusta oraciones a 12–18 palabras y limita tecnicismos con breve explicación.",
+        "B3": "Usa 18–25 palabras por oración, permite frases subordinadas y vocabulario más técnico.",
+    }
+    msg = f"""Reescribe el texto para que cumpla la banda {band}:
+- {adjustments[band]}
+- Mantén fidelidad al contenido.
+Devuelve solo el texto revisado, sin comentarios."""
+    r = client.chat.completions.create(
+        model="gpt-4.1-mini",
+        messages=[
+            {"role": "system", "content": PROMPTS_ES[band]},
+            {"role": "user", "content": text},
+            {"role": "user", "content": msg}
+        ],
+        temperature=0.3,
+    )
+    return r.choices[0].message.content.strip()
+
+def build_synthetic_dataset(input_path, output_path, max_samples=None):
+    """Generate synthetic dataset from a JSON file with {fulltext, summary}"""
+    results = []
+    seen_articles = set()
+    if os.path.exists(output_path):
+        with open(output_path, 'r') as f:
+            results = json.load(f)
+            seen_articles = set(r['article'] for r in results)
+    with open(input_path, "r") as f:
+        data = json.load(f)
+        for item in tqdm.tqdm(data):
+            if max_samples and len(results) >= max_samples:
+                break
+            article, gold = item["fulltext"], item["summary"]
+            if article in seen_articles:
+                continue
+            temp = {}
+            for band in ["B1", "B2", "B3"]:
+                synthetic = generate_synthetic_summary(article, gold, band)
+                fh = fernandez_huerta(synthetic)
+                lo, hi = FH_TARGETS[band]
+                if fh is None or not (lo <= fh <= hi):
+                    synthetic = revise_to_band(synthetic, band)
+                temp[band] = synthetic
+            results.append({
+                "article": article,
+                "gold_summary": gold,
+                "synthetic_summary": temp
+            })
+            seen_articles.add(article)
+            if len(results) % 5 == 0:
+                print(f"Processed {len(results)} samples, saving progress...")
+                with open(output_path, "w") as f:
+                    json.dump(results, f, ensure_ascii=False, indent=4)
+    with open(output_path, "w") as f:
+        json.dump(results, f, ensure_ascii=False, indent=4)
+
+# Example usage:
+lang = "es"
+path = f"/home/mshahidul/readctrl/data/testing_data_gs/multiclinsum_gs_train_{lang}.json"
+build_synthetic_dataset(path, f"/home/mshahidul/readctrl/generating_data/{lang}_synthetic.json", max_samples=100)
\ No newline at end of file
diff --git a/code/reasoning/reasoning.py b/code/reasoning/reasoning.py
new file mode 100644
index 0000000000000000000000000000000000000000..37d78d209560d430447dddf66d23276b843af2e5
--- /dev/null
+++ b/code/reasoning/reasoning.py
@@ -0,0 +1,114 @@
+import os
+import json
+import tqdm
+from openai import OpenAI
+
+# --- CONFIGURATION ---
+MODEL_PATH = "/home/mshahidul/readctrl_model/full_model/qwen3-32B_subclaims-support-check-8b_ctx_v2-bf16"
+API_URL = "http://172.16.34.29:8004/v1" 
+API_KEY = "EMPTY"
+
+client = OpenAI(base_url=API_URL, api_key=API_KEY)
+
+def get_reasoning_prompt_json(source_text, gold_summary, generated_text, subclaim, level):
+    """
+    Forces the model to output a machine-readable JSON object for clinical logic validation.
+    """
+    return f"""You are a clinical logic validator auditing medical text simplification.
+
+### Context & Goals:
+- **Target Literacy Level:** {level}
+
+1. Level: Low Health Literacy (High Readability)
+
+Target: Individuals needing the simplest terms for immediate action.
+
+Linguistic Goal: Use "living room" language. Replace all medical jargon with functional descriptions (e.g., "renal" becomes "kidney").
+
+Information Density: Focus strictly on the "need-to-know" info found in the Gold Summary.
+
+Strategy: High paraphrasing using analogies. One idea per sentence.
+
+Faithfulness: Must align perfectly with the Gold Summary.
+
+2. Level: Intermediate Health Literacy (Medium Readability)
+
+Target: The general public (news-reading level).
+
+Linguistic Goal: Standard vocabulary. Common medical terms are okay, but technical "doctor-speak" must be simplified.
+
+Information Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.
+
+Strategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.
+
+Faithfulness: Maintains the main narrative of the Gold Summary.
+
+3. Level: Proficient Health Literacy (Low Readability)
+
+Target: Researchers, clinicians, or highly informed patients.
+
+Linguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.
+
+Information Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.
+
+Strategy: Minimal paraphrasing. Retain all original technical terminology.
+
+Faithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.
+
+### Input Data:
+1. **Source Text:** {source_text}
+2. **Gold Summary (Reference):** {gold_summary}
+3. **Generated Text (Output):** {generated_text}
+4. **Subclaim to Evaluate:** {subclaim}
+
+### Task:
+Evaluate the Subclaim's status in the Generated Text compared to the Source and Gold Summary. Output ONLY a JSON object.
+
+### Classification Categories:
+- "reasonable_removal": Subclaim in Source, but NOT in Gold (non-essential).
+- "reasonable_modification": Subclaim simplified correctly for the {level} goal.
+- "unreasonable_removal": Subclaim in Gold but MISSING from Generated (critical loss).
+- "unreasonable_addition": Subclaim in Generated but NOT in Source/Gold (hallucination).
+- "preserved": Fact maintained with high fidelity.
+
+### JSON Schema Requirement:
+{{
+  "category": "string (reasonable_removal | reasonable_modification | unreasonable_removal | unreasonable_addition | preserved)",
+  "action": "string (added | removed | modified | preserved)",
+  "presence_in_gold": "boolean",
+  "presence_in_generated": "boolean",
+  "verdict": "string (one sentence clinical justification)"
+}}
+
+Output JSON:"""
+
+def evaluate_reasoning_json(source, gold, generated, subclaim, level):
+    prompt = get_reasoning_prompt_json(source, gold, generated, subclaim, level)
+    
+    try:
+        response = client.chat.completions.create(
+            model=MODEL_PATH,
+            messages=[{"role": "user", "content": prompt}],
+            max_tokens=400,
+            temperature=0.1,
+            # If your vLLM setup supports JSON mode, you can add response_format={"type": "json_object"}
+        )
+        content = response.choices[0].message.content.strip()
+        
+        # Clean potential markdown formatting if model outputs ```json ... ```
+        if content.startswith("```json"):
+            content = content.replace("```json", "").replace("```", "").strip()
+        
+        return json.loads(content)
+    except Exception as e:
+        return {
+            "category": "error",
+            "action": "error",
+            "verdict": f"API or Parsing Error: {str(e)}"
+        }
+
+# -----------------------------
+# Example Usage in your Main Loop:
+# -----------------------------
+# result = evaluate_reasoning_json(full_text, ref_summary, summary_at_level, sc, level)
+# print(result['category'])
\ No newline at end of file
diff --git a/code/reasoning/reasoning_completeness_sourceCov.py b/code/reasoning/reasoning_completeness_sourceCov.py
new file mode 100644
index 0000000000000000000000000000000000000000..563d5f316b656facc07fecfa47c6d56e8f59ae13
--- /dev/null
+++ b/code/reasoning/reasoning_completeness_sourceCov.py
@@ -0,0 +1,183 @@
+import os
+import json
+import tqdm
+from openai import OpenAI
+
+# --- CONFIGURATION ---
+MODEL_PATH = "Qwen/Qwen3-30B-A3B-Instruct-2507"
+API_URL = "http://172.16.34.29:8004/v1" 
+API_KEY = "EMPTY"
+
+# Input Files
+EVAL_FILE = "/home/mshahidul/readctrl/data/reasoning/REFINED_full_details_evaluation_0_20_qwen3-32B_v2.json"
+RAW_DATA_FILE = "/home/mshahidul/readctrl/data/extracting_subclaim/extracted_subclaims_syn_data_with_gs_summary_en.json"
+# Output File
+file_name=os.path.basename(EVAL_FILE)
+UPDATED_FILE = f"/home/mshahidul/readctrl/data/reasoning/reasoned_updated_results_v2_{file_name}"
+
+client = OpenAI(base_url=API_URL, api_key=API_KEY)
+
+# -----------------------------
+#  REASONING CORE
+# -----------------------------
+def get_clinical_reasoning(source, gold, generated, subclaim, level):
+    # Map your specific label info to the prompt context
+    level_guidelines = {
+        "low_health_literacy": """
+            - Goal: 'Living room' language; replace jargon (e.g., 'renal' -> 'kidney').
+            - Density: Focus ONLY on 'need-to-know' info from Gold Summary.
+            - Strategy: One idea per sentence.
+            - Reasonable Omission: Technical jargon or details NOT in the Gold Summary.
+        """,
+        "intermediate_health_literacy": """
+            - Goal: Standard vocabulary; common medical terms are okay.
+            - Density: Gold Summary as lead + necessary Source Text context.
+            - Strategy: Remove minor technical details to avoid overload.
+            - Reasonable Omission: Minor technical nuances or physiological mechanisms.
+        """,
+        "proficient_health_literacy": """
+            - Goal: Technical/Academic language; prioritize clinical nuance.
+            - Density: High; include data, mechanisms, and statistics from Full Source.
+            - Strategy: Retain all original technical terminology.
+            - Reasonable Omission: Almost none; should adhere closely to Full Source.
+        """
+    }
+
+    guideline = level_guidelines.get(level, "Follow standard medical summarization principles.")
+
+#     prompt = f"""You are a clinical logic validator auditing medical text simplification.
+# A subclaim is currently 'not_supported' in the generated text.
+
+# ### Target Level Guidelines: {level}
+# {guideline}
+
+# ### Inputs:
+# 1. Source Text (Full Paper): {source}
+# 2. Gold Summary (Expert Reference): {gold}
+# 3. Generated Text (Model Output): {generated}
+# 4. Subclaim to Evaluate: {subclaim}
+
+# ### Task:
+# Determine if the absence of this subclaim in the Generated Text is justified based on the {level} strategy.
+
+# - CATEGORY 'reasonable': Omission aligns with the linguistic goals (e.g., removing jargon for Low literacy or filtering minor details for Intermediate).
+# - CATEGORY 'unreasonable': Omission results in clinical information loss that violates the target density (e.g., missing a diagnosis or omitting technical data for Proficient level).
+
+# Output ONLY JSON:
+# {{
+#   "category": "reasonable" | "unreasonable",
+#   "reason": "jargon_reduction" | "detail_filtering" | "clinical_info_loss",
+#   "explanation": "One sentence justification matching the {level} strategy."
+# }}
+# JSON:"""
+    prompt = f"""You are a clinical logic validator auditing medical text simplification.
+
+        A subclaim is currently labeled 'not_supported' in the generated text. Your job is to decide whether
+        its omission is acceptable for the target literacy level.
+
+        ### Target Level Guidelines: {level}
+        {guideline}
+
+        ### Inputs:
+        1) Source Text (Full Paper): {source}
+        2) Gold Summary (Expert Reference): {gold}
+        3) Generated Text (Model Output): {generated}
+        4) Subclaim to Evaluate: {subclaim}
+
+        ### Decision rules (MUST follow):
+        A) First, determine whether the subclaim is present in or required by the Gold Summary.
+        - If the Gold Summary includes this subclaim (or an equivalent idea), then omitting it is usually UNREASONABLE
+            even for low health literacy, because low literacy still must retain "need-to-know" gold content.
+        B) Check for outcome-critical content.
+        - If the subclaim is about outcomes/prognosis (e.g., recovery, no sequelae, disability, death, major complications),
+            treat it as clinically important. Omission is UNREASONABLE unless the Gold Summary clearly omits it and
+            the generated text already conveys the same outcome clearly.
+        C) Check time scope.
+        - If the subclaim could apply only to a specific time window (e.g., "no sequelae after initial event"),
+            infer whether the generated text covers that window. If the generated text describes later deterioration/death,
+            do NOT assume that supports "no sequelae." If the time scope is unclear, err toward UNREASONABLE.
+        D) Only mark REASONABLE if:
+        - The subclaim is NOT in the Gold Summary (or is clearly non-essential there), AND
+        - It is mainly anatomical/technical detail, jargon, or minor nuance for this literacy level, AND
+        - Omitting it does not change the clinical interpretation.
+
+        ### Output ONLY JSON:
+        {{
+        "category": "reasonable" | "unreasonable",
+        "reason": "jargon_reduction" | "detail_filtering" | "clinical_info_loss",
+        "explanation": "One sentence justification referencing Gold Summary importance and (if relevant) time/outcome."
+        }}
+        JSON:"""
+    try:
+        response = client.chat.completions.create(
+            model=MODEL_PATH,
+            messages=[{"role": "user", "content": prompt}],
+            max_tokens=250,
+            temperature=0.1
+        )
+        content = response.choices[0].message.content.strip()
+        if "```json" in content:
+            content = content.split("```json")[-1].split("```")[0].strip()
+        return json.loads(content)
+    except:
+        return {"category": "unreasonable", "explanation": "API parsing error"}
+
+# -----------------------------
+#  MAIN PROCESSING LOOP
+# -----------------------------
+def process_and_update_details():
+    # 1. Load Datasets
+    with open(EVAL_FILE, 'r') as f:
+        eval_data = json.load(f)
+    with open(RAW_DATA_FILE, 'r') as f:
+        raw_lookup = {item['index']: item for item in json.load(f)}
+
+    # 2. Iterate through index and literacy levels
+    for entry in tqdm.tqdm(eval_data, desc="Updating Subclaim Details"):
+        idx = entry['index']
+        raw_item = raw_lookup.get(idx)
+        if not raw_item: continue
+
+        source_text = raw_item['fulltext']
+        gold_summary = raw_item['summary']
+
+        for level, lvl_content in entry['literacy_levels'].items():
+            gen_text = raw_item['diff_label_texts'].get(level, "")
+            
+            # --- UPDATE COMPLETENESS DETAILS ---
+            comp_list = lvl_content['details']['completeness']
+            comp_corrected = 0
+            for fact_obj in comp_list:
+                if fact_obj['status'] == 'not_supported':
+                    res = get_clinical_reasoning(source=source_text, gold=gold_summary, generated=gen_text, subclaim=fact_obj['source_fact'], level=level)
+                    # Update status and add reasoning metadata
+                    if res['category'] == 'reasonable':
+                        fact_obj['status'] = 'reasonable_omission'
+                        comp_corrected += 1
+                    fact_obj['reasoning_audit'] = res
+                else:
+                    comp_corrected += 1
+            lvl_content['scores']['completeness'] = comp_corrected / len(comp_list) if comp_list else 0
+
+            # --- UPDATE SOURCE COVERAGE DETAILS ---
+            sc_list = lvl_content['details']['source_coverage']
+            sc_corrected = 0
+            for sc_obj in sc_list:
+                if sc_obj['status'] == 'not_supported':
+                    res = get_clinical_reasoning(source=source_text, gold=gold_summary, generated=gen_text, subclaim=sc_obj['source_subclaim'], level=level)
+                    # Update status and add reasoning metadata
+                    if res['category'] == 'reasonable':
+                        sc_obj['status'] = 'reasonable_omission'
+                        sc_corrected += 1
+                    sc_obj['reasoning_audit'] = res
+                else:
+                    sc_corrected += 1
+            lvl_content['scores']['source_coverage'] = sc_corrected / len(sc_list) if sc_list else 0
+
+    # 3. Save the modified full structure
+    with open(UPDATED_FILE, 'w') as f:
+        json.dump(eval_data, f, indent=2)
+    print(f"\nUpdate complete. Detailed status and scores saved to: {UPDATED_FILE}")
+
+if __name__ == "__main__":
+    process_and_update_details()
\ No newline at end of file
diff --git a/code/reasoning/ressoning_qwen3-30B-a3b.py b/code/reasoning/ressoning_qwen3-30B-a3b.py
new file mode 100644
index 0000000000000000000000000000000000000000..4277dd06504e0405daa7f5bf6efdd17cf36ec3e5
--- /dev/null
+++ b/code/reasoning/ressoning_qwen3-30B-a3b.py
@@ -0,0 +1,112 @@
+import os
+import json
+import tqdm
+import argparse
+from openai import OpenAI
+import re
+
+# -----------------------------
+#  CONFIGURATION
+# -----------------------------
+# Pointing to your ALREADY RUNNING vLLM server (Qwen3-30B-A3B-Instruct)
+API_URL = "http://172.16.34.29:8004/v1" 
+API_KEY = "EMPTY"
+# This model name should match what vLLM expects (often the path or the alias)
+MODEL_NAME = "Qwen/Qwen3-30B-A3B-Instruct-2507" 
+
+client = OpenAI(base_url=API_URL, api_key=API_KEY)
+
+# -----------------------------
+#  REASONING PROMPT
+# -----------------------------
+def reasoning_prompt(text, subclaim):
+    return f"""You are a senior clinical data validator. A previous automated system flagged a subclaim as 'not_supported'. Your job is to perform a deep-dive reasoning to verify if that judgment was correct.
+
+### CONTEXT:
+Medical Text: {text}
+Subclaim: {subclaim}
+
+### TASK:
+1. Analyze the text for any paraphrased evidence, synonyms, or implicit support for the subclaim.
+2. Determine if the previous 'not_supported' label was a "False Negative" (it actually is supported) or a "True Negative" (it is definitely not in the text).
+3. Be strict: If the text truly doesn't mention the specifics, stick with 'not_supported'.
+
+### OUTPUT FORMAT:
+Provide your internal reasoning first, then conclude with exactly one word: 'supported' or 'not_supported'."""
+
+# -----------------------------
+#  LOGIC TO EXTRACT THINKING & LABEL
+# -----------------------------
+def get_reasoned_verdict(text: str, subclaim: str):
+    prompt = reasoning_prompt(text, subclaim)
+    
+    try:
+        response = client.chat.completions.create(
+            model=MODEL_NAME,
+            messages=[{"role": "user", "content": prompt}],
+            temperature=0.1, # Keep it low for consistency
+        )
+        full_content = response.choices[0].message.content
+        
+        # Extract reasoning (vLLM usually includes <think> tags for Qwen3-A3B)
+        reasoning = ""
+        if "<think>" in full_content and "</think>" in full_content:
+            reasoning = re.search(r"<think>(.*?)</think>", full_content, re.DOTALL).group(1).strip()
+            final_output = full_content.split("</think>")[-1].strip().lower()
+        else:
+            # Fallback if tags aren't present
+            reasoning = "No explicit <think> tags provided."
+            final_output = full_content.strip().lower()
+
+        # Final label extraction
+        if "not_supported" in final_output:
+            label = "not_supported"
+        elif "supported" in final_output:
+            label = "supported"
+        else:
+            label = "inconclusive"
+
+        return reasoning, label
+
+    except Exception as e:
+        print(f"Error: {e}")
+        return str(e), "error_api"
+
+# -----------------------------
+#  MAIN PROCESSING
+# -----------------------------
+if __name__ == "__main__":
+    parser = argparse.ArgumentParser()
+    # Provide the path to the JSON generated by your FIRST script
+    parser.add_argument("--input_file", type=str, required=True) 
+    parser.add_argument("--save_path", type=str, default="/home/mshahidul/readctrl/data/reasoning/")
+    args = parser.parse_args()
+
+    with open(args.input_file, "r") as f:
+        data = json.load(f)
+    save_path = args.save_path+f"refined_{os.path.basename(args.input_file)}"
+    print(f"Loaded {len(data)} documents. Starting reasoning audit...")
+
+    for doc in tqdm.tqdm(data):
+        full_text = doc.get('fulltext', '')
+        
+        for eval_item in doc.get('subclaim_evaluations', []):
+            # Only process if the first model said 'not_supported'
+            if eval_item['support_label'] == "not_supported":
+                subclaim = eval_item['subclaim']
+                
+                reasoning, new_label = get_reasoned_verdict(full_text, subclaim)
+                
+                # Update the entry with the new insights
+                eval_item['original_label'] = "not_supported"
+                eval_item['reasoning_audit'] = reasoning
+                eval_item['support_label'] = new_label # Overwriting with refined label
+                eval_item['is_refined'] = True
+            else:
+                eval_item['is_refined'] = False
+
+        # Save every document to avoid data loss
+        with open(save_path, "w") as f:
+            json.dump(data, f, indent=2, ensure_ascii=False)
+
+    print(f"Refinement complete. Saved to {save_path}")
\ No newline at end of file
diff --git a/code/reasoning/ressoning_qwen3-30B-a3b_cover_all.py b/code/reasoning/ressoning_qwen3-30B-a3b_cover_all.py
new file mode 100644
index 0000000000000000000000000000000000000000..fb1cdddfe6a66991d52a7f5c084c1fb77189df39
--- /dev/null
+++ b/code/reasoning/ressoning_qwen3-30B-a3b_cover_all.py
@@ -0,0 +1,247 @@
+import os
+import json
+import tqdm
+import argparse
+import re
+from openai import OpenAI
+
+# -----------------------------
+#  CONFIGURATION
+# -----------------------------
+API_URL = "http://172.16.34.29:8004/v1" 
+API_KEY = "EMPTY"
+MODEL_NAME = "Qwen/Qwen3-30B-A3B-Instruct-2507" 
+
+client = OpenAI(base_url=API_URL, api_key=API_KEY)
+
+# -----------------------------
+#  REASONING PROMPTS
+# -----------------------------
+def get_audit_prompt(task_type, reference_text, subclaim, literacy_level):
+    level_guidelines = {
+        "low_health_literacy": """
+        Level: Low Health Literacy (High Readability)
+        Target: Individuals needing simple terms.
+        Goal: 'Living room' language. Replace jargon (e.g., 'renal' -> 'kidney').
+        Density: Strictly 'need-to-know' info from Gold Summary.
+        Strategy: High paraphrasing, analogies, one idea per sentence.
+        Faithfulness: Must align with Gold Summary.""",
+        
+        "intermediate_health_literacy": """
+        Level: Intermediate Health Literacy (Medium Readability)
+        Target: General public.
+        Goal: Standard vocabulary. Common medical terms okay; technical speak simplified.
+        Density: Balanced. Use Gold Summary as lead, supplemented by context from Source.
+        Strategy: Moderate paraphrasing. Remove minor technical details.
+        Faithfulness: Maintain main narrative of Gold Summary.""",
+        
+        "proficient_health_literacy": """
+        Level: Proficient Health Literacy (Low Readability)
+        Target: Researchers/Clinicians.
+        Goal: Technical/Academic. Prioritize clinical nuance and accuracy.
+        Density: High. Include data, physiological mechanisms, and statistics from Source.
+        Strategy: Minimal paraphrasing. Retain original technical terminology.
+        Faithfulness: Adhere to Source Text; add deeper scientific context."""
+    }
+
+    guidelines = level_guidelines.get(literacy_level, "Follow standard medical audit practices.")
+    level_desc = literacy_level.replace("_", " ")
+
+    base_instructions = f"""
+### Literacy Level Context:
+{guidelines}
+
+### Task Instructions:"""
+
+#     if task_type == "attribution":
+#         return f"""{base_instructions}
+# 1. Compare the Subclaim against the Source Text.
+# 2. Flag as 'supported' if the Source contains this claim, even if highly paraphrased for {level_desc}.
+# SOURCE: {reference_text}
+# SUBCLAIM: {subclaim}
+# Provide reasoning in <reasoning> tags, then output: 'supported' or 'not_supported'."""
+    if task_type == "attribution":
+        return f"""{base_instructions}
+        1. Compare the Subclaim against the Source Text.
+        2. Mark 'supported' ONLY IF:
+        - The Source Text explicitly states the claim, OR
+        - The claim is clearly conveyed through a faithful paraphrase that preserves its meaning.
+        3. Do NOT infer support from silence, omission, or related but non-equivalent statements.
+        4. For negative or exclusionary claims (e.g., "no complications," "no family history," "absence of signs"),
+        the Source Text must explicitly indicate absence.
+        5. Mark 'not_supported' if:
+        - The claim is missing, OR
+        - The Source discusses a related concept but does not confirm the specific claim.
+
+        SOURCE: {reference_text}
+        SUBCLAIM: {subclaim}
+
+        Provide reasoning in <reasoning> tags, then output: 'supported' or 'not_supported'.
+        """
+
+
+#     elif task_type == "completeness":
+#         return f"""{base_instructions}
+# 1. Is this Fact from the Gold Standard missing from the {level_desc} summary?
+# 2. Mark 'supported' if: The info is present (paraphrased) OR if the info was omitted because it is too complex for {level_desc} guidelines.
+# SUMMARY: {reference_text}
+# FACT: {subclaim}
+# Provide reasoning in <reasoning> tags, then output: 'supported' or 'not_supported'."""
+    elif task_type == "completeness":
+        return f"""{base_instructions}
+    1. Determine whether this Fact from the Gold Standard is covered in the {level_desc} summary.
+    2. Mark 'supported' ONLY IF:
+    - The fact is explicitly stated in the summary, OR
+    - The fact is clearly paraphrased or simplified in a way that preserves its meaning.
+    3. Do NOT mark 'supported' based solely on omission.
+    - Absence of mention does NOT imply intentional exclusion.
+    - Negative or exclusionary facts (e.g., "no complications," "no family history," "no systemic signs") must be explicitly conveyed.
+    4. Mark 'not_supported' if:
+    - The fact is completely omitted, OR
+    - The summary discusses related information but does not confirm the specific fact.
+    5. Literacy-based simplification is allowed, but factual meaning must be preserved.
+
+    SUMMARY: {reference_text}
+    FACT: {subclaim}
+
+    Provide reasoning in <reasoning> tags, then output: 'supported' or 'not_supported'.
+    """
+
+
+#     elif task_type == "conciseness":
+#         return f"""{base_instructions}
+# 1. The Subclaim exists in the summary but NOT in the Gold Reference. Is this okay?
+# 2. Mark 'supported' if: The info adds necessary definitions or scientific depth appropriate for {level_desc}.
+# REFERENCE: {reference_text}
+# SUBCLAIM: {subclaim}
+# Provide reasoning in <reasoning> tags, then output: 'supported' or 'not_supported'."""
+    elif task_type == "conciseness":
+        return f"""{base_instructions}
+            1. The Subclaim appears in the summary but NOT in the Gold Reference.
+            2. Determine whether this addition is acceptable.
+            3. Mark 'supported' ONLY IF:
+            - The information is a definition, clarification, or explanatory restatement
+                of concepts already present in the Gold Reference, AND
+            - It does NOT introduce new clinical findings, test results, diagnoses,
+                causes, outcomes, or exclusions.
+            4. Do NOT mark 'supported' if the Subclaim:
+            - Adds a new medical fact not found in the Gold Reference, OR
+            - Draws clinical conclusions or inferences beyond what the source states.
+            5. Literacy-based explanation is allowed, but factual content must remain unchanged.
+
+            REFERENCE: {reference_text}
+            SUBCLAIM: {subclaim}
+
+            Provide reasoning in <reasoning> tags, then output: 'supported' or 'not_supported'.
+            """
+
+
+    # NEW: Source Coverage Prompt
+#     elif task_type == "source_coverage":
+#         return f"""{base_instructions}
+# 1. Check if the following Fact from the ORIGINAL Source Text is covered in the generated {level_desc} summary.
+# 2. Mark 'supported' if the summary includes this information, even if it is simplified or combined with other points.
+# 3. Mark 'not_supported' if the summary completely omits this specific medical fact.
+# GENERATED SUMMARY: {reference_text}
+# SOURCE FACT: {subclaim}
+# Provide reasoning in <reasoning> tags, then output: 'supported' or 'not_supported'."""
+    elif task_type == "source_coverage":
+        return f"""{base_instructions}
+        1. Check whether the following Fact from the ORIGINAL Source Text is explicitly covered in the generated {level_desc} summary.
+        2. Mark 'supported' ONLY IF:
+        - The summary clearly states the fact, OR
+        - The fact is conveyed through an explicit paraphrase or simplification that preserves its meaning.
+        3. Do NOT infer support from silence or omission.
+        - Absence of mention does NOT count as support.
+        - Especially for negative or exclusionary facts (e.g., "no family history," "no extra-renal signs," "no complications"), the summary must explicitly indicate absence.
+        4. Mark 'not_supported' if:
+        - The summary omits the fact entirely, OR
+        - The summary discusses related topics but does not clearly confirm the specific fact.
+        5. Simplification for literacy level is allowed, but factual meaning must be preserved.
+
+        GENERATED SUMMARY: {reference_text}
+        SOURCE FACT: {subclaim}
+
+        Provide reasoning in <reasoning> tags, then output: 'supported' or 'not_supported'.
+        """
+
+# -----------------------------
+#  LOGIC
+# -----------------------------
+def get_reasoned_verdict(reference, statement, task_type, literacy_level):
+    prompt = get_audit_prompt(task_type, reference, statement, literacy_level)
+    try:
+        response = client.chat.completions.create(
+            model=MODEL_NAME,
+            messages=[{"role": "user", "content": prompt}],
+            temperature=0.1,
+        )
+        content = response.choices[0].message.content
+        
+        # Extracts reasoning from <reasoning> tags specifically
+        reasoning = re.search(r"<reasoning>(.*?)</reasoning>", content, re.DOTALL).group(1).strip() if "<reasoning>" in content else "N/A"
+        final_text = content.split("</reasoning>")[-1].lower()
+        
+        label = "supported" if "supported" in final_text and "not_supported" not in final_text else "not_supported"
+        return reasoning, label
+    except:
+        return "API Error", "not_supported"
+
+# -----------------------------
+#  MAIN PROCESSING
+# -----------------------------
+if __name__ == "__main__":
+    parser = argparse.ArgumentParser()
+    parser.add_argument("--eval_file", type=str, default="/home/mshahidul/readctrl/data/factual_testing/full_details_evaluation_0_20_qwen3-32B_v2.json")
+    parser.add_argument("--source_file", type=str, default="/home/mshahidul/readctrl/data/extracting_subclaim/extracted_subclaims_syn_data_with_gs_summary_en.json")
+    parser.add_argument("--save_path", type=str, default="/home/mshahidul/readctrl/data/reasoning/")
+    args = parser.parse_args()
+
+    os.makedirs(args.save_path, exist_ok=True)
+
+    with open(args.eval_file, "r") as f: eval_data = json.load(f)
+    with open(args.source_file, "r") as f: source_data = {item['index']: item for item in json.load(f)}
+
+    for doc in tqdm.tqdm(eval_data):
+        idx = doc['index']
+        original = source_data.get(idx, {})
+        
+        for level, content in doc['literacy_levels'].items():
+            details = content['details']
+            gen_text = original.get('diff_label_texts', {}).get(level, '')
+            
+            # 1. Audit Attribution
+            for item in details.get('attribution', []):
+                if item['status'] == "not_supported":
+                    res, lbl = get_reasoned_verdict(original.get('fulltext'), item['subclaim'], "attribution", level)
+                    item.update({"reasoning": res, "status": lbl, "refined": True})
+
+            # 2. Audit Conciseness
+            for item in details.get('conciseness', []):
+                if item['status'] == "not_supported":
+                    res, lbl = get_reasoned_verdict(original.get('summary'), item['subclaim'], "conciseness", level)
+                    item.update({"reasoning": res, "status": lbl, "refined": True})
+
+            # 3. Audit Completeness
+            for item in details.get('completeness', []):
+                if item['status'] == "not_supported":
+                    res, lbl = get_reasoned_verdict(gen_text, item['source_fact'], "completeness", level)
+                    item.update({"reasoning": res, "status": lbl, "refined": True})
+
+            # 4. NEW: Audit Source Coverage
+            for item in details.get('source_coverage', []):
+                if item['status'] == "not_supported":
+                    # Comparing Source Fact against the Generated Text
+                    res, lbl = get_reasoned_verdict(gen_text, item['source_subclaim'], "source_coverage", level)
+                    item.update({"reasoning": res, "status": lbl, "refined": True})
+
+            # Recalculate Scores
+            metrics = ['factual_attribution', 'conciseness', 'completeness', 'source_coverage']
+            for m in metrics:
+                if m in details:
+                    content['scores'][m] = sum(1 for x in details[m] if x['status'] == 'supported') / len(details[m]) if details[m] else 0
+
+    save_path = os.path.join(args.save_path, f"REFINED_{os.path.basename(args.eval_file)}")
+    with open(save_path, "w") as f:
+        json.dump(eval_data, f, indent=2)
+    print(f"Refinement complete. Saved to {save_path}")
\ No newline at end of file
diff --git a/code/reasoning/ressoning_qwen3-30B-a3b_v2.py b/code/reasoning/ressoning_qwen3-30B-a3b_v2.py
new file mode 100644
index 0000000000000000000000000000000000000000..9aec36428db6f9ebb8bc1a219d5d4bc78e5e004a
--- /dev/null
+++ b/code/reasoning/ressoning_qwen3-30B-a3b_v2.py
@@ -0,0 +1,136 @@
+import os
+import json
+import tqdm
+import argparse
+from openai import OpenAI
+import re
+
+# -----------------------------
+#  CONFIGURATION
+# -----------------------------
+API_URL = "http://172.16.34.29:8004/v1" 
+API_KEY = "EMPTY"
+MODEL_NAME = "Qwen/Qwen3-30B-A3B-Instruct-2507" 
+
+client = OpenAI(base_url=API_URL, api_key=API_KEY)
+
+# -----------------------------
+#  REASONING PROMPT
+# -----------------------------
+def reasoning_prompt(reference_text, statement, task_type="attribution"):
+    if task_type == "attribution":
+        # Checking if a summary subclaim is supported by the source medical text
+        return f"""You are a senior clinical data validator. A previous system flagged a subclaim as 'not_supported' by the medical text. 
+Verify if this is a False Negative.
+
+### CONTEXT:
+Medical Text (Source): {reference_text}
+Subclaim (from Summary): {statement}
+
+### TASK:
+1. Search the Medical Text for paraphrased evidence or implicit support for the Subclaim.
+2. Determine if it is 'supported' or 'not_supported'.
+
+### OUTPUT FORMAT:
+Provide internal reasoning in <think> tags, then conclude with exactly one word: 'supported' or 'not_supported'."""
+    else:
+        # Checking if a source fact is actually present in the summary (Completeness)
+        return f"""You are a senior clinical data validator. A system flagged that a specific fact from the source medical text is missing ('not_supported') from the summary.
+Verify if the summary actually contains this information.
+
+### CONTEXT:
+Summary Text: {reference_text}
+Source Fact: {statement}
+
+### TASK:
+1. Search the Summary Text for the Source Fact. Look for synonyms or condensed mentions.
+2. If the summary contains the info, label it 'supported'. If truly missing, label it 'not_supported'.
+
+### OUTPUT FORMAT:
+Provide internal reasoning in <think> tags, then conclude with exactly one word: 'supported' or 'not_supported'."""
+
+# -----------------------------
+#  LOGIC TO EXTRACT THINKING & LABEL
+# -----------------------------
+def get_reasoned_verdict(reference: str, statement: str, task_type: str):
+    prompt = reasoning_prompt(reference, statement, task_type)
+    
+    try:
+        response = client.chat.completions.create(
+            model=MODEL_NAME,
+            messages=[{"role": "user", "content": prompt}],
+            temperature=0.1,
+        )
+        full_content = response.choices[0].message.content
+        
+        reasoning = ""
+        if "<think>" in full_content and "</think>" in full_content:
+            reasoning = re.search(r"<think>(.*?)</think>", full_content, re.DOTALL).group(1).strip()
+            final_output = full_content.split("</think>")[-1].strip().lower()
+        else:
+            reasoning = "No explicit <think> tags provided."
+            final_output = full_content.strip().lower()
+
+        if "not_supported" in final_output:
+            label = "not_supported"
+        elif "supported" in final_output:
+            label = "supported"
+        else:
+            label = "inconclusive"
+
+        return reasoning, label
+
+    except Exception as e:
+        return str(e), "error_api"
+
+# -----------------------------
+#  MAIN PROCESSING
+# -----------------------------
+if __name__ == "__main__":
+    parser = argparse.ArgumentParser()
+    parser.add_argument("--input_file", type=str, required=True) 
+    parser.add_argument("--save_path", type=str, default="/home/mshahidul/readctrl/data/reasoning/")
+    args = parser.parse_args()
+
+    os.makedirs(args.save_path, exist_ok=True)
+
+    with open(args.input_file, "r") as f:
+        data = json.load(f)
+        
+    save_filename = f"refined_v2_{os.path.basename(args.input_file)}"
+    full_save_path = os.path.join(args.save_path, save_filename)
+    
+    print(f"Processing {len(data)} documents...")
+
+    for doc in tqdm.tqdm(data):
+        # We need the source text for Attribution and the summary text for Completeness
+        # Assuming 'fulltext' is the source and 'summary' is the generated summary
+        source_text = doc.get('fulltext', '')
+        summary_text = doc.get('summary', '') # Ensure this key matches your JSON
+
+        # 1. Audit Attribution Details
+        if 'attribution_details' in doc:
+            for item in doc['attribution_details']:
+                if item.get('label') == "not_supported":
+                    reasoning, new_label = get_reasoned_verdict(source_text, item.get('subclaim', ''), "attribution")
+                    item['original_label'] = "not_supported"
+                    item['reasoning_audit'] = reasoning
+                    item['label'] = new_label
+                    item['is_refined'] = True
+
+        # 2. Audit Completeness Details
+        if 'completeness_details' in doc:
+            for item in doc['completeness_details']:
+                if item.get('present_in_summary') == "not_supported":
+                    # Here we check if the 'source_fact' is in the 'summary_text'
+                    reasoning, new_label = get_reasoned_verdict(summary_text, item.get('source_fact', ''), "completeness")
+                    item['original_label'] = "not_supported"
+                    item['reasoning_audit'] = reasoning
+                    item['present_in_summary'] = new_label
+                    item['is_refined'] = True
+
+        # Save state periodically
+        with open(full_save_path, "w") as f:
+            json.dump(data, f, indent=2, ensure_ascii=False)
+
+    print(f"Refinement complete. Saved to {full_save_path}")
\ No newline at end of file
diff --git a/code/reasoning/ressoning_qwen3-30B-a3b_v3.py b/code/reasoning/ressoning_qwen3-30B-a3b_v3.py
new file mode 100644
index 0000000000000000000000000000000000000000..689cee23f2d215a67536ac5e689b6dd257a149d8
--- /dev/null
+++ b/code/reasoning/ressoning_qwen3-30B-a3b_v3.py
@@ -0,0 +1,158 @@
+import os
+import json
+import tqdm
+import argparse
+import re
+from openai import OpenAI
+
+# -----------------------------
+#  CONFIGURATION
+# -----------------------------
+API_URL = "http://172.16.34.29:8004/v1" 
+API_KEY = "EMPTY"
+MODEL_NAME = "Qwen/Qwen3-30B-A3B-Instruct-2507" 
+
+client = OpenAI(base_url=API_URL, api_key=API_KEY)
+
+# -----------------------------
+#  REASONING PROMPTS
+# -----------------------------
+def get_audit_prompt(task_type, reference_text, subclaim, literacy_level):
+    # Mapping the specific literacy guidelines to the prompt context
+    level_guidelines = {
+        "low_health_literacy": """
+        Level: Low Health Literacy (High Readability)
+        Target: Individuals needing simple terms.
+        Goal: 'Living room' language. Replace jargon (e.g., 'renal' -> 'kidney').
+        Density: Strictly 'need-to-know' info from Gold Summary.
+        Strategy: High paraphrasing, analogies, one idea per sentence.
+        Faithfulness: Must align with Gold Summary.""",
+        
+        "intermediate_health_literacy": """
+        Level: Intermediate Health Literacy (Medium Readability)
+        Target: General public.
+        Goal: Standard vocabulary. Common medical terms okay; technical speak simplified.
+        Density: Balanced. Use Gold Summary as lead, supplemented by context from Source.
+        Strategy: Moderate paraphrasing. Remove minor technical details.
+        Faithfulness: Maintain main narrative of Gold Summary.""",
+        
+        "proficient_health_literacy": """
+        Level: Proficient Health Literacy (Low Readability)
+        Target: Researchers/Clinicians.
+        Goal: Technical/Academic. Prioritize clinical nuance and accuracy.
+        Density: High. Include data, physiological mechanisms, and statistics from Source.
+        Strategy: Minimal paraphrasing. Retain original technical terminology.
+        Faithfulness: Adhere to Source Text; add deeper scientific context."""
+    }
+
+    guidelines = level_guidelines.get(literacy_level, "Follow standard medical audit practices.")
+    level_desc = literacy_level.replace("_", " ")
+
+    # Base instructions for the reasoning model
+    base_instructions = f"""
+### Literacy Level Context:
+{guidelines}
+
+### Task Instructions:"""
+
+    if task_type == "attribution":
+        return f"""{base_instructions}
+1. Compare the Subclaim against the Source Text.
+2. Flag as 'supported' if the Source contains this claim, even if highly paraphrased for {level_desc}.
+3. Note: Proficient level summaries should be strictly accurate, while Low level summaries use analogies.
+SOURCE: {reference_text}
+SUBCLAIM: {subclaim}
+Provide reasoning in <think> tags, then output: 'supported' or 'not_supported'."""
+
+    elif task_type == "completeness":
+        return f"""{base_instructions}
+1. Is this Fact from the Gold Standard missing from the {level_desc} summary?
+2. Mark 'supported' if: The info is present (paraphrased) OR if the info was omitted because it is too complex/technical for the {level_desc} guidelines.
+3. Mark 'not_supported' ONLY if a critical safety fact or 'need-to-know' item is truly missing.
+SUMMARY: {reference_text}
+FACT: {subclaim}
+Provide reasoning in <think> tags, then output: 'supported' or 'not_supported'."""
+
+    elif task_type == "conciseness":
+        return f"""{base_instructions}
+1. The Subclaim exists in the summary but NOT in the Gold Reference. Is this okay?
+2. Mark 'supported' if: The info adds necessary definitions for Low/Intermediate readers, or adds scientific depth for Proficient readers.
+3. Mark 'not_supported' if: The info is a hallucination or irrelevant 'fluff' that violates the Information Density rules.
+REFERENCE: {reference_text}
+SUBCLAIM: {subclaim}
+Provide reasoning in <think> tags, then output: 'supported' or 'not_supported'."""
+
+# -----------------------------
+#  LOGIC
+# -----------------------------
+def get_reasoned_verdict(reference, statement, task_type, literacy_level):
+    prompt = get_audit_prompt(task_type, reference, statement, literacy_level)
+    try:
+        response = client.chat.completions.create(
+            model=MODEL_NAME,
+            messages=[{"role": "user", "content": prompt}],
+            temperature=0.1,
+        )
+        content = response.choices[0].message.content
+        # import ipdb; ipdb.set_trace()
+        reasoning = re.search(r"<reasoning>(.*?)</reasoning>", content, re.DOTALL).group(1).strip() if "<reasoning>" in content else "N/A"
+        final_text = content.split("</reasoning>")[-1].lower()
+        
+        label = "supported" if "supported" in final_text and "not_supported" not in final_text else "not_supported"
+        return reasoning, label
+    except:
+        return "API Error", "not_supported"
+
+# -----------------------------
+#  MAIN PROCESSING
+# -----------------------------
+if __name__ == "__main__":
+    parser = argparse.ArgumentParser()
+    # Path to the output of your previous generation script
+    parser.add_argument("--eval_file", type=str, default="/home/mshahidul/readctrl/data/factual_testing/full_details_evaluation_0_20_qwen3-32B.json")
+    # Path to the original data file containing 'fulltext' and 'summary'
+    parser.add_argument("--source_file", type=str, default="/home/mshahidul/readctrl/data/extracting_subclaim/extracted_subclaims_syn_data_with_gs_summary_en.json")
+    parser.add_argument("--save_path", type=str, default="/home/mshahidul/readctrl/data/reasoning/")
+    args = parser.parse_args()
+
+    os.makedirs(args.save_path, exist_ok=True)
+
+    with open(args.eval_file, "r") as f: eval_data = json.load(f)
+    with open(args.source_file, "r") as f: source_data = {item['index']: item for item in json.load(f)}
+
+    for doc in tqdm.tqdm(eval_data):
+        idx = doc['index']
+        original = source_data.get(idx, {})
+        
+        for level, content in doc['literacy_levels'].items():
+            details = content['details']
+            # import ipdb; ipdb.set_trace()
+            
+            # 1. Audit Attribution (Check against Full Text)
+            for item in details['attribution']:
+                if item['status'] == "not_supported":
+                    res, lbl = get_reasoned_verdict(original.get('fulltext'), item['subclaim'], "attribution", level)
+                    item.update({"reasoning": res, "status": lbl, "refined": True})
+
+            # 2. Audit Conciseness (Check against Ref Summary)
+            for item in details['conciseness']:
+                if item['status'] == "not_supported":
+                    res, lbl = get_reasoned_verdict(original.get('summary'), item['subclaim'], "conciseness", level)
+                    item.update({"reasoning": res, "status": lbl, "refined": True})
+
+            # 3. Audit Completeness (Check Ref facts against Gen Text)
+            gen_text = original.get('diff_label_texts', {}).get(level, '')
+            for item in details['completeness']:
+                if item['status'] == "not_supported":
+                    res, lbl = get_reasoned_verdict(gen_text, item['source_fact'], "completeness", level)
+                    item.update({"reasoning": res, "status": lbl, "refined": True})
+
+            # Recalculate Scores after refinement
+            content['scores']['attribution'] = sum(1 for x in details['attribution'] if x['status'] == 'supported') / len(details['attribution']) if details['attribution'] else 0
+            content['scores']['conciseness'] = sum(1 for x in details['conciseness'] if x['status'] == 'supported') / len(details['conciseness']) if details['conciseness'] else 0
+            content['scores']['completeness'] = sum(1 for x in details['completeness'] if x['status'] == 'supported') / len(details['completeness']) if details['completeness'] else 0
+
+    save_path = os.path.join(args.save_path, f"REFINED_{os.path.basename(args.eval_file)}")
+    with open(save_path, "w") as f:
+        json.dump(eval_data, f, indent=2)
+    print(f"Refinement complete. Saved to {save_path}")
\ No newline at end of file
diff --git a/code/reasoning/ressoning_qwen3-30B-a3b_v5.py b/code/reasoning/ressoning_qwen3-30B-a3b_v5.py
new file mode 100644
index 0000000000000000000000000000000000000000..ce12dfedaf5136c6915a43a30d69d8dacbdb7b17
--- /dev/null
+++ b/code/reasoning/ressoning_qwen3-30B-a3b_v5.py
@@ -0,0 +1,169 @@
+import os
+import json
+import tqdm
+import argparse
+import re
+from openai import OpenAI
+
+# -----------------------------
+#  CONFIGURATION
+# -----------------------------
+API_URL = "http://172.16.34.29:8004/v1" 
+API_KEY = "EMPTY"
+MODEL_NAME = "Qwen/Qwen3-30B-A3B-Instruct-2507" 
+
+client = OpenAI(base_url=API_URL, api_key=API_KEY)
+
+# -----------------------------
+#  REASONING PROMPTS
+# -----------------------------
+def get_audit_prompt(task_type, reference_text, subclaim, literacy_level):
+    level_guidelines = {
+        "low_health_literacy": """
+        Level: Low Health Literacy (High Readability)
+        Target: Individuals needing simple terms.
+        Goal: 'Living room' language. Replace jargon (e.g., 'renal' -> 'kidney').
+        Density: Strictly 'need-to-know' info from Gold Summary.
+        Strategy: High paraphrasing, analogies, one idea per sentence.
+        Faithfulness: Must align with Gold Summary.""",
+        
+        "intermediate_health_literacy": """
+        Level: Intermediate Health Literacy (Medium Readability)
+        Target: General public.
+        Goal: Standard vocabulary. Common medical terms okay; technical speak simplified.
+        Density: Balanced. Use Gold Summary as lead, supplemented by context from Source.
+        Strategy: Moderate paraphrasing. Remove minor technical details.
+        Faithfulness: Maintain main narrative of Gold Summary.""",
+        
+        "proficient_health_literacy": """
+        Level: Proficient Health Literacy (Low Readability)
+        Target: Researchers/Clinicians.
+        Goal: Technical/Academic. Prioritize clinical nuance and accuracy.
+        Density: High. Include data, physiological mechanisms, and statistics from Source.
+        Strategy: Minimal paraphrasing. Retain original technical terminology.
+        Faithfulness: Adhere to Source Text; add deeper scientific context."""
+    }
+
+    guidelines = level_guidelines.get(literacy_level, "Follow standard medical audit practices.")
+    level_desc = literacy_level.replace("_", " ")
+
+    base_instructions = f"""
+### Literacy Level Context:
+{guidelines}
+
+### Task Instructions:"""
+
+    if task_type == "attribution":
+        return f"""{base_instructions}
+1. Compare the Subclaim against the Source Text.
+2. Flag as 'supported' if the Source contains this claim, even if highly paraphrased for {level_desc}.
+SOURCE: {reference_text}
+SUBCLAIM: {subclaim}
+Provide reasoning in <reasoning> tags, then output: 'supported' or 'not_supported'."""
+
+    elif task_type == "completeness":
+        return f"""{base_instructions}
+1. Is this Fact from the Gold Standard missing from the {level_desc} summary?
+2. Mark 'supported' if: The info is present (paraphrased) OR if the info was omitted because it is too complex for {level_desc} guidelines.
+SUMMARY: {reference_text}
+FACT: {subclaim}
+Provide reasoning in <reasoning> tags, then output: 'supported' or 'not_supported'."""
+
+    elif task_type == "conciseness":
+        return f"""{base_instructions}
+1. The Subclaim exists in the summary but NOT in the Gold Reference. Is this okay?
+2. Mark 'supported' if: The info adds necessary definitions or scientific depth appropriate for {level_desc}.
+REFERENCE: {reference_text}
+SUBCLAIM: {subclaim}
+Provide reasoning in <reasoning> tags, then output: 'supported' or 'not_supported'."""
+
+    # NEW: Source Coverage Prompt
+    elif task_type == "source_coverage":
+        return f"""{base_instructions}
+1. Check if the following Fact from the ORIGINAL Source Text is covered in the generated {level_desc} summary.
+2. Mark 'supported' if the summary includes this information, even if it is simplified or combined with other points.
+3. Mark 'not_supported' if the summary completely omits this specific medical fact.
+GENERATED SUMMARY: {reference_text}
+SOURCE FACT: {subclaim}
+Provide reasoning in <reasoning> tags, then output: 'supported' or 'not_supported'."""
+
+# -----------------------------
+#  LOGIC
+# -----------------------------
+def get_reasoned_verdict(reference, statement, task_type, literacy_level):
+    prompt = get_audit_prompt(task_type, reference, statement, literacy_level)
+    try:
+        response = client.chat.completions.create(
+            model=MODEL_NAME,
+            messages=[{"role": "user", "content": prompt}],
+            temperature=0.1,
+        )
+        content = response.choices[0].message.content
+        
+        # Extracts reasoning from <reasoning> tags specifically
+        reasoning = re.search(r"<reasoning>(.*?)</reasoning>", content, re.DOTALL).group(1).strip() if "<reasoning>" in content else "N/A"
+        final_text = content.split("</reasoning>")[-1].lower()
+        
+        label = "supported" if "supported" in final_text and "not_supported" not in final_text else "not_supported"
+        return reasoning, label
+    except:
+        return "API Error", "not_supported"
+
+# -----------------------------
+#  MAIN PROCESSING
+# -----------------------------
+if __name__ == "__main__":
+    parser = argparse.ArgumentParser()
+    parser.add_argument("--eval_file", type=str, default="/home/mshahidul/readctrl/data/reasoning/reasoned_updated_results_0_20.json")
+    parser.add_argument("--source_file", type=str, default="/home/mshahidul/readctrl/data/extracting_subclaim/extracted_subclaims_syn_data_with_gs_summary_en.json")
+    parser.add_argument("--save_path", type=str, default="/home/mshahidul/readctrl/data/reasoning/")
+    args = parser.parse_args()
+
+    os.makedirs(args.save_path, exist_ok=True)
+
+    with open(args.eval_file, "r") as f: eval_data = json.load(f)
+    with open(args.source_file, "r") as f: source_data = {item['index']: item for item in json.load(f)}
+
+    for doc in tqdm.tqdm(eval_data):
+        idx = doc['index']
+        original = source_data.get(idx, {})
+        
+        for level, content in doc['literacy_levels'].items():
+            details = content['details']
+            gen_text = original.get('diff_label_texts', {}).get(level, '')
+            
+            # 1. Audit Attribution
+            for item in details.get('attribution', []):
+                if item['status'] == "not_supported":
+                    res, lbl = get_reasoned_verdict(original.get('fulltext'), item['subclaim'], "attribution", level)
+                    item.update({"reasoning": res, "status": lbl, "refined": True})
+
+            # 2. Audit Conciseness
+            for item in details.get('conciseness', []):
+                if item['status'] == "not_supported":
+                    res, lbl = get_reasoned_verdict(original.get('summary'), item['subclaim'], "conciseness", level)
+                    item.update({"reasoning": res, "status": lbl, "refined": True})
+
+            # 3. Audit Completeness
+            # for item in details.get('completeness', []):
+            #     if item['status'] == "not_supported":
+            #         res, lbl = get_reasoned_verdict(gen_text, item['source_fact'], "completeness", level)
+            #         item.update({"reasoning": res, "status": lbl, "refined": True})
+
+            # 4. NEW: Audit Source Coverage
+            # for item in details.get('source_coverage', []):
+            #     if item['status'] == "not_supported":
+            #         # Comparing Source Fact against the Generated Text
+            #         res, lbl = get_reasoned_verdict(gen_text, item['source_subclaim'], "source_coverage", level)
+            #         item.update({"reasoning": res, "status": lbl, "refined": True})
+
+            # Recalculate Scores
+            metrics = ['factual_attribution', 'conciseness']
+            for m in metrics:
+                if m in details:
+                    content['scores'][m] = sum(1 for x in details[m] if x['status'] == 'supported') / len(details[m]) if details[m] else 0
+
+    save_path = os.path.join(args.save_path, f"REFINED_attr_concise_{os.path.basename(args.eval_file)}")
+    with open(save_path, "w") as f:
+        json.dump(eval_data, f, indent=2)
+    print(f"Refinement complete. Saved to {save_path}")
\ No newline at end of file
diff --git a/code/rl_inference/run_gpt5mini_nano_inference.py b/code/rl_inference/run_gpt5mini_nano_inference.py
new file mode 100644
index 0000000000000000000000000000000000000000..611be3f58fadf5ba750efd704b45a633b5afccf2
--- /dev/null
+++ b/code/rl_inference/run_gpt5mini_nano_inference.py
@@ -0,0 +1,351 @@
+import argparse
+import json
+import os
+import time
+import urllib.error
+import urllib.request
+from datetime import datetime
+from typing import Any, Dict, List, Optional
+
+from tqdm import tqdm  # pyright: ignore[reportMissingModuleSource]
+
+
+api_file = "/home/mshahidul/api_new.json"
+with open(api_file, "r", encoding="utf-8") as f:
+    api_keys = json.load(f)
+
+DEFAULT_API_BASE = "https://api.openai.com/v1"
+DEFAULT_INPUT_PATH = (
+    "/home/mshahidul/readctrl/data/annotators_validate_data_(20_80)/combine/"
+    "verified_combined_0-80.json"
+)
+DEFAULT_OUTPUT_DIR = "/home/mshahidul/readctrl/code/rl_inference/test_result"
+DEFAULT_PROMPT_LOW_PATH = (
+    "/home/mshahidul/readctrl/code/RL_model/verl/verl_train/dataset/prompt_low"
+)
+DEFAULT_PROMPT_INTERMEDIATE_PATH = (
+    "/home/mshahidul/readctrl/code/RL_model/verl/verl_train/dataset/prompt_intermediate"
+)
+DEFAULT_PROMPT_PROFICIENT_PATH = (
+    "/home/mshahidul/readctrl/code/RL_model/verl/verl_train/dataset/prompt_proficient"
+)
+DEFAULT_MODELS = "gpt-5-mini,gpt-5-nano"
+
+VALID_LABELS = {
+    "low_health_literacy",
+    "intermediate_health_literacy",
+    "proficient_health_literacy",
+}
+
+
+def parse_args() -> argparse.Namespace:
+    parser = argparse.ArgumentParser(
+        description=(
+            "Generate outputs with gpt-5-mini and gpt-5-nano using "
+            "verified_combined dataset and literacy-level prompts."
+        )
+    )
+    parser.add_argument("--api-base", default=os.environ.get("OPENAI_API_BASE", DEFAULT_API_BASE))
+    parser.add_argument(
+        "--api-key",
+        default=os.environ.get("OPENAI_API_KEY", api_keys["openai"]),
+    )
+    parser.add_argument("--models", default=DEFAULT_MODELS, help="Comma-separated model list.")
+    parser.add_argument("--input-path", default=DEFAULT_INPUT_PATH)
+    parser.add_argument("--output-dir", default=DEFAULT_OUTPUT_DIR)
+    parser.add_argument("--prompt-low-path", default=DEFAULT_PROMPT_LOW_PATH)
+    parser.add_argument(
+        "--prompt-intermediate-path",
+        default=DEFAULT_PROMPT_INTERMEDIATE_PATH,
+    )
+    parser.add_argument(
+        "--prompt-proficient-path",
+        default=DEFAULT_PROMPT_PROFICIENT_PATH,
+    )
+    parser.add_argument(
+        "--max-samples",
+        type=int,
+        default=-1,
+        help="Use -1 for all rows.",
+    )
+    parser.add_argument("--temperature", type=float, default=0.0)
+    parser.add_argument("--timeout-seconds", type=int, default=120)
+    parser.add_argument("--max-retries", type=int, default=2)
+    parser.add_argument("--retry-wait-seconds", type=float, default=2.0)
+    return parser.parse_args()
+
+
+def check_api_base(api_base: str, api_key: str, timeout_seconds: int) -> None:
+    models_url = api_base.rstrip("/") + "/models"
+    req = urllib.request.Request(models_url, method="GET")
+    if api_key:
+        req.add_header("Authorization", f"Bearer {api_key}")
+    try:
+        with urllib.request.urlopen(req, timeout=timeout_seconds) as resp:
+            if resp.status >= 400:
+                raise RuntimeError(
+                    f"Endpoint reachable but unhealthy: {models_url} (status={resp.status})"
+                )
+    except urllib.error.URLError as exc:
+        raise ConnectionError(
+            "Cannot reach OpenAI-compatible endpoint. "
+            f"api_base={api_base}. Check network/API base/API key."
+        ) from exc
+
+
+def load_prompt_templates(args: argparse.Namespace) -> Dict[str, str]:
+    prompt_path_by_label = {
+        "low_health_literacy": args.prompt_low_path,
+        "intermediate_health_literacy": args.prompt_intermediate_path,
+        "proficient_health_literacy": args.prompt_proficient_path,
+    }
+    templates: Dict[str, str] = {}
+    for label, path in prompt_path_by_label.items():
+        if not os.path.exists(path):
+            raise FileNotFoundError(f"Prompt file not found: {path}")
+        with open(path, "r", encoding="utf-8") as f:
+            templates[label] = f.read()
+    return templates
+
+
+def infer_source_lang(fulltext: str) -> str:
+    if fulltext and any("a" <= ch.lower() <= "z" for ch in fulltext):
+        return "English"
+    return "Unknown"
+
+
+def build_prompt(template: str, fulltext: str, summary: str, source_lang: str) -> str:
+    return (
+        template.replace("{source_lang}", source_lang)
+        .replace("{gold_summary}", summary)
+        .replace("{full_text}", fulltext)
+    )
+
+
+def load_verified_rows(path: str) -> List[Dict[str, Any]]:
+    if not os.path.exists(path):
+        raise FileNotFoundError(f"Input file not found: {path}")
+    with open(path, "r", encoding="utf-8") as f:
+        parsed = json.load(f)
+    if not isinstance(parsed, list):
+        raise ValueError(f"Expected top-level JSON array in {path}")
+    return [row for row in parsed if isinstance(row, dict)]
+
+
+def parse_models(models_arg: str) -> List[str]:
+    models = [m.strip() for m in models_arg.split(",") if m.strip()]
+    if not models:
+        raise ValueError("No models provided. Example: --models gpt-5-mini,gpt-5-nano")
+    return models
+
+
+def _clean_json_block(text: str) -> str:
+    cleaned = text.strip()
+    if "```json" in cleaned:
+        cleaned = cleaned.split("```json", 1)[1].split("```", 1)[0].strip()
+    elif "```" in cleaned:
+        cleaned = cleaned.split("```", 1)[1].split("```", 1)[0].strip()
+    return cleaned
+
+
+def extract_generated_text(raw_response: str, expected_label: str) -> str:
+    cleaned = _clean_json_block(raw_response)
+    try:
+        parsed = json.loads(cleaned)
+    except json.JSONDecodeError:
+        return raw_response.strip()
+
+    if isinstance(parsed, dict):
+        value = parsed.get(expected_label)
+        if isinstance(value, str) and value.strip():
+            return value.strip()
+    return raw_response.strip()
+
+
+def call_chat_completion(
+    *,
+    api_base: str,
+    api_key: str,
+    model: str,
+    prompt: str,
+    temperature: float,
+    timeout_seconds: int,
+    max_retries: int,
+    retry_wait_seconds: float,
+) -> str:
+    url = api_base.rstrip("/") + "/chat/completions"
+    payload = {
+        "model": model,
+        "messages": [{"role": "user", "content": prompt}],
+    }
+    data = json.dumps(payload).encode("utf-8")
+
+    last_error: Optional[Exception] = None
+    for attempt in range(max_retries + 1):
+        req = urllib.request.Request(url, data=data, method="POST")
+        req.add_header("Content-Type", "application/json")
+        if api_key:
+            req.add_header("Authorization", f"Bearer {api_key}")
+        try:
+            with urllib.request.urlopen(req, timeout=timeout_seconds) as resp:
+                body = resp.read().decode("utf-8")
+            parsed = json.loads(body)
+            return str(parsed["choices"][0]["message"]["content"]).strip()
+        except urllib.error.HTTPError as exc:
+            retriable = exc.code in (408, 409, 429, 500, 502, 503, 504)
+            last_error = exc
+            if attempt < max_retries and retriable:
+                time.sleep(retry_wait_seconds)
+                continue
+            raise
+        except (urllib.error.URLError, KeyError, IndexError, json.JSONDecodeError) as exc:
+            last_error = exc
+            if attempt < max_retries:
+                time.sleep(retry_wait_seconds)
+                continue
+            raise
+
+    if last_error:
+        raise last_error
+    raise RuntimeError("Unknown error during chat completion call.")
+
+
+def main() -> None:
+    args = parse_args()
+    if not args.api_key:
+        raise ValueError("Missing API key. Set OPENAI_API_KEY or pass --api-key.")
+
+    for path in (
+        args.prompt_low_path,
+        args.prompt_intermediate_path,
+        args.prompt_proficient_path,
+    ):
+        if not os.path.exists(path):
+            raise FileNotFoundError(f"Prompt file not found: {path}")
+
+    check_api_base(args.api_base, args.api_key, args.timeout_seconds)
+    models = parse_models(args.models)
+    templates = load_prompt_templates(args)
+    rows = load_verified_rows(args.input_path)
+
+    parsed_items: List[Dict[str, Any]] = []
+    for idx, row in enumerate(rows):
+        gold_label = str(row.get("label", "")).strip()
+        fulltext = str(row.get("fulltext", "")).strip()
+        summary = str(row.get("summary", "")).strip()
+        if gold_label not in VALID_LABELS:
+            continue
+        if not fulltext or not summary:
+            continue
+        source_lang = infer_source_lang(fulltext)
+        prompt = build_prompt(
+            template=templates[gold_label],
+            fulltext=fulltext,
+            summary=summary,
+            source_lang=source_lang,
+        )
+        parsed_items.append(
+            {
+                "row_index": idx,
+                "doc_id": row.get("doc_id"),
+                "gold_label": gold_label,
+                "source_lang": source_lang,
+                "prompt": prompt,
+            }
+        )
+
+    if args.max_samples > 0:
+        parsed_items = parsed_items[: args.max_samples]
+    if not parsed_items:
+        raise RuntimeError("No valid rows found in input file.")
+
+    ts = datetime.now().strftime("%Y%m%d_%H%M%S")
+    os.makedirs(args.output_dir, exist_ok=True)
+    summary_path = os.path.join(args.output_dir, f"gpt5_inference_summary_{ts}.json")
+    combined_path = os.path.join(args.output_dir, f"gpt5_inference_all_{ts}.jsonl")
+
+    combined_records: List[Dict[str, Any]] = []
+    model_stats: Dict[str, Dict[str, Any]] = {}
+
+    for model in models:
+        model_slug = model.replace("/", "_")
+        model_output_path = os.path.join(
+            args.output_dir, f"gpt5_inference_{model_slug}_{ts}.jsonl"
+        )
+        success_count = 0
+        error_count = 0
+
+        with open(model_output_path, "w", encoding="utf-8") as f_model:
+            total = len(parsed_items)
+            progress_iter = tqdm(
+                parsed_items,
+                total=total,
+                desc=f"{model}",
+                unit="item",
+            )
+            for item in progress_iter:
+
+                record: Dict[str, Any] = {
+                    "model": model,
+                    "row_index": item["row_index"],
+                    "doc_id": item.get("doc_id"),
+                    "gold_label": item["gold_label"],
+                    "source_lang": item["source_lang"],
+                    "prompt": item["prompt"],
+                }
+                try:
+                    raw_response = call_chat_completion(
+                        api_base=args.api_base,
+                        api_key=args.api_key,
+                        model=model,
+                        prompt=item["prompt"],
+                        temperature=args.temperature,
+                        timeout_seconds=args.timeout_seconds,
+                        max_retries=args.max_retries,
+                        retry_wait_seconds=args.retry_wait_seconds,
+                    )
+                    generated_text = extract_generated_text(raw_response, item["gold_label"])
+                    record["prediction"] = raw_response
+                    record["generated_text"] = generated_text
+                    record["error"] = ""
+                    success_count += 1
+                except Exception as exc:
+                    record["prediction"] = ""
+                    record["generated_text"] = ""
+                    record["error"] = f"{type(exc).__name__}: {exc}"
+                    error_count += 1
+
+                f_model.write(json.dumps(record, ensure_ascii=False) + "\n")
+                combined_records.append(record)
+
+        model_stats[model] = {
+            "output_path": model_output_path,
+            "total_rows": len(parsed_items),
+            "success_count": success_count,
+            "error_count": error_count,
+        }
+        print(f"[DONE] {model} output: {model_output_path}")
+
+    with open(combined_path, "w", encoding="utf-8") as f_all:
+        for record in combined_records:
+            f_all.write(json.dumps(record, ensure_ascii=False) + "\n")
+
+    summary_obj = {
+        "input_path": args.input_path,
+        "api_base": args.api_base,
+        "models": models,
+        "max_samples": args.max_samples,
+        "temperature": args.temperature,
+        "total_dataset_rows_used": len(parsed_items),
+        "combined_output_path": combined_path,
+        "model_stats": model_stats,
+    }
+    with open(summary_path, "w", encoding="utf-8") as f_summary:
+        json.dump(summary_obj, f_summary, ensure_ascii=False, indent=2)
+
+    print(f"[DONE] Combined output: {combined_path}")
+    print(f"[DONE] Summary output: {summary_path}")
+
+
+if __name__ == "__main__":
+    main()
diff --git a/code/rl_inference/run_inference_vllm_server.py b/code/rl_inference/run_inference_vllm_server.py
new file mode 100644
index 0000000000000000000000000000000000000000..a8479f602c427f1b1dc5f6e599bd75b4f68bd780
--- /dev/null
+++ b/code/rl_inference/run_inference_vllm_server.py
@@ -0,0 +1,324 @@
+import argparse
+import json
+import os
+import re
+from datetime import datetime
+from typing import Any, Dict, List, Optional
+
+import pandas as pd
+import requests
+from tqdm import tqdm
+from transformers import AutoTokenizer
+
+
+DEFAULT_MODEL_PATH = "Qwen/Qwen3-4B-Instruct-2507"
+DEFAULT_DATASET_PATH = (
+    "/home/mshahidul/readctrl/code/text_classifier/data/verified_combined_0-80_clean200.json"
+)
+DEFAULT_OUTPUT_DIR = "/home/mshahidul/readctrl/code/RL_model/inference_data"
+DEFAULT_BASE_URL = "http://127.0.0.1:8001/v1"
+DEFAULT_SERVED_MODEL_NAME = "inference"
+DEFAULT_PROMPT_LOW_PATH = (
+    "/home/mshahidul/readctrl/code/RL_model/verl/verl_train/dataset/prompt_low"
+)
+DEFAULT_PROMPT_INTERMEDIATE_PATH = (
+    "/home/mshahidul/readctrl/code/RL_model/verl/verl_train/dataset/prompt_intermediate"
+)
+DEFAULT_PROMPT_PROFICIENT_PATH = (
+    "/home/mshahidul/readctrl/code/RL_model/verl/verl_train/dataset/prompt_proficient"
+)
+VALID_LABELS = {
+    "low_health_literacy",
+    "intermediate_health_literacy",
+    "proficient_health_literacy",
+}
+
+
+def parse_args() -> argparse.Namespace:
+    parser = argparse.ArgumentParser(description="Run batched inference via vLLM OpenAI-compatible server.")
+    parser.add_argument("--model_path", type=str, default=DEFAULT_MODEL_PATH, help="Local path for tokenizer/chat template.")
+    parser.add_argument("--dataset_path", type=str, default=DEFAULT_DATASET_PATH)
+    parser.add_argument("--prompt-low-path", type=str, default=DEFAULT_PROMPT_LOW_PATH)
+    parser.add_argument("--prompt-intermediate-path", type=str, default=DEFAULT_PROMPT_INTERMEDIATE_PATH)
+    parser.add_argument("--prompt-proficient-path", type=str, default=DEFAULT_PROMPT_PROFICIENT_PATH)
+    parser.add_argument("--output_dir", type=str, default=DEFAULT_OUTPUT_DIR)
+    parser.add_argument("--base_url", type=str, default=DEFAULT_BASE_URL, help="vLLM OpenAI base URL, e.g. http://127.0.0.1:8000/v1")
+    parser.add_argument("--served_model_name", type=str, default=DEFAULT_SERVED_MODEL_NAME, help="Model name exposed by vLLM server.")
+    parser.add_argument("--batch_size", type=int, default=8)
+    parser.add_argument("--max_samples", type=int, default=-1, help="Use -1 for full dataset.")
+    parser.add_argument("--max_tokens", type=int, default=1024)
+    parser.add_argument("--temperature", type=float, default=0.7)
+    parser.add_argument("--top_p", type=float, default=0.8)
+    parser.add_argument("--api_key", type=str, default="EMPTY")
+    parser.add_argument("--timeout_sec", type=int, default=300)
+    return parser.parse_args()
+
+
+def load_prompt_templates(args: argparse.Namespace) -> Dict[str, str]:
+    prompt_path_by_label = {
+        "low_health_literacy": args.prompt_low_path,
+        "intermediate_health_literacy": args.prompt_intermediate_path,
+        "proficient_health_literacy": args.prompt_proficient_path,
+    }
+    templates: Dict[str, str] = {}
+    for label, path in prompt_path_by_label.items():
+        if not os.path.exists(path):
+            raise FileNotFoundError(f"Prompt file not found: {path}")
+        with open(path, "r", encoding="utf-8") as f:
+            templates[label] = f.read()
+    return templates
+
+
+def load_verified_rows(path: str) -> List[Dict[str, Any]]:
+    if not os.path.exists(path):
+        raise FileNotFoundError(f"Input file not found: {path}")
+    with open(path, "r", encoding="utf-8") as f:
+        parsed = json.load(f)
+    if not isinstance(parsed, list):
+        raise ValueError(f"Expected top-level JSON array in {path}")
+    return [row for row in parsed if isinstance(row, dict)]
+
+
+def infer_source_lang(fulltext: str) -> str:
+    if fulltext and any("a" <= ch.lower() <= "z" for ch in fulltext):
+        return "English"
+    return "Unknown"
+
+
+def build_prompt(template: str, fulltext: str, summary: str, source_lang: str) -> str:
+    return (
+        template.replace("{source_lang}", source_lang)
+        .replace("{gold_summary}", summary)
+        .replace("{full_text}", fulltext)
+    )
+
+
+def _clean_json_block(text: str) -> str:
+    cleaned = text.strip()
+    if "```json" in cleaned:
+        cleaned = cleaned.split("```json", 1)[1].split("```", 1)[0].strip()
+    elif "```" in cleaned:
+        cleaned = cleaned.split("```", 1)[1].split("```", 1)[0].strip()
+    return cleaned
+
+
+def extract_generated_text(raw_response: str, expected_label: str) -> str:
+    cleaned = _clean_json_block(raw_response)
+    try:
+        parsed = json.loads(cleaned)
+    except json.JSONDecodeError:
+        return raw_response.strip()
+
+    if isinstance(parsed, dict):
+        value = parsed.get(expected_label)
+        if isinstance(value, str) and value.strip():
+            return value.strip()
+    return raw_response.strip()
+
+
+def _normalize_messages(prompt_obj: Any) -> List[Dict[str, str]]:
+    if hasattr(prompt_obj, "tolist"):
+        prompt_obj = prompt_obj.tolist()
+
+    if isinstance(prompt_obj, dict):
+        if "role" in prompt_obj and "content" in prompt_obj:
+            return [{"role": str(prompt_obj["role"]), "content": str(prompt_obj["content"])}]
+        return [{"role": "user", "content": json.dumps(prompt_obj, ensure_ascii=False)}]
+
+    if isinstance(prompt_obj, list):
+        messages = []
+        for item in prompt_obj:
+            if isinstance(item, dict) and "role" in item and "content" in item:
+                messages.append({"role": str(item["role"]), "content": str(item["content"])})
+            else:
+                messages.append({"role": "user", "content": str(item)})
+        if messages:
+            return messages
+
+    return [{"role": "user", "content": str(prompt_obj)}]
+
+
+def build_prompt_text(tokenizer: AutoTokenizer, prompt_obj: Any) -> str:
+    messages = _normalize_messages(prompt_obj)
+    if tokenizer.chat_template:
+        return tokenizer.apply_chat_template(messages, tokenize=False, add_generation_prompt=True)
+    return "\n".join(m["content"] for m in messages) + "\n\nAssistant:"
+
+
+def sanitize_model_tag(model_path: str, max_len: int = 80) -> str:
+    tag = re.sub(r"[^A-Za-z0-9]+", "-", model_path).strip("-").lower()
+    if not tag:
+        return "unknown-model"
+    if len(tag) > max_len:
+        return tag[:max_len].rstrip("-")
+    return tag
+
+
+def check_server(base_url: str, headers: Dict[str, str], timeout_sec: int) -> Optional[List[Dict[str, Any]]]:
+    models_url = f"{base_url.rstrip('/')}/models"
+    resp = requests.get(models_url, headers=headers, timeout=timeout_sec)
+    resp.raise_for_status()
+    payload = resp.json()
+    return payload.get("data", [])
+
+
+def batched_completion_request(
+    base_url: str,
+    headers: Dict[str, str],
+    model_name: str,
+    prompts: List[str],
+    max_tokens: int,
+    temperature: float,
+    top_p: float,
+    timeout_sec: int,
+) -> List[str]:
+    payload = {
+        "model": model_name,
+        "prompt": prompts,
+        "max_tokens": max_tokens,
+        "temperature": temperature,
+        "top_p": top_p,
+    }
+    url = f"{base_url.rstrip('/')}/completions"
+    resp = requests.post(url, headers=headers, json=payload, timeout=timeout_sec)
+    resp.raise_for_status()
+    data = resp.json()
+    choices = data.get("choices", [])
+
+    preds = [""] * len(prompts)
+    for choice in choices:
+        idx = choice.get("index", None)
+        text = str(choice.get("text", "")).strip()
+        if isinstance(idx, int) and 0 <= idx < len(preds) and not preds[idx]:
+            preds[idx] = text
+
+    if any(not p for p in preds):
+        fallback_texts = [str(c.get("text", "")).strip() for c in choices]
+        for i in range(len(preds)):
+            if not preds[i]:
+                preds[i] = fallback_texts[i] if i < len(fallback_texts) else ""
+
+    return preds
+
+
+def main() -> None:
+    args = parse_args()
+    os.makedirs(args.output_dir, exist_ok=True)
+
+    run_ts = datetime.now().strftime("%Y%m%d_%H%M%S")
+    model_tag = sanitize_model_tag(args.model_path)
+    output_jsonl = os.path.join(args.output_dir, f"vllm_inference_{model_tag}_{run_ts}.jsonl")
+    output_parquet = os.path.join(args.output_dir, f"vllm_inference_{model_tag}_{run_ts}.parquet")
+    meta_path = os.path.join(args.output_dir, f"vllm_inference_{model_tag}_{run_ts}_meta.json")
+
+    headers = {
+        "Authorization": f"Bearer {args.api_key}",
+        "Content-Type": "application/json",
+    }
+
+    print(f"[INFO] Checking vLLM server: {args.base_url}")
+    models = check_server(args.base_url, headers=headers, timeout_sec=args.timeout_sec)
+    available_model_ids = [m.get("id", "") for m in models or []]
+    print(f"[INFO] Server models: {available_model_ids}")
+    if args.served_model_name not in available_model_ids:
+        print(
+            f"[WARN] Served model '{args.served_model_name}' not found in /models. "
+            "Will still try requests with provided name."
+        )
+
+    print(f"[INFO] Loading tokenizer from: {args.model_path}")
+    tokenizer = AutoTokenizer.from_pretrained(args.model_path, trust_remote_code=True)
+
+    print(f"[INFO] Reading dataset: {args.dataset_path}")
+    templates = load_prompt_templates(args)
+    rows = load_verified_rows(args.dataset_path)
+    parsed_items: List[Dict[str, Any]] = []
+    for idx, row in enumerate(rows):
+        gold_label = str(row.get("label", "")).strip()
+        fulltext = str(row.get("fulltext", "")).strip()
+        summary = str(row.get("summary", "")).strip()
+        if gold_label not in VALID_LABELS:
+            continue
+        if not fulltext or not summary:
+            continue
+        source_lang = infer_source_lang(fulltext)
+        prompt = build_prompt(
+            template=templates[gold_label],
+            fulltext=fulltext,
+            summary=summary,
+            source_lang=source_lang,
+        )
+        parsed_items.append(
+            {
+                "row_index": idx,
+                "doc_id": row.get("doc_id"),
+                "gold_label": gold_label,
+                "source_lang": source_lang,
+                "prompt": prompt,
+            }
+        )
+
+    df = pd.DataFrame(parsed_items)
+    if args.max_samples > 0:
+        df = df.head(args.max_samples)
+    print(f"[INFO] Rows to process: {len(df)}")
+    if df.empty:
+        raise RuntimeError("No valid rows found in input file.")
+
+    outputs: List[Dict[str, Any]] = []
+    with open(output_jsonl, "w", encoding="utf-8") as f_out:
+        for start in tqdm(range(0, len(df), args.batch_size), desc="Batches"):
+            batch_df = df.iloc[start : start + args.batch_size]
+            prompts = [build_prompt_text(tokenizer, row.get("prompt", "")) for _, row in batch_df.iterrows()]
+
+            preds = batched_completion_request(
+                base_url=args.base_url,
+                headers=headers,
+                model_name=args.served_model_name,
+                prompts=prompts,
+                max_tokens=args.max_tokens,
+                temperature=args.temperature,
+                top_p=args.top_p,
+                timeout_sec=args.timeout_sec,
+            )
+
+            for (row_idx, row), pred in zip(batch_df.iterrows(), preds):
+                gold_label = str(row.get("gold_label", ""))
+                record = {
+                    "row_index": int(row.get("row_index", row_idx)),
+                    "doc_id": row.get("doc_id"),
+                    "gold_label": gold_label,
+                    "source_lang": row.get("source_lang"),
+                    "prediction": pred,
+                    "generated_text": extract_generated_text(pred, gold_label) if gold_label else pred.strip(),
+                }
+                outputs.append(record)
+                f_out.write(json.dumps(record, ensure_ascii=False) + "\n")
+
+    pd.DataFrame(outputs).to_parquet(output_parquet, index=False)
+
+    with open(meta_path, "w", encoding="utf-8") as f_meta:
+        json.dump(
+            {
+                "model_path_for_tokenizer": args.model_path,
+                "dataset_path": args.dataset_path,
+                "base_url": args.base_url,
+                "served_model_name": args.served_model_name,
+                "batch_size": args.batch_size,
+                "num_samples": len(outputs),
+                "output_jsonl": output_jsonl,
+                "output_parquet": output_parquet,
+            },
+            f_meta,
+            ensure_ascii=False,
+            indent=2,
+        )
+
+    print("[DONE] vLLM batch inference complete.")
+    print(f"[DONE] JSONL: {output_jsonl}")
+    print(f"[DONE] Parquet: {output_parquet}")
+    print(f"[DONE] Meta: {meta_path}")
+
+
+if __name__ == "__main__":
+    main()
diff --git a/code/rl_inference/script.sh b/code/rl_inference/script.sh
new file mode 100644
index 0000000000000000000000000000000000000000..64849095e79c398dcc723c9e45dbb0e1e2752b96
--- /dev/null
+++ b/code/rl_inference/script.sh
@@ -0,0 +1,25 @@
+cd /home/mshahidul/readctrl/code/RL_model/verl/verl_train
+python scripts/legacy_model_merger.py merge \
+    --backend fsdp \
+    --local_dir /home/mshahidul/readctrl/code/RL_model/RL_model_subclaim_classifier/global_step_45/actor \
+    --target_dir /home/mshahidul/readctrl/code/RL_model/converted_model/v1
+
+
+CUDA_DEVICE_ORDER=PCI_BUS_ID CUDA_VISIBLE_DEVICES=2 python -m vllm.entrypoints.openai.api_server \
+  --model /home/mshahidul/readctrl/code/RL_model/converted_model/v1 \
+  --served-model-name inference \
+  --dtype bfloat16 \
+  --port 8001
+# Qwen/Qwen3-4B-Instruct-2507
+# /home/mshahidul/readctrl/code/RL_model/models/converted_model/v1
+VLLM_USE_V1=0 CUDA_VISIBLE_DEVICES=2 python -m vllm.entrypoints.openai.api_server \
+  --model Qwen/Qwen3-4B-Instruct-2507 \
+  --served-model-name inference \
+  --dtype float16 \
+  --port 8001 \
+  --max-model-len 16384
+
+python /home/mshahidul/readctrl/code/rl_inference/run_inference_vllm_server.py \
+  --base_url http://127.0.0.1:8001/v1 \
+  --served_model_name inference \
+  --batch_size 8
\ No newline at end of file
diff --git a/code/rl_inference/test_classifier_on_gpt5_outputs.py b/code/rl_inference/test_classifier_on_gpt5_outputs.py
new file mode 100644
index 0000000000000000000000000000000000000000..17104eff05305acddc1a9ecf130c788a1c378959
--- /dev/null
+++ b/code/rl_inference/test_classifier_on_gpt5_outputs.py
@@ -0,0 +1,274 @@
+import argparse
+import glob
+import json
+import os
+import traceback
+import urllib.error
+import urllib.request
+from collections import defaultdict
+from datetime import datetime
+from typing import Any, DefaultDict, Dict, List
+
+import dspy
+from tqdm import tqdm
+
+
+DEFAULT_API_BASE = "http://172.16.34.22:8040/v1"
+DEFAULT_MODEL_PATH = (
+    "/home/mshahidul/readctrl/code/text_classifier/"
+    "dspy_model/vllm-Meta-Llama-3.1-8B-Instruct_teacher-gpt5_v1/model.json"
+)
+DEFAULT_OUTPUT_DIR = "/home/mshahidul/readctrl/code/rl_inference/test_result"
+
+VALID_LABELS = {
+    "low_health_literacy",
+    "intermediate_health_literacy",
+    "proficient_health_literacy",
+}
+
+
+class HealthLiteracySignature(dspy.Signature):
+    generated_text = dspy.InputField(
+        desc="A version of the source text rewritten for a specific audience."
+    )
+    literacy_label = dspy.OutputField(
+        desc=(
+            "Classification: low_health_literacy (simple words, no jargon), "
+            "intermediate_health_literacy (moderate technicality), or "
+            "proficient_health_literacy (highly technical/original level)."
+        )
+    )
+
+
+class HealthLiteracyClassifier(dspy.Module):
+    def __init__(self):
+        super().__init__()
+        self.classifier = dspy.ChainOfThought(HealthLiteracySignature)
+
+    def forward(self, generated_text):
+        return self.classifier(generated_text=generated_text)
+
+
+def parse_args() -> argparse.Namespace:
+    parser = argparse.ArgumentParser(
+        description="Evaluate GPT output files with saved DSPy health literacy classifier."
+    )
+    parser.add_argument("--model-path", default=DEFAULT_MODEL_PATH)
+    parser.add_argument(
+        "--input-path",
+        default="",
+        help=(
+            "Path to GPT output JSONL (e.g. gpt5_inference_all_*.jsonl). "
+            "If omitted, auto-select latest file in test_result."
+        ),
+    )
+    parser.add_argument(
+        "--api-base",
+        default=os.environ.get("VLLM_API_BASE", DEFAULT_API_BASE),
+    )
+    parser.add_argument("--output-dir", default=DEFAULT_OUTPUT_DIR)
+    parser.add_argument(
+        "--max-samples",
+        type=int,
+        default=-1,
+        help="Use -1 for all valid rows.",
+    )
+    parser.add_argument(
+        "--provide-traceback",
+        action="store_true",
+        help="Print full traceback if runtime error happens.",
+    )
+    return parser.parse_args()
+
+
+def resolve_input_path(input_path: str, search_dir: str) -> str:
+    if input_path and os.path.exists(input_path):
+        return input_path
+    if input_path:
+        raise FileNotFoundError(f"Input file not found: {input_path}")
+
+    candidates = sorted(glob.glob(os.path.join(search_dir, "gpt5_inference_all_*.jsonl")), key=os.path.getmtime)
+    if not candidates:
+        # Fallback: allow evaluating model-specific inference outputs too.
+        candidates = sorted(
+            glob.glob(os.path.join(search_dir, "gpt5_inference_*_*.jsonl")),
+            key=os.path.getmtime,
+        )
+    if not candidates:
+        raise FileNotFoundError(
+            "No GPT output file found. Expected pattern: "
+            f"{search_dir}/gpt5_inference_all_*.jsonl "
+            "or gpt5_inference_*_*.jsonl"
+        )
+    return candidates[-1]
+
+
+def check_api_base(api_base: str) -> None:
+    models_url = api_base.rstrip("/") + "/models"
+    req = urllib.request.Request(models_url, method="GET")
+    try:
+        with urllib.request.urlopen(req, timeout=5) as resp:
+            if resp.status >= 400:
+                raise RuntimeError(
+                    f"Endpoint reachable but unhealthy: {models_url} (status={resp.status})"
+                )
+    except urllib.error.URLError as exc:
+        raise ConnectionError(
+            "Cannot reach OpenAI-compatible endpoint. "
+            f"api_base={api_base}. "
+            "Start your vLLM server or pass correct --api-base."
+        ) from exc
+
+
+def load_compiled_classifier(path: str):
+    if hasattr(dspy, "load"):
+        try:
+            return dspy.load(path)
+        except Exception:
+            pass
+
+    classifier = HealthLiteracyClassifier()
+    try:
+        classifier.load(path)
+    except Exception as exc:
+        raise RuntimeError(f"Failed to load compiled model from {path}") from exc
+    return classifier
+
+
+def normalize_pred_label(pred_obj: Any) -> str:
+    if not pred_obj or not hasattr(pred_obj, "literacy_label"):
+        return ""
+    return str(pred_obj.literacy_label).strip().lower()
+
+
+def load_eval_items(path: str) -> List[Dict[str, Any]]:
+    items: List[Dict[str, Any]] = []
+    with open(path, "r", encoding="utf-8") as f:
+        for line_no, line in enumerate(f, start=1):
+            if not line.strip():
+                continue
+            row = json.loads(line)
+            gold_label = str(row.get("gold_label", "")).strip()
+            generated_text = str(row.get("generated_text", "")).strip()
+            err_msg = str(row.get("error", "")).strip()
+
+            if gold_label not in VALID_LABELS:
+                continue
+            if err_msg:
+                continue
+            if not generated_text:
+                continue
+
+            items.append(
+                {
+                    "line_no": line_no,
+                    "model": str(row.get("model", "")).strip() or "unknown_model",
+                    "row_index": row.get("row_index"),
+                    "doc_id": row.get("doc_id"),
+                    "gold_label": gold_label,
+                    "generated_text": generated_text,
+                }
+            )
+    return items
+
+
+def main() -> None:
+    args = parse_args()
+    args.input_path = resolve_input_path(args.input_path, args.output_dir)
+
+    if not os.path.exists(args.model_path):
+        raise FileNotFoundError(f"Model file not found: {args.model_path}")
+
+    try:
+        check_api_base(args.api_base)
+        lm = dspy.LM(
+            model="openai/dspy",
+            api_base=args.api_base,
+            api_key="EMPTY",
+            temperature=0.0,
+        )
+        dspy.configure(lm=lm)
+        classifier = load_compiled_classifier(args.model_path)
+        print(f"[INFO] Using input file: {args.input_path}")
+
+        eval_items = load_eval_items(args.input_path)
+        if args.max_samples > 0:
+            eval_items = eval_items[: args.max_samples]
+        if not eval_items:
+            raise RuntimeError("No valid rows found for evaluation.")
+
+        results: List[Dict[str, Any]] = []
+        model_total: DefaultDict[str, int] = defaultdict(int)
+        model_correct: DefaultDict[str, int] = defaultdict(int)
+
+        for item in tqdm(eval_items, desc="Classifying"):
+            pred = classifier(generated_text=item["generated_text"])
+            pred_label = normalize_pred_label(pred)
+            is_correct = item["gold_label"] in pred_label
+
+            model_name = item["model"]
+            model_total[model_name] += 1
+            model_correct[model_name] += int(is_correct)
+
+            results.append(
+                {
+                    "line_no": item["line_no"],
+                    "model": model_name,
+                    "row_index": item["row_index"],
+                    "doc_id": item["doc_id"],
+                    "gold_label": item["gold_label"],
+                    "pred_label": pred_label,
+                    "is_correct": is_correct,
+                }
+            )
+
+        total = len(results)
+        correct = sum(1 for r in results if r["is_correct"])
+        overall_accuracy = correct / total if total else 0.0
+
+        per_model: Dict[str, Dict[str, Any]] = {}
+        for model_name in sorted(model_total.keys()):
+            m_total = model_total[model_name]
+            m_correct = model_correct[model_name]
+            per_model[model_name] = {
+                "total_samples": m_total,
+                "correct_samples": m_correct,
+                "accuracy_score": (m_correct / m_total) if m_total else 0.0,
+            }
+
+        ts = datetime.now().strftime("%Y%m%d_%H%M%S")
+        os.makedirs(args.output_dir, exist_ok=True)
+        summary_path = os.path.join(args.output_dir, f"classifier_eval_gpt5_{ts}.json")
+        details_path = os.path.join(args.output_dir, f"classifier_eval_gpt5_{ts}.jsonl")
+
+        summary_obj = {
+            "model_path": args.model_path,
+            "input_path": args.input_path,
+            "api_base": args.api_base,
+            "total_samples": total,
+            "correct_samples": correct,
+            "accuracy_score": overall_accuracy,
+            "per_model": per_model,
+            "details_path": details_path,
+        }
+
+        with open(summary_path, "w", encoding="utf-8") as f:
+            json.dump(summary_obj, f, indent=2, ensure_ascii=False)
+
+        with open(details_path, "w", encoding="utf-8") as f:
+            for record in results:
+                f.write(json.dumps(record, ensure_ascii=False) + "\n")
+
+        print(json.dumps(summary_obj, indent=2, ensure_ascii=False))
+        print(f"[DONE] Summary saved: {summary_path}")
+        print(f"[DONE] Details saved: {details_path}")
+
+    except Exception as exc:
+        print(f"[error] {type(exc).__name__}: {exc}")
+        if args.provide_traceback:
+            traceback.print_exc()
+        raise
+
+
+if __name__ == "__main__":
+    main()
diff --git a/code/rl_inference/test_classifier_on_gpt5_outputs_with_subclaim_thresholds.py b/code/rl_inference/test_classifier_on_gpt5_outputs_with_subclaim_thresholds.py
new file mode 100644
index 0000000000000000000000000000000000000000..6641b17baa138b175db9865c7512fe69917c9483
--- /dev/null
+++ b/code/rl_inference/test_classifier_on_gpt5_outputs_with_subclaim_thresholds.py
@@ -0,0 +1,554 @@
+import argparse
+import glob
+import json
+import os
+import re
+import traceback
+import urllib.error
+import urllib.request
+from collections import defaultdict
+from datetime import datetime
+from typing import Any, DefaultDict, Dict, List, Tuple
+
+import dspy
+from openai import OpenAI
+from tqdm import tqdm
+
+
+DEFAULT_CLASSIFIER_API_BASE = "http://172.16.34.22:8040/v1"
+DEFAULT_SUPPORT_API_BASE = "http://172.16.34.22:3090/v1"
+DEFAULT_MODEL_PATH = (
+    "/home/mshahidul/readctrl/code/text_classifier/"
+    "dspy_model/vllm-Meta-Llama-3.1-8B-Instruct_teacher-gpt5_v1/model.json"
+)
+DEFAULT_INPUT_FILE = (
+    "/home/mshahidul/readctrl/code/rl_inference/test_result/"
+    "gpt5_inference_gpt-5-mini_20260213_025254_cleaned_by_verified_combined_0-80_clean200.jsonl"
+)
+DEFAULT_OUTPUT_DIR = "/home/mshahidul/readctrl/code/rl_inference/test_result_v2"
+DEFAULT_REFERENCE_SUBCLAIMS_FILE = (
+    "/home/mshahidul/readctrl/code/text_classifier/data/"
+    "verified_combined_0-80_clean200_with_subclaims.json"
+)
+
+CHAT_TEMPLATE = (
+    "<|begin_of_text|><|start_header_id|>system<|end_header_id|>\n\n"
+    "Cutting Knowledge Date: December 2023\n"
+    "Today Date: 26 July 2024\n\n"
+    "<|eot_id|><|start_header_id|>user<|end_header_id|>\n\n"
+    "{user_prompt}"
+    "<|eot_id|><|start_header_id|>assistant<|end_header_id|>\n\n"
+)
+
+VALID_LABELS = {
+    "low_health_literacy",
+    "intermediate_health_literacy",
+    "proficient_health_literacy",
+}
+
+
+class HealthLiteracySignature(dspy.Signature):
+    generated_text = dspy.InputField(
+        desc="A version of the source text rewritten for a specific audience."
+    )
+    literacy_label = dspy.OutputField(
+        desc=(
+            "Classification: low_health_literacy (simple words, no jargon), "
+            "intermediate_health_literacy (moderate technicality), or "
+            "proficient_health_literacy (highly technical/original level)."
+        )
+    )
+
+
+class HealthLiteracyClassifier(dspy.Module):
+    def __init__(self):
+        super().__init__()
+        self.classifier = dspy.ChainOfThought(HealthLiteracySignature)
+
+    def forward(self, generated_text):
+        return self.classifier(generated_text=generated_text)
+
+
+class MedicalClaimVerifier:
+    def __init__(self, base_url: str, model_name: str):
+        self.model_name = model_name
+        self.base_url = base_url
+        self.client = OpenAI(api_key="EMPTY", base_url=self.base_url)
+        self.cov_iqr_ranges = {
+            "low": (0.1765, 0.3226),
+            "intermediate": (0.1818, 0.4091),
+            "proficient": (0.7725, 0.9347),
+        }
+
+    def build_user_prompt(self, text: str, subclaims: List[str]) -> str:
+        numbered_subclaims = "\n".join(
+            f"{idx + 1}. {subclaim}" for idx, subclaim in enumerate(subclaims)
+        )
+        return (
+            "You are a medical evidence checker.\n"
+            "Given a medical passage and a list of subclaims, return labels for each "
+            "subclaim in the same order.\n\n"
+            "Allowed labels: supported, not_supported.\n"
+            "Output format: a JSON array of strings only.\n\n"
+            f"Medical text:\n{text}\n\n"
+            f"Subclaims:\n{numbered_subclaims}"
+        )
+
+    def render_chat_prompt(self, user_prompt: str) -> str:
+        return CHAT_TEMPLATE.format(user_prompt=user_prompt)
+
+    def extract_label_list(self, text: str) -> List[str]:
+        cleaned = text.strip()
+        try:
+            parsed = json.loads(cleaned)
+            if isinstance(parsed, list):
+                return parsed
+        except json.JSONDecodeError:
+            pass
+
+        match = re.search(r"\[[\s\S]*\]", cleaned)
+        if match:
+            try:
+                parsed = json.loads(match.group(0))
+                if isinstance(parsed, list):
+                    return parsed
+            except json.JSONDecodeError:
+                return []
+        return []
+
+    def check_support_api(self, context: str, subclaims: List[str]) -> List[str]:
+        if not context or not subclaims:
+            return []
+
+        user_prompt = self.build_user_prompt(context, subclaims)
+        prompt = self.render_chat_prompt(user_prompt)
+        try:
+            response = self.client.completions.create(
+                model=self.model_name,
+                prompt=prompt,
+                max_tokens=256,
+                temperature=0,
+            )
+            pred_text = response.choices[0].text.strip()
+            labels = self.extract_label_list(pred_text)
+            return [str(x).strip().lower() for x in labels]
+        except Exception:
+            return []
+
+    @staticmethod
+    def average_supported(labels: List[str], expected_len: int) -> float:
+        if expected_len <= 0:
+            return 0.0
+        normalized = [str(x).strip().lower() for x in labels]
+        if len(normalized) < expected_len:
+            normalized.extend(["invalid"] * (expected_len - len(normalized)))
+        elif len(normalized) > expected_len:
+            normalized = normalized[:expected_len]
+        supported_count = sum(1 for item in normalized if item == "supported")
+        return supported_count / expected_len
+
+    def evaluate_level(
+        self, gen_text: str, gold_subs: List[str], full_subs: List[str]
+    ) -> Tuple[float, float]:
+        if not gen_text or not gold_subs or not full_subs:
+            return 0.0, 0.0
+        comp_labels = self.check_support_api(gen_text, gold_subs)
+        cov_labels = self.check_support_api(gen_text, full_subs)
+        comp_score = self.average_supported(comp_labels, len(gold_subs))
+        cov_score = self.average_supported(cov_labels, len(full_subs))
+        return comp_score, cov_score
+
+
+def parse_args() -> argparse.Namespace:
+    parser = argparse.ArgumentParser(
+        description=(
+            "Evaluate GPT outputs with classifier + subclaim threshold checks "
+            "(completeness + coverage)."
+        )
+    )
+    parser.add_argument("--model-path", default=DEFAULT_MODEL_PATH)
+    parser.add_argument(
+        "--input-file",
+        default=DEFAULT_INPUT_FILE,
+        help=(
+            "Path to GPT output JSONL (e.g. gpt5_inference_all_*.jsonl). "
+            "If empty, auto-select latest file in --output-dir."
+        ),
+    )
+    parser.add_argument("--output-dir", default=DEFAULT_OUTPUT_DIR)
+    parser.add_argument(
+        "--reference-subclaims-file",
+        default=DEFAULT_REFERENCE_SUBCLAIMS_FILE,
+        help=(
+            "JSON list file that contains subclaims per sample "
+            "(e.g., verified_combined_0-80_clean200_with_subclaims.json)."
+        ),
+    )
+    parser.add_argument(
+        "--classifier-api-base",
+        default=os.environ.get("VLLM_API_BASE", DEFAULT_CLASSIFIER_API_BASE),
+    )
+    parser.add_argument(
+        "--support-api-base",
+        default=os.environ.get("SUPPORT_API_BASE", DEFAULT_SUPPORT_API_BASE),
+    )
+    parser.add_argument(
+        "--support-model",
+        default=os.environ.get("VLLM_MODEL", "sc"),
+    )
+    parser.add_argument(
+        "--comp-min-threshold",
+        type=float,
+        default=0.9,
+        help="Completeness pass lower bound (inclusive).",
+    )
+    parser.add_argument(
+        "--comp-max-threshold",
+        type=float,
+        default=1.0,
+        help="Completeness pass upper bound (inclusive).",
+    )
+    parser.add_argument(
+        "--max-samples",
+        type=int,
+        default=-1,
+        help="Use -1 for all valid rows.",
+    )
+    parser.add_argument(
+        "--provide-traceback",
+        action="store_true",
+        help="Print full traceback if runtime error happens.",
+    )
+    return parser.parse_args()
+
+
+def resolve_input_path(input_path: str, search_dir: str) -> str:
+    if input_path and os.path.exists(input_path):
+        return input_path
+    if input_path:
+        raise FileNotFoundError(f"Input file not found: {input_path}")
+
+    candidates = sorted(
+        glob.glob(os.path.join(search_dir, "gpt5_inference_all_*.jsonl")),
+        key=os.path.getmtime,
+    )
+    if not candidates:
+        candidates = sorted(
+            glob.glob(os.path.join(search_dir, "gpt5_inference_*_*.jsonl")),
+            key=os.path.getmtime,
+        )
+    if not candidates:
+        raise FileNotFoundError(
+            "No GPT output file found. Expected pattern: "
+            f"{search_dir}/gpt5_inference_all_*.jsonl "
+            "or gpt5_inference_*_*.jsonl"
+        )
+    return candidates[-1]
+
+
+def check_api_base(api_base: str) -> None:
+    models_url = api_base.rstrip("/") + "/models"
+    req = urllib.request.Request(models_url, method="GET")
+    try:
+        with urllib.request.urlopen(req, timeout=5) as resp:
+            if resp.status >= 400:
+                raise RuntimeError(
+                    f"Endpoint reachable but unhealthy: {models_url} (status={resp.status})"
+                )
+    except urllib.error.URLError as exc:
+        raise ConnectionError(
+            "Cannot reach OpenAI-compatible endpoint. "
+            f"api_base={api_base}. "
+            "Start your vLLM server or pass correct api base."
+        ) from exc
+
+
+def load_compiled_classifier(path: str):
+    if hasattr(dspy, "load"):
+        try:
+            return dspy.load(path)
+        except Exception:
+            pass
+
+    classifier = HealthLiteracyClassifier()
+    try:
+        classifier.load(path)
+    except Exception as exc:
+        raise RuntimeError(f"Failed to load compiled model from {path}") from exc
+    return classifier
+
+
+def normalize_pred_label(pred_obj: Any) -> str:
+    if not pred_obj or not hasattr(pred_obj, "literacy_label"):
+        return ""
+    return str(pred_obj.literacy_label).strip().lower()
+
+
+def to_level_key(label: str) -> str:
+    mapping = {
+        "low_health_literacy": "low",
+        "intermediate_health_literacy": "intermediate",
+        "proficient_health_literacy": "proficient",
+    }
+    return mapping.get(label, "")
+
+
+def in_range(value: float, lower: float, upper: float) -> bool:
+    return lower <= value <= upper
+
+
+def load_subclaim_lookup(
+    reference_path: str,
+) -> Dict[Tuple[Any, str], Tuple[List[str], List[str]]]:
+    with open(reference_path, "r", encoding="utf-8") as f:
+        rows = json.load(f)
+    if not isinstance(rows, list):
+        raise ValueError("Reference subclaims file must be a JSON list.")
+
+    lookup: Dict[Tuple[Any, str], Tuple[List[str], List[str]]] = {}
+    for row in rows:
+        doc_id = row.get("doc_id")
+        label = str(row.get("label", "")).strip()
+        gold_subs = row.get("summary_subclaims", [])
+        full_subs = row.get("fulltext_subclaims", [])
+        if label not in VALID_LABELS:
+            continue
+        if not isinstance(gold_subs, list) or not isinstance(full_subs, list):
+            continue
+        if not gold_subs or not full_subs:
+            continue
+        key = (doc_id, label)
+        if key not in lookup:
+            lookup[key] = (gold_subs, full_subs)
+    return lookup
+
+
+def load_eval_items(path: str) -> List[Dict[str, Any]]:
+    items: List[Dict[str, Any]] = []
+    with open(path, "r", encoding="utf-8") as f:
+        for line_no, line in enumerate(f, start=1):
+            if not line.strip():
+                continue
+            row = json.loads(line)
+            gold_label = str(row.get("gold_label", "")).strip()
+            generated_text = str(row.get("generated_text", "")).strip()
+            err_msg = str(row.get("error", "")).strip()
+
+            if gold_label not in VALID_LABELS:
+                continue
+            if err_msg:
+                continue
+            if not generated_text:
+                continue
+
+            items.append(
+                {
+                    "line_no": line_no,
+                    "model": str(row.get("model", "")).strip() or "unknown_model",
+                    "row_index": row.get("row_index"),
+                    "doc_id": row.get("doc_id"),
+                    "gold_label": gold_label,
+                    "generated_text": generated_text,
+                }
+            )
+    return items
+
+
+def main() -> None:
+    args = parse_args()
+    args.input_file = resolve_input_path(args.input_file, args.output_dir)
+
+    if not os.path.exists(args.model_path):
+        raise FileNotFoundError(f"Model file not found: {args.model_path}")
+    if not os.path.exists(args.reference_subclaims_file):
+        raise FileNotFoundError(
+            f"Reference subclaims file not found: {args.reference_subclaims_file}"
+        )
+
+    try:
+        check_api_base(args.classifier_api_base)
+        check_api_base(args.support_api_base)
+
+        lm = dspy.LM(
+            model="openai/dspy",
+            api_base=args.classifier_api_base,
+            api_key="EMPTY",
+            temperature=0.0,
+        )
+        dspy.configure(lm=lm)
+        classifier = load_compiled_classifier(args.model_path)
+        verifier = MedicalClaimVerifier(
+            base_url=args.support_api_base,
+            model_name=args.support_model,
+        )
+        subclaim_lookup = load_subclaim_lookup(args.reference_subclaims_file)
+
+        print(f"[INFO] Using input file: {args.input_file}")
+        print(f"[INFO] Using reference subclaims: {args.reference_subclaims_file}")
+        eval_items = load_eval_items(args.input_file)
+        if args.max_samples > 0:
+            eval_items = eval_items[: args.max_samples]
+        if not eval_items:
+            raise RuntimeError("No valid rows found for evaluation.")
+
+        results: List[Dict[str, Any]] = []
+        unmatched_rows = 0
+        total = 0
+        classifier_correct = 0
+        comp_pass_count = 0
+        cov_pass_count = 0
+        cls_and_comp_pass_count = 0
+        cls_comp_cov_pass_count = 0
+
+        model_total: DefaultDict[str, int] = defaultdict(int)
+        model_cls_correct: DefaultDict[str, int] = defaultdict(int)
+        model_comp_pass: DefaultDict[str, int] = defaultdict(int)
+        model_cov_pass: DefaultDict[str, int] = defaultdict(int)
+        model_cls_comp_pass: DefaultDict[str, int] = defaultdict(int)
+        model_cls_comp_cov_pass: DefaultDict[str, int] = defaultdict(int)
+
+        for item in tqdm(eval_items, desc="Evaluating"):
+            key = (item.get("doc_id"), item["gold_label"])
+            subclaims = subclaim_lookup.get(key)
+            if not subclaims:
+                unmatched_rows += 1
+                continue
+
+            gold_subs, full_subs = subclaims
+            total += 1
+            model_name = item["model"]
+            model_total[model_name] += 1
+
+            pred = classifier(generated_text=item["generated_text"])
+            pred_label = normalize_pred_label(pred)
+            is_cls_correct = item["gold_label"] in pred_label
+            classifier_correct += int(is_cls_correct)
+            model_cls_correct[model_name] += int(is_cls_correct)
+
+            comp_score, cov_score = verifier.evaluate_level(
+                gen_text=item["generated_text"],
+                gold_subs=gold_subs,
+                full_subs=full_subs,
+            )
+            comp_pass = in_range(
+                comp_score, args.comp_min_threshold, args.comp_max_threshold
+            )
+            comp_pass_count += int(comp_pass)
+            model_comp_pass[model_name] += int(comp_pass)
+
+            level_key = to_level_key(item["gold_label"])
+            cov_low, cov_high = verifier.cov_iqr_ranges[level_key]
+            cov_pass = in_range(cov_score, cov_low, cov_high)
+            cov_pass_count += int(cov_pass)
+            model_cov_pass[model_name] += int(cov_pass)
+
+            cls_and_comp_pass = is_cls_correct and comp_pass
+            cls_comp_cov_pass = cls_and_comp_pass and cov_pass
+            cls_and_comp_pass_count += int(cls_and_comp_pass)
+            cls_comp_cov_pass_count += int(cls_comp_cov_pass)
+            model_cls_comp_pass[model_name] += int(cls_and_comp_pass)
+            model_cls_comp_cov_pass[model_name] += int(cls_comp_cov_pass)
+
+            results.append(
+                {
+                    "line_no": item["line_no"],
+                    "model": model_name,
+                    "row_index": item["row_index"],
+                    "doc_id": item["doc_id"],
+                    "gold_label": item["gold_label"],
+                    "pred_label": pred_label,
+                    "classifier_correct": is_cls_correct,
+                    "completeness_score": comp_score,
+                    "coverage_score": cov_score,
+                    "completeness_threshold": [
+                        args.comp_min_threshold,
+                        args.comp_max_threshold,
+                    ],
+                    "completeness_pass": comp_pass,
+                    "coverage_iqr_threshold": [cov_low, cov_high],
+                    "coverage_pass": cov_pass,
+                    "pass_cls_and_completeness": cls_and_comp_pass,
+                    "pass_cls_comp_cov": cls_comp_cov_pass,
+                }
+            )
+
+        if total == 0:
+            raise RuntimeError(
+                "No matched rows were found. Could not join GPT rows with "
+                "reference subclaims by (doc_id, gold_label)."
+            )
+
+        def safe_rate(n: int, d: int) -> float:
+            return (n / d) if d else 0.0
+
+        per_model: Dict[str, Dict[str, Any]] = {}
+        for model_name in sorted(model_total.keys()):
+            m_total = model_total[model_name]
+            per_model[model_name] = {
+                "total_samples": m_total,
+                "classifier_only_accuracy": safe_rate(
+                    model_cls_correct[model_name], m_total
+                ),
+                "completeness_pass_rate": safe_rate(model_comp_pass[model_name], m_total),
+                "coverage_pass_rate": safe_rate(model_cov_pass[model_name], m_total),
+                "accuracy_cls_and_completeness_threshold": safe_rate(
+                    model_cls_comp_pass[model_name], m_total
+                ),
+                "accuracy_cls_completeness_coverage_threshold": safe_rate(
+                    model_cls_comp_cov_pass[model_name], m_total
+                ),
+            }
+
+        ts = datetime.now().strftime("%Y%m%d_%H%M%S")
+        os.makedirs(args.output_dir, exist_ok=True)
+        summary_path = os.path.join(
+            args.output_dir, f"classifier_subclaim_threshold_eval_gpt5_{ts}.json"
+        )
+        details_path = os.path.join(
+            args.output_dir, f"classifier_subclaim_threshold_eval_gpt5_{ts}.jsonl"
+        )
+
+        summary_obj = {
+            "model_path": args.model_path,
+            "input_file": args.input_file,
+            "reference_subclaims_file": args.reference_subclaims_file,
+            "classifier_api_base": args.classifier_api_base,
+            "support_api_base": args.support_api_base,
+            "support_model": args.support_model,
+            "total_samples": total,
+            "unmatched_rows": unmatched_rows,
+            "classifier_only_accuracy": safe_rate(classifier_correct, total),
+            "completeness_pass_rate": safe_rate(comp_pass_count, total),
+            "coverage_pass_rate": safe_rate(cov_pass_count, total),
+            "accuracy_cls_and_completeness_threshold": safe_rate(
+                cls_and_comp_pass_count, total
+            ),
+            "accuracy_cls_completeness_coverage_threshold": safe_rate(
+                cls_comp_cov_pass_count, total
+            ),
+            "completeness_threshold": [args.comp_min_threshold, args.comp_max_threshold],
+            "coverage_thresholds": verifier.cov_iqr_ranges,
+            "per_model": per_model,
+            "details_path": details_path,
+        }
+
+        with open(summary_path, "w", encoding="utf-8") as f:
+            json.dump(summary_obj, f, indent=2, ensure_ascii=False)
+
+        with open(details_path, "w", encoding="utf-8") as f:
+            for record in results:
+                f.write(json.dumps(record, ensure_ascii=False) + "\n")
+
+        print(json.dumps(summary_obj, indent=2, ensure_ascii=False))
+        print(f"[DONE] Summary saved: {summary_path}")
+        print(f"[DONE] Details saved: {details_path}")
+
+    except Exception as exc:
+        print(f"[error] {type(exc).__name__}: {exc}")
+        if args.provide_traceback:
+            traceback.print_exc()
+        raise
+
+
+if __name__ == "__main__":
+    main()
diff --git a/code/rl_inference/test_classifier_on_vllm_outputs.py b/code/rl_inference/test_classifier_on_vllm_outputs.py
new file mode 100644
index 0000000000000000000000000000000000000000..117e71a4b41faba083658340fd79107d29c4d967
--- /dev/null
+++ b/code/rl_inference/test_classifier_on_vllm_outputs.py
@@ -0,0 +1,262 @@
+import argparse
+import glob
+import json
+import os
+import traceback
+import urllib.error
+import urllib.request
+from datetime import datetime
+from typing import Any, Dict, List
+
+import dspy
+from tqdm import tqdm
+
+
+DEFAULT_API_BASE = "http://172.16.34.21:8040/v1"
+DEFAULT_MODEL_PATH = (
+    "/home/mshahidul/readctrl/code/text_classifier/"
+    "dspy_model/vllm-Meta-Llama-3.1-8B-Instruct_teacher-gpt5_v1/model.json"
+)
+DEFAULT_INPUT_PATH = "/home/mshahidul/readctrl/code/RL_model/inference_data"
+DEFAULT_INPUT_FILE = (
+    "/home/mshahidul/readctrl/code/RL_model/inference_data/"
+    "vllm_inference_qwen-qwen3-4b-instruct-2507_20260213_173334.jsonl"
+)
+DEFAULT_OUTPUT_DIR = "/home/mshahidul/readctrl/code/rl_inference/test_result"
+
+VALID_LABELS = {
+    "low_health_literacy",
+    "intermediate_health_literacy",
+    "proficient_health_literacy",
+}
+
+
+class HealthLiteracySignature(dspy.Signature):
+    generated_text = dspy.InputField(
+        desc="A version of the source text rewritten for a specific audience."
+    )
+    literacy_label = dspy.OutputField(
+        desc=(
+            "Classification: low_health_literacy (simple words, no jargon), "
+            "intermediate_health_literacy (moderate technicality), or "
+            "proficient_health_literacy (highly technical/original level)."
+        )
+    )
+
+
+class HealthLiteracyClassifier(dspy.Module):
+    def __init__(self):
+        super().__init__()
+        self.classifier = dspy.ChainOfThought(HealthLiteracySignature)
+
+    def forward(self, generated_text):
+        return self.classifier(generated_text=generated_text)
+
+
+def parse_args() -> argparse.Namespace:
+    parser = argparse.ArgumentParser(
+        description="Evaluate saved DSPy classifier on saved vLLM inference outputs."
+    )
+    parser.add_argument("--model-path", default=DEFAULT_MODEL_PATH)
+    parser.add_argument(
+        "--input-path",
+        default=DEFAULT_INPUT_FILE,
+        help=(
+            "Path to vLLM output JSONL (e.g. vllm_inference_*.jsonl). "
+            "Set to empty string to auto-select latest file in --search-dir."
+        ),
+    )
+    parser.add_argument(
+        "--search-dir",
+        default=DEFAULT_INPUT_PATH,
+        help="Directory to auto-search for vllm_inference_*.jsonl",
+    )
+    parser.add_argument(
+        "--api-base",
+        default=os.environ.get("VLLM_API_BASE", DEFAULT_API_BASE),
+    )
+    parser.add_argument("--output-dir", default=DEFAULT_OUTPUT_DIR)
+    parser.add_argument(
+        "--max-samples",
+        type=int,
+        default=-1,
+        help="Use -1 for all rows.",
+    )
+    parser.add_argument(
+        "--provide-traceback",
+        action="store_true",
+        help="Print full traceback if runtime error happens.",
+    )
+    return parser.parse_args()
+
+
+def check_api_base(api_base: str) -> None:
+    models_url = api_base.rstrip("/") + "/models"
+    req = urllib.request.Request(models_url, method="GET")
+    try:
+        with urllib.request.urlopen(req, timeout=5) as resp:
+            if resp.status >= 400:
+                raise RuntimeError(
+                    f"Endpoint reachable but unhealthy: {models_url} (status={resp.status})"
+                )
+    except urllib.error.URLError as exc:
+        raise ConnectionError(
+            "Cannot reach OpenAI-compatible endpoint. "
+            f"api_base={api_base}. "
+            "Start your vLLM server or pass correct --api-base."
+        ) from exc
+
+
+def resolve_input_path(input_path: str, search_dir: str) -> str:
+    if input_path and os.path.exists(input_path):
+        return input_path
+    if input_path:
+        raise FileNotFoundError(f"Input file not found: {input_path}")
+
+    candidates = sorted(
+        glob.glob(os.path.join(search_dir, "vllm_inference_*.jsonl")),
+        key=os.path.getmtime,
+    )
+    if not candidates:
+        raise FileNotFoundError(
+            "No vLLM output file found. Expected pattern: "
+            f"{search_dir}/vllm_inference_*.jsonl"
+        )
+    return candidates[-1]
+
+
+def load_compiled_classifier(path: str):
+    if hasattr(dspy, "load"):
+        try:
+            return dspy.load(path)
+        except Exception:
+            pass
+
+    classifier = HealthLiteracyClassifier()
+    try:
+        classifier.load(path)
+    except Exception as exc:
+        raise RuntimeError(f"Failed to load compiled model from {path}") from exc
+    return classifier
+
+
+def normalize_pred_label(pred_obj: Any) -> str:
+    if not pred_obj or not hasattr(pred_obj, "literacy_label"):
+        return ""
+    return str(pred_obj.literacy_label).strip().lower()
+
+
+def load_eval_items(path: str) -> List[Dict[str, Any]]:
+    items: List[Dict[str, Any]] = []
+    with open(path, "r", encoding="utf-8") as f:
+        for line_no, line in enumerate(f, start=1):
+            if not line.strip():
+                continue
+            row = json.loads(line)
+            gold_label = str(row.get("gold_label", "")).strip()
+            generated_text = str(row.get("generated_text", "")).strip()
+            if not generated_text:
+                generated_text = str(row.get("prediction", "")).strip()
+            err_msg = str(row.get("error", "")).strip()
+
+            if gold_label not in VALID_LABELS:
+                continue
+            if err_msg:
+                continue
+            if not generated_text:
+                continue
+
+            items.append(
+                {
+                    "line_no": line_no,
+                    "row_index": row.get("row_index"),
+                    "doc_id": row.get("doc_id"),
+                    "gold_label": gold_label,
+                    "generated_text": generated_text,
+                }
+            )
+    return items
+
+
+def main() -> None:
+    args = parse_args()
+    args.input_path = resolve_input_path(args.input_path, args.search_dir)
+
+    if not os.path.exists(args.model_path):
+        raise FileNotFoundError(f"Model file not found: {args.model_path}")
+
+    try:
+        check_api_base(args.api_base)
+        lm = dspy.LM(
+            model="openai/dspy",
+            api_base=args.api_base,
+            api_key="EMPTY",
+            temperature=0.0,
+        )
+        dspy.configure(lm=lm)
+        classifier = load_compiled_classifier(args.model_path)
+        print(f"[INFO] Using input file: {args.input_path}")
+        parsed_items = load_eval_items(args.input_path)
+        if args.max_samples > 0:
+            parsed_items = parsed_items[: args.max_samples]
+
+        if not parsed_items:
+            raise RuntimeError("No valid rows found in input file for classifier evaluation.")
+
+        correct = 0
+        results: List[Dict[str, Any]] = []
+        for item in tqdm(parsed_items, desc="Classifying"):
+            pred = classifier(generated_text=item["generated_text"])
+            pred_label = normalize_pred_label(pred)
+            is_correct = item["gold_label"] in pred_label
+            correct += int(is_correct)
+            results.append(
+                {
+                    "line_no": item["line_no"],
+                    "row_index": item["row_index"],
+                    "doc_id": item.get("doc_id"),
+                    "gold_label": item["gold_label"],
+                    "pred_label": pred_label,
+                    "is_correct": is_correct,
+                }
+            )
+
+        total = len(results)
+        accuracy = correct / total if total else 0.0
+        ts = datetime.now().strftime("%Y%m%d_%H%M%S")
+        os.makedirs(args.output_dir, exist_ok=True)
+        summary_path = os.path.join(args.output_dir, f"classifier_eval_vllm_{ts}.json")
+        details_path = os.path.join(args.output_dir, f"classifier_eval_vllm_{ts}.jsonl")
+
+        with open(summary_path, "w", encoding="utf-8") as f:
+            json.dump(
+                {
+                    "model_path": args.model_path,
+                    "input_path": args.input_path,
+                    "api_base": args.api_base,
+                    "total_samples": total,
+                    "correct_samples": correct,
+                    "accuracy_score": accuracy,
+                    "details_path": details_path,
+                },
+                f,
+                indent=2,
+            )
+
+        with open(details_path, "w", encoding="utf-8") as f:
+            for r in results:
+                f.write(json.dumps(r, ensure_ascii=False) + "\n")
+
+        print(json.dumps({"total_samples": total, "accuracy_score": accuracy}, indent=2))
+        print(f"[DONE] Summary saved: {summary_path}")
+        print(f"[DONE] Details saved: {details_path}")
+
+    except Exception as exc:
+        print(f"[error] {type(exc).__name__}: {exc}")
+        if args.provide_traceback:
+            traceback.print_exc()
+        raise
+
+
+if __name__ == "__main__":
+    main()
diff --git a/code/rl_inference/test_classifier_with_subclaim_thresholds.py b/code/rl_inference/test_classifier_with_subclaim_thresholds.py
new file mode 100644
index 0000000000000000000000000000000000000000..312cddd1cfd5adc4b328356e07983e635bd4c010
--- /dev/null
+++ b/code/rl_inference/test_classifier_with_subclaim_thresholds.py
@@ -0,0 +1,483 @@
+import argparse
+import json
+import os
+import re
+import traceback
+import urllib.error
+import urllib.request
+from datetime import datetime
+from typing import Any, Dict, List, Tuple
+
+import dspy
+from openai import OpenAI
+from tqdm import tqdm
+
+
+DEFAULT_CLASSIFIER_API_BASE = "http://172.16.34.22:8040/v1"
+DEFAULT_SUPPORT_API_BASE = "http://172.16.34.22:3090/v1"
+DEFAULT_MODEL_PATH = (
+    "/home/mshahidul/readctrl/code/text_classifier/"
+    "dspy_model/vllm-Meta-Llama-3.1-8B-Instruct_teacher-gpt5_v1/model.json"
+)
+DEFAULT_INPUT_FILE = (
+    "/home/mshahidul/readctrl/code/RL_model/inference_data/"
+    "RL_model_inference_v1.jsonl"
+)
+DEFAULT_REFERENCE_SUBCLAIMS_FILE = (
+    "/home/mshahidul/readctrl/code/text_classifier/data/"
+    "verified_combined_0-80_clean200_with_subclaims.json"
+)
+DEFAULT_OUTPUT_DIR = "/home/mshahidul/readctrl/code/rl_inference/test_result_v2"
+
+CHAT_TEMPLATE = (
+    "<|begin_of_text|><|start_header_id|>system<|end_header_id|>\n\n"
+    "Cutting Knowledge Date: December 2023\n"
+    "Today Date: 26 July 2024\n\n"
+    "<|eot_id|><|start_header_id|>user<|end_header_id|>\n\n"
+    "{user_prompt}"
+    "<|eot_id|><|start_header_id|>assistant<|end_header_id|>\n\n"
+)
+
+VALID_LABELS = {
+    "low_health_literacy",
+    "intermediate_health_literacy",
+    "proficient_health_literacy",
+}
+
+
+class HealthLiteracySignature(dspy.Signature):
+    generated_text = dspy.InputField(
+        desc="A version of the source text rewritten for a specific audience."
+    )
+    literacy_label = dspy.OutputField(
+        desc=(
+            "Classification: low_health_literacy (simple words, no jargon), "
+            "intermediate_health_literacy (moderate technicality), or "
+            "proficient_health_literacy (highly technical/original level)."
+        )
+    )
+
+
+class HealthLiteracyClassifier(dspy.Module):
+    def __init__(self):
+        super().__init__()
+        self.classifier = dspy.ChainOfThought(HealthLiteracySignature)
+
+    def forward(self, generated_text):
+        return self.classifier(generated_text=generated_text)
+
+
+class MedicalClaimVerifier:
+    def __init__(self, base_url: str, model_name: str):
+        self.model_name = model_name
+        self.base_url = base_url
+        self.client = OpenAI(api_key="EMPTY", base_url=self.base_url)
+        self.cov_iqr_ranges = {
+            "low": (0.1765, 0.3226),
+            "intermediate": (0.1818, 0.4091),
+            "proficient": (0.7725, 0.9347),
+        }
+
+    def build_user_prompt(self, text: str, subclaims: List[str]) -> str:
+        numbered_subclaims = "\n".join(
+            f"{idx + 1}. {subclaim}" for idx, subclaim in enumerate(subclaims)
+        )
+        return (
+            "You are a medical evidence checker.\n"
+            "Given a medical passage and a list of subclaims, return labels for each "
+            "subclaim in the same order.\n\n"
+            "Allowed labels: supported, not_supported.\n"
+            "Output format: a JSON array of strings only.\n\n"
+            f"Medical text:\n{text}\n\n"
+            f"Subclaims:\n{numbered_subclaims}"
+        )
+
+    def render_chat_prompt(self, user_prompt: str) -> str:
+        return CHAT_TEMPLATE.format(user_prompt=user_prompt)
+
+    def extract_label_list(self, text: str) -> List[str]:
+        cleaned = text.strip()
+        try:
+            parsed = json.loads(cleaned)
+            if isinstance(parsed, list):
+                return parsed
+        except json.JSONDecodeError:
+            pass
+
+        match = re.search(r"\[[\s\S]*\]", cleaned)
+        if match:
+            try:
+                parsed = json.loads(match.group(0))
+                if isinstance(parsed, list):
+                    return parsed
+            except json.JSONDecodeError:
+                return []
+        return []
+
+    def check_support_api(self, context: str, subclaims: List[str]) -> List[str]:
+        if not context or not subclaims:
+            return []
+
+        user_prompt = self.build_user_prompt(context, subclaims)
+        prompt = self.render_chat_prompt(user_prompt)
+        try:
+            response = self.client.completions.create(
+                model=self.model_name,
+                prompt=prompt,
+                max_tokens=256,
+                temperature=0,
+            )
+            pred_text = response.choices[0].text.strip()
+            labels = self.extract_label_list(pred_text)
+            return [str(x).strip().lower() for x in labels]
+        except Exception:
+            return []
+
+    @staticmethod
+    def average_supported(labels: List[str], expected_len: int) -> float:
+        if expected_len <= 0:
+            return 0.0
+        normalized = [str(x).strip().lower() for x in labels]
+        if len(normalized) < expected_len:
+            normalized.extend(["invalid"] * (expected_len - len(normalized)))
+        elif len(normalized) > expected_len:
+            normalized = normalized[:expected_len]
+        supported_count = sum(1 for item in normalized if item == "supported")
+        return supported_count / expected_len
+
+    def evaluate_level(
+        self, gen_text: str, gold_subs: List[str], full_subs: List[str]
+    ) -> Tuple[float, float]:
+        if not gen_text or not gold_subs or not full_subs:
+            return 0.0, 0.0
+        comp_labels = self.check_support_api(gen_text, gold_subs)
+        cov_labels = self.check_support_api(gen_text, full_subs)
+        comp_score = self.average_supported(comp_labels, len(gold_subs))
+        cov_score = self.average_supported(cov_labels, len(full_subs))
+        return comp_score, cov_score
+
+
+def parse_args() -> argparse.Namespace:
+    parser = argparse.ArgumentParser(
+        description=(
+            "Evaluate classifier accuracy plus subclaim support thresholds "
+            "(completeness + coverage)."
+        )
+    )
+    parser.add_argument("--model-path", default=DEFAULT_MODEL_PATH)
+    parser.add_argument(
+        "--input-file",
+        default=DEFAULT_INPUT_FILE,
+        help="Path to RL inference JSONL (e.g. RL_model_inference_v1.jsonl).",
+    )
+    parser.add_argument(
+        "--reference-subclaims-file",
+        default=DEFAULT_REFERENCE_SUBCLAIMS_FILE,
+        help=(
+            "JSON list file that contains summary_subclaims/fulltext_subclaims "
+            "(used for lookup by doc_id + label)."
+        ),
+    )
+    parser.add_argument(
+        "--classifier-api-base",
+        default=os.environ.get("VLLM_API_BASE", DEFAULT_CLASSIFIER_API_BASE),
+    )
+    parser.add_argument(
+        "--support-api-base",
+        default=os.environ.get("SUPPORT_API_BASE", DEFAULT_SUPPORT_API_BASE),
+    )
+    parser.add_argument(
+        "--support-model",
+        default=os.environ.get("VLLM_MODEL", "sc"),
+    )
+    parser.add_argument("--output-dir", default=DEFAULT_OUTPUT_DIR)
+    parser.add_argument(
+        "--generated-text-key",
+        default="generated_text",
+        help="Field name to evaluate text from input JSONL.",
+    )
+    parser.add_argument(
+        "--comp-min-threshold",
+        type=float,
+        default=0.9,
+        help="Completeness pass lower bound (inclusive).",
+    )
+    parser.add_argument(
+        "--comp-max-threshold",
+        type=float,
+        default=1.0,
+        help="Completeness pass upper bound (inclusive).",
+    )
+    parser.add_argument(
+        "--max-samples",
+        type=int,
+        default=-1,
+        help="Use -1 for all rows.",
+    )
+    parser.add_argument(
+        "--provide-traceback",
+        action="store_true",
+        help="Print full traceback if runtime error happens.",
+    )
+    return parser.parse_args()
+
+
+def check_api_base(api_base: str) -> None:
+    models_url = api_base.rstrip("/") + "/models"
+    req = urllib.request.Request(models_url, method="GET")
+    try:
+        with urllib.request.urlopen(req, timeout=5) as resp:
+            if resp.status >= 400:
+                raise RuntimeError(
+                    f"Endpoint reachable but unhealthy: {models_url} (status={resp.status})"
+                )
+    except urllib.error.URLError as exc:
+        raise ConnectionError(
+            "Cannot reach OpenAI-compatible endpoint. "
+            f"api_base={api_base}. "
+            "Start your vLLM server or pass correct api base."
+        ) from exc
+
+
+def load_compiled_classifier(path: str):
+    if hasattr(dspy, "load"):
+        try:
+            return dspy.load(path)
+        except Exception:
+            pass
+    classifier = HealthLiteracyClassifier()
+    try:
+        classifier.load(path)
+    except Exception as exc:
+        raise RuntimeError(f"Failed to load compiled model from {path}") from exc
+    return classifier
+
+
+def normalize_pred_label(pred_obj: Any) -> str:
+    if not pred_obj or not hasattr(pred_obj, "literacy_label"):
+        return ""
+    return str(pred_obj.literacy_label).strip().lower()
+
+
+def load_items(path: str) -> List[Dict[str, Any]]:
+    items: List[Dict[str, Any]] = []
+    with open(path, "r", encoding="utf-8") as f:
+        for line_no, line in enumerate(f, start=1):
+            if not line.strip():
+                continue
+            row = json.loads(line)
+            items.append(
+                {
+                    "line_no": line_no,
+                    "row_index": row.get("row_index"),
+                    "doc_id": row.get("doc_id"),
+                    "gold_label": str(row.get("gold_label", "")).strip(),
+                    "generated_text": str(row.get("generated_text", "")).strip(),
+                }
+            )
+    return items
+
+
+def load_subclaim_lookup(
+    reference_path: str,
+) -> Dict[Tuple[Any, str], Tuple[List[str], List[str]]]:
+    with open(reference_path, "r", encoding="utf-8") as f:
+        rows = json.load(f)
+    if not isinstance(rows, list):
+        raise ValueError("Reference subclaims file must be a JSON list.")
+
+    lookup: Dict[Tuple[Any, str], Tuple[List[str], List[str]]] = {}
+    for row in rows:
+        doc_id = row.get("doc_id")
+        label = str(row.get("label", "")).strip()
+        gold_subs = row.get("summary_subclaims", [])
+        full_subs = row.get("fulltext_subclaims", [])
+        if label not in VALID_LABELS:
+            continue
+        if not isinstance(gold_subs, list) or not isinstance(full_subs, list):
+            continue
+        if not gold_subs or not full_subs:
+            continue
+        key = (doc_id, label)
+        if key not in lookup:
+            lookup[key] = (gold_subs, full_subs)
+    return lookup
+
+
+def to_level_key(label: str) -> str:
+    mapping = {
+        "low_health_literacy": "low",
+        "intermediate_health_literacy": "intermediate",
+        "proficient_health_literacy": "proficient",
+    }
+    return mapping.get(label, "")
+
+
+def in_range(value: float, lower: float, upper: float) -> bool:
+    return lower <= value <= upper
+
+
+def main() -> None:
+    args = parse_args()
+    if not os.path.exists(args.model_path):
+        raise FileNotFoundError(f"Model file not found: {args.model_path}")
+    if not os.path.exists(args.input_file):
+        raise FileNotFoundError(f"Input file not found: {args.input_file}")
+    if not os.path.exists(args.reference_subclaims_file):
+        raise FileNotFoundError(
+            f"Reference subclaims file not found: {args.reference_subclaims_file}"
+        )
+
+    try:
+        check_api_base(args.classifier_api_base)
+        check_api_base(args.support_api_base)
+
+        lm = dspy.LM(
+            model="openai/dspy",
+            api_base=args.classifier_api_base,
+            api_key="EMPTY",
+            temperature=0.0,
+        )
+        dspy.configure(lm=lm)
+        classifier = load_compiled_classifier(args.model_path)
+        verifier = MedicalClaimVerifier(
+            base_url=args.support_api_base,
+            model_name=args.support_model,
+        )
+        subclaim_lookup = load_subclaim_lookup(args.reference_subclaims_file)
+
+        rows = load_items(args.input_file)
+        if args.max_samples > 0:
+            rows = rows[: args.max_samples]
+
+        unmatched_rows = 0
+        total = 0
+        classifier_correct = 0
+        comp_pass_count = 0
+        cov_pass_count = 0
+        cls_and_comp_pass_count = 0
+        cls_comp_cov_pass_count = 0
+        details: List[Dict[str, Any]] = []
+
+        for idx, row in enumerate(tqdm(rows, desc="Evaluating"), start=1):
+            gold_label = str(row.get("gold_label", "")).strip()
+            if gold_label not in VALID_LABELS:
+                continue
+
+            generated_text = str(row.get(args.generated_text_key, "")).strip()
+            subclaims = subclaim_lookup.get((row.get("doc_id"), gold_label))
+            if not generated_text or not subclaims:
+                if not subclaims:
+                    unmatched_rows += 1
+                continue
+            gold_subs, full_subs = subclaims
+
+            total += 1
+            pred = classifier(generated_text=generated_text)
+            pred_label = normalize_pred_label(pred)
+            is_cls_correct = gold_label in pred_label
+            classifier_correct += int(is_cls_correct)
+
+            comp_score, cov_score = verifier.evaluate_level(
+                gen_text=generated_text,
+                gold_subs=gold_subs,
+                full_subs=full_subs,
+            )
+
+            comp_pass = in_range(
+                comp_score, args.comp_min_threshold, args.comp_max_threshold
+            )
+            comp_pass_count += int(comp_pass)
+
+            level_key = to_level_key(gold_label)
+            cov_low, cov_high = verifier.cov_iqr_ranges[level_key]
+            cov_pass = in_range(cov_score, cov_low, cov_high)
+            cov_pass_count += int(cov_pass)
+
+            cls_and_comp_pass = is_cls_correct and comp_pass
+            cls_comp_cov_pass = cls_and_comp_pass and cov_pass
+            cls_and_comp_pass_count += int(cls_and_comp_pass)
+            cls_comp_cov_pass_count += int(cls_comp_cov_pass)
+
+            details.append(
+                {
+                    "idx": idx,
+                    "line_no": row.get("line_no"),
+                    "row_index": row.get("row_index"),
+                    "doc_id": row.get("doc_id"),
+                    "gold_label": gold_label,
+                    "pred_label": pred_label,
+                    "classifier_correct": is_cls_correct,
+                    "completeness_score": comp_score,
+                    "coverage_score": cov_score,
+                    "completeness_threshold": [
+                        args.comp_min_threshold,
+                        args.comp_max_threshold,
+                    ],
+                    "completeness_pass": comp_pass,
+                    "coverage_iqr_threshold": [cov_low, cov_high],
+                    "coverage_pass": cov_pass,
+                    "pass_cls_and_completeness": cls_and_comp_pass,
+                    "pass_cls_comp_cov": cls_comp_cov_pass,
+                }
+            )
+
+        if total == 0:
+            raise RuntimeError("No valid rows were found for evaluation.")
+
+        def safe_rate(n: int) -> float:
+            return n / total if total else 0.0
+
+        os.makedirs(args.output_dir, exist_ok=True)
+        ts = datetime.now().strftime("%Y%m%d_%H%M%S")
+        summary_path = os.path.join(
+            args.output_dir, f"classifier_subclaim_threshold_eval_{ts}.json"
+        )
+        details_path = os.path.join(
+            args.output_dir, f"classifier_subclaim_threshold_eval_{ts}.jsonl"
+        )
+
+        summary = {
+            "model_path": args.model_path,
+            "input_file": args.input_file,
+            "reference_subclaims_file": args.reference_subclaims_file,
+            "generated_text_key": args.generated_text_key,
+            "classifier_api_base": args.classifier_api_base,
+            "support_api_base": args.support_api_base,
+            "support_model": args.support_model,
+            "total_samples": total,
+            "unmatched_rows": unmatched_rows,
+            "classifier_only_accuracy": safe_rate(classifier_correct),
+            "completeness_pass_rate": safe_rate(comp_pass_count),
+            "coverage_pass_rate": safe_rate(cov_pass_count),
+            "accuracy_cls_and_completeness_threshold": safe_rate(
+                cls_and_comp_pass_count
+            ),
+            "accuracy_cls_completeness_coverage_threshold": safe_rate(
+                cls_comp_cov_pass_count
+            ),
+            "completeness_threshold": [args.comp_min_threshold, args.comp_max_threshold],
+            "coverage_thresholds": verifier.cov_iqr_ranges,
+            "details_path": details_path,
+        }
+
+        with open(summary_path, "w", encoding="utf-8") as f:
+            json.dump(summary, f, indent=2)
+
+        with open(details_path, "w", encoding="utf-8") as f:
+            for item in details:
+                f.write(json.dumps(item, ensure_ascii=False) + "\n")
+
+        print(json.dumps(summary, indent=2))
+        print(f"[DONE] Summary saved: {summary_path}")
+        print(f"[DONE] Details saved: {details_path}")
+
+    except Exception as exc:
+        print(f"[error] {type(exc).__name__}: {exc}")
+        if args.provide_traceback:
+            traceback.print_exc()
+        raise
+
+
+if __name__ == "__main__":
+    main()
diff --git a/code/rl_inference/verified_combined_0-80_clean200.json b/code/rl_inference/verified_combined_0-80_clean200.json
new file mode 100644
index 0000000000000000000000000000000000000000..f128ae175b341b5515cb7672ba17e82e71df9f89
--- /dev/null
+++ b/code/rl_inference/verified_combined_0-80_clean200.json
@@ -0,0 +1,1402 @@
+[
+  {
+    "doc_id": 20,
+    "label": "low_health_literacy",
+    "fulltext": "Patient A.P., female, born in 1979, has been diagnosed with dilatation cardiomyopathy in 1996. Anamnestically, disease started with tonsillitis, possible myocarditis (which was never proven), with pronounced symptoms of heart failure and general symptoms. She was hospitalized and after one month, the left ventricular ejection fraction was 10% with the aforementioned signs of congestive heart failure. She was hospitalized for 10 months and 9 days, with standard therapy for vitally endangered patient, oxygen support, numerous adjuvant therapy, and intensive monitoring. Therapy was administered (ACE inhibitor - ramipril, cardiotonic - digoxin, beta-blockers - metoprolol and combination of diuretics - furosemide and spironolactone), with the indication of heart transplantation. Clinical improvement occured with an ejection fraction that was gradually increasing and at the age of 21 she entered in remission or stabilization phase, with the ejection fraction value of 48-57% (regular echocardiography was performed every three months). For the following four years therapy remained the same, but in Jun 2004 (after an episode of low immunity), ejection fraction fell to 25%, with a clinical deterioration of the disease. The patient was hospitalized for a period of two months, and the condition stabilized, and she was discharged with therapy that was the same but without cardiotonic. Ejection fraction was stabilized, and in year 2006 it was 50%. At the age of 27, the patient decided on the first pregnancy that was successful with beta blocker (metoprolol) in therapy. After the first pregnancy, the ejection fraction was 40% and she was treated with the same therapy with eplerenone (25 mg) instead of spironolactone. The ejection fraction was controlled and did not fall below 45%. At the end of 2015 the patient became pregnant for the second time, and the pregnancy went neatly until eighth month (35 weeks), when she was urgently admitted to hospital, due to sense of suffocation and inability to walk. Ejection fraction decreased to 18% (brain natriuretic peptide (BNP) was 2600 pg/ mL (reference values are 100-400 pg/ mL)). During pregnancy she received only metoprolol in therapy. Physicians decide to continue with her pregnancy, in the 39th week they performed c-section, and the condition stabilized again after twenty days. In October 2016 new mode of therapy was administered, ramipril (2.5 mg, in the morning), metoprolol (47.5 mg, in the morning), spironolactone (50 mg, once a day) and ivabradine (5 mg, twice a day) with torasemide (5 mg, once a day). LifeVest Defibrillator was carried from 06 December 2016 until 27 February 2017 when it was removed. When removed and after examination (ejection fraction was 44%) she continued with ramipril therapy (1.25 mg) metoprolol (23.75 mg), torasemide (5 mg), spironolactone (25 mg) and ivabradine (7.5 mg, twice a day) with potassium supplements, and compliance with non-pharmacological measures (fluid intake restricted to 1.5 L/ day). The echocardiographic finding in March 2017 showed left ventricular dilatation with moderately reduced left ventricular function and left ventricular wall hypokinesia with ejection fraction of 44% (insignificant pericardial effusion was present, inferior vena cava with physiological flow, preserved valves function - Dopler sonography showed slight insufficiency of mitral valve with dilatation of anulus). Evaluation of a patient with ejection fraction 44% showed no indication for an implantable cardioverter defibrillator (ICD), and conservative procedure and medication therapy were recommended. Regular check-ups and body mass reduction, regular control of renal function parameters and electrolytes were recommended. She is led under the diagnosis of dilated cardiomyopathy and heart failure NYHA stage II without any indication for the ICD prophylactic implantation.",
+    "diff_label_texts": "A.P. is a 38‑year‑old woman. At age 17, her heart became big and weak. This may have started after a bad throat infection.\nShe stayed in the hospital for 10 months and 10 days. She was very sick and waiting for a new heart. Her heart rhythm was not dangerously abnormal. Her heart’s pump was very weak.\nDoctors treated her heart failure. They also tried to prevent dangerous heart rhythms and blood clots.\nHer heart got better. This kind of recovery happens in about 16 out of 100 people. The better phase lasted 4 years.\nThen the disease got worse for 2 years.\nAfter that, she was stable. She had her first baby, and the pregnancy was normal.\nIn the middle of her second pregnancy, her heart got worse again. It improved a few months after the birth.\nIn May 2017, she was doing well on medicines. These medicines relax blood vessels, slow the heart, help the body get rid of extra water, and slow the heart’s natural pacemaker. She had no limits in daily activity. She is a mother of two. She did not have a job.",
+    "summary": "Patient A.P., female, 38 years old, had symptoms of dilated cardiomyopathy (with possible infectious myocarditis in the background) at age 17. After hospitalization for ten months and ten days, while waiting for heart transplantation (with threatening death outcome), without a clearly pronounced threatening arrhythmia, but with a low ejection fraction and a poor general condition, remission occurred. The therapy focused primarily on the treatment of heart failure, prevention of arrhythmia and thromboembolism. Normalization of the disease by improving the function of the left ventricle (expected in 16% of patients) occurred and lasted for 4 years, followed by an exacerbation of the disease that lasted for two years. In the next few years the patient was stable, had a first child with normal pregnancy. During the second trimester of the second pregnancy, there was an exacerbation (postpartum dilatation cardiomyopathy) lasting for couple of months. At the time of case report (May 2017), the patient is stable on therapy (ACE inhibitor, beta blocker, diuretics, If channel blocker), without limitation of physical capacity, mother of two children, unemployed."
+  },
+  {
+    "doc_id": 21,
+    "label": "low_health_literacy",
+    "fulltext": "27-year-old male patient with a history of fibrous dysplasia in the right proximal femur, which was managed prophylactically to reduce the risk of fracture 20 years ago by curettage (intralesional resection), application of bone graft and fixation with osteosynthesis material, which was removed one year after the fixation. Two weeks before admission to hospital, the patient experienced pain after a fall with low energy mechanism characterised by axial load and rotational component of the right hip, which resulted in pain intensity 8/10 on the visual analogue scale (VAS) at the level of the inguinal fold and right thigh, which incapacitated him for walking. Radiological control was performed at four weeks, observing all prosthetic components adequately. The patient was discharged clinically and haemodynamically stable, without the need for transfusion of blood products. During his follow-up in the postoperative period (612 weeks), the patient continued with partial support until day 20, in which he began with full support even accompanied by a walker. Radiological control was performed at four weeks, observing all prosthetic components adequately. The patient is currently carrying out daily activities with slight limitation due to claudicatio intermittens caused by the incision in the middle gluteus. However, he was able to participate in low-impact sports activities, such as walking and expressed great satisfaction with the functional outcome of the procedure.\n",
+    "diff_label_texts": "A 27-year-old man came to the emergency room with a break at the top of his right thigh bone, near the hip. The break happened after a small fall that twisted his hip and pushed straight down on it. As a child, he had a bone problem in that same area and had surgery to help prevent breaks. The doctors scraped out the weak bone, added graft bone, and used metal to hold it for a time. That metal was removed a year later. To fix the new break for good, the doctors removed the damaged top part of the thigh bone and put in a new artificial hip. They also used metal bands to help hold things steady. They sent a piece of the bone to the lab. The test showed he still had the same bone condition from childhood.",
+    "summary": "We present the case of a 27-year-old male patient who presented to the emergency department with a fracture of the right femur at the base of the neck in pathological ground Garden II Pauwells III AO 31B2.3r, after a low energy mechanism of injury characterized by axial load with rotational component of the right hip. The patient had a history of intralesional resection, application of bone graft and prophylactic fixation with unspecified osteosynthesis material in the pertrochanteric region 20 years ago; the biopsy later showed DF; one year later, the osteosynthesis material was removed. Due to the characteristics of the fracture and as a definitive and curative therapeutic method, it was decided to carry out a wide resection of the proximal femur and total arthroplasty of the hip with a modular prosthesis with placement of cerclage, as well as a excisional biopsy that later corroborated that it was the same DF treated in childhood.\n"
+  },
+  {
+    "doc_id": 21,
+    "label": "intermediate_health_literacy",
+    "fulltext": "27-year-old male patient with a history of fibrous dysplasia in the right proximal femur, which was managed prophylactically to reduce the risk of fracture 20 years ago by curettage (intralesional resection), application of bone graft and fixation with osteosynthesis material, which was removed one year after the fixation. Two weeks before admission to hospital, the patient experienced pain after a fall with low energy mechanism characterised by axial load and rotational component of the right hip, which resulted in pain intensity 8/10 on the visual analogue scale (VAS) at the level of the inguinal fold and right thigh, which incapacitated him for walking. Radiological control was performed at four weeks, observing all prosthetic components adequately. The patient was discharged clinically and haemodynamically stable, without the need for transfusion of blood products. During his follow-up in the postoperative period (612 weeks), the patient continued with partial support until day 20, in which he began with full support even accompanied by a walker. Radiological control was performed at four weeks, observing all prosthetic components adequately. The patient is currently carrying out daily activities with slight limitation due to claudicatio intermittens caused by the incision in the middle gluteus. However, he was able to participate in low-impact sports activities, such as walking and expressed great satisfaction with the functional outcome of the procedure.\n",
+    "diff_label_texts": "A 27-year-old man presented to the emergency department with a fracture at the base of the neck of the right femur after a low-energy fall that involved axial loading and a twisting motion of the right hip. He had a known history of fibrous dysplasia in the right proximal femur and, 20 years earlier, underwent curettage, bone grafting, and prophylactic fixation; the hardware was removed one year later, and biopsy at that time confirmed fibrous dysplasia. Given the pattern and pathologic nature of the current fracture, the team proceeded with a definitive treatment: wide resection of the proximal femur and a total hip replacement using a modular prosthesis, along with cerclage to secure the construct. An excisional biopsy performed during surgery confirmed the same fibrous dysplasia that had been treated in childhood. He recovered well: imaging at four weeks showed the components in good position, and he progressed from partial weight-bearing to full weight-bearing with a walker around day 20. He returned to daily activities with a mild, intermittent limp related to the gluteus medius incision and was able to do low-impact activities such as walking, reporting high satisfaction with the outcome.",
+    "summary": "We present the case of a 27-year-old male patient who presented to the emergency department with a fracture of the right femur at the base of the neck in pathological ground Garden II Pauwells III AO 31B2.3r, after a low energy mechanism of injury characterized by axial load with rotational component of the right hip. The patient had a history of intralesional resection, application of bone graft and prophylactic fixation with unspecified osteosynthesis material in the pertrochanteric region 20 years ago; the biopsy later showed DF; one year later, the osteosynthesis material was removed. Due to the characteristics of the fracture and as a definitive and curative therapeutic method, it was decided to carry out a wide resection of the proximal femur and total arthroplasty of the hip with a modular prosthesis with placement of cerclage, as well as a excisional biopsy that later corroborated that it was the same DF treated in childhood.\n"
+  },
+  {
+    "doc_id": 22,
+    "label": "intermediate_health_literacy",
+    "fulltext": "A 4-year-old boy with stage IV neuroblastoma received four cycles of chemotherapy, including high-dose chemotherapy including busulfan and melphalan, followed by autologous peripheral blood stem cell transplantation with autologous bone marrow supplementation. After eight additional cycles of chemotherapy consisting of temozolomide and irinotecan, which led to stable disease, the patient underwent preparative conditioning with fludarabine (150 mg/m2), melphalan (140 mg/m2), and 12 Gy of TBI for subsequent allogeneic CBT. The patient received tacrolimus and a short-term course of methotrexate for GVHD prophylaxis. The patient underwent engraftment on day 17. He then developed grade 3 GVHD, which was managed by increasing the prednisolone dose and was later discharged on day 85. The patient also received proton beam therapy (39.6 Gy) from days 121 to 150 post-transplantation for a right supra-mediastinum tumor with residual I123-MIBG accumulation in the right adrenal gland.\n\nThe patient remained healthy with no evidence of GVHD until presentation at our hospital with a productive cough on day 159. As his older brother displayed similar cold symptoms, a rapid antigen test for RSV was performed, which revealed a positive result. His respiratory symptoms gradually worsened, and he revisited our hospital on day 194 with dyspnea and intercostal retractions. Upon admission, he was given 0.7-1.0 mg/kg of prednisolone, which failed to improve his respiratory condition. Chest computed tomography on day 231 revealed infiltration, ground-glass opacity, and septal thickening in the bilateral lung fields along with right pleural effusion. Echocardiography showed an elevated tricuspid regurgitation peak velocity of 4.1 m/s and an interventricular septum close to the isobaric, indicating the presence of PH. In addition, pericardial effusion was detected. On day 231, the patient was transferred to the pediatric intensive care unit, where mechanical ventilation and inhaled nitric oxide (NO) were initiated. Thoracoscopic lung biopsy on day 244 revealed diffuse intra-alveolar hemorrhage and edema on hematoxylin-eosin (HE)-stained samples. Elastica van Gieson staining revealed diffuse obstructive lesions due to fibrocellular components with plump endothelial cells in the pre-septal pulmonary veins and venules. While pulmonary muscular arteries and arterioles showed mild medial hypertrophy and focal intimal thickening (Heath-Edwards Grade 2), severe stenosis with concentric intimal fibrosis or plexiform lesions was present. Based on these results, the patient was diagnosed with PVOD with mild pulmonary arterial/arteriolar lesions. Of note, HE staining also revealed enlarged type II pneumocytes with multinucleated and giant cell-like features, indicating the presence of prior lung injury that was likely attributable to his preceding viral infection.",
+    "diff_label_texts": "A 4-year-old boy with metastatic neuroblastoma received intensive treatment, including chemotherapy, an autologous stem cell transplant, and then an allogeneic cord blood transplant. About a month after he developed upper respiratory symptoms and tested positive for RSV, he presented on day 194 post–cord blood transplant with worsening breathing problems and was ultimately diagnosed with pulmonary veno-occlusive disease (PVOD), a rare form of pulmonary hypertension caused by blockage of small lung veins. Lung biopsy not only confirmed PVOD-related changes but also showed lung injury patterns consistent with a recent viral infection. Taken together, the timing of his RSV infection and the biopsy findings suggest RSV may have contributed to the onset of PVOD.",
+    "summary": "A 4-year-old boy was diagnosed with metastatic neuroblastoma and underwent intensive chemotherapy, autologous HSCT, and allogeneic cord blood transplantation (CBT). He experienced PVOD on day 194 following CBT after displaying upper respiratory symptoms and positive RSV antigen test results approximately one month prior. Pathological examination of a lung biopsy specimen revealed lung injury suspected to be associated with viral infection in addition to PVOD-related findings, suggesting that RSV infection might have contributed to the onset of PVOD."
+  },
+  {
+    "doc_id": 23,
+    "label": "low_health_literacy",
+    "fulltext": "65-year-old male with no personal or family history of pathology of relevance. His condition began in 2020 with productive cough that intensified and was accompanied by shortness of breath with small to medium effort; as well as loss of 10 kg of weight in a period of 4 months. He went to a doctor who requested a chest X-ray that showed massive, multilocular right pleural effusion with right bronchial obstruction and mediastinal lymphadenopathy. A thoracocentesis was performed with a biopsy of the right lung and parietal pleura. The histopathological study reported an adeno-squamous carcinoma. His evolution was bad, which is why he was referred to our institution. On admission, a physical examination found him cachectic, with right pulmonary hypoventilation, 92% oxygen saturation and pneumokoccal dysfunction, with no evidence of systemic or haemodynamic compromise. A chest X-ray was performed that showed complete opacity of the right hemithorax, and a pleural catheter was placed with a serohematic flow. In the histopathological study of the revision material, the lung parenchyma was replaced by a poorly differentiated neoplasm with a solid mantle and syncytia, surrounded by abundant lymphocytes and plasma cells. The neoplastic cells had large, ovoid nuclei, fine chromatin, prominent nucleolus and wide, poorly defined cytoplasm. An immunohistochemical study was performed that was positive for CKAE1/AE3, CK 5/6, p63, EBER ISH, and negative for Napsina A, TTF-1 and CK 7, which ruled out the reference diagnosis of adeno-squamous carcinoma and established the diagnosis of CTLP. Molecular study in the paraffin block was positive for PD-L1 (SP263) +++ in approximately 100% of the neoplastic cells, and negative for EGFR, K-RAS, ALK, ROS1. In order to confirm the pulmonary origin of the neoplasm, a nasopharyngeal examination was performed that was negative. In April 2021, a PET-CT was performed that reported a heterogeneous parahilary pulmonary lesion that compromised the main bronchus and caused atelectasis; as well as multiple cervical, mediastinal and peri-gastric lymphadenopathies. The catheter was removed due to partial resolution of the effusion and chemotherapy treatment with gemcitabine/cisplatin was initiated. He received 6 cycles, however, the patient reported hearing loss and AKIN I acute renal failure was documented, so cisplatin was changed to carboplatin, and maintenance durvalumab was continued. In December 2021, disease progression was documented and he died in January 2022 due to respiratory failure.\n",
+    "diff_label_texts": "A 65-year-old man had a cough, trouble breathing, and lost weight. A chest scan showed a spot in the right lung. A needle test of the spot showed it was a kind of lung cancer. Under the microscope, the cancer cells were large and sat among many infection-fighting cells. Lab tests fit this cancer type and ruled out other common lung cancers. A virus called Epstein–Barr was found inside the tumor cells. Another test showed a protein called PD-L1 was very high on the cancer cells. He was treated with strong chemotherapy and an immune therapy (gemcitabine, cisplatin, and durvalumab). The cancer kept growing. He died 9 months after diagnosis.",
+    "summary": "We report the case of a 65-year-old man with a pulmonary lymphoepithelioma-like carcinoma, who presented with cough, dyspnea, and weight loss. A chest CT scan showed a poorly defined nodule located in the right lung. A trans-thoracic biopsy of the lesion was performed, and microscopic examination revealed large polygonal cells arranged in sheets, infiltrated by abundant lymphocytes and plasma cells, around the interstitium. The neoplastic cells were positive for cytokeratin 5/6 and p63, and negative for Napsina A and thyroid transcription factor 1 (TTF-1). PD-L1 expression was positive (approximately 100%) by immunohistochemistry; as was the nucleus of the neoplastic cells by in situ hybridization for Epstein-Barr virus-encoded RNA (EBER-ISH). The patient received six cycles of a combination chemotherapy regimen based on platinum (gemcitabine/cisplatin) plus durvalumab. He progressed and ultimately died 9 months after diagnosis.\n"
+  },
+  {
+    "doc_id": 24,
+    "label": "low_health_literacy",
+    "fulltext": "A 13-year-old male patient was admitted to the Children’s Hospital in Damascus after noticing a palpable enlarged mass in the left inguinal region. His medical history was unremarkable except for a surgical intervention on his spine 6 years ago due to an accident, which resulted in the loss of motor function and sensation in both of his lower extremities.\n\nDue to the long period he had spent in bed, the patient developed decubitus sores on his left foot. The only finding on clinical examination was a mass in the left inguinal area, which was movable on deep structures and so was the overlaying skin on it. The mass was not tender on palpation, and no signs of local inflammation were observed.\n\nLaboratory tests revealed an Elevated ESR (119 mm/h in the first hour). Other Basic Laboratory tests including (Complete Blood Count, Liver function tests, electrolytes, Urea, Creatinine and LDH) were ordered and were within normal ranges for age. Ordering these tests was essential to rule out systemic diseases. Given the absence of indicative physical findings for systemic disorders or immunodeficiencies, additional tests like those for HIV or Direct Antiglobulin were deemed unnecessary.\n\nA CT of the abdomen, chest, and pelvis showed enlarged lymph nodes inferior to the inguinal ligament, with the largest measuring approximately (3.5 × 2.4 cm). Other organs and nodes were within normal limits.\n\nAll of the above-mentioned investigations were essential to rule other high-risk diagnosis including lymphoma and leukemia. However, these were not sufficient to reach the definite diagnosis, so a decision of surgical resection of the nodes was taken.\n\nTo confirm the diagnoses and exclude other potential differentials presenting with enlarged lymph nodes, surgical removal of all of these enlarged nodes was performed under general anesthesia, and biopsies were sent for microscopic study.\n\nThe biopsy showed hyperplastic nodal architecture with proliferation of histiocytes and plasma cells with vascular proliferation, consistent with Plasma cell subtype of Castleman’s Disease.\n\nThe patient was discharged from the hospital after 14-day period after ensuring that there were no remaining enlarged lymph nodes. The only recommendation was oral prednisolone. The patient underwent follow-up using a whole-body CT scan every three months. During each hospital visit, a comprehensive clinical examination and laboratory tests (e.g. Complete Blood Test, ESR, C-reactive protein, liver function tests, renal function tests) were performed in addition to the CT scan. After a 12-month follow-up period, the patient reported no new symptoms or enlarged lymph nodes. Additionally, no abnormalities were observed during clinical examination or in laboratory tests.",
+    "diff_label_texts": "A 13-year-old boy felt a lump in his left groin, where the leg meets the body. He felt fine otherwise. The doctors took the lump out to make sure it was not something dangerous. Tests on the lump showed Castleman disease, plasma cell type. This type is very rare in children. This is the first known case of a single Castleman disease lump in the groin. The boy was checked for 12 months after surgery. No new swollen glands or symptoms showed up.",
+    "summary": "We report a unique case of a 13-year-old boy who presented with a palpable enlarged mass in the left inguinal region without any constitutional symptoms. Surgical removal of this mass was essential to exclude worrying causes. Pathologic examination revealed proliferative changes consistent with Castleman's disease plasma cell type which is one of the rarest forms of the disease in children. To our knowledge, this case is the first reported case of Unicentric Castleman Disease (UCD) in the inguinal area. During a 12-month-period of follow-up, no additional lymph node enlargements or other symptoms were reported."
+  },
+  {
+    "doc_id": 25,
+    "label": "proficient_health_literacy",
+    "fulltext": "The medical records of patients with a diagnosis of congenital myotonia studied and followed in the pediatric neurology consultation in a third-level hospital between 2015 and 2020 were reviewed. The inclusion criteria were to present a clinical diagnosis – myotonia, warm-up phenomenon, characteristic electromyographic pattern and/or family history – and/or a molecular diagnosis (mutation in the CLCN1 gene). The clinical signs and symptoms, as well as the results of the complementary explorations and the genetic mutation found, were collected by reviewing the medical record. Demographic variables (age and sex), course of the disease (age of onset, symptoms and signs, time elapsed until diagnosis and clinical evolution), family history and evaluation of the response to treatment were collected.\n\nFive cases with clinical diagnosis of congenital myotonia were identified (three with Becker's disease and two with Thomsen's disease). The incidence in relation to the number of births was estimated at 1:15,000 newborns for cases with Becker's phenotype and 1:21,000 newborns for Thomsen's phenotypes.\n\nMost of our patients were female, and the male was the only one who started before the age of six. The initial clinical presentation included myotonia in the lower limbs in four of the five patients and in the upper limbs in all but one. The age at onset ranged from 22 months to 12 years, with a median of 6 years. Genetic diagnosis was performed in all cases approximately two years after onset, and the family of one patient refused to have it performed. All had a worsening with cold, but the warming phenomenon was only in those with the Becker phenotype.\n\nPatients with recessive congenital myotonia showed some progression. As a family history, it is worth noting that patients 2 and 3 were sisters, without the parents showing any clinical signs, and that the mother of patient 1 showed mild clinical signs that were doubtful with the cold. The patient who refused the study had a history of myotonia in the maternal branch.\n\nBlood tests did not show elevated creatine kinase in any of the patients. The electromyogram was abnormal in all patients except the first one at 2.8/12 years of age. The test was not repeated later because it was not considered necessary.\n\nThe most used treatment initially was oxcarbazepine (in patients with recessive form), with a good response in general. In case 2 it lost efficacy with time and mexiletine was initiated. Patient 4 initiated several drugs without success due to loss of efficacy or side effects. Patient 5 rejected treatment due to mild clinical presentation.\n\nPatient 1 had a previously undescribed, likely pathogenic mutation (CLCN1: c.824T>C) inherited from his mother. Cases 1 to 3 had the Becker phenotype with composite heterozygosity mutations, and cases 4 and 5 had the Thomsen phenotype. Case 5 declined genetic testing.\n",
+    "diff_label_texts": "We retrospectively reviewed medical records from a pediatric neurology consultation at a third‑level hospital (2015–2020) for patients with congenital myotonia. Inclusion criteria comprised a clinical diagnosis (myotonia, warm‑up phenomenon, characteristic electromyographic pattern and/or family history) and/or a molecular diagnosis (CLCN1 mutation). For each patient we abstracted demographics (age, sex), disease course (age of onset, symptoms and signs, time to diagnosis, clinical evolution), family history, and treatment response, along with complementary testing and genotypes. Five cases with a clinical diagnosis of congenital myotonia were identified: three with Becker’s disease (recessive phenotype) and two with Thomsen’s disease (dominant phenotype). Incidence relative to births was estimated at 1:15,000 for Becker phenotypes and 1:21,000 for Thomsen phenotypes. Most patients were female; the single male was the only child with onset before age six. Initial presentation included myotonia in the lower limbs in four of five patients and in the upper limbs in all but one. Age at onset ranged from 22 months to 12 years (median 6 years). Genetic diagnosis was pursued approximately two years after onset; one family declined testing. All patients reported worsening with cold; the warming phenomenon was noted only in those with the Becker phenotype. Patients with recessive congenital myotonia showed some progression. Family history included: patients 2 and 3 were sisters with unaffected parents; the mother of patient 1 had mild, cold‑provoked, doubtful clinical signs; the patient who declined genetic testing had a maternal‑line history of myotonia. Serum creatine kinase was not elevated in any case. The electromyogram was abnormal in all patients except the first one at 2.8/12 years of age (not repeated). Initial therapy most often used was oxcarbazepine in the recessive form, with generally good response; in case 2 it lost efficacy and mexiletine was initiated. Case 4 trialed several drugs without success due to loss of efficacy or adverse effects. Case 5 declined treatment given mild symptoms. Patient 1 harbored a previously undescribed, likely pathogenic variant, CLCN1: c.824T>C, maternally inherited. Cases 1–3 (Becker phenotype) carried composite heterozygosity mutations; cases 4–5 had the Thomsen phenotype, and case 5 declined genetic testing.",
+    "summary": "The medical records of patients with a diagnosis of congenital myotonia studied and followed in the pediatric neurology consultation in a third-level hospital between 2015 and 2020 were reviewed. Demographic variables (age and sex), course of the disease (age of onset, symptoms and signs, time elapsed until diagnosis and clinical evolution), family history and evaluation of the response to treatment were collected. Five cases with a clinical diagnosis of congenital myotonia were identified (three with Becker disease and two with Thomsen disease). The incidence in relation to the number of births was estimated at 1:15,000 newborns for cases with a Becker phenotype and 1:21,000 newborns for Thomsen phenotypes. We found a probably pathogenic mutation not previously described (CLCN1: c.824T>C).\n"
+  },
+  {
+    "doc_id": 26,
+    "label": "low_health_literacy",
+    "fulltext": "A 67-year-old female patient presented with a six-year history of recurrent swelling in the left lower limb. One year prior, she was diagnosed with an AVM in the lower limb at another hospital. Two months before hospitalization, the patient underwent embolization treatment, which included the placement of two coils (20 mm x 40 cm, BSX, USA). Despite this intervention, the patient’s left lower limb swelling did not show any improvement. The patient has been experiencing fatigue and difficulty of breathing for a month. As these symptoms of heart failure progressed and worsened, the patient was transferred to Chengdu University of Traditional Chinese Medicine Hospital for further evaluation and treatment. The patient had no prior history of cardiovascular diseases, injuries, or surgeries. However, she reported a history of oral estrogen use for menopausal syndrome seven years ago.\n\nShe exhibited significant edema and skin sclerosis in the left lower limb. Additionally, absent pulses were observed in the popliteal artery and distal regions. A noticeable tremor was also present in the left thigh. The patient was seated during the examination. Echocardiography revealed cardiac enlargement, along with moderate mitral regurgitation and severe tricuspid regurgitation. The left ventricular ejection fraction (EF) was measured at 60%, and there was an elevation in b-type natriuretic peptide (BNP) levels to 2853 ng/L. The electrocardiogram showed a sinus rhythm with a heart rate of 105 beats per minute and evidence of left atrial enlargement. Chest CT scans confirmed cardiac enlargement, while no respiratory system abnormalities were detected. Preoperative computed tomography angiography (CTA) provided further insights, revealing a left iliac artery aneurysm, a significantly enlarged femoral artery, and complex AVMs in the superficial femoral artery. Additionally, the femoral and superficial veins appeared significantly enlarged on arterial phase imaging. Notably, the left lower limb popliteal artery and anterior tibial artery were not visualized. Based on these findings, the patient was diagnosed with complex congenital lower limb AVMs, acute exacerbation of chronic heart failure, and classified as NYHA Class IV.\n\nThe patient exhibits distinct symptoms of acute heart failure, and preoperative ultrasound assessment has revealed a volume flow of 3400 ml/min in the CFA. Given that embolization using coils may not effectively reduce the flow rate of the AVMs, the utilization of covered stents is a viable option. These stents effectively decrease the flow of lower limb AVMs, thereby improving the patient’s heart failure condition. Additionally, staged embolization treatment can further enhance the treatment outcome by improving the nidus of the lower limb AVMs.\n\nCTA of the patient revealed significant dilatation of blood vessels, with a maximum diameter of 32 mm for the iliac artery, 27 mm for the common femoral artery (CFA), and 22 mm for the superficial femoral artery (SFA). To minimize access site complications, antegrade access was achieved through a surgical approach of the CFA. Under general anesthesia, intravascular covered stents were inserted through an open femoral artery approach, utilizing 14 F (Cook Medical, USA) catheter sheaths intraoperatively. complex AVMs were visualized in the superficial femoral artery and profunda femoris artery, accompanied by early visualization of an enlarged femoral vein.\n\nPreoperative CTA measurements indicated a diameter of 19 mm for the middle segment of the SFA, leading to the selection of a 20 mm–12 mm/120 mm aorto-uni-iliac covered stent (MicroPort, China). A 0.035 guidewire, in conjunction with a single-curve catheter, was used to access the popliteal artery. Subsequently, it was replaced with a 0.035 super-hard guidewire to provide support during the implantation of the stent graft. The stent was deployed precisely at the distal end of the superficial femoral artery, the location with the highest concentration of AVMs. Completion angiography revealed a significant reduction in venous opacification around the stent and clear visualization of the popliteal artery. Postoperatively, the left femoral artery was sutured using a 6 − 0 vascular risk suture, resulting in a significant improvement in the patient’s heart failure symptoms. The patient has heart failure, so the surgery duration should not be excessive. It is planned to perform embolization treatment in the second phase.\n\nOne week post-treatment, ultrasound examination revealed a reduction in volume flow to 1600 ml/min in the CFA, with a BNP level of 1198ug/l. Targeting the nidus with embolization therapy is expected to further decrease the flow velocity of arteriovenous malformations. The right CFA was punctured, allowing the insertion of a 5 F arterial sheath and a 5 F catheter for angiographic examination. Guided by ultrasound, the drainage vein of the AVM was punctured, and a 5 F vascular sheath was introduced. The contrast agent confirmed the presence of a nidus and its draining veins. The embolization procedure of the draining veins involved the use of a coil (18–20 mm x 40 cm, BSX, USA), two microcoils (4 mm x 42 mm, 5 mm x 10 mm, USA), 3% polidocanol (6 mL Kruelle, Germany), and 99% anhydrous ethanol (10 mL).\n\nCompletion angiography showed a significant reduction in the visualization of AVMs and draining veins, indicating their disappearance. During the one-year follow-up, the patient exhibited notable improvement in lower limb swelling and cardiac function. The volume flow in the CFA decreased to 780 ml/min. Echocardiography revealed minor enlargement of the left and right atria, slight mitral and tricuspid regurgitation, and a left ventricular ejection fraction (EF) of 71%. Notably, BNP levels decreased significantly.",
+    "diff_label_texts": "This report is about a woman with abnormal blood vessel connections in her left leg that she was born with. Her left leg stayed swollen for a long time. She then started having signs of heart trouble. At age 67, doctors confirmed the leg problem was complex and present since birth. The team used a special tube made for the big belly artery, plus a blocking procedure, to slow the bad blood flow in her leg. This was done to help her sudden heart failure caused by the leg problem. The report explains what worked well and what did not.",
+    "summary": "We present a case involving a patient with congenital AVMs in the lower limb, who had suffered from prolonged swelling in the left lower limb and recently developed symptoms of heart failure. At the age of 67, the patient was definitively diagnosed with a complex congenital AVMs in the lower limb. This article delves into the practical experiences and limitations encountered in employing an abdominal aortic stent graft, coupled with embolization, to address acute heart failure caused by complex congenital AVMs in the lower limb."
+  },
+  {
+    "doc_id": 26,
+    "label": "intermediate_health_literacy",
+    "fulltext": "A 67-year-old female patient presented with a six-year history of recurrent swelling in the left lower limb. One year prior, she was diagnosed with an AVM in the lower limb at another hospital. Two months before hospitalization, the patient underwent embolization treatment, which included the placement of two coils (20 mm x 40 cm, BSX, USA). Despite this intervention, the patient’s left lower limb swelling did not show any improvement. The patient has been experiencing fatigue and difficulty of breathing for a month. As these symptoms of heart failure progressed and worsened, the patient was transferred to Chengdu University of Traditional Chinese Medicine Hospital for further evaluation and treatment. The patient had no prior history of cardiovascular diseases, injuries, or surgeries. However, she reported a history of oral estrogen use for menopausal syndrome seven years ago.\n\nShe exhibited significant edema and skin sclerosis in the left lower limb. Additionally, absent pulses were observed in the popliteal artery and distal regions. A noticeable tremor was also present in the left thigh. The patient was seated during the examination. Echocardiography revealed cardiac enlargement, along with moderate mitral regurgitation and severe tricuspid regurgitation. The left ventricular ejection fraction (EF) was measured at 60%, and there was an elevation in b-type natriuretic peptide (BNP) levels to 2853 ng/L. The electrocardiogram showed a sinus rhythm with a heart rate of 105 beats per minute and evidence of left atrial enlargement. Chest CT scans confirmed cardiac enlargement, while no respiratory system abnormalities were detected. Preoperative computed tomography angiography (CTA) provided further insights, revealing a left iliac artery aneurysm, a significantly enlarged femoral artery, and complex AVMs in the superficial femoral artery. Additionally, the femoral and superficial veins appeared significantly enlarged on arterial phase imaging. Notably, the left lower limb popliteal artery and anterior tibial artery were not visualized. Based on these findings, the patient was diagnosed with complex congenital lower limb AVMs, acute exacerbation of chronic heart failure, and classified as NYHA Class IV.\n\nThe patient exhibits distinct symptoms of acute heart failure, and preoperative ultrasound assessment has revealed a volume flow of 3400 ml/min in the CFA. Given that embolization using coils may not effectively reduce the flow rate of the AVMs, the utilization of covered stents is a viable option. These stents effectively decrease the flow of lower limb AVMs, thereby improving the patient’s heart failure condition. Additionally, staged embolization treatment can further enhance the treatment outcome by improving the nidus of the lower limb AVMs.\n\nCTA of the patient revealed significant dilatation of blood vessels, with a maximum diameter of 32 mm for the iliac artery, 27 mm for the common femoral artery (CFA), and 22 mm for the superficial femoral artery (SFA). To minimize access site complications, antegrade access was achieved through a surgical approach of the CFA. Under general anesthesia, intravascular covered stents were inserted through an open femoral artery approach, utilizing 14 F (Cook Medical, USA) catheter sheaths intraoperatively. complex AVMs were visualized in the superficial femoral artery and profunda femoris artery, accompanied by early visualization of an enlarged femoral vein.\n\nPreoperative CTA measurements indicated a diameter of 19 mm for the middle segment of the SFA, leading to the selection of a 20 mm–12 mm/120 mm aorto-uni-iliac covered stent (MicroPort, China). A 0.035 guidewire, in conjunction with a single-curve catheter, was used to access the popliteal artery. Subsequently, it was replaced with a 0.035 super-hard guidewire to provide support during the implantation of the stent graft. The stent was deployed precisely at the distal end of the superficial femoral artery, the location with the highest concentration of AVMs. Completion angiography revealed a significant reduction in venous opacification around the stent and clear visualization of the popliteal artery. Postoperatively, the left femoral artery was sutured using a 6 − 0 vascular risk suture, resulting in a significant improvement in the patient’s heart failure symptoms. The patient has heart failure, so the surgery duration should not be excessive. It is planned to perform embolization treatment in the second phase.\n\nOne week post-treatment, ultrasound examination revealed a reduction in volume flow to 1600 ml/min in the CFA, with a BNP level of 1198ug/l. Targeting the nidus with embolization therapy is expected to further decrease the flow velocity of arteriovenous malformations. The right CFA was punctured, allowing the insertion of a 5 F arterial sheath and a 5 F catheter for angiographic examination. Guided by ultrasound, the drainage vein of the AVM was punctured, and a 5 F vascular sheath was introduced. The contrast agent confirmed the presence of a nidus and its draining veins. The embolization procedure of the draining veins involved the use of a coil (18–20 mm x 40 cm, BSX, USA), two microcoils (4 mm x 42 mm, 5 mm x 10 mm, USA), 3% polidocanol (6 mL Kruelle, Germany), and 99% anhydrous ethanol (10 mL).\n\nCompletion angiography showed a significant reduction in the visualization of AVMs and draining veins, indicating their disappearance. During the one-year follow-up, the patient exhibited notable improvement in lower limb swelling and cardiac function. The volume flow in the CFA decreased to 780 ml/min. Echocardiography revealed minor enlargement of the left and right atria, slight mitral and tricuspid regurgitation, and a left ventricular ejection fraction (EF) of 71%. Notably, BNP levels decreased significantly.",
+    "diff_label_texts": "A 67-year-old woman with years of left leg swelling developed new symptoms of heart failure and was diagnosed with complex, congenital arteriovenous malformations (AVMs) in the lower limb. These abnormal vessel connections create high-flow shunts that can overload the heart. After a prior coil embolization failed to help, the team used an abdominal aortic stent graft (repurposed in the leg) to quickly reduce blood flow through the AVM, then performed staged embolization to target the AVM nidus and draining veins. Her heart failure and leg swelling improved, with blood flow in the common femoral artery falling stepwise and heart function markers getting better over time. The article highlights real-world lessons and limits: coils alone may not control very high-flow AVMs; covered stents can promptly lower shunt flow but usually need follow-up embolization; and staging helps reduce risk in patients with severe (acute) heart failure.",
+    "summary": "We present a case involving a patient with congenital AVMs in the lower limb, who had suffered from prolonged swelling in the left lower limb and recently developed symptoms of heart failure. At the age of 67, the patient was definitively diagnosed with a complex congenital AVMs in the lower limb. This article delves into the practical experiences and limitations encountered in employing an abdominal aortic stent graft, coupled with embolization, to address acute heart failure caused by complex congenital AVMs in the lower limb."
+  },
+  {
+    "doc_id": 26,
+    "label": "proficient_health_literacy",
+    "fulltext": "A 67-year-old female patient presented with a six-year history of recurrent swelling in the left lower limb. One year prior, she was diagnosed with an AVM in the lower limb at another hospital. Two months before hospitalization, the patient underwent embolization treatment, which included the placement of two coils (20 mm x 40 cm, BSX, USA). Despite this intervention, the patient’s left lower limb swelling did not show any improvement. The patient has been experiencing fatigue and difficulty of breathing for a month. As these symptoms of heart failure progressed and worsened, the patient was transferred to Chengdu University of Traditional Chinese Medicine Hospital for further evaluation and treatment. The patient had no prior history of cardiovascular diseases, injuries, or surgeries. However, she reported a history of oral estrogen use for menopausal syndrome seven years ago.\n\nShe exhibited significant edema and skin sclerosis in the left lower limb. Additionally, absent pulses were observed in the popliteal artery and distal regions. A noticeable tremor was also present in the left thigh. The patient was seated during the examination. Echocardiography revealed cardiac enlargement, along with moderate mitral regurgitation and severe tricuspid regurgitation. The left ventricular ejection fraction (EF) was measured at 60%, and there was an elevation in b-type natriuretic peptide (BNP) levels to 2853 ng/L. The electrocardiogram showed a sinus rhythm with a heart rate of 105 beats per minute and evidence of left atrial enlargement. Chest CT scans confirmed cardiac enlargement, while no respiratory system abnormalities were detected. Preoperative computed tomography angiography (CTA) provided further insights, revealing a left iliac artery aneurysm, a significantly enlarged femoral artery, and complex AVMs in the superficial femoral artery. Additionally, the femoral and superficial veins appeared significantly enlarged on arterial phase imaging. Notably, the left lower limb popliteal artery and anterior tibial artery were not visualized. Based on these findings, the patient was diagnosed with complex congenital lower limb AVMs, acute exacerbation of chronic heart failure, and classified as NYHA Class IV.\n\nThe patient exhibits distinct symptoms of acute heart failure, and preoperative ultrasound assessment has revealed a volume flow of 3400 ml/min in the CFA. Given that embolization using coils may not effectively reduce the flow rate of the AVMs, the utilization of covered stents is a viable option. These stents effectively decrease the flow of lower limb AVMs, thereby improving the patient’s heart failure condition. Additionally, staged embolization treatment can further enhance the treatment outcome by improving the nidus of the lower limb AVMs.\n\nCTA of the patient revealed significant dilatation of blood vessels, with a maximum diameter of 32 mm for the iliac artery, 27 mm for the common femoral artery (CFA), and 22 mm for the superficial femoral artery (SFA). To minimize access site complications, antegrade access was achieved through a surgical approach of the CFA. Under general anesthesia, intravascular covered stents were inserted through an open femoral artery approach, utilizing 14 F (Cook Medical, USA) catheter sheaths intraoperatively. complex AVMs were visualized in the superficial femoral artery and profunda femoris artery, accompanied by early visualization of an enlarged femoral vein.\n\nPreoperative CTA measurements indicated a diameter of 19 mm for the middle segment of the SFA, leading to the selection of a 20 mm–12 mm/120 mm aorto-uni-iliac covered stent (MicroPort, China). A 0.035 guidewire, in conjunction with a single-curve catheter, was used to access the popliteal artery. Subsequently, it was replaced with a 0.035 super-hard guidewire to provide support during the implantation of the stent graft. The stent was deployed precisely at the distal end of the superficial femoral artery, the location with the highest concentration of AVMs. Completion angiography revealed a significant reduction in venous opacification around the stent and clear visualization of the popliteal artery. Postoperatively, the left femoral artery was sutured using a 6 − 0 vascular risk suture, resulting in a significant improvement in the patient’s heart failure symptoms. The patient has heart failure, so the surgery duration should not be excessive. It is planned to perform embolization treatment in the second phase.\n\nOne week post-treatment, ultrasound examination revealed a reduction in volume flow to 1600 ml/min in the CFA, with a BNP level of 1198ug/l. Targeting the nidus with embolization therapy is expected to further decrease the flow velocity of arteriovenous malformations. The right CFA was punctured, allowing the insertion of a 5 F arterial sheath and a 5 F catheter for angiographic examination. Guided by ultrasound, the drainage vein of the AVM was punctured, and a 5 F vascular sheath was introduced. The contrast agent confirmed the presence of a nidus and its draining veins. The embolization procedure of the draining veins involved the use of a coil (18–20 mm x 40 cm, BSX, USA), two microcoils (4 mm x 42 mm, 5 mm x 10 mm, USA), 3% polidocanol (6 mL Kruelle, Germany), and 99% anhydrous ethanol (10 mL).\n\nCompletion angiography showed a significant reduction in the visualization of AVMs and draining veins, indicating their disappearance. During the one-year follow-up, the patient exhibited notable improvement in lower limb swelling and cardiac function. The volume flow in the CFA decreased to 780 ml/min. Echocardiography revealed minor enlargement of the left and right atria, slight mitral and tricuspid regurgitation, and a left ventricular ejection fraction (EF) of 71%. Notably, BNP levels decreased significantly.",
+    "diff_label_texts": "Case summary: A 67-year-old woman with a six-year history of recurrent left lower limb swelling presented with one month of progressive dyspnea and fatigue consistent with acute exacerbation of chronic heart failure. She had no prior cardiovascular disease, trauma, or surgery; remote oral estrogen use occurred seven years earlier. Examination showed marked left leg edema, skin sclerosis, absent popliteal and distal pulses, and a palpable thrill/tremor in the left thigh. Echocardiography demonstrated cardiomegaly with moderate mitral regurgitation, severe tricuspid regurgitation, and LVEF 60%. BNP was 2853 ng/L. ECG showed sinus tachycardia (105 bpm) with left atrial enlargement. Chest CT confirmed cardiomegaly without pulmonary parenchymal disease. CTA revealed a left iliac artery aneurysm (max 32 mm), marked dilation of the CFA (27 mm) and SFA (22 mm), complex AVMs centered on the SFA with early opacification of an enlarged femoral vein, and nonvisualization of the popliteal and anterior tibial arteries. She was diagnosed with complex congenital lower-limb AVMs and acute exacerbation of chronic heart failure, NYHA class IV.\n\nRationale and strategy: Preoperative duplex showed CFA volume flow of 3400 ml/min, indicating a high-flow shunt. Given prior coil embolization (two coils, 20 mm x 40 cm) failed to reduce flow or swelling, the team prioritized rapid shunt reduction using a covered stent, with staged embolization to address the nidus. This approach repurposed an abdominal aortic stent graft to reduce AVM inflow and improve cardiac load while limiting operative time in the setting of heart failure.\n\nProcedure details: To minimize access complications in dilated vessels (iliac 32 mm, CFA 27 mm, SFA 22 mm), antegrade surgical exposure of the CFA was performed under general anesthesia, placing a 14 F sheath. Complex AVMs were visualized in the SFA and profunda femoris with early venous filling. Based on a preoperative SFA mid-segment diameter of 19 mm, a 20–12 mm/120 mm aorto-uni-iliac abdominal aortic covered stent graft (MicroPort, China) was advanced over a 0.035 super-stiff wire (after popliteal access with a single-curve catheter) and deployed at the distal SFA to span the highest AVM density. Completion angiography showed marked reduction of peri-stent venous opacification with clear visualization of the popliteal artery. The femoral arteriotomy was closed with 6-0 vascular suture. The patient’s heart failure symptoms improved postoperatively, and a staged embolization was planned to limit procedure time.\n\nSecond stage and outcomes: At one week, CFA flow decreased to 1600 ml/min and BNP to 1198 µg/L. Transvenous embolization targeted the nidus and draining veins via right CFA arterial access (5 F sheath/catheter) and ultrasound-guided puncture of the AVM drainage vein (5 F venous sheath). Embolic materials included one 18–20 mm x 40 cm coil, two microcoils (4 x 42 mm, 5 x 10 mm), 3% polidocanol (6 mL), and 99% anhydrous ethanol (10 mL). Completion angiography demonstrated near-complete disappearance of AVM/shunting. At one year, leg swelling and cardiac function improved substantially: CFA flow was 780 ml/min; echocardiography showed only mild biatrial enlargement, mild mitral and tricuspid regurgitation, and LVEF 71%; BNP declined markedly.\n\nPractical experience and limitations: In very high-flow, complex congenital lower-limb AVMs causing high-output heart failure, coil-only embolization may be insufficient to meaningfully reduce shunt volume. A covered stent can rapidly downregulate inflow and unload the heart, but often requires adjunctive embolization of the nidus and draining veins to consolidate results. Repurposing an abdominal aortic aorto-uni-iliac covered stent in the SFA is technically feasible but off-label, demands large-bore access (14 F) with surgical exposure, and may be limited by vessel size mismatch, landing zone adequacy, and the need to preserve distal perfusion. Staging is advisable in NYHA IV patients to shorten anesthesia time and manage hemodynamics. This case illustrates that an abdominal aortic stent graft coupled with targeted embolization can effectively address acute heart failure driven by complex congenital lower-limb AVMs, while highlighting device-selection and access considerations that may constrain its use.",
+    "summary": "We present a case involving a patient with congenital AVMs in the lower limb, who had suffered from prolonged swelling in the left lower limb and recently developed symptoms of heart failure. At the age of 67, the patient was definitively diagnosed with a complex congenital AVMs in the lower limb. This article delves into the practical experiences and limitations encountered in employing an abdominal aortic stent graft, coupled with embolization, to address acute heart failure caused by complex congenital AVMs in the lower limb."
+  },
+  {
+    "doc_id": 27,
+    "label": "low_health_literacy",
+    "fulltext": "28-year-old male patient with no significant history presented to the dermatology department with a 48-hour history of a skin condition characterized by two erythematous plaques with central vesicles and superficial ulceration located on the flexor surface of the right arm and forearm equidistant from the elbow crease, accompanied by a burning sensation and pruritus at the site of the lesions. He did not have systemic symptoms or self-medicate. As a background, he reported that he was on vacation in the coastal region of Ecuador at the time of the lesions. An incisional biopsy was performed that reported epidermis with acanthosis, parakeratosis and spongiosis, neutrophils in the stratum corneum and perivascular lymphocyte infiltration in the superficial, middle and deep dermis. Based on the clinical characteristics, the background of travel to a tropical region and the histological findings, a diagnosis of Paederus dermatitis was made. Treatment with antihistamines, topical steroids and cold compresses was indicated. After 8 days of treatment, the lesions resolved, leaving a post-inflammatory hyperpigmentation.\n",
+    "diff_label_texts": "A 28-year-old man had two red patches with small blisters and shallow sores on the inner part of his right arm and forearm for 2 days. The spots burned and itched. He had been on vacation on the coast of Ecuador when this started. The doctor took a small piece of skin to test. The diagnosis was a type of skin irritation called Paederus dermatitis. He was treated with allergy pills, a steroid cream, and cold packs. After 8 days, the rash went away. It left dark marks on the skin.",
+    "summary": "The case of a 28-year-old male patient who presented to the dermatology department with a 48-hour history of two erythematous plaques with central vesicles and superficial ulceration located on the flexor surface of the right arm and forearm, accompanied by a burning sensation and pruritus at the site of the lesions, without accompanying symptoms, is reported. As a background, he stated that he was on vacation in the coastal region of Ecuador at the time of the lesions. An incisional biopsy was performed and, due to the clinical characteristics and the background of travel to a tropical region, the diagnosis was made as dermatitis by Paederus and treatment with antihistamines, topical steroids and cold compresses was indicated. After 8 days of treatment, the lesions subsided, leaving a post-inflammatory hyperpigmentation.\n"
+  },
+  {
+    "doc_id": 27,
+    "label": "proficient_health_literacy",
+    "fulltext": "28-year-old male patient with no significant history presented to the dermatology department with a 48-hour history of a skin condition characterized by two erythematous plaques with central vesicles and superficial ulceration located on the flexor surface of the right arm and forearm equidistant from the elbow crease, accompanied by a burning sensation and pruritus at the site of the lesions. He did not have systemic symptoms or self-medicate. As a background, he reported that he was on vacation in the coastal region of Ecuador at the time of the lesions. An incisional biopsy was performed that reported epidermis with acanthosis, parakeratosis and spongiosis, neutrophils in the stratum corneum and perivascular lymphocyte infiltration in the superficial, middle and deep dermis. Based on the clinical characteristics, the background of travel to a tropical region and the histological findings, a diagnosis of Paederus dermatitis was made. Treatment with antihistamines, topical steroids and cold compresses was indicated. After 8 days of treatment, the lesions resolved, leaving a post-inflammatory hyperpigmentation.\n",
+    "diff_label_texts": "A 28-year-old male with no significant past medical history presented with a 48-hour history of two erythematous plaques with central vesicles and superficial ulceration on the flexor surface of the right arm and forearm, equidistant from the antecubital crease, associated with burning and pruritus. He denied systemic symptoms and had not self-medicated. He reported being on vacation in coastal Ecuador at the time of onset. Incisional biopsy demonstrated epidermal acanthosis, parakeratosis, and spongiosis, neutrophils within the stratum corneum, and perivascular lymphocytic infiltrates in the superficial, mid, and deep dermis. Integrating the clinical morphology, tropical travel history, and histopathology, the diagnosis of Paederus dermatitis was made. Management included antihistamines, topical corticosteroids, and cold compresses. By day 8, the eruption resolved, with residual post-inflammatory hyperpigmentation. Paederus dermatitis is an irritant contact dermatitis due to exposure to Paederus species toxin (pederin), typically producing burning, vesiculation, and superficial erosions; the histologic pattern here (spongiotic dermatitis with mixed inflammatory infiltrates) is consistent with this mechanism.",
+    "summary": "The case of a 28-year-old male patient who presented to the dermatology department with a 48-hour history of two erythematous plaques with central vesicles and superficial ulceration located on the flexor surface of the right arm and forearm, accompanied by a burning sensation and pruritus at the site of the lesions, without accompanying symptoms, is reported. As a background, he stated that he was on vacation in the coastal region of Ecuador at the time of the lesions. An incisional biopsy was performed and, due to the clinical characteristics and the background of travel to a tropical region, the diagnosis was made as dermatitis by Paederus and treatment with antihistamines, topical steroids and cold compresses was indicated. After 8 days of treatment, the lesions subsided, leaving a post-inflammatory hyperpigmentation.\n"
+  },
+  {
+    "doc_id": 28,
+    "label": "low_health_literacy",
+    "fulltext": "Technique\nInformation about the procedure of TFD.\nThe patient receives intravenous photosensitizer (Photogen®, King of Prussia, PA, USA - 1.5 mg/kg) 24 h before the procedure. Its peak light absorption is at the wavelength of 630 nm. The procedure begins with standard duodenoscopy (Olympus TJF-180) under general anesthesia. After the identification of the greater duodenal papilla and the retrograde cannulation, the digital cholangioscope (SpyGlassTM DS, Boston Scientific, Natick, MA) is introduced into the common bile duct. Then the cholangioscopic examination helps to identify the neoplastic stenosis. Under direct visualization, the illumination catheter (Medlight S.A., RD10-323, Switzerland) is advanced through the cholangioscope. This consists of a typical three-way cannula. The first port has a 1 cm long cylindrical light diffuser at the end. Two black radiopaque marks demarcate the limits of the diffuser. The second port accommodates a 0.025 inch guidewire and the third is a portal for injection. After positioning under cholangioscopic guidance, illumination is initiated. The dose is 90 J/cm², with a power of 70 mW/cm². Repositioning is recommended every centimeter to cover the entire stenosed area. At the end of the procedure, new cholangioscopy evaluates the bile duct for immediate outcome and adverse events.\n\nPost-procedure care\nThe patient is fasted for the next 24 h. If no adverse event is detected, oral diet is initiated. Discharge from hospital is done under strict guidance on photoprotection (prevention of exposure to light and use of sunglasses), especially during the first week after the session of TFD.\n\nRESULTS\nThis procedure was performed in an 82-year-old man who presented to our tertiary center with obstructive jaundice and weight loss over the previous two months. Endoscopic ultrasound (EUS) revealed severe dilation of the common bile duct associated with choledocholithiasis. ERCP confirmed these findings but was unable to remove the stones due to the disproportionate dilation of the common bile duct. Therefore, a plastic biliary stent was chosen. The patient showed improvement in his clinical condition, but the cholestasis returned 45 days after the first procedure. Two other ERCPs failed to remove the stones. During the third procedure, a long irregular stenosis of the common hepatic duct was apparent and he was referred for another echoendoscopic evaluation.\n\nIn addition to the choledocholithiasis, the new EUS revealed a dilated common hepatic duct with a well-circumscribed hypoechoic solid mass measuring 1.8x2 cm, which was compressing the common hepatic duct. The mass appeared to also involve the common hepatic artery. An ultrasound-guided needle biopsy confirmed the diagnosis of moderately differentiated cholangiocarcinoma (Bismuth I).\n\nAfter staging, the mass was considered inoperable and the patient was referred for palliative treatment. After a multidisciplinary meeting with the oncology team, adjunctive PDT was proposed to treat the recurrent biliary obstruction. The procedure went without complications and lasted 150 minutes. At the end, a biliary drainage was performed with a 10 Fr plastic stent, since a self-expanding metal stent was not available at that time.\n\nThe patient showed no signs or symptoms of photosensitivity in the following week. There was, however, early recurrence of cholestasis complicated with cholangitis. ERCP revealed obstruction of the stent with debris and biliary sludge secondary to tumor necrosis. A biliary scan followed by new drainage resolved the patient's acute condition. Subsequently, he remained asymptomatic for three months, the longest period since the onset of the disease. At his next recurrence, he was drained with a self-expanding metal stent. He continued with systemic treatment and eventually required a duodenal stent for palliation of dysphagia. He died due to complications of pulmonary metastases two years after the onset of symptoms and 15 months after the session of TFD.\n",
+    "diff_label_texts": "One day before the treatment, you get a light‑activated medicine through a vein. During the visit, the doctor slides a flexible camera through your mouth into your gut. They find the small drain where bile comes out. They thread a tiny camera up into the main bile tube. They look for a tight spot caused by a tumor. They slide a thin light cable to that spot while watching on the screen. They turn on the light and move the cable a small step, about 1 centimeter, each time to cover the whole tight area. At the end, they look again to see how it went and to check for any problems. This treatment was used for an 82‑year‑old man who had yellow skin from blocked bile for two months. Tests showed the main bile tube was very wide and had stones. They also found a firm lump about 1.8 by 2 centimeters pressing on the liver’s main bile tube. Surgery could not fix it. He got this light treatment to ease the blockage. He felt well for three months. He died from complications 15 months after the light treatment.",
+    "summary": "Patient receives intravenous photosensitizer 24 h before the procedure which begins with regular duodenoscopy. After identification of the main papilla and retrograde cannulation, the digital cholangioscope is introduced into the common bile duct. Then the cholangioscopic examination helps to identify neoplastic stenosis. Under direct visualization, the illumination catheter is advanced through the cholangioscope. Repositioning is done every centimeter. At the end of cholangioscopy, the bile duct is evaluated for immediate outcome and adverse events.\n\nResult: This procedure was performed in an 82-year-old man with obstructive jaundice for the past two months. EUS and ERCP revealed severe dilation of the common bile duct associated with choledocholithiasis. In addition, there was dilation of the hepatic duct to a well-circumscribed hypoechoic solid mass measuring 1.8x2 cm, compressing the common hepatic duct. It was considered inoperable and the patient was referred for palliative treatment with PDT, which remained asymptomatic for three months. He died of complications 15 months after the PDT session.\n"
+  },
+  {
+    "doc_id": 28,
+    "label": "proficient_health_literacy",
+    "fulltext": "Technique\nInformation about the procedure of TFD.\nThe patient receives intravenous photosensitizer (Photogen®, King of Prussia, PA, USA - 1.5 mg/kg) 24 h before the procedure. Its peak light absorption is at the wavelength of 630 nm. The procedure begins with standard duodenoscopy (Olympus TJF-180) under general anesthesia. After the identification of the greater duodenal papilla and the retrograde cannulation, the digital cholangioscope (SpyGlassTM DS, Boston Scientific, Natick, MA) is introduced into the common bile duct. Then the cholangioscopic examination helps to identify the neoplastic stenosis. Under direct visualization, the illumination catheter (Medlight S.A., RD10-323, Switzerland) is advanced through the cholangioscope. This consists of a typical three-way cannula. The first port has a 1 cm long cylindrical light diffuser at the end. Two black radiopaque marks demarcate the limits of the diffuser. The second port accommodates a 0.025 inch guidewire and the third is a portal for injection. After positioning under cholangioscopic guidance, illumination is initiated. The dose is 90 J/cm², with a power of 70 mW/cm². Repositioning is recommended every centimeter to cover the entire stenosed area. At the end of the procedure, new cholangioscopy evaluates the bile duct for immediate outcome and adverse events.\n\nPost-procedure care\nThe patient is fasted for the next 24 h. If no adverse event is detected, oral diet is initiated. Discharge from hospital is done under strict guidance on photoprotection (prevention of exposure to light and use of sunglasses), especially during the first week after the session of TFD.\n\nRESULTS\nThis procedure was performed in an 82-year-old man who presented to our tertiary center with obstructive jaundice and weight loss over the previous two months. Endoscopic ultrasound (EUS) revealed severe dilation of the common bile duct associated with choledocholithiasis. ERCP confirmed these findings but was unable to remove the stones due to the disproportionate dilation of the common bile duct. Therefore, a plastic biliary stent was chosen. The patient showed improvement in his clinical condition, but the cholestasis returned 45 days after the first procedure. Two other ERCPs failed to remove the stones. During the third procedure, a long irregular stenosis of the common hepatic duct was apparent and he was referred for another echoendoscopic evaluation.\n\nIn addition to the choledocholithiasis, the new EUS revealed a dilated common hepatic duct with a well-circumscribed hypoechoic solid mass measuring 1.8x2 cm, which was compressing the common hepatic duct. The mass appeared to also involve the common hepatic artery. An ultrasound-guided needle biopsy confirmed the diagnosis of moderately differentiated cholangiocarcinoma (Bismuth I).\n\nAfter staging, the mass was considered inoperable and the patient was referred for palliative treatment. After a multidisciplinary meeting with the oncology team, adjunctive PDT was proposed to treat the recurrent biliary obstruction. The procedure went without complications and lasted 150 minutes. At the end, a biliary drainage was performed with a 10 Fr plastic stent, since a self-expanding metal stent was not available at that time.\n\nThe patient showed no signs or symptoms of photosensitivity in the following week. There was, however, early recurrence of cholestasis complicated with cholangitis. ERCP revealed obstruction of the stent with debris and biliary sludge secondary to tumor necrosis. A biliary scan followed by new drainage resolved the patient's acute condition. Subsequently, he remained asymptomatic for three months, the longest period since the onset of the disease. At his next recurrence, he was drained with a self-expanding metal stent. He continued with systemic treatment and eventually required a duodenal stent for palliation of dysphagia. He died due to complications of pulmonary metastases two years after the onset of symptoms and 15 months after the session of TFD.\n",
+    "diff_label_texts": "Technique (TFD/PDT): The patient receives intravenous photosensitizer (Photogen, 1.5 mg/kg) 24 h pre‑procedure; peak absorption is 630 nm. Under general anesthesia, standard duodenoscopy (Olympus TJF‑180) is performed. After identification of the greater duodenal papilla and retrograde cannulation, a digital cholangioscope (SpyGlass DS, Boston Scientific) is introduced into the common bile duct. Cholangioscopy is used to identify the neoplastic stenosis. Under direct visualization, the illumination catheter (Medlight S.A., RD10‑323) is advanced through the cholangioscope. The catheter is a three‑way cannula: port 1 carries a 1‑cm cylindrical light diffuser with two black radiopaque markers denoting its limits; port 2 accommodates a 0.025‑inch guidewire; port 3 is an injection portal. Following cholangioscopic positioning, illumination is delivered at 90 J/cm² with power of 70 mW/cm², with 1‑cm stepwise repositioning to cover the entire stenosed segment. Completion cholangioscopy assesses immediate outcome and adverse events. Post‑procedure care: patients are fasted for 24 h; if no adverse events occur, oral intake is resumed. Discharge includes strict photoprotection instructions (avoidance of light exposure and use of sunglasses), especially during the first week after TFD. Results/Case: An 82‑year‑old man presented with a 2‑month history of obstructive jaundice and weight loss. EUS showed severe dilation of the common bile duct with choledocholithiasis; ERCP confirmed these findings but stone extraction was unsuccessful due to disproportionate ductal dilation, so a plastic biliary stent was placed. Cholestasis recurred 45 days later; two additional ERCPs failed to clear stones. During the third ERCP, a long irregular CHD stenosis was noted, prompting repeat EUS. Repeat EUS revealed a well‑circumscribed hypoechoic solid mass (1.8 × 2 cm) compressing the common hepatic duct, with apparent involvement of the common hepatic artery. Ultrasound‑guided needle biopsy confirmed moderately differentiated cholangiocarcinoma (Bismuth I). After staging, the lesion was deemed unresectable and the patient was referred for palliative therapy. Following multidisciplinary discussion, adjunctive PDT was performed to treat recurrent biliary obstruction. The procedure lasted 150 minutes without complications. A 10 Fr plastic stent was placed for biliary drainage (SEMS unavailable at that time). No photosensitivity occurred in the subsequent week. Early recurrence of cholestasis with cholangitis ensued; ERCP demonstrated stent occlusion by debris and biliary sludge secondary to tumor necrosis. A biliary scan and re‑drainage resolved the acute episode. He then remained asymptomatic for three months—the longest interval since symptom onset. At subsequent recurrence, a self‑expanding metal stent was placed. He continued systemic therapy and later required a duodenal stent for palliation of dysphagia. He died from complications of pulmonary metastases two years after symptom onset and 15 months after the TFD session. Mechanistic context: PDT activates the photosensitizer at 630 nm to generate reactive oxygen species, inducing localized tumor cytotoxicity and microvascular damage, which can debulk malignant biliary strictures and improve ductal patency.",
+    "summary": "Patient receives intravenous photosensitizer 24 h before the procedure which begins with regular duodenoscopy. After identification of the main papilla and retrograde cannulation, the digital cholangioscope is introduced into the common bile duct. Then the cholangioscopic examination helps to identify neoplastic stenosis. Under direct visualization, the illumination catheter is advanced through the cholangioscope. Repositioning is done every centimeter. At the end of cholangioscopy, the bile duct is evaluated for immediate outcome and adverse events.\n\nResult: This procedure was performed in an 82-year-old man with obstructive jaundice for the past two months. EUS and ERCP revealed severe dilation of the common bile duct associated with choledocholithiasis. In addition, there was dilation of the hepatic duct to a well-circumscribed hypoechoic solid mass measuring 1.8x2 cm, compressing the common hepatic duct. It was considered inoperable and the patient was referred for palliative treatment with PDT, which remained asymptomatic for three months. He died of complications 15 months after the PDT session.\n"
+  },
+  {
+    "doc_id": 29,
+    "label": "proficient_health_literacy",
+    "fulltext": "A 77-year-old woman with haematemesis presented to the emergency room. Her medical history included only hypertension and dyslipidaemia. When she presented to the emergency room, her vital signs indicated shock (heart rate: 100 beats/min, blood pressure: 79/56 mmHg), and blood tests revealed anaemia (haemoglobin: 9.6 g/dL), which suggested upper gastrointestinal bleeding.\n\nNon-contrast-enhanced CT was performed immediately because of renal dysfunction. CT revealed that the third part of the duodenum flexed steeply on the right side of the aorta and ran caudally, without crossing anterior to the aorta. The jejunum was located on the patient’s right side. The second part of the duodenum and the stomach were dilated, and there were high-density gastric contents that were considered to indicate a haematoma.\n\nUpper gastrointestinal endoscopy was performed following the CT examination, which revealed a mucosal laceration at the gastric cardia. Bleeding from lacerations of the cardia of the stomach as a result of forceful vomiting was first reported by Mallory and Weiss in 1929.1 In our case, the third part of the duodenum flexed steeply, and the lumen was narrowed, which caused an obstruction. As a result, repeat vomiting was considered to have caused Mallory–Weiss syndrome.\n\nOn the basis of the CT findings showing that the duodenal-jejunal junction was located in the right hemi-abdomen, intestinal malrotation was suspected.2 However, 7 days later, when CT was repeated, spontaneous resolution of the malpositioned jejunum was seen. The patient was then discharged from the hospital. However, months later, she was rushed to the emergency room for repeat haematemesis. Dynamic CT was performed before upper gastrointestinal endoscopy, on admission, and revealed contrast extravasation in the dilated stomach. Additionally, the third part of the duodenum was flexed on the right side of the aorta, and the duodenal-jejunal junction and jejunum were again located in the right hemi-abdomen. Upper gastrointestinal endoscopy revealed a laceration at the gastric cardia, as in the previous endoscopy, which was considered Mallory–Weiss syndrome.\n\nTwo months after the second episode of haematemesis, the patient presented to the emergency room with nausea. Non-contrast-enhanced CT revealed no abnormalities in the duodenal positioning, but there was oedematous wall thickening in the second part of the duodenum. If we had not had previous CT images, we would have suspected duodenitis, but on the basis of all of the CT findings, we suspected the possibility of an underlying condition after the right-sided deviation of the small intestine had resolved spontaneously.\n\nIn summary, CT was performed 4 times over 5 months. The third and fourth parts of the duodenum and the jejunum deviated repeatedly, but this resolved spontaneously, which is not indicative of intestinal malrotation. Therefore, we diagnosed dysplasia of the ligament of Treitz.\n\nClinical outcomes\nThe patient underwent laparotomy, which revealed no abnormalities in the relative position of the duodenum to the jejunum. Additionally, the jejunum was located on the patient’s left side, and there was no intestinal malrotation. The ligament of Treitz was formed; however, its fixation in the upper jejunum was incomplete as it was attached only to the duodenum. The duodenal-jejunal junction was not fixed to the retroperitoneum, and the jejunum folded easily with the ligament of Treitz as a fulcrum. Surgically, the upper jejunum was fixed with 4 sutures to the retroperitoneum on the patient’s left side. The postoperative course was good, and the patient has remained symptom-free.",
+    "diff_label_texts": "A 77-year-old woman with haematemesis presented in shock (heart rate 100 beats/min, blood pressure 79/56 mmHg) with anaemia (haemoglobin 9.6 g/dL), consistent with upper gastrointestinal bleeding. Because of renal dysfunction, non-contrast CT was obtained and demonstrated the third portion of the duodenum flexed steeply on the right side of the aorta and coursing caudally without crossing anterior to the aorta. The duodenojejunal (DJ) junction and the jejunum were in the right hemi-abdomen. The second portion of the duodenum and the stomach were dilated, and high-density gastric contents suggested haematoma. Esophagogastroduodenoscopy showed a mucosal laceration at the gastric cardia, consistent with Mallory–Weiss syndrome; in this case, steep flexion with luminal narrowing of the third portion likely caused transient obstruction and repeated vomiting precipitating the tear. Seven days later, repeat CT showed spontaneous resolution of the malpositioned jejunum. Months later she re-presented with haematemesis; dynamic CT on admission demonstrated contrast extravasation in a dilated stomach and again showed the third portion of the duodenum flexed on the right of the aorta with the DJ junction and jejunum in the right hemi-abdomen. Endoscopy again revealed a cardia laceration. Two months after the second haematemesis, she presented with nausea; non-contrast CT showed normal duodenal positioning but oedematous wall thickening in the second portion. Over four CT examinations spanning five months, the third and fourth portions of the duodenum and the jejunum repeatedly deviated to the right and then spontaneously returned to normal position, a pattern incompatible with fixed intestinal malrotation. Dysplasia (incomplete fixation) of the ligament of Treitz was diagnosed. Laparotomy found no intestinal malrotation: the ligament of Treitz was formed, but fixation in the upper jejunum was incomplete (attached only to the duodenum); the DJ junction was not fixed to the retroperitoneum, and the jejunum folded readily with the ligament as a fulcrum. CT also indicated a loosely fixed, mobile anterior pararenal space. These anatomic factors likely permitted intermittent right-sided deviation of the small intestine. Surgically, the upper jejunum was fixed with four sutures to the left retroperitoneum; the postoperative course was uneventful, and she remained symptom-free.",
+    "summary": "A 77-year-old woman underwent CT to evaluate haematemesis. The images showed that the third part of the duodenum flexed steeply on the right side of the aorta and ran caudally, without crossing anterior to the aorta. The duodenal-jejunal junction and jejunum were located on the patient's right side. Upper gastrointestinal endoscopy revealed a laceration at the gastric cardia, and a diagnosis of Mallory-Weiss syndrome was made. Repeat CT 7 days later revealed that the abnormal positioning of the intestinal tract had resolved spontaneously. Two months later, the patient experienced another episode of haematemesis, and CT revealed repeat deviation of the duodenal-jejunal junction and jejunum to her right side. Upper gastrointestinal endoscopy revealed another laceration at the gastric cardia, as in the previous study. On the basis of the initial CT findings showing the duodenal-jejunal junction in the right hemi-abdomen, intestinal malrotation was suspected. However, because the jejunum deviated repeatedly to the right side but resolved spontaneously, we diagnosed dysplasia of the ligament of Treitz. Laparotomy revealed a formed ligament of Treitz; however, fixation in the upper jejunum was incomplete. Additionally, CT revealed that the anterior pararenal space was loosely fixed and mobile. These factors may have caused the right-sided deviation of the small intestine."
+  },
+  {
+    "doc_id": 30,
+    "label": "low_health_literacy",
+    "fulltext": "Patient and observation\nPatient information (presentation of the patient): he is a 28-year-old single man without children, an active military. He has been present for 5 weeks with progressive abdominal pain, more marked in the epigastrium and the right hypochondrium, followed shortly after by a non-quantified fever, chills, profuse sweats in a context of anorexia and weight loss of 6 kg. Note that the patient is not a drinker or smoker, vaccinated with BCG and has no other contributing personal or family history.\n\nClinical findings: On admission, the physical examination found the patient in a general altered state, asthenic with a weight loss of 6 kg in one month. A clinical systemic inflammatory response syndrome was present with the following elements: a fever of 39.1 °C, tachycardia (124 beats/min), polypnea (22 cycles/min). The pulmonary examination and exploration of the superficial lymph node areas were without particularity. In the abdominal area, moderate sensitivity in the right hypochondrium with hepatomegaly was found.\n\nChronology: dates back to February 2022 with the onset of diffuse abdominal pain with diarrhea-constipation transit disorder, all in a context of preservation of general condition with low-grade fever predominantly at night. A syntagmatic treatment was unsuccessfully initiated. The evolution is marked by the persistence of low-grade fever associated with anorexia and progressive weight loss of 12 kg over three months. In the face of this transit disorder with unexplained fever and the deterioration of the general condition, the patient will be admitted to the emergency department for further investigation.\n\nDiagnostic approach: upon admission, a biological infectious syndrome was reported with a neutrophilic predominant hyperleucocytosis (17800 cells/mm3) and a high C-reactive protein of 323 mg/L.\n\nIn the face of his abdominal pain, the lipase and troponin tests were normal at 38 IU/L (VN: <3 78 IU/L) and 4 ng/L (VN: 2 to 16 ng/L) respectively. The liver function was stable with ALT (alanine amino transferase) at 22 IU/L (VN: < 40UI/L), AST (aspartate amino transferase) at 17 IU/L (VN: < 35UI/L), GGT (gamma glutamyl transferase) at 42 IU/L (VN: < 50UI/L), PAL (alkaline phosphatase) at 115 IU/L (VN: 40- 150 IU/L) and normal bilirubinemia. The liver function was normal with a prothrombin rate of 78% and an albuminemia of 39 g/L. The blood ionogram and renal function were normal. The chest radiograph and abdominal ultrasound were without particularity.\n\nWith a procalcitonin positive at 4.1 ng/L, an infectious disease assessment to search for the infectious focus was initiated, including a cytobacteriological examination of urine and blood cultures during the febrile peaks at 39°C, which were both negative. The hepatitis viral B, C and HIV serologies, as well as the syphilis serology performed in hospital were all negative. The lactate dehydrogenase (LDH) and beta-2 microglobulin were normal at 231 IU/L and 2.28 mg/L respectively. The GeneXpert to search for the Mycobacterium on these bioptic pieces was negative. The quantiferon was negative. The search for the Mycobacterium on the morning expectorations of 3 consecutive days was negative.\n\nOn the morphological level, a thoraco-abdomino-pelvic scan showed an enlarged liver (hepatic arrow at 17 cm), the site of multiple, well-defined, rounded hypodensities, which were not enhanced after injection of the contrast agent. The largest lesions were in segment I (21 x 16 mm) and segment V (36 x 27 mm). No suspicious lesions were detected in the thoracic and pelvic levels. The first liver biopsies obtained by echo-guided puncture revealed subacute, fibro-inflammatory liver lesions, with no histological evidence of specificity or malignancy.\n\nA liver MRI following the scan objectified a dysmorphic liver, the site of lesions in heterogeneous signal T2 surrounded by a wall in hyper signal T2, enhanced in the periphery after injection of the contrast agent, the largest of which is located in segment I (20 x 22 mm) and in segment V (33 x 31 mm). No deep lymphadenopathy had been objectified, either in the scan or in the MRI. A diagnostic laparoscopy performed on the hepatic nodules, the histological examination found epithelioid and gigantocellular granulomas of varying size with caseous necrosis in favour of a hepatic tuberculosis.\n\nTherapeutic intervention: the patient was put on anti-tuberculosis treatment according to the standard protocol for months: Phase 1: quadritherapy (Isoniazide + Rifampicine + Pyrazinamide + Ethambutol) in a single oral intake each morning on an empty stomach for 2 months. Phase 2: bithrapia (Isoniazide + Rifampicine) in a single oral intake each morning on an empty stomach for 4 months\n\nFollow-up and results of therapeutic interventions: from the first days of treatment, a good response was obtained with disappearance of the inflammatory syndrome with systemic response both clinically and biologically. After three months of treatment, a control scan of the liver showed a decrease in the number and volume of liver lesions.\n",
+    "diff_label_texts": "A young man from Morocco had strong liver pain for about a month. He also had mild signs that can come with TB infection. Scans of his belly showed small spots in his liver. Doctors used a small camera surgery to take a tiny piece from one of the spots. The test on that piece proved the spots were TB in the liver. He started TB medicines. He felt better, and his blood tests got better too.",
+    "summary": "This clinical case was reported in a young Moroccan, presenting a picture of hepatic colic that had been developing for a month, associated with subtle signs of tuberculous infection. Non-specific hepatic nodular lesions were revealed on the scanner and on the hepatic magnetic resonance imaging (MRI). The diagnosis of focal hepatic tuberculosis was confirmed after pathological analysis of hepatic nodule biopsies obtained after a laparoscopy. After the start of well-conducted anti-bacillary treatment, a good clinical-biological improvement was obtained.\n"
+  },
+  {
+    "doc_id": 30,
+    "label": "intermediate_health_literacy",
+    "fulltext": "Patient and observation\nPatient information (presentation of the patient): he is a 28-year-old single man without children, an active military. He has been present for 5 weeks with progressive abdominal pain, more marked in the epigastrium and the right hypochondrium, followed shortly after by a non-quantified fever, chills, profuse sweats in a context of anorexia and weight loss of 6 kg. Note that the patient is not a drinker or smoker, vaccinated with BCG and has no other contributing personal or family history.\n\nClinical findings: On admission, the physical examination found the patient in a general altered state, asthenic with a weight loss of 6 kg in one month. A clinical systemic inflammatory response syndrome was present with the following elements: a fever of 39.1 °C, tachycardia (124 beats/min), polypnea (22 cycles/min). The pulmonary examination and exploration of the superficial lymph node areas were without particularity. In the abdominal area, moderate sensitivity in the right hypochondrium with hepatomegaly was found.\n\nChronology: dates back to February 2022 with the onset of diffuse abdominal pain with diarrhea-constipation transit disorder, all in a context of preservation of general condition with low-grade fever predominantly at night. A syntagmatic treatment was unsuccessfully initiated. The evolution is marked by the persistence of low-grade fever associated with anorexia and progressive weight loss of 12 kg over three months. In the face of this transit disorder with unexplained fever and the deterioration of the general condition, the patient will be admitted to the emergency department for further investigation.\n\nDiagnostic approach: upon admission, a biological infectious syndrome was reported with a neutrophilic predominant hyperleucocytosis (17800 cells/mm3) and a high C-reactive protein of 323 mg/L.\n\nIn the face of his abdominal pain, the lipase and troponin tests were normal at 38 IU/L (VN: <3 78 IU/L) and 4 ng/L (VN: 2 to 16 ng/L) respectively. The liver function was stable with ALT (alanine amino transferase) at 22 IU/L (VN: < 40UI/L), AST (aspartate amino transferase) at 17 IU/L (VN: < 35UI/L), GGT (gamma glutamyl transferase) at 42 IU/L (VN: < 50UI/L), PAL (alkaline phosphatase) at 115 IU/L (VN: 40- 150 IU/L) and normal bilirubinemia. The liver function was normal with a prothrombin rate of 78% and an albuminemia of 39 g/L. The blood ionogram and renal function were normal. The chest radiograph and abdominal ultrasound were without particularity.\n\nWith a procalcitonin positive at 4.1 ng/L, an infectious disease assessment to search for the infectious focus was initiated, including a cytobacteriological examination of urine and blood cultures during the febrile peaks at 39°C, which were both negative. The hepatitis viral B, C and HIV serologies, as well as the syphilis serology performed in hospital were all negative. The lactate dehydrogenase (LDH) and beta-2 microglobulin were normal at 231 IU/L and 2.28 mg/L respectively. The GeneXpert to search for the Mycobacterium on these bioptic pieces was negative. The quantiferon was negative. The search for the Mycobacterium on the morning expectorations of 3 consecutive days was negative.\n\nOn the morphological level, a thoraco-abdomino-pelvic scan showed an enlarged liver (hepatic arrow at 17 cm), the site of multiple, well-defined, rounded hypodensities, which were not enhanced after injection of the contrast agent. The largest lesions were in segment I (21 x 16 mm) and segment V (36 x 27 mm). No suspicious lesions were detected in the thoracic and pelvic levels. The first liver biopsies obtained by echo-guided puncture revealed subacute, fibro-inflammatory liver lesions, with no histological evidence of specificity or malignancy.\n\nA liver MRI following the scan objectified a dysmorphic liver, the site of lesions in heterogeneous signal T2 surrounded by a wall in hyper signal T2, enhanced in the periphery after injection of the contrast agent, the largest of which is located in segment I (20 x 22 mm) and in segment V (33 x 31 mm). No deep lymphadenopathy had been objectified, either in the scan or in the MRI. A diagnostic laparoscopy performed on the hepatic nodules, the histological examination found epithelioid and gigantocellular granulomas of varying size with caseous necrosis in favour of a hepatic tuberculosis.\n\nTherapeutic intervention: the patient was put on anti-tuberculosis treatment according to the standard protocol for months: Phase 1: quadritherapy (Isoniazide + Rifampicine + Pyrazinamide + Ethambutol) in a single oral intake each morning on an empty stomach for 2 months. Phase 2: bithrapia (Isoniazide + Rifampicine) in a single oral intake each morning on an empty stomach for 4 months\n\nFollow-up and results of therapeutic interventions: from the first days of treatment, a good response was obtained with disappearance of the inflammatory syndrome with systemic response both clinically and biologically. After three months of treatment, a control scan of the liver showed a decrease in the number and volume of liver lesions.\n",
+    "diff_label_texts": "A 28-year-old Moroccan man developed about a month of liver-area pain along with fever, night sweats, and weight loss, which are symptoms that can suggest tuberculosis. CT and MRI showed multiple non-specific nodules in the liver. An initial needle biopsy was not conclusive, so doctors performed a laparoscopy to obtain better tissue samples. Pathology showed granulomas with caseous necrosis, confirming focal hepatic tuberculosis. He started standard anti-tuberculosis therapy: two months of four drugs, then four months of two drugs. He improved quickly, both in how he felt and in his lab results. A follow-up scan at three months showed that the liver nodules were fewer and smaller.",
+    "summary": "This clinical case was reported in a young Moroccan, presenting a picture of hepatic colic that had been developing for a month, associated with subtle signs of tuberculous infection. Non-specific hepatic nodular lesions were revealed on the scanner and on the hepatic magnetic resonance imaging (MRI). The diagnosis of focal hepatic tuberculosis was confirmed after pathological analysis of hepatic nodule biopsies obtained after a laparoscopy. After the start of well-conducted anti-bacillary treatment, a good clinical-biological improvement was obtained.\n"
+  },
+  {
+    "doc_id": 30,
+    "label": "proficient_health_literacy",
+    "fulltext": "Patient and observation\nPatient information (presentation of the patient): he is a 28-year-old single man without children, an active military. He has been present for 5 weeks with progressive abdominal pain, more marked in the epigastrium and the right hypochondrium, followed shortly after by a non-quantified fever, chills, profuse sweats in a context of anorexia and weight loss of 6 kg. Note that the patient is not a drinker or smoker, vaccinated with BCG and has no other contributing personal or family history.\n\nClinical findings: On admission, the physical examination found the patient in a general altered state, asthenic with a weight loss of 6 kg in one month. A clinical systemic inflammatory response syndrome was present with the following elements: a fever of 39.1 °C, tachycardia (124 beats/min), polypnea (22 cycles/min). The pulmonary examination and exploration of the superficial lymph node areas were without particularity. In the abdominal area, moderate sensitivity in the right hypochondrium with hepatomegaly was found.\n\nChronology: dates back to February 2022 with the onset of diffuse abdominal pain with diarrhea-constipation transit disorder, all in a context of preservation of general condition with low-grade fever predominantly at night. A syntagmatic treatment was unsuccessfully initiated. The evolution is marked by the persistence of low-grade fever associated with anorexia and progressive weight loss of 12 kg over three months. In the face of this transit disorder with unexplained fever and the deterioration of the general condition, the patient will be admitted to the emergency department for further investigation.\n\nDiagnostic approach: upon admission, a biological infectious syndrome was reported with a neutrophilic predominant hyperleucocytosis (17800 cells/mm3) and a high C-reactive protein of 323 mg/L.\n\nIn the face of his abdominal pain, the lipase and troponin tests were normal at 38 IU/L (VN: <3 78 IU/L) and 4 ng/L (VN: 2 to 16 ng/L) respectively. The liver function was stable with ALT (alanine amino transferase) at 22 IU/L (VN: < 40UI/L), AST (aspartate amino transferase) at 17 IU/L (VN: < 35UI/L), GGT (gamma glutamyl transferase) at 42 IU/L (VN: < 50UI/L), PAL (alkaline phosphatase) at 115 IU/L (VN: 40- 150 IU/L) and normal bilirubinemia. The liver function was normal with a prothrombin rate of 78% and an albuminemia of 39 g/L. The blood ionogram and renal function were normal. The chest radiograph and abdominal ultrasound were without particularity.\n\nWith a procalcitonin positive at 4.1 ng/L, an infectious disease assessment to search for the infectious focus was initiated, including a cytobacteriological examination of urine and blood cultures during the febrile peaks at 39°C, which were both negative. The hepatitis viral B, C and HIV serologies, as well as the syphilis serology performed in hospital were all negative. The lactate dehydrogenase (LDH) and beta-2 microglobulin were normal at 231 IU/L and 2.28 mg/L respectively. The GeneXpert to search for the Mycobacterium on these bioptic pieces was negative. The quantiferon was negative. The search for the Mycobacterium on the morning expectorations of 3 consecutive days was negative.\n\nOn the morphological level, a thoraco-abdomino-pelvic scan showed an enlarged liver (hepatic arrow at 17 cm), the site of multiple, well-defined, rounded hypodensities, which were not enhanced after injection of the contrast agent. The largest lesions were in segment I (21 x 16 mm) and segment V (36 x 27 mm). No suspicious lesions were detected in the thoracic and pelvic levels. The first liver biopsies obtained by echo-guided puncture revealed subacute, fibro-inflammatory liver lesions, with no histological evidence of specificity or malignancy.\n\nA liver MRI following the scan objectified a dysmorphic liver, the site of lesions in heterogeneous signal T2 surrounded by a wall in hyper signal T2, enhanced in the periphery after injection of the contrast agent, the largest of which is located in segment I (20 x 22 mm) and in segment V (33 x 31 mm). No deep lymphadenopathy had been objectified, either in the scan or in the MRI. A diagnostic laparoscopy performed on the hepatic nodules, the histological examination found epithelioid and gigantocellular granulomas of varying size with caseous necrosis in favour of a hepatic tuberculosis.\n\nTherapeutic intervention: the patient was put on anti-tuberculosis treatment according to the standard protocol for months: Phase 1: quadritherapy (Isoniazide + Rifampicine + Pyrazinamide + Ethambutol) in a single oral intake each morning on an empty stomach for 2 months. Phase 2: bithrapia (Isoniazide + Rifampicine) in a single oral intake each morning on an empty stomach for 4 months\n\nFollow-up and results of therapeutic interventions: from the first days of treatment, a good response was obtained with disappearance of the inflammatory syndrome with systemic response both clinically and biologically. After three months of treatment, a control scan of the liver showed a decrease in the number and volume of liver lesions.\n",
+    "diff_label_texts": "A 28-year-old Moroccan active-duty military male, BCG-vaccinated and without alcohol or tobacco use or relevant comorbidities, presented after 5 weeks of progressive abdominal pain maximal in the epigastrium and right hypochondrium, accompanied by fever, chills, profuse sweats, anorexia, and weight loss. On admission, he had SIRS with T 39.1 °C, HR 124 bpm, RR 22/min, and right hypochondrial tenderness with hepatomegaly; pulmonary exam and superficial lymph node survey were unremarkable. Laboratory data showed neutrophil-predominant leukocytosis (17,800/mm3) and markedly elevated CRP (323 mg/L), with normal lipase (38 IU/L), troponin (4 ng/L), LFTs (ALT 22 IU/L, AST 17 IU/L, GGT 42 IU/L, ALP 115 IU/L, normal bilirubin), PT 78%, albumin 39 g/L, normal electrolytes and renal function, LDH 231 IU/L, and beta-2 microglobulin 2.28 mg/L. Procalcitonin was 4.1 ng/L. Infectious workup including blood and urine cultures during febrile peaks, HBV/HCV/HIV and syphilis serologies, Quantiferon, GeneXpert on biopsy material, and three consecutive morning sputum examinations for mycobacteria were negative. Chest radiograph and abdominal ultrasound were unrevealing.\n\nCross-sectional imaging demonstrated non-specific focal hepatic lesions. Thoraco-abdomino-pelvic CT showed hepatomegaly (liver long axis 17 cm) with multiple, well-circumscribed rounded hypodense lesions lacking post-contrast enhancement; largest lesions were in segment I (21 × 16 mm) and segment V (36 × 27 mm). No suspicious thoracic or pelvic lesions were identified. Initial echo-guided liver biopsies showed subacute fibro-inflammatory changes without specific histology or malignancy. Liver MRI revealed a dysmorphic liver containing lesions with heterogeneous T2 signal, a hyperintense T2 rim, and peripheral enhancement after contrast; the largest lesions were in segment I (20 × 22 mm) and segment V (33 × 31 mm). No deep lymphadenopathy was seen on CT or MRI. Diagnostic laparoscopy with targeted biopsies demonstrated epithelioid and multinucleated giant-cell granulomas of varying size with caseous necrosis, confirming focal hepatic tuberculosis.\n\nTreatment followed a standard anti-tuberculosis regimen: Phase 1 with isoniazid, rifampicin, pyrazinamide, and ethambutol once daily fasting for 2 months, followed by Phase 2 with isoniazid and rifampicin once daily fasting for 4 months. Clinical and biological improvement occurred within days, with resolution of the inflammatory response. At 3 months, control CT showed a decrease in both number and size of the hepatic lesions. This case underscores that focal hepatic TB can present with non-specific hepatic nodules on imaging and often requires histopathologic confirmation when microbiological tests are negative.",
+    "summary": "This clinical case was reported in a young Moroccan, presenting a picture of hepatic colic that had been developing for a month, associated with subtle signs of tuberculous infection. Non-specific hepatic nodular lesions were revealed on the scanner and on the hepatic magnetic resonance imaging (MRI). The diagnosis of focal hepatic tuberculosis was confirmed after pathological analysis of hepatic nodule biopsies obtained after a laparoscopy. After the start of well-conducted anti-bacillary treatment, a good clinical-biological improvement was obtained.\n"
+  },
+  {
+    "doc_id": 31,
+    "label": "low_health_literacy",
+    "fulltext": "A 12-year-old boy with Down Syndrome and motoric disorders was referred from the Pediatric Department to the Oral Medicine Department of RS Hasan Sadikin Bandung. The patient was diagnosed with Down Syndrome and myeloradiculopathy. The patient’s mother said that the patient was admitted to the hospital because of weakness in both patient’s hands and feet. The patient had a history of falling down about one year ago. The patient’s mother also had a difficulty in cleaning the patient’s oral cavity regularly.\n\nIn the extraoral examination, the patient had a dysmorphic face. The patient also had a cracking and desquamative condition of the vermillion border of the lips. Lymph node examination could not be assessed because the patient wore a cervical collar. The intraoral examination showed an irregular ulcer with 1×0.7 cm in diameter, indurated margin, and white-yellowish base at the right lateral border of the tongue. There was dentinal caries on 63 tooth and also the tooth remnants on 55, 62, 74, and 85 teeth. The upper and lower tooth remnants were suggested to be extracted by pediatric dentist. The space of the extracted teeth will be maintained using a space maintainer. The 55 tooth was sharp and caused an occlusion trauma to the right lateral border of the tongue.\n\nLaboratory examination showed a decrease in sodium value (130 mEq/L) and an increase in lymphocyte value (46%). The MRI examination was performed in the Radiology Department to determine the presence of abnormalities in the cervical spine. The results of the MRI examination showed a dislocation of the patient’s cervical spine. The patient’s mother provided informed consent to publish the patient’s case details and any accompanying images.\n\nBased on the history review, the clinical examination, and appropriate investigation, the patient was diagnosed with a chronic traumatic ulcer mimicking OSCC, exfoliative cheilitis, reversible pulpitis of 63 teeth, and radix gangrene on 55, 62, 74, and 85 teeth. The diagnosis of the chronic ulcer was based on clinical examination. There was an indurated margin in the traumatic lesion, which mimicked Oral Squamous Cell Carcinoma clinically. The patient has been hospitalized for 4 days and was given paracetamol 120 mg/5 mL oral suspension and amoxicillin 125 mg/5 mL oral suspension from the Pediatric Department. The patient also was given sodium chloride 0.9% solution, povidone-iodine mouthwash 1%, and petroleum jelly from the Oral Medicine Department. The patient’s mother was instructed to clean the patient’s oral cavity using gauze soaked in sodium chloride 0.9% solution, compress the ulcer using povidone-iodine mouthwashes 1% three times a day as an antiseptic and anti-inflammatory agent to the oral ulcer, and apply petroleum jelly to moisturize the patient’s lips. The patient was also suggested to extract the 55, 62, 74, and 85 teeth.\n\nIn the second visit (3 days follow-up), oral lesions already showed improvement. In the third visit (1-week follow-up), the size of the oral ulcer at the lateral border of the tongue was getting smaller and the lesion of the lips had some improvement.\n\nIn the fourth visit (10 days follow-up), the size of the oral ulcer at the lateral border of the tongue already had significant improvement. Two days after the fourth visit, the patient underwent neurosurgery. The patient was observed in the Pediatric Intensive Care Unit postoperatively. After two weeks of observation in the Pediatric Intensive Care Unit, the experienced respiratory failure and was declared dead.",
+    "diff_label_texts": "A 12-year-old boy with Down Syndrome and movement problems went to the mouth doctor. His face looked different. His lips were very dry. The doctor could not feel the neck glands because he wore a neck brace. Inside his mouth, there was a sore on the right side of his tongue. It was about 1 by 0.7 centimeters. The edge felt hard. The bottom looked white-yellow. A sharp baby tooth kept rubbing and biting that spot on his tongue. This made a long-lasting injury sore that can look like mouth cancer, but it was from repeated rubbing. The team gave 0.9% salt-water solution, 1% iodine mouthwash, and petroleum jelly for his lips.",
+    "summary": "A 12-year-old boy with Down Syndrome and motoric disorders was referred to Oral Medicine Department. In the extraoral examination, the patient had a dysmorphic face and dry lips. Lymph node examination could not be assessed because the patient wore a cervical collar. The intraoral examination showed an irregular ulcer with 1×0.7 cm in diameter, indurated margin, and white-yellowish base at the right lateral border of the tongue. The 55 teeth were sharp and caused an occlusion trauma to the right lateral border of the tongue. The patient was diagnosed with a chronic traumatic ulcer mimicking OSCC based on clinical examination. The medication given to the patient were sodium chloride 0.9%, povidone-iodine mouthwash 1%, and petroleum jelly."
+  },
+  {
+    "doc_id": 31,
+    "label": "proficient_health_literacy",
+    "fulltext": "A 12-year-old boy with Down Syndrome and motoric disorders was referred from the Pediatric Department to the Oral Medicine Department of RS Hasan Sadikin Bandung. The patient was diagnosed with Down Syndrome and myeloradiculopathy. The patient’s mother said that the patient was admitted to the hospital because of weakness in both patient’s hands and feet. The patient had a history of falling down about one year ago. The patient’s mother also had a difficulty in cleaning the patient’s oral cavity regularly.\n\nIn the extraoral examination, the patient had a dysmorphic face. The patient also had a cracking and desquamative condition of the vermillion border of the lips. Lymph node examination could not be assessed because the patient wore a cervical collar. The intraoral examination showed an irregular ulcer with 1×0.7 cm in diameter, indurated margin, and white-yellowish base at the right lateral border of the tongue. There was dentinal caries on 63 tooth and also the tooth remnants on 55, 62, 74, and 85 teeth. The upper and lower tooth remnants were suggested to be extracted by pediatric dentist. The space of the extracted teeth will be maintained using a space maintainer. The 55 tooth was sharp and caused an occlusion trauma to the right lateral border of the tongue.\n\nLaboratory examination showed a decrease in sodium value (130 mEq/L) and an increase in lymphocyte value (46%). The MRI examination was performed in the Radiology Department to determine the presence of abnormalities in the cervical spine. The results of the MRI examination showed a dislocation of the patient’s cervical spine. The patient’s mother provided informed consent to publish the patient’s case details and any accompanying images.\n\nBased on the history review, the clinical examination, and appropriate investigation, the patient was diagnosed with a chronic traumatic ulcer mimicking OSCC, exfoliative cheilitis, reversible pulpitis of 63 teeth, and radix gangrene on 55, 62, 74, and 85 teeth. The diagnosis of the chronic ulcer was based on clinical examination. There was an indurated margin in the traumatic lesion, which mimicked Oral Squamous Cell Carcinoma clinically. The patient has been hospitalized for 4 days and was given paracetamol 120 mg/5 mL oral suspension and amoxicillin 125 mg/5 mL oral suspension from the Pediatric Department. The patient also was given sodium chloride 0.9% solution, povidone-iodine mouthwash 1%, and petroleum jelly from the Oral Medicine Department. The patient’s mother was instructed to clean the patient’s oral cavity using gauze soaked in sodium chloride 0.9% solution, compress the ulcer using povidone-iodine mouthwashes 1% three times a day as an antiseptic and anti-inflammatory agent to the oral ulcer, and apply petroleum jelly to moisturize the patient’s lips. The patient was also suggested to extract the 55, 62, 74, and 85 teeth.\n\nIn the second visit (3 days follow-up), oral lesions already showed improvement. In the third visit (1-week follow-up), the size of the oral ulcer at the lateral border of the tongue was getting smaller and the lesion of the lips had some improvement.\n\nIn the fourth visit (10 days follow-up), the size of the oral ulcer at the lateral border of the tongue already had significant improvement. Two days after the fourth visit, the patient underwent neurosurgery. The patient was observed in the Pediatric Intensive Care Unit postoperatively. After two weeks of observation in the Pediatric Intensive Care Unit, the experienced respiratory failure and was declared dead.",
+    "diff_label_texts": "A 12-year-old boy with Down Syndrome and motoric disorders (diagnosed with myeloradiculopathy) was referred from Pediatrics to the Oral Medicine Department (RS Hasan Sadikin Bandung) for oral evaluation. The mother reported hospitalization for weakness of both hands and feet and difficulty maintaining the child’s oral hygiene; there was a history of a fall approximately one year prior. Extraoral findings: dysmorphic facies; cracking and desquamation of the vermilion border; cervical collar in place, precluding lymph node assessment. Intraorally, there was an irregular 1×0.7 cm ulcer with an indurated margin and a white‑yellowish base on the right lateral tongue. Additional findings included dentinal caries on tooth 63 and tooth remnants on 55, 62, 74, and 85. The 55 tooth had a sharp cusp causing occlusal trauma to the right lateral tongue. Pediatric dentistry recommended extraction of the upper and lower tooth remnants with subsequent space maintenance. Laboratory data: hyponatremia (Na 130 mEq/L) and relative lymphocytosis (46%). MRI of the cervical spine demonstrated dislocation; the mother provided informed consent for publication. Working diagnoses, based on history, clinical examination, and investigations: chronic traumatic ulcer mimicking OSCC (clinical diagnosis; indurated margin raised concern for oral squamous cell carcinoma), exfoliative cheilitis, reversible pulpitis of 63, and radix gangrene on 55, 62, 74, and 85. The patient had been hospitalized for 4 days and received paracetamol 120 mg/5 mL oral suspension and amoxicillin 125 mg/5 mL oral suspension from Pediatrics. Oral Medicine management included sodium chloride 0.9% solution, 1% povidone‑iodine mouthwash, and petroleum jelly. Caregiver instructions: cleanse the oral cavity with gauze soaked in 0.9% saline; apply 1% povidone‑iodine compresses to the ulcer three times daily as an antiseptic/anti‑inflammatory; apply petroleum jelly to moisturize the lips. Extractions of 55, 62, 74, and 85 were advised. Follow-up: at 3 days, oral lesions showed improvement; at 1 week, the lateral tongue ulcer decreased in size and lip lesions improved; at 10 days, the ulcer showed significant improvement. Two days later, the patient underwent neurosurgery and was observed in the Pediatric ICU. After two weeks in the ICU, he developed respiratory failure and died.",
+    "summary": "A 12-year-old boy with Down Syndrome and motoric disorders was referred to Oral Medicine Department. In the extraoral examination, the patient had a dysmorphic face and dry lips. Lymph node examination could not be assessed because the patient wore a cervical collar. The intraoral examination showed an irregular ulcer with 1×0.7 cm in diameter, indurated margin, and white-yellowish base at the right lateral border of the tongue. The 55 teeth were sharp and caused an occlusion trauma to the right lateral border of the tongue. The patient was diagnosed with a chronic traumatic ulcer mimicking OSCC based on clinical examination. The medication given to the patient were sodium chloride 0.9%, povidone-iodine mouthwash 1%, and petroleum jelly."
+  },
+  {
+    "doc_id": 32,
+    "label": "low_health_literacy",
+    "fulltext": "We present a case of a 59-year-old lady with a twelve-year history of secondary progressive multiple sclerosis who was referred to ophthalmology with a few weeks’ history of bilateral blurring of vision.\n\nThe patient had no past ophthalmic history and no drug history other than the anti-epileptic medications related to her multiple sclerosis. Previously documented ophthalmic examinations did not reveal any signs of Fuchs' endothelial corneal dystrophy, and the patient has no family history of corneal pathology.\n\nThe patient had been on amantadine therapy at a dose of 100mg twice daily for the past 7 years and was started on levetiracetam 250mg twice daily as an add-on agent. Visual deterioration was experienced shortly after commencement of levetiracetam therapy for a breakthrough seizure.\n\nOn examination, the patient’s best corrected visual acuity was 0.5 logMAR right eye and 0.5 logMAR left eye. Slit-lamp examination revealed corneal edema involving both eyes and absence of uveitis. Corrected intraocular pressures were 16mmHg right eye and 18mmHg left eye. Corneal topography was performed which confirmed bilateral significant corneal thickening with a right central corneal thickness of 936μm and left central corneal thickness of 1134μm. The rest of the eye examination was normal.\n\nSince amantadine is a known cause of corneal edema, it was agreed with the patient and her caring neurologist to switch from amantadine to lamotrigine. Levetiracetam therapy was continued at this stage. No improvement in vision was noted two months after this change in treatment. The patient expressed the wish to temporarily stop levetiracetam on a trial basis in view of the direct temporal association between the onset of symptoms and the commencement of the medication.\n\nAmantadine was re-introduced, while levetiracetam dose was tapered. Improvement in vision was noted a few days after levetiracetam dose reduction. Levetiracetam was stopped altogether, and the patient remained on amantadine and lamotrigine. A provisional diagnosis of levetiracetam-induced corneal edema was made at this stage. Her vision normalized and repeat corneal topography six months after stopping the levetiracetam showed a right central corneal thickness of 567μm and a left central corneal thickness of 573μm, and a visual acuity of 0.2 logMAR both eyes. Slit-lamp examination confirmed clear cornea and the absence of corneal guttata in either eye.\n\nThe patient was examined again thirteen months after the first presentation. No further changes in her medications were made, and her vision had remained stable at 0.2 logMAR in both eyes. Repeat corneal topography showed no further changes.",
+    "diff_label_texts": "A 59-year-old woman has multiple sclerosis. She started a new seizure medicine called levetiracetam. A few weeks later, her vision in both eyes became blurry. The eye doctor found swelling in the clear front window of both eyes. A special eye scan confirmed the swelling. They lowered the dose of the new medicine. Her vision started to get better. They then stopped the medicine. Her vision went back to normal. The swelling went away.",
+    "summary": "A 59-year-old woman was referred to the ophthalmology department with a few weeks’ history of bilateral blurring of vision. She is a known case of secondary progressive multiple sclerosis, and she was started on levetiracetam by her neurologist a few weeks prior to referral in view of new seizure activity. Examination revealed bilateral clinically evident corneal edema, which was documented on corneal topography.\n\nResults\nUpon levetiracetam dose reduction, symptoms started to improve and eventually the medication was stopped altogether. The patient’s vision and corneal edema normalized on follow-up."
+  },
+  {
+    "doc_id": 32,
+    "label": "intermediate_health_literacy",
+    "fulltext": "We present a case of a 59-year-old lady with a twelve-year history of secondary progressive multiple sclerosis who was referred to ophthalmology with a few weeks’ history of bilateral blurring of vision.\n\nThe patient had no past ophthalmic history and no drug history other than the anti-epileptic medications related to her multiple sclerosis. Previously documented ophthalmic examinations did not reveal any signs of Fuchs' endothelial corneal dystrophy, and the patient has no family history of corneal pathology.\n\nThe patient had been on amantadine therapy at a dose of 100mg twice daily for the past 7 years and was started on levetiracetam 250mg twice daily as an add-on agent. Visual deterioration was experienced shortly after commencement of levetiracetam therapy for a breakthrough seizure.\n\nOn examination, the patient’s best corrected visual acuity was 0.5 logMAR right eye and 0.5 logMAR left eye. Slit-lamp examination revealed corneal edema involving both eyes and absence of uveitis. Corrected intraocular pressures were 16mmHg right eye and 18mmHg left eye. Corneal topography was performed which confirmed bilateral significant corneal thickening with a right central corneal thickness of 936μm and left central corneal thickness of 1134μm. The rest of the eye examination was normal.\n\nSince amantadine is a known cause of corneal edema, it was agreed with the patient and her caring neurologist to switch from amantadine to lamotrigine. Levetiracetam therapy was continued at this stage. No improvement in vision was noted two months after this change in treatment. The patient expressed the wish to temporarily stop levetiracetam on a trial basis in view of the direct temporal association between the onset of symptoms and the commencement of the medication.\n\nAmantadine was re-introduced, while levetiracetam dose was tapered. Improvement in vision was noted a few days after levetiracetam dose reduction. Levetiracetam was stopped altogether, and the patient remained on amantadine and lamotrigine. A provisional diagnosis of levetiracetam-induced corneal edema was made at this stage. Her vision normalized and repeat corneal topography six months after stopping the levetiracetam showed a right central corneal thickness of 567μm and a left central corneal thickness of 573μm, and a visual acuity of 0.2 logMAR both eyes. Slit-lamp examination confirmed clear cornea and the absence of corneal guttata in either eye.\n\nThe patient was examined again thirteen months after the first presentation. No further changes in her medications were made, and her vision had remained stable at 0.2 logMAR in both eyes. Repeat corneal topography showed no further changes.",
+    "diff_label_texts": "A 59-year-old woman with secondary progressive multiple sclerosis developed a few weeks of blurry vision in both eyes shortly after starting levetiracetam for new seizures. Eye examination showed corneal edema in both eyes, confirmed by corneal topography. When the levetiracetam dose was reduced, her symptoms improved, and the drug was then stopped. On follow-up, both her vision and the corneal swelling returned to normal. She had no prior eye disease or family history of corneal problems, and changes to other medications did not help beforehand, supporting levetiracetam as the likely cause.",
+    "summary": "A 59-year-old woman was referred to the ophthalmology department with a few weeks’ history of bilateral blurring of vision. She is a known case of secondary progressive multiple sclerosis, and she was started on levetiracetam by her neurologist a few weeks prior to referral in view of new seizure activity. Examination revealed bilateral clinically evident corneal edema, which was documented on corneal topography.\n\nResults\nUpon levetiracetam dose reduction, symptoms started to improve and eventually the medication was stopped altogether. The patient’s vision and corneal edema normalized on follow-up."
+  },
+  {
+    "doc_id": 32,
+    "label": "proficient_health_literacy",
+    "fulltext": "We present a case of a 59-year-old lady with a twelve-year history of secondary progressive multiple sclerosis who was referred to ophthalmology with a few weeks’ history of bilateral blurring of vision.\n\nThe patient had no past ophthalmic history and no drug history other than the anti-epileptic medications related to her multiple sclerosis. Previously documented ophthalmic examinations did not reveal any signs of Fuchs' endothelial corneal dystrophy, and the patient has no family history of corneal pathology.\n\nThe patient had been on amantadine therapy at a dose of 100mg twice daily for the past 7 years and was started on levetiracetam 250mg twice daily as an add-on agent. Visual deterioration was experienced shortly after commencement of levetiracetam therapy for a breakthrough seizure.\n\nOn examination, the patient’s best corrected visual acuity was 0.5 logMAR right eye and 0.5 logMAR left eye. Slit-lamp examination revealed corneal edema involving both eyes and absence of uveitis. Corrected intraocular pressures were 16mmHg right eye and 18mmHg left eye. Corneal topography was performed which confirmed bilateral significant corneal thickening with a right central corneal thickness of 936μm and left central corneal thickness of 1134μm. The rest of the eye examination was normal.\n\nSince amantadine is a known cause of corneal edema, it was agreed with the patient and her caring neurologist to switch from amantadine to lamotrigine. Levetiracetam therapy was continued at this stage. No improvement in vision was noted two months after this change in treatment. The patient expressed the wish to temporarily stop levetiracetam on a trial basis in view of the direct temporal association between the onset of symptoms and the commencement of the medication.\n\nAmantadine was re-introduced, while levetiracetam dose was tapered. Improvement in vision was noted a few days after levetiracetam dose reduction. Levetiracetam was stopped altogether, and the patient remained on amantadine and lamotrigine. A provisional diagnosis of levetiracetam-induced corneal edema was made at this stage. Her vision normalized and repeat corneal topography six months after stopping the levetiracetam showed a right central corneal thickness of 567μm and a left central corneal thickness of 573μm, and a visual acuity of 0.2 logMAR both eyes. Slit-lamp examination confirmed clear cornea and the absence of corneal guttata in either eye.\n\nThe patient was examined again thirteen months after the first presentation. No further changes in her medications were made, and her vision had remained stable at 0.2 logMAR in both eyes. Repeat corneal topography showed no further changes.",
+    "diff_label_texts": "A 59-year-old woman with a 12-year history of secondary progressive multiple sclerosis presented with several weeks of bilateral blurred vision. Past ophthalmic history was unremarkable; there was no family history of corneal pathology, and prior examinations showed no signs of Fuchs' endothelial corneal dystrophy. She had been on amantadine 100 mg twice daily for 7 years and was started on levetiracetam 250 mg twice daily as an add-on agent after a breakthrough seizure; visual deterioration occurred shortly after levetiracetam initiation. On examination, BCVA was 0.5 logMAR OU. Slit-lamp examination revealed bilateral corneal edema without uveitis; IOPs were 16 mmHg OD and 18 mmHg OS. Corneal topography confirmed significant bilateral corneal thickening with CCT 936 μm OD and 1134 μm OS; the remainder of the ocular examination was normal. Because amantadine is a known cause of corneal edema, it was switched to lamotrigine while levetiracetam was continued, but there was no improvement after two months. Amantadine was then reintroduced and levetiracetam was tapered; visual improvement was noted within days of levetiracetam dose reduction. Levetiracetam was subsequently discontinued, and the patient remained on amantadine and lamotrigine. A provisional diagnosis of levetiracetam-induced corneal edema was made. Six months after stopping levetiracetam, BCVA improved to 0.2 logMAR OU; corneal topography showed CCT 567 μm OD and 573 μm OS, and slit-lamp confirmed clear corneas without guttata. At 13 months after initial presentation, medications were unchanged, vision remained stable at 0.2 logMAR OU, and repeat corneal topography was unchanged. The clinical course is consistent with a drug-induced, reversible corneal endothelial dysfunction temporally related to levetiracetam exposure, with no response to amantadine withdrawal.",
+    "summary": "A 59-year-old woman was referred to the ophthalmology department with a few weeks’ history of bilateral blurring of vision. She is a known case of secondary progressive multiple sclerosis, and she was started on levetiracetam by her neurologist a few weeks prior to referral in view of new seizure activity. Examination revealed bilateral clinically evident corneal edema, which was documented on corneal topography.\n\nResults\nUpon levetiracetam dose reduction, symptoms started to improve and eventually the medication was stopped altogether. The patient’s vision and corneal edema normalized on follow-up."
+  },
+  {
+    "doc_id": 33,
+    "label": "low_health_literacy",
+    "fulltext": "A 77-year-old male patient presented with a history of moderate cognitive impairment. The patient was admitted to the emergency department for a tonic-clonic seizure at home. The patient presented hemodynamically unstable in the context of a postcritical state and suspected intrapelvic bleeding. The code for a polytraumatized patient was activated, not because of the mechanism of injury, but because of the patient's hemodynamic status.  He was stabilized and optimized in the emergency department with intravenous fluid and transfusion of packed red blood cells. A pelvic girdle was placed. Once hemodynamic stability was achieved, a physical examination was performed. Clinically, the patient presented a shortening of the lower limb compared to the contralateral limb, external rotation and joint blockage when performing the log roll test in both limbs. He presented functional impotence in both hips. Given the patient's condition when he arrived at the emergency department, it was not possible to assess the neurological status. He had no signs of external injuries or bruises. Distal pulses were present at the foot level. He could move his upper limbs. A chest and anteroposterior pelvic radiograph was performed as part of the code for a polytraumatized patient, pending completion of an abdominal-pelvic computed tomography (CT) study. A bilateral femoral dislocation was diagnosed in the pelvic radiograph. The patient underwent a procedure to correct the dislocation.\n\n\n\nComputed tomography angiography to rule out vascular lesions given the instability in hemodynamic that presented itself on admission. Vascular lesions were ruled out after the angiography. In the 3D-CT reconstruction of the pelvis, a bilateral transverse acetabular fracture was found, according to the classification of Letournel and a bilateral longitudinal fracture of the iliac wing was found, along with intrapelvic protrusion of both femoral heads. After initial evaluation, supracondylar traction was placed on the femoral head in both extremities and the pelvic traction was removed. The patient was admitted to the recovery unit until surgery, where he remained with the traction supracondylar femoral head in both extremities and the pelvic traction was removed. The patient was operated on the eighth day of admission. In our service, the acetabular fractures were ruled out after seven days waiting for the formation of a fibrosis in the focus of fracture and the decrease of intraoperative bleeding during surgical procedures. It was decided to perform the surgery in two stages due to the long duration of each intervention. Both surgeries were performed with general anaesthesia, tranexamic acid was administered to prevent intraoperative bleeding and decrease blood transfusions in relation to the surgeries; and antibiotic (cefazolin 2 g preoperatively and 1 g of cefazolin every 8 hours postoperatively for 24 hours) as an intrahospital protocol. During the postoperative period, enoxaparin 40 mg was administered subcutaneously every 24 hours for seven weeks. Initially, the surgery of the left hemipelvis was performed since, at the radiographic level, it presented greater pelvic protrusion and it was not desirable that a hematoma in the soft tissue phase could generate complications at the time of extraction of the femoral head (vascular injuries, intraoperative bleeding). The supracondylar traction was removed. The patient was placed in lateral decubitus, and a posterior lateral approach was performed with a Moore's autograft in the acetabular background (fracture focus). Subsequently, the anti-protrusion ring was implanted (Burch SchneiderTM Reinforcement Cage, Zimmer Biomet) anchored to the ischium and ilium. Prior to the implantation of the ring, it was necessary to perform dissection of the gluteal musculature (gluteus minimus and medius) to correctly place the femoral head. The medial ischial fracture of the ring was also anchored with screws. The check was performed under the control of a scope to verify the correct implantation. Subsequently, a double mobility cementaed acetabular ring was implanted and then the non-cemented femoral stem was implanted. After finishing the placement of the components, the capsule and pelvic musculature were closed by means of transosseous trochanteric points. The surgery of the right hemipelvis was performed seven days later. The patient was placed in lateral decubitus. To address the longitudinal fracture of the iliac wing, the first window of the ilio-inguinal approach was performed. It was synthesised with a six-hole anatomical plate. Subsequently, the same procedure as the previous surgery was performed, using an anti-protrusion ring with a double mobility cemented femoral stem and non-cemented femoral stem. This type of anti-protrusion rings are used when there are acetabular fractures that could be equivalent to a pelvic disjunction (type IV classification of acetabular defects of the AAOS) and an anchorage in the ischium and ilium of the ring is needed to support the ring. They are not indicated for isolated fractures of the anterior or posterior wall of the acetabulum where there is no involvement of the acetabular background. During admission, the patient remained in bed and was mobilised to avoid decubitus ulcers. Once the second intervention was performed and when the patient tolerated it clinically, he began to transfer with the use of a wheelchair. In bed he was allowed to have a full range of motion without restriction. The patient was discharged four weeks later and did not begin to load or walk until six weeks. He began to load with the use of a walking stick. We decided to delay loading because, despite the use of arthroplasty as a treatment, it was decided to wait until there was an initial consolidation of the graft in the acetabular background that provided better support for the ring. It was also added that the patient presented bilateral involvement and it would be difficult to start partial loading, given that he did not have a healthy hip to support. During the follow-up of the patient, at 12 months of the intervention he was already doing full load with the use of a walking stick, with a Harris hip score of 79 in the left hip and 77 in the right hip; and a score of 12 on the WOMAC scale. He has not presented any postoperative complications to date. The patient is satisfied clinically, he reports occasional discomfort and a slight limp of the right side. He has a full range of motion in the examination and does not report having had any episode of instability since the surgery.\n",
+    "diff_label_texts": "A 77-year-old man has memory and thinking problems. He had a big seizure. Both hip joints popped inward into the pelvis. In the emergency room, his right leg looked shorter than the left. Both legs were turned outward. Both hips were stuck when staff gently rolled his legs. Scans and medical checks were done to get him ready for surgery. The surgeries were done in two steps. The left hip was done on day 8. The right hip was done on day 15. In both surgeries, doctors put in a support ring and a special hip socket that helps keep the joint stable. They also put in a new thigh-bone piece that does not use cement. Right after surgery, there were no problems from the operation. At 12 months, he could put full weight on his legs. His right hip score was 77. His left hip score was 79. His WOMAC score was 12. He has had no problems since the surgery.",
+    "summary": "77-year-old patient with a history of moderate cognitive impairment who suffered bilateral central dislocation of the hip in the context of a generalized convulsive seizure. Clinically, upon arrival in the emergency department, the patient presented a shortening of the lower right limb compared to the contralateral limb, external rotation and joint blockage when performing the log roll test in both limbs. Imaging and clinical optimization study was performed prior to surgery. It was performed in two stages: first the left hip on the eighth day of admission and the right hip on the fifteenth. In both surgeries the same procedure was performed by implanting an anti-protrusive ring and prosthesis with double mobility acetabulum with non-cemented femoral stem. In the immediate postoperative period, the patient did not present any complications associated with the surgery. In the 12-month follow-up, the patient performed a full load with a Harris hip score (HHS) of 77 in the right hip and 79 in the left; 12 points in the WOMAC scale. He has not presented any postoperative complications to date.\n"
+  },
+  {
+    "doc_id": 33,
+    "label": "proficient_health_literacy",
+    "fulltext": "A 77-year-old male patient presented with a history of moderate cognitive impairment. The patient was admitted to the emergency department for a tonic-clonic seizure at home. The patient presented hemodynamically unstable in the context of a postcritical state and suspected intrapelvic bleeding. The code for a polytraumatized patient was activated, not because of the mechanism of injury, but because of the patient's hemodynamic status.  He was stabilized and optimized in the emergency department with intravenous fluid and transfusion of packed red blood cells. A pelvic girdle was placed. Once hemodynamic stability was achieved, a physical examination was performed. Clinically, the patient presented a shortening of the lower limb compared to the contralateral limb, external rotation and joint blockage when performing the log roll test in both limbs. He presented functional impotence in both hips. Given the patient's condition when he arrived at the emergency department, it was not possible to assess the neurological status. He had no signs of external injuries or bruises. Distal pulses were present at the foot level. He could move his upper limbs. A chest and anteroposterior pelvic radiograph was performed as part of the code for a polytraumatized patient, pending completion of an abdominal-pelvic computed tomography (CT) study. A bilateral femoral dislocation was diagnosed in the pelvic radiograph. The patient underwent a procedure to correct the dislocation.\n\n\n\nComputed tomography angiography to rule out vascular lesions given the instability in hemodynamic that presented itself on admission. Vascular lesions were ruled out after the angiography. In the 3D-CT reconstruction of the pelvis, a bilateral transverse acetabular fracture was found, according to the classification of Letournel and a bilateral longitudinal fracture of the iliac wing was found, along with intrapelvic protrusion of both femoral heads. After initial evaluation, supracondylar traction was placed on the femoral head in both extremities and the pelvic traction was removed. The patient was admitted to the recovery unit until surgery, where he remained with the traction supracondylar femoral head in both extremities and the pelvic traction was removed. The patient was operated on the eighth day of admission. In our service, the acetabular fractures were ruled out after seven days waiting for the formation of a fibrosis in the focus of fracture and the decrease of intraoperative bleeding during surgical procedures. It was decided to perform the surgery in two stages due to the long duration of each intervention. Both surgeries were performed with general anaesthesia, tranexamic acid was administered to prevent intraoperative bleeding and decrease blood transfusions in relation to the surgeries; and antibiotic (cefazolin 2 g preoperatively and 1 g of cefazolin every 8 hours postoperatively for 24 hours) as an intrahospital protocol. During the postoperative period, enoxaparin 40 mg was administered subcutaneously every 24 hours for seven weeks. Initially, the surgery of the left hemipelvis was performed since, at the radiographic level, it presented greater pelvic protrusion and it was not desirable that a hematoma in the soft tissue phase could generate complications at the time of extraction of the femoral head (vascular injuries, intraoperative bleeding). The supracondylar traction was removed. The patient was placed in lateral decubitus, and a posterior lateral approach was performed with a Moore's autograft in the acetabular background (fracture focus). Subsequently, the anti-protrusion ring was implanted (Burch SchneiderTM Reinforcement Cage, Zimmer Biomet) anchored to the ischium and ilium. Prior to the implantation of the ring, it was necessary to perform dissection of the gluteal musculature (gluteus minimus and medius) to correctly place the femoral head. The medial ischial fracture of the ring was also anchored with screws. The check was performed under the control of a scope to verify the correct implantation. Subsequently, a double mobility cementaed acetabular ring was implanted and then the non-cemented femoral stem was implanted. After finishing the placement of the components, the capsule and pelvic musculature were closed by means of transosseous trochanteric points. The surgery of the right hemipelvis was performed seven days later. The patient was placed in lateral decubitus. To address the longitudinal fracture of the iliac wing, the first window of the ilio-inguinal approach was performed. It was synthesised with a six-hole anatomical plate. Subsequently, the same procedure as the previous surgery was performed, using an anti-protrusion ring with a double mobility cemented femoral stem and non-cemented femoral stem. This type of anti-protrusion rings are used when there are acetabular fractures that could be equivalent to a pelvic disjunction (type IV classification of acetabular defects of the AAOS) and an anchorage in the ischium and ilium of the ring is needed to support the ring. They are not indicated for isolated fractures of the anterior or posterior wall of the acetabulum where there is no involvement of the acetabular background. During admission, the patient remained in bed and was mobilised to avoid decubitus ulcers. Once the second intervention was performed and when the patient tolerated it clinically, he began to transfer with the use of a wheelchair. In bed he was allowed to have a full range of motion without restriction. The patient was discharged four weeks later and did not begin to load or walk until six weeks. He began to load with the use of a walking stick. We decided to delay loading because, despite the use of arthroplasty as a treatment, it was decided to wait until there was an initial consolidation of the graft in the acetabular background that provided better support for the ring. It was also added that the patient presented bilateral involvement and it would be difficult to start partial loading, given that he did not have a healthy hip to support. During the follow-up of the patient, at 12 months of the intervention he was already doing full load with the use of a walking stick, with a Harris hip score of 79 in the left hip and 77 in the right hip; and a score of 12 on the WOMAC scale. He has not presented any postoperative complications to date. The patient is satisfied clinically, he reports occasional discomfort and a slight limp of the right side. He has a full range of motion in the examination and does not report having had any episode of instability since the surgery.\n",
+    "diff_label_texts": "A 77-year-old male with a history of moderate cognitive impairment presented after a tonic–clonic seizure at home. On arrival to the ED he was hemodynamically unstable in a postictal state with suspected intrapelvic bleeding, triggering activation of the polytrauma code (for physiology rather than mechanism). He was stabilized with intravenous fluids and transfusion of packed red blood cells, and a pelvic girdle was applied. Once stable, examination showed shortening of the lower limb compared with the contralateral side, external rotation, and joint blockage on log-roll testing in both limbs, with functional impotence of both hips. Neurologic assessment was initially limited. There were no external injuries; distal foot pulses were present, and he could move his upper limbs. Chest and AP pelvic radiographs were obtained; the pelvic film demonstrated bilateral femoral dislocation, and a reduction procedure was performed. Computed tomography angiography was then used to exclude vascular injury (none identified). 3D-CT reconstructions revealed bilateral transverse acetabular fractures per Letournel, bilateral longitudinal iliac wing fractures, and intrapelvic protrusion of both femoral heads. Bilateral supracondylar femoral traction was applied and pelvic traction was removed. The patient was operated on hospital day 8, in accordance with the service protocol to delay acetabular fracture surgery approximately 7 days to allow fibrosis at the fracture site and reduce intraoperative bleeding. Given anticipated operative duration, a staged approach was selected. Perioperatively, both procedures were performed under general anesthesia with tranexamic acid to limit bleeding and cefazolin prophylaxis (2 g pre-op, then 1 g q8h for 24 h). Postoperatively, enoxaparin 40 mg SC daily was administered for 7 weeks. The left hemipelvis was addressed first due to greater radiographic protrusion and concern that a soft-tissue hematoma could complicate femoral head extraction (risk of vascular injury/bleeding). With the patient in lateral decubitus, a posterolateral approach was used. A Moore’s autograft was placed in the acetabular background (fracture focus). A Burch-Schneider Reinforcement Cage (Zimmer Biomet) was implanted, anchored to the ischium and ilium; dissection of the gluteus minimus and medius was required to position the femoral head. The ischial fixation was secured with screws, and fluoroscopy confirmed component positioning. A cemented dual-mobility acetabular construct was then implanted, followed by a non-cemented femoral stem. Closure included the capsule and pelvic musculature with transosseous trochanteric sutures. Seven days later, the right side was performed in lateral decubitus. The longitudinal iliac wing fracture was addressed first via the first window of the ilioinguinal approach and fixed with a six-hole anatomical plate. The hip reconstruction then mirrored the left: anti-protrusion ring with a cemented dual-mobility acetabular component and a non-cemented femoral stem. The authors note that anti-protrusion rings are indicated for acetabular fractures equivalent to pelvic discontinuity (AAOS type IV acetabular defects), requiring ischial and iliac anchorage, and are not indicated for isolated anterior or posterior wall fractures without acetabular floor involvement. During admission, the patient remained in bed with mobilization to prevent pressure ulcers. After the second operation and as tolerated, he transferred using a wheelchair; in bed he had unrestricted range of motion. He was discharged at 4 weeks and remained non–weight bearing until 6 weeks, then progressed to loading with a cane. Loading was delayed to allow initial consolidation of the acetabular background graft to support the ring and because bilateral involvement precluded practical partial weight bearing. At 12 months, he was fully weight bearing with a cane, with Harris Hip Scores of 79 (left) and 77 (right), WOMAC 12, and no postoperative complications. He reported occasional discomfort and a mild right-sided limp, had full range of motion on examination, and no episodes of instability since surgery.",
+    "summary": "77-year-old patient with a history of moderate cognitive impairment who suffered bilateral central dislocation of the hip in the context of a generalized convulsive seizure. Clinically, upon arrival in the emergency department, the patient presented a shortening of the lower right limb compared to the contralateral limb, external rotation and joint blockage when performing the log roll test in both limbs. Imaging and clinical optimization study was performed prior to surgery. It was performed in two stages: first the left hip on the eighth day of admission and the right hip on the fifteenth. In both surgeries the same procedure was performed by implanting an anti-protrusive ring and prosthesis with double mobility acetabulum with non-cemented femoral stem. In the immediate postoperative period, the patient did not present any complications associated with the surgery. In the 12-month follow-up, the patient performed a full load with a Harris hip score (HHS) of 77 in the right hip and 79 in the left; 12 points in the WOMAC scale. He has not presented any postoperative complications to date.\n"
+  },
+  {
+    "doc_id": 34,
+    "label": "low_health_literacy",
+    "fulltext": "A 19-month-old boy was admitted to the Emergency Department because he fell from his baby feeding highchair. This fall occurred in apparent well-being, without the presence of anticipatory signs or symptoms. First, he fell on his gluteus and then he banged his head (occiput) on the ground. He presented with vomiting (three episodes) and he was very irritable. His respiratory rate and heart rate were >60 breaths and >150 beats per minute, while oxygen saturation was <80%. Upon physical examination, the child was hydrated and conscious, but irritable. More importantly, we noted subcostal retractions, and, at the auscultation, decreased breath sounds in the left basal part of chest. The patient was ventilated with an AMBU balloon connected to an oxygen source and monitored with a pulse oximeter. Despite our intervention, oxygen saturation fell below 70% and the more we ventilated, the more the saturation dropped down. The lung ultrasound showed the absence of the typical A lines and the consolidation of the lung, which was directly visualized as a solid parenchyma. On the basis of the poor clinical condition, the patient underwent orotracheal intubation with a cuffed endotracheal tube. After the baby was stabilized, he underwent a chest computed tomography (CT) showing complete atelectasis of the left lung with an interruption of the main left bronchus at 12 cm from bronchial bifurcation. An FBA was suspected as the mother also stated that the baby in the previous days had an intensive cough attack and disappeared within 24 h without any treatment. Therefore, a rigid bronchoscopy was performed and an almond of 2 cm in diameter in the main left bronchus was found and promptly removed.\n\nThe patient had never consumed almonds or other nuts before and in this circumstance ingested the almond by chance.\n\nThe baby had a progressive clinical improvement, and after 24 h, he was extubated and discharged from intensive care to be admitted to the general pediatrics ward for a few days with gradual and a total respiratory function recovery.",
+    "diff_label_texts": "A 19‑month‑old boy went to the emergency room because he hit his head. Doctors saw that he was fighting to breathe. They put in a breathing tube to help him. The team believed the breathing problem likely started first. It may have made him less alert, and then he fell and hit his head. Scans showed the left lung was not filling with air, like a balloon that stays flat. This made doctors think something was stuck in his airway. A CT scan showed a sudden stop in the main airway to the left lung. Doctors used a small camera to look inside. They found and removed a 2‑cm almond that was blocking the airway.",
+    "summary": "We describe the case of a 19-month-old boy who accessed the emergency room initially for a head trauma. The clinical evaluation, however, revealed an unexplained serious respiratory distress needing tracheal intubation. After our evaluation, we hypothesized that the severe respiratory distress determined an altered state of consciousness with following head trauma. The radiological findings raised the suspicion of foreign body aspiration for the presence of an atelectasis of the entire left lung. The computed tomography showed an abrupt interruption of the main bronchus at 12 mm from the hull. The following bronchoscopy identified an almond of 2 cm."
+  },
+  {
+    "doc_id": 34,
+    "label": "proficient_health_literacy",
+    "fulltext": "A 19-month-old boy was admitted to the Emergency Department because he fell from his baby feeding highchair. This fall occurred in apparent well-being, without the presence of anticipatory signs or symptoms. First, he fell on his gluteus and then he banged his head (occiput) on the ground. He presented with vomiting (three episodes) and he was very irritable. His respiratory rate and heart rate were >60 breaths and >150 beats per minute, while oxygen saturation was <80%. Upon physical examination, the child was hydrated and conscious, but irritable. More importantly, we noted subcostal retractions, and, at the auscultation, decreased breath sounds in the left basal part of chest. The patient was ventilated with an AMBU balloon connected to an oxygen source and monitored with a pulse oximeter. Despite our intervention, oxygen saturation fell below 70% and the more we ventilated, the more the saturation dropped down. The lung ultrasound showed the absence of the typical A lines and the consolidation of the lung, which was directly visualized as a solid parenchyma. On the basis of the poor clinical condition, the patient underwent orotracheal intubation with a cuffed endotracheal tube. After the baby was stabilized, he underwent a chest computed tomography (CT) showing complete atelectasis of the left lung with an interruption of the main left bronchus at 12 cm from bronchial bifurcation. An FBA was suspected as the mother also stated that the baby in the previous days had an intensive cough attack and disappeared within 24 h without any treatment. Therefore, a rigid bronchoscopy was performed and an almond of 2 cm in diameter in the main left bronchus was found and promptly removed.\n\nThe patient had never consumed almonds or other nuts before and in this circumstance ingested the almond by chance.\n\nThe baby had a progressive clinical improvement, and after 24 h, he was extubated and discharged from intensive care to be admitted to the general pediatrics ward for a few days with gradual and a total respiratory function recovery.",
+    "diff_label_texts": "A 19‑month‑old boy was admitted following a fall from a feeding highchair, landing on his gluteal region and striking the occiput. He had three episodes of vomiting, marked irritability, RR >60/min, HR >150/min, and SpO2 <80%. On exam, he was hydrated and conscious but irritable, with subcostal retractions and decreased breath sounds at the left base. Bag‑mask ventilation with supplemental oxygen and pulse oximetry monitoring were initiated; paradoxically, SpO2 fell below 70% with ongoing ventilation. Lung ultrasound demonstrated absent A‑lines and consolidation, visualizing the lung as solid parenchyma. Given the poor clinical condition, orotracheal intubation with a cuffed endotracheal tube was performed. Post‑stabilization chest CT revealed complete atelectasis of the left lung with interruption of the main left bronchus at 12 cm from the bronchial bifurcation. In the context of maternal history of an intensive coughing episode in the preceding days that resolved spontaneously within 24 h, foreign body aspiration was suspected. Rigid bronchoscopy identified and removed a 2‑cm almond lodged in the left main bronchus. The patient improved progressively, was extubated at 24 h, transferred from intensive care to the general pediatrics ward, and achieved full recovery of respiratory function. Based on the clinical course, the team hypothesized that severe respiratory compromise likely preceded the event, causing altered consciousness and subsequent head trauma.",
+    "summary": "We describe the case of a 19-month-old boy who accessed the emergency room initially for a head trauma. The clinical evaluation, however, revealed an unexplained serious respiratory distress needing tracheal intubation. After our evaluation, we hypothesized that the severe respiratory distress determined an altered state of consciousness with following head trauma. The radiological findings raised the suspicion of foreign body aspiration for the presence of an atelectasis of the entire left lung. The computed tomography showed an abrupt interruption of the main bronchus at 12 mm from the hull. The following bronchoscopy identified an almond of 2 cm."
+  },
+  {
+    "doc_id": 35,
+    "label": "proficient_health_literacy",
+    "fulltext": "The patient was a 4-month-old male from central Mexico with two healthy male siblings. His mother was hypothyroid during the first trimester of pregnancy and took drugs. The infant was born with normal weight and size, was breast-fed, and received the BCG vaccine with no scarring. The mother of the patient was a prisoner in a jail cell with the infant in a crowded cell with two others.At 4 months, the patient was medically evaluated for a painful tumor in the left axilla. A chest X-ray showed suggestive images of rib fractures; the mother was suspected of child abuse, and the infant was admitted to a pediatric hospital. The infant was weighed (4,190 g) and measured (58 cm) below the third percentile, oxygen saturation of 70%, fever, cough, increased volume in the left axilla, and pain, redness, and warmth. The blood count showed: hemoglobin of 8.8 g/dL (11.0-12.6), 29.3 × 109 leukocytes/L (6.0-17.5), 18.4 × 109 neutrophils/L (1.0-8.5), 7.0 × 109 lymphocytes/L (4.0-13.5), 3.5 × 109 monocytes/L, 459 × 109 platelets/L (150-350), and C-reactive protein of 16 mg/L (< 3.0). The first thoracoabdominal tomography showed an abscess in the left axilla, lytic lesions in ribs 3-6, left apical pneumonia, pulmonary nodules in both lungs, and enlarged cervical and mediastinal lymph nodes. The biopsy of the left axilla abscess reported myositis and suppurative panniculitis. Only the culture for bacteria from the bronchoalveolar liquid was negative, and the PCR for the Mycobacterium tuberculosis complex was negative. After 41 days of hospitalization and receiving two antimicrobial regimens of ceftriaxone-clindamycin and cefepime-vancomycin, the patient was discharged.\n\nTwo months later, at eight months of age, he was readmitted to hospital with a fever, irritability and a suppurating abscess in the left scapula. The blood count showed haemoglobin of 10.8 g/dl (10.5-12), 21.2 × 109 leukocytes/L (6-17), 12.2 × 109 neutrophils/L (1.5-8.5), 7.5 × 109 lymphocytes/L (4-10.5), 1.2 × 109 monocytes/L (600), and 583 × 109 platelets/L (150-350); the serum test for HIV was negative. A left apical consolidation, bronchiectasis, lytic lesions in ribs 2-7 and dorsal vertebrae 2-7, and a multilocular fluid collection were observed on a chest scan; ultrasound showed a fistula associated with the scapular abscess. The patient received piperacillin-tazobactam, which was later replaced with voriconazole after Aspergillus fumigatus was detected in the secretion sample culture. Given the recurrence and severity of the infection, an innate immunity defect was suspected. The dihydrorhodamine test showed no production of reactive oxygen species and the gp91phox expression in neutrophils was absent, establishing a diagnosis of X-linked chronic granulomatous disease. The pathogenic variant detected by next-generation sequencing was c.80_83del/Y (p.Val27Glyfs*33) in CYBB. The mother was a carrier of the variant (c.80_83del/WT). The two older male siblings, who were apparently healthy, could not be genetically tested. The patient was discharged after 65 days of hospitalisation and 28 days of voriconazole treatment. Daily antibiotic prophylaxis with trimethoprim-sulfamethoxazole and antifungal prophylaxis with fluconazole twice a week were initiated. Two months later, at one year of age, the infant was readmitted due to multifocal pneumonia, for which mechanical respiratory assistance was required. The galactomannan antigen was detected in the serum and A. fumigatus was detected in the culture of the lavage fluid, so treatment with voriconazole was initiated again. The patient suffered a multiple organ failure and died one month after admission.\n",
+    "diff_label_texts": "A 4‑month‑old male from central Mexico with two apparently healthy older male siblings presented with a painful tumor in the left axilla while living with his hypothyroid mother in a crowded prison cell. He was born appropriate for gestational age, was breast‑fed, and had received BCG without scarring. On admission he was below the 3rd percentile for weight (4,190 g) and length (58 cm), with oxygen saturation of 70%, fever, cough, and a tender, erythematous, warm left axillary mass. CBC: hemoglobin 8.8 g/dL (11.0–12.6), leukocytes 29.3 × 10^9/L (6.0–17.5), neutrophils 18.4 × 10^9/L (1.0–8.5), lymphocytes 7.0 × 10^9/L (4.0–13.5), monocytes 3.5 × 10^9/L, platelets 459 × 10^9/L (150–350), CRP 16 mg/L (< 3.0). Chest radiography showed images suggestive of rib fractures, prompting concern for child abuse and admission. Thoracoabdominal CT demonstrated a left axillary abscess, lytic lesions of ribs 3–6, left apical pneumonia, bilateral pulmonary nodules, and enlarged cervical and mediastinal lymph nodes. Biopsy of the axillary lesion showed myositis and suppurative panniculitis. BAL bacterial culture was negative, and PCR for Mycobacterium tuberculosis complex was negative. He received ceftriaxone–clindamycin, then cefepime–vancomycin, and was discharged after 41 days. \n\nAt 8 months, he was readmitted with fever, irritability, and a suppurating abscess over the left scapula. CBC: hemoglobin 10.8 g/dL (10.5–12), leukocytes 21.2 × 10^9/L (6–17), neutrophils 12.2 × 10^9/L (1.5–8.5), lymphocytes 7.5 × 10^9/L (4–10.5), monocytes 1.2 × 10^9/L (~0.6), platelets 583 × 10^9/L (150–350); HIV serology was negative. Chest imaging showed left apical consolidation, bronchiectasis, lytic lesions in ribs 2–7 and thoracic vertebrae T2–T7, and a multilocular fluid collection; ultrasound identified a fistula linked to the scapular abscess. Initial piperacillin–tazobactam was switched to voriconazole when Aspergillus fumigatus grew from abscess secretion culture, establishing invasive aspergillosis. Given the recurrence and severity, an innate immune defect was suspected. Dihydrorhodamine (DHR) testing demonstrated absent reactive oxygen species production with absent gp91phox expression in neutrophils, confirming X‑linked chronic granulomatous disease. Next‑generation sequencing identified CYBB c.80_83del/Y (p.Val27Glyfs*33); the mother was a heterozygous carrier (c.80_83del/WT). The patient was discharged after 65 days of hospitalization, including 28 days of voriconazole, and was started on prophylaxis with daily trimethoprim–sulfamethoxazole and fluconazole twice weekly. \n\nAt 12 months, he was readmitted with multifocal pneumonia requiring mechanical respiratory assistance. Serum galactomannan was positive, and A. fumigatus was recovered from lavage fluid; voriconazole was re‑initiated. Despite therapy, he developed multiple organ failure and died one month after admission. \n\nContext: CGD is caused by NADPH oxidase dysfunction in phagocytes, leading to impaired oxidative burst and susceptibility to catalase‑positive organisms, especially Aspergillus spp. X‑linked CYBB variants frequently present in infancy with invasive aspergillosis and osteolytic lesions; A. fumigatus remains a leading cause of mortality in CGD.",
+    "summary": "A case of infant with chronic granulomatous disease and invasive aspergillosis is reported. The infant was a 4-month-old male infant living with his mother in a prison cell. The infant had tumors in the left axillary region and a chest X-ray suggested rib fractures; he was hospitalized on suspicion of child abuse. A chest X-ray showed an axillary abscess, osteolysis of ribs, pneumonia and pulmonary nodules; the patient received broad spectrum antibiotics and was discharged. At 8 months, he was readmitted with fever and extension of the purulent abscess to the left shoulder region; a chest X-ray showed worsening of the condition. Aspergillus fumigatus was isolated from the secretion of the abscess and invasive aspergillosis was diagnosed; voriconazole was initiated for 28 days. A dihydro rhodamine test was performed and a diagnosis of chronic granulomatous disease caused by the pathogenic variant c.80_83del/Y of the CYBB gene, carried by the mother (c.80_83del/WT), was made. At 12 months, the patient was readmitted with invasive aspergillosis, resistant to treatment, with fatal outcome.\n"
+  },
+  {
+    "doc_id": 36,
+    "label": "proficient_health_literacy",
+    "fulltext": "Male patient, 25 years old, Sundanese, presented at the Dental Hospital of the Faculty of Dentistry Universitas Padjadjaran with the chief complaint of mouth sores, which are painful on the upper and lower lips and exacerbated when eating and talking. Initially, four days ago, canker sores started in the oral cavity, then appeared on the lips two days later. The patient tried to self-medicate by applying petroleum jelly which he used to relieve his symptoms, but it did not improve. The patient replaced the drug with triamcinolone acetonide 0.1% in orabase ointment purchased at the pharmacy and applied it once a day. Canker sores were getting better but did not cure.\n\nThe patient had history a of fever for about a week before the canker sores appeared and there were no lesions on other parts of the body. He stated that the workload was quite heavy and he had not consumed a balanced nutritional diet for about one and a half months. He had no medical history, history of food allergies, or history of taking medication. He had no history of alcohol consumption or smoking, but he had a frequent habit of licking his lips. He also had a history of chickenpox when he was a child.\n\nThe patient had no fever with all vital signs within normal limits on general examination. Extra-oral examination showed no abnormalities in the lymph nodes. There were serosanguineous crusts that felt painful and bleed easily on the lips. Intra-oral examination revealed erythematous lesions, irregular in shape, and had diffuse borders, accompanied by pain in the upper and lower labial mucosa. Hyperkeratotic white plaque that could not be scraped off, irregular in shape, has diffuse borders, without pain in the region of tooth 38 left buccal mucosa. Yellowish-white plaques were seen on 1/3 of the posterior surface of the dorsal tongue, which could be scraped off without leaving an erythematous area, and there were indentations in the form of dental impressions without pain on the lateral right and left sides of the tongue. A painless hard nodule about 2×1 x 0.5 cm in size was seen in the midline of the hard palate. Several teeth were found in caries, radix, and edentulous conditions in all regions. The oral hygiene was poor.\n\nExamination of psychological conditions was evaluated using the DASS-21 questionnaire and showed normal depression level (score 0), normal anxiety level (score 6), and normal stress level (score 6). Based on history and clinical examination, the working diagnosis was suspected HAEM, accompanied by the coated tongue, frictional keratosis, crenated tongue, torus palatinus, reversible pulpitis of tooth 18, irreversible pulpitis of tooth 47, chronic apical periodontitis et causa radix of tooth 15, and edentulous teeth 28, 37, 36, and 46. The differential diagnosis of suspected HAEM lesions on the lips was exfoliative cheilitis. However, exfoliative cheilitis did not have herpes virus involvement. The patient was indicated for serological testing (IgG anti-HSV-1) to confirm the diagnosis. Oral health-related quality of life was measured, and the results of the OHIP-14 examination at the first visit were 35 (moderate OHRQol).\n\nThe non-pharmacological therapy included instruction to maintain oral hygiene by brushing the teeth and tongue using a soft-bristled toothbrush two times a day and using non-detergent toothpaste. Education was given such as increasing the intake of water by at least two liters per day, consuming a balanced nutritional diet, avoiding acidic, spicy, hard, and monosodium glutamate-containing foods, and stopping the bad habit of licking and peeling the skin of the lips. The pharmacological therapy included topical and systemic medications. The topical medications included instructions to compress the lips with gauze moistened with 0.9% NaCl solution at least three times a day and to apply a thin layer of triamcinolone acetonide 0.1% in orabase to the lips three times a day. The systemic medications included instruction to take a multivitamin once a day.\n\nThe progress of improvement was visible in the first follow-up, two days after the initial visit. The pain in the lips was reduced, but the canker sores have not healed. Extra-oral examination revealed serosanguinous crusts on the lips which were still painful and bled easily. The serological test result (IgG anti-HSV-1) was positive with a ratio of: 6.32 (positive: ratio > 1.1). The definitive diagnosis was established based on the history, clinical examination, and serological tests as HAEM. The non-pharmacological and pharmacological therapy was continued, and systemic medication was added in the form of instructions to consume acyclovir 200 mg tablets five times a day for one week.\n\nSignificant improvement was visible in the second follow-up, five days after the previous visit, showing excellent healing in all of the patient’s oral lesions. The OHIP-14 result at the last visit was 4 (good OHRQoL). The patient’s physical, psychological, and social conditions showed improvement and returned to normal after 7 days of treatment. Patient was referred to continue dental and oral care in the periodontics, dental conservation, oral surgery, and prosthodontics departments. The patient has approved and written informed consent for the case details to be published included publication of the images, and the institution has also approved for publication. This case had complied with the Declaration of Helsinki.",
+    "diff_label_texts": "A 25-year-old Sundanese male presented to the Dental Hospital, Faculty of Dentistry, Universitas Padjadjaran with a 4-day history of painful oral ulcerations that appeared intraorally first and extended to the lips 2 days later, exacerbated by eating and speaking. He initially self-treated with petroleum jelly without benefit, then applied triamcinolone acetonide 0.1% in orabase once daily from a pharmacy, with partial but incomplete improvement. One week prior to lesion onset he reported a febrile episode; he also reported heavy workload and approximately 1.5 months of suboptimal nutrition. He denied systemic disease, drug or food allergies, alcohol, and tobacco, but reported frequent lip-licking; childhood varicella was noted.\n\nGeneral examination showed normal vital signs and no lymphadenopathy. Extraoral findings: serosanguineous crusts on the lips that were painful and bled easily. Intraoral findings: irregular, diffuse-bordered erythematous lesions with pain on the upper and lower labial mucosa. Additional findings included a non-scrapable hyperkeratotic white plaque of irregular shape with diffuse borders on the left buccal mucosa near tooth 38; scrapable yellowish-white plaques on the posterior third of the dorsal tongue without underlying erythema; crenated tongue with dental impressions laterally; a painless, hard torus palatinus (~2 × 1 × 0.5 cm) at the hard palate midline; multiple teeth with caries, radix, and edentulous areas; poor oral hygiene.\n\nPsychological assessment (DASS-21): normal depression (0), anxiety (6), and stress (6). Working diagnosis: suspected HAEM, with concurrent findings of coated tongue, frictional keratosis, crenated tongue, torus palatinus, reversible pulpitis (tooth 18), irreversible pulpitis (tooth 47), chronic apical periodontitis et causa radix (tooth 15), and edentulous teeth 28, 37, 36, and 46. Differential diagnosis for the lip lesions included exfoliative cheilitis, which lacks herpesvirus involvement. Serologic testing (IgG anti–HSV-1) was indicated to support the diagnosis. Baseline OHRQoL (OHIP-14) was 35 (moderate).\n\nInitial management combined non-pharmacologic and pharmacologic therapy. Non-pharmacologic: oral hygiene instructions (brush teeth and tongue twice daily with a soft-bristled brush and non-detergent toothpaste), hydrate with ≥2 L water/day, consume a balanced diet, avoid acidic, spicy, hard, and MSG-containing foods, and cease lip-licking and peeling. Pharmacologic: topical lip compresses with 0.9% NaCl at least three times daily and triamcinolone acetonide 0.1% in orabase applied thinly to the lips three times daily; a daily multivitamin was prescribed.\n\nAt 2-day follow-up, pain had decreased though serosanguineous crusts persisted. Serology returned positive for anti–HSV-1 IgG, ratio 6.32 (positive >1.1). A definitive diagnosis of HAEM (herpes-associated erythema multiforme) was established based on history, clinical findings, and serology. Existing therapy was continued, and acyclovir 200 mg orally five times daily for 7 days was added.\n\nAt 5 days after the prior visit, there was significant improvement with excellent healing of all oral lesions. Final OHIP-14 was 4, and physical, psychological, and social conditions normalized after 7 days of treatment. The patient was referred for definitive dental and oral care in periodontics, dental conservation, oral surgery, and prosthodontics. Written informed consent and institutional approval were obtained; the case complies with the Declaration of Helsinki.\n\nContext: HAEM is an immune-mediated mucocutaneous reaction pattern commonly triggered by HSV-1. Positive HSV-1 serology in the appropriate clinical context, together with characteristic labial crusting and diffuse labial mucosal erythema, supports the diagnosis. Management typically combines topical corticosteroids and systemic antiviral therapy, along with supportive oral care and trigger avoidance.",
+    "summary": "A 25-year-old male patient came to the Department of Oral Medicine with the chief complaint of painful canker sores on the lips. Extra-oral examination revealed serosanguineous crusts on the lips that were painful and easily bleed. Intra-oral examination showed diffused and painful irregular erythematous lesions on the upper and lower labial mucosa. The anti-HSV1 IgG test was positive. The patient was diagnosed with HAEM.\n\nCase management: Pharmacological therapy included triamcinolone acetonide 0.1% in orabase, acyclovir tablets, multivitamins, and 0.9% NaCl. Non-pharmacological therapy included advice on maintaining good oral hygiene, avoiding spicy and sour foods, and breaking the bad habit of licking the lips."
+  },
+  {
+    "doc_id": 37,
+    "label": "proficient_health_literacy",
+    "fulltext": "A 29-year-old woman, Para 1, with abnormal vaginal bleeding of one-month duration presented to the gynecology outpatient department of a level 2 hospital. She was HIV positive, commenced on antiretroviral treatment following diagnosis, but had defaulted the antiretroviral treatment for one month when she became ill with vaginal bleeding, resulting in virological and immunological failures (viral load 37400 copies/mL and CD4 count 26 cells/μL). Of note, it was unclear when the patient first started showing HIV symptoms. However, she was diagnosed with HIV about a year prior to presentation. Physical examination revealed a large mass on the cervix measuring 8 × 8 cm extending to the parametrium and to the pelvic side walls bilaterally. There was bleeding on contact and foul-smelling vaginal discharge. Ultrasonography detected a bulky cervix and bilateral hydronephrosis. The patient was clinically diagnosed with cervical malignancy stage 3B. She was recommenced on antiretroviral therapy with a treatment change from TLD (Tenofovir-Lamivudine-Dolutegravir combination) to a preferable renal friendly regimen (Lamivudine-Abacavir-Dolutegravir combination). A punch biopsy of the cervix was performed, and the histopathological report revealed the diagnosis of an extra-nodal BL. The immunohistochemical and in situ hybridization confirmed the diagnosis, with CD20, CD75a, CD10, PAX5 and Bcl-6 positive. In addition, the CD44 and c-Myc were positive, with the EBER-ISH demonstrating focal positivity. The Ki67 demonstrated a proliferation index of almost 100% and PAX5 moderately positive BCL6. She had white cell count of 2.67 x109/L, haemoglobin of 5.7g/dl and platelet count of 71 × 109/L. Results of other investigations were serum creatinine 187 mmol/L, urea 11.1 mmol/l, albumin 21 g/l, aspartate transaminase 41 U/l and alkaline phosphatase 100 U/l.\n\nFollowing histological confirmation of the diagnosis and review at an oncology multidisciplinary meeting, she spent 43 days waiting to start treatment at oncology unit. The delay was due to long waiting list. This delay exceeded the 48 hours waiting period during which oncological treatment for BL should commence following diagnosis. The treatment plan was chemo-radiation therapy, and the patient gave written informed consent for the case to be published. However, she demised in the gynaecological ward on the 43rd day while waiting to start the treatment. During the 43 days, further imaging could not be performed due to poor functionality of the available CT and MRI machines. In addition to antiretroviral therapy, the patient received other supportive care such as blood transfusion and analgesia. Again, the number of days between the diagnosis of the BL and her death was 43 days. Histopathological postmortem was not performed as the diagnoses (BL and retroviral disease) were known. We reckon that the main primary cause of death is challenging to assign because of the multiple principal diagnoses. Because BL has rapid progression and high mortality rate in persons living with HIV particularly with high viral load, the attending physician certifying the death assigned BL as the most likely cause of death. However, the secondary cause of death was multiple organ failure (renal and haematological inclusive).",
+    "diff_label_texts": "A 29-year-old woman, Para 1, presented with one month of abnormal vaginal bleeding to a level 2 hospital. She was HIV positive, had been commenced on antiretroviral therapy (ART) after diagnosis approximately one year earlier, but defaulted ART for one month when she became ill with vaginal bleeding, resulting in virological and immunological failure (viral load 37,400 copies/mL; CD4 26 cells/μL). On exam, there was an 8 × 8 cm friable cervical mass extending to the parametrium and bilaterally to the pelvic sidewalls, with contact bleeding and foul-smelling discharge. Ultrasonography showed a bulky cervix and bilateral hydronephrosis. She was clinically staged as FIGO stage 3B cervical malignancy based on pelvic wall involvement and hydronephrosis. ART was re-initiated with a switch from TLD (Tenofovir–Lamivudine–Dolutegravir) to a renal-friendly regimen (Lamivudine–Abacavir–Dolutegravir). A punch cervical biopsy revealed extra-nodal BL (Burkitt lymphoma). Immunohistochemistry and in situ hybridization confirmed the diagnosis: CD20, CD75a, CD10, PAX5, and Bcl-6 positive; CD44 and c-Myc positive; EBER-ISH focally positive. Ki-67 showed an almost 100% proliferation index, and PAX5 moderately positive BCL6. Baseline labs included WBC 2.67 × 10^9/L, hemoglobin 5.7 g/dL, platelets 71 × 10^9/L; creatinine 187 mmol/L, urea 11.1 mmol/L, albumin 21 g/L, AST 41 U/L, ALP 100 U/L. After histologic confirmation and multidisciplinary review, the plan was chemoradiation. She then waited 43 days to start treatment at the oncology unit due to a long waiting list—exceeding the recommended ≤48-hour window for initiating BL therapy. During this interval, further CT/MRI imaging could not be performed due to equipment dysfunction. Supportive care included ART, blood transfusion, and analgesia. She died on day 43 post-diagnosis while awaiting treatment and received no chemoradiation. No histopathological postmortem was performed because BL and HIV were established. Given BL’s rapid progression and high mortality in people with HIV and high viral load, the attending physician certified BL as the most likely primary cause of death, with multiple organ failure (including renal and hematologic) as a secondary cause.",
+    "summary": "The patient was a 29-year-old woman, Para 1, with abnormal vaginal bleeding for a month and living with HIV and had a CD4 of 26 cells/μL. The histological examination of the cervical biopsy confirmed an extra-nodal BL. She had International Federation of Gynecology and Obstetrics (FIGO) stage 3B cervical cancer based on presence of hydronephrosis and pelvic wall involvement. The patient was reviewed at the oncology multidisciplinary meeting and required chemoradiation. There was delay in her management due to a long waiting list for chemoradiation at oncology unit in the referral center and the patient demised 43 days after diagnosis and did not receive the treatment."
+  },
+  {
+    "doc_id": 38,
+    "label": "proficient_health_literacy",
+    "fulltext": "A 56-year-old female patient presented with complaints of dyspnea that required oxygen supplementation. Her medical history dates back to July 2013 when she was hospitalized in the chest ward for dyspnea and cough with yellow sputum. She was subsequently diagnosed with Sjogren’s syndrome complicated with interstitial lung disease (ILD) and PAH (Table I). Her chest X-ray at that time showed vascular markings with interstitial thickening, costophrenic (CP) angle blunting and cardiomegaly. An echocardiogram revealed a pulmonary arterial (PA) systolic pressure of 99 mmHg, enlargement of the right atrium and ventricle, D-shaped left ventricle (LV), and severe tricuspid regurgitation. Chest CNYCT showed no filling defects, excluding pulmonary embolism; it also displayed an enlarged pulmonary trunk, right atrium (RA), and right ventricle (RV), further evidencing pulmonary hypertension. Symptoms of dry mouth, dry eyes, and cracked tongue mucosa, with a Schirmer’s test showing <5 cm, oculus uterque (OU). A positive minor salivary gland biopsy, nuclear medicine scan showing impaired salivary gland function, and a positive anti-Ro test, confirmed Sjogren’s syndrome. She started on Revatio (Sildenafil) 20 mg three times a day (TID) for pulmonary hypertension control, adding Tracleer (Bosentan) in 2016 due to disease progression. A right heart catheterization (RHC) revealed a mean pulmonary arterial pressure (PAP) of 39 mmHg, pulmonary vascular resistance (PVR) nearly 15 Woods, and a wedge pressure of 4, indicating pre-capillary type, group I, CTD-related PAH in 2017. The right heart catheterization (RHC) report allowed for insurance coverage of Opsumit (Macitentan) 10 mg once a day (QD), replacing Tracleer (Bosentan) in 2017. From 2017 to 2020, she was hospitalized multiple times for steroid treatments to manage her underlying Sjogren’s syndrome.\n\nPulmonary hypertension treatment is risk-based, and until 2017, the patient was considered low to intermediate risk, controlled with two medications (Sildenafil + Macitentan). Her condition remained stable until October 2020, when she experienced worsened dyspnea accompanied by cough and expectoration of white sputum, suggestive of infection. On November 10, 2020, the patient experienced severe dyspnea, cold sweats, and cyanosis, with SpO2 dropping to 70%, necessitating 100% O2 via face tent. Blood gas and lab tests revealed a lactate level of 5.2 mmol/l and brain natriuretic peptide (BNP) over 10,000 pg/ml, strongly suggesting cardiogenic shock. She was prepped for intensive care unit (ICU) admission, intubated, and initiated on four pulmonary hypertension medications. Her condition stabilized and showed improvement, preventing further deterioration. On November 12, 2020, evaluation for heart-lung transplantation began. Her condition continued to improve with off vasopressors on November 13, 2020, and extubating on November 14, 2020, and transferred to a general ward on November 21, 2020, with O2 tapered to nasal cannula 2l/min. A follow-up RHC continued to show elevated pulmonary artery pressure, likely attributed to chronic hypertension leading to right heart strain and eventual failure. After intensive care unit (ICU) treatment, she was referred to National Taiwan University Hospital for evaluation for heart-lung transplant.\n\nReviewing the records since the onset of her illness, it was evident that pulmonary artery pressure had steadily increased, and the distance covered in the 6-minute walk test was progressively shortened. Currently, the patient is classified as high risk. She continues regular hospitalizations for control. Despite the relatively stable condition, her chief complaint during the admission is still dyspnea. The physical examination revealed mild rhonchi ILD and a pansystolic murmur indicative of severe valvular heart disease, with no other significant findings. Ventavis (Iloprost) 10 mcg/ml 2 ml was added in 2020. Molecular hydrogen therapy (1 capsule/day) was initiated in May 2023. Hydrogen capsules (PURE HYDROGEN) were purchased from HoHo Biotech Co., Ltd. (Taipei, Taiwan, ROC). Each capsule contained 170 mg of hydrogen-rich coral calcium containing 1.7×1,021 molecules of hydrogen, which is equivalent to 24 cups of water with 1,200 ppb of hydrogen or 0.6 mM of hydrogen per 200 ml of water. Adjuvant therapy with hydrogen capsules resulted in increased CD127 + Treg, decreased anti-Ro antibody, decreased B cell subsets, and stabilization of clinical symptoms and signs was observed following the addition of hydrogen therapy in this patient. No adverse reactions or events were observed following the administration of hydrogen capsules. Flow cytometry and serological examination were employed for whole-blood analysis to assess changes in immune cells and autoantibody before and after hydrogen therapy. For subsequent whole-blood analysis via flow cytometry, blood samples were prepared using standard fluorescent dye preparation methods and fluorescent antibody reagent kits with dried reagents (Beckman Coulter, Brea, CA, USA). The methods, steps, immunophenotypic analysis, and cell gating were conducted following previously described procedures. Our analysis of immunophenotypic markers before and after hydrogen therapy revealed increased CD127 + Treg and decreased B cell subsets after treatment. Moreover, this study adheres to the CARE reporting guidelines (2013 CARE Checklist).",
+    "diff_label_texts": "A 56-year-old female with CTD-PAH secondary to Sjogren’s syndrome (diagnosed 2013) complicated by ILD initially presented with dyspnea. Early studies showed interstitial changes and cardiomegaly on chest X-ray; echocardiography demonstrated PASP 99 mmHg, RA/RV enlargement, D-shaped LV, and severe TR. Chest CNYCT showed no filling defects to suggest PE, with enlarged pulmonary trunk, RA, and RV, consistent with PH. Sjogren’s was confirmed by sicca symptoms with Schirmer’s <5 cm OU, positive minor salivary gland biopsy, impaired salivary gland function on nuclear medicine scan, and positive anti-Ro. She began Revatio (sildenafil) 20 mg TID in 2013; Tracleer (bosentan) was added in 2016. Right heart catheterization in 2017 showed mPAP 39 mmHg, PVR nearly 15 Woods, and wedge 4 mmHg, indicating pre-capillary, group I CTD-PAH; Opsumit (macitentan) 10 mg QD replaced bosentan. From 2017 to 2020 she required repeated steroid hospitalizations for Sjogren’s control. Her risk status was low-to-intermediate on dual therapy until October–November 2020, when she developed worsened dyspnea and signs of infection, then severe decompensation on November 10 with SpO2 70% requiring 100% O2 via face tent, lactate 5.2 mmol/L, and BNP >10,000 pg/mL, consistent with cardiogenic shock. She was intubated in the ICU, started on four PH agents, stabilized, and improved; heart–lung transplant evaluation began November 12, vasopressors were discontinued November 13, she was extubated November 14, and transferred to the ward November 21 on nasal cannula 2 L/min. Follow-up RHC showed persistently elevated PA pressures attributed to chronic PH with right heart strain. She was reclassified as high risk; Ventavis (iloprost) 10 mcg/ml 2 ml was added in 2020. In May 2023, molecular hydrogen was initiated as adjuvant therapy: 1 capsule/day (PURE HYDROGEN; HoHo Biotech, Taipei, Taiwan), each containing 170 mg of hydrogen-rich coral calcium with 1.7×1,021 molecules of hydrogen, equivalent to 24 cups of water at 1,200 ppb H2 or 0.6 mM H2 per 200 ml water. Flow cytometry and serology (standard fluorescent dye preparation; dried reagent kits, Beckman Coulter; immunophenotyping and gating per prior methods) before and after hydrogen therapy demonstrated increased CD127+ Treg populations and decreased B cell subsets; anti-Ro antibody levels declined. Clinically, signs and symptoms stabilized following the addition of hydrogen therapy, and no adverse reactions occurred. The case adheres to CARE reporting guidelines (2013 CARE Checklist).",
+    "summary": "We present the case of a 56-year-old female with CTD-PAH, diagnosed in 2013 with Sjogren’s syndrome complicated by interstitial lung disease (ILD) and PAH. Despite treatment with sildenafil, bosentan, macitentan, iloprost, and corticosteroids, her condition deteriorated, resulting in severe dyspnea and cardiogenic shock in 2020. In May 2023, molecular hydrogen therapy was initiated as an adjuvant treatment. The patient received daily hydrogen capsules, which led to increased CD127+ Treg cells, reduced anti-Ro antibodies, and decreased B cell subsets. Her clinical symptoms stabilized without adverse effects."
+  },
+  {
+    "doc_id": 39,
+    "label": "low_health_literacy",
+    "fulltext": "The patient was a 45-year-old male born in Pakistan who had resided in Portugal for 7 years. He had a history of grade 3 obesity, with no other known personal history or usual pharmacological therapy.\n\nThe patient sought emergency care for fever, dry cough, dyspnea, chest pain, dysgeusia, headache and myalgia with 4 days of evolution. In the summary neurological examination at admission, there were no reported changes. In the evaluation of the respiratory system, tachypnea and pulmonary auscultation with bilateral rough vesicular murmur, without other adventitious sounds, were noted. The remainder of the objective examination showed no changes.\n\nOf the complementary diagnostic tests performed at admission, there was a slight increase in inflammatory parameters and in arterial blood gases under an inspired oxygen fraction (FiO2) of 21%, with type 1 respiratory failure and extensive predominant bilateral, peripheral and basal opacities on chest teleradiography. After a positive reverse-transcription real-time polymerase chain reaction (RT-PCR) test for SARS-CoV-2 (nasal and oropharyngeal exudate) and negative tests for influenza A and B, Streptococcus pneumoniae and Legionella pneumophila, a diagnosis of pneumonia by SARS-CoV-2 infection was established.\n\nOver the first 48 hours, progressive worsening of fatigue, dyspnea and type 1 respiratory failure, requiring an increase in supplemental oxygen therapy, were observed. Due to the lack of improvement, noninvasive mechanical ventilation was initiated; however, due to poor adherence, high-flow oxygen therapy was initiated through a nasal cannula, without a response to therapy.\n\nIn this context, the patient was admitted to the intensive care unit (ICU), level III, where he underwent sedoanalgesia and orotracheal intubation with connection to invasive mechanical ventilation.\n\nOn the eleventh day of hospitalization, treatment with remdesivir, dexamethasone, enoxaparin and empirical antibiotic therapy with amoxicillin/clavulanic acid and azithromycin, administered on suspicion of bacterial overinfection, was continued. During this period, sustained fever was observed, with a weak response to antipyretic therapy, with improvements in inflammatory parameters after the third day of hospitalization in the ICU.\n\nTo exclude any concomitant infectious etiology, intravenous devices were replaced, and blood cultures, cultures of the tip of the central catheter and bronchial secretions, urinalysis, urine culture and transthoracic echocardiography were performed. Among the cultures, the blood culture yielded the only positive result, i.e., Klebsiella pneumoniae, which is sensitive to amoxicillin/clavulanic acid, which the patient was already receiving. The summary echocardiogram did not reveal valve changes suggestive of endocarditis, but the patient presented hypokinesia of the lateral wall and left ventricular apex, as well as poor biventricular function. A slight increase in troponins (1.8ng/mL) and ST-segment depression in leads I and aVL were confirmed, suggesting the existence of acute coronary syndrome or septic cardiomyopathy.\n\nOther noninfectious causes of febrile symptoms in the critically ill patient were excluded, including treatment with neuroleptics or altered thyroid function.\n\nNotably, there was a need for inotropic support with dobutamine in the ventilatory weaning phase as well as noninvasive ventilatory support after orotracheal extubation, which occurred on the fifteenth day of hospitalization.\n\nOn the sixteenth day of hospitalization (nineteenth day of confirmed disease), there was an episode of altered state of consciousness, conjugated deviation of gaze to the right and myoclonus of the face and thoracic region to the left followed by a generalized tonic-clonic seizure crisis, which ceased after midazolam therapy. The hypothesis that the seizure occurred in the context of a hypoxic-ischemic event was excluded because the patient remained normotensive, there was never a peri-event or hypoxemia, serum lactate level was normal, and diuresis remained preserved. Any ionic or glycemic disorders that could explain the inaugural seizure episode were excluded.\n\nIn the post-critical period, there was an absence of eye opening, no verbal response, failure to localize to pain (coma scale of Glasgow 7), and persistent left hemiparesis grade 3 out of 5. Due to the need for airway protection, the patient was sedated, subjected to orotracheal intubation and started on anticonvulsant therapy.\n\nIn the process of diagnosis of the convulsive episode, after cranial computed tomography confirmed no changes, the patient was subjected to lumbar puncture, with turbid CSF output and mild proteinorrachia but without pleocytosis and with normal opening pressure. In the CSF, neurotropic virus and venereal disease research laboratory (VDRL), acid-alcohol resistant bacteria tests and an RT-PCR test for SARS-CoV-2 were requested, and samples were collected for culture. Electroencephalography was performed 1 hour after propofol suspension and under fentanyl, with a single record and total duration of 13 minutes; the findings indicated no changes.\n\nAfter confirmation of a positive RT-PCR test for SARS-CoV-2 RNA in the CSF, without CSF pleiocytosis, the hypothesis of bacterial but nonviral meningitis was excluded, considering the hypothesis of encephalitis. Magnetic resonance imaging (MRI) performed on the seventeenth day of hospitalization showed multiple image artifacts associated with patient movement during the procedure, suggesting the need to repeat the examination.\n\nAfter discontinuation of sedoanalgesia, a change in consciousness was observed, with a Glasgow coma scale score of 14, persistent left hemiparesis with muscle strength grade 4 in 5 and an absence of involuntary movements, allowing safe orotracheal extubation in 24 hours. Given the favorable clinical outcome, brain biopsy was excluded. On the twenty-first day of hospitalization, the patient was transferred to the ward.\n\nThe patient maintained apyrexia without altered state of consciousness. No new episodes of involuntary movements were observed, and on the twenty-sixth day of hospitalization, he underwent a reassessment MRI, which revealed no pathological changes. As he maintained a favorable clinical evolution, the patient was discharged on the thirty-first day of hospitalization without antiepileptic drugs and with an appointment for follow-up with the internal medicine department.\n",
+    "diff_label_texts": "A 45-year-old man was in the hospital with lung infection from the virus that causes COVID-19. He had no past brain or nerve problems. On day 16 in the hospital, he suddenly became less awake. Both eyes pulled to the right. His left face and chest had quick jerks. Then he had a full-body seizure. After that, the left side of his body stayed weak. A lab test on the fluid around his brain and spine found the COVID-19 virus. He slowly got better, and the final result was good.",
+    "summary": "The authors present the clinical case of a 45-year-old man admitted for pneumonia with a positive result for SARS-CoV-2, with no neurological history, who, on the 16th day of admission, presented a sudden change in consciousness accompanied by a conjugate deviation of the gaze to the right and myoclonia of the face and thoracic region to the left, followed by a generalized tonic-clonic convulsive seizure, associated with persistent left hemiparesis. From the study carried out, the existence of RT-PCR for SARS-CoV-2 in the cerebrospinal fluid is highlighted. The patient presented a clinical evolution with gradual improvement, and the outcome was favourable.\n"
+  },
+  {
+    "doc_id": 39,
+    "label": "intermediate_health_literacy",
+    "fulltext": "The patient was a 45-year-old male born in Pakistan who had resided in Portugal for 7 years. He had a history of grade 3 obesity, with no other known personal history or usual pharmacological therapy.\n\nThe patient sought emergency care for fever, dry cough, dyspnea, chest pain, dysgeusia, headache and myalgia with 4 days of evolution. In the summary neurological examination at admission, there were no reported changes. In the evaluation of the respiratory system, tachypnea and pulmonary auscultation with bilateral rough vesicular murmur, without other adventitious sounds, were noted. The remainder of the objective examination showed no changes.\n\nOf the complementary diagnostic tests performed at admission, there was a slight increase in inflammatory parameters and in arterial blood gases under an inspired oxygen fraction (FiO2) of 21%, with type 1 respiratory failure and extensive predominant bilateral, peripheral and basal opacities on chest teleradiography. After a positive reverse-transcription real-time polymerase chain reaction (RT-PCR) test for SARS-CoV-2 (nasal and oropharyngeal exudate) and negative tests for influenza A and B, Streptococcus pneumoniae and Legionella pneumophila, a diagnosis of pneumonia by SARS-CoV-2 infection was established.\n\nOver the first 48 hours, progressive worsening of fatigue, dyspnea and type 1 respiratory failure, requiring an increase in supplemental oxygen therapy, were observed. Due to the lack of improvement, noninvasive mechanical ventilation was initiated; however, due to poor adherence, high-flow oxygen therapy was initiated through a nasal cannula, without a response to therapy.\n\nIn this context, the patient was admitted to the intensive care unit (ICU), level III, where he underwent sedoanalgesia and orotracheal intubation with connection to invasive mechanical ventilation.\n\nOn the eleventh day of hospitalization, treatment with remdesivir, dexamethasone, enoxaparin and empirical antibiotic therapy with amoxicillin/clavulanic acid and azithromycin, administered on suspicion of bacterial overinfection, was continued. During this period, sustained fever was observed, with a weak response to antipyretic therapy, with improvements in inflammatory parameters after the third day of hospitalization in the ICU.\n\nTo exclude any concomitant infectious etiology, intravenous devices were replaced, and blood cultures, cultures of the tip of the central catheter and bronchial secretions, urinalysis, urine culture and transthoracic echocardiography were performed. Among the cultures, the blood culture yielded the only positive result, i.e., Klebsiella pneumoniae, which is sensitive to amoxicillin/clavulanic acid, which the patient was already receiving. The summary echocardiogram did not reveal valve changes suggestive of endocarditis, but the patient presented hypokinesia of the lateral wall and left ventricular apex, as well as poor biventricular function. A slight increase in troponins (1.8ng/mL) and ST-segment depression in leads I and aVL were confirmed, suggesting the existence of acute coronary syndrome or septic cardiomyopathy.\n\nOther noninfectious causes of febrile symptoms in the critically ill patient were excluded, including treatment with neuroleptics or altered thyroid function.\n\nNotably, there was a need for inotropic support with dobutamine in the ventilatory weaning phase as well as noninvasive ventilatory support after orotracheal extubation, which occurred on the fifteenth day of hospitalization.\n\nOn the sixteenth day of hospitalization (nineteenth day of confirmed disease), there was an episode of altered state of consciousness, conjugated deviation of gaze to the right and myoclonus of the face and thoracic region to the left followed by a generalized tonic-clonic seizure crisis, which ceased after midazolam therapy. The hypothesis that the seizure occurred in the context of a hypoxic-ischemic event was excluded because the patient remained normotensive, there was never a peri-event or hypoxemia, serum lactate level was normal, and diuresis remained preserved. Any ionic or glycemic disorders that could explain the inaugural seizure episode were excluded.\n\nIn the post-critical period, there was an absence of eye opening, no verbal response, failure to localize to pain (coma scale of Glasgow 7), and persistent left hemiparesis grade 3 out of 5. Due to the need for airway protection, the patient was sedated, subjected to orotracheal intubation and started on anticonvulsant therapy.\n\nIn the process of diagnosis of the convulsive episode, after cranial computed tomography confirmed no changes, the patient was subjected to lumbar puncture, with turbid CSF output and mild proteinorrachia but without pleocytosis and with normal opening pressure. In the CSF, neurotropic virus and venereal disease research laboratory (VDRL), acid-alcohol resistant bacteria tests and an RT-PCR test for SARS-CoV-2 were requested, and samples were collected for culture. Electroencephalography was performed 1 hour after propofol suspension and under fentanyl, with a single record and total duration of 13 minutes; the findings indicated no changes.\n\nAfter confirmation of a positive RT-PCR test for SARS-CoV-2 RNA in the CSF, without CSF pleiocytosis, the hypothesis of bacterial but nonviral meningitis was excluded, considering the hypothesis of encephalitis. Magnetic resonance imaging (MRI) performed on the seventeenth day of hospitalization showed multiple image artifacts associated with patient movement during the procedure, suggesting the need to repeat the examination.\n\nAfter discontinuation of sedoanalgesia, a change in consciousness was observed, with a Glasgow coma scale score of 14, persistent left hemiparesis with muscle strength grade 4 in 5 and an absence of involuntary movements, allowing safe orotracheal extubation in 24 hours. Given the favorable clinical outcome, brain biopsy was excluded. On the twenty-first day of hospitalization, the patient was transferred to the ward.\n\nThe patient maintained apyrexia without altered state of consciousness. No new episodes of involuntary movements were observed, and on the twenty-sixth day of hospitalization, he underwent a reassessment MRI, which revealed no pathological changes. As he maintained a favorable clinical evolution, the patient was discharged on the thirty-first day of hospitalization without antiepileptic drugs and with an appointment for follow-up with the internal medicine department.\n",
+    "diff_label_texts": "A 45-year-old man was hospitalized with COVID-19 pneumonia and had no prior neurologic history. On hospital day 16, he suddenly developed reduced consciousness, his eyes deviated to the right, and he had jerking movements on the left side of his face and chest, followed by a generalized tonic–clonic seizure. After the seizure, he was left with persistent weakness on the left side (left hemiparesis). Brain CT was normal, and a spinal tap showed slightly elevated protein but no increase in white blood cells. Importantly, the cerebrospinal fluid tested positive for SARS-CoV-2 by RT-PCR, making viral involvement of the brain (encephalitis) likely and bacterial meningitis unlikely. An EEG did not show clear abnormalities, and later MRI was also unremarkable. He improved gradually, his condition stabilized, and his overall outcome was favorable.",
+    "summary": "The authors present the clinical case of a 45-year-old man admitted for pneumonia with a positive result for SARS-CoV-2, with no neurological history, who, on the 16th day of admission, presented a sudden change in consciousness accompanied by a conjugate deviation of the gaze to the right and myoclonia of the face and thoracic region to the left, followed by a generalized tonic-clonic convulsive seizure, associated with persistent left hemiparesis. From the study carried out, the existence of RT-PCR for SARS-CoV-2 in the cerebrospinal fluid is highlighted. The patient presented a clinical evolution with gradual improvement, and the outcome was favourable.\n"
+  },
+  {
+    "doc_id": 39,
+    "label": "proficient_health_literacy",
+    "fulltext": "The patient was a 45-year-old male born in Pakistan who had resided in Portugal for 7 years. He had a history of grade 3 obesity, with no other known personal history or usual pharmacological therapy.\n\nThe patient sought emergency care for fever, dry cough, dyspnea, chest pain, dysgeusia, headache and myalgia with 4 days of evolution. In the summary neurological examination at admission, there were no reported changes. In the evaluation of the respiratory system, tachypnea and pulmonary auscultation with bilateral rough vesicular murmur, without other adventitious sounds, were noted. The remainder of the objective examination showed no changes.\n\nOf the complementary diagnostic tests performed at admission, there was a slight increase in inflammatory parameters and in arterial blood gases under an inspired oxygen fraction (FiO2) of 21%, with type 1 respiratory failure and extensive predominant bilateral, peripheral and basal opacities on chest teleradiography. After a positive reverse-transcription real-time polymerase chain reaction (RT-PCR) test for SARS-CoV-2 (nasal and oropharyngeal exudate) and negative tests for influenza A and B, Streptococcus pneumoniae and Legionella pneumophila, a diagnosis of pneumonia by SARS-CoV-2 infection was established.\n\nOver the first 48 hours, progressive worsening of fatigue, dyspnea and type 1 respiratory failure, requiring an increase in supplemental oxygen therapy, were observed. Due to the lack of improvement, noninvasive mechanical ventilation was initiated; however, due to poor adherence, high-flow oxygen therapy was initiated through a nasal cannula, without a response to therapy.\n\nIn this context, the patient was admitted to the intensive care unit (ICU), level III, where he underwent sedoanalgesia and orotracheal intubation with connection to invasive mechanical ventilation.\n\nOn the eleventh day of hospitalization, treatment with remdesivir, dexamethasone, enoxaparin and empirical antibiotic therapy with amoxicillin/clavulanic acid and azithromycin, administered on suspicion of bacterial overinfection, was continued. During this period, sustained fever was observed, with a weak response to antipyretic therapy, with improvements in inflammatory parameters after the third day of hospitalization in the ICU.\n\nTo exclude any concomitant infectious etiology, intravenous devices were replaced, and blood cultures, cultures of the tip of the central catheter and bronchial secretions, urinalysis, urine culture and transthoracic echocardiography were performed. Among the cultures, the blood culture yielded the only positive result, i.e., Klebsiella pneumoniae, which is sensitive to amoxicillin/clavulanic acid, which the patient was already receiving. The summary echocardiogram did not reveal valve changes suggestive of endocarditis, but the patient presented hypokinesia of the lateral wall and left ventricular apex, as well as poor biventricular function. A slight increase in troponins (1.8ng/mL) and ST-segment depression in leads I and aVL were confirmed, suggesting the existence of acute coronary syndrome or septic cardiomyopathy.\n\nOther noninfectious causes of febrile symptoms in the critically ill patient were excluded, including treatment with neuroleptics or altered thyroid function.\n\nNotably, there was a need for inotropic support with dobutamine in the ventilatory weaning phase as well as noninvasive ventilatory support after orotracheal extubation, which occurred on the fifteenth day of hospitalization.\n\nOn the sixteenth day of hospitalization (nineteenth day of confirmed disease), there was an episode of altered state of consciousness, conjugated deviation of gaze to the right and myoclonus of the face and thoracic region to the left followed by a generalized tonic-clonic seizure crisis, which ceased after midazolam therapy. The hypothesis that the seizure occurred in the context of a hypoxic-ischemic event was excluded because the patient remained normotensive, there was never a peri-event or hypoxemia, serum lactate level was normal, and diuresis remained preserved. Any ionic or glycemic disorders that could explain the inaugural seizure episode were excluded.\n\nIn the post-critical period, there was an absence of eye opening, no verbal response, failure to localize to pain (coma scale of Glasgow 7), and persistent left hemiparesis grade 3 out of 5. Due to the need for airway protection, the patient was sedated, subjected to orotracheal intubation and started on anticonvulsant therapy.\n\nIn the process of diagnosis of the convulsive episode, after cranial computed tomography confirmed no changes, the patient was subjected to lumbar puncture, with turbid CSF output and mild proteinorrachia but without pleocytosis and with normal opening pressure. In the CSF, neurotropic virus and venereal disease research laboratory (VDRL), acid-alcohol resistant bacteria tests and an RT-PCR test for SARS-CoV-2 were requested, and samples were collected for culture. Electroencephalography was performed 1 hour after propofol suspension and under fentanyl, with a single record and total duration of 13 minutes; the findings indicated no changes.\n\nAfter confirmation of a positive RT-PCR test for SARS-CoV-2 RNA in the CSF, without CSF pleiocytosis, the hypothesis of bacterial but nonviral meningitis was excluded, considering the hypothesis of encephalitis. Magnetic resonance imaging (MRI) performed on the seventeenth day of hospitalization showed multiple image artifacts associated with patient movement during the procedure, suggesting the need to repeat the examination.\n\nAfter discontinuation of sedoanalgesia, a change in consciousness was observed, with a Glasgow coma scale score of 14, persistent left hemiparesis with muscle strength grade 4 in 5 and an absence of involuntary movements, allowing safe orotracheal extubation in 24 hours. Given the favorable clinical outcome, brain biopsy was excluded. On the twenty-first day of hospitalization, the patient was transferred to the ward.\n\nThe patient maintained apyrexia without altered state of consciousness. No new episodes of involuntary movements were observed, and on the twenty-sixth day of hospitalization, he underwent a reassessment MRI, which revealed no pathological changes. As he maintained a favorable clinical evolution, the patient was discharged on the thirty-first day of hospitalization without antiepileptic drugs and with an appointment for follow-up with the internal medicine department.\n",
+    "diff_label_texts": "A 45-year-old male (Pakistan-born, 7 years in Portugal) with grade 3 obesity and no neurologic history presented with 4 days of fever, dry cough, dyspnea, chest pain, dysgeusia, headache, and myalgia. Admission exam: no focal neurologic findings; tachypnea; bilateral rough vesicular murmur; otherwise unremarkable. Labs showed mildly elevated inflammatory markers; on room air (FiO2 21%) arterial gases were consistent with type 1 respiratory failure. Chest teleradiography: extensive bilateral, predominantly peripheral and basal opacities. Nasal/oropharyngeal RT-PCR for SARS-CoV-2 was positive; influenza A/B, Streptococcus pneumoniae, and Legionella pneumophila tests were negative, confirming COVID-19 pneumonia. Respiratory status worsened over 48 hours, escalating from supplemental O2 to noninvasive ventilation, then high-flow nasal cannula without response. He was transferred to a level III ICU for sedoanalgesia, orotracheal intubation, and invasive mechanical ventilation.\nBy ICU day 11, he was on remdesivir, dexamethasone, enoxaparin, and empirical amoxicillin/clavulanic acid plus azithromycin for suspected bacterial superinfection. He had sustained fever with poor antipyretic response; inflammatory markers improved by ICU day 3. A sepsis workup included line changes; blood, catheter tip, bronchial secretion, urine cultures; urinalysis; and transthoracic echocardiography. Only blood cultures were positive (Klebsiella pneumoniae), sensitive to amoxicillin/clavulanic acid already in use. Echocardiogram: no valvular vegetations; hypokinesia of the lateral wall and LV apex with poor biventricular function. Troponin was mildly elevated (1.8 ng/mL) with ST-segment depression in leads I and aVL, raising concern for ACS vs septic cardiomyopathy. Noninfectious fever causes (e.g., neuroleptics, thyroid dysfunction) were excluded. He required dobutamine during ventilatory weaning and needed noninvasive ventilatory support post-extubation; first extubation occurred on hospital day 15.\nOn hospital day 16 (day 19 of illness), he developed an acute alteration in consciousness with conjugate rightward gaze deviation and left facial and thoracic myoclonus, progressing to a generalized tonic–clonic seizure that terminated after midazolam. Hypoxic-ischemic seizure etiology was deemed unlikely: he remained normotensive, without peri-event hypoxemia, had normal serum lactate, and preserved diuresis. No ionic or glycemic disturbances were identified. Postictally: no eye opening, no verbal response, no localization to pain (GCS 7), and persistent left hemiparesis (3/5). For airway protection, he was resedated, reintubated, and started on anticonvulsant therapy. Head CT was unremarkable. Lumbar puncture yielded turbid CSF with mild proteinorrachia, no pleocytosis, and normal opening pressure. CSF studies included panels for neurotropic viruses, VDRL, acid–alcohol resistant bacteria, cultures, and RT-PCR for SARS-CoV-2. EEG performed 1 hour after propofol discontinuation (under fentanyl; single 13-minute recording) showed no significant abnormalities. CSF RT-PCR returned positive for SARS-CoV-2 RNA, and in the absence of CSF pleocytosis, bacterial (but not viral) meningitis was excluded; encephalitis was considered the leading diagnosis. Brain MRI on hospital day 17 was limited by motion artifacts. After withdrawal of sedoanalgesia, his mental status improved (GCS 14); left hemiparesis improved to 4/5; no recurrent involuntary movements; he was safely extubated within 24 hours. Given the favorable trajectory, brain biopsy was not pursued. He was transferred to the ward on day 21, remained afebrile with stable mentation, had no further seizures or myoclonus, and a repeat MRI on day 26 was normal. He was discharged home on day 31 without antiepileptic drugs, with internal medicine follow-up. This case highlights COVID-19–associated encephalitic presentation with a generalized seizure and persistent unilateral deficits, supported by detection of SARS-CoV-2 RNA in CSF despite absent pleocytosis, and a favorable clinical outcome with gradual recovery.",
+    "summary": "The authors present the clinical case of a 45-year-old man admitted for pneumonia with a positive result for SARS-CoV-2, with no neurological history, who, on the 16th day of admission, presented a sudden change in consciousness accompanied by a conjugate deviation of the gaze to the right and myoclonia of the face and thoracic region to the left, followed by a generalized tonic-clonic convulsive seizure, associated with persistent left hemiparesis. From the study carried out, the existence of RT-PCR for SARS-CoV-2 in the cerebrospinal fluid is highlighted. The patient presented a clinical evolution with gradual improvement, and the outcome was favourable.\n"
+  },
+  {
+    "doc_id": 40,
+    "label": "low_health_literacy",
+    "fulltext": "This is a 32-year-old patient, a baker, from Bamako, who was admitted to the Infectious and Tropical Diseases department of the CHU du Point G (Bamako, Mali) on 27 April 2023 for chronic productive cough, otalgia and a chronic right-sided purulent otorrhea.\n\nThe symptomatology would be of progressive installation in 1 month, initially treated in a medical center with artésunate, paracetamol and unspecified antibiotics for confirmed malaria and acute otitis media, without success. He is immunosuppressed by a HIV1 infection, diagnosed and put on a tritherapy antiretroviral (TARV) Tenofovir/Lamivudine/Dolutégravir 7 months ago, not observed due to denial of his illness.\n\nThe general physical examination found a fever (38.2 °C), altered general condition, otalgia, purulent right foul-smelling otorrhea, a right basal pulmonary condensation syndrome, a normal neurological examination, without the involvement of the cranial nerves, mainly the facial nerve VII and the VIII cochleovestibular nerve.\n\nIn the ENT examination, the otoscopy of the right ear showed an inflammatory external auditory canal with purulent secretions and the presence of a single tympanic perforation in the anterior-inferior quadrant. The left ear is normal. The Rinne and Weber test is in favor of a right conductive hearing loss.\n\nImmuno-virological evaluation shows a CD4 count of 118 cells/pl and a viral load of 12,370 copies/ml at the time of diagnosis of HIV infection, compared to a viral load of 9,460 copies/ml and a CD4 lymphocyte count of 193 cells/pl at the 6th month of antiretroviral treatment. At the time of diagnosis of tuberculosis at the 7th month, the immuno-virological evaluation shows a CD4 count of 89 cells/pl and a viral load of 10,230 copies/ml.\n\nThe Ziehl Neelsen bacilloscopy was positive with a cross in the gastric washings on admission and 19 days later in the right ear swab because of the persistent otorrhea. The Xpert-MTB/GeneXpert test did not detect rifampicin-resistant Mycobacterium tuberculosis.\n\nThe frontal chest radiograph shows a more accentuated bronchovascular network at the base of the right lung.\n\nThe diagnosis of tuberculosis of the middle ear concomitant to a pulmonary localization in the field of immunosuppression by HIV1 is therefore retained.\n\nThe patient is put on oral first-line anti-tuberculosis for 6 months, a fixed dose of a quadra-therapy in the intensive phase of isoniazid, rifampicin, pyrazinamide and ethambutol for 2 months (2RHZE), followed by a bi-therapy in the maintenance phase of isoniazid and rifampicin for 4 months (4RH) at a dose of 3 tablets/day in the morning on an empty stomach, associated with vitamin B6 (1 tablet/day). He benefits from two sessions of therapeutic reinforcement with anti-retroviral drugs. The ART is restarted on 4 May 2023 with his consent, given the good tolerance of the anti-tuberculosis drugs, with the combination of tenofovir/lamivudine/dolutegravir at a dose of 1 tablet/day associated with dolutegravir 50 mg as a supplement (1 tablet/day) according to the protocol for the management of HIV/AIDS. A chemoprophylaxis with cotrimoxazole 960 mg (1 tablet/day) is undertaken as well as a cleaning of the external auditory canal by aspiration and the instillation of ciprofloxacin ear drops (2 drops 3 times a day) for 14 days.\n\nThe evolution is favorable after 14 days of treatment, marked by a pyrexia, a good general state, the amendment of the cough and otorrhea with the negativation of the bacilloscopy in the gastric tube liquid and the swab of the pus of the right ear. At the end of the maintenance anti-tuberculosis treatment, the clinical healing is complete with a normal ENT and neurological examination. The bacilloscopy associated with the Xpert-MTB/GeneXpert test at the end of the 2nd month of the intensive phase, during the 5th month and at the end of the 6th month of the maintenance phase were negative. The HIV viral load performed after 3 months of ART is 329 copies/ml.\n",
+    "diff_label_texts": "You had a long-lasting cough with mucus. Your right ear hurt and kept leaking pus.\nDoctors looked for TB germs. They found these germs in fluid taken from a tube from your stomach and in the pus from your right ear.\nYou took TB medicine for 6 months, along with other helpful medicines. You got completely better.",
+    "summary": "The patient presented with a chronic productive cough, otalgia and a chronic right-sided purulent otorrhea. The search for acid-fast bacilli was positive by direct examination in the gastric tube liquid and the swab of the auricular pus.\n\nAn anti-tuberculosis treatment of 6 months, associated with adjuvants, led to the patient's complete recovery.\n"
+  },
+  {
+    "doc_id": 40,
+    "label": "intermediate_health_literacy",
+    "fulltext": "This is a 32-year-old patient, a baker, from Bamako, who was admitted to the Infectious and Tropical Diseases department of the CHU du Point G (Bamako, Mali) on 27 April 2023 for chronic productive cough, otalgia and a chronic right-sided purulent otorrhea.\n\nThe symptomatology would be of progressive installation in 1 month, initially treated in a medical center with artésunate, paracetamol and unspecified antibiotics for confirmed malaria and acute otitis media, without success. He is immunosuppressed by a HIV1 infection, diagnosed and put on a tritherapy antiretroviral (TARV) Tenofovir/Lamivudine/Dolutégravir 7 months ago, not observed due to denial of his illness.\n\nThe general physical examination found a fever (38.2 °C), altered general condition, otalgia, purulent right foul-smelling otorrhea, a right basal pulmonary condensation syndrome, a normal neurological examination, without the involvement of the cranial nerves, mainly the facial nerve VII and the VIII cochleovestibular nerve.\n\nIn the ENT examination, the otoscopy of the right ear showed an inflammatory external auditory canal with purulent secretions and the presence of a single tympanic perforation in the anterior-inferior quadrant. The left ear is normal. The Rinne and Weber test is in favor of a right conductive hearing loss.\n\nImmuno-virological evaluation shows a CD4 count of 118 cells/pl and a viral load of 12,370 copies/ml at the time of diagnosis of HIV infection, compared to a viral load of 9,460 copies/ml and a CD4 lymphocyte count of 193 cells/pl at the 6th month of antiretroviral treatment. At the time of diagnosis of tuberculosis at the 7th month, the immuno-virological evaluation shows a CD4 count of 89 cells/pl and a viral load of 10,230 copies/ml.\n\nThe Ziehl Neelsen bacilloscopy was positive with a cross in the gastric washings on admission and 19 days later in the right ear swab because of the persistent otorrhea. The Xpert-MTB/GeneXpert test did not detect rifampicin-resistant Mycobacterium tuberculosis.\n\nThe frontal chest radiograph shows a more accentuated bronchovascular network at the base of the right lung.\n\nThe diagnosis of tuberculosis of the middle ear concomitant to a pulmonary localization in the field of immunosuppression by HIV1 is therefore retained.\n\nThe patient is put on oral first-line anti-tuberculosis for 6 months, a fixed dose of a quadra-therapy in the intensive phase of isoniazid, rifampicin, pyrazinamide and ethambutol for 2 months (2RHZE), followed by a bi-therapy in the maintenance phase of isoniazid and rifampicin for 4 months (4RH) at a dose of 3 tablets/day in the morning on an empty stomach, associated with vitamin B6 (1 tablet/day). He benefits from two sessions of therapeutic reinforcement with anti-retroviral drugs. The ART is restarted on 4 May 2023 with his consent, given the good tolerance of the anti-tuberculosis drugs, with the combination of tenofovir/lamivudine/dolutegravir at a dose of 1 tablet/day associated with dolutegravir 50 mg as a supplement (1 tablet/day) according to the protocol for the management of HIV/AIDS. A chemoprophylaxis with cotrimoxazole 960 mg (1 tablet/day) is undertaken as well as a cleaning of the external auditory canal by aspiration and the instillation of ciprofloxacin ear drops (2 drops 3 times a day) for 14 days.\n\nThe evolution is favorable after 14 days of treatment, marked by a pyrexia, a good general state, the amendment of the cough and otorrhea with the negativation of the bacilloscopy in the gastric tube liquid and the swab of the pus of the right ear. At the end of the maintenance anti-tuberculosis treatment, the clinical healing is complete with a normal ENT and neurological examination. The bacilloscopy associated with the Xpert-MTB/GeneXpert test at the end of the 2nd month of the intensive phase, during the 5th month and at the end of the 6th month of the maintenance phase were negative. The HIV viral load performed after 3 months of ART is 329 copies/ml.\n",
+    "diff_label_texts": "You developed a month of productive cough, ear pain, and a long-lasting pus discharge from the right ear. Tests showed tuberculosis bacteria: the direct smear for acid-fast bacilli (AFB) was positive in a gastric aspirate (stomach fluid) and in a swab of the pus from the right ear. This supported TB affecting the middle ear, with likely lung involvement.\nYou were treated with standard anti-tuberculosis therapy for 6 months, along with supportive care. The treatment cleared the infection, and you made a complete recovery.",
+    "summary": "The patient presented with a chronic productive cough, otalgia and a chronic right-sided purulent otorrhea. The search for acid-fast bacilli was positive by direct examination in the gastric tube liquid and the swab of the auricular pus.\n\nAn anti-tuberculosis treatment of 6 months, associated with adjuvants, led to the patient's complete recovery.\n"
+  },
+  {
+    "doc_id": 40,
+    "label": "proficient_health_literacy",
+    "fulltext": "This is a 32-year-old patient, a baker, from Bamako, who was admitted to the Infectious and Tropical Diseases department of the CHU du Point G (Bamako, Mali) on 27 April 2023 for chronic productive cough, otalgia and a chronic right-sided purulent otorrhea.\n\nThe symptomatology would be of progressive installation in 1 month, initially treated in a medical center with artésunate, paracetamol and unspecified antibiotics for confirmed malaria and acute otitis media, without success. He is immunosuppressed by a HIV1 infection, diagnosed and put on a tritherapy antiretroviral (TARV) Tenofovir/Lamivudine/Dolutégravir 7 months ago, not observed due to denial of his illness.\n\nThe general physical examination found a fever (38.2 °C), altered general condition, otalgia, purulent right foul-smelling otorrhea, a right basal pulmonary condensation syndrome, a normal neurological examination, without the involvement of the cranial nerves, mainly the facial nerve VII and the VIII cochleovestibular nerve.\n\nIn the ENT examination, the otoscopy of the right ear showed an inflammatory external auditory canal with purulent secretions and the presence of a single tympanic perforation in the anterior-inferior quadrant. The left ear is normal. The Rinne and Weber test is in favor of a right conductive hearing loss.\n\nImmuno-virological evaluation shows a CD4 count of 118 cells/pl and a viral load of 12,370 copies/ml at the time of diagnosis of HIV infection, compared to a viral load of 9,460 copies/ml and a CD4 lymphocyte count of 193 cells/pl at the 6th month of antiretroviral treatment. At the time of diagnosis of tuberculosis at the 7th month, the immuno-virological evaluation shows a CD4 count of 89 cells/pl and a viral load of 10,230 copies/ml.\n\nThe Ziehl Neelsen bacilloscopy was positive with a cross in the gastric washings on admission and 19 days later in the right ear swab because of the persistent otorrhea. The Xpert-MTB/GeneXpert test did not detect rifampicin-resistant Mycobacterium tuberculosis.\n\nThe frontal chest radiograph shows a more accentuated bronchovascular network at the base of the right lung.\n\nThe diagnosis of tuberculosis of the middle ear concomitant to a pulmonary localization in the field of immunosuppression by HIV1 is therefore retained.\n\nThe patient is put on oral first-line anti-tuberculosis for 6 months, a fixed dose of a quadra-therapy in the intensive phase of isoniazid, rifampicin, pyrazinamide and ethambutol for 2 months (2RHZE), followed by a bi-therapy in the maintenance phase of isoniazid and rifampicin for 4 months (4RH) at a dose of 3 tablets/day in the morning on an empty stomach, associated with vitamin B6 (1 tablet/day). He benefits from two sessions of therapeutic reinforcement with anti-retroviral drugs. The ART is restarted on 4 May 2023 with his consent, given the good tolerance of the anti-tuberculosis drugs, with the combination of tenofovir/lamivudine/dolutegravir at a dose of 1 tablet/day associated with dolutegravir 50 mg as a supplement (1 tablet/day) according to the protocol for the management of HIV/AIDS. A chemoprophylaxis with cotrimoxazole 960 mg (1 tablet/day) is undertaken as well as a cleaning of the external auditory canal by aspiration and the instillation of ciprofloxacin ear drops (2 drops 3 times a day) for 14 days.\n\nThe evolution is favorable after 14 days of treatment, marked by a pyrexia, a good general state, the amendment of the cough and otorrhea with the negativation of the bacilloscopy in the gastric tube liquid and the swab of the pus of the right ear. At the end of the maintenance anti-tuberculosis treatment, the clinical healing is complete with a normal ENT and neurological examination. The bacilloscopy associated with the Xpert-MTB/GeneXpert test at the end of the 2nd month of the intensive phase, during the 5th month and at the end of the 6th month of the maintenance phase were negative. The HIV viral load performed after 3 months of ART is 329 copies/ml.\n",
+    "diff_label_texts": "A 32-year-old male baker from Bamako presented on 27 April 2023 with a 1-month history of chronic productive cough, otalgia, and chronic right-sided purulent otorrhea. He had been treated elsewhere for confirmed malaria and acute otitis media with artesunate, paracetamol, and unspecified antibiotics without improvement. He is HIV-1 positive, started on TDF/3TC/DTG 7 months prior but was non-adherent due to denial of illness.\nOn exam: T 38.2 °C, altered general condition, right foul-smelling purulent otorrhea and otalgia, right basal pulmonary condensation syndrome; neurological exam normal with no cranial nerve involvement (VII, VIII intact). ENT: right EAC inflammation with purulent secretions and a single tympanic membrane perforation in the anterior-inferior quadrant; left ear normal. Rinne and Weber favored right conductive hearing loss.\nImmunovirology: at HIV diagnosis CD4 118 cells/µl, VL 12,370 copies/ml; at 6 months on ART CD4 193 cells/µl, VL 9,460 copies/ml; at TB diagnosis (month 7) CD4 89 cells/µl, VL 10,230 copies/ml.\nMicrobiology: Ziehl–Neelsen bacilloscopy positive (one cross) in gastric washings at admission; due to persistent otorrhea, repeat testing 19 days later showed a positive smear on the right ear swab. Xpert MTB/RIF detected M. tuberculosis without rifampicin resistance. Chest radiograph: accentuated bronchovascular markings at the right lung base. Diagnosis: tuberculous otitis media (middle ear TB) with concomitant pulmonary involvement in the context of HIV-1–related immunosuppression.\nTreatment: first-line anti-tuberculosis therapy for 6 months—intensive phase 2 months of isoniazid, rifampicin, pyrazinamide, ethambutol (2RHZE), then 4 months of isoniazid and rifampicin (4RH); fixed-dose combination, 3 tablets each morning fasting; pyridoxine (vitamin B6) 1 tablet daily. Two sessions of adherence reinforcement for ART. ART was restarted 4 May 2023 with tenofovir/lamivudine/dolutegravir 1 tablet daily plus supplemental dolutegravir 50 mg daily per protocol. Cotrimoxazole prophylaxis 960 mg daily. Local ear care included suctioning of the external auditory canal and ciprofloxacin ear drops, 2 drops three times daily for 14 days.\nOutcome: by day 14 there was clinical improvement with resolution of cough and otorrhea, and smear conversion to negative in both the gastric aspirate and the right ear swab. End-of-treatment status: complete clinical healing with normal ENT and neurological exams. Serial bacilloscopies with Xpert MTB/RIF at the end of month 2 (intensive phase), during month 5, and at the end of month 6 were negative. HIV viral load after 3 months of resumed ART was 329 copies/ml.",
+    "summary": "The patient presented with a chronic productive cough, otalgia and a chronic right-sided purulent otorrhea. The search for acid-fast bacilli was positive by direct examination in the gastric tube liquid and the swab of the auricular pus.\n\nAn anti-tuberculosis treatment of 6 months, associated with adjuvants, led to the patient's complete recovery.\n"
+  },
+  {
+    "doc_id": 41,
+    "label": "low_health_literacy",
+    "fulltext": "A 23-month-old boy with hypoxic-ischaemic encephalopathy at birth with good brain motor potential and normal psychomotor development. He had a personal history of restrictive cardiomyopathy and was included in a cardiac transplant programme when he was 16 months old. He also required the implantation of an external Berlin Heart biventricular support device. In order to prevent embolic events, double antiplatelet and anticoagulant treatment was administered. When he was 23 month old presented with disconnection and right hemiparesis. A computerised tomography (CT) scan showed a hyperdense left middle cerebral artery (MCA), as well as a chronic right parietotemporal infarction. His blood analysis showed: red cells 4.16 × 106 µ/L; haemoglobin 11.4 g/gL; activated partial thromboplastin time (APTT) 93 seconds and international normalised ratio (INR) 1.08.\n\nIntravenous thrombolytic treatment was contraindicated due to double antiplatelet and anticoagulant treatment at full dose with heparin, so an intra-arterial thrombectomy was performed. Although the patient was 23 months old, he was in the third percentile of the weight curve (10 kg). Under general anaesthesia, the right femoral artery was punctured and an 11 cm long 4F sheath (Cordis, Ireland) was placed. A 4F vertebral Radiofocus catheter (Glidecath of Terumo, Belgium) was used to confirm the occlusion of the M1 segment of the left MCA. The artery was recanalised by mechanical thrombectomy with a stentriever using the 4F vertebral catheter as a tutor, positioning it in the petrous segment of the carotid artery. A 3 mm × 20 mm Trevo XP Pro Vue device (Stryker, The Netherlands) was used, with a straight Rapid Transit microcatheter (Codman Neurovascular, UK), opening the artery in one pass. The whole system was removed (tutor catheter, microcatheter and stentriever) simultaneously. In the control run, an iatrogenic dissection of the left internal carotid artery was detected, which had no clinical significance, however, as the left hemisphere was irrigated through the anterior communicant artery.\n\nOne month later, his heart transplant was carried out successfully. Neurologically, the only long-term sequel that came as a result of the stroke was a right upper limb spasticity.",
+    "diff_label_texts": "At 16 months, a boy had a stiff heart muscle and was put on the heart transplant list. At 20 months, he needed an external heart pump (Berlin Heart) to help both sides of his heart. At 23 months, he had a stroke on the left side of his brain. Doctors treated the clot from inside an artery, like snaking a drain. The treatment worked well. One month later, he got a new heart, and the surgery went well.",
+    "summary": "A 16-month-old boy with restrictive cardiomyopathy who was listed for a cardiac transplant. At 20 months he required an implantation of an external biventricular support device (Berlin Heart) and had a left hemisphere stroke at 23 months. An intra-arterial approach was used and produced good clinical results. One month later, a heart transplant was performed successfully."
+  },
+  {
+    "doc_id": 41,
+    "label": "proficient_health_literacy",
+    "fulltext": "A 23-month-old boy with hypoxic-ischaemic encephalopathy at birth with good brain motor potential and normal psychomotor development. He had a personal history of restrictive cardiomyopathy and was included in a cardiac transplant programme when he was 16 months old. He also required the implantation of an external Berlin Heart biventricular support device. In order to prevent embolic events, double antiplatelet and anticoagulant treatment was administered. When he was 23 month old presented with disconnection and right hemiparesis. A computerised tomography (CT) scan showed a hyperdense left middle cerebral artery (MCA), as well as a chronic right parietotemporal infarction. His blood analysis showed: red cells 4.16 × 106 µ/L; haemoglobin 11.4 g/gL; activated partial thromboplastin time (APTT) 93 seconds and international normalised ratio (INR) 1.08.\n\nIntravenous thrombolytic treatment was contraindicated due to double antiplatelet and anticoagulant treatment at full dose with heparin, so an intra-arterial thrombectomy was performed. Although the patient was 23 months old, he was in the third percentile of the weight curve (10 kg). Under general anaesthesia, the right femoral artery was punctured and an 11 cm long 4F sheath (Cordis, Ireland) was placed. A 4F vertebral Radiofocus catheter (Glidecath of Terumo, Belgium) was used to confirm the occlusion of the M1 segment of the left MCA. The artery was recanalised by mechanical thrombectomy with a stentriever using the 4F vertebral catheter as a tutor, positioning it in the petrous segment of the carotid artery. A 3 mm × 20 mm Trevo XP Pro Vue device (Stryker, The Netherlands) was used, with a straight Rapid Transit microcatheter (Codman Neurovascular, UK), opening the artery in one pass. The whole system was removed (tutor catheter, microcatheter and stentriever) simultaneously. In the control run, an iatrogenic dissection of the left internal carotid artery was detected, which had no clinical significance, however, as the left hemisphere was irrigated through the anterior communicant artery.\n\nOne month later, his heart transplant was carried out successfully. Neurologically, the only long-term sequel that came as a result of the stroke was a right upper limb spasticity.",
+    "diff_label_texts": "A 23-month-old boy with hypoxic-ischemic encephalopathy at birth but normal psychomotor development had restrictive cardiomyopathy and was listed for cardiac transplantation at 16 months. At 20 months he required implantation of an external Berlin Heart biventricular support device; to prevent embolic events he was maintained on dual antiplatelet therapy plus full-dose heparin anticoagulation. At 23 months he presented with disconnection and right hemiparesis. CT demonstrated a hyperdense left middle cerebral artery (M1) sign and a chronic right parietotemporal infarction. Laboratory studies showed RBC 4.16 × 10^6/µL, hemoglobin 11.4 g/dL, APTT 93 s, and INR 1.08. Intravenous thrombolysis was contraindicated, so intra-arterial mechanical thrombectomy was undertaken. Despite his age, he weighed 10 kg (3rd percentile). Under general anesthesia, the right femoral artery was accessed and an 11 cm 4F sheath (Cordis, Ireland) was placed. A 4F vertebral Radiofocus catheter (Glidecath, Terumo, Belgium) confirmed occlusion of the M1 segment of the left MCA. Recanalization was achieved with a stentriever, using the 4F vertebral catheter as a tutor positioned in the petrous internal carotid artery. A 3 mm × 20 mm Trevo XP Pro Vue device (Stryker, The Netherlands) was delivered via a straight Rapid Transit microcatheter (Codman Neurovascular, UK), reopening the artery in a single pass; the tutor catheter, microcatheter, and stent retriever were removed simultaneously. The control run revealed an iatrogenic dissection of the left internal carotid artery without clinical repercussions, as the left hemisphere was perfused through the anterior communicating artery. One month later, cardiac transplantation was performed successfully. The only long-term neurological sequel was right upper-limb spasticity.",
+    "summary": "A 16-month-old boy with restrictive cardiomyopathy who was listed for a cardiac transplant. At 20 months he required an implantation of an external biventricular support device (Berlin Heart) and had a left hemisphere stroke at 23 months. An intra-arterial approach was used and produced good clinical results. One month later, a heart transplant was performed successfully."
+  },
+  {
+    "doc_id": 42,
+    "label": "low_health_literacy",
+    "fulltext": "52-year-old male patient with no medical history, transferred from a lower-level hospital to our institution due to a tonic-clonic seizure secondary to alcohol withdrawal and non-reduced right LFGHP. He was evaluated by a traumatologist 24 hours after admission, and was found to be conscious, with bilateral ecchymosis of the shoulders and severe limitation of passive external rotation on both sides. In addition, the patient was restrained physically at this point, with both feet and his left hand held down by intermittent psychomotor agitation.\n\nThe initial evaluation included a thorough review of the patient's admission radiographs, which showed a right LFGHP and a left simple posterior dislocation. This second injury (simple posterior dislocation of the left shoulder) was not diagnosed at the referring facility, and took approximately 48 hours to be diagnosed at our facility.\n\nComputed tomography (CT) of both shoulders was requested to better characterize the injuries. These images showed a marked worsening of the left shoulder injury since the time of the first radiographic study, possibly secondary to the physical restraint of the patient. This evidence of progression from a simple left posterior glenohumeral dislocation on admission radiographs to a LFGHP on the CT taken 48 hours later.\n\n\nPlanning\n\nThe preoperative study of the right shoulder showed bone indemnity of the glenoid and 40% involvement of the articular surface of the humerus, but with a large fragment with the possibility of osteosynthesis in continuity with the lesser tuberosity, so it was planned to fix this fragment by spongeous screw 4.0 mm partial thread and high strength sutures. In the left shoulder, no significant bone defect was evidenced in the glenoid and the defect of the articular surface of the humerus was 20%, so it was planned to fill the defect with the fragment of the lesser tuberosity at the time of osteosynthesis (imitating the surgery of McLaughlin).\n\n\nSurgical technique\n\nOpen reduction and internal fixation with bilateral locked-plate is decided. The patient is placed in a beach chair position and the surgical fields are prepared in the usual way for the right shoulder. The fracture focus is accessed by a classic deltopectoral approach. A digital maneuver is performed to reduce the posterior fragment of the humeral head with a posterior mini-open incision of the size of a standard diagnostic arthroscopy portal. A provisional reduction of the fracture is achieved using high-strength sutures and needles. A partial 4.0 mm spongy screw and high-strength sutures are used to fix both fragments of the humeral head. Definitive fixation of the fracture with a Philos (Depuy Synthes®) plate achieves adequate reduction and stability of fragments. Fixation is increased with high-strength sutures to the tendons of the rotator cuff that are tied to the plate. Closure by planes of the right shoulder, healing and immobilization of the extremity with a universal shoulder immobilizer.\nThe surgical field of the left shoulder is immediately prepared. Classic deltopectoral approach is performed again to reach the fracture focus using an accessory posterior portal for digital manipulation and reduction of the humeral head. Fixation and osteosynthesis are performed in the same way as described for the right shoulder with the exception of the spongiosa screw, as the anterior fragment could be adequately fixed only with the use of high strength sutures.\nPostoperative management consisted of the use of bilateral shoulder immobilizer for four weeks. A pendular exercise of flexion-extension of the elbow and exercises of the fist were given to be performed from the second postoperative week to tolerance (according to the level of pain). In the radiographic control of the first month, loss of reduction of the greater left tuberosity was observed. It was decided to perform revision surgery achieving adequate fixation of the fragment with high-strength sutures.\nThe patient is left with a shoulder immobilizer for an additional four weeks on the left shoulder. The self-administered exercise regimen is restarted as described previously from the second postoperative week on a bilateral basis. At the sixth week after the revision surgery, face-to-face kinesiological therapy is initiated twice a week. After 30 sessions of kinesiological rehabilitation, the patient is able to return to work five months after the initial injury.\nFollow-up one year after the initial surgery shows that the patient has recovered strength and mobility in the right shoulder. The left shoulder still has severe limitations in the range of motion, especially in external rotation. At this point, it is decided to perform arthroscopic joint release surgery and remove the osteosynthesis in the left shoulder.\nIn his last check-up two years after the trauma, the patient showed a favorable evolution, consistent with the functional scales evaluated.\n",
+    "diff_label_texts": "A 52-year-old man had a seizure and was sent to a big hospital. X-rays showed a bad break-and-dislocation in his right shoulder. The same X-rays also found that his left shoulder had popped out of the socket in the back, which had been missed before. A later CT scan showed both shoulders had a break-and-dislocation, and the left shoulder got worse while he was in the hospital. Surgeons fixed both shoulders in one operation and held the bones with metal plates. The left shoulder needed two more surgeries: one because the repair failed, and another to free a stiff joint. Two years later, he was doing well. His arm disability score was 5% on QuickDASH. His shoulder scores (Constant) were 72 on the left and 76 on the right.",
+    "summary": "52-year-old male patient, transferred to a high-complexity center for a tonic-clonic convulsion and a right LFGHP. In the initial study with radiographs, a right shoulder injury was confirmed and a simple posterior glenohumeral dislocation of the left shoulder was diagnosed, which had not been previously detected. The study was complemented with a computed tomography (CT) of both shoulders, showing a bilateral LFGHP, which demonstrated intrahospital aggravation of the injury of the left shoulder. An open reduction and osteosynthesis with a bilateral blocked plate was performed in one time. The left shoulder required two reinterventions, one for osteosynthesis failure and another for joint release. Two years after the procedure, the patient was satisfactorily progressing with a 5% on the Quick DASH scale and a score of 72 and 76 on the Constant scale in the left and right shoulder, respectively.\n"
+  },
+  {
+    "doc_id": 42,
+    "label": "intermediate_health_literacy",
+    "fulltext": "52-year-old male patient with no medical history, transferred from a lower-level hospital to our institution due to a tonic-clonic seizure secondary to alcohol withdrawal and non-reduced right LFGHP. He was evaluated by a traumatologist 24 hours after admission, and was found to be conscious, with bilateral ecchymosis of the shoulders and severe limitation of passive external rotation on both sides. In addition, the patient was restrained physically at this point, with both feet and his left hand held down by intermittent psychomotor agitation.\n\nThe initial evaluation included a thorough review of the patient's admission radiographs, which showed a right LFGHP and a left simple posterior dislocation. This second injury (simple posterior dislocation of the left shoulder) was not diagnosed at the referring facility, and took approximately 48 hours to be diagnosed at our facility.\n\nComputed tomography (CT) of both shoulders was requested to better characterize the injuries. These images showed a marked worsening of the left shoulder injury since the time of the first radiographic study, possibly secondary to the physical restraint of the patient. This evidence of progression from a simple left posterior glenohumeral dislocation on admission radiographs to a LFGHP on the CT taken 48 hours later.\n\n\nPlanning\n\nThe preoperative study of the right shoulder showed bone indemnity of the glenoid and 40% involvement of the articular surface of the humerus, but with a large fragment with the possibility of osteosynthesis in continuity with the lesser tuberosity, so it was planned to fix this fragment by spongeous screw 4.0 mm partial thread and high strength sutures. In the left shoulder, no significant bone defect was evidenced in the glenoid and the defect of the articular surface of the humerus was 20%, so it was planned to fill the defect with the fragment of the lesser tuberosity at the time of osteosynthesis (imitating the surgery of McLaughlin).\n\n\nSurgical technique\n\nOpen reduction and internal fixation with bilateral locked-plate is decided. The patient is placed in a beach chair position and the surgical fields are prepared in the usual way for the right shoulder. The fracture focus is accessed by a classic deltopectoral approach. A digital maneuver is performed to reduce the posterior fragment of the humeral head with a posterior mini-open incision of the size of a standard diagnostic arthroscopy portal. A provisional reduction of the fracture is achieved using high-strength sutures and needles. A partial 4.0 mm spongy screw and high-strength sutures are used to fix both fragments of the humeral head. Definitive fixation of the fracture with a Philos (Depuy Synthes®) plate achieves adequate reduction and stability of fragments. Fixation is increased with high-strength sutures to the tendons of the rotator cuff that are tied to the plate. Closure by planes of the right shoulder, healing and immobilization of the extremity with a universal shoulder immobilizer.\nThe surgical field of the left shoulder is immediately prepared. Classic deltopectoral approach is performed again to reach the fracture focus using an accessory posterior portal for digital manipulation and reduction of the humeral head. Fixation and osteosynthesis are performed in the same way as described for the right shoulder with the exception of the spongiosa screw, as the anterior fragment could be adequately fixed only with the use of high strength sutures.\nPostoperative management consisted of the use of bilateral shoulder immobilizer for four weeks. A pendular exercise of flexion-extension of the elbow and exercises of the fist were given to be performed from the second postoperative week to tolerance (according to the level of pain). In the radiographic control of the first month, loss of reduction of the greater left tuberosity was observed. It was decided to perform revision surgery achieving adequate fixation of the fragment with high-strength sutures.\nThe patient is left with a shoulder immobilizer for an additional four weeks on the left shoulder. The self-administered exercise regimen is restarted as described previously from the second postoperative week on a bilateral basis. At the sixth week after the revision surgery, face-to-face kinesiological therapy is initiated twice a week. After 30 sessions of kinesiological rehabilitation, the patient is able to return to work five months after the initial injury.\nFollow-up one year after the initial surgery shows that the patient has recovered strength and mobility in the right shoulder. The left shoulder still has severe limitations in the range of motion, especially in external rotation. At this point, it is decided to perform arthroscopic joint release surgery and remove the osteosynthesis in the left shoulder.\nIn his last check-up two years after the trauma, the patient showed a favorable evolution, consistent with the functional scales evaluated.\n",
+    "diff_label_texts": "A 52-year-old man was transferred to a tertiary center after a tonic-clonic seizure. Initial radiographs confirmed a serious right shoulder injury and also revealed a previously missed simple posterior dislocation of the left shoulder. Follow-up CT scans of both shoulders showed bilateral posterior fracture-dislocations, indicating that the left shoulder had worsened during the hospital stay. He underwent a single-stage open reduction and internal fixation of both shoulders using locked plates. The left shoulder later required two additional procedures: one to address failure of the initial fixation (osteosynthesis failure) and another arthroscopic procedure to release a stiff joint. At two years, his recovery was favorable: QuickDASH showed 5% disability, and Constant scores were 72 on the left and 76 on the right.",
+    "summary": "52-year-old male patient, transferred to a high-complexity center for a tonic-clonic convulsion and a right LFGHP. In the initial study with radiographs, a right shoulder injury was confirmed and a simple posterior glenohumeral dislocation of the left shoulder was diagnosed, which had not been previously detected. The study was complemented with a computed tomography (CT) of both shoulders, showing a bilateral LFGHP, which demonstrated intrahospital aggravation of the injury of the left shoulder. An open reduction and osteosynthesis with a bilateral blocked plate was performed in one time. The left shoulder required two reinterventions, one for osteosynthesis failure and another for joint release. Two years after the procedure, the patient was satisfactorily progressing with a 5% on the Quick DASH scale and a score of 72 and 76 on the Constant scale in the left and right shoulder, respectively.\n"
+  },
+  {
+    "doc_id": 42,
+    "label": "proficient_health_literacy",
+    "fulltext": "52-year-old male patient with no medical history, transferred from a lower-level hospital to our institution due to a tonic-clonic seizure secondary to alcohol withdrawal and non-reduced right LFGHP. He was evaluated by a traumatologist 24 hours after admission, and was found to be conscious, with bilateral ecchymosis of the shoulders and severe limitation of passive external rotation on both sides. In addition, the patient was restrained physically at this point, with both feet and his left hand held down by intermittent psychomotor agitation.\n\nThe initial evaluation included a thorough review of the patient's admission radiographs, which showed a right LFGHP and a left simple posterior dislocation. This second injury (simple posterior dislocation of the left shoulder) was not diagnosed at the referring facility, and took approximately 48 hours to be diagnosed at our facility.\n\nComputed tomography (CT) of both shoulders was requested to better characterize the injuries. These images showed a marked worsening of the left shoulder injury since the time of the first radiographic study, possibly secondary to the physical restraint of the patient. This evidence of progression from a simple left posterior glenohumeral dislocation on admission radiographs to a LFGHP on the CT taken 48 hours later.\n\n\nPlanning\n\nThe preoperative study of the right shoulder showed bone indemnity of the glenoid and 40% involvement of the articular surface of the humerus, but with a large fragment with the possibility of osteosynthesis in continuity with the lesser tuberosity, so it was planned to fix this fragment by spongeous screw 4.0 mm partial thread and high strength sutures. In the left shoulder, no significant bone defect was evidenced in the glenoid and the defect of the articular surface of the humerus was 20%, so it was planned to fill the defect with the fragment of the lesser tuberosity at the time of osteosynthesis (imitating the surgery of McLaughlin).\n\n\nSurgical technique\n\nOpen reduction and internal fixation with bilateral locked-plate is decided. The patient is placed in a beach chair position and the surgical fields are prepared in the usual way for the right shoulder. The fracture focus is accessed by a classic deltopectoral approach. A digital maneuver is performed to reduce the posterior fragment of the humeral head with a posterior mini-open incision of the size of a standard diagnostic arthroscopy portal. A provisional reduction of the fracture is achieved using high-strength sutures and needles. A partial 4.0 mm spongy screw and high-strength sutures are used to fix both fragments of the humeral head. Definitive fixation of the fracture with a Philos (Depuy Synthes®) plate achieves adequate reduction and stability of fragments. Fixation is increased with high-strength sutures to the tendons of the rotator cuff that are tied to the plate. Closure by planes of the right shoulder, healing and immobilization of the extremity with a universal shoulder immobilizer.\nThe surgical field of the left shoulder is immediately prepared. Classic deltopectoral approach is performed again to reach the fracture focus using an accessory posterior portal for digital manipulation and reduction of the humeral head. Fixation and osteosynthesis are performed in the same way as described for the right shoulder with the exception of the spongiosa screw, as the anterior fragment could be adequately fixed only with the use of high strength sutures.\nPostoperative management consisted of the use of bilateral shoulder immobilizer for four weeks. A pendular exercise of flexion-extension of the elbow and exercises of the fist were given to be performed from the second postoperative week to tolerance (according to the level of pain). In the radiographic control of the first month, loss of reduction of the greater left tuberosity was observed. It was decided to perform revision surgery achieving adequate fixation of the fragment with high-strength sutures.\nThe patient is left with a shoulder immobilizer for an additional four weeks on the left shoulder. The self-administered exercise regimen is restarted as described previously from the second postoperative week on a bilateral basis. At the sixth week after the revision surgery, face-to-face kinesiological therapy is initiated twice a week. After 30 sessions of kinesiological rehabilitation, the patient is able to return to work five months after the initial injury.\nFollow-up one year after the initial surgery shows that the patient has recovered strength and mobility in the right shoulder. The left shoulder still has severe limitations in the range of motion, especially in external rotation. At this point, it is decided to perform arthroscopic joint release surgery and remove the osteosynthesis in the left shoulder.\nIn his last check-up two years after the trauma, the patient showed a favorable evolution, consistent with the functional scales evaluated.\n",
+    "diff_label_texts": "A 52-year-old male with no prior medical history was transferred from a lower-level facility for a tonic–clonic seizure secondary to alcohol withdrawal and a non-reduced right LFGHP. He was evaluated by traumatology 24 hours after admission: he was conscious, with bilateral shoulder ecchymosis and severe limitation of passive external rotation bilaterally. At that time, he was physically restrained (both feet and the left hand) due to intermittent psychomotor agitation. Admission radiographs reviewed at our center showed a right LFGHP and a simple posterior dislocation of the left shoulder that had been missed at the referring facility; the left-sided posterior dislocation was diagnosed approximately 48 hours after arrival. CT of both shoulders was then obtained and demonstrated interval progression of the left injury from a simple posterior glenohumeral dislocation on the initial radiographs to an LFGHP on CT 48 hours later, possibly related to the period of physical restraint, i.e., intrahospital aggravation.\n\nPreoperative planning: On the right, the glenoid was intact; humeral head articular surface involvement was 40% with a large fragment continuous with the lesser tuberosity, amenable to osteosynthesis using a 4.0 mm partial-thread spongy screw plus high-strength sutures. On the left, there was no significant glenoid defect and the humeral head defect was 20%; the plan was to fill the defect using the lesser tuberosity fragment at the time of osteosynthesis (McLaughlin-type strategy).\n\nSurgical technique: A single-session bilateral open reduction and internal fixation with locked plates was performed. The patient was positioned in a beach-chair position. For the right shoulder, a classic deltopectoral approach was used. A posterior mini-open incision (arthroscopy portal size) permitted digital maneuvering to reduce the posterior humeral head fragment. Provisional reduction was achieved with high-strength sutures and needles. Definitive fixation employed a partial 4.0 mm spongy screw and high-strength sutures to secure humeral head fragments, followed by a Philos (Depuy Synthes) locked plate to achieve stable reduction; rotator cuff tendons were tied to the plate with high-strength sutures. The wound was closed in layers and the arm immobilized. The left shoulder was addressed immediately afterward via the same deltopectoral approach with an accessory posterior portal for digital manipulation and reduction; fixation mirrored the right but without a spongiosa screw, as the anterior fragment was adequately stabilized with high-strength sutures alone.\n\nPostoperative course: Bilateral shoulder immobilizers were used for four weeks. From the second postoperative week, elbow pendulum flexion–extension and hand exercises were started to pain tolerance. At the one-month radiographic control, loss of reduction of the greater tuberosity on the left was observed; revision surgery achieved stable fixation with high-strength sutures. The left shoulder was re-immobilized for an additional four weeks, then the home exercise program was restarted from week two post-revision. Six weeks after the revision, supervised kinesiologic therapy was initiated twice weekly; after 30 sessions, the patient returned to work five months after the initial injury. At one year, the right shoulder had recovered strength and mobility, whereas the left had marked ROM limitations, especially external rotation; arthroscopic capsular release and hardware removal were performed on the left. At two years post-trauma, evolution was favorable and consistent with functional scales: QuickDASH 5% and Constant scores of 72 (left) and 76 (right).",
+    "summary": "52-year-old male patient, transferred to a high-complexity center for a tonic-clonic convulsion and a right LFGHP. In the initial study with radiographs, a right shoulder injury was confirmed and a simple posterior glenohumeral dislocation of the left shoulder was diagnosed, which had not been previously detected. The study was complemented with a computed tomography (CT) of both shoulders, showing a bilateral LFGHP, which demonstrated intrahospital aggravation of the injury of the left shoulder. An open reduction and osteosynthesis with a bilateral blocked plate was performed in one time. The left shoulder required two reinterventions, one for osteosynthesis failure and another for joint release. Two years after the procedure, the patient was satisfactorily progressing with a 5% on the Quick DASH scale and a score of 72 and 76 on the Constant scale in the left and right shoulder, respectively.\n"
+  },
+  {
+    "doc_id": 43,
+    "label": "low_health_literacy",
+    "fulltext": "A 70-year-old white man was treated for severe symptomatic aortic regurgitation due to healed endocarditis using TAVI from the apical approach. TAVI was performed at that time because he was considered a high-risk surgical patient due to secondary pulmonary hypertension, severely impaired left ventricular function with a left ventricular ejection fraction (LVEF) of 20%, chronic renal failure, and a logistic EuroSCORE I of 24.36%. At the time he was treated by diuretics (torasemide 20 mg once a day), an angiotensin-converting enzyme (ACE) inhibitor (ramipril 5 mg once a day), a ß-blocker (bisoprolol 2.5 mg twice a day), and an aldosterone antagonist (12.5 mg once a day). On admission he had cardiac decompensation and resulting dyspnea (temperature 36.7 °C, pulse 99/minute, blood pressure 109/48 mmHg) but his emotional status and neurological constitution were good. The laboratory results were unremarkable except for: a mild increase in liver enzymes, aspartate aminotransferase (AST) 59 U/l and alanine aminotransferase (ALT) 67 U/l; a known chronic renal insufficiency (creatinine 2.1 mg/dl); and a mild decrease in hemoglobin (Hb) 10.7 g/dl. No urine analysis was done. Due to normal C-reactive protein and normal count of leukocytes no microbiological examination was performed. After interdisciplinary discussion of the case (including a normal coronary angiography that was performed a few days before) and cardiac recompensation, he was initially treated with an implantation of a JenaValve 27 mm self-expandable valve. Despite a good result after implantation with the JenaValve and minimal transvalvular central insufficiency, he presented recurrent cardiac decompensation due to his severely impaired LVEF. His case was discussed again at an interdisciplinary meeting: 4 weeks after TAVI he underwent the implantation of a LVAD system (Thoratec® HeartMate II). His postoperative course was uneventful. He remained asymptomatic for 1 year until the LVAD system showed recurrent significant high flow alarms. Echocardiography examinations during this year showed a continuous increase in transvalvular central insufficiency to the level of a severe regurgitation without any sign for structural alteration of the leaflets of the JenaValve prosthesis. Treatment options were discussed and a new TAVI as valve-in-valve was decided.\n\nThe procedure was performed under general anesthesia using a CoreValve Evolut R 29 mm prosthesis. The prosthesis was implanted without prior valvuloplasty. The flow rate of LVAD was reduced to minimum and pacing with a frequency of 140 beats/minute was applied during placement of the valve prosthesis. Positioning was done with great care using fluoroscopic and transesophageal echocardiography (TEE) guidance with the aim of having the ventricular strut end of the CoreValve Evolut R prosthesis between the ventricular end and the “cusp feelers” of the JenaValve prosthesis. This position was obtained because of JenaValve structure and individual computed tomography analysis of our patient which had shown the ventricular edge of the JenaValve well positioned in left ventricular outflow tract (LVOT). The first positioning was successful with no need for repositioning. After the last fluoroscopic control the CoreValve Evolut R was released successfully in the planned position. Slow rapid pacing was stopped and the LVAD flow was increased and required good hemodynamic under normal LVAD flow. His postoperative course was uneventful and he has shown a very good recovery. A second TEE did not show any change regarding the performance of the valve-in-valve and only marginal residual insufficiency. At 12-month follow-up our patient had no complaints and had a satisfactory capacity in daily life. Echocardiography showed no relevant aortic regurgitation and an increase of LVEF to 33%. At that time the 6-minute walk test was significantly increased to 381 m (compared to 148 m on admission).",
+    "diff_label_texts": "A 70-year-old man had a bad leak in his main heart valve. Doctors placed a new valve through a small opening near the tip of his heart. Four weeks later, his heart got worse again. Doctors added a heart pump to help move blood. About a year later, a heart scan showed the valve was leaking badly through the middle. The team put a second valve inside the first one, like stacking one cup inside another. They turned the heart pump down to its lowest setting during the procedure. They also made his heart beat fast at 140 beats per minute to keep the new valve steady. The result was excellent. One year later, he felt well and the valve leak was no longer a problem.",
+    "summary": "We report the case of a 70-year-old white man who was treated for severe symptomatic aortic regurgitation using transcatheter aortic valve implantation from the apical approach. Because of recurrent cardiac decompensation 4 weeks after implantation he underwent the implantation of a left ventricular assist device system. A year later echocardiography showed a severe transvalvular central insufficiency. Our heart team decided to choose a valve-in-valve approach while reducing the flow rate of left ventricular assist device to minimum and pacing with a frequency of 140 beats/minute. There was an excellent result and our patient is doing well with no relevant insufficiency of the aortic valve at 12-month follow-up."
+  },
+  {
+    "doc_id": 43,
+    "label": "intermediate_health_literacy",
+    "fulltext": "A 70-year-old white man was treated for severe symptomatic aortic regurgitation due to healed endocarditis using TAVI from the apical approach. TAVI was performed at that time because he was considered a high-risk surgical patient due to secondary pulmonary hypertension, severely impaired left ventricular function with a left ventricular ejection fraction (LVEF) of 20%, chronic renal failure, and a logistic EuroSCORE I of 24.36%. At the time he was treated by diuretics (torasemide 20 mg once a day), an angiotensin-converting enzyme (ACE) inhibitor (ramipril 5 mg once a day), a ß-blocker (bisoprolol 2.5 mg twice a day), and an aldosterone antagonist (12.5 mg once a day). On admission he had cardiac decompensation and resulting dyspnea (temperature 36.7 °C, pulse 99/minute, blood pressure 109/48 mmHg) but his emotional status and neurological constitution were good. The laboratory results were unremarkable except for: a mild increase in liver enzymes, aspartate aminotransferase (AST) 59 U/l and alanine aminotransferase (ALT) 67 U/l; a known chronic renal insufficiency (creatinine 2.1 mg/dl); and a mild decrease in hemoglobin (Hb) 10.7 g/dl. No urine analysis was done. Due to normal C-reactive protein and normal count of leukocytes no microbiological examination was performed. After interdisciplinary discussion of the case (including a normal coronary angiography that was performed a few days before) and cardiac recompensation, he was initially treated with an implantation of a JenaValve 27 mm self-expandable valve. Despite a good result after implantation with the JenaValve and minimal transvalvular central insufficiency, he presented recurrent cardiac decompensation due to his severely impaired LVEF. His case was discussed again at an interdisciplinary meeting: 4 weeks after TAVI he underwent the implantation of a LVAD system (Thoratec® HeartMate II). His postoperative course was uneventful. He remained asymptomatic for 1 year until the LVAD system showed recurrent significant high flow alarms. Echocardiography examinations during this year showed a continuous increase in transvalvular central insufficiency to the level of a severe regurgitation without any sign for structural alteration of the leaflets of the JenaValve prosthesis. Treatment options were discussed and a new TAVI as valve-in-valve was decided.\n\nThe procedure was performed under general anesthesia using a CoreValve Evolut R 29 mm prosthesis. The prosthesis was implanted without prior valvuloplasty. The flow rate of LVAD was reduced to minimum and pacing with a frequency of 140 beats/minute was applied during placement of the valve prosthesis. Positioning was done with great care using fluoroscopic and transesophageal echocardiography (TEE) guidance with the aim of having the ventricular strut end of the CoreValve Evolut R prosthesis between the ventricular end and the “cusp feelers” of the JenaValve prosthesis. This position was obtained because of JenaValve structure and individual computed tomography analysis of our patient which had shown the ventricular edge of the JenaValve well positioned in left ventricular outflow tract (LVOT). The first positioning was successful with no need for repositioning. After the last fluoroscopic control the CoreValve Evolut R was released successfully in the planned position. Slow rapid pacing was stopped and the LVAD flow was increased and required good hemodynamic under normal LVAD flow. His postoperative course was uneventful and he has shown a very good recovery. A second TEE did not show any change regarding the performance of the valve-in-valve and only marginal residual insufficiency. At 12-month follow-up our patient had no complaints and had a satisfactory capacity in daily life. Echocardiography showed no relevant aortic regurgitation and an increase of LVEF to 33%. At that time the 6-minute walk test was significantly increased to 381 m (compared to 148 m on admission).",
+    "diff_label_texts": "A 70-year-old man with severe aortic regurgitation was treated with a transcatheter aortic valve implantation (TAVI) through the tip of the heart (apical approach) because he was high risk for open surgery. Four weeks later, he developed recurrent heart failure, so a left ventricular assist device (LVAD) was implanted. He remained stable for about a year, but echocardiography then showed severe central leakage through the valve. The heart team chose a valve-in-valve TAVI to fix the problem. During the procedure, they reduced the LVAD flow to a minimum and used rapid pacing at 140 beats per minute to stabilize the new valve during placement. The outcome was excellent: at 12 months, he was doing well with no significant aortic valve leak.",
+    "summary": "We report the case of a 70-year-old white man who was treated for severe symptomatic aortic regurgitation using transcatheter aortic valve implantation from the apical approach. Because of recurrent cardiac decompensation 4 weeks after implantation he underwent the implantation of a left ventricular assist device system. A year later echocardiography showed a severe transvalvular central insufficiency. Our heart team decided to choose a valve-in-valve approach while reducing the flow rate of left ventricular assist device to minimum and pacing with a frequency of 140 beats/minute. There was an excellent result and our patient is doing well with no relevant insufficiency of the aortic valve at 12-month follow-up."
+  },
+  {
+    "doc_id": 43,
+    "label": "proficient_health_literacy",
+    "fulltext": "A 70-year-old white man was treated for severe symptomatic aortic regurgitation due to healed endocarditis using TAVI from the apical approach. TAVI was performed at that time because he was considered a high-risk surgical patient due to secondary pulmonary hypertension, severely impaired left ventricular function with a left ventricular ejection fraction (LVEF) of 20%, chronic renal failure, and a logistic EuroSCORE I of 24.36%. At the time he was treated by diuretics (torasemide 20 mg once a day), an angiotensin-converting enzyme (ACE) inhibitor (ramipril 5 mg once a day), a ß-blocker (bisoprolol 2.5 mg twice a day), and an aldosterone antagonist (12.5 mg once a day). On admission he had cardiac decompensation and resulting dyspnea (temperature 36.7 °C, pulse 99/minute, blood pressure 109/48 mmHg) but his emotional status and neurological constitution were good. The laboratory results were unremarkable except for: a mild increase in liver enzymes, aspartate aminotransferase (AST) 59 U/l and alanine aminotransferase (ALT) 67 U/l; a known chronic renal insufficiency (creatinine 2.1 mg/dl); and a mild decrease in hemoglobin (Hb) 10.7 g/dl. No urine analysis was done. Due to normal C-reactive protein and normal count of leukocytes no microbiological examination was performed. After interdisciplinary discussion of the case (including a normal coronary angiography that was performed a few days before) and cardiac recompensation, he was initially treated with an implantation of a JenaValve 27 mm self-expandable valve. Despite a good result after implantation with the JenaValve and minimal transvalvular central insufficiency, he presented recurrent cardiac decompensation due to his severely impaired LVEF. His case was discussed again at an interdisciplinary meeting: 4 weeks after TAVI he underwent the implantation of a LVAD system (Thoratec® HeartMate II). His postoperative course was uneventful. He remained asymptomatic for 1 year until the LVAD system showed recurrent significant high flow alarms. Echocardiography examinations during this year showed a continuous increase in transvalvular central insufficiency to the level of a severe regurgitation without any sign for structural alteration of the leaflets of the JenaValve prosthesis. Treatment options were discussed and a new TAVI as valve-in-valve was decided.\n\nThe procedure was performed under general anesthesia using a CoreValve Evolut R 29 mm prosthesis. The prosthesis was implanted without prior valvuloplasty. The flow rate of LVAD was reduced to minimum and pacing with a frequency of 140 beats/minute was applied during placement of the valve prosthesis. Positioning was done with great care using fluoroscopic and transesophageal echocardiography (TEE) guidance with the aim of having the ventricular strut end of the CoreValve Evolut R prosthesis between the ventricular end and the “cusp feelers” of the JenaValve prosthesis. This position was obtained because of JenaValve structure and individual computed tomography analysis of our patient which had shown the ventricular edge of the JenaValve well positioned in left ventricular outflow tract (LVOT). The first positioning was successful with no need for repositioning. After the last fluoroscopic control the CoreValve Evolut R was released successfully in the planned position. Slow rapid pacing was stopped and the LVAD flow was increased and required good hemodynamic under normal LVAD flow. His postoperative course was uneventful and he has shown a very good recovery. A second TEE did not show any change regarding the performance of the valve-in-valve and only marginal residual insufficiency. At 12-month follow-up our patient had no complaints and had a satisfactory capacity in daily life. Echocardiography showed no relevant aortic regurgitation and an increase of LVEF to 33%. At that time the 6-minute walk test was significantly increased to 381 m (compared to 148 m on admission).",
+    "diff_label_texts": "A 70-year-old white man with severe symptomatic aortic regurgitation due to healed endocarditis underwent transapical TAVI because of prohibitive surgical risk (secondary pulmonary hypertension, severely impaired LV function with LVEF 20%, chronic renal failure, logistic EuroSCORE I 24.36%). Home medications included torasemide 20 mg qd, ramipril 5 mg qd, bisoprolol 2.5 mg bid, and an aldosterone antagonist 12.5 mg qd. On admission he had decompensated heart failure with dyspnea (T 36.7 °C, HR 99 bpm, BP 109/48 mmHg). Labs were notable for AST 59 U/L, ALT 67 U/L, creatinine 2.1 mg/dL, and Hb 10.7 g/dL; CRP and leukocyte count were normal; urine was not analyzed; coronary angiography was normal. After multidisciplinary discussion and recompensation, a 27-mm JenaValve self-expandable prosthesis was implanted with a good immediate result and minimal central transvalvular insufficiency. Despite this, he had recurrent cardiac decompensation attributed to severely impaired LVEF; 4 weeks after TAVI, a Thoratec HeartMate II LVAD was implanted, and the postoperative course was uneventful. He remained asymptomatic for 1 year until recurrent significant high-flow alarms occurred on the LVAD. Serial echocardiography over that year demonstrated progressive central transvalvular insufficiency culminating in severe regurgitation without structural leaflet alteration of the JenaValve.\n\nA valve-in-valve TAVI was performed under general anesthesia using a 29-mm CoreValve Evolut R without prior valvuloplasty. During deployment, LVAD flow was reduced to minimum and rapid pacing at 140 bpm was applied. Fluoroscopy and TEE guided positioning targeted placement of the ventricular strut end of the CoreValve Evolut R between the ventricular end and the cusp feelers of the JenaValve, informed by CT showing the JenaValve ventricular edge well positioned in the LVOT. Initial positioning was successful without need for repositioning; after final fluoroscopic confirmation, the device was released, rapid pacing was stopped, and LVAD flow was increased, resulting in stable hemodynamics. The postoperative course was uneventful. Follow-up TEE showed only marginal residual insufficiency. At 12 months, the patient reported no complaints, echocardiography showed no relevant aortic regurgitation, LVEF improved to 33%, and the 6-minute walk distance increased to 381 m from 148 m at admission.",
+    "summary": "We report the case of a 70-year-old white man who was treated for severe symptomatic aortic regurgitation using transcatheter aortic valve implantation from the apical approach. Because of recurrent cardiac decompensation 4 weeks after implantation he underwent the implantation of a left ventricular assist device system. A year later echocardiography showed a severe transvalvular central insufficiency. Our heart team decided to choose a valve-in-valve approach while reducing the flow rate of left ventricular assist device to minimum and pacing with a frequency of 140 beats/minute. There was an excellent result and our patient is doing well with no relevant insufficiency of the aortic valve at 12-month follow-up."
+  },
+  {
+    "doc_id": 44,
+    "label": "low_health_literacy",
+    "fulltext": "A 12-year-old boy was brought to our department exhibiting sudden onset symptoms of headache and polyuria-polydipsia syndrome, which began one week prior to his initial visit. The child had no significant medical history. During the first clinical evaluation, he measured 146.5 cm in height (M) and weighed 30 kg (-1.4 SD). There were no observed signs of adrenal insufficiency or hypothyroidism. He was at the onset of puberty, with gonad sizes measuring 3.2 cm on each side and a penis length of 6.2 cm (M). Notably, the patient experienced polyuria-polydipsia syndrome, with fluid excretion reaching up to 113ml/kg/day, nocturnal enuresis, and an excessive liquid intake of 3.8 liters/m². Ophthalmologic examination yielded expected results, with no visual impairments detected and normal optical coherence tomography (OCT) findings.\n\nThe biological assessment revealed DI, with a serum sodium level of 140 mEq/l and plasma osmolality of 287 mosm/kg, while the urine osmolality was significantly low at 179 mosm/kg. Furthermore, his serum levels of insulin-like growth factor-1 (IGF1), prolactin (PRL), free T4, cortisol, follicle-stimulating hormone (FSH), and luteinizing hormone (LH) were all within the normal range.\n\nMRI scans with and without contrast highlighted apoplexy in an RCC, showing a spontaneous hyperintensity on T1 and T2 sequences measuring 15x6x11 mm. The anterior pituitary gland displayed homogeneous contrast uptake. However, we observed a loss of the typical hyperintensity of the posterior pituitary gland, with no radiological indications of a craniopharyngioma. Therefore, during the initial hormonal evaluation, the only hormone deficiency identified in our case was DI, which showed significant improvement under vasopressin treatment. The case was reviewed in a multidisciplinary meeting, including an endocrinologist, neurosurgeon, and radiologist. Given the absence of clinical or biological signs other than DI and the stability of the RCC apoplexy over nine months of MRI monitoring—with measurements of 12 × 11 × 10 mm—a conservative management approach with regular follow-ups was chosen.\n\nThe child was monitored for three years, during which he displayed normal puberty development and maintained a stable hormonal profile (Table 1). Visual evaluations revealed no abnormalities. However, a decrease in growth velocity was noted, dropping from -0.8 SD to -1.1 SD. This necessitated an investigation for acquired growth hormone (GH) deficiency. At the age of 14 years and nine months, the child was readmitted to undergo two GH stimulation tests: A propranolol-glucagon test and an Insulin Tolerance Test, which indicated a partial GH deficiency with peaks of 19.3 µUI/ml and 10.0 µUI/ml, respectively. After receiving GH treatment, the patient experienced a notable increase in growth velocity, improving from -1.1 SD to 0.2 SD over one year.\n\nSubsequently, MRI monitoring showed a stable appearance of the RCC apoplexy after two years (11 × 12 × 11 mm), with a slight decrease in size observed at the three-year follow-up, measuring 7 × 10 × 6 mm. It is important to note that the radiological follow-up was consistently conducted at the same MRI center, with the same radiologist interpreting both recent and previous MRI findings during multidisciplinary meetings that included an endocrinologist and a neurosurgeon.",
+    "diff_label_texts": "A 12-year-old boy suddenly had headaches. He also peed a lot and was very thirsty. A brain scan found a small cyst near the body’s hormone control center that had changed suddenly. It was not pressing on his brain or eyes. He was just starting puberty. His basic hormone tests looked normal. The doctors chose watchful waiting with regular checkups, blood tests, and scans. He went through puberty normally. He had no hormone problems except a partial shortage of growth hormone.",
+    "summary": "We present the case of a 12-year-old boy admitted due to the recent onset of headaches and diabetes insipidus. Magnetic resonance imaging revealed Rathke cleft cyst apoplexy. Given the absence of compressive symptoms in a child at the early stages of puberty and without abnormalities in basic endocrine tests, a conservative strategy was employed, involving regular clinical, biological, and radiological follow-ups. The child experienced normal puberty without any endocrine deficiencies except for a partial growth hormone deficiency."
+  },
+  {
+    "doc_id": 44,
+    "label": "proficient_health_literacy",
+    "fulltext": "A 12-year-old boy was brought to our department exhibiting sudden onset symptoms of headache and polyuria-polydipsia syndrome, which began one week prior to his initial visit. The child had no significant medical history. During the first clinical evaluation, he measured 146.5 cm in height (M) and weighed 30 kg (-1.4 SD). There were no observed signs of adrenal insufficiency or hypothyroidism. He was at the onset of puberty, with gonad sizes measuring 3.2 cm on each side and a penis length of 6.2 cm (M). Notably, the patient experienced polyuria-polydipsia syndrome, with fluid excretion reaching up to 113ml/kg/day, nocturnal enuresis, and an excessive liquid intake of 3.8 liters/m². Ophthalmologic examination yielded expected results, with no visual impairments detected and normal optical coherence tomography (OCT) findings.\n\nThe biological assessment revealed DI, with a serum sodium level of 140 mEq/l and plasma osmolality of 287 mosm/kg, while the urine osmolality was significantly low at 179 mosm/kg. Furthermore, his serum levels of insulin-like growth factor-1 (IGF1), prolactin (PRL), free T4, cortisol, follicle-stimulating hormone (FSH), and luteinizing hormone (LH) were all within the normal range.\n\nMRI scans with and without contrast highlighted apoplexy in an RCC, showing a spontaneous hyperintensity on T1 and T2 sequences measuring 15x6x11 mm. The anterior pituitary gland displayed homogeneous contrast uptake. However, we observed a loss of the typical hyperintensity of the posterior pituitary gland, with no radiological indications of a craniopharyngioma. Therefore, during the initial hormonal evaluation, the only hormone deficiency identified in our case was DI, which showed significant improvement under vasopressin treatment. The case was reviewed in a multidisciplinary meeting, including an endocrinologist, neurosurgeon, and radiologist. Given the absence of clinical or biological signs other than DI and the stability of the RCC apoplexy over nine months of MRI monitoring—with measurements of 12 × 11 × 10 mm—a conservative management approach with regular follow-ups was chosen.\n\nThe child was monitored for three years, during which he displayed normal puberty development and maintained a stable hormonal profile (Table 1). Visual evaluations revealed no abnormalities. However, a decrease in growth velocity was noted, dropping from -0.8 SD to -1.1 SD. This necessitated an investigation for acquired growth hormone (GH) deficiency. At the age of 14 years and nine months, the child was readmitted to undergo two GH stimulation tests: A propranolol-glucagon test and an Insulin Tolerance Test, which indicated a partial GH deficiency with peaks of 19.3 µUI/ml and 10.0 µUI/ml, respectively. After receiving GH treatment, the patient experienced a notable increase in growth velocity, improving from -1.1 SD to 0.2 SD over one year.\n\nSubsequently, MRI monitoring showed a stable appearance of the RCC apoplexy after two years (11 × 12 × 11 mm), with a slight decrease in size observed at the three-year follow-up, measuring 7 × 10 × 6 mm. It is important to note that the radiological follow-up was consistently conducted at the same MRI center, with the same radiologist interpreting both recent and previous MRI findings during multidisciplinary meetings that included an endocrinologist and a neurosurgeon.",
+    "diff_label_texts": "A 12-year-old boy presented with one week of acute-onset headache and polyuria–polydipsia. Past history was unremarkable. On first assessment: height 146.5 cm (M), weight 30 kg (−1.4 SD). He was at the onset of puberty with bilateral gonadal length 3.2 cm and penile length 6.2 cm (M). Visual assessment, including OCT, was normal. Polyuria reached 113 ml/kg/day with nocturnal enuresis and intake approximately 3.8 L/m²/day. Initial labs were consistent with central diabetes insipidus: serum sodium 140 mEq/L, plasma osmolality 287 mOsm/kg, urine osmolality 179 mOsm/kg. Basal pituitary axes were otherwise intact: IGF-1, PRL, free T4, cortisol, FSH, and LH within reference ranges. MRI with and without contrast demonstrated apoplexy within a Rathke cleft cyst (T1/T2 hyperintense lesion measuring 15 × 6 × 11 mm). The anterior pituitary enhanced homogeneously. The posterior pituitary bright spot was absent. There were no radiologic features suggestive of craniopharyngioma. DI improved significantly with vasopressin therapy. A multidisciplinary team (endocrinology, neurosurgery, radiology) elected conservative management given the absence of compressive symptoms, early pubertal status, and normal baseline endocrine testing apart from DI. Serial MRI over nine months showed stability (12 × 11 × 10 mm), and subsequent surveillance at two years remained stable (11 × 12 × 11 mm) with slight size reduction at three years (7 × 10 × 6 mm). Over three years, the patient maintained normal pubertal progression and a stable hormonal profile on routine testing, with persistently normal vision. Growth velocity declined from −0.8 SD to −1.1 SD, prompting evaluation for acquired GH deficiency. At 14 years 9 months, two GH stimulation tests demonstrated partial GH deficiency: propranolol–glucagon peak 19.3 µUI/ml and insulin tolerance test peak 10.0 µUI/ml. GH therapy led to improved growth velocity from −1.1 SD to 0.2 SD over one year. Overall, this case illustrates that RCC apoplexy in a pubertal child can present with abrupt DI due to posterior pituitary/stalk dysfunction, while sparing anterior pituitary function initially. In the absence of mass effect or broader hypopituitarism, conservative management with structured clinical, biochemical, and radiologic follow-up is appropriate; delayed, isolated partial GH deficiency may emerge, warranting dynamic testing and treatment.",
+    "summary": "We present the case of a 12-year-old boy admitted due to the recent onset of headaches and diabetes insipidus. Magnetic resonance imaging revealed Rathke cleft cyst apoplexy. Given the absence of compressive symptoms in a child at the early stages of puberty and without abnormalities in basic endocrine tests, a conservative strategy was employed, involving regular clinical, biological, and radiological follow-ups. The child experienced normal puberty without any endocrine deficiencies except for a partial growth hormone deficiency."
+  },
+  {
+    "doc_id": 45,
+    "label": "proficient_health_literacy",
+    "fulltext": "Patient and observation\nPatient information: This was a 67-year-old patient with no medical history who presented with dysphagia, dysphonia and altered general condition.\n\nClinical findings: initial clinical examination found a conscious patient with a Glasgow score of 15/15, apyrexia, blood pressure of 12/07 cmHg, oxygen saturation of 100%, heart rate of 80/min, conjunctivae of normal colour with a large mass in the cavum. There was no hepatomegaly or splenomegaly, the lymph node areas were free, the rest of the physical examination was normal.\n\nChronology: the patient had been experiencing difficulty swallowing with dysphonia for 6 months, the clinical picture worsened with the development of dysphagia for solids with a deterioration in general condition (weight loss of 15kg/6 months).\n\nDiagnostic approach: cervico-thoraco-abdomino-pelvic CT scan showed a 70 mm x 40 mm nasopharyngeal mass extending to 60 mm. The patient's blood work was normal (white blood cell count, renal and hepatic function, lactate dehydrogenase and HIV, HCV and HBV serologies). The histological and immunohistochemical study of the nasopharyngeal biopsy was in favour of a grade 1,2 CD20+; CD19+; CD79a+; CD10+ follicular B-cell NHL in 2 readings in 2 different laboratories. The bone marrow biopsy was normal as was the pre-therapeutic work-up.\n\nTherapeutic intervention: the patient received 4 RCHOP 21 cures (rituximab 375mg/m2 intravenous (iv), cyclophosphamide 750 mg/m2 iv, oncovin 2 mg iv, prednisolone 100 mg orally, and doxorubicin 50 mg/m2 (iv) with no response and then 3 RDHAOX cures (rituximab 375 mg/m2 intravenous (iv) on day 1, high dose aracytine 2 g/m2 x 2 iv on day 2, dexamethasone 40 mg from day 1 to day 4, and oxalipatine 100 mg/m2 on day 1) with no clinical response.\n\nFollow-up and results of therapeutic interventions: the persistence and increase of the nasopharyngeal mass led to the realization of the tracheotomy, the biopsy of the nasopharyngeal mass objectified the disappearance of the lymphoid B infiltration with presence of the amyloid deposits AL type kappa.\n\nImmune electrophoresis of plasma proteins showed the presence of immunoglobulin M kappa, the dosage of light chains was not performed due to lack of resources, the myelogram and a second bone marrow biopsy were normal, the TEP scan objectified a hypermetabolic nasopharyngeal process without other anomalies, the cardiac evaluation (ECG, natriuretic peptides, troponin, echocore) and renal were without particularities, the patient is currently under protocol bortezomib, prednisone and bendamustine with good clinical evolution after the first treatment.\n",
+    "diff_label_texts": "A 67-year-old patient with no medical history presented with a 6‑month course of dysphagia and dysphonia and deterioration of general condition (15 kg weight loss over 6 months). On examination: GCS 15/15, afebrile, BP 12/07 cmHg, SpO2 100%, HR 80/min, normal conjunctivae, and a large mass in the cavum; no hepatosplenomegaly or peripheral adenopathy; otherwise unremarkable exam. Cervico-thoraco-abdomino-pelvic CT identified a 70 × 40 mm nasopharyngeal mass extending to 60 mm. Laboratory studies were normal (WBC, renal and hepatic function, LDH) with negative HIV, HCV, and HBV serologies. Nasopharyngeal biopsy with histology and immunohistochemistry in two independent readings supported a grade 1–2 follicular B‑cell NHL: CD20+, CD19+, CD79a+, CD10+. Bone marrow biopsy and the pre‑therapeutic work‑up were normal. The patient received 4 cures of R‑CHOP‑21 (rituximab 375 mg/m2 IV, cyclophosphamide 750 mg/m2 IV, oncovin 2 mg IV, prednisolone 100 mg PO, doxorubicin 50 mg/m2 IV) without response, followed by 3 cures of R‑DHAOX (rituximab 375 mg/m2 IV D1, high‑dose aracytine 2 g/m2 × 2 IV D2, dexamethasone 40 mg D1–D4, oxaliplatine 100 mg/m2 D1) with no clinical response. Due to persistence and increase of the nasopharyngeal mass, a tracheotomy was performed. Repeat biopsy of the mass objectified disappearance of lymphoid B infiltration with presence of AL‑type kappa amyloid deposits. Immune electrophoresis of plasma proteins revealed immunoglobulin M kappa; serum free light chains were not dosed due to resource limitations. Myelogram and a second bone marrow biopsy were normal. PET (TEP) showed a hypermetabolic nasopharyngeal process without other anomalies. Cardiac evaluation (ECG, natriuretic peptides, troponin, echocore) and renal assessment were unremarkable. The patient is currently under a bortezomib, prednisone, and bendamustine protocol, with good clinical evolution after the first treatment. This trajectory suggests an IgM‑associated localized AL amyloid process emerging in the site of the prior follicular lymphoma, despite systemic evaluations (including marrow and organ assessments) remaining normal.",
+    "summary": "We report the case of a 67-year-old patient without pathological CDDs who presented with a deterioration of general condition with progressive dysphonia and dysphagia with a large mass in the neck that was biopsy-proven to be a grade 1 and 2 follicular non-Hodgkin lymphoma. A cervico-thoraco-abdomino-pelvic CT scan showed a 70 mm x 40 mm nasopharyngeal mass extending to 60 mm. Bone marrow biopsy was normal and the pre-therapeutic evaluation was normal. The patient received 4 courses of rituximab plus CHOP (cyclophosphamide, adriamycin, prednisone and oncovin) without response and then 3 courses of rituximab plus DHAOX (dexamethasone, high dose ara-cytin and oxalipatin) with persistence of the mass. The biopsy of the latter showed the disappearance of the B lymphocyte infiltration with presence of the AL amyloid deposits. The immunoelectrophoresis of plasma proteins showed the presence of immunoglobulin M. A positron emission tomography (PET) scan showed a hypermetabolic nasopharyngeal process. The patient is currently receiving a protocol of bortezomib, prednisone and bendamustine.\n"
+  },
+  {
+    "doc_id": 46,
+    "label": "low_health_literacy",
+    "fulltext": "46-year-old Haitian male, residing in Chile for one year. In Haiti he was a livestock farmer. He presented a one-and-a-half-year history of a lesion that began as a papule on the anterior aspect of the right leg, which increased in size progressively. Initially asymptomatic, three months prior to the consultation he developed pruritus, pain, superficial ulceration and yellowish discharge. On physical examination, the patient was found to be of phototype V, with 1 x 1 cm, 2 x 2 cm and 3 x 2 cm warty plaques on the anterior aspect of the right leg. A dermatoscopy revealed a hyperkeratotic mass with ulcerated center, with reddish-black dots and congested hemorrhagic vessels. The general laboratory was normal; VDRL, HIV and PPD were non-reactive. Tissue samples were taken by a punch biopsy, including epidermis, dermis and subcutaneous tissue, and stained with Gram, routine bacteriological culture and anaerobic culture, which were negative. Bacilloscopy and Koch culture of the same tissue were also negative. The histopathological study was performed with hematoxylin and eosin stain, and showed a pseudoepitheliomatous epidermis with irregular hyperplasia, a dermis with abundant mixed inflammatory infiltrate with suppurative foci and giant cells of the foreign body type, some of which contained round cells with a thick brown wall, compatible with muriform cells; these cells were more evident when evaluated with PAS stain. Fungal culture was performed on Sabouraud dextrose agar at 25°C, which showed, after 15 days of incubation, the growth of black or dematiaceous, elevated, well-defined, velvety colonies. Direct microscopic examination with 20% KOH showed long, branched, sometimes tortuous, hyphae, and short chains of acropetal conidia, suggestive of Fonsecaea spp. Itraconazole was administered at 100 mg every 12 h for six months, in association with physical measures, which consisted of cryotherapy (liquid nitrogen) application to hypertrophic areas every six to eight weeks. Due to local complications, such as erosion or ulceration of the lesions, frequent healing was performed with application of mupirocin ointment topically for signs of bacterial superinfection.\n\nThe patient had a favorable evolution, with regression of the lesions and no evidence of relapses to date, remaining with a mild local hypopigmentation, expected in areas of treatment with cryotherapy.\n",
+    "diff_label_texts": "A 46-year-old man from Haiti now lives in Chile. He had wart-like bumps on the front of his shin for about a year. Tests showed a long-lasting skin fungus called chromoblastomycosis. The skin sample had special cells that prove this infection. The lab also grew dark-colored fungus from the sample. Under the microscope, the germ looked like a kind called Fonsecaea. He took antifungal pills and got freezing treatments on the spots. Treatment lasted six months. All the bumps went away.",
+    "summary": "A 46-year-old Haitian man, residing in Chile, presented with warty plaques in the anterior tibial region that had been present for one year. The diagnosis of chromoblastomycosis was confirmed by the presence of muriform cells in the histopathology and dematiaceous colonies in the mycological culture. In addition, conidia compatible with Fonsecaea spp. were observed in direct microscopy. After six months of treatment with systemic antimycotics and cryotherapy, complete remission of the lesions was achieved.\n"
+  },
+  {
+    "doc_id": 46,
+    "label": "intermediate_health_literacy",
+    "fulltext": "46-year-old Haitian male, residing in Chile for one year. In Haiti he was a livestock farmer. He presented a one-and-a-half-year history of a lesion that began as a papule on the anterior aspect of the right leg, which increased in size progressively. Initially asymptomatic, three months prior to the consultation he developed pruritus, pain, superficial ulceration and yellowish discharge. On physical examination, the patient was found to be of phototype V, with 1 x 1 cm, 2 x 2 cm and 3 x 2 cm warty plaques on the anterior aspect of the right leg. A dermatoscopy revealed a hyperkeratotic mass with ulcerated center, with reddish-black dots and congested hemorrhagic vessels. The general laboratory was normal; VDRL, HIV and PPD were non-reactive. Tissue samples were taken by a punch biopsy, including epidermis, dermis and subcutaneous tissue, and stained with Gram, routine bacteriological culture and anaerobic culture, which were negative. Bacilloscopy and Koch culture of the same tissue were also negative. The histopathological study was performed with hematoxylin and eosin stain, and showed a pseudoepitheliomatous epidermis with irregular hyperplasia, a dermis with abundant mixed inflammatory infiltrate with suppurative foci and giant cells of the foreign body type, some of which contained round cells with a thick brown wall, compatible with muriform cells; these cells were more evident when evaluated with PAS stain. Fungal culture was performed on Sabouraud dextrose agar at 25°C, which showed, after 15 days of incubation, the growth of black or dematiaceous, elevated, well-defined, velvety colonies. Direct microscopic examination with 20% KOH showed long, branched, sometimes tortuous, hyphae, and short chains of acropetal conidia, suggestive of Fonsecaea spp. Itraconazole was administered at 100 mg every 12 h for six months, in association with physical measures, which consisted of cryotherapy (liquid nitrogen) application to hypertrophic areas every six to eight weeks. Due to local complications, such as erosion or ulceration of the lesions, frequent healing was performed with application of mupirocin ointment topically for signs of bacterial superinfection.\n\nThe patient had a favorable evolution, with regression of the lesions and no evidence of relapses to date, remaining with a mild local hypopigmentation, expected in areas of treatment with cryotherapy.\n",
+    "diff_label_texts": "A 46-year-old Haitian man living in Chile developed wart-like plaques on the front of his right shin for about a year. Doctors diagnosed chromoblastomycosis after a skin biopsy showed the characteristic cells of this infection and a fungal culture grew dark (dematiaceous) colonies; direct microscopy suggested a Fonsecaea-type fungus. He was treated for six months with itraconazole taken twice daily and cryotherapy to the thickened areas. The lesions cleared completely. Additional context: The problem began as a small bump that slowly enlarged, later causing itch, pain, shallow ulcers, and yellowish drainage. Routine blood tests and screening for syphilis, HIV, and tuberculosis were negative. Local wound care was provided, including antibiotic ointment when signs of bacterial infection appeared. After therapy, there has been no relapse, with only mild lightening of the treated skin, which is expected after cryotherapy.",
+    "summary": "A 46-year-old Haitian man, residing in Chile, presented with warty plaques in the anterior tibial region that had been present for one year. The diagnosis of chromoblastomycosis was confirmed by the presence of muriform cells in the histopathology and dematiaceous colonies in the mycological culture. In addition, conidia compatible with Fonsecaea spp. were observed in direct microscopy. After six months of treatment with systemic antimycotics and cryotherapy, complete remission of the lesions was achieved.\n"
+  },
+  {
+    "doc_id": 46,
+    "label": "proficient_health_literacy",
+    "fulltext": "46-year-old Haitian male, residing in Chile for one year. In Haiti he was a livestock farmer. He presented a one-and-a-half-year history of a lesion that began as a papule on the anterior aspect of the right leg, which increased in size progressively. Initially asymptomatic, three months prior to the consultation he developed pruritus, pain, superficial ulceration and yellowish discharge. On physical examination, the patient was found to be of phototype V, with 1 x 1 cm, 2 x 2 cm and 3 x 2 cm warty plaques on the anterior aspect of the right leg. A dermatoscopy revealed a hyperkeratotic mass with ulcerated center, with reddish-black dots and congested hemorrhagic vessels. The general laboratory was normal; VDRL, HIV and PPD were non-reactive. Tissue samples were taken by a punch biopsy, including epidermis, dermis and subcutaneous tissue, and stained with Gram, routine bacteriological culture and anaerobic culture, which were negative. Bacilloscopy and Koch culture of the same tissue were also negative. The histopathological study was performed with hematoxylin and eosin stain, and showed a pseudoepitheliomatous epidermis with irregular hyperplasia, a dermis with abundant mixed inflammatory infiltrate with suppurative foci and giant cells of the foreign body type, some of which contained round cells with a thick brown wall, compatible with muriform cells; these cells were more evident when evaluated with PAS stain. Fungal culture was performed on Sabouraud dextrose agar at 25°C, which showed, after 15 days of incubation, the growth of black or dematiaceous, elevated, well-defined, velvety colonies. Direct microscopic examination with 20% KOH showed long, branched, sometimes tortuous, hyphae, and short chains of acropetal conidia, suggestive of Fonsecaea spp. Itraconazole was administered at 100 mg every 12 h for six months, in association with physical measures, which consisted of cryotherapy (liquid nitrogen) application to hypertrophic areas every six to eight weeks. Due to local complications, such as erosion or ulceration of the lesions, frequent healing was performed with application of mupirocin ointment topically for signs of bacterial superinfection.\n\nThe patient had a favorable evolution, with regression of the lesions and no evidence of relapses to date, remaining with a mild local hypopigmentation, expected in areas of treatment with cryotherapy.\n",
+    "diff_label_texts": "A 46-year-old Haitian male, residing in Chile for one year, presented with a one-and-a-half-year history of a lesion that began as a papule on the anterior aspect of the right leg, with progressive enlargement. Initially asymptomatic, pruritus, pain, superficial ulceration, and yellowish discharge developed three months prior to consultation. On examination (phototype V), there were warty plaques measuring 1 × 1 cm, 2 × 2 cm, and 3 × 2 cm on the anterior right leg. Dermatoscopy revealed a hyperkeratotic mass with an ulcerated center, reddish-black dots, and congested hemorrhagic vessels. General laboratories were normal; VDRL, HIV, and PPD were non-reactive. Punch biopsy including epidermis, dermis, and subcutis was performed; Gram stain, routine bacteriological culture, and anaerobic culture were negative. Bacilloscopy and Koch culture were also negative. Histopathology (hematoxylin and eosin) showed pseudoepitheliomatous epidermal hyperplasia with irregular hyperplasia; the dermis contained abundant mixed inflammatory infiltrate with suppurative foci and foreign body-type giant cells, some containing round, thick-walled brown cells compatible with muriform (sclerotic) cells; these were more evident with PAS stain. Fungal culture on Sabouraud dextrose agar at 25°C demonstrated, after 15 days, growth of black/dematiaceous, elevated, well-defined, velvety colonies. Direct microscopic examination with 20% KOH showed long, branched, sometimes tortuous hyphae and short chains of acropetal conidia, suggestive of Fonsecaea spp. The diagnosis was chromoblastomycosis. Treatment included itraconazole 100 mg every 12 hours for six months, combined with physical measures consisting of cryotherapy (liquid nitrogen) applied to hypertrophic areas every 6–8 weeks. Due to local complications (erosion/ulceration), frequent wound care was provided, with topical mupirocin for signs of bacterial superinfection. The patient had a favorable evolution, with regression of lesions and no evidence of relapse to date, remaining with mild local hypopigmentation expected after cryotherapy. Contextual note: Chromoblastomycosis is a chronic cutaneous and subcutaneous mycosis caused by dematiaceous fungi (classically Fonsecaea, Cladophialophora, and Phialophora), with muriform cells being pathognomonic; combined antifungal therapy and cryotherapy are standard strategies, with itraconazole commonly dosed at 200 mg/day as used here.",
+    "summary": "A 46-year-old Haitian man, residing in Chile, presented with warty plaques in the anterior tibial region that had been present for one year. The diagnosis of chromoblastomycosis was confirmed by the presence of muriform cells in the histopathology and dematiaceous colonies in the mycological culture. In addition, conidia compatible with Fonsecaea spp. were observed in direct microscopy. After six months of treatment with systemic antimycotics and cryotherapy, complete remission of the lesions was achieved.\n"
+  },
+  {
+    "doc_id": 47,
+    "label": "low_health_literacy",
+    "fulltext": "Patient information: A 19-year-old male with no significant medical history was admitted to our department with a painful left scrotal mass that had been present for 8 months and had not improved with antibiotics for pyogenic organisms. The patient reported intermittent low grade fever, night sweats, anorexia and unexplained weight loss since the onset of symptoms. He did not have a cough, sputum or haemoptysis. There was no history of tuberculosis in his personal or family medical history. He was vaccinated against tuberculosis at birth.\n\nClinical findings: Physical examination revealed a large, painful, slightly hot left bursa and two elongated, poorly defined, firm, painful subcutaneous formations in the anterior thoracic wall, 3 to 4 cm long. There were no rales on auscultation. The remainder of the examination was normal. Laboratory studies revealed a high c-reactive protein of 90 mg/dl. The blood count, creatinine, blood glucose and liver function tests were within normal limits. The standard chest X-ray showed reticulonodular infiltrates in both lung fields.\n\nDiagnostic approach: In the presence of an ultrasound finding in favour of an epididymal tumour, the patient underwent a left orchidectomy. However, the pathological examination of the surgical specimen showed a granulomatous epitheloid necrosis of the epididymis, suggestive of active epididymal tuberculosis involving the body and tail of the epididymis and sparing the head and testicle. The intradermal tuberculin reaction was positive. The search for acid-fast bacilli (AFB) in sputum and urine for 3 consecutive days was negative on direct examination and culture. The serologies for human immunodeficiency virus (HIV), hepatitis B virus (HBV), hepatitis C virus (HCV) and Wright's stain were also negative. In search of other tuberculous sites, a thoraco-abdomino-pelvic tomodensitometry was performed, which showed a miliary tuberculosis, coelo-mesenteric necrotic adenopathies, two thoracic parietal collections (at the expense of the external oblique muscles measuring 33 × 10 mm on the right and 45 × 10 mm on the left) and a focal osteolysis of D11 and L5, suggestive of a spondylodiscitis in the early stages. The magnetic resonance imaging (MRI) of the spinal cord confirmed the existence of a spondylodiscitis at the level of D7, D11, L4 and L5. The diagnosis of disseminated tuberculosis with epididymal, pulmonary, parietal, ganglionary and osteo-articular sites was retained.\n\nTherapeutic intervention: a poly-chemotherapy for tuberculosis with isoniazid, rifampicin, ethambutol and pyrazinamide for 2 months, followed by the association of isoniazid and rifampicin, was initiated.\n\nFollow-up and results: however, at the 4th month of treatment, the patient had presented generalised tonic-clonic convulsive seizures. A brain MRI was performed, showing multiple nodular lesions above and below the tentorial membrane corresponding to tuberculomas. The patient was put on anticonvulsive treatment and anti-tuberculosis treatment was continued. The evolution was favourable with recovery of the general condition and weight gain from the first months of treatment as well as a disappearance of thoracic parietal formations, adenopathies and tuberculous milia on the tomodensitometry with absence of recurrence of convulsive seizures. However, the slow decrease of the size of the tuberculomas obliged us to continue the anti-tuberculosis treatment for a long period. Finally, the patient was declared cured, without sequelae, at the end of the 234th month of treatment with a 2-year follow-up.\n",
+    "diff_label_texts": "A 19-year-old man had a painful lump in his left scrotum for 8 months. Doctors removed the left testicle. Lab tests showed the lump was from TB in the small tube behind the testicle that carries sperm. Scans showed the TB germs had also spread to his lymph nodes, lungs, chest wall, and his bones and joints. He started TB medicines. After 4 months, he had seizures. A brain scan showed small TB lumps in his brain. The doctors kept the TB treatment and added seizure medicine. He got better, and his scans looked better too.",
+    "summary": "A 19-year-old man with no significant history was admitted to hospital with a painful left scrotal mass that had been present for 8 months. He had undergone an orchidectomy and the pathological examination was in favour of epididymal tuberculosis. A radiological examination had shown other sites of infection: lymph nodes, lungs, parietal and osteoarticular. An anti-tuberculosis treatment was initiated. However, in the 4th month of treatment, the patient had convulsive seizures. A brain MRI was performed and concluded that there were brain tuberculomas. The anti-tuberculosis treatment was continued in association with an anticonvulsant with good clinical and radiological evolution.\n"
+  },
+  {
+    "doc_id": 47,
+    "label": "intermediate_health_literacy",
+    "fulltext": "Patient information: A 19-year-old male with no significant medical history was admitted to our department with a painful left scrotal mass that had been present for 8 months and had not improved with antibiotics for pyogenic organisms. The patient reported intermittent low grade fever, night sweats, anorexia and unexplained weight loss since the onset of symptoms. He did not have a cough, sputum or haemoptysis. There was no history of tuberculosis in his personal or family medical history. He was vaccinated against tuberculosis at birth.\n\nClinical findings: Physical examination revealed a large, painful, slightly hot left bursa and two elongated, poorly defined, firm, painful subcutaneous formations in the anterior thoracic wall, 3 to 4 cm long. There were no rales on auscultation. The remainder of the examination was normal. Laboratory studies revealed a high c-reactive protein of 90 mg/dl. The blood count, creatinine, blood glucose and liver function tests were within normal limits. The standard chest X-ray showed reticulonodular infiltrates in both lung fields.\n\nDiagnostic approach: In the presence of an ultrasound finding in favour of an epididymal tumour, the patient underwent a left orchidectomy. However, the pathological examination of the surgical specimen showed a granulomatous epitheloid necrosis of the epididymis, suggestive of active epididymal tuberculosis involving the body and tail of the epididymis and sparing the head and testicle. The intradermal tuberculin reaction was positive. The search for acid-fast bacilli (AFB) in sputum and urine for 3 consecutive days was negative on direct examination and culture. The serologies for human immunodeficiency virus (HIV), hepatitis B virus (HBV), hepatitis C virus (HCV) and Wright's stain were also negative. In search of other tuberculous sites, a thoraco-abdomino-pelvic tomodensitometry was performed, which showed a miliary tuberculosis, coelo-mesenteric necrotic adenopathies, two thoracic parietal collections (at the expense of the external oblique muscles measuring 33 × 10 mm on the right and 45 × 10 mm on the left) and a focal osteolysis of D11 and L5, suggestive of a spondylodiscitis in the early stages. The magnetic resonance imaging (MRI) of the spinal cord confirmed the existence of a spondylodiscitis at the level of D7, D11, L4 and L5. The diagnosis of disseminated tuberculosis with epididymal, pulmonary, parietal, ganglionary and osteo-articular sites was retained.\n\nTherapeutic intervention: a poly-chemotherapy for tuberculosis with isoniazid, rifampicin, ethambutol and pyrazinamide for 2 months, followed by the association of isoniazid and rifampicin, was initiated.\n\nFollow-up and results: however, at the 4th month of treatment, the patient had presented generalised tonic-clonic convulsive seizures. A brain MRI was performed, showing multiple nodular lesions above and below the tentorial membrane corresponding to tuberculomas. The patient was put on anticonvulsive treatment and anti-tuberculosis treatment was continued. The evolution was favourable with recovery of the general condition and weight gain from the first months of treatment as well as a disappearance of thoracic parietal formations, adenopathies and tuberculous milia on the tomodensitometry with absence of recurrence of convulsive seizures. However, the slow decrease of the size of the tuberculomas obliged us to continue the anti-tuberculosis treatment for a long period. Finally, the patient was declared cured, without sequelae, at the end of the 234th month of treatment with a 2-year follow-up.\n",
+    "diff_label_texts": "A 19-year-old man was admitted with an 8-month history of a painful left scrotal mass. He underwent an orchidectomy, and pathology favored epididymal tuberculosis. Imaging then revealed additional TB sites: lymph nodes, lungs, the chest wall (parietal), and the bones and joints (osteoarticular). Standard anti-tuberculosis therapy was started. In the fourth month of treatment he developed generalized seizures, and brain MRI showed tuberculomas. Treatment was continued along with an anticonvulsant, leading to good clinical and radiologic improvement.",
+    "summary": "A 19-year-old man with no significant history was admitted to hospital with a painful left scrotal mass that had been present for 8 months. He had undergone an orchidectomy and the pathological examination was in favour of epididymal tuberculosis. A radiological examination had shown other sites of infection: lymph nodes, lungs, parietal and osteoarticular. An anti-tuberculosis treatment was initiated. However, in the 4th month of treatment, the patient had convulsive seizures. A brain MRI was performed and concluded that there were brain tuberculomas. The anti-tuberculosis treatment was continued in association with an anticonvulsant with good clinical and radiological evolution.\n"
+  },
+  {
+    "doc_id": 47,
+    "label": "proficient_health_literacy",
+    "fulltext": "Patient information: A 19-year-old male with no significant medical history was admitted to our department with a painful left scrotal mass that had been present for 8 months and had not improved with antibiotics for pyogenic organisms. The patient reported intermittent low grade fever, night sweats, anorexia and unexplained weight loss since the onset of symptoms. He did not have a cough, sputum or haemoptysis. There was no history of tuberculosis in his personal or family medical history. He was vaccinated against tuberculosis at birth.\n\nClinical findings: Physical examination revealed a large, painful, slightly hot left bursa and two elongated, poorly defined, firm, painful subcutaneous formations in the anterior thoracic wall, 3 to 4 cm long. There were no rales on auscultation. The remainder of the examination was normal. Laboratory studies revealed a high c-reactive protein of 90 mg/dl. The blood count, creatinine, blood glucose and liver function tests were within normal limits. The standard chest X-ray showed reticulonodular infiltrates in both lung fields.\n\nDiagnostic approach: In the presence of an ultrasound finding in favour of an epididymal tumour, the patient underwent a left orchidectomy. However, the pathological examination of the surgical specimen showed a granulomatous epitheloid necrosis of the epididymis, suggestive of active epididymal tuberculosis involving the body and tail of the epididymis and sparing the head and testicle. The intradermal tuberculin reaction was positive. The search for acid-fast bacilli (AFB) in sputum and urine for 3 consecutive days was negative on direct examination and culture. The serologies for human immunodeficiency virus (HIV), hepatitis B virus (HBV), hepatitis C virus (HCV) and Wright's stain were also negative. In search of other tuberculous sites, a thoraco-abdomino-pelvic tomodensitometry was performed, which showed a miliary tuberculosis, coelo-mesenteric necrotic adenopathies, two thoracic parietal collections (at the expense of the external oblique muscles measuring 33 × 10 mm on the right and 45 × 10 mm on the left) and a focal osteolysis of D11 and L5, suggestive of a spondylodiscitis in the early stages. The magnetic resonance imaging (MRI) of the spinal cord confirmed the existence of a spondylodiscitis at the level of D7, D11, L4 and L5. The diagnosis of disseminated tuberculosis with epididymal, pulmonary, parietal, ganglionary and osteo-articular sites was retained.\n\nTherapeutic intervention: a poly-chemotherapy for tuberculosis with isoniazid, rifampicin, ethambutol and pyrazinamide for 2 months, followed by the association of isoniazid and rifampicin, was initiated.\n\nFollow-up and results: however, at the 4th month of treatment, the patient had presented generalised tonic-clonic convulsive seizures. A brain MRI was performed, showing multiple nodular lesions above and below the tentorial membrane corresponding to tuberculomas. The patient was put on anticonvulsive treatment and anti-tuberculosis treatment was continued. The evolution was favourable with recovery of the general condition and weight gain from the first months of treatment as well as a disappearance of thoracic parietal formations, adenopathies and tuberculous milia on the tomodensitometry with absence of recurrence of convulsive seizures. However, the slow decrease of the size of the tuberculomas obliged us to continue the anti-tuberculosis treatment for a long period. Finally, the patient was declared cured, without sequelae, at the end of the 234th month of treatment with a 2-year follow-up.\n",
+    "diff_label_texts": "A 19-year-old male with no significant history presented with an 8-month painful left scrotal mass unresponsive to antibiotics for presumed pyogenic infection, along with intermittent low-grade fever, night sweats, anorexia, and weight loss. Exam showed a large, painful, slightly warm left bursa and two firm, painful subcutaneous formations on the anterior thoracic wall (3–4 cm). CRP was 90 mg/dl; CBC, creatinine, glucose, and liver function tests were normal. Chest radiograph demonstrated bilateral reticulonodular infiltrates. Scrotal ultrasound suggested an epididymal tumor, and a left orchidectomy was performed. Histopathology revealed granulomatous epithelioid necrosis of the epididymis, consistent with active epididymal tuberculosis involving the body and tail and sparing the head and testis. The tuberculin skin test was positive. AFB studies of sputum and urine on 3 consecutive days were negative on direct smear and culture. HIV, HBV, HCV serologies and Wright's were negative. Thoraco-abdomino-pelvic CT identified miliary tuberculosis, coelo-mesenteric necrotic adenopathies, two thoracic parietal collections within the external oblique muscles (33 × 10 mm right, 45 × 10 mm left), and focal osteolysis of D11 and L5 suggestive of early spondylodiscitis; spinal MRI confirmed spondylodiscitis at D7, D11, L4, and L5. The diagnosis was disseminated tuberculosis with epididymal, pulmonary, parietal, ganglionary, and osteo-articular involvement. Treatment consisted of isoniazid, rifampicin, ethambutol, and pyrazinamide for 2 months, followed by isoniazid plus rifampicin. At month 4 of therapy he developed generalized tonic-clonic seizures; brain MRI showed multiple supra- and infratentorial nodular lesions compatible with tuberculomas. An anticonvulsant was added and anti-tuberculous therapy was continued. Evolution was favorable with early weight gain and disappearance of thoracic parietal formations, adenopathies, and miliary lesions on CT; there was no recurrence of seizures. Because the tuberculomas regressed slowly, therapy was prolonged; he was ultimately declared cured without sequelae at the end of the 234th month of treatment (as reported) with 2-year follow-up. Context: Epididymal tuberculosis can mimic neoplasm and may occur with negative AFB studies; CNS tuberculomas emerging during therapy are a recognized phenomenon, typically managed by continuing anti-tuberculous treatment with seizure control.",
+    "summary": "A 19-year-old man with no significant history was admitted to hospital with a painful left scrotal mass that had been present for 8 months. He had undergone an orchidectomy and the pathological examination was in favour of epididymal tuberculosis. A radiological examination had shown other sites of infection: lymph nodes, lungs, parietal and osteoarticular. An anti-tuberculosis treatment was initiated. However, in the 4th month of treatment, the patient had convulsive seizures. A brain MRI was performed and concluded that there were brain tuberculomas. The anti-tuberculosis treatment was continued in association with an anticonvulsant with good clinical and radiological evolution.\n"
+  },
+  {
+    "doc_id": 48,
+    "label": "low_health_literacy",
+    "fulltext": "We present the case of a 10-year-old male diagnosed with high-risk early T-cell acute lymphoblastic leukaemia, who was treated according to the LAL SEHOP-PETHEMA 2013 protocol. Two years after diagnosis, he developed an early CNS relapse, so he was treated according to the InteReALL HR 2010 protocol with bortezomib. During induction, after being neutropenic for four weeks (20 neutrophils/μL), he was receiving prophylaxis with cefepime, cotrimoxazole and fluconazole. In addition, he was being treated with acyclovir for a herpes simplex virus 1 skin infection. In this context, he developed a severe headache that did not respond to usual analgesia. A cranial computed tomographic scan was performed that showed a hypodens lesion in the right temporal lobe. When the possibility of an infectious origin was considered, a lumbar puncture was performed and cefepime was replaced with meropenem and vancomycin.\n\nDespite remaining afebrile, he developed signs of septic shock on the first day after admission to the clinic and was transferred to the paediatric intensive care unit for inotropic and vasoactive support. In addition, the antimicrobial spectrum was extended with gentamicin and caspofungin.\n\nThe blood analysis showed a progressive increase in C-reactive protein and procalcitonin (up to 312 mg/L and 47.58 ng/mL, respectively, on the third day of evolution), with no other relevant biochemical alterations. The blood count showed pancytopenia due to chemotherapy. The blood cultures ruled out bacteremia and fungemia, and herpes virus serologies were negative. The urine culture and the fecal culture were also negative. The biochemical analysis of the cerebrospinal fluid was completely normal (glucose, 63 mg/dL; proteins, 16 mg/dL; leukocytes 1/µL), but the presence of B. cereus was detected in the microbiological study (sensitive to meropenem, vancomycin, linezolid and ciprofloxacin). The presence of herpes simplex 1 and 2, herpes virus 6, cytomegalovirus, varicella-zoster virus, enterovirus, parechovirus, toxoplasma, Neisseria meningitidis, Listeria monocytogenes, Streptococcus pneumoniae and Cryptococcus was ruled out in the cerebrospinal fluid.\n\nThe EEG showed diffuse slowing of brain activity with no clear epileptiform activity. On day 4, after the haemodynamic support was removed, a cranial MRI showed two hyperintense lesions in T2 and FLAIR that involved the subcortical region of the right temporal and parietal lobes. The parietal lesion had ring enhancement after administration of gadolinium and both lesions showed peripheral diffusion restriction. In addition, small haemorrhagic foci were observed scattered in the brain parenchyma. The image suggested a bacterial origin with an atypical germ, and these findings, together with those of the cerebrospinal fluid, led to the diagnosis of B. cereus abscess.\n\nAfter two weeks of treatment, the patient had a favorable outcome with resolution of the headache and no neurological findings. A follow-up MRI showed a decrease in the size of the lesions. Vancomycin and acyclovir were discontinued after three weeks and meropenem was continued for six weeks.\n",
+    "diff_label_texts": "A 10-year-old boy was getting cancer medicine for leukemia. During the first phase of treatment, he got a pocket of infection in his brain. The germ was called Bacillus cereus. Doctors found it with brain scans and by testing the fluid around his brain and spine. He got better after taking antibiotics.",
+    "summary": "We present the case of a 10-year-old boy undergoing chemotherapy for acute lymphoblastic leukaemia. During the induction period he developed a cerebral abscess caused by B. cereus that was diagnosed by imaging tests and direct detection in the cerebrospinal fluid. His evolution was favourable with antibiotic treatment.\n"
+  },
+  {
+    "doc_id": 48,
+    "label": "intermediate_health_literacy",
+    "fulltext": "We present the case of a 10-year-old male diagnosed with high-risk early T-cell acute lymphoblastic leukaemia, who was treated according to the LAL SEHOP-PETHEMA 2013 protocol. Two years after diagnosis, he developed an early CNS relapse, so he was treated according to the InteReALL HR 2010 protocol with bortezomib. During induction, after being neutropenic for four weeks (20 neutrophils/μL), he was receiving prophylaxis with cefepime, cotrimoxazole and fluconazole. In addition, he was being treated with acyclovir for a herpes simplex virus 1 skin infection. In this context, he developed a severe headache that did not respond to usual analgesia. A cranial computed tomographic scan was performed that showed a hypodens lesion in the right temporal lobe. When the possibility of an infectious origin was considered, a lumbar puncture was performed and cefepime was replaced with meropenem and vancomycin.\n\nDespite remaining afebrile, he developed signs of septic shock on the first day after admission to the clinic and was transferred to the paediatric intensive care unit for inotropic and vasoactive support. In addition, the antimicrobial spectrum was extended with gentamicin and caspofungin.\n\nThe blood analysis showed a progressive increase in C-reactive protein and procalcitonin (up to 312 mg/L and 47.58 ng/mL, respectively, on the third day of evolution), with no other relevant biochemical alterations. The blood count showed pancytopenia due to chemotherapy. The blood cultures ruled out bacteremia and fungemia, and herpes virus serologies were negative. The urine culture and the fecal culture were also negative. The biochemical analysis of the cerebrospinal fluid was completely normal (glucose, 63 mg/dL; proteins, 16 mg/dL; leukocytes 1/µL), but the presence of B. cereus was detected in the microbiological study (sensitive to meropenem, vancomycin, linezolid and ciprofloxacin). The presence of herpes simplex 1 and 2, herpes virus 6, cytomegalovirus, varicella-zoster virus, enterovirus, parechovirus, toxoplasma, Neisseria meningitidis, Listeria monocytogenes, Streptococcus pneumoniae and Cryptococcus was ruled out in the cerebrospinal fluid.\n\nThe EEG showed diffuse slowing of brain activity with no clear epileptiform activity. On day 4, after the haemodynamic support was removed, a cranial MRI showed two hyperintense lesions in T2 and FLAIR that involved the subcortical region of the right temporal and parietal lobes. The parietal lesion had ring enhancement after administration of gadolinium and both lesions showed peripheral diffusion restriction. In addition, small haemorrhagic foci were observed scattered in the brain parenchyma. The image suggested a bacterial origin with an atypical germ, and these findings, together with those of the cerebrospinal fluid, led to the diagnosis of B. cereus abscess.\n\nAfter two weeks of treatment, the patient had a favorable outcome with resolution of the headache and no neurological findings. A follow-up MRI showed a decrease in the size of the lesions. Vancomycin and acyclovir were discontinued after three weeks and meropenem was continued for six weeks.\n",
+    "diff_label_texts": "A 10-year-old boy receiving chemotherapy for acute lymphoblastic leukemia developed a brain abscess during induction therapy. He had a severe headache, and brain scans (CT/MRI) showed lesions that looked like an infection. Tests on his spinal fluid directly detected Bacillus cereus, confirming the cause. He was treated with antibiotics (such as meropenem and vancomycin). His symptoms resolved, follow-up imaging showed the abscess shrinking, and he recovered well.",
+    "summary": "We present the case of a 10-year-old boy undergoing chemotherapy for acute lymphoblastic leukaemia. During the induction period he developed a cerebral abscess caused by B. cereus that was diagnosed by imaging tests and direct detection in the cerebrospinal fluid. His evolution was favourable with antibiotic treatment.\n"
+  },
+  {
+    "doc_id": 48,
+    "label": "proficient_health_literacy",
+    "fulltext": "We present the case of a 10-year-old male diagnosed with high-risk early T-cell acute lymphoblastic leukaemia, who was treated according to the LAL SEHOP-PETHEMA 2013 protocol. Two years after diagnosis, he developed an early CNS relapse, so he was treated according to the InteReALL HR 2010 protocol with bortezomib. During induction, after being neutropenic for four weeks (20 neutrophils/μL), he was receiving prophylaxis with cefepime, cotrimoxazole and fluconazole. In addition, he was being treated with acyclovir for a herpes simplex virus 1 skin infection. In this context, he developed a severe headache that did not respond to usual analgesia. A cranial computed tomographic scan was performed that showed a hypodens lesion in the right temporal lobe. When the possibility of an infectious origin was considered, a lumbar puncture was performed and cefepime was replaced with meropenem and vancomycin.\n\nDespite remaining afebrile, he developed signs of septic shock on the first day after admission to the clinic and was transferred to the paediatric intensive care unit for inotropic and vasoactive support. In addition, the antimicrobial spectrum was extended with gentamicin and caspofungin.\n\nThe blood analysis showed a progressive increase in C-reactive protein and procalcitonin (up to 312 mg/L and 47.58 ng/mL, respectively, on the third day of evolution), with no other relevant biochemical alterations. The blood count showed pancytopenia due to chemotherapy. The blood cultures ruled out bacteremia and fungemia, and herpes virus serologies were negative. The urine culture and the fecal culture were also negative. The biochemical analysis of the cerebrospinal fluid was completely normal (glucose, 63 mg/dL; proteins, 16 mg/dL; leukocytes 1/µL), but the presence of B. cereus was detected in the microbiological study (sensitive to meropenem, vancomycin, linezolid and ciprofloxacin). The presence of herpes simplex 1 and 2, herpes virus 6, cytomegalovirus, varicella-zoster virus, enterovirus, parechovirus, toxoplasma, Neisseria meningitidis, Listeria monocytogenes, Streptococcus pneumoniae and Cryptococcus was ruled out in the cerebrospinal fluid.\n\nThe EEG showed diffuse slowing of brain activity with no clear epileptiform activity. On day 4, after the haemodynamic support was removed, a cranial MRI showed two hyperintense lesions in T2 and FLAIR that involved the subcortical region of the right temporal and parietal lobes. The parietal lesion had ring enhancement after administration of gadolinium and both lesions showed peripheral diffusion restriction. In addition, small haemorrhagic foci were observed scattered in the brain parenchyma. The image suggested a bacterial origin with an atypical germ, and these findings, together with those of the cerebrospinal fluid, led to the diagnosis of B. cereus abscess.\n\nAfter two weeks of treatment, the patient had a favorable outcome with resolution of the headache and no neurological findings. A follow-up MRI showed a decrease in the size of the lesions. Vancomycin and acyclovir were discontinued after three weeks and meropenem was continued for six weeks.\n",
+    "diff_label_texts": "A 10-year-old male with high-risk early T-cell acute lymphoblastic leukaemia (initially treated per LAL SEHOP-PETHEMA 2013) experienced an early CNS relapse two years after diagnosis and began InteReALL HR 2010 induction with bortezomib. After four weeks of profound neutropenia (20 neutrophils/µL) on prophylaxis (cefepime, cotrimoxazole, fluconazole) and acyclovir for HSV-1 skin infection, he developed a severe, analgesia-refractory headache. Head CT revealed a right temporal hypodense lesion. Suspecting infection, a lumbar puncture was performed and cefepime was switched to meropenem plus vancomycin. Despite being afebrile, he showed signs of septic shock on day 1 and required PICU admission for inotropic/vasoactive support; antimicrobials were broadened with gentamicin and caspofungin. Inflammatory markers rose (CRP 312 mg/L, procalcitonin 47.58 ng/mL by day 3), with pancytopenia attributable to chemotherapy and no other major biochemical abnormalities. Blood, urine, and fecal cultures were negative; viral serologies were negative. CSF biochemistry was normal (glucose 63 mg/dL; protein 16 mg/dL; leukocytes 1/µL), but microbiology detected Bacillus cereus, susceptible to meropenem, vancomycin, linezolid, and ciprofloxacin; CSF PCR/assays were negative for HSV-1/2, HHV-6, CMV, VZV, enterovirus, parechovirus, Toxoplasma, Neisseria meningitidis, Listeria monocytogenes, Streptococcus pneumoniae, and Cryptococcus. EEG showed diffuse slowing without epileptiform activity. On day 4, once off haemodynamic support, brain MRI demonstrated two T2/FLAIR hyperintense subcortical lesions in the right temporal and parietal lobes; the parietal lesion exhibited ring enhancement post-gadolinium, both lesions had peripheral diffusion restriction, and scattered parenchymal microhaemorrhages were present—an appearance suggestive of bacterial abscess due to an atypical pathogen. Integrating imaging with direct CSF detection established the diagnosis of B. cereus cerebral abscess. After two weeks of therapy, his headache resolved with no focal neurological deficits; interval MRI showed lesion size reduction. Vancomycin and acyclovir were discontinued after three weeks, and meropenem was continued to complete six weeks, with a favourable clinical course.",
+    "summary": "We present the case of a 10-year-old boy undergoing chemotherapy for acute lymphoblastic leukaemia. During the induction period he developed a cerebral abscess caused by B. cereus that was diagnosed by imaging tests and direct detection in the cerebrospinal fluid. His evolution was favourable with antibiotic treatment.\n"
+  },
+  {
+    "doc_id": 49,
+    "label": "low_health_literacy",
+    "fulltext": "Female patient, 16 years old, presenting a depressed gray plaque of 10.5 × 8.0 cm interspersed with hypochromic areas in the lower lateral part of the left thigh. Telangiectatic vessels overlap the lesion peripherally, with visible veins close to it. The plaque was present from birth, but was initially violaceous. It evolved with the passing of the years, with lightening and depression. There is no discrepancy in the length of the lower limbs.\n\nAngioresonance showed vascular malformations in the skin and subcutaneous tissue supplied by intermuscular branches of the popliteal artery. Early venous filling was found in both the region and the malformations, suggesting early venous shunting. Dilated draining veins were not documented, except for a superficial draining vein running along the subcutaneous cellular tissue of the anterior thigh. In addition, thinning of the subcutaneous tissue was noted in the topography of the vascular alteration, but without intramuscular or bone extension.\n",
+    "diff_label_texts": "A 16-year-old girl has a sunken, gray patch on her left thigh. A special scan that looks at blood vessels showed a blood vessel problem in the skin and in the layer just under the skin.",
+    "summary": "16-year-old girl with a depressed gray plaque on the left thigh, with a vascular malformation affecting the skin and subcutaneous tissue evident by angioresonance.\n"
+  },
+  {
+    "doc_id": 49,
+    "label": "proficient_health_literacy",
+    "fulltext": "Female patient, 16 years old, presenting a depressed gray plaque of 10.5 × 8.0 cm interspersed with hypochromic areas in the lower lateral part of the left thigh. Telangiectatic vessels overlap the lesion peripherally, with visible veins close to it. The plaque was present from birth, but was initially violaceous. It evolved with the passing of the years, with lightening and depression. There is no discrepancy in the length of the lower limbs.\n\nAngioresonance showed vascular malformations in the skin and subcutaneous tissue supplied by intermuscular branches of the popliteal artery. Early venous filling was found in both the region and the malformations, suggesting early venous shunting. Dilated draining veins were not documented, except for a superficial draining vein running along the subcutaneous cellular tissue of the anterior thigh. In addition, thinning of the subcutaneous tissue was noted in the topography of the vascular alteration, but without intramuscular or bone extension.\n",
+    "diff_label_texts": "Female patient, 16 years old, with a depressed gray plaque measuring 10.5 × 8.0 cm, interspersed with hypochromic areas on the lower lateral left thigh. Telangiectatic vessels overlap the lesion peripherally, with visible veins adjacent to it. The plaque has been present since birth, initially violaceous, and evolved over the years with lightening and progressive depression. No discrepancy in lower limb length. Angioresonance demonstrated vascular malformations confined to the skin and subcutaneous tissue, supplied by intermuscular branches of the popliteal artery. There is early venous filling in both the region and the malformations, suggesting early venous shunting. Dilated draining veins were not documented, except for a superficial draining vein coursing along the subcutaneous cellular tissue of the anterior thigh. There is thinning of the subcutaneous tissue at the site of the vascular alteration, without intramuscular or bone extension.",
+    "summary": "16-year-old girl with a depressed gray plaque on the left thigh, with a vascular malformation affecting the skin and subcutaneous tissue evident by angioresonance.\n"
+  },
+  {
+    "doc_id": 50,
+    "label": "intermediate_health_literacy",
+    "fulltext": "A 57-year-old woman with a 14-year history of asthma and allergic rhinitis, on salmeterol/fluticasone, was hospitalized for recurrent abdominal pain that began two months earlier. The pain was intermittent and dull, accompanied by nausea, anorexia, malaise, and a weight loss of 5 kg. There was no fever, blood / mucus in the stool, or respiratory symptoms (rhinorrhea, wheezing, coughing). She had no history of alcohol/tobacco use or traditional herbal medicines. Six weeks before admission, she was diagnosed with an intestinal infection in a local clinic after a complete blood count (CBC) revealed leukocytosis and significant eosinophilia (25.61 G/L, 77.8% eosinophils). She received antibiotics and mebendazole without relief of symptoms. At presentation, the patient was alerted and oriented with stable vitals (BP 110/70 mmHg, T 37°C, HR 88 bpm, RR 18 bpm). She had a BMI of 16.6 kg/m² and sarcopenia, but no skin rash, lymphadenopathy, or edema. The abdominal exam showed tenderness in the epigastric and umbilical regions without guarding. CBC revealed leukocytosis and significant eosinophilia (20.8 G/L, with a total white blood cell count of 26.8 G/L, comprising 77.8% eosinophils). Peripheral blood film examination showed normal eosinophils. Bone marrow aspiration reveals 48% eosinophils without blasts, atypical cells. Fluorescence in situ hybridization (FISH) for CHIC2 deletion as a surrogate marker for FIP1L1-PDGFRA showed no rearrangements of the PDGFRA gene. Autoimmune and vasculitis screenings (ANA, anti-dsDNA, p-ANCA, c-ANCA) were negative. Elevated serum IgG (2760 mg/dL; normal range, 700–1600 mg/dL) and IgG4 (1260 mg/dL; normal range, 3.9–86.4 mg/dL), slightly elevated IgE (137.5 IU/mL; normal range, <100 IU/mL) and high RF (144.4 IU/mL; normal range, <20 IU/mL) were observed. Other parameters were normal, including aminotransferase, blood urea nitrogen, serum creatinine, complement C3, complement C4, vitamin B12, serum cortisol, and NT-proBNP. ECG and echocardiogram were normal. Chest CT scans showed mild fibrosis and bronchiectasis. Sputum AFB smears and bronchoscopy were negative. The cytology of the bronchoalveolar lavage fluid showed 35% neutrophils, no eosinophils. Spirometry indicated severe obstruction with bronchodilator response. The fractional exhaled nitric oxide (FeNO) level was 15 ppb. Stool samples were tested positive for leukocytes, with no signs of ova or parasites. Serology tests were positive for toxocariasis (positive IgG of Toxocara canis at 54.2 NovaTec-Units) but negative for Strongyloides stercoralis, Fasciola sp., Toxoplasma gondii, Trichinella spiralis, Ancylostoma sp., Angiostrongylus cantonensis, Ascaris lumbricoides, Clonorchis sinensis, Paragonimus sp., Gnathostoma sp., Entamoeba histolytica, cysticercosis, filariasis, and HIV. An abdominal contrast-enhanced computed tomography scan revealed gallbladder stones without acute cholecystitis and showed no gastrointestinal tract abnormalities. The upper gastrointestinal endoscopy showed unremarkable results with a normal appearance. Colonoscopy showed mucosal inflammation in the sigmoid, left, transverse, and right colon with systemic biopsy. A five-day course of albendazole (400 mg twice daily) for suspected toxocariasis was ineffective. Colonic biopsies revealed significant eosinophilic infiltration (>85 eosinophils/High-power field (HPF) in the left colon, >100 eosinophils/HPF in the transverse and right colon). Given the patient’s nonresponse to toxocariasis treatment and the significant eosinophilic infiltration observed in the colon mucosa biopsy, a diagnosis of eosinophilic colitis was confirmed. The patient was treated with oral methylprednisolone (16 mg) and montelukast (5 mg). Symptoms resolved in two weeks and eosinophil counts normalized (0.3 G/L). The corticosteroid was reduced and discontinued, and the patient was maintained on montelukast for three months without symptom recurrence.",
+    "diff_label_texts": "A 57-year-old woman with longstanding asthma and allergic rhinitis developed recurrent abdominal pain. Blood tests showed marked eosinophilia (very high levels of allergy-type white blood cells) and an elevated IgG4 level. After doctors ruled out blood cancers and other secondary causes of eosinophilia, they performed a colon biopsy. The biopsy showed an excess of eosinophils in the colon lining, confirming eosinophilic colitis. She improved quickly on corticosteroids and was then maintained on montelukast. Over the next three months, her symptoms did not return.",
+    "summary": "We present a unique case of a 57-year-old patient with a medical history of asthma and allergic rhinitis who presented recurrent abdominal pain, significant blood eosinophilia, and elevated levels of Immunoglobulin G4. After ruling out hematological and secondary causes of eosinophilia, a biopsy of the colon mucosa revealed an excess of tissue eosinophils, confirming the diagnosis of EoC. The patient responded well to corticosteroids and was subsequently maintained on montelukast, with no recurrence of symptoms over 3 months."
+  },
+  {
+    "doc_id": 50,
+    "label": "proficient_health_literacy",
+    "fulltext": "A 57-year-old woman with a 14-year history of asthma and allergic rhinitis, on salmeterol/fluticasone, was hospitalized for recurrent abdominal pain that began two months earlier. The pain was intermittent and dull, accompanied by nausea, anorexia, malaise, and a weight loss of 5 kg. There was no fever, blood / mucus in the stool, or respiratory symptoms (rhinorrhea, wheezing, coughing). She had no history of alcohol/tobacco use or traditional herbal medicines. Six weeks before admission, she was diagnosed with an intestinal infection in a local clinic after a complete blood count (CBC) revealed leukocytosis and significant eosinophilia (25.61 G/L, 77.8% eosinophils). She received antibiotics and mebendazole without relief of symptoms. At presentation, the patient was alerted and oriented with stable vitals (BP 110/70 mmHg, T 37°C, HR 88 bpm, RR 18 bpm). She had a BMI of 16.6 kg/m² and sarcopenia, but no skin rash, lymphadenopathy, or edema. The abdominal exam showed tenderness in the epigastric and umbilical regions without guarding. CBC revealed leukocytosis and significant eosinophilia (20.8 G/L, with a total white blood cell count of 26.8 G/L, comprising 77.8% eosinophils). Peripheral blood film examination showed normal eosinophils. Bone marrow aspiration reveals 48% eosinophils without blasts, atypical cells. Fluorescence in situ hybridization (FISH) for CHIC2 deletion as a surrogate marker for FIP1L1-PDGFRA showed no rearrangements of the PDGFRA gene. Autoimmune and vasculitis screenings (ANA, anti-dsDNA, p-ANCA, c-ANCA) were negative. Elevated serum IgG (2760 mg/dL; normal range, 700–1600 mg/dL) and IgG4 (1260 mg/dL; normal range, 3.9–86.4 mg/dL), slightly elevated IgE (137.5 IU/mL; normal range, <100 IU/mL) and high RF (144.4 IU/mL; normal range, <20 IU/mL) were observed. Other parameters were normal, including aminotransferase, blood urea nitrogen, serum creatinine, complement C3, complement C4, vitamin B12, serum cortisol, and NT-proBNP. ECG and echocardiogram were normal. Chest CT scans showed mild fibrosis and bronchiectasis. Sputum AFB smears and bronchoscopy were negative. The cytology of the bronchoalveolar lavage fluid showed 35% neutrophils, no eosinophils. Spirometry indicated severe obstruction with bronchodilator response. The fractional exhaled nitric oxide (FeNO) level was 15 ppb. Stool samples were tested positive for leukocytes, with no signs of ova or parasites. Serology tests were positive for toxocariasis (positive IgG of Toxocara canis at 54.2 NovaTec-Units) but negative for Strongyloides stercoralis, Fasciola sp., Toxoplasma gondii, Trichinella spiralis, Ancylostoma sp., Angiostrongylus cantonensis, Ascaris lumbricoides, Clonorchis sinensis, Paragonimus sp., Gnathostoma sp., Entamoeba histolytica, cysticercosis, filariasis, and HIV. An abdominal contrast-enhanced computed tomography scan revealed gallbladder stones without acute cholecystitis and showed no gastrointestinal tract abnormalities. The upper gastrointestinal endoscopy showed unremarkable results with a normal appearance. Colonoscopy showed mucosal inflammation in the sigmoid, left, transverse, and right colon with systemic biopsy. A five-day course of albendazole (400 mg twice daily) for suspected toxocariasis was ineffective. Colonic biopsies revealed significant eosinophilic infiltration (>85 eosinophils/High-power field (HPF) in the left colon, >100 eosinophils/HPF in the transverse and right colon). Given the patient’s nonresponse to toxocariasis treatment and the significant eosinophilic infiltration observed in the colon mucosa biopsy, a diagnosis of eosinophilic colitis was confirmed. The patient was treated with oral methylprednisolone (16 mg) and montelukast (5 mg). Symptoms resolved in two weeks and eosinophil counts normalized (0.3 G/L). The corticosteroid was reduced and discontinued, and the patient was maintained on montelukast for three months without symptom recurrence.",
+    "diff_label_texts": "A 57-year-old woman with a 14-year history of asthma and allergic rhinitis on salmeterol/fluticasone presented with two months of intermittent, dull abdominal pain, nausea, anorexia, malaise, and 5-kg weight loss. She was afebrile, hemodynamically stable, underweight (BMI 16.6 kg/m²) with sarcopenia, and had epigastric/umbilical tenderness without guarding. CBC showed leukocytosis with marked eosinophilia (WBC 26.8 G/L with 20.8 G/L eosinophils; 77.8%). Peripheral smear showed morphologically normal eosinophils. Bone marrow aspiration revealed 48% eosinophils without blasts or atypia. FISH for CHIC2 deletion (surrogate for FIP1L1-PDGFRA) was negative. Autoimmune/vasculitis screens (ANA, anti-dsDNA, p-ANCA, c-ANCA) were negative. Serum immunoglobulins demonstrated elevated IgG (2760 mg/dL) and IgG4 (1260 mg/dL), mildly elevated IgE (137.5 IU/mL), and high RF (144.4 IU/mL). Liver enzymes, BUN/creatinine, C3/C4, vitamin B12, cortisol, and NT-proBNP were within normal limits. ECG/echocardiogram were normal. Chest CT showed mild fibrosis and bronchiectasis. Bronchoscopy and AFB smears were negative; BAL cytology had 35% neutrophils and no eosinophils. Spirometry demonstrated severe obstruction with bronchodilator responsiveness; FeNO was 15 ppb. Stool leukocytes were present, but ova/parasite exams were negative. Serology was positive for Toxocara canis IgG (54.2 NovaTec-Units) and negative for other helminths and HIV. Empiric albendazole (400 mg twice daily for 5 days) was ineffective. Abdominal contrast-enhanced CT showed cholelithiasis without cholecystitis and no GI structural abnormality. Upper GI endoscopy was unremarkable. Colonoscopy demonstrated mucosal inflammation in the sigmoid, left, transverse, and right colon. Systematic colonic biopsies showed dense eosinophilic infiltration (>85 eosinophils/HPF in the left colon; >100 eosinophils/HPF in the transverse and right colon). Given the exclusion of hematologic neoplasms and secondary causes (including lack of response to anti-parasitic therapy and negative work-up for vasculitis/autoimmune disease), the findings were diagnostic of eosinophilic colitis. She was treated with oral methylprednisolone 16 mg and montelukast 5 mg. Symptoms resolved within two weeks with normalization of eosinophils to 0.3 G/L. Corticosteroids were tapered and discontinued, and montelukast was continued for three months with no symptom recurrence. This case illustrates eosinophilic colitis in an atopic patient with marked peripheral and tissue eosinophilia, elevated IgG4, negative myeloid neoplasm markers, and steroid-responsiveness, consistent with primary eosinophilic gastrointestinal disease after exclusion of secondary etiologies.",
+    "summary": "We present a unique case of a 57-year-old patient with a medical history of asthma and allergic rhinitis who presented recurrent abdominal pain, significant blood eosinophilia, and elevated levels of Immunoglobulin G4. After ruling out hematological and secondary causes of eosinophilia, a biopsy of the colon mucosa revealed an excess of tissue eosinophils, confirming the diagnosis of EoC. The patient responded well to corticosteroids and was subsequently maintained on montelukast, with no recurrence of symptoms over 3 months."
+  },
+  {
+    "doc_id": 51,
+    "label": "low_health_literacy",
+    "fulltext": "A 38-year-old male presented to the hospital with chest tightness and shortness of breath. Three years prior, he had experienced similar symptoms post-activity and received treatment at our hospital. Outpatient echocardiography indicated a left heart echomass suggestive of a myxoma, which led to his admission for further evaluation. Physical examination revealed pigmentation of the patient’s ears characterized by multiple small brown and black spots. Abdominal computed tomography (CT) showed multiple livers and small cysts in the left kidney. Genetic testing identified mutations in the TTN and PRKAR1A genes. The diagnosis of CNC was confirmed through clinical examination, imaging, and genetic testing. Following symptomatic treatment, the patient’s condition improved; however, he refused surgical intervention. On September 20, 2023, the patient presented to our hospital with exacerbated chest tightness and dyspnea. He reported difficulty lying supine and needing to sit upright to breathe. Physical examination revealed jugular vein distension, leftward and downward displacement of the heart boundary, irregular heart rhythm on auscultation, and a mitral valve murmur of intensity 2/6–3/6 in the fourth intercostal space along the left sternal margin. Wet rales were audible in both middle and lower lung fields. Palpation revealed a firm liver extending three fingers below the xiphoid process and two fingers below the rib cage, along with mild pitting edema in both lower limbs. Echocardiographic images indicated global heart enlargement, dilation of the aortic sinus and pulmonary artery, small-to-moderate mitral valve regurgitation, and an irregular echoic mass measuring 54 mm ×43 mm in the left chamber attached to the atrial septum. The left ventricular (LV) ejection fraction (EF) was 23.1%, with fractional shortening (FS) of 10.9%. Electrocardiography demonstrated atrial fibrillation (average ventricular rate, 150 beats/min) and abnormal Q waves in leads V1-V3. Based on the patient’s history, the diagnosis included DCM and CNC with cardiac myxoma. Given the presence of end-stage heart failure and concurrent cardiac myxoma, the patient was hospitalized, and heart transplantation was considered a viable therapeutic option to address both conditions simultaneously. A suitable donor heart became available for immediate transplantation on October 1, 2024.\n\n\nSurgical procedure\n\nThe skin and subcutaneous tissues were carefully incised layer-by-layer through a median sternotomy. The sternum was sawed longitudinally open, and bleeding was controlled using electrocoagulation and bone wax. Extracardiac exploration uncovered global heart enlargement, most prominent in the LV. The heart showed diminished contractile strength. The aorta and the main pulmonary artery (PA) were dissected from the supravalvular region. Some tissues were preserved for posterior suturing, whereas most diseased right atrium, left atrium(LA), right ventricle, and LV were excised. Resection revealed a greyish-white mucoid mass. The donor and residual recipient LA tissues were sutured using double continuous 3/0 Prolene threads. The anastomosis was meticulously inspected multiple times, and no significant bleeding was observed. Similarly, end-to-end anastomosis of the donor ascending aorta and recipient PA was performed using continuous 5/0 Prolene sutures, and careful inspection revealed no bleeding.\n\nFurthermore, the donor’s LA and recipient’s PA were securely closed using double continuous 5/0 Prolene sutures. The inferior vena cava tissues of both the donor and recipient were similarly sutured with 5/0 Prolene sutures, and several inspections were performed to confirm no significant bleeding was present. The left side of the heart was then deflated, and as rewarming commenced, oxygenation was restored, the ascending aorta was unclamped, and the heart spontaneously returned to sinus rhythm. Continuous suturing with 5/0 Prolene was applied to both the donor and recipient’s superior vena cava and diligently inspected to ensure the absence of significant bleeding. After the successful discontinuation of assisted circulation, the venous cavity was decannulated. Tissue samples from the patient’s left heart and gray matter were collected for histopathological examination, and the diagnosis of DCM and cardiac myxoma were confirmed.\n\n\nPostoperative management\n\nOn the first day after heart transplantation, the patient produced 1200 ml of urine. Laboratory tests revealed a hypersensitive troponin T level of 796.70ng/L and an NT-proBNP level of 10798pg/ml. The complete blood count showed white blood cells at 17.15 × 109/L, with no significant abnormalities in other test results. The echocardiograph displayed an LVEF of 65%, FS of 35%, normal ventricular wall thickness and echogenicity, and no discernible abnormalities in valve morphology and structure. After heart transplantation, Methylprednisolone Sodium Succinate (0.25 g)intravenous hormone therapy was administered to enhance immunity, and Cefoperazone and Sulbactam Sodium (2 g) intravenous anti-infection treatment was provided. The patient was given a nutrient solution and liver and tiopronin on the first day post-surgery. On postoperative day three, Methylprednisolone Sodium Succinate was replaced with oral Prednisone Acetate (25 mg). Mycophenolate Mofetil capsules (0.5 g) were administered orally to minimize heart rejection, and (50 mg) of Carpofungin Acetate was administered intravenously to prevent fungal infections. The patient’s urine output was 2000 ml, with hypersensitive troponin T levels of 390ng/L, NT-proBNP levels of 7877pg/ml, and a leukocyte count of 12.15 × 109/L. On the 7th day post-surgery, tacrolimus capsules were introduced at an oral dose of (1 mg) to minimize the patient’s rejection of the donor heart, with careful monitoring of blood concentrations. Subsequently, the oral dosage of Prednisone Acetate was gradually decreased to (10 mg) while adjusting the tacrolimus blood concentration to 10.90ng/ml. The patient’s recovery improved. On October 20, 2023, follow-up echocardiography (Fig. 6) indicated no abnormalities, with troponin levels of 85 ng/L, NT-proBNP of 210pg/ml, and all other test results within normal ranges. The patient exhibited excellent postoperative recovery and was discharged. Regular follow-up visits to our department after discharge showed that the patient remains in good condition.",
+    "diff_label_texts": "This is the story of a 35-year-old man with a rare condition called Carney syndrome. This condition led to a growth in his heart (a myxoma) and made his heart large and weak (dilated cardiomyopathy). Three years ago, he went to the hospital for sudden chest tightness and shortness of breath. Heart pictures showed the growth. Exams and genetic tests confirmed Carney syndrome. His symptoms got better with medicines, and he went home. No surgery was done then. Later, his chest tightness and shortness of breath got much worse. Doctors said he had very severe heart failure. Tests showed the weak, enlarged heart was still there along with the heart growth. He received a heart transplant. The transplant successfully treated his heart failure.",
+    "summary": "Herein, we report a case of heart failure due to Carney syndrome that resulted in cardiac myxoma combined with dilated cardiomyopathy. A 35-year-old male was admitted to the hospital three years ago because of sudden chest tightness and shortness of breath. Echocardiography indicated myxoma, and a combination of genetic screening and physical examination confirmed Carney syndrome with cardiac myxoma. Following symptomatic management, he was discharged. Surgical interventions were not considered at the time. However, the patient’s chest tightness and shortness of breath symptoms worsened, and he returned to the hospital. A New York Heart Association grade IV heart function was confirmed, and echocardiography indicated the presence of dilated cardiomyopathy accompanied by cardiac myxoma. Ultimately, the patient’s heart failure was successfully treated with heart transplantation."
+  },
+  {
+    "doc_id": 51,
+    "label": "intermediate_health_literacy",
+    "fulltext": "A 38-year-old male presented to the hospital with chest tightness and shortness of breath. Three years prior, he had experienced similar symptoms post-activity and received treatment at our hospital. Outpatient echocardiography indicated a left heart echomass suggestive of a myxoma, which led to his admission for further evaluation. Physical examination revealed pigmentation of the patient’s ears characterized by multiple small brown and black spots. Abdominal computed tomography (CT) showed multiple livers and small cysts in the left kidney. Genetic testing identified mutations in the TTN and PRKAR1A genes. The diagnosis of CNC was confirmed through clinical examination, imaging, and genetic testing. Following symptomatic treatment, the patient’s condition improved; however, he refused surgical intervention. On September 20, 2023, the patient presented to our hospital with exacerbated chest tightness and dyspnea. He reported difficulty lying supine and needing to sit upright to breathe. Physical examination revealed jugular vein distension, leftward and downward displacement of the heart boundary, irregular heart rhythm on auscultation, and a mitral valve murmur of intensity 2/6–3/6 in the fourth intercostal space along the left sternal margin. Wet rales were audible in both middle and lower lung fields. Palpation revealed a firm liver extending three fingers below the xiphoid process and two fingers below the rib cage, along with mild pitting edema in both lower limbs. Echocardiographic images indicated global heart enlargement, dilation of the aortic sinus and pulmonary artery, small-to-moderate mitral valve regurgitation, and an irregular echoic mass measuring 54 mm ×43 mm in the left chamber attached to the atrial septum. The left ventricular (LV) ejection fraction (EF) was 23.1%, with fractional shortening (FS) of 10.9%. Electrocardiography demonstrated atrial fibrillation (average ventricular rate, 150 beats/min) and abnormal Q waves in leads V1-V3. Based on the patient’s history, the diagnosis included DCM and CNC with cardiac myxoma. Given the presence of end-stage heart failure and concurrent cardiac myxoma, the patient was hospitalized, and heart transplantation was considered a viable therapeutic option to address both conditions simultaneously. A suitable donor heart became available for immediate transplantation on October 1, 2024.\n\n\nSurgical procedure\n\nThe skin and subcutaneous tissues were carefully incised layer-by-layer through a median sternotomy. The sternum was sawed longitudinally open, and bleeding was controlled using electrocoagulation and bone wax. Extracardiac exploration uncovered global heart enlargement, most prominent in the LV. The heart showed diminished contractile strength. The aorta and the main pulmonary artery (PA) were dissected from the supravalvular region. Some tissues were preserved for posterior suturing, whereas most diseased right atrium, left atrium(LA), right ventricle, and LV were excised. Resection revealed a greyish-white mucoid mass. The donor and residual recipient LA tissues were sutured using double continuous 3/0 Prolene threads. The anastomosis was meticulously inspected multiple times, and no significant bleeding was observed. Similarly, end-to-end anastomosis of the donor ascending aorta and recipient PA was performed using continuous 5/0 Prolene sutures, and careful inspection revealed no bleeding.\n\nFurthermore, the donor’s LA and recipient’s PA were securely closed using double continuous 5/0 Prolene sutures. The inferior vena cava tissues of both the donor and recipient were similarly sutured with 5/0 Prolene sutures, and several inspections were performed to confirm no significant bleeding was present. The left side of the heart was then deflated, and as rewarming commenced, oxygenation was restored, the ascending aorta was unclamped, and the heart spontaneously returned to sinus rhythm. Continuous suturing with 5/0 Prolene was applied to both the donor and recipient’s superior vena cava and diligently inspected to ensure the absence of significant bleeding. After the successful discontinuation of assisted circulation, the venous cavity was decannulated. Tissue samples from the patient’s left heart and gray matter were collected for histopathological examination, and the diagnosis of DCM and cardiac myxoma were confirmed.\n\n\nPostoperative management\n\nOn the first day after heart transplantation, the patient produced 1200 ml of urine. Laboratory tests revealed a hypersensitive troponin T level of 796.70ng/L and an NT-proBNP level of 10798pg/ml. The complete blood count showed white blood cells at 17.15 × 109/L, with no significant abnormalities in other test results. The echocardiograph displayed an LVEF of 65%, FS of 35%, normal ventricular wall thickness and echogenicity, and no discernible abnormalities in valve morphology and structure. After heart transplantation, Methylprednisolone Sodium Succinate (0.25 g)intravenous hormone therapy was administered to enhance immunity, and Cefoperazone and Sulbactam Sodium (2 g) intravenous anti-infection treatment was provided. The patient was given a nutrient solution and liver and tiopronin on the first day post-surgery. On postoperative day three, Methylprednisolone Sodium Succinate was replaced with oral Prednisone Acetate (25 mg). Mycophenolate Mofetil capsules (0.5 g) were administered orally to minimize heart rejection, and (50 mg) of Carpofungin Acetate was administered intravenously to prevent fungal infections. The patient’s urine output was 2000 ml, with hypersensitive troponin T levels of 390ng/L, NT-proBNP levels of 7877pg/ml, and a leukocyte count of 12.15 × 109/L. On the 7th day post-surgery, tacrolimus capsules were introduced at an oral dose of (1 mg) to minimize the patient’s rejection of the donor heart, with careful monitoring of blood concentrations. Subsequently, the oral dosage of Prednisone Acetate was gradually decreased to (10 mg) while adjusting the tacrolimus blood concentration to 10.90ng/ml. The patient’s recovery improved. On October 20, 2023, follow-up echocardiography (Fig. 6) indicated no abnormalities, with troponin levels of 85 ng/L, NT-proBNP of 210pg/ml, and all other test results within normal ranges. The patient exhibited excellent postoperative recovery and was discharged. Regular follow-up visits to our department after discharge showed that the patient remains in good condition.",
+    "diff_label_texts": "A 35-year-old man developed heart failure due to Carney syndrome, which caused a cardiac myxoma and dilated cardiomyopathy. Three years earlier, he presented with sudden chest tightness and shortness of breath. Echocardiography suggested a myxoma, and the diagnosis of Carney syndrome with cardiac myxoma was confirmed by physical examination and genetic screening. He improved with symptomatic treatment and was discharged; surgery was not performed at that time. His symptoms later worsened, and he returned with severe (New York Heart Association class IV) heart failure. Echocardiography then showed dilated cardiomyopathy accompanied by a cardiac myxoma. He ultimately underwent heart transplantation, which successfully treated his heart failure.",
+    "summary": "Herein, we report a case of heart failure due to Carney syndrome that resulted in cardiac myxoma combined with dilated cardiomyopathy. A 35-year-old male was admitted to the hospital three years ago because of sudden chest tightness and shortness of breath. Echocardiography indicated myxoma, and a combination of genetic screening and physical examination confirmed Carney syndrome with cardiac myxoma. Following symptomatic management, he was discharged. Surgical interventions were not considered at the time. However, the patient’s chest tightness and shortness of breath symptoms worsened, and he returned to the hospital. A New York Heart Association grade IV heart function was confirmed, and echocardiography indicated the presence of dilated cardiomyopathy accompanied by cardiac myxoma. Ultimately, the patient’s heart failure was successfully treated with heart transplantation."
+  },
+  {
+    "doc_id": 51,
+    "label": "proficient_health_literacy",
+    "fulltext": "A 38-year-old male presented to the hospital with chest tightness and shortness of breath. Three years prior, he had experienced similar symptoms post-activity and received treatment at our hospital. Outpatient echocardiography indicated a left heart echomass suggestive of a myxoma, which led to his admission for further evaluation. Physical examination revealed pigmentation of the patient’s ears characterized by multiple small brown and black spots. Abdominal computed tomography (CT) showed multiple livers and small cysts in the left kidney. Genetic testing identified mutations in the TTN and PRKAR1A genes. The diagnosis of CNC was confirmed through clinical examination, imaging, and genetic testing. Following symptomatic treatment, the patient’s condition improved; however, he refused surgical intervention. On September 20, 2023, the patient presented to our hospital with exacerbated chest tightness and dyspnea. He reported difficulty lying supine and needing to sit upright to breathe. Physical examination revealed jugular vein distension, leftward and downward displacement of the heart boundary, irregular heart rhythm on auscultation, and a mitral valve murmur of intensity 2/6–3/6 in the fourth intercostal space along the left sternal margin. Wet rales were audible in both middle and lower lung fields. Palpation revealed a firm liver extending three fingers below the xiphoid process and two fingers below the rib cage, along with mild pitting edema in both lower limbs. Echocardiographic images indicated global heart enlargement, dilation of the aortic sinus and pulmonary artery, small-to-moderate mitral valve regurgitation, and an irregular echoic mass measuring 54 mm ×43 mm in the left chamber attached to the atrial septum. The left ventricular (LV) ejection fraction (EF) was 23.1%, with fractional shortening (FS) of 10.9%. Electrocardiography demonstrated atrial fibrillation (average ventricular rate, 150 beats/min) and abnormal Q waves in leads V1-V3. Based on the patient’s history, the diagnosis included DCM and CNC with cardiac myxoma. Given the presence of end-stage heart failure and concurrent cardiac myxoma, the patient was hospitalized, and heart transplantation was considered a viable therapeutic option to address both conditions simultaneously. A suitable donor heart became available for immediate transplantation on October 1, 2024.\n\n\nSurgical procedure\n\nThe skin and subcutaneous tissues were carefully incised layer-by-layer through a median sternotomy. The sternum was sawed longitudinally open, and bleeding was controlled using electrocoagulation and bone wax. Extracardiac exploration uncovered global heart enlargement, most prominent in the LV. The heart showed diminished contractile strength. The aorta and the main pulmonary artery (PA) were dissected from the supravalvular region. Some tissues were preserved for posterior suturing, whereas most diseased right atrium, left atrium(LA), right ventricle, and LV were excised. Resection revealed a greyish-white mucoid mass. The donor and residual recipient LA tissues were sutured using double continuous 3/0 Prolene threads. The anastomosis was meticulously inspected multiple times, and no significant bleeding was observed. Similarly, end-to-end anastomosis of the donor ascending aorta and recipient PA was performed using continuous 5/0 Prolene sutures, and careful inspection revealed no bleeding.\n\nFurthermore, the donor’s LA and recipient’s PA were securely closed using double continuous 5/0 Prolene sutures. The inferior vena cava tissues of both the donor and recipient were similarly sutured with 5/0 Prolene sutures, and several inspections were performed to confirm no significant bleeding was present. The left side of the heart was then deflated, and as rewarming commenced, oxygenation was restored, the ascending aorta was unclamped, and the heart spontaneously returned to sinus rhythm. Continuous suturing with 5/0 Prolene was applied to both the donor and recipient’s superior vena cava and diligently inspected to ensure the absence of significant bleeding. After the successful discontinuation of assisted circulation, the venous cavity was decannulated. Tissue samples from the patient’s left heart and gray matter were collected for histopathological examination, and the diagnosis of DCM and cardiac myxoma were confirmed.\n\n\nPostoperative management\n\nOn the first day after heart transplantation, the patient produced 1200 ml of urine. Laboratory tests revealed a hypersensitive troponin T level of 796.70ng/L and an NT-proBNP level of 10798pg/ml. The complete blood count showed white blood cells at 17.15 × 109/L, with no significant abnormalities in other test results. The echocardiograph displayed an LVEF of 65%, FS of 35%, normal ventricular wall thickness and echogenicity, and no discernible abnormalities in valve morphology and structure. After heart transplantation, Methylprednisolone Sodium Succinate (0.25 g)intravenous hormone therapy was administered to enhance immunity, and Cefoperazone and Sulbactam Sodium (2 g) intravenous anti-infection treatment was provided. The patient was given a nutrient solution and liver and tiopronin on the first day post-surgery. On postoperative day three, Methylprednisolone Sodium Succinate was replaced with oral Prednisone Acetate (25 mg). Mycophenolate Mofetil capsules (0.5 g) were administered orally to minimize heart rejection, and (50 mg) of Carpofungin Acetate was administered intravenously to prevent fungal infections. The patient’s urine output was 2000 ml, with hypersensitive troponin T levels of 390ng/L, NT-proBNP levels of 7877pg/ml, and a leukocyte count of 12.15 × 109/L. On the 7th day post-surgery, tacrolimus capsules were introduced at an oral dose of (1 mg) to minimize the patient’s rejection of the donor heart, with careful monitoring of blood concentrations. Subsequently, the oral dosage of Prednisone Acetate was gradually decreased to (10 mg) while adjusting the tacrolimus blood concentration to 10.90ng/ml. The patient’s recovery improved. On October 20, 2023, follow-up echocardiography (Fig. 6) indicated no abnormalities, with troponin levels of 85 ng/L, NT-proBNP of 210pg/ml, and all other test results within normal ranges. The patient exhibited excellent postoperative recovery and was discharged. Regular follow-up visits to our department after discharge showed that the patient remains in good condition.",
+    "diff_label_texts": "A 38-year-old male with a three-year history of exertional chest tightness and dyspnea re-presented with progressive orthopnea and decompensated heart failure. Three years prior, outpatient echocardiography had identified a left-sided intracardiac echogenic mass consistent with myxoma, prompting admission. Physical examination at that time noted auricular hyperpigmentation with multiple brown-black macules. Abdominal imaging reported extracardiac findings, and genetic testing revealed TTN and PRKAR1A mutations. The diagnosis of Carney complex (CNC) with cardiac myxoma was established by clinical findings, imaging, and genetics. He improved with symptomatic therapy but declined definitive surgery. \n\nOn re-presentation (September 20, 2023), exam showed jugular venous distension, cardiomegaly with leftward/downward displacement, an irregular rhythm, a 2/6–3/6 mitral murmur at the left sternal border (fourth intercostal space), bilateral mid-to-lower lung wet rales, hepatomegaly (firm liver palpable 3 fingerbreadths below the xiphoid and 2 fingerbreadths below the costal margin), and mild bilateral pitting edema. ECG demonstrated atrial fibrillation (average ventricular rate ~150 bpm) with abnormal Q waves in V1–V3. Transthoracic echocardiography showed global cardiac enlargement, dilation of the aortic sinus and main pulmonary artery, small-to-moderate mitral regurgitation, and an irregular echogenic mass measuring 54 × 43 mm in the left chamber attached to the atrial septum. LV systolic function was severely depressed (LVEF 23.1%, FS 10.9%). The working diagnosis was end-stage heart failure due to dilated cardiomyopathy (DCM) in the setting of CNC with a cardiac myxoma. Given concomitant end-stage DCM and intracardiac tumor, heart transplantation was pursued when a suitable donor became available.\n\nOperative course: Median sternotomy was performed with cardiopulmonary bypass. Exploration confirmed global cardiomegaly, most pronounced in the LV, with poor contractility. Diseased native right atrium, left atrium, right ventricle, and left ventricle were resected, revealing a gray-white mucoid mass consistent with myxoma. Standard orthotopic heart transplantation anastomoses were completed (including left atrial cuff, great vessels, and caval anastomoses) using continuous Prolene sutures (3/0 and 5/0), with meticulous hemostasis. After rewarming and aortic unclamping, the graft resumed sinus rhythm spontaneously. Assisted circulation was weaned uneventfully. Histopathology of the explanted tissues confirmed DCM and cardiac myxoma.\n\nPostoperative course: On postoperative day (POD) 1, urine output was 1200 mL; hs‑troponin T was 796.70 ng/L; NT‑proBNP 10,798 pg/mL; WBC 17.15 × 10^9/L. Echocardiography demonstrated normal ventricular wall thickness and morphology with LVEF 65% (FS 35%). Immunosuppression and anti-infective therapy included IV methylprednisolone sodium succinate 0.25 g, cefoperazone/sulbactam 2 g, supportive nutrition, and hepatoprotective therapy. On POD 3, steroids were transitioned to oral prednisone acetate 25 mg; mycophenolate mofetil 0.5 g PO was initiated for rejection prophylaxis; caspofungin acetate 50 mg IV was added for antifungal prophylaxis. Urine output increased to 2000 mL; hs‑troponin T decreased to 390 ng/L; NT‑proBNP decreased to 7877 pg/mL; WBC 12.15 × 10^9/L. On POD 7, tacrolimus 1 mg PO was introduced with therapeutic drug monitoring (blood level 10.90 ng/mL), and prednisone was tapered to 10 mg. Clinical status steadily improved. By late postoperative follow-up (October 20, 2023), echocardiography was unremarkable; hs‑troponin T was 85 ng/L; NT‑proBNP 210 pg/mL; other labs were within normal limits. The patient was discharged in excellent condition and has remained clinically stable on outpatient follow-up.\n\nInterpretation: This case illustrates CNC with PRKAR1A mutation manifesting as atrial myxoma and end-stage DCM, compounded by atrial fibrillation and severe LV systolic dysfunction (LVEF 23.1%). Orthotopic heart transplantation effectively addressed both the intracardiac tumor and the refractory heart failure, with prompt normalization of graft function and favorable early outcomes under standard triple immunosuppression.",
+    "summary": "Herein, we report a case of heart failure due to Carney syndrome that resulted in cardiac myxoma combined with dilated cardiomyopathy. A 35-year-old male was admitted to the hospital three years ago because of sudden chest tightness and shortness of breath. Echocardiography indicated myxoma, and a combination of genetic screening and physical examination confirmed Carney syndrome with cardiac myxoma. Following symptomatic management, he was discharged. Surgical interventions were not considered at the time. However, the patient’s chest tightness and shortness of breath symptoms worsened, and he returned to the hospital. A New York Heart Association grade IV heart function was confirmed, and echocardiography indicated the presence of dilated cardiomyopathy accompanied by cardiac myxoma. Ultimately, the patient’s heart failure was successfully treated with heart transplantation."
+  },
+  {
+    "doc_id": 52,
+    "label": "low_health_literacy",
+    "fulltext": "2 years 6 months old female pre-schooler with a previous diagnosis of NF1. She consulted due to a 4 week diarrhea with blood streaks (5 to 10 episodes a day). A week after the onset of the diarrhea she consulted the emergency department, where rotavirus (+) was detected, with low inflammatory parameters, negative coproculture and normal abdominal ultrasound. She was hospitalized for 3 days to manage dehydration and was discharged without bleeding, with persistence of semi-liquid stools. 10 days after discharge she presented diarrhea with blood streaks, associated with low intake and weight loss of 1 kg reported by parents. They consulted a pediatric gastroenterologist who requested a polymerase chain reaction (PCR) panel of gastrointestinal pathogens and PCR of Clostridium difficile (which were negative) and indicated hospitalization for study.\n\nOn direct questioning, the parents reported no fever, abdominal pain, vomiting, respiratory or urinary symptoms, arthralgia, or new skin lesions. They did not own pets, and there was no history of travel or recent dietary changes.\n\nThe patient was diagnosed with confirmed NF1 at 8 months of age by genetic testing with the heterozygous pathogenic variant c.5606_5627del (p.Gly1869Valfs*28). She has skin involvement (café con leche spots) and bone involvement. At 18 months she required ankle arthrodesis for tibial curvature. She has no family history of NF1 or inflammatory bowel disease.\n\nOn physical examination, the abdomen was soft and indistinct, with increased air-bubble murmurs, without masses or visceral enlargement. The perianal examination was normal. There were multiple brown-coffee stains on the lower extremities and back. General examinations were performed, including a blood count with moderate microcytic-hypochromic anaemia (Hb 9.6 g/dL), leukocytosis with left shift (leukocytes 13,900), and discretely elevated inflammatory parameters (CRP 1.37 mg/dL, normal value up to 0.5 mg/dL).\n\nA colonoscopy was performed, the rectum, sigmoid and various segments of the colon were examined up to the cecum, visualizing the ileocecal valve and the appendicular orifice. The last few centimeters of the distal ileum were also inspected. The mucosa from the anal margin to the cecum was observed to be erythematous, with loss of vascular transparency, unlike the cecal mucosa, which appeared normal. No lesions were identified in the anal canal or cecum.\n\nBiopsies of the small intestine (ileon) and large intestine were taken. Microscopic examination showed mucosa of ileal type with preserved villous architecture and adequate epithelial differentiation, with a non-inflamed lamina propria. The mucosa of the large intestine had a mild distortion of architecture and adequate epithelial differentiation, a swollen lamina propria with a mild mixed inflammatory infiltrate and hyperplasia of lymphoid follicles. Isolated foci of microabscesses were recognized. The biopsy was consistent with mild colitis, with signs suggesting chronicity.\n\nIn addition, a PCR study for cytomegalovirus (CMV) was requested in a colon biopsy, which was positive.\n\nGiven a positive PCR for CMV, CMV IgG and IgM and CMV viral load in blood were requested, resulting in a positive IgG, negative IgM, and CMV viral load of 79.7 IU/ml. Further laboratory studies included PCR for gastrointestinal pathogens and PCR for Clostridium difficile in stool, both of which were negative. In the colon biopsy, Gram stain microbiological studies were requested, which showed +++ leukocytes without bacteria; biopsy culture showed S. gallolyticus/equinus complex in very low amount (interpreted as bacterial flora); acridine orange, Ziehl-Neelsen, Koch culture, and ADV PCR were negative.\n\nEndoscopy and histology suggestive of UC was reported in the context of a patient with moderate symptoms (PUCAI 50) who was started on Mesalazine (70 mg/kg/day three times daily) and a request for a faecal calprotectin was made which was greater than 600 ug/g.\n\nThe immunology team evaluated the patient for suspected immunodeficiency. The parents did not report a history of infections, they reported that they were vaccinated, that they had good weight gain, no family history of immunodeficiencies, auto-immunity or early deaths. A study with lymphocyte subpopulations (normal), immunoglobulins (normal), HIV (negative), memory T lymphocytes (with alterations expected in the context of CMV viremia) and lymphoproliferation test (normal) was requested. In addition, a genetic panel of primary immunodeficiencies (Invitae) was performed, which contains 429 genes, of which 68 make up the panel of monogenic inflammatory intestinal disease. 7 variants of uncertain significance were obtained, none included in the panel of monogenic IBD.\n\nGanciclovir was initiated intravenous for CMV infection and continued for 15 days. The last PCR CMV control prior to discharge reported undetectable load.\n\nThe patient improved during the hospital stay with decreased frequency of stools and increased consistency, no rectal bleeding, no nocturnal stools and no abdominal pain, with PUCAI 0 at discharge.\n\nTwo months later, he presented with a reactivation of IBD with bloody diarrhea (PUCAI 35). A blood count was performed (normal), a panel of gastrointestinal pathogens was performed (–), PCR for Clostridium difficile was performed (+), and CMV load was undetectable. He was treated with oral metronidazole. However, he persisted with diarrhea with blood streaks, so he was hospitalized again.\n\nA colonoscopy was performed, where erythematous mucous was observed in a diffuse form from the rectum to the cecum, with nodularity and loss of vascular transparency in the submucosa, greater in the left and transverse colon segments. No focal lesions were observed. The mucosa of the ileum and anal canal were observed without lesions.\n\nBiopsy of the terminal ileum, right colon and left colon was performed. Microscopic examination of the ileal-type mucosa showed preserved villous architecture and adequate epithelial differentiation. The lamina propria showed no signs of inflammation. There were no aphthous erosions or granulomas. The mucosa of the large intestine showed mild distortion of architecture and epithelial dedifferentiation. The lamina propria was expanded by mixed inflammatory infiltrate, transmucosal distribution. Foci of cryptitis and cryptitic microabscesses and hyperplasia of reactive lymphoid follicles were recognized. No granulomas, viral or parasitic cytopathic changes were observed. All fragments of the left colon sample presented a similar histopathological picture.\n\nShe was given oral treatment with Vancomycin and Prednisone (1 mg/kg/day) with a good response and a favorable evolution. She was discharged with a decrease in the frequency of bowel movements. She persists with mild symptoms (PUCAI 5) in outpatient control, so the dose of corticosteroids is progressively decreased and she remains on treatment with Mesalazina.\n",
+    "diff_label_texts": "This child is 2 and a half years old and has a condition called NF1. She had diarrhea with blood. Doctors used a small camera to look inside her large intestine. The inner lining looked red and irritated from the bottom (anus) to the start of the large intestine (cecum). The usual fine pattern of tiny blood vessels was hard to see. Small tissue samples showed long-lasting swelling. This fits a disease of the large intestine called ulcerative colitis. A special lab test (PCR) on the tissue found a virus called CMV.",
+    "summary": "2.5-year-old pre-schooler with a history of NF1 presenting with bloody diarrhea. On endoscopic examination, the mucosa from the anal margin to the cecum was erythematous with loss of vascular transparency. Colon mucosal biopsies showed signs of chronic inflammation consistent with a diagnosis of ulcerative colitis and CMV infection was diagnosed by PCR.\n"
+  },
+  {
+    "doc_id": 52,
+    "label": "proficient_health_literacy",
+    "fulltext": "2 years 6 months old female pre-schooler with a previous diagnosis of NF1. She consulted due to a 4 week diarrhea with blood streaks (5 to 10 episodes a day). A week after the onset of the diarrhea she consulted the emergency department, where rotavirus (+) was detected, with low inflammatory parameters, negative coproculture and normal abdominal ultrasound. She was hospitalized for 3 days to manage dehydration and was discharged without bleeding, with persistence of semi-liquid stools. 10 days after discharge she presented diarrhea with blood streaks, associated with low intake and weight loss of 1 kg reported by parents. They consulted a pediatric gastroenterologist who requested a polymerase chain reaction (PCR) panel of gastrointestinal pathogens and PCR of Clostridium difficile (which were negative) and indicated hospitalization for study.\n\nOn direct questioning, the parents reported no fever, abdominal pain, vomiting, respiratory or urinary symptoms, arthralgia, or new skin lesions. They did not own pets, and there was no history of travel or recent dietary changes.\n\nThe patient was diagnosed with confirmed NF1 at 8 months of age by genetic testing with the heterozygous pathogenic variant c.5606_5627del (p.Gly1869Valfs*28). She has skin involvement (café con leche spots) and bone involvement. At 18 months she required ankle arthrodesis for tibial curvature. She has no family history of NF1 or inflammatory bowel disease.\n\nOn physical examination, the abdomen was soft and indistinct, with increased air-bubble murmurs, without masses or visceral enlargement. The perianal examination was normal. There were multiple brown-coffee stains on the lower extremities and back. General examinations were performed, including a blood count with moderate microcytic-hypochromic anaemia (Hb 9.6 g/dL), leukocytosis with left shift (leukocytes 13,900), and discretely elevated inflammatory parameters (CRP 1.37 mg/dL, normal value up to 0.5 mg/dL).\n\nA colonoscopy was performed, the rectum, sigmoid and various segments of the colon were examined up to the cecum, visualizing the ileocecal valve and the appendicular orifice. The last few centimeters of the distal ileum were also inspected. The mucosa from the anal margin to the cecum was observed to be erythematous, with loss of vascular transparency, unlike the cecal mucosa, which appeared normal. No lesions were identified in the anal canal or cecum.\n\nBiopsies of the small intestine (ileon) and large intestine were taken. Microscopic examination showed mucosa of ileal type with preserved villous architecture and adequate epithelial differentiation, with a non-inflamed lamina propria. The mucosa of the large intestine had a mild distortion of architecture and adequate epithelial differentiation, a swollen lamina propria with a mild mixed inflammatory infiltrate and hyperplasia of lymphoid follicles. Isolated foci of microabscesses were recognized. The biopsy was consistent with mild colitis, with signs suggesting chronicity.\n\nIn addition, a PCR study for cytomegalovirus (CMV) was requested in a colon biopsy, which was positive.\n\nGiven a positive PCR for CMV, CMV IgG and IgM and CMV viral load in blood were requested, resulting in a positive IgG, negative IgM, and CMV viral load of 79.7 IU/ml. Further laboratory studies included PCR for gastrointestinal pathogens and PCR for Clostridium difficile in stool, both of which were negative. In the colon biopsy, Gram stain microbiological studies were requested, which showed +++ leukocytes without bacteria; biopsy culture showed S. gallolyticus/equinus complex in very low amount (interpreted as bacterial flora); acridine orange, Ziehl-Neelsen, Koch culture, and ADV PCR were negative.\n\nEndoscopy and histology suggestive of UC was reported in the context of a patient with moderate symptoms (PUCAI 50) who was started on Mesalazine (70 mg/kg/day three times daily) and a request for a faecal calprotectin was made which was greater than 600 ug/g.\n\nThe immunology team evaluated the patient for suspected immunodeficiency. The parents did not report a history of infections, they reported that they were vaccinated, that they had good weight gain, no family history of immunodeficiencies, auto-immunity or early deaths. A study with lymphocyte subpopulations (normal), immunoglobulins (normal), HIV (negative), memory T lymphocytes (with alterations expected in the context of CMV viremia) and lymphoproliferation test (normal) was requested. In addition, a genetic panel of primary immunodeficiencies (Invitae) was performed, which contains 429 genes, of which 68 make up the panel of monogenic inflammatory intestinal disease. 7 variants of uncertain significance were obtained, none included in the panel of monogenic IBD.\n\nGanciclovir was initiated intravenous for CMV infection and continued for 15 days. The last PCR CMV control prior to discharge reported undetectable load.\n\nThe patient improved during the hospital stay with decreased frequency of stools and increased consistency, no rectal bleeding, no nocturnal stools and no abdominal pain, with PUCAI 0 at discharge.\n\nTwo months later, he presented with a reactivation of IBD with bloody diarrhea (PUCAI 35). A blood count was performed (normal), a panel of gastrointestinal pathogens was performed (–), PCR for Clostridium difficile was performed (+), and CMV load was undetectable. He was treated with oral metronidazole. However, he persisted with diarrhea with blood streaks, so he was hospitalized again.\n\nA colonoscopy was performed, where erythematous mucous was observed in a diffuse form from the rectum to the cecum, with nodularity and loss of vascular transparency in the submucosa, greater in the left and transverse colon segments. No focal lesions were observed. The mucosa of the ileum and anal canal were observed without lesions.\n\nBiopsy of the terminal ileum, right colon and left colon was performed. Microscopic examination of the ileal-type mucosa showed preserved villous architecture and adequate epithelial differentiation. The lamina propria showed no signs of inflammation. There were no aphthous erosions or granulomas. The mucosa of the large intestine showed mild distortion of architecture and epithelial dedifferentiation. The lamina propria was expanded by mixed inflammatory infiltrate, transmucosal distribution. Foci of cryptitis and cryptitic microabscesses and hyperplasia of reactive lymphoid follicles were recognized. No granulomas, viral or parasitic cytopathic changes were observed. All fragments of the left colon sample presented a similar histopathological picture.\n\nShe was given oral treatment with Vancomycin and Prednisone (1 mg/kg/day) with a good response and a favorable evolution. She was discharged with a decrease in the frequency of bowel movements. She persists with mild symptoms (PUCAI 5) in outpatient control, so the dose of corticosteroids is progressively decreased and she remains on treatment with Mesalazina.\n",
+    "diff_label_texts": "A 2 years 6 months old female with genetically confirmed NF1 (heterozygous pathogenic variant c.5606_5627del [p.Gly1869Valfs*28]) presented with 4 weeks of blood-streaked diarrhea (5–10/day). Initial ED evaluation showed rotavirus positive, low inflammatory markers, negative coproculture, and a normal abdominal ultrasound; she was hospitalized 3 days for dehydration and discharged with persistent semi-liquid stools. Ten days later she recurred with blood-streaked diarrhea, decreased intake, and ~1 kg weight loss, prompting admission for further workup after outpatient GI pathogen and C. difficile PCR panels were negative. There was no fever, abdominal pain, vomiting, respiratory/urinary symptoms, arthralgia, pet exposure, travel, or dietary changes. NF1 phenotype included café-au-lait macules and osseous involvement; she underwent ankle arthrodesis at 18 months for tibial bowing; no family history of NF1 or IBD. Exam: soft, non-tender abdomen with increased bowel sounds; perianal exam normal; multiple café-au-lait macules. Labs: microcytic–hypochromic anemia (Hb 9.6 g/dL), leukocytosis with left shift (13,900/µL), CRP 1.37 mg/dL (ULN 0.5).\n\nIndex colonoscopy evaluated rectum, sigmoid, and colon to cecum; distal ileum was also inspected. The colonic mucosa from the anal margin to the cecum was erythematous with loss of vascular transparency; the cecal mucosa itself appeared normal; no lesions in the anal canal or cecum. Biopsies: ileal mucosa with preserved villous architecture, adequate epithelial differentiation, and non-inflamed lamina propria. Colonic mucosa showed mild architectural distortion, adequate epithelial differentiation, lamina propria edema with a mild mixed inflammatory infiltrate, lymphoid follicular hyperplasia, and isolated crypt microabscesses—consistent with mild colitis with features suggesting chronicity. CMV PCR on colon biopsy was positive. Additional virology: CMV IgG positive, IgM negative; plasma CMV viral load 79.7 IU/mL. Stool GI pathogen panel and C. difficile PCR were negative. Biopsy microbiology: Gram stain +++ leukocytes without bacteria; culture with very low S. gallolyticus/equinus interpreted as flora; acridine orange, Ziehl–Neelsen, Koch culture, and adenovirus PCR were negative. Clinical impression: endoscopy and histology suggestive of ulcerative colitis (UC) in the setting of moderate activity (PUCAI 50). Mesalazine 70 mg/kg/day tid initiated; fecal calprotectin >600 µg/g. Immunology workup for suspected PID: normal lymphocyte subsets and immunoglobulins; HIV negative; memory T-cell abnormalities attributed to CMV viremia; lymphoproliferation normal. Invitae PID panel (429 genes; 68 monogenic IBD) returned 7 VUS, none in monogenic IBD genes.\n\nTreatment with IV ganciclovir for 15 days led to clinical improvement; CMV PCR was undetectable prior to discharge. She achieved PUCAI 0 at discharge with normalized stool frequency/consistency and no rectal bleeding, nocturnal stools, or abdominal pain. Two months later she had an IBD flare with bloody diarrhea (PUCAI 35); CBC normal, GI pathogen panel negative, C. difficile PCR positive, and CMV load undetectable. She received oral metronidazole but persisted with blood-streaked diarrhea and was re-hospitalized. Repeat colonoscopy showed diffuse erythematous mucosa from rectum to cecum with nodularity and loss of vascular transparency, more prominent in the left and transverse colon; no focal lesions; ileum and anal canal without lesions. Histology (terminal ileum, right and left colon): ileal architecture preserved without inflammation; colon with mild architectural distortion and epithelial dedifferentiation; lamina propria expanded by mixed inflammatory infiltrate with transmucosal distribution; foci of cryptitis and crypt abscesses; reactive lymphoid follicular hyperplasia; no granulomas or viral/parasitic cytopathic changes. She was treated with oral vancomycin and prednisone 1 mg/kg/day with good response and was discharged with reduced stool frequency. At outpatient follow-up she has mild residual symptoms (PUCAI 5); corticosteroids are being tapered and mesalazine maintained.\n\nOverall, this case represents pediatric UC in an NF1 patient with tissue CMV positivity at presentation and low-level viremia, responsive to ganciclovir and 5-ASA, followed by a subsequent flare associated with C. difficile infection that improved with vancomycin and corticosteroids; CMV remained undetectable thereafter.",
+    "summary": "2.5-year-old pre-schooler with a history of NF1 presenting with bloody diarrhea. On endoscopic examination, the mucosa from the anal margin to the cecum was erythematous with loss of vascular transparency. Colon mucosal biopsies showed signs of chronic inflammation consistent with a diagnosis of ulcerative colitis and CMV infection was diagnosed by PCR.\n"
+  },
+  {
+    "doc_id": 53,
+    "label": "proficient_health_literacy",
+    "fulltext": "40-year-old HIV-positive man with regular adherence to treatment (viral load 4500/mm3 and CD4 70/mm3 from the previous year), consulted for intermittent fever of two years' evolution that did not respect the standard time and gave way to transient antinflammatory non-steroidal drugs. He added in the last two months diffuse abdominal pain with predominance in the upper right lobe where he acquired a configuration of a tree in bud and bilateral pleural effusion, and at the abdominal level, marked increase of hepato-splenomegaly associated with ascites. After 48 hours of his suspension, he presented fulminant hepatic failure and was transferred to the intensive care unit. Tracheal aspirate was performed and after transfusion support a liver biopsy was obtained by puncture.  The patient died a few hours later. The postmortem culture of the tracheal aspirate was positive for Mycobacterium tuberculosis and the liver biopsy was performed with non-necrotizing granulomas and the rest of the parenchyma preserved. This work was carried out in accordance with the principles laid out in the ethical code of the WHO (Helsinki Declaration).\n",
+    "diff_label_texts": "A 40-year-old HIV-positive man with reported regular ART adherence (prior year viral load 4,500 and CD4 70/mm3) presented with a two-year history of intermittent, noncyclical febrile episodes that transiently responded to NSAIDs. Over the preceding two months, he developed progressive, diffuse abdominal pain and generalized adenomegaly. Laboratory evaluation showed pancytopenia, coagulopathy, hypoalbuminemia, and elevated acute phase reactants. Initial CT of the thorax, abdomen, and pelvis demonstrated hepatosplenomegaly and generalized adenomegaly without additional parenchymal findings. A broad microbiologic workup was undertaken, including mycobacterial cultures from multiple specimen types; all were negative except an RT-PCR positive for HHV-8. Excisional biopsy of a left iliac lymph node showed features consistent with Castleman’s disease. Despite reinitiating antiretroviral therapy, clinical status deteriorated, prompting initiation of corticosteroids and ganciclovir. After approximately one week, the patient developed multiorgan failure with anasarca, rendering the instituted therapies contraindicated and necessitating discontinuation. Repeat chest CT revealed right upper lobe tree-in-bud infiltrates with bilateral pleural effusions. Concurrent abdominal imaging showed progression of hepatosplenomegaly and new-onset ascites. Forty-eight hours later, he developed fulminant hepatic failure and was transferred to the intensive care unit. He expired within hours. Tracheal aspirate culture, finalized postmortem, grew Mycobacterium tuberculosis. A percutaneous liver biopsy performed with transfusion support demonstrated non-necrotizing granulomas with otherwise preserved parenchyma. The case management and reporting adhered to the ethical principles of the WHO/Declaration of Helsinki.",
+    "summary": "We present the case of a 40-year-old HIV-positive man with regular adherence to treatment, who consulted for intermittent febrile episodes of two years' evolution, adding in the last two months progressive diffuse abdominal pain and generalized adenomegaly. In the laboratory, he presented pancytopenia, coagulopathy, hypoalbuminemia and increased acute phase reactants. The computed tomography (CT) of the thorax, abdomen and pelvis only showed hepato-splenomegaly and generalized adenomegaly. Multiple microbiological examinations were performed, including cultures for Mycobacterium sp. of different samples, all with negative results, with the exception of RT-PCR for HHV-8. A left iliac ganglion biopsy was performed with findings consistent with Castleman's disease. Despite restarting antiretroviral therapy, the symptomatology progressed, initiating treatment with corticosteroids and ganciclovir. After a week, he developed multiple organ failure and anasarca, which contraindicated the drugs initiated. A new chest CT was performed that showed infiltrates with a tree-like pattern in the upper right lobe associated with bilateral pleural effusion, and at the abdominal level, progression of hepato-splenomegaly and ascites. He passed to the intensive care unit 48 hours later due to fulminant hepatic failure. The patient died within a few hours. A postmortem culture of the tracheal aspirate was received positive for Mycobacterium tuberculosis and a liver biopsy with non-necrotizing granulomas.\n"
+  },
+  {
+    "doc_id": 54,
+    "label": "proficient_health_literacy",
+    "fulltext": "4-month-old indigenous lactating mother from the rural area of the interior of Panama, from the town of Urracá, 3 hours by canoe from the nearest health center. Her background included being the fourth daughter, born by vaginal delivery at home by a relative, without prenatal controls, her weight, height and Apgar score at birth are unknown. She did not breastfeed and was fed with powdered milk formula with iron for children under 6 months, receiving 3 ounces every 4 hours.\n\nThe nuclear family was composed of 6 people (parents and 4 children) who lived in a house with walls and floor of boards and palm roof, 2 rooms, without electricity, they were illuminated with kerosene lamps, water from a well, excreta in a river and they burned the garbage, their economic income came from subsistence agriculture.\n\nHe had no health care in his first 4 months of life and did not receive the vaccinations included in the national expanded programme of immunizations. According to his parents, his neurodevelopment was normal until his hospitalization.\n\nThe minor consulted in a health center with a history of 4 days of diarrhoea, without mucus or blood associated with vomiting of food content (the mother gave her tea because she could not tolerate milk), afebrile and without respiratory symptoms. Oral fluids and 4 doses of Enterogermina® (B. clausii: two billion spores/5 mL) were administered. Due to the lack of supplies (they did not have catheters, or intraosseous for the administration of intravenous fluids) she was transferred to a second-level hospital in the provincial capital and then to our institution in Panama City with a diagnosis of acute gastroenteritis and severe dehydration.\n\nHe presented to the emergency department with a consciousness compromise, dehydration characterised by a tearless cry, dry oral mucosa. He had oedema of +++ hands, feet, abdomen and face. He was afebrile and had signs of shock, capillary refill time > 2 seconds, cold extremities, filiform pulse and marble skin, heart rate 170 bpm, respiratory rate 55 bpm, blood pressure 91/37 mmHg, oxygen saturation 99%. He weighed 4.7 kg and was 56 cm tall at admission, Z-score height/age -2.52, weight/height and weight/age Z-scores were not quantifiable due to severe dehydration. On segmental examination, there were fine crepitus in both lung bases and erythematous-squamous lesions with desquamation of skin and others with hypopigmentation of trunk and upper limbs (interpreted as pellagroid dermatosis).\n\nLactate Ringer bolus was given at 10 ml/kg in the emergency department, followed by 5% Dextrose in 0.33% Saline 500 ml at an infusion rate of 29 ml/h over 6 hours without KCL until diuresis was obtained. She was started on Ceftriaxone 50 mg/kg/day for suspected sepsis, stabilised and sent to the ward where she continued to receive 500 ml of 5% Dextrose in 0.9% Saline at 20 ml/hr.\n\nAmong the examinations, a blood count revealed leukocytosis at 39.0 x 103/uL, severe anaemia 5.6 g/dL, thrombocytosis 502 x 103/uL, the rest of the results are detailed in. He was transfused with 50 ml of filtered and leuko-reduced red blood cells and 40 cc of fresh frozen plasma due to altered coagulation times. Enteral feeding was initiated by nasogastric tube and infusion was decreased to 15 ml/h of 5% Dextrose in 0.9% Saline 500 cc, and continued with negative water balance.\n\nOn day 2, initial peripheral blood culture was reported as Gram positive cocci in clusters, Oxacillin was added at 200 mg/kg/day, Ceftriaxone was increased to 75-100 mg/kg/day, total fluids to 120 ml/kg/day and calcium was corrected (value received 6.38 mg/dL).\n\nOn her 3rd day she lost venous access, so a central venous catheter (CVC) was placed. She was hypovolemic with subhydrated oral mucosa, increased respiratory work, cold extremities and capillary refill time of 3-4 seconds. Ringer's lactate was given at a load of 20 ml/kg in one hour. Arterial blood gas revealed uncompensated metabolic acidosis with pH 7.26, HCO3 13 mmol/L, PCO2 28.4 mmHg, PO2 39.2 mmHg, lactate 2.8 mmol/L. She was intubated and transferred to the paediatric intensive care unit (PICU) where she was placed on mechanical ventilation.\n\nTotal fluids of 100 cc/kg, infused epinephrine, low-salt albumin, and 10% calcium gluconate were administered, and fentanyl was changed to remifentanil due to elevated liver enzymes.\n\nThe blood culture of admission reported growth of methicillin-resistant Staphylococcus aureus (MRSA), Oxacillin was omitted and Clindamycin was added at 40 mg/kg/day; the blood culture of admission on the second day of admission to the ICU with Gram-negative bacillus smear was positive, and Ceftriaxone was changed to Ceftazidime at 150 mg/kg/day.\n\nOn his first day in the ICU, a substantial increase in serum biomarkers of cardiac damage was documented, the echocardiogram showed mild mitral and tricuspid regurgitation, left ventricular dilatation, left ventricular ejection fraction (LVEF) 58%, no evidence of thrombi, vegetations or pericardial effusion, and he was diagnosed with acute myocarditis. Milrinone was started at 0.4 mcg/kg/min, furosemide and IV immunoglobulin 1 g/kg single dose.\n\nThe second day blood culture the germ was identified as Bacillus clausii, identified by the system (VYTEK 2TM), the susceptibility profile was not performed because the team did not have cut points for this germ, for this reason the antibiotic coverage was adjusted, considering it was not a contaminant, Ceftazidime was changed to Ciprofloxacin at 30 mg/kg/day and Ceftaroline was added at 8 mg/kg every 8 hours along with Clindamycin for MRSA. The 3 subsequent blood cultures with intervals of 48 hours between each were positive in both peripheral blood and CVC for isolation of B. clausii.\n\nOn his 6th day in hospital, the gastrointestinal panel (Maripoc gastro test methodology) performed on the second day detected Clostridiodes difficile toxin A/B, the tests for Campylobacteryeyuni, Norovirus GI, Norovirus GII.4, Adenovirus and Rotavirus were negative. Following these findings, therapy was escalated to IV Vancomycin at a dose of 60 mg/kg/day and metronidazole was added orally. Ceftaroline, clindamycin and ciprofloxacin were omitted, covering both B. clausii and C. difficile and MRSA .\n\nHIV testing, serology for Chagas and SARS-CoV-2 antigen by immunofluorescence (FIA) were negative, immunoglobulins were within normal limits.\n\nOn the seventh day, arterial hypertension was reported and spirinolactone was added to the management.\n\nOn the 8th day, the laboratory tests showed altered coagulation times and increased azotaemia associated with anuria that had lasted for 12 hours. However, due to the patient's condition, a peritoneal catheter was not placed, the vancomycin dose was adjusted and vitamin K was administered. The patient continued to have anuria and anasarca, and she developed sustained hypotension. Noradrenaline was added, but her condition deteriorated with multisystem organ failure and she died twelve days after admission. No autopsy was performed because the mother refused permission for cultural reasons.\n",
+    "diff_label_texts": "A 4‑month‑old Indigenous infant from Urracá, rural Panama (approximately 3 hours by canoe from the nearest health subcenter), with protein‑calorie malnutrition and no prior healthcare or vaccinations, presented with 4 days of non‑bloody diarrhea and vomiting, progressing to moderate–severe dehydration. At the initial health center she received oral fluids and 4 doses of Enterogermina (Bacillus clausii: two billion spores/5 mL), but due to supply limitations was transferred to a second‑level facility and then to a tertiary hospital in Panama City with a working diagnosis of acute gastroenteritis and severe dehydration.\n\nOn arrival to the ED she had altered mental status, signs of shock (tearless cry, dry mucosa, cold extremities, capillary refill >2 s, filiform pulse, mottling), tachycardia 170 bpm, tachypnea 55/min, BP 91/37 mmHg, SpO2 99%, generalized edema (+++) of hands, feet, abdomen, and face, and skin changes suggestive of pellagroid dermatosis. Anthropometrics: weight 4.7 kg, length 56 cm, H/A Z −2.52 (W/H and W/A not quantifiable due to severe dehydration). Chest exam had fine basal crackles. Initial management included LR 10 mL/kg bolus, followed by 5% dextrose/0.33% saline then 5% dextrose/0.9% saline; empiric ceftriaxone 50 mg/kg/day for suspected sepsis. CBC showed leukocytosis 39×10^3/µL, severe anemia Hgb 5.6 g/dL, thrombocytosis 502×10^3/µL. She received 50 mL filtered, leukoreduced PRBCs and 40 cc FFP for coagulopathy. Enteral feeds were started via NGT; fluids were titrated with ongoing negative balance.\n\nOn hospital day (HD) 2, the initial peripheral blood culture signaled Gram‑positive cocci in clusters; oxacillin 200 mg/kg/day was added and ceftriaxone increased to 75–100 mg/kg/day. Hypocalcemia (Ca 6.38 mg/dL) was corrected. On HD3 she lost peripheral access; a central venous catheter (CVC) was placed. She remained hypovolemic with worsening work of breathing; LR 20 mL/kg was given. ABG: pH 7.26, HCO3− 13 mmol/L, pCO2 28.4 mmHg, pO2 39.2 mmHg, lactate 2.8 mmol/L. She was intubated and transferred to PICU for mechanical ventilation. Management included total fluids ~100 mL/kg, epinephrine infusion, low‑salt albumin, 10% calcium gluconate; analgesia/sedation was switched from fentanyl to remifentanil due to elevated transaminases.\n\nThe admission blood culture grew methicillin‑resistant Staphylococcus aureus (MRSA); oxacillin was discontinued and clindamycin 40 mg/kg/day was added. A subsequent blood culture smear showing Gram‑negative bacilli prompted a change from ceftriaxone to ceftazidime 150 mg/kg/day. On PICU day 1 there was a marked rise in cardiac injury biomarkers; echocardiogram showed mild MR/TR, LV dilation, LVEF 58%, without thrombi, vegetations, or pericardial effusion, consistent with acute myocarditis. She received milrinone 0.4 mcg/kg/min, furosemide, and IVIG 1 g/kg once.\n\nBy HD4–5, the second‑day blood culture identified Bacillus clausii via VITEK 2; no susceptibility profile was generated (no interpretive breakpoints). Considering it was not a contaminant, antimicrobial therapy was adjusted: ceftazidime was changed to ciprofloxacin 30 mg/kg/day and ceftaroline 8 mg/kg q8h was added, with clindamycin continued for MRSA coverage. Three subsequent blood cultures at 48‑hour intervals remained positive for B. clausii from both peripheral blood and the CVC. On HD6, a GI panel (Maripoc) detected Clostridioides difficile toxin A/B; tests for Campylobacter jejuni, Norovirus GI/GII.4, Adenovirus, and Rotavirus were negative. Therapy was escalated to IV vancomycin 60 mg/kg/day plus oral metronidazole; ceftaroline, clindamycin, and ciprofloxacin were discontinued to streamline coverage for MRSA, B. clausii, and C. difficile. HIV, Chagas serology, and SARS‑CoV‑2 antigen (FIA) were negative; immunoglobulins were within reference ranges.\n\nOn HD7, arterial hypertension developed and spironolactone was initiated. By HD8, coagulopathy worsened and azotemia with 12 hours of anuria was documented; vancomycin dosing was adjusted and vitamin K administered. Due to clinical instability, peritoneal dialysis catheter placement was deferred. She progressed to anasarca and sustained hypotension; norepinephrine was added. Despite intensive care and multiple antibiotic regimens, she developed refractory septic shock and multisystem organ failure. She died 12 days after admission. No autopsy was performed due to family cultural objections.\n\nKey microbiologic findings were: (1) initial MRSA bacteremia; (2) GI panel positive for C. difficile toxin; and (3) persistent Bacillus clausii bacteremia documented in serial peripheral and CVC cultures after prior administration of Enterogermina. The clinical course was marked by severe malnutrition, shock, myocarditis, evolving renal failure with anuria, coagulopathy, and ultimate multiorgan failure despite escalated antimicrobial and organ support.",
+    "summary": "4-month-old lactating infant, indigenous ethnicity, from the rural interior of Panama, 3 hours by canoe from the nearest health subcenter, with protein-caloric malnutrition, who presented with acute diarrhea and moderate-severe dehydration, receiving Enterogermina as part of the initial treatment. She was transferred to a third-level hospital, where she arrived with respiratory distress and signs of shock. The initial blood culture reported growth of methicillin-resistant Staphylococcus aureus (MRSA), the gastrointestinal panel was positive for Clostridiodes difficile, and later growth was confirmed in serial blood cultures of peripheral blood and central venous catheter, of Bacillus clausii. With a torpid evolution and resistance to multiple antibiotic regimens, she died of multisystem organ failure twelve days after admission.\n"
+  },
+  {
+    "doc_id": 55,
+    "label": "low_health_literacy",
+    "fulltext": "A 2-year-old female presented with a 1-year history of painless left progressive proptosis with no reported systemic diseases or family history. Ophthalmologic examination revealed light sensation as the only vision in the left eye, along with proptosis, inward and upward eyeball displacement, and restricted extraocular muscle movements in downward and outward directions. An irregularly shaped, well-defined soft mass was palpable in the inferior aspect of the left orbit, accompanied by left lower eyelid ectropion. The pupil was enlarged (4 mm in diameter), and pupillary reaction was absent. The remaining anterior segment examination showed no apparent abnormalities. Fundus examination was challenging due to the child’s size. Hertel exophthalmometry readings measured 10.5 mm in the right eye and 18 mm in the left. Magnetic resonance imaging (MRI) revealed a well-circumscribed mass, displaying hypointense signals on T1-weighted images and hyperintense signals on T2-weighted images. Contrast-enhanced imaging demonstrated no significant improvement. A transconjunctival approach via the inferior fornix with canthotomy and cantholysis was performed, revealing a grayish-white cystic mass with a distinct boundary from surrounding tissues. During posterior separation to the eyeballs’ posterior part, tight adhesion to the optic nerve was observed. Due to the mass’s substantial size and the restricted surgical field, volume reduction was necessary. Approximately 12.5 mL of the fluid was aspirated, and the mass was completely excised. Histopathological examination disclosed a fibrous capsule wall covered with squamous and glandular epithelium, along with visible brain tissue and a cartilage-like matrix consistent with orbital teratoma. One month postsurgery, the patient exhibited enophthalmos, conjunctival hyperemia, and keratitis on ocular examination. This was attributed to the mass’s prior enlargement of the orbital cavity, resulting in postoperative enophthalmos. The cornea could not adhere to the eyelids, creating a space and causing corneal inflammation. After obtaining the consent of the patient’s guardian, a second operation involved the implantation of an allogeneic sclera into the orbit to increase the orbital volume, alleviate fossa pitting and restore keratitis to normal. No recurrence of the teratomas was noted during the 1-year follow-up. The patient still had minor enophthalmos and outer canthus abnormality. The visual acuity remained consistent with pre-operation levels. Hertel exophthalmometry readings measured 10.5 mm in the right eye and 8 mm in the left. The remaining anterior segment examination showed no apparent abnormalities.",
+    "diff_label_texts": "A 2-year-old girl had a bulging left eye. The eye was pushed inward and upward. An MRI scan showed a clear lump. It looked dark on one kind of picture and bright on another. Tests on the tissue, including special lab tests, proved it was a teratoma (a type of growth). Doctors removed the lump through the inside of the lower eyelid and made small cuts at the outer corner to make room. One month later, the eye looked sunken. The white part was red. The clear front of the eye was inflamed. Doctors did a second surgery. They put donated eye-white tissue into the eye socket to add space, smooth the hollow, and help the eye surface heal. After one year, the growth did not come back, and there were no other problems.",
+    "summary": "Patient concerns: A 2-year-old female child was presented exhibiting proptosis and inward and upward eyeball displacement. Enhanced magnetic resonance imaging revealed a well-circumscribed mass, persisting with hypointense signals on T1-weighted images (T1WI) and hyperintense signals on T2-weighted images (T2WI).\n\nDiagnoses: The diagnosis of teratoma was confirmed finally through histological and immunohistochemical exams.\n\nInterventions: A transconjunctival approach via the inferior fornix, coupled with canthotomy and cantholysis, was performed. However, a month postsurgery, the patient developed enophthalmos, conjunctival hyperemia, and keratitis upon ocular examination. A second operation involved the implantation of allogeneic sclera into the orbit to increase orbital volume, improve the pitting of the fossa, and restore keratitis to normal.\n\nOutcomes: No recurrence and other complications were noted during the 1-year follow-up."
+  },
+  {
+    "doc_id": 55,
+    "label": "proficient_health_literacy",
+    "fulltext": "A 2-year-old female presented with a 1-year history of painless left progressive proptosis with no reported systemic diseases or family history. Ophthalmologic examination revealed light sensation as the only vision in the left eye, along with proptosis, inward and upward eyeball displacement, and restricted extraocular muscle movements in downward and outward directions. An irregularly shaped, well-defined soft mass was palpable in the inferior aspect of the left orbit, accompanied by left lower eyelid ectropion. The pupil was enlarged (4 mm in diameter), and pupillary reaction was absent. The remaining anterior segment examination showed no apparent abnormalities. Fundus examination was challenging due to the child’s size. Hertel exophthalmometry readings measured 10.5 mm in the right eye and 18 mm in the left. Magnetic resonance imaging (MRI) revealed a well-circumscribed mass, displaying hypointense signals on T1-weighted images and hyperintense signals on T2-weighted images. Contrast-enhanced imaging demonstrated no significant improvement. A transconjunctival approach via the inferior fornix with canthotomy and cantholysis was performed, revealing a grayish-white cystic mass with a distinct boundary from surrounding tissues. During posterior separation to the eyeballs’ posterior part, tight adhesion to the optic nerve was observed. Due to the mass’s substantial size and the restricted surgical field, volume reduction was necessary. Approximately 12.5 mL of the fluid was aspirated, and the mass was completely excised. Histopathological examination disclosed a fibrous capsule wall covered with squamous and glandular epithelium, along with visible brain tissue and a cartilage-like matrix consistent with orbital teratoma. One month postsurgery, the patient exhibited enophthalmos, conjunctival hyperemia, and keratitis on ocular examination. This was attributed to the mass’s prior enlargement of the orbital cavity, resulting in postoperative enophthalmos. The cornea could not adhere to the eyelids, creating a space and causing corneal inflammation. After obtaining the consent of the patient’s guardian, a second operation involved the implantation of an allogeneic sclera into the orbit to increase the orbital volume, alleviate fossa pitting and restore keratitis to normal. No recurrence of the teratomas was noted during the 1-year follow-up. The patient still had minor enophthalmos and outer canthus abnormality. The visual acuity remained consistent with pre-operation levels. Hertel exophthalmometry readings measured 10.5 mm in the right eye and 8 mm in the left. The remaining anterior segment examination showed no apparent abnormalities.",
+    "diff_label_texts": "A 2-year-old female with a 1-year history of painless, progressive left proptosis and no systemic disease or family history presented with light perception only in the left eye. Examination showed proptosis with inward and upward globe displacement; restricted extraocular movements in downward and outward gaze; a palpable, irregular, well-defined soft mass in the inferior orbit; left lower lid ectropion; a 4 mm mydriatic, nonreactive pupil; and otherwise unremarkable anterior segment (fundus view limited by age). Hertel exophthalmometry: OD 10.5 mm, OS 18 mm. MRI demonstrated a well-circumscribed mass, hypointense on T1WI and hyperintense on T2WI; contrast-enhanced imaging demonstrated no significant improvement. The lesion was excised via a transconjunctival approach through the inferior fornix with canthotomy and cantholysis. Intraoperatively, a grayish-white cystic mass with a distinct boundary was identified; posterior dissection revealed tight adhesion to the optic nerve. Due to lesion size and limited exposure, volume reduction was performed with aspiration of approximately 12.5 mL of fluid, followed by complete excision. Histopathology showed a fibrous capsule lined by squamous and glandular epithelium with visible brain tissue and cartilage-like matrix, consistent with orbital teratoma; immunohistochemical examination corroborated the diagnosis. One month postoperatively, the patient developed enophthalmos, conjunctival hyperemia, and keratitis, attributed to prior orbital cavity enlargement by the mass leading to postoperative volume deficit; corneal nonapposition to the lids created a gap and corneal inflammation. After guardian consent, a second operation implanted allogeneic sclera to augment orbital volume, alleviate fossa pitting, and normalize keratitis. At 1-year follow-up, there was no recurrence of the teratoma. Residual findings included minor enophthalmos and outer canthus abnormality; visual acuity remained at preoperative levels. Hertel measurements were OD 10.5 mm and OS 8 mm; the remaining anterior segment examination was unremarkable.",
+    "summary": "Patient concerns: A 2-year-old female child was presented exhibiting proptosis and inward and upward eyeball displacement. Enhanced magnetic resonance imaging revealed a well-circumscribed mass, persisting with hypointense signals on T1-weighted images (T1WI) and hyperintense signals on T2-weighted images (T2WI).\n\nDiagnoses: The diagnosis of teratoma was confirmed finally through histological and immunohistochemical exams.\n\nInterventions: A transconjunctival approach via the inferior fornix, coupled with canthotomy and cantholysis, was performed. However, a month postsurgery, the patient developed enophthalmos, conjunctival hyperemia, and keratitis upon ocular examination. A second operation involved the implantation of allogeneic sclera into the orbit to increase orbital volume, improve the pitting of the fossa, and restore keratitis to normal.\n\nOutcomes: No recurrence and other complications were noted during the 1-year follow-up."
+  },
+  {
+    "doc_id": 56,
+    "label": "low_health_literacy",
+    "fulltext": "A 78-year-old woman, who came to collect her blister pack with her medication reconstituted in a personalised dosage system (PDS) from the community pharmacy, informed us that for some months she had been suffering from tiredness, weakness, dizziness and confusion. These symptoms were preventing her from leaving her home to walk as often as she normally did. In view of this situation, she was invited to the personalised care area to review the degree of knowledge that the patient had of her medication and the use she made of it, to analyse whether any of her medication could be related to the health problem described.\n\nPharmacological treatment of the patient\n\nMedication  Dose  Dosage  Health issue  Start date\nDoxazosin  2 mg/24 h  0-0-1  Hypertension  2014\nLosartan  100 mg/24 h  1-0-0  Hypertension  2014\nManidipine  20 mg/24 h  0-1-0  Hypertension  2014\nSimvastatin  40 mg/24 h  0-0-1  Hypercholesterolemia  2014\nAcetylsalicylic acid  100 mg/24 h  1-0-0  Secondary prophylaxis  2014\nOmeprazole  20 mg/24 h  1-0-0  Prevention of peptic ulcer  2014\nPregabalin  100 mg/12 h  1-0-1  Neuralgia  2019\nTorasemide  10 mg/24 h  1-0-0  Edema  2023\nDulaglutide  1.5 mg/week  1 time/week  Diabetes  2014\nInsulin glargine  74 IU/24 h  1-0-0  Diabetes  2014\nInsulin lispro  20 IU/24 h  0-1-0  Diabetes  2014\nBrimonidine  1 drop/12 h  1-0-1  Ocular hypertension  2018\n\nStudy and evaluation\nThe interview revealed that there was no new medication and that it did not appear in the SPD service register. Given the suspicion of a possible hypotension, her blood pressure was measured with an Omron Complete device, with the following values: Systolic Blood Pressure (SBP) 96 mmHg, Diastolic Blood Pressure (DBP) 52 mmHg and Heart Rate (HR) 69 beats per minute. Given these values, it was suggested that her blood pressure be monitored and the influence of her medication on these values and the symptoms described by the patient be analysed.\n\nThe patient's medication doses, starting with antihypertensive medications, are reviewed to adjust to the patient's estimated glomerular filtration rate (eGFR) and to see if hypotension is related to the dosage of these medications. The patient's eGFR value, calculated using the Chronic Kidney Disease-Epidemiology Collaboration (CKD-EPI) formula, is 30 ml/min/1.73 m2.\n\nThe guidelines for the revision of the dose according to the value of the eGFR are the product information for the medicinal products and the consensus guidelines for the use of medicinal products in renal impairment of the teaching and research group in the field of practical pharmacy of the Faculty of Pharmacy of the University of Barcelona, which is available on the Internet. This guide has been prepared from the analysis of the most dispensed medicinal products in community pharmacies. They have been organised by therapeutic groups according to the ATC (Anatomical-Therapeutic-Chemical) classification, information on the symptoms of overdose has been included and it has been agreed to categorise the risk to the patient of taking these medicinal products according to their eGFR as low, moderate or high.\n\nAfter the medication review was performed according to the eGFR value of 30 ml/min/1.73 m2, the results were obtained.\n\nFollowing the study of the medication, our intervention focuses on the dosage of the following medicines: losartan, manidipine, torasemide and pregabalin. The antihypertensive medicines, losartan and manidipine, and pregabalin require a dose adjustment depending on the patient's eGFR value, while the diuretic torasemide can influence blood pressure values.\n\nInitially, it was decided to intervene in the dosage of losartan and manidipine. There is the possibility of reducing the dose of pregabalin, but the pharmaceutical team agreed with the patient to assess the influence of this medication after the possible adjustment of the dose of antihypertensive during the evolution and follow-up of the patient.\n\nIntervention\nThe information is used to prepare a report for the doctor (see annex), recommending a reduction in the dose of losartan and manidipine, as the available information recommends a reduction in the dose to 50-75% of losartan for eGFR of 30-59 ml/min/1.73 m2 and adjusting the dose of manidipine for eGFR of 15-30 ml/min/1.73 m2.\n\nThe proposed intervention was explained to the patient and the report was given to the primary care doctor, explaining the possibility of adjusting the dose of losartan and manidipine to improve the patient's condition (table 4). When this information reached the doctor, he opted to reduce the dose of losartan to 50 mg/24 hours and manidipine to 10 mg/24 hours. Pregabalin 100 mg/12 hours was also replaced with gabapentin 300 mg/12 hours.\n\nFollow-up\nFollowing this change in the patient's treatment and after a follow-up of two months, the patient showed an improvement in blood pressure values (table 5) and a remission of the symptoms described. It was reviewed whether the gabapentin dose of 300 mg/12 hours was adequate for the eGFR value of 30 ml/min/1.73 m2, and it was correct (eGFR between 30 and 60, recommended total daily dose 300-900 mg).\n\n",
+    "diff_label_texts": "You are 78 and take many medicines in a pre-packed pill system (SPD). For months, you felt very tired, weak, dizzy, and confused. We checked your medicines. We looked closely at pills that the kidneys help clear, using your kidney filter number (eGFR). We wrote a note to your family doctor. We asked to lower the dose of two blood pressure pills: losartan and manidipine, based on your eGFR. Your doctor lowered the doses. We kept an eye on you. Your symptoms went away.",
+    "summary": "78-year-old patient, taking many medicines and included in the Personalised Medication Dosage System (SPD). When she came to collect her medication, she informed us that for some months she had been suffering from tiredness, weakness, dizziness and confusion. A review of the medication was carried out, focusing on the dosage of the medicines metabolised or eliminated by the kidneys, depending on the patient's estimated glomerular filtration rate (EGFR). A referral was made to the Primary Care Physician (PCP) by means of a report, in which the reduction of the dose of losartan and manidipine was recommended, depending on the patient's estimated glomerular filtration rate (EGFR). The PCP reduced the dose of the antihypertensive medicines. The case was monitored, which allowed us to observe that the patient no longer presented the symptoms described initially.\n"
+  },
+  {
+    "doc_id": 56,
+    "label": "intermediate_health_literacy",
+    "fulltext": "A 78-year-old woman, who came to collect her blister pack with her medication reconstituted in a personalised dosage system (PDS) from the community pharmacy, informed us that for some months she had been suffering from tiredness, weakness, dizziness and confusion. These symptoms were preventing her from leaving her home to walk as often as she normally did. In view of this situation, she was invited to the personalised care area to review the degree of knowledge that the patient had of her medication and the use she made of it, to analyse whether any of her medication could be related to the health problem described.\n\nPharmacological treatment of the patient\n\nMedication  Dose  Dosage  Health issue  Start date\nDoxazosin  2 mg/24 h  0-0-1  Hypertension  2014\nLosartan  100 mg/24 h  1-0-0  Hypertension  2014\nManidipine  20 mg/24 h  0-1-0  Hypertension  2014\nSimvastatin  40 mg/24 h  0-0-1  Hypercholesterolemia  2014\nAcetylsalicylic acid  100 mg/24 h  1-0-0  Secondary prophylaxis  2014\nOmeprazole  20 mg/24 h  1-0-0  Prevention of peptic ulcer  2014\nPregabalin  100 mg/12 h  1-0-1  Neuralgia  2019\nTorasemide  10 mg/24 h  1-0-0  Edema  2023\nDulaglutide  1.5 mg/week  1 time/week  Diabetes  2014\nInsulin glargine  74 IU/24 h  1-0-0  Diabetes  2014\nInsulin lispro  20 IU/24 h  0-1-0  Diabetes  2014\nBrimonidine  1 drop/12 h  1-0-1  Ocular hypertension  2018\n\nStudy and evaluation\nThe interview revealed that there was no new medication and that it did not appear in the SPD service register. Given the suspicion of a possible hypotension, her blood pressure was measured with an Omron Complete device, with the following values: Systolic Blood Pressure (SBP) 96 mmHg, Diastolic Blood Pressure (DBP) 52 mmHg and Heart Rate (HR) 69 beats per minute. Given these values, it was suggested that her blood pressure be monitored and the influence of her medication on these values and the symptoms described by the patient be analysed.\n\nThe patient's medication doses, starting with antihypertensive medications, are reviewed to adjust to the patient's estimated glomerular filtration rate (eGFR) and to see if hypotension is related to the dosage of these medications. The patient's eGFR value, calculated using the Chronic Kidney Disease-Epidemiology Collaboration (CKD-EPI) formula, is 30 ml/min/1.73 m2.\n\nThe guidelines for the revision of the dose according to the value of the eGFR are the product information for the medicinal products and the consensus guidelines for the use of medicinal products in renal impairment of the teaching and research group in the field of practical pharmacy of the Faculty of Pharmacy of the University of Barcelona, which is available on the Internet. This guide has been prepared from the analysis of the most dispensed medicinal products in community pharmacies. They have been organised by therapeutic groups according to the ATC (Anatomical-Therapeutic-Chemical) classification, information on the symptoms of overdose has been included and it has been agreed to categorise the risk to the patient of taking these medicinal products according to their eGFR as low, moderate or high.\n\nAfter the medication review was performed according to the eGFR value of 30 ml/min/1.73 m2, the results were obtained.\n\nFollowing the study of the medication, our intervention focuses on the dosage of the following medicines: losartan, manidipine, torasemide and pregabalin. The antihypertensive medicines, losartan and manidipine, and pregabalin require a dose adjustment depending on the patient's eGFR value, while the diuretic torasemide can influence blood pressure values.\n\nInitially, it was decided to intervene in the dosage of losartan and manidipine. There is the possibility of reducing the dose of pregabalin, but the pharmaceutical team agreed with the patient to assess the influence of this medication after the possible adjustment of the dose of antihypertensive during the evolution and follow-up of the patient.\n\nIntervention\nThe information is used to prepare a report for the doctor (see annex), recommending a reduction in the dose of losartan and manidipine, as the available information recommends a reduction in the dose to 50-75% of losartan for eGFR of 30-59 ml/min/1.73 m2 and adjusting the dose of manidipine for eGFR of 15-30 ml/min/1.73 m2.\n\nThe proposed intervention was explained to the patient and the report was given to the primary care doctor, explaining the possibility of adjusting the dose of losartan and manidipine to improve the patient's condition (table 4). When this information reached the doctor, he opted to reduce the dose of losartan to 50 mg/24 hours and manidipine to 10 mg/24 hours. Pregabalin 100 mg/12 hours was also replaced with gabapentin 300 mg/12 hours.\n\nFollow-up\nFollowing this change in the patient's treatment and after a follow-up of two months, the patient showed an improvement in blood pressure values (table 5) and a remission of the symptoms described. It was reviewed whether the gabapentin dose of 300 mg/12 hours was adequate for the eGFR value of 30 ml/min/1.73 m2, and it was correct (eGFR between 30 and 60, recommended total daily dose 300-900 mg).\n\n",
+    "diff_label_texts": "A 78-year-old woman using a prefilled blister pack service (SPD) reported several months of tiredness, weakness, dizziness, and confusion that limited her usual walks. The pharmacy team suspected medication-related low blood pressure and reviewed her treatment, focusing on drugs cleared by the kidneys and on her blood pressure medicines. Her kidney function (eGFR) was about 30, so doses that depend on kidney clearance needed reassessment. The pharmacist prepared a report for the primary care physician recommending lowering the doses of losartan and manidipine according to renal dosing guidance. The physician reduced the doses of these antihypertensives. With follow-up, her blood pressure improved and the earlier symptoms resolved.",
+    "summary": "78-year-old patient, taking many medicines and included in the Personalised Medication Dosage System (SPD). When she came to collect her medication, she informed us that for some months she had been suffering from tiredness, weakness, dizziness and confusion. A review of the medication was carried out, focusing on the dosage of the medicines metabolised or eliminated by the kidneys, depending on the patient's estimated glomerular filtration rate (EGFR). A referral was made to the Primary Care Physician (PCP) by means of a report, in which the reduction of the dose of losartan and manidipine was recommended, depending on the patient's estimated glomerular filtration rate (EGFR). The PCP reduced the dose of the antihypertensive medicines. The case was monitored, which allowed us to observe that the patient no longer presented the symptoms described initially.\n"
+  },
+  {
+    "doc_id": 56,
+    "label": "proficient_health_literacy",
+    "fulltext": "A 78-year-old woman, who came to collect her blister pack with her medication reconstituted in a personalised dosage system (PDS) from the community pharmacy, informed us that for some months she had been suffering from tiredness, weakness, dizziness and confusion. These symptoms were preventing her from leaving her home to walk as often as she normally did. In view of this situation, she was invited to the personalised care area to review the degree of knowledge that the patient had of her medication and the use she made of it, to analyse whether any of her medication could be related to the health problem described.\n\nPharmacological treatment of the patient\n\nMedication  Dose  Dosage  Health issue  Start date\nDoxazosin  2 mg/24 h  0-0-1  Hypertension  2014\nLosartan  100 mg/24 h  1-0-0  Hypertension  2014\nManidipine  20 mg/24 h  0-1-0  Hypertension  2014\nSimvastatin  40 mg/24 h  0-0-1  Hypercholesterolemia  2014\nAcetylsalicylic acid  100 mg/24 h  1-0-0  Secondary prophylaxis  2014\nOmeprazole  20 mg/24 h  1-0-0  Prevention of peptic ulcer  2014\nPregabalin  100 mg/12 h  1-0-1  Neuralgia  2019\nTorasemide  10 mg/24 h  1-0-0  Edema  2023\nDulaglutide  1.5 mg/week  1 time/week  Diabetes  2014\nInsulin glargine  74 IU/24 h  1-0-0  Diabetes  2014\nInsulin lispro  20 IU/24 h  0-1-0  Diabetes  2014\nBrimonidine  1 drop/12 h  1-0-1  Ocular hypertension  2018\n\nStudy and evaluation\nThe interview revealed that there was no new medication and that it did not appear in the SPD service register. Given the suspicion of a possible hypotension, her blood pressure was measured with an Omron Complete device, with the following values: Systolic Blood Pressure (SBP) 96 mmHg, Diastolic Blood Pressure (DBP) 52 mmHg and Heart Rate (HR) 69 beats per minute. Given these values, it was suggested that her blood pressure be monitored and the influence of her medication on these values and the symptoms described by the patient be analysed.\n\nThe patient's medication doses, starting with antihypertensive medications, are reviewed to adjust to the patient's estimated glomerular filtration rate (eGFR) and to see if hypotension is related to the dosage of these medications. The patient's eGFR value, calculated using the Chronic Kidney Disease-Epidemiology Collaboration (CKD-EPI) formula, is 30 ml/min/1.73 m2.\n\nThe guidelines for the revision of the dose according to the value of the eGFR are the product information for the medicinal products and the consensus guidelines for the use of medicinal products in renal impairment of the teaching and research group in the field of practical pharmacy of the Faculty of Pharmacy of the University of Barcelona, which is available on the Internet. This guide has been prepared from the analysis of the most dispensed medicinal products in community pharmacies. They have been organised by therapeutic groups according to the ATC (Anatomical-Therapeutic-Chemical) classification, information on the symptoms of overdose has been included and it has been agreed to categorise the risk to the patient of taking these medicinal products according to their eGFR as low, moderate or high.\n\nAfter the medication review was performed according to the eGFR value of 30 ml/min/1.73 m2, the results were obtained.\n\nFollowing the study of the medication, our intervention focuses on the dosage of the following medicines: losartan, manidipine, torasemide and pregabalin. The antihypertensive medicines, losartan and manidipine, and pregabalin require a dose adjustment depending on the patient's eGFR value, while the diuretic torasemide can influence blood pressure values.\n\nInitially, it was decided to intervene in the dosage of losartan and manidipine. There is the possibility of reducing the dose of pregabalin, but the pharmaceutical team agreed with the patient to assess the influence of this medication after the possible adjustment of the dose of antihypertensive during the evolution and follow-up of the patient.\n\nIntervention\nThe information is used to prepare a report for the doctor (see annex), recommending a reduction in the dose of losartan and manidipine, as the available information recommends a reduction in the dose to 50-75% of losartan for eGFR of 30-59 ml/min/1.73 m2 and adjusting the dose of manidipine for eGFR of 15-30 ml/min/1.73 m2.\n\nThe proposed intervention was explained to the patient and the report was given to the primary care doctor, explaining the possibility of adjusting the dose of losartan and manidipine to improve the patient's condition (table 4). When this information reached the doctor, he opted to reduce the dose of losartan to 50 mg/24 hours and manidipine to 10 mg/24 hours. Pregabalin 100 mg/12 hours was also replaced with gabapentin 300 mg/12 hours.\n\nFollow-up\nFollowing this change in the patient's treatment and after a follow-up of two months, the patient showed an improvement in blood pressure values (table 5) and a remission of the symptoms described. It was reviewed whether the gabapentin dose of 300 mg/12 hours was adequate for the eGFR value of 30 ml/min/1.73 m2, and it was correct (eGFR between 30 and 60, recommended total daily dose 300-900 mg).\n\n",
+    "diff_label_texts": "A 78-year-old woman enrolled in a community pharmacy personalised dosage system (PDS/SPD) presented at medication pickup reporting several months of asthenia, weakness, dizziness, and confusion, limiting her usual ambulation. There were no new medicines in the SPD register. On-site vitals with an Omron Complete device showed SBP 96 mmHg, DBP 52 mmHg, HR 69 bpm, raising concern for symptomatic hypotension possibly related to her regimen. Her active medications and doses were: doxazosin 2 mg q24h (0-0-1) for hypertension; losartan 100 mg q24h (1-0-0) for hypertension; manidipine 20 mg q24h (0-1-0) for hypertension; simvastatin 40 mg q24h (0-0-1) for hypercholesterolemia; acetylsalicylic acid 100 mg q24h (1-0-0) for secondary prophylaxis; omeprazole 20 mg q24h (1-0-0) for ulcer prevention; pregabalin 100 mg q12h (1-0-1) for neuralgia; torasemide 10 mg q24h (1-0-0) for edema; dulaglutide 1.5 mg weekly; insulin glargine 74 IU q24h (1-0-0); insulin lispro 20 IU q24h (0-1-0) for diabetes; brimonidine 1 drop q12h (1-0-1) for ocular hypertension.\n\nRenal function by CKD-EPI yielded eGFR 30 ml/min/1.73 m2. Dose appropriateness was assessed against product information and a consensus guideline for drug use in renal impairment from the University of Barcelona Faculty of Pharmacy practical pharmacy group (ATC-organised, with overdose symptom summaries and risk stratification by eGFR). Based on eGFR 30 ml/min/1.73 m2, antihypertensive agents losartan and manidipine required dose adjustment; pregabalin also warranted renal dosing, and torasemide was recognised as potentially contributing to low BP. The team prioritised adjusting antihypertensives first and proposed deferring changes to pregabalin until after reassessing response.\n\nIntervention: A report to the primary care physician recommended reducing losartan to 50–75% of standard dose for eGFR 30–59 ml/min/1.73 m2 and adjusting manidipine for eGFR 15–30 ml/min/1.73 m2. The PCP implemented losartan 50 mg q24h and manidipine 10 mg q24h. The PCP also substituted pregabalin 100 mg q12h with gabapentin 300 mg q12h.\n\nFollow-up over two months showed improved BP values and resolution of the initial symptoms. Gabapentin 300 mg q12h was verified as appropriate for eGFR ~30 ml/min/1.73 m2 (recommended total daily dose 300–900 mg for eGFR 30–60). Overall, the case suggests symptomatic hypotension related to cumulative antihypertensive effect in the setting of stage 3b CKD by eGFR, with clinical improvement after renal dose adjustment of losartan and manidipine and subsequent regimen optimisation.",
+    "summary": "78-year-old patient, taking many medicines and included in the Personalised Medication Dosage System (SPD). When she came to collect her medication, she informed us that for some months she had been suffering from tiredness, weakness, dizziness and confusion. A review of the medication was carried out, focusing on the dosage of the medicines metabolised or eliminated by the kidneys, depending on the patient's estimated glomerular filtration rate (EGFR). A referral was made to the Primary Care Physician (PCP) by means of a report, in which the reduction of the dose of losartan and manidipine was recommended, depending on the patient's estimated glomerular filtration rate (EGFR). The PCP reduced the dose of the antihypertensive medicines. The case was monitored, which allowed us to observe that the patient no longer presented the symptoms described initially.\n"
+  },
+  {
+    "doc_id": 57,
+    "label": "low_health_literacy",
+    "fulltext": "It is a case study, approved by the Research Ethics Committee (CEP) under number 1.012.635. The prior authorization of the relatives and the participant was requested from the signature of the Free and Informed Consent (TCLE) and the Free and Informed Consent (TALE).\n\nThe participant in this study is a female student in the 3rd year of elementary school. In the first evaluation, in 2018, the child was 8 years and 2 months old, while in the second evaluation, in 2019, she was 9 years and 6 months old. The interval between the evaluations occurred due to the fact that it is a public service. Thus, the laboratory was absent from activities during the holidays. In addition, it is important to consider that the appointments were only made once a week and, during that period, the participant was absent, which also prolonged the process. As for her history, she was born at term and presented adequate neuropsychomotor and linguistic development. The child was born and lived in a French-speaking country until the age of 2 years, but had exposure to another language at home, since her parents are Brazilian Portuguese speakers. However, her first words were in French. When she returned to Brazil, she went through two private schools. In the first school, she was unable to communicate, as she only expressed herself in French. After that experience, at the age of 3, she began studying in a French school, still in Brazil. Over the years, she presented difficulty in acquiring reading and writing; for that reason, she repeated the 1st year of elementary school, at the request of her mother. At the age of 6, she began studying in a bilingual Portuguese-English school. At the age of 8 years old, she underwent evaluation by an interdisciplinary team in the areas of speech therapy and neuropsychology, finding the diagnosis of developmental dyslexia (DD) and high abilities/giftedness (AH/S). Soon after, she was referred to the evaluation of reading and writing in the Laboratory of Written Language, Interdisciplinarity and Learning - LEIA/UFRN.\n\nPhases of the study: four assessment sessions for each moment - pre and post intervention (T1 and T2, respectively) - and 20 sessions of phonological remediation, once a week for 60 minutes. The intervention took place in the second semester of 2018, where parents were not very engaged due to work demands.\n\nAssessments were conducted individually over a one-hour period. They included tasks to assess performance in phonological processing - phonological working memory, phonological awareness and mental lexical access - reading and writing.\n\nThe following protocols were used to evaluate the child:\n\nPhonological awareness: to evaluate this ability, the Consciência Fonológica Instrumento de Avaliação Sequencial - CONFIAS (11) was used. This protocol proposes tasks of synthesis, segmentation, rhyme, alliteration, initial and final syllable identification, exclusion and transposition. First, syllabic awareness, formed by nine items, is analyzed, followed by phonemic awareness, formed by seven items. Each hit is equivalent to one point, with 40 for syllabic awareness and 30 for phonemic awareness, totaling 70 points. Its results should be compared with the expected writing hypotheses based on Ferreiro and Teberosky (12). In this way, the following normal values were used: for the syllabic-alphabetic writing hypothesis, 27, 12 and 39 for the syllabic, phonemic and total score, respectively; for the alphabetic writing hypothesis, 31, 15 and 46.\n\nPhonological working memory: The Phonological Working Memory Test was used (13). In the application of this protocol, the assessor should begin with the non-word test, which consists of 40 invented words. The assessor should then say each word in the list, asking the child to repeat it immediately. The child has two attempts to repeat the words correctly. In the first attempt, each correct answer is worth two points, in the second attempt, the child is awarded one point, and in the third attempt, the child is awarded zero points. After this, the assessor should move on to the test of digits in direct and reverse order, which is scored in the same way as the pseudo-words. Depending on the age of the participant at the time of the assessments, the normal values of 69, 13 and 6 were used for pseudo-words, direct and reverse digits, respectively.\n\nAccess to the mental lexicon: the Rapid Automatic Naming Test (RAN)(14) was used in the evaluation and the Automatic Naming Test (TENA)(15) in the re-evaluation. Both tests aim to estimate the individual's ability to name a sequence of stimuli, that is, to measure the speed at which the child can verbalize a visual stimulus quickly. Two protocols were used, since the TENA had not yet been published at the time of the first evaluation. In addition, the TENA is a current and more complete protocol for the verification of normality, as it allows analysis according to age and months. The two tests used have similar application and are divided into four boards, where the child must name colors, objects, letters and digits. The naming must be done with the same movement that is used for reading - from left to right and from top to bottom. For T1, which used the RAN, the normality values correspond to children aged between 8 years and 8 years and 11 months, due to the age of the participant in that period, thus, it should have a score of 28, 29, 52 and 46 seconds for the subtests of digits, letters, objects and colors, respectively. For T2, the normality values of the age of 9 years and 6 months of the protocol (TENA) were used, with an expected score of 35, 32, 50, 53 seconds for the subtests of digits, letters, objects and colors, respectively.\n\nReading: First, the Protocol for the Assessment of Reading of Words/Pseudowords Isolated – LPI(16) was used, in which the child is asked to read aloud words and pseudowords, which are scored. 19 regular words, 20 irregular words and 20 pseudowords are arranged in black Arial font, size 24 and white background. The child may obtain a total of 59 points, since each correct reading is worth one point. After this, the Protocol for the Assessment of Reading of Expository Texts was used(17). This instrument aims to assess reading comprehension through directed questions about texts compatible with the subject's school year. It assesses and times patterns of silent and oral reading. This allows the reading level to be verified and compared. In addition, the number of words read per minute is averaged, allowing the reading speed to be verified and compared.\n\nWriting: To evaluate the writing, the child was asked to produce a text on a topic of their interest. After finishing the story, the professional asked the child to read out loud what was written. Furthermore, the child was asked to write the target words of the LPI(16) on a separate sheet, in order to carry out a dictation of words and pseudo-words. With this, a qualitative investigation of the writing was carried out, based on the orthographic analysis of Zorzi and Ciasca(18).\n\nThe remediation was based on a program used for children with dyslexia(19) and included activities that aimed to improve phonological abilities, such as: identification of graphemes and phonemes, phoneme pairs, syllable pairs, word pairs, addition and subtraction of phonemes, syllabic and phonemic manipulation, rhymes, alliteration, access to mental lexicon, visual working memory, auditory working memory and reading training. In all sessions, these activities were explored in a playful way, mainly directed to the metalinguistic aspects of phonological awareness. In reading training, the child was exposed to children's books from the Mico Maneco collection. This collection has various stories that increase the level of complexity of words, so it is possible to follow the child's progress. The activities performed and the child's evolution were described in his/her medical record at the end of each session.\n\nAnalysing the results found, with regard to performance in phonological awareness, in both assessments the child presented performance consistent with the hypotheses of writing presented in each period. In the first assessment, he received the syllabic-alphabetic writing hypothesis and in the second, the alphabetic one, demonstrating progress. The performance score progressed in both categories of the skill, syllabic (T1 = 35; T2 = 37) and phonemic (T1 = 14; T2 = 20) (Table 1). The progress of 4 successes in the phonemic level is highlighted, which can be explained due to the phonological remediation having been performed with focus on the phonemic level.\n\nThe results of phonological working memory at the time prior to phonological remediation expressed below-expected performance for the pseudo-word category, with 66 points in T1, with expected performance for T1 (ET1) of 69, and for the reverse-order digits category (T1 = 04; ET1 = 06) (Table 1). Despite this, it presented results within the expected range for the reverse-order digits category (T1 = 20; ET1 = 13). In the post-intervention evaluation (T2), the results are adequate for the age. It is also possible to notice advances in this skill in all categories, pseudo-word (T1 = 66; T2 = 69), reverse-order digits (T1 = 04; T2 = 12) (Table 1), which requires aspects of executive functions that assist in the rapid storage of the response, a differential aspect in high abilities.\n\nAs for the automatic rapid naming, it is noted that in T1, the performance is inadequate for the standards of normality in all subtests. It is also possible to say that, in T2, the performance was below the expected for the categories of digits (T2 = 41; ET2 = 35), objects (T2 = 59; ET2 = 50) and colors (T2 = 56; ET2 = 53). Only the category of letters presented results within the expected (T2 = 29; ET2 = 32). On the other hand, the advance in the speed of naming is visible for the subtests of letters (T1 = 37; T2 = 29), objects (T1 = 62; T2 = 59) and colors (T1 = 60; T2 = 56), with the exception of digits (T1 = 37; T2 = 41) (Table 1). With the decrease of the time of naming of the stimuli, it is possible to say that the child becomes more effective to access the mental lexicon at the level of the phonological and visual representation, which is also not usual in isolated dyslexia.\n\nAs for reading, in T1 she presented an alphabetic level and in T2 an orthographic level. In the first test, it was noted that there was difficulty mainly with visually similar letters and phonologically close. In addition, the student used sub-vocal support to decode and had an average reading of 20 words per minute, which demonstrates extremely slow decoding and is far below what is expected for her schooling. In the reassessment, she had an average of 94.4 words per minute in oral reading, which is considered adequate for her schooling. She demonstrated presence of prosody, rhythm, global reading, interest and adequate understanding. Qualitatively, it is observed that the child, even with adequate performance, read with a low intensity of speech, still demonstrating insecurity in carrying out the task.\n\nIn writing, it can be observed that in T1 the child had inadequate pencil grip, imprecise writing, with letter changes, omissions, hyper and hyposegments, repetition of words and low use of cohesive elements. In this period, it was shown with writing in the transition from the syllabic-alphabetic phase to the alphabetic phase. In T2 no significant change was observed, since his writing continued to be imprecise, with little intelligibility of the content, visual similarities between letters (such as “d” and “b”) and lack of punctuation. According to the sample collected, it was shown in the alphabetic phase of writing, although difficulties not expected for his age persisted. Despite this, it is noted that he used a greater repertoire in the use of vocabulary for the lexicon of visual input.\n\nAfter the analysis of the results in their entirety, it can be observed that the written language skills advanced during the interval between the evaluations, despite the persistence of consonant characteristics with dyslexia, as it still presents performance below the expected in the access to the mental lexicon and in writing - with the presence of exchanges between phonemes that are audibly and visually similar in a persistent way, omission of letters and hypersegmentation.\n",
+    "diff_label_texts": "This report tells the story of one 9-year-old girl. She is very bright and also has dyslexia. The team tested how she handles speech sounds, how she reads, and how she writes. They tested her before and after sound-based help. Before help, she read by sounding out letters. Her writing was between early sound-by-sound writing and full letter-by-letter writing. She had trouble with tasks that use the sounds in words. After help, her sound skills got better. Her writing became steady at the letter-by-letter stage. Her reading moved up to the next stage, where she could recognize whole words and common spelling patterns.",
+    "summary": "This study is a case report of the evaluation and intervention process of a 9-year-old child with the paradoxical combination of high abilities associated with dyslexia. The objective was to compare the performance in the tasks of phonological processing, reading and writing before and after phonological remediation. In the first evaluation, the child presented an alphabetic level in reading, a transition phase between the syllabic-alphabetic and alphabetic levels in writing and a performance below the expected level in phonological processing abilities. After the intervention, there was an improvement in phonological processing abilities, consolidation of alphabetic writing and of the orthographic level of reading.\n"
+  },
+  {
+    "doc_id": 57,
+    "label": "proficient_health_literacy",
+    "fulltext": "It is a case study, approved by the Research Ethics Committee (CEP) under number 1.012.635. The prior authorization of the relatives and the participant was requested from the signature of the Free and Informed Consent (TCLE) and the Free and Informed Consent (TALE).\n\nThe participant in this study is a female student in the 3rd year of elementary school. In the first evaluation, in 2018, the child was 8 years and 2 months old, while in the second evaluation, in 2019, she was 9 years and 6 months old. The interval between the evaluations occurred due to the fact that it is a public service. Thus, the laboratory was absent from activities during the holidays. In addition, it is important to consider that the appointments were only made once a week and, during that period, the participant was absent, which also prolonged the process. As for her history, she was born at term and presented adequate neuropsychomotor and linguistic development. The child was born and lived in a French-speaking country until the age of 2 years, but had exposure to another language at home, since her parents are Brazilian Portuguese speakers. However, her first words were in French. When she returned to Brazil, she went through two private schools. In the first school, she was unable to communicate, as she only expressed herself in French. After that experience, at the age of 3, she began studying in a French school, still in Brazil. Over the years, she presented difficulty in acquiring reading and writing; for that reason, she repeated the 1st year of elementary school, at the request of her mother. At the age of 6, she began studying in a bilingual Portuguese-English school. At the age of 8 years old, she underwent evaluation by an interdisciplinary team in the areas of speech therapy and neuropsychology, finding the diagnosis of developmental dyslexia (DD) and high abilities/giftedness (AH/S). Soon after, she was referred to the evaluation of reading and writing in the Laboratory of Written Language, Interdisciplinarity and Learning - LEIA/UFRN.\n\nPhases of the study: four assessment sessions for each moment - pre and post intervention (T1 and T2, respectively) - and 20 sessions of phonological remediation, once a week for 60 minutes. The intervention took place in the second semester of 2018, where parents were not very engaged due to work demands.\n\nAssessments were conducted individually over a one-hour period. They included tasks to assess performance in phonological processing - phonological working memory, phonological awareness and mental lexical access - reading and writing.\n\nThe following protocols were used to evaluate the child:\n\nPhonological awareness: to evaluate this ability, the Consciência Fonológica Instrumento de Avaliação Sequencial - CONFIAS (11) was used. This protocol proposes tasks of synthesis, segmentation, rhyme, alliteration, initial and final syllable identification, exclusion and transposition. First, syllabic awareness, formed by nine items, is analyzed, followed by phonemic awareness, formed by seven items. Each hit is equivalent to one point, with 40 for syllabic awareness and 30 for phonemic awareness, totaling 70 points. Its results should be compared with the expected writing hypotheses based on Ferreiro and Teberosky (12). In this way, the following normal values were used: for the syllabic-alphabetic writing hypothesis, 27, 12 and 39 for the syllabic, phonemic and total score, respectively; for the alphabetic writing hypothesis, 31, 15 and 46.\n\nPhonological working memory: The Phonological Working Memory Test was used (13). In the application of this protocol, the assessor should begin with the non-word test, which consists of 40 invented words. The assessor should then say each word in the list, asking the child to repeat it immediately. The child has two attempts to repeat the words correctly. In the first attempt, each correct answer is worth two points, in the second attempt, the child is awarded one point, and in the third attempt, the child is awarded zero points. After this, the assessor should move on to the test of digits in direct and reverse order, which is scored in the same way as the pseudo-words. Depending on the age of the participant at the time of the assessments, the normal values of 69, 13 and 6 were used for pseudo-words, direct and reverse digits, respectively.\n\nAccess to the mental lexicon: the Rapid Automatic Naming Test (RAN)(14) was used in the evaluation and the Automatic Naming Test (TENA)(15) in the re-evaluation. Both tests aim to estimate the individual's ability to name a sequence of stimuli, that is, to measure the speed at which the child can verbalize a visual stimulus quickly. Two protocols were used, since the TENA had not yet been published at the time of the first evaluation. In addition, the TENA is a current and more complete protocol for the verification of normality, as it allows analysis according to age and months. The two tests used have similar application and are divided into four boards, where the child must name colors, objects, letters and digits. The naming must be done with the same movement that is used for reading - from left to right and from top to bottom. For T1, which used the RAN, the normality values correspond to children aged between 8 years and 8 years and 11 months, due to the age of the participant in that period, thus, it should have a score of 28, 29, 52 and 46 seconds for the subtests of digits, letters, objects and colors, respectively. For T2, the normality values of the age of 9 years and 6 months of the protocol (TENA) were used, with an expected score of 35, 32, 50, 53 seconds for the subtests of digits, letters, objects and colors, respectively.\n\nReading: First, the Protocol for the Assessment of Reading of Words/Pseudowords Isolated – LPI(16) was used, in which the child is asked to read aloud words and pseudowords, which are scored. 19 regular words, 20 irregular words and 20 pseudowords are arranged in black Arial font, size 24 and white background. The child may obtain a total of 59 points, since each correct reading is worth one point. After this, the Protocol for the Assessment of Reading of Expository Texts was used(17). This instrument aims to assess reading comprehension through directed questions about texts compatible with the subject's school year. It assesses and times patterns of silent and oral reading. This allows the reading level to be verified and compared. In addition, the number of words read per minute is averaged, allowing the reading speed to be verified and compared.\n\nWriting: To evaluate the writing, the child was asked to produce a text on a topic of their interest. After finishing the story, the professional asked the child to read out loud what was written. Furthermore, the child was asked to write the target words of the LPI(16) on a separate sheet, in order to carry out a dictation of words and pseudo-words. With this, a qualitative investigation of the writing was carried out, based on the orthographic analysis of Zorzi and Ciasca(18).\n\nThe remediation was based on a program used for children with dyslexia(19) and included activities that aimed to improve phonological abilities, such as: identification of graphemes and phonemes, phoneme pairs, syllable pairs, word pairs, addition and subtraction of phonemes, syllabic and phonemic manipulation, rhymes, alliteration, access to mental lexicon, visual working memory, auditory working memory and reading training. In all sessions, these activities were explored in a playful way, mainly directed to the metalinguistic aspects of phonological awareness. In reading training, the child was exposed to children's books from the Mico Maneco collection. This collection has various stories that increase the level of complexity of words, so it is possible to follow the child's progress. The activities performed and the child's evolution were described in his/her medical record at the end of each session.\n\nAnalysing the results found, with regard to performance in phonological awareness, in both assessments the child presented performance consistent with the hypotheses of writing presented in each period. In the first assessment, he received the syllabic-alphabetic writing hypothesis and in the second, the alphabetic one, demonstrating progress. The performance score progressed in both categories of the skill, syllabic (T1 = 35; T2 = 37) and phonemic (T1 = 14; T2 = 20) (Table 1). The progress of 4 successes in the phonemic level is highlighted, which can be explained due to the phonological remediation having been performed with focus on the phonemic level.\n\nThe results of phonological working memory at the time prior to phonological remediation expressed below-expected performance for the pseudo-word category, with 66 points in T1, with expected performance for T1 (ET1) of 69, and for the reverse-order digits category (T1 = 04; ET1 = 06) (Table 1). Despite this, it presented results within the expected range for the reverse-order digits category (T1 = 20; ET1 = 13). In the post-intervention evaluation (T2), the results are adequate for the age. It is also possible to notice advances in this skill in all categories, pseudo-word (T1 = 66; T2 = 69), reverse-order digits (T1 = 04; T2 = 12) (Table 1), which requires aspects of executive functions that assist in the rapid storage of the response, a differential aspect in high abilities.\n\nAs for the automatic rapid naming, it is noted that in T1, the performance is inadequate for the standards of normality in all subtests. It is also possible to say that, in T2, the performance was below the expected for the categories of digits (T2 = 41; ET2 = 35), objects (T2 = 59; ET2 = 50) and colors (T2 = 56; ET2 = 53). Only the category of letters presented results within the expected (T2 = 29; ET2 = 32). On the other hand, the advance in the speed of naming is visible for the subtests of letters (T1 = 37; T2 = 29), objects (T1 = 62; T2 = 59) and colors (T1 = 60; T2 = 56), with the exception of digits (T1 = 37; T2 = 41) (Table 1). With the decrease of the time of naming of the stimuli, it is possible to say that the child becomes more effective to access the mental lexicon at the level of the phonological and visual representation, which is also not usual in isolated dyslexia.\n\nAs for reading, in T1 she presented an alphabetic level and in T2 an orthographic level. In the first test, it was noted that there was difficulty mainly with visually similar letters and phonologically close. In addition, the student used sub-vocal support to decode and had an average reading of 20 words per minute, which demonstrates extremely slow decoding and is far below what is expected for her schooling. In the reassessment, she had an average of 94.4 words per minute in oral reading, which is considered adequate for her schooling. She demonstrated presence of prosody, rhythm, global reading, interest and adequate understanding. Qualitatively, it is observed that the child, even with adequate performance, read with a low intensity of speech, still demonstrating insecurity in carrying out the task.\n\nIn writing, it can be observed that in T1 the child had inadequate pencil grip, imprecise writing, with letter changes, omissions, hyper and hyposegments, repetition of words and low use of cohesive elements. In this period, it was shown with writing in the transition from the syllabic-alphabetic phase to the alphabetic phase. In T2 no significant change was observed, since his writing continued to be imprecise, with little intelligibility of the content, visual similarities between letters (such as “d” and “b”) and lack of punctuation. According to the sample collected, it was shown in the alphabetic phase of writing, although difficulties not expected for his age persisted. Despite this, it is noted that he used a greater repertoire in the use of vocabulary for the lexicon of visual input.\n\nAfter the analysis of the results in their entirety, it can be observed that the written language skills advanced during the interval between the evaluations, despite the persistence of consonant characteristics with dyslexia, as it still presents performance below the expected in the access to the mental lexicon and in writing - with the presence of exchanges between phonemes that are audibly and visually similar in a persistent way, omission of letters and hypersegmentation.\n",
+    "diff_label_texts": "This is a single-case report of a female third-grade student with developmental dyslexia (DD) and high abilities/giftedness (AH/S), evaluated pre- and post-phonological remediation. Ethical approval: CEP 1.012.635; informed consent/assent obtained. The first evaluation (T1) occurred at 8y2m (2018) and the second (T2) at 9y6m (2019). History: term birth; typical neuropsychomotor and language development; early bilingual exposure (French first words; Brazilian Portuguese at home); school transitions including French and later Portuguese–English bilingual schooling; interdisciplinary diagnosis of DD and AH/S at age 8; referral to LEIA/UFRN. Protocol: four assessment sessions at each time point (T1, T2) and 20 weekly 60-minute phonological remediation sessions (2H2018); limited parental engagement due to work. Assessments targeted phonological processing (phonological awareness, phonological working memory, rapid naming), reading, and writing. Measures: CONFIAS for phonological awareness; Phonological Working Memory Test (nonword repetition; digit span direct/reverse); RAN at T1 and TENA at T2 for rapid automatic naming; LPI (isolated word/pseudoword reading) and an expository text protocol (accuracy, oral/silent modes, comprehension, words/minute) for reading; spontaneous text plus dictation of LPI target words with Zorzi & Ciasca orthographic analysis for writing.\nResults—phonological awareness (CONFIAS): performance aligned with the writing hypothesis at each time point. T1 scores: syllabic = 35; phonemic = 14 (consistent with a syllabic–alphabetic writing hypothesis). T2 scores: syllabic = 37; phonemic = 20 (consistent with an alphabetic writing hypothesis). The 4-point gain at the phonemic level likely reflects the remediation focus on phonemic skills.\nPhonological working memory: At T1, nonwords were below expected (66 vs ET1 69) and reverse digits were below expected (4 vs ET1 6); direct-order digits were within/above expected (20 vs ET1 13). At T2, age-appropriate performance was documented with gains across categories: nonwords 69; reverse digits 12. The improvement in reverse span implicates executive mechanisms supporting rapid storage/manipulation, consistent with a strength often observed in high-ability profiles.\nRapid naming: T1 RAN performance was below normal across all subtests. At T2 (TENA), digits (41 vs ET2 35), objects (59 vs ET2 50), and colors (56 vs ET2 53) remained below expected; letters were within expected (29 vs ET2 32). Naming speed improved for letters (37→29 s), objects (62→59 s), and colors (60→56 s), but worsened for digits (37→41 s). Reduced naming latencies indicate more efficient access to the phonological/visual lexicon, though residual RAN deficits persisted—typical in DD.\nReading: T1 showed an alphabetic level with reliance on sub-vocal decoding, confusions for visually/phonologically similar letters, and very slow rate (≈20 words/min), well below grade expectations. T2 advanced to an orthographic level with oral reading ≈94.4 words/min, adequate prosody, rhythm, global reading, interest, and comprehension; low speech intensity suggested residual task-related insecurity.\nWriting: T1 reflected a transition from syllabic–alphabetic to alphabetic, with maladaptive pencil grip, imprecision, letter substitutions/omissions, hyper-/hyposegmentation, word repetition, and limited cohesion. T2 remained qualitatively imprecise with low intelligibility, visual letter confusions (e.g., b/d), and limited punctuation; however, the sample was consistent with an alphabetic phase, with a broader vocabulary repertoire (visual input lexicon). Overall, alphabetic writing consolidated but orthographic accuracy lagged.\nConclusion: After phonological remediation, the child demonstrated gains in phonological processing (awareness and working memory) and progressed from alphabetic to orthographic reading, while consolidating alphabetic writing. Nevertheless, characteristic dyslexic features persisted, particularly reduced efficiency in rapid access to the mental lexicon (RAN) and ongoing orthographic/spelling errors (confusions, omissions, hypersegmentation).",
+    "summary": "This study is a case report of the evaluation and intervention process of a 9-year-old child with the paradoxical combination of high abilities associated with dyslexia. The objective was to compare the performance in the tasks of phonological processing, reading and writing before and after phonological remediation. In the first evaluation, the child presented an alphabetic level in reading, a transition phase between the syllabic-alphabetic and alphabetic levels in writing and a performance below the expected level in phonological processing abilities. After the intervention, there was an improvement in phonological processing abilities, consolidation of alphabetic writing and of the orthographic level of reading.\n"
+  },
+  {
+    "doc_id": 58,
+    "label": "low_health_literacy",
+    "fulltext": "65-year-old woman with no relevant personal or family history. In August 2022, a posterior mediastinal tumour was found in the preoperative assessment for a knee surgery, which was why she was referred for evaluation and treatment. On admission, the physical examination was not relevant and the laboratory studies were within normal parameters. A chest CT scan was performed that showed a tumour located in the posterior right mediastinum measuring 6.5 × 4.2 cm, with well-defined borders, with a fat and solid density, with no evidence of bone erosion or infiltration of surrounding tissue. A biopsy of the lesion was performed using a 18G × 250 mm semiautomatic cutting needle, with image guidance, through a posterior approach. In the histopathological study, a benign neoplasm consisting of mature adipose tissue with areas of haemorrhage alternating with haematopoietic elements, predominantly precursors of the red series, was observed, as well as elements of the myeloid series in different stages of maturation and megakaryocytes, which established the diagnosis of MPM.  Finally, with the diagnosis established and the characteristics of the lesion, conservative management was decided. The patient evolved satisfactorily and was discharged without complications.\n",
+    "diff_label_texts": "A 65-year-old woman had a lump in the back part of the space between her lungs. A chest scan showed it was oval like an egg, had smooth edges, and measured about 6.5 by 4.2 centimeters. Doctors took a small sample with a needle through the chest. Under the microscope, it had fat and blood-making cells. This means the lump was a myelolipoma in the area between the lungs.",
+    "summary": "We present the case of a 65-year-old woman with a primary mediastinal myelolipoma. Computed tomography of the chest showed an ovoid, well-defined bordered tumor of 6.5 × 4.2 cm, located in the posterior mediastinum. A trans-thoracic biopsy of the lesion was performed and microscopic examination revealed haemopoietic elements and mature adipose tissue.\n"
+  },
+  {
+    "doc_id": 58,
+    "label": "intermediate_health_literacy",
+    "fulltext": "65-year-old woman with no relevant personal or family history. In August 2022, a posterior mediastinal tumour was found in the preoperative assessment for a knee surgery, which was why she was referred for evaluation and treatment. On admission, the physical examination was not relevant and the laboratory studies were within normal parameters. A chest CT scan was performed that showed a tumour located in the posterior right mediastinum measuring 6.5 × 4.2 cm, with well-defined borders, with a fat and solid density, with no evidence of bone erosion or infiltration of surrounding tissue. A biopsy of the lesion was performed using a 18G × 250 mm semiautomatic cutting needle, with image guidance, through a posterior approach. In the histopathological study, a benign neoplasm consisting of mature adipose tissue with areas of haemorrhage alternating with haematopoietic elements, predominantly precursors of the red series, was observed, as well as elements of the myeloid series in different stages of maturation and megakaryocytes, which established the diagnosis of MPM.  Finally, with the diagnosis established and the characteristics of the lesion, conservative management was decided. The patient evolved satisfactorily and was discharged without complications.\n",
+    "diff_label_texts": "A 65-year-old woman was found to have an incidental mass in the back part of the chest between the lungs (posterior mediastinum). Chest CT showed an oval, well-defined tumor measuring 6.5 × 4.2 cm. A transthoracic needle biopsy was performed. Microscopy revealed mature fat and blood-forming tissue, confirming a primary mediastinal myelolipoma. Imaging showed no invasion of nearby structures, and the lesion was managed conservatively with a good outcome.",
+    "summary": "We present the case of a 65-year-old woman with a primary mediastinal myelolipoma. Computed tomography of the chest showed an ovoid, well-defined bordered tumor of 6.5 × 4.2 cm, located in the posterior mediastinum. A trans-thoracic biopsy of the lesion was performed and microscopic examination revealed haemopoietic elements and mature adipose tissue.\n"
+  },
+  {
+    "doc_id": 58,
+    "label": "proficient_health_literacy",
+    "fulltext": "65-year-old woman with no relevant personal or family history. In August 2022, a posterior mediastinal tumour was found in the preoperative assessment for a knee surgery, which was why she was referred for evaluation and treatment. On admission, the physical examination was not relevant and the laboratory studies were within normal parameters. A chest CT scan was performed that showed a tumour located in the posterior right mediastinum measuring 6.5 × 4.2 cm, with well-defined borders, with a fat and solid density, with no evidence of bone erosion or infiltration of surrounding tissue. A biopsy of the lesion was performed using a 18G × 250 mm semiautomatic cutting needle, with image guidance, through a posterior approach. In the histopathological study, a benign neoplasm consisting of mature adipose tissue with areas of haemorrhage alternating with haematopoietic elements, predominantly precursors of the red series, was observed, as well as elements of the myeloid series in different stages of maturation and megakaryocytes, which established the diagnosis of MPM.  Finally, with the diagnosis established and the characteristics of the lesion, conservative management was decided. The patient evolved satisfactorily and was discharged without complications.\n",
+    "diff_label_texts": "A 65-year-old woman with no relevant personal or family history had a posterior mediastinal tumour detected incidentally during preoperative assessment for knee surgery (August 2022). On admission, physical examination was noncontributory and laboratory studies were within normal parameters. Chest CT demonstrated a tumour in the posterior right mediastinum measuring 6.5 × 4.2 cm with well-defined borders and mixed fat and solid density, without bone erosion or infiltration of surrounding tissues. An image-guided biopsy was obtained via a posterior approach using an 18G × 250 mm semiautomatic cutting needle. Histopathology showed a benign neoplasm composed of mature adipose tissue with areas of haemorrhage alternating with haemopoietic elements, predominantly erythroid precursors, along with myeloid elements at varying stages of maturation and megakaryocytes, establishing the diagnosis of primary mediastinal myelolipoma (MPM). Given the diagnosis and lesion characteristics, conservative management was chosen. The patient had an uncomplicated course and was discharged in good condition.",
+    "summary": "We present the case of a 65-year-old woman with a primary mediastinal myelolipoma. Computed tomography of the chest showed an ovoid, well-defined bordered tumor of 6.5 × 4.2 cm, located in the posterior mediastinum. A trans-thoracic biopsy of the lesion was performed and microscopic examination revealed haemopoietic elements and mature adipose tissue.\n"
+  },
+  {
+    "doc_id": 59,
+    "label": "low_health_literacy",
+    "fulltext": "The 52-year-old man tested positive for SARS-CoV-2 using a self-test kit after having a cold. He returned to work without fever after resting for two days, but lost consciousness while working outdoors in an ambient temperature of 35°C for five hours. Upon admission to the local hospital’s emergency department, his core temperature (Tc) was recorded as 40°C. The patient presented with persistent coma, dyspnea and gastrointestinal hemorrhage. No underlying diseases and relative family history was noted. Based on the characteristic presentation of hyperpyrexia, coma and multiple organ damage, a diagnosis of HS was established. He was admitted to emergency intensive care unit (ICU) of the local hospital and then received mechanical ventilation. The test results indicated the presence of pulmonary infection, hepatic and renal dysfunction, myocardial ischemia and coagulation disorders. The patient received initial management including rehydration (intravenously infused Lactated Ringer’s solution and normal saline at a rate of 2.5mL/kg∙h), intravenous administration of Piperacillin Sodium and Tazobactam Sodium, vasoactive medications for blood pressure support, continuous mechanical ventilation, and continuous renal replacement therapy (CRRT) to manage subsequent anuria. The patient received plasma transfusion and was administered Tranexamic acid on day 5. The worsening of his condition led to his admission to the medical ICU of our hospital 7 days after HS.\n\nFollowing admission, Reverse-transcription polymerase chain reaction (RT-PCR) testing of a nasopharyngeal swab yielded positive results for SARS-CoV-2. The patient was diagnosed with HS and severe COVID-19 based on China’s COVID-19 Diagnosis and Treatment Program (trial version 10): 1. real-time fluorescent RT-PCR detection of SARS-CoV-2 nucleic acid is positive; 2. respiratory failure and requires mechanical ventilation; 3. shock; 4. combined with multiple organ failure requiring intensive care. The patient had no contact with COVID-19 diagnosed patients or healthcare workers in the hospital, indicating community-acquired infection. The physical examination showed a Glasgow Coma Scale (GCS) score of 3/15, with scores of 1 for eye-opening, verbal response, and motor response. Additionally, the pupils were symmetrical and non-reactive. The heart rate was recorded at 106 bpm and blood pressure was maintained at 126/77 mmHg by continuously infusing norepinephrine at a rate of 0.4 ug/kg·min. The laboratory test results indicated a severe infection, along with anemia, thrombocytopenia, disseminated intravascular coagulation (DIC), as well as acute liver and kidney injury. The white blood cell count (WBC) decreased from 3.55×109/L to 3.13×109/L, lymphocytes significantly decreased from 0.25×109/L to 0.1×109/L, and neutrophil percentage (N%) increased to 85.3%. The Procalcitonin level measured 2.81 ng/mL and C-reactive protein (CRP) level was 32.6 mg/L. Sputum culture testing yielded Stenotrophomonas Maltophilia and Candida lipolytica. The central venous catheter culture test detected Staphylococcus epidermidis, but the continuous blood culture test yielded no positive results. The Computed Tomography (CT) scan revealed bilateral frontal subdural effusion, consolidation and atelectasis in the lower lungs, inflammation in the right upper lobe, bilateral pleural effusion, and a small amount of abdominal fluid.\n\nThe patient received synchronized intermittent mandatory ventilation with a positive end expiratory pressure of 5 mmH2O and an oxygen concentration of 80% and continuous administration of norepinephrine and pituitrin to sustain normal blood pressure. Polyene phosphatidylcholine, adenosylmethionine budisulfonate, ulinastatin, and hemofiltration have been employed for the management of hepatic and renal dysfunction. The antibiotic was substituted with Meropenem and Thymalfasin was administered for 20 days to augment immune function. Mannitol was used to alleviate intracranial pressure for 3 days. To improve coagulation dysfunction, the patient received plasma and cryoprecipitate transfusions, continuous intravenous infusion of heparin sodium at 6000u/day and CRRT with sodium citrate for anticoagulant (8g/day) on day 7. Platelet transfusion was administered after 9 days of HS. His Tc fluctuated between 36 °C and 38.5 °C. CRRT was administered without anticoagulant on day 8. The patient had gastrointestinal hemorrhage and fever after 9 days of HS, but electronic gastroenteroscopy showed no signs of active bleeding. He underwent red blood cell suspension transfusion, hemostasis treatment and gastric acid suppression. Teicoplanin was added due to the presence of Methicillin-resistant Staphylococcus aureus isolated from sputum culture. The patient regained consciousness on day 13 with a GCS score of 14/15 and presented with a moderate fever. Gastrointestinal hemorrhage was not observed. Mechanical ventilation was discontinued and the tracheal tube was removed. But the creatinine levels increased following the suspension of CRRT on day 12.\n\nOn day 17, he developed sudden dyspnea with desaturation (oxygen saturation <85%) followed by a high fever (Tc: 39.3°C), necessitating reintubation and mechanical ventilation. Bronchoscopy revealed less sputum in both lungs and subbranches. He experienced a recurrence of coma, with a GCS score of 3/15. WBC increased to 14.94×109/L and NEU increased to 13.77×109/L. The levels of serum total bilirubin rose to 235.2 µmol/L, while creatinine increased to 441µmol/L. The brain CT scan revealed an ischemic stroke in the right frontal lobe and a hemorrhagic infarction in the right occipital lobe. The patient underwent cooling therapy using CRRT with ice-cold replacement fluid, along with persistent administration of Meropenem and Teicoplanin for anti-infection treatment. Carpofungin was added on day 18 due to the observed elevation in serum levels of Aspergillus galactomannan, Aspergillus IgG antibody, and Candida mannan. The RT-PCR testing for SARS-CoV-2 returned negative results.\n\nThe patient’s fever and infection improved on day 20, but he subsequently developed cerebral hemorrhage and hernia with bilateral dilated pupils. The dehydration therapy was used to reduce intracranial pressure, as surgery was refused by his family. On day 22, indicators of infection, levels of aspartate aminotransferase and creatinine increased again. Carbapenem-resistant Acinetobacter baumannii and A. fumigatus were cultured in the bronchoalveolar lavage fluid. The combination of Meropenem, Teicoplanin, and Carpofungine was administered for anti-infective therapy. The patient’s condition progressively worsened over the next 7 days, ultimately resulting in his demise on day 29. The patients’ inflammatory indicators, cytokines, and coagulation indicators are presented in Table 1.",
+    "diff_label_texts": "This is the first known report of heatstroke happening at the same time as infection with the virus that causes COVID-19 in a 52-year-old man. Doctors gave him antibiotics through a vein. They used treatments to protect his organs. They also treated his blood-clotting problems. His fever went down, and he woke up from the coma. A few days later, he had trouble breathing. He also had bleeding in his brain. He got a lung infection from several germs, and his blood did not clot the way it should. Many organs stopped working. He died.",
+    "summary": "We report the first case of heatstroke comorbid with Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection in a 52-year-old male. After receiving intravenous antibiotics, organ protection measures, and treatment for coagulation disorders, his fever and coma resolved. However, he developed dyspnea and cerebral hemorrhage after several days. This patient experienced a multi-pathogen pulmonary infection and an intractable coagulopathy that ultimately resulted in MODS and death."
+  },
+  {
+    "doc_id": 59,
+    "label": "proficient_health_literacy",
+    "fulltext": "The 52-year-old man tested positive for SARS-CoV-2 using a self-test kit after having a cold. He returned to work without fever after resting for two days, but lost consciousness while working outdoors in an ambient temperature of 35°C for five hours. Upon admission to the local hospital’s emergency department, his core temperature (Tc) was recorded as 40°C. The patient presented with persistent coma, dyspnea and gastrointestinal hemorrhage. No underlying diseases and relative family history was noted. Based on the characteristic presentation of hyperpyrexia, coma and multiple organ damage, a diagnosis of HS was established. He was admitted to emergency intensive care unit (ICU) of the local hospital and then received mechanical ventilation. The test results indicated the presence of pulmonary infection, hepatic and renal dysfunction, myocardial ischemia and coagulation disorders. The patient received initial management including rehydration (intravenously infused Lactated Ringer’s solution and normal saline at a rate of 2.5mL/kg∙h), intravenous administration of Piperacillin Sodium and Tazobactam Sodium, vasoactive medications for blood pressure support, continuous mechanical ventilation, and continuous renal replacement therapy (CRRT) to manage subsequent anuria. The patient received plasma transfusion and was administered Tranexamic acid on day 5. The worsening of his condition led to his admission to the medical ICU of our hospital 7 days after HS.\n\nFollowing admission, Reverse-transcription polymerase chain reaction (RT-PCR) testing of a nasopharyngeal swab yielded positive results for SARS-CoV-2. The patient was diagnosed with HS and severe COVID-19 based on China’s COVID-19 Diagnosis and Treatment Program (trial version 10): 1. real-time fluorescent RT-PCR detection of SARS-CoV-2 nucleic acid is positive; 2. respiratory failure and requires mechanical ventilation; 3. shock; 4. combined with multiple organ failure requiring intensive care. The patient had no contact with COVID-19 diagnosed patients or healthcare workers in the hospital, indicating community-acquired infection. The physical examination showed a Glasgow Coma Scale (GCS) score of 3/15, with scores of 1 for eye-opening, verbal response, and motor response. Additionally, the pupils were symmetrical and non-reactive. The heart rate was recorded at 106 bpm and blood pressure was maintained at 126/77 mmHg by continuously infusing norepinephrine at a rate of 0.4 ug/kg·min. The laboratory test results indicated a severe infection, along with anemia, thrombocytopenia, disseminated intravascular coagulation (DIC), as well as acute liver and kidney injury. The white blood cell count (WBC) decreased from 3.55×109/L to 3.13×109/L, lymphocytes significantly decreased from 0.25×109/L to 0.1×109/L, and neutrophil percentage (N%) increased to 85.3%. The Procalcitonin level measured 2.81 ng/mL and C-reactive protein (CRP) level was 32.6 mg/L. Sputum culture testing yielded Stenotrophomonas Maltophilia and Candida lipolytica. The central venous catheter culture test detected Staphylococcus epidermidis, but the continuous blood culture test yielded no positive results. The Computed Tomography (CT) scan revealed bilateral frontal subdural effusion, consolidation and atelectasis in the lower lungs, inflammation in the right upper lobe, bilateral pleural effusion, and a small amount of abdominal fluid.\n\nThe patient received synchronized intermittent mandatory ventilation with a positive end expiratory pressure of 5 mmH2O and an oxygen concentration of 80% and continuous administration of norepinephrine and pituitrin to sustain normal blood pressure. Polyene phosphatidylcholine, adenosylmethionine budisulfonate, ulinastatin, and hemofiltration have been employed for the management of hepatic and renal dysfunction. The antibiotic was substituted with Meropenem and Thymalfasin was administered for 20 days to augment immune function. Mannitol was used to alleviate intracranial pressure for 3 days. To improve coagulation dysfunction, the patient received plasma and cryoprecipitate transfusions, continuous intravenous infusion of heparin sodium at 6000u/day and CRRT with sodium citrate for anticoagulant (8g/day) on day 7. Platelet transfusion was administered after 9 days of HS. His Tc fluctuated between 36 °C and 38.5 °C. CRRT was administered without anticoagulant on day 8. The patient had gastrointestinal hemorrhage and fever after 9 days of HS, but electronic gastroenteroscopy showed no signs of active bleeding. He underwent red blood cell suspension transfusion, hemostasis treatment and gastric acid suppression. Teicoplanin was added due to the presence of Methicillin-resistant Staphylococcus aureus isolated from sputum culture. The patient regained consciousness on day 13 with a GCS score of 14/15 and presented with a moderate fever. Gastrointestinal hemorrhage was not observed. Mechanical ventilation was discontinued and the tracheal tube was removed. But the creatinine levels increased following the suspension of CRRT on day 12.\n\nOn day 17, he developed sudden dyspnea with desaturation (oxygen saturation <85%) followed by a high fever (Tc: 39.3°C), necessitating reintubation and mechanical ventilation. Bronchoscopy revealed less sputum in both lungs and subbranches. He experienced a recurrence of coma, with a GCS score of 3/15. WBC increased to 14.94×109/L and NEU increased to 13.77×109/L. The levels of serum total bilirubin rose to 235.2 µmol/L, while creatinine increased to 441µmol/L. The brain CT scan revealed an ischemic stroke in the right frontal lobe and a hemorrhagic infarction in the right occipital lobe. The patient underwent cooling therapy using CRRT with ice-cold replacement fluid, along with persistent administration of Meropenem and Teicoplanin for anti-infection treatment. Carpofungin was added on day 18 due to the observed elevation in serum levels of Aspergillus galactomannan, Aspergillus IgG antibody, and Candida mannan. The RT-PCR testing for SARS-CoV-2 returned negative results.\n\nThe patient’s fever and infection improved on day 20, but he subsequently developed cerebral hemorrhage and hernia with bilateral dilated pupils. The dehydration therapy was used to reduce intracranial pressure, as surgery was refused by his family. On day 22, indicators of infection, levels of aspartate aminotransferase and creatinine increased again. Carbapenem-resistant Acinetobacter baumannii and A. fumigatus were cultured in the bronchoalveolar lavage fluid. The combination of Meropenem, Teicoplanin, and Carpofungine was administered for anti-infective therapy. The patient’s condition progressively worsened over the next 7 days, ultimately resulting in his demise on day 29. The patients’ inflammatory indicators, cytokines, and coagulation indicators are presented in Table 1.",
+    "diff_label_texts": "We report the first case of heatstroke (HS) comorbid with SARS-CoV-2 infection in a 52-year-old male. He self-tested positive for SARS-CoV-2 after a cold, then lost consciousness while working outdoors (ambient 35°C for 5 h). On ED arrival, core temperature was 40°C with persistent coma, dyspnea, and gastrointestinal hemorrhage. HS was diagnosed based on hyperpyrexia, coma, and multiorgan injury. Initial management at the local ICU included mechanical ventilation; fluid resuscitation with Lactated Ringer’s and normal saline at 2.5 mL/kg·h; piperacillin–tazobactam; vasoactive support; and continuous renal replacement therapy (CRRT) for anuria. He received plasma transfusion and tranexamic acid on day 5, but clinical worsening prompted transfer on day 7.\n\nOn admission to our medical ICU, nasopharyngeal RT-PCR was positive for SARS-CoV-2, meeting criteria for severe COVID-19 (respiratory failure requiring mechanical ventilation, shock, and multiorgan failure requiring ICU). He had no in-hospital exposures, consistent with community-acquired infection. Examination: GCS 3/15 with bilaterally nonreactive, symmetric pupils; HR 106 bpm; BP 126/77 mmHg on norepinephrine 0.4 µg/kg·min. Laboratory data showed severe infection, anemia, thrombocytopenia, DIC, and acute hepatic and renal injury: WBC 3.55→3.13×10^9/L, lymphocytes 0.25→0.1×10^9/L, N% 85.3%, procalcitonin 2.81 ng/mL, CRP 32.6 mg/L. Microbiology: sputum grew Stenotrophomonas maltophilia and Candida lipolytica; central venous catheter culture grew Staphylococcus epidermidis; serial blood cultures were negative. CT demonstrated bilateral frontal subdural effusion; lower-lobe consolidation and atelectasis; right upper lobe inflammation; bilateral pleural effusions; and small-volume ascites.\n\nICU course included SIMV with PEEP 5 mmH2O and FiO2 0.80; continuous norepinephrine and pituitrin for hemodynamic support; hepatic/renal support with polyene phosphatidylcholine, adenosylmethionine budisulfonate, ulinastatin, and hemofiltration; antimicrobial escalation to meropenem; Thymalfasin for 20 days; mannitol for 3 days for intracranial pressure; and coagulopathy management with plasma and cryoprecipitate transfusions, continuous IV heparin 6000 U/day, and CRRT with sodium citrate anticoagulation 8 g/day (day 7). Platelet transfusion was given on day 9. Tc fluctuated between 36–38.5°C. CRRT was continued without anticoagulation on day 8. On day 9 he developed GI hemorrhage and fever; EGD showed no active bleeding. He received RBC transfusion, hemostatic therapy, and acid suppression. Teicoplanin was added after MRSA was isolated from sputum. By day 13 he regained consciousness (GCS 14/15) with moderate fever; GI bleeding had ceased; he was extubated. Creatinine rose after CRRT was stopped on day 12.\n\nOn day 17 he acutely deteriorated with dyspnea, SpO2 <85%, and fever to 39.3°C, necessitating reintubation. Bronchoscopy showed scant sputum. Coma recurred (GCS 3/15). Labs: WBC 14.94×10^9/L, NEU 13.77×10^9/L; total bilirubin 235.2 µmol/L; creatinine 441 µmol/L. Brain CT: right frontal ischemic stroke and right occipital hemorrhagic infarction. Cooling was provided via CRRT with ice-cold replacement fluid. Meropenem and teicoplanin were continued. Carpofungin was started on day 18 for elevated serum Aspergillus galactomannan, Aspergillus IgG, and Candida mannan. SARS-CoV-2 RT-PCR subsequently turned negative.\n\nBy day 20, fever and infection indices improved, but he developed cerebral hemorrhage with herniation (bilateral fixed dilated pupils). Dehydration therapy for intracranial hypertension was given; neurosurgery was declined. On day 22, infection markers and AST/creatinine rose again; BALF cultured carbapenem-resistant Acinetobacter baumannii and Aspergillus fumigatus. Combination therapy with meropenem, teicoplanin, and Carpofungine was continued. Despite comprehensive antimicrobial therapy, organ support, and repeated attempts to correct a refractory coagulopathy, he progressed to multi-pathogen pulmonary infection, intractable coagulopathy, MODS, and died on day 29.",
+    "summary": "We report the first case of heatstroke comorbid with Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection in a 52-year-old male. After receiving intravenous antibiotics, organ protection measures, and treatment for coagulation disorders, his fever and coma resolved. However, he developed dyspnea and cerebral hemorrhage after several days. This patient experienced a multi-pathogen pulmonary infection and an intractable coagulopathy that ultimately resulted in MODS and death."
+  },
+  {
+    "doc_id": 60,
+    "label": "proficient_health_literacy",
+    "fulltext": "A 19-year-old female presented to our hospital’s emergency room with a chief complaint of a two-day history of headache, accompanied by recurrent nausea, vomiting, and a one-day fever. On admission, her physical examination revealed a high fever of 39.1°C, elevated blood pressure at 189/120 mmHg, and a pulse rate of 148 beats per minute. Laboratory results indicated an elevated white blood cell count of 14.77×10^9/L and a neutrophil count of 13.55×10^9/L, suggesting a possible infection or inflammatory response. Initial empirical treatment with antibiotics was administered due to suspected infection, but her symptoms persisted. Given her abnormal vital signs, elevated inflammatory markers, and lack of symptom improvement, the patient was admitted for further diagnostic evaluation and transferred to the intensive care unit for close monitoring. A year prior, the patient had presented with similar symptoms and was diagnosed with myocarditis at a local hospital based on clinical findings at that time. During that hospitalization, she was also diagnosed with hypertension and prescribed antihypertensive medications. However, after discharge, the patient did not adhere to the prescribed antihypertensive therapy and did not regularly monitor her blood pressure. Additionally, it is notable that her father had a history of sudden, unexplained death.\n\nTo investigate the underlying etiology of the patient’s symptoms, a chest computed tomography (CT) scan was performed. Incidentally, this scan revealed a left adrenal mass with soft tissue density, measuring 43 mm × 36 mm. No pathological findings were observed in the head and chest CT scans. The electrocardiogram demonstrated sinus tachycardia with a shortened PR interval and tall, peaked P-waves in leads II, III, and aVF. Transthoracic echocardiography did not reveal any significant abnormalities.\n\nOn the second day of admission, the patient exhibited rising levels of brain natriuretic peptide (BNP) and Troponin I (TnI). The cardiologist provisionally diagnosed the patient with myocarditis of uncertain etiology, based on clinical presentation, elevated cardiac biomarkers (BNP and TnI), and supportive electrocardiogram findings. Treatment was initiated with methylprednisolone (0.25 g daily) to address potential myocardial inflammation due to suspected myocarditis. Furosemide (20 mg every 12 hours) and spironolactone (20 mg every 12 hours) were administered as diuretics to manage fluid retention and reduce cardiac workload. Perindopril amlodipine (10 mg: 5 mg daily) was prescribed as an angiotensin-converting enzyme inhibitor and calcium channel blocker combination to control blood pressure and reduce afterload. Metoprolol tartrate (25 mg every 12 hours) was used to manage heart rate and decrease myocardial oxygen demand, while esmolol (0.2 g/hour intravenous infusion), a short-acting beta-blocker, was administered for additional acute heart rate control due to sinus tachycardia. Due to concerns about a potential infection, moxifloxacin was added as empiric antibiotic therapy.\n\nGiven the patient’s presentation with an adrenal mass and hypertension, the endocrinologist recommended an evaluation of the aldosterone-to-renin ratio, plasma cortisol, plasma catecholamines, and 24-hour urinary catecholamines along with their metabolites. In the recumbent position, plasma and urinary catecholamine levels were markedly elevated (Table 1), including plasma dopamine at 524.5 pmol/L, norepinephrine at 83975 pmol/L, and epinephrine at 10579.3 pmol/L. Additionally, the 24-hour urinary levels showed free adrenaline at 4368.89 nmol/24 hours, free norepinephrine exceeding 12697.60 nmol/24 hours, normetanephrine at 8312 nmol/24 hours, metanephrines at 4078 nmol/24 hours, and vanillylmandelic acid at 58.1 mg/24 hours. These findings supported a clinical diagnosis of pheochromocytoma. On the fifth day post-admission, glucocorticoid therapy was discontinued, and perindopril amlodipine was substituted with terazosin for more targeted blood pressure management.\n\nAn enhanced abdominal CT scan further confirmed a left adrenal mass, highly suggestive of pheochromocytoma. Additionally, after obtaining informed consent, whole-exome sequencing was performed, revealing a heterozygous missense mutation, c.1900T > C: p. Cys634Arg, in the RET gene, leading to a substitution of cysteine with arginine at codon 634. This mutation raised suspicion for multiple endocrine neoplasia syndrome, prompting further evaluation of the thyroid and parathyroid glands. Thyroid color Doppler ultrasound identified a hypoechoic mass measuring 6 mm × 4 mm in the left thyroid lobe, and a mild elevation in calcitonin levels was noted. No additional significant abnormalities were detected.\n\nAs the patient’s condition gradually improved, plasma cortisol and ACTH levels returned to normal. The patient was subsequently discharged with a prescription for metoprolol tartrate (100 mg every 12 hours) and ivabradine hydrochloride (5 mg every 12 hours) for home management. Three months later, after achieving stable clinical status, the patient underwent resection of the left adrenal tumor, which measured 50 mm × 40 mm × 30 mm. Immunohistochemical analysis confirmed positive staining for Vim, CD56, Syn, CgA, and NSE, with S-100 positive in Sertoli cells, while CKpan, CD10, MART-1/Melan-A, and Melan-A were negative. The Ki67 index was 1%, leading to a definitive diagnosis of adrenal pheochromocytoma. The patient was discharged without further medications and has since been regularly followed up postoperatively without recurrence of symptoms. Over a 15-month postoperative follow-up, the patient exhibited persistently mild hypercalcitoninemia with stable thyroid nodule size, while PTH and serum calcium levels showed a progressive increase (Table 2). Further parathyroid scintigraphy using 99mTc-MIBI was performed, and the conclusion was a negative result for parathyroid adenoma.",
+    "diff_label_texts": "A 19-year-old female presented with a 2-day history of headache plus recurrent nausea/vomiting and a 1-day fever. On admission: T 39.1°C, BP 189/120 mmHg, HR 148 bpm. Laboratory testing showed WBC 14.77×10^9/L and neutrophils 13.55×10^9/L. She received empiric antibiotics and was admitted to the ICU. One year prior she had similar symptoms and was diagnosed with myocarditis; hypertension was diagnosed at that time, but she was nonadherent post-discharge. Family history was notable for her father’s sudden unexplained death.\n\nChest CT incidentally identified a left adrenal soft-tissue mass measuring 43 × 36 mm; head and chest CT had no other pathologies. ECG showed sinus tachycardia with a shortened PR interval and tall, peaked P waves in II, III, and aVF. Transthoracic echocardiography was without significant abnormalities.\n\nOn hospital day 2, BNP and troponin I increased. Cardiology provisionally diagnosed myocarditis of uncertain etiology. She was treated with methylprednisolone 0.25 g daily, furosemide 20 mg q12h, spironolactone 20 mg q12h, perindopril amlodipine (10 mg:5 mg daily), metoprolol tartrate 25 mg q12h, and an esmolol infusion at 0.2 g/h; moxifloxacin was added empirically. Despite high-dose glucocorticoids, she did not develop a catecholamine crisis.\n\nGiven the adrenal mass and hypertension, endocrine testing was pursued. In the recumbent position, plasma catecholamines were markedly elevated: dopamine 524.5 pmol/L, norepinephrine 83,975 pmol/L, epinephrine 10,579.3 pmol/L. Twenty-four-hour urine showed free adrenaline 4,368.89 nmol/24 h, free norepinephrine >12,697.60 nmol/24 h, normetanephrine 8,312 nmol/24 h, metanephrines 4,078 nmol/24 h, and vanillylmandelic acid 58.1 mg/24 h, supporting pheochromocytoma. On day 5, glucocorticoids were discontinued and perindopril/amlodipine was changed to terazosin for targeted blood pressure control. Contrast-enhanced abdominal CT confirmed a left adrenal mass highly suggestive of pheochromocytoma.\n\nWhole-exome sequencing identified a heterozygous missense RET mutation, c.1900T > C: p.Cys634Arg, prompting MEN2 evaluation. Thyroid Doppler ultrasound showed a 6 × 4 mm hypoechoic nodule in the left lobe with mildly elevated calcitonin; no other significant abnormalities were detected.\n\nAs her condition improved, plasma cortisol and ACTH normalized. She was discharged on metoprolol tartrate 100 mg q12h and ivabradine 5 mg q12h. Three months later, she underwent resection of a 50 × 40 × 30 mm left adrenal tumor. Immunohistochemistry was positive for Vim, CD56, Syn, CgA, and NSE; S-100 was positive in Sertoli cells; CKpan, CD10, MART-1/Melan-A, and Melan-A were negative. Ki-67 was 1%. The final diagnosis was adrenal pheochromocytoma. She was discharged without medications and remained asymptomatic on follow-up.\n\nOver 15 months postoperatively, she had persistently mild hypercalcitoninemia with stable thyroid nodule size, while PTH and serum calcium progressively increased. 99mTc-MIBI parathyroid scintigraphy was negative for parathyroid adenoma.\n\nContext and implications: Glucocorticoids are recognized precipitants of hypertensive crisis in pheochromocytoma, yet no crisis occurred here despite a significant tumor and high-dose methylprednisolone. The RET c.1900T > C (p.Cys634Arg) variant is classically associated with MEN2A, which confers high penetrance of medullary thyroid carcinoma and pheochromocytoma and variable primary hyperparathyroidism. The rising PTH and serum calcium with a negative MIBI scan are compatible with early or multigland parathyroid disease, which is common in MEN2A and may be scintigraphically occult when glands are small or hyperplastic.",
+    "summary": "We report the case of a 19-year-old female who presented with pheochromocytoma without experiencing a crisis, despite having a significant adrenal mass and undergoing high-dose glucocorticoid treatment. Genetic testing revealed a heterozygous missense mutation in the RET gene (c.1900T > C: p. Cys634Arg), associated with MEN2A. Further endocrine evaluation identified a thyroid nodule with mildly elevated calcitonin levels, but normal electrolyte and parathyroid hormone levels. Over a 15-month postoperative follow-up, the patient exhibited persistently mild hypercalcitoninemia with stable thyroid nodule size, while PTH and serum calcium levels showed a progressive increase. Further parathyroid scintigraphy using 99mTc-MIBI was performed, yielding a negative result for parathyroid adenoma."
+  },
+  {
+    "doc_id": 61,
+    "label": "low_health_literacy",
+    "fulltext": "February 2020, a 36-year-old with no significant past medical history presented with 5 years history of left sided penoscrotal mass. He has no lower urinary tract symptoms. No History of trauma or infections and he denied any history of weight loss, anorexia or fever. On examination, there is a smooth surface, tender cystic lesion around 20 mm ∗ 20 mm attached to the left side of the bulbar urethra at the penoscrotal junction, it was deep without any skin tethering and not related to the left spermatic cord and it was partially mobile.\n\nDoppler ultrasonography showed a well-defined hypoechoic mass measuring 2.7 ∗ 3.1 ∗ 2.0 cm with significantly increased vascularity at the left of penoscrotal junction. Pelvis Magnetic resonance imaging revealed a mass in the left inferolateral side of the base of the penis with a clear fat plane, which is isointense to the testes in the T2 weighted imaging, T1 weighted imaging and Diffusion-weighted imaging and it was connected to the vas deferens, no lymphadenopathy was noted. Alpha fetoprotein and beta-human chronic gonadotrophin levels were all in the normal range. Given the results of workup and the pain experienced by the patient, a decision was made to proceed with surgical removal of the mass for both diagnostic and therapeutic purposes. During surgery, a mass was seen in the left posterolateral of the scrotum and it was resected completely and sent for histopathology.\n\nHistopathology of the mass showed cellular spindle cell tumour arranged into interlacing fascicle, the cells have spindle to oval vesicular nuclei with evenly dispersed chromatin and inconspicuous nucleoli. The tumour showed high mitotic activity reaching up to 3/High-power field. Immunohistochemistry analysis was consistent with synovial sarcoma, revealing a positive TLE-1, CD99, B-cell lymphoma 2 (BLC2), Focal cytokeratin and focal epithelial membrane antigen (EMA). The material was sent for Fluorescence in situ hybridization (FISH) and reported a rearrangement of the SS18 gene at 18q11.2 which has been observed in synovial sarcomas. The mass margins were difficult to be assessed by histopathology as the sample had fragmented margins.\n\nThe patient presented to the clinic after 2 weeks and given the histopathology report, a re-resection with wider margin was discussed with the patient and he agreed. Positron emission tomography – Computed tomography (PET/CT) was done for Head and Neck, Chest, Abdomen, Pelvis and musculoskeletal structures. Only a 29 ∗ 27 mm thyroid nodule in the lower pole of the left thyroid lobe with moderate hypermetabolism at standardized uptake values (SUVs) of 4.9. Thyroid US showed a solid isoechoic well-defined nodule in the lower pole of the left thyroid lobe with no echogenic foci, Thyroid Imaging Reporting and Data System (TIRADS) was TR3.\n\nA second resection was made 3 weeks from the first one. The whole specimen was resected from both cords bilaterally which was deepened until reaching the corpus spongiosum which was shaved superiorly up to the urethra. The specimen was sent for histopathology. The resected mass was 6.0 ∗ 6.0 ∗ 3.0 cm in size, and it was negative for any pathology. The patient then went into active surveillance and after 16 months of active surveillance he was found to have metastatic lesions in the sixth liver segment and L1 vertebral body. Oncology team started chemotherapy regimen of Ifosfamide and Doxorubicin for 6 cycles with no improvement in the liver lesion. Surgical resection was made for the Fifth and Sixth liver sections with cholecystectomy. Patient then developed a new lung lesion and was started on Pazopanib and Stereotactic Body Radiation Therapy SBRT. The patient then underwent surveillance for 6 months then developed new liver and lung lesions then chemotherapy regimen of Gemcitabine and Docetaxel combination for 3 cycles and progressed then he was started 2 cycles of Dacarbazine and progressed then 2 cycles of Pembrolizumab and progressed. The patient then was shifted to palliative care, and he stopped following up.",
+    "diff_label_texts": "A 36-year-old man had a painful lump where the penis meets the scrotum for five years. Doctors took the lump out with surgery. Lab tests on the tissue confirmed it was a tumor. He had a second surgery to remove more tissue. Even with these surgeries, the disease spread to other parts of his body. It kept getting worse even after trying different chemotherapy medicines.",
+    "summary": "A 36-year-old man presented with a tender penoscrotal mass for 5 years. The patient underwent surgical resection of the mass. Histopathology revealed cellular spindle cell tumour arranged into interlacing fascicle, Immunohistochemistry analysis revealed a positive TLE-1, CD99, B-cell lymphoma 2 (BLC2), Focal cytokeratin and focal epithelial membrane antigen (EMA). In our case, the patient was aggressively treated with two surgical resections and still progressed and metastasized and continued progressing even after different chemotherapy regimens."
+  },
+  {
+    "doc_id": 61,
+    "label": "intermediate_health_literacy",
+    "fulltext": "February 2020, a 36-year-old with no significant past medical history presented with 5 years history of left sided penoscrotal mass. He has no lower urinary tract symptoms. No History of trauma or infections and he denied any history of weight loss, anorexia or fever. On examination, there is a smooth surface, tender cystic lesion around 20 mm ∗ 20 mm attached to the left side of the bulbar urethra at the penoscrotal junction, it was deep without any skin tethering and not related to the left spermatic cord and it was partially mobile.\n\nDoppler ultrasonography showed a well-defined hypoechoic mass measuring 2.7 ∗ 3.1 ∗ 2.0 cm with significantly increased vascularity at the left of penoscrotal junction. Pelvis Magnetic resonance imaging revealed a mass in the left inferolateral side of the base of the penis with a clear fat plane, which is isointense to the testes in the T2 weighted imaging, T1 weighted imaging and Diffusion-weighted imaging and it was connected to the vas deferens, no lymphadenopathy was noted. Alpha fetoprotein and beta-human chronic gonadotrophin levels were all in the normal range. Given the results of workup and the pain experienced by the patient, a decision was made to proceed with surgical removal of the mass for both diagnostic and therapeutic purposes. During surgery, a mass was seen in the left posterolateral of the scrotum and it was resected completely and sent for histopathology.\n\nHistopathology of the mass showed cellular spindle cell tumour arranged into interlacing fascicle, the cells have spindle to oval vesicular nuclei with evenly dispersed chromatin and inconspicuous nucleoli. The tumour showed high mitotic activity reaching up to 3/High-power field. Immunohistochemistry analysis was consistent with synovial sarcoma, revealing a positive TLE-1, CD99, B-cell lymphoma 2 (BLC2), Focal cytokeratin and focal epithelial membrane antigen (EMA). The material was sent for Fluorescence in situ hybridization (FISH) and reported a rearrangement of the SS18 gene at 18q11.2 which has been observed in synovial sarcomas. The mass margins were difficult to be assessed by histopathology as the sample had fragmented margins.\n\nThe patient presented to the clinic after 2 weeks and given the histopathology report, a re-resection with wider margin was discussed with the patient and he agreed. Positron emission tomography – Computed tomography (PET/CT) was done for Head and Neck, Chest, Abdomen, Pelvis and musculoskeletal structures. Only a 29 ∗ 27 mm thyroid nodule in the lower pole of the left thyroid lobe with moderate hypermetabolism at standardized uptake values (SUVs) of 4.9. Thyroid US showed a solid isoechoic well-defined nodule in the lower pole of the left thyroid lobe with no echogenic foci, Thyroid Imaging Reporting and Data System (TIRADS) was TR3.\n\nA second resection was made 3 weeks from the first one. The whole specimen was resected from both cords bilaterally which was deepened until reaching the corpus spongiosum which was shaved superiorly up to the urethra. The specimen was sent for histopathology. The resected mass was 6.0 ∗ 6.0 ∗ 3.0 cm in size, and it was negative for any pathology. The patient then went into active surveillance and after 16 months of active surveillance he was found to have metastatic lesions in the sixth liver segment and L1 vertebral body. Oncology team started chemotherapy regimen of Ifosfamide and Doxorubicin for 6 cycles with no improvement in the liver lesion. Surgical resection was made for the Fifth and Sixth liver sections with cholecystectomy. Patient then developed a new lung lesion and was started on Pazopanib and Stereotactic Body Radiation Therapy SBRT. The patient then underwent surveillance for 6 months then developed new liver and lung lesions then chemotherapy regimen of Gemcitabine and Docetaxel combination for 3 cycles and progressed then he was started 2 cycles of Dacarbazine and progressed then 2 cycles of Pembrolizumab and progressed. The patient then was shifted to palliative care, and he stopped following up.",
+    "diff_label_texts": "A 36-year-old man had a tender lump at the junction of the penis and scrotum for five years. Surgeons removed the mass. Under the microscope, it was a spindle cell tumor, and special staining supported a diagnosis consistent with synovial sarcoma. He then had a second, wider surgery. Despite these aggressive steps, the cancer spread to other parts of the body and kept progressing even after multiple chemotherapy treatments.",
+    "summary": "A 36-year-old man presented with a tender penoscrotal mass for 5 years. The patient underwent surgical resection of the mass. Histopathology revealed cellular spindle cell tumour arranged into interlacing fascicle, Immunohistochemistry analysis revealed a positive TLE-1, CD99, B-cell lymphoma 2 (BLC2), Focal cytokeratin and focal epithelial membrane antigen (EMA). In our case, the patient was aggressively treated with two surgical resections and still progressed and metastasized and continued progressing even after different chemotherapy regimens."
+  },
+  {
+    "doc_id": 61,
+    "label": "proficient_health_literacy",
+    "fulltext": "February 2020, a 36-year-old with no significant past medical history presented with 5 years history of left sided penoscrotal mass. He has no lower urinary tract symptoms. No History of trauma or infections and he denied any history of weight loss, anorexia or fever. On examination, there is a smooth surface, tender cystic lesion around 20 mm ∗ 20 mm attached to the left side of the bulbar urethra at the penoscrotal junction, it was deep without any skin tethering and not related to the left spermatic cord and it was partially mobile.\n\nDoppler ultrasonography showed a well-defined hypoechoic mass measuring 2.7 ∗ 3.1 ∗ 2.0 cm with significantly increased vascularity at the left of penoscrotal junction. Pelvis Magnetic resonance imaging revealed a mass in the left inferolateral side of the base of the penis with a clear fat plane, which is isointense to the testes in the T2 weighted imaging, T1 weighted imaging and Diffusion-weighted imaging and it was connected to the vas deferens, no lymphadenopathy was noted. Alpha fetoprotein and beta-human chronic gonadotrophin levels were all in the normal range. Given the results of workup and the pain experienced by the patient, a decision was made to proceed with surgical removal of the mass for both diagnostic and therapeutic purposes. During surgery, a mass was seen in the left posterolateral of the scrotum and it was resected completely and sent for histopathology.\n\nHistopathology of the mass showed cellular spindle cell tumour arranged into interlacing fascicle, the cells have spindle to oval vesicular nuclei with evenly dispersed chromatin and inconspicuous nucleoli. The tumour showed high mitotic activity reaching up to 3/High-power field. Immunohistochemistry analysis was consistent with synovial sarcoma, revealing a positive TLE-1, CD99, B-cell lymphoma 2 (BLC2), Focal cytokeratin and focal epithelial membrane antigen (EMA). The material was sent for Fluorescence in situ hybridization (FISH) and reported a rearrangement of the SS18 gene at 18q11.2 which has been observed in synovial sarcomas. The mass margins were difficult to be assessed by histopathology as the sample had fragmented margins.\n\nThe patient presented to the clinic after 2 weeks and given the histopathology report, a re-resection with wider margin was discussed with the patient and he agreed. Positron emission tomography – Computed tomography (PET/CT) was done for Head and Neck, Chest, Abdomen, Pelvis and musculoskeletal structures. Only a 29 ∗ 27 mm thyroid nodule in the lower pole of the left thyroid lobe with moderate hypermetabolism at standardized uptake values (SUVs) of 4.9. Thyroid US showed a solid isoechoic well-defined nodule in the lower pole of the left thyroid lobe with no echogenic foci, Thyroid Imaging Reporting and Data System (TIRADS) was TR3.\n\nA second resection was made 3 weeks from the first one. The whole specimen was resected from both cords bilaterally which was deepened until reaching the corpus spongiosum which was shaved superiorly up to the urethra. The specimen was sent for histopathology. The resected mass was 6.0 ∗ 6.0 ∗ 3.0 cm in size, and it was negative for any pathology. The patient then went into active surveillance and after 16 months of active surveillance he was found to have metastatic lesions in the sixth liver segment and L1 vertebral body. Oncology team started chemotherapy regimen of Ifosfamide and Doxorubicin for 6 cycles with no improvement in the liver lesion. Surgical resection was made for the Fifth and Sixth liver sections with cholecystectomy. Patient then developed a new lung lesion and was started on Pazopanib and Stereotactic Body Radiation Therapy SBRT. The patient then underwent surveillance for 6 months then developed new liver and lung lesions then chemotherapy regimen of Gemcitabine and Docetaxel combination for 3 cycles and progressed then he was started 2 cycles of Dacarbazine and progressed then 2 cycles of Pembrolizumab and progressed. The patient then was shifted to palliative care, and he stopped following up.",
+    "diff_label_texts": "A 36-year-old man presented with a 5-year history of a tender left penoscrotal mass attached to the left side of the bulbar urethra at the penoscrotal junction; on exam it was a deep, smooth, tender, partially mobile cystic lesion (~20 × 20 mm) without skin tethering and not involving the spermatic cord. Doppler ultrasound showed a well-defined hypoechoic mass (2.7 × 3.1 × 2.0 cm) with marked vascularity. Pelvic MRI demonstrated a mass at the left inferolateral base of the penis with a clear fat plane, isointense to the testes on T1, T2, and diffusion-weighted sequences, connected to the vas deferens, without lymphadenopathy. Serum AFP and β-hCG were normal. The mass was excised for diagnosis and symptom control. Pathology revealed a cellular spindle cell tumor arranged in interlacing fascicles with spindle-to-oval vesicular nuclei, evenly dispersed chromatin, and inconspicuous nucleoli; mitotic activity reached up to 3/HPF. Immunohistochemistry was positive for TLE-1, CD99, and BCL2 with focal cytokeratin and focal EMA, supporting synovial sarcoma. FISH demonstrated SS18 gene rearrangement at 18q11.2, confirming the diagnosis. Margins were difficult to assess due to specimen fragmentation. Two weeks later, a wider re-resection was performed; the specimen (6.0 × 6.0 × 3.0 cm), resected deeply to the corpus spongiosum with shaving up to the urethra, showed no residual tumor. Staging PET/CT was notable only for an incidental left thyroid nodule (29 × 27 mm, SUV 4.9; TR3 on ultrasound). After 16 months of surveillance, metastatic disease developed in liver segment VI and the L1 vertebral body. Systemic ifosfamide/doxorubicin (6 cycles) produced no response in the liver lesion. He subsequently underwent hepatic resection of segments V and VI with cholecystectomy. New pulmonary lesions later emerged; therapy included pazopanib and stereotactic body radiation therapy, followed by gemcitabine/docetaxel (3 cycles), dacarbazine (2 cycles), and pembrolizumab (2 cycles), with continued progression. He was transitioned to palliative care and was lost to follow-up. Overall, this case represents a primary penoscrotal synovial sarcoma with SS18 rearrangement and an aggressive, treatment-refractory course despite two surgical resections and multiple systemic regimens.",
+    "summary": "A 36-year-old man presented with a tender penoscrotal mass for 5 years. The patient underwent surgical resection of the mass. Histopathology revealed cellular spindle cell tumour arranged into interlacing fascicle, Immunohistochemistry analysis revealed a positive TLE-1, CD99, B-cell lymphoma 2 (BLC2), Focal cytokeratin and focal epithelial membrane antigen (EMA). In our case, the patient was aggressively treated with two surgical resections and still progressed and metastasized and continued progressing even after different chemotherapy regimens."
+  },
+  {
+    "doc_id": 62,
+    "label": "low_health_literacy",
+    "fulltext": "A 13-year-old adolescent male, with no significant previous medical history, presented to the emergency department with a 3-day history of acute bilateral pleuritic chest pain associated with mild non-productive cough and no dyspnea. Associated with this, he had mild rhinorrhea and a single febrile episode that day (temperature of 38ºC). Chest pain was localized to the costal margin region and worsened with cough, without diurnal variation. The patient-reported relief with paracetamol. There were no complaints of joint pain, weight loss, anorexia, fatigue, episodes of syncope or exercise restriction. In fact, he practiced sports regularly—canoeing 2 times a week. No evidence of an infectious exposure or contact with household or environmental fumes, dust, or mineral oils was described. There was no known family history of cardiopulmonary conditions. He had a chest radiograph taken 4 years earlier during an acute illness, which showed a marked interstitial infiltrate that was presumptively treated with azithromycin with no further clinical symptoms and no further follow-up.\n\nOn admission, the patient’s temperature was 37.8°C with normal peripheral oxygen saturation (99%) in room air. His heart (93 beats per minute) and respiratory rate (15 breaths per minute) were normal and blood pressure was on the 85th percentile (115/66 mmHg). Physical examination revealed diminished breath sounds in the lower two thirds of the chest with no adventitious sounds. No respiratory distress, finger clubbing, cyanosis, abnormal heart sounds, or other findings were present. Chest radiograph revealed a marked interstitial infiltrate, comparable with his previous examination. A thoracic computed tomography (CT) revealed multiple bilateral areas of ground-glass opacities involving > 65% of lung parenchyma, suggestive of PAP. Respiratory viral testing was negative, and he remained stable throughout his monitoring in the emergency department. He was discharged with empiric antibiotics (amoxicillin-clavulanic acid and azithromycin) to cover a potential respiratory infection, with clinical resolution of symptoms and was sent for follow-up at the pediatric respiratory clinic.\n\nUpon further investigation in the outpatient setting, positive antinuclear antibodies (ANAs) at a titer of 1/89 with a fine speckled pattern were detected, while other autoantibodies tested negative and immunoglobulin levels remained within normal limits. Bronchoalveolar lavage revealed fluid with a milky appearance and positive periodic acid-Schiff staining; microbiological examination, including for mycobacteria, returned negative results. Spirometry indicated a mild restrictive pattern with reduced forced vital capacity (FVC) at 2.92 L (77%) and forced expiratory volume in 1 second (FEV1) at 3.21 L (69.9%), alongside a normal FEV1/FVC ratio (109%). In addition, the DLCO single breath (SB) showed a moderate decrease at 13.8 ml/min/mmHg (48.6%). Suspecting PAP, a genetic panel was conducted, which showed no mutations associated with surfactant dysfunction. Subsequently, GM-CSF antibody testing was performed with a positive result, raising suspicion for AI-PAP. At 20 months of follow-up, the patient remains asymptomatic and continues to exercise regularly. He repeated spirometry testing with normal FVC at 4.03 L (81.3%); FEV1 at 3.71 L (87.5%); FEV1/FVC ratio at 91.96% and DLCO SB at 25.54 ml/min/mmHg (83.7%). As the patient remains stable with no respiratory symptoms, we decided to defer treatment and continue monitoring with regular clinic visits.",
+    "diff_label_texts": "This report is about a 13-year-old boy. He came to the ER with sharp chest pain that hurt more when he took a deep breath. He did not feel sick otherwise. His oxygen level was normal at 98% on room air. The lower parts of his chest sounded quieter when the doctor listened. A chest X-ray looked like one he had 4 years earlier. A CT scan showed many hazy and crisscross areas in both lungs, covering more than half of the lungs. This pointed to a rare lung problem called PAP, where material builds up in the air sacs. Tests for viruses, including COVID-19, were negative. A gentle lung wash showed milky fluid, and a special lab stain was positive. Breathing tests showed his lungs held a little less air than expected and moved oxygen less well. A gene test did not find a known cause. A blood test found strong antibodies that mean the body’s own immune system is likely causing this problem. About 20 months later, he feels well, and his breathing tests are normal.",
+    "summary": "We describe the case of a 13-year-old adolescent male who presented to the emergency department with acute pleuritic chest pain not associated with systemic complaints. On examination, he had diminished breath sounds in the lower two thirds of the chest with no other abnormal findings; SpO2 (oxygen saturation) was 98% on room air. Chest radiograph revealed a marked interstitial infiltrate, comparable with the one taken 4 years earlier during an acute illness that was presumptively treated with azithromycin. A computed tomography (CT) scan revealed multiple bilateral areas of ground-glass opacities with areas of crazy paving, involving > 65% of lung parenchyma, suggestive of pulmonary alveolar proteinosis (PAP). Respiratory viral testing, including for coronavirus (SARS-CoV2), was negative. Bronchoalveolar lavage performed in the outpatient setting revealed a milky fluid and positive periodic acid-Schiff staining. Spirometry indicated a mild restrictive pattern (forced vital capacity [FVC] = 77%) and diffusing capacity of the lungs for carbon monoxide (DLCO) showed a moderate decrease at 48.6%. No mutations associated with surfactant dysfunction were found on the genetic panel. Anti-granulocyte macrophage colony-stimulating factor (GM-CSF) antibody testing was strongly positive, raising suspicion for autoimmune PAP. At 20 months of follow-up, the patient remains asymptomatic with a normal spirometry."
+  },
+  {
+    "doc_id": 62,
+    "label": "proficient_health_literacy",
+    "fulltext": "A 13-year-old adolescent male, with no significant previous medical history, presented to the emergency department with a 3-day history of acute bilateral pleuritic chest pain associated with mild non-productive cough and no dyspnea. Associated with this, he had mild rhinorrhea and a single febrile episode that day (temperature of 38ºC). Chest pain was localized to the costal margin region and worsened with cough, without diurnal variation. The patient-reported relief with paracetamol. There were no complaints of joint pain, weight loss, anorexia, fatigue, episodes of syncope or exercise restriction. In fact, he practiced sports regularly—canoeing 2 times a week. No evidence of an infectious exposure or contact with household or environmental fumes, dust, or mineral oils was described. There was no known family history of cardiopulmonary conditions. He had a chest radiograph taken 4 years earlier during an acute illness, which showed a marked interstitial infiltrate that was presumptively treated with azithromycin with no further clinical symptoms and no further follow-up.\n\nOn admission, the patient’s temperature was 37.8°C with normal peripheral oxygen saturation (99%) in room air. His heart (93 beats per minute) and respiratory rate (15 breaths per minute) were normal and blood pressure was on the 85th percentile (115/66 mmHg). Physical examination revealed diminished breath sounds in the lower two thirds of the chest with no adventitious sounds. No respiratory distress, finger clubbing, cyanosis, abnormal heart sounds, or other findings were present. Chest radiograph revealed a marked interstitial infiltrate, comparable with his previous examination. A thoracic computed tomography (CT) revealed multiple bilateral areas of ground-glass opacities involving > 65% of lung parenchyma, suggestive of PAP. Respiratory viral testing was negative, and he remained stable throughout his monitoring in the emergency department. He was discharged with empiric antibiotics (amoxicillin-clavulanic acid and azithromycin) to cover a potential respiratory infection, with clinical resolution of symptoms and was sent for follow-up at the pediatric respiratory clinic.\n\nUpon further investigation in the outpatient setting, positive antinuclear antibodies (ANAs) at a titer of 1/89 with a fine speckled pattern were detected, while other autoantibodies tested negative and immunoglobulin levels remained within normal limits. Bronchoalveolar lavage revealed fluid with a milky appearance and positive periodic acid-Schiff staining; microbiological examination, including for mycobacteria, returned negative results. Spirometry indicated a mild restrictive pattern with reduced forced vital capacity (FVC) at 2.92 L (77%) and forced expiratory volume in 1 second (FEV1) at 3.21 L (69.9%), alongside a normal FEV1/FVC ratio (109%). In addition, the DLCO single breath (SB) showed a moderate decrease at 13.8 ml/min/mmHg (48.6%). Suspecting PAP, a genetic panel was conducted, which showed no mutations associated with surfactant dysfunction. Subsequently, GM-CSF antibody testing was performed with a positive result, raising suspicion for AI-PAP. At 20 months of follow-up, the patient remains asymptomatic and continues to exercise regularly. He repeated spirometry testing with normal FVC at 4.03 L (81.3%); FEV1 at 3.71 L (87.5%); FEV1/FVC ratio at 91.96% and DLCO SB at 25.54 ml/min/mmHg (83.7%). As the patient remains stable with no respiratory symptoms, we decided to defer treatment and continue monitoring with regular clinic visits.",
+    "diff_label_texts": "A previously healthy 13-year-old male presented with 3 days of acute bilateral pleuritic chest pain, mild non-productive cough, no dyspnea, mild rhinorrhea, and a single febrile episode (38°C). Pain localized to the costal margins, was worse with cough, and improved with paracetamol. He denied constitutional symptoms, syncope, or exercise limitation and regularly canoed twice weekly. There were no reported infectious exposures, environmental/occupational inhalational exposures, or family history of cardiopulmonary disease. A prior chest radiograph 4 years earlier during an acute illness showed a marked interstitial infiltrate; he was presumptively treated with azithromycin and had no follow-up.\nOn admission, temperature was 37.8°C, SpO2 99% on room air, HR 93 bpm, RR 15/min, and BP 115/66 mmHg (85th percentile). Exam revealed diminished breath sounds in the lower two thirds of the chest without adventitious sounds; there was no respiratory distress, clubbing, cyanosis, or abnormal heart sounds. Chest radiograph again showed a marked interstitial infiltrate comparable to the prior film. Thoracic CT demonstrated multiple bilateral ground-glass opacities involving >65% of the lung parenchyma, suggestive of pulmonary alveolar proteinosis (PAP). Respiratory viral testing was negative, and he remained clinically stable in the ED. He was discharged on empiric amoxicillin–clavulanate and azithromycin with symptom resolution and referred to a pediatric respiratory clinic.\nOutpatient workup showed positive ANA at 1/89 (fine speckled) with other autoantibodies negative and immunoglobulins within normal limits. Bronchoalveolar lavage returned milky fluid with positive periodic acid–Schiff staining; microbiology including mycobacterial studies was negative. Spirometry demonstrated a mild restrictive ventilatory defect with reduced FVC 2.92 L (77% predicted) and FEV1 3.21 L (69.9% predicted) with a normal FEV1/FVC ratio (109%). DLCO (SB) was moderately reduced at 13.8 ml/min/mmHg (48.6% predicted). A surfactant dysfunction genetic panel identified no pathogenic variants. GM-CSF antibody testing was positive, supporting a diagnosis of autoimmune PAP (AI-PAP). At 20 months, he remains asymptomatic and physically active; repeat testing showed FVC 4.03 L (81.3%), FEV1 3.71 L (87.5%), FEV1/FVC 91.96%, and DLCO (SB) 25.54 ml/min/mmHg (83.7%). Given stable, improving physiology and absence of symptoms, treatment was deferred with ongoing surveillance.\nContext: AI-PAP is mediated by neutralizing anti–GM-CSF antibodies that impair alveolar macrophage–mediated surfactant clearance, producing intra-alveolar lipoproteinaceous material that is PAS-positive and radiographically manifests as diffuse bilateral ground-glass opacities (often with a “crazy paving” pattern). Standard therapies include whole lung lavage and GM-CSF replacement; however, observation is appropriate in stable, minimally symptomatic patients, as in this case.",
+    "summary": "We describe the case of a 13-year-old adolescent male who presented to the emergency department with acute pleuritic chest pain not associated with systemic complaints. On examination, he had diminished breath sounds in the lower two thirds of the chest with no other abnormal findings; SpO2 (oxygen saturation) was 98% on room air. Chest radiograph revealed a marked interstitial infiltrate, comparable with the one taken 4 years earlier during an acute illness that was presumptively treated with azithromycin. A computed tomography (CT) scan revealed multiple bilateral areas of ground-glass opacities with areas of crazy paving, involving > 65% of lung parenchyma, suggestive of pulmonary alveolar proteinosis (PAP). Respiratory viral testing, including for coronavirus (SARS-CoV2), was negative. Bronchoalveolar lavage performed in the outpatient setting revealed a milky fluid and positive periodic acid-Schiff staining. Spirometry indicated a mild restrictive pattern (forced vital capacity [FVC] = 77%) and diffusing capacity of the lungs for carbon monoxide (DLCO) showed a moderate decrease at 48.6%. No mutations associated with surfactant dysfunction were found on the genetic panel. Anti-granulocyte macrophage colony-stimulating factor (GM-CSF) antibody testing was strongly positive, raising suspicion for autoimmune PAP. At 20 months of follow-up, the patient remains asymptomatic with a normal spirometry."
+  },
+  {
+    "doc_id": 63,
+    "label": "low_health_literacy",
+    "fulltext": "27-year-old woman with a history of uncontrolled asthma, mild SARS-CoV-2 infection. In March 2021, she consulted a doctor for pain in the left hemicara and trismus. She reported having completed 48 hours before the antibiotic treatment with phenoxymethyl penicillin 1,000,000 IU daily orally for five days for a peritonsillar abscess. She was hemodynamically stable at the physical examination, without the need for supplemental oxygen, and without relevant findings in respiratory symptoms. The head and neck examination showed a soft, painful, cervical adenopathy, palpable and painful, predominantly homolateral and trismus. Complementary studies were performed. The admission laboratory reported leukocytosis, platelopenia, increased acute phase reactants and the rest of the parameters within normal values. An angiotomy of the craniofacial mass was performed, where a large thrombus was found in the internal and external carotid arteries. Studies were completed with a chest tomography and arterial Doppler ultrasound of neck vessels with no relevant findings. Early intravenous antibiotic treatment was initiated with ceftriaxone 1 g every 12 hours, clindamycin 300 mg every 6 hours and anticoagulation with enoxaparin adjusted to body weight and renal function, 60 mg subcutaneously every 12 hours. The patient evolved 72 hours after initiating the directed treatment with a fever of 38.5 °C and increased leukocytosis, so new complementary studies were performed, including a Doppler ultrasound of the heart without finding cardiac vegetations and a chest tomography where bilateral pulmonary septic emboli were found. With the admission hemocultures negative, a new admission of 3 units, culture of pharyngeal exudate and rotation of ceftriaxone to piperacillin tazobactam 4.5 g every 6 hours intravenous was decided. The patient evolved favorably, without rescue of germs in cultures. After 14 days of initiating the new therapeutic scheme, and with a control chest tomography without pulmonary lesions, it was decided to continue antibiotic treatment with oral clindamycin 300 mg every 6 hours, anticoagulation with acenocumarol adjusted to body weight and hospital discharge.\n",
+    "diff_label_texts": "A 27-year-old woman got face swelling and a tight jaw two days after finishing penicillin for a tooth infection. A blood clot is like a plug that blocks a pipe. A scan of her neck found a big clot in a neck vein. A scan of her chest showed the infection had sent clots to her lungs. Doctors gave strong antibiotics through a vein right away. They also gave blood thinners to treat the clot.",
+    "summary": "A 27-year-old woman presented with facial oedema and trismus 48 hours after completing treatment with phenoxymethylpenicillin for an odontogenic infection. A head and neck CT scan showed a large thrombus in the internal jugular vein and a chest CT scan showed pulmonary septic embolism. Treatment consisted of early intravenous broad spectrum antibiotics and anticoagulation.\n"
+  },
+  {
+    "doc_id": 63,
+    "label": "intermediate_health_literacy",
+    "fulltext": "27-year-old woman with a history of uncontrolled asthma, mild SARS-CoV-2 infection. In March 2021, she consulted a doctor for pain in the left hemicara and trismus. She reported having completed 48 hours before the antibiotic treatment with phenoxymethyl penicillin 1,000,000 IU daily orally for five days for a peritonsillar abscess. She was hemodynamically stable at the physical examination, without the need for supplemental oxygen, and without relevant findings in respiratory symptoms. The head and neck examination showed a soft, painful, cervical adenopathy, palpable and painful, predominantly homolateral and trismus. Complementary studies were performed. The admission laboratory reported leukocytosis, platelopenia, increased acute phase reactants and the rest of the parameters within normal values. An angiotomy of the craniofacial mass was performed, where a large thrombus was found in the internal and external carotid arteries. Studies were completed with a chest tomography and arterial Doppler ultrasound of neck vessels with no relevant findings. Early intravenous antibiotic treatment was initiated with ceftriaxone 1 g every 12 hours, clindamycin 300 mg every 6 hours and anticoagulation with enoxaparin adjusted to body weight and renal function, 60 mg subcutaneously every 12 hours. The patient evolved 72 hours after initiating the directed treatment with a fever of 38.5 °C and increased leukocytosis, so new complementary studies were performed, including a Doppler ultrasound of the heart without finding cardiac vegetations and a chest tomography where bilateral pulmonary septic emboli were found. With the admission hemocultures negative, a new admission of 3 units, culture of pharyngeal exudate and rotation of ceftriaxone to piperacillin tazobactam 4.5 g every 6 hours intravenous was decided. The patient evolved favorably, without rescue of germs in cultures. After 14 days of initiating the new therapeutic scheme, and with a control chest tomography without pulmonary lesions, it was decided to continue antibiotic treatment with oral clindamycin 300 mg every 6 hours, anticoagulation with acenocumarol adjusted to body weight and hospital discharge.\n",
+    "diff_label_texts": "A 27-year-old woman developed facial swelling and trismus 48 hours after finishing phenoxymethylpenicillin for a dental infection. A head and neck CT showed a large blood clot in the internal jugular vein. A chest CT showed septic emboli in the lungs. She was treated promptly with intravenous broad-spectrum antibiotics and anticoagulation. She improved with care and continued treatment after discharge.",
+    "summary": "A 27-year-old woman presented with facial oedema and trismus 48 hours after completing treatment with phenoxymethylpenicillin for an odontogenic infection. A head and neck CT scan showed a large thrombus in the internal jugular vein and a chest CT scan showed pulmonary septic embolism. Treatment consisted of early intravenous broad spectrum antibiotics and anticoagulation.\n"
+  },
+  {
+    "doc_id": 63,
+    "label": "proficient_health_literacy",
+    "fulltext": "27-year-old woman with a history of uncontrolled asthma, mild SARS-CoV-2 infection. In March 2021, she consulted a doctor for pain in the left hemicara and trismus. She reported having completed 48 hours before the antibiotic treatment with phenoxymethyl penicillin 1,000,000 IU daily orally for five days for a peritonsillar abscess. She was hemodynamically stable at the physical examination, without the need for supplemental oxygen, and without relevant findings in respiratory symptoms. The head and neck examination showed a soft, painful, cervical adenopathy, palpable and painful, predominantly homolateral and trismus. Complementary studies were performed. The admission laboratory reported leukocytosis, platelopenia, increased acute phase reactants and the rest of the parameters within normal values. An angiotomy of the craniofacial mass was performed, where a large thrombus was found in the internal and external carotid arteries. Studies were completed with a chest tomography and arterial Doppler ultrasound of neck vessels with no relevant findings. Early intravenous antibiotic treatment was initiated with ceftriaxone 1 g every 12 hours, clindamycin 300 mg every 6 hours and anticoagulation with enoxaparin adjusted to body weight and renal function, 60 mg subcutaneously every 12 hours. The patient evolved 72 hours after initiating the directed treatment with a fever of 38.5 °C and increased leukocytosis, so new complementary studies were performed, including a Doppler ultrasound of the heart without finding cardiac vegetations and a chest tomography where bilateral pulmonary septic emboli were found. With the admission hemocultures negative, a new admission of 3 units, culture of pharyngeal exudate and rotation of ceftriaxone to piperacillin tazobactam 4.5 g every 6 hours intravenous was decided. The patient evolved favorably, without rescue of germs in cultures. After 14 days of initiating the new therapeutic scheme, and with a control chest tomography without pulmonary lesions, it was decided to continue antibiotic treatment with oral clindamycin 300 mg every 6 hours, anticoagulation with acenocumarol adjusted to body weight and hospital discharge.\n",
+    "diff_label_texts": "A 27-year-old woman with uncontrolled asthma and recent mild SARS-CoV-2 infection presented in March 2021 with left hemifacial pain and trismus 48 hours after completing phenoxymethylpenicillin 1,000,000 IU orally once daily for five days for a peritonsillar/oropharyngeal infection. She was hemodynamically stable, without oxygen requirement. Examination showed tender ipsilateral cervical lymphadenopathy and trismus. Admission labs demonstrated leukocytosis, thrombocytopenia, and elevated acute phase reactants; other parameters were within normal limits. Head and neck CT angiography identified a large thrombus within the internal jugular vein. Initial Doppler assessment of neck vessels did not add further actionable findings. Chest CT demonstrated bilateral septic pulmonary emboli. Management included immediate intravenous broad-spectrum antibiotics (ceftriaxone 1 g every 12 hours plus clindamycin 300 mg every 6 hours initially) and therapeutic anticoagulation with enoxaparin 60 mg subcutaneously every 12 hours, dose-adjusted to body weight and renal function. At 72 hours, she developed fever to 38.5 °C with rising leukocytosis; transthoracic echocardiography showed no valvular vegetations. Blood cultures remained negative and a pharyngeal exudate culture was obtained. Antibiotics were escalated to piperacillin–tazobactam 4.5 g IV every 6 hours, with subsequent clinical improvement and no organisms isolated. After 14 days of the revised regimen, follow-up chest CT showed resolution of pulmonary lesions. She was transitioned to oral clindamycin 300 mg every 6 hours and oral anticoagulation with acenocoumarol (dose-adjusted to body weight) and discharged. The presentation and imaging were consistent with internal jugular vein thrombosis complicated by septic pulmonary emboli.",
+    "summary": "A 27-year-old woman presented with facial oedema and trismus 48 hours after completing treatment with phenoxymethylpenicillin for an odontogenic infection. A head and neck CT scan showed a large thrombus in the internal jugular vein and a chest CT scan showed pulmonary septic embolism. Treatment consisted of early intravenous broad spectrum antibiotics and anticoagulation.\n"
+  },
+  {
+    "doc_id": 64,
+    "label": "low_health_literacy",
+    "fulltext": "A 5-year-old presented to the paediatric emergency department (ED) having ingested chlorpyriphos 13 hours prior to presentation, followed by abnormal jerks, fast breathing and difficulty with breathing. The history was also comprised of excessive sweating and urination, mouth secretions and involuntary movement of the limbs. Vomiting followed the ingestion of crushed charcoal and palm oil. The patient had lapsed into coma prior to presentation. The temperature at presentation was 38.3°C, Glasgow coma score was 3, pupils were pinpoint pupils and there was hypotonia in all limbs. In addition, the patient was severely dyspneic, tachypneic (respiratory rate of 48/minute with intermittent sighing breaths), a saturation of 88% and widespread crackles. The pulse rate was 180/minute, blood pressure 120/80 mmHg, and random blood glucose 14 mg/dl. Serum lactate and cholinesterase tests were not done due to lack of facilities.\n\nThe patient was diagnosed with severe organophosphate poisoning (OPP) and aspiration pneumonitis. As ICU care was beyond the affordability of the parents, non-invasive ventilation (NIV) was administered using bubble continuous positive airway pressure (b-CPAP) causing his saturation to increase to 99%–100%. Hypoglycemia was corrected with a bolus of dextrose solution and tachycardia was treated with 20 ml/kg of normal saline. Intravenous Dexamethasone, Mannitol and IV Atropine at 0.02 mg/kg/dose were also administered. Empirical intravenous antibiotics were administered for aspiration pneumonitis. Pralidoxime was not given due to unavailability. Within 3 hours of presentation, the patient had fresh-whole-blood exchange-blood-transfusion (FWB-EBT) with 500mls of blood.\n\nThe patient’s GCS appreciated to 9/15 but IV Atropine was discontinued after the first dose due to a rapid increase in the heart rate. The blood glucose fluctuated between 41 to 259 mg/dl in the first 15 hours of admission and subsequently normalized with treatment. By the second day on admission, the patient developed thready pulses and hypotension for which another bolus of normal saline was administered. Dopamine infusion was commenced at 5mcg/kg/min using a peripheral vein and IV Mannitol discontinued. A second aliquot of FWB-EBT was administered with 500mls of blood.\n\nOver the first 30 hours of admission, the consciousness level improved and respiratory distress slowly declined. However, the patient developed rhonchi which was treated with nebulized Salbutamol and Budesonide and was subsequently transited to Oxygen therapy with nasal prongs with clinical improvement. The saturation remained stable at 97%. On Day 2 of admission, a chest radiograph was done which showed bilateral infiltrates in keeping with pneumonia.\n\nThe patient regained full consciousness by the 39th hour of admission. Intravenous Vitamin C and B, as well as oral Vitamin E and Zinc were commenced for their antioxidant effects, and regular diet was recommenced in a graded manner over the subsequent 48 hours. The patient’s clinical condition progressively improved and was discharged home after 10 days but was subsequently lost to follow-up.",
+    "diff_label_texts": "A 5-year-old drank a farm bug killer called chlorpyrifos. Some charcoal and palm oil were later breathed into the lungs. The child got very sick. Breathing failed. The body went into shock. The child was in a coma. There was an early kind of paralysis (type 1). In the emergency room, a mask machine helped with breathing. Doctors swapped out some blood and put in new blood more than once. They gave atropine through a vein. They used a drip to help the heart and blood pressure. They also gave antibiotics and steroids. The child got better quickly. The child did not get the delayed muscle weakness that can happen later. The child went home after 10 days in the hospital.",
+    "summary": "We present the case of a 5-year-old with severe organophosphate poisoning from ingestion of chlorpyrifos, further worsened by aspiration of a charcoal-palm oil mixture. The clinical illness was marked by respiratory failure, shock, coma and type I paralysis. The patient was treated in the emergency department with noninvasive ventilation, multiple episodes of exchange transfusion, intravenous atropine, inotrope infusion, antibiotics and steroids. The patient responded rapidly to treatment, did not develop intermediate syndrome and was discharged after 10 days of admission."
+  },
+  {
+    "doc_id": 64,
+    "label": "intermediate_health_literacy",
+    "fulltext": "A 5-year-old presented to the paediatric emergency department (ED) having ingested chlorpyriphos 13 hours prior to presentation, followed by abnormal jerks, fast breathing and difficulty with breathing. The history was also comprised of excessive sweating and urination, mouth secretions and involuntary movement of the limbs. Vomiting followed the ingestion of crushed charcoal and palm oil. The patient had lapsed into coma prior to presentation. The temperature at presentation was 38.3°C, Glasgow coma score was 3, pupils were pinpoint pupils and there was hypotonia in all limbs. In addition, the patient was severely dyspneic, tachypneic (respiratory rate of 48/minute with intermittent sighing breaths), a saturation of 88% and widespread crackles. The pulse rate was 180/minute, blood pressure 120/80 mmHg, and random blood glucose 14 mg/dl. Serum lactate and cholinesterase tests were not done due to lack of facilities.\n\nThe patient was diagnosed with severe organophosphate poisoning (OPP) and aspiration pneumonitis. As ICU care was beyond the affordability of the parents, non-invasive ventilation (NIV) was administered using bubble continuous positive airway pressure (b-CPAP) causing his saturation to increase to 99%–100%. Hypoglycemia was corrected with a bolus of dextrose solution and tachycardia was treated with 20 ml/kg of normal saline. Intravenous Dexamethasone, Mannitol and IV Atropine at 0.02 mg/kg/dose were also administered. Empirical intravenous antibiotics were administered for aspiration pneumonitis. Pralidoxime was not given due to unavailability. Within 3 hours of presentation, the patient had fresh-whole-blood exchange-blood-transfusion (FWB-EBT) with 500mls of blood.\n\nThe patient’s GCS appreciated to 9/15 but IV Atropine was discontinued after the first dose due to a rapid increase in the heart rate. The blood glucose fluctuated between 41 to 259 mg/dl in the first 15 hours of admission and subsequently normalized with treatment. By the second day on admission, the patient developed thready pulses and hypotension for which another bolus of normal saline was administered. Dopamine infusion was commenced at 5mcg/kg/min using a peripheral vein and IV Mannitol discontinued. A second aliquot of FWB-EBT was administered with 500mls of blood.\n\nOver the first 30 hours of admission, the consciousness level improved and respiratory distress slowly declined. However, the patient developed rhonchi which was treated with nebulized Salbutamol and Budesonide and was subsequently transited to Oxygen therapy with nasal prongs with clinical improvement. The saturation remained stable at 97%. On Day 2 of admission, a chest radiograph was done which showed bilateral infiltrates in keeping with pneumonia.\n\nThe patient regained full consciousness by the 39th hour of admission. Intravenous Vitamin C and B, as well as oral Vitamin E and Zinc were commenced for their antioxidant effects, and regular diet was recommenced in a graded manner over the subsequent 48 hours. The patient’s clinical condition progressively improved and was discharged home after 10 days but was subsequently lost to follow-up.",
+    "diff_label_texts": "A 5-year-old developed severe organophosphate poisoning after ingesting chlorpyrifos and then aspirated a charcoal–palm oil mixture. The illness progressed to respiratory failure, shock, coma, and acute (type I) paralysis. In the emergency department, the child received noninvasive ventilation, repeated exchange transfusions, intravenous atropine, and an inotrope infusion to support blood pressure, along with antibiotics and steroids. The child improved rapidly, did not develop intermediate syndrome (the delayed muscle weakness sometimes seen after organophosphate poisoning), and was discharged after a 10-day hospitalization. Additional context: the child arrived about 13 hours after ingestion with heavy secretions, pinpoint pupils, fast breathing, low oxygen, and crackles on chest exam. Pralidoxime was unavailable. Blood sugar was low at first and then fluctuated before stabilizing. A chest X-ray on day 2 showed pneumonia. Consciousness returned by about 39 hours, oxygen was weaned to nasal prongs, and recovery continued to discharge.",
+    "summary": "We present the case of a 5-year-old with severe organophosphate poisoning from ingestion of chlorpyrifos, further worsened by aspiration of a charcoal-palm oil mixture. The clinical illness was marked by respiratory failure, shock, coma and type I paralysis. The patient was treated in the emergency department with noninvasive ventilation, multiple episodes of exchange transfusion, intravenous atropine, inotrope infusion, antibiotics and steroids. The patient responded rapidly to treatment, did not develop intermediate syndrome and was discharged after 10 days of admission."
+  },
+  {
+    "doc_id": 64,
+    "label": "proficient_health_literacy",
+    "fulltext": "A 5-year-old presented to the paediatric emergency department (ED) having ingested chlorpyriphos 13 hours prior to presentation, followed by abnormal jerks, fast breathing and difficulty with breathing. The history was also comprised of excessive sweating and urination, mouth secretions and involuntary movement of the limbs. Vomiting followed the ingestion of crushed charcoal and palm oil. The patient had lapsed into coma prior to presentation. The temperature at presentation was 38.3°C, Glasgow coma score was 3, pupils were pinpoint pupils and there was hypotonia in all limbs. In addition, the patient was severely dyspneic, tachypneic (respiratory rate of 48/minute with intermittent sighing breaths), a saturation of 88% and widespread crackles. The pulse rate was 180/minute, blood pressure 120/80 mmHg, and random blood glucose 14 mg/dl. Serum lactate and cholinesterase tests were not done due to lack of facilities.\n\nThe patient was diagnosed with severe organophosphate poisoning (OPP) and aspiration pneumonitis. As ICU care was beyond the affordability of the parents, non-invasive ventilation (NIV) was administered using bubble continuous positive airway pressure (b-CPAP) causing his saturation to increase to 99%–100%. Hypoglycemia was corrected with a bolus of dextrose solution and tachycardia was treated with 20 ml/kg of normal saline. Intravenous Dexamethasone, Mannitol and IV Atropine at 0.02 mg/kg/dose were also administered. Empirical intravenous antibiotics were administered for aspiration pneumonitis. Pralidoxime was not given due to unavailability. Within 3 hours of presentation, the patient had fresh-whole-blood exchange-blood-transfusion (FWB-EBT) with 500mls of blood.\n\nThe patient’s GCS appreciated to 9/15 but IV Atropine was discontinued after the first dose due to a rapid increase in the heart rate. The blood glucose fluctuated between 41 to 259 mg/dl in the first 15 hours of admission and subsequently normalized with treatment. By the second day on admission, the patient developed thready pulses and hypotension for which another bolus of normal saline was administered. Dopamine infusion was commenced at 5mcg/kg/min using a peripheral vein and IV Mannitol discontinued. A second aliquot of FWB-EBT was administered with 500mls of blood.\n\nOver the first 30 hours of admission, the consciousness level improved and respiratory distress slowly declined. However, the patient developed rhonchi which was treated with nebulized Salbutamol and Budesonide and was subsequently transited to Oxygen therapy with nasal prongs with clinical improvement. The saturation remained stable at 97%. On Day 2 of admission, a chest radiograph was done which showed bilateral infiltrates in keeping with pneumonia.\n\nThe patient regained full consciousness by the 39th hour of admission. Intravenous Vitamin C and B, as well as oral Vitamin E and Zinc were commenced for their antioxidant effects, and regular diet was recommenced in a graded manner over the subsequent 48 hours. The patient’s clinical condition progressively improved and was discharged home after 10 days but was subsequently lost to follow-up.",
+    "diff_label_texts": "A 5-year-old presented to the pediatric ED 13 hours after ingesting chlorpyrifos with abnormal jerks, severe dyspnea, tachypnea (RR 48/min with intermittent sighs), diaphoresis, salivation, polyuria, vomiting, and subsequent aspiration of a charcoal–palm oil mixture. On arrival: T 38.3°C, GCS 3/15, pinpoint pupils, generalized hypotonia, SpO2 88% with widespread crackles, HR 180/min, BP 120/80 mmHg, random blood glucose 14 mg/dl. Serum lactate and cholinesterase levels were unavailable. The working diagnoses were severe organophosphate poisoning (cholinergic crisis with type I paralysis), aspiration pneumonitis, respiratory failure, and impending shock. Because ICU care was unaffordable, NIV via bubble CPAP was initiated, improving SpO2 to 99–100%. Hypoglycemia was corrected with a dextrose bolus; 20 ml/kg normal saline was given for tachycardia. The patient received IV dexamethasone, mannitol, and atropine 0.02 mg/kg (discontinued after the first dose due to rapid tachycardia), plus empiric IV antibiotics for aspiration pneumonitis; pralidoxime was unavailable. Within 3 hours, a 500 mL fresh whole blood exchange transfusion (FWB-EBT) was performed, after which GCS improved to 9/15. Blood glucose fluctuated between 41–259 mg/dl during the first 15 hours and subsequently normalized. By hospital day 2, the patient developed thready pulses and hypotension; an additional NS bolus was administered and dopamine was started at 5 mcg/kg/min via a peripheral vein. Mannitol was discontinued. A second 500 mL FWB-EBT was performed. Over the first 30 hours, consciousness and respiratory distress improved, though rhonchi developed and were treated with nebulized salbutamol and budesonide; the patient was transitioned to oxygen via nasal prongs with SpO2 ~97%. A day-2 chest radiograph showed bilateral infiltrates consistent with pneumonia. Full consciousness returned by hour 39. Antioxidants (IV vitamins C and B; oral vitamin E and zinc) were started, and diet was advanced over 48 hours. The patient responded rapidly overall, did not develop intermediate syndrome, and was discharged on hospital day 10; follow-up was lost. Exchange transfusion was utilized as a detoxification strategy in the absence of oximes and may have contributed to clinical stabilization by reducing circulating toxin and replenishing cholinesterase activity, alongside atropinization, ventilatory support, fluids, and inotropic therapy.",
+    "summary": "We present the case of a 5-year-old with severe organophosphate poisoning from ingestion of chlorpyrifos, further worsened by aspiration of a charcoal-palm oil mixture. The clinical illness was marked by respiratory failure, shock, coma and type I paralysis. The patient was treated in the emergency department with noninvasive ventilation, multiple episodes of exchange transfusion, intravenous atropine, inotrope infusion, antibiotics and steroids. The patient responded rapidly to treatment, did not develop intermediate syndrome and was discharged after 10 days of admission."
+  },
+  {
+    "doc_id": 65,
+    "label": "low_health_literacy",
+    "fulltext": "A 19-year-old woman presented to the emergency department of our institution for acute onset of palpitations. An electrocardiogram (ECG) showed ventricular tachycardia, with right branch bundle block associated to left posterior hemiblock, and T waves inversion in the inferior and precordial leads. Blood test showed elevated troponin (27 ng/L, normal values <14 ng/L) and NT-pro BNP (aminoterminal pro B-Type Natriuretic Peptide) levels (2225 pg/mL, normal values <130 pg/mL). Hence, she was admitted to the coronary care unit.\n\nAbout 5 years before, she had already presented to the emergency department with cardiogenic shock due to fascicular ventricular tachycardia; she was subsequently hospitalized and underwent cardiac magnetic resonance (CMR) and a transoesophageal electrophysiological study, both with inconclusive results. She was discharged with a diagnosis of tachycardiomiopathy, with the prescription of a standard medical therapy (angiotensin-converting enzyme inhibitors, mineralocorticoid receptor antagonist, and beta blockers), and a follow-up was planned. Her subsequent clinical history was uneventful.\n\nDuring the present hospitalization, no further episodes of hyperkinetic arrhythmias were detected. Basal 12-lead ECG. Echocardiography showed diffuse hypokinesia of both the left and the right ventricles, and CMR was once again inconclusive. Then, the patient was advised to undergo cardiac computed tomography angiography (CCTA) to evaluate the anatomy of the coronary tree, under the suspicion of an undiagnosed congenital cardiac anomaly. CCTA was performed with a GE Lightspeed unit (GE HealthCare, Chicago, United States), with retrospective gating, at 100 kVp and 696 mAs, with a gantry rotation time of 0.35 s, and 0.625 mm slice thickness, with intravenous injection of 70 mL of Iomeron 400 mgI/mL (Bracco Imaging, Milan, Italy).\n\nDifferential diagnosis\nCardiogenic shock, namely a shock caused by inadequate blood flow, may be caused by different pathologies such as myocardial infarction, arrhythmias, or other cardiomyopathies. Undiagnosed congenital heart disease is a non-negligible cause of cardiogenic shock in otherwise healthy adult patients. Once myocardial infarction is ruled out by a 12-lead ECG, and an underlying cardiomyopathy has been excluded by an inconclusive CMR examination, CCTA is the technique of choice for the differential diagnosis among diverse causes of cardiogenic shock.\n\nInvestigations/imaging findings\nThe CCTA examination showed regular origin of the left main coronary artery, the left anterior descending artery, which presented a wide ramus intermedium, 2 diagonal branches, and the left circumflex artery, which appeared thin and non-dominant. Among all these vessels, there was no evidence of obstructive coronary artery disease. However, the ostium and the proximal portion of the right coronary artery (RCA) were absent, whereas its mid and distal portions were supplied by a wide collateral branch originating from the distal left anterior descending artery, which then surrounded the lateral wall of the right ventricle, ran through the distal part of the atrioventricular groove, finally giving rise to thin posterior interventricular and posterolateral arteries. Furthermore, a thin branch going from the mid left anterior descending artery to the sinoatrial node was observed.\n\nTreatment, outcome, and follow-up\nIn view of the CCTA findings, the patient underwent an echo-stress test, which confirmed the presence of inducible myocardial ischaemia in the inferior wall, in line with the positioning of the arrhythmic focus. After being transferred to a specialized centre for the diagnosis and treatment of congenital heart disease, the patient underwent transcatheter radiofrequency ablation of sustained ventricular tachycardia originating by the posteromedial papillary muscle. Then, she was discharged with medical therapy (Acetylsalicylic acid and Verapamil). At her 6-month follow-up, she has always been asymptomatic, with no further signs of arrhythmias.",
+    "diff_label_texts": "A 19-year-old woman went to the emergency room. Her heart was beating fast and uneven. Her body showed signs that her heart was not pumping enough blood. A heart tracing test showed she was not having a heart attack. A heart MRI did not show a disease of the heart muscle. A special heart CT scan then looked at her heart arteries. It showed the normal opening to her right heart artery was missing from birth. She was sent to a center that treats heart problems people are born with. Doctors did an electrical test inside her heart. They found a small hot spot on a tiny muscle that helps a heart valve. That spot was starting the bad rhythm, like a faulty spark. The team gently burned that spot to stop it. She has had no symptoms since.",
+    "summary": "A 19-year-old woman presented to the emergency department with arrhythmia and signs of cardiogenic shock. After a 12-lead electrocardiogram ruled out acute myocardial infarction, and cardiac magnetic resonance showed no sign of cardiomyopathy, cardiac computed tomography angiography (CCTA) was performed, displaying ostial atresia of the right coronary artery. She was thus referred to a specialist centre for congenital cardiovascular disease, where an electrophysiological study observed an arrhythmogenic focus on the posteromedial papillary muscle, which was ablated, and she has been asymptomatic since."
+  },
+  {
+    "doc_id": 65,
+    "label": "intermediate_health_literacy",
+    "fulltext": "A 19-year-old woman presented to the emergency department of our institution for acute onset of palpitations. An electrocardiogram (ECG) showed ventricular tachycardia, with right branch bundle block associated to left posterior hemiblock, and T waves inversion in the inferior and precordial leads. Blood test showed elevated troponin (27 ng/L, normal values <14 ng/L) and NT-pro BNP (aminoterminal pro B-Type Natriuretic Peptide) levels (2225 pg/mL, normal values <130 pg/mL). Hence, she was admitted to the coronary care unit.\n\nAbout 5 years before, she had already presented to the emergency department with cardiogenic shock due to fascicular ventricular tachycardia; she was subsequently hospitalized and underwent cardiac magnetic resonance (CMR) and a transoesophageal electrophysiological study, both with inconclusive results. She was discharged with a diagnosis of tachycardiomiopathy, with the prescription of a standard medical therapy (angiotensin-converting enzyme inhibitors, mineralocorticoid receptor antagonist, and beta blockers), and a follow-up was planned. Her subsequent clinical history was uneventful.\n\nDuring the present hospitalization, no further episodes of hyperkinetic arrhythmias were detected. Basal 12-lead ECG. Echocardiography showed diffuse hypokinesia of both the left and the right ventricles, and CMR was once again inconclusive. Then, the patient was advised to undergo cardiac computed tomography angiography (CCTA) to evaluate the anatomy of the coronary tree, under the suspicion of an undiagnosed congenital cardiac anomaly. CCTA was performed with a GE Lightspeed unit (GE HealthCare, Chicago, United States), with retrospective gating, at 100 kVp and 696 mAs, with a gantry rotation time of 0.35 s, and 0.625 mm slice thickness, with intravenous injection of 70 mL of Iomeron 400 mgI/mL (Bracco Imaging, Milan, Italy).\n\nDifferential diagnosis\nCardiogenic shock, namely a shock caused by inadequate blood flow, may be caused by different pathologies such as myocardial infarction, arrhythmias, or other cardiomyopathies. Undiagnosed congenital heart disease is a non-negligible cause of cardiogenic shock in otherwise healthy adult patients. Once myocardial infarction is ruled out by a 12-lead ECG, and an underlying cardiomyopathy has been excluded by an inconclusive CMR examination, CCTA is the technique of choice for the differential diagnosis among diverse causes of cardiogenic shock.\n\nInvestigations/imaging findings\nThe CCTA examination showed regular origin of the left main coronary artery, the left anterior descending artery, which presented a wide ramus intermedium, 2 diagonal branches, and the left circumflex artery, which appeared thin and non-dominant. Among all these vessels, there was no evidence of obstructive coronary artery disease. However, the ostium and the proximal portion of the right coronary artery (RCA) were absent, whereas its mid and distal portions were supplied by a wide collateral branch originating from the distal left anterior descending artery, which then surrounded the lateral wall of the right ventricle, ran through the distal part of the atrioventricular groove, finally giving rise to thin posterior interventricular and posterolateral arteries. Furthermore, a thin branch going from the mid left anterior descending artery to the sinoatrial node was observed.\n\nTreatment, outcome, and follow-up\nIn view of the CCTA findings, the patient underwent an echo-stress test, which confirmed the presence of inducible myocardial ischaemia in the inferior wall, in line with the positioning of the arrhythmic focus. After being transferred to a specialized centre for the diagnosis and treatment of congenital heart disease, the patient underwent transcatheter radiofrequency ablation of sustained ventricular tachycardia originating by the posteromedial papillary muscle. Then, she was discharged with medical therapy (Acetylsalicylic acid and Verapamil). At her 6-month follow-up, she has always been asymptomatic, with no further signs of arrhythmias.",
+    "diff_label_texts": "A 19-year-old woman came to the emergency department with a dangerous arrhythmia and signs that her heart was failing to pump well (cardiogenic shock). An ECG ruled out an acute heart attack, and cardiac MRI did not show cardiomyopathy. Because a hidden congenital issue was suspected, she underwent cardiac CT angiography. The scan showed ostial atresia of the right coronary artery—the opening of the right coronary artery was absent. She was referred to a specialized congenital heart disease center. An electrophysiology study pinpointed the arrhythmia to the posteromedial papillary muscle, and the focus was treated with catheter ablation. She has remained symptom-free since.",
+    "summary": "A 19-year-old woman presented to the emergency department with arrhythmia and signs of cardiogenic shock. After a 12-lead electrocardiogram ruled out acute myocardial infarction, and cardiac magnetic resonance showed no sign of cardiomyopathy, cardiac computed tomography angiography (CCTA) was performed, displaying ostial atresia of the right coronary artery. She was thus referred to a specialist centre for congenital cardiovascular disease, where an electrophysiological study observed an arrhythmogenic focus on the posteromedial papillary muscle, which was ablated, and she has been asymptomatic since."
+  },
+  {
+    "doc_id": 65,
+    "label": "proficient_health_literacy",
+    "fulltext": "A 19-year-old woman presented to the emergency department of our institution for acute onset of palpitations. An electrocardiogram (ECG) showed ventricular tachycardia, with right branch bundle block associated to left posterior hemiblock, and T waves inversion in the inferior and precordial leads. Blood test showed elevated troponin (27 ng/L, normal values <14 ng/L) and NT-pro BNP (aminoterminal pro B-Type Natriuretic Peptide) levels (2225 pg/mL, normal values <130 pg/mL). Hence, she was admitted to the coronary care unit.\n\nAbout 5 years before, she had already presented to the emergency department with cardiogenic shock due to fascicular ventricular tachycardia; she was subsequently hospitalized and underwent cardiac magnetic resonance (CMR) and a transoesophageal electrophysiological study, both with inconclusive results. She was discharged with a diagnosis of tachycardiomiopathy, with the prescription of a standard medical therapy (angiotensin-converting enzyme inhibitors, mineralocorticoid receptor antagonist, and beta blockers), and a follow-up was planned. Her subsequent clinical history was uneventful.\n\nDuring the present hospitalization, no further episodes of hyperkinetic arrhythmias were detected. Basal 12-lead ECG. Echocardiography showed diffuse hypokinesia of both the left and the right ventricles, and CMR was once again inconclusive. Then, the patient was advised to undergo cardiac computed tomography angiography (CCTA) to evaluate the anatomy of the coronary tree, under the suspicion of an undiagnosed congenital cardiac anomaly. CCTA was performed with a GE Lightspeed unit (GE HealthCare, Chicago, United States), with retrospective gating, at 100 kVp and 696 mAs, with a gantry rotation time of 0.35 s, and 0.625 mm slice thickness, with intravenous injection of 70 mL of Iomeron 400 mgI/mL (Bracco Imaging, Milan, Italy).\n\nDifferential diagnosis\nCardiogenic shock, namely a shock caused by inadequate blood flow, may be caused by different pathologies such as myocardial infarction, arrhythmias, or other cardiomyopathies. Undiagnosed congenital heart disease is a non-negligible cause of cardiogenic shock in otherwise healthy adult patients. Once myocardial infarction is ruled out by a 12-lead ECG, and an underlying cardiomyopathy has been excluded by an inconclusive CMR examination, CCTA is the technique of choice for the differential diagnosis among diverse causes of cardiogenic shock.\n\nInvestigations/imaging findings\nThe CCTA examination showed regular origin of the left main coronary artery, the left anterior descending artery, which presented a wide ramus intermedium, 2 diagonal branches, and the left circumflex artery, which appeared thin and non-dominant. Among all these vessels, there was no evidence of obstructive coronary artery disease. However, the ostium and the proximal portion of the right coronary artery (RCA) were absent, whereas its mid and distal portions were supplied by a wide collateral branch originating from the distal left anterior descending artery, which then surrounded the lateral wall of the right ventricle, ran through the distal part of the atrioventricular groove, finally giving rise to thin posterior interventricular and posterolateral arteries. Furthermore, a thin branch going from the mid left anterior descending artery to the sinoatrial node was observed.\n\nTreatment, outcome, and follow-up\nIn view of the CCTA findings, the patient underwent an echo-stress test, which confirmed the presence of inducible myocardial ischaemia in the inferior wall, in line with the positioning of the arrhythmic focus. After being transferred to a specialized centre for the diagnosis and treatment of congenital heart disease, the patient underwent transcatheter radiofrequency ablation of sustained ventricular tachycardia originating by the posteromedial papillary muscle. Then, she was discharged with medical therapy (Acetylsalicylic acid and Verapamil). At her 6-month follow-up, she has always been asymptomatic, with no further signs of arrhythmias.",
+    "diff_label_texts": "A 19-year-old woman presented with acute palpitations. The initial ECG demonstrated ventricular tachycardia with right bundle branch block morphology associated with left posterior hemiblock, and T-wave inversion in the inferior and precordial leads. Biomarkers were elevated (troponin 27 ng/L, normal <14 ng/L; NT-proBNP 2225 pg/mL, normal <130 pg/mL). She was admitted to the coronary care unit. Five years earlier, she had presented with cardiogenic shock due to fascicular ventricular tachycardia; CMR and a transoesophageal electrophysiological study at that time were inconclusive. She was discharged with a diagnosis of tachycardiomyopathy on ACE inhibitors, a mineralocorticoid receptor antagonist, and beta blockers, with an uneventful interval thereafter.\n\nDuring the current hospitalization, there were no further hyperkinetic arrhythmias. Basal 12-lead ECG was obtained. Echocardiography showed diffuse hypokinesia of both ventricles. CMR was again inconclusive, and an undiagnosed congenital cardiac anomaly was suspected. Cardiac computed tomography angiography (CCTA) was performed (GE Lightspeed, retrospective gating, 100 kVp, 696 mAs, gantry rotation 0.35 s, 0.625 mm slice thickness; 70 mL Iomeron 400 mgI/mL IV). The left main and left anterior descending (with a wide ramus intermedius and two diagonal branches) and a thin, non-dominant left circumflex showed no obstructive coronary artery disease. The right coronary artery ostium and proximal segment were absent (ostial atresia); the mid and distal RCA were supplied by a large collateral from the distal LAD that coursed around the lateral right ventricular wall, traversed the distal atrioventricular groove, and gave rise to thin posterior interventricular and posterolateral branches. A thin branch from the mid LAD to the sinoatrial node was also observed.\n\nIn the differential for cardiogenic shock in otherwise healthy adults, once acute myocardial infarction is ruled out on 12-lead ECG and cardiomyopathy is not demonstrated on CMR, CCTA is the modality of choice to evaluate for congenital coronary anomalies and other causes. In this case, an echo-stress test confirmed inducible ischemia in the inferior wall, concordant with the arrhythmic focus location. The patient was transferred to a specialist congenital heart disease center, where she underwent transcatheter radiofrequency ablation of sustained ventricular tachycardia arising from the posteromedial papillary muscle. She was discharged on acetylsalicylic acid and verapamil. At 6-month follow-up she remained asymptomatic, without recurrent arrhythmias.",
+    "summary": "A 19-year-old woman presented to the emergency department with arrhythmia and signs of cardiogenic shock. After a 12-lead electrocardiogram ruled out acute myocardial infarction, and cardiac magnetic resonance showed no sign of cardiomyopathy, cardiac computed tomography angiography (CCTA) was performed, displaying ostial atresia of the right coronary artery. She was thus referred to a specialist centre for congenital cardiovascular disease, where an electrophysiological study observed an arrhythmogenic focus on the posteromedial papillary muscle, which was ablated, and she has been asymptomatic since."
+  },
+  {
+    "doc_id": 66,
+    "label": "low_health_literacy",
+    "fulltext": "A 17-year-old male with no significant past medical or family history was referred to our clinic from the dental department following an incidental finding of a NFB during preoperative orthodontic planning, including dental x-rays and cone beam computed tomography (CBCT) without contrast. The patient was entirely asymptomatic and denied any history of nasal obstruction, rhinorrhea, epistaxis, foul odor, hyposmia, halitosis, facial pain, discomfort, or sleep disturbances. The patient's parents recalled an event when their son was seven, where he inserted an object into his nose. They sought medical advice, where no imaging was performed and an anterior rhinoscopy was utilized for diagnoses but due to the child's non-cooperation during the examination, the physician recommended the removal of the foreign body under sedation. However, the family did not follow up, and since the child remained asymptomatic, they assumed the foreign body had fallen out on its own. On endoscopic examination of the right nasal cavity, a deviated nasal septum with inferior turbinate hypertrophy was noted. The mucosa appeared erythematous and slightly edematous. A foreign body was visualized, lodged, and adhered to the floor of the nasal cavity beneath the inferior turbinate. The object was partially covered with mucus and possibly some crusted material and had a shiny appearance, indicating a metallic nature. Radiographic evaluation, including lateral and frontal X-rays, revealed a circular radiopaque object consistent with a metallic snap button located along the floor of the nasal cavity. The surrounding bony structures appeared normal. A CBCT confirmed the presence of the foreign body with associated mild inflammation, but no significant bony damage or sinus involvement was observed. With informed consent from the patient's parent, the foreign body was removed under local anesthesia in a semi-sitting position to reduce the risk of dislodgment to the airway. After decongesting the nasal cavity with Xylometazoline 0.1 % and administering Lidocaine spray (10 mg/spray) in the right nostril, a hook was utilized to disengage the foreign body, which was then retrieved using bayonet forceps. The procedure was uncomplicated, with minimal bleeding, easily controlled with saline irrigation. Post-removal examination showed no significant tissue damage. The retrieved object, a metallic snap button measuring 1 cm in diameter, exhibited signs of long-term exposure, including substantial corrosion and biological deposits. The patient was discharged in stable condition and prescribed nasal rinses with a sodium chloride irrigation solution (0.9 %). The patient was doing well at his two-week follow-up with an unremarkable examination.",
+    "diff_label_texts": "A 17-year-old boy felt fine. A routine dental x-ray found something in his right nose by accident. He did not have a stuffy nose, nosebleeds, or pain. The pictures showed a bright spot in his right nose. It was a small metal snap button, like one on clothing. It was stuck low on the floor of the right side of his nose. It had probably been there for more than 10 years.",
+    "summary": "We present the case of a 17-year-old male with an asymptomatic NFB discovered incidentally during routine dental radiography. The patient denied any history of nasal obstruction, epistaxis, or discomfort. Imaging revealed a radiopaque object in the right nasal cavity, later identified as a metallic snap button embedded in the floor of the nasal cavity. The foreign body had likely been retained for over a decade."
+  },
+  {
+    "doc_id": 67,
+    "label": "proficient_health_literacy",
+    "fulltext": "An 18-year-old hispanic male patient with no significant medical history presents to the emergency department (ED) complaining of substernal, non-radiated chest pain, orthopnoea, dry and non-productive cough, and subjective fevers at home, for the last 3–4 days. Family history remarkable for paternal grandfather diagnosed with non-ischaemic cardiomyopathy and a pacemaker at age 86 years old. Patient lives with both parents and denies any smoking, ethanol consumption, recreational drug use, abuse or neglect at home. He worked at auto-part shop and planned to start college soon.\n\n\nInvestigations\n\n\nIn the ED, serum troponin I levels were found to be elevated and ECG showed diffuse ST-segment elevation. He was admitted to the local hospital and initial workup was remarkable for an enlarged cardiac silhouette and mild pulmonary oedema observed on chest X-ray, a transthoracic echocardiogram (TTE) demonstrating left ventricular ejection fraction (LVEF) of 40%, with severe left ventricular (LV) concentric hypertrophy and mild posterior pericardial effusion. Additionally, the patient was found to have elevated titres for Coxsackie virus A and B. His symptoms initially improved with the initiation of ibuprofen and colchicine. Cardiac catheterisation was performed, which revealed no evidence of coronary artery disease. Repeat TTE showed an LVEF of 40%–45%, hypokinesis of anteroapical and inferolateral wall, with an elevated LV end-diastolic pressure, consistent with diastolic dysfunction. Chest CT angiogram showed evidence of pneumonitis and a pericardial effusion. And at this point, the constellation of symptoms was thought to be secondary to Coxsackie myopericarditis, for which he continued to receive medical treatment as previously mentioned.\n\nOn the fourth day of admission, the patient became diaphoretic, tachycardic and hypotensive with an undetectable blood pressure. Emergent TTE showed large pericardial effusion with impending cardiac tamponade features, and pericardiocentesis was performed. During the procedure, the patient developed pulseless electrical activity (PEA) cardiac arrest and received advanced cardiovascular support for 30 min. Ultimately patient was intubated, placed on venous-arterial extracorporeal membrane oxygenation (VA ECMO) and started on vasopressor support (norepinephrine 5 mcg/min and vasopressin 0.05 units/min), with numerous transfusions (9 packed red bloodcells, 10 units of platelets, 10 units of cryoprecipitate and 4 units of fresh frozen plasma) due to significant oozing of blood from the ECMO cannula. He was transferred to our hospital where endomyocardial biopsy (EMB) was then obtained due to concern of fulminant myocarditis and to test for other infiltrative cardiomyopathies. Pathology reports showed no signs suggestive of inflammatory or infiltrative process in the endomyocardium. Coxsackie Abs were repeated and were positive for Cox A type 9, Coxsackie B2 and Coxsackie B6, and an elevated Epstein-Barr virus (EBV) DNA quantitative PCR at 133 000 IU/mL. At this point, another TTE was done, which showed a severely decreased ejection fraction (EF) of 10%–15% with previously noted severe LV concentric hypertrophy (1.9 cm septum and 2.2 cm in the inferolateral wall).\n\nThe patient was started on intravenous immunoglobulin (IVIG) for treatment of Coxsackie myocarditis, and broad-spectrum antibiotics due to worsening leucocytosis, but with no identified infectious focus. Colchicine was discontinued due to concern for rhabdomyolysis, with elevation of serum creatine kinase level to 2874 unit/L. Vasopressors were then discontinued and the patient was extubated. He also developed episode of flushing, fever, dyspnoea and decreasing oxygen saturation, with chest X-ray showing congested lung parenchyma with concerns for ARDS, therefore, IVIG was stopped.\n\nGiven improvement of cardiac function in another TTE with LVEF of 25%–30%, it was decided to attempt to remove the ECMO, which was unsuccessful. The patient remained on ECMO support and emergent discussion with heart failure team took place to determine best approach. The patient was evaluated for possible left ventricle assist device, however, deemed not a candidate due to significant global concentric LV hypertrophy, and the multidisciplinary team agreed to facilitate emergency listing for heart transplantation, with consideration to transition to another cardiovascular support such as intra-aortic balloon pump, with potential inotrope support.\n\nDuring further evaluation for possible heart transplant, an incisional biopsy of a 1×1 inch palpable, painless, rubbery, mobile mass in the right arm was done and sent for pathology. The patient mentioned he first noticed this lesion approximately 2–3 months before presenting to the ED. Pathology report of the right upper extremity mass showed aggressive EBV (+) NK/T-cell lymphoma with a cytotoxic immunophenotype (positive for CD 2, CD3, CD56, BCL2, granzyme B, TIA1, MUM1 and diffuse coexpression of Epstein-Barr virus-encoded small RNAs by in situ hybridisation), and a modified SMILE (Steroids, Methotrexate with leucovorin, Ifosfamide with mesna, L-asparaginase and Etoposide) chemotherapy regimen was started. In situ hybridisation of the EMB previously obtained were negative for EBV-RNA.\n\nCardiac MRI was obtained, which revealed hypokinesis of the inferolateral and anterolateral wall, as previously described by TTE, delayed enhancement in the subendocardial and transmural distribution in these regions, with relative sparing of the septum. Additionally, avid enhancement and thickening of the pericardium, without a mass identified, and a pocket of pericardial fluid with septations, concerning for loculations, were also noted.\n\n\nDifferential diagnosis\n\nThe constellation of symptoms (shortness of breath, orthopnoea, hypotension and subjective fevers), with findings such as diffuse ST-segment elevation on ECG, leakages of cardiac markers (troponin), elevated Coxsackie virus titres (both of serotype A and B), as well as echocardiographic findings of pericardial effusion; all seemed to correlate with a classic presentation of viral pericarditis clinical due to Coxackie virus. However, despite medical treatment with colchicine, the patient continued to decompensate and eventually required pericardiocentesis due to cardiac tamponade, then developed cardiac arrest and ultimately requires ECMO support, for what seems acute onset heart failure. In this setting, fulminant myocarditis secondary to Coxsackie virus was considered. Cardiotropic RNA virus, such as Coxackie viruses, induce receptor-mediated endocytosis, with viral replication contributing to cellular dysfunction and ultimately apoptosis of the cell.1 When susceptible individuals are infected with highly virulent viral strains, maladaptive immunologic activity can occur, leading to persistent activation of T cells and continued antibody-mediated myocyte destruction, which can ultimately lead to fulminant myocarditis. EBV myocarditis could also explain the rapid deterioration in the setting of a positive EBV PCR, which is a more sensitivity test than traditional serologies for detection of acute infection.2 However, in situ hybridisation was negative for EBV-RNA.\n\nNevertheless, the significant concentric hypertrophy observed on the initial TTEs and the atypical delayed enhancement observed on the cardiac MRI are not explained by this diagnosis. Additionally, the EMB did not show an inflammatory process.\n\nFortuitous finding of EBV (+) NK/T-cell lymphoma by incisional biopsy of the right upper extremity allowed for a more fitting diagnosis for this case. The pericardial effusion, unresponsive to initial medical treatment and new acute heart failure with concentric hypertrophic cardiomyopathy, in the setting of newly diagnosed NK/T-cell lymphoma, raises the possibility of NK/T-cell lymphoma with involvement of the myocardium and pericardium as the most adequate diagnosis in this scenario, which englobes all the features previously mentioned in this case.\n\nOther differentials taken into consideration include infiltrative cardiomyopathy such as amyloidosis. However, Congo red staining of the EMB samples failed to demonstrate deposition of amyloid.\n\n\nTreatment\n\nGiven the diagnosis of extranodal NK/T-cell lymphoma (ENKTCL) with suspected pericardial involvement and no bone marrow involvement, modified SMILE regimen was desired as the first-line chemotherapy regimen. This regimen includes dexamethasone, ifosfamide, mesna and etoposide, and excluded methotrexate, due to evidence of third-spacing and effusions, which could lead to delayed excretion and increased risk of toxicity.\n\nHowever, due to his compromised cardiac function, it was believed that the patient would not tolerate cytotoxic chemotherapy which requires aggressive intravenous, and alternatively, emergent chemotherapy regimen was instituted: carboplatin (day 1–day 3), etoposide (day 1–day 5) and dexamethasone. Peg-asparaginase was later introduced in the regimen (day 7–day 21). This regimen proved effective, as evidenced by rapid recovery of the LV function and overall haemodynamic stability, and decision was made to incorporate a modified SMILE chemotherapy regimen, of which he received two cycles. Then chemotherapy regimen was changed to dexamethasone, gemcitabine, carboplatin and peg-asparaginase (DDGP). The patient received two cycles of DDGP. A full body positron emission tomography (PET) scan was negative for lymphoma. The plan is to continue two more cycles of chemotherapy (to complete six total cycles of chemotherapy). Currently, the patient is considering radiation therapy and possible stem cell transplant, after completion of the chemotherapy regimen. Additionally, the patient is currently on guideline-directed medical therapy for heart failure and has completed cardiac rehabilitation.\n\n\nOutcome and follow-up\n\nThe patient has completed five out of six chemotherapy sessions with the previously mentioned regimens. After initiation of chemotherapy and optimal medical treatment for heart failure, the patient has recovered much of his cardiac function, as evidenced by an LVEF of 55%, no wall motion abnormalities and normal myocardial wall thickness on his most recent TTE. He continues to be followed by heart failure/cardiology team and oncology team in clinic.",
+    "diff_label_texts": "An 18-year-old Hispanic male with no prior medical history presented with 3–4 days of substernal, nonradiating chest pain, orthopnoea, dry cough, and subjective fevers. Initial ED workup showed elevated troponin I and diffuse ST-segment elevation. Chest X-ray demonstrated an enlarged cardiac silhouette with mild pulmonary oedema. TTE revealed LVEF 40% with severe LV concentric hypertrophy and a mild posterior pericardial effusion. Coxsackie A and B titres were elevated. Symptoms transiently improved on ibuprofen and colchicine. Coronary angiography showed no CAD. Repeat TTE showed LVEF 40–45%, anteroapical and inferolateral hypokinesis, and elevated LVEDP consistent with diastolic dysfunction. Chest CT angiography showed pneumonitis and a pericardial effusion. Working diagnosis was Coxsackie myopericarditis. On hospital day 4 he acutely decompensated (diaphoresis, tachycardia, undetectable BP). Emergent TTE showed a large pericardial effusion with impending tamponade; pericardiocentesis was performed but was complicated by PEA arrest requiring ~30 minutes of ACLS. He was intubated, cannulated to VA-ECMO, and started on vasopressors (norepinephrine 5 mcg/min, vasopressin 0.05 units/min) with substantial transfusion requirements (9 PRBC, 10 platelets, 10 cryoprecipitate, 4 FFP) due to cannula site oozing. At the receiving centre, EMB was obtained for suspected fulminant myocarditis/infiltrative disease and was negative for inflammatory or infiltrative pathology. Repeat serology showed Coxsackie A type 9 and Coxsackie B2/B6 positivity and EBV DNA PCR 133,000 IU/mL. TTE now showed EF 10–15% with persistent severe LV concentric hypertrophy (septum 1.9 cm, inferolateral wall 2.2 cm). He was started on IVIG for presumed Coxsackie myocarditis and broad-spectrum antibiotics for worsening leucocytosis without a clear source; colchicine was stopped for concern of rhabdomyolysis (CK 2874 U/L). He subsequently developed flushing, fever, dyspnoea, and hypoxaemia with CXR consistent with pulmonary congestion/concern for ARDS, and IVIG was discontinued. Vasopressors were weaned off and he was extubated. Attempted ECMO decannulation failed; due to global concentric LV hypertrophy he was not an LVAD candidate. Emergency heart transplant listing and possible transition to IABP with inotropes were discussed. During transplant evaluation, an incisional biopsy of a 1×1 inch, painless, mobile right arm mass disclosed aggressive EBV(+) NK/T-cell lymphoma with a cytotoxic immunophenotype (CD2+, CD3+, CD56+, BCL2+, granzyme B+, TIA1+, MUM1+, diffuse EBER positivity). In situ hybridisation of the prior EMB was negative for EBV-RNA. Cardiac MRI demonstrated inferolateral and anterolateral hypokinesis with subendocardial to transmural LGE in those territories with relative septal sparing, marked pericardial thickening with avid enhancement, and a loculated pericardial effusion; no discrete mass was identified. Differential included Coxsackie myopericarditis and EBV myocarditis (noting EBV PCR is more sensitive than serology), but the absence of myocardial inflammation on EMB, marked concentric hypertrophy, and atypical LGE pattern argued against primary viral myocarditis. Amyloidosis was considered, but Congo red staining on EMB was negative. The overall picture—pericardial effusion refractory to initial therapy, acute heart failure with concentric hypertrophy, and the new diagnosis of EBV(+) NK/T-cell lymphoma—favoured pericardial/myocardial involvement by ENKTCL. Given ENKTCL without marrow involvement and concern for third spacing, a modified SMILE was planned (excluding methotrexate). Because of haemodynamic instability and concerns about tolerating cytotoxic therapy, induction was initiated with carboplatin (days 1–3), etoposide (days 1–5), and dexamethasone; peg-asparaginase was added (days 7–21). This regimen led to rapid improvement in LV function and haemodynamic stability, after which two cycles of modified SMILE were administered, followed by two cycles of DDGP (dexamethasone, gemcitabine, carboplatin, peg-asparaginase). Whole-body PET was negative. The treatment plan is to complete six total cycles and consider radiotherapy and possible stem cell transplantation. He is on guideline-directed medical therapy for heart failure and has completed cardiac rehabilitation. Outcome: after initiation of chemotherapy and optimisation of HF therapy, TTE showed recovery of LVEF to 55%, normal wall motion, and normal myocardial wall thickness, with resolution of the pericardial effusion and regression of hypertrophy. He continues multidisciplinary follow-up with cardiology/heart failure and oncology. Pathophysiologic context: cardiotropic RNA viruses such as Coxsackie can trigger receptor-mediated endocytosis and replication, leading to myocyte dysfunction and apoptosis; in susceptible hosts, maladaptive immune activation (persistent T-cell activation and antibody-mediated myocyte injury) can precipitate fulminant myocarditis. In this case, however, the lack of myocardial inflammation on EMB and the imaging phenotype supported lymphoma-associated cardiac involvement rather than primary viral myocarditis.",
+    "summary": "An 18-year-old male patient presented to the emergency department complaining of new onset chest pain, fever and orthopnoea. Initial workup was remarkable for elevated troponin, diffuse ST-segment elevation on ECG and chest X-ray with enlarged cardiac silhouette. Transthoracic echocardiogram (TTE) demonstrates severe biventricular concentric hypertrophy and pericardial effusion. Also, Coxsackie virus A and B titres were positive, concerning for a classic viral pericarditis. However, despite medical management, the patient became dyspnoeic and hypotensive. Impending cardiac tamponade was observed on repeat TTE, and pericardiocentesis was performed, complicated by pulseless electrical activity cardiac arrest, and ultimately patient requiring venoarterial extracorporeal membrane oxygenation support. Emergent endomyocardial biopsy showed no inflammatory process, and a skin biopsy of a small lesion in the right arm showed unexpected diagnosis of Epstein-Barr virus (+) natural killer/T-cell lymphoma. On initiation of chemotherapy, clinical improvement was observed as evidenced by improving ejection fraction, resolution of pericardial effusion and gradual decrease in myocardial hypertrophy."
+  },
+  {
+    "doc_id": 68,
+    "label": "low_health_literacy",
+    "fulltext": "We report a rare case of euthyroid unilateral GO with early massive mono-muscular fibrosis in a 50-year-old male patient. The patient had a family history of cardiovascular disease, type 2 diabetes mellitus, and myasthenia gravis but no family or personal history of thyroid autoimmune disease. The patient was a smoker of 20 cigarettes a day from the age of 30 and presented dyslipidemia for several years. Since June 2020, he experienced rapid and progressive swelling of the soft tissues in the right orbit, moderate pain during ocular globe movements, redness of eyelids and diplopia. Visual acuity was normal in both eyes. In October 2020, the patient was evaluated in our outpatient clinic. Moderate right orbit active inflammation was confirmed by Clinical Activity Score 3/7 (CAS),3 and eyelid edema was moderate. The eyelid aperture was 14 mm in the right orbit and 10 mm in the left orbit, and the Hertel measurements were 24 mm and 18 mm in the right and left orbits, respectively. In addition, the patient presented a severe reduction in elevation, persistent depression in the primary position of the right ocular globe and constant diplopia, as scored according to the Gorman score.4 The quality of life evaluated by Graves’ Ophthalmopathy quality of life questionnaire (GO-QOL)5 was reduced in both appearance and functional subscales. However, the functional subscale was reduced with respect to the appearance subscale, as the values were 12.5 and 50, respectively (considering 0 = worse condition and 100 = the best health state). Visual acuity was normal, and color vision by Ishihara tables was 16/17 and 17/17 in the right and left eyes, respectively. Evaluation of extraocular muscles by computer tomography (CT) scan (contiguous 1.25 mm thick slices, 200 mA, 120 kV, pitch 0.5) showed severe enlargement of the lower rectal body to the edge of the insertion tendon in the right orbit. Remarkably, the morphology of the other extraocular muscles in both orbits was normal. The muscle orbit area ratio measured in the right eyes was 0.25 Autocad units (in-house method; vn ≤ 0.20±0.03).6 Thyroid function was normal with a slight increase in TSH-R-Ab: 1.75 mU/l (n.v. < 1.5 mU/l). The amplitude of the p100 wave was slightly reduced by electrophysiology evaluation in the right eye. A thyroid ultrasound scan of the thyroid gland showed a thyroiditis pattern. Biochemical and clinical evaluations were negative for hematological or other systemic diseases. Routine clinical tests were normal, but the total cholesterol levels that were 220 mg/dl, triglyceride levels were 297 mg/dl, and high-density lipoprotein cholesterol (HDL) levels were 38 mg/dl.\n\nThe patient was treated by intravenous corticosteroid pulse therapy (Solumedrol; Pfizer, Karlsruhe, Germany) with a cumulative dose of 4500 mg over 12 weeks, leading to the resolution of inflammatory signs and symptoms. However, GO-QOL, Hertel measurements and diplopia remained unchanged; in contrast, electrophysiology evaluation and visual acuity worsened. Two-wall orbital surgical decompression plus parenteral glucocorticoids was chosen as the second-line treatment for GO. In that context, a biopsy of the right inferior rectus muscle revealed massive fibrosis with adipose tissue infiltration of this extraocular muscle.",
+    "diff_label_texts": "This is a rare kind of thyroid eye disease that affected just one eye muscle. The person was 50, smoked, and had high blood fats. His thyroid levels were normal. A thyroid antibody in his blood was only a little high. His right eye lost movement very fast and stayed pulled down. He saw double all the time, and glasses could not fix it. This hurt his daily life a lot. Doctors gave strong steroids through a vein. The swelling got better, but the double vision did not. He then needed two surgeries to make more space in the eye socket. A small sample from the tight eye muscle showed a lot of scar-like tissue in the lower right eye muscle.",
+    "summary": "Here, we present a rare case of euthyroid single muscular GO in a 50-year-old patient who was a smoker and had dyslipidemia for several years. The patient experienced a very rapid and severe depression of ocular motility of the right eye that caused uncorrectable and constant diplopia, severely affecting his quality of life. He was euthyroid, and TSH-R-Ab plasmatic levels were only slightly elevated. Intravenous corticosteroid pulse therapy was partially effective, and two rounds of wall orbital surgical decompression were necessary. Massive mono-muscular fibrosis was evidenced by biopsy of the right inferior rectus muscle."
+  },
+  {
+    "doc_id": 68,
+    "label": "intermediate_health_literacy",
+    "fulltext": "We report a rare case of euthyroid unilateral GO with early massive mono-muscular fibrosis in a 50-year-old male patient. The patient had a family history of cardiovascular disease, type 2 diabetes mellitus, and myasthenia gravis but no family or personal history of thyroid autoimmune disease. The patient was a smoker of 20 cigarettes a day from the age of 30 and presented dyslipidemia for several years. Since June 2020, he experienced rapid and progressive swelling of the soft tissues in the right orbit, moderate pain during ocular globe movements, redness of eyelids and diplopia. Visual acuity was normal in both eyes. In October 2020, the patient was evaluated in our outpatient clinic. Moderate right orbit active inflammation was confirmed by Clinical Activity Score 3/7 (CAS),3 and eyelid edema was moderate. The eyelid aperture was 14 mm in the right orbit and 10 mm in the left orbit, and the Hertel measurements were 24 mm and 18 mm in the right and left orbits, respectively. In addition, the patient presented a severe reduction in elevation, persistent depression in the primary position of the right ocular globe and constant diplopia, as scored according to the Gorman score.4 The quality of life evaluated by Graves’ Ophthalmopathy quality of life questionnaire (GO-QOL)5 was reduced in both appearance and functional subscales. However, the functional subscale was reduced with respect to the appearance subscale, as the values were 12.5 and 50, respectively (considering 0 = worse condition and 100 = the best health state). Visual acuity was normal, and color vision by Ishihara tables was 16/17 and 17/17 in the right and left eyes, respectively. Evaluation of extraocular muscles by computer tomography (CT) scan (contiguous 1.25 mm thick slices, 200 mA, 120 kV, pitch 0.5) showed severe enlargement of the lower rectal body to the edge of the insertion tendon in the right orbit. Remarkably, the morphology of the other extraocular muscles in both orbits was normal. The muscle orbit area ratio measured in the right eyes was 0.25 Autocad units (in-house method; vn ≤ 0.20±0.03).6 Thyroid function was normal with a slight increase in TSH-R-Ab: 1.75 mU/l (n.v. < 1.5 mU/l). The amplitude of the p100 wave was slightly reduced by electrophysiology evaluation in the right eye. A thyroid ultrasound scan of the thyroid gland showed a thyroiditis pattern. Biochemical and clinical evaluations were negative for hematological or other systemic diseases. Routine clinical tests were normal, but the total cholesterol levels that were 220 mg/dl, triglyceride levels were 297 mg/dl, and high-density lipoprotein cholesterol (HDL) levels were 38 mg/dl.\n\nThe patient was treated by intravenous corticosteroid pulse therapy (Solumedrol; Pfizer, Karlsruhe, Germany) with a cumulative dose of 4500 mg over 12 weeks, leading to the resolution of inflammatory signs and symptoms. However, GO-QOL, Hertel measurements and diplopia remained unchanged; in contrast, electrophysiology evaluation and visual acuity worsened. Two-wall orbital surgical decompression plus parenteral glucocorticoids was chosen as the second-line treatment for GO. In that context, a biopsy of the right inferior rectus muscle revealed massive fibrosis with adipose tissue infiltration of this extraocular muscle.",
+    "diff_label_texts": "We describe a rare case of euthyroid, single-muscle thyroid eye disease (Graves’ orbitopathy) in a 50-year-old man who smoked and had dyslipidemia. He developed a very rapid and severe loss of upward movement in the right eye, producing constant, uncorrectable double vision and major quality-of-life impact. Thyroid function was normal, and TSH receptor antibodies were only slightly elevated. Imaging showed isolated enlargement of the right inferior rectus muscle; the other eye muscles were normal. Intravenous steroid pulses reduced inflammation but did not improve the diplopia or eye position. He ultimately required two orbital decompression surgeries. A biopsy of the right inferior rectus confirmed massive fibrosis with fat infiltration, consistent with single-muscle involvement.",
+    "summary": "Here, we present a rare case of euthyroid single muscular GO in a 50-year-old patient who was a smoker and had dyslipidemia for several years. The patient experienced a very rapid and severe depression of ocular motility of the right eye that caused uncorrectable and constant diplopia, severely affecting his quality of life. He was euthyroid, and TSH-R-Ab plasmatic levels were only slightly elevated. Intravenous corticosteroid pulse therapy was partially effective, and two rounds of wall orbital surgical decompression were necessary. Massive mono-muscular fibrosis was evidenced by biopsy of the right inferior rectus muscle."
+  },
+  {
+    "doc_id": 68,
+    "label": "proficient_health_literacy",
+    "fulltext": "We report a rare case of euthyroid unilateral GO with early massive mono-muscular fibrosis in a 50-year-old male patient. The patient had a family history of cardiovascular disease, type 2 diabetes mellitus, and myasthenia gravis but no family or personal history of thyroid autoimmune disease. The patient was a smoker of 20 cigarettes a day from the age of 30 and presented dyslipidemia for several years. Since June 2020, he experienced rapid and progressive swelling of the soft tissues in the right orbit, moderate pain during ocular globe movements, redness of eyelids and diplopia. Visual acuity was normal in both eyes. In October 2020, the patient was evaluated in our outpatient clinic. Moderate right orbit active inflammation was confirmed by Clinical Activity Score 3/7 (CAS),3 and eyelid edema was moderate. The eyelid aperture was 14 mm in the right orbit and 10 mm in the left orbit, and the Hertel measurements were 24 mm and 18 mm in the right and left orbits, respectively. In addition, the patient presented a severe reduction in elevation, persistent depression in the primary position of the right ocular globe and constant diplopia, as scored according to the Gorman score.4 The quality of life evaluated by Graves’ Ophthalmopathy quality of life questionnaire (GO-QOL)5 was reduced in both appearance and functional subscales. However, the functional subscale was reduced with respect to the appearance subscale, as the values were 12.5 and 50, respectively (considering 0 = worse condition and 100 = the best health state). Visual acuity was normal, and color vision by Ishihara tables was 16/17 and 17/17 in the right and left eyes, respectively. Evaluation of extraocular muscles by computer tomography (CT) scan (contiguous 1.25 mm thick slices, 200 mA, 120 kV, pitch 0.5) showed severe enlargement of the lower rectal body to the edge of the insertion tendon in the right orbit. Remarkably, the morphology of the other extraocular muscles in both orbits was normal. The muscle orbit area ratio measured in the right eyes was 0.25 Autocad units (in-house method; vn ≤ 0.20±0.03).6 Thyroid function was normal with a slight increase in TSH-R-Ab: 1.75 mU/l (n.v. < 1.5 mU/l). The amplitude of the p100 wave was slightly reduced by electrophysiology evaluation in the right eye. A thyroid ultrasound scan of the thyroid gland showed a thyroiditis pattern. Biochemical and clinical evaluations were negative for hematological or other systemic diseases. Routine clinical tests were normal, but the total cholesterol levels that were 220 mg/dl, triglyceride levels were 297 mg/dl, and high-density lipoprotein cholesterol (HDL) levels were 38 mg/dl.\n\nThe patient was treated by intravenous corticosteroid pulse therapy (Solumedrol; Pfizer, Karlsruhe, Germany) with a cumulative dose of 4500 mg over 12 weeks, leading to the resolution of inflammatory signs and symptoms. However, GO-QOL, Hertel measurements and diplopia remained unchanged; in contrast, electrophysiology evaluation and visual acuity worsened. Two-wall orbital surgical decompression plus parenteral glucocorticoids was chosen as the second-line treatment for GO. In that context, a biopsy of the right inferior rectus muscle revealed massive fibrosis with adipose tissue infiltration of this extraocular muscle.",
+    "diff_label_texts": "We report a rare case of euthyroid unilateral GO with early massive mono-muscular fibrosis in a 50-year-old male. Family history included cardiovascular disease, type 2 diabetes mellitus, and myasthenia gravis, with no family or personal history of thyroid autoimmune disease. He smoked 20 cigarettes/day since age 30 and had longstanding dyslipidemia. Beginning June 2020, he developed rapid, progressive right orbital soft-tissue swelling, pain on ocular movements, eyelid redness, and diplopia; visual acuity was initially normal OU. In October 2020, examination showed active right orbital inflammation (CAS 3/7) with moderate eyelid edema. Palpebral fissure height was 14 mm OD and 10 mm OS. Hertel exophthalmometry was 24 mm OD and 18 mm OS. There was severe limitation of elevation, persistent depression in primary position OD, and constant diplopia per the Gorman score. GO-QOL was reduced in both subscales, with a greater decrement in function (12.5) than appearance (50) on a 0–100 scale. Color vision by Ishihara was 16/17 OD and 17/17 OS. CT (contiguous 1.25 mm slices, 200 mA, 120 kV, pitch 0.5) demonstrated severe enlargement of the right inferior rectus to the tendon insertion; all other extraocular muscles were normal OU. The muscle–orbit area ratio OD was 0.25 AutoCAD units (vn ≤ 0.20 ± 0.03). Thyroid function was normal with slightly increased TSH-R-Ab at 1.75 mU/L (n.v. < 1.5 mU/L). Electrophysiology showed a slight reduction in p100 amplitude OD. Thyroid ultrasound displayed a thyroiditis pattern. Hematologic and systemic evaluations were negative. Routine labs were unremarkable aside from dyslipidemia (total cholesterol 220 mg/dl, triglycerides 297 mg/dl, HDL 38 mg/dl).\n\nTreatment with intravenous corticosteroid pulse therapy (methylprednisolone; cumulative 4,500 mg over 12 weeks) resolved inflammatory signs and symptoms; however, GO-QOL, Hertel exophthalmometry, and diplopia remained unchanged, and both visual acuity and electrophysiology worsened. As second-line therapy, two-wall orbital surgical decompression plus parenteral glucocorticoids was performed. Intraoperative biopsy of the right inferior rectus revealed massive fibrosis with adipose tissue infiltration.\n\nThis case exemplifies euthyroid unilateral GO with isolated inferior rectus involvement and early fibrotic transformation despite only mildly elevated TSH-R-Ab, producing a profound motility deficit and constant diplopia that was refractory to IV steroids and required bony decompression.",
+    "summary": "Here, we present a rare case of euthyroid single muscular GO in a 50-year-old patient who was a smoker and had dyslipidemia for several years. The patient experienced a very rapid and severe depression of ocular motility of the right eye that caused uncorrectable and constant diplopia, severely affecting his quality of life. He was euthyroid, and TSH-R-Ab plasmatic levels were only slightly elevated. Intravenous corticosteroid pulse therapy was partially effective, and two rounds of wall orbital surgical decompression were necessary. Massive mono-muscular fibrosis was evidenced by biopsy of the right inferior rectus muscle."
+  },
+  {
+    "doc_id": 69,
+    "label": "low_health_literacy",
+    "fulltext": "We present the clinical case of a 15-year-old male with no medical history or previous interventions, who presented to the paediatric emergency department with a history of vomiting and epigastric abdominal pain of four days' duration, remaining afebrile during the course of the illness.\n\nInitially treated as gastroenteritis, but with no improvement, and with persistence of epigastric abdominal pain and biliary vomiting, he was admitted to the emergency department for further evaluation.\n\nOn physical examination, the patient was in acceptable general condition, afebrile, with mild signs of dehydration. The abdomen was distended, without signs of peritonism and with decreased hydroaerolic sounds. The laboratory tests did not present significant findings, and an abdominal radiograph was performed with findings suggestive of intestinal obstruction.\n\nGiven the evolution, an urgent computed tomography was performed, which showed the presence of ascites and significant dilation of small intestine loops, suggesting the interposition of a small intestine loop at the beginning of the transcavity of the epiplons, with a change in caliber at the level of the hiatus of Winslow.\n\nUrgent surgical intervention was performed, initially by exploratory laparoscopy. Dilated loops of small intestine and terminal ileum, cecum and ascending colon of normal calibre but located in the right hypochondrium, with the cecum very mobile and without presenting adhesions to the right parietocolic space, were observed. Following the terminal ileum proximally, loops of small intestine of different calibre were observed from the depth of the theoretical location of the hiatus of Winslow. It was possible to pull the cecum and terminal ileum until they were displaced to the right iliac fossa, but without correctly identifying the point of change of calibre, since the interposition of the lower edge of the liver and the distension of loops of small intestine hampered the technique. An attempt was made to improve visualization by percutaneous puncture of a dilated loop to empty the gas, without improvement. To ensure the resolution of the obstructive picture, a supraumbilical mid-laparotomy was decided. When accessing the cavity, the change of calibre in the ileum was evident, about 40 centimetres from the ileocecal valve, with signs compatible with hernia of a section of about five centimetres of the ileum through the hiatus of Winslow. In both ends of the herniated loop, we observed the congestive imprint of the hiatus on the loop (Fig. 3). The normal calibre of the hiatus of Winslow was identified, so no preventive technique was performed to reduce the risk of recurrence.\n\nDuring the first days of the postoperative period, the patient presented a paralytic ileus, and the nasogastric tube could be removed five days after surgery and oral tolerance was initiated with a good response. Simultaneously, he developed a pelvic collection that was managed conservatively with antibiotics, with a good evolution. Finally, the patient was discharged ten days after the intervention, with preserved transit, remaining afebrile and with a good general state.\n\nThe patient is currently being followed up in the outpatient department of paediatric surgery.\n",
+    "diff_label_texts": "A 15-year-old boy had bad belly pain and was throwing up. A CT scan showed his small intestine was blocked because a loop slipped through a small opening deep in the upper belly. Doctors first tried surgery with a small camera. They could not see well. They changed to a bigger cut down the middle above his belly button. They moved the trapped intestine back where it belongs. The intestine looked healthy, so nothing had to be removed. They did not do an extra step to try to stop this from happening again. After surgery, he got a pocket of fluid in the lower belly. It was treated with antibiotics. He is going to follow-up visits in the children’s surgery clinic.",
+    "summary": "We present the clinical case of a 15-year-old adolescent male with no previous surgical history, who presented with abdominal pain and vomiting, and whose computed tomography suggested a picture of intestinal obstruction due to internal hernia at the level of the Winslow hiatus. He required surgical intervention by exploratory laparoscopy, converted to a supraumbilical midline laparotomy due to poor visualization, for reduction of the herniated ileal loop. This presented a good appearance and intestinal resection was not necessary. No preventive technique was performed to reduce the risk of recurrence. Postoperatively, the patient presented a pelvic collection managed conservatively with antibiotics. He is currently being monitored in outpatient paediatric surgery.\n"
+  },
+  {
+    "doc_id": 69,
+    "label": "intermediate_health_literacy",
+    "fulltext": "We present the clinical case of a 15-year-old male with no medical history or previous interventions, who presented to the paediatric emergency department with a history of vomiting and epigastric abdominal pain of four days' duration, remaining afebrile during the course of the illness.\n\nInitially treated as gastroenteritis, but with no improvement, and with persistence of epigastric abdominal pain and biliary vomiting, he was admitted to the emergency department for further evaluation.\n\nOn physical examination, the patient was in acceptable general condition, afebrile, with mild signs of dehydration. The abdomen was distended, without signs of peritonism and with decreased hydroaerolic sounds. The laboratory tests did not present significant findings, and an abdominal radiograph was performed with findings suggestive of intestinal obstruction.\n\nGiven the evolution, an urgent computed tomography was performed, which showed the presence of ascites and significant dilation of small intestine loops, suggesting the interposition of a small intestine loop at the beginning of the transcavity of the epiplons, with a change in caliber at the level of the hiatus of Winslow.\n\nUrgent surgical intervention was performed, initially by exploratory laparoscopy. Dilated loops of small intestine and terminal ileum, cecum and ascending colon of normal calibre but located in the right hypochondrium, with the cecum very mobile and without presenting adhesions to the right parietocolic space, were observed. Following the terminal ileum proximally, loops of small intestine of different calibre were observed from the depth of the theoretical location of the hiatus of Winslow. It was possible to pull the cecum and terminal ileum until they were displaced to the right iliac fossa, but without correctly identifying the point of change of calibre, since the interposition of the lower edge of the liver and the distension of loops of small intestine hampered the technique. An attempt was made to improve visualization by percutaneous puncture of a dilated loop to empty the gas, without improvement. To ensure the resolution of the obstructive picture, a supraumbilical mid-laparotomy was decided. When accessing the cavity, the change of calibre in the ileum was evident, about 40 centimetres from the ileocecal valve, with signs compatible with hernia of a section of about five centimetres of the ileum through the hiatus of Winslow. In both ends of the herniated loop, we observed the congestive imprint of the hiatus on the loop (Fig. 3). The normal calibre of the hiatus of Winslow was identified, so no preventive technique was performed to reduce the risk of recurrence.\n\nDuring the first days of the postoperative period, the patient presented a paralytic ileus, and the nasogastric tube could be removed five days after surgery and oral tolerance was initiated with a good response. Simultaneously, he developed a pelvic collection that was managed conservatively with antibiotics, with a good evolution. Finally, the patient was discharged ten days after the intervention, with preserved transit, remaining afebrile and with a good general state.\n\nThe patient is currently being followed up in the outpatient department of paediatric surgery.\n",
+    "diff_label_texts": "A 15-year-old male with no prior surgeries developed four days of abdominal pain and vomiting. CT suggested a small-bowel obstruction from an internal hernia through the foramen (hiatus) of Winslow, an opening behind the stomach. He underwent urgent surgery that began as a diagnostic laparoscopy but was converted to a supraumbilical midline laparotomy because the view was poor. The surgeons reduced a herniated ileal loop; the bowel looked viable, so no resection was needed. They did not perform a preventive maneuver to lower the risk of recurrence. After surgery, he developed a pelvic fluid collection that was managed with antibiotics alone. He is currently followed in the outpatient pediatric surgery clinic.",
+    "summary": "We present the clinical case of a 15-year-old adolescent male with no previous surgical history, who presented with abdominal pain and vomiting, and whose computed tomography suggested a picture of intestinal obstruction due to internal hernia at the level of the Winslow hiatus. He required surgical intervention by exploratory laparoscopy, converted to a supraumbilical midline laparotomy due to poor visualization, for reduction of the herniated ileal loop. This presented a good appearance and intestinal resection was not necessary. No preventive technique was performed to reduce the risk of recurrence. Postoperatively, the patient presented a pelvic collection managed conservatively with antibiotics. He is currently being monitored in outpatient paediatric surgery.\n"
+  },
+  {
+    "doc_id": 69,
+    "label": "proficient_health_literacy",
+    "fulltext": "We present the clinical case of a 15-year-old male with no medical history or previous interventions, who presented to the paediatric emergency department with a history of vomiting and epigastric abdominal pain of four days' duration, remaining afebrile during the course of the illness.\n\nInitially treated as gastroenteritis, but with no improvement, and with persistence of epigastric abdominal pain and biliary vomiting, he was admitted to the emergency department for further evaluation.\n\nOn physical examination, the patient was in acceptable general condition, afebrile, with mild signs of dehydration. The abdomen was distended, without signs of peritonism and with decreased hydroaerolic sounds. The laboratory tests did not present significant findings, and an abdominal radiograph was performed with findings suggestive of intestinal obstruction.\n\nGiven the evolution, an urgent computed tomography was performed, which showed the presence of ascites and significant dilation of small intestine loops, suggesting the interposition of a small intestine loop at the beginning of the transcavity of the epiplons, with a change in caliber at the level of the hiatus of Winslow.\n\nUrgent surgical intervention was performed, initially by exploratory laparoscopy. Dilated loops of small intestine and terminal ileum, cecum and ascending colon of normal calibre but located in the right hypochondrium, with the cecum very mobile and without presenting adhesions to the right parietocolic space, were observed. Following the terminal ileum proximally, loops of small intestine of different calibre were observed from the depth of the theoretical location of the hiatus of Winslow. It was possible to pull the cecum and terminal ileum until they were displaced to the right iliac fossa, but without correctly identifying the point of change of calibre, since the interposition of the lower edge of the liver and the distension of loops of small intestine hampered the technique. An attempt was made to improve visualization by percutaneous puncture of a dilated loop to empty the gas, without improvement. To ensure the resolution of the obstructive picture, a supraumbilical mid-laparotomy was decided. When accessing the cavity, the change of calibre in the ileum was evident, about 40 centimetres from the ileocecal valve, with signs compatible with hernia of a section of about five centimetres of the ileum through the hiatus of Winslow. In both ends of the herniated loop, we observed the congestive imprint of the hiatus on the loop (Fig. 3). The normal calibre of the hiatus of Winslow was identified, so no preventive technique was performed to reduce the risk of recurrence.\n\nDuring the first days of the postoperative period, the patient presented a paralytic ileus, and the nasogastric tube could be removed five days after surgery and oral tolerance was initiated with a good response. Simultaneously, he developed a pelvic collection that was managed conservatively with antibiotics, with a good evolution. Finally, the patient was discharged ten days after the intervention, with preserved transit, remaining afebrile and with a good general state.\n\nThe patient is currently being followed up in the outpatient department of paediatric surgery.\n",
+    "diff_label_texts": "A 15-year-old male with no medical history or prior interventions presented to the pediatric emergency department with 4 days of epigastric abdominal pain and bilious vomiting; he remained afebrile. Examination showed mild dehydration, abdominal distension without peritonism, and decreased hydroaeric sounds. Laboratory tests were unremarkable. An abdominal radiograph was suggestive of intestinal obstruction. Urgent CT demonstrated ascites and marked dilation of small-intestinal loops, with interposition of a small-intestinal loop at the entrance to the transcavity of the epiplons and a caliber change at the level of the hiatus (foramen) of Winslow—compatible with small-bowel obstruction due to an internal hernia.\n\nUrgent exploratory laparoscopy was performed. Intraoperatively, dilated small-bowel loops were seen; the terminal ileum, cecum, and ascending colon were of normal caliber but located in the right hypochondrium, with a very mobile cecum and no adhesions to the right parietocolic space. Following the terminal ileum proximally revealed small-bowel loops of differing caliber arising from the depth of the theoretical location of the hiatus of Winslow. Traction on the cecum and terminal ileum allowed displacement toward the right iliac fossa, but the point of caliber change could not be identified due to the interposition of the inferior hepatic edge and small-bowel distension. Percutaneous puncture of a dilated loop for gas decompression did not improve visualization. To ensure definitive management, conversion to a supraumbilical midline laparotomy was undertaken. On entering the cavity, a caliber change in the ileum was evident ~40 cm from the ileocecal valve, with findings consistent with herniation of an approximately 5-cm ileal segment through the hiatus of Winslow; both ends of the herniated loop bore a congestive imprint from the hiatus. The hiatus of Winslow was of normal caliber; no preventive technique (e.g., narrowing or closure) was performed to reduce recurrence risk. The herniated loop was reduced; it appeared viable, and intestinal resection was not necessary.\n\nPostoperatively, the patient developed a paralytic ileus; the nasogastric tube was removed on postoperative day 5, and oral intake was initiated with good tolerance. A pelvic collection occurred and was managed conservatively with antibiotics, with favorable evolution. He was discharged on postoperative day 10 with preserved transit, afebrile, and in good general condition. He is being followed in the outpatient pediatric surgery clinic.\n\nContext: Internal herniation through the foramen of Winslow is an uncommon cause of small-bowel obstruction; CT identification of a transition at the foramen supports prompt operative reduction, and bowel viability often permits avoidance of resection.",
+    "summary": "We present the clinical case of a 15-year-old adolescent male with no previous surgical history, who presented with abdominal pain and vomiting, and whose computed tomography suggested a picture of intestinal obstruction due to internal hernia at the level of the Winslow hiatus. He required surgical intervention by exploratory laparoscopy, converted to a supraumbilical midline laparotomy due to poor visualization, for reduction of the herniated ileal loop. This presented a good appearance and intestinal resection was not necessary. No preventive technique was performed to reduce the risk of recurrence. Postoperatively, the patient presented a pelvic collection managed conservatively with antibiotics. He is currently being monitored in outpatient paediatric surgery.\n"
+  },
+  {
+    "doc_id": 70,
+    "label": "low_health_literacy",
+    "fulltext": "This is a 75-year-old para 6 patient from Western Ethiopia who saw her last menses 25 years back. Her age at giving birth to her 1st child and menopause were 18 and 50 years, respectively. She had occasional pelvic pain for the last 3 years for which she was visiting different health facilities. Currently, she presented to Nekemte Specialized Hospital with exacerbation of lower abdominal pain for 3 weeks. She feels discomfort in her vagina but no protrusion of mass through her vagina. She has no history of fever, abdominal swelling, vaginal discharge, or bleeding. All her previous deliveries were normal vaginal deliveries. Upon enquiring about the history of family planning utilization, she reported that the intrauterine device was inserted 40 years back at a public hospital. Since then, she had no history of gynecologic evaluation for a checkup. She had no history of gynecologic procedures, pelvic or abdominal surgery. The patient has no history of medical problems like diabetes mellitus, hypertension, cardiac or renal problems.\n\nOn examination, she was acutely sick-looking. Her vital signs were blood pressure (BP) = 120/80mmHg, pulse rate (PR) = 82 beats per minute, respiratory rate (RR) = 18 breaths per minute, and temperature of 37.1°C. She had pink conjunctivae. Lymph glandular system, chest, and cardiovascular system were normal. On abdominal examination, there was no mass, organomegaly, area of tenderness, or signs of fluid collection. Inspection of external genitalia showed no vulvar mass or lesion. On speculum examination, there is a foreign body at the external cervical os. However, there is no other cervical mass or lesion. On bimanual examination, the uterus was not enlarged and there was no adnexal mass or tenderness. On the integumentary system, she had no palmar pallor. On neurologic examination, she was oriented to time, person, and place. She had normal reflexes and no neurologic deficits.\n\nOn laboratory investigation, an ultrasound examination was done by a radiologist and showed unremarkable pelvic findings. Urinalysis, complete blood count, and serum blood glucose level were normal. With the final diagnosis of postmenopausal pelvic pain secondary to the retained intrauterine device, the patient was prepared and taken to the gynecology procedure room. In the lithotomy position, the speculum was inserted and the intrauterine device was easily removed with spongy forceps. The mother was observed for 4 hours and discharged with analgesia and doxycycline 100 mg PO twice a day for three days. Upon follow-up, the pelvic pain was resolved.",
+    "diff_label_texts": "A 75-year-old woman in Western Ethiopia had a birth control loop in her womb for 40 years. She had lower belly pain after her periods had stopped. Doctors looked inside the vagina with a small tool. They saw part of the loop at the opening of the womb. They gently pulled it out with a soft clamp. She went home with pain medicine. She also took an antibiotic called doxycycline two times a day for 3 days.",
+    "summary": "We present the case of retained Lippes loop IUD for 40 years in a 75-year-old postmenopausal patient from Western Ethiopia. The patient presented to the hospital with postmenopausal pelvic pain. Speculum exam showed part of loop at external cervical os. The loop was easily removed with spongy forceps. The patient was discharged with analgesia and doxycycline twice a day for 3 days."
+  },
+  {
+    "doc_id": 70,
+    "label": "intermediate_health_literacy",
+    "fulltext": "This is a 75-year-old para 6 patient from Western Ethiopia who saw her last menses 25 years back. Her age at giving birth to her 1st child and menopause were 18 and 50 years, respectively. She had occasional pelvic pain for the last 3 years for which she was visiting different health facilities. Currently, she presented to Nekemte Specialized Hospital with exacerbation of lower abdominal pain for 3 weeks. She feels discomfort in her vagina but no protrusion of mass through her vagina. She has no history of fever, abdominal swelling, vaginal discharge, or bleeding. All her previous deliveries were normal vaginal deliveries. Upon enquiring about the history of family planning utilization, she reported that the intrauterine device was inserted 40 years back at a public hospital. Since then, she had no history of gynecologic evaluation for a checkup. She had no history of gynecologic procedures, pelvic or abdominal surgery. The patient has no history of medical problems like diabetes mellitus, hypertension, cardiac or renal problems.\n\nOn examination, she was acutely sick-looking. Her vital signs were blood pressure (BP) = 120/80mmHg, pulse rate (PR) = 82 beats per minute, respiratory rate (RR) = 18 breaths per minute, and temperature of 37.1°C. She had pink conjunctivae. Lymph glandular system, chest, and cardiovascular system were normal. On abdominal examination, there was no mass, organomegaly, area of tenderness, or signs of fluid collection. Inspection of external genitalia showed no vulvar mass or lesion. On speculum examination, there is a foreign body at the external cervical os. However, there is no other cervical mass or lesion. On bimanual examination, the uterus was not enlarged and there was no adnexal mass or tenderness. On the integumentary system, she had no palmar pallor. On neurologic examination, she was oriented to time, person, and place. She had normal reflexes and no neurologic deficits.\n\nOn laboratory investigation, an ultrasound examination was done by a radiologist and showed unremarkable pelvic findings. Urinalysis, complete blood count, and serum blood glucose level were normal. With the final diagnosis of postmenopausal pelvic pain secondary to the retained intrauterine device, the patient was prepared and taken to the gynecology procedure room. In the lithotomy position, the speculum was inserted and the intrauterine device was easily removed with spongy forceps. The mother was observed for 4 hours and discharged with analgesia and doxycycline 100 mg PO twice a day for three days. Upon follow-up, the pelvic pain was resolved.",
+    "diff_label_texts": "A 75-year-old postmenopausal woman from Western Ethiopia had a Lippes loop IUD retained for 40 years and came in with pelvic pain. On speculum exam, part of the loop was seen at the external opening of the cervix. The device was removed easily with spongy forceps. She was discharged with pain medication and doxycycline twice a day for 3 days. Additional context: She reported no fever, bleeding, or vaginal discharge; her exam and pelvic ultrasound were otherwise unremarkable. She was observed for a few hours after removal, then sent home. On follow-up, her pelvic pain resolved.",
+    "summary": "We present the case of retained Lippes loop IUD for 40 years in a 75-year-old postmenopausal patient from Western Ethiopia. The patient presented to the hospital with postmenopausal pelvic pain. Speculum exam showed part of loop at external cervical os. The loop was easily removed with spongy forceps. The patient was discharged with analgesia and doxycycline twice a day for 3 days."
+  },
+  {
+    "doc_id": 71,
+    "label": "low_health_literacy",
+    "fulltext": "A 71-year-old patient with a history of untreated vitiligo presented with visual loss in the right eye 6 months prior to admission accompanied by bilateral hearing loss with a predominance in the right ear. Chronic headaches and intermittent fever were also reported, although the patient denied a history of drug use or prior infections. He was evaluated by our department due to the presence of significant and unintentional weight loss, generalized weakness and thickening of the skin. On initial ophthalmologic examination, visual acuity in the right eye (RO) was reduced to light perception and color discrimination, and visual acuity in the left eye (LO) was 20/200 with afferent pupillary defect in both eyes with hyperemic margins of the eyelid. On examination of the RO, it was found to have a hyperemic bulbar conjunctiva, ciliary injection, cornea with peripheral, nummular, subepithelial infiltrates, aqueous anterior chamber (AAC) without cellularity, normal iris and lens with nuclear opacities. On examination of the left eye, it was found to have a hyperemic bulbar conjunctiva, ciliary injection, cornea with peripheral, nummular, subepithelial infiltrates, AAC, aqueous without cellularity, normal iris and lens with nuclear opacities. On examination of the right fundus, a round, pale ++ papilla was found with a 50% excavation, slightly blunt nasal border, with a raised and thinned vascular pattern, with macular area and scattered pigment. On the left fundus, a vitreous haze 2+ was found with edematous papilla, blurred borders, hyperemic, peripapillary, streaked hemorrhages, and an unevaluable excavation with a thinned vascular pattern and macular area with scattered pigment, with right optic atrophy and left anterior optic neuritis.\n\nDue to ocular involvement, weight loss and neurological symptoms, additional testing was performed to rule out causes such as tuberculosis, herpes, ANCA and non-ANCA vasculitis, and sarcoidosis. As for the management of the neurological condition, a lumbar puncture was performed and an opening pressure within normal limits and a proteinocracy of 54 mg/dL was found. Due to distal symmetric polyneuropathy, nerve conduction velocities (NCV) were performed, which showed a pattern of polyradiculoneuropathy with moderate to severe axonal degeneration, involving all 4 extremities with a predominance of the lower extremities; the contrasted magnetic resonance imaging (MRI) of the skull and orbit did not show enhancement of the optic nerve or brain tumors; however, it did show sinusitis and meningeal enhancement. Within the management, sarcoidosis was ruled out, with angiotensin converting enzyme (ACE) within normal parameters, as well as a whole body gamma scan, without enhancement or boosting. After all the study and clinical evaluation of the patient, a second ophthalmological assessment was performed in which persistence and progression of the ocular condition was found, with optic atrophy in the right eye and anterior optic neuritis in the left eye. Because of this, high dose pulse steroid treatment was initiated, followed by a gradual reduction of the dose and the patient was referred for follow-up in the Outpatient Department. A clinical and functional improvement was observed, mainly at the neurological and ophthalmological level.\n",
+    "diff_label_texts": "A 71-year-old man had vitiligo for many years. He lost vision in his right eye about six months before he came to the hospital. He also had hearing loss in both ears, worse on the right. While in the hospital, he had ongoing headaches. He had fevers. He lost a lot of weight without trying. The eye exam showed the right eye could only sense light. The white part of the right eye looked very red. The left eye could see at 20/200, which is very blurry. The back of the right eye had small specks of color. The back of the left eye showed a swollen nerve. The nerve of the right eye looked damaged.",
+    "summary": "A 71-year-old man with a history of long-standing vitiligo who had experienced visual loss in his right eye six months prior to admission, along with bilateral hearing loss, predominantly in the right ear. During his hospital stay, he presented with chronic headaches, fever, and significant involuntary weight loss. On ophthalmologic examination, the right eye was light sensitive with hyperemic bulbar conjunctiva, while the left eye had a visual acuity of 20/200. The fundus of the right eye had scattered pigmentation, while the left eye had a swollen optic disc and right optic atrophy.\n"
+  },
+  {
+    "doc_id": 71,
+    "label": "intermediate_health_literacy",
+    "fulltext": "A 71-year-old patient with a history of untreated vitiligo presented with visual loss in the right eye 6 months prior to admission accompanied by bilateral hearing loss with a predominance in the right ear. Chronic headaches and intermittent fever were also reported, although the patient denied a history of drug use or prior infections. He was evaluated by our department due to the presence of significant and unintentional weight loss, generalized weakness and thickening of the skin. On initial ophthalmologic examination, visual acuity in the right eye (RO) was reduced to light perception and color discrimination, and visual acuity in the left eye (LO) was 20/200 with afferent pupillary defect in both eyes with hyperemic margins of the eyelid. On examination of the RO, it was found to have a hyperemic bulbar conjunctiva, ciliary injection, cornea with peripheral, nummular, subepithelial infiltrates, aqueous anterior chamber (AAC) without cellularity, normal iris and lens with nuclear opacities. On examination of the left eye, it was found to have a hyperemic bulbar conjunctiva, ciliary injection, cornea with peripheral, nummular, subepithelial infiltrates, AAC, aqueous without cellularity, normal iris and lens with nuclear opacities. On examination of the right fundus, a round, pale ++ papilla was found with a 50% excavation, slightly blunt nasal border, with a raised and thinned vascular pattern, with macular area and scattered pigment. On the left fundus, a vitreous haze 2+ was found with edematous papilla, blurred borders, hyperemic, peripapillary, streaked hemorrhages, and an unevaluable excavation with a thinned vascular pattern and macular area with scattered pigment, with right optic atrophy and left anterior optic neuritis.\n\nDue to ocular involvement, weight loss and neurological symptoms, additional testing was performed to rule out causes such as tuberculosis, herpes, ANCA and non-ANCA vasculitis, and sarcoidosis. As for the management of the neurological condition, a lumbar puncture was performed and an opening pressure within normal limits and a proteinocracy of 54 mg/dL was found. Due to distal symmetric polyneuropathy, nerve conduction velocities (NCV) were performed, which showed a pattern of polyradiculoneuropathy with moderate to severe axonal degeneration, involving all 4 extremities with a predominance of the lower extremities; the contrasted magnetic resonance imaging (MRI) of the skull and orbit did not show enhancement of the optic nerve or brain tumors; however, it did show sinusitis and meningeal enhancement. Within the management, sarcoidosis was ruled out, with angiotensin converting enzyme (ACE) within normal parameters, as well as a whole body gamma scan, without enhancement or boosting. After all the study and clinical evaluation of the patient, a second ophthalmological assessment was performed in which persistence and progression of the ocular condition was found, with optic atrophy in the right eye and anterior optic neuritis in the left eye. Because of this, high dose pulse steroid treatment was initiated, followed by a gradual reduction of the dose and the patient was referred for follow-up in the Outpatient Department. A clinical and functional improvement was observed, mainly at the neurological and ophthalmological level.\n",
+    "diff_label_texts": "A 71-year-old man with long-standing vitiligo reported six months of visual loss in the right eye and hearing loss in both ears, worse on the right. During hospitalization, he had chronic headaches, fever, and marked unintentional weight loss. On eye exam, the right eye was reduced to light perception and the white of the eye was notably red; the left eye had a visual acuity of 20/200. Fundus findings showed scattered pigmentation in the right eye, a swollen optic disc in the left eye, and evidence of optic atrophy on the right.",
+    "summary": "A 71-year-old man with a history of long-standing vitiligo who had experienced visual loss in his right eye six months prior to admission, along with bilateral hearing loss, predominantly in the right ear. During his hospital stay, he presented with chronic headaches, fever, and significant involuntary weight loss. On ophthalmologic examination, the right eye was light sensitive with hyperemic bulbar conjunctiva, while the left eye had a visual acuity of 20/200. The fundus of the right eye had scattered pigmentation, while the left eye had a swollen optic disc and right optic atrophy.\n"
+  },
+  {
+    "doc_id": 71,
+    "label": "proficient_health_literacy",
+    "fulltext": "A 71-year-old patient with a history of untreated vitiligo presented with visual loss in the right eye 6 months prior to admission accompanied by bilateral hearing loss with a predominance in the right ear. Chronic headaches and intermittent fever were also reported, although the patient denied a history of drug use or prior infections. He was evaluated by our department due to the presence of significant and unintentional weight loss, generalized weakness and thickening of the skin. On initial ophthalmologic examination, visual acuity in the right eye (RO) was reduced to light perception and color discrimination, and visual acuity in the left eye (LO) was 20/200 with afferent pupillary defect in both eyes with hyperemic margins of the eyelid. On examination of the RO, it was found to have a hyperemic bulbar conjunctiva, ciliary injection, cornea with peripheral, nummular, subepithelial infiltrates, aqueous anterior chamber (AAC) without cellularity, normal iris and lens with nuclear opacities. On examination of the left eye, it was found to have a hyperemic bulbar conjunctiva, ciliary injection, cornea with peripheral, nummular, subepithelial infiltrates, AAC, aqueous without cellularity, normal iris and lens with nuclear opacities. On examination of the right fundus, a round, pale ++ papilla was found with a 50% excavation, slightly blunt nasal border, with a raised and thinned vascular pattern, with macular area and scattered pigment. On the left fundus, a vitreous haze 2+ was found with edematous papilla, blurred borders, hyperemic, peripapillary, streaked hemorrhages, and an unevaluable excavation with a thinned vascular pattern and macular area with scattered pigment, with right optic atrophy and left anterior optic neuritis.\n\nDue to ocular involvement, weight loss and neurological symptoms, additional testing was performed to rule out causes such as tuberculosis, herpes, ANCA and non-ANCA vasculitis, and sarcoidosis. As for the management of the neurological condition, a lumbar puncture was performed and an opening pressure within normal limits and a proteinocracy of 54 mg/dL was found. Due to distal symmetric polyneuropathy, nerve conduction velocities (NCV) were performed, which showed a pattern of polyradiculoneuropathy with moderate to severe axonal degeneration, involving all 4 extremities with a predominance of the lower extremities; the contrasted magnetic resonance imaging (MRI) of the skull and orbit did not show enhancement of the optic nerve or brain tumors; however, it did show sinusitis and meningeal enhancement. Within the management, sarcoidosis was ruled out, with angiotensin converting enzyme (ACE) within normal parameters, as well as a whole body gamma scan, without enhancement or boosting. After all the study and clinical evaluation of the patient, a second ophthalmological assessment was performed in which persistence and progression of the ocular condition was found, with optic atrophy in the right eye and anterior optic neuritis in the left eye. Because of this, high dose pulse steroid treatment was initiated, followed by a gradual reduction of the dose and the patient was referred for follow-up in the Outpatient Department. A clinical and functional improvement was observed, mainly at the neurological and ophthalmological level.\n",
+    "diff_label_texts": "A 71-year-old patient with untreated, long-standing vitiligo presented with a 6-month history of right-eye visual loss and bilateral hearing loss, right-predominant. During admission he endorsed chronic headaches, intermittent fever, significant unintentional weight loss, generalized asthenia, and skin thickening. Initial ophthalmologic assessment: RO visual acuity reduced to light perception with impaired color discrimination; LO visual acuity 20/200. There was an afferent pupillary defect in both eyes and hyperemic eyelid margins. Anterior segment (both eyes): hyperemic bulbar conjunctiva, ciliary injection, cornea with peripheral nummular subepithelial infiltrates, aqueous anterior chamber without cellularity, normal iris, and lenses with nuclear opacities. Fundus, RO: pale (++) optic disc with approximately 50% excavation, slightly blunted nasal margin, attenuated/“raised and thinned” vasculature, macular area with scattered pigment. Fundus, LO: 2+ vitreous haze; edematous, hyperemic optic disc with blurred margins; peripapillary streaked hemorrhages; excavation not assessable; thinned vasculature; macular area with scattered pigment. Impression at that time documented right optic atrophy and left anterior optic neuritis. Workup for ocular–neurologic disease included evaluation to exclude tuberculosis, herpes, ANCA and non-ANCA vasculitides, and sarcoidosis. Lumbar puncture: opening pressure within normal limits; CSF protein 54 mg/dL. Nerve conduction velocities showed a polyradiculoneuropathy with moderate–severe axonal degeneration involving all four extremities, greater in the lower limbs. Contrast-enhanced MRI of the brain and orbits showed no optic nerve enhancement and no intracranial masses, but did reveal sinusitis and meningeal enhancement. Sarcoidosis was further disfavored by a normal ACE level and a whole-body gamma scan without hypermetabolic foci. On repeat ophthalmologic evaluation, there was progression with persistent right optic atrophy and left anterior optic neuritis. High-dose pulse corticosteroids were initiated, followed by a taper. The patient experienced clinical and functional improvement, particularly in neurologic and ophthalmologic parameters.",
+    "summary": "A 71-year-old man with a history of long-standing vitiligo who had experienced visual loss in his right eye six months prior to admission, along with bilateral hearing loss, predominantly in the right ear. During his hospital stay, he presented with chronic headaches, fever, and significant involuntary weight loss. On ophthalmologic examination, the right eye was light sensitive with hyperemic bulbar conjunctiva, while the left eye had a visual acuity of 20/200. The fundus of the right eye had scattered pigmentation, while the left eye had a swollen optic disc and right optic atrophy.\n"
+  },
+  {
+    "doc_id": 72,
+    "label": "proficient_health_literacy",
+    "fulltext": "A 39-year-old woman with a diagnosis of peripartum cardiomyopathy who received a heart transplant in October 2014. She received induction with Basiliximab and methylprednisolone. She also received maintenance treatment with tacrolimus XL prolonged release 7 mg daily, everolimus 1 mg twice daily, and prednisolone 5 mg/day. She had two episodes of acute rejection during the first year post-transplant, and was controlled with methylprednisolone pulse therapy with good results. There was no history of renal disease and her renal function was stable with creatinine of 0.88 mg/dL and a glomerular filtration rate (GFR) of 102 mL/min/1.73m2 during the first year post-transplant. Follow-up was done exclusively by the heart transplant group and routine polyomavirus viral load BK or urinary cytology was not performed. In 2016, she presented a creatinine serum elevation of up to 1.9 mg/dL, with a GFR of 32.6 mL/min/1.73m2. At that time, the minimum tacrolimus level was 7.2 ng/mL and everolimus, 5.2 ng/mL. Anticalcineurin toxicity was suspected; therefore, tacrolimus was reduced to 4 mg daily and creatinine returned to near baseline (creatinine 1.25 mg/dL, GFR 54.1 mL/min/1.73m2); no renal biopsy was performed. In March 2017, creatinine increased to 2.69 mg/dL, with a GFR of 21.4 mL/min/1.73m2, for which she was hospitalized. The patient stated that she did not have any symptoms. During physical examination, she was in good general condition, heart rate of 80 beats per minute, blood pressure of 130/90 mmHg, respiratory rate of 15 per minute, afebrile. Further studies were performed: renal tract ultrasound showed normal renal size but increased echogenicity; urinalysis and urine cultures were negative, without haematuria, pyuria or casts; echocardiogram with adequate cardiac function; HIV, syphilis, hepatitis B and C serologic tests were negative; minimum tacrolimus level of 5.2 ng/mL, and everolimus of 5.98 ng/mL. Control was initiated with intravenous hydration, and tacrolimus XL dose was reduced to 2 mg daily, but there was no improvement in renal function; a renal biopsy was planned.\n\nRenal biopsy revealed active chronic interstitial nephritis associated with advanced poliomyelitis virus nephritis. BK virus PCR was performed and was positive at 33,800 copies/mL in blood (log 4.5). Tacrolimus was discontinued; creatinine levels stabilized between 2.2 and 2.4 mg/dL, with no further elevation in post-discharge controls. Her viral load began to decline to undetectable levels. The patient did not have episodes of cardiac rejection in 3 years of follow-up; the last creatinine measurement was 2.5 mg/dL, corresponding to a GFR of 23.4 mL/min/1.73m2.\n",
+    "diff_label_texts": "A 39-year-old woman with peripartum cardiomyopathy underwent orthotopic heart transplantation in October 2014. Induction was basiliximab plus methylprednisolone. Maintenance immunosuppression included tacrolimus XL 7 mg daily, everolimus 1 mg twice daily, and prednisolone 5 mg/day. She had two episodes of acute rejection in the first post-transplant year, managed with methylprednisolone pulse therapy. Baseline renal function during year one was normal (creatinine 0.88 mg/dL; eGFR 102 mL/min/1.73m2). Follow-up was by the heart transplant team; routine BK polyomavirus screening (plasma PCR or urine cytology) was not performed.\n\nIn 2016, creatinine rose to 1.9 mg/dL (eGFR 32.6), with tacrolimus trough 7.2 ng/mL and everolimus 5.2 ng/mL. Calcineurin inhibitor toxicity was suspected; tacrolimus was reduced to 4 mg daily, and creatinine improved to 1.25 mg/dL (eGFR 54.1); no biopsy was obtained. In March 2017, creatinine increased to 2.69 mg/dL (eGFR 21.4) without symptoms. Vitals and exam were unremarkable; renal ultrasound showed normal size with increased echogenicity; urinalysis/culture were negative (no hematuria, pyuria, or casts); echocardiogram showed adequate cardiac function; HIV, syphilis, HBV, and HCV serologies were negative. Tacrolimus and everolimus troughs were 5.2 ng/mL and 5.98 ng/mL, respectively. Despite IV hydration and reducing tacrolimus XL to 2 mg daily, renal function did not improve, prompting biopsy.\n\nRenal biopsy demonstrated active chronic interstitial (tubulointerstitial) nephritis associated with advanced polyomavirus nephritis. Plasma BK virus PCR was positive at 33,800 copies/mL (log 4.5). Tacrolimus was discontinued; creatinine stabilized between 2.2 and 2.4 mg/dL with declining BK viremia to undetectable. Over three years, there were no further cardiac rejection episodes. At two years of follow-up from diagnosis of BKVN, renal function was stable with creatinine 2.5 mg/dL (eGFR 23.4 mL/min/1.73m2).\n\nContext: BK polyomavirus nephropathy, while classically described in kidney transplant recipients, can occur in non-renal solid organ transplant recipients under potent immunosuppression. Management centers on reduction of immunosuppression; maintaining an mTOR inhibitor (everolimus) while withdrawing the calcineurin inhibitor can aid viral clearance, at the potential cost of rejection risk, which was not observed here. Plasma BK viral load (log 4.5) plus biopsy-proven late-stage BKVN established the diagnosis and guided therapy.",
+    "summary": "We report a case of BK virus nephropathy in a patient who underwent heart transplantation due to peripartum cardiomyopathy. The renal biopsy reported active chronic tubulointerstitial nephritis associated with late-stage BK virus nephritis and the blood viral load for BK virus was positive (log 4.5). The immunosuppressive treatment was reduced, and after two years of follow-up, the patient had stable renal function with serum creatinine of 2.5 mg/dL (GFR of 23.4 mL/min/1.73m2).\n"
+  },
+  {
+    "doc_id": 73,
+    "label": "low_health_literacy",
+    "fulltext": "14-year-old previously healthy adolescent who presented to the Primary Emergency Care Service (PEC) of Osorno with a 11-day history of a predominantly nocturnal irritative cough. Symptomatic treatment was indicated, evolving with dyspnoea and orthopnoea. He presented to the Emergency Department of the Osorno Base Hospital (OBH), with severe respiratory distress, intolerance to supine position, and abdominal pain. He was admitted to the Paediatric Intensive Care Unit (PICU), tachycardic, hypertensive, polypneic, oxygen saturation 96% with FiO2 35%, rosy, hydrated and well perfused, with flat jugular veins, small bilateral supraclavicular lymphadenopathies. The thorax was without retraction of soft tissue, maintained in a genupectoral position, with decreased pulmonary murmurs in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The soft abdomen was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and\n\nA nephrological evaluation was performed, which confirmed renal failure secondary to tumor lysis syndrome, without dialysis urgency and tendency to hypertension, with creatinine 1.54 mg/dL, phosphemia 11 mg/dL, without hypernatremia. It continued with hyperhydration, diuretic (furosemide) and antihypertensive (amlodipine). From the respiratory point of view, it presented oxygen requirement, with FIO2 35% by mask of Venturi, suspending this supply on the third day of admission. It evolved with episodes of psychomotor agitation, associated to the diagnosis in process, which was treated according to the institutional protocol of psychomotor agitation, with psychological and psychiatric support, with satisfactory evolution. On the third day of admission and treatment a CT scan of the thorax, abdomen and pelvis was performed with contrast, observing an increase in the size of the thymus, of homogeneous aspect, probably in the context of a lymphoproliferative process and findings suggestive of pulmonary thromboembolism. The angioCT of the thorax showed thrombosis of the jugular vein, extensive bilateral pleural effusion associated to atelectatic phenomena in both bases, with signs of medical bilateral nephrosis. Anticoagulation with enoxaparin (1 mg/kg dose, every 12 hours) was indicated for twenty days. Then the angioCT of control showed resolution of the thrombosis.On the fourth day of admission and treatment, a diagnostic and extension study was performed, which included, among others, a complete biochemical profile including lipid profile, granulopoietic hyperplasia of the bone marrow (myelogram), flow cytometry (bone marrow) in which no cells with a predominant clonal or neoplastic immunophenotype of haemological lineage were observed, flow cytometry in peripheral blood negative for neoplastic cells, cytological of pleural fluid negative for neoplastic cells, flow cytometry of pleural fluid without evidence of haemological neoplasia. It was presented to the paediatric oncological committee, highlighting that it was not possible to take a biopsy of the tumour given that the mediastinal mass disappeared with the cytoreductive treatment, assuming the diagnosis of lymphoblastic lymphoma by the clinical picture and the response to treatment, according to the PINDA 0516 protocol. This protocol contemplates in Induction IA eight doses of Lasp E. coli of 10,000 IU/m2. Having received seven doses of L-asp and with a cumulative dose of ninety thousand international units plus glucocorticoid (prednisone), presented a picture of decline, vomiting, abdominal pain and mild dehydration. There was suspicion of pancreatitis, which was ruled out by normal amylase/lipase values and normal hepatic tests. At that time it had plasma electrolyte profile with hyponatraemia of 126 mOsm/kg and urinary osmolality of 510 mOsm/kg, both normal values. With hyponatraemia and hypertriglyceridaemia, there was suspicion of RAM of pseudohyponatraemia secondary to hypertriglyceridaemia associated to L-asp. It was evaluated by Gastroenterology and Endocrinology, indicating a diet low in refined sugars and rich in fiber, fibrates (ciprofibrato 100 mg oral daily) and omega 3 (4 g oral daily), until triglyceride values of 300 mg/dL were achieved. Two weeks later the triglycerides had a value of 79 mg/dL. Ciprofibrato and omega3 were suspended, indicating prophylactic use associated to corticoid and L-asp treatment. A total of twelve doses of L-asp were completed with a cumulative dose of one hundred and eighty four thousand international units corresponding to the induction protocol. The suspicion of RAM was subjected to causality evaluation, with the modified Karch and Lasagna algorithm by WHO5, which resulted in “Definitive” RAM for the association of L-asp and Prednisone\n",
+    "diff_label_texts": "A teenager was getting treatment for a blood cancer called non-Hodgkin lymphoma. He developed very high blood fats (triglycerides). This made a lab test say his sodium was low, even though his body sodium was okay. Think of it like the blood looked milky with fat, which can trick the test. Doctors thought this was a side effect from two cancer medicines: asparaginase and a steroid (prednisone). They used a standard checklist and decided the side effect was definitely from those medicines. He was treated with a low-fat eating plan and medicines that lower blood fats. The cancer drugs were not stopped because that part of his treatment had already reached its planned end. His blood fats went back to normal in about two weeks, and he had no problems.",
+    "summary": "A teenager who developed pseudohyponatraemia and hypertriglyceridaemia during treatment for non-Hodgkin lymphoma (NHL) was suspected to have a drug reaction (ADR). This suspicion of ADR was evaluated according to the modified causality algorithm (Karch and Lasagna), resulting in a \"definitive\" ADR for the association of L-asp and corticosteroids. He received treatment with a low-fat diet and lipid-modifying medicines. L-asp and prednisone were not discontinued due to the end of the indication, according to the protocol. The hypertriglyceridaemia recovered without complications after 14 days of treatment.\n"
+  },
+  {
+    "doc_id": 73,
+    "label": "intermediate_health_literacy",
+    "fulltext": "14-year-old previously healthy adolescent who presented to the Primary Emergency Care Service (PEC) of Osorno with a 11-day history of a predominantly nocturnal irritative cough. Symptomatic treatment was indicated, evolving with dyspnoea and orthopnoea. He presented to the Emergency Department of the Osorno Base Hospital (OBH), with severe respiratory distress, intolerance to supine position, and abdominal pain. He was admitted to the Paediatric Intensive Care Unit (PICU), tachycardic, hypertensive, polypneic, oxygen saturation 96% with FiO2 35%, rosy, hydrated and well perfused, with flat jugular veins, small bilateral supraclavicular lymphadenopathies. The thorax was without retraction of soft tissue, maintained in a genupectoral position, with decreased pulmonary murmurs in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The soft abdomen was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and\n\nA nephrological evaluation was performed, which confirmed renal failure secondary to tumor lysis syndrome, without dialysis urgency and tendency to hypertension, with creatinine 1.54 mg/dL, phosphemia 11 mg/dL, without hypernatremia. It continued with hyperhydration, diuretic (furosemide) and antihypertensive (amlodipine). From the respiratory point of view, it presented oxygen requirement, with FIO2 35% by mask of Venturi, suspending this supply on the third day of admission. It evolved with episodes of psychomotor agitation, associated to the diagnosis in process, which was treated according to the institutional protocol of psychomotor agitation, with psychological and psychiatric support, with satisfactory evolution. On the third day of admission and treatment a CT scan of the thorax, abdomen and pelvis was performed with contrast, observing an increase in the size of the thymus, of homogeneous aspect, probably in the context of a lymphoproliferative process and findings suggestive of pulmonary thromboembolism. The angioCT of the thorax showed thrombosis of the jugular vein, extensive bilateral pleural effusion associated to atelectatic phenomena in both bases, with signs of medical bilateral nephrosis. Anticoagulation with enoxaparin (1 mg/kg dose, every 12 hours) was indicated for twenty days. Then the angioCT of control showed resolution of the thrombosis.On the fourth day of admission and treatment, a diagnostic and extension study was performed, which included, among others, a complete biochemical profile including lipid profile, granulopoietic hyperplasia of the bone marrow (myelogram), flow cytometry (bone marrow) in which no cells with a predominant clonal or neoplastic immunophenotype of haemological lineage were observed, flow cytometry in peripheral blood negative for neoplastic cells, cytological of pleural fluid negative for neoplastic cells, flow cytometry of pleural fluid without evidence of haemological neoplasia. It was presented to the paediatric oncological committee, highlighting that it was not possible to take a biopsy of the tumour given that the mediastinal mass disappeared with the cytoreductive treatment, assuming the diagnosis of lymphoblastic lymphoma by the clinical picture and the response to treatment, according to the PINDA 0516 protocol. This protocol contemplates in Induction IA eight doses of Lasp E. coli of 10,000 IU/m2. Having received seven doses of L-asp and with a cumulative dose of ninety thousand international units plus glucocorticoid (prednisone), presented a picture of decline, vomiting, abdominal pain and mild dehydration. There was suspicion of pancreatitis, which was ruled out by normal amylase/lipase values and normal hepatic tests. At that time it had plasma electrolyte profile with hyponatraemia of 126 mOsm/kg and urinary osmolality of 510 mOsm/kg, both normal values. With hyponatraemia and hypertriglyceridaemia, there was suspicion of RAM of pseudohyponatraemia secondary to hypertriglyceridaemia associated to L-asp. It was evaluated by Gastroenterology and Endocrinology, indicating a diet low in refined sugars and rich in fiber, fibrates (ciprofibrato 100 mg oral daily) and omega 3 (4 g oral daily), until triglyceride values of 300 mg/dL were achieved. Two weeks later the triglycerides had a value of 79 mg/dL. Ciprofibrato and omega3 were suspended, indicating prophylactic use associated to corticoid and L-asp treatment. A total of twelve doses of L-asp were completed with a cumulative dose of one hundred and eighty four thousand international units corresponding to the induction protocol. The suspicion of RAM was subjected to causality evaluation, with the modified Karch and Lasagna algorithm by WHO5, which resulted in “Definitive” RAM for the association of L-asp and Prednisone\n",
+    "diff_label_texts": "A 14-year-old treated for non-Hodgkin lymphoma developed hypertriglyceridaemia and pseudohyponatraemia after multiple doses of L-asparaginase with prednisone. Pseudohyponatraemia means the sodium result looks low because very high blood lipids interfere with the lab method; the body’s actual sodium status is not truly low. Clinicians suspected an adverse drug reaction and, using the modified Karch and Lasagna causality algorithm, classified the reaction as definitive for the combination of L-asparaginase and corticosteroids. Management included diet changes (low fat/low refined sugars, high fiber) and lipid-lowering therapy with a fibrate (ciprofibrate 100 mg daily) plus omega-3 fatty acids (4 g daily). Per protocol, L-asparaginase and prednisone were not discontinued because the indicated treatment phase had reached its end; the patient completed the planned doses. Triglycerides fell to 79 mg/dL within 14 days, and the episode resolved without complications.",
+    "summary": "A teenager who developed pseudohyponatraemia and hypertriglyceridaemia during treatment for non-Hodgkin lymphoma (NHL) was suspected to have a drug reaction (ADR). This suspicion of ADR was evaluated according to the modified causality algorithm (Karch and Lasagna), resulting in a \"definitive\" ADR for the association of L-asp and corticosteroids. He received treatment with a low-fat diet and lipid-modifying medicines. L-asp and prednisone were not discontinued due to the end of the indication, according to the protocol. The hypertriglyceridaemia recovered without complications after 14 days of treatment.\n"
+  },
+  {
+    "doc_id": 73,
+    "label": "proficient_health_literacy",
+    "fulltext": "14-year-old previously healthy adolescent who presented to the Primary Emergency Care Service (PEC) of Osorno with a 11-day history of a predominantly nocturnal irritative cough. Symptomatic treatment was indicated, evolving with dyspnoea and orthopnoea. He presented to the Emergency Department of the Osorno Base Hospital (OBH), with severe respiratory distress, intolerance to supine position, and abdominal pain. He was admitted to the Paediatric Intensive Care Unit (PICU), tachycardic, hypertensive, polypneic, oxygen saturation 96% with FiO2 35%, rosy, hydrated and well perfused, with flat jugular veins, small bilateral supraclavicular lymphadenopathies. The thorax was without retraction of soft tissue, maintained in a genupectoral position, with decreased pulmonary murmurs in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The soft abdomen was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and the cardiac auscultation had muffled tones, without breath sounds. The abdominal soft tissue was not easily depressible and sensitive in both hypochondria, with doubtful visceral enlargements and no injuries. The chest radiograph showed a superior mediastinal mass and atelectasis of the right middle lobe associated with ipsilateral pleural effusion. Contrast-enhanced chest X-ray was not performed due to contraindication of anaesthesia, as stated in the summary of transfer from OBH. He was transferred in a serious condition to the PICU HBV, with a Mediastinal Compression Syndrome, with clinical suspicion of non-Hodgkin lymphoma. He was evaluated by the paediatric haemato-oncology, paediatric surgery, paediatric intensive care, imaging, radiotherapy and paediatric oncology teams, with a normal pulmonary murmur in both bases, and\n\nA nephrological evaluation was performed, which confirmed renal failure secondary to tumor lysis syndrome, without dialysis urgency and tendency to hypertension, with creatinine 1.54 mg/dL, phosphemia 11 mg/dL, without hypernatremia. It continued with hyperhydration, diuretic (furosemide) and antihypertensive (amlodipine). From the respiratory point of view, it presented oxygen requirement, with FIO2 35% by mask of Venturi, suspending this supply on the third day of admission. It evolved with episodes of psychomotor agitation, associated to the diagnosis in process, which was treated according to the institutional protocol of psychomotor agitation, with psychological and psychiatric support, with satisfactory evolution. On the third day of admission and treatment a CT scan of the thorax, abdomen and pelvis was performed with contrast, observing an increase in the size of the thymus, of homogeneous aspect, probably in the context of a lymphoproliferative process and findings suggestive of pulmonary thromboembolism. The angioCT of the thorax showed thrombosis of the jugular vein, extensive bilateral pleural effusion associated to atelectatic phenomena in both bases, with signs of medical bilateral nephrosis. Anticoagulation with enoxaparin (1 mg/kg dose, every 12 hours) was indicated for twenty days. Then the angioCT of control showed resolution of the thrombosis.On the fourth day of admission and treatment, a diagnostic and extension study was performed, which included, among others, a complete biochemical profile including lipid profile, granulopoietic hyperplasia of the bone marrow (myelogram), flow cytometry (bone marrow) in which no cells with a predominant clonal or neoplastic immunophenotype of haemological lineage were observed, flow cytometry in peripheral blood negative for neoplastic cells, cytological of pleural fluid negative for neoplastic cells, flow cytometry of pleural fluid without evidence of haemological neoplasia. It was presented to the paediatric oncological committee, highlighting that it was not possible to take a biopsy of the tumour given that the mediastinal mass disappeared with the cytoreductive treatment, assuming the diagnosis of lymphoblastic lymphoma by the clinical picture and the response to treatment, according to the PINDA 0516 protocol. This protocol contemplates in Induction IA eight doses of Lasp E. coli of 10,000 IU/m2. Having received seven doses of L-asp and with a cumulative dose of ninety thousand international units plus glucocorticoid (prednisone), presented a picture of decline, vomiting, abdominal pain and mild dehydration. There was suspicion of pancreatitis, which was ruled out by normal amylase/lipase values and normal hepatic tests. At that time it had plasma electrolyte profile with hyponatraemia of 126 mOsm/kg and urinary osmolality of 510 mOsm/kg, both normal values. With hyponatraemia and hypertriglyceridaemia, there was suspicion of RAM of pseudohyponatraemia secondary to hypertriglyceridaemia associated to L-asp. It was evaluated by Gastroenterology and Endocrinology, indicating a diet low in refined sugars and rich in fiber, fibrates (ciprofibrato 100 mg oral daily) and omega 3 (4 g oral daily), until triglyceride values of 300 mg/dL were achieved. Two weeks later the triglycerides had a value of 79 mg/dL. Ciprofibrato and omega3 were suspended, indicating prophylactic use associated to corticoid and L-asp treatment. A total of twelve doses of L-asp were completed with a cumulative dose of one hundred and eighty four thousand international units corresponding to the induction protocol. The suspicion of RAM was subjected to causality evaluation, with the modified Karch and Lasagna algorithm by WHO5, which resulted in “Definitive” RAM for the association of L-asp and Prednisone\n",
+    "diff_label_texts": "A 14-year-old with suspected lymphoblastic non-Hodgkin lymphoma on protocolized induction (PINDA 0516) received L-asp E. coli 10,000 IU/m2 plus a glucocorticoid (prednisone). After seven doses of L-asp (cumulative ~90,000 IU) he developed clinical decline with vomiting, abdominal pain, and mild dehydration. Pancreatitis was suspected but excluded (amylase/lipase normal; liver tests normal). Laboratory assessment showed hyponatraemia (reported as 126 mOsm/kg) with urinary osmolality 510 mOsm/kg and concurrent hypertriglyceridaemia, prompting the diagnosis of pseudohyponatraemia secondary to hypertriglyceridaemia associated with L-asp plus corticosteroids. He was managed by Gastroenterology and Endocrinology with a diet low in refined sugars and rich in fiber, fibrates (ciprofibrato/ciprofibrate 100 mg PO daily), and omega-3 fatty acids (4 g PO daily), targeting triglycerides ≤300 mg/dL. Two weeks later triglycerides were 79 mg/dL; ciprofibrato and omega-3 were discontinued with advice for prophylactic use during subsequent corticosteroid/L-asp exposure. The patient ultimately completed 12 total doses of L-asp (cumulative 184,000 IU) for induction; L-asp and prednisone were not discontinued due to the end of indication per protocol. Causality assessment for the adverse drug reaction (ADR) using the modified Karch and Lasagna algorithm (WHO) was Definitive for the association of L-asp plus prednisone. No complications occurred, and the hypertriglyceridaemia resolved within 14 days. Mechanistically, L-asparaginase can reduce lipoprotein lipase activity and increase VLDL, while corticosteroids augment hepatic VLDL production; marked lipaemia then produces pseudohyponatraemia via indirect ion-selective electrode dilutional error, with normalization as triglycerides fall.",
+    "summary": "A teenager who developed pseudohyponatraemia and hypertriglyceridaemia during treatment for non-Hodgkin lymphoma (NHL) was suspected to have a drug reaction (ADR). This suspicion of ADR was evaluated according to the modified causality algorithm (Karch and Lasagna), resulting in a \"definitive\" ADR for the association of L-asp and corticosteroids. He received treatment with a low-fat diet and lipid-modifying medicines. L-asp and prednisone were not discontinued due to the end of the indication, according to the protocol. The hypertriglyceridaemia recovered without complications after 14 days of treatment.\n"
+  },
+  {
+    "doc_id": 74,
+    "label": "proficient_health_literacy",
+    "fulltext": "A 56-year-old Italian female patient with β-thalassemia major presented to the radiology department to undergo MRI to quantify myocardial, hepatic, and pancreatic iron deposition. The clinical history of the patient included a transfusion-dependent β-thalassemia condition (genotype HBB:c.118C > T/ HBB:c.93-21G > A), diagnosed at the age of 7 years, despite the fact that the first transfusion was carried out at 2 years. As a consequence of β-thalassemia, the patient underwent splenectomy and cholecystectomy.\n\nAt the moment of MRI, she had a negative HCV-RNA (Hepatitis C virus-Ribonucleic acid) test, no osteoporosis or other endocrine, cardiac, or hepatic complications, and good iron levels. The patient’s therapy included iron chelation with deferasirox, vitamin D, and luspatercept, an erythropoiesis modulator started 2 years before the MRI examination (good response, with an increase of about 35% of transfusion interval duration). Transfusion therapy included two units of concentrated and filtered red blood cells every 25 days with pre-transfusion hemoglobin values of 10–10.5 g/dl.\n\nOn MRI, a solid mass with lobulated and regular contours was incidentally identified within the prevascular compartment of the mediastinum.\n\nThe lesion was mildly hyperintense on T2-weighted images (T2-wi) and isointense on T1-wi. The mediastinal mass in question was discernible in a prior MRI examination conducted for the same purpose in 2020 before starting luspatercept therapy, albeit with a marginal enlargement.\n\nThere were no other apparent abnormalities observed in the remaining mediastinal compartments. No pleural or pericardial effusions were present.\n\nThe neurological examination was unremarkable, and in the preceding months, the patient exhibited no symptoms of mediastinal syndrome associated with compression of the adjacent neurovascular structures. Moreover, she did not exhibit any fever or experience any weight loss.\n\nFor further evaluation, the patient underwent 18F-deoxyglucose (18FDG) positron emission tomography (PET)-computed tomography (CT) and chest CT with contrast media. On PET-CT, the mediastinal mass showed only mild FDG uptake (SUVmax = 4.3); no other sites of abnormal radiotracer uptake were reported in the neck, chest, abdomen, and skeleton. On CT images, the lesion presented regular margins, solid density, and mild contrast enhancement. The adjacent structures did not exhibit any signs of invasion, and lymphadenopathies or extra-thoracic disease were not present. Such radiological features, the indolent behaviour over time, the absence of systemic symptoms, and the lack of avid FDG uptake on PET-CT scan made the diagnosis of thymoma probable.\n\nHowever, on lung window visualization, multiple rounded areas of parenchymal lucency, consistent with thin-walled cysts distributed symmetrically throughout both lungs, with normal intervening parenchyma, were evident.\n\nNo nodules or other interstitial abnormalities were associated with the cysts. No pneumothorax was detected. Coherently with thalassemic bone disease, the ribs appeared widened, and the spine displayed mild platyspondyly. The remaining portion of the chest and visible upper abdomen were unremarkable. The radiological findings were consistent with cystic lung disease, most likely LAM.\n\nThe patient was then referred to the pulmonary clinic for further evaluation. She was a never-smoker and did not report any respiratory symptoms. In particular, she denied a history of chronic cough, recurrent respiratory infections, or pneumothorax. No cutaneous lesions, notably facial fibrofolliculomas, were evident. On chest examination, the lung fields were clear. Peripheral capillary oxygen saturation was normal (98%), with a heart rate of 75 beats per minute. Pulmonary function tests revealed a substantial reduction in diffusing capacity of the lungs for carbon monoxide (DLCO; 42% of the predicted value), partly imputable to the condition of anemia, with a carbon monoxide transfer coefficient (KCO) of 73% of the predicted value. After discussion in a multidisciplinary tumor board setting, including a pulmonologist, the patient underwent left thoracoscopic thymectomy and concomitant lingual segment wedge resection. The histopathological report revealed a morphological finding and immunohistochemical pattern referable to type B2 thymoma with focal infiltration of the capsule. Extracapsular extension was not evident. However, the lesion was present at the resection margin (stage IIa according to Masaoka–Koga; stage 1a according to the tumor, node, metastasis [TNM] classification).\n\nRegarding the lung parenchyma, histopathologic analysis described lung parenchyma with cysts of variable size lined by spindle cells in myoid habit with immunohistochemical reactivity for actin, estrogen, progesterone receptors, and HMB45 (focal positivity). Modest chronic interstitial inflammation, vascular congestion, and recent blood extravasation were evident. These morphological findings were compatible with pulmonary LAM.\n\nA final histological diagnosis of thymoma and pulmonary LAM was made. For the neoplastic condition, the patient was a candidate for adjuvant radiation therapy due to the microscopically incomplete resection (R1). For LAM with concomitant β-thalassemia, treatment with sirolimus was recommended.",
+    "diff_label_texts": "A 56-year-old Italian female with transfusion-dependent β-thalassemia major (genotype HBB:c.118C > T/HBB:c.93-21G > A), diagnosed at age 7 years with first transfusion at age 2, presented for MRI quantification of myocardial, hepatic, and pancreatic iron. Past history included splenectomy and cholecystectomy. At the time of MRI, HCV-RNA was negative; there were no osteoporosis or other endocrine, cardiac, or hepatic complications; and iron levels were good. Ongoing therapy included deferasirox, vitamin D, and luspatercept started 2 years prior with a good response (approximately 35% increase in transfusion interval). Transfusion regimen was two units of concentrated, filtered RBCs every 25 days with pre-transfusion hemoglobin 10–10.5 g/dL.\nOn MRI, an incidental solid mass with lobulated, regular contours was identified in the prevascular mediastinum. The lesion was mildly hyperintense on T2-weighted imaging and isointense on T1-weighted imaging. It had been visible on a prior MRI in 2020 (before luspatercept) with marginal enlargement over time. No other mediastinal abnormalities and no pleural or pericardial effusions were present. Neurological examination was unremarkable, and there were no symptoms of mediastinal compression, fever, or weight loss.\nFurther evaluation with 18F-FDG PET-CT and contrast-enhanced chest CT showed mild FDG uptake of the mediastinal mass (SUVmax 4.3) with no other abnormal uptake in the neck, chest, abdomen, or skeleton. On CT, the mass had regular margins, solid density, mild contrast enhancement, no invasion of adjacent structures, and no lymphadenopathies or extra-thoracic disease. Lung window images revealed multiple, symmetrically distributed, thin-walled cysts with normal intervening parenchyma, without nodules, additional interstitial abnormalities, or pneumothorax. Skeletal findings coherent with thalassemic bone disease included widened ribs and mild platyspondyly. Overall, these findings were consistent with cystic lung disease, most likely lymphangioleiomyomatosis (LAM).\nPulmonary evaluation noted a never-smoker with no respiratory symptoms, no history of chronic cough, recurrent infections, or pneumothorax, and no cutaneous lesions such as facial fibrofolliculomas. Lung fields were clear on exam; SpO2 was 98% and heart rate 75 bpm. Pulmonary function testing showed reduced DLCO at 42% predicted, partially attributable to anemia, with KCO at 73% predicted.\nAfter multidisciplinary tumor board discussion (including a pulmonologist), the patient underwent left thoracoscopic thymectomy with concomitant lingual segment wedge resection. Histopathology demonstrated a type B2 thymoma with focal capsular infiltration, no extracapsular extension, but tumor at the resection margin (R1), corresponding to Masaoka–Koga stage IIa and TNM stage 1a. Lung parenchyma showed cysts of variable size lined by spindle cells with myoid habit and immunohistochemical reactivity for actin, estrogen and progesterone receptors, and focal HMB45 positivity, with modest chronic interstitial inflammation, vascular congestion, and recent blood extravasation, consistent with pulmonary LAM.\nFinal diagnosis: type B2 thymoma and pulmonary LAM. Management recommendations included adjuvant radiation therapy for the microscopically incomplete thymoma resection (R1) and sirolimus for LAM in the context of concomitant β-thalassemia.\nContextual considerations: B2 thymoma with R1 margins is generally managed with adjuvant radiotherapy to reduce local recurrence risk. LAM is a cystic lung disease characterized by aberrant smooth muscle-like cell proliferation with mTOR pathway activation; sirolimus (an mTOR inhibitor) is standard therapy to stabilize lung function and reduce disease progression. Luspatercept, an erythroid maturation agent, can reduce transfusion burden in transfusion-dependent β-thalassemia, as reflected by the patient’s 35% prolongation of the transfusion interval.",
+    "summary": "A 56-year-old Italian female patient with β-thalassemia major underwent magnetic resonance imaging to quantify myocardial, hepatic, and pancreatic iron deposition. Her medical history included transfusion-dependent β-thalassemia, splenectomy, and cholecystectomy. At the time of magnetic resonance imaging, she had no significant endocrine, cardiac, or hepatic complications and was on deferasirox, vitamin D, and luspatercept. Magnetic resonance imaging revealed a lobulated mass in the prevascular mediastinum, which showed mild radiotracer uptake on positron emission tomography. Chest computed tomography revealed multiple thin-walled cysts in the lungs, indicating lymphangioleiomyomatosis. Following multidisciplinary evaluation, the patient underwent thoracoscopic thymectomy and lung wedge resection. Histopathology confirmed type B2 thymoma and pulmonary lymphangioleiomyomatosis. Post-surgery, the patient was recommended for adjuvant radiation therapy and sirolimus treatment."
+  },
+  {
+    "doc_id": 75,
+    "label": "low_health_literacy",
+    "fulltext": "We present a case of a 49-year-old woman with renal and heart failure following a long-term (lasting from 13 years of age) SLE prepared for kidney transplantation. Due to LN (class III, then IV), starting at childhood, she was treated with steroids, together with cyclophosphamide, replaced later by methotrexate and then azathioprine. Hence, the partial remission of nephrotic syndrome was achieved and from 2002 the patient did not receive any immunosuppressive therapy. She was also HBV and HCV positive. SLE involvement of circulatory system presented with early coronary atherosclerosis, ischemic heart disease, and myocardial infarction at the age of 20. In 2007, because of deterioration of kidney function with a serum creatinine concentration of 2.2 mg/dL and proteinuria of 2 g/day, the kidney biopsy was performed. The biopsy showed active and sclerotic focal proliferative lupus nephritis nevertheless immunosuppressive therapy was not introduced for the reason of active replication of HCV. The kidney function was gradually deteriorating over time. Despite cardiac intervention (PCI RCA), the patient developed severe post-infarction and dilated cardiomyopathy and required ICD implantation in primary prevention in 2009. Later, on lupus and secondary cardiomyopathic background, the patient developed severe MV and TV regurgitation. For this reason, the patient underwent mitral and tricuspid valve repair and left ventricle volume reduction surgery complicated by low cardiac output syndrome with a need for intra-aortic balloon pump use (2014). In the postoperative period, the kidney function deteriorated, requiring the initiation of renal replacement therapy. The patient has been on dialysis for 4 years. While being on active waiting list for kidney transplantation presented remission of laboratory indices of lupus (complement splits within normal limits: C3–0,93 g/l, C4–0,4 g/l, ANA negative) and persisting circulatory insufficiency with markedly reduced stair-climbing capacity (to one flight of stairs) with elevated BNP 619 pg/ml (n. 0–100). In transthoracic echocardiography, performed before renal transplantation, the left ventricle and the left atrium were significantly enlarged and the left ventricular systolic function was significantly reduced with LVEF 26% and GLS -3. Due to the implantation of the mitral ring, it was not possible to assess the left ventricular diastolic function. The high tricuspid regurgitant flow gradient with widened and poorly respiratory mobile inferior vena cava indicated a high probability of pulmonary hypertension. Furthermore, while preparing the patient for the surgical procedure, it was decided to include cardioprotective therapy with Levosimendan. Due to the time frame associated with the transplantation procedure, the drug infusion was started as soon as possible after cross-match results were known, immediately after the dialysis session. The infusion at a dose of 0.1 μg/kg/min was continued after surgery for a total of 24 h. The patient’s anesthesia for kidney transplantation and perioperative care included the aspect of optimizing transplanted kidney perfusion, avoiding the use of renal toxic drugs and those excreted by properly functioning kidneys, as well as the use of nephroprotective agents. Because of the patient’s cardiological burden, including recurrent episodes of extrasystole proceeding with decompensation of the circulatory system, together with the need of ICD turning off for the transplantation period, the Swan-Ganz catheter for hemodynamic assessment was not used. Anesthesia monitoring was limited the to ECG, central catheter with CVP assessment, direct blood pressure measurement from the cannula inserted into the radial artery, and cardiac ultrasound. In the perioperative period the CVP parameter was used to assess the volatility, and in the postoperative period, a cardiac ultrasound was used along with the assessment of VCI respiratory fill and motility. The therapy was aimed at the standard of fluid therapy called Goal Directed Therapy (GDT). During general anesthesia, fentanyl, triacrium, propofol, desflurane, antibiotic therapy, and standard immunosuppressive treatment were used as well as 25 g of mannitol infusion was administered as a nephroprotective treatment and 0.9% NaCl as a fluid therapy. In the course of postoperative immunosuppression, she received steroids, tacrolimus with mycophenolate mofetil which was stopped due to persistent leukopenia and cytomegalovirus infection. Furthermore delayed graft function was observed with a need for hemodialysis for almost 6 weeks (mostly due to fluid retention). BNP levels raised to 2996 pg/ml and then slowly decreased. The kidney biopsy performed 2 weeks after transplantation revealed acute rejection (AR II B Banff 2015) with ATN. Finally, the patient was discharged from the hospital on the 67th POD with the serum creatinine concentration of 1.4 mg/dL and BNP level of 1794 pg/ml. One month after kidney transplantation, there was a reduction in left ventricular dimensions, improved systolic function in the EF (increase to 30%) and GLS (decrease to − 6) assessment. In addition, there was a decrease in the tricuspid regurgitant flow gradient with normal width and respiratory motility of the IVC, which indicates a low probability of pulmonary hypertension. The improvement of echocardiographic parameters also reflected the simultaneous improvement of exercise capacity in the recipient from NYHA III/IV to NYHA II. In the 5-month observation, further improvement of heart function with a drop of BNP to 1066 pg/ml and normal kidney function were noted.",
+    "diff_label_texts": "This story is about a 49-year-old woman who had lupus for many years. Over time, her kidneys and her heart got weaker. She needed dialysis to do the work of her kidneys for 4 years until she could get a kidney transplant. Her heart pump was very weak before surgery. To help her heart get through the operation, doctors gave her a heart-helping medicine called levosimendan. The time after surgery had some ups and downs. But she got through it. At about one month after surgery, her heart started to work better, and her new kidney worked normally. At about five months, her heart kept improving, and her kidney function stayed normal.",
+    "summary": "We present a case of a 49-year-old woman with renal and heart failure following a long-term SLE prepared for kidney transplantation. During the SLE course, the function of the heart and kidneys gradually deteriorated. The patient required the initiation of renal replacement therapy and was dialyzed until a kidney transplantation for 4 years. In the preparation of the patient for the surgical procedure, due to the extremely low ejection fraction, it was decided to include cardioprotective treatment with Levosimendan. The postoperative period was not straightforward but successful. In the monthly and five-month follow-up, a continuous improvement of heart function with normal renal function was noted."
+  },
+  {
+    "doc_id": 75,
+    "label": "proficient_health_literacy",
+    "fulltext": "We present a case of a 49-year-old woman with renal and heart failure following a long-term (lasting from 13 years of age) SLE prepared for kidney transplantation. Due to LN (class III, then IV), starting at childhood, she was treated with steroids, together with cyclophosphamide, replaced later by methotrexate and then azathioprine. Hence, the partial remission of nephrotic syndrome was achieved and from 2002 the patient did not receive any immunosuppressive therapy. She was also HBV and HCV positive. SLE involvement of circulatory system presented with early coronary atherosclerosis, ischemic heart disease, and myocardial infarction at the age of 20. In 2007, because of deterioration of kidney function with a serum creatinine concentration of 2.2 mg/dL and proteinuria of 2 g/day, the kidney biopsy was performed. The biopsy showed active and sclerotic focal proliferative lupus nephritis nevertheless immunosuppressive therapy was not introduced for the reason of active replication of HCV. The kidney function was gradually deteriorating over time. Despite cardiac intervention (PCI RCA), the patient developed severe post-infarction and dilated cardiomyopathy and required ICD implantation in primary prevention in 2009. Later, on lupus and secondary cardiomyopathic background, the patient developed severe MV and TV regurgitation. For this reason, the patient underwent mitral and tricuspid valve repair and left ventricle volume reduction surgery complicated by low cardiac output syndrome with a need for intra-aortic balloon pump use (2014). In the postoperative period, the kidney function deteriorated, requiring the initiation of renal replacement therapy. The patient has been on dialysis for 4 years. While being on active waiting list for kidney transplantation presented remission of laboratory indices of lupus (complement splits within normal limits: C3–0,93 g/l, C4–0,4 g/l, ANA negative) and persisting circulatory insufficiency with markedly reduced stair-climbing capacity (to one flight of stairs) with elevated BNP 619 pg/ml (n. 0–100). In transthoracic echocardiography, performed before renal transplantation, the left ventricle and the left atrium were significantly enlarged and the left ventricular systolic function was significantly reduced with LVEF 26% and GLS -3. Due to the implantation of the mitral ring, it was not possible to assess the left ventricular diastolic function. The high tricuspid regurgitant flow gradient with widened and poorly respiratory mobile inferior vena cava indicated a high probability of pulmonary hypertension. Furthermore, while preparing the patient for the surgical procedure, it was decided to include cardioprotective therapy with Levosimendan. Due to the time frame associated with the transplantation procedure, the drug infusion was started as soon as possible after cross-match results were known, immediately after the dialysis session. The infusion at a dose of 0.1 μg/kg/min was continued after surgery for a total of 24 h. The patient’s anesthesia for kidney transplantation and perioperative care included the aspect of optimizing transplanted kidney perfusion, avoiding the use of renal toxic drugs and those excreted by properly functioning kidneys, as well as the use of nephroprotective agents. Because of the patient’s cardiological burden, including recurrent episodes of extrasystole proceeding with decompensation of the circulatory system, together with the need of ICD turning off for the transplantation period, the Swan-Ganz catheter for hemodynamic assessment was not used. Anesthesia monitoring was limited the to ECG, central catheter with CVP assessment, direct blood pressure measurement from the cannula inserted into the radial artery, and cardiac ultrasound. In the perioperative period the CVP parameter was used to assess the volatility, and in the postoperative period, a cardiac ultrasound was used along with the assessment of VCI respiratory fill and motility. The therapy was aimed at the standard of fluid therapy called Goal Directed Therapy (GDT). During general anesthesia, fentanyl, triacrium, propofol, desflurane, antibiotic therapy, and standard immunosuppressive treatment were used as well as 25 g of mannitol infusion was administered as a nephroprotective treatment and 0.9% NaCl as a fluid therapy. In the course of postoperative immunosuppression, she received steroids, tacrolimus with mycophenolate mofetil which was stopped due to persistent leukopenia and cytomegalovirus infection. Furthermore delayed graft function was observed with a need for hemodialysis for almost 6 weeks (mostly due to fluid retention). BNP levels raised to 2996 pg/ml and then slowly decreased. The kidney biopsy performed 2 weeks after transplantation revealed acute rejection (AR II B Banff 2015) with ATN. Finally, the patient was discharged from the hospital on the 67th POD with the serum creatinine concentration of 1.4 mg/dL and BNP level of 1794 pg/ml. One month after kidney transplantation, there was a reduction in left ventricular dimensions, improved systolic function in the EF (increase to 30%) and GLS (decrease to − 6) assessment. In addition, there was a decrease in the tricuspid regurgitant flow gradient with normal width and respiratory motility of the IVC, which indicates a low probability of pulmonary hypertension. The improvement of echocardiographic parameters also reflected the simultaneous improvement of exercise capacity in the recipient from NYHA III/IV to NYHA II. In the 5-month observation, further improvement of heart function with a drop of BNP to 1066 pg/ml and normal kidney function were noted.",
+    "diff_label_texts": "We report a 49-year-old woman with end-stage renal disease and advanced heart failure secondary to long-standing systemic lupus erythematosus (SLE, onset at age 13) and lupus nephritis (LN class III, then IV). Childhood LN was treated with steroids plus cyclophosphamide, later transitioned to methotrexate and then azathioprine, achieving partial remission of nephrotic syndrome; she had no immunosuppression after 2002. She was HBV- and HCV-positive. Cardiovascular SLE involvement included early coronary atherosclerosis, ischemic heart disease, and myocardial infarction at age 20. In 2007, with creatinine 2.2 mg/dL and proteinuria 2 g/day, kidney biopsy showed active and sclerotic focal proliferative LN; immunosuppression was withheld due to active HCV replication. Renal function progressively declined. Despite PCI to the RCA, she developed severe post-infarction and dilated cardiomyopathy, requiring primary-prevention ICD implantation in 2009. On a lupus and secondary cardiomyopathic background, she developed severe mitral and tricuspid regurgitation. In 2014 she underwent mitral and tricuspid valve repair and left ventricular volume reduction surgery, complicated by low cardiac output syndrome necessitating intra-aortic balloon pump support. Postoperatively, renal function worsened, prompting initiation of renal replacement therapy; she remained on dialysis for four years.\n\nWhile listed for kidney transplantation, laboratory indices indicated lupus remission (C3 0.93 g/L, C4 0.4 g/L, ANA negative) but persistent circulatory insufficiency with markedly reduced functional capacity (limited to one flight of stairs) and elevated BNP 619 pg/mL (n 0–100). Pre-transplant transthoracic echocardiography demonstrated markedly enlarged LV and LA, severely reduced LV systolic function (LVEF 26%, GLS −3). Mitral ring precluded diastolic assessment. High tricuspid regurgitant flow gradient with a dilated, poorly respiratory mobile IVC suggested high probability of pulmonary hypertension.\n\nGiven the extremely low ejection fraction, cardioprotective therapy with levosimendan (a calcium sensitizer/inodilator) was instituted perioperatively. Due to transplant timing constraints, infusion (0.1 μg/kg/min) began as soon as crossmatch results were available, immediately post-dialysis, and was continued through the operation for a total of 24 h. Anesthetic management prioritized optimization of allograft perfusion, avoidance of nephrotoxins and renally excreted agents, and use of nephroprotective measures. Because of recurrent extrasystoles with prior decompensation and the need to deactivate the ICD during transplantation, a Swan-Ganz catheter was not placed. Monitoring included ECG, central venous catheter with CVP, invasive arterial blood pressure via radial arterial cannula, and cardiac ultrasound. CVP guided intravascular volume during anesthesia, and postoperative assessments incorporated focused cardiac ultrasound with IVC diameter and respirophasic variability. Fluid management followed a Goal Directed Therapy paradigm. Agents included fentanyl, triacrium, propofol, desflurane, antibiotic prophylaxis, standard immunosuppression, mannitol 25 g for nephroprotection, and 0.9% NaCl for fluid therapy.\n\nPostoperatively, immunosuppression comprised steroids and tacrolimus; mycophenolate mofetil was discontinued due to persistent leukopenia and cytomegalovirus infection. Delayed graft function occurred, necessitating hemodialysis for almost six weeks (largely due to fluid retention). BNP rose to 2996 pg/mL and then gradually declined. Allograft biopsy at postoperative week two revealed acute rejection (AR II B, Banff 2015) with acute tubular necrosis. She was discharged on postoperative day 67 with serum creatinine 1.4 mg/dL and BNP 1794 pg/mL.\n\nAt one month post-transplant, echocardiography showed reduced LV dimensions and improved systolic performance (EF increased to 30%, GLS to −6). Tricuspid regurgitant gradient decreased, and IVC caliber and respirophasic motion normalized, indicating low probability of pulmonary hypertension. Functional status improved from NYHA III/IV to NYHA II. At five months, there was continued cardiac improvement with BNP down to 1066 pg/mL and normalization of renal function. Overall, despite a nontrivial postoperative course, perioperative levosimendan support and tailored hemodynamic and nephroprotective strategies were associated with successful kidney transplantation, progressive recovery of LV function, and stable, normal allograft function at short-term follow-up.",
+    "summary": "We present a case of a 49-year-old woman with renal and heart failure following a long-term SLE prepared for kidney transplantation. During the SLE course, the function of the heart and kidneys gradually deteriorated. The patient required the initiation of renal replacement therapy and was dialyzed until a kidney transplantation for 4 years. In the preparation of the patient for the surgical procedure, due to the extremely low ejection fraction, it was decided to include cardioprotective treatment with Levosimendan. The postoperative period was not straightforward but successful. In the monthly and five-month follow-up, a continuous improvement of heart function with normal renal function was noted."
+  },
+  {
+    "doc_id": 76,
+    "label": "low_health_literacy",
+    "fulltext": "The patient was a 42-year-old woman with a history of menstrual migraine, Hashimoto Thyroiditis, Familial Mediterian Fever (FMF), and dyspepsia. She was taking 75 mg of levothyroxine, 30 mg of lansoprazole, and 1.5 mg of colchicine daily. In February of 2023, she was diagnosed with acute bronchitis, which was treated with antibiotics and bronchodilators. She developed a daily headache after two weeks, manifesting as more than ten short-lasting attacks per day provoked by coughing, straining, and lifting. The duration of each attack was 30 minutes, and the pain was bilaterally distributed from the neck to the top of the head. The headache was sharp and severe. She described the attack as a sensation of storm-like fluid movement in the head. She did not suffer any of the symptoms associated with previous migraine attacks, such as phonophobia, photophobia, vomiting, or throbbing. The severity of the attack was determined using a numeric rating scale (NRS) with a score of 9 out of 10. These attacks typically necessitated a visit to the emergency room. The results of her physical and neurological exams were unremarkable. The laboratory tests, including those for thyroid hormones, electrolytes, liver and kidney function, and serology, were negative. Brain and cervical spinal magnetic resonance imaging (MRI) with and without contrast, magnetic resonance venography (MRV), and angiography (MRA) were all normal. She did not give consent for a lumbar puncture. When we first encountered her in the clinic, she was taking 25 mg of indomethacin per day. Her attacks stopped after putting her on 60 mg of lansoprazole and increasing her daily dose of indomethacin to 150 mg. However, she encountered gastrointestinal side effects, so the indomethacin was discontinued on day three. Due to the adverse effects, she was unable to take topiramate and propranolol.\n\nShe came to the clinic 15 days after her initial visit with an NRS score of 9/10. She was taken to the local operating room. We used a GE Healthcare, Voluson™ E6, ultrasonography system with a linear 13–5 MHz probe for unilateral PGONB. The patient’s neck was prone to flexion. The linear probe was initially transversely positioned on the occipital protuberance and then advanced caudally, demonstrating that the C2 spinous process resembled the two horns. Through lateral probe movement, the inferior muscles of the obliquus capitis and semispinalis capitis were located. Here, the superior to the inferior oblique capitis muscle and beneath the semispinalis capitis muscle were identified to be the greater occipital neuron (GON). From this location, a 22-gauge spinal needle and 3 ccs of bupivacaine at a concentration of 0.5% were used to perform GON blocking. The intensity of her attack decreased from 9/10 to 2/10 after the first 20 minutes of the block. Throughout a month, the blocks were repeated once a week. In the second month, the frequency of her attacks decreased to two per month, with an intensity of 4/10. She did not encounter any attacks in the sixth month.\n\n",
+    "diff_label_texts": "A 42-year-old woman had a hard-to-treat headache condition. Headache pills made her feel sick, so she could not take them. She came to the clinic with very strong pain, 9 out of 10. We took her to a small operating room. We used ultrasound, like a live picture, to guide a numbing shot to a nerve at the back of her head. The numbing medicine made her pain drop to 2 out of 10 within minutes. We repeated the same shot once a week for four weeks. After two months, her headaches happened less often and hurt less. She had no side effects.",
+    "summary": "Herein, we report that a 42-year-old female patient with PCH who could not use the oral medication because of side effects. When she came to the pain clinic with an attack with intensity of 9/10 , we took her to the local operating room. The ultrasound (US) guided proximal greater occipital nerve block with bupivacaine was performed and the intensity of the attack was reduced to 2/10. The blockage was repeated once a week for a month. After two months, both the intensity of headache and number of attacks decreased and no adverse effect was observed."
+  },
+  {
+    "doc_id": 76,
+    "label": "proficient_health_literacy",
+    "fulltext": "The patient was a 42-year-old woman with a history of menstrual migraine, Hashimoto Thyroiditis, Familial Mediterian Fever (FMF), and dyspepsia. She was taking 75 mg of levothyroxine, 30 mg of lansoprazole, and 1.5 mg of colchicine daily. In February of 2023, she was diagnosed with acute bronchitis, which was treated with antibiotics and bronchodilators. She developed a daily headache after two weeks, manifesting as more than ten short-lasting attacks per day provoked by coughing, straining, and lifting. The duration of each attack was 30 minutes, and the pain was bilaterally distributed from the neck to the top of the head. The headache was sharp and severe. She described the attack as a sensation of storm-like fluid movement in the head. She did not suffer any of the symptoms associated with previous migraine attacks, such as phonophobia, photophobia, vomiting, or throbbing. The severity of the attack was determined using a numeric rating scale (NRS) with a score of 9 out of 10. These attacks typically necessitated a visit to the emergency room. The results of her physical and neurological exams were unremarkable. The laboratory tests, including those for thyroid hormones, electrolytes, liver and kidney function, and serology, were negative. Brain and cervical spinal magnetic resonance imaging (MRI) with and without contrast, magnetic resonance venography (MRV), and angiography (MRA) were all normal. She did not give consent for a lumbar puncture. When we first encountered her in the clinic, she was taking 25 mg of indomethacin per day. Her attacks stopped after putting her on 60 mg of lansoprazole and increasing her daily dose of indomethacin to 150 mg. However, she encountered gastrointestinal side effects, so the indomethacin was discontinued on day three. Due to the adverse effects, she was unable to take topiramate and propranolol.\n\nShe came to the clinic 15 days after her initial visit with an NRS score of 9/10. She was taken to the local operating room. We used a GE Healthcare, Voluson™ E6, ultrasonography system with a linear 13–5 MHz probe for unilateral PGONB. The patient’s neck was prone to flexion. The linear probe was initially transversely positioned on the occipital protuberance and then advanced caudally, demonstrating that the C2 spinous process resembled the two horns. Through lateral probe movement, the inferior muscles of the obliquus capitis and semispinalis capitis were located. Here, the superior to the inferior oblique capitis muscle and beneath the semispinalis capitis muscle were identified to be the greater occipital neuron (GON). From this location, a 22-gauge spinal needle and 3 ccs of bupivacaine at a concentration of 0.5% were used to perform GON blocking. The intensity of her attack decreased from 9/10 to 2/10 after the first 20 minutes of the block. Throughout a month, the blocks were repeated once a week. In the second month, the frequency of her attacks decreased to two per month, with an intensity of 4/10. She did not encounter any attacks in the sixth month.\n\n",
+    "diff_label_texts": "A 42-year-old woman with a history of menstrual migraine, Hashimoto thyroiditis, familial Mediterranean fever, and dyspepsia developed daily, short-lasting headache attacks approximately two weeks after an episode of acute bronchitis treated with antibiotics and bronchodilators. Attacks were provoked by coughing, straining, and lifting; occurred more than ten times per day; lasted about 30 minutes; were bilaterally distributed from the neck to the vertex; and were described as sharp, severe, with a sensation of storm-like fluid movement. She denied prior migraine-associated symptoms (no phonophobia, photophobia, vomiting, or throbbing). Neurological examination and laboratory studies (thyroid hormones, electrolytes, liver/kidney function, serologies) were unremarkable. Brain and cervical spine MRI with and without contrast, MRV, and MRA were normal. She declined lumbar puncture. At initial clinic contact, she was taking indomethacin 25 mg/day; increasing indomethacin to 150 mg/day with lansoprazole 60 mg/day aborted attacks, but gastrointestinal adverse effects led to discontinuation on day 3. She was unable to take topiramate and propranolol due to adverse effects. Fifteen days later she returned with an NRS 9/10 attack and was brought to the local operating room for an ultrasound-guided proximal greater occipital nerve block (PGONB). Using a GE Healthcare Voluson E6 system with a 13–5 MHz linear probe, the patient was positioned prone with neck flexed. The probe was placed transversely at the external occipital protuberance and moved caudally to identify the C2 spinous process (“two horns” appearance). Via lateral probe movement, the obliquus capitis inferior and semispinalis capitis were visualized; the greater occipital nerve was identified superior to the obliquus capitis inferior and beneath the semispinalis capitis. A 22-gauge spinal needle was advanced, and 3 mL of 0.5% bupivacaine was injected for GON blockade. Pain intensity decreased from 9/10 to 2/10 within 20 minutes. The block was repeated weekly for one month. By the second month, attack frequency decreased to two per month with intensity 4/10; no adverse effects were observed. At month six, she reported no further attacks.",
+    "summary": "Herein, we report that a 42-year-old female patient with PCH who could not use the oral medication because of side effects. When she came to the pain clinic with an attack with intensity of 9/10 , we took her to the local operating room. The ultrasound (US) guided proximal greater occipital nerve block with bupivacaine was performed and the intensity of the attack was reduced to 2/10. The blockage was repeated once a week for a month. After two months, both the intensity of headache and number of attacks decreased and no adverse effect was observed."
+  },
+  {
+    "doc_id": 77,
+    "label": "low_health_literacy",
+    "fulltext": "Patient information\nA 20-year-old male Arabic martial artist (weight 91.5 kg, height 180 cm, and body mas index (BMI) 28.24) presented with pain in the back of the left thigh for the past 5 weeks and underwent pharmacological and physiotherapeutic intervention; however, he did not responded well to symptomatic treatment. He reported that the symptoms first appeared during a short sprint while playing soccer and heard a pop in the back of his thigh. The pain was so bad that he withdrew from the game soon after his injury and noted no bruising on the back of his thigh or significant swelling in that area. However, he reported progressive loss of flexibility in the left knee and inability to flex and extend the knee joint while the knee remained flexed at a 15° angle, whether standing or having the leg in the air. He denied any previous history of lower back pain but could barely support the weight of the affected limb. There was no history of alcohol, smoking, diabetes, high blood pressure, or other serious genetic diseases.\n\nClinical findings and diagnostic assessment\nThe patient reported having received icing and elevation of the affected leg while lying down following the injury as therapeutic interventions. He had a crepe bandage applied to his affected thigh to support him while standing and walking. He used crutches for ambulation and to go for a little longer distance. To climb the stairs, he had to use one step at a time, relying on his right lower extremity. He also reported adopting a sitting position at the edge of the chair as direct pressure on the thigh from the chair caused him discomfort. He denied ever hurting his legs or back in sports. As a result, the patient withdrew from all activities, such as playing sports, owing to the pain, and his knee was mildly bent most of the time. Despite taking medication (nonsteroidal antiinflammatory drugs (NSAIDs)), the pain worsened over time. Since the patient did not respond well to cryotherapy, compression bandages, and medications, he decided to see a doctor for further diagnosis and treatment before meeting with us.\n\nOn further evaluation, he presented with limited knee extension and flexion and exhibited an analgesic gait with a reduced heel strike phase. Active range of motion (AROM) of the left knee was 10–15° compared with 0–130°degrees in the right knee. Palpation revealed tenderness and firmness in the middle third of the semimembranosus and semitendinosus muscles.\n\nManual muscle testing and isometrics could not be performed owing to persistent discomfort. The patient reported pain at rest, rated 5/10, and during activity it was rated 7/10. Further, clinical evaluation rule out lumbar disc involvement or gluteal and ischial tunnel syndrome [4, 6].\n\nThe best way to screen nerve tension for peripheral pain in the lower extremities is with a slump test [17]. However, the result of the slump test in this patient was negative.\n\nTherapeutic interventions\nDespite the patient’s current clinical presentation, which was suggestive of HSI, the authors decided to treat him with neural glide technique on the basis of the structural and functional proximity of nerve to the lower limb flexibility through a novel neurodynamic tension technique [18, 19]. The scientific rationale for this neural approach was detailed to the patient and consent was obtained.\n\nThe patient was directed to sit with arms folded behind his back and knees and ankles held in extension and dorsiflexion, respectively, while a therapist guided the patient to flex his thoracic and cervical spine and extend his knee joint to the maximum tolerable limit. Next, the patient was instructed to move his neck forward and backward as much as possible while also moving his ankle up and down 15 times to help with nerve glide.\n\nThis was done in three sets each day. The therapist then helped the patient bend their middle and upper back as much as possible until the patient felt pain in the knee area. Then, the process was repeated. By the 3rd day, the patient’s active knee extension improved from 5° to 10° and then to a 15° degree bent position. In addition, the standing posture also got better.\n\nSubsequently, the patient was instructed in executing a set of posture re-education workouts, which involved doing active chin flexion, engaging in passive stretching of the cervical extensors while lying down in prone, and building up the shoulder retractors, arm from positions T to Y, then from Y to W with the limb’s weight while lying down.\n\nTo address the kyphotic posture, active chest stretches were taught at wall corners. The patient was instructed to increase the duration of the exercises from 5 to 10 seconds, doing 10 reps and 3 sets daily.\n\nOutcomes and follow-up\nThe results were assessed using a numeric pain rating scale (NPRS) and Knee Society score (KSS). Substantial enhancement in clinical outcome measures such as pain and function were achieved within 3 successive days of therapy. The use of pain medication was discontinued.\n\nThe patient continued his self-neural glides and postural reduction exercises at home and was advised for a follow-up after 4 weeks or to contact us if symptoms worsened. On the 3rd follow-up day, the patient’s NPRS from 5 at rest and 7 with activity to 2 at rest and 4 with activity. The KSS increased from 22 to 61 and from 30 to 80 in the functional domain. At the end of the 2-week home program, the patient reported to have full active straight leg raise (SLR). The patient had fully recovered from his knee dysfunction and pain at the 2-month follow-up.",
+    "diff_label_texts": "Who: A 20-year-old Arabic man who practices martial arts. Problem: Pain in the back of his left thigh for 5 weeks. He tried medicines and physical therapy, but they did not help. Doctors said it was not a trapped-nerve problem in the hamstring. He stopped all sports. Treatment: He did a gentle seated nerve-glide exercise four times a day for three days in a row. He also learned better posture. Pain before treatment: 5 out of 10 at rest. 7 out of 10 with activity. Pain after 3 days: 2 out of 10 at rest. 4 out of 10 with activity. Knee scores got better. Pain part went from 22 to 61. Function part went from 30 to 80. After 2 months, he felt fully recovered and returned to sports with no problems.",
+    "summary": "A 20-year-old male Arabic martial artist had a history of left hamstring strain for the past 5 weeks. He had undergone pharmacological and physiotherapeutic interventions for his clinical conditions but had not responded favorably. Further clinical assessment had ruled out hamstring syndrome. The patient refrained from all sports activities.\n\nIntervention: The patient was treated using a modified slump mobilization technique with four repetitions for 3 consecutive days, together with postural retraining. Results of the numeric pain rating scale and Knee Society score before and after the interventions were obtained.\n\nResults and discussion: Pre-intervention score of the numeric pain rating scale was 5/10 and 7/10 at rest and with activity, respectively. Assessment on the 3rd consecutive day of intervention, the numeric pain rating scale decreased to 2/10 and 4/10 at rest and with activity, respectively. Similarly, the pre- and post-intervention Knee Society score improved from 22 to 61 in pain and from 30 to 80 in function. At the 2-month follow-up, the patient reported a complete recovery from symptoms and resumed his sports activities without any disruption."
+  },
+  {
+    "doc_id": 77,
+    "label": "intermediate_health_literacy",
+    "fulltext": "Patient information\nA 20-year-old male Arabic martial artist (weight 91.5 kg, height 180 cm, and body mas index (BMI) 28.24) presented with pain in the back of the left thigh for the past 5 weeks and underwent pharmacological and physiotherapeutic intervention; however, he did not responded well to symptomatic treatment. He reported that the symptoms first appeared during a short sprint while playing soccer and heard a pop in the back of his thigh. The pain was so bad that he withdrew from the game soon after his injury and noted no bruising on the back of his thigh or significant swelling in that area. However, he reported progressive loss of flexibility in the left knee and inability to flex and extend the knee joint while the knee remained flexed at a 15° angle, whether standing or having the leg in the air. He denied any previous history of lower back pain but could barely support the weight of the affected limb. There was no history of alcohol, smoking, diabetes, high blood pressure, or other serious genetic diseases.\n\nClinical findings and diagnostic assessment\nThe patient reported having received icing and elevation of the affected leg while lying down following the injury as therapeutic interventions. He had a crepe bandage applied to his affected thigh to support him while standing and walking. He used crutches for ambulation and to go for a little longer distance. To climb the stairs, he had to use one step at a time, relying on his right lower extremity. He also reported adopting a sitting position at the edge of the chair as direct pressure on the thigh from the chair caused him discomfort. He denied ever hurting his legs or back in sports. As a result, the patient withdrew from all activities, such as playing sports, owing to the pain, and his knee was mildly bent most of the time. Despite taking medication (nonsteroidal antiinflammatory drugs (NSAIDs)), the pain worsened over time. Since the patient did not respond well to cryotherapy, compression bandages, and medications, he decided to see a doctor for further diagnosis and treatment before meeting with us.\n\nOn further evaluation, he presented with limited knee extension and flexion and exhibited an analgesic gait with a reduced heel strike phase. Active range of motion (AROM) of the left knee was 10–15° compared with 0–130°degrees in the right knee. Palpation revealed tenderness and firmness in the middle third of the semimembranosus and semitendinosus muscles.\n\nManual muscle testing and isometrics could not be performed owing to persistent discomfort. The patient reported pain at rest, rated 5/10, and during activity it was rated 7/10. Further, clinical evaluation rule out lumbar disc involvement or gluteal and ischial tunnel syndrome [4, 6].\n\nThe best way to screen nerve tension for peripheral pain in the lower extremities is with a slump test [17]. However, the result of the slump test in this patient was negative.\n\nTherapeutic interventions\nDespite the patient’s current clinical presentation, which was suggestive of HSI, the authors decided to treat him with neural glide technique on the basis of the structural and functional proximity of nerve to the lower limb flexibility through a novel neurodynamic tension technique [18, 19]. The scientific rationale for this neural approach was detailed to the patient and consent was obtained.\n\nThe patient was directed to sit with arms folded behind his back and knees and ankles held in extension and dorsiflexion, respectively, while a therapist guided the patient to flex his thoracic and cervical spine and extend his knee joint to the maximum tolerable limit. Next, the patient was instructed to move his neck forward and backward as much as possible while also moving his ankle up and down 15 times to help with nerve glide.\n\nThis was done in three sets each day. The therapist then helped the patient bend their middle and upper back as much as possible until the patient felt pain in the knee area. Then, the process was repeated. By the 3rd day, the patient’s active knee extension improved from 5° to 10° and then to a 15° degree bent position. In addition, the standing posture also got better.\n\nSubsequently, the patient was instructed in executing a set of posture re-education workouts, which involved doing active chin flexion, engaging in passive stretching of the cervical extensors while lying down in prone, and building up the shoulder retractors, arm from positions T to Y, then from Y to W with the limb’s weight while lying down.\n\nTo address the kyphotic posture, active chest stretches were taught at wall corners. The patient was instructed to increase the duration of the exercises from 5 to 10 seconds, doing 10 reps and 3 sets daily.\n\nOutcomes and follow-up\nThe results were assessed using a numeric pain rating scale (NPRS) and Knee Society score (KSS). Substantial enhancement in clinical outcome measures such as pain and function were achieved within 3 successive days of therapy. The use of pain medication was discontinued.\n\nThe patient continued his self-neural glides and postural reduction exercises at home and was advised for a follow-up after 4 weeks or to contact us if symptoms worsened. On the 3rd follow-up day, the patient’s NPRS from 5 at rest and 7 with activity to 2 at rest and 4 with activity. The KSS increased from 22 to 61 and from 30 to 80 in the functional domain. At the end of the 2-week home program, the patient reported to have full active straight leg raise (SLR). The patient had fully recovered from his knee dysfunction and pain at the 2-month follow-up.",
+    "diff_label_texts": "A 20-year-old Arabic male martial artist had 5 weeks of left hamstring pain after a sports injury and did not improve with medications or physiotherapy. Hamstring syndrome was ruled out, and he stopped all sports during recovery. Intervention: a modified slump mobilization (a seated nerve-gliding technique) was performed with four repetitions on 3 consecutive days, along with postural retraining. Outcomes: Pain on the numeric pain rating scale improved from 5/10 at rest and 7/10 with activity to 2/10 at rest and 4/10 with activity by day 3. The Knee Society Score also improved: pain from 22 to 61 and function from 30 to 80. At 2 months, he reported complete symptom resolution and returned to sports without limitation.",
+    "summary": "A 20-year-old male Arabic martial artist had a history of left hamstring strain for the past 5 weeks. He had undergone pharmacological and physiotherapeutic interventions for his clinical conditions but had not responded favorably. Further clinical assessment had ruled out hamstring syndrome. The patient refrained from all sports activities.\n\nIntervention: The patient was treated using a modified slump mobilization technique with four repetitions for 3 consecutive days, together with postural retraining. Results of the numeric pain rating scale and Knee Society score before and after the interventions were obtained.\n\nResults and discussion: Pre-intervention score of the numeric pain rating scale was 5/10 and 7/10 at rest and with activity, respectively. Assessment on the 3rd consecutive day of intervention, the numeric pain rating scale decreased to 2/10 and 4/10 at rest and with activity, respectively. Similarly, the pre- and post-intervention Knee Society score improved from 22 to 61 in pain and from 30 to 80 in function. At the 2-month follow-up, the patient reported a complete recovery from symptoms and resumed his sports activities without any disruption."
+  },
+  {
+    "doc_id": 77,
+    "label": "proficient_health_literacy",
+    "fulltext": "Patient information\nA 20-year-old male Arabic martial artist (weight 91.5 kg, height 180 cm, and body mas index (BMI) 28.24) presented with pain in the back of the left thigh for the past 5 weeks and underwent pharmacological and physiotherapeutic intervention; however, he did not responded well to symptomatic treatment. He reported that the symptoms first appeared during a short sprint while playing soccer and heard a pop in the back of his thigh. The pain was so bad that he withdrew from the game soon after his injury and noted no bruising on the back of his thigh or significant swelling in that area. However, he reported progressive loss of flexibility in the left knee and inability to flex and extend the knee joint while the knee remained flexed at a 15° angle, whether standing or having the leg in the air. He denied any previous history of lower back pain but could barely support the weight of the affected limb. There was no history of alcohol, smoking, diabetes, high blood pressure, or other serious genetic diseases.\n\nClinical findings and diagnostic assessment\nThe patient reported having received icing and elevation of the affected leg while lying down following the injury as therapeutic interventions. He had a crepe bandage applied to his affected thigh to support him while standing and walking. He used crutches for ambulation and to go for a little longer distance. To climb the stairs, he had to use one step at a time, relying on his right lower extremity. He also reported adopting a sitting position at the edge of the chair as direct pressure on the thigh from the chair caused him discomfort. He denied ever hurting his legs or back in sports. As a result, the patient withdrew from all activities, such as playing sports, owing to the pain, and his knee was mildly bent most of the time. Despite taking medication (nonsteroidal antiinflammatory drugs (NSAIDs)), the pain worsened over time. Since the patient did not respond well to cryotherapy, compression bandages, and medications, he decided to see a doctor for further diagnosis and treatment before meeting with us.\n\nOn further evaluation, he presented with limited knee extension and flexion and exhibited an analgesic gait with a reduced heel strike phase. Active range of motion (AROM) of the left knee was 10–15° compared with 0–130°degrees in the right knee. Palpation revealed tenderness and firmness in the middle third of the semimembranosus and semitendinosus muscles.\n\nManual muscle testing and isometrics could not be performed owing to persistent discomfort. The patient reported pain at rest, rated 5/10, and during activity it was rated 7/10. Further, clinical evaluation rule out lumbar disc involvement or gluteal and ischial tunnel syndrome [4, 6].\n\nThe best way to screen nerve tension for peripheral pain in the lower extremities is with a slump test [17]. However, the result of the slump test in this patient was negative.\n\nTherapeutic interventions\nDespite the patient’s current clinical presentation, which was suggestive of HSI, the authors decided to treat him with neural glide technique on the basis of the structural and functional proximity of nerve to the lower limb flexibility through a novel neurodynamic tension technique [18, 19]. The scientific rationale for this neural approach was detailed to the patient and consent was obtained.\n\nThe patient was directed to sit with arms folded behind his back and knees and ankles held in extension and dorsiflexion, respectively, while a therapist guided the patient to flex his thoracic and cervical spine and extend his knee joint to the maximum tolerable limit. Next, the patient was instructed to move his neck forward and backward as much as possible while also moving his ankle up and down 15 times to help with nerve glide.\n\nThis was done in three sets each day. The therapist then helped the patient bend their middle and upper back as much as possible until the patient felt pain in the knee area. Then, the process was repeated. By the 3rd day, the patient’s active knee extension improved from 5° to 10° and then to a 15° degree bent position. In addition, the standing posture also got better.\n\nSubsequently, the patient was instructed in executing a set of posture re-education workouts, which involved doing active chin flexion, engaging in passive stretching of the cervical extensors while lying down in prone, and building up the shoulder retractors, arm from positions T to Y, then from Y to W with the limb’s weight while lying down.\n\nTo address the kyphotic posture, active chest stretches were taught at wall corners. The patient was instructed to increase the duration of the exercises from 5 to 10 seconds, doing 10 reps and 3 sets daily.\n\nOutcomes and follow-up\nThe results were assessed using a numeric pain rating scale (NPRS) and Knee Society score (KSS). Substantial enhancement in clinical outcome measures such as pain and function were achieved within 3 successive days of therapy. The use of pain medication was discontinued.\n\nThe patient continued his self-neural glides and postural reduction exercises at home and was advised for a follow-up after 4 weeks or to contact us if symptoms worsened. On the 3rd follow-up day, the patient’s NPRS from 5 at rest and 7 with activity to 2 at rest and 4 with activity. The KSS increased from 22 to 61 and from 30 to 80 in the functional domain. At the end of the 2-week home program, the patient reported to have full active straight leg raise (SLR). The patient had fully recovered from his knee dysfunction and pain at the 2-month follow-up.",
+    "diff_label_texts": "A 20-year-old Arabic male martial artist (91.5 kg, 180 cm, BMI 28.24) presented with 5 weeks of posterior left thigh pain after a short sprint during soccer, described as an acute “pop,” followed by progressive loss of knee flexibility and inability to fully flex or extend the knee; the knee rested in approximately 15° of flexion. He reported no ecchymosis or significant swelling, could barely weight-bear on the affected limb, and withdrew from all sport. Initial self-management included icing, elevation, a crepe bandage, crutches, and step-to stair negotiation; NSAIDs, cryotherapy, and compression provided little relief. He denied prior lumbar symptoms and had no notable medical comorbidities (no alcohol use, smoking, diabetes, hypertension, or hereditary disease). Examination showed an analgesic gait with reduced heel strike; AROM of the left knee was 10–15° versus 0–130° on the right. Palpation identified tenderness and firmness in the middle third of the semimembranosus and semitendinosus. Manual muscle testing and isometrics were deferred due to discomfort. NPRS was 5/10 at rest and 7/10 with activity. Clinical evaluation ruled out lumbar disc involvement and gluteal/ischial tunnel syndromes. Although the slump test is a standard screen for lower-limb neurodynamic mechanosensitivity, it was negative in this patient. Despite a presentation suggestive of hamstring strain injury, the team implemented a neural glide based on neurodynamic principles and the anatomical/functional proximity of peripheral nerve structures to hamstring flexibility. Technique: seated with arms folded behind the back; knees extended and ankles dorsiflexed; therapist-guided thoracic and cervical flexion with knee extension to the patient’s tolerance, followed by active cervical flexion–extension coordinated with ankle dorsiflexion–plantarflexion (15 repetitions) to facilitate nerve gliding. Three sets were performed daily over 3 consecutive days. The therapist also facilitated progressive thoracic/cervical flexion until knee-area pain was provoked and then repeated the sequence. By day 3, active knee extension improved from approximately 5° to 10° and then to a 15°-bent position, and standing posture improved. Postural re-education included active chin flexion, prone passive stretching of cervical extensors, and progressive scapular retractor strengthening (arm positions T→Y→W) in prone with limb weight. To address kyphotic posture, active pectoral stretches at wall corners were prescribed, progressing hold time from 5 to 10 seconds, 10 repetitions, 3 sets daily. Outcomes: Measured by NPRS and Knee Society Score (KSS). Within 3 treatment days, substantial improvement was observed; pain medication was discontinued. NPRS decreased from 5/10 (rest) and 7/10 (activity) to 2/10 and 4/10, respectively. KSS improved from 22 to 61 (pain domain) and from 30 to 80 (function). After a 2-week home program, the patient achieved full active straight leg raise. At 2-month follow-up, he reported full recovery of knee function and pain resolution and had returned to sport without disruption. This case suggests that, even with a negative slump test, targeted neurodynamic mobilization combined with postural retraining may rapidly improve pain and function in select hamstring strain presentations; proposed mechanisms include reduced intraneural/extraneural adhesions, improved neural excursion, and modulation of nociceptive input.",
+    "summary": "A 20-year-old male Arabic martial artist had a history of left hamstring strain for the past 5 weeks. He had undergone pharmacological and physiotherapeutic interventions for his clinical conditions but had not responded favorably. Further clinical assessment had ruled out hamstring syndrome. The patient refrained from all sports activities.\n\nIntervention: The patient was treated using a modified slump mobilization technique with four repetitions for 3 consecutive days, together with postural retraining. Results of the numeric pain rating scale and Knee Society score before and after the interventions were obtained.\n\nResults and discussion: Pre-intervention score of the numeric pain rating scale was 5/10 and 7/10 at rest and with activity, respectively. Assessment on the 3rd consecutive day of intervention, the numeric pain rating scale decreased to 2/10 and 4/10 at rest and with activity, respectively. Similarly, the pre- and post-intervention Knee Society score improved from 22 to 61 in pain and from 30 to 80 in function. At the 2-month follow-up, the patient reported a complete recovery from symptoms and resumed his sports activities without any disruption."
+  },
+  {
+    "doc_id": 78,
+    "label": "proficient_health_literacy",
+    "fulltext": "A male was born via an emergency cesarean section due to fetal distress at 40 weeks of gestational age. The mother's age was 33 years, with gravida 1 and para 1 parity. Both the parents and brother had no family history of congenital anomalies, aortic-related diseases, or sudden death. Based on the results of the prenatal ultrasonography at the end of the second trimester, the femur length of the fetus was found to be 1 to 3 weeks longer than the supposed length of the actual gestational age. Fetal echocardiography showed cardiomegaly with a fetal cardiothoracic circumference ratio of 0.5 or higher based on the baby's term. Moreover, the size of the foramen ovale was larger than normal, and left aortic constriction was seen next to the subclavian artery basin. Furthermore, no other abnormalities were found on prenatal ultrasound.\n\nAt birth, the weight was 3560 g (75 percentile), the length was 56.5 cm (over 90 percentile), and the head circumference was 36 cm (over 90 percentile). Apgar scores at 1 and 5 minutes were 4 and 6 points, respectively. In the delivery room, the patient had no spontaneous breathing and had bradycardia and cyanosis. After being admitted to the neonatal intensive care unit, various musculoskeletal malformations were confirmed via physical examination. Severe arachnodactyly and camptodactyly were observed in both hands and feet, and the soles of the feet were flat. The elbow and knee joints were not fully extended. The face had malar hypoplasia with senile facial appearance. The eye was deeply settled with a down-slanting palpebral fissure, and the ear with hypoplastic cartilage was poorly settled and crumpled. The patient presented with a sagging mouth, prominent coronal suture, and brachycephaly. A grade V/VI systolic murmur was heard at both the upper sternal border and left lower sternal border with grade III parasternal heave. Echocardiography showed poor cardiac contractility, severe pulmonary hypertension, dilated aortic sinus (20.2 mm) (Z-score; 8.08 by Boston, 6.37 by Detroit, or 5.97 by Halifax), and multiple intracardiac valvular dysfunction with valve prolapses (moderate aortic regurgitation, severe mitral regurgitation, moderate tricuspid regurgitation, and moderate pulmonary valve regurgitation). And the ophthalmologic examination results showed ectopia lentis in both eyes as well as lens subluxation. Liver herniation was confirmed using abdominal X-ray and ultrasound. The systemic score of the musculoskeletal manifestation was 11 points, according to the Ghent criteria (international diagnostic criteria for MFS).\n\nFor genetic diagnosis, Sanger sequencing and polymerase chain reaction were performed on the nucleotide sequence as reference for the FBN1 gene. As a result, a mutation in which G, the first base of the 32nd intron in the form of a heterogeneous mutation, was substituted with T (c.3964 + 1G > T). This was confirmed as the likely pathogen variant based on the 2015 ACMG/AMP guideline. The location of the mutation was included in the site previously known as the neonatal region of MFS (exons 24–32). The patient could be diagnosed with neonatal MFS with a novel FBN1 gene mutation within 2 weeks of life.\n\nOn the first day of life, differential cyanosis was found to show refractory hypoxemia despite more than 60% oxygen supply and signs of low cardiac output. The patient was managed medically for improving the low cardiac output according to severe mitral regurgitation and aortic regurgitation. Afterload reduction including milrinone continuous infusion, full sedation using fentanyl continuous infusion, and use of diuretic were attempt to improve the oliguria and heart failure. Despite the medical management, the patient presented with respiratory failure, heart failure, and severe pulmonary hypertension requiring continuous invasive mechanical ventilation. Aortic regurgitation, mitral regurgitation, pulmonary hypertension, and cardiac contractility got worse. After several consultations with the patient's family and medical staff about the treatment plan, palliative care was continued instead of surgical treatment. As a result, hepatic and pulmonary congestion accompanied by pulmonary hemorrhage had progressed as well. Eventually, it had progressed to multiple organ dysfunction syndrome, and the patient died 32 days after the birth.",
+    "diff_label_texts": "A male infant was delivered at 40 weeks via emergency cesarean section for fetal distress to a 33-year-old G1P1 mother. Family history was negative for congenital anomalies, aortic disease, or sudden death. Prenatal imaging showed advanced femur length (by 1–3 weeks), cardiomegaly with a cardiothoracic circumference ratio ≥0.5, an enlarged foramen ovale, and left aortic constriction near the subclavian artery basin; no other anomalies were noted. Birth measurements: 3560 g (75th percentile), length 56.5 cm (>90th), head circumference 36 cm (>90th). Apgars were 4 and 6 at 1 and 5 minutes. In the delivery room he had no spontaneous respirations, bradycardia, and cyanosis, prompting NICU admission. Physical exam revealed multiple musculoskeletal and craniofacial anomalies: severe arachnodactyly and camptodactyly of all extremities with flat soles; elbow and knee contractures; malar hypoplasia with senile facial appearance; deep-set eyes with down-slanting palpebral fissures; hypoplastic, crumpled auricular cartilage; sagging mouth; prominent coronal suture; and brachycephaly. A grade V/VI systolic murmur was audible at both upper sternal borders and the left lower sternal border with a grade III parasternal heave. The Ghent systemic score for musculoskeletal features was 11. Echocardiography demonstrated poor contractility, severe pulmonary hypertension, a dilated aortic sinus measuring 20.2 mm (Z-score 8.08 Boston, 6.37 Detroit, 5.97 Halifax), and multivalvular prolapse with dysfunction: moderate aortic regurgitation, severe mitral regurgitation, moderate tricuspid regurgitation, and moderate pulmonary valve regurgitation. Ophthalmology confirmed bilateral ectopia lentis with lens subluxation. Abdominal radiography and ultrasound identified liver herniation.\n\nMolecular testing (Sanger sequencing/PCR) of FBN1 detected a heterozygous donor splice-site variant, c.3964+1G>T in intron 32, classified as likely pathogenic per the 2015 ACMG/AMP guideline. The variant resides within the established neonatal region of FBN1 (exons 24–32) associated with the severe neonatal Marfan phenotype. Mechanistically, splice-site variants at this locus are expected to disrupt normal FBN1 splicing, compromising microfibril integrity and driving the aggressive cardiovascular phenotype observed in neonatal MFS (notably early aortic root dilation and severe atrioventricular valve regurgitation).\n\nOn day 1, he exhibited differential cyanosis with refractory hypoxemia despite >60% oxygen and clinical signs of low cardiac output. Medical management targeted afterload reduction (continuous milrinone infusion), full sedation (continuous fentanyl infusion), and diuresis to address oliguria and heart failure. Despite these measures, he progressed to respiratory failure and severe pulmonary hypertension requiring continuous invasive mechanical ventilation. Aortic and mitral regurgitation worsened, pulmonary hypertension escalated, and cardiac contractility deteriorated. Given the grave trajectory and the expectation that surgical intervention would be essential to prolong life but with limited prospects in the face of rapid progression, the family elected palliative care after multidisciplinary discussions. He developed hepatic and pulmonary congestion with pulmonary hemorrhage, progressed to multiple organ dysfunction syndrome, and died 32 days after birth.\n\nThis case documents a novel FBN1 c.3964+1G>T splice-site variant in the neonatal region, concordant with the classic neonatal MFS phenotype: severe early valvulopathy, aortic root dilation, ectopia lentis, characteristic skeletal/craniodysmorphic features, and a fulminant cardiorespiratory course with death in early infancy.",
+    "summary": "Patient concerns:\nA newborn with neonatal MFS and severe cardiac involvement. He presented various severe clinical features such as arachnodactyly, camptodactyly, elbow and knee joint contracture, senile facial appearance, and deep settling with down-slanting palpebral fissure, hypoplastic ear cartilage, sagging mouth, brachycephaly, and ectopia lentis.\n\nDiagnosis:\nGenetic analysis revealed a novel mutation at nucleotide 3964 (c.3964 + 1 G > T) in intron 32 of the fibrillin-1 gene. This mutation is identified to be in the so-called neonatal region of fibrillin-1 exon 24 to 32, as reported previously.\n\nInterventions:\nThe patient was managed medically for improving the low cardiac output according to severe mitral regurgitation and aortic regurgitation. Afterload reduction, full sedation, and use of diuretic were attempted to improve the oliguria and heart failure.\n\nOutcomes:\nDespite the medical management, aortic regurgitation, mitral regurgitation, pulmonary hypertension, and cardiac contractility got worse. Surgical treatment is essential to prolong the patient's life, however, considerations for the grave progression of the disease make families decide to continue palliative care instead of surgical treatment. A few months after birth, he presented with rapidly progressive aortic regurgitation, mitral regurgitation, and congestive heart failure leading to death."
+  },
+  {
+    "doc_id": 79,
+    "label": "low_health_literacy",
+    "fulltext": "A 27-year-old woman with beta-thalassemia major since 24 years and 16 weeks of pregnancy was referred from the Internal Medicine Department to the Oral Medicine Department with complaints of swelling, bleeding gums since early pregnancy, and bad breath. The patient was hospitalized with complaints of pain in her knee so he could not move. She was admitted to hospital with complaints of pain in her knees so she could not move and was diagnosed with Arthritis ar Genue Sinistra related to Thalassemia by an internal medicine specialist, sub division of rheumatology. General condition patient was weak, sick, and difficult to move during the approximately two weeks, when she was hospitalized. Patient has never visited a dentist, either before or now, with complaints about her oral cavity. The patient had a splenectomy in 2009. Her beta-thalassemia major was treated with routine blood transfusions once a month and iron anti- chelation drugs (deferoxamine); however, it was stopped due to pregnancy. There was no history of other systemic disease in this patient. A family history of the same disease was ruled out. History of recurrent stomatitis and drug or food allergies was ruled out.\n\nThe patient’s general condition weak, with normal vital signs; however, the patient had fever. Intraoral examination revealed gingival hyperplasia; erythema; soft consistency; a dark red, rounded gingival margin; tendencies to bleed on the labial, buccal, palatal, and lingual areas; and pain. Oral hygiene index-simplified (OHIS) score was poor (5.7) and there were true pockets in all regions. Peripheral blood morphology result: (1) erythrocytes: polychromacy in anisochrome populations (hypochrome, normochrome), anisopoikilocytosis (ovalocytes, target); (2) leukocytes: sufficient quantity, hypersegmentation (+); (3) platelet count: numbers increase, spread out; Interpretation: moderate anemia et causa thalassemia major accompanied by signs of increased erythropoiesis activity with suspected infection. The diagnosis was made based on the history, clinical features, and examination, as well as additional examinations, namely gingival enlargement accompanied by chronic periodontitis associated to pregnancy with β-thalassemia major and exfoliative cheilitis of the lips. The classification of periodontal disease in this patient is chronic periodontitis with gingival enlargement associated with pregnancy and beta-thalassemia major. The prognosis in this case was good because the patient was cooperative and followed the directions of the Oral Medicine Department. In this case, multidisciplinary therapy was a collaboration between an oral medicine specialist, a periodontist, and an internist. Dental therapy consisted of spooling with 3% hydrogen peroxide (H2O2) solution, chlorine dioxide spray mouthwash (Oxyfresh®, USA), antibiotics (amoxicillin 500 mg tablet, and metronidazole 300 mg tablet), and scaling/root planning. Spooling of H2O2 3% solution was performed at every visit; chlorine dioxide spray mouthwash was used three times a day after meals, and antibiotics were administered for seven days at third visit. Scaling and root planning were performed by the periodontist after the general condition was controlled and after the gingival hyperplasia and spontaneous bleeding improved. Blood transfusions to remove packed red cell buffy coat (PRC BCR) are also carried out routinely once a month. Non-pharmacological therapy, including oral hygiene instructions, was still given to patients. Oral complaints in this case occurred due to the poor oral hygiene, β-thalassemia major, and pregnancy, were also informed to the patient as education.\n\nThis patient had eight follow-up visits, consisting of two inpatient and six outpatient visits, with the following details:\n\nFirst Visit\nThe first visit was carried out one day after the initial inpatient visit (day +1). Intraoral bleeding still exists in the lingual-anterior part of the mandible, but bleeding in the anterior part of the maxilla has stopped. The patient still had a fever. Medications previously provided were used accordingly. Pharmacological were continued, including spooling 3% H2O2 on all parts of the gingiva, using chlorine dioxide as a mouthwash, and applying a thin layer of petroleum jelly to the lips. A blood transfusion was carried out last night. Oral hygiene instructions are still given to patients.\n\nSecond Visit\nThe second visit was performed two days after the initial visit (day +2). Intraoral bleeding Follow-up visits should be conducted in outpatient settings. Pharmacological therapy including spooling 3% H2O2 on all parts of the gingiva, using chlorine dioxide as a mouthwash, and applying a thin layer of petroleum jelly to the lips. A blood transfusion was carried out last night. Oral hygiene instructions are still given to patients.\n\nThird Visit\nNine days after the initial visit (Day+9). First outpatient treatment. Oral symptoms appeared to improve; bad breath was greatly reduced, but the gums were still swollen. The chlorine dioxide spray mouthwash was still being used and had run out. The patient could brush her teeth with a soft toothbrush but still experienced bleeding. Spooling was performed with 3% H2O2. The previous therapy was continued, antibiotics were prescribed 3x/day for seven days, and a blood transfusion was planned as a preparation for scaling the dental calculus. Oral hygiene instructions are still given to patients.\n\nFourth Visit\nOne month after the first visit (Day+30). Oral complaints improved significantly, bad breath was absent, gingiva enlargement decreased, and spontaneous bleeding ceased. The patient did not experience bleeding when brushing her teeth. Transfusions were performed between visits H+9 and H+30. During this visit, laboratory hematology tests and subsequent blood transfusions were performed. Antibiotics were no longer administered, 3% H2O2, chlorine dioxide, petroleum jelly and oral hygiene instructions were continued.\n\nFifth Visit\nOne week after the 4th visit (day +37), the oral complaints improved, but pharmacological and non-pharmacological therapy continued, including spooling 3% H2O2 on all parts of the gingiva, chlorine dioxide as a mouthwash, and applying a thin layer of petroleum jelly to the lips. Oral hygiene instructions are still given to patients. Supragingival scaling was planned two weeks later or after routine transfusions were administered.\n\nSixth Visit\nTwo months after the initial visit (day +60), the oral complaints improved. The gingival hyperplasia in some areas was no longer present, although in other areas still present, but they have undergone improvement. The transfusion had already been performed one week previously. Pharmacological therapy was continued, including 3% H2O2 spooling, chlorine dioxide spray mouthwash, and petroleum jelly. Non-pharmacological therapy namely oral hygiene instructions and an interdental toothbrush was suggested. Supra- and subgival scaling were performed.\n\nSeventh Visit\nTwo weeks after the 6th visit (Day+74), all the complaints improved. Gingival hyperplasia mostly resolved after scaling. Pharmacological includes 3% H2O2 spooling, chlorine dioxide spray mouthwash, and petroleum jelly as well as non-pharmacological therapy, consisting of oral hygiene instructions and the use of an interdental toothbrush.\n\nEighth Visit\nThree months after the initial visit (day +90), routine blood transfusions were performed one week before the visit. The patient is no longer presented with any oral complaints. All patients with gingival hyperplasia recovered optimally. The spooling process was stopped with 3% H2O2. Supra- and subgival scaling were performed again in all maxillary and mandibular regions. Instructions for the use of an interdental toothbrush, chlorine dioxide spray mouthwash, and petroleum jelly are still provided.",
+    "diff_label_texts": "Who: A 27-year-old woman, 16 weeks pregnant. She has a blood problem called beta thalassemia major. She gets a blood transfusion every month. She stopped her iron-removing medicine because she is pregnant.\n\nMain mouth problems: Her gums are swollen, red, soft, and bleed easily. She has bad breath. Her lips are very dry and peeling. There are deep spaces like pockets around her teeth that trap germs and cause pain all around her mouth. She had never seen a dentist before. Her blood test showed anemia and signs of an infection.\n\nWhat the dentists called it: Swollen gums and long-term gum disease linked to pregnancy and her blood problem.\n\nCare plan: Rinse the mouth with 3% hydrogen peroxide. Use a chlorine dioxide spray mouthwash. Take antibiotics. Get a professional teeth cleaning to remove hard buildup. Follow simple daily mouth-care steps at home. Keep getting monthly blood transfusions. Do not take the iron-removing medicine during pregnancy.\n\nResult: After three months of care by a dental and medical team, her mouth got much better.",
+    "summary": "A 27-year-old woman, suffering from beta thalassemia major who is undergoing therapy in the form of routine blood transfusions every month and taking anti-chelation drugs but is currently stopping this because she is pregnant, currently 16 weeks pregnant, complains complained of swollen gums, bleeding, and bad breath. Extraoral examination revealed dry, exfoliative lips. Intraoral examination revealed gingival hyperplasia with erythema, soft consistency, dark red rounded gingival margins, bleeding, true pockets and pain throughout the labial, buccal, palatal, and lingual. There was no history of systemic disease in this patient. Patient has never visited a dentist, either before or now, with complaints about her oral cavity. Hematological parameters showed abnormalities, and peripheral blood examination revealed an infection. The oral diagnoses included gingival enlargement and chronic periodontitis associated with pregnancy and β- thalassemia major.\n\nCase Management\nDental management consisted of spooling with 3% hydrogen peroxide (H2O2) spooling, chlorine dioxide spray mouthwash, antibiotics, calculus removal, and oral hygiene instructions. Blood transfusions were administered once a month, and anti-chelation therapy was stopped during pregnancy. After three months of multidisciplinary management, the results were satisfactory."
+  },
+  {
+    "doc_id": 79,
+    "label": "intermediate_health_literacy",
+    "fulltext": "A 27-year-old woman with beta-thalassemia major since 24 years and 16 weeks of pregnancy was referred from the Internal Medicine Department to the Oral Medicine Department with complaints of swelling, bleeding gums since early pregnancy, and bad breath. The patient was hospitalized with complaints of pain in her knee so he could not move. She was admitted to hospital with complaints of pain in her knees so she could not move and was diagnosed with Arthritis ar Genue Sinistra related to Thalassemia by an internal medicine specialist, sub division of rheumatology. General condition patient was weak, sick, and difficult to move during the approximately two weeks, when she was hospitalized. Patient has never visited a dentist, either before or now, with complaints about her oral cavity. The patient had a splenectomy in 2009. Her beta-thalassemia major was treated with routine blood transfusions once a month and iron anti- chelation drugs (deferoxamine); however, it was stopped due to pregnancy. There was no history of other systemic disease in this patient. A family history of the same disease was ruled out. History of recurrent stomatitis and drug or food allergies was ruled out.\n\nThe patient’s general condition weak, with normal vital signs; however, the patient had fever. Intraoral examination revealed gingival hyperplasia; erythema; soft consistency; a dark red, rounded gingival margin; tendencies to bleed on the labial, buccal, palatal, and lingual areas; and pain. Oral hygiene index-simplified (OHIS) score was poor (5.7) and there were true pockets in all regions. Peripheral blood morphology result: (1) erythrocytes: polychromacy in anisochrome populations (hypochrome, normochrome), anisopoikilocytosis (ovalocytes, target); (2) leukocytes: sufficient quantity, hypersegmentation (+); (3) platelet count: numbers increase, spread out; Interpretation: moderate anemia et causa thalassemia major accompanied by signs of increased erythropoiesis activity with suspected infection. The diagnosis was made based on the history, clinical features, and examination, as well as additional examinations, namely gingival enlargement accompanied by chronic periodontitis associated to pregnancy with β-thalassemia major and exfoliative cheilitis of the lips. The classification of periodontal disease in this patient is chronic periodontitis with gingival enlargement associated with pregnancy and beta-thalassemia major. The prognosis in this case was good because the patient was cooperative and followed the directions of the Oral Medicine Department. In this case, multidisciplinary therapy was a collaboration between an oral medicine specialist, a periodontist, and an internist. Dental therapy consisted of spooling with 3% hydrogen peroxide (H2O2) solution, chlorine dioxide spray mouthwash (Oxyfresh®, USA), antibiotics (amoxicillin 500 mg tablet, and metronidazole 300 mg tablet), and scaling/root planning. Spooling of H2O2 3% solution was performed at every visit; chlorine dioxide spray mouthwash was used three times a day after meals, and antibiotics were administered for seven days at third visit. Scaling and root planning were performed by the periodontist after the general condition was controlled and after the gingival hyperplasia and spontaneous bleeding improved. Blood transfusions to remove packed red cell buffy coat (PRC BCR) are also carried out routinely once a month. Non-pharmacological therapy, including oral hygiene instructions, was still given to patients. Oral complaints in this case occurred due to the poor oral hygiene, β-thalassemia major, and pregnancy, were also informed to the patient as education.\n\nThis patient had eight follow-up visits, consisting of two inpatient and six outpatient visits, with the following details:\n\nFirst Visit\nThe first visit was carried out one day after the initial inpatient visit (day +1). Intraoral bleeding still exists in the lingual-anterior part of the mandible, but bleeding in the anterior part of the maxilla has stopped. The patient still had a fever. Medications previously provided were used accordingly. Pharmacological were continued, including spooling 3% H2O2 on all parts of the gingiva, using chlorine dioxide as a mouthwash, and applying a thin layer of petroleum jelly to the lips. A blood transfusion was carried out last night. Oral hygiene instructions are still given to patients.\n\nSecond Visit\nThe second visit was performed two days after the initial visit (day +2). Intraoral bleeding Follow-up visits should be conducted in outpatient settings. Pharmacological therapy including spooling 3% H2O2 on all parts of the gingiva, using chlorine dioxide as a mouthwash, and applying a thin layer of petroleum jelly to the lips. A blood transfusion was carried out last night. Oral hygiene instructions are still given to patients.\n\nThird Visit\nNine days after the initial visit (Day+9). First outpatient treatment. Oral symptoms appeared to improve; bad breath was greatly reduced, but the gums were still swollen. The chlorine dioxide spray mouthwash was still being used and had run out. The patient could brush her teeth with a soft toothbrush but still experienced bleeding. Spooling was performed with 3% H2O2. The previous therapy was continued, antibiotics were prescribed 3x/day for seven days, and a blood transfusion was planned as a preparation for scaling the dental calculus. Oral hygiene instructions are still given to patients.\n\nFourth Visit\nOne month after the first visit (Day+30). Oral complaints improved significantly, bad breath was absent, gingiva enlargement decreased, and spontaneous bleeding ceased. The patient did not experience bleeding when brushing her teeth. Transfusions were performed between visits H+9 and H+30. During this visit, laboratory hematology tests and subsequent blood transfusions were performed. Antibiotics were no longer administered, 3% H2O2, chlorine dioxide, petroleum jelly and oral hygiene instructions were continued.\n\nFifth Visit\nOne week after the 4th visit (day +37), the oral complaints improved, but pharmacological and non-pharmacological therapy continued, including spooling 3% H2O2 on all parts of the gingiva, chlorine dioxide as a mouthwash, and applying a thin layer of petroleum jelly to the lips. Oral hygiene instructions are still given to patients. Supragingival scaling was planned two weeks later or after routine transfusions were administered.\n\nSixth Visit\nTwo months after the initial visit (day +60), the oral complaints improved. The gingival hyperplasia in some areas was no longer present, although in other areas still present, but they have undergone improvement. The transfusion had already been performed one week previously. Pharmacological therapy was continued, including 3% H2O2 spooling, chlorine dioxide spray mouthwash, and petroleum jelly. Non-pharmacological therapy namely oral hygiene instructions and an interdental toothbrush was suggested. Supra- and subgival scaling were performed.\n\nSeventh Visit\nTwo weeks after the 6th visit (Day+74), all the complaints improved. Gingival hyperplasia mostly resolved after scaling. Pharmacological includes 3% H2O2 spooling, chlorine dioxide spray mouthwash, and petroleum jelly as well as non-pharmacological therapy, consisting of oral hygiene instructions and the use of an interdental toothbrush.\n\nEighth Visit\nThree months after the initial visit (day +90), routine blood transfusions were performed one week before the visit. The patient is no longer presented with any oral complaints. All patients with gingival hyperplasia recovered optimally. The spooling process was stopped with 3% H2O2. Supra- and subgival scaling were performed again in all maxillary and mandibular regions. Instructions for the use of an interdental toothbrush, chlorine dioxide spray mouthwash, and petroleum jelly are still provided.",
+    "diff_label_texts": "Patient: 27-year-old woman, 16 weeks pregnant, with beta thalassemia major on monthly transfusions. Iron chelation was stopped during pregnancy.\n\nPresenting concerns: Since early pregnancy she had swollen, bleeding gums and bad breath. Exam showed dry, exfoliative lips and generalized gingival enlargement with redness, soft tissue, dark red rounded margins, easy bleeding, pain, and true periodontal pockets on the labial, buccal, palatal, and lingual surfaces. She had never seen a dentist for these issues. No other systemic illnesses were reported. Hematology showed anemia with abnormalities and evidence suggesting infection.\n\nAssessment: Gingival enlargement and chronic periodontitis associated with pregnancy and beta thalassemia major.\n\nManagement: Multidisciplinary dental care included 3% hydrogen peroxide rinses, a chlorine dioxide spray mouthwash, a course of antibiotics, professional calculus removal (scaling/root planing), and oral hygiene instructions. Medical care continued monthly transfusions; iron chelation remained on hold during pregnancy.\n\nOutcome: After about three months of coordinated care, symptoms and clinical findings improved satisfactorily.",
+    "summary": "A 27-year-old woman, suffering from beta thalassemia major who is undergoing therapy in the form of routine blood transfusions every month and taking anti-chelation drugs but is currently stopping this because she is pregnant, currently 16 weeks pregnant, complains complained of swollen gums, bleeding, and bad breath. Extraoral examination revealed dry, exfoliative lips. Intraoral examination revealed gingival hyperplasia with erythema, soft consistency, dark red rounded gingival margins, bleeding, true pockets and pain throughout the labial, buccal, palatal, and lingual. There was no history of systemic disease in this patient. Patient has never visited a dentist, either before or now, with complaints about her oral cavity. Hematological parameters showed abnormalities, and peripheral blood examination revealed an infection. The oral diagnoses included gingival enlargement and chronic periodontitis associated with pregnancy and β- thalassemia major.\n\nCase Management\nDental management consisted of spooling with 3% hydrogen peroxide (H2O2) spooling, chlorine dioxide spray mouthwash, antibiotics, calculus removal, and oral hygiene instructions. Blood transfusions were administered once a month, and anti-chelation therapy was stopped during pregnancy. After three months of multidisciplinary management, the results were satisfactory."
+  },
+  {
+    "doc_id": 20,
+    "label": "intermediate_health_literacy",
+    "fulltext": "Patient A.P., female, born in 1979, has been diagnosed with dilatation cardiomyopathy in 1996. Anamnestically, disease started with tonsillitis, possible myocarditis (which was never proven), with pronounced symptoms of heart failure and general symptoms. She was hospitalized and after one month, the left ventricular ejection fraction was 10% with the aforementioned signs of congestive heart failure. She was hospitalized for 10 months and 9 days, with standard therapy for vitally endangered patient, oxygen support, numerous adjuvant therapy, and intensive monitoring. Therapy was administered (ACE inhibitor - ramipril, cardiotonic - digoxin, beta-blockers - metoprolol and combination of diuretics - furosemide and spironolactone), with the indication of heart transplantation. Clinical improvement occured with an ejection fraction that was gradually increasing and at the age of 21 she entered in remission or stabilization phase, with the ejection fraction value of 48-57% (regular echocardiography was performed every three months). For the following four years therapy remained the same, but in Jun 2004 (after an episode of low immunity), ejection fraction fell to 25%, with a clinical deterioration of the disease. The patient was hospitalized for a period of two months, and the condition stabilized, and she was discharged with therapy that was the same but without cardiotonic. Ejection fraction was stabilized, and in year 2006 it was 50%. At the age of 27, the patient decided on the first pregnancy that was successful with beta blocker (metoprolol) in therapy. After the first pregnancy, the ejection fraction was 40% and she was treated with the same therapy with eplerenone (25 mg) instead of spironolactone. The ejection fraction was controlled and did not fall below 45%. At the end of 2015 the patient became pregnant for the second time, and the pregnancy went neatly until eighth month (35 weeks), when she was urgently admitted to hospital, due to sense of suffocation and inability to walk. Ejection fraction decreased to 18% (brain natriuretic peptide (BNP) was 2600 pg/ mL (reference values are 100-400 pg/ mL)). During pregnancy she received only metoprolol in therapy. Physicians decide to continue with her pregnancy, in the 39th week they performed c-section, and the condition stabilized again after twenty days. In October 2016 new mode of therapy was administered, ramipril (2.5 mg, in the morning), metoprolol (47.5 mg, in the morning), spironolactone (50 mg, once a day) and ivabradine (5 mg, twice a day) with torasemide (5 mg, once a day). LifeVest Defibrillator was carried from 06 December 2016 until 27 February 2017 when it was removed. When removed and after examination (ejection fraction was 44%) she continued with ramipril therapy (1.25 mg) metoprolol (23.75 mg), torasemide (5 mg), spironolactone (25 mg) and ivabradine (7.5 mg, twice a day) with potassium supplements, and compliance with non-pharmacological measures (fluid intake restricted to 1.5 L/ day). The echocardiographic finding in March 2017 showed left ventricular dilatation with moderately reduced left ventricular function and left ventricular wall hypokinesia with ejection fraction of 44% (insignificant pericardial effusion was present, inferior vena cava with physiological flow, preserved valves function - Dopler sonography showed slight insufficiency of mitral valve with dilatation of anulus). Evaluation of a patient with ejection fraction 44% showed no indication for an implantable cardioverter defibrillator (ICD), and conservative procedure and medication therapy were recommended. Regular check-ups and body mass reduction, regular control of renal function parameters and electrolytes were recommended. She is led under the diagnosis of dilated cardiomyopathy and heart failure NYHA stage II without any indication for the ICD prophylactic implantation.",
+    "diff_label_texts": "A.P. is a 38‑year‑old woman who developed dilated cardiomyopathy at age 17, likely on the background of infectious myocarditis after a throat infection. She was hospitalized for 10 months and 10 days with severe heart failure and a very low ejection fraction while being evaluated for heart transplantation. There was no clearly dangerous arrhythmia. Treatment focused on heart failure care and on preventing arrhythmias and blood clots.\nHer heart function recovered—a remission seen in about 16% of patients—and that improvement lasted 4 years. She then had a two‑year worsening, followed by several stable years and a normal first pregnancy. During her second pregnancy, she experienced a flare in the second trimester with postpartum dilated cardiomyopathy that lasted a couple of months, then improved.\nAs of May 2017, she was stable on guideline‑based therapy (an ACE inhibitor, a beta‑blocker, diuretics, and an If‑channel blocker), reported no limitation in physical activity, and was a mother of two and unemployed.",
+    "summary": "Patient A.P., female, 38 years old, had symptoms of dilated cardiomyopathy (with possible infectious myocarditis in the background) at age 17. After hospitalization for ten months and ten days, while waiting for heart transplantation (with threatening death outcome), without a clearly pronounced threatening arrhythmia, but with a low ejection fraction and a poor general condition, remission occurred. The therapy focused primarily on the treatment of heart failure, prevention of arrhythmia and thromboembolism. Normalization of the disease by improving the function of the left ventricle (expected in 16% of patients) occurred and lasted for 4 years, followed by an exacerbation of the disease that lasted for two years. In the next few years the patient was stable, had a first child with normal pregnancy. During the second trimester of the second pregnancy, there was an exacerbation (postpartum dilatation cardiomyopathy) lasting for couple of months. At the time of case report (May 2017), the patient is stable on therapy (ACE inhibitor, beta blocker, diuretics, If channel blocker), without limitation of physical capacity, mother of two children, unemployed."
+  },
+  {
+    "doc_id": 24,
+    "label": "intermediate_health_literacy",
+    "fulltext": "A 13-year-old male patient was admitted to the Children’s Hospital in Damascus after noticing a palpable enlarged mass in the left inguinal region. His medical history was unremarkable except for a surgical intervention on his spine 6 years ago due to an accident, which resulted in the loss of motor function and sensation in both of his lower extremities.\n\nDue to the long period he had spent in bed, the patient developed decubitus sores on his left foot. The only finding on clinical examination was a mass in the left inguinal area, which was movable on deep structures and so was the overlaying skin on it. The mass was not tender on palpation, and no signs of local inflammation were observed.\n\nLaboratory tests revealed an Elevated ESR (119 mm/h in the first hour). Other Basic Laboratory tests including (Complete Blood Count, Liver function tests, electrolytes, Urea, Creatinine and LDH) were ordered and were within normal ranges for age. Ordering these tests was essential to rule out systemic diseases. Given the absence of indicative physical findings for systemic disorders or immunodeficiencies, additional tests like those for HIV or Direct Antiglobulin were deemed unnecessary.\n\nA CT of the abdomen, chest, and pelvis showed enlarged lymph nodes inferior to the inguinal ligament, with the largest measuring approximately (3.5 × 2.4 cm). Other organs and nodes were within normal limits.\n\nAll of the above-mentioned investigations were essential to rule other high-risk diagnosis including lymphoma and leukemia. However, these were not sufficient to reach the definite diagnosis, so a decision of surgical resection of the nodes was taken.\n\nTo confirm the diagnoses and exclude other potential differentials presenting with enlarged lymph nodes, surgical removal of all of these enlarged nodes was performed under general anesthesia, and biopsies were sent for microscopic study.\n\nThe biopsy showed hyperplastic nodal architecture with proliferation of histiocytes and plasma cells with vascular proliferation, consistent with Plasma cell subtype of Castleman’s Disease.\n\nThe patient was discharged from the hospital after 14-day period after ensuring that there were no remaining enlarged lymph nodes. The only recommendation was oral prednisolone. The patient underwent follow-up using a whole-body CT scan every three months. During each hospital visit, a comprehensive clinical examination and laboratory tests (e.g. Complete Blood Test, ESR, C-reactive protein, liver function tests, renal function tests) were performed in addition to the CT scan. After a 12-month follow-up period, the patient reported no new symptoms or enlarged lymph nodes. Additionally, no abnormalities were observed during clinical examination or in laboratory tests.",
+    "diff_label_texts": "We report a unique case of a 13-year-old boy who presented with a palpable, painless mass in the left inguinal (groin) area and no other constitutional symptoms. His medical history included prior spinal surgery with resulting immobility and a pressure sore on the left foot, but otherwise he was well. Routine blood tests were normal except for a very high erythrocyte sedimentation rate (ESR 119 mm/h), and CT scans of the chest, abdomen and pelvis showed enlarged lymph nodes below the inguinal ligament, the largest about 3.5 × 2.4 cm. Because imaging and blood tests could not rule out malignancy (for example lymphoma or leukemia), the enlarged nodes were surgically removed for definitive diagnosis. Pathology showed features consistent with unicentric Castleman disease, plasma-cell type — one of the rarest forms in children and, to our knowledge, the first reported unicentric Castleman case in the inguinal area. The patient was discharged after 14 days with a course of oral prednisolone and was followed with clinical exams, laboratory tests and whole-body CT scans every three months. After 12 months of follow-up there were no new symptoms, no new enlarged lymph nodes on exam or imaging, and no abnormal laboratory findings.",
+    "summary": "We report a unique case of a 13-year-old boy who presented with a palpable enlarged mass in the left inguinal region without any constitutional symptoms. Surgical removal of this mass was essential to exclude worrying causes. Pathologic examination revealed proliferative changes consistent with Castleman's disease plasma cell type which is one of the rarest forms of the disease in children. To our knowledge, this case is the first reported case of Unicentric Castleman Disease (UCD) in the inguinal area. During a 12-month-period of follow-up, no additional lymph node enlargements or other symptoms were reported."
+  },
+  {
+    "doc_id": 27,
+    "label": "intermediate_health_literacy",
+    "fulltext": "28-year-old male patient with no significant history presented to the dermatology department with a 48-hour history of a skin condition characterized by two erythematous plaques with central vesicles and superficial ulceration located on the flexor surface of the right arm and forearm equidistant from the elbow crease, accompanied by a burning sensation and pruritus at the site of the lesions. He did not have systemic symptoms or self-medicate. As a background, he reported that he was on vacation in the coastal region of Ecuador at the time of the lesions. An incisional biopsy was performed that reported epidermis with acanthosis, parakeratosis and spongiosis, neutrophils in the stratum corneum and perivascular lymphocyte infiltration in the superficial, middle and deep dermis. Based on the clinical characteristics, the background of travel to a tropical region and the histological findings, a diagnosis of Paederus dermatitis was made. Treatment with antihistamines, topical steroids and cold compresses was indicated. After 8 days of treatment, the lesions resolved, leaving a post-inflammatory hyperpigmentation.\n",
+    "diff_label_texts": "A 28-year-old man presented to dermatology with a 48-hour history of two red patches with central blisters and shallow ulcers on the inner (flexor) side of his right arm and forearm. He described burning and itching at the sites, had no other systemic symptoms, and had not self‑medicated. He reported being on vacation in the coastal region of Ecuador when the lesions appeared. A skin biopsy showed changes consistent with an acute inflammatory reaction, and, together with the clinical picture and recent travel, the diagnosis of Paederus dermatitis (skin injury caused by contact with certain rove beetles) was made. He was treated with oral antihistamines, topical corticosteroids and cold compresses. After 8 days the lesions resolved, leaving post‑inflammatory hyperpigmentation.",
+    "summary": "The case of a 28-year-old male patient who presented to the dermatology department with a 48-hour history of two erythematous plaques with central vesicles and superficial ulceration located on the flexor surface of the right arm and forearm, accompanied by a burning sensation and pruritus at the site of the lesions, without accompanying symptoms, is reported. As a background, he stated that he was on vacation in the coastal region of Ecuador at the time of the lesions. An incisional biopsy was performed and, due to the clinical characteristics and the background of travel to a tropical region, the diagnosis was made as dermatitis by Paederus and treatment with antihistamines, topical steroids and cold compresses was indicated. After 8 days of treatment, the lesions subsided, leaving a post-inflammatory hyperpigmentation.\n"
+  },
+  {
+    "doc_id": 29,
+    "label": "intermediate_health_literacy",
+    "fulltext": "A 77-year-old woman with haematemesis presented to the emergency room. Her medical history included only hypertension and dyslipidaemia. When she presented to the emergency room, her vital signs indicated shock (heart rate: 100 beats/min, blood pressure: 79/56 mmHg), and blood tests revealed anaemia (haemoglobin: 9.6 g/dL), which suggested upper gastrointestinal bleeding.\n\nNon-contrast-enhanced CT was performed immediately because of renal dysfunction. CT revealed that the third part of the duodenum flexed steeply on the right side of the aorta and ran caudally, without crossing anterior to the aorta. The jejunum was located on the patient’s right side. The second part of the duodenum and the stomach were dilated, and there were high-density gastric contents that were considered to indicate a haematoma.\n\nUpper gastrointestinal endoscopy was performed following the CT examination, which revealed a mucosal laceration at the gastric cardia. Bleeding from lacerations of the cardia of the stomach as a result of forceful vomiting was first reported by Mallory and Weiss in 1929.1 In our case, the third part of the duodenum flexed steeply, and the lumen was narrowed, which caused an obstruction. As a result, repeat vomiting was considered to have caused Mallory–Weiss syndrome.\n\nOn the basis of the CT findings showing that the duodenal-jejunal junction was located in the right hemi-abdomen, intestinal malrotation was suspected.2 However, 7 days later, when CT was repeated, spontaneous resolution of the malpositioned jejunum was seen. The patient was then discharged from the hospital. However, months later, she was rushed to the emergency room for repeat haematemesis. Dynamic CT was performed before upper gastrointestinal endoscopy, on admission, and revealed contrast extravasation in the dilated stomach. Additionally, the third part of the duodenum was flexed on the right side of the aorta, and the duodenal-jejunal junction and jejunum were again located in the right hemi-abdomen. Upper gastrointestinal endoscopy revealed a laceration at the gastric cardia, as in the previous endoscopy, which was considered Mallory–Weiss syndrome.\n\nTwo months after the second episode of haematemesis, the patient presented to the emergency room with nausea. Non-contrast-enhanced CT revealed no abnormalities in the duodenal positioning, but there was oedematous wall thickening in the second part of the duodenum. If we had not had previous CT images, we would have suspected duodenitis, but on the basis of all of the CT findings, we suspected the possibility of an underlying condition after the right-sided deviation of the small intestine had resolved spontaneously.\n\nIn summary, CT was performed 4 times over 5 months. The third and fourth parts of the duodenum and the jejunum deviated repeatedly, but this resolved spontaneously, which is not indicative of intestinal malrotation. Therefore, we diagnosed dysplasia of the ligament of Treitz.\n\nClinical outcomes\nThe patient underwent laparotomy, which revealed no abnormalities in the relative position of the duodenum to the jejunum. Additionally, the jejunum was located on the patient’s left side, and there was no intestinal malrotation. The ligament of Treitz was formed; however, its fixation in the upper jejunum was incomplete as it was attached only to the duodenum. The duodenal-jejunal junction was not fixed to the retroperitoneum, and the jejunum folded easily with the ligament of Treitz as a fulcrum. Surgically, the upper jejunum was fixed with 4 sutures to the retroperitoneum on the patient’s left side. The postoperative course was good, and the patient has remained symptom-free.",
+    "diff_label_texts": "A 77-year-old woman was admitted with haematemesis. CT scans showed that the third part of her duodenum bent sharply on the right side of the aorta and ran downward without crossing in front of it; the duodenojejunal junction and much of the jejunum were located on the right side of the abdomen. Upper GI endoscopy found a mucosal tear at the gastric cardia consistent with Mallory–Weiss syndrome. Seven days after the first scan the abnormal right-sided position resolved on CT, but two months later the patient had another episode of haematemesis and the duodenojejunal junction and jejunum had again shifted to the right. Because the small bowel moved back and forth rather than staying in the wrong position, true intestinal malrotation was considered unlikely. The working diagnosis was dysplasia (abnormal development) of the ligament of Treitz, meaning the ligament that normally helps fix the upper small intestine was not holding the jejunum securely. At laparotomy the ligament of Treitz was present but did not fully fix the upper jejunum to the back wall of the abdomen (retroperitoneum); the pararenal area also appeared loosely fixed and mobile on CT. These factors probably allowed the jejunum to fold and deviate to the right. Surgically the upper jejunum was tacked to the left retroperitoneum with sutures, the postoperative course was good, and the patient has remained symptom-free.",
+    "summary": "A 77-year-old woman underwent CT to evaluate haematemesis. The images showed that the third part of the duodenum flexed steeply on the right side of the aorta and ran caudally, without crossing anterior to the aorta. The duodenal-jejunal junction and jejunum were located on the patient's right side. Upper gastrointestinal endoscopy revealed a laceration at the gastric cardia, and a diagnosis of Mallory-Weiss syndrome was made. Repeat CT 7 days later revealed that the abnormal positioning of the intestinal tract had resolved spontaneously. Two months later, the patient experienced another episode of haematemesis, and CT revealed repeat deviation of the duodenal-jejunal junction and jejunum to her right side. Upper gastrointestinal endoscopy revealed another laceration at the gastric cardia, as in the previous study. On the basis of the initial CT findings showing the duodenal-jejunal junction in the right hemi-abdomen, intestinal malrotation was suspected. However, because the jejunum deviated repeatedly to the right side but resolved spontaneously, we diagnosed dysplasia of the ligament of Treitz. Laparotomy revealed a formed ligament of Treitz; however, fixation in the upper jejunum was incomplete. Additionally, CT revealed that the anterior pararenal space was loosely fixed and mobile. These factors may have caused the right-sided deviation of the small intestine."
+  },
+  {
+    "doc_id": 31,
+    "label": "intermediate_health_literacy",
+    "fulltext": "A 12-year-old boy with Down Syndrome and motoric disorders was referred from the Pediatric Department to the Oral Medicine Department of RS Hasan Sadikin Bandung. The patient was diagnosed with Down Syndrome and myeloradiculopathy. The patient’s mother said that the patient was admitted to the hospital because of weakness in both patient’s hands and feet. The patient had a history of falling down about one year ago. The patient’s mother also had a difficulty in cleaning the patient’s oral cavity regularly.\n\nIn the extraoral examination, the patient had a dysmorphic face. The patient also had a cracking and desquamative condition of the vermillion border of the lips. Lymph node examination could not be assessed because the patient wore a cervical collar. The intraoral examination showed an irregular ulcer with 1×0.7 cm in diameter, indurated margin, and white-yellowish base at the right lateral border of the tongue. There was dentinal caries on 63 tooth and also the tooth remnants on 55, 62, 74, and 85 teeth. The upper and lower tooth remnants were suggested to be extracted by pediatric dentist. The space of the extracted teeth will be maintained using a space maintainer. The 55 tooth was sharp and caused an occlusion trauma to the right lateral border of the tongue.\n\nLaboratory examination showed a decrease in sodium value (130 mEq/L) and an increase in lymphocyte value (46%). The MRI examination was performed in the Radiology Department to determine the presence of abnormalities in the cervical spine. The results of the MRI examination showed a dislocation of the patient’s cervical spine. The patient’s mother provided informed consent to publish the patient’s case details and any accompanying images.\n\nBased on the history review, the clinical examination, and appropriate investigation, the patient was diagnosed with a chronic traumatic ulcer mimicking OSCC, exfoliative cheilitis, reversible pulpitis of 63 teeth, and radix gangrene on 55, 62, 74, and 85 teeth. The diagnosis of the chronic ulcer was based on clinical examination. There was an indurated margin in the traumatic lesion, which mimicked Oral Squamous Cell Carcinoma clinically. The patient has been hospitalized for 4 days and was given paracetamol 120 mg/5 mL oral suspension and amoxicillin 125 mg/5 mL oral suspension from the Pediatric Department. The patient also was given sodium chloride 0.9% solution, povidone-iodine mouthwash 1%, and petroleum jelly from the Oral Medicine Department. The patient’s mother was instructed to clean the patient’s oral cavity using gauze soaked in sodium chloride 0.9% solution, compress the ulcer using povidone-iodine mouthwashes 1% three times a day as an antiseptic and anti-inflammatory agent to the oral ulcer, and apply petroleum jelly to moisturize the patient’s lips. The patient was also suggested to extract the 55, 62, 74, and 85 teeth.\n\nIn the second visit (3 days follow-up), oral lesions already showed improvement. In the third visit (1-week follow-up), the size of the oral ulcer at the lateral border of the tongue was getting smaller and the lesion of the lips had some improvement.\n\nIn the fourth visit (10 days follow-up), the size of the oral ulcer at the lateral border of the tongue already had significant improvement. Two days after the fourth visit, the patient underwent neurosurgery. The patient was observed in the Pediatric Intensive Care Unit postoperatively. After two weeks of observation in the Pediatric Intensive Care Unit, the experienced respiratory failure and was declared dead.",
+    "diff_label_texts": "A 12-year-old boy with Down syndrome and motor disorders was referred to the Oral Medicine clinic. On exam he had a dysmorphic face and dry, cracked lips; a cervical collar prevented assessment of his neck lymph nodes. Inside the mouth there was an irregular ulcer on the right lateral border of the tongue measuring about 1 × 0.7 cm, with a firm (indurated) edge and a white-yellow base. A sharp remnant of tooth 55 was causing repeated trauma to that part of the tongue. Based on the history and exam, the team diagnosed a chronic traumatic ulcer that clinically looked like oral squamous cell carcinoma (OSCC). Other dental problems included caries and several tooth remnants (63, 55, 62, 74, 85) that were recommended for extraction and later space maintenance. Blood tests showed low sodium and a mildly raised lymphocyte percentage, and MRI revealed a cervical spine dislocation; the patient later had neurosurgery. Treatment in hospital included paracetamol and amoxicillin, and local oral care from the Oral Medicine team: saline rinses (0.9% sodium chloride), 1% povidone-iodine mouthwash as an antiseptic, and petroleum jelly for the lips. The mother was instructed to clean the mouth with gauze soaked in saline, apply the povidone-iodine compress to the ulcer three times daily, and use petroleum jelly to moisturize the lips. The oral lesions improved over follow-up visits at 3 days, 1 week, and 10 days. After neurosurgery the patient was observed in the pediatric intensive care unit but developed respiratory failure and died.",
+    "summary": "A 12-year-old boy with Down Syndrome and motoric disorders was referred to Oral Medicine Department. In the extraoral examination, the patient had a dysmorphic face and dry lips. Lymph node examination could not be assessed because the patient wore a cervical collar. The intraoral examination showed an irregular ulcer with 1×0.7 cm in diameter, indurated margin, and white-yellowish base at the right lateral border of the tongue. The 55 teeth were sharp and caused an occlusion trauma to the right lateral border of the tongue. The patient was diagnosed with a chronic traumatic ulcer mimicking OSCC based on clinical examination. The medication given to the patient were sodium chloride 0.9%, povidone-iodine mouthwash 1%, and petroleum jelly."
+  },
+  {
+    "doc_id": 34,
+    "label": "intermediate_health_literacy",
+    "fulltext": "A 19-month-old boy was admitted to the Emergency Department because he fell from his baby feeding highchair. This fall occurred in apparent well-being, without the presence of anticipatory signs or symptoms. First, he fell on his gluteus and then he banged his head (occiput) on the ground. He presented with vomiting (three episodes) and he was very irritable. His respiratory rate and heart rate were >60 breaths and >150 beats per minute, while oxygen saturation was <80%. Upon physical examination, the child was hydrated and conscious, but irritable. More importantly, we noted subcostal retractions, and, at the auscultation, decreased breath sounds in the left basal part of chest. The patient was ventilated with an AMBU balloon connected to an oxygen source and monitored with a pulse oximeter. Despite our intervention, oxygen saturation fell below 70% and the more we ventilated, the more the saturation dropped down. The lung ultrasound showed the absence of the typical A lines and the consolidation of the lung, which was directly visualized as a solid parenchyma. On the basis of the poor clinical condition, the patient underwent orotracheal intubation with a cuffed endotracheal tube. After the baby was stabilized, he underwent a chest computed tomography (CT) showing complete atelectasis of the left lung with an interruption of the main left bronchus at 12 cm from bronchial bifurcation. An FBA was suspected as the mother also stated that the baby in the previous days had an intensive cough attack and disappeared within 24 h without any treatment. Therefore, a rigid bronchoscopy was performed and an almond of 2 cm in diameter in the main left bronchus was found and promptly removed.\n\nThe patient had never consumed almonds or other nuts before and in this circumstance ingested the almond by chance.\n\nThe baby had a progressive clinical improvement, and after 24 h, he was extubated and discharged from intensive care to be admitted to the general pediatrics ward for a few days with gradual and a total respiratory function recovery.",
+    "diff_label_texts": "A 19-month-old boy came to the emergency department after falling from a highchair and hitting his head. On exam he had severe, unexplained breathing trouble that required tracheal intubation (a tube placed into the windpipe to help him breathe). The team suspected that the breathing problem had caused an altered state of consciousness and led to the fall and head injury. Imaging of the chest showed complete collapse (atelectasis) of the entire left lung and an abrupt cutoff of the left main bronchus about 12 mm from the lung hilum (the area where the bronchus enters the lung). Rigid bronchoscopy found and removed a 2 cm almond that was stuck in the left main bronchus. Earlier signs included very fast breathing and heart rate, low oxygen levels despite bag-mask ventilation, visible chest retractions, and decreased breath sounds on the left. The mother reported the child had an intense coughing episode a few days earlier that resolved without treatment; the child had never eaten almonds before and likely swallowed this one by accident. After the almond was removed the child improved steadily, was extubated 24 hours later, moved from intensive care to the pediatric ward, and made a full recovery of respiratory function.",
+    "summary": "We describe the case of a 19-month-old boy who accessed the emergency room initially for a head trauma. The clinical evaluation, however, revealed an unexplained serious respiratory distress needing tracheal intubation. After our evaluation, we hypothesized that the severe respiratory distress determined an altered state of consciousness with following head trauma. The radiological findings raised the suspicion of foreign body aspiration for the presence of an atelectasis of the entire left lung. The computed tomography showed an abrupt interruption of the main bronchus at 12 mm from the hull. The following bronchoscopy identified an almond of 2 cm."
+  },
+  {
+    "doc_id": 35,
+    "label": "low_health_literacy",
+    "fulltext": "The patient was a 4-month-old male from central Mexico with two healthy male siblings. His mother was hypothyroid during the first trimester of pregnancy and took drugs. The infant was born with normal weight and size, was breast-fed, and received the BCG vaccine with no scarring. The mother of the patient was a prisoner in a jail cell with the infant in a crowded cell with two others.At 4 months, the patient was medically evaluated for a painful tumor in the left axilla. A chest X-ray showed suggestive images of rib fractures; the mother was suspected of child abuse, and the infant was admitted to a pediatric hospital. The infant was weighed (4,190 g) and measured (58 cm) below the third percentile, oxygen saturation of 70%, fever, cough, increased volume in the left axilla, and pain, redness, and warmth. The blood count showed: hemoglobin of 8.8 g/dL (11.0-12.6), 29.3 × 109 leukocytes/L (6.0-17.5), 18.4 × 109 neutrophils/L (1.0-8.5), 7.0 × 109 lymphocytes/L (4.0-13.5), 3.5 × 109 monocytes/L, 459 × 109 platelets/L (150-350), and C-reactive protein of 16 mg/L (< 3.0). The first thoracoabdominal tomography showed an abscess in the left axilla, lytic lesions in ribs 3-6, left apical pneumonia, pulmonary nodules in both lungs, and enlarged cervical and mediastinal lymph nodes. The biopsy of the left axilla abscess reported myositis and suppurative panniculitis. Only the culture for bacteria from the bronchoalveolar liquid was negative, and the PCR for the Mycobacterium tuberculosis complex was negative. After 41 days of hospitalization and receiving two antimicrobial regimens of ceftriaxone-clindamycin and cefepime-vancomycin, the patient was discharged.\n\nTwo months later, at eight months of age, he was readmitted to hospital with a fever, irritability and a suppurating abscess in the left scapula. The blood count showed haemoglobin of 10.8 g/dl (10.5-12), 21.2 × 109 leukocytes/L (6-17), 12.2 × 109 neutrophils/L (1.5-8.5), 7.5 × 109 lymphocytes/L (4-10.5), 1.2 × 109 monocytes/L (600), and 583 × 109 platelets/L (150-350); the serum test for HIV was negative. A left apical consolidation, bronchiectasis, lytic lesions in ribs 2-7 and dorsal vertebrae 2-7, and a multilocular fluid collection were observed on a chest scan; ultrasound showed a fistula associated with the scapular abscess. The patient received piperacillin-tazobactam, which was later replaced with voriconazole after Aspergillus fumigatus was detected in the secretion sample culture. Given the recurrence and severity of the infection, an innate immunity defect was suspected. The dihydrorhodamine test showed no production of reactive oxygen species and the gp91phox expression in neutrophils was absent, establishing a diagnosis of X-linked chronic granulomatous disease. The pathogenic variant detected by next-generation sequencing was c.80_83del/Y (p.Val27Glyfs*33) in CYBB. The mother was a carrier of the variant (c.80_83del/WT). The two older male siblings, who were apparently healthy, could not be genetically tested. The patient was discharged after 65 days of hospitalisation and 28 days of voriconazole treatment. Daily antibiotic prophylaxis with trimethoprim-sulfamethoxazole and antifungal prophylaxis with fluconazole twice a week were initiated. Two months later, at one year of age, the infant was readmitted due to multifocal pneumonia, for which mechanical respiratory assistance was required. The galactomannan antigen was detected in the serum and A. fumigatus was detected in the culture of the lavage fluid, so treatment with voriconazole was initiated again. The patient suffered a multiple organ failure and died one month after admission.\n",
+    "diff_label_texts": "A baby boy was 4 months old. He lived with his mother in a prison cell. A painful lump grew in his left armpit. A chest X-ray looked like some ribs were broken. Doctors worried he might have been hurt. The pictures also showed a pocket of pus in his armpit, damage to his ribs, a lung infection, and small spots in his lungs. He got strong antibiotics. He went home. When he was 8 months old, he got a fever. The pus spread toward his left shoulder. New chest pictures looked worse. Tests found a mold called Aspergillus fumigatus in the pus. The doctors said he had a serious mold infection. He took a strong antifungal medicine called voriconazole for 28 days. A special blood test showed his germ-fighting cells did not work well. He had a rare immune problem called chronic granulomatous disease. It was caused by a change in a gene called CYBB. His mother carried this gene change. When he was 12 months old, the mold infection came back. The treatments did not work. He died.",
+    "summary": "A case of infant with chronic granulomatous disease and invasive aspergillosis is reported. The infant was a 4-month-old male infant living with his mother in a prison cell. The infant had tumors in the left axillary region and a chest X-ray suggested rib fractures; he was hospitalized on suspicion of child abuse. A chest X-ray showed an axillary abscess, osteolysis of ribs, pneumonia and pulmonary nodules; the patient received broad spectrum antibiotics and was discharged. At 8 months, he was readmitted with fever and extension of the purulent abscess to the left shoulder region; a chest X-ray showed worsening of the condition. Aspergillus fumigatus was isolated from the secretion of the abscess and invasive aspergillosis was diagnosed; voriconazole was initiated for 28 days. A dihydro rhodamine test was performed and a diagnosis of chronic granulomatous disease caused by the pathogenic variant c.80_83del/Y of the CYBB gene, carried by the mother (c.80_83del/WT), was made. At 12 months, the patient was readmitted with invasive aspergillosis, resistant to treatment, with fatal outcome.\n"
+  },
+  {
+    "doc_id": 36,
+    "label": "low_health_literacy",
+    "fulltext": "Male patient, 25 years old, Sundanese, presented at the Dental Hospital of the Faculty of Dentistry Universitas Padjadjaran with the chief complaint of mouth sores, which are painful on the upper and lower lips and exacerbated when eating and talking. Initially, four days ago, canker sores started in the oral cavity, then appeared on the lips two days later. The patient tried to self-medicate by applying petroleum jelly which he used to relieve his symptoms, but it did not improve. The patient replaced the drug with triamcinolone acetonide 0.1% in orabase ointment purchased at the pharmacy and applied it once a day. Canker sores were getting better but did not cure.\n\nThe patient had history a of fever for about a week before the canker sores appeared and there were no lesions on other parts of the body. He stated that the workload was quite heavy and he had not consumed a balanced nutritional diet for about one and a half months. He had no medical history, history of food allergies, or history of taking medication. He had no history of alcohol consumption or smoking, but he had a frequent habit of licking his lips. He also had a history of chickenpox when he was a child.\n\nThe patient had no fever with all vital signs within normal limits on general examination. Extra-oral examination showed no abnormalities in the lymph nodes. There were serosanguineous crusts that felt painful and bleed easily on the lips. Intra-oral examination revealed erythematous lesions, irregular in shape, and had diffuse borders, accompanied by pain in the upper and lower labial mucosa. Hyperkeratotic white plaque that could not be scraped off, irregular in shape, has diffuse borders, without pain in the region of tooth 38 left buccal mucosa. Yellowish-white plaques were seen on 1/3 of the posterior surface of the dorsal tongue, which could be scraped off without leaving an erythematous area, and there were indentations in the form of dental impressions without pain on the lateral right and left sides of the tongue. A painless hard nodule about 2×1 x 0.5 cm in size was seen in the midline of the hard palate. Several teeth were found in caries, radix, and edentulous conditions in all regions. The oral hygiene was poor.\n\nExamination of psychological conditions was evaluated using the DASS-21 questionnaire and showed normal depression level (score 0), normal anxiety level (score 6), and normal stress level (score 6). Based on history and clinical examination, the working diagnosis was suspected HAEM, accompanied by the coated tongue, frictional keratosis, crenated tongue, torus palatinus, reversible pulpitis of tooth 18, irreversible pulpitis of tooth 47, chronic apical periodontitis et causa radix of tooth 15, and edentulous teeth 28, 37, 36, and 46. The differential diagnosis of suspected HAEM lesions on the lips was exfoliative cheilitis. However, exfoliative cheilitis did not have herpes virus involvement. The patient was indicated for serological testing (IgG anti-HSV-1) to confirm the diagnosis. Oral health-related quality of life was measured, and the results of the OHIP-14 examination at the first visit were 35 (moderate OHRQol).\n\nThe non-pharmacological therapy included instruction to maintain oral hygiene by brushing the teeth and tongue using a soft-bristled toothbrush two times a day and using non-detergent toothpaste. Education was given such as increasing the intake of water by at least two liters per day, consuming a balanced nutritional diet, avoiding acidic, spicy, hard, and monosodium glutamate-containing foods, and stopping the bad habit of licking and peeling the skin of the lips. The pharmacological therapy included topical and systemic medications. The topical medications included instructions to compress the lips with gauze moistened with 0.9% NaCl solution at least three times a day and to apply a thin layer of triamcinolone acetonide 0.1% in orabase to the lips three times a day. The systemic medications included instruction to take a multivitamin once a day.\n\nThe progress of improvement was visible in the first follow-up, two days after the initial visit. The pain in the lips was reduced, but the canker sores have not healed. Extra-oral examination revealed serosanguinous crusts on the lips which were still painful and bled easily. The serological test result (IgG anti-HSV-1) was positive with a ratio of: 6.32 (positive: ratio > 1.1). The definitive diagnosis was established based on the history, clinical examination, and serological tests as HAEM. The non-pharmacological and pharmacological therapy was continued, and systemic medication was added in the form of instructions to consume acyclovir 200 mg tablets five times a day for one week.\n\nSignificant improvement was visible in the second follow-up, five days after the previous visit, showing excellent healing in all of the patient’s oral lesions. The OHIP-14 result at the last visit was 4 (good OHRQoL). The patient’s physical, psychological, and social conditions showed improvement and returned to normal after 7 days of treatment. Patient was referred to continue dental and oral care in the periodontics, dental conservation, oral surgery, and prosthodontics departments. The patient has approved and written informed consent for the case details to be published included publication of the images, and the institution has also approved for publication. This case had complied with the Declaration of Helsinki.",
+    "diff_label_texts": "A 25-year-old man went to the mouth clinic because he had painful canker sores on his lips. The outside of his lips had crusty scabs that hurt and bled easily. Inside his mouth, the inner parts of his upper and lower lips had red, sore, uneven patches. A blood test for the cold sore virus (HSV-1) was positive. The doctor said he had a condition called HAEM. His treatment included a steroid mouth paste (triamcinolone acetonide 0.1% in orabase), acyclovir pills, multivitamins, and salt-water (0.9% NaCl). He was also told to keep his mouth clean, avoid spicy and sour foods, and stop licking his lips.",
+    "summary": "A 25-year-old male patient came to the Department of Oral Medicine with the chief complaint of painful canker sores on the lips. Extra-oral examination revealed serosanguineous crusts on the lips that were painful and easily bleed. Intra-oral examination showed diffused and painful irregular erythematous lesions on the upper and lower labial mucosa. The anti-HSV1 IgG test was positive. The patient was diagnosed with HAEM.\n\nCase management: Pharmacological therapy included triamcinolone acetonide 0.1% in orabase, acyclovir tablets, multivitamins, and 0.9% NaCl. Non-pharmacological therapy included advice on maintaining good oral hygiene, avoiding spicy and sour foods, and breaking the bad habit of licking the lips."
+  },
+  {
+    "doc_id": 36,
+    "label": "intermediate_health_literacy",
+    "fulltext": "Male patient, 25 years old, Sundanese, presented at the Dental Hospital of the Faculty of Dentistry Universitas Padjadjaran with the chief complaint of mouth sores, which are painful on the upper and lower lips and exacerbated when eating and talking. Initially, four days ago, canker sores started in the oral cavity, then appeared on the lips two days later. The patient tried to self-medicate by applying petroleum jelly which he used to relieve his symptoms, but it did not improve. The patient replaced the drug with triamcinolone acetonide 0.1% in orabase ointment purchased at the pharmacy and applied it once a day. Canker sores were getting better but did not cure.\n\nThe patient had history a of fever for about a week before the canker sores appeared and there were no lesions on other parts of the body. He stated that the workload was quite heavy and he had not consumed a balanced nutritional diet for about one and a half months. He had no medical history, history of food allergies, or history of taking medication. He had no history of alcohol consumption or smoking, but he had a frequent habit of licking his lips. He also had a history of chickenpox when he was a child.\n\nThe patient had no fever with all vital signs within normal limits on general examination. Extra-oral examination showed no abnormalities in the lymph nodes. There were serosanguineous crusts that felt painful and bleed easily on the lips. Intra-oral examination revealed erythematous lesions, irregular in shape, and had diffuse borders, accompanied by pain in the upper and lower labial mucosa. Hyperkeratotic white plaque that could not be scraped off, irregular in shape, has diffuse borders, without pain in the region of tooth 38 left buccal mucosa. Yellowish-white plaques were seen on 1/3 of the posterior surface of the dorsal tongue, which could be scraped off without leaving an erythematous area, and there were indentations in the form of dental impressions without pain on the lateral right and left sides of the tongue. A painless hard nodule about 2×1 x 0.5 cm in size was seen in the midline of the hard palate. Several teeth were found in caries, radix, and edentulous conditions in all regions. The oral hygiene was poor.\n\nExamination of psychological conditions was evaluated using the DASS-21 questionnaire and showed normal depression level (score 0), normal anxiety level (score 6), and normal stress level (score 6). Based on history and clinical examination, the working diagnosis was suspected HAEM, accompanied by the coated tongue, frictional keratosis, crenated tongue, torus palatinus, reversible pulpitis of tooth 18, irreversible pulpitis of tooth 47, chronic apical periodontitis et causa radix of tooth 15, and edentulous teeth 28, 37, 36, and 46. The differential diagnosis of suspected HAEM lesions on the lips was exfoliative cheilitis. However, exfoliative cheilitis did not have herpes virus involvement. The patient was indicated for serological testing (IgG anti-HSV-1) to confirm the diagnosis. Oral health-related quality of life was measured, and the results of the OHIP-14 examination at the first visit were 35 (moderate OHRQol).\n\nThe non-pharmacological therapy included instruction to maintain oral hygiene by brushing the teeth and tongue using a soft-bristled toothbrush two times a day and using non-detergent toothpaste. Education was given such as increasing the intake of water by at least two liters per day, consuming a balanced nutritional diet, avoiding acidic, spicy, hard, and monosodium glutamate-containing foods, and stopping the bad habit of licking and peeling the skin of the lips. The pharmacological therapy included topical and systemic medications. The topical medications included instructions to compress the lips with gauze moistened with 0.9% NaCl solution at least three times a day and to apply a thin layer of triamcinolone acetonide 0.1% in orabase to the lips three times a day. The systemic medications included instruction to take a multivitamin once a day.\n\nThe progress of improvement was visible in the first follow-up, two days after the initial visit. The pain in the lips was reduced, but the canker sores have not healed. Extra-oral examination revealed serosanguinous crusts on the lips which were still painful and bled easily. The serological test result (IgG anti-HSV-1) was positive with a ratio of: 6.32 (positive: ratio > 1.1). The definitive diagnosis was established based on the history, clinical examination, and serological tests as HAEM. The non-pharmacological and pharmacological therapy was continued, and systemic medication was added in the form of instructions to consume acyclovir 200 mg tablets five times a day for one week.\n\nSignificant improvement was visible in the second follow-up, five days after the previous visit, showing excellent healing in all of the patient’s oral lesions. The OHIP-14 result at the last visit was 4 (good OHRQoL). The patient’s physical, psychological, and social conditions showed improvement and returned to normal after 7 days of treatment. Patient was referred to continue dental and oral care in the periodontics, dental conservation, oral surgery, and prosthodontics departments. The patient has approved and written informed consent for the case details to be published included publication of the images, and the institution has also approved for publication. This case had complied with the Declaration of Helsinki.",
+    "diff_label_texts": "A 25-year-old man came to the oral medicine clinic with painful canker sores on his lips that started in the mouth four days earlier and involved the lips two days later. On exam there were blood-tinged crusts on the lips that bled easily, and diffuse, painful red lesions on the inside of the upper and lower lips. He had reported a fever about a week before the sores appeared, a period of heavy workload and poor diet, and a habit of frequently licking his lips. Initial tests showed a positive anti-HSV-1 IgG (ratio 6.32), supporting herpes virus involvement, and the working diagnosis was HAEM. Exfoliative cheilitis was considered but less likely because it does not involve the herpes virus. Other findings included poor oral hygiene and several unrelated dental problems. Treatment combined topical and systemic care: topical steroid ointment (triamcinolone acetonide 0.1% in orabase), warm compresses with 0.9% saline, oral acyclovir tablets (200 mg, five times daily for one week), and a daily multivitamin. Patients were also advised on non-drug measures: brush teeth and tongue twice daily with a soft brush and non‑detergent toothpaste, drink more water, eat a balanced diet, avoid acidic, spicy or hard foods (and foods with MSG), and stop licking or peeling the lips. Two days after the first visit pain was reduced but lesions remained; after starting acyclovir there was marked healing by the next follow-up and complete clinical recovery after 7 days. Oral-health–related quality of life improved (OHIP-14 score from 35 to 4). The patient was referred for further dental care (periodontics, restorative, oral surgery, and prosthodontics) and gave consent for publication.",
+    "summary": "A 25-year-old male patient came to the Department of Oral Medicine with the chief complaint of painful canker sores on the lips. Extra-oral examination revealed serosanguineous crusts on the lips that were painful and easily bleed. Intra-oral examination showed diffused and painful irregular erythematous lesions on the upper and lower labial mucosa. The anti-HSV1 IgG test was positive. The patient was diagnosed with HAEM.\n\nCase management: Pharmacological therapy included triamcinolone acetonide 0.1% in orabase, acyclovir tablets, multivitamins, and 0.9% NaCl. Non-pharmacological therapy included advice on maintaining good oral hygiene, avoiding spicy and sour foods, and breaking the bad habit of licking the lips."
+  },
+  {
+    "doc_id": 37,
+    "label": "low_health_literacy",
+    "fulltext": "A 29-year-old woman, Para 1, with abnormal vaginal bleeding of one-month duration presented to the gynecology outpatient department of a level 2 hospital. She was HIV positive, commenced on antiretroviral treatment following diagnosis, but had defaulted the antiretroviral treatment for one month when she became ill with vaginal bleeding, resulting in virological and immunological failures (viral load 37400 copies/mL and CD4 count 26 cells/μL). Of note, it was unclear when the patient first started showing HIV symptoms. However, she was diagnosed with HIV about a year prior to presentation. Physical examination revealed a large mass on the cervix measuring 8 × 8 cm extending to the parametrium and to the pelvic side walls bilaterally. There was bleeding on contact and foul-smelling vaginal discharge. Ultrasonography detected a bulky cervix and bilateral hydronephrosis. The patient was clinically diagnosed with cervical malignancy stage 3B. She was recommenced on antiretroviral therapy with a treatment change from TLD (Tenofovir-Lamivudine-Dolutegravir combination) to a preferable renal friendly regimen (Lamivudine-Abacavir-Dolutegravir combination). A punch biopsy of the cervix was performed, and the histopathological report revealed the diagnosis of an extra-nodal BL. The immunohistochemical and in situ hybridization confirmed the diagnosis, with CD20, CD75a, CD10, PAX5 and Bcl-6 positive. In addition, the CD44 and c-Myc were positive, with the EBER-ISH demonstrating focal positivity. The Ki67 demonstrated a proliferation index of almost 100% and PAX5 moderately positive BCL6. She had white cell count of 2.67 x109/L, haemoglobin of 5.7g/dl and platelet count of 71 × 109/L. Results of other investigations were serum creatinine 187 mmol/L, urea 11.1 mmol/l, albumin 21 g/l, aspartate transaminase 41 U/l and alkaline phosphatase 100 U/l.\n\nFollowing histological confirmation of the diagnosis and review at an oncology multidisciplinary meeting, she spent 43 days waiting to start treatment at oncology unit. The delay was due to long waiting list. This delay exceeded the 48 hours waiting period during which oncological treatment for BL should commence following diagnosis. The treatment plan was chemo-radiation therapy, and the patient gave written informed consent for the case to be published. However, she demised in the gynaecological ward on the 43rd day while waiting to start the treatment. During the 43 days, further imaging could not be performed due to poor functionality of the available CT and MRI machines. In addition to antiretroviral therapy, the patient received other supportive care such as blood transfusion and analgesia. Again, the number of days between the diagnosis of the BL and her death was 43 days. Histopathological postmortem was not performed as the diagnoses (BL and retroviral disease) were known. We reckon that the main primary cause of death is challenging to assign because of the multiple principal diagnoses. Because BL has rapid progression and high mortality rate in persons living with HIV particularly with high viral load, the attending physician certifying the death assigned BL as the most likely cause of death. However, the secondary cause of death was multiple organ failure (renal and haematological inclusive).",
+    "diff_label_texts": "She was 29 years old and had one child. She had HIV and a very weak immune system (CD4 count of 26). She had abnormal vaginal bleeding for one month. A tissue test from her cervix showed a blood cancer called Burkitt lymphoma in the cervix, outside the lymph nodes. Doctors also said the cervical cancer was stage 3B because it reached the pelvic wall and caused the kidneys to swell from blocked urine. A team of cancer doctors said she needed chemotherapy and radiation together. There was a long waiting list for this treatment. The start of care was delayed. She died 43 days after the diagnosis. She did not get the planned treatment.",
+    "summary": "The patient was a 29-year-old woman, Para 1, with abnormal vaginal bleeding for a month and living with HIV and had a CD4 of 26 cells/μL. The histological examination of the cervical biopsy confirmed an extra-nodal BL. She had International Federation of Gynecology and Obstetrics (FIGO) stage 3B cervical cancer based on presence of hydronephrosis and pelvic wall involvement. The patient was reviewed at the oncology multidisciplinary meeting and required chemoradiation. There was delay in her management due to a long waiting list for chemoradiation at oncology unit in the referral center and the patient demised 43 days after diagnosis and did not receive the treatment."
+  },
+  {
+    "doc_id": 38,
+    "label": "intermediate_health_literacy",
+    "fulltext": "A 56-year-old female patient presented with complaints of dyspnea that required oxygen supplementation. Her medical history dates back to July 2013 when she was hospitalized in the chest ward for dyspnea and cough with yellow sputum. She was subsequently diagnosed with Sjogren’s syndrome complicated with interstitial lung disease (ILD) and PAH (Table I). Her chest X-ray at that time showed vascular markings with interstitial thickening, costophrenic (CP) angle blunting and cardiomegaly. An echocardiogram revealed a pulmonary arterial (PA) systolic pressure of 99 mmHg, enlargement of the right atrium and ventricle, D-shaped left ventricle (LV), and severe tricuspid regurgitation. Chest CNYCT showed no filling defects, excluding pulmonary embolism; it also displayed an enlarged pulmonary trunk, right atrium (RA), and right ventricle (RV), further evidencing pulmonary hypertension. Symptoms of dry mouth, dry eyes, and cracked tongue mucosa, with a Schirmer’s test showing <5 cm, oculus uterque (OU). A positive minor salivary gland biopsy, nuclear medicine scan showing impaired salivary gland function, and a positive anti-Ro test, confirmed Sjogren’s syndrome. She started on Revatio (Sildenafil) 20 mg three times a day (TID) for pulmonary hypertension control, adding Tracleer (Bosentan) in 2016 due to disease progression. A right heart catheterization (RHC) revealed a mean pulmonary arterial pressure (PAP) of 39 mmHg, pulmonary vascular resistance (PVR) nearly 15 Woods, and a wedge pressure of 4, indicating pre-capillary type, group I, CTD-related PAH in 2017. The right heart catheterization (RHC) report allowed for insurance coverage of Opsumit (Macitentan) 10 mg once a day (QD), replacing Tracleer (Bosentan) in 2017. From 2017 to 2020, she was hospitalized multiple times for steroid treatments to manage her underlying Sjogren’s syndrome.\n\nPulmonary hypertension treatment is risk-based, and until 2017, the patient was considered low to intermediate risk, controlled with two medications (Sildenafil + Macitentan). Her condition remained stable until October 2020, when she experienced worsened dyspnea accompanied by cough and expectoration of white sputum, suggestive of infection. On November 10, 2020, the patient experienced severe dyspnea, cold sweats, and cyanosis, with SpO2 dropping to 70%, necessitating 100% O2 via face tent. Blood gas and lab tests revealed a lactate level of 5.2 mmol/l and brain natriuretic peptide (BNP) over 10,000 pg/ml, strongly suggesting cardiogenic shock. She was prepped for intensive care unit (ICU) admission, intubated, and initiated on four pulmonary hypertension medications. Her condition stabilized and showed improvement, preventing further deterioration. On November 12, 2020, evaluation for heart-lung transplantation began. Her condition continued to improve with off vasopressors on November 13, 2020, and extubating on November 14, 2020, and transferred to a general ward on November 21, 2020, with O2 tapered to nasal cannula 2l/min. A follow-up RHC continued to show elevated pulmonary artery pressure, likely attributed to chronic hypertension leading to right heart strain and eventual failure. After intensive care unit (ICU) treatment, she was referred to National Taiwan University Hospital for evaluation for heart-lung transplant.\n\nReviewing the records since the onset of her illness, it was evident that pulmonary artery pressure had steadily increased, and the distance covered in the 6-minute walk test was progressively shortened. Currently, the patient is classified as high risk. She continues regular hospitalizations for control. Despite the relatively stable condition, her chief complaint during the admission is still dyspnea. The physical examination revealed mild rhonchi ILD and a pansystolic murmur indicative of severe valvular heart disease, with no other significant findings. Ventavis (Iloprost) 10 mcg/ml 2 ml was added in 2020. Molecular hydrogen therapy (1 capsule/day) was initiated in May 2023. Hydrogen capsules (PURE HYDROGEN) were purchased from HoHo Biotech Co., Ltd. (Taipei, Taiwan, ROC). Each capsule contained 170 mg of hydrogen-rich coral calcium containing 1.7×1,021 molecules of hydrogen, which is equivalent to 24 cups of water with 1,200 ppb of hydrogen or 0.6 mM of hydrogen per 200 ml of water. Adjuvant therapy with hydrogen capsules resulted in increased CD127 + Treg, decreased anti-Ro antibody, decreased B cell subsets, and stabilization of clinical symptoms and signs was observed following the addition of hydrogen therapy in this patient. No adverse reactions or events were observed following the administration of hydrogen capsules. Flow cytometry and serological examination were employed for whole-blood analysis to assess changes in immune cells and autoantibody before and after hydrogen therapy. For subsequent whole-blood analysis via flow cytometry, blood samples were prepared using standard fluorescent dye preparation methods and fluorescent antibody reagent kits with dried reagents (Beckman Coulter, Brea, CA, USA). The methods, steps, immunophenotypic analysis, and cell gating were conducted following previously described procedures. Our analysis of immunophenotypic markers before and after hydrogen therapy revealed increased CD127 + Treg and decreased B cell subsets after treatment. Moreover, this study adheres to the CARE reporting guidelines (2013 CARE Checklist).",
+    "diff_label_texts": "A 56-year-old woman was diagnosed in 2013 with Sjogren’s syndrome, an autoimmune disease that also caused scarring in her lungs (interstitial lung disease). She developed pulmonary arterial hypertension, which means high blood pressure in the blood vessels of her lungs. Over the years she took many medicines for her lung pressure and autoimmune disease, including sildenafil, bosentan, macitentan, iloprost, and steroid drugs, but her condition got worse. In 2020 she had very bad shortness of breath and her heart began to fail, a life-threatening problem called cardiogenic shock. In May 2023 she started taking one hydrogen capsule each day as an extra treatment. After she began the hydrogen capsules, tests showed she had more of a calming immune cell called CD127+ regulatory T cells. The tests also showed lower levels of anti-Ro antibodies, which are harmful antibodies linked to Sjogren’s syndrome. The tests showed fewer B cells, which are the immune system’s antibody-making cells. Her symptoms became stable and she did not have any side effects from the hydrogen capsules.",
+    "summary": "We present the case of a 56-year-old female with CTD-PAH, diagnosed in 2013 with Sjogren’s syndrome complicated by interstitial lung disease (ILD) and PAH. Despite treatment with sildenafil, bosentan, macitentan, iloprost, and corticosteroids, her condition deteriorated, resulting in severe dyspnea and cardiogenic shock in 2020. In May 2023, molecular hydrogen therapy was initiated as an adjuvant treatment. The patient received daily hydrogen capsules, which led to increased CD127+ Treg cells, reduced anti-Ro antibodies, and decreased B cell subsets. Her clinical symptoms stabilized without adverse effects."
+  },
+  {
+    "doc_id": 44,
+    "label": "intermediate_health_literacy",
+    "fulltext": "A 12-year-old boy was brought to our department exhibiting sudden onset symptoms of headache and polyuria-polydipsia syndrome, which began one week prior to his initial visit. The child had no significant medical history. During the first clinical evaluation, he measured 146.5 cm in height (M) and weighed 30 kg (-1.4 SD). There were no observed signs of adrenal insufficiency or hypothyroidism. He was at the onset of puberty, with gonad sizes measuring 3.2 cm on each side and a penis length of 6.2 cm (M). Notably, the patient experienced polyuria-polydipsia syndrome, with fluid excretion reaching up to 113ml/kg/day, nocturnal enuresis, and an excessive liquid intake of 3.8 liters/m². Ophthalmologic examination yielded expected results, with no visual impairments detected and normal optical coherence tomography (OCT) findings.\n\nThe biological assessment revealed DI, with a serum sodium level of 140 mEq/l and plasma osmolality of 287 mosm/kg, while the urine osmolality was significantly low at 179 mosm/kg. Furthermore, his serum levels of insulin-like growth factor-1 (IGF1), prolactin (PRL), free T4, cortisol, follicle-stimulating hormone (FSH), and luteinizing hormone (LH) were all within the normal range.\n\nMRI scans with and without contrast highlighted apoplexy in an RCC, showing a spontaneous hyperintensity on T1 and T2 sequences measuring 15x6x11 mm. The anterior pituitary gland displayed homogeneous contrast uptake. However, we observed a loss of the typical hyperintensity of the posterior pituitary gland, with no radiological indications of a craniopharyngioma. Therefore, during the initial hormonal evaluation, the only hormone deficiency identified in our case was DI, which showed significant improvement under vasopressin treatment. The case was reviewed in a multidisciplinary meeting, including an endocrinologist, neurosurgeon, and radiologist. Given the absence of clinical or biological signs other than DI and the stability of the RCC apoplexy over nine months of MRI monitoring—with measurements of 12 × 11 × 10 mm—a conservative management approach with regular follow-ups was chosen.\n\nThe child was monitored for three years, during which he displayed normal puberty development and maintained a stable hormonal profile (Table 1). Visual evaluations revealed no abnormalities. However, a decrease in growth velocity was noted, dropping from -0.8 SD to -1.1 SD. This necessitated an investigation for acquired growth hormone (GH) deficiency. At the age of 14 years and nine months, the child was readmitted to undergo two GH stimulation tests: A propranolol-glucagon test and an Insulin Tolerance Test, which indicated a partial GH deficiency with peaks of 19.3 µUI/ml and 10.0 µUI/ml, respectively. After receiving GH treatment, the patient experienced a notable increase in growth velocity, improving from -1.1 SD to 0.2 SD over one year.\n\nSubsequently, MRI monitoring showed a stable appearance of the RCC apoplexy after two years (11 × 12 × 11 mm), with a slight decrease in size observed at the three-year follow-up, measuring 7 × 10 × 6 mm. It is important to note that the radiological follow-up was consistently conducted at the same MRI center, with the same radiologist interpreting both recent and previous MRI findings during multidisciplinary meetings that included an endocrinologist and a neurosurgeon.",
+    "diff_label_texts": "A 12-year-old boy was admitted with sudden headaches and a week-long history of excessive urination and thirst. Tests showed central diabetes insipidus (low urine concentration with normal blood sodium and plasma osmolality), and MRI identified apoplexy (bleeding or sudden change) in a Rathke cleft cyst measuring about 15 × 6 × 11 mm; the normal bright signal of the posterior pituitary was lost but the anterior pituitary enhanced normally. He had no visual problems and routine pituitary hormone tests were otherwise normal. Because he was early in puberty, had no compressive symptoms, and basic endocrine tests were normal, a multidisciplinary team chose conservative management: clinical, hormonal and MRI follow-up, and treatment of the diabetes insipidus with vasopressin. Over three years the cyst remained stable then decreased in size (about 12 × 11 × 10 mm at nine months, 11 × 12 × 11 mm at two years, and 7 × 10 × 6 mm at three years), puberty progressed normally, and vision stayed normal. During follow-up his growth slowed, and stimulation tests at age 14 years 9 months showed a partial growth hormone deficiency; after starting growth hormone therapy his growth rate improved markedly. Overall, conservative follow-up was effective: the Rathke cleft cyst apoplexy stabilized and shrank, diabetes insipidus was controlled, and the only long-term endocrine issue was a treatable partial GH deficiency.",
+    "summary": "We present the case of a 12-year-old boy admitted due to the recent onset of headaches and diabetes insipidus. Magnetic resonance imaging revealed Rathke cleft cyst apoplexy. Given the absence of compressive symptoms in a child at the early stages of puberty and without abnormalities in basic endocrine tests, a conservative strategy was employed, involving regular clinical, biological, and radiological follow-ups. The child experienced normal puberty without any endocrine deficiencies except for a partial growth hormone deficiency."
+  },
+  {
+    "doc_id": 45,
+    "label": "intermediate_health_literacy",
+    "fulltext": "Patient and observation\nPatient information: This was a 67-year-old patient with no medical history who presented with dysphagia, dysphonia and altered general condition.\n\nClinical findings: initial clinical examination found a conscious patient with a Glasgow score of 15/15, apyrexia, blood pressure of 12/07 cmHg, oxygen saturation of 100%, heart rate of 80/min, conjunctivae of normal colour with a large mass in the cavum. There was no hepatomegaly or splenomegaly, the lymph node areas were free, the rest of the physical examination was normal.\n\nChronology: the patient had been experiencing difficulty swallowing with dysphonia for 6 months, the clinical picture worsened with the development of dysphagia for solids with a deterioration in general condition (weight loss of 15kg/6 months).\n\nDiagnostic approach: cervico-thoraco-abdomino-pelvic CT scan showed a 70 mm x 40 mm nasopharyngeal mass extending to 60 mm. The patient's blood work was normal (white blood cell count, renal and hepatic function, lactate dehydrogenase and HIV, HCV and HBV serologies). The histological and immunohistochemical study of the nasopharyngeal biopsy was in favour of a grade 1,2 CD20+; CD19+; CD79a+; CD10+ follicular B-cell NHL in 2 readings in 2 different laboratories. The bone marrow biopsy was normal as was the pre-therapeutic work-up.\n\nTherapeutic intervention: the patient received 4 RCHOP 21 cures (rituximab 375mg/m2 intravenous (iv), cyclophosphamide 750 mg/m2 iv, oncovin 2 mg iv, prednisolone 100 mg orally, and doxorubicin 50 mg/m2 (iv) with no response and then 3 RDHAOX cures (rituximab 375 mg/m2 intravenous (iv) on day 1, high dose aracytine 2 g/m2 x 2 iv on day 2, dexamethasone 40 mg from day 1 to day 4, and oxalipatine 100 mg/m2 on day 1) with no clinical response.\n\nFollow-up and results of therapeutic interventions: the persistence and increase of the nasopharyngeal mass led to the realization of the tracheotomy, the biopsy of the nasopharyngeal mass objectified the disappearance of the lymphoid B infiltration with presence of the amyloid deposits AL type kappa.\n\nImmune electrophoresis of plasma proteins showed the presence of immunoglobulin M kappa, the dosage of light chains was not performed due to lack of resources, the myelogram and a second bone marrow biopsy were normal, the TEP scan objectified a hypermetabolic nasopharyngeal process without other anomalies, the cardiac evaluation (ECG, natriuretic peptides, troponin, echocore) and renal were without particularities, the patient is currently under protocol bortezomib, prednisone and bendamustine with good clinical evolution after the first treatment.\n",
+    "diff_label_texts": "A 67-year-old patient with no significant past medical history presented with declining overall health marked by progressive hoarseness (dysphonia) and difficulty swallowing (dysphagia). Imaging showed a large nasopharyngeal/neck mass. Biopsy confirmed grade 1–2 follicular non-Hodgkin lymphoma. CT of the neck, chest, abdomen, and pelvis found a nasopharyngeal mass measuring about 70 × 40 mm with extension to 60 mm. Bone marrow biopsy and the pre-treatment evaluation were normal. The patient received four cycles of rituximab plus CHOP without response, followed by three cycles of rituximab plus DHAOX, with persistence of the mass. Repeat biopsy then showed loss of B‑cell infiltration and the presence of AL amyloid deposits. Serum protein immunoelectrophoresis detected immunoglobulin M. PET imaging demonstrated a hypermetabolic nasopharyngeal process. The patient is currently being treated with bortezomib, prednisone, and bendamustine.",
+    "summary": "We report the case of a 67-year-old patient without pathological CDDs who presented with a deterioration of general condition with progressive dysphonia and dysphagia with a large mass in the neck that was biopsy-proven to be a grade 1 and 2 follicular non-Hodgkin lymphoma. A cervico-thoraco-abdomino-pelvic CT scan showed a 70 mm x 40 mm nasopharyngeal mass extending to 60 mm. Bone marrow biopsy was normal and the pre-therapeutic evaluation was normal. The patient received 4 courses of rituximab plus CHOP (cyclophosphamide, adriamycin, prednisone and oncovin) without response and then 3 courses of rituximab plus DHAOX (dexamethasone, high dose ara-cytin and oxalipatin) with persistence of the mass. The biopsy of the latter showed the disappearance of the B lymphocyte infiltration with presence of the AL amyloid deposits. The immunoelectrophoresis of plasma proteins showed the presence of immunoglobulin M. A positron emission tomography (PET) scan showed a hypermetabolic nasopharyngeal process. The patient is currently receiving a protocol of bortezomib, prednisone and bendamustine.\n"
+  },
+  {
+    "doc_id": 49,
+    "label": "intermediate_health_literacy",
+    "fulltext": "Female patient, 16 years old, presenting a depressed gray plaque of 10.5 × 8.0 cm interspersed with hypochromic areas in the lower lateral part of the left thigh. Telangiectatic vessels overlap the lesion peripherally, with visible veins close to it. The plaque was present from birth, but was initially violaceous. It evolved with the passing of the years, with lightening and depression. There is no discrepancy in the length of the lower limbs.\n\nAngioresonance showed vascular malformations in the skin and subcutaneous tissue supplied by intermuscular branches of the popliteal artery. Early venous filling was found in both the region and the malformations, suggesting early venous shunting. Dilated draining veins were not documented, except for a superficial draining vein running along the subcutaneous cellular tissue of the anterior thigh. In addition, thinning of the subcutaneous tissue was noted in the topography of the vascular alteration, but without intramuscular or bone extension.\n",
+    "diff_label_texts": "A 16-year-old girl has a depressed gray plaque on the lower outer (lateral) part of her left thigh, about 10.5 × 8.0 cm. The area includes lighter patches and small dilated surface blood vessels (telangiectasias) around the edges, and some nearby veins are visible. The lesion has been present since birth—it was initially purplish (violaceous) and over the years became lighter and sunken. There is no difference in leg length. Vascular imaging (angioresonance) shows a vascular malformation involving the skin and the fat under the skin in that area, supplied by branches of the popliteal artery. The scan showed early filling of veins, which suggests early venous shunting; no markedly dilated draining veins were found except for a superficial draining vein along the front of the thigh. The subcutaneous tissue beneath the plaque is thinner, and there is no extension into muscle or bone.",
+    "summary": "16-year-old girl with a depressed gray plaque on the left thigh, with a vascular malformation affecting the skin and subcutaneous tissue evident by angioresonance.\n"
+  },
+  {
+    "doc_id": 50,
+    "label": "low_health_literacy",
+    "fulltext": "A 57-year-old woman with a 14-year history of asthma and allergic rhinitis, on salmeterol/fluticasone, was hospitalized for recurrent abdominal pain that began two months earlier. The pain was intermittent and dull, accompanied by nausea, anorexia, malaise, and a weight loss of 5 kg. There was no fever, blood / mucus in the stool, or respiratory symptoms (rhinorrhea, wheezing, coughing). She had no history of alcohol/tobacco use or traditional herbal medicines. Six weeks before admission, she was diagnosed with an intestinal infection in a local clinic after a complete blood count (CBC) revealed leukocytosis and significant eosinophilia (25.61 G/L, 77.8% eosinophils). She received antibiotics and mebendazole without relief of symptoms. At presentation, the patient was alerted and oriented with stable vitals (BP 110/70 mmHg, T 37°C, HR 88 bpm, RR 18 bpm). She had a BMI of 16.6 kg/m² and sarcopenia, but no skin rash, lymphadenopathy, or edema. The abdominal exam showed tenderness in the epigastric and umbilical regions without guarding. CBC revealed leukocytosis and significant eosinophilia (20.8 G/L, with a total white blood cell count of 26.8 G/L, comprising 77.8% eosinophils). Peripheral blood film examination showed normal eosinophils. Bone marrow aspiration reveals 48% eosinophils without blasts, atypical cells. Fluorescence in situ hybridization (FISH) for CHIC2 deletion as a surrogate marker for FIP1L1-PDGFRA showed no rearrangements of the PDGFRA gene. Autoimmune and vasculitis screenings (ANA, anti-dsDNA, p-ANCA, c-ANCA) were negative. Elevated serum IgG (2760 mg/dL; normal range, 700–1600 mg/dL) and IgG4 (1260 mg/dL; normal range, 3.9–86.4 mg/dL), slightly elevated IgE (137.5 IU/mL; normal range, <100 IU/mL) and high RF (144.4 IU/mL; normal range, <20 IU/mL) were observed. Other parameters were normal, including aminotransferase, blood urea nitrogen, serum creatinine, complement C3, complement C4, vitamin B12, serum cortisol, and NT-proBNP. ECG and echocardiogram were normal. Chest CT scans showed mild fibrosis and bronchiectasis. Sputum AFB smears and bronchoscopy were negative. The cytology of the bronchoalveolar lavage fluid showed 35% neutrophils, no eosinophils. Spirometry indicated severe obstruction with bronchodilator response. The fractional exhaled nitric oxide (FeNO) level was 15 ppb. Stool samples were tested positive for leukocytes, with no signs of ova or parasites. Serology tests were positive for toxocariasis (positive IgG of Toxocara canis at 54.2 NovaTec-Units) but negative for Strongyloides stercoralis, Fasciola sp., Toxoplasma gondii, Trichinella spiralis, Ancylostoma sp., Angiostrongylus cantonensis, Ascaris lumbricoides, Clonorchis sinensis, Paragonimus sp., Gnathostoma sp., Entamoeba histolytica, cysticercosis, filariasis, and HIV. An abdominal contrast-enhanced computed tomography scan revealed gallbladder stones without acute cholecystitis and showed no gastrointestinal tract abnormalities. The upper gastrointestinal endoscopy showed unremarkable results with a normal appearance. Colonoscopy showed mucosal inflammation in the sigmoid, left, transverse, and right colon with systemic biopsy. A five-day course of albendazole (400 mg twice daily) for suspected toxocariasis was ineffective. Colonic biopsies revealed significant eosinophilic infiltration (>85 eosinophils/High-power field (HPF) in the left colon, >100 eosinophils/HPF in the transverse and right colon). Given the patient’s nonresponse to toxocariasis treatment and the significant eosinophilic infiltration observed in the colon mucosa biopsy, a diagnosis of eosinophilic colitis was confirmed. The patient was treated with oral methylprednisolone (16 mg) and montelukast (5 mg). Symptoms resolved in two weeks and eosinophil counts normalized (0.3 G/L). The corticosteroid was reduced and discontinued, and the patient was maintained on montelukast for three months without symptom recurrence.",
+    "diff_label_texts": "A 57-year-old patient had asthma and nose allergies. She kept having stomach pain. Her blood showed very high levels of allergy-fighting white cells. A certain immune protein (IgG4) was also high. The doctors checked for blood cancers and other causes and did not find them. They gently took tiny samples from the lining of her large intestine. The samples showed too many of those allergy cells sitting in the tissue. This meant she had eosinophilic colitis, which is swelling of the colon from a build-up of allergy cells. She took a steroid medicine to calm the swelling. Then she stayed on montelukast to keep the problem quiet. Her pain went away and did not come back for three months.",
+    "summary": "We present a unique case of a 57-year-old patient with a medical history of asthma and allergic rhinitis who presented recurrent abdominal pain, significant blood eosinophilia, and elevated levels of Immunoglobulin G4. After ruling out hematological and secondary causes of eosinophilia, a biopsy of the colon mucosa revealed an excess of tissue eosinophils, confirming the diagnosis of EoC. The patient responded well to corticosteroids and was subsequently maintained on montelukast, with no recurrence of symptoms over 3 months."
+  },
+  {
+    "doc_id": 52,
+    "label": "intermediate_health_literacy",
+    "fulltext": "2 years 6 months old female pre-schooler with a previous diagnosis of NF1. She consulted due to a 4 week diarrhea with blood streaks (5 to 10 episodes a day). A week after the onset of the diarrhea she consulted the emergency department, where rotavirus (+) was detected, with low inflammatory parameters, negative coproculture and normal abdominal ultrasound. She was hospitalized for 3 days to manage dehydration and was discharged without bleeding, with persistence of semi-liquid stools. 10 days after discharge she presented diarrhea with blood streaks, associated with low intake and weight loss of 1 kg reported by parents. They consulted a pediatric gastroenterologist who requested a polymerase chain reaction (PCR) panel of gastrointestinal pathogens and PCR of Clostridium difficile (which were negative) and indicated hospitalization for study.\n\nOn direct questioning, the parents reported no fever, abdominal pain, vomiting, respiratory or urinary symptoms, arthralgia, or new skin lesions. They did not own pets, and there was no history of travel or recent dietary changes.\n\nThe patient was diagnosed with confirmed NF1 at 8 months of age by genetic testing with the heterozygous pathogenic variant c.5606_5627del (p.Gly1869Valfs*28). She has skin involvement (café con leche spots) and bone involvement. At 18 months she required ankle arthrodesis for tibial curvature. She has no family history of NF1 or inflammatory bowel disease.\n\nOn physical examination, the abdomen was soft and indistinct, with increased air-bubble murmurs, without masses or visceral enlargement. The perianal examination was normal. There were multiple brown-coffee stains on the lower extremities and back. General examinations were performed, including a blood count with moderate microcytic-hypochromic anaemia (Hb 9.6 g/dL), leukocytosis with left shift (leukocytes 13,900), and discretely elevated inflammatory parameters (CRP 1.37 mg/dL, normal value up to 0.5 mg/dL).\n\nA colonoscopy was performed, the rectum, sigmoid and various segments of the colon were examined up to the cecum, visualizing the ileocecal valve and the appendicular orifice. The last few centimeters of the distal ileum were also inspected. The mucosa from the anal margin to the cecum was observed to be erythematous, with loss of vascular transparency, unlike the cecal mucosa, which appeared normal. No lesions were identified in the anal canal or cecum.\n\nBiopsies of the small intestine (ileon) and large intestine were taken. Microscopic examination showed mucosa of ileal type with preserved villous architecture and adequate epithelial differentiation, with a non-inflamed lamina propria. The mucosa of the large intestine had a mild distortion of architecture and adequate epithelial differentiation, a swollen lamina propria with a mild mixed inflammatory infiltrate and hyperplasia of lymphoid follicles. Isolated foci of microabscesses were recognized. The biopsy was consistent with mild colitis, with signs suggesting chronicity.\n\nIn addition, a PCR study for cytomegalovirus (CMV) was requested in a colon biopsy, which was positive.\n\nGiven a positive PCR for CMV, CMV IgG and IgM and CMV viral load in blood were requested, resulting in a positive IgG, negative IgM, and CMV viral load of 79.7 IU/ml. Further laboratory studies included PCR for gastrointestinal pathogens and PCR for Clostridium difficile in stool, both of which were negative. In the colon biopsy, Gram stain microbiological studies were requested, which showed +++ leukocytes without bacteria; biopsy culture showed S. gallolyticus/equinus complex in very low amount (interpreted as bacterial flora); acridine orange, Ziehl-Neelsen, Koch culture, and ADV PCR were negative.\n\nEndoscopy and histology suggestive of UC was reported in the context of a patient with moderate symptoms (PUCAI 50) who was started on Mesalazine (70 mg/kg/day three times daily) and a request for a faecal calprotectin was made which was greater than 600 ug/g.\n\nThe immunology team evaluated the patient for suspected immunodeficiency. The parents did not report a history of infections, they reported that they were vaccinated, that they had good weight gain, no family history of immunodeficiencies, auto-immunity or early deaths. A study with lymphocyte subpopulations (normal), immunoglobulins (normal), HIV (negative), memory T lymphocytes (with alterations expected in the context of CMV viremia) and lymphoproliferation test (normal) was requested. In addition, a genetic panel of primary immunodeficiencies (Invitae) was performed, which contains 429 genes, of which 68 make up the panel of monogenic inflammatory intestinal disease. 7 variants of uncertain significance were obtained, none included in the panel of monogenic IBD.\n\nGanciclovir was initiated intravenous for CMV infection and continued for 15 days. The last PCR CMV control prior to discharge reported undetectable load.\n\nThe patient improved during the hospital stay with decreased frequency of stools and increased consistency, no rectal bleeding, no nocturnal stools and no abdominal pain, with PUCAI 0 at discharge.\n\nTwo months later, he presented with a reactivation of IBD with bloody diarrhea (PUCAI 35). A blood count was performed (normal), a panel of gastrointestinal pathogens was performed (–), PCR for Clostridium difficile was performed (+), and CMV load was undetectable. He was treated with oral metronidazole. However, he persisted with diarrhea with blood streaks, so he was hospitalized again.\n\nA colonoscopy was performed, where erythematous mucous was observed in a diffuse form from the rectum to the cecum, with nodularity and loss of vascular transparency in the submucosa, greater in the left and transverse colon segments. No focal lesions were observed. The mucosa of the ileum and anal canal were observed without lesions.\n\nBiopsy of the terminal ileum, right colon and left colon was performed. Microscopic examination of the ileal-type mucosa showed preserved villous architecture and adequate epithelial differentiation. The lamina propria showed no signs of inflammation. There were no aphthous erosions or granulomas. The mucosa of the large intestine showed mild distortion of architecture and epithelial dedifferentiation. The lamina propria was expanded by mixed inflammatory infiltrate, transmucosal distribution. Foci of cryptitis and cryptitic microabscesses and hyperplasia of reactive lymphoid follicles were recognized. No granulomas, viral or parasitic cytopathic changes were observed. All fragments of the left colon sample presented a similar histopathological picture.\n\nShe was given oral treatment with Vancomycin and Prednisone (1 mg/kg/day) with a good response and a favorable evolution. She was discharged with a decrease in the frequency of bowel movements. She persists with mild symptoms (PUCAI 5) in outpatient control, so the dose of corticosteroids is progressively decreased and she remains on treatment with Mesalazina.\n",
+    "diff_label_texts": "A 2.5-year-old girl with a known diagnosis of neurofibromatosis type 1 (NF1) developed four weeks of watery diarrhea that became bloody. She was initially treated for dehydration after a rotavirus infection but continued to have bloody stools and weight loss. Colonoscopy showed red, inflamed mucosa from the anal margin through the colon up to the cecum, with loss of the normal visible blood vessels. Biopsies of the colon showed chronic inflammation with cryptitis and microabscesses, findings consistent with ulcerative colitis (UC). A PCR test on the colon tissue was positive for cytomegalovirus (CMV); blood testing showed past CMV exposure (IgG positive), no IgM, and a low CMV viral load. Blood tests showed mild anemia, a raised white count, and slightly increased CRP; faecal calprotectin was >600 µg/g, supporting active intestinal inflammation. Immunology testing and a broad genetic panel for monogenic immune causes were essentially normal. She was treated with mesalazine and received 15 days of intravenous ganciclovir for CMV, with clinical improvement and undetectable CMV on repeat testing at discharge. Two months later she had a flare with bloody diarrhea; stool testing showed Clostridioides difficile and CMV was undetectable. She was treated with antibiotics and prednisone, improved, and is maintained on mesalazine with only mild ongoing symptoms.",
+    "summary": "2.5-year-old pre-schooler with a history of NF1 presenting with bloody diarrhea. On endoscopic examination, the mucosa from the anal margin to the cecum was erythematous with loss of vascular transparency. Colon mucosal biopsies showed signs of chronic inflammation consistent with a diagnosis of ulcerative colitis and CMV infection was diagnosed by PCR.\n"
+  },
+  {
+    "doc_id": 53,
+    "label": "low_health_literacy",
+    "fulltext": "40-year-old HIV-positive man with regular adherence to treatment (viral load 4500/mm3 and CD4 70/mm3 from the previous year), consulted for intermittent fever of two years' evolution that did not respect the standard time and gave way to transient antinflammatory non-steroidal drugs. He added in the last two months diffuse abdominal pain with predominance in the upper right lobe where he acquired a configuration of a tree in bud and bilateral pleural effusion, and at the abdominal level, marked increase of hepato-splenomegaly associated with ascites. After 48 hours of his suspension, he presented fulminant hepatic failure and was transferred to the intensive care unit. Tracheal aspirate was performed and after transfusion support a liver biopsy was obtained by puncture.  The patient died a few hours later. The postmortem culture of the tracheal aspirate was positive for Mycobacterium tuberculosis and the liver biopsy was performed with non-necrotizing granulomas and the rest of the parenchyma preserved. This work was carried out in accordance with the principles laid out in the ethical code of the WHO (Helsinki Declaration).\n",
+    "diff_label_texts": "A 40-year-old man has HIV and takes his medicines regularly. For two years, he had fevers that came and went. In the last two months, he also had spreading belly pain and many swollen glands. Blood tests showed very low blood cells, blood that did not clot well, low blood protein, and strong signs of inflammation. A body scan showed a big liver and spleen and many swollen glands. Many germ tests were done and were negative, except one that found the HHV-8 virus. A gland sample showed a rare illness called Castleman’s disease. Even after restarting his HIV drugs, he got worse. Doctors tried steroids and an antiviral called ganciclovir. A week later, many organs started to fail and he swelled all over, so those drugs had to be stopped. A new chest scan showed small branch-like spots in the right lung and fluid around both lungs. The belly scan showed the liver and spleen got bigger and there was fluid in the belly. He went to intensive care because his liver suddenly failed. He died soon after. After his death, a lung sample grew tuberculosis. A liver sample showed tiny immune lumps called granulomas.",
+    "summary": "We present the case of a 40-year-old HIV-positive man with regular adherence to treatment, who consulted for intermittent febrile episodes of two years' evolution, adding in the last two months progressive diffuse abdominal pain and generalized adenomegaly. In the laboratory, he presented pancytopenia, coagulopathy, hypoalbuminemia and increased acute phase reactants. The computed tomography (CT) of the thorax, abdomen and pelvis only showed hepato-splenomegaly and generalized adenomegaly. Multiple microbiological examinations were performed, including cultures for Mycobacterium sp. of different samples, all with negative results, with the exception of RT-PCR for HHV-8. A left iliac ganglion biopsy was performed with findings consistent with Castleman's disease. Despite restarting antiretroviral therapy, the symptomatology progressed, initiating treatment with corticosteroids and ganciclovir. After a week, he developed multiple organ failure and anasarca, which contraindicated the drugs initiated. A new chest CT was performed that showed infiltrates with a tree-like pattern in the upper right lobe associated with bilateral pleural effusion, and at the abdominal level, progression of hepato-splenomegaly and ascites. He passed to the intensive care unit 48 hours later due to fulminant hepatic failure. The patient died within a few hours. A postmortem culture of the tracheal aspirate was received positive for Mycobacterium tuberculosis and a liver biopsy with non-necrotizing granulomas.\n"
+  },
+  {
+    "doc_id": 53,
+    "label": "intermediate_health_literacy",
+    "fulltext": "40-year-old HIV-positive man with regular adherence to treatment (viral load 4500/mm3 and CD4 70/mm3 from the previous year), consulted for intermittent fever of two years' evolution that did not respect the standard time and gave way to transient antinflammatory non-steroidal drugs. He added in the last two months diffuse abdominal pain with predominance in the upper right lobe where he acquired a configuration of a tree in bud and bilateral pleural effusion, and at the abdominal level, marked increase of hepato-splenomegaly associated with ascites. After 48 hours of his suspension, he presented fulminant hepatic failure and was transferred to the intensive care unit. Tracheal aspirate was performed and after transfusion support a liver biopsy was obtained by puncture.  The patient died a few hours later. The postmortem culture of the tracheal aspirate was positive for Mycobacterium tuberculosis and the liver biopsy was performed with non-necrotizing granulomas and the rest of the parenchyma preserved. This work was carried out in accordance with the principles laid out in the ethical code of the WHO (Helsinki Declaration).\n",
+    "diff_label_texts": "A 40-year-old man with HIV on treatment presented with intermittent fevers for two years. Over the prior two months, he developed progressive, diffuse abdominal pain and generalized lymphadenopathy. Laboratory tests showed pancytopenia, coagulopathy, hypoalbuminemia, and elevated inflammatory markers. CT of the chest, abdomen, and pelvis revealed only hepatosplenomegaly and widespread adenopathy. Broad infectious workup, including mycobacterial cultures from multiple specimens, was negative except for a positive HHV-8 RT-PCR. A left iliac lymph node biopsy was consistent with Castleman’s disease. Despite restarting antiretroviral therapy, his condition worsened, so clinicians initiated corticosteroids and ganciclovir. After one week he developed multiorgan failure with anasarca, making those medications unsafe. Repeat chest CT showed right upper lobe tree-in-bud infiltrates with bilateral pleural effusions; abdominal imaging showed worsening hepatosplenomegaly and new ascites. He was transferred to the ICU 48 hours later for fulminant hepatic failure and died shortly afterward. Postmortem testing grew Mycobacterium tuberculosis from a tracheal aspirate, and liver biopsy showed non-necrotizing granulomas.",
+    "summary": "We present the case of a 40-year-old HIV-positive man with regular adherence to treatment, who consulted for intermittent febrile episodes of two years' evolution, adding in the last two months progressive diffuse abdominal pain and generalized adenomegaly. In the laboratory, he presented pancytopenia, coagulopathy, hypoalbuminemia and increased acute phase reactants. The computed tomography (CT) of the thorax, abdomen and pelvis only showed hepato-splenomegaly and generalized adenomegaly. Multiple microbiological examinations were performed, including cultures for Mycobacterium sp. of different samples, all with negative results, with the exception of RT-PCR for HHV-8. A left iliac ganglion biopsy was performed with findings consistent with Castleman's disease. Despite restarting antiretroviral therapy, the symptomatology progressed, initiating treatment with corticosteroids and ganciclovir. After a week, he developed multiple organ failure and anasarca, which contraindicated the drugs initiated. A new chest CT was performed that showed infiltrates with a tree-like pattern in the upper right lobe associated with bilateral pleural effusion, and at the abdominal level, progression of hepato-splenomegaly and ascites. He passed to the intensive care unit 48 hours later due to fulminant hepatic failure. The patient died within a few hours. A postmortem culture of the tracheal aspirate was received positive for Mycobacterium tuberculosis and a liver biopsy with non-necrotizing granulomas.\n"
+  },
+  {
+    "doc_id": 54,
+    "label": "low_health_literacy",
+    "fulltext": "4-month-old indigenous lactating mother from the rural area of the interior of Panama, from the town of Urracá, 3 hours by canoe from the nearest health center. Her background included being the fourth daughter, born by vaginal delivery at home by a relative, without prenatal controls, her weight, height and Apgar score at birth are unknown. She did not breastfeed and was fed with powdered milk formula with iron for children under 6 months, receiving 3 ounces every 4 hours.\n\nThe nuclear family was composed of 6 people (parents and 4 children) who lived in a house with walls and floor of boards and palm roof, 2 rooms, without electricity, they were illuminated with kerosene lamps, water from a well, excreta in a river and they burned the garbage, their economic income came from subsistence agriculture.\n\nHe had no health care in his first 4 months of life and did not receive the vaccinations included in the national expanded programme of immunizations. According to his parents, his neurodevelopment was normal until his hospitalization.\n\nThe minor consulted in a health center with a history of 4 days of diarrhoea, without mucus or blood associated with vomiting of food content (the mother gave her tea because she could not tolerate milk), afebrile and without respiratory symptoms. Oral fluids and 4 doses of Enterogermina® (B. clausii: two billion spores/5 mL) were administered. Due to the lack of supplies (they did not have catheters, or intraosseous for the administration of intravenous fluids) she was transferred to a second-level hospital in the provincial capital and then to our institution in Panama City with a diagnosis of acute gastroenteritis and severe dehydration.\n\nHe presented to the emergency department with a consciousness compromise, dehydration characterised by a tearless cry, dry oral mucosa. He had oedema of +++ hands, feet, abdomen and face. He was afebrile and had signs of shock, capillary refill time > 2 seconds, cold extremities, filiform pulse and marble skin, heart rate 170 bpm, respiratory rate 55 bpm, blood pressure 91/37 mmHg, oxygen saturation 99%. He weighed 4.7 kg and was 56 cm tall at admission, Z-score height/age -2.52, weight/height and weight/age Z-scores were not quantifiable due to severe dehydration. On segmental examination, there were fine crepitus in both lung bases and erythematous-squamous lesions with desquamation of skin and others with hypopigmentation of trunk and upper limbs (interpreted as pellagroid dermatosis).\n\nLactate Ringer bolus was given at 10 ml/kg in the emergency department, followed by 5% Dextrose in 0.33% Saline 500 ml at an infusion rate of 29 ml/h over 6 hours without KCL until diuresis was obtained. She was started on Ceftriaxone 50 mg/kg/day for suspected sepsis, stabilised and sent to the ward where she continued to receive 500 ml of 5% Dextrose in 0.9% Saline at 20 ml/hr.\n\nAmong the examinations, a blood count revealed leukocytosis at 39.0 x 103/uL, severe anaemia 5.6 g/dL, thrombocytosis 502 x 103/uL, the rest of the results are detailed in. He was transfused with 50 ml of filtered and leuko-reduced red blood cells and 40 cc of fresh frozen plasma due to altered coagulation times. Enteral feeding was initiated by nasogastric tube and infusion was decreased to 15 ml/h of 5% Dextrose in 0.9% Saline 500 cc, and continued with negative water balance.\n\nOn day 2, initial peripheral blood culture was reported as Gram positive cocci in clusters, Oxacillin was added at 200 mg/kg/day, Ceftriaxone was increased to 75-100 mg/kg/day, total fluids to 120 ml/kg/day and calcium was corrected (value received 6.38 mg/dL).\n\nOn her 3rd day she lost venous access, so a central venous catheter (CVC) was placed. She was hypovolemic with subhydrated oral mucosa, increased respiratory work, cold extremities and capillary refill time of 3-4 seconds. Ringer's lactate was given at a load of 20 ml/kg in one hour. Arterial blood gas revealed uncompensated metabolic acidosis with pH 7.26, HCO3 13 mmol/L, PCO2 28.4 mmHg, PO2 39.2 mmHg, lactate 2.8 mmol/L. She was intubated and transferred to the paediatric intensive care unit (PICU) where she was placed on mechanical ventilation.\n\nTotal fluids of 100 cc/kg, infused epinephrine, low-salt albumin, and 10% calcium gluconate were administered, and fentanyl was changed to remifentanil due to elevated liver enzymes.\n\nThe blood culture of admission reported growth of methicillin-resistant Staphylococcus aureus (MRSA), Oxacillin was omitted and Clindamycin was added at 40 mg/kg/day; the blood culture of admission on the second day of admission to the ICU with Gram-negative bacillus smear was positive, and Ceftriaxone was changed to Ceftazidime at 150 mg/kg/day.\n\nOn his first day in the ICU, a substantial increase in serum biomarkers of cardiac damage was documented, the echocardiogram showed mild mitral and tricuspid regurgitation, left ventricular dilatation, left ventricular ejection fraction (LVEF) 58%, no evidence of thrombi, vegetations or pericardial effusion, and he was diagnosed with acute myocarditis. Milrinone was started at 0.4 mcg/kg/min, furosemide and IV immunoglobulin 1 g/kg single dose.\n\nThe second day blood culture the germ was identified as Bacillus clausii, identified by the system (VYTEK 2TM), the susceptibility profile was not performed because the team did not have cut points for this germ, for this reason the antibiotic coverage was adjusted, considering it was not a contaminant, Ceftazidime was changed to Ciprofloxacin at 30 mg/kg/day and Ceftaroline was added at 8 mg/kg every 8 hours along with Clindamycin for MRSA. The 3 subsequent blood cultures with intervals of 48 hours between each were positive in both peripheral blood and CVC for isolation of B. clausii.\n\nOn his 6th day in hospital, the gastrointestinal panel (Maripoc gastro test methodology) performed on the second day detected Clostridiodes difficile toxin A/B, the tests for Campylobacteryeyuni, Norovirus GI, Norovirus GII.4, Adenovirus and Rotavirus were negative. Following these findings, therapy was escalated to IV Vancomycin at a dose of 60 mg/kg/day and metronidazole was added orally. Ceftaroline, clindamycin and ciprofloxacin were omitted, covering both B. clausii and C. difficile and MRSA .\n\nHIV testing, serology for Chagas and SARS-CoV-2 antigen by immunofluorescence (FIA) were negative, immunoglobulins were within normal limits.\n\nOn the seventh day, arterial hypertension was reported and spirinolactone was added to the management.\n\nOn the 8th day, the laboratory tests showed altered coagulation times and increased azotaemia associated with anuria that had lasted for 12 hours. However, due to the patient's condition, a peritoneal catheter was not placed, the vancomycin dose was adjusted and vitamin K was administered. The patient continued to have anuria and anasarca, and she developed sustained hypotension. Noradrenaline was added, but her condition deteriorated with multisystem organ failure and she died twelve days after admission. No autopsy was performed because the mother refused permission for cultural reasons.\n",
+    "diff_label_texts": "This story is about a 4‑month‑old baby girl from an Indigenous community in rural Panama. The nearest clinic was three hours away by canoe. She was not getting enough protein and calories. She suddenly had bad diarrhea. She got very dehydrated, like a plant without water. A probiotic medicine called Enterogermina was given at the start. She was moved to a large hospital. She arrived breathing hard. She was in shock, which means her blood was not carrying enough to her organs. A blood test found a hard‑to‑treat germ called MRSA. A stool test found a germ called C. difficile that can cause diarrhea. Later blood tests from her arm and from a central line found Bacillus clausii. Doctors tried many antibiotics, but the germs did not respond. Her organs began to fail. She died 12 days after she got to the hospital.",
+    "summary": "4-month-old lactating infant, indigenous ethnicity, from the rural interior of Panama, 3 hours by canoe from the nearest health subcenter, with protein-caloric malnutrition, who presented with acute diarrhea and moderate-severe dehydration, receiving Enterogermina as part of the initial treatment. She was transferred to a third-level hospital, where she arrived with respiratory distress and signs of shock. The initial blood culture reported growth of methicillin-resistant Staphylococcus aureus (MRSA), the gastrointestinal panel was positive for Clostridiodes difficile, and later growth was confirmed in serial blood cultures of peripheral blood and central venous catheter, of Bacillus clausii. With a torpid evolution and resistance to multiple antibiotic regimens, she died of multisystem organ failure twelve days after admission.\n"
+  },
+  {
+    "doc_id": 54,
+    "label": "intermediate_health_literacy",
+    "fulltext": "4-month-old indigenous lactating mother from the rural area of the interior of Panama, from the town of Urracá, 3 hours by canoe from the nearest health center. Her background included being the fourth daughter, born by vaginal delivery at home by a relative, without prenatal controls, her weight, height and Apgar score at birth are unknown. She did not breastfeed and was fed with powdered milk formula with iron for children under 6 months, receiving 3 ounces every 4 hours.\n\nThe nuclear family was composed of 6 people (parents and 4 children) who lived in a house with walls and floor of boards and palm roof, 2 rooms, without electricity, they were illuminated with kerosene lamps, water from a well, excreta in a river and they burned the garbage, their economic income came from subsistence agriculture.\n\nHe had no health care in his first 4 months of life and did not receive the vaccinations included in the national expanded programme of immunizations. According to his parents, his neurodevelopment was normal until his hospitalization.\n\nThe minor consulted in a health center with a history of 4 days of diarrhoea, without mucus or blood associated with vomiting of food content (the mother gave her tea because she could not tolerate milk), afebrile and without respiratory symptoms. Oral fluids and 4 doses of Enterogermina® (B. clausii: two billion spores/5 mL) were administered. Due to the lack of supplies (they did not have catheters, or intraosseous for the administration of intravenous fluids) she was transferred to a second-level hospital in the provincial capital and then to our institution in Panama City with a diagnosis of acute gastroenteritis and severe dehydration.\n\nHe presented to the emergency department with a consciousness compromise, dehydration characterised by a tearless cry, dry oral mucosa. He had oedema of +++ hands, feet, abdomen and face. He was afebrile and had signs of shock, capillary refill time > 2 seconds, cold extremities, filiform pulse and marble skin, heart rate 170 bpm, respiratory rate 55 bpm, blood pressure 91/37 mmHg, oxygen saturation 99%. He weighed 4.7 kg and was 56 cm tall at admission, Z-score height/age -2.52, weight/height and weight/age Z-scores were not quantifiable due to severe dehydration. On segmental examination, there were fine crepitus in both lung bases and erythematous-squamous lesions with desquamation of skin and others with hypopigmentation of trunk and upper limbs (interpreted as pellagroid dermatosis).\n\nLactate Ringer bolus was given at 10 ml/kg in the emergency department, followed by 5% Dextrose in 0.33% Saline 500 ml at an infusion rate of 29 ml/h over 6 hours without KCL until diuresis was obtained. She was started on Ceftriaxone 50 mg/kg/day for suspected sepsis, stabilised and sent to the ward where she continued to receive 500 ml of 5% Dextrose in 0.9% Saline at 20 ml/hr.\n\nAmong the examinations, a blood count revealed leukocytosis at 39.0 x 103/uL, severe anaemia 5.6 g/dL, thrombocytosis 502 x 103/uL, the rest of the results are detailed in. He was transfused with 50 ml of filtered and leuko-reduced red blood cells and 40 cc of fresh frozen plasma due to altered coagulation times. Enteral feeding was initiated by nasogastric tube and infusion was decreased to 15 ml/h of 5% Dextrose in 0.9% Saline 500 cc, and continued with negative water balance.\n\nOn day 2, initial peripheral blood culture was reported as Gram positive cocci in clusters, Oxacillin was added at 200 mg/kg/day, Ceftriaxone was increased to 75-100 mg/kg/day, total fluids to 120 ml/kg/day and calcium was corrected (value received 6.38 mg/dL).\n\nOn her 3rd day she lost venous access, so a central venous catheter (CVC) was placed. She was hypovolemic with subhydrated oral mucosa, increased respiratory work, cold extremities and capillary refill time of 3-4 seconds. Ringer's lactate was given at a load of 20 ml/kg in one hour. Arterial blood gas revealed uncompensated metabolic acidosis with pH 7.26, HCO3 13 mmol/L, PCO2 28.4 mmHg, PO2 39.2 mmHg, lactate 2.8 mmol/L. She was intubated and transferred to the paediatric intensive care unit (PICU) where she was placed on mechanical ventilation.\n\nTotal fluids of 100 cc/kg, infused epinephrine, low-salt albumin, and 10% calcium gluconate were administered, and fentanyl was changed to remifentanil due to elevated liver enzymes.\n\nThe blood culture of admission reported growth of methicillin-resistant Staphylococcus aureus (MRSA), Oxacillin was omitted and Clindamycin was added at 40 mg/kg/day; the blood culture of admission on the second day of admission to the ICU with Gram-negative bacillus smear was positive, and Ceftriaxone was changed to Ceftazidime at 150 mg/kg/day.\n\nOn his first day in the ICU, a substantial increase in serum biomarkers of cardiac damage was documented, the echocardiogram showed mild mitral and tricuspid regurgitation, left ventricular dilatation, left ventricular ejection fraction (LVEF) 58%, no evidence of thrombi, vegetations or pericardial effusion, and he was diagnosed with acute myocarditis. Milrinone was started at 0.4 mcg/kg/min, furosemide and IV immunoglobulin 1 g/kg single dose.\n\nThe second day blood culture the germ was identified as Bacillus clausii, identified by the system (VYTEK 2TM), the susceptibility profile was not performed because the team did not have cut points for this germ, for this reason the antibiotic coverage was adjusted, considering it was not a contaminant, Ceftazidime was changed to Ciprofloxacin at 30 mg/kg/day and Ceftaroline was added at 8 mg/kg every 8 hours along with Clindamycin for MRSA. The 3 subsequent blood cultures with intervals of 48 hours between each were positive in both peripheral blood and CVC for isolation of B. clausii.\n\nOn his 6th day in hospital, the gastrointestinal panel (Maripoc gastro test methodology) performed on the second day detected Clostridiodes difficile toxin A/B, the tests for Campylobacteryeyuni, Norovirus GI, Norovirus GII.4, Adenovirus and Rotavirus were negative. Following these findings, therapy was escalated to IV Vancomycin at a dose of 60 mg/kg/day and metronidazole was added orally. Ceftaroline, clindamycin and ciprofloxacin were omitted, covering both B. clausii and C. difficile and MRSA .\n\nHIV testing, serology for Chagas and SARS-CoV-2 antigen by immunofluorescence (FIA) were negative, immunoglobulins were within normal limits.\n\nOn the seventh day, arterial hypertension was reported and spirinolactone was added to the management.\n\nOn the 8th day, the laboratory tests showed altered coagulation times and increased azotaemia associated with anuria that had lasted for 12 hours. However, due to the patient's condition, a peritoneal catheter was not placed, the vancomycin dose was adjusted and vitamin K was administered. The patient continued to have anuria and anasarca, and she developed sustained hypotension. Noradrenaline was added, but her condition deteriorated with multisystem organ failure and she died twelve days after admission. No autopsy was performed because the mother refused permission for cultural reasons.\n",
+    "diff_label_texts": "A 4‑month‑old indigenous infant from a remote rural area of Panama (about three hours by canoe from the nearest health subcenter) with protein‑calorie malnutrition presented with acute diarrhea and moderate‑to‑severe dehydration. She had limited prior health care, had not received routine vaccinations, and was initially given Enterogermina (Bacillus clausii spores) and oral rehydration before being transferred to higher‑level hospitals because local facilities lacked supplies. On arrival at a third‑level hospital she had respiratory distress and signs of shock and was admitted to the pediatric intensive care unit, intubated, and treated with fluids, blood products, and multiple antibiotics. Initial blood culture grew methicillin‑resistant Staphylococcus aureus (MRSA); a gastrointestinal panel later detected Clostridioides difficile. Subsequent serial blood cultures from both peripheral blood and the central venous catheter repeatedly grew Bacillus clausii. Despite changes to antibiotic therapy to cover MRSA, C. difficile, and B. clausii, she developed worsening multisystem organ failure, including cardiac and kidney dysfunction, and died twelve days after admission.",
+    "summary": "4-month-old lactating infant, indigenous ethnicity, from the rural interior of Panama, 3 hours by canoe from the nearest health subcenter, with protein-caloric malnutrition, who presented with acute diarrhea and moderate-severe dehydration, receiving Enterogermina as part of the initial treatment. She was transferred to a third-level hospital, where she arrived with respiratory distress and signs of shock. The initial blood culture reported growth of methicillin-resistant Staphylococcus aureus (MRSA), the gastrointestinal panel was positive for Clostridiodes difficile, and later growth was confirmed in serial blood cultures of peripheral blood and central venous catheter, of Bacillus clausii. With a torpid evolution and resistance to multiple antibiotic regimens, she died of multisystem organ failure twelve days after admission.\n"
+  },
+  {
+    "doc_id": 55,
+    "label": "intermediate_health_literacy",
+    "fulltext": "A 2-year-old female presented with a 1-year history of painless left progressive proptosis with no reported systemic diseases or family history. Ophthalmologic examination revealed light sensation as the only vision in the left eye, along with proptosis, inward and upward eyeball displacement, and restricted extraocular muscle movements in downward and outward directions. An irregularly shaped, well-defined soft mass was palpable in the inferior aspect of the left orbit, accompanied by left lower eyelid ectropion. The pupil was enlarged (4 mm in diameter), and pupillary reaction was absent. The remaining anterior segment examination showed no apparent abnormalities. Fundus examination was challenging due to the child’s size. Hertel exophthalmometry readings measured 10.5 mm in the right eye and 18 mm in the left. Magnetic resonance imaging (MRI) revealed a well-circumscribed mass, displaying hypointense signals on T1-weighted images and hyperintense signals on T2-weighted images. Contrast-enhanced imaging demonstrated no significant improvement. A transconjunctival approach via the inferior fornix with canthotomy and cantholysis was performed, revealing a grayish-white cystic mass with a distinct boundary from surrounding tissues. During posterior separation to the eyeballs’ posterior part, tight adhesion to the optic nerve was observed. Due to the mass’s substantial size and the restricted surgical field, volume reduction was necessary. Approximately 12.5 mL of the fluid was aspirated, and the mass was completely excised. Histopathological examination disclosed a fibrous capsule wall covered with squamous and glandular epithelium, along with visible brain tissue and a cartilage-like matrix consistent with orbital teratoma. One month postsurgery, the patient exhibited enophthalmos, conjunctival hyperemia, and keratitis on ocular examination. This was attributed to the mass’s prior enlargement of the orbital cavity, resulting in postoperative enophthalmos. The cornea could not adhere to the eyelids, creating a space and causing corneal inflammation. After obtaining the consent of the patient’s guardian, a second operation involved the implantation of an allogeneic sclera into the orbit to increase the orbital volume, alleviate fossa pitting and restore keratitis to normal. No recurrence of the teratomas was noted during the 1-year follow-up. The patient still had minor enophthalmos and outer canthus abnormality. The visual acuity remained consistent with pre-operation levels. Hertel exophthalmometry readings measured 10.5 mm in the right eye and 8 mm in the left. The remaining anterior segment examination showed no apparent abnormalities.",
+    "diff_label_texts": "A 2-year-old girl had a 1-year history of painless, progressive protrusion of the left eye with the eye displaced inward and upward; vision in that eye was only light perception. MRI showed a well-defined mass in the orbit that was dark on T1-weighted images and bright on T2-weighted images, with no clear contrast enhancement. The mass was removed through the lower eyelid conjunctiva using a transconjunctival approach with canthotomy and cantholysis to widen the surgical field; the tumor was cystic, gray‑white, and tightly adherent to the optic nerve, so about 12.5 mL of fluid was aspirated to reduce its size before complete excision. Histology and immunohistochemistry confirmed an orbital teratoma, showing squamous and glandular epithelium, brain tissue, and cartilage‑like material. One month after the first surgery the child developed enophthalmos (a sunken eye), conjunctival redness, and keratitis because removal of the large mass left reduced orbital volume and the cornea could not fully close. A second operation implanted donor (allogeneic) scleral tissue into the orbit to increase volume, correct the posterior fossa indentation, and allow the cornea to recover. At 1-year follow-up there was no tumor recurrence; vision remained at the preoperative level and the child had only minor residual enophthalmos and an outer canthus abnormality.",
+    "summary": "Patient concerns: A 2-year-old female child was presented exhibiting proptosis and inward and upward eyeball displacement. Enhanced magnetic resonance imaging revealed a well-circumscribed mass, persisting with hypointense signals on T1-weighted images (T1WI) and hyperintense signals on T2-weighted images (T2WI).\n\nDiagnoses: The diagnosis of teratoma was confirmed finally through histological and immunohistochemical exams.\n\nInterventions: A transconjunctival approach via the inferior fornix, coupled with canthotomy and cantholysis, was performed. However, a month postsurgery, the patient developed enophthalmos, conjunctival hyperemia, and keratitis upon ocular examination. A second operation involved the implantation of allogeneic sclera into the orbit to increase orbital volume, improve the pitting of the fossa, and restore keratitis to normal.\n\nOutcomes: No recurrence and other complications were noted during the 1-year follow-up."
+  },
+  {
+    "doc_id": 57,
+    "label": "intermediate_health_literacy",
+    "fulltext": "It is a case study, approved by the Research Ethics Committee (CEP) under number 1.012.635. The prior authorization of the relatives and the participant was requested from the signature of the Free and Informed Consent (TCLE) and the Free and Informed Consent (TALE).\n\nThe participant in this study is a female student in the 3rd year of elementary school. In the first evaluation, in 2018, the child was 8 years and 2 months old, while in the second evaluation, in 2019, she was 9 years and 6 months old. The interval between the evaluations occurred due to the fact that it is a public service. Thus, the laboratory was absent from activities during the holidays. In addition, it is important to consider that the appointments were only made once a week and, during that period, the participant was absent, which also prolonged the process. As for her history, she was born at term and presented adequate neuropsychomotor and linguistic development. The child was born and lived in a French-speaking country until the age of 2 years, but had exposure to another language at home, since her parents are Brazilian Portuguese speakers. However, her first words were in French. When she returned to Brazil, she went through two private schools. In the first school, she was unable to communicate, as she only expressed herself in French. After that experience, at the age of 3, she began studying in a French school, still in Brazil. Over the years, she presented difficulty in acquiring reading and writing; for that reason, she repeated the 1st year of elementary school, at the request of her mother. At the age of 6, she began studying in a bilingual Portuguese-English school. At the age of 8 years old, she underwent evaluation by an interdisciplinary team in the areas of speech therapy and neuropsychology, finding the diagnosis of developmental dyslexia (DD) and high abilities/giftedness (AH/S). Soon after, she was referred to the evaluation of reading and writing in the Laboratory of Written Language, Interdisciplinarity and Learning - LEIA/UFRN.\n\nPhases of the study: four assessment sessions for each moment - pre and post intervention (T1 and T2, respectively) - and 20 sessions of phonological remediation, once a week for 60 minutes. The intervention took place in the second semester of 2018, where parents were not very engaged due to work demands.\n\nAssessments were conducted individually over a one-hour period. They included tasks to assess performance in phonological processing - phonological working memory, phonological awareness and mental lexical access - reading and writing.\n\nThe following protocols were used to evaluate the child:\n\nPhonological awareness: to evaluate this ability, the Consciência Fonológica Instrumento de Avaliação Sequencial - CONFIAS (11) was used. This protocol proposes tasks of synthesis, segmentation, rhyme, alliteration, initial and final syllable identification, exclusion and transposition. First, syllabic awareness, formed by nine items, is analyzed, followed by phonemic awareness, formed by seven items. Each hit is equivalent to one point, with 40 for syllabic awareness and 30 for phonemic awareness, totaling 70 points. Its results should be compared with the expected writing hypotheses based on Ferreiro and Teberosky (12). In this way, the following normal values were used: for the syllabic-alphabetic writing hypothesis, 27, 12 and 39 for the syllabic, phonemic and total score, respectively; for the alphabetic writing hypothesis, 31, 15 and 46.\n\nPhonological working memory: The Phonological Working Memory Test was used (13). In the application of this protocol, the assessor should begin with the non-word test, which consists of 40 invented words. The assessor should then say each word in the list, asking the child to repeat it immediately. The child has two attempts to repeat the words correctly. In the first attempt, each correct answer is worth two points, in the second attempt, the child is awarded one point, and in the third attempt, the child is awarded zero points. After this, the assessor should move on to the test of digits in direct and reverse order, which is scored in the same way as the pseudo-words. Depending on the age of the participant at the time of the assessments, the normal values of 69, 13 and 6 were used for pseudo-words, direct and reverse digits, respectively.\n\nAccess to the mental lexicon: the Rapid Automatic Naming Test (RAN)(14) was used in the evaluation and the Automatic Naming Test (TENA)(15) in the re-evaluation. Both tests aim to estimate the individual's ability to name a sequence of stimuli, that is, to measure the speed at which the child can verbalize a visual stimulus quickly. Two protocols were used, since the TENA had not yet been published at the time of the first evaluation. In addition, the TENA is a current and more complete protocol for the verification of normality, as it allows analysis according to age and months. The two tests used have similar application and are divided into four boards, where the child must name colors, objects, letters and digits. The naming must be done with the same movement that is used for reading - from left to right and from top to bottom. For T1, which used the RAN, the normality values correspond to children aged between 8 years and 8 years and 11 months, due to the age of the participant in that period, thus, it should have a score of 28, 29, 52 and 46 seconds for the subtests of digits, letters, objects and colors, respectively. For T2, the normality values of the age of 9 years and 6 months of the protocol (TENA) were used, with an expected score of 35, 32, 50, 53 seconds for the subtests of digits, letters, objects and colors, respectively.\n\nReading: First, the Protocol for the Assessment of Reading of Words/Pseudowords Isolated – LPI(16) was used, in which the child is asked to read aloud words and pseudowords, which are scored. 19 regular words, 20 irregular words and 20 pseudowords are arranged in black Arial font, size 24 and white background. The child may obtain a total of 59 points, since each correct reading is worth one point. After this, the Protocol for the Assessment of Reading of Expository Texts was used(17). This instrument aims to assess reading comprehension through directed questions about texts compatible with the subject's school year. It assesses and times patterns of silent and oral reading. This allows the reading level to be verified and compared. In addition, the number of words read per minute is averaged, allowing the reading speed to be verified and compared.\n\nWriting: To evaluate the writing, the child was asked to produce a text on a topic of their interest. After finishing the story, the professional asked the child to read out loud what was written. Furthermore, the child was asked to write the target words of the LPI(16) on a separate sheet, in order to carry out a dictation of words and pseudo-words. With this, a qualitative investigation of the writing was carried out, based on the orthographic analysis of Zorzi and Ciasca(18).\n\nThe remediation was based on a program used for children with dyslexia(19) and included activities that aimed to improve phonological abilities, such as: identification of graphemes and phonemes, phoneme pairs, syllable pairs, word pairs, addition and subtraction of phonemes, syllabic and phonemic manipulation, rhymes, alliteration, access to mental lexicon, visual working memory, auditory working memory and reading training. In all sessions, these activities were explored in a playful way, mainly directed to the metalinguistic aspects of phonological awareness. In reading training, the child was exposed to children's books from the Mico Maneco collection. This collection has various stories that increase the level of complexity of words, so it is possible to follow the child's progress. The activities performed and the child's evolution were described in his/her medical record at the end of each session.\n\nAnalysing the results found, with regard to performance in phonological awareness, in both assessments the child presented performance consistent with the hypotheses of writing presented in each period. In the first assessment, he received the syllabic-alphabetic writing hypothesis and in the second, the alphabetic one, demonstrating progress. The performance score progressed in both categories of the skill, syllabic (T1 = 35; T2 = 37) and phonemic (T1 = 14; T2 = 20) (Table 1). The progress of 4 successes in the phonemic level is highlighted, which can be explained due to the phonological remediation having been performed with focus on the phonemic level.\n\nThe results of phonological working memory at the time prior to phonological remediation expressed below-expected performance for the pseudo-word category, with 66 points in T1, with expected performance for T1 (ET1) of 69, and for the reverse-order digits category (T1 = 04; ET1 = 06) (Table 1). Despite this, it presented results within the expected range for the reverse-order digits category (T1 = 20; ET1 = 13). In the post-intervention evaluation (T2), the results are adequate for the age. It is also possible to notice advances in this skill in all categories, pseudo-word (T1 = 66; T2 = 69), reverse-order digits (T1 = 04; T2 = 12) (Table 1), which requires aspects of executive functions that assist in the rapid storage of the response, a differential aspect in high abilities.\n\nAs for the automatic rapid naming, it is noted that in T1, the performance is inadequate for the standards of normality in all subtests. It is also possible to say that, in T2, the performance was below the expected for the categories of digits (T2 = 41; ET2 = 35), objects (T2 = 59; ET2 = 50) and colors (T2 = 56; ET2 = 53). Only the category of letters presented results within the expected (T2 = 29; ET2 = 32). On the other hand, the advance in the speed of naming is visible for the subtests of letters (T1 = 37; T2 = 29), objects (T1 = 62; T2 = 59) and colors (T1 = 60; T2 = 56), with the exception of digits (T1 = 37; T2 = 41) (Table 1). With the decrease of the time of naming of the stimuli, it is possible to say that the child becomes more effective to access the mental lexicon at the level of the phonological and visual representation, which is also not usual in isolated dyslexia.\n\nAs for reading, in T1 she presented an alphabetic level and in T2 an orthographic level. In the first test, it was noted that there was difficulty mainly with visually similar letters and phonologically close. In addition, the student used sub-vocal support to decode and had an average reading of 20 words per minute, which demonstrates extremely slow decoding and is far below what is expected for her schooling. In the reassessment, she had an average of 94.4 words per minute in oral reading, which is considered adequate for her schooling. She demonstrated presence of prosody, rhythm, global reading, interest and adequate understanding. Qualitatively, it is observed that the child, even with adequate performance, read with a low intensity of speech, still demonstrating insecurity in carrying out the task.\n\nIn writing, it can be observed that in T1 the child had inadequate pencil grip, imprecise writing, with letter changes, omissions, hyper and hyposegments, repetition of words and low use of cohesive elements. In this period, it was shown with writing in the transition from the syllabic-alphabetic phase to the alphabetic phase. In T2 no significant change was observed, since his writing continued to be imprecise, with little intelligibility of the content, visual similarities between letters (such as “d” and “b”) and lack of punctuation. According to the sample collected, it was shown in the alphabetic phase of writing, although difficulties not expected for his age persisted. Despite this, it is noted that he used a greater repertoire in the use of vocabulary for the lexicon of visual input.\n\nAfter the analysis of the results in their entirety, it can be observed that the written language skills advanced during the interval between the evaluations, despite the persistence of consonant characteristics with dyslexia, as it still presents performance below the expected in the access to the mental lexicon and in writing - with the presence of exchanges between phonemes that are audibly and visually similar in a persistent way, omission of letters and hypersegmentation.\n",
+    "diff_label_texts": "This case report describes a 9-year-old girl who was diagnosed with developmental dyslexia alongside high abilities (giftedness). The team compared her phonological processing, reading and writing before and after a program of 20 weekly phonological remediation sessions. Before intervention (age 8y2m) she showed weak phonological processing, reading at an alphabetic level, and writing in transition between syllabic-alphabetic and alphabetic stages. The remediation targeted phonological awareness, working memory, rapid naming and reading practice. After treatment (age 9y6m) phonological skills improved (notably phonemic awareness), phonological working memory reached age-appropriate levels, and rapid naming times improved for letters, objects and colors (digits stayed below expectation). Her reading advanced from an alphabetic to an orthographic level: oral reading rate rose from about 20 words per minute to about 94 words per minute, with better prosody and comprehension. Writing also showed gains and was classified at the alphabetic phase, but remained imprecise with letter reversals, omissions and segmentation errors that reflect persistent dyslexic features. In summary, phonological remediation produced clear gains in phonology and reading fluency, and helped consolidate alphabetic writing, but some difficulties in lexical access and accurate spelling persisted.",
+    "summary": "This study is a case report of the evaluation and intervention process of a 9-year-old child with the paradoxical combination of high abilities associated with dyslexia. The objective was to compare the performance in the tasks of phonological processing, reading and writing before and after phonological remediation. In the first evaluation, the child presented an alphabetic level in reading, a transition phase between the syllabic-alphabetic and alphabetic levels in writing and a performance below the expected level in phonological processing abilities. After the intervention, there was an improvement in phonological processing abilities, consolidation of alphabetic writing and of the orthographic level of reading.\n"
+  },
+  {
+    "doc_id": 59,
+    "label": "intermediate_health_literacy",
+    "fulltext": "The 52-year-old man tested positive for SARS-CoV-2 using a self-test kit after having a cold. He returned to work without fever after resting for two days, but lost consciousness while working outdoors in an ambient temperature of 35°C for five hours. Upon admission to the local hospital’s emergency department, his core temperature (Tc) was recorded as 40°C. The patient presented with persistent coma, dyspnea and gastrointestinal hemorrhage. No underlying diseases and relative family history was noted. Based on the characteristic presentation of hyperpyrexia, coma and multiple organ damage, a diagnosis of HS was established. He was admitted to emergency intensive care unit (ICU) of the local hospital and then received mechanical ventilation. The test results indicated the presence of pulmonary infection, hepatic and renal dysfunction, myocardial ischemia and coagulation disorders. The patient received initial management including rehydration (intravenously infused Lactated Ringer’s solution and normal saline at a rate of 2.5mL/kg∙h), intravenous administration of Piperacillin Sodium and Tazobactam Sodium, vasoactive medications for blood pressure support, continuous mechanical ventilation, and continuous renal replacement therapy (CRRT) to manage subsequent anuria. The patient received plasma transfusion and was administered Tranexamic acid on day 5. The worsening of his condition led to his admission to the medical ICU of our hospital 7 days after HS.\n\nFollowing admission, Reverse-transcription polymerase chain reaction (RT-PCR) testing of a nasopharyngeal swab yielded positive results for SARS-CoV-2. The patient was diagnosed with HS and severe COVID-19 based on China’s COVID-19 Diagnosis and Treatment Program (trial version 10): 1. real-time fluorescent RT-PCR detection of SARS-CoV-2 nucleic acid is positive; 2. respiratory failure and requires mechanical ventilation; 3. shock; 4. combined with multiple organ failure requiring intensive care. The patient had no contact with COVID-19 diagnosed patients or healthcare workers in the hospital, indicating community-acquired infection. The physical examination showed a Glasgow Coma Scale (GCS) score of 3/15, with scores of 1 for eye-opening, verbal response, and motor response. Additionally, the pupils were symmetrical and non-reactive. The heart rate was recorded at 106 bpm and blood pressure was maintained at 126/77 mmHg by continuously infusing norepinephrine at a rate of 0.4 ug/kg·min. The laboratory test results indicated a severe infection, along with anemia, thrombocytopenia, disseminated intravascular coagulation (DIC), as well as acute liver and kidney injury. The white blood cell count (WBC) decreased from 3.55×109/L to 3.13×109/L, lymphocytes significantly decreased from 0.25×109/L to 0.1×109/L, and neutrophil percentage (N%) increased to 85.3%. The Procalcitonin level measured 2.81 ng/mL and C-reactive protein (CRP) level was 32.6 mg/L. Sputum culture testing yielded Stenotrophomonas Maltophilia and Candida lipolytica. The central venous catheter culture test detected Staphylococcus epidermidis, but the continuous blood culture test yielded no positive results. The Computed Tomography (CT) scan revealed bilateral frontal subdural effusion, consolidation and atelectasis in the lower lungs, inflammation in the right upper lobe, bilateral pleural effusion, and a small amount of abdominal fluid.\n\nThe patient received synchronized intermittent mandatory ventilation with a positive end expiratory pressure of 5 mmH2O and an oxygen concentration of 80% and continuous administration of norepinephrine and pituitrin to sustain normal blood pressure. Polyene phosphatidylcholine, adenosylmethionine budisulfonate, ulinastatin, and hemofiltration have been employed for the management of hepatic and renal dysfunction. The antibiotic was substituted with Meropenem and Thymalfasin was administered for 20 days to augment immune function. Mannitol was used to alleviate intracranial pressure for 3 days. To improve coagulation dysfunction, the patient received plasma and cryoprecipitate transfusions, continuous intravenous infusion of heparin sodium at 6000u/day and CRRT with sodium citrate for anticoagulant (8g/day) on day 7. Platelet transfusion was administered after 9 days of HS. His Tc fluctuated between 36 °C and 38.5 °C. CRRT was administered without anticoagulant on day 8. The patient had gastrointestinal hemorrhage and fever after 9 days of HS, but electronic gastroenteroscopy showed no signs of active bleeding. He underwent red blood cell suspension transfusion, hemostasis treatment and gastric acid suppression. Teicoplanin was added due to the presence of Methicillin-resistant Staphylococcus aureus isolated from sputum culture. The patient regained consciousness on day 13 with a GCS score of 14/15 and presented with a moderate fever. Gastrointestinal hemorrhage was not observed. Mechanical ventilation was discontinued and the tracheal tube was removed. But the creatinine levels increased following the suspension of CRRT on day 12.\n\nOn day 17, he developed sudden dyspnea with desaturation (oxygen saturation <85%) followed by a high fever (Tc: 39.3°C), necessitating reintubation and mechanical ventilation. Bronchoscopy revealed less sputum in both lungs and subbranches. He experienced a recurrence of coma, with a GCS score of 3/15. WBC increased to 14.94×109/L and NEU increased to 13.77×109/L. The levels of serum total bilirubin rose to 235.2 µmol/L, while creatinine increased to 441µmol/L. The brain CT scan revealed an ischemic stroke in the right frontal lobe and a hemorrhagic infarction in the right occipital lobe. The patient underwent cooling therapy using CRRT with ice-cold replacement fluid, along with persistent administration of Meropenem and Teicoplanin for anti-infection treatment. Carpofungin was added on day 18 due to the observed elevation in serum levels of Aspergillus galactomannan, Aspergillus IgG antibody, and Candida mannan. The RT-PCR testing for SARS-CoV-2 returned negative results.\n\nThe patient’s fever and infection improved on day 20, but he subsequently developed cerebral hemorrhage and hernia with bilateral dilated pupils. The dehydration therapy was used to reduce intracranial pressure, as surgery was refused by his family. On day 22, indicators of infection, levels of aspartate aminotransferase and creatinine increased again. Carbapenem-resistant Acinetobacter baumannii and A. fumigatus were cultured in the bronchoalveolar lavage fluid. The combination of Meropenem, Teicoplanin, and Carpofungine was administered for anti-infective therapy. The patient’s condition progressively worsened over the next 7 days, ultimately resulting in his demise on day 29. The patients’ inflammatory indicators, cytokines, and coagulation indicators are presented in Table 1.",
+    "diff_label_texts": "This report describes the first known case of heatstroke occurring together with SARS‑CoV‑2 infection in a 52‑year‑old man. He had a recent cold and a positive self-test for COVID‑19, then returned to work and lost consciousness after five hours outdoors in 35°C heat. On arrival at the hospital his core temperature was 40°C and he was comatose with breathing problems and gastrointestinal bleeding; clinicians diagnosed heatstroke. He was admitted to the ICU, placed on a ventilator, given IV fluids, antibiotics, blood‑pressure support, and continuous renal replacement therapy when his kidneys failed. Laboratory tests showed severe infection, low platelets and a severe clotting disorder (disseminated intravascular coagulation), plus liver, kidney and heart injury. Sputum and airway cultures later grew several pathogens (including Stenotrophomonas, Candida, MRSA, Acinetobacter and Aspergillus), and he was treated with broad antibiotics, antifungals, plasma and blood products, and anticoagulation as needed. After these treatments his fever subsided and he regained consciousness by about day 13 and was briefly taken off the ventilator. Several days later he suddenly worsened with respiratory failure, high fever and a return to coma; brain imaging showed an ischemic stroke and a hemorrhagic infarct. Despite further intensive care, he developed a large cerebral hemorrhage with brain herniation; surgery was not performed and his condition progressed to multiple organ dysfunction syndrome (MODS). The combination of multi‑pathogen pulmonary infection and an intractable coagulopathy ultimately led to MODS and death on day 29.",
+    "summary": "We report the first case of heatstroke comorbid with Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection in a 52-year-old male. After receiving intravenous antibiotics, organ protection measures, and treatment for coagulation disorders, his fever and coma resolved. However, he developed dyspnea and cerebral hemorrhage after several days. This patient experienced a multi-pathogen pulmonary infection and an intractable coagulopathy that ultimately resulted in MODS and death."
+  },
+  {
+    "doc_id": 60,
+    "label": "intermediate_health_literacy",
+    "fulltext": "A 19-year-old female presented to our hospital’s emergency room with a chief complaint of a two-day history of headache, accompanied by recurrent nausea, vomiting, and a one-day fever. On admission, her physical examination revealed a high fever of 39.1°C, elevated blood pressure at 189/120 mmHg, and a pulse rate of 148 beats per minute. Laboratory results indicated an elevated white blood cell count of 14.77×10^9/L and a neutrophil count of 13.55×10^9/L, suggesting a possible infection or inflammatory response. Initial empirical treatment with antibiotics was administered due to suspected infection, but her symptoms persisted. Given her abnormal vital signs, elevated inflammatory markers, and lack of symptom improvement, the patient was admitted for further diagnostic evaluation and transferred to the intensive care unit for close monitoring. A year prior, the patient had presented with similar symptoms and was diagnosed with myocarditis at a local hospital based on clinical findings at that time. During that hospitalization, she was also diagnosed with hypertension and prescribed antihypertensive medications. However, after discharge, the patient did not adhere to the prescribed antihypertensive therapy and did not regularly monitor her blood pressure. Additionally, it is notable that her father had a history of sudden, unexplained death.\n\nTo investigate the underlying etiology of the patient’s symptoms, a chest computed tomography (CT) scan was performed. Incidentally, this scan revealed a left adrenal mass with soft tissue density, measuring 43 mm × 36 mm. No pathological findings were observed in the head and chest CT scans. The electrocardiogram demonstrated sinus tachycardia with a shortened PR interval and tall, peaked P-waves in leads II, III, and aVF. Transthoracic echocardiography did not reveal any significant abnormalities.\n\nOn the second day of admission, the patient exhibited rising levels of brain natriuretic peptide (BNP) and Troponin I (TnI). The cardiologist provisionally diagnosed the patient with myocarditis of uncertain etiology, based on clinical presentation, elevated cardiac biomarkers (BNP and TnI), and supportive electrocardiogram findings. Treatment was initiated with methylprednisolone (0.25 g daily) to address potential myocardial inflammation due to suspected myocarditis. Furosemide (20 mg every 12 hours) and spironolactone (20 mg every 12 hours) were administered as diuretics to manage fluid retention and reduce cardiac workload. Perindopril amlodipine (10 mg: 5 mg daily) was prescribed as an angiotensin-converting enzyme inhibitor and calcium channel blocker combination to control blood pressure and reduce afterload. Metoprolol tartrate (25 mg every 12 hours) was used to manage heart rate and decrease myocardial oxygen demand, while esmolol (0.2 g/hour intravenous infusion), a short-acting beta-blocker, was administered for additional acute heart rate control due to sinus tachycardia. Due to concerns about a potential infection, moxifloxacin was added as empiric antibiotic therapy.\n\nGiven the patient’s presentation with an adrenal mass and hypertension, the endocrinologist recommended an evaluation of the aldosterone-to-renin ratio, plasma cortisol, plasma catecholamines, and 24-hour urinary catecholamines along with their metabolites. In the recumbent position, plasma and urinary catecholamine levels were markedly elevated (Table 1), including plasma dopamine at 524.5 pmol/L, norepinephrine at 83975 pmol/L, and epinephrine at 10579.3 pmol/L. Additionally, the 24-hour urinary levels showed free adrenaline at 4368.89 nmol/24 hours, free norepinephrine exceeding 12697.60 nmol/24 hours, normetanephrine at 8312 nmol/24 hours, metanephrines at 4078 nmol/24 hours, and vanillylmandelic acid at 58.1 mg/24 hours. These findings supported a clinical diagnosis of pheochromocytoma. On the fifth day post-admission, glucocorticoid therapy was discontinued, and perindopril amlodipine was substituted with terazosin for more targeted blood pressure management.\n\nAn enhanced abdominal CT scan further confirmed a left adrenal mass, highly suggestive of pheochromocytoma. Additionally, after obtaining informed consent, whole-exome sequencing was performed, revealing a heterozygous missense mutation, c.1900T > C: p. Cys634Arg, in the RET gene, leading to a substitution of cysteine with arginine at codon 634. This mutation raised suspicion for multiple endocrine neoplasia syndrome, prompting further evaluation of the thyroid and parathyroid glands. Thyroid color Doppler ultrasound identified a hypoechoic mass measuring 6 mm × 4 mm in the left thyroid lobe, and a mild elevation in calcitonin levels was noted. No additional significant abnormalities were detected.\n\nAs the patient’s condition gradually improved, plasma cortisol and ACTH levels returned to normal. The patient was subsequently discharged with a prescription for metoprolol tartrate (100 mg every 12 hours) and ivabradine hydrochloride (5 mg every 12 hours) for home management. Three months later, after achieving stable clinical status, the patient underwent resection of the left adrenal tumor, which measured 50 mm × 40 mm × 30 mm. Immunohistochemical analysis confirmed positive staining for Vim, CD56, Syn, CgA, and NSE, with S-100 positive in Sertoli cells, while CKpan, CD10, MART-1/Melan-A, and Melan-A were negative. The Ki67 index was 1%, leading to a definitive diagnosis of adrenal pheochromocytoma. The patient was discharged without further medications and has since been regularly followed up postoperatively without recurrence of symptoms. Over a 15-month postoperative follow-up, the patient exhibited persistently mild hypercalcitoninemia with stable thyroid nodule size, while PTH and serum calcium levels showed a progressive increase (Table 2). Further parathyroid scintigraphy using 99mTc-MIBI was performed, and the conclusion was a negative result for parathyroid adenoma.",
+    "diff_label_texts": "A 19-year-old woman came to the emergency room with headache, nausea, vomiting and fever and was found to have very high blood pressure and a fast heart rate. Imaging incidentally showed a large mass on her left adrenal gland, and blood and 24-hour urine tests showed markedly raised catecholamines and their metabolites, confirming a diagnosis of pheochromocytoma. Despite the size of the tumor and receiving high‑dose glucocorticoid treatment early in her stay, she did not develop a hypertensive crisis. She had a past episode a year earlier diagnosed as myocarditis and a family history of sudden unexplained death. Genetic testing identified a pathogenic RET gene mutation (c.1900T>C, p.Cys634Arg) consistent with multiple endocrine neoplasia type 2A (MEN2A), so the thyroid and parathyroid glands were evaluated. Thyroid ultrasound found a small nodule and blood tests showed mildly raised calcitonin, while initial electrolytes and parathyroid hormone (PTH) were within the normal range. Three months later she underwent removal of the left adrenal tumor; pathology confirmed pheochromocytoma, and she recovered without recurrence of symptoms. Over 15 months of follow-up she continued to have mildly elevated calcitonin with a stable thyroid nodule, but PTH and serum calcium levels rose progressively. A 99mTc‑MIBI parathyroid scan did not show a parathyroid adenoma.",
+    "summary": "We report the case of a 19-year-old female who presented with pheochromocytoma without experiencing a crisis, despite having a significant adrenal mass and undergoing high-dose glucocorticoid treatment. Genetic testing revealed a heterozygous missense mutation in the RET gene (c.1900T > C: p. Cys634Arg), associated with MEN2A. Further endocrine evaluation identified a thyroid nodule with mildly elevated calcitonin levels, but normal electrolyte and parathyroid hormone levels. Over a 15-month postoperative follow-up, the patient exhibited persistently mild hypercalcitoninemia with stable thyroid nodule size, while PTH and serum calcium levels showed a progressive increase. Further parathyroid scintigraphy using 99mTc-MIBI was performed, yielding a negative result for parathyroid adenoma."
+  },
+  {
+    "doc_id": 62,
+    "label": "intermediate_health_literacy",
+    "fulltext": "A 13-year-old adolescent male, with no significant previous medical history, presented to the emergency department with a 3-day history of acute bilateral pleuritic chest pain associated with mild non-productive cough and no dyspnea. Associated with this, he had mild rhinorrhea and a single febrile episode that day (temperature of 38ºC). Chest pain was localized to the costal margin region and worsened with cough, without diurnal variation. The patient-reported relief with paracetamol. There were no complaints of joint pain, weight loss, anorexia, fatigue, episodes of syncope or exercise restriction. In fact, he practiced sports regularly—canoeing 2 times a week. No evidence of an infectious exposure or contact with household or environmental fumes, dust, or mineral oils was described. There was no known family history of cardiopulmonary conditions. He had a chest radiograph taken 4 years earlier during an acute illness, which showed a marked interstitial infiltrate that was presumptively treated with azithromycin with no further clinical symptoms and no further follow-up.\n\nOn admission, the patient’s temperature was 37.8°C with normal peripheral oxygen saturation (99%) in room air. His heart (93 beats per minute) and respiratory rate (15 breaths per minute) were normal and blood pressure was on the 85th percentile (115/66 mmHg). Physical examination revealed diminished breath sounds in the lower two thirds of the chest with no adventitious sounds. No respiratory distress, finger clubbing, cyanosis, abnormal heart sounds, or other findings were present. Chest radiograph revealed a marked interstitial infiltrate, comparable with his previous examination. A thoracic computed tomography (CT) revealed multiple bilateral areas of ground-glass opacities involving > 65% of lung parenchyma, suggestive of PAP. Respiratory viral testing was negative, and he remained stable throughout his monitoring in the emergency department. He was discharged with empiric antibiotics (amoxicillin-clavulanic acid and azithromycin) to cover a potential respiratory infection, with clinical resolution of symptoms and was sent for follow-up at the pediatric respiratory clinic.\n\nUpon further investigation in the outpatient setting, positive antinuclear antibodies (ANAs) at a titer of 1/89 with a fine speckled pattern were detected, while other autoantibodies tested negative and immunoglobulin levels remained within normal limits. Bronchoalveolar lavage revealed fluid with a milky appearance and positive periodic acid-Schiff staining; microbiological examination, including for mycobacteria, returned negative results. Spirometry indicated a mild restrictive pattern with reduced forced vital capacity (FVC) at 2.92 L (77%) and forced expiratory volume in 1 second (FEV1) at 3.21 L (69.9%), alongside a normal FEV1/FVC ratio (109%). In addition, the DLCO single breath (SB) showed a moderate decrease at 13.8 ml/min/mmHg (48.6%). Suspecting PAP, a genetic panel was conducted, which showed no mutations associated with surfactant dysfunction. Subsequently, GM-CSF antibody testing was performed with a positive result, raising suspicion for AI-PAP. At 20 months of follow-up, the patient remains asymptomatic and continues to exercise regularly. He repeated spirometry testing with normal FVC at 4.03 L (81.3%); FEV1 at 3.71 L (87.5%); FEV1/FVC ratio at 91.96% and DLCO SB at 25.54 ml/min/mmHg (83.7%). As the patient remains stable with no respiratory symptoms, we decided to defer treatment and continue monitoring with regular clinic visits.",
+    "diff_label_texts": "A 13-year-old boy presented with acute pleuritic chest pain but no other systemic symptoms. On exam, he had diminished breath sounds over the lower two thirds of the chest, and his oxygen saturation was normal (98% on room air). Chest X-ray showed a marked interstitial infiltrate similar to an image taken 4 years earlier during an illness treated presumptively with azithromycin. Chest CT demonstrated multiple bilateral ground-glass opacities with areas of “crazy paving,” involving more than 65% of the lung, which raised concern for pulmonary alveolar proteinosis (PAP). Respiratory viral testing, including SARS-CoV-2, was negative. Bronchoalveolar lavage yielded milky fluid with positive periodic acid–Schiff staining. Pulmonary function testing showed a mild restrictive pattern (FVC 77%) and a moderately reduced diffusing capacity (DLCO 48.6%). A genetic panel found no mutations linked to surfactant dysfunction. Anti–GM-CSF antibodies were strongly positive, supporting autoimmune PAP. At 20 months, he remains asymptomatic, and spirometry has normalized.",
+    "summary": "We describe the case of a 13-year-old adolescent male who presented to the emergency department with acute pleuritic chest pain not associated with systemic complaints. On examination, he had diminished breath sounds in the lower two thirds of the chest with no other abnormal findings; SpO2 (oxygen saturation) was 98% on room air. Chest radiograph revealed a marked interstitial infiltrate, comparable with the one taken 4 years earlier during an acute illness that was presumptively treated with azithromycin. A computed tomography (CT) scan revealed multiple bilateral areas of ground-glass opacities with areas of crazy paving, involving > 65% of lung parenchyma, suggestive of pulmonary alveolar proteinosis (PAP). Respiratory viral testing, including for coronavirus (SARS-CoV2), was negative. Bronchoalveolar lavage performed in the outpatient setting revealed a milky fluid and positive periodic acid-Schiff staining. Spirometry indicated a mild restrictive pattern (forced vital capacity [FVC] = 77%) and diffusing capacity of the lungs for carbon monoxide (DLCO) showed a moderate decrease at 48.6%. No mutations associated with surfactant dysfunction were found on the genetic panel. Anti-granulocyte macrophage colony-stimulating factor (GM-CSF) antibody testing was strongly positive, raising suspicion for autoimmune PAP. At 20 months of follow-up, the patient remains asymptomatic with a normal spirometry."
+  },
+  {
+    "doc_id": 66,
+    "label": "intermediate_health_literacy",
+    "fulltext": "A 17-year-old male with no significant past medical or family history was referred to our clinic from the dental department following an incidental finding of a NFB during preoperative orthodontic planning, including dental x-rays and cone beam computed tomography (CBCT) without contrast. The patient was entirely asymptomatic and denied any history of nasal obstruction, rhinorrhea, epistaxis, foul odor, hyposmia, halitosis, facial pain, discomfort, or sleep disturbances. The patient's parents recalled an event when their son was seven, where he inserted an object into his nose. They sought medical advice, where no imaging was performed and an anterior rhinoscopy was utilized for diagnoses but due to the child's non-cooperation during the examination, the physician recommended the removal of the foreign body under sedation. However, the family did not follow up, and since the child remained asymptomatic, they assumed the foreign body had fallen out on its own. On endoscopic examination of the right nasal cavity, a deviated nasal septum with inferior turbinate hypertrophy was noted. The mucosa appeared erythematous and slightly edematous. A foreign body was visualized, lodged, and adhered to the floor of the nasal cavity beneath the inferior turbinate. The object was partially covered with mucus and possibly some crusted material and had a shiny appearance, indicating a metallic nature. Radiographic evaluation, including lateral and frontal X-rays, revealed a circular radiopaque object consistent with a metallic snap button located along the floor of the nasal cavity. The surrounding bony structures appeared normal. A CBCT confirmed the presence of the foreign body with associated mild inflammation, but no significant bony damage or sinus involvement was observed. With informed consent from the patient's parent, the foreign body was removed under local anesthesia in a semi-sitting position to reduce the risk of dislodgment to the airway. After decongesting the nasal cavity with Xylometazoline 0.1 % and administering Lidocaine spray (10 mg/spray) in the right nostril, a hook was utilized to disengage the foreign body, which was then retrieved using bayonet forceps. The procedure was uncomplicated, with minimal bleeding, easily controlled with saline irrigation. Post-removal examination showed no significant tissue damage. The retrieved object, a metallic snap button measuring 1 cm in diameter, exhibited signs of long-term exposure, including substantial corrosion and biological deposits. The patient was discharged in stable condition and prescribed nasal rinses with a sodium chloride irrigation solution (0.9 %). The patient was doing well at his two-week follow-up with an unremarkable examination.",
+    "diff_label_texts": "A 17-year-old male had an asymptomatic nasal foreign body (NFB) found incidentally on routine dental x-rays and cone beam CT during orthodontic planning. He denied any nasal blockage, nosebleeds, or discomfort. His parents recalled that at age seven he had put something in his nose; the family had been advised at the time to remove it under sedation but did not follow up, assuming it had fallen out. Endoscopic exam showed a deviated septum and enlargement of the lower nasal turbinate, with mild redness and swelling of the nasal lining. A shiny object was seen stuck to the floor of the right nasal cavity beneath the inferior turbinate and was partly covered with mucus and crust. X-rays and CBCT confirmed a circular radiopaque object consistent with a metallic snap button about 1 cm across, with mild surrounding inflammation but no damage to the nearby bone or sinuses. With parental consent, the button was removed in the clinic under local anesthesia and nasal decongestion while the patient was semi‑upright to reduce the risk of it moving toward the airway; removal with a hook and forceps was uncomplicated, with only minimal bleeding. The retrieved snap button showed corrosion and biological deposits, consistent with being present for many years. The patient was discharged in stable condition, advised to use saline nasal rinses, and was doing well with a normal exam at two-week follow-up.",
+    "summary": "We present the case of a 17-year-old male with an asymptomatic NFB discovered incidentally during routine dental radiography. The patient denied any history of nasal obstruction, epistaxis, or discomfort. Imaging revealed a radiopaque object in the right nasal cavity, later identified as a metallic snap button embedded in the floor of the nasal cavity. The foreign body had likely been retained for over a decade."
+  },
+  {
+    "doc_id": 66,
+    "label": "proficient_health_literacy",
+    "fulltext": "A 17-year-old male with no significant past medical or family history was referred to our clinic from the dental department following an incidental finding of a NFB during preoperative orthodontic planning, including dental x-rays and cone beam computed tomography (CBCT) without contrast. The patient was entirely asymptomatic and denied any history of nasal obstruction, rhinorrhea, epistaxis, foul odor, hyposmia, halitosis, facial pain, discomfort, or sleep disturbances. The patient's parents recalled an event when their son was seven, where he inserted an object into his nose. They sought medical advice, where no imaging was performed and an anterior rhinoscopy was utilized for diagnoses but due to the child's non-cooperation during the examination, the physician recommended the removal of the foreign body under sedation. However, the family did not follow up, and since the child remained asymptomatic, they assumed the foreign body had fallen out on its own. On endoscopic examination of the right nasal cavity, a deviated nasal septum with inferior turbinate hypertrophy was noted. The mucosa appeared erythematous and slightly edematous. A foreign body was visualized, lodged, and adhered to the floor of the nasal cavity beneath the inferior turbinate. The object was partially covered with mucus and possibly some crusted material and had a shiny appearance, indicating a metallic nature. Radiographic evaluation, including lateral and frontal X-rays, revealed a circular radiopaque object consistent with a metallic snap button located along the floor of the nasal cavity. The surrounding bony structures appeared normal. A CBCT confirmed the presence of the foreign body with associated mild inflammation, but no significant bony damage or sinus involvement was observed. With informed consent from the patient's parent, the foreign body was removed under local anesthesia in a semi-sitting position to reduce the risk of dislodgment to the airway. After decongesting the nasal cavity with Xylometazoline 0.1 % and administering Lidocaine spray (10 mg/spray) in the right nostril, a hook was utilized to disengage the foreign body, which was then retrieved using bayonet forceps. The procedure was uncomplicated, with minimal bleeding, easily controlled with saline irrigation. Post-removal examination showed no significant tissue damage. The retrieved object, a metallic snap button measuring 1 cm in diameter, exhibited signs of long-term exposure, including substantial corrosion and biological deposits. The patient was discharged in stable condition and prescribed nasal rinses with a sodium chloride irrigation solution (0.9 %). The patient was doing well at his two-week follow-up with an unremarkable examination.",
+    "diff_label_texts": "A 17-year-old male with no significant past medical or family history was referred from Dentistry after an incidental nasal foreign body (NFB) was detected during preoperative orthodontic planning with dental radiographs and cone beam computed tomography (CBCT) without contrast. He was entirely asymptomatic, denying nasal obstruction, rhinorrhea, epistaxis, foul odor, hyposmia, halitosis, facial pain, discomfort, or sleep disturbances. The parents recalled a prior event at age seven when he inserted an object into his nose; an anterior rhinoscopy was attempted at that time, and removal under sedation was recommended, but the family did not follow up and assumed spontaneous expulsion given the absence of symptoms. Nasal endoscopy of the right cavity showed a deviated nasal septum with inferior turbinate hypertrophy; the mucosa was erythematous and mildly edematous. A foreign body was visualized, lodged and adherent to the floor of the nasal cavity beneath the inferior turbinate, partially covered with mucus/crust, with a shiny surface suggesting a metallic nature. Lateral and frontal radiographs demonstrated a circular radiopaque object along the nasal floor consistent with a metallic snap button; adjacent bony structures were normal. CBCT confirmed the foreign body and mild surrounding inflammation, without significant bony erosion or sinus involvement. With informed consent, removal was performed under local anesthesia in a semi-sitting position to mitigate the risk of airway dislodgment. After decongestion with xylometazoline 0.1% and topical anesthesia with lidocaine spray (10 mg/spray) in the right nostril, a hook was used to disengage the foreign body, which was then extracted with bayonet forceps. The procedure was uncomplicated with minimal bleeding controlled by saline irrigation, and post-removal inspection showed no significant tissue injury. The retrieved object was a metallic snap button (1 cm diameter) with substantial corrosion and biological deposits, consistent with long-term retention—likely over a decade. The patient was discharged in stable condition with 0.9% sodium chloride nasal irrigations and had an unremarkable two-week follow-up.",
+    "summary": "We present the case of a 17-year-old male with an asymptomatic NFB discovered incidentally during routine dental radiography. The patient denied any history of nasal obstruction, epistaxis, or discomfort. Imaging revealed a radiopaque object in the right nasal cavity, later identified as a metallic snap button embedded in the floor of the nasal cavity. The foreign body had likely been retained for over a decade."
+  },
+  {
+    "doc_id": 67,
+    "label": "low_health_literacy",
+    "fulltext": "An 18-year-old hispanic male patient with no significant medical history presents to the emergency department (ED) complaining of substernal, non-radiated chest pain, orthopnoea, dry and non-productive cough, and subjective fevers at home, for the last 3–4 days. Family history remarkable for paternal grandfather diagnosed with non-ischaemic cardiomyopathy and a pacemaker at age 86 years old. Patient lives with both parents and denies any smoking, ethanol consumption, recreational drug use, abuse or neglect at home. He worked at auto-part shop and planned to start college soon.\n\n\nInvestigations\n\n\nIn the ED, serum troponin I levels were found to be elevated and ECG showed diffuse ST-segment elevation. He was admitted to the local hospital and initial workup was remarkable for an enlarged cardiac silhouette and mild pulmonary oedema observed on chest X-ray, a transthoracic echocardiogram (TTE) demonstrating left ventricular ejection fraction (LVEF) of 40%, with severe left ventricular (LV) concentric hypertrophy and mild posterior pericardial effusion. Additionally, the patient was found to have elevated titres for Coxsackie virus A and B. His symptoms initially improved with the initiation of ibuprofen and colchicine. Cardiac catheterisation was performed, which revealed no evidence of coronary artery disease. Repeat TTE showed an LVEF of 40%–45%, hypokinesis of anteroapical and inferolateral wall, with an elevated LV end-diastolic pressure, consistent with diastolic dysfunction. Chest CT angiogram showed evidence of pneumonitis and a pericardial effusion. And at this point, the constellation of symptoms was thought to be secondary to Coxsackie myopericarditis, for which he continued to receive medical treatment as previously mentioned.\n\nOn the fourth day of admission, the patient became diaphoretic, tachycardic and hypotensive with an undetectable blood pressure. Emergent TTE showed large pericardial effusion with impending cardiac tamponade features, and pericardiocentesis was performed. During the procedure, the patient developed pulseless electrical activity (PEA) cardiac arrest and received advanced cardiovascular support for 30 min. Ultimately patient was intubated, placed on venous-arterial extracorporeal membrane oxygenation (VA ECMO) and started on vasopressor support (norepinephrine 5 mcg/min and vasopressin 0.05 units/min), with numerous transfusions (9 packed red bloodcells, 10 units of platelets, 10 units of cryoprecipitate and 4 units of fresh frozen plasma) due to significant oozing of blood from the ECMO cannula. He was transferred to our hospital where endomyocardial biopsy (EMB) was then obtained due to concern of fulminant myocarditis and to test for other infiltrative cardiomyopathies. Pathology reports showed no signs suggestive of inflammatory or infiltrative process in the endomyocardium. Coxsackie Abs were repeated and were positive for Cox A type 9, Coxsackie B2 and Coxsackie B6, and an elevated Epstein-Barr virus (EBV) DNA quantitative PCR at 133 000 IU/mL. At this point, another TTE was done, which showed a severely decreased ejection fraction (EF) of 10%–15% with previously noted severe LV concentric hypertrophy (1.9 cm septum and 2.2 cm in the inferolateral wall).\n\nThe patient was started on intravenous immunoglobulin (IVIG) for treatment of Coxsackie myocarditis, and broad-spectrum antibiotics due to worsening leucocytosis, but with no identified infectious focus. Colchicine was discontinued due to concern for rhabdomyolysis, with elevation of serum creatine kinase level to 2874 unit/L. Vasopressors were then discontinued and the patient was extubated. He also developed episode of flushing, fever, dyspnoea and decreasing oxygen saturation, with chest X-ray showing congested lung parenchyma with concerns for ARDS, therefore, IVIG was stopped.\n\nGiven improvement of cardiac function in another TTE with LVEF of 25%–30%, it was decided to attempt to remove the ECMO, which was unsuccessful. The patient remained on ECMO support and emergent discussion with heart failure team took place to determine best approach. The patient was evaluated for possible left ventricle assist device, however, deemed not a candidate due to significant global concentric LV hypertrophy, and the multidisciplinary team agreed to facilitate emergency listing for heart transplantation, with consideration to transition to another cardiovascular support such as intra-aortic balloon pump, with potential inotrope support.\n\nDuring further evaluation for possible heart transplant, an incisional biopsy of a 1×1 inch palpable, painless, rubbery, mobile mass in the right arm was done and sent for pathology. The patient mentioned he first noticed this lesion approximately 2–3 months before presenting to the ED. Pathology report of the right upper extremity mass showed aggressive EBV (+) NK/T-cell lymphoma with a cytotoxic immunophenotype (positive for CD 2, CD3, CD56, BCL2, granzyme B, TIA1, MUM1 and diffuse coexpression of Epstein-Barr virus-encoded small RNAs by in situ hybridisation), and a modified SMILE (Steroids, Methotrexate with leucovorin, Ifosfamide with mesna, L-asparaginase and Etoposide) chemotherapy regimen was started. In situ hybridisation of the EMB previously obtained were negative for EBV-RNA.\n\nCardiac MRI was obtained, which revealed hypokinesis of the inferolateral and anterolateral wall, as previously described by TTE, delayed enhancement in the subendocardial and transmural distribution in these regions, with relative sparing of the septum. Additionally, avid enhancement and thickening of the pericardium, without a mass identified, and a pocket of pericardial fluid with septations, concerning for loculations, were also noted.\n\n\nDifferential diagnosis\n\nThe constellation of symptoms (shortness of breath, orthopnoea, hypotension and subjective fevers), with findings such as diffuse ST-segment elevation on ECG, leakages of cardiac markers (troponin), elevated Coxsackie virus titres (both of serotype A and B), as well as echocardiographic findings of pericardial effusion; all seemed to correlate with a classic presentation of viral pericarditis clinical due to Coxackie virus. However, despite medical treatment with colchicine, the patient continued to decompensate and eventually required pericardiocentesis due to cardiac tamponade, then developed cardiac arrest and ultimately requires ECMO support, for what seems acute onset heart failure. In this setting, fulminant myocarditis secondary to Coxsackie virus was considered. Cardiotropic RNA virus, such as Coxackie viruses, induce receptor-mediated endocytosis, with viral replication contributing to cellular dysfunction and ultimately apoptosis of the cell.1 When susceptible individuals are infected with highly virulent viral strains, maladaptive immunologic activity can occur, leading to persistent activation of T cells and continued antibody-mediated myocyte destruction, which can ultimately lead to fulminant myocarditis. EBV myocarditis could also explain the rapid deterioration in the setting of a positive EBV PCR, which is a more sensitivity test than traditional serologies for detection of acute infection.2 However, in situ hybridisation was negative for EBV-RNA.\n\nNevertheless, the significant concentric hypertrophy observed on the initial TTEs and the atypical delayed enhancement observed on the cardiac MRI are not explained by this diagnosis. Additionally, the EMB did not show an inflammatory process.\n\nFortuitous finding of EBV (+) NK/T-cell lymphoma by incisional biopsy of the right upper extremity allowed for a more fitting diagnosis for this case. The pericardial effusion, unresponsive to initial medical treatment and new acute heart failure with concentric hypertrophic cardiomyopathy, in the setting of newly diagnosed NK/T-cell lymphoma, raises the possibility of NK/T-cell lymphoma with involvement of the myocardium and pericardium as the most adequate diagnosis in this scenario, which englobes all the features previously mentioned in this case.\n\nOther differentials taken into consideration include infiltrative cardiomyopathy such as amyloidosis. However, Congo red staining of the EMB samples failed to demonstrate deposition of amyloid.\n\n\nTreatment\n\nGiven the diagnosis of extranodal NK/T-cell lymphoma (ENKTCL) with suspected pericardial involvement and no bone marrow involvement, modified SMILE regimen was desired as the first-line chemotherapy regimen. This regimen includes dexamethasone, ifosfamide, mesna and etoposide, and excluded methotrexate, due to evidence of third-spacing and effusions, which could lead to delayed excretion and increased risk of toxicity.\n\nHowever, due to his compromised cardiac function, it was believed that the patient would not tolerate cytotoxic chemotherapy which requires aggressive intravenous, and alternatively, emergent chemotherapy regimen was instituted: carboplatin (day 1–day 3), etoposide (day 1–day 5) and dexamethasone. Peg-asparaginase was later introduced in the regimen (day 7–day 21). This regimen proved effective, as evidenced by rapid recovery of the LV function and overall haemodynamic stability, and decision was made to incorporate a modified SMILE chemotherapy regimen, of which he received two cycles. Then chemotherapy regimen was changed to dexamethasone, gemcitabine, carboplatin and peg-asparaginase (DDGP). The patient received two cycles of DDGP. A full body positron emission tomography (PET) scan was negative for lymphoma. The plan is to continue two more cycles of chemotherapy (to complete six total cycles of chemotherapy). Currently, the patient is considering radiation therapy and possible stem cell transplant, after completion of the chemotherapy regimen. Additionally, the patient is currently on guideline-directed medical therapy for heart failure and has completed cardiac rehabilitation.\n\n\nOutcome and follow-up\n\nThe patient has completed five out of six chemotherapy sessions with the previously mentioned regimens. After initiation of chemotherapy and optimal medical treatment for heart failure, the patient has recovered much of his cardiac function, as evidenced by an LVEF of 55%, no wall motion abnormalities and normal myocardial wall thickness on his most recent TTE. He continues to be followed by heart failure/cardiology team and oncology team in clinic.",
+    "diff_label_texts": "An 18-year-old man came to the emergency room with new chest pain, fever, and trouble breathing when he lay down. A blood test showed strain on his heart. His heart tracing had changes that can happen when the heart is irritated. His chest X-ray made the heart look bigger than normal. An ultrasound showed the heart muscle was very thick on both sides. It also showed fluid around the heart. Blood tests pointed to a common virus called Coxsackie, which can inflame the sac around the heart. Doctors treated him, but he got worse with shortness of breath and very low blood pressure. A new heart ultrasound showed the fluid was starting to squeeze his heart, like a tight jacket. Doctors drained the fluid, but his heart stopped, and he needed a heart-lung machine to stay alive. A small piece of heart tissue did not show infection. A small skin lump on his right arm was tested. It showed a rare blood cancer linked to the Epstein–Barr virus. He started cancer medicines. His heart pumping got better. The fluid around his heart went away. The thick heart muscle slowly went back toward normal.",
+    "summary": "An 18-year-old male patient presented to the emergency department complaining of new onset chest pain, fever and orthopnoea. Initial workup was remarkable for elevated troponin, diffuse ST-segment elevation on ECG and chest X-ray with enlarged cardiac silhouette. Transthoracic echocardiogram (TTE) demonstrates severe biventricular concentric hypertrophy and pericardial effusion. Also, Coxsackie virus A and B titres were positive, concerning for a classic viral pericarditis. However, despite medical management, the patient became dyspnoeic and hypotensive. Impending cardiac tamponade was observed on repeat TTE, and pericardiocentesis was performed, complicated by pulseless electrical activity cardiac arrest, and ultimately patient requiring venoarterial extracorporeal membrane oxygenation support. Emergent endomyocardial biopsy showed no inflammatory process, and a skin biopsy of a small lesion in the right arm showed unexpected diagnosis of Epstein-Barr virus (+) natural killer/T-cell lymphoma. On initiation of chemotherapy, clinical improvement was observed as evidenced by improving ejection fraction, resolution of pericardial effusion and gradual decrease in myocardial hypertrophy."
+  },
+  {
+    "doc_id": 67,
+    "label": "intermediate_health_literacy",
+    "fulltext": "An 18-year-old hispanic male patient with no significant medical history presents to the emergency department (ED) complaining of substernal, non-radiated chest pain, orthopnoea, dry and non-productive cough, and subjective fevers at home, for the last 3–4 days. Family history remarkable for paternal grandfather diagnosed with non-ischaemic cardiomyopathy and a pacemaker at age 86 years old. Patient lives with both parents and denies any smoking, ethanol consumption, recreational drug use, abuse or neglect at home. He worked at auto-part shop and planned to start college soon.\n\n\nInvestigations\n\n\nIn the ED, serum troponin I levels were found to be elevated and ECG showed diffuse ST-segment elevation. He was admitted to the local hospital and initial workup was remarkable for an enlarged cardiac silhouette and mild pulmonary oedema observed on chest X-ray, a transthoracic echocardiogram (TTE) demonstrating left ventricular ejection fraction (LVEF) of 40%, with severe left ventricular (LV) concentric hypertrophy and mild posterior pericardial effusion. Additionally, the patient was found to have elevated titres for Coxsackie virus A and B. His symptoms initially improved with the initiation of ibuprofen and colchicine. Cardiac catheterisation was performed, which revealed no evidence of coronary artery disease. Repeat TTE showed an LVEF of 40%–45%, hypokinesis of anteroapical and inferolateral wall, with an elevated LV end-diastolic pressure, consistent with diastolic dysfunction. Chest CT angiogram showed evidence of pneumonitis and a pericardial effusion. And at this point, the constellation of symptoms was thought to be secondary to Coxsackie myopericarditis, for which he continued to receive medical treatment as previously mentioned.\n\nOn the fourth day of admission, the patient became diaphoretic, tachycardic and hypotensive with an undetectable blood pressure. Emergent TTE showed large pericardial effusion with impending cardiac tamponade features, and pericardiocentesis was performed. During the procedure, the patient developed pulseless electrical activity (PEA) cardiac arrest and received advanced cardiovascular support for 30 min. Ultimately patient was intubated, placed on venous-arterial extracorporeal membrane oxygenation (VA ECMO) and started on vasopressor support (norepinephrine 5 mcg/min and vasopressin 0.05 units/min), with numerous transfusions (9 packed red bloodcells, 10 units of platelets, 10 units of cryoprecipitate and 4 units of fresh frozen plasma) due to significant oozing of blood from the ECMO cannula. He was transferred to our hospital where endomyocardial biopsy (EMB) was then obtained due to concern of fulminant myocarditis and to test for other infiltrative cardiomyopathies. Pathology reports showed no signs suggestive of inflammatory or infiltrative process in the endomyocardium. Coxsackie Abs were repeated and were positive for Cox A type 9, Coxsackie B2 and Coxsackie B6, and an elevated Epstein-Barr virus (EBV) DNA quantitative PCR at 133 000 IU/mL. At this point, another TTE was done, which showed a severely decreased ejection fraction (EF) of 10%–15% with previously noted severe LV concentric hypertrophy (1.9 cm septum and 2.2 cm in the inferolateral wall).\n\nThe patient was started on intravenous immunoglobulin (IVIG) for treatment of Coxsackie myocarditis, and broad-spectrum antibiotics due to worsening leucocytosis, but with no identified infectious focus. Colchicine was discontinued due to concern for rhabdomyolysis, with elevation of serum creatine kinase level to 2874 unit/L. Vasopressors were then discontinued and the patient was extubated. He also developed episode of flushing, fever, dyspnoea and decreasing oxygen saturation, with chest X-ray showing congested lung parenchyma with concerns for ARDS, therefore, IVIG was stopped.\n\nGiven improvement of cardiac function in another TTE with LVEF of 25%–30%, it was decided to attempt to remove the ECMO, which was unsuccessful. The patient remained on ECMO support and emergent discussion with heart failure team took place to determine best approach. The patient was evaluated for possible left ventricle assist device, however, deemed not a candidate due to significant global concentric LV hypertrophy, and the multidisciplinary team agreed to facilitate emergency listing for heart transplantation, with consideration to transition to another cardiovascular support such as intra-aortic balloon pump, with potential inotrope support.\n\nDuring further evaluation for possible heart transplant, an incisional biopsy of a 1×1 inch palpable, painless, rubbery, mobile mass in the right arm was done and sent for pathology. The patient mentioned he first noticed this lesion approximately 2–3 months before presenting to the ED. Pathology report of the right upper extremity mass showed aggressive EBV (+) NK/T-cell lymphoma with a cytotoxic immunophenotype (positive for CD 2, CD3, CD56, BCL2, granzyme B, TIA1, MUM1 and diffuse coexpression of Epstein-Barr virus-encoded small RNAs by in situ hybridisation), and a modified SMILE (Steroids, Methotrexate with leucovorin, Ifosfamide with mesna, L-asparaginase and Etoposide) chemotherapy regimen was started. In situ hybridisation of the EMB previously obtained were negative for EBV-RNA.\n\nCardiac MRI was obtained, which revealed hypokinesis of the inferolateral and anterolateral wall, as previously described by TTE, delayed enhancement in the subendocardial and transmural distribution in these regions, with relative sparing of the septum. Additionally, avid enhancement and thickening of the pericardium, without a mass identified, and a pocket of pericardial fluid with septations, concerning for loculations, were also noted.\n\n\nDifferential diagnosis\n\nThe constellation of symptoms (shortness of breath, orthopnoea, hypotension and subjective fevers), with findings such as diffuse ST-segment elevation on ECG, leakages of cardiac markers (troponin), elevated Coxsackie virus titres (both of serotype A and B), as well as echocardiographic findings of pericardial effusion; all seemed to correlate with a classic presentation of viral pericarditis clinical due to Coxackie virus. However, despite medical treatment with colchicine, the patient continued to decompensate and eventually required pericardiocentesis due to cardiac tamponade, then developed cardiac arrest and ultimately requires ECMO support, for what seems acute onset heart failure. In this setting, fulminant myocarditis secondary to Coxsackie virus was considered. Cardiotropic RNA virus, such as Coxackie viruses, induce receptor-mediated endocytosis, with viral replication contributing to cellular dysfunction and ultimately apoptosis of the cell.1 When susceptible individuals are infected with highly virulent viral strains, maladaptive immunologic activity can occur, leading to persistent activation of T cells and continued antibody-mediated myocyte destruction, which can ultimately lead to fulminant myocarditis. EBV myocarditis could also explain the rapid deterioration in the setting of a positive EBV PCR, which is a more sensitivity test than traditional serologies for detection of acute infection.2 However, in situ hybridisation was negative for EBV-RNA.\n\nNevertheless, the significant concentric hypertrophy observed on the initial TTEs and the atypical delayed enhancement observed on the cardiac MRI are not explained by this diagnosis. Additionally, the EMB did not show an inflammatory process.\n\nFortuitous finding of EBV (+) NK/T-cell lymphoma by incisional biopsy of the right upper extremity allowed for a more fitting diagnosis for this case. The pericardial effusion, unresponsive to initial medical treatment and new acute heart failure with concentric hypertrophic cardiomyopathy, in the setting of newly diagnosed NK/T-cell lymphoma, raises the possibility of NK/T-cell lymphoma with involvement of the myocardium and pericardium as the most adequate diagnosis in this scenario, which englobes all the features previously mentioned in this case.\n\nOther differentials taken into consideration include infiltrative cardiomyopathy such as amyloidosis. However, Congo red staining of the EMB samples failed to demonstrate deposition of amyloid.\n\n\nTreatment\n\nGiven the diagnosis of extranodal NK/T-cell lymphoma (ENKTCL) with suspected pericardial involvement and no bone marrow involvement, modified SMILE regimen was desired as the first-line chemotherapy regimen. This regimen includes dexamethasone, ifosfamide, mesna and etoposide, and excluded methotrexate, due to evidence of third-spacing and effusions, which could lead to delayed excretion and increased risk of toxicity.\n\nHowever, due to his compromised cardiac function, it was believed that the patient would not tolerate cytotoxic chemotherapy which requires aggressive intravenous, and alternatively, emergent chemotherapy regimen was instituted: carboplatin (day 1–day 3), etoposide (day 1–day 5) and dexamethasone. Peg-asparaginase was later introduced in the regimen (day 7–day 21). This regimen proved effective, as evidenced by rapid recovery of the LV function and overall haemodynamic stability, and decision was made to incorporate a modified SMILE chemotherapy regimen, of which he received two cycles. Then chemotherapy regimen was changed to dexamethasone, gemcitabine, carboplatin and peg-asparaginase (DDGP). The patient received two cycles of DDGP. A full body positron emission tomography (PET) scan was negative for lymphoma. The plan is to continue two more cycles of chemotherapy (to complete six total cycles of chemotherapy). Currently, the patient is considering radiation therapy and possible stem cell transplant, after completion of the chemotherapy regimen. Additionally, the patient is currently on guideline-directed medical therapy for heart failure and has completed cardiac rehabilitation.\n\n\nOutcome and follow-up\n\nThe patient has completed five out of six chemotherapy sessions with the previously mentioned regimens. After initiation of chemotherapy and optimal medical treatment for heart failure, the patient has recovered much of his cardiac function, as evidenced by an LVEF of 55%, no wall motion abnormalities and normal myocardial wall thickness on his most recent TTE. He continues to be followed by heart failure/cardiology team and oncology team in clinic.",
+    "diff_label_texts": "An 18-year-old man came to the emergency department with new chest pain, fever, shortness of breath when lying flat (orthopnoea) and a dry cough for several days. Initial tests showed an elevated troponin, diffuse ST-segment elevations on ECG, and an enlarged heart on chest X-ray. Transthoracic echocardiogram (TTE) showed severe concentric thickening of both ventricles and a pericardial effusion; Coxsackie A and B antibody titres were also positive, so clinicians initially treated him for viral myopericarditis with anti-inflammatory medications. Despite treatment he acutely worsened on day four, becoming hypotensive and short of breath; repeat TTE showed impending cardiac tamponade and he underwent pericardiocentesis. The procedure was complicated by a pulseless electrical activity cardiac arrest, and he required intubation and venoarterial extracorporeal membrane oxygenation (VA-ECMO) for circulatory support. An endomyocardial biopsy did not show inflammation, and blood testing found a very high Epstein–Barr virus (EBV) PCR. A separate biopsy of a small painless mass on his right arm unexpectedly showed EBV-positive natural killer/T‑cell lymphoma. With a working diagnosis of lymphoma involving the heart and pericardium, he was started on systemic chemotherapy (initially an emergency regimen followed by modified lymphoma protocols). After treatment his heart function steadily improved: ejection fraction recovered to normal range, the pericardial effusion resolved, and the abnormal myocardial thickening decreased. He completed most planned chemotherapy cycles and continues follow-up with cardiology and oncology.",
+    "summary": "An 18-year-old male patient presented to the emergency department complaining of new onset chest pain, fever and orthopnoea. Initial workup was remarkable for elevated troponin, diffuse ST-segment elevation on ECG and chest X-ray with enlarged cardiac silhouette. Transthoracic echocardiogram (TTE) demonstrates severe biventricular concentric hypertrophy and pericardial effusion. Also, Coxsackie virus A and B titres were positive, concerning for a classic viral pericarditis. However, despite medical management, the patient became dyspnoeic and hypotensive. Impending cardiac tamponade was observed on repeat TTE, and pericardiocentesis was performed, complicated by pulseless electrical activity cardiac arrest, and ultimately patient requiring venoarterial extracorporeal membrane oxygenation support. Emergent endomyocardial biopsy showed no inflammatory process, and a skin biopsy of a small lesion in the right arm showed unexpected diagnosis of Epstein-Barr virus (+) natural killer/T-cell lymphoma. On initiation of chemotherapy, clinical improvement was observed as evidenced by improving ejection fraction, resolution of pericardial effusion and gradual decrease in myocardial hypertrophy."
+  },
+  {
+    "doc_id": 72,
+    "label": "low_health_literacy",
+    "fulltext": "A 39-year-old woman with a diagnosis of peripartum cardiomyopathy who received a heart transplant in October 2014. She received induction with Basiliximab and methylprednisolone. She also received maintenance treatment with tacrolimus XL prolonged release 7 mg daily, everolimus 1 mg twice daily, and prednisolone 5 mg/day. She had two episodes of acute rejection during the first year post-transplant, and was controlled with methylprednisolone pulse therapy with good results. There was no history of renal disease and her renal function was stable with creatinine of 0.88 mg/dL and a glomerular filtration rate (GFR) of 102 mL/min/1.73m2 during the first year post-transplant. Follow-up was done exclusively by the heart transplant group and routine polyomavirus viral load BK or urinary cytology was not performed. In 2016, she presented a creatinine serum elevation of up to 1.9 mg/dL, with a GFR of 32.6 mL/min/1.73m2. At that time, the minimum tacrolimus level was 7.2 ng/mL and everolimus, 5.2 ng/mL. Anticalcineurin toxicity was suspected; therefore, tacrolimus was reduced to 4 mg daily and creatinine returned to near baseline (creatinine 1.25 mg/dL, GFR 54.1 mL/min/1.73m2); no renal biopsy was performed. In March 2017, creatinine increased to 2.69 mg/dL, with a GFR of 21.4 mL/min/1.73m2, for which she was hospitalized. The patient stated that she did not have any symptoms. During physical examination, she was in good general condition, heart rate of 80 beats per minute, blood pressure of 130/90 mmHg, respiratory rate of 15 per minute, afebrile. Further studies were performed: renal tract ultrasound showed normal renal size but increased echogenicity; urinalysis and urine cultures were negative, without haematuria, pyuria or casts; echocardiogram with adequate cardiac function; HIV, syphilis, hepatitis B and C serologic tests were negative; minimum tacrolimus level of 5.2 ng/mL, and everolimus of 5.98 ng/mL. Control was initiated with intravenous hydration, and tacrolimus XL dose was reduced to 2 mg daily, but there was no improvement in renal function; a renal biopsy was planned.\n\nRenal biopsy revealed active chronic interstitial nephritis associated with advanced poliomyelitis virus nephritis. BK virus PCR was performed and was positive at 33,800 copies/mL in blood (log 4.5). Tacrolimus was discontinued; creatinine levels stabilized between 2.2 and 2.4 mg/dL, with no further elevation in post-discharge controls. Her viral load began to decline to undetectable levels. The patient did not have episodes of cardiac rejection in 3 years of follow-up; the last creatinine measurement was 2.5 mg/dL, corresponding to a GFR of 23.4 mL/min/1.73m2.\n",
+    "diff_label_texts": "She had a heart transplant because her heart got very weak after pregnancy. Later, her kidneys—the body’s filters—were hurt by a germ called BK virus. A small kidney sample showed long‑lasting irritation and damage from this virus. A blood test also showed a high amount of BK virus (log 4.5). Her doctors turned down her anti‑rejection medicines to help. After about two years, her kidney numbers stayed steady. Her creatinine was 2.5 mg/dL and her GFR was 23.4 mL/min/1.73m2.",
+    "summary": "We report a case of BK virus nephropathy in a patient who underwent heart transplantation due to peripartum cardiomyopathy. The renal biopsy reported active chronic tubulointerstitial nephritis associated with late-stage BK virus nephritis and the blood viral load for BK virus was positive (log 4.5). The immunosuppressive treatment was reduced, and after two years of follow-up, the patient had stable renal function with serum creatinine of 2.5 mg/dL (GFR of 23.4 mL/min/1.73m2).\n"
+  },
+  {
+    "doc_id": 72,
+    "label": "intermediate_health_literacy",
+    "fulltext": "A 39-year-old woman with a diagnosis of peripartum cardiomyopathy who received a heart transplant in October 2014. She received induction with Basiliximab and methylprednisolone. She also received maintenance treatment with tacrolimus XL prolonged release 7 mg daily, everolimus 1 mg twice daily, and prednisolone 5 mg/day. She had two episodes of acute rejection during the first year post-transplant, and was controlled with methylprednisolone pulse therapy with good results. There was no history of renal disease and her renal function was stable with creatinine of 0.88 mg/dL and a glomerular filtration rate (GFR) of 102 mL/min/1.73m2 during the first year post-transplant. Follow-up was done exclusively by the heart transplant group and routine polyomavirus viral load BK or urinary cytology was not performed. In 2016, she presented a creatinine serum elevation of up to 1.9 mg/dL, with a GFR of 32.6 mL/min/1.73m2. At that time, the minimum tacrolimus level was 7.2 ng/mL and everolimus, 5.2 ng/mL. Anticalcineurin toxicity was suspected; therefore, tacrolimus was reduced to 4 mg daily and creatinine returned to near baseline (creatinine 1.25 mg/dL, GFR 54.1 mL/min/1.73m2); no renal biopsy was performed. In March 2017, creatinine increased to 2.69 mg/dL, with a GFR of 21.4 mL/min/1.73m2, for which she was hospitalized. The patient stated that she did not have any symptoms. During physical examination, she was in good general condition, heart rate of 80 beats per minute, blood pressure of 130/90 mmHg, respiratory rate of 15 per minute, afebrile. Further studies were performed: renal tract ultrasound showed normal renal size but increased echogenicity; urinalysis and urine cultures were negative, without haematuria, pyuria or casts; echocardiogram with adequate cardiac function; HIV, syphilis, hepatitis B and C serologic tests were negative; minimum tacrolimus level of 5.2 ng/mL, and everolimus of 5.98 ng/mL. Control was initiated with intravenous hydration, and tacrolimus XL dose was reduced to 2 mg daily, but there was no improvement in renal function; a renal biopsy was planned.\n\nRenal biopsy revealed active chronic interstitial nephritis associated with advanced poliomyelitis virus nephritis. BK virus PCR was performed and was positive at 33,800 copies/mL in blood (log 4.5). Tacrolimus was discontinued; creatinine levels stabilized between 2.2 and 2.4 mg/dL, with no further elevation in post-discharge controls. Her viral load began to decline to undetectable levels. The patient did not have episodes of cardiac rejection in 3 years of follow-up; the last creatinine measurement was 2.5 mg/dL, corresponding to a GFR of 23.4 mL/min/1.73m2.\n",
+    "diff_label_texts": "A 39-year-old woman had a heart transplant in 2014 for peripartum cardiomyopathy and was treated with standard immunosuppression (basiliximab induction, then tacrolimus, everolimus and low‑dose prednisone). She had two treated episodes of rejection in the first year and initially normal kidney function. Routine BK virus monitoring was not done. Over the next two to three years her serum creatinine rose: first to 1.9 mg/dL in 2016 (which improved after lowering tacrolimus), then to 2.69 mg/dL in March 2017, when she was hospitalized. Workup including ultrasound and urine tests was unrevealing, so a kidney biopsy was performed. The biopsy showed chronic tubulointerstitial nephritis with late-stage BK virus nephropathy, and blood BK viral load was positive at about 33,800 copies/mL (log 4.5). Tacrolimus was stopped and her creatinine stabilized between 2.2 and 2.5 mg/dL while the BK viral load fell to undetectable levels. After two years of follow-up she had stable renal function with a creatinine of 2.5 mg/dL (estimated GFR about 23.4 mL/min/1.73 m2) and no further cardiac rejection.",
+    "summary": "We report a case of BK virus nephropathy in a patient who underwent heart transplantation due to peripartum cardiomyopathy. The renal biopsy reported active chronic tubulointerstitial nephritis associated with late-stage BK virus nephritis and the blood viral load for BK virus was positive (log 4.5). The immunosuppressive treatment was reduced, and after two years of follow-up, the patient had stable renal function with serum creatinine of 2.5 mg/dL (GFR of 23.4 mL/min/1.73m2).\n"
+  },
+  {
+    "doc_id": 74,
+    "label": "intermediate_health_literacy",
+    "fulltext": "A 56-year-old Italian female patient with β-thalassemia major presented to the radiology department to undergo MRI to quantify myocardial, hepatic, and pancreatic iron deposition. The clinical history of the patient included a transfusion-dependent β-thalassemia condition (genotype HBB:c.118C > T/ HBB:c.93-21G > A), diagnosed at the age of 7 years, despite the fact that the first transfusion was carried out at 2 years. As a consequence of β-thalassemia, the patient underwent splenectomy and cholecystectomy.\n\nAt the moment of MRI, she had a negative HCV-RNA (Hepatitis C virus-Ribonucleic acid) test, no osteoporosis or other endocrine, cardiac, or hepatic complications, and good iron levels. The patient’s therapy included iron chelation with deferasirox, vitamin D, and luspatercept, an erythropoiesis modulator started 2 years before the MRI examination (good response, with an increase of about 35% of transfusion interval duration). Transfusion therapy included two units of concentrated and filtered red blood cells every 25 days with pre-transfusion hemoglobin values of 10–10.5 g/dl.\n\nOn MRI, a solid mass with lobulated and regular contours was incidentally identified within the prevascular compartment of the mediastinum.\n\nThe lesion was mildly hyperintense on T2-weighted images (T2-wi) and isointense on T1-wi. The mediastinal mass in question was discernible in a prior MRI examination conducted for the same purpose in 2020 before starting luspatercept therapy, albeit with a marginal enlargement.\n\nThere were no other apparent abnormalities observed in the remaining mediastinal compartments. No pleural or pericardial effusions were present.\n\nThe neurological examination was unremarkable, and in the preceding months, the patient exhibited no symptoms of mediastinal syndrome associated with compression of the adjacent neurovascular structures. Moreover, she did not exhibit any fever or experience any weight loss.\n\nFor further evaluation, the patient underwent 18F-deoxyglucose (18FDG) positron emission tomography (PET)-computed tomography (CT) and chest CT with contrast media. On PET-CT, the mediastinal mass showed only mild FDG uptake (SUVmax = 4.3); no other sites of abnormal radiotracer uptake were reported in the neck, chest, abdomen, and skeleton. On CT images, the lesion presented regular margins, solid density, and mild contrast enhancement. The adjacent structures did not exhibit any signs of invasion, and lymphadenopathies or extra-thoracic disease were not present. Such radiological features, the indolent behaviour over time, the absence of systemic symptoms, and the lack of avid FDG uptake on PET-CT scan made the diagnosis of thymoma probable.\n\nHowever, on lung window visualization, multiple rounded areas of parenchymal lucency, consistent with thin-walled cysts distributed symmetrically throughout both lungs, with normal intervening parenchyma, were evident.\n\nNo nodules or other interstitial abnormalities were associated with the cysts. No pneumothorax was detected. Coherently with thalassemic bone disease, the ribs appeared widened, and the spine displayed mild platyspondyly. The remaining portion of the chest and visible upper abdomen were unremarkable. The radiological findings were consistent with cystic lung disease, most likely LAM.\n\nThe patient was then referred to the pulmonary clinic for further evaluation. She was a never-smoker and did not report any respiratory symptoms. In particular, she denied a history of chronic cough, recurrent respiratory infections, or pneumothorax. No cutaneous lesions, notably facial fibrofolliculomas, were evident. On chest examination, the lung fields were clear. Peripheral capillary oxygen saturation was normal (98%), with a heart rate of 75 beats per minute. Pulmonary function tests revealed a substantial reduction in diffusing capacity of the lungs for carbon monoxide (DLCO; 42% of the predicted value), partly imputable to the condition of anemia, with a carbon monoxide transfer coefficient (KCO) of 73% of the predicted value. After discussion in a multidisciplinary tumor board setting, including a pulmonologist, the patient underwent left thoracoscopic thymectomy and concomitant lingual segment wedge resection. The histopathological report revealed a morphological finding and immunohistochemical pattern referable to type B2 thymoma with focal infiltration of the capsule. Extracapsular extension was not evident. However, the lesion was present at the resection margin (stage IIa according to Masaoka–Koga; stage 1a according to the tumor, node, metastasis [TNM] classification).\n\nRegarding the lung parenchyma, histopathologic analysis described lung parenchyma with cysts of variable size lined by spindle cells in myoid habit with immunohistochemical reactivity for actin, estrogen, progesterone receptors, and HMB45 (focal positivity). Modest chronic interstitial inflammation, vascular congestion, and recent blood extravasation were evident. These morphological findings were compatible with pulmonary LAM.\n\nA final histological diagnosis of thymoma and pulmonary LAM was made. For the neoplastic condition, the patient was a candidate for adjuvant radiation therapy due to the microscopically incomplete resection (R1). For LAM with concomitant β-thalassemia, treatment with sirolimus was recommended.",
+    "diff_label_texts": "A 56-year-old Italian woman with transfusion-dependent beta-thalassemia major (with prior splenectomy and cholecystectomy) underwent MRI to measure iron in the heart, liver, and pancreas. At the time of imaging, she had no significant endocrine, cardiac, or hepatic complications and was taking deferasirox, vitamin D, and luspatercept. The MRI incidentally revealed a lobulated mass in the prevascular mediastinum. PET showed only mild FDG uptake, and chest CT identified multiple thin-walled cysts throughout both lungs, a pattern consistent with lymphangioleiomyomatosis (LAM). After multidisciplinary review, she had thoracoscopic thymectomy and a lung wedge resection. Pathology confirmed type B2 thymoma and pulmonary LAM. Based on these findings, adjuvant radiation therapy was recommended for the thymoma, and sirolimus was advised for LAM.",
+    "summary": "A 56-year-old Italian female patient with β-thalassemia major underwent magnetic resonance imaging to quantify myocardial, hepatic, and pancreatic iron deposition. Her medical history included transfusion-dependent β-thalassemia, splenectomy, and cholecystectomy. At the time of magnetic resonance imaging, she had no significant endocrine, cardiac, or hepatic complications and was on deferasirox, vitamin D, and luspatercept. Magnetic resonance imaging revealed a lobulated mass in the prevascular mediastinum, which showed mild radiotracer uptake on positron emission tomography. Chest computed tomography revealed multiple thin-walled cysts in the lungs, indicating lymphangioleiomyomatosis. Following multidisciplinary evaluation, the patient underwent thoracoscopic thymectomy and lung wedge resection. Histopathology confirmed type B2 thymoma and pulmonary lymphangioleiomyomatosis. Post-surgery, the patient was recommended for adjuvant radiation therapy and sirolimus treatment."
+  },
+  {
+    "doc_id": 75,
+    "label": "intermediate_health_literacy",
+    "fulltext": "We present a case of a 49-year-old woman with renal and heart failure following a long-term (lasting from 13 years of age) SLE prepared for kidney transplantation. Due to LN (class III, then IV), starting at childhood, she was treated with steroids, together with cyclophosphamide, replaced later by methotrexate and then azathioprine. Hence, the partial remission of nephrotic syndrome was achieved and from 2002 the patient did not receive any immunosuppressive therapy. She was also HBV and HCV positive. SLE involvement of circulatory system presented with early coronary atherosclerosis, ischemic heart disease, and myocardial infarction at the age of 20. In 2007, because of deterioration of kidney function with a serum creatinine concentration of 2.2 mg/dL and proteinuria of 2 g/day, the kidney biopsy was performed. The biopsy showed active and sclerotic focal proliferative lupus nephritis nevertheless immunosuppressive therapy was not introduced for the reason of active replication of HCV. The kidney function was gradually deteriorating over time. Despite cardiac intervention (PCI RCA), the patient developed severe post-infarction and dilated cardiomyopathy and required ICD implantation in primary prevention in 2009. Later, on lupus and secondary cardiomyopathic background, the patient developed severe MV and TV regurgitation. For this reason, the patient underwent mitral and tricuspid valve repair and left ventricle volume reduction surgery complicated by low cardiac output syndrome with a need for intra-aortic balloon pump use (2014). In the postoperative period, the kidney function deteriorated, requiring the initiation of renal replacement therapy. The patient has been on dialysis for 4 years. While being on active waiting list for kidney transplantation presented remission of laboratory indices of lupus (complement splits within normal limits: C3–0,93 g/l, C4–0,4 g/l, ANA negative) and persisting circulatory insufficiency with markedly reduced stair-climbing capacity (to one flight of stairs) with elevated BNP 619 pg/ml (n. 0–100). In transthoracic echocardiography, performed before renal transplantation, the left ventricle and the left atrium were significantly enlarged and the left ventricular systolic function was significantly reduced with LVEF 26% and GLS -3. Due to the implantation of the mitral ring, it was not possible to assess the left ventricular diastolic function. The high tricuspid regurgitant flow gradient with widened and poorly respiratory mobile inferior vena cava indicated a high probability of pulmonary hypertension. Furthermore, while preparing the patient for the surgical procedure, it was decided to include cardioprotective therapy with Levosimendan. Due to the time frame associated with the transplantation procedure, the drug infusion was started as soon as possible after cross-match results were known, immediately after the dialysis session. The infusion at a dose of 0.1 μg/kg/min was continued after surgery for a total of 24 h. The patient’s anesthesia for kidney transplantation and perioperative care included the aspect of optimizing transplanted kidney perfusion, avoiding the use of renal toxic drugs and those excreted by properly functioning kidneys, as well as the use of nephroprotective agents. Because of the patient’s cardiological burden, including recurrent episodes of extrasystole proceeding with decompensation of the circulatory system, together with the need of ICD turning off for the transplantation period, the Swan-Ganz catheter for hemodynamic assessment was not used. Anesthesia monitoring was limited the to ECG, central catheter with CVP assessment, direct blood pressure measurement from the cannula inserted into the radial artery, and cardiac ultrasound. In the perioperative period the CVP parameter was used to assess the volatility, and in the postoperative period, a cardiac ultrasound was used along with the assessment of VCI respiratory fill and motility. The therapy was aimed at the standard of fluid therapy called Goal Directed Therapy (GDT). During general anesthesia, fentanyl, triacrium, propofol, desflurane, antibiotic therapy, and standard immunosuppressive treatment were used as well as 25 g of mannitol infusion was administered as a nephroprotective treatment and 0.9% NaCl as a fluid therapy. In the course of postoperative immunosuppression, she received steroids, tacrolimus with mycophenolate mofetil which was stopped due to persistent leukopenia and cytomegalovirus infection. Furthermore delayed graft function was observed with a need for hemodialysis for almost 6 weeks (mostly due to fluid retention). BNP levels raised to 2996 pg/ml and then slowly decreased. The kidney biopsy performed 2 weeks after transplantation revealed acute rejection (AR II B Banff 2015) with ATN. Finally, the patient was discharged from the hospital on the 67th POD with the serum creatinine concentration of 1.4 mg/dL and BNP level of 1794 pg/ml. One month after kidney transplantation, there was a reduction in left ventricular dimensions, improved systolic function in the EF (increase to 30%) and GLS (decrease to − 6) assessment. In addition, there was a decrease in the tricuspid regurgitant flow gradient with normal width and respiratory motility of the IVC, which indicates a low probability of pulmonary hypertension. The improvement of echocardiographic parameters also reflected the simultaneous improvement of exercise capacity in the recipient from NYHA III/IV to NYHA II. In the 5-month observation, further improvement of heart function with a drop of BNP to 1066 pg/ml and normal kidney function were noted.",
+    "diff_label_texts": "This report describes a 49-year-old woman with long‑standing systemic lupus erythematosus (SLE) who developed progressive kidney and heart failure and was listed for kidney transplantation after four years on dialysis. Her SLE began in childhood with lupus nephritis and she had prior immunosuppressive treatments; she was also hepatitis B and C positive. She had early heart disease, including a heart attack at age 20, later developed ischemic and dilated cardiomyopathy, received an ICD, and underwent mitral and tricuspid valve repair with left‑ventricle surgery; after that operation her kidney function worsened and dialysis was started. Before transplant she had severe heart dysfunction (LVEF about 26%, high BNP) and signs suggesting possible pulmonary hypertension, so the team added perioperative cardioprotective therapy with levosimendan. Levosimendan infusion (0.1 µg/kg/min) began after a dialysis session when the donor match was confirmed and continued through the first 24 hours after surgery. Anesthesia and postoperative care focused on protecting the new kidney and careful fluid and hemodynamic management; invasive pulmonary artery catheterization was avoided because of her ICD and unstable rhythm history. The postoperative course was complicated: she experienced delayed graft function requiring hemodialysis for roughly six weeks, had a biopsy‑proven acute rejection episode with acute tubular necrosis, and developed leukopenia and cytomegalovirus infection that led to changes in immunosuppression. BNP rose after surgery but then gradually fell; she was discharged on day 67 with serum creatinine 1.4 mg/dL. By one month after transplant there was measurable improvement in heart size and function (EF up to ~30%, better strain measurements), lower pressures suggesting less pulmonary hypertension, and better exercise tolerance (NYHA III/IV to II). At five months she had continued improvement in heart function, BNP down to about 1066 pg/mL, and normal kidney function.",
+    "summary": "We present a case of a 49-year-old woman with renal and heart failure following a long-term SLE prepared for kidney transplantation. During the SLE course, the function of the heart and kidneys gradually deteriorated. The patient required the initiation of renal replacement therapy and was dialyzed until a kidney transplantation for 4 years. In the preparation of the patient for the surgical procedure, due to the extremely low ejection fraction, it was decided to include cardioprotective treatment with Levosimendan. The postoperative period was not straightforward but successful. In the monthly and five-month follow-up, a continuous improvement of heart function with normal renal function was noted."
+  },
+  {
+    "doc_id": 76,
+    "label": "intermediate_health_literacy",
+    "fulltext": "The patient was a 42-year-old woman with a history of menstrual migraine, Hashimoto Thyroiditis, Familial Mediterian Fever (FMF), and dyspepsia. She was taking 75 mg of levothyroxine, 30 mg of lansoprazole, and 1.5 mg of colchicine daily. In February of 2023, she was diagnosed with acute bronchitis, which was treated with antibiotics and bronchodilators. She developed a daily headache after two weeks, manifesting as more than ten short-lasting attacks per day provoked by coughing, straining, and lifting. The duration of each attack was 30 minutes, and the pain was bilaterally distributed from the neck to the top of the head. The headache was sharp and severe. She described the attack as a sensation of storm-like fluid movement in the head. She did not suffer any of the symptoms associated with previous migraine attacks, such as phonophobia, photophobia, vomiting, or throbbing. The severity of the attack was determined using a numeric rating scale (NRS) with a score of 9 out of 10. These attacks typically necessitated a visit to the emergency room. The results of her physical and neurological exams were unremarkable. The laboratory tests, including those for thyroid hormones, electrolytes, liver and kidney function, and serology, were negative. Brain and cervical spinal magnetic resonance imaging (MRI) with and without contrast, magnetic resonance venography (MRV), and angiography (MRA) were all normal. She did not give consent for a lumbar puncture. When we first encountered her in the clinic, she was taking 25 mg of indomethacin per day. Her attacks stopped after putting her on 60 mg of lansoprazole and increasing her daily dose of indomethacin to 150 mg. However, she encountered gastrointestinal side effects, so the indomethacin was discontinued on day three. Due to the adverse effects, she was unable to take topiramate and propranolol.\n\nShe came to the clinic 15 days after her initial visit with an NRS score of 9/10. She was taken to the local operating room. We used a GE Healthcare, Voluson™ E6, ultrasonography system with a linear 13–5 MHz probe for unilateral PGONB. The patient’s neck was prone to flexion. The linear probe was initially transversely positioned on the occipital protuberance and then advanced caudally, demonstrating that the C2 spinous process resembled the two horns. Through lateral probe movement, the inferior muscles of the obliquus capitis and semispinalis capitis were located. Here, the superior to the inferior oblique capitis muscle and beneath the semispinalis capitis muscle were identified to be the greater occipital neuron (GON). From this location, a 22-gauge spinal needle and 3 ccs of bupivacaine at a concentration of 0.5% were used to perform GON blocking. The intensity of her attack decreased from 9/10 to 2/10 after the first 20 minutes of the block. Throughout a month, the blocks were repeated once a week. In the second month, the frequency of her attacks decreased to two per month, with an intensity of 4/10. She did not encounter any attacks in the sixth month.\n\n",
+    "diff_label_texts": "A 42-year-old woman with primary cough headache (PCH) could not tolerate oral preventive medicines because of side effects. She developed more than ten short, severe headache attacks a day after a bout of bronchitis; each attack lasted about 30 minutes, was triggered by coughing, straining or lifting, and reached 9/10 on a pain scale. Neurological exam and brain and neck imaging were normal, and she declined a lumbar puncture. Because she could not keep taking indomethacin and could not use other oral options, we offered an ultrasound-guided proximal greater occipital nerve block (PGONB) using bupivacaine. After a single, unilateral block the pain fell from 9/10 to 2/10 within 20 minutes. The block was repeated once weekly for a month; at two months both the number of attacks and their intensity had declined (about two attacks per month at 4/10), and by six months she reported no attacks. No adverse effects from the nerve blocks were observed, suggesting ultrasound-guided GON blockade can be an effective option when oral drugs are not tolerated.",
+    "summary": "Herein, we report that a 42-year-old female patient with PCH who could not use the oral medication because of side effects. When she came to the pain clinic with an attack with intensity of 9/10 , we took her to the local operating room. The ultrasound (US) guided proximal greater occipital nerve block with bupivacaine was performed and the intensity of the attack was reduced to 2/10. The blockage was repeated once a week for a month. After two months, both the intensity of headache and number of attacks decreased and no adverse effect was observed."
+  },
+  {
+    "doc_id": 78,
+    "label": "low_health_literacy",
+    "fulltext": "A male was born via an emergency cesarean section due to fetal distress at 40 weeks of gestational age. The mother's age was 33 years, with gravida 1 and para 1 parity. Both the parents and brother had no family history of congenital anomalies, aortic-related diseases, or sudden death. Based on the results of the prenatal ultrasonography at the end of the second trimester, the femur length of the fetus was found to be 1 to 3 weeks longer than the supposed length of the actual gestational age. Fetal echocardiography showed cardiomegaly with a fetal cardiothoracic circumference ratio of 0.5 or higher based on the baby's term. Moreover, the size of the foramen ovale was larger than normal, and left aortic constriction was seen next to the subclavian artery basin. Furthermore, no other abnormalities were found on prenatal ultrasound.\n\nAt birth, the weight was 3560 g (75 percentile), the length was 56.5 cm (over 90 percentile), and the head circumference was 36 cm (over 90 percentile). Apgar scores at 1 and 5 minutes were 4 and 6 points, respectively. In the delivery room, the patient had no spontaneous breathing and had bradycardia and cyanosis. After being admitted to the neonatal intensive care unit, various musculoskeletal malformations were confirmed via physical examination. Severe arachnodactyly and camptodactyly were observed in both hands and feet, and the soles of the feet were flat. The elbow and knee joints were not fully extended. The face had malar hypoplasia with senile facial appearance. The eye was deeply settled with a down-slanting palpebral fissure, and the ear with hypoplastic cartilage was poorly settled and crumpled. The patient presented with a sagging mouth, prominent coronal suture, and brachycephaly. A grade V/VI systolic murmur was heard at both the upper sternal border and left lower sternal border with grade III parasternal heave. Echocardiography showed poor cardiac contractility, severe pulmonary hypertension, dilated aortic sinus (20.2 mm) (Z-score; 8.08 by Boston, 6.37 by Detroit, or 5.97 by Halifax), and multiple intracardiac valvular dysfunction with valve prolapses (moderate aortic regurgitation, severe mitral regurgitation, moderate tricuspid regurgitation, and moderate pulmonary valve regurgitation). And the ophthalmologic examination results showed ectopia lentis in both eyes as well as lens subluxation. Liver herniation was confirmed using abdominal X-ray and ultrasound. The systemic score of the musculoskeletal manifestation was 11 points, according to the Ghent criteria (international diagnostic criteria for MFS).\n\nFor genetic diagnosis, Sanger sequencing and polymerase chain reaction were performed on the nucleotide sequence as reference for the FBN1 gene. As a result, a mutation in which G, the first base of the 32nd intron in the form of a heterogeneous mutation, was substituted with T (c.3964 + 1G > T). This was confirmed as the likely pathogen variant based on the 2015 ACMG/AMP guideline. The location of the mutation was included in the site previously known as the neonatal region of MFS (exons 24–32). The patient could be diagnosed with neonatal MFS with a novel FBN1 gene mutation within 2 weeks of life.\n\nOn the first day of life, differential cyanosis was found to show refractory hypoxemia despite more than 60% oxygen supply and signs of low cardiac output. The patient was managed medically for improving the low cardiac output according to severe mitral regurgitation and aortic regurgitation. Afterload reduction including milrinone continuous infusion, full sedation using fentanyl continuous infusion, and use of diuretic were attempt to improve the oliguria and heart failure. Despite the medical management, the patient presented with respiratory failure, heart failure, and severe pulmonary hypertension requiring continuous invasive mechanical ventilation. Aortic regurgitation, mitral regurgitation, pulmonary hypertension, and cardiac contractility got worse. After several consultations with the patient's family and medical staff about the treatment plan, palliative care was continued instead of surgical treatment. As a result, hepatic and pulmonary congestion accompanied by pulmonary hemorrhage had progressed as well. Eventually, it had progressed to multiple organ dysfunction syndrome, and the patient died 32 days after the birth.",
+    "diff_label_texts": "This newborn had a very serious genetic condition called neonatal Marfan syndrome. It badly affected his heart. His fingers and toes were very long like spider legs. Some fingers and toes were stuck in a bent position. His elbows and knees could not fully straighten. His face looked old for a baby. His eyes were deep set and tilted downward. His ears were soft and not well formed. His mouth sagged. His head was short and wide. The clear lenses in his eyes were out of place. A DNA test found a new change in the fibrillin-1 gene in a spot linked to the newborn form of this condition. Doctors tried medicines to lower the heart’s workload, kept him deeply sedated to reduce strain, and gave water pills to help him pee and move extra fluid. Even with this care, the heart valve leaks and high pressure in the lungs got worse, and the heart grew weaker. Surgery would have been needed to help him live longer. Because the disease was getting worse very fast, the family chose comfort care. A few months after birth, his heart failure worsened and he died.",
+    "summary": "Patient concerns:\nA newborn with neonatal MFS and severe cardiac involvement. He presented various severe clinical features such as arachnodactyly, camptodactyly, elbow and knee joint contracture, senile facial appearance, and deep settling with down-slanting palpebral fissure, hypoplastic ear cartilage, sagging mouth, brachycephaly, and ectopia lentis.\n\nDiagnosis:\nGenetic analysis revealed a novel mutation at nucleotide 3964 (c.3964 + 1 G > T) in intron 32 of the fibrillin-1 gene. This mutation is identified to be in the so-called neonatal region of fibrillin-1 exon 24 to 32, as reported previously.\n\nInterventions:\nThe patient was managed medically for improving the low cardiac output according to severe mitral regurgitation and aortic regurgitation. Afterload reduction, full sedation, and use of diuretic were attempted to improve the oliguria and heart failure.\n\nOutcomes:\nDespite the medical management, aortic regurgitation, mitral regurgitation, pulmonary hypertension, and cardiac contractility got worse. Surgical treatment is essential to prolong the patient's life, however, considerations for the grave progression of the disease make families decide to continue palliative care instead of surgical treatment. A few months after birth, he presented with rapidly progressive aortic regurgitation, mitral regurgitation, and congestive heart failure leading to death."
+  },
+  {
+    "doc_id": 78,
+    "label": "intermediate_health_literacy",
+    "fulltext": "A male was born via an emergency cesarean section due to fetal distress at 40 weeks of gestational age. The mother's age was 33 years, with gravida 1 and para 1 parity. Both the parents and brother had no family history of congenital anomalies, aortic-related diseases, or sudden death. Based on the results of the prenatal ultrasonography at the end of the second trimester, the femur length of the fetus was found to be 1 to 3 weeks longer than the supposed length of the actual gestational age. Fetal echocardiography showed cardiomegaly with a fetal cardiothoracic circumference ratio of 0.5 or higher based on the baby's term. Moreover, the size of the foramen ovale was larger than normal, and left aortic constriction was seen next to the subclavian artery basin. Furthermore, no other abnormalities were found on prenatal ultrasound.\n\nAt birth, the weight was 3560 g (75 percentile), the length was 56.5 cm (over 90 percentile), and the head circumference was 36 cm (over 90 percentile). Apgar scores at 1 and 5 minutes were 4 and 6 points, respectively. In the delivery room, the patient had no spontaneous breathing and had bradycardia and cyanosis. After being admitted to the neonatal intensive care unit, various musculoskeletal malformations were confirmed via physical examination. Severe arachnodactyly and camptodactyly were observed in both hands and feet, and the soles of the feet were flat. The elbow and knee joints were not fully extended. The face had malar hypoplasia with senile facial appearance. The eye was deeply settled with a down-slanting palpebral fissure, and the ear with hypoplastic cartilage was poorly settled and crumpled. The patient presented with a sagging mouth, prominent coronal suture, and brachycephaly. A grade V/VI systolic murmur was heard at both the upper sternal border and left lower sternal border with grade III parasternal heave. Echocardiography showed poor cardiac contractility, severe pulmonary hypertension, dilated aortic sinus (20.2 mm) (Z-score; 8.08 by Boston, 6.37 by Detroit, or 5.97 by Halifax), and multiple intracardiac valvular dysfunction with valve prolapses (moderate aortic regurgitation, severe mitral regurgitation, moderate tricuspid regurgitation, and moderate pulmonary valve regurgitation). And the ophthalmologic examination results showed ectopia lentis in both eyes as well as lens subluxation. Liver herniation was confirmed using abdominal X-ray and ultrasound. The systemic score of the musculoskeletal manifestation was 11 points, according to the Ghent criteria (international diagnostic criteria for MFS).\n\nFor genetic diagnosis, Sanger sequencing and polymerase chain reaction were performed on the nucleotide sequence as reference for the FBN1 gene. As a result, a mutation in which G, the first base of the 32nd intron in the form of a heterogeneous mutation, was substituted with T (c.3964 + 1G > T). This was confirmed as the likely pathogen variant based on the 2015 ACMG/AMP guideline. The location of the mutation was included in the site previously known as the neonatal region of MFS (exons 24–32). The patient could be diagnosed with neonatal MFS with a novel FBN1 gene mutation within 2 weeks of life.\n\nOn the first day of life, differential cyanosis was found to show refractory hypoxemia despite more than 60% oxygen supply and signs of low cardiac output. The patient was managed medically for improving the low cardiac output according to severe mitral regurgitation and aortic regurgitation. Afterload reduction including milrinone continuous infusion, full sedation using fentanyl continuous infusion, and use of diuretic were attempt to improve the oliguria and heart failure. Despite the medical management, the patient presented with respiratory failure, heart failure, and severe pulmonary hypertension requiring continuous invasive mechanical ventilation. Aortic regurgitation, mitral regurgitation, pulmonary hypertension, and cardiac contractility got worse. After several consultations with the patient's family and medical staff about the treatment plan, palliative care was continued instead of surgical treatment. As a result, hepatic and pulmonary congestion accompanied by pulmonary hemorrhage had progressed as well. Eventually, it had progressed to multiple organ dysfunction syndrome, and the patient died 32 days after the birth.",
+    "diff_label_texts": "A term newborn boy had neonatal Marfan syndrome with severe heart involvement. He showed typical features: very long fingers and toes (arachnodactyly), bent fingers and toes (camptodactyly), elbow and knee contractures, an aged facial appearance, deep-set downward-slanting eyes, underdeveloped ear cartilage with a sagging mouth, a short-wide head shape (brachycephaly), and ectopia lentis (displaced eye lenses). Genetic testing identified a new FBN1 mutation affecting a splice site (c.3964+1G>T in intron 32) within the known neonatal region (exons 24–32). He developed low cardiac output due to severe mitral and aortic regurgitation and also had pulmonary hypertension. Medical management focused on afterload reduction, deep sedation to lessen cardiac work, and diuretics to treat fluid overload and low urine output. Despite treatment, the valve regurgitation, pulmonary hypertension, and poor heart pumping worsened. Surgery would likely have been required to extend survival, but given the rapid and grave progression, the family chose palliative care. Within a few months after birth, he experienced rapidly progressive heart failure and died.",
+    "summary": "Patient concerns:\nA newborn with neonatal MFS and severe cardiac involvement. He presented various severe clinical features such as arachnodactyly, camptodactyly, elbow and knee joint contracture, senile facial appearance, and deep settling with down-slanting palpebral fissure, hypoplastic ear cartilage, sagging mouth, brachycephaly, and ectopia lentis.\n\nDiagnosis:\nGenetic analysis revealed a novel mutation at nucleotide 3964 (c.3964 + 1 G > T) in intron 32 of the fibrillin-1 gene. This mutation is identified to be in the so-called neonatal region of fibrillin-1 exon 24 to 32, as reported previously.\n\nInterventions:\nThe patient was managed medically for improving the low cardiac output according to severe mitral regurgitation and aortic regurgitation. Afterload reduction, full sedation, and use of diuretic were attempted to improve the oliguria and heart failure.\n\nOutcomes:\nDespite the medical management, aortic regurgitation, mitral regurgitation, pulmonary hypertension, and cardiac contractility got worse. Surgical treatment is essential to prolong the patient's life, however, considerations for the grave progression of the disease make families decide to continue palliative care instead of surgical treatment. A few months after birth, he presented with rapidly progressive aortic regurgitation, mitral regurgitation, and congestive heart failure leading to death."
+  },
+  {
+    "doc_id": 0,
+    "label": "intermediate_health_literacy",
+    "fulltext": "A 20-year-old woman was followed up since the age of eight for idiopathic NS inaugurated by cerebral venous thrombosis extended to the right jugular vein with a massive pulmonary embolism. The patient did not have any sequelae. She had no other medical or surgical history. A family history of thrombosis has not been reported. The patient was not biopsied because she had no kidney failure nor gross hematuria, or hypertension at first presentation; added to that, she had no extra renal signs suggestive of a secondary nephrotic syndrome. She was accordingly put on anticoagulant therapy (Oral vitamin K antagonist) and oral corticosteroid therapy with good evolution. Thereafter, the patient received several cures of high-dose corticosteroids for steroid-dependent relapses of NS. She was, hence, put on mycophenolate mofetil (MMF) as a background therapy to avoid corticosteroids and ensure normal growth. An exhaustive assessment of thrombophilia was performed and did not show any abnormality. Homocysteine rate, blood fibrinogen rate, Protein C, protein S, antithrombin III, factor V Leiden mutation, JAK-2 mutation, cryoglobulins, anticardiolipin antibodies, lupus anticoagulant and beta-1-glycoprotein antibodies were normal. The anticoagulant treatment was stopped after nine years. The evolution was enameled by the occurrence of several relapses of her disease controlled by oral corticosteroid therapy. Remission of NS has been noted since 2017, so MMF was gradually stopped in 2019 and the patient remained asymptomatic and without any relapse.\n\nOne year later, the patient came up to our emergency department for acute intense diffuse abdominal pain without any particular irradiation associated with postprandial vomiting and bilateral lower limb edema for the last six hours. The physical examination revealed an intense epigastric tenderness with normal vital signs (arterial pressure of 120/70 mm Hg, heart rate of 83 bpm, and oxygen saturation at 100% on room air). The patient was afebrile with normal consciousness. The rest of the physical examination was unremarkable. The urinalysis with labstix revealed proteinuria. The hemogasanalysis results showed metabolic acidosis with respiratory compensation. Further laboratory tests revealed hypoalbuminemia, hypercholesterolemia, a prothrombin time at 90%, high levels of D-dimer, lactate dehydrogenase, and creatine phosphokinase as well as a biological inflammatory syndrome with a CRP of 37 mg/L, and leucocytosis at 26.4 x 103/µL. Renal and liver functions were normal.\n\nThe patient was hospitalized in an intensive care unit with close monitoring of vital signs and initiation of resuscitation measures. An abdominal ultrasound was performed urgently showing an intra-abdominal effusion of low to moderate abundance. An abdominal CT scan revealed acute thrombosis of the superior mesenteric artery with acute mesenteric ischemia. The patient was immediately routed to the operating room. Intraoperative exploration confirmed mesenteric ischemia with extensive necrosis of almost entirely of the small bowel making their resections incompatible with life shown in Figure 3. The patient died after 48 hours.",
+    "diff_label_texts": "A 20‑year‑old woman had a 12‑year history of idiopathic nephrotic syndrome that initially presented with extensive cerebral venous thrombosis and pulmonary embolism. She was treated with anticoagulation and oral corticosteroids, then mycophenolate mofetil as a steroid‑sparing agent. A comprehensive thrombophilia work‑up was negative. She experienced multiple relapses controlled with steroids until 2017, then remained in remission; anticoagulation and MMF were discontinued. One year later, she developed sudden diffuse abdominal pain with postprandial vomiting and bilateral leg edema. Laboratory tests confirmed a relapse of nephrotic syndrome. Abdominal CT showed acute superior mesenteric artery thrombosis causing acute mesenteric ischemia. At surgery, there was extensive small‑bowel necrosis not compatible with survival. She died 48 hours later.",
+    "summary": "We present the case of a 20-year-old woman with a 12-year history of idiopathic NS revealed by extensive cerebral venous thrombosis with pulmonary embolism treated with anticoagulation therapy and oral corticosteroid therapy followed by mycophenolate mofetil (MMF). The thrombophilia assessment did not show any abnormalities. The evolution was marked by the occurrence of several NS relapses controlled by oral corticosteroid therapy until 2017. Subsequently, the patient had not presented a relapse of her disease. The anticoagulant treatment and the MMF were therefore stopped. One year later, the patient presented with severe diffuse acute abdominal pain associated with postprandial vomiting and bilateral lower limb edema. Laboratory results confirmed a NS relapse. An abdominal CT scan revealed acute thrombosis of the superior mesenteric artery with acute mesenteric ischemia. Intraoperative exploration showed mesenteric ischemia with extensive necrosis of the small intestine making their resections incompatible with life. The patient died after 48 hours."
+  },
+  {
+    "doc_id": 0,
+    "label": "low_health_literacy",
+    "fulltext": "A 20-year-old woman was followed up since the age of eight for idiopathic NS inaugurated by cerebral venous thrombosis extended to the right jugular vein with a massive pulmonary embolism. The patient did not have any sequelae. She had no other medical or surgical history. A family history of thrombosis has not been reported. The patient was not biopsied because she had no kidney failure nor gross hematuria, or hypertension at first presentation; added to that, she had no extra renal signs suggestive of a secondary nephrotic syndrome. She was accordingly put on anticoagulant therapy (Oral vitamin K antagonist) and oral corticosteroid therapy with good evolution. Thereafter, the patient received several cures of high-dose corticosteroids for steroid-dependent relapses of NS. She was, hence, put on mycophenolate mofetil (MMF) as a background therapy to avoid corticosteroids and ensure normal growth. An exhaustive assessment of thrombophilia was performed and did not show any abnormality. Homocysteine rate, blood fibrinogen rate, Protein C, protein S, antithrombin III, factor V Leiden mutation, JAK-2 mutation, cryoglobulins, anticardiolipin antibodies, lupus anticoagulant and beta-1-glycoprotein antibodies were normal. The anticoagulant treatment was stopped after nine years. The evolution was enameled by the occurrence of several relapses of her disease controlled by oral corticosteroid therapy. Remission of NS has been noted since 2017, so MMF was gradually stopped in 2019 and the patient remained asymptomatic and without any relapse.\n\nOne year later, the patient came up to our emergency department for acute intense diffuse abdominal pain without any particular irradiation associated with postprandial vomiting and bilateral lower limb edema for the last six hours. The physical examination revealed an intense epigastric tenderness with normal vital signs (arterial pressure of 120/70 mm Hg, heart rate of 83 bpm, and oxygen saturation at 100% on room air). The patient was afebrile with normal consciousness. The rest of the physical examination was unremarkable. The urinalysis with labstix revealed proteinuria. The hemogasanalysis results showed metabolic acidosis with respiratory compensation. Further laboratory tests revealed hypoalbuminemia, hypercholesterolemia, a prothrombin time at 90%, high levels of D-dimer, lactate dehydrogenase, and creatine phosphokinase as well as a biological inflammatory syndrome with a CRP of 37 mg/L, and leucocytosis at 26.4 x 103/µL. Renal and liver functions were normal.\n\nThe patient was hospitalized in an intensive care unit with close monitoring of vital signs and initiation of resuscitation measures. An abdominal ultrasound was performed urgently showing an intra-abdominal effusion of low to moderate abundance. An abdominal CT scan revealed acute thrombosis of the superior mesenteric artery with acute mesenteric ischemia. The patient was immediately routed to the operating room. Intraoperative exploration confirmed mesenteric ischemia with extensive necrosis of almost entirely of the small bowel making their resections incompatible with life shown in Figure 3. The patient died after 48 hours.",
+    "diff_label_texts": "This is about a 20-year-old woman. She had a kidney problem since age eight that made protein leak into her urine. The problem first showed up when a big blood clot blocked veins in her brain, and a clot also went to her lungs. She took blood thinners and steroid pills. Later she took a medicine that calms the immune system to help her use fewer steroids. Tests showed no inherited blood-clotting problem. She had several flare-ups of the kidney problem. Steroid pills controlled them until 2017. After that she had no relapses. Her doctors stopped the blood thinner and the immune-calming medicine. One year later she had sudden, very bad belly pain all over. She threw up after eating. Both legs were swollen. Tests showed the kidney problem was back. A special X-ray picture (CT scan) showed a new clot in the main artery that feeds the small intestine. It was like a plug in a pipe that stops water. Blood could not reach the intestines. In surgery, most of her small intestine was dead. Taking out that much bowel would not allow life. She died 48 hours later.",
+    "summary": "We present the case of a 20-year-old woman with a 12-year history of idiopathic NS revealed by extensive cerebral venous thrombosis with pulmonary embolism treated with anticoagulation therapy and oral corticosteroid therapy followed by mycophenolate mofetil (MMF). The thrombophilia assessment did not show any abnormalities. The evolution was marked by the occurrence of several NS relapses controlled by oral corticosteroid therapy until 2017. Subsequently, the patient had not presented a relapse of her disease. The anticoagulant treatment and the MMF were therefore stopped. One year later, the patient presented with severe diffuse acute abdominal pain associated with postprandial vomiting and bilateral lower limb edema. Laboratory results confirmed a NS relapse. An abdominal CT scan revealed acute thrombosis of the superior mesenteric artery with acute mesenteric ischemia. Intraoperative exploration showed mesenteric ischemia with extensive necrosis of the small intestine making their resections incompatible with life. The patient died after 48 hours."
+  },
+  {
+    "doc_id": 0,
+    "label": "proficient_health_literacy",
+    "fulltext": "A 20-year-old woman was followed up since the age of eight for idiopathic NS inaugurated by cerebral venous thrombosis extended to the right jugular vein with a massive pulmonary embolism. The patient did not have any sequelae. She had no other medical or surgical history. A family history of thrombosis has not been reported. The patient was not biopsied because she had no kidney failure nor gross hematuria, or hypertension at first presentation; added to that, she had no extra renal signs suggestive of a secondary nephrotic syndrome. She was accordingly put on anticoagulant therapy (Oral vitamin K antagonist) and oral corticosteroid therapy with good evolution. Thereafter, the patient received several cures of high-dose corticosteroids for steroid-dependent relapses of NS. She was, hence, put on mycophenolate mofetil (MMF) as a background therapy to avoid corticosteroids and ensure normal growth. An exhaustive assessment of thrombophilia was performed and did not show any abnormality. Homocysteine rate, blood fibrinogen rate, Protein C, protein S, antithrombin III, factor V Leiden mutation, JAK-2 mutation, cryoglobulins, anticardiolipin antibodies, lupus anticoagulant and beta-1-glycoprotein antibodies were normal. The anticoagulant treatment was stopped after nine years. The evolution was enameled by the occurrence of several relapses of her disease controlled by oral corticosteroid therapy. Remission of NS has been noted since 2017, so MMF was gradually stopped in 2019 and the patient remained asymptomatic and without any relapse.\n\nOne year later, the patient came up to our emergency department for acute intense diffuse abdominal pain without any particular irradiation associated with postprandial vomiting and bilateral lower limb edema for the last six hours. The physical examination revealed an intense epigastric tenderness with normal vital signs (arterial pressure of 120/70 mm Hg, heart rate of 83 bpm, and oxygen saturation at 100% on room air). The patient was afebrile with normal consciousness. The rest of the physical examination was unremarkable. The urinalysis with labstix revealed proteinuria. The hemogasanalysis results showed metabolic acidosis with respiratory compensation. Further laboratory tests revealed hypoalbuminemia, hypercholesterolemia, a prothrombin time at 90%, high levels of D-dimer, lactate dehydrogenase, and creatine phosphokinase as well as a biological inflammatory syndrome with a CRP of 37 mg/L, and leucocytosis at 26.4 x 103/µL. Renal and liver functions were normal.\n\nThe patient was hospitalized in an intensive care unit with close monitoring of vital signs and initiation of resuscitation measures. An abdominal ultrasound was performed urgently showing an intra-abdominal effusion of low to moderate abundance. An abdominal CT scan revealed acute thrombosis of the superior mesenteric artery with acute mesenteric ischemia. The patient was immediately routed to the operating room. Intraoperative exploration confirmed mesenteric ischemia with extensive necrosis of almost entirely of the small bowel making their resections incompatible with life shown in Figure 3. The patient died after 48 hours.",
+    "diff_label_texts": "A 20‑year‑old woman had been followed since age eight for idiopathic nephrotic syndrome (NS) inaugurated by cerebral venous thrombosis extended to the right jugular vein with a massive pulmonary embolism, without sequelae and without personal or family thrombotic history. Kidney biopsy was deferred because there was no kidney failure, gross hematuria, hypertension, or extra‑renal signs suggestive of secondary NS at presentation. She was treated with an oral vitamin K antagonist and oral corticosteroids with good evolution. Subsequently, she had multiple steroid‑dependent relapses and was started on mycophenolate mofetil (MMF) as background therapy to spare corticosteroids and ensure normal growth. An exhaustive thrombophilia assessment was negative: homocysteine, fibrinogen, protein C, protein S, antithrombin III, factor V Leiden, JAK‑2, cryoglobulins, anticardiolipin antibodies, lupus anticoagulant, and anti‑β2‑glycoprotein I antibodies were all normal. Anticoagulation was stopped after nine years. Several relapses occurred but were controlled with oral corticosteroids. NS remission was documented from 2017; MMF was gradually discontinued in 2019, and she remained asymptomatic without relapse.\n\nOne year later, she presented to the emergency department with acute intense diffuse abdominal pain without irradiation, associated with postprandial vomiting and bilateral lower‑limb edema for six hours. Examination showed intense epigastric tenderness with normal vital signs (BP 120/70 mm Hg, HR 83 bpm, SpO2 100% on room air) and no fever or neurological impairment. Urinalysis detected proteinuria. Hemogasanalysis showed metabolic acidosis with respiratory compensation. Labs revealed hypoalbuminemia, hypercholesterolemia, prothrombin time 90%, elevated D‑dimer, LDH, and creatine phosphokinase, with inflammatory markers (CRP 37 mg/L) and leukocytosis (26.4 × 10^3/µL); renal and liver function were normal. Urgent abdominal ultrasound showed a low‑to‑moderate intra‑abdominal effusion. Contrast‑enhanced CT demonstrated acute thrombosis of the superior mesenteric artery with acute mesenteric ischemia. She underwent emergency laparotomy: intraoperative exploration confirmed mesenteric ischemia with extensive necrosis of almost the entire small bowel, rendering resection incompatible with life. She died 48 hours later.\n\nThis case illustrates catastrophic arterial thrombosis in the setting of NS despite a negative thrombophilia work‑up. NS is a hypercoagulable state with multifactorial mechanisms, including urinary loss of anticoagulant proteins (e.g., antithrombin III, protein S), increased fibrinogen, hemoconcentration, dyslipidemia, and systemic inflammation. While venous thromboembolism is more common in NS, superior mesenteric artery thrombosis is rare but often fatal, underscoring the need for high clinical suspicion and rapid imaging when severe acute abdominal pain occurs in patients with active or relapsing NS.",
+    "summary": "We present the case of a 20-year-old woman with a 12-year history of idiopathic NS revealed by extensive cerebral venous thrombosis with pulmonary embolism treated with anticoagulation therapy and oral corticosteroid therapy followed by mycophenolate mofetil (MMF). The thrombophilia assessment did not show any abnormalities. The evolution was marked by the occurrence of several NS relapses controlled by oral corticosteroid therapy until 2017. Subsequently, the patient had not presented a relapse of her disease. The anticoagulant treatment and the MMF were therefore stopped. One year later, the patient presented with severe diffuse acute abdominal pain associated with postprandial vomiting and bilateral lower limb edema. Laboratory results confirmed a NS relapse. An abdominal CT scan revealed acute thrombosis of the superior mesenteric artery with acute mesenteric ischemia. Intraoperative exploration showed mesenteric ischemia with extensive necrosis of the small intestine making their resections incompatible with life. The patient died after 48 hours."
+  },
+  {
+    "doc_id": 1,
+    "label": "low_health_literacy",
+    "fulltext": "We present the case of a 34-year-old woman, eight weeks pregnant with no other personal history of interest, who presents to the emergency department with generalized convulsions with dysarthria in the postcritical period, which resolve progressively in less than two hours. On physical examination, she is conscious, oriented, with no language or motor or sensory deficits. Only signs of a right lateral tongue bite are observed.\n\nThe complementary tests, such as blood tests or the electrocardiogram, are normal. Given that the episode corresponds with a first epileptic seizure and the patient is pregnant, an urgent magnetic resonance of the skull is requested.\n\nThe usual protocol was performed and 3D T1 sequences without and with intravenous contrast were obtained in axial, coronal and sagital planes, axial FLAIR, axial T2, VEN BOLD and magnetic susceptibility sequences, as well as axial diffusion and apparent diffusion coefficient map. The MRI identified multiple venous cortico-medullary vascular structures converging centripetally to a large central venous structure draining through the inferior anastomotic vein into the left transverse sinus, forming the classic ‘Medusa head’ sign. In the T1 sequences, the drainage vein was seen to be increased in signal with central hyphocaptation after contrast administration, suggesting partial thrombosis versus slow flow. In addition, in T2 and FLAIR sequences, the brain tissue surrounding the drainage vein was seen to be hyperintense, without diffusion restriction and compatible with edema.\n\nThese findings are suggestive of a venous anomaly of development with signs of partial peripheral thrombosis and slow flow more proximal, which cause edema of the surrounding tissue. She is started on clexane 60 mg/12 hours and levetiracetam 500 mg/12 hours and the patient shows improvement and symptomatic stability after one week.\n",
+    "diff_label_texts": "She is 34 years old and pregnant. She had a seizure and trouble speaking clearly. She was sent right away for a head MRI scan. The scan showed a pattern doctors call the “Medusa head.” This means the veins in her brain are arranged in an unusual way that she was born with. There is a small blood clot at the outer part of this vein pattern. The blood is also moving slowly closer to the main vein.",
+    "summary": "A 34-year-old pregnant woman presents with seizures and dysarthria and is urgently referred for a cranial MRI. The classic ‘Medusa head’ sign is seen and the diagnosis is made as a venous anomaly of development with peripheral partial thrombosis and proximal slow flow.\n"
+  },
+  {
+    "doc_id": 2,
+    "label": "intermediate_health_literacy",
+    "fulltext": "A 22-year-old woman came to the Department of Oral Medicine with complaints of mouth ulcers causing pain and eating and drinking difficulty persisting for a duration of one month. This condition begins with a fever and appears like pimples on the lips. Based on the anamnesis, it was discovered that she had been using pod-type vapes for about a year but had never experienced complaints like when she came for treatment. She had never smoked traditional cigarettes before starting to vape. She said the reason for trying vaping was out of curiosity, and she quite often tried different types of e-liquid with different flavors. Before her complaint, she had simply changed the type of e-liquid to a different flavor without mentioning the brand. She vapes almost every day, but not all day, only in her free time or with friends. She was a healthy individual, and before this condition appeared, she had no history of taking medications, including antibiotics, analgesics, anticonvulsants, non-steroidal anti-inflammatory drugs, and antifungals. She also had no history of drug or food allergies, but the patient has unhealthy eating habits (eating irregularly and not consuming vegetables and fruit). Extraoral examination showed no lesions on other parts of the body, while the lips of the patient had serosanguineous crusts and an erosive area at the corner of the mouth, and tended to bleed. Intraoral examination revealed white ulcers with yellowish edges, irregular, varying sizes, and pain on the labial, buccal, lateral, and ventral mucosa of the tongue and floor of the mouth.\n\nBased on the medical history of the patient and physical examination, which revealed oral mucosal involvement but no symptoms elsewhere in the body, as well as the non-reactive anti-HSV1 IgG results, the diagnosis of vaping-related oral erythema multiforme was established. The medical condition has been classified as minor erythema multiforme. The oral conditions were treated with 0.9% NaCl, which was moistened in gauze and placed on the lips three times a day. The patient was instructed to gargle 1 mg of dexamethasone in 10 mL of hyaluronic acid three times a day and avoid eating or drinking for at least 30 minutes after gargling. She was also given 2% miconazole cream applied to the wound in the right corner of the mouth twice a day, as well as vaseline album cream for dry lips. To maintain good oral hygiene, she was advised to brush her teeth and tongue twice a day, after breakfast and before bed. She was also instructed to stop vaping and avoid foods containing monosodium glutamate (MSG). The control was carried out after a week following therapy and showed that oral condition had improved. Written informed consent for the publication of details was obtained from the patient. This case report conformed with the Helsinki Declaration. The publication of this case report has also been approved by the institution.",
+    "diff_label_texts": "A 22-year-old woman presented with a month of painful stomatitis that made eating and drinking difficult. The illness began with a fever and pimple-like lesions on the lips. She had been vaping regularly for about one year. Examination showed no skin lesions elsewhere. The lips had serosanguineous crusts and erosions at the labial commissures that tended to bleed. Intraorally, there were multiple irregular white ulcers with yellowish borders on several sites of the oral mucosa. Anti–HSV-1 IgG was non-reactive. The diagnosis was oral erythema multiforme, likely related to vaping. Management included normal saline compresses to the lips, a dexamethasone mouth rinse mixed with hyaluronic acid, 2% miconazole cream applied to the lip corner, petroleum jelly for dry lips, and stopping vaping. Her oral condition improved within one week.",
+    "summary": "A 22-year-old woman came to the Oral Medicine Department with complaints of stomatitis causing pain, eating, and drinking difficulty, which started with fever and pimple-like on the lips. She was an active vape user for one year. Extraoral examination revealed no lesions on other body parts. The serosanguinolent crusts on the lips, an erosive area on the labial commissures and tended to bleed. Intraoral examination revealed white ulcers with yellowish edges and irregular, varying sizes in several parts of the oral mucosa. The anti-HSV-1 IgG laboratory results showed non-reactive, leading to a diagnosis of oral erythema multiforme. Management of oral conditions using 0.9% NaCl compress, dexamethasone mouthwash, and hyaluronic acid, applying 2% miconazole cream on labial commissures and vaseline album cream on the dry lips, and stopping vaping. Oral condition improved in a week of therapy."
+  },
+  {
+    "doc_id": 3,
+    "label": "low_health_literacy",
+    "fulltext": "A 29-year-old gravida V par IV (all alive, 3 spontaneous vaginal deliveries, and the last child was delivered by cesarean section for the indication of a failed induction 4 years prior to the current pregnancy) came for ANC follow-up at a gestational age of 32 weeks from her LNMP.\n\nAfter taking a medical history, it was discovered that all four of her children are healthy, doing well in school, and have no known history of genetic or seizure disorders. She was investigated with the Venereal Disease Research Laboratory (VDRL), Hepatitis B surface antigen (HBSag), and urine analysis, all of which were negative. All cell lines in the CBC were normal, her blood group is A, and Rh is positive, according to the Complete Blood Count (CBC), blood group, and RH. Obstetric ultrasound was also performed showing normal anatomical scan of the all body parts of the fetus except the heart. Detailed fetal echocardiography evaluation was done with findings of: both atria have comparable size and normal situs. Both atrioventricular and semilunar valves are normally positioned with normal opening and closure. Both ventricles are comparable in size and contractility; in both 2D and color flow, the left ventricle forms the apex of the heart without any ventricular septal defect. But on the papillary muscles of the left ventricle there were two circumscribed, round, echogenic mass measuring 18.2 mm by 8.3mm and 13.5mm by 8.3 mm. Upon evaluation of the outflow tract, both the LVOT (left ventricular outflow tract) and RVOT (right ventricular outflow tract) have normal anatomy and function using 2D and CF ultrasound evaluation. According to the fetal echo finding, a diagnosis of cardiac rhabdomyoma was made. Since there is a high chance of tuberous sclerosis in cardiac rhabdomyoma, detailed neurosonography and other system exams were done to look for other signs of tuberous sclerosis. Despite searching for the other features of tuberous sclerosis, no other sign of it was found other than the tumor. She had regular ANC follow-up from 32 weeks of gestation up to 39 weeks without any complications.\n\nAt gestational age of 39 weeks plus 1 day, she underwent a cesarean section for the indication of full-term pregnancy plus a request for a repeat cesarean section, with the outcome of a 3200-gram female with an APGAR score of 10 and 10 at the 1st and 5th minutes. Both the mother and the neonate had a smooth post-operative period and were discharged on the third day.\n\nAfter delivery, the neonate was evaluated on the 1st, 7th, and 30th days for any regression or increment of the mass, emergence of skin lesions, or seizure. All physical examination results were normal, and the mass size was similar to the antepartal evaluation.\n\nAt her 7th month, the child was evaluated again, and upon history inquiries, the infant was doing great developmentally for her age group. The infant was examined for neurodevelopmental delay, and the child was growing appropriately for her age. An echocardiography study by a pediatric cardiologist revealed well-circumscribed hyperechoic masses on both left ventricular papillary muscles, each measuring 21.8 mm by 9.2 mm and 14.7 mm by 8.5 mm and creating no left ventricular inflow obstruction.\n\nA history from the family was obtained, and a physical examination with anthropometric measurements was performed to assess her developmental condition during her first-year evaluation. The child was developing normally, as other children her age were. Except for the heart, all of the systems examined were unremarkable. An echocardiography study has revealed well-circumscribed hyperechoic masses on both left ventricular papillary muscles with no size increment and creating no left ventricular inflow obstruction.",
+    "diff_label_texts": "At 32 weeks of pregnancy, a routine scan found one small lump inside the baby’s heart. It caused no symptoms. This was the only problem seen. Doctors watched it with clinic visits until 39 weeks plus 1 day. Then the baby was delivered by C-section (a surgery to deliver the baby). After birth, the child had checkups on day 1, day 7, day 30, month 7, and month 12. At each visit, the child’s growth and behavior were healthy for age. The heart lump stayed the same size; it did not grow or shrink. By 1 year old, there were no signs of a related condition called tuberous sclerosis complex.",
+    "summary": "We are reporting an isolated, asymptomatic fetal intra-cardiac mass (rhabdomyoma) that was discovered at 32 weeks of gestation and was followed as an outpatient until 39 weeks plus one day, at which point a cesarean section was performed. After delivery, the child underwent evaluations at the 1st day, 7th day, 30th day, 7th month, and 12th month of age. Following a checkup, the child's anthropometric and neurobehavioral growth were both healthy. Except for the tumor, which was neither growing nor shrinking in size, none of the clinical diagnostic criteria for tuberous sclerosis complex were met for this child up to the age of one year."
+  },
+  {
+    "doc_id": 3,
+    "label": "proficient_health_literacy",
+    "fulltext": "A 29-year-old gravida V par IV (all alive, 3 spontaneous vaginal deliveries, and the last child was delivered by cesarean section for the indication of a failed induction 4 years prior to the current pregnancy) came for ANC follow-up at a gestational age of 32 weeks from her LNMP.\n\nAfter taking a medical history, it was discovered that all four of her children are healthy, doing well in school, and have no known history of genetic or seizure disorders. She was investigated with the Venereal Disease Research Laboratory (VDRL), Hepatitis B surface antigen (HBSag), and urine analysis, all of which were negative. All cell lines in the CBC were normal, her blood group is A, and Rh is positive, according to the Complete Blood Count (CBC), blood group, and RH. Obstetric ultrasound was also performed showing normal anatomical scan of the all body parts of the fetus except the heart. Detailed fetal echocardiography evaluation was done with findings of: both atria have comparable size and normal situs. Both atrioventricular and semilunar valves are normally positioned with normal opening and closure. Both ventricles are comparable in size and contractility; in both 2D and color flow, the left ventricle forms the apex of the heart without any ventricular septal defect. But on the papillary muscles of the left ventricle there were two circumscribed, round, echogenic mass measuring 18.2 mm by 8.3mm and 13.5mm by 8.3 mm. Upon evaluation of the outflow tract, both the LVOT (left ventricular outflow tract) and RVOT (right ventricular outflow tract) have normal anatomy and function using 2D and CF ultrasound evaluation. According to the fetal echo finding, a diagnosis of cardiac rhabdomyoma was made. Since there is a high chance of tuberous sclerosis in cardiac rhabdomyoma, detailed neurosonography and other system exams were done to look for other signs of tuberous sclerosis. Despite searching for the other features of tuberous sclerosis, no other sign of it was found other than the tumor. She had regular ANC follow-up from 32 weeks of gestation up to 39 weeks without any complications.\n\nAt gestational age of 39 weeks plus 1 day, she underwent a cesarean section for the indication of full-term pregnancy plus a request for a repeat cesarean section, with the outcome of a 3200-gram female with an APGAR score of 10 and 10 at the 1st and 5th minutes. Both the mother and the neonate had a smooth post-operative period and were discharged on the third day.\n\nAfter delivery, the neonate was evaluated on the 1st, 7th, and 30th days for any regression or increment of the mass, emergence of skin lesions, or seizure. All physical examination results were normal, and the mass size was similar to the antepartal evaluation.\n\nAt her 7th month, the child was evaluated again, and upon history inquiries, the infant was doing great developmentally for her age group. The infant was examined for neurodevelopmental delay, and the child was growing appropriately for her age. An echocardiography study by a pediatric cardiologist revealed well-circumscribed hyperechoic masses on both left ventricular papillary muscles, each measuring 21.8 mm by 9.2 mm and 14.7 mm by 8.5 mm and creating no left ventricular inflow obstruction.\n\nA history from the family was obtained, and a physical examination with anthropometric measurements was performed to assess her developmental condition during her first-year evaluation. The child was developing normally, as other children her age were. Except for the heart, all of the systems examined were unremarkable. An echocardiography study has revealed well-circumscribed hyperechoic masses on both left ventricular papillary muscles with no size increment and creating no left ventricular inflow obstruction.",
+    "diff_label_texts": "A 29-year-old gravida V para IV (3 spontaneous vaginal deliveries, prior cesarean for failed induction 4 years earlier) presented for ANC at 32 weeks by LNMP. Maternal labs: VDRL, HBsAg, and urinalysis negative; CBC within normal limits; blood group A Rh-positive. Obstetric ultrasound revealed normal fetal anatomy except the heart. Fetal echocardiography showed normal situs; atria of comparable size; normally positioned atrioventricular and semilunar valves with normal motion; ventricles comparable in size and contractility; left ventricle forming the apex; no ventricular septal defect. Two circumscribed, round, echogenic masses were noted on the left ventricular papillary muscles, measuring 18.2 × 8.3 mm and 13.5 × 8.3 mm. LVOT and RVOT anatomy and function were normal on 2D and color flow. Impression: cardiac rhabdomyoma. Given the association with tuberous sclerosis complex (TSC), detailed neurosonography and systemic evaluation were performed and were unremarkable. She continued routine ANC without complications to 39 weeks. At 39 weeks + 1 day, a cesarean section (repeat on request at term) delivered a 3200 g female, Apgar 10 and 10 at 1 and 5 minutes. Postoperative courses for mother and neonate were uneventful; discharge occurred on postoperative day 3. The neonate was evaluated on days 1, 7, and 30: physical examinations were normal; no seizure activity or new cutaneous lesions; mass dimensions were similar to the antenatal findings. At 7 months, development was age-appropriate; pediatric echocardiography showed well-circumscribed hyperechoic masses on both left ventricular papillary muscles measuring 21.8 × 9.2 mm and 14.7 × 8.5 mm, without left ventricular inflow obstruction. At 12 months, anthropometric and neurobehavioral development remained normal. Echocardiography again demonstrated well-circumscribed hyperechoic masses on both left ventricular papillary muscles with no size increment and no left ventricular inflow obstruction. Up to one year of age, apart from the persistent intracardiac rhabdomyomas, the child met none of the clinical diagnostic criteria for TSC. Notably, while cardiac rhabdomyomas often regress spontaneously in infancy, these lesions were stable through 12 months.",
+    "summary": "We are reporting an isolated, asymptomatic fetal intra-cardiac mass (rhabdomyoma) that was discovered at 32 weeks of gestation and was followed as an outpatient until 39 weeks plus one day, at which point a cesarean section was performed. After delivery, the child underwent evaluations at the 1st day, 7th day, 30th day, 7th month, and 12th month of age. Following a checkup, the child's anthropometric and neurobehavioral growth were both healthy. Except for the tumor, which was neither growing nor shrinking in size, none of the clinical diagnostic criteria for tuberous sclerosis complex were met for this child up to the age of one year."
+  },
+  {
+    "doc_id": 4,
+    "label": "low_health_literacy",
+    "fulltext": "13-year-old boy from Cusco with a history of laryngeal papillomatosis since the age of two (at the age of three he required a tracheostomy) and a mother with a history of genital papilloma. The patient was admitted to the San Borja National Institute of Child Health in Lima, after a 16-day illness characterised by respiratory difficulties predominantly at night, inspiratory laryngeal stridor and moderate dysphonia; he previously received azithromycin and oxygen support, without improvement.\n\nThe physical examination revealed mild subcostal retraction, decreased vesicular murmurs in the left hemithorax and scanty wheezy breath sounds with predominance in the right hemithorax, which required oxygen support with a binasal cannula at 4 liters. The rest of the evaluation had no relevant findings. At the laboratory level, leukocytes were found at 8.03 × 103/u, platelets 209 × 103/u, hemoglobin 13.2 g/dL, C-reactive protein at 36.6 mg/L. As part of the imaging studies, a chest radiograph and a head and neck tomography were performed.\n\n48 hours after admission, she presented with increased stridor and respiratory difficulty, so admission to the emergency operating room for tracheostomy, microsurgery and excision of papillomatosis lesions was decided. An appendicular tumour of papillomatose appearance with ventricular bands in the epiglottis, glottic face, vocal cords, subglottis and trachea up to ring 5 was evident. The anatomopathological report reported coilocitic atypia due to HPV and mild focal dysplasia.\n\nIn the immediate postoperative period, he was transferred to the paediatric intensive care unit for respiratory monitoring, with weaning from oxygen at 48 hours. He received a single dose of bevacizumab 400 mg intravenous and subsequently improved clinically. The patient remained hospitalised for seven days, achieving clinical stability through normalisation of oxygen saturation levels and progressive weaning from oxygen, and was subsequently referred to the hospital in Breña to continue his management. Telemonitoring was carried out after eight months and the family indicated that there was no evidence of relapse or other intercurrences.\n",
+    "diff_label_texts": "This is about a 13-year-old boy. He has had small growths in his throat since he was two years old. The growths were in his voice box and windpipe. They narrowed his breathing tube, so he had trouble breathing. It was like trying to breathe through a pinched straw. A chest scan showed several small cysts in his lungs. Doctors removed the throat growths. They also placed a breathing tube through a small hole in his neck to help him breathe. He got one dose of a medicine called bevacizumab (400 mg) through a vein. He also had breathing therapy. He got better. The problem has not come back during follow-up.",
+    "summary": "A 13-year-old boy with a history of laryngeal papillomatosis since the age of two years was presented. The patient presented respiratory distress and multiple stenosing nodules in the larynx and trachea, and several pulmonary cysts were visualized on a chest tomography. The patient underwent exeresis of the papillomatosis lesions and tracheostomy. He received a single dose of 400 mg bevacizumab intravenous and respiratory therapy with a favorable evolution, without recurrence in the follow-up.\n"
+  },
+  {
+    "doc_id": 4,
+    "label": "proficient_health_literacy",
+    "fulltext": "13-year-old boy from Cusco with a history of laryngeal papillomatosis since the age of two (at the age of three he required a tracheostomy) and a mother with a history of genital papilloma. The patient was admitted to the San Borja National Institute of Child Health in Lima, after a 16-day illness characterised by respiratory difficulties predominantly at night, inspiratory laryngeal stridor and moderate dysphonia; he previously received azithromycin and oxygen support, without improvement.\n\nThe physical examination revealed mild subcostal retraction, decreased vesicular murmurs in the left hemithorax and scanty wheezy breath sounds with predominance in the right hemithorax, which required oxygen support with a binasal cannula at 4 liters. The rest of the evaluation had no relevant findings. At the laboratory level, leukocytes were found at 8.03 × 103/u, platelets 209 × 103/u, hemoglobin 13.2 g/dL, C-reactive protein at 36.6 mg/L. As part of the imaging studies, a chest radiograph and a head and neck tomography were performed.\n\n48 hours after admission, she presented with increased stridor and respiratory difficulty, so admission to the emergency operating room for tracheostomy, microsurgery and excision of papillomatosis lesions was decided. An appendicular tumour of papillomatose appearance with ventricular bands in the epiglottis, glottic face, vocal cords, subglottis and trachea up to ring 5 was evident. The anatomopathological report reported coilocitic atypia due to HPV and mild focal dysplasia.\n\nIn the immediate postoperative period, he was transferred to the paediatric intensive care unit for respiratory monitoring, with weaning from oxygen at 48 hours. He received a single dose of bevacizumab 400 mg intravenous and subsequently improved clinically. The patient remained hospitalised for seven days, achieving clinical stability through normalisation of oxygen saturation levels and progressive weaning from oxygen, and was subsequently referred to the hospital in Breña to continue his management. Telemonitoring was carried out after eight months and the family indicated that there was no evidence of relapse or other intercurrences.\n",
+    "diff_label_texts": "A 13-year-old male from Cusco with recurrent respiratory papillomatosis (RRP) since age two (tracheostomy at age three) and a maternal history of genital papilloma presented after 16 days of predominantly nocturnal respiratory difficulty, inspiratory laryngeal stridor, and moderate dysphonia. He had previously received azithromycin and supplemental oxygen without improvement. On exam, there was mild subcostal retraction, decreased vesicular breath sounds over the left hemithorax, and scant wheezes predominating on the right; he required 4 L/min oxygen via binasal cannula. Laboratory studies showed WBC 8.03 × 10^3/μL, platelets 209 × 10^3/μL, hemoglobin 13.2 g/dL, and CRP 36.6 mg/L. Imaging included a chest study and head and neck tomography; chest tomography visualized several pulmonary cysts. Forty-eight hours after admission, he developed worsening stridor and respiratory distress, prompting emergent OR transfer for tracheostomy, microlaryngoscopy, and excision of papillomatous lesions. Intraoperative findings demonstrated extensive papillomatous disease with appendicular tumor-like lesions and ventricular bands involving the epiglottis, glottic surface, vocal cords, subglottis, and trachea to ring 5. Histopathology showed koilocytotic atypia consistent with HPV and mild focal dysplasia. Postoperatively, he was managed in the PICU with respiratory monitoring and was weaned off oxygen within 48 hours. He received a single intravenous dose of bevacizumab 400 mg and showed prompt clinical improvement. He completed a seven-day hospitalization with normalization of oxygen saturation and progressive oxygen weaning, then was transferred for ongoing care. He also received respiratory therapy. On telemonitoring at eight months, there was no evidence of recurrence or intercurrent events. Clinical context: RRP is typically HPV-related (often low-risk types) and can cause multifocal papillomas leading to airway stenosis; anti-VEGF therapy such as bevacizumab is used off-label to reduce angiogenesis and disease recurrence, and in this case was associated with a favorable short- to mid-term outcome.",
+    "summary": "A 13-year-old boy with a history of laryngeal papillomatosis since the age of two years was presented. The patient presented respiratory distress and multiple stenosing nodules in the larynx and trachea, and several pulmonary cysts were visualized on a chest tomography. The patient underwent exeresis of the papillomatosis lesions and tracheostomy. He received a single dose of 400 mg bevacizumab intravenous and respiratory therapy with a favorable evolution, without recurrence in the follow-up.\n"
+  },
+  {
+    "doc_id": 5,
+    "label": "low_health_literacy",
+    "fulltext": "A 54-year-old male who had a medical history of membranous nephropathy II with nephrotic syndrome was administered with long-term oral glucocorticoids and immunosuppressants. The patient had a 20 pack-year history of smoking, and denied a family history of hereditary diseases. Chest x-ray demonstrated normal findings at one month before admission. On August 8, 2016, the patient was hospitalized for fever accompanied by progressive dyspnea, cough, and expectoration for 5 days. On admission, the BMI of the patient was 24.5 kg/m2, and his body temperature was 39.0°C. Furthermore, the patient had symptoms of tachypnea (35 bpm) and severe hypoxemia (SaO2 86%). On auscultation, the patient had good air entrance bilaterally with scattered diffuse crackles and rhonchi. Furthermore, the chest CT scan revealed multiple ground-glass opacities, and laboratory tests revealed normal white blood cell (WBC) count, but with elevated neutrophil count, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and (1→3)-β-D-glucan. The patient was diagnosed as RSV infection on the fourth day of hospitalization when positive RSV-Ab was detected.\n\nOn admission, the patient was immediately given respiratory monitoring and supplemental oxygen to improve the low oxygen saturation, as well as antibiotics (moxifloxacin for 4 days, followed by cefminoxine for 8 days), and antifungal therapy (voriconazole for 10 days). The dose of the glucocorticoids and immunosuppressants remained largely unchanged. After 10 days of treatment, the patient's condition became worse. Chest CT revealed the progression of the disease, and oxygen partial pressure was further decreased. The patient was transferred to the Emergency Intensive Care Unit, where the patient was intensively treated, including noninvasive mechanical ventilation, broad-spectrum antibiotics (i.v. meropenem, oral moxifloxacin, and cotrimoxazole), antifungal therapy (micafungin), corticosteroids (methylprednisolone 40 mg bid iv) to relieve the inflammation, and other supportive treatment. Ganciclovir was also prescribed due to a possibility of viral infection, such as cytomegalovirus. Five days later, the patient's condition was further aggravated based on the chest x-ray evaluation. Despite receiving another round of treatments, including invasive ventilator-assisted ventilation therapy, methylprednisolone (80 mg bid), antibacterial agents (cefoperazone sulbactam, tigecycline, and cotrimoxazole) and antifungal (micafungin) therapy, the patient eventually died after 2 days.",
+    "diff_label_texts": "This 54-year-old man had long-term kidney disease. He took steroids and other medicines that weaken the body’s defenses for a long time. He came to the lung department with fever, cough with mucus, and trouble breathing. A scan showed many cloudy spots in both lungs, like frosted glass. Blood tests showed a lot of inflammation. This suggested an infection from germs such as bacteria, a virus, or a fungus. A blood test was positive for RSV antibodies. Tests for other germs were not positive. His immune system was weak. His antibody level (IgG) was low. His infection-fighting T cells (CD4 and CD8) were also low. Doctors gave strong medicines for infection and support to help his breathing. His illness got worse quickly. He died from breathing failure.",
+    "summary": "Patient concerns:\nA 54-year-old male patient with chronic nephropathy, who received long-term immunosuppressants, was admitted to the Department of Respiratory Medicine due to the symptoms of fever, cough, expectoration, and dyspnea.\n\nDiagnoses:\nPulmonary radiology revealed multiple bilateral ground-glass opacity. Laboratory tests revealed elevated inflammation indicators, implying infection with bacteria, viruses, and/or fungi. Furthermore, the patient was positive for RSV antibodies, without positive results for other pathogens. Moreover, the patient was immunocompromised due to the long-term use of corticosteroids and immunosuppressants, as evidenced by decreased total IgG levels and reduced CD4 and CD8 T-lymphocyte counts.\n\nInterventions and outcome:\nDespite the intensive anti-infection treatment and respiratory support, the patient developed rapid progression, and subsequently died of respiratory failure."
+  },
+  {
+    "doc_id": 6,
+    "label": "low_health_literacy",
+    "fulltext": "A 34-year-old patient with a disease duration of four weeks. Two months earlier, she had a cesarean section in the 37th week of pregnancy and had persistent bleeding from the surgical wound. She denied a history of bleeding in childhood or adolescence. Three years earlier, she had given birth to her first child (also by cesarean section), who died due to a chromosome disorder (referred to by the patient). She also stated that she was allergic to tramadol.\n\nThe clinical picture began with lower back pain due to bilateral renal lithiasis. Subsequently, he managed to expel a stone and after that he presented haematuria for three days, for which he received tranexamic acid c/12 h. Three weeks later, he presented pain in the lower region of the left thigh that increased in intensity, with hardening of the area. Due to persistence of the symptoms, he was given diclofenac intramuscularly, which caused ecchymosis and bleeding in the gluteal area and persists despite the compression with gauze.\n\nThe patient underwent a particular Doppler ultrasound that revealed deep venous thrombosis of the left lower limb, and went to the hospital in her locality with these results. She was given anticoagulation with enoxaparin 30 mg/24 h subcutaneously, in addition to morphine for pain management and was hospitalized. The next day, she presented epigastralgia, blurred vision, heart rate of 117 beats/min, blood pressure of 113/85 mmHg and saturation of 93%. It was decided to discontinue enoxaparin. The blood count revealed a hemoglobin of 6.4 g/dl, which represented a difference of 4 g/dl from the result one day before admission, which was 10.4 g/dl. Because of the above, two blood transfusions were given. Due to the suspicion of vasculitis, methylprednisolone was indicated and she was referred to our hospital for further study.\n\nOn admission, the physical examination revealed severe pallor, extensive ecchymosis on the left thigh and lateral knee, and a haematoma on the right thigh. The haemogram showed moderate anaemia (Hb = 9.8 g/dl), normocytic and normochromic. The biochemical examination showed glucose values of 160 mg/dl. The liver enzymes AST and ALT were at 52 U/L and 86 U/L, respectively. The coagulation profile showed a prolonged activated partial thromboplastin time (APTT) of 91.2 s. The rest of the haemogram, biochemical, electrolyte, liver profile and coagulation profile were normal. The ultrasound of soft parts of the right gluteal region revealed a collection at the level of the subcutaneous cellular tissue (TCSC) and oedema up to the upper third of the thigh. The Doppler ultrasound in the left lower limb showed adequate flowometry without signs of thrombosis in the common femoral vein, superficial and deep.\n\nSymptomatic treatment was initiated and blood and urine cultures were requested and were negative. Antinuclear antibody (ANA) values, complement C3 and C4 and ferritin were within the reference range.\n\nIn the face of suspected acquired haemophilia, studies were requested for confirmation, where a partial correction of aPTT was found in the mixing test. Factor VIII was measured and its activity was found to be decreased (<1.0 U/dl) and the presence of a factor VIII inhibitor was demonstrated: 8.64 Bethesda units/ml. The above allowed the diagnosis of acquired haemophilia to be confirmed, which was related to the postpartum period due to the onset of symptoms.\n\nPrednisone 50 mg orally at breakfast and 10 mg orally at lunch, cyclophosphamide 50 mg 2 tablets orally every 24 hours and anti-inhibitor coagulant complex for haemophilia (FEIBA) were initiated. Five days later, the latter was discontinued due to chest tightness, dyspnoea and nausea (possible adverse drug reaction) and replaced with activated recombinant factor VII (NovoSeven).\n\nThe patient's clinical evolution was favorable, with a decrease in ecchymosis and no other symptoms, so she was discharged from the hospital.\n",
+    "diff_label_texts": "A 34-year-old woman had new lower back pain. She saw blood in her urine. She also had a big bruise under the skin on her right buttock. She had never had bleeding problems before. Because these bleeding signs were serious, she was sent to the emergency room. Doctors did blood-clotting tests. One test mixed her blood with normal blood to see how it clotted. Another test looked for a blocker against a clotting protein called factor eight. These tests confirmed the diagnosis.",
+    "summary": "A 34-year-old female patient presented with lower back pain, haematuria and a haematoma in the right gluteal region, with no previous history of bleeding. Due to the extent of the haemorrhagic manifestations, she was transferred to the emergency department. The coagulation profile, mixing test and measurement of the factor VIII inhibitor titres confirmed the diagnosis.\n"
+  },
+  {
+    "doc_id": 7,
+    "label": "intermediate_health_literacy",
+    "fulltext": "We present here the case of a two-day old neonate with in-born right scrotal swelling admitted at Children’s hospital. The patient was born at term via cesarean section at a private hospital. He was kept in the nursery for one day. The examining doctor referred them for urgent surgical care, but it took them one day to arrive at our hospital. Upon arrival in the emergency department, he was well hydrated, pink at room temperature with good perfusion. Upon examination, the right testis was found to be enlarged, tense, non-tender visibly reddish with overlying skin excoriation. Trans-illumination was negative in the right but positive in the contralateral testis. Both hernial orifices were normal. All the laboratory investigations were performed with an urgent Doppler ultrasound of the inguinoscrotal area. The ultrasound examination found the right testis to be enlarged (15.6*9.4 mm) and showed heterogeneous hypoechoic texture with prominent rete testis and no flow on color Doppler analysis. Left testis appeared normal in size, shape and echotexture with minimal hydrocele. An urgent scrotal exploration was undertaken. Intra-operatively, there was frank necrotic right testis with intravaginal torsion of the testis with minimal hydrocele. A right orchidectomy and contralateral orchidopexy was then performed.",
+    "diff_label_texts": "A full‑term male newborn, 2 days old and delivered by cesarean section, presented with a congenital right scrotal swelling. On arrival he appeared well perfused and stable. Examination showed the right testis was enlarged, tense, non‑tender, and visibly reddish with excoriated overlying skin. Transillumination was negative on the right and positive on the left; both hernia openings were normal. Doppler ultrasound showed the right testis was enlarged with a heterogeneous, darker appearance and no detectable blood flow; the left testis looked normal, with only a small amount of fluid. He was taken urgently to surgery. Intra‑operatively, the right testis was frankly nonviable due to intravaginal torsion, with minimal hydrocele. Surgeons removed the right testis (orchidectomy) and fixed the left testis in place (contralateral orchidopexy) to reduce the risk of future twisting.",
+    "summary": "We present here the case of a two-day old neonate with in-born right scrotal swelling admitted at Children’s hospital. The patient was born at term via cesarean section at a private hospital. Upon arrival in the emergency department, he was well hydrated, pink at room temperature with good perfusion. Upon examination, the right testis was found to be enlarged, tense, non-tender visibly reddish with overlying skin excoriation. Trans-illumination was negative in right but positive in the contralateral testis. Both hernial orifices were normal. Doppler ultrasound of the inguinoscrotal area found the right testis to be enlarged (15.6*9.4 mm) and showed heterogeneous hypoechoic texture with prominent rete testis and no flow on color doppler analysis. An urgent scrotal exploration was undertaken. Intra-operatively there was frank necrotic right testis with intravaginal torsion of the testis and minimal hydrocele. A right orchidectomy and contralateral orchidopexy were performed."
+  },
+  {
+    "doc_id": 7,
+    "label": "low_health_literacy",
+    "fulltext": "We present here the case of a two-day old neonate with in-born right scrotal swelling admitted at Children’s hospital. The patient was born at term via cesarean section at a private hospital. He was kept in the nursery for one day. The examining doctor referred them for urgent surgical care, but it took them one day to arrive at our hospital. Upon arrival in the emergency department, he was well hydrated, pink at room temperature with good perfusion. Upon examination, the right testis was found to be enlarged, tense, non-tender visibly reddish with overlying skin excoriation. Trans-illumination was negative in the right but positive in the contralateral testis. Both hernial orifices were normal. All the laboratory investigations were performed with an urgent Doppler ultrasound of the inguinoscrotal area. The ultrasound examination found the right testis to be enlarged (15.6*9.4 mm) and showed heterogeneous hypoechoic texture with prominent rete testis and no flow on color Doppler analysis. Left testis appeared normal in size, shape and echotexture with minimal hydrocele. An urgent scrotal exploration was undertaken. Intra-operatively, there was frank necrotic right testis with intravaginal torsion of the testis with minimal hydrocele. A right orchidectomy and contralateral orchidopexy was then performed.",
+    "diff_label_texts": "This is about a 2-day-old newborn boy. He was born at full term by C-section at a private hospital. He came to the children’s hospital because the right side of his scrotum (the sack that holds the testicles) was swollen since birth. In the emergency room, he looked well. His skin was pink and warm. His blood flow looked good. On exam, the right testicle was big and tight. It was not sore when touched. The skin was red and looked rubbed. A light test did not shine through the right side. The light did shine through the left side. There were no signs of a hernia. An urgent ultrasound scan was done. The scan showed the right testicle was larger and looked uneven inside. No blood was flowing to it. The doctors took him quickly to surgery to look inside the scrotum. In surgery, the right testicle was dead because it had twisted, like a kinked hose that stops flow. There was a small amount of fluid. They removed the right testicle. They fixed the left testicle in place to help prevent twisting.",
+    "summary": "We present here the case of a two-day old neonate with in-born right scrotal swelling admitted at Children’s hospital. The patient was born at term via cesarean section at a private hospital. Upon arrival in the emergency department, he was well hydrated, pink at room temperature with good perfusion. Upon examination, the right testis was found to be enlarged, tense, non-tender visibly reddish with overlying skin excoriation. Trans-illumination was negative in right but positive in the contralateral testis. Both hernial orifices were normal. Doppler ultrasound of the inguinoscrotal area found the right testis to be enlarged (15.6*9.4 mm) and showed heterogeneous hypoechoic texture with prominent rete testis and no flow on color doppler analysis. An urgent scrotal exploration was undertaken. Intra-operatively there was frank necrotic right testis with intravaginal torsion of the testis and minimal hydrocele. A right orchidectomy and contralateral orchidopexy were performed."
+  },
+  {
+    "doc_id": 7,
+    "label": "proficient_health_literacy",
+    "fulltext": "We present here the case of a two-day old neonate with in-born right scrotal swelling admitted at Children’s hospital. The patient was born at term via cesarean section at a private hospital. He was kept in the nursery for one day. The examining doctor referred them for urgent surgical care, but it took them one day to arrive at our hospital. Upon arrival in the emergency department, he was well hydrated, pink at room temperature with good perfusion. Upon examination, the right testis was found to be enlarged, tense, non-tender visibly reddish with overlying skin excoriation. Trans-illumination was negative in the right but positive in the contralateral testis. Both hernial orifices were normal. All the laboratory investigations were performed with an urgent Doppler ultrasound of the inguinoscrotal area. The ultrasound examination found the right testis to be enlarged (15.6*9.4 mm) and showed heterogeneous hypoechoic texture with prominent rete testis and no flow on color Doppler analysis. Left testis appeared normal in size, shape and echotexture with minimal hydrocele. An urgent scrotal exploration was undertaken. Intra-operatively, there was frank necrotic right testis with intravaginal torsion of the testis with minimal hydrocele. A right orchidectomy and contralateral orchidopexy was then performed.",
+    "diff_label_texts": "A 2‑day‑old term male neonate, delivered by cesarean section at a private hospital, was referred for a congenital right scrotal swelling and presented to our children’s hospital one day later. On ED arrival he was well hydrated, pink on room air with good perfusion. Physical exam: right hemiscrotum with an enlarged, tense, non‑tender, visibly reddish testis and overlying skin excoriation; transillumination negative on the right and positive contralaterally; both hernial orifices normal. Laboratory studies were obtained, and urgent inguinoscrotal Doppler ultrasonography demonstrated an enlarged right testis measuring 15.6 × 9.4 mm with heterogeneous hypoechoic echotexture, prominent rete testis, and absent intratesticular color Doppler flow. The left testis was normal in size, shape, and echotexture; there was minimal hydrocele. The patient underwent urgent scrotal exploration. Intra‑operatively there was frank necrosis of the right testis secondary to intravaginal testicular torsion, with minimal hydrocele. A right orchidectomy and contralateral orchidopexy were performed. Contextually, perinatal testicular torsion often presents at or shortly after birth and Doppler evidence of absent flow with heterogeneous hypoechoic parenchyma correlates with nonviability; salvage rates are low when presentation is delayed. Contralateral orchidopexy is commonly performed to mitigate future torsion risk.",
+    "summary": "We present here the case of a two-day old neonate with in-born right scrotal swelling admitted at Children’s hospital. The patient was born at term via cesarean section at a private hospital. Upon arrival in the emergency department, he was well hydrated, pink at room temperature with good perfusion. Upon examination, the right testis was found to be enlarged, tense, non-tender visibly reddish with overlying skin excoriation. Trans-illumination was negative in right but positive in the contralateral testis. Both hernial orifices were normal. Doppler ultrasound of the inguinoscrotal area found the right testis to be enlarged (15.6*9.4 mm) and showed heterogeneous hypoechoic texture with prominent rete testis and no flow on color doppler analysis. An urgent scrotal exploration was undertaken. Intra-operatively there was frank necrotic right testis with intravaginal torsion of the testis and minimal hydrocele. A right orchidectomy and contralateral orchidopexy were performed."
+  },
+  {
+    "doc_id": 8,
+    "label": "low_health_literacy",
+    "fulltext": "4-year-old male patient with a history of nasal impetigo two weeks before admission (treated with topical mupirocin and oral cefadroxil; dose, duration and adherence to treatment unknown), with no other morbid history, who presented macroscopic glomerular haematuria associated with oedema of the lower extremities of 5 days' evolution, with the last 12 hours prior to the consultation adding headaches, nausea and vomiting. He went to the emergency department (ED) in convulsive status, after 20 minutes of generalised tonic-clonic convulsions.\n\nOn admission to the ED, the patient was afebrile, with non-evaluable blood pressure, with quantitative consciousness impairment associated with generalized hypertonia and bilateral and pretibial oedema. Endotracheal intubation was decided and phenobarbital (10 mg/kg) was administered to manage the convulsive status.\n\nOn physical examination in the intensive care unit (ICU), blood pressure was 134/94 mmHg (BP 110 mmHg) (p95 for patient 108/66 mmHg, p95+12 120/78 mmHg).\n\nInitial laboratory parameters included: complete urine with haematuria (> 100 erythrocytes per field), proteinuria 3+ and leucocyturia 10-25 per field, creatinemia 0.3 mg/dL, anaemia with haematocrit (HTO) 21%, haemoglobin (Hb) 7 g/dL, with normal mean corpuscular volume (VCM) and mean corpuscular haemoglobin concentration (CHCM), leukocytosis of 23,900 cells/mm3, thrombocytosis of 756,000/mm3, without elevation of acute phase reactants, hypocomplementemia with complement C3 level at 25 mg/dL (normal value, VN: 80-150 mg/dL) and normal C4. The rapid antigen test for Streptococcus beta-haemolytic group A (Streptococcus pyogenes) in pharynx was positive and the Anti-streptolysin O (ASO) was (+). The non-contrast brain computed tomography showed no acute changes. The renal ultrasound concluded bilateral nephromegaly with increased cortical echogenicity and decreased corticomedullar differentiation.\n\nThe patient was diagnosed with nephritic syndrome due to complicated GNAPE with hypertensive emergency - convulsive status.\n\nWithin the first 24 hours of his ICU stay, the patient required mechanical ventilation (MV) and anticonvulsant therapy with phenobarbital. He progressed without seizures, with a normal electroencephalogram (EEG) (on the day following admission) and a normal cerebrospinal fluid study. Antibiotic therapy was initiated for eradication of Streptococcus pyogenes with cefotaxime and diuretic therapy with furosemide.\n\nThe next day, he developed renal impairment with creatinine elevation to 0.99 mg/dL, hypertension and 24 hour proteinuria of 36.6 mg/m2/h, without oliguria. He initiated antihypertensive therapy with amlodipine and intravenous labetalol, with good initial control.\n\nWith favorable evolution, extubation was performed at 48 hours, which was well tolerated from the ventilatory point of view. However, after 24 hours of extubation, the patient's consciousness deteriorated, with both ocular opening and withdrawal of limb only in response to painful stimulus and poor verbal response (Glasgow Coma Scale 8), and developed blood pressure figures > p95+12 despite receiving therapy with labetalol in continuous infusion (up to 3 mg/kg/h), amlodipine (10 mg/day) and furosemide, which required the reintroduction of mechanical ventilation and infusion of sodium nitroprusside (up to 3 mcg/kg/min), with the aim of achieving gradual reduction of blood pressure figures (25% daily) to prevent secondary neurological damage. Given the presence of acute neurological symptomatology associated with HTA in a patient with glomerulonephritis, the diagnosis of PRES was suspected, which was confirmed by magnetic resonance imaging (MRI) of the brain (day 5), which showed an increase in the subcortical signal in bilateral and symmetric occipital region, without restriction in diffusion, which was compatible with vasogenic edema (PRES). Ophthalmological evaluation was normal and a new EEG evidenced occasional episodes of generalized voltage depression.\n\nAdding enalapril to the treatment. Finally, after 10 days with a slow pharmacological weaning, normalization of blood pressure was achieved. The control MRI (day 12) revealed regression of the previously described findings. Successful extubation was achieved after 5 days.\n\nDuring his stay in the ICU, the hemoglobin level dropped to 5 g/dL, with normal mean corpuscular volume and mean corpuscular hemoglobin concentration, without plateletopenia, so hemolytic anemia was suspected given a positive direct Coombs test and hemoglobinuria. He required red blood cell transfusions twice. Steroid therapy with methylprednisolone (1 mg/kg/d) was initiated for 72 hours. The coproculture was negative, as was the urinary antigen for Streptococcus pneumoniae. Epstein-Barr virus and Parvovirus B19 serology, extractable nuclear antigen (ENA) profile, anti-neutrophil cytoplasmic antibodies (ANCA), anti-DNA antibodies, anti-B2 glycoprotein 1 antibodies, anti-cardiolipin antibodies and lupus anticoagulant were all negative. All cultures were negative (blood cultures, urine cultures, cultures of endotracheal aspirate and pharyngeal cultures). ANA (antinuclear antibodies) was positive 1/160.\n\nThe patient improved with blood pressure normalization, increased complement levels, and a urine test without proteinuria or hematuria. The direct Coombs test remained positive on the 9th day of hospitalization.\n\nOn day 31, the patient was discharged normotensive, without anaemia, with preserved renal function, without proteinuria or haematuria, with normalisation of C3 levels and asymptomatic from the neurological point of view. He was discharged with pharmacological therapy with prednisone, amlodipine, enalapril and folic acid. The patient did not present recurrence and remained asymptomatic 6 months after discharge.\n",
+    "diff_label_texts": "A 4-year-old boy had blood in his pee and swelling for 5 days. He then had headaches, nausea, and vomiting. He came to the hospital with seizures and very high blood pressure. Blood tests showed a low level of a protein called C3 and signs of a recent strep infection. This meant his kidney filters were inflamed after strep. His brain was affected by the very high blood pressure. Doctors suspected a problem called PRES, which is brain swelling from high pressure. A brain MRI confirmed this. His immune system also attacked his red blood cells. This made his blood level drop very low, to 5 g/dL. He was treated with medicines to lower his blood pressure, steps to protect his brain, and steroid medicines. He left the hospital after 31 days. Six months later, he had no symptoms.",
+    "summary": "4-year-old male patient with a history of 5 days of haematuria and oedema, with additional headaches, nausea and vomiting, who entered a convulsive state and hypertensive crisis. Laboratory tests showed hypocomplementemia C3 and elevated Anti-Streptolysin O titers, which was interpreted as GNAPE. He developed encephalopathy, which led to suspicion of secondary PRES due to hypertensive emergency, which was finally confirmed by magnetic resonance of the brain. He also developed autoimmune haemolytic anaemia with haemoglobin up to 5 g/dL. His treatment was based on antihypertensive therapy, neuroprotection measures and steroid treatment. He was discharged after 31 days of hospitalisation, asymptomatic 6 months after discharge.\n"
+  },
+  {
+    "doc_id": 8,
+    "label": "proficient_health_literacy",
+    "fulltext": "4-year-old male patient with a history of nasal impetigo two weeks before admission (treated with topical mupirocin and oral cefadroxil; dose, duration and adherence to treatment unknown), with no other morbid history, who presented macroscopic glomerular haematuria associated with oedema of the lower extremities of 5 days' evolution, with the last 12 hours prior to the consultation adding headaches, nausea and vomiting. He went to the emergency department (ED) in convulsive status, after 20 minutes of generalised tonic-clonic convulsions.\n\nOn admission to the ED, the patient was afebrile, with non-evaluable blood pressure, with quantitative consciousness impairment associated with generalized hypertonia and bilateral and pretibial oedema. Endotracheal intubation was decided and phenobarbital (10 mg/kg) was administered to manage the convulsive status.\n\nOn physical examination in the intensive care unit (ICU), blood pressure was 134/94 mmHg (BP 110 mmHg) (p95 for patient 108/66 mmHg, p95+12 120/78 mmHg).\n\nInitial laboratory parameters included: complete urine with haematuria (> 100 erythrocytes per field), proteinuria 3+ and leucocyturia 10-25 per field, creatinemia 0.3 mg/dL, anaemia with haematocrit (HTO) 21%, haemoglobin (Hb) 7 g/dL, with normal mean corpuscular volume (VCM) and mean corpuscular haemoglobin concentration (CHCM), leukocytosis of 23,900 cells/mm3, thrombocytosis of 756,000/mm3, without elevation of acute phase reactants, hypocomplementemia with complement C3 level at 25 mg/dL (normal value, VN: 80-150 mg/dL) and normal C4. The rapid antigen test for Streptococcus beta-haemolytic group A (Streptococcus pyogenes) in pharynx was positive and the Anti-streptolysin O (ASO) was (+). The non-contrast brain computed tomography showed no acute changes. The renal ultrasound concluded bilateral nephromegaly with increased cortical echogenicity and decreased corticomedullar differentiation.\n\nThe patient was diagnosed with nephritic syndrome due to complicated GNAPE with hypertensive emergency - convulsive status.\n\nWithin the first 24 hours of his ICU stay, the patient required mechanical ventilation (MV) and anticonvulsant therapy with phenobarbital. He progressed without seizures, with a normal electroencephalogram (EEG) (on the day following admission) and a normal cerebrospinal fluid study. Antibiotic therapy was initiated for eradication of Streptococcus pyogenes with cefotaxime and diuretic therapy with furosemide.\n\nThe next day, he developed renal impairment with creatinine elevation to 0.99 mg/dL, hypertension and 24 hour proteinuria of 36.6 mg/m2/h, without oliguria. He initiated antihypertensive therapy with amlodipine and intravenous labetalol, with good initial control.\n\nWith favorable evolution, extubation was performed at 48 hours, which was well tolerated from the ventilatory point of view. However, after 24 hours of extubation, the patient's consciousness deteriorated, with both ocular opening and withdrawal of limb only in response to painful stimulus and poor verbal response (Glasgow Coma Scale 8), and developed blood pressure figures > p95+12 despite receiving therapy with labetalol in continuous infusion (up to 3 mg/kg/h), amlodipine (10 mg/day) and furosemide, which required the reintroduction of mechanical ventilation and infusion of sodium nitroprusside (up to 3 mcg/kg/min), with the aim of achieving gradual reduction of blood pressure figures (25% daily) to prevent secondary neurological damage. Given the presence of acute neurological symptomatology associated with HTA in a patient with glomerulonephritis, the diagnosis of PRES was suspected, which was confirmed by magnetic resonance imaging (MRI) of the brain (day 5), which showed an increase in the subcortical signal in bilateral and symmetric occipital region, without restriction in diffusion, which was compatible with vasogenic edema (PRES). Ophthalmological evaluation was normal and a new EEG evidenced occasional episodes of generalized voltage depression.\n\nAdding enalapril to the treatment. Finally, after 10 days with a slow pharmacological weaning, normalization of blood pressure was achieved. The control MRI (day 12) revealed regression of the previously described findings. Successful extubation was achieved after 5 days.\n\nDuring his stay in the ICU, the hemoglobin level dropped to 5 g/dL, with normal mean corpuscular volume and mean corpuscular hemoglobin concentration, without plateletopenia, so hemolytic anemia was suspected given a positive direct Coombs test and hemoglobinuria. He required red blood cell transfusions twice. Steroid therapy with methylprednisolone (1 mg/kg/d) was initiated for 72 hours. The coproculture was negative, as was the urinary antigen for Streptococcus pneumoniae. Epstein-Barr virus and Parvovirus B19 serology, extractable nuclear antigen (ENA) profile, anti-neutrophil cytoplasmic antibodies (ANCA), anti-DNA antibodies, anti-B2 glycoprotein 1 antibodies, anti-cardiolipin antibodies and lupus anticoagulant were all negative. All cultures were negative (blood cultures, urine cultures, cultures of endotracheal aspirate and pharyngeal cultures). ANA (antinuclear antibodies) was positive 1/160.\n\nThe patient improved with blood pressure normalization, increased complement levels, and a urine test without proteinuria or hematuria. The direct Coombs test remained positive on the 9th day of hospitalization.\n\nOn day 31, the patient was discharged normotensive, without anaemia, with preserved renal function, without proteinuria or haematuria, with normalisation of C3 levels and asymptomatic from the neurological point of view. He was discharged with pharmacological therapy with prednisone, amlodipine, enalapril and folic acid. The patient did not present recurrence and remained asymptomatic 6 months after discharge.\n",
+    "diff_label_texts": "A 4-year-old male, two weeks post nasal impetigo treated with topical mupirocin and oral cefadroxil (dose/duration/adherence unknown), presented with 5 days of macroscopic glomerular haematuria and lower-extremity oedema, followed by 12 hours of headache, nausea, and vomiting, and arrived to the ED in convulsive status after 20 minutes of generalized tonic–clonic seizures. On ED arrival he was afebrile, with non-evaluable BP, depressed consciousness, generalized hypertonia, and bilateral pretibial oedema. He was intubated and loaded with phenobarbital 10 mg/kg. In the ICU, BP was 134/94 mmHg (p95 for age 108/66; p95+12 120/78), consistent with hypertensive emergency. Initial labs: urinalysis with haematuria (>100 RBC/hpf), proteinuria 3+, leucocyturia 10–25/hpf; creatinine 0.3 mg/dL; anaemia Hct 21%, Hb 7 g/dL with normocytic, normochromic indices; leukocytosis 23,900/mm3; thrombocytosis 756,000/mm3; no elevation of acute-phase reactants; hypocomplementemia with C3 25 mg/dL (VN 80–150) and normal C4. Throat rapid antigen for group A Streptococcus was positive and ASO positive. Non-contrast head CT was unremarkable. Renal ultrasound showed bilateral nephromegaly with increased cortical echogenicity and decreased corticomedullary differentiation. The working diagnosis was nephritic syndrome due to complicated GNAPE with hypertensive emergency and status epilepticus. He required mechanical ventilation and phenobarbital; EEG the next day was normal; CSF was normal. Cefotaxime was started for Streptococcus pyogenes eradication and furosemide for diuresis. By day 2 he developed AKI (creatinine 0.99 mg/dL), hypertension, and 24-hour proteinuria 36.6 mg/m2/h without oliguria. Antihypertensive therapy included amlodipine and IV labetalol with initial control. After extubation at 48 hours, he deteriorated neurologically within 24 hours (GCS 8) with BP > p95+12 despite labetalol infusion up to 3 mg/kg/h, amlodipine 10 mg/day, and furosemide, necessitating reintubation and sodium nitroprusside infusion up to 3 mcg/kg/min with a planned gradual BP reduction of 25% per day to mitigate secondary neurologic injury. Given acute neurologic deficits with severe HTN in GN, PRES was suspected and confirmed by brain MRI on day 5 showing increased subcortical T2/FLAIR signal in bilateral symmetric occipital regions without diffusion restriction, consistent with vasogenic edema. Ophthalmologic exam was normal; repeat EEG showed occasional generalized voltage depression. Enalapril was added. Over 10 days, BP normalized with slow pharmacologic weaning; follow-up MRI on day 12 showed radiologic regression, and he was successfully extubated after 5 days. During the ICU course, Hb fell to 5 g/dL with normocytic, normochromic indices and no thrombocytopenia; hemolytic anemia was diagnosed given a positive direct Coombs test and hemoglobinuria. He required two packed RBC transfusions. Methylprednisolone 1 mg/kg/day was given for 72 hours. Stool culture and urinary antigen for Streptococcus pneumoniae were negative. Serologies for EBV and Parvovirus B19, ENA profile, ANCA, anti-dsDNA, anti-β2 glycoprotein I, anticardiolipin, and lupus anticoagulant were all negative; all cultures (blood, urine, endotracheal aspirate, pharyngeal) were negative. ANA was positive at 1:160. Clinical status improved with BP control, rising complement levels, and resolution of proteinuria and haematuria; the direct Coombs remained positive on hospital day 9. He was discharged on day 31 normotensive, non-anaemic, with preserved renal function, no proteinuria or haematuria, normalized C3, and asymptomatic neurologically. Discharge medications: prednisone, amlodipine, enalapril, and folic acid. He remained asymptomatic with no recurrence at 6 months. Overall, the case represents GNAPE with hypocomplementemia (low C3) and elevated ASO complicated by hypertensive emergency causing encephalopathy and secondary PRES, plus autoimmune hemolytic anemia with Hb nadir 5 g/dL, successfully managed with antihypertensives, neuroprotective measures, and corticosteroids, with full clinical and radiologic recovery.",
+    "summary": "4-year-old male patient with a history of 5 days of haematuria and oedema, with additional headaches, nausea and vomiting, who entered a convulsive state and hypertensive crisis. Laboratory tests showed hypocomplementemia C3 and elevated Anti-Streptolysin O titers, which was interpreted as GNAPE. He developed encephalopathy, which led to suspicion of secondary PRES due to hypertensive emergency, which was finally confirmed by magnetic resonance of the brain. He also developed autoimmune haemolytic anaemia with haemoglobin up to 5 g/dL. His treatment was based on antihypertensive therapy, neuroprotection measures and steroid treatment. He was discharged after 31 days of hospitalisation, asymptomatic 6 months after discharge.\n"
+  },
+  {
+    "doc_id": 9,
+    "label": "intermediate_health_literacy",
+    "fulltext": "A 69-year-old male with prior history of CABG presented with severe dyspnea at mild exertion (NYHA III) of 2 months duration was admitted in our center. The electrocardiogram showed ST depression in leads II, III, aVF, and V4-6, and blood examination revealed elevation of plasma N-terminal pro-B-type natriuretic peptide levels (2640 pg/mL). Echocardiogram showed left ventricular systolic dysfunction and low left ventricular ejection fraction (30%). The patient had inferior ST-segment-elevation myocardial infarction in 2009, when he was 59 years old, with angiographic evidence of severe 3 vessels disease (coronary angiography showed CTO in proximal left anterior descending artery (LAD), 90% stenosis in mid and distal left circumflex artery, and 95% stenosis in mid RCA. The patient underwent CABG with left internal mammary artery (LIMA) to LAD, and sequential SVG to 1st obtuse marginal branch (OM1), 2nd obtuse marginal branch (OM2), and posterolateral branch (PL) in 2009.\n\nCoronary angiography was performed via 6 French (Fr) left radial artery access and demonstrated patency of LIMA to LAD and SVG to OM1, OM2 conduits, but a complete occlusion of sequential SVG to PL conduit. Native left main coronary artery was occluded in ostium and native RCA was occluded in the mid portion with bridging collaterals. We decided to treat the native RCA CTO. Dual arterial access was achieved with another 6 Fr sheath in right femoral artery. The left and right coronary arteries were intubated with 6 Fr AL 0.75 (Launcher; Medtronic; USA) and 6 Fr EBU 3.5 (Launcher; Medtronic; USA) guide catheters, respectively. An antegrade approach via left radial artery was attempted; however, neither Fielder XTR wire (Asahi Intec, Japan) nor Gaia 3 wire (Asahi Intec, Japan) with Finecross microcatheter (Terumo, Japan) reached the true lumen in distal RCA. Then, parallel wire technique with Crusade microcatheter (Kaneka, Japan) and two Gaia 3 wires (Asahi Intec, Japan) were attempted, but also failed. We therefore switched to the retrograde approach using septal channel from LAD through occluded left coronary artery. Gaia 3 wire (Asahi Intec, Japan) crossed occluded left main (LM) and LAD, and finally reached true lumen in distal LAD. Sion wire was exchanged by Finecross microcatheter (Terumo, Japan) into dital LAD, and dilation of LM and proximal LAD with a 2.0 × 15 mm balloon was performed. Then, septal surfing technique (SST) was used for septal crossing. We tried different septal channels originating from proximal to distal LAD, and delivered Sion wire (Asahi Intec, Japan) retrogradely through distal septal branch into distal RCA supported by a 150-cm Finecross microcatheter (Terumo, Japan). Gaia 3 wire (Asahi Intec, Japan) crossed CTO lesion retrogradely into the true lumen in proximal RCA, and was advanced into Guidezilla guide extension catheter (Boston Scientific, USA) positioned in the antegrade guiding catheter. The Finecross microcatheter (Terumo, Japan) was delivered to the antegrade catheter and a RG3 wire (Asahi Intec, Japan) was externalized. The CTO was then predilated by a 2.0 × 15 mm balloon and stented with 2 overlapping drug-eluting stents (2.5 × 38 mm and 3.0 × 38 mm) with excellent angiographic result and TIMI3 flow in all distal branches.\n\nDyspnea was relieved at discharge. At 6-month follow-up, the patient had no recurrence of dyspnea.",
+    "diff_label_texts": "A 69-year-old man with prior coronary bypass surgery presented with two months of severe shortness of breath with mild activity (NYHA class III). He was diagnosed with heart failure due to ischemia after failure of a saphenous vein graft to the right coronary artery. This was supported by an abnormal ECG, elevated NT-proBNP, and a coronary angiogram; echocardiography also showed reduced pumping function. The team reopened a chronic total occlusion in the native right coronary artery using a retrograde approach through septal channels (septal surfing). To enable that route, they first re-opened the totally occluded left coronary artery. After the procedure, his dyspnea improved before discharge, and at 6 months he had no recurrence of shortness of breath.",
+    "summary": "Patient concerns:\nThis is a 69-year-old male with prior history of coronary artery bypass grafting presented with severe dyspnea at mild exertion (NYHA III) of 2 months duration.\n\nDiagnosis:\nThe patient was diagnosed as heart failure caused by ischemia after SVG failure (SVG to right coronary artery) according to electrocardiogram, plasma N-terminal pro-B-type natriuretic peptide levels, and coronary angiogram.\n\nInterventions:\nWe recanalized native right coronary artery CTO by retrograde approach using septal collaterals by surfing technique after recanalization of totally occluded left coronary artery.\n\nOutcomes:\nDyspnea was relieved at discharge. At 6-month follow-up, the patient had no recurrence of dyspnea."
+  },
+  {
+    "doc_id": 9,
+    "label": "low_health_literacy",
+    "fulltext": "A 69-year-old male with prior history of CABG presented with severe dyspnea at mild exertion (NYHA III) of 2 months duration was admitted in our center. The electrocardiogram showed ST depression in leads II, III, aVF, and V4-6, and blood examination revealed elevation of plasma N-terminal pro-B-type natriuretic peptide levels (2640 pg/mL). Echocardiogram showed left ventricular systolic dysfunction and low left ventricular ejection fraction (30%). The patient had inferior ST-segment-elevation myocardial infarction in 2009, when he was 59 years old, with angiographic evidence of severe 3 vessels disease (coronary angiography showed CTO in proximal left anterior descending artery (LAD), 90% stenosis in mid and distal left circumflex artery, and 95% stenosis in mid RCA. The patient underwent CABG with left internal mammary artery (LIMA) to LAD, and sequential SVG to 1st obtuse marginal branch (OM1), 2nd obtuse marginal branch (OM2), and posterolateral branch (PL) in 2009.\n\nCoronary angiography was performed via 6 French (Fr) left radial artery access and demonstrated patency of LIMA to LAD and SVG to OM1, OM2 conduits, but a complete occlusion of sequential SVG to PL conduit. Native left main coronary artery was occluded in ostium and native RCA was occluded in the mid portion with bridging collaterals. We decided to treat the native RCA CTO. Dual arterial access was achieved with another 6 Fr sheath in right femoral artery. The left and right coronary arteries were intubated with 6 Fr AL 0.75 (Launcher; Medtronic; USA) and 6 Fr EBU 3.5 (Launcher; Medtronic; USA) guide catheters, respectively. An antegrade approach via left radial artery was attempted; however, neither Fielder XTR wire (Asahi Intec, Japan) nor Gaia 3 wire (Asahi Intec, Japan) with Finecross microcatheter (Terumo, Japan) reached the true lumen in distal RCA. Then, parallel wire technique with Crusade microcatheter (Kaneka, Japan) and two Gaia 3 wires (Asahi Intec, Japan) were attempted, but also failed. We therefore switched to the retrograde approach using septal channel from LAD through occluded left coronary artery. Gaia 3 wire (Asahi Intec, Japan) crossed occluded left main (LM) and LAD, and finally reached true lumen in distal LAD. Sion wire was exchanged by Finecross microcatheter (Terumo, Japan) into dital LAD, and dilation of LM and proximal LAD with a 2.0 × 15 mm balloon was performed. Then, septal surfing technique (SST) was used for septal crossing. We tried different septal channels originating from proximal to distal LAD, and delivered Sion wire (Asahi Intec, Japan) retrogradely through distal septal branch into distal RCA supported by a 150-cm Finecross microcatheter (Terumo, Japan). Gaia 3 wire (Asahi Intec, Japan) crossed CTO lesion retrogradely into the true lumen in proximal RCA, and was advanced into Guidezilla guide extension catheter (Boston Scientific, USA) positioned in the antegrade guiding catheter. The Finecross microcatheter (Terumo, Japan) was delivered to the antegrade catheter and a RG3 wire (Asahi Intec, Japan) was externalized. The CTO was then predilated by a 2.0 × 15 mm balloon and stented with 2 overlapping drug-eluting stents (2.5 × 38 mm and 3.0 × 38 mm) with excellent angiographic result and TIMI3 flow in all distal branches.\n\nDyspnea was relieved at discharge. At 6-month follow-up, the patient had no recurrence of dyspnea.",
+    "diff_label_texts": "This 69-year-old man had heart bypass surgery in the past. For 2 months, he got very short of breath with light activity. Tests—a heart tracing, a blood test, and an X-ray movie with dye of the heart arteries—showed heart failure from poor blood flow after a bypass vein to the right heart artery failed. Doctors first opened a totally blocked artery on the left side of his heart. Then they used tiny natural detours between heart arteries to reach the right heart artery from the far end and open it. His breathing was better when he left the hospital. Six months later, his shortness of breath had not come back.",
+    "summary": "Patient concerns:\nThis is a 69-year-old male with prior history of coronary artery bypass grafting presented with severe dyspnea at mild exertion (NYHA III) of 2 months duration.\n\nDiagnosis:\nThe patient was diagnosed as heart failure caused by ischemia after SVG failure (SVG to right coronary artery) according to electrocardiogram, plasma N-terminal pro-B-type natriuretic peptide levels, and coronary angiogram.\n\nInterventions:\nWe recanalized native right coronary artery CTO by retrograde approach using septal collaterals by surfing technique after recanalization of totally occluded left coronary artery.\n\nOutcomes:\nDyspnea was relieved at discharge. At 6-month follow-up, the patient had no recurrence of dyspnea."
+  },
+  {
+    "doc_id": 9,
+    "label": "proficient_health_literacy",
+    "fulltext": "A 69-year-old male with prior history of CABG presented with severe dyspnea at mild exertion (NYHA III) of 2 months duration was admitted in our center. The electrocardiogram showed ST depression in leads II, III, aVF, and V4-6, and blood examination revealed elevation of plasma N-terminal pro-B-type natriuretic peptide levels (2640 pg/mL). Echocardiogram showed left ventricular systolic dysfunction and low left ventricular ejection fraction (30%). The patient had inferior ST-segment-elevation myocardial infarction in 2009, when he was 59 years old, with angiographic evidence of severe 3 vessels disease (coronary angiography showed CTO in proximal left anterior descending artery (LAD), 90% stenosis in mid and distal left circumflex artery, and 95% stenosis in mid RCA. The patient underwent CABG with left internal mammary artery (LIMA) to LAD, and sequential SVG to 1st obtuse marginal branch (OM1), 2nd obtuse marginal branch (OM2), and posterolateral branch (PL) in 2009.\n\nCoronary angiography was performed via 6 French (Fr) left radial artery access and demonstrated patency of LIMA to LAD and SVG to OM1, OM2 conduits, but a complete occlusion of sequential SVG to PL conduit. Native left main coronary artery was occluded in ostium and native RCA was occluded in the mid portion with bridging collaterals. We decided to treat the native RCA CTO. Dual arterial access was achieved with another 6 Fr sheath in right femoral artery. The left and right coronary arteries were intubated with 6 Fr AL 0.75 (Launcher; Medtronic; USA) and 6 Fr EBU 3.5 (Launcher; Medtronic; USA) guide catheters, respectively. An antegrade approach via left radial artery was attempted; however, neither Fielder XTR wire (Asahi Intec, Japan) nor Gaia 3 wire (Asahi Intec, Japan) with Finecross microcatheter (Terumo, Japan) reached the true lumen in distal RCA. Then, parallel wire technique with Crusade microcatheter (Kaneka, Japan) and two Gaia 3 wires (Asahi Intec, Japan) were attempted, but also failed. We therefore switched to the retrograde approach using septal channel from LAD through occluded left coronary artery. Gaia 3 wire (Asahi Intec, Japan) crossed occluded left main (LM) and LAD, and finally reached true lumen in distal LAD. Sion wire was exchanged by Finecross microcatheter (Terumo, Japan) into dital LAD, and dilation of LM and proximal LAD with a 2.0 × 15 mm balloon was performed. Then, septal surfing technique (SST) was used for septal crossing. We tried different septal channels originating from proximal to distal LAD, and delivered Sion wire (Asahi Intec, Japan) retrogradely through distal septal branch into distal RCA supported by a 150-cm Finecross microcatheter (Terumo, Japan). Gaia 3 wire (Asahi Intec, Japan) crossed CTO lesion retrogradely into the true lumen in proximal RCA, and was advanced into Guidezilla guide extension catheter (Boston Scientific, USA) positioned in the antegrade guiding catheter. The Finecross microcatheter (Terumo, Japan) was delivered to the antegrade catheter and a RG3 wire (Asahi Intec, Japan) was externalized. The CTO was then predilated by a 2.0 × 15 mm balloon and stented with 2 overlapping drug-eluting stents (2.5 × 38 mm and 3.0 × 38 mm) with excellent angiographic result and TIMI3 flow in all distal branches.\n\nDyspnea was relieved at discharge. At 6-month follow-up, the patient had no recurrence of dyspnea.",
+    "diff_label_texts": "A 69-year-old male with prior CABG presented with 2 months of severe dyspnea on mild exertion (NYHA III). ECG showed ST depression in II, III, aVF, and V4–6; NT-proBNP was 2640 pg/mL. Echocardiography demonstrated LV systolic dysfunction with LVEF 30%. His history included an inferior STEMI in 2009 with severe 3-vessel disease (proximal LAD CTO, 90% mid/distal LCx stenoses, 95% mid RCA stenosis) treated with CABG (LIMA–LAD; sequential SVG to OM1, OM2, and PL). Current angiography via 6 Fr left radial access showed patent LIMA–LAD and SVG–OM1/OM2, but complete occlusion of the sequential SVG to PL. The native LM was occluded at the ostium and the native RCA was occluded in the mid segment with bridging collaterals. The strategy was to treat the native RCA CTO. Dual arterial access was obtained with an additional 6 Fr right femoral sheath. The right and left coronaries were engaged with 6 Fr AL 0.75 (Launcher; Medtronic) and 6 Fr EBU 3.5 (Launcher; Medtronic) guide catheters, respectively. An antegrade approach from the left radial artery failed: neither a Fielder XTR nor a Gaia 3 with a Finecross microcatheter could enter the distal true lumen. A parallel wire technique with a Crusade microcatheter and two Gaia 3 wires also failed. The team then switched to a retrograde approach via septal channels from the LAD through the occluded left coronary system. A Gaia 3 crossed the occluded LM and LAD to reach the distal LAD true lumen. A Sion wire was exchanged via a Finecross into the distal LAD, followed by dilation of the LM and proximal LAD with a 2.0 × 15 mm balloon. Septal surfing technique (SST) was then used to identify a viable septal channel. A Sion wire, supported by a 150-cm Finecross, was advanced retrogradely through a distal septal branch into the distal RCA. A Gaia 3 traversed the RCA CTO retrogradely into the proximal RCA true lumen and was advanced into a Guidezilla guide extension catheter positioned in the antegrade guide. The Finecross was delivered to the antegrade guide and an RG3 wire was externalized. The CTO segment was predilated with a 2.0 × 15 mm balloon and stented with two overlapping DES (2.5 × 38 mm and 3.0 × 38 mm), achieving an excellent angiographic result with TIMI 3 flow in all distal branches. Dyspnea was relieved at discharge, and at 6-month follow-up there was no recurrence of dyspnea.",
+    "summary": "Patient concerns:\nThis is a 69-year-old male with prior history of coronary artery bypass grafting presented with severe dyspnea at mild exertion (NYHA III) of 2 months duration.\n\nDiagnosis:\nThe patient was diagnosed as heart failure caused by ischemia after SVG failure (SVG to right coronary artery) according to electrocardiogram, plasma N-terminal pro-B-type natriuretic peptide levels, and coronary angiogram.\n\nInterventions:\nWe recanalized native right coronary artery CTO by retrograde approach using septal collaterals by surfing technique after recanalization of totally occluded left coronary artery.\n\nOutcomes:\nDyspnea was relieved at discharge. At 6-month follow-up, the patient had no recurrence of dyspnea."
+  },
+  {
+    "doc_id": 10,
+    "label": "intermediate_health_literacy",
+    "fulltext": "A 51-year-old male patient presented to us with acute painful visual loss of his left eye (LE) from 3 days ago. The best-corrected distance visual acuity (BCDVA) was 20/20, and hand motion (HM) detection for the right eye (RE) and LE, respectively. The ocular movement was normal in both eyes. Anterior segment examination was unremarkable for both eyes. The LE fundus examination showed ONH swelling, choroidal bulging, multiple patches of subretinal fluid accumulation, and retinal pigment epithelial (RPE) corrugations. Fundus examination of the RE was unremarkable.\n\nWe used multimodal imaging including Optical coherence tomography (OCT) (OptoVue, Inc., Fremont, CA, USA, software version: 2018,0,0,18), fundus blue-autofluorescence (BAF), fluorescein angiography (FA) (Heidelberg Eye Explorer version 1.9.13.0, Spectralis Viewing Module 6.5.2.0; Heidelberg Engineering), Indocyanin green angiography (ICGA), and B-scan ultrasonography for further evaluation. Besides, orbital and brain MRIs with gadolinium enhancement were ordered. The OCT image revealed a mild RPE and choroidal bulging, RPE hyper-reflectivity with back shadowing, subretinal and intraretinal fluid accumulation, and mild retinal thickening. A geographic area of macular hypocyanescence was apparent in the ICGA image of the left eye. BAF showed a geographic area with a speckled autofluorescence pattern at the macula. Optic nerve enlargement was found in the B-scan ultrasonography. In FA images, vascular leakage was apparent at the ONH (hot disc). Besides, a geographic patchy hypofluorescent area with speckled hyperfluorescent margins with a size of three disc diameters (DD) was detected. Orbital and brain MRI showed a retrobulbar nodular mass with gadolinium enhancement at the junction of the optic nerve and sclera. An oncology consultation was done with no remarkable finding.\n\nConsidering the suspicion of malignancy and the presence of an enhancing nodular mass in the orbit, the patient underwent transconjunctival lateral orbitotomy one week after the presentation. A pink localized scleral nodule with edematous tenon was found. Sub-tenon triamcinolone acetonide was injected with the clinical diagnosis of nodular posterior scleritis. The patient refused admission and intravenous corticosteroid injection as the treatment order. Oral prednisolone 50 mg/Kg was started. Rheumatology consultation and screening lab results, including PPD test (tuberculosis), chest X-ray, serum ACE level (sarcoidosis), and C-ANCA level (Wegner granulomatosis), were unremarkable. At the last follow-up examination (one week after the surgery), the patient’s BCDVA was 20/20, and counting fingers at 2 meters for the RE and LE, respectively. Furthermore, SRF was absorbed, and the macula became atrophic. Oral prednisolone was tapered off slowly for three months.",
+    "diff_label_texts": "A 51-year-old man presented with 3 days of sudden, painful vision loss in the left eye. Visual acuity was 20/20 in the right eye and hand motion in the left eye. Left fundus findings included optic nerve head swelling, choroidal bulging, multiple areas of subretinal fluid, and RPE corrugations. Orbital/brain MRI with gadolinium showed a retrobulbar nodular mass enhancing at the junction of the optic nerve and sclera. Oncology and rheumatology evaluations were unremarkable. The clinical diagnosis was nodular posterior scleritis, and oral prednisolone was started.",
+    "summary": "A 51-year-old male patient presented to us with acute painful visual loss of his left eye (LE) from 3 days ago. The best-corrected distance visual acuity (BCDVA) was 20/20 and hand motion (HM) for the right eye (RE) and LE, respectively. Fundus examination of the LE showed ONH swelling, choroidal bulging, multiple patches of subretinal fluid accumulation, and retinal pigment epithelial (RPE) corrugations. Orbital and brain MRI showed a retrobulbar nodular mass with gadolinium enhancement at the optic nerve and sclera junction. Oncology and rheumatology work-ups were unremarkable. With the clinical diagnosis of nodular posterior scleritis oral prednisolone 50 mg/Kg was started."
+  },
+  {
+    "doc_id": 10,
+    "label": "low_health_literacy",
+    "fulltext": "A 51-year-old male patient presented to us with acute painful visual loss of his left eye (LE) from 3 days ago. The best-corrected distance visual acuity (BCDVA) was 20/20, and hand motion (HM) detection for the right eye (RE) and LE, respectively. The ocular movement was normal in both eyes. Anterior segment examination was unremarkable for both eyes. The LE fundus examination showed ONH swelling, choroidal bulging, multiple patches of subretinal fluid accumulation, and retinal pigment epithelial (RPE) corrugations. Fundus examination of the RE was unremarkable.\n\nWe used multimodal imaging including Optical coherence tomography (OCT) (OptoVue, Inc., Fremont, CA, USA, software version: 2018,0,0,18), fundus blue-autofluorescence (BAF), fluorescein angiography (FA) (Heidelberg Eye Explorer version 1.9.13.0, Spectralis Viewing Module 6.5.2.0; Heidelberg Engineering), Indocyanin green angiography (ICGA), and B-scan ultrasonography for further evaluation. Besides, orbital and brain MRIs with gadolinium enhancement were ordered. The OCT image revealed a mild RPE and choroidal bulging, RPE hyper-reflectivity with back shadowing, subretinal and intraretinal fluid accumulation, and mild retinal thickening. A geographic area of macular hypocyanescence was apparent in the ICGA image of the left eye. BAF showed a geographic area with a speckled autofluorescence pattern at the macula. Optic nerve enlargement was found in the B-scan ultrasonography. In FA images, vascular leakage was apparent at the ONH (hot disc). Besides, a geographic patchy hypofluorescent area with speckled hyperfluorescent margins with a size of three disc diameters (DD) was detected. Orbital and brain MRI showed a retrobulbar nodular mass with gadolinium enhancement at the junction of the optic nerve and sclera. An oncology consultation was done with no remarkable finding.\n\nConsidering the suspicion of malignancy and the presence of an enhancing nodular mass in the orbit, the patient underwent transconjunctival lateral orbitotomy one week after the presentation. A pink localized scleral nodule with edematous tenon was found. Sub-tenon triamcinolone acetonide was injected with the clinical diagnosis of nodular posterior scleritis. The patient refused admission and intravenous corticosteroid injection as the treatment order. Oral prednisolone 50 mg/Kg was started. Rheumatology consultation and screening lab results, including PPD test (tuberculosis), chest X-ray, serum ACE level (sarcoidosis), and C-ANCA level (Wegner granulomatosis), were unremarkable. At the last follow-up examination (one week after the surgery), the patient’s BCDVA was 20/20, and counting fingers at 2 meters for the RE and LE, respectively. Furthermore, SRF was absorbed, and the macula became atrophic. Oral prednisolone was tapered off slowly for three months.",
+    "diff_label_texts": "A 51-year-old man came to us with sudden, painful vision loss in his left eye for three days. His right eye could see clearly (20/20). His left eye could only see hand movements. The back of his left eye showed swelling of the seeing nerve, a bulge in the layer under the retina, several patches of fluid under the retina, and wrinkles in the thin lining there. An MRI scan with contrast dye of the eyes and brain showed a small lump behind the eye where the eye nerve meets the white part of the eye. Tests for cancer and immune diseases were normal. The doctors diagnosed inflammation in the back part of the eye’s white coat that forms a small lump (nodular posterior scleritis). They started high-dose steroid pills by mouth (prednisolone).",
+    "summary": "A 51-year-old male patient presented to us with acute painful visual loss of his left eye (LE) from 3 days ago. The best-corrected distance visual acuity (BCDVA) was 20/20 and hand motion (HM) for the right eye (RE) and LE, respectively. Fundus examination of the LE showed ONH swelling, choroidal bulging, multiple patches of subretinal fluid accumulation, and retinal pigment epithelial (RPE) corrugations. Orbital and brain MRI showed a retrobulbar nodular mass with gadolinium enhancement at the optic nerve and sclera junction. Oncology and rheumatology work-ups were unremarkable. With the clinical diagnosis of nodular posterior scleritis oral prednisolone 50 mg/Kg was started."
+  },
+  {
+    "doc_id": 10,
+    "label": "proficient_health_literacy",
+    "fulltext": "A 51-year-old male patient presented to us with acute painful visual loss of his left eye (LE) from 3 days ago. The best-corrected distance visual acuity (BCDVA) was 20/20, and hand motion (HM) detection for the right eye (RE) and LE, respectively. The ocular movement was normal in both eyes. Anterior segment examination was unremarkable for both eyes. The LE fundus examination showed ONH swelling, choroidal bulging, multiple patches of subretinal fluid accumulation, and retinal pigment epithelial (RPE) corrugations. Fundus examination of the RE was unremarkable.\n\nWe used multimodal imaging including Optical coherence tomography (OCT) (OptoVue, Inc., Fremont, CA, USA, software version: 2018,0,0,18), fundus blue-autofluorescence (BAF), fluorescein angiography (FA) (Heidelberg Eye Explorer version 1.9.13.0, Spectralis Viewing Module 6.5.2.0; Heidelberg Engineering), Indocyanin green angiography (ICGA), and B-scan ultrasonography for further evaluation. Besides, orbital and brain MRIs with gadolinium enhancement were ordered. The OCT image revealed a mild RPE and choroidal bulging, RPE hyper-reflectivity with back shadowing, subretinal and intraretinal fluid accumulation, and mild retinal thickening. A geographic area of macular hypocyanescence was apparent in the ICGA image of the left eye. BAF showed a geographic area with a speckled autofluorescence pattern at the macula. Optic nerve enlargement was found in the B-scan ultrasonography. In FA images, vascular leakage was apparent at the ONH (hot disc). Besides, a geographic patchy hypofluorescent area with speckled hyperfluorescent margins with a size of three disc diameters (DD) was detected. Orbital and brain MRI showed a retrobulbar nodular mass with gadolinium enhancement at the junction of the optic nerve and sclera. An oncology consultation was done with no remarkable finding.\n\nConsidering the suspicion of malignancy and the presence of an enhancing nodular mass in the orbit, the patient underwent transconjunctival lateral orbitotomy one week after the presentation. A pink localized scleral nodule with edematous tenon was found. Sub-tenon triamcinolone acetonide was injected with the clinical diagnosis of nodular posterior scleritis. The patient refused admission and intravenous corticosteroid injection as the treatment order. Oral prednisolone 50 mg/Kg was started. Rheumatology consultation and screening lab results, including PPD test (tuberculosis), chest X-ray, serum ACE level (sarcoidosis), and C-ANCA level (Wegner granulomatosis), were unremarkable. At the last follow-up examination (one week after the surgery), the patient’s BCDVA was 20/20, and counting fingers at 2 meters for the RE and LE, respectively. Furthermore, SRF was absorbed, and the macula became atrophic. Oral prednisolone was tapered off slowly for three months.",
+    "diff_label_texts": "A 51-year-old male presented with acute, painful visual loss of the left eye (LE) for 3 days. Best-corrected distance visual acuity (BCDVA) was 20/20 OD and hand motion (HM) OS. Ocular motility and anterior segment were unremarkable OU. Fundus OS showed optic nerve head (ONH) swelling, choroidal bulging, multiple patches of subretinal fluid (SRF), and retinal pigment epithelial (RPE) corrugations; OD fundus was unremarkable.\n\nMultimodal imaging was obtained: OCT (OptoVue, Inc., Fremont, CA, USA; software version 2018.0.0.18) demonstrated mild RPE and choroidal bulging, RPE hyper-reflectivity with back shadowing, subretinal and intraretinal fluid, and mild retinal thickening. Indocyanine green angiography (ICGA) showed a geographic macular hypocyanescent area OS. Blue-autofluorescence (BAF) revealed a geographic macular area with speckled autofluorescence. B-scan ultrasonography showed optic nerve enlargement. Fluorescein angiography (FA) demonstrated vascular leakage at the ONH (hot disc) and a geographic patchy hypofluorescent area with speckled hyperfluorescent margins measuring approximately three disc diameters. Orbital and brain MRI with gadolinium revealed a retrobulbar nodular enhancing mass at the optic nerve–sclera junction. Oncology consultation was unremarkable.\n\nGiven concern for malignancy and the enhancing orbital nodule, the patient underwent transconjunctival lateral orbitotomy one week after presentation. Intraoperatively, a pink localized scleral nodule with edematous Tenon was identified. With a clinical diagnosis of nodular posterior scleritis, sub-Tenon triamcinolone acetonide was administered. The patient declined admission and intravenous corticosteroids; oral prednisolone 50 mg/Kg was initiated. Rheumatologic and infectious work-up, including PPD (tuberculosis), chest X-ray, serum ACE (sarcoidosis), and C-ANCA (Wegener granulomatosis), was unremarkable.\n\nAt the one-week postoperative follow-up, BCDVA was 20/20 OD and counting fingers at 2 meters OS. SRF had resolved, and the macula was atrophic. Oral prednisolone was tapered over three months.",
+    "summary": "A 51-year-old male patient presented to us with acute painful visual loss of his left eye (LE) from 3 days ago. The best-corrected distance visual acuity (BCDVA) was 20/20 and hand motion (HM) for the right eye (RE) and LE, respectively. Fundus examination of the LE showed ONH swelling, choroidal bulging, multiple patches of subretinal fluid accumulation, and retinal pigment epithelial (RPE) corrugations. Orbital and brain MRI showed a retrobulbar nodular mass with gadolinium enhancement at the optic nerve and sclera junction. Oncology and rheumatology work-ups were unremarkable. With the clinical diagnosis of nodular posterior scleritis oral prednisolone 50 mg/Kg was started."
+  },
+  {
+    "doc_id": 11,
+    "label": "intermediate_health_literacy",
+    "fulltext": "An elderly 78-year-old patient from the Amhara region of Ethiopia, who has had a permanent cardiac pacemaker for 7 years, was scheduled for retropubic prostatectomy due to benign prostatic hyperplasia (BPH). This condition developed following a previous transurethral resection of the prostate 3 months earlier. The patient in the preoperative anesthesia evaluation was fully evaluated, and all the routine investigations required for the proposed surgery, which were within normal limits, were investigated. The patient presented with a history of frequency, urgency, nocturia, and dribbling for the past 2 months. Additionally, the patient had been known to have hypertension for the past 16 years and was taking amlodipine 5 mg orally daily, enalapril 10 mg orally twice daily (BID), and atorvastatin 10 mg orally daily. He had also been known to have type II diabetes mellitus for the past 25 years and was on metformin 500 mg orally BID and neutral protamine Hagedorn (NPH) 20 IU and 10 IU. He was admitted to a hospital for further evaluation, and complete bundle branch block (BBB) was detected via electrocardiogram (ECG). In an electrophysiology study, the patient was diagnosed with left ventricular hypertrophy secondary to hypertensive heart disease, mild diastolic dysfunction, and an ejection fraction of 62%. Abdominal ultrasound revealed an enlarged prostate size of 82 ml; anterior–posterior (AP) chest X-ray revealed a normal chest region with a left-side pacemaker in situ, and all the other blood parameters, including electrolytes and serum troponin levels, were within normal limits.\n\nA cardiologist was involved preoperatively as a multidisciplinary approach and risk determination tool for cardiac risk assessment. The patient had a frailty score of 5.5 with a poor functional cardiopulmonary reserve of metabolic equivalent (MET) = 3.4 and Revised Cardiac Risk Index (RCRI) class III, which accounts for 10.1% of major cardiac adverse events (myocardial infarction [MI], cardiac arrest, or death) within 30 days of the postoperative period, and intermediate risk on the basis of surgery type and patient risk factors. After preoperative evaluation and risk disclosure regarding the un-reprogrammed pacemaker and the associated complications during anesthesia and surgery, the patient was unable to afford the necessary health coverage for pacemaker reprogramming. This is because the cardiac surgery was performed in Addis Ababa, Ethiopia, which has a long waiting list with few cardiac surgeons for millions of people and is a considerable distance from the patient’s home institution, and there is a period of monitoring after pacemaker reprogramming for considerable post-reprogramming complication. As a result, the patient chose to proceed with the surgery, accepting the potential risks and harm associated with the situation. Continuous cardiac monitoring during the intraoperative period is highly advocated. Despite these factors, the patient did not experience cardiorespiratory failure, and he was stable. The patient continued on medication until the day of surgery, which included amlodipine, enalapril, atorvastatin, and a morning lower dose of two-thirds of the NPH. He also took 5 mg of diazepam orally for anxiolytics at midnight before the day of surgery.\n\nOn the day of surgery, the patient’s random blood sugar (RBS) was measured, and sliding scale glycemic control was implemented. Communication among the anesthetist, surgeon, and nurses was emphasized, ensuring that the cautery pad was placed away from the pacemaker, and that emergency drugs and a defibrillator were ready. The patient was premedicated with dexamethasone for nausea prophylaxis and paracetamol for pain relief as preemptive analgesia. American Society of Anesthesiology (ASA) standard monitoring was applied, and baseline parameters were recorded. Combined epidural–spinal anesthesia was administered via 0.5% isobaric bupivacaine (12.5 mg) and 50 µg fentanyl at the L3–L4 interspace. The block achieved anesthesia up to the umbilicus, and the sensory block was performed at T7. The surgery involved a midline incision below the umbilicus, with monopolar cautery used at low voltage (20 mA). Hemostasis was achieved through bipolar low-voltage cautery. Throughout the procedure, the patient’s vital signs remained stable. The patient’s vital signs did not change by more than 10% from the baseline vital signs. The intravenous fluid was resuscitated intraoperatively. During the postoperative period, the patient was transferred to the postanesthesia care unit (PACU) with vigilant monitoring, and 10 ml of 0.125% epidural top-up analgesia was given. Postop investigations were within normal limits. The patient was observed in the PACU for 12 hours and later transferred to the ward in stable condition with regular follow-up with the cardiology team. After 88th day of postsurgery the patient was discharged and advised to have regular checkups for pacemaker’s in situ status.",
+    "diff_label_texts": "A 78-year-old man from the Amhara region, Ethiopia, with a permanent pacemaker placed for complete heart block was scheduled for retropubic prostatectomy. The anesthesia and cardiology teams recommended switching his dual-chamber, rate‑modulated pacemaker to an asynchronous mode perioperatively to reduce the risk of electromagnetic interference during surgery. He could not afford reprogramming and chose to proceed with the existing plan after informed consent; permission to publish the case was obtained after the operation. He received combined spinal–epidural anesthesia at L3–L4 using 0.5% isobaric bupivacaine 2.5 ml (12.5 mg) plus fentanyl 50 µg. Standard ASA monitoring was applied with special attention to cardiac stability. Intraoperatively, he remained stable with minimal changes in vital signs; blood pressure was supported with isotonic saline as needed. Postoperatively, he was monitored in the PACU, received analgesia at 4 hours with an epidural top‑up, and was transferred to the ward about 6 hours after surgery in stable condition. Epidural analgesia was continued for 72 hours. He was discharged at the 88th postoperative hour in good condition.",
+    "summary": "A 78-year-old male from the Amhara region, Ethiopia, with a permanent pacemaker for complete heart block was scheduled for retropubic prostatectomy. Preoperative assessments by the anesthetist and cardiologist recommended reprogramming the pacemaker to asynchronous mode to reduce risks related to its dual-chamber, rate-modulated mode setting. However, the patient could not afford reprogramming and opted to proceed with the existing perioperative plan. Informed consent was obtained, and case report publication permission was obtained after operation. The patient received combined epidural-spinal anesthesia with 2.50 ml of 0.5% isobaric bupivacaine and 50 µg fentanyl at the L3-L4 interspace. Standard American Society of Anesthesiology monitoring was applied, with a focus on cardiac stability. The patient remained stable with minimal vital sign fluctuations and maintained adequate blood pressure using isotonic saline. Postoperatively, the patient was transferred to the postanesthesia care unit, receiving analgesia after 4 hours and an epidural top-up. After 6 hours, he was transferred to the ward in stable condition. Epidural analgesia was continued for 72 hours, and the patient was discharged on the 88th postoperative hour in stable condition."
+  },
+  {
+    "doc_id": 11,
+    "label": "low_health_literacy",
+    "fulltext": "An elderly 78-year-old patient from the Amhara region of Ethiopia, who has had a permanent cardiac pacemaker for 7 years, was scheduled for retropubic prostatectomy due to benign prostatic hyperplasia (BPH). This condition developed following a previous transurethral resection of the prostate 3 months earlier. The patient in the preoperative anesthesia evaluation was fully evaluated, and all the routine investigations required for the proposed surgery, which were within normal limits, were investigated. The patient presented with a history of frequency, urgency, nocturia, and dribbling for the past 2 months. Additionally, the patient had been known to have hypertension for the past 16 years and was taking amlodipine 5 mg orally daily, enalapril 10 mg orally twice daily (BID), and atorvastatin 10 mg orally daily. He had also been known to have type II diabetes mellitus for the past 25 years and was on metformin 500 mg orally BID and neutral protamine Hagedorn (NPH) 20 IU and 10 IU. He was admitted to a hospital for further evaluation, and complete bundle branch block (BBB) was detected via electrocardiogram (ECG). In an electrophysiology study, the patient was diagnosed with left ventricular hypertrophy secondary to hypertensive heart disease, mild diastolic dysfunction, and an ejection fraction of 62%. Abdominal ultrasound revealed an enlarged prostate size of 82 ml; anterior–posterior (AP) chest X-ray revealed a normal chest region with a left-side pacemaker in situ, and all the other blood parameters, including electrolytes and serum troponin levels, were within normal limits.\n\nA cardiologist was involved preoperatively as a multidisciplinary approach and risk determination tool for cardiac risk assessment. The patient had a frailty score of 5.5 with a poor functional cardiopulmonary reserve of metabolic equivalent (MET) = 3.4 and Revised Cardiac Risk Index (RCRI) class III, which accounts for 10.1% of major cardiac adverse events (myocardial infarction [MI], cardiac arrest, or death) within 30 days of the postoperative period, and intermediate risk on the basis of surgery type and patient risk factors. After preoperative evaluation and risk disclosure regarding the un-reprogrammed pacemaker and the associated complications during anesthesia and surgery, the patient was unable to afford the necessary health coverage for pacemaker reprogramming. This is because the cardiac surgery was performed in Addis Ababa, Ethiopia, which has a long waiting list with few cardiac surgeons for millions of people and is a considerable distance from the patient’s home institution, and there is a period of monitoring after pacemaker reprogramming for considerable post-reprogramming complication. As a result, the patient chose to proceed with the surgery, accepting the potential risks and harm associated with the situation. Continuous cardiac monitoring during the intraoperative period is highly advocated. Despite these factors, the patient did not experience cardiorespiratory failure, and he was stable. The patient continued on medication until the day of surgery, which included amlodipine, enalapril, atorvastatin, and a morning lower dose of two-thirds of the NPH. He also took 5 mg of diazepam orally for anxiolytics at midnight before the day of surgery.\n\nOn the day of surgery, the patient’s random blood sugar (RBS) was measured, and sliding scale glycemic control was implemented. Communication among the anesthetist, surgeon, and nurses was emphasized, ensuring that the cautery pad was placed away from the pacemaker, and that emergency drugs and a defibrillator were ready. The patient was premedicated with dexamethasone for nausea prophylaxis and paracetamol for pain relief as preemptive analgesia. American Society of Anesthesiology (ASA) standard monitoring was applied, and baseline parameters were recorded. Combined epidural–spinal anesthesia was administered via 0.5% isobaric bupivacaine (12.5 mg) and 50 µg fentanyl at the L3–L4 interspace. The block achieved anesthesia up to the umbilicus, and the sensory block was performed at T7. The surgery involved a midline incision below the umbilicus, with monopolar cautery used at low voltage (20 mA). Hemostasis was achieved through bipolar low-voltage cautery. Throughout the procedure, the patient’s vital signs remained stable. The patient’s vital signs did not change by more than 10% from the baseline vital signs. The intravenous fluid was resuscitated intraoperatively. During the postoperative period, the patient was transferred to the postanesthesia care unit (PACU) with vigilant monitoring, and 10 ml of 0.125% epidural top-up analgesia was given. Postop investigations were within normal limits. The patient was observed in the PACU for 12 hours and later transferred to the ward in stable condition with regular follow-up with the cardiology team. After 88th day of postsurgery the patient was discharged and advised to have regular checkups for pacemaker’s in situ status.",
+    "diff_label_texts": "A 78-year-old man from the Amhara region of Ethiopia had a permanent heart pacemaker because of a complete heart block. He was scheduled for prostate surgery. Before surgery, the anesthesia and heart doctors advised switching his pacemaker to a steady, fixed beat to lower the chance of problems. He could not afford that change. He chose to go ahead with the operation. He signed consent for the plan. After surgery, he also gave permission to share his case. For anesthesia, he got a numbing injection in the lower back (a combined spinal–epidural). The team used 2.5 ml of strong numbing medicine (0.5% bupivacaine) and a tiny dose of fentanyl (50 micrograms). Standard monitors were used, and his heart was watched closely. His vital signs stayed steady, with only small changes. His blood pressure stayed good with IV salt water. After surgery, he went to the recovery room. He got pain medicine after 4 hours and an extra dose through the epidural. Six hours after surgery, he moved to the ward in stable condition. The epidural pain control continued for 72 hours. He went home in stable condition about 88 hours after surgery.",
+    "summary": "A 78-year-old male from the Amhara region, Ethiopia, with a permanent pacemaker for complete heart block was scheduled for retropubic prostatectomy. Preoperative assessments by the anesthetist and cardiologist recommended reprogramming the pacemaker to asynchronous mode to reduce risks related to its dual-chamber, rate-modulated mode setting. However, the patient could not afford reprogramming and opted to proceed with the existing perioperative plan. Informed consent was obtained, and case report publication permission was obtained after operation. The patient received combined epidural-spinal anesthesia with 2.50 ml of 0.5% isobaric bupivacaine and 50 µg fentanyl at the L3-L4 interspace. Standard American Society of Anesthesiology monitoring was applied, with a focus on cardiac stability. The patient remained stable with minimal vital sign fluctuations and maintained adequate blood pressure using isotonic saline. Postoperatively, the patient was transferred to the postanesthesia care unit, receiving analgesia after 4 hours and an epidural top-up. After 6 hours, he was transferred to the ward in stable condition. Epidural analgesia was continued for 72 hours, and the patient was discharged on the 88th postoperative hour in stable condition."
+  },
+  {
+    "doc_id": 12,
+    "label": "low_health_literacy",
+    "fulltext": "A 52-year-old woman referred to the urology clinic with urinary complaints. Her symptoms began three years ago with frequency, dysuria and dribbling. She also mentioned the frequent passage of red and black thread-like substances in her urine. Moreover, during these discharges, she had headache, fever and chills. Intermittent periurethral and genital itching was another complaint of hers. She had been treated by several specialists with the diagnosis of recurrent urinary tract infections, with no clinical improvement. The patient denied recent travel, camping, hiking, farming, swimming and insect bites. She had positive history of pilonidal sinus surgery and hysterectomy, 8 and 7 years earlier, respectively. Two years prior to the current visit, she had been hospitalized for assessment. On physical examination, she was well-appearing with normal vital signs. All her laboratory tests, including cell blood count, urine analysis and biochemistries were in normal ranges. Abdominopelvic computed tomography (CT) scan revealed no abnormalities. Hence, she underwent cystoscopy, which demonstrated erythema and hyperemia of the bladder mucosa, suspended debris, and dilation of the left ureteral orifice. During consultation with an infectious diseases’ specialist, schistosomiasis was suspected, Therefore, she was treated with Praziquantel with the appropriate dose and duration and was discharged from the hospital.\n\nHowever, her symptoms did not subside. She was revisited by another infectious disease specialist, who prescribed her ivermectin due to suspicion to urinary myiasis. Nevertheless, no improvement was observed. She was readmitted to undergo bladder irrigation with polyethylene glycol, but the bladder washfluid did not contain any visible larvae. This procedure was followed by a two-day hematuria with spontaneous cessation. She was discharged home and advised to repeat the urine analysis one months later. Her random urine analysis was normal, so she collected her 24-h urine and sent it to the laboratory for analysis, in which a live larva was demonstrated under light microscope by the pathologist. The larva was isolated and sent to an entomologist to be identified morphologically. Finally, it was determined that the larva belonged to the species Sarcophaga. The patient was advised to take personal hygiene and consume at least 3 L of water daily.",
+    "diff_label_texts": "A 52-year-old woman had burning when she peed and had to pee very often for a long time. She tried many treatments for bladder infections, but the problem did not go away. Regular scans and lab tests looked normal. A camera test that looked inside her bladder showed the lining was red and irritated, with tiny bits floating in the urine. Later, the lab saw a live larva (a baby insect) in her urine under the microscope. That finding explained her symptoms. She was told to keep very clean. She was also told to drink plenty of water every day.",
+    "summary": "We report a 52-year-old woman with persistent dysuria, frequency despite multiple treatments for suspected infections. Cystoscopy revealed erythema and debris, but imaging and laboratory tests were unremarkable. A live larva was identified in urine analysis, confirming the diagnosis. Treatment involved improved hygiene and hydration."
+  },
+  {
+    "doc_id": 13,
+    "label": "intermediate_health_literacy",
+    "fulltext": "A 36-year-old female patient with a history of ulcerative colitis and good disease control on sulfasalazine, ferrous fumarate and intermittent prednisone for flare-ups is presented.\n\nHe was admitted to the emergency unit with a 1 week history of progressive oppressive precordial pain associated with dyspnea and neurovegetative symptoms. On admission, an electrocardiogram was performed in sinus rhythm, with finding of supradesnivel of the ST segment in the lower wall.\n\nThe patient reported a 6-month history of general disorders, fatigue and night sweats. She had previously presented episodes of precordial pain in relation to effort that progressed to rest. The physical examination was without murmurs or alterations of the peripheral pulses.\n\nAn emergency coronary angiography was performed, which revealed severe 2-vessel disease: severe ostial lesion 90% in the left coronary trunk and severe subocclusive lesion 99-100% at the ostial level in the right coronary artery (culprit vessel). Primary angioplasty of the right coronary artery was performed with successful installation of a medicated stent. The hemodynamicist was impressed by a possible aortitis due to involvement of the arch and friability of the vessels when the balloon was advanced, so he suggested an etiological study oriented to inflammatory disease, prior to surgical resolution of the lesion of the left coronary trunk.\n\nLaboratory tests showed mild anaemia (haemoglobin: 11.6 g/dL), mild leukocytosis (13,800/mm3), elevated erythrocyte sedimentation rate (ESR): 42 mm/h and C-reactive protein (CRP): 4.9 mg/L (normal value <1) and elevated ultrasensitive troponin. From the autoimmunity study, normal levels of complement C3 and C4, negative anti-nuclear antibodies (ANA), anti-DNA, negative extracellular nuclear antigen (ENA) profile and non-reactive VDRL were rescued.\n\nCardiac magnetic resonance (MRI) with contrast was completed with findings of acute infarction of the left ventricular inferior wall non-transmural myocardium and subendocardial ischemia in the anteroseptoapical resting of the left ventricle. Mild aortic and mitral insufficiency. Preserved biventricular systolic function.\n\nComputed tomography angiography (CTA) of the chest, abdomen and pelvis showed periaortic fibrotic wall thickening involving the root, aortic arch and abdominal aorta with severe left coronary trunk stenosis and mild left subclavian, left vertebral artery stenosis and severe lower mesenteric artery stenosis. Immune globulin G (IgG) 4 deposition disease or Takayasu's arteritis was suggested.\n\nWithin the differential diagnosis study, IgG levels were performed at 1,600 mg/dl (reference values: 700-1,600), and its subclasses: IgG1: 1024 mg/dl (elevated), and the rest in normal range (IgG2: 456 mg/dl; IgG3: 98.8 mg/dl and IgG4: 13.6 mg/dl).\n\nTakayasu arteritis was diagnosed clinically and by imaging and treatment was initiated with prednisone 60 mg daily, methotrexate 20 mg weekly by injection and folic acid 1 mg daily. After 3 weeks of treatment she underwent myocardial revascularisation surgery with use of the left internal mammary artery (LIMA) as a graft to the descending anterior artery (DA) and aortocoronary bypass to circumflex artery. It was noted intraoperatively that the root of the aorta and the ascending aorta presented a healthy appearance. The patient is currently at home in good general condition and under ambulatory follow-up.\n",
+    "diff_label_texts": "A 36-year-old woman with ulcerative colitis developed a week of worsening chest pressure with autonomic symptoms (such as sweating and nausea). Her electrocardiogram showed ST-segment elevation in the inferior leads, consistent with an inferior-wall heart attack. She also reported several months of fatigue and night sweats.\n\nUrgent coronary angiography found severe two-vessel coronary artery disease. The right coronary artery was the culprit lesion and was opened successfully with a stent. Because the interventional team suspected inflammation of the aorta (aortitis), additional workup was done. Inflammatory markers were mildly elevated, and CT angiography showed fibrotic thickening around the aorta with significant narrowing in multiple arteries, pointing to Takayasu arteritis.\n\nShe started treatment with prednisone and methotrexate. After stabilization, she underwent delayed coronary bypass surgery and did well.",
+    "summary": "A 36-year-old woman with ulcerative colitis presented with progressive precordial pain and neurovegetative symptoms. The electrocardiogram showed a ST segment elevation in the inferior wall. The patient had a history of fatigue and night sweats. She underwent a coronary angiography that revealed severe disease in two coronary arteries, with successful primary angioplasty of the culprit artery. Aortitis was suspected, which led to additional studies, including a mild elevation of inflammatory activity indices and a computed tomographic angiography with periaortic fibrotic thickening and significant stenosis in multiple arteries, suggesting Takayasu arteritis. She was treated with prednisone, methotrexate, and underwent delayed myocardial revascularization surgery with good results.\n"
+  },
+  {
+    "doc_id": 13,
+    "label": "low_health_literacy",
+    "fulltext": "A 36-year-old female patient with a history of ulcerative colitis and good disease control on sulfasalazine, ferrous fumarate and intermittent prednisone for flare-ups is presented.\n\nHe was admitted to the emergency unit with a 1 week history of progressive oppressive precordial pain associated with dyspnea and neurovegetative symptoms. On admission, an electrocardiogram was performed in sinus rhythm, with finding of supradesnivel of the ST segment in the lower wall.\n\nThe patient reported a 6-month history of general disorders, fatigue and night sweats. She had previously presented episodes of precordial pain in relation to effort that progressed to rest. The physical examination was without murmurs or alterations of the peripheral pulses.\n\nAn emergency coronary angiography was performed, which revealed severe 2-vessel disease: severe ostial lesion 90% in the left coronary trunk and severe subocclusive lesion 99-100% at the ostial level in the right coronary artery (culprit vessel). Primary angioplasty of the right coronary artery was performed with successful installation of a medicated stent. The hemodynamicist was impressed by a possible aortitis due to involvement of the arch and friability of the vessels when the balloon was advanced, so he suggested an etiological study oriented to inflammatory disease, prior to surgical resolution of the lesion of the left coronary trunk.\n\nLaboratory tests showed mild anaemia (haemoglobin: 11.6 g/dL), mild leukocytosis (13,800/mm3), elevated erythrocyte sedimentation rate (ESR): 42 mm/h and C-reactive protein (CRP): 4.9 mg/L (normal value <1) and elevated ultrasensitive troponin. From the autoimmunity study, normal levels of complement C3 and C4, negative anti-nuclear antibodies (ANA), anti-DNA, negative extracellular nuclear antigen (ENA) profile and non-reactive VDRL were rescued.\n\nCardiac magnetic resonance (MRI) with contrast was completed with findings of acute infarction of the left ventricular inferior wall non-transmural myocardium and subendocardial ischemia in the anteroseptoapical resting of the left ventricle. Mild aortic and mitral insufficiency. Preserved biventricular systolic function.\n\nComputed tomography angiography (CTA) of the chest, abdomen and pelvis showed periaortic fibrotic wall thickening involving the root, aortic arch and abdominal aorta with severe left coronary trunk stenosis and mild left subclavian, left vertebral artery stenosis and severe lower mesenteric artery stenosis. Immune globulin G (IgG) 4 deposition disease or Takayasu's arteritis was suggested.\n\nWithin the differential diagnosis study, IgG levels were performed at 1,600 mg/dl (reference values: 700-1,600), and its subclasses: IgG1: 1024 mg/dl (elevated), and the rest in normal range (IgG2: 456 mg/dl; IgG3: 98.8 mg/dl and IgG4: 13.6 mg/dl).\n\nTakayasu arteritis was diagnosed clinically and by imaging and treatment was initiated with prednisone 60 mg daily, methotrexate 20 mg weekly by injection and folic acid 1 mg daily. After 3 weeks of treatment she underwent myocardial revascularisation surgery with use of the left internal mammary artery (LIMA) as a graft to the descending anterior artery (DA) and aortocoronary bypass to circumflex artery. It was noted intraoperatively that the root of the aorta and the ascending aorta presented a healthy appearance. The patient is currently at home in good general condition and under ambulatory follow-up.\n",
+    "diff_label_texts": "A 36-year-old woman had a long-term bowel disease (ulcerative colitis). She came in with chest pain that kept getting worse. She also had shortness of breath, sweating, and felt sick to her stomach. For months she had felt very tired and had night sweats. Her heart test (EKG) showed signs of a heart attack in the lower part of the heart. Doctors did a dye X-ray to look at the heart arteries. It showed bad blockages in two heart pipes. They opened the most blocked pipe right away with a balloon and a tiny mesh tube (stent). While looking, the team worried the main body artery (aorta) was swollen. Blood tests showed mild inflammation. A special CT scan showed the aorta wall looked thick and scarred, with tight narrow spots in several arteries. This pointed to a rare illness that causes swollen big arteries, called Takayasu arteritis. She started strong anti-inflammatory and immune medicines (prednisone and methotrexate). Later she had heart bypass surgery to improve blood flow. She did well after treatment.",
+    "summary": "A 36-year-old woman with ulcerative colitis presented with progressive precordial pain and neurovegetative symptoms. The electrocardiogram showed a ST segment elevation in the inferior wall. The patient had a history of fatigue and night sweats. She underwent a coronary angiography that revealed severe disease in two coronary arteries, with successful primary angioplasty of the culprit artery. Aortitis was suspected, which led to additional studies, including a mild elevation of inflammatory activity indices and a computed tomographic angiography with periaortic fibrotic thickening and significant stenosis in multiple arteries, suggesting Takayasu arteritis. She was treated with prednisone, methotrexate, and underwent delayed myocardial revascularization surgery with good results.\n"
+  },
+  {
+    "doc_id": 13,
+    "label": "proficient_health_literacy",
+    "fulltext": "A 36-year-old female patient with a history of ulcerative colitis and good disease control on sulfasalazine, ferrous fumarate and intermittent prednisone for flare-ups is presented.\n\nHe was admitted to the emergency unit with a 1 week history of progressive oppressive precordial pain associated with dyspnea and neurovegetative symptoms. On admission, an electrocardiogram was performed in sinus rhythm, with finding of supradesnivel of the ST segment in the lower wall.\n\nThe patient reported a 6-month history of general disorders, fatigue and night sweats. She had previously presented episodes of precordial pain in relation to effort that progressed to rest. The physical examination was without murmurs or alterations of the peripheral pulses.\n\nAn emergency coronary angiography was performed, which revealed severe 2-vessel disease: severe ostial lesion 90% in the left coronary trunk and severe subocclusive lesion 99-100% at the ostial level in the right coronary artery (culprit vessel). Primary angioplasty of the right coronary artery was performed with successful installation of a medicated stent. The hemodynamicist was impressed by a possible aortitis due to involvement of the arch and friability of the vessels when the balloon was advanced, so he suggested an etiological study oriented to inflammatory disease, prior to surgical resolution of the lesion of the left coronary trunk.\n\nLaboratory tests showed mild anaemia (haemoglobin: 11.6 g/dL), mild leukocytosis (13,800/mm3), elevated erythrocyte sedimentation rate (ESR): 42 mm/h and C-reactive protein (CRP): 4.9 mg/L (normal value <1) and elevated ultrasensitive troponin. From the autoimmunity study, normal levels of complement C3 and C4, negative anti-nuclear antibodies (ANA), anti-DNA, negative extracellular nuclear antigen (ENA) profile and non-reactive VDRL were rescued.\n\nCardiac magnetic resonance (MRI) with contrast was completed with findings of acute infarction of the left ventricular inferior wall non-transmural myocardium and subendocardial ischemia in the anteroseptoapical resting of the left ventricle. Mild aortic and mitral insufficiency. Preserved biventricular systolic function.\n\nComputed tomography angiography (CTA) of the chest, abdomen and pelvis showed periaortic fibrotic wall thickening involving the root, aortic arch and abdominal aorta with severe left coronary trunk stenosis and mild left subclavian, left vertebral artery stenosis and severe lower mesenteric artery stenosis. Immune globulin G (IgG) 4 deposition disease or Takayasu's arteritis was suggested.\n\nWithin the differential diagnosis study, IgG levels were performed at 1,600 mg/dl (reference values: 700-1,600), and its subclasses: IgG1: 1024 mg/dl (elevated), and the rest in normal range (IgG2: 456 mg/dl; IgG3: 98.8 mg/dl and IgG4: 13.6 mg/dl).\n\nTakayasu arteritis was diagnosed clinically and by imaging and treatment was initiated with prednisone 60 mg daily, methotrexate 20 mg weekly by injection and folic acid 1 mg daily. After 3 weeks of treatment she underwent myocardial revascularisation surgery with use of the left internal mammary artery (LIMA) as a graft to the descending anterior artery (DA) and aortocoronary bypass to circumflex artery. It was noted intraoperatively that the root of the aorta and the ascending aorta presented a healthy appearance. The patient is currently at home in good general condition and under ambulatory follow-up.\n",
+    "diff_label_texts": "A 36-year-old female with ulcerative colitis (well controlled on sulfasalazine, ferrous fumarate, and intermittent prednisone for flares) presented with 1 week of progressive oppressive precordial pain associated with dyspnea and neurovegetative symptoms. On admission, the ECG was in sinus rhythm with ST-segment elevation in the inferior wall. She endorsed a 6-month history of general malaise, fatigue, and night sweats, and had experienced exertional precordial pain that progressed to occur at rest. Physical examination revealed no murmurs or peripheral pulse abnormalities.\n\nEmergency coronary angiography demonstrated severe 2-vessel coronary disease: a severe 90% ostial lesion in the left coronary trunk (left main) and a severe 99–100% subocclusive ostial lesion in the right coronary artery (culprit vessel). Primary angioplasty of the right coronary artery was performed with successful placement of a drug-eluting stent. The hemodynamicist noted possible aortitis given arch involvement and vessel friability during balloon advancement and recommended an inflammatory/etiologic evaluation prior to definitive management of the left main lesion.\n\nLaboratory testing showed mild anemia (hemoglobin 11.6 g/dL), mild leukocytosis (13,800/mm3), elevated ESR 42 mm/h, CRP 4.9 mg/L (normal <1), and elevated high-sensitivity troponin. Autoimmunity panel: normal complement C3/C4, negative ANA, anti-DNA, and ENA profile; non-reactive VDRL. Cardiac MRI with contrast demonstrated acute non-transmural infarction of the left ventricular inferior wall and subendocardial ischemia in the anteroseptoapical region at rest, with mild aortic and mitral insufficiency and preserved biventricular systolic function.\n\nComputed tomographic angiography of the chest/abdomen/pelvis showed periaortic fibrotic wall thickening involving the aortic root, arch, and abdominal aorta, with severe left coronary trunk stenosis, mild left subclavian and left vertebral artery stenoses, and severe inferior mesenteric artery stenosis. The differential included IgG4-related disease versus Takayasu arteritis. Total IgG was 1,600 mg/dL (ref 700–1,600) with IgG1 1,024 mg/dL (elevated) and normal IgG2 456 mg/dL, IgG3 98.8 mg/dL, and IgG4 13.6 mg/dL, findings not supportive of IgG4-related aortitis. Takayasu arteritis was diagnosed clinically and by imaging.\n\nImmunosuppression was initiated with prednisone 60 mg daily and methotrexate 20 mg weekly (parenteral) with folic acid 1 mg daily. After 3 weeks of therapy, she underwent myocardial revascularization surgery using the left internal mammary artery graft to the descending anterior artery (LAD) and an aortocoronary bypass to the circumflex artery. Intraoperatively, the aortic root and ascending aorta appeared healthy. She was discharged home in good general condition and remains under ambulatory follow-up.\n\nContext: Takayasu arteritis is a large-vessel granulomatous vasculitis affecting the aorta and its major branches that can produce aorto-ostial coronary lesions (as in this case, involving the left main and right coronary ostia), leading to myocardial ischemia/infarction. The mildly elevated inflammatory indices, periaortic fibrotic thickening, and multifocal arterial stenoses on CTA are characteristic, and the lack of IgG4 elevation argues against IgG4-related aortitis. The staged approach—urgent culprit-vessel PCI followed by immunosuppression and delayed CABG—is consistent with management principles aiming to control vascular inflammation before definitive surgical revascularization.",
+    "summary": "A 36-year-old woman with ulcerative colitis presented with progressive precordial pain and neurovegetative symptoms. The electrocardiogram showed a ST segment elevation in the inferior wall. The patient had a history of fatigue and night sweats. She underwent a coronary angiography that revealed severe disease in two coronary arteries, with successful primary angioplasty of the culprit artery. Aortitis was suspected, which led to additional studies, including a mild elevation of inflammatory activity indices and a computed tomographic angiography with periaortic fibrotic thickening and significant stenosis in multiple arteries, suggesting Takayasu arteritis. She was treated with prednisone, methotrexate, and underwent delayed myocardial revascularization surgery with good results.\n"
+  },
+  {
+    "doc_id": 14,
+    "label": "intermediate_health_literacy",
+    "fulltext": "A 36-year-old female patient complained of dysphagia with longstanding cervical and upper thoracic pain. She also had a multinodular goiter with no other significant history. Esophagogastroduodenal transit was performed. It showed a posterior and lateral right impression of the proximal esophagus after ingestion of baryte, extending 3.5 cm cephalocaudal. A maximum esophageal stenosis of 60% was estimated. A cervical and thoracic CT scan revealed a congenital anomaly of the aortic arch: a mirror image of the right aortic arch. The aortic arch originates from the root of the aorta and runs above the right stem bronchus, giving rise to the three supra-aortic trunks as follows: the first is the left brachiocephalic artery (which gives rise to the left common carotid artery and the left subclavian artery); the second is the right common carotid artery; and the third is the right subclavian artery. The aortic arch then enters posteriorly to the esophagus and gives rise to a small anterior saccule of 1.3 cm, known as the Kommerell diverticulum. This configuration forms a ring around the tracheo-esophageal pair, whose edges are formed posterior-lateral to the right by the aortic arch, posterior-lateral to the left by the Kommerell diverticulum, lateral to the left by the arteriosum ligamentum (or arterial ligament), and anteriorly by the left brachiocephalic artery. A gastroscopy confirmed the endoluminal impact of extrinsic compression. In view of minimal clinical repercussions and the absence of nutritional disorders, no surgical cure was ultimately performed. The evolution was favorable with, according to the patient, a spontaneous amelioration of symptoms.\n",
+    "diff_label_texts": "A 36-year-old woman had dysphagia due to a congenital right aortic arch with mirror-image branching.\nIn this rare pattern, the aorta runs to the right, wraps around the right main bronchus, and the head-and-arm arteries branch in the reverse order of normal.\nMost people have no symptoms unless the aorta or an associated bulge compresses the esophagus or trachea.\nSurgery is considered for major airway or esophageal compression, aneurysmal disease, thoracic aortic dissection, or a Kommerell diverticulum larger than 2 cm.\nThere is no standard operation; treatment is tailored to the person’s anatomy and symptoms.\nIn this case, imaging showed external compression of the upper esophagus with a small Kommerell diverticulum (about 1.3 cm), so no intervention was performed and her symptoms improved.",
+    "summary": "We report the case of a 36-year-old female patient whose dysphagia presented a congenital anomaly of the thoracic aorta: the right aortic arch with mirror image. This is a rare anomaly of embryonic development where the aorta winds around the right stem bronchus and the supra-aortic trunks emerge from the crown in the reverse and opposite order to normal. The vast majority of patients are asymptomatic unless there is a compression of the mediastinal structures. Major compression of the esophagus or trachea, aneurysmal disease, thoracic aortic dissection or the presence of a Kommerell diverticulum of more than 2 cm may warrant surgical intervention. There is no standard treatment and it must be adapted to the clinical presentation and anatomical configuration of the patient. Our patient did not receive any treatment for her condition.\n"
+  },
+  {
+    "doc_id": 14,
+    "label": "low_health_literacy",
+    "fulltext": "A 36-year-old female patient complained of dysphagia with longstanding cervical and upper thoracic pain. She also had a multinodular goiter with no other significant history. Esophagogastroduodenal transit was performed. It showed a posterior and lateral right impression of the proximal esophagus after ingestion of baryte, extending 3.5 cm cephalocaudal. A maximum esophageal stenosis of 60% was estimated. A cervical and thoracic CT scan revealed a congenital anomaly of the aortic arch: a mirror image of the right aortic arch. The aortic arch originates from the root of the aorta and runs above the right stem bronchus, giving rise to the three supra-aortic trunks as follows: the first is the left brachiocephalic artery (which gives rise to the left common carotid artery and the left subclavian artery); the second is the right common carotid artery; and the third is the right subclavian artery. The aortic arch then enters posteriorly to the esophagus and gives rise to a small anterior saccule of 1.3 cm, known as the Kommerell diverticulum. This configuration forms a ring around the tracheo-esophageal pair, whose edges are formed posterior-lateral to the right by the aortic arch, posterior-lateral to the left by the Kommerell diverticulum, lateral to the left by the arteriosum ligamentum (or arterial ligament), and anteriorly by the left brachiocephalic artery. A gastroscopy confirmed the endoluminal impact of extrinsic compression. In view of minimal clinical repercussions and the absence of nutritional disorders, no surgical cure was ultimately performed. The evolution was favorable with, according to the patient, a spontaneous amelioration of symptoms.\n",
+    "diff_label_texts": "A 36-year-old woman had trouble swallowing. Tests found she was born with an unusual shape of the main body artery in her chest. The artery curves to the right in a mirror-image pattern. It wraps around a main branch of the airway. The side branches of the artery come off in the reverse order from normal. Most people with this have no symptoms. Problems happen only if the artery squeezes the space in the middle of the chest. This can press on the food pipe or the windpipe. Surgery may be needed if there is strong pressure on these tubes, a bulge or a tear in the chest artery, or a pouch on the artery bigger than 2 cm. There is no one-size-fits-all treatment. Care is tailored to the person’s symptoms and body anatomy. This patient did not receive any treatment.",
+    "summary": "We report the case of a 36-year-old female patient whose dysphagia presented a congenital anomaly of the thoracic aorta: the right aortic arch with mirror image. This is a rare anomaly of embryonic development where the aorta winds around the right stem bronchus and the supra-aortic trunks emerge from the crown in the reverse and opposite order to normal. The vast majority of patients are asymptomatic unless there is a compression of the mediastinal structures. Major compression of the esophagus or trachea, aneurysmal disease, thoracic aortic dissection or the presence of a Kommerell diverticulum of more than 2 cm may warrant surgical intervention. There is no standard treatment and it must be adapted to the clinical presentation and anatomical configuration of the patient. Our patient did not receive any treatment for her condition.\n"
+  },
+  {
+    "doc_id": 15,
+    "label": "intermediate_health_literacy",
+    "fulltext": "A 62-year-old Tunisian Arab postmenopausal female diagnosed with Von Hippel–Lindau disease in 2021 presented with various manifestations related to the disease. She had a history of multiple surgeries, primarily for renal, adrenal, and pancreatic tumors, with incidental findings of ovarian masses.\n\nThe patient was asymptomatic from a gynecological standpoint, but primarily complained of headaches before undergoing brain surgery. She had no significant family or psychosocial history.\n\nHer surgical history included\n2021: A non-operable tumor (6 cm) of the left petrous bone endolymphatic sac, managed with radiotherapy.\n\n2021: Left adrenalectomy for a 6 cm pheochromocytoma. Pathological examination revealed pheochromocytoma.\n\n2021: Left nephrectomy for a ruptured left renal tumor. Microscopy showed multifocal clear-cell renal carcinoma of nuclear grade 2.\n\n2022: Cephalic duodenopancreatectomy for a mass in the pancreas. Histological examination confirmed three serous cystadenomas and two well-differentiated neuroendocrine tumors.\n\nIn January 2021, during postoperative surveillance with an abdominal–pelvic computed tomography (CT) scan, a 4 cm solid cystic left adnexal mass was incidentally discovered, which raised suspicion of malignancy. The mass was confirmed by transvaginal ultrasound and pelvic MRI, classified as Ovarian-Adnexal Reporting and Data System (O-RADS) 5 (high suspicion for malignancy).\n\nGynecological examination and surgical history\nPhysical examination: No abdominal–pelvic mass detected.\n\nSpeculum examination: Healthy cervix observed.\n\nSurgical scars from previous left nephrectomy and cephalic duodenopancreatectomy were noted.\n\nA multidisciplinary staff meeting concluded that surgery was necessary. A laparotomy was performed via a midline incision below the umbilicus, revealing a well-defined solid cystic mass in the left adnexa. No ascites or signs of peritoneal carcinomatosis were present, and the right adnexa appeared normal, with no macroscopic signs of malignancy observed intraoperatively, including the absence of exocystic vegetations.\n\nCytology was performed along with left adnexectomy, and the specimen was sent for frozen section examination. The results were inconclusive, raising the possibility of borderline tumors or tumors specific to Von Hippel–Lindau syndrome. Considering the patient’s postmenopausal status, a right adnexectomy and total hysterectomy were performed.\n\nHistological examination later revealed bilateral clear-cell papillary cystadenomas of the Fallopian Tubes and broad ligament, characteristic of Von Hippel–Lindau disease (0.5 cm on the right side and 4 cm on the left side).The tumors consisted of tightly packed papillae with fibrous cores, covered by monolayered epithelium.\n\nThe immediate postoperative period was uneventful, and at the 1-month follow-up, no abnormalities were detected. The patient has since been followed up with every 4 months with normal pelvic ultrasounds. During these 2 years of follow-up, no complications have arisen, but the patient was recently readmitted to the neurosurgery department for recurrence of a brain tumor.",
+    "diff_label_texts": "A 62-year-old white North African woman with Von Hippel–Lindau (VHL) disease diagnosed in 2021 developed several VHL-related tumors: a left petrous bone tumor, a left pheochromocytoma, left renal cell carcinoma, a multicystic right kidney, and pancreatic masses. She was treated with radiotherapy to the petrous bone lesion, left adrenalectomy, left nephrectomy, and cephalic duodenopancreatectomy for the pancreatic tumors. During surveillance, ultrasound and MRI showed a solid–cystic mass in the left adnexal (ovary/tube) region. Laparoscopy then identified cystic tumors in the mesosalpinx on both the right and left sides. She underwent hysterectomy with removal of both adnexa. Pathology confirmed bilateral clear-cell papillary cystadenomas of the mesosalpinx and broad ligament, a pattern consistent with VHL.",
+    "summary": "A 62-year-old white North African woman diagnosed with Von Hippel-Lindau disease in 2021 presented with multiple manifestations, including a left petrous bone tumor, left pheochromocytoma, left renal cell carcinoma, multi-cystic right kidney, and pancreatic masses. She underwent various treatments, including radiotherapy, adrenalectomy, nephrectomy, and cephalic duodenopancreatectomy. Ultrasonographic and magnetic resonance imaging examinations revealed a solid cystic mass in the left adnexal region. Laparoscopy identified cystic tumors in the right and left mesosalpinx. Following a hysterectomy with bilateral adnexectomy, histological examination revealed bilateral clear-cell papillary cystadenomas of the mesosalpinx and broad ligament, consistent with Von Hippel-Lindau disease."
+  },
+  {
+    "doc_id": 15,
+    "label": "low_health_literacy",
+    "fulltext": "A 62-year-old Tunisian Arab postmenopausal female diagnosed with Von Hippel–Lindau disease in 2021 presented with various manifestations related to the disease. She had a history of multiple surgeries, primarily for renal, adrenal, and pancreatic tumors, with incidental findings of ovarian masses.\n\nThe patient was asymptomatic from a gynecological standpoint, but primarily complained of headaches before undergoing brain surgery. She had no significant family or psychosocial history.\n\nHer surgical history included\n2021: A non-operable tumor (6 cm) of the left petrous bone endolymphatic sac, managed with radiotherapy.\n\n2021: Left adrenalectomy for a 6 cm pheochromocytoma. Pathological examination revealed pheochromocytoma.\n\n2021: Left nephrectomy for a ruptured left renal tumor. Microscopy showed multifocal clear-cell renal carcinoma of nuclear grade 2.\n\n2022: Cephalic duodenopancreatectomy for a mass in the pancreas. Histological examination confirmed three serous cystadenomas and two well-differentiated neuroendocrine tumors.\n\nIn January 2021, during postoperative surveillance with an abdominal–pelvic computed tomography (CT) scan, a 4 cm solid cystic left adnexal mass was incidentally discovered, which raised suspicion of malignancy. The mass was confirmed by transvaginal ultrasound and pelvic MRI, classified as Ovarian-Adnexal Reporting and Data System (O-RADS) 5 (high suspicion for malignancy).\n\nGynecological examination and surgical history\nPhysical examination: No abdominal–pelvic mass detected.\n\nSpeculum examination: Healthy cervix observed.\n\nSurgical scars from previous left nephrectomy and cephalic duodenopancreatectomy were noted.\n\nA multidisciplinary staff meeting concluded that surgery was necessary. A laparotomy was performed via a midline incision below the umbilicus, revealing a well-defined solid cystic mass in the left adnexa. No ascites or signs of peritoneal carcinomatosis were present, and the right adnexa appeared normal, with no macroscopic signs of malignancy observed intraoperatively, including the absence of exocystic vegetations.\n\nCytology was performed along with left adnexectomy, and the specimen was sent for frozen section examination. The results were inconclusive, raising the possibility of borderline tumors or tumors specific to Von Hippel–Lindau syndrome. Considering the patient’s postmenopausal status, a right adnexectomy and total hysterectomy were performed.\n\nHistological examination later revealed bilateral clear-cell papillary cystadenomas of the Fallopian Tubes and broad ligament, characteristic of Von Hippel–Lindau disease (0.5 cm on the right side and 4 cm on the left side).The tumors consisted of tightly packed papillae with fibrous cores, covered by monolayered epithelium.\n\nThe immediate postoperative period was uneventful, and at the 1-month follow-up, no abnormalities were detected. The patient has since been followed up with every 4 months with normal pelvic ultrasounds. During these 2 years of follow-up, no complications have arisen, but the patient was recently readmitted to the neurosurgery department for recurrence of a brain tumor.",
+    "diff_label_texts": "This story is about a 62-year-old white North African woman. She was diagnosed in 2021 with a rare condition called Von Hippel–Lindau disease. This condition caused growths in several parts of her body. She had a tumor in a bone near her left ear. She had a tumor in the left adrenal gland, which sits above the kidney. She had cancer in her left kidney. Her right kidney had many cysts. She also had growths in her pancreas. She received several treatments. She had radiation treatment. She had surgery to remove the left adrenal gland. She had surgery to remove the left kidney. She had major surgery on the pancreas and nearby small intestine. Later, ultrasound and MRI scans showed a lump with both fluid and solid parts near the left ovary and tube. Keyhole surgery looked inside the pelvis. It found cyst-type tumors in the thin support tissue next to both fallopian tubes. Doctors then removed the uterus and both ovaries and tubes. The lab checked the tissue. It showed tumors of the same type on both sides in the thin support tissue around the tubes and the uterus. These findings fit with Von Hippel–Lindau disease.",
+    "summary": "A 62-year-old white North African woman diagnosed with Von Hippel-Lindau disease in 2021 presented with multiple manifestations, including a left petrous bone tumor, left pheochromocytoma, left renal cell carcinoma, multi-cystic right kidney, and pancreatic masses. She underwent various treatments, including radiotherapy, adrenalectomy, nephrectomy, and cephalic duodenopancreatectomy. Ultrasonographic and magnetic resonance imaging examinations revealed a solid cystic mass in the left adnexal region. Laparoscopy identified cystic tumors in the right and left mesosalpinx. Following a hysterectomy with bilateral adnexectomy, histological examination revealed bilateral clear-cell papillary cystadenomas of the mesosalpinx and broad ligament, consistent with Von Hippel-Lindau disease."
+  },
+  {
+    "doc_id": 16,
+    "label": "intermediate_health_literacy",
+    "fulltext": "The patient was a 59-year-old Japanese man with a 28-year history of type 1 diabetes. He visited our hospital monthly for management of diabetes with intensive therapy employing multiple-dose insulin injections. His height and body weight were 168 cm and 52 kg (body mass index: 18.4 kg/m2), respectively. He showed depleted insulin secretion (serum C-peptide level was below the limit of detection), such that his blood glucose levels fluctuated severely, and his hemoglobin A1c (HbA1c) level was around 9.0% despite intensive insulin therapy. He had been diagnosed with asymptomatic chronic severe (grade III) aortic regurgitation (AR) 16 years before the current presentation but had declined follow-up for the AR. He had never undergone surgery nor the implantation of any prosthetic devices.\n\nEight days after his regular hospital visit, he visited an emergency clinic complaining of breathing difficulty and had a fever above 38℃. Until that day, he had not noticed any fever, chills, weakness, or any other symptoms. His blood pressure and pulse rate were 192/82 mmHg and 118/min, respectively. He showed orthopnea, and his oxygen saturation (SpO2) was 80%. He was transported to the emergency department of our hospital. A physical examination revealed a Levine 3/6 systolic murmur, although his cardiac murmur had not been checked at regular hospital visits. No physical findings suggesting IE, such as Osler nodes, Janeway lesions, or conjunctival petechiae, were recognized. His white blood cell (WBC) count was markedly increased to 20,800 /μL, and his C-reactive protein (CRP) was elevated to 6.06 mg/dL. Serum creatine phosphokinase MB was within the normal range, at 6.0 IU/L, and troponin T was negative. Chest X-ray showed pulmonary congestion with cardiac enlargement (cardiothoracic ratio: 55%). Electrocardiography revealed ST elevation on V1-V4, but emergency echocardiography showed no dysfunction of cardiac contractility. He was diagnosed with acute heart failure due to valvular disease, and treatment with non-invasive positive pressure ventilation and nitrates was initiated.\n\nAfter hospital admission, a detailed examination by transthoracic echocardiography showed severe aortic regurgitation, severe mitral regurgitation, and a mobile vegetation on the mitral valve. Transesophageal echocardiography revealed a 16.5×6-mm mobile vegetation on the anterior leaflet of the mitral valve and an 11.2×5-mm nonmobile vegetation on the noncoronary cusp of the aortic valve. These findings raised strong suspicion of NVE. In this case, head computed tomography (CT) and magnetic resonance imaging revealed no cerebral infarction or hemorrhaging, although a mobile vegetation was detected.\n\nOn reviewing the clinical course until hospitalization, we noted that at the visit four months before admission, his WBC count had been slightly elevated. The following month, his albumin (Alb) level decreased to 3.0 g/dL, and his hemoglobin (Hb) level had shown a gradual decline over the 2 months prior to admission. During this period, he had experienced a 4-kg weight loss. Esophagogastroduodenoscopy and whole-body CT were performed, but no abnormalities were detected. One month later, he had regained some weight, and the laboratory findings had nearly normalized, except for a slightly elevated CRP level (0.54 mg/dL). At the last visit (8 days before admission), his WBC count had again risen to 9,300 /μL, while his Hb and Alb levels had again decreased to 13.1 g/dL and 3.0 g/dL, respectively. Furthermore, his CRP level had increased to 4.18 mg/dL. At that time, his diastolic blood pressure has shown an obvious decrease. Thus far, he had not experienced a fever or any symptoms other than weight loss. We suspected diseases of infectious and/or malignant origin and initiated comprehensive examinations to identify the source of his clinical findings.\n\nAfter heart failure treatment had been started, his clinical symptoms showed rapid improvement, and his hemodynamic stability was maintained during the first six hours. He initially received empirical intravenous antibiotic therapy consisting of 12 g/day of ampicillin sulbactam (ABPC/S) and 120 mg/day of gentamycin (GM). Three blood culture sets were obtained on the admission, and all were positive for S. warneri [minimum inhibitory concentration (MIC) to ABPC/S ≤8 μg/mL; MIC to GM ≤1 μg/mL; MIC to cefazolin (CEZ) ≤2 μg/mL]. Thus, IE caused by this organism was diagnosed.\n\nAccording to the clinical guideline established by the Japanese Circulation Society, emergency surgery is generally recommended for heart failure of NYHA III to IV or urgent surgery for NVE mobile vegetation exceeding 10 mm and severe valve dysfunction. In this case, however, his heart failure was successfully improved. Based on the guideline, the risk of embolism was considered to have been reduced by the administration of appropriate antibiotic therapy. In addition, the patient had type 1 diabetes, and his glycemic control was so poor that we were concerned that double-valve surgery would be a high-risk procedure. Therefore, we planned elective surgery after sufficient control of both infection and diabetes.\n\nBased on the blood culture results, the antibiotic regimen was switched to 6 g/day of CEZ. A detailed dental examination revealed no abnormalities, such as periodontitis. After four weeks of antibiotic therapy, he underwent surgical therapy. His aortic valve was found to be bicuspid, and the aortic and mitral annuli were intact without abscess formation. Large vegetations were exenterated, and the mitral and aortic valves were both replaced with mechanical valves. He experienced no postoperative complications and was discharged on the 22nd day after the operation without apparent embolism. He has not had any recurrence in over two years since the operation.",
+    "diff_label_texts": "A 59-year-old man with long-standing type 1 diabetes presented with acute heart failure. An echocardiogram showed large vegetations on the mitral and aortic valves. Blood cultures were positive for Staphylococcus warneri, a coagulase‑negative staphylococcus commonly found on the skin. He was diagnosed with native valve endocarditis. After medical stabilization, he ultimately underwent replacement of both the mitral and aortic valves. In retrospect, mild laboratory abnormalities and several months of weight loss beginning about four months earlier were likely early signs of endocarditis. He had no history of immunosuppressive therapy and no implanted medical devices.",
+    "summary": "A 59-year-old man with type 1 diabetes presented with heart failure. Echocardiography showed large vegetations on the mitral and aortic valves. Blood bacterial culture was positive for Staphylococcus warneri, a coagulase-negative staphylococcus (CoNS) family member. He was diagnosed with native valve endocarditis (NVE) induced by the resident bacteria and ultimately underwent double valve replacement. Retrospectively, slight laboratory data abnormalities and weight loss beginning four months before may have been signs of NVE. He had no history of immunosuppressive therapies or medical device implantation. "
+  },
+  {
+    "doc_id": 16,
+    "label": "low_health_literacy",
+    "fulltext": "The patient was a 59-year-old Japanese man with a 28-year history of type 1 diabetes. He visited our hospital monthly for management of diabetes with intensive therapy employing multiple-dose insulin injections. His height and body weight were 168 cm and 52 kg (body mass index: 18.4 kg/m2), respectively. He showed depleted insulin secretion (serum C-peptide level was below the limit of detection), such that his blood glucose levels fluctuated severely, and his hemoglobin A1c (HbA1c) level was around 9.0% despite intensive insulin therapy. He had been diagnosed with asymptomatic chronic severe (grade III) aortic regurgitation (AR) 16 years before the current presentation but had declined follow-up for the AR. He had never undergone surgery nor the implantation of any prosthetic devices.\n\nEight days after his regular hospital visit, he visited an emergency clinic complaining of breathing difficulty and had a fever above 38℃. Until that day, he had not noticed any fever, chills, weakness, or any other symptoms. His blood pressure and pulse rate were 192/82 mmHg and 118/min, respectively. He showed orthopnea, and his oxygen saturation (SpO2) was 80%. He was transported to the emergency department of our hospital. A physical examination revealed a Levine 3/6 systolic murmur, although his cardiac murmur had not been checked at regular hospital visits. No physical findings suggesting IE, such as Osler nodes, Janeway lesions, or conjunctival petechiae, were recognized. His white blood cell (WBC) count was markedly increased to 20,800 /μL, and his C-reactive protein (CRP) was elevated to 6.06 mg/dL. Serum creatine phosphokinase MB was within the normal range, at 6.0 IU/L, and troponin T was negative. Chest X-ray showed pulmonary congestion with cardiac enlargement (cardiothoracic ratio: 55%). Electrocardiography revealed ST elevation on V1-V4, but emergency echocardiography showed no dysfunction of cardiac contractility. He was diagnosed with acute heart failure due to valvular disease, and treatment with non-invasive positive pressure ventilation and nitrates was initiated.\n\nAfter hospital admission, a detailed examination by transthoracic echocardiography showed severe aortic regurgitation, severe mitral regurgitation, and a mobile vegetation on the mitral valve. Transesophageal echocardiography revealed a 16.5×6-mm mobile vegetation on the anterior leaflet of the mitral valve and an 11.2×5-mm nonmobile vegetation on the noncoronary cusp of the aortic valve. These findings raised strong suspicion of NVE. In this case, head computed tomography (CT) and magnetic resonance imaging revealed no cerebral infarction or hemorrhaging, although a mobile vegetation was detected.\n\nOn reviewing the clinical course until hospitalization, we noted that at the visit four months before admission, his WBC count had been slightly elevated. The following month, his albumin (Alb) level decreased to 3.0 g/dL, and his hemoglobin (Hb) level had shown a gradual decline over the 2 months prior to admission. During this period, he had experienced a 4-kg weight loss. Esophagogastroduodenoscopy and whole-body CT were performed, but no abnormalities were detected. One month later, he had regained some weight, and the laboratory findings had nearly normalized, except for a slightly elevated CRP level (0.54 mg/dL). At the last visit (8 days before admission), his WBC count had again risen to 9,300 /μL, while his Hb and Alb levels had again decreased to 13.1 g/dL and 3.0 g/dL, respectively. Furthermore, his CRP level had increased to 4.18 mg/dL. At that time, his diastolic blood pressure has shown an obvious decrease. Thus far, he had not experienced a fever or any symptoms other than weight loss. We suspected diseases of infectious and/or malignant origin and initiated comprehensive examinations to identify the source of his clinical findings.\n\nAfter heart failure treatment had been started, his clinical symptoms showed rapid improvement, and his hemodynamic stability was maintained during the first six hours. He initially received empirical intravenous antibiotic therapy consisting of 12 g/day of ampicillin sulbactam (ABPC/S) and 120 mg/day of gentamycin (GM). Three blood culture sets were obtained on the admission, and all were positive for S. warneri [minimum inhibitory concentration (MIC) to ABPC/S ≤8 μg/mL; MIC to GM ≤1 μg/mL; MIC to cefazolin (CEZ) ≤2 μg/mL]. Thus, IE caused by this organism was diagnosed.\n\nAccording to the clinical guideline established by the Japanese Circulation Society, emergency surgery is generally recommended for heart failure of NYHA III to IV or urgent surgery for NVE mobile vegetation exceeding 10 mm and severe valve dysfunction. In this case, however, his heart failure was successfully improved. Based on the guideline, the risk of embolism was considered to have been reduced by the administration of appropriate antibiotic therapy. In addition, the patient had type 1 diabetes, and his glycemic control was so poor that we were concerned that double-valve surgery would be a high-risk procedure. Therefore, we planned elective surgery after sufficient control of both infection and diabetes.\n\nBased on the blood culture results, the antibiotic regimen was switched to 6 g/day of CEZ. A detailed dental examination revealed no abnormalities, such as periodontitis. After four weeks of antibiotic therapy, he underwent surgical therapy. His aortic valve was found to be bicuspid, and the aortic and mitral annuli were intact without abscess formation. Large vegetations were exenterated, and the mitral and aortic valves were both replaced with mechanical valves. He experienced no postoperative complications and was discharged on the 22nd day after the operation without apparent embolism. He has not had any recurrence in over two years since the operation.",
+    "diff_label_texts": "A 59-year-old man with type 1 diabetes came to the hospital with heart failure. A heart ultrasound showed big clumps of germs stuck to two heart valves, the mitral and the aortic valves. His blood test grew a germ called Staphylococcus warneri. This is a kind of staph that usually lives on the skin and is normally harmless. Doctors found he had an infection on his own heart valves (native valve endocarditis). He later had surgery to replace both the mitral and the aortic valves. Looking back, small lab changes and weight loss that began about four months earlier may have been early warning signs. He had not been on immune-weakening medicines and did not have any implanted medical devices.",
+    "summary": "A 59-year-old man with type 1 diabetes presented with heart failure. Echocardiography showed large vegetations on the mitral and aortic valves. Blood bacterial culture was positive for Staphylococcus warneri, a coagulase-negative staphylococcus (CoNS) family member. He was diagnosed with native valve endocarditis (NVE) induced by the resident bacteria and ultimately underwent double valve replacement. Retrospectively, slight laboratory data abnormalities and weight loss beginning four months before may have been signs of NVE. He had no history of immunosuppressive therapies or medical device implantation. "
+  },
+  {
+    "doc_id": 16,
+    "label": "proficient_health_literacy",
+    "fulltext": "The patient was a 59-year-old Japanese man with a 28-year history of type 1 diabetes. He visited our hospital monthly for management of diabetes with intensive therapy employing multiple-dose insulin injections. His height and body weight were 168 cm and 52 kg (body mass index: 18.4 kg/m2), respectively. He showed depleted insulin secretion (serum C-peptide level was below the limit of detection), such that his blood glucose levels fluctuated severely, and his hemoglobin A1c (HbA1c) level was around 9.0% despite intensive insulin therapy. He had been diagnosed with asymptomatic chronic severe (grade III) aortic regurgitation (AR) 16 years before the current presentation but had declined follow-up for the AR. He had never undergone surgery nor the implantation of any prosthetic devices.\n\nEight days after his regular hospital visit, he visited an emergency clinic complaining of breathing difficulty and had a fever above 38℃. Until that day, he had not noticed any fever, chills, weakness, or any other symptoms. His blood pressure and pulse rate were 192/82 mmHg and 118/min, respectively. He showed orthopnea, and his oxygen saturation (SpO2) was 80%. He was transported to the emergency department of our hospital. A physical examination revealed a Levine 3/6 systolic murmur, although his cardiac murmur had not been checked at regular hospital visits. No physical findings suggesting IE, such as Osler nodes, Janeway lesions, or conjunctival petechiae, were recognized. His white blood cell (WBC) count was markedly increased to 20,800 /μL, and his C-reactive protein (CRP) was elevated to 6.06 mg/dL. Serum creatine phosphokinase MB was within the normal range, at 6.0 IU/L, and troponin T was negative. Chest X-ray showed pulmonary congestion with cardiac enlargement (cardiothoracic ratio: 55%). Electrocardiography revealed ST elevation on V1-V4, but emergency echocardiography showed no dysfunction of cardiac contractility. He was diagnosed with acute heart failure due to valvular disease, and treatment with non-invasive positive pressure ventilation and nitrates was initiated.\n\nAfter hospital admission, a detailed examination by transthoracic echocardiography showed severe aortic regurgitation, severe mitral regurgitation, and a mobile vegetation on the mitral valve. Transesophageal echocardiography revealed a 16.5×6-mm mobile vegetation on the anterior leaflet of the mitral valve and an 11.2×5-mm nonmobile vegetation on the noncoronary cusp of the aortic valve. These findings raised strong suspicion of NVE. In this case, head computed tomography (CT) and magnetic resonance imaging revealed no cerebral infarction or hemorrhaging, although a mobile vegetation was detected.\n\nOn reviewing the clinical course until hospitalization, we noted that at the visit four months before admission, his WBC count had been slightly elevated. The following month, his albumin (Alb) level decreased to 3.0 g/dL, and his hemoglobin (Hb) level had shown a gradual decline over the 2 months prior to admission. During this period, he had experienced a 4-kg weight loss. Esophagogastroduodenoscopy and whole-body CT were performed, but no abnormalities were detected. One month later, he had regained some weight, and the laboratory findings had nearly normalized, except for a slightly elevated CRP level (0.54 mg/dL). At the last visit (8 days before admission), his WBC count had again risen to 9,300 /μL, while his Hb and Alb levels had again decreased to 13.1 g/dL and 3.0 g/dL, respectively. Furthermore, his CRP level had increased to 4.18 mg/dL. At that time, his diastolic blood pressure has shown an obvious decrease. Thus far, he had not experienced a fever or any symptoms other than weight loss. We suspected diseases of infectious and/or malignant origin and initiated comprehensive examinations to identify the source of his clinical findings.\n\nAfter heart failure treatment had been started, his clinical symptoms showed rapid improvement, and his hemodynamic stability was maintained during the first six hours. He initially received empirical intravenous antibiotic therapy consisting of 12 g/day of ampicillin sulbactam (ABPC/S) and 120 mg/day of gentamycin (GM). Three blood culture sets were obtained on the admission, and all were positive for S. warneri [minimum inhibitory concentration (MIC) to ABPC/S ≤8 μg/mL; MIC to GM ≤1 μg/mL; MIC to cefazolin (CEZ) ≤2 μg/mL]. Thus, IE caused by this organism was diagnosed.\n\nAccording to the clinical guideline established by the Japanese Circulation Society, emergency surgery is generally recommended for heart failure of NYHA III to IV or urgent surgery for NVE mobile vegetation exceeding 10 mm and severe valve dysfunction. In this case, however, his heart failure was successfully improved. Based on the guideline, the risk of embolism was considered to have been reduced by the administration of appropriate antibiotic therapy. In addition, the patient had type 1 diabetes, and his glycemic control was so poor that we were concerned that double-valve surgery would be a high-risk procedure. Therefore, we planned elective surgery after sufficient control of both infection and diabetes.\n\nBased on the blood culture results, the antibiotic regimen was switched to 6 g/day of CEZ. A detailed dental examination revealed no abnormalities, such as periodontitis. After four weeks of antibiotic therapy, he underwent surgical therapy. His aortic valve was found to be bicuspid, and the aortic and mitral annuli were intact without abscess formation. Large vegetations were exenterated, and the mitral and aortic valves were both replaced with mechanical valves. He experienced no postoperative complications and was discharged on the 22nd day after the operation without apparent embolism. He has not had any recurrence in over two years since the operation.",
+    "diff_label_texts": "A 59-year-old Japanese man with a 28-year history of type 1 diabetes on intensive multiple-dose insulin therapy (BMI 18.4 kg/m2, undetectable C‑peptide, HbA1c ~9.0%) and remote, asymptomatic chronic severe (grade III) aortic regurgitation (diagnosed 16 years earlier without subsequent follow‑up) presented with acute decompensated heart failure. He had never undergone surgery or prosthetic device implantation and had no history of immunosuppressive therapies.\n\nEight days after a routine visit, he developed dyspnea and fever >38℃. On arrival: BP 192/82 mmHg, HR 118/min, orthopnea, SpO2 80%. Exam: Levine 3/6 systolic murmur; no Osler nodes, Janeway lesions, or conjunctival petechiae. Labs: WBC 20,800/μL, CRP 6.06 mg/dL, CK‑MB 6.0 IU/L, troponin T negative. CXR showed pulmonary congestion with cardiomegaly (CTR 55%). ECG had ST elevation in V1–V4, but emergent echocardiography showed no systolic dysfunction. He was diagnosed with acute heart failure due to valvular disease and treated with non‑invasive positive pressure ventilation and nitrates.\n\nTransthoracic echocardiography demonstrated severe aortic regurgitation and severe mitral regurgitation with a mobile mitral vegetation. Transesophageal echocardiography identified a 16.5×6‑mm mobile vegetation on the anterior leaflet of the mitral valve and an 11.2×5‑mm nonmobile vegetation on the noncoronary cusp of the aortic valve, raising strong suspicion for native valve endocarditis (NVE). Head CT and MRI showed no cerebral infarction or hemorrhage.\n\nRetrospective review revealed subtle abnormalities starting four months pre‑admission: mildly elevated WBC, albumin decreased to 3.0 g/dL the following month, and gradual hemoglobin decline over two months, with a 4‑kg weight loss. EGD and whole‑body CT were unrevealing. He partially regained weight and labs nearly normalized except for a CRP of 0.54 mg/dL. At the last pre‑admission visit (8 days prior), WBC was 9,300/μL, Hb 13.1 g/dL, Alb 3.0 g/dL, CRP 4.18 mg/dL, and diastolic BP had fallen; he remained afebrile and asymptomatic aside from weight loss.\n\nEmpiric antibiotics were initiated with ampicillin–sulbactam 12 g/day plus gentamicin 120 mg/day. Three admission blood culture sets all grew Staphylococcus warneri, a coagulase‑negative staphylococcus (CoNS) and resident skin flora (MICs: ABPC/S ≤8 μg/mL; GM ≤1 μg/mL; CEZ ≤2 μg/mL), confirming S. warneri IE. Per Japanese Circulation Society guidance, emergency surgery is generally recommended for NYHA III–IV heart failure or urgent surgery for NVE with mobile vegetation >10 mm and severe valve dysfunction. Because heart failure improved rapidly and appropriate antibiotics were started (reducing embolic risk), and given poorly controlled type 1 diabetes increasing operative risk, elective surgery was planned after stabilization of infection and glycemia. Antibiotics were narrowed to cefazolin 6 g/day; dental evaluation showed no periodontitis.\n\nAfter four weeks of antibiotics, surgery revealed a bicuspid aortic valve with intact aortic and mitral annuli and no abscess. Large vegetations were exenterated, and both valves were replaced with mechanical prostheses. The postoperative course was uneventful; he was discharged on postoperative day 22 without apparent embolism and has remained recurrence‑free for over two years. This case represents NVE due to the resident CoNS S. warneri in a patient without prosthetic material or immunosuppression, with prodromal laboratory abnormalities and weight loss evident up to four months before presentation.",
+    "summary": "A 59-year-old man with type 1 diabetes presented with heart failure. Echocardiography showed large vegetations on the mitral and aortic valves. Blood bacterial culture was positive for Staphylococcus warneri, a coagulase-negative staphylococcus (CoNS) family member. He was diagnosed with native valve endocarditis (NVE) induced by the resident bacteria and ultimately underwent double valve replacement. Retrospectively, slight laboratory data abnormalities and weight loss beginning four months before may have been signs of NVE. He had no history of immunosuppressive therapies or medical device implantation. "
+  },
+  {
+    "doc_id": 17,
+    "label": "intermediate_health_literacy",
+    "fulltext": "A 27-year-old woman with multiple colorectal cancers on a background of FAP was presented to our department. Notably, a large lesion was detected in the ascending, transverse, and sigmoid colon and the upper rectum, and pathological examination confirmed some of them as adenocarcinoma. Preoperative computed tomography revealed multiple lymph node swellings along the inferior mesenteric artery (IMA) and middle colic artery, without any evidence of distant metastases. After a comprehensive evaluation by a multidisciplinary cancer board, we decided to perform TPC with lymph node dissection of the entire colorectal region, using the Hugo RAS system as a surgical device.\n\nRobot-assisted TPC using the Hugo RAS system was approved by the Evaluating Committee for Highly Difficult New Medical Technologies (approval number H-0051) and the Institutional Review Board at Kyoto University.\n\nUnder general anesthesia, the patient was placed in a lithotomy position with the arms tucked. After a 5-cm vertical skin incision was made at the umbilicus, a wound-protecting device was applied. After pneumoperitoneum, 4 robotic trocars and 2 assistant trocars were placed. The instruments used in robot-assisted TPC with Hugo were a camera, monopolar curved shears for the right hand, bipolar fenestrated forceps for the left hand, and Cadiere/double fenestrated forceps for the reserve arm. Robot-assisted TPC with Hugo consists of 3 distinct steps, followed by transanal specimen extraction, ileal pouch construction through a small laparotomy, and ileal pouch-anus anastomosis (IPAA). Two table positions, Trendelenburg and flat, were required, each with specific docking tilts but the same angles of the arm carts throughout the robotic procedure. The detailed operative procedure is presented in Supplementary Videos.\n\nStep 1: Ascending colon complete mesocolic excision (CME)\n\nThe ascending colon CME from the caudal approach proceeded until the completion of the hepatic flexure mobilization (Supplementary Video S1).\n\nStep 2: Central vessel ligation (CVL) of the IMA, descending colon CME, and total mesorectal excision (TME)\n\nAfter CVL of the IMA, descending colon CME proceeded until the completion of splenic flexure mobilization, followed by TME until the intersphincteric space was fully exposed (Supplementary Video S2).\n\nStep 3: CVL along the superior mesenteric artery (SMA)\n\nAfter undocking all the robotic arms, the patient was placed in a flat position. Then, CVL along the SMA was performed to ligate the ileocolic, right colic, and middle colic vessels (Supplementary Video S3). The final step of this procedure was the ligation of the inferior mesenteric vein (IMV) at its root, which was exposed in Step 2.\n\nTransanal and small laparotomy procedures\nAfter transection of the terminal ileum, we extracted the specimen transanally by excising the rectal mucosa entirely from just below the dentate line because of multiple adenomas in the anal canal. After constructing the ileal pouch through the small umbilical incision and confirming that the ileal pouch could reach the bottom of the anal canal for anastomosis, transanal hand-sewn IPAA was performed. A diverting ileostomy was not performed.\n\nAll 3 steps were completed without conversion to open surgery. After undocking Hugo when we finished Step 3, we performed a laparoscopy to confirm hemostasis, specimen extraction, and appropriate anastomosis. The operative time was 632 min (36 min for Step 1, 160 min for Step 2, 188 min for Step 3, and 248 min for other procedures such as positioning, docking, specimen extraction, and anastomosis), with a minimal intraoperative estimated blood loss of 20 mL. The patient exhibited an uneventful postoperative recovery, with gas passage and initiation of liquid nutrition on postoperative day 1 (POD 1) and a solid diet on POD 3 with a functional ileal pouch and satisfactory anal function. Pathological examination revealed 2 sigmoid colon cancers (S1, Type 0-Ip, 55 × 50 mm, tub1, T1b, ly0, v0; S2, Type 0-Isp, 55 × 50 mm, tub1, Tis, ly0, v0) and 1 rectal cancer (R1, Type 0-Ip, 40 × 35 mm, tub1, Tis, ly0, v0). It also revealed 18 out of 89 positive lymph nodes, all of which belonged to the sigmoid colon and rectosigmoid lesions (stations #241, 242, and 251), resulting in UICC pT1bN2b stage.",
+    "diff_label_texts": "A 27-year-old woman with familial adenomatous polyposis and multiple colorectal cancers underwent robot-assisted total proctocolectomy with complete lymph node dissection using the Hugo RAS system. The robotic work was organized into three steps: 1) in Trendelenburg position, ascending colon complete mesocolic excision up to the hepatic flexure; 2) descending colon complete mesocolic excision and total mesorectal excision with D3 lymph node dissection; and 3) in a flat position, central vessel ligation along the superior mesenteric artery. After undocking, the specimen was removed transanally. An ileal pouch was created through a small umbilical incision and then connected to the anus (ileal pouch–anal anastomosis). The operation lasted 632 minutes with minimal blood loss, and the postoperative course was uneventful.",
+    "summary": "A 27-year-old woman with multiple colorectal cancers with a background of familial adenomatous polyposis underwent robot-assisted TPC, including lymph node dissection of the entire colorectal region using the Hugo RAS system. The robotic procedure was divided into 3 steps: 1) Trendelenburg position to perform ascending colon complete mesocolic excision (CME) to the hepatic flexure, 2) descending colon CME and total mesorectal excision with D3 lymph node dissection, and 3) flat position to perform central vessel ligation along the superior mesenteric artery. After undocking, the specimen was extracted transanally, and an ileal pouch was constructed from a small laparotomy at the umbilical incision, followed by ileal pouch-anal anastomosis. The operative time was 632 min, and the estimated blood loss was minimal. The postoperative period was uneventful."
+  },
+  {
+    "doc_id": 18,
+    "label": "intermediate_health_literacy",
+    "fulltext": "A 65-year-old male presented with swelling and boutonniere deformity on the right middle finger for six months after a motorcycle accident on January 1st, 2023. Initially, he managed the injury with painkillers and did not seek medical attention. After six months of persistent symptoms, including an inability to fully extend the finger and noticeable edema, he sought treatment.\n\nClinical findings\nThe inspection of the right hand showed the presence of deformity with edema. The active range of motion (ROM) was impaired in PIP joint in digiti III of the right hand. The active ROM of PIP joint digiti III of the right hand 45–110 degrees. The passive ROM of PIP joint digiti III of the right hand within normal.\n\nDiagnostic assessment\nWe performed X-ray of the right hand AP/Lateral which showed there are no abnormality in the bone and we diagnosed the deformity from soft tissue which is central slip injury.\n\nSurgical technique\nA central slip defect reconstruction utilizing partial ulnar side of flexor digitorum superficial tendon was performed. Under anesthesia, the patient was positioned supine with a tourniquet applied to the upper arm. A midlateral incision was made on the ulnar aspect of the right middle phalanx, centered at the PIP joint. The incision extended dorsally in an oblique manner. A transverse incision was made over the MCP joint flexion crease, just proximal to the A1 pulley. The procedure involves identifying and protecting the ulnar digital neurovascular bundle, exposing the central slip and extensor tendon to the PIPJ, full-thickness dorsal flaps are elevated. Scar tissue and pseudotendinous tissue is identified and excised. The central slip cannot be repaired primarily, so the ulnar slip of the FDS tendon is used for reconstruction. The ulnar neurovascular bundle is mobilized to visualize the periosteal insertion of the A3 pulley.\n\nThe extensor tendon is mobilized and tenolyzed, followed by incision of the dorsal capsule of the PIP joint and removal of interposed tissue. The A3 pulley's periosteal insertion is incised longitudinally, and the PIP joint's volar capsule is incised longitudinally. The ulnar slip of the FDS tendon is identified and a 2–0 non-absorbable, monofilament suture is placed around it. A transverse incision is made at the MCP joint flexion crease, proximal to the A1 pulley revealing the flexor tendon sheath. The tendon sheath and A1 pulley are incised longitudinally. The FDS tendon is identified. The ulnar slip of the FDS tendon is isolated and transected to release the ulnar slip, avoiding entrapment or catching of the radial slip. The 2–0 suture that was placed around the ulnar slip at the level of the PIP joint is used to release distally based FDS tendon slip and deliver the ulnar slip of the FDS tendon distally.\n\nA 2.8-mm drill is used to create a vertically oriented bone tunnel dorsal to volar. An elevator is placed between the flexor digitorum profundus tendon, volar plate, and volar aspect of the base of the middle phalanx protecting the volar anatomic structures. The FDS tendon slip passes through the tunnel while maintaining the PIP joint in extension and reduced position. The FDS tendon slip passed through the intact proximal section of the central slip and extensor tendon. A tendon weaver completes a Pulvertaft weave, confirming the appropriate tension with the PIPJ in the reduced, full extension position. A 3–0 non-absorbable suture secures the pulvertaft weave. The margins of the capsule and central slip reconstruction are approximated across the PIP joint, and adhesions are released and the lateral bands mobilized.\n\nThe overall posture, stability, and motion with tenodesis assessed. All the incisions are copiously irrigated. The tourniquet is deflated and hemostasis is obtained. Capillary refill of all fingers is assessed. The skin is closed using horizontal mattress stiches. A sterile dressing is applied with an appropriately padded PIP joint extension splint to allow for early DIP joint and MCP joint motion.\n\nFollow-up and outcomes\nFirst follow-up was done 4 days after for wound treatment. The patient was given oral meloxicam 7,5 mg twice a day and doxycycline 100 mg twice a day for 3 days. The second follow-up was done 3 days after for wound treatment. After 2 weeks, we remove the back slab, remove the external suture and begin the active and passive ROM exercise. After 3 weeks, the wound was healed, and we found the ROM of PIP joint 0 to 90 degrees. And after a month, the patient came with improved ROM of PIP joint 0 to 100 degrees, and improved functional outcome. After 7 weeks of physical rehabilitation, patients already back to work with improve ROM of PIP joint 0 to 110 degrees. The function of the patient's right hand is evaluated with DASH score, which improves significantly from 50 to 4.2.",
+    "diff_label_texts": "A 65-year-old man developed persistent swelling and a boutonniere deformity of the right middle finger after a motorcycle fall six months earlier. He could not fully extend the finger. On exam, the finger showed edema with flexion at the proximal interphalangeal (PIP) joint and hyperextension at the distal interphalangeal (DIP) joint. Active PIP range of motion (ROM) was 45–110 degrees. X‑rays of the right hand (AP/oblique) showed no bone injury, indicating a soft-tissue problem consistent with a central slip injury. The patient underwent reconstruction of the central slip using a partial ulnar slip of the flexor digitorum superficialis (FDS) tendon. A PIP extension splint was used for 2 weeks. Active and passive PIP ROM exercises began after 2 weeks. One month after surgery, PIP ROM improved to 0–90 degrees, and by 2 months it returned to normal. Hand function, measured by the DASH score, improved markedly from 50 to 4.2.",
+    "summary": "A 65-year-old male patient presented with swelling and boutonniere deformity on the digiti III of the right hand. The patient had previously fallen from a motorcycle, and the patient's right middle finger got was by a motorcycle six months ago. After the incident, the patient's right middle finger cannot be fully extended. The patient's right hand showed edema with flexion of the interphalangeal (PIP) joint and hyperextension of the distal interphalangeal (DIP) joint. The Range of Motion (ROM) of the PIP joint right middle finger was 45-110 degrees. The X-ray of the right hand AP/oblique showed no bone involvement in the deformity. The patient underwent central slip defect reconstruction utilizing the partial ulnar side of the flexor digitorum superficial tendon. A PIP joint extension splint was applied for 2 weeks. Active and passive exercise of the ROM of the PIP joint began after 2 weeks of PIP extension joint splinting. The patient's ROM of the PIP joint (0-90 degrees) significantly improved 1 month after surgery. The patient's ROM of the PIP joint returned to normal after 2 months after surgery. The function of the patient's right hand is evaluated with the DASH score, which improves significantly from 50 to 4.2."
+  },
+  {
+    "doc_id": 18,
+    "label": "proficient_health_literacy",
+    "fulltext": "A 65-year-old male presented with swelling and boutonniere deformity on the right middle finger for six months after a motorcycle accident on January 1st, 2023. Initially, he managed the injury with painkillers and did not seek medical attention. After six months of persistent symptoms, including an inability to fully extend the finger and noticeable edema, he sought treatment.\n\nClinical findings\nThe inspection of the right hand showed the presence of deformity with edema. The active range of motion (ROM) was impaired in PIP joint in digiti III of the right hand. The active ROM of PIP joint digiti III of the right hand 45–110 degrees. The passive ROM of PIP joint digiti III of the right hand within normal.\n\nDiagnostic assessment\nWe performed X-ray of the right hand AP/Lateral which showed there are no abnormality in the bone and we diagnosed the deformity from soft tissue which is central slip injury.\n\nSurgical technique\nA central slip defect reconstruction utilizing partial ulnar side of flexor digitorum superficial tendon was performed. Under anesthesia, the patient was positioned supine with a tourniquet applied to the upper arm. A midlateral incision was made on the ulnar aspect of the right middle phalanx, centered at the PIP joint. The incision extended dorsally in an oblique manner. A transverse incision was made over the MCP joint flexion crease, just proximal to the A1 pulley. The procedure involves identifying and protecting the ulnar digital neurovascular bundle, exposing the central slip and extensor tendon to the PIPJ, full-thickness dorsal flaps are elevated. Scar tissue and pseudotendinous tissue is identified and excised. The central slip cannot be repaired primarily, so the ulnar slip of the FDS tendon is used for reconstruction. The ulnar neurovascular bundle is mobilized to visualize the periosteal insertion of the A3 pulley.\n\nThe extensor tendon is mobilized and tenolyzed, followed by incision of the dorsal capsule of the PIP joint and removal of interposed tissue. The A3 pulley's periosteal insertion is incised longitudinally, and the PIP joint's volar capsule is incised longitudinally. The ulnar slip of the FDS tendon is identified and a 2–0 non-absorbable, monofilament suture is placed around it. A transverse incision is made at the MCP joint flexion crease, proximal to the A1 pulley revealing the flexor tendon sheath. The tendon sheath and A1 pulley are incised longitudinally. The FDS tendon is identified. The ulnar slip of the FDS tendon is isolated and transected to release the ulnar slip, avoiding entrapment or catching of the radial slip. The 2–0 suture that was placed around the ulnar slip at the level of the PIP joint is used to release distally based FDS tendon slip and deliver the ulnar slip of the FDS tendon distally.\n\nA 2.8-mm drill is used to create a vertically oriented bone tunnel dorsal to volar. An elevator is placed between the flexor digitorum profundus tendon, volar plate, and volar aspect of the base of the middle phalanx protecting the volar anatomic structures. The FDS tendon slip passes through the tunnel while maintaining the PIP joint in extension and reduced position. The FDS tendon slip passed through the intact proximal section of the central slip and extensor tendon. A tendon weaver completes a Pulvertaft weave, confirming the appropriate tension with the PIPJ in the reduced, full extension position. A 3–0 non-absorbable suture secures the pulvertaft weave. The margins of the capsule and central slip reconstruction are approximated across the PIP joint, and adhesions are released and the lateral bands mobilized.\n\nThe overall posture, stability, and motion with tenodesis assessed. All the incisions are copiously irrigated. The tourniquet is deflated and hemostasis is obtained. Capillary refill of all fingers is assessed. The skin is closed using horizontal mattress stiches. A sterile dressing is applied with an appropriately padded PIP joint extension splint to allow for early DIP joint and MCP joint motion.\n\nFollow-up and outcomes\nFirst follow-up was done 4 days after for wound treatment. The patient was given oral meloxicam 7,5 mg twice a day and doxycycline 100 mg twice a day for 3 days. The second follow-up was done 3 days after for wound treatment. After 2 weeks, we remove the back slab, remove the external suture and begin the active and passive ROM exercise. After 3 weeks, the wound was healed, and we found the ROM of PIP joint 0 to 90 degrees. And after a month, the patient came with improved ROM of PIP joint 0 to 100 degrees, and improved functional outcome. After 7 weeks of physical rehabilitation, patients already back to work with improve ROM of PIP joint 0 to 110 degrees. The function of the patient's right hand is evaluated with DASH score, which improves significantly from 50 to 4.2.",
+    "diff_label_texts": "A 65-year-old male presented with six months of swelling and boutonniere deformity of the right digit III following a motorcycle accident on January 1, 2023. He initially self-managed with analgesics and did not seek care. He reported inability to fully extend the right middle finger. Examination demonstrated edema and a boutonniere posture (PIP flexion, DIP hyperextension). Active PIP ROM was 45–110 degrees, with passive PIP ROM within normal limits. Radiographs of the right hand (AP/lateral) revealed no osseous pathology, supporting a soft-tissue etiology consistent with a central slip injury. \n\nSurgical technique: Central slip defect reconstruction was performed using the partial ulnar slip of the flexor digitorum superficialis (FDS) tendon. Under anesthesia and tourniquet control in the supine position, a midlateral incision was made on the ulnar aspect of the middle phalanx centered at the PIP joint with dorsal oblique extension, and a transverse incision was made over the MCP flexion crease proximal to the A1 pulley. The ulnar digital neurovascular bundle was identified and protected. Full-thickness dorsal flaps were elevated to expose the central slip and extensor mechanism to the PIPJ. Scar and pseudotendinous tissue were excised. The central slip was not amenable to primary repair; therefore, the ulnar slip of the FDS was selected for reconstruction. The ulnar neurovascular bundle was mobilized to visualize the periosteal insertion of the A3 pulley. The extensor tendon was mobilized and tenolyzed; the dorsal PIP capsule was incised with removal of interposed tissue. The A3 pulley periosteal insertion and the volar capsule of the PIP joint were incised longitudinally. A 2–0 non-absorbable monofilament suture was placed around the ulnar FDS slip at the PIP level. Through the proximal incision, the flexor sheath and A1 pulley were incised longitudinally to expose the FDS; the ulnar slip was isolated and transected, preserving the radial slip. The previously placed 2–0 suture facilitated delivery of the distally based ulnar FDS slip distally. A 2.8‑mm dorsal-to-volar bone tunnel was drilled at the base of the middle phalanx; an elevator protected the FDP, volar plate, and volar structures. With the PIP reduced in full extension, the FDS slip was passed through the tunnel and routed through the intact proximal segment of the central slip/extensor tendon. A tendon weaver completed a Pulvertaft weave under appropriate tension with the PIP in full extension and reduction, secured with 3–0 non-absorbable suture. The capsule and central slip reconstruction margins were approximated; adhesions were released and lateral bands mobilized. Tenodesis effect, posture, stability, and motion were assessed. Wounds were irrigated, the tourniquet deflated, hemostasis obtained, and capillary refill confirmed. Skin was closed with horizontal mattress sutures. A sterile dressing and a well-padded PIP extension splint were applied to allow early DIP and MCP motion.\n\nPostoperative course: First wound check at postoperative day 4; the patient received meloxicam 7.5 mg PO BID and doxycycline 100 mg PO BID for 3 days. A second wound visit occurred 3 days later. At 2 weeks, the back slab and external sutures were removed, and active and passive PIP ROM exercises were initiated. By 3 weeks, the wound had healed and PIP ROM was 0–90 degrees. At 1 month, PIP ROM improved to 0–100 degrees, with continued functional gains. After 7 weeks of rehabilitation, he returned to work with PIP ROM 0–110 degrees. Overall function improved substantially, with the DASH score decreasing from 50 to 4.2.\n\nInterpretation: Clinical and radiographic findings were concordant with a chronic central slip injury producing boutonniere deformity (PIP flexion, DIP hyperextension due to dorsal apparatus disruption and volar migration of lateral bands). Reconstruction using an ulnar FDS slip via bone tunnel and Pulvertaft weave restored PIP extension and yielded progressive ROM gains and marked functional recovery.",
+    "summary": "A 65-year-old male patient presented with swelling and boutonniere deformity on the digiti III of the right hand. The patient had previously fallen from a motorcycle, and the patient's right middle finger got was by a motorcycle six months ago. After the incident, the patient's right middle finger cannot be fully extended. The patient's right hand showed edema with flexion of the interphalangeal (PIP) joint and hyperextension of the distal interphalangeal (DIP) joint. The Range of Motion (ROM) of the PIP joint right middle finger was 45-110 degrees. The X-ray of the right hand AP/oblique showed no bone involvement in the deformity. The patient underwent central slip defect reconstruction utilizing the partial ulnar side of the flexor digitorum superficial tendon. A PIP joint extension splint was applied for 2 weeks. Active and passive exercise of the ROM of the PIP joint began after 2 weeks of PIP extension joint splinting. The patient's ROM of the PIP joint (0-90 degrees) significantly improved 1 month after surgery. The patient's ROM of the PIP joint returned to normal after 2 months after surgery. The function of the patient's right hand is evaluated with the DASH score, which improves significantly from 50 to 4.2."
+  },
+  {
+    "doc_id": 19,
+    "label": "intermediate_health_literacy",
+    "fulltext": "A 23-year-old male patient presented to the emergency department with a sudden onset of severe frontal headache lasting for 2 h. He experienced associated symptoms of nausea, vomiting, and chest heaviness. He has a unremarkable medical record and denies the use of illicit drugs. However, he is a smoker with a history of 23 pack-years but does not consume alcohol.\n\nOn physical examination, the young male appeared distressed but was fully conscious and oriented to time, place, and person. Chest auscultation revealed normal vesicular breathing sounds, while cardiovascular and abdominal examinations were inconclusive. Neurological examinations demonstrated neck stiffness, dilated pupils reactive to light, normal plantar reflexes, and no focal neurological deficits.\n\nHis vital signs were as follows: blood pressure 178/103 mmHg, respiratory rate 26 breaths/min, temperature 38.9°C, heart rate 87 beats/min, and oxygen saturation of 94%.\n\nEmergency tests were initiated. An ECG revealed ST segment elevation >2 mm in leads V2-V5, consistent with STEMI as the top of our differential diagnosis, requiring confirmation by cardiac markers. With prompt referral to a tertiary cardiac centre implemented, the patient received a 300 mg aspirin load while being transferred to the catheter lab. Troponin levels were significantly elevated at 1.48 mg/dl (normal <0.16 mg/dl).\n\nPercutaneous coronary intervention was performed via the femoral artery, and the result showed normal coronary arteries with thrombolysis in myocardial infarction (TIMI) flow grade of 3.\n\nHis ECG after coronary angiography revealed normal sinus rhythm with left ventricular hypertrophy LVH. An echocardiogram was performed, revealing normal ventricular function with no regional wall motion abnormalities (RWMA).\n\nFollowing coronary intervention, he was admitted to the medical ward for further assessment and investigation. Blood samples were drawn for a complete blood count, random blood sugar, renal function tests, and CRP. The results revealed lymphocytosis and mildly elevated CRP.\n\nWe proceeded further with CT brain to exclude serious cause of headache. His brain CT showed cisternal subarachnoid haemorrhage SAH with extension anterior to the right temporal lobe. Abdominal ultrasound screening was performed to rule out polycystic kidney disease which was negative and cerebral CT angiography was scheduled to exclude cerebral aneurysm Nimodipine 60 mg every 4 h was initiated, with a target blood pressure of 160/100 mmHg.\n\nOn the second day, his condition suddenly deteriorated, culminating with cardiac arrest. Therefore, cardiopulmonary resuscitation (CPR), resulting in a Glasgow Coma Scale score (GCS) of 6. The patient was subsequently, intubated and placed on mechanical ventilation in the Intensive Care Unit (ICU). Due to his unstable condition in the ICU, we could not perform a repeated CT brain scan or the planned cerebral CT angiography.\n\nOver the next 7 days, we diligently monitored him with a strict multidisciplinary team. A nasogastric tube was inserted for feeding and fluid replacement. His medications included intravenous fluids, antibiotics, proton pump inhibitors, and nimodipine.\n\nOn the 8th day, he suddenly developed ventricular fibrillation, and despite CPR with more than five defibrillations, we were unable to revive him and death was the final outcome.39734686",
+    "diff_label_texts": "A 23-year-old man came to the emergency department with a sudden severe headache, nausea, vomiting, and chest heaviness. His initial vital signs showed high blood pressure and a fast breathing rate. An emergency ECG showed a heart attack pattern (STEMI), so he was urgently sent for percutaneous coronary intervention; the angiogram revealed normal coronary arteries. Further evaluation with a brain CT identified a cisternal subarachnoid hemorrhage (bleeding around the brain). Despite coordinated care by multiple teams, his condition rapidly worsened, leading to cardiac arrest and death.",
+    "summary": "We present a case detailing the diagnostic challenges of a 23-year-old male presenting with a sudden severe headache, nausea, vomiting, and chest heaviness. Initial evaluation showed elevated blood pressure and respiratory rate. An emergency electrocardiogram (ECG) indicated ST-segment elevation myocardial infarction (STEMI), leading to immediate referral for percutaneous coronary intervention, which revealed normal coronary arteries. Further investigations identified a cisternal subarachnoid haemorrhage (SAH) on CT brain imaging. Despite multidisciplinary management, the patient's condition rapidly deteriorated, resulting in cardiac arrest and mortality."
+  },
+  {
+    "doc_id": 19,
+    "label": "low_health_literacy",
+    "fulltext": "A 23-year-old male patient presented to the emergency department with a sudden onset of severe frontal headache lasting for 2 h. He experienced associated symptoms of nausea, vomiting, and chest heaviness. He has a unremarkable medical record and denies the use of illicit drugs. However, he is a smoker with a history of 23 pack-years but does not consume alcohol.\n\nOn physical examination, the young male appeared distressed but was fully conscious and oriented to time, place, and person. Chest auscultation revealed normal vesicular breathing sounds, while cardiovascular and abdominal examinations were inconclusive. Neurological examinations demonstrated neck stiffness, dilated pupils reactive to light, normal plantar reflexes, and no focal neurological deficits.\n\nHis vital signs were as follows: blood pressure 178/103 mmHg, respiratory rate 26 breaths/min, temperature 38.9°C, heart rate 87 beats/min, and oxygen saturation of 94%.\n\nEmergency tests were initiated. An ECG revealed ST segment elevation >2 mm in leads V2-V5, consistent with STEMI as the top of our differential diagnosis, requiring confirmation by cardiac markers. With prompt referral to a tertiary cardiac centre implemented, the patient received a 300 mg aspirin load while being transferred to the catheter lab. Troponin levels were significantly elevated at 1.48 mg/dl (normal <0.16 mg/dl).\n\nPercutaneous coronary intervention was performed via the femoral artery, and the result showed normal coronary arteries with thrombolysis in myocardial infarction (TIMI) flow grade of 3.\n\nHis ECG after coronary angiography revealed normal sinus rhythm with left ventricular hypertrophy LVH. An echocardiogram was performed, revealing normal ventricular function with no regional wall motion abnormalities (RWMA).\n\nFollowing coronary intervention, he was admitted to the medical ward for further assessment and investigation. Blood samples were drawn for a complete blood count, random blood sugar, renal function tests, and CRP. The results revealed lymphocytosis and mildly elevated CRP.\n\nWe proceeded further with CT brain to exclude serious cause of headache. His brain CT showed cisternal subarachnoid haemorrhage SAH with extension anterior to the right temporal lobe. Abdominal ultrasound screening was performed to rule out polycystic kidney disease which was negative and cerebral CT angiography was scheduled to exclude cerebral aneurysm Nimodipine 60 mg every 4 h was initiated, with a target blood pressure of 160/100 mmHg.\n\nOn the second day, his condition suddenly deteriorated, culminating with cardiac arrest. Therefore, cardiopulmonary resuscitation (CPR), resulting in a Glasgow Coma Scale score (GCS) of 6. The patient was subsequently, intubated and placed on mechanical ventilation in the Intensive Care Unit (ICU). Due to his unstable condition in the ICU, we could not perform a repeated CT brain scan or the planned cerebral CT angiography.\n\nOver the next 7 days, we diligently monitored him with a strict multidisciplinary team. A nasogastric tube was inserted for feeding and fluid replacement. His medications included intravenous fluids, antibiotics, proton pump inhibitors, and nimodipine.\n\nOn the 8th day, he suddenly developed ventricular fibrillation, and despite CPR with more than five defibrillations, we were unable to revive him and death was the final outcome.39734686",
+    "diff_label_texts": "A 23-year-old man came to the emergency room with a sudden, very bad headache. He also felt sick, threw up, and felt heavy pressure in his chest. His blood pressure was high and he was breathing fast. A quick heart test looked like a major heart attack. He was rushed for a procedure to check and open the heart arteries. The heart arteries looked normal. A head CT scan then showed bleeding in the space around his brain. A team of specialists cared for him, but he got worse quickly. He went into cardiac arrest and died.",
+    "summary": "We present a case detailing the diagnostic challenges of a 23-year-old male presenting with a sudden severe headache, nausea, vomiting, and chest heaviness. Initial evaluation showed elevated blood pressure and respiratory rate. An emergency electrocardiogram (ECG) indicated ST-segment elevation myocardial infarction (STEMI), leading to immediate referral for percutaneous coronary intervention, which revealed normal coronary arteries. Further investigations identified a cisternal subarachnoid haemorrhage (SAH) on CT brain imaging. Despite multidisciplinary management, the patient's condition rapidly deteriorated, resulting in cardiac arrest and mortality."
+  },
+  {
+    "doc_id": 19,
+    "label": "proficient_health_literacy",
+    "fulltext": "A 23-year-old male patient presented to the emergency department with a sudden onset of severe frontal headache lasting for 2 h. He experienced associated symptoms of nausea, vomiting, and chest heaviness. He has a unremarkable medical record and denies the use of illicit drugs. However, he is a smoker with a history of 23 pack-years but does not consume alcohol.\n\nOn physical examination, the young male appeared distressed but was fully conscious and oriented to time, place, and person. Chest auscultation revealed normal vesicular breathing sounds, while cardiovascular and abdominal examinations were inconclusive. Neurological examinations demonstrated neck stiffness, dilated pupils reactive to light, normal plantar reflexes, and no focal neurological deficits.\n\nHis vital signs were as follows: blood pressure 178/103 mmHg, respiratory rate 26 breaths/min, temperature 38.9°C, heart rate 87 beats/min, and oxygen saturation of 94%.\n\nEmergency tests were initiated. An ECG revealed ST segment elevation >2 mm in leads V2-V5, consistent with STEMI as the top of our differential diagnosis, requiring confirmation by cardiac markers. With prompt referral to a tertiary cardiac centre implemented, the patient received a 300 mg aspirin load while being transferred to the catheter lab. Troponin levels were significantly elevated at 1.48 mg/dl (normal <0.16 mg/dl).\n\nPercutaneous coronary intervention was performed via the femoral artery, and the result showed normal coronary arteries with thrombolysis in myocardial infarction (TIMI) flow grade of 3.\n\nHis ECG after coronary angiography revealed normal sinus rhythm with left ventricular hypertrophy LVH. An echocardiogram was performed, revealing normal ventricular function with no regional wall motion abnormalities (RWMA).\n\nFollowing coronary intervention, he was admitted to the medical ward for further assessment and investigation. Blood samples were drawn for a complete blood count, random blood sugar, renal function tests, and CRP. The results revealed lymphocytosis and mildly elevated CRP.\n\nWe proceeded further with CT brain to exclude serious cause of headache. His brain CT showed cisternal subarachnoid haemorrhage SAH with extension anterior to the right temporal lobe. Abdominal ultrasound screening was performed to rule out polycystic kidney disease which was negative and cerebral CT angiography was scheduled to exclude cerebral aneurysm Nimodipine 60 mg every 4 h was initiated, with a target blood pressure of 160/100 mmHg.\n\nOn the second day, his condition suddenly deteriorated, culminating with cardiac arrest. Therefore, cardiopulmonary resuscitation (CPR), resulting in a Glasgow Coma Scale score (GCS) of 6. The patient was subsequently, intubated and placed on mechanical ventilation in the Intensive Care Unit (ICU). Due to his unstable condition in the ICU, we could not perform a repeated CT brain scan or the planned cerebral CT angiography.\n\nOver the next 7 days, we diligently monitored him with a strict multidisciplinary team. A nasogastric tube was inserted for feeding and fluid replacement. His medications included intravenous fluids, antibiotics, proton pump inhibitors, and nimodipine.\n\nOn the 8th day, he suddenly developed ventricular fibrillation, and despite CPR with more than five defibrillations, we were unable to revive him and death was the final outcome.39734686",
+    "diff_label_texts": "A 23-year-old male with a 23 pack-year smoking history, no alcohol use, and no illicit drug use presented with 2 hours of sudden severe frontal headache, nausea, vomiting, and chest heaviness. He was distressed but alert and oriented. Vitals: BP 178/103 mmHg, RR 26/min, T 38.9°C, HR 87/min, SpO2 94%. Exam: normal vesicular breath sounds; cardiovascular and abdominal exams inconclusive; neurological exam notable for neck stiffness, dilated but light-reactive pupils, normal plantar reflexes, and no focal deficits. ECG showed ST-segment elevation >2 mm in V2–V5, consistent with STEMI; he received a 300 mg aspirin load and was urgently transferred for PCI. Troponin was elevated at 1.48 mg/dl (normal <0.16 mg/dl). Femoral-access coronary angiography demonstrated normal coronary arteries with TIMI 3 flow. Post-angiography ECG showed normal sinus rhythm with LVH; echocardiography revealed normal ventricular function without RWMA. Subsequent workup found lymphocytosis and mildly elevated CRP. Non-contrast CT brain demonstrated a cisternal subarachnoid haemorrhage with extension anterior to the right temporal lobe. Abdominal ultrasound was negative for polycystic kidney disease; cerebral CT angiography was planned to exclude aneurysm. Nimodipine 60 mg q4h was initiated with a BP target of 160/100 mmHg. On day 2, he acutely deteriorated with cardiac arrest; after CPR, GCS was 6, and he was intubated and mechanically ventilated in the ICU. Owing to instability, repeat CT brain and planned cerebral CTA were not performed. He received multidisciplinary ICU care with NG feeding, IV fluids, antibiotics, a proton pump inhibitor, and nimodipine. On day 8, he developed ventricular fibrillation and, despite CPR and more than five defibrillation attempts, could not be resuscitated and died.",
+    "summary": "We present a case detailing the diagnostic challenges of a 23-year-old male presenting with a sudden severe headache, nausea, vomiting, and chest heaviness. Initial evaluation showed elevated blood pressure and respiratory rate. An emergency electrocardiogram (ECG) indicated ST-segment elevation myocardial infarction (STEMI), leading to immediate referral for percutaneous coronary intervention, which revealed normal coronary arteries. Further investigations identified a cisternal subarachnoid haemorrhage (SAH) on CT brain imaging. Despite multidisciplinary management, the patient's condition rapidly deteriorated, resulting in cardiac arrest and mortality."
+  }
+]
\ No newline at end of file
diff --git a/code/support_check/dataset_process.py b/code/support_check/dataset_process.py
new file mode 100644
index 0000000000000000000000000000000000000000..f888e8ec0eeabcc044079cec94308b26f16d3a73
--- /dev/null
+++ b/code/support_check/dataset_process.py
@@ -0,0 +1,74 @@
+import json
+from pathlib import Path
+
+# Input file (synthetic subclaims dataset)
+DATA_PATH = Path(
+    "/home/mshahidul/readctrl/data/extracting_subclaim/synthetic_subclaims_first200.json"
+)
+OUTPUT_PATH = Path(
+    "/home/mshahidul/readctrl/data/finetuning_data/dataset_for_sft_support_check_list_new.json"
+)
+
+
+def training_prompt(medical_text, subclaims, labels):
+    numbered_subclaims = "\n".join(
+        [f"{idx + 1}. {claim}" for idx, claim in enumerate(subclaims)]
+    )
+    
+    system_prompt = f"""
+You are an expert medical adjudicator. Determine if the 'Medical Passage' contains the core factual information of each 'Subclaim', even if the passage uses simpler language or layperson terms.
+Rules:
+- Label 'supported' if the essential meaning is present.
+- Label 'not_supported' only if the information is missing or contradicted.
+Output: JSON array of strings ['supported', 'not_supported', ...]
+
+Medical text:
+{medical_text}
+
+Subclaims:
+{numbered_subclaims}
+"""
+
+    conversation = {}
+    conversation["conversations"] = (
+        {"from": "user", "content": system_prompt},
+        {"from": "assistant", "content": json.dumps(labels, ensure_ascii=False)},
+    )
+    return conversation
+
+
+def load_conversation_dataset(data_path=DATA_PATH):
+    with Path(data_path).open("r", encoding="utf-8") as f:
+        raw_data = json.load(f)
+
+    formatted_data = []
+    for record in raw_data:
+        generated = record.get("generated", {})
+        medical_text = generated.get("passage", "")
+        raw_subclaims = generated.get("subclaims", [])
+
+        subclaims = []
+        labels = []
+        for subclaim in raw_subclaims:
+            claim_text = subclaim.get("claim_text", "").strip()
+            if not claim_text:
+                continue
+            subclaims.append(claim_text)
+            labels.append(subclaim.get("label", "not_supported"))
+
+        if not medical_text or not subclaims:
+            continue
+
+        formatted_data.append(training_prompt(medical_text, subclaims, labels))
+
+    return formatted_data
+
+
+# Example usage:
+dataset_for_sft = load_conversation_dataset()
+
+with OUTPUT_PATH.open("w", encoding="utf-8") as f:
+    json.dump(dataset_for_sft, f, ensure_ascii=False, indent=2)
+
+print(len(dataset_for_sft))
+print(dataset_for_sft[0])
\ No newline at end of file
diff --git a/code/support_check/test.py b/code/support_check/test.py
new file mode 100644
index 0000000000000000000000000000000000000000..89188b67c812ed9351134a4a3be04e9df8f30d52
--- /dev/null
+++ b/code/support_check/test.py
@@ -0,0 +1,94 @@
+import json
+from pathlib import Path
+from openai import OpenAI
+from datasets import load_dataset
+from transformers import AutoTokenizer
+from unsloth.chat_templates import get_chat_template
+
+# Configuration
+API_BASE = "http://172.16.34.22:8086/v1"
+MODEL_PATH = "sc"
+TOKENIZER_NAME = "meta-llama/Llama-3.1-8B-Instruct"
+DATASET_FILE = Path("/home/mshahidul/readctrl/data/finetuning_data/finetune_dataset_subclaim_support_v2.json")
+TEXT_VARIANT = "hard_text"
+
+# 1. Initialize OpenAI Client
+client = OpenAI(api_key="EMPTY", base_url=API_BASE)
+tokenizer = AutoTokenizer.from_pretrained(TOKENIZER_NAME)
+tokenizer = get_chat_template(tokenizer, chat_template="llama-3.1")
+
+
+def render_chat_prompt(user_prompt: str) -> str:
+    messages = [{"role": "user", "content": user_prompt}]
+    template = tokenizer.apply_chat_template(
+        messages,
+        tokenize=False,
+        add_generation_prompt=True,
+    )
+    import ipdb; ipdb.set_trace()
+    print(template)
+    return template
+
+def build_user_prompt(text: str, subclaims: list[str]) -> str:
+    numbered_subclaims = "\n".join(f"{idx + 1}. {s}" for idx, s in enumerate(subclaims))
+    return (
+        "You are a medical evidence checker.\n"
+        "Given a medical passage and a list of subclaims, return labels for each "
+        "subclaim in the same order.\n\n"
+        "Allowed labels: supported, not_supported.\n"
+        "Output format: a JSON array of strings only.\n\n"
+        f"Medical text:\n{text}\n\n"
+        f"Subclaims:\n{numbered_subclaims}"
+    )
+
+def main():
+    # 2. Load the original dataset
+    raw_dataset = load_dataset("json", data_files=str(DATASET_FILE), split="train")
+    
+    # 3. Re-create the test split (using your same seed/ratio)
+    splits = raw_dataset.train_test_split(test_size=0.1, seed=3407, shuffle=True)
+    test_split = splits["test"]
+
+    print(f"Running inference on {len(test_split)} samples...")
+
+    results = []
+    for row in test_split:
+        for item in row.get("items", []):
+            text = item.get(TEXT_VARIANT, "").strip()
+            subclaims = [s["subclaim"] for s in item.get("subclaims", [])]
+            gold_labels = [s["label"] for s in item.get("subclaims", [])]
+            # print("--------------------------------")
+            # print(text)
+            # print(subclaims)
+            # print(gold_labels)
+            # print("--------------------------------")
+
+            if not text or not subclaims:
+                continue
+
+            # 4. Render Llama chat template locally and request inference from vLLM.
+            prompt = render_chat_prompt(build_user_prompt(text, subclaims))
+            response = client.completions.create(
+                model=MODEL_PATH,
+                prompt=prompt,
+                temperature=0,  # Keep it deterministic
+                max_tokens=256
+            )
+
+            pred_text = response.choices[0].text.strip()
+            
+            print(f"--- Sample ---")
+            print(f"Pred: {pred_text}")
+            print(f"Gold: {gold_labels}")
+            
+            results.append({
+                "predicted": pred_text,
+                "gold": gold_labels
+            })
+
+    # Save results
+    with open("inference_results.json", "w") as f:
+        json.dump(results, f, indent=4)
+
+if __name__ == "__main__":
+    main()
\ No newline at end of file
diff --git a/code/support_check/test_v2.py b/code/support_check/test_v2.py
new file mode 100644
index 0000000000000000000000000000000000000000..a2a7a7d2d81574ad6d2bdd447340c07c9854e8d6
--- /dev/null
+++ b/code/support_check/test_v2.py
@@ -0,0 +1,90 @@
+import json
+from pathlib import Path
+from openai import OpenAI
+from datasets import load_dataset
+
+# Configuration
+API_BASE = "http://172.16.34.22:3090/v1"
+MODEL_PATH = "sc"
+DATASET_FILE = Path("/home/mshahidul/readctrl/data/finetuning_data/finetune_dataset_subclaim_support_v2.json")
+TEXT_VARIANT = "hard_text"
+
+# 1. Initialize OpenAI Client
+client = OpenAI(api_key="EMPTY", base_url=API_BASE)
+
+CHAT_TEMPLATE = (
+    "<|begin_of_text|><|start_header_id|>system<|end_header_id|>\n\n"
+    "Cutting Knowledge Date: December 2023\n"
+    "Today Date: 26 July 2024\n\n"
+    "<|eot_id|><|start_header_id|>user<|end_header_id|>\n\n"
+    "{user_prompt}"
+    "<|eot_id|><|start_header_id|>assistant<|end_header_id|>\n\n"
+)
+
+
+def render_chat_prompt(user_prompt: str) -> str:
+    return CHAT_TEMPLATE.format(user_prompt=user_prompt)
+
+def build_user_prompt(text: str, subclaims: list[str]) -> str:
+    numbered_subclaims = "\n".join(f"{idx + 1}. {s}" for idx, s in enumerate(subclaims))
+    return (
+        "You are a medical evidence checker.\n"
+        "Given a medical passage and a list of subclaims, return labels for each "
+        "subclaim in the same order.\n\n"
+        "Allowed labels: supported, not_supported.\n"
+        "Output format: a JSON array of strings only.\n\n"
+        f"Medical text:\n{text}\n\n"
+        f"Subclaims:\n{numbered_subclaims}"
+    )
+
+def main():
+    # 2. Load the original dataset
+    raw_dataset = load_dataset("json", data_files=str(DATASET_FILE), split="train")
+    
+    # 3. Re-create the test split (using your same seed/ratio)
+    splits = raw_dataset.train_test_split(test_size=0.1, seed=3407, shuffle=True)
+    test_split = splits["test"]
+
+    print(f"Running inference on {len(test_split)} samples...")
+
+    results = []
+    for row in test_split:
+        for item in row.get("items", []):
+            text = item.get(TEXT_VARIANT, "").strip()
+            subclaims = [s["subclaim"] for s in item.get("subclaims", [])]
+            gold_labels = [s["label"] for s in item.get("subclaims", [])]
+            # print("--------------------------------")
+            # print(text)
+            # print(subclaims)
+            # print(gold_labels)
+            # print("--------------------------------")
+
+            if not text or not subclaims:
+                continue
+
+            # 4. Render Llama chat template locally and request inference from vLLM.
+            prompt = render_chat_prompt(build_user_prompt(text, subclaims))
+            response = client.completions.create(
+                model=MODEL_PATH,
+                prompt=prompt,
+                temperature=0,  # Keep it deterministic
+                max_tokens=256
+            )
+
+            pred_text = response.choices[0].text.strip()
+            
+            print(f"--- Sample ---")
+            print(f"Pred: {pred_text}")
+            print(f"Gold: {gold_labels}")
+            
+            results.append({
+                "predicted": pred_text,
+                "gold": gold_labels
+            })
+
+    # Save results
+    with open("inference_results.json", "w") as f:
+        json.dump(results, f, indent=4)
+
+if __name__ == "__main__":
+    main()
\ No newline at end of file
diff --git a/code/translation/download_translategemma_model.py b/code/translation/download_translategemma_model.py
new file mode 100644
index 0000000000000000000000000000000000000000..bfdd8a95157a9a5aa23870c64212838461e48f1f
--- /dev/null
+++ b/code/translation/download_translategemma_model.py
@@ -0,0 +1,24 @@
+import sys
+
+from huggingface_hub import hf_hub_download
+
+
+def main() -> int:
+    try:
+        hf_hub_download(
+            repo_id="bullerwins/translategemma-27b-it-GGUF",
+            filename="translategemma-27b-it-Q8_0.gguf",
+            local_dir="/home/mshahidul/readctrl/models",
+            local_dir_use_symlinks=False,
+        )
+        return 0
+    except ImportError:
+        print("huggingface_hub not found. Install it and try again.", file=sys.stderr)
+        return 1
+    except Exception as exc:
+        print(str(exc), file=sys.stderr)
+        return 1
+
+
+if __name__ == "__main__":
+    raise SystemExit(main())
diff --git a/code/translation/misc/translate_multiclinsum_en2bn_v2.py b/code/translation/misc/translate_multiclinsum_en2bn_v2.py
new file mode 100644
index 0000000000000000000000000000000000000000..7d1333a02484f67fee1ab73ba85aecd71e54dfbf
--- /dev/null
+++ b/code/translation/misc/translate_multiclinsum_en2bn_v2.py
@@ -0,0 +1,331 @@
+import os
+os.environ["CUDA_DEVICE_ORDER"] = "PCI_BUS_ID"
+os.environ["CUDA_VISIBLE_DEVICES"] = "2"
+
+import argparse
+import json
+import re
+import time
+import unicodedata
+import urllib.error
+import urllib.request
+from typing import Dict, List, Tuple
+
+from openai import OpenAI
+from tqdm import tqdm
+
+
+DATA_PATH = "/home/mshahidul/readctrl/data/testing_data_gs/multiclinsum_gs_train_en.json"
+OUT_PATH = "/home/mshahidul/readctrl/data/translated_data/multiclinsum_gs_train_en2bn_gemma(0_200).json"
+
+# Tune if you hit model input limits.
+MAX_CHARS_PER_CHUNK = 1500
+MAX_NEW_TOKENS = 512
+SAVE_EVERY = 10
+
+OPENAI_BASE_URL = os.environ.get("OPENAI_BASE_URL", "http://localhost:8081/v1")
+OPENAI_API_KEY = os.environ.get("OPENAI_API_KEY", "no-key-required")
+OPENAI_MODEL = os.environ.get("OPENAI_MODEL", "translate_gemma")
+OPENAI_TIMEOUT_SEC = float(os.environ.get("OPENAI_TIMEOUT_SEC", "60"))
+
+VLLM_BASE_URL = os.environ.get("VLLM_BASE_URL", "http://localhost:8004/v1")
+JUDGE_MODEL = os.environ.get("JUDGE_MODEL", "Qwen/Qwen3-30B-A3B-Instruct-2507")
+JUDGE_MAX_RETRIES = 3
+JUDGE_TIMEOUT_SEC = 60
+JUDGE_TEMPERATURE = 0.0
+
+_BENGALI_RANGE = (0x0980, 0x09FF)
+_ALLOWED_PUNCT = set(" \n\t\r.,;:!?-—()[]{}\"'`~")
+_ALLOWED_EN_WORDS = {
+    w.strip().lower()
+    for w in os.environ.get("ALLOWED_EN_WORDS", "").split(",")
+    if w.strip()
+}
+
+
+def chunk_text(text: str, max_chars: int) -> List[str]:
+    if len(text) <= max_chars:
+        return [text]
+
+    chunks: List[str] = []
+    paragraphs = [p for p in text.split("\n\n") if p.strip()]
+    for para in paragraphs:
+        if len(para) <= max_chars:
+            chunks.append(para)
+            continue
+
+        sentences = [s.strip() for s in para.split(". ") if s.strip()]
+        current = ""
+        for sentence in sentences:
+            sentence = sentence if sentence.endswith(".") else f"{sentence}."
+            if not current:
+                current = sentence
+                continue
+
+            if len(current) + 1 + len(sentence) <= max_chars:
+                current = f"{current} {sentence}"
+            else:
+                chunks.append(current)
+                current = sentence
+
+        if current:
+            chunks.append(current)
+
+    return chunks
+
+
+def translate_text(client: OpenAI, text: str) -> str:
+    if not text.strip():
+        return text
+
+    chunks = chunk_text(text, MAX_CHARS_PER_CHUNK)
+    if len(chunks) == 1:
+        messages = [
+            {
+                "role": "user",
+                "content": (
+                    "Translate the following text from English to Bengali:\n\n"
+                    f"{chunks[0]}"
+                ),
+            }
+        ]
+        completion = client.chat.completions.create(
+            model=OPENAI_MODEL,
+            messages=messages,
+            max_tokens=MAX_NEW_TOKENS,
+            stream=False,
+        )
+        return completion.choices[0].message.content
+
+    def _translate_chunk(chunk: str) -> str:
+        messages = [
+            {
+                "role": "user",
+                "content": (
+                    "Translate the following text from English to Bengali:\n\n"
+                    f"{chunk}"
+                ),
+            }
+        ]
+        completion = client.chat.completions.create(
+            model=OPENAI_MODEL,
+            messages=messages,
+            max_tokens=MAX_NEW_TOKENS,
+            stream=False,
+        )
+        return completion.choices[0].message.content
+
+    translated_chunks: List[str] = []
+    for chunk in chunks:
+        translated_chunks.append(_translate_chunk(chunk))
+
+    return "\n\n".join(translated_chunks)
+
+
+def _strip_code_fences(text: str) -> str:
+    text = text.strip()
+    if text.startswith("```"):
+        text = re.sub(r"^```[a-zA-Z]*\n?", "", text)
+        text = re.sub(r"\n?```$", "", text)
+    return text.strip()
+
+
+def _extract_json_payload(text: str) -> Dict:
+    cleaned = _strip_code_fences(text)
+    try:
+        return json.loads(cleaned)
+    except json.JSONDecodeError:
+        match = re.search(r"\{.*\}", cleaned, flags=re.DOTALL)
+        if match:
+            return json.loads(match.group(0))
+    return {}
+
+
+def _contains_disallowed_chars(text: str) -> Tuple[bool, str]:
+    # Allow common medical/tech symbols that might be marked as 'S' (Symbol)
+    # like ±, μ, §, ©, or mathematical operators.
+    allowed_extra_symbols = {"±", "μ", "°", "%", "+", "=", "<", ">", "/", "\\"}
+    
+    for ch in text:
+        code = ord(ch)
+        # 1. Allow Bengali Range
+        if _BENGALI_RANGE[0] <= code <= _BENGALI_RANGE[1]:
+            continue
+        # 2. Allow Basic Latin (English + Punctuation)
+        if 0x0000 <= code <= 0x007F:
+            continue
+        # 3. Allow specifically whitelisted symbols
+        if ch in allowed_extra_symbols:
+            continue
+            
+        category = unicodedata.category(ch)
+        # Only fail if it's a 'Other, Not Assigned' or 'Private Use' character (junk)
+        if category in ["Cn", "Co"]:
+            return True, f"Corrupted character detected: {ch} (U+{code:04X})"
+            
+    return False, ""
+
+
+def _call_judge_model(source_text: str, translated_text: str) -> Dict:
+    url = f"{VLLM_BASE_URL}/chat/completions"
+    prompt = (
+        "You are a strict judge for Bengali translations. "
+        "Return JSON only with keys ok (true/false) and reason. "
+        "Check if the Bengali translation contains any non-Bengali, "
+        "non-English letters, or strange symbols. "
+        "Allow Bengali punctuation, Bengali digits, and common punctuation. "
+        "English words and keywords are allowed. "
+        "Minor punctuation differences are acceptable."
+        "Allow common medical/tech symbols that might be marked as 'S' (Symbol) like ±, μ, §, ©, or mathematical operators."
+        "If any issue exists, ok must be false.\n\n"
+        f"English:\n{source_text}\n\nBengali:\n{translated_text}"
+    )
+    payload = {
+        "model": JUDGE_MODEL,
+        "messages": [
+            {"role": "system", "content": "Respond with JSON only."},
+            {"role": "user", "content": prompt},
+        ],
+        "temperature": JUDGE_TEMPERATURE,
+        "max_tokens": 256,
+    }
+    data = json.dumps(payload).encode("utf-8")
+    req = urllib.request.Request(
+        url,
+        data=data,
+        headers={"Content-Type": "application/json"},
+        method="POST",
+    )
+    with urllib.request.urlopen(req, timeout=JUDGE_TIMEOUT_SEC) as resp:
+        response_json = json.loads(resp.read().decode("utf-8"))
+    content = response_json["choices"][0]["message"]["content"]
+    return _extract_json_payload(content)
+
+
+def _judge_translation(source_text: str, translated_text: str) -> Tuple[bool, str]:
+    if not translated_text.strip():
+        return False, "Empty translation"
+
+    try:
+        response = _call_judge_model(source_text, translated_text)
+        ok = bool(response.get("ok", False))
+        reason = str(response.get("reason", ""))
+    except (urllib.error.URLError, json.JSONDecodeError, KeyError, TimeoutError) as exc:
+        ok = False
+        reason = f"Judge call failed: {exc}"
+
+    disallowed, disallowed_reason = _contains_disallowed_chars(translated_text)
+    if disallowed:
+        return False, disallowed_reason
+    if not ok:
+        return False, reason or "Judge rejected translation"
+    return True, ""
+
+
+def translate_with_judge(
+    client: OpenAI, source_text: str, field_name: str, record_id: str
+) -> str:
+    if not source_text.strip():
+        return source_text
+
+    for attempt in range(1, JUDGE_MAX_RETRIES + 1):
+        translated = translate_text(client, source_text)
+        ok, reason = _judge_translation(source_text, translated)
+        if ok:
+            return translated
+        print(
+            f"[Judge] id={record_id} field={field_name} attempt={attempt} failed: {reason}"
+        )
+        time.sleep(1)
+
+    print(
+        f"[Judge] id={record_id} field={field_name} failed after "
+        f"{JUDGE_MAX_RETRIES} attempts. Leaving empty for re-translation."
+    )
+    return ""
+
+
+def load_json(path: str) -> List[Dict]:
+    with open(path, "r", encoding="utf-8") as f:
+        return json.load(f)
+
+
+def save_json(path: str, data: List[Dict]) -> None:
+    os.makedirs(os.path.dirname(path), exist_ok=True)
+    with open(path, "w", encoding="utf-8") as f:
+        json.dump(data, f, ensure_ascii=False, indent=2)
+
+
+def parse_args() -> argparse.Namespace:
+    parser = argparse.ArgumentParser(
+        description="Translate MultiClinSum EN to BN."
+    )
+    parser.add_argument(
+        "--limit",
+        type=int,
+        default=200,
+        help="Only translate the first N instances.",
+    )
+    return parser.parse_args()
+
+
+def main() -> None:
+    args = parse_args()
+    data = load_json(DATA_PATH)
+    if args.limit is not None:
+        data = data[: args.limit]
+
+    existing: Dict[str, Dict] = {}
+    existing_list: List[Dict] = []
+    resume_index = 0
+    if os.path.exists(OUT_PATH):
+        existing_list = load_json(OUT_PATH)
+        for item in existing_list:
+            existing[item["id"]] = item
+        if existing_list:
+            prefix_ids = [item.get("id") for item in existing_list]
+            data_prefix_ids = [item.get("id") for item in data[: len(prefix_ids)]]
+            if prefix_ids == data_prefix_ids:
+                resume_index = len(existing_list)
+
+    client = OpenAI(
+        base_url=OPENAI_BASE_URL,
+        api_key=OPENAI_API_KEY,
+        timeout=OPENAI_TIMEOUT_SEC,
+    )
+
+    translated: List[Dict] = existing_list.copy()
+    for idx, item in enumerate(
+        tqdm(data[resume_index:], desc="Translating", unit="record"),
+        start=resume_index + 1,
+    ):
+        if item["id"] in existing:
+            translated.append(existing[item["id"]])
+        else:
+            record_id = str(item.get("id", ""))
+            fulltext_bn = translate_with_judge(
+                client, item.get("fulltext", ""), "fulltext", record_id
+            )
+            summary_bn = translate_with_judge(
+                client, item.get("summary", ""), "summary", record_id
+            )
+            translated.append(
+                {
+                    "id": item.get("id"),
+                    "fulltext_en": item.get("fulltext", ""),
+                    "summary_en": item.get("summary", ""),
+                    "fulltext_bn": fulltext_bn,
+                    "summary_bn": summary_bn,
+                }
+            )
+
+        if idx % SAVE_EVERY == 0:
+            save_json(OUT_PATH, translated)
+            print(f"Saved {idx}/{len(data)} records to {OUT_PATH}")
+
+    save_json(OUT_PATH, translated)
+    print(f"Done. Saved {len(translated)} records to {OUT_PATH}")
+
+
+if __name__ == "__main__":
+    main()
diff --git a/code/translation/misc/translate_multiclinsum_en2bn_v3.py b/code/translation/misc/translate_multiclinsum_en2bn_v3.py
new file mode 100644
index 0000000000000000000000000000000000000000..b739d7e2450d78f61a1304b7413c9ec181016093
--- /dev/null
+++ b/code/translation/misc/translate_multiclinsum_en2bn_v3.py
@@ -0,0 +1,133 @@
+import os
+import json
+import time
+from tqdm import tqdm
+from openai import OpenAI
+from transformers import AutoProcessor
+model_id = "google/translategemma-27b-it"
+processor = AutoProcessor.from_pretrained(model_id)
+
+# ---- Configuration ----
+DATA_PATH = "/home/mshahidul/readctrl/data/testing_data_gs/multiclinsum_gs_train_en.json"
+OUT_PATH = "/home/mshahidul/readctrl/data/translated_data/multiclinsum_gs_train_en2bn_gemma(0_200).json"
+
+# Translation API
+TRANSLATE_BASE_URL = "http://localhost:8081/v1"
+# Judge API
+VLLM_BASE_URL = os.environ.get("VLLM_BASE_URL", "http://localhost:8004/v1")
+JUDGE_MODEL = os.environ.get("JUDGE_MODEL", "Qwen/Qwen3-30B-A3B-Instruct-2507")
+
+# Initialize Clients
+translate_client = OpenAI(base_url=TRANSLATE_BASE_URL, api_key="no-key-required")
+judge_client = OpenAI(base_url=VLLM_BASE_URL, api_key="no-key-required")
+
+def translate_text(text, source_lang="en", target_lang="bn"):
+    """
+    Sends a single string to the Gemma translation endpoint.
+    """
+    # Note: If your local server supports batching natively in the completions call, 
+    # you can pass a list of messages. Otherwise, we loop within the batch processor.
+    try:
+        messages = [{
+            "role": "user",
+            "content": [
+                {
+                    "type": "text",
+                    "source_lang_code": source_lang,
+                    "target_lang_code": target_lang,
+                    "text": text,
+                }
+            ],
+        }]
+        
+        prompt = processor.apply_chat_template(
+                messages, tokenize=False, add_generation_prompt=True
+            )
+        
+        # Note: We assume the template application is handled by the server 
+        # or simplified here for the API call.
+        completion = translate_client.chat.completions.create(
+            model="translate_gemma",
+            messages=prompt,
+            temperature=0.1
+        )
+        return completion.choices[0].message.content.strip()
+    except Exception as e:
+        print(f"Translation error: {e}")
+        return None
+
+def judge_translation(original, translated):
+    """
+    Uses Qwen to check for hallucinations or mixed-language issues.
+    Returns True if passed, False otherwise.
+    """
+    prompt = f"""
+    You are a linguistic judge. Evaluate the following Bengali translation of an English medical text.
+    Check for:
+    1. Presence of any language other than Bengali or English medical terms.
+    2. Hallucinated keywords not present in the original.
+    
+    Original English: {original}
+    Translated Bengali: {translated}
+    
+    Does this translation pass? Respond with ONLY 'PASS' or 'FAIL'.
+    """
+    try:
+        response = judge_client.chat.completions.create(
+            model=JUDGE_MODEL,
+            messages=[{"role": "user", "content": prompt}],
+            max_tokens=5
+        )
+        result = response.choices[0].message.content.strip().upper()
+        return "PASS" in result
+    except Exception as e:
+        print(f"Judge error: {e}")
+        return True # Default to True to avoid getting stuck
+
+def process_batch(data_slice):
+    results = []
+    for record in data_slice:
+        # Translate Fulltext
+        bn_fulltext = translate_text(record['fulltext'])
+        # Translate Summary
+        bn_summary = translate_text(record['summary'])
+        
+        # Verify with Judge
+        is_valid_full = judge_translation(record['fulltext'], bn_fulltext)
+        is_valid_sum = judge_translation(record['summary'], bn_summary)
+        
+        record['translated_fulltext'] = bn_fulltext
+        record['translated_summary'] = bn_summary
+        record['judge_pass'] = is_valid_full and is_valid_sum
+        
+        results.append(record)
+    return results
+
+# ---- Main Execution ----
+def main():
+    # Load data
+    with open(DATA_PATH, 'r', encoding='utf-8') as f:
+        data = json.load(f)
+
+    # Slice data for (0_200) as per your filename
+    subset = data[0:200]
+    
+    translated_data = []
+    batch_size = 10 # Adjust based on your VRAM/Server capacity
+
+    print(f"Starting translation for {len(subset)} records...")
+    
+    for i in tqdm(range(0, len(subset), batch_size)):
+        batch = subset[i:i+batch_size]
+        processed_batch = process_batch(batch)
+        translated_data.extend(processed_batch)
+        
+        # Intermediate save to avoid data loss
+        os.makedirs(os.path.dirname(OUT_PATH), exist_ok=True)
+        with open(OUT_PATH, 'w', encoding='utf-8') as f:
+            json.dump(translated_data, f, ensure_ascii=False, indent=4)
+
+    print(f"Processing complete. Saved to {OUT_PATH}")
+
+if __name__ == "__main__":
+    main()
\ No newline at end of file
diff --git a/code/translation/misc/translate_multiclinsum_en2bn_v4.py b/code/translation/misc/translate_multiclinsum_en2bn_v4.py
new file mode 100644
index 0000000000000000000000000000000000000000..c2a4278c0f9262214fe31b4c3ece67e5e1c8cb89
--- /dev/null
+++ b/code/translation/misc/translate_multiclinsum_en2bn_v4.py
@@ -0,0 +1,143 @@
+import os
+import json
+import asyncio
+import httpx
+from tqdm.asyncio import tqdm
+from transformers import AutoProcessor
+
+# ---- Configuration ----
+DATA_PATH = "/home/mshahidul/readctrl/data/testing_data_gs/multiclinsum_gs_train_en.json"
+OUT_PATH = "/home/mshahidul/readctrl/data/translated_data/multiclinsum_gs_train_en2bn_gemma(0_200).json"
+
+TRANSLATE_URL = "http://localhost:8081/v1/chat/completions"
+JUDGE_URL = "http://localhost:8004/v1/chat/completions"
+CONCURRENCY_LIMIT = 8  # Matches your server's "-np" or "--parallel" value
+
+model_id = "google/translategemma-27b-it"
+processor = AutoProcessor.from_pretrained(model_id)
+
+semaphore = asyncio.Semaphore(CONCURRENCY_LIMIT)
+
+async def call_llm(client, url, model, messages, temperature=0.1, max_tokens=None):
+    """Generic async caller for both Translation and Judge."""
+    async with semaphore:
+        try:
+            payload = {
+                "model": model,
+                "messages": messages,
+                "temperature": temperature
+            }
+            if max_tokens is not None:
+                payload["max_tokens"] = max_tokens
+            response = await client.post(url, json=payload, timeout=60.0)
+            result = response.json()
+            return result['choices'][0]['message']['content'].strip()
+        except Exception as e:
+            return None
+
+def build_gemma_prompt(text, source_lang="en", target_lang="bn"):
+    messages = [{
+        "role": "user",
+        "content": [
+            {
+                "type": "text",
+                "source_lang_code": source_lang,
+                "target_lang_code": target_lang,
+                "text": text,
+            }
+        ],
+    }]
+    prompt = processor.apply_chat_template(
+        messages, tokenize=False, add_generation_prompt=True
+    )
+    messages=[{"role": "user", "content": prompt}]
+    return messages
+
+async def process_record(client, record):
+    """Translates and judges a single JSON record."""
+    # 1. Translate Fulltext & Summary
+    # (Using the prompt format your local server expects)
+    bn_fulltext_prompt = build_gemma_prompt(record['fulltext'])
+    bn_summary_prompt = build_gemma_prompt(record['summary'])
+    bn_fulltext = await call_llm(
+        client, TRANSLATE_URL, "translate_gemma", bn_fulltext_prompt, max_tokens=1024
+    )
+    bn_summary = await call_llm(
+        client, TRANSLATE_URL, "translate_gemma", bn_summary_prompt, max_tokens=512
+    )
+
+    # 2. Judge Phase
+    judge_prompt = f"""
+    You are a linguistic judge. Evaluate the following Bengali translation of an English medical text.
+    Check for:
+    1. Presence of any language other than Bengali or English medical terms.
+    2. Hallucinated keywords not present in the original.
+
+    Original English: {record['fulltext']}
+    Translated Bengali: {bn_fulltext} 
+
+    Does this translation pass? Respond with ONLY 'PASS' or 'FAIL'.
+    """
+    judge_pass = False
+    for _ in range(3):
+        judge_res = await call_llm(client, JUDGE_URL, "Qwen/Qwen3-30B-A3B-Instruct-2507", [
+            {"role": "user", "content": judge_prompt}
+        ])
+        judge_pass = "PASS" in (judge_res or "").upper()
+        if judge_pass:
+            break
+
+    if not judge_pass:
+        return None
+
+    record['translated_fulltext'] = bn_fulltext
+    record['translated_summary'] = bn_summary
+    record['judge_pass'] = True
+    return record
+
+def record_key(record):
+    record_id = record.get("id")
+    if record_id is not None:
+        return str(record_id)
+    return f"{record.get('fulltext', '')}||{record.get('summary', '')}"
+
+async def main():
+    with open(DATA_PATH, 'r', encoding='utf-8') as f:
+        data = json.load(f)[0:200]
+
+    async with httpx.AsyncClient() as client:
+        existing_results = []
+        if os.path.exists(OUT_PATH):
+            with open(OUT_PATH, 'r', encoding='utf-8') as f:
+                existing_results = json.load(f)
+
+        existing_by_key = {record_key(rec): rec for rec in existing_results}
+        output_results = []
+
+        batch_size = 10
+        for i in tqdm(range(0, len(data), batch_size)):
+            batch = data[i:i + batch_size]
+            pending = []
+            pending_keys = []
+
+            for rec in batch:
+                key = record_key(rec)
+                if key in existing_by_key:
+                    output_results.append(existing_by_key[key])
+                else:
+                    pending.append(process_record(client, rec))
+                    pending_keys.append(key)
+
+            if pending:
+                processed = await asyncio.gather(*pending)
+                for key, rec in zip(pending_keys, processed):
+                    if rec is not None:
+                        existing_by_key[key] = rec
+                        output_results.append(rec)
+
+            os.makedirs(os.path.dirname(OUT_PATH), exist_ok=True)
+            with open(OUT_PATH, 'w', encoding='utf-8') as f:
+                json.dump(output_results, f, ensure_ascii=False, indent=4)
+
+if __name__ == "__main__":
+    asyncio.run(main())
\ No newline at end of file
diff --git a/code/translation/misc/translate_test.py b/code/translation/misc/translate_test.py
new file mode 100644
index 0000000000000000000000000000000000000000..d6008996d2f876ff52760e63a6242bfaa8251215
--- /dev/null
+++ b/code/translation/misc/translate_test.py
@@ -0,0 +1,34 @@
+import os
+import json
+os.environ["CUDA_DEVICE_ORDER"] = "PCI_BUS_ID"
+os.environ["CUDA_VISIBLE_DEVICES"] = "2"
+import torch
+from transformers import AutoModelForImageTextToText, AutoProcessor
+
+model_id = "google/translategemma-27b-it"
+processor = AutoProcessor.from_pretrained(model_id)
+# model = AutoModelForImageTextToText.from_pretrained(model_id, device_map="auto")
+
+
+# ---- Text Translation ----
+messages = [
+    {
+        "role": "user",
+        "content": [
+            {
+                "type": "text",
+                "source_lang_code": "cs",
+                "target_lang_code": "de-DE",
+                "text": "V nejhorším případě i k prasknutí čočky.",
+            }
+        ],
+    }
+]
+
+inputs = processor.apply_chat_template(
+    messages, tokenize=False, add_generation_prompt=True, return_dict=True, return_tensors="pt"
+)
+
+
+
+print(inputs)
diff --git a/code/translation/retranslate_fulltext_by_index_or_id.py b/code/translation/retranslate_fulltext_by_index_or_id.py
new file mode 100644
index 0000000000000000000000000000000000000000..671fae5355c1238ad8003b559ea5d9195710aa24
--- /dev/null
+++ b/code/translation/retranslate_fulltext_by_index_or_id.py
@@ -0,0 +1,212 @@
+import argparse
+import json
+from pathlib import Path
+from typing import Any
+
+from openai import OpenAI
+
+
+PROMPT_PATH = Path("/home/mshahidul/readctrl/prompts/translation_prompt.txt")
+API_KEY_PATH = Path("/home/mshahidul/api_new.json")
+
+
+def parse_csv_list(raw: str) -> list[str]:
+    if not raw:
+        return []
+    return [part.strip() for part in raw.split(",") if part.strip()]
+
+
+def parse_indices(raw: str) -> list[int]:
+    out: list[int] = []
+    for part in parse_csv_list(raw):
+        try:
+            out.append(int(part))
+        except ValueError as exc:
+            raise ValueError(f"Invalid index '{part}'. Indices must be integers.") from exc
+    return out
+
+
+def load_json(path: Path) -> Any:
+    with path.open("r", encoding="utf-8") as f:
+        return json.load(f)
+
+
+def save_json(path: Path, data: Any) -> None:
+    with path.open("w", encoding="utf-8") as f:
+        json.dump(data, f, indent=2, ensure_ascii=False)
+
+
+def build_prompt(
+    prompt_template: str,
+    medical_text: str,
+    source_language: str,
+    target_language: str,
+) -> str:
+    return (
+        prompt_template.replace("<MEDICAL_TEXT>", medical_text)
+        .replace("<SOURCE_LANGUAGE>", source_language)
+        .replace("<TARGET_LANGUAGE>", target_language)
+    )
+
+
+def translate_text(
+    client: OpenAI,
+    prompt: str,
+    model: str = "gpt-5",
+) -> str | None:
+    try:
+        response = client.chat.completions.create(
+            model=model,
+            messages=[
+                {
+                    "role": "system",
+                    "content": "You are a helpful assistant that outputs only valid JSON.",
+                },
+                {"role": "user", "content": prompt},
+            ],
+            response_format={"type": "json_object"},
+        )
+        content = response.choices[0].message.content.strip()
+        cleaned = content.replace("```json", "").replace("```", "").strip()
+        parsed = json.loads(cleaned)
+        if isinstance(parsed, dict):
+            return parsed.get("translated_medical_note")
+        return None
+    except Exception as exc:
+        print(f"[WARN] API/parsing error: {exc}")
+        return None
+
+
+def get_target_positions(
+    data: list[dict[str, Any]],
+    target_indices: set[int],
+    target_ids: set[str],
+) -> list[int]:
+    positions: set[int] = set()
+
+    # Match by array position and by item["index"].
+    for pos, item in enumerate(data):
+        if pos in target_indices:
+            positions.add(pos)
+        item_index = item.get("index")
+        if isinstance(item_index, int) and item_index in target_indices:
+            positions.add(pos)
+
+    # Match by item["id"].
+    for pos, item in enumerate(data):
+        item_id = item.get("id")
+        if item_id is not None and str(item_id) in target_ids:
+            positions.add(pos)
+
+    return sorted(positions)
+
+
+def main() -> None:
+    parser = argparse.ArgumentParser(
+        description=(
+            "Retranslate selected records' fulltext using gpt-5, "
+            "selected by array index/item index and/or id."
+        )
+    )
+    parser.add_argument(
+        "--input",
+        required=True,
+        help="Path to JSON file (list of records).",
+    )
+    parser.add_argument(
+        "--output",
+        default=None,
+        help="Optional output path. Defaults to in-place overwrite of --input.",
+    )
+    parser.add_argument(
+        "--indices",
+        default="36,40,44,48",
+        help="Comma-separated list of indices (e.g., 36,40,44,48).",
+    )
+    parser.add_argument(
+        "--ids",
+        default="",
+        help='Comma-separated list of ids (e.g., "a.txt,b.txt").',
+    )
+    parser.add_argument(
+        "--source-language",
+        default="English",
+        help="Source language name for prompt replacement.",
+    )
+    parser.add_argument(
+        "--target-language",
+        default="Bengali",
+        help="Target language name for prompt replacement.",
+    )
+    parser.add_argument(
+        "--model",
+        default="gpt-5",
+        help="OpenAI model name (default: gpt-5).",
+    )
+    parser.add_argument(
+        "--save-every",
+        type=int,
+        default=1,
+        help="Incremental save frequency in processed items (default: 1).",
+    )
+    args = parser.parse_args()
+
+    input_path = Path(args.input)
+    output_path = Path(args.output) if args.output else input_path
+
+    data = load_json(input_path)
+    if not isinstance(data, list):
+        raise ValueError("Input JSON must be a list of records.")
+
+    indices = set(parse_indices(args.indices))
+    ids = set(parse_csv_list(args.ids))
+    if not indices and not ids:
+        raise ValueError("Provide at least one selector: --indices and/or --ids.")
+
+    prompt_template = PROMPT_PATH.read_text(encoding="utf-8")
+    api_keys = load_json(API_KEY_PATH)
+    openai_api_key = api_keys["openai"]
+    client = OpenAI(api_key=openai_api_key)
+
+    target_positions = get_target_positions(data, indices, ids)
+    if not target_positions:
+        print("No matching records found for provided indices/ids.")
+        return
+
+    print(f"Matched {len(target_positions)} record(s): {target_positions}")
+    processed = 0
+
+    for pos in target_positions:
+        item = data[pos]
+        fulltext = item.get("fulltext")
+        if not isinstance(fulltext, str) or not fulltext.strip():
+            print(f"[SKIP] pos={pos} id={item.get('id')} has empty fulltext.")
+            continue
+
+        prompt = build_prompt(
+            prompt_template=prompt_template,
+            medical_text=fulltext,
+            source_language=args.source_language,
+            target_language=args.target_language,
+        )
+        translated = translate_text(client=client, prompt=prompt, model=args.model)
+        if translated is None:
+            print(f"[WARN] pos={pos} id={item.get('id')} translation failed.")
+            continue
+
+        item["translated_fulltext"] = translated
+        processed += 1
+        print(f"[OK] pos={pos} id={item.get('id')} translated_fulltext updated.")
+
+        if processed % max(args.save_every, 1) == 0:
+            save_json(output_path, data)
+            print(f"[SAVE] Incremental save after {processed} item(s) -> {output_path}")
+
+    save_json(output_path, data)
+    print(f"Done. Total updated records: {processed}. Saved to: {output_path}")
+
+
+if __name__ == "__main__":
+    main()
+
+
diff --git a/code/translation/translate_Gemma.py b/code/translation/translate_Gemma.py
new file mode 100644
index 0000000000000000000000000000000000000000..ef7268bf8e3d12e5322038d8fcc5b83d5ae250df
--- /dev/null
+++ b/code/translation/translate_Gemma.py
@@ -0,0 +1,38 @@
+from openai import OpenAI
+
+# Initialize client pointing to your local server
+client = OpenAI(base_url="http://localhost:8081/v1", api_key="no-key-required")
+# messages = [
+#     {
+#         "role": "user",
+#         "content": "Translate the following text from English to Bengali:\n\nA 20-year-old woman was followed up since the age of eight for idiopathic NS inaugurated by cerebral venous thrombosis extended to the right jugular vein with a massive pulmonary embolism. The patient did not have any sequelae. She had no other medical or surgical history. A family history of thrombosis has not been reported. The patient was not biopsied because she had no kidney failure nor gross hematuria, or hypertension at first presentation; added to that, she had no extra renal signs suggestive of a secondary nephrotic syndrome. She was accordingly put on anticoagulant therapy (Oral vitamin K antagonist) and oral corticosteroid therapy with good evolution. Thereafter, the patient received several cures of high-dose corticosteroids for steroid-dependent relapses of NS. She was, hence, put on mycophenolate mofetil (MMF) as a background therapy to avoid corticosteroids and ensure normal growth. An exhaustive assessment of thrombophilia was performed and did not show any abnormality. Homocysteine rate, blood fibrinogen rate, Protein C, protein S, antithrombin III, factor V Leiden mutation, JAK-2 mutation, cryoglobulins, anticardiolipin antibodies, lupus anticoagulant and beta-1-glycoprotein antibodies were normal. The anticoagulant treatment was stopped after nine years. The evolution was enameled by the occurrence of several relapses of her disease controlled by oral corticosteroid therapy. Remission of NS has been noted since 2017, so MMF was gradually stopped in 2019 and the patient remained asymptomatic and without any relapse.\n\nOne year later, the patient came up to our emergency department for acute intense diffuse abdominal pain without any particular irradiation associated with postprandial vomiting and bilateral lower limb edema for the last six hours. The physical examination revealed an intense epigastric tenderness with normal vital signs (arterial pressure of 120/70 mm Hg, heart rate of 83 bpm, and oxygen saturation at 100% on room air). The patient was afebrile with normal consciousness. The rest of the physical examination was unremarkable. The urinalysis with labstix revealed proteinuria. The hemogasanalysis results showed metabolic acidosis with respiratory compensation. Further laboratory tests revealed hypoalbuminemia, hypercholesterolemia, a prothrombin time at 90%, high levels of D-dimer, lactate dehydrogenase, and creatine phosphokinase as well as a biological inflammatory syndrome with a CRP of 37 mg/L, and leucocytosis at 26.4 x 103/µL. Renal and liver functions were normal.\n\nThe patient was hospitalized in an intensive care unit with close monitoring of vital signs and initiation of resuscitation measures. An abdominal ultrasound was performed urgently showing an intra-abdominal effusion of low to moderate abundance. An abdominal CT scan revealed acute thrombosis of the superior mesenteric artery with acute mesenteric ischemia. The patient was immediately routed to the operating room. Intraoperative exploration confirmed mesenteric ischemia with extensive necrosis of almost entirely of the small bowel making their resections incompatible with life shown in Figure 3. The patient died after 48 hours."
+#     }
+# ]
+messages = [
+    {
+        "role": "user",
+        "content": [
+            {
+                "type": "text",
+                "source_lang_code": "cs",
+                "target_lang_code": "de-DE",
+                "text": "V nejhorším případě i k prasknutí čočky.",
+            }
+        ],
+    }
+]
+
+
+
+completion = client.chat.completions.create(
+    model="translate_gemma",
+    messages=messages,
+    stream=False
+)
+
+print(completion.choices[0].message.content)
+
+# for chunk in completion:
+#     if chunk.choices[0].delta.content:
+#         print(chunk.choices[0].delta.content, end="", flush=True)
+# print()
\ No newline at end of file
diff --git a/code/translation/translate_correction_gpt5.py b/code/translation/translate_correction_gpt5.py
new file mode 100644
index 0000000000000000000000000000000000000000..6270cb30c4efa85fbfa903594326559a7b4e6f18
--- /dev/null
+++ b/code/translation/translate_correction_gpt5.py
@@ -0,0 +1,200 @@
+#!/usr/bin/env python3
+import argparse
+import json
+import os
+import re
+import time
+from typing import Dict, Any, Tuple
+
+from openai import OpenAI
+from tqdm import tqdm
+
+
+def load_prompt_template(path: str) -> str:
+    with open(path, "r", encoding="utf-8") as f:
+        return f.read()
+
+
+def load_api_key_from_json(path: str, key_name: str) -> str:
+    with open(path, "r", encoding="utf-8") as f:
+        data = json.load(f)
+    api_key = data.get(key_name, "")
+    if not api_key:
+        raise SystemExit(f"API key '{key_name}' not found in {path}.")
+    return api_key
+
+
+def build_prompt(template: str, src_text: str, target_language: str, target_translation: str) -> str:
+    return (
+        template.replace("{SRC_TEXT}", src_text)
+        .replace("{TARGET_LANGUAGE}", target_language)
+        .replace("{TARGET_TRANSLATION}", target_translation)
+    )
+
+
+def extract_json(text: str) -> Dict[str, Any]:
+    try:
+        return json.loads(text)
+    except json.JSONDecodeError:
+        match = re.search(r"\{.*\}", text, re.DOTALL)
+        if not match:
+            raise
+        return json.loads(match.group(0))
+
+
+def call_gpt5(client: OpenAI, model: str, prompt: str, max_retries: int = 5) -> Dict[str, Any]:
+    last_err = None
+    for attempt in range(1, max_retries + 1):
+        try:
+            resp = client.responses.create(
+                model=model,
+                input=[{"role": "user", "content": prompt}],
+            )
+            return extract_json(resp.output_text)
+        except Exception as err:
+            last_err = err
+            sleep_s = min(2 ** attempt, 30)
+            time.sleep(sleep_s)
+    raise last_err
+
+
+def process_record(
+    client: OpenAI,
+    model: str,
+    template: str,
+    target_language: str,
+    record: Dict[str, Any],
+    src_key: str,
+    tgt_key: str,
+    out_key: str,
+) -> Tuple[str, Dict[str, Any]]:
+    src_text = record.get(src_key, "")
+    tgt_text = record.get(tgt_key, "")
+    if not src_text or not tgt_text:
+        return out_key, {"translated_text": tgt_text}
+    prompt = build_prompt(template, src_text, target_language, tgt_text)
+    return out_key, call_gpt5(client, model, prompt)
+
+
+def write_batch(output_dir: str, base_name: str, batch_start: int, batch_end: int, batch: list) -> None:
+    os.makedirs(output_dir, exist_ok=True)
+    out_name = f"{base_name}_{batch_start:04d}_{batch_end - 1:04d}.json"
+    out_path = os.path.join(output_dir, out_name)
+    with open(out_path, "w", encoding="utf-8") as out_f:
+        json.dump(batch, out_f, ensure_ascii=False, indent=2)
+
+
+def main() -> None:
+    parser = argparse.ArgumentParser(description="GPT-5 translation correction runner")
+    parser.add_argument(
+        "--input",
+        default="/home/mshahidul/readctrl/data/translated_data/translation_wo_judge/multiclinsum_gs_train_en2bn_gemma(0_200).json",
+        help="Path to input JSON file",
+    )
+    parser.add_argument(
+        "--output-dir",
+        default="/home/mshahidul/readctrl/data/translated_data/dataset_correction_gpt5",
+        help="Output directory (writes one file per 2 instances)",
+    )
+    parser.add_argument(
+        "--batch-size",
+        type=int,
+        default=2,
+        help="Number of instances per output file",
+    )
+    parser.add_argument(
+        "--prompt",
+        default="/home/mshahidul/readctrl/prompts/translation_correction_prompt",
+        help="Path to prompt template",
+    )
+    parser.add_argument(
+        "--target-language",
+        default="Bengali",
+        help="Target language name",
+    )
+    parser.add_argument(
+        "--model",
+        default="gpt-5",
+        help="OpenAI model name",
+    )
+    parser.add_argument(
+        "--api-json",
+        default="/home/mshahidul/api_new.json",
+        help="Path to JSON file containing API keys",
+    )
+    parser.add_argument(
+        "--api-json-key",
+        default="openai",
+        help="Key name inside the JSON file",
+    )
+    parser.add_argument(
+        "--start",
+        type=int,
+        default=0,
+        help="Start index (0-based)",
+    )
+    parser.add_argument(
+        "--end",
+        type=int,
+        default=None,
+        help="End index (exclusive)",
+    )
+    args = parser.parse_args()
+
+    api_key = os.getenv("OPENAI_API_KEY")
+    if not api_key:
+        api_key = load_api_key_from_json(args.api_json, args.api_json_key)
+    client = OpenAI(api_key=api_key)
+
+    with open(args.input, "r", encoding="utf-8") as f:
+        data = json.load(f)
+
+    template = load_prompt_template(args.prompt)
+
+    src_map = {
+        "translated_fulltext": "fulltext",
+        "translated_summary": "summary",
+    }
+    out_map = {
+        "translated_fulltext": "corrected_translated_fulltext",
+        "translated_summary": "corrected_translated_summary",
+    }
+
+    start = args.start
+    end = args.end if args.end is not None else len(data)
+
+    base_name = os.path.splitext(os.path.basename(args.input))[0]
+    batch_start = start
+    batch = []
+
+    for idx in tqdm(range(start, min(end, len(data))), desc="Processing", unit="item"):
+        record = data[idx]
+        for tgt_key, src_key in src_map.items():
+            out_key = out_map[tgt_key]
+            if out_key in record:
+                continue
+            out_key, result = process_record(
+                client,
+                args.model,
+                template,
+                args.target_language,
+                record,
+                src_key,
+                tgt_key,
+                out_key,
+            )
+            record[out_key] = result.get("translated_text", record.get(tgt_key, ""))
+
+        batch.append(record)
+
+        if len(batch) >= args.batch_size:
+            write_batch(args.output_dir, base_name, batch_start, idx + 1, batch)
+            batch = []
+            batch_start = idx + 1
+
+    if batch:
+        write_batch(args.output_dir, base_name, batch_start, min(end, len(data)), batch)
+
+
+if __name__ == "__main__":
+    main()
diff --git a/code/translation/translate_multiclinsum_all_lang_judge_strict.py b/code/translation/translate_multiclinsum_all_lang_judge_strict.py
new file mode 100644
index 0000000000000000000000000000000000000000..183ce11c4d001c77e2da1cd343af5a382ef8e4a6
--- /dev/null
+++ b/code/translation/translate_multiclinsum_all_lang_judge_strict.py
@@ -0,0 +1,187 @@
+import os
+import json
+import asyncio
+import argparse
+import httpx
+from tqdm.asyncio import tqdm
+from transformers import AutoProcessor
+
+# ---- Configuration ----
+DATA_PATH = "/home/mshahidul/readctrl/data/testing_data_gs/multiclinsum_gs_train_en.json"
+OUT_PATH_TEMPLATE = (
+    "/home/mshahidul/readctrl/data/translated_data/"
+    "multiclinsum_gs_train_{source_lang}2{target_lang}_gemma(0_200).json"
+)
+
+TRANSLATE_URL = "http://localhost:8081/v1/chat/completions"
+JUDGE_URL = "http://localhost:8004/v1/chat/completions"
+CONCURRENCY_LIMIT = 8  # Matches your server's "-np" or "--parallel" value
+
+model_id = "google/translategemma-27b-it"
+processor = AutoProcessor.from_pretrained(model_id)
+
+semaphore = asyncio.Semaphore(CONCURRENCY_LIMIT)
+
+async def call_llm(client, url, model, messages, temperature=0.1, max_tokens=None):
+    """Generic async caller for both Translation and Judge."""
+    async with semaphore:
+        try:
+            payload = {
+                "model": model,
+                "messages": messages,
+                "temperature": temperature
+            }
+            if max_tokens is not None:
+                payload["max_tokens"] = max_tokens
+            response = await client.post(url, json=payload, timeout=60.0)
+            result = response.json()
+            return result['choices'][0]['message']['content'].strip()
+        except Exception as e:
+            return None
+
+def build_gemma_prompt(text, source_lang="en", target_lang="bn"):
+    messages = [{
+        "role": "user",
+        "content": [
+            {
+                "type": "text",
+                "source_lang_code": source_lang,
+                "target_lang_code": target_lang,
+                "text": text,
+            }
+        ],
+    }]
+    prompt = processor.apply_chat_template(
+        messages, tokenize=False, add_generation_prompt=True
+    )
+    messages=[{"role": "user", "content": prompt}]
+    return messages
+
+def describe_lang(code):
+    lang_names = {
+        "en": "English",
+        "bn": "Bengali",
+        "zh": "Chinese",
+        "vi": "Vietnamese",
+        "hi": "Hindi"
+    }
+    return lang_names.get(code, "Unknown Language")
+
+async def process_record(client, record, source_lang, target_lang):
+    """Translates and judges a single JSON record."""
+    # 1. Translate Fulltext & Summary
+    # (Using the prompt format your local server expects)
+    translated_fulltext_prompt = build_gemma_prompt(
+        record['fulltext'], source_lang=source_lang, target_lang=target_lang
+    )
+    translated_summary_prompt = build_gemma_prompt(
+        record['summary'], source_lang=source_lang, target_lang=target_lang
+    )
+    translated_fulltext = await call_llm(
+        client, TRANSLATE_URL, "translate_gemma", translated_fulltext_prompt, max_tokens=1024
+    )
+    translated_summary = await call_llm(
+        client, TRANSLATE_URL, "translate_gemma", translated_summary_prompt, max_tokens=512
+    )
+
+    # 2. Judge Phase
+    source_lang_label = describe_lang(source_lang)
+    target_lang_label = describe_lang(target_lang)
+    judge_prompt = f"""
+    You are a strict linguistic judge. Evaluate the {target_lang_label} translation of a
+    {source_lang_label} medical text and summary.
+
+    Rules (FAIL if any rule is violated):
+    1. The translation must be entirely in {target_lang_label} script, except for:
+       - Standard medical abbreviations (e.g., ICU, HIV), numeric values, and units.
+       - English medical words or keywords that are present in the original text.
+       - Proper nouns that must remain in {source_lang_label}.
+    2. No words from any other language (e.g., Hindi/Arabic/Chinese) are allowed.
+    3. No mixed-script words (e.g., combining Latin + {target_lang_label} in one word).
+    4. No hallucinated keywords not present in the original.
+
+    Original {source_lang_label} Fulltext: {record['fulltext']}
+    Translated {target_lang_label} Fulltext: {translated_fulltext}
+
+    Original {source_lang_label} Summary: {record['summary']}
+    Translated {target_lang_label} Summary: {translated_summary}
+
+    Does this translation pass? Respond with ONLY 'PASS' or 'FAIL'.
+    """
+    judge_pass = False
+    for _ in range(3):
+        judge_res = await call_llm(client, JUDGE_URL, "Qwen/Qwen3-30B-A3B-Instruct-2507", [
+            {"role": "user", "content": judge_prompt}
+        ], max_tokens=200)
+        judge_pass = "PASS" in (judge_res or "").upper()
+        if judge_pass:
+            break
+
+    if not judge_pass:
+        return None
+
+    record['translated_fulltext'] = translated_fulltext
+    record['translated_summary'] = translated_summary
+    record['judge_pass'] = True
+    return record
+
+def record_key(record):
+    record_id = record.get("id")
+    if record_id is not None:
+        return str(record_id)
+    return f"{record.get('fulltext', '')}||{record.get('summary', '')}"
+
+async def main():
+    parser = argparse.ArgumentParser(description="Translate Multiclinsum dataset.")
+    parser.add_argument("--source-lang", default="en", help="Source language code")
+    parser.add_argument("--target-lang", default="bn", help="Target language code")
+    args = parser.parse_args()
+
+    out_path = OUT_PATH_TEMPLATE.format(
+        source_lang=args.source_lang, target_lang=args.target_lang
+    )
+
+    with open(DATA_PATH, 'r', encoding='utf-8') as f:
+        data = json.load(f)[0:200]
+
+    async with httpx.AsyncClient() as client:
+        existing_results = []
+        if os.path.exists(out_path):
+            with open(out_path, 'r', encoding='utf-8') as f:
+                existing_results = json.load(f)
+
+        existing_by_key = {record_key(rec): rec for rec in existing_results}
+        output_results = []
+
+        batch_size = 10
+        for i in tqdm(range(0, len(data), batch_size)):
+            batch = data[i:i + batch_size]
+            pending = []
+            pending_keys = []
+            new_generated = 0
+
+            for rec in batch:
+                key = record_key(rec)
+                if key in existing_by_key:
+                    output_results.append(existing_by_key[key])
+                else:
+                    pending.append(process_record(client, rec, args.source_lang, args.target_lang))
+                    pending_keys.append(key)
+
+            if pending:
+                processed = await asyncio.gather(*pending)
+                for key, rec in zip(pending_keys, processed):
+                    if rec is not None:
+                        existing_by_key[key] = rec
+                        output_results.append(rec)
+                        new_generated += 1
+
+            os.makedirs(os.path.dirname(out_path), exist_ok=True)
+            with open(out_path, 'w', encoding='utf-8') as f:
+                json.dump(output_results, f, ensure_ascii=False, indent=4)
+            print(
+                f"Batch {i // batch_size + 1}: new={new_generated}, total={len(output_results)}"
+            )
+
+if __name__ == "__main__":
+    asyncio.run(main())
\ No newline at end of file
diff --git a/code/translation/translate_multiclinsum_all_lang_judge_strict_v2.py b/code/translation/translate_multiclinsum_all_lang_judge_strict_v2.py
new file mode 100644
index 0000000000000000000000000000000000000000..f3362b59130ecbead097f23d95479f08f494235f
--- /dev/null
+++ b/code/translation/translate_multiclinsum_all_lang_judge_strict_v2.py
@@ -0,0 +1,151 @@
+import os
+import json
+import asyncio
+import argparse
+import httpx
+from tqdm.asyncio import tqdm
+from transformers import AutoProcessor
+
+# ---- Configuration ----
+DATA_PATH = "/home/mshahidul/readctrl/data/testing_data_gs/multiclinsum_gs_train_en.json"
+OUT_PATH_TEMPLATE = (
+    "/home/mshahidul/readctrl/data/translated_data/translation_wo_judge_v2/"
+    "multiclinsum_gs_train_{source_lang}2{target_lang}_gemma(0_200).json"
+)
+
+TRANSLATE_URL = "http://172.16.34.29:8081/v1/chat/completions"
+CONCURRENCY_LIMIT = 8  # Matches your server's "-np" or "--parallel" value
+
+model_id = "google/translategemma-27b-it"
+processor = AutoProcessor.from_pretrained(model_id)
+
+semaphore = asyncio.Semaphore(CONCURRENCY_LIMIT)
+
+async def call_llm(client, url, model, messages, temperature=0.1, max_tokens=None):
+    """Generic async caller for both Translation and Judge."""
+    async with semaphore:
+        try:
+            payload = {
+                "model": model,
+                "messages": messages,
+                "temperature": temperature
+            }
+            if max_tokens is not None:
+                payload["max_tokens"] = max_tokens
+            response = await client.post(url, json=payload, timeout=60.0)
+            result = response.json()
+            return result['choices'][0]['message']['content'].strip()
+        except Exception as e:
+            return None
+
+def build_gemma_prompt(text, source_lang="en", target_lang="bn"):
+    messages = [{
+        "role": "user",
+        "content": [
+            {
+                "type": "text",
+                "source_lang_code": source_lang,
+                "target_lang_code": target_lang,
+                "text": text,
+            }
+        ],
+    }]
+    prompt = processor.apply_chat_template(
+        messages, tokenize=False, add_generation_prompt=True
+    )
+    messages=[{"role": "user", "content": prompt}]
+    return messages
+
+async def process_record(client, record, source_lang, target_lang):
+    """Translates a single JSON record."""
+    # 1. Translate Fulltext & Summary
+    # (Using the prompt format your local server expects)
+    translated_fulltext_prompt = build_gemma_prompt(
+        record['fulltext'], source_lang=source_lang, target_lang=target_lang
+    )
+    translated_summary_prompt = build_gemma_prompt(
+        record['summary'], source_lang=source_lang, target_lang=target_lang
+    )
+    translated_fulltext = await call_llm(
+        client, TRANSLATE_URL, "translate_gemma", translated_fulltext_prompt, max_tokens=4092
+    )
+    translated_summary = await call_llm(
+        client, TRANSLATE_URL, "translate_gemma", translated_summary_prompt, max_tokens=1024
+    )
+
+    record['translated_fulltext'] = translated_fulltext
+    record['translated_summary'] = translated_summary
+    return record
+
+def record_key(record):
+    record_id = record.get("id")
+    if record_id is not None:
+        return str(record_id)
+    return f"{record.get('fulltext', '')}||{record.get('summary', '')}"
+
+def has_valid_translation(record):
+    translated_fulltext = record.get("translated_fulltext")
+    translated_summary = record.get("translated_summary")
+    return translated_fulltext is not None and translated_summary is not None
+
+async def main():
+    parser = argparse.ArgumentParser(description="Translate Multiclinsum dataset.")
+    parser.add_argument("--source-lang", default="en", help="Source language code")
+    parser.add_argument("--target-lang", default="bn", help="Target language code")
+    args = parser.parse_args()
+
+    out_path = OUT_PATH_TEMPLATE.format(
+        source_lang=args.source_lang, target_lang=args.target_lang
+    )
+
+    with open(DATA_PATH, 'r', encoding='utf-8') as f:
+        data = json.load(f)[0:80]
+
+    async with httpx.AsyncClient() as client:
+        existing_results = []
+        if os.path.exists(out_path):
+            with open(out_path, 'r', encoding='utf-8') as f:
+                existing_results = json.load(f)
+
+        existing_by_key = {record_key(rec): rec for rec in existing_results}
+        output_results = []
+
+        batch_size = 10
+        max_regen = 80
+        regenerated = 0
+        for i in tqdm(range(0, len(data), batch_size)):
+            batch = data[i:i + batch_size]
+            pending = []
+            pending_keys = []
+            new_generated = 0
+
+            for rec in batch:
+                key = record_key(rec)
+                existing = existing_by_key.get(key)
+                if existing and has_valid_translation(existing):
+                    output_results.append(existing)
+                else:
+                    if regenerated < max_regen:
+                        pending.append(process_record(client, rec, args.source_lang, args.target_lang))
+                        pending_keys.append(key)
+                        regenerated += 1
+                    elif existing:
+                        output_results.append(existing)
+
+            if pending:
+                processed = await asyncio.gather(*pending)
+                for key, rec in zip(pending_keys, processed):
+                    if rec is not None:
+                        existing_by_key[key] = rec
+                        output_results.append(rec)
+                        new_generated += 1
+
+            os.makedirs(os.path.dirname(out_path), exist_ok=True)
+            with open(out_path, 'w', encoding='utf-8') as f:
+                json.dump(output_results, f, ensure_ascii=False, indent=4)
+            print(
+                f"Batch {i // batch_size + 1}: new={new_generated}, total={len(output_results)}"
+            )
+
+if __name__ == "__main__":
+    asyncio.run(main())
\ No newline at end of file
diff --git a/code/translation/translate_multiclinsum_all_lang_v5.py b/code/translation/translate_multiclinsum_all_lang_v5.py
new file mode 100644
index 0000000000000000000000000000000000000000..30d06a1618e9da76acc3d341895178339dc3b5ce
--- /dev/null
+++ b/code/translation/translate_multiclinsum_all_lang_v5.py
@@ -0,0 +1,172 @@
+import os
+import json
+import asyncio
+import argparse
+import httpx
+from tqdm.asyncio import tqdm
+from transformers import AutoProcessor
+
+# ---- Configuration ----
+DATA_PATH = "/home/mshahidul/readctrl/data/testing_data_gs/multiclinsum_gs_train_en.json"
+OUT_PATH_TEMPLATE = (
+    "/home/mshahidul/readctrl/data/translated_data/"
+    "multiclinsum_gs_train_{source_lang}2{target_lang}_gemma(0_200).json"
+)
+
+TRANSLATE_URL = "http://localhost:8081/v1/chat/completions"
+JUDGE_URL = "http://localhost:8004/v1/chat/completions"
+CONCURRENCY_LIMIT = 8  # Matches your server's "-np" or "--parallel" value
+
+model_id = "google/translategemma-27b-it"
+processor = AutoProcessor.from_pretrained(model_id)
+
+semaphore = asyncio.Semaphore(CONCURRENCY_LIMIT)
+
+async def call_llm(client, url, model, messages, temperature=0.1, max_tokens=None):
+    """Generic async caller for both Translation and Judge."""
+    async with semaphore:
+        try:
+            payload = {
+                "model": model,
+                "messages": messages,
+                "temperature": temperature
+            }
+            if max_tokens is not None:
+                payload["max_tokens"] = max_tokens
+            response = await client.post(url, json=payload, timeout=60.0)
+            result = response.json()
+            return result['choices'][0]['message']['content'].strip()
+        except Exception as e:
+            return None
+
+def build_gemma_prompt(text, source_lang="en", target_lang="bn"):
+    messages = [{
+        "role": "user",
+        "content": [
+            {
+                "type": "text",
+                "source_lang_code": source_lang,
+                "target_lang_code": target_lang,
+                "text": text,
+            }
+        ],
+    }]
+    prompt = processor.apply_chat_template(
+        messages, tokenize=False, add_generation_prompt=True
+    )
+    messages=[{"role": "user", "content": prompt}]
+    return messages
+
+def describe_lang(code):
+    lang_names = {
+        "en": "English",
+        "bn": "Bengali",
+        "zh": "Chinese",
+        "vi": "Vietnamese",
+        "hi": "Hindi"
+    }
+    return lang_names.get(code, "Unknown Language")
+
+async def process_record(client, record, source_lang, target_lang):
+    """Translates and judges a single JSON record."""
+    # 1. Translate Fulltext & Summary
+    # (Using the prompt format your local server expects)
+    translated_fulltext_prompt = build_gemma_prompt(
+        record['fulltext'], source_lang=source_lang, target_lang=target_lang
+    )
+    translated_summary_prompt = build_gemma_prompt(
+        record['summary'], source_lang=source_lang, target_lang=target_lang
+    )
+    translated_fulltext = await call_llm(
+        client, TRANSLATE_URL, "translate_gemma", translated_fulltext_prompt, max_tokens=1024
+    )
+    translated_summary = await call_llm(
+        client, TRANSLATE_URL, "translate_gemma", translated_summary_prompt, max_tokens=512
+    )
+
+    # 2. Judge Phase
+    source_lang_label = describe_lang(source_lang)
+    target_lang_label = describe_lang(target_lang)
+    judge_prompt = f"""
+    You are a linguistic judge. Evaluate the following {target_lang_label} translation of a {source_lang_label} medical text.
+    Check for:
+    1. Presence of any language other than {target_lang_label} or {source_lang_label} medical terms.
+    2. Hallucinated keywords not present in the original.
+
+    Original {source_lang_label}: {record['fulltext']}
+    Translated {target_lang_label}: {translated_fulltext} 
+
+    Does this translation pass? Respond with ONLY 'PASS' or 'FAIL'.
+    """
+    judge_pass = False
+    for _ in range(3):
+        judge_res = await call_llm(client, JUDGE_URL, "Qwen/Qwen3-30B-A3B-Instruct-2507", [
+            {"role": "user", "content": judge_prompt}
+        ])
+        judge_pass = "PASS" in (judge_res or "").upper()
+        if judge_pass:
+            break
+
+    if not judge_pass:
+        return None
+
+    record['translated_fulltext'] = translated_fulltext
+    record['translated_summary'] = translated_summary
+    record['judge_pass'] = True
+    return record
+
+def record_key(record):
+    record_id = record.get("id")
+    if record_id is not None:
+        return str(record_id)
+    return f"{record.get('fulltext', '')}||{record.get('summary', '')}"
+
+async def main():
+    parser = argparse.ArgumentParser(description="Translate Multiclinsum dataset.")
+    parser.add_argument("--source-lang", default="en", help="Source language code")
+    parser.add_argument("--target-lang", default="bn", help="Target language code")
+    args = parser.parse_args()
+
+    out_path = OUT_PATH_TEMPLATE.format(
+        source_lang=args.source_lang, target_lang=args.target_lang
+    )
+
+    with open(DATA_PATH, 'r', encoding='utf-8') as f:
+        data = json.load(f)[0:200]
+
+    async with httpx.AsyncClient() as client:
+        existing_results = []
+        if os.path.exists(out_path):
+            with open(out_path, 'r', encoding='utf-8') as f:
+                existing_results = json.load(f)
+
+        existing_by_key = {record_key(rec): rec for rec in existing_results}
+        output_results = []
+
+        batch_size = 10
+        for i in tqdm(range(0, len(data), batch_size)):
+            batch = data[i:i + batch_size]
+            pending = []
+            pending_keys = []
+
+            for rec in batch:
+                key = record_key(rec)
+                if key in existing_by_key:
+                    output_results.append(existing_by_key[key])
+                else:
+                    pending.append(process_record(client, rec, args.source_lang, args.target_lang))
+                    pending_keys.append(key)
+
+            if pending:
+                processed = await asyncio.gather(*pending)
+                for key, rec in zip(pending_keys, processed):
+                    if rec is not None:
+                        existing_by_key[key] = rec
+                        output_results.append(rec)
+
+            os.makedirs(os.path.dirname(out_path), exist_ok=True)
+            with open(out_path, 'w', encoding='utf-8') as f:
+                json.dump(output_results, f, ensure_ascii=False, indent=4)
+
+if __name__ == "__main__":
+    asyncio.run(main())
\ No newline at end of file
diff --git a/code/translation/translate_multiclinsum_en2bn.py b/code/translation/translate_multiclinsum_en2bn.py
new file mode 100644
index 0000000000000000000000000000000000000000..5a6a68b38a69965473bdc73ed1295d673005eb60
--- /dev/null
+++ b/code/translation/translate_multiclinsum_en2bn.py
@@ -0,0 +1,322 @@
+import os
+os.environ["CUDA_DEVICE_ORDER"] = "PCI_BUS_ID"
+os.environ["CUDA_VISIBLE_DEVICES"] = "2"
+
+import argparse
+import json
+import re
+import time
+import unicodedata
+import urllib.error
+import urllib.request
+from typing import Dict, List, Tuple
+
+import torch
+from tqdm import tqdm
+from transformers import pipeline
+
+
+DATA_PATH = "/home/mshahidul/readctrl/data/testing_data_gs/multiclinsum_gs_train_en.json"
+OUT_PATH = "/home/mshahidul/readctrl/data/translated_data/multiclinsum_gs_train_en2bn(0_200).json"
+
+SOURCE_LANG = "en"
+TARGET_LANG = "bn"
+
+# Tune if you hit model input limits.
+MAX_CHARS_PER_CHUNK = 1500
+MAX_NEW_TOKENS = 512
+SAVE_EVERY = 10
+BATCH_SIZE = int(os.environ.get("BATCH_SIZE", "16"))
+
+VLLM_BASE_URL = os.environ.get("VLLM_BASE_URL", "http://localhost:8004/v1")
+JUDGE_MODEL = os.environ.get("JUDGE_MODEL", "Qwen/Qwen3-30B-A3B-Instruct-2507")
+JUDGE_MAX_RETRIES = 3
+JUDGE_TIMEOUT_SEC = 60
+JUDGE_TEMPERATURE = 0.0
+
+_BENGALI_RANGE = (0x0980, 0x09FF)
+_ALLOWED_PUNCT = set(" \n\t\r.,;:!?-—()[]{}\"'`~")
+_ALLOWED_EN_WORDS = {
+    w.strip().lower()
+    for w in os.environ.get("ALLOWED_EN_WORDS", "").split(",")
+    if w.strip()
+}
+
+
+def chunk_text(text: str, max_chars: int) -> List[str]:
+    if len(text) <= max_chars:
+        return [text]
+
+    chunks: List[str] = []
+    paragraphs = [p for p in text.split("\n\n") if p.strip()]
+    for para in paragraphs:
+        if len(para) <= max_chars:
+            chunks.append(para)
+            continue
+
+        sentences = [s.strip() for s in para.split(". ") if s.strip()]
+        current = ""
+        for sentence in sentences:
+            sentence = sentence if sentence.endswith(".") else f"{sentence}."
+            if not current:
+                current = sentence
+                continue
+
+            if len(current) + 1 + len(sentence) <= max_chars:
+                current = f"{current} {sentence}"
+            else:
+                chunks.append(current)
+                current = sentence
+
+        if current:
+            chunks.append(current)
+
+    return chunks
+
+
+def translate_text(pipe, text: str) -> str:
+    if not text.strip():
+        return text
+
+    chunks = chunk_text(text, MAX_CHARS_PER_CHUNK)
+    translated_chunks: List[str] = []
+    messages_list = []
+    for chunk in chunks:
+        messages_list.append(
+            [
+                {
+                    "role": "user",
+                    "content": [
+                        {
+                            "type": "text",
+                            "source_lang_code": SOURCE_LANG,
+                            "target_lang_code": TARGET_LANG,
+                            "text": chunk,
+                        }
+                    ],
+                }
+            ]
+        )
+
+    for start in range(0, len(messages_list), BATCH_SIZE):
+        batch = messages_list[start : start + BATCH_SIZE]
+        outputs = pipe(
+            text=batch,
+            max_new_tokens=MAX_NEW_TOKENS,
+            batch_size=BATCH_SIZE,
+        )
+        for output in outputs:
+            if isinstance(output, list):
+                output = output[0]
+            translated_chunks.append(output["generated_text"][-1]["content"])
+
+    return "\n\n".join(translated_chunks)
+
+
+def _strip_code_fences(text: str) -> str:
+    text = text.strip()
+    if text.startswith("```"):
+        text = re.sub(r"^```[a-zA-Z]*\n?", "", text)
+        text = re.sub(r"\n?```$", "", text)
+    return text.strip()
+
+
+def _extract_json_payload(text: str) -> Dict:
+    cleaned = _strip_code_fences(text)
+    try:
+        return json.loads(cleaned)
+    except json.JSONDecodeError:
+        match = re.search(r"\{.*\}", cleaned, flags=re.DOTALL)
+        if match:
+            return json.loads(match.group(0))
+    return {}
+
+
+def _contains_disallowed_chars(text: str) -> Tuple[bool, str]:
+    if _ALLOWED_EN_WORDS:
+        normalized = re.sub(r"[^\w\s]", " ", text.lower())
+        for token in normalized.split():
+            if token.isalpha() and token in _ALLOWED_EN_WORDS:
+                text = re.sub(rf"\b{re.escape(token)}\b", "", text, flags=re.IGNORECASE)
+
+    for ch in text:
+        if ch.isalpha():
+            code = ord(ch)
+            if _BENGALI_RANGE[0] <= code <= _BENGALI_RANGE[1]:
+                continue
+            if ("A" <= ch <= "Z") or ("a" <= ch <= "z"):
+                continue
+            return True, f"Non-Bengali/English letter detected: {ch}"
+
+        category = unicodedata.category(ch)
+        if category.startswith("S"):
+            return True, f"Symbol detected: {ch}"
+        if ch.isdigit():
+            continue
+        if category.startswith("P") or category.startswith("Z"):
+            continue
+        if ch in _ALLOWED_PUNCT:
+            continue
+    return False, ""
+
+
+def _call_judge_model(source_text: str, translated_text: str) -> Dict:
+    url = f"{VLLM_BASE_URL}/chat/completions"
+    prompt = (
+        "You are a strict judge for Bengali translations. "
+        "Return JSON only with keys ok (true/false) and reason. "
+        "Check if the Bengali translation contains any non-Bengali, "
+        "non-English letters, or strange symbols. "
+        "Allow Bengali punctuation, Bengali digits, and common punctuation. "
+        "English words and keywords are allowed. "
+        "If any issue exists, ok must be false.\n\n"
+        f"English:\n{source_text}\n\nBengali:\n{translated_text}"
+    )
+    payload = {
+        "model": JUDGE_MODEL,
+        "messages": [
+            {"role": "system", "content": "Respond with JSON only."},
+            {"role": "user", "content": prompt},
+        ],
+        "temperature": JUDGE_TEMPERATURE,
+        "max_tokens": 256,
+    }
+    data = json.dumps(payload).encode("utf-8")
+    req = urllib.request.Request(
+        url,
+        data=data,
+        headers={"Content-Type": "application/json"},
+        method="POST",
+    )
+    with urllib.request.urlopen(req, timeout=JUDGE_TIMEOUT_SEC) as resp:
+        response_json = json.loads(resp.read().decode("utf-8"))
+    content = response_json["choices"][0]["message"]["content"]
+    return _extract_json_payload(content)
+
+
+def _judge_translation(source_text: str, translated_text: str) -> Tuple[bool, str]:
+    if not translated_text.strip():
+        return False, "Empty translation"
+
+    try:
+        response = _call_judge_model(source_text, translated_text)
+        ok = bool(response.get("ok", False))
+        reason = str(response.get("reason", ""))
+    except (urllib.error.URLError, json.JSONDecodeError, KeyError, TimeoutError) as exc:
+        ok = False
+        reason = f"Judge call failed: {exc}"
+
+    disallowed, disallowed_reason = _contains_disallowed_chars(translated_text)
+    if disallowed:
+        return False, disallowed_reason
+    if not ok:
+        return False, reason or "Judge rejected translation"
+    return True, ""
+
+
+def translate_with_judge(pipe, source_text: str, field_name: str, record_id: str) -> str:
+    if not source_text.strip():
+        return source_text
+
+    for attempt in range(1, JUDGE_MAX_RETRIES + 1):
+        translated = translate_text(pipe, source_text)
+        ok, reason = _judge_translation(source_text, translated)
+        if ok:
+            return translated
+        print(
+            f"[Judge] id={record_id} field={field_name} attempt={attempt} failed: {reason}"
+        )
+        time.sleep(1)
+
+    print(
+        f"[Judge] id={record_id} field={field_name} failed after "
+        f"{JUDGE_MAX_RETRIES} attempts. Leaving empty for re-translation."
+    )
+    return ""
+
+
+def load_json(path: str) -> List[Dict]:
+    with open(path, "r", encoding="utf-8") as f:
+        return json.load(f)
+
+
+def save_json(path: str, data: List[Dict]) -> None:
+    os.makedirs(os.path.dirname(path), exist_ok=True)
+    with open(path, "w", encoding="utf-8") as f:
+        json.dump(data, f, ensure_ascii=False, indent=2)
+
+
+def parse_args() -> argparse.Namespace:
+    parser = argparse.ArgumentParser(
+        description="Translate MultiClinSum EN to BN."
+    )
+    parser.add_argument(
+        "--limit",
+        type=int,
+        default=200,
+        help="Only translate the first N instances.",
+    )
+    return parser.parse_args()
+
+
+def main() -> None:
+    args = parse_args()
+    data = load_json(DATA_PATH)
+    if args.limit is not None:
+        data = data[: args.limit]
+
+    existing: Dict[str, Dict] = {}
+    existing_list: List[Dict] = []
+    resume_index = 0
+    if os.path.exists(OUT_PATH):
+        existing_list = load_json(OUT_PATH)
+        for item in existing_list:
+            existing[item["id"]] = item
+        if existing_list:
+            prefix_ids = [item.get("id") for item in existing_list]
+            data_prefix_ids = [item.get("id") for item in data[: len(prefix_ids)]]
+            if prefix_ids == data_prefix_ids:
+                resume_index = len(existing_list)
+
+    pipe = pipeline(
+        "image-text-to-text",
+        model="google/translategemma-27b-it",
+        device="cuda",
+        dtype=torch.bfloat16,
+    )
+
+    translated: List[Dict] = existing_list.copy()
+    for idx, item in enumerate(
+        tqdm(data[resume_index:], desc="Translating", unit="record"),
+        start=resume_index + 1,
+    ):
+        if item["id"] in existing:
+            translated.append(existing[item["id"]])
+        else:
+            record_id = str(item.get("id", ""))
+            fulltext_bn = translate_with_judge(
+                pipe, item.get("fulltext", ""), "fulltext", record_id
+            )
+            summary_bn = translate_with_judge(
+                pipe, item.get("summary", ""), "summary", record_id
+            )
+            translated.append(
+                {
+                    "id": item.get("id"),
+                    "fulltext_en": item.get("fulltext", ""),
+                    "summary_en": item.get("summary", ""),
+                    "fulltext_bn": fulltext_bn,
+                    "summary_bn": summary_bn,
+                }
+            )
+
+        if idx % SAVE_EVERY == 0:
+            save_json(OUT_PATH, translated)
+            print(f"Saved {idx}/{len(data)} records to {OUT_PATH}")
+
+    save_json(OUT_PATH, translated)
+    print(f"Done. Saved {len(translated)} records to {OUT_PATH}")
+
+
+if __name__ == "__main__":
+    main()
diff --git a/code/translation/translate_test_v2.py b/code/translation/translate_test_v2.py
new file mode 100644
index 0000000000000000000000000000000000000000..b32fa3d988c3a78734ca21b8937b931e1233f180
--- /dev/null
+++ b/code/translation/translate_test_v2.py
@@ -0,0 +1,39 @@
+import os
+import json
+from openai import OpenAI
+os.environ["CUDA_DEVICE_ORDER"] = "PCI_BUS_ID"
+os.environ["CUDA_VISIBLE_DEVICES"] = "2"
+import torch
+from transformers import AutoModelForImageTextToText, AutoProcessor
+
+model_id = "google/translategemma-27b-it"
+processor = AutoProcessor.from_pretrained(model_id)
+# model = AutoModelForImageTextToText.from_pretrained(model_id, device_map="auto")
+
+client = OpenAI(base_url="http://localhost:8081/v1", api_key="no-key-required")
+
+# ---- Text Translation ----
+messages = [
+    {
+        "role": "user",
+        "content": [
+            {
+                "type": "text",
+                "source_lang_code": "en",
+                "target_lang_code": "bn",
+                "text": "Patient A.P., female, born in 1979, has been diagnosed with dilatation cardiomyopathy in 1996. Anamnestically, disease started with tonsillitis, possible myocarditis (which was never proven), with pronounced symptoms of heart failure and general symptoms. She was hospitalized and after one month, the left ventricular ejection fraction was 10% with the aforementioned signs of congestive heart failure. She was hospitalized for 10 months and 9 days, with standard therapy for vitally endangered patient, oxygen support, numerous adjuvant therapy, and intensive monitoring. Therapy was administered (ACE inhibitor - ramipril, cardiotonic - digoxin, beta-blockers - metoprolol and combination of diuretics - furosemide and spironolactone), with the indication of heart transplantation. Clinical improvement occured with an ejection fraction that was gradually increasing and at the age of 21 she entered in remission or stabilization phase, with the ejection fraction value of 48-57% (regular echocardiography was performed every three months). For the following four years therapy remained the same, but in Jun 2004 (after an episode of low immunity), ejection fraction fell to 25%, with a clinical deterioration of the disease. The patient was hospitalized for a period of two months, and the condition stabilized, and she was discharged with therapy that was the same but without cardiotonic. Ejection fraction was stabilized, and in year 2006 it was 50%. At the age of 27, the patient decided on the first pregnancy that was successful with beta blocker (metoprolol) in therapy. After the first pregnancy, the ejection fraction was 40% and she was treated with the same therapy with eplerenone (25 mg) instead of spironolactone. The ejection fraction was controlled and did not fall below 45%. At the end of 2015 the patient became pregnant for the second time, and the pregnancy went neatly until eighth month (35 weeks), when she was urgently admitted to hospital, due to sense of suffocation and inability to walk. Ejection fraction decreased to 18% (brain natriuretic peptide (BNP) was 2600 pg/ mL (reference values are 100-400 pg/ mL)). During pregnancy she received only metoprolol in therapy. Physicians decide to continue with her pregnancy, in the 39th week they performed c-section, and the condition stabilized again after twenty days. In October 2016 new mode of therapy was administered, ramipril (2.5 mg, in the morning), metoprolol (47.5 mg, in the morning), spironolactone (50 mg, once a day) and ivabradine (5 mg, twice a day) with torasemide (5 mg, once a day). LifeVest Defibrillator was carried from 06 December 2016 until 27 February 2017 when it was removed. When removed and after examination (ejection fraction was 44%) she continued with ramipril therapy (1.25 mg) metoprolol (23.75 mg), torasemide (5 mg), spironolactone (25 mg) and ivabradine (7.5 mg, twice a day) with potassium supplements, and compliance with non-pharmacological measures (fluid intake restricted to 1.5 L/ day). The echocardiographic finding in March 2017 showed left ventricular dilatation with moderately reduced left ventricular function and left ventricular wall hypokinesia with ejection fraction of 44% (insignificant pericardial effusion was present, inferior vena cava with physiological flow, preserved valves function - Dopler sonography showed slight insufficiency of mitral valve with dilatation of anulus). Evaluation of a patient with ejection fraction 44% showed no indication for an implantable cardioverter defibrillator (ICD), and conservative procedure and medication therapy were recommended. Regular check-ups and body mass reduction, regular control of renal function parameters and electrolytes were recommended. She is led under the diagnosis of dilated cardiomyopathy and heart failure NYHA stage II without any indication for the ICD prophylactic implantation.",
+            }
+        ],
+    }
+]
+
+prompt = processor.apply_chat_template(
+    messages, tokenize=False, add_generation_prompt=True
+)
+completion = client.chat.completions.create(
+    model="translate_gemma",
+    messages=[{"role": "user", "content": prompt}],
+    stream=False
+)
+
+print(completion.choices[0].message.content)
diff --git a/code/translation/translate_test_v3.py b/code/translation/translate_test_v3.py
new file mode 100644
index 0000000000000000000000000000000000000000..b32fa3d988c3a78734ca21b8937b931e1233f180
--- /dev/null
+++ b/code/translation/translate_test_v3.py
@@ -0,0 +1,39 @@
+import os
+import json
+from openai import OpenAI
+os.environ["CUDA_DEVICE_ORDER"] = "PCI_BUS_ID"
+os.environ["CUDA_VISIBLE_DEVICES"] = "2"
+import torch
+from transformers import AutoModelForImageTextToText, AutoProcessor
+
+model_id = "google/translategemma-27b-it"
+processor = AutoProcessor.from_pretrained(model_id)
+# model = AutoModelForImageTextToText.from_pretrained(model_id, device_map="auto")
+
+client = OpenAI(base_url="http://localhost:8081/v1", api_key="no-key-required")
+
+# ---- Text Translation ----
+messages = [
+    {
+        "role": "user",
+        "content": [
+            {
+                "type": "text",
+                "source_lang_code": "en",
+                "target_lang_code": "bn",
+                "text": "Patient A.P., female, born in 1979, has been diagnosed with dilatation cardiomyopathy in 1996. Anamnestically, disease started with tonsillitis, possible myocarditis (which was never proven), with pronounced symptoms of heart failure and general symptoms. She was hospitalized and after one month, the left ventricular ejection fraction was 10% with the aforementioned signs of congestive heart failure. She was hospitalized for 10 months and 9 days, with standard therapy for vitally endangered patient, oxygen support, numerous adjuvant therapy, and intensive monitoring. Therapy was administered (ACE inhibitor - ramipril, cardiotonic - digoxin, beta-blockers - metoprolol and combination of diuretics - furosemide and spironolactone), with the indication of heart transplantation. Clinical improvement occured with an ejection fraction that was gradually increasing and at the age of 21 she entered in remission or stabilization phase, with the ejection fraction value of 48-57% (regular echocardiography was performed every three months). For the following four years therapy remained the same, but in Jun 2004 (after an episode of low immunity), ejection fraction fell to 25%, with a clinical deterioration of the disease. The patient was hospitalized for a period of two months, and the condition stabilized, and she was discharged with therapy that was the same but without cardiotonic. Ejection fraction was stabilized, and in year 2006 it was 50%. At the age of 27, the patient decided on the first pregnancy that was successful with beta blocker (metoprolol) in therapy. After the first pregnancy, the ejection fraction was 40% and she was treated with the same therapy with eplerenone (25 mg) instead of spironolactone. The ejection fraction was controlled and did not fall below 45%. At the end of 2015 the patient became pregnant for the second time, and the pregnancy went neatly until eighth month (35 weeks), when she was urgently admitted to hospital, due to sense of suffocation and inability to walk. Ejection fraction decreased to 18% (brain natriuretic peptide (BNP) was 2600 pg/ mL (reference values are 100-400 pg/ mL)). During pregnancy she received only metoprolol in therapy. Physicians decide to continue with her pregnancy, in the 39th week they performed c-section, and the condition stabilized again after twenty days. In October 2016 new mode of therapy was administered, ramipril (2.5 mg, in the morning), metoprolol (47.5 mg, in the morning), spironolactone (50 mg, once a day) and ivabradine (5 mg, twice a day) with torasemide (5 mg, once a day). LifeVest Defibrillator was carried from 06 December 2016 until 27 February 2017 when it was removed. When removed and after examination (ejection fraction was 44%) she continued with ramipril therapy (1.25 mg) metoprolol (23.75 mg), torasemide (5 mg), spironolactone (25 mg) and ivabradine (7.5 mg, twice a day) with potassium supplements, and compliance with non-pharmacological measures (fluid intake restricted to 1.5 L/ day). The echocardiographic finding in March 2017 showed left ventricular dilatation with moderately reduced left ventricular function and left ventricular wall hypokinesia with ejection fraction of 44% (insignificant pericardial effusion was present, inferior vena cava with physiological flow, preserved valves function - Dopler sonography showed slight insufficiency of mitral valve with dilatation of anulus). Evaluation of a patient with ejection fraction 44% showed no indication for an implantable cardioverter defibrillator (ICD), and conservative procedure and medication therapy were recommended. Regular check-ups and body mass reduction, regular control of renal function parameters and electrolytes were recommended. She is led under the diagnosis of dilated cardiomyopathy and heart failure NYHA stage II without any indication for the ICD prophylactic implantation.",
+            }
+        ],
+    }
+]
+
+prompt = processor.apply_chat_template(
+    messages, tokenize=False, add_generation_prompt=True
+)
+completion = client.chat.completions.create(
+    model="translate_gemma",
+    messages=[{"role": "user", "content": prompt}],
+    stream=False
+)
+
+print(completion.choices[0].message.content)
diff --git a/code/translation/translation_review_gradio.py b/code/translation/translation_review_gradio.py
new file mode 100644
index 0000000000000000000000000000000000000000..4de273ec5753b339e4046548161e9204b59e31da
--- /dev/null
+++ b/code/translation/translation_review_gradio.py
@@ -0,0 +1,276 @@
+import json
+import os
+from typing import List, Tuple
+
+import gradio as gr
+import httpx
+from transformers import AutoProcessor
+
+DATA_PATH = (
+    "/home/mshahidul/readctrl/data/translated_data/translation_wo_judge/"
+    "multiclinsum_gs_train_en2bn_gemma(0_200).json"
+)
+
+TRANSLATE_URL = "http://172.16.34.29:8081/v1/chat/completions"
+SOURCE_LANG = "en"
+TARGET_LANG = "bn"
+
+MODEL_ID = "google/translategemma-27b-it"
+SERVER_MODEL_NAME = "translate_gemma"
+
+MAX_INSTANCES = 80
+
+processor = AutoProcessor.from_pretrained(MODEL_ID)
+
+
+def load_data(path: str) -> List[dict]:
+    with open(path, "r", encoding="utf-8") as f:
+        return json.load(f)
+
+
+def save_data(path: str, data: List[dict]) -> None:
+    os.makedirs(os.path.dirname(path), exist_ok=True)
+    with open(path, "w", encoding="utf-8") as f:
+        json.dump(data, f, ensure_ascii=False, indent=4)
+
+
+def build_gemma_prompt(text: str, source_lang: str, target_lang: str) -> List[dict]:
+    messages = [
+        {
+            "role": "user",
+            "content": [
+                {
+                    "type": "text",
+                    "source_lang_code": source_lang,
+                    "target_lang_code": target_lang,
+                    "text": text,
+                }
+            ],
+        }
+    ]
+    prompt = processor.apply_chat_template(
+        messages, tokenize=False, add_generation_prompt=True
+    )
+    return [{"role": "user", "content": prompt}]
+
+
+def call_llm(
+    text: str,
+    temperature: float = 0.1,
+    max_tokens: int | None = None,
+    source_lang: str = SOURCE_LANG,
+    target_lang: str = TARGET_LANG,
+) -> Tuple[str | None, str | None]:
+    if not text:
+        return None, "Empty source text."
+    messages = build_gemma_prompt(text, source_lang=source_lang, target_lang=target_lang)
+    payload = {
+        "model": SERVER_MODEL_NAME,
+        "messages": messages,
+        "temperature": float(temperature),
+    }
+    if max_tokens is not None:
+        payload["max_tokens"] = int(max_tokens)
+    try:
+        response = httpx.post(TRANSLATE_URL, json=payload, timeout=60.0)
+        result = response.json()
+        content = result["choices"][0]["message"]["content"].strip()
+        return content, None
+    except Exception as exc:
+        return None, f"LLM call failed: {exc}"
+
+
+data = load_data(DATA_PATH)
+limit = min(MAX_INSTANCES, len(data))
+options = [(f"{i:03d} | {data[i].get('id', 'no-id')}", i) for i in range(limit)]
+
+
+def get_record(idx: int) -> dict:
+    return data[idx]
+
+
+def record_to_fields(idx: int):
+    rec = get_record(idx)
+    return (
+        idx,
+        rec.get("id", ""),
+        rec.get("fulltext", ""),
+        rec.get("summary", ""),
+        rec.get("translated_fulltext") or "",
+        rec.get("translated_summary") or "",
+        f"Loaded index {idx}.",
+    )
+
+
+def goto_index(idx: int):
+    return record_to_fields(int(idx))
+
+
+def step_index(idx: int, delta: int):
+    new_idx = max(0, min(limit - 1, int(idx) + delta))
+    return record_to_fields(new_idx)
+
+
+def regenerate_fulltext(idx: int, temperature: float, max_tokens: int):
+    rec = get_record(int(idx))
+    translated, error = call_llm(
+        rec.get("fulltext", ""),
+        temperature=temperature,
+        max_tokens=max_tokens,
+    )
+    if translated is not None:
+        rec["translated_fulltext"] = translated
+        return translated, f"Regenerated fulltext at index {idx}."
+    return rec.get("translated_fulltext") or "", error or "Regenerate failed."
+
+
+def regenerate_summary(idx: int, temperature: float, max_tokens: int):
+    rec = get_record(int(idx))
+    translated, error = call_llm(
+        rec.get("summary", ""),
+        temperature=temperature,
+        max_tokens=max_tokens,
+    )
+    if translated is not None:
+        rec["translated_summary"] = translated
+        return translated, f"Regenerated summary at index {idx}."
+    return rec.get("translated_summary") or "", error or "Regenerate failed."
+
+
+def regenerate_both(idx: int, temperature: float, max_tokens_full: int, max_tokens_sum: int):
+    fulltext, full_error = regenerate_fulltext(idx, temperature, max_tokens_full)
+    summary, sum_error = regenerate_summary(idx, temperature, max_tokens_sum)
+    status = "Regenerated fulltext and summary."
+    if full_error or sum_error:
+        errors = "; ".join([e for e in [full_error, sum_error] if e])
+        status = f"Partial regenerate: {errors}"
+    return fulltext, summary, status
+
+
+def save_record(idx: int, translated_fulltext: str, translated_summary: str):
+    rec = get_record(int(idx))
+    rec["translated_fulltext"] = translated_fulltext or None
+    rec["translated_summary"] = translated_summary or None
+    save_data(DATA_PATH, data)
+    gr.Info(f"Saved index {idx} to file.")
+    return f"Saved index {idx} to file."
+
+
+with gr.Blocks(title="Translation Review") as demo:
+    gr.Markdown("## Translation review for first 80 instances")
+
+    with gr.Row():
+        record_select = gr.Dropdown(
+            label="Record",
+            choices=options,
+            value=0,
+            interactive=True,
+        )
+        status = gr.Textbox(label="Status", value="Ready.", interactive=False)
+
+    with gr.Row():
+        prev_btn = gr.Button("Prev")
+        next_btn = gr.Button("Next")
+
+    record_id = gr.Textbox(label="Record ID", interactive=False)
+    fulltext = gr.Textbox(label="Fulltext (source)", lines=8, interactive=False)
+    summary = gr.Textbox(label="Summary (source)", lines=6, interactive=False)
+
+    with gr.Row():
+        temperature = gr.Slider(
+            minimum=0.0,
+            maximum=1.5,
+            value=0.2,
+            step=0.05,
+            label="Temperature",
+        )
+        max_tokens_full = gr.Number(value=2048, precision=0, label="Max tokens (fulltext)")
+        max_tokens_sum = gr.Number(value=1024, precision=0, label="Max tokens (summary)")
+
+    translated_fulltext = gr.Textbox(label="Translated fulltext", lines=8)
+    translated_summary = gr.Textbox(label="Translated summary", lines=6)
+
+    with gr.Row():
+        regen_full_btn = gr.Button("Regenerate Fulltext")
+        regen_sum_btn = gr.Button("Regenerate Summary")
+        regen_both_btn = gr.Button("Regenerate Both")
+        save_btn = gr.Button("Save to file")
+
+    record_select.change(
+        goto_index,
+        inputs=[record_select],
+        outputs=[
+            record_select,
+            record_id,
+            fulltext,
+            summary,
+            translated_fulltext,
+            translated_summary,
+            status,
+        ],
+    )
+    prev_btn.click(
+        lambda idx: step_index(idx, -1),
+        inputs=[record_select],
+        outputs=[
+            record_select,
+            record_id,
+            fulltext,
+            summary,
+            translated_fulltext,
+            translated_summary,
+            status,
+        ],
+    )
+    next_btn.click(
+        lambda idx: step_index(idx, 1),
+        inputs=[record_select],
+        outputs=[
+            record_select,
+            record_id,
+            fulltext,
+            summary,
+            translated_fulltext,
+            translated_summary,
+            status,
+        ],
+    )
+
+    regen_full_btn.click(
+        regenerate_fulltext,
+        inputs=[record_select, temperature, max_tokens_full],
+        outputs=[translated_fulltext, status],
+    )
+    regen_sum_btn.click(
+        regenerate_summary,
+        inputs=[record_select, temperature, max_tokens_sum],
+        outputs=[translated_summary, status],
+    )
+    regen_both_btn.click(
+        regenerate_both,
+        inputs=[record_select, temperature, max_tokens_full, max_tokens_sum],
+        outputs=[translated_fulltext, translated_summary, status],
+    )
+    save_btn.click(
+        save_record,
+        inputs=[record_select, translated_fulltext, translated_summary],
+        outputs=[status],
+    )
+
+    demo.load(
+        goto_index,
+        inputs=[record_select],
+        outputs=[
+            record_select,
+            record_id,
+            fulltext,
+            summary,
+            translated_fulltext,
+            translated_summary,
+            status,
+        ],
+    )
+
+
+if __name__ == "__main__":
+    demo.launch(share=True)
diff --git a/code/translation/translation_using_gpt5.py b/code/translation/translation_using_gpt5.py
new file mode 100644
index 0000000000000000000000000000000000000000..58b6d4ab172492542b78da09986b3a1387063ac9
--- /dev/null
+++ b/code/translation/translation_using_gpt5.py
@@ -0,0 +1,58 @@
+from openai import OpenAI
+import json, os
+
+source_language = "English"
+target_language = "Hindi"
+print(f"Translating from {source_language} to {target_language}")
+with open("/home/mshahidul/readctrl/prompts/translation_prompt.txt", "r") as f:
+    prompt_template = f.read()
+
+
+api_file = "/home/mshahidul/api_new.json"
+with open(api_file, "r") as f:
+    api_keys = json.load(f)
+openai_api_key = api_keys["openai"]
+
+client = OpenAI(api_key=openai_api_key)
+
+
+def openai_return(prompt, model="gpt-5"):
+    """Send a prompt to GPT and parse JSON."""
+    response = client.chat.completions.create(
+        model=model,
+        messages=[
+            {"role": "system", "content": "You are a helpful assistant."},
+            {"role": "user", "content": prompt}
+        ]
+    )
+    content = response.choices[0].message.content.strip()
+    cleaned = content.replace("```json", "").replace("```", "").strip()
+    try:
+        return json.loads(cleaned)
+    except json.JSONDecodeError:
+        print("⚠️ JSON parse failed — storing raw text.")
+        return cleaned
+
+save_path=f"/home/mshahidul/readctrl/data/translated_data/translation_{source_language[:2].lower()}2{target_language[:2].lower()}_v1.json"
+res=[]
+if os.path.exists(save_path):
+    with open(save_path, "r") as f:
+        res = json.load(f)
+import tqdm
+with open("/home/mshahidul/readctrl/data/testing_data_gs/multiclinsum_gs_train_en.json", "r") as f:
+    data = json.load(f)
+for item in tqdm.tqdm(data[:15]):
+    prompt=prompt_template.replace("<MEDICAL_TEXT>", item["fulltext"]).replace("<SOURCE_LANGUAGE>", source_language).replace("<TARGET_LANGUAGE>", target_language)
+    # import ipdb; ipdb.set_trace()
+    sample = openai_return(prompt, model="gpt-5")
+
+    res.append(sample)
+
+    if len(res) % 2 == 0:
+        with open(save_path, "w") as f:
+            json.dump(res, f, indent=2, ensure_ascii=False)
+        print(f"Saved {len(res)} samples so far.")
+
+with open(save_path, "w") as f:
+    json.dump(res, f, indent=2, ensure_ascii=False)
+
diff --git a/code/translation/translation_using_gpt5_v2.py b/code/translation/translation_using_gpt5_v2.py
new file mode 100644
index 0000000000000000000000000000000000000000..569b9c444fb1d4981a14eb66080ffc7c7a3e24f3
--- /dev/null
+++ b/code/translation/translation_using_gpt5_v2.py
@@ -0,0 +1,98 @@
+import json
+import os
+import tqdm
+from pathlib import Path
+from openai import OpenAI
+
+# --- Configuration ---
+source_language = "English"
+target_language = "Bangla"
+save_dir = "/home/mshahidul/readctrl/data/translated_data"
+save_path = os.path.join(save_dir, f"translation_{source_language.lower()}2{target_language.lower()}_v1.json")
+
+# Ensure the directory exists
+Path(save_dir).mkdir(parents=True, exist_ok=True)
+
+print(f"Translating from {source_language} to {target_language}")
+
+# Load Prompt Template
+with open("/home/mshahidul/readctrl/prompts/translation_prompt.txt", "r") as f:
+    prompt_template = f.read()
+
+# API Setup
+api_file = "/home/mshahidul/api_new.json"
+with open(api_file, "r") as f:
+    api_keys = json.load(f)
+openai_api_key = api_keys["openai"]
+
+client = OpenAI(api_key=openai_api_key)
+
+def openai_return(prompt, model="gpt-5"):
+    """Send a prompt to GPT and parse JSON."""
+    try:
+        response = client.chat.completions.create(
+            model=model,
+            messages=[
+                {"role": "system", "content": "You are a helpful assistant that outputs only valid JSON."},
+                {"role": "user", "content": prompt}
+            ],
+            response_format={"type": "json_object"} # Ensuring JSON mode if supported
+        )
+        content = response.choices[0].message.content.strip()
+        # Clean up possible markdown artifacts
+        cleaned = content.replace("```json", "").replace("```", "").strip()
+        return json.loads(cleaned)
+    except Exception as e:
+        print(f"⚠️ Error during API call or parsing: {e}")
+        return content
+
+# Load existing results if they exist to resume progress
+res = []
+if os.path.exists(save_path):
+    with open(save_path, "r") as f:
+        res = json.load(f)
+
+# Load Source Data
+with open("/home/mshahidul/readctrl/data/testing_data_gs/multiclinsum_gs_train_en.json", "r") as f:
+    data = json.load(f)
+
+# --- Translation Loop ---
+# Start from the number of already processed items
+start_index = len(res)
+for item in tqdm.tqdm(data[start_index:200]):
+    
+    # Helper to generate prompt and call API
+    def get_translation(text):
+        formatted_prompt = (prompt_template
+                            .replace("<MEDICAL_TEXT>", text)
+                            .replace("<SOURCE_LANGUAGE>", source_language)
+                            .replace("<TARGET_LANGUAGE>", target_language))
+        return openai_return(formatted_prompt, model="gpt-5")
+
+    # Translate Fulltext
+    translated_full = get_translation(item["fulltext"])
+    
+    # Translate Summary
+    translated_sum = get_translation(item["summary"])
+
+    # Create the translated object
+    translated_item = {
+        "id": item["id"],
+        "fulltext_translated": translated_full,
+        "summary_translated": translated_sum,
+        "original_id": item["id"]
+    }
+
+    res.append(translated_item)
+
+    # Incremental save every 2 items
+    if len(res) % 2 == 0:
+        with open(save_path, "w", encoding='utf-8') as f:
+            json.dump(res, f, indent=2, ensure_ascii=False)
+        print(f" Saved {len(res)} samples so far.")
+
+# Final Save
+with open(save_path, "w", encoding='utf-8') as f:
+    json.dump(res, f, indent=2, ensure_ascii=False)
+
+print(f"✅ Processing complete. Data saved to {save_path}")
\ No newline at end of file
diff --git a/code/translation/translation_using_gpt5_v3_correct_null.py b/code/translation/translation_using_gpt5_v3_correct_null.py
new file mode 100644
index 0000000000000000000000000000000000000000..ce4a166cdfe337b550dbae74f3121522ac3f4e4b
--- /dev/null
+++ b/code/translation/translation_using_gpt5_v3_correct_null.py
@@ -0,0 +1,85 @@
+import json
+import os
+import tqdm
+from pathlib import Path
+from openai import OpenAI
+
+# --- Configuration ---
+source_language = "English"
+target_language = "Chinese"
+input_path = "/home/mshahidul/readctrl/data/translated_data/translation_wo_judge/multiclinsum_gs_train_en2zh_gemma(0_200).json"
+save_path = input_path
+
+print(f"Fixing null translations from {source_language} to {target_language}")
+
+# Load Prompt Template
+with open("/home/mshahidul/readctrl/prompts/translation_prompt.txt", "r") as f:
+    prompt_template = f.read()
+
+# API Setup
+api_file = "/home/mshahidul/api_new.json"
+with open(api_file, "r") as f:
+    api_keys = json.load(f)
+openai_api_key = api_keys["openai"]
+
+client = OpenAI(api_key=openai_api_key)
+
+def openai_return(prompt, model="gpt-5"):
+    """Send a prompt to GPT and parse JSON."""
+    try:
+        response = client.chat.completions.create(
+            model=model,
+            messages=[
+                {"role": "system", "content": "You are a helpful assistant that outputs only valid JSON."},
+                {"role": "user", "content": prompt}
+            ],
+            response_format={"type": "json_object"} # Ensuring JSON mode if supported
+        )
+        content = response.choices[0].message.content.strip()
+        # Clean up possible markdown artifacts
+        cleaned = content.replace("```json", "").replace("```", "").strip()
+        return json.loads(cleaned)
+    except Exception as e:
+        print(f"⚠️ Error during API call or parsing: {e}")
+        return {"translated_medical_note": None}
+
+def extract_translation(result):
+    if isinstance(result, dict):
+        return result.get("translated_medical_note")
+    return None
+
+# Load Source Data (existing translations)
+with open(input_path, "r") as f:
+    data = json.load(f)
+
+# --- Translation Loop ---
+for idx, item in tqdm.tqdm(enumerate(data), total=len(data)):
+    
+    # Helper to generate prompt and call API
+    def get_translation(text):
+        formatted_prompt = (prompt_template
+                            .replace("<MEDICAL_TEXT>", text)
+                            .replace("<SOURCE_LANGUAGE>", source_language)
+                            .replace("<TARGET_LANGUAGE>", target_language))
+        return openai_return(formatted_prompt, model="gpt-5")
+
+    # Fix only null translations
+    if item.get("translated_fulltext") is None:
+        translated_full = extract_translation(get_translation(item["fulltext"]))
+        item["translated_fulltext"] = translated_full
+
+    if item.get("translated_summary") is None:
+        translated_sum = extract_translation(get_translation(item["summary"]))
+        item["translated_summary"] = translated_sum
+
+    # Incremental save every 2 items
+    if idx % 2 == 0:
+        with open(save_path, "w", encoding='utf-8') as f:
+            json.dump(data, f, indent=2, ensure_ascii=False)
+        print(f" Saved up to index {idx}.")
+
+# Final Save
+with open(save_path, "w", encoding='utf-8') as f:
+    json.dump(data, f, indent=2, ensure_ascii=False)
+
+print(f"✅ Processing complete. Data saved to {save_path}")
\ No newline at end of file
diff --git a/code/vectordb_build/data_annotate_data_prep copy.py b/code/vectordb_build/data_annotate_data_prep copy.py
new file mode 100644
index 0000000000000000000000000000000000000000..bb2696135d5d826d85608e615dd82b0f3be7e351
--- /dev/null
+++ b/code/vectordb_build/data_annotate_data_prep copy.py	
@@ -0,0 +1,128 @@
+import os
+# Environment Setup
+# os.environ["CUDA_DEVICE_ORDER"] = "PCI_BUS_ID"
+os.environ["CUDA_VISIBLE_DEVICES"] = "4"
+import json
+import tqdm
+import numpy as np
+import pandas as pd
+import textstat
+import spacy
+import torch
+from sentence_transformers import SentenceTransformer, util
+from datasets import load_dataset
+
+
+device = "cuda" if torch.cuda.is_available() else "cpu"
+
+# 1. Load Models Efficiently
+model = SentenceTransformer('Qwen/Qwen3-Embedding-0.6B').to(device)
+# Disable unnecessary components in Spacy to save time/memory
+nlp = spacy.load("en_core_web_sm", disable=["ner", "lemmatizer", "attribute_ruler"])
+
+def get_parse_tree_stats(text):
+    doc = nlp(text)
+    depths = []
+    for sent in doc.sents:
+        def walk_tree(node, depth):
+            if not list(node.children): return depth
+            return max(walk_tree(child, depth + 1) for child in node.children)
+        depths.append(walk_tree(sent.root, 1))
+    return np.mean(depths) if depths else 0
+
+# 2. Data Loading
+ds = load_dataset("wikimedia/wikipedia", "20231101.en", split='train', streaming=True)
+# Taking a subset for the anchor pool to keep memory manageable
+wiki_list = [item['text'] for item in ds.take(1000000)] 
+
+# 3. PRE-PROCESS WIKI ANCHORS (Do this ONCE)
+print("Chunking and Encoding Wikipedia...")
+wiki_chunks = []
+for text in wiki_list:
+    paragraphs = [p.strip() for p in text.split('\n\n') if len(p.split()) > 20]
+    wiki_chunks.extend(paragraphs)
+
+# Encode all chunks at once and keep on GPU
+chunk_embs = model.encode(wiki_chunks, convert_to_tensor=True, show_progress_bar=True).to(device)
+
+# 4. Load Target Docs
+with open("/home/mshahidul/readctrl/data/synthetic_dataset_diff_labels/syn_data_diff_labels_en_v1.json", "r") as f:
+    res = json.load(f)
+
+my_target_documents = []
+for item in res:
+    for key, value in item['diff_label_texts'].items():
+        my_target_documents.append({"index": item['index'], "label": key, "text": value})
+
+# Load Progress
+save_path = "/home/mshahidul/readctrl/data/data_annotator_data/crowdsourcing_input_en_v2.json"
+processed_data = []
+if os.path.exists(save_path):
+    with open(save_path, "r") as f:
+        processed_data = json.load(f)
+processed_keys = {(d['index'], d['label']) for d in processed_data}
+
+# 5. Process with Batching logic where possible
+print("Starting Matching Loop...")
+for doc in tqdm.tqdm(my_target_documents):
+    if (doc['index'], doc['label']) in processed_keys:
+        continue
+
+    # A. Robust Anchor Finding (Optimized)
+    doc_emb = model.encode(doc['text'], convert_to_tensor=True).to(device)
+    doc_len = len(doc['text'].split())
+    
+    hits = util.semantic_search(doc_emb, chunk_embs, top_k=25)[0]
+    
+    wiki_anchor = None
+    best_fallback = None
+    min_delta = float('inf')
+
+    for hit in hits:
+        cand_text = wiki_chunks[hit['corpus_id']]
+        cand_len = len(cand_text.split())
+        len_diff = abs(cand_len - doc_len)
+        
+        # Track fallback while looking for strict match
+        if len_diff < min_delta:
+            min_delta = len_diff
+            best_fallback = cand_text
+            
+        if 0.8 <= (cand_len / doc_len) <= 1.2:
+            wiki_anchor = cand_text
+            break
+    
+    if not wiki_anchor:
+        wiki_anchor = best_fallback
+
+    # B. Calculate Metrics
+    doc_metrics = {
+        "fkgl": textstat.flesch_kincaid_grade(doc['text']),
+        "word_count": doc_len
+    }
+    wiki_metrics = {
+        "fkgl": textstat.flesch_kincaid_grade(wiki_anchor),
+        "word_count": len(wiki_anchor.split())
+    }
+    
+    # C. Store results
+    processed_data.append({
+        "index": doc['index'],
+        "label": doc['label'],
+        "original_doc": doc['text'],
+        "wiki_anchor": wiki_anchor,
+        "doc_fkgl": doc_metrics['fkgl'],
+        "wiki_fkgl": wiki_metrics['fkgl'],
+        "doc_tree_depth": get_parse_tree_stats(doc['text']),
+        "wiki_tree_depth": get_parse_tree_stats(wiki_anchor),
+        "fkgl_delta": doc_metrics['fkgl'] - wiki_metrics['fkgl']
+    })
+
+    # Save every 20 to reduce disk I/O overhead
+    if len(processed_data) % 20 == 0:
+        with open(save_path, "w") as f:
+            json.dump(processed_data, f, indent=2)
+
+# Final Save
+with open(save_path, "w") as f:
+    json.dump(processed_data, f, indent=2)
\ No newline at end of file
diff --git a/code/vectordb_build/data_annotate_data_prep_test_v3.py b/code/vectordb_build/data_annotate_data_prep_test_v3.py
new file mode 100644
index 0000000000000000000000000000000000000000..4de30a8f874b89b8123d70db4a430714f97ef53e
--- /dev/null
+++ b/code/vectordb_build/data_annotate_data_prep_test_v3.py
@@ -0,0 +1,125 @@
+import os
+import argparse
+parser = argparse.ArgumentParser()
+parser.add_argument("--lang", type=str, default="en", help="language code")
+parser.add_argument("--cuda", type=str, default="3", help="CUDA device ID to use")
+args = parser.parse_args()
+
+lang_code = args.lang
+os.environ["CUDA_DEVICE_ORDER"] = "PCI_BUS_ID"
+os.environ["CUDA_VISIBLE_DEVICES"] = args.cuda
+import json
+import tqdm
+import numpy as np
+import pandas as pd
+import textstat
+import spacy
+import torch
+import glob
+from sentence_transformers import SentenceTransformer, util
+
+
+
+# 1. Load Models
+model = SentenceTransformer('all-MiniLM-L6-v2')
+nlp = spacy.load(f"{lang_code}_core_web_sm", disable=["ner", "lemmatizer", "attribute_ruler"])
+
+def get_parse_tree_stats(text):
+    doc = nlp(text)
+    depths = []
+    for sent in doc.sents:
+        def walk_tree(node, depth):
+            if not list(node.children): return depth
+            return max(walk_tree(child, depth + 1) for child in node.children)
+        depths.append(walk_tree(sent.root, 1))
+    return np.mean(depths) if depths else 0
+
+# 2. Load and Merge All Shards
+print("Loading and merging all shards...")
+shard_pattern = f"/home/mshahidul/readctrl/data/wiki_chunks/wiki_chunks_{lang_code}_shard_*.parquet"
+shard_files = sorted(glob.glob(shard_pattern))
+
+all_dfs = []
+for f in shard_files:
+    all_dfs.append(pd.read_parquet(f))
+
+df_merged = pd.concat(all_dfs, ignore_index=True)
+wiki_chunks = df_merged['text'].tolist()
+print(f"Total wiki chunks loaded: {len(wiki_chunks)}")
+
+# 3. Encode Merged Chunks (Keep on GPU)
+print("Encoding merged chunks...")
+chunk_embs = model.encode(wiki_chunks, convert_to_tensor=True, show_progress_bar=True)
+
+# 4. Load Target Docs
+with open(f"/home/mshahidul/readctrl/data/synthetic_dataset_diff_labels/syn_data_diff_labels_{lang_code}_v1.json", "r") as f:
+    res = json.load(f)
+
+my_target_documents = []
+for item in res:
+    for key, value in item['diff_label_texts'].items():
+        my_target_documents.append({"index": item['index'], "label": key, "text": value})
+
+# 5. Output Path (Removed shard_id from filename)
+save_path = f"/home/mshahidul/readctrl/data/data_annotator_data/new_v2/crowdsourcing_input_{lang_code}_merged_v1.json"
+os.makedirs(os.path.dirname(save_path), exist_ok=True)
+
+processed_data = []
+if os.path.exists(save_path):
+    with open(save_path, "r") as f:
+        processed_data = json.load(f)
+processed_keys = {(d['index'], d['label']) for d in processed_data}
+
+# 6. Process Loop
+print(f"Starting Matching Loop for {len(my_target_documents)} documents...")
+for doc in tqdm.tqdm(my_target_documents):
+    if (doc['index'], doc['label']) in processed_keys:
+        continue
+
+    doc_emb = model.encode(doc['text'], convert_to_tensor=True)
+    doc_len = len(doc['text'].split())
+    
+    # Search across the entire merged corpus
+    hits = util.semantic_search(doc_emb, chunk_embs, top_k=25)[0]
+    
+    wiki_anchor = None
+    best_fallback = None
+    min_delta = float('inf')
+
+    for hit in hits:
+        cand_text = wiki_chunks[hit['corpus_id']]
+        cand_len = len(cand_text.split())
+        len_diff = abs(cand_len - doc_len)
+        
+        if len_diff < min_delta:
+            min_delta = len_diff
+            best_fallback = cand_text
+            
+        if 0.8 <= (cand_len / doc_len) <= 1.2:
+            wiki_anchor = cand_text
+            break
+    
+    if not wiki_anchor:
+        wiki_anchor = best_fallback
+
+    # Calculate Metrics
+    processed_data.append({
+        "index": doc['index'],
+        "label": doc['label'],
+        "original_doc": doc['text'],
+        "wiki_anchor": wiki_anchor,
+        "doc_fkgl": textstat.flesch_kincaid_grade(doc['text']),
+        "wiki_fkgl": textstat.flesch_kincaid_grade(wiki_anchor),
+        "doc_tree_depth": get_parse_tree_stats(doc['text']),
+        "wiki_tree_depth": get_parse_tree_stats(wiki_anchor),
+        "fkgl_delta": textstat.flesch_kincaid_grade(doc['text']) - textstat.flesch_kincaid_grade(wiki_anchor)
+    })
+
+    if len(processed_data) % 20 == 0:
+        with open(save_path, "w") as f:
+            json.dump(processed_data, f, indent=2)
+
+# Final Save
+with open(save_path, "w") as f:
+    json.dump(processed_data, f, indent=2)
+print(f"Processing complete. Saved to {save_path}")
\ No newline at end of file
diff --git a/code/vectordb_build/data_annotate_data_prep_test_v4.py b/code/vectordb_build/data_annotate_data_prep_test_v4.py
new file mode 100644
index 0000000000000000000000000000000000000000..9a5319420b640a916bf8c2a09fd11d96b0828523
--- /dev/null
+++ b/code/vectordb_build/data_annotate_data_prep_test_v4.py
@@ -0,0 +1,131 @@
+import os
+import argparse
+# 1. Setup Arguments
+parser = argparse.ArgumentParser()
+parser.add_argument("--lang", type=str, default="en")
+parser.add_argument("--num_shards", type=int, default=20)
+parser.add_argument("--cuda", type=str, default="0")
+args = parser.parse_args()
+os.environ["CUDA_DEVICE_ORDER"] = "PCI_BUS_ID"
+os.environ["CUDA_VISIBLE_DEVICES"] = args.cuda
+import json
+import tqdm
+import numpy as np
+import pandas as pd
+import textstat
+import spacy
+import torch
+import pickle  # Added for saving text chunks efficiently
+from sentence_transformers import SentenceTransformer, util
+
+
+# device = "cuda" if torch.cuda.is_available() else "cpu"
+
+# Define Paths for the "Vector Database"
+db_dir = "/home/mshahidul/readctrl/data/vector_db"
+os.makedirs(db_dir, exist_ok=True)
+embs_cache_path = os.path.join(db_dir, f"wiki_{args.lang}_embs.pt")
+text_cache_path = os.path.join(db_dir, f"wiki_{args.lang}_chunks.pkl")
+
+# 2. Load Models
+model = SentenceTransformer('all-MiniLM-L6-v2')
+nlp = spacy.load(f"{args.lang}_core_web_sm", disable=["ner", "lemmatizer", "attribute_ruler"])
+
+# (Helper functions get_parse_tree_stats and walk_tree remain the same...)
+def walk_tree(node, depth):
+    if not list(node.children): return depth
+    return max([walk_tree(child, depth + 1) for child in node.children], default=depth)
+
+def get_parse_tree_stats(text):
+    doc = nlp(text)
+    depths = [walk_tree(sent.root, 1) for sent in doc.sents]
+    return np.mean(depths) if depths else 0
+
+# ---------------------------------------------------------
+# 3. Step 1 & 2: Load or Create Vector Database
+# ---------------------------------------------------------
+if os.path.exists(embs_cache_path) and os.path.exists(text_cache_path):
+    print("Loading cached vector database...")
+    all_chunk_embs = torch.load(embs_cache_path)
+    with open(text_cache_path, "rb") as f:
+        all_wiki_chunks = pickle.load(f)
+    print(f"Loaded {len(all_wiki_chunks)} chunks from cache.")
+else:
+    print(f"Cache not found. Merging {args.num_shards} shards and encoding...")
+    all_wiki_chunks = []
+    for i in range(args.num_shards):
+        path = f"/home/mshahidul/readctrl/data/wiki_chunks/wiki_chunks_{args.lang}_shard_{i}.parquet"
+        if os.path.exists(path):
+            df_shard = pd.read_parquet(path)
+            all_wiki_chunks.extend(df_shard['text'].tolist())
+
+    print(f"Total merged chunks: {len(all_wiki_chunks)}")
+    
+    # Encoding
+    all_chunk_embs = model.encode(all_wiki_chunks, convert_to_tensor=True, show_progress_bar=True)
+    
+    # SAVE the vector database
+    print("Saving vector database for future use...")
+    torch.save(all_chunk_embs, embs_cache_path)
+    with open(text_cache_path, "wb") as f:
+        pickle.dump(all_wiki_chunks, f)
+    print("Database saved successfully.")
+
+# ---------------------------------------------------------
+# 4. Step 3: Run Target Documents
+# ---------------------------------------------------------
+# (The rest of your target processing logic remains the same)
+with open(f"/home/mshahidul/readctrl/data/synthetic_dataset_diff_labels/syn_data_diff_labels_{args.lang}_v1.json", "r") as f:
+    res = json.load(f)
+
+my_targets = []
+for item in res:
+    for key, val in item['diff_label_texts'].items():
+        my_targets.append({"index": item['index'], "label": key, "text": val})
+
+target_texts = [d['text'] for d in my_targets]
+target_embs = model.encode(target_texts, convert_to_tensor=True)
+
+print("Running semantic search...")
+search_results = util.semantic_search(target_embs, all_chunk_embs, top_k=25)
+
+processed_data = []
+for i, hits in enumerate(tqdm.tqdm(search_results)):
+    doc = my_targets[i]
+    doc_len = len(doc['text'].split())
+    
+    wiki_anchor = None
+    best_fallback = None
+    min_delta = float('inf')
+
+    for hit in hits:
+        cand_text = all_wiki_chunks[hit['corpus_id']]
+        cand_len = len(cand_text.split())
+        len_diff = abs(cand_len - doc_len)
+        
+        if len_diff < min_delta:
+            min_delta = len_diff
+            best_fallback = cand_text
+            
+        if 0.8 <= (cand_len / doc_len) <= 1.2:
+            wiki_anchor = cand_text
+            break
+    
+    final_anchor = wiki_anchor if wiki_anchor else best_fallback
+
+    processed_data.append({
+        "index": doc['index'],
+        "label": doc['label'],
+        "original_doc": doc['text'],
+        "wiki_anchor": final_anchor,
+        "doc_fkgl": textstat.flesch_kincaid_grade(doc['text']),
+        "wiki_fkgl": textstat.flesch_kincaid_grade(final_anchor),
+        "doc_tree_depth": get_parse_tree_stats(doc['text']),
+        "wiki_tree_depth": get_parse_tree_stats(final_anchor)
+    })
+
+final_save_path = f"/home/mshahidul/readctrl/data/data_annotator_data/new_v1/crowdsourcing_input_{args.lang}_fully_merged_v2.json"
+with open(final_save_path, "w") as f:
+    json.dump(processed_data, f, indent=2)
+
+print(f"Done! Results saved to {final_save_path}")
\ No newline at end of file
diff --git a/code/vectordb_build/data_annotate_data_prep_test_v4_multiThread.py b/code/vectordb_build/data_annotate_data_prep_test_v4_multiThread.py
new file mode 100644
index 0000000000000000000000000000000000000000..6508daddd37c25a638895f4285f495df0a1c054d
--- /dev/null
+++ b/code/vectordb_build/data_annotate_data_prep_test_v4_multiThread.py
@@ -0,0 +1,135 @@
+import os
+import argparse
+import json
+import tqdm
+import numpy as np
+import pandas as pd
+import textstat
+import spacy
+import torch
+import pickle
+from sentence_transformers import SentenceTransformer, util
+
+# Define helper functions OUTSIDE the if __name__ block
+def walk_tree(node, depth):
+    if not list(node.children): return depth
+    return max([walk_tree(child, depth + 1) for child in node.children], default=depth)
+
+def get_parse_tree_stats(nlp, text):
+    doc = nlp(text)
+    depths = [walk_tree(sent.root, 1) for sent in doc.sents]
+    return np.mean(depths) if depths else 0
+
+def main():
+    # 1. Setup Arguments
+    parser = argparse.ArgumentParser()
+    parser.add_argument("--lang", type=str, default="en")
+    parser.add_argument("--num_shards", type=int, default=20)
+    parser.add_argument("--cuda", type=str, default="0")
+    args = parser.parse_args()
+
+    os.environ["CUDA_DEVICE_ORDER"] = "PCI_BUS_ID"
+    os.environ["CUDA_VISIBLE_DEVICES"] = args.cuda
+
+    # Define Paths
+    db_dir = "/home/mshahidul/readctrl/data/vector_db"
+    os.makedirs(db_dir, exist_ok=True)
+    embs_cache_path = os.path.join(db_dir, f"wiki_{args.lang}_embs.pt")
+    text_cache_path = os.path.join(db_dir, f"wiki_{args.lang}_chunks.pkl")
+
+    # 2. Load Models
+    model = SentenceTransformer('all-MiniLM-L6-v2')
+    # Load spacy here so workers don't necessarily need to load it unless used in parallel
+    nlp = spacy.load(f"{args.lang}_core_web_sm", disable=["ner", "lemmatizer", "attribute_ruler"])
+
+    # 3. Load or Create Vector Database
+    if os.path.exists(embs_cache_path) and os.path.exists(text_cache_path):
+        print("Loading cached vector database...")
+        all_chunk_embs = torch.load(embs_cache_path, map_location='cuda')
+        with open(text_cache_path, "rb") as f:
+            all_wiki_chunks = pickle.load(f)
+    else:
+        print(f"Merging {args.num_shards} shards and encoding on A100...")
+        all_wiki_chunks = []
+        for i in range(args.num_shards):
+            path = f"/home/mshahidul/readctrl/data/wiki_chunks/wiki_chunks_{args.lang}_shard_{i}.parquet"
+            if os.path.exists(path):
+                df_shard = pd.read_parquet(path)
+                all_wiki_chunks.extend(df_shard['text'].tolist())
+
+        # MULTI-PROCESS ENCODING
+        pool = model.start_multi_process_pool()
+        all_chunk_embs_np = model.encode_multi_process(
+            all_wiki_chunks, 
+            pool, 
+            batch_size=512
+        )
+        model.stop_multi_process_pool(pool)
+        
+        all_chunk_embs = torch.from_numpy(all_chunk_embs_np).to("cuda")
+        
+        torch.save(all_chunk_embs, embs_cache_path)
+        with open(text_cache_path, "wb") as f:
+            pickle.dump(all_wiki_chunks, f)
+
+    # 4. Run Target Documents
+    input_path = f"/home/mshahidul/readctrl/data/synthetic_dataset_diff_labels/syn_data_diff_labels_{args.lang}_v1.json"
+    with open(input_path, "r") as f:
+        res = json.load(f)
+
+    my_targets = []
+    for item in res:
+        for key, val in item['diff_label_texts'].items():
+            my_targets.append({"index": item['index'], "label": key, "text": val})
+
+    target_texts = [d['text'] for d in my_targets]
+    target_embs = model.encode(target_texts, convert_to_tensor=True)
+
+    print("Running semantic search...")
+    search_results = util.semantic_search(target_embs, all_chunk_embs, top_k=25)
+
+    processed_data = []
+    for i, hits in enumerate(tqdm.tqdm(search_results)):
+        doc = my_targets[i]
+        doc_len = len(doc['text'].split())
+        
+        wiki_anchor = None
+        best_fallback = None
+        min_delta = float('inf')
+
+        for hit in hits:
+            cand_text = all_wiki_chunks[hit['corpus_id']]
+            cand_len = len(cand_text.split())
+            len_diff = abs(cand_len - doc_len)
+            
+            if len_diff < min_delta:
+                min_delta = len_diff
+                best_fallback = cand_text
+                
+            if 0.8 <= (cand_len / doc_len) <= 1.2:
+                wiki_anchor = cand_text
+                break
+        
+        final_anchor = wiki_anchor if wiki_anchor else best_fallback
+
+        processed_data.append({
+            "index": doc['index'],
+            "label": doc['label'],
+            "original_doc": doc['text'],
+            "wiki_anchor": final_anchor,
+            "doc_fkgl": textstat.flesch_kincaid_grade(doc['text']),
+            "wiki_fkgl": textstat.flesch_kincaid_grade(final_anchor),
+            "doc_tree_depth": get_parse_tree_stats(nlp, doc['text']),
+            "wiki_tree_depth": get_parse_tree_stats(nlp, final_anchor)
+        })
+
+    final_save_path = f"/home/mshahidul/readctrl/data/data_annotator_data/new_v1/crowdsourcing_input_{args.lang}_fully_merged.json"
+    os.makedirs(os.path.dirname(final_save_path), exist_ok=True)
+    with open(final_save_path, "w") as f:
+        json.dump(processed_data, f, indent=2)
+
+    print(f"Done! Results saved to {final_save_path}")
+
+# This is the crucial part that fixes the RuntimeError
+if __name__ == '__main__':
+    main()
\ No newline at end of file
diff --git a/code/vectordb_build/process.py b/code/vectordb_build/process.py
new file mode 100644
index 0000000000000000000000000000000000000000..1ba03d587e3f21b1035b7208c188da62c029e593
--- /dev/null
+++ b/code/vectordb_build/process.py
@@ -0,0 +1,41 @@
+import subprocess
+import time
+
+# --- CONFIGURATION ---
+LANG = "en"
+TOTAL_SHARDS = 20
+MAX_CHUNKS_PER_ARTICLE = 5
+# ---------------------
+
+def run_preprocessing():
+    start_time = time.time()
+    
+    for shard_id in range(TOTAL_SHARDS):
+        print(f"\n{'='*40}")
+        print(f"STARTING SHARD {shard_id + 1} OF {TOTAL_SHARDS}")
+        print(f"{'='*40}\n")
+        
+        # Build the command to call your existing script
+        command = [
+            "python", "/home/mshahidul/readctrl/code/vectordb_build/t.py",
+            "--lang", LANG,
+            "--shard_id", str(shard_id),
+            "--num_shards", str(TOTAL_SHARDS),
+            "--max_chunks", str(MAX_CHUNKS_PER_ARTICLE)
+        ]
+        
+        # Run the process and wait for it to finish before starting the next
+        try:
+            subprocess.run(command, check=True)
+            print(f"\nSuccessfully finished Shard {shard_id}")
+        except subprocess.CalledProcessError as e:
+            print(f"\nError occurred while processing Shard {shard_id}: {e}")
+            # Optional: break if you want to stop on error
+            # break 
+
+    end_time = time.time()
+    duration = (end_time - start_time) / 60
+    print(f"\nAll {TOTAL_SHARDS} shards processed in {duration:.2f} minutes.")
+
+if __name__ == "__main__":
+    run_preprocessing()
\ No newline at end of file
diff --git a/code/vectordb_build/qwen_embed_v3.py b/code/vectordb_build/qwen_embed_v3.py
new file mode 100644
index 0000000000000000000000000000000000000000..c11072fb1fbd6cd4e64f65f05c57c3befb86ef82
--- /dev/null
+++ b/code/vectordb_build/qwen_embed_v3.py
@@ -0,0 +1,93 @@
+import os
+# 1. Environment & Configuration
+import argparse
+parser = argparse.ArgumentParser()
+parser.add_argument("--lang", type=str, default="en", help="language code")
+parser.add_argument("--shard_id", type=int, required=True, help="Shard ID for this run")
+parser.add_argument("--num_shards", type=int, default=20, help="Total number of shards")
+parser.add_argument("--batch_size", type=int, default=16, help="Batch size for embedding")
+parser.add_argument("--cuda", type=str, default="none", help="CUDA device ID to use")
+args = parser.parse_args()
+
+if args.cuda == "none":
+    os.environ["CUDA_DEVICE_ORDER"] = "PCI_BUS_ID"
+    os.environ["CUDA_VISIBLE_DEVICES"] = "2"
+else:
+    # os.environ["CUDA_DEVICE_ORDER"] = "PCI_BUS_ID"
+    os.environ["CUDA_VISIBLE_DEVICES"] = args.cuda
+
+
+import gc
+import torch
+import faiss
+import numpy as np
+from datasets import load_dataset
+from sentence_transformers import SentenceTransformer
+import pandas as pd
+
+
+# --- SHARDING CONFIG ---
+# SHARD_ID = 2  # Change this for each run (e.g., 0, 1, 2, 3...)
+NUM_SHARDS = args.num_shards # Total number of parts to split Wikipedia into
+SHARD_ID = args.shard_id
+batch_size = args.batch_size
+lang_code = args.lang
+# -----------------------
+
+model_id = "Qwen/Qwen3-Embedding-4B"
+save_path = f"/home/mshahidul/readctrl/data/vector_db/qwen_em/shard_{SHARD_ID}_{lang_code}.faiss"
+# batch_size = 64 #16  # Keep small for 4B model to avoid OOM
+
+# 2. Load Model with Memory Optimizations
+print("Loading model...")
+model = SentenceTransformer(
+    model_id, 
+    trust_remote_code=True, 
+    device="cuda",
+    model_kwargs={"torch_dtype": torch.bfloat16} # Use half-precision
+)
+model.max_seq_length = 1024 # Truncate long paragraphs to save VRAM
+
+
+load_path = f"/home/mshahidul/readctrl/data/wiki_chunks/wiki_chunks_{lang_code}_shard_{SHARD_ID}.parquet"
+df = pd.read_parquet(load_path)
+wiki_chunks = df['text'].tolist()
+
+# 5. Embedding Function
+def build_faiss_index(chunks, model, batch_size):
+    index = None
+    total_chunks = len(chunks)
+    
+    print(f"Starting embedding process for {total_chunks} chunks...")
+    import tqdm
+    for i in tqdm.tqdm(range(0, total_chunks, batch_size)):
+        batch = chunks[i : i + batch_size]
+        
+        # Generate Embeddings
+        with torch.no_grad():
+            embeddings = model.encode(
+                batch, 
+                show_progress_bar=False,
+                convert_to_numpy=True
+            ).astype('float32')
+        
+        # Initialize FAISS index on first batch
+        if index is None:
+            dimension = embeddings.shape[1]
+            index = faiss.IndexFlatL2(dimension)
+            # Optional: If you have a massive dataset, consider using faiss.IndexIVFFlat 
+            # for faster search, though IndexFlatL2 is most accurate.
+        
+        index.add(embeddings)
+        
+        if i % 1000 == 0:
+            print(f"Processed {i}/{total_chunks} chunks...")
+
+    return index
+
+# 6. Run and Save
+vector_index = build_faiss_index(wiki_chunks, model, batch_size)
+
+print(f"Saving index to {save_path}...")
+faiss.write_index(vector_index, save_path)
+print("Done!")
\ No newline at end of file
diff --git a/code/vectordb_build/t.py b/code/vectordb_build/t.py
new file mode 100644
index 0000000000000000000000000000000000000000..7e7b81661976693405f1273ed71ac262b265441a
--- /dev/null
+++ b/code/vectordb_build/t.py
@@ -0,0 +1,52 @@
+import argparse
+import tqdm
+import pandas as pd
+import gc
+from datasets import load_dataset
+
+def main():
+    parser = argparse.ArgumentParser()
+    parser.add_argument("--lang", type=str, default="en")
+    parser.add_argument("--shard_id", type=int, required=True)
+    parser.add_argument("--num_shards", type=int, default=20)
+    parser.add_argument("--max_chunks", type=int, default=15)
+    args = parser.parse_args()
+
+    # 1. Load Shard
+    print(f"Loading {args.lang} Wikipedia shard {args.shard_id}...")
+    ds = load_dataset("wikimedia/wikipedia", f"20231101.{args.lang}", split='train')
+    ds_shard = ds.shard(num_shards=args.num_shards, index=args.shard_id)
+
+    # 2. Cleaning & Chunking
+    STOP_HEADERS = ["\nReferences", "\nSee also", "\nExternal links", "\nNotes", "\nFurther reading", "\nBibliography"]
+    wiki_chunks = []
+    
+    # Track which original article each chunk came from (optional but helpful)
+    for article in tqdm.tqdm(ds_shard):
+        text = article['text']
+        
+        # Clean: Remove reference sections
+        clean_text = text
+        for header in STOP_HEADERS:
+            if header in clean_text:
+                clean_text = clean_text.split(header)[0]
+        
+        # Split into paragraphs
+        paragraphs = [p.strip() for p in clean_text.split('\n\n') if len(p.split()) > 20]
+        
+        # Cap chunks per article
+        if len(paragraphs) > args.max_chunks:
+            paragraphs = paragraphs[:args.max_chunks]
+            
+        wiki_chunks.extend(paragraphs)
+
+    # 3. Save to Parquet
+    # Saving as a DataFrame is highly efficient for loading later
+    df = pd.DataFrame({"text": wiki_chunks})
+    save_path = f"/home/mshahidul/readctrl/data/wiki_chunks/wiki_chunks_{args.lang}_shard_{args.shard_id}.parquet"
+    df.to_parquet(save_path, compression='snappy')
+    
+    print(f"Saved {len(wiki_chunks)} chunks to {save_path}")
+
+if __name__ == "__main__":
+    main()
\ No newline at end of file
diff --git a/code/vectordb_build/testing.ipynb b/code/vectordb_build/testing.ipynb
new file mode 100644
index 0000000000000000000000000000000000000000..f5f56cd35373daabc7be6817d9193f5b872badbf
--- /dev/null
+++ b/code/vectordb_build/testing.ipynb
@@ -0,0 +1,141 @@
+{
+ "cells": [
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "61997615",
+   "metadata": {},
+   "outputs": [],
+   "source": []
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "baa55c98",
+   "metadata": {},
+   "outputs": [],
+   "source": [
+    "import faiss\n",
+    "\n",
+    "merged_index = faiss.read_index(\"/home/mshahidul/readctrl/data/vector_db/qwen_em/shard_0_en.faiss\")\n",
+    "for i in range(1, NUM_SHARDS):\n",
+    "    next_index = faiss.read_index(f\"/home/mshahidul/readctrl/data/vector_db/qwen_em/shard_{i}_en.faiss\")\n",
+    "    merged_index.merge_from(next_index)\n",
+    "\n",
+    "faiss.write_index(merged_index, \"full_wikipedia_index.faiss\")"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 1,
+   "id": "c8c08129",
+   "metadata": {},
+   "outputs": [
+    {
+     "name": "stdout",
+     "output_type": "stream",
+     "text": [
+      "Successfully loaded. Type: <class 'list'>\n"
+     ]
+    }
+   ],
+   "source": [
+    "import json\n",
+    "\n",
+    "file_path = '/home/mshahidul/readctrl/data/testing_data_gs/multiclinsum_gs_train_en.json'\n",
+    "\n",
+    "try:\n",
+    "    with open(file_path, 'r', encoding='utf-8') as file:\n",
+    "        data = json.load(file)\n",
+    "    \n",
+    "    # Success: 'data' is now a Python object\n",
+    "    print(f\"Successfully loaded. Type: {type(data)}\")\n",
+    "    \n",
+    "except FileNotFoundError:\n",
+    "    print(\"Error: The file path was not found.\")\n",
+    "except json.JSONDecodeError:\n",
+    "    print(\"Error: Failed to decode JSON. Check if the file is formatted correctly.\")"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 6,
+   "id": "055e14be",
+   "metadata": {},
+   "outputs": [
+    {
+     "name": "stdout",
+     "output_type": "stream",
+     "text": [
+      "summary 1========================================\n",
+      "We present the case of a 20-year-old woman with a 12-year history of idiopathic NS revealed by extensive cerebral venous thrombosis with pulmonary embolism treated with anticoagulation therapy and oral corticosteroid therapy followed by mycophenolate mofetil (MMF). The thrombophilia assessment did not show any abnormalities. The evolution was marked by the occurrence of several NS relapses controlled by oral corticosteroid therapy until 2017. Subsequently, the patient had not presented a relapse of her disease. The anticoagulant treatment and the MMF were therefore stopped. One year later, the patient presented with severe diffuse acute abdominal pain associated with postprandial vomiting and bilateral lower limb edema. Laboratory results confirmed a NS relapse. An abdominal CT scan revealed acute thrombosis of the superior mesenteric artery with acute mesenteric ischemia. Intraoperative exploration showed mesenteric ischemia with extensive necrosis of the small intestine making their resections incompatible with life. The patient died after 48 hours.\n",
+      "summary 2========================================\n",
+      "A 34-year-old pregnant woman presents with seizures and dysarthria and is urgently referred for a cranial MRI. The classic ‘Medusa head’ sign is seen and the diagnosis is made as a venous anomaly of development with peripheral partial thrombosis and proximal slow flow.\n",
+      "\n",
+      "summary 3========================================\n",
+      "A 22-year-old woman came to the Oral Medicine Department with complaints of stomatitis causing pain, eating, and drinking difficulty, which started with fever and pimple-like on the lips. She was an active vape user for one year. Extraoral examination revealed no lesions on other body parts. The serosanguinolent crusts on the lips, an erosive area on the labial commissures and tended to bleed. Intraoral examination revealed white ulcers with yellowish edges and irregular, varying sizes in several parts of the oral mucosa. The anti-HSV-1 IgG laboratory results showed non-reactive, leading to a diagnosis of oral erythema multiforme. Management of oral conditions using 0.9% NaCl compress, dexamethasone mouthwash, and hyaluronic acid, applying 2% miconazole cream on labial commissures and vaseline album cream on the dry lips, and stopping vaping. Oral condition improved in a week of therapy.\n",
+      "summary 4========================================\n",
+      "We are reporting an isolated, asymptomatic fetal intra-cardiac mass (rhabdomyoma) that was discovered at 32 weeks of gestation and was followed as an outpatient until 39 weeks plus one day, at which point a cesarean section was performed. After delivery, the child underwent evaluations at the 1st day, 7th day, 30th day, 7th month, and 12th month of age. Following a checkup, the child's anthropometric and neurobehavioral growth were both healthy. Except for the tumor, which was neither growing nor shrinking in size, none of the clinical diagnostic criteria for tuberous sclerosis complex were met for this child up to the age of one year.\n"
+     ]
+    }
+   ],
+   "source": [
+    "for i,x in enumerate(data[:4]):\n",
+    "    print(f\"summary {i+1}========================================\")\n",
+    "    print(x['summary'])"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": 7,
+   "id": "94ad4f5d",
+   "metadata": {},
+   "outputs": [
+    {
+     "data": {
+      "text/plain": [
+       "{'id': 'multiclinsum_gs_en_27.txt',\n",
+       " 'fulltext': 'A 20-year-old woman was followed up since the age of eight for idiopathic NS inaugurated by cerebral venous thrombosis extended to the right jugular vein with a massive pulmonary embolism. The patient did not have any sequelae. She had no other medical or surgical history. A family history of thrombosis has not been reported. The patient was not biopsied because she had no kidney failure nor gross hematuria, or hypertension at first presentation; added to that, she had no extra renal signs suggestive of a secondary nephrotic syndrome. She was accordingly put on anticoagulant therapy (Oral vitamin K antagonist) and oral corticosteroid therapy with good evolution. Thereafter, the patient received several cures of high-dose corticosteroids for steroid-dependent relapses of NS. She was, hence, put on mycophenolate mofetil (MMF) as a background therapy to avoid corticosteroids and ensure normal growth. An exhaustive assessment of thrombophilia was performed and did not show any abnormality. Homocysteine rate, blood fibrinogen rate, Protein C, protein S, antithrombin III, factor V Leiden mutation, JAK-2 mutation, cryoglobulins, anticardiolipin antibodies, lupus anticoagulant and beta-1-glycoprotein antibodies were normal. The anticoagulant treatment was stopped after nine years. The evolution was enameled by the occurrence of several relapses of her disease controlled by oral corticosteroid therapy. Remission of NS has been noted since 2017, so MMF was gradually stopped in 2019 and the patient remained asymptomatic and without any relapse.\\n\\nOne year later, the patient came up to our emergency department for acute intense diffuse abdominal pain without any particular irradiation associated with postprandial vomiting and bilateral lower limb edema for the last six hours. The physical examination revealed an intense epigastric tenderness with normal vital signs (arterial pressure of 120/70 mm Hg, heart rate of 83 bpm, and oxygen saturation at 100% on room air). The patient was afebrile with normal consciousness. The rest of the physical examination was unremarkable. The urinalysis with labstix revealed proteinuria. The hemogasanalysis results showed metabolic acidosis with respiratory compensation. Further laboratory tests revealed hypoalbuminemia, hypercholesterolemia, a prothrombin time at 90%, high levels of D-dimer, lactate dehydrogenase, and creatine phosphokinase as well as a biological inflammatory syndrome with a CRP of 37 mg/L, and leucocytosis at 26.4 x 103/µL. Renal and liver functions were normal.\\n\\nThe patient was hospitalized in an intensive care unit with close monitoring of vital signs and initiation of resuscitation measures. An abdominal ultrasound was performed urgently showing an intra-abdominal effusion of low to moderate abundance. An abdominal CT scan revealed acute thrombosis of the superior mesenteric artery with acute mesenteric ischemia. The patient was immediately routed to the operating room. Intraoperative exploration confirmed mesenteric ischemia with extensive necrosis of almost entirely of the small bowel making their resections incompatible with life shown in Figure 3. The patient died after 48 hours.',\n",
+       " 'summary': 'We present the case of a 20-year-old woman with a 12-year history of idiopathic NS revealed by extensive cerebral venous thrombosis with pulmonary embolism treated with anticoagulation therapy and oral corticosteroid therapy followed by mycophenolate mofetil (MMF). The thrombophilia assessment did not show any abnormalities. The evolution was marked by the occurrence of several NS relapses controlled by oral corticosteroid therapy until 2017. Subsequently, the patient had not presented a relapse of her disease. The anticoagulant treatment and the MMF were therefore stopped. One year later, the patient presented with severe diffuse acute abdominal pain associated with postprandial vomiting and bilateral lower limb edema. Laboratory results confirmed a NS relapse. An abdominal CT scan revealed acute thrombosis of the superior mesenteric artery with acute mesenteric ischemia. Intraoperative exploration showed mesenteric ischemia with extensive necrosis of the small intestine making their resections incompatible with life. The patient died after 48 hours.'}"
+      ]
+     },
+     "execution_count": 7,
+     "metadata": {},
+     "output_type": "execute_result"
+    }
+   ],
+   "source": [
+    "data[0]"
+   ]
+  },
+  {
+   "cell_type": "code",
+   "execution_count": null,
+   "id": "2b2eead1",
+   "metadata": {},
+   "outputs": [],
+   "source": []
+  }
+ ],
+ "metadata": {
+  "kernelspec": {
+   "display_name": "un",
+   "language": "python",
+   "name": "python3"
+  },
+  "language_info": {
+   "codemirror_mode": {
+    "name": "ipython",
+    "version": 3
+   },
+   "file_extension": ".py",
+   "mimetype": "text/x-python",
+   "name": "python",
+   "nbconvert_exporter": "python",
+   "pygments_lexer": "ipython3",
+   "version": "3.11.14"
+  }
+ },
+ "nbformat": 4,
+ "nbformat_minor": 5
+}
diff --git a/code/vectordb_build/vector_db_build.py b/code/vectordb_build/vector_db_build.py
new file mode 100644
index 0000000000000000000000000000000000000000..56488a13503136253c47000dc189772c891f2803
--- /dev/null
+++ b/code/vectordb_build/vector_db_build.py
@@ -0,0 +1,82 @@
+import os
+# Environment Setup
+os.environ["CUDA_DEVICE_ORDER"] = "PCI_BUS_ID"
+os.environ["CUDA_VISIBLE_DEVICES"] = "2"
+import chromadb
+from chromadb.utils import embedding_functions
+from datasets import load_dataset
+import argparse
+
+# 1. Setup
+parser = argparse.ArgumentParser()
+parser.add_argument("--lang", type=str, default="pt", help="language code")
+args = parser.parse_args()
+lang_code = args.lang
+
+db_path = f"/home/mshahidul/readctrl/data/vector_db/{lang_code}_v2"
+
+# 2. Initialize Client and Embedding Function
+client = chromadb.PersistentClient(path=db_path)
+# Qwen3-Embedding-4B is heavy; ensure your GPU has ~10GB+ VRAM
+ef = embedding_functions.SentenceTransformerEmbeddingFunction(
+    model_name='Qwen/Qwen3-Embedding-4B',
+    device="cuda"
+)
+
+collection = client.get_or_create_collection(name="wiki_collection", embedding_function=ef)
+
+# 3. Logic to Add New Data
+if collection.count() == 0:
+    print(f"Database empty. Processing Wikipedia ({lang_code})...")
+    
+    # Use streaming to avoid loading the whole dataset into RAM
+    ds = load_dataset("wikimedia/wikipedia", f"20231101.{lang_code}", split='train', streaming=True)
+    
+    batch_docs = []
+    batch_ids = []
+    chunk_count = 0
+    # Process a subset (e.g., 50,000 articles) to avoid massive processing times
+    # 1,000,000 articles might result in 10,000,000+ chunks.
+    max_articles = 500000
+    import tqdm
+    for i, item in tqdm.tqdm(enumerate(ds.take(max_articles))):
+        text = item['text']
+        # Simple paragraph chunking
+        paragraphs = [p.strip() for p in text.split('\n\n') if len(p.split()) > 20]
+        
+        for p_idx, para in tqdm.tqdm(enumerate(paragraphs)):
+            batch_docs.append(para)
+            batch_ids.append(f"art_{i}_p_{p_idx}")
+            
+            # 4. Batch Upload to Chroma (Every 100 chunks)
+            # This prevents memory overflow and allows for incremental saving
+            if len(batch_docs) >= 100:
+                collection.add(
+                    documents=batch_docs,
+                    ids=batch_ids
+                )
+                chunk_count += len(batch_docs)
+                batch_docs = []
+                batch_ids = []
+                
+        if i % 500 == 0:
+            print(f"Processed {i} articles... Total chunks in DB: {collection.count()}")
+
+    # Add remaining documents
+    if batch_docs:
+        collection.add(documents=batch_docs, ids=batch_ids)
+    
+    print(f"Finished! Total documents in DB: {collection.count()}")
+else:
+    print(f"Database already exists with {collection.count()} documents. Loading...")
+
+# 5. Search
+query = "Tell me about history" # Adjust based on your language
+results = collection.query(
+    query_texts=[query],
+    n_results=3
+)
+
+print(f"\nQuery: {query}")
+for i, doc in enumerate(results['documents'][0]):
+    print(f"Result {i+1}: {doc[:200]}...") # Print first 200 chars
\ No newline at end of file
diff --git a/code/vectordb_build/vector_db_select.py b/code/vectordb_build/vector_db_select.py
new file mode 100644
index 0000000000000000000000000000000000000000..b752c8ee34f80222beace5ce25bf1b305fa74416
--- /dev/null
+++ b/code/vectordb_build/vector_db_select.py
@@ -0,0 +1,164 @@
+import os
+os.environ["CUDA_DEVICE_ORDER"] = "PCI_BUS_ID"
+os.environ["CUDA_VISIBLE_DEVICES"] = "0"
+import json
+import torch
+import pickle
+import gradio as gr
+import textstat
+from sentence_transformers import SentenceTransformer, util
+
+# --- Configuration & Paths ---
+LANG_CODE = "en" 
+CHUNKS_PATH = f"/home/mshahidul/readctrl/data/vector_db/db_model/wiki_{LANG_CODE}_chunks.pkl"
+EMBS_PATH = f"/home/mshahidul/readctrl/data/vector_db/db_model/wiki_{LANG_CODE}_embs.pt"
+TARGET_DOCS_PATH = f"/home/mshahidul/readctrl/data/synthetic_dataset_diff_labels/syn_data_diff_labels_{LANG_CODE}_v1.json"
+SAVE_PATH = f"/home/mshahidul/readctrl/data/data_annotator_data/manual_selections_{LANG_CODE}.json"
+
+# --- 1. Load Resources ---
+print("Loading Model and Tensors...")
+model = SentenceTransformer('all-MiniLM-L6-v2')
+
+with open(CHUNKS_PATH, "rb") as f:
+    wiki_chunks = pickle.load(f)
+
+device = "cuda" if torch.cuda.is_available() else "cpu"
+wiki_embs = torch.load(EMBS_PATH).to(device)
+
+with open(TARGET_DOCS_PATH, "r") as f:
+    raw_targets = json.load(f)
+
+target_list = []
+for item in raw_targets:
+    for label, text in item['diff_label_texts'].items():
+        target_list.append({
+            "index": item['index'],
+            "label": label,
+            "text": text
+        })
+
+# --- 2. Logic Functions ---
+def get_candidates(target_text, top_k=20):
+    query_emb = model.encode(target_text, convert_to_tensor=True).to(device)
+    hits = util.semantic_search(query_emb, wiki_embs, top_k=top_k)[0]
+    
+    candidates = []
+    for hit in hits:
+        candidates.append(wiki_chunks[hit['corpus_id']])
+    return candidates
+
+def calculate_stats(text):
+    if not text: return "N/A"
+    wc = len(text.split())
+    fk = textstat.flesch_kincaid_grade(text)
+    return f"📏 Words: {wc} | 🎓 FKGL: {fk}"
+
+def save_selection(target_idx, label, original_text, selected_wiki):
+    entry = {
+        "index": target_idx,
+        "label": label,
+        "original_text": original_text,
+        "selected_wiki_anchor": selected_wiki,
+        "wiki_fkgl": textstat.flesch_kincaid_grade(selected_wiki),
+        "doc_fkgl": textstat.flesch_kincaid_grade(original_text)
+    }
+    
+    existing_data = []
+    if os.path.exists(SAVE_PATH):
+        try:
+            with open(SAVE_PATH, "r") as f:
+                existing_data = json.load(f)
+        except:
+            existing_data = []
+    
+    existing_data = [d for d in existing_data if not (d['index'] == target_idx and d['label'] == label)]
+    existing_data.append(entry)
+    
+    with open(SAVE_PATH, "w") as f:
+        json.dump(existing_data, f, indent=2)
+    gr.Info(f"Successfully saved ID {target_idx} ({label})")
+    return f"✅ Saved: ID {target_idx} ({label})"
+
+# --- 3. Gradio UI ---
+with gr.Blocks(theme=gr.themes.Soft(), title="Wiki Anchor Selector") as demo:
+    gr.Markdown(f"# 🔍 ReadCtrl: Anchor Selection (Numeric View)")
+    
+    current_idx = gr.State(0)
+    
+    with gr.Row():
+        # Left Panel
+        with gr.Column(scale=1):
+            target_info = gr.Markdown("### Loading...")
+            # Changed from HighlightedText to Textbox for stability
+            label_display = gr.Textbox(label="Target Readability Level", interactive=False)
+            display_text = gr.Textbox(label="Medical Text", lines=12, interactive=False)
+            target_stats = gr.Markdown("Stats: ...")
+            
+        # Right Panel
+        with gr.Column(scale=2):
+            wiki_dropdown = gr.Dropdown(
+                label="Select Candidate Number", 
+                choices=[], 
+                interactive=True
+            )
+            full_wiki_view = gr.Textbox(label="Wikipedia Chunk Preview", lines=12, interactive=False)
+            wiki_stats = gr.Markdown("Stats: ...")
+
+    status_msg = gr.Markdown("### *Status: Ready*")
+
+    with gr.Row():
+        prev_btn = gr.Button("⬅️ Previous")
+        save_btn = gr.Button("💾 Confirm & Save", variant="primary")
+        next_btn = gr.Button("Next / Skip ➡️")
+
+    # --- UI Logic ---
+    def load_item(idx):
+        if not (0 <= idx < len(target_list)):
+            return "End", "None", "", "", gr.update(choices=[], value=None), "", "", "Finished!"
+        
+        doc = target_list[idx]
+        candidates = get_candidates(doc['text'], top_k=20)
+        
+        info = f"### Document {idx + 1} of {len(target_list)} (ID: {doc['index']})"
+        t_stats = calculate_stats(doc['text'])
+        
+        dropdown_choices = [(f"Candidate {i+1}", c) for i, c in enumerate(candidates)]
+        
+        return (
+            info, 
+            doc['label'].upper(), # Simple string for the Label Textbox
+            doc['text'], 
+            t_stats, 
+            gr.update(choices=dropdown_choices, value=candidates[0]), 
+            candidates[0], 
+            calculate_stats(candidates[0]), 
+            ""
+        )
+
+    def on_dropdown_change(selected_text):
+        if not selected_text: return "", ""
+        return selected_text, calculate_stats(selected_text)
+
+    def handle_next(idx):
+        new_idx = min(len(target_list) - 1, idx + 1)
+        return [new_idx] + list(load_item(new_idx))
+
+    def handle_prev(idx):
+        new_idx = max(0, idx - 1)
+        return [new_idx] + list(load_item(new_idx))
+
+    # --- Event Bindings ---
+    demo.load(load_item, inputs=[current_idx], 
+              outputs=[target_info, label_display, display_text, target_stats, wiki_dropdown, full_wiki_view, wiki_stats, status_msg])
+    
+    wiki_dropdown.change(on_dropdown_change, inputs=wiki_dropdown, outputs=[full_wiki_view, wiki_stats])
+    
+    save_btn.click(lambda i, t, w: save_selection(target_list[i]['index'], target_list[i]['label'], t, w), 
+                   inputs=[current_idx, display_text, wiki_dropdown], 
+                   outputs=[status_msg])
+    
+    next_btn.click(handle_next, inputs=[current_idx], outputs=[current_idx, target_info, label_display, display_text, target_stats, wiki_dropdown, full_wiki_view, wiki_stats, status_msg])
+    prev_btn.click(handle_prev, inputs=[current_idx], outputs=[current_idx, target_info, label_display, display_text, target_stats, wiki_dropdown, full_wiki_view, wiki_stats, status_msg])
+
+if __name__ == "__main__":
+    demo.launch(server_name="0.0.0.0", server_port=7861,share=True)
\ No newline at end of file
diff --git a/generating_data/raw_file/es_syntheticV1.json b/generating_data/raw_file/es_syntheticV1.json
new file mode 100644
index 0000000000000000000000000000000000000000..bc010d2c9d52a589ac6384d3ef118c33029fb34b
--- /dev/null
+++ b/generating_data/raw_file/es_syntheticV1.json
@@ -0,0 +1,902 @@
+[
+    {
+        "article": "Información para el paciente\nUn hombre de 27 años y fumador estuvo involucrado en un accidente de tráfico; se cayó de su motocicleta sin casco. El hombre llevó la motocicleta al hospital e informó de un dolor de cabeza y heridas hemorrágicas en la frente.\n\nEl paciente no tiene antecedentes patológicos y trabaja en una zona rural.\n\nHallazgos clínicos\nTras su ingreso en urgencias, perdió el conocimiento y sufrió dos convulsiones. En la exploración física, la escala de coma de Glasgow fue de 6/15 (no abrió los ojos, se retiró al sentir dolor, no respondió verbalmente) con midriasis bilateral, dificultad hemodinámica y buena saturación. Se identificó una lesión craneal penetrante con una profusa hemorragia intracraneal.\n\nLínea de tiempo\nTras caerse de la motocicleta, el paciente volvió a montarse en ella e inmediatamente fue al hospital, quejándose de dolores de cabeza y de una herida en la frente por la que sangraba. Recibió tratamiento de urgencia para estabilizar sus funciones respiratorias y hemodinámicas. Ese mismo día, fue trasladado inconsciente a un centro mejor equipado, donde se le realizó un TAC y se sometió a una operación quirúrgica con éxito.\n\nEvaluación diagnóstica\nSu nivel de hemoglobina era de 6 g/dL y su grupo sanguíneo era O positivo. El hospital no tenía ni una unidad de cuidados intensivos ni un escáner. El único diagnóstico sugerido fue el de traumatismo agudo en la cabeza, complicado por hemorragia intracraneal que provocó shock y convulsiones. El pronóstico vital, basado en la presentación clínica, era malo.\n\nIntervención terapéutica\nUna intervención inicial consiste en un relleno intracraneal a través de la fractura craneal, seguido de un vendaje cefálico que ayuda a detener el sangrado. El tratamiento involucró la estabilización de la columna cervical, intubación orotraqueal con oxígeno a 6 L por minuto y la inserción de un catéter Foley. Se usaron dos puertos venosos periféricos para administrar NaCl 0.9 % 1000 CC, Geloplasma* 500 CC, Manitol 20 % 250 CC; Phenobarbital inj 40 mg/2 ml: 100 mg, luego Thiopental 250 mg: bolo de 100 mg × 2 debido a otras convulsiones; Amoxicillin + Clavulanic Acid injection 2 g; Gentamycin 160 mg intramuscularmente. Se realizó un suero antitetánico de 1500 IU y una transfusión de 450 CC de sangre.\n\nEl paciente fue trasladado inconsciente a un equipo en un hospital de primera categoría, sin intubación y en un estado hemodinámico estable.\n\nEl primer día después de la transferencia, el paciente evolucionó bien; estaba consciente y podía caminar, sin problemas neurológicos, hemodinámicos o respiratorios. La tomografía computarizada reveló un edema bifrontal agudo, una contusión hemorrágica del parénquima predominantemente en el lado derecho, una capa de hematoma subdural agudo (3 mm) en la región fronto-parieto-temporo-occipital izquierda, una hernia subfalcular izquierda de 5 mm, una compresión discreta del ventrículo lateral derecho, una hemorragia subaracnoidea superior bifrontal aguda, una fractura frontal deprimida con rotura osteomeníngea y una fractura de la tercera vértebra cervical con compresión de la médula espinal. El paciente se sometió a una operación exitosa en el hospital de primera categoría.\n\nSeguimiento y resultados\nEl período postoperatorio estuvo marcado por convulsiones, para las cuales se le administró anticonvulsivos al paciente, con un buen resultado.\n",
+        "gold_summary": "Un hombre de 27 años, fumador sin antecedentes patológicos, estuvo involucrado en un accidente de tráfico, al caerse de una motocicleta sin casco. En el ingreso al hospital de nuestro distrito rural, la escala de coma de Glasgow durante el examen físico fue de 6/15 con midriasis bilateral, distrés hemodinámico y buena saturación. Se identificó una lesión penetrante en la cabeza con profusa hemorragia intracraneal. Se usó el relleno intracraneal conocido en la neurocirugía de control de daños para taponar la hemorragia intracraneal grave y que es una maniobra neuroquirúrgica que salva vidas. El paciente fue trasladado inconsciente a un hospital de primera categoría, libre de intubación y en un estado hemodinámico estable. El período postoperatorio estuvo marcado por convulsiones, por lo que el paciente fue puesto en anticonvulsivos con un buen resultado.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre de 27 años se cayó de su motocicleta sin casco. Se golpeó muy fuerte la cabeza y sangraba por la frente. Al llegar al hospital quedó muy dormido y tuvo dos convulsiones (ataques o “fits”). Tenía la sangre muy baja y estaba en peligro.\n\nEn el hospital pequeño no había todo lo que necesita la gente con heridas así. Los médicos taparon la herida dentro del cráneo para detener la sangre. Le pusieron líquidos, medicinas, y le dieron sangre. Luego lo llevaron a un hospital grande para más ayuda.\n\nEn el hospital grande le hicieron una prueba especial (una tomografía) y vieron golpes y hinchazón en el cerebro, una fractura en la frente y otra en el cuello. Le operaron con éxito. Después de la operación todavía tuvo convulsiones, pero le dieron medicinas para controlarlas. Al final mejoró: recuperó la conciencia y pudo caminar. Los médicos dicen que su resultado fue bueno.",
+            "B2": "Resumen (nivel B2, lenguaje claro y comprensible)\n\nUn hombre de 27 años que fuma sufrió una caída de una motocicleta sin llevar casco. Al llegar al hospital de su zona rural estaba en mal estado: la escala de coma de Glasgow era 6/15 (esto indica que estaba muy inconsciente), tenía las pupilas dilatadas en ambos ojos (un signo de lesión cerebral grave), y presentaba inestabilidad hemodinámica (problemas para mantener la presión y el flujo de sangre). Se detectó una lesión penetrante en la cabeza con hemorragia dentro del cráneo.\n\nEn ese hospital se realizó una maniobra de emergencia llamada relleno intracraneal o “taponamiento” para controlar la hemorragia; es una técnica de neurocirugía de control de daños que puede salvar la vida al detener sangrados cerebrales masivos. Posteriormente el paciente fue llevado, aún inconsciente, a un centro de mayor complejidad para cirugía. Llegó sin intubación y en un estado hemodinámico estable.\n\nDespués de la operación tuvo episodios de convulsiones, que se trataron con medicamentos anticonvulsivos, y la evolución fue buena. Este caso muestra cómo una intervención rápida para controlar la hemorragia puede ser determinante y subraya la importancia de medidas preventivas como el uso del casco al conducir una motocicleta.",
+            "B3": "Resumen (nivel lector universitario)\n\nPaciente\n- Hombre de 27 años, fumador, sin antecedentes médicos conocidos. Sufrió una caída de motocicleta sin casco.\n\nPresentación inicial (hallazgos anormales y normales)\n- Al ingreso en el hospital rural: pérdida de conciencia y dos convulsiones. Glasgow Coma Scale 6/15 (no abre ojos, retirada a dolor, sin respuesta verbal) — esto indica un daño cerebral grave.  \n- Midriasis bilateral (dilatación de pupilas) y distrés hemodinámico (inestabilidad de la presión/ritmo circulatorio) — signos de lesión neurológica y estado crítico.  \n- Buena saturación de oxígeno (hallazgo relativamente normal), pero hemoglobina muy baja: 6 g/dL (anemia grave).  \n- Se constató una lesión craneal penetrante con hemorragia intracraneal profusa.\n\nActuación inicial en el centro rural\n- Medidas de soporte: inmovilización cervical, intubación orotraqueal y oxígeno, acceso venoso y reposición de líquidos, administración de manitol (para disminuir presión intracraneal), anticonvulsivantes (fenobarbital, thiopental), antibióticos, suero antitetánico y transfusión sanguínea parcial.  \n- Se practicó un taponamiento (relleno) a través de la fractura craneal para controlar la hemorragia — una maniobra de control de daños neuroquirúrgico destinada a detener sangrado masivo cuando no hay recursos avanzados.  \n- El hospital rural no disponía de TAC ni de unidad de cuidados intensivos, por lo que el paciente fue trasladado a un centro de mayor complejidad estando inconsciente pero hemodinámicamente estable tras la estabilización inicial.\n\nEvaluación en el hospital de referencia y hallazgos por TAC (anormales relevantes)\n- Edema bifrontal agudo y contusión hemorrágica del parénquima, predominante en el lado derecho.  \n- Hematoma subdural agudo (capa de 3 mm) en la región fronto-parieto-temporo-occipital izquierda.  \n- Hernia subfalcular izquierda de 5 mm (desplazamiento del tejido cerebral hacia la línea media), con compresión moderada del ventrículo lateral derecho — ambos son signos de aumento de la presión intracraneal y riesgo de lesión cerebral adicional.  \n- Hemorragia subaracnoidea bifrontal superior.  \n- Fractura frontal deprimida con ruptura osteomeníngea (fractura que comunica el cráneo con las meninges), lo que aumenta el riesgo de infección y fuga de líquido cefalorraquídeo.  \n- Fractura de la tercera vértebra cervical (C3) con compresión de la médula espinal — lesión adicional que requiere manejo espinal especializado.\n\nTratamiento definitivo y evolución\n- El paciente fue intervenido quirúrgicamente con éxito en el hospital de referencia.  \n- En el postoperatorio presentó convulsiones recurrentes, que fueron tratadas con anticonvulsivantes. Bajo ese tratamiento tuvo buena evolución clínica: al primer día tras la transferencia se informó que estaba consciente y caminando, sin déficit neurológico, hemodinámico o respiratorio evidente.\n\nImplicaciones y pasos a seguir recomendados\n- El cuadro inicial era de muy mal pronóstico, pero la intervención de control de daño y la cirugía definitiva permitieron una recuperación inicial favorable.  \n- Seguimiento necesario: continuidad de la terapia anticonvulsivante y vigilancia neurológica para detectar convulsiones tardías o déficits cognitivos/neurológicos; control de la fractura craneal abierta por riesgo de infección y posible reparación adicional si hay fuga de líquido cefalorraquídeo; evaluación y manejo específico de la fractura cervical y de la médula (riesgo de lesión medular tardía, rehabilitación y posible cirugía vertebral según evaluación neuroquirúrgica/ortopédica); control imagenológico de evolución (TAC o RMN) y rehabilitación física/neurológica según necesidades.  \n- También es importante continuar la vigilancia hematológica (recuperación de la anemia) y la prevención de complicaciones infecciosas.\n\nComentario empático\n- Se trata de un adulto joven sin enfermedades previas que sufrió lesiones cerebrales y medulares graves. Recibió intervenciones de emergencia que resultaron en una recuperación inicial notable, pero requiere seguimiento especializado y rehabilitación para maximizar la recuperación y reducir riesgos futuros."
+        }
+    },
+    {
+        "article": "La paciente era una madre de 54 años que provenía de una zona rural y que llegó al Hospital Especializado de Compresión de Nekemte con la queja de una masa en su vagina de 3 años de duración. Hace tres años, encontró una protuberancia de masa a través de su vagina, que gradualmente creció en tamaño con el tiempo. Había tenido dos bebés, el último hace 12 años. Ambos partos fueron en casa, ya que el centro de salud está demasiado lejos de su área de residencia, y fue asistida por una comadrona tradicional. Ella afirmó que todo había sido sin problemas. Inicialmente, hace tres años, hubo sangrado y una descarga ofensiva de la masa, pero eso se detuvo en el último año. Desarrolló laceraciones en la masa hace seis meses. Por esta razón, se divorció y se aisló de toda la vida social durante este largo período de tiempo. Ahora, su hermana mayor y otro familiar la trajeron al hospital específicamente por la laceración de la masa. No tenía ninguna otra enfermedad médica crónica conocida.\n\nHallazgo pertinente del PE\nSigno vital: PA = 100/60 mm hg, FC = 84 lpm, FR = 20 lpm, T° = 36.5°C, peso = 47 kg.\n\nGUS: hay una masa rosada en la vagina que se encuentra a unos 7 cm del anillo del himen.\n\nEl fondo uterino es la parte principal de la masa.\n\nHabía una laceración longitudinal de unos 5 cm en el lado derecho de la masa.\n\nNo hubo sangrado ni secreción de la masa ni del área de la laceración.\n\nLaboratorio\nCBC: hemoglobina = 12 g/dl, PLT = 285 mil, neutrófilos = 74%.\n\nAnálisis de orina: resultado normal.\n\nGrupo sanguíneo = A, RH = positivo.\n\nPrueba de VIH = negativa.\n\nHBSAg = negativo.\n\nEcografía: vejiga parcialmente llena visible en el abdomen, útero no visible en el abdomen. Por lo demás, no se observaron otros hallazgos pertinentes.\n\nRadiografía de tórax: radiografía de tórax normal.\n\nPor este motivo, se le diagnosticó una inversión uterina crónica. Se tomaron imágenes preoperatorias y postoperatorias, el fondo uterino era el punto principal de la masa que sobresalía completamente a través de la vagina y había una laceración crónica desarrollada en la superficie endometrial. Después de la operación, se observó un canal vaginal normal. Después de revisar las opciones de tratamiento con ella y su familia, se programó una cirugía y se realizó una histerectomía abdominal al día siguiente. Era una cirugía abdominal y era fácil introducir el útero en el abdomen. Como el tejido era redundante y distorsionado, es difícil identificar la referencia anatómica y los puntos de referencia quirúrgicos. Debido a esto, la cirugía fue difícil y hubo una lesión ureteral derecha transaccional intraoperatoria y se realizó una anastomosis de extremo a extremo. Se dio de alta el décimo día de la operación y se encontró que estaba mejorando. Se le dio una cita de seguimiento dos semanas después y cuando se evaluó se encontró que estaba bien.\n",
+        "gold_summary": "Una mujer de 54 años de edad acudió a nuestro hospital con la queja de una masa indolora en su vagina de 3 años de duración. Hace tres años, encontró una protuberancia de masa a través de su vagina, que gradualmente creció en tamaño con el tiempo. En el examen físico, el fondo uterino fue el punto principal de la masa y sobresalía 7 cm por debajo del anillo del himen. Como resultado, se le diagnosticó inversión uterina crónica y se le sometió a una histerectomía abdominal. Fue dada de alta en casa mejorada. Presentamos este caso debido a un factor no identificado que provocó la inversión uterina, la presentación tardía de la enfermedad y la dificultad en el tratamiento quirúrgico.\n",
+        "synthetic_summary": {
+            "B1": "Esta es la historia de una mamá de 54 años que vivía en el campo. Hace tres años notó una bolita que salía por su vagina. La bolita fue creciendo poco a poco. Al final, era la parte superior del útero (el lugar donde crecen los bebés) que se había dado vuelta y salido por la vagina. Esto se llama inversión uterina.\n\nTenía una grieta en esa zona desde hace meses. Vivía lejos del hospital y no pidió ayuda antes. Su hermana la llevó cuando la herida empeoró.\n\nLos médicos la revisaron y le hicieron estudios. Todo lo demás estaba bien. Le explicaron las opciones y la operaron al día siguiente. Le quitaron el útero con una cirugía por el abdomen. La operación fue difícil porque los órganos estaban muy cambiados. Durante la cirugía, se cortó sin querer un tubito que lleva la orina del riñón a la vejiga (eso se llama uréter). Los cirujanos lo arreglaron uniendo los dos extremos.\n\nElla mejoró después de la operación. Salió del hospital diez días después y en la cita de control estaba bien. Los médicos compartieron el caso porque la causa de que el útero se volteara no quedó clara y porque la operación fue complicada.",
+            "B2": "Resumen comprensible (nivel secundaria)\n\nUna mujer de 54 años que vive en una zona rural llegó al hospital porque tenía desde hacía 3 años una masa que le salía por la vagina. Al principio la masa sangraba y tenía mal olor, pero eso paró hace aproximadamente un año. Hace seis meses se le abrió una herida (laceración) en la masa, lo que la aisló socialmente y la llevó incluso a un divorcio. No tenía otras enfermedades crónicas conocidas.\n\nEn la exploración, la parte superior del útero (llamada fondo uterino) era la parte principal de la masa y sobresalía por la vagina unos 7 cm más allá del anillo del himen. Esto llevó al diagnóstico de inversión uterina crónica. La inversión uterina ocurre cuando el útero se voltea hacia dentro y puede salir por la vagina; es algo raro en mujeres no embarazadas y suele requerir tratamiento quirúrgico si es crónica.\n\nSe hicieron pruebas: hemoglobina y otros análisis fueron normales, la ecografía no mostró el útero en el abdomen (porque estaba fuera) y las pruebas de VIH y hepatitis B fueron negativas. Tras hablar con la paciente y su familia, se realizó una histerectomía abdominal (operación para quitar el útero). Durante la cirugía fue difícil reconocer las estructuras porque los tejidos estaban muy deformados; esto causó una lesión accidental en el uréter derecho (el conducto que lleva la orina del riñón a la vejiga), que se reparó con una sutura de extremo a extremo.\n\nLa paciente mejoró después de la operación, estuvo ingresada diez días y en la consulta de control dos semanas después estaba bien. Este caso llama la atención por la causa no identificada de la inversión, la presentación tardía (probablemente influida por el acceso limitado a servicios de salud) y las dificultades técnicas durante la cirugía.",
+            "B3": "Presentación clínica\nUna mujer de 54 años, procedente de zona rural, consultó por una masa vaginal que había notado desde hacía 3 años y que fue creciendo gradualmente. Inicialmente la masa produjo sangrado y secreción fétida (que cesaron en el último año); hace seis meses se desarrolló una laceración sobre la masa. Por esta condición la paciente sufrió aislamiento social y divorcio y acudió al hospital acompañada por familiares. No refería otras enfermedades crónicas conocidas.\n\nExamen físico y pruebas\n- Signos vitales estables (PA 100/60 mmHg, FC 84 lpm, FR 20, T 36.5 °C). Peso 47 kg.  \n- Inspección genital: masa rosada que protruye por la vagina y cuyo punto principal es el fondo uterino, ubicado 7 cm por debajo del anillo himenal. Se observó una laceración longitudinal de unos 5 cm en el lado derecho de la masa sin sangrado activo ni secreción en el momento del examen.  \n- Analítica: hemoglobina 12 g/dl, plaquetas 285.000/µl, neutrófilos 74%. Orina normal. Serologías: VIH negativo, HBsAg negativo. Grupo sanguíneo A Rh+.  \n- Imagen: ecografía abdominal no visualizó el útero en su localización habitual; radiografía de tórax normal.\n\nDiagnóstico y tratamiento\nCon estos hallazgos se diagnosticó inversión uterina crónica: el útero estaba volteado de manera que su fondo sobresalía a través de la vagina. Tras discutir opciones, se realizó una histerectomía abdominal programada al día siguiente. Durante la cirugía el útero pudo reintegrarse al abdomen, pero el tejido estaba muy redundante y distorsionado, lo que dificultó identificar referencias anatómicas. Esto provocó una lesión transaccional del uréter derecho, que se reparó mediante anastomosis término-terminal intraoperatoria. La paciente evolucionó bien, fue dada de alta al décimo día y en la cita de control a las dos semanas se encontró sin problemas aparentes.\n\nInterpretación y consideraciones\n- Hallazgos normales: signos vitales y pruebas básicas (hemograma, orina, radiografía de tórax) sin alteraciones importantes; ausencia de infección por VIH o hepatitis B.  \n- Hallazgos anormales: inversión uterina crónica con protrusión del fondo uterino y laceración endometrial crónica; distorsión anatómica que complicó la cirugía y conllevó lesión ureteral iatrogénica tratada en el mismo acto.  \n- Etiología: la causa precisa de la inversión no pudo establecerse. La inversión uterina crónica suele relacionarse con eventos obstétricos (p. ej., manipulación uterina) pero en este caso la paciente no informó de un episodio agudo claro en el puerperio —su último parto fue hace 12 años, en casa— lo que sugiere un caso de presentación tardía o una causa no identificada.  \n- Impacto psicosocial: la larga evolución, la secreción y la laceración contribuyeron al estigma social y aislamiento de la paciente, subrayando barreras de acceso a la atención en áreas rurales.\n\nRecomendaciones y seguimiento\n- Seguimiento urológico para vigilar la viabilidad y el drenaje del uréter derecho (evaluación clínica, creatinina renal y, si procede, imagen como urografía por TC o ecografía renal).  \n- Control ginecológico de la herida y recuperación posoperatoria.  \n- Apoyo psicosocial y, si procede, orientación para acceso a servicios de salud reproductiva y atención primaria para prevenir demoras en futuros problemas.  \n- Documentación y discusión multidisciplinaria de casos similares pueden ayudar a identificar factores de riesgo y mejorar la atención en áreas con acceso limitado.\n\nResumen breve\nMujer de 54 años con inversión uterina crónica que protruyó por la vagina durante 3 años, tratada mediante histerectomía abdominal. La cirugía fue compleja por la alteración anatómica y se asoció a lesión ureteral reparada intraoperatoriamente. La paciente mejoró y presentó buena evolución en controles. El caso destaca la presentación tardía, la dificultad quirúrgica y las consecuencias psicosociales en un entorno rural con acceso limitado a atención obstétrica."
+        }
+    },
+    {
+        "article": "Varón de 20 años, HIV negativo, con TB pulmonar y tratamiento irregular en 2020-2021. Se internó por síndrome de impregnación bacilar, dolor e impotencia funcional del hombro derecho. Presentaba mal estado general, adelgazado, hipotrofia muscular grave, lesiones tumorales frías fluctuantes fistulizadas en dorso, calota craneana y tórax anterior con secreción caseosa, sin presentar déficits motores ni sensitivos. El examen molecular rápido (GeneXpert Mtb/Rif) de secreción del tórax fue positivo para Mycobacterium tuberculosis, sensible a rifampicina (el antibiograma fenotípico mostró una cepa pansensible). La TC demostró consolidaciones pulmonares y árbol en brote, junto con el compromiso óseo de columna cervical, dorsal y lumbar con imágenes líticas y colecciones pre y paraespinales. En la RMN se observaron imágenes infiltrativas desde C4 a C6; D4 a D6, D9 a D12; fractura patológica de D6 y D10 e infiltración en L1, L2 y L3. Inició tratamiento anti-TB con esquema estándar de primera línea (isoniacida, rifampicina, pirazinamida, etambutol). Dada la extensa destrucción y el peligro de cuadriplejía/paraplejía por el compromiso cervical y/o dorsal, se indicó posición decúbito dorsal permanente, collar de Filadelfia, asistencia kinésica y conducta neuroquirúrgica en forma programada en los niveles cervicales, D6 y D10. Previo a la cirugía programada presentó un cuadro agudo de paraplejía con nivel sensitivo D8, con compromiso vesical. Se interpretó como nivel de compresión aguda en D6. Se indicó neurocirugía de urgencia con descompresión medular vía posterior con laminectomía dorsal 6 y parcialmente D5 y 7 y evacuación de una colección epidural. Fue recuperando la función motora y sensitiva en forma progresiva. Posteriormente se realizó la cirugía programada cervical vía anterior con corporectomía de C4, C5, C6 y C7 más artrodesis de C3 a D1 con reemplazo de cuerpo vertebral más injerto autólogo, placa y tornillos. En la TC de control se evidenció luxación posterior de D6 con compresión del canal espinal y deterioro neurológico por compresión medular. Se reconsideró la táctica quirúrgica debido a la inestabilidad mecánica y neurológica. Se realizó descompresión y alineación del nivel luxado con artrodesis posterior de los tres niveles espinales no adyacentes, cervical, dorsal 6 y dorsal 10 en un solo tiempo quirúrgico. Se fijó desde  C3 hasta D12 con tornillos poliaxiales y barra de transición cervicodorsal. En cada tiempo quirúrgico se evidenció evacuación espontánea de material caseoso, BAAR positivo, y se realizaron lavados profusos.  Presentó mejoría clínica, bacteriológica y resolución de las lesiones pulmonares. Recuperó movilidad con rehabilitación kinésica sumada al tratamiento específico (3 meses de primera fase e indicación de continuación con isoniacida y rifampicina hasta completar los 12 meses). Egresó caminando por sus propios medios, luego de una prolongada internación de 5 meses.",
+        "gold_summary": "Se presenta el caso de un varón de 20 años con espondilitis tuberculosa multinivel no contigua (cervical, dorsal 6, dorsal 10 y lumbar). Se trata de un paciente HIV negativo con tuberculosis diseminada con grave compromiso de su estado general y múltiples localizaciones de la enfermedad. Algunas tenían fistulas que secretaban caseum. El paciente presentó paraplejía aguda que requirió, teniendo en cuenta el nivel sensitivo a nivel dorsal 6, una primera cirugía urgente de descompresión por vía posterior. Luego se efectuó la cirugía programada. En primera instancia, la región cervical por vía anterior, con corporectomía, colocación de reemplazo de cuerpo vertebral más injerto autólogo y placa con tornillos. Posteriormente se evidenció luxación del nivel dorsal 6 hacia atrás comprimiendo la médula espinal y, dada la inestabilidad mecánica, se indicó un tercer tiempo quirúrgico por vía posterior que comprendió reducción, descompresión y fijación, resolviendo los tres niveles por vía posterior con barras y tornillos. El tratamiento quirúrgico, médico y kinésico de esta forma poco frecuente del mal de Pott fue exitoso, con recuperación de su estabilidad mecánica y progresiva recuperación de su estado neurológico.",
+        "synthetic_summary": {
+            "B1": "Un joven de 20 años tuvo tuberculosis que se extendió a los pulmones y a varios huesos de la columna. Tenía heridas que supuraban material blando y estaba muy delgado y débil. \n\nEmpezó tratamiento contra la tuberculosis con antibióticos especiales. Pero un día perdió fuerza en las piernas y no podía controlar la vejiga. Los médicos vieron que la médula espinal estaba siendo aplastada en la parte media de la espalda. Hicieron una cirugía urgente por detrás para quitar la presión y drenar una colección de material infectado. Después de esa operación fue mejorando poco a poco.\n\nLuego le hicieron una cirugía programada en el cuello por delante. Le quitaron partes de varias vértebras enfermas y las reemplazaron, con injerto y una placa para dejar el cuello firme. Más tarde se comprobó que una vértebra de la espalda se había movido hacia atrás y volvía a apretar la médula. Por eso hicieron otra operación desde atrás para alinear, descomprimir y fijar la columna con tornillos y barras, abarcando los niveles afectados.\n\nEn las operaciones encontraron material típico de la tuberculosis y lo lavaron bien. Con los medicamentos antituberculosos (incluyendo isoniacida y rifampicina) y la rehabilitación con fisioterapia, el joven mejoró mucho. Sus pulmones también sanaron. Continuó el tratamiento hasta completar 12 meses. Tras cinco meses de hospital, salió caminando por sus propios medios.",
+            "B2": "This is the case of a 20-year-old man with widespread tuberculosis (TB) that affected his lungs and many parts of his spine. He was HIV-negative and had a history of not finishing TB treatment. He was very weak and thin, and had several soft swellings on his back, skull, and chest that leaked a thick, cheese-like fluid (this is dead tissue caused by TB).\n\nTests on the chest fluid confirmed Mycobacterium tuberculosis that was sensitive to usual drugs. Scans showed lung damage and multiple areas of bone destruction in the cervical (neck), dorsal (upper and mid-back), and lumbar (lower back) spine. MRI also found broken vertebrae and collections of infected material pressing near the spinal cord.\n\nDoctors began standard first-line TB medicine (isoniazid, rifampicin, pyrazinamide, ethambutol). Because the spine was badly damaged and there was a real risk of losing movement (paralysis), they planned spinal surgery and kept him in a stable position with a neck collar while preparing.\n\nBefore the planned surgery, he suddenly developed paraplegia (loss of leg movement) and a sensory level at the mid-back, with bladder problems. This was judged to be sudden spinal cord compression at the sixth dorsal vertebra (D6). He had emergency posterior surgery to relieve the pressure (laminectomy, which means removing part of the back of the vertebra) and the surgeons drained an epidural collection of infected material. He recovered some movement and feeling after that operation.\n\nLater, the team performed the planned neck surgery from the front: they removed damaged vertebral bodies in the neck (corporectomy of C4–C7), replaced them, and fused the spine from C3 to D1 using the patient’s bone graft and metal hardware. In a follow-up scan, D6 had shifted backwards and was again pressing on the spinal cord, causing new neurologic problems. Because the spine was mechanically unstable, surgeons performed another operation from the back to realign, decompress, and stabilize the damaged levels. In total, they fixed the spine from C3 down to D12 with rods and screws in a combined approach.\n\nThroughout the surgeries, the teams found and washed out caseous (cheesy) TB material; samples were positive for TB bacteria. With combined medical therapy, repeated surgical drainage and stabilization, and intensive physical rehabilitation, the patient improved. His lung infections healed, bacteria tests became negative, and he regained the ability to walk. He continued TB medication to complete a year of treatment and was discharged walking after a five-month hospital stay.\n\nThis case shows a severe, multi-level form of spinal TB (Pott disease) that required urgent and staged surgical care together with long-term antibiotics and rehab. The combined approach led to recovery of spinal stability and gradual neurological improvement.",
+            "B3": "Resumen clínico breve (empatía y contexto)\n- Paciente: varón de 20 años, VIH negativo, con antecedente de tratamiento antituberculoso irregular en 2020–2021.\n- Presentación: deterioro general marcado, pérdida de peso y atrofia muscular; lesiones frias fistulizadas en dorso, calota y tórax con secreción caseosa. Inicialmente sin déficit neurológico motor o sensitivo, pero con dolor e impotencia funcional del hombro derecho.\n\nHallazgos diagnósticos principales\n- Microbiología: GeneXpert positivo para Mycobacterium tuberculosis sensible a rifampicina; cultivos/antibiograma fenotípico: cepa pansensible.\n- Imágenes torácicas: consolidaciones y patrón árbol en brote (típico de TB pulmonar).\n- Columna: lesiones líticas y colecciones pre/paraespinales en niveles cervical, dorsal y lumbar. RMN con infiltración en C4–C6; D4–D6; D9–D12; fracturas patológicas en D6 y D10; compromiso de L1–L3.\n- Diagnóstico anatómico: espondilitis tuberculosa multisegmentaria no contigua (mal de Pott), con abscesos epidurales que amenazaban la médula.\n\nTratamiento realizado (médico, quirúrgico y rehabilitador)\n- Tratamiento antituberculoso inicial estándar de primera línea (isoniacida, rifampicina, pirazinamida, etambutol); esquema prolongado hasta 12 meses (fase intensiva 3 meses, continuación con isoniacida + rifampicina).\n- Manejo preventivo inicial: posición supina, collar cervical de Filadelfia y kinesiterapia, plan quirúrgico programado por compromiso multisegmentario.\n- Evento agudo: antes de la cirugía programada el paciente desarrolló paraplejía aguda con nivel sensitivo en D8 y trastorno vesical → interpretado como compresión aguda en D6.\n  - Urgencia: descompresión posterior con laminectomía (D6 ± D5–D7) y evacuación de colección epidural → recuperación progresiva sensitivo-motora.\n- Cirugías programadas posteriores:\n  1) Vía anterior cervical: corporectomías cervicales (C4–C7), reemplazo de cuerpos vertebrales con injerto autólogo, artrodesis C3–D1 y fijación anterior (placa y tornillos).\n  2) Tras observar luxación posterior en D6 con nueva compresión y inestabilidad, se realizó en un solo tiempo posterior: reducción/descompresión y artrodesis posterior que incluyó fijación desde C3 hasta D12 con tornillos poliaxiales y barra de transición cervicodorsal; se abordaron los tres niveles comprometidos (cervical, D6 y D10). En todas las cirugías se evacuó material caseoso y se comprobó BAAR positivo.\n- Rehabilitación kinésica intensiva complementaria.\n\nEvolución y resultado\n- Mejoría clínica y microbiológica: resolución de lesiones pulmonares y negativización progresiva.\n- Recuperación neurológica: recuperación de la función motora y sensitiva de forma progresiva; al alta el paciente caminaba por sus propios medios.\n- Hospitalización prolongada: 5 meses; seguimiento con continuidad del tratamiento antituberculoso hasta completar 12 meses.\n\nImplicaciones clínicas y lecciones principales\n- Este caso ilustra una forma poco frecuente y grave de TB ósea: espondilitis tuberculosa multisegmentaria no contigua con abscesos epidurales y riesgo real de lesión medular irreversible.\n- Mensajes relevantes:\n  - Ante déficit neurológico agudo por compresión medular por TB, la descompresión urgente puede permitir recuperación neurológica.\n  - Las lesiones tuberculosas vertebrales pueden requerir una combinación de abordajes (anterior para reconstrucción vertebral y posterior para estabilización) y fijación extensa cuando hay inestabilidad mecánica.\n  - El tratamiento antibiótico prolongado y la rehabilitación son esenciales para la resolución infectológica y funcional.\n  - La adherencia al tratamiento antituberculoso y el seguimiento son claves para prevenir diseminación y complicaciones graves.\n\nComentario final (empatía)\nEl caso muestra que, aun frente a una TB diseminada y compromiso medular serio, la combinación de tratamiento antituberculoso apropiado, intervenciones quirúrgicas oportunas y rehabilitación puede conducir a una recuperación funcional significativa."
+        }
+    },
+    {
+        "article": "Un hombre japonés de 23 años fue admitido en nuestro hospital debido al empeoramiento de la disnea de esfuerzo. Había mostrado dificultad para correr a los dos años y se le diagnosticó EDMD con una mutación genética de LMNA (Lamin A/C) en el exón 1 de leucina 102 a prolina. De acuerdo con las manifestaciones típicas de EDMD, sus codos, rodillas y tendones de Aquiles se habían contraído a los cinco años, y sus músculos cervicales posteriores se habían vuelto rígidos; sin embargo, continuó con su vida diaria habitual, aunque con una leve restricción de ejercicio. Su padre también había sido diagnosticado con EDMD y murió repentinamente a los 40 años.\n\nCuando el paciente tenía 19 años, fue admitido en un hospital por primera vez debido a una insuficiencia cardiaca congestiva. Los signos de insuficiencia de la RV, tales como edema de las piernas y congestión hepática, fueron prominentes, como lo indica el alto nivel de bilirrubina en sangre (2,5 mg/dL). La ecocardiografía mostró que la excursión sistólica del plano anular tricúspide (TAPSE) era de 5,7 mm, la velocidad de la RV de 5,1 cm/s y el cambio del área fraccional de la RV (RVFAC) del 19 %, lo que indica una marcada disfunción de la RV. Se introdujeron diuréticos de alta dosis además de carvedilol (10 mg/día) y enalapril (2,5 mg/día). A pesar de esos medicamentos, fue readmitido debido al empeoramiento de la insuficiencia de la RV.\n\nA los 22 años, se le implantó un desfibrilador cardioversor implantable (ICD) debido a su taquicardia ventricular no sostenida (VT) y a la historia familiar de muerte súbita cardiaca. En este momento, el cateterismo cardiaco derecho (RHC) mostró una presión de la cuña de la arteria pulmonar (PAWP) de 22 mmHg, presión auricular derecha (RAP) de 17 mmHg, e índice de trabajo de accidente cerebrovascular ventricular derecho (RVSWI) de 6.47, lo que sugiere una disfunción severa sostenida del RV. Como tal, el fallo del RV probablemente fue la principal condición patológica a lo largo de su curso clínico.\n\nTenía insuficiencia cardiaca sintomática con la clasificación III de la New York Heart Association con dosis máximas de medicación guiada por directrices, y su electrocardiograma mostraba un ritmo sinusal regular y bloqueo de rama izquierda con ancho QRS (150 ms). Su fracción de eyección del ventrículo izquierdo (LVEF) era ≤35 % en la ecocardiografía. Por lo tanto, se consideró que estaba indicado para CRT y se le actualizó a ICD a los 23 años.\n\nAl ingreso, su presión arterial era de 106/65 mmHg y su frecuencia cardíaca de 60 latidos/min con un ritmo regular. El examen físico reveló un tercer sonido cardíaco y un soplo pan sistólico (Levine II/VI) en la región apical. Los sonidos respiratorios eran claros, mientras que una vena yugular distendida y un edema de miembros inferiores eran evidentes. La radiografía de tórax indicó un aumento de la relación cardiotorácica (59%) sin congestión pulmonar.\n\nEl electrocardiograma mostró un ritmo biventricular debido a la TRC. La ecocardiografía reveló una ligera dilatación en ambos ventrículos (diámetro final diastólico del LV: 54 mm, diámetro del RV: 50 mm) con una reducción de la LVEF (30%). La función del RV también se redujo, como lo indican una reducción de la RVFAC (11%) y un bajo TAPSE (8 mm). Ambos ventrículos agrandados causaron una pérdida de sujeción y coaptación de las valvas que resultó en una regurgitación mitral moderada y una regurgitación tricuspídea severa. La vena cava inferior se dilató a 23 mm con una reducción de la fluctuación respiratoria.\n\nEn los hallazgos histológicos de los músculos cervicales posteriores realizados más tarde en la autopsia, se observó un aumento en la variación del tamaño de la fibra muscular con una infiltración moderada de tejido conectivo, lo que fue compatible con la EDMD. Los análisis de sangre revelaron péptido natriurético cerebral (BNP) 196.1 pg/mL, bilirrubina total 1.4 mg/dL, aspartato aminotransferasa (AST) 39 U/L, alanina aminotransferasa (ALT) 43 U/L, y gamma glutamil transpeptidasa (gamma-GTP) 451 U/L, lo que sugirió una disfunción hepática. Aunque las arterias coronarias estaban intactas en la angiografía, una biopsia endocárdica del VD reveló una hipertrofia cardiaca con un aumento de la magnitud del núcleo y el miocardio.\n\nLa microscopía electrónica demostró hallazgos típicos de la EDMD: un número reducido de miofibrillas, necrosis y la formación de pseudo- o verdaderas inclusiones. Dado que se descartaron otras cardiomiopatías secundarias mediante estos hallazgos clínicos e histológicos, diagnosticamos una cardiomiopatía relacionada con la EDMD.\n\n\nEl curso clínico del paciente. El cateterismo cardiaco derecho (RHC) en el día 11 mostró disfunción y congestión severa del LV/RV, y se iniciaron algunos inótropos. Aunque la hemodinámica del paciente mejoró, su función renal empeoró progresivamente en el día 38. Preocupados por el empeoramiento de su función renal debido a la disminución de la presión arterial, se iniciaron la dopamina y el soporte mecánico (IABP y CRRT), y la función renal y la hemodinámica del paciente mejoraron. Sin embargo, desarrolló insuficiencia hepática aguda junto con insuficiencia severa del RV indicada por los datos del RHC en el día 68. Aunque se introdujo ECMO veno-atrial en el día 71, la disfunción hepática y la DIC causaron diátesis hemorrágica sistémica, y el paciente falleció por fallo multiorgánico en el día 100. CRRT: terapia de reemplazo renal continua, DIC: coagulación intravascular diseminada, ECMO: oxigenación por membrana extracorpórea, IABP: bombeo de globo intraaórtico, LV: ventrículo izquierdo, RV: ventrículo derecho\n\nEl RHC en el día 11 mostró que el índice cardiaco (IC) era de 2,0 L/min/m2 (método de Fick), y la PAP era de 15 mmHg, lo que indicaba un subgrupo IV de Forrester. La presión arterial pulmonar (PAP) era de 29/12 (18) mmHg, y la RAP era de 15 mmHg. El RVSWI, uno de los parámetros hemodinámicos para la función del RV, se calculó con la siguiente fórmula: RVSWI (g·m/m2/latido)=[presión arterial pulmonar media (mPAP)-presión atrial derecha media (mRAP)]×índice de volumen de latido (SVI)×0.0136. Su RVSWI era de 1.36 g·m/m2/latido, lo que indicaba una disfunción severa del RV. Para compensar el síndrome de baja producción del paciente y la congestión, comenzamos una infusión continua de dobutamina (3.0 μg/kg/min) y añadimos milrinona (0.125 μg/kg/min) en el día 16.\n\n\nEn el día 32, los datos de RHC mejoraron, con un aumento del IC (2,48 L/min/m2), una reducción de la PAWP (13 mmHg) y un aumento de la RVSWI (2,8 g·m/m2/latido). Sin embargo, en el día 38, la función renal del paciente empeoró progresivamente, posiblemente debido a una presión venosa central alta (CVP) e hipotensión, ya que la presión arterial había sido de alrededor de 70/40 mmHg varios días antes del empeoramiento de la función renal. Para aumentar su presión arterial, se inició una infusión continua de dopamina (2,0 μg/kg/min); se redujo la milrinona y se interrumpieron el enalapril y la eplerenona. Además, se necesitaron temporalmente el bombeo de globo intraaórtico (IABP) y la terapia de reemplazo renal continuo (CRRT). A medida que la hemodinámica del paciente mejoró en respuesta al aumento de la saturación de oxígeno venoso mixto (SvO2, 70-80%) y el IC (3,0-3,5 L/min/m2), se retiraron el IABP y la CRRT en el día 45.\n\nSin embargo, el día 68, el IC volvió a disminuir a 1,25 l/min/m2 y la congestión pulmonar y la retención de fluidos del paciente se deterioraron; la PAWP era tan alta como la RAP, a 22 mmHg. Además, los niveles de bilirrubina en suero y las transaminasas hepáticas del paciente aumentaron drásticamente, lo que sugiere el desarrollo de insuficiencia hepática. El día 71, se inició la ECMO VA a través de una vena femoral a la arteria subclavia, pero debido a la diátesis hemorrágica sistémica acompañada por la coagulación intravascular diseminada (CID), el paciente falleció de insuficiencia multiorgánica el día 100.\n\nUna autopsia realizada con el consentimiento informado de la familia del paciente reveló un agrandamiento eferente en ambos ventrículos con un espesor de pared delgado. El examen histopatológico reveló que la hipertrofia miocárdica leve a moderada y la fibrosis severa eran evidentes en el RV y el LV. El peso del hígado aumentó significativamente a 2298 g, y se detectaron congestión hepática macroscópica y colestasis. En las imágenes microscópicas, el área de la vena porta apenas cambió, y se observó atrofia o pérdida de hepatocitos alrededor de las venas centrales, lo que indica un «hígado de shock». En los pulmones, se observó una hemorragia alveolar extensa, y se observó una colección de macrófagos que habían ingerido hemosiderina, lo que refleja una diátesis hemorrágica sistémica.\n\nMH - Adulto\nMH - Insuficiencia cardiaca/*etiología/fisiopatología/terapia\nMH - Humanos\nMH - Lamin tipo A/genética\nMH - Hombre\nMH - Distrofia muscular, Emery-Dreifuss/*complicaciones/diagnóstico/genética/terapia\nMH - Mutación\n",
+        "gold_summary": "Un hombre de 23 años tenía debilidad muscular progresiva y distrofia muscular de Emery-Dreifuss (EDMD) debido a una mutación de LMNA (lamina A/C). Insuficiencia cardiaca congestiva diagnosticada a los 19 años de edad. El tratamiento farmacológico máximo/resincronización cardiaca no logró mejorar la función cardiaca. Por lo tanto, fue hospitalizado debido a insuficiencia cardiaca. A pesar de la oxigenación por membrana extracorpórea, desarrolló una disfunción cardiaca derecha grave y falleció (fallo multiorgánico).\n",
+        "synthetic_summary": {
+            "B1": "Había un joven japonés de 23 años con una enfermedad heredada llamada distrofia muscular de Emery-Dreifuss. Esta enfermedad hace que los músculos y también el corazón se debiliten. Desde niño tuvo problemas para moverse y con el tiempo su corazón empezó a fallar.\n\nA los 19 años su corazón ya no bombeaba bien, sobre todo el lado derecho. Le dieron medicinas y le pusieron un aparato que protege el corazón y otro que ayuda a que los dos lados latan al mismo tiempo. Aun así su estado empeoró y lo ingresaron al hospital.\n\nLos médicos usaron muchos tratamientos fuertes. Le dieron medicinas que ayudan al corazón, una máquina para apoyar la circulación, una máquina para limpiar la sangre cuando los riñones fallan y otra para ayudar a los pulmones y al corazón. Al principio mejoró, pero después su hígado y otros órganos sufrieron mucho.\n\nLamentablemente, después de varios días con cuidados intensivos presentó sangrados y una falla de varios órganos, y falleció. La autopsia mostró que los dos ventrículos del corazón estaban agrandados y con mucho daño, y que el hígado y los pulmones también estaban muy dañados por la mala circulación. Su caso muestra cómo esta forma de distrofia muscular puede afectar gravemente al corazón y a todo el cuerpo.",
+            "B2": "Here is a clear, compassionate summary of the case:\n\nA 23-year-old Japanese man had Emery–Dreifuss muscular dystrophy (EDMD). EDMD is a genetic disease that weakens muscles and causes stiff joints. His condition came from a change (mutation) in the LMNA gene, which makes a protein important for cell structure. He had muscle problems and joint contractures from early childhood, and his father—who also had EDMD—died suddenly at 40.\n\nAt 19 he developed congestive heart failure. This means his heart could not pump blood well, and fluid built up in his body. Tests showed the right side of his heart (the right ventricle, RV) was especially weak. He needed strong medicines for heart failure, but his condition later got worse again. At 22 he received an implantable cardioverter-defibrillator (ICD) because of dangerous heart rhythms and family history of sudden death. At 23, because his left heart pumping (left ventricular ejection fraction) was low and he had severe symptoms, his device was upgraded to cardiac resynchronization therapy (CRT) to try to help both sides of the heart work together.\n\nDuring the hospital stay his blood pressures and heart pressures showed severe right and left heart failure. Doctors tried many treatments: inotropic medicines (drugs that help the heart pump), dopamine and dobutamine, milrinone, a balloon pump placed in the aorta (IABP) to support circulation, continuous dialysis (CRRT) when his kidneys failed, and finally veno-arterial extracorporeal membrane oxygenation (VA-ECMO), which is an external machine that supports heart and lung function. At times his condition improved, but he later developed worsening kidney failure, then severe liver failure and a disorder of blood clotting (disseminated intravascular coagulation, DIC) that caused bleeding throughout the body.\n\nDespite all treatments, he died on day 100 of multiorgan failure. An autopsy showed both heart ventricles were enlarged with thin walls and had severe scarring (fibrosis). The liver was very congested and showed changes called “shock liver” from poor blood flow. The lungs had bleeding and signs of widespread bleeding problems.\n\nDoctors concluded his heart disease was a cardiomyopathy caused by EDMD (linked to the LMNA mutation). This report shows how a genetic muscle disease can especially damage the heart and, despite many advanced treatments, can lead to fatal heart and organ failure. My condolences to his family—this was a serious, progressive illness that proved hard to control.",
+            "B3": "Resumen clínico (lectores universitarios)\n\nPaciente: hombre japonés, 23 años. Historia familiar relevante: padre con diagnóstico de distrofia muscular de Emery–Dreifuss (EDMD) que falleció súbitamente a los 40 años. Genética: mutación heterocigota en LMNA (lamina A/C), cambio L102P (leucina 102 → prolina, exón 1).\n\nAntecedentes musculares y diagnóstico\n- Desde la infancia presentó debilidad muscular progresiva y contracturas típicas de EDMD (codos, rodillas, tendones de Aquiles; rigidez cervical), diagnóstico confirmado por hallazgos histológicos musculares (variación del tamaño de fibras y fibrosis) en la autopsia.\n- La mutación en LMNA explica la combinación de miopatía, afectación del sistema de conducción y cardiomiopatía.\n\nCurso cardíaco y hallazgos iniciales\n- A los 19 años ingresó por insuficiencia cardiaca congestiva con signos predominantes de insuficiencia del ventrículo derecho (RV): edema, congestión hepática y bilirrubina elevada (2,5 mg/dL).\n- Ecocardiografía inicial: marcada disfunción del RV (TAPSE 5,7 mm; velocidad tisular RV 5,1 cm/s; RVFAC 19%).\n- Se inició tratamiento médico (diuréticos, carvedilol, enalapril) pero con episodios recurrentes de descompensación.\n\nArritmias y dispositivos\n- A los 22 años recibió un desfibrilador cardioversor implantable (ICD) por taquicardia ventricular no sostenida y antecedentes familiares de muerte súbita.\n- Debido a insuficiencia cardiaca sintomática (NYHA III), LVEF ≤35% y bloqueo de rama izquierda con QRS ancho (150 ms), se actualizó a resincronizador (CRT‑D) a los 23 años.\n\nIngreso y evaluación hemodinámica reciente\n- Al ingreso presentaba hipotensión relativa (106/65 mmHg), ritmo biventricular por CRT, hepatomegalia congestiva, vena yugular distendida y edema. Radiografía: cardiomegalia (ITC 59%) sin edema pulmonar marcado.\n- Ecocardiograma: dilatación leve de ambos ventrículos, LVEF ≈30%, RV muy deteriorado (RVFAC 11%, TAPSE 8 mm), insuficiencia tricuspídea severa secundaria a dilatación.\n- Laboratorio: BNP elevado (196 pg/mL), enzimas hepáticas y gamma‑GTP marcadamente elevadas (gamma‑GTP 451 U/L), signos de disfunción hepática.\n- Angiografía coronaria normal; biopsia endomiocárdica del RV mostró hipertrofia miocárdica, necrosis y en la microscopía electrónica hallazgos característicos de EDMD (pérdida de miofibrillas e inclusiones).\n\nEvolución hospitalaria y terapias avanzadas\n- RHC (día 11): bajo índice cardíaco (IC 2,0 L/min/m2 por Fick), RAP y PAWP elevadas; RVSWI muy reducido (1,36 g·m/m2/latido), consistente con insuficiencia grave del RV. Se inició dobutamina y luego milrinona.\n- Respuesta transitoria: mejoría hemodinámica (IC 2,48 L/min/m2, RVSWI 2,8 g·m/m2/día 32). Posteriormente empeoramiento renal (probablemente por hipotensión sostenida y alta presión venosa central) → dopamina, suspensión de inhibidores del SRA, IABP e inicio de terapia de reemplazo renal continua (CRRT). Estas medidas mejoraron la hemodinámica y se retiraron IABP/CRRT.\n- Recaída y órgano terminal: en día 68 nuevo descenso del IC (1,25 L/min/m2), agravamiento de congestión y colestasis/hepatopatía aguda. Se instauró ECMO veno‑arterial (día 71), pero el paciente desarrolló coagulación intravascular diseminada (CID) con diátesis hemorrágica y falleció por fallo multiorgánico en el día 100.\n\nHallazgos post‑mortem\n- Corazón: dilatación biventricular con paredes adelgazadas; histología con fibrosis severa y moderada hipertrofia en ambos ventrículos.\n- Hígado: peso aumentado (2298 g), congestión macroscópica, colestasis y atrofia centrolobulillar de hepatocitos compatible con “hígado de shock” por congestión/hipoperfusión.\n- Pulmones: hemorragia alveolar extensa y macrófagos con hemosiderina (reflejan diátesis hemorrágica).\n- Musculatura cervical: cambios compatibles con EDMD.\n\nInterpretación y lecciones clínicas (implicaciones)\n- En esta persona la cardiomiopatía relacionada con LMNA/EDMD se presentó con afectación dominante del ventrículo derecho y evolución fulminante pese a terapia médica óptima y resincronización. Las mutaciones en LMNA predisponen a arritmias malignas y a una cardiomiopatía progresiva que puede no responder a terapias convencionales.\n- Puntos clínicos relevantes para casos similares: vigilancia temprana y seriada de la función del RV (ecocardiografía y, si procede, RHC), consideración precoz de derivación a trasplante o asistencia ventricular cuando existe disfunción biventricular progresiva y falla orgánica recurrente, y cribado genético/familiar y asesoramiento genético por el riesgo hereditario.\n- El caso también subraya las limitaciones de las terapias de soporte (inótropos, IABP, ECMO) cuando la miocardiopatía está avanzada y la fibrosis es extensa, y los riesgos de complicaciones como CID y fallo multiorgánico.\n\nComentario humano y empatía\nEste caso ejemplifica la carga grave y rápida que puede comportar la cardiomiopatía por LMNA en pacientes jóvenes con EDMD. A pesar de intervenciones agresivas y tecnología avanzada, la enfermedad puede progresar a insuficiencia orgánica irreversible. El manejo óptimo incluye vigilancia cardiaca estrecha, planificación anticipada de terapias avanzadas y apoyo a la familia con información y asesoramiento genético."
+        }
+    },
+    {
+        "article": "Mujer de 65 años sin antecedentes patológicos destacables que en 2004 inició paroxismos lancinantes en los territorios V2 y V3 derechos, con desencadenantes clásicos, por lo que se le diagnosticó una neuralgia del trigémino derecho. En las resonancias magnéticas cerebrales hasta 2021 no se habían realizado las secuencias que permiten identificar si hay un cruce neurovascular. Desde el inicio, el control del dolor con carboxamidas fue difícil. En 2021 presentó exacerbación de los paroxismos previos que aparecieron en V1. La neuralgia se volvió refractaria, sin respuesta a las carboxamidas y la lamotrigina, y muy escasa al clonacepam, por lo que requirió perfusiones de fenitoína y/o lidocaína en las exacerbaciones graves. Simultáneamente inició paroxismos lancinantes en la parte posterior de la lengua y la pared lateral derecha de la orofaringe, que se exacerbaron con la deglución y que aumentaron progresivamente en intensidad y frecuencia. Se orientó como el inicio de una neuralgia del nervio glosofaríngeo derecho. Se repitió la resonancia magnética cerebral con secuencia CISS (del inglés, constructive interference in steady state), que mostró un contacto arterial significativo entre la arteria cerebelosa superior derecha y el origen del V par craneal derecho, y de la arteria cerebelosa anteroinferior con el origen de los pares craneales bajos derechos. Ante un caso de neuralgia del nervio trigémino y neuralgia del nervio glosofaríngeo clásicas, concomitantes y refractarias, se planteó una doble descompresión microvascular en un tiempo como mejor opción terapéutica.\n\nEn marzo de 2021 se realizó una craniectomía retrosigmoidea derecha con exposición de la cisterna perimesencefálica y las cisternas basales. Se procedió a la liberación del V par craneal, y se apreció un íntimo contacto con la arteria cerebelosa superior en su parte sensitiva y adelgazamiento en la zona de entrada de la raíz nerviosa. Se procedió a la colocación de teflón entre la arteria cerebelosa superior y el V par craneal en todo su trayecto. Posteriormente, se exploró la cisterna basal y se apreció loop vascular de la arteria cerebelosa anteroinferior en íntimo contacto con el IX par craneal, donde se colocó teflón y sellante dural encima. El postoperatorio cursó sin incidencias, con resolución completa de la neuralgia del nervio trigémino y reducción >50% de la intensidad de los paroxismos en el territorio glosofaríngeo. A los dos años continúa sin paroxismos trigeminales y presenta <1 paroxismo/mes de intensidad tolerable en el territorio glosofaríngeo desencadenado con la deglución. El tratamiento farmacológico continúa en pauta descendente sin que ello haya supuesto la reaparición de los paroxismos.",
+        "gold_summary": "Mujer de 65 años con NT derecho (inicialmente en V2-V3) desde 2004 con control regular con carboxamidas. Diecisiete años después empeoraron los paroxismos en V2-V3, aparecieron también en V1 y en el territorio del nervio glosofaríngeo derecho (oído derecho y fosa amigdalar al hablar y deglutir). La resonancia magnética cerebral mostró contacto arterial significativo entre arteria cerebelosa superior (ACS) con origen del V par craneal derecho y de la arteria cerebelosa antero-inferior (AICA) con el origen de pares craneales bajos derechos. Se realizó DMV de ambos pares craneales en un mismo tiempo quirúrgico mediante craniectomía retrosigmoidea, y se procedió a la liberación del V par craneal, en contacto íntimo con la ACS, y del IX par craneal en contacto con la AICA derecha, para lo que se puso teflón entre ellas. La paciente tuvo una resolución inmediata de los paroxismos trigeminales y una mejoría considerable en intensidad y frecuencia de los glosofaríngeos. A los 2 años de la intervención continúa la desescalada de tratamiento neuromodulador con buena respuesta.",
+        "synthetic_summary": {
+            "B1": "Esta es la historia de una mujer de 65 años que tuvo dolores muy fuertes y repentinos en la cara desde 2004. Esos dolores se llaman neuralgia del trigémino. Al principio los medicamentos ayudaban, pero con los años los dolores empeoraron. En 2021 empezó también a tener pinchazos muy fuertes en la parte de atrás de la lengua y la garganta al tragar. Los medicamentos ya no bastaban.\n\nLos médicos hicieron una resonancia especial y vieron que dos arterias tocaban los nervios que causaban el dolor. Esto puede provocar esos pinchazos. Decidieron hacer una operación pequeña en la parte de atrás de la cabeza. Durante la cirugía separaron las arterias de los nervios y pusieron una pequeña almohadilla de material (teflón) para que no se volvieran a rozar.\n\nDespués de la operación se fue el dolor de la cara por completo. Los pinchazos en la lengua y la garganta bajaron mucho (más del 50%). Dos años después sigue sin dolor en la cara y casi no tiene ataques en la garganta (menos de uno al mes y tolerable). Los médicos han bajado poco a poco los medicamentos y ella está bien.",
+            "B2": "Resumen comprensible (nivel B2)\n\nUna mujer de 65 años empezó en 2004 con episodios de dolor punzante, breves y muy intensos en la cara, localizados en las zonas V2 y V3 del nervio trigémino derecho (V2 = zona media de la cara, V3 = mandíbula). Al principio los analgésicos habituales (como la carbamazepina) funcionaban con dificultad. En 2021 el dolor empeoró: los episodios aparecieron también en V1 (zona superior de la cara) y comenzaron además dolores parecidos en la parte posterior de la lengua y la pared lateral derecha de la garganta al tragar, compatibles con neuralgia del nervio glosofaríngeo. Los medicamentos dejaron de controlar bien los ataques; en crisis graves requirió perfusiones de fenitoína o lidocaína.\n\nSe repitió una resonancia magnética con una secuencia especial (CISS) que permitió ver contactos importantes entre vasos sanguíneos y nervios: la arteria cerebelosa superior tocaba el origen del nervio trigémino derecho, y la arteria cerebelosa antero-inferior estaba en íntimo contacto con los nervios craneales bajos (incluido el glosofaríngeo) del lado derecho. Este tipo de contacto vascular puede causar los dolores paroxísticos.\n\nComo los dos tipos de neuralgia eran clásicos, simultáneos y resistentes a fármacos, se decidió realizar una descompresión microvascular (cirugía para separar el vaso del nervio). En marzo de 2021 se hizo una craniectomía retrosigmoidea derecha (acceso por detrás del oído). Durante la operación se colocaron pequeñas almohadillas de teflón entre la arteria y cada nervio para evitar el roce directo.\n\nEl postoperatorio fue bueno. El dolor trigeminal desapareció por completo y el dolor glosofaríngeo mejoró más del 50% en intensidad y frecuencia. A los dos años la paciente sigue sin ataques trigeminales y tiene menos de uno por mes de dolor en la garganta, de intensidad tolerable y desencadenado al tragar. Los medicamentos se están reduciendo progresivamente sin que los dolores reaparezcan.\n\nComentario final: La descompresión microvascular puede ser una opción eficaz cuando la neuralgia facial o glosofaríngea está causada por el roce de una arteria sobre el nervio y no responde a medicación. El seguimiento clínico y la disminución controlada de fármacos son pasos habituales tras una buena respuesta quirúrgica.",
+            "B3": "Resumen clínico (nivel universitario, lectura B3)\n\nPresentación\n- Paciente: mujer de 65 años, sin antecedentes relevantes.\n- Historia: desde 2004 presentó neuralgia del trigémino derecho con paroxismos lancinantes en los territorios V2 y V3, con desencadenantes típicos (p. ej., tacto, masticación). El dolor fue difícil de controlar con carboxamidas (p. ej., carbamazepina).\n- En 2021 hubo empeoramiento: los paroxismos se extendieron a V1 y aparecieron además episodios dolorosos en la parte posterior de la lengua y la pared lateral derecha de la orofaringe, provocados y agravados por la deglución. Estos hallazgos orientaron a neuralgia glosofaríngea derecha concomitante.\n\nInvestigaciones\n- Resonancias magnéticas previas no incluían secuencias de alta resolución para ver un contacto neurovascular.\n- Se repitió la RM con secuencia CISS (secuencia de alta resolución que muestra bien vasos y raíces nerviosas). Encontró:\n  - Compresión significativa del nervio trigémino derecho por la arteria cerebelosa superior (ACS) en su zona sensitiva, con adelgazamiento de la raíz.\n  - Un asa de la arteria cerebelosa anteroinferior (AICA) en íntimo contacto con las raíces de los pares craneales bajos derechos (incluido el IX).\n\nTratamiento quirúrgico\n- En marzo de 2021 se realizó una descompresión microvascular (DMV) por vía retrosigmoidea derecha en un solo tiempo para ambos nervios.\n- Hallazgos operatorios: contacto íntimo y daño por compresión del V por la ACS; asa de AICA en contacto con el IX.\n- Procedimiento: se colocó material de teflón entre cada arteria y la raíz nerviosa afectada (con sellante dural sobre la colocación en la zona del IX).\n\nEvolución y resultado\n- Postoperatorio sin complicaciones inmediatas.\n- Resultado precoz: resolución completa de los paroxismos trigeminales y reducción >50% de la intensidad de los episodios glosofaríngeos.\n- A los 2 años: ausencia de paroxismos trigeminales; menos de 1 paroxismo glosofaríngeo por mes, de intensidad tolerable y desencadenado por la deglución. El tratamiento farmacológico se ha ido reduciendo (desescalada) sin recrudecimiento de los síntomas.\n\nInterpretación y consideraciones\n- El caso ilustra una neuralgia trigeminal y una neuralgia glosofaríngea clásicas causadas por conflicto neurovascular (arterias en contacto directo con la raíz nerviosa). Estas condiciones pueden volverse refractarias a medicación y requerir intervención quirúrgica.\n- La descompresión microvascular, que separa el vaso de la raíz nerviosa y coloca un acolchado (teflón), es una opción terapéutica eficaz en casos refractarios y en este caso logró un control clínico sostenido a 2 años.\n- Seguimiento recomendável: control neurológico y neuroquirúrgico para monitorizar recurrencias, manejo gradual de fármacos y vigilancia de posibles complicaciones tardías aunque la paciente no las presentó hasta el momento informado."
+        }
+    },
+    {
+        "article": "Hombre de 36 años, bisexual, en profilaxis antirretroviral de pre-exposición al HIV, sin antecedentes de viaje, que refirió haber asistido a un evento donde tuvo contactos con parejas ocasionales cuya identidad y antecedentes se desconocen. Diez días después comenzó con fiebre, odinofagia y dolor cervical por lo que consultó en varias oportunidades, hasta que a los siete días del inicio de los síntomas se internó por persistencia de los mismos a pesar del tratamiento antibiótico indicado. Al ingreso presentó exudado faríngeo, adenopatías cervicales bilaterales dolorosas y pápulas umbilicadas en escroto y pene y pústulas en cara de cinco días de evolución. Se realizó tomografía computarizada de cuello con contraste endovenoso que descartó colección, ecografía abdominal con leve hepatoesplenomegalia, e inició tratamiento empírico con ceftriaxona y azitromicina. Se tomaron muestras para cultivo, para serologías, y escarificación de dos lesiones de la cara que se enviaron al Laboratorio Nacional de Referencia, INEI-ANLIS Dr. Carlos G. Malbrán, para PCR de punto final para Orthopoxvirus, con resultado DETECTABLE, confirmando así el diagnóstico de viruela símica. La secuenciación arrojó un alto porcentaje de homología con secuencias del clado de África Occidental (MPV-ARG003-2022, Genbank_ID ON800897). Otros diagnósticos diferenciales fueron descartados. El paciente evolucionó con aparición de una úlcera en lengua y nuevas lesiones asincrónicas en glúteos, región perianal, inguinal derecha, umbilical, frontal, cuello, mano derecha y dorso de pie en un total de no más de 25. En el laboratorio se constató un aumento de transaminasas en 2.2 veces el valor normal, sin otros datos significativos.  Por persistencia del dolor cervical se solicitó nueva tomografía computarizada a los 14 días del inicio de los síntomas que evidenció adenomegalias con centro hipodenso de aspecto necrótico, que no requirieron drenaje quirúrgico. Al día 17 se realizó PCR en muestras de exudado de fauces y semen las que también resultaron positivas para virus de viruela símica. Se externó con franca mejoría clínica dos días después. El paciente dio su consentimiento informado escrito para la publicación de este informe de caso y las imágenes que lo acompañan.",
+        "gold_summary": "Se trata de un hombre joven, bisexual, en profilaxis antirretroviral de pre-exposición al HIV, cuya forma de presentación fue faringitis exudativa sin otra etiología documentada y adenopatías que evolucionaron a la necrosis, presencia de lesiones asincrónicas características en cara, cuello, abdomen, extremidades y genitales. El diagnóstico fue por detección de ADN viral por reacción en cadena de la polimerasa en lesiones de piel, exudado de fauces y semen. El compromiso faríngeo con presencia de exudado luego del descarte de otras infecciones, podría ser una rareza para la forma epidémica de la enfermedad. El hallazgo del virus en semen ya reportado en otras publicaciones no es suficiente aún para confirmar la vía sexual como forma de trasmisión.",
+        "synthetic_summary": {
+            "B1": "This is a simple story about a man of 36 years. He takes medicine to help prevent HIV. He went to an event and had contact with people he did not know. Ten days later he had fever, sore throat, and neck pain.\n\nWhen he went to the hospital, doctors found white stuff in his throat, painful swollen neck glands, and small bumps and pus spots on his face and private parts. Scans showed no pus collection, but his liver and spleen were a little big. Blood tests showed his liver enzymes were a bit high.\n\nDoctors tested skin sores and other samples. A lab test found monkeypox virus. The virus’s genetic code matched the West African type. The virus was also found in a throat sample and in semen. Finding the virus in semen does not prove that sex is how it spreads.\n\nHe developed new skin sores in several places, and one sore on his tongue. Some neck glands looked damaged on a later scan, but they did not need surgery. He got better with time and went home two days after the last test. Other possible illnesses were ruled out.",
+            "B2": "Resumen claro y amable:\n\nUn hombre de 36 años que usa profilaxis previa al VIH (PrEP) asistió a un evento donde tuvo contacto con parejas ocasionales. Diez días después empezó con fiebre, dolor de garganta y dolor en el cuello. Siete días tras el inicio de los síntomas fue internado porque no mejoraba con antibióticos.\n\nAl ingreso tenía pus en la garganta (exudado), ganglios dolorosos en ambos lados del cuello y lesiones en piel: pequeñas pápulas con hoyuelo en escroto y pene, y pústulas en la cara. Se hicieron estudios por imágenes: una tomografía de cuello descartó una colección purulenta y una ecografía abdominal mostró el hígado y bazo algo aumentados. Empezó tratamiento antibiótico mientras se recogían muestras para pruebas.\n\nEl laboratorio nacional detectó ADN de Orthopoxvirus por PCR en dos lesiones de la cara, confirmando infección por viruela símica (mpox). La secuenciación del virus mostró gran semejanza con el clado (variante) de África Occidental. Otros diagnósticos posibles fueron descartados. Durante la evolución apareció una úlcera en la lengua y nuevas lesiones en glúteos, región perianal, ingle, ombligo, frente, cuello, mano y pie, hasta unas 25 en total. Un análisis de sangre mostró aumento moderado de las enzimas hepáticas.\n\nA los 14 días una nueva tomografía mostró ganglios con zonas de aspecto necrosado (áreas donde el tejido estaba dañado), pero no fue necesario realizar cirugía. El día 17 se encontró PCR positiva para el virus en exudado de garganta y en semen. Dos días después el paciente fue dado de alta por clara mejoría. El hallazgo del virus en semen se ha visto en otros estudios, pero por ahora no basta para probar que la transmisión sea sexual. La presentación con pus en la garganta, tras descartar otras infecciones, puede ser menos común en los brotes actuales.",
+            "B3": "Resumen clínico breve\nUn hombre de 36 años, bisexual y en profilaxis preexposición para VIH (PrEP), asistió a un evento con contactos sexuales ocasionales. Diez días después desarrolló fiebre, odinofagia (dolor al tragar) y dolor cervical. Siete días tras el inicio de los síntomas fue internado por persistencia pese a tratamiento antibiótico.\n\nHallazgos clave al ingreso\n- Exudado faríngeo y adenopatías cervicales bilaterales dolorosas.  \n- Lesiones cutáneas: pápulas umbilicadas en escroto y pene; pústulas en la cara (5 días de evolución).  \n- Tomografía de cuello inicial: sin colección. Ecografía abdominal: leve hepatoesplenomegalia.  \n- Laboratorio: aumento moderado de transaminasas (≈2,2× el valor normal); resto sin hallazgos significativos.\n\nDiagnóstico microbiológico y genético\n- PCR final para Orthopoxvirus en lesiones cutáneas: detectable → diagnóstico confirmado de viruela símica (monkeypox).  \n- Secuenciación: alta homología con el clado de África Occidental (MPV-ARG003-2022, Genbank ID ON800897).  \n- PCR posterior positiva también en exudado de fauces y en semen.\n\nEvolución clínica\n- Aparecieron nuevas lesiones asincrónicas (máx. 25 en total) en lengua (úlcera), glúteos, región perianal, inguinal, abdomen, cara, cuello y extremidades.  \n- A los 14 días, nueva TC mostró adenomegalias con centros hipodensos de aspecto necrótico; no requirieron drenaje quirúrgico.  \n- Mejoría clínica progresiva; egresó dos días después de la PCR positiva en orina y semen. El paciente prestó consentimiento para la publicación del caso.\n\nInterpretación y consideraciones prácticas\n- Presentación atípica: la afectación faríngea con exudado como manifestación predominante, después de descartar otras infecciones, es poco frecuente en la forma epidémica descrita de viruela símica y debe alertar al clínico.  \n- Detección viral en semen confirma presencia de ARN/ADN viral en ese fluido, pero no prueba por sí sola la vía sexual de transmisión; otros estudios epidemiológicos y virológicos son necesarios para documentarla.  \n- La evolución fue moderada y no requirió intervenciones invasivas ni terapia antiviral específica en este caso; hubo un aumento leve-moderado de transaminasas que conviene monitorizar.  \n- Implicaciones de salud pública: identificar y notificar contactos sexuales, ofrecer pruebas a parejas potencialmente expuestas y aconsejar medidas de aislamiento y prácticas sexuales seguras hasta resolución de lesiones son pasos razonables en la gestión de casos confirmados.\n\nRecomendaciones para manejo y seguimiento (generales)\n- Confirmar diagnóstico por PCR en lesiones cutáneas; considerar muestreo adicional (fauces, semen) según contexto clínico.  \n- Vigilar signos de complicación (infección secundaria, compromiso mucoso extenso, linfadenopatía necrotizante, alteración hepática).  \n- Control de laboratorio seriado (función hepática) y seguimiento clínico hasta cicatrización completa de las lesiones.  \n- Notificar a salud pública y realizar rastreo de contactos sexuales; ofrecer consejería sobre reducción de riesgo y pruebas para ITS/VIH según corresponda.\n\nTono final\nEl caso ilustra una forma de presentación algo atípica de viruela símica —predominio de faringitis exudativa y adenopatías que evolucionaron a necrosis— y subraya la importancia de considerar este diagnóstico ante la combinación de síntomas sistémicos, adenopatías y lesiones genitales o cutáneas; asimismo muestra que la detección del virus en semen, aunque relevante, no aclara por sí sola las rutas de transmisión."
+        }
+    },
+    {
+        "article": "Paciente de sexo masculino de 23 años, natural de Itagüí - Colombia, antecedente familiar de muerte súbita de etiología no clara en abuelo a los 50 años, sin otros antecedentes familiares o personales de importancia. Venía en seguimiento externo por episodios sincopales a repetición con diagnóstico desde la infancia de disfunción del nodo sinusal sintomática por lo que se le implantó un marcapaso.\n\nDurante controles posteriores no hay reporte de deterioro de clase funcional hasta el año 2012 en Guayaquil-Ecuador. Durante su hospitalización se realiza el cambio de generador; en el primer mes postoperatorio presenta como complicación temprana una infección de bolsillo de marcapaso por lo que requirió el explante de la unidad generadora con posterior abandono de electrodo ventricular previamente implantado. Se realiza un nuevo implante de marcapaso en el lado contralateral sin complicaciones ni registro de nuevos eventos sincopales en los siguientes 10 años de seguimiento.\n\nSeis meses antes del ingreso presentaba deterioro de clase funcional NYHA III, sin otros síntomas y sin reportes de evaluaciones por servicio de electrofisiología desde el último implante de generador de marcapaso en 2012. Durante controles ambulatorios se reportó la suspensión del tratamiento con beta bloqueador debido a la pobre tolerancia.\n\nAl examen físico se encontró soplo sistólico en foco aórtico II/VI sin irradiación, no presentó signos de congestión central o periférica. Dentro de los laboratorios no se evidenció alteración en función renal, electrolítica ni del perfil hematológico. Se programó el marcapaso con evidencia de agotamiento de la batería de generador. Se realizó un ecocardiograma transtorácico donde se encontró hipertrofia concéntrica severa del septum interventricular a nivel medio ventricular, de 26 mm con gradiente intracavitario pico de 117 mmHg y movimiento sistólico anterior del velo mitral (SAM) el cual generaba una regurgitación mitral leve.\n\nFue evaluado por Heart Team, debido al score de riesgo de muerte súbita (16,8%) además de tener antecedentes familiares de muerte súbita considerando EUROSCORE II 0,67%; en cuanto a los electrodos abandonados previamente y la contraindicación de realización de resonancia magnética cardiaca, dado a la incompatibilidad del marcapaso, se realiza un estudio tomográfico y se consideró la realización de miectomía por sintomatología y variante documentada.\n\nFue programado para realización de miectomía medio ventricular por abordaje transapical con retiro de electrodos; se realizó la ventriculotomía izquierda en el ápex, con posterior resección del septum desde el parte medio ventricular hasta la base, con posterior retiro de electrodos adheridos a velo septal tricúspideo. No hubo complicaciones intraoperatorias y posteriormente se presentó disminución del gradiente intracavitario sin presencia del fenómeno SAM. Durante su estancia en Unidad de Cuidados Intensivos el paciente cursó con dos episodios documentados de taquicardia ventricular con inestabilidad hemodinámica por lo cual se le colocó un cardiodesfibrilador implantable (CDI) compatible con resonancia magnética (MRI) ST Jude sin presentar nuevos episodios de TV. El paciente cursó sin nuevas intercurrencias y se iniciaron los estudios ambulatorios de estudio genético debido a sus antecedente familiares.\n\nEl paciente presentó una evolución posoperatoria favorable luego del implante de CDI. En los estudios genéticos se encontró una variante, probablemente patogénica, en heterocigosis del FLNC, c 4636G>A consistente con miocardiopatía familiar hipertrófica tipo 26 autosómica dominante.\n\nActualmente, el paciente se encuentra en clase funcional I, sin arritmias evidenciadas en la telemetría y en tratamiento regular con Bisoprolol 5 mg. Se inició ampliación de estudio genético a familiares directos, sin embargo, debido al difícil acceso a servicios de salud su ejecución fue limitada.",
+        "gold_summary": "A continuación, se presenta el caso de un paciente sexo masculino de 23 años con diagnóstico de cardiomiopatía hipertrófica variante medio apical, en quien se documenta variante de la filamina C, ante la inadecuada respuesta y persistencia de sintomatología frente al manejo médico, se realizó el procedimiento de miectomía con abordaje transapical, con posterior mejoría de sintomatología clínica y obstrucción al tracto de salida.",
+        "synthetic_summary": {
+            "B1": "Este es un resumen sencillo y amable del caso.\n\nUn joven de 23 años tenía desde niño desmayos porque su corazón a veces no marcaba bien el ritmo. Le pusieron un marcapasos, que es una pequeña máquina que ayuda al corazón a latir. Más tarde tuvo una infección en el lugar del marcapasos y le cambiaron el aparato y los cables.\n\nA los 23 años empezó a cansarse mucho al hacer cosas normales. Un ecocardiograma (una ecografía del corazón) mostró que el músculo del corazón, sobre todo en el tabique entre las dos cámaras, estaba muy grueso. Ese músculo grueso hacía que la sangre se encontrara con una “pared” dentro del corazón. También una parte de la válvula se movía de forma incorrecta y dejaba pasar un poco de sangre. Todo esto podía explicar por qué se cansaba y tenía riesgo de problemas con el ritmo del corazón.\n\nLos médicos decidieron hacer una operación llamada miectomía. En esa operación quitaron una parte del músculo muy grueso para dejar más espacio para la sangre. También retiraron unos cables viejos que estaban pegados. La operación salió bien. Después de la cirugía el flujo de sangre mejoró y la válvula dejó de moverse mal.\n\nEn cuidados intensivos tuvo dos episodios de latidos peligrosos llamados taquicardia ventricular. Para cuidarlo mejor le pusieron un desfibrilador implantable (un aparato que puede dar una descarga si el corazón tiene un latido muy peligroso). Luego no presentó más episodios.\n\nLos estudios genéticos mostraron un cambio en un gen llamado FLNC. Ese cambio puede causar una forma de “miocardiopatía hipertrófica”, que significa que el músculo del corazón tiende a volverse más grueso. Esta enfermedad puede pasar de padres a hijos. Por eso empezaron a ofrecer pruebas a la familia, aunque fue difícil que todos pudieran hacerse los estudios.\n\nHoy el paciente está bien. Se cansa menos y está en buena clase funcional. Toma un medicamento para el corazón (bisoprolol). Los médicos siguen revisándolo y buscan ayudar a su familia con las pruebas genéticas.\n\nSi tienes preguntas sobre alguna palabra, puedo explicarla con más calma.",
+            "B2": "Resumen (nivel B2, lenguaje claro y cuidado)\n\nSe presenta el caso de un hombre de 23 años con antecedentes de desmayos desde la infancia por un problema del nodo sinusal (el marcapasos natural del corazón), por lo que tenía un marcapasos. Tenía además antecedente familiar de muerte súbita en un abuelo. Tras un recambio de generador en 2012 sufrió infección del bolsillo del marcapasos, se retiró el generador y se dejó un electrodo ventricular abandonado; se colocó después un nuevo marcapasos en el otro lado y estuvo sin eventos durante 10 años.\n\nSeis meses antes del ingreso empeoró su capacidad para hacer actividad física (clase funcional NYHA III). Un ecocardiograma mostró hipertrofia severa del tabique entre los ventrículos (26 mm) con una obstrucción dentro de la cavidad del ventrículo izquierdo que producía un gradiente elevado (117 mmHg). Además había movimiento sistólico anterior (SAM) de la válvula mitral, que favoreció una insuficiencia mitral leve. El marcapasos y los electrodos abandonados impedían hacer una resonancia magnética, por lo que se solicitó una tomografía.\n\nEl equipo médico decidió una miectomía medio-ventricular por vía transapical (cirugía para resecar el músculo hipertrofiado desde el ápex —la punta— del corazón) y retirar los electrodos adheridos. La cirugía transcurrió sin complicaciones y redujo la obstrucción; el fenómeno SAM desapareció. En el posoperatorio presentó dos episodios de taquicardia ventricular con inestabilidad (arritmias peligrosas), por lo que se le implantó un desfibrilador automático implantable (CDI) compatible con resonancia magnética. Tras el implante no tuvo nuevas arritmias.\n\nEl estudio genético mostró una variante probablemente patogénica en el gen FLNC (miocardiopatía hipertrófica tipo 26, herencia autosómica dominante). Se inició el rastreo genético en familiares, aunque el acceso a pruebas fue limitado. Actualmente el paciente está en clase funcional I (sintomático mínimo o ninguno), toma bisoprolol 5 mg y no se han registrado arritmias en la monitorización.\n\nComentarios finales sencillos\n- La cirugía (miectomía) fue necesaria porque el músculo del corazón estaba obstruyendo el flujo y los síntomas empeoraban pese al tratamiento médico.  \n- La variante genética encontrada puede explicar la enfermedad y hace importante ofrecer pruebas a familiares directos.  \n- El desfibrilador se colocó como prevención ante el riesgo de arritmias graves y muerte súbita.  \n\nSi tienes dudas sobre algún término médico, puedo explicarlo con más detalle.",
+            "B3": "Resumen clínico\n\nPaciente masculino de 23 años, con antecedente de síncopes desde la infancia que motivaron el implante de un marcapasos por disfunción del nodo sinusal. Historia importante: cambio de generador en 2012 complicado por infección de bolsillo que obligó a explante del generador y abandono del electrodo ventricular; luego se implantó un nuevo marcapasos en el lado contralateral y estuvo estable 10 años. Antecedente familiar relevante: abuelo con muerte súbita a los 50 años.\n\nPresentación y hallazgos principales\n- Seis meses antes del ingreso el paciente empeoró su clase funcional a NYHA III (disnea con actividad cotidiana). Se había suspendido un betabloqueador por mala tolerancia.  \n- En el examen físico solo se objetivó un soplo sistólico aórtico II/VI; sin signos de congestión.  \n- Ecocardiograma transtorácico: hipertrofia septal concéntrica severa (septum 26 mm), gradiente intraventricular pico 117 mmHg (obstrucción importante del tracto de salida del ventrículo izquierdo) y presencia de movimiento sistólico anterior (SAM) de la valva mitral, con regurgitación mitral leve.  \n- El marcapasos mostraba agotamiento de batería; además, los electrodos abandonados y la incompatibilidad con resonancia magnética llevaron a realizar un estudio tomográfico para evaluar la anatomía.  \n- Score de riesgo de muerte súbita calculado en 16,8% (riesgo aumentado); EUROSCORE II 0,67% (bajo riesgo quirúrgico).\n\nDecisión terapéutica y procedimiento\n- Tras evaluación por Heart Team y dada la sintomatología refractaria y la obstrucción documentada, se decidió realizar una miectomía medio-ventricular por abordaje transapical y retirar los electrodos abandonados.  \n- Durante la cirugía se hizo ventriculotomía apical izquierda, resección del septum desde la zona media hasta la base y extracción de electrodos adheridos. No hubo complicaciones intraoperatorias y el SAM desapareció con disminución del gradiente intraventricular.\n\nEventos posoperatorios y manejo adicional\n- En UCI presentó dos episodios de taquicardia ventricular con inestabilidad hemodinámica; por esto se implantó un cardiodesfibrilador implantable (CDI) compatible con resonancia magnética (marca St. Jude). Tras el implante no se registraron nuevas taquiarritmias.  \n- Evolución posterior favorable: paciente en clase funcional I, sin arritmias en telemetría y en tratamiento con bisoprolol 5 mg.\n\nHallazgo genético y recomendaciones\n- El estudio genético detectó una variante probablemente patogénica heterocigota en FLNC (c.4636G>A), consistente con miocardiopatía hipertrófica familiar tipo 26 de herencia autosómica dominante.  \n- Implicaciones: la variante en FLNC explica la cardiomiopatía y aumenta el riesgo arrítmico; se recomienda estudio genético y seguimiento cardiológico en familiares de primer grado (cribado y consejería genética). En este caso, la extensión del estudio familiar fue limitada por dificultades de acceso a servicios de salud.\n\nInterpretación y pasos siguientes\n- Diagnóstico final: miocardiopatía hipertrófica con obstrucción septal medio-ventricular, complicación arrítmica posoperatoria que requirió CDI, y variante probablemente patogénica en FLNC.  \n- El procedimiento quirúrgico resolvió la obstrucción y mejoró la capacidad funcional; el CDI fue necesario por episodios de taquicardia ventricular.  \n- Recomendaciones clínicas: seguimiento cardiológico periódico (función ventricular, síntomas, registro de arritmias por el CDI), optimización del tratamiento farmacológico según tolerancia, y realización de estudio genético y evaluación cardiológica a familiares directos para detección precoz y manejo preventivo.\n\nComentario empático\nEl paciente tuvo una mejora clínica clara tras la cirugía y el control de arritmias, pero el hallazgo genético tiene implicaciones familiares importantes. Se sugiere apoyo para facilitar el acceso al cribado y a la consejería genética de sus familiares cercanos, dado el potencial riesgo hereditario."
+        }
+    },
+    {
+        "article": "Varón de 32 años, con antecedentes de infección por VIH en terapia anti-retroviral (carga viral indetectable y recuento de CD4 de 454 céls/mm3) y consumo de tabaco y drogas (marihuana, éxtasis y ketamina). Consultó en nuestra unidad de salud sexual por una historia de dos semanas de secreción uretral de aspecto mucoso con escaso ardor local, asociado a una úlcera eritematosa indurada en el surco balanoprepucial de 1,5 cm de diámetro, dolorosa y exudativa. Al examen físico presentaba una adenopatía inguinal izquierda de 2 cm, sensible a palpación, blanda, no adherida a planos profundos ni asociada a signos inflamatorios cutáneos. No presentaba fiebre ni otros síntomas asociados. En la anamnesis dirigida, refirió 20 parejas sexuales hombres en el último año, con relaciones sexuales orales y anales insertivas y receptivas, con uso ocasional de preservativo. No tenía antecedente de viajes fuera de Chile. Cuatro semanas antes del inicio de los síntomas, había tenido un contacto sexual de riesgo sin preservativo con una pareja contactada mediante una aplicación de telefonía móvil. Con el diagnóstico presuntivo de una sífilis primaria y uretritis en estudio, se tomaron muestras de sangre y secreción uretral para estudio microbiológico. Por la conducta sexual de alto riesgo, se tomó también un hisopado anorrectal para tinción de Gram y cultivo. De acuerdo con la norma vigente en Chile, se administraron tres dosis de 2,4 millones de UI de penicilina benzatina intramuscular separadas por una semana, además de 250 mg de ceftriaxona intramuscular y 1 g de azitromicina oral, ambas por una vez. El estudio de laboratorio confirmó el diagnóstico de sífilis, con un VDRL (Venereal disease research laboratory) reactivo con dilución de 1:2 y MHA-TP (Microhemagglutination assay for antibody to Treponema pallidum) reactivo. La tinción de Gram y los cultivos de secreción uretral (agar sangre y Thayer Martin) fueron negativos. La muestra anorrectal mostró escasos diplococos gramnegativos en la tinción de Gram, con desarrollo abundante de N. meningitidis y microbiota comensal en el cultivo corriente. La identificación bacteriana se realizó a través de espectrometría de masas MALDI-TOF MS. El paciente evolucionó favorablemente, sin secreción uretral y con regresión de la lesión ulcerada genital y la adenopatía inguinal a las dos semanas de seguimiento. Las tinciones de Gram y los cultivos de control de secreción uretral, faríngea y anorrectal resultaron negativos. Se citó al contacto sexual reciente para estudio y tratamiento. Sin embargo, éste se encontraba asintomático y los cultivos faríngeo, anorrectal y uretral realizados fueron negativos.",
+        "gold_summary": "Presentamos el caso de un HSH con infección por VIH, que consultó por un cuadro de uretritis y sifilis primaria, en el cual se aisló N. meningitidis en una muestra anorectal. Fue tratado en forma empírica con ceftriaxona y azitromicina, realizándose un cultivo de control post-tratamiento que fue negativo.",
+        "synthetic_summary": {
+            "B1": "Un hombre de 32 años con VIH controlado vino al consultorio porque tenía una secreción en la uretra y una llaga dolorosa en el glande. También tenía un ganglio inflamado en la ingle. Había tenido muchas parejas y un encuentro sin preservativo unas semanas antes.\n\nLos médicos pensaron que podía ser sífilis, que es una infección que causa llagas. Le hicieron análisis de sangre y muestras de la secreción y del recto. Los exámenes confirmaron sífilis. En la muestra del recto encontraron otra bacteria llamada Neisseria meningitidis, que normalmente vive en la garganta pero a veces aparece en otras partes del cuerpo.\n\nRecibió antibióticos por inyección y una pastilla. En dos semanas la secreción desapareció, la llaga y el ganglio mejoraron, y los controles dieron negativo. También llamaron a la pareja reciente para que le hicieran pruebas y tratamiento; esa persona estaba sin síntomas y los cultivos salieron negativos.",
+            "B2": "Resumen claro y directo:\n\nUn hombre de 32 años con VIH controlado (carga viral indetectable y recuento de defensas razonable) consultó por dos semanas de secreción uretral y una úlcera dolorosa en el pene. En los exámenes se confirmó sífilis (pruebas VDRL y MHA-TP positivas). Además, en un cultivo de la muestra anorrectal se aisló Neisseria meningitidis, una bacteria que normalmente vive en la garganta pero que a veces puede aparecer en la zona genital o anal y causar infección.\n\nPor el cuadro y el riesgo sexual se le dio tratamiento empírico con antibióticos (ceftriaxona y azitromicina) y, según la norma local para sífilis, recibió tres dosis semanales de penicilina benzatina. A las dos semanas mejoró clínicamente: la secreción desapareció y la úlcera y la adenopatía (ganglio inflamado) disminuyeron. Los cultivos de control (uretral, faríngeo y anorrectal) fueron negativos después del tratamiento. El contacto sexual reciente fue citado para estudio y tratamiento; estaba sin síntomas y sus cultivos resultaron negativos.",
+            "B3": "Resumen clínico\n\nContexto y presentación\nUn hombre de 32 años, con infección por VIH en tratamiento antirretroviral (carga viral indetectable, recuento de CD4 454 céls/mm3) y consumo de tabaco y drogas recreativas, consultó por dos semanas de secreción uretral mucosa con leve ardor y una úlcera eritematosa, indurada y dolorosa de 1,5 cm en el surco balanoprepucial. Además presentó una adenopatía inguinal izquierda sensible de 2 cm. No había fiebre ni otros síntomas sistémicos. En la anamnesis refirió múltiples parejas sexuales masculinas y prácticas de riesgo con uso ocasional de preservativo; cuatro semanas antes había tenido un contacto sexual sin protección por una aplicación móvil.\n\nInvestigaciones y diagnóstico\nSe investigaron causas de uretritis y lesiones genitales. Se tomaron muestras de sangre, secreción uretral y un hisopado anorrectal. Los serológicos confirmaron sífilis (VDRL reactivo 1:2 y MHA-TP reactivo). La tinción de Gram y los cultivos de la secreción uretral resultaron negativos. En la muestra anorrectal se observaron escasos diplococos gramnegativos en la tinción, y el cultivo mostró crecimiento abundante de Neisseria meningitidis junto con flora comensal; la identificación se realizó mediante espectrometría de masas (MALDI-TOF MS).\n\nTratamiento inicial\nSiguiendo la normativa local, se administraron: tres dosis semanales de penicilina benzatina 2,4 millones UI intramuscular (tratamiento para sífilis) y, de forma empírica por uretritis/posible gonorrea, una dosis única de ceftriaxona 250 mg IM y una dosis única de azitromicina 1 g VO.\n\nEvolución y control\nA las dos semanas el paciente mostró resolución de la secreción uretral y regresión de la úlcera y la adenopatía. Los controles microbiológicos (tinciones y cultivos de secreción uretral, faríngea y anorrectal) fueron negativos tras el tratamiento. El contacto sexual reciente fue citado, estaba asintomático y sus cultivos faríngeo, anorrectal y uretral resultaron negativos.\n\nImplicaciones y observaciones\n- Encontrar N. meningitidis en un hisopado anorrectal es notable: aunque esta especie es clásica como agente de meningitis/sepsis, puede colonizar o infectar mucosas urogenitales y anorectales y en la práctica puede confundirse con Neisseria gonorrhoeae.  \n- En este caso el aislamiento en anorrectal podría representar colonización o infección local; no hubo evidencia de infección invasiva.  \n- El tratamiento empírico con ceftriaxona (utilizado para sospecha de gonorrea) es activo frente a muchas cepas de N. meningitidis, y el paciente respondió clínicamente.  \n- Es importante identificar la especie mediante métodos como MALDI-TOF y, cuando sea posible, realizar pruebas de susceptibilidad para orientar terapias y vigilancia epidemiológica.\n\nRecomendaciones prácticas (derivadas del caso)\n- Considerar N. meningitidis en el diagnóstico diferencial de infecciones anorrectales/urogenitales en hombres que tienen sexo con hombres (HSH) u otras poblaciones con prácticas de riesgo.  \n- Notificar y estudiar contactos sexuales según protocolos locales.  \n- Seguimiento serológico de sífilis y control clínico si persisten síntomas.  \n\nEl caso ilustra la utilidad de la identificación bacteriana precisa y la importancia del abordaje integral (tratamiento empírico, confirmación diagnóstica y estudio de contactos) en infecciones de transmisión sexual en redes de alto riesgo."
+        }
+    },
+    {
+        "article": "Un paciente hispanoparlante de 63 años de edad se presentó en el hospital como una emergencia con inicio repentino de dificultad respiratoria severa, palpitaciones y sudoración profusa. Estaba en su estado habitual de salud y podía deambular con actividades independientes de la vida diaria hasta 30 minutos antes de su llegada a la sala de urgencias. Tenía un historial de 20 años de hipertensión, un historial de 15 años de diabetes mellitus, enfermedad de la arteria coronaria que requería la inserción de un stent de la arteria coronaria cinco años antes, un historial de diez años de insuficiencia cardiaca de la clase II de la New York Heart Association (NYHA) con una fracción de eyección reducida (EF) del 35 %, enfermedad renal crónica (CKD) en estadio 3B. Al ingresar en el hospital, sus medicamentos incluían carvedilol (25 mg dos veces al día), lisinopril (20 mg diario), espironolactona (25 mg diario), furosemida (20 mg diario), insulina glargina (20 unidades al acostarse), inyección de insulina lispro (7 unidades tres veces al día), atorvastatina (40 mg diario), y aspirina (81 mg diario), sin alergias a medicamentos conocidas.\n\nAl examen, su presión arterial era de 205/110 mmHg, su frecuencia respiratoria de 29 respiraciones/min, su frecuencia cardíaca de 118 latidos/min, la oximetría de pulso era de 82% (en aire ambiente) y su temperatura de 36.2°C. Su peso era de 72 kg y su estatura de 68 pulgadas, lo que resultó en un índice de masa corporal (IMC) de 24.13 kg/m2. Al examen físico, el paciente estaba en grave dificultad respiratoria, sudaba y no podía hablar con claridad. Su presión venosa yugular era elevada, como se muestra por la distensión de la vena yugular (3+). Al auscultar el tórax, se observaron crepitaciones bilaterales en todos los campos pulmonares. La auscultación cardíaca fue notable por un galope con una frecuencia regular y un murmullo sistólico 3/6 que se oía en la línea medioclavicular izquierda, al nivel del quinto espacio intercostal. El punto de impulso cardíaco máximo se desplazó hacia la izquierda (en la línea medioaxilar anterior) y no se observó distensión abdominal ni ascitis, con edema de los miembros inferiores (1+) hasta el nivel de la mitad de la pantorrilla.\n\nEl paciente fue trasladado a la zona de reanimación cardiopulmonar (RCP), donde se midieron los gases sanguíneos en el aire y se solicitaron pruebas de laboratorio. El paciente fue tratado con oxígeno al 100% utilizando una máscara no reanadora y se le colocó en posición de 90°, lo que produjo una mejora en la oximetría de pulso, que aumentó hasta el 90%. Un electrocardiograma (ECG) mostró taquicardia sinusal, depresión del ST del conductor lateral (de 1 mV), desviación del eje izquierdo e hipertrofia del ventrículo izquierdo. Se obtuvo una radiografía de tórax portátil que fue notable por una silueta cardiaca agrandada, señal de asta de ciervo de desviación venosa pulmonar del lóbulo superior (cefalización), y líneas B de Kerley, que indican edema intersticial.\n\nAunque se solicitaron pruebas de laboratorio, debido a que el paciente estaba gravemente enfermo y no se podía demorar el tratamiento, se inició un tratamiento inicial basado en los hallazgos clínicos, el historial clínico, el ECG, los gases arteriales en sangre y los hallazgos de rayos X. En vista de los hallazgos de las investigaciones iniciales y la ausencia de fiebre, se descartó la neumonía y se realizó un diagnóstico de edema pulmonar cardiogénico hipertensivo. Se inició un tratamiento intravenoso (IV) con nitroglicerina, comenzando a 30 mcg/min y aumentando en 15 mcg/min cada 3 minutos, con oximetría de pulso continua y monitoreo de los signos vitales cada 3 minutos. Después de 18 minutos, se tituló la nitroglicerina hasta 120 mcg/min y su presión arterial disminuyó a 148/82 mmHg, su presión arterial sistólica se redujo en un 29%, su presión arterial diastólica se redujo en un 25%, y su frecuencia cardíaca disminuyó a 87 latidos por minuto. Se hizo una rápida mejora clínica y el paciente pudo comunicarse con oraciones completas y pudo respirar sin el uso de músculos accesorios. La oximetría de pulso mostró una saturación de oxígeno >97%, y la suplementación de oxígeno continuó con el uso de una cánula nasal a 3 L/min y la medición de la oximetría de pulso del paciente fue >96%.\n\nDespués de 25 minutos, el paciente fue tratado con enalapril (2,5 mg IV) combinado con furosemida (20 mg IV). La nitroglicerina se redujo a una tasa de 10 mcg/min cada 5 minutos hasta que se interrumpió, seguido de una dosis oral de isosorbida dinitrato (30 mg). Después de la estabilización clínica completa, los resultados de los laboratorios mostraron un recuento de glóbulos blancos (WBC) de 11,43 × 109/uL, hemoglobina de 10,9 g/dl, hematocrito de 31,8%, plaquetas de 74 × 109/L, sodio de 144 mmol/L, potasio de 3,9 mmol/L, cloruro de 107 mmol/L, dióxido de carbono (CO2) de 25 mmol/L, nitrógeno ureico en sangre (BUN) de 27 mg/dL, creatinina de 1,4 mg/dL, péptido natriurético cerebral (BNP) de 3,452 pg/ml, y troponina I <0,05 ng/ml. Las mediciones de gases en sangre en aire incluyeron pH de 7,381, pCO2 de 44,8 mmHg, pO2 de 57 mmHg, HCO3 de 25,8 mmol/L, y saturación de oxígeno de 84%.\n\nSe evaluó al paciente para detectar la presencia de una posible embolia pulmonar (EP) subyacente, utilizando los criterios de estratificación de riesgo de EP de Wells, y se lo estratificó como de bajo riesgo, con una evaluación posterior con un nivel de dímero D de 340 ng/ml, que se interpretó como negativo. La evaluación para detectar hipertiroidismo mostró un valor normal de la medición ultrasensible del ensayo de la hormona estimulante de la tiroides en plasma (usTSH) de 2,56 μU/mL y tiroxina libre (T4) de 6,87 μU/mL.\n\nEl paciente fue admitido en la sala de hospital de medicina interna con un diagnóstico de edema pulmonar cardiogénico hipertensivo y fue dado de alta 48 horas después. Al momento del alta hospitalaria, su medicación incluía furosemida (40 mg diarios), carvedilol (12.5 mg dos veces al día), sacubitril/valsartan (24 mg/26 mg dos veces al día), espironolactona (25 mg diarios) e isosorbida mononitrato (60 mg diarios). El paciente fue sometido a seguimiento semanal por su cardiólogo, quien optimizó la terapia medicinal. No se registraron visitas a urgencias ni hospitalizaciones, al menos durante los siguientes 60 días.\n\nMH - Insuficiencia cardiaca/*complicaciones\nMH - Humanos\nMH - Hipertensión/*complicaciones\nMH - Infusiones, intravenosas\nMH - Hombre\nMH - Edad Media\nMH - Nitroglicerina/*administración y dosificación\nMH - Edema pulmonar/*terapia farmacológica/etiología\nMH - Insuficiencia respiratoria/*terapia farmacológica/etiología\nMH - Agentes vasodilatadores/*administración y dosificación\n",
+        "gold_summary": "Paciente: Hombre, 63 años\n\nDiagnóstico final: Edema pulmonar cardiovenoso hipertensivo\n\nSíntomas: falta de aire\n\nMedicación: —\n\nProcedimiento clínico: —\n\nEspecialidad: Medicina general e interna\n\nUn hombre hispano de 63 años con antecedentes de hipertensión, enfermedad de las arterias coronarias, insuficiencia cardiaca con una fracción de eyección reducida del 35 %, enfermedad renal crónica (ERC) y diabetes mellitus, se presentó como una emergencia con disnea aguda y grave. El paciente fue tratado inicialmente con 100 % de oxígeno suplementario y nitroglicerina intravenosa (IV) en dosis altas (30 mcg/min), que se ajustó cada 3 minutos, aumentando en 15 mcg/min hasta que se alcanzó una dosis de 120 mcg/min. Después de 18 minutos de terapia agresiva, la condición del paciente mejoró y ya no necesitaba ventilación mecánica.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre hispano de 63 años, con presión alta, diabetes, problemas del corazón y del riñón, llegó al hospital porque de pronto no podía respirar bien. Tenía mucha sudoración y palpitaciones. \n\nEn la sala su tensión arterial estaba muy alta y su oxígeno en la sangre estaba bajo. Al escucharlo, los médicos oyeron líquido en sus pulmones y signos de que el corazón no estaba trabajando bien. Esto se llama edema pulmonar cardiogénico: es cuando el corazón no bombea bien y se acumula líquido en los pulmones.\n\nLe dieron oxígeno y un medicamento por la vena llamado nitroglicerina. Ese medicamento ayuda a relajar las venas y bajar la presión. En unos 18 minutos empezó a sentirse mucho mejor. Pudo hablar y respirar con menos esfuerzo. Después recibió otros medicamentos y fue cuidado en el hospital.\n\nLas pruebas mostraron que el corazón estaba muy cargado, pero no había un ataque al corazón. Fue dado de alta a las 48 horas con medicinas nuevas y seguimiento con su cardiólogo. No volvió a urgencias en los siguientes 60 días. \n\nFue una situación grave y asustadora, pero recibió tratamiento rápido y mejoró.",
+            "B2": "Resumen comprensible y amable\n\nPaciente: hombre de 63 años.\n\nQué pasó: Llegó al servicio de urgencias con una falta de aire muy fuerte, palpitaciones y sudoración. Hasta media hora antes estaba bien y podía caminar solo.\n\nAntecedentes importantes: tenía hipertensión (20 años), diabetes (15 años), enfermedad coronaria con un stent (hace 5 años), insuficiencia cardiaca crónica con función reducida del corazón (fracción de eyección 35 %) y enfermedad renal crónica (estadio 3B).\n\nQué encontraron al llegar:\n- Presión arterial muy alta (205/110 mmHg), respiración rápida y saturación de oxígeno baja (82 % en aire).\n- Venas del cuello hinchadas, crepitaciones en ambos pulmones (ruidos que sugieren líquido) y un sonido extra en el corazón (galope). También tenía un soplo y algo de hinchazón en las piernas.\n- Radiografía de tórax: corazón agrandado y signos de acumulación de líquido en los pulmones.\n- ECG: ritmo sinusal rápido y señales de sobrecarga del ventrículo izquierdo.\n- Análisis: péptido natriurético (BNP) muy alto (3,452 pg/ml), lo que indica estrés o fallo del corazón; troponina baja (sin evidencia de infarto); plaquetas bajas (74 × 10^9/L) y anemia leve. Gasometría arterial mostró bajo oxígeno en sangre al aire ambiente.\n\nDiagnóstico: edema pulmonar cardiogénico hipertensivo (es decir, líquido en los pulmones provocado por que el corazón no estaba manejando bien la presión alta).\n\nTratamiento inicial y evolución:\n- Se le dio oxígeno al 100 % y se colocó erguido; luego se administró nitroglicerina por vía intravenosa (un medicamento que dilata los vasos y reduce la carga del corazón). La dosis se aumentó rápidamente hasta 120 mcg/min.\n- En 18 minutos mejoró mucho: bajó la presión arterial, la frecuencia cardíaca y su respiración; pudo hablar en oraciones y la saturación subió por encima del 97 %. Luego se mantuvo con cánula nasal a 3 L/min.\n- Después se le dio enalapril IV y furosemida IV (diurético para eliminar líquido). La nitroglicerina se fue retirando y se inició medicación oral para mantener el control.\n\nResultados y seguimiento:\n- Fue ingresado en medicina interna y dado de alta a las 48 horas con tratamiento oral actualizado: diurético (furosemida), betabloqueante (carvedilol, dosis reducida), sacubitril/valsartán (medicamento para la insuficiencia cardiaca), espironolactona e isosorbida mononitrato.\n- Se programaron controles semanales con su cardiólogo y no tuvo nuevas visitas a urgencias ni reingresos durante, al menos, los siguientes 60 días.\n\nComentario en palabras sencillas: El paciente tuvo una emergencia por acumulación de líquido en los pulmones causada por presión arterial muy alta y un corazón que ya estaba debilitado. Con oxígeno y medicamentos que bajaron la presión y ayudaron al corazón y a eliminar líquido, mejoró rápido y pudo volver a casa bajo control médico. Algunas pruebas mostraron otros datos (por ejemplo, plaquetas bajas y anemia leve) que requerirán seguimiento con su equipo de salud.",
+            "B3": "Summary — Hypertensive cardiogenic pulmonary edema in a 63-year-old man\n\nBrief clinical picture\n- A 63-year-old Hispanic man with long-standing hypertension (20 years), type 2 diabetes, coronary artery disease with prior stent, chronic heart failure (NYHA class II, LVEF ≈35%), and chronic kidney disease (stage 3B) presented suddenly with severe shortness of breath, palpitations and heavy sweating. He had been independent and ambulatory until about 30 minutes before arrival.\n\nImportant abnormal findings on arrival\n- Vital signs: blood pressure 205/110 mmHg (severely elevated), heart rate 118/min (tachycardia), respiratory rate 29/min, O2 saturation 82% on room air.\n- Exam: marked respiratory distress, jugular venous distension (JVD 3+), bilateral crackles throughout the lungs, an S3 gallop and a 3/6 systolic murmur, displaced point of maximal impulse, mild bilateral leg edema.\n- Chest x-ray: enlarged cardiac silhouette, cephalization of pulmonary vessels and Kerley B lines — consistent with pulmonary interstitial edema.\n- ECG: sinus tachycardia, left axis deviation, left ventricular hypertrophy, and lateral ST depression.\n- Arterial blood gas (on room air): pO2 57 mmHg, O2 saturation 84% (hypoxemia).\n- Blood tests after initial stabilization: BNP 3,452 pg/mL (markedly elevated → supports acute cardiac failure), troponin I <0.05 ng/mL (no biochemical evidence of acute myocardial infarction), creatinine 1.4 mg/dL (mildly elevated for CKD), mild anemia (Hb 10.9 g/dL) and thrombocytopenia (platelets 74 × 10^9/L) — both notable and require follow-up. WBC slightly elevated (11.4 × 10^9/L). D-dimer 340 ng/mL (not suggestive of pulmonary embolism in this low-risk patient). Thyroid tests normal.\n\nWorking diagnosis\n- Hypertensive cardiogenic (cardiogenic) pulmonary edema — acute heart-failure exacerbation driven by very high blood pressure, with resultant pulmonary congestion and hypoxemia. Infection and pulmonary embolism were considered unlikely based on clinical course, absence of fever, and negative testing.\n\nTreatment and response\n- Immediate care: high-flow oxygen (initially 100% by non-rebreather), upright positioning, and rapid medical therapy targeted at lowering afterload and relieving pulmonary congestion.\n- Nitroglycerin IV was started at 30 mcg/min and titrated every 3 minutes by 15 mcg/min to 120 mcg/min. Within 18 minutes the patient’s blood pressure fell to 148/82 mmHg, heart rate slowed to 87/min, breathing and mental status improved rapidly, and oxygen saturation rose to >97% on supplemental oxygen. Aggressive IV nitrates likely reduced preload/afterload and avoided need for mechanical ventilation.\n- Additional therapy included IV enalapril 2.5 mg and IV furosemide 20 mg to promote diuresis. Nitroglycerin was tapered and transitioned to oral nitrates (isosorbide dinitrate then long-acting isosorbide mononitrate).\n- No evidence of acute myocardial infarction; treatment focused on decongestion and blood-pressure control.\n\nHospital course and disposition\n- Admitted to internal medicine, clinically stabilized within 48 hours and discharged home.\n- Discharge medications included: furosemide 40 mg daily, carvedilol 12.5 mg twice daily, sacubitril/valsartan 24/26 mg twice daily (ARNI added/optimized), spironolactone 25 mg daily, and isosorbide mononitrate 60 mg daily.\n- Outpatient cardiology follow-up was arranged weekly for medication optimization. No emergency visits or readmissions were reported during at least the subsequent 60 days.\n\nKey points, implications and recommended follow-up\n- This was an acute, severe hypertensive cardiogenic pulmonary edema responding rapidly to high-dose IV nitrates plus diuretic and afterload reduction — demonstrating that early vasodilator therapy can reverse life‑threatening pulmonary congestion and avoid intubation when used carefully.\n- Important supportive findings that helped exclude other causes: very high BNP (supports heart-failure cause), negative troponin (argues against large acute MI), low Wells score and negative D-dimer (makes pulmonary embolism unlikely), and no fever or focal consolidation on imaging (less likely pneumonia).\n- Issues requiring ongoing attention: his chronic kidney disease (monitor renal function, BUN/creatinine, and electrolytes with diuretics and RAAS/ARNI therapy); new or unexplained thrombocytopenia and mild anemia (needs hematology review and repeat testing to identify cause); blood-pressure control and optimization of heart‑failure medications; careful outpatient monitoring for hypotension, renal effects, and potassium abnormalities after starting sacubitril/valsartan and spironolactone.\n- Follow-up with cardiology and primary care, with repeat labs and clinical checks in the near term, is appropriate to ensure safe medication titration and to investigate low platelets and anemia.\n\nIf you would like, I can produce a brief patient-facing version (simpler language) for explanation to the patient or a checklist for the outpatient follow-up plan."
+        }
+    },
+    {
+        "article": "Historial clínico\nUn niño de 12 años se presentó en nuestro hospital con un mes de historia de sensación de cuerpo extraño y una masa conjuntival pedunculada carnosa que creció con el tiempo. No había historia de trauma o lesiones similares en el otro lado del cuerpo. Se descubrió una masa pedunculada carnosa rosácea de 15 mm de la conjuntiva palpebral derecha durante un examen oftalmológico. La agudeza visual estaba dentro de los límites normales. Se diagnosticó al niño como papiloma de células escamosas pedunculadas y se le realizó una biopsia excisional de la lesión.\n\nHallazgos macroscópicos y microscópicos\nRecibimos un fragmento de tejido blanco grisáceo, pequeño, firme, ovoide, fijado en formalina, de 1,5 x 1 cm, para su análisis patológico. En las secciones microscópicas se encontró una lesión poliopóidea hiperplásica con múltiples quistes globulares en la submucosa conjuntival, junto con una importante infiltración inflamatoria constituida por linfocitos, células plasmáticas y neutrófilos, así como enormes esporangios de paredes gruesas con numerosas endosporas. Las endosporas se liberaron después de que algunos de los esporangios maduros se rompieran. La rinosporidiosis conjuntival se diagnosticó histopatológicamente. No hubo recurrencia ni signo de rinosporidiosis en el ojo ni en ninguna otra área del cuerpo en el último examen del paciente, que fue 7 meses después de la escisión quirúrgica.\n",
+        "gold_summary": "Un niño de 12 años con una masa conjuntival pedunculada carnosa fue llevado al Centro Médico de la Universidad de Jimma con un historial de un mes de sensación de cuerpo extraño. Al paciente se le diagnosticó un papiloma pedunculado de células escamosas y se le realizó una biopsia excisional de la lesión. Se encontró que la masa era una lesión polipoide hiperplásica con numerosos quistes globulares dentro de la submucosa conjuntival, rodeados por un infiltrado inflamatorio pesado de linfocitos, células plasmáticas y neutrófilos, así como grandes esporas de paredes gruesas con numerosas endosporas en secciones microscópicas. Se diagnosticó histopatológicamente rinosporidiosis conjuntival.\n",
+        "synthetic_summary": {
+            "B1": "Un niño de 12 años tenía desde hace un mes una bolita carnosa dentro del párpado derecho. Decía que sentía algo en el ojo, pero su vista estaba bien. Los médicos quitaron la bolita y la miraron con un microscopio. Vieron muchas bolsitas grandes llenas de pequeñas esporas y mucho material de defensa del cuerpo alrededor. Esto se llama rinosporidiosis, una infección rara que hace crecer bultos en la conjuntiva del ojo. Después de la operación el niño se recuperó. Siete meses más tarde no había vuelto a aparecer y no había señales de la infección en otras partes.",
+            "B2": "A 12-year-old boy had one month of feeling something in his right eye and a slowly growing, fleshy bump on the inner surface of his eyelid. His sight was normal. Doctors first thought it was a benign papilloma (a wart-like growth) and removed the lump by excisional biopsy.\n\nUnder the microscope, the tissue showed a polyp-like overgrowth with many round, cyst-like spaces under the surface, and a heavy inflammatory reaction (lots of immune cells). Pathologists also saw large, thick-walled sacs filled with many smaller spores; some sacs had burst and released those spores. These changes are typical of conjunctival rinosporidiosis — an infection that causes polyp-like growths on mucous membranes and is diagnosed by finding these distinctive spore-filled sacs.\n\nThe lesion had been completely removed, and at a follow-up exam 7 months later there was no sign of the infection coming back. Surgical removal is the usual step, and continued follow-up is recommended because these growths can sometimes recur.",
+            "B3": "Resumen clínico y hallazgos principales\n\n- Paciente: niño de 12 años con un mes de sensación de cuerpo extraño en el ojo derecho y una masa conjuntival pedunculada, carnosa, rosácea de 15 mm. La agudeza visual era normal.\n- Manejo inicial: la lesión se interpretó clínicamente como un papiloma escamoso pedunculado y se realizó biopsia excisional.\n\nHallazgos macroscópicos y microscópicos\n\n- Macroscópico: fragmento de tejido fijo, blanco‑grisáceo, firme, ovoide, de 1,5 × 1 cm.\n- Microscópico: lesión polipoidea hiperplásica de la conjuntiva con múltiples quistes globulares en la submucosa y un infiltrado inflamatorio intenso (linfocitos, células plasmáticas y neutrófilos). Se observaron grandes esporangios de pared gruesa conteniendo numerosas endosporas; algunos esporangios maduros se habían roto liberando endosporas.\n- Diagnóstico histopatológico: rinosporidiosis conjuntival.\n\nEvolución y consideraciones clínicas\n\n- El paciente no presentó recurrencia ni signos de rinosporidiosis en el ojo ni en otras localizaciones a los 7 meses tras la escisión.\n- La rinosporidiosis es una infección granulomatosa crónica que suele identificarse por la presencia característica de esporangios y endosporas en el tejido; el tratamiento habitual es la escisión quirúrgica completa, y existe riesgo de recurrencia si la extirpación es incompleta.\n- Recomendaciones prácticas (habituales en este contexto): vigilancia clínica periódica de la misma zona y evaluación de otras mucosas (por ejemplo cavidad nasal) para buscar lesiones adicionales; aconsejar medidas para reducir la exposición a posibles fuentes de contagio según la epidemiología local.  \n\nSi desea, puedo redactar una versión breve para familiares o añadir sugerencias específicas de seguimiento y prevención adaptadas al entorno del paciente."
+        }
+    },
+    {
+        "article": "Presentamos el caso clínico de un varón de quince años, sin antecedentes médicos ni intervenciones previas, que acude al servicio de urgencias de pediatría con clínica de vómitos y dolor abdominal epigástrico de cuatro días de evolución, manteniéndose afebril durante la evolución del cuadro.\n\nInicialmente fue manejado como gastroenteritis, pero ante la ausencia de mejoría, con persistencia del dolor abdominal de tipo cólico a nivel epigástrico y de los vómitos de aspecto bilioso, acude a urgencias para nueva valoración.\n\nA la exploración física el paciente presentaba aceptable estado general, se encontraba afebril, con signos leves de deshidratación. El abdomen se encontraba distendido, sin datos de peritonismo y con ruidos hidroaéreos disminuidos. La analítica no presentaba hallazgos significativos, realizándose una radiografía de abdomen con hallazgos sugestivos de obstrucción intestinal.\n\nDada la evolución se decide realizar una tomografía computarizada urgente, en la que se observó presencia de ascitis e importante dilatación de asas de intestino delgado, sugiriendo la interposición de un asa de intestino delgado en el inicio de la transcavidad de los epiplones, con cambio de calibre a nivel del hiato de Winslow.\n\nSe realizó intervención quirúrgica urgente, realizando inicialmente una laparoscopia exploradora. Se observaban asas de intestino delgado dilatadas, e íleon terminal, ciego y colon ascendente de calibre normal pero localizados en hipocondrio derecho, con el ciego muy móvil y sin presentar adherencias al espacio parietocólico derecho. Siguiendo proximalmente el íleon terminal, se observaron asas de intestino delgado de distinto calibre desde la profundidad de la teórica localización del hiato de Winslow. Se consiguió traccionar de ciego e íleon terminal hasta desplazarlos a fosa iliaca derecha, pero sin llegar a identificar correctamente el punto de cambio de calibre, ya que la interposición del borde inferior del hígado y la distensión de asas de intestino delgado dificultaban la técnica. Se intentó mejorar la visualización mediante punción percutánea de un asa dilatada para vaciar el gas, sin mejoría. Para asegurar la resolución del cuadro obstructivo se decidió realizar una laparotomía media supraumbilical. Al acceder a cavidad se evidenciaba el cambio de calibre en íleon, a unos 40 centímetros de la válvula ileocecal, con signos compatibles con herniación de un tramo de unos cinco centímetros de íleon a través de hiato de Winslow. En ambos extremos del asa herniada observamos la impronta congestiva del hiato sobre el asa (Fig. 3). Se identificó el hiato de Winslow, de calibre normal, por lo que no se realizó ninguna técnica preventiva para disminuir el riesgo de recidiva.\n\nDurante los primeros días del postoperatorio el paciente presentó un íleo paralítico, pudiendo retirar la sonda nasogástrica a los cinco días de la cirugía e iniciando tolerancia oral con buena respuesta. Simultáneamente desarrolló una colección pélvica que se manejó de forma conservadora con antibióticos, con buena evolución. Finalmente, el paciente fue dado de alta a los diez días de la intervención, con tránsito conservado, manteniéndose afebril y con buen estado general.\n\nActualmente el paciente está en seguimiento en consultas externas de cirugía pediátrica.",
+        "gold_summary": "Presentamos el caso clínico de un varón adolescente de 15 años sin antecedentes quirúrgicos previos, con clínica de dolor abdominal y vómitos, en el que la tomografía computarizada sugería un cuadro de obstrucción intestinal a causa de hernia interna a nivel del hiato de Winslow. Precisó de intervención quirúrgica mediante laparoscopia exploradora, reconvertida por mala visualización a laparotomía media supraumbilical, para reducción del asa de íleon herniada. Esta presentaba buen aspecto y no fue necesaria la resección intestinal. No se realizó ninguna técnica preventiva para disminuir el riesgo de recidiva. Postoperatoriamente, el paciente presentó una colección pélvica manejada de manera conservadora con antibióticos. Actualmente se encuentra en seguimiento en consultas externas de cirugía pediátrica.",
+        "synthetic_summary": {
+            "B1": "Este es el caso de un chico de 15 años que empezó con dolor de barriga y vómitos. Al principio pensaron que era una infección del estómago, pero no mejoró. Una tomografía (una imagen del interior del cuerpo) mostró que parte del intestino estaba atascado porque se metió por un pequeño agujero dentro del abdomen cerca del hígado.  \n\nLos médicos operaron para mirar dentro con una cámara y luego abrieron un poco más para poder sacar el trozo de intestino. El intestino estaba sano y no hubo que quitar ninguna parte. No se hizo ninguna técnica extra para evitar que vuelva a ocurrir.  \n\nDespués de la operación tuvo el intestino un poco lento y también una pequeña bolsa de líquido en la pelvis. Le quitaron la sonda del estómago a los cinco días y trataron la bolsa con antibióticos. Salió del hospital a los diez días, sin fiebre y en buen estado. Ahora sigue en controles con los médicos para ver cómo va.",
+            "B2": "Resumen claro y comprensible:\n\nUn chico de 15 años, sin cirugías previas, acudió por varios días de vómitos y dolor en la parte alta del abdomen. Al principio se pensó que tenía una gastroenteritis, pero como no mejoró y los vómitos eran biliosos (con contenido del intestino), le hicieron pruebas de imagen. La tomografía mostró líquido en la barriga y asas delgadas del intestino muy dilatadas, lo que sugería una obstrucción por una hernia interna a través del hiato de Winslow (una abertura dentro del abdomen donde, raramente, puede quedar atrapada una porción del intestino).\n\nEl equipo realizó primero una laparoscopia (cirugía con pequeñas incisiones y cámara), pero por mala visualización la convirtieron en una laparotomía media (incisión abdominal mayor). Encontraron un tramo de íleon (la parte final del intestino delgado) de unos 5 cm atrapado en el hiato; lo redujeron (lo sacaron) y el intestino estaba viable, por lo que no fue necesario cortar ninguna porción. No se practicó ninguna maniobra adicional para intentar evitar que la hernia vuelva a ocurrir.\n\nEn los días posteriores presentó un íleo paralítico (cuando el intestino se mueve muy poco de forma temporal) y desarrolló una colección en la pelvis que se trató con antibióticos y observación. Se le retiró la sonda nasogástrica al quinto día, empezó a tolerar alimentos y fue dado de alta al décimo día con buena evolución. Actualmente sigue en revisión en consultas de cirugía pediátrica.",
+            "B3": "Presentación clínica\nUn varón de 15 años sin antecedentes médicos ni cirugías previas acudió por 4 días de vómitos y dolor abdominal epigástrico. Inicialmente fue tratado como gastroenteritis, pero los síntomas persistieron y el vómito se volvió bilioso. A la exploración estaba afebril, con leve deshidratación, abdomen distendido, ruidos hidroaéreos disminuidos y sin signos de peritonismo.\n\nHallazgos diagnósticos\n- Analítica: sin hallazgos relevantes.  \n- Radiografía abdominal: imágenes sugestivas de obstrucción intestinal.  \n- Tomografía computarizada urgente: ascitis, marcada dilatación de asas de intestino delgado y un cambio de calibre a nivel del hiato (foramen) de Winslow, hallazgos compatibles con una herniación interna de asa ileal hacia la cavidad del epiplón menor.\n\nProcedimiento quirúrgico y hallazgos intraoperatorios\nSe realizó laparoscopia exploradora que mostró asas delgado dilatadas y ciego/íleon terminal móviles, localizados en hipocondrio derecho. La visualización quedó limitada por el borde hepático y la distensión intestinal; se intentó descomprimir una asa por punción sin éxito visual. Se convirtió a laparotomía media supraumbilical. Al abrir la cavidad se identificó un cambio de calibre en el íleon a unos 40 cm de la válvula ileocecal: un segmento de aproximadamente 5 cm de íleon había herniado a través del hiato de Winslow. Se observaron impresiones congestivas en los extremos del asa herniada. El foramen de Winslow tenía calibre normal. El asa reducida tenía buena viabilidad, por lo que no fue necesaria resección intestinal. No se realizó maniobra preventiva adicional para reducir el riesgo de recurrencia dado el aspecto y el calibre normal del hiato.\n\nEvolución postoperatoria\nEl postoperatorio inmediato cursó con íleo paralítico; la sonda nasogástrica se retiró al quinto día y se inició tolerancia oral progresiva con buena respuesta. Además desarrolló una colección pélvica que se manejó de forma conservadora con antibióticos, con buena evolución clínica. Fue dado de alta al décimo día tras mantener tránsito intestinal y buen estado general. Actualmente está en seguimiento en consultas externas de cirugía pediátrica.\n\nImplicaciones y recomendaciones\n- Diagnóstico: hernia interna a través del foramen de Winslow provocando obstrucción intestinal; es una causa poco frecuente de obstrucción en pacientes sin cirugía previa.  \n- Manejo realizado: reducción quirúrgica por laparotomía tras intento laparoscópico; no hubo necrosis intestinal ni resección.  \n- Seguimiento: vigilancia clínica en consultas de cirugía para detectar signos de recurrencia (dolor abdominal agudo, vómitos biliosos, distensión) o complicaciones infecciosas residuales. Si reaparecen síntomas, estaría indicado estudio por imagen y valoración quirúrgica precoz.  \n- Riesgo de recidiva: no se practicó cierre ni fijación específica del hiato en esta intervención porque el foramen tenía aspecto normal; el equipo mantiene seguimiento por si fuera necesario intervenir en el futuro.\n\nResumen empático\nSe trata de un adolescente previamente sano con una hernia interna poco habitual por el foramen de Winslow que provocó obstrucción intestinal. Gracias al diagnóstico por TC y la intervención oportuna se redujo el asa intestinal sin necesidad de resección, y el paciente evolucionó favorablemente tras un inicio postoperatorio complicado pero controlado. Continúa en seguimiento para asegurar recuperación completa y detectar cualquier signo de recurrencia."
+        }
+    },
+    {
+        "article": "Un niño de 23 meses de edad con encefalopatía isquémica hipóxica al nacer, con buen potencial motor cerebral y desarrollo psicomotor normal. Tenía antecedentes personales de miocardiopatía restrictiva y fue incluido en un programa de trasplante cardiaco cuando tenía 16 meses de edad. También fue necesario implantarle un dispositivo de asistencia biventricular Berlin Heart externo. Para evitar eventos embólicos, se le administró un tratamiento antiplaquetario doble y anticoagulante. Cuando tenía 23 meses de edad, presentó desconexión y hemiparesia derecha. Una tomografía computarizada (TC) mostró una arteria cerebral media (ACM) izquierda hiperdensa, así como un infarto parietotemporal derecho crónico. Su análisis de sangre mostró: glóbulos rojos 4.16 × 106 µ/L; hemoglobina 11.4 g/gL; tiempo de tromboplastina parcial activada (TTPA) 93 segundos y relación internacional normalizada (INR) 1.08.\n\nEl tratamiento trombolítico intravenoso estaba contraindicado debido al doble tratamiento antiplaquetario y anticoagulante a la dosis completa con heparina, por lo que se realizó una trombectomía intraarterial. Aunque el paciente tenía 23 meses de edad, se encontraba en el tercer percentil de la curva de peso (10 kg). Bajo anestesia general, se perforó la arteria femoral derecha y se colocó una funda 4F de 11 cm de largo (Cordis, Irlanda). Se usó un catéter vertebral Radiofocus 4F (Glidecath de Terumo, Bélgica) para confirmar la oclusión del segmento M1 de la MCA izquierda. La arteria se recanalizó mediante trombectomía mecánica con un stentriever utilizando el catéter vertebral 4F como tutor, colocándolo en el segmento petroso de la arteria carótida. Se usó un dispositivo Trevo XP Pro Vue de 3 mm x 20 mm (Stryker, Países Bajos), con un microcatéter Rapid Transit recto (Codman Neurovascular, Reino Unido), abriendo la arteria en una sola pasada. Se retiró todo el sistema (catéter tutor, microcatéter y stentriever) simultáneamente. En la prueba de control, se detectó una disección iatrogénica de la arteria carótida interna izquierda, que no tuvo importancia clínica, ya que el hemisferio izquierdo se irrigaba a través de la arteria comunicante anterior.\n\nUn mes después, se realizó con éxito el trasplante de corazón. La única secuela neurológica a largo plazo que surgió como resultado del accidente cerebrovascular fue la espasticidad del miembro superior derecho.\n\nMH - Cardiomiopatía, Dilatada/complicaciones/cirugía\nMH - Cardiomiopatía, restrictiva/complicaciones/cirugía\nMH - Angiografía cerebral\nMH - Procedimientos/métodos endovasculares\nMH - Mujer\nMH - Estudios de seguimiento\nMH - Insuficiencia cardiaca/*complicaciones/tratamiento\nMH - Trasplante de corazón\nMH - *Dispositivos de asistencia cardíaca\nMH - Humanos\nMH - Infantil\nMH - Hombre\nMH - Arteria cerebral media/imágenes diagnósticas\nMH - Estudios Retrospectivos\nMH - Ictus/complicaciones/diagnóstico por imágenes/cirugía\nMH - Resultado del tratamiento\n",
+        "gold_summary": "Un niño de 16 meses de edad con cardiomiopatía restrictiva que fue incluido en una lista para un trasplante cardiaco. A los 20 meses de edad, requirió un implante de un dispositivo de asistencia biventricular externo (Berlin Heart) y tuvo un accidente cerebrovascular en el hemisferio izquierdo a los 23 meses. Se utilizó un enfoque intraarterial y produjo buenos resultados clínicos. Un mes después, se realizó con éxito un trasplante cardiaco.\n",
+        "synthetic_summary": {
+            "B1": "Este es el resumen de la historia de un niño pequeño contado con palabras sencillas.\n\n- Cuando nació tuvo un problema en el cerebro por falta de oxígeno, pero creció con un desarrollo normal y movía bien su cuerpo.\n- Tenía una enfermedad del corazón llamada cardiomiopatía. A los 16 meses lo pusieron en la lista para un trasplante de corazón.\n- Más tarde le pusieron una máquina externa (Berlin Heart) para ayudar a su corazón a bombear. Por eso tomaba medicinas para hacer la sangre menos pegajosa.\n- A los 23 meses tuvo un accidente cerebrovascular (un coágulo que tapó una arteria del lado izquierdo del cerebro). Esto hizo que su brazo y pierna derechos quedaran débiles.\n- Los médicos no pudieron darle la medicina que disuelve coágulos porque ya estaba con medicinas que adelgazan la sangre. En vez de eso, hicieron una operación por dentro de los vasos.\n- Introdujeron un catéter por la pierna, llegaron hasta la arteria del cerebro y usaron un pequeño aparato para sacar el coágulo. Lo lograron en una sola vez.\n- Durante el procedimiento apareció una pequeña rotura en una arteria del cuello. No fue grave porque otra arteria seguía dando sangre al cerebro.\n- Un mes después le hicieron el trasplante de corazón con éxito. La única secuela que le quedó fue rigidez (espasticidad) en el brazo derecho.\n- En general, los doctores pudieron arreglar el problema de la arteria y después recibió el nuevo corazón. Esto ayudó mucho a su salud.",
+            "B2": "Resumen comprensible para lectores jóvenes (11–17 años):\n\nUn niño de 23 meses que había sufrido una lesión cerebral por falta de oxígeno al nacer (pero que se había desarrollado bien en cuanto al movimiento y al desarrollo general) tenía una cardiomiopatía restrictiva —una enfermedad del corazón que dificulta que el ventrículo se llene bien— y fue incluido en la lista para un trasplante de corazón cuando tenía 16 meses. Más adelante necesitó un dispositivo de asistencia cardiaca externo (llamado Berlin Heart) para ayudar al corazón a bombear.\n\nPara evitar coágulos, recibía dos medicamentos antiplaquetarios y también anticoagulación completa con heparina. A los 23 meses presentó una pérdida súbita de conciencia y debilidad marcada en el lado derecho del cuerpo. Una tomografía mostró lo que parecía ser un coágulo en la arteria cerebral media izquierda (la arteria que lleva sangre a gran parte del lado izquierdo del cerebro). Debido a los medicamentos que estaba tomando, no se pudo dar el tratamiento trombolítico por vía intravenosa (el fármaco que disuelve coágulos). Por eso los médicos realizaron una trombectomía mecánica intraarterial: introdujeron catéteres por la arteria femoral, llegaron hasta la arteria bloqueada y retiraron el coágulo con un dispositivo especial llamado stent retriever. Abrieron la arteria en una sola pasada.\n\nDurante el procedimiento se produjo una pequeña disección iatrogénica (un desgarro en la pared de la arteria causado por el procedimiento), pero no causó problemas porque la parte izquierda del cerebro seguía recibiendo sangre por otra vía (la arteria comunicante anterior). Un mes después el niño pudo recibir con éxito el trasplante de corazón. La única secuela neurológica duradera fue espasticidad (rigidez y tensión) en el brazo derecho.\n\nQué significa esto de forma sencilla:\n- Cuando hay un coágulo grande en una arteria cerebral, a veces no puede usarse el tratamiento que disuelve coágulos si el paciente ya toma anticoagulantes; entonces los médicos pueden quitar el coágulo usando instrumentos que llegan por dentro de las arterias.\n- Aunque el procedimiento tuvo una pequeña complicación en la arteria, la circulación alternativa protegió el cerebro.\n- El niño se recuperó lo suficiente para recibir el trasplante, pero quedó con algo de rigidez en el brazo derecho.",
+            "B3": "Resumen\n\nUn niño de 23 meses con antecedentes de encefalopatía hipóxico-isquémica neonatal (con desarrollo psicomotor y función motora cerebral considerados buenos) y cardiomiopatía restrictiva fue incluido en lista para trasplante cardiaco en la infancia y recibió un dispositivo de asistencia biventricular externo (Berlin Heart). Pesaba 10 kg, en el tercer percentil para su edad.\n\nPresentación y hallazgos\n- A los 23 meses tuvo una desconexión neurológica y hemiparesia derecha.  \n- La TC craneal mostró una arteria cerebral media (ACM) izquierda hiperdensa compatible con oclusión aguda; además existía un infarto crónico en el hemisferio derecho (parietotemporal).  \n- Analíticas: hematíes 4.16 × 10^6/µL, hemoglobina 11.4 g/dL; tiempo de tromboplastina parcial activada (TTPA) prolongado a 93 s (por anticoagulación con heparina) e INR 1.08.  \n\nDecisiones terapéuticas\n- La terapia trombolítica intravenosa se consideró contraindicada por estar en tratamiento antiplaquetario doble y anticoagulación a dosis completa.  \n- Se optó por una trombectomía mecánica endovascular, procedimiento dirigido a retirar el trombo y restaurar el flujo arterial.\n\nProcedimiento\n- Bajo anestesia general, se accedió por arteria femoral derecha con una vaina 4F y se navegó hasta la carótida para confirmar oclusión del segmento M1 de la ACM izquierda.  \n- Se realizó trombectomía con un stent-retriever (Trevo XP ProVue 3 × 20 mm) colocado mediante microcatéter; la arteria se recanalizó en una sola pasada.  \n- Tras la retirada simultánea del sistema, se identificó una disección iatrogénica de la arteria carótida interna izquierda, pero ésta no produjo déficit clínico porque el hemisferio izquierdo seguía recibiendo irrigación por la arteria comunicante anterior.\n\nEvolución y resultados\n- La recanalización fue exitosa y permitió la resolución del evento isquémico agudo.  \n- Un mes después se realizó con éxito el trasplante cardiaco.  \n- A largo plazo la única secuela neurológica señalada fue espasticidad del miembro superior derecho.\n\nImplicaciones y consideraciones\n- Este caso muestra que la trombectomía mecánica puede ser factible y eficaz en lactantes pequeños con ictus isquémico agudo, incluso cuando la trombólisis sistémica está contraindicada por anticoagulación/antiplaquetarios.  \n- Riesgos específicos incluyen lesión o disección vascular iatrogénica; por eso estos procedimientos requieren equipos y experiencia en neurointervencionismo pediátrico y acceso vascular adaptado al tamaño del niño.  \n- El seguimiento debe incluir rehabilitación neurológica dirigida a la espasticidad (fisioterapia, terapias del tono, y si procede, intervención rehabilitadora adicional) y vigilancia neurovascular y neurofuncional tras el trasplante.\n\nEste informe es esperanzador respecto a la posibilidad de tratar ictus isquémicos en niños muy pequeños con técnicas endovasculares cuando la trombólisis no es una opción, pero subraya la necesidad de centros especializados y un seguimiento rehabilitador estrecho."
+        }
+    },
+    {
+        "article": "Una mujer de 23 años de edad se presentó al departamento de urgencias con pérdida de conciencia y exceso de secreciones orales 2 horas después de la ingestión de un veneno no especificado. No tenía movimientos corporales anormales, fiebre, diarrea, vómitos o sudoración. Inicialmente la habían llevado a un hospital primario cercano, donde fue tratada por posible intoxicación por OP con atropina y cimetidina durante 3 días, antes de ser trasladada al hospital Saint Peter. Después de un interrogatorio exhaustivo, se descubrió que la paciente había consumido unos 30 ml de 2,4-D en un intento de suicidio, precipitado por problemas financieros. No tenía antecedentes conocidos de enfermedad psiquiátrica, intentos de suicidio, episodios depresivos o abuso de sustancias. No se observaron trastornos cardíacos, renales o metabólicos previos.\n\nAl llegar al departamento de urgencias, la paciente estaba inconsciente. Sus constantes vitales eran PR 110/min, BP 120/70 mmHg, RR 21/min, y SPO2 96% en aire ambiente. Los resultados del examen físico fueron notables: un GCS de 6 sobre 15, pupilas dilatadas y reactivas, extremidades inferiores hipertónicas e hiperreflexivas, y reflejo plantar ascendente. Tras la investigación inicial, el recuento completo de células sanguíneas, la prueba de la función renal, la prueba de la función hepática, y la glucosa en sangre aleatoria fueron normales. Su electrocardiograma mostró taquicardia sinusal, mientras que la radiografía de tórax no fue notable. El análisis de gases en sangre arterial y el nivel sérico de la toxina no pudieron determinarse, ya que ninguno de los medios de prueba estaba disponible en el hospital.\n\nLa paciente fue trasladada a la unidad de cuidados intensivos (UCI), se le introdujo una sonda para proteger las vías respiratorias y se le inició inmediatamente una diuresis alcalina forzada. Su evolución en la UCI fue notable por el desarrollo de una insuficiencia renal (creatinina 3,1 ml/dL [intervalo de referencia 0,5-1,2 mg/dL], BUN 133 mg/dL [intervalo de referencia 16,6-48,5 mg/dL], análisis de orina 3+ hemoglobina y muchos glóbulos rojos), debido a una rabdomiolisis inducida por toxinas (nivel de creatina fosfocinasa de 1330 µg/L). Posteriormente, la paciente se volvió hipotensa y se le inició un tratamiento con vasopresores. La ecocardiografía y la ecografía abdominal no fueron significativas. A pesar de estos esfuerzos, falleció por colapso circulatorio el tercer día de estancia en la UCI.\n",
+        "gold_summary": "Aquí se informa sobre el caso de una joven granjera de la zona rural de Etiopía que fue internada en un hospital local tras perder el conocimiento y presentar exceso de secreciones orales 2 horas después de haber ingerido, de manera suicida, un agente tóxico desconocido. Originalmente, se la trató por intoxicación con organofosforados y luego se la trasladó al Hospital Saint Peter's en Addis Abeba para recibir atención médica más intensiva. Allí, se confirmó la ingesta de 2,4-D y se le brindó atención médica de apoyo, ventilación mecánica y diuresis alcalina forzada. A pesar de estas intervenciones, falleció varios días después.\n",
+        "synthetic_summary": {
+            "B1": "Una mujer de 23 años tomó 30 ml de 2,4-D, un veneno que se usa contra las malas hierbas. Lo hizo porque tenía problemas de dinero. Dos horas después la encontraron inconsciente y con mucha saliva. La llevaron a un hospital pequeño. Allí pensaron que era otro veneno y le dieron medicinas. Luego la trasladaron a un hospital más grande.\n\nAl llegar estaba muy dormida y no respondía. Al principio sus análisis de sangre y la radiografía no mostraron problemas grandes. En la unidad de cuidados intensivos le pusieron una sonda para proteger su respiración y le dieron líquidos y medicinas para ayudar a sacar el veneno por la orina.\n\nPero su situación empeoró. Los músculos se dañaron, y eso lesionó sus riñones. Empezó a orinar sangre y sus riñones dejaron de funcionar bien. También bajó demasiado su presión y tuvo que recibir medicinas para subirla. A pesar de los tratamientos, falleció al tercer día por un fallo circulatorio.\n\nEs una historia triste. Los médicos hicieron lo posible, pero algunos venenos son muy peligrosos y difíciles de tratar.",
+            "B2": "Resumen clínico (nivel B2, lectura para adolescentes)\n\nUna mujer de 23 años intentó suicidarse bebiendo cerca de 30 ml de 2,4-D, un herbicida (un producto para matar malezas). Dos horas después fue llevada al servicio de urgencias porque había perdido el conocimiento y tenía mucha saliva en la boca. Al principio la trataron en un hospital cercano pensando que se había intoxicado con organofosforados (otro tipo de veneno) y le dieron atropina y cimetidina durante 3 días antes de transferirla a un hospital más grande.\n\nAl llegar al Hospital Saint Peter:\n- Estaba inconsciente con una puntuación de 6/15 en la escala de Glasgow (una forma de medir el nivel de conciencia).\n- Tenía pupilas dilatadas pero que respondían a la luz, y las piernas estaban rígidas y con reflejos exagerados; el reflejo plantar estaba anormal (signo de daño en la vía nerviosa).\n- Ritmo cardiaco rápido (taquicardia) y otras pruebas iniciales (sangre, hígado, glucosa) salieron normales.\n- No se pudo medir el gas en sangre ni el nivel de la toxina porque el hospital no tenía esas pruebas.\n\nQué se hizo y cómo evolucionó:\n- Fue llevada a cuidados intensivos, se le puso un tubo para proteger la vía aérea y se inició diuresis alcalina forzada (una medida para intentar eliminar el veneno por la orina).\n- Desarrolló rabdomiólisis: las células musculares se dañaron y liberaron sustancias al torrente sanguíneo (el valor de creatina quinasa estaba alto), lo que dañó los riñones.\n- Apareció insuficiencia renal: la creatinina y el nitrógeno ureico en sangre (BUN), que muestran función renal, se elevaron mucho; en la orina se veía hemoglobina y muchos glóbulos rojos.\n- Se volvió hipotensa (presión arterial baja) y necesitaron medicación para subir la presión (vasopresores).\n- Ecocardiograma y ecografía abdominal no mostraron hallazgos importantes.\n- A pesar de las medidas de apoyo, falleció por colapso circulatorio al tercer día en la UCI.\n\nComentario y lecciones importantes (explicado con calma):\n- El 2,4-D es un herbicida que no tiene un antídoto específico; el tratamiento es sobre todo de soporte: proteger la respiración, controlar la presión, eliminar la toxina si es posible y cuidar los riñones.\n- En este caso hubo limitaciones en las pruebas disponibles (no se pudo medir la sustancia ni el gasometría), lo que complica el manejo.\n- La rabdomiólisis y la insuficiencia renal fueron complicaciones graves que contribuyeron al empeoramiento.\n- En intoxicaciones graves como esta, además de la atención intensiva, a veces se considera diálisis para ayudar a eliminar la toxina y apoyar los riñones.\n\nEs una situación triste: una joven sin antecedentes psiquiátricos que tomó esta decisión por problemas económicos. Casos así recuerdan la importancia de tener acceso rápido a pruebas y tratamientos específicos, así como apoyo emocional y social para prevenir intentos de suicidio.",
+            "B3": "Resumen clínico (paciente: mujer, 23 años)\n\nBreve introducción\n- Se presenta el caso de una mujer joven que intentó suicidarse ingiriendo aproximadamente 30 ml de 2,4-diclorofenoxiacético (2,4‑D), un herbicida. Fue llevada al servicio de urgencias 2 horas después de la ingestión y, tras tratamiento inicial en un hospital local por sospecha de intoxicación por organofosforados, fue trasladada a un centro terciario para manejo intensivo.\n\nAntecedentes y motivo de la ingesta\n- Intento de suicidio motivado por problemas financieros.\n- Sin antecedentes documentados de enfermedad psiquiátrica, consumo de tóxicos, intentos previos ni enfermedad cardíaca, renal o metabólica conocida.\n\nHallazgos al ingreso\n- Estado neurológico: conciencia gravemente alterada (GCS 6/15), pupilas dilatadas pero reactivas, hipertonicidad e hiperreflexia en miembros inferiores con signo de extensión plantar (anormal).\n- Signos vitales: frecuencia cardiaca 110/min, presión arterial 120/70 mmHg, frecuencia respiratoria 21/min, saturación de O2 96% en aire ambiente.\n- Pruebas iniciales normales: hemograma, pruebas hepáticas, pruebas renales y glucemia al ingreso fueron normales. ECG: taquicardia sinusal. Radiografía de tórax sin hallazgos.\n- No fue posible medir gases arteriales ni niveles séricos del tóxico por falta de disponibilidad.\n\nTratamiento inicial y medidas en UCI\n- Protección de vía aérea con tubo endotraqueal.\n- Diuresis alcalina forzada como medida para aumentar eliminación renal del tóxico.\n- Antes del traslado, recibió atropina y cimetidina en el hospital local por sospecha de organofosforados.\n\nEvolución y complicaciones\n- Desarrollo de rabdomiólisis: creatina fosfocinasa elevada (1.330 µg/L).\n- Insuficiencia renal aguda: creatinina 3,1 mg/dL (valor referencia 0,5–1,2), BUN 133 mg/dL (ref. 16,6–48,5). Análisis de orina: 3+ hemoglobina y numerosos glóbulos rojos.\n- Posteriormente se volvió hipotensa y requirió vasopresores.\n- Ecocardiograma y ecografía abdominal sin hallazgos relevantes.\n- Falleció por colapso circulatorio al tercer día en la UCI.\n\nInterpretación y puntos clave\n- 2,4‑D puede causar afectación neurológica severa, daño muscular (rabdomiólisis), fallo renal y alteraciones hemodinámicas; en este caso la progresión fue rápida y fatal a pesar de medidas de soporte intensivo.\n- La ausencia de pruebas toxicológicas y de gasometría limitó la monitorización específica del envenenamiento.\n- El diagnóstico inicial por error como intoxicación por organofosforados motivó tratamiento empírico (atropina), lo que ilustra cómo la identificación temprana del agente es importante para orientar intervenciones específicas.\n\nLecciones prácticas y siguientes pasos razonables (generales)\n- En intoxicaciones por herbicidas como 2,4‑D, la atención es mayoritariamente de soporte: estabilizar vía aérea, circulación y función renal; medidas de descontaminación precoz cuando procede; y considerar diálisis o soporte renal de reemplazo si hay insuficiencia renal grave o acumulación del tóxico.\n- Contar con pruebas analíticas (niveles séricos del tóxico, gasometría) facilita el manejo y el pronóstico.\n- Es clave la evaluación y el soporte psiquiátrico tras intentos de suicidio para prevención secundaria.\n\nComentario final\nEste caso ilustra la gravedad potencial de la ingestión de 2,4‑D y los límites que imponen la presentación tardía o el diagnóstico incierto y la falta de recursos diagnósticos. Lamento la trágica evolución de la paciente; el reporte subraya la necesidad de recursos de toxicología, acceso a terapias de reemplazo renal y servicios de salud mental en entornos con exposiciones a pesticidas."
+        }
+    },
+    {
+        "article": "Una paciente etíope de 35 años de edad se presentó en el departamento de urgencias del Colegio Médico del Hospital Yekatitit 12 con síntomas de falta de aire en reposo, ortopnea, disnea paroxística nocturna significativa, dolor torácico, tos productiva teñida de sangre y vómitos de materia ingerida (2-3 episodios por día) durante 2 semanas. Presentaba una hinchazón progresiva del cuerpo que comenzó en las extremidades inferiores y luego afectó a todo el cuerpo, fatigabilidad fácil, pérdida de apetito, fiebre intermitente de alto grado y sensación de ardor epigástrico durante la misma semana y con la misma duración. La paciente también experimentó una pérdida de peso y fatiga no especificadas durante los últimos 2 meses. Por lo demás, no tenía comorbilidades conocidas, ni comportamientos de riesgo, como fumar o beber alcohol, medicamentos o antecedentes familiares de neoplasia. Estaba casada, tenía cuatro hijos y no tenía antecedentes obstétricos negativos. Su ocupación era la agricultura y había vivido en una zona rural. Nunca había sido admitida por una queja similar.\n\nLa escala de coma de Glasgow (GCS) de la paciente fue de 15 sobre 15, y no había anormalidades de memoria, potencia o tono. La paciente estaba en grave dificultad respiratoria con saturación de oxígeno del 70% con aire atmosférico, frecuencia respiratoria de 30-35 latidos/minuto, y frecuencia del pulso de 120 por minuto. Tenía registros de fiebre de alto grado hasta el nivel de 39.5 0C y puede mantener su presión arterial. El examen de mama con ultrasonido y mamografía fue supuestamente normal. No se detectó linfadenopatía en áreas accesibles.\n\nEl examen del tórax reveló signos de derrame pleural que también se observaron en las imágenes y se analizaron. Una tomografía computarizada (TC) del tórax con contraste mostró derrame pericárdico y neumonía multifocal. La angiografía por TC mostró un defecto de llenado arterial pulmonar segmentario del lóbulo inferior en ambos lados, lo que sugiere embolia pulmonar y derrame pleural en ambos lados. Los frotis citológicos se informaron con láminas de células mesoteliales, neutrófilos y grupos dispersos de células grandes atípicas con nucleolos prominentes que sugieren derrame maligno. El análisis del líquido pleural mostró un líquido con predominio linfocítico con glucosa normal (82 mg/dl), proteínas (2,2 g/dl) y lactato deshidrogenasa (LDH) de 592 mg/dl.\n\nLa presión venosa yugular aumentó con los sonidos cardiacos apagados. La ecocardiografía mostró derrame pericárdico masivo con características de taponamiento cardiaco, fracción de eyección preservada (65%), y excursión sistólica del plano anular tricuspídeo (TAPSE) mayor a 18 mm. Un electrocardiograma (ECG) reveló solo taquicardia sinusal y desviación del eje. Se realizó una pericardiocentesis inmediata, se extrajo un drenaje de aproximadamente 250 ml de fluido hemorrágico y se aseguró la ventana pericárdica. La repetida ecocardiografía reveló una reducción del tamaño. El informe de citología del fluido pericárdico mostró numerosos linfocitos junto con células malignas atípicas que tenían prominentes nucleolos, lo que sugería un derrame maligno.\n\nEn el examen abdominal, mostró signos positivos de acumulación de fluidos sin órgano hinchable. La tomografía computarizada abdominal y pélvica mostró un aumento en el tamaño del hígado con múltiples lesiones hepáticas hipointensas que sugerían metástasis. Los órganos pélvicos, incluidos los ovarios y el útero, no presentaron lesiones identificadas. Se realizó una biopsia con aguja de la lesión hepática y los resultados revelaron un adenocarcinoma secundario.\n\nSe realizó un diagnóstico de insuficiencia cardíaca causada por una efusión pericárdica masiva maligna secundaria a un adenocarcinoma diseminado y un carcinoma de origen primario desconocido que afectaba al pulmón, la pleura, el pericardio y el tracto gastrointestinal. Se le diagnosticó a la paciente una trombosis venosa profunda extensa en la extremidad superior izquierda, una embolia pulmonar bilateral y segmentaria, posiblemente debido a la CUP diseminada. Los hallazgos también mostraron una neumonía multifocal superpuesta y una anemia leve de enfermedad crónica.\n\nEl recuento sanguíneo completo inicial reveló leucocitosis con un recuento de glóbulos blancos de 24 × 103 por ml, neutrófilos predominantes (91%), recuento de glóbulos rojos de 3.7 × 106 por µl, anemia normocítica leve (hemoglobina (Hgb) 11.2 mg/dl), volumen corpuscular medio (MCV) de 81.2 fl, y trombocitopenia severa (66 × 103/µl). Después del tratamiento antibiótico para neumonía, el recuento sanguíneo completo volvió a la normalidad (excepto para Hgb). Con niveles normales de bilirrubina, la aspartato aminotransferasa (AST) aumentó más de siete veces (263 U/L), mientras que la alanina transaminasa (ALT) aumentó más de nueve veces (332 U/L). Los electrolitos séricos (excepto para Na + con hiponatremia leve, 129 mEq/L) y las pruebas de función renal fueron normales. La albúmina era baja (2.12 g/dl). Los niveles de lactato deshidrogenasa (LDH) aumentaron casi dos veces desde el inicio (592 U/L). Los virus del virus de inmunodeficiencia humana, hepatitis B y hepatitis C no fueron reactivos. La sangre y el cultivo del líquido pleural no tuvieron crecimiento. Un antígeno carcinoembrionario (CEA) aumentó más de 400 veces (1000 µg/L) del inicio.\n\nLa paciente fue admitida en la sala general. Se realizó una ventana pericárdica y una inserción de un tubo torácico derecho con un cirujano cardiotorácico junto con un cardiólogo (ver la cantidad de aspirado antes). Se realizó una aspiración pleural terapéutica intermitente para el derrame pleural maligno. Una vez que la dosis de carga (60 mg) de frusemida produjo suficiente producción de orina, esta dosis se mantuvo tres veces (TID) al día. Esto se redujo y se dio de alta a la paciente con una dosis oral de 20 mg dos veces al día (BID). Se inició una dosis estándar de enoxaparina para el tromboembolismo pulmonar y la trombosis venosa profunda aguda extensa en la extremidad superior izquierda. Se administró enoxaparina por vía subcutánea 40 mg BID durante la hospitalización, que se cambió a 5 mg de warfarina oral diaria durante el alta debido a problemas financieros. La neumonía multifocal se trató con ceftazidima (1 g intravenoso TID) y vancomicina (1 g intravenoso BID) según el protocolo de tratamiento estándar nacional. El dolor se controló con un potente medicamento contra el dolor (morfina 5 mg intravenosa TID) y se redujo y suspendió. También estaba en la profilaxis de la úlcera. La paciente fue dada de alta de la sala médica con una mejora significativa después de 14 días de hospitalización y fue asignada a la unidad de oncología del hospital. Por lo tanto, para el cáncer de origen primario desconocido, se le dio un ciclo de quimioterapia (carboplatino/paclitaxel). Se perdió el seguimiento debido a problemas financieros, y la paciente murió en su casa cuatro meses después del alta.\n\nMH - Humanos\nMH - Mujer\nMH - *Insuficiencia cardiaca/etiología\nMH - Adulto\nMH - *Neoplasias, complicaciones/primaria desconocida",
+        "gold_summary": "Una mujer negra de 35 años se presentó con falta de aire en reposo, ortopnea, disnea paroxística nocturna, dolor torácico, tos productiva teñida de sangre y fiebre durante 2 semanas. También tenía hinchazón progresiva del cuerpo, fatigabilidad fácil, pérdida de apetito y dolor abdominal durante la misma semana. La imagen corporal reveló grandes derrames pleurales y pericárdicos, lesiones hepáticas metastásicas y defectos de llenado segmentarios y subsegmentarios vasculares pulmonares bilaterales. La citología de los fluidos pericardio y pleural sugieren derrame maligno. Las lesiones hepáticas y la biopsia con aguja indicaron adenocarcinoma de origen desconocido, y el nivel de antígeno carcinoembriónico también aumentó significativamente.\n",
+        "synthetic_summary": {
+            "B1": "Una mujer de 35 años fue al hospital porque le costaba mucho respirar. Tenía dolor en el pecho, tos con algo de sangre, fiebre, hinchazón por todo el cuerpo, y se sentía muy cansada y había bajado de peso.\n\nLos médicos encontraron mucho líquido alrededor de sus pulmones y alrededor del corazón. El líquido alrededor del corazón estaba apretando el corazón y por eso le costaba respirar. Le sacaron ese líquido y ella mejoró. Al mirar ese líquido, vieron células de cáncer.\n\nLas pruebas y una biopsia (un pequeño pedazo de tejido tomado con una aguja) mostraron que el cáncer había llegado al hígado y a las membranas del pecho y del corazón. No pudieron encontrar con seguridad de dónde empezó el cáncer. También tuvo coágulos de sangre en una vena del brazo y en los pulmones.\n\nLa trataron en el hospital. Le hicieron una pequeña operación para drenar el líquido del corazón y le pusieron un tubo en el pecho para sacar el líquido de los pulmones. Le dieron antibióticos para la infección, medicinas para bajar la hinchazón, calmantes y medicinas para los coágulos. Le dieron una sesión de quimioterapia (medicinas fuertes para tratar el cáncer).\n\nDespués de 14 días en el hospital, ella estaba mejor y salió a su casa. No pudo seguir el tratamiento por problemas de dinero. Cuatro meses después murió en su casa. Fue un caso triste de cáncer que ya se había extendido y que fue difícil de curar.",
+            "B2": "Summary (upper-intermediate / suitable for ages 14–17)\n\nA 35-year-old Ethiopian woman went to the emergency room with two weeks of worsening breathlessness (even at rest), trouble breathing when lying flat (orthopnea), sudden night-time breathlessness, chest pain, coughing up blood-stained mucus, vomiting, fever, and swelling that began in her legs and spread through her body. She had also lost weight and felt tired for about two months.\n\nImportant findings and tests\n- She was very sick on arrival: low oxygen (about 70%), fast breathing and heart rate, and high fever.\n- Chest scans showed large amounts of fluid around both lungs (pleural effusion) and around the heart (pericardial effusion). There was also pneumonia in several places and small blood clots in lung arteries (pulmonary emboli).\n- The heart ultrasound showed a large pericardial effusion causing cardiac tamponade. Cardiac tamponade means the fluid was pressing on the heart and stopping it from working normally.\n- Doctors drained blood-stained fluid from around the heart (about 250 ml) with a needle (pericardiocentesis) and made a surgical opening (pericardial window) so fluid could drain more easily.\n- Cell studies (cytology) of the fluid around the heart and lungs showed cancer cells, which suggested the effusions were caused by cancer.\n- An abdominal CT scan showed an enlarged liver with many lesions. A needle biopsy of a liver lesion showed metastatic adenocarcinoma — a common type of cancer that started somewhere else and spread to the liver.\n- Blood tests showed high white blood cells (infection/inflammation), low platelets at first (which later improved), low blood protein (albumin), very high liver enzymes, and a very high carcinoembryonic antigen (CEA), a marker often raised in some cancers.\n\nDiagnosis and other problems\n- The team diagnosed heart failure caused by a large malignant pericardial effusion, due to widely spread adenocarcinoma of unknown primary origin (called cancer of unknown primary, CUP). The cancer involved the lungs, pleura (lining of the lungs), pericardium (lining of the heart), and likely the digestive tract.\n- She also had a large blood clot in a vein of her left arm (deep vein thrombosis), pulmonary emboli (clots in the lungs), and multifocal pneumonia.\n\nTreatment and outcome\n- Emergency drainage of the heart and chest was done, repeated draining of the pleural fluid was performed, and a chest tube was placed.\n- She received diuretics (to remove extra fluid), antibiotics for pneumonia, strong pain relief, and blood thinners for the clots (started with enoxaparin, later changed to warfarin for cost reasons).\n- After 14 days in hospital she improved and was sent to the oncology unit. She began chemotherapy (carboplatin and paclitaxel) aimed at the cancer of unknown primary.\n- Due to financial difficulties she stopped follow-up care and died at home four months after leaving the hospital.\n\nWhat this means (in simple terms)\n- The patient had an aggressive cancer that spread to several places in her body and caused dangerous fluid build-up around her heart and lungs. Drainage and medical treatments helped in hospital, but the cancer was advanced and the exact original site could not be found. Financial and access problems affected ongoing care, and she died a few months later.\n\nThis case shows how cancer can present first with life-threatening fluid around the heart and lungs, and how serious complications (like clots and liver spread) make treatment harder. The medical team acted quickly to relieve the pressure on her heart and to treat infections and clots, but the advanced stage of disease made the outlook poor.",
+            "B3": "Resumen clínico (nivel lector universitario)\n\nPresentación y síntoma principal\n- Mujer etíope de 35 años acudió por reciente insuficiencia respiratoria: disnea en reposo, ortopnea y disnea paroxística nocturna durante 2 semanas, acompañadas de dolor torácico, tos productiva con sangre, vómitos alimentarios, fiebre intermitente y edema progresivo generalizado. Además refirió pérdida de peso y fatigabilidad durante 2 meses.\n\nHallazgos iniciales y examen físico\n- Estado neurológico intacto (GCS 15), sin déficit motor o de memoria. Estaba taquipneica (FR 30–35/min), taquicárdica (pulso 120/min) y con saturación de oxígeno del 70% en aire ambiente. Tenía fiebre hasta 39.5 °C pero tensión arterial mantenida.\n- No se palparon adenopatías accesibles; examen mamario (ecografía y mamografía) informados como normales.\n\nImágenes y procedimientos urgentes\n- TC torácica con contraste: derrame pericárdico masivo, neumonía multifocal y derrames pleurales bilaterales. Angio-TC mostró defectos de llenado segmentarios bilaterales en arterias pulmonares, compatibles con embolia pulmonar.\n- Ecocardiograma: derrame pericárdico masivo con signos de taponamiento cardiaco; fracción de eyección conservada (~65%).\n- Se practicó pericardiocentesis urgente y se creó una ventana pericárdica; se extrajeron ≈250 ml de líquido hemorrágico, con reducción del derrame en la ecografía posterior. Se colocó drenaje torácico derecho y se realizaron aspiraciones pleurales terapéuticas.\n\nLaboratorio y citología\n- Sangre: leucocitosis marcada (24 × 10^3/µL) con neutrofilia (91%), anemia leve normocítica (Hb 11.2 g/dL), trombocitopenia severa inicial (66 × 10^3/µL) que luego mejoró tras tratamiento.\n- Bioquímica: elevación notable de transaminasas (AST 263 U/L, ALT 332 U/L), LDH aumentada (~592 U/L), albúmina baja (2.12 g/dL) e hiponatremia leve (Na+ 129 mEq/L). Pruebas virales (VIH, hepatitis B y C) negativas. Hemocultivos y cultivo de líquido pleural negativos.\n- Marcador tumoral: antígeno carcinoembrionario (CEA) muy elevado (>1000 µg/L).\n- Citología de líquido pleural y pericárdico: presencia de células malignas atípicas con nucleolos prominentes; líquido pleural linfocítico con glucosa normal, proteína aumentada y LDH elevada — compatibles con derrame maligno.\n\nHallazgos abdominales y diagnóstico histológico\n- TAC abdominopélvico: hepatomegalia con múltiples lesiones hipointensas en hígado sugestivas de metástasis; ovarios y útero sin lesiones identificadas.\n- Biopsia hepática por aguja: adenocarcinoma metastásico.\n- Se diagnosticó cáncer de origen primario desconocido (CUP) con afectación pleuro-pericárdica, pulmonar y hepática.\n\nComplicaciones adicionales\n- Trombosis venosa profunda extensa en miembro superior izquierdo y embolia pulmonar bilateral segmentaria, atribuibles al estado pro-trombótico paraneoplásico.\n- Neumonía multifocal superpuesta y anemia de enfermedad crónica.\n\nTratamiento y evolución\n- Manejo agudo: pericardiocentesis y ventana pericárdica, drenaje pleural derecho, diuréticos (furosemida) para congestión, anticoagulación con enoxaparina (cambiada a warfarina al alta por limitaciones económicas), y antibióticos (ceftazidima + vancomicina) para la neumonía. Analgesia y profilaxis de úlcera también.\n- Oncología: un ciclo de quimioterapia con carboplatino/paclitaxel para cáncer de origen desconocido.\n- Alta tras 14 días con mejoría clínica, pero la paciente perdió seguimiento por dificultades económicas y falleció en su domicilio cuatro meses después.\n\nInterpretación y implicaciones\n- El cuadro es compatible con un adenocarcinoma metastásico avanzado que se presentó inicialmente por complicaciones cardiopulmonares (derrame pericárdico maligno con taponamiento y derrames pleurales), además de tromboembolismo venoso masivo. La elevación muy marcada del CEA y la citología positiva apoyan origen adenocarcinomatoso, pero no se identificó de forma concluyente el tumor primario.\n- El pronóstico en este contexto era reservado/malo: derrame pericárdico maligno con taponamiento y enfermedad metastásica múltiple suelen asociarse a supervivencia limitada, a pesar del control sintomático y la quimioterapia paliativa.\n\nPasos diagnósticos y terapéuticos razonables (general)\n- En casos similares valorar tinción inmunohistoquímica de la biopsia hepática e investigación molecular para intentar identificar el tumor primario y detectar alteraciones tratables (cuando los recursos lo permitan).\n- PET-CT y estudios dirigidos según el panel inmunohistoquímico pueden ayudar a localizar el primario.\n- Enfoque multidisciplinario (oncología, cardiología, cuidados paliativos) para control sintomático, tratamiento antitromboembólico y planificación oncológica según estado funcional y objetivos de la paciente.\n\nComentario final (tono empático)\n- Esta paciente joven presentó una forma agresiva y avanzada de cáncer con complicaciones potencialmente mortales (taponamiento cardíaco, embolia pulmonar y metástasis hepáticas). A pesar de intervenciones urgentes y tratamiento paliativo, la enfermedad era sistémica y el desenlace fue fatal pocos meses después del alta. La atención integrada y el acceso a estudios diagnósticos y terapias más amplios pueden, en otros casos, ayudar a orientar tratamientos más específicos, aunque el pronóstico sigue siendo a menudo reservado en CUP con derrames malignos extensos."
+        }
+    },
+    {
+        "article": "Paciente del sexo femenino de 17 años con diagnóstico de enfermedad de Graves con bocio difuso, la cual negó otros antecedentes de importancia.\n\nSu cuadro comenzó seis meses antes con pérdida de peso progresiva, episodios de ansiedad y agitación, temperaturas de 37.4 a 37.9 ºC, palpitaciones, dolor abdominal y diarrea intermitente. A los dos meses se agregó como síntoma el crecimiento de la cara anterior del cuello; al tercer mes presentó taquicardia de hasta 130 latidos por minuto. Al ser valorada por Endocrinología se le administró tiamazol de 15 mg cada 8 horas, el cual fue suspendido por cuadro de agranulocitosis. Por lo tanto, se le comenzó a administrar lugol y propanol de 20 mg cada 8 horas, sin respuesta adecuada. Por ende, se decidió aplicar una dosis terapéutica de yodo 131 (I-131) 10 mcU.\n\n\nExploración física\nA la exploración física, la paciente presentó como signos basales una presión arterial no invasiva (PANI) 137/75 mmHg, frecuencia cardiaca (FC) 105 lpm, frecuencia respiratoria (FR) 16 rpm, SpO2 95%, temperatura 37.4ºC. La paciente ingresó deambulando, con agitación leve, con actitud cooperadora; estaba hidratada y sin datos clínicos de vía aérea difícil, pero no se valoró movilidad de tráquea por crecimiento tiroideo de aproximadamente 7.5 x 7 x 10 cm). La superficie del cuello era regular y su movilidad tenía una adecuada extensión. A la auscultación cardiopulmonar no hubo ruidos agregados y la paciente tenía ruidos cardiacos aumentados en frecuencia; asimismo, abdomen blando, depresible, no doloroso, con peristalsis presente. Extremidades integras, sensibilidad con aumento de la percepción del calor, hiperhidrosis palmar, fuerza 5/5, y temblor fino.\n\nSe empleó la escala de Burch y Wartofsky y se obtuvieron 40 puntos con elevada probabilidad de tormenta tiroidea, por lo cual se decidió manejo con anestesia multimodal.\n\nEn la monitorización tipo 2 la paciente presentó signos vitales iniciales PANI 137/75 mmHg, frecuencia cardiaca 96 latidos por minuto, frecuencia respiratoria 16 respiraciones por minuto, 95% Spo2, monitoreo invasivo de tensión arterial.\n\nPor inducción endovenosa se le administraron a la paciente 2 mg de midazolam; 150 mcg de fentanilo; 5 mg de cisatracurio y 50 mg de propofol.\n\nEl abordaje de la vía aérea se hizo con videolaringoscopía Glide Scope con hoja hiperangular 3 sin complicaciones. La ventilación mecánica invasiva modo volumen presentó flujos bajos FIO2 (40%).\n\nSe llevó a cabo bloqueo cervical superficial bilateral ecoguiado con 4 mL de ropivacaina al 0.2% en cada lado (16 mg en total).\n\nPara el mantenimiento se empleó sevoflorano CAM 0.8, infusión de dexmedetomedina 0.7 a 0.4 mcg/kg/hora, infusión de lidocaína 25 mcg/kg/hora, concentración plasmática de fentanilo 0.001 mcg/mL.\n\nEn cuanto a los adyuvantes se empleó paracetamol 750 mg + parecoxib 40 mg + ketorolaco intravenoso 30 + sulfato de magnesio 1250 g en infusión para una hora. El balance de líquidos fue negativo. El tiempo anestésico fue de 215 minutos. En el transoperatorio, la paciente estuvo hemodinámicamente estable, con presión arterial media de 67 a 75 mmHg, que se considera adecuada para la perfusión de órganos.\n\nEn el postoperatorio la paciente presentó analgesia durante 12 horas. Rescate con 1 g de metamizol por razón necesaria, utilizando un solo rescate. Disfonía postoperatoria persistente, sin presencia de odinofagia.",
+        "gold_summary": "Adolescente de 17 años con enfermedad de Graves con manifestaciones clínicas descontroladas, la cual no respondió a tratamiento médico y se programó para tiroidectomia radical. Se obtuvieron 35 puntos en la Escala de Burch y Wartofsky. Se manejó con anestesia general y fueron disminuyendo los estímulos para control de vía aérea y regional a fin de disminuir los estímulos quirúrgicos. Se usaron medicamentos adyuvantes como sulfato de magnesio para la estabilidad transoperatoria.",
+        "synthetic_summary": {
+            "B1": "Esta es la historia de una chica de 17 años con una enfermedad llamada Graves. En Graves la tiroides, que está en el cuello, trabaja demasiado y hace que el cuerpo se acelere. Ella perdió peso, se sentía muy nerviosa y agitada, tenía el pulso rápido, sudaba y su cuello se hizo grande porque la tiroides creció.\n\nLe dieron un medicamento para bajar la tiroides, pero tuvo un problema serio en la sangre y el médico tuvo que dejar de dárselo. Probaron otros tratamientos que no funcionaron bien. Por eso decidieron quitar la tiroides con una operación.\n\nAntes de la operación, los médicos vieron que tenía alto riesgo de una complicación llamada “tormenta tiroidea”, que es cuando el cuerpo se altera mucho por la tiroides. Por eso prepararon todo con mucho cuidado.\n\nDurante la operación:\n- Le pusieron anestesia para que durmiera y no sintiera dolor.\n- Le cuidaron la respiración con una cámara especial para ver la garganta.\n- Pusieron medicinas que ayudan a mantener el corazón y la presión estables.\n- También usaron una inyección cerca del cuello para reducir el dolor.\n- La operación duró más de tres horas y la paciente estuvo estable todo el tiempo.\n\nDespués de la operación:\n- Estuvo sin dolor por 12 horas. Solo necesitó una medicina extra para el dolor una vez.\n- Quedó con la voz ronca por un tiempo, pero no tenía dolor al tragar.\n\nEn resumen: la chica tenía la tiroides muy activa y la medicina le causó un problema. Por eso le quitaron la tiroides con una operación. Los médicos la cuidaron muy bien antes, durante y después de la cirugía.",
+            "B2": "Here is a clear, caring summary written for a teenage reader:\n\n- Patient: 17-year-old girl with Graves disease. Graves disease is an autoimmune condition that makes the thyroid gland overactive and often causes the gland to grow (a goiter).\n\n- Symptoms before surgery: Over six months she lost weight, felt anxious and agitated, had mild fevers (about 37.4–37.9 °C), fast heartbeats (up to 130 beats/min), belly pain and intermittent diarrhea, and noticed a growing lump at the front of her neck. On exam she had a fast heartbeat, sweating, a fine tremor, and an enlarged thyroid about 7.5 × 7 × 10 cm.\n\n- Treatments tried: She was given thiamazole (a medicine that lowers thyroid hormone) but developed agranulocytosis, a serious drop in white blood cells, so that drug had to be stopped. She then received iodine and propranolol (a medicine to slow the heart), but her condition did not improve enough. A dose of radioactive iodine (I-131) was given, and because medical treatment was not controlling the disease, surgery to remove the thyroid (thyroidectomy) was planned.\n\n- Risk before surgery: Doctors used the Burch and Wartofsky score, a checklist that estimates the chance of a dangerous complication called “thyroid storm” (a sudden, severe increase in thyroid effects). Her score was 40, which means a high risk. Because of this, the anesthesia team prepared extra measures to keep her safe.\n\n- Anesthesia and pain control: She received general anesthesia using a combination of medicines to sedate her, control pain, and relax her muscles. Her airway was managed successfully with a video laryngoscope (a device that helps place the breathing tube) without problems. The team also performed a guided bilateral superficial cervical block (a local anesthetic injected around the neck) to reduce surgical pain and stress. Other medicines given during surgery helped keep her blood pressure and heart rate stable and decreased pain after surgery.\n\n- How she did during surgery: The operation and anesthesia lasted about 215 minutes (just over 3.5 hours). She remained hemodynamically stable (blood pressure and circulation were adequate), with a mean arterial pressure of about 67–75 mmHg, which is acceptable for organ blood flow. Fluid balance was slightly negative. There were no breathing or heart complications recorded during the operation.\n\n- After surgery: She had good pain relief for about 12 hours and needed only one extra dose of pain medicine (1 g metamizole). She had persistent hoarseness (voice change) after the operation but did not have painful swallowing. No other major problems were reported.\n\nTakeaway: This teenager had a severe, hard-to-control form of hyperthyroidism. Because medicines either caused a bad side effect or did not work well, surgery was chosen. The anesthesia team used several drug strategies and a local neck block to keep her safe and comfortable. She recovered from surgery without major complications, although she had lasting hoarseness that will need follow-up.",
+            "B3": "Resumen clínico\n\nPaciente femenina de 17 años con enfermedad de Graves y bocio difuso que consultó por seis meses de síntomas progresivos: pérdida de peso, episodios de ansiedad y agitación, febrícula (37.4–37.9 ºC), palpitaciones, dolor abdominal y diarrea intermitente. A los 2–3 meses apareció aumento del tamaño del cuello y taquicardia hasta 130 lpm. El tratamiento antitiroideo con tiamazol se suspendió por agranulocitosis (una reacción grave que disminuye los glóbulos blancos); los bloqueantes adrenérgicos y lugol no fueron suficientes, por lo que se administró yodo-131 y se programó tiroidectomía radical.\n\nHallazgos relevantes antes y durante la cirugía\n- Signos vitales preoperatorios: PA 137/75 mmHg, FC 105 lpm, T 37.4 ºC, SpO2 95%.  \n- Examen físico: paciente levemente agitada, hidratada, sin signos de dificultad respiratoria evidente; bocio grande (aprox. 7.5 x 7 x 10 cm). No se valoró movilidad traqueal debido al volumen tiroideo. Presentaba intolerancia al calor, hiperhidrosis palmar y temblor fino.  \n- Escala de Burch y Wartofsky: 40 puntos, valor que indica alta probabilidad de tormenta tiroidea — por ello se planificó manejo anestésico multimodal para minimizar riesgo hemodinámico-perioperatorio.  \n- Monitorización: invasiva para tensión arterial. Inducción con midazolam, fentanilo, propofol y cisatracurio; intubación con videolaringoscopio GlideScope sin complicaciones. Ventilación mecánica con FiO2 40%.  \n- Bloqueo cervical superficial bilateral bajo ecografía con ropivacaína 0,2% (4 mL por lado; 16 mg total).  \n- Mantenimiento anestésico: sevoflurano, infusión de dexmedetomidina (0.7→0.4 mcg/kg/h), lidocaína IV (25 mcg/kg/h) y fentanilo (concentración plasmática reportada).  \n- Adyuvantes analgésicos y estabilizadores: paracetamol 750 mg, parecoxib 40 mg, ketorolaco 30 mg IV y sulfato de magnesio (el informe menciona \"1250 g\", lo más probable es que sea 1250 mg = 1,25 g; parece un error tipográfico). Balance hídrico intraoperatorio fue negativo; tiempo anestésico 215 minutos.  \n- Transoperatoriamente la paciente permaneció hemodinámicamente estable; presión arterial media entre 67–75 mmHg (adecuada para perfusión).  \n\nEvolución postoperatoria\n- Analgesia efectiva por 12 horas; requirió un rescate único con 1 g de metamizol.  \n- Presentó disfonía persistente en el postoperatorio sin odinofagia (sin dolor al tragar). No se reportó tormenta tiroidea ni complicaciones hemodinámicas mayores.\n\nInterpretación y posibles pasos siguientes (implicaciones)\n- El manejo anestésico multimodal y la intubación guiada facilitaron una cirugía segura en una paciente con tirotoxicosis severa y riesgo elevado de tormenta tiroidea.  \n- La disfonía postoperatoria puede reflejar irritación o lesión temporal del nervio laríngeo recurrente o edema de cuerdas vocales; se recomienda evaluación otorrinolaringológica con laringoscopia y seguimiento vocal.  \n- Tras tiroidectomía es importante monitorizar calcio sérico (por riesgo de hipocalcemia por afectación de paratiroides), signos de hipotiroidismo y ajustar terapia de reemplazo hormonal tiroidea cuando proceda.  \n- Dado el antecedente de agranulocitosis por tiamazol, debe evitarse reexposición a ese fármaco y documentarse la alergia/efecto adverso en la historia clínica.\n\nComentario final\nLa intervención se desarrolló sin eventos hemodinámicos mayores y con control del dolor postoperatorio; sin embargo la paciente precisa seguimiento para la disfonía y vigilancia de complicaciones propias de la tiroidectomía (calcemia, función tiroidea y evaluación de nervio laríngeo). Si desea, puedo formular un plan de seguimiento detallado o una explicación más amplia sobre los riesgos habituales después de una tiroidectomía."
+        }
+    },
+    {
+        "article": "Una mujer de 30 años de edad, embarazada de 3, para 3, se presentó con disminución de la micción, dolor en el flanco izquierdo y fiebre durante 2 días después de una cesárea de emergencia por primera vez, indicada debido a la angustia materna y fetal secundaria al trabajo de parto prolongado y sangrado vaginal prolongado en el hospital Al-Thora, Ibb, Yemen. A pesar de los esfuerzos de reanimación, su recién nacido falleció después de 45 minutos. Durante la cesárea, se identificaron severas adherencias uterinas (ya que había lesiones de endometriosis y adherencias entre la pared posterior del útero y el colon sigmoide), y una pérdida de sangre estimada de 1500 cc, según el informe del ginecólogo. La paciente no recibió atención prenatal durante su embarazo. No es fumadora y negó condiciones médicas crónicas, abuso de drogas, intoxicación accidental o antecedentes quirúrgicos previos.\n\nEn el examen físico, el paciente se veía pálido, enfermo y febril durante la evaluación inicial, con una temperatura oral de 38 °C, pulso de 80 latidos por minuto y presión arterial de 95/70 mm Hg. El abdomen del paciente estaba levemente distendido, con sensibilidad moderada, principalmente en el cuadrante inferior izquierdo.\n\nLos datos de laboratorio fueron los siguientes: el recuento de glóbulos blancos (WBC) fue de 15,3 × 103/mL, con 90% de neutrófilos polimórficos (leucocitosis con predominio neutrofílico), la hemoglobina fue de 7,5 g/dL, el recuento de plaquetas fue de 200 × 103/µL, el nitrógeno ureico en sangre (BUN) fue de 23 mg/dl y la creatinina fue de 3,8 mg/dl. Otros análisis de sangre, como los de la función hepática y los de coagulación, estuvieron dentro de los rangos normales. La ecografía (US) mostró una hidronefrosis izquierda grave y un fluido libre moderado en la cavidad abdominal. Se realizó la aspiración de la punción abdominal y la creatinina en el punto fue de 52 mg/dL, lo que indica que el fluido era orina.\n\nLa paciente fue resucitada con glóbulos rojos concentrados y una amplia cobertura antibiótica. Después de esto, se le realizó una ureteroscopia urgente que mostró una oclusión total del uréter izquierdo. Se tomó la decisión de realizar una exploración quirúrgica, dada la inestabilidad hemodinámica, la falta de equipos de nefrostomía percutánea y la evidencia de contaminación intraabdominal. Durante la operación, se encontró fluido libre moderado en la cavidad abdominal. El uréter izquierdo fue aplastado y ligado con una sutura Vicryl (5 agujas) a unos 5 cm de su parte distal. Después de evacuar el fluido, se extirpó el segmento lesionado del uréter y se realizó una ureteroneocistostomía de forma refluyente tras distender la vejiga con solución salina a través del catéter. Además, diseccionamos el uréter, con cuidado, de los tejidos circundantes en dirección cefálica, espatulamos el extremo distal del uréter e insertamos un stent doble. Se implantó el uréter en la cúpula posterior de la vejiga urinaria con anastomosis sin tensión y se suturó con Vicryl 4-0 a través del uréter de espesor completo, luego la capa mucosa de la vejiga y la capa detrusora. Se insertó un drenaje Jackson-Pratt (JP) cerca de la anastomosis y se cerró la pared abdominal tras evaluar el contenido intraperitoneal.\n\n\nSeguimiento y resultado\nSe iniciaron líquidos transparentes el segundo día postoperatorio. La paciente tenía distensión abdominal leve, dolor y náuseas. El tercer día postoperatorio, tenía una distensión abdominal creciente y dejó de expulsar flatos. La ecografía abdominal mostró una gran cantidad de acumulación en la cavidad peritoneal. Los datos de laboratorio de sangre mostraron una leucocitosis (WBC de 22 × 103/mL con un cambio a la izquierda).\n\nUna tomografía computarizada (TC) del abdomen y la pelvis con contraste reveló una cantidad significativa de aire libre y líquido en todo el abdomen y la pelvis adyacente a la pared abdominal anterior. También se observaron múltiples localizaciones de gas libre en el mesenterio, con realce de contraste de múltiples bucles intestinales pequeños, sin evidencia de extravasación de contraste. Los hallazgos sugirieron una víscera perforada. Después de consultar al equipo de cirugía general, la paciente fue llevada inmediatamente al quirófano para una laparotomía exploratoria, que reveló una pequeña perforación en la parte rectosigmoidea con algo de derrame, peritonitis con edema del asa intestinal y alteración de la anastomosis ureteral. La complejidad de este caso nos obligó a realizar intervenciones en varias etapas de manera multidisciplinaria. En primer lugar, el ginecólogo realizó una histerectomía debido a endometritis (confirmada histopatológicamente), supuración severa y alteración de la sutura del útero. En segundo lugar, un urólogo realizó una derivación ureterocutánea del uréter izquierdo y se creó una urostomía en el lado izquierdo. Por último, el cirujano general realizó el procedimiento de colostomía después de reparar la lesión del colon y se creó una colostomía en el lado izquierdo. En el quinto día postoperatorio, se produjo retracción de la colostomía con infección de la herida y se observó comunicación entre la colostomía y la urostomía. Se decidió realizar una reexploración para reubicar la colostomía sigmoidea y se realizó una colostomía transversal derecha. Una semana después de la operación, la paciente experimentó una infección superficial de la pared abdominal complicada con dehiscencia de la herida e hipoalbuminemia (albúmina: 2 g/dL) que requirió tratamiento con varios desbridamientos, irrigación de la herida, antibióticos y terapia de apoyo. Los antibióticos recomendados fueron linezolid (600 mg IV cada 12 horas durante 7 días), luego cambiaron a ceftriaxona (1 g IV cada 12 horas durante 5 días) más metronidazol (500 mg IV cada 12 horas durante 5 días) y cambiaron a ciprofloxacina oral (500 mg cada 12 horas por vía oral durante 7 días). Gradualmente, reanudó su dieta normal y fue dada de alta 30 días después en condiciones estables. Requería atención domiciliaria para ayudarla con la colostomía, la ureterostomía y la deambulación.\n\nSeis meses después, se cerró la colostomía y se anastomosó el uréter mediante el procedimiento de colgajo de vejiga tabular de Boari (la vejiga se abrió en su superficie anterior y se volteó un colgajo de vejiga de espesor completo caudalmente y se tabularizó para anastomosis al segmento ureteral proximal después de la inserción de la endoprótesis doble J). Después de una recuperación postoperatoria sin incidentes, se dio de alta a la paciente el séptimo día postoperatorio. El seguimiento de un mes mediante ecografía y cistouretrografía miccional mostró un aspecto normal de la vejiga con capacidad vesical adecuada y un sistema del tracto urinario superior normal. Tres meses después, la ureteroscopia retrógrada mostró un calibre adecuado del uréter. Se hizo un seguimiento regular de la paciente con ecografía durante 3 meses durante un año. La paciente no tuvo síntomas irritativos o gastrointestinales en los 2 años de seguimiento.\n",
+        "gold_summary": "Una mujer de 30 años presentó disminución de la micción durante 2 días después de una cesárea. La ecografía mostró una hidronefrosis izquierda grave y un fluido abdominal libre moderado. Una ureteroscopia reveló una oclusión total del uréter izquierdo y, posteriormente, se realizó una ureteroneocistostomía. Dos días después, la paciente presentó complicaciones con distensión abdominal que requirieron una nueva exploración. La exploración reveló lesiones en el colon (recto-sigmoide), peritonitis, endometritis y alteración de la anastomosis ureteral. Se realizó una colostomía, reparación de lesiones en el colon, histerectomía y derivación ureterocutánea. La estancia hospitalaria de la paciente fue complicada, con retracción estomal que requirió revisión quirúrgica y dehiscencia de la herida, que se trató de forma conservadora. Después de 6 meses, se cerró la colostomía y se anastomosó el uréter mediante el procedimiento de colgajo de Boari.\n",
+        "synthetic_summary": {
+            "B1": "Había una mujer de 30 años que tuvo una cesárea de emergencia. Después de la operación, habló que orinaba menos, tenía dolor en el lado izquierdo y fiebre. \n\nLos médicos vieron que el riñón izquierdo estaba muy hinchado porque el conducto que lleva la orina (el uréter) estaba totalmente tapado. También había líquido en la barriga que resultó ser orina. Hicieron una operación para quitar la parte dañada del uréter y unirlo al lugar correcto en la vejiga. Pusieron un pequeño tubo dentro para que la orina pasara bien.\n\nUnos días después, la mujer tuvo mucho dolor y la barriga se puso peor. Un examen mostró que había una perforación, es decir, un orificio en el intestino (parte rectosigmoidea) y una infección dentro de la barriga llamada peritonitis. También había infección en el útero y el arreglo del uréter se había estropeado. \n\nPor la gravedad del problema, varios médicos trabajaron juntos. Hicieron:\n- una histerectomía (quitaron el útero) por infección,\n- una colostomía (hicieron que las heces salieran a una bolsa en la piel) tras reparar el intestino,\n- y una derivación del uréter a la piel (para que la orina saliera a una bolsa).\n\nTuvo más problemas: la colostomía se retrajo y la herida se infectó. Recibió más operaciones, limpieza de la herida y antibióticos. Poco a poco mejoró y salió del hospital a los 30 días. Necesitó ayuda en casa para cuidar las bolsas y caminar.\n\nSeis meses después le cerraron la colostomía y reconstruyeron el uréter usando un colgajo de la vejiga (llamado procedimiento de Boari). Le pusieron un stent temporal y la operación fue bien. En los controles posteriores, la vejiga y los riñones estaban normales. Tras un año y más, la mujer no tenía problemas y estaba bien.  \n\nAunque fue una situación muy difícil, al final recibió varias operaciones y cuidados, y se recuperó.",
+            "B2": "Summary (readability: upper-intermediate, for ages 11–17)\n\nA 30-year-old woman who had no prenatal care had an emergency cesarean section after a long labor and heavy bleeding. Sadly, her baby died shortly after birth. During the cesarean the surgeons found severe scar tissue in the pelvis (from endometriosis) and she lost a large amount of blood.\n\nTwo days after surgery she had very little urine, left-side belly pain, fever, and felt unwell. Blood tests showed infection (high white blood cells), severe anemia (low hemoglobin), and kidney injury (high creatinine). An ultrasound showed a very swollen left kidney (hydronephrosis — this means urine was backing up into the kidney) and fluid in the belly. The fluid was tested and found to be urine, meaning the urinary tract had been damaged and urine was leaking into the abdomen.\n\nShe received blood transfusions and antibiotics. An urgent scope of the ureter (the tube that carries urine from the kidney to the bladder) showed the left ureter was completely blocked. Because she was unstable and a tube from the kidney to the skin (nephrostomy) was not available, the team opened her belly. They removed the injured segment of the left ureter and reconnected the ureter to the bladder (ureteroneocystostomy) and put in a stent to keep it open. A drain was left near the repair.\n\nA few days later her belly became much more swollen, she stopped passing gas, and her white blood cell count rose. A CT scan showed free air and fluid in the abdomen, suggesting a hole in the bowel. Emergency surgery found a small perforation in the rectosigmoid (part of the colon), peritonitis (infection and inflammation of the abdominal cavity), an infected uterus, and a problem with the ureter repair.\n\nBecause of these problems, several teams operated together. The gynecologist removed the uterus (hysterectomy) because of severe infection. The urologist created a left ureterostomy (bringing the ureter to the skin to drain urine into a bag). The general surgeon repaired the colon and made a left colostomy (bringing part of the colon to the skin to divert stool). The patient then had more problems: the colostomy retracted and became infected, and there was communication between the colostomy and the urostomy. The team re-explored and moved the colostomy to the right side. She also developed a wound infection and the surgical wound partly opened; low blood protein (hypoalbuminemia) made healing harder. She was treated with antibiotics, repeated wound cleaning, and supportive care.\n\nAfter a difficult hospital stay of 30 days she was discharged in stable condition with help at home to manage the colostomy and urostomy. Six months later the surgeons closed the colostomy and repaired the ureter using a Boari flap (a piece of bladder tissue is reshaped and used to bridge the gap to the ureter) with a new stent. Her recovery after that operation was smooth. Follow-up tests over the next months showed normal bladder capacity and normal upper urinary tract, and ureteroscopy showed the ureter was wide enough. At two years after these events she had no urinary or bowel symptoms.\n\nOverall outcome: despite a very serious and complex course with multiple operations and complications, the patient recovered well, had her stomas closed, and had normal urinary and bowel function on follow-up. The case shows how pelvic scarring, heavy bleeding, and surgery can lead to accidental injury of the urinary tract and bowel, and how staged, team-based surgery and close follow-up can restore function.",
+            "B3": "Resumen clínico — caso de lesión ureteral compleja tras cesárea\n\nPresentación y contexto\n- Paciente: mujer de 30 años, embarazada de término, sin controles prenatales, sometida a cesárea de urgencia por trabajo de parto prolongado y sangrado vaginal. Durante la cesárea hubo pérdidas sanguíneas importantes (≈1.500 ml) y se describieron adherencias severas por endometriosis. El recién nacido falleció; la paciente presentó 2 días después disminución de la micción, dolor en flanco izquierdo y fiebre.\n\nHallazgos iniciales (anormales)\n- Signos vitales: febril (38 °C), algo hipotensa (PA 95/70 mm Hg).\n- Laboratorio: leucocitosis (WBC 15,3 ×10^3/µL, 90% neutrófilos), anemia grave (Hb 7,5 g/dL), elevación de creatinina sérica (3,8 mg/dL) y BUN 23 mg/dL — compatible con daño renal agudo y sepsis/hipoperfusión.\n- Ecografía: hidronefrosis izquierda severa y líquido libre abdominal moderado.\n- Análisis del líquido abdominal: creatinina 52 mg/dL (muy superior a la sérica) — esto confirma que el fluido era orina (urinoma) por lesión ureteral.\n- Ureteroscopia urgente: oclusión total del uréter izquierdo.\n\nIntervenciones iniciales\n- Reanimación con glóbulos rojos concentrados y antibióticos de amplio espectro.\n- Dadas la inestabilidad hemodinámica, la falta de acceso a nefrostomía percutánea y la contaminación abdominal, se optó por laparotomía urgente. Se encontró el uréter izquierdo aplastado y ligado a 5 cm de su porción distal. Se reseca el segmento lesionado y se realizó ureteroneocistostomía refluyente con colocación de stent doble J y drenaje JP.\n\nEvolución y complicaciones posteriores\n- A los 3 días: distensión abdominal progresiva, ileo (sin expulsión de flatos), incremento de leucocitos (WBC 22 ×10^3/µL).\n- TC abdominal: abundante líquido y aire libre en peritoneo, con gas en mesenterio y realce de asas intestinales — sugerente de perforación visceral.\n- Laparotomía exploratoria: perforación en rectosigma, peritonitis, edema intestinal y compromiso de la anastomosis ureteral.\n- Manejo multidisciplinario en varias etapas:\n  1. Histerectomía por endometritis y sutura uterina deteriorada (confirmada histopatológicamente).\n  2. Derivación ureterocutánea del uréter izquierdo (urostomía) por fallo de la anastomosis ureteral.\n  3. Reparación de la lesión colónica y colostomía izquierda.\n- Complicaciones posoperatorias: retracción de la colostomía con infección de herida y comunicación entre colostomía y urostomía; se reexploró y se reubicó la colostomía a transversal derecha. Posteriormente presentó infección superficial de la pared abdominal con dehiscencia y hipoalbuminemia (albúmina 2 g/dL), tratadas con desbridamientos, irrigación, antibióticos y soporte nutricional.\n\nAlta y reconstrucciones diferidas\n- La paciente fue dada de alta estable 30 días después, con cuidados en domicilio para colostomía y ureterostomía.\n- A los 6 meses se cerró la colostomía y se reconstruyó el uréter mediante colgajo de Boari (flap vesical tabularizado) con colocación de doble J. Recuperación postoperatoria sin incidentes; dada de alta al 7.º día.\n- Controles por imagen (ecografía, cistouretrografía miccional) a 1 mes mostraron vejiga con capacidad adecuada y tracto urinario superior normal. Ureteroscopia a los 3 meses mostró calibre ureteral adecuado. Seguimiento clínico/por ecografía hasta 1 año y evaluación clínica a 2 años sin síntomas urinarios o gastrointestinales.\n\nImplicaciones y puntos clave\n- Este caso ejemplifica una lesión ureteral iatrogénica grave tras cesárea complicada por adherencias y sangrado, que fue inicialmente reconocida por oliguria, dolor en flanco e hidronefrosis y confirmada por análisis de líquido abdominal (elevada creatinina).\n- La ausencia de recursos (no disponibilidad de nefrostomía percutánea) y la inestabilidad hemodinámica condicionaron la necesidad de terapia quirúrgica inmediata.\n- La anastomosis ureteral primaria fracasó en el contexto de contaminación abdominal y sepsis, obligando a derivaciones temporales (urostomía y colostomía) y posterior reconstrucción diferida (Boari flap), que dio buen resultado a largo plazo.\n- Complicaciones serias incluyeron peritonitis por perforación colo-rectal, infección de herida, dehiscencia y hipoalbuminemia; todas requirieron manejo multidisciplinario intensivo.\n\nConsejos prácticos (para pacientes y cuidadores)\n- La recuperación fue prolongada y requirió cuidados especializados de estomas y rehabilitación; la planificación precoz de apoyo nutricional y cuidado de la herida es importante en casos similares.\n- Cuando hay disminución de la orina, dolor lumbar y fiebre después de cirugía pélvica, es crítico investigar lesión ureteral o urinoma cuanto antes para reducir riesgo de sepsis y daño renal definitivo.\n\nTono final\n- La paciente tuvo un curso muy complejo y doloroso, pero gracias a intervenciones secuenciales y manejo multidisciplinario se logró restaurar la anatomía y la función urinaria y digestiva con buena recuperación a largo plazo."
+        }
+    },
+    {
+        "article": "Mujer de 43 años, con antecedente de hipertensión arterial con tratamiento con losartán, dos cesáreas y oclusión tubaria bilateral. Ingresó a nuestro hospital y refirió dolor de 24 horas de evolución, tipo cólico en hipogastrio e irradiación a fosa iliaca izquierda, además de náusea y vómito en dos ocasiones. Se agregaron evacuaciones semilíquidas en forma inicial y posteriormente cese en las evacuaciones y en la canalización de gases. A la exploración física, la paciente presentó dolor en el abdomen, así como distensión, especialmente hacia el flanco izquierdo. En el mesogastrio y el flanco izquierdo hubo la presencia de timpanismo. La peristalsis estaba presente, mínima, abolida en flanco izquierdo y mesogastrio. La irritación peritoneal estuvo ausente. Se colocó sonda nasogástrica, con gasto mínimo gástrico y sin mejoría en la sintomatología. Los estudios de laboratorio demostraron: 9700 leucocitos con un 87% de neutrófilos, creatinina de 0.7 mg/dL, urea de 22 mg/dL y proteína C reactiva de 5.0 mg/L. En la radiografía simple de abdomen presentó dilatación importante del lado izquierdo del colon, con niveles hidroaéreos. La tomografía muestra la dilatación del colon del lado izquierdo, con imagen que simula grano de café en el corte coronal.\n\nAnte estos hallazgos clínicos y de imagen, se decidió hacer laparotomía de urgencia ante la sospecha de la presencia de vólvulo de sigmoides o de síndrome adherencial complicado. Durante la cirugía se evidenció un ciego flexionado hacia adelante y a la izquierda, carente de fijación retroperitoneal. El punto de flexión fue producido por una banda de adherencia colocada sobre el colon ascendente. Se realizó liberación de la adherencia y se corroboró continuidad adecuada hacia el colon distal. No se evidenció la presencia de isquemia, necrosis o perforación del ciego. Se realizó apendicectomía con descompresión del ciego a través de base apendicular y posteriormente ligadura de esta. Se llevó a cabo cecopexia hacia pared de fosa iliaca derecha. Después de la cirugía, hubo mejoría clínica de la paciente, que tuvo evacuaciones presentes normales. La paciente siguió controles correctos en consulta externa de cirugía y se mantuvo asintomática.",
+        "gold_summary": "Mujer de 43 años que ingresó a un servicio de urgencias con datos de obstrucción intestinal. Se realizó tomografía simple de abdomen donde se identificó dilatación del colon e imagen que semejaba un grano de café invertido. Se hizo laparotomía exploradora y se identificó vólvulo cecal del tipo báscula, sin compromiso vascular. Se realizó desvolvulación, descompresión a través de apendicectomía, y cecopexia. Posterior a evento quirúrgico, la paciente se recuperó sin incidentes y fue dada de alta con controles adecuados por consulta externa.",
+        "synthetic_summary": {
+            "B1": "Una mujer de 43 años llegó al hospital con dolor de barriga, náuseas, vómitos y que no podía hacer caca ni sacar gases. Las radiografías y la tomografía mostraron que una parte del intestino grueso estaba muy hinchada y parecía torcida.  \n\nEn la operación se encontró que el ciego (el inicio del intestino grueso, que normalmente está en la parte derecha) se había doblado y girado hacia la izquierda por una banda de tejido que lo tenía pegado. Esa torsión se llama vólvulo y puede tapar el paso dentro del intestino. Por suerte, el intestino no estaba dañado ni muerto.  \n\nLos médicos quitaron la banda que pegaba el intestino, sacaron el apéndice para poder desinflar el ciego y fijaron el ciego a la pared para que no volviera a moverse. Después de la cirugía la mujer mejoró, empezó a evacuar normalmente y se fue a casa con controles. Está bien y no ha vuelto a tener problemas.",
+            "B2": "Mujer de 43 años que llegó al hospital con dolor abdominal, náuseas y vómitos, y luego dejó de tener deposiciones y expulsión de gases, signos que sugerían una obstrucción intestinal. La radiografía y la tomografía mostraron una gran dilatación del colon izquierdo y una imagen en \"grano de café\" que sugiere un intestino girado o comprimido. Ante la falta de mejoría con medidas iniciales se decidió operar de urgencia.\n\nEn la cirugía se encontró el ciego (la primera parte del colon, donde se une el intestino delgado) plegado hacia adelante y hacia la izquierda porque una banda de adherencia lo doblaba. Esto se describió como un vólvulo cecal del tipo “báscula” (el ciego se volcó o se giró sobre sí mismo). No había evidencia de falta de riego sanguíneo (isquemia), necrosis ni perforación. Los cirujanos liberaron la adherencia, descomprimieron el ciego quitando el apéndice (apendicectomía para vaciar el intestino por su base) y fijaron el ciego a la pared abdominal (cecopexia) para evitar que volviera a girarse.\n\nLa paciente mejoró después de la operación: recuperó las deposiciones normales y, en controles posteriores, permaneció sin síntomas. En resumen, se trató un vólvulo cecal sin daño tisular mediante desvolvulación, descompresión y fijación, con buena recuperación.",
+            "B3": "Resumen clínico (nivel universitario)\n\nPaciente: mujer de 43 años con hipertensión arterial tratada con losartán; antecedentes quirúrgicos: dos cesáreas y oclusión tubaria bilateral.\n\nPresentación y examen:\n- Cuadro de 24 horas de evolución con dolor cólico en hipogastrio que irradiaba a la fosa ilíaca izquierda, náuseas, dos vómitos y cambio en las deposiciones: al inicio heces semilíquidas y luego detención de las evacuaciones y de la eliminación de gases (íleo obstructivo).\n- Exploración: distensión abdominal predominante en hemiabdomen izquierdo, timpanismo en mesogastrio y flanco izquierdo, peristalsis presente pero muy disminuida (prácticamente abolida en mesogastrio y flanco izquierdo). No hubo signos de irritación peritoneal.\n- Sonda nasogástrica con escaso drenaje y sin mejoría sintomática.\n\nPruebas complementarias:\n- Laboratorio: leucocitos 9 700/µL con 87% neutrófilos (predominio neutrofílico), creatinina y urea normales, PCR 5,0 mg/L (ligera elevación de marcador inflamatorio).\n- Radiografía de abdomen: importante dilatación del colon izquierdo con niveles hidroaéreos.\n- Tomografía abdominal: dilatación colónica izquierda con imagen en \"grano de café\" en cortes coronales, sugestiva de volvulus (torsión intestinal).\n\nDiagnóstico presuntivo y conducta:\n- Se planteó vólvulo de sigma versus obstrucción por adherencias complicada; por la gravedad del cuadro se realizó laparotomía exploradora urgente.\n\nHallazgos intraoperatorios y tratamiento:\n- Se identificó un vólvulo cecal del tipo báscula: el ciego estaba plegado hacia adelante y hacia la izquierda y carecía de su fijación retroperitoneal habitual.\n- El punto de flexión fue producido por una banda de adherencia sobre el colon ascendente. No había isquemia, necrosis ni perforación del ciego.\n- Se liberó la adherencia, se confirmó la continuidad intestinal distal y se procedió a desvolvulación. Para descompresión del ciego se realizó apendicectomía con descompresión por la base apendicular y posterior ligadura. Finalmente se realizó cecopexia (fijación del ciego a la pared abdominal en fosa iliaca derecha) para reducir el riesgo de recurrencia.\n\nEvolución y pronóstico:\n- La paciente mejoró clínicamente tras la cirugía; recuperó deposiciones normales y fue seguida en consulta externa de cirugía sin síntomas residuales.\n- Al no existir compromiso vascular del ciego no fue necesaria la resección intestinal, lo que favorece un pronóstico bueno a corto y medio plazo.\n\nImplicaciones y consideraciones:\n- El vólvulo cecal puede simular otros cuadros obstructivos; la imagen en \"grano de café\" en TC y la presentación clínica orientan al diagnóstico, pero la confirmación y el manejo definitivo pueden requerir cirugía urgente.\n- En ausencia de isquemia, las maniobras conservadoras de desvolvulación, descompresión y fijación (cecopexia) son adecuadas; cuando existe necrosis o perforación está indicada la resección.\n- Seguimiento ambulatorio y vigilancia ante signos de obstrucción recurrente o complicaciones posoperatorias son necesarios. Se puede considerar medidas para reducir formación de nuevas adherencias según la práctica quirúrgica."
+        }
+    },
+    {
+        "article": "Paciente de sexo femenino de 10 años, sin historia familiar de enfermedad tiroidea, portadora de bocio diagnosticado a los 9 años (ecografía tiroidea con sig nos compatibles de tiroiditis crónica) con presencia de anticuerpos antitiroideos positivos. Sin tratamiento al momento del ingreso hospitalario. Consultó por orina de aspecto espumoso de 5 días de evolución, asociado a dolor abdominal, vómitos profusos y diarrea. Evo lucionó con edema palpebral y de extremidades, disminución de la diuresis, decaimiento y fiebre de 38° C el día previo a su ingreso. Al momento de su eva luación en el servicio de urgencia destacó una pacien te con edema palpebral bilateral y pretibial, con bocio evidente (indoloro y sin nódulos palpables) y presen cia de soplo sistólico eyectivo en foco pulmonar IV/VI sin irradiación. Resto del examen sin alteraciones de significancia. Presión arterial 120/78 mmHg (percentil 95), temperatura 38,1°C, peso: 33.9 Kg, talla: 131,5 cm (p7), IMC 19,8 (p83).\n\nDentro de sus exámenes de admisión destacaron examen de orina completa con proteinuria +++, sin bacterias, sin nitritos, leucocitos 7 cel/uL (VN: 0-10 cel/uL), eritrocitos 4 cel/uL (VN: 0-15 cel/uL), índice proteinuria/creatininuria (IPC) 2 mg/mg, proteínas totales de 3.8 g/dL, hipoalbuminemia de 2,1 g/dL, hipercolesterolemia de 416 mg/dL, hipertrigliceridemia de 127 mg/dL y creatinina plasmática de 0,46 mg/dL (aclaramiento de creatinina calculado por fórmula de Schwartz: 125 ml/min/1,73 m2). Gases venosos, elec trolitos plasmáticos y hemograma dentro de rangos normales. En cuanto al estudio inmunológico destacó: inmunoglobulina A 181 mg/dL (VN 45-236), inmunoglobulina M 131 mg/dL (VN 52-242), inmunoglobulina G 208 (VN 608-1572) mg/dL, C3 125 mg/dL (VN 80-150), C4 37,3 mg/dL (VN 12-36). Ecografía renal normal. Se ingresó a la paciente con diagnóstico de SN y tiroiditis autoinmune.\n\nEn el contexto de SN se inició tratamiento con prednisona (60 mg/m2/día), con buena respuesta, logrando fundir edema y disminuir progresivamente la proteinuria hasta alcanzar rangos normales previo al egreso (IPC de egreso: 0.09, a los 6 días).\n\nDel punto de vista de función tiroidea su estudio mostró hormona tiroestimulante (TSH) 4,4 UI/ml (VN: 0,67-4,16 UI/ml), tiroxina (T4) libre 0,80 ng/ dL (VN: 0,86-1,4 ng/dL), anticuerpos antiperoxidasa (Anti Tpo) 120 U/ml (VN: 0-60 U/ml), anticuerpos antitiroglobulina (Anti-Tg) 82 U/ml (VN: 0-60 U/ ml), por lo que se inició terapia de sustitución con levotiroxina (25 mcg/día). La ecografía tiroidea descri bió tiroides de tamaño normal con leve aumento de vascularización difusa al Doppler, sin lesiones focales sólidas ni quísticas, siendo estos hallazgos sugerentes de tiroiditis. Resto del estudio (PCR para SARS CoV-2, anticuerpos anti citoplasma de neutrófilos, anticuer pos anti nucleares, anticuerpos anti DNA, anticuerpos anti estreptolisina O, anticuerpos anticardiolipinas, anticuerpos anti mieloperoxidasa y anticuerpos anti proteinasa 3) resultó negativo.\n\nA los 6 días de ingresada la paciente se encontraba en buenas condiciones, siendo dada de alta con prednisona (60 mg al día) y levotiroxina (25 ucg al día). En el seguimiento a los 12 meses la paciente se encontraba asintomática, con su patología tiroidea bajo control (TSH 1,11 UI/ml) con tratamiento de sustitución. No ha presentado recaídas del SN (examen de orina sin proteinuria y creatinina 0,44 mg/dL).",
+        "gold_summary": "Paciente de 10 años que se presenta con síndrome nefrótico y bocio. Se pesquisa antecedente de tiroiditis autoinmu ne e hipotiroidismo no tratado. Se inicia terapia corticoidal y hormonal de sustitución (levotiroxina), logrando buena respuesta clínica y de laboratorio.",
+        "synthetic_summary": {
+            "B1": "Había una niña de 10 años que tenía un bulto en el cuello porque su tiroides (la glándula del cuello) no trabajaba bien por una enfermedad del sistema que cuida al cuerpo. Un día llegó al hospital porque su orina estaba espumosa, tenía dolor de panza, vómitos, diarrea y después le salieron hinchazón en los párpados y las piernas. Los médicos encontraron que sus riñones perdían mucha proteína en la orina. Esa pérdida hizo que tuviera poco proteína en la sangre y mucho colesterol. \n\nLa niña recibió dos medicinas: una pastilla que baja la inflamación (prednisona) para cuidar los riñones, y otra que reemplaza la hormona de la tiroides (levotiroxina). Con las medicinas la hinchazón bajó y la orina dejó de tener tanta proteína en pocos días. Fue dada de alta y, al año, estaba muy bien: la tiroides funcionaba con la pastilla y los riñones no habían vuelto a fallar. Los médicos vieron que todo estaba bajo control y ella no tuvo recaídas.",
+            "B2": "Resumen claro y amable:\n\nSe trata de una niña de 10 años que llegó al hospital con orina espumosa, dolor abdominal, vómitos, diarrea y aparición de hinchazón en párpados y piernas. Tenía desde los 9 años un bocio (aumento de la glándula tiroides) diagnosticado como tiroiditis autoinmune —es decir, el propio sistema inmunitario ataca la tiroides— pero no estaba recibiendo tratamiento.\n\nDiagnósticos principales\n- Síndrome nefrótico: esto es un cuadro en el que los riñones pierden mucha proteína en la orina, lo que produce hinchazón, baja proteína en la sangre y niveles altos de colesterol. En esta paciente se confirmó por proteinuria alta (índice proteinuria/creatinina 2 mg/mg), albúmina baja (2,1 g/dL) y colesterol elevado (416 mg/dL). La función renal (creatinina) estaba normal y la ecografía renal no mostró alteraciones.\n- Tiroiditis autoinmune con hipotiroidismo leve: tenía anticuerpos tiroideos positivos y pruebas que mostraron TSH algo alta y T4 libre algo baja, por lo que se consideró necesario iniciar tratamiento.\n\nTratamiento y evolución\n- Para el síndrome nefrótico se le dio prednisona (un corticoide) a dosis alta. Respondió muy bien: la hinchazón cedió y la proteinuria mejoró hasta valores normales en seis días.\n- Para la tiroiditis se inició levotiroxina (hormona tiroidea) en dosis de 25 µg/día. La ecografía tiroidea apoyó el diagnóstico de tiroiditis.\n- Otros estudios de autoinmunidad fueron negativos.\n\nAlta y seguimiento\n- Fue dada de alta a los 6 días tomando prednisona y levotiroxina. A los 12 meses estaba asintomática, la función tiroidea controlada con el tratamiento (TSH 1,11 UI/ml) y sin recaídas del síndrome nefrótico (orina sin proteinuria).\n\nComentario final (calmado y práctico)\nLa niña tuvo dos problemas relacionados con el sistema inmune: uno que afectó la tiroides y otro que afectó los riñones. Ambos se trataron con medicamentos apropiados y la respuesta fue buena. Es importante el seguimiento médico para ajustar la hormona tiroidea y vigilar que el síndrome nefrótico no reaparezca.",
+            "B3": "Resumen clínico (empatético y claro)\n\nPaciente: niña de 10 años con antecedente de bocio e investigación previa compatible con tiroiditis crónica autoinmune (anticuerpos antitiroideos positivos), sin tratamiento hormonal al ingreso.\n\nPresentación y evolución inicial\n- Síntomas de 5 días: orina espumosa, dolor abdominal, vómitos profusos y diarrea. Posteriormente desarrolló edema palpebral y de extremidades, menor diuresis, decaimiento y fiebre (≈38 °C).\n- En el examen: edema palpebral bilateral y pretibial, bocio visible (indoloro, sin nódulos) y soplo sistólico eyectivo grado IV/VI en foco pulmonar. Presión arterial 120/78 mmHg (alrededor del percentil 95 para su edad), temperatura 38,1 °C, IMC en percentil 83.\n\nHallazgos de laboratorio y estudio imagenológico\n- Orina: proteinuria marcada (+++); cociente proteína/creatinina (IPC) en orina 2 mg/mg (rango nefrótico).\n- Sangre: proteínas totales 3,8 g/dL, albúmina 2,1 g/dL (hipoalbuminemia), colesterol total 416 mg/dL (hipercolesterolemia), triglicéridos 127 mg/dL; creatinina 0,46 mg/dL (aclaramiento según Schwartz ≈125 ml/min/1,73 m2).\n- Inmunología: IgG baja (208 mg/dL; rango referido 608–1572), IgA e IgM en rangos normales; C3 y C4 sin alteraciones clínicamente relevantes. La disminución de IgG es coherente con pérdidas urinarias en síndrome nefrótico.\n- Tiroides: TSH 4,4 UI/ml (ligeramente elevada), T4 libre 0,80 ng/dL (límite bajo), anti-TPO 120 U/ml y anti-Tg 82 U/ml (ambos positivos). Ecografía tiroidea: tamaño normal con aumento difuso de la vascularización (compatible con tiroiditis).\n- Ecografía renal normal. Estudios serológicos/autoinmunes adicionales (ANA, ANCA, anti‑DNA, PCR SARS‑CoV‑2, etc.) negativos.\n\nDiagnóstico\n- Síndrome nefrótico (probablemente de tipo minimal change o similar por rápida respuesta a corticoides), asociado a tiroiditis autoinmune con disfunción tiroidea leve/incipiente (hipotiroidismo subclínico/levemente franco).\n\nTratamiento y evolución\n- Se inició prednisona 60 mg/m2/día. Respuesta rápida y completa: desaparición del edema y normalización progresiva de la proteinuria; IPC al alta 0,09 (normal) a los 6 días.\n- Se inició levotiroxina 25 µg/día por alteración de la función tiroidea y anticuerpos positivos.\n- Alta hospitalaria al día 6 con prednisona y levotiroxina.\n- Seguimiento a 12 meses: asintomática, función tiroidea controlada con TSH 1,11 UI/ml en terapia de reemplazo; sin recaídas de síndrome nefrótico (orina sin proteinuria) y creatinina estable.\n\nImplicaciones y recomendaciones prácticas\n- El cuadro ilustra la coexistencia de enfermedad renal con pérdida proteica y una tiroiditis autoinmune que requiere tratamiento de reemplazo. En el síndrome nefrótico es habitual la pérdida urinaria de proteínas plasmáticas (albúmina, inmunoglobulinas, proteínas transportadoras) que puede agravar o revelar trastornos tiroideos y aumentar el riesgo de infecciones.\n- Buen pronóstico inmediato por la respuesta completa a esteroides; es necesario seguimiento continuado para:\n  - Vigilar recaídas del síndrome nefrótico y adaptación de la terapia esteroidea si aparecen recaídas o efectos adversos.\n  - Controlar función tiroidea y ajustar levotiroxina según crecimiento y cambios puberales.\n  - Monitorizar parámetros cardiovasculares y lípidos (dada la hiperlipidemia), estado vacunal y riesgo trombótico asociado con síndrome nefrótico.\n- En conjunto, la niña evolucionó favorablemente y permanece estable a 12 meses, pero requiere seguimiento pediátrico/nefrológico y endocrinológico periódicos.\n\nSi desea, puedo redactar una versión más breve para familiares o una hoja de seguimiento con los controles y signos de alarma que deben observar."
+        }
+    },
+    {
+        "article": "La exploración neurológica exhaustiva puso de manifiesto una apariencia facial característica: mirada fija con los ojos muy abiertos, fruncimiento de la frente con una expresión de ceño fruncido (signo del procerus) y expresión fija de la parte inferior de la cara. La paciente presentaba hipocinesia-rigidez simétrica de predominio axial con postura retrocólica del tronco y el cuello. El examen de la deambulación reveló un patrón de la marcha del nivel superior caracterizado por una llamativa vacilación inicial que requería ayuda de objetos/personas cercanas. Una vez que comenzaba a caminar, los pasos mejoraban relativamente, pero volvía a aparecer una marcha inefectiva cuando intentaba girar. Exhibía zancadas cortas, congelación, base amplia de sustentación, desequilibrio, movimiento lento de los miembros inferiores, arrastre de los pies y pérdida de la fluidez normal del tronco y las extremidades. Los reflejos posturales estaban alterados. Asimismo, existía una dificultad grave para la bipedestación tras la sedestación y dificultad para darse la vuelta en la cama. Sin embargo, los signos frontales, como la rigidez paratónica, los reflejos de prensión, la incontinencia urinaria y las características de los déficits cognitivos frontales (por ejemplo, cambios disejecutivos y de personalidad e impulsividad) estaban ausentes, excepto por un estado apático progresivo. Los movimientos oculares sacádicos verticales estaban alterados, con amplitudes relativamente normales y movimientos sacádicos horizontales. Se evidenciaron sacadas de onda cuadrada y una oftalmoplejía supranuclear. La resonancia magnética del cerebro reveló atrofia del mesencéfalo, dilatación del acueducto de Silvio y del III ventrículo y atrofia de los lóbulos frontales, y los signos típicos del colibrí y de la gloria de la mañana. Finalmente, la paciente fue diagnosticada de una PSP probable.",
+        "gold_summary": "Mujer de 58 años sana que consultó por un trastorno de la marcha con caídas. La exploración neurológica mostró una apariencia facial característica (mirada fija, ojos muy abiertos, ceño fruncido y expresión fija hemifacial inferior), e hipocinesia-rigidez simétrica de predominio axial (postura retrocólica del tronco y el cuello). La exploración de la marcha reveló un trastorno de la marcha del nivel superior, caracterizado por una significativa vacilación inicial, que precisaba ayuda de objetos/personas cercanos. Al iniciar la marcha, los pasos mejoraban relativamente, pero reaparecía una deambulación inefectiva al girar. Presentaba zancadas cortas, congelación, base amplia de sustentación, desequilibrio, movimiento lento de las piernas, arrastre de los pies, y pérdida de la cadencia normal del tronco y las extremidades. Los reflejos posturales estaban alterados. La resonancia magnética cerebral desveló atrofia mesencefálica, dilatación de acueducto de Silvio y III ventrículo, atrofia frontal bilateral y el signo típico del colibrí. Finalmente, la paciente fue diagnosticada de una PSP probable.",
+        "synthetic_summary": {
+            "B1": "Una mujer de 58 años fue a la consulta porque tenía problemas para caminar y se caía.  \nSu cara parecía rígida: miraba fijamente, tenía los ojos muy abiertos y el ceño fruncido.  \nEl cuerpo y el cuello estaban tiesos y se movía muy despacio.  \nAl empezar a andar, dudaba mucho y necesitaba apoyarse en cosas o en otras personas.  \nCuando ya llevaba unos pasos, caminaba un poco mejor, pero al girar volvía a fallar.  \nSus pasos eran cortos, a veces se quedaba “pegada” (congelación), arrastraba los pies y perdía el equilibrio.  \nLe costaba ponerse de pie después de estar sentada y también girarse en la cama.  \nLos movimientos de los ojos hacia arriba y abajo estaban alterados.  \nLa resonancia mostró que algunas partes del cerebro estaban más pequeñas y que unos espacios con líquido estaban más grandes.  \nLos médicos vieron cambios en la imagen que son típicos de una enfermedad llamada PSP.  \nPSP es una enfermedad que afecta el movimiento, el equilibrio y la mirada.  \nPor todo esto, la diagnosis final fue de PSP probable. Esto puede ser duro, y la persona necesita apoyo y cuidados.",
+            "B2": "Here is a clear summary written for readers at an upper-intermediate (B2) level:\n\nA 58-year-old woman went to the doctor because she had trouble walking and had fallen. On exam she had a striking facial look: a fixed stare, very wide-open eyes, a deeply furrowed brow (called the procerus sign), and a lower face that looked less expressive. She moved more slowly and was stiff, especially in the trunk and neck, which were bent slightly backward.\n\nHer walking showed a typical “higher-level” gait problem: she hesitated a lot before starting to walk and often needed to hold on to things or people to begin. Once she started, her steps improved a bit, but she had trouble when turning and her walking became ineffective again. Other features were short steps, episodes of “freezing” where she could not start stepping, a wide stance for balance, unsteadiness, slow leg movements, dragging of the feet, and loss of normal smooth movement of the trunk and limbs. Her automatic balance reactions (postural reflexes) were reduced, and she had trouble standing up from a sitting position and turning over in bed.\n\nEye movement testing showed problems with vertical saccades (quick up-and-down eye movements) and signs of supranuclear ophthalmoplegia — an eye movement disorder caused by brain control problems rather than muscle weakness. Small involuntary eye movements called square-wave jerks were also seen. Brain MRI showed shrinkage (atrophy) in the midbrain and frontal lobes, enlargement of fluid-filled spaces including the aqueduct of Sylvius and the third ventricle, and imaging patterns often called the “hummingbird” and “morning glory” signs, which are typical in this condition.\n\nPutting these findings together, the doctors diagnosed probable progressive supranuclear palsy (PSP). PSP is a neurodegenerative disease that mainly affects balance, walking, posture, and eye movements. The MRI and the clinical signs supported this diagnosis.",
+            "B3": "Resumen clínico (nivel universitario, lectura B3)\n\nPaciente: mujer de 58 años que consultó por alteración de la marcha con caídas.\n\nHallazgos principales\n- Apariencia facial característica: mirada fija con ojos muy abiertos, ceño fruncido (signo del procerus) y expresión fija en la parte inferior de la cara — un patrón distintivo en ciertas enfermedades neurodegenerativas.\n- Trastorno motor axial simétrico: hipocinesia (movimiento reducido) y rigidez predominantemente en el tronco y el cuello, con postura retrocólica (el tronco y la cabeza inclinados hacia atrás).\n- Trastorno de la marcha de “nivel superior”: inicio vacilante que requiere apoyo, mejoría relativa al comenzar a andar pero marcada dificultad al girar; pasos cortos, episodios de congelación, base de sustentación amplia, arrastre de los pies, lentitud de las piernas y pérdida de la cadencia normal. Los reflejos posturales estaban alterados; también había dificultad importante para ponerse de pie desde la sedestación y para darse la vuelta en la cama.\n- Función frontal: no se documentaron los signos frontales típicos (rigidez paratónica, reflejos de prensión, incontinencia urinaria ni déficits cognitivos frontales claros como desinhibición o impulsividad). Sí existía un cuadro de apatía progresiva.\n- Oculomotricidad: alteración de las sacadas verticales con presencia de sacadas “onda cuadrada” y oftalmoplejía supranuclear (limitación de los movimientos oculares por un defecto supranuclear), mientras que las sacadas horizontales eran relativamente preservadas.\n- Imagen por resonancia magnética (RM): atrofia del mesencéfalo (signo del “colibrí” o “hummingbird”), dilatación del acueducto de Silvio y del tercer ventrículo y atrofia frontal bilateral (también descrito como el signo de la “gloria de la mañana”).\n\nImpresión diagnóstica\n- Diagnóstico final: probable PSP (parálisis supranuclear progresiva), una enfermedad neurodegenerativa que típicamente produce problemas de equilibrio y marcha, alteraciones de la mirada supranuclear (especialmente vertical) y cambios en el comportamiento o la motivación.\n\nImplicaciones y pasos siguientes sugeridos\n- Pronóstico: progresiva a lo largo de varios años, con aumento del riesgo de caídas y limitación funcional; la progresión y el tiempo varían entre pacientes.\n- Manejo inmediato y a medio plazo: evaluación por un equipo de trastornos del movimiento (neurólogo especialista), fisioterapia enfocada en equilibrio y estrategias para disminuir caídas, terapia ocupacional para adaptar actividades y el hogar, evaluación de la deglución y terapia del habla según necesidad, y apoyo psicológico/social para paciente y cuidadores.\n- Tratamiento farmacológico: no existe cura; algunos fármacos (p. ej., prueba con levodopa) pueden probarse pero la respuesta suele ser limitada. El tratamiento es mayormente sintomático y de soporte.\n- Seguimiento: controles periódicos para monitorizar progresión, ajustar medidas de seguridad y planificar cuidados a largo plazo; considerar derivación a servicios de cuidados paliativos cuando los síntomas sean avanzados.\n\nComentario empático\nEsta situación suele ser difícil para la paciente y su familia. Es importante ofrecer información clara, apoyo multidisciplinario y medidas concretas para reducir el riesgo de caídas y mantener la autonomía el mayor tiempo posible."
+        }
+    },
+    {
+        "article": "Una mujer de 36 años, previamente sana, fue picada una vez por un insecto Hymenoptera desconocido, lo que le provocó hinchazón y eritema en la parte dorsal de la mano derecha. La fiebre punzante apareció en un plazo de 6 horas, a pesar de que el sitio de la picadura se volvió irreconocible gradualmente. Acudió a una clínica local donde le recetaron esteroides orales (prednisolona 20 mg/día) y antibióticos. Tres días después, acudió a nuestro departamento de urgencias por una fiebre intermitente. Presentaba una temperatura elevada (38,9°C), taquicardia e hipotensión (presión arterial 80/52 mmHg) en el momento de la clasificación. La electrocardiografía mostró fibrilación auricular con una frecuencia ventricular rápida de alrededor de 130 latidos por minuto y elevación difusa del ST. La radiografía de tórax mostró una relación cardiotorácica normal sin signos de infiltración o congestión. El hemograma no mostró eosinofilia, leucocitosis, leucopenia o desviación a la izquierda. La isoenzima MB de creatina cinasa (CK-MB) y la troponina cardíaca I se elevaron a 96,0 ng/mL y 8,0 ng/mL, respectivamente. La proteína C reactiva fue de 10,5 mg/L y la procalcitonina fue de 0,32 ng/mL. El NT-proBNP fue de 20 700 pg/mL. La ecocardiografía mostró una hipocinesia global del ventrículo izquierdo con una fracción de eyección del 30,6% y sin derrame pericárdico. El cateterismo cardíaco emergente no reveló lesiones de las arterias coronarias o vasospasmo. Se insertó un globo intraaórtico durante el procedimiento para el shock cardiogénico. La hipotensión progresó acompañada de taquicardia ventricular y fibrilación ventricular, y luego se produjo un paro cardíaco intrahospitalario. La reanimación cardiopulmonar manual no tuvo éxito durante 25 minutos y se usó el soporte cardiopulmonar percutáneo (PCPS, CAPIOX® Centrifugal Pump Controller SP-200, Terumo). La circulación espontánea se estableció 25 minutos después con una recuperación total de la conciencia.\n\nLa prueba rápida de antígeno de influenza (Directigen EZ Flu A+B; BD, Franklin Lakes, NJ, EE. UU.), los cultivos de esputo, los cultivos de sangre y los exámenes serológicos para los virus respiratorios recolectados al ingreso fueron negativos. En el día 2 del ingreso, los niveles séricos de CK-MB y troponina I alcanzaron un máximo de >303 ng/ml y >81 ng/ml, respectivamente. La ecocardiografía de seguimiento 24 horas después del inicio del PCPS mostró deterioro de la función ventricular izquierda, cierre persistente de las válvulas aórticas y trombos intracardiacos en la aurícula izquierda y el ventrículo izquierdo, aproximadamente 24 horas después del inicio del soporte mecánico. En el día 3, el shock progresó con falla multiorgánica. Se aplicó hemodiálisis venovenosa continua debido a la acidosis metabólica y oliguria. En el día 4, la función ventricular derecha también se deterioró gravemente y la actividad eléctrica del corazón desapareció gradualmente. El PCPS se cambió a soportes mecánicos bi-ventriculares a través de canalizaciones hacia la aurícula derecha, el tronco pulmonar, el ápex del ventrículo izquierdo y la aorta ascendente. Ambos sistemas se establecieron utilizando bombas de sangre centrífugas MEDTRONIC Affinity CP. Debido a la hemorragia pulmonar con consolidación bilateral severa de los pulmones, se usó un oxigenador de membrana para lograr una oxigenación adecuada. El flujo sanguíneo se estableció a 3.5 L/minuto, lo que podría mantener la presión arterial media en torno a 65 mmHg. Se realizó una biopsia endomiocárdica del ventrículo izquierdo y la patología reveló una inflamación significativa compuesta principalmente por linfocitos y algunos eosinófilos. El daño miocárdico con necrosis estuvo presente, pero no extenso. En términos de ajustes de ventilador, la presión de conducción y la presión de meseta se establecieron en torno a 15 y 30 cmH2O respectivamente para la protección pulmonar. Se usó la fibra broncoscopia repetidamente para eliminar los coágulos de sangre que obstruían las vías respiratorias principales. En el día 13 del ingreso, la actividad eléctrica del corazón del paciente permaneció ausente y ambas bombas de sangre se cambiaron a los sistemas de asistencia ventricular Levitronix Centri-Mag (Levitronix LLC, Waltham, MA, EE. UU.) para un mejor soporte. El paciente fue trasladado a un centro de trasplantes y se registró como candidato para un trasplante de corazón. En el día 14 se insertó otra cánula en la vena femoral común izquierda para aumentar el flujo de entrada del VAD derecho. Desde el día 14 hasta el día 48, el paciente sufrió episodios de sangrado masivo del mediastino y la vagina, infección de la herida esternal con formación de abscesos, infecciones por úlceras de presión y progresiva hiperbilirrubinemia. Su condición se estabilizó después de desbridamiento, hemostasia quirúrgica y uso de antibióticos fuertes. Se sometió a 5 cursos de intercambio de plasma terapéutico para evitar el rechazo mediado por anticuerpos y recibió un trasplante de corazón ortotópico el día 49. El estudio patológico del corazón del paciente mostró pancarditis de ambos ventrículos y ninguna alteración específica de las 3 arterias coronarias. La ECMO de VA se mantuvo hasta el día 58 para el apoyo postoperatorio del fallo cardiaco. La biopsia endomiocárdica repetida después del trasplante no mostró evidencia de rechazo celular o humoral. La paciente experimentó episodios de shock séptico bajo inmunosupresión y se sometió a una laparoscopia exploratoria y apendicectomía el día 93. La extubación se realizó el día 96 y se dio de alta el día 101. La paciente permaneció clínicamente estable en el seguimiento de 3 meses.\n\nMH - Adulto\nMH - Animales\nMH - Abejas\nMH - Picaduras y mordeduras/*complicaciones\nMH - Oxigenación por membrana extracorpórea\nMH - Mujer\nMH - Paro cardiaco/*etiología/tratamiento\nMH - Insuficiencia cardiaca/*etiología/terapia\nMH - *Trasplante de corazón\nMH - Dispositivos de asistencia cardiaca\nMH - Humanos\nMH - Hipersensibilidad/*diagnóstico\nMH - Miocarditis/*diagnóstico\nMH - Shock, Cardiogénico/*etiología/terapia\n",
+        "gold_summary": "Paciente: Mujer, 36 años\n\nDiagnóstico final: Shock cardiogénico • miocarditis\n\nSíntomas: Fiebre\n\nMedicación: —\n\nProcedimiento clínico: soporte circulatorio mecánico\n\nEspecialidad: Cirugía\n\n\nInforme del caso:\n\nReportamos el caso de una mujer de 36 años que desarrolló fiebre y shock cardiogénico 3 días después de una picadura de abeja. La angiografía cardíaca mostró arterias coronarias permeables y una función ventricular izquierda gravemente comprometida. Su hemodinámica permaneció inestable bajo una dosis alta de agentes inotrópicos y apoyo con un balón intraaórtico. El paro cardíaco intrahospitalario ocurrió 4 horas después del ingreso y recibió reanimación cardiopulmonar extracorpórea. Su oxigenación de membrana extracorpórea venosa periférica (VA ECMO) se cambió a dispositivos de asistencia ventricular bilateral (VAD) debido a una insuficiencia cardíaca derecha progresiva. El resultado de la biopsia endomiocárdica fue compatible con el cuadro de miocarditis por hipersensibilidad. Su corazón entró en paro persistente bajo apoyo circulatorio mecánico. Se sometió a un trasplante de corazón el día 49 del ingreso y permaneció clínicamente estable 6 meses después del alta.\n",
+        "synthetic_summary": {
+            "B1": "Había una mujer de 36 años que fue picada por un insecto en la mano. La picadura se hinchó y poco después ella tuvo fiebre. Tres días más tarde fue al hospital porque estuvo muy enferma. Tenía el pulso muy rápido y la presión baja. Su corazón no podía bombear bien la sangre. Los médicos vieron que las arterias del corazón estaban normales, pero el músculo del corazón estaba inflamado. Esto se llama miocarditis. Es como si algunas células del cuerpo hubieran atacado al corazón.\n\nLa mujer sufrió un paro cardíaco dentro del hospital. Recibió muchos cuidados y se usó una máquina que bombea y oxigena la sangre por fuera del cuerpo. También le pusieron otros dispositivos para ayudar los dos lados del corazón. Durante su enfermedad tuvo sangrados, infecciones y problemas con los riñones. Los médicos llegaron a la conclusión de que su corazón no iba a mejorar. Por eso, después de muchos días le hicieron un trasplante de corazón nuevo.\n\nDespués de la operación, la mujer fue cuidada mucho tiempo. Mejoró poco a poco. Salió del hospital y estuvo estable meses después. Los médicos creen que la inflamación del corazón pudo estar relacionada con la reacción a la picadura. Aunque fue un caso muy grave, recibió tratamiento y finalmente pudo recuperarse.",
+            "B2": "Resumen (nivel B2, para lectores de 11–17 años)\n\nQué pasó\n- Una mujer de 36 años recibió la picadura de un insecto del grupo Hymenoptera (por ejemplo, una abeja). En las horas siguientes tuvo hinchazón y enrojecimiento en la mano y empezó a tener fiebre.\n- Tres días después acudió al hospital con fiebre, pulso muy rápido y presión arterial baja. En el electrocardiograma tenía una arritmia (fibrilación auricular) y cambios que sugerían daño al corazón.\n- Las pruebas de sangre mostraron elevación marcada de las enzimas cardíacas (troponina y CK‑MB), que indican lesión del músculo del corazón. La ecocardiografía mostró que el ventrículo izquierdo funcionaba muy mal (fracción de eyección baja).\n\nDiagnóstico probable\n- Los médicos concluyeron que tenía miocarditis, es decir, inflamación del músculo cardíaco. En este caso parecía ser miocarditis por hipersensibilidad: una reacción del sistema inmune (posible reacción alérgica) que daña el corazón después de la picadura.\n\nQué tratamientos recibió\n- Le hicieron un cateterismo para ver las arterias coronarias; estaban abiertas, por lo que no había ataque al corazón por obstrucción.\n- Empezó con soporte farmacológico y un balón intraaórtico, pero su situación empeoró: sufrió arritmias graves y paro cardíaco dentro del hospital.\n- La reanimación manual no fue suficiente, por lo que se conectó a soporte cardiopulmonar percutáneo (ECMO/PCPS), una máquina que hace temporalmente el trabajo del corazón y los pulmones.\n- Su corazón empeoró y desarrolló trombos dentro de las cámaras y fallo de ambos ventrículos, por lo que el equipo cambió a dispositivos de asistencia ventricular (VAD) para mantener la circulación.\n- A lo largo de su ingreso tuvo complicaciones (sangrados graves, infecciones, fallo renal que necesitó diálisis). Se le practicaron biopsias del corazón que mostraron inflamación con linfocitos y algunos eosinófilos, compatible con miocarditis por hipersensibilidad.\n- Fue incluida en lista para trasplante y recibió un trasplante de corazón el día 49. Tras el trasplante no mostró rechazo en las biopsias posteriores.\n\nEvolución y resultado\n- Tras el trasplante y cuidados intensivos prolongados (incluyendo soporte ECMO temporal), la paciente mejoró. Tuvo episodios de infección que requirieron cirugía, pero fue extubada el día 96 y dada de alta el día 101.\n- En el seguimiento a 3 meses estaba clínicamente estable.\n\nMensaje clave (explicado con calma)\n- La picadura de un insecto rara vez puede desencadenar una reacción inmunológica grave que dañe el corazón (miocarditis).  \n- La miocarditis puede provocar fallo cardíaco y paro, y a veces necesita soporte mecánico largo y hasta un trasplante de corazón.  \n- Gracias a la atención intensiva y al trasplante, esta paciente sobrevivió y mejoró con el tiempo.\n\nSi tienes preguntas sobre alguno de los términos (miocarditis, ECMO, VAD), puedo explicarlos con más detalle.",
+            "B3": "Resumen clínico (nivel universitario, lenguaje no especializado)\n\nCaso y presentación\n- Paciente: mujer de 36 años, previamente sana.\n- Antecedente inmediato: picadura única por un insecto del orden Hymenoptera (probablemente abeja) con eritema y edema local.\n- Curso temprano: en las siguientes 6 horas desarrolló fiebre; 3 días después consultó por fiebre intermitente y signos de insuficiencia hemodinámica.\n\nHallazgos iniciales y pruebas\n- Signos vitales al ingreso: fiebre 38,9 °C, taquicardia, hipotensión (PA 80/52 mmHg).\n- ECG: fibrilación auricular con respuesta ventricular rápida (~130 lpm) y elevación difusa del segmento ST.\n- Radiografía de tórax: sin congestión ni infiltrados al ingreso.\n- Marcadores cardíacos: CK‑MB y troponina I marcadamente elevados (CK‑MB 96 ng/mL al ingreso, pico >303 ng/mL; troponina I 8,0 ng/mL al ingreso, pico >81 ng/mL). NT‑proBNP 20.700 pg/mL.\n- Hemograma: sin eosinofilia ni leucocitosis significativa.\n- Microbiología: pruebas iniciales (antígeno de influenza, cultivos de sangre y esputo, serologías respiratorias) negativas.\n- Ecocardiograma: hipocinesia global del ventrículo izquierdo, fracción de eyección ≈30,6%, sin derrame pericárdico.\n- Angiografía coronaria emergente: arterias coronarias sin lesiones ni vasoespasmo (descarta infarto coronario como causa primaria).\n\nEvolución clínica y tratamientos empleados\n- Shock cardiogénico progresivo a pesar de inotrópicos y balón intraaórtico; evolución a paro cardíaco intrahospitalario con taquicardia ventricular/fibrilación ventricular.\n- Reanimación: reanimación avanzada sin retorno inmediato; se inició soporte cardiopulmonar percutáneo (PCPS/VA‑ECMO) y se obtuvo retorno de la circulación tras ~25 minutos.\n- Complicaciones tempranas: empeoramiento de la función ventricular izquierda, aparición de trombos intracardiacos (aurícula y ventrículo izquierdo) 24 horas tras iniciar soporte mecánico.\n- Progresión a insuficiencia multiorgánica: oliguria y acidosis que requirieron hemodiálisis venovenosa continua.\n- Deterioro de la función ventricular derecha → cambio de soporte a dispositivos de asistencia ventricular biventricular (VADs) y uso de oxigenador de membrana para soporte respiratorio por hemorragia pulmonar y consolidación bilateral.\n- Manejo quirúrgico y procedimientos adicionales: extracción repetida de coágulos por broncoscopia, desbridamiento y control quirúrgico de sangrados, intercambio plasmático terapéutico (5 sesiones) para reducir riesgo de rechazo inmunológico cuando se planificó trasplante.\n- A lo largo del ingreso presentó episodios de sangrados masivos (mediastino, vagina), infección de herida esternal con absceso, úlceras por presión e hiperbilirrubinemia; recibió antibioticoterapia dirigida y cuidados quirúrgicos.\n\nPatología y diagnóstico etiológico\n- Biopsia endomiocárdica del ventrículo izquierdo: inflamación significativa formada principalmente por linfocitos con presencia de algunos eosinófilos; daño miocárdico con necrosis focal (no extensa).\n- Estudio patológico del corazón explantado tras trasplante: pancarditis de ambos ventrículos; coronarias sin lesiones.\n- Interpretación final: miocarditis de tipo hipersensibilidad (probable relación temporal con la picadura de insecto), que provocó fallo cardiaco fulminante y shock cardiogénico refractario.\n\nResultado y seguimiento\n- Debido a paro cardíaco persistente y fallo biventricular refractario, se realizó trasplante cardíaco ortotópico el día 49 de ingreso.\n- Soporte mecánico posoperatorio (ECMO venoarterial) mantenido hasta el día 58.\n- Biopsias endomiocárdicas posteriores al trasplante: sin evidencia de rechazo celular o humoral.\n- Complicaciones tardías: episodios sépticos bajo inmunosupresión; laparoscopia exploratoria y apendicectomía en día 93.\n- Alta hospitalaria en día 101; paciente clínicamente estable en el control a 3 meses.\n\nImplicaciones clínicas y lecciones\n- Una reacción sistémica a una picadura de insecto puede, en casos raros, desencadenar una miocarditis por hipersensibilidad que progresa rápidamente a fracaso cardiaco fulminante.\n- En pacientes con insuficiencia cardíaca aguda y marcadores de daño miocárdico elevados pero coronarias normales, la miocarditis debe sospecharse; la biopsia endomiocárdica puede aportar diagnóstico histológico.\n- La ausencia de eosinofilia periférica no excluye la miocarditis por hipersensibilidad (en este caso hubo pocos eosinófilos en la biopsia).\n- El manejo puede requerir escalada a soporte circulatorio mecánico avanzado (ECMO, VAD biventricular) y, cuando la recuperación miocárdica es imposible, trasplante cardíaco.\n- Este caso subraya la rapidez con la que puede evolucionar la enfermedad y la necesidad de un abordaje multidisciplinario (cardiología, cirugía cardiaca, cuidados intensivos, infectología, cirugía).\n\nTono final\nEste caso describe una complicación rara pero grave tras una picadura de insecto que llevó a miocarditis fulminante y a la necesidad de soporte mecánico prolongado y trasplante. La paciente sobrevivió y estaba estable a los 3 meses, lo que ilustra tanto la gravedad potencial de la miocarditis por hipersensibilidad como la eficacia del tratamiento intensivo y del trasplante en centros especializados."
+        }
+    },
+    {
+        "article": "Un hombre de 24 años con complicaciones cardiovasculares relacionadas con MFS fue admitido en nuestro departamento de medicina interna debido a 3 episodios consecutivos de insuficiencia cardiaca aguda descompensada con fracción de eyección reducida (ADHFrEF) de 2014 a 2017. Su historia médica restante incluye hipertensión arterial, dislipidemia, hipertiroidismo, shock anafiláctico debido a flecainida y hábito tabágico previo.\n\nEl diagnóstico de MFS se realizó en 2010, cuando se llevó a cabo la sustitución de la aorta ascendente y la válvula aórtica con prótesis mecánica debido a una disección aórtica aguda tipo A en presencia de antecedentes familiares (madre, padre y 3 hijos con MFS). Durante el período intraoperatorio, se produjo un síndrome coronario agudo inferior y se trató con cirugía de injerto de derivación de la arteria coronaria.\n\nEn mayo de 2014, se realizó la implantación de una prótesis mecánica de aorta descendente y arco aórtico debido a un aneurisma disecante crónico. El hematoma peri-aórtico y la isquemia medular complicaron la cirugía y causaron paraplejia de las extremidades inferiores, dolor y hipoestesia térmica, e incontinencia rectal. Después de 2 meses, durante su primera admisión por ADHFrEF, las pruebas de laboratorio fueron notables para N-terminal pro-BNP (NT-proBNP) de 12,000 pg/mL y el ecocardiograma transtorácico mostró una función de la prótesis normal, dilatación de todas las cámaras cardiacas (principalmente las izquierdas) con insuficiencia mitral y tricuspídea moderada, hipertrofia ventricular izquierda, acinesia de la pared inferior, discinesia septal e hipocinesia de las paredes restantes con reducción severa de la fracción de eyección ventricular izquierda (LVEF) −20%. Se le trató con diuréticos intravenosos y desfibrilador cardiaco interno (St. Jude Ellipse DR, modo DDD) sin terapia de resincronización cardiaca (criterios de electrocardiograma no cumplidos) y se le dio de alta con la máxima terapia médica (furosemida, carvedilol, ramipril, espironolactona, digoxina y amlodipina).\n\nEn agosto de 2017, se produjo un nuevo episodio de ADHFrEF. Los valores de laboratorio de admisión notables incluían NT-proBNP de 2719 pg/mL y midregional-proadrenomedullin (MR-proADM) de 1.61 nmol/L, mientras que el ecocardiograma transtorácico y transesofágico mostró un LVEF de 35%, función de prótesis normal, severa regurgitación tricuspídea, y ruptura de la valva anterior de la chorda tendineae con severa regurgitación mitral. Los pacientes fueron tratados con diuréticos intravenosos y digoxina y dados de alta con una terapia médica óptima (furosemida, carvedilol, ramipril, espironolactona, digoxina, y amlodipina).\n\nPor último, volvió a ser admitido en nuestro departamento de medicina interna en noviembre de 2017 debido a un tercer episodio de ADHFrEF y una acumulación de líquido mediastinal infectado secundaria a una corrección quirúrgica de insuficiencia valvular severa un mes antes con implantación de prótesis mecánica mitral (31 mm ST Jude) y anuloplastia tricúspide De Vega.\n\nEl examen físico reveló una presión arterial de 120/80 mm Hg, pulso de 82 bpm, frecuencia respiratoria de 26 apm, saturación de O2 de 87% en aire ambiente con posición ortopneica obligatoria, y un habitus marfanoide (peso de 147 kg, altura de 2.2 m). La evaluación cardiopulmonar reveló un segundo sonido cardíaco metálico, percusión opaca con reducción del frémito vocal táctil y crepitaciones en la base de los pulmones, disminución amplia de los sonidos respiratorios vesiculares, presencia de ascitis abundante e hinchazón de las piernas.\n\nLos valores de laboratorio notables incluyeron NT-proBNP de 10,132 pg/mL y MR-proADM de 2,36 nmoL/mL.\n\nEl análisis de gases arteriales reveló una hipoxemia grave con alcalosis respiratoria y metabólica (pH 7,56, pO2 46 mm Hg, pCO2 24,8 mm Hg, HCO3− 21,9 mm mol/L, gradiente alveolar-arterial 31 mm Hg). Aunque el electrocardiograma resaltó fibrilación auricular con frecuencia ventricular de 80 bpm, hipertrofia ventricular izquierda e isquemia subepicárdica infralateral, el ecocardiograma transtorácico mostró las mismas características que el anterior, excepto por una FEVI de 30 %, presencia de prótesis mecánicas mitrales con fuga paravalvular y gradiente medio de 9 mm Hg, e insuficiencia tricuspídea leve.\n\n\nEn la radiografía de tórax y en la tomografía computarizada de alta resolución se observa una congestión hilar con cardiomegalia, consolidación pulmonar en el lóbulo superior derecho y acumulación de líquido mediastínico infectado.\n\nEl paciente fue tratado con 250 mg de furosemida intravenosa por día, 100 mg de canrenona por día, 4,5 g de piperacilina/tazobactam cada 6 horas y 12 mg/kg de teicoplanina por día, y luego 12 mg/kg por día. El día 9, una vez alcanzada la estabilización hemodinámica, se agregó una dosis intermedia de sacubitril/valsartan de 49/51 mg por día a 3,125 mg de carvedilol por día, 100 mg de espironolactona por día, 250 mg de furosemida por día y 0,25 mg de digoxina por día.\n\nEn el seguimiento de 1 mes, sacubitril/valsartan se aumentó a 97/103 mg b.i.d. para la buena condición clínica del paciente, lo que permitió una reducción persistente y progresiva de los parámetros clínicos, de laboratorio (reducción de NT-proBNP e incremento de MR-proADM), de los parámetros ecocardiográficos (aumento del EFV final del ventrículo izquierdo (42 % vs 30 %), del diámetro final del ventrículo izquierdo, del diámetro diastólico final del ventrículo izquierdo, de la masa del ventrículo izquierdo y del índice de masa del ventrículo izquierdo) y una mejora de la calidad de vida sin nuevos episodios de ADHFrEF hasta el seguimiento de 9 meses (Fig. (Fig.1B1B y D; Tabla 1).1). Debido a la falta de un régimen de dosificación específico para sacubitril/valsartan en la miocardiopatía relacionada con la EM, utilizamos el esquema terapéutico recomendado.\n\nMH - Aminobutiratos/uso terapéutico\nMH - Antagonistas de los receptores de la angiotensina/*uso terapéutico\nMH - Compuestos de bifenilo\nMH - Combinaciones de fármacos\nMH - Insuficiencia cardiaca/*terapia farmacológica/*etiología\nMH - Humanos\nMH - Hombre\nMH - Síndrome de Marfan/*complicaciones\nMH - Tetrazoles/uso terapéutico\nMH - Resultado del tratamiento\nMH - Valsartán\nMH - Adultos jóvenes\n",
+        "gold_summary": "Preocupaciones de los pacientes:\nUn hombre de 24 años fue admitido en nuestro departamento de medicina interna debido a disnea, ascitis e hinchazón de las piernas. El análisis de gases en sangre arterial reveló una hipoxemia grave con alcalosis respiratoria y metabólica. La radiografía de tórax mostró una congestión hilar.\n\nDiagnósticos:\nInsuficiencia cardíaca aguda descompensada recurrente con fracción de eyección reducida a pesar de la terapia médica óptima en la cardiomiopatía relacionada con el síndrome de Marfan.\n\nIntervenciones y resultados:\nSe agregó sacubitril/valsartan a la terapia médica óptima después de la estabilización hemodinámica, lo que permitió una mejora clínica, de laboratorio y ecocardiográfica progresiva. El paciente mantuvo una supervivencia libre de insuficiencia cardiaca y una buena calidad de vida hasta el seguimiento de 9 meses.\n",
+        "synthetic_summary": {
+            "B1": "Había un hombre joven de 24 años con síndrome de Marfan. Esto es una condición que puede hacer que las paredes de los vasos y las válvulas del corazón sean débiles. Él ya había tenido varias operaciones en el corazón y en la aorta. Después de una operación quedó sin poder mover bien las piernas y con menos sensibilidad en ellas.\n\nDurante varios años tuvo episodios en los que su corazón fallaba y no bombeaba suficiente sangre. Esto le causaba falta de aire, líquido en el abdomen y en los pulmones, y mucho hinchazón en las piernas. También tenía infección en líquido cerca del corazón y necesitó antibióticos.\n\nLos médicos le dieron muchos medicamentos para el corazón y lo estabilizaron. Cuando estuvo más estable, le añadieron un medicamento nuevo llamado sacubitril/valsartan. Con ese cambio, su respiración mejoró. El líquido en el cuerpo bajó. Las pruebas y el ecocardiograma mostraron que su corazón empezó a bombear mejor. No tuvo nuevos ataques de falla del corazón durante por lo menos nueve meses y su calidad de vida mejoró.\n\nEn resumen: era un joven con muchas operaciones y problemas cardíacos. Tras estabilizarlo, los médicos usaron un medicamento nuevo que ayudó a que se sintiera mejor y que su corazón trabajara con más fuerza.",
+            "B2": "Resumen para lectores jóvenes (nivel secundaria — B2)\n\nEste informe cuenta la historia de un hombre de 24 años con síndrome de Marfan, una enfermedad genética que afecta el tejido conectivo y suele dañar la aorta y las válvulas del corazón. Desde 2010 ha tenido varias cirugías mayores en el corazón y la aorta, y complicaciones importantes: en una operación sufrió un infarto y requirió un bypass coronario; en otra intervención de la aorta descendente quedó con paraplejia (pérdida de movimiento de las piernas), dolor y problemas de sensibilidad e incontinencia.\n\nProblema principal\nEntre 2014 y 2017 el paciente presentó tres episodios de insuficiencia cardíaca aguda descompensada con fracción de eyección reducida. La fracción de eyección (FE) es una medida de la capacidad del corazón para bombear sangre; valores bajos (por ejemplo 20–35 %) indican fallo importante del bombeo. En sus ingresos se detectaron también niveles muy altos de NT‑proBNP, un análisis de sangre que sube cuando el corazón está estresado.\n\nQué le pasó en la última hospitalización (noviembre de 2017)\n- Allí tenía dificultad para respirar, ascitis (líquido en el abdomen) e hinchazón de piernas. Su saturación de oxígeno era baja.\n- Tenía prótesis mecánicas en válvulas cardíacas y fugas alrededor de una prótesis (fuga paravalvular).\n- Además se encontró una acumulación de líquido mediastínico infectado (líquido infectado en el área entre los pulmones), que se trató con antibióticos fuertes.\n- Tras estabilizarlo con diuréticos y tratamiento para la infección, se añadió sacubitril/valsartán —un fármaco combinado recomendado para ciertos tipos de insuficiencia cardíaca— a la terapia ya óptima que estaba recibiendo (betabloqueante, espironolactona, diuréticos, digoxina, entre otros).\n\nResultados tras la nueva medicación\n- En el seguimiento a 1 mes y hasta 9 meses, el paciente mejoró de forma sostenida: mejor estado clínico, menos signos en sangre de fallo cardíaco (NT‑proBNP disminuyó) y mejorías en el ecocardiograma.\n- La fracción de eyección del ventrículo izquierdo aumentó de alrededor del 30 % a 42 %, lo que significa que el corazón bombeaba mejor.\n- No tuvo nuevos episodios de insuficiencia cardíaca aguda hasta el control a 9 meses y su calidad de vida mejoró.\n\nImportancia y enseñanza\nEste caso muestra a una persona joven con síndrome de Marfan y cardiomiopatía severa que, a pesar de muchas cirugías y complicaciones, tuvo mejoría clínica y ecocardiográfica tras añadir sacubitril/valsartán a la terapia médica óptima. En pacientes con enfermedades complejas como ésta, los cambios en el tratamiento pueden traducirse en mejor función cardíaca y menos hospitalizaciones, aunque se necesita vigilancia continua y adaptación del tratamiento individualmente.",
+            "B3": "Paciente\nUn hombre de 24 años con síndrome de Marfan (antecedente familiar claro) que ha sufrido varias cirugías aórticas y valvulares y complicaciones graves (incluida paraplejia tras cirugía de aorta en 2014) ingresó por disnea intensa, ortopnea, ascitis y edemas de piernas. Tenía saturación de O2 en aire ambiente del 87% y signos clínicos de congestión pulmonar y sobrecarga sistémica.\n\nAntecedentes relevantes\n- Diagnóstico de síndrome de Marfan en 2010; cirugía de sustitución de aorta ascendente y válvula aórtica por disección tipo A, con injerto coronario tras infarto intraoperatorio.  \n- En 2014 reemplazo de aorta descendente y arco aórtico por aneurisma disecante; complicaciones: hematoma peri-aórtico, isquemia medular y paraplejia.  \n- Implante previo de desfibrilador (St. Jude Ellipse DR); múltiples episodios previos de insuficiencia cardiaca aguda descompensada con fracción de eyección reducida (HFrEF).  \n- Un mes antes del ingreso más reciente se había colocado una prótesis mecánica mitral (31 mm) y se realizó anuloplastia tricuspídea De Vega; luego presentó colección mediastínica infectada.\n\nHallazgos clínicos y pruebas\n- Gasometría: hipoxemia grave (pO2 46 mm Hg) con alcalosis respiratoria y metabólica (pH 7,56).  \n- ECG: fibrilación auricular con respuesta ventricular lenta (~80 lpm), hipertrofia ventricular izquierda e isquemia subepicárdica infralateral.  \n- Ecocardiograma: fracción de eyección del ventrículo izquierdo (LVEF) reducida (30% en el ingreso más reciente), prótesis valvulares presentes con fuga paravalvular mitral y gradiente medio 9 mm Hg; regurgitación tricuspídea variable en los episodios previos.  \n- Marcadores: NT‑proBNP marcadamente elevado en episodios (12,000 pg/mL en 2014; 2,719 pg/mL en agosto de 2017; 10,132 pg/mL en noviembre de 2017), MR‑proADM también elevado (1.61 nmol/L en agosto 2017, 2.36 nmol/L en noviembre 2017).  \n- Imagen torácica: cardiomegalia, congestión hilar y consolidación pulmonar; colección mediastínica infectada confirmada por TC.\n\nTratamiento durante esta hospitalización\n- Manejo inicial: diuréticos intravenosos intensivos (furosemida 250 mg/día), antagonistas mineralocorticoides (canrenona/espironolactona), control de ritmo/anticongestión y antibióticos para mediastinitis (piperacilina/tazobactam y teicoplanina).  \n- Tras estabilización hemodinámica (día 9) se añadió sacubitril/valsartán (inhibidor de neprilisina + valsartán) 49/51 mg/día junto con la terapia médica óptima ya en curso (carvedilol, espironolactona, digoxina, diuréticos).  \n- A 1 mes se incrementó sacubitril/valsartán a 97/103 mg dos veces al día siguiendo el esquema recomendado para insuficiencia cardiaca con fracción reducida.\n\nEvolución y resultados\n- Clínicamente mejoró de forma sostenida: reducción de disnea y congestión, mejor tolerancia funcional y mejor calidad de vida.  \n- Biológicamente disminuyó el NT‑proBNP (marcador de tensión cardiaca). MR‑proADM aumentó (el significado pronóstico de este cambio en este contexto no está del todo aclarado).  \n- Ecocardiograma de control mostró aumento de LVEF de ~30% a 42% y cambios favorables en parámetros del ventrículo izquierdo.  \n- A los 9 meses de seguimiento no presentó nuevos episodios de insuficiencia cardiaca aguda descompensada.\n\nInterpretación y recomendaciones\n- En este paciente joven con cardiomiopatía asociada a síndrome de Marfan y HFrEF recurrente, la adición de sacubitril/valsartán a la terapia médica óptima se asoció a mejoría clínica, descenso de NT‑proBNP y recuperación parcial de la función ventricular izquierda.  \n- Limitaciones importantes: se trata de un único caso observacional; no puede establecerse causalidad ni generalizarse la eficacia o seguridad del tratamiento para todos los pacientes con Marfan. Además, no existe un régimen de dosificación específico para la miocardiopatía relacionada con Marfan, por lo que se siguió el esquema estándar para HFrEF.  \n- Pasos siguientes razonables para pacientes similares: seguimiento estrecho (función renal, potasio, tensión arterial), monitorizar prótesis valvulares y complicaciones infecciosas, considerar indicaciones para terapia de resincronización o intervenciones sobre fugas paravalvulares si persisten, y evaluar la acumulación de evidencia mediante series de casos o estudios controlados.\n\nComentario final (tono empático)\nEste caso sugiere que, en circunstancias seleccionadas y con monitorización cuidadosa, un inhibidor de neprilisina/ARA II (sacubitril/valsartán) puede ayudar a recuperar función ventricular y mejorar síntomas en HFrEF asociada a Marfan. Es alentador para el paciente y su equipo tratar de alcanzar estabilidad y calidad de vida, pero se necesitan más datos sistemáticos para confirmar este enfoque en poblaciones similares."
+        }
+    },
+    {
+        "article": "Paciente masculino de 41 años de edad quien ingresó en 2016 al servicio de urgencia con politraumatismo producto de accidente de tránsito; con trauma en miembros inferioA B res, en los rayos X se observa fractura de platillos tibiales izquierdos y fractura subtrocanteriana derecha, trauma toracoabdominal y trauma craneoencefálico leve.\nSe le practica osteosíntesis de fémur con clavo cefalomedular largo a foco cerrado corrigiendo la fractura subtrocanteriana y se le aplica tutor externo transarticular de rodilla como medida de control de daño local provisional; 15 días después se realiza osteosíntesis definitiva de su fractura de platillos tibiales. Evolución adecuada y satisfactoria de platillos tibiales.\nEntre 2016 y 2019 tuvo episodios esporádicos de dolor en cadera derecha que cedían fácilmente al manejo con antiinflamatorios y analgésicos sin limitar las actividades de la vida diaria y en la toma de rayos X se observaba fatiga de los bloqueos distales con dudas de la consolidación de la fractura.\nEn 2020 se incrementa el dolor en la cadera que no cede con el tratamiento médico y se acompaña de limitación funcional. En los rayos X de control se evidencia ruptura del clavo cefalomedular en su tercio proximal y no unión de la fractura subtrocantérica.\nEn Febrero de 2020 intento fallido de extracción de material de osteosíntesis (extrainstitucional), por lo que es remitido a nuestra institución. Se lleva a cirugía el 8 de Febrero, se realiza retiro de material de osteosíntesis, curetaje y toma de cultivo de foco de no unión. Cultivo positivo para Klebsiella pneumoniae recibiendo tratamiento con meropenem intravenoso por 10 días. Posteriormente se le realizó un lavado quirúrgico con drenaje de hematoma para el 20 de Febrero realizar nueva osteosíntesis con clavo cefalomedular + injerto óseo autólogo (tomado de ambas crestas iliacas) en foco de no unión.\nReactivación de la infección en Marzo de 2020, requiriendo nuevamente cirugía para lavados y desbridamiento quirúrgicos seriados (#5). Se aísla nueva bacteria Enterobacter que es manejada con vancomicina y meropenem. A f inales de Abril completa tratamiento médico y se le da salida en condiciones estables.\nEn Mayo de 2020 por persistencia de la infección se retira el material de osteosíntesis, se deja un clavo TENS endomedular recubierto de cemento con antibióticos (gentamicina).\nA finales de Mayo después de dos lavados quirúrgicos se retiró el clavo TENS, resección de bordes de fractura (hasta hueso sano) injerto óseo endomedular con un segmento de 10 cm de peroné no vascularizado (autólogo) y fijación de la fractura con una placa de soporte condíleo de fémur distal; colocación de sistema VAC y cierre definitivo de la herida en un segundo tiempo el 28 de Mayo de 2020. El paciente evolucionó adecuadamente, la herida quirúrgica cicatrizó por completo hasta el día de hoy con infección en remisión y evidencia radiológica de consolidación de la fractura, además paciente asintomático con función preservada de la extremidad.",
+        "gold_summary": "Masculino de 41 años de edad que sufre fractura subtrocantérica derecha producto de un accidente de tránsito que requirió manejo de osteosíntesis. Con posterior ruptura del clavo cefalomedular en su tercio proximal, no unión de la fractura e infecciones en sitio de la fractura. Fue tratado con múltiples lavados quirúrgicos, antibioticoterapia y un procedimiento ortopédico y quirúrgico poco convencional como el uso de una placa de soporte condíleo de fémur distal y un injerto óseo endomedular con un segmento de 10 cm de peroné no vascularizado. Paciente con evolución satisfactoria y favorable.",
+        "synthetic_summary": {
+            "B1": "Un hombre de 41 años se rompió el hueso del muslo derecho en un accidente de coche en 2016. Le pusieron un clavo dentro del hueso para sujetar la fractura. También le hicieron otras operaciones en la rodilla y la tibia.\n\nEn los años siguientes tuvo dolor a veces. En 2020 el clavo se rompió y el hueso no había sanado. Le operaron para quitar el material y tomaron muestras. Salieron bacterias (gérmenes) en los análisis. Recibió antibióticos fuertes por vía intravenosa.\n\nSe le hicieron varios lavados y limpiezas quirúrgicas porque la infección volvió. Le pusieron y quitaron distintos dispositivos con antibióticos. Finalmente le quitaron el material roto y pusieron un injerto de hueso: un trozo de 10 cm del peroné del propio paciente, metido dentro del hueso para ayudar a que sane. También le pusieron una placa metálica grande para dar soporte. Usaron un sistema de vacío (VAC) para ayudar a cerrar la herida.\n\nEl proceso fue largo y requirió varias cirugías y medicinas. Al final la infección desapareció. La herida cicatrizó bien. Las radiografías muestran que el hueso consolidó. El paciente está sin dolor y puede usar la pierna. Esto fue un buen resultado después de un tratamiento difícil.",
+            "B2": "Resumen (nivel B2, claro y empático)\n\nHombre de 41 años que en 2016 sufrió un accidente de tráfico con varias fracturas, entre ellas una fractura subtrocantérea del fémur derecho (justo debajo del trocánter, una parte de la cadera). Inicialmente se le colocó un clavo cefalomedular largo (un clavo metálico dentro del hueso para sujetar la fractura) y otros dispositivos para controlar el daño.\n\nEntre 2016 y 2019 tuvo dolor intermitente en la cadera; en 2020 el dolor aumentó y la fractura no había consolidado (no unión = el hueso no había cicatrizado). Además, el clavo se rompió en su tercio proximal. Tras un intento fallido de extracción del material, fue operado en febrero de 2020: se retiró el material, se limpió la zona afectada (curetaje) y se tomaron cultivos, que dieron positivo para Klebsiella pneumoniae. Recibió antibióticos intravenosos (meropenem) y se le colocó de nuevo un clavo junto con injerto óseo autólogo (hueso propio de las crestas ilíacas).\n\nEn marzo la infección reapareció; requirió varios lavados y desbridamientos (cirugías para limpiar tejido infectado) y se aisló una nueva bacteria, Enterobacter, tratada con vancomicina y meropenem. A pesar del tratamiento, la infección persistió y en mayo se retiró el material de osteosíntesis y se dejó temporalmente un clavo TENS recubierto con cemento que contiene antibiótico (esto ayuda a dar estabilidad y liberar antibiótico localmente).\n\nA finales de mayo se decidió un tratamiento reconstructivo: retirada del clavo TENS, resección de los bordes de la fractura hasta hueso sano, colocación de un injerto endomedular con un segmento de 10 cm del peroné del propio paciente (injerto no vascularizado = hueso sin reconexión directa de vasos sanguíneos) y fijación con una placa de soporte condílea en el fémur distal. Se utilizó también sistema VAC (terapia de presión negativa para ayudar a que la herida sane) y el cierre definitivo se hizo en un segundo tiempo. \n\nEvolución final: la herida cicatrizó completamente, la infección quedó en remisión y las imágenes radiológicas mostraron consolidación de la fractura. El paciente está asintomático y mantiene función en la extremidad. Este caso muestra el uso combinado de limpiezas repetidas, antibióticos y técnicas reconstructivas poco convencionales para controlar infección y lograr la curación ósea.",
+            "B3": "Resumen clínico (nivel universitario)\n\n- Presentación inicial\n  - Hombre de 41 años con politraumatismo por accidente de tránsito en 2016. Entre sus lesiones destacaron una fractura subtrocantérica derecha (por debajo del trocánter femoral), fractura de platillos tibiales izquierdos y fractura subtrocantérica derecha; además trauma toracoabdominal y craneoencefálico leve.\n  - Tratamiento agudo: osteosíntesis del fémur con clavo cefalomedular largo (clavo intramedular que estabiliza el cuello y la diáfisis femoral) y tutor externo transarticular de rodilla; 15 días después se fijaron los platillos tibiales. Evolución inicial satisfactoria de la tibia.\n\n- Curso clínico y complicaciones\n  - Entre 2016 y 2019 tuvo dolor intermitente en cadera derecha controlable con AINEs. Radiografías mostraban fatiga de los bloqueos distales del clavo y duda de consolidación.\n  - En 2020 empeoró el dolor y la función; radiografías mostraron ruptura del clavo cefalomedular en su tercio proximal y ausencia de unión de la fractura (no unión).\n\n- Manejo en 2020\n  - Febrero 2020: intento fallido extradicional de extracción del material; fue remitido y el 8 de febrero se retiró el material, se realizó curetaje y se tomó cultivo del foco de no unión. Cultivo positivo para Klebsiella pneumoniae → tratamiento con meropenem IV 10 días.\n  - Segunda cirugía: lavado y drenaje de hematoma; el 20 de febrero se realizó nueva osteosíntesis con clavo cefalomedular y injerto óseo autólogo tomado de ambas crestas ilíacas.\n  - Marzo 2020: reactivación de infección, necesitó múltiples lavados y desbridamientos seriados (cinco procedimientos). Se aisló Enterobacter; se trató con vancomicina y meropenem. Alta clínica estable a finales de abril.\n  - Mayo 2020: por persistencia de infección se retiró el material; se colocó temporalmente un clavo TENS endomedular recubierto con cemento impregnado de gentamicina (técnica para administrar antibiótico local).\n  - Finales de mayo 2020: tras dos lavados adicionales se retiró el clavo TENS, se resecaron los bordes de fractura hasta hueso sano, se colocó un injerto óseo endomedular con un segmento autólogo de peroné no vascularizado de 10 cm (injerto interpuesto dentro del canal medular) y se fijó la fractura con una placa soporte condílea de fémur distal. Se usó sistema VAC (vacío) y cierre definitivo el 28 de mayo.\n\n- Hallazgos y desenlace\n  - Tras estos procedimientos el paciente evolucionó favorablemente: la herida cicatrizó completamente, la infección está en remisión, hay evidencia radiológica de consolidación ósea y el paciente está asintomático con función preservada de la extremidad.\n\n- Interpretación y consideraciones\n  - Problema principal: no unión de fractura subtrocantérica complicada por infección posoperatoria y fractura/ruptura del implante, lo que requirió manejo secuencial: control de infección (desbridamiento, antibióticos sistémicos y locales), retirada y sustitución de material, y reconstrucción ósea con injerto autólogo.\n  - Técnicas destacadas: uso temporal de clavo con cemento antibiótico para control local de infección, injerto endomedular con peroné no vascularizado y fijación con placa de soporte inusual para esta localización — todas medidas de salvamento que evitaron resultados más adversos como la pérdida funcional o amputación.\n\n- Recomendaciones posteriores (seguimiento)\n  - Continuar seguimiento clínico y radiológico para detectar recidiva de infección o fallo de consolidación.\n  - Monitorizar marcadores inflamatorios/infecciosos si hay signos sugestivos.\n  - Programa de rehabilitación para potenciar la recuperación funcional y control del dolor.\n  - Considerar control ortopédico periódico y evaluación por rehabilitación y, si procede, por infectología para manejo a largo plazo.\n\nLa evolución final fue satisfactoria: infección en remisión, consolidación radiológica y función de la extremidad preservada. Si desea, puedo preparar una versión más breve o una explicación de cualquiera de los procedimientos y términos usados."
+        }
+    },
+    {
+        "article": "Una adolescente de 17 años se presentó en nuestra clínica con una historia de dos meses de dolor torácico en el lado izquierdo y una historia de una semana de dolor en la espalda en el nivel de T7. El dolor torácico se acompañaba de palpitaciones y disnea que ocurrían de tres a cuatro días por semana. Una semana antes de la primera visita, las palpitaciones y la disnea se hicieron menos frecuentes, y desarrolló un dolor sordo diario intermitente en el lado izquierdo del pecho y la parte media de la espalda sin radiación, en la mayoría de los casos. El dolor ocurría tanto con el ejercicio como en reposo, y duraba horas, sin factores agravantes o atenuantes. Informó una intensidad del dolor de 2 a 6 en una escala de 10 puntos. La intensidad cambiaba durante un ataque, y el promedio era 4. Estaba sana por lo demás. No había limitación en la vida diaria. Visitó a un médico local un mes antes de visitar nuestra clínica. Los resultados de los exámenes electrocardiográficos y de laboratorio de Holter fueron normales. Su historial médico incluía migraña durante tres años. Sus medicamentos regulares eran lomerizina, loxoprofen y naratriptan para la prevención y el tratamiento agudo de la migraña. Su migraña estaba bien controlada, y rara vez experimentaba ataques. Negó trauma o cirugías previas. Negó síntomas sospechosos o antecedentes familiares de afecciones autoinmunes o inflamatorias.\n\nSu presión arterial era de 107/60 mmHg y su pulso de 62 latidos/min. Medía 162 cm de altura y pesaba 43 kg, con un índice de masa corporal de 16,4 kg/m2. No se escuchaba ningún murmullo ni arritmia en su examen cardiovascular. Los pulmones estaban limpios a la auscultación bilateral. La palpación del tórax provocó un dolor local no reproducible en las articulaciones inferiores esterno-costales; la maniobra de tracción del brazo horizontal y la maniobra del gallo cantando no provocaron dolor. No había sensibilidad en los músculos y huesos de la parte superior del cuerpo.\n\nLos hallazgos electrocardiográficos y de laboratorio, incluida la función tiroidea, fueron normales. El examen radiográfico torácico y torácico mostró el enderezamiento de la columna torácica superior y una pérdida de la curvatura cifótica normal. Las radiografías de las costillas inferiores no revelaron fractura ni neumotórax. Sospechamos un síndrome de la espalda recta, de acuerdo con los dos criterios diagnósticos diferentes propuestos por Davies et al. y DeLeon et al. La distancia entre la mitad del borde anterior de T8 y una línea vertical que conecta T4 a T12 fue de 0.91 cm. El diámetro anteroposterior fue de 74.0 cm, y el diámetro transversal fue de 243.2 cm. Le aconsejamos que comenzara y continuara la terapia quiropráctica para aumentar la cifosis torácica. Procedimos con una espera vigilante durante un mes en atención ambulatoria.\n\nDespués de esta primera visita, el dolor de pecho y de espalda se alivió gradualmente. Las palpitaciones y la disnea apenas se produjeron. Todos los síntomas desaparecieron en tres semanas. En la visita de seguimiento de un mes, se realizó una ecocardiografía, que reveló una regurgitación mitral trivial sin prolapso. Confirmamos el diagnóstico de síndrome de espalda recta. Reaseguramos a la paciente de que la enfermedad es benigna y le aconsejamos que continuara con la terapia quiropráctica. No ha tenido recaída de síntomas graves ni necesidad de visitar el hospital. Nunca volvió a visitar nuestra clínica en el año siguiente.\n",
+        "gold_summary": "Una adolescente de 17 años se presentó con su madre en nuestra clínica con un historial de dos meses de dolor en el pecho izquierdo y un historial de una semana de dolor en la parte media de la espalda. Diagnosticamos el síndrome de la columna vertebral basado en los hallazgos radiográficos del pecho y la columna vertebral y los síntomas de dolor en el pecho, palpitaciones y disnea. Tranquilizamos a la paciente de que la enfermedad era benigna y le aconsejamos que iniciara y continuara con la terapia quiropráctica. Todos los síntomas, incluido el dolor de espalda, desaparecieron en tres semanas.\n",
+        "synthetic_summary": {
+            "B1": "Una chica de 17 años vino con su mamá porque tenía dolor en el lado izquierdo del pecho desde hace dos meses y dolor en la mitad de la espalda desde hace una semana. También sentía a veces que el corazón le latía fuerte y que le faltaba el aire. Las pruebas del corazón y la sangre salieron normales. Las radiografías mostraron que la parte de la columna en el pecho estaba demasiado recta. Los médicos dijeron que tenía “síndrome de la espalda recta”, que puede causar esos dolores y molestias pero no es grave. Le recomendaron terapia quiropráctica y vigilancia. En tres semanas todos los síntomas desaparecieron. Los médicos la tranquilizaron y no volvió a tener problemas en el año siguiente.",
+            "B2": "A 17-year-old girl came to the clinic with two months of left-sided chest pain and one week of dull mid‑back pain. She also had episodes of palpitations (feelings of a fast or strong heartbeat) and shortness of breath, but heart rhythm tests and blood work were normal. Chest and spine X‑rays showed a loss of the normal upper‑back curve, a finding consistent with straight‑back syndrome — a harmless condition in which the upper spine is unusually straight and can sometimes cause chest symptoms. The team advised chiropractic therapy to help restore the thoracic curve and watched her as an outpatient. Her chest and back pain and the palpitations improved and then completely went away within three weeks. A follow‑up heart ultrasound (echocardiogram) showed only a very small leak in the mitral valve (trivial mitral regurgitation) without valve prolapse, which is not expected to cause problems. She was reassured that the condition is benign, advised to continue therapy, and had no serious recurrence during the next year.",
+            "B3": "Presentación\nUna adolescente de 17 años acudió con dolor en el lado izquierdo del pecho durante dos meses y dolor intermitente en la parte media de la espalda (nivel T7) desde hace una semana. Inicialmente también presentaba palpitaciones y disnea tres o cuatro días por semana; con el tiempo estas molestias respiratorias disminuyeron y quedó un dolor sordo diario en el pecho y la espalda (intensidad media 4/10). No refería traumatismo ni antecedentes familiares relevantes; tenía una historia de migraña controlada con medicación.\n\nExploración y pruebas\n- Signos vitales dentro de límites normales (PA 107/60 mmHg, pulso 62/min); índice de masa corporal 16,4 kg/m2.\n- Examen cardiopulmonar sin soplos ni ruidos patológicos; palpación torácica provocó dolor local no reproducible en articulaciones esternocostales inferiores.\n- ECG, monitor Holter y análisis de laboratorio, incluida la función tiroidea, normales.\n- Radiografías de tórax/columna mostraron rectificación de la columna torácica superior y pérdida de la curvatura cifótica normal; radiografías de costillas sin fractura ni neumotórax.\n- Ecocardiograma realizado en el seguimiento mostró una regurgitación mitral trivial sin prolapso.\n\nDiagnóstico\nCon base en los hallazgos clínicos y radiográficos se diagnosticó síndrome de la espalda recta (straight back syndrome): una disminución de la curvatura cifótica torácica que puede asociarse a síntomas torácicos y palpitaciones pero suele ser benigno.\n\nTratamiento y evolución\nSe recomendó iniciar y continuar terapia quiropráctica dirigida a restaurar la cifosis torácica y se realizó vigilancia ambulatoria. Los síntomas (dolor torácico, dolor dorsal, palpitaciones y disnea) mejoraron gradualmente y desaparecieron en tres semanas. A un año no hubo recaídas que requirieran atención hospitalaria.\n\nImplicaciones y recomendaciones\n- El cuadro fue benigno y respondió a manejo conservador; la ecocardiografía descartó una afección estructural cardiaca significativa.\n- Recomendaciones prácticas: continuar la terapia postural/quiropraxia y vigilancia; solicitar nueva evaluación (incluida ecocardiografía) si reaparecen palpitaciones intensas, disnea persistente, síncope o dolor torácico severo.\n- Aunque infrecuente, cuando los síntomas torácicos y palpitaciones aparecen en pacientes jóvenes, conviene correlacionar examen clínico, ECG y radiografías para diferenciar causas musculoesqueléticas/estructurales benignas de enfermedades cardiacas."
+        }
+    },
+    {
+        "article": "Una mujer de 59 años con urolitiasis bilateral recurrente se presentó con dolor en el flanco derecho, fiebre y fatiga. Se le había colocado un stent doble J derecho un año antes para una piedra pélvica sintomática, pero no se le dio seguimiento. Tenía insuficiencia cardíaca derecha, diabetes tipo 2 mal controlada y enfermedad renal crónica (nadir de creatinina: 18 mg/L).\nEstable clínicamente, tenía una escala de coma de Glasgow de 14/15 (respuesta verbal ligeramente alterada), fiebre (38,3 °C), sensibilidad en el flanco derecho y una producción de orina de 800 cc en 24 horas.\nLos resultados de laboratorio revelaron una lesión renal aguda, con un nivel de creatinina sérica de 107 mg/L (normal: 6-12 mg/L) y urea sanguínea de 3 g/L (normal: 0.15-0.45 g/L). Los marcadores inflamatorios estaban elevados, con un nivel de proteína C reactiva de 300 mg/L (normal: <5 mg/L) y un recuento de glóbulos blancos de 17,000/mm3 (normal: 4000-10,000/mm3). Además, el paciente exhibió anemia normocítica (hemoglobina: 7.6 g/dL; normal: 12-16 g/dL) e hipercalemia leve (potasio sérico: 5.4 mEq/L; normal: 3.5-5.1 mEq/L). El análisis de orina y el cultivo de orina fueron negativos para infección bacteriana.\nUna tomografía computarizada abdominal y pélvica sin contraste reveló una hidronefrosis del lado derecho, un stent de doble J calcificado en espiral en ambos extremos y una piedra en la pelvis derecha de 35 × 28 mm (588 UH). El riñón izquierdo está reducido en tamaño, con hidronefrosis y una piedra en la pelvis de 12 × 7 mm (531 UH).\n\nDebido a la obstructiva severa de la pielonefritis, en particular causada por la endoprótesis incrustada, se realizó una nefrostomía percutánea bilateral urgente, lo que produjo una importante mejora clínica y normalización de los marcadores inflamatorios y la función renal.\nTres días después, la paciente experimentó una convulsión generalizada asociada con disartria. Una tomografía computarizada urgente del cerebro mostró lesiones isquémicas en los lóbulos occipitales izquierdo y frontal derecho, lo que indicaba un accidente cerebrovascular embólico. Se le inició un tratamiento con enoxaparina (0,4 cc diarios) y Kardegic (160 mg diarios) para la prevención de accidentes cerebrovasculares.\nA pesar de la mejora neurológica, cuatro días después, la paciente desarrolló palidez mucocutánea progresiva, taquicardia (110 latidos por minuto), hipotensión (80/50 mmHg) y hematuria macroscópica por el catéter urinario. Los niveles de hemoglobina descendieron de 7,5 g/dL a 4,4 g/dL, lo que levantó sospechas de hemorragia activa. Se administró fluidoterapia, vasopresores intravenosos y transfusiones de sangre, estabilizando su estado para una exploración de angiografía por TAC con contraste.\nLa tomografía computarizada reveló una colección polar media heterogénea de 17 mm de espesor con extravasación de contraste en las fases arterial y portal, lo que indica una hemorragia activa de las arterias del polo superior y medio. También había coágulos intraluminales en la pelvis renal y la vejiga. Se hizo un diagnóstico de fístula arteriovenosa postnefrostomía, exacerbada por la terapia anticoagulante para el accidente cerebrovascular.\nSe realizó una arteriografía renal urgente a través del acceso a la arteria femoral derecha, utilizando un catéter de diagnóstico de calibre 5. La angiografía selectiva reveló una FAV en el polo inferior del riñón con drenaje venoso temprano hacia la vena cava inferior, junto con un pequeño pseudoaneurisma. La embolización superselectiva con microespirales de 3 mm y 5 mm logró ocluir con éxito la fístula, y se usaron partículas de Gelfoam para evitar el sangrado retrógrado. Una inyección final de contraste confirmó la oclusión completa de la fístula, restaurando la integridad arterial y deteniendo la hemorragia.\n\nDespués de la embolización, se vigiló de cerca al paciente en la UCI. La hemodinámica se mantuvo estable y se tomó la decisión colegiada de reintroducir la anticoagulación con monitorización del INR para controlar el accidente cerebrovascular isquémico mientras se equilibraba el riesgo de hemorragia. La hematuria se resolvió, la función renal se normalizó y la nefrostomía siguió siendo funcional.\nSe adoptó un enfoque multidisciplinario para el tratamiento definitivo. La primera etapa involucró la litotripsia endoscópica con láser del bucle inferior calcificado del stent de JJ, la inserción de un segundo stent de JJ en paralelo con el incrustado y la extracción de la nefrostomía, que se completó con éxito. La segunda etapa, programada seis semanas después, incluyó una ureteroscopia derecha flexible para liberar el bucle superior del stent de JJ calcificado, la fragmentación de la piedra pélvica derecha mediante litotripsia con láser y la extracción completa del stent incrustado. Lamentablemente, la salud del paciente se deterioró debido a múltiples factores, entre ellos, insuficiencia cardíaca, diabetes mal controlada, enfermedad renal crónica y un accidente cerebrovascular previo, lo que demoró la finalización de la segunda etapa del tratamiento planificado.\n",
+        "gold_summary": "Una mujer de 59 años con urolitiasis bilateral recurrente, insuficiencia cardiaca derecha, diabetes tipo 2 mal controlada y enfermedad renal crónica se presentó con dolor en el flanco derecho, fiebre y fatiga. Previamente se le había colocado un stent doble J derecho, pero se perdió su seguimiento. Una tomografía computarizada reveló una hidronefrosis, un stent calcificado y una piedra pélvica de 22 mm, lo que llevó a la realización de una nefrostomía percutánea. La paciente desarrolló un accidente cerebrovascular embólico tres días después y posteriormente presentó hematuria, hipotensión y anemia significativa. La angiografía por TC confirmó una FAV con sangrado activo, que se trató con éxito con embolización.\n",
+        "synthetic_summary": {
+            "B1": "Una mujer de 59 años con problemas de salud y piedras en los riñones vino al hospital con dolor en el costado, fiebre y cansancio. Tenía un pequeño tubo llamado stent en el riñón que se le había puesto antes, pero nadie lo revisó después. Las pruebas y una tomografía mostraron que el stent estaba lleno de calcio y que había piedras grandes que bloqueaban el paso de la orina. Esto hacía que el riñón se hinchara y se infectara.\n\nLos médicos pusieron tubos desde la piel hasta los riñones (nefrostomías) para drenar la orina. Esto ayudó y la infección mejoró. Tres días después, la mujer tuvo una convulsión y luego un pequeño derrame cerebral por un coágulo. Le dieron medicinas para evitar más coágulos.\n\nMás tarde empezó a sangrar mucho por la orina, se puso muy pálida y su presión bajó. Las pruebas mostraron que había una conexión anormal entre una arteria y una vena en el riñón (llamada fístula arteriovenosa), que probablemente apareció después de poner los tubos y se empeoró por las medicinas para el coágulo. Los médicos hicieron una angiografía (una prueba que mira las arterias) y cerraron la conexión con pequeños espirales y material que hace tapón. Esto paró el sangrado.\n\nDespués del procedimiento ella estuvo en la UCI y se recuperó: la sangre en la orina desapareció y la función del riñón volvió a la normalidad. Los médicos planearon dos pasos para quitar el stent calcificado y romper las piedras con láser. La primera parte se hizo con éxito. La segunda parte se programó más tarde, pero se demoró porque la mujer tenía otros problemas de salud (corazón, diabetes y riñones) que la hicieron más frágil.",
+            "B2": "A 59-year-old woman with a history of repeated kidney stones, right-sided heart failure, poorly controlled type 2 diabetes, and chronic kidney disease came to the hospital with right-side flank pain, fever, and tiredness. A CT scan showed a large stone in the right kidney (about 35 × 28 mm), swelling of the right kidney from blocked urine flow (hydronephrosis), and a calcified “double‑J” ureteral stent on the right that had been left in place a year earlier. Because she had signs of an infected, obstructed kidney, doctors put in urgent percutaneous nephrostomies (tubes through the skin into each kidney to drain urine). Her infection and kidney tests improved after drainage.\n\nThree days later she had a generalized seizure and imaging showed embolic strokes (small clots in the brain). She was started on blood thinners for stroke prevention. A few days after that she developed heavy visible blood in the urine, fast heartbeat, low blood pressure, and a sharp drop in hemoglobin, indicating major bleeding. CT angiography found active bleeding from an arteriovenous fistula (an abnormal connection between an artery and a vein) in the kidney, likely created by the nephrostomy and made worse by anticoagulation.\n\nInterventional radiology performed a superselective renal angiography and treated the bleeding with coil embolization and Gelfoam particles to block the abnormal vessel. The procedure stopped the hemorrhage, the visible blood in the urine resolved, and kidney function returned to normal. Anticoagulation was restarted carefully with close monitoring because of her stroke.\n\nA multidisciplinary plan was made to remove the heavily calcified stent and treat the kidney stones in two stages using endoscopic laser procedures. The first stage (breaking the lower stent loop, adding a parallel stent, and removing the nephrostomy) was done successfully. The second stage (freeing the upper loop, fragmenting the pelvic stone, and removing the remaining stent) was planned for six weeks later but was delayed because her overall health—heart failure, poorly controlled diabetes, chronic kidney disease, and the recent stroke—worsened. The bleeding complication was managed successfully, but her complex medical problems made completing definitive treatment more difficult.",
+            "B3": "Resumen clínico (nivel universitario, lectura cuidada y empática)\n\nPaciente: mujer de 59 años con antecedentes importantes: urolitiasis bilateral recurrente, insuficiencia cardíaca derecha, diabetes tipo 2 mal controlada y enfermedad renal crónica.\n\nPresentación y hallazgos iniciales\n- Síntomas: dolor en flanco derecho, fiebre y fatiga. Tenía un stent ureteral doble J derecho colocado un año antes y sin seguimiento; el stent estaba muy calcificado.\n- Pruebas: TAC abdominopélvico mostró hidronefrosis derecha, stent doble J con incrustación en ambos extremos y una litiasis pélvica derecha grande (aprox. 35 × 28 mm). El riñón izquierdo estaba atrófico con hidronefrosis y otra piedra menor.\n- Laboratorio: marcadores inflamatorios marcadamente elevados (p. ej., PCR muy alta) y leucocitosis, lesión renal aguda con elevación de creatinina y urea, anemia normocítica y ligera hipercaliemia. El urocultivo fue negativo.\n\nPrimer manejo y respuesta\n- Por la obstrucción severa y la sospecha de pielonefritis obstructiva causada por el stent incrustado se colocaron nefrostomías percutáneas bilaterales de urgencia. Tras esto hubo mejoría clínica importante y normalización de inflamación y función renal.\n\nComplicaciones posteriores\n- A los tres días tuvo un accidente cerebrovascular isquémico embólico (lesiones en lóbulos occipital y frontal). Se inició anticoagulación (enoxaparina) y antiagregación (ácido acetilsalicílico) para prevención secundaria.\n- Cuatro días después desarrolló hematuria macroscópica, hipotensión, taquicardia y una caída rápida de la hemoglobina (de ~7,5 a 4,4 g/dL), compatible con hemorragia activa. Se estabilizó con líquidos, vasopresores y transfusiones.\n- La angio-TAC mostró extravasación de contraste desde ramas renales (hemorragia activa) y coágulos intraluminales. Se diagnosticó una fístula arteriovenosa (FAV) post-nefrostomía, posiblemente favorecida por la anticoagulación.\n\nTratamiento definitivo de la hemorragia\n- Se realizó arteriografía selectiva y embolización superselectiva (microespirales + Gelfoam). La oclusión de la fístula y del pseudoaneurisma fue exitosa y detuvo la hemorragia. Tras la embolización la hemodinámica y la hematuria se resolvieron; la nefrostomía siguió funcionando y la función renal se normalizó.\n\nPlan urológico y evolución\n- Se decidió un enfoque multidisciplinario en dos etapas: 1) litotripsia endoscópica y corte/fragmentación del asa inferior calcificada del stent, colocación de un segundo stent paralelo y retirada de la nefrostomía; 2) seis semanas después, ureteroscopia flexible para liberar y extraer el asa superior calcificada y fragmentar la litiasis pélvica derecha. La primera etapa se completó con éxito; la segunda se retrasó y no se realizó por deterioro clínico global relacionado con sus comorbilidades (insuficiencia cardíaca, diabetes mal controlada, enfermedad renal crónica y el ACV).\n\nPuntos clave e implicaciones\n- El stent ureteral retenido y muy incrustado produjo obstrucción e infección que requirieron drenaje urgente. La falta de seguimiento de los stents puede causar complicaciones graves.\n- La nefrostomía percutánea salvó la función renal y la vida al aliviar la obstrucción, pero la punción renal puede producir complicaciones vasculares raras como fístulas arteriovenosas; estas pueden sangrar de forma masiva, especialmente si el paciente recibe anticoagulación.\n- La embolización arterial selectiva es una opción eficaz y preservadora de órgano para controlar hemorragias renales por FAV/pseudoaneurisma.\n- El manejo en estos casos exige coordinación estrecha entre urólogos, radiólogos intervencionistas, intensivistas y neurológos, y un delicado balance entre prevenir eventos embólicos (requiriendo anticoagulación) y minimizar riesgo de sangrado.\n\nEmpatía y pronóstico\nEste caso ilustra la complejidad de manejar pacientes con múltiples enfermedades crónicas y procedimientos urológicos retenidos. Aunque las intervenciones endovasculares y endourológicas fueron exitosas para las complicaciones inmediatas, las comorbilidades y el ACV complicaron la recuperación y retrasaron el tratamiento definitivo. La prevención (seguimiento y extracción programada de stents) y la vigilancia estrecha tras procedimientos invasivos son medidas esenciales para evitar desenlaces similares."
+        }
+    },
+    {
+        "article": "Un hombre de 52 años fue admitido en un hospital debido a palpitaciones repentinas y fatiga general. La electrocardiografía reveló taquicardia ventricular con una frecuencia cardíaca de 180 lpm. Su ritmo cardíaco volvió a un ritmo sinusal después de una cardioversión inmediata y luego fue derivado a nuestra institución para una investigación adicional. Su historial médico pasado incluía reconstrucción del tracto de salida del ventrículo derecho utilizando un injerto homólogo y cierre de un defecto septal ventricular para TOF, que se realizó 47 años antes. Sin embargo, se perdió su seguimiento posterior. Tras ser derivado a nuestra institución, su presión arterial era de 116/70 mmHg, frecuencia cardíaca de 80 lpm, y saturación de oxígeno del 99% (con aire ambiente). Al inspeccionar la pulsación de la vena yugular, se observaron claramente una onda prominente y un descenso profundo, que eran consistentes con el aumento de la presión de llenado del ventrículo derecho y la compensación del aumento de la contracción de la RA. Cabe destacar que la auscultación reveló un murmullo diastólico regurgitante agudo en el tercer espacio intercostal izquierdo, un primer sonido cardíaco ampliamente dividido (S1) y un segundo sonido cardíaco (S2), lo que indicaba un ventrículo derecho severamente dilatado debido a la liberación de PR libre y la presencia de una válvula pulmonar no funcional. Además, se auscultó un tercer sonido cardíaco (S3) en el cuarto borde paraesternal, que era consistente con un S3 derecho. El electrocardiograma reveló bloqueo completo del haz de rama derecha, con una duración de QRS de 200 lpm. La radiografía de tórax mostró cardiomegalia con dilatación de las arterias pulmonares bilaterales. La ecocardiografía transtorácica reveló una regresión completa de la válvula pulmonar, que resultó en PR libre y una dilatación prominente del ventrículo derecho. La evaluación volumétrica del ventrículo derecho se realizó utilizando una resonancia magnética cardíaca, que reveló un volumen final diastólico del ventrículo derecho de 428 ml (índice de volumen final diastólico del ventrículo derecho de 240 ml/m2), una fracción de eyección del ventrículo derecho del 36% y una fracción de eyección de PR del 74%. Además, la tomografía computarizada multidetector mostró claramente una regresión completa de la válvula pulmonar del injerto homólogo.\n\nEl paciente se sometió a un examen con catéter para investigar más a fondo su estado hemodinámico. Su forma de onda de presión RA fue particularmente notable, ya que consistía en una onda a prominente y un descenso y, que coincidían con el cuarto sonido cardiaco (S4) y S3 en un fonocardiograma, respectivamente. Además, se reveló que la presión arterial pulmonar final diastólica y la presión final diastólica del VD eran casi idénticas debido al PR libre. Por lo tanto, la evaluación clínica del «quinteto de sonidos cardiacos», que incluye un murmullo diastólico regurgitante agudo, un S1 ampliamente dividido, un S2 único y la presencia de un S3 y un S4 derechos, se confirmó mediante una evaluación hemodinámica y anatómica multimodal como insuficiencia cardiaca derecha grave concomitante con un VD significativamente dilatado debido a la regresión completa de la válvula pulmonar y el PR libre resultante.\n\nDespués del reemplazo de la válvula pulmonar, el «quinteto de sonidos del corazón» se resolvió por completo.\n\nMH - Insuficiencia cardiaca/*etiología\nMH - Murmullos cardiacos/*diagnóstico\nMH - *Sonidos del corazón\nMH - Humanos\nMH - Hombre\nMH - Edad Media\nMH - Insuficiencia de la válvula pulmonar/*complicaciones/diagnóstico\nMH - Taquicardia, ventricular/etiología\nMH - Tetralogía de Fallot/*cirugía\nMH - Disfunción ventricular, derecha/etiología\n",
+        "gold_summary": "Un hombre de 52 años fue derivado a nuestra institución para la evaluación de una taquicardia ventricular de inicio súbito. Su historia clínica incluía una reconstrucción del tracto de salida del ventrículo derecho a los 5 años de edad. La auscultación reveló un murmullo diastólico regurgitante agudo, un primer sonido cardiaco (S1) ampliamente dividido y un segundo sonido cardiaco (S2) único, lo que indicaba un ventrículo derecho severamente dilatado debido a una regurgitación pulmonar (RP) grave y la presencia de una válvula pulmonar no funcional. Además, el tercer sonido cardiaco (S3) y el cuarto sonido cardiaco (S4) del lado derecho estaban presentes, lo que era coherente con una presión de llenado del ventrículo derecho elevada y la presencia de un ventrículo derecho no conforme. Finalmente, el mencionado «quinteto de sonidos cardiacos» se confirmó mediante una evaluación multimodal como insuficiencia cardiaca del lado derecho con un ventrículo derecho concomitantemente severamente dilatado debido a la regresión completa de la válvula pulmonar y la consiguiente RP libre.\n",
+        "synthetic_summary": {
+            "B1": "Había un hombre de 52 años que llegó al hospital porque su corazón empezó a latir muy, muy rápido y se sentía muy cansado. Los médicos lo trataron para que el latido volviera a la normalidad. \n\nCuando le escucharon el pecho, oyeron ruidos raros. Esos ruidos decían que la válvula que va del corazón a los pulmones no funcionaba. Esa válvula estaba rota y dejaba que la sangre volviera hacia atrás. Por eso, la parte derecha del corazón (la que manda sangre a los pulmones) estaba muy grande y cansada.\n\nLos médicos hicieron ecografías, una tomografía y una resonancia. También pasaron un tubito fino para medir las presiones dentro del corazón. Todo mostró lo mismo: la válvula estaba fallando por completo y el lado derecho del corazón trabajaba mal.\n\nLe cambiaron la válvula por una nueva. Después de la operación, los ruidos raros desaparecieron. En resumen: su corazón tuvo un problema grande por una válvula rota. Los médicos lo arreglaron con una operación y eso solucionó los sonidos y la falla del corazón.",
+            "B2": "Here is a clear, patient summary you can understand at a high-school level.\n\nWhat happened\n- A 52-year-old man went to the hospital because he suddenly felt very fast heartbeats (ventricular tachycardia) and was tired. Doctors restored his normal heart rhythm with an emergency shock (cardioversion).\n- As a child he had surgery for tetralogy of Fallot (a congenital heart defect). That surgery included rebuilding the outlet of the right ventricle and placing a homograft (a donated valve). He did not have follow-up care after that.\n\nKey findings and what they mean\n- Physical exam found a loud blowing sound during the heart’s filling phase (a diastolic regurgitant murmur). This comes from blood leaking backward through the pulmonary valve into the right ventricle. This leak is called pulmonary regurgitation (PR).\n- Additional heart sounds were unusual: a widely split first heart sound (S1), a single second heart sound (S2), and two extra low-pitched sounds on the right side called S3 and S4. These signs together (the authors call them a “quintet” of heart sounds) point to a severely dilated, poorly working right ventricle with high filling pressure.\n- Imaging tests confirmed the problem:\n  - Chest X-ray showed an enlarged heart and big pulmonary arteries.\n  - Echocardiography and CT showed the homograft pulmonary valve had completely failed (no working leaflets), causing free pulmonary regurgitation.\n  - Cardiac MRI measured a very large right ventricle: end-diastolic volume 428 ml (indexed 240 ml/m2) — much larger than normal — and right ventricular ejection fraction 36% (reduced pump function). The regurgitation fraction was 74% (meaning most blood was leaking back).\n- A catheter study (direct pressure measurements from inside the heart) supported these findings. Pressures in the pulmonary artery and right ventricle were almost the same at end-diastole because blood flowed freely backward through the failed valve. The wave patterns in the right atrium matched the S4 and S3 sounds heard with the stethoscope.\n\nDiagnosis and outcome\n- The team diagnosed severe right-sided heart failure caused by complete degeneration of the pulmonary homograft and massive pulmonary regurgitation. This also likely contributed to the episode of ventricular tachycardia.\n- The patient had the failed pulmonary valve replaced. After surgery, the unusual “quintet” of heart sounds disappeared, showing the valve replacement fixed the abnormal blood flow and reduced the load on the right ventricle.\n\nTakeaway (in simple terms)\n- A valve placed in childhood can wear out decades later and cause the right side of the heart to become very large and weak if not checked.\n- Symptoms can include fast, dangerous heart rhythms and tiredness. Careful physical exam, imaging, and pressure measurements can show the problem.\n- Replacing the failed valve can stop the backward leak and improve the heart’s function and sounds. Regular long-term follow-up after congenital heart surgery is important to catch valve failure early.",
+            "B3": "Resumen clínico (nivel universitario)\n\nUn hombre de 52 años ingresó tras un episodio de taquicardia ventricular súbita (180 lpm) que requirió cardioversión eléctrica. Tenía antecedentes de reparación de la tetralogía de Fallot a los 5 años (reconstrucción del tracto de salida del ventrículo derecho con un injerto homólogo y cierre de un defecto septal ventricular) y había perdido el seguimiento desde entonces.\n\nHallazgos clínicos y pruebas\n- Signos vitales al ingreso: PA 116/70 mmHg, FC 80 lpm, SaO2 99% en aire ambiente.\n- Inspección: pulso yugular con una onda prominente y un descenso profundo, compatibles con aumento de la presión de llenado del ventrículo derecho (VD) y mayor contracción auricular derecha.\n- Auscultación: \"quinteto\" de hallazgos anormales — un soplo diastólico regurgitante agudo (compatible con insuficiencia pulmonar libre), primer ruido cardíaco (S1) ampliamente dividido, segundo ruido (S2) único (ausencia de componente pulmonar), y ruidos del lado derecho S3 y S4. Estos signos apuntaban a un VD severamente dilatado y a insuficiencia cardíaca derecha.\n- ECG: bloqueo completo de rama derecha con QRS muy ancho (200 ms).\n- Radiografía de tórax: cardiomegalia y dilatación de las arterias pulmonares.\n- Ecocardiografía transtorácica y TC multicorte: regresión completa/degeneración de la válvula pulmonar del injerto homólogo y regurgitación pulmonar (RP) libre, con dilatación prominente del VD.\n- Resonancia cardíaca (evaluación volumétrica): volumen telesistólico/diastólico derecho muy aumentado — volumen telediastólico del VD 428 ml (índice 240 ml/m2), fracción de eyección del VD 36%; fracción regurgitante pulmonar 74% (indicativa de RP severa).\n- Cateterismo derecho: la onda auricular derecha mostró a una prominente y un descenso pronunciado que se correlacionaron con S4 y S3 en el fonocardiograma; la presión diastólica final pulmonar y la presión diastólica final del VD fueron casi iguales, hallazgo esperado en RP libre.\n\nInterpretación y significado\n- La regresión/degeneración completa de la válvula pulmonar del injerto causó regurgitación pulmonar libre, lo que produjo sobrecarga de volumen crónica del VD. Esto llevó a dilatación ventricular derecha marcada, disfunción sistólica (RVEF reducida) y elevación de las presiones de llenado derechas.\n- La dilatación y la alteración de la geometría ventricular, junto con la conducción alterada (QRS ancho), explican la presentación con arritmia ventricular y aumentan el riesgo de eventos arrítmicos.\n- El conjunto característico de cinco hallazgos auscultatorios (soplo diastólico regurgitante agudo, S1 ampliamente dividido, S2 único, S3 y S4 derechos) fue confirmado por estudios hemodinámicos e imagenológicos como manifestación clínica de insuficiencia cardíaca derecha por RP severa.\n\nTratamiento y evolución\n- Se realizó reemplazo de la válvula pulmonar. Tras la cirugía, los cinco hallazgos auscultatorios desaparecieron por completo, lo que refleja la corrección inmediata de la regurgitación y la mejora hemodinámica.\n\nImplicaciones prácticas\n- Los pacientes reparados de tetralogía de Fallot necesitan seguimiento cardiológico de por vida; la degeneración tardía de válvulas biológicas o injertos puede causar RP progresiva, dilatación del VD y arritmias potencialmente graves.\n- La evaluación periódica con ecocardiografía y, cuando sea necesario, resonancia cardíaca permite detectar indicación de reemplazo valvular pulmonar antes de un deterioro irreversible del VD.\n- En pacientes con RP severa y VD dilatado o síntomas/taquiarritmias, el reemplazo valvular pulmonar puede normalizar la hemodinámica y reducir los síntomas y riesgos arrítmicos.\n\nComentario empático\nEste caso ilustra la importancia del seguimiento a largo plazo después de la reparación de cardiopatías congénitas. El diagnóstico y tratamiento oportunos permitieron revertir hallazgos clínicos claros y mejorar la situación hemodinámica del paciente."
+        }
+    },
+    {
+        "article": "Un hombre de 62 años con antecedentes médicos de cardiopatía no isquémica que derivó en insuficiencia cardíaca, en estado postoperatorio de un dispositivo de asistencia ventricular izquierdo, se sometió a un trasplante cardíaco ortotópico. Mientras se recuperaba en la UCI quirúrgica, desarrolló un empeoramiento de la distensión abdominal, sensibilidad y leucocitosis, lo que motivó la evaluación por el equipo de cirugía general 6 días después del trasplante. El paciente no había evacuado ni expulsado gases desde su cirugía y no había respondido a los enemas administrados ni a la metoclopramida oral por un presunto íleo posoperatorio. Se realizó una tomografía computarizada del abdomen y la pelvis, que reveló múltiples bucles intestinales dilatados con niveles de aire-líquido y un punto de transición en el intestino delgado proximal en el cuadrante superior izquierdo, lo que generó preocupación por una obstrucción. En función de estos hallazgos y del hecho de que el paciente no había sido sometido a cirugías abdominales previas, lo que hacía que la obstrucción intestinal fuera secundaria a las adherencias, se llevó al paciente al quirófano para una laparotomía exploratoria. En el quirófano, se encontró que el intestino estaba dilatado de forma difusa sin ninguna área de isquemia aparente. Se encontró que una porción del intestino delgado estaba adherida a la pared abdominal anterior en el cuadrante superior izquierdo. Tras una exploración adicional, se encontró que una línea motriz de LVAD retenida estaba tunelizada en la cavidad peritoneal, estrangulando un bucle de intestino delgado en el cuadrante superior izquierdo. La línea motriz se liberó de la pared abdominal y se retiró, y se liberó el bucle de intestino afectado. Se encontró que era viable después de unos minutos de reperfusión. Se examinó el intestino delgado en su totalidad, desde el ligamento de Trietz distalmente hasta el intestino ciego, y se encontró que estaba dilatado pero en general era normal. Se reparó una pequeña área de desgarro seroso en el punto de adhesión a la línea motriz, principalmente. Se devolvió el intestino a la cavidad abdominal y se cerró la fascia y la piel con suturas corrientes y grapas cutáneas.\n\nMH - *Eliminación de dispositivo\nMH - Migración de cuerpos extraños/*complicaciones\nMH - Insuficiencia cardiaca/*terapia\nMH - *Trasplante de corazón\nMH - Dispositivos de asistencia cardíaca/*efectos adversos\nMH - Humanos\nMH - Obstrucción intestinal/diagnóstico por imágenes/*etiología\nMH - Laparotomía\nMH - Hombre\nMH - Edad Media\nMH - Tomografía computarizada por rayos X\nMH - Estados Unidos\n",
+        "gold_summary": "Un hombre de 62 años con antecedentes de insuficiencia cardiaca inducida por cardiomiopatía no isquémica, post-puente de asistencia ventricular izquierda y trasplante cardiaco ortotópico, presentó distensión abdominal, dolor y leucocitosis seis días después del trasplante. La TAC de abdomen y pelvis reveló bucles intestinales dilatados, niveles de aire-líquido y un punto de transición en el intestino delgado proximal. Se diagnosticó al paciente una obstrucción intestinal y se le realizó una laparotomía exploratoria. Se encontró que tenía un conducto de LVAD intraabdominal retenido que estrangulaba un bucle de intestino delgado en el cuadrante superior izquierdo. Se retiró el conducto y se liberó la sección de intestino con el retorno de la perfusión.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre de 62 años tuvo un trasplante de corazón. Antes, llevaba un aparato de asistencia que tenía un cable que salía del cuerpo. Seis días después de la operación, su barriga se hinchó, le dolía y no podía hacer caca ni expulsar gases. Los médicos vieron en una tomografía que su intestino estaba bloqueado.\n\nAbrieron la barriga para mirar. Encontraron que el cable del aparato había quedado dentro y rodeaba un tramo del intestino. El cable estaba apretando el intestino. Los cirujanos quitaron el cable y soltaron el intestino. Después de unos minutos la sangre volvió a correr y el intestino estaba bien. Repararon una pequeña rotura en la superficie y cerraron la herida.\n\nLos médicos resolvieron el problema y el intestino quedó sano. Esto muestra que a veces partes de aparatos antiguos pueden causar problemas, pero los médicos pueden encontrarlos y corregirlos.",
+            "B2": "Here is a clear summary in plain language:\n\nA 62-year-old man who had severe heart failure and previously used a left ventricular assist device (LVAD) received a new heart (orthotopic heart transplant). Six days after the transplant he developed increasing belly swelling, pain, and a high white blood cell count. He had not passed stool or gas since the surgery and did not improve with enemas or medicines for a suspected postoperative ileus (an ileus is when the intestines are slow or stopped but not blocked).\n\nA CT scan of the belly showed many dilated small-bowel loops, air–fluid levels, and a clear “transition point” in the upper left side of the small intestine — findings that suggested a mechanical bowel obstruction. Because he had not had previous abdominal surgery (making adhesions less likely), the team took him to the operating room for an exploratory laparotomy (surgically opening the abdomen to look inside).\n\nDuring surgery the small intestine was very dilated. The surgeons found that a portion of small bowel was stuck to the front abdominal wall. Further inspection revealed that the retained LVAD driveline (the cable that connects the LVAD pump to outside power) had been tunneled into the abdominal cavity and was strangling a loop of small intestine. The driveline was freed from the wall and removed, and the trapped bowel loop was released. After a few minutes of restoring blood flow (reperfusion), the affected bowel looked viable (alive and likely to recover). The surgeons checked the rest of the small intestine from the ligament of Treitz down to the cecum; it was dilated but otherwise normal. A small tear in the bowel’s outer layer where it had adhered to the driveline was repaired. The abdomen was closed.\n\nIn short: a retained LVAD driveline caused a strangulating small-bowel obstruction after heart transplant. The driveline was removed and the bowel was saved. The patient would be monitored afterward for return of bowel function, signs of infection, and healing.",
+            "B3": "Resumen (nivel universitario)\n\nUn hombre de 62 años, con insuficiencia cardiaca por miocardiopatía no isquémica que había recibido previamente un dispositivo de asistencia ventricular izquierdo (LVAD) y posteriormente un trasplante cardíaco ortotópico, desarrolló seis días después del trasplante distensión abdominal progresiva, dolor y leucocitosis. No había evacuado ni expulsado gases desde la cirugía y no respondió a medidas conservadoras (enemas y metoclopramida), por lo que se solicitó una tomografía abdominal.\n\nLa TC mostró múltiples asas intestinales dilatadas con niveles hidroaéreos y un punto de transición en el intestino delgado proximal, hallazgos compatibles con una obstrucción del intestino delgado. Dado que el paciente no tenía cirugías abdominales previas que explicaran adherencias, se decidió una laparotomía exploratoria.\n\nEn quirófano se observó dilatación intestinal generalizada pero sin zonas necróticas. El hallazgo clave fue que una línea motriz (driveline) del LVAD, retenida y tunelizada hacia la cavidad peritoneal, estaba estrangulando un asa de intestino delgado en el cuadrante superior izquierdo. El equipo liberó y retiró la línea motriz de la pared abdominal y desestranguló el asa intestinal; tras unos minutos de reperfusión la víscera quedó viable, por lo que no fue necesaria resección. Se reparó una pequeña rotura serosa en el punto de adherencia y se cerró la pared abdominal.\n\nImplicaciones y recomendaciones prácticas\n- Este caso ilustra que cuerpos extraños o componentes retenidos de dispositivos cardíacos (como la línea motriz de un LVAD) pueden migrar y producir una obstrucción mecánica por estrangulación, incluso en pacientes sin cirugías abdominales previas.  \n- La ausencia de isquemia intestinal y la recuperación tras la liberación son resultados favorables; sin embargo, la situación exigió intervención quirúrgica urgente para evitar necrosis intestinal.  \n- Es importante la revisión y eliminación completa de componentes extracorpóreos al retirar o explantar dispositivos, y mantener alta sospecha clínica de obstrucción mecánica cuando un paciente con dispositivo implantado presenta distensión y ausencia de tránsito intestinal.  \n- El seguimiento debe incluir vigilancia de la función intestinal, signos de infección o complicaciones de la herida y control cardíaco postrasplante.  \n\nSe reporta un desenlace inmediato favorable tras la intervención, con preservación del intestino afectado."
+        }
+    },
+    {
+        "article": "Un paciente de 13 años de edad, del sexo masculino, fue admitido en el Hospital de Niños de Damasco tras notar una masa palpable agrandada en la región inguinal izquierda. Su historial médico no fue notable, excepto por una intervención quirúrgica en su columna vertebral 6 años atrás, debido a un accidente, que resultó en la pérdida de la función motora y la sensación en ambas extremidades inferiores.\n\nDebido al largo período que había pasado en la cama, el paciente desarrolló úlceras de decúbito en su pie izquierdo. El único hallazgo en el examen clínico fue una masa en el área inguinal izquierda, que era móvil en las estructuras profundas y también lo era la piel que la cubría. La masa no era sensible a la palpación y no se observaron signos de inflamación local.\n\nLos exámenes de laboratorio revelaron una ESR elevada (119 mm/h en la primera hora). Se solicitaron otros exámenes básicos de laboratorio, que incluían (recuento sanguíneo completo, pruebas de función hepática, electrolitos, urea, creatinina y LDH) y estaban dentro de los rangos normales para la edad. La realización de estos exámenes fue esencial para descartar enfermedades sistémicas. Dada la ausencia de hallazgos físicos indicativos de trastornos sistémicos o inmunodeficiencias, se consideró innecesario realizar exámenes adicionales como los de VIH o antiglobulina directa.\n\nLa tomografía computarizada del abdomen, el tórax y la pelvis mostró ganglios linfáticos agrandados por debajo del ligamento inguinal, el más grande de aproximadamente 3,5 por 2,4 cm. Otros órganos y ganglios estaban dentro de los límites normales.\n\nTodas las investigaciones mencionadas fueron esenciales para descartar otros diagnósticos de alto riesgo, como linfoma y leucemia. Sin embargo, no fueron suficientes para llegar al diagnóstico definitivo, por lo que se tomó la decisión de realizar una resección quirúrgica de los ganglios.\n\nPara confirmar los diagnósticos y descartar otras posibles diferencias que pudieran presentarse con ganglios linfáticos agrandados, se realizó la extirpación quirúrgica de todos estos ganglios agrandados bajo anestesia general y se enviaron biopsias para su estudio microscópico.\n\nLa biopsia mostró una arquitectura ganglionar hiperplásica con proliferación de histiocitos y células plasmáticas con proliferación vascular, lo que es compatible con el subtipo de enfermedad de Castleman de células plasmáticas.\n\nEl paciente fue dado de alta del hospital después de 14 días, tras comprobar que no había ganglios linfáticos agrandados. La única recomendación fue prednisolona oral. El paciente se sometió a un seguimiento mediante TAC de cuerpo entero cada tres meses. Durante cada visita al hospital, se realizó un examen clínico exhaustivo y pruebas de laboratorio (por ejemplo, análisis de sangre completo, VSG, proteína C reactiva, pruebas de función hepática, pruebas de función renal), además del TAC. Después de un período de seguimiento de 12 meses, el paciente no informó de nuevos síntomas o ganglios linfáticos agrandados. Además, no se observaron anomalías durante el examen clínico o en las pruebas de laboratorio.\n",
+        "gold_summary": "Reportamos un caso único de un niño de 13 años que presentó una masa palpable agrandada en la región inguinal izquierda sin ningún síntoma constitucional. La extirpación quirúrgica de esta masa fue esencial para descartar causas preocupantes. El examen patológico reveló cambios proliferativos consistentes con el tipo de célula plasmática de la enfermedad de Castleman, que es una de las formas más raras de la enfermedad en niños. Hasta donde sabemos, este caso es el primer caso reportado de enfermedad de Castleman unicéntrica (UCD) en el área inguinal. Durante un período de seguimiento de 12 meses, no se reportaron agrandamientos adicionales de los ganglios linfáticos u otros síntomas.\n",
+        "synthetic_summary": {
+            "B1": "Había un niño de 13 años que encontró un bulto en la ingle izquierda. El bulto no dolía. El niño había pasado mucho tiempo en cama antes y tenía una úlcera en el pie, pero por lo demás estaba bien.\n\nLos médicos hicieron análisis de sangre. Una prueba mostró algo de inflamación. Otras pruebas estaban normales. También le hicieron una tomografía (una foto grande del cuerpo) y vieron ganglios linfáticos agrandados en la ingle. Los ganglios son pequeños “guardianes” que ayudan al cuerpo a luchar contra gérmenes.\n\nLos médicos sacaron los ganglios con cirugía para ver qué eran. Miraron el tejido con un microscopio. Dijeron que era enfermedad de Castleman, tipo de células plasmáticas. Esto es una enfermedad rara donde un ganglio crece más de lo normal, pero no es lo mismo que un cáncer. En este niño, solo un grupo de ganglios estaba afectado (esto se llama “unicéntrica”). Es muy raro en niños y puede ser el primer caso descrito en la ingle.\n\nEl niño salió del hospital a las dos semanas. Le dieron un medicamento para bajar la inflamación. Lo revisaron con pruebas y tomografías cada tres meses. Después de un año no tenía nuevos bultos ni otros problemas. Esto es una buena noticia.",
+            "B2": "Resumen para lectores jóvenes (nivel B2, 11–17 años)\n\nUn niño de 13 años acudió al hospital porque notó una masa en la ingle izquierda. El chico había perdido la movilidad y la sensibilidad en las piernas años antes tras un accidente y una operación de columna, por lo que pasó mucho tiempo en cama y tenía úlceras por presión en el pie. Aparte de eso, no tenía otros síntomas como fiebre, pérdida de peso ni cansancio extremo.\n\nQué encontraron los médicos\n- En la exploración física solo se vio una masa en la ingle: era móvil, no dolorosa y la piel sobre ella estaba normal.  \n- Un análisis de sangre mostró la velocidad de sedimentación globular (VSG) elevada, que indica inflamación, pero el resto de las pruebas básicas salió dentro de lo esperado.  \n- La tomografía (TAC) reveló ganglios linfáticos agrandados por debajo del ligamento inguinal; el mayor medía 3,5 × 2,4 cm. No había agrandamiento en otros órganos o ganglios.\n\nQué hicieron y por qué\n- Para descartar enfermedades graves como linfoma o leucemia y para saber exactamente qué era la masa, los médicos decidieron extirpar quirúrgicamente los ganglios agrandados y enviarlos a estudio microscópico (biopsia).  \n- La biopsia mostró un patrón llamado “subtipo de células plasmáticas” de la enfermedad de Castleman. La enfermedad de Castleman es un trastorno raro en el que los ganglios linfáticos se agrandan por cambios en las células del sistema inmune. Cuando afecta a un solo grupo de ganglios se llama “unicéntrica”.\n\nTratamiento y seguimiento\n- El paciente recibió prednisolona oral y quedó ingresado 14 días antes del alta.  \n- Se programaron controles completos cada tres meses que incluyeron TAC de cuerpo entero y análisis de sangre (para vigilar inflamación y función de órganos).  \n- Tras 12 meses de seguimiento no hubo nuevos ganglios aumentados, ni síntomas ni alteraciones en las pruebas.\n\nImportancia del caso\n- La resección quirúrgica fue clave tanto para lograr el diagnóstico como para excluir enfermedades más graves.  \n- Según los autores, este sería el primer caso descrito de enfermedad de Castleman unicéntrica en la región inguinal en un niño.\n\nSi tienes preguntas sobre esto: es normal sentir curiosidad o preocupación por enfermedades raras. Los médicos suelen usar imágenes y biopsias para saber exactamente qué ocurre y así ofrecer el mejor tratamiento.",
+            "B3": "Resumen clínico — enfermedad de Castleman unicéntrica (subtipo plasmocítico) en un niño de 13 años\n\nPresentación y antecedentes\n- Paciente: varón de 13 años, sin antecedentes médicos relevantes salvo una cirugía vertebral 6 años antes que lo dejó con pérdida de función motora y sensibilidad en ambas piernas. Por inmovilidad prolongada tenía úlceras por presión en el pie izquierdo.\n- Motivo de consulta: masa palpable en la región inguinal izquierda, indolora, móvil respecto a las estructuras profundas y a la piel, sin signos locales de inflamación ni síntomas generales (febrícula, pérdida de peso, sudoración nocturna).\n\nHallazgos iniciales\n- Laboratorio: velocidad de sedimentación globular (VSG/ESR) muy elevada (119 mm/h), lo que indica inflamación sistémica. Resto de pruebas básicas (hemograma, función hepática, electrolitos, urea, creatinina, LDH) dentro de rangos normales.\n- Imagen: tomografía computarizada (abdomen, tórax y pelvis) mostró ganglios linfáticos aumentados de volumen por debajo del ligamento inguinal; el mayor medía ≈ 3,5 × 2,4 cm. Otros órganos y ganglios normales.\n\nQué se hizo y por qué\n- Dada la preocupación por diagnósticos de alto riesgo (linfoma, leucemia) y la imposibilidad de diagnosticar con certeza solo con pruebas de imagen y laboratorio, se decidió la resección quirúrgica de los ganglios agrandados.\n- La cirugía tuvo finalidad diagnóstica y terapéutica: extirpación completa de las adenopatías con envío de biopsias para estudio histológico.\n\nDiagnóstico final (biopsia)\n- Anatomía patológica: arquitectura ganglionar hiperplásica con proliferación de histiocitos y abundantes células plasmáticas junto con proliferación vascular.\n- Interpretación: compatible con enfermedad de Castleman unicéntrica, subtipo plasmocítico. Breve nota explicativa: la enfermedad de Castleman es un trastorno linfoproliferativo poco frecuente; la forma unicéntrica afecta a un solo grupo ganglionar y suele curarse con la extirpación completa. El subtipo plasmocítico se caracteriza por abundantes células plasmáticas e inflamación.\n\nTratamiento, seguimiento y evolución\n- Alta hospitalaria: a los 14 días, sin adenopatías palpables. Se indicó prednisolona oral.\n- Vigilancia: tomografía corporal cada 3 meses y controles clínicos y analíticos regulares (hemograma, VSG, proteína C reactiva, función hepática y renal).\n- Resultado a 12 meses: asintomático, sin recurrencia de adenopatías ni alteraciones en el examen físico o en las pruebas de laboratorio.\n\nImplicaciones y puntos clave\n- La resección quirúrgica fue clave tanto para establecer el diagnóstico definitivo como para tratar la enfermedad; en la enfermedad de Castleman unicéntrica la extirpación completa suele ser curativa.\n- La VSG muy elevada señaló un proceso inflamatorio aunque el niño no mostró síntomas sistémicos.\n- Se descartaron causas graves como linfoma o leucemia mediante imagen y, finalmente, por la histología.\n- Según los autores, este es el primer caso reportado de enfermedad de Castleman unicéntrica localizada en la región inguinal en un niño, lo que subraya su rareza.\n- Recomendación razonable: continuar seguimiento periódico para detectar recurrencia o aparición de enfermedad multicéntrica, aunque el pronóstico tras resección completa es generalmente bueno.\n\nEmpatía\n- El diagnóstico fue infrecuente pero tratable. El paciente respondió bien al tratamiento y permanece sin evidencia de enfermedad a los 12 meses. Es importante que las familias mantengan el seguimiento médico programado y consulten ante cualquier nuevo bulto, fiebre persistente o pérdida de peso."
+        }
+    },
+    {
+        "article": "Un hombre asiático de 55 años de edad, que había estado recibiendo tratamiento irregularmente (el paciente no cumplía con el tratamiento) para DCMP durante los últimos 6 meses, acudió con quejas de disnea al hacer ejercicio durante 1 semana y disminución de la producción de orina durante 2 días. El paciente aparentemente estaba bien hace 1 semana cuando empezó a desarrollar disnea, inicio insidioso, gradualmente progresiva, inicialmente de grado II de la New York Heart Association (NYHA) pero progresó a grado IV de la NYHA asociada con pesadez en el pecho. La historia de ortopnea y disnea nocturna paroxística estuvo presente. Esto estuvo asociado con tos con una cantidad moderada de expectoración espumosa, no purulenta. El paciente también se quejó de hinchazón de las extremidades inferiores bilaterales. No hubo historia de hinchazón periorbital, orina espumosa o hematuria. No hubo historia de palpitación, síncope, dolor de pecho o hemoptisis. El paciente también dio una historia de una sensación de hormigueo en ambas manos y pies durante 1 mes.\n\nEl paciente había tenido un episodio similar 6 meses atrás, por el que fue hospitalizado y tratado de manera conservadora como un caso de DCMP. Se le había practicado una cirugía de cataratas en ambos ojos 15 años atrás.\n\nEn el examen físico general, el paciente estaba consciente y orientado en cuanto al tiempo, el lugar y la persona, y afebril con una presión arterial de 90/60 mmHg en el brazo derecho en posición supina y una frecuencia de pulso de 110/min, que era de bajo volumen y todos los pulsos periféricos eran palpables. Presentaba taquipnea con una frecuencia respiratoria de 28/min y palidez. Tenía un edema de pedal B/L, que era de tipo lento con presión venosa yugular elevada (JVP). No se observó ictericia, cianosis, clubbing ni linfadenopatía. Mientras se medía la presión arterial, el paciente empezó a tener espasmos en la muñeca, lo que nos dio una pista para examinar más a fondo y revelar un signo de Chvostek positivo. El signo de Trousseau también fue positivo a los 10 segundos.\n\nEl examen del sistema cardiovascular reveló un latido apical localizado en el sexto espacio intercostal izquierdo, a 1 cm fuera de la línea medioclavicular, de carácter hiperdinámico. Se escucharon S1 y S2 con normalidad en todas las áreas.\n\nEl examen del sistema respiratorio reveló una reducción de la entrada de aire en las bases pulmonares bilaterales con crepitación fina al final de la inspiración bilateral. El examen del sistema nervioso abdominal y central no reveló nada de interés.\n\n\nInvestigaciones\n\nEn el momento del ingreso, el ECG mostró bloqueo completo de rama izquierda (B-R) con un intervalo QT prolongado. La hemoglobina era de 58 g/l (133-162) con un cuadro dimórfico. El volumen corpuscular medio era de 110 fL (80,0-100,0 fL), la hemoglobina corpuscular media era de 34 pg/mL (27,0-32,0 pg/mL), la concentración media de hemoglobina corpuscular era de 36,2 g/dL (32,0-35,0 g/dL). Otros análisis revelaron niveles séricos de vitamina B12 de 135 pg/mL (211-911 pg/mL). El nivel sérico de ácido fólico era de 5,40 ng/mL (>5,38 ng/mL). El nitrógeno ureico en sangre era de 53 mg/dL (10-50) con creatinina de 0,8 mg/dL (0,7-1,3). Los resultados de las pruebas de función hepática (LFT) estaban dentro de los límites normales. El perfil de calcio mostró 4,3 mg/dL de S.calcium (8,5-10,5), fosfato 7,1 mg/dL (2,5-4,5), 3,06 g/dL de S.albumin (3,5-5,5). En vista de la hipocalcemia e hiperfosfatemia, se realizó un estudio del nivel de hormona paratiroidea intacta, que resultó ser <0,23 ng/mL (14-72). El S.magnesium era de 2,0 mg/dL (1,7-2,2). El análisis de gases en sangre arterial (ABG) fue sugestivo de una acidosis metabólica leve. El perfil tiroideo y los niveles de IgAtTG estaban dentro de los límites normales. Los niveles de ferritina y ceruloplasmina séricos estaban dentro de los límites normales. El ultrasonido abdominal y torácico mostró derrame pleural bilateral en posición supina. La vena cava inferior (IVC) y las venas hepáticas eran prominentes. El reposo dentro de los límites normales. La radiografía de tórax mostró un aplanamiento de los ángulos costofrénicos bilaterales que sugería derrame pleural bilateral. La ecocardiografía reveló un ventrículo izquierdo dilatado (LV) con una fracción de eyección del ventrículo izquierdo del 15 %, que sugería DCMP con disfunción severa del LV. Se realizó un arteriograma coronario basal que fue normal. La TC sin contraste de la cabeza mostró calcificación simétrica bilateral (B/L) en el hemisferio cerebeloso B/L, ganglios basales B/L y calcificación cortical/subcortical en la región B/L fronto-parieto-occipital. El reposo dentro de los límites normales.\n\n\nTratamiento\n\nPara el CHF, se inició al paciente con dobutamina intravenosa a una dosis de 6 µg/kg y furosemida intravenosa 20 mg BD para la descongestión. Sin embargo, el paciente no mostró una mejora significativa con el tratamiento anterior. En vista de la hipocalcemia con hiperfosfatemia y bajos niveles de hormona paratiroidea, se consideró un diagnóstico de cardiomiopatía hipocalcemica con hipoparatiroidismo y se inició al paciente con inyección de gluconato de calcio 1 g (90 mg de calcio elemental) administrado por vía intravenosa seguido de infusión de gluconato de calcio en 500 ml de dextrosa al 5% a una velocidad de 37,5 mg/hora de calcio elemental. El paciente mostró una mejora significativa después de iniciar el gluconato de calcio. El paciente fue dado de alta en condiciones estables con comprimidos de calcio por vía oral 3 g/día junto con calcitriol 0,5 µg/día. También se inició con benzotiazida con triamtereno (25/50 mg) OD, ramipril 5 mg una vez al día y carvedilol 3,125 mg dos veces al día. Para la anemia megaloblástica, se administraron inyecciones de cianocobalamina según el protocolo.\n\n\nResultado y seguimiento\n\nAl cabo de tres meses, el paciente había mejorado notablemente.\n\nLas investigaciones mostraron S.calcium 7.7, S.phosphate 6.0 y albúmina 3.6. La hemoglobina fue de 10.1 g/dL. El eco mostró una mejora en la función del LV con una fracción de eyección del 25%. Se planificó una biopsia endomiocardial, pero el paciente se negó, por lo que no pudo realizarse.\n\nMH - Gluconato de calcio/administración y dosificación/uso terapéutico\nMH - Cardiomiopatía, Dilatada/*complicaciones/diagnóstico\nMH - Ecocardiografía/métodos\nMH - Insuficiencia cardiaca/terapia farmacológica/*etiología/fisiopatología\nMH - Humanos\nMH - Hipocalcemia/*complicaciones/diagnóstico/terapia farmacológica/fisiopatología\nMH - Hipoparatiroidismo/*complicaciones/terapia farmacológica\nMH - Hombre\nMH - Edad Media\nMH - Volumen de carrera\nMH - Resultado del tratamiento\nMH - Disfunción ventricular izquierda/diagnóstico por imágenes\n",
+        "gold_summary": "Presentamos el caso de un hombre asiático de 55 años que había tenido un caso conocido de miocardiopatía dilatada durante 6 meses, que se presentó con las principales quejas de falta de aire al hacer ejercicio y disminución de la producción de orina. En el examen físico general, se observaron características que sugerían una ICC. El signo de Chvostek y Trousseau fue positivo. El paciente tenía antecedentes de cirugía de cataratas en ambos ojos 15 años atrás. Otras investigaciones revelaron una hipocalcemia. La ecografía mostró una grave hipocinesia global del ventrículo izquierdo con una fracción de eyección del ventrículo izquierdo del 15%. Esta ICC fue refractaria al tratamiento convencional, aunque, con la suplementación de calcio, el paciente mejoró sintomáticamente. En el seguimiento después de 3 meses, se observó una mejora en los parámetros ecocardiográficos con una fracción de eyección que mejoró al 25%.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre de 55 años llegó al hospital porque le costaba respirar al hacer esfuerzo y había reducido la cantidad de orina. También tenía hinchazón en las piernas y tos con algo de esputo espumoso.\n\nLos médicos vieron que su corazón estaba muy débil. Esto se llama miocardiopatía dilatada. Su corazón estaba agrandado y no bombeaba bien. También tenía signos de falta de calcio en la sangre. Por ejemplo, se le contrajo la mano cuando le pusieron la presión y tuvo pequeños espasmos en la cara. Los exámenes mostraron calcio muy bajo y una hormona llamada paratiroidea muy baja. Tenía además anemia por falta de vitamina B12.\n\nLos médicos le dieron calcio por la vena y medicinas para el corazón. También le dieron vitamina B12. Después de empezar el calcio por vía intravenosa, mejoró rápido. Tres meses después estaba mucho mejor. Su sangre y sus niveles de calcio habían mejorado. La ecografía del corazón mostró que ahora bombeaba mejor (mejoró de 15% a 25% de fracción de eyección).\n\nEn resumen: su corazón estaba débil por falta de calcio causada por un problema en las glándulas paratiroides. Al darle calcio y otros tratamientos, el paciente mejoró y se sentía mucho mejor después de tres meses.",
+            "B2": "Here is a clear, caring summary of the case:\n\nA 55-year-old man with a known weak, enlarged heart (dilated cardiomyopathy — a condition where the heart cannot pump well) came to the hospital with worsening shortness of breath, trouble breathing when lying down, swollen legs, and reduced urine output. On exam he had signs of heart failure and low blood pressure. He also had two physical signs (Chvostek and Trousseau) that suggest very low blood calcium.\n\nImportant test results:\n- Very low blood calcium (4.3 mg/dL; normal is about 8.5–10.5), high blood phosphate, and a very low parathyroid hormone (PTH) level — this points to hypoparathyroidism (the parathyroid glands are not making enough hormone, which causes low calcium).\n- Severe anemia and low vitamin B12.\n- ECG showed changes (left bundle branch block and a prolonged QT interval) that can happen with low calcium.\n- Echocardiogram showed a very weak left ventricle with ejection fraction (EF) 15% (normal EF is ~55–70%).\n- Brain CT showed symmetric calcium deposits in several brain areas, which can occur with long-standing low calcium.\n\nCourse and treatment:\nStandard heart-failure medicines and a drip to support the heart did not help much at first. When doctors started intravenous calcium (calcium gluconate) because of the low calcium and low PTH, the patient improved noticeably. He was sent home on oral calcium, active vitamin D (calcitriol), heart-failure medicines, and vitamin B12 injections. A heart biopsy was offered later but the patient declined.\n\nOutcome:\nAfter three months the patient was doing much better. His calcium had risen, hemoglobin improved, and heart function showed partial recovery (EF rose to 25%). The findings suggest his severe heart weakness was at least partly caused by very low calcium from hypoparathyroidism, and correcting the calcium helped the heart.\n\nWhat this means and possible next steps:\n- Low blood calcium can cause serious heart problems; treating the calcium deficiency can improve heart function.\n- Ongoing follow-up is needed to keep calcium and phosphate balanced, to monitor heart function, and to continue treating anemia and vitamin B12 deficiency.\n- If uncertainty about the heart’s cause remains, a biopsy can be considered, but it requires patient consent.",
+            "B3": "Resumen clínico (nivel universitario — lectura avanzada)\n\nPresentación y contexto\n- Hombre asiático de 55 años con miocardiopatía dilatada (DCMP) conocida durante 6 meses y tratamiento irregular.\n- Ingresó por empeoramiento rápido de la insuficiencia cardíaca: disnea progresiva (de NYHA II a IV en una semana), ortopnea, disnea paroxística nocturna, tos con esputo espumoso y disminución del volumen urinario durante 2 días. También refería parestesias en manos y pies durante el último mes.\n- Antecedente relevante: cirugía de cataratas bilateral hace 15 años. Hospitalizado previamente por DCMP hace 6 meses.\n\nExploración física y hallazgos relevantes\n- Signos de insuficiencia cardiacas: taquipnea (FR 28/min), taquicardia (FC 110/min), hipotensión (PA 90/60 mmHg), ingurgitación yugular, edema periférico bilateral y crepitantes finos basales pulmonares.\n- Signos neuromusculares positivos para hipocalcemia: Chvostek y Trousseau positivos.\n- Latido apical desplazado (indicador de corazón dilatado).\n- ECG: bloqueo completo de rama izquierda y QT prolongado.\n- Radiografía/ultrasonido: derrame pleural bilateral.\n\nPruebas de laboratorio e imagen\n- Anemia severa: hemoglobina 58 g/L (5.8 g/dL) con cuadro dimórfico y macrocitosis (VCM 110 fL). Niveles bajos de vitamina B12 (135 pg/mL) — compatible con anemia megaloblástica.\n- Función renal y hepática: creatinina normal (0,8 mg/dL), BUN algo elevado (53 mg/dL), LFT dentro de límites normales.\n- Alteraciones electrolíticas críticas:\n  - Calcio sérico total muy bajo: 4.3 mg/dL (normal 8.5–10.5).\n  - Fósforo elevado: 7.1 mg/dL (normal 2.5–4.5).\n  - Albúmina baja: 3.06 g/dL.\n  - Hormona paratiroidea intacta (PTH) suprimida: <0.23 ng/mL (normal 14–72) — indica hipoparatiroidismo.\n  - Magnesio normal.\n- Ecocardiograma: ventrículo izquierdo dilatado con fracción de eyección (FE) del 15% — disfunción ventricular izquierda severa.\n- Coronariografía: arterias coronarias normales (descarta isquemia coronaria como causa principal).\n- TAC craneal: calcificaciones bilaterales en ganglios basales, cerebelo y córtico-subcortical fronto-parieto-occipital — hallazgo compatible con hipoparatiroidismo crónico.\n\nDiagnóstico clínico\n- Insuficiencia cardíaca por miocardiopatía dilatada agravada por hipocalcemia severa: cardiomiopatía hipocalcémica secundaria a hipoparatiroidismo.\n- Anemia megaloblástica por déficit de vitamina B12.\n\nTratamiento y evolución\n- Terapia inicial para insuficiencia cardíaca (dobutamina IV y furosemida) proporcionó respuesta clínica insuficiente.\n- Tras identificar hipocalcemia con PTH baja, se inició reposición con gluconato de calcio IV (bolo 1 g seguido de infusión continua) y posteriormente suplemento oral de calcio (3 g/día) y calcitriol (0,5 µg/día).\n- También recibió tratamiento para la anemia con inyecciones de cianocobalamina.\n- Se añadieron terapia establecida para insuficiencia cardíaca (ramipril, carvedilol, tiazídico combinado con triamtereno).\n- Respuesta: mejoría clínica rápida tras la corrección de calcio; a los 3 meses, calcio sérico 7.7 mg/dL, fósforo 6.0 mg/dL, Hb 10.1 g/dL y FE del VI aumentó a 25% (mejoría parcial). Se planeó biopsia endomiocárdica, pero el paciente la rechazó.\n\nInterpretación e implicaciones\n- La hipocalcemia grave por hipoparatiroidismo fue el factor reversible que agravó la función ventricular en este paciente. La normalidad arterial coronaria y la mejoría de la FE tras corregir el calcio apoyan la relación causal (cardiomiopatía hipocalcémica).\n- Las calcificaciones intracraneales y la presencia de signos clínicos de hipocalcemia (Chvostek/Trousseau) sugieren un hipoparatiroidismo de larga evolución.\n- La anemia megaloblástica coexistente probablemente contribuyó a la fatiga y la anemia severa al ingreso; mejoró con suplementación de vitamina B12.\n\nRecomendaciones y próximos pasos clínicos (prácticos)\n- Continuar substitución oral de calcio y calcitriol, con controles periódicos de calcio total y calcio corregido por albúmina, fósforo, magnesio y función renal.\n- Vigilar signos de exceso de tratamiento (hipercalcemia, hiperparatiroidismo secundario renal, riesgo de nefrolitiasis) y realizar control de calcio urinario si procede.\n- Investigar la causa subyacente del hipoparatiroidismo (quirúrgica, autoinmune, genética, etc.) y considerar pruebas específicas según la sospecha clínica.\n- Seguimiento cardiológico con ecocardiogramas seriados para valorar recuperación ventricular y ajuste de terapia para insuficiencia cardíaca.\n- Adherencia al tratamiento y educación del paciente sobre síntomas de hipocalcemia/hipercalcemia.\n- Evaluación continua y suplementación para la anemia por déficit de B12 si persiste.\n\nComentario final (tono humano)\nEste caso ilustra que causas metabólicas tratables, como la hipocalcemia por hipoparatiroidismo, pueden precipitar o agravar una miocardiopatía grave. La identificación y corrección de la alteración electrolítica permitió una mejoría clínica y parcial recuperación de la función cardíaca. Es importante el seguimiento estrecho y la investigación de la causa del hipoparatiroidismo para evitar recurrencias y complicaciones a largo plazo."
+        }
+    },
+    {
+        "article": "Una mujer de 54 años de edad, libanesa, en hemodiálisis (HD) de mantenimiento tres veces por semana para glomeruloesclerosis segmentaria focal (GSF) fue admitida en el departamento de urgencias, luego de haber sido sometida a su HD programada la noche anterior, debido al inicio repentino de un dolor lumbar agudo en el lado izquierdo, náuseas y vómitos. El dolor había comenzado repentinamente cerca de 12 horas antes de su presentación y se agravó rápidamente. En una nota al margen, un hiperparatiroidismo secundario grave con calcificación cutánea vascular fue tratado con cinacalcet durante 3 años sin respuesta, lo que demandó una paratiroidectomía (hiperplasia de cuatro glándulas) 8 meses antes de su presentación actual. Cinco días antes de su presentación, fue admitida en el hospital debido a anemia grave y rectorragia. Su evaluación por ultrasonido renal mostró riñones bilaterales pequeños con parénquima delgado que contenía quistes de hasta 3 cm y calcificaciones vasculares sin hidronefrosis. Cuatro días antes de su presentación, la colonoscopia a través del íleo terminal reveló un pólipo de 7 mm en el colon descendente izquierdo, que fue removido por mucosectomía. La microscopía volvió como adenoma tubular sésil con displasia de bajo grado. La paciente negó fiebre o antecedentes de trauma. No hubo antecedentes previos de uso de antiplaquetarios. En la emergencia, su presión arterial y pulso fueron de 112/65 mmHg y 96 bpm, su temperatura fue de 36.8°C y presentaba abdomen levemente distendido, con dolor importante en el ángulo costovertebral izquierdo. Los hallazgos de laboratorio mostraron hemoglobina de 9.0 g/dL mientras que el hematocrito fue de 29.7%, recuento total de leucocitos 12.2 × 1000/microlitro, creatinina de 6.06 mg/dL, y nivel de proteína C reactiva de 6 mg/L. Además, el TP fue de 83% y el INR fue de 1.13. En el día de la presentación (es decir, 4 días después de la colonoscopia), se realizó una tomografía computarizada (TC) multifásica del tórax, abdomen y pelvis con y sin contraste intravenoso. El examen reveló un gran quiste y enormes hematomas intraparenquimatosos perirrenales izquierdos con una colección subcapsular de hasta 1,8 cm de espesor con colección hemática en todo el compartimiento renal que alcanzaba un diámetro de más de 9 × 4 cm, hidronefrosis izquierda y edema alrededor de la grasa en todo el flanco y calcificaciones en el hilo. Para la descompresión del sistema pélvico renal y drenaje, optamos por tratarla con inserción retrógrada de doble stent ureteral a la izquierda, que identificó un coágulo en la parte media del uréter izquierdo. Se realizaron cultivo de orina y citología y los resultados fueron negativos. Una simple radiografía del abdomen mostró el doble J en su lugar. La paciente permaneció hemodinámicamente estable, pero presentó una nueva caída en la hemoglobina (6.1 g/dL) la misma noche, lo que exigió una transfusión de una unidad de concentrado de eritrocitos leucodepleados para estabilización. Se tomó la decisión de explorar quirúrgicamente con diagnóstico presuntivo de hematoma perirrenal izquierdo subagudo y para excluir una malignidad subyacente. Se sometió a una sesión de HD sin heparina. En el tercer día, se sometió a una nefrectomía radical abierta a la izquierda con conservación de la glándula suprarrenal. Recibió 2 unidades más de concentrado de eritrocitos leucodepleados durante la intervención. El parénquima renal fue casi totalmente reemplazado por un hematoma que medía 9 × 9 × 7 cm y se extendía hasta la grasa perirrenal. Una pequeña masa papilar fue enviada por separado para análisis. La evaluación histopatológica detallada reveló un parénquima renal con lesiones de nefritis crónica mutilada por grandes áreas hemorrágicas que se extendían hasta la grasa perirrenal. Además, había una proliferación neoplásica de 2 mm, con arquitectura papilar cubierta por pequeñas células cúbicas atípicas y macrófagos espumosos en el eje, compatibles con adenoma papilar. Al día siguiente de la operación, la paciente fue sometida a HD y recibió un paquete de eritrocitos leucodepleados. El período postoperatorio fue sin intercorrerencias. El nivel de hemoglobina se mantuvo alrededor de 10 g/dL. La paciente se recuperó sin signos o síntomas de sangrado. La paciente permanece bien y asintomática y actualmente se encuentra en HD de mantenimiento regular.\n",
+        "gold_summary": "A continuación, se describe un caso inusual de una paciente con HD de 54 años de edad que presentó HPE pocos días después de una colonoscopia. La causa de la HPE fue la ruptura de un quiste de DRCA. Consideramos que la colonoscopia fue un factor desencadenante y planteamos hipótesis sobre su etiopatogenia. La paciente se sometió a una nefrectomía izquierda exitosa.\n",
+        "synthetic_summary": {
+            "B1": "Esta es la historia en palabras sencillas.\n\nUna mujer de 54 años hacía diálisis tres veces por semana. La diálisis es cuando una máquina limpia su sangre porque sus riñones no trabajan bien.\n\nCuatro días después de hacerse una colonoscopia (un examen del intestino), comenzó a sentir un dolor fuerte en el costado izquierdo. También tenía náuseas y vómitos. Fue al hospital.\n\nLas pruebas por imágenes mostraron que tenía un gran coágulo de sangre alrededor del riñón izquierdo. Esto ocurrió porque se rompió un quiste (una bolsita con líquido) en ese riñón. Los médicos piensan que la colonoscopia pudo haber sido la causa que lo desencadenó.\n\nPrimero le pusieron un tubo para ayudar a drenar la orina y un coágulo dentro del uréter. Pero como el riñón estaba muy dañado y lleno de sangre, la tuvieron que sacar en una operación (nefrectomía), es decir, remover el riñón izquierdo. Durante la cirugía recibió transfusiones de sangre.\n\nEl estudio del riñón mostró que había mucho daño por sangrado. También encontraron una pequeña masa que resultó ser un adenoma papilar, que es un tumor pequeño y benigno (no canceroso).\n\nDespués de la operación, la mujer se recuperó bien. No volvió a sangrar y su hemoglobina se mantuvo estable. Sigue en diálisis regular. Los médicos la vigilan y está bien ahora.",
+            "B2": "Here is a clear, patient-friendly summary of the case.\n\nA 54-year-old woman on long-term hemodialysis (dialysis is a machine treatment that filters the blood when the kidneys do not work) came to the emergency room with sudden, severe pain in her left side, nausea, and vomiting. This happened four days after she had a colonoscopy in which a small polyp was removed.\n\nKey findings and what the doctors did\n- A CT scan showed a large bleed around and inside her left kidney (a perirenal and intraparenchymal hematoma). There was also fluid collecting under the kidney capsule and swelling of the kidney collecting system (hydronephrosis).\n- The team placed a ureteral stent (a small tube that helps urine drain from the kidney to the bladder) and found a blood clot in the ureter. She received blood transfusions because her hemoglobin dropped dangerously low.\n- Because the kidney was mostly replaced by the blood collection and the cause needed to be clarified, the doctors performed a left radical nephrectomy (surgical removal of the left kidney). The adrenal gland was left in place.\n\nWhat the tests showed\n- Pathology (microscope examination) found that the kidney had chronic damage from long-term kidney disease and large hemorrhagic (bleeding) areas that extended into the fat around the kidney.\n- A tiny 2 mm papillary adenoma (a small benign tumor) was also found, but no cancer was identified.\n- The bleeding was caused by rupture of a cyst related to acquired cystic kidney disease (this is common in people on long-term dialysis and means small cysts form in the kidneys).\n\nOutcome and possible cause\n- After surgery she recovered without complications, received further dialysis and blood transfusion as needed, and remained stable with no more signs of bleeding.\n- The team thinks the recent colonoscopy may have triggered the cyst rupture and bleeding, although the exact reason is uncertain.\n\nIn simple terms: a woman on long-term dialysis developed a sudden, serious kidney bleed a few days after a colonoscopy. Treatment included a drain tube, blood transfusions, and removal of the damaged kidney. She recovered well, and the bleeding was linked to a ruptured dialysis-related kidney cyst.",
+            "B3": "Resumen clínico (nivel universitario — lectura avanzada)\n\nPresentación y antecedentes\n- Paciente: mujer libanesa de 54 años en hemodiálisis crónica (3 veces/semana) por esclerosis focal y segmentaria.\n- Antecedentes relevantes: enfermedad renal crónica con riñones pequeños y quistes (en ecografía), múltiples calcificaciones vasculares; hiperparatiroidismo secundario tratado finalmente con paratiroidectomía 8 meses antes. No tomaba antiplaquetarios.\n- Procedimientos recientes: 5 días antes tuvo anemia y rectorragia; 4 días antes se le realizó colonoscopia con polipectomía (pólipo de 7 mm, adenoma tubular sésil con displasia de bajo grado).\n\nCuadro actual y hallazgos iniciales\n- Motivo de ingreso: dolor lumbar izquierdo agudo, náuseas y vómitos con inicio súbito ~12 horas antes de la consulta.\n- Signos vitales: hemodinámica relativamente estable; dolor a la palpación en ángulo costovertebral izquierdo.\n- Laboratorio: anemia (Hb 9 g/dL al ingreso), leucocitosis leve, creatinina elevada (6.06 mg/dL — esperado en paciente en HD), inflamación leve (PCR 6 mg/L), coagulación dentro de límites aceptables (INR 1.13).\n- Imagen: TC multifásica mostró hematoma intrarrenal e importante colección hemática perirrenal izquierda (subcapsular y que ocupaba el compartimento renal, hasta >9 × 4 cm), quiste renal grande, hidronefrosis izquierda y edema de la grasa perirrenal.\n\nManejo inicial\n- Se realizó colocación retrógrada de stent ureteral doble-J izquierdo para descomprimir el sistema pielocalicial; se observó un coágulo en el uréter medio.\n- Cultivo urinario y citología: negativos.\n- A pesar de estabilidad hemodinámica inicial, la paciente presentó caída de hemoglobina a 6.1 g/dL la misma noche, que requirió transfusión de glóbulos rojos leucodepletados.\n\nDecisión terapéutica y hallazgos quirúrgicos\n- Dado el hematoma perirrenal subagudo de gran tamaño y la necesidad de excluir una lesión maligna subyacente, se optó por cirugía exploratoria.\n- Tercero día: nefrectomía radical izquierda abierta (suprarrenal preservada). Durante la intervención se transfundieron 2 unidades adicionales.\n- Hallazgo operatorio: el parénquima renal casi totalmente reemplazado por un hematoma de 9 × 9 × 7 cm que se extendía a la grasa perirrenal; se remitió además una pequeña masa papilar para estudio.\n\nAnatomía patológica y diagnóstico final\n- Macroscópicamente y microscópicamente: riñón con cambios crónicos (nefritis crónica) y áreas extensas de hemorragia que invadían la grasa perirrenal.\n- pequeña lesión neoplásica (2 mm) con arquitectura papilar y células cúbicas atípicas, compatible con adenoma papilar (lesión benigna).\n- Conclusión clínica: hematoma perirrenal izquierdo secundario a ruptura de un quiste asociado a enfermedad renal quística adquirida (DRCA/ACKD) en un paciente en hemodiálisis.\n\nEvolución y desenlace\n- Postoperatorio sin complicaciones significativas; pacientes continuó en HD (sin heparina previa a la cirugía) y recibió transfusiones según necesidad.\n- Hemoglobina estabilizada alrededor de 10 g/dL; sin signos de sangrado recurrente.\n- Actualmente asintomática y en hemodiálisis de mantenimiento.\n\nInterpretación y puntos clave (implicaciones clínicas)\n- Complicación rara pero grave: la rotura espontánea de quistes renales en pacientes con enfermedad renal crónica en diálisis puede producir hematoma intrarrenal/perirrenal masivo que amenaza la estabilidad y puede requerir nefrectomía.\n- Factores predisponentes: enfermedad renal crónica avanzada con quistes (ACKD), alteraciones vasculares y procedimientos recientes (en este caso se plantea que la colonoscopia/polipectomía pudo ser un factor desencadenante, aunque la relación causal no puede probarse definitivamente).\n- Manejo recomendado en casos similares: evaluación rápida con TC, estabilización hemodinámica y transfusional, medidas de descompresión si procede (p. ej., stent ureteral) y, cuando existe hemorragia extensa o duda sobre malignidad, exploración quirúrgica/nephrectomía. La histología es esencial para descartar cáncer renal, que tiene mayor incidencia en ACKD.\n- Resultado favorable en este caso: resolución del sangrado, lesión papilar benigna en anatomía patológica y recuperación sin recurrencia de hemorragia.\n\nComentario empático\nLa paciente presentó un evento agudo grave que exigió intervenciones rápidas y finalmente una nefrectomía. Aunque la situación fue seria, la atención multidisciplinaria permitió controlar la hemorragia, confirmar el diagnóstico y lograr una buena recuperación. Este caso resalta la importancia de la vigilancia en pacientes en diálisis con quistes renales y la necesidad de considerar complicaciones hemorrágicas después de procedimientos endoscópicos, aun cuando la relación causal no esté confirmada."
+        }
+    },
+    {
+        "article": "Se evaluó a una mujer de 30 años de edad con antecedentes de dos meses de dolor progresivo y disminución de la visión OD. Dos semanas antes del desarrollo de los síntomas oculares, la paciente comenzó a disminuir la prednisona como tratamiento para sus síntomas inflamatorios sistémicos. Los antecedentes médicos incluyen artritis inflamatoria, síntomas gastrointestinales que sugieren enfermedad intestinal inflamatoria y pérdida de peso de 20 libras antes de la presentación. Los detalles completos del caso de la paciente se informaron previamente y se resumen aquí junto con análisis adicionales de quimiocina y citoquina de fluido ocular.13\n\nEn el examen, las BCVAs fueron 20/40 OD y 20/20 OS, y las pupilas fueron 9 mm y akinéticas OD y 5 mm con una rápida reactividad a la luz OS. Las presiones intraoculares fueron 65 mmHg OD y 21 mmHg OS. El examen con lámpara de hendidura mostró precipitados queráticos granulomatosos pigmentados (KP) dentro de la córnea inferior, 3+ células de la cámara anterior, atrofia difusa del iris con pigmento en las zónulas, y ectropion uvea OD, y OS fue normal. La gonioscopia mostró 3+ células pigmentadas dentro del ángulo inferior OD. El examen del fondo fue normal en ambos ojos. Una paracentesis anterior diagnóstica fue positiva para ADN de VZV mediante pruebas de PCR, y las pruebas serológicas fueron positivas para anticuerpos IgG de VZV. Posteriormente, se le diagnosticó uveítis anterior hipertensiva asociada a VZV, lo que provocó el inicio de acetazolamida oral y timolol oftálmico, dorzolamida, y brimonidina para la hipertensión ocular, así como valaciclovir 1 g TID y acetato de prednisolona 1% cada 2 horas. El curso de la enfermedad de la paciente y otros detalles de su tratamiento se describieron previamente.13\n\nLa paciente fue diagnosticada con un accidente cerebrovascular (ACV), que se cree que se debe a una vasculopatía del SNC asociada al VVZ, y fue hospitalizada durante 2 semanas, durante las cuales sus síntomas oculares mejoraron gradualmente. Sin embargo, dos meses después de su ACV, desarrolló un empeoramiento del dolor y la visión en el ojo derecho, y su BCVA disminuyó a 20/100 con una PIO elevada de 39 mmHg OD. El examen reveló una inyección ciliar 1+ y 3+ células de la cámara anterior, y se cambió de prednisolona a difluprednato con una mejora mínima. Posteriormente, se sometió a un procedimiento de filtración de glaucoma con una derivación de Ahmed debido a su PIO elevada persistente a pesar de la máxima tolerancia de la terapia ocular hipertensiva. Se obtuvo una muestra de humor acuoso del ojo derecho durante la cirugía de filtración para un análisis de perfil de quimiocina/citoquina. Se estimaron los niveles de 22 citoquinas y quimioquinas, incluidos IFN-Y, IL-10, IL-12p70, IL-17A, IL-1B, IL-2, IL-5, IL-6, IL-8, TNF-a, IL-18, IL-1RA, IL-1a, IL-1a, IP-10, MCP-1, MIP-1a, MIP-1B, SDF-1a, IL-21, IL-22, IL-23 e IL-27, utilizando la técnica de inmunoensayo de perlas múltiplex. Se detectaron niveles de concentración de 7 citoquinas/quimioquinas, incluidos IL-6, IL-8, IL-18, MIP-1b, IP-10, MCP-1, e IL-1RA. La IL-1RA fue la citoquina más abundante (1000 pg/mL), mientras que IP-10 y MCP-1 fueron las segundas citoquinas más abundantes (150–200 pg/mL). Se detectaron niveles de 10–20 pg/mL de IL-18 y MCP-1b, pero a niveles mínimos en esta muestra de AqH. Se detectaron niveles de IL-6 e IL-8, pero se encontró que eran las citoquinas menos abundantes, cada una con niveles de <10 pg/mL.\n\n",
+        "gold_summary": "El caso 2 fue el de una mujer de 30 años con antecedentes de dos meses de dolor progresivo y disminución de la visión en el ojo derecho. Se le diagnosticó uveítis anterior hipertensiva tras una paracentesis diagnóstica de la cámara anterior. A pesar de la terapia exitosa para la uveítis anterior, su presión intraocular se mantuvo elevada y requirió un procedimiento de filtración de glaucoma. Se recolectó una muestra de fluido ocular en el momento de la cirugía para el análisis de perfiles de citoquinas/quimioquinas, y se detectaron niveles de 7 citoquinas/quimioquinas, entre ellas, IL-6, IL-8, IL-18, MIP-1B, IP-10, MCP-1 e IL-1RA, siendo IL-1RA la citoquina más abundante.\n",
+        "synthetic_summary": {
+            "B1": "This is a simple and kind summary of the case.\n\nA 30-year-old woman had two months of pain and worse sight in her right eye. She also had body inflammation and had been lowering her steroid medicine. Doctors found her right eye was very inflamed and the eye pressure was very high. A special test found varicella zoster virus (the chickenpox/shingles virus) in the front part of her eye. This caused “anterior hypertensive uveitis,” which means the front of the eye was inflamed and the eye pressure went up.\n\nShe was given medicine for the virus, eye drops, and steroid drops. Later she had a stroke that doctors thought was linked to the same virus. Her eye got a little better, but the eye pressure stayed high. Because the pressure would not fall with medicines, she had glaucoma surgery (an Ahmed valve) to help drain fluid and lower the pressure.\n\nDuring the surgery, doctors took a tiny sample of eye fluid to study inflammation signals called cytokines and chemokines. They tested for 22 different signals and found 7 of them. The most common signal was IL-1RA (about 1000 units). Two others (IP-10 and MCP-1) were next highest (about 150–200). Several others were present at low amounts.\n\nWhat this means: the virus caused inflammation in the eye and high pressure. The surgery was needed because medicines could not control the pressure. The fluid test helped doctors see which inflammation signals were active in her eye.",
+            "B2": "Here is a clear summary of the case in plain, caring language.\n\nA 30-year-old woman had two months of increasing pain and worsening vision in her right eye. She also had a history of inflammatory arthritis, gut symptoms that suggested inflammatory bowel disease, and recent weight loss. Two weeks before her eye problems began she had reduced the dose of prednisone, a steroid she had been taking for inflammation.\n\nOn exam her right vision was worse than the left and her right pupil was large and not reacting to light. The pressure inside her right eye was very high (65 mmHg; normal is under about 21 mmHg). The front part of the eye showed signs of inflammation: pigmented deposits on the cornea, many inflammatory cells in the front chamber, and damage to the iris. A small sample of fluid from the front of the eye (an anterior chamber paracentesis) tested positive by PCR for varicella zoster virus (VZV), the virus that causes chickenpox and shingles. This led to a diagnosis of VZV-associated hypertensive anterior uveitis. (“Uveitis” means inflammation inside the eye; “hypertensive” here means it caused high eye pressure.)\n\nShe was treated with antiviral medication (valacyclovir), topical and oral medicines to lower eye pressure, and steroid eye drops to reduce inflammation. While hospitalized later with a stroke believed to be caused by VZV affecting blood vessels in the brain, her eye symptoms improved. But two months after the stroke she had a flare: increased pain, worse vision in the right eye (20/100), and a high pressure of 39 mmHg despite strong medical therapy. Steroid drops were switched with little benefit, so she underwent glaucoma filtration surgery with an Ahmed drainage valve to control the pressure.\n\nAt the time of surgery a sample of the eye fluid was tested for immune signaling proteins called cytokines and chemokines. These small proteins help the immune system communicate during inflammation. Of 22 tested, seven were detected: IL-6, IL-8, IL-18, MIP-1β, IP-10, MCP-1, and IL-1RA. The most abundant was IL-1RA (about 1,000 pg/mL), a natural blocker that can reduce inflammation. IP-10 and MCP-1 were present at moderate levels (around 150–200 pg/mL). IL-18 and MIP-1β were low (about 10–20 pg/mL), and IL-6 and IL-8 were very low (<10 pg/mL).\n\nIn short: this patient had VZV-related inflammation inside the eye that led to very high eye pressure and eventually required surgical drainage. Testing of her eye fluid showed a mix of immune signals, with IL-1RA notably high, which may reflect the eye’s attempt to limit inflammation. Continued antiviral treatment and pressure control were key parts of her care.",
+            "B3": "Resumen (nivel B3)\n\nPresentación y antecedentes\n- Mujer de 30 años con dos meses de dolor progresivo y pérdida de visión en el ojo derecho (OD). Dos semanas antes de los síntomas oculares había reducido la prednisona que tomaba por cuadros inflamatorios sistémicos (artritis, síntomas gastrointestinales y pérdida de peso).\n- Importante antecedente: evolución posterior complicada por un accidente cerebrovascular (ACV), atribuido a vasculopatía del sistema nervioso central asociada a varicela zóster (VVZ).\n\nHallazgos clínicos clave\n- Agudeza visual mejor corregida: 20/40 OD (ojo afectado) y 20/20 OS (ojo izquierdo).\n- Pupila derecha dilatada (9 mm) y acinética; pupil izquierda con reacción rápida.\n- Presiones intraoculares: 65 mmHg OD (muy alta; normal ≈ 10–21 mmHg) y 21 mmHg OS.\n- Examen con lámpara de hendidura en OD: precipitados queráticos granulomatosos pigmentados, 3+ células en cámara anterior (inflamación activa), atrofia difusa del iris con pigmento en zónulas y ectropion uvea. Gonioscopia: células pigmentadas en el ángulo. Fondo de ojo normal en ambos.\n- Prueba diagnóstica en humor acuoso positiva por PCR para ADN de VVZ; serología positiva para IgG de VVZ.\n\nDiagnóstico y tratamiento\n- Diagnóstico: uveítis anterior hipertensiva secundaria a infección por VVZ, con hipertonía ocular persistente a pesar de terapia médica máxima.\n- Tratamiento inicial: antivírico oral (valaciclovir 1 g tres veces al día), corticoides tópicos (acetato de prednisolona 1% cada 2 horas, luego cambio a difluprednato), y múltiples fármacos para reducir la presión intraocular (acetazolamida oral; timolol, dorzolamida y brimonidina tópicas).\n- Debido a la presión intraocular refractaria (persistió elevada tras tratamiento), se realizó cirugía filtrante con implante de válvula de Ahmed. Durante la cirugía se obtuvo humor acuoso para análisis de citoquinas/quimioquinas.\n\nAnálisis de citoquinas/quimioquinas en humor acuoso\n- Se midieron 22 mediadores; se detectaron 7: IL-1RA, IP-10 (CXCL10), MCP-1 (CCL2), IL-18, MIP-1β, IL-6 e IL-8.\n- Concentraciones observadas (aprox.):\n  - IL-1RA: la más alta, ~1000 pg/mL.\n  - IP-10 y MCP-1: segundas más abundantes, ~150–200 pg/mL.\n  - IL-18 y MIP-1β: ~10–20 pg/mL (niveles bajos).\n  - IL-6 e IL-8: <10 pg/mL (las menos abundantes en esta muestra).\n- Interpretación preliminar: el alto nivel de IL-1RA (antagonista de la señalización proinflamatoria de IL-1) sugiere una fuerte respuesta antiinflamatoria compensatoria en el ojo. IP-10 y MCP-1 son quimioquinas relacionadas con reclutamiento de linfocitos T y monocitos, consistentes con una respuesta inmune dirigida frente a infección viral. Niveles bajos de IL-6/IL-8 son llamativos y pueden reflejar la fase de la enfermedad, efecto del tratamiento o particularidades de la respuesta inmune local en VVZ.\n\nImplicaciones y pasos a seguir\n- Clínicamente, la paciente necesitó cirugía por glaucoma secundario a uveítis por VVZ; el ACV atribuido a vasculopatía por VVZ subraya la naturaleza sistémica y potencialmente grave de la infección.\n- El perfil de citoquinas aporta información sobre la inflamación intraocular: la elevada IL-1RA podría indicar control parcial de la inflamación, mientras que IP-10 y MCP-1 respaldan la participación de respuestas celulares frente al virus.\n- Recomendaciones prácticas: seguimiento estrecho de la presión intraocular y de la función visual, mantenimiento/ajuste del tratamiento antiviral según evolución, control neurológico por riesgo de recurrencia de vasculopatía por VVZ, y considerar investigación adicional (serie de pacientes) para correlacionar perfiles de citoquinas con pronóstico y respuesta terapéutica.\n\nComentario empático\n- Este caso muestra cómo una infección por VVZ ocular puede provocar inflamación intensa, glaucoma secundario y complicaciones sistémicas graves. Es comprensible que la situación haya sido angustiante; el manejo incluyó terapia antiviral, antiinflamatoria y cirugía para proteger la visión, y los hallazgos de laboratorio ayudan a entender la respuesta inmunitaria local."
+        }
+    },
+    {
+        "article": "Un varón negro de 2021 g de peso nació a las 35 semanas y tres días de edad gestacional estimada por repetición de cesárea debido a la preocupación por la disminución del movimiento fetal en el contexto de una puntuación de perfil biofísico baja (basada en el tono muscular, la frecuencia cardíaca, el movimiento, la respiración y el volumen de líquido amniótico). La historia materna fue notable por el rasgo de células falciformes, la edad materna avanzada y la obesidad. La historia del embarazo fue notable por oligohidramnios observados por ultrasonografía a las 31 semanas. La ecografía fetal también mostró distensión de la vejiga, hidroceles bilaterales, dilatación de la uretra y ascitis abdominal preocupantes por la obstrucción del tracto urinario inferior y la posible ruptura de la vejiga. La ruptura de membranas ocurrió al momento del parto.\n\nAl nacer, el bebé experimentó dificultad respiratoria y fue tratado con ventilación con presión positiva, oxígeno suplementario e intubación. Las puntuaciones de Apgar fueron de dos y siete a un minuto y cinco minutos de vida, respectivamente. El examen mostró hematomas sustanciales y oscurecimiento de la extremidad superior izquierda. El bebé fue trasladado a la unidad de cuidados intensivos neonatales para el tratamiento de la dificultad respiratoria y sospecha de obstrucción del tracto urinario inferior. En la evaluación realizada dentro de la hora posterior al nacimiento por especialistas en ortopedia y cirugía plástica, el tercio distal del antebrazo y la mano estaban cianóticos, y una gran ampolla y área circundante de descamación eran evidentes en el dorso de la mano. No se observó movimiento espontáneo de la extremidad superior izquierda, y no se provocó la retirada o respuesta a los estímulos. La ecografía Doppler mostró flujo arterial al nivel de la fosa antecubital, pero no se detectaron pulsos radiales o cubitales. Los hallazgos del examen físico fueron consistentes con NCS, probablemente debido a la compresión de la pared uterina debido a oligohidramnios durante el embarazo.\n\nDespués de aproximadamente 5 horas de exámenes en serie, así como una amplia discusión con los equipos de ortopedia, cirugía plástica, neonatología y anestesia pediátrica, así como con los padres del bebé, se tomó la decisión de realizar una fasciotomía descompresiva del antebrazo, la mano y el túnel carpiano para permitir el rescate de la extremidad. La fasciotomía se realizó aproximadamente 6 horas después del nacimiento. El bebé fue monitoreado de cerca durante los siguientes días. La apariencia de la extremidad superior izquierda mejoró gradualmente. Al tercer día de vida, el antebrazo y la mano habían mejorado notablemente en color y parecían bien vascularizados. Las señales Doppler estaban presentes en todo momento, desde la arteria braquial hasta cada dedo. Se permitió que las heridas de la fasciotomía se curaran por intención secundaria, y se aplicó una férula personalizada con la muñeca en posición neutra y los dedos extendidos. No hubo signos de infección o isquemia en curso. Las heridas se curaron bien a las seis semanas de edad. En la visita de seguimiento a los cuatro meses de edad, las heridas se curaron por completo. El paciente tenía un rango de movimiento pasivo completo de la muñeca y los dedos. Se observó que tenía una ligera flexión y extensión del dedo anular y meñique, pero por lo demás, un movimiento activo mínimo de la muñeca o la mano en este momento. Tenía un movimiento activo del hombro y el codo. El paciente continuará recibiendo terapia ocupacional, así como férulas y masaje de cicatrices para prevenir/minimizar las contracturas. Los equipos multidisciplinarios continuarán siguiendo su progreso y recuperación de cerca.\n",
+        "gold_summary": "Presentamos un caso de NCS diagnosticado y tratado en base a los hallazgos del examen físico. La ecografía fetal mostró distensión de la vejiga, hidroceles bilaterales, dilatación de la uretra y ascitis abdominal que preocupaban por la obstrucción del tracto urinario inferior y posible ruptura de la vejiga. Una hora después del nacimiento, el examen de la extremidad superior izquierda del lactante no mostró movimiento espontáneo, la mano y el antebrazo parecían oscuros y la mano tenía una gran ampolla con descamación. No se detectó pulso distal a la fosa antecubital mediante ecografía Doppler. Se diagnosticó al lactante con NCS y se le practicó una fasciotomía urgente. La apariencia clínica y la perfusión de la extremidad superior izquierda mejoraron gradualmente. A los cuatro meses de edad, las heridas se habían curado y el paciente tenía un rango de movimiento pasivo completo de la extremidad superior izquierda. La recuperación del movimiento activo está en curso.\n",
+        "synthetic_summary": {
+            "B1": "Un bebé nació un poco antes de tiempo. Antes de nacer, las ecografías mostraron poco líquido alrededor del bebé y problemas en su barriga. Los médicos pensaron que eso pudo haber apretado al bebé dentro de la mamá.\n\nAl nacer, la mano y el antebrazo izquierdos del bebé estaban muy oscuros. No se movían. Los médicos creyeron que había mucha presión dentro del brazo. Esto puede dañar músculos y nervios. A eso se le llama síndrome compartimental neonatal. Para salvar el brazo, le hicieron una operación urgente llamada fasciotomía. En esa operación se cortan unas capas muy apretadas para que la sangre pueda volver a pasar.\n\nDespués de la operación, el brazo mejoró poco a poco. En los primeros días el color y la circulación mejoraron. Las heridas sanaron bien en unas semanas. A los cuatro meses, las cicatrices estaban cerradas y el brazo podía moverse pasivamente (otra persona podía moverlo) completamente. El bebé ya movía un poco algunos dedos, pero todavía tenía poco movimiento por sí mismo en la mano y la muñeca. \n\nLos médicos y terapeutas seguirán cuidando al bebé. Hará terapia de manos y usará férulas para ayudar su recuperación. Los doctores esperan que siga mejorando con tiempo y tratamiento.",
+            "B2": "Presentamos el caso de un recién nacido que desarrolló un problema serio en el brazo izquierdo debido a presión prolongada dentro del útero. La madre tenía un embarazo con pocas semanas de gestación restantes y se había observado oligohidramnios (poco líquido amniótico). En una ecografía prenatal se vio la vejiga muy distendida, hidroceles en ambos lados (acumulación de líquido en el escroto), dilatación de la uretra y ascitis (líquido en el abdomen), hallazgos que hacían sospechar una obstrucción del aparato urinario fetal y posible ruptura de la vejiga. Por disminución del movimiento fetal y una prueba llamada perfil biofísico baja, se decidió realizar una cesárea.\n\nAl nacer, el bebé necesitó ayuda para respirar y mostró un brazo izquierdo muy pálido/azulado, sin movimiento espontáneo, con una ampolla grande en la mano. Un examen con Doppler (una ecografía que mide el flujo sanguíneo) mostró flujo en la parte superior del brazo pero no en las arterias del antebrazo y la mano. Los especialistas concluyeron que el bebé tenía un síndrome compartimental neonatal (NCS). Esto significa que la presión dentro del antebrazo era tan alta que comprimía los vasos sanguíneos y los nervios, poniendo en riesgo la viabilidad de la extremidad.\n\nPara salvar el brazo se realizó una fasciotomía de emergencia unas seis horas después del nacimiento. La fasciotomía es una operación en la que se abre la fascia (la cubierta de los músculos) para aliviar la presión y restablecer la circulación. Tras la cirugía la apariencia y la perfusión (flujo sanguíneo) del brazo mejoraron de forma gradual; los registros por Doppler mostraron flujo hasta los dedos. Las heridas se dejaron curar poco a poco (por segunda intención) y se colocó una férula para mantener la mano en buena posición.\n\nA las seis semanas las heridas estaban bien curadas y, a los cuatro meses, la piel estaba completamente cicatrizada. El bebé tenía movilidad pasiva completa de la muñeca y los dedos (puede moverse con ayuda), y movimiento activo en el hombro y el codo. Por ahora muestra poco movimiento activo de la muñeca y la mano, salvo una ligera función de dos dedos; esto puede mejorar con el tiempo. El plan es continuar con terapia ocupacional, usar férulas y masajes en la cicatriz para prevenir contracturas, y que el equipo multidisciplinario siga de cerca su recuperación.\n\nEste caso muestra la importancia de reconocer y tratar rápidamente el síndrome compartimental en recién nacidos: una intervención temprana puede ayudar a salvar la extremidad y mejorar el resultado funcional.",
+            "B3": "Resumen clínico (nivel lector universitario)\n\nAntecedentes y presentación\n- Recién nacido masculino, 35+3 semanas, peso 2 021 g. Cesárea repetida por disminución del movimiento fetal y perfil biofísico bajo.\n- Embarazo complicado por oligohidramnios (ecografía a 31 semanas) y hallazgos fetales sugestivos de obstrucción del tracto urinario inferior (vejiga distendida, hidrocéles bilaterales, dilatación de la uretra y ascitis), con posible ruptura vesical.\n- Madre con rasgo falciforme, edad materna avanzada y obesidad.\n\nEvento al nacimiento\n- Dificultad respiratoria al nacer: precisó ventilación a presión positiva, oxígeno e intubación. Apgar 2 y 7 al minuto y a los cinco minutos.\n- Desde la primera hora de vida, la extremidad superior izquierda era cianótica en su tercio distal; existía una gran ampolla dorsal con descamación, sin movimiento espontáneo ni respuesta a estímulos. No se palparon pulsos radiales ni cubitales; Doppler mostró flujo arterial a nivel de la fosa antecubital pero ausencia de señales distales.\n- Diagnóstico clínico: síndrome compartimental neonatal (NCS), probablemente secundario a compresión intrauterina asociada a oligohidramnios.\n\nTratamiento\n- Tras evaluación multidisciplinaria (ortopedia, cirugía plástica, neonatología, anestesia) y discusión con la familia, se realizó fasciotomía descompresiva del antebrazo, mano y túnel carpiano aproximadamente 6 horas tras el nacimiento para intentar salvar la extremidad.\n- Las heridas se dejaron cerrar por intención secundaria y se colocó una férula personalizada con muñeca neutra y dedos extendidos.\n\nEvolución y resultados\n- Mejoría progresiva de la perfusión y del color de la extremidad en los días siguientes. En todo momento hubo señales Doppler desde la arteria braquial hasta cada dedo.\n- No hubo signos de infección ni isquemia continuada. Cicatrización buena a las 6 semanas.\n- A los 4 meses: heridas completamente cerradas; rango de movimiento pasivo completo en muñeca y dedos. Movilidad activa limitada en mano y muñeca (leve flexo-extensión del anular y meñique), con movimiento activo preservado en hombro y codo.\n\nPlan y consideraciones\n- Continuará terapia ocupacional, uso de férulas y masaje de cicatrices para reducir el riesgo de contracturas y favorecer la recuperación funcional.\n- Seguimiento multidisciplinario continuo para monitorizar la recuperación motora a largo plazo.\n- Nota clave: el NCS neonatal es una emergencia; el reconocimiento temprano y la fasciotomía descompresiva pueden restaurar la perfusión y salvar tejido, pero la recuperación motora puede ser parcial y requiere rehabilitación prolongada."
+        }
+    },
+    {
+        "article": "Una mujer de 38 años de edad fue admitida en la sala de cirugía en noviembre de 2022 con la principal queja de una hinchazón abdominal progresiva que se asoció con un dolor abdominal leve y una saciedad precoz durante cinco meses. No tenía síntomas sistémicos como pérdida de peso, estreñimiento, diarrea, deseo de alimentos salados, fatigabilidad fácil o dolor de cabeza.\nEn el examen, parecía estar bien alimentada, pero presentaba una gran distensión abdominal, un leve palidez, afebril y con un tinte de ictericia en la esclerótica.\nLa palpación abdominal reveló una gran masa intraabdominal, no dolorosa, que ocupaba todo el abdomen inferior y se extendía hacia el superior, sin signos de irritación peritoneal u organomegalia.\nLos análisis de sangre mostraron un recuento de glóbulos blancos (5,7 × 109/l), hemoglobina (9,8 g/dl), bilirrubina (103 mg/dl) con recuentos normales de plaquetas (393 × 109/l). Las enzimas hepáticas, AST (24,0 U/l), ALT (21,0 U/l), albúmina 42,7 g/l. Creatinina sérica (53 μmol/l) y ESR (80 mm/h). Todos los demás análisis de sangre fueron normales. Una ecografía abdominal reveló un complejo quiste abdominal, ambos riñones eran de tamaño normal y con una ecografía normal, el hígado parecía normal. La TC abdominal y pélvica de contraste, vistas axiales y coronales, demostraron un gran quiste suprarrenal de paredes delgadas (flechas azules) que medía aproximadamente 23,5 cm (AP) x 20,3 cm (T) x 32,2 cm (CC) con un volumen de 8 l. El gran quiste desplaza el riñón derecho (flechas rojas) inferomedial a través de la línea media y ejerce presión sobre el hígado, la vesícula biliar, el páncreas y los intestinos delgados. Se extiende hasta la fosa ilíaca derecha. Como había un tinte de esclerosis ictérica, pero la masa era separada del hígado, el páncreas, los conductos biliares y el riñón derecho. Dado el tamaño del quiste y sus efectos compresivos, se planificó una intervención quirúrgica. Se eligió un enfoque quirúrgico abierto.\n\nSe le practicó una laparotomía al paciente. Se le hizo una incisión abdominal en la línea media, bajo anestesia general, y tras abrir las capas de la pared abdominal, se identificó un enorme quiste retroperitoneal que ocupaba toda la cavidad abdominal.\n\nSe abrió el quiste para acceder al fluido que se aspiraba, como se demostró en la cistectomía que se realizó con éxito. Se aspiraron unos 8 l de fluido de color marrón de la masa. Se enviaron muestras de la pared quística y del fluido para su análisis histológico.\n\nLa paciente se recuperó sin incidentes y fue dada de alta el día 7 después de la operación. El seguimiento a los 6 y 12 meses no mostró recurrencia ni complicaciones. El examen citológico de la muestra informó la presencia de material amorfo, no hubo evidencia de malignidad. Los resultados histológicos indicaron que la pared quística contenía tejido suprarrenal sin atipia, había infiltración de la pared quística por células inflamatorias mononucleares. La superficie interna de la pared no estaba revestida por células específicas reconocibles. En cuanto a los hallazgos clínicos intraoperativos, donde el origen del quiste era incierto, los hallazgos fueron más sugerentes de un quiste gigante idiopático retroperitoneal.\n\n",
+        "gold_summary": "Una mujer de 38 años se presentó con distensión abdominal progresiva. Las imágenes revelaron un quiste retroperitoneal gigante. Debido a los recursos limitados, se realizó una laparotomía abierta y se extirpó completamente un quiste de 33 cm que contenía 8 l de líquido transparente. La histopatología confirmó un quiste retroperitoneal idiopático gigante.\n",
+        "synthetic_summary": {
+            "B1": "Una mujer de 38 años vino al hospital porque su barriga había crecido mucho y se sentía llena. Los médicos hicieron pruebas y encontraron un quiste grande. Un quiste es una bolsita llena de líquido. Este quiste estaba detrás de los órganos de la barriga y empujaba todo a su alrededor.\n\nLos médicos abrieron la barriga con una operación y sacaron el quiste. Del quiste salieron unos 8 litros de líquido. Mandaron partes del quiste y el líquido al laboratorio. Allí no vieron cáncer. El tejido parecía venir de una glándula cerca del riñón y había un poco de inflamación.\n\nLa mujer se recuperó bien. Salió del hospital al séptimo día. A los 6 y 12 meses no había vuelto a aparecer el quiste. Esto fue una buena noticia.",
+            "B2": "Resumen (nivel B2)\n\nUna mujer de 38 años consultó por una hinchazón abdominal progresiva durante cinco meses, con dolor leve y sensación de llenura temprana. En la exploración se observó gran distensión abdominal, ligera palidez y tinción amarilla de las escleróticas (ictericia). Los análisis mostraron una anemia leve y una velocidad de sedimentación elevada; las pruebas de función hepática estaban dentro de límites normales.\n\nLa ecografía y la tomografía computarizada revelaron un quiste grande en el espacio retroperitoneal (zona detrás de los órganos abdominales) que medía alrededor de 23–33 cm y contenía unos 8 litros de líquido, desplazando riñón, hígado y otros órganos. Por el tamaño y el efecto compresivo se decidió una cirugía abierta (laparotomía), se drenó y retiró el quiste por completo; se extrajeron aproximadamente 8 litros de líquido marrón y se enviaron muestras para análisis.\n\nLa paciente tuvo una recuperación sin complicaciones y recibió el alta al séptimo día; a los controles a los 6 y 12 meses no hubo recidiva. Los estudios de la pared quística mostraron tejido suprarrenal sin signos de malignidad y células inflamatorias; la citología del líquido no detectó tumor. En conjunto, los hallazgos fueron compatibles con un quiste retroperitoneal gigante idiopático (es decir, de causa desconocida).",
+            "B3": "Resumen clínico (nivel universitario, lectura B3)\n\nPresentación\n- Paciente: mujer de 38 años.\n- Síntomas: distensión abdominal progresiva durante 5 meses, dolor abdominal leve y saciedad precoz. No refirió pérdida de peso ni otros síntomas sistémicos significativos.\n- Examen: gran distensión abdominal con una masa intraabdominal no dolorosa que ocupaba gran parte del abdomen; ligera palidez y tinción ictérica de la esclerótica. No hubo signos de irritación peritoneal.\n\nInvestigaciones\n- Analíticas: leucocitos dentro de rango, anemia moderada (Hb 9,8 g/dl), elevación marcada de bilirrubina (correlando con la ictericia) y velocidad de sedimentación elevada (ESR 80 mm/h). Función hepática (AST/ALT) y albúmina normales; creatinina normal.\n- Imagen: ecografía detectó un quiste abdominal complejo. La tomografía contrastada mostró un quiste retroperitoneal de pared delgada, muy grande (aprox. 23,5 × 20,3 × 32,2 cm; volumen estimado ≈ 8 L) que desplazaba el riñón derecho y comprimía hígado, vesícula, páncreas e intestino delgado. El quiste estaba separado de órganos sólidos y conductos biliares.\n\nTratamiento\n- Se realizó laparotomía media abierta (decisión influida por recursos limitados) y resección del quiste.\n- Durante la cirugía se aspiraron ≈ 8 L de líquido marrón desde el quiste y se completó la cistectomía.\n\nHallazgos anatomopatológicos\n- Citología del líquido: material amorfo, sin evidencia de malignidad.\n- Anatomía patológica de la pared quística: presencia de tejido suprarrenal sin atipia y infiltrado inflamatorio mononuclear; la superficie interna no mostró un revestimiento celular específico reconocible.\n- Dado que el origen exacto no pudo confirmarse intraoperatoriamente, los hallazgos se interpretaron como un quiste retroperitoneal gigante idiopático, con elementos sugestivos de origen suprarrenal pero sin signos de malignidad.\n\nEvolución y pronóstico\n- Recuperación postoperatoria sin complicaciones; alta al día 7.\n- Seguimiento a 6 y 12 meses sin recurrencia ni problemas detectados.\n- Prognosis favorable: resección completa y ausencia de malignidad sugieren bajo riesgo de recidiva, aunque se recomienda vigilancia clínica/imaginológica periódica.\n\nInterpretación y pasos a considerar\n- Este caso es un ejemplo de un quiste retroperitoneal gigante que, por su tamaño, produjo síntomas por efecto compresivo aunque sin evidencia de invasión maligna.\n- Hallazgos clave a vigilar: recuperación de la anemia, normalización de la bilirrubina y control imagenológico para descartar recurrencia.\n- En general, el tratamiento definitivo de quistes retroperitoneales sintomáticos es quirúrgico; la histología confirma la naturaleza benigna en este caso, por lo que no se precisó tratamiento oncológico adicional.\n\nNota empática: la paciente recibió atención quirúrgica oportuna y evolucionó bien; el pronóstico a medio plazo es bueno, pero las revisiones periódicas son razonables para asegurar que no haya recurrencia."
+        }
+    },
+    {
+        "article": "Un hombre de 71 años con diabetes y enfermedad de Chagas había perdido recientemente mucho peso (60 kg). La investigación clínica dio lugar a un diagnóstico de megaesófago asociado a una obstrucción significativa a nivel del cardias. Se realizó una dilatación esofágica con balón, recuperando con éxito el tránsito digestivo. Mientras tanto, durante la evaluación del riesgo quirúrgico, el paciente también presentó dolor torácico con el mínimo esfuerzo. La angiografía por tomografía computarizada coronaria realizada tres años antes mostró una enfermedad multivascular muy calcificada que afectaba a la arteria coronaria izquierda; en ese momento no se había realizado ninguna otra investigación. Esta vez, se lo derivó a nosotros para un cateterismo cardíaco.\nEl examen realizado el 16 de febrero de 2016 mostró: arteria coronaria derecha (RCA) con importante calcificación y una lesión del 50% en el tercio medio; arteria descendente posterior (PDA) y arteria posterolateral derecha (RPLA), con severa calcificación y lesiones del 80% y 70%, respectivamente; LM con 80% de lesiones calcificadas en el tercio distal; arteria descendente anterior izquierda (LAD) con significativa calcificación y 90% de lesión en el tercio medio; ramas diagonales (DG1 y DG2) con lesiones calcificadas del 70% y 80%, en el origen y en el tercio proximal, respectivamente; y arteria circunfleja izquierda (LCx) ocluida y calcificada, recibiendo colaterales grado II de múltiples orígenes. El volumen ventricular izquierdo y la contractilidad se conservaron.\n\nCon esta imagen angiográfica, una puntuación de riesgo de la Society of Thoracic Surgeons del 15,8 % para morbilidad o mortalidad, una puntuación EuroSCORE II del 4,67 %, y una debilidad significativa debido a una pérdida de peso importante y reciente, el equipo cardiaco decidió realizar una intervención coronaria percutánea (ICP) de la LM, LAD, DG1 y DG2 inicialmente y, en un segundo procedimiento después de 30 días, una ICP de las ramas de la RCA. En ambos procedimientos, también se indicó una RA debido a una calcificación significativa. No se abordaría la LCx, ya que angiográficamente el vaso no estaba tan gravemente afectado y también considerando la dificultad técnica de la recanalización, debido a la longitud del CTO y también a las paredes muy calcificadas (puntuación J-CTO 4). La LCx ya estaba recibiendo una circulación collateral de grado II.\nEl 19 de febrero de 2016, tras comenzar una terapia antiplaquetaria dual con aspirina y clopidogrel, el paciente se sometió a una angioplastia de la arteria descendente anterior, la arteria circunfleja y la arteria descendente derecha con una fresa de 1,5 mm, seguida de una predilatación con un balón de 3,0 mm x 20 mm a 14 atm y la implantación de stents liberadores de fármacos en la arteria descendente derecha y la arteria circunfleja, utilizando una técnica de mini-aplastamiento y un balón de contacto al final. Se realizó un balón de contacto en la bifurcación de la arteria descendente derecha/arteria circunfleja y, finalmente, se implantó el tercer stent liberador de fármacos desde el origen de la arteria descendente derecha para superponerse con el stent de la arteria descendente derecha. Se logró un éxito procedimental con un flujo TIMI de 3 y sin complicaciones clínicas o angiográficas.\nEl 22 de marzo de 2016, el paciente volvió para una PCI con un RotaWire PCI en el PDA y RPLA con una fresa de 1,5 mm, seguido por la implantación de dos DES de 2,75 mm x 20 mm y 2,75 mm x 16 mm a 12 atm en el PDA y RPLA, respectivamente, sin ninguna predilatación adicional. También observamos la presencia de una disección larga y severa en el tercio medio del RCA, sin duda causada por un manejo excesivo e intentos de remover la fresa, lo que causó una penetración profunda por el catéter guía 7F. Esta disección se corrigió rápidamente con la implantación de un tercer DES de 4,0 mm x 32 mm, y se obtuvo un flujo TIMI 3 final sin complicaciones clínicas o electrocardiográficas. Los dos sitios de punción femoral se ocluyeron con dispositivos AngioSeal 8F y 6F, respectivamente. El paciente permaneció en la unidad de cuidados intensivos durante 48 horas, la única anormalidad fue la elevación de CK-MB (el doble del valor de referencia). Fue dado de alta el día 3 en excelentes condiciones generales. El ecocardiograma de control mostró una contractilidad ventricular izquierda normal.\n",
+        "gold_summary": "Un hombre de 71 años con enfermedad de Chagas y angina estable en esfuerzo mínimo se sometió a una angiografía por tomografía computarizada y cineangiografía que reveló una enfermedad multivascular muy calcificada que afectaba a la arteria descendente anterior izquierda (LM). Debido al grado de calcificación, se decidió realizar una rotablation. La primera etapa de la intervención coronaria percutánea (ICP) con rotablation se realizó en la arteria descendente anterior izquierda (LM), la arteria descendente anterior izquierda y la segunda rama diagonal sin complicaciones. Casi 30 días después, volvió para una ICP de la arteria coronaria derecha (RCA). La estrategia propuesta fue la aterectomía rotativa en la arteria descendente anterior posterior (PDA) y la arteria posterolateral derecha (RPLA) con una fresa de 1,5 mm, seguida por la implantación de dos stents liberadores de fármacos (DES). A través del acceso a la arteria femoral derecha, la lesión de la RPLA se extirpó con éxito. Como no había signos de disección y se mantuvo el flujo TIMI 3, se reposicionó el RotaWire de 0,009″ para cruzar la lesión de la PDA y se realizó la extirpación de la lesión. Después de dos intentos, logramos cruzar la lesión con la fresa de 1,5 mm, sin embargo, se produjo el atrapamiento de la misma. El sistema se retiró hasta que el catéter guía penetró profundamente en la RCA, y se hicieron intentos para liberar el Rotablator moviéndolo hacia adelante y hacia atrás, pero la fresa ni siquiera giró. La arteria femoral contralateral se perforó y se insertó un catéter guía 6F JR, con el fin de mover un alambre guía y un pequeño globo de angioplastia tangencialmente a la fresa, pero sin éxito. Finalmente, avanzamos el alambre guía utilizando la técnica de «nudillo», aprovechando la torsión de la porción distal del alambre guía PT2, realizando una disección subintimal y reentrada, y pudimos cruzar fácilmente el globo, inflarlo y liberar la fresa atrapada. A través del sistema 6F, se implantaron dos DES programados y uno de rescate con éxito en la PDA, RPLA y RCA, obteniendo un flujo TIMI 3 final sin complicaciones.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre de 71 años con enfermedad de Chagas y mucho adelgazamiento tenía dolor en el pecho con poco esfuerzo. Las pruebas mostraron que varias arterias del corazón estaban muy duras y estrechas por la calcificación. Los médicos decidieron abrirlas en dos veces usando una técnica especial.\n\nPrimero, le hicieron una angioplastia con rotablación. Rotablación es usar una pequeña fresa que quita el calcio de las arterias. Después pusieron stents, que son tubitos pequeños que mantienen la arteria abierta. Esta primera intervención salió bien. La sangre fluía bien y no hubo problemas.\n\nUnas cuatro semanas después volvieron a tratar otras arterias del lado derecho del corazón. En esa segunda intervención también usaron la fresa y pusieron más stents. Durante el procedimiento se formó una rasgadura en la arteria por el manejo de los instrumentos. Los médicos la arreglaron rápido poniendo un stent más grande. Al final la circulación quedó buena.\n\nEl paciente estuvo 48 horas en cuidados intensivos. Solo subió un poco una prueba de sangre del corazón. Fue dado de alta al tercer día en buen estado. El ecocardiograma mostró que su corazón latía y se movía normalmente.",
+            "B2": "Resumen claro y comprensible:\n\nUn hombre de 71 años con enfermedad de Chagas y pérdida de peso importante tuvo dolor en el pecho al mínimo esfuerzo. Un estudio de imagen y una arteriografía mostraron enfermedad coronaria muy calcificada en múltiples vasos (arterias que llevan sangre al corazón). Su función del ventrículo izquierdo (la principal cámara del corazón) estaba conservada, pero el riesgo de cirugía abierta era alto, así que el equipo decidió tratar las lesiones con intervenciones coronarias percutáneas (ICP) en dos etapas usando además rotablación (una técnica que usa una pequeña fresa giratoria para “lijar” la calcificación dentro de la arteria) y luego colocando stents liberadores de fármaco (pequeños tubos metálicos recubiertos que mantienen la arteria abierta y liberan medicamento para reducir la reestenosis).\n\nPrimera sesión (19 de febrero de 2016)\n- Se inició terapia antiplaquetaria dual (aspirina y clopidogrel) y se realizó rotablación con fresa de 1,5 mm y angioplastia con balón.  \n- Se implantaron varios stents liberadores de fármaco en las arterias tratadas usando técnicas especiales para bifurcaciones.  \n- El procedimiento fue exitoso con flujo sanguíneo final normal (TIMI 3) y sin complicaciones clínicas.\n\nSegunda sesión (22 de marzo de 2016)\n- Se usó de nuevo rotablación en la arteria descendente posterior (PDA) y la arteria posterolateral derecha (RPLA) y se colocaron dos stents DES en esas ramas.  \n- Durante el procedimiento apareció una disección larga y severa (una rotura o desgarro en la capa interna de la arteria), probablemente por manipulación excesiva al intentar retirar la fresa.  \n- La disección se trató rápidamente con la colocación de un stent de rescate más grande (4,0 mm x 32 mm), con buen resultado y flujo TIMI 3 final.\n\nCuidados posteriores y resultado\n- Los accesos femorales se cerraron con dispositivos hemostáticos. El paciente estuvo 48 horas en la unidad de cuidados intensivos; la única anomalía fue un aumento moderado de una enzima cardíaca (CK‑MB).  \n- Fue dado de alta al tercer día en buen estado general. El ecocardiograma de control mostró función ventricular izquierda normal.\n\nInterpretación y próxima etapa\n- En un corazón con mucha calcificación, la rotablación seguida de stent es una estrategia usada para facilitar la apertura de las arterias.  \n- Aunque hubo una complicación (disección), se manejó con éxito en la misma intervención. El resultado inmediato fue bueno, con recuperación rápida y función cardíaca preservada.  \n- El equipo decidió no intentar recanalizar una arteria circunfleja muy calcificada y crónicamente ocluida porque ya recibía circulación colateral y la intervención habría sido técnicamente muy difícil.\n\nEn resumen: el paciente de 71 años con enfermedad coronaria severa y muy calcificada fue tratado en dos procedimientos mediante rotablación y colocación de stents. A pesar de una complicación tratada con éxito, terminó con buen flujo coronario y fue dado de alta con función cardíaca normal.",
+            "B3": "Resumen (nivel universitario, lectura clara y empática)\n\nPaciente y contexto\n- Hombre de 71 años con diabetes y enfermedad de Chagas. Había sufrido una pérdida de peso importante y reciente (60 kg) y recibió tratamiento por megaesófago antes de la evaluación cardiológica.\n- Consultó por dolor torácico al mínimo esfuerzo. Tres años antes ya tenía una tomografía coronaria que mostraba enfermedad coronaria calcificada multivaso.\n\nHallazgos principales\n- Coronariografía (16 feb 2016): enfermedad coronaria multivaso muy calcificada:\n  - LM: lesión calcificada del 80% en tercio distal.\n  - LAD: lesión del 90% en tercio medio; DG1 y DG2 con lesiones calcificadas del 70–80%.\n  - RCA: lesión del 50% en tercio medio; PDA 80% y RPLA 70% (ambas muy calcificadas).\n  - LCx: ocluida y muy calcificada, con circulación colateral grado II desde otras arterias.\n- Función ventricular: volumen y contractilidad del ventrículo izquierdo conservados (es decir, función global preservada).\n\nRazonamiento terapéutico\n- El paciente tenía alto riesgo quirúrgico (STS 15,8% para morbimortalidad) y cierta fragilidad por la pérdida de peso; por ello el equipo eligió una estrategia percutánea y escalonada en dos tiempos, en lugar de cirugía cardíaca.\n- Debido a la calcificación severa, las intervenciones incluyeron aterectomía rotatoria (rotablación) antes de implantar stents liberadores de fármaco (DES).\n- No se intentó recanalizar la LCx porque era una oclusión crónica larga y muy calcificada (J‑CTO 4) y ya recibía colaterales; esto aumentaría notablemente la complejidad y el riesgo.\n\nProcedimientos y resultado\n1) Primera sesión (19 feb 2016)\n   - Se inició doble antiagregación (aspirina + clopidogrel).\n   - Rotablación con fresa 1,5 mm y predilatación con balón (3,0 × 20 mm a 14 atm).\n   - Implante de DES en arterias afectadas (incluida técnica de mini‑crush en bifurcación y balón de contacto final).\n   - Resultado: flujo TIMI 3, sin complicaciones clínicas ni angiográficas inmediatas.\n\n2) Segunda sesión (22 mar 2016)\n   - Rotablación en PDA y RPLA con fresa 1,5 mm; se implantaron dos DES (2,75 × 20 mm y 2,75 × 16 mm) sin predilatación adicional.\n   - Durante el procedimiento apareció una disección larga y severa en el tercio medio de la RCA, atribuida a manipulación excesiva y a la penetración profunda del catéter guía.\n   - La disección se trató rápidamente con un tercer DES (4,0 × 32 mm).\n   - Resultado final: flujo TIMI 3, sin complicaciones clínicas ni cambios electrocardiográficos relevantes.\n\nEvolución hospitalaria y controles\n- Hemostasia de los accesos femorales con AngioSeal (8F y 6F).\n- Permaneció 48 horas en UCI; la única alteración fue elevación moderada de CK‑MB (≈2 veces el valor de referencia).\n- Ecocardiograma de control mostró contractilidad ventricular izquierda normal.\n- Alta al tercer día en muy buenas condiciones generales.\n\nImplicaciones y pasos siguientes (interpretación)\n- Lo positivo: revascularización percutánea multivaso con rotablación fue técnicamente exitosa y dejó flujo coronario normal (TIMI 3) conservando la función ventricular; el paciente salió en buen estado.\n- Riesgos y elementos a vigilar: la calcificación extensa y la oclusión crónica de la LCx dejan una parte de la enfermedad sin tratamiento directo; la disección de la RCA durante la intervención muestra la complejidad y el riesgo procedimental en arterias muy calcificadas. La elevación de CK‑MB indica lesión miocárdica procedimental leve a moderada.\n- Seguimiento razonable: continuar doble antiagregación según indicación cardiológica, control clínico y electrocardiográfico, vigilancia de marcadores cardíacos si reaparecen síntomas, ecocardiograma de control y rehabilitación cardiaca. Si reaparecen síntomas anginosos o hay isquemia recurrente, valorar estrategias adicionales (reintervención percutánea en otros segmentos o reconsiderar cirugía en un equipo multidisciplinario, aunque el riesgo quirúrgico sigue siendo alto).\n\nComentario final (empatía)\nEste fue un caso complejo por la edad, la comorbilidad y la calcificación difusa de las arterias. El equipo adaptó la estrategia al riesgo del paciente y logró una revascularización percutánea eficaz con buena recuperación inicial; sin embargo, precisa seguimiento estrecho y manejo multidisciplinario."
+        }
+    },
+    {
+        "article": "Una paciente de 29 años se presentó al departamento de urología con dolor intermittent en el flanco derecho durante un año y sensación de ardor urinaria ocasional sin hematuria; su estado general era estable. La paciente no mostró signos de tos, fatiga, pérdida de peso, no había tenido cirugías previas, pero había estado expuesta frecuentemente a ovejas. A pesar de los exámenes de laboratorio normales, el examen de anticuerpos de equinococos arrojó un resultado positivo. El ultrasonido abdominal posterior reveló una lesión quística grande en el riñón derecho, que medía aproximadamente 63 mm con paredes gruesas y sin flujo de doppler significativo. La tomografía computarizada con contraste, tanto en vista transversal como coronal, reveló una masa quística con septos en el lado lateral del riñón derecho, que presentaba una pared gruesa y regular que se intensificaba con el contraste. Esta lesión se clasificó como categoría 4 de Bosniak, con imágenes de tomografía computarizada en vista coronal que mostraban la participación del sistema colector y el contacto con el hígado. Se sospechó de HC en base a las evaluaciones clínicas y radiológicas. Los hallazgos de la radiografía de tórax no fueron significativos, sin evidencia de quistes pulmonares. Después de un régimen de tres meses de albendazol 400 mg administrado dos veces al día, la paciente se sometió a una intervención quirúrgica. Se realizó un procedimiento abierto a través de una incisión subcostal derecha de Kocher, lo que resultó en una nefrectomía derecha y una resección hepática parcial debido a las adherencias. El espécimen, que pesaba 372 g y medía 13 × 8 × 6 cm, mostró un gran quiste blanco con paredes delgadas que contenían una membrana desprendida, que afectaba los cálices renales y la pelvis. El diagnóstico final fue HC del riñón acompañado de pielonefritis crónica. Los exámenes de laboratorio posteriores al procedimiento mostraron resultados normales, con una producción urinaria estable y signos vitales. El catéter urinario se retiró después de 24 horas debido a una producción urinaria adecuada (2 L). El drenaje renal se retiró después de 3 días, con volúmenes de drenaje de 200 ml, 100 ml y ninguno en días consecutivos. La paciente volvió a sus actividades normales sin complicaciones.\n",
+        "gold_summary": "Se diagnosticó a una mujer de 29 años con dolor intermitente en el flanco derecho y ardor urinario un quiste hidatídico (HC) de categoría 4 de Bosniak, tras dar positivo en anticuerpos de equinococo. Las imágenes confirmaron el diagnóstico, lo que derivó en un tratamiento de tres meses con albendazol, seguido de una nefrectomía derecha y una resección hepática parcial. El análisis histopatológico confirmó un HC y una pielonefritis crónica. La paciente se recuperó sin incidentes y volvió a sus actividades normales.\n",
+        "synthetic_summary": {
+            "B1": "Había una mujer de 29 años que tuvo dolor en el costado derecho y a veces ardor al orinar durante un año. Vivía cerca de ovejas. Esto es importante porque un parásito que vive en ovejas puede causar un quiste en los órganos.\n\nLas pruebas de sangre mostraron que su cuerpo había visto ese parásito. Las ecografías y la tomografía mostraron un quiste grande en el riñón derecho. Los médicos dijeron que era “Bosniak 4”, que quiere decir que el quiste parecía serio y necesitaba tratamiento.\n\nLa mujer tomó un medicamento llamado albendazol durante tres meses. Este medicamento ayuda a matar al parásito. Luego tuvo una operación. Le quitaron todo el riñón derecho y también sacaron una parte pequeña del hígado porque el quiste estaba pegado allí.\n\nEl examen del quiste confirmó que era un quiste hidatídico (un saco con una membrana causado por el parásito) y además había una infección crónica del riñón llamada pielonefritis. Después de la operación estuvo bien. No tuvo problemas, le quitaron los tubos y volvió a sus actividades normales.",
+            "B2": "Here is a clear, caring summary written for a high-school reader:\n\nA 29-year-old woman had on-and-off pain in her right side for about a year and sometimes felt a burning when she urinated. She had often been around sheep, which is important because certain parasites carried by sheep can infect people. Blood tests were otherwise normal, but a test for antibodies against the Echinococcus parasite (which causes hydatid disease) was positive.\n\nAn ultrasound and a contrast CT scan showed a large cystic mass (about 6.3 cm) in the right kidney with thick walls and internal divisions. Radiologists labeled it Bosniak category 4 — this means the cyst looked complex and suspicious on imaging, so surgery was recommended. No abnormal cysts were seen in the lungs.\n\nThe medical team gave the patient albendazole (an anti-parasite medicine) for three months before surgery. She then had an open operation through a right-sided Kocher incision. Because the kidney cyst was stuck to the nearby liver, the surgeons removed the whole right kidney (right nephrectomy) and part of the liver. The removed tissue contained a large white cyst with a detached inner membrane — a typical finding for a hydatid cyst.\n\nLab examination of the removed tissue confirmed a hydatid cyst (caused by Echinococcus) and chronic pyelonephritis (long-standing kidney inflammation/infection). After surgery her lab tests and urine output were good, tubes and drains were removed over the next few days, and she recovered without complications. She returned to normal activities.\n\nKey points to remember:\n- A hydatid cyst is a parasitic cyst that can form after contact with animals like sheep.  \n- Imaging sometimes makes these cysts look like dangerous kidney tumors, so surgery is often needed to be sure and to treat the problem.  \n- Pretreatment with albendazole helps reduce the risk of spreading the parasite during surgery.  \n\nIf you have questions about any term or step in the treatment, I can explain it in more detail.",
+            "B3": "Resumen clínico (nivel universitario — lectura B3)\n\nPresentación\n- Mujer de 29 años con un año de dolor intermitente en el flanco derecho y episodios ocasionales de ardor al orinar. No presentó fiebre, tos, fatiga ni pérdida de peso, y no tenía antecedentes quirúrgicos relevantes.\n- Antecedente epidemiológico: exposición frecuente a ovejas, factor de riesgo para enfermedad por Echinococcus (hidatidosis).\n\nExploraciones y hallazgos\n- Laboratorio: resultados generales normales; no hubo hematuria.\n- Serología: anticuerpos contra Echinococcus positivos, lo que sugiere infección hidatídica.\n- Ecografía abdominal: lesión quística derecha grande (~63 mm) con paredes gruesas y sin flujo Doppler significativo.\n- Tomografía computarizada con contraste: quiste renal complejo con tabiques y pared gruesa que realzaba con contraste; se clasificó como Bosniak 4 (categoría que habitualmente sugiere una lesión quística con alto riesgo de malignidad). La imagen mostró además contacto con el hígado y compromiso del sistema colector renal.\n- Radiografía de tórax: sin signos de quistes pulmonares.\n\nImpresión diagnóstica antes de la cirugía\n- Sospecha de quiste hidatídico renal (HC) sobre la base de la serología, la imagen y los antecedentes; la lesión simulaba una lesión quística compleja (Bosniak 4), lo que motivó manejo quirúrgico por riesgo de enfermedad grave o malignidad.\n\nTratamiento\n- Terapia antiparasitaria preoperatoria: albendazol 400 mg, dos veces al día durante 3 meses.\n- Intervención quirúrgica abierta por incisión subcostal derecha (Kocher): se realizó nefrectomía derecha y resección hepática parcial debido a adherencias entre el quiste y el hígado.\n\nHallazgos anatomopatológicos y diagnóstico definitivo\n- Especimen: 372 g, 13 × 8 × 6 cm; gran quiste blanco con membrana desprendida, que afectaba cálices y pelvis renales.\n- Diagnóstico final: quiste hidatídico renal (HC) asociado a pielonefritis crónica (inflamación/infección crónica del parénquima renal).\n\nEvolución y alta\n- Postoperatorio sin complicaciones: parámetros hemodinámicos y laboratorios dentro de la normalidad, adecuada producción de orina (alrededor de 2 L) — catéter retirado a las 24 h; drenaje renal retirado a los 3 días.\n- La paciente se recuperó y retomó sus actividades habituales.\n\nComentarios e implicaciones\n- La hidatidosis renal es rara y puede imitar radiológicamente lesiones quísticas complejas (Bosniak 4), que suelen hacer pensar en cáncer renal; por ello la combinación de antecedentes epidemiológicos y serología fue clave para orientar el diagnóstico.\n- El tratamiento combinó terapia antiparasitaria preoperatoria y resección quirúrgica extensa, lo cual es apropiado para reducir riesgo de diseminación y tratar la lesión que comprometía la función renal.\n- Recomendaciones prácticas (no detalladas en el informe, pero usualmente indicadas): seguimiento clínico y por imagen para vigilar recidiva, control de la función hepática y renal, y considerar controles serológicos periódicos según protocolo local.\n\nEmpatía\n- La paciente recibió tratamiento dirigido y se recuperó sin complicaciones; el manejo multidisciplinario (urología, cirugía y tratamiento antiparasitario) contribuyó a este buen resultado."
+        }
+    },
+    {
+        "article": "Una paciente de 46 años de edad fue admitida en nuestro hospital debido a opresión en el pecho y falta de aire que había durado más de un mes. Su historial médico incluía una tiroidectomía parcial, y no tenía antecedentes de tabaquismo o consumo de alcohol. Fue tratada con medicamentos regulares (comprimidos de liberación prolongada de succinato de metoprolol, comprimidos de sacubitril valsartán sodio, espironolactona, comprimidos de dapagliflozina) para la IC, pero la respuesta fue pobre. Durante el examen físico, la paciente estaba consciente y bien orientada. Su frecuencia cardíaca era de 68 latidos por minuto, la presión arterial era de 150/98 mm Hg, la frecuencia respiratoria era de 20 latidos por minuto. No había signos de sangrado o ictericia en la piel o membranas mucosas, y no se observó distensión de la vena yugular. La glándula tiroides no estaba agrandada. Los sonidos respiratorios eran gruesos en ambos pulmones, con roncus húmedos presentes en las bases pulmonares. La frecuencia cardíaca era de 68 lpm con un ritmo regular. El abdomen era suave, sin sensibilidad o sensibilidad de rebote, y el hígado y el bazo no eran palpables por debajo de la caja torácica. El signo de reflujo hepatoyugular fue negativo, pero había edema en ambas extremidades inferiores.\n\nLa paciente fue hospitalizada y se le realizaron los exámenes pertinentes. Los análisis bioquímicos mostraron una hormona estimulante de la tiroides (TSH) de 7,190 uIU/mL, triglicéridos de 0,81 mmol/L, colesterol de lipoproteínas de baja densidad (LDL-C) de 2,61 mmol/L, lipoproteína (a) de suero de 435 mg/L y NT-proBNP de 6245 pg/mL. Un examen de electrocardiograma (ECG) mostró bradicardia sinusal, anomalías de la onda T-U y duración del QRS de 90 ms. Un examen ecocardiográfico transtorácico posterior reveló un diámetro de la aurícula izquierda (LA) (anteroposterior) de 41 mm, un diámetro del ventrículo izquierdo (LVD) (anteroposterior) de 54 mm, un espesor del tabique interventricular en diástole (IVSD) de 9 mm, un espesor de la pared posterior del ventrículo izquierdo en la fase final de la diástole (LVPWd) de 9 mm, una fracción de eyección del ventrículo izquierdo (LVEF) del 28% (M-mode), una fracción de acortamiento (FS) del 13% y una presión de la arteria pulmonar de 29 mm Hg. No se observaron lesiones coronarias significativas en la angiografía coronaria computarizada (CCA). Se diagnosticó a la paciente con cardiomiopatía dilatada, insuficiencia cardiaca de clase III con LVEF reducida según la New York Heart Association (NYHA). En combinación con los parámetros, se puede observar que los volúmenes de la aurícula izquierda y el ventrículo izquierdo se reducen gradualmente, lo que indica que la función diastólica del ventrículo izquierdo está mejorando. El tratamiento con CCM revierte la remodelación miocárdica. Además, E/e′ refleja la presión de llenado ventricular izquierdo. El valor normal debe ser inferior a 8. Se puede observar que en este caso, E/e′ vuelve al valor normal tres meses después de la implantación de CCM. Estos dos puntos reflejan el papel de CCM en la mejora de la función diastólica miocárdica en el tratamiento de la insuficiencia cardiaca. En resumen, la paciente tenía las siguientes características: (1) LVEF mejoró pero se mantuvo tan bajo como el 30% después de la terapia óptima para la insuficiencia cardiaca; (2) opresión en el pecho y malestar con ligera actividad, grado de función cardiaca III; (3) ECG muestra QRS estrecho. Teniendo en cuenta el resultado positivo de la prueba preoperatoria de levosimendan, después de una discusión general y una comunicación completa con el paciente y su familia, se decidió realizar el tratamiento con CCM.\n\nEl procedimiento de implantación del CCM fue similar al de la implantación de un marcapasos tradicional. El paciente se colocó en posición supina, se desinfectó con una toalla y se perforó la vena subclavia izquierda dos veces bajo anestesia local, y se hizo la bolsa capsular después de insertar el alambre guía. Bajo la guía del alambre guía, se introdujeron dos vainas de desprendimiento, y se introdujeron dos cables de estimulación ventricular (Medtronic 3830-69) a través de la vaina, y se ajustó la posición de los cables a la superficie del tabique ventricular derecho con una distancia de 3 cm. Durante la operación, se probó el electrodo de campo cercano (RV), que mostró un umbral de estimulación de 0,5 V, una amplitud de la onda R detectada mayor de 10 mV, y una impedancia del cable de 1080 Ω; el electrodo de campo lejano (LS) mostró un umbral de estimulación de 0,5 V, una amplitud de la onda R detectada mayor de 15 mV, y una impedancia del cable de 900 Ω. Estas mediciones cumplieron los criterios para una implantación exitosa del electrodo. Ambos cables se anclaron de forma segura en el tabique ventricular derecho. Después de asegurarse de que no había estimulación diafragmática palpable con un pulso de estimulación de 10 V y una anchura de pulso de 0,4 ms, se conectaron los cables al generador de impulsos Optimizer Smart. Posteriormente, se ajustaron los impulsos de salida y se programaron y optimizaron los parámetros.\n\nLa monitorización del ECG postoperatorio inmediato indicó un suministro normal de impulsos CCM (Figura 1C). Observamos la respuesta de los pacientes al CCM al adherirnos a un protocolo de seguimiento estandarizado. Utilizando una amplia variedad de herramientas de evaluación, que incluían ultrasonografía Doppler cardiaca a color, análisis de sangre NT-ProBNP, pruebas de caminata de seis minutos (6MW) y el Cuestionario de Minnesota para Vivir con Insuficiencia Cardiaca (MLHFQ), evaluamos sistemáticamente el estado clínico de los pacientes. El paciente no experimentó opresión en el pecho ni falta de aire, y hubo una marcada mejora en la tolerancia al ejercicio y la calidad de vida.\n",
+        "gold_summary": "Presentamos a una paciente de 46 años que fue admitida en nuestro hospital debido a opresión torácica y falta de aire que duró más de un mes. La ecocardiografía reveló un diámetro del ventrículo izquierdo (anteroposterior) de 54 mm, el electrocardiograma mostró bradicardia sinusal y duración del QRS de 90 ms. La paciente no experimentó opresión torácica o falta de aire, y hubo una marcada mejora en la tolerancia al ejercicio y calidad de vida después de la implantación de la modulación de la contractilidad cardiaca.\n",
+        "synthetic_summary": {
+            "B1": "Esta es la historia de una mujer de 46 años que se sentía con el pecho apretado y le faltaba el aire por más de un mes. Los médicos vieron que su corazón estaba débil y no bombeaba bien. En una ecografía su corazón tenía una fracción de eyección baja (esto quiere decir que no soltaba suficiente sangre cada latido). No tenía vasos del corazón tapados.\n\nLe pusieron un aparato llamado CCM. Este aparato se pone como un marcapasos. Envía pequeñas señales al músculo del corazón para ayudarle a contraerse mejor. La operación fue bien y las pruebas durante la cirugía salieron normales.\n\nTras poner el aparato, la mujer empezó a sentirse mucho mejor. Ya no tenía la opresión en el pecho y podía hacer más ejercicio sin cansarse tanto. Las ecografías y otras pruebas mostraron que la función del corazón fue mejorando con el tiempo. En resumen: recibió un tratamiento con un dispositivo que ayudó a su corazón y mejoró su vida.",
+            "B2": "Resumen para lectores de nivel B2 (adolescentes):\n\nUna mujer de 46 años ingresó por más de un mes con sensación de opresión en el pecho y falta de aire. Tenía antecedente de tiroidectomía parcial y estaba recibiendo tratamiento médico estándar para insuficiencia cardiaca, pero no mejoró lo suficiente. Las pruebas mostraron: una fracción de eyección del ventrículo izquierdo (LVEF) muy baja (28%), marcadores de insuficiencia cardiaca elevados (NT‑proBNP 6245 pg/mL) y un electrocardiograma con bradicardia sinusal y un QRS estrecho (90 ms). La angiografía coronaria no mostró obstrucciones importantes, por lo que se diagnosticó miocardiopatía dilatada con insuficiencia cardiaca clase III (NYHA).\n\nTras una prueba positiva con levosimendan (un fármaco que ayuda a predecir la respuesta a terapias eléctricas), se decidió implantar un dispositivo de modulación de la contractilidad cardiaca (CCM). El implante es similar al de un marcapasos: se colocaron dos electrodos en el tabique del ventrículo derecho y se conectaron a un generador. Las mediciones durante la cirugía fueron adecuadas y no hubo estimulación del diafragma.\n\nEn el seguimiento, con ecocardiografías, análisis de sangre, la prueba de caminata de seis minutos y cuestionarios de calidad de vida, la paciente mostró mejoría clara: desapareció la opresión torácica y la disnea, mejoró la tolerancia al ejercicio y su calidad de vida. Además, indicadores ecocardiográficos de función diastólica (como E/e′) volvieron a valores normales a los tres meses, y los volúmenes del corazón disminuyeron, lo que sugiere una reversión favorable del remodelado cardiaco tras la terapia CCM. En conjunto, el tratamiento fue seguro y produjo una mejora clínica importante en esta paciente con insuficiencia cardiaca avanzada.",
+            "B3": "Resumen clínico conciso y comprensible\n\nCaso\n- Mujer de 46 años ingresada por opresión torácica y disnea persistentes >1 mes. Antecedente de tiroidectomía parcial; no fumadora ni consumidora de alcohol. Recibía tratamiento farmacológico óptimo para insuficiencia cardiaca (metoprolol de liberación prolongada, sacubitril/valsartán, espironolactona, dapagliflozina) pero con mala respuesta sintomática.\n\nExploración y pruebas iniciales (hallazgos relevantes)\n- Signos vitales: FC 68 lpm (normal), TA 150/98 mm Hg (elevada), FR 20 rpm (límite alto).\n- Examen: crepitantes y roncus húmedos en bases pulmonares; edema en ambas piernas; sin distensión yugular ni hepatomegalia.\n- Analítica: TSH 7,19 μIU/mL (elevada → sugiere hipotiroidismo subyacente), NT‑proBNP 6.245 pg/mL (muy elevado, indica fallo cardiaco), lipoproteína (a) 435 mg/L (elevada, factor de riesgo).\n- ECG: bradicardia sinusal, alteraciones de onda T‑U, QRS estrecho (90 ms).\n- Ecocardiograma: aurícula izquierda 41 mm, ventrículo izquierdo diástole 54 mm, fracción de eyección (LVEF) 28% (disfunción sistólica importante), acortamiento (FS) 13%, presión arterial pulmonar 29 mm Hg.\n- Angio‑TC coronaria: sin lesiones coronarias significativas.\n\nDiagnóstico\n- Miocardiopatía dilatada con insuficiencia cardiaca sistólica (HFrEF), clase funcional NYHA III (síntomas con actividad ligera).\n\nRazonamiento para la intervención\n- Persistencia de LVEF reducida (~30%) y síntomas limitantes a pesar de terapia médica óptima.\n- QRS estrecho contraindica o reduce la probabilidad de respuesta a resincronización (CRT).\n- Prueba preoperatoria con levosimendan fue positiva, lo que apoyó la probabilidad de respuesta a terapia eléctrica dirigida a mejorar la contractilidad.\n\nIntervención: implantación de modulación de la contractilidad cardiaca (CCM)\n- Procedimiento similar al de un marcapasos: vías de abordaje por vena subclavia izquierda, colocación de dos electrodos (Medtronic 3830‑69) fijados en el tabique ventricular derecho con 3 cm de separación, y conexión al generador Optimizer Smart.\n- Parámetros intraoperatorios: umbrales de estimulación bajos (0,5 V), buena detección de ondas R (>10–15 mV) e impedancias dentro de rango; ausencia de estimulación diafragmática con estimulación hasta 10 V.\n- Implantación técnica satisfactoria y entrega correcta de impulsos CCM en el ECG postoperatorio.\n\nEvolución y seguimiento\n- Evaluaciones seriadas incluyeron ecocardiografía Doppler, NT‑proBNP, prueba de caminata de 6 minutos y cuestionario MLHFQ.\n- A los 3 meses: reducción progresiva de volúmenes auricular y ventricular izquierdos y normalización del cociente E/e′ (marcador de presión de llenado diastólico), lo que indica mejora de la función diastólica; desaparición de opresión torácica y disnea; aumento de la tolerancia al ejercicio y mejora clara en calidad de vida.\n- No se describieron complicaciones agudas relacionadas con el implante.\n\nImplicaciones y próximos pasos recomendados\n- La CCM puede ser una opción útil en pacientes con HFrEF sintomática, LVEF moderadamente baja y QRS estrecho que no responden a terapia médica y no son candidatos claros para CRT.\n- Seguimiento a largo plazo: monitorizar función clínica, pruebas serológicas (NT‑proBNP), ecocardiografía y control del dispositivo (umbrales, detección, ausencia de estimulación diafragmática).\n- Tratar condiciones asociadas que pueden influir en el pronóstico: ajustar manejo tiroideo (TSH elevada), control de factores de riesgo lipídico (LDL y lipoproteína (a) elevada) y optimización farmacológica según guías.\n- Comunicación continua con la paciente sobre expectativas, señalización de síntomas de alarma y adherencia al seguimiento.\n\nConclusión\nEn esta paciente con miocardiopatía dilatada y LVEF severamente reducida, la implantación de CCM fue técnicamente exitosa y se asoció a mejoría objetiva de la función cardiaca (sistólica y diastólica) y a alivio sintomático significativo. Esto sugiere que la CCM puede revertir parcialmente la remodelación miocárdica y mejorar la calidad de vida en pacientes seleccionados con insuficiencia cardiaca refractaria a tratamiento médico."
+        }
+    },
+    {
+        "article": "Paciente de sexo femenino, 61 años, caucásica, casada, dos hijos, informó empeoramiento de los síntomas de la psoriasis tras el inicio de L-metilfolato 15 mg al día para tratamiento coadyuvante de la depresión. Informó depresión y psoriasis desde los 20 años. Desde los 41 años, la paciente no había tenido recidivas de las lesiones psoriáticas.\n\nPor su historial de depresiones, se le indicó carbonato de litio, pero no lo tomó debido a la psoriasis. En 2000, su cuadro depresivo mejoró con venlafaxina 225 mg al día. En 2016, debido a las oscilaciones de humor, se le agregó lamotrigina 100 mg al día y, para mejorar el sueño, se le sumó quetiapina 50 mg al día.\n\nEstas fueron las dosis actuales, con una mejora en la depresión, la calidad de vida y sin efectos adversos significativos.\n\nEn enero de 2019, se detectó polimorfismo en el gen MTHFR, con una mutación heterozigótica en C677T, y se le recetó a la paciente 15 mg diarios de L-metilfolato. Antes de que finalizara la primera semana de uso de L-metilfolato, aparecieron lesiones psoriáticas que no se habían manifestado en 20 años. Se informó lo ocurrido al psiquiatra, quien retiró la medicación y, 4 días después, las lesiones psoriáticas comenzaron a remitir, desapareciendo por completo al cabo de unas semanas. La paciente no volvió a registrar manifestaciones hasta principios de 2020.\n",
+        "gold_summary": "Paciente de sexo femenino, de 61 años, que había estado en remisión de psoriasis durante 20 años. Sufrió una recaída de psoriasis en forma de placa pocos días después de comenzar el tratamiento con L-metilfolato a una dosis diaria de 15 mg.\n",
+        "synthetic_summary": {
+            "B1": "Una mujer de 61 años tenía psoriasis y depresión desde joven. Durante 20 años no tuvo brotes de psoriasis. Tomaba medicinas para la depresión que le iban bien.\n\nLe hicieron una prueba y vieron un cambio en un gen llamado MTHFR. Eso puede cambiar cómo el cuerpo usa una vitamina llamada folato. Por eso le recetaron L‑metilfolato, que es una forma de esa vitamina, 15 mg al día.\n\nA los pocos días de tomarlo le volvieron las placas de psoriasis. Se lo contó al médico y dejaron de darle L‑metilfolato. Cuatro días después las manchas empezaron a mejorar y, en unas semanas, desaparecieron. No volvió a tener brotes hasta principios de 2020.\n\nParece que, en este caso, el L‑metilfolato pudo haber causado la recaída de la psoriasis.",
+            "B2": "Resumen breve y claro:\n\nUna mujer de 61 años, con antecedentes de depresión desde los 20 años y psoriasis (una enfermedad de la piel que causa placas rojas y escamosas), estuvo 20 años sin brotes de psoriasis. En enero de 2019, se le encontró una variante del gen MTHFR (que puede cambiar cómo el cuerpo usa el folato, una vitamina) y le recetaron L‑metilfolato 15 mg al día. L‑metilfolato es la forma activa del folato y a veces se añade para ayudar con la depresión.\n\nA menos de una semana de comenzar L‑metilfolato aparecieron de nuevo las lesiones de psoriasis. Su psiquiatra suspendió el medicamento y, cuatro días después, las lesiones empezaron a mejorar y desaparecieron por completo en pocas semanas. Antes de esto, su tratamiento con venlafaxina, lamotrigina y quetiapina estaba controlando bien la depresión sin efectos adversos importantes.\n\nEsto sugiere que el inicio de L‑metilfolato se asoció en el tiempo con la recaída de psoriasis, ya que las lesiones remitieron al retirar el fármaco. Un paso razonable en casos así es detener el medicamento sospechoso y vigilar la respuesta; también puede considerarse consultar con un dermatólogo y discutir alternativas para el tratamiento de la depresión.",
+            "B3": "Resumen clínico\n\nPaciente mujer de 61 años, con antecedentes de psoriasis desde los 20 años y en remisión completa durante aproximadamente 20 años (desde los 41). También presenta episodio(s) depresivo(s) crónico(s) controlados con medicación psiquiátrica estable: venlafaxina 225 mg/día, lamotrigina 100 mg/día y quetiapina 50 mg/día. Por motivos de tratamiento adyuvante de la depresión y tras detectarse un polimorfismo heterocigoto C677T en el gen MTHFR, se le prescribió L‑metilfolato 15 mg/día.\n\nDescripción del evento adverso\n- Normal previo: psoriasis en remisión durante 20 años; estado depresivo relativamente estable con la medicación actual y sin efectos adversos importantes.\n- Evento anómalo: a los pocos días (antes de finalizar la primera semana) de iniciar L‑metilfolato 15 mg/día, la paciente desarrolló lesiones psoriáticas en placa, reaparición que no había ocurrido en dos décadas.\n- Curso tras suspensión: el psiquiatra retiró L‑metilfolato; cuatro días después las lesiones comenzaron a remitir y desaparecieron por completo en unas semanas. La paciente no volvió a presentar manifestaciones cutáneas hasta principios de 2020.\n\nInterpretación y significado clínico\n- La temporalidad (inicio de la psoriasis pocos días después de comenzar L‑metilfolato) y la resolución tras la suspensión (dechallenge positivo) sugieren una relación probable entre L‑metilfolato 15 mg/día y la recaída psoriásica en esta paciente.\n- No se identificaron otros cambios en medicación o factores obvios que expliquen la reactivación, y las terapias psiquiátricas previas se toleraban bien.\n- Aunque no se puede probar causalidad definitiva con un solo caso, el patrón temporal hace razonable considerar el L‑metilfolato como el desencadenante más probable.\n\nRecomendaciones prácticas\n- Para pacientes con historia de psoriasis, especialmente de larga evolución, considerar con cautela el uso de altas dosis de L‑metilfolato y discutir el balance riesgo/beneficio.\n- Si se decide iniciar L‑metilfolato, recomendar seguimiento dermatológico estrecho y vigilancia temprana de cualquier signo cutáneo.\n- Ante reaparición de lesiones, suspender el fármaco y coordinar con dermatología y psiquiatría para alternativas antidepresivas seguras.\n- Notificar el evento adverso a los registros farmacovigilantes para mejorar la información sobre seguridad.\n\nComentario final\nEste caso subraya la importancia de revisar antecedentes dermatológicos antes de introducir suplementos o fármacos nuevos. La paciente tuvo resolución completa tras retirar L‑metilfolato, lo que permitió controlar la recaída; seguir un plan conjunto entre psiquiatría y dermatología ayudará a mantener tanto la salud mental como la cutánea de forma segura."
+        }
+    },
+    {
+        "article": "Se diagnosticó osteoartritis bilateral de las articulaciones de la cadera en un paciente de 61 años de edad con tratamiento con esteroides para la artritis reumatoide y dolencias en la ingle bilateral. [9] Recibió una inyección intraarticular bilateral de ácido hialurónico y se presentó doce semanas después en nuestro departamento de urgencias con fiebre, un estado general reducido y un dolor cada vez más incapacitante. Las radiografías de la pelvis mostraron una destrucción progresiva y rápida de ambas articulaciones de la cadera con una osteólisis extensa, subluxación concomitante y un defecto óseo acetabular del lado izquierdo. La aspiración de la articulación mostró pus en ambas articulaciones de la cadera y se hizo el diagnóstico de artritis séptica bilateral progresiva rápida. Se realizó una resección bilateral de ambas cabezas femorales con desbridamiento de la articulación de la cadera y la implantación de espaciadores de PMMA cargados con antibióticos a través de un enfoque anterolateral mínimamente invasivo.\n\nSe inició un tratamiento antibiótico sistémico empírico con vancomicina y ampicilina por vía intravenosa. Se detectó E. coli en muestras de tejido de ambas articulaciones de la cadera y se adaptó el tratamiento antibiótico sistémico a meropenem por vía intravenosa. Se realizaron dos procedimientos quirúrgicos de seguimiento con intercambio de los espaciadores de PMMA cargados con antibiótico para controlar la infección debido al drenaje persistente.\n\nDoce semanas después de la resección de la cabeza femoral y el control exitoso de la infección, el paciente recibió una artroplastia total de cadera con el uso adicional de un revestimiento multicapa de plata (HyProtect®, Bio-Gate, Nürnberg, Alemania). Este revestimiento consiste en una capa de siloxano ultrafina directamente sobre la superficie del implante (10 a 30 nm), de la que se liberan iones de plata.\n\n12 semanas después de la resección de la cabeza femoral, se realizó una artroplastia total de cadera en el lado derecho con una copa estándar sin cemento (Allofit®, ZimmerBiomet, Varsovia, EE. UU.) y un vástago femoral sin cemento (Avenir®, ZimmerBiomet, Varsovia, EE. UU.) a través del enfoque anterolateral mínimamente invasivo previamente utilizado con este revestimiento multicapa de plata ultrafino. Tanto la superficie posterior de la copa como todo el eje femoral se revistieron con plata.\n\nLa cadera izquierda se trató 18 semanas después de la resección de la cabeza femoral con una jaula de refuerzo recubierta de plata (Burch-Schneider®, ZimmerBiomet, Varsovia, EE. UU.) para un defecto acetabular tipo IIB de Paprosky y una copa de polietileno cementada (Durasul®, ZimmerBiomet, Varsovia, EE. UU.). El vástago femoral sin cemento (Avenir®, ZimmerBiomet, Varsovia, EE. UU.) también se recubrió de plata en toda su parte intramedular. Esta intervención también se realizó mediante el enfoque anterolateral mínimamente invasivo utilizado previamente. El paciente se sometió a una terapia antibiótica sistémica durante un período de tratamiento total de 18 semanas después de la implantación del lado derecho. Se aplicó ertapenem 1 g por vía intravenosa durante este período de tiempo una vez al día, después de la descarga en un entorno ambulatorio. Esto permitió una cobertura antibiótica del lado derecho de 18 semanas y del lado izquierdo de 12 semanas de tratamiento antibiótico.\n\nSe recomendó el uso parcial de peso con 20 kg en el lado operado y el uso de muletas durante 6 semanas después de las intervenciones.\n\nLas heridas de ambos lados se curaron sin incidentes. El paciente fue visto regularmente para un seguimiento clínico y radiológico. Se logró el apoyo total del peso sin el uso de muletas 7 semanas después de la operación en ambos lados. No hubo signos de PIJ y no fue necesaria una cirugía de revisión adicional.\n\nEn un seguimiento final tres años después de la implantación de las prótesis recubiertas de plata, la paciente mostró un aspecto normal de la piel con mínimas cicatrices después de enfoques antero-laterales mínimamente invasivos en ambos lados sin signos de argiria. Hubo un excelente resultado funcional de ambas caderas con marcha normal y una puntuación WOMAC de 6 en ambos lados (dolor: 0, rigidez: 0, función física: 6). El recuento de leucocitos en sangre fue de 7,29/nl (referencia: 4,23-9,1) y el nivel de proteína C reactiva (PCR) fue de 12,4 mg/l (referencia: <5 mg/l). El nivel ligeramente elevado de PCR es atribuible a la artritis reumatoide subyacente de la paciente. Las radiografías revelaron componentes protésicos de cadera bien integrados y no sueltos en ambos lados tres años después de la implantación con una articulación correcta.\n",
+        "gold_summary": "Este informe de caso se refiere a un paciente de 61 años con destrucción rápida de ambas articulaciones de la cadera debido a una artritis séptica que se trató con éxito con una implantación por etapas de prótesis de cadera recubiertas con plata con un recubrimiento ultrafino multicapa de plata. En un seguimiento de tres años, no hubo signos de infección, se observó un buen estado de todos los componentes protésicos y el resultado funcional fue excelente.\n",
+        "synthetic_summary": {
+            "B1": "Un paciente de 61 años tuvo una infección grave en las dos caderas. Antes tenía artritis y tomaba medicinas con esteroides. Después de una inyección en las caderas, se puso muy enfermo. Tenía fiebre y mucho dolor. Las radiografías mostraron que las caderas se estaban destruyendo. Al sacar líquido de las caderas, los médicos encontraron pus. Esto quería decir que había una infección con gusanos (gérmenes).\n\nPrimero le quitaron las partes dañadas del hueso y limpiaron las caderas. Pusieron piezas temporales con antibiótico para combatir los gérmenes. Le dieron antibióticos por la vena. Más tarde, cuando la infección estuvo controlada, le pusieron reemplazos de cadera permanentes. Las piezas nuevas tenían un recubrimiento muy fino con plata. La plata ayuda a impedir que vuelvan las infecciones.\n\nEl paciente usó muletas y caminó con cuidado al principio. Las heridas sanaron bien. Tres años después estaba muy bien. Caminaba normalmente y no tenía señales de infección. La piel se veía normal y las prótesis estaban firmes. Los análisis de sangre estaban casi normales; una prueba pequeña estaba un poco alta porque todavía tenía artritis. En resumen: los médicos controlaron la infección y las nuevas caderas funcionaron muy bien.",
+            "B2": "Resumen comprensible (nivel B2)\n\nUn hombre de 61 años con artritis reumatoide y que estaba tomando esteroides desarrolló dolor en ambas ingles y tenía artrosis de cadera. Recibió inyecciones en las articulaciones y, 12 semanas después, llegó a urgencias con fiebre, empeoramiento general y dolor muy intenso. Las radiografías mostraron una destrucción rápida de las dos caderas y la extracción de líquido articular mostró pus; se diagnosticó artritis séptica, es decir, infección grave dentro de ambas articulaciones.\n\nPara controlar la infección se retiraron las cabezas femorales (parte superior del hueso del muslo) y se limpiaron las articulaciones. Se colocaron espaciadores de PMMA (una especie de cemento que libera antibiótico localmente) y se inició tratamiento antibiótico por vía intravenosa. Las muestras de tejido crecieron E. coli, por lo que los antibióticos se adaptaron a ese germen. Debido a drenaje persistente, se cambiaron los espaciadores en dos ocasiones antes de considerar la reconstrucción definitiva.\n\nCuando la infección estuvo controlada, se realizó la artroplastia total de cadera en dos tiempos: primero el lado derecho y después el izquierdo. Las prótesis y algunos refuerzos usados en la cirugía recibieron un recubrimiento multicapa muy fino de plata, que libera iones de plata y ayuda a reducir el riesgo de que las bacterias vuelvan a crecer. Además, el paciente recibió antibióticos intravenosos durante varias semanas tras las cirugías y caminó con apoyo parcial durante las primeras semanas.\n\nLas heridas cicatrizaron bien y, a las siete semanas, pudo apoyar todo el peso sin muletas. Tres años después las caderas funcionaban muy bien (puntuación WOMAC de 6 en cada lado), no hubo signos de nueva infección ni problemas por la plata en la piel, los implantes estaban bien fijados en las radiografías y las pruebas de sangre fueron razonables (la PCR algo elevada se atribuyó a su artritis reumatoide). En resumen, el tratamiento por etapas con espaciadores antibióticos, antibióticos intravenosos prolongados y prótesis recubiertas de plata logró controlar la infección y obtuvo un buen resultado funcional a tres años.",
+            "B3": "Summary (readability band B3)\n\nPatient and presentation\n- A 61-year-old patient with rheumatoid arthritis on long-term steroids developed bilateral groin pain and was treated with intra‑articular hyaluronic acid injections. Twelve weeks later they presented with fever, worsening general condition and progressive, severe hip pain.\n- Imaging showed rapid, destructive changes in both hip joints with extensive bone loss and subluxation. Joint aspiration yielded pus from both hips, and the diagnosis was rapidly progressive bilateral septic arthritis.\n\nTreatment course\n- Initial surgery: both femoral heads were resected, the hips were extensively debrided, and antibiotic‑loaded polymethylmethacrylate (PMMA) spacers were placed via a minimally invasive anterolateral approach.\n- Empiric intravenous antibiotics (vancomycin + ampicillin) were started. Cultures from joint tissue grew Escherichia coli, so systemic therapy was changed to meropenem. Because drainage persisted, two additional operations were done to exchange the antibiotic spacers.\n- After infection control, staged total hip arthroplasties were performed: the right hip 12 weeks after resection and the left hip 18 weeks after resection. Both procedures used implants with a multilayer ultrathin silver coating (a siloxane layer that releases silver ions). The left side required a silver‑coated reinforcement cage for a Paprosky type IIB acetabular defect and a cemented polyethylene cup.\n- Systemic intravenous ertapenem 1 g daily was continued as outpatient therapy for a total of 18 weeks after the right‑side implantation (resulting in 18 weeks of antibiotic coverage for the right hip and 12 weeks for the left).\n\nRecovery and follow‑up\n- The surgical wounds healed without complication. The patient progressed to full weight bearing without crutches by seven weeks after each operation.\n- At three years after implantation there were no clinical or radiographic signs of recurrent periprosthetic joint infection. The hips showed well‑integrated, stable prosthetic components.\n- Function was excellent: normal gait and a WOMAC score of 6 on each side (pain 0, stiffness 0, physical function 6). There were no signs of argyria (skin discoloration from silver).\n- Laboratory tests at three years: normal white blood cell count (7.29/nl) and a mildly elevated C‑reactive protein (CRP 12.4 mg/L), attributed to the patient’s underlying rheumatoid arthritis rather than implant infection.\n\nInterpretation and implications\n- This case demonstrates successful management of bilateral, rapidly destructive septic arthritis in an immunosuppressed patient using a staged approach: aggressive debridement with antibiotic spacers, culture‑directed prolonged IV antibiotics, and delayed total hip arthroplasty using implants with an ultrathin silver coating.\n- The silver coating was well tolerated in this patient (no argyria) and infection did not recur over three years, suggesting that silver‑coated implants can be a useful adjunct in high‑risk or previously infected reconstructions. However, this is a single case—broader studies are needed to define safety, long‑term outcomes and comparative effectiveness.\n- Practical points for similar cases: obtain culture guidance, use staged exchange with antibiotic spacers when infection is active, provide prolonged culture‑directed antibiotics, monitor clinical, radiographic and laboratory markers for recurrence, and counsel patients about the risks and uncertain long‑term benefits of silver‑coated implants."
+        }
+    },
+    {
+        "article": "Una niña africana de raza negra, con 1000 g de peso, nacida a las 32 semanas de gestación, de madre viva, fue derivada a nuestra unidad de cuidados intensivos neonatales debido a múltiples anomalías congénitas y dificultad respiratoria moderada. La madre tiene 32 años y está en un matrimonio no consanguíneo. La madre no buscó atención médica hasta el inicio del tercer trimestre de embarazo, debido a un desprendimiento de placenta. El primer ultrasonido prenatal reveló oligohidramnios severos. No era diabética (la glucosa en sangre aleatoria fue de 5.1 mmol/L) y no recibió suplementos de ácido fólico durante el embarazo.\n\nAl ingreso, la bebé estaba alerta con características leves del síndrome de dificultad respiratoria. Presentaba múltiples rasgos dismórficos, entre ellos, microcefalia (circunferencia de la cabeza < 10%), occipucio prominente, orejas bajas, paladar hendido y labio derecho, micrognatia, contractura bilateral de los codos e inferiores más cortos.\n\n\nEl peso al nacer fue de 1000 g, la longitud del bebé fue de 40 cm y la circunferencia occipitofrontal fue de 30 cm.\n\nInvestigaciones\nLa radiografía esquelética mostró aplanamiento de las costillas, aplasia del fémur derecho e hipoplasia del fémur izquierdo. Los análisis de laboratorio incluyeron: hemograma completo, proteína C reactiva, creatinina, urea en sangre y electrolitos, todos dentro de los valores normales. La ecografía craneal fue normal, pero la ecocardiografía reveló un pequeño conducto arterioso permeable.\n\nDiagnóstico diferencial\nLa paciente presentaba aplasia femoral bilateral y facies inusuales. Estas características clínicas llevaron al diagnóstico de síndrome femoro-facial.\n\nLa similitud en la etiopatogénesis hace que el síndrome de regresión caudal sea el diagnóstico diferencial común. Ambos pueden ser causados por una hiperglucemia materna mal controlada. Sin embargo, los defectos faciales están ausentes en el síndrome de regresión caudal, la característica diagnóstica clave.\n\nLa hipoplasia femoral focal proximal y las anomalías craneofaciales suelen estar ausentes.\n\nEntre las condiciones que pueden provocar el labio leporino se incluye el síndrome de banda amniótica grave.\n\nTratamiento\nEl bebé recibió asistencia respiratoria y antibióticos empíricos. Participaron un cirujano ortopédico, un otorrinolaringólogo y un fisioterapeuta. Está previsto reparar quirúrgicamente el paladar hendido a los 6 meses de edad. La rehabilitación funcional está prevista antes de que el paciente comience a deambular. La cirugía de alargamiento de extremidades no se realiza actualmente en nuestro entorno.\n\nResultado y seguimiento\nEl paciente falleció a la edad de un mes por complicaciones de una sepsis neonatal grave de inicio tardío.\n",
+        "gold_summary": "Una niña africana de raza negra bantú de 1 día de vida fue admitida en la unidad neonatal debido a múltiples anomalías congénitas. La madre no buscó atención médica hasta el inicio del tercer trimestre, cuando tuvo un desprendimiento de placenta. La madre nunca recibió suplementos de ácido fólico prenatal. La niña tenía microcefalia, orejas bajas, paladar hendido derecho y labio, micrognatia, contractura y extremidades más cortas. Una radiografía esquelética mostró hipoplasia femoral. Presentamos este caso poco habitual y destacamos los retos en el diagnóstico y el tratamiento.\n",
+        "synthetic_summary": {
+            "B1": "Esta es la historia de una bebé muy pequeña. Nació antes de tiempo, a las 32 semanas. Pesó 1 kilo. La mamá tiene 32 años y no tuvo controles con el médico hasta muy tarde en el embarazo. No tomó ácido fólico. Durante el embarazo hubo poco líquido alrededor del bebé.\n\nAl nacer, la niña estaba despierta pero respiraba con dificultad leve. Tenía la cabeza más pequeña de lo esperado. Tenía orejas bajas, un labio y paladar partidos en el lado derecho (esto se llama paladar hendido), y la mandíbula pequeña. También tenía los codos apretados y las piernas más cortas.\n\nLas radiografías mostraron que faltaba el hueso del muslo derecho y que el muslo izquierdo estaba pequeño. El ultrasonido de la cabeza fue normal, y algunas pruebas de sangre también estuvieron dentro de lo esperado. El corazón tenía un pequeño orificio llamado ductus arterioso persistente.\n\nLos médicos pensaron que tenía un problema llamado síndrome femoro-facial. Trataron a la bebé con ayuda para respirar y con antibióticos. También la vieron un cirujano de huesos, un especialista de oídos y garganta, y un fisioterapeuta. Planeaban arreglar el paladar cuando tuviera 6 meses y hacer terapia para ayudarla a caminar.\n\nCon mucho dolor, la bebé murió a la edad de un mes por una infección grave en la sangre. Es una historia triste. Los médicos aprendieron sobre un caso poco común y los desafíos para cuidar a bebés con muchos problemas al nacer.",
+            "B2": "Resumen claro y amable\n\nPresentación\nUna recién nacida africana de 32 semanas (muy prematura) y 1 000 g fue ingresada en la unidad neonatal por varias malformaciones congénitas y dificultad respiratoria leve. La madre tenía 32 años, no recibió control prenatal hasta el tercer trimestre porque presentó un desprendimiento de la placenta, y no tomó suplementos de ácido fólico durante el embarazo. El primer ultrasonido mostró oligohidramnios severo (poco líquido alrededor del feto).\n\nHallazgos en la bebé\n- Cabeza pequeña (microcefalia: circunferencia por debajo del rango esperado).\n- Occipucio prominente (parte posterior de la cabeza más sobresaliente).\n- Orejas bajas.\n- Labio y paladar hendidos en el lado derecho (hendidura en el labio y en el techo de la boca).\n- Micrognatia (mandíbula pequeña).\n- Contracciones en ambas articulaciones de los codos y extremidades inferiores más cortas de lo habitual.\n- Radiografía ósea: ausencia del fémur derecho y fémur izquierdo más pequeño (aplasia e hipoplasia femoral).\n- Ecocardiograma: pequeño conducto arterioso permeable (PDA), que es un vaso que normalmente se cierra después del nacimiento.\n- Ecografía cerebral y pruebas de sangre básicas dentro de la normalidad al ingreso.\n\nDiagnóstico y consideraciones\nLos médicos consideraron el síndrome femoro-facial, que combina problemas en los huesos del muslo con rasgos faciales anormales. Como diagnóstico alternativo se evaluó el síndrome de regresión caudal (otro trastorno relacionado con la formación de la parte baja del cuerpo), pero este último generalmente no tiene defectos faciales, lo que apoyó el diagnóstico de femoro-facial en este caso. Algunas condiciones como bandas amnióticas pueden causar labio leporino, por lo que también se tuvieron en cuenta otras causas. Aunque algunos síndromes se han asociado con diabetes materna mal controlada, en este caso la madre no era diabética según la glucosa registrada.\n\nTratamiento y seguimiento\nLa bebé recibió soporte respiratorio y antibióticos empíricos. Fueron consultados ortopedia, otorrinolaringología y fisioterapia. Se planificó reparar el paladar hendido a los 6 meses y comenzar rehabilitación antes de que la niña empezara a caminar. Algunas operaciones complejas, como alargamiento de las extremidades, no estaban disponibles en el centro.\n\nResultado\nLa bebé falleció a la edad de un mes por una sepsis neonatal severa de inicio tardío (infección generalizada grave adquirida después del período inmediato del nacimiento).\n\nComentario final (empatía y contexto)\nEste caso muestra un cuadro poco frecuente y los retos que existen para diagnosticar y tratar malformaciones complejas en recién nacidos, especialmente cuando el control prenatal es tardío y hay limitaciones de recursos. Es una situación triste; las decisiones médicas intentaron ofrecer apoyo y planificar intervenciones futuras, pero la infección grave complicó el curso.",
+            "B3": "Case summary\nA preterm Black African female infant (32 weeks’ gestation, birth weight 1,000 g, length 40 cm, head circumference 30 cm) was referred to the neonatal intensive care unit on day 1 of life for multiple congenital anomalies and moderate respiratory distress. The mother (32 years) had no consanguinity with the father, sought prenatal care late (first seen in the third trimester after placental abruption), had severe oligohydramnios on ultrasound, did not take prenatal folic acid, and was not known to be diabetic (random maternal glucose 5.1 mmol/L).\n\nAbnormal findings (clinical and imaging)\n- Craniofacial and head: microcephaly (head circumference <10th centile), prominent occiput, low-set ears, right-sided cleft lip and cleft palate, and micrognathia (small lower jaw).  \n- Limbs and musculoskeletal: bilateral elbow contractures and markedly shortened lower limbs. Skeletal X-ray showed right femoral aplasia (absence) and left femoral hypoplasia, with flattened ribs.  \n- Cardiac: small patent ductus arteriosus on echocardiography.  \n- Respiratory: mild features of neonatal respiratory distress syndrome requiring respiratory support.\n\nNormal or unremarkable findings\n- Basic laboratory tests, including complete blood count, C-reactive protein, renal function (creatinine, urea) and electrolytes, were within reference ranges at admission.  \n- Cranial ultrasound was normal.\n\nWorking diagnosis and differential\n- The clinical picture (proximal femoral deficiency with characteristic facial anomalies) led to a diagnosis of femoral-facial syndrome.  \n- Caudal regression syndrome is an important differential because both disorders can be associated with maternal hyperglycemia; however, caudal regression typically lacks the facial anomalies seen here.  \n- Severe amniotic band syndrome can cause cleft lip/palate and other limb defects and was considered as another differential.\n\nManagement and course\n- Initial care included respiratory support and empirical antibiotics. Multidisciplinary involvement included orthopedics, otolaryngology, and physiotherapy.  \n- Planned interventions included surgical repair of the cleft palate at about 6 months of age and pre-ambulation functional rehabilitation. Limb-lengthening or advanced orthopedic reconstruction was not available in the treating center.  \n- The infant developed late-onset neonatal sepsis and died at one month of age.\n\nImplications and recommendations\n- This is a rare and severe presentation of femoral-facial syndrome, highlighting diagnostic challenges and limited therapeutic options in a resource-constrained setting.  \n- Important preventive and investigational points for future pregnancies: timely prenatal care, folic acid supplementation, and screening for maternal diabetes (since maternal hyperglycemia can be associated with similar anomalies).  \n- Families should be offered multidisciplinary counseling (genetic counseling when available, discussion of recurrence risk, and psychosocial support).  \n- Where possible, referral to specialized centers for orthopedic planning and advanced neonatal surgical care can improve access to reconstructive options and long-term rehabilitation.\n\nTone and context\n- The case illustrates both the medical complexity of congenital limb–facial syndromes and the vulnerability of neonates to infectious complications. The outcome was tragic; compassionate follow-up and support for the family are important components of care."
+        }
+    },
+    {
+        "article": "Paciente de sexo masculino de 18 años, con diag nóstico clínico de Neurofibromatosis tipo 1 desde el primer año de vida. Entre sus antecedentes destaca que tiene educación completa, sus padres no son consan guíneos, y no tiene antecedentes familiares de manchas café con leche. Desde el punto de vista neurológico desarrolló durante la infancia retraso del desarrollo psicomotor fino y grueso, trastorno del lenguaje de predominio expresivo, con alteración fonológica y semántica del lenguaje, por lo que fue manejado con fonoaudiología en Escuela de Lenguaje, además de ki- nesioterapia y terapia ocupacional durante la infancia. Durante la adolescencia se le diagnosticó Trastorno por Déficit Atencional e Hiperactividad, que fue manejado con metilfenidato, manteniendo regular rendimiento escolar. Tuvo desarrollo puberal normal. Oftalmológi camente presentó nódulos de Lisch desde los 4 años de edad, euriblefaron y astigmatismo. Se mantuvo en control anual en Oftalmología y Neuropediatría. Su última Resonancia Magnética de cerebro fue realiza da 6 meses previo a la consulta en Dermatología, sin hallazgos patológicos y en la Resonancia Magnética de columna se evidenció discopatía L5-S1 y realce perifacetario en T11-T12 y T12-L1. A los 16 años se reali zó estudio genético que demostró deleción de exones 5-47 del gen NF1.\n\nA los 18 años consultó en servicio de Dermatología del Centro de Referencia en Salud Peñalolén Cordille ra Oriente por aparición de nueva mancha en muslo izquierdo de 1 año evolución, asintomática. Además, refirió aparición de nódulos en muñeca derecha, su praciliar derecho y cuero cabelludo, de unos meses de evolución, asintomáticos.\n\nAl examen físico destacaba presión arterial normal, macrocefalia (CC: 60 cm) y múltiples manchas café con leche generalizadas, efélides en axilas, y en zona supraciliar derecha, occipital y muñeca derecha nódulos subcutáneos ovalados de 0,5 cm, bien delimitados, móviles. En muslo izquierdo lateral pre sentaba placa de 25 mm algo rosada, con pérdida de anexos, y de consistencia blanda. Por último, en zona lumbar y pectoral, múltiples máculas rojo- azuladas pequeñas, de menos de 5 mm cada una, algu nas levemente deprimidas.\n\nSe realizó biopsia cutánea de máculas azuladas en pecho y de placa muslo, resultando ambas compatibles con NF. Se realizó una ecografía de nódulos supraciliar y occipital que resultó compatible con NF nodular subcutáneo.\n\nUsando la clasificación clínica de García-Martínez et al.1 se diagnosticó al paciente con NF superficial sub cutáneo nodular en zona supraciliar derecha, occipital y muñeca derecha, NF superficial cutáneo pseudoatró fico en muslo izquierdo lateral y NF superficial cutáneo rojo azulado en zona lumbar y pectoral.",
+        "gold_summary": "Paciente masculino de 18 años con diagnóstico desde la infancia de NF-1 que presenta múltiples nodulos ovalados en cara, zona occipital y muñeca, máculas rojo-azuladas en dorso y placa rosada atrófica en muslo. El estudio ecográfico de los nódulos fue compatible con neurofibromas y el estudio histopatológico de las lesiones de dorso y muslo compatibles con neurofibromas cutáneos.",
+        "synthetic_summary": {
+            "B1": "Resumen simple y amable:\n\nEste joven tiene 18 años y desde bebé sabe que tiene neurofibromatosis tipo 1. Esa enfermedad causa manchas en la piel y a veces bultos pequeños.\n\nCuando era niño recibió terapia del habla, fisioterapia y apoyo escolar. También le diagnosticaron TDAH y tomó medicina para eso. Tiene nódulos en los ojos llamados nódulos de Lisch y la cabeza un poco más grande de lo habitual.\n\nA los 17–18 años le salieron nuevas lesiones en la piel. Apareció una mancha rosada en el muslo que mide unos 2,5 cm. También notó bultitos pequeños y móviles en la frente, la nuca y la muñeca derecha. Además había pequeñas manchas rojo-azuladas en la espalda y el pecho. Los bultos no le dolían.\n\nHicieron estudios: la ecografía de los nódulos y las biopsias de la mancha del muslo y de las manchas del pecho mostraron que son neurofibromas. La resonancia del cerebro fue normal. La resonancia de la columna mostró cambios en un disco y en unas articulaciones. Un estudio genético confirmó un cambio en el gen NF1, que explica la enfermedad.\n\nEn resumen: tiene múltiples neurofibromas en la piel y algunas manchas. Los exámenes confirmaron que las nuevas lesiones son parte de su neurofibromatosis.",
+            "B2": "Resumen comprensible (nivel secundaria — B2)\n\nEste informe describe a un joven de 18 años con diagnóstico de neurofibromatosis tipo 1 (NF1) desde el primer año de vida. NF1 es una condición genética que causa manchas en la piel y tumores benignos que nacen de los nervios (estos tumores se llaman neurofibromas).\n\nAntecedentes importantes\n- Tuvo retrasos en el desarrollo motor y en el lenguaje en la infancia; recibió terapia del lenguaje, fisioterapia y terapia ocupacional.  \n- Durante la adolescencia fue diagnosticado con TDAH y recibió metilfenidato.  \n- Tuvo pubertad normal.  \n- Desde los 4 años tenía nódulos en el iris del ojo llamados nódulos de Lisch (manchitas en el ojo que suelen aparecer en NF1), además de astigmatismo y una diferencia en el párpado (euriblefaron).  \n- Estudio genético a los 16 años mostró una eliminación grande en el gen NF1 (deleción de exones 5-47), lo que confirma la causa genética de su NF1.  \n- La resonancia del cerebro hecha 6 meses antes fue normal; la de columna mostró algo de desgaste de disco en L5-S1.\n\nQué consultó ahora\n- Nueva mancha en el muslo izquierdo que apareció hace 1 año (no duele ni molesta).  \n- Nódulos pequeños en la frente (sobre la ceja derecha), en la nuca (occipucio) y en la muñeca derecha que salieron hace meses, también sin dolor.  \n- Varias manchas rojo-azuladas pequeñas en la espalda y el pecho.\n\nHallazgos al examen y estudios\n- Múltiples manchas “café con leche” y efélides (pecas) en las axilas. Cabeza mayor de lo habitual (microcefalia no, sino macrocefalia: circunferencia 60 cm).  \n- Nódulos subcutáneos ovalados, móviles, de ~0,5 cm en frente, nuca y muñeca.  \n- Placa en muslo izquierdo de 25 mm, algo rosada, con pérdida de pelo local y consistencia blanda.  \n- Pequeñas máculas rojo-azuladas (<5 mm) en zona lumbar y pectoral, algunas ligeramente hundidas.  \n- Ecografía de los nódulos y biopsias de la zona del pecho y del muslo: todos los hallazgos fueron compatibles con neurofibromas (tumores benignos asociados a NF1).\n\nDiagnóstico final (clasificación clínica)\n- Neurofibromas subcutáneos nodulares: frente (supraciliar derecha), occipucio y muñeca derecha.  \n- Neurofibroma cutáneo pseudoatrófico: placa rosada en muslo izquierdo.  \n- Neurofibromas cutáneos rojo-azulados: zonas lumbar y pectoral.\n\nQué significa y siguientes pasos\n- Las lesiones encontradas son compatibes con los tipos comunes de neurofibromas en NF1 y actualmente son asintomáticas.  \n- Es importante mantener seguimiento médico regular (dermatología, neurología y oftalmología).  \n- Se vigilarán cambios en tamaño, dolor, sangrado o pérdida de función; si alguno aparece, se puede considerar extirpar el tumor o hacer estudios adicionales para descartar complicaciones.  \n- Dado que la prueba genética mostró una deleción grande en NF1, también puede ser recomendable asesoría genética para la familia.\n\nSi tienes preguntas sobre qué observar en casa o sobre opciones de tratamiento, los médicos del equipo pueden explicar los riesgos, beneficios y pasos siguientes de forma clara y paciente.",
+            "B3": "Resumen clínico breve (nivel universitario)\n\nAntecedentes relevantes\n- Paciente masculino de 18 años, con diagnóstico clínico de neurofibromatosis tipo 1 (NF1) desde el primer año de vida. El estudio genético a los 16 años mostró una deleción de los exones 5–47 del gen NF1, confirmando la enfermedad a nivel molecular.\n- Desarrollo neurológico: retraso psicomotor fino y grueso en la infancia, trastorno del lenguaje (predominio expresivo) tratado con fonoaudiología, kinesioterapia y terapia ocupacional. Diagnosticado luego con trastorno por déficit de atención e hiperactividad (TDAH) tratado con metilfenidato.\n- Ojos: nódulos de Lisch (pequeñas lesiones en el iris) desde los 4 años. Pubertad y presión arterial normales.\n- Imágenes: resonancia magnética cerebral hecha 6 meses antes de la consulta sin hallazgos patológicos; resonancia de columna con discopatía L5–S1 y realce perifacetario en T11–T12 y T12–L1.\n\nPresentación actual\n- Consulta por aparición, durante el último año, de una nueva placa en el muslo izquierdo (asintomática) y, durante meses, de nódulos subcutáneos asintomáticos en la región supraciliar derecha, cuero cabelludo (occipital) y muñeca derecha.\n- Examen físico: macrocefalia (circunferencia craneal 60 cm), múltiples manchas café con leche y efélides axilares. Nódulos subcutáneos ovalados, bien delimitados y móviles (≈0,5 cm). Placa en muslo lateral izquierdo de 25 mm, de aspecto algo rosado, con pérdida de anexos (pelo) y consistencia blanda. Varias máculas rojo‑azuladas pequeñas (<5 mm) en región lumbar y pectoral, algunas levemente deprimidas.\n\nEstudios realizados y diagnóstico\n- Biopsias cutáneas de las máculas rojo‑azuladas del pecho y de la placa del muslo: resultados compatibles con neurofibromas cutáneos.\n- Ecografía de los nódulos supraciliar y occipital: compatible con neurofibromas subcutáneos nodulares.\n- Clasificación clínica (según García‑Martínez et al.): coexistencia de tres fenotipos cutáneos en este paciente — NF superficial subcutáneo nodular (supraciliar derecho, occipital, muñeca derecha), NF superficial cutáneo pseudoatrófico (muslo izquierdo lateral) y NF superficial cutáneo rojo‑azulado (zona lumbar y pectoral).\n\nQué es normal y qué es anómalo aquí\n- Coincide con NF1: macrocefalia, manchas café‑con‑leche, efélides axilares, nódulos (neurofibromas) y nódulos de Lisch son hallazgos típicos de NF1.\n- Anómalo o relevante para seguimiento: aparición de nuevas lesiones cutáneas y subcutáneas confirmadas como neurofibromas; la deleción amplia en NF1 (exones 5–47) puede asociarse con mayor carga de enfermedad en algunos casos, por lo que requiere vigilancia más estrecha.\n\nImplicaciones y recomendaciones prácticas\n- Seguimiento multidisciplinario continuo: control dermatológico, neurología/neuropediatría y oftalmología según protocolo de NF1. Dada la genética confirmada, ofrecer asesoría genética si considera tener descendencia.\n- Vigilancia activa de lesiones: indicar control y reevaluación si cualquier neurofibroma crece rápidamente, duele, causa déficit neurológico o cambia de aspecto (motivos para imagen adicional y posible derivación a cirugía). Biopsia o resección se justifica si hay duda diagnóstica o sintomas.\n- Imagen y clínica de columna: correlacionar con síntomas de dolor o signos neurológicos; la discopatía y el realce facetario pueden requerir manejo ortopédico/neuroquirúrgico si hay clínica.\n- Riesgos a explicar al paciente: aunque la mayoría de los neurofibromas son benignos, existe un riesgo (bajo) de transformación maligna en algunos casos (tumor maligno de la vaina nerviosa); por eso la observación periódica es importante.\n- Soporte psicosocial y educativo: dado el antecedente de dificultades del desarrollo y TDAH, mantener soporte rehabilitador y educativo según necesidad.\n\nComentario final (empático)\nUsted presenta las manifestaciones cutáneas y sistémicas esperables de NF1, confirmadas por estudios histológicos y por la deleción genética amplia. Lo más importante ahora es mantener controles periódicos con los especialistas, vigilar cambios en las lesiones cutáneas o síntomas nuevos, y recibir orientación genética si planea tener hijos. Si desea, puedo ayudar a redactar preguntas para llevar a la próxima consulta o a preparar una lista de señales de alarma que justifiquen consultar antes."
+        }
+    },
+    {
+        "article": "Un hombre de 38 años de edad fue ingresado en el hospital por traumatismo torácico contundente. El paciente estaba generalmente sano y no tenía factores de riesgo de enfermedad coronaria. Fue golpeado en el pecho por un tornillo de alta velocidad que tenía aproximadamente 6 cm de diámetro mientras trabajaba en una fábrica. Voló aproximadamente 4 metros de distancia debido a la fuerza y presión del tornillo de alta velocidad. Perdió el conocimiento de inmediato, pero recuperó la conciencia varios minutos después. Fue trasladado inmediatamente a la sala de urgencias de un hospital local. Su puntaje en la escala de coma de Glasgow fue de 15. Se quejó de dolor torácico intenso y persistente, opresión y disnea. La tomografía computarizada del tórax mostró derrame pleural bilateral y fracturas de esternón y costillas. Por lo tanto, se insertó un tubo torácico durante varios días. Luego, fue dado de alta sin someterse a un electrocardiograma (ECG) u otros exámenes cardiovasculares.\n\nTres meses después del alta hospitalaria, durante un chequeo de seguimiento de rutina, todavía había presencia de derrame pleural con síntomas acompañantes de opresión en el pecho, falta de aire después de la actividad física, e incluso disnea por la noche, lo que motivó su ingreso en nuestro hospital. Sus constantes vitales durante el ingreso fueron las siguientes: frecuencia cardíaca regular de 98 latidos/min, presión arterial de 110/70 mmHg, y frecuencia respiratoria de 20 respiraciones/min. El examen físico mostró una pulsación carotídea y yugular normal. El movimiento respiratorio torácico bilateral y la actividad fueron normales, la fibrilación del lenguaje táctil del pulmón derecho disminuyó, la percusión del pulmón derecho presentó un sonido sordo, y los sonidos respiratorios disminuyeron. No hubo roncus ni estertores evidentes durante la auscultación pulmonar. No hubo murmullos en la auscultación cardíaca. Los exámenes del abdomen y las extremidades revelaron hallazgos normales. El primer ECG mostró evaluación ST e inversión de la onda T en las derivaciones I, aVL y V2-V5 y en el bloqueo de rama anterior izquierdo. La prueba de troponina-I fue negativa, y el nivel de NT-proBNP fue de 706 pg/ml (rango normal: 0-104 pg/ml), lo que sugiere un infarto de miocardio anterior antiguo. La ecocardiografía transtorácica mostró una aurícula izquierda de 26,4 mm, un ventrículo izquierdo de 51,8 mm, y una fracción de eyección ventricular izquierda (EF) del 32% (modo M). La pared anterior del LV e interventricular septum mostraron adelgazamiento a 6,6 mm, con un eco de movimiento notablemente reducido.\n\nAl examinar las arterias carótidas, intracraneales y de las extremidades inferiores del paciente, no se encontraron placas ateroscleróticas evidentes. Todos los hallazgos apoyaron el diagnóstico de infarto de miocardio antiguo (OMI), en lugar de arteriosclerosis. Sin embargo, el paciente era hemodinámicamente estable. Después de someterse a una terapia diurética, se le administraron bloqueadores beta, estatinas y estimulantes cardíacos, lo que alivió su malestar. La angiografía por tomografía computarizada coronaria mostró una estenosis moderada en la arteria LAD proximal. Para confirmar la estenosis y examinar el estado de la íntima coronaria, se realizó CAG 3 meses después del traumatismo torácico, que mostró un estrechamiento aproximado del 70% del lumen en la LAD proximal y el segmento coronario tenía una lesión curva. La arteria circunfleja izquierda (LCX) y la arteria coronaria derecha (RCA) eran normales. Los resultados de CAG confirmaron el diagnóstico de OMI, pero debido a la carga de costos, el paciente rechazó el examen IVUS. El paciente se sometió a una terapia conservadora y fue dado de alta del hospital varios días después.\n\nUn mes después, el 9 de diciembre de 2014, volvió al hospital para someterse a una intervención coronaria percutánea (ICP). Después de someterse a una terapia con fármacos, sus condiciones habían mejorado ligeramente. El examen físico y el ECG revelaron resultados casi normales. La ecocardiografía transtorácica mostró una mejora en la función sistólica del LV y EF del 45%. Se sometió a otra CAG 4 meses después del traumatismo torácico, que mostró una ligera mejora de la estenosis. Había aproximadamente un 60% de estrechamiento del lumen. Se realizó un IVUS y reveló que la gravedad de la lesión era del 55.9%, y la placa de bajo eco apareció antes de la formación de trombos después de la rotura subintimal. Completamos el examen sin más intervención porque solo se encontró un 55.9% de estrechamiento del lumen y el paciente tenía una hemodinámica estable sin evidencia de isquemia miocárdica constante. Se le recetó al paciente la medicación óptima, y su incomodidad se alivió gradualmente. El 17 de julio de 2018, 4 años después del traumatismo, la evaluación de seguimiento reveló que el paciente todavía experimentaba dificultad para respirar después de trabajar, pero se alivió poco después de descansar. El examen físico mostró los siguientes resultados: presión arterial de 114/80 mmHg, frecuencia cardíaca de 66 latidos/min, ausencia de anomalías obvias en la auscultación pulmonar y cardíaca; y ausencia de edema obvio en ambas extremidades inferiores. El ECG de seguimiento reveló los siguientes hallazgos: rS en las derivaciones V2-V4, inversión de la onda T en las derivaciones I, AVL y V2-V5 y bloqueo de rama izquierda. La ecocardiografía transtorácica mostró agrandamiento del ventrículo izquierdo con una aurícula izquierda de 39 mm, un ventrículo izquierdo de 54.7 mm y una EF del LV del 41% (Simpson's). También se observó adelgazamiento de la pared anterior del LV y del tabique interventricular, con la parte más delgada de 4.7 mm; el movimiento casi había desaparecido y el eco se había mejorado. Sin embargo, las arterias carótidas, intracraneales y de las extremidades inferiores seguían siendo normales. Además, descubrimos que los medicamentos recetados para tratar la insuficiencia cardíaca no se tomaron religiosamente después del alta; por lo tanto, recetamos 23.75 mg de metoprolol, 2.5 mg de benazepril y 20 mg de espironolactona para tomar una vez al día, y coenzima para tomar cada 10 horas.\n\nMH - Adulto\nMH - Errores de diagnóstico\nMH - Insuficiencia cardiaca/etiología\nMH - Humanos\nMH - Hombre\nMH - Infarto de miocardio/complicaciones/*etiología\nMH - Lesiones torácicas/*complicaciones\nMH - Tiempo hasta el tratamiento\nMH - Heridas, no penetrantes/complicaciones\n",
+        "gold_summary": "Preocupaciones de los pacientes:\nUn hombre de 38 años, previamente sano, fue admitido en nuestro hospital con una queja de disnea. Tenía un historial de haber sido golpeado en el pecho por un tornillo de alta velocidad mientras trabajaba en una fábrica 3 meses antes de ser admitido en el hospital.\n\nDiagnóstico:\nLuego de realizarse una angiografía coronaria y una ecocardiografía, finalmente se le diagnosticó un infarto de miocardio.\n\nIntervenciones:\nRecibió medicamentos optimizados, entre ellos, diuréticos, bloqueadores beta y estimulantes cardíacos.\n\nResultados:\nAl cabo de cuatro años de seguimiento, se le diagnosticó al paciente una insuficiencia cardíaca crónica con una fracción de eyección reducida.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre de 38 años se golpeó muy fuerte el pecho con un tornillo mientras trabajaba. Perdió el conocimiento por un rato y tuvo mucho dolor en el pecho. Primero lo atendieron en el hospital, pero no le hicieron pruebas del corazón.\n\nTres meses después todavía tenía falta de aire. Los médicos le hicieron imágenes especiales del corazón. Descubrieron que había tenido un ataque al corazón cuando se lastimó el pecho. Eso dañó una parte del corazón y lo dejó más débil.\n\nLe dieron medicinas para ayudar al corazón y para quitarle líquido del cuerpo. Mejoró un poco, pero el corazón no volvió a ser del todo fuerte. Cuatro años después seguía con el corazón débil y tenía lo que llaman insuficiencia cardíaca crónica. También se notó que no siempre tomaba sus medicinas como debía, por eso los doctores le recetaron nuevos medicamentos y le pidieron que los tome todos los días.",
+            "B2": "Patient story (in simple terms)\nA previously healthy 38-year-old man was hit hard in the chest by a large, high-speed screw while working in a factory. He lost consciousness briefly and had broken ribs and a broken breastbone. He was treated for chest injuries and a fluid build-up around the lungs, then sent home. No heart tests were done at that first discharge.\n\nWhat happened next\nThree months later he still had chest tightness and shortness of breath. Tests at our hospital showed changes on his ECG (a heart tracing) and a high NT-proBNP blood level (a marker that can mean the heart is strained). An ultrasound of the heart (echocardiogram) showed the front wall of his left heart was thin and not moving well, and his left ventricular ejection fraction (EF) — the percent of blood the heart pumps out each beat — was low (about 32%). These findings meant he had an old heart attack (myocardial infarction), most likely caused by the blunt chest trauma rather than usual artery disease, because scans did not show plaque elsewhere.\n\nFurther checks and treatment\nCoronary imaging (angiography and later CT angiography) showed the left anterior descending (LAD) artery had a significant narrowing. At first he considered a stent procedure (percutaneous coronary intervention), but he was treated with medicines (diuretics, beta blocker, statin and other heart drugs). Later, intravascular ultrasound (IVUS) measured the narrowing at about 56%, which is moderate; because he was stable and not having ongoing chest pain or clear signs of ongoing ischemia (lack of blood flow), no stent was placed. He was sent home on optimal medical therapy.\n\nOutcome and follow-up\nOver four years he continued to have some breathlessness with activity. His heart size was slightly larger and EF stayed reduced (about 41%), so he developed chronic heart failure with reduced ejection fraction — a long-term effect of the earlier heart attack. It was also noted he had not always taken his heart medicines as prescribed, so doctors restarted guideline medications (a beta blocker, an ACE inhibitor, and spironolactone).\n\nWhat this means and next steps\nBlunt chest trauma can sometimes injure a coronary artery and cause a heart attack. Important steps are close follow-up, taking prescribed medicines, lifestyle changes, and regular cardiology checks (including repeat imaging or stress tests if symptoms change). Staying on medications and keeping appointments can help protect heart function and reduce symptoms.",
+            "B3": "Resumen clínico (nivel universitario, lectura B3)\n\nPresentación y antecedente inmediato\n- Hombre de 38 años, previamente sano, recibió un fuerte golpe en el pecho por un tornillo de alta velocidad durante el trabajo; perdió la conciencia brevemente. \n- En el hospital inicial se identificaron derrame pleural bilateral y fracturas de esternón y costillas; se colocó tubo torácico. Fue dado de alta sin electrocardiograma (ECG) ni evaluación coronaria.\n\nSíntomas y hallazgos al ingreso a los 3 meses\n- Motivo de ingreso: disnea de esfuerzo persistente, opresión torácica y derrame pleural residual.\n- Signos vitales relativamente estables (FC ≈ 98 lpm, PA 110/70 mmHg).\n- ECG: alteraciones de la repolarización (inversión de onda T en I, aVL y V2–V5) y bloqueo de rama izquierda anterior — cambios sugestivos de lesión miocárdica previa.\n- Troponina I negativa (no lesión aguda evidente en ese momento); NT‑proBNP elevado (706 pg/ml; normal 0–104) — compatible con estrés ventricular/insuficiencia cardiaca.\n- Ecocardiograma transtorácico: ventrículo izquierdo dilatado, fracción de eyección (FE) reducida (32% por modo M) y adelgazamiento / movilidad severamente reducida de la pared anterior y del septo interventricular — hallazgos consistentes con infarto de miocardio antiguo (OMI).\n\nEvaluación coronaria y etiología\n- Arterias carotídeas, intracraneales y de extremidades sin placas ateroscleróticas significativas, lo que sugiere que la causa no fue una aterosclerosis difusa.\n- Tomografía coronaria y posteriormente angiografía coronaria (CAG) mostraron estenosis en la arteria descendente anterior (LAD) proximal: ~70% en la primera CAG realizada 3 meses tras el trauma. LCX y RCA normales.\n- IVUS (realizado más tarde) mostró que la lesión tenía un 55.9% de estrechamiento y una placa hipoecoica antes de formación trombótica por ruptura subintimal. Esto sugiere lesión intimal/traumática de la LAD seguida de trombosis y embolización que causó el infarto, en lugar de enfermedad aterosclerótica crónica.\n\nTratamiento y evolución\n- Inicialmente manejo médico conservador: diuréticos, betabloqueantes, estatinas y fármacos inotrópicos según necesidad; luego terapia óptima para insuficiencia cardíaca.\n- No se realizó intervención revascularizadora inmediata por falta de evidencia de isquemia persistente y por el grado moderado de estenosis en IVUS; además, el paciente rechazó IVUS en una ocasión por motivos económicos.\n- Tras terapia médica la función mejoró parcialmente (FE hasta 45% un mes después; luego estabilizada alrededor de 41% a los 4 años), pero persistió disnea de esfuerzo leve-moderada.\n- A los 4 años se constató insuficiencia cardíaca crónica con FE reducida, ventrículo izquierdo dilatado y zonas akiné­ticas/adelgazadas en pared anterior; se documentó además incumplimiento terapéutico intermitente.\n\nInterpretación clínica y lecciones\n- Probable lesión coronaria traumática (LAD) secundaria a trauma torácico cerrado que llevó a ruptura intimal, trombosis y un infarto de miocardio que no fue detectado ni tratado en el momento agudo.\n- Hallazgos normales en otras arterias y la historia clínica del trauma apoyan la etiología traumática más que la aterosclerótica.\n- El retraso en la sospecha/diagnóstico coronario tras traumatismo torácico tuvo como consecuencia daño miocárdico irreversible y evolución a insuficiencia cardíaca crónica con FE reducida.\n\nImplicaciones y recomendaciones prácticas\n- Tras traumatismo torácico de alta energía, es importante realizar evaluación cardíaca precoz: ECG seriados, troponinas y ecocardiograma según la clínica. Si hay sospecha de lesión coronaria, considerar angiografía y/o imagen intracoronaria (IVUS/OCT) para guiar la revascularización.\n- En pacientes con disfunción ventricular tras posible infarto, instaurar y garantizar adherencia a terapia cardioprotectora y para insuficiencia cardíaca (betabloqueantes, IEC/ARA-II, antagonistas de aldosterona, estatinas cuando indicada).\n- Seguimiento prolongado: monitorizar función ventricular, síntomas, adherencia a tratamiento y considerar revascularización si hay isquemia documentada o progresión de la lesión; valorar terapia dispositivo si persiste FE ≤35% pese a terapia óptima.\n- Educar al paciente sobre la importancia de la adherencia farmacológica y seguimiento cardiológico para mejorar pronóstico.\n\nTono final\nEste caso subraya la posibilidad, aunque poco frecuente, de lesión coronaria por traumatismo cerrado del tórax y la importancia de una evaluación cardiológica temprana. Con una detección y manejo oportunos se puede reducir el riesgo de daño miocárdico irreversible y de progresión a insuficiencia cardíaca crónica. Se recomienda atención continuada y cumplimiento estricto de la terapia guiada por las guías."
+        }
+    },
+    {
+        "article": "La paciente era una recién nacida de 0 días de edad, de etnia Han, que nació a las 36 semanas de gestación de una mujer embarazada de 3, para 2, con un peso de 2650 g. Se le practicó una cesárea de urgencia debido a la angustia fetal, con puntuaciones de Apgar de 6 a 1 min y 5 min. Su grupo sanguíneo era O y RhD positivo. Al nacer, presentaba palidez, equimosis dispersas en múltiples áreas del cuerpo, sangrado de las mucosas e insuficiencia respiratoria, con un leve flujo de sangre hemorrágica también observado en los sitios de punción venosa. El análisis de gases en sangre de la arteria umbilical mostró un hematocrito de 0.08 y una hemoglobina de 23 g/L. La paciente requirió intubación endotraqueal y ventilación mecánica. Después de la transfusión de una suspensión de glóbulos rojos, los recuentos sanguíneos iniciales revelaron una trombocitopenia severa (recuento de plaquetas de 12 × 109/L), anemia (hemoglobina de 46 g/L) y leucopenia (recuento de leucocitos de 1.11 × 109/L).\n\nLa paciente fue ingresada en la unidad de cuidados intensivos neonatales a las 3 horas de vida para recibir tratamiento adicional. Durante la hospitalización, se le diagnosticó coagulación intravascular diseminada (CID), con tiempo de tromboplastina parcial activada (TTPA) de 73,10 segundos, tiempo de protrombina (TP) de 25,4 segundos, fibrinógeno (FIB) de 1,01 g/L, razón internacional normalizada (INR) de 2,26 y dímero D > 20 mg/L. Se le administró ventilación mecánica, corrección de la acidosis y transfusión de plasma fresco congelado. A pesar de múltiples transfusiones de glóbulos rojos y plaquetas, los niveles de hemoglobina y plaquetas permanecieron por debajo de lo normal (hemoglobina 106 g/L y plaquetas 11 × 109/L el día 3). También recibió tratamiento antiinfeccioso, cardiotónico, vasopresor y otro tratamiento sintomático. Un frotis periférico mostró áreas de tinción pálida agrandadas de glóbulos rojos, con una proporción de reticulocitos del 1,5% y un resultado negativo en la prueba directa de Coombs. No se realizó aspiración de médula ósea debido a su grave estado. No hubo evidencia clínica o de laboratorio de sepsis neonatal, y las pruebas para toxoplasma, rubéola, citomegalovirus y virus del herpes simple (TORCH); virus de hepatitis; y Treponema pallidum fueron negativas. El examen físico de admisión reveló un estado mental deficiente, disminución del tono muscular en las extremidades y reflejo pupilar lento a la luz. Todos los demás hallazgos fueron normales. El ultrasonido craneal y electroencefalograma de cabecera revelaron hemorragia intracraneal grave y bajo voltaje, respectivamente. Los hallazgos del ecocardiograma sugirieron un conducto arterioso patente, foramen oval permeable e hipertensión pulmonar. El ultrasonido abdominal indicó hemorragia gastrointestinal. A pesar de todos los esfuerzos, la paciente falleció el tercer día de vida debido a falla multiorgánica y hemorragia intracraneal masiva (la información detallada se puede encontrar en el Informe Suplementario).\n\nLos padres de la paciente no eran consanguíneos y ambos tenían talasemia. La madre, que compartía el mismo tipo de sangre que la paciente, tuvo una anemia leve durante el embarazo (nivel de hemoglobina de 97 g/L) y un historial de aborto inducido. Los exámenes prenatales no mostraron anomalías, ni tampoco hidrops fetal, y no recibió ninguna medicación durante el embarazo que pudiera provocar una enfermedad hemorrágica de inicio temprano en el recién nacido. La paciente también tenía un hermano de 1 año que gozaba de buena salud. Su abuelo tenía un historial de anemia leve (detalles desconocidos).\n\nSe obtuvo el consentimiento informado de los padres del paciente y se realizó un secuenciamiento de Sanger para descubrir la causa de la enfermedad. Se detectó una nueva mutación de MECOM de desplazamiento de marco heterocigótica [NM_001105078: c.157_158del (p.Met53Glyfs*2)] en el probando. Esta variante cambió el aminoácido 53 de metionina (codón ATG) a glicina (codón GGT), seguido de una terminación temprana. La mutación no se encontró en los padres o en el hermano mayor. La variante se clasificó como patogénica según las directrices del Colegio Americano de Genética Médica (ACMG) [14]. El algoritmo “AutoPVS1” brindó un fuerte apoyo para la interpretación de PVS1 de p.Met53Glyfs*2, lo que indica patogenicidad. La variante no se ha informado previamente en la Base de Datos de Mutación Genética Humana (HGMD) o en Clinvar. El análisis de conservación mostró que el residuo Met53 está altamente conservado en todas las especies de mamíferos (incluidos humanos, ratones, ratas, chimpancés y bovinos) utilizando Clustal Omega. Se generaron modelos de estructura de proteínas tridimensionales de las proteínas MECOM de tipo salvaje y mutantes utilizando SWISS-MODEL, lo que indica que la mutación de desplazamiento de marco causó una terminación temprana de la síntesis de aminoácidos, alterando significativamente la estructura de la proteína.\n",
+        "gold_summary": "Reportamos el caso de una neonata Han china de 0 días de vida que presentó trombocitopenia grave y hemorragia intracraneal, y que finalmente falleció por fallo multiorgánico e intracraneal el tercer día después del nacimiento. La secuenciación genética identificó una variante de cambio de marco heterocigótica, c.157_158del, dentro del gen MECOM. Esta variante condujo a una sustitución del 53.º aminoácido de metionina a glicina, terminando en el 54.º aminoácido. Una revisión exhaustiva de la literatura indicó que las mutaciones del gen MECOM incluían mutaciones sin sentido (68.3%), deleción (8.5%), sitio de empalme (8.5%), cambio de marco (7.3%) y sin sentido (7.3%). Las pacientes con mutaciones sin sentido frecuentemente presentaban sinostosis radiocubital, mientras que el fallo de la médula ósea se asociaba más comúnmente con los otros cuatro tipos de mutaciones.\n",
+        "synthetic_summary": {
+            "B1": "Esta es la historia de una bebé que nació muy débil a las pocas semanas de embarazo.  \nAl nacer estaba muy pálida, tenía moretones por todo el cuerpo y sangraba. También tenía problemas para respirar y necesitó ayuda con un tubo y una máquina para respirar.\n\nLos médicos encontraron que tenía muy pocas plaquetas. Las plaquetas son pequeñas partes de la sangre que ayudan a detener el sangrado. También tenía pocos glóbulos rojos, que llevan el oxígeno por el cuerpo. A pesar de recibir transfusiones y medicinas, la bebé sufrió una hemorragia grande en el cerebro y fallaron varios órganos. Murió al tercer día de vida. Esto fue muy triste para la familia y para el equipo médico.\n\nBuscaron la causa y no encontraron infección. Hicieron un estudio del ADN y hallaron un cambio nuevo en un gen llamado MECOM. Un gen es como una instrucción que le dice al cuerpo cómo funcionar. Ese cambio hizo que las instrucciones no funcionaran bien. Por eso su cuerpo no pudo producir bien las células de la sangre y no pudo parar las hemorragias.  \nEl cambio no estaba en la mamá, el papá ni en su hermano, así que apareció por primera vez en ella.\n\nLos médicos creen que este tipo de cambios en el gen MECOM puede causar problemas graves en la médula ósea y en la sangre. Lamentamos mucho la pérdida de la bebé.",
+            "B2": "Summary (clear, age 11–17 level)\n\nThis report describes a newborn baby girl of Han Chinese background who was born at 36 weeks by emergency cesarean because of fetal distress. Soon after birth she looked very pale, had bruises and bleeding from her mouth and from IV sites, and had trouble breathing. Blood tests showed very low red blood cells, very low white blood cells, and a critically low number of platelets (platelets are the blood cells that help stop bleeding). scans showed a large bleed inside her brain. Despite breathing support, many blood transfusions, and other intensive care treatments, she died on the third day of life from multiple organ failure and massive brain bleeding.\n\nDoctors tested for infections and other common causes of newborn bleeding; these were negative. Her lab tests also showed disseminated intravascular coagulation (DIC) — a serious condition where the clotting system becomes overactive and then fails, causing both dangerous clots and severe bleeding. An ultrasound of her belly showed bleeding in the gut, and an ultrasound of the heart showed small birth-related openings and high pressure in the lung blood vessels.\n\nGenetic testing (Sanger sequencing) found a new, harmful change in one copy of the gene called MECOM. This change is a small deletion (called c.157_158del) that shifts the gene’s “reading frame” so the protein is cut off very early (written p.Met53Glyfs*2). Because the change causes early termination of the protein, it is predicted to stop the protein from working properly. The same mutation was not found in either parent or her older brother, so it likely happened for the first time in this baby (a de novo mutation). Computer analyses showed the affected part of the protein is conserved in mammals and that the mutation severely alters the protein’s 3D structure. Using standard clinical guidelines, the change was classified as pathogenic (disease-causing).\n\nPutting this case in context, other reports of MECOM mutations show several types of changes: most are nonsense mutations (which also make a short, nonworking protein), and others include deletions, splice-site changes, frameshifts, and missense changes (which swap one amino acid for another). People with nonsense mutations often have bone and limb findings such as radioulnar synostosis (fusion of forearm bones), while bone marrow failure and very low blood counts are more commonly seen with the other mutation types.\n\nWhy this matters (kind note)\nThis baby’s illness was caused by a new harmful change in MECOM that led to rapid bone marrow failure and life‑threatening bleeding. Reporting new mutations helps doctors recognize similar cases sooner, offer genetic counseling to families, and improve understanding of how MECOM variants lead to disease. I’m sorry for this tragic outcome; the information may help prevent or better treat future cases.",
+            "B3": "Summary\n\nThis report describes a full-term–near (36 weeks) Han Chinese neonate who presented at birth with severe bleeding and bone‑marrow failure and died on day 3 of life from multiorgan failure and massive intracranial hemorrhage. The case was caused by a de novo, heterozygous frameshift mutation in the MECOM gene (c.157_158del; p.Met53Glyfs*2), classified as pathogenic.\n\nClinical course and key findings\n- Delivery and immediate condition: emergency cesarean for fetal distress; Apgar scores 6 and 5. The newborn was pale with widespread bruising, mucosal bleeding, respiratory failure, and active bleeding from venipuncture sites.  \n- Hematology at birth and early life: umbilical arterial gas analysis showed extremely low hematocrit and hemoglobin; after transfusion the neonate had severe thrombocytopenia (platelets 12 × 10^9/L), marked anemia (hemoglobin 46 g/L), and leukopenia (WBC 1.11 × 10^9/L). Reticulocyte proportion 1.5%; direct Coombs test negative.  \n- Coagulopathy and organ involvement: diagnosed with disseminated intravascular coagulation (prolonged PT/TTPA, low fibrinogen, D‑dimer >20 mg/L). Cranial ultrasound and EEG showed major intracranial hemorrhage and low-voltage activity. Echocardiography revealed patent ductus arteriosus, patent foramen ovale, and pulmonary hypertension. Abdominal ultrasound suggested gastrointestinal bleeding. The patient required intubation, mechanical ventilation, blood product support (RBCs, plasma, platelets), antibiotics, inotropes and vasopressors, and correction of acidosis. Bone marrow aspiration was not performed because the infant was clinically unstable. Despite aggressive support, the infant died on day 3.\n\nInvestigations for cause\n- Infectious and metabolic workup was negative: cultures/markers for neonatal sepsis, TORCH infections, hepatitis viruses and syphilis were negative.  \n- Family history: parents nonconsanguineous; both reported to have thalassemia (mother had mild antenatal anemia). An older sibling is well. The MECOM variant was not detected in either parent or the sibling, indicating a de novo mutation.\n\nGenetic result and interpretation\n- A novel heterozygous frameshift deletion in MECOM (c.157_158del, p.Met53Glyfs*2) was identified by Sanger sequencing. The change introduces a premature stop codon soon after residue 53. The altered residue (Met53) is highly conserved across mammals. In silico structural modeling predicted major disruption of the MECOM protein. The variant was classified pathogenic under ACMG criteria with strong PVS1 support and is not reported in public mutation databases.\n\nClinical implications and recommended next steps\n- MECOM encodes transcriptional regulators (including EVI1) required for normal hematopoiesis. Pathogenic MECOM variants are a recognized cause of congenital bone‑marrow failure syndromes, often presenting as severe thrombocytopenia and risk of life‑threatening bleeding in the neonatal period. Some variant types are also associated with skeletal anomalies (for example, radioulnar synostosis) though findings are variable.  \n- For the family: this appears to be a de novo event, so recurrence risk for future pregnancies is low but not zero (gonadal mosaicism is possible). Genetic counseling is indicated. Options to discuss include targeted prenatal testing or preimplantation testing in future pregnancies.  \n- For clinicians: in suspected neonatal bone‑marrow failure, early genetic testing can clarify diagnosis and guide planning (for example, timing of hematopoietic stem cell transplant for survivors). When infants survive initial instability, hematology referral and consideration of definitive therapy (HSCT) may be necessary. Reporting novel pathogenic variants to databases and considering autopsy or postmortem genetic/hematopathology when feasible can improve knowledge for future cases.\n\nThe case underscores how a de novo MECOM loss‑of‑function variant can produce catastrophic neonatal marrow failure and bleeding despite intensive supportive care. Condolences to the family for this tragic outcome."
+        }
+    },
+    {
+        "article": "La paciente es una mujer de 74 años de edad, físicamente activa, que practica senderismo y equitación. Un mes después del tratamiento con inyección de cortisona de la tendinopatía insercional de Aquiles, sufrió una rotura total del tendón de Aquiles insercional al intentar dar un paso mientras montaba en bicicleta. Esta rotura se trató de forma conservadora con una bota de Walker durante 8 semanas. Después, mientras montaba a caballo, un intento de dar un paso provocó una nueva rotura total del tendón de Aquiles en la inserción. La rotura se trató quirúrgicamente con reinserción del tendón de Aquiles en el calcáneo, utilizando anclajes de sutura. Esto fue seguido por inmovilización en un yeso. Después de la operación, la paciente sufrió una infección profunda que no respondía a los antibióticos, signos de sepsis, y se indicó exploración quirúrgica. Durante la cirugía, se encontró que todo el tendón de Aquiles estaba gravemente afectado por la infección, más o menos destruido, y hubo que retirar el tendón de Aquiles distal de 7 cm (todo el tendón libre de Aquiles). Esto dejó una gran herida sin tejido tendinoso, y la piel se suturó sobre la herida. Después de este procedimiento, la inmovilización y el tratamiento con antibióticos de cloxacilina curaron la infección y la herida se curó adecuadamente. El pie se inmovilizó en un yeso durante las primeras 10 semanas, desde la máxima flexión plantar inicialmente, y luego la flexión plantar disminuyó gradualmente hasta alcanzar la posición neutra. Esto fue seguido por inmovilización en un yeso dorsal, evitando la extensión del tendón de Aquiles en flexión plantar, durante otros 3 meses. Se le dijo que aumentara gradualmente la carga al caminar, pero que evitara la extensión durante un total de 6 meses. Después de 6 meses se le ofreció reconstrucción quirúrgica con un injerto de flexor hallucis longus, pero como entonces tenía una función satisfactoria, decidió esperar y ver. Su función mejoró gradualmente, y un año después de la operación, cuando buscó ayuda por el dolor en el otro tendón de Aquiles, se notó la buena función en el lado operado. La exploración por ultrasonido mostró sorprendentemente un tendón que se parecía mucho a un tendón de Aquiles ligeramente tendinopático.\n",
+        "gold_summary": "Esta señora de 74 años padecía tendinopatía insercional de Aquiles. Después del tratamiento con una inyección local de cortisona, sufrió una rotura total del tendón de Aquiles insercional. Esta rotura se trató de forma conservadora y, después del tratamiento, el tendón de Aquiles volvió a romperse en la zona de inserción. La rotura se trató entonces con reinserción en la zona de inserción calcánea. Al poco tiempo del postoperatorio, la paciente sufrió una infección de herida quirúrgica profunda y sepsis. Debido al pobre efecto del tratamiento con antibióticos y a la destrucción total del tendón, se extirpó todo el tendón de Aquiles. Después de la extirpación, se inmovilizó en un yeso, seguido de movilización y aumento gradual de la carga. En un seguimiento de un año, la paciente caminaba sin cojera, podía levantar el talón hasta la mitad mientras estaba de pie sobre una pierna, había un tendón de Aquiles palpable y el escaneado por ultrasonido mostró una estructura muy similar a un tendón de Aquiles tendinopático y ligeramente engrosado. Había una regeneración evidente de todo el tendón de Aquiles y la función del tendón era sorprendentemente buena.\n",
+        "synthetic_summary": {
+            "B1": "Había una señora de 74 años que hacía ejercicio y montaba a caballo. Tenía dolor en el lugar donde el tendón de Aquiles se une al talón. El tendón de Aquiles es una cuerda fuerte detrás del tobillo que ayuda a caminar y saltar.\n\nLe pusieron una inyección para el dolor. Un mes después, al dar un paso en la bicicleta, el tendón se rompió por completo. La trataron con una bota especial durante ocho semanas. Más tarde, al montar a caballo, el tendón volvió a romperse en el mismo sitio. Entonces le hicieron una operación para volver a fijar el tendón al hueso del talón.\n\nDespués de la operación, la herida se infectó. La infección fue grave y no mejoró con antibióticos. Los médicos tuvieron que quitar todo el tendón de Aquiles que estaba dañado. Cerraron la piel sobre la herida y siguieron con antibióticos y yesos hasta que la infección sanó.\n\nLa pierna estuvo inmovilizada muchos meses. Poco a poco la mujer empezó a apoyar el pie y caminar de nuevo. Le ofrecieron otra operación para reconstruir el tendón, pero ella tenía suficiente función y decidió esperar.\n\nUn año después caminaba sin cojear. Podía subir el talón a la mitad estando en una pierna. La ecografía (una imagen con sonido) mostró algo que se parecía mucho a un tendón, aunque algo engrosado. Fue sorprendente ver que se formó tejido parecido al tendón y que la función del pie era buena después de tanto problema.",
+            "B2": "Resumen comprensible (nivel B2, pensado para lectores de 11–17 años)\n\nUna mujer activa de 74 años, que practica senderismo y monta a caballo, tenía una tendinopatía insercional del tendón de Aquiles (es decir, dolor y daño en la parte donde el tendón se une al hueso del talón). Recibió una inyección local de cortisona (un antiinflamatorio) y, un mes después, sufrió una rotura completa del tendón de Aquiles en la inserción al intentar dar un paso. Esa primera rotura se trató de forma conservadora con una bota de apoyo durante 8 semanas. Más tarde, al montar a caballo, volvió a romperse el tendón en la misma zona. Entonces se operó para reinsertar el tendón en el hueso del talón usando anclajes de sutura.\n\nPoco después de la operación apareció una infección profunda de la herida y signos de sepsis (una infección grave que afecta a todo el cuerpo). Como los antibióticos no controlaron bien la infección, fue necesaria una nueva cirugía. En esa intervención se halló que casi todo el tendón había quedado destruido por la infección, por lo que se retiró por completo el segmento distal libre del tendón (unos 7 cm). La herida se cerró y, con antibióticos (cloxacilina) y reposo en yeso, la infección sanó.\n\nEl pie se inmovilizó durante muchos meses para proteger la zona: primero 10 semanas en una posición con el pie apuntando hacia abajo (flexión plantar), y después se fue llevando poco a poco a posición neutra; más tarde se usó un yeso que impedía estirar el tendón otros 3 meses. En total se le indicó evitar la extensión del tendón durante 6 meses y aumentar la carga al caminar de forma gradual. A los 6 meses le ofrecieron reconstruir el tendón con un injerto del músculo flexor largo del dedo gordo del pie (es una operación que usa otro tendón para reemplazar el que falta), pero como su función ya era aceptable, ella prefirió esperar.\n\nA los 12 meses del último tratamiento estaba caminando sin cojear, podía levantarse sobre una pierna y elevar el talón hasta la mitad, y se notaba un tendón al palpar. La ecografía mostró una estructura sorprendentemente parecida a un tendón de Aquiles algo tendinopático y engrosado, lo que indica que hubo una regeneración importante del tendón y que su función final fue mejor de lo esperado.\n\nComentario final suave: aunque la paciente pasó por complicaciones serias (roturas repetidas e infección que obligó a retirar el tendón), con cirugía, antibióticos y una reeducación lenta, consiguió recuperar una función sorprendentemente buena. Se le ofreció una reconstrucción adicional, pero decidió esperar porque su capacidad para caminar y ponerse de puntillas era satisfactoria.",
+            "B3": "Resumen clínico (nivel lector universitario)\n\nPaciente: mujer de 74 años, físicamente activa (senderismo y equitación).\n\nAntecedente inicial\n- Tenía tendinopatía insercional del tendón de Aquiles (dolor y degeneración en la zona donde el tendón se une al hueso del talón).\n- Recibió una inyección local de cortisona para esa tendinopatía.\n\nEpisodios posteriores y tratamientos\n1. Primer evento (1 mes después de la inyección): rotura total del tendón de Aquiles en la inserción al intentar dar un paso. Tratamiento inicial conservador: bota tipo “walker” durante 8 semanas.\n2. Recaída: meses después, al montar a caballo, volvió a romperse el tendón en la misma zona. Se realizó una reinserción quirúrgica en el calcáneo con anclajes de sutura.\n3. Complicación postoperatoria grave: desarrolló infección profunda de la herida y signos de sepsis que no respondieron bien a antibióticos. En la exploración quirúrgica se observó que el tendón estaba gravemente destruido; se retiró la porción distal afectada (unos 7 cm, es decir, la totalidad del “tendón libre” distal).\n4. Manejo de la infección y rehabilitación inicial: cierre de la piel sobre la herida, tratamiento con cloxacilina y prolongada inmovilización en yeso: primero en máxima flexión plantar y progresivamente hacia neutro durante ~10 semanas, seguido de un yeso dorsal que evitaba la extensión durante alrededor de 3 meses más. Se indicó aumento gradual de carga al caminar y evitar la extensión forzada del tobillo durante unos 6 meses en total.\n5. Oferta de reconstrucción: a los 6 meses se ofreció reconstrucción mediante trasferencia de tendón flexor hallucis longus (FHL), pero la paciente tenía función satisfactoria y prefirió esperar.\n\nEvolución y hallazgos al año\n- A 1 año, la paciente caminaba sin cojear y podía levantar el talón hasta la mitad en apoyo monopodal (prueba funcional útil para valorar la fuerza del tríceps sural).\n- A la palpación había una estructura en la región posterior del tobillo que se asemejaba a un tendón.\n- Ecografía: mostró una estructura muy parecida a un tendón de Aquiles con cambios compatibles con tendinopatía leve y engrosamiento.\n- Conclusión clínica: hubo regeneración o reemplazo por tejido que aporta función tendinosa suficiente; la recuperación funcional fue sorprendentemente buena pese a la extirpación completa del tendón libre distal.\n\nPuntos importantes y consideraciones\n- Riesgos asociados: la inyección local de cortisona en tendones insercionales puede debilitar tejido y aumentar el riesgo de rotura; la cirugía de reinserción tiene riesgo de infección profunda, la cual puede requerir desbridamiento extenso e incluso pérdida del tendón.\n- Recuperación sin reconstrucción: en este caso, a pesar de la extirpación del tendón, la paciente obtuvo una recuperación funcional satisfactoria sin injerto reconstructivo; esto sugiere que, en algunos pacientes, la cicatrización y remodelado pueden restaurar función suficiente.\n- Seguimiento y opciones futuras: si apareciese debilidad funcional persistente o dolor incapacitante, la reconstrucción con transferencia tendinosa (por ejemplo FHL) sigue siendo una opción razonable. La rehabilitación progresiva y ejercicios de fortalecimiento son claves para optimizar la función.\n- Prevención y alerta temprana: ante signos de infección postoperatoria (fiebre, enrojecimiento intenso, dolor creciente, secreción) se debe actuar rápido: cultivo, antibióticos dirigidos y, si es necesario, limpieza quirúrgica.\n\nTono y mensaje final\nEsta paciente vivió complicaciones graves (roturas recurrentes e infección con pérdida del tendón), pero con manejo quirúrgico/agresivo de la infección, inmovilización adecuada y rehabilitación coherente consiguió una recuperación funcional notable a un año. El caso recuerda la necesidad de evaluar riesgos y beneficios de inyecciones de cortisona en tendones, la vigilancia estrecha tras cirugía y la posibilidad de resultados funcionales aceptables incluso después de pérdidas anatómicas importantes."
+        }
+    },
+    {
+        "article": "Una mujer de 47 años con antecedentes de CHB congénita se presentó con quejas de dolor en el cuello del lado izquierdo y dolor en el oído izquierdo. Aproximadamente 30 meses antes de la presentación, la paciente había notado una pequeña masa en el lado izquierdo de su cuello, que había aumentado gradualmente de tamaño. El dolor se localizó inicialmente en la región del cuello, pero se intensificó con el tiempo y se extendió al área del oído izquierdo.\nInicialmente, debido al dolor en el oído izquierdo, el paciente consultó a varios otorrinolaringólogos y fue tratado por un diagnóstico preliminar de otitis media. Sin embargo, a pesar de los tratamientos, el dolor persistió. Finalmente, un otorrinolaringólogo derivó al paciente para una ecografía, que reveló una masa en el lado izquierdo del cuello, lo que llevó a una derivación quirúrgica. Después de las evaluaciones iniciales, se solicitó una angiografía por TC, que reveló una masa de forma ovalada que medía 30 por 50 mm en la bifurcación de la arteria carótida izquierda, lo que sugiere un CBT tipo II de Shamblin.\n\nEvaluaciones cardiovasculares preoperatorias\nDada la historia del paciente de CHB congénita, se realizó una evaluación cardiovascular preoperatoria exhaustiva. Esto incluyó un electrocardiograma (ECG) de 12 derivaciones, que confirmó la presencia de CHB con un ritmo de escape ventricular estable. Se realizó una ecocardiografía transtorácica para evaluar la estructura y función cardiaca, revelando una función sistólica ventricular normal sin evidencia de anormalidades estructurales. Además, se obtuvo una consulta de cardiología para evaluar la aptitud del paciente para la cirugía y optimizar el manejo perioperatorio.\n\nConsideraciones anestésicas\nDebido a la CHB congénita del paciente y al potencial de inestabilidad hemodinámica durante la cirugía, se formuló un plan anestésico detallado. El paciente fue clasificado como estado físico III de la Sociedad Estadounidense de Anestesiología (ASA). Preoperativamente, se le colocó un marcapasos externo temporal para garantizar un control adecuado de la frecuencia cardíaca y se le insertó un catéter arterial para el monitoreo continuo de la presión arterial. La inducción de la anestesia se realizó utilizando una combinación de etomidato (0,3 mg/kg) y fentanilo (2 μg/kg) para minimizar las fluctuaciones hemodinámicas. El mantenimiento se logró con sevoflurano (1-2 %) y rocuronio (0,6 mg/kg) para la relajación muscular. Los parámetros hemodinámicos, incluida la frecuencia cardíaca, la presión arterial y la saturación de oxígeno, se controlaron de forma continua. Además, se le colocó un catéter venoso central para monitorear la presión venosa central y administrar medicamentos vasoactivos si fuera necesario. El equipo de anestesia mantuvo una comunicación estrecha con el equipo quirúrgico para abordar de forma inmediata cualquier cambio hemodinámico intraoperatorio.\n\nEnfoque quirúrgico\nEl paciente fue sometido a cirugía el 19 de mayo de 2024, después de la localización precisa de la TCC mediante angiografía por TC. El enfoque quirúrgico se eligió en base a la clasificación de Shamblin tipo II, que indica un encasamiento parcial de las arterias carótidas. Dada la proximidad del tumor a estructuras neurovasculares críticas, incluidos los nervios vago e hipogloso, se consideró que el enfoque quirúrgico abierto era el más apropiado para garantizar una resección completa y minimizar las complicaciones.\nTras la inducción de la anestesia general, se colocó al paciente en posición supina con el cuello extendido y rotado hacia la derecha. Se realizó una incisión oblicua paralela al músculo esternocleidomastoideo izquierdo, que se extendía desde la apófisis mastoidea hasta la escotadura esternal. Tras la incisión de la piel y la disección del platisma, se expuso con cuidado la vaina carotídea. Se identificaron la arteria carótida común y su bifurcación en las arterias carótidas internas y externas. Se observó el tumor, de 30 × 50 mm, en la bifurcación carotídea y se diseccionó con cuidado de los tejidos circundantes.\n\nManobras y precauciones específicas\n1.\nSe aplicaron pinzas vasculares temporales en las arterias carótidas internas y externas para controlar el flujo sanguíneo durante la disección del tumor. Esto minimizó el sangrado y proporcionó un campo quirúrgico despejado.\n2.\nSe utilizó neuromonitorización intraoperativa para evaluar la integridad de los nervios vago e hipogloso. La retroalimentación continua garantizó que las estructuras neurales se preservaran durante la disección.\n3.\nEl tumor se separó cuidadosamente de las arterias carótidas y las estructuras neurales circundantes, mediante una combinación de disección aguda y roma. Se logró la hemostasis mediante cauterización bipolar y pinzas quirúrgicas para minimizar el sangrado.\n4.\nEl marcapasos externo se monitoreó activamente durante todo el procedimiento para garantizar un ritmo cardíaco estable. El equipo de anestesia estaba preparado para administrar atropina o epinefrina si se producía una bradicardia o hipotensión significativas.\n2.5. Manejo postoperatorio\nTras asegurarse de que no había hemorragia activa y restablecer el flujo sanguíneo, se devolvieron los tejidos a su posición original y se cerró la herida en múltiples capas. Se aplicó un vendaje apropiado. La cirugía se completó sin complicaciones y con un sangrado mínimo en 2 h y 10 min. El paciente fue trasladado a la UCI vascular para una estrecha monitorización.\nDespués de la operación, se controló al paciente en la UCI durante 24 horas y, más tarde, se le trasladó a la planta general tras mejorar su estado clínico. El marcapasos externo se retiró el día 1 después de la operación, ya que el paciente mantenía un ritmo de escape ventricular estable. El paciente fue dado de alta en buenas condiciones generales el día 3 después de la operación, sin quejas específicas.\n2.6. Seguimiento y resultados a largo plazo\nEl examen histopatológico confirmó el diagnóstico definitivo de TCC en la paciente. Se realizaron evaluaciones de seguimiento a las 2 semanas, 1 mes, 6 meses y 1 año posteriores a la cirugía para evaluar los resultados quirúrgicos y cardíacos. En cada visita, la paciente se sometió a un ECG de 12 derivaciones para monitorear el CHB congénito, que permaneció sin cambios durante todo el período de seguimiento. Se repitió la ecocardiografía transtorácica a los 6 meses y un año, sin deterioro de la función cardíaca y con una función sistólica ventricular estable.\n\nPara evaluar el impacto de la extirpación del tumor en la función cardiaca, se realizó un análisis de la variabilidad de la frecuencia cardiaca (VFC) antes de la operación y a los 6 meses después de la misma. El análisis de la VFC antes de la operación demostró una reducción de la actividad parasimpática, probablemente debido a la compresión del nervio vago por el tumor. El análisis de la VFC después de la operación mostró una mejora significativa del tono parasimpático, lo que sugiere que la extirpación del tumor alivió la compresión del nervio vago y restauró la función autónoma normal.\nAsimismo, el paciente manifestó que el dolor en el cuello y en el oído había desaparecido por completo después de la cirugía, sin que se produjera una reaparición de los síntomas durante el período de seguimiento. Se realizaron estudios de imagen, que incluyeron ultrasonido Doppler y angiografía por TAC, a los 6 meses y al año, que no mostraron evidencia de reaparición del tumor o complicaciones vasculares.\n",
+        "gold_summary": "Describimos el caso de una mujer de 47 años con antecedentes de dolor en el cuello izquierdo y en el oído, acompañado por una masa en el cuello que había ido aumentando gradualmente durante 2,5 años. Después de las evaluaciones iniciales y de múltiples diagnósticos diferenciales, la angiografía por TC reveló una masa ovalada de 30 × 50 mm en la bifurcación carotídea izquierda, lo que confirmó un CCT tipo II de Shamblin. Las evaluaciones preoperatorias demostraron CHB congénita en el electrocardiograma y la ecocardiografía. La paciente se sometió a una resección completa del tumor con todas las precauciones necesarias, incluida la colocación temporal de un marcapasos y un cuidadoso seguimiento.\n",
+        "synthetic_summary": {
+            "B1": "Había una mujer de 47 años que tenía una bola en el lado izquierdo del cuello. La bola creció poco a poco por unos 2 años y medio. También le dolía el cuello y el oído izquierdo. Al principio pensaron que era una infección del oído, pero los tratamientos no ayudaron.\n\nUnos médicos le hicieron una ecografía y una angiografía por TAC. Vieron una masa de 3 x 5 cm en la división de la arteria del cuello. Los médicos dijeron que era un tumor llamado cuerpo carotídeo (un tipo de tumor cerca de la arteria). Estaba muy cerca de nervios y vasos importantes.\n\nAntes de la operación, revisaron su corazón. Ella tenía un bloqueo cardíaco desde que nació. Esto significa que el corazón late con un ritmo diferente, pero su función estaba bien. Los cardiólogos ayudaron a preparar todo para la cirugía.\n\nPara la operación, los médicos pusieron un marcapasos temporal por fuera para cuidar el latido del corazón. Durante la cirugía cuidaron mucho las arterias y los nervios. Usaron monitoreo para ver los nervios en tiempo real. Quitaron el tumor con cuidado. La operación duró unas 2 horas y 10 minutos y hubo poco sangrado.\n\nDespués de la operación, la mujer estuvo en la unidad de cuidados intensivos 24 horas. El marcapasos temporal se retiró al día siguiente porque su ritmo era estable. Ella salió del hospital al tercer día en buen estado.\n\nEl estudio del tumor confirmó el diagnóstico. En las visitas de control a las 2 semanas, 1 mes, 6 meses y 1 año, estaba bien. El dolor del cuello y del oído desapareció. El bloqueo del corazón no empeoró y la función del corazón se mantuvo normal. Pruebas mostraron que un nervio que estaba comprimido por el tumor mejoró después de quitarlo. No hubo señal de que el tumor volviera.",
+            "B2": "Resumen comprensible y atento\n\nPresentamos el caso de una mujer de 47 años que notó una pequeña masa en el lado izquierdo del cuello que creció durante unos 30 meses y acabó causando dolor en el cuello y en el oído izquierdo. Al principio fue tratada como una otitis (infección del oído), pero el dolor no cedió. Una ecografía y luego una angiografía por TC mostraron una masa ovalada de 30 × 50 mm en la bifurcación de la arteria carótida izquierda. Esto fue diagnosticado como un tumor del cuerpo carotídeo (también llamado paraganglioma o CBT) tipo II de Shamblin, lo que significa que el tumor rodeaba parcialmente las arterias carótidas.\n\nAntecedentes cardíacos y preparaciones\nLa paciente tenía un bloqueo cardíaco completo congénito (CHB). Esto es un problema del ritmo del corazón en el que las señales eléctricas entre las partes superiores e inferiores del corazón no pasan con normalidad; la paciente tenía un “ritmo de escape” ventricular estable que mantenía el latido, pero requería precaución. Antes de la operación se hicieron un ECG y una ecocardiografía: la función de bombeo del corazón era normal. Un equipo de cardiología revisó al caso para asegurar que la paciente era apta para la cirugía y para planear cuidados especiales.\n\nCuidados durante la anestesia y la cirugía\nPor seguridad se colocó un marcapasos externo temporal y un catéter arterial para monitorizar la presión arterial constantemente. La anestesia fue cuidadosamente elegida para evitar cambios bruscos en la presión o la frecuencia cardíaca; también se colocó un catéter venoso central por si era necesario dar medicación para el corazón. Se mantuvo comunicación estrecha entre anestesiólogos y cirujanos durante todo el procedimiento.\n\nLa cirugía se realizó por vía abierta (incisión en el lado izquierdo del cuello) debido a la cercanía del tumor a vasos y nervios importantes. Se usaron pinzas vasculares temporales para controlar el sangrado y monitorización neurológica intraoperatoria para proteger nervios importantes como el vago (que ayuda a controlar funciones como la frecuencia cardíaca) y el hipogloso (que mueve la lengua). La operación duró 2 horas y 10 minutos, con sangrado mínimo, y se completó sin complicaciones.\n\nRecuperación y controles\nLa paciente pasó 24 horas en la UCI vascular y luego fue a planta. El marcapasos externo se retiró al día 1 porque el ritmo de escape ventricular siguió siendo estable. Fue dada de alta al tercer día en buen estado y sin dolor en cuello ni oído. El examen de laboratorio confirmó que la masa era un tumor del cuerpo carotídeo.\n\nA largo plazo se hicieron seguimientos a las 2 semanas, 1 mes, 6 meses y 1 año. El bloqueo cardíaco congénito no empeoró y la función del corazón se mantuvo estable en ecocardiografías repetidas. Además, antes de la operación el análisis de la variabilidad de la frecuencia cardíaca (una forma de medir el balance del sistema nervioso que controla el corazón) mostró menos actividad del sistema parasimpático, probablemente porque el tumor comprimía el nervio vago. Se observó una mejora en esa medida a los 6 meses tras la extirpación, lo que sugiere que quitar el tumor alivió la compresión nerviosa. Las imágenes de control (Doppler y angiografía por TC) a los 6 meses y 1 año no mostraron recurrencia del tumor ni problemas vasculares.\n\nConclusión práctica\nEste caso muestra que, incluso con un bloqueo cardíaco congénito, una planificación cuidadosa (marcapasos temporal, monitorización intensiva y comunicación entre equipos) permite realizar con seguridad la resección de un tumor carotídeo. La paciente se recuperó bien, el dolor desapareció y las pruebas mostraron mejora en la función nerviosa relacionada con el corazón y ausencia de recurrencia tumoral en el primer año.",
+            "B3": "Resumen clínico (lenguaje dirigido a lector universitario)\n\nPresentación y diagnóstico\n- Paciente: mujer de 47 años con bloqueo auriculoventricular completo (CHB) congénito.\n- Síntomas: masa progresiva en el lado izquierdo del cuello por ~30 meses, dolor cervical izquierdo y otalgia (dolor de oído) que no respondieron a tratamientos para otitis media.\n- Estudios de imagen: angiografía por tomografía computarizada (angio‑TAC) mostró una masa ovalada de 30 × 50 mm en la bifurcación de la arteria carótida izquierda, compatible con tumor del cuerpo carotídeo (TCC, paraganglioma) Shamblin tipo II (encasamiento parcial de las carótidas).\n\nEvaluación preoperatoria y consideraciones cardíacas\n- ECG de 12 derivaciones confirmó CHB con ritmo de escape ventricular estable (hallazgo anormal, pero hemodinámicamente tolerado).\n- Ecocardiograma transtorácico: función sistólica ventricular normal (hallazgo normal).\n- Consulta cardiológica para valorar aptitud para cirugía y planificar manejo perioperatorio.\n\nPlan anestésico y medidas de seguridad\n- Clasificada ASA III por su cardiopatía.\n- Se colocó un marcapasos externo temporal y un catéter arterial para monitorización continua; además se insertó catéter venoso central.\n- Inducción con etomidato y fentanilo para minimizar cambios hemodinámicos; mantenimiento con sevoflurano y rocuronio.\n- Monitorización continua de ritmo, presión arterial y saturación; preparación para tratamiento rápido de bradicardia o hipotensión.\n\nCirugía y técnicas intraoperatorias\n- Fecha: 19 de mayo de 2024. Enfoque abierto por la localización y relación del tumor con estructuras neurovasculares (vago e hipogloso).\n- Incisión paralela al esternocleidomastoideo izquierdo; exposición de la bifurcación carotídea y disección cuidadosa del tumor.\n- Medidas específicas: clampaje temporal de arterias carótidas interna y externa para controlar flujo, neuromonitorización intraoperatoria de nervios craneales, disección combinada (aguda y roma), hemostasia con cauterio bipolar.\n- El marcapasos externo se monitorizó activamente durante todo el procedimiento.\n- Duración: 2 h 10 min; sangrado mínimo; resección completa sin complicaciones inmediatas.\n\nEvolución postoperatoria y seguimiento\n- Postoperatorio inmediato: vigilancia en UCI vascular 24 h; marcapasos externo retirado al día 1 porque persistía ritmo de escape ventricular estable.\n- Alta hospitalaria al día 3 en buenas condiciones y sin síntomas.\n- Anatomía patológica confirmó TCC.\n- Seguimiento a 2 semanas, 1 mes, 6 meses y 1 año: ECG mostró CHB sin cambios (estable); ecocardiogramas a 6 meses y 1 año sin deterioro de función ventricular.\n- Estudios de imagen (Doppler y angio‑TAC) a 6 meses y 1 año sin recidiva tumoral ni complicaciones vasculares.\n- Análisis de variabilidad de la frecuencia cardíaca: antes de la cirugía hubo disminución del tono parasimpático (probablemente por compresión del nervio vago por el tumor); a los 6 meses se observó mejoría significativa, lo que sugiere alivio de la compresión vagal tras la resección.\n- Síntomas (dolor cervical y otalgia) desaparecieron y no recurrieron durante el seguimiento.\n\nImplicaciones y puntos clave\n- El caso muestra que un TCC carotídeo mayor, parcialmente encasante (Shamblin II), puede producir síntomas vagales y afectar la regulación autonómica; su resección puede restaurar función parasimpática.\n- En pacientes con CHB congénito, la planificación perioperatoria cuidadosa (marcapasos temporal, monitorización invasiva, equipo coordinado) permitió una cirugía segura sin necesidad inmediata de marcapasos definitivo, dado el ritmo de escape estable.\n- Riesgos potenciales de este tipo de cirugía incluyen lesión de nervios craneales, sangrado, isquemia cerebral o necesidad de reconstrucción vascular; ninguno de estos ocurrió en este caso.\n- Recomendaciones prácticas: continuar con vigilancia cardiológica (evaluar necesidad de marcapasos permanente si el ritmo se vuelve inestable o aparecen síntomas) y con imágenes periódicas para detectar recidiva del paraganglioma."
+        }
+    },
+    {
+        "article": "Una mujer de 19 años de edad acudió al servicio de urgencias de nuestro hospital con una queja principal de dos días de historia de cefalea, acompañada de náuseas recurrentes, vómitos y fiebre de un día. En el ingreso, su examen físico reveló una fiebre alta de 39.1°C, presión arterial elevada de 189/120 mmHg y una frecuencia cardíaca de 148 latidos por minuto. Los resultados de laboratorio indicaron un recuento de glóbulos blancos elevado de 14.77×10^9/L y un recuento de neutrófilos de 13.55×10^9/L, lo que sugiere una posible infección o respuesta inflamatoria. Se administró un tratamiento empírico inicial con antibióticos debido a la sospecha de infección, pero sus síntomas persistieron. Dados sus signos vitales anormales, marcadores inflamatorios elevados y falta de mejora de los síntomas, la paciente fue admitida para una evaluación diagnóstica adicional y transferida a la unidad de cuidados intensivos para una estrecha monitorización. Un año antes, la paciente había presentado síntomas similares y se le diagnosticó miocarditis en un hospital local en base a los hallazgos clínicos en ese momento. Durante esa hospitalización, también se le diagnosticó hipertensión y se le prescribieron medicamentos antihipertensivos. Sin embargo, después del alta, la paciente no se adhirió al tratamiento antihipertensivo prescrito y no controló regularmente su presión arterial. Además, es notable que su padre tenía antecedentes de muerte súbita inexplicable.\n\nPara investigar la etiología subyacente de los síntomas del paciente, se realizó una tomografía computarizada (TC) de tórax. De forma incidental, esta exploración reveló una masa suprarrenal izquierda con densidad de tejido blando, que medía 43 mm × 36 mm. No se observaron hallazgos patológicos en las exploraciones de TC de cabeza y tórax. El electrocardiograma demostró taquicardia sinusal con un intervalo PR acortado y ondas P altas y puntiagudas en las derivaciones II, III y aVF. La ecocardiografía transtorácica no reveló ninguna anomalía significativa.\n\nEn el segundo día de ingreso, el paciente mostró niveles crecientes de péptido natriurético cerebral (BNP) y troponina I (TnI). El cardiólogo diagnosticó provisionalmente al paciente con miocarditis de etiología incierta, basándose en la presentación clínica, los biomarcadores cardiacos elevados (BNP y TnI) y los hallazgos del electrocardiograma de apoyo. Se inició el tratamiento con metilprednisolona (0,25 g diarios) para abordar la posible inflamación miocárdica debida a la sospecha de miocarditis. Se administraron furosemida (20 mg cada 12 horas) y espironolactona (20 mg cada 12 horas) como diuréticos para controlar la retención de líquidos y reducir la carga de trabajo cardiaco. Se prescribió perindopril amlodipina (10 mg: 5 mg diarios) como inhibidor de la enzima convertidora de la angiotensina y bloqueador del canal del calcio para controlar la presión arterial y reducir la poscarga. Se usó tartrato de metoprolol (25 mg cada 12 horas) para controlar la frecuencia cardiaca y disminuir la demanda de oxígeno miocárdico, mientras que se administró esmolol (0,2 g/hora por infusión intravenosa), un bloqueador beta de acción corta, para controlar la frecuencia cardiaca aguda adicional debido a la taquicardia sinusal. Debido a la preocupación por una posible infección, se agregó moxifloxacina como terapia antibiótica empírica.\n\nDada la presentación del paciente con una masa suprarrenal e hipertensión, el endocrinólogo recomendó una evaluación de la relación aldosterona/renina, cortisol plasmático, catecolaminas plasmáticas y catecolaminas urinarias de 24 horas, junto con sus metabolitos. En posición supina, los niveles de catecolaminas plasmáticas y urinarias estaban marcadamente elevados (Tabla 1), incluyendo dopamina plasmática a 524,5 pmol/L, norepinefrina a 83975 pmol/L y epinefrina a 10579,3 pmol/L. Además, los niveles urinarios de 24 horas mostraron adrenalina libre a 4368,89 nmol/24 horas, norepinefrina libre superior a 12697,60 nmol/24 horas, normetaneprina a 8312 nmol/24 horas, metaneprinas a 4078 nmol/24 horas y ácido vanilmandélico a 58,1 mg/24 horas. Estos hallazgos apoyaron un diagnóstico clínico de feocromocitoma. En el quinto día posterior al ingreso, se interrumpió la terapia glucocorticoide y se sustituyó perindopril amlodipina con terazosin para un control más dirigido de la presión arterial.\n\nUna tomografía computarizada abdominal mejorada confirmó una masa suprarrenal izquierda, muy sugestiva de feocromocitoma. Además, después de obtener el consentimiento informado, se realizó una secuenciación del exoma completo, que reveló una mutación sin sentido heterocigótica, c.1900T > C: p. Cys634Arg, en el gen RET, que conduce a una sustitución de cisteína por arginina en el codón 634. Esta mutación levantó sospechas de un síndrome de neoplasia endocrina múltiple, lo que impulsó una evaluación adicional de las glándulas tiroides y paratiroides. La ecografía Doppler en color de la tiroides identificó una masa hipoecoica que medía 6 mm × 4 mm en el lóbulo tiroideo izquierdo, y se observó una leve elevación en los niveles de calcitonina. No se detectaron anormalidades significativas adicionales.\n\nA medida que la condición del paciente mejoró gradualmente, los niveles de cortisol en plasma y ACTH volvieron a la normalidad. El paciente fue dado de alta con una prescripción de tartrato de metoprolol (100 mg cada 12 horas) e hidrocloruro de ivabradina (5 mg cada 12 horas) para el tratamiento en el hogar. Tres meses después, después de lograr un estado clínico estable, el paciente se sometió a una resección del tumor suprarrenal izquierdo, que medía 50 mm × 40 mm × 30 mm. El análisis inmunohistoquímico confirmó una tinción positiva para Vim, CD56, Syn, CgA y NSE, con S-100 positivo en las células de Sertoli, mientras que CKpan, CD10, MART-1/Melan-A y Melan-A fueron negativos. El índice Ki67 fue del 1 %, lo que llevó a un diagnóstico definitivo de feocromocitoma suprarrenal. El paciente fue dado de alta sin más medicamentos y desde entonces se le ha dado seguimiento regular postoperatorio sin recurrencia de síntomas. Durante un seguimiento postoperatorio de 15 meses, el paciente exhibió hipercalcinotemia persistente leve con un tamaño de nódulo tiroideo estable, mientras que los niveles de PTH y calcio en suero mostraron un aumento progresivo (Tabla 2). Se realizó una gammagrafía paratiroidea adicional utilizando 99mTc-MIBI, y la conclusión fue un resultado negativo para el adenoma paratiroideo.\n",
+        "gold_summary": "Reportamos el caso de una mujer de 19 años que presentó feocromocitoma sin experimentar una crisis, a pesar de tener una masa suprarrenal significativa y someterse a un tratamiento glucocorticoide de alta dosis. Las pruebas genéticas revelaron una mutación de sentido erróneo heterocigótica en el gen RET (c.1900T > C: p. Cys634Arg), asociada con MEN2A. La evaluación endocrina adicional identificó un nódulo tiroideo con niveles de calcitonina levemente elevados, pero niveles normales de electrolitos y hormona paratiroidea. Durante un seguimiento postoperatorio de 15 meses, la paciente exhibió hipercalcitonemia persistente leve con tamaño de nódulo tiroideo estable, mientras que la PTH y los niveles de calcio sérico mostraron un aumento progresivo. Se realizó una gammagrafía paratiroidea adicional utilizando 99mTc-MIBI, que arrojó un resultado negativo para el adenoma paratiroideo.\n",
+        "synthetic_summary": {
+            "B1": "Esta es la historia de una joven de 19 años. Ella vino al hospital con dolor de cabeza, náuseas, vómitos y fiebre. Tenía la presión muy alta y el corazón latía muy rápido. Al principio pensaron que tenía infección y le dieron antibióticos, pero no mejoró.\n\nUna tomografía mostró por casualidad un bulto en una glándula encima del riñón. Esa glándula se llama suprarrenal. Esos bultos a veces hacen muchas “hormonas del estrés”. Las pruebas de sangre y orina mostraron que tenía muchísima de esas hormonas. Por eso los médicos dijeron que el bulto era muy probablemente un feocromocitoma. Un feocromocitoma es un tumor que hace hormonas que suben la presión y aceleran el corazón.\n\nTambién le hicieron pruebas del corazón. Unos análisis del músculo del corazón estaban un poco altos, y por eso la cuidaron en intensivo y le dieron medicinas para bajar la presión y el ritmo del corazón. Una ecografía del corazón salió normal, lo cual fue una buena noticia.\n\nSe hizo un examen genético. Encontraron un cambio en el gen RET que puede pasar en familias. Ese cambio está ligado a un síndrome llamado MEN2A. MEN2A hace que a veces aparezcan tumores en la tiroides, las glándulas paratiroides y las suprarrenales. Por eso buscaron en la tiroides y hallaron un pequeño nódulo y un leve aumento de una sustancia llamada calcitonina.\n\nTres meses después, cuando estuvo mejor, le sacaron el tumor de la suprarrenal con cirugía. La biopsia confirmó que era un feocromocitoma. Después de la operación se fue recuperando bien y no tuvo más síntomas por ahora.\n\nEn el seguimiento de más de un año, la calcitonina siguió algo alta y los niveles de PTH y calcio subieron un poco. Hicieron una prueba para buscar un problema en las paratiroides y no encontraron un tumor allí. Los médicos siguen controlándola porque el cambio genético puede afectar otras glándulas con el tiempo.\n\nEn resumen:\n- Tenía un tumor en la suprarrenal que producía muchas hormonas del estrés (feocromocitoma).\n- Le quitaron el tumor y mejoró.\n- Tiene una mutación genética que necesita controles médicos continuos.\n- Los médicos la siguen de cerca para vigilar la tiroides y las paratiroides.",
+            "B2": "Resumen comprensible y amable:\n\nUna mujer de 19 años llegó al hospital con dolor de cabeza, náuseas, vómitos y fiebre. En la exploración tenía presión arterial muy alta y latidos rápidos del corazón. Una tomografía detectó, de forma accidental, una masa en la glándula suprarrenal izquierda (las glándulas suprarrenales están encima de los riñones y pueden producir hormonas). Las pruebas de sangre y orina mostraron niveles muy altos de catecolaminas, que son hormonas como la adrenalina y la noradrenalina. Estos resultados apoyaron el diagnóstico de feocromocitoma, un tumor de la glándula suprarrenal que produce esas hormonas y puede causar presión alta y palpitaciones.\n\nAdemás, se hizo una prueba genética y se encontró una mutación en el gen RET (c.1900T>C, p.Cys634Arg). Esta mutación está asociada con un síndrome hereditario llamado MEN2A (neoplasia endocrina múltiple tipo 2A). En MEN2A suelen aparecer tres problemas: feocromocitoma, cáncer medular de tiroides y enfermedades de las glándulas paratiroides. Por ello, los médicos estudiaron también la tiroides y las paratiroides: encontraron un pequeño nódulo tiroideo y una leve elevación de calcitonina (una hormona producida por la tiroides que puede subir si hay enfermedad tiroidea), pero no hallaron un adenoma claro de la paratiroides en la gammagrafía (una prueba que busca tumores paratiroideos).\n\nAntes de la cirugía, la paciente recibió medicamentos para controlar la presión y la frecuencia cardíaca y también un tratamiento breve con glucocorticoides. A pesar del tamaño del tumor y de ese tratamiento, no sufrió una crisis por la liberación masiva de hormonas (lo que a veces ocurre con los feocromocitomas). Tras estabilizarse, se realizó la extirpación del tumor suprarrenal. El examen del tejido confirmó que se trataba de un feocromocitoma benigno.\n\nEn el control a 15 meses después de la operación, la paciente seguía sin recurrencia del tumor suprarrenal. Tenía una calcitonina ligeramente alta y un nódulo tiroideo estable; además, los niveles de hormona paratiroidea (PTH) y calcio en sangre fueron aumentando con el tiempo, aunque la gammagrafía no mostró un adenoma paratiroideo claro. Estos hallazgos sugieren la necesidad de seguimiento continuo para vigilar la tiroides y las paratiroides, porque la mutación RET aumenta el riesgo de problemas en esas glándulas.\n\nQué significa esto para la paciente:\n- El diagnóstico de feocromocitoma fue tratado con éxito mediante cirugía.\n- La mutación genética encontrada implica que necesita seguimiento endocrinológico a largo plazo (control de tiroides y paratiroides) y consejo genético; familiares pueden necesitar hacerse pruebas.\n- Los médicos continuarán monitorizando calcitonina, calcio y PTH, y harán más estudios si los resultados cambian.\n\nSi tienes preguntas sobre alguno de los términos o sobre lo que sigue para esta paciente, te lo explico con gusto.",
+            "B3": "Resumen clínico (nivel de lectura universitario)\n\nPaciente y presentación inicial\n- Mujer de 19 años que acudió por 2 días de cefalea, náuseas, vómitos y un día de fiebre. Al ingreso presentaba hipertensión severa (189/120 mmHg), taquicardia (148 lpm) y fiebre (39.1 °C). Tenía leucocitosis (WBC 14.77×10^9/L), lo que orientó inicialmente a posible infección.\n- Ante la persistencia de la taquicardia y el aumento de biomarcadores cardíacos (BNP y troponina I), el equipo consideró miocarditis y se inició tratamiento con glucocorticoides, diuréticos, bloqueadores beta y fármacos para la presión arterial.\n\nHallazgos relevantes y diagnóstico de feocromocitoma\n- Una tomografía toraco-abdominal realizada para investigar la causa mostró de forma incidental una masa suprarrenal izquierda de ≈43 × 36 mm. Estudios bioquímicos en decúbito supino revelaron elevaciones marcadas de catecolaminas plasmáticas y en orina de 24 h (adrenalina, noradrenalina, metanefrinas, ácido vanilmandélico), compatibles con feocromocitoma —un tumor de la médula suprarrenal que secreta catecolaminas.\n- Tras la confirmación bioquímica, se cambió la estrategia antihipertensiva a bloqueo alfa (terazosina) antes de la cirugía, y se suspendieron los glucocorticoides.\n\nTratamiento y anatomía patológica\n- Tres meses después de estabilizarse, la paciente se sometió a adrenalectomía izquierda. La pieza medía 50 × 40 × 30 mm; la inmunohistoquímica fue compatible con feocromocitoma (marcadores neuroendocrinos positivos) y el índice Ki-67 fue bajo (1 %). Tras la cirugía no requirió medicación antihipertensiva y no hubo recurrencia clínica en el seguimiento inicial.\n\nHallazgo genético y evaluación endocrina asociada\n- La secuenciación del exoma mostró una mutación heterocigota de sentido erróneo en el gen RET (c.1900T>C; p.Cys634Arg). Esta variante está asociada con el síndrome de neoplasia endocrina múltiple tipo 2A (MEN2A), cuyo espectro incluye feocromocitoma, carcinoma medular de tiroides (MTC) y hiperparatiroidismo primario.\n- La ecografía tiroidea mostró un nódulo hipoecoico pequeño (6 × 4 mm) y la calcitonina sérica estaba ligeramente elevada, hallazgos que plantean la posibilidad de enfermedad tiroidea medular incipiente.\n- Durante 15 meses de seguimiento postoperatorio persistió una leve hipercalcitoninemia y, de forma preocupante, hubo un aumento progresivo de PTH y calcio séricos, lo que sugiere desarrollo de hiperparatiroidismo primario. Una gammagrafía paratiroidea con 99mTc‑MIBI fue negativa para adenoma localizado, lo que no descarta hiperplasia o adenomas pequeños.\n\nInterpretación y implicaciones clínicas\n- El cuadro inicial que parecía miocarditis probablemente incluyó contribuciones de catecolaminas (cardiomiopatía por exceso de catecolaminas), dado el feocromocitoma subyacente. Los esteroides pueden precipitar crisis adrenérgicas en pacientes con feocromocitoma, pero en este caso la paciente no desarrolló una crisis aguda a pesar de dosis altas.\n- La mutación RET p.Cys634Arg es de alto riesgo para MTC y se asocia con aparición temprana y mayor agresividad. Por ello, la combinación de feocromocitoma + mutación RET obliga a vigilancia y manejo proactivo de la tiroides y las paratiroides.\n\nRecomendaciones prácticas y seguimiento sugerido\n- Consulta genética y asesoramiento familiar: ofrecer prueba genética a familiares de primer grado (por la mutación RET) y consejo reproductivo.\n- Vigilancia tiroidea: monitoreo estrecho de calcitonina y CEA, ecografías tiroideas periódicas; en mutaciones de alto riesgo como Cys634 suele considerarse tiroidectomía profiláctica temprana o evaluar su necesidad según tendencias de calcitonina y hallazgos ecográficos, en discusión con endocrinología y cirugía.\n- Evaluación de paratiroides: seguimiento de calcio y PTH; si la hipercalcemia y/o síntomas progresan, valorar imagenología adicional (p. ej., sustracción selectiva o PET/CT con trazadores específicos) y discusión quirúrgica, ya que el MIBI negativo no excluye enfermedad paratiroidea.\n- Seguimiento por endocrinología de por vida: controles periódicos para detectar recurrencia de feocromocitoma, progresión de MTC o aparición de hiperparatiroidismo, y ajuste de intervenciones según evolución.\n- Evaluación cardiológica continua hasta normalización completa de función y biomarcadores.\n\nTono y pronóstico\n- La paciente respondió bien al tratamiento del feocromocitoma y la cirugía fue curativa para el tumor suprarrenal. Sin embargo, la mutación RET implica riesgo real de enfermedad tiroidea y paratiroidea futura; con vigilancia apropiada y manejo temprano (incluyendo opciones quirúrgicas cuando esté indicado), el pronóstico puede ser favorable. Es importante el seguimiento estrecho y la implicación familiar en el rastreo genético y clínico.\n\nSi desea, puedo preparar un resumen para familiares que explique qué es MEN2A, qué pruebas deben hacerse a los parientes, y qué señales clínicas deben vigilarse."
+        }
+    },
+    {
+        "article": "Una refugiada etíope embarazada de 39 años (Gravida 3 Para 2+0) fue derivada a nuestro departamento de urgencias de medicina interna en el Hospital Universitario de Gadarif, Gadarif State, Sudán, con hinchazón generalizada progresiva, falta de aire y fatiga durante 6 semanas y una revisión sistémica sin importancia. La paciente fue admitida en el sitio de admisión de casos críticos y su historia, tomada con la ayuda de un intérprete de idiomas más tarde en la admisión, reveló un episodio remoto inicialmente no revelado de tres convulsiones tónico-clónicas generalizadas no provocadas hace 21 años que se trataron tradicionalmente. Sin embargo, no había antecedentes de traumatismo craneal o antecedentes familiares de convulsiones. El examen general de la paciente reveló un PWS del lado izquierdo que involucraba la división oftálmica del nervio trigémino. Sin embargo, este hallazgo se perdió inicialmente en la inspección pero luego fue confirmado por el cónyuge de la paciente para estar presente desde el nacimiento. La paciente también estaba muy pálida y tenía derrames pleurales bilaterales, hepatomegalia blanda e hinchazón bilateral de las extremidades inferiores.\n\nLas investigaciones iniciales revelaron un nivel de hemoglobina de 8,84 g/dl. Por lo tanto, se diagnosticó insuficiencia cardíaca debido a anemia y se trató a la paciente en consecuencia. Sin embargo, ocho días después de su ingreso, la paciente había desarrollado aproximadamente seis episodios de convulsiones tónico-clónicas focales a bilaterales que respondieron bien a la fenitoína, pero que dejaron a la paciente en un estado comatoso profundo con un GCS de tres. Fue posteriormente admitida en la unidad de cuidados intensivos (UCI) y se le insertó un tubo nasogástrico para ayudarla con su nutrición y administración de fármacos. Además, para evitar más convulsiones, se le inició un tratamiento con comprimidos de carbamazepina de 200 mg administrados a través del tubo nasogástrico.\n\nSe retrasó una tomografía computarizada (TC) sin contraste del cerebro para el día posterior a la estabilización, ya que solo había una máquina de tomografía computarizada en el estado de Gadarif y funcionaba de forma intermitente debido a la falta de un número suficiente de técnicos radiólogos. La tomografía computarizada reveló calcificaciones corticales en la parte posterior del área parietal izquierda, lo que planteó el diagnóstico diferencial de SWS. En consecuencia, se realizó un examen físico de repetición, que mostró la presencia de una lesión plana de color rojo púrpura en la frente y el ojo. Al interrogar al cónyuge, se confirmó la presencia de esta lesión y que no había cambiado desde el nacimiento, lo que nos ayudó a descartar el diagnóstico de una mancha salmón, ya que esta lesión no se desvaneció, por lo que se diagnosticó como PWS. Además, no tenía características de megalencefalia, síndrome de malformación capilar que por lo general incluye un gran tamaño de la cabeza o del cerebro, problemas en las articulaciones y malformaciones capilares en la piel. Tampoco tenía hipertrofia de extremidades, anomalías del drenaje linfático o excrecencias óseas o de tejidos blandos que sugieran el síndrome de Klippel-Trenaunay-Weber. Por lo tanto, en función de los hallazgos de la tomografía computarizada y la presentación típica, llegamos a la conclusión del diagnóstico de SWS.\n\nDos días después de ingresar en la UCI, la paciente experimentó un cambio fluctuante en su estado de conciencia y una nueva aparición de hemiparesia contralateral (contralateral al SPW), así como afasia y labilidad emocional. Desafortunadamente, cuatro días después de ingresar en la UCI, la paciente empezó a experimentar sangrado vaginal; por ello, se consultó al departamento de obstetricia y ginecología y se descubrió que la paciente tenía un embarazo no viable (28 semanas + 1 día) y se realizó una inducción sin incidentes. Durante el mismo período, la paciente se volvió combativa y poco cooperativa, lo que llevó a que se la inmovilizara físicamente. Tres días después, la paciente desarrolló nuevos ataques focales bilaterales que comenzaron como episodios mioclónicos faciales y, tras consultar con el departamento de neurología, se aumentó la dosis de carbamazepina de la paciente a 1000 mg diarios, lo que ayudó a prevenir la recurrencia de los ataques. Cabe mencionar que, en su segundo trimestre y antes de recibir el resultado de la tomografía computarizada, se exploró un diagnóstico de eclampsia, pero sus constantes lecturas de presión arterial con una presión sistólica superior a la normal de 139 la mayoría de los días y una presión diastólica con un máximo de 97 mmHg y un rango bajo de proteinuria, así como la ausencia de características sistémicas como deterioro renal o hepático, excluyeron este diagnóstico. Después de alcanzar el diagnóstico de SW, se puso en juego un enfoque multidisciplinario; por ello, se realizó una consulta oftalmológica para descartar glaucoma. Sin embargo, la paciente estaba muy irritable y era difícil realizar un examen de fondo de ojo. Además, la paciente fue trasladada a la sala de medicina interna tras la estabilización.\n",
+        "gold_summary": "Presentamos el caso de una refugiada de 39 años, no diabética y no hipertensa, que inicialmente presentó insuficiencia cardiaca debido a anemia, por lo que recibió transfusiones de sangre. Más adelante, al ingresar, desarrolló convulsiones múltiples focales bilaterales, irritabilidad severa, afasia y hemiplejía derecha, lo que motivó su ingreso a la UCI. Un examen y un historial médico repetidos revelaron una mancha de vino de Oporto ocular izquierda leve que inicialmente pasó desapercibida y un historial remoto de convulsiones no provocadas 20 años atrás. Las imágenes revelaron calcificaciones parietales y confirmaron el diagnóstico de SWS. Por lo tanto, se adoptó un enfoque multidisciplinario para comprender plenamente el diagnóstico de la paciente y determinar una estrategia de tratamiento, que incluyó consultas con los departamentos de neurología, oftalmología, otorrinolaringología y fisioterapia. Se logró un control exitoso de las convulsiones mediante la administración de fenitoína IV durante 3 días y el aumento gradual de la carbamazepina oral a 1 g diario a través de una sonda nasogástrica. Lamentablemente, debido a la falta de personal o recursos, no se pudieron realizar otras evaluaciones importantes para pacientes con SWS, como evaluaciones avanzadas de neuroimagen, psiquiátricas, de cirugía plástica y neurocirugía, así como revisiones dentales.\n",
+        "synthetic_summary": {
+            "B1": "Esta es la historia de una mujer de 39 años que había huido de su país. Llegó al hospital porque estaba muy cansada y tenía hinchazón. Tenía anemia, que hizo que su corazón trabajara mal. Le dieron sangre para ayudarla.\n\nAl poco tiempo empezó a tener ataques: convulsiones son movimientos fuertes y pérdida de lo que hace la persona. Fue llevada a la unidad de cuidados intensivos (una sala para pacientes muy enfermos). Los médicos encontraron que tenía desde niña una mancha roja en la frente y el ojo izquierdo. También dijo que tuvo convulsiones hace muchos años.\n\nUna exploración del cerebro mostró pequeñas zonas duras llamadas calcificaciones. Juntos, la mancha en la cara y las cosas del cerebro hicieron que los médicos pensaran en el síndrome de Sturge‑Weber. Este síndrome es algo con lo que se nace. Puede causar convulsiones y problemas con el lado del cuerpo opuesto a la mancha.\n\nLos médicos usaron medicinas para parar las convulsiones. Primero le dieron fenitoína en la vena. Luego le subieron la dosis de carbamazepina hasta 1.000 mg al día por una sonda en la nariz. Con eso las convulsiones se controlaron. También la vieron especialistas de neurología, oftalmología, otorrinolaringología y fisioterapia para ayudarla.\n\nLa paciente estaba embarazada, pero desgraciadamente el embarazo no siguió adelante y se hizo la inducción. Por falta de personal y recursos, no pudieron hacer algunas pruebas y tratamientos más complejos que a veces se hacen para este síndrome.\n\nEn resumen: la mujer tenía anemia y convulsiones. Los médicos diagnosticaron síndrome de Sturge‑Weber por la mancha y las pruebas. Controlaron las convulsiones con medicinas y la atendió un equipo de especialistas, aunque faltaron recursos para más estudios.",
+            "B2": "Resumen comprensible y amable:\n\nPresentamos el caso de una mujer refugiada de 39 años que llegó al hospital embarazada y con síntomas de fatiga, dificultad para respirar e hinchazón generalizada. Al principio se pensó que tenía insuficiencia cardíaca por anemia severa y recibió tratamiento con transfusiones. Más tarde, durante la hospitalización, sufrió varias crisis convulsivas (ataques cerebrales que causan movimientos incontrolados y pérdida de conciencia) y quedó en coma breve con un GCS muy bajo (GCS 3 indica nivel de conciencia muy reducido).\n\nAl investigar más a fondo se descubrió una mancha rojiza plana en la frente y el ojo izquierdo presente desde el nacimiento, llamada mancha en “vino de Oporto” (port-wine stain). Una tomografía computarizada (TC) mostró calcificaciones en la parte parietal del cerebro. Estos hallazgos, junto con la historia de convulsiones antiguas, llevaron al diagnóstico de síndrome de Sturge–Weber (SWS). SWS es una condición congénita (desde el nacimiento) que afecta los vasos sanguíneos de la piel, el cerebro y a veces el ojo; puede causar manchas en la piel, convulsiones y aumentar el riesgo de problemas oculares como el glaucoma (aumento de la presión en el ojo).\n\nDurante la estancia la paciente desarrolló debilidad en la mitad del cuerpo opuesta a la mancha (hemiparesia), dificultades para hablar (afasia) y cambios emocionales. El embarazo resultó no viable a las 28 semanas y se indujo el parto. Para controlar las convulsiones se administró fenitoína por vía intravenosa y después se aumentó la carbamazepina oral hasta 1 g al día a través de una sonda nasogástrica; con esto las convulsiones quedaron mejor controladas. Se hicieron consultas con neurología y oftalmología, y se empleó un enfoque multidisciplinario que también incluyó fisioterapia.\n\nDebido a limitaciones de recursos y personal, no se pudieron realizar otras pruebas importantes para SWS (como estudios de neuroimagen más avanzados, valoración psiquiátrica, cirugía plástica o estudios dentales). En estos casos, los próximos pasos recomendables suelen incluir seguimiento neurológico y oftalmológico regular (para vigilar glaucoma), rehabilitación para la debilidad, ajustes de medicación anticonvulsiva y, cuando sea posible, estudios adicionales de imagen y consultas con cirugía o psiquiatría para planificar cuidados a largo plazo.\n\nSentimos la difícil situación de la paciente; el equipo logró estabilizar y controlar sus convulsiones, pero destacó la necesidad de más recursos para completar una evaluación y seguimiento completos del síndrome de Sturge–Weber.",
+            "B3": "Summary — Sturge‑Weber syndrome (SWS) diagnosed in a pregnant refugee with new seizures\n\nPatient and presentation\n- A 39‑year‑old Ethiopian refugee (gravida 3, para 2) presented with 6 weeks of progressive generalized swelling, shortness of breath and fatigue. She was markedly pale (hemoglobin 8.8 g/dL) and had bilateral pleural effusions and soft hepatomegaly. These findings led initially to a working diagnosis of heart failure secondary to severe anemia and she received supportive care and blood transfusion.\n- Her history—obtained later with an interpreter—included three unprovoked generalized tonic‑clonic seizures about 20–21 years earlier (treated outside conventional medicine), a detail not disclosed at first.\n\nCritical deterioration and neurological findings\n- On hospital day 8 she developed multiple focal‑onset seizures that generalized. Seizures responded to IV phenytoin but she became deeply comatose (GCS 3) and required ICU care with nasogastric feeding and anticonvulsant therapy.\n- Repeated examination revealed a left‑sided port‑wine stain (PWS) in the territory of the ophthalmic branch of the trigeminal nerve; the lesion had been present since birth and had been missed on initial inspection.\n- Non‑contrast CT brain (delayed because of intermittent CT availability) showed cortical calcifications in the left parietal region, consistent with leptomeningeal vascular malformation.\n- Over the ICU stay she developed fluctuating consciousness, new right‑sided hemiparesis, aphasia and emotional lability — all signs of focal brain dysfunction contralateral to the facial PWS.\n\nDiagnosis and management\n- The combination of a congenital facial port‑wine stain in the V1 (ophthalmic) distribution, remote seizure history, recent focal seizures with neurologic deficits, and ipsilateral cortical calcifications led to a clinical diagnosis of Sturge‑Weber syndrome (SWS).\n- Seizures were treated acutely with IV phenytoin and later with enteral carbamazepine via the nasogastric tube, gradually increased to 1,000 mg/day, which helped control recurrent attacks.\n- An ophthalmology consult was arranged to evaluate for glaucoma (a known risk in SWS), but a complete eye exam was limited by the patient’s agitation.\n- Obstetric evaluation: at 28 weeks + 1 day she developed vaginal bleeding and the fetus was judged nonviable; induction was performed without incident. Eclampsia was considered earlier but deemed unlikely because blood pressures were only mildly elevated at times, proteinuria was low and there were no renal or hepatic dysfunction signs.\n\nImportant exclusions and resource limits\n- The team excluded other syndromes that can produce vascular skin lesions and limb or brain overgrowth (for example, Klippel‑Trenaunay‑Weber and megalencephaly‑capillary malformation) based on the absence of limb hypertrophy, lymphatic abnormalities or large head size.\n- Advanced investigations and specialist input (MRI with contrast, detailed neuroimaging, formal EEG, psychiatric assessment, plastic surgery, neurosurgery and dental review) were not available or were limited by staffing and resources.\n\nWhat this implies and suggested next steps\n- SWS is a congenital neurocutaneous disorder caused by leptomeningeal and facial vascular malformations; main concerns are refractory seizures, stroke‑like neurological deficits, and glaucoma. Early and ongoing multidisciplinary care improves outcomes.\n- In this patient, priorities going forward (as resources permit) would include:\n  - Complete neuroimaging (MRI with contrast) and EEG to better define the extent of leptomeningeal disease and seizure focus.\n  - Full ophthalmologic assessment including intraocular pressure and optic nerve evaluation to detect glaucoma.\n  - Neurology follow‑up to optimize antiseizure therapy and consider surgical options if seizures remain medically refractory.\n  - Rehabilitation (physiotherapy, speech therapy) for hemiparesis and aphasia.\n  - Psychosocial support and counseling, including reproductive counseling and coordination of care given refugee status and limited local resources.\n- If advanced care is not locally available, referral pathways to centers with pediatric/adult neurovascular and neurosurgical expertise should be sought.\n\nTone and context\n- The case highlights diagnostic delay because the facial PWS and remote seizure history were initially missed, and illustrates how limited imaging access and staffing can restrict comprehensive care. The clinical team used a pragmatic multidisciplinary approach to control seizures and stabilize the patient despite resource constraints.\n\nIf you would like, I can produce a one‑page clinical snapshot for clinicians (timeline, key investigations, medications and recommended referrals) or a patient‑facing explanation of SWS and its implications."
+        }
+    },
+    {
+        "article": "Una paciente de 69 años se quejaba de una pérdida progresiva de la visión. Sus padres eran primos hermanos. Le habían diagnosticado retinitis pigmentosa 27 años antes. La paciente había fumado durante 15 años. Tenía antecedentes de hiperlipidemia e hipotiroidismo.\n\nTras una evaluación oftalmológica completa, se determinó que el paciente tenía una agudeza visual corregida (AVC) de contar los dedos a 5’ y 3’ en los ojos derecho e izquierdo, respectivamente. La retinoscopia mostró una refracción de –1.00 + 0.50×70 y –2.00 + 1.00×5 en los ojos derecho e izquierdo, respectivamente. El paciente tenía discos ópticos pálidos con una atrofia profunda extensa de la mácula central, hiperplasia del pigmento epitelial y otras áreas de atrofia multifocal en el ojo derecho. Además, el paciente tenía atrofia macular en el ojo izquierdo. En la imagen de autofluorescencia del fondo del ojo (FAF) del paciente, había evidencia de una hipoautofluorescencia central de la mácula, con una extensión centrífuga difusa desde su centro hasta su periferia.\n\nLa tomografía de coherencia óptica macular (OCT) determinó que el espesor macular promedio era de 191 µM y 193 µM en los ojos derecho e izquierdo, respectivamente. El volumen macular era de 6.9 mm3 y 7.0 mm3 en los ojos derecho e izquierdo, respectivamente. No se encontró edema macular, quistes o fluido subretinal en ninguno de los ojos.\n\nUna prueba de campo visual reveló que el paciente tenía desviaciones medias de –23.75 dB y –24.56 dB en los ojos derecho e izquierdo, respectivamente. Las desviaciones estándar de patrón fueron de +3.69 dB y +4.69 dB en los ojos derecho e izquierdo, respectivamente. Los resultados de un electrorretinograma de campo completo (ERG) mostraron una respuesta normal de bastones y una respuesta de conos disminuida, bilateralmente. Por estas razones, se realizó un diagnóstico clínico de enfermedad STGD1.\n\nSe encontró una variante patogénica homocigótica intrónica c.5714+5G>A del gen ABCA4 tras el análisis de secuenciación y eliminación/duplicación utilizando secuenciación de próxima generación (Invitae Corporation, San Francisco, California). Tenía seis variantes adicionales de significación incierta (VUS) en los genes CACNA1F, EYS, KCNV2, KLHL7, MKKS y USH2A.\n",
+        "gold_summary": "Una paciente de 69 años de edad se presentó en la clínica quejándose de una pérdida progresiva de la visión. La evaluación oftálmica fue notable para una mejor agudeza visual corregida de contar los dedos a 5' en el ojo derecho y 3' en el ojo izquierdo. Las imágenes revelaron una atrofia profunda y extensa de la mácula central, una hiperplasia del pigmento epitelial y otras áreas de atrofia multifocal en el ojo derecho. Además, las imágenes de autofluorescencia del fondo de la mácula mostraron una hipoautofluorescencia central con expansión bilateral a la periferia en ambos ojos. Un electrorretinograma de campo completo mostró una respuesta normal de los bastones, con una respuesta disminuida de los conos, bilateralmente. Las pruebas genéticas fueron positivas para una mutación inotrópica homocigótica en el gen ABCA4 de la variante c.5714+5G>A.\n",
+        "synthetic_summary": {
+            "B1": "Una mujer de 69 años tenía pérdida de la vista que empeoraba con el tiempo. Esto la hacía ver solo grandes cosas: podía contar dedos a poca distancia. Los médicos miraron sus ojos con muchas pruebas. Vieron que la parte central de la retina (la mácula), que nos ayuda a ver caras y detalles, estaba muy dañada en los dos ojos. No había hinchazón ni líquido en la mácula, lo cual es algo bueno.\n\nUna prueba llamada ERG mostró que las células que nos ayudan a ver con poca luz (bastones) funcionaban bien. Pero las células que nos ayudan a ver colores y detalles (conos) estaban dañadas. Por eso tiene problemas para ver con claridad y para distinguir detalles.\n\nLos médicos dijeron que tiene enfermedad de Stargardt (STGD1). Esta es una enfermedad heredada que afecta la visión central. La prueba genética encontró un cambio en el gen ABCA4 que explica su enfermedad. Los padres de la paciente eran primos, y eso puede aumentar la probabilidad de tener el mismo cambio en ambos genes. También se hallaron otras pequeñas variantes en varios genes, pero su importancia no está clara.",
+            "B2": "Resumen claro y amable:\n\nUna mujer de 69 años acudió por una pérdida progresiva de visión. Tenía antecedentes familiares cercanos (sus padres eran primos) y otros problemas de salud como hiperlipidemia e hipotiroidismo. En la exploración oftalmológica su agudeza visual corregida era muy reducida: podía contar dedos a 5 pies en el ojo derecho y a 3 pies en el izquierdo. Las imágenes de la retina mostraron una atrofia profunda de la mácula, que es la zona central de la retina responsable de la visión fina y de los detalles, y cambios en el epitelio pigmentario (capa que apoya a las células de la retina). La autofluorescencia del fondo de ojo mostró una área oscura (hipoautofluorescencia) en la mácula que se extendía hacia la periferia, lo que indica daño y pérdida de tejido macular.\n\nEl electrorretinograma (ERG), una prueba que mide la respuesta eléctrica de la retina, encontró respuestas normales de los bastones (células que ayudan a ver en la oscuridad) y respuestas disminuidas de los conos (células que permiten ver los colores y los detalles), lo que explica la pérdida de visión central.\n\nEl estudio genético encontró que la paciente es homocigótica para una variante patogénica (dañina) en el gen ABCA4 (c.5714+5G>A). \"Homocigótica\" significa que la misma variante proviene de ambos progenitores, lo que aumenta la probabilidad de enfermedad hereditaria. Esta mutación se asoció con un diagnóstico clínico de enfermedad STGD1 (Stargardt), una forma hereditaria de degeneración macular juvenil-adulta que causa pérdida de la visión central. También se hallaron seis variantes adicionales de significado incierto en otros genes; estas requieren más estudio para saber si tienen importancia.\n\nQué puede seguirse haciendo (pasos razonables):\n- Derivación a consejo genético para explicar el resultado, sus implicaciones familiares y la posibilidad de hacer pruebas a familiares.\n- Soporte de baja visión (ayudas ópticas y rehabilitación) para mejorar la independencia en las actividades diarias.\n- Seguimiento oftalmológico regular para vigilar la progresión.\n- Considerar evaluación para ensayos clínicos o terapias en investigación si procede.\n\nSi necesita, puedo ayudar a redactar preguntas para el equipo médico o explicar con más detalle qué significan las pruebas.",
+            "B3": "Resumen clínico (nivel universitario)\n\nPresentación y antecedentes\n- Mujer de 69 años con pérdida progresiva de la visión. Sus padres eran primos hermanos (consanguinidad).\n- Historia previa de retinitis pigmentosa diagnosticada hace 27 años. Fumó durante 15 años. Antecedentes médicos: hiperlipidemia e hipotiroidismo.\n\nHallazgos oftalmológicos clave\n- Agudeza visual corregida: contar los dedos a 5 pies (ojo derecho) y a 3 pies (ojo izquierdo) — pérdida visual central marcada.\n- Exploración del segmento posterior: discos ópticos pálidos; atrofia macular central profunda y extensa con hiperplasia del epitelio pigmentario y áreas de atrofia multifocal especialmente en el ojo derecho; atrofia macular también en el izquierdo.\n- Autofluorescencia del fondo (FAF): hipoautofluorescencia central de la mácula con extensión centrifuga difusa hacia la periferia — hallazgo anormal compatible con pérdida del epitelio pigmentario y de los fotorreceptores en la región macular.\n- Tomografía de coherencia óptica (OCT) macular: espesor macular promedio ~191–193 µm y volúmenes 6.9–7.0 mm3; no se observaron edema macular, quistes ni líquido subretinal (esto indica ausencia de edema o exudación activa).\n- Campo visual: desviaciones medias severas (−23.75 dB y −24.56 dB), compatible con importante pérdida del campo funcional.\n- Electrorretinograma (ERG) global: respuesta de bastones (visión escotópica) normal; respuesta de conos (visión fotópica/central y color) disminuida bilateralmente — patrón típico de afectación predominantemente de conos.\n\nDiagnóstico clínico y genético\n- Diagnóstico clínico final: enfermedad STGD1 (Stargardt tipo 1), enfermedad hereditaria de la mácula que provoca atrofia macular y pérdida de visión central.\n- Genética: se identificó una variante homocigótica intrónica c.5714+5G>A en el gen ABCA4, reportada como patogénica. Además se hallaron seis variantes de significado incierto (VUS) en CACNA1F, EYS, KCNV2, KLHL7, MKKS y USH2A.\n- Interpretación genética: la variante homocigótica en ABCA4 confirma que la enfermedad es causada por mutaciones en ABCA4 (forma autosómica recesiva), y la consanguinidad parental aumenta la probabilidad de homocigosidad. Las VUS requieren más estudio para determinar si contribuyen a la enfermedad.\n\nImplicaciones clínicas y pasos recomendados\n- Pronóstico: enfermedad progresiva con deterioro persistente de la visión central; la preservación de la función de bastones sugiere que la visión periférica y la adaptación a la oscuridad pueden conservarse más tiempo, pero la visión central y la agudeza seguirán comprometiéndose.\n- Manejo inmediato razonable: derivación a servicios de baja visión (rehabilitación visual, ayudas ópticas), protección solar y fotoprotección, control de factores modificables (p. ej., cesación del tabaquismo si procede).\n- Seguimiento y estudios adicionales: consulta de genética clínica para asesoramiento familiar y oferta de prueba genética a parientes (pruebas de portador/cascade testing); considerar confirmación funcional o segregación familiar para las VUS. Evaluación periódica oftalmológica para detectar complicaciones (p. ej. neovascularización coroidea) y para seguimiento de la progresión.\n- Investigación y ensayos: información sobre ensayos clínicos en enfermedades ABCA4/STGD1 y registro en bases de pacientes podría ofrecer acceso a terapias experimentales en el futuro.\n\nComentario final (tono empático)\nLos hallazgos estructurales (atrofia macular extensa y cambios en FAF) junto con la pérdida selectiva de la función de conos y la variante patogénica homocigota en ABCA4 respaldan fuertemente el diagnóstico de Stargardt (STGD1). Entiendo que esta es una noticia difícil; el paso siguiente más útil es coordinar atención multidisciplinaria (oftalmología, genética, baja visión) para optimizar la calidad de vida y explorar opciones de apoyo y, cuando proceda, participación en investigación."
+        }
+    },
+    {
+        "article": "Un niño de 19 meses de edad fue admitido en el departamento de urgencias porque se cayó de la trona en la que comía. Esta caída ocurrió en un aparente bienestar, sin la presencia de signos o síntomas anticipados. Primero, se cayó sobre su glúteo y luego se golpeó la cabeza (occipucio) contra el suelo. Vomitó (tres episodios) y estaba muy irritable. Su frecuencia respiratoria y cardíaca eran >60 respiraciones y >150 latidos por minuto, mientras que la saturación de oxígeno era <80%. Tras el examen físico, el niño estaba hidratado y consciente, pero irritable. Más importante aún, observamos retracciones subcostal y, al auscultar, disminución de los sonidos respiratorios en la parte basal izquierda del tórax. El paciente fue ventilado con un balón de AMBU conectado a una fuente de oxígeno y monitorizado con un oxímetro de pulso. A pesar de nuestra intervención, la saturación de oxígeno cayó por debajo del 70% y cuanto más ventilábamos, más caía la saturación. La ecografía pulmonar mostró la ausencia de las típicas líneas A y la consolidación del pulmón, que se visualizó directamente como un parénquima sólido. Sobre la base del mal estado clínico, el paciente se sometió a intubación orotraqueal con un tubo endotraqueal con manguito. Después de que el bebé se estabilizó, se sometió a una tomografía computarizada (TC) de tórax que mostró una atelectasia completa del pulmón izquierdo con una interrupción del bronquio izquierdo principal a 12 cm de la bifurcación bronquial. Se sospechó un FBA ya que la madre también declaró que el bebé en los días anteriores había tenido un ataque de tos intenso y desapareció en 24 h sin ningún tratamiento. Por lo tanto, se realizó una broncoscopia rígida y se encontró y se eliminó rápidamente una almendra de 2 cm de diámetro en el bronquio izquierdo principal.\n\nEl paciente nunca había consumido antes almendras u otros frutos secos y, en esta ocasión, ingirió la almendra por accidente.\n\nEl bebé mostró una mejora clínica progresiva y, después de 24 horas, se le retiró la sonda y se le dio de alta de la unidad de cuidados intensivos para ser ingresado en la sala de pediatría general durante unos días, con una recuperación gradual y total de la función respiratoria.\n",
+        "gold_summary": "Describimos el caso de un niño de 19 meses que llegó a la sala de urgencias por un traumatismo en la cabeza. La evaluación clínica, sin embargo, reveló una dificultad respiratoria grave inexplicable que requería intubación traqueal. Después de nuestra evaluación, planteamos la hipótesis de que la dificultad respiratoria grave determinó un estado alterado de conciencia con el consiguiente traumatismo en la cabeza. Los hallazgos radiológicos levantaron la sospecha de aspiración de cuerpo extraño por la presencia de una atelectasia de todo el pulmón izquierdo. La tomografía computarizada mostró una interrupción abrupta del bronquio principal a 12 mm del casco. La siguiente broncoscopia identificó una amígdala de 2 cm.\n",
+        "synthetic_summary": {
+            "B1": "Un niño de 19 meses se cayó de la trona y se golpeó la cabeza. Vomitó varias veces y estaba muy irritable. También tenía mucha dificultad para respirar y el nivel de oxígeno en su sangre estaba muy bajo.\n\nLos médicos escucharon menos aire en el lado izquierdo del pecho. Le pusieron una máscara y luego un tubo para ayudarle a respirar. Una tomografía mostró que todo el pulmón izquierdo estaba colapsado. Esto pasó porque algo tapaba el bronquio principal izquierdo, que es el conducto por donde entra el aire al pulmón.\n\nLa madre contó que el niño había tenido una tos fuerte unos días antes. Por eso los médicos pensaron que podía haber inhalado algo sin querer. Hicieron una broncoscopia, que es meter una pequeña cámara por la garganta para ver los pulmones. Encontraron y sacaron una almendra de 2 cm que estaba atascada.\n\nEl niño mejoró poco a poco. Al día siguiente le quitaron el tubo y, después de unos días en el hospital, se recuperó totalmente. No había comido almendras antes; se la tragó por accidente.",
+            "B2": "Resumen para alumnos (nivel B2, edad 11–17)\n\nUn niño de 19 meses llegó a urgencias tras caerse de la trona y golpearse la cabeza. Aunque parecía consciente, tenía problemas para respirar: respiraba muy rápido (>60 respiraciones/min), su corazón latía muy deprisa (>150 lpm) y su saturación de oxígeno estaba muy baja (<80% y luego <70%), incluso cuando se le ventilaba con una bolsa de oxígeno. En la exploración se vieron retracciones debajo de las costillas (señal de dificultad para respirar) y menos sonidos respiratorios en la parte baja del pulmón izquierdo.\n\nSe le puso un tubo en la tráquea para ayudarle a respirar (intubación). Una ecografía y después una tomografía del tórax mostraron que todo el pulmón izquierdo estaba colapsado (atelectasia: cuando una parte del pulmón deja de llenarse de aire) y que el conducto principal del pulmón (bronquio izquierdo) estaba bloqueado poco después de la bifurcación de las vías aéreas, a aproximadamente 1 cm. La familia recordó que el niño había tenido un episodio intenso de tos días antes que se resolvió solo, lo que hizo sospechar que había aspirado (tragado) algo.\n\nSe realizó una broncoscopia rígida (una exploración con un tubo rígido por la vía aérea) y se extrajo inmediatamente una almendra de unos 2 cm atrapada en el bronquio izquierdo. El niño no había comido almendras antes; la ingesta fue accidental. Tras la retirada del cuerpo extraño mejoró rápidamente: se le retiró el tubo tras 24 horas y fue trasladado de la UCI a planta, recuperando por completo la función respiratoria.\n\nMensaje final: la inhalación de alimentos o objetos pequeños puede causar bloqueo grave de una vía aérea. Si un niño tiene dificultad respiratoria, tos intensa o colapso de un pulmón en las pruebas, los médicos pueden necesitar imágenes y una broncoscopia para encontrar y quitar el cuerpo extraño.",
+            "B3": "Presentación clínica\nUn niño de 19 meses fue traído a urgencias tras caerse de la trona y golpearse la nuca. En el examen inicial estaba hidratado y consciente pero muy irritable. Tenía signos vitales anormales: taquipnea (>60 respiraciones/min), taquicardia (>150 lpm) y saturación de oxígeno marcadamente baja (<80%, llegando por debajo del 70% a pesar de ventilación con bolsa y oxígeno). Además presentaba retracciones subcostales y disminución de los ruidos respiratorios en la base del hemitórax izquierdo.\n\nHallazgos de imagen y procedimientos\n- Ecografía pulmonar: ausencia de las líneas A normales y presencia de consolidación en el pulmón izquierdo, visualizada como parénquima sólido.  \n- Debido al deterioro respiratorio se realizó intubación orotraqueal.  \n- Tomografía torácica: atelectasia completa del pulmón izquierdo y un corte abrupto del bronquio principal izquierdo situado a 12 mm (≈1,2 cm) desde la carina, lo que sugiere obstrucción bronquial.  \n- Ante la sospecha de aspiración de cuerpo extraño (la madre refirió un episodio reciente de tos intensa que cedió espontáneamente), se realizó broncoscopia rígida: se extrajo una almendra de 2 cm alojada en el bronquio principal izquierdo.\n\nDiagnóstico e interpretación\nEl cuadro corresponde a una obstrucción bronquial por cuerpo extraño (almendra) que provocó atelectasia total del pulmón izquierdo y una insuficiencia respiratoria grave. Es plausible que el episodio respiratorio agudo (hipoxia/alteración del nivel de conciencia) precediera y causara la caída y el traumatismo craneal, más que al revés.\n\nTratamiento y evolución\nLa extracción endoscópica del objeto fue curativa. El niño mejoró progresivamente, fue extubado a las 24 horas, trasladado a planta y tuvo recuperación completa de la función respiratoria en los días siguientes.\n\nImplicaciones y recomendaciones\n- En niños pequeños con insuficiencia respiratoria aguda, hipoxemia inexplicable o atelectasia unilateral, debe considerarse de inmediato la posibilidad de aspiración de cuerpo extraño.  \n- La tomografía y la ecografía pueden orientar, pero la broncoscopia rígida es diagnóstica y terapéutica.  \n- Prevención: los frutos secos enteros representan un riesgo alto de aspiración en menores de 3–4 años; es importante evitar darles nueces o almendras enteras y vigilar la alimentación.\n\nNota final (tono humano)\nEl caso subraya cuán rápido y grave puede ser la aspiración de un cuerpo extraño en lactantes y la importancia de una respuesta urgente. Afortunadamente, en este caso la extracción fue efectiva y el niño se recuperó completamente."
+        }
+    },
+    {
+        "article": "Una mujer nulípara de 35 años con antecedentes de infertilidad se presentó en la consulta externa. Informó de un antecedente de tres años de dolor sordo cíclico en el ombligo. El dolor se asoció a un nódulo umbilical que sangraba durante la menstruación. Cabe destacar que el dolor empeoraba durante la menstruación y se aliviaba con analgésicos. La paciente también informó de dismenorrea, menorragia y dispareunia. La paciente se había insertado un DIU de cobre 3 años antes y había estado usando Zinnia P (levonorgestrel y etinilestradiol) durante los últimos 3-4 meses para intentar aliviar el dolor. Su historial ginecológico previo no fue notable y tenía un ciclo menstrual regular. No había antecedentes médicos, quirúrgicos o sociales de importancia.\nAl examinarla, sus constantes vitales eran estables. Se observó una hinchazón hiperpigmentada (3 × 2 cm) en el ombligo al examinar el abdomen. La hinchazón era firme, inmóvil, no dolorosa, no reductible y no estaba ligada a estructuras subyacentes. Una resonancia magnética abdominal reveló una masa de mejora mal definida que medía 3 × 4 × 6 cm ubicada a lo largo de la pared abdominal anterior derecha y estaba conectada a un tracto sinusal que se extendía hacia la región suprapúbica, pero no se comunicaba con la cavidad peritoneal, hallazgos que sugieren endometriosis. El diagnóstico diferencial fue amplio, incluida una hernia umbilical, granuloma, cicatriz queloide, neoplasias malignas nodulares y anomalías embriológicas. Además, se observaron lesiones anexiales bilaterales, eran hiperintensas con áreas hipointensas focales y restricciones variables, la lesión del lado derecho medía 1,6 × 1,7 cm y la lesión del lado izquierdo medía 2,0 × 0,8 cm, hallazgos consistentes con endometriosis ovárica bilateral.\n\nSe programó al paciente para la extirpación quirúrgica del nódulo umbilical. La muestra se envió para un examen histopatológico. Los resultados revelaron una epidermis normal con glándulas endometriales dispersas y estroma dentro de la dermis. La fotomicroscopía resaltó la presencia de estroma endometrial y tejido graso subcutáneo. Esta morfología es consistente con la endometriosis. La recuperación postoperatoria de la paciente fue sin incidentes, y se la consideró apta para el alta el día 2 postoperatorio. Recibió asesoramiento sobre su fertilidad futura y la posibilidad de FIV, riesgo de recurrencia y se programó una visita de seguimiento en dos semanas. Se le inició con Dienogest, Visanne y un anticonceptivo oral combinado para el tratamiento de la endometriosis. Se la ha monitoreado clínicamente cada cuatro semanas, y no se han observado síntomas o signos de recurrencia local durante el período de seguimiento de 8 meses. Cabe destacar que, a pesar de que su condición permaneció estable después del tratamiento, no concibió en el transcurso del año siguiente.\n",
+        "gold_summary": "Presentamos el caso de una mujer nulípara de 35 años de edad del norte de Tanzania con un historial de infertilidad de 10 años. Al presentarse, la paciente informó de un historial de tres años de dolor cíclico asociado a una masa umbilical. Una resonancia magnética abdominal reveló una masa mal definida que se intensificaba y medía 3 × 4 × 6 cm, localizada a lo largo de la pared abdominal anterior derecha. La masa estaba conectada a un tracto sinusal que se extendía hacia la región suprapúbica, pero no mostraba comunicación con la cavidad peritoneal, lo que sugería endometriosis. Además, las lesiones anexiales bilaterales demostraron señales hiperintensas con áreas hipointensas focales y restricciones variables, consistentes con endometriomas ováricos bilaterales. La paciente se sometió a la extirpación de la masa umbilical y el examen histopatológico confirmó el diagnóstico de endometriosis umbilical primaria. A pesar de su condición estable después del tratamiento, no concibió durante el año siguiente.\n",
+        "synthetic_summary": {
+            "B1": "A 35-year-old woman who had not had children came to the clinic. She had three years of dull pain at her belly button. The pain got worse and the small lump at the belly button bled when she had her period. She also had painful and heavy periods.\n\nAn MRI scan showed a lump at the belly button and spots on both ovaries. Doctors thought this was endometriosis. Endometriosis is when tissue like the inside of the womb grows where it should not. This can make pain and bleeding.\n\nThe doctors removed the belly-button lump with a small operation. The lab looked at the removed tissue and found womb-like tissue in the skin. That confirmed endometriosis. The woman healed well and went home two days after surgery.\n\nShe was given hormone medicines to help keep the endometriosis quiet. She had check-ups every month. There was no sign that the lump came back for eight months. Even so, she did not become pregnant during the next year. Doctors talked with her about her future fertility and possible help such as IVF.",
+            "B2": "Summary (clear, age-appropriate)\n\nA 35-year-old woman who had never given birth and had been unable to get pregnant for many years came to clinic because she had three years of a dull, monthly pain at her belly button. The spot at her belly button sometimes formed a small lump that bled during her periods. She also had painful periods, heavy bleeding, and pain during sex.\n\nExams and scans\n- On physical exam the doctors saw a firm, darkened lump at the belly button.\n- An MRI scan showed a larger mass in the front abdominal wall connected by a small tract toward the lower belly. The scan did not show the mass opening into the main belly cavity. The MRI also showed small cyst-like lesions on both ovaries. These findings suggested endometriosis. \n- Endometriosis means tissue similar to the lining of the uterus grows outside the uterus. This can cause pain, bleeding, and sometimes ovarian cysts (called endometriomas).\n\nTreatment and outcome\n- The doctors surgically removed the belly-button lump. Looking at the removed tissue under a microscope (histopathology) showed endometrial glands and stroma in the skin — confirming primary umbilical endometriosis, a rare form of the condition.\n- She recovered well and left the hospital two days after surgery. She was given hormonal medicines (including dienogest and a combined birth-control pill) to help control endometriosis and was advised about future fertility options such as in vitro fertilization (IVF) and the chance the disease could come back.\n- During follow-up over eight months there were no signs that the belly-button problem had returned. However, she did not become pregnant in the year after treatment.\n\nThis case shows how endometriosis can sometimes appear in unusual places, such as the belly button, and how doctors use scans, surgery, and tissue tests to find and treat it.",
+            "B3": "Presentación breve\nUna mujer nulípara de 35 años con antecedentes de infertilidad consultó por un nódulo umbilical doloroso de aparición cíclica. El dolor era sordo, empeoraba durante la menstruación y el nódulo llegaba a sangrar en esos episodios. También refería dismenorrea (dolor menstrual intenso), menorragia (sangrado abundante) y dispareunia (dolor con las relaciones sexuales).\n\nHallazgos clínicos y de imagen\n- Exploración: lesión umbilical hiperpigmentada, firme, inmóvil, de unos 3 × 2 cm; no reducible y sin clara conexión con estructuras profundas a la palpación.\n- Resonancia magnética abdominal: masa mal definida de 3 × 4 × 6 cm en la pared abdominal anterior derecha, conectada por un tracto sinusal hacia la región suprapúbica pero sin comunicación con la cavidad peritoneal — hallazgos compatibles con endometriosis cutánea. Además, lesiones anexiales bilaterales con características (hiperintensas/hipo-intensas) compatibles con endometriomas ováricos (derecha 1,6 × 1,7 cm; izquierda 2,0 × 0,8 cm).\n\nDiagnóstico diferencial considerado\nhernia umbilical, granuloma, queloide, nódulos malignos o malformaciones congénitas. La combinación de clínica cíclica y hallazgos por imagen orientó hacia endometriosis umbilical (endometriosis primaria de la pared) asociada a enfermedad ovárica.\n\nTratamiento y confirmación diagnóstica\nSe realizó exéresis quirúrgica del nódulo umbilical. El examen histopatológico mostró epidermis normal con glándulas endometriales y estroma en la dermis y tejido graso subcutáneo, confirmando endometriosis umbilical primaria.\n\nEvolución y manejo posterior\n- Recuperación postoperatoria sin incidencias; alta al segundo día.\n- Inicio de tratamiento médico con dienogest (Visanne) y anticonceptivo oral combinado.\n- Consejería sobre fertilidad futura, posibilidad de FIV y riesgo de recurrencia; seguimiento clínico cada 4 semanas.\n- Durante 8 meses de seguimiento no hubo signos clínicos de recurrencia local. A pesar del tratamiento, la paciente no logró concebir en el año siguiente.\n\nImplicaciones y recomendaciones prácticas\n- La endometriosis umbilical primaria es poco frecuente pero debe sospecharse ante un nódulo umbilical con dolor y sangrado cíclico.  \n- La presencia simultánea de endometriomas ováricos sugiere enfermedad pélvica relacionada, lo que puede contribuir a la infertilidad.  \n- El manejo eficaz suele combinar cirugía (exéresis completa) y terapia hormonal para reducir síntomas y riesgo de recurrencia.  \n- Para pacientes que desean embarazo, es razonable la derivación a reproducción asistida (incluida la valoración para FIV) y la coordinación entre ginecología quirúrgica y reproducción asistida.  \n- Mantener seguimiento clínico e imagenológico si aparecen síntomas nuevos, por el riesgo —aunque bajo— de recurrencia o complicaciones.\n\nSi desea, puedo preparar un resumen más breve para uso clínico, una lista de preguntas para la consulta de fertilidad, o una explicación más detallada sobre los tratamientos hormonales y sus efectos sobre la fertilidad."
+        }
+    },
+    {
+        "article": "Presentamos a un recién nacido de 15 minutos de edad, hijo de una madre para-cuatro que no recordaba su LNMP pero que afirmaba haber estado amenorreica durante los últimos nueve meses. Su madre había recibido atención prenatal en el centro de salud cercano dos veces y no había tenido incidentes. Sin embargo, no se le había realizado un ultrasonido obstétrico temprano. Por lo demás, no tiene antecedentes de enfermedades crónicas como diabetes mellitus e hipertensión. Durante su embarazo actual, no tuvo fiebre, dolor de cabeza o visión borrosa. Nunca había usado ninguna droga aparte de sulfato ferroso durante este embarazo. Sus hijos anteriores están todos sanos y vivos. A su llegada a nuestro hospital, tuvo una hemorragia vaginal de dos horas de duración. Posteriormente, fue admitida con un diagnóstico de embarazo de tercer trimestre más multigravida más hemorragia anteparto secundaria a desprendimiento de placenta más oligohidramnios severo más presentación de nalgas.\n\nEn el examen pélvico, tenía un sangrado vaginal activo. Se le realizó una ecografía obstétrica al llegar. En consecuencia, la edad gestacional era de 34 semanas, la placenta estaba en el fondo con un coágulo retroplacentario y el líquido amniótico había disminuido significativamente con un único bolsillo más profundo de 1,5 cm. El peso fetal estimado era de 2,4 kg y presentación de nalgas. Otras investigaciones de la madre son grupo sanguíneo AB+, VDRL=negativo, RBS=120 mg/dL, en CBC, glóbulos blancos=9000, hemoglobina=11 gm/dL, plaqueta=180,000 y neutrófilo=60%.\n\nTras obtener el consentimiento informado por escrito, se realizó una cesárea de urgencia por las indicaciones ya mencionadas para extraer un neonato vivo de 2,01 kg de peso con puntuaciones de 5 y 6 en las pruebas de Apgar en el primer y el quinto minuto, respectivamente.\n\nEl neonato no lloró y fue reanimado durante cinco minutos. Luego fue trasladado a la unidad de cuidados intensivos neonatales para recibir atención e investigaciones adicionales. Al llegar, el neonato estaba en dificultad respiratoria. Sus signos vitales eran de 160 latidos por minuto, 70 respiraciones por minuto, temperatura de 33,4 grados centígrados y saturación de oxígeno del 60%. La fontanela anterior del neonato medía 2 cm por 2 cm y tenía micrognatia y cuello corto. En el sistema respiratorio, había retracciones intercostales y subcostales, respiración trabajosa y gruñidos. En el examen precordial, se escucharon bien los sonidos s1 y s2, no había murmullo ni ritmo de galope. En el sistema musculoesquelético, había acortamiento bilateral de las extremidades superiores, la extremidad inferior derecha estaba normal en posición y estructura, la pierna izquierda giraba hacia adentro (flexión mediolateral) en la articulación de la rodilla y la estructura del pie era normal. En el examen neurológico, estaba letárgico, el tono era normotónico en la extremidad inferior derecha y el reflejo de Moro era difícil de evaluar. La investigación de laboratorio mostró grupo sanguíneo = A+, CRP = reactivo, WBC = 30,000, neutrófilos = 54%, linfocitos = 21.1%, HGB = 8 gm/dL y plaquetas = 150,000. Se realizó una radiografía que mostró un acortamiento extremo de las extremidades superiores. La extremidad inferior izquierda estaba internamente girada. La ecocardiografía fue normal. Con una evaluación de prematuro tardío (34-36 semanas por puntaje de Ballard) más bajo peso al nacer más apropiado para la edad gestacional más focomelia más asfixia perinatal más sepsis neonatal temprana, se manejó con apoyo de oxígeno, fluido de mantenimiento e antibióticos intravenosos. El neonato murió después de tres días de hospitalización.\n",
+        "gold_summary": "Presentamos a un neonato de 15 minutos de vida, hijo de una madre para-cuatro que no recordaba su LNMP pero que afirmaba estar amenorreica desde hacía nueve meses. El modo de parto fue por cesárea para extraer al neonato vivo, que pesaba 2,01 kg y tenía puntuaciones APGAR de 5 y 6 en el primer y quinto minutos, respectivamente. El neonato no lloró y fue reanimado durante cinco minutos. Después se lo trasladó a la unidad de cuidados intensivos neonatales para continuar con el tratamiento y las investigaciones. Sus signos vitales eran: pulso de 160 latidos por minuto, frecuencia respiratoria de 70 respiraciones por minuto, temperatura de 33,4 grados centígrados y saturación de oxígeno del 60%. La fontanela anterior del neonato medía 2 cm por 2 cm y tenía micrognatia y cuello corto. En el sistema respiratorio había retracciones intercostales y subcostales, respiración trabajosa y gruñidos. En el sistema musculoesquelético había acortamiento bilateral de la extremidad superior, la pierna derecha tenía una posición y estructura normales, la pierna izquierda giraba hacia adentro (se doblaba hacia la parte media) en la articulación de la rodilla y el pie tenía una estructura normal.\n",
+        "synthetic_summary": {
+            "B1": "Resumen sencillo y amable:\n\nUna madre llegó al hospital con sangrado antes del parto. Le hicieron una cesárea de urgencia porque la placenta se había separado y el bebé estaba en presentación de nalgas. La madre había tenido poco control prenatal y no se hizo una ecografía temprana.\n\nNació un bebé que pesó 2,01 kg. Al nacer tuvo puntuaciones de Apgar 5 y 6, no lloró y tuvo que ser reanimado por cinco minutos. Lo llevaron a la unidad de cuidados intensivos neonatales.\n\nEl bebé tenía dificultad para respirar. Tenía la piel fría y la temperatura era baja (33,4 °C). Su oxígeno en la sangre era muy bajo (60%). Tenía la frente blanda (fontanela 2 x 2 cm), la mandíbula pequeña (micrognatia) y el cuello corto. Se le veía respirar con esfuerzo y hacía gruñidos.\n\nEn el cuerpo se encontró que los brazos estaban muy cortos en ambos lados (esto se llama focomelia). La pierna izquierda estaba girada hacia adentro. La ecografía del corazón fue normal. Los análisis de sangre mostraron signos de infección y anemia.\n\nEl equipo le dio oxígeno, líquidos y antibióticos por vena. A pesar de los cuidados, el bebé falleció después de tres días en el hospital. Es una noticia triste, y los médicos actuaron rápido para intentar ayudar.",
+            "B2": "This report describes a baby born by emergency cesarean section after the mother had heavy vaginal bleeding caused by a placental abruption (the placenta partly detaching from the uterus). The mother had limited prenatal checks and an ultrasound at arrival showed the pregnancy was about 34 weeks, the baby was in breech position, and the amniotic fluid was very low (oligohydramnios).\n\nThe baby was alive at birth but weak, weighing 2.01 kg, and had low Apgar scores (5 at 1 minute, 6 at 5 minutes), which are quick tests of a newborn’s health. The infant did not cry at first and needed five minutes of resuscitation. In the neonatal intensive care unit the baby had serious breathing problems: fast breathing, chest retractions, grunting, low oxygen saturation (60%), and a low body temperature (33.4 °C). These signs show respiratory distress and possible birth-related oxygen shortage (perinatal asphyxia).\n\nOn exam and X-ray the baby had very short upper arms (phocomelia, a condition where parts of the limbs are missing or very shortened), a small lower jaw (micrognathia), and a short neck. One lower leg was turned inward at the knee. Heart ultrasound was normal. Blood tests suggested infection (high white blood cell count and positive CRP) and anemia (hemoglobin 8 g/dL).\n\nDoctors treated the newborn with oxygen, fluids, and intravenous antibiotics for suspected early neonatal sepsis (a bloodstream infection). Despite care, the baby died after three days in hospital.\n\nWhen infants have severe limb differences and early problems like these, doctors often consider further investigations such as genetic testing and specialist counseling for the family, along with explaining the causes, likely outcomes, and options for future pregnancies. The tone of this case is one of serious illness and sadness; families in similar situations are usually offered support, clear information, and follow-up care.",
+            "B3": "Resumen clínico (nivel universitario, tono empático)\n\nPresentación y antecedentes maternos\n- Madre multípara (para 4) con dos controles prenatales en centro de salud; no se hizo ecografía temprana. No refiere enfermedades crónicas ni uso de fármacos teratógenos declarados (solo sulfato ferroso). Reportó amenorrea de nueve meses.\n- Acudió por hemorragia vaginal de 2 horas; fue diagnosticada de probable desprendimiento de placenta con oligohidramnios severo y presentación de nalgas. Ecografía al ingreso: edad gestacional estimada 34 semanas, placenta fundal con colección retroplacentaria, bolsillo amniótico más profundo 1,5 cm, peso fetal estimado 2,4 kg.\n\nParto y reanimación\n- Se realizó cesárea de urgencia por las indicaciones maternas/fetales. Se extrajo un neonato vivo que pesó 2,01 kg (APGAR 5 al 1’ y 6 al 5’). No lloró al nacer y precisó reanimación por 5 minutos antes de traslado a UCI neonatal.\n\nExamen inicial del neonato y hallazgos relevantes\n- Signos vitales al ingreso: FC 160/min, FR 70/min, temperatura 33,4 °C (hipotermia), SaO2 60% (hipoxia).\n- Estado general: dificultad respiratoria con retracciones inter- y subcostales y gruñidos; letárgico.\n- Cabeza/cara/cuello: fontanela anterior 2 × 2 cm, micrognatia (mandíbula pequeña) y cuello corto.\n- Sistema cardiovascular: sonidos normales sin soplos.\n- Sistema musculoesquelético: acortamiento bilateral marcado de ambas extremidades superiores (focomelia en radiografía). Extremidad inferior derecha con aspecto normal; extremidad inferior izquierda con rotación interna en la rodilla, pie con estructura normal.\n- Neurológico: tono conservado en la extremidad inferior derecha; reflejo de Moro difícil de evaluar.\n- Laboratorio: grupo sanguíneo A+; CRP reactiva; leucocitos 30 000/µL, neutrófilos 54%, linfocitos 21.1%; hemoglobina 8 g/dL; plaquetas 150 000/µL.\n- Ecocardiograma normal. Radiografía confirmó acortamiento extremo de los miembros superiores.\n\nDiagnóstico y manejo inicial\n- Diagnósticos planteados: recién nacido prematuro tardío (≈34 semanas), bajo peso al nacer (2,01 kg), apropiado para la edad gestacional según evaluación, focomelia bilateral de miembros superiores, asfixia perinatal, y sospecha de sepsis neonatal temprana (CRP alta, leucocitosis).\n- Tratamiento: soporte con oxígeno, control térmico, líquidos de mantenimiento y antibióticos intravenosos empíricos.\n- Evolución: fallecimiento tras 3 días de hospitalización.\n\nInterpretación y consideraciones importantes\n- Los hallazgos estructurales (focomelia bilateral de miembros superiores y malposición de la pierna izquierda) indican una malformación congénita significativa. Las causas posibles incluyen alteraciones en el desarrollo embrionario por factores genéticos, alteraciones vasculares durante la organogénesis o exposición a teratógenos (p. ej., fármacos como talidomida), aunque la madre negó uso de fármacos distintos al hierro. No se puede concluir la causa sin estudios adicionales.\n- La combinación de desprendimiento placentario, oligohidramnios, parto pretérmino y las anomalías respiratorias y térmicas contribuía a la asfixia perinatal y al riesgo de sepsis. La anemia (Hb 8 g/dL) y la hipoxia/hipotermia empeoran el pronóstico neonatal.\n- La discordancia entre el peso fetal estimado por ecografía (2,4 kg) y el peso real (2,01 kg) sugiere estimación prenatal imprecisa o pérdida de peso por las condiciones perinatales.\n\nRecomendaciones y pasos siguientes sugeridos (para la familia y el equipo clínico)\n- Considerar estudio postmortem (autopsia) y examen patológico de la placenta para investigar desprendimiento, infecciones o causas vasculares.\n- Estudios genéticos y/o consulta con genética clínica para evaluar etiologías hereditarias o síndromes asociados a focomelia.\n- Revisión detallada de la historia de exposición materna a medicamentos, sustancias o infecciones durante el embarazo.\n- Cultivos y PCR para agentes infecciosos (si no se hicieron) y revisión de resultados microbiológicos para confirmar o descartar sepsis neonatal.\n- Apoyo psicosocial y consejería para la familia sobre hallazgos, pruebas adicionales y planificación de embarazos futuros.\n\nLamento profundamente la pérdida de este recién nacido. Si la familia o el equipo clínico lo desean, los pasos descritos pueden ayudar a aclarar la causa y orientar el manejo en futuros embarazos; el apoyo emocional y la comunicación clara son fundamentales en este proceso."
+        }
+    },
+    {
+        "article": "Mujer de 61 años con antecedente de carcinoma escamocelular de cuello uterino estadio FIGO IIB, diagnosticado en febrero de 2019, tratada en un hospital privado de cuarto nivel de atención, donde se ofrece cuidado ambulatorio y hospitalario para pacientes con condiciones complejas oncológicas y no oncológicas. Al momento del diagnóstico se realizó histerectomía radical con linfadenectomía pélvica, que descartó compromiso nodal. El tratamiento complementario de primera línea incluyó seis ciclos de quimioterapia con cisplatino, y braquiterapia y radioterapia, alcanzando una respuesta tumoral completa. En 2021, tras detectarse una recaída aislada en la región ilíaca, mediante tomografía, se administró cisplatino y 30 sesiones de radioterapia, logrando una nueva respuesta completa. En septiembre de 2022, una tomografía reveló otra recaída con compromiso del parametrio izquierdo, el uréter y la cadena ilíaca ipsilateral, por lo que se decidió primera línea para enfermedad recurrente con carboplatino, paclitaxel y pembrolizumab. Durante este régimen, la paciente presentó hipersensibilidad al platino en el quinto ciclo, gestionada con un protocolo de desensibilización, continuando con el pembrolizumab. En septiembre de 2023, ante la progresión en imágenes de una masa retroperitoneal única, debido a la falta de respuesta óptima, se inició gemcitabina, según guías de manejo, segunda línea de enfermedad recurrente, recibiendo una dosis acumulada de 8.544 mg/m2 hasta enero de 2024. Sin embargo, desarrolló síntomas de isquemia digital en manos, por lo que el tratamiento fue suspendido tras la segunda dosis del tercer ciclo, acumulando 11.744 mg/m2 de gemcitabina.\n\nEn febrero de 2024, la paciente ingresó al servicio de urgencias del mismo hospital donde era valorada de forma ambulatoria, remitida por oncología debido a progresión de los síntomas en sus extremidades. La paciente refería dolor lancinante y coloración azulada en dedos de manos; al examen físico se evidencia necrosis en el segundo dedo de la mano derecha, coloración ocre y fenómeno de Raynaud en los dedos de la mano izquierda. Las extremidades inferiores mostraban edema grado II en el miembro inferior izquierdo y pulsos presentes. Los estudios para autoinmunidad y vasculitis resultaron negativos, incluyendo anticuerpos anticitoplasma de neutrófilos (ANCAS), anticuerpos antinucleares (ANAS), anticuerpos antidesoxirribonucleicos (anti-DNA), cardiolipinas, prueba confirmatoria de anticoagulante lúpico, perfil de anticuerpos contra antígenos nucleares extraíbles (ENAS), anticuerpos contra proteinasa 3, anticuerpos antimieloperoxidasa y anticuerpos dirigidos contra la ADN topoisomerasa I (antiSCL). Además, el factor reumatoide y los niveles de complemento 3 (C3) y complemento 4 (C4) también fueron normales. Prueba serológica para sífilis (VDRL - Venereal Disease Research Laboratory) negativa, ecocardiograma transtorácico sin hallazgos de un foco cardioembólico.\n\nSe inició anticoagulación con heparina de bajo peso molecular, junto con ácido acetilsalicílico, estatina y un calcioantagonista. El equipo de cirugía de mano realizó amputación del segundo dedo de la mano derecha, confirmando necrosis por licuefacción en el estudio histopatológico.\n\nDurante el posoperatorio se agregó sildenafil al tratamiento, logrando una mejoría progresiva en los signos de isquemia de los dedos restantes. Durante la hospitalización, la paciente presenta complicación por sangrado vaginal masivo, requiriendo embolización de arterias uterinas.\n\nEl servicio de reumatología aplicó la escala de causalidad de Naranjo para determinar el papel de la gemcitabina en la vasculitis, con un puntaje de 8, lo que indicó que el medicamento probablemente provocó la necrosis.\n\nPosteriormente, a los 20 días de ingreso a hospitalización desarrolló deterioro neurológico, sin hallazgos significativos en la tomografía de cráneo. Evaluada por cuidados paliativos, su estado funcional se clasificó con un Barthel de 0/30, ECOG de 4 y Karnofsky de 10 %, con pronóstico de vida inferior a tres semanas según el Índice Pronóstico de Paciente (PPI: + 6 puntos). En consenso con la familia, se suspendieron estudios adicionales y se implementó un manejo paliativo integral. La paciente falleció tras el alta hospitalaria.",
+        "gold_summary": "Oaciente de 61 años tratada con gemcitabina (11.744 mg/m² acumulados) por enfermedad metastásica, en un hospital general de cuarto nivel, privado, no oncológico, donde venía siendo manejada de forma ambulatoria. Presentó necrosis distal del segundo dedo de la mano derecha, por lo que se suspendió el tratamiento y se requirió amputación de este dedo. Se realizó una búsqueda en Embase, Medline y Lilacs. Se buscaron estudios de reporte y series de casos sobre necrosis distal inducida por gemcitabina. Se extrajeron datos de dosis, diagnóstico y tratamiento.",
+        "synthetic_summary": {
+            "B1": "Había una mujer de 61 años que había tenido cáncer en la parte baja del vientre. Los médicos le dieron muchos tratamientos con medicina fuerte (quimioterapia). Cuando volvió a empeorar, le dieron un medicamento llamado gemcitabina.\n\nDespués de varias dosis, empezó a tener mucho dolor y sus dedos de las manos se pusieron de color azul y después algunas partes se murieron (necrosis). Los médicos hicieron muchas pruebas para ver si otra enfermedad estaba causando eso. Esas pruebas salieron normales. También revisaron el corazón y no encontraron que hubiera coágulos saliendo del corazón.\n\nLos médicos pensaron, usando una lista de comprobación, que probablemente la gemcitabina causó el problema. Dejaron de dar ese medicamento. Tuvieron que quitar el segundo dedo de la mano derecha porque esa parte estaba muerta. Le dieron otras medicinas y, con eso, los otros dedos mejoraron un poco.\n\nMientras estuvo en el hospital sufrió un sangrado fuerte en la zona del vientre y los médicos tuvieron que hacer un procedimiento para parar la sangre. Más tarde empezó a empeorar mucho de salud en general. La familia y el equipo médico acordaron darle cuidados de confort para que no sufriera más. Poco después de salir del hospital, la mujer falleció.\n\nLo importante: los médicos creen que un medicamento pudo haber causado que un dedo se dañara. Buscaron otras causas y no las encontraron. Los cuidaron y, al final, decidieron darle alivio y acompañamiento.",
+            "B2": "Here is a clear, gentle summary of the case written for a teenage reader.\n\nSummary:\n- A 61-year-old woman had a type of cervical cancer (squamous cell carcinoma) first treated successfully with surgery, chemotherapy, and radiotherapy. After two separate recurrences over several years, she received different chemotherapy drugs.\n- In September 2023 her cancer progressed and doctors started gemcitabine, a chemotherapy drug. By January 2024 she had received a total dose of 11,744 mg/m² of gemcitabine when she developed problems in her hands.\n- She came to the hospital with severe, stabbing pain and blue coloring of her fingers. On exam, the right index finger (second finger) was dead tissue (necrosis), and the left hand showed a Raynaud-like pattern (fingers turning pale or blue when stressed). Her lower legs had some swelling but blood pulses were present.\n- Doctors checked for other causes that can block blood flow or cause inflammation of vessels (vasculitis). Tests for autoimmune diseases and infections (for example, ANCA, ANA, anti-DNA, antiphospholipid tests, complements C3/C4, and syphilis test) were all negative. A heart ultrasound showed no blood-clot source from the heart.\n- Because of the worsening ischemia (lack of blood flow), the medical team stopped gemcitabine. They started blood thinners (low-molecular-weight heparin), aspirin, a cholesterol-lowering drug (statin), and a calcium-channel blocker to try to open blood vessels. The damaged right index finger was surgically removed; the tissue exam confirmed liquefactive necrosis (tissue breakdown due to lack of blood).\n- After surgery doctors added sildenafil (a drug that can help improve blood flow) and the remaining fingers gradually improved. During the hospital stay she also had heavy vaginal bleeding that required embolization (a procedure to block the bleeding uterine artery).\n- Rheumatology used the Naranjo scale (a standard checklist) to see whether gemcitabine likely caused the blood-vessel damage. The score was 8, which means it was a probable cause.\n- About 20 days after admission she developed sudden neurological decline. Brain CT did not show a clear cause. Her overall condition became very poor: she could not perform daily activities and scores used to measure function and prognosis indicated a very limited life expectancy (under three weeks). After discussion with her family, further invasive testing was stopped and palliative (comfort-focused) care was started. The patient died after discharge.\n\nWhat this means (in simple terms):\n- Gemcitabine is a chemotherapy drug that can, rarely, cause severe problems with blood flow to the fingers and toes, leading to pain, color change, and sometimes tissue death. In this case the pattern, the timing after gemcitabine, and the negative tests for other causes made the drug the most likely reason.\n- When such signs appear, doctors usually stop the suspected drug, use medicines to improve blood flow and prevent clots, and may need surgery for dead tissue. If a patient’s overall health worsens, the focus may shift to comfort care in discussion with the family.\n\nThis case shows how rare but serious side effects of chemotherapy can develop, and how teams work together to diagnose, treat, and support the patient and family.",
+            "B3": "Resumen clínico (lectores universitarios)\n\nAntecedentes y tratamiento oncológico\n- Mujer de 61 años con carcinoma epidermoide de cuello uterino estadio FIGO IIB diagnosticado en 2019. Fue sometida a histerectomía radical y linfadenectomía pélvica (sin afectación nodal) y recibió quimioterapia con cisplatino, braquiterapia y radioterapia, con respuesta completa.\n- En 2021 presentó recurrencia ilíaca tratada con cisplatino y radioterapia (respuesta completa). En 2022 hubo nueva recaída con compromiso del parametrio izquierdo, uréter y cadena ilíaca ipsilateral; se inició carboplatino + paclitaxel + pembrolizumab. Se documentó hipersensibilidad al platino en el 5.º ciclo, manejada con desensibilización.\n- Por progresión en 2023 se inició gemcitabina como segunda línea. La paciente recibió una dosis acumulada total de 11.744 mg/m² antes de suspender el fármaco por aparición de síntomas isquémicos en las manos.\n\nPresentación y hallazgos\n- En febrero de 2024 consultó por dolor intenso y acrocianosis en los dedos. Al examen: necrosis del segundo dedo de la mano derecha, coloración ocre y fenómeno de Raynaud en la mano izquierda; miembros inferiores con edema grado II y pulsos presentes.\n- Se descartaron causas autoinmunes y vasculitis: pruebas negativas (ANCA, ANA, anti‑DNA, ENA, anticardiolipinas, anticoagulante lúpico, anti‑PR3, anti‑MPO, anti‑Scl‑70), factor reumatoide y C3/C4 normales. Serología para sífilis negativa. Ecocardiograma transtorácico sin foco cardioembólico.\n\nManejo realizado\n- Suspensión de gemcitabina. Inicio de anticoagulación con heparina de bajo peso molecular, ácido acetilsalicílico, estatina y un calcioantagonista (vasodilatador).\n- Amputación del segundo dedo derecho por necrosis; anatomía patológica compatible con necrosis por licuefacción.\n- Posteriormente se añadió sildenafil (vasodilatador), con mejoría progresiva de la isquemia en los dedos restantes.\n- Complicación durante la hospitalización: hemorragia vaginal masiva que requirió embolización de las arterias uterinas.\n\nCausalidad y evolución\n- El equipo de reumatología aplicó la escala de Naranjo (herramienta para estimar probabilidad de reacción adversa a un fármaco); el puntaje fue 8, lo que sugiere que gemcitabina fue una causa probable de la vasculopatía/digital necrosis.\n- A los 20 días de hospitalización la paciente presentó deterioro neurológico sin hallazgos significativos en la tomografía cerebral. Su estado funcional empeoró (Barthel 0/30, ECOG 4, Karnofsky 10 %) y el índice pronóstico (PPI) indicó expectativa de vida inferior a tres semanas.\n- En consenso con la familia se limitaron estudios y se inició manejo paliativo integral. La paciente falleció tras el egreso.\n\nInterpretación y consideraciones\n- Se trata de un cuadro de isquemia digital grave y necrosis distal aparecido durante tratamiento con gemcitabina, tras excluir causas autoinmunes y cardioembólicas. Aunque raro, la gemcitabina se ha asociado con vasculopatías y fenómenos tromboembólicos que pueden ocasionar isquemia tisular.\n- Implicaciones prácticas: ante signos tempranos de isquemia digital en pacientes que reciben gemcitabina, debe considerarse la suspensión inmediata del fármaco, evaluación exhaustiva para excluir otras causas (trombosis, embolia, vasculitis), tratamiento médico con anticoagulación y vasodilatadores, y cirugía cuando exista necrosis establecida. La notificación del evento adverso y la evaluación de causalidad son recomendables.\n- En pacientes con enfermedad avanzada y deterioro funcional marcado, la atención paliativa temprana y la toma de decisiones compartida con la familia son fundamentales.\n\nEmpatía\n- Este caso ilustra una complicación grave y devastadora en el contexto de cáncer avanzado. La toma rápida de decisiones terapéuticas y el apoyo paliativo fueron elementos clave en el manejo hacia el final de la vida."
+        }
+    },
+    {
+        "article": "Mujer de 53 años, con antecedente de AR de 15 años de diagnóstico en tratamiento con metotrexato, resto de antecedentes sin datos de importancia, la cual presentó cuadro clínico 8 meses antes (de acudir a nuestro servicio) con astenia y adinamia de forma progresiva, palidez de tegumentos, alzas térmicas no cuantificadas de predominio nocturno, pérdida de peso no intencionada de 15 kg en 6 meses aproximadamente, sin valoración ni seguimiento médico, a lo que se agregó 3 meses después disnea de grandes a medianos esfuerzos, y cuya sintomatología se agudizó 5 días antes (de acudir a nuestro servicio), aunada a sangrado de tubo digestivo alto (STDA), caracterizado por evacuaciones melénicas abundantes, 3 evacuaciones en 24 horas, hematemesis en 2 ocasiones, escasas, sin causa aparente. La paciente negó consumo de analgésicos no esteroideos (AINE) y tuvo aumento de volumen en la pierna izquierda, la cual le dolía y tenía la presencia de edema y eritema, con limitación a la movilidad, motivo por el cual acudió a (nuestro) Servicio de Urgencias.\n\nDurante su hospitalización con anemia severa sin repercusión hemodinámica, se transfundieron 3 concentrados eritrocitarios sin complicaciones aparentes. Después de su estabilización, se inició abordaje diagnóstico para síndrome consuntivo. Por el cuadro clínico de miembro inferior izquierdo se hizo US Doppler que evidenció trombosis venosa profunda. Se realizó ultrasonido de abdomen por probable hepatopatía por metotrexato, el cual reportó infartos esplénicos y hepáticos, así como presencia de cambios crónicos hepáticos. Se llevó a cabo endoscopía con evidencia de varices pequeñas, sin sangrado activo. Debido a la sospecha de neoplasia por los antecedentes y el cuadro clínico de la paciente, se llevó a cabo tomografía axial simple y contrastada de tórax y abdomen y se encontró hepatoesplenomegalia y múltiples conglomerados ganglionares axilares, mediastinales y paraaórticos que sugerían actividad infiltrativa. Esto se valoró por el Servicio de Cirugía General para la realización de biopsia de ganglio axilar derecho, donde se reportó proliferación neoplásica de células linfoides. Posteriormente se valoró por el Servicio de Hematología de la unidad, se solicitaron estudios de laboratorio (cuadro I) y se realizó aspirado de médula ósea en el que se evidenciaron células plasmáticas displásicas y células reticulares, por lo cual se concluyó que había la presencia de infiltración linfoplasmocitaria. Con los antecedentes, el cuadro clínico y los estudios complementarios se diagnosticó LNH estadio IV y la paciente fue enviada a hospital de tercer nivel para realización de inmunohistoquímica, estadificación e inicio de tratamiento. En tercer nivel se identificó linfoma difuso de células B con inmunofenotipo B CD20 con sobrecrecimiento de células dendríticas, y la paciente fue valorada para inicio de tratamiento con quimioterapia.",
+        "gold_summary": "Mujer de 55 años con antecedente de AR que ingresó a un servicio de medicina interna por sangrado de tubo digestivo; presentó datos clínicos de trombosis venosa profunda en miembro pélvico izquierdo y síndrome consuntivo en estudio. Durante su abordaje se identificó con infartos esplénicos y hepáticos, así como múltiples conglomerados ganglionares, por lo que se practicó biopsia de ganglio axilar que reportó proliferación neoplásica de células linfoides y aspirado de médula ósea con presencia de infiltración linfoplasmocitaria, con lo que se determinó diagnóstico de linfoma no Hodgkin estadio IV. La paciente fue enviada a un hospital de tercer nivel para inicio de tratamiento.",
+        "synthetic_summary": {
+            "B1": "Una mujer de 53 años llegó al hospital porque estaba muy cansada, había bajado mucho de peso y tenía fiebre por las noches. También tenía sangre en las heces y vomitó sangre. Su pierna izquierda se hinchó y le dolía. \n\nEn el hospital le pusieron sangre porque estaba muy baja de sangre. Hicieron muchas pruebas. En la pierna encontraron un coágulo en una vena. En el abdomen vieron zonas del bazo y del hígado que dejaron de recibir sangre. También encontraron muchos ganglios inflamados en el cuerpo. \n\nSacaron una muestra de un ganglio y del hueso para mirar las células. Vieron que unas células del sistema inmune estaban creciendo sin control. Por eso diagnosticaron linfoma no Hodgkin en estadio IV. Esto es un tipo de cáncer que afecta ganglios y médula. \n\nLa enviaron a un hospital más grande para hacer más estudios y empezar tratamiento con quimioterapia. Los médicos la estaban cuidando y le darán el tratamiento que necesita.",
+            "B2": "Resumen claro y amable:\n\nUna mujer de 53 años con artritis reumatoide tratada con metotrexato llegó al hospital por cansancio progresivo, pérdida de peso fuerte (unos 15 kg en 6 meses), palidez, fiebre nocturna y dificultad para respirar. Cinco días antes de la consulta presentó además sangrado digestivo alto: heces negras por sangre (melena) y dos episodios de vómito con sangre (hematemesis). También tenía hinchazón, dolor y enrojecimiento en la pierna izquierda, que limitaban su movimiento.\n\nEn el hospital presentaba anemia severa y recibió tres transfusiones de sangre. Un ecodoppler de la pierna mostró una trombosis venosa profunda (un coágulo en una vena profunda). Un ecografía abdominal encontró infartos en el bazo y el hígado y cambios hepáticos crónicos. La endoscopia mostró varices pequeñas sin sangrado activo. La tomografía (TAC) mostró aumento de tamaño del hígado y del bazo (hepatosplenomegalia) y muchos ganglios agrandados en axilas, mediastino y alrededor de la aorta, lo que sugirió una enfermedad infiltrativa (posible tumor).\n\nSe tomó una biopsia de un ganglio axilar y un aspirado de médula ósea (muestras para mirar las células al microscopio). Estos estudios mostraron proliferación de células linfoides e infiltración linfoplasmocitaria, por lo que se diagnosticó un linfoma no Hodgkin en estadio IV (un tipo de cáncer de los linfocitos que ya afecta varios órganos). La paciente fue enviada a un hospital de tercer nivel para confirmar el diagnóstico con inmunohistoquímica; allí identificaron un linfoma difuso de células B positivo para CD20 y se planificó el inicio de quimioterapia.\n\nQué significa esto y próximos pasos: la paciente tiene un cáncer del sistema inmunitario que requiere tratamiento especializado (quimioterapia). Ya se completaron estudios diagnósticos y fue derivada para recibir tratamiento y seguimiento en un centro con experiencia.",
+            "B3": "Resumen clínico (nivel universitario)\n\nPaciente: mujer de 53 años con artritis reumatoide de 15 años en tratamiento con metotrexato.\n\nPresentación y evolución\n- Hace 8 meses inició astenia progresiva, pérdida de fuerza, palidez, febrículas nocturnas y pérdida de peso no intencional de ~15 kg. No recibió seguimiento médico inicial.\n- A los 3 meses apareció disnea a esfuerzos moderados.\n- Cinco días antes del ingreso presentó sangrado digestivo alto: evacuaciones melénicas abundantes (3 en 24 h) y dos episodios de hematemesis leves. Negó consumo de AINE.\n- También refirió aumento de volumen, dolor, eritema y edema en la pierna izquierda con limitación funcional.\n\nHallazgos durante la hospitalización\n- Anemia severa que requirió transfusión de 3 concentrados eritrocitarios sin complicaciones hemodinámicas aparentes.\n- Doppler venoso de miembro inferior izquierdo: trombosis venosa profunda (complicación trombótica confirmada).\n- Endoscopia digestiva alta: varices pequeñas sin sangrado activo en el momento del estudio.\n- Ecografía abdominal (realizada por sospecha de hepatopatía relacionada con metotrexato): infartos esplénicos y hepáticos y signos de cambios hepáticos crónicos.\n- Tomografía (tórax y abdomen, con contraste): hepatoesplenomegalia y múltiples conglomerados ganglionares axilares, mediastinales y paraaórticos, sugestivos de proceso infiltrativo/linfoproliferativo.\n- Biopsia de ganglio axilar derecho: proliferación neoplásica de células linfoides.\n- Aspirado de médula ósea: presencia de células plasmáticas displásicas y células reticulares; se documentó infiltración linfoplasmocitaria.\n\nDiagnóstico y manejo inicial\n- Con los antecedentes, la clínica y los estudios anatomopatológicos se diagnosticó linfoma no Hodgkin (LNH) en estadio IV.\n- Fue remitida a un hospital de tercer nivel para completar inmunohistoquímica, estadificación definitiva e inicio de tratamiento. En el centro de referencia se identificó linfoma difuso de células B CD20+, con sobrecrecimiento de células dendríticas, y se valoró el inicio de quimioterapia.\n\nImplicaciones clínicas y consideraciones importantes\n- El cuadro combina complicaciones graves: sangrado digestivo, anemia significativa, trombosis venosa profunda e infartos esplénicos/hepáticos, todas ellas asociadas al proceso neoplásico sistémico y que requieren manejo multidisciplinario.\n- Necesidades inmediatas y siguientes pasos esperables: confirmación inmunohistoquímica y estadificación completa (para planificar quimioterapia), discusión del riesgo/beneficio de anticoagulación por la trombosis frente al reciente sangrado digestivo, soporte transfusional y manejo de complicaciones infecciosas y hepáticas, y valoración por hematología/oncología para iniciar esquema específico dirigido a LNH difuso de células B (CD20+).\n- La historia de tratamiento con metotrexato es relevante porque la inmunosupresión crónica puede aumentar el riesgo de linfomas, pero la relación causal debe evaluarse en el contexto clínico y patológico.\n\nResumen empático\nSe trata de una mujer con pérdida progresiva de salud y complicaciones serias atribuibles a un linfoma sistémico avanzado. Fue correctamente evaluada y derivada para confirmación diagnóstica y tratamiento oncohematológico especializado. El enfoque inmediato combina control de complicaciones (anemia, sangrado, trombosis) y el inicio temprano de quimioterapia apropiada según la subclasificación del linfoma."
+        }
+    },
+    {
+        "article": "Un hombre de 56 años se presentó en el departamento de urgencias de nuestro hospital debido a una falta de aire repentina y un episodio de síncope mientras caminaba dentro de su casa. Se sometió a una prostatectomía laparoscópica asistida por robot para el carcinoma de próstata, 5 días antes de su presentación en el departamento de urgencias. Su curso postoperatorio en el hospital fue sin incidentes. En el departamento de urgencias, su presión arterial era de 94/54 mmHg, frecuencia cardiaca de 121 latidos por minuto, frecuencia respiratoria de 20 respiraciones por minuto, no tenía fiebre y su saturación de oxígeno era de 92% con 6 L por minuto de oxígeno a través de una cánula nasal. El examen cardiaco reveló S1S2, regular, taquicardia, sin murmullos/galopes/ruidos respiratorios. El examen respiratorio reveló ruidos respiratorios vesiculares normales bilaterales. Se observó que tenía edema de extremidad inferior izquierdo asimétrico. El electrocardiograma (ECG) reveló taquicardia sinusal, sin cambios en la onda ST-T. La troponina estaba levemente elevada a 0.120 ng/mL (rango de referencia: 0 a 0.020). La angiografía por tomografía computarizada (CTA) del tórax mostró embolia pulmonar bilateral extensa, con una gran carga de coágulos en ambas arterias pulmonares principales, evidencia de insuficiencia ventricular derecha aguda. El examen dúplex venoso mostró trombosis venosa profunda izquierda aguda. El ecocardiograma mostró fracción de eyección ventricular izquierda normal del 60% al 65%, movimiento septal anormal y aplanamiento del tabique interventricular, presión sistólica ventricular derecha de 49.7 mmHg, ventrículo derecho moderadamente dilatado, función ventricular derecha disminuida, excursión sistólica tricuspídea de 12.1 mm (normal 15 a 20 mm). Como la mayoría de la carga de coágulos era distal, no se consideró susceptible de extracción quirúrgica, ya que la cirugía reciente era una contraindicación importante para la trombólisis. El paciente comenzó con un goteo de heparina e inhaló óxido nítrico a 20 ppm junto con 40 mg de sildenafil oral cada 8 horas. Al día siguiente, el paciente estaba hemodinámicamente estable y su óxido nítrico inhalado se redujo. Repetir el ecocardiograma 48 horas desde la presentación inicial mostró un tamaño y función del ventrículo derecho mejorados. Su presión sistólica ventricular derecha disminuyó a 22.4 mmHg y su excursión sistólica tricuspídea mejoró a 17.8 mm. Recomendamos que continuara con sildenafil durante el mes siguiente después del alta junto con anticoagulación oral con un plan de seguimiento como paciente ambulatorio. El paciente dio su consentimiento por escrito para el tratamiento durante su hospitalización. El paciente y sus familiares estaban bien informados sobre el plan de atención completo y estuvieron de acuerdo con el plan de atención.\n\nMH - Insuficiencia cardiaca/*terapia farmacológica/etiología\nMH - Humanos\nMH - Hombre\nMH - Edad Media\nMH - Inhibidores de la fosfodiesterasa 5/*uso terapéutico\nMH - Embolismo pulmonar/*complicaciones\nMH - Agentes vasodilatadores/*uso terapéutico\nMH - Disfunción ventricular, derecha/terapia/etiología\n",
+        "gold_summary": "Paciente: Hombre, 56 años\n\nDiagnóstico final: Insuficiencia cardíaca derecha por embolia pulmonar\n\nSíntomas: síncope\n\nMedicación: —\n\nProcedimiento clínico: —\n\nEspecialidad: Cardiología\n\nSe trata de un informe de caso en el que se utilizó sildenafil como agente de rescate para lograr una mejora en el tamaño y la función del ventrículo derecho en un caso de inicio agudo de embolia pulmonar masiva con insuficiencia aguda del ventrículo derecho en el escenario en el que la terapia trombolítica sistémica estaba contraindicada.\n",
+        "synthetic_summary": {
+            "B1": "Resumen sencillo\n\nUn hombre de 56 años tuvo una emergencia. Cinco días antes, se había operado de la próstata. Mientras caminaba en su casa, de repente no podía respirar bien y se desmayó.\n\nQué tenía:\n- Tenía una trombosis en la pierna izquierda (un coágulo de sangre).\n- Ese coágulo viajó a sus pulmones. Esto se llama embolia pulmonar. Los médicos encontraron muchos coágulos en ambos pulmones.\n- La parte derecha del corazón estaba muy estresada y un poco agrandada por los coágulos. La parte izquierda del corazón estaba normal.\n\nQué le hicieron los médicos:\n- No le pudieron dar el remedio fuerte para disolver coágulos porque acababa de operarse. Eso sería peligroso.\n- Le pusieron un medicamento que evita que la sangre forme más coágulos (heparina).\n- También le dieron óxido nítrico para respirar y un medicamento por boca llamado sildenafil. Estos ayudan a abrir los vasos en los pulmones y a que el corazón derecho trabaje mejor.\n\nQué pasó después:\n- Al día siguiente estaba más estable.\n- Dos días después el corazón derecho estaba más pequeño y funcionaba mejor.\n- Lo dieron de alta con pastillas para seguir abriendo los vasos y con anticoagulantes (medicina para que no se formen más coágulos). Debía volver a control con los médicos.\n\nMensaje amable:\nLos médicos cuidaron al paciente con cuidado porque no podían usar el tratamiento habitual por su cirugía reciente. Con otros medicamentos, él mejoró y pudo volver a casa.",
+            "B2": "Resumen para lectores jóvenes (nivel B2)\n\nUn hombre de 56 años llegó a urgencias 5 días después de una operación de próstata por haber sentido una falta de aire repentina y desmayarse mientras caminaba. Tenía la presión baja y el pulso alto. Además se notó que su pierna izquierda estaba más hinchada que la derecha.\n\nQué encontraron los médicos\n- Una tomografía del tórax mostró grandes coágulos en ambas arterias pulmonares: esto se llama embolia pulmonar. Significa que fragmentos de coágulos (normalmente venas de las piernas) viajaron hasta los pulmones y bloquearon el flujo de sangre.\n- Un estudio de las venas de la pierna encontró una trombosis venosa profunda (coágulo) en la pierna izquierda.\n- El ecocardiograma (una ecografía del corazón) mostró que el ventrículo izquierdo funcionaba bien, pero el ventrículo derecho estaba agrandado y no trabajaba bien. Esto indica insuficiencia o “agotamiento” del ventrículo derecho por la carga que pusieron los coágulos en los pulmones.\n  - Medidas importantes: presión sistólica del ventrículo derecho elevada (49.7 mmHg) y una medida de movimiento del ventrículo derecho baja (TAPSE 12.1 mm; lo normal es 15–20 mm).\n\nPor qué no se usó trombólisis (disolver coágulos)\n- Aunque en algunos casos graves se usan medicamentos para disolver los coágulos o se sacan quirúrgicamente, el paciente había tenido una cirugía reciente. Eso aumentaba mucho el riesgo de sangrado, por lo que esos tratamientos no eran seguros.\n\nTratamiento que recibió\n- Anticoagulación con heparina (para evitar que se formen más coágulos).\n- Óxido nítrico inhalado (un vasodilatador que ayuda a bajar la presión en las arterias pulmonares y alivia al ventrículo derecho).\n- Sildenafil oral (un medicamento que también dilata los vasos sanguíneos pulmonares) 40 mg cada 8 horas como terapia de rescate.\n\nEvolución y alta\n- Al día siguiente el paciente estaba más estable y se redujo el óxido nítrico inhalado.\n- A las 48 horas, el ecocardiograma mostró mejoría del tamaño y la función del ventrículo derecho: la presión descendió a 22.4 mmHg y el TAPSE mejoró a 17.8 mm.\n- Se le dio el alta con anticoagulante oral y se recomendó continuar sildenafil durante un mes, con seguimiento ambulatorio.\n\nConclusión simple y amable\nEste caso muestra que, cuando no se pueden usar tratamientos que disuelven coágulos por riesgo de sangrado después de una cirugía, combinar anticoagulación con medidas que bajan la presión en las arterias pulmonares (óxido nítrico y sildenafil) puede ayudar al ventrículo derecho a recuperarse. El equipo explicó todo al paciente y su familia y obtuvo su consentimiento para el tratamiento.",
+            "B3": "Resumen clínico (nivel universitario, tono empático)\n\nPaciente\n- Hombre de 56 años, cinco días después de prostatectomía laparoscópica asistida por robot por cáncer de próstata.\n\nPresentación\n- Llegó a urgencias con disnea súbita y un episodio de síncope mientras caminaba en su casa.\n- Signos iniciales: PA 94/54 mmHg, FC 121 lpm, FR 20 rpm, SatO2 92% con 6 L/min por cánula nasal.\n\nHallazgos relevantes\n- Exploración: taquicardia sin otros ruidos cardíacos anormales; ruidos respiratorios vesiculares bilaterales conservados; edema asimétrico en la pierna izquierda.\n- ECG: taquicardia sinusal sin cambios isquémicos.\n- Troponina: levemente elevada (0,120 ng/mL; referencia 0–0,020).\n- Angio-TC torácica: embolia pulmonar bilateral extensa con gran carga de trombos en ambas arterias pulmonares principales y signos de insuficiencia ventricular derecha aguda.\n- Eco-Doppler venoso: trombosis venosa profunda (Trombosis venosa profunda) aguda en miembro inferior izquierdo.\n- Ecocardiograma: \n  - Fracción de eyección del ventrículo izquierdo normal (60–65%).\n  - Aplanamiento del septo interventricular y movimiento septal anormal (señales de sobrecarga derecha).\n  - Ventrículo derecho moderadamente dilatado y función reducida.\n  - Presión sistólica ventricular derecha estimada 49.7 mmHg (elevada).\n  - TAPSE (excursión sistólica tricuspídea) 12.1 mm (normal 15–20 mm) — indicador de función sistólica del ventrículo derecho disminuida.\n\nDiagnóstico\n- Insuficiencia ventricular derecha aguda secundaria a embolia pulmonar masiva, con TEP secundario a TEP venosa profunda postoperatoria.\n\nRazonamiento terapéutico y tratamiento aplicado\n- El paciente no fue candidato a trombólisis sistémica por la cirugía reciente (riesgo alto de sangrado) y la mayoría de los trombos eran demasiado distales para extracción quirúrgica.\n- Se inició:\n  - Heparina intravenosa (anticoagulación).\n  - Óxido nítrico inhalado (20 ppm) como vasodilatador pulmonar selectivo.\n  - Sildenafil oral 40 mg cada 8 horas (inhibidor de la fosfodiesterasa tipo 5, usado aquí como vasodilatador pulmonar de rescate) — uso fuera de ficha técnica en este contexto, empleado para reducir la poscarga del ventrículo derecho.\n- Consentimiento informado obtenido.\n\nEvolución y resultado\n- A las 24 horas el paciente estaba hemodinámicamente estable y se redujo la dosis de óxido nítrico inhalado.\n- A las 48 horas, ecocardiograma mostró mejoría significativa del ventrículo derecho: presión sistólica derecha disminuyó a 22.4 mmHg y TAPSE mejoró a 17.8 mm.\n- Alta hospitalaria con plan de continuar sildenafil durante un mes y anticoagulación oral indefinida según seguimiento ambulatorio.\n\nImplicaciones prácticas y consideraciones\n- Este caso ilustra el uso de vasodilatadores pulmonares (sildenafil e óxido nítrico inhalado) como medida de rescate en insuficiencia ventricular derecha aguda por embolia pulmonar cuando la trombólisis está contraindicada.\n- Mecanismo: la vasodilatación pulmonar reduce la resistencia vascular pulmonar y la poscarga del ventrículo derecho, permitiendo recuperación funcional.\n- Limitaciones: evidencia basada en un caso clínico; no prueba causal definitiva. El uso de sildenafil en este contexto es off-label y requiere monitorización estrecha por riesgo de hipotensión y contraindicaciones (por ejemplo, nitratos sistémicos).\n- Seguimiento recomendado: control clínico y ecocardiográfico, manejo continuo de anticoagulación y vigilancia de efectos adversos.\n\nComentario final (empático)\nEl equipo tratante adoptó una estrategia terapéutica prudente y multidisciplinaria frente a una situación de alto riesgo (TEP masivo con contraindicación para trombólisis). El paciente respondió bien al tratamiento combinado, con recuperación rápida de la función del ventrículo derecho. Casos como este subrayan la necesidad de más estudios para definir el papel de fármacos vasodilatadores sistémicos u inhalados como terapia puente o de rescate en pacientes con embolia pulmonar y falla ventricular derecha cuando las opciones estándar están limitadas."
+        }
+    },
+    {
+        "article": "Presentamos el caso de un hombre de 78 años con antecedentes conocidos de fibrilación auricular crónica, cardiopatía hipertensiva y miocardiopatía no isquémica. Tenía una reducción global de la fracción de eyección del ventrículo izquierdo del 40-45 %, y su ecocardiograma no mostraba anomalías significativas. El paciente había sido seguido en la clínica de cardiología ambulatoria, donde fue tratado por insuficiencia cardiaca crónica en estadio C del Colegio Americano de Cardiología (ACC) con síntomas de clase III de la Asociación del Corazón de Nueva York (NYHA). A pesar de varios cambios en sus diuréticos e intentos de controlar su estado de líquidos, ganó 40 libras de peso en un período de 3 meses, con un aumento significativo de la falta de aire. A medida que su descompensación de la insuficiencia cardiaca progresó, fue hospitalizado durante 8 días y tratado con furosemida intravenosa (IV). Debido a su clasificación de la NYHA y su ingreso al hospital por exacerbación de la insuficiencia cardiaca, se indicó y se realizó un monitoreo hemodinámico invasivo con implantación de CardioMEMS. La implantación de su CardioMEMS se realizó en Grand Blanc, Michigan, a una altitud de 837 pies con una presión atmosférica de 731.2 el 9 de abril de 2019. Las mediciones hemodinámicas iniciales del cateterismo cardiaco mostraron una presión sistólica PA de 45 mmHg, presión diastólica PA de 16 mmHg y una presión PA media de 30 mmHg. La presión auricular derecha fue de 21 mmHg, presión ventricular derecha de 44/17 mmHg y la presión media de la cuña pulmonar fue de 24 mmHg. El procedimiento se completó sin complicaciones y el paciente fue dado de alta el mismo día.\n\nTras la implantación de CardioMEMS, el paciente permaneció estable durante 4 semanas sin empeoramiento de los síntomas de insuficiencia cardiaca. Cumplió con las lecturas diarias de CardioMEMS con una PA media que osciló entre 27 y 31 mmHg, y una presión diastólica de PA de 17 a 21 mmHg. Estos hallazgos hemodinámicos globales fueron estables en comparación con los del momento de la implantación.\n\nEl paciente viajó a Denver, Colorado, durante cuatro días a una altitud de 5280 pies con una presión atmosférica de 596.8 atm el 5 de mayo de 2019. Las grabaciones del primer día de su visita mostraron un aumento de la presión sistólica de 44 mmHg a 73 mmHg, un aumento de la presión media de 30 mmHg a 53 mmHg y un aumento de la presión diastólica de 20 mmHg a 40 mmHg. Al mismo tiempo, notó un aumento significativo de la falta de aire y la hinchazón de las extremidades inferiores. No buscó atención médica, sino que se contactó con su cardiólogo primario en Michigan. Su oxígeno nasal de referencia se incrementó de 1 litro a 2 litros y su dosis de furosemida se duplicó de 40 mg diarios a dos veces al día. Afortunadamente, este tratamiento mejoró los síntomas del paciente y evitó la admisión hospitalaria. Debido a que se evitó la admisión hospitalaria, no se dispuso de valores de laboratorio, imágenes de diagnóstico y signos vitales clínicos.\n\nDurante su estancia hospitalaria de 4 días, sus presiones invasivas se mantuvieron altas, pero disminuyeron lentamente y se estabilizaron con una PA sistólica de 72 mmHg, una PA media de 49 mmHg y una PA diastólica de 35 mmHg el día previo a su regreso a Michigan. El quinto día, volvió a Michigan y sus mediciones de presión invasiva se normalizaron rápidamente, con una presión PA media de 29 mmHg y una presión PA diastólica de 20 mmHg. Ha seguido estando bien mientras estuvo en Michigan con diuréticos de mantenimiento continuos y un control diario de las presiones PA con su dispositivo CardioMEMS.\n\nMH - Envejecido\nMH - *Altitud\nMH - Monitoreo de presión arterial, ambulatorio\nMH - *Insuficiencia cardiaca/diagnóstico/etiología\nMH - Hospitalización\nMH - Humanos\nMH - Hombre\nMH - Arteria Pulmonar\n",
+        "gold_summary": "Presentamos el caso de un hombre de 78 años con una exacerbación de la insuficiencia cardiaca mientras viajaba a gran altitud. Se detectó un aumento de sus presiones arteriales pulmonares (PA) mediante su dispositivo CardioMEMS implantado. La comprensión del cambio esperado en los registros de presión de la PA ayudó a identificar una verdadera exacerbación de la insuficiencia cardiaca en nuestro paciente. Esto llevó a un cambio rápido en la terapia médica, que en última instancia evitó la hospitalización.\n",
+        "synthetic_summary": {
+            "B1": "Este cuento habla de un hombre de 78 años con problemas del corazón. Le pusieron un pequeño sensor dentro de una arteria del pulmón. El sensor mide la presión y ayuda a los médicos a ver cómo está su corazón.\n\nDurante un mes estuvo estable. Luego viajó a Denver, que está muy alto sobre el nivel del mar. Allí el sensor mostró que la presión en sus pulmones subió mucho. Él tuvo más falta de aire y las piernas se le hincharon.\n\nNo fue al hospital. Llamó a su médico. Le subieron el oxígeno y le dieron más pastillas para sacar el líquido del cuerpo. Con eso mejoró y no tuvo que quedarse en el hospital. Cuando volvió a su ciudad, la presión volvió a la normalidad.\n\nEl sensor ayudó a encontrar el problema rápido. Gracias a eso cambiaron su tratamiento a tiempo y él se recuperó sin entrar al hospital.",
+            "B2": "Resumen para lectores jóvenes (nivel secundaria)\n\nPresentamos el caso de un hombre de 78 años con insuficiencia cardiaca crónica que llevaba implantado un pequeño sensor llamado CardioMEMS. CardioMEMS se coloca en la arteria pulmonar (el vaso que lleva la sangre del corazón a los pulmones) y mide la presión allí cada día. Los médicos usan esas cifras para ver si el corazón está trabajando bien o si hay acumulación de líquido en el cuerpo.\n\nAntes del viaje, sus lecturas eran estables: la presión media en la arteria pulmonar estaba alrededor de 27–31 mmHg. Viajó a Denver (5.280 pies de altitud) y, durante los primeros días, el sensor mostró un aumento grande de las presiones (por ejemplo, la presión media subió de 30 a 53 mmHg). Al mismo tiempo, el paciente tuvo más dificultad para respirar y notó hinchazón en las piernas. La elevación de la presión pulmonar puede deberse al cambio de altitud, pero también puede señalar que la insuficiencia cardiaca empeora.\n\nEl paciente llamó a su cardiólogo. Le aumentaron el oxígeno y duplicaron la dosis de furosemida (un diurético que ayuda a eliminar el exceso de líquido). Con ese tratamiento, sus síntomas mejoraron y se evitó la hospitalización. Mientras estuvo en Denver las presiones fueron bajando lentamente; al volver a la altitud baja, las lecturas del CardioMEMS volvieron rápidamente a valores cercanos a los iniciales.\n\nQué podemos aprender de este caso\n- El monitoreo remoto con CardioMEMS permitió detectar rápido un aumento importante de la presión pulmonar y relacionarlo con síntomas reales.\n- El viaje a gran altitud puede aumentar las presiones pulmonares, pero ante síntomas (más falta de aire y edema) es importante tratar como una descompensación de insuficiencia cardiaca.\n- La comunicación rápida con el equipo médico y ajustes de tratamiento (más oxígeno y diuréticos) pueden evitar la hospitalización.\n- Seguir con controles y diuréticos de mantenimiento fue clave para mantener al paciente estable después del regreso.\n\nEste caso muestra cómo la vigilancia continua y respuestas médicas rápidas ayudan a cuidar a personas con insuficiencia cardiaca, especialmente cuando viajan a lugares de mucha altitud.",
+            "B3": "Presentamos el caso de un hombre de 78 años con fibrilación auricular crónica, cardiopatía hipertensiva y miocardiopatía no isquémica, seguido por insuficiencia cardíaca crónica estadio C (NYHA clase III). Su fracción de eyección del ventrículo izquierdo era de 40–45 % y el ecocardiograma no mostraba hallazgos significativos. Debido a una descompensación con ganancia de peso y empeoramiento de la disnea después de intentos de manejo ambulatorio, se implantó un sensor CardioMEMS para monitorización invasiva ambulatoria de la presión arterial pulmonar (PA) el 9 de abril de 2019 en Grand Blanc, Michigan (altitud 837 pies).\n\nHallazgos hemodinámicos y evolución\n- Mediciones iniciales en el cateterismo: PA sistólica 45 mmHg, PA diastólica 16 mmHg, PA media 30 mmHg; presión auricular derecha 21 mmHg; presión de cuña 24 mmHg. El procedimiento fue sin complicaciones.\n- En las 4 semanas posteriores a la implantación, las lecturas diarias del CardioMEMS se mantuvieron estables (PA media 27–31 mmHg; PA diastólica 17–21 mmHg) y el paciente se encontró clínicamente estable.\n- El 5 de mayo de 2019 el paciente viajó a Denver (altitud 5.280 pies). Ese mismo día el CardioMEMS mostró un aumento marcado de las presiones: PA sistólica de 44→73 mmHg, PA media de 30→53 mmHg, PA diastólica de 20→40 mmHg. Coincidiendo con estos cambios, el paciente presentó incremento significativo de disnea e edema en miembros inferiores.\n- No requirió ingreso: el cardiólogo aumentó el oxígeno domiciliario de 1 L a 2 L y duplicó la furosemida oral (de 40 mg una vez diaria a 40 mg dos veces al día). Los síntomas mejoraron y el paciente evitó hospitalización.\n- Durante su estancia en Denver las presiones se mantuvieron elevadas pero fueron descendiendo lentamente (el día antes del regreso PA sistólica ≈72 mmHg, PA media 49 mmHg, PA diastólica 35 mmHg). Tras volver a Michigan las lecturas se normalizaron rápidamente (PA media 29 mmHg, PA diastólica 20 mmHg) y el paciente permaneció estable con tratamiento de mantenimiento.\n\nInterpretación y puntos clave\n- Lo anormal: aumentos agudos y marcados en las presiones arteriales pulmonares durante la estancia en altitud elevada, acompañados de empeoramiento sintomático (disnea y edema), indicaron una verdadera descompensación hemodinámica.\n- Probable mecanismo: la hipoxia asociada con la altitud alta produce vasoconstricción pulmonar, lo que eleva las resistencias y las presiones en la circulación pulmonar; en un paciente con insuficiencia cardíaca esto puede precipitar o agravar la congestión.\n- Papel del CardioMEMS: la monitorización invasiva ambulatoria permitió detección inmediata del cambio hemodinámico mientras el paciente estaba fuera de su centro habitual, lo que facilitó ajustes médicos remotos rápidos y evitó la hospitalización.\n\nImplicaciones clínicas y recomendaciones prácticas\n- Para pacientes con insuficiencia cardíaca y dispositivos de monitorización hemodinámica: considerar el efecto de la altitud en las lecturas del dispositivo y en la clínica del paciente; interpretar cambios absolutos en contexto (síntomas, uso de oxígeno, altitud).\n- Antes de viajar a altitudes altas, aconsejar evaluación y planificación: posible ajuste profiláctico de diuréticos, disponer de oxígeno suplementario si está indicado, y acordar un plan de contacto y manejo remoto con el equipo de cardiología.\n- El monitoreo remoto invasivo puede mejorar la seguridad de pacientes con insuficiencia cardíaca al permitir intervenciones tempranas y reducir admissions, pero se necesitan datos adicionales para guiar protocolos específicos sobre viajes a altitud.\n\nConclusión\nEn este caso, el aumento de las presiones pulmonares detectado por CardioMEMS durante un viaje a gran altitud se correlacionó con empeoramiento clínico; la intervención médica precoz y ambulatoria (más oxígeno y mayor diurético) estabilizó al paciente y evitó la hospitalización. Este caso ilustra la importancia de reconocer cómo factores ambientales como la altitud pueden afectar las mediciones hemodinámicas y el curso de la insuficiencia cardíaca."
+        }
+    },
+    {
+        "article": "Un hombre de 55 años, previamente sano, fue derivado al servicio de urgencias por su médico de cabecera, quejándose de una fiebre de 3 semanas de evolución, tos productiva, disnea y sibilancias. Tenía un historial de 80 paquetes-año de consumo de tabaco y un historial familiar positivo de cáncer de pulmón. Había sido tratado por su médico de cabecera con un ciclo de amoxicilina oral y prednisona oral, pero sus síntomas empeoraron. Cuando llegó al servicio de urgencias, su recuento de glóbulos blancos era de 16,4 × 109/L (rango normal: 4,0-10,0 × 109/L), el recuento de neutrófilos de 13,8 × 109/L (rango normal: 2,0-7,0 × 109/L), la proteína C reactiva era de 118 mg/L (normal: 0-5 mg/L) y el sodio sérico era de 112 mmol/L (rango normal: 136-145 mmol/L). Otros marcadores bioquímicos estaban dentro de los límites normales. Una radiografía de tórax mostró consolidación del lóbulo medio e inferior derecho con derrame pleural moderado asociado. Fue admitido y tratado como neumonía adquirida en la comunidad y el estudio confirmó el diagnóstico de SIADH.\n\nEl paciente empeoró a pesar de la administración intravenosa de piperacilina-tazobactam y de claritromicina oral, con empeoramiento de la consolidación en la repetición de la radiografía de tórax. El paciente fue trasladado a la unidad de cuidados intensivos y, posteriormente, se le realizó una intubación y ventilación. Una tomografía computarizada (TC) de su tórax reveló una masa hilar derecha con afectación mediastinal y adenopatía hilar derecha con consolidación de espacio aéreo extenso superpuesta. Una biopsia realizada durante la broncoscopia reveló células pequeñas, histológicamente monótonas, con núcleos ovoides oscuros. No se observaron nucleolos, y varias figuras mitóticas estaban presentes. Las células tienen un citoplasma estrecho y mal definido. La inmunohistoquímica realizada en las células tumorales mostró negatividad a CD45, AE1/AE3, positividad a TTF1. También se observaron sinapsina mínima focal y positividad a cromogranina A. Este perfil inmunohistoquímico fue consistente con un diagnóstico de cáncer de pulmón de células pequeñas.\n\nLa estadificación completa, que consistió en una tomografía computarizada del cerebro y tórax-abdomen-pelvis, confirmó una enfermedad en estadio extenso con metástasis suprarrenales. El estado funcional ECOG de la paciente era deficiente debido a una combinación de SCLC y dificultad respiratoria que requería ventilación artificial. Como las tasas de respuesta con quimioterapia en SCLC son generalmente altas, se inició un tratamiento quimioterápico doble en forma de carboplatino y etopósido mientras la paciente estaba intubada en la UCI.\n\nEl paciente respondió bien al tratamiento y fue extubado y trasladado a la sala de ventilación no invasiva. Una nueva tomografía computarizada de tórax después de 1 ciclo mostró una buena respuesta parcial al tratamiento.\n\nEn el día 3 del ciclo 2 de quimioterapia, la paciente desarrolló dolor en la parte inferior de la espalda y debilidad bilateral en las extremidades inferiores. El examen identificó paresia motora bilateral en las extremidades inferiores (grado 3 del Consejo de Investigación Médica [MRC]) y paresia sensorial. El examen sensorial reveló ausencia de tacto ligero, pinchazo, coordinación y propiocepción en las extremidades inferiores. El día 3 de etopósido se retrasó como resultado de los nuevos hallazgos neurológicos.\n\nSe realizaron un TAC cerebral, resonancia magnética (RM) cerebral y resonancia magnética (RM) de la columna para investigar los nuevos hallazgos neurológicos. Todos los resultados radiológicos fueron normales, sin evidencia de metástasis intracerebrales, accidente cerebrovascular, mielitis o enfermedad leptomeníngea. Además, no hubo evidencia radiográfica obvia de compresión de la médula espinal, ya sea por compresión extrínseca por depósito metastásico óseo o depósitos intramedulares o leptomeníngeos.\n\nDos días después, un examen neurológico de seguimiento reveló tetraplejía, MRC grado 0 en las extremidades superiores e inferiores. Todos los reflejos tendinosos profundos estaban ausentes. Los músculos de la cabeza y el cuello, la cognición y el habla no se vieron afectados, y el examen de los nervios craneales fue normal.\n\nLos análisis de sangre de rutina, incluida la proteína C reactiva y la velocidad de sedimentación de eritrocitos, fueron normales. Los análisis de sangre específicos, incluidos los de vitamina B12 en suero, folato, serología del VIH, serología de la enfermedad de Lyme, serología del virus de Epstein-Barr, serología de Brucella, anticuerpos tiroideos, pruebas de función tiroidea, ANCA, ENA, ANA y electroforesis de proteínas séricas, fueron negativos o normales. Se enviaron anticuerpos para las pruebas de sangre Hu, Ri y Yo, y todos fueron negativos. En este momento, se sospechó un diagnóstico de polineuropatía simétrica ascendente aguda motora y sensorial y se realizó una punción lumbar. Los resultados del líquido cefalorraquídeo (LCR) revelaron una proteína total elevada de 3.32 g/L (normal 0.15–0.45), y otros parámetros fueron normales, con una repetición 3 días después que mostró resultados similares. La citología del LCR fue negativa para la malignidad y el cultivo del LCR también fue negativo.\n\nLa electromiografía fue consistente con una polineuropatía difusa predominantemente motora; los potenciales sensoriales se conservaron, pero fueron de pequeña amplitud. Las conducciones motoras mostraron características axonales/desmielinizantes mixtas, que no eran típicas del síndrome de Guillain-Barré.\n\nSe realizaron estudios de electromiografía y conducción nerviosa para investigar la polineuropatía motora y sensorial aguda del paciente. Los estudios de conducción nerviosa revelaron lo siguiente:\n\n•Nervios motores:\n◦Las amplitudes del potencial de acción muscular compuesto (CMAP) se redujeron notablemente en los nervios tibial y cubital de forma bilateral (tibial: 1,2 mV; normal > 4 mV; cubital: 0,8 mV; normal > 3 mV).\n◦Las velocidades de conducción motora (MCV) se desaceleraron en los nervios tibial y cubital (tibial: 30 m/s; normal > 40 m/s; cubital: 34 m/s; normal > 50 m/s), lo que es coherente con la desmielinización.\n◦Las latencias motoras distales se prolongaron, con un patrón mixto axonal y desmielinizante.\n•Nervios sensoriales:\n◦Las amplitudes del potencial de acción nerviosa sensorial (SNAP) se conservaron, pero fueron de poca amplitud en los nervios surales y medianos (sural: 4 μV; normal > 10 μV; mediano: 6 μV; normal > 15 μV).\n◦Las velocidades de conducción sensorial (VCS) se encontraban dentro de los límites normales.\nLos hallazgos electrofisiológicos revelaron una polineuropatía predominantemente motora con características axonales y desmielinizantes mixtas, atípicas para los síndromes paraneoplásicos clásicos, que generalmente son predominantemente sensoriales y se caracterizan por la ausencia de SNAP.\n\nMientras tanto, mientras estas investigaciones estaban en curso, se inició al paciente con dexametasona intravenosa y 0.4 g/kg/día de inmunoglobulina intravenosa sin ninguna mejora sintomática.\n\n3. Resultados y seguimiento\nA pesar de una importante respuesta oncológica inicial a la quimioterapia, el estado neurológico del paciente se deterioró rápidamente. Después de 1 ciclo de carboplatino y etopósido, las imágenes confirmaron una respuesta parcial con una reducción en el tamaño del tumor. Sin embargo, el inicio de una polineuropatía motora y sensorial grave y ascendente condujo a un compromiso respiratorio. Esta disociación entre las respuestas oncológicas y neurológicas destaca la naturaleza agresiva y refractaria del SNP, incluso cuando el tratamiento del cáncer es efectivo. Aunque la dexametasona intravenosa y la inmunoglobulina intravenosa se administraron rápidamente, no lograron mejorar los resultados neurológicos.\n\nSe llevaron a cabo largas y repetidas discusiones multidisciplinares con el paciente y su familia sobre la admisión en la unidad de cuidados intensivos para recibir apoyo ventilatorio. El paciente estaba bien informado y consciente de que era poco probable que sus síntomas neurológicos fueran reversibles y, por lo tanto, optó por el mejor tratamiento de apoyo. El paciente falleció 3 semanas después de los síntomas iniciales. La decisión del paciente de rechazar el apoyo ventilatorio invasivo en favor de los cuidados paliativos pone de relieve las consideraciones éticas que rodean la calidad de vida en los síndromes paraneoplásicos de progresión rápida.\n",
+        "gold_summary": "Preocupaciones del paciente: Un hombre de 55 años con un historial de 80 años fumando presenta al hospital con un historial de 3 semanas de fiebres, tos productiva, disnea y sibilancias. No tenía comorbilidades significativas.\n\nDiagnóstico: Extensas investigaciones radiológicas revelaron una gran masa en el hilum derecho que comprimía el bronquio inferior derecho con depósitos suprarrenales metastásicos. Las investigaciones bioquímicas confirmaron el síndrome de secreción inadecuada de la hormona antidiurética, y la histología identificó un CPCP.\n\nIntervenciones: A pesar de iniciar una quimioterapia combinada con carboplatino y etopósido, el paciente desarrolló parálisis motora progresiva y pérdida sensorial en el transcurso de 4 días, lo que derivó en un diagnóstico de polineuropatía motora y sensorial aguda paraneoplásica.\n\nResultados: Su estado empeoró rápidamente y falleció 14 días después de la aparición de los síntomas debido a una insuficiencia respiratoria, lo que pone de relieve la agresividad de los síndromes paraneoplásicos.\n",
+        "synthetic_summary": {
+            "B1": "Había un hombre de 55 años que fumaba mucho. Durante tres semanas tuvo fiebre, tos y le faltaba el aire. Su doctor le dio antibióticos y pastillas, pero no mejoró.\n\nEn el hospital le hicieron una radiografía y un escáner. Tenía una masa grande en el pulmón derecho y la enfermedad ya había llegado a las glándulas suprarrenales. Un trocito de la masa (biopsia) mostró que era cáncer de pulmón de células pequeñas. También tenía la sangre con muy poco sodio, un problema llamado SIADH.\n\nEmpezó quimioterapia mientras estaba en la unidad de cuidados intensivos. El tumor se hizo más pequeño con el primer ciclo de tratamiento. Pero después, en el segundo ciclo, empezó a perder fuerza en las piernas. En pocos días quedó paralizado en brazos y piernas. También perdió la sensibilidad de abajo hacia arriba.\n\nHicieron muchas pruebas. Las imágenes del cerebro y de la médula fueron normales. El líquido que rodea el cerebro y la médula tenía mucha proteína, pero no había células de cáncer. Los estudios de los nervios mostraron daño serio. Los médicos pensaron que su propio cuerpo estaba atacando los nervios por culpa del cáncer; esto se llama síndrome paraneoplásico, y a veces pasa con este tipo de cáncer.\n\nLe dieron medicinas para el sistema inmune, pero no mejoró. La respiración empeoró. El paciente habló con su familia y decidió no recibir más respiración artificial. Recibió cuidados para estar cómodo y murió unas tres semanas después de que empezaron los problemas de los nervios.\n\nEste caso muestra que, aunque el cáncer pudiera responder al tratamiento, a veces las enfermedades que el cáncer provoca en los nervios pueden avanzar muy rápido y ser fatales. Los médicos y la familia tomaron las decisiones cuidando lo que él quería.",
+            "B2": "Summary (for older children / teens)\n\nWhat happened\n- A 55-year-old man who had smoked heavily came to hospital after 3 weeks of fever, a cough that made mucus, shortness of breath and wheeze. Initial antibiotics and steroids did not help.\n- Tests showed infection-like blood changes, very low blood sodium (112 mmol/L) caused by SIADH — a condition where the body makes too much antidiuretic hormone and keeps extra water — and a chest X-ray with a blockage and fluid in the right lung.\n- A CT scan and a biopsy showed small cell lung cancer (a fast-growing type of lung cancer) that had already spread to the adrenal glands. He became very breathless and needed ventilator support in the intensive care unit.\n\nTreatment and tumour response\n- Because small cell lung cancer often responds to chemotherapy, doctors started carboplatin and etoposide while he remained in hospital on a ventilator.\n- The cancer did shrink with treatment and he was able to come off the ventilator to less invasive breathing support.\n\nNew and serious neurological problems\n- During the second cycle of chemotherapy, he developed sudden lower back pain and weakness in both legs. Over two days the weakness spread to all four limbs and he lost reflexes, though his thinking and cranial nerves (face and head muscles) stayed normal.\n- Brain and spine scans were normal — there was no stroke, no tumour pressing on the spinal cord, and no obvious spread into the brain or spinal fluid on imaging.\n- A lumbar puncture (spinal tap) showed very high protein in the cerebrospinal fluid, but no cancer cells or infection.\n- Nerve tests (EMG and nerve conduction studies) showed a widespread nerve problem that mainly affected motor nerves and had both axonal (nerve-fibre) and demyelinating (insulation) features. Sensory nerve signals were reduced but not completely absent. This pattern was not typical for the usual paraneoplastic nerve syndromes, which are often mainly sensory.\n- Blood tests for common paraneoplastic antibodies (Hu, Ri, Yo) and many other causes were negative.\n\nResponse to immune treatment and outcome\n- Doctors gave high-dose steroids (dexamethasone) and intravenous immunoglobulin (IVIG), treatments used for immune-related nerve damage, but he did not improve.\n- The neurologic condition led to breathing failure despite the cancer responding to chemotherapy. After long discussions with his family, he chose comfort-focused care rather than further invasive ventilator support. He died three weeks after his first symptoms.\n\nWhat this shows\n- This case shows a rare, very fast, and severe paraneoplastic peripheral neuropathy — a nerve disease caused by the body’s reaction to a cancer — that can progress quickly and not get better with usual immune treatments.\n- It also highlights a difficult situation where the cancer itself responds to treatment, but the immune-related neurological damage continues to get worse, which can lead to serious disability and life-threatening breathing failure.\n- Decisions about aggressive life support are personal and were made here after careful discussion with the patient and family.",
+            "B3": "Resumen clínico (nivel lector universitario)\n\nPresentación\n- Hombre de 55 años, fumador importante (80 paquetes-año), sin comorbilidades previas conocidas.\n- Síntomas iniciales: fiebre durante 3 semanas, tos productiva, disnea y sibilancias. Tratado en atención primaria con amoxicilina y prednisona sin mejora.\n\nHallazgos clave y diagnóstico oncológico\n- Analíticas anormales al ingreso: leucocitosis (16,4 × 10^9/L), neutrofilia (13,8 × 10^9/L), proteína C reactiva elevada (118 mg/L) e hiponatremia marcada (Na 112 mmol/L) consistente con SIADH (síndrome de secreción inadecuada de hormona antidiurética).\n- Radiografía/TC torácica: consolidación extensa en lóbulo medio e inferior derecho, derrame pleural moderado y masa hiliar derecha con afectación mediastinal y adenopatía.\n- Biopsia broncoscópica: tumor de células pequeñas de pulmón (small‑cell lung cancer, SCLC) — inmunohistoquímica: TTF1 positiva, CD45 y AE1/AE3 negativas; sinapsina focal mínima y cromogranina A positiva.\n- Estadificación: enfermedad en estadio extenso con metástasis suprarrenales.\n- Situación funcional comprometida por insuficiencia respiratoria que precisó ventilación mecánica.\n\nTratamiento inicial y respuesta tumoral\n- Se inició quimioterapia combinada (carboplatino + etopósido) incluso mientras el paciente estaba intubado, dado que SCLC suele responder a quimioterapia.\n- Buena respuesta oncológica inicial: reducción tumoral documentada tras 1 ciclo y posibilitó extubación.\n\nDesarrollo neurológico agudo\n- Durante el ciclo 2 (día 3) apareció dolor lumbar y debilidad bilateral de las piernas, progresando en 48–72 horas a tetraplejía completa con arreflexia generalizada; función bulbar, nervios craneales y cognición preservadas.\n- Estudios por imagen (TC cerebral, RNM cerebral y de columna) normales: sin metástasis intracraneal, compresión medular, mielitis ni enfermedad leptomeníngea evidente.\n- Punción lumbar: proteína total muy elevada (3,32 g/L) con recuento celular normal — hallazgo de “disociación albúmino-citológica”.\n- Citología y cultivos de LCR negativos para malignidad o infección.\n- Serologías y panel extendido (incluyendo anticuerpos paraneoplásicos Hu, Ri, Yo) negativos; otras causas metabólicas/infecciosas/autoinmunes descartadas por pruebas de rutina.\n- Electrofisiología (EMG/velocidades de conducción): polineuropatía difusa predominantemente motora con rasgos mixtos axonal y desmielinizante; potenciales sensoriales conservados pero de baja amplitud. Estos hallazgos no eran típicos de los síndromes paraneoplásicos clásicos (que suelen ser predominantemente sensoriales con ausencia de SNAP).\n- Diagnóstico clínico: polineuropatía motora y sensorial aguda de probable origen paraneoplásico, atípica en su patrón electrofisiológico y de evolución muy rápida.\n\nTratamiento neurológico y resultado\n- Se administraron dexametasona IV e inmunoglobulina IV (0,4 g/kg/día) sin mejoría neurológica.\n- El cuadro progresó rápidamente hasta provocar insuficiencia respiratoria por debilidad respiratoria. Tras discusión multidisciplinaria y conversación informada con el paciente y su familia, el paciente optó por cuidados de soporte y no reintubación invasiva.\n- Falleció tres semanas después del inicio de los síntomas neurológicos.\n\nInterpretación e implicaciones\n- Este caso muestra una disociación clínica importante: tumor pulmonar de células pequeñas con buena respuesta inicial a quimioterapia, pero aparición de una polineuropatía paraneoplásica motora-sensorial fulminante que no respondió a inmunoterapia aguda y condujo al fallecimiento.\n- Hallazgos que apoyan origen paraneoplásico: inicio subagudo en contexto de cáncer de pulmón de células pequeñas, LCR con proteinorraquia aislada y exclusión de otras causas (infección, metástasis, compresión medular). Sin embargo, la ausencia de anticuerpos paraneoplásicos conocidos y el patrón electrofisiológico mixto hacen el caso atípico.\n- Pronóstico: las neuropatías paraneoplásicas pueden ser rápidamente debilitantes y, en algunos subtipos, refractarias al tratamiento inmunomodulador; cuando afectan la musculatura respiratoria, el pronóstico es pobre.\n\nRecomendaciones generales para casos similares\n- Evaluación precoz y urgente ante signos de debilidad progresiva en pacientes oncológicos: neuroimagen, LCR, estudio electrofisiológico y pruebas serológicas paraneoplásicas.\n- Tratamiento temprano con inmunoterapia (IVIG, plasmaféresis, esteroides) suele intentarse, aunque la respuesta es variable; la identificación temprana no garantiza recuperación.\n- Discutir de forma proactiva las metas de tratamiento y preferencias del paciente (incluido soporte ventilatorio) dada la posibilidad de deterioro rápido.\n- Considerar manejo multidisciplinario (oncología, neurología, cuidados intensivos, cuidados paliativos) desde fases tempranas.\n\nComentario final (tono humano)\nLamento el desenlace de este caso. A pesar de un tratamiento oncológico eficaz sobre la lesión primaria, la aparición de una neuropatía paraneoplásica fulminante mostró cómo las complicaciones neurológicas pueden ser devastadoras y poco previsibles. En situaciones así, las conversaciones honestas sobre pronóstico y las decisiones compartidas con el paciente y la familia son fundamentales."
+        }
+    },
+    {
+        "article": "El paciente presentado firmó el Consentimiento Informado y se cumplieron los demás principios éticos, respetando la Resolución 466/12 del Consejo Nacional de Ética en Investigación. Este informe de caso fue aprobado por el Comité de Ética en Investigación de la Universidad Federal de São Paulo (UNIFESP), bajo el dictamen número 4.455.365.\n\nEl paciente, de 66 años de edad y sexo masculino, acudió a una consulta de otorrinolaringología por presentar disfagia tipo atragantamiento con sólidos y reflujo nasal de alimentos desde hacía un año. Había sufrido un accidente automovilístico 13 años atrás y era diabético. Se le realizó una videoendoscopia de la deglución (VED), en la que se observó, en la evaluación estructural, una protuberancia de la pared posterior de la hipofaringe con residuo salival sobre la lesión. En la evaluación funcional, tras la ingesta de alimentos sólidos, se observó una restricción de la retroflexión de la epiglotis, una limitación de la elevación de la laringe y un reflujo nasal de alimentos, con gran cantidad de residuo alimentario por encima de la lesión, en la pared posterior de la faringe. En la prueba de maniobras posturales, empeoró la disfagia al extender el cuello y mejoró la eliminación al flexionar la cabeza. Se le realizó una tomografía computarizada (TC) de la columna cervical, solicitada para evaluar la naturaleza de la lesión, que mostró la presencia de osteofitos cervicales anteriores entre las vértebras C3 y C6, el mayor de 12 milímetros (mm) de longitud, que estrechaba la columna aérea al nivel de la orofaringe e hipofaringe. Se descartaron otras causas de disfagia y se trató al paciente con terapia de deglución y omeprazol, dirigido al reflujo faringolaríngeo. Se realizaron 6 sesiones de terapia de deglución individualizada, con el objetivo de compensar el mecanismo de deglución ante un obstáculo mecánico en la región faríngea. Los principales aspectos trabajados fueron: modificación de la textura de la dieta, evitando alimentos sólidos y secos; maniobras posturales de deglución, probadas durante la VED, especialmente el chin tuck (“cabeza hacia abajo” o “flexión de la cabeza”), que aumenta el espacio de la válvula (“abre la válvula”) y mejora la presión de transferencia faríngea del alimento; y ejercicios de fortalecimiento de la lengua, para superar la barrera mecánica de la orofaringe durante la expulsión del alimento. Se recomendó, si fuera necesario, alternar la ingesta de alimentos sólidos con líquidos, ante la percepción de alimentos estancados en la faringe. Se le indicó que repitiera los ejercicios de lengua en el hogar, 2 a 3 veces al día. Después de las sesiones iniciales, el paciente presentó una respuesta satisfactoria, y se lo controló trimestralmente durante el primer año y semestralmente a partir del segundo año. Se lo derivó para una evaluación ortopédica para analizar la viabilidad quirúrgica, y se optó por un tratamiento conservador debido a la buena compensación con medidas clínicas. Sigue en seguimiento ambulatorio desde hace 2 años, y mantiene una deglución eficiente, sin incidencia de complicaciones relacionadas con la disfagia. Se optó por mantener reevaluaciones periódicas, al menos una vez al año, para detectar precozmente un posible nuevo desequilibrio de la homeostasis de la deglución relacionado con el deterioro gradual de las funciones en el contexto de la presbifagia o el surgimiento de un nuevo factor agresor.\n",
+        "gold_summary": "Se describió el caso de un paciente de 66 años con disfagia por atragantamiento con sólidos y reflujo nasal de alimentos desde hacía un año. La videoendoscopia de la deglución mostró una protuberancia en la pared posterior de la faringe y, al ofrecer alimentos sólidos, una restricción de la retroflexión de la epiglotis, reflujo nasal de alimentos y una gran cantidad de residuos de alimentos sobre la lesión. La tomografía computarizada de la columna cervical identificó la presencia de osteofitos cervicales anteriores entre las vértebras C3 y C6, el más grande con una longitud anteroposterior de 12 milímetros, que estrechaba la columna aérea a nivel de la orofaringe e hipofaringe. El paciente fue tratado adecuadamente con fonoterapia para la deglución.\n",
+        "synthetic_summary": {
+            "B1": "Había un hombre de 66 años que tenía dificultad para tragar alimentos sólidos y a veces la comida subía por la nariz desde hacía un año. Le hicieron una cámara para ver la garganta cuando tragaba. Vieron un bulto en la parte de atrás de la garganta. También notaron que una pequeña “tapa” que cierra la entrada de la tráquea (epiglotis) no se movía bien y que había mucha comida parada encima del bulto. Cuando estiraba el cuello, le iba peor; cuando bajaba la cabeza (chin tuck), mejoraba.\n\nLuego le hicieron una tomografía del cuello. Encontraron unos “bultos de hueso” en las vértebras del cuello (osteofitos) entre C3 y C6. Uno era bastante grande (unos 1,2 cm) y estrechaba el paso del aire y de la comida en la parte de atrás de la garganta.\n\nLos médicos descartaron otras causas. No operaron. Le dieron terapia para aprender a tragar mejor y medicina para el reflujo. En las sesiones le enseñaron a comer alimentos más blandos, a usar la postura de “cabeza hacia abajo” y a hacer ejercicios con la lengua. También tenía ejercicios para hacer en casa.\n\nDespués de seis sesiones mejoró mucho. Sigue con controles médicos desde hace dos años y puede tragar bien. Los médicos pidieron que siga con revisiones al menos una vez al año para revisar que todo siga bien.",
+            "B2": "Resumen comprensible (nivel B2, lectura para jóvenes)\n\nEste caso describe a un hombre de 66 años que llevaba un año teniendo problemas para tragar alimentos sólidos y a veces le regresaban alimentos por la nariz. El paciente dio su consentimiento y el informe contó con aprobación ética.\n\nQué encontraron los doctores\n- En la evaluación con endoscopia de la deglución (una cámara pequeña para ver la garganta) vieron una protuberancia en la parte posterior de la faringe y restos de saliva y comida encima de esa zona.\n- Al darle alimentos sólidos, la epiglotis (una tapa de cartílago que protege la vía aérea cuando tragamos) no se doblaba bien hacia atrás, la laringe no subía lo suficiente y parte de la comida subía hacia la nariz. Todo esto hacía que se acumulara mucha comida sobre la protuberancia.\n- En la tomografía de la columna cervical encontraron osteofitos anteriores entre las vértebras C3 y C6. Los osteofitos son pequeñas crestas o \"protuberancias\" de hueso (a veces llamadas bone spurs). El mayor medía 12 mm y estrechaba el espacio por donde pasa el alimento en la parte alta de la garganta.\n\nTratamiento y resultado\n- Los médicos descartaron otras causas de la dificultad para tragar y trataron al paciente con terapia de la deglución (ejercicios y maniobras prácticas) y omeprazol para controlar el reflujo hacia la garganta.\n- Hicieron 6 sesiones individuales de terapia: cambiaron la textura de la dieta (evitando alimentos sólidos y secos), enseñaron maniobras posturales que probó en la endoscopia (especialmente el \"chin tuck\" o flexionar la cabeza hacia adelante, que ayuda a empujar la comida y a proteger la vía aérea) y ejercicios para fortalecer la lengua.\n- Le recomendaron alternar sólidos con líquidos si sentía que la comida se atascaba, y repetir los ejercicios en casa 2–3 veces al día.\n\nSeguimiento\n- El paciente respondió bien al tratamiento. Se le revisó cada tres meses el primer año y cada seis meses después. Fue valorado por ortopedia para estudiar cirugía, pero se decidió manejarlo de forma conservadora porque la terapia daba buenos resultados.\n- Lleva 2 años en seguimiento ambulatorio con una deglución eficiente y sin complicaciones. Mantendrán controles periódicos, al menos una vez al año, para detectar cambios tempranos relacionados con el envejecimiento de la deglución (presbifagia) o nuevos problemas.\n\nEn resumen: la dificultad para tragar se debió a protuberancias óseas en la columna cervical que estrechaban la parte alta de la garganta. Con terapia de deglución dirigida y medidas para el reflujo, el paciente mejoró y se optó por evitar la cirugía mientras siga estable.",
+            "B3": "Resumen clínico (nivel universitario)\n\nContexto y aspectos éticos\n- Se presentó un paciente varón de 66 años con consentimiento informado; el caso contó con aprobación del comité de ética de la UNIFESP.  \n\nPresentación clínica\n- Síntomas: disfagia del tipo “atragantamiento” con alimentos sólidos y reflujo nasal de alimentos de aproximadamente 1 año de evolución.  \n- Antecedentes relevantes: accidente de tráfico hace 13 años y diabetes mellitus.\n\nExploraciones y hallazgos (normales vs anormales)\n- Videoendoscopia de la deglución (VED): hallazgo estructural anormal — protuberancia en la pared posterior de la hipofaringe con residuo salival sobre ella. Evaluación funcional anormal al ofrecer sólidos: restricción de la retroflexión de la epiglotis (la epiglotis no se pliega con normalidad para proteger la vía aérea), limitación de la elevación laríngea, reflujo nasal de alimento y gran cantidad de residuo por encima de la lesión.  \n- Maniobras posturales: la extensión de cuello empeoró la disfagia; la flexión del cuello (chin tuck) mejoró la eliminación del alimento.  \n- Tomografía computarizada cervical: hallazgo anatómico anormal — osteofitos anteriores (excrecencias óseas) entre C3 y C6, el mayor de 12 mm, que estrechaban el paso aéreo a nivel de orofaringe e hipofaringe.  \n- Se descartaron otras causas de disfagia en el estudio.\n\nDiagnóstico funcional y etiológico\n- Disfagia mecánica secundaria a osteofitos cervicales anteriores que generan una barrera en la región faríngea, con compromiso protector de la vía aérea (epiglotis y elevación laríngea) y reflujo faringolaríngeo concurrente.\n\nTratamiento aplicado\n- Manejo conservador elegido por buena respuesta clínica:\n  - Terapia fonoaudiológica de deglución: 6 sesiones individualizadas centradas en:\n    - Modificación de la textura dietética (evitar sólidos secos; alternativas liquidar/mezclar según percepción de estancamiento).\n    - Maniobras posturales validadas por VED, sobre todo el chin tuck, que reduce el espacio afectado y mejora la transferencia faríngea.\n    - Ejercicios de fortalecimiento lingual para ayudar a vencer la barrera mecánica durante la propulsión del bolo.\n    - Repetición domiciliaria de ejercicios 2–3 veces/día y recomendaciones para alternar sólidos con líquidos si hay sensación de retención.\n  - Omeprazol para control del reflujo faringolaríngeo.\n  - Derivación a ortopedia para valorar viabilidad quirúrgica (se consideró, pero se optó por conducta conservadora).\n\nEvolución y seguimiento\n- Respuesta clínica satisfactoria tras las sesiones iniciales.  \n- Seguimiento ambulatorio: controles trimestrales el primer año y semestrales desde el segundo año; al cabo de 2 años mantiene deglución eficiente sin complicaciones relacionadas con la disfagia.  \n- Plan: reevaluaciones periódicas, al menos anuales, para detectar precozmente empeoramiento (por ejemplo por presbifagia —cambios por envejecimiento— o aparición de nuevos factores).\n\nImplicaciones clínicas y recomendaciones prácticas\n- Los osteofitos cervicales pueden producir una obstrucción mecánica de la faringe y aumentar el riesgo de aspiración y residuos alimentarios; en casos graves existe la opción quirúrgica (osteofitectomía anterior), pero la terapia rehabilitadora y las modificaciones dietéticas pueden ser eficaces cuando el paciente compensa bien.  \n- Señales de alarma que justificarían revaluación urgente: pérdida de peso, infecciones respiratorias recurrentes (neumonía por aspiración), empeoramiento marcado de la disfagia o incapacidad para hidratarse/alimentarse.  \n- Mantener las medidas aprendidas (ejercicios y posturas) y controles periódicos para preservar la seguridad alimentaria y la calidad de vida.\n\nComentario empático\n- El manejo multidisciplinario y la adherencia a la terapia permitieron al paciente recuperar una deglución funcional sin cirugía. Es razonable y prudente mantener vigilancia periódica para detectar cambios precoces y adaptar el tratamiento si la situación evoluciona."
+        }
+    },
+    {
+        "article": "Una paciente caucásica de 18 años de edad se presentó en nuestra clínica con quejas de múltiples bultos palpables en sus senos bilateralmente. En el examen físico, la paciente tenía múltiples lesiones pigmentadas lentigosas en su cara, cuerpo y esclerótica bilateralmente, nevos azules en su tronco y extremidades superiores y una cara redonda con forma de luna.\n\nTras la evaluación ultrasonográfica, se encontraron múltiples nódulos compactos (fibroadenomas) en ambos senos, siendo el más grande en el cuadrante superior externo del seno izquierdo, con un diámetro de 7,8 cm.\n\nEn 2018, se le había practicado una tiroidectomía total con el diagnóstico de adenoma folicular y la extirpación de un nódulo grande del seno izquierdo, debido a su gran tamaño y al dolor que causaba, con un informe de histopatología que sugería un fibroadenoma con estroma mixóide.\n\nSe realizó una biopsia por escisión de dos nódulos de la mama derecha con diagnóstico de fibroadenoma mixto, lo que respaldó nuestro diagnóstico de complejo de Carney.\n\nEn la resonancia magnética se encontraron múltiples fibroadenomas compactos en ambos senos, con alta intensidad de señal en las imágenes T2 y T2/FS, con tabiques internos sin restricción de difusión, compatibles con múltiples fibroadenomas mixoides.\n\nAdemás, había un par de ganglios linfáticos axilares y prominentes ganglios linfáticos mamarios internos bilaterales.\n\nAdemás, se observó una anomalía en la densidad de los tejidos blandos en el mediastino anterior, que medía 11 mm de espesor máximo, lo que sugería un timo prominente.\n\nTodos los hallazgos anteriores sugerían la posibilidad de un complejo de Carney. Se realizó una evaluación adicional en el laboratorio. Los análisis hormonales no mostraron anomalías en los niveles de testosterona, prolactina, PTH y DHEA-S.\n\nLuego se realizó un análisis genético que arrojó como resultado la mutación del gen PRHAR1A, heterocigótico para una variante sin sentido de significancia incierta en el exón 3 de este gen. Esta mutación nunca se había informado en la base de datos gnomAD.\n\nSe realizaron pruebas genéticas a los padres y se determinó que solo el padre era portador de la misma mutación genética.\n\nSe discutieron con la paciente varios planes de tratamiento conservadores, pero ninguno demostró proporcionar una solución/tratamiento definitivo. En el pasado se realizó la extirpación de los lóbulos grandes con alivio temporal de los síntomas de dolor de la paciente y las cirugías recurrentes estaban afectando su calidad de vida. La paciente también tuvo varias sesiones con la psicóloga de nuestra clínica y fue evaluada a fondo antes de decidir la solución final de una mastectomía bilateral.\n\nLa paciente se sometió a una mastectomía bilateral con conservación de la piel y colocación subcutánea de expansores de tejidos (suave, Motiva Flora®). La histopatología informó múltiples fibroadenomas mixóides en ambos senos, compatibles con el síndrome de Carney, con interrupción de la arquitectura normal del parénquima mamario. Las figuras muestran el fibroadenoma de forma macroscópica e histológica.\n\nEl cuidado de la herida fue mínimo, se le recomendó a la paciente usar un sujetador médico y visitas regulares a la clínica ambulatoria para seguimiento y rellenado adicional de los expansores de tejidos a intervalos regulares hasta que se alcanzó el tamaño deseado. Paciente antes y después de la mastectomía. Después de un año se realizó una segunda cirugía y los expansores se reemplazaron con implantes de silicona permanentes (suaves, Motiva Ergonomic®) submusculares, con los mismos requisitos mínimos de cuidado de la herida y colocación del sujetador.\n",
+        "gold_summary": "Una paciente de 18 años de edad se presentó en nuestra clínica con múltiples bultos palpables en sus senos bilateralmente. En el examen físico, la paciente también tenía múltiples lesiones pigmentadas lentigosas en su cara, cuerpo y esclerótica, nevos azules en su tronco y extremidades superiores y un rostro redondo con forma de luna. El diagnóstico del síndrome de Carney se decidió mediante imágenes, biopsias y análisis genético. La paciente se sometió a una mastectomía bilateral como plan de tratamiento profiláctico con colocación de expansores de tejidos.\n",
+        "synthetic_summary": {
+            "B1": "Había una paciente de 18 años que notó muchos bultos en los dos pechos. También tenía manchas oscuras en la piel, lunares azules y una cara redonda.  \n\nLos doctores hicieron exámenes y biopsias. Descubrieron que los bultos eran fibroadenomas. Eso quiere decir que eran bolitas no cancerosas, pero grandes y que le dolían.  \n\nLe hicieron pruebas de sangre y las hormonas salieron normales. También hicieron un estudio del ADN y encontraron un cambio en un gen que puede causar este conjunto de problemas. El padre tenía el mismo cambio.  \n\nLa joven ya había tenido otras cirugías que ayudaban solo por un tiempo. Ella se sentía cansada de las operaciones repetidas y habló con psicólogos. Al final decidió quitarse los pechos para evitar más problemas.  \n\nLe hicieron una mastectomía en los dos pechos y pusieron unas bolsitas temporales llamadas expansores. Después, un año más tarde, cambiaron las bolsitas por implantes de silicona. La herida sanó bien y la paciente siguió controles médicos.  \n\nEsta operación era para mejorar su salud y su vida diaria. Los doctores la acompañaron con cuidado y apoyo durante todo el proceso.",
+            "B2": "An 18-year-old woman came to the clinic because she felt many lumps in both breasts. On exam she also had many small dark spots on her skin and eyes (lentigines), blue‑colored moles (blue nevi), and a round, “moon‑shaped” face. She had previously had her thyroid removed in 2018 for a benign tumor.\n\nImaging with ultrasound and MRI showed many compact breast tumors called fibroadenomas (benign lumps made of gland and fibrous tissue). The largest lump was 7.8 cm in the upper outer part of the left breast. Some nearby lymph nodes looked larger than usual and there was a slightly prominent thymus (a small gland in the chest). Biopsies of breast nodules confirmed mixed (myxoid) fibroadenomas — “myxoid” means the tissue has a soft, jelly‑like stroma.\n\nThese findings suggested Carney complex, a rare genetic condition that can cause skin spots, benign tumors, and endocrine problems. Blood hormone tests were normal. Genetic testing found a previously unreported change (a heterozygous nonsense variant of uncertain significance) in the PRHAR1A gene; the same change was also found in her father. This supports an inherited cause, so family genetic counseling was offered.\n\nBecause repeated lump removals had only given temporary relief and were affecting her quality of life, after psychological support she chose a preventive surgery: bilateral mastectomy with skin preservation and temporary tissue expanders placed under the skin. Pathology of the removed breasts confirmed multiple myxoid fibroadenomas that had disrupted the normal breast tissue, which fits with Carney complex. One year later the expanders were replaced with permanent silicone implants under the muscle. Wound healing was uncomplicated and she continues outpatient follow‑up and implant care.\n\nThis approach aimed to stop the cycle of repeated surgeries, reduce pain and distress, and improve her quality of life. Genetic counseling and follow‑up for other possible features of Carney complex remain important for her and her family.",
+            "B3": "Presentación y contexto\nUna mujer caucásica de 18 años acudió por múltiples nódulos palpables en ambos senos. En el examen físico también se observaron múltiples lentigos pigmentados en cara, cuerpo y esclerótica, nevos azules en tronco y extremidades superiores y una facies redondeada tipo “luna”. En 2018 había recibido tiroidectomía total por un adenoma folicular y, en el pasado, se extirpó un gran nódulo mamario izquierdo por dolor.\n\nHallazgos clínicos, de imagen y anatomía patológica\n- Imágenes (ecografía y resonancia): múltiples nódulos compactos en ambos senos compatibles con fibroadenomas mixoides; el mayor medía 7,8 cm en el cuadrante superior externo izquierdo. En RM los nódulos eran hiperintensos en T2/T2-FS, con tabiques internos y sin restricción en difusión. Se informaron además ganglios axilares e internos mamarios prominentes y una densidad de tejidos blandos de 11 mm en mediastino anterior sugestiva de timo prominente.\n- Biopsias y pieza quirúrgica: resecciones previas y biopsia por escisión de nódulos confirmaron fibroadenomas mixtos/mixoides. La histología definitiva tras la segunda intervención mostró múltiples fibroadenomas mixoides y alteración de la arquitectura normal del parénquima mamario.\n- Laboratorio endocrino: niveles normales de testosterona, prolactina, PTH y DHEA‑S.\n- Genética: se identificó una variante heterocigota sin sentido de significado incierto en el exón 3 del gen reportado en el artículo como PRHAR1A (probablemente correspondiente al gen PRKAR1A, conocido por asociarse al complejo de Carney). La variante no estaba en la base de datos gnomAD. El mismo cambio genético fue hallado en el padre de la paciente.\n\nDiagnóstico y decisión terapéutica\n- Conjuntamente, los hallazgos clínicos, radiológicos, histológicos y la variante genética apoyaron el diagnóstico de complejo de Carney (síndrome que asocia lentigos, tumores mamarios mixoides/fibroadenomas, neoplasias y alteraciones endocrinas).\n- Se discutieron opciones conservadoras, pero las resecciones repetidas daban solo alivio temporal y afectaban la calidad de vida. Tras valoración psicológica y consenso informado, la paciente optó por una mastectomía bilateral profiláctica con conservación de piel.\n\nTratamiento y evolución\n- Primera intervención: mastectomía bilateral skin‑sparing y colocación subcutánea de expansores de tejidos (Motiva Flora®). Cuidados posoperatorios mínimos, uso de sujetador médico y controles para relleno progresivo de expansores.\n- Segunda intervención (un año después): sustitución de expansores por implantes de silicona submusculares permanentes (Motiva Ergonomic®). La anatomía patológica confirmó la presencia de múltiples fibroadenomas mixoides bilaterales.\n\nImplicaciones y recomendaciones razonables\n- El hallazgo genético (variante sin sentido heterocigota no reportada previamente) y la identificación de la misma variante en el padre sugieren una forma familiar del complejo de Carney, aunque la variante fue catalogada como de significado incierto; se requieren más datos para clasificarla definitivamente.\n- Dado el diagnóstico de complejo de Carney, se recomiendan seguimientos dirigidos a detectar otras manifestaciones del síndrome: cribado cardiológico (ecocardiograma para excluir mixomas cardiacos), vigilancia endocrina periódica (tiroides, glándulas suprarrenales, etc.), examen dermatológico y controles ginecológicos según indicación. También se aconseja asesoramiento genético para la paciente y la familia.\n- Los ganglios mamarios y axilares descritos eran prominentes en imagen pero no se informó malignidad; la ausencia de restricción en difusión en la RM favorece benignidad, aunque el seguimiento es pertinente.\n\nTono y conclusión\nLa paciente recibió un tratamiento definitivo que alivió el problema recurrente y la carga sintomática de lesiones mamarias extensas. Dado el carácter genético y sistémico del complejo de Carney, el pronóstico dependerá del control y la detección precoz de otras posibles lesiones asociadas; el seguimiento multidisciplinario y el consejo genético son pasos clave. Lamento la carga emocional y física que esta enfermedad ha supuesto para la paciente y destaco la importancia del apoyo psicológico y de un plan de vigilancia a largo plazo."
+        }
+    },
+    {
+        "article": "Una adolescente femenino de 13 años sin antecedentes médico-quirúrgicos de interés acude a Urgencias por dolor e impotencia funcional en muñeca izquierda tras caída mientras patinaba. Diagnosticada de lesión en torus metafisaria con extensión fisaria de radio distal clasificada como lesión Peterson tipo I, es inmovilizada durante cuatro semanas con férula antebraquiopalmar. Dos semanas después de la retirada de la férula, acude nuevamente a Urgencias al sentir un crujido en la muñeca, sin sobreesfuerzo asociado e impotencia para movilizar el primer dedo de la mano izquierda. Clínicamente presenta déficit de extensión activa interfalángica, efecto tenodesis patológico, edema local y asimetría macroscópica a la comparación con la extremidad contralateral. Se estudia con resonancia magnética nuclear (RMN), identificando imagen de solución de continuidad del EPL. Con la paciente bajo anestesia general, se procede al tratamiento quirúrgico mediante transferencia tendinosa del extensor propio del índice (EPI) al remanente distal del EPL con sutura tipo Pulvertaft de monofilamento no absorbible. En el postoperatorio se inmovilizó la extremidad las cuatro primeras semanas.\n\nTras cuatro semanas, se autorizó movilidad evidenciando recuperación de extensión del primer dedo de la mano izquierda y cicatrices discretamente hipertróficas, sin dolor. El seguimiento a la sexta, duodécima semana y al año no reporta complicaciones, con una restitución completa de la función y una puntuación de 0 en la escala PRWE (Patient Rated Wrist Evaluation).",
+        "gold_summary": "Se presenta el caso de una paciente adolescente femenino que, tras tratamiento conservador con férula de una fractura fisaria Peterson tipo I en radio, sufre a las seis semanas déficit agudo de extensión del pulgar, diagnosticada mediante examen clínico radiológico de rotura espontánea del extensor pollicis longus. Es tratada por medio de transferencia del extensor propio del índice (EPI) con resultados satisfactorios y recuperación de su actividad habitual al mes postoperatorio.",
+        "synthetic_summary": {
+            "B1": "Una niña de 13 años se cayó mientras patinaba y se lastimó la muñeca. Los médicos le pusieron una férula y la inmovilizaron por cuatro semanas porque se había hecho una pequeña fractura en el hueso cerca de la muñeca.  \n\nDos semanas después de quitar la férula, notó un crujido en la muñeca y no pudo mover el pulgar. Al hacer pruebas y una imagen por resonancia, vieron que se había roto un tendón que sirve para levantar el pulgar.  \n\nLe hicieron una operación. Los cirujanos usaron un tendón del dedo índice para reemplazar el tendón roto del pulgar. El brazo quedó quieto otra vez durante cuatro semanas para sanar.  \n\nA las cuatro semanas después de la cirugía, pudo mover el pulgar otra vez y no tenía dolor. Quedó con una pequeña cicatriz. En los controles a las 6 y 12 semanas y al año, no hubo problemas y recuperó totalmente la función de la mano.",
+            "B2": "Resumen\n\nUna adolescente de 13 años se presentó tras una caída mientras patinaba con una fractura en la parte distal del radio (clasificada como lesión de torus con extensión a la fisis, Peterson tipo I). Se trató de forma conservadora con una férula antebraquiopalmar durante cuatro semanas. Dos semanas después de retirar la férula (seis semanas tras la caída) notó un “crujido” en la muñeca y perdió la capacidad para extender el pulgar: el examen mostró imposibilidad de extender la articulación interfalángica del pulgar, edema local y asimetría con la mano sana. La resonancia magnética confirmó la rotura del tendón extensor largo del pulgar (EPL).\n\nCon la paciente bajo anestesia general se realizó una transferencia tendinosa, utilizando el extensor propio del índice (EPI) para reemplazar la función del EPL, suturando los tendones con la técnica de Pulvertaft (una forma firme de unir tendones). La muñeca se inmovilizó cuatro semanas después de la cirugía. A las cuatro semanas la paciente había recuperado la extensión del pulgar, con cicatrices levemente sobreelevadas y sin dolor. En los controles a las 6 y 12 semanas y al año no hubo complicaciones y la función se restauró por completo; la paciente obtuvo 0 puntos en la escala PRWE (una puntuación de 0 indica ausencia de dolor y limitación funcional). En resumen, una rotura espontánea del EPL tras una fractura distal del radio fue resuelta con éxito mediante transferencia tendinosa, permitiendo la recuperación completa de la actividad habitual.",
+            "B3": "Resumen clínico (nivel B3)\n\nPresentación\n- Paciente: adolescente femenina de 13 años, sin antecedentes relevantes.\n- Evento inicial: caída mientras patinaba → dolor e incapacidad funcional de la muñeca izquierda.\n- Diagnóstico inicial: lesión en torus metafisaria con extensión fisaria del radio distal (Peterson tipo I).\n- Tratamiento inicial: inmovilización con férula antebraquiopalmar durante 4 semanas.\n\nEvolución y hallazgos anormales\n- Dos semanas tras retirar la férula (6 semanas desde la fractura) la paciente siente un crujido en la muñeca y presenta incapacidad para extender el pulgar izquierdo.\n- Examen clínico: déficit de extensión interfalángica del pulgar, efecto tenodesis patológico (movimientos pasivos que no se traducen en extensión activa), edema local y asimetría evidente respecto al lado sano.\n- Imagen: resonancia magnética (RMN) mostró solución de continuidad (rotura) del extensor pollicis longus (EPL), el tendón encargado de la extensión del pulgar.\n\nTratamiento realizado\n- Bajo anestesia general se efectuó transferencia tendinosa: se tomó el extensor propio del índice (EPI) y se suturó al remanente distal del EPL mediante técnica de Pulvertaft con monofilamento no absorbible.\n- Postoperatorio: inmovilización de la extremidad durante las primeras 4 semanas.\n\nResultados y seguimiento\n- A las 4 semanas postoperatorias se permitió movilización: recuperación de la extensión del pulgar y cicatrices ligeramente hipertróficas, sin dolor.\n- Controles a 6 y 12 semanas y a 1 año: sin complicaciones, restitución completa de la función, puntuación 0 en la escala PRWE (Patient Rated Wrist Evaluation), es decir, ausencia de limitación percibida por la paciente.\n\nInterpretación y puntos clave\n- La ruptura espontánea del EPL es una complicación conocida tras fracturas distales de radio, incluso cuando la fractura es leve o tratada de forma conservadora. Mecanismos posibles: daño directo, pinzamiento sobre callo óseo o alteración del aporte vascular al tendón.\n- La transferencia del EPI es una solución quirúrgica bien establecida y eficaz: restituye la extensión del pulgar con mínima pérdida funcional del índice.\n- En pacientes con fractura distal de radio que desarrollan pérdida aguda de extensión del pulgar debe sospecharse lesión de EPL; la RMN o la ecografía ayudan a confirmar la rotura y guiar el tratamiento.\n- El pronóstico tras una transferencia tendinosa orientada y una rehabilitación adecuada suele ser excelente, como se observó en este caso.\n\nRecomendaciones prácticas\n- Vigilar la función tendinosa del pulgar tras fracturas distales de radio y valorar imágenes si aparece déficit funcional.\n- Derivar a cirugía de mano/rehabilitación temprana cuando se confirma rotura tendinosa.\n- Informar al paciente y a la familia sobre la alta probabilidad de recuperación funcional tras transferencia tendinosa y sobre el posible cambio mínimo en la función del índice."
+        }
+    },
+    {
+        "article": "Se remitió a un hombre de 73 años para una SAVR para tratar la regurgitación valvular aórtica sintomática (AR). Dos años antes, había presentado múltiples lesiones exantématicas. Una biopsia de piel reveló infiltración de células plasmáticas, lo que motivó la derivación a un hematólogo. La tomografía computarizada reveló linfadenopatía sistémica y hepatoesplenomegalia. Una biopsia renal realizada por disfunción renal confirmó la amiloidosis AA; una biopsia de ganglios linfáticos mostró plasmocitosis interfolicular y un centro germinal hiperplásico, consistente con el subtipo plasmático de iMCD, apoyado por niveles elevados de IL-6 en plasma. Se administró al paciente TCZ intravenoso (640 mg cada 2 semanas), junto con prednisolona (10 mg diarios). La erupción cutánea y la linfadenopatía se resolvieron. La ecocardiografía reveló AR puro moderado y agrandamiento ventricular izquierdo. Dado que el paciente experimentó gradualmente disnea de esfuerzo con agrandamiento ventricular izquierdo progresivo, se consideró necesaria la SAVR.\n\nDebido al sangrado por hemorroides y a la hepatosplenomegalia, se consultó a un hepatólogo; se diagnosticó cirrosis hepática de Child-Pugh grado A y varices esofágicas. Se realizó una conferencia preoperatoria del equipo, en la que participaron un intensivista y un farmacéutico, en la que se revisaron los mecanismos de acción de TCZ, las posibles complicaciones y el tratamiento perioperatorio. La cirugía se realizó 26 días después de la última dosis de TCZ. Durante el período perioperatorio, se suspendió el tratamiento con TCZ, mientras que se continuó con los esteroides por vía oral o intravenosa. Las medidas preventivas para las infecciones del sitio quirúrgico (SSI) incluyeron la detección de portadores nasales de Staphylococcus aureus resistentes a la meticilina, la preparación antiséptica de la piel, la terapia antibiótica profiláctica y el control de la hiperglucemia. El cultivo nasal fue positivo para Staphylococcus coagulasa negativo. Se realizó el reemplazo de la válvula aórtica quirúrgica a través de una esternotomía media bajo circulación extracorpórea, con 65 minutos de tiempo de isquemia cardiaca y 128 minutos de tiempo de circulación extracorpórea. Se requirieron transfusiones de sangre, incluidos glóbulos rojos, plasma y plaquetas; el paciente fue extubado al día siguiente. Los hallazgos patológicos revelaron un espesamiento fibroso focal sin depósitos amiloides.\n\nLa herida quirúrgica no mostró signos de infección en el día 2 postoperatorio; se inició la terapia de presión negativa en la herida (NPWT) en la herida quirúrgica cerrada para evitar SSI. La terapia de presión negativa en la herida se interrumpió en el día 13 postoperatorio, sin aparente SSI. El paciente fue dado de alta en el día 17 postoperatorio sin ningún signo de infección.\n\nAunque los niveles de IL-6 aumentaron temporalmente los días 1 y 2 después de la operación, disminuyeron progresivamente hasta el día 24 después de la operación, y luego volvieron a aumentar al reanudarse el tratamiento con TCZ. Los niveles de proteína C reactiva (PCR) estaban ligeramente elevados, alcanzando un máximo de 0,56 mg/dL el día 2 después de la operación. Para el día 24 después de la operación, la PCR había aumentado a 1,06 mg/dL sin infección. Antes del aumento de la PCR, los niveles del factor de crecimiento endotelial vascular aumentaron el día 13 después de la operación.\n\nEl paciente no experimentó recurrencia de erupción cutánea o linfadenopatía durante el período perioperatorio. Los niveles de creatinina postoperatorios aumentaron temporalmente, pero volvieron a los niveles preoperatorios el día 24. Se reanudó el tratamiento con tocilizumab el día 30 postoperatorio tras confirmar la ausencia de infección, incluida la IFI.\n",
+        "gold_summary": "Un hombre de 73 años con enfermedad de Castleman, tratado con TCZ, se sometió a un reemplazo de la válvula aórtica por medio de esternotomía mediana para la regurgitación de la válvula aórtica con falta de aire al hacer ejercicio. Se implementaron medidas integrales para prevenir la infección del sitio quirúrgico junto con un examen minucioso durante el período perioperatorio. Tocilizumab se interrumpió 26 días antes de la cirugía y se reanudó 30 días después de la cirugía, durante los cuales los niveles de IL-6 en plasma disminuyeron. No hubo evidencia de infección o exacerbación de la enfermedad de Castleman. Los niveles del factor de crecimiento endotelial vascular aumentaron antes de un aumento en los niveles de proteína C reactiva después del alta hospitalaria y antes de la reanudación de TCZ.\n",
+        "synthetic_summary": {
+            "B1": "Resumen sencillo:\n\nUn hombre de 73 años tenía una enfermedad llamada Castleman. Esa enfermedad le hacía hinchar los ganglios y tener sarpullido, pero mejoró con una medicina llamada tocilizumab (TCZ).\n\nTenía problemas en una válvula del corazón. Esto le daba falta de aire al caminar. Los médicos le hicieron una operación para cambiar la válvula por una nueva.\n\nAntes de la operación, dejaron de darle TCZ unas cuatro semanas. Hicieron muchas cosas para evitar infecciones. Revisaron si tenía gérmenes en la nariz, limpiaron bien la piel, dieron antibiótico para prevenir infecciones y cuidaron su azúcar en la sangre.\n\nLa operación salió bien. No hubo infección en la herida. El hombre salió del hospital 17 días después de la operación.\n\nReanudaron la medicina TCZ cerca de 4 semanas después de la operación, cuando comprobaron que no había infección. Las pruebas de sangre mostraron que una sustancia llamada IL-6 bajó mientras la medicina estuvo parada y volvió a subir cuando la medicina se reanudó. Otra prueba (PCR) subió un poco más tarde, pero no hubo infección ni empeoramiento de la enfermedad.\n\nEn pocas palabras: la operación fue necesaria y se hizo con cuidado para evitar infecciones. El paciente se recuperó bien y volvió a su tratamiento sin que su enfermedad empeorara.",
+            "B2": "Resumen sencillo y claro\n\nUn hombre de 73 años con enfermedad de Castleman multicéntrica (una enfermedad en la que el sistema inmunitario está alterado) y amiloidosis AA (acumulación anormal de proteína en órganos) necesitó un reemplazo de la válvula aórtica porque tenía regurgitación aórtica (la válvula no cerraba bien) y dificultad para respirar al hacer ejercicio.\n\nTratamiento previo y preparación para la cirugía\n- Recibía tocilizumab (TCZ), un medicamento que bloquea la proteína inflamatoria IL‑6, y prednisolona (un esteroide).\n- Tenía también hepatomegalia y cirrosis hepática leve (Child‑Pugh A) y várices esofágicas, por lo que un equipo médico evaluó cuidadosamente los riesgos.\n- El equipo decidió suspender TCZ 26 días antes de la operación; los esteroides se mantuvieron. La cirugía se hizo por esternotomía media con circulación extracorpórea (máquina corazón‑pulmón).\n\nMedidas para evitar infección y cuidados quirúrgicos\n- Se tomaron varias precauciones para prevenir infecciones de la herida: búsqueda de portadores nasales de bacterias, antisepsia de la piel, antibiótico profiláctico y control de la glucosa.\n- Tras la operación, se usó terapia de presión negativa sobre la herida (un vendaje con succión que ayuda a prevenir infección). Esta terapia se interrumpió el día 13 sin problemas y el paciente salió del hospital al día 17 sin signos de infección.\n\nEvolución de pruebas y medicamentos después de la operación\n- Tras la cirugía, los niveles de IL‑6 subieron de forma temporal en los primeros días y luego bajaron hasta el día 24; aumentaron otra vez cuando se reanudó TCZ.\n- La proteína C reactiva (PCR), un marcador de inflamación, se elevó levemente (máximo 0,56 mg/dL el día 2) y luego a 1,06 mg/dL el día 24, también sin evidencia de infección.\n- El factor de crecimiento endotelial vascular (VEGF) subió antes del segundo aumento de la PCR.\n- La función renal mostró un aumento temporal de creatinina que regresó a los valores previos al día 24.\n- No reaparecieron la erupción cutánea ni la linfadenopatía relacionadas con la enfermedad de Castleman.\n- TCZ se reanudó el día 30 tras comprobar que no había infección, incluida infección fúngica invasiva.\n\nResultados y conclusión\n- La operación fue técnicamente exitosa; la biopsia de la válvula mostró fibrosis localizada pero sin depósitos de amiloide.\n- Con las medidas tomadas, no hubo infección de la herida ni empeoramiento de la enfermedad de Castleman durante el periodo perioperatorio.\n- En resumen: la suspensión planificada de TCZ antes de la cirugía, la vigilancia estrecha y las medidas preventivas permitieron realizar el reemplazo valvular con buena recuperación y reanudar el tratamiento inmunológico de forma segura.",
+            "B3": "Resumen clínico (nivel lector universitario)\n\nPresentación y antecedentes\n- Paciente: hombre de 73 años con enfermedad de Castleman multicéntrica idiopática (subtipo plasmocítico) confirmada por biopsia de ganglio y niveles elevados de IL‑6, y amiloidosis AA secundaria (biopsia renal). Tenía antecedentes de erupciones cutáneas y hepatoesplenomegalia.\n- Tratamiento crónico previo a la cirugía: tocilizumab intravenoso (640 mg cada 2 semanas) más prednisolona 10 mg/día. La terapia con tocilizumab controló la erupción y la linfadenopatía.\n- Motivo de la cirugía: insuficiencia aórtica (regurgitación aórtica pura moderada) con dilatación ventricular izquierda y progresiva disnea de esfuerzo → decisión de realizar reemplazo quirúrgico de válvula aórtica (SAVR).\n\nEvaluación preoperatoria y riesgos\n- Hallazgos relevantes: sangrado por hemorroides, hepatólogo diagnosticó cirrosis hepática Child‑Pugh A y varices esofágicas.\n- Gestión del riesgo inmunosupresor: discusión multidisciplinaria (incluyendo intensivista y farmacéutico) sobre los efectos de tocilizumab y estrategias perioperatorias.\n- Plan: suspender tocilizumab antes de la cirugía (última dosis 26 días antes) y mantener esteroides; aplicar medidas intensivas para prevenir infección del sitio quirúrgico (screening nasal para Staphylococcus aureus resistente, antisepsia cutánea, antibiótico profiláctico, control de glucemia). Cultivo nasal positivo para estafilococos coagulasa‑negativos.\n\nCurso quirúrgico y postoperatorio\n- Procedimiento: reemplazo valvular aórtico por esternotomía media bajo circulación extracorpórea (tiempo de isquemia 65 min; circulación 128 min). Requirió transfusiones y fue extubado al día siguiente.\n- Anatomía patológica de la válvula: engrosamiento fibroso focal sin depósitos amiloides.\n- Herida y complicaciones infecciosas: sin signos clínicos de infección; se empleó terapia de presión negativa en herida cerrada (NPWT) desde el día 2 al 13 postoperatorio; alta hospitalaria en el día 17 sin infección aparente.\n- Función renal: creatinina aumentó transitoriamente pero volvió al nivel preoperatorio al día 24.\n\nBiomarcadores y reanudación de tocilizumab\n- IL‑6: aumento transitorio en los días 1–2 posoperatorios, luego disminución progresiva hasta el día 24; aumentó de nuevo tras la reintroducción de tocilizumab.\n- PCR (proteína C reactiva): ligera elevación máxima 0,56 mg/dL el día 2; subió a 1,06 mg/dL al día 24 sin evidencia de infección.\n- VEGF: aumento detectado el día 13, precediendo el incremento de la PCR.\n- Reinicio de tocilizumab: se reanudó el día 30 postoperatorio tras confirmar ausencia de infección, incluida la infección fúngica invasora (IFI).\n- Clínica de Castleman: sin recurrencia de erupción ni linfadenopatía durante el período perioperatorio.\n\nInterpretación y puntos prácticos\n- Resultado: SAVR exitoso sin infección del sitio quirúrgico ni reactivación clínica de la enfermedad de Castleman, gracias a una planificación perioperatoria cuidadosa.\n- Implicaciones:\n  - Suspender tocilizumab varias semanas antes de cirugía y reanudarlo después de confirmar ausencia de infección fue una estrategia segura en este caso, pero debe individualizarse según el riesgo infeccioso y la gravedad de la enfermedad subyacente.\n  - Monitorizar biomarcadores (IL‑6, PCR, VEGF) puede ayudar a distinguir respuestas inflamatorias posoperatorias esperadas de infecciones o actividad de la enfermedad; sin embargo, los inmunomoduladores cambian la interpretación de estos marcadores.\n  - Medidas preventivas (screening nasal, antisepsia, profilaxis antibiótica, control glucémico) y el uso de NPWT en herida cerrada pueden contribuir a reducir el riesgo de SSI en pacientes inmunocomprometidos.\n  - La decisión sobre timing de suspensión/rehabilitación de agentes biológicos requiere un enfoque multidisciplinario, especialmente cuando hay comorbilidades como cirrosis.\n\nComentario empático\nEste caso muestra que, con evaluación y coordinación cuidadosas, es posible realizar cirugías mayores en pacientes con enfermedades inflamatorias tratadas con biológicos sin provocar infección ni reactivación clínica. Las decisiones sobre manejo perioperatorio de inmunosupresión deben discutirse de forma individualizada y con seguimiento estrecho."
+        }
+    },
+    {
+        "article": "Se trata de un paciente de sexo masculino de cuatro meses de edad, originario del centro de México y con dos hermanos hombres sanos. Durante el primer trimestre de gestación, su madre hipotiroidea consumió drogas. No obstante, el infante nació con peso y talla adecuados, fue alimentado con leche materna y recibió la vacuna del bacilo de Calmette-Guérin (BCG), sin desarrollo de cicatriz. La madre del paciente era prisionera en una cárcel y, junto con el bebé, compartían una celda insalubre con dos personas más.A los cuatro meses, el paciente fue valorado médicamente por un tumor doloroso en la región axilar izquierda. En la radiografía de tórax se observaron imágenes sugestivas de fracturas costales; se sospechó de maltrato infantil por parte de la madre, y el infante fue hospitalizado en un hospital pediátrico. Se determinó el peso (4.190 g) y la talla (58 cm) –por debajo del percentil tres–, saturación de oxígeno del 70 %, fiebre, tos, aumento de volumen en la región axilar izquierda, además de dolor, rubor y calor. En el cuadro hemático se encontró: hemoglobina de 8,8 g/dl (11,0 - 12,6), 29,3 × 109 leucocitos/L (6,0 - 17,5), 18,4 × 109 neutrófilos/L (1,0 - 8,5), 7,0 × 109 linfocitos/L (4,0 - 13,5), 3,5 × 109 monocitos/L, 459 × 109 plaquetas/L (150 - 350) y proteína C reactiva igual a 16 mg/L (< 3,0). En la primera tomografía toracoabdominal se observaron imágenes de un absceso en la región axilar izquierda, lesiones líticas en las costillas 3 a 6, neumonía apical izquierda, nódulos pulmonares en ambos pulmones y ganglios linfáticos cervicales y mediastinales incrementados de tamaño. En la biopsia del absceso axilar izquierdo se reportó miositis y paniculitis supurativa. Solo se hizo cultivo para bacterias del líquido broncoalveolar, el cual fue negativo, y la PCR para el complejo Mycobacterium tuberculosis fue negativa. Después de 41 días de hospitalización y de haber recibido dos esquemas de antimicrobianos –ceftriaxona-clindamicina y cefepima-vancomicina–, el paciente fue dado de alta.\n\nDos meses después, a los ocho meses de edad, reingresó al hospital por fiebre, irritabilidad y un absceso supurante en la escápula izquierda. En el cuadro hemático se encontró: hemoglobina de 10,8 g/dl (10,5 - 12), 21,2 × 109 leucocitos/L (6 - 17), 12,2 × 109 neutrófilos/L (1,5 - 8,5), 7,5 × 109 linfocitos/L (4 - 10,5), 1,2 × 109 monocitos/L (600), y 583 × 109 plaquetas/L (150 - 350); la prueba para la detección sérica de HIV fue negativa. En la tomografía de tórax se observó una consolidación apical izquierda, bronquiectasias, lesiones líticas en las costillas 2 a 7 y en las vértebras dorsales 2 a 7, además de una colección de líquido multiloculado; en el ultrasonido se encontró una fístula asociada con el absceso escapular. El paciente recibió piperacilina-tazobactam, que se sustituyó después por voriconazol al detectarse Aspergillus fumigatus en el cultivo de la muestra de secreción del absceso. Dada la recurrencia y la gravedad de la infección, se sospechó un error innato de la inmunidad. La prueba de dihidrorrodamina resultó sin producción de especies reactivas de oxígeno y la expresión de gp91phox en los neutrófilos fue nula, estableciéndose así el diagnóstico de enfermedad granulomatosa crónica ligada al cromosoma X. La variante patógena detectada por la secuenciación de nueva generación fue c.80_83del/Y (p.Val27Glyfs*33) en CYBB. La madre resultó portadora de la variante (c.80_83del/WT). No fue posible estudiar genéticamente a sus dos hermanos mayores, de sexo masculino, y aparentemente sanos. El paciente fue dado de alta después de 65 días de hospitalización y tratamiento con voriconazol por 28 días. Se inició profilaxis antibiótica diaria con trimetoprim-sulfametoxazol y profilaxis antifúngica con fluconazol dos veces a la semana. Dos meses después, al año de edad, el infante reingresó debido a una neumonía multifocal, por la cual requirió asistencia respiratoria mecánica. Se detectó el antígeno galactomanano en el suero y A. fumigatusen el cultivo del líquido del lavado broncoalveolar, por lo que se inició nuevamente tratamiento con voriconazol. El paciente sufrió una falla orgánica múltiple y falleció un mes después de su ingreso.\n",
+        "gold_summary": "Se presenta el caso de un infante con enfermedad granulomatosa crónica y aspergilosis invasiva. Se trata de un lactante de sexo masculino de cuatro meses de edad, de madre hipotiroidea y con quien convive en la celda de la cárcel. El infante presentó tumores en la región axilar izquierda y la radiografía de tórax sugirió fracturas costales; fue hospitalizado ante la sospecha de maltrato infantil. En la tomografía de tórax se observó un absceso axilar, osteólisis de costillas, neumonía y nódulos pulmonares; el paciente recibió antibióticos de amplio espectro y fue dado de alta. A los ocho meses, reingresó por fiebre y extensión del absceso purulento hacia la región escapular izquierda; en la tomografía se observaron imágenes de empeoramiento de la condición. Se aisló Aspergillus fumigatus de la secreción del absceso y se diagnosticó aspergilosis invasiva; se inició tratamiento con voriconazol por 28 días. Mediante la prueba de dihidrorrodamina, se diagnosticó enfermedad granulomatosa crónica causada por la variante patógena c.80_83del/Y del gen CYBB, portada por la madre (c.80_83del/WT). A los 12 meses, el paciente reingresó nuevamente por aspergilosis invasiva, resistente al tratamiento, con desenlace fatal.",
+        "synthetic_summary": {
+            "B1": "Este es el cuento triste de un bebé que nació con un problema en sus defensas.\n\nEl niño era un bebé varón. Vivía con su mamá en una celda sucia. Cuando tenía cuatro meses, apareció un bulto doloroso en la axila. También le dolía el pecho y tenía fiebre. Los médicos pensaron al principio que podía haber sido maltrato porque se vieron lesiones en las costillas. Lo ingresaron al hospital y le dieron antibióticos.\n\nEl bebé mejoró un poco y salió del hospital. Pero a los ocho meses volvió con fiebre y un absceso que supuraba cerca del omóplato. En el cultivo del pus crecieron hongos llamados Aspergillus. Le dieron un medicamento para los hongos, pero la infección seguía preocupando a los médicos.\n\nLos especialistas pensaron que el niño no podía luchar bien contra gérmenes y le hicieron pruebas. Descubrieron que sus glóbulos blancos no funcionaban para matar microbios. Esto se llama enfermedad granulomatosa crónica (CGD). Es un problema en un gen llamado CYBB. La mamá era portadora de ese cambio en el gen. Por eso el bebé nació con este problema.\n\nLe dieron medicinas para prevenir infecciones y para el hongo. Aun así, al año volvió muy enfermo con neumonía por el mismo hongo. Necesitó respirador y, a pesar del tratamiento, su cuerpo dejó de trabajar y murió un mes después.\n\nEs una historia triste. El bebé sufrió por muchas infecciones porque su sistema de defensa no funcionaba. Los médicos encontraron la causa y cuidaron de él, pero no fue suficiente.",
+            "B2": "This is the story of a baby boy who became very sick from a rare immune problem and a serious fungal infection.\n\nBackground and first illness\n- The child was born apparently healthy and lived with his mother, who had thyroid disease, in a poor and crowded jail cell. At 4 months old he developed a painful swollen lump under his left armpit. A chest X‑ray also suggested broken ribs, so doctors first worried about possible child abuse and admitted him to hospital.\n- At admission he was very small for his age, had low oxygen levels, fever, cough, and a painful, red axillary (armpit) abscess. Blood tests showed anemia and signs of infection. A CT scan found an abscess under the arm, areas where the ribs had been destroyed, pneumonia in the top of the left lung, small lung nodules, and enlarged lymph nodes. A biopsy of the abscess showed inflammation and pus. Tests for common bacteria and for tuberculosis were negative.\n- He received broad‑spectrum antibiotics in hospital and was sent home after about six weeks.\n\nSecond illness, diagnosis, and treatment\n- At 8 months he returned with fever, irritability, and a new draining abscess near his left shoulder blade. Imaging showed worse lung disease (including bronchiectasis, which means damaged airways), more bone destruction of ribs and spinal vertebrae, and collections of infected fluid with a fistula (an abnormal draining tract).\n- A fungus called Aspergillus fumigatus grew from the abscess. Treatment was changed to the antifungal drug voriconazole. Because the infections kept coming back and were unusual for an infant, doctors tested his immune system.\n- A dihydrorhodamine (DHR) test showed his white blood cells could not produce reactive oxygen species—chemicals immune cells normally use to kill certain germs. A further test showed no gp91phox protein. Genetic testing found a damaging change (called c.80_83del in the CYBB gene) that explains the condition: X‑linked chronic granulomatous disease (CGD). In CGD, some immune cells cannot destroy certain bacteria and fungi, so people get repeated, severe infections. The mother was found to be a carrier of the same gene change.\n\nFinal course and outcome\n- He received antifungal therapy and daily antibiotic prevention (trimethoprim‑sulfamethoxazole) plus twice‑weekly fluconazole to try to prevent new infections. Despite this, at about 12 months he was readmitted with widespread pneumonia, needed a breathing machine, and tests again found Aspergillus in his lungs. He developed multiple organ failure and died about one month later.\n\nWhat this means (calmly)\n- This case shows how CGD, an inherited immune defect that mainly affects boys when it is X‑linked, can lead to life‑threatening infections with organisms like Aspergillus. Early diagnosis of primary immunodeficiency can allow targeted care (antifungal and antibiotic treatment, infection prevention, and sometimes bone marrow transplant) that might improve outcomes. The medical team also had to consider and rule out other problems, such as child abuse, because of the unusual bone findings. The situation was made harder by the child’s difficult living conditions and the delayed recognition of the underlying immune disorder.",
+            "B3": "Resumen clínico empatético y orientado a no especialistas (nivel lector universitario)\n\nPaciente y contexto\n- Lactante masculino, originario del centro de México. Madre con hipotiroidismo, privada de libertad; vivían en una celda con condiciones insalubres. Nacimiento con peso y talla adecuados; lactancia materna y vacuna BCG aplicada sin formación de cicatriz.\n- Dos hermanos varones aparentemente sanos, no fue posible estudiarles genéticamente.\n\nCurso clínico y hallazgos principales\n1) Primer ingreso (4 meses)\n- Motivo: tumor doloroso en la axila izquierda. Radiografía de tórax sugirió fracturas costales, por lo que se consideró inicialmente maltrato infantil.\n- Signos anormales: saturación de oxígeno 70% (muy baja), fiebre, crecimiento por debajo del percentil 3, dolor e inflamación axilar.\n- Laboratorio: anemia (Hb 8,8 g/dl), leucocitosis marcada (29,3 ×10^9/L) con neutrofilia, PCR elevada (16 mg/L) y trombocitosis.\n- Imágenes: tomografía mostró absceso axilar izquierdo, lesiones líticas en costillas (3–6), neumonía apical izquierda, nódulos pulmonares bilaterales y adenopatías cervicales y mediastinales.\n- Biopsia del absceso: miositis y paniculitis supurativa. Cultivo de LBA y PCR para Mycobacterium tuberculosis negativos.\n- Tratamiento: antibióticos de amplio espectro (esquemas secuenciales). Alta tras 41 días.\n\n2) Segundo ingreso (8 meses)\n- Motivo: fiebre y absceso supurante en región escapular izquierda que formó fístula.\n- Hallazgos: nuevas lesiones líticas en costillas y vértebras (D2–D7), bronquiectasias, colección multiloculada en tórax.\n- Microbiología: Aspergillus fumigatus aislado del secreción del absceso. Se cambió a voriconazol.\n- Dada la recurrencia y gravedad, se sospechó inmunodeficiencia.\n\nDiagnóstico de enfermedad granulomatosa crónica (EGC)\n- Prueba de dihidrorrodamina (DHR): ausencia de producción de especies reactivas de oxígeno en neutrófilos.\n- Flujo: ausencia de expresión de gp91phox.\n- Genética: secuenciación identificó una variante patógena en el gen CYBB: c.80_83del (p.Val27Glyfs*33), consistente con EGC ligada al cromosoma X. La madre resultó portadora de la misma variante.\n- Explicación breve: la EGC es un defecto hereditario del complejo NADPH oxidasa de los fagocitos; impide la producción de especies reactivas necesarias para matar ciertos bacterias y hongos, por lo que hay infecciones recurrentes, especialmente por organismos como Aspergillus.\n\nTratamiento, profilaxis y desenlace\n- Tras el segundo ingreso se administró voriconazol (28 días) y se instauró profilaxis diaria con trimetoprim‑sulfametoxazol y antifúngico profiláctico (fluconazol dos veces por semana).\n- A los 12 meses presentó neumonía multifocal por A. fumigatus (galactomanano sérico positivo), requirió ventilación mecánica, evolucionó a falla multiorgánica y falleció un mes después.\n\nImplicaciones clínicas y lecciones\n- Signos que deben alertar sobre una inmunodeficiencia primaria en lactantes: infecciones graves o recurrentes por hongos u otros patógenos inusuales, abscesos recurrentes, osteólisis/osteomielitis y mala respuesta a tratamientos convencionales.\n- La DHR es una prueba diagnóstica rápida y sensible para EGC; la confirmación genética permite identificar portadores y ofrecer consejo genético.\n- Manejo recomendado en EGC: profilaxis antibiótica/antifúngica, tratamiento agresivo de infecciones invasivas, evaluación para trasplante de progenitores hematopoyéticos (terapia potencialmente curativa) y seguimiento familiar. En este caso, el diagnóstico llegó después de infecciones ya avanzadas y aunque se iniciaron medidas profilácticas, no fue suficiente para evitar el desenlace fatal.\n- Es importante evaluar y ofrecer estudio genético a hermanos varones y apoyo social/psicosocial dada la situación familiar y el riesgo para otros varones portadores.\n\nComentario final (empático)\nEste caso ilustra cómo una enfermedad genética del sistema inmune (EGC ligada al X) puede manifestarse precozmente con infecciones fúngicas y lesiones óseas graves. El diagnóstico temprano y la coordinación entre microbiología, inmunología, genética y cuidado social son claves para ofrecer intervenciones que puedan cambiar el pronóstico. Lamento el desenlace desfavorable para el lactante y subrayo la importancia del estudio y consejo genético para la familia."
+        }
+    },
+    {
+        "article": "Se trata de un hombre de 66 años de edad que vive en la ciudad de Juan Bautista Alberdi de la provincia de Buenos Aires, con antecedentes de hipertensión arterial y trastorno obsesivo compulsivo. Su medicación habitual incluía amlodipina, quetiapina, venlafaxina y ácido valproico. Consultó por presentar fiebre de 39ºC de cuatro días de evolución sin síntomas asociados y se internó para estudio en sala general. Al examen de ingreso se constató un paciente lúcido, sin foco motor, sin trastorno sensitivo ni rigidez de nuca (escala de coma de Glasgow (GCS) 15/15). El resto del examen físico y el laboratorio general no presentaron particularidades. Los cultivos de sangre y orina resultaron negativos, y la tomografía computarizada de encéfalo, tórax, abdomen y pelvis no mostró afecciones. A las 24 horas agregó episodios de desorientación témporo-espacial que alternaban con otros de somnolencia (GCS 13/15). Al examen físico se constató temblor grueso distal en los cuatro miembros. El examen del LCR informó: líquido incoloro, límpido, y aspecto post centrifugado también límpido. Recuento de leucocitos 310/mm3 (mononucleares 54%, polimorfonucleares 46%), hematíes < de 1000/mm3, proteínas 0.76 g/l, glucosa 54 mg/dl (glucemia 120 mg/dl), y ácido láctico 21 mg/dl. Se inició tratamiento empírico con aciclovir 10 mg/kg endovenoso cada 8 horas. Se solicitaron en LCR: PCR para virus de herpes simple (VHS) y para virus de encefalopatía equina del oeste (VEEO) que resultaron no reactivas. Sin embargo, la IgM (ELISA) para EEO resultó positiva en suero y en LCR a los diez días. La RMN de encéfalo evidenció aumento en la intensidad en secuencias FLAIR y T2 a nivel de la región dorsal del tronco encefálico (tanto protuberancial, como también bulbar y mesencefálico), ambos pedúnculos cerebrales y ganglios de la base, con afectación bilateral y ligero predominio ganglio basal derecho. También se observaron múltiples imágenes focales hiperintensas en la sustancia blanca de ambos hemisferios cerebrales. El paciente evolucionó con deterioro del sensorio (GCS 8/15), sin protección de la vía aérea, por lo que ingresó a UTI. Requirió intubación y ventilación mecánica, con utilización de sedación y analgesia. Al ingreso a UTI presentaba: estado ácido-base (EAB) arterial: pH 7.11, pCO2 136 mmHg, pO2 75 mmHg, bicarbonato 43 mEq/l, exceso de base 11 mEq/l, saturación 88% (Con FIO2 21%), ácido láctico 11.5 mg/dl. Se inició la ventilación mecánica con un volumen minuto respiratorio (VMR) de 9.8 litros (volumen tidal 490 ml que corresponde a 6 ml/kg de peso teórico, frecuencia respiratoria 20 por minuto, presión positiva al final de espiración (PEEP) 5 cmH2 O, fracción inspirada de oxígeno 30%) se extrajo sangre para EAB arterial: pH 7.40, pCO2 41 mmHg, pO2 65 mmHg, bicarbonato 28 mEq/l, exceso de base 0 mEq/l, saturación 93%, PAFI 216. Evolucionó sin fiebre, estable hemodinámicamente, con adecuada oxigenación y ritmo diurético. Al suspender sedantes presentó GCS de 3 puntos sobre 10 (correspondiente con evaluación ocular 1 y motor 2 puntos), con rigidez generalizada y reflejos osteotendinosos adecuados, con movimientos rítmicos linguales y peribucales. El electroencefalograma de 12 canales no evidenció descargas patológicas. Al décimo día de inicio de los síntomas presentó apertura ocular y menor rigidez, pero no toleraba la modalidad respiratoria espontánea por hipoventilación e hipercapnia que lo llevaron a hipoxemia transitoria. En el EAB arterial presentó: pH 7.31, pCO2 70 mmHg, pO2 76 mmHg, bicarbonato 35 mEq/l, exceso de base 8 mEq/l bajo asistencia ventilatoria en modalidad espontánea de presión soporte de 5 cmH2 O, frecuencia respiratoria 6 por minuto, PEEP 5 cmH2 O y volumen tidal entre 120-150 ml. Los siguientes días el paciente se conectó, respondiendo órdenes simples y complejas, y movilizó simétricamente los miembros con cierta debilidad. Por intolerancia a las pruebas ventilatorias espontáneas fue traqueostomizado. En la evaluación funcional respiratoria presentaba presión inspiratoria máxima menor a -40 cm de H2 O, presión espiratoria máxima mayor a 80 cm de H2 O, pero continuaba con hipercapnia en la prueba ventilatoria espontánea, por lo que requirió soporte ventilatorio con modalidad controlada. Se realizó ecocardiograma transtorácico que informó cavidades derechas normales, sin signos de hipertensión pulmonar. En la nueva RMN de encéfalo se evidenció disminución de las áreas hiperintensas en secuencias FLAIR y T2 visibles previamente.\n\nEl enfermo evolucionó con requerimiento de menor soporte ventilatorio en forma progresiva al momento del desarrollo de este informe.",
+        "gold_summary": "Presentamos el caso de un varón de 66 años de edad oriundo de la ciudad Juan Bautista Alberdi de la provincia de Buenos Aires con antecedentes de hipertensión arterial y trastorno obsesivo compulsivo. Consultó por fiebre súbita de cuatro días de evolución, con desarrollo de encefalopatía durante su internación. La punción lumbar mostró un líquido cefalorraquídeo cristalino, aunque inflamatorio de predominio mononuclear. La RMN de encéfalo informó hiperintensidad en secuencias FLAIR y T2 en el dorso del tronco encefálico. Ingresó a terapia intensiva por deterioro neurológico y acidosis respiratoria grave, requiriendo asistencia ventilatoria mecánica. Luego de 10 días presentó mejoría neurológica, sin déficit motor pero con hipoventilación alveolar que dificultaron el destete del respirador.",
+        "synthetic_summary": {
+            "B1": "Un hombre de 66 años llegó al hospital con fiebre. Tenía presión alta y un problema de ansiedad. Al principio estaba despierto y sin signos de infección en el cuerpo.  \n\nAl día siguiente empezó a estar confundido y muy somnoliento. Le hicieron una punción lumbar (sacaron líquido de la espalda) y ese líquido mostró signos de infección. Le hicieron una resonancia del cerebro (una prueba por imágenes) y vieron cambios en el tronco del cerebro y otras áreas. Los médicos pensaron que tenía una infección viral del cerebro llamada encefalitis. Pruebas en sangre y en el líquido de la espalda mostraron anticuerpos que apoyaron la idea de una infección por el virus de la encefalitis equina del este.  \n\nEl paciente empeoró y perdió parte de su capacidad para respirar solo. Lo conectaron a un respirador en la unidad de cuidados intensivos. Con el tiempo mejoró en la parte del cerebro: abrió los ojos y respondía. Pero seguía respirando de forma lenta y no podía dejar el respirador, por lo que le hicieron una pequeña apertura en la garganta (traqueostomía) para ayudarle a respirar mejor.  \n\nLa segunda resonancia mostró que las áreas dañadas empezaban a mejorar. Al momento del informe, necesitaba menos ayuda del respirador y su estado general estaba mejorando. Aunque había mejoría, seguía con debilidad y problemas para respirar por su cuenta. Los médicos continuaban cuidándolo y dándole apoyo.",
+            "B2": "Resumen amable y claro:\n\nUn hombre de 66 años, con hipertensión y trastorno obsesivo-compulsivo, consultó por fiebre de cuatro días y fue hospitalizado. Al principio estaba lúcido, pero al día siguiente comenzó con desorientación y somnolencia, además de temblor en las manos y pies.\n\nSe le practicó una punción lumbar (extracción de líquido que rodea el cerebro y la médula, llamado líquido cefalorraquídeo o LCR). El LCR estaba claro pero mostraba signos de inflamación (aumento de glóbulos blancos y proteínas), lo que sugiere infección o inflamación en el sistema nervioso. Se inició tratamiento empírico con aciclovir (un antiviral usado para sospecha de infección por herpes) mientras se hacían pruebas. La PCR para virus herpes y otro virus equino fue negativa, pero a los diez días la prueba de anticuerpos IgM fue positiva tanto en sangre como en LCR, lo que indica una infección reciente por un virus equino (virus de encefalitis equina del oeste).\n\nLa resonancia magnética (RMN) del cerebro mostró zonas anormales en la parte posterior del tronco encefálico (incluyendo puente, bulbo y mesencéfalo), en los pedúnculos cerebrales y en los ganglios basales, además de algunas lesiones en la sustancia blanca de ambos hemisferios. Estas imágenes son compatibles con inflamación del cerebro por virus.\n\nPor empeoramiento neurológico (bajó el nivel de conciencia) y una respiración muy insuficiente con retención de dióxido de carbono (hipercapnia), fue trasladado a la unidad de cuidados intensivos y conectado a ventilación mecánica (respirador). Tras estabilizar los gases sanguíneos y suspender sedación, estuvo con reflejos y movimientos anormales, y el electroencefalograma no mostró crisis epilépticas. Diez días después empezó a mejorar neurocognitivamente (respondía órdenes y movía los brazos y piernas), pero no podía respirar bien por sí mismo: respiraba muy despacio y con volúmenes pequeños, lo que causaba alta CO2 y episodios de baja oxigenación. Por eso se le practicó traqueostomía (una abertura en la garganta para ayudar la ventilación) y siguió recibiendo apoyo ventilatorio.\n\nUna resonancia de control mostró reducción de las zonas anormales, y al momento del informe requería cada vez menos asistencia del respirador, aunque aún no estaba totalmente independiente para respirar solo.\n\nQué significa y posibles pasos siguientes:\n- El cuadro es compatible con una encefalitis viral (inflamación del cerebro) por un virus de encefalitis equina occidental, confirmada por anticuerpos IgM.  \n- El tratamiento principal fue de soporte en UCI (respirador, control de gases, cuidado neurológico); no existe un tratamiento específico para algunos de estos virus, por eso el manejo es de apoyo.  \n- Los próximos pasos suelen incluir rehabilitación respiratoria y neurológica, seguimiento con nuevas imágenes y control clínico para ver la recuperación funcional y respiratoria.\n\nEs comprensible que este proceso sea angustiante; la evolución mostrada aquí es alentadora porque hubo mejoría neurológica y disminución de las lesiones en la RMN, aunque aún requiere cuidado para lograr el alta completa.",
+            "B3": "Resumen clínico (nivel universitario — lectura avanzada, tono empático)\n\nPresentación\n- Paciente: varón de 66 años, antecedentes de hipertensión arterial y trastorno obsesivo‑compulsivo; toma amlodipina, quetiapina, venlafaxina y ácido valproico.\n- Motivo de consulta: fiebre de 39 °C durante 4 días, sin focalidad infecciosa aparente al ingreso.\n- Inicialmente lúcido (GCS 15/15), sin rigidez de nuca ni déficit neurológico focal. Estudios iniciales (cultivos de sangre y orina, tomografías de cráneo, tórax, abdomen y pelvis) sin hallazgos.\n\nHallazgos clínicos y de laboratorio relevantes\n- A las 24 horas desarrolló desorientación témporo‑espacial y somnolencia intermitente, con temblor grueso distal en las cuatro extremidades.\n- Punción lumbar: LCR claro pero inflamatorio — pleocitosis 310 leucocitos/mm3 (predominio mononuclear 54%), proteínas elevadas (0.76 g/L), glucosa 54 mg/dL (glicemia concomitante 120 mg/dL), hematíes <1000/mm3. Estos valores indican inflamación meníngea/encefálica.\n- PCR en LCR para virus herpes simple y para virus equino (pruebas realizadas inicialmente) negativas.\n- Serología (ELISA IgM) para encefalitis equina oriental (EEO) positiva en suero y en LCR a los 10 días, lo que apoya infección aguda por este arbovirus (presencia de IgM en LCR sugiere producción intratecal).\n- EEG de 12 canales sin descargas epileptiformes, a pesar de movimientos periorales rítmicos y rigidez generalizada.\n\nImagenología\n- RMN cerebral: hiperintensidades en FLAIR y T2 en el dorso del tronco encefálico (protuberancia, bulbo y mesencéfalo), ambos pedúnculos cerebrales y núcleos de la base (predominio relativo en el ganglio basal derecho), además de múltiples focos en la sustancia blanca de ambos hemisferios. Estos hallazgos son compatibles con encefalitis que afecta preferentemente tronco cerebral y ganglios basales.\n- RMN de control mostró reducción de las áreas hiperintensas, coincidiendo con mejoría radiológica.\n\nEvolución clínica y manejo\n- Deterioro neurológico progresivo hasta GCS 8/15; ingreso a unidad de terapia intensiva e intubación por pérdida de protección de vía aérea.\n- Presentó acidosis respiratoria grave por hipoventilación (pCO2 muy elevado) y requirió ventilación mecánica; después de ventilación controlada los gases arteriales se normalizaron.\n- Tras suspensión de sedación, persistió un bajo nivel de conciencia (GCS reducido) con rigidez y movimientos orofaciales; no hubo evidencia electroencefalográfica de estatus epiléptico.\n- A los 10 días mejoría neurológica: apertura ocular y disminución de rigidez; sin embargo, hipoventilación alveolar (central) persistente que dificultó el destete ventilatorio. Se realizó traqueostomía por intolerancia a las pruebas de ventilación espontánea.\n- Ecocardiograma transtorácico sin alteraciones significativas.\n- En el momento del informe, el paciente requería progresivamente menos soporte ventilatorio.\n\nInterpretación y puntos clave\n- Diagnóstico probable: encefalitis por virus de la encefalitis equina oriental (EEO/“Eastern equine encephalitis”), confirmado por IgM positiva en suero y LCR. La PCR puede ser negativa por baja carga viral o ventana temporal de muestreo; la serología IgM en LCR respalda infección activa del SNC.\n- La localización predominantemente en el dorso del tronco encefálico explica la insuficiencia ventilatoria central (afección de centros respiratorios bulboprotuberanciales) y la necesidad de ventilación prolongada.\n- La ausencia de foco infeccioso sistémico y la imagen típica en RMN, junto con la pleocitosis del LCR, son concordantes con encefalitis viral.\n- Tratamiento específico para EEO es de soporte; a su ingreso se inició aciclovir empírico hasta descartar herpesvirus, pero no existe terapia antiviral eficaz específica para EEO establecida en práctica clínica.\n\nImplicaciones y recomendaciones prácticas\n- Pronóstico: la encefalitis por EEO puede tener evolución grave y mortalidad elevada; sin embargo, algunos pacientes muestran recuperación parcial o gradual, como en este caso donde hubo mejoría neurológica pero persistió hipoventilación. El pronóstico funcional dependerá de la extensión del daño encefálico y de complicaciones respiratorias y neurológicas residuales.\n- Seguimiento: ventilatorio prolongado y rehabilitación neurológica motora y respiratoria; control seriado por neuroimagen y evaluación neurofisiológica si cambian los movimientos anormales; vigilancia de complicaciones nosocomiales en UTI.\n- Consideraciones epidemiológicas: notificar a salud pública y evaluar riesgo de transmisión vectorial en la región, ya que EEO es un arbovirus transmitido por mosquitos.\n\nTono final\nEste caso ilustra una forma severa de encefalitis viral con compromiso troncoencefálico y falla ventilatoria central, confirmada por serología en LCR. El cuidado ha sido predominantemente de soporte intensivo y manejo de complicaciones; la mejora clínica y la disminución de las lesiones en la RMN son alentadoras, aunque la capacidad respiratoria central comprometida requerirá tiempo y rehabilitación especializada. Si desea, puedo preparar una versión más técnica orientada a médicos o una guía de seguimiento y rehabilitación para el equipo tratante."
+        }
+    },
+    {
+        "article": "Mujer de 27 años de edad oriunda del interior de la Provincia de Buenos Aires sin antecedentes personales o familiares de relevancia, consultó por sangrado vaginal. El estudio colposcópico evidenció formación polipoide que protruía por el orificio cervical externo (OCE). Se arribó clínicamente al diagnóstico de mioma nascens y se tomó una muestra de biopsia para su evaluación. Ante el diagnóstico patológico de sarcoma, se instauró quimioterapia, con el fin de reducir la masa lesional. Una vez lograda la reducción del tamaño, se decidió derivarla a nuestra institución para realizar tratamiento quirúrgico. Se recibió una pieza de histerectomía total con anexos, f ijada en formol al 10%. Cuerpo de 5 × 5 × 3.2 cm, cuello de 3.5 × 3 × 2 cm, ambas trompas de 4.5 × 0.7 cm y ovarios de 4 × 2.5 × 2.5 cm. A la apertura de la pieza, se observó a nivel de la unión cérvico-ístmica una formación polipoide pediculada de 8.5 cm de diámetro, que emergía hacia el canal endocervical y se exteriorizaba por el OCE. La superficie externa era parda, lobulada, con sectores rojizos. Al corte, se observaba blanquecina, blanda, con sectores de aspecto gelatinoso y formaciones quísticas de hasta 0,6 cm de dimensión máxima. Luego del procesamiento de rutina, se efectuaron secciones histológicas y se colorearon con hematoxilina-eosina (H-E), las cuales evidenciaron sectores celulares alternados por áreas laxas, mixoides junto a glándulas ístmico-endometriales típicas. La proliferación, predominantemente fusocelular atípica se disponía en nidos, constituidos por células de amplio citoplasma eosinófilo y núcleos excéntricos con cromatina homogénea, algunos pleomórficos. Se apreciaron estriaciones citoplasmáticas transversales en dichas células. El estroma era ampliamente mixoide y ricamente vascularizado. Se destacaban focalmente áreas celulares densamente condensadas inmediatas y próximas al revestimiento epitelial intacto, pero separadas de él, por una fina capa de estroma laxo. Esto se conoce como cambium layer o capa cambial. Se realizaron técnicas de inmunohistoquímica para desmina, actina músculo específico (AME) y miogenina (MYF4), las cuales resultaron positivas, mientras que la actina músculo liso fue negativa. Esta inmunomarcación permitió comprobar la estirpe muscular estriada y en última instancia arribar al diagnóstico, junto al cuadro morfológico, de RMS embrionario. Asimismo, la presencia de rabdomioblastos agrupados constituyendo la capa cambial a nivel subepitelial resultó fundamental y necesario para tipificar al RMS embrionario como botrioide, independientemente de la presentación macroscópica en forma de racimos polipoides.",
+        "gold_summary": "Presentamos el caso de una mujer de 27 años que consultó por sangrado vaginal y en quien se evidenció en la colposcopia, una lesión polipoide blanquecina que se exteriorizaba a través del orificio cervical externo. El estudio histológico reveló sectores celulares alternados por áreas laxas, mixoides, junto a glándulas ístmico-endometriales típicas. La proliferación fusocelular atípica, se disponía en nidos, constituidos por células de amplio citoplasma eosinófilo con estriaciones citoplasmáticas transversales y núcleos excéntricos con cromatina homogénea. Se exhibían áreas de células densamente condensadas inmediatas y próximas al revestimiento epitelial intacto, pero separadas de él, por una fina capa de estroma laxo (capa cambial). El perfil de inmunomarcación resultó positivo para desmina, actina músculo específico y miogenina, y negativo para actina músculo liso. Se realizó diagnóstico de rabdomiosarcoma embrionario botroide de cuerpo uterino.",
+        "synthetic_summary": {
+            "B1": "Una mujer de 27 años fue a la consulta porque tenía sangrado por la vagina.  \nLos médicos miraron el cuello del útero y vieron una especie de bulto que salía por el orificio del cuello.  \nTomaron un pedacito del bulto (biopsia) para verlo en el microscopio.  \nEn el laboratorio encontraron que el bulto era un cáncer raro que nace de células del músculo. Ese cáncer se llama rabdomiosarcoma.  \nAntes de operar, le dieron quimioterapia para hacerlo más pequeño. Luego le quitaron el útero con sus anexos.  \nAl abrir la pieza y al mirarla con el microscopio, vieron un tumor polipoide grande con zonas gelatinosas y quistes pequeños.  \nTambién encontraron una capa muy delgada de muchas células del tumor justo debajo de la capa interna: eso se llama “capa cambial” y ayuda a identificar un tipo especial del tumor.  \nHicieron pruebas con colorantes especiales que detectan proteínas de músculo y esas pruebas salieron positivas.  \nCon todo eso, los médicos dieron el diagnóstico de rabdomiosarcoma embrionario tipo botrioide. “Botrioide” significa que el tumor tiene aspecto parecido a racimos o a uvas.  \nLos médicos actuaron con pruebas y tratamientos para manejar este problema de manera cuidadosa.",
+            "B2": "A 27-year-old woman from the Buenos Aires province went to the doctor for vaginal bleeding. On exam, a polyp-like mass was seen coming through the cervical opening. At first it was thought to be a type of fibroid, but a biopsy showed a sarcoma (a cancer of soft-tissue cells). She received chemotherapy to shrink the tumor and was then referred for surgery.\n\nThe removed uterus showed a pedunculated (on a stalk) polypoid mass about 8.5 cm wide at the cervico-isthmic area that projected through the cervical opening. On cut section the lesion was soft, partly gelatinous, and had small cystic spaces.\n\nUnder the microscope, the tumor had areas of loose, myxoid (mucus-like) stroma mixed with denser cellular nests. Tumor cells were spindle-shaped to rounded, had abundant pink (eosinophilic) cytoplasm and eccentric nuclei, and some showed transverse striations—features suggesting muscle-type cells. Right beneath the intact surface epithelium there was a dense layer of tumor cells separated from the epithelium by a thin loose stroma; this dense zone is called a cambium layer and is characteristic of the botryoid form of certain tumors.\n\nSpecial stains (immunohistochemistry) were positive for desmin, muscle-specific actin, and myogenin, and negative for smooth muscle actin. These results point to a skeletal muscle cell origin rather than smooth muscle, supporting the diagnosis.\n\nPutting the microscopic appearance and the immunostains together, the final diagnosis was embryonal rhabdomyosarcoma, botryoid type, of the uterine cervix. Rhabdomyosarcoma is a cancer that shows skeletal muscle features; the botryoid type often forms grape-like polypoid masses and is identified by the cambium layer. The patient was treated with chemotherapy followed by total hysterectomy (removal of the uterus and nearby reproductive structures). Ongoing cancer follow-up and care by a specialist team are needed to monitor recovery and any further treatment.",
+            "B3": "Resumen clínico y patológico\n\nPresentamos el caso de una mujer de 27 años sin antecedentes relevantes que consultó por sangrado vaginal. En la colposcopia se mostró una formación polipoide que protruyó por el orificio cervical externo y fue inicialmente interpretada como un mioma nascens; se tomó biopsia y, ante el resultado de sarcoma, se indicó quimioterapia neoadyuvante para reducir la masa antes del tratamiento definitivo. Tras disminución del tumor, se practicó histerectomía total con anexos.\n\nHallazgos macroscópicos: pieza con tumor polipoide pediculado de 8,5 cm en la unión cérvico-ístmica, de superficie parda y lobulada; en el corte, tejido blanquecino con áreas blandas, gelatinosas y quistes de hasta 0,6 cm.\n\nHallazgos histológicos e inmunohistoquímicos: el tumor mostró zonas celulares alternando con estroma laxo y mixoide, y glándulas ístmico-endometriales adyacentes. La proliferación fusocelular atípica se organizó en nidos con células de citoplasma eosinófilo, núcleos excéntricos y estriaciones citoplasmáticas transversales (rhabdomioblastos). Se observó una capa cambial —una banda subepitelial de células densamente condensadas—, característica del tipo botrioide. La inmunohistoquímica fue positiva para desmina, actina músculo-específica y miogenina, y negativa para actina de músculo liso, confirmando diferenciación hacia músculo estriado. En conjunto, estos hallazgos permiten el diagnóstico de rabdomiosarcoma embrionario, variante botrioide, del cuerpo uterino.\n\nImplicaciones y recomendaciones: el rabdomiosarcoma uterino es raro en adultas; la variante botrioide tiene rasgos morfológicos característicos pero requiere manejo oncológico multidisciplinario. Dado que la paciente recibió histerectomía, existe pérdida de fertilidad; se recomienda seguimiento oncológico estrecho (estadificación por imagen si no realizada, valoración en oncología médica y radioterápica según protocolos locales, vigilancia por recidiva). El pronóstico y el tratamiento adyuvante dependen del estadío, la resección completa y la respuesta a quimioterapia, por lo que es importante coordinar un plan terapéutico individualizado."
+        }
+    },
+    {
+        "article": "Un hombre de 53 años de edad, que inició diálisis por disfunción renal en etapa terminal debido a nefropatía diabética o nefroesclerosis en nuestro departamento de nefrología 10 años antes, se sometió a una ecocardiografía de seguimiento anual para estenosis valvular aórtica progresiva (AVS) y regurgitación moderada con fracción de eyección ventricular izquierda (LVEF) normal. Un año antes, se observaron calcificaciones que sugerían MAC en el anillo mitral posterior, que no se habían visto dos años antes. En el último seguimiento, la ecocardiografía reveló una masa redonda de superficie lisa de 22 × 17 mm con alta ecogenicidad en el área circundante y un brillo interno ligeramente disminuido en el anillo mitral posterior del lado auricular izquierdo. El paciente no tenía síntomas significativos ni hallazgos físicos, excepto un soplo sistólico.\n\nLa ecocardiografía también reveló una VS moderada con un flujo de pico valvular transaórtico de 3,76 m/s y una regurgitación valvular aórtica moderada. Se observó una regurgitación mitral leve pero no estenosis. El patrón de velocidad de flujo de entrada del VI mostró un patrón pseudo-normal con un agrandamiento de la aurícula izquierda de 47 mm de diámetro. La ecocardiografía en serie durante dos años reveló un agrandamiento del VI y una disminución de la FEVI. El diámetro final diastólico/final sistólico del VI y la FEVI fueron de 50/33 mm y 64 %, respectivamente, hace dos años; 57/41 mm y 52 % hace un año; y 59/47 mm y 42 % en el último seguimiento.\n\nTeniendo en cuenta el estado de la hemodiálisis, predijimos la progresión a una AVS casi severa, con empeoramiento de la disfunción sistólica del LV, que se convertiría en una indicación para el reemplazo de la válvula aórtica (AVR) en un futuro cercano.\n\nLa tomografía computarizada (TC) reveló una masa de alta densidad sin realce de contraste. La resonancia magnética (MRI) mostró una masa bien definida de alta intensidad en el centro, con un borde hipointenso en la imagen T1 y una señal desprovista en T2. Se excluyeron los neoplasmas, incluidos los mixomas y los fibroelastomas papilares, en función de sus características de imagen. Los hallazgos de laboratorio no indicaron infección, y no se sospechó de vegetación con endocarditis infecciosa. Teniendo en cuenta la disfunción renal en etapa terminal en la hemodiálisis y los hallazgos de imagen, se sospechó CCMA. El rápido agrandamiento de la masa generó preocupación sobre una potencial embolia. En consecuencia, la masa se resecó con AVR.\n\nLa incisión del atrio izquierdo reveló una masa por debajo del endocardio auricular en el anillo de la válvula mitral (P1-2); se observaron sustancias cremosas en la incisión de la masa, lo que sugiere CCMA. Después de la extirpación y desbridamiento del tejido, el sitio de la incisión se suturó con prolina. Se realizó el reemplazo de la válvula aórtica utilizando una válvula SJM de 21 mm. La retirada del bypass cardiopulmonar fue relativamente suave. Al momento del alta, se prescribió warfarina y aspirina, junto con bisoprolol para la fibrilación auricular paroxística después de la cirugía.\n\nNo se observaron eventos embólicos antes o después de la cirugía.\n\nEl examen histopatológico reveló calcificaciones granulares y nodulares dispersas, que consistían principalmente en infiltración de células inflamatorias y proliferación vascular de neutrófilos, linfocitos, células espumosas, macrófagos tisulares y células plasmáticas, con osificación parcial compatible con CICM. La biopsia miocárdica LV para descartar cardiomiopatía secundaria y la válvula aórtica resecada mostraron células inflamatorias similares a las observadas en CICM. Por lo tanto, se diagnosticó CICM en base a la disminución del movimiento de la pared y la fibrosis miocárdica, con infiltración de células inflamatorias > 14 mm2, células T CD3 positivas > 7/mm2 y negatividad de tenascina C (4C8).7 Sin embargo, no se pudo determinar la causa de CICM.\n\nLa ecocardiografía 6 meses después de la resección no mostró recurrencia del tumor (ver material complementario en línea), ni progresión de la regurgitación mitral, función normal de la válvula aórtica protésica y ninguna mejora de la FEVI (41 %)\n\n",
+        "gold_summary": "Un hombre de 52 años con insuficiencia renal en fase terminal que requería hemodiálisis se sometió a una ecocardiografía anual de seguimiento para detectar una disfunción valvular aórtica. La ecocardiografía reveló una masa circular bien definida de 22 × 17 mm en el anillo de la valva mitral posterior que no se había detectado 2 años antes. En función de las características de la imagen, se sospechó que la masa era un CCMA. Se había agrandado rápidamente y suponía un riesgo potencial de embolia; por lo tanto, se extirpó al mismo tiempo que la sustitución de la válvula aórtica. Aunque se sospechó un CCMA en función de los hallazgos intraoperativos, el diagnóstico histopatológico fue un CAT. Tras el análisis histológico de la muestra de miocardio del ventrículo izquierdo y la válvula aórtica extirpada, se observó una infiltración de células inflamatorias crónicas; por lo tanto, se diagnosticó una cardiomiopatía inflamatoria crónica.\n",
+        "synthetic_summary": {
+            "B1": "Había un hombre de 53 años que necesitaba hemodiálisis. Eso quiere decir que una máquina limpiaba su sangre porque sus riñones estaban muy enfermos. Los médicos le hacían una ecografía del corazón cada año para ver sus válvulas.\n\nUn año vieron un bulto nuevo cerca de una válvula del corazón. El bulto medía como 2 cm. El hombre no tenía dolor, sólo un sonido extraño cuando el corazón latía. Las pruebas con tomografía y resonancia mostraron que el bulto tenía calcio y no parecía un tumor ni una infección. Los médicos temieron que el bulto pudiera soltar algo y viajar por la sangre. Por eso lo quitaron con cirugía. También cambiaron la válvula aórtica por una nueva.\n\nDentro del bulto hallaron una sustancia cremosa y calcio. El examen con el microscopio mostró muchas células de inflamación. Los médicos dijeron que tenía una inflamación crónica del corazón. No hubo señales de que algo se hubiera desprendido antes o después de la operación. Tras la operación, el hombre recibió medicinas para el ritmo del corazón y para evitar coágulos.\n\nSeis meses después, la ecografía mostró que el bulto no volvió. La válvula nueva funcionaba bien. Pero la fuerza del corazón no había mejorado mucho. Los médicos siguen cuidándolo y dándole medicinas.",
+            "B2": "Here is a clear, kind summary written for a secondary-school reader:\n\nA 53-year-old man who has been on hemodialysis for kidney failure had routine heart scans because of worsening aortic valve disease. Over two years his left heart pumping function (called left ventricular ejection fraction, or LVEF) fell from 64% to about 42%. In the most recent scan doctors found a new, round 22 × 17 mm mass on the back part of the ring of the mitral valve. The patient had no new symptoms besides a heart murmur.\n\nImaging tests (CT and MRI) suggested the mass might be “caseous calcification of the mitral annulus” (CCMA). CCMA is a rare, non-cancerous lump where calcium and other material build up in the valve ring. Because the mass had grown quickly and might break off and cause an embolus (a dangerous blockage), the team removed it during surgery and also replaced the aortic valve at the same time.\n\nUnder the microscope the removed mass looked like a calcified amorphous tumor (CAT) — another non-cancerous, calcium-containing mass — and showed many inflammatory cells. Samples from the left heart muscle and the removed aortic valve also had similar chronic inflammation. Based on these findings, doctors diagnosed chronic inflammatory cardiomyopathy (a long-lasting inflammation of the heart muscle) as the reason for the reduced heart function. The exact cause of that inflammation was not found.\n\nThe patient recovered from surgery without any embolic events. He went home on blood thinners (warfarin and aspirin) and a beta-blocker for occasional atrial fibrillation. Six months later there was no sign the mass had come back, the artificial aortic valve worked well, and mitral valve leakage had not worsened — but the heart’s pumping function had not improved.\n\nTakeaway: The team treated a new, quickly growing calcified mass in the mitral valve ring with surgery because of embolic risk. Pathology showed a non-cancerous calcified tumor and chronic inflammation of the heart muscle, which likely explains the falling heart function. Continued follow-up and medical care are needed to monitor heart function and look for causes of the inflammation.",
+            "B3": "Summary\n\nBackground and context\n- A 53-year-old man on chronic hemodialysis for end‑stage renal disease (ESRD) — started 10 years earlier for diabetic nephropathy or nephroesclerosis — was followed with annual echocardiography for progressive aortic valve disease (aortic stenosis and moderate regurgitation).\n\nKey findings (what was normal and what was abnormal)\n- Symptoms and exam: the patient had no new symptoms and only a systolic murmur on exam.\n- Echocardiography (latest): a new, smooth, round mass 22 × 17 mm located at the posterior mitral annulus on the left‑atrial side; the mass was highly echogenic with slightly reduced internal brightness. Other findings: moderate aortic stenosis (peak transaortic velocity 3.76 m/s), moderate aortic regurgitation, mild mitral regurgitation without stenosis, a pseudonormal LV inflow pattern, and left atrial enlargement (47 mm).\n- Serial LV measurements (progressive worsening over 2 years): \n  - 2 years ago: LV end‑diastolic/systolic diameters 50/33 mm, LVEF 64%\n  - 1 year ago: 57/41 mm, LVEF 52%\n  - Latest: 59/47 mm, LVEF 42% (clear progressive LV dilation and falling ejection fraction).\n- CT: high‑density (calcified) mass without contrast enhancement.\n- Cardiac MRI: well‑defined central high signal with a hypointense rim on T1 and signal void on T2 — Imaging features argued against cardiac tumors (myxoma, papillary fibroelastoma) and against infective vegetation. Laboratory testing did not indicate infection.\n\nWorking diagnosis before surgery\n- Because the mass appeared calcified, grew rapidly, and the patient has ESRD (a risk factor for mitral annular calcification), the team suspected caseous calcification of the mitral annulus (CCMA). Rapid enlargement raised concern for embolic risk and, together with predicted near‑severe aortic stenosis and worsening LV dysfunction, led to a decision for surgery.\n\nTreatment and surgical findings\n- The patient underwent resection of the mitral‑annulus mass at the time of aortic valve replacement (AVR) with a mechanical 21 mm SJM valve.\n- Intraoperative appearance: mass beneath the left atrial endocardium at the posterior mitral annulus (P1–2) contained a creamy substance — an appearance suggestive of CCMA.\n- Postoperative course: uneventful weaning from bypass. Discharged on warfarin and aspirin (for the mechanical valve) and bisoprolol for new paroxysmal atrial fibrillation. No clinical embolic events occurred before or after surgery.\n\nPathology and final diagnosis\n- Histopathology of the resected specimen showed dispersed granular and nodular calcifications with abundant inflammatory cell infiltrates (neutrophils, lymphocytes, foam cells, tissue macrophages, plasma cells), vascular proliferation and partial ossification.\n- Similar inflammatory findings were present in the left ventricular biopsy and in the excised aortic valve tissue.\n- Based on wall‑motion abnormalities, myocardial fibrosis and quantitative inflammatory cell criteria (inflammatory cell infiltration and CD3+ T‑cell density above diagnostic thresholds), the final diagnosis was chronic inflammatory cardiomyopathy (CICM). The exact cause of the inflammatory cardiomyopathy remained unknown.\n\nOutcomes and follow‑up\n- Six months after surgery: echocardiography showed no recurrence of the mitral annulus mass, no progression of mitral regurgitation, normal prosthetic aortic valve function, but persistent LV systolic dysfunction (LVEF ~41%) with no improvement in ejection fraction.\n\nImplications and reasonable next steps\n- What this means: the mass was initially suspected to be a benign caseous calcification of the mitral annulus based on imaging and intraoperative appearance, but histology demonstrated a chronic inflammatory process involving both the annulus and myocardium. The patient also has progressive LV systolic dysfunction consistent with inflammatory cardiomyopathy.\n- Clinical implications: persistent LV dysfunction despite removal of the mass suggests that myocardial inflammation and fibrosis are established and are the likely drivers of heart failure risk. ESRD patients are prone to annular calcification and complex valve pathology; the presence of inflammatory cardiomyopathy complicates prognosis.\n- Reasonable next steps in care (individualized by the treating team):\n  - Ongoing surveillance of LV function and valve prosthesis by echocardiography.\n  - Guideline‑directed heart failure management as appropriate (medications, rate/rhythm control for atrial fibrillation).\n  - Further evaluation to seek an underlying cause of the inflammatory cardiomyopathy if clinically indicated (infectious, autoimmune, metabolic, or drug‑related causes), and consideration of specialty input (cardiology with heart failure and possibly myocarditis/inflammatory cardiomyopathy expertise).\n  - Long‑term monitoring for embolic events and prosthetic valve management (anticoagulation).\n\nEmpathy note\n- The team acted preemptively because of the mass’s rapid growth and the patient’s declining cardiac function, aiming to reduce embolic risk and address worsening aortic valve disease. Although surgery removed the mass and replaced the aortic valve successfully, the persistent LV dysfunction highlights the need for careful long‑term cardiology follow‑up and targeted management of the underlying inflammatory cardiomyopathy."
+        }
+    },
+    {
+        "article": "Paciente masculino de 28 años, sin antecedentes de importancia, acude a consulta de dermatología con un cuadro cutáneo de 48 horas de evolución caracterizado por dos placas eritematosas con ampollas centrales más ulceración superficial localizadas en cara flexora de brazo y antebrazo derecho equidistantes del pliegue del codo, acompañadas de una sensación de ardor y prurito en el lugar de las lesiones. No presentó síntomas sistémicos ni se automedicó. Como antecedente refiere que se encontraba de vacaciones en la región costera de Ecuador al momento de aparecer las lesiones. Se realizó una biopsia incisional que reportó epidermis con acantosis, paraqueratosis y espongiosis, neutrófilos en estrato córneo e infiltrado linfocitario perivascular en dermis superficial, media y profunda. Por las características clínicas, el antecedente de viaje a una región tropical y los hallazgos histológicos se diagnosticó como dermatitis por Paederus. Se indicó tratamiento con antihistamínicos, esteroides tópicos y compresas frías. Después de 8 días de tratamiento, las lesiones remitieron dejando una hiperpigmentación postinflamatoria.",
+        "gold_summary": "Se comunica el caso de un paciente masculino de 28 años, que acude a consulta de dermatología con cuadro de 48 horas de evolución de dos placas eritematosas con ampollas centrales más ulceración superficial localizadas en cara flexora de brazo y antebrazo derecho, acompañadas de una sensación de ardor y prurito en el lugar de las lesiones, sin síntomas acompañantes. Como antecedente refiere que se encontraba de vacaciones en la región costera de Ecuador al momento de aparecer las lesiones. Se realizó una biopsia incisional y por las características clínicas y el antecedente de viaje a una región tropical se diagnosticó como dermatitis por Paederus y se indicó tratamiento con antihistamínicos, esteroides tópicos y compresas frías. Después de 8 días de tratamiento, las lesiones remitieron dejando una hiperpigmentación postinflamatoria.",
+        "synthetic_summary": {
+            "B1": "Un hombre de 28 años fue al doctor por dos manchas rojas en el brazo y el antebrazo derecho. Tenían ampollas en el centro y un poco de herida. Le dolía y le picaba. No tuvo fiebre ni otros problemas. Él había estado de vacaciones en la costa de Ecuador cuando aparecieron las lesiones.\n\nLos médicos hicieron una pequeña prueba en la piel que mostró inflamación. Juntando eso con su viaje, dijeron que era dermatitis por Paederus. Esto ocurre cuando un insecto pequeño (un escarabajo llamado Paederus) toca la piel y deja una sustancia que la irrita.\n\nLe dieron antihistamínicos para la picazón, cremas con esteroide para bajar la inflamación y compresas frías. Después de 8 días las heridas mejoraron, pero quedó una mancha más oscura en la piel donde estuvieron las lesiones.",
+            "B2": "A 28-year-old man went to a skin doctor after 48 hours of two red patches on the inner (flexor) side of his right upper arm and forearm. Each patch had a central blister and a shallow ulcer, and he felt burning and itching where the lesions were. He had no other symptoms and had not treated the spots himself; he said the lesions began while he was on vacation in coastal Ecuador. A skin biopsy showed changes that mean inflammation of the outer skin layers and a band of immune cells around blood vessels in the deeper skin. Based on the look of the lesions, the biopsy, and the travel to a tropical area, doctors diagnosed Paederus dermatitis — a skin reaction that can happen after contact with a small beetle that releases a toxin. He was treated with antihistamines (to reduce itching), topical steroids (to lower inflammation), and cold compresses. After eight days the lesions improved, leaving a darker area of skin called postinflammatory hyperpigmentation.",
+            "B3": "Resumen clínico (nivel universitario, tono empático)\n\nPresentación y síntomas:\nUn hombre de 28 años, sin antecedentes relevantes, consultó por lesiones cutáneas de 48 horas de evolución: dos placas eritematosas con ampollas centrales y ulceración superficial en la cara flexora del brazo y antebrazo derechos, equidistantes del pliegue del codo. Las lesiones producían ardor y prurito local; no hubo síntomas sistémicos ni automedicación. Como antecedente relevante, el paciente estaba de vacaciones en la zona costera de Ecuador cuando aparecieron las lesiones.\n\nHallazgos histológicos:\nSe realizó una biopsia incisional. El informe describió: engrosamiento epidérmico (acantosis), retención de núcleos en la capa córnea (parakeratosis), edema intercelular epidérmico (espongiosis), presencia de neutrófilos en el estrato córneo y un infiltrado linfocitario perivascular que afectaba dermis superficial, media y profunda. Estos cambios son compatibles con una reacción inflamatoria aguda de la piel.\n\nDiagnóstico y explicación breve:\nPor la apariencia clínica, el antecedente de exposición en una región tropical y los hallazgos histológicos, se diagnosticó dermatitis por Paederus. Esta es una dermatitis irritativa causada por la liberación del tóxico pederina cuando se aplasta un escarabajo del género Paederus; típicamente provoca placas eritematosas, ampollas o lesiones lineales en áreas expuestas.\n\nTratamiento y evolución:\nSe indicó manejo conservador: antihistamínicos para el prurito, esteroides tópicos y compresas frías. Tras 8 días de tratamiento las lesiones remitieron, dejando hiperpigmentación postinflamatoria en la zona.\n\nImplicaciones y recomendaciones prácticas:\n- Prognóstico: buena respuesta al tratamiento en este caso; la hiperpigmentación postinflamatoria puede tardar semanas o meses en atenuarse.  \n- Seguimiento: acudir si las lesiones se extienden, aparecen signos de infección (dolor creciente, supuración, fiebre) o si la pigmentación persiste y causa preocupación estética.  \n- Prevención: evitar aplastar escarabajos Paederus en la piel (si contacta con uno, lavar con agua y jabón y no frotar), usar mosquiteros y minimizar la luz nocturna directa que atrae a estos insectos en regiones endémicas.  \n- Tratamientos adicionales: para hiperpigmentación persistente pueden considerarse medidas dermatológicas (fotoprotección, cremas despigmentantes, procedimientos) tras valoración por dermatólogo.\n\nSi desea, puedo redactar una versión aún más breve para registro clínico o preparar materiales para el paciente con recomendaciones de cuidado de la piel y prevención."
+        }
+    },
+    {
+        "article": "Un hombre de 35 años de edad, herido en un accidente de tráfico, fue trasladado a nuestro hospital, que está equipado con un ER híbrido. Había sufrido una lesión potencialmente mortal, con su pierna derecha acortada y girada. Los signos vitales del paciente a su llegada fueron los siguientes: frecuencia respiratoria de 24 respiraciones/min, saturación de oxígeno del 99 % con 12 L de administración de oxígeno, frecuencia cardiaca de 143 latidos/min, presión arterial de 80/40 mmHg, y puntuación de Glasgow Coma Scale de E4V4M6. Intentamos realizar un TAC y resucitar al paciente. El TAC reveló un hemotórax izquierdo, ensanchamiento del mediastino, y fractura pélvica. Como la presión arterial del paciente cayó rápidamente antes del TAC, se administraron procedimientos de salvamento, como intubación de emergencia, preperitoneal pelvic packing, y transfusión masiva, con un cuidadoso control de la presión arterial en el ER híbrido. Después de la estabilización de los signos vitales con estos procedimientos, el TAC con contraste reveló una fractura de BTAI de grado IV que se extendía hacia la cavidad torácica izquierda. La embolización arterial transcatéter (TAE) para la fractura pélvica y la fijación esquelética externa de la fractura del fémur derecho se realizaron primero, ya que el radiólogo y el cirujano cardiovascular, que realizan TEVAR en nuestro centro médico, no estaban disponibles en ese momento. Posteriormente, se realizó TEVAR utilizando un injerto de stent (GORE C-TAG 26 × 150 mm; WL Gore & Associates, Flagstaff, Arizona, EE. UU.) en el ER híbrido sin transferir al paciente. Se desplegó un injerto de stent justo distal de la arteria carótida común izquierda (zona II) y el extremo distal del injerto de stent se posicionó en el nivel de Th 8. Decidimos sacrificar LSCA ya que el flujo sanguíneo de la arteria vertebral izquierda fue suficiente según lo evaluado por angiografía. El paciente no tuvo síntomas que sugirieran isquemia después de TEVER. Durante la cirugía, se administraron 50 unidades/kg (3000 unidades) de heparina. El paciente fue trasladado a un hospital de rehabilitación el día 41 postoperatorio.\n",
+        "gold_summary": "Un hombre de 35 años de edad sufrió múltiples lesiones tras un accidente de tráfico y fue trasladado a nuestro hospital en estado de shock. La tomografía computarizada reveló una fractura de TAI de grado IV que se extendía hasta la cavidad torácica y una fractura pélvica. Poco tiempo después de realizar un relleno pélvico preperitoneal y una embolización arterial transcatéter para la fractura pélvica, se realizó un TEVAR en el quirófano híbrido sin trasladar al paciente. El paciente fue trasladado a un hospital de rehabilitación el día 41 después de la operación.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre de 35 años tuvo un choque de coche y llegó muy herido. Tenía el muslo derecho roto y el cuerpo herido por dentro. Los médicos vieron que tenía sangre en el pecho y una grave rotura en una arteria del tórax. También tenía una fractura en la pelvis.\n\nPrimero los doctores lo ayudaron a respirar con un tubo y le dieron mucha sangre. Pusieron compresas dentro de la pelvis para detener la hemorragia. Luego cerraron los vasos de la pelvis con un catéter para parar el sangrado y pusieron una fijación externa en la pierna rota.\n\nDespués, sin moverlo del cuarto de urgencias, los médicos arreglaron la arteria rota en el pecho colocando un injerto por dentro de la arteria. Para eso usaron un “tubo” especial que evita que la arteria siga perdiendo sangre. Tuvieron que cerrar una rama pequeña de la arteria, pero otra arteria daba suficiente sangre, y el paciente no tuvo problemas por eso. También le dieron un medicamento para evitar coágulos durante la cirugía.\n\nEl hombre se recuperó y, 41 días después, lo enviaron a un hospital de rehabilitación para seguir mejorando.",
+            "B2": "Un hombre de 35 años llegó al hospital después de un accidente de tráfico con la pierna derecha visiblemente dañada y signos de shock (pulso rápido y presión arterial muy baja). En la tomografía se vio sangre en el pecho (hemotórax izquierdo), ensanchamiento del mediastino (un hallazgo que puede indicar lesión de un gran vaso) y una fractura pélvica. Como su presión arterial bajó rápido, el equipo realizó maniobras de emergencia en la sala híbrida (una sala con imagen y recursos quirúrgicos): intubación para ayudar a respirar, colocaron compresas en la pelvis para detener el sangrado y le dieron una transfusión masiva.\n\nTras estabilizarlo, la tomografía con contraste mostró una lesión grave en la aorta torácica (fractura de aorta por traumatismo, grado IV). Primero controlaron el sangrado de la pelvis con embolización (bloqueo de vasos desde un catéter) y fijaron la fractura del fémur. Luego realizaron una reparación endovascular de la aorta (TEVAR): colocaron un injerto o “stent” dentro de la aorta en la misma sala híbrida sin mover al paciente. Para asegurar el flujo cerebral, decidieron cerrar la arteria subclavia izquierda porque la arteria vertebral izquierda suministraba suficiente sangre; el paciente no presentó síntomas de falta de riego después del procedimiento. Durante la operación se usó heparina para evitar coágulos.\n\nEl paciente evolucionó bien y fue trasladado a un hospital de rehabilitación 41 días después de la cirugía.",
+            "B3": "Resumen clínico (lectores con formación universitaria)\n\nPresentación\n- Hombre de 35 años, víctima de accidente de tráfico, ingresó en estado de choque con la pierna derecha acortada y girada. A su llegada presentaba taquicardia (FC 143/min), hipotensión (PA 80/40 mmHg), frecuencia respiratoria 24/min y puntuación de Glasgow 14 (E4V4M6). Recibía 12 L de oxígeno con saturación del 99 %.\n\nHallazgos radiológicos y lesiones principales (anormales)\n- Tomografía computarizada (TAC) mostró hemotórax izquierdo, ensanchamiento del mediastino y fractura pélvica.\n- TAC con contraste posterior evidenció una lesión aórtica por traumatismo torácico (BTAI) grado IV que se extendía hacia la cavidad torácica izquierda — lesión potencialmente letal.\n\nIntervenciones realizadas\n- Manejo inicial de emergencia en el servicio de urgencias híbrido: intubación, preperitoneal pelvic packing (para controlar sangrado pélvico) y transfusión masiva, logrando estabilizar hemodinámicamente al paciente.\n- Procedimientos por prioridad: embolización arterial transcatéter (TAE) para la fractura pélvica y fijación externa de la fractura femoral derecha (realizados primero porque el equipo de TEVAR no estaba disponible inmediatamente).\n- Una vez disponible el equipo, se realizó TEVAR (colocación endovascular de stent endoluminal) en el quirófano/ER híbrido sin traslado del paciente. Se usó un graft GORE C-TAG 26 × 150 mm, implantado desde justo distal a la arteria carótida común izquierda (zona II) hasta aproximadamente T8.\n- Se decidió cubrir (sacrificar) la arteria subclavia izquierda (LSCA) porque la angiografía mostró flujo vertebral izquierdo suficiente. Durante el procedimiento se administraron 50 U/kg de heparina (3.000 U).\n\nResultados y evolución\n- No aparecieron síntomas sugestivos de isquemia vertebrobasilar o de miembro superior tras la cobertura de la LSCA.\n- El paciente fue trasladado a un centro de rehabilitación al día 41 posoperatorio.\n\nComentarios e implicaciones\n- El manejo escalonado —control urgente del sangrado pélvico y estabilización hemodinámica, seguido de reparación endovascular de la lesión aórtica— fue decisivo para la supervivencia.\n- La cobertura de la subclavia izquierda es una decisión frecuente cuando es necesario para lograr un sellado aórtico; requiere evaluar el flujo vertebral y vigilancia posterior por riesgo teórico de isquemia cerebral posterior, del brazo o de la médula espinal. En este caso no hubo signos clínicos de complicaciones inmediatas.\n- El uso del ER híbrido permitió realizar intervenciones simultáneas y evitar traslados riesgosos en un paciente inestable.\n\nSi desea, puedo añadir una breve explicación sobre qué implican las clasificaciones de lesiones aórticas (grado IV) o sobre los riesgos a medio-largo plazo tras TEVAR."
+        }
+    },
+    {
+        "article": "Hombre de 31 años con antecedentes de consumo de alcohol, tabaco, cocaína inhalada, tuberculosis pulmonar tratada, nefrectomía izquierda y esplenectomía post-traumática. Consultó al servicio de urgencias por cuadro de una semana de evolución que inició inmediatamente posterior a la aplicación intramuscular de penicilina por contacto sexual con pareja con sífilis, caracterizado por dolor en región glútea derecha que irradiaba hasta pie, con posterior aparición de dermatosis purpúrica relacionada con sitio de inyección, siendo una lesión tipo placa configurada en forma anular, con bordes irregulares y distribución racemosa que medía 15 centímetros (cm), con piel sana en su interior. También presentaba una pequeña escara escrotal y una extensa lesión plantar derecha de aspecto livedoide desde la zona talar hasta la punta de los dedos que no respetaba margen estricto. Se realizó ecografía del glúteo mayor, que mostró pérdida del patrón fibrilar heterogéneo, aumento del espesor del mismo a nivel de su tercio medio de aspecto edematoso, además de edema del tejido celular subcutáneo (TCS); en región plantar homolateral y en escroto edema de TCS. En el laboratorio presentó leucocitosis de 13.7 × 109/L, proteína C reactiva de 3.2 mg/dL (normal hasta 0.5 mg/dL), que se interpretaron como reactantes de fase aguda, también aumento de transaminasas con aspartato aminotransferasa de 175 UI/L (normal hasta 32), alanino aminotransferasa de 245 UI/L (normal hasta 33), creatina kinasa con un valor de 2741 UI/L (normal hasta 170) y lactato deshidrogenasa de 2499 UI/L (normal hasta 250) representando compromiso muscular. Se realizaron serologías completas para sífilis, con venereal disease research laboratory (VDRL y anticuerpos treponémicos), virus de la inmunodeficiencia humana (HIV) hepatitis B, hepatitis C, con resultados negativos. La cronología, las manifestaciones clínicas y la posterior biopsia, respaldaron el diagnóstico de síndrome de Nicolau, para lo cual se inició anticoagulación con enoxaparina 1 mg/ kg c/12 hs vía subcutánea, cilostazol 100 mg cada 12 horas y tramadol, por 10 días. Se realizó biopsia de piel de glúteo que evidenció necrosis epidérmica y extensión a epitelio folicular, con formación de ampolla secundaria a reepitelización, sin vasculitis ni trombosis vascular, vinculable a embolia cutis medicamentosa en fase aguda, hubo franca mejoría con descenso de valores de transaminasas, con aspartato aminotransferasa de 39 UI/L, alanino aminotransferasa de 77 UI/L y creatin kinasa de 167 UI/L.  No se solicitó perfil inmunológico, basados en que nuestro diagnóstico presuntivo inicial no justificaba la búsqueda de otras etiologías. Se otorgó alta con cilostazol y analgésicos, control ambulatorio a los 3 meses con mejoría del dolor y de las lesiones, quedando en glúteo derecho cicatriz discrómica con presencia de descamación fina y en pie derecho cicatriz discrómica con zonas de descamación gruesas en región de apoyo tarso metatarsiano asociado a mínimas lesiones livedoides en planta del mismo pie.",
+        "gold_summary": "Se reporta el caso de un hombre de 31 años que presenta este síndrome luego de la aplicación de penicilina benzatínica intramuscular. La biopsia apoyó el diagnóstico. Recibió tratamiento con enoxaparina y cilostazol con posterior mejoría.",
+        "synthetic_summary": {
+            "B1": "Un hombre de 31 años recibió una inyección de penicilina en la nalga. Poco después tuvo mucho dolor en esa zona y apareció una mancha grande y morada en la piel. También tuvo una pequeña llaga en el escroto y una lesión en la planta del pie.\n\nLas pruebas de sangre mostraron inflamación y que algunos músculos y el hígado estaban dañados. Las pruebas para sífilis y otros virus fueron negativas. Los médicos pensaron que tenía síndrome de Nicolau. Esto es una reacción rara después de una inyección que puede dañar la piel y el músculo.\n\nLe hicieron una biopsia (tomaron un pedacito de piel) que mostró daño en la piel y apoyó el diagnóstico. Lo trataron con medicamentos para mejorar la circulación y evitar coágulos (enoxaparina), con otro que ayuda la sangre a fluir mejor (cilostazol) y con analgésicos para el dolor. Con el tratamiento mejoró mucho. Las pruebas de sangre volvieron casi a la normalidad.\n\nAl salir del hospital quedó con pequeñas cicatrices y algo de piel seca en la nalga y en la planta del pie, y tenía menos dolor. Fue un caso raro, pero con tratamiento el hombre se recuperó. Si alguien siente mucho dolor o ve una lesión después de una inyección, debe avisar al médico.",
+            "B2": "Here is a clear, reader-friendly summary of the case:\n\nA 31-year-old man developed a painful skin and muscle problem after receiving an intramuscular injection of benzathine penicillin. He had pain in his right buttock that spread down to his foot. At the injection site a large purplish, ring-shaped plaque formed (15 cm across), with healthy-looking skin in the middle. He also had a small scab on the scrotum and a wide, net-like discolored area on the sole of the right foot.\n\nTests and imaging\n- Ultrasound of the buttock showed swelling and loss of the normal muscle pattern, and swelling under the skin. Swelling was also seen in the sole and scrotum.\n- Blood tests showed signs of inflammation and marked muscle injury: white blood cell count slightly high, CRP (an inflammation marker) elevated, and very high muscle enzymes (creatine kinase and LDH). Liver enzymes were also raised but later improved.\n- Tests for syphilis, HIV, hepatitis B and C were negative.\n\nDiagnosis and what it means\n- Based on the timing, how the symptoms developed, and a skin biopsy, doctors diagnosed Nicolau syndrome (also called medicamentous cutaneous embolism). This is a rare reaction after an injection that can cause blockage of small blood vessels and local tissue damage, leading to severe pain, skin necrosis (dead skin), and swelling.\n\nTreatment and outcome\n- He was treated with a blood thinner (enoxaparin), cilostazol (a medicine that can improve blood flow), and pain control (tramadol) for 10 days. The skin biopsy showed dead skin cells and damage around hair follicles, but no clear blood-vessel inflammation or clot in the sampled tissue, which fit the diagnosis.\n- His pain and lab tests improved: muscle and liver enzymes fell toward normal. He was discharged with cilostazol and pain medicines.\n- At 3-month follow-up he was much better. The main lasting effects were discolored scars at the right buttock and foot, with some flaky skin and small remaining mottled areas on the sole.\n\nNotes for readers\n- Nicolau syndrome is uncommon but can happen after injections. Early recognition and treatment can limit damage. If someone has severe pain, changing color, or skin breakdown after an injection, they should seek medical care right away.",
+            "B3": "Resumen clínico (nivel universitario)\n\nPresentación\n- Hombre de 31 años con antecedentes de consumo de alcohol, tabaco y cocaína inhalada, tuberculosis pulmonar tratada, nefrectomía izquierda y esplenectomía por trauma.\n- Una semana después de recibir una inyección intramuscular de penicilina benzatínica (administrada por exposición sexual a una pareja con sífilis), desarrolló dolor intenso en glúteo derecho irradiado al pie y, posteriormente, lesiones cutáneas purpúricas en el sitio de inyección.\n\nHallazgos clínicos y complementarios\n- Lesión principal: placa anular de 15 cm en glúteo derecho, bordes irregulares y aspecto racemoso, con piel sana en el centro.\n- Otras lesiones: pequeña escara escrotal y extensa lesión livedoide en la planta del pie derecho que abarcaba desde la región talar hasta las puntas de los dedos.\n- Ecografía: pérdida del patrón fibrilar y engrosamiento edematoso del glúteo mayor en su tercio medio; edema del tejido celular subcutáneo en zona plantar y escrotal.\n- Laboratorio: leucocitosis (13.7 × 10^9/L) y proteína C reactiva elevada (3.2 mg/dL) —indicadores de reacción inflamatoria—; marcadores de daño muscular marcadamente altos: AST 175 UI/L, ALT 245 UI/L, CK 2741 UI/L, LDH 2499 UI/L.\n- Serologías para sífilis (VDRL y pruebas treponémicas), VIH, hepatitis B y C: todas negativas.\n\nDiagnóstico\n- La combinación de inicio inmediato tras la inyección, la apariencia cutánea y la biopsia condujeron al diagnóstico de síndrome de Nicolau (también llamado embolia cutis medicamentosa).  \n- Biopsia cutánea: necrosis epidérmica que llega hasta epitelio folicular y formación de ampolla secundaria a reepitelización; no se observó vasculitis ni trombosis vascular, hallazgo compatible con fase aguda de embolia cutis medicamentosa.\n\nTratamiento y evolución\n- Tratamiento instaurado: anticoagulación con enoxaparina subcutánea (1 mg/kg cada 12 h), cilostazol 100 mg cada 12 h y analgesia (tramadol) durante 10 días.\n- Respuesta: mejoría clínica y marcadores bioquímicos (AST 39 UI/L, ALT 77 UI/L, CK 167 UI/L), alta hospitalaria con cilostazol y analgésicos.\n- Seguimiento a 3 meses: disminución del dolor y de las lesiones; secuelas residuales: cicatriz discrómica y descamación fina en glúteo derecho; en planta del pie derecho cicatriz discrómica con descamación gruesa en zona de apoyo tarsometatarsiana y pequeñas áreas livedoides.\n\nPuntos clave e implicaciones\n- El síndrome de Nicolau es una complicación rara pero grave de inyecciones intramusculares que provoca isquemia y necrosis en el tejido local; el diagnóstico se basa en la historia temporal, el examen y la biopsia.\n- En este caso hubo afectación muscular y elevación enzimática importante, lo que sugiere compromiso más allá de la piel; la respuesta favorable a anticoagulación y vasodilatación (cilostazol) es consistente con un proceso isquémico/embólico reversible en su fase aguda.\n- Las serologías negativas indican que la penicilina se administró por exposición, no por confirmación serológica de sífilis.\n- No se completó un perfil inmunológico porque el equipo consideró que la presentación clínica y la biopsia justificaban el diagnóstico sin buscar otras etiologías.\n\nRecomendaciones prácticas (consideraciones para el seguimiento)\n- Continuar vigilancia clínica de las secuelas cutáneas y dolor; cuidado local de la piel para evitar infección.  \n- Valoración por dermatología y, si la cicatriz es funcional o estéticamente problemática, considerar evaluación por cirugía plástica.  \n- Si aparecieran signos de infección o empeoramiento, reconsulta urgente.  \n- En futuros procedimientos intramusculares, notificar a los profesionales de salud sobre este antecedente para evitar riesgo de recurrencia.\n\nEste resumen respeta la evolución y decisiones del equipo tratante y subraya que el paciente mejoró con tratamiento conservador, quedando secuelas cutáneas residuales que requieren manejo y seguimiento."
+        }
+    },
+    {
+        "article": "Un varón de cuatro días de edad, nacido a las 39 semanas y 4 días de gestación, acude a un servicio de urgencias con un empeoramiento de la dificultad respiratoria y el estridor, que se ve agravado por la alimentación y la posición supina.\n\nNació de una madre de 31 años con serología significativa para una prueba de Coomb positiva indirecta, con un parto vaginal sin complicaciones y puntuaciones de APGAR de ocho y nueve en el primer y quinto minuto, respectivamente. Su peso al nacer fue de 3050 g. La ecografía fetal mostró preocupación por un foco intracardíaco, con un embarazo sin complicaciones. El curso de enfermería fue significativo solo por una prueba de audición bilateral fallida y un ecocardiograma normal. El bebé fue dado de alta en el día dos de vida. Se observó que tenía congestión nasal en el momento de la descarga. Se instruyó a la familia para que le aspirara la nariz y usara gotas salinas según fuera necesario.\n\nEn el día cuatro de vida, la madre del lactante notó estridor asociado con dificultad para alimentarse y el pediatra lo derivó al servicio de urgencias. El examen en el servicio de urgencias es significativo para el estridor inspiratorio agudo con tirones traqueales y retracciones subcostal. Además, se observa que tiene pectus excavatum. El estridor y el aumento del trabajo respiratorio mejoran con la posición prona o lateral. La evaluación de laboratorio es significativa para la acidosis respiratoria en el gas sanguíneo venoso [pH 7.18 y CO2 73 mmHg (9,732 Pa)] y el análisis de orina que revela bacterias moderadas y 11-20 glóbulos blancos sin la presencia de nitrito urinario o esterasa leucocitaria. Un recuento sanguíneo completo es tranquilizador. Se le coloca una cánula nasal de alto flujo y se inicia con ampicilina y gentamicina después de obtener cultivos de sangre.\n\nSe le aumentó la presión positiva continua en la vía aérea (CPAP) y se lo trasladó a una unidad de cuidados intensivos neonatales de nivel III para continuar con el tratamiento y la evaluación de otorrinolaringología. Se le introdujo un tubo nasogástrico por las dos fosas nasales sin dificultad. La laringoscopia flexible mostró una cuerda vocal izquierda inmóvil y cavidades nasales estrechas con edema de los cornetes nasales, aritenoides bilaterales y cuerdas vocales. La broncoscopia no reveló ninguna otra anormalidad. El examen físico posterior se caracterizó por rasgos dismórficos sutiles, que incluían orejas de implantación baja, retromicrognatia, microftalmia y clinodactilia de los dedos de los pies. Se interrumpió el tratamiento antibiótico empírico tras un examen infeccioso tranquilizador. Se consultó a un equipo multidisciplinario.\n\nEl paciente finalmente requirió intubación a las dos semanas de vida debido al empeoramiento del fallo respiratorio. Se administraron ciprofloxacina nasal y dexametasona para el edema de las vías respiratorias superiores. Una resonancia magnética del cerebro, cuello y tórax mostró un curso normal de los nervios laríngeos recurrentes. La evaluación genética incluyó un análisis de microarreglo cromosómico normal (CMA). La prueba adicional del panel genético fue positiva para la variante patogénica en el gen CHD7, consistente con el síndrome CHARGE. En este caso, el VFP se atribuyó a la asociación conocida con el síndrome CHARGE. La evaluación continua reveló otras características consistentes con el síndrome CHARGE, incluidos colobomas bilaterales, glaucoma, pérdida auditiva confirmada y anomalías genitales.\n\nLa repetición de la broncoscopia en el día 42 de vida demostró una mejora en el edema laríngeo general, pero continuó con un edema leve de las cuerdas vocales bilaterales. El paciente fue extubado después de la broncoscopia en el marco de un edema de las vías respiratorias mejorado. Sin embargo, fue re-intubado el día 46 de vida debido al empeoramiento de la insuficiencia respiratoria. La repetición de la laringoscopia ese día mostró un edema continuado. En este momento, el paciente ya había recibido múltiples ciclos cortos de Dexamethasone en un intento de disminuir el edema de las vías respiratorias. Debido a la necesidad de re-intubación, fue tratado con Tobramycin tópico y Dexamethasone aplicado directamente a las cuerdas vocales mediante laringoscopia directa durante cinco días. Después de este tratamiento, fue extubado con éxito a los dos meses de edad y se le colocó un tubo de gastrostomía a los tres meses.\n\nEn el momento de la colocación del tubo de gastrotomía, se le realizó una broncoscopia y una microlaringoscopia adicionales que demostraron que la cuerda vocal izquierda afectada originalmente era totalmente móvil, pero que mostraba una nueva inmovilidad de la cuerda derecha; la etiología de esto no está clara. Ambas cuerdas vocales seguían estando ligeramente edematosas, pero habían mejorado mucho desde la evaluación anterior. El paciente fue dado de alta en aire ambiente a los cuatro meses de edad y continúa siendo seguido de cerca por el otorrinolaringólogo. En la laringoscopia ambulatoria de repetición a los cuatro meses de edad, ambas cuerdas aparecían móviles con un edema de las vías respiratorias continuado.\n\n",
+        "gold_summary": "Un bebé de cuatro días de edad, a término, varón, nacido por parto vaginal sin complicaciones, con un curso de enfermería significativo para la falta de audición, se presentó en un departamento de emergencias (DE) con dificultad respiratoria y estridor en aumento. Fue trasladado a una unidad de cuidados intensivos neonatales (UCIN) de nivel III para una evaluación posterior y se le practicó una intubación debido a la hipercarbia progresiva. La laringoscopia reveló una parálisis unilateral de las cuerdas vocales (PCV) del lado izquierdo. Se le sometió a una evaluación posterior que incluyó un cerebro, cuello y tórax normales en una resonancia magnética. Se consultó a genética por la preocupación de los rasgos dismórficos en el examen físico. Después de las pruebas del panel de genes, la PCV se atribuyó a la asociación conocida con el síndrome CHARGE. Se observó un edema de las vías respiratorias en la laringoscopia que impidió la extubación hasta los dos meses de edad. Se identificaron otras características del síndrome CHARGE, incluidos los colobomas, el glaucoma, la pérdida auditiva neurosensorial y las anomalías genitales. Se le dio de alta con aire ambiente y después de la colocación de un tubo de gastrostomía con seguimiento de otorrinolaringología.\n",
+        "synthetic_summary": {
+            "B1": "Este es un resumen sencillo y amable del caso.\n\nUn bebé de cuatro días tenía mucha dificultad para respirar. Hacía un sonido fuerte al respirar (estridor). Comía mal y estaba peor cuando lo acostaban boca arriba. Nació a término y al principio parecía bien. En el hospital le hicieron pruebas y vieron que tenía mucho CO2 en la sangre, lo que significa que no respiraba bien.\n\nLos médicos usaron una máquina para ayudarle a respirar. Miraron dentro de su garganta con una cámara y vieron que una cuerda vocal (una de las dos pequeñas “telitas” que ayudan a hablar y a respirar) no se movía y que había hinchazón en la garganta. Le pusieron antibióticos al principio, pero luego los dejaron cuando las pruebas no mostraron infección.\n\nA las dos semanas el bebé empeoró y le pusieron un tubo para ayudarle a respirar mejor (intubación). Le hicieron una resonancia y los nervios grandes estaban normales, lo cual fue una buena noticia. También hicieron pruebas genéticas y encontraron un cambio en un gen llamado CHD7. Ese cambio explica que el bebé tiene el síndrome CHARGE. Ese síndrome puede causar problemas en los ojos, la audición, la garganta y otras partes del cuerpo. En este bebé también encontraron problemas en los ojos, pérdida de audición y algunas diferencias en los genitales.\n\nLa hinchazón en la garganta hizo difícil quitar el tubo por varias semanas. Usaron medicinas y trataron la garganta directamente con medicamentos. A los dos meses pudieron quitar el tubo y a los tres meses le pusieron un tubito para darle comida directo al estómago porque comer seguía siendo difícil. Al principio solo la cuerda vocal izquierda estaba paralizada, luego mejoró, y por un tiempo la cuerda derecha también dejó de moverse; los médicos no saben por qué pasó eso. Al final, a los cuatro meses, las dos cuerdas vocales ya se movían y el bebé pudo irse a casa respirando aire normal. Sigue con control del otorrinolaringólogo (especialista de garganta y oídos).\n\nEn palabras simples: el bebé tuvo problemas de respiración por la hinchazón y por una cuerda vocal que no se movía. Los médicos le ayudaron a respirar, lo cuidaron con medicinas y pruebas, y encontraron que tenía el síndrome CHARGE. Poco a poco mejoró y pudo volver a casa.",
+            "B2": "Summary (B2 level)\n\nA baby boy, born at full term and healthy at birth, came to the emergency room at four days old because he had loud noisy breathing (called stridor) and trouble feeding. The noisy breathing was worse when he lay on his back and during feeding, and got better when he was placed on his side or stomach.\n\nOn arrival he had signs of poor breathing and a blood test showed respiratory acidosis (high carbon dioxide in the blood), so he was given support with high-flow oxygen and later CPAP (a breathing machine that helps keep the airway open). Ear–nose–throat doctors (ENT) looked inside his throat with a flexible scope and found that his left vocal cord was not moving (vocal fold paralysis). When a vocal cord does not move it can make breathing and swallowing hard. His nasal passages were also narrow and swollen. Other small physical differences were found, for example low-set ears, small jaw, small eyes, and toe differences.\n\nBecause of worsening breathing, he needed a breathing tube (intubation) at two weeks of age. An MRI of the brain, neck and chest was normal for the nerves that go to the larynx. Genetic tests first showed a normal chromosome microarray, but a later gene panel found a disease-causing change in the CHD7 gene, which confirmed CHARGE syndrome. CHARGE is a genetic condition that can cause eye problems (colobomas), hearing loss, heart and genital differences, and facial and airway anomalies. In this baby the diagnosis explained the vocal cord paralysis and other features (colobomas, glaucoma, confirmed hearing loss, and genital differences).\n\nHe had repeated scopes and treatment for airway swelling, including steroid medicine and topical antibiotic applied to the vocal cords. Over time the swelling got much better. The left cord, which had been immobile, later moved again, and at times both cords were moving on follow-up exams. He was successfully taken off the breathing tube at about two months. Because he had ongoing feeding problems, a feeding tube into the stomach (gastrostomy) was placed at three months. He was discharged home breathing room air at four months and continues close follow-up with ENT and genetics.\n\nWhat this means and next steps\n- Vocal cord paralysis in newborns can cause serious breathing and feeding problems. In this case it was part of CHARGE syndrome.  \n- Children with CHARGE need multiple specialists: ENT, genetics, eye and hearing doctors, and feeding teams.  \n- The baby received breathing support, medicines to reduce airway swelling, and a feeding tube until he could feed safely. Ongoing follow-up will monitor breathing, voice, hearing, vision and development, and help plan future care.  \n\nThis was a stressful and complex condition for the family, but the team managed the airway and feeding needs while identifying the underlying genetic cause so the baby can get the right long-term care.",
+            "B3": "Resumen clínico (lectores universitarios)\n\nPresentación y curso inicial\nUn recién nacido varón a término (39+4 semanas), con parto eutócico y pruebas de Apgar normales, fue dado de alta al día 2 pero reingresó a los 4 días por estridor inspiratorio y dificultad para alimentarse, empeoradas en decúbito supino y al alimentarse. En urgencias presentaba tiraje y signos de insuficiencia respiratoria; la gasometría mostró acidosis respiratoria (pH 7,18; pCO2 73 mmHg). Se inició soporte respiratorio (cánula nasal de alto flujo y luego CPAP), se obtuvieron cultivos y se administraron antibióticos empíricos que se suspendieron tras descartar infección significativa.\n\nHallazgos otorrinolaringológicos y anatómicos\nLa laringoscopia flexible mostró parálisis de la cuerda vocal izquierda (parálisis vocal unilateral) junto con edema laríngeo y estrechez nasal por edema de los cornetes. La broncoscopia no mostró otras anormalidades. Estudios por imagen (RM de cerebro, cuello y tórax) no identificaron anomalía en el trayecto de los nervios laríngeos recurrentes. El examen físico también reveló rasgos dismórficos sutiles: orejas de implantación baja, retromicrognatia, microftalmia y clinodactilia podal.\n\nEvolución y manejo\nA las dos semanas el paciente precisó intubación por empeoramiento respiratorio. Se administraron corticoides sistémicos y tratamientos tópicos (antibiótico nasal y posteriormente aplicación directa de dexametasona y tobramicina sobre las cuerdas vocales) para reducir el edema laríngeo. Tras varios intentos de extubación exitosos y reintubaciones, finalmente fue extubado de forma sostenida alrededor de los 2 meses. Se colocó una sonda de gastrostomía a los 3 meses por seguridad alimentaria. Repetidas laringoscopias mostraron mejoría progresiva del edema; la movilidad de las cuerdas vocales cambió en el tiempo (recuperación de la izquierda y, de forma transitoria, inmovilidad derecha), y a los 4 meses ambas cuerdas eran móviles con edema residual. El alta se produjo en aire ambiente con seguimiento otorrinolaringológico ambulatorio.\n\nDiagnóstico etiológico y hallazgos asociados\nEl cariotipo microarray fue normal, pero un panel genético identificó una variante patogénica en el gen CHD7, diagnóstico compatible con síndrome CHARGE. Tras esto se detectaron otras manifestaciones típicas del síndrome: colobomas bilaterales, glaucoma, hipoacusia confirmada y anomalías genitales. La parálisis vocal en este caso se interpretó como parte de las manifestaciones del síndrome CHARGE más que como lesión quirúrgica o nerviosa focal identificable por imagen.\n\nImplicaciones y seguimiento\n- Las parálisis de cuerdas vocales en recién nacidos pueden provocar compromiso respiratorio y dificultades de alimentación; requieren manejo multidisciplinario urgente (neonatología, otorrinolaringología, genética, audiología, oftalmología y, según el caso, cirugía pediátrica/urología).  \n- El diagnóstico de CHARGE implica vigilancia y tratamiento multisistémico a largo plazo: corrección/rehabilitación visual y auditiva, control del crecimiento y desarrollo, manejo de anomalías genitales y nutricionales, y planificación de soporte respiratorio o intervenciones laríngeas si la obstrucción persiste.  \n- El pronóstico laríngeo es variable; en este caso hubo recuperación funcional con tratamiento conservador y procedimientos endoscópicos locales, pero algunos pacientes precisan traqueostomía o intervenciones quirúrgicas si la obstrucción o la aspiración alimentaria son persistentes.\n\nComentario final (empático)\nEste caso ilustra cómo una presentación respiratoria neonatal aparentemente aislada puede ser la primera señal de un síndrome genético multisistémico. La coordinación rápida entre equipos y el diagnóstico genético permitieron orientar el seguimiento y las intervenciones necesarias para proteger la vía aérea, la nutrición y el desarrollo del niño."
+        }
+    },
+    {
+        "article": "Mujer de 17 años oriunda de Tucumán, acudió a la consulta por cuadro de vías aéreas superiores y hemoptisis leve. La tomografía computarizada de tórax informó, en lóbulo superior derecho, una imagen redondeada de paredes regulares y lisas de 25x24x24 mm, rodeado de un tenue halo periférico en vidrio esmerilado. No se observaba realce ante la administración de contraste endovenoso. Se sugirió un posible quiste broncogénico, por lo que se realizó una RMN de tórax que informó imagen redondeada de paredes regulares y lisas que alcanzó un diámetro anteroposterior de 25 x 24 x 24.5 mm con intensidad de señal líquida. Debido a la localización central de la lesión, se realizó una lobectomía superior derecha videoasistida. Dado que el estudio anatomopatológico intraoperatorio fue indeterminado, se complementó la resección pulmonar con un vaciamiento ganglionar mediastínico. La anatomía patológica definitiva informó neumocitoma esclerosante de 2 x 1.7 cm. La inmunomarcación fue positiva para TTF1, CK, CK7 y napsina.",
+        "gold_summary": "Describimos aquí el caso de una paciente de 17 años con diagnóstico de neumocitoma esclerosante con presentación infrecuente.",
+        "synthetic_summary": {
+            "B1": "Resumen sencillo y amable:\n\n- Una joven de 17 años vino al médico porque tenía mocos y tos. También sacó un poco de sangre al toser.  \n- Le hicieron una tomografía y una resonancia. Vieron una bolita redonda de unos 2.5 cm en la parte superior del pulmón derecho.  \n- Al principio pensaron que podía ser un quiste. Como la bolita estaba en una zona difícil, los médicos quitaron la parte superior del pulmón derecho usando una cirugía con cámara (una operación menos grande que la abierta).  \n- Durante la operación, la prueba rápida no dio un resultado claro. Por eso, además quitaron algunos ganglios cercanos para estudiar mejor.  \n- El examen final del tejido dijo que la bolita era un neumocitoma esclerosante. Es un tipo de tumor del pulmón que se encontró en esta paciente.  \n- Hicieron pruebas especiales en el tumor que dieron positivo para varias proteínas (TTF1, CK, CK7 y napsina). Esas pruebas ayudaron a confirmar el diagnóstico.  \n\nEste caso muestra a una persona joven con un tumor poco común en el pulmón. La cirugía permitió quitar la lesión y obtener el diagnóstico.",
+            "B2": "A 17-year-old woman from Tucumán went to the doctor because of upper respiratory symptoms and a small amount of coughing up blood. A chest CT scan found a round, smooth-walled lesion about 2.5 cm wide in the right upper lung lobe, with a faint “ground-glass” halo around it. The lesion did not take up contrast, so doctors first thought it might be a bronchogenic cyst (a fluid-filled birth-related lung cyst). An MRI showed the mass had a fluid-like signal and the same size.\n\nBecause the lesion was centrally located in the lung, surgeons removed the right upper lobe using a minimally invasive video-assisted technique (VATS lobectomy). The quick exam of tissue taken during surgery (frozen section) could not give a clear diagnosis, so the team also removed nearby mediastinal lymph nodes to check for spread. The final pathology report identified the tumor as a sclerosing pneumocytoma (also called pneumocitoma esclerosante) measuring about 2 x 1.7 cm. This is a rare lung tumor that is usually benign; special lab stains (TTF‑1, cytokeratins CK and CK7, and napsin) were positive and supported a lung origin.\n\nThis case is unusual because sclerosing pneumocytoma typically appears in older adults, not teenagers. The standard treatment is surgical removal, which was done here. After a complete resection with negative lymph nodes, the usual next steps are routine follow-up visits and imaging to watch for any recurrence. Overall prognosis is generally good after full removal.",
+            "B3": "Presentamos el caso de una mujer de 17 años que consultó por síntomas de vías respiratorias superiores y hemoptisis leve. La tomografía computada de tórax mostró en el lóbulo superior derecho una lesión redondeada, de paredes lisas, de aproximadamente 25 x 24 x 24 mm, con un tenue halo periférico en vidrio esmerilado; no hubo realce tras contraste intravenoso. Una resonancia confirmó una lesión bien delimitada con señal compatible con contenido líquido. Inicialmente se planteó como posible quiste broncogénico, pero por la localización central de la lesión se decidió realizar una lobectomía superior derecha asistida por video (VATS).\n\nDurante la cirugía, el estudio anatomopatológico intraoperatorio (congelación) no fue concluyente, por lo que se completó la resección con vaciamiento ganglionar mediastínico. El examen histopatológico definitivo identificó un neumocitoma esclerosante de 2 x 1,7 cm. La inmunohistoquímica fue positiva para TTF‑1, CK, CK7 y napsina A, un perfil que apoya el origen pneumocítico de la lesión.\n\nComentarios clínicos y manejo: el neumocitoma esclerosante es un tumor pulmonar poco frecuente que suele aparecer en mujeres jóvenes y suele comportarse de forma benigna; sin embargo, puede simular quistes o neoplasias malignas en estudios por imagen. La resección quirúrgica completa suele ser curativa y, cuando el diagnóstico no es claro en el intraoperatorio, puede justificarse ampliar el acto quirúrgico (por ejemplo, con vaciamiento ganglionar) para asegurar un tratamiento definitivo. El pronóstico después de resección completa es generalmente excelente, aunque se recomienda seguimiento clínico e imágenes periódicas para vigilar recidiva o complicaciones."
+        }
+    },
+    {
+        "article": "Una mujer asiática de 28 años fue admitida en el hospital para el tratamiento de «una masa pélvica durante 10 meses» el 11 de noviembre de 2018. La paciente solía tener menstruación regular, volumen menstrual moderado, dismenorrea y un G1P0L0A1. Examen ginecológico: la parte posterior del útero tenía aproximadamente 8 cm de diámetro con poca actividad y sensibilidad, pero no se observaron otras anomalías. La paciente no tenía una causa obvia de dolor abdominal durante los primeros 10 meses previos al ingreso. El examen de ultrasonido reveló una masa heterogénea en la parte superior derecha del útero con un diámetro de aproximadamente 4 cm, un nódulo del epiplón mayor con un diámetro de aproximadamente 2 cm y un nivel de CA125 sérico de 416 mU/mL. Se diagnosticó como «endometriosis, masas pélvicas inflamatorias». Se administró una terapia de rehidratación antiinfecciosa y se dio de alta a la paciente con alivio del dolor. Dos semanas después del alta, el nivel de CA125 sérico de la paciente disminuyó a 106 mU/mL y volvió a la normalidad después de 6 semanas. Sin embargo, la masa pélvica aumentó gradualmente. El reexamen de la ecografía pélvica realizada mostró una masa ecoica mixta de 7.7 cm x 7.4 cm x 8.2 cm en el lado derecho del útero con un límite claro, eco puntiforme fino en el quiste y derrame abdominal y pélvico. La ecografía de contraste mostró que la pared del quiste de la masa pélvica estaba significativamente mejorada, se sospechaba malignidad y se recomendó un tratamiento quirúrgico. El 14 de noviembre de 2018, la paciente se sometió a liberación de adherencias pélvicas e intestinales transabdominales, omento, ovarios bilaterales, peritoneo multipunto y múltiples adenomiosis y histerectomía. Durante la operación, se aspiraron aproximadamente 600 ml de ascitis hemorrágica. Tras la exploración, se observó una masa de color rojo grisáceo con un diámetro de aproximadamente 8 cm en la superficie del epiplón mayor, que era suave y se asemejaba a carne podrida. Se encontraron depósitos de celulosa marrón difusos en la superficie del útero, ovarios bilaterales, pared abdominal, tracto intestinal, surco lateral del recto y pared anterior del recto. Las lesiones no se eliminaron por completo y algunas áreas se electrocoagularon. El examen patológico de la muestra resecada mostró endometriosis del tejido retiniano con vasodilatación, ampollas, infiltración linfocítica difusa y focal, folículos ováricos císticos bilaterales, fibrosis peritoneal dentro de la necrosis del tejido adiposo, proliferación de fibroblastos, aumento de la infiltración de células espumosas y adenomiosis uterina. La patología de ascitis mostró muchos glóbulos rojos, un pequeño número de linfocitos y neutrófilos y ninguna célula tumoral. Después de la operación, la paciente se recuperó sin problemas y se trató con agonista de la hormona liberadora de gonadotropina (GnRH-α). Se inició leuprorelina una vez al mes durante 6 meses, seguido de dienogest oral (DNG) durante 3 años, después de lo cual se interrumpió la medicación durante 3 meses. La paciente concibió de forma natural y tuvo un embarazo normal. Se dio a luz a un bebé de 3300 g por vía vaginal a las 39 semanas + 3 días de gestación. Tanto la madre como el bebé estaban sanos, sin recurrencia ni reacciones adversas durante el seguimiento.\n\nMH - Humanos\nMH - Mujer\nMH - *Endometriosis/complicaciones/terapia\nMH - Adulto",
+        "gold_summary": "Preocupaciones de la paciente: Una mujer de 28 años de edad vino a nuestro hospital para recibir tratamiento debido al descubrimiento de una masa pélvica 10 meses antes. Después de la admisión, la paciente se sometió a tratamiento quirúrgico y fue dada de alta en 1 semana. Recibió tratamiento médico durante 3 años después del alta. Después de la retirada de la medicación, la paciente quedó embarazada y dio a luz a un niño sin recurrencia durante el seguimiento.\n\nDiagnósticos: Los diagnósticos iniciales al ingreso fueron «¿masa pelviana inflamatoria?» y «¿endometriosis?». Después de 10 meses, la paciente volvió a ser internada en el hospital debido a un aumento gradual de la masa, y se le diagnosticó endometriosis.\n\nIntervenciones: El paciente fue tratado con terapia antiinfecciosa de rehidratación por primera vez, y el paciente fue tratado quirúrgicamente por segunda vez, seguido de agonista de la hormona liberadora de gonadotropina (GnRH-α) y tratamiento con dienogest (DNG) después de la cirugía.\n\nResultados: Después de 6 ciclos de tratamiento con GnRH-α y 3 años de tratamiento con DNG, un hijo nació con éxito tras la interrupción de la medicación y, hasta ahora, no se han producido reacciones adversas ni recurrencias durante el período de seguimiento.\n",
+        "synthetic_summary": {
+            "B1": "Una mujer de 28 años tuvo una bolita y dolor en la tripa durante 10 meses. Los médicos vieron en una ecografía una masa cerca del útero. También midieron una prueba en la sangre que estaba alta al principio, pero volvió a la normalidad después.\n\nLos médicos pensaron que era endometriosis. Eso quiere decir que un tejido que normalmente está dentro del útero estaba creciendo en otros sitios del cuerpo. A veces esto causa bultos, dolor y líquido en la barriga.\n\nLa mujer tuvo una operación. Se sacó líquido de la barriga y se quitó la masa que encontraron. Los exámenes del tejido demostraron que no había cáncer. Confirmaron que era endometriosis.\n\nDespués de la operación recibió medicinas para controlar la endometriosis: inyecciones una vez al mes durante 6 meses y luego una pastilla por 3 años. Tres meses después de dejar las medicinas, quedó embarazada de forma natural. Tuvo un parto normal a las 39 semanas. El bebé pesó 3300 g. Madre y bebé están sanos. No ha vuelto la enfermedad durante el seguimiento.",
+            "B2": "Resumen claro y amable\n\nQué sentía la paciente:\n- Una mujer de 28 años acudió al hospital porque le habían encontrado una masa en la pelvis hacía 10 meses. Tenía regla regular, dolor menstrual (dismenorrea) y no había una causa clara para su dolor abdominal al principio.\n\nQué encontraron los médicos:\n- Ecografía inicial: una masa heterogénea cerca del útero (unos 4 cm) y un pequeño nódulo en el epiplón (2 cm).\n- Análisis de sangre: CA125 elevado (416 mU/mL). CA125 es una sustancia que puede aumentar en enfermedades como la endometriosis o en algunos cánceres, pero no es una prueba definitiva.\n- Tras un primer tratamiento para aliviar el dolor e infección, el CA125 bajó y se normalizó en unas semanas. Sin embargo, la masa siguió creciendo hasta medir alrededor de 8 cm, y hubo líquido en el abdomen (ascitis).\n\nDecisión y operación:\n- Debido al crecimiento de la masa y a que la imagen sugería posible malignidad, se realizó una cirugía el 14 de noviembre de 2018.\n- En la operación se encontraron aproximadamente 600 ml de líquido con sangre en el abdomen y una masa en el epiplón (tejido graso del abdomen). Había además muchas pequeñas lesiones oscuras (depósitos de «celulosa» típicos de endometriosis) en la superficie del útero, ovarios, peritoneo y partes del intestino.\n- No se pudieron quitar todas las lesiones; algunas se trataron con electrocoagulación (quemado controlado para destruir tejido).\n\nResultados de la biopsia:\n- El examen de los tejidos confirmó endometriosis en el epiplón y cambios relacionados (fibrosis, necrosis grasa, células inflamatorias). También se observó adenomiosis (cuando tejido parecido al que recubre el útero crece dentro del músculo uterino).\n- El líquido del abdomen no mostró células tumorales, lo que ayuda a descartar cáncer.\n\nTratamiento después de la operación:\n- Buena recuperación postoperatoria.\n- Tratamiento hormonal: 6 inyecciones mensuales de un agonista de la hormona liberadora de gonadotropina (GnRH-α, leuprorelina) y luego dienogest por vía oral durante 3 años. Estas medicaciones reducen la actividad de la endometriosis y el dolor.\n\nEvolución y resultado final:\n- Tras suspender la medicación durante 3 meses, la paciente quedó embarazada de manera natural.\n- Tuvo un embarazo normal y dio a luz por vía vaginal a término a un bebé sano de 3300 g.\n- En el seguimiento no hubo recurrencia de la enfermedad ni efectos adversos reportados.\n\nMensaje final (con calma):\n- Este caso muestra que la endometriosis puede producir masas grandes y líquido en el abdomen, pero con cirugía adecuada, confirmación por biopsia y tratamiento hormonal prolongado, una mujer joven pudo recuperarse y lograr un embarazo sano. Si te interesa saber más sobre qué es la endometriosis o cómo afectan estos tratamientos a la fertilidad, puedo explicarlo de forma sencilla.",
+            "B3": "Summary (college-level, empathetic tone)\n\nPresentation and background\n- A 28‑year‑old Asian woman presented with a pelvic mass that had been present for about 10 months. She reported regular menstrual cycles with moderate flow and painful periods (dysmenorrhea). There was no clear trigger for abdominal pain during the initial 10 months.\n\nKey findings (abnormal vs normal)\n- Abnormal:\n  - Pelvic mass on ultrasound that grew from about 4 cm to roughly 8 cm over time.\n  - An omental nodule (~2–8 cm) and approximately 600 mL of hemorrhagic ascites (blood‑tinged fluid in the abdomen) found at surgery.\n  - Serum CA125 was markedly elevated to 416 U/mL on admission, fell to 106 U/mL two weeks later and normalized by six weeks.\n  - Contrast ultrasound suggested cyst wall enhancement and raised concern for possible malignancy.\n- Normal/benign findings:\n  - Cytology of the ascitic fluid showed many red blood cells and only small numbers of inflammatory cells; no malignant cells were found.\n\nInterventions\n- Initial conservative treatment included rehydration and anti‑infective therapy, which relieved pain and reduced CA125 levels.\n- Because the pelvic mass enlarged and imaging raised concern, she underwent abdominal surgery for release of pelvic and intestinal adhesions, removal or treatment of omental and peritoneal lesions, and coagulation of residual implants. (The operative report described multiple brown “powder‑burn” implants typical of endometriosis.)\n- Post‑operative medical therapy to suppress endometriosis was given: monthly GnRH‑agonist (leuprorelin) for 6 months, followed by oral dienogest for 3 years.\n\nPathology\n- Surgical specimens showed extensive endometriosis involving the omentum and peritoneum, with vascular dilation, inflammatory cell infiltrates, peritoneal fibrosis and foamy cell changes; the uterus showed adenomyosis (endometrial tissue within the uterine muscle). No cancer cells were identified in the ascitic fluid.\n\nOutcome\n- Recovery from surgery was uncomplicated.\n- After finishing hormonal treatment and a 3‑month medication break, the patient conceived naturally and had an uneventful full‑term vaginal delivery (3,300 g infant) at 39+3 weeks.\n- During follow‑up there was no reported recurrence of disease or treatment‑related adverse effects.\n\nClinical points and implications\n- Endometriosis can mimic ovarian or peritoneal malignancy on imaging and can produce very high CA125 and hemorrhagic ascites; these findings are not specific for cancer and require tissue diagnosis when imaging is suspicious.\n- The case illustrates effective combined management: surgical removal or ablation of disease burden followed by prolonged hormonal suppression to reduce recurrence risk and preserve fertility.\n- For patients with similar findings, recommended next steps typically include regular follow‑up (clinical exam and symptom assessment, targeted imaging as needed), fertility counselling if pregnancy is desired, and discussion of long‑term medical options to manage recurrence and symptoms.\n\nIf you would like, I can summarize the pathology in simpler terms, outline the typical side effects and monitoring needs for leuprorelin and dienogest, or suggest key questions to discuss with a treating gynecologist."
+        }
+    },
+    {
+        "article": "Presentamos una paciente de 76 años de edad, que es traída al servicio de urgencias por bajo nivel de conciencia con tendencia al sueño.\n\nComo antecedentes médicos de interés destaca una enfermedad pulmonar intersticial difusa, dislipemia e hipertensión arterial.\n\nA la exploración física el paciente se encuentra estuporosa, arreactiva, con atonía de las 4 extremidades y desviación conjugada de la mirada hacia la derecha, sin fiebre y con una leve sequedad en piel y mucosas. La analítica sanguínea no muestra alteraciones significativas.\n\nEl paciente es valorado por el servicio de neurología que considera la realización de una TC cerebral urgente ante la sospecha de patología intracraneal de evolución aguda. Las pruebas de imagen ponen de manifiesto la presencia de numerosas burbujas aéreas que se disponen en los surcos cerebrales, cuerpo calloso y ambos tálamos así como áreas hipodensas cortico-subcorticales de distribución parcheada en hemisferio cerebeloso izquierdo y parietooccipitales bilaterales, todo ello compatible con isquemia cerebral subaguda secundaria a embolismo gaseoso.\n\nAnte los antecedentes personales de enfermedad pulmonar intersticial difusa se decide también realizar una placa de tórax en proyección anteroposterior y una TC torácica que objetivan un neumotórax apical izquierdo y aire ectópico en mediastino superior.\n\nSe decide el ingreso en la Unidad de Ictus del centro para control estrecho de constantes, sin embargo, la paciente presenta una evolución tórpida con el fallecimiento el segundo día de ingreso debido a fracaso multiorgánico.",
+        "gold_summary": "Paciente de 76 años con una enfermedad pulmonar intersticial difusa preexistente, que experimentó un ictus masivo debido a un neumomediastino espontáneo. Su presentación incluyó confusión, convulsiones y debilidad motora. Las pruebas de imagen revelaron burbujas de aire en los surcos cerebrales y áreas hipodensas en el cerebelo y parietooccipitales. Además, se observó neumotórax y aire en el mediastino superior en las radiografías de tórax y la tomografía torácica. A pesar de las medidas terapéuticas como el oxígeno hiperbárico, la paciente lamentablemente falleció debido al fallo multiorgánico.",
+        "synthetic_summary": {
+            "B1": "Esta historia trata de una mujer de 76 años que llegó al hospital porque estaba muy dormida y no respondía bien.\n\nElla ya tenía una enfermedad en los pulmones, además de colesterol alto y tensión alta. En la consulta estaba muy atontada, con los brazos y piernas muy flojos y la mirada fija hacia la derecha. Los análisis de sangre salieron normales.\n\nLas pruebas de imagen de la cabeza mostraron muchas burbujas de aire dentro del cerebro y zonas donde el cerebro no recibía bien la sangre. Los médicos dijeron que esto era un ictus provocado por burbujas de aire que viajaron por la sangre y taparon vasos del cerebro.\n\nComo ella tenía enfermedad pulmonar, hicieron placas y una tomografía del tórax. Vieron aire fuera del pulmón izquierdo (neumotórax) y aire en el espacio del medio del pecho (neumomediastino). Es probable que ese aire escapado de los pulmones haya entrado en la sangre y causado el problema en el cerebro.\n\nLa ingresaron en la unidad de ictus para vigilarla muy de cerca. Aun así, la paciente empeoró y falleció al segundo día por un fallo de varios órganos. Fue un caso grave y muy triste.",
+            "B2": "Resumen claro y cordial:\n\nUna mujer de 76 años con enfermedad pulmonar intersticial (una afección crónica del pulmón que daña el tejido y dificulta la respiración) fue traída a urgencias porque estaba muy somnolienta y con nivel de conciencia bajo. En la exploración estaba en estupor, no respondía bien, tenía flacidez en los cuatro miembros y la mirada desviada hacia la derecha. La analítica de sangre no mostró alteraciones relevantes.\n\nLa tomografía craneal urgente mostró muchas burbujas de aire dentro del cerebro (embolia gaseosa) y áreas oscuras en el cerebelo y en zonas parietooccipitales, hallazgos compatibles con lesiones por falta de riego sanguíneo (isquemia) debidas a esos émbolos de aire. Dado su antecedente pulmonar, se hicieron también radiografía y tomografía de tórax, que revelaron un neumotórax apical izquierdo (colapso parcial del pulmón por aire en el espacio pleural) y aire en el mediastino superior (neumomediastino).\n\nLa paciente ingresó en la Unidad de Ictus para vigilancia estrecha, pero su estado empeoró y falleció al segundo día por fallo multiorgánico. En casos como este, los médicos suelen investigar las causas del aire en el tórax y valorar medidas urgentes para intentar limitar el daño cerebral, aunque en este informe no se detallan otras intervenciones concretas. Lamento la triste evolución de la paciente.",
+            "B3": "Resumen clínico (nivel universitario)\n\nCaso: mujer de 76 años con enfermedad pulmonar intersticial difusa, dislipemia e hipertensión arterial, que ingresó por disminución del nivel de conciencia y somnolencia progresiva.\n\nExploración y pruebas:\n- Examen: estupor, no reactiva, hipotono en las cuatro extremidades y desviación conjugada de la mirada hacia la derecha; sin fiebre; leve sequedad de piel y mucosas.\n- Analítica sanguínea: sin alteraciones significativas.\n- TAC cerebral urgente: numerosas burbujas de aire en los surcos corticales, cuerpo calloso y ambos tálamos, y áreas hipodensas parcheadas cortico-subcorticales en el hemisferio cerebeloso izquierdo y en regiones parietooccipitales bilaterales. Estos hallazgos son compatibles con isquemia cerebral subaguda secundaria a embolismo gaseoso (embolismo por aire).\n- Radiografía y TAC torácica: neumotórax apical izquierdo y aire ectópico en el mediastino superior (neumomediastino).\n\nInterpretación y relación causal:\n- El cuadro se interpretó como un ictus masivo por embolismo aéreo cerebral, probablemente secundario a ruptura alveolar relacionada con la enfermedad pulmonar intersticial, que provocó neumotórax y aire en el mediastino y facilitó el paso de burbujas de aire a la circulación cerebral.\n- Mecanismo plausible: aire que atraviesa el circuito pulmonar (por rotura alveolar, fistulización o por un shunt derecho-izquierdo) alcanza la circulación arterial y ocluye vasos cerebrales, produciendo isquemia.\n\nEvolución y resultado:\n- Ingreso en la Unidad de Ictus para monitorización intensiva. Evolución tórpida; fallecimiento al segundo día por fracaso multiorgánico.\n\nImplicaciones clínicas y lecciones:\n- En pacientes con enfermedad pulmonar crónica, la aparición súbita de déficit neurológico o alteración del nivel de conciencia debe hacer sospechar embolismo gaseoso si hay antecedentes de neumotórax o neumomediastino.\n- El diagnóstico precoz mediante TAC y la identificación del origen torácico son cruciales. Las medidas que se consideran en estos casos incluyen oxigenoterapia de alto flujo, tratamiento del neumotórax/neumomediastino y, cuando está indicado y disponible, oxigenoterapia hiperbárica; sin embargo, el pronóstico depende del volumen de aire y de la extensión del daño cerebral.\n- Este caso ilustra la gravedad potencial del neumomediastino/neumotórax espontáneo en pacientes con enfermedad pulmonar intersticial y la necesidad de alta sospecha clínica.\n\nLamento la pérdida de la paciente; el caso subraya la rapidez con la que puede progresar un embolismo aéreo cerebral y la dificultad de tratamiento cuando el compromiso es extenso."
+        }
+    },
+    {
+        "article": "Un hombre de 24 años de edad, de etnia persa, presentó una queja principal de mal olor bucal después de un período de recuperación de la enfermedad leve por coronavirus 2019 (COVID-19), que quería resolver lo antes posible. Su dentista notó pérdida ósea y sangrado al explorar el área interproximal de los dientes número 18 y 19 clínicamente. Se realizó un escalamiento y un aplanamiento radicular, y se ordenaron radiografías periapicales y panorámicas para la evaluación del paciente. Sin embargo, el paciente se negó a tomar radiografías. La halitosis del paciente disminuyó después de 1 semana de tratamiento. Después de 2 meses, el paciente volvió a su dentista con la queja principal de sensibilidad al frío en sus incisivos mandibulares. El dentista realizó una prueba de vitalidad, y los dientes eran vitales excepto los números 23 y 24. El dentista tomó una radiografía periapical, y una lesión radiolucente en la mandíbula anterior era evidente.\n\nEn la radiografía panorámica, se evidenció una lesión radiolúcida lítica grande y bien definida con bordes festoneados que se extendían desde el diente número 31 en el lado derecho hasta el ramus ascendente izquierdo. Un estudio posterior de tomografía computarizada de haz cónico (TCFC) reveló una lesión lítica multilocular grande, con un margen relativamente distinto, que causó adelgazamiento y perforación de los cortexes bucales y linguales y signos de festoneado.\n\nTras el examen, se remitió al paciente a un cirujano oral y maxilofacial. En la entrevista médica, el paciente explicó su prolapso de la válvula mitral; antecedentes de episodios recurrentes de otitis desde el primer año de vida; antecedentes de septicemia de origen desconocido cuando tenía un año de edad, tras episodios de diarrea y vómitos; antecedentes de uso de broncodilatadores para la alergia estacional; antecedentes de uso de levotiroxina, cabergolina, acetato de desmopresina (DDAVP) en spray y gel de testosterona durante 4 años tras el diagnóstico de síndrome de silla turca vacía, tras poliúria y polidipsia; y, por último, antecedentes de infección reciente por COVID-19 (3 meses antes). Su historia familiar reveló tiroiditis de Hashimoto en su familia materna; su abuelo, su madre y sus tres tías padecían este tipo de hipotiroidismo. El historial quirúrgico previo del paciente incluía una reparación de una hernia inguinal 10 años antes sin complicaciones. Además, el paciente era obeso, con un índice de masa corporal (IMC) de 34,5.\n\nEn el examen clínico, los hallazgos extraorales e intraorales no fueron relevantes. Los exámenes de laboratorio, incluido el recuento sanguíneo completo (CBC), fueron normales, excepto por un aumento en la velocidad de sedimentación globular (ESR) y los niveles de proteína C reactiva (CRP). Se realizó una biopsia incisional en la mandíbula anterior y la muestra se envió al departamento de patología oral y maxilofacial de la Universidad de Ciencias Médicas Shahid Beheshti. Las secciones mostraron una infiltración difusa de grandes células de tinción pálida, como los histiocitos, con eosinófilos dentados y numerosos en el fondo fibroso. Un examen de inmunohistoquímica (IHC) reveló un positivo disperso para el grupo de diferenciación 1a (CD-1a) (+ +), un positivo fuerte para Langerin (CD-207) (+ + +), y más del 50% positivo para S-100.\n\nDe acuerdo con los datos clínicos, radiológicos e histopatológicos, se llegó al diagnóstico de LCH. Los diagnósticos diferenciales fueron osteomielitis, granuloma eosinófilo y metástasis ósea. Sin embargo, debido a las pruebas de laboratorio, los datos radiológicos y el historial clínico, se confirmó el diagnóstico de LCH. Por lo tanto, para un examen más a fondo, el paciente fue derivado al departamento de medicina nuclear para una tomografía por emisión de positrones con fluor-2-desoxiglucosa y una tomografía computarizada (FDG PET/CT), que reveló lesiones líticas hipermetabólicas en la mandíbula, el parietal derecho, el frontal izquierdo y el esfenoidal izquierdo, y opacidad hipermetabólica en el seno etmoidal izquierdo. Además, se observó una actividad metabólica aumentada en la región sellar, hidrocefalia comunicante y amígdalas palatinas hipermetabólicas prominentes. Además, se evidenció una actividad metabólica heterogénea aumentada en las tibias y fémures bilaterales.\n\nUna resonancia magnética del cerebro reveló una notable ampliación de la intensidad del material del líquido cefalorraquídeo (LCR) que contiene la silla turca. La adenohipófisis apareció como una capa delgada en la base de la silla turca agrandada, y se observaron cambios homogéneos e inflamatorios en las células aéreas mastoideas izquierdas. Se observó la extensión de la inflamación hacia el oído medio izquierdo (es de destacar que el paciente había sufrido de otitis durante muchos años). De acuerdo con la implicación multifocal de la enfermedad y su pronóstico cuestionable, el paciente fue derivado al departamento de oncología para quimioterapia sistémica. Pruebas posteriores revelaron mutaciones en el oncogen BRAF y no se detectaron mutaciones en KRAS y NRAS. El oncólogo eligió un régimen de denosumab, vinblastina, etopósido, 6-mercaptopurina, metotrexato y pegfilgrastim; sin embargo, el seguimiento no fue posible ya que el paciente falleció tras un accidente.\n",
+        "gold_summary": "Un paciente de 24 años de edad, de etnia persa, se presentó con una queja principal de halitosis tras recuperarse de la enfermedad por coronavirus 2019 en el consultorio de su dentista general. Los exámenes intraorales y extraorales no revelaron ningún problema específico. En la sesión de seguimiento tras el tratamiento periodontal de fase I, la sensibilidad de los dientes al estímulo frío era evidente, y las radiografías revelaron una gran lesión intraósea lítica en la mandíbula. Una biopsia incisional reveló células de Langerhans y una reacción positiva a Langerina y al grupo de diferenciación 1a, por lo que se le diagnosticó histiocitosis de células de Langerhans. Después de realizar una tomografía por emisión de positrones con fluoro-2-desoxiglucosa y una tomografía computarizada, una resonancia magnética y una tomografía computarizada de haz cónico, debido a la implicación generalizada de la enfermedad, el paciente fue derivado a un oncólogo. En última instancia, se descubrió que los problemas de salud infantil del paciente, incluidos los problemas endocrinos, probablemente fueron causados por una histiocitosis de células de Langerhans no diagnosticada. El oncólogo eligió un régimen de denosumab, vinblastina, etopósido, 6-mercaptopurina, metotrexato y pegfilgrastim. El seguimiento no fue posible ya que el paciente falleció tras un accidente.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre de 24 años fue al dentista porque tenía mal olor en la boca después de recuperarse del COVID-19. El dentista vio pérdida de hueso cerca de unos dientes y, después, el paciente tuvo dolor con el frío. Las radiografías mostraron una gran zona dañada en la mandíbula.\n\nLos médicos tomaron una pequeña muestra del hueso (biopsia). Al mirar esa muestra al microscopio, encontraron un tipo especial de células. Con eso dieron el diagnóstico de histiocitosis de células de Langerhans (LCH). LCH es una enfermedad rara en la que ciertas células del cuerpo crecen de más y pueden hacer daño en los huesos y en otros órganos.\n\nHicieron más pruebas de imagen y vieron que la enfermedad estaba en varias partes del cuerpo: huesos de la cara y del cráneo, senos nasales, piernas y la zona de la hipófisis en el cerebro. Los médicos pensaron que los problemas de salud que el paciente tuvo cuando era niño (como problemas hormonales y muchas otitis) probablemente fueron por esta misma enfermedad sin ser diagnosticada.\n\nDebido a que la enfermedad afectaba muchas zonas, lo derivaron a oncología para tratamiento con medicamentos fuertes. Sin embargo, el seguimiento no fue posible porque el paciente murió en un accidente.",
+            "B2": "Resumen comprensible (nivel B2)\n\nUn hombre persa de 24 años acudió al dentista porque tenía mal aliento (halitosis) poco después de recuperarse de una infección leve por COVID-19. Al explorar la zona entre dos muelas, el dentista notó pérdida de hueso y sangrado. Se hizo un tratamiento periodontal básico (raspado y alisado radicular) y el mal aliento mejoró. El paciente rehusó radiografías en esa primera visita.\n\nDos meses después regresó por sensibilidad al frío en los incisivos inferiores. Entonces se le practicaron radiografías y se vio una gran lesión en la mandíbula. Una tomografía computarizada con haz cónico (un tipo de imagen 3D, parecida a un TAC) mostró una lesión con varias “cavidades” que estaba haciendo el hueso más delgado y hasta lo perforaba. Se tomó una biopsia (pequeña muestra de tejido) de la lesión.\n\nEl examen microscópico y las pruebas de inmunohistoquímica mostraron células de Langerhans (un tipo de célula del sistema inmune) positivas para marcadores como CD1a y Langerina. Esos hallazgos llevaron al diagnóstico de histiocitosis de células de Langerhans (LCH), una enfermedad rara en la que este tipo de células se acumulan y dañan hueso u otros tejidos.\n\nAntes y después del diagnóstico se recogió más información clínica: tenía antecedentes desde la infancia de otitis (infecciones de oído) y una septicemia de niño; le habían diagnosticado “silla turca vacía” (una forma en la que la glándula pituitaria queda muy aplanada, lo que puede afectar hormonas) y recibía varios tratamientos hormonales. Era obeso (IMC 34,5) y tenía antecedes familiares de tiroiditis de Hashimoto. En análisis sanguíneos, los marcadores de inflamación (velocidad de sedimentación y proteína C reactiva) estaban elevados.\n\nPara buscar más lesiones, se hizo una FDG PET/CT (una exploración que detecta zonas metabólicamente activas). Esta prueba mostró lesiones líticas activas en la mandíbula y en varios huesos del cráneo, además de cambios en el seno etmoidal y actividad aumentada en fémures y tibias. Una resonancia magnética del cráneo confirmó cambios en la silla turca y signos de inflamación en las celdillas mastoideas izquierdas, lo que concuerda con sus episodios crónicos de otitis.\n\nDado que la enfermedad afectaba varias áreas (enfermedad multifocal) y tenía un pronóstico incierto, fue derivado a oncología para tratamiento sistémico. Se detectó una mutación en el gen BRAF, y el equipo decidió un régimen que incluía denosumab (que actúa en el hueso) y varios fármacos de quimioterapia (vinblastina, etopósido, 6‑mercaptopurina, metotrexato) junto con pegfilgrastim (para proteger las células blancas). No se llegó a documentar el seguimiento del tratamiento porque el paciente falleció en un accidente.\n\nPuntos clave y explicación breve de términos\n- Histiocitosis de células de Langerhans (LCH): enfermedad rara donde células del sistema inmune llamadas células de Langerhans se acumulan y dañan hueso u otros órganos.  \n- Biopsia e inmunohistoquímica: la biopsia permite ver las células al microscopio; las pruebas de inmunohistoquímica usan marcadores (CD1a, Langerina, S‑100) para confirmar el tipo celular.  \n- FDG PET/CT: imagen que muestra áreas con actividad metabólica alta, útil para detectar lesiones en todo el cuerpo.  \n- Silla turca vacía: la glándula pituitaria aparece muy aplanada en su cavidad; puede explicar problemas hormonales.\n\nEste caso muestra cómo un problema dental puede ser la primera señal de una enfermedad más amplia. El diagnóstico requirió imágenes, biopsia y estudios adicionales, y el tratamiento planificado fue sistémico por la afectación multifocal.",
+            "B3": "Summary\n\nA 24-year-old Persian man first saw his dentist because of new bad breath (halitosis) shortly after recovering from a mild COVID-19 infection. Initial oral and extraoral exams were essentially normal, and his halitosis improved after routine periodontal treatment. Two months later he developed cold sensitivity in his lower front teeth. Dental vitality testing and imaging then revealed a large, destructive bone lesion in the lower jaw.\n\nKey findings\n- Clinical: initially unremarkable oral exam; later cold sensitivity of mandibular incisors.  \n- Imaging: periapical and panoramic radiographs showed a large, well-defined multilocular radiolucent lesion of the mandible with scalloped borders; cone-beam CT confirmed a multilocular lytic mass causing cortical thinning and perforation.  \n- Laboratory: routine blood count normal; inflammatory markers elevated (ESR and CRP).  \n- Pathology: incisional biopsy showed sheets of pale histiocyte-like cells with numerous eosinophils. Immunohistochemistry was strongly positive for Langerin (CD207), positive for CD1a, and >50% positive for S-100—findings diagnostic of Langerhans cell histiocytosis (LCH).  \n- Staging: FDG PET/CT showed additional hypermetabolic lytic lesions in skull bones (right parietal, left frontal, left sphenoid), hypermetabolic opacity in the left ethmoid sinus, increased activity in the sellar region, and increased uptake in both tibias and femurs. Brain MRI showed an enlarged, CSF-filled (empty) sella turcica with a thin anterior pituitary and inflammatory changes in the left mastoid and middle ear.\n\nRelevant medical history\n- Longstanding issues that likely relate to LCH involvement of the pituitary/central nervous system: empty-sella syndrome, years of polyuria/polydipsia requiring desmopressin (DDAVP), and four years of hormone replacement (levothyroxine and testosterone).  \n- Recurrent childhood otitis media and an episode of infantile sepsis.  \n- Mitral valve prolapse and obesity (BMI 34.5).  \n- Family history of Hashimoto thyroiditis.  \n- Recent COVID-19 infection three months before presentation.\n\nDiagnosis and management\n- A final diagnosis of multifocal Langerhans cell histiocytosis was made based on clinical, radiologic, and histopathologic evidence. Differential diagnoses such as osteomyelitis and metastatic disease were considered but excluded by the combined findings.  \n- Molecular testing identified a BRAF oncogene mutation (KRAS and NRAS were negative). BRAF status can influence therapy choices because targeted BRAF inhibitors may be effective in some patients.  \n- Because disease involved multiple bones and the central skull base/pituitary region, the patient was referred for systemic therapy. The oncology team planned a multiagent treatment regimen (denosumab, vinblastine, etoposide, 6‑mercaptopurine, methotrexate, and pegfilgrastim). No clinical follow-up of treatment response was possible because the patient later died in an unrelated accident.\n\nInterpretation and implications\n- This case illustrates LCH presenting first to dental care with a jaw lesion discovered after a trivial symptom (halitosis) and a normal initial exam.  \n- The patient’s prior endocrine problems (empty sella, diabetes insipidus treated with DDAVP, long‑term hormone replacement) and chronic otitis are most consistent with longstanding, previously unrecognized LCH involving the pituitary and temporal bones. Such involvement can cause permanent endocrine dysfunction and often signifies more extensive disease.  \n- Elevated inflammatory markers and multifocal PET/CT uptake confirm systemic activity and justify systemic therapy rather than local treatment alone. BRAF mutation offers a potential option for targeted therapy in appropriate cases.\n\nEmpathetic note\nThis was a complex and progressive illness that affected multiple systems and ultimately required coordinated care across dentistry, oral surgery, radiology, pathology, endocrinology, and oncology. The report underscores the importance of careful investigation of unusual oral findings, thorough systemic staging of LCH, and early multidisciplinary management when pituitary or multifocal bone involvement is suspected."
+        }
+    },
+    {
+        "article": "La paciente es una mujer de 66 años de edad que goza de buena salud. A mediados de la década de 1980, recibió varias sesiones de tratamiento con rayos grenz en el cuero cabelludo para aliviar el picor asociado con la psoriasis del cuero cabelludo. Con un tratamiento regular de aproximadamente una sesión al mes durante un período de 5 años, que se complementó de vez en cuando con alquitrán de hulla, ácido salicílico y prednisona, logró cierto alivio de su enfermedad. Con el tiempo, su cabello se adelgazó; la piel en toda el área del cuero cabelludo se volvió sensible al dolor y se produjo cicatrización. Los tratamientos con rayos grenz se habían administrado en una clínica privada; no se disponía de detalles del tratamiento, como la dosis única y acumulada. No había sufrido radiodermitis.\n\nEn un período muy breve en 2020, unos 35 años después de que cesara el tratamiento de radiación, aparecieron numerosos BCC y queratosis actínicas premalignas (AK) en su cuero cabelludo. Se inició un régimen de tratamiento de extirpación quirúrgica de BCC verificado por histología preoperatoria y crioterapia de AK por evaluación del médico. La terapia fotodinámica o los tratamientos tópicos no eran aplicables debido a la sensibilidad al dolor y las secuelas de la cirugía. De 2020 a 2022, recibió varios tratamientos de criocirugía y curetaje y un total de 13 extirpaciones quirúrgicas de BCC por cirugía de Mohs. Se estima que su número total de extirpaciones a lo largo del tiempo es de unos 30. Los BCC recalcitrantes y de novo en el cuero cabelludo cada vez más dañado, obviamente, son un desafío eterno; por lo tanto, los cirujanos plásticos y los dermatólogos buscaban otra modalidad de tratamiento con un mejor índice terapéutico.\n\nEn septiembre de 2022, aparecieron nuevos CCB confirmados histológicamente en el cuero cabelludo. La exploración por ultrasonido (DermaScan C, Cortex Technology ApS, Aalborg, Dinamarca) mostró tumores ecolucidos de 0,5-1,3 mm de espesor en ambos sitios analizados histológicamente, así como en algunas lesiones adicionales que pudieron identificarse en base al examen clínico y dermatoscópico. La paciente, tras ser informada, dio su consentimiento por escrito para el tratamiento con HIFU, con o sin biopsia de pretratamiento de las lesiones sospechosas.\n\nSe delinearon las lesiones elegibles para el tratamiento con un rotulador impermeable, incluyendo un margen perilesional de 2 mm. Se mapeó cada lesión seleccionada en una lámina transparente para ayudar a determinar la ubicación precisa en el seguimiento. Se usó el ultrasonido de 20 MHz para confirmar la profundidad de las lesiones identificadas al inicio y en las visitas de seguimiento posteriores. Debido al estado del cuero cabelludo conocido por ser sensible al dolor, se administró anestesia local (lidocaína 25 mg/ml + adrenalina 5 mg/ml, Amgros I/S, Copenhagen, Dinamarca) a todas las lesiones 10-15 minutos antes del tratamiento.\n\nLas lesiones fueron tratadas con HIFU utilizando la sonda de 1.3 mm; ajustes de 150 ms/dosis y energía acústica de 0.9 J/dosis. Se aplicaron 20-200 dosis a las lesiones, dependiendo de la extensión de la lesión. Las lesiones tratadas se curaron de forma espontánea sin complicaciones o necesidad de tratamiento especial. Se programaron visitas de seguimiento cada 3-6 meses para controlar la tasa de curación/recaída, tolerancia local y lesiones nuevas no identificadas anteriormente.\n\nDurante los 15 meses posteriores a la limpieza inicial con HIFU, se trataron con HIFU un total de 10 lesiones que, de acuerdo con las rutinas, hubieran requerido una biopsia seguida de una cirugía de escisión, en sesiones de unos 30 minutos. Las lesiones se curaron en unos pocos días sin complicaciones ni necesidad de intervención. Se observó una limpieza total en 7 de 8 lesiones de BCC tratadas y en ambas lesiones de AK. La única lesión recurrente de BCC de pequeño tamaño se observó después de 15 meses entre las primeras seis lesiones tratadas; la lesión se volvió a tratar con HIFU. Ejemplos de lesiones curadas 15 meses después del tratamiento con HIFU; el tumor con recurrencia.\n",
+        "gold_summary": "Una mujer de 66 años que en la década de 1980 había recibido varios tratamientos de rayos gamma en el cuero cabelludo desarrolló múltiples carcinomas basocelulares en la zona. Se le habían realizado más de 30 cirugías de escisión, incluida la cirugía de Mohs, en el pasado, con muchas complicaciones locales, pero, no obstante, los cánceres recurrentes. Los tratamientos con HIFU aplicados a ocho carcinomas basocelulares y dos lesiones precancerosas dieron como resultado una limpieza completa en el control a los 12 meses, pero una recurrencia después de 15 meses.\n",
+        "synthetic_summary": {
+            "B1": "Esta es la historia de una mujer de 66 años. Cuando era más joven recibió radiación en el cuero cabelludo para tratar la psoriasis. Con el tiempo eso dejó la piel más fina, con cicatrices y dolor. Muchas décadas después le salieron muchas lesiones en la piel del cuero cabelludo. Algunas eran cáncer de piel llamado carcinoma basocelular (BCC). Otras eran manchas que a veces pueden volverse cáncer, llamadas queratosis actínicas (AK).\n\nLa paciente tuvo muchas cirugías antes (más de 30), incluidas varias con una técnica especial llamada Mohs. Aun así, los problemas seguían apareciendo. En 2022 los médicos probaron otro método llamado HIFU. HIFU usa ultrasonido para calentar y destruir la lesión sin cortar la piel. Buscaron las lesiones con una ecografía y pusieron anestesia local para que no doliera.\n\nTrataron 10 lesiones con HIFU (8 BCC y 2 AK). Las sesiones duraban alrededor de 30 minutos. Las heridas se curaron en pocos días y no hubo problemas importantes. Después de revisar a la paciente hasta 15 meses, encontraron que 7 de los 8 BCC y las 2 AK habían desaparecido. Una lesión pequeña volvió a aparecer a los 15 meses y la trataron otra vez con HIFU.\n\nEn resumen: muchos problemas de piel parecían estar relacionados con la radiación antigua. El HIFU ayudó a curar la mayoría de las lesiones en este caso. El tratamiento fue rápido y bien tolerado. Una lesión volvió a aparecer y se volvió a tratar.",
+            "B2": "Here is a clear, student-level summary of the case report:\n\nA 66-year-old woman who had repeated low-dose X-ray treatment to her scalp in the 1980s developed many skin problems decades later. The earlier radiation, given for scalp psoriasis, left her scalp thin, sensitive, and scarred. About 35 years after those treatments, multiple basal cell carcinomas (BCCs — a common type of skin cancer) and actinic keratoses (AKs — rough, sun-related patches that can become cancerous) appeared on her scalp. Over the years she had about 30 surgical removals, including Mohs surgery, but new and recurring tumors kept appearing.\n\nIn 2022 doctors tried a different approach: high-intensity focused ultrasound (HIFU). HIFU uses tightly focused sound waves to heat and destroy small tumors without cutting the skin. Before treatment, doctors used a 20 MHz ultrasound to measure how deep each lesion was (they were 0.5–1.3 mm thick) and marked the spots. Because her scalp was sensitive, each area was numbed with local anesthetic. The HIFU settings used a small 1.3 mm probe, short pulses (150 ms) and a set energy for each pulse; each lesion received between about 20 and 200 pulses depending on size.\n\nOver 15 months of follow-up, ten lesions that otherwise would have needed biopsy and surgery were treated with HIFU in short (≈30-minute) sessions. The treated spots healed in a few days without complications or extra care. Of eight BCCs treated, seven showed complete clearance at follow-up. Both AKs also cleared. One small BCC recurred after 15 months and was treated again with HIFU.\n\nWhat this means: In this single case, HIFU was well tolerated and cleared most small, thin BCCs and AKs on a previously damaged scalp. The results are promising, but this is a small series with limited follow-up. Longer monitoring and more patients are needed to know how well HIFU compares to standard treatments and how often recurrences happen. For this patient, ongoing check-ups and the option to re-treat with HIFU were used to manage new or returning lesions.",
+            "B3": "Resumen clínico (nivel universitario, lectura B3)\n\nPaciente y antecedentes\n- Mujer de 66 años, por lo demás en buena salud.\n- En la década de 1980 recibió sesiones repetidas de radioterapia superficial (rayos grenz) en el cuero cabelludo durante unos 5 años (aprox. una sesión/mes), además de tratamientos tópicos ocasionales (alquitrán de hulla, ácido salicílico) y corticoide sistémico (prednisona). No hay datos sobre dosis acumulada y no refirió radiodermitis aguda.\n- A largo plazo desarrolló adelgazamiento del cabello, piel del cuero cabelludo dolorosa y cicatrizada.\n\nProblema actual\n- Unos 35 años después de la radioterapia (alrededor de 2020) apareció un brote de múltiples carcinomas basocelulares (BCC) y queratosis actínicas (AK, lesiones precancerosas) en el cuero cabelludo.\n- Entre 2020 y 2022 recibió múltiples tratamientos quirúrgicos (incluidas 13 resecciones por cirugía de Mohs) y criocirugía; se estiman unas 30 extirpaciones a lo largo del tiempo, con recidivas y aparición de lesiones nuevas.\n\nNueva estrategia terapéutica: HIFU\n- En septiembre de 2022 se documentaron nuevos BCC confirmados por biopsia. La ecografía cutánea (20 MHz) mostró tumores con espesor entre 0,5 y 1,3 mm.\n- La paciente consintió tratamiento con HIFU (ultrasonido focalizado de alta intensidad), seleccionándose y mapeando las lesiones con un margen perilesional de 2 mm.\n- Por sensibilidad dolorosa del cuero cabelludo se administró anestesia local (lidocaína con adrenalina) antes del procedimiento.\n- Parámetros de HIFU: sonda 1,3 mm, 150 ms por disparo, 0,9 J por disparo; se aplicaron entre 20 y 200 disparos según el tamaño de la lesión. Cada sesión duró aproximadamente 30 minutos.\n\nResultados\n- Durante 15 meses de seguimiento se trataron con HIFU 10 lesiones que, según la práctica habitual, habrían precisado biopsia y escisión.\n- Las zonas tratadas cicatrizaron espontáneamente en pocos días sin complicaciones locales ni necesidad de cuidados especiales.\n- Resultado clínico: limpieza total observada en 7 de 8 BCC tratados y en las 2 AK tratadas. Una lesión BCC pequeña recidivó a los 15 meses entre las primeras seis tratadas y fue nuevamente tratada con HIFU.\n- Controles programados cada 3–6 meses con ecografía para vigilar curación, recidiva y aparición de nuevas lesiones.\n\nInterpretación y consideraciones prácticas\n- HIFU se mostró como una opción local no quirúrgica, bien tolerada y rápida, capaz de conseguir resolución clínica en la mayoría de las lesiones pequeñas (espesor ≤1,3 mm) en este caso particular de cuero cabelludo previamente irradiado y doloroso.\n- Ventajas observadas: tratamiento ambulatorio corto, curación rápida, mínima morbilidad y posibilidad de repetir el tratamiento en caso de recidiva.\n- Limitaciones importantes: serie de un solo paciente, número pequeño de lesiones tratadas, seguimiento limitado (15 meses) y ausencia de datos completos sobre la radiación previa (dosis acumulada). La confirmación histológica de curación a largo plazo no consta en todos los casos.\n\nRecomendaciones y próximos pasos\n- Mantener vigilancia dermatológica estrecha con examen clínico y ecografía; biopsiar cualquier lesión sospechosa o recurrente.\n- Considerar HIFU como alternativa en pacientes con múltiples lesiones superficiales pequeñas o en cueros cabelludos con secuelas de radiación donde la cirugía es difícil o dolorosa.\n- Se necesitan series más amplias y con seguimiento prolongado para evaluar la eficacia real, la seguridad a largo plazo y comparar HIFU con terapias estándar (cirugía, tratamientos tópicos, fotodinámica).\n\nNota empática\n- El manejo de múltiples BCC en un cuero cabelludo previamente irradiado es complejo y puede ser emocionalmente agotador para la paciente. Las opciones que minimizan las intervenciones quirúrgicas y el dolor, como HIFU en este caso, pueden mejorar la calidad de vida, pero requieren seguimiento atento y comunicación clara entre paciente y equipo médico."
+        }
+    },
+    {
+        "article": "Se realizó un trasplante cardíaco ortotópico a una niña de 12 años con insuficiencia cardíaca en fase terminal debido a una miocardiopatía restrictiva. Durante la operación, se presentó una disfunción primaria grave del injerto, que requirió el uso de oxigenación por membrana extracorpórea venosa arterial. La función cardíaca se recuperó completamente después de 4 días, y su período postoperatorio se complicó por una insuficiencia renal aguda transitoria y un bloqueo auriculoventricular completo que duró >3 semanas después de la operación. Para evitar la disincronía del ventrículo izquierdo y el posible daño de la derivación del ventrículo derecho debido a las biopsias endomiocárdicas de vigilancia de rechazo múltiple, se indicó un marcapasos biventricular transvenoso que utiliza un marcapasos del ventrículo izquierdo aislado a través de la vena coronaria.\n\nBajo anestesia local y sedación suave, se cortó la vena cefálica izquierda y se introdujo un catéter guía en la vena subclavia y se colocó en el seno coronario inicialmente para realizar un venograma cardiaco. Se implantó un electrodo de estimulación endocárdica de elución de esteroides unipolar con mecanismo de fijación activa (Attain StarFix® 4195, Medtronic, Minneapolis, MN) en la rama de la vena interventricular anterior. Las medidas en el momento del implante fueron las siguientes: umbral 2 V a 0,4 ms, onda R 6 mV e impedancia 300 Ω a 4,8 mA. Se implantó un segundo electrodo de estimulación endocárdica de elución de esteroides bipolar con fijación activa (2088T®, St. Jude Medical, Minneapolis, MN) en la aurícula derecha.\n\nAmbos cables se aseguraron y se conectaron a un marcapasos adaptable a la frecuencia (Accent DR®, St. Jude Medical, Minneapolis, MN) que se colocó en una bolsa muscular infraclavicular izquierda y se programó a VDD. Las mediciones de los cables electrofisiológicos fueron estables después del implante: umbral ventricular 1.5 V a 0.7 ms, onda R 4.5 mV, onda P 4.3 mV (bipolar), impedancia ventricular 260 Ω y vida útil estimada de la batería de 5 años.\n\nEl electrocardiograma posterior al implante mostró complejos de morfología de bloqueo de rama derecha, y la evaluación ecocardiográfica mostró ausencia de disincronías auriculoventriculares, interventriculares e intraventriculares. En el seguimiento a 5 años, el paciente permaneció en Clase Funcional I con el mismo sistema de estimulación y conservó la función ventricular.\n\nMH - Bloqueo auriculoventricular/etiología/*terapia\nMH - Niño\nMH - Sinus coronario\nMH - Mujer\nMH - Insuficiencia cardiaca/cirugía\nMH - Trasplante de corazón/*efectos adversos\nMH - Ventrículos del corazón\nMH - Humanos\nMH - *Marcapasos, artificial\nMH - Disfunción/complicaciones/tratamiento del injerto primario\n",
+        "gold_summary": "Se sometió a un trasplante de corazón ortotópico a un niño de 12 años con insuficiencia cardiaca en fase terminal debido a una miocardiopatía restrictiva. La disfunción primaria del injerto precisó oxigenación con membrana extracorpórea venosa arterial. La función cardiaca se normalizó, pero el bloqueo auriculoventricular completo persistió después de 3 semanas. Se realizó un marcapaso bicameral con marcapaso transvenoso del ventrículo izquierdo a través del seno coronario. Tras 5 años de seguimiento, el paciente se encuentra estable con el mismo sistema de marcapaso y con la función ventricular preservada.\n",
+        "synthetic_summary": {
+            "B1": "Una niña de 12 años recibió un trasplante de corazón porque su propio corazón estaba muy enfermo.  \nDurante la operación, el corazón nuevo no funcionó bien al principio. Los médicos usaron una máquina que ayuda al corazón y a los pulmones (ECMO) durante cuatro días. Después de eso, el corazón se recuperó por completo.  \n\nLa niña tuvo dos problemas después: el riñón dejó de funcionar bien por un tiempo y las señales eléctricas del corazón no pasaban normalmente (esto se llama bloqueo auriculoventricular). Ese bloqueo duró más de tres semanas.  \n\nPara ayudar, los médicos le pusieron un marcapasos. Un marcapasos es un aparato con cables que envía pequeñas señales para que el corazón lata al ritmo correcto. Uno de los cables fue colocado en una vena del lado izquierdo del corazón para que los dos lados del corazón latan juntos y no se dañara el lado derecho con muchas pruebas. El procedimiento se hizo con anestesia local y sedación suave.  \n\nDespués de poner el marcapasos, las ecografías mostraron que el corazón latía de forma sincronizada y funcionaba bien. Cinco años después, la niña está bien, hace sus actividades y el marcapasos sigue funcionando correctamente.",
+            "B2": "Resumen claro y amable:\n\nUna niña de 12 años con insuficiencia cardíaca terminal por una miocardiopatía restrictiva (el corazón está muy rígido y no se llena bien) recibió un trasplante de corazón. Tras la operación el nuevo corazón tuvo una insuficiencia primaria grave y fue necesario conectarla a circulación extracorpórea (ECMO veno‑arterial), un soporte que sustituye temporalmente la función del corazón y los pulmones. La función cardíaca se recuperó completamente en 4 días.\n\nEn el postoperatorio tuvo una insuficiencia renal aguda transitoria y desarrolló un bloqueo auriculoventricular completo (el impulso eléctrico entre las aurículas y los ventrículos no pasaba) que persistió más de 3 semanas. Para tratar ese bloqueo y, al mismo tiempo, evitar que el ventrículo izquierdo se desincronizara —y también para proteger el ventrículo derecho de posibles daños por las biopsias que se hacen para vigilar el rechazo— se decidió implantar un marcapasos transvenoso especial que estimula el ventrículo izquierdo a través de la vena coronaria.\n\nEl procedimiento se realizó con sedación leve y anestesia local. Por la vena cefálica/subclavia se accedió al seno coronario y se colocó un cable activo de fijación para el ventrículo izquierdo en una rama de la vena interventricular anterior. Se colocó otro cable en la aurícula derecha. Ambos cables se conectaron a un marcapasos colocado en una bolsa muscular bajo la clavícula izquierda y se programó para asegurar una buena coordinación entre las cámaras del corazón.\n\nLas pruebas inmediatas mostraron parámetros eléctricos estables y, en la ecocardiografía, no había desincronía entre las cámaras del corazón. En el electrocardiograma apareció una morfología de bloqueo de rama derecha, lo cual es un hallazgo esperado después de este tipo de implantación. A los 5 años de seguimiento, la niña estaba estable en Clase Funcional I (sin limitación de la actividad), mantenía el mismo sistema de estimulación y tenía función ventricular preservada.\n\nComentario breve y humano: aunque tuvo complicaciones serias al principio, el equipo usó soportes temporales y un marcapasos diseñado para proteger la función del nuevo corazón. El resultado a medio plazo fue muy bueno, y la paciente siguió con buena calidad de vida.",
+            "B3": "Resumen clínico (nivel universitario, lectura B3)\n\nUna niña de 12 años con miocardiopatía restrictiva en insuficiencia cardiaca terminal recibió un trasplante cardiaco ortotópico. Durante la cirugía presentó una disfunción primaria grave del injerto que exigió soporte con oxigenación por membrana extracorpórea veno‑arterial (VA‑ECMO). La función cardíaca se recuperó completamente en 4 días. En el posoperatorio inmediato hubo además una insuficiencia renal aguda transitoria. No obstante, persistió un bloqueo auriculoventricular completo durante más de 3 semanas.\n\nPor dos motivos se evitó implantar un cable ventricular derecho: (1) prevenir la disincronía del ventrículo izquierdo que puede derivarse del marcapaseo ventricular derecho exclusivo, y (2) reducir el riesgo de daño del electrodo derecho por las repetidas biopsias endomiocárdicas necesarias para el control del rechazo en trasplante. Se decidió, por tanto, un sistema transvenoso que estimulase el ventrículo izquierdo a través de la vena coronaria, combinado con estimulación auricular.\n\nProcedimiento y hallazgos técnicos\n- Bajo anestesia local y sedación ligera se abordó la vena cefálica izquierda y, tras cateterizar la subclavia y localizar el seno coronario con venograma, se implantó:\n  - Un electrodo unipolar de fijación activa y liberación de esteroides (Attain StarFix® 4195, Medtronic) en una rama de la vena interventricular anterior (vía coronaria) para estimular el ventrículo izquierdo. Parámetros iniciales: umbral 2 V a 0,4 ms; onda R 6 mV; impedancia 300 Ω.\n  - Un electrodo bipolar de fijación activa y liberación de esteroides (2088T®, St. Jude) en la aurícula derecha.\n- Ambos cables se aseguraron y se conectaron a un generador bicameral con adaptación de frecuencia (Accent DR®, St. Jude), ubicado en bolsa muscular infraclavicular izquierda y programado en modo VDD (sensado auricular con estimulación ventricular).\n- Mediciones posoperatorias: umbral ventricular 1,5 V a 0,7 ms; onda R 4,5 mV; onda P (bipolar) 4,3 mV; impedancia ventricular 260 Ω; autonomía estimada de la batería ≈ 5 años.\n\nEvolución y control\n- El electrocardiograma posimplante mostró complejos con morfología de bloqueo de rama derecha (compatible con estimulación ventricular izquierda).\n- Ecocardiografía: no se evidenciaron disincronías auriculoventriculares, interventriculares ni intraventriculares.\n- Seguimiento a 5 años: la paciente permaneció en clase funcional I (sin limitación clínica), conservó la función ventricular y seguía con el mismo sistema de estimulación.\n\nInterpretación y consideraciones\n- Este caso muestra que, en un niño trasplantado con bloqueo auriculoventricular persistente y necesidad de biopsias frecuentes, la estimulación ventricular izquierda transvenosa (a través del seno coronario) puede ser una alternativa eficaz para evitar disincronía y el riesgo de lesión del electrodo derecho.\n- Factores a considerar al valorar esta estrategia: anatomía coronaria favorable para colocación del cable, estabilidad del electrodo coronario, posibles complicaciones (p. ej., estimulación faríngea/frenica, desplazamiento del cable, problemas de umbral a largo plazo) y la vida útil del generador.\n- En este caso concreto, la solución fue bien tolerada y estable a mediano-largo plazo, con recuperación funcional y sin evidencia de disincronía.\n\nEmpatía y conclusión\nLa paciente superó una complicación grave del trasplante y, tras recibir un sistema de marcapaseo diseñado para minimizar riesgos en el contexto del trasplante, logró una recuperación funcional completa y estable a 5 años. Este enfoque aporta una opción valiosa cuando el riesgo de daño del electrodo derecho por biopsias o la posibilidad de disincronía ventricular hacen preferible estimular el ventrículo izquierdo por vía coronaria."
+        }
+    },
+    {
+        "article": "Una paciente de 20 años de edad se presentó con distensión abdominal progresiva asociada con calambres abdominales, incapacidad para expulsar flatos y heces, así como vómitos frecuentes de materia ingerida y biliar de un día de duración. El día anterior, dio a luz por cesárea por una indicación de bradicardia fetal severa. También tenía preeclampsia sin signos de gravedad y desnutrición de inicio en la edad adulta con un índice de masa corporal (IMC) de 16,5 kg/M2. No tenía antecedentes de cirugía abdominal previa. Negó cualquier queja similar en el pasado o antecedentes de cambio de hábitos intestinales o estreñimiento con paso de heces sanguinolentas. No tenía ninguna enfermedad médica crónica conocida.\n\nEn el examen físico, la paciente se veía enferma y con dolor. Su presión arterial era de 90/70 mmHg, su pulso oscilaba entre 116 y 120 latidos por minuto, y su frecuencia respiratoria era de 22 a 24 respiraciones por minuto. No se registró fiebre. Su abdomen estaba muy distendido y simétrico, con visibles movimientos intestinales peristálticos. Había una difusa sensibilidad directa en todo su abdomen, más en el cuadrante inferior derecho. Había un signo positivo de acumulación de fluido intraperitoneal con opacidad cambiante. Había una herida quirúrgica suprapúbica bien aproximada con un vendaje limpio. El examen rectal digital no mostró nada destacable. Tenía una herida superficial lineal de 3 cm de largo, orientada verticalmente, en su labio mayor izquierdo, que el equipo de obstetricia pensó inicialmente que era una quemadura de yodo en la piel.\n\nSe le introdujo un catéter y se le resucitó con dos bolsas de solución salina normal y produjo 200 ml de orina en una hora. Se le introdujo una sonda nasogástrica (NGT) pero no hubo una salida significativa. Se le realizó un hemograma completo y una radiografía abdominal simple. Su recuento de glóbulos blancos era de 1780 células/µl con predominio de neutrófilos del 88 %, hemoglobina de 12,7 mg/dl y un recuento de plaquetas de 78 x 103/ µl. Su prueba de función renal era normal y sus enzimas hepáticas estaban ligeramente elevadas por encima del rango normal pero no fue significativo. Su radiografía abdominal simple muestra múltiples niveles de aire-líquido ubicados centralmente con un bucle intestinal grande dilatado ubicado periféricamente y blanqueamiento del espacio pélvico que indica una acumulación de líquido. No se solicitó una tomografía computarizada abdominal (CT) porque trabajamos en un entorno con recursos limitados y para pacientes con obstrucción intestinal, solicitamos una tomografía computarizada cuando existe la posibilidad de un diagnóstico alternativo o cuando se sospecha una obstrucción tumoral.\n\nTras obtener el consentimiento informado por escrito, se exploró a la paciente bajo anestesia general con un diagnóstico de abdomen agudo secundario a obstrucción intestinal mixta secundaria a vólvulo del intestino delgado. El hallazgo intraoperatorio fue un íleon distal que rodeaba el ciego y el colon ascendente proximal, ambos móviles y no adheridos a la pared abdominal posterolateral derecha. Tanto el íleon como el ciego, así como el colon ascendente, eran viables. La punta del apéndice estaba enredada con el nudo ileal y estaba gangrenoso. El intestino delgado proximal y el intestino grueso distal estaban muy distendidos, pero en su ubicación normal. Había unos cuatro litros de líquido intraperitoneal seroso.\n\nDurante la operación, la paciente se mantuvo hipotensa (80/50 mmHg) desde que se le indujo la anestesia y se le administró un vasopresor. Debido a la inestabilidad de la paciente y a la viabilidad de los intestinos afectados por el nudo, se procedió a una hemicolectomía derecha. Se realizó una descompresión proximal y distal de los intestinos delgado y grueso distendidos, respectivamente. Se fijó el ciego y el colon ascendente a la pared abdominal posterolateral derecha con suturas seromusculares interrumpidas con hilo no absorbible (Silk 2-0).\n\nDespués del procedimiento, se le retiró la intubación y se le dio alimentación por vía oral (NPO) durante 24 horas y se le administró un fluido de mantenimiento con reposición de la pérdida. A pesar de la reanimación con fluidos y el apoyo con vasopresores, ella se encontraba persistentemente hipotensa, por lo que se le administró un tratamiento antibiótico doble con ceftriaxona 1 g, IV, BID y metronidazol 500 mg, IV, TID, en vista de un posible shock séptico de origen genitourinario. Su estado empeoró gradualmente y, tras una nueva evaluación el primer día postoperatorio, la herida superficial en su vulva se había extendido hacia la zona suprapúbica con signos clínicos de gangrena de Fournier. Por ello, revisamos su tratamiento antibiótico a meropenem 1 g, IV, BID, vancomicina 1 g, IV, BID y metronidazol 500 mg, IV, TID. Después de obtener el consentimiento informado por escrito, se la volvió a llevar al quirófano para un desbridamiento radical de la gangrena de Fournier y, posteriormente, se la trasladó a la unidad de cuidados intensivos quirúrgicos (ICU) intubada debido a un shock séptico persistente y un retraso en la recuperación de la anestesia. Lamentablemente, falleció con fallo multiorgánico debido a un shock séptico refractario en su segundo día postoperatorio, después de la exploración inicial.\n",
+        "gold_summary": "Presentamos un caso de nudos ileocecales en una paciente posparto con distensión abdominal, vómitos y ausencia de heces y flatos. La radiografía abdominal simple reveló bucles intestinales dilatados con múltiples niveles de aire y fluidos. Se realizó una laparotomía exploratoria con hallazgo intraoperatorio de nudos ileocecales con intestino viable, ciego móvil y colon ascendente y punta gangrenosa del apéndice. Deshicimos el nudo y realizamos una apendectomía. Debido a la inestabilidad intraoperatoria de los signos vitales de la paciente, se aplazó la hemicolectomía derecha y se fijaron el ciego y el colon ascendente a la pared abdominal posterolateral derecha.\n",
+        "synthetic_summary": {
+            "B1": "Este es el caso de una mujer joven que acababa de tener un bebé. Tenía la barriga muy hinchada, vomitaba y no podía expulsar gases ni hacer caca.  \nLa radiografía mostró muchos huecos con aire y líquido en los intestinos. Eso dejó claro que algo bloqueaba el paso en su tripa.  \n\nEn la operación encontraron un nudo entre el intestino delgado y la parte de inicio del intestino grueso (el ciego). El nudo se llama \"nudo ileocecal\". La parte del intestino que estaba en el nudo estaba viva, pero la punta del apéndice estaba dañada.  \nLos cirujanos deshicieron el nudo y sacaron el apéndice enfermo. Como la paciente estaba muy inestable, no pudieron quitar una parte grande del colon. En vez de eso, fijaron el ciego y el colon a la pared para que no se movieran.  \n\nEs un problema raro y serio. Los médicos actuaron rápido para salvar el intestino y cuidar a la paciente.",
+            "B2": "Presentamos el caso de una paciente posparto que acudió con distensión abdominal, vómitos y ausencia de expulsión de gases y heces. La radiografía abdominal mostró asas intestinales muy dilatadas con varios niveles de aire y líquido, hallazgos compatibles con una obstrucción intestinal. Al abrir el abdomen (laparotomía exploradora) se encontró un nudo entre el íleon (la parte final del intestino delgado) y la región ileocecal; el intestino afectado estaba todavía viable (es decir, con buena circulación), el ciego y el colon ascendente eran móviles, y la punta del apéndice estaba gangrenosa (tejido muerto). Se deshizo el nudo y se realizó una apendicectomía (extirpación del apéndice). Dado que la paciente presentó inestabilidad de las constantes vitales durante la operación, se decidió posponer una hemicolectomía derecha (extirpar la porción derecha del colon) y, en su lugar, fijar el ciego y el colon ascendente a la pared abdominal para prevenir nueva torsión.",
+            "B3": "Resumen clínico (nivel lector universitario)\n\nPresentación y antecedentes\n- Mujer de 20 años, un día después de una cesárea por bradicardia fetal severa. Antecedentes relevantes: preeclampsia (sin signos de gravedad) y desnutrición crónica reciente (IMC 16,5 kg/m2). Sin cirugías abdominales previas.\n- Síntomas al ingreso: distensión abdominal progresiva, calambres, ausencia de flatos y deposiciones (obstipación), vómitos alimentarios y biliosos de 1 día de evolución.\n\nExamen físico y pruebas iniciales\n- Signos vitales anormales: hipotensión (90/70 mmHg), taquicardia (116–120 lpm), taquipnea (22–24 rpm), afebril.\n- Abdomen: muy distendido, movimientos peristálticos visibles, sensibilidad generalizada con mayor dolor en cuadrante inferior derecho; signo de onda de líquido positivo (sugiere líquido intraperitoneal).\n- Hallazgo cutáneo inicial: lesión lineal superficial de 3 cm en labio mayor izquierdo, interpretada en primera instancia como quemadura de yodo.\n- Laboratorio: leucopenia marcada (GB 1.780/µl) con predominio de neutrófilos (88%), hemoglobina 12,7 g/dl, trombocitopenia (plaquetas 78 x10^3/µl). Función renal normal; enzimas hepáticas ligeramente elevadas.\n- Radiografía abdominal simple: múltiples niveles hidroaéreos centrales y asas dilatadas; borramiento del espacio pélvico compatible con líquido libre/colección. No se realizó TC por limitaciones de recursos.\n\nDiagnóstico preoperatorio\n- Abdomen agudo por sospecha de obstrucción intestinal por vólvulo del intestino delgado (obstrucción alta).\n\nHallazgos y conducta intraoperatoria\n- Exploración con anestesia general: nudo ileocecal (íleon distal enroscado alrededor del ciego y colon ascendente proximal). El íleon, el ciego y el colon ascendente eran móviles y, en apariencia, viables. La punta del apéndice estaba enredada en el nudo y presentaba gangrena local. Existían ≈4 litros de líquido seroso intraperitoneal.\n- Durante la cirugía la paciente se volvió hemodinámicamente inestable (PA 80/50 mmHg) y requirió vasopresores. Según el informe, se procedió a una hemicolectomía derecha, descompresión proximal y distal de los tramos intestinales dilatados, y fijación (cecopexia) del ciego y colon ascendente a la pared abdominal posterolateral.  \n\nEvolución postoperatoria y desenlace\n- Inicialmente fue extubada y mantenida NPO; recibió reposición hídrica y soporte vasopresor. Persistió hipotensa a pesar de líquidos y vasopresores.\n- Se inició terapia antibiótica empírica (ceftriaxona + metronidazol) por sospecha de shock séptico de posible origen genitourinario.\n- En el primer día posoperatorio la lesión vulvar se extendió hacia la región suprapúbica con signos clínicos compatibles con gangrena de Fournier (necrosis de tejidos blandos del periné). Antibióticos escalados a meropenem + vancomicina + metronidazol.\n- Se realizó desbridamiento radical de la zona afectada y la paciente fue trasladada a UCI quirúrgica intubada por shock séptico persistente y retraso en la recuperación anestésica.\n- Falleció en el segundo día posoperatorio por shock séptico refractario y fallo multiorgánico.\n\nInterpretación y puntos clave\n- Diagnóstico anatómico: nudo ileocecal (ileocecal knot) que produjo obstrucción intestinal aguda; apéndice con gangrena focal por enredo. El nudo puede causar compromiso vascular rápido y requiere manejo quirúrgico urgente.\n- Complicaciones críticas en este caso: inestabilidad hemodinámica intraoperatoria, insuficiencia de respuesta a resucitación, y evolución hacia gangrena de Fournier con sepsis rápida y refractaria.\n- Factores que probablemente contribuyeron al desenlace adverso: estado posparto inmediato, desnutrición, citopenias (leucopenia y trombocitopenia), posible foco infeccioso perineal precoz y limitaciones en recursos diagnósticos (no TC). La leucopenia con neutrofilia relativa y la trombocitopenia sugieren un estado sistémico grave que pudo empeorar la capacidad de respuesta a la infección.\n- Enseñanzas prácticas: el nudo ileocecal es una causa rara pero potencialmente letal de obstrucción intestinal; requiere diagnóstico y tratamiento quirúrgicos rápidos. Una lesión perineal aparentemente menor en un contexto posoperatorio o posparto debe vigilarse estrechamente porque puede progresar a infección necrotizante (Fournier) con rapidez. En entornos con recursos limitados, la vigilancia clínica y la intervención temprana son decisivas, pero aun así existe alto riesgo de mortalidad cuando concurren factores de riesgo sistémicos.\n\nEmpatía final\nEste caso ilustra cómo una complicación intestinal aguda combinada con una infección necrotizante del periné y un estado sistémico comprometido pueden evolucionar rápidamente a sepsis refractaria, pese a intervención quirúrgica activa. Es una pérdida trágica de una paciente joven; reconozco el impacto emocional y clínico que este desenlace tiene para la familia y el equipo tratante."
+        }
+    },
+    {
+        "article": "Un hombre de 38 años se presentó en el hospital con opresión en el pecho y falta de aire. Tres años antes, había experimentado síntomas similares después de la actividad y recibió tratamiento en nuestro hospital. La ecocardiografía ambulatoria indicó una masa de eco del corazón izquierdo que sugería un mixoma, lo que llevó a su ingreso para una evaluación adicional. El examen físico reveló pigmentación de las orejas del paciente caracterizada por múltiples puntos pequeños de color café y negro. La tomografía computarizada abdominal (TC) mostró múltiples hígados y pequeños quistes en el riñón izquierdo. Las pruebas genéticas identificaron mutaciones en los genes TTN y PRKAR1A. El diagnóstico de CNC se confirmó mediante examen clínico, imágenes y pruebas genéticas. Después del tratamiento sintomático, la condición del paciente mejoró; sin embargo, rechazó la intervención quirúrgica. El 20 de septiembre de 2023, el paciente se presentó en nuestro hospital con opresión en el pecho y falta de aire exacerbadas. Informó dificultad para permanecer acostado boca arriba y necesidad de sentarse erguido para respirar. El examen físico reveló distensión de la vena yugular, desplazamiento hacia la izquierda y hacia abajo del límite del corazón, ritmo cardíaco irregular en la auscultación y un murmullo de la válvula mitral de intensidad 2/6-3/6 en el cuarto espacio intercostal a lo largo del margen izquierdo del esternón. Se escucharon estertores húmedos en ambos campos pulmonares medio e inferior. La palpación reveló un hígado firme que se extendía tres dedos por debajo del proceso xifoides y dos dedos por debajo de la caja torácica, junto con un edema de pitting leve en ambas extremidades inferiores. Las imágenes ecocardiográficas indicaron un agrandamiento global del corazón, dilatación del seno aórtico y arteria pulmonar, regurgitación mitral pequeña a moderada y una masa ecógena irregular que medía 54 mm × 43 mm en la cámara izquierda unida al tabique auricular. La fracción de eyección del ventrículo izquierdo (FEVI) fue del 23,1 %, con acortamiento fraccional (FS) del 10,9 %. La electrocardiografía demostró fibrilación auricular (frecuencia ventricular promedio, 150 latidos/min) y ondas Q anormales en las derivaciones V1-V3. Basándose en la historia del paciente, el diagnóstico incluyó DCM y CNC con mixoma cardíaco. Dada la presencia de insuficiencia cardíaca en etapa terminal y mixoma cardíaco concurrente, el paciente fue hospitalizado y se consideró el trasplante de corazón como una opción terapéutica viable para abordar ambas afecciones simultáneamente. Un corazón de donante adecuado estuvo disponible para su trasplante inmediato el 1 de octubre de 2024.\n\n\nProcedimiento quirúrgico\n\nLa piel y los tejidos subcutáneos se incisionaron cuidadosamente capa por capa a través de una esternotomía media. El esternón se abrió longitudinalmente y se controló el sangrado mediante electrocoagulación y cera ósea. La exploración extracardíaca reveló un agrandamiento global del corazón, más prominente en el ventrículo izquierdo. El corazón mostró una disminución de la fuerza contráctil. La aorta y la arteria pulmonar principal (AP) se diseccionaron desde la región supravalvular. Algunos tejidos se conservaron para suturarlos posteriormente, mientras que la mayor parte de la aurícula derecha enferma, la aurícula izquierda (AL), el ventrículo derecho y el ventrículo izquierdo se extirparon. La resección reveló una masa mucoide de color blanco grisáceo. Los tejidos de la aurícula izquierda del donante y del receptor se suturaron utilizando hilos Prolene 3/0 dobles continuos. La anastomosis se inspeccionó meticulosamente varias veces y no se observó sangrado significativo. De forma similar, la anastomosis término-terminal de la aorta ascendente del donante y la arteria pulmonar del receptor se realizó utilizando suturas Prolene 5/0 continuas, y una inspección cuidadosa no reveló sangrado.\n\nAdemás, la LA del donante y la PA del receptor se cerraron de forma segura utilizando suturas Prolene 5/0 dobles y continuas. Los tejidos de la vena cava inferior tanto del donante como del receptor se suturaron de forma similar con suturas Prolene 5/0, y se realizaron varias inspecciones para confirmar que no había presencia de sangrado significativo. El lado izquierdo del corazón se desinfló y, a medida que comenzó el recalentamiento, se restableció la oxigenación, se soltó la aorta ascendente y el corazón volvió espontáneamente al ritmo sinusal. Se aplicó sutura continua con Prolene 5/0 tanto a la vena cava superior del donante como del receptor y se inspeccionó de forma diligente para garantizar la ausencia de sangrado significativo. Después de la interrupción exitosa de la circulación asistida, se descanuló la cavidad venosa. Se recogieron muestras de tejido del corazón izquierdo y de la materia gris del paciente para un examen histopatológico, y se confirmó el diagnóstico de DCM y mixoma cardiaco.\n\n\nManejo postoperatorio\n\nEl primer día después del trasplante de corazón, el paciente produjo 1200 ml de orina. Los exámenes de laboratorio revelaron un nivel de troponina T hipersensible de 796.70 ng/L y un nivel de NT-proBNP de 10798 pg/ml. El recuento completo de sangre mostró un recuento de glóbulos blancos de 17.15 × 109/L, sin anomalías significativas en otros resultados de exámenes. El ecocardiógrafo mostró un EFV del 65 %, FS del 35 %, un espesor de la pared ventricular normal y ecogenicidad, y no se observaron anomalías discernibles en la morfología y estructura de la válvula. Después del trasplante de corazón, se administró una terapia hormonal intravenosa de succinato sódico de metilprednisolona (0.25 g) para mejorar la inmunidad, y se proporcionó un tratamiento intravenoso antiinfeccioso con cefoperazona y sulbactam sódico (2 g). El paciente recibió una solución nutriente y tiopronina en el primer día después de la cirugía. En el día tres postoperatorio, se reemplazó el succinato sódico de metilprednisolona con acetato de prednisona oral (25 mg). Se administraron cápsulas de micofenolato de mofetilo (0.5 g) por vía oral para minimizar el rechazo del corazón, y se administró acetato de carpofénico intravenoso (50 mg) para prevenir infecciones fúngicas. La producción de orina del paciente fue de 2000 ml, con niveles de troponina T hipersensible de 390 ng/L, niveles de NT-proBNP de 7877 pg/ml, y un recuento de leucocitos de 12.15 × 109/L. En el día siete postoperatorio, se introdujeron cápsulas de tacrolimus a una dosis oral de (1 mg) para minimizar el rechazo del paciente al corazón del donante, con un cuidadoso monitoreo de las concentraciones sanguíneas. Subsiguientemente, la dosis oral de acetato de prednisona se redujo gradualmente a (10 mg) mientras se ajustaba la concentración sanguínea de tacrolimus a 10.90 ng/L. La recuperación del paciente mejoró. El 20 de octubre de 2023, la ecocardiografía de seguimiento (Fig. 6) no mostró anomalías, con niveles de troponina T de 85 ng/L, NT-proBNP de 210 pg/ml, y todos los demás resultados de exámenes dentro de los rangos normales. El paciente exhibió una excelente recuperación postoperatoria y fue dado de alta. Las visitas regulares de seguimiento a nuestro departamento después del alta mostraron que el paciente permanece en buen estado.\n\nMH - Humanos\nMH - *Cardiomiopatía, Dilatada/cirugía/etiología/diagnóstico/diagnóstico por imágenes\nMH - Hombre\nMH - *Complejo de Carney/genética/diagnóstico/cirugía/complicaciones\nMH - Adulto\nMH - *Trasplante de corazón\nMH - *Mixoma/complicaciones/cirugía/diagnóstico por imágenes/diagnóstico/genética\nMH - *Insuficiencia cardiaca/etiología/diagnóstico/cirugía\nMH - *Neoplasias cardiacas/cirugía/complicaciones/diagnóstico por imágenes/diagnóstico/genética\nMH - Resultado del tratamiento\nMH - Subunidad/genética de la proteína quinasa Rlalpha dependiente de AMP cíclico\n",
+        "gold_summary": "Aquí, reportamos un caso de insuficiencia cardiaca debido al síndrome de Carney que resultó en mixoma cardiaco combinado con cardiomiopatía dilatada. Un hombre de 35 años de edad fue admitido en el hospital hace tres años debido a opresión torácica repentina y falta de aire. La ecocardiografía indicó mixoma, y una combinación de cribado genético y examen físico confirmó el síndrome de Carney con mixoma cardiaco. Después del tratamiento sintomático, fue dado de alta. Las intervenciones quirúrgicas no fueron consideradas en ese momento. Sin embargo, la opresión torácica y los síntomas de falta de aire del paciente empeoraron, y volvió al hospital. Se confirmó una función cardiaca de grado IV de la New York Heart Association, y la ecocardiografía indicó la presencia de cardiomiopatía dilatada acompañada de mixoma cardiaco. En última instancia, la insuficiencia cardiaca del paciente fue tratada con éxito con un trasplante cardiaco.\n",
+        "synthetic_summary": {
+            "B1": "Este es el cuento de un hombre que tuvo problemas con su corazón. Tenía 38 años y se sentía con opresión en el pecho y le costaba respirar. Hace tres años ya había tenido síntomas parecidos. Los médicos vieron en una ecografía que tenía una masa dentro del corazón. Esa masa se llama mixoma, que es un tumor que crece en el corazón.\n\nTambién tenía pequeñas manchas oscuras en las orejas y quistes en el hígado y en un riñón. Las pruebas de genética mostraron cambios en dos genes. Todo eso ayudó a los médicos a decir que tenía el síndrome de Carney. El síndrome de Carney es una condición que puede causar manchas en la piel y tumores como el mixoma.\n\nCon el tiempo, su corazón se hizo muy grande y se volvió muy débil. Esto se llama cardiomiopatía dilatada. Sus síntomas empeoraron mucho hasta que ya no podía acostarse boca arriba sin sentirse mal. Los médicos pensaron que la mejor opción era darle un corazón nuevo.\n\nEl 1 de octubre de 2024 recibió un trasplante de corazón. La operación fue compleja, pero salió bien. Después de la cirugía, su nuevo corazón funcionó correctamente. Recibió medicinas para evitar infecciones y para que su cuerpo no rechazara el nuevo corazón. Con el tiempo, sus pruebas volvieron a la normalidad y se recuperó muy bien.\n\nHoy está en buen estado y sigue con controles médicos regulares. Los médicos lo vigilan para asegurarse de que siga mejorando.",
+            "B2": "Resumen comprensible (nivel B2, para lectores de 11–17 años)\n\nUn hombre de 38 años llegó al hospital porque sentía opresión en el pecho y le costaba respirar. Tres años antes había presentado síntomas parecidos y, tras pruebas, se detectó en su corazón una masa que parecía un mixoma, un tumor benigno que puede crecer dentro de las cavidades del corazón y causar problemas.\n\nAl explorarlo, los médicos vieron que tenía manchas oscuras en las orejas y que en una tomografía abdominal había pequeños quistes en el hígado y el riñón. Las pruebas genéticas encontraron cambios en dos genes: PRKAR1A, que se asocia con el síndrome de Carney (una enfermedad hereditaria que puede causar tumores y pigmentación de la piel), y TTN, que puede relacionarse con debilidad del músculo cardíaco. Con estos datos —los hallazgos físicos, las imágenes y los genes— se confirmó el diagnóstico de síndrome de Carney con mixoma cardíaco y además cardiomiopatía dilatada (DCM), que significa que el corazón estaba agrandado y no latía con suficiente fuerza.\n\nCon el paso del tiempo, los síntomas empeoraron: el paciente ya no podía estar tumbado boca arriba porque le costaba respirar y tenía signos de insuficiencia cardíaca grave, como hinchazón en las piernas y acumulación de líquido en los pulmones. Las pruebas mostraron una fracción de eyección del ventrículo izquierdo muy baja (23 %) —esto indica que el corazón bombeaba poco— y fibrilación auricular (un ritmo cardíaco irregular). Dado que tenía insuficiencia cardíaca en fase terminal y un mixoma, los médicos consideraron el trasplante de corazón la mejor opción para tratar las dos condiciones a la vez.\n\nUn corazón de donante adecuado estuvo disponible y se realizó el trasplante. En la operación, se retiró el corazón enfermo y se implantó el corazón del donante. Los cirujanos revisaron cuidadosamente las uniones entre vasos y cavidades para evitar sangrado. Se tomaron muestras del tejido retirado y el examen posterior confirmó la cardiomiopatía dilatada y el mixoma.\n\nDespués de la cirugía, el paciente recibió cuidados intensivos: medicamentos para prevenir el rechazo del nuevo corazón (inmunosupresores como prednisona, micofenolato y tacrolimus), antibióticos y fármacos para evitar infecciones fúngicas. En los primeros días había marcadores cardíacos y algunas cifras inflamatorias elevadas, lo cual es esperado tras una cirugía mayor, pero con el tratamiento esos valores bajaron. La ecocardiografía mostró que el nuevo corazón funcionaba bien (fracción de eyección alrededor del 65 %) y no había problemas visibles con las válvulas o la estructura. El paciente se recuperó bien, fue dado de alta y, en los controles posteriores, permaneció en buen estado.\n\nQué significa esto y próximos pasos: el trasplante resolvió tanto la falla del músculo cardíaco como el problema del mixoma. El paciente necesitará controles médicos regulares y tratamiento con medicamentos inmunosupresores de por vida para prevenir el rechazo del órgano. También será importante el seguimiento por genética y para detectar posibles otros problemas relacionados con el síndrome de Carney.\n\nEste caso muestra cómo una enfermedad genética poco frecuente puede afectar al corazón y cómo, en casos graves, el trasplante puede ser una solución que salva la vida. El equipo médico actuó con cuidado durante la cirugía y en el manejo posterior, y el paciente tuvo una buena recuperación.",
+            "B3": "Resumen clínico comprensible y empático\n\nPaciente y presentación\n- Hombre de 38 años con episodios recurrentes de opresión torácica y disnea. Tres años antes ya había presentado síntomas similares; en ese momento una ecocardiografía ambulatoria detectó una masa en el corazón izquierdo compatible con mixoma.\n- La exploración reveló pigmentación cutánea en las orejas (múltiples máculas café/negro). La tomografía abdominal mostró alteraciones hepáticas y pequeños quistes renales. El estudio genético identificó mutaciones en PRKAR1A y TTN.\n- Con esos hallazgos —masa cardiaca, pigmentación cutánea y mutación en PRKAR1A— se confirmó el diagnóstico de complejo de Carney (CNC). La mutación en TTN apoyó la presencia de una miocardiopatía dilatada (DCM).\n\nCómo progresó la enfermedad\n- Tras tratamiento sintomático inicial el paciente mejoró pero rechazó cirugía en ese momento. Más tarde volvió con empeoramiento marcado: ortopnea (incapacidad para permanecer acostado por dificultad respiratoria), ingurgitación yugular, soplo mitral, estertores pulmonares, hepatomegalia y edema periférico.\n- Ecocardiograma: corazón globalmente dilatado, dilatación de seno aórtico y arteria pulmonar, regurgitación mitral leve-moderada y una masa ecogénica de 54 × 43 mm en la aurícula izquierda adherida al septo interauricular. Función sistólica muy reducida: fracción de eyección del ventrículo izquierdo (FEVI) 23,1% (normal ≈55–70%).\n- ECG: fibrilación auricular con respuesta ventricular rápida (≈150 lpm) y ondas Q patológicas en V1–V3.\n- Diagnóstico final antes de cirugía: miocardiopatía dilatada terminal con mixoma cardíaco en el contexto de complejo de Carney.\n\nDecisión terapéutica y cirugía\n- Debido a insuficiencia cardíaca en estadio terminal y a la masa intracardíaca, se consideró el trasplante cardíaco como la opción que podía resolver simultáneamente ambos problemas. Se obtuvo un corazón donante y se realizó trasplante por esternotomía media con técnica bicava/anastomosis habituales.\n- Durante la intervención se extirpó el corazón enfermo; la pieza mostró mixoma mucoide grisáceo. La anatomía y las anastomosis fueron verificadas varias veces sin sangrado significativo.\n- El examen histopatológico confirmó la miocardiopatía dilatada y el mixoma.\n\nEvolución postoperatoria\n- En las primeras 48–72 horas hubo elevación esperable de marcadores (troponina T y NT-proBNP) y leucocitosis, pero buena diuresis. La ecocardiografía temprana mostró FEVI normalizada (≈65%) y grosor de pared ventricular normal, sin alteraciones valvulares.\n- Esquema de inmunosupresión e profilaxis: metilprednisolona intravenosa inicialmente, transición a prednisona oral, micofenolato de mofetilo y, desde el día 7, tacrolimus con control de niveles sanguíneos. Antibióticos y antifúngicos de profilaxis también administrados.\n- Progresivamente los marcadores cardiacos y los síntomas mejoraron; en el control el corazón funcionaba bien, los valores de troponina y NT-proBNP descendieron y el paciente fue dado de alta en buen estado. Seguimientos ambulatorios posteriores mostraron recuperación sostenida.\n\nSignificado clínico y recomendaciones\n- Qué significa el diagnóstico: el complejo de Carney es un síndrome genético (frecuentemente por mutaciones en PRKAR1A) que predispone a mixomas cardíacos, pigmentación cutánea y tumores endocrinos u otras neoplasias. La mutación en TTN está asociada a miocardiopatía dilatada familiar. Ambos hallazgos explican la combinación de tumor cardíaco y fallo ventricular en este paciente.\n- Por qué se eligió el trasplante: el paciente tenía insuficiencia cardíaca avanzada con función ventricular gravemente reducida; el trasplante resolvió la falla mecánica y eliminó la masa tumoral intracardíaca.\n- Qué sigue para el paciente: vigilancia y manejo a largo plazo incluyen\n  - Terapia inmunosupresora de por vida con monitorización de niveles (p. ej., tacrolimus), y vigilancia estrecha para rechazo, infecciones y efectos adversos.\n  - Controles cardiológicos periódicos (ecocardiogramas, marcadores).\n  - Seguimiento por genética y cribado familiar: las mutaciones identificadas justifican consejo genético y estudio de familiares de primer grado.\n  - Vigilancia para otras manifestaciones del CNC (evaluación endocrinológica y cribado para nuevos tumores).\n  - Atención a la adherencia a la medicación y campañas de prevención (vacunación, profilaxis según indicación).\n\nComentario empático final\nEste caso muestra cómo una enfermedad genética poco frecuente puede combinar un tumor cardiaco benigno pero potencialmente peligroso (mixoma) con una miocardiopatía que progresa a insuficiencia terminal. El trasplante permitió recuperar función cardíaca y síntomas, pero impone una nueva etapa de cuidados crónicos y seguimiento multidisciplinario. El equipo clínico y el paciente han logrado una recuperación favorable hasta la última visita de control."
+        }
+    },
+    {
+        "article": "Un paciente de 52 años de edad con un diagnóstico inicial de arteria pulmonar fue admitido en el departamento de cardiología para una evaluación médica y una decisión sobre el tratamiento posterior. El paciente tenía un historial de neumotórax espontáneo del lado derecho, tratado con toracocentesis y drenaje por vacío 35 años antes. El paciente sentía una disnea creciente al hacer ejercicio. También se quejaba de signos de insuficiencia ventricular derecha y cianosis. Cuatro años antes, el paciente fue hospitalizado tres veces por fibrilación auricular paroxística que se convirtió en ritmo sinusal por cardioversión eléctrica, además de que el examen electrocardiográfico era normal.\n\nEn ese mismo año, la angiografía coronaria indicó arterias coronarias normales. La ecocardiografía reveló una hipertensión pulmonar leve con una presión sistólica calculada en el ventrículo derecho de 36 mmHg sin dilatación de ese ventrículo.\n\nEn los años siguientes, se observó insuficiencia cardiaca progresiva con aumento de la presión arterial pulmonar en la ecocardiografía. Se realizó angio-CT en dos ocasiones y se excluyó la hipertensión pulmonar tromboembólica crónica en cada ocasión. La tomografía computarizada de alta resolución excluyó la patología pulmonar intersticial. La espirometría fue normal. La detección de enfermedades autoinmunes y la infección por VIH fue negativa.\n\n\nLínea de tiempo: historia, curso de la enfermedad, diagnóstico y tratamiento\n\n1976  neumotórax derecho\n2007 Hospitalizado tres veces por fibrilación auricular e insuficiencia cardiaca. Se le realizaron ecocardiografías, cardioversiones y coronografías. En cada ocasión, fue dado de alta de los servicios con diagnósticos de fibrilación auricular, insuficiencia cardiaca e insuficiencia cardiaca de clase II de la NYHA.\n2010-2011: Aumento de la falta de aire y síntomas de insuficiencia cardiaca. El paciente fue hospitalizado tres veces. Se detectaron características indirectas de hipertensión pulmonar en ecocardiografía. Se realizó tres veces un examen de tórax por TAC; se excluyó la embolia pulmonar o la hipertensión arterial pulmonar tromboembólica crónica (2 x angio-TAC) o la fibrosis pulmonar (tomografía computarizada de alta resolución).\nSe estableció el diagnóstico de hipertensión pulmonar, clase III de la OMS.\nDEC-2011 Admisión a la clínica de cardiología – ecocardiografía (TTE, TEE), prueba de caminata de 6 minutos, NT-proBNP, cateterización cardiaca derecha, prueba de vasoreactividad pulmonar.\nSe estableció el diagnóstico de hipertensión pulmonar arterial irreversible.\nSe ha iniciado el tratamiento con iloprost y sildenafil\nEn enero de 2012, visita de control: mejora en la clase de la OMS, disminución de la concentración de NT-proBNP e incremento de la distancia en la prueba de 6 minutos.\nMAY-2012. Control RHC. La SaO2 de las muestras de sangre obtenidas durante el RHC de la arteria del lóbulo superior del pulmón derecho fue del 87 %.\nEl diagnóstico angiográfico de las arterias pulmonares reveló fístulas de HAP entre las arterias subclavianas y el lóbulo superior del pulmón derecho.\nJUN 2012  angiografía por TC de las arterias sistémicas reveló la presencia adicional de fístulas arteriales bronquiales en el lóbulo superior de las arterias del pulmón derecho\nIII-2013 Embolización de fístulas\nVI-2013. Muerte como resultado del empeoramiento de la insuficiencia cardiaca, combinado con neumonía.\n\n\n\nEn el ingreso a nuestra clínica, la clase funcional del paciente fue evaluada como OMS III. En el examen físico, el segundo sonido cardiaco (S2) fue acentuado con S2 dividido ensanchado. Además, la auscultación cardiaca indicó un murmullo holosistólico de regurgitación tricuspídea. La auscultación del tórax no mostró un murmullo vascular. La cianosis periférica y central fue marcada. Se examinaron la hepatomegalia, el edema periférico y las venas varicosas bilateralmente.\n\nLa SaO2 obtenida por el método de oximetría de pulso se redujo al 88 %. La electrocardiografía reveló fibrilación auricular, desviación del eje derecho y onda T negativa en las derivaciones precordiales v1-v3. Las pruebas adicionales fueron las siguientes: concentración de NT-proBNP - 3383 pg/ml, distancia de la prueba de caminata de seis minutos - 373 m con 7/10 puntos en la escala de disnea de Borg.\n\nLa ecocardiografía mostró características de hipertensión pulmonar grave: agrandamiento del ventrículo derecho a 44 mm (cuatro cámaras), con función deprimida del TAPSE del ventrículo derecho de 9 mm, agrandamiento del área de la aurícula derecha a 40 cm2, regurgitación tricuspídea grave (++++), aumento del PSVR calculado a 112 mmHg, acortamiento del tiempo de aceleración de la arteria pulmonar a 60 ms y derrame pericárdico leve. No hubo defecto en el tabique interventricular. La ecocardiografía transesofágica tampoco mostró un defecto en el tabique auricular, lo que se confirmó más tarde con angio-TAC.\n\n\nLa SaO2 de la sangre obtenida de la arteria radial se redujo al 87,8%. Se realizó un cateterismo cardiaco derecho. La SaO2 de las muestras de sangre obtenidas durante el RHC de la vena cava superior, la vena cava inferior, la aurícula derecha, el tronco pulmonar, la arteria del lóbulo medio del pulmón derecho y la arteria pulmonar izquierda ascendieron respectivamente a: 64,8%; 77,4%; 73,2%; 70,2%; 69,3%; 71,2% y no indicaron la presencia de un shunt de izquierda a derecha.\n\nLas mediciones hemodinámicas mostraron una hipertensión pulmonar precapilar grave, irreversible en las pruebas de vasoreactividad con óxido nítrico inhalado (80 ppm) y una combinación de sildenafil oral (50 mg) y óxido nítrico inhalado (80 ppm).\n\nEn base a todos los datos clínicos y los resultados de la RHC, se estableció un diagnóstico de hipertensión pulmonar idiopática irreversible.\n\nSe inició el tratamiento con iloprost inhalado (Ventavis) 6 × 5 µg y sildenafil (Revatio) por vía oral 3 × 20 mg. Además, se administraron digoxina (0,1 mg diarios), warfarina (INR rango: 2-3), furosemida (40 mg por vía oral diarios) y espironolactona (100 mg diarios).\n\nUn mes después se realizó un seguimiento no invasivo. El paciente manifestó una mejoría en la capacidad física, clase II según la OMS, concentración de NT-proBNP: 1014 pg/ml. Distancia en la prueba de caminata de seis minutos: 471 m.\n\nCinco meses después se realizó una evaluación invasiva. La RHC mostró valores de PAP más elevados que en las mediciones iniciales [75,4/51,8 (59,7) mm Hg] y PVR (13,4 WU) (Tabla 22 – control RHC).\n\nLa saturación de oxígeno de las muestras de sangre obtenidas durante la RHC de la arteria lobular superior del pulmón derecho fue elevada y ascendió al 89.7%.\n\nEn la angiografía pulmonar se detectó la reducción del trazo vascular periférico típico de la hipertensión arterial pulmonar y la falta de contraste de la arteria del lóbulo superior derecho. Además, se encontró evidencia de flujo sanguíneo retrógrado visible como un contraste negativo en la arteria pulmonar derecha. Después, se realizó una arteriografía de la arteria subclavia derecha y se detectó una enorme malformación vascular que se comunicaba con la arteria del lóbulo superior derecho.\n\nLa angio-TC de las arterias sistémicas confirmó la presencia de las fístulas previamente descritas y reveló la presencia adicional de fístulas de la arteria bronquial en el lóbulo superior de las arterias del pulmón derecho.\n\nSe realizó embolización selectiva de las fístulas (mezcla al 50% de Lipiodol y pegamento monomérico de n-butil-2-cianoacrilato). La embolización no produjo ningún cambio clínico en el estado del paciente.\n\nMH - Fístula arterio-arterial/*complicaciones\nMH - *Cateterización cardiaca\nMH - Angiografía por tomografía computarizada\nMH - Hipertensión pulmonar primaria familiar/*diagnóstico/terapia farmacológica\nMH - Resultado fatal\nMH - Insuficiencia cardiaca/fisiopatología\nMH - Humanos",
+        "gold_summary": "Un paciente caucásico de 52 años de edad con hipertensión pulmonar (HP) confirmada por ecocardiografía fue admitido en el departamento de cardiología debido a disnea de esfuerzo y signos de insuficiencia ventricular derecha. La exploración rutinaria para detectar causas de HP secundaria fue negativa. El cateterismo cardiaco derecho (CCR) confirmó una HP arterial de alto grado [presión arterial pulmonar media (PAPm); 50,6 mmHg, presión de enclavamiento pulmonar (PWP); 11,3 mmHg, resistencia vascular pulmonar (PVR); 11,9 unidades de Wood (UW)] irreversible en la prueba con óxido nítrico inhalado. La saturación de oxígeno (SaO2) de las muestras de sangre obtenidas durante el primer CCR osciló entre 69,3 y 73,2%. Se diagnosticó hipertensión arterial pulmonar idiopática. Se inició el tratamiento con iloprost inhalado y sildenafil.\n\nEl control RHC, realizado 5 meses después, mostró valores de mPAP (59,7 mmHg) y PVR (13,4 WU) más altos en comparación con la medición inicial. El SaO2 de sangre obtenida durante el RHC de la arteria del lóbulo superior del pulmón derecho fue elevado y ascendió al 89,7 %.\n\nLuego se realizó una arteriografía pulmonar. Se encontró falta de contraste en la arteria del lóbulo superior derecho con evidencia de flujo sanguíneo retrógrado visible como contraste negativo en la arteria pulmonar derecha. Después, una arteriografía de la arteria subclavia derecha detectó una enorme malformación vascular que se comunicaba con la arteria del lóbulo superior derecho. Después, un angiograma por tomografía computarizada (angio-CT) reveló adicionalmente el agrandamiento de las arterias bronquiales que se originaban en las fístulas hacia la arteria pulmonar del lóbulo superior derecho.\n\nA pesar del tratamiento farmacológico intensivo, que incluyó la terapia de la hipertensión pulmonar y la embolización percutánea de las fístulas, el estado del paciente siguió deteriorándose. Falleció tres meses después de la embolización debido a una insuficiencia cardiaca grave complicada por neumonía.\n",
+        "synthetic_summary": {
+            "B1": "Este es el cuento de un hombre de 52 años que tuvo mucha dificultad para respirar y problemas en el lado derecho del corazón.\n\nQué le pasaba\n- Tenía cada vez más falta de aire cuando caminaba o hacía esfuerzos.  \n- Su piel se veía un poco azulada por falta de oxígeno.  \n- El lado derecho del corazón estaba cansado y tenía líquido en el cuerpo (hinchazón).\n\nQué hicieron los médicos\n- Le hicieron muchas pruebas para buscar una causa. No encontraron trombos en los pulmones ni otras enfermedades del pulmón.  \n- Mediante una prueba especial con un catéter en el corazón comprobaron que la presión en las arterias del pulmón era muy alta. Eso se llama hipertensión pulmonar. Es como si las tuberías del pulmón tuvieran mucha presión y el corazón tuviera que esforzarse mucho.  \n- Los médicos pensaron que era una forma sin causa clara (hipertensión arterial pulmonar idiopática). Le dieron medicinas para bajar la presión en los pulmones y ayudar al corazón. Al principio se sintió mejor.\n\nQué encontraron después\n- Más tarde, vieron que la sangre en una parte del pulmón derecho tenía más oxígeno de lo esperado.  \n- Nuevas pruebas de imagen mostraron vasos sanguíneos anormales que conectaban arterias grandes del cuerpo con una arteria del pulmón derecho. Esas conexiones se llaman fístulas. Por allí pasaba sangre de forma equivocada.  \n- Intentaron cerrar esas fístulas con un procedimiento llamado embolización. Esto consiste en introducir material para taponar los vasos anormales.\n\nQué pasó al final\n- Aunque intentaron tratarlo con medicinas y con la embolización, su estado empeoró.  \n- Murió tres meses después por fallo del corazón y una infección en los pulmones.\n\nMensaje final (con cariño)\n- Los médicos hicieron muchas pruebas y trataron de ayudarlo.  \n- A veces, las enfermedades del corazón y de los pulmones son difíciles de curar.  \n- Es triste que este paciente no mejorara, pero su historia ayuda a los médicos a entender mejor estas situaciones para ayudar a otros en el futuro.",
+            "B2": "Here is a clear, gentle summary of the case:\n\nA 52-year-old man developed gradually worsening shortness of breath and signs of right‑sided heart failure. He had a past right lung collapse (pneumothorax) decades earlier and episodes of irregular heartbeat (atrial fibrillation). Over several years doctors ruled out common causes of lung blood‑vessel disease: repeated CT scans excluded chronic blood clots in the lungs and high‑resolution CT showed no lung scarring. Blood tests for autoimmune disease and HIV were negative, and basic lung function tests were normal.\n\nTests and key findings\n- Echocardiograms showed severe pulmonary hypertension (high pressure in the lung arteries) with a large, poorly working right ventricle and severe leakage of the tricuspid valve. He was cyanotic (bluish skin) and had low oxygen levels by pulse oximetry (~88%).\n- Right heart catheterization (RHC), a test that directly measures pressures inside the heart and lung arteries, confirmed very high pulmonary artery pressure and very high vascular resistance. These findings were not improved by inhaled nitric oxide, so the hypertension was judged irreversible.\n  - Initial RHC: mean pulmonary artery pressure about 50.6 mmHg (normal is much lower) and pulmonary vascular resistance 11.9 Wood units (very high).\n  - Five months later: pressures and resistance were even higher (mean pressure ~59.7 mmHg, resistance 13.4 WU).\n- Oxygen measurements from blood samples taken in the heart and lungs were generally low (around 69–73%), but an unusually high oxygen level (about 89.7%) was found in the artery that supplies the right upper lung. A high oxygen level in a pulmonary artery is abnormal and suggested that oxygenated blood from the body’s arteries was entering the pulmonary circulation.\n- Detailed angiography (imaging of blood vessels) showed large abnormal connections (fistulas) between systemic arteries (including the right subclavian artery and enlarged bronchial arteries) and the right upper-lobe pulmonary artery. These are direct vascular shunts that let oxygen-rich blood from the body’s arteries flow into the lung arteries.\n\nDiagnosis and treatment\n- The working diagnosis was idiopathic pulmonary arterial hypertension that had become irreversible. In addition, large systemic-to-pulmonary arterial fistulas were found in the right upper lung.\n- He was started on targeted pulmonary hypertension medications (inhaled iloprost and oral sildenafil) plus standard heart‑failure medicines (digoxin, diuretics, anticoagulation).\n- He initially felt better: after one month his walking distance and heart‑failure blood marker (NT‑proBNP) improved.\n- After the worsening seen on repeat RHC, the fistulas were treated by selective embolization (a minimally invasive procedure that blocks abnormal vessels using glue-like material). The embolization itself did not improve his symptoms.\n\nOutcome\n- Despite medical therapy and embolization, his heart failure progressed. He died three months after the embolization from worsening heart failure complicated by pneumonia.\n\nSimple explanations of a few terms\n- Pulmonary hypertension: high blood pressure inside the arteries that carry blood through the lungs; this makes the right side of the heart work harder and can lead to heart failure.\n- Right heart catheterization (RHC): a test where thin tubes measure pressures and oxygen levels inside the heart and lung arteries; it gives exact information about how severe the problem is.\n- Fistula: an abnormal connection between two blood vessels; here, arteries that normally belong to the systemic circulation were directly connected to lung arteries.\n- Embolization: a procedure to block an abnormal blood vessel to stop unwanted blood flow.\n\nOverall message\nThis was a complex case of severe pulmonary arterial hypertension that was made worse by hidden abnormal blood vessel connections in the right upper lung. Even with advanced medications and a targeted procedure to block the abnormal vessels, the disease progressed and the patient died. The case highlights how rare vascular abnormalities can complicate pulmonary hypertension and how difficult some forms of this disease are to treat. My condolences to the patient’s family — this was a serious, heartbreaking illness.",
+            "B3": "Resumen clínico breve y comprensible\n\nPaciente varón caucásico de 52 años con disnea progresiva al esfuerzo, cianosis y signos de insuficiencia ventricular derecha. Antecedentes relevantes: neumotórax espontáneo derecho hace 35 años y episodios previos de fibrilación auricular que precisaron cardioversión.\n\nPresentación y hallazgos iniciales\n- Clase funcional OMS III a la admisión; SaO2 por pulsioximetría ≈ 88 % (hipoxemia).\n- Exploración: acentuación del segundo ruido cardiaco, soplo holosistólico por insuficiencia tricuspídea severa, hepatomegalia y edemas periféricos.\n- Ecocardiografía: hipertensión pulmonar grave con ventrículo derecho dilatado (44 mm), función sistólica derecha deprimida (TAPSE 9 mm), aurícula derecha aumentada (40 cm2), insuficiencia tricuspídea cuantiosa y PAsistólica estimada elevada (PSVR ≈ 112 mmHg). Pequeño derrame pericárdico.\n- Analítica: NT‑proBNP elevado 3.383 pg/ml (marcador de sobrecarga cardiaca). Prueba de caminata de 6 minutos: 373 m.\n\nInvestigaciones diagnósticas\n- Estudios para causas secundarias de hipertensión pulmonar (embolia crónica, enfermedad pulmonar intersticial, autoinmunidad, VIH) fueron negativos.\n- Cateterismo cardiaco derecho (RHC) inicial confirmó hipertensión pulmonar precapilar severa: presión arterial pulmonar media (mPAP) ≈ 50,6 mmHg, presión de enclavamiento pulmonar 11,3 mmHg, resistencia vascular pulmonar (PVR) ≈ 11,9 Wood units. Prueba de vasorreactividad negativa → lesión vascular irreversible.\n- Saturaciones durante el primer RHC no mostraron shunt izquierda‑derecha.\n- Tras tratamiento médico hubo mejoría clínica y biomarcadores a 1 mes (NT‑proBNP descendió a 1.014 pg/ml; 6MWD aumentó a 471 m).\n- A los 5 meses, RHC de control mostró empeoramiento hemodinámico (mPAP ≈ 59,7 mmHg, PVR 13,4 WU). Llama la atención una saturación anormalmente alta (≈ 89,7 %) en la arteria lobar superior derecha.\n- Arteriografía y angio‑TAC sistémica demostraron fístulas arteriales sistémico → pulmonar: una gran malformación entre la arteria subclavia derecha y la arteria del lóbulo superior derecho, además de fístulas de arterias bronquiales hacia la misma arteria pulmonar.\n\nDiagnóstico y tratamiento\n- Diagnóstico final: hipertensión arterial pulmonar de alto grado inicialmente catalogada como idiopática/irrevocable, sobreañadida a una malformación arteriovenosa/arterio‑arterial sistémico → pulmonar en el lóbulo superior derecho.\n- Terapia médica para hipertensión pulmonar iniciada: iloprost inhalado (6 × 5 µg) y sildenafil oral (3 × 20 mg); además digoxina, anticoagulación con warfarina, furosemida y espironolactona.\n- Se realizó embolización selectiva de las fístulas con mezcla 50 % Lipiodol y adhesivo (n‑butil‑2‑cianoacrilato). La embolización no produjo mejoría clínica evidente.\n\nEvolución y desenlace\n- Pese al tratamiento médico y a la embolización, el paciente continuó deteriorándose y falleció tres meses después de la embolización por insuficiencia cardiaca descompensada complicada con neumonía.\n\nInterpretación y puntos clave para clínicos y pacientes\n- El paciente presentó hipertensión pulmonar precapilar severa e irreversible con repercusión derecha importante. Aunque inicialmente se clasificó como idiopática, las imágenes y la elevada saturación localizada en la arteria lobar superior derecha revelaron fístulas sistémico → pulmonar que pueden haber contribuido o agravado la hipertensión y la sobrecarga derecha.\n- Las fístulas arteriales sistémico → pulmonar (incluidas malformaciones de arteria bronquial o conexión desde la subclavia) pueden introducir flujo arterial sistémico en la circulación pulmonar, alterar las saturaciones y aumentar la carga hemodinámica. Su detección requiere alto índice de sospecha y estudios angiográficos dirigidos.\n- La prueba de vasorreactividad negativa y las cifras de PVR altas indicaron daño vascular establecido, lo que limita la reversibilidad con vasodilatadores. La embolización puede ser una opción, pero no siempre revierte la insuficiencia cardiaca si la hipertensión y la remodelación vascular están avanzadas.\n- En pacientes con hipertensión pulmonar severa y hallazgos discordantes de saturación o ausencia de contraste en un segmento pulmonar, es razonable investigar fístulas arteriales sistémicas mediante angio‑TAC/arteriografía sistémica lo antes posible, porque su cierre precoz podría modificar el curso en algunos casos.\n\nEmpatía\nEste caso ilustra la complejidad de la hipertensión pulmonar avanzada y cómo una malformación vascular poco frecuente puede complicar el diagnóstico y el tratamiento. A pesar de los esfuerzos terapéuticos, la enfermedad puede progresar rápidamente; el enfoque multidisciplinario precoz y la exploración angiográfica dirigida son importantes cuando aparece evidencia clínica o radiológica sugestiva de comunicaciones vasculares anómalas."
+        }
+    },
+    {
+        "article": "Paciente de 73 años, diagnosticada de enfermedad pulmonar obstructiva crónica (EPOC), hipertensión arterial (HTA), trastorno bipolar, ansiedad, depresión, hipotiroidismo y artritis reumatoide, condiciones para las cuales tiene prescrito el tratamiento reflejado en el Anexo I.\n\nRealiza una llamada telefónica a la farmacia comunitaria para solicitar información sobre una nueva medicación prescrita para el tratamiento de una infección de orina y un déficit de vitamina D, diagnosticados tras la realización de una analítica completa en el servicio de urgencias de un hospital privado.\n\nLa paciente es totalmente dependiente y no sale de casa, siendo su cuidadora la persona que siempre va a retirar su medicación y elabora los pastilleros semanales.\n\nLos fármacos prescritos para el tratamiento de la infección de orina fueron cefuroxima 250 mg (1 comprimido cada 12 horas durante 5 días) y butilescopolamina 10 mg (1 comprimido en la mañana si presentaba molestias).\n\nPara el déficit de vitamina D se le prescribió colecalciferol 50.000 U.I. (1 cápsula una vez al mes durante dos meses) y colecalciferol 25.000 UI (1 cápsula una vez al mes tras finalizar el envase de 50.000 U.I.).\n\nESTUDIO Y EVALUACIÓN\nSe lleva a cabo el servicio de dispensación (SD) sin incidencias, siguiendo la metodología expuesta en la Guía práctica para los Servicios Profesionales Farmacéuticos Asistenciales en la Farmacia Comunitaria. Posteriormente, la paciente contacta con la farmacia comunitaria, preocupada porque la nueva medicación le ha generado confusión, ya que ella tomaba unas cápsulas naranjas para su déficit de vitamina D prescritas por su médico de Atención Primaria hace unos meses y en la parte del informe de urgencias en la que figura el tratamiento venía reflejado una medicación nueva para ese mismo problema de salud. Además, coincidió con que su cuidadora habitual ya no podrá trabajar más con ella y no la podrá ayudar con su medicación. Por ello, se le propone a la paciente el servicio de Revisión del Uso del Medicamento (RUM) con el objetivo de evaluar el grado de conocimiento que tienen la paciente con respecto a sus patologías y su tratamiento, a la par que poder resolver posibles errores en la administración de los distintos fármacos que forman parte del mismo. Se le explica en qué consiste todo el procedimiento y decide aceptar.\n\nTras esto, se procedió a citar a la cuidadora en la farmacia con la tarjeta sanitaria de la paciente, su bolsa de medicación para hacer una revisión exhaustiva de su botiquín y el último informe de urgencias con el objetivo de recopilar toda la información necesaria para realizar el servicio asistencial vía telefónica. Durante la llamada con la paciente, se procede a cumplimentar el formulario RUM, el cual se volcó posteriormente en la plataforma SEFAC e_XPERT ®. Además, para poder evaluar correctamente todo el tratamiento farmacológico, se emplearon herramientas como el CIMA (donde se consultaron las fichas técnicas de los medicamentos) y el BotPlus (donde se consultaron las posibles interacciones farmacológicas).\n\nINTERVENCIÓN\nTras la primera toma de contacto a través de la entrevista telefónica y hacer revisión del botiquín, se pudo detectar que la paciente y su cuidadora no estaban haciendo una gestión apropiada de la medicación. Tras la revisión de su botiquín, se hallaron envases caducados y con anotaciones erróneas sobre su uso, blísteres con comprimidos partidos que no deberían de estarlo y acúmulo de varios envases de un mismo fármaco. Al tratarse de una paciente dependiente, polimedicada y con problemas para gestionar correctamente su tratamiento antes y durante la ausencia de su cuidadora habitual se decidió con el fin de garantizar la seguridad farmacoterapéutica y mejorar la adherencia al tratamiento derivar al servicio de sistema personalizado de dosificación (SPD). A través de la plataforma de SEFAC e_XPERT ® se procedió a redactar un informe de derivación a su médico de Atención Primaria (MAP) del Sistema Nacional de Salud (SNS) (ver Anexo II), donde se detallaba la inclusión de la paciente en el servicio de Revisión del Uso de la Medicación y su posterior derivación al servicio de SPD. Además, quedaron recogidas las siguientes propuestas de intervención:\n\nRevisión de la pauta posológica de tramadol 50 mg de liberación retardada por la existencia de un posible error en la prescripción.\n\nRevisión del tratamiento prescrito para el déficit de vitamina D por la existencia de una duplicidad terapéutica.\n\nCambio del absorbente de incontinencia de tipo pants a elástico alegando la situación de dependencia de la paciente y las dificultades para realizar una correcta colocación por parte de la cuidadora al pasar encamada la mayor parte del tiempo. Se aportaron los Códigos Nacionales (CN) correspondientes.\n\nRevisión del tratamiento para la EPOC por dificultades de empleo del inhalador y falta de adherencia terapéutica.\n\nRESULTADOS\nDurante la cita médica, la médico de atención primaria recibe el informe de derivación entregado a la cuidadora donde, además, se solicita contacto con la farmacia comunitaria para poder iniciar de forma correcta el servicio de SPD. Tras hablar con ella vía telefónica, se realizaron los siguientes cambios en su tratamiento:\n\nDéficit de vitamina D: anulación de calcifediol y sustitución por colecalciferol prescrito en el Servicio de Urgencias.\n\nArtritis reumatoide: modificación de pauta de tramadol de liberación prolongada a 1-0-1 y empleo de paracetamol 1000 mg 1-1-1 si precisa.\n\nIncontinencia urinaria: sustitución de absorbente tipo pants por elástico.\n\nEPOC: no se realizó un cambio de tratamiento. La médico de atención primaria consideró oportuno llevar a cabo una supervisión diaria por parte de la cuidadora en cada una de las tomas del inhalador.",
+        "gold_summary": "Paciente 73 años, dependiente, polimedicada y pluripatológica contacta telefónicamente con la farmacia comunitaria para solicitar información sobre un tratamiento de nueva prescripción para una infección de orina y un déficit de vitamina D. La dispensación de la medicación a su cuidadora deriva en mayores dudas a la paciente, por lo que se le ofrece el servicio de revisión del uso del medicamento (RUM). Durante la prestación del servicio se detectan varias incidencias en su tratamiento, por lo que se decide realizar un informe de derivación al médico de atención primaria para una revisión completa del tratamiento y poder así derivar a la paciente al servicio de Sistema Personalizado de Dosificación (SPD) con el fin de garantizar la seguridad farmacoterapéutica de la paciente y mejorar su adherencia al tratamiento.",
+        "synthetic_summary": {
+            "B1": "La señora tiene 73 años y muchas enfermedades. No puede salir de casa. Su cuidadora siempre le daba las medicinas, pero ahora ya no podrá ayudarla.\n\nFue al servicio de urgencias por una infección de orina y le dijeron que tiene falta de vitamina D (una vitamina que ayuda a los huesos). Le dieron medicinas nuevas. La paciente y su cuidadora se confundieron con las pastillas.\n\nLa farmacia ofreció revisar todas sus medicinas. Encontraron problemas: algunos envases estaban caducados, había notas equivocadas, pastillas partidas y medicinas repetidas. La paciente toma muchos medicamentos y tiene dificultad para organizarlos sola.\n\nLa farmacia habló con la doctora de su centro de salud y pidió cambiar y coordinar tratamientos. Hicieron estos cambios:\n- Quitaron una de las medicinas de vitamina D y dejaron la que le dio urgencias.\n- Cambiaron la forma de tomar el medicamento para el dolor.\n- Pusieron paracetamol (si necesita) para dolor leve.\n- Cambiaron el tipo de protector para la incontinencia por otro más fácil de poner.\n- Para el inhalador del pulmón, la doctora pidió que la cuidadora supervise cada toma.\n\nTambién la enviaron al servicio de Sistema Personalizado de Dosificación (SPD). En ese servicio la farmacia prepara las pastillas en pastilleros por días y tomas. Así es más fácil y seguro tomar las medicinas correctas.\n\nTodo esto se hizo para que la señora tome sus medicinas bien y no haya errores. La doctora y la farmacia hablaron para ayudarla.",
+            "B2": "Resumen claro y amable\n\nUna mujer de 73 años, con varias enfermedades crónicas (como EPOC —problemas para respirar—, hipertensión, artritis reumatoide y otras) vive completamente dependiente y recibe ayuda de una cuidadora para sus medicinas. Tras una analítica en urgencias le recetaron tratamiento para una infección de orina (cefuroxima y un antiespasmódico) y suplementos de vitamina D (colecalciferol). La paciente se puso confusa porque ya tomaba otras cápsulas para la vitamina D y su cuidadora habitual dejó de poder ayudarla.\n\nQué hizo la farmacia\n- La farmacia ofreció un servicio llamado Revisión del Uso del Medicamento (RUM): es una entrevista y revisión para ver si la persona entiende sus medicinas y si hay problemas que puedan causar errores.\n- La cuidadora llevó la bolsa con todos los envases y la tarjeta sanitaria; la farmacia revisó los medicamentos y habló con la paciente por teléfono.\n- Encontraron varios problemas: envases caducados, instrucciones equivocadas, pastillas partido que no deberían partirse y duplicidad de medicamentos (más de un envase para la misma cosa).\n\nProblemas detectados y propuestas\n- Duplicidad en el tratamiento de la vitamina D (dos medicamentos para lo mismo).\n- Posible error o necesidad de revisar la dosis de tramadol (analgésico para el dolor).\n- Dificultad para poner los absorbentes de incontinencia tipo “pants” debido a que la paciente está encamada; propusieron cambiar a absorbentes elásticos más fáciles de poner.\n- Problemas con el uso del inhalador para la EPOC y falta de supervisión para garantizar que lo use correctamente.\n\nAcciones con el médico y resultados\n- La farmacia envió un informe al médico de Atención Primaria y propuso incluir a la paciente en un servicio llamado Sistema Personalizado de Dosificación (SPD). SPD significa que los medicamentos se organizan en pastilleros por día y hora para evitar errores y mejorar el cumplimiento.\n- El médico aceptó las recomendaciones: anuló un medicamento duplicado para la vitamina D y dejó el colecalciferol recetado en urgencias; cambió la pauta del tramadol (ahora 1-0-1, es decir una dosis por la mañana y otra por la noche) y recomendó paracetamol si hace falta; sustituyó los absorbentes por otros elásticos; y decidió no cambiar la medicación de la EPOC pero pidió que la cuidadora supervise cada uso del inhalador.\n\nPor qué es importante\nEstas acciones ayudan a reducir la confusión, evitar errores en la medicación y mejorar la seguridad de la paciente. El SPD y la supervisión diaria del inhalador buscan que la mujer reciba las medicinas correctas en el momento correcto, lo que es especialmente importante cuando depende de otros para su cuidado.",
+            "B3": "Resumen clínico (nivel universitario, lectura B3)\n\nPaciente: mujer de 73 años, totalmente dependiente, polimedicada y con múltiples patologías crónicas: EPOC, hipertensión, trastorno bipolar, ansiedad, depresión, hipotiroidismo y artritis reumatoide. Vive en casa y su cuidadora habitual gestionaba la medicación; la cuidadora ha comunicado que dejará de prestar cuidados, lo que aumenta el riesgo sobre el manejo de fármacos.\n\nMotivo de contacto: la paciente llamó a la farmacia preocupada por confusión tras una receta nueva emitida en urgencias para una infección urinaria y un déficit de vitamina D. Ella recordaba cápsulas naranjas previas para vitamina D prescritas por su médico de Atención Primaria, y el informe de urgencias parecía duplicar ese tratamiento. Aceptó una Revisión del Uso del Medicamento (RUM).\n\nQué hizo la farmacia\n- Servicio de dispensación realizado sin incidencias iniciales.  \n- Se ofreció y realizó una RUM: entrevista telefónica con la paciente, revisión del botiquín (con la cuidadora en farmacia) y consulta de bases de datos (CIMA, BotPlus) para fichas técnicas e interacciones.  \n- Se detectaron problemas de gestión de la medicación: envases caducados, anotaciones erróneas, comprimidos partidos que no deberían partirse y duplicidad/acumulación de envases de un mismo fármaco.\n\nProblemas clínicos detectados (anormales)\n- Duplicidad en el tratamiento para déficit de vitamina D (medicación previa de Atención Primaria y nueva prescripción de urgencias). Esto incrementa riesgo teórico de sobredosificación y efectos adversos (p. ej., hipercalcemia).  \n- Posible error en la pauta de tramadol de liberación prolongada (riesgo de dosis inadecuada, efectos adversos y posibles interacciones con los psicofármacos de la paciente).  \n- Dificultades prácticas para el manejo del absorbente tipo pants por dependencia de la paciente (problemas en colocación y confort).  \n- Problemas de manejo y adherencia del tratamiento inhalatorio para EPOC por dificultades con el inhalador.\n\nIntervenciones realizadas\n- Elaboración y envío de un informe de derivación al médico de Atención Primaria solicitando revisión y propuesta de inclusión en el Servicio Personalizado de Dosificación (SPD; blísteres preparados por dosis).  \n- Propuestas concretas a AP: revisar tramadol, corregir duplicidad de vitamina D, cambiar tipo de absorbente y revisar EPOC/inhalador.  \n- Plan de derivación al SPD para mejorar seguridad y adherencia dada la dependencia y polimedicación.\n\nResultados tras contacto con el médico de Atención Primaria\n- Vitamina D: anulación de calcifediol y sustitución por colecalciferol recetado en urgencias (eliminó la duplicidad).  \n- Artritis y dolor: modificación de tramadol de liberación prolongada a pauta 1-0-1 (mañana-noche) y recomendación de paracetamol 1 g hasta tres veces al día si precisa.  \n- Incontinencia: cambio de absorbente tipo pants por absorbente elástico (más fácil de colocar en paciente dependiente).  \n- EPOC: no se cambió la medicación, pero se estableció que la cuidadora supervise diariamente la administración del inhalador para mejorar adherencia y técnica.  \n- Se acordó iniciar el proceso para el SPD contactando farmacia y AP.\n\nImplicaciones y siguientes pasos recomendados\n- Inicio del SPD para centralizar y simplificar tomas: expectable mejora de seguridad (evitar dosis erróneas, duplicidades) y adherencia.  \n- Monitorizar los niveles clínicos y efectos adversos: vigilar síntomas de hipercalcemia tras ajuste de vitamina D (aunque la duplicidad fue corregida), evaluar eficacia y tolerancia del nuevo esquema de tramadol/paracetamol, y controlar efectos sobre el ánimo dado el historial psiquiátrico.  \n- Formación y coordinación: instruir a la nueva cuidadora (o redes de apoyo) sobre el SPD, supervisión del inhalador y señales de alarma (sueño excesivo, confusión, signos de hipercalcemia, empeoramiento respiratorio).  \n- Seguimiento farmacéutico periódico (RUM o consulta en farmacia) para revisar adherencia, interacciones y necesidad de ajustes.\n\nMensaje final (empatía)\nLa intervención farmacéutica detectó problemas prácticos y clínicos que aumentaban el riesgo para esta paciente dependiente. Las correcciones acordadas con el médico (eliminación de duplicidad de vitamina D, ajuste del analgesia, cambio de absorbente y supervisión del inhalador) y la derivación al SPD son medidas concretas que reducen riesgos y facilitan la gestión diaria. Es importante mantener seguimiento cercano mientras se incorpora a un nuevo cuidador y se inicia el SPD."
+        }
+    },
+    {
+        "article": "Nuestra paciente era una mujer japonesa de 83 años con insuficiencia cardiaca crónica (fracción de eyección: aproximadamente 30 %) que inició un tratamiento con empagliflozina 10 mg diarios unos 8 meses antes de su ingreso. Nunca se le había diagnosticado diabetes mellitus (HbA1c 5.9 % antes de iniciar el tratamiento con empagliflozina). Unos 6 meses antes de su ingreso, su tratamiento se cambió a dapagliflozina 5 mg. Sus diuréticos y otros medicamentos cardiacos no se ajustaron durante ese tiempo. Dos semanas antes de su ingreso, tropezó y cayó, sufriendo fracturas vertebrales y de costillas. La paciente se debilitó significativamente por el dolor de las fracturas, lo que le causó dificultad para caminar y anorexia. Solo podía comer el 50-70 % de su ingesta dietética habitual. Esto empeoró en la semana siguiente, cuando también desarrolló náuseas y vómitos y redujo aún más su ingesta de alimentos a solo el 10-20 % de la cantidad habitual. Durante este período, continuó tomando dapagliflozina. Fue ingresada en el hospital.\nAl ingreso, la paciente estaba consciente con una temperatura corporal de 37.4°C, presión arterial de 124/68 mmHg, frecuencia cardiaca de 91 bpm y saturación de oxígeno de 98% en aire ambiente. Los análisis de sangre revelaron un nivel de glucosa en sangre de 124 mg/dL, pH de 7.3, concentración de HCO3– de 14 mmol/L, exceso de base de -10 mEq/L, brecha aniónica de 20 mEq/L y concentración de b-hidroxibutirato de 5150 umol/L (Tabla 1). Estos hallazgos fueron consistentes con el diagnóstico de cetoacidosis normoglucémica. La paciente no tenía antecedentes de consumo de alcohol, tabaquismo o uso de drogas.\nSe descartaron otras causas de acidosis con alto déficit aniónico. Su nivel de péptido C era coherente con los niveles de glucosa en sangre en el ingreso, lo que indicaba que tenía una secreción de insulina adecuada; por lo tanto, no se inició la administración de insulina. Se interrumpió el uso de inhibidores de SGLT2 y la paciente se trató inicialmente con solución salina isotónica y una infusión de mantenimiento de aproximadamente 170 g de glucosa diarios.\nA pesar de no haber iniciado la insulina, su pH (7.418), concentración de HCO3– (20.7 mmol/L) y brecha aniónica (13.3 mEq/L) mejoraron al día siguiente de su ingreso. Se inició la dieta Carb 60, pero se continuaron las infusiones intravenosas de glucosa porque la ingesta de alimentos de la paciente era escasa. La cantidad de infusión de glucosa administrada se ajustó según su ingesta de alimentos. En el cuarto día de hospitalización, las cetonas urinarias desaparecieron.\nLa infusión de glucosa se interrumpió el día 12 de la hospitalización, una vez que el paciente pudo comer comidas completas. Aunque el nivel de glucosa en sangre del paciente estaba dentro del rango normal, la excreción de glucosa en la orina fue de 3+ (>500 mg/dL) durante 8 días después de la última dosis de dapagliflozina.\nAl ingreso, la paciente no podía caminar debido al dolor de la fractura, la fatiga general y el síndrome de desuso, pero después de la rehabilitación pudo hacerlo de forma independiente. Fue dada de alta el día 19 de hospitalización, tras someterse a rehabilitación.\nLos inhibidores de SGLT2 no se reiniciaron.\n\nMH - Humanos\nMH - Mujer\nMH - *Insuficiencia cardiaca/inducida químicamente\nMH - *Inhibidores del transportador de glucosa y sodio 2/efectos adversos\nMH - Edad 80 años y más\nMH - Cetosis/químicamente inducida\nMH - glucósidos/efectos adversos\nMH - Cetoacidosis diabética/inducida químicamente\n",
+        "gold_summary": "A continuación, describimos un caso de cetoacidosis en una mujer japonesa de 83 años sin diabetes a la que se le administraron inhibidores de SGLT2 para la insuficiencia cardiaca (fracción de eyección: aproximadamente 30 %). Dos semanas antes de su ingreso, había sufrido una fractura vertebral y una fractura de costilla debido a una caída, a la que siguió una anorexia, pero continuó tomando inhibidores de SGLT2. En el momento del ingreso, los resultados de los análisis de sangre revelaron un nivel de glucosa en sangre de 124 mg/dL, un nivel de hemoglobina A1C del 5,9 %, un pH de 7,329, una concentración de HCO₃⁻ de 14,3 mmol/L y una concentración de β-hidroxibutirato de 5150 μmol/L, lo que condujo a un diagnóstico de cetoacidosis euglucémica. El nivel de péptido C de la paciente coincidía con los niveles de glucosa en sangre en el momento del ingreso, lo que indicaba que tenía una secreción de insulina adecuada. La paciente fue tratada únicamente con administración de glucosa sin insulina y fue dada de alta tras la interrupción del inhibidor de SGLT2.\n",
+        "synthetic_summary": {
+            "B1": "Esta es la historia de una mujer japonesa de 83 años. Tenía enfermedad del corazón y tomaba un medicamento llamado inhibidor de SGLT2. Este medicamento ayuda al corazón y hace que el riñón saque azúcar en la orina. Ella no tenía diabetes (su HbA1c fue 5,9 % antes de empezar el medicamento).\n\nHace poco se cayó y se rompió una vértebra y algunas costillas. El dolor le quitó las ganas de comer. Cada vez comía menos. Igual siguió tomando el medicamento.\n\nCuando llegó al hospital estaba consciente pero débil. Su azúcar en sangre estaba casi normal (124 mg/dL). Aun así, su sangre estaba demasiado ácida porque su cuerpo había hecho muchas cetonas. Las cetonas son unas sustancias que el cuerpo usa cuando no recibe comida suficiente. Esto se llama cetoacidosis, y en su caso la azúcar estaba casi normal, por eso se llama “cetoacidosis con azúcar normal”.\n\nLos médicos pararon el medicamento SGLT2. No le pusieron insulina porque su cuerpo todavía fabricaba algo de insulina. Le dieron líquidos y azúcar por vía intravenosa para que su cuerpo dejara de hacer cetonas. Al día siguiente su sangre empezó a mejorar. Después de algunos días las cetonas desaparecieron. Aunque su azúcar en sangre estaba normal, su orina siguió mostrando azúcar durante varios días.\n\nHizo rehabilitación para poder caminar otra vez. Mejoró y salió del hospital el día 19. No le volvieron a dar el medicamento SGLT2.",
+            "B2": "Resumen sencillo y amable\n\nPresentamos el caso de una mujer japonesa de 83 años con insuficiencia cardiaca que recibía un medicamento llamado inhibidor de SGLT2 (se cambió de empagliflozina a dapagliflozina). Estos fármacos se usan para el corazón y también en la diabetes, pero esta paciente no tenía diabetes (su HbA1c antes del tratamiento era 5,9 %, un valor normal).\n\nDos semanas antes de ir al hospital, se cayó y se fracturó la columna y varias costillas. El dolor la dejó muy débil y comió mucho menos de lo habitual; luego empezó con náuseas y vómitos y llegó a comer solo el 10–20 % de lo normal. Durante ese tiempo siguió tomando dapagliflozina.\n\nAl ingresar, tenía la glucosa en sangre casi normal (124 mg/dL) pero presentaba acidosis metabólica (pH bajo y bicarbonato bajo) y niveles muy altos de una cetona llamada β-hidroxibutirato (5150 µmol/L). Esto llevó al diagnóstico de cetoacidosis euglucémica: es cetoacidosis (acumulación de ácidos llamados cetonas) que ocurre con glucosa en sangre normal o solo ligeramente elevada. El péptido C, una medida que refleja si el cuerpo produce insulina, estaba acorde con su glucosa, lo que sugiere que no tenía falta importante de insulina.\n\nTratamiento y evolución\n- Se suspendió el inhibidor de SGLT2.  \n- No se administró insulina porque la secreción de insulina no parecía insuficiente.  \n- Se le dio suero y una infusión de glucosa para corregir el problema y prevenir más formación de cetonas mientras no comía bien.  \n- Los cuerpos cetónicos en orina desaparecieron al cuarto día.  \n- La infusión de glucosa se retiró al día 12, cuando la paciente volvió a comer normalmente.  \n- Aunque su glucosa en sangre fue normal, la orina mostró glucosa alta durante 8 días después de la última dosis de dapagliflozina (esto puede pasar porque el fármaco actúa varios días).  \n- Tras rehabilitación por las fracturas y la debilidad, pudo caminar y fue dada de alta el día 19. El medicamento SGLT2 no se reanudó.\n\nMensaje importante (explicado con calma)\nLos inhibidores de SGLT2 pueden, en casos raros, provocar cetoacidosis incluso en personas sin diabetes, sobre todo si están enfermas, comen muy poco o tienen estrés físico (como fracturas). Si alguien que toma estos fármacos deja de comer, tiene vómitos o está muy debilitado, es importante que los profesionales de la salud consideren suspender el medicamento y tratar con líquidos y glucosa.",
+            "B3": "Resumen del caso\nUna mujer japonesa de 83 años con insuficiencia cardiaca (fracción de eyección ~30 %) que no tenía diabetes diagnosticada (HbA1c 5,9 %) estaba recibiendo inhibidores de SGLT2 para su insuficiencia cardiaca: empagliflozina 10 mg durante unos 8 meses y, desde 6 meses antes del ingreso, dapagliflozina 5 mg. Dos semanas antes de la hospitalización sufrió una caída con fracturas vertebrales y costales; el dolor y las náuseas la dejaron con apetito muy reducido (10–70 % de lo habitual) durante días, pero continuó tomando dapagliflozina. Fue ingresada por debilidad progresiva.\n\nHallazgos principales (normales vs anormales)\n- Signos vitales: estables en admisión (temperatura 37.4 °C, PA 124/68 mmHg, FC 91 lpm, Sat O2 98 %).  \n- Glucemia: 124 mg/dL (normal).  \n- Metabólicos: pH 7,30 (acidemia), HCO3– 14 mmol/L (bajo), exceso de base –10 mEq/L, brecha aniónica 20 mEq/L (elevada).  \n- Cetosis: β-hidroxibutirato 5.150 μmol/L (marcadamente elevado) → diagnóstico de cetoacidosis normoglucémica (euglucémica).  \n- Péptido C: coherente con la glucemia de ingreso, indicando secreción de insulina endógena adecuada.  \n- Historia: sin consumo de alcohol ni drogas; se descartaron otras causas de acidosis aniónica elevada.\n\nTratamiento y evolución\n- Se interrumpió el inhibidor de SGLT2.  \n- Recibió solución salina isotónica y una perfusión de glucosa de mantenimiento (≈170 g/día), ajustada según la ingesta oral. No se administró insulina debido a la evidencia de secreción de insulina adecuada.  \n- Mejoría rápida: al día siguiente pH 7,418, HCO3– 20,7 mmol/L, brecha aniónica 13,3 mEq/L.  \n- Dieta Carb 60 iniciada; las perfusiones de glucosa continuaron hasta que pudo alimentarse por completo. Las cetonas urinarias desaparecieron en el día 4.  \n- La glucosuria persistió (3+ en tira >500 mg/dL) durante 8 días después de la última dosis de dapagliflozina.  \n- Rehabilitación mejoró la movilidad; alta al día 19. No se reiniciaron los inhibidores de SGLT2.\n\nImplicaciones clínicas y recomendaciones prácticas\n- Los inhibidores de SGLT2 pueden provocar cetoacidosis euglucémica incluso en pacientes sin diabetes, sobre todo en situaciones de ingesta reducida, estrés agudo, enfermedad o tras un traumatismo.  \n- Signos de alerta: náuseas/vómitos, anorexia, fatiga y dolor con cetonas elevadas aunque la glucosa esté normal o ligeramente elevada.  \n- Manejo apropiado incluye suspender el SGLT2, corregir la volemia, aportar glucosa (para frenar la cetogénesis) y monitorizar cetonas, electrólitos y equilibrio ácido-base. La insulina puede no ser necesaria si hay secreción endógena suficiente, pero la decisión debe basarse en la evaluación clínica y de laboratorio.  \n- La glucosuria puede persistir días después de suspender el fármaco, por lo que no excluirá la responsabilidad del SGLT2.  \n- Prevención: evitar o suspender inhibidores de SGLT2 durante periodos de ayuno, enfermedad aguda, cirugía o trauma; educar al paciente y cuidadores sobre señales de alarma y cuándo buscar atención.\n\nTono y resultado\nLa paciente respondió bien al tratamiento conservador (fluido y glucosa), recuperó la capacidad de caminar con rehabilitación y fue dada de alta sin reiniciar los inhibidores de SGLT2. Este caso subraya la necesidad de precaución al usar SGLT2 en personas mayores o en quienes pueden presentar pérdida de ingesta o estrés fisiológico."
+        }
+    },
+    {
+        "article": "Una recién nacida fue evaluada en la sala de neonatos poco tiempo después del parto debido a la presencia de extensas lesiones similares a cicatrices en sus flancos y muslos superiores. La bebé, nacida de una madre asiática de 28 años a las 39 semanas de gestación, formaba parte de un embarazo gemelar espontáneo. Su madre, que ya había tenido cinco hijos, había tenido un aborto espontáneo en el primer trimestre durante su segundo embarazo.\n\nLos padres eran primos hermanos y no habían tenido problemas de salud en sus tres hijos vivos. La ecografía a las 13 semanas confirmó un embarazo bicorial y diacítico y la ausencia de actividad cardíaca en uno de los gemelos. Las ecografías posteriores mostraron un feto que se desarrollaba con normalidad junto a un gemelo no viable.\n\nDurante el embarazo, la madre no informó sobre el uso de medicamentos o síntomas como fiebre y erupción cutánea. Dio negativo para estreptococo del grupo B y fue admitida en el departamento de urgencias obstétricas con dolores de parto. La niña fue entregada por vía vaginal, pesando 2,83 kg, y fue vigorosa al nacer. A la placenta se le unió un remanente fetal no viable comprimido que medía 6 × 2 cm. La placenta pesaba 460 g y parecía normal al examen.\n\nLa niña presentaba lesiones cutáneas extensas e irregulares, que se caracterizaban por un aspecto estrellado en ambos flancos, que se extendían lateralmente sobre la zona glútea y el muslo superior. Las lesiones eran simétricas en ambos flancos. No obstante, las lesiones en los muslos eran notablemente más leves en el lado izquierdo. Sus constantes vitales eran estables y no presentaba otras anomalías externas. El examen clínico de sus sistemas respiratorio, cardiovascular, gastrointestinal y neurológico reveló resultados normales, y no se observaron otras anomalías cutáneas, incluida la ausencia de lesiones ampollosas.\n\nDada la naturaleza simétrica de las anomalías cutáneas y el contexto de embarazo de mellizos con FP, se realizó un diagnóstico de aplasia cutis congénita grupo V. Los exámenes de laboratorio, que incluían hemograma completo, electrolitos y pruebas de función renal e hepática, arrojaron resultados normales. Los exámenes de detección de toxoplasmosis, rubéola, citomegalovirus, herpes simple y VIH (TORCH) arrojaron resultados negativos. La ecografía del cerebro, abdomen y corazón no reveló anomalías.\n\nDado que las lesiones se curaron en el útero, solo se prescribieron emolientes locales. Después de 48 horas de observación, el bebé fue dado de alta en su casa, con derivaciones a clínicas de dermatología pediátrica y cirugía plástica. En el seguimiento de 2 semanas, no se observaron cambios en las lesiones de la piel ni nuevos síntomas. Su análisis de microarreglo cromosómico fue reportado como normal.\n",
+        "gold_summary": "Informamos sobre un neonato al que se le diagnosticó ACC de grupo G-V asociado con fetus papyraceus de un embarazo gemelar di-coriónico y di-amniótico. Nacida de una madre asiática de 28 años, esta niña presentaba lesiones extensas, cicatrizadas, similares a las cicatrices en sus flancos y muslos superiores. Estas lesiones eran consistentes con la distribución en forma de «H» comúnmente descrita en ACC ligada a fetus papyraceus. A pesar de las manifestaciones dermatológicas significativas, la niña no mostró otras anormalidades externas o implicación sistémica, y las evaluaciones exhaustivas, incluidos los ultrasonidos y el microarray cromosómico, fueron normales.\n",
+        "synthetic_summary": {
+            "B1": "A baby girl was born with wide, scar-like marks on both sides of her tummy and top of her legs. The marks looked like an H shape. She was strong when she was born and had no other problems.\n\nBefore she was born, she was one of two twins. The other twin had died early in the pregnancy and was very small and pressed against the placenta. This can sometimes cause the kind of skin marks the baby had.\n\nDoctors checked the baby carefully. Blood tests, scans of her brain, belly, and heart, and a chromosome test all came back normal. The doctors said the marks were a type of birth skin problem called aplasia cutis congenita group V (this means skin was missing or scarred in places because of the twin situation). The baby only needed soft skin cream. She went home after two days and stayed well on follow-up.",
+            "B2": "Resumen (nivel B2, para lectores jóvenes)\n\nUn recién nacido fue diagnosticado con aplasia cutis congénita (ACC) grupo V, una condición en la que faltan partes de la piel desde el nacimiento. En este caso, las lesiones eran simétricas y extensas en los flancos y la parte superior de los muslos, formando una distribución en “H” que a menudo se ve cuando hay un fetus papyraceus: un gemelo que murió antes del nacimiento y quedó aplastado y reducido dentro del útero.\n\nLa niña nació a término, pesó 2,83 kg y estaba vigorosa. No había otras anomalías externas ni problemas en los sistemas respiratorio, cardíaco, digestivo o neurológico. Pruebas de laboratorio básicas, ecografías del cerebro, abdomen y corazón, análisis para infecciones comunes en embarazos (TORCH) y un estudio genético por microarreglo resultaron normales. Los médicos consideraron que las lesiones ya se habían curado parcialmente en el útero, por lo que solo se prescribieron emolientes (cremas hidratantes) y seguimiento por dermatología pediátrica y cirugía plástica.\n\nTras 48 horas de observación la bebé fue dada de alta; a las dos semanas no hubo cambios ni nuevos síntomas. En conjunto, a pesar de las marcas en la piel, la bebé estaba bien y no hubo afectación sistémica evidente.",
+            "B3": "Resumen clínico (nivel B3, lectura universitaria)\n\nPresentamos el caso de una recién nacida de 39 semanas, producto de un embarazo gemelar bicorial y biamniótico, en el que uno de los gemelos había fallecido en el primer trimestre y quedó como un remanente fetal comprimido (fetus papyraceus) adherido a la placenta. La madre, de 28 años, no refirió antecedentes infecciosos ni uso de fármacos relevantes durante la gestación; los padres son primos hermanos.\n\nHallazgos principales (anormales)\n- La niña mostró, al nacer, extensas lesiones cutáneas simétricas en ambos flancos y en la región glútea y muslos superiores. Las lesiones tenían aspecto cicatricial y seguían la distribución en “H” típica de la aplasia cutis congénita (ACC) grupo V, una forma de pérdida localizada de piel asociada a la presencia de un fetus papyraceus. Las lesiones en el muslo izquierdo eran algo menos marcadas.\n\nHallazgos normales (sin implicación sistémica)\n- La paciente estaba vigorosa al nacer, con constantes estables y sin otras anomalías externas. Exámenes dirigidos —hemograma, electrolitos, función renal y hepática— fueron normales. Pruebas infecciosas TORCH y VIH fueron negativas. Ecografías cerebrales, abdominales y cardiacas no mostraron alteraciones. El microarreglo cromosómico fue normal.\n\nInterpretación y manejo\n- El cuadro es coherente con ACC grupo V secundaria a fetus papyraceus: se interpreta como una lesión localizada por un evento intrauterino (probablemente alteración vascular relacionada con la muerte del gemelo) más que por una causa genética o infección sistémica. Dado que no hubo compromiso sistemático, el manejo inicial fue conservador: cuidados locales con emolientes. La paciente fue dada de alta tras 48 horas y derivada a dermatología pediátrica y cirugía plástica.\n\nPronóstico y pasos a seguir\n- El pronóstico funcional inmediato es bueno porque no hay afectación interna ni signos de infección. Sin embargo, las cicatrices pueden persistir y, según la evolución estética o funcional, podría considerarse tratamiento reconstructivo en el futuro. Se recomienda seguimiento por dermatología y cirugía plástica para vigilancia del área afectada, control del crecimiento y desarrollo, y para planificar intervenciones si son necesarias."
+        }
+    },
+    {
+        "article": "Información para el paciente\nUn hombre de 44 años de edad fue ingresado en nuestro hospital con quejas principales de neumaturia y cistitis repetida. El paciente también tenía antecedentes de hipotiroidismo.\n\nLa tomografía computarizada con contraste mejorado reveló múltiples divertículos del colon sigmoide, y el límite entre el divertículo y la vejiga no estaba claro. La endoscopia gastrointestinal inferior reveló una fístula en el colon rectosigmoide aproximadamente a 15 cm del borde anal. La cistoscopia reveló una fístula en la pared posterior izquierda de la vejiga. Se diagnosticó una fístula vesicovaginal y se planificó una cirugía laparoscópica. Los hallazgos intraoperatorios revelaron una inflamación severa alrededor de la fístula vesicovaginal, y también se habían formado adhesiones severas entre el íleon y la vejiga. El íleon y la vejiga eran difíciles de exfoliar debido a las adhesiones severas. Por lo tanto, decidimos realizar una resección intestinal combinada. El colon rectosigmoide, incluida la fístula, se movilizó y se resecó. La fístula vesical se seccionó y se cerró con una sutura de púas sin nudos (V-LocTM 180, Covidien, Mansfield). La anastomosis sigmoide-rectal se reconstruyó utilizando la técnica de doble grapado. La resección parcial del íleon se reconstruyó con una anastomosis funcional de extremo a extremo (FEEA). Además de la presencia de una anastomosis de 2 sitios, había una inflamación severa en el área circundante, y considerando el riesgo de fuga anastomótica, se creó una ileostomía de derivación 30 cm proximal a la anastomosis ileo-ileal.\n\nLos procedimientos quirúrgicos incluyeron resección anterior alta laparoscópica, resección parcial del intestino delgado, cistectomía parcial y derivación en forma de asa. La operación duró 236 minutos y la pérdida de sangre fue de 50 ml. El curso postoperatorio fue sin incidentes y el cierre de la ileostomía se planificó 1 mes después de la cirugía inicial. Con ayuda laparoscópica, se eliminaron las adherencias entre el omento y la pared abdominal alrededor del estoma. Se realizó una movilización completa alrededor del estoma y el intestino se sacó hacia afuera. El íleon se reconstruyó utilizando FEEA. El procedimiento quirúrgico implicó el cierre de la ileostomía asistida por laparoscopia. La operación duró 100 minutos y la pérdida de sangre fue de 30 ml.\n\nHallazgos clínicos\nAl día siguiente de la cirugía, se produjo un shock sintomático debido a la presión arterial baja (<80 mm Hg) y la taquicardia. Los análisis de sangre mostraron que la hemoglobina disminuyó de 15.3 antes de la cirugía a 8.6 g/dL después de la cirugía.\n\nEvaluación diagnóstica\nLa tomografía computarizada abdominal (TC) reveló una gran cantidad de fluido de alta densidad en la cavidad abdominal. El diagnóstico fue sangrado posoperatorio y shock hemorrágico. Se insertó un catéter venoso central y se administraron 8 unidades de glóbulos rojos y 8 unidades de plasma fresco congelado para estabilizar los signos vitales. Los signos vitales se estabilizaron y no se observó progresión de la anemia después de eso. Aunque se logró la hemostasia, la distensión abdominal severa y los altos niveles de respuesta inflamatoria (proteína C reactiva [CRP] a 42.9 mg/dL y recuento de glóbulos blancos [WBC] de 18,500/uL) persistieron 7 días después de la cirugía.\n\nLa TC con contraste reveló que el hematoma intraabdominal se localizaba en el abdomen inferior izquierdo y derecho, y se consideró posible el drenaje percutáneo. En el día 8 posoperatorio, se insertaron tubos de drenaje de 18 Fr en el abdomen inferior izquierdo y derecho a través de una punción guiada por TC, y se drenó una gran cantidad de sangre antigua. Después del drenaje, la reacción inflamatoria y la distensión abdominal causadas por la infección del hematoma residual mejoraron (CRP a 1,9 mg/dL y WBC de 5000/μL). No se observó progresión de la anemia. En el día 14 posoperatorio, el drenaje en el abdomen inferior derecho cambió de sangre antigua a jugo intestinal. Una angiografía de drenaje reveló fuga anastomótica tardía en el sitio de cierre de la ileostomía. No hubo signos de peritonitis con buen drenaje, pero el drenaje fue de aproximadamente 100 a 200 ml, y el flato del drenaje continuó. No se observó disminución del drenaje durante los siguientes 14 días.\n\nIntervención terapéutica\nAunque se consideró la posibilidad de una nueva operación, se esperaban adhesiones intraabdominales severas debido a la historia de cirugías anteriores, sangrado postoperatorio y fuga anastomótica. Por lo tanto, se consideró que la nueva operación era un procedimiento de alto riesgo. La tomografía computarizada con contraste mostró que un hematoma organizado permanecía en el mesenterio del intestino delgado y el íleon en el lado distal de 10 cm de la anastomosis estaba comprimido cerca del hematoma restante. Teniendo en cuenta la estenosis del íleon en el lado anal de la anastomosis debido a un hematoma residual como la causa de fuga anastomótica, se intentó la dilatación radioscópica del área de estenosis a través del drenaje en el día 24 postoperatorio. Se colocó un introductor de funda Cordis BRITE TIP® (8 Fr × 23 cm) en la fístula donde ocurrió la fuga anastomótica después del drenaje angiográfico. Se usó un hilo radioscópico GT (0.016 pulgadas, 180 cm, 90°) (Terumo, Tokio, Japón) y un microcatéter Renegade HI-FLO (135 × 20 cm) (Boston Scientific, Tokio, Japón) para alcanzar el íleon terminal. Usando el catéter Selecon MP II (6 Fr, 80 cm, φ20 mm) (Terumo), se identificó el área de estenosis en el íleon debido a la compresión del hematoma donde el globo no podía pasar.\n\nSe realizó dilatación con globo fluoroscópica en la estenosis del íleo utilizando un globo guiado por alambre CRE PRO GI (180 cm, 15-18 mm) (Boston Scientific), inflado a 16,5 mm de diámetro a 4,5 atm durante 3 minutos.\n\nSeguimiento y resultados\nDesde el día posterior a la dilatación con globo, la cantidad de drenaje disminuyó notablemente, y se observaron flatos y defecaciones desde el ano. Una semana después de la dilatación con globo, el drenaje fue casi nulo, y se determinó que la fuga anastomótica se había resuelto. El drenaje se eliminó gradualmente. La ingesta oral fue buena, y tuvo movimientos intestinales regulares. Fue dado de alta el día 45 posterior a la operación. Desde entonces, no se ha informado de ninguna recurrencia de la estenosis o fuga anastomótica.\n",
+        "gold_summary": "Preocupaciones del paciente: Presentamos el caso de un hombre de 44 años con fuga anastomótica tardía después del cierre de la ileostomía, causada por la compresión de un hematoma intraabdominal que se curó rápidamente después de la dilatación fluoroscópica con globo del área de la estenosis intestinal.\n\nDiagnósticos: Se produjo sangrado postoperatorio y shock hemorrágico el día 1 postoperatorio tras el cierre de la ileostomía. Los signos vitales se estabilizaron tras la transfusión de sangre, y se realizó con éxito un drenaje guiado por tomografía computarizada para reducir el volumen del hematoma. Sin embargo, el hematoma residual comprimió el íleon en el lado anal de la anastomosis, lo que provocó una fuga anastomótica tardía.\n\nIntervenciones/resultados: Se realizó con éxito la dilatación con balón fluoroscópico del área estenótica a través del drenaje y la fuga anastomótica se curó rápidamente.\n",
+        "synthetic_summary": {
+            "B1": "Había un hombre de 44 años que tuvo una operación para reparar el intestino. Después, le cerraron una ileostomía. La ileostomía es una salida en la barriga para que las heces salgan a una bolsa mientras el intestino se cura.\n\nAl día siguiente tuvo un sangrado fuerte dentro de la barriga. Los médicos le dieron sangre y le pusieron tubos para sacar la sangre acumulada. Ese líquido pegado (hematoma) quedó en un sitio cerca del intestino y apretó una parte del intestino. Esto hizo que la unión del intestino (donde se habían cosido dos trozos) se abriera y saliera líquido por el tubo de drenaje. Eso se llama fuga.\n\nHacer otra operación era muy peligroso porque había mucha cicatriz y riesgo de sangrar otra vez. Entonces los médicos usaron rayos X para ver y pasaron un pequeño globo por el tubo. Inflaron el globo en la parte apretada para abrirla. Después de eso, el drenaje bajó mucho. El hombre pudo expulsar gases y hacer caca por el ano. La fuga se cerró y fue dado de alta al día 45 después de la operación. No ha vuelto a tener ese problema.",
+            "B2": "Here is a clear, kind summary of the case:\n\nWhat happened first\n- A 44-year-old man went to the hospital because he had air in his urine (neumaturia) and repeated bladder infections. Scans showed many diverticula (small pouches) in the sigmoid colon and a fistula (an abnormal connection) between his colon and bladder.  \n- He had laparoscopic surgery to remove the diseased part of the colon, repair the bladder, remove a small part of the small intestine (ileum) that was stuck to the bladder, and make a temporary ileostomy. An ileostomy is a short-term opening of the small intestine to the skin so waste can leave the body while the inside heals.\n\nWhat happened after closing the ileostomy\n- One month later the ileostomy was closed (the two ends of intestine were reconnected). The next day he went into hemorrhagic shock — his blood pressure fell and his hemoglobin dropped a lot because of bleeding inside the belly. He received blood and plasma and his vital signs stabilized.\n- Scans showed a large blood collection (hematoma) inside the abdomen. On day 8 after the closure, doctors drained much of this old blood through tubes placed with CT imaging. This improved his inflammation and belly swelling.\n\nThe late leak and why it happened\n- On day 14 the right-side drain began to show intestinal juice instead of blood. Imaging showed a late anastomotic leak where the bowel had been reconnected. The leak was caused because a remaining, organized hematoma was pressing on the ileum below the anastomosis and creating a narrowing (stenosis). This pressure caused the join to fail and leak.\n- Because the patient already had difficult surgeries, bleeding, and likely severe scar tissue (adhesions), another open operation would be high risk.\n\nHow the team fixed it without major surgery\n- On day 24, the team used the already placed drain route to reach the narrowed part of the ileum under X-ray guidance (fluoroscopy). They passed wires and tiny catheters to the narrowed area and inflated a balloon inside the ileum to stretch the narrowed segment. This is called balloon (or dilatation) treatment.\n- The balloon was inflated to widen the area that the hematoma had compressed.\n\nResult and follow-up\n- The day after balloon dilatation the amount of drainage fell a lot, and the patient had gas and bowel movements again. One week later the drain output was nearly zero and the leak was judged to be healed. The drains were removed gradually.\n- He ate well, had normal bowel movements, and was discharged on postoperative day 45. There was no return of the narrowing or leak during follow-up.\n\nWhy this matters\n- This case shows that a late leak after ileostomy closure can be caused by an internal blood clot pressing on the bowel. In a patient for whom another major operation is risky, a minimally invasive approach — draining the hematoma and dilating the narrowed bowel with a balloon under X-ray — can treat the problem and avoid reoperation.",
+            "B3": "Resumen clínico (edad 44)\n\nMotivo de consulta\nUn hombre de 44 años fue ingresado inicialmente por neumaturia y cistitis recurrente; se diagnosticó una fístula colo-vesical y se realizó cirugía laparoscópica mayor (resección sigmoide-rectal, resección parcial de íleon, cierre de fístula vesical y creación de ileostomía de derivación).\n\nCurso inmediato y complicaciones\n- Tras el cierre de la ileostomía, al día siguiente presentó shock hemorrágico: presión arterial <80 mmHg, taquicardia y caída de hemoglobina de 15.3 a 8.6 g/dL.  \n- Se diagnosticó sangrado posoperatorio y se logró hemostasia; el paciente recibió 8 unidades de glóbulos rojos y 8 unidades de plasma fresco congelado para estabilizarlo.  \n- Persistió distensión abdominal e inflamación intensa (CRP 42.9 mg/dL, WBC 18.500/µL). La TAC mostró hematoma intraabdominal en ambos cuadrantes inferiores.\n\nIntervenciones no quirúrgicas tempranas\n- Día 8: drenajes percutáneos guiados por TAC colocados en ambos cuadrantes inferiores; drenaron abundante sangre antigua y mejoraron la inflamación (CRP 1.9 mg/dL, WBC 5.000/µL).  \n- Día 14: el drenaje derecho cambió a contenido intestinal; la angiografía de drenaje confirmó una fuga anastomótica tardía en el sitio de cierre de la ileostomía. El drenaje continuó (≈100–200 ml/día) durante 2 semanas sin signos de peritonitis.\n\nCausa de la fuga y razonamiento terapéutico\n- La TAC mostró un hematoma organizado en el mesenterio que comprimía el íleon en el lado distal (10 cm desde la anastomosis). Se interpretó que esa compresión provocó estenosis intestinal distal, aumento de presión y finalmente fuga anastomótica.  \n- Debido a múltiples cirugías previas, sangrado y riesgo elevado por adherencias extensas, una reoperación se consideró de alto riesgo. Se optó por una estrategia mínimamente invasiva: dilatación con balón por vía radiológica a través del tracto de drenaje.\n\nProcedimiento de dilatación (día 24 posoperatorio)\n- Se accedió a la fístula a través del drenaje; se avanzaron hilo guía y microcatéter hasta el íleon terminal y se localizó la estenosis.  \n- Se realizó dilatación fluoroscópica con balón (diámetro inflado 16.5 mm, 4.5 atm, 3 minutos).\n\nResultados y seguimiento\n- A partir del día siguiente a la dilatación disminuyó marcadamente el volumen de drenaje; se observaron expulsión de flatos y heces por vía natural.  \n- Una semana después, el drenaje fue casi nulo y se consideró resuelta la fuga anastomótica; los tubos se retiraron progresivamente.  \n- El paciente toleró la vía oral, recuperó tránsito intestinal normal y fue dado de alta al día 45 posoperatorio. No se ha registrado recidiva de estenosis ni de la fuga hasta el último seguimiento.\n\nLecciones y recomendaciones prácticas\n- Una fuga anastomótica tardía puede deberse no solo a fallo técnico, sino a estenosis distal por compresión (p. ej., hematoma organizado).  \n- En pacientes con alto riesgo de reintervención, la dilatación endovascular/fluoroscópica de una estenosis compresiva puede ser una alternativa eficaz y menos invasiva para permitir el drenaje y la cicatrización de la anastomosis.  \n- Seguimiento clínico e imagenológico estrecho es necesario tras la resolución; si la estenosis o la fuga persisten, puede precisarse intervención quirúrgica. También conviene monitorizar nutrición, infección y función intestinal.\n\nComentario empático\nEl equipo tratante evitó una reoperación de alto riesgo y consiguió la resolución mediante técnicas percutáneas y endovasculares. Este enfoque permitió al paciente recuperarse sin nueva cirugía mayor; sin embargo, requiere vigilancia continua para detectar recurrencias y asegurar una recuperación completa."
+        }
+    },
+    {
+        "article": "Paciente femenino de 23 años, ASA I, acude al Centro de Salud de la Universidad Peruana de Ciencias Aplicadas (CUS-UPC) para colocarle un implante en la zona edéntula de la pieza 1.6. Durante la evaluación, la paciente refiere que hace unos meses se le fracturó la primera molar superior derecha y, como consecuencia, le realizaron la exodoncia atraumática de dicha pieza dentaria.\n\nTras la inspección clínica, se observó la ausencia de la pieza dentaria 1.6, fenotipo gingival delgado y disminución en altura de reborde edéntulo Seibert tipo II 13. Tomográficamente, se registraron medidas de la altura del reborde óseo residual en relación con el piso del seno maxilar (6 mm) y el ancho de la cresta ósea a nivel cervical (11,20 mm), medio (11,80 mm) y apical (12,40 mm), con lo que se identifica la presencia de un seno maxilar ovoide, según Nie et al. Se realizó la planificación quirúrgica para la realización de una elevación del seno maxilar con abordaje transcrestal y la colocación de un implante dental de 4,8 x 8 mm.\n\nSe inició el procedimiento quirúrgico, que consistió en lo siguiente:\n\n• Asepsia y antisepsia\n\n• Técnica anestesia infiltrativa por vestibular y palatino de la zona edéntula 1.6 utilizando 2 cartuchos de lidocaína al 2% con epinefrina 1:80.000.\n\n• Incisión supracrestal en la zona edéntula 1.6 e incisiones sulculares en mesial de la pieza dentaria 1.7 y en distal de la pieza dentaria 1.5.\n\n• Decolado del colgajo a espesor parcial y, luego, se procedió a probar la guía quirúrgica para realizar la secuencia de fresado hasta una longitud de 6 mm, dejando 1 mm de distancia al piso del seno maxilar, el cual fue comprobado con los calibradores de profundidad, según el diámetro de la fresa que se utilizó durante la osteotomía. La secuencia de fresado se realizó hasta la fresa 3,5 mm de diámetro y luego se procedió a realizar el levantamiento de 2 mm del seno maxilar con la técnica de abordaje transcrestal mediante el uso de un osteótomo, hasta llegar a una longitud de 8 mm.\n\n• Colocación del implante φ 4,8 x 8 mm (Bone Level tapered, Straumann®) y tornillo de cierre, ambos con un torque de inserción de 20 N.\n\n• Sutura con puntos interrumpidos con ácido poliglicólico 5/0 y lavado de la zona quirúrgica con suero fisiológico al 0,09%.\n\n• Radiografía posquirúrgica del implante en zona edéntula 1.6.\n\n• Indicación de tomar amoxicilina de 500 mg + ácido clavulánico 125 mg cada 8 horas durante 7 días, ketorolaco de 10 mg cada 8 horas por 3 días, cetirizina de 10 mg cada 24 horas por 3 días y clorhexidina al 0,12%, 2 veces al día, por 10 días. Entre las indicaciones posquirúrgicas se le indicó a la paciente reposo absoluto, sin esfuerzo físico, dieta blanda, no sonarse la nariz, no succionar líquidos por dos semanas, no sumergir la cabeza en agua, tampoco estornudar o toser con la boca abierta, mantener la cabeza elevada y aplicarse compresas de hielo durante las primeras 4 horas.\n\nSe realizó un control posquirúrgico a los 7 días, el cual evidenció tejidos blandos en proceso de cicatrización, por lo que se procedió al retiro de puntos y lavado con suero fisiológico al 0,9%, y se realizó una tomografía de control que evidenció la elevación de seno maxilar, con 2,83 mm aproximadamente. Asimismo, se realizaron controles posquirúrgicos a los 35 y 56 días, en los cueles se hallaron tejidos blandos en completo proceso de cicatrización.",
+        "gold_summary": "Se realizó un levantamiento de seno maxilar sin injerto óseo en una paciente de sexo femenino de 23 años que requería la colocación de un implante dental en la zona edéntula de la pieza 16. La evaluación clínica y tomográfica permitieron planificar y realizar la elevación de seno maxilar mediante el abordaje transcrestal y sin la necesidad de injerto óseo. El reborde residual de 6 mm permitió la colocación de un implante dental simultáneo. Luego de 6 meses de seguimiento tomográfico, antes de la carga protésica, se consiguió una altura ósea vertical de 8,83 mm, lo que dio como resultado una ganancia ósea vertical de 2,83 mm. Adicionalmente, se observa una adecuada integración del implante dental sin complicaciones posoperatorias.",
+        "synthetic_summary": {
+            "B1": "Había una joven de 23 años que necesitaba poner un implante en el lugar donde le habían sacado un molar arriba a la derecha. Debajo de ese diente hay un espacio con aire llamado seno. Para poner el implante había que levantar un poco el suelo de ese espacio.  \n\nLos doctores vieron en la radiografía que quedaba 6 mm de hueso. Eso era suficiente para hacer la operación sin añadir hueso extra. Durante la cirugía limpiaron y adormecieron la zona. Con cuidado levantaron 2 mm del piso del seno por la misma abertura donde iba el implante. Pusieron un implante pequeño (4,8 x 8 mm) y cerraron la encía con puntos. Le dieron medicinas y le explicaron cómo cuidarse en casa.  \n\nA los 7 días la herida estaba sanando y quitaron los puntos. En controles posteriores la encía siguió cicatrizando bien. A los 6 meses, la radiografía mostró que había crecido casi 3 mm de hueso más, quedando cerca de 9 mm. El implante estaba integrado y no hubo problemas.  \n\nTodo salió bien y la paciente se recuperó sin complicaciones.",
+            "B2": "Resumen (nivel B2, lenguaje claro y amable)\n\nUna mujer de 23 años acudió para colocar un implante dental en el lugar donde faltaba la muela superior derecha (pieza 1.6), después de una extracción previa. La evaluación clínica y una tomografía mostraron que había 6 mm de hueso vertical entre la cresta alveolar y el suelo del seno maxilar (una cavidad aérea situada sobre las muelas), y un ancho de cresta suficiente (unos 11–12 mm). Por estas medidas se planificó un levantamiento de seno maxilar por vía transcrestal (es decir, accediendo desde la propia cresta donde va el implante) y la colocación simultánea de un implante de 4,8 x 8 mm, sin usar injerto óseo.\n\nDurante la cirugía se usó anestesia local y se talló un colgajo parcial. Se fresó hasta 6 mm de profundidad (dejando 1 mm del suelo del seno), y con un osteótomo se elevó el piso del seno alrededor de 2 mm para alcanzar la longitud necesaria. Se colocó el implante con un par de inserción de 20 N·cm y se suturó la zona. Se indicaron antibióticos, analgésicos, enjuague con clorhexidina y medidas postoperatorias cuidadosas (reposo, dieta blanda, evitar sonarse la nariz o succionar, mantener la cabeza elevada, hielo las primeras horas) para proteger la elevación del seno.\n\nEn el control a los 7 días la herida evolucionaba bien; la tomografía mostró una elevación del seno de aproximadamente 2,83 mm. En controles posteriores (35 y 56 días) la cicatrización fue completa. Tras seguimiento tomográfico antes de la carga protésica se reportó una altura ósea vertical final de 8,83 mm, lo que supone una ganancia ósea de 2,83 mm. No se registraron complicaciones y el implante mostró buena integración.\n\nComentario final (claro y tranquilizador): en este caso, debido a la altura residual de hueso, fue posible levantar el seno y colocar el implante al mismo tiempo sin usar injerto. La ganancia ósea y la buena cicatrización indican un resultado exitoso y sin problemas inmediatos.",
+            "B3": "Resumen clínico (nivel universitario)\n\nPaciente y motivo\n- Mujer de 23 años, ASA I, que acudió para la colocación de un implante en el espacio edéntulo del primer molar superior derecho (pieza 1.6). Refería exodoncia atraumática previa de esa pieza tras una fractura.\n\nHallazgos iniciales\n- Examen clínico: ausencia de la pieza 1.6, fenotipo gingival delgado y reducción del reborde edéntulo tipo Seibert II (pérdida moderada de altura).\n- Tomografía (CBCT): altura ósea residual de 6 mm desde la cresta hasta el piso del seno maxilar; anchos crestal de 11,20 mm (cervical), 11,80 mm (medio) y 12,40 mm (apical). Se describió un seno maxilar de morfología ovoide (criterios de Nie et al.).\n\nPlan y técnica quirúrgica\n- Se planificó una elevación de seno maxilar por abordaje transcrestal sin injerto óseo y la colocación inmediata de un implante.\n- Procedimiento relevante:\n  - Anestesia infiltrativa vestibular y palatina con lidocaína 2% + epinefrina.\n  - Incisión supracrestal y despegamiento de espesor parcial.\n  - Fresado guiado hasta 6 mm (1 mm por debajo del piso sin perforar), luego osteotomía con osteótomo para elevar 2 mm el piso del seno y alcanzar una profundidad total de 8 mm.\n  - Colocación de implante Bone Level tapered Straumann de 4,8 x 8 mm y tornillo de cierre con torque de inserción registrado de 20 N.\n  - Sutura con puntos interrumpidos (ácido poliglicólico 5/0) y lavado con suero fisiológico.\n\nTratamiento posoperatorio y cuidados\n- Medicación: amoxicilina/ácido clavulánico 500/125 mg cada 8 h por 7 días; ketorolaco 10 mg cada 8 h por 3 días; cetirizina 10 mg cada 24 h por 3 días; enjuagues con clorhexidina 0,12% dos veces al día por 10 días.\n- Indicaciones: reposo, dieta blanda, evitar sonarse la nariz, succión, inmersión en agua, estornudar o toser con la boca cerrada, mantener la cabeza elevada y aplicar frío local las primeras 4 horas.\n\nEvolución y resultados\n- Control a los 7 días: buena cicatrización de tejidos blandos; retirada de puntos. CBCT de control mostró una elevación del seno de aproximadamente 2,83 mm respecto al piso previo.\n- Controles a los 35 y 56 días: tejidos blandos en completo proceso de cicatrización.\n- Antes de la carga protésica, a los 6 meses de seguimiento tomográfico, se constató una altura ósea vertical total de ~8,83 mm (ganancia vertical ≈ 2,83 mm) y buena integración del implante sin complicaciones clínicas registradas.\n\nInterpretación e implicaciones\n- Con una altura residual de 6 mm, la técnica transcrestal sin relleno fue suficiente para elevar el piso sin injerto y colocar el implante simultáneamente, logrando una ganancia ósea vertical cercana a 3 mm y estabilidad sin evidencia de complicaciones en el seguimiento reportado.\n- Esta estrategia puede ser una alternativa menos invasiva cuando la altura residual permite soporte primario del implante; reduce el uso de biomateriales y la morbilidad asociada a procedimientos más extensos.\n\nRecomendaciones y consideraciones\n- Seguimiento prolongado (radiográfico y clínico) hasta la carga definitiva y más allá para confirmar estabilidad a largo plazo del hueso y del implante.\n- Vigilar signos de complicación: dolor persistente, aumento de inflamación, secreción purulenta, o síntomas de sinusitis que podrían indicar perforación de la membrana, infección o fracaso de la osteointegración.\n- Antes de la rehabilitación protésica final, confirmar por CBCT y pruebas clínicas la integración y la calidad ósea obtenida.\n\nComentario final (tono empático)\nEl procedimiento fue exitoso en esta paciente joven, con buena cicatrización y aumento óseo suficiente para la rehabilitación protésica planificada. Es importante mantener controles periódicos y seguir las recomendaciones para minimizar riesgos y asegurar un resultado funcional y estable a largo plazo."
+        }
+    },
+    {
+        "article": "Una paciente de 42 años de edad fue remitida a nuestro centro terciario de cáncer con antecedentes de seroma recurrente del seno izquierdo. La paciente se había sometido a una extracción bilateral de implantes mamarios con una capsulotomía parcial 11 meses antes de su primera visita a nuestro centro. La paciente no presentaba ninguna comorbilidad notable y tenía antecedentes de aumento bilateral de senos con implantes mamarios en el plano submuscular en 2003, a la edad de 21 años. No se pudo localizar ninguna información sobre el tipo de implantes que había recibido originalmente. La paciente volvió a consultar al mismo cirujano en 2008, quejándose de seroma bilateral, para someterse a un primer reemplazo bilateral de implantes mamarios con implantes mamarios anatómicos texturados de 425 cc (Sebbin LSA TF 425). En 2013, se sometió a un segundo procedimiento de reemplazo de implantes para aumentar el tamaño con implantes mamarios de 480 cc del mismo fabricante (Sebbin LSA TF 480). En 2017, la paciente volvió para una revisión en la que se quejaba de dolor y aumento del volumen del seno bilateralmente. En ese momento, se le realizó una exploración por ultrasonido que identificó efusiones periprostéticas bilaterales sin linfadenopatía o masas palpables en las regiones mamarias. Las efusiones se drenaron sin análisis, pero reaparecieron a lo largo de los años, cuando la paciente buscó ayuda del mismo cirujano y se sometió a un tercer procedimiento de revisión en 2022, con un reemplazo bilateral de implantes mamarios y una toma de muestras de la cápsula anterior. El cirujano envió dos especímenes desde el lado derecho (9 x 1 cm y 3 x 3 cm) y uno desde el lado izquierdo (2 x 1 cm). El informe histopatológico del espécimen encontró «material proteico amorfo celular acellular» en el lado derecho y «tejido fibroso escleroso con inflamación de linfocitos-monocitos, que requiere correlación con la presentación clínica» en el lado izquierdo. A pesar de la extracción, el seroma reapareció en el lado izquierdo, y se envió para pruebas citopatológicas que identificaron «una población de células pleomórficas atípicas irregulares con contornos irregulares que sugieren un proceso linfoproliferativo con CD30+ elementos» para los que se recomendaron pruebas diagnósticas adicionales. Por esta razón, la paciente buscó tratamiento en nuestra institución, donde el caso fue gestionado por un equipo multidisciplinario (MDT) que incluía a un cirujano plástico, un hematopatólogo, un hematólogo, un oncólogo, un radioterapeuta, un oncólogo quirúrgico y un radiólogo de mama. El espécimen histopatológico original de la toma de la cápsula se revisó por un hematopatólogo de nuestro centro de referencia, que identificó células CD30+ grandes y escasas atípicas con contornos irregulares que se consideraron compatibles con el diagnóstico de BIA-ALCL. Las células presentaron el siguiente fenotipo: CD30+, CD3-, CD7-, CD5-, CD4-, CD8-, Granzima B+/-, TIA1-, ALK1-, PAX5-, CD79a-, CD68-, CD15-/+. La paciente recibió una exploración por ultrasonido con aspiración por aguja fina y citopatología de la efusión recurrente que confirmó un proceso CD30+ linfoproliferativo atípico con captación de 18F-FDG (fluorodeoxiglucosa) (SUV máx. 1,8). No se pudieron localizar otras áreas de captación en todos los demás segmentos corporales explorados. La paciente también recibió una exploración por resonancia magnética de ambos senos con medio de contraste para completar la estadificación preoperativa, confirmando el seroma del lado izquierdo. Los portaobjetos del espécimen de la cirugía anterior se revisaron por el hematopatólogo que consideró los hallazgos suficientes para identificar BIA-ALCL con infiltración temprana de la cápsula periprostética (pT2 según el sistema de estadificación MD Anderson-TNM). Tres semanas después de la visita inicial, la paciente se sometió a cirugía radical con capsulotomía en bloque que contenía solo 150 cc de efusión serosa sin implante. El contenido líquido se envió para cultivo y citopatología, mientras que el espécimen sólido se envió para examen histopatológico. Además, la paciente se sometió a biopsia de ganglio linfático centinela de 2 ganglios axilares identificados preoperativamente a través de linfografía segmentaria. Los ganglios linfáticos presentaron una linfadenopatía silicona-asociada reactiva crónica sin signos de linfadenopatía metastásica. El informe histopatológico de la cápsula reveló agregados celulares infiltrantes en la cápsula periprostética, pero márgenes de resección claros y sin signos de infiltración más allá de la cápsula. Como tal, la paciente recibió un estadio IC (pT3pN0M0). El curso postoperatorio fue sin incidentes, y no se consideraron necesarios más tratamientos adyuvantes por el MDT. La paciente continuó su estricto protocolo de seguimiento, con PET/CT de 6, 12 y 18 meses posteriores a la cirugía que no mostró signos de recurrencia de enfermedad local o distante. Como está, la paciente continúa sus visitas de seguimiento y exploraciones, con supervivencia libre de enfermedad más allá de 18 meses.\n",
+        "gold_summary": "Describimos el caso de una mujer de 42 años con antecedentes de aumento de senos bilateral con fines cosméticos 21 años antes, que desarrolló seroma recurrente del lado izquierdo. Buscó ayuda de su primer cirujano, quien realizó 2 procedimientos de intercambio de implantes mamarios, colocando dispositivos texturados y, finalmente, una extracción bilateral de implantes mamarios en el transcurso de dos décadas. La paciente no recibió capsulectomías en los intercambios de implantes anteriores y recibió una muestra de la cápsula anterior en el último procedimiento, donde se diagnosticó BIA-ALCL en el lado izquierdo. Fue derivada a un centro de cáncer terciario donde el examen preoperatorio confirmó la presencia de enfermedad residual local. Después de la gestión del equipo multidisciplinario, se sometió a una revisión de capsulectomía en bloque del lado izquierdo sin necesidad de tratamientos adicionales. El curso postoperatorio fue sin incidentes y sin signos de recurrencias locales a los 18 meses de seguimiento.\n",
+        "synthetic_summary": {
+            "B1": "Esta es la historia de una mujer de 42 años que se había puesto implantes de seno cuando era joven. Con los años tuvo varias cirugías y a veces se le formó líquido alrededor del implante en el seno izquierdo. Ese líquido volvió muchas veces.\n\nCuando le quitaron los implantes y mandaron a mirar el tejido, los médicos encontraron un tipo raro de cáncer llamado BIA-ALCL. Eso es un cáncer de las células del sistema que a veces aparece cerca de implantes de seno. Los médicos la mandaron a un centro especializado para estudiar mejor el caso.\n\nAllí le hicieron más pruebas y vieron que el cáncer estaba solo en la cápsula (el tejido cicatricial) alrededor del seno izquierdo. Le hicieron una cirugía para quitar toda la cápsula y el líquido de una sola vez. También revisaron los ganglios (pequeñas bolitas que revisan si el cáncer se ha movido) y no encontraron cáncer en ellos. Los márgenes de la cirugía quedaron limpios, es decir, quitó todo lo que hacía falta.\n\nDespués de la operación no necesitó más tratamientos. Los controles con imágenes a los 6, 12 y 18 meses no mostraron enfermedad. La paciente sigue controlándose y, hasta ahora, está libre de cáncer más de 18 meses después.",
+            "B2": "Resumen claro y amable:\n\nUna mujer de 42 años que había recibido implantes mamarios por estética desde los 21 años desarrolló repetidos acúmulos de líquido (seromas) en el seno izquierdo. Un seroma es una acumulación de líquido que puede formarse alrededor de un implante. A lo largo de casi dos décadas la paciente tuvo varios recambios de implantes y en 2022 se le retiraron los implantes y se tomaron muestras de la cápsula (la bolsa de tejido fibroso que el cuerpo forma alrededor del implante).\n\nTras la extracción, el seroma volvió a aparecer en el lado izquierdo. El examen del líquido y de la cápsula encontró células anormales que daban positivo para una proteína llamada CD30. Eso hizo sospechar un tipo raro de linfoma asociado a implantes mamarios, llamado BIA‑ALCL (un linfoma no Hodgkin que puede aparecer en el líquido o la cápsula alrededor de implantes). El caso fue enviado a un equipo especializado (cirujanos, hematólogos, patólogos, radiólogos y oncólogos) para decidir el mejor tratamiento.\n\nLas pruebas por imagen (ecografía, PET/CT y resonancia magnética) mostraron enfermedad localizada en el seno izquierdo sin signos de extensión a otras partes del cuerpo. Los patólogos revisaron las muestras y vieron células CD30+ compatibles con BIA‑ALCL con infiltración temprana de la cápsula.\n\nTres semanas después de la evaluación, la paciente se sometió a una cirugía para retirar en bloque la cápsula afectada y el líquido acumulado (capsulectomía en bloque). También se hicieron biopsias de los ganglios linfáticos sentinel para comprobar si el cáncer se había diseminado. Los ganglios mostraron cambios reactivos por la silicona, pero no había metástasis. La pieza quirúrgica tenía márgenes limpios y no se encontró enfermedad fuera de la cápsula.\n\nEl diagnóstico final fue BIA‑ALCL en estadio local (estadio IC, pT3 pN0 M0), y el equipo decidió que no eran necesarias más terapias (quimioterapia o radioterapia). La recuperación fue buena y las revisiones con PET/CT a los 6, 12 y 18 meses no mostraron recurrencia. Al momento del informe la paciente seguía libre de enfermedad más allá de 18 meses.\n\nComentario y pasos a seguir: BIA‑ALCL es raro y a menudo se identifica por seromas tardíos alrededor de implantes. El manejo ideal cuando la enfermedad está limitada a la cápsula suele ser cirugía completa para retirar la cápsula y el implante, seguida de controles periódicos por imagen. En este caso la respuesta fue buena y el seguimiento hasta ahora es favorable.",
+            "B3": "Resumen clínico (nivel lector universitario)\n\nPresentación y antecedentes\n- Mujer de 42 años con antecedente de aumento mamario en 2003 y múltiples revisiones/reemplazos de implantes durante las dos décadas siguientes. En 2008 y 2013 se usaron implantes anatómicos texturados (Sebbin LSA TF 425 y 480). No se dispone de datos del implante original de 2003.\n- Desde 2017 presentó efusiones (seromas) periprotésicos recurrentes del lado izquierdo que se drenaron en varias ocasiones. En 2022 se realizó un tercer procedimiento de revisión; 11 meses antes de la derivación al centro terciario se hicieron extracción bilateral de implantes con capsulotomía parcial.\n- Tras la extracción persistió el seroma izquierdo, y la citología detectó una población atípica CD30+ que orientó a un proceso linfoproliferativo.\n\nEvaluaciones diagnósticas\n- Revisión por un equipo multidisciplinario en el centro oncológico; examen histopatológico y revisión por hematopatólogo identificaron células grandes CD30+ y ALK-, hallazgo compatible con BIA‑ALCL (linfoma anaplásico de células grandes asociado a implante mamario).\n- Inmunofenotipo relevante: CD30+, ALK1–, negativos para marcadores B (PAX5, CD79a) y en su mayoría para marcadores T habituales (CD3, CD4, CD5, CD7, CD8); granzima B variable.\n- Ecografía con punción aspirativa del derrame confirmó proceso linfoproliferativo CD30+. PET/CT mostró captación de FDG limitada al foco mamario izquierdo (SUV máx 1,8) sin otras lesiones a distancia. RM con contraste confirmó el seroma izquierdo.\n- Biopsia de ganglios centinela axilares (2 ganglios) mostró linfadenopatía reactiva crónica asociada a silicona, sin compromiso metastásico.\n\nTratamiento y estadificación\n- Se realizó capsulotomía en bloque lateral izquierdo (extirpación completa de la cápsula periprotésica con el contenido seroso —150 cc—). El examen histológico mostró agregados celulares infiltrantes en la cápsula, márgenes quirúrgicos libres y ausencia de extensión más allá de la cápsula.\n- Estadio postoperatorio informado: IC (pT3 pN0 M0) según el sistema MD Anderson–TNM. El equipo multidisciplinario consideró que, dada la resección completa y la ausencia de afectación ganglionar o a distancia, no se requerían tratamientos adyuvantes (quimioterapia o radioterapia).\n\nEvolución y seguimiento\n- Recuperación postoperatoria sin complicaciones.\n- Vigilancia con PET/CT a los 6, 12 y 18 meses: sin evidencia de recidiva local ni enfermedad a distancia.\n- Actualmente la paciente permanece en seguimiento activo, con supervivencia libre de enfermedad >18 meses.\n\nInterpretación y puntos prácticos\n- BIA‑ALCL es un linfoma raro asociado con implantes mamarios, con mayor relación reportada en implantes texturados; se caracteriza por células CD30+ y generalmente ALK–.\n- En este caso, la enfermedad estuvo confinada a la cápsula periprotésica y fue tratada con resección en bloque completa, lo que se asocia con buen pronóstico cuando la resección es completa y no hay afectación ganglionar o sistémica.\n- Importa la vigilancia continua: seguimiento clínico e imagenológico para detectar recurrencia precoz. El manejo se beneficia de un enfoque multidisciplinario que incluye cirugía, hematopatología e imagen.\n\nNota empática\n- La paciente atravesó múltiples revisiones y procedimientos antes del diagnóstico definitivo. El resultado temprano y localizado, la intervención quirúrgica completa y el seguimiento riguroso han permitido hasta ahora una evolución favorable."
+        }
+    },
+    {
+        "article": "Se trata de un paciente de 50 años que se presentó con una queja de dolor e hinchazón de la lengua de tres días de duración. Asociado a esto, tenía dolor al tragar, dificultad para abrir la boca, falta de aire y babeo. Asimismo, tenía fiebre alta y un tipo de dolor de cabeza global. Por lo demás, no tenía traumatismo en la lengua, ni procedimientos dentales u orales recientes, ni antecedentes de tabaquismo ni de enfermedad médica crónica como diabetes mellitus, enfermedad cardiaca e hipertensión. Históricamente, había tenido un dolor dental agudo en los últimos seis meses antes de su queja actual. Había masticado khat desde su niñez y tenía una mala higiene oral.\n\nEn el examen físico, se veía muy enfermo y sus signos vitales eran: presión arterial 115 por 70 mmHg, pulso 120 latidos por minuto, frecuencia respiratoria 20, temperatura 39 grados centígrados y saturación de oxígeno 92% de oxígeno. En el examen HEENT, había una hinchazón significativa de la lengua en el área anterolateral izquierdo, fluctuante a la palpación, y tenía un borde eritematoso. Hay múltiples caries en las áreas maxilares y mandibulares. No hubo hallazgos pertinentes en los sistemas restantes.\n\nTras obtener el consentimiento informado, el paciente fue trasladado al quirófano con el diagnóstico de absceso lingual. Posteriormente, se realizó la incisión y el drenaje bajo anestesia general, y se drenaron unos 30 ml de pus espeso. La bolsa se lavó con solución salina normal y peróxido de hidrógeno al 2 %. El paciente fue trasladado a la sala de cirugía con signos vitales estables y había tomado ceftriaxona 1 g por vía intravenosa dos veces al día y metronidazol 500 mg por vía intravenosa tres veces al día durante dos días. Fue dado de alta después de dos días de estancia en el hospital con mejoría y Augmentin 625 mg por vía oral tres veces al día durante cinco días.\n",
+        "gold_summary": "Se trata de un paciente de 50 años que se presentó con una queja de dolor e hinchazón de la lengua de tres días de duración. Asociado a esto, tenía dolor al tragar, dificultad para abrir la boca, falta de aire y babeo. Asimismo, tenía fiebre alta y un tipo de dolor de cabeza global. En el examen físico, había una hinchazón significativa de la lengua en el área anterolateral izquierda, fluctuante a la palpación, y tenía un borde eritematoso. Después de que se tomó el consentimiento informado, el paciente fue trasladado al quirófano con el diagnóstico de absceso de la lengua. Posteriormente, se hizo una incisión y drenaje bajo anestesia general, y se drenaron unos 30 ml de pus espeso. El bolsillo se lavó con solución salina normal y peróxido de hidrógeno al 2%. El paciente fue trasladado a la sala de cirugía con signos vitales estables y había estado tomando antibióticos. Fue dado de alta después de dos días de estancia en el hospital.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre de 50 años llegó al hospital porque tenía la lengua hinchada y dolorida desde hacía tres días. Le dolía al tragar. Tenía dificultad para abrir la boca, le salía saliva y le costaba un poco respirar. También tenía fiebre y dolor de cabeza.\n\nEn la boca se vio una hinchazón grande en la parte izquierda de la lengua. Esa zona estaba blanda y al tocarla parecía haber líquido dentro. Los médicos dijeron que era un absceso de la lengua. Un absceso es una bolsa con pus, que es líquido amarillo que se forma cuando hay infección.\n\nCon el permiso del paciente, lo llevaron al quirófano. Lo pusieron a dormir para la operación. Le hicieron un pequeño corte y sacaron unos 30 ml de pus espeso. Limpiaron la herida con agua salada y peróxido de hidrógeno al 2 %. Después lo cuidaron con antibióticos por vía intravenosa en el hospital.\n\nEl hombre mejoró y, tras dos días, lo dejaron ir a su casa con más antibiótico para tomar por cinco días. Está bien decir que recibió tratamiento y mejoró.",
+            "B2": "Resumen sencillo y claro:\n\nUn hombre de 50 años llegó al hospital porque desde hacía tres días tenía dolor e hinchazón en la lengua. También le dolía al tragar, tenía dificultad para abrir la boca, le salía saliva sin control (babeo), se quedaba sin aliento y tenía fiebre alta y dolor de cabeza general. No había sufrido un golpe en la lengua ni se había hecho tratamientos dentales recientes. No tenía enfermedades crónicas conocidas como diabetes o problemas del corazón, ni fumaba. Sí había tenido un dolor dental agudo en los últimos seis meses, masticaba khat y tenía mala higiene bucal.\n\nAl examinarlo se veía muy enfermo. Sus signos vitales fueron: presión 115/70 mmHg, pulso rápido 120 latidos por minuto, respiración 20 por minuto, temperatura 39 °C y saturación de oxígeno 92%. En la boca se observó una hinchazón importante en el lado izquierdo y hacia la parte frontal de la lengua; esa zona se sentía blanda y llena de líquido al tocarla (fluctuación) y tenía el borde enrojecido. Además había muchas caries en los dientes superiores e inferiores.\n\nEl diagnóstico fue absceso de la lengua. Un absceso es una acumulación de pus causada por una infección. Bajo anestesia general se hizo una incisión para abrir y drenar el absceso; salieron unos 30 ml de pus espeso. La cavidad se limpió con suero salino y peróxido de hidrógeno al 2%. Después del procedimiento el paciente quedó estable y recibió antibióticos por vía intravenosa (ceftriaxona y metronidazol) durante dos días.\n\nFue dado de alta tras dos días en el hospital porque mejoró. Al salir recibió antibiótico oral (Augmentin 625 mg, tres veces al día por cinco días).\n\nQué significa y próximos pasos prácticos:\n- El problema principal era una infección localizada que necesitó drenaje y antibióticos, lo que suele resolver la infección.  \n- Es importante seguir la receta y volver si empeora la hinchazón, aparece dificultad para respirar más grave, fiebre alta persistente o dolor que no cede.  \n- También se recomienda atención dental y mejorar la higiene bucal para evitar que caries o infecciones dentales vuelvan a provocar problemas.",
+            "B3": "Resumen clínico (nivel B3)\n\n- Presentación: Hombre de 50 años con 3 días de dolor e hinchazón de la lengua, asociados a odinofagia (dolor al tragar), dificultad para abrir la boca (trismo), disnea leve y babeo. También tuvo fiebre alta y cefalea difusa.\n\n- Antecedentes relevantes: No refirió traumatismo lingual ni procedimientos dentales u orales recientes, ni enfermedades crónicas conocidas (por ejemplo diabetes, cardiopatía o hipertensión). Historia de dolor dental agudo en los últimos seis meses, masticación crónica de khat y mala higiene bucal, lo que sugiere una probable fuente odontogénica de la infección.\n\n- Exploración: Paciente en estado general comprometido. Signos vitales anormales: taquicardia (FC 120/min), fiebre (39 °C) y saturación de oxígeno algo reducida (92%); tensión arterial y frecuencia respiratoria dentro de límites aceptables. En HEENT hallazgo clave: masa fluctuante y eritematosa en la región anterolateral izquierda de la lengua (absceso lingual). Múltiples caries dentales en maxilar y mandíbula. No se reportaron otros hallazgos sistémicos importantes.\n\n- Diagnóstico y manejo inmediato: Diagnóstico de absceso lingual. Tras consentimiento informado, se realizó drenaje quirúrgico bajo anestesia general; se evacuaron aproximadamente 30 ml de pus espeso y el bolsillo se irrigó con solución salina y peróxido de hidrógeno al 2%. Se inició antibioterapia empírica intravenosa: ceftriaxona 1 g cada 12 horas y metronidazol 500 mg cada 8 horas durante 2 días.\n\n- Evolución y alta: Mejoró tras el drenaje y la terapia intravenosa; fue trasladado a sala quirúrgica en situación estable y dado de alta tras 48 horas con tratamiento oral (amoxicilina/ácido clavulánico 625 mg cada 8 horas por 5 días).\n\n- Interpretación y puntos a considerar: El absceso lingual es una infección rara pero potencialmente grave por riesgo de compromiso de la vía aérea y extensión a espacios profundos del cuello. En este caso, la presencia de múltiples caries y antecedente de dolor dental hacen probable un origen odontogénico. La saturación de 92% y la taquicardia justificaron manejo urgente y vigilancia del estado respiratorio. No se mencionó cultivo del pus ni pruebas metabólicas (p. ej., glucemia) en el informe; obtener cultivo y evaluar factores de riesgo inmunológicos puede ser útil en casos similares para orientar el tratamiento antimicrobiano y prevenir recurrencias.\n\n- Recomendaciones sugeridas tras el alta: seguimiento dental para tratar la fuente (caries), mejora de higiene oral, consejo para suspender masticación de khat y control ambulatorio para confirmar resolución completa y vigilar signos de recurrencia o extensión (fiebre persistente, empeoramiento de la respiración, dolor cervical). Si aparecieran nuevos síntomas, reconsulta urgente por riesgo de complicaciones."
+        }
+    },
+    {
+        "article": "Hombre de 73 años de edad de origen latinoamericano, con antecedente de madre con diagnóstico de demencia tipo Alzheimer con panel genético negativo; hermano con diagnóstico de ELA; hermana con diagnóstico de enfermedad de Parkinson. La sintomatología progresiva comenzó desde el año 2016 y se caracterizó por síntomas progresivos de hiposmia, hipoacusia, estreñimiento e insomnio, los cuales ameritaron valoración por otorrinolaringología y audiología, sin conclusión diagnóstica. En el año 2020 los familiares notaron que el paciente presentaba problemas en la memoria episódica, olvidos de objetos de la vida cotidiana, problemas de ganancias en su negocio (de comercio). Estos síntomas fueron progresivos hasta que el paciente empezó a tener limitación en las tareas diarias, como al manejar y al cambiar las velocidades, además de al salir de su casa. A finales de ese año el paciente comenzó a presentar debilidad muscular distal, manifestada al abrir botellas, cepillarse los dientes, lo cual progresó de forma insidiosa, no fluctuante, sin predominio de horario.\n\nEn enero de 2021 el paciente comenzó con alteraciones de la marcha, las cuales condicionaron caídas frecuentes hasta más de 6 veces a la semana, esto debido a inestabilidad postural. El paciente acudió a valoración en mayo. Se le hizo test de MoCA de 16 puntos con alteraciones en la fluidez del lenguaje y repetición de oraciones; en la abstracción, recuerdo diferido y problemas visuoespaciales y disejecutivos. El test de Luria dio positivo. El paciente presentó facie hipomímica, emitió con hipofonía, entrecortado y lento, y presentó reflejo nauseoso disminuido, rigidez generalizada de predominio izquierdo, hipotrofia generalizada, bradicinesia de predominio izquierdo, fuerza 4/5 generalizada, reflejos de estiramientos musculares 3/4, reflejos abdominocutáneos abolidos, signos de Hoffmann y Trömner presentes de forma bilateral, respuesta plantar extensora bilateral, fasciculaciones en extremidades inferiores evocadas al tacto, marcha con pasos cortos, congelamiento de la marcha al giro, pull test positivo (inestabilidad postural). Se manejó con levodopa carbidopa a una dosis gradual. Al seguimiento a los 3 meses el paciente había presentado nula mejoría en cuanto a los síntomas parkinsónicos, aumento de la debilidad muscular y persistieron los datos de motoneurona inferior y superior. Con estos hallazgos se realizó resonancia magnética (RM) del encéfalo. La velocidad de neuroconducción (VCN) presentó neuropatía axonal motora de miembros torácicos en relación con atrofia y neuroconducción sensitiva sin alteraciones. La electromiografía (EMG) presentó datos de denervación activa (aumento de actividad insercional, potenciales de fibrilación, fasciculación) y reinervación crónica (potenciales de acción de la unidad motora polifásicos, y bajo reclutamiento a la contracción máxima) en los 5 segmentos corporales, lo cual es compatible con enfermedad de motoneurona.\n\n\nLa EMG mostró un aumento de actividad insercional en músculos deltoides, bíceps, tríceps, extensor digital común bilateral y músculos linguales de forma bilateral. Se observaron abundantes potenciales de fibrilación y predominó la fasciculación en los músculos de los miembros torácicos. Durante la contracción, se observó una activación del potencial de acción de la unidad motora (PAUM) de forma polifásica y de gran amplitud. Y a máxima contracción se observó una disminución del reclutamiento en la mayoría de los músculos evaluados.\n\nEl paciente perdió seguimiento un año. Al vover a valoración se encontraba con postración en cama, afásico, aumento de los datos de parkinsonismo y síndrome de motoneurona. Se decidió realizar panel genético que resultó negativo para C9ORF72, así como para 143 genes más involucrados en enfermedades neuromusculares y neurodegenerativas, incluidos los genes VCP, MAT3, asociados a ELA, NOTCH3, asociado a demencia frontotemporal, sin alteraciones. Se reportó resultado de variante patogénica para el gen POLG: C.2209G>C, p.(Gly737Arg), relacionado con síndrome de depleción mitocondrial autosómico dominante y recesivo. Se realizó sesión de asesoramiento genético y el paciente fue informado. En mayo de 2022, el paciente presentaba disfagia y acudió en silla de ruedas, por lo que fue enviado a que se le practicara una gastrostomía.",
+        "gold_summary": "Presentamos un caso de origen latinoamericano que inicialmente se manifestó con síntomas sistémicos de más de 6 años de evolución, con posteriores alteraciones cognitivas. Después presentó alteraciones de la marcha y síntomas motores sugestivos de parkinsonismo con datos atípicos y datos de enfermedad de motoneurona. Se hicieron estudios de extensión que confirmaron hallazgos compatibles con afectación en motoneurona superior e inferior. Observamos mutación en gen POLG, relacionada con síndrome de depleción mitocondrial.",
+        "synthetic_summary": {
+            "B1": "Este es el cuento de un hombre de 73 años. Al principio, hace varios años, empezó a perder el olfato y algo de oído. También tenía estreñimiento y no podía dormir bien. Con el tiempo tuvo problemas para recordar cosas y eso le afectó su trabajo y la vida diaria.\n\nLuego le costó abrir frascos y cepillarse los dientes. Empezó a caerse muchas veces cuando caminaba. Los médicos le hicieron pruebas. Una prueba de la memoria y el pensamiento salió baja. Las pruebas que miran los nervios y los músculos mostraron que muchas células que mandan órdenes a los músculos estaban dañadas. Eso explica la debilidad y los temblores que tuvo.\n\nLe probaron un medicamento para el Parkinson, pero no mejoró. También le hicieron un examen de los genes. En muchos genes no encontraron cambios. Sí hallaron un cambio en un gen llamado POLG. Ese gen ayuda a las \"baterías\" de las células (mitocondrias). Cuando ese gen cambia, las células pueden quedarse sin energía y eso causa problemas.\n\nCon el tiempo se puso peor. Quedó en cama, perdió el habla y tuvo dificultad para tragar. Los médicos le pusieron una sonda para poder darle comida directamente al estómago.\n\nEn resumen: tenía problemas de memoria y de movimiento. Tenía señales de dos cosas: un tipo de problema parecido al Parkinson y también daño en las células que mueven los músculos. Los médicos encontraron un cambio en el gen POLG que puede explicar por qué las células no tenían energía. Fue una enfermedad difícil y fue empeorando con el tiempo.",
+            "B2": "Resumen comprensible y amable:\n\nPresentamos el caso de un hombre latinoamericano de 73 años cuya enfermedad comenzó de forma lenta desde 2016. Al principio tuvo pérdida del olfato (hiposmia), disminución de la audición, estreñimiento e insomnio. En 2020 la familia notó problemas de memoria para eventos recientes y olvidos que afectaron su trabajo. Más adelante empezó a presentar debilidad en manos y brazos, que fue empeorando sin aparecer y desaparecer.\n\nEn enero de 2021 tuvo dificultades para caminar y caídas frecuentes por inestabilidad. En la valoración neurológica obtuvo 16/30 en la prueba MoCA, con problemas en el lenguaje, memoria diferida, funciones visuoespaciales y planificación. El examen mostró rasgos de parkinsonismo (cara con poca expresión, voz baja y lenta, rigidez y lentitud de movimientos), junto con signos de afectación de la motoneurona superior e inferior: reflejos anormales, respuesta plantar extensora, fasciculaciones (contracciones musculares visibles) y debilidad. Al darle levodopa-carbidopa no mejoró el parkinsonismo.\n\nSe hicieron estudios eléctricos: la velocidad de conducción nerviosa mostró daño axonal motor en los brazos y la electromiografía (EMG) mostró signos de denervación activa (fibrilaciones y fasciculaciones) y cambios de reinervación crónica en varios segmentos del cuerpo. Estos hallazgos son compatibles con enfermedad de la motoneurona (un grupo de enfermedades que incluye a la ELA). Posteriormente el paciente empeoró: quedó en cama, con dificultad para hablar (afasia) y problemas para tragar, lo que requirió la colocación de una gastrostomía (tubo para alimentar directamente al estómago).\n\nSe realizó un estudio genético extenso. No se encontraron alteraciones en genes habitualmente asociados a ELA u otras demencias (por ejemplo C9ORF72, VCP, NOTCH3). Sí se identificó una variante patogénica en el gen POLG (c.2209G>C, p.Gly737Arg). Mutaciones en POLG se asocian con síndromes de depleción mitocondrial, que afectan la función de las mitocondrias (las “plantas de energía” de las células) y pueden provocar síntomas neurológicos. El equipo ofreció asesoría genética al paciente y la familia.\n\nQué significa todo esto, en términos sencillos:\n- El cuadro clínico combina signos de parkinsonismo que no respondieron a levodopa y criterios eléctricos que indican daño tanto de la motoneurona superior como inferior.\n- La variante en POLG podría estar relacionada con el problema, pero su papel exacto debe interpretarse junto con la clínica y otros estudios por especialistas en genética y neurología.\n- El manejo ya incluyó terapia sintomática y soporte nutricional; los siguientes pasos suelen ser seguimiento neurológico, apoyo multidisciplinario (rehabilitación, nutrición, cuidados respiratorios si hace falta) y valoración genética familiar si procede.\n\nLamento la situación difícil del paciente y su familia; este caso ilustra cómo enfermedades neurológicas complejas pueden superponerse y por qué se necesitan estudios clínicos, eléctricos e genéticos para entenderlas mejor.",
+            "B3": "Presentamos el caso de un hombre latinoamericano de 73 años con un cuadro progresivo multisistémico que comenzó en 2016 y que, a lo largo de varios años, combinó síntomas motores, cognitivos y autonómicos.\n\nCronología y síntomas principales\n- 2016 en adelante: síntomas prodrómicos no específicos pero relevantes — hiposmia (pérdida del olfato), hipoacusia, estreñimiento e insomnio. Fueron evaluados por otorrinolaringología y audiología sin diagnóstico concluyente.  \n- 2020: inicio de deterioro cognitivo episódico (olvidos de objetos, problemas en la gestión de su negocio) que progresó hasta afectar las actividades diarias (conducción, salir de casa).  \n- Finales 2020: debilidad distal insidiosa (dificultad para abrir botellas, cepillarse los dientes).  \n- Enero 2021: alteración de la marcha con inestabilidad postural y caídas frecuentes (>6/semana).  \n- Mayo 2021: valoración neurológica con MoCA 16/30 (déficits en fluidez verbal, repetición, abstracción, memoria retrasada, visoespacial y funciones ejecutivas). Signos clínicos notables: facie hipomímica, hipofonía, rigidez generalizada (predominio izquierdo), bradicinesia (predominio izquierdo), hipotrofia muscular, reflejos profundos aumentados, abolición de reflejos abdominales cutáneos, signos de neurona motora superior (Hoffmann, Trömner, respuesta plantar extensora bilateral), fasciculaciones en miembros inferiores, marcha con pasos cortos y congelamiento al girar, test de pull positivo. Se inició levodopa-carbidopa sin mejoría.  \n- Empeoramiento electromiográfico y neurofisiológico compatible con enfermedad de motoneurona (ver abajo).  \n- Pérdida de seguimiento durante un año; al retorno estaba postrado, afásico y con agravamiento del parkinsonismo y del síndrome de motoneurona. En mayo 2022 presentaba disfagia y necesitó gastrostomía.\n\nEstudios complementarios relevantes\n- Velocidad de conducción nerviosa: neuropatía axonal motora en miembros superiores (asociada a atrofia); conducción sensitiva normal.  \n- Electromiografía (EMG): actividad de denervación activa (aumento de la actividad insercional, fibrilaciones, fasciculaciones) y signos de reinervación crónica (potenciales de unidad motora polifásicos y bajo reclutamiento) en los cinco segmentos estudiados — hallazgos compatibles con afectación de motoneurona superior e inferior (fenotipo similar a esclerosis lateral amiotrófica / enfermedad motoneurona). Se observó afectación de músculos deltoides, bíceps, tríceps, extensores digitales y lengua.  \n- Resonancia magnética cerebral: mencionada, sin detalles en el informe resumido.  \n- Panel genético amplio (144 genes) y prueba para expansión C9ORF72: negativos para genes clásicos de ELA (incluidos VCP, MATR3) y para NOTCH3.  \n- Se identificó una variante patogénica en POLG: c.2209G>C, p.(Gly737Arg), asociada a síndromes por depleción mitocondrial (herencia autosómica dominante y recesiva). Se brindó asesoramiento genético.\n\nInterpretación y consideraciones\n- El paciente presentó una combinación atípica de parkinsonismo (con pobre respuesta a levodopa), deterioro cognitivo y signos claros de enfermedad de motoneurona. Este patrón sugiere traslapo clínico entre trastornos extrapiramidales y enfermedades de la motoneurona; no se identificó la causa genética clásica de ELA/FTD (C9ORF72 negativo).  \n- La presencia de una variante patogénica en POLG introduce una posible explicación alternativa: las mutaciones en POLG producen alteraciones del ADN mitocondrial y pueden dar síndromes neuromusculares y neurodegenerativos variados (neuropatía, ataxia, parkinsonismo, miopatía, epilepsia, depleción de ADN mitocondrial). No obstante, la relación causal entre la variante POLG encontrada y el cuadro clínico concreto requiere evaluación adicional (correlación fenotípica, estudios funcionales, análisis de linaje familiar y pruebas complementarias de mitocondria).  \n- Dada la rápida progresión hasta la dependencia funcional (afasia, postración, disfagia), el pronóstico fue grave y exigió intervención de soporte nutricional (gastrostomía).\n\nRecomendaciones y pasos siguientes plausibles (según práctica clínica)\n- Confirmación y caracterización de la afectación mitocondrial: determinación de lactato en sangre/CSF, estudio de ADN mitocondrial (carga heteroplásmica), conteo de copias de mtDNA y, si procede, biopsia muscular con estudios bioquímicos mitocondriales.  \n- Revisión y seguimiento genético familiar: ofrecer prueba dirigida a parientes para la variante POLG y asesoramiento genético, dado el hallazgo patogénico y las implicaciones familiares.  \n- Manejo multidisciplinario: cuidados paliativos/rehabilitación, nutrición (gastrostomía ya realizada), fisioterapia, terapia del lenguaje, manejo de complicaciones respiratorias y control sintomático del parkinsonismo y de la rigidez.  \n- Considerar derivación a centros especializados en enfermedades mitocondriales y en enfermedades de motoneurona para discusión de diagnóstico y posibilidades de investigación/ensayos clínicos.\n\nConclusión\nEste paciente mayor presentó un cuadro progresivo complejo que asoció síntomas prodrómicos (olfato, audición, función autonómica), deterioro cognitivo y un síndrome mixto de parkinsonismo y enfermedad de motoneurona. Los estudios neurofisiológicos confirmaron compromiso de motoneurona superior e inferior. El hallazgo de una variante patogénica en POLG abre la posibilidad de un trastorno mitocondrial como explicación o contribución genética al fenotipo, aunque la relación causal no está totalmente establecida sin estudios funcionales y correlación familiar. El caso subraya la importancia de una evaluación genética amplia y de un manejo multidisciplinario en cuadros neurodegenerativos atípicos."
+        }
+    },
+    {
+        "article": "Mujer de 33 años, previamente sana, presentó disnea progresiva, fiebre alta, sudores nocturnos y pérdida de peso en diciembre de 2017. Después de un mes de evolución, fue ingresada en un hospital general con insuficiencia respiratoria aguda y shock séptico con infiltrados alveolares difusos, ictericia, hemoptisis y petequias en las extremidades inferiores. Fue intubada y necesitó soporte hemodinámico. Se detectó un soplo sistólico mitral a la ausculta del precordio. Había leucocitosis acentuada con desviación a la izquierda, plaquetopenia, disfunción hepática y renal asociada a proteinuria subnefrótica y consumo de complemento. El resultado de los anticuerpos antinucleares fue de 1/80, a pesar de los niveles normales de anti-DNA de doble cadena, anti-SM y anti-PR3. Después de la administración de ceftriaxona, mejoró clínicamente. Fiebre amarilla, dengue, chikungunya, leptospirosis, VIH y hepatitis virales fueron descartados. Las hemoculturas fueron positivas para Haemophilus spp. en las seis muestras recolectadas. El ecocardiograma transtorácico (ETT) demostró una masa ecogénica amorfa con superficie irregular y algunos elementos móviles que envolvían ambos folletos de la válvula mitral, midiendo 20x17 mm en el folleto anterior y 19 mm en su mayor diámetro en los folletos posteriores, resultando en regurgitación grave por flail mitral y perforación. La resonancia magnética mostró pequeños abscesos esplénicos, tratados de manera conservadora. Un aneurisma micótico no complicado de la arteria cerebral media izquierda fue tratado por embolización percutánea. Treinta días después de la hospitalización, se sometió a un reemplazo de la válvula mitral con éxito por una prótesis valvular biológica de tamaño 29 mm y después de una extensa resección del tumor. Se evidenció regurgitación aórtica moderada debido a lesión de la fibrosa intervalvar mitroaórtica y retracción de la cúspide no coronaria, tratada de manera conservadora. El examen patológico confirmó la presencia de un mixoma valvular mitral infectado. La paciente completó 28 días de ceftriaxona y gentamicina, recibiendo el alta hospitalaria asintomática. En el seguimiento de un año, no hubo evidencia de recurrencia y se constató solamente regurgitación aórtica leve. Los mixomas infectados presentan mayor riesgo de eventos embólicos, aunque las manifestaciones clínicas son indistinguibles de tumores no infectados.2 El presente caso parece ser el sexto de mixoma valvular mitral infectado relatado en la literatura, llenando criterios definitivos para el diagnóstico, y el tercero causado por un microorganismo del grupo HACEK.3 - 8 De los 64 mixomas valvulares mitrales publicados de 2006 a 2012, los síntomas eran cardiovasculares en 36,7%; 9,5 a 21,6% de los mixomas de la válvula mitral fueron sometidos al cambio de válvula y el tiempo del diagnóstico hasta la cirugía varió de algunas horas a 42 días.2 , 9 La mortalidad operatoria y general fue relatada como siendo, respectivamente, 2,6 a 3% y 5,1 a 21%.2 , 10 En la presente serie, la mayoría de los pacientes presentó insuficiencia cardiaca sintomática, fueron sometidos al cambio de válvula mitral y todos presentaron buenos resultados en el seguimiento.\n",
+        "gold_summary": "Una mujer de 33 años de edad, con antecedentes de fiebre y disnea de unos pocos días de evolución, fue hospitalizada con un síndrome lupoide, con hemocultivos positivos para Haemophilus spp. El ecocardiograma reveló una masa gigante que involucraba ambas valvas mitrales, con una severa regurgitación mitral que requería un reemplazo valvular mitral biológico. La microscopía reveló un mixoma infectado y la paciente fue dada de alta asintomática tras finalizar la terapia con antibióticos. Ella tuvo un buen seguimiento.\n",
+        "synthetic_summary": {
+            "B1": "Había una mujer de 33 años que se sentía muy enferma. Tenía fiebre, dificultad para respirar y perdía peso. Llegó al hospital con una infección grave y tuvo que usar una máquina para ayudarla a respirar.\n\nLos médicos encontraron gérmenes en su sangre. También vieron en el corazón una masa grande en la válvula mitral. La válvula es como una puerta que ayuda a la sangre a ir en la dirección correcta. La masa estaba dañando la puerta y la sangre no circulaba bien.\n\nElla recibió antibióticos fuertes y los médicos trataron otros problemas, como un pequeño absceso en el bazo y un aneurisma en una arteria del cerebro (eso es una bolita en una arteria que puede ser peligrosa; la arreglaron con un procedimiento sin abrir la cabeza). Un mes después le cambiaron la válvula mitral por una nueva de material biológico y quitaron la masa.\n\nEl examen del tejido mostró que la masa era un mixoma infectado. Después de 28 días de antibióticos, la mujer salió del hospital sin síntomas. Un año después estaba bien y no había vuelto a aparecer la masa. Los médicos dicen que estos mixomas infectados son raros, pero pueden ser graves. Gracias al tratamiento a tiempo, ella se recuperó.",
+            "B2": "Resumen comprensible y amable:\n\nUna mujer sana de 33 años comenzó con fiebre, pérdida de peso y dificultad para respirar. Al mes empeoró y fue hospitalizada con insuficiencia respiratoria y shock séptico; además presentó tos con sangre, ictericia (piel y ojos amarillos) y pequeñas manchas en las piernas llamadas petequias. Los análisis mostraron infección y afectación del hígado y los riñones, y los hemocultivos crecieron Haemophilus spp., una bacteria que puede infectar el corazón.\n\nUna ecocardiografía mostró una masa grande y irregular en la válvula mitral (la válvula entre dos cámaras del corazón) que dañaba ambos velos y producía una regurgitación grave: la sangre volvía en lugar de seguir su camino normal. Se detectaron también pequeños abscesos en el bazo y un aneurisma micótico (una dilatación de una arteria causada por la infección) en una arteria cerebral, que se trató con embolización.\n\nTras estabilizarla con antibióticos (ceftriaxona y gentamicina) y tratar las complicaciones, a los 30 días se le sustituyó la válvula mitral por una prótesis biológica y se resecaron los tejidos infectados. El examen microscópico confirmó que la masa era un mixoma (un tumor benigno del corazón) que estaba infectado. Completó 28 días de antibióticos, recibió el alta sin síntomas y, al año, no había recurrencia; solo quedó una insuficiencia aórtica leve.\n\nComentario final: los mixomas infectados son raros y tienen mayor riesgo de que fragmentos viajen por la sangre y provoquen embolias, pero sus síntomas suelen ser parecidos a los de los mixomas no infectados. En este caso el tratamiento combinado (antibióticos y cirugía) fue exitoso.",
+            "B3": "Resumen clínico (nivel universitario)\n\nCaso: mujer de 33 años previamente sana que consultó por disnea progresiva, fiebre alta, sudores nocturnos y pérdida de peso. Tras aproximadamente un mes empeoró hasta ingreso por insuficiencia respiratoria aguda y shock séptico, con infiltrados alveolares difusos, ictericia, hemoptisis y petequias en las piernas. Requirió intubación y soporte hemodinámico.\n\nHallazgos importantes\n- Signos y laboratorio: soplo sistólico mitral al examen; leucocitosis con desviación a la izquierda, trombocitopenia, disfunción hepática y renal, proteinuria subnefrótica y consumo de complemento. Anticuerpos antinucleares 1/80, demás autoanticuerpos relevantes negativos.\n- Microbiología: hemocultivos positivos en las seis muestras para Haemophilus spp. (miembro del grupo HACEK).\n- Ecocardiografía transtorácica: masa ecogénica, irregular y parcialmente móvil que involucraba ambas valvas mitrales (aprox. 20×17 mm), con flail y perforación de la válvula causando regurgitación mitral grave.\n- Complicaciones y procedimientos: pequeños abscesos esplénicos (tratados de forma conservadora) y un aneurisma micótico de la arteria cerebral media izquierda tratado por embolización percutánea.\n- Tratamiento y evolución: recibió ceftriaxona (y gentamicina), mejoró clínicamente; a los 30 días se realizó resección extensa y reemplazo de la válvula mitral por una prótesis biológica de 29 mm. Se observó regurgitación aórtica moderada por lesión de la zona intervalvar mitroaórtica, manejada conservadoramente.\n- Anatomía patológica: confirmación de mixoma (tumor cardiacógeno) de la válvula mitral infectado.\n- Alta y seguimiento: completó 28 días de antibioterapia, egresó asintomática; a 1 año no hubo recidiva del mixoma y quedó con regurgitación aórtica leve.\n\nInterpretación y puntos clave\n- Se trató de un mixoma valvular mitral infectado por Haemophilus spp., un cuadro raro (pocos casos descritos) que combina infección sistémica grave y afectación valvular tumoral. Aunque clínicamente los mixomas infectados pueden parecerse a los no infectados, la infección aumenta el riesgo de embolias y complicaciones sépticas.\n- El diagnóstico combinó hallazgos clínicos, hemocultivos positivos, imágenes (ecocardiograma) y confirmación histológica —cumpliendo criterios definitivos.\n- Manejo efectivo incluyó antibioterapia dirigida, tratamiento de complicaciones embólicas/aneurismas y tratamiento quirúrgico (resección y reemplazo valvular) cuando fue necesario.\n\nImplicaciones prácticas y recomendaciones razonables\n- Los mixomas valvulares infectados requieren un enfoque multidisciplinario: cardiología, cirugía cardíaca, infectología y neurología/intervencionismo si hay aneurismas o embolias cerebrales.\n- Tras el alta, el seguimiento debe centrarse en: controles seriados por ecocardiografía para vigilar la prótesis y la regurgitación aórtica, vigilancia neurológica por el antecedente de aneurisma micótico, y control clínico/infectológico para detectar recurrencia o complicaciones tardías.\n- En infecciones por HACEK, ceftriaxona es tratamiento apropiado; la duración y combinación con aminoglucósidos varía según la situación clínica, el tipo de intervención y la respuesta.\n\nPronóstico\n- En este caso la paciente evolucionó favorablemente: recuperación clínica, resección del tumor infectado, y ausencia de recidiva a 1 año, aunque persiste regurgitación aórtica leve que requiere seguimiento.\n\nComentario final (empatía)\nEste fue un cuadro grave y poco frecuente cuyo manejo coordinado —antibiótico adecuado, tratamiento de complicaciones y cirugía valvular— permitió una recuperación completa y sin recidiva a un año. Para la paciente, el seguimiento cardiológico y neurológico continuo será importante para vigilar la función valvular y prevenir complicaciones futuras."
+        }
+    },
+    {
+        "article": "Mujer de 71 años, que fue atendida en urgencias del Hospital de Mataró (Barcelona, España) el 9 de septiembre de 2020 con debilidad progresiva, por lo que se decidió su ingreso en neurología. Como antecedentes patológicos destacaban hipertensión arterial, temblor esencial, artrosis y trastorno de ansiedad leve, en tratamiento con gabapentina, sertralina y tramadol. La paciente había consultado a su médico de cabecera el 1 de septiembre de 2020 por dolor abdominal, junto con diarrea leve que duró 24 horas. Al día siguiente comenzó a sentirse débil y, a lo largo de los días siguientes, apareció disnea y disfagia, por lo que se sospechó laringitis y se le recetó prednisona. El 8 de septiembre de 2020 fue visitada nuevamente por su médico de cabecera por empeoramiento global de la debilidad; presentaba, además, disartria, disfagia y ptosis bilateral, por lo que fue derivada a urgencias del hospital.\n\nA su llegada no presentaba fiebre, la presión arterial y la frecuencia cardíaca eran normales, y la exploración física era normal, a excepción de taquipnea moderada. El examen neurológico mostró ptosis palpebral bilateral, parálisis facial bilateral, midriasis bilateral arreactiva a la luz y a la acomodación, oftalmoparesia bilateral tanto para la suprainfraversión como para la mirada horizontal bilateral, tetraparesia moderada en las extremidades (3/5), y disfonía y disfagia graves. Ella estaba consciente y el contenido del lenguaje era normal, al igual que los reflejos miotáticos, la sensibilidad y la coordinación. Las maniobras de fatigabilidad no fueron concluyentes y se realizó la prueba del hielo, que resultó positiva, mejorando –transitoriamente– la ptosis.\n\nLa reacción en cadena de la polimerasa (PCR) para el SARS-CoV-2 fue repetidamente negativa (en su ambulatorio y en el hospital). La gasometría arterial mostró hipoxemia: 75, con SO2 al 95%, y el resto de las exploraciones realizadas en urgencias resultaron normales (radiografía de tórax, análisis de sangre de rutina, electrocardiograma).\n\nSe inició tratamiento de soporte con oxígeno, sueroterapia, nutrición por sonda nasogástrica y medidas encaminadas a la prevención de complicaciones. El cuadro se estabilizó el tercer día del ingreso en planta, sin requerir soporte ventilatorio avanzado, y comenzó una mejoría lenta a partir del octavo día, iniciando tolerancia a la dieta adaptada de disfagia. Durante la primera semana presentaba hipotensión arterial, que fue corrigiéndose con la sueroterapia. A partir de la segunda semana, pudo iniciar rehabilitación física, con buena evolución, por lo que fue trasladada a un centro específico de rehabilitación al 19.º día, y entonces fue capaz de deambular con ayuda bilateral. En la visita de control en consultas externas de neurología seis semanas después, la paciente estaba completamente recuperada.",
+        "gold_summary": "Describimos el caso confirmado de botulismo alimentario en una paciente atendida en nuestro hospital en septiembre de 2020. La instauración en pocos días de una afectación bilateral de pares craneales, incluyendo disfagia, disnea y disartria, junto con midriasis y tetraparesia graves, precedida de diarrea, constituyó la presentación clínica en el primer caso; mientras que en su familiar cursó con síntomas inespecíficos y transitorios. Constatamos disautonomía consistente en hipotensión arterial. Teniendo en cuenta la situación pandémica en aquel momento, se descartó repetidamente la infección por SARS-CoV-2 antes de plantear alternativas diagnósticas. La neurotoxina B de C. botulinum fue detectada en las heces de la paciente, confirmando el diagnóstico de botulismo, que relacionamos con la ingesta de una conserva casera de alubias. Se completó el diagnóstico diferencial del cuadro descartando otras posibles etiologías.",
+        "synthetic_summary": {
+            "B1": "Esta es la historia de una mujer de 71 años que se puso muy débil después de tener diarrea. Al principio tenía dolor de barriga y un día de diarrea. Luego empezó a sentirse débil, con dificultad para respirar, tragar y hablar. La vieron en urgencias y la ingresaron en neurología.\n\nEn el hospital tenía los párpados caídos en los dos ojos, la cara muy floja, las pupilas grandes que no cambiaban con la luz, y los ojos casi no se movían. También tenía debilidad en los cuatro brazos y piernas y mucha dificultad para tragar y hablar. Estaba despierta y pensaba con normalidad. Le hicieron una prueba con hielo y los párpados mejoraron un rato.\n\nLe hicieron pruebas para COVID y salieron negativas. Tenía el oxígeno un poco bajo, pero la radiografía de tórax y las analíticas salieron bien. Empezaron cuidados con oxígeno, sueros y nutrición por sonda para que no se atragantara. No necesitó respirador.\n\nAl tercer día se estabilizó. Empezó a mejorar despacio desde el octavo día. Tuvo bajadas de tensión que mejoraron con sueros. En la segunda semana pudo empezar rehabilitación. El día 19 la llevaron a un centro de rehabilitación y pudo andar con ayuda. Se recuperó por completo a las seis semanas.\n\nLos médicos encontraron la toxina B de Clostridium botulinum en sus heces. Esto confirmó que tuvo botulismo alimentario. Creen que fue por comer una conserva casera de alubias. Un familiar tuvo síntomas leves y breves. Los médicos descartaron otras causas antes de dar el diagnóstico.\n\nResumen claro: fue un botulismo por comida. La paciente recibió cuidados y rehabilitación. Al final se recuperó totalmente.",
+            "B2": "Resumen para alumnos de secundaria (lectura clara y amable)\n\nEste informe cuenta el caso de una mujer de 71 años que en septiembre de 2020 desarrolló debilidad y problemas para mover los ojos y la cara, así como dificultad para hablar, tragar y respirar. Antes de estos síntomas tuvo un episodio breve de diarrea. Al llegar al hospital se descartó repetidamente que tuviera COVID-19 (las PCR fueron negativas).\n\nLos médicos observaron que tenía afectación de varios nervios craneales (es decir, los nervios que controlan los ojos, la cara, la deglución y la voz), pupilas dilatadas que no reaccionaban a la luz, debilidad en los cuatro miembros y baja presión arterial. Estos signos sugirieron botulismo alimentario: una intoxicación causada por una toxina producida por la bacteria Clostridium botulinum que puede provocar parálisis y afectar funciones automáticas del cuerpo (como la presión arterial).\n\nEl diagnóstico se confirmó al encontrar la neurotoxina B de C. botulinum en las heces de la paciente. Se relacionó el caso con la ingesta de una conserva casera de judías (alubias). Otra persona de su familia sólo tuvo síntomas leves y pasajeros.\n\nEl tratamiento fue principalmente de apoyo: oxígeno, líquidos por vía venosa, alimentación por sonda mientras no podía tragar y medidas para prevenir complicaciones. No necesitó ventilación invasiva. Empezó rehabilitación física en la segunda semana, mejoró poco a poco y fue trasladada a un centro de rehabilitación. Se recuperó completamente en unas seis semanas. Los médicos también descartaron otras causas posibles antes de llegar a este diagnóstico.",
+            "B3": "Resumen clínico (nivel lector universitario)\n\nPresentación y antecedente inmediato\n- Paciente mujer de 71 años, con hipertensión, temblor esencial, artrosis y ansiedad, en tratamiento con gabapentina, sertralina y tramadol.\n- El 1 de septiembre de 2020 consultó por dolor abdominal y diarrea leve de 24 horas. Desde el día siguiente empezó con debilidad progresiva; en los días posteriores apareció disnea y disfagia. Inicialmente se sospechó laringitis y se le pautó prednisona. El 8 de septiembre presentó empeoramiento: disartria, disfagia y ptosis bilateral, por lo que fue derivada al hospital; ingresó el 9 de septiembre.\n\nExploración y hallazgos clave\n- Signos vitales: sin fiebre; presión arterial y frecuencia cardiaca dentro de límites normales al ingreso; respiración algo acelerada. Gasometría arterial con leve hipoxemia (PaO2 ≈ 75 mmHg; saturación ≈ 95%).\n- Estado neurológico: consciente, lenguaje con contenido normal; reflejos tendinosos, sensibilidad y coordinación preservados.\n- Defectos motores y neurológicos importantes y bilaterales: ptosis palpebral, parálisis facial, midriasis bilateral no reactiva a la luz ni a la acomodación, oftalmoparesia (movimientos oculares limitados vertical y horizontalmente), tetraparesia moderada (fuerza 3/5) y disfonía y disfagia graves.\n- Prueba del hielo positiva (mejora transitoria de la ptosis), maniobras de fatigabilidad no concluyentes.\n- Pruebas de imagen y analítica de rutina sin alteraciones significativas; PCR para SARS‑CoV‑2 repetidamente negativa.\n\nEvolución clínica y tratamiento\n- Se instauró tratamiento de soporte: oxígeno, fluidoterapia, nutrición por sonda nasogástrica y medidas para prevenir complicaciones.\n- No requirió ventilación mecánica avanzada. Presentó hipotensión durante la primera semana, que se corrigió con fluidos.\n- Estabilización al tercer día; mejoría lenta desde el día 8 con progresiva tolerancia oral. Inició rehabilitación en la segunda semana; fue transferida a un centro de rehabilitación el día 19 y pudo deambular con ayuda bilateral.\n- En la consulta de neurología a las seis semanas la paciente estaba completamente recuperada.\n\nDiagnóstico y etiología\n- Se confirmó botulismo alimentario: se detectó neurotoxina tipo B de Clostridium botulinum en las heces de la paciente. La intoxicación se relacionó con la ingestión de una conserva casera de alubias.\n- Se documentó además disautonomía (hipotensión). Un familiar presentó síntomas leves y transitorios.\n- Se completó el diagnóstico diferencial y se descartaron otras etiologías relevantes, incluidas repetidas pruebas de COVID‑19 en el contexto pandémico.\n\nBreve explicación del mecanismo (para comprensión)\n- El botulismo alimentario es causado por una toxina que bloquea la liberación de acetilcolina en la unión neuromuscular y en sinapsis autonómicas, provocando una parálisis motora descendente y posible afectación autonómica. Suele comenzar con síntomas cráneo‑bulbares (ptosis, diplopía, disfagia, disartria) y puede progresar a debilidad generalizada y riesgo respiratorio.\n\nImplicaciones prácticas\n- Ante un cuadro agudo de pares craneales bilaterales con debilidad y antecedentes de ingestión de conservas caseras, debe considerarse botulismo y recogerse muestras de heces y alimentos para análisis. El manejo inmediato es sobre todo soporte respiratorio y nutricional, monitorización estrecha y rehabilitación; la identificación del alimento implicado es clave para medidas de salud pública.\n- La recuperación completa es posible pero puede requerir semanas de soporte y rehabilitación, como ilustra este caso.\n\nComentario final\nEste caso muestra una presentación clásica de botulismo alimentario con recuperación completa tras manejo de soporte y rehabilitación. La evaluación incluyó descartar infecciones prevalentes en la época (SARS‑CoV‑2) antes de confirmar la etiología por toxina B de C. botulinum."
+        }
+    },
+    {
+        "article": "Un hombre de 52 años presentó pérdida de agudeza visual en su ojo derecho (OD) dos días después de una inyección intravenosa no complicada de ranibizumab con una aguja de 30 G. Su historial médico incluía PE, miopía alta y vitrectomía pars plana en el OD debido a desprendimiento de retina. Recibía tratamiento mensual con ranibizumab debido a neovascularización coroidea secundaria a estrías angioides, con 78 inyecciones previas en el OD. En el momento de la presentación, su BCVA era de 6/18 y la presión intraocular (IOP) era de 3 mmHg. El examen con lámpara de hendidura del segmento anterior no mostró nada de particular. El examen de fondo de ojo y los escaneos OCT revelaron pliegues corio-retinianos posteriores. En conjunto, la baja presión intraocular y los hallazgos del fondo de ojo llevaron al diagnóstico de hipotensión maculopatía. Se prescribió dexametasona tópica y atropina para mejorar la función del cuerpo ciliar. La IOP se normalizó en tres días con recuperación de la agudeza visual y resolución de los pliegues corio-retinianos. Cuatro meses después, se realizó una nueva inyección intravenosa anti-VEGF en el cuadrante inferolateral y el paciente informó disminución de la agudeza visual en el día siguiente a la inyección. La BCVA era contar los dedos y la IOP era de 2 mmHg. Los pliegues corio-retinianos en el polo posterior estaban presentes, incluso más prominentemente esta vez. El examen con lámpara de hendidura reveló una herida abierta en la esclerótica en el sitio de la inyección. La herida se suturó con monofilamento 10-0 y se prescribió dexametasona tópica y atropina. El paciente se recuperó bien y presentó una BCVA de 6/12 y una IOP de 12 mmHg.\n",
+        "gold_summary": "Un hombre de 52 años se quejó de pérdida de visión en el ojo derecho (OD) dos días después de un IVI anti-VEGF sin complicaciones para el tratamiento de la neovascularización coroidea secundaria a estrías angioides. Su historial médico incluía PE, miopía patológica y una vitrectomía pars plana (PPV) previa debido a un desprendimiento de retina. La agudeza visual mejor corregida (BCVA) en el OD disminuyó de 6/12 a 6/18 después del IVI. La presión intraocular (IOP) era de 3 mmHg y se observaron pliegues corio-retinianos en el polo posterior. Se prescribió dexametasona tópica y atropina, y se observó una recuperación completa después de tres días. Cuatro meses después, el paciente desarrolló un nuevo episodio de pérdida de visión después de otro IVI. Su BCVA era contar los dedos, la IOP era de 2 mmHg, y se observaron pliegues corio-retinianos más evidentes. Esta vez, una herida escleral abierta en el sitio de inyección era evidente y fue necesaria una sutura escleral. Una vez más, el paciente se recuperó bien.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre de 52 años perdió visión en su ojo derecho dos días después de que le pusieran una inyección dentro del ojo para tratar vasos anormales. Él ya había tenido antes una operación en ese ojo y usa estas inyecciones desde hace tiempo.\n\nDespués de la primera inyección, el ojo tenía muy baja presión. Esto hizo que la parte de atrás del ojo tuviera pliegues y que viera menos. Los médicos le dieron gotas para ayudar al ojo a curarse y a subir la presión. Tres días después, la presión volvió a la normalidad y su vista mejoró.\n\nCuatro meses después, volvió a tener pérdida de visión después de otra inyección. Esta vez la presión era aún más baja. Al mirar con lupa encontraron una pequeña herida en la pared blanca del ojo donde se había puesto la inyección. Los médicos cerraron la herida con una puntada y le dieron las mismas gotas. El ojo sanó y su vista volvió a mejorar.\n\nEn resumen: las inyecciones dentro del ojo causaron que la presión bajara y que la visión empeorara. Con tratamiento rápido, primero con gotas y luego con una puntada cuando hubo una fuga, el ojo se recuperó bien.",
+            "B2": "This report describes a 52-year-old man who had two episodes of sudden vision loss in his right eye shortly after routine intravitreal injections (IVIs) of an anti-VEGF drug (ranibizumab). Anti-VEGF injections are medicines placed inside the eye to stop abnormal new blood vessels; he was receiving these monthly for choroidal neovascularization (abnormal blood vessel growth under the retina) caused by angioid streaks. His eye history included high myopia (strong nearsightedness) and a past pars plana vitrectomy (surgery that removed the eye’s inner gel) for a retinal detachment. He had already had many injections in that eye.\n\nFirst episode\n- Two days after an injection, his corrected vision fell from 6/12 to 6/18 and his intraocular pressure (IOP) was very low (3 mmHg). Low IOP is called hypotony.\n- The front of the eye looked normal, but retinal imaging showed chorioretinal folds (wrinkles in the layers at the back of the eye).\n- These findings led to the diagnosis of hypotony maculopathy — vision problems caused by very low eye pressure that distort the central retina.\n- He was treated with topical dexamethasone (a steroid) and atropine (a medicine that relaxes the eye’s focusing muscle). His pressure and vision returned to normal within three days and the retinal folds resolved.\n\nSecond episode (four months later)\n- After another injection, he had rapid vision loss the next day (vision reduced to counting fingers) and a very low IOP (2 mmHg). The retinal folds were more obvious.\n- This time the exam found an open wound in the sclera (the white wall of the eye) at the injection site. A leaking wound can cause hypotony.\n- The wound was closed with a very fine suture and he received the same topical treatments. He recovered well, with vision improving to 6/12 and IOP rising to 12 mmHg.\n\nKey points and lessons\n- Repeated injections, prior vitrectomy, and high myopia can raise the risk that an injection site might leak and cause hypotony.\n- Hypotony maculopathy can often be treated successfully by sealing a leak (if present) and using medicines to reduce inflammation and help the eye’s ciliary body restore normal pressure.\n- Prompt examination and treatment after sudden vision change following an injection are important and can lead to full recovery, as happened in this case.\n\nIf you or someone notices sudden vision loss after an eye injection, they should seek urgent eye care so the cause can be checked and treated quickly.",
+            "B3": "Resumen clínico (nivel universitario)\n\nUn hombre de 52 años sufrió pérdida aguda de visión en su ojo derecho (OD) dos días después de una inyección intravítrea (IVI) de ranibizumab con aguja 30 G, administrada como parte de un tratamiento mensual por neovascularización coroidea secundaria a estrías angioides (había recibido 78 inyecciones previas en ese ojo). Sus antecedentes incluían miopía alta y una vitrectomía pars plana previa por desprendimiento de retina.\n\nPrimer episodio\n- Presentación: agudeza visual mejor corregida (BCVA) bajó a 6/18; presión intraocular (PIO) muy baja, 3 mmHg.  \n- Examen: segmento anterior sin hallazgos relevantes; fondo de ojo y OCT mostraron pliegues corio-retinianos en el polo posterior.  \n- Interpretación: conjunto de hipotensión ocular con maculopatía (hipotonía macular) secundaria a fuga/defecto de la pared ocular tras la IVI.  \n- Tratamiento y evolución: terapia tópica con dexametasona y atropina para mejorar la función del cuerpo ciliar y controlar la inflamación. La PIO se normalizó en tres días, con resolución de los pliegues y recuperación de la agudeza visual.\n\nSegundo episodio (4 meses después)\n- Tras una nueva IVI en el cuadrante inferolateral, el paciente refirió disminución de visión al día siguiente. BCVA fue contar dedos, PIO 2 mmHg. Los pliegues corio-retinianos eran ahora más prominentes.  \n- Examen con lámpara de hendidura mostró una herida escleral abierta en el sitio de la inyección.  \n- Manejo: sutura escleral con monofilamento 10-0 y nuevamente dexametasona tópica y atropina. Resultado favorable: recuperación a BCVA 6/12 e IOP 12 mmHg.\n\nComentarios y enseñanzas clave (implicaciones)\n- La hipotensión ocular tras IVI puede presentarse con visión reducida y pliegues corio-retinianos en el polo posterior; la PIO baja es un dato crítico para el diagnóstico.  \n- En ojos vitrectomizados y/o miopes altos existe mayor riesgo de fuga por el sitio de inyección y de hipotensión prolongada.  \n- El manejo inicial puede ser conservador (ciclopléjicos y antiinflamatorios tópicos) si la fuga es mínima y la PIO se recupera; cuando hay una herida escleral franca o fuga persistente, es necesaria reparación quirúrgica (sutura).  \n- Vigilancia estrecha tras IVI —evaluación de la PIO y del sitio de inyección— permite detectar y tratar la hipotensión antes de que cause daño macular permanente.\n\nEmpático cierre\nEl paciente evolucionó bien tras ambos episodios gracias a la detección rápida y al tratamiento apropiado. Para pacientes con características de alto riesgo (vitrectomía previa, miopía patológica) es razonable una vigilancia más cuidadosa tras las IVI y discutir con el equipo las medidas preventivas y las alternativas terapéuticas."
+        }
+    },
+    {
+        "article": "Una mujer de 82 años acudió al servicio de urgencias por dolor abdominal, diarrea, confusión y deterioro de su estado general de varios días de evolución. Entre sus antecedentes médicos destacaban hipertensión arterial tratada e hipotiroidismo en tratamiento sustitutivo. No se recogieron antecedentes quirúrgicos ni hábitos tóxicos de interés. A la exploración física, la frecuencia cardíaca era de 84 lpm, tensión arterial de 105/82 mmHg, temperatura de 38 °C y saturación de oxígeno de 95% en aire ambiente. Las mucosas estaban secas y el abdomen era difusamente doloroso a la palpación sin masas palpables ni reacción peritoneal. La analítica realizada mostró una hemoglobina de 13.1 g/dL, proteína C reactiva a 122.9 mg/L sin leucocitosis (8.9 × 10^9/L), hiponatremia (130 mmol/L), hipopotasemia (2.9 mmol/L), pruebas de función renal, hepáticas, lipasa y enzimas cardiacas normales. El frotis para SARSCoV-2 fue negativo. La orina era maloliente con presencia de nitritos positivos, hematíes (+++) y leucocitos (+) por lo que se envió la muestra para cultivo microbiológico. Ante estos hallazgos se inició antibioticoterapia probabilista con ceftriaxona ante la sospecha de una posible infección urinaria y se decidió realizar una tomografía tóraco-abdomino-pélvica para descartar la presencia de un foco infeccioso profundo. Este examen reveló la presencia de signos de broncopatía crónica y una neumatosis vesical parietal a nivel abdominal compatible con una cistitis enfisematosa. El cultivo de orina reveló la presencia de Escherichia coli (> 100 000 UFC/m) sensible a la antibioticoterapia prescrita empíricamente y los hemocultivos fueron positivos al mismo germen. Se decidió el ingreso de la paciente en servicio de medicina interna y se continuó el tratamiento antibiótico durante 7 días con una evolución favorable desde el punto de vista clínico y analítico, permitiendo el alta hospitalaria.",
+        "gold_summary": "Una mujer de 82 años con antecedentes de hipertensión arterial e hipotiroidismo acudió al servicio de urgencias por dolor abdominal, diarrea, confusión y deterioro de su estado general de varios días de evolución. A su admisión, la paciente se encontraba febril y la analítica mostró una elevación de la proteína C reactiva sin leucocitosis (8.9 × 10^9/L). En ese contexto se realizó exudado nasofaríngeo para SARS-CoV-2 que fue negativo. Con estos resultados, la sospecha inicial era la de un cuadro infeccioso de origen digestivo. La muestra de orina era maloliente con presencia de leucocitos y nitritos enviándose a cultivo microbiológico. Se inició tratamiento antibiótico empírico con una cefalosporina de tercera generación ante la sospecha de une posible infección urinaria. Se decidió la realización de una tomografía tóraco-abdomino-pélvica con el objetivo de evaluar la presencia de otros focos infecciosos en una paciente de edad avanzada. Este estudio mostró una cistitis enfisematosa, una enfermedad poco frecuente en una paciente sin ninguno de los factores de riesgo clásicos para esta entidad. Los cultivos de orina y sangre fueron positivos para Escherichia coli sensible al antibiótico empírico por lo que se continuó para completar 7 días de tratamiento. La evolución clínica fue favorable.",
+        "synthetic_summary": {
+            "B1": "Una mujer de 82 años fue al hospital porque tenía dolor de barriga, diarrea y estaba confundida. Llevaba varios días encontrándose mal y tenía un poco de fiebre.\n\nLa orina olía mal y las pruebas mostraron signos de infección. Los médicos empezaron un antibiótico mientras esperaban los resultados. Hicieron una radiografía especial (tomografía) y vieron gas en la pared de la vejiga. Eso se llama cistitis enfisematosa. Es una infección rara en la vejiga que puede formar gas.\n\nLas muestras de orina y de sangre mostraron que la bacteria Escherichia coli causaba la infección. Esa bacteria respondió bien al antibiótico que le dieron. La mujer estuvo ingresada y recibió antibióticos durante 7 días. Mejoró con el tratamiento y pudo volver a casa.",
+            "B2": "Una mujer de 82 años con hipertensión e hipotiroidismo llegó a urgencias tras varios días con dolor abdominal, diarrea, confusión y empeoramiento general. Tenía fiebre (38 °C), mucosas secas y dolor abdominal difuso a la palpación.\n\nEn los análisis destacó una proteína C reactiva elevada (marcador de inflamación), sin aumento del recuento de glóbulos blancos, además de sodio y potasio bajos. La orina olía mal y en el examen se detectaron nitritos y leucocitos, hallazgos que suelen indicar infección urinaria; por eso se envió la orina a cultivo y se empezó tratamiento antibiótico empírico con ceftriaxona.\n\nSe realizó una tomografía toraco-abdominopélvica para buscar focos de infección más profundos. El estudio mostró neumatosis de la pared vesical, es decir, gas en la pared de la vejiga, hallazgo compatible con cistitis enfisematosa. La cistitis enfisematosa es una infección de la vejiga que produce gas en la pared y suele ser más frecuente en pacientes con factores de riesgo (por ejemplo, diabetes), aunque en esta paciente no había esos factores clásicos.\n\nLos cultivos confirmaron Escherichia coli en orina (>100 000 UFC/mL) y en sangre, sensible al antibiótico iniciado. La presencia de E. coli en sangre indica que la infección llegó a la circulación (bacteriemia), por lo que la paciente fue ingresada y continuó con antibiótico durante 7 días.\n\nLa evolución fue favorable desde el punto de vista clínico y analítico, y la paciente pudo recibir el alta. En resumen: infección urinaria complicada por cistitis enfisematosa y bacteriemia por E. coli, tratada con antibiótico adecuado con buena respuesta.",
+            "B3": "Resumen clínico (nivel lector universitario)\n\nPresentación\n- Mujer de 82 años que consultó por varios días de dolor abdominal, diarrea, confusión y deterioro del estado general.\n- Antecedentes: hipertensión arterial e hipotiroidismo en tratamiento. No se refirieron antecedentes quirúrgicos ni hábitos tóxicos relevantes.\n\nExploración y pruebas iniciales\n- Signos vitales: taquicardia moderada (84 lpm), tensión arterial 105/82 mmHg, febrícula (38 °C) y saturación de O2 95% en aire ambiente. Mucosas secas; abdomen doloroso de manera difusa sin defensa ni signos de peritonismo.\n- Analítica: hemoglobina 13.1 g/dL; proteína C reactiva elevada (122.9 mg/L); recuento de leucocitos dentro de rango (8.9 × 10^9/L). Alteraciones electrolíticas: hiponatremia leve (Na 130 mmol/L) e hipopotasemia (K 2.9 mmol/L). Función renal, hepática, lipasa y enzimas cardiacas normales.\n- Frotis nasofaríngeo para SARS‑CoV‑2: negativo.\n- Orina maloliente con nitritos positivos, hematíes y leucocitos; se envió cultivo urinario.\n\nHallazgos de imagen y microbiología\n- Tomografía tóraco-abdomino-pélvica: signos de broncopatía crónica y neumatosis parietal vesical compatible con cistitis enfisematosa (presencia de gas en la pared de la vejiga).\n- Cultivos: urocultivo con Escherichia coli (>100 000 UFC/mL) sensible a la ceftriaxona; hemocultivos también positivos para el mismo germen (bacteriemia por E. coli).\n\nDiagnóstico y manejo\n- Diagnóstico principal: cistitis enfisematosa complicada por bacteriemia por Escherichia coli.\n- Tratamiento: antibioterapia empírica inicial con ceftriaxona (cefalosporina de tercera generación), que resultó adecuada según la sensibilidad; antibioticoterapia mantenida durante 7 días.\n- Evolución: respuesta clínica y analítica favorable, con alta hospitalaria.\n\nPuntos clave e implicaciones\n- La cistitis enfisematosa es una infección del tracto urinario poco frecuente, caracterizada por formación de gas en la pared vesical. Suele asociarse a factores de riesgo como diabetes mellitus o inmunosupresión; en este caso no se describieron esos factores clásicos.\n- La presencia de bacteriemia (hemocultivos positivos) indica infección sistémica y justifica la hospitalización y tratamiento intravenoso hasta control clínico.\n- Hallazgos relevantes que requirieron seguimiento: hipopotasemia significativa (K 2.9 mmol/L) e hiponatremia leve, que deben corregirse y monitorizarse; y la necesidad de vigilar la resolución de la infección y posibles complicaciones.\n- Consideraciones prácticas tras el alta: control clínico y analítico para confirmar resolución, valorar investigación de factores predisponentes (por ejemplo, despistaje de diabetes si no se ha realizado) y medidas para prevenir recurrencias del tracto urinario.\n\nComentario final (tono empático)\nLa paciente anciana presentó una forma rara pero tratable de infección urinaria complicada, con detección rápida del germen y respuesta favorable al tratamiento antibiótico. Es comprensible la preocupación ante una infecció n sistémica en edad avanzada; el manejo oportuno y el seguimiento han permitido una evolución positiva."
+        }
+    },
+    {
+        "article": "Varón nacido a las 38 semanas de gestación y sin controles obstétricos prenatales, producto de un parto eutócico sin complicaciones con un peso de 2.678 g y Apgar 7 y 8 al minuto y a los cinco minutos de vida, respectivamente; derivado por sospecha de enterocolitis necrotizante a los siete días de vida. Al nacimiento, en su hospital de origen, se descartaron malformaciones congénitas externas y se colocó una sonda orogástrica para verificar la permeabilidad esofágica, obteniendo 200 mL de líquido amniótico. Posteriormente inició alimentación vía oral pero debido a succión débil y vómitos biliosos fue ingresado en la unidad de cuidados intensivos neonatales. A las 4 horas de vida se realizó radiografía abdominal observando una imagen de doble burbuja atípica, por lo cual realizaron un control radiológico 48 horas después identificando gas intestinal aparentemente distal, y presentó meconiorrexis a las 50 horas de vida. Dos días después reinició la alimentación oral, tras lo cual presentó nuevamente vómitos de aspecto biliar y distensión abdominal que mejoró con el ayuno y sonda orogástrica; por lo cual se sospechó enterocolitis necrotizante indicándose dieta absoluta, nutrición parenteral total y antibioterapia con ampicilina y amikacina. A los siete días de vida y debido a la persistencia de los síntomas pese al tratamiento instaurado, fue derivado a nuestro centro. A su llegada presentaba distensión abdominal, sin ruidos intestinales ni signos de irritación peritoneal, por lo que se realizó tránsito intestinal sin progresión distal y colon por enema con hallazgo de microcolon, todo ello sugestivo de atresia intestinal yeyunoileal. Tras la realización de los estudios de imagen y con la sospecha de atresia intestinal se realizó una laparotomía exploradora mediante abordaje supraumbilical transverso, observando adherencias hepatoileales, una hernia interna a través de un defecto mesentérico con incarceración de un asa yeyunal y atresia yeyunoileal tipo IV. Se identificaron dos sitios de atresia a 56 cm del ángulo de Treitz y a 36 cm de la válvula ileocecal, con un segmento interatrésico de 10 cm con meconio intraluminal y cambios de coloración con aspecto violáceo pero sin perforación; la diferencia de diámetros intestinales proximal a distal tenía una relación 3:1. Se decidió disecar el mesenterio y resecar el asa ciega (10 cm) para realizar una anastomosis término-oblicua yeyunoileal, corroborando la permeabilidad distal con sonda intraluminal y administración de solución fisiológica hasta que presentó evacuación rectal. El reporte de histopatología confirmó una atresia yeyunoileal tipo IV con enteritis crónica leve. El paciente evolucionó favorablemente y al 5º día postoperatorio inició alimentación oral con adecuada tolerancia progresiva y descenso paulatino de la nutrición parenteral total con retirada al 8º día postoperatorio. Al 6° día de la intervención presentó deposiciones espontáneas y a los 20 días de vida fue dado de alta sin complicaciones. Doce meses después el paciente continúa asintomático con adecuada ganancia ponderal y tolerancia a la alimentación complementaria con deposiciones diarias de características normales.",
+        "gold_summary": "Recién nacido de sexo masculino, nacido a término, derivado por vómitos, evacuaciones escasas y distensión abdominal. A los 8 días de vida y tras excluir diversas causas de distensión abdominal se sometió a laparotomía exploradora, identificando una hernia transmesentérica y dos sitios de atresia intestinal. Se realizó resección del segmento atrésico y anastomosis primaria, con buena evolución.",
+        "synthetic_summary": {
+            "B1": "Un bebé varón nació a término. Tenía vómitos, pocas deposiciones y la barriga hinchada. A los 8 días no mejoró y lo llevaron a cirugía. Al abrir la barriga, los médicos encontraron una hernia en el mesenterio (un hueco que dejó pasar parte del intestino) y dos zonas del intestino que estaban cerradas, es decir, bloqueadas (atresias). Quitaron la parte dañada y unieron los extremos del intestino para que volviera a funcionar. El bebé se recuperó bien. Empezó a comer poco a poco y salió del hospital sin problemas. A los 12 meses seguía sano, comiendo bien y subiendo de peso.",
+            "B2": "Resumen para lectores jóvenes (nivel B2)\n\nUn recién nacido varón, nacido a término (38 semanas) y sin controles prenatales, presentó desde los primeros días vómitos con bilis, distensión abdominal y poca cantidad de deposiciones. Inicialmente se sospechó una enterocolitis necrotizante (una infección/inflamación grave del intestino en recién nacidos) y se trató con ayuno, nutrición por vena y antibióticos, pero los síntomas persistieron. Las radiografías y un enema mostraron un colon muy pequeño (microcolon) y ausencia de paso de contraste hacia el intestino distal, lo que hizo sospechar una atresia intestinal (cuando una parte del intestino está ausente o cerrada).\n\nSe realizó una cirugía exploradora en la que encontraron una hernia interna a través del mesenterio (un defecto en el tejido que sostiene el intestino) que tenía un asa intestinal atrapada, y además hallaron atresias múltiples del intestino delgado (atresia yeyunoileal tipo IV). Se resecaron los segmentos no funcionales y se unieron los extremos sanos del intestino (anastomosis). El informe de biopsia confirmó la atresia múltiple y cambios leves de inflamación.\n\nLa recuperación fue buena: empezó a tomar por boca al quinto día después de la operación, la nutrición por vía venosa se retiró al octavo día, tuvo deposiciones normales y fue dado de alta a los 20 días de vida. A los 12 meses seguía sin síntomas, con buen aumento de peso y alimentación normal.",
+            "B3": "Resumen clínico (nivel B3)\n\nPaciente: recién nacido varón, nacido a término (38 semanas) sin controles prenatales, parto eutócico, peso 2.678 g, Apgar 7/8. Al nacimiento no se observaron malformaciones externas; se colocó sonda orogástrica para comprobar permeabilidad esofágica y se aspiraron 200 mL de líquido amniótico.\n\nPresentación y evolución inicial: en las primeras horas de vida presentó succión débil y vómitos biliosos, por lo que fue ingresado en la unidad neonatal. La radiografía abdominal inicial mostró una imagen de “doble burbuja” atípica; 48 h después apareció gas intestinal distal y hubo eliminación de meconio a las ~50 h de vida. Tras reiniciar alimentación reaparecieron vómitos biliosos y distensión abdominal que cedieron con ayuno y sonda orogástrica. Por sospecha de enterocolitis necrotizante se instituyeron dieta absoluta, nutrición parenteral total (NPT) y antibióticos (ampicilina + amikacina). Al persistir los síntomas fue transferido a otro centro al día 7 de vida.\n\nHallazgos al ingreso y estudios: a su llegada había distensión abdominal, ausencia de ruidos intestinales y sin signos de peritonitis. El tránsito intestinal no mostró progresión distal y el enema opaco evidenció microcolon. Estos hallazgos son sugestivos de obstrucción intestinal alta (p. ej. atresia yeyunoileal): el microcolon indica un colon poco utilizado por una obstrucción proximal.\n\nIntervención quirúrgica y hallazgos intraoperatorios: se realizó laparotomía exploradora por abordaje supraumbilical transverso. Se encontraron adherencias hepatoileales, una hernia interna por defecto mesentérico con encarcelamiento de un asa yeyunal y atresia yeyunoileal tipo IV (atresias múltiples). Se identificaron dos atresias: una a 56 cm del ángulo de Treitz y otra a 36 cm de la válvula ileocecal, con un segmento interatrésico de 10 cm lleno de meconio y con coloración violácea, pero sin perforación. La relación de calibre proximal:distal era aproximadamente 3:1. Se resecaron 10 cm del asa ciega y se realizó una anastomosis término-oblicua yeyunoileal; se comprobó la permeabilidad distal mediante sonda y lavado salino hasta evacuación rectal. La histopatología confirmó atresia yeyunoileal tipo IV con enteritis crónica leve.\n\nCurso postoperatorio y seguimiento: evolución favorable. Inició alimentación oral al 5º día postoperatorio con buena tolerancia; la NPT se retiró al 8º día. Tuvo deposiciones espontáneas al 6º día postoperatorio y fue dado de alta a los 20 días de vida sin complicaciones. A los 12 meses permanece asintomático, con ganancia ponderal adecuada y tolerancia a alimentación complementaria; deposiciones diarias normales.\n\nInterpretación y puntos clave (implicaciones):\n- Diagnóstico final: atresia yeyunoileal múltiple (tipo IV) asociada a hernia transmesentérica con encarcelamiento de asa intestinal. Las atresias intestinales en neonatos suelen relacionarse con eventos isquémicos intraútero o perinatales que interrumpen la vascularización; la hernia transmesentérica pudo contribuir al compromiso vascular/ischemia y a la aparición de atresias.\n- Diagnóstico diferencial inicial incluyó enterocolitis necrotizante; la falta de respuesta al manejo médico y las imágenes (microcolon, ausencia de progresión distal) orientaron hacia obstrucción congénita que requiere corrección quirúrgica.\n- Buen pronóstico en este caso: preservación suficiente de longitud intestinal para evitar síndrome de intestino corto, anastomosis primaria satisfactoria y recuperación sin secuelas en el primer año. Sin embargo, los pacientes con atresias múltiples requieren seguimiento para vigilar complicaciones tardías (estenosis anastomótica, problemas de motilidad, retraso de crecimiento), por lo que el control pediátrico y nutricional es importante.\n\nComentario empático: el bebé recibió diagnóstico y tratamiento quirúrgico oportuno y ha mostrado una recuperación excelente. Es comprensible la preocupación de la familia frente a vómitos biliosos y la necesidad de cirugía en los primeros días de vida; el seguimiento continuo ha confirmado una evolución favorable."
+        }
+    },
+    {
+        "article": "Se remitió a un hombre de 86 años para que se le implantara una válvula aórtica transfemoral.\n\nLa historia significativa incluyó el hecho de fumar 40 cajetillas al año (hasta fines de la década de 1980) y la fibrilación auricular paroxística que requería anticoagulación con Coumadin desde 1999, seguida poco después por la implantación de un marcapasos ventricular debido a bradicardia. Fue admitido por síncope en mayo de 2011 y se le diagnosticó una estenosis aórtica calcificada severa. Era eupneico y no mostraba signos de insuficiencia cardiaca o retención de líquidos. La ecocardiografía transtorácica reveló una estenosis aórtica severa (gradiente medio: 58 mmHg, área de la válvula aórtica: 0,4 cm2) con hipertrofia ventricular izquierda, fracción de eyección ventricular izquierda deteriorada (29%), acinesia inferior apical y obstrucción septal subvalvular (septum: 18 mm) con dilatación biauricular e hipertensión pulmonar con dilatación de la vena cava.\n\nLa angiografía coronaria mostró una estenosis del 75% de la arteria descendente anterior izquierda. El examen de eco-Doppler encontró vasos normales en el cuello. Se agregó aspirina 80 mg diariamente a su tratamiento; el paciente fue programado para un reemplazo de la válvula aórtica, pero no llegó hasta agosto, cuando fue readmitido en urgencias por disnea aguda y confusión. Había ganado 6 kg de peso, con edemas en las piernas y signos clínicos de derrame pleural. En ese momento, su SpO2 era del 92% y la proteína B-natriurética estaba elevada a 2336 pg·mL−1 (normal < 100 pg·mL−1).\n\nTras la terapia diurética y la eliminación de 850 ml de derrame pleural, se realizó una valvuloplastia de balón percutáneo aórtico de emergencia (Cristal Balloon, 23 mm) e inmediatamente después se le implantó un stent de metal desnudo (Biotronik-Pro-Kinetic 2.74 × 10.0) en la arteria descendente anterior izquierda. El gradiente medio transvalvular disminuyó de 59 a 38 mmHg. Se observaron algunas torsades de pointe el día 6 después de la intervención, que desaparecieron cuando la frecuencia más baja del marcapasos se aceleró a 80 latidos/min. Su estado mejoró drásticamente y se le dio el alta con furosemida, aldactazina y clopidogrel. Tras una revisión cuidadosa del expediente del paciente por parte del equipo cardiaco, se consideró que el riesgo de una cirugía valvular era demasiado alto (Euroscore logístico: 51%), y se propuso al paciente un implante de válvula aórtica transfemoral.\n\nLas notas de las enfermeras mencionan la hiperventilación nocturna y las crisis de ansiedad. El paciente era semiautónomo y vivía con su hija.\n\nLa implantación de la válvula aórtica transfemoral se programó para octubre de 2011. En el ingreso, 2 días antes del procedimiento, el paciente se describió como «ansioso e hiperventilante»; su peso era de 67 kg para una altura de 168 cm; el volumen espiratorio forzado en 1 s (FEV1) era de 1,1 L (50% del valor previsto) y la capacidad vital forzada de 1,7 L (55%); la presión arterial sistémica era de 120/60 mmHg; la concentración de hemoglobina era de 167 g·L−1; la creatinina era de 12,7 g·L−1; la tasa de filtración glomerular se calculó en 54 ml·min−1·m−2; el potasio era de 3,7 mEq·L−1; el sodio era de 141 mEq·L−1; el bicarbonato era de 22 mEq·L−1; y la proteína B natriurética era de 2.073 pg·mL−1. La ecografía describió un área de superficie de la válvula aórtica de 0,5 cm2 con un gradiente aórtico medio de 55 mmHg y acinesia inferoapical en el ventrículo izquierdo. La fracción de eyección se midió en 27% por el método Simpson biplano con regurgitación mitral moderada con dilatación biauricular y se estimó la presión pulmonar sistólica en >69 mmHg. La radiografía de tórax no mostró derrame pleural significativo. El paciente era totalmente dependiente del marcapasos.\n\nDos horas antes de la intervención, el paciente recibió 1 g de acetaminofeno por vía oral. Al llegar al quirófano, el paciente, plenamente consciente, presentaba respiración de Cheyne-Stokes periódica; cada ciclo duraba unos 85 s, con apneas de entre 15 y 20 s y grandes oscilaciones de la SpO2 entre el 88 % y el 99 %. Se le colocó dos catéteres intravenosos periféricos y uno arterial. El trazado arterial también mostraba oscilaciones de 85 s y una presión sistólica de 130 a 150 mmHg. Se le aplicó una máscara facial de oxígeno al 40 % con ventilación no invasiva; la SpO2 alcanzó un rango más estable (92 %-99 %). Diez minutos después, los análisis de gases en sangre mostraron un pH de 7,39, Pao2 de 108 mmHg, Paco2 de 40 mmHg, SaO2 del 97 %, y oscilaciones de lactato de 1,2 mEq·L−1. Se instaló una línea de muestreo capnógrafo dentro de la máscara facial para monitorizar la frecuencia respiratoria (Carescape Monitor B650, GE Healthcare, Helsinki, Finlandia). La monitorización también incluía un ECG de 12 derivaciones, oximetría de pulso, y oximetría cerebral regional (rSO2) mediante espectroscopia infrarroja cercana en el frente (INVOS, Somanetics). La capnografía reveló que las oscilaciones de la presión arterial eran sincrónicas con el ritmo de la respiración y que la presión disminuía durante los períodos apneicos e hipopneicos y aumentaba durante la hiperventilación; la rSO2 seguía el mismo patrón, a pesar de que la SpO2 del dedo permanecía a un nivel constante de 99 %. Se inició una infusión de propofol a una concentración objetivo de 0,2 µg·mL−1; se administraron 2,5 µg de sufentanilo antes de que los operadores infiltraran cada ingle con 200 mg de mepivacaína; el paciente se quedó dormido pero se mantuvo despierto al menor contacto con su cara o cuando su nombre se susurraba al oído; se administraron otros 2,5 µg de sufentanilo antes de la dilatación femoral de la arteria, un procedimiento requerido antes del reemplazo de la válvula. Los ciclos de ventilación se desaceleraron a un máximo de 120 s con 24 s de apneas centrales. Cuando la angiografía y los catéteres operativos estaban en su lugar en la aorta ascendente y se introdujo un marcapasos temporal en el ventrículo derecho, se indujo un ritmo rápido de 200 latidos/min para permitir una nueva dilatación de la válvula calcificada. Este procedimiento duró <25 s, durante el cual el paciente permaneció consciente y continuó respirando de la forma habitual, el ritmo se indujo justo después del final de un período apneico. Se preparó una válvula de 26 mm (SAPIEN, Edwards Lifesciences) y se introdujo en el orificio aórtico. Se dio una señal a los operadores una vez que la respiración se reanudó al final de un período apneico; se inició un ritmo ventricular rápido que llevó a la asistolia a una presión arterial media de 45 mmHg, y la válvula se expandió con balón y la angiografía confirmó la ausencia de fuga paravalvular. El balón se desinfló justo antes de que se detuviera el ritmo rápido, y el corazón volvió a latir a 80 latidos/min bajo la estimulación del marcapasos implantado. La secuencia completa se filmó; duró 31 s, durante los cuales el paciente siguió respirando regularmente (8 veces durante la detención circulatoria, es decir, una tasa de 16 veces por minuto) y no se despertó. Las expulsiones de sangre se reanudaron inmediatamente después de la deflación del balón, con una presión sistólica de 80 mmHg. Después de unas respiraciones profundas, la respiración se hizo regular; no se produjeron nuevos períodos apneicos ni oscilaciones de la presión arterial o rSO2. La hipertensión sistémica se desarrolló rápidamente, culminando después de 1 min a 190 mmHg y se controló con 40 mg de urapidil intravenoso durante los siguientes 15 min. La ecografía transtorácica midió el área valvular a 1,6 cm2 y el gradiente transvalvular máximo a 15 mmHg. La estimación de la presión arterial pulmonar mediante ecografía transtorácica mostró un gradiente sistólico de la presión ventricular derecha-aurícula derecha de 69 mmHg 1 día antes del procedimiento y 45 mmHg 2 días después. Un mes después, era de 28 mmHg. La evolución posterior no tuvo incidentes, y el paciente fue dado de alta 72 h después sin haber vuelto a la respiración periódica.\n\nMH - Edad 80 años y más\nMH - Cirugía de la válvula aórtica\nMH - *Estenosis/cirugía de la válvula aórtica\nMH - *Respiración de Cheyne-Stokes\nMH - Ecocardiografía\nMH - *Insuficiencia cardiaca\nMH - *Implantación de prótesis valvulares cardíacas\nMH - Hemodinámica\nMH - Humanos\nMH - Hombre\nMH - Resultado del tratamiento\n",
+        "gold_summary": "Se remitió a un hombre de 86 años para la implantación de una válvula aórtica transfemoral. La ecocardiografía transtorácica reveló una estenosis grave (gradiente medio: 58 mmHg, área de la válvula aórtica: 0,4 cm2), y después de una discusión multidisciplinaria, se consideró que el riesgo de la cirugía era demasiado alto (Euroscore logístico: 51%), y se propuso al paciente para la implantación de una válvula aórtica transfemoral (TAVI). Al llegar al quirófano, se observó que el paciente, completamente consciente, tenía respiración de Cheyne-Stokes (CSB), que persistió después de la administración de oxígeno al 40%. El procedimiento TAVI fue exitoso, y el patrón CSB se interrumpió en 8 s.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre de 86 años tenía la válvula del corazón muy estrecha. Los médicos dijeron que una operación grande era demasiado peligrosa. En lugar de eso, le pusieron una válvula nueva usando un tubo por la pierna.  \n\nAntes de la operación y durante el procedimiento notaron que respiraba de forma muy irregular. A esto se le llama respiración de Cheyne‑Stokes. Significa que a veces respiraba muy rápido y otras veces dejaba de respirar por un rato. Le dieron oxígeno y cuidado para mantenerlo tranquilo. \n\nPara colocar la nueva válvula, los médicos pararon el latido del corazón por un momento de forma controlada. El corazón volvió a latir bien y la válvula quedó en su sitio. Después del procedimiento, su respiración volvió a ser normal y no volvió a tener los episodios raros. Se recuperó bien y salió del hospital a los pocos días.",
+            "B2": "Here is a clear, caring summary of the case written for readers aged about 11–17:\n\nAn 86-year-old man with severe heart disease was treated with a less-invasive aortic valve replacement called TAVI (transfemoral transcatheter aortic valve implantation). He had very tight narrowing of his aortic valve (the valve that blood leaves the heart through), with the valve opening area only about 0.4–0.5 cm² (normal is much larger). He also had a weak left heart pump (ejection fraction about 27–29%), high pressure in his lungs, and a serious blockage (75%) in one of the heart arteries. Because he was frail and had a very high risk for open-heart surgery, doctors chose TAVI instead.\n\nBefore the procedure, the medical team noticed the patient was breathing in a Cheyne–Stokes pattern. Cheyne–Stokes breathing is a type of “periodic” breathing seen in people with advanced heart failure: it causes cycles of faster, deeper breaths followed by short pauses (central apneas). This can make the oxygen level and blood pressure swing up and down and is a sign of unstable heart and breathing control.\n\nDuring TAVI the team used light sedation and gave oxygen. To place and expand the new valve they briefly switched the heart into a very fast paced rhythm for about 25–31 seconds so the valve could be positioned safely. Even during that brief period of almost stopped circulation, the patient continued to breathe fairly regularly and did not suffer a bad event. After the valve was deployed, blood flow and valve measurements improved (valve area increased to about 1.6 cm² and pressure gradients dropped). The Cheyne–Stokes breathing pattern stopped soon after the procedure and did not come back. The patient’s lung blood pressure also fell over the next days and weeks. He recovered without further problems and was discharged three days later.\n\nWhy this matters: The patient had severe valve disease and heart failure, and Cheyne–Stokes breathing showed his circulation and breathing control were unstable. The team successfully used a less-invasive valve procedure, which quickly improved blood flow and stopped the dangerous breathing pattern. The outcome was good.",
+            "B3": "Resumen clínico (nivel universitario)\n\nPresentación y contexto\n- Paciente: hombre de 86 años con estenosis aórtica calcificada grave, fibrilación auricular anticoagulada, marcapasos ventricular por bradicardia y fracción de eyección baja (FEVI ≈ 27–29%). Tenía además estenosis coronaria significativa en la arteria descendente anterior.\n- Antecedentes inmediatos: ingreso previo por insuficiencia cardiaca aguda que requirió diuréticos, evacuación de derrame pleural, valvuloplastia con balón de urgencia y colocación de un stent en la arteria descendente anterior. La cirugía abierta valvular fue considerada de muy alto riesgo (Euroscore logístico 51%), por lo que se planificó un implante transcatéter de válvula aórtica transfemoral (TAVI).\n\nHallazgos preoperatorios relevantes\n- Ecocardiograma: estenosis aórtica severa (área valvular 0,4–0,5 cm2; gradiente medio 55–59 mmHg), FEVI 27–29%, acinesia inferoapical, regurgitación mitral moderada, dilatación auricular y presión pulmonar elevada.\n- Función respiratoria moderadamente reducida (FEV1 ≈ 50% previsto).\n- Durante la evaluación preoperatoria y en quirófano el paciente presentó respiración de Cheyne‑Stokes (respiración periódica con ciclos de hiperventilación seguidos de apneas centrales). Los ciclos duraban ~85 s, con apneas centrales de 15–24 s y oscilaciones marcadas en la presión arterial y en la saturación cerebral regional (rSO2), aunque la SpO2 periférica permanecía alta. La respiración periódica persistió a pesar de oxígeno al 40%.\n\nProcedimiento y monitorización\n- Anestesia y sedación: sedación ligera con propofol a baja concentración y dosis pequeñas de opioide; analgesia local para acceso femoral. Monitorización exhaustiva incluyó ECG de 12 derivaciones, oximetría periférica, oximetría cerebral por infrarrojo cercano (rSO2), capnografía perimascara y línea arterial.\n- Durante la implantación de la prótesis (válvula SAPIEN 26 mm), se indujo ritmo de marcapasos ventricular rápido (≈200 latidos/min) para inmovilizar el corazón y permitir la expansión valvular. Esta maniobra provocó una parada circulatoria breve y una presión arterial media muy baja durante la inflación del balón.\n- Duración total de la secuencia de parada y expansión: 31 s. El paciente permaneció espontáneamente respirando (8 inspiraciones en esos 31 s), no se despertó ni requirió ventilación asistida durante el episodio.\n\nEvolución inmediata y resultados\n- La válvula se implantó con éxito y sin fuga paravalvular significativa. El área valvular mejoró a 1,6 cm2 y el gradiente máximo transvalvular descendió (ej. gradiente máximo 15 mmHg postoperatorio).\n- Tras el procedimiento hubo recuperación inmediata del latido con presión sistólica inicial baja (≈80 mmHg), seguida de hipertensión transitoria controlada con urapidil. La presión pulmonar estimada disminuyó rápidamente en los días siguientes (ej.: estimación ecocardiográfica de la presión sistólica pulmonar: 69 mmHg preop, 45 mmHg 2 días después, 28 mmHg a 1 mes).\n- Importante: el patrón de respiración de Cheyne‑Stokes desapareció tras la corrección de la estenosis aórtica y no reapareció durante la hospitalización; el paciente fue dado de alta 72 h después sin recurrencia.\n\nInterpretación y puntos clave\n- Cheyne‑Stokes (respiración periódica con apneas centrales) se asocia en pacientes con insuficiencia cardiaca y baja fracción de eyección. En este caso era clínicamente evidente y producía fluctuaciones hemodinámicas y de perfusión cerebral que se correlacionaban con la ventilación.\n- La corrección de la obstrucción aórtica mediante TAVI mejoró rápidamente la hemodinámica (mayor gasto cardiaco, reducción de presiones pulmonares) y se asoció a la desaparición del patrón respiratorio anómalo. Esto sugiere que la insuficiencia cardiaca avanzada y la inestabilidad hemodinámica eran mecanismos importantes de la respiración de Cheyne‑Stokes en este paciente.\n- La maniobra de estimulación ventricular rápida (breve parada circulatoria) durante la implantación no llevó a despertar ni a paro respiratorio significativo, probablemente porque el paciente tuvo respiración espontánea mantenida y se monitorizó estrechamente (capnografía, rSO2). La supervisión neurológica y hemodinámica fue clave para la seguridad del procedimiento.\n\nImplicaciones clínicas y recomendaciones\n- En pacientes con estenosis aórtica severa e insuficiencia cardiaca, la TAVI puede corregir no solo la válvula sino también reducir la apnea central relacionada con la insuficiencia cardiaca.\n- Para enfermos con respiración periódica es esencial monitorizar no solo la SpO2 periférica sino también la capnografía y la oxigenación cerebral (rSO2), ya que la saturación periférica puede permanecer normal mientras la perfusión cerebral y la presión arterial oscilan.\n- Vigilancia postoperatoria: control hemodinámico, ajuste de la terapia antiarrítmica y del marcapasos según necesidad, y seguimiento ecocardiográfico y de la presión pulmonar. Si las alteraciones respiratorias persistieran, considerar evaluación por sueño y tratamiento específico.\n\nTono final\nEl caso muestra que, con adecuada selección y monitorización, el TAVI puede realizarse de forma segura en un paciente anciano con respiración de Cheyne‑Stokes y disfunción ventricular severa, y que la corrección valvular puede resolver la apnea central secundaria a la insuficiencia cardiaca. Se requirió una estrecha vigilancia multidisciplinaria y medios de monitorización avanzados para garantizar un resultado favorable."
+        }
+    },
+    {
+        "article": "Una mujer árabe tunecina de 62 años, diagnosticada con la enfermedad de Von Hippel-Lindau en 2021, presentó varias manifestaciones relacionadas con la enfermedad. Tenía antecedentes de múltiples cirugías, principalmente por tumores renales, suprarrenales y pancreáticos, con hallazgos incidentales de masas ováricas.\n\nLa paciente no presentaba síntomas desde el punto de vista ginecológico, pero se quejaba principalmente de dolores de cabeza antes de someterse a una cirugía cerebral. No tenía antecedentes familiares o psicosociales significativos.\n\nSu historial quirúrgico incluye\n2021: Un tumor no operable (6 cm) del saco endolinfático del hueso petroso izquierdo, tratado con radioterapia.\n\n2021: Adrenalectomía izquierda por un feocromocitoma de 6 cm. El examen patológico reveló un feocromocitoma.\n\n2021: Nefrectomía izquierda por un tumor renal izquierdo roto. La microscopía mostró un carcinoma renal multifocal de células claras de grado nuclear 2.\n\n2022: Duodenopancreatectomía cefálica por una masa en el páncreas. El examen histológico confirmó tres cistadenomas serosos y dos tumores neuroendocrinos bien diferenciados.\n\nEn enero de 2021, durante la vigilancia posoperatoria con una tomografía computarizada (TC) abdominal-pélvica, se descubrió incidentalmente una masa anexial izquierda sólida de 4 cm, lo que levantó sospechas de malignidad. La masa se confirmó mediante ultrasonido transvaginal e IRM pélvica, clasificada como Sistema de Reporte y Datos Ováricos-Anexiales (O-RADS) 5 (alta sospecha de malignidad).\n\nExamen ginecológico e historial quirúrgico\nExamen físico: No se detectó masa abdominal-pélvica.\n\nExamen con espéculo: cuello uterino sano.\n\nSe observaron cicatrices quirúrgicas de una nefrectomía izquierda y una duodenopancreatectomía cefálica anteriores.\n\nUna reunión multidisciplinaria del personal concluyó que era necesaria la cirugía. Se realizó una laparotomía a través de una incisión en la línea media por debajo del ombligo, que reveló una masa quística sólida bien definida en el anexo izquierdo. No había ascitis ni signos de carcinomatosis peritoneal, y el anexo derecho parecía normal, sin signos macroscópicos de malignidad observados intraoperatoriamente, incluida la ausencia de vegetaciones exocísticas.\n\nSe realizó una citología junto con una anexectomía izquierda y la muestra se envió para un examen de sección congelada. Los resultados no fueron concluyentes, lo que planteó la posibilidad de tumores de margen o específicos del síndrome de Von Hippel-Lindau. Teniendo en cuenta el estado posmenopáusico de la paciente, se realizó una anexectomía derecha y una histerectomía total.\n\nEl examen histológico posterior reveló cistadenomas papilares de células claras bilaterales de las trompas de Falopio y el ligamento ancho, característicos de la enfermedad de Von Hippel-Lindau (0,5 cm en el lado derecho y 4 cm en el lado izquierdo). Los tumores consistían en papilas densamente compactadas con núcleos fibrosos, cubiertos por un epitelio monocapa.\n\nEl período postoperatorio inmediato transcurrió sin incidentes y, en el seguimiento de 1 mes, no se detectaron anomalías. Desde entonces, se ha hecho un seguimiento al paciente cada 4 meses con ecografías pélvicas normales. Durante estos 2 años de seguimiento, no han surgido complicaciones, pero el paciente fue readmitido recientemente en el departamento de neurocirugía por la recurrencia de un tumor cerebral.\n",
+        "gold_summary": "Una mujer blanca norteafricana de 62 años de edad, diagnosticada con la enfermedad de Von Hippel-Lindau en 2021, presentó múltiples manifestaciones, entre ellas, un tumor del hueso petroso izquierdo, feocromocitoma izquierdo, carcinoma de células renales izquierdo, riñón derecho con múltiples quistes y masas pancreáticas. Se sometió a varios tratamientos, entre ellos, radioterapia, adrenalectomía, nefrectomía y duodenopancreatectomía cefálica. Los exámenes de ultrasonografía y resonancia magnética revelaron una masa quística sólida en la región anexial izquierda. La laparoscopia identificó tumores quísticos en la mesosalpinx derecha e izquierda. Después de una histerectomía con anexectomía bilateral, el examen histológico reveló cistadenomas papilares de células claras bilaterales de la mesosalpinx y el ligamento ancho, compatibles con la enfermedad de Von Hippel-Lindau.\n",
+        "synthetic_summary": {
+            "B1": "Here is a short, easy-to-understand summary:\n\nA 62-year-old woman from Tunisia has a condition called Von Hippel-Lindau (VHL). VHL is a problem some people are born with that can cause many different tumors in the body.\n\nSince 2021 she had several health problems and surgeries. Doctors treated tumors in her brain area, her left adrenal gland, her left kidney, and her pancreas. During a follow-up scan, they also found a new lump near her left ovary.\n\nShe did not have belly pain or other symptoms from this lump. Scans showed the lump might be cancer, so doctors did surgery. They removed her uterus and both adnexa (the left and right fallopian tube/ovary areas). In the operation they did not see signs that the cancer had spread.\n\nThe lab tests on the removed tissue showed small growths called clear cell papillary cystadenomas. These growths are known to happen with VHL. One was 4 cm on the left and a small one (0.5 cm) on the right.\n\nAfter the operation she recovered well. Follow-up checks every 4 months with pelvic ultrasound were normal for two years. Recently she went back to the hospital because a brain tumor came back and she is being treated by neurosurgery.\n\nOverall: the pelvic surgery worked and the pelvic scans stayed normal. But because VHL can cause tumors in many places, she needs ongoing care.",
+            "B2": "Resumen comprensible (nivel B2, dirigido a lectores de secundaria)\n\nUna mujer tunecina de 62 años fue diagnosticada en 2021 con la enfermedad de Von Hippel–Lindau (VHL). VHL es un trastorno genético que predispone a desarrollar varios tipos de tumores en diferentes órganos.\n\nAntes y desde el diagnóstico tuvo varios problemas relacionados con VHL:\n- Tumor del saco endolinfático en el hueso petroso izquierdo tratado con radioterapia.\n- Feocromocitoma (un tumor de la glándula suprarrenal) en el lado izquierdo, extirpado mediante cirugía.\n- Carcinoma renal de células claras multifocal en el riñón izquierdo, por el que se realizó una nefrectomía.\n- Masas en el páncreas que requirieron una duodenopancreatectomía; el tejido mostró cistadenomas serosos y dos tumores neuroendocrinos bien diferenciados.\n\nEn enero de 2021, durante un control con tomografía abdominal-pélvica se encontró por casualidad una masa sólida y quística de 4 cm en el anexo izquierdo (zona de ovario/trompa). Las ecografías y una resonancia la clasificaron como O-RADS 5, que indica alta sospecha de malignidad en la imagen.\n\nLa paciente no tenía síntomas ginecológicos ni masa palpable en la exploración. Se decidió operar y, durante una laparotomía, se vio una masa quística sólida bien definida en el anexo izquierdo. No había líquido de ascitis ni signos abiertos de cáncer en la cavidad abdominal; el anexo derecho parecía normal a simple vista.\n\nSe tomó una muestra para citología y se realizó una sección congelada durante la operación, pero los resultados fueron inconclusos. Dado que la paciente era posmenopáusica y para evitar dejar tejido enfermo, se completó la cirugía con anexectomía derecha (retirada de ambos anexos) y una histerectomía total.\n\nEl examen definitivo del tejido mostró cistadenomas papilares de células claras en ambas trompas de Falopio y en el ligamento ancho (mesosalpinx): lesiones benignas pero típicas de la enfermedad de Von Hippel–Lindau (0,5 cm a la derecha y 4 cm a la izquierda). Estas formaciones estaban hechas de papilas compactas cubiertas por una sola capa de células.\n\nLa recuperación inmediata fue buena. Al mes no se encontraron anomalías, y durante dos años se hizo seguimiento con ecografías pélvicas cada cuatro meses que permanecieron normales. No hubo complicaciones relacionadas con la cirugía pélvica. Recientemente la paciente volvió a ingresar en neurocirugía por la recurrencia de un tumor cerebral, lo que sugiere que seguirá recibiendo tratamiento y controles específicos para ese problema.\n\nComentario final: en personas con VHL es común encontrar tumores en distintas partes del cuerpo. Aunque las imágenes podían parecer sospechosas de cáncer, en este caso las lesiones pélvicas resultaron ser cistadenomas asociados al síndrome. El manejo incluyó cirugía para quitar las lesiones y control estrecho con imágenes; la paciente se mantiene en seguimiento por sus otras afecciones relacionadas con VHL.",
+            "B3": "Resumen clínico (nivel universitario)\n\nPaciente: mujer tunecina árabe de 62 años, diagnosticada con la enfermedad de Von Hippel–Lindau (VHL) en 2021.\n\nAntecedentes relevantes\n- Enfermedad de VHL con múltiples manifestaciones tratadas previamente:\n  - Tumor del saco endolinfático del hueso petroso izquierdo (6 cm), no resecable → radioterapia.\n  - Feocromocitoma izquierdo (glándula suprarrenal) → adrenalectomía; confirmación patológica.\n  - Carcinoma renal de células claras multifocal del riñón izquierdo → nefrectomía izquierda.\n  - Masa pancreática → duodenopancreatectomía cefálica; hallazgos: cistadenomas serosos y dos tumores neuroendocrinos bien diferenciados.\n- Sin síntomas ginecológicos reportados y sin antecedentes familiares o psicosociales relevantes.\n\nHallazgo actual que motivó intervención\n- En una tomografía abdominal-pélvica de control (enero 2021) se detectó una masa anexial izquierda sólida de 4 cm, confirmada por ecografía transvaginal y resonancia magnética pélvica. Clasificada como O-RADS 5, lo que indica alta sospecha de malignidad.\n- Examen físico y ginecológico: sin masa palpable ni anormalidades del cuello uterino.\n\nIntervención quirúrgica y hallazgos intraoperatorios\n- Se realizó laparotomía por línea media infraumbilical. Se encontró una masa quístico-sólida bien delimitada en el anexo izquierdo; no había ascitis ni signos macroscópicos de carcinomatosis peritoneal. El anexo derecho parecía macroscópicamente normal.\n- Se tomaron citología y se practicó anexectomía izquierda con envío a sección congelada; el resultado intraoperatorio fue no concluyente.\n- Dado que la paciente estaba posmenopáusica y ante la incertidumbre diagnóstica, se completó histerectomía total con anexectomía derecha.\n\nResultado histológico definitivo\n- Lesiones bilaterales localizadas en la mesosalpinx y ligamento ancho (no en el ovario): papilares cistadenomas de células claras, compatibles con la VHL.\n  - Tamaños: 4 cm en el anexo izquierdo y 0,5 cm en el derecho.\n  - Morfología: papilas densamente compactadas con núcleos en el eje fibroso, revestidas por epitelio monocapa.\n- Estas lesiones tienen un patrón característico descrito en pacientes con VHL.\n\nEvolución y seguimiento\n- Período postoperatorio inmediato sin complicaciones.\n- Control al mes sin anomalías.\n- Seguimiento con ecografías pélvicas cada 4 meses durante 2 años, todas normales.\n- Reciente reingreso en neurocirugía por recurrencia de un tumor cerebral (relacionado con la VHL).\n\nInterpretación y consideraciones\n- Normal vs anormal: el examen ginecológico fue normal, pero la imagen detectó una masa anexial que resultó ser un tumor asociado a VHL. No hubo evidencia macroscópica de diseminación peritoneal ni signos de malignidad intraoperatorios; la histología describió lesiones benignas típicas de VHL.\n- Implicaciones: las cistadenomas papilares de células claras en la mesosalpinx son lesiones asociadas a VHL y, en este contexto, su hallazgo es coherente con la naturaleza multiorgánica de la enfermedad. La decisión de extirpar ambos anexos y el útero fue razonable dada la edad posmenopáusica y la inconclusión de la biopsia intraoperatoria.\n- Próximos pasos prudentes: continuar vigilancia multidisciplinaria para VHL (incluyendo control neurológico por la recurrencia cerebral, imágenes periódicas renales, suprarrenales y pancreáticas, y vigilancia por si aparecen nuevas lesiones), además de manejo específico del tumor cerebral recurrente por neurocirugía.\n\nComentario final (empatía)\nLa paciente ha recibido un manejo integral frente a una enfermedad sistémica compleja. El hallazgo pélvico se resolvió con tratamiento quirúrgico y la evolución inmediata fue favorable; sin embargo, la naturaleza heterogénea y recidivante de la VHL exige seguimiento estrecho y coordinación entre especialidades."
+        }
+    },
+    {
+        "article": "Una mujer embarazada de 31 años que había sido sometida a una cesárea fue derivada a la unidad de ultrasonido de nuestro departamento para un examen de ultrasonido morfológico de segundo trimestre. La paciente no tenía antecedentes familiares destacables y no había tomado medicamentos ni había estado expuesta a teratógenos durante el primer trimestre del embarazo. Los exámenes serológicos para diversas enfermedades infecciosas fueron negativos y un examen de ultrasonido previo a las 14 semanas fue normal. El triple examen para anomalías fetales también fue negativo a las 16 semanas.\n\nDurante la ecografía de la semana 20, se observó un feto masculino con una edad sonográfica compuesta de 20 semanas y 2 días que presentaba un edema significativo de las extremidades inferiores y líquido amniótico normal. Se recomendó un examen de seguimiento en 2 semanas, junto con pruebas de TORCH y pruebas de Coombs indirectas.\n\nSin embargo, se observó nuevamente edema subcutáneo en ambas extremidades inferiores durante la ecografía morfológica de la semana 23, lo que sugiere un posible diagnóstico de EM. Debido al linfedema persistente en las extremidades inferiores, se realizó una amniocentesis.\n\nLos exámenes posteriores revelaron que el cariotipo masculino era normal (46, XY), y el análisis molecular para el síndrome de Noonan fue negativo. Se realizó la secuenciación de nucleótidos del líquido amniótico con la secuenciación Illumina de 150 bases. Se aplicó el sistema de bioinformática (North-Oehler Aligarh, GATX) mientras se verificaba adicionalmente la existencia de deleciones/duplicaciones/CNV (Copy Number Variations) en el gen FLT4. El análisis identificó una mutación c.3116C>A p. (Ala1039Asp), que es una variante patogénica no conocida en el gen FLT4, lo que confirma el diagnóstico de linfedema hereditario tipo 1A – enfermedad de Milroy. El análisis de sangre materno confirmó la mutación materna y se realizó el asesoramiento genético.\n\nLa cesárea se realizó a las 38 semanas y 6 días de gestación y nació un neonato de sexo masculino que pesaba 3850 g y medía 46 cm con una puntuación de Apgar de 9/10. Después del parto se reconoció un edema en la extremidad inferior. El examen histopatológico de la placenta, el cordón umbilical y el saco amniótico no mostró signos de corioamnionitis u otra patología.\n",
+        "gold_summary": "Presentamos un informe de caso de una primera mutación descrita de un feto masculino diagnosticado prenatalmente con síndrome de Milroy a través de amniocentesis. El feto tenía edema bilateral de miembros inferiores, y las pruebas genéticas confirmaron el diagnóstico de síndrome de Milroy. La paciente fue monitoreada de cerca durante todo el embarazo, y después del parto, el lactante fue tratado con terapias apropiadas, incluyendo prendas de compresión y drenaje linfático manual. Los padres recibieron asesoramiento y apoyo apropiados.\n",
+        "synthetic_summary": {
+            "B1": "Una mujer embarazada de 31 años tuvo controles normales al principio del embarazo. A las 20 semanas, el bebé en su vientre mostró hinchazón en las piernas. Esto se llama linfedema. Los médicos volvieron a ver la hinchazón a las 23 semanas y pidieron una prueba del líquido que rodea al bebé (amniocentesis).  \n\nLas pruebas de los genes mostraron un cambio en un gen llamado FLT4. Ese cambio confirma un tipo de linfedema que se llama enfermedad de Milroy. La misma cambio se vio también en la sangre de la mamá, por eso se dijo que la condición es heredada. Los padres tuvieron explicación y apoyo con información genética.  \n\nEl bebé nació por cesárea a las 38 semanas y pesó 3850 g. Nació sano en general (puntuación de Apgar 9/10), pero tenía hinchazón en una pierna, como se esperaba. La placenta y los tejidos alrededor del bebé estaban normales.  \n\nDespués del nacimiento, al bebé le dieron cuidados para ayudar a bajar la hinchazón. Le pusieron prendas de compresión y le hicieron drenaje linfático manual, que son tratamientos para que el líquido salga y las piernas se sientan mejor. Los padres siguen recibiendo apoyo y consejos para cuidar al bebé.",
+            "B2": "This report describes a pregnant 31-year-old woman whose baby was found to have swelling in both lower legs on routine ultrasound in the second trimester. Because the swelling (called lymphedema — extra fluid that builds up when the body’s lymph vessels do not drain well) persisted, doctors performed an amniocentesis (a test that takes a small sample of the fluid around the baby to check the baby’s genes).\n\nStandard chromosome testing (karyotype) and tests for Noonan syndrome were normal, but detailed gene sequencing found a new harmful change in the FLT4 gene. Changes in FLT4 are known to cause Milroy disease, a hereditary form of lymphedema (type 1A). Blood testing showed the mother carried the same mutation, so the condition was inherited. The family received genetic counseling and support.\n\nThe baby was delivered by cesarean at 38 weeks and 6 days, weighing 3850 g, with good Apgar scores (9 and 10). The newborn had the same leg swelling at birth; the placenta and umbilical cord appeared normal. After birth the infant was treated with helpful measures such as compression garments and manual lymphatic drainage to reduce swelling. Early diagnosis allowed the team to plan appropriate care and provide the parents with information and support.",
+            "B3": "Resumen (nivel B3)\n\nPresentación y antecedentes\n- Mujer de 31 años con cesárea previa, embarazo controlado sin exposición a teratógenos ni historias familiares relevantes.\n- Serologías maternas y cribado bioquímico (triple test a las 16 semanas) fueron normales; ecografía previa a las 14 semanas sin hallazgos.\n\nHallazgos prenatales y pruebas realizadas\n- A las 20 semanas se detectó edema significativo en las extremidades inferiores del feto masculino (edad gestacional ecográfica 20+2), con líquido amniótico normal. Se programó control.\n- A las 23 semanas el edema subcutáneo en ambas piernas persistió, lo que orientó a linfedema fetal. Debido a la persistencia del linfedema se practicó amniocentesis.\n- Cariotipo fetal normal (46,XY). Test molecular para síndrome de Noonan negativo.\n- Secuenciación del ADN del líquido amniótico (Illumina, lectura de 150 pb) e inspección de variaciones en número de copias en el gen FLT4 revelaron la variante c.3116C>A p.(Ala1039Asp) en FLT4, no previamente descrita y considerada patogénica. Diagnóstico: linfedema hereditario tipo 1A (enfermedad de Milroy).\n- Análisis genético materno confirmó que la madre portaba la misma mutación; se dio asesoramiento genético.\n\nNacimiento y evolución postnatal\n- Cesárea a las 38+6 semanas; recién nacido masculino de 3.850 g, 46 cm, Apgar 9/10.\n- Al nacimiento se observó edema en las extremidades inferiores, concordante con la sospecha prenatal.\n- Anatomía patológica de placenta, cordón y saco amniótico sin signos de infección o patología (no corioamnionitis).\n\nImplicaciones clínicas y manejo\n- La enfermedad de Milroy es un linfedema hereditario por alteración del desarrollo de los vasos linfáticos (mutaciones en FLT4/VEGFR3). Se manifiesta por edema crónico de las extremidades, que puede detectarse prenatalmente cuando es evidente en ecografía.\n- No hay cura definitiva; el tratamiento es de soporte y sintomático: cuidados de la piel, prendas de compresión, drenaje linfático manual y seguimiento con especialistas en linfedema y genética. En el caso descrito, el lactante recibió terapias conservadoras adecuadas.\n- La confirmación de la misma mutación en la madre indica herencia autosómica dominante y permite estimar riesgo de recurrencia en futuros embarazos y la posibilidad de evaluar a otros familiares.\n- El diagnóstico prenatal mediante ecografía seguido de estudio genético permitió planificación perinatal, consejo genético y preparación para el manejo neonatal.\n\nComentario final (tono empático)\nEste caso ilustra cómo un edema fetal persistente en ecografía puede conducir a un diagnóstico genético temprano de linfedema hereditario (Milroy). La identificación de una mutación patogénica, incluida su confirmación en la madre, permitió ofrecer a la familia información concreta, apoyo y opciones de manejo desde la etapa prenatal. Aunque el linfedema será probablemente una condición crónica, el control especializado y las medidas conservadoras pueden mejorar la calidad de vida del niño."
+        }
+    },
+    {
+        "article": "Un paciente de 50 años con antecedentes médicos conocidos de diabetes mellitus (DM) e hipertensión (HTN), que se manejaba de manera irregular, se presentó en nuestro hospital en la ciudad de Sana’a, Yemen, el 25 de mayo de 2022, a las 5:30 p. m. El paciente fue derivado a otro hospital y manifestó un dolor abdominal agudo que había durado una semana antes del ingreso. El dolor se localizaba en la región epigástrica, de inicio repentino, empeoramiento progresivo y radiación hacia la espalda. Además, el paciente experimentó distensión abdominal generalizada, náuseas, vómitos y fatiga significativa. También se informó un historial de melena y vómitos relacionados con los alimentos durante el mes pasado. Dos días antes del ingreso, el paciente había recibido una transfusión de sangre de 2 unidades. No había antecedentes de cirugías previas ni antecedentes familiares de neoplasias.\n\nAl examinar al paciente, se constató que estaba consciente y alerta, pero que presentaba un aspecto pálido. La presión arterial era de 90/60 mmHg y el pulso de 120 latidos por minuto. Se observó distensión abdominal generalizada, particularmente prominente en la región supraumbilical con desplazamiento hacia abajo del ombligo. Se constató una leve sensibilidad en la zona epigástrica, junto con sonidos intestinales positivos, el examen rectal digital reveló un tono normal del esfínter anal y no se detectó ninguna masa palpable.\n\nLos exámenes hematológicos y bioquímicos revelaron anemia microcítica hipocrómica con un nivel de hemoglobina de 6 g/dL (rango normal: 12-15.5 g/dL), un recuento de glóbulos blancos de 16,000 (rango normal: 4-10,000), y un recuento de plaquetas de 303. El nivel de nitrógeno ureico en sangre fue de 7 mg/dL (rango normal: 10-20 mg/dL), la creatinina fue de 0.49 mg/dL (rango normal: 0.7-1.5% / dL), el índice internacional normalizado fue de 1.34 (rango normal: 0.62-1.3), el tiempo de protrombina (PT) fue de 16.9, el tiempo de tromboplastina parcial (PTT) fue de 30, el calcio fue de 8.0 mg/dL (rango normal: 8.5-10.1 mg / dL) y el ácido láctico fue de 1.9 mmol/L (rango normal: 0.5-2.2% / L). Los niveles de enzimas hepáticas y amilasa estuvieron dentro de los límites normales.\n\nSe realizaron estudios de diagnóstico por imágenes, que incluyeron una radiografía de tórax y una ecografía abdominal. La radiografía de tórax no reveló aire subdiafragmático, pero se observó una elevación en el diafragma izquierdo. La ecografía abdominal demostró la presencia de una acumulación de líquido intraabdominal. Posteriormente, se realizó una angiografía por TC abdominal, que reveló un hematoma de aproximadamente 14,3 × 8,8 cm en la región paraumbilical. En el interior del hematoma, se identificó un aneurisma arterial de 3,4 × 2,2 cm conectado a la arteria gastroduodenal, acompañado de cambios edematosos circundantes. Estos hallazgos sugieren la presencia de un aneurisma trombosado grande en la arteria gastroduodenal. Además, se observó la evisceración del diafragma izquierdo, que contiene el bazo y parte del estómago, junto con una acumulación de líquido intraperitoneal leve a moderada. No se detectó evidencia de un aneurisma aórtico.\n\nPara estabilizar al paciente, se inició la reanimación con 1000 ml de lactato de Ringer y se transfundieron tres unidades de sangre fresca. Se obtuvo el consentimiento informado para la intervención de alto riesgo y el paciente fue llevado inmediatamente al quirófano. Bajo anestesia general, en posición supina y con estricta adhesión a las técnicas asépticas, se realizó una incisión de laparotomía en la línea media. Cuando se abrió el peritoneo, se evacuó aproximadamente 2000 ml de sangre, revelando una masa pulsátil ocluida en el duodeno. Se logró una exposición adecuada utilizando un retractor auto-reforzado. La flexión del hígado y el colon transverso se movilizaron inferiormente desde la cabeza del páncreas y se eliminó la sangre coagulada del intestino delgado. Se realizó una disección meticulosa sobre el gran aneurisma ocluido pulsátil en la arteria gastroduodenal abriendo el ligamento gastrohepático. La movilización del píloro y el duodeno lejos de la cabeza del páncreas expuso una fístula que conectaba el duodeno y el aneurisma, sin contenido digestivo. Después de la heparinización, se realizó un pinzamiento proximal y distal de la arteria gastroduodenal. Posteriormente, se abrió el pseudoaneurisma y se evacuó una cantidad significativa de trombo. Se realizó una aneurismorrafía utilizando suturas de prolina 7.0. La perforación en la primera parte del duodeno se reparó en dos capas y se insertó una sonda nasogástrica más allá de la perforación. Se logró una irrigación exhaustiva con solución salina normal y una hemostasia meticulosa. Se colocó un drenaje abdominal y se cerró la incisión abdominal en capas. El paciente fue trasladado a la unidad de cuidados intensivos (UCI) para una estrecha monitorización y observación.\n\nDurante el período postoperatorio, el drenaje abdominal recolectó aproximadamente 100 ml de fluido seroso, que se eliminó el tercer día después de la operación. La recuperación de la paciente progresó sin complicaciones. Diez días después de la cirugía, la paciente fue dada de alta en condiciones favorables. Se programaron citas de seguimiento en el departamento ambulatorio y se mantuvo una comunicación regular por teléfono, con la condición de la paciente reportada como satisfactoria.\n",
+        "gold_summary": "Un hombre de 50 años se presentó con dolor abdominal agudo, anemia y signos de inestabilidad hemodinámica. Las imágenes de diagnóstico, incluida la CTA, revelaron un aneurisma de la arteria gastroduodenal grande y trombosado con evidencia de ruptura. El paciente se sometió a exploración y reparación quirúrgica abierta para abordar tanto el aneurisma como la perforación duodenal. La recuperación del paciente fue satisfactoria y fue dado de alta en condiciones estables.\n",
+        "synthetic_summary": {
+            "B1": "Un señor de 50 años llegó al hospital porque tenía muchísimos dolores en la panza que se iban hacia la espalda. También estaba muy cansado, vomitaba y había perdido sangre en las heces. Tenía la presión baja y estaba pálido.\n\nLos médicos hicieron estudios y vieron una gran bolita en una arteria cerca del estómago. Esa bolita era como un globo en la pared de la arteria y tenía dentro coágulos (sangre pegada). Esa bolita se había roto y había hecho un hoyo en la primera parte del intestino (duodeno). Por eso había mucha sangre dentro de la panza.\n\nLo llevaron de urgencia al quirófano. Abrieron el abdomen, sacaron mucha sangre y arreglaron la arteria y el hoyo del intestino. Le pusieron sangre para ayudarlo y lo cuidaron en la unidad de cuidados intensivos.\n\nSe recuperó bien después de la operación. Diez días más tarde pudo irse a su casa y volvió a sus citas de control. Los médicos dijeron que su estado era estable y que mejoraba.",
+            "B2": "Here is a clear, kind summary of the case:\n\nA 50-year-old man with diabetes and high blood pressure came to the hospital with one week of sudden, severe upper-abdominal pain that spread to his back. He also had belly swelling, nausea, vomiting, tiredness, and black stools (melena), and he was already very anemic from bleeding. On arrival he looked pale, his blood pressure was low and his heart rate fast, and blood tests showed a very low hemoglobin (6 g/dL) and a raised white blood cell count.\n\nImaging with a CT angiogram showed a large blood collection (hematoma) near the belly and a 3.4 × 2.2 cm aneurysm of the gastroduodenal artery. An aneurysm is a ballooning or bulge in an artery. This aneurysm was partly filled with clot (thrombosed) and had likely ruptured, causing internal bleeding. The scan also showed that part of the spleen and stomach had moved upward through the left side of the diaphragm (a type of herniation) and there was a moderate amount of fluid inside the abdomen.\n\nBecause of ongoing bleeding and the patient’s unstable condition, the team gave fluids and several units of blood and took him immediately to emergency surgery. During an open operation (a midline laparotomy), the surgeons removed about 2 liters of blood from the abdomen and found a pulsating mass connected to the duodenum (first part of the small intestine). They discovered a fistula — an abnormal hole or connection — between the aneurysm and the duodenum. After temporarily controlling the artery, they opened the aneurysm, removed the clot, repaired the artery, and stitched the hole in the duodenum in two layers. They placed a drain and a nasogastric tube (a tube through the nose into the stomach) and moved him to the intensive care unit for close monitoring.\n\nThe patient recovered well after surgery. The abdominal drain produced a small amount of clear fluid and was removed on day 3. He had no major complications and was discharged in good condition on day 10, with outpatient follow-up arranged.\n\nIn short: the patient had a ruptured, partly clot-filled aneurysm of the gastroduodenal artery that caused major internal bleeding. Emergency open surgery successfully controlled the bleeding, repaired the artery and the duodenal injury, and the patient recovered.",
+            "B3": "Resumen clínico\n\nUn hombre de 50 años con diabetes e hipertensión mal controladas llegó al hospital con una semana de dolor epigástrico intenso y de inicio súbito que irradiaba a la espalda, distensión abdominal, náuseas, vómitos y fatiga. También refería melena (heces oscuras por sangrado) y había recibido transfusión sanguínea días antes. Al ingreso estaba pálido, hipotenso (90/60 mmHg) y taquicárdico (120 lpm), lo que indica inestabilidad hemodinámica.\n\nHallazgos clave (anormales)\n- Hemoglobina muy baja: 6 g/dL (anemia microcítica hipocrómica severa).\n- Leucocitosis: 16.000 /µL (inflamación o reacción al sangrado).\n- Radiografía: elevación del hemidiafragma izquierdo, sin aire libre subdiafragmático.\n- Ecografía: líquido intraabdominal (anfiperitoneo).\n- Angio-TC abdominal: hematoma paraumbilical grande (14,3 × 8,8 cm) y un aneurisma de la arteria gastroduodenal de 3,4 × 2,2 cm, parcialmente trombosado, con signos de ruptura hacia el peritoneo. Se observó además herniación del bazo y parte del estómago a través del hemidiafragma izquierdo.\n\nDiagnóstico y manejo\n- Diagnóstico principal: aneurisma roto (pseudoaneurisma) de la arteria gastroduodenal con hemoperitoneo y fístula hacia el duodeno.\n- Manejo inmediato: reanimación con líquidos y transfusión de sangre; consentimiento y traslado urgente a quirófano.\n- Procedimiento quirúrgico: laparotomía media con evacuación de ~2000 mL de sangre; identificación de un aneurisma ocluido en relación con el duodeno y una fístula duodenal. Tras heparinización, se pinzó la arteria gastroduodenal proximal y distal, se abrió el pseudoaneurisma y se evacuó trombo; se reparó el saco aneurismático (aneurismorrafia) y se suturó la perforación duodenal en dos capas; se colocó sonda nasogástrica y drenaje abdominal.\n\nEvolución y pronóstico\n- Postoperatorio sin complicaciones significativas: drenaje seroso retirado al tercer día; alta al décimo día en condiciones estables.\n- Se programaron controles ambulatorios y seguimiento telefónico, con reporte de buena recuperación.\n\nImplicaciones y recomendaciones prácticas\n- Este caso muestra una causa rara pero potencialmente mortal de dolor abdominal agudo: ruptura de un aneurisma visceral (arteria gastroduodenal), que requiere diagnóstico rápido y control quirúrgico u endovascular inmediato.\n- Pasos razonables a seguir tras el alta: control estricto de los factores de riesgo cardiovascular (mejorar control de diabetes e hipertensión), corrección y seguimiento de la anemia, y vigilancia por imagen (según indicación del equipo tratante) para asegurar que no haya recurrencia o nuevos aneurismas.  \n- La coordinación con cirugía vascular/gastroenterología en consultas de seguimiento es recomendable.\n\nEstoy disponible si desea una versión más breve, una lista de términos explicados con más detalle, o recomendaciones específicas para el control de factores de riesgo."
+        }
+    },
+    {
+        "article": "Una mujer de 60 años fue admitida en el departamento de nefrología con dolor epigástrico, hematemesis y edema en la pierna. La presión arterial era de 90/50 mmHg, dentro del rango normal para esta paciente.\nLos resultados de laboratorio fueron notables para las enzimas hepáticas alteradas con un patrón colestático: los niveles de alanina amino transferasa (ALT) y aspartato amino transferasa (AST) fueron ligeramente elevados a 28 U/L y 61 U/L, respectivamente, mientras que los niveles de fosfatasa alcalina (388 U/L) y gamma glutamiltransferasa (291 U/L) fueron muy elevados. Los niveles de albúmina en suero fueron de 24 g/L y el índice internacional normalizado fue normal a 1.02.\nOtros resultados de laboratorio, incluidos la bilirrubina total (0,32 mg/dL), la bilirrubina directa (0,26 mg/dL), el recuento total de plaquetas (176 000 plaquetas por microlitro) y el recuento de glóbulos blancos (8400 células por microlitro), se encontraban dentro de los valores normales.\nEl paciente tenía un extenso historial de enfermedades cardiacas y renales. A los 11 años, se le diagnosticó estenosis congénita de la válvula pulmonar, por lo que se le practicó una valvulotomía. Más adelante, desarrolló fibrilación auricular y aleteo auricular, que no toleró bien y para los que se intentó, sin éxito, la ablación del aleteo. Como el paciente seguía teniendo síntomas, se le practicó una ablación del nódulo auriculoventricular con colocación de un marcapasos.\nSe inició anticoagulación oral con fenprocoumon debido a una puntuación CHA2DS2-Vasc de 3 (mujer, insuficiencia cardiaca y enfermedad vascular periférica). A la edad de 55 años, se desarrolló una insuficiencia cardiaca derecha manifiesta y la paciente continuó luchando con ascitis y edemas periféricos que requerían múltiples ingresos hospitalarios. Además, también desarrolló un problema de efusiones pleurales transudativas recurrentes de etiología poco clara.\nLa ecocardiografía en ese momento mostró una severa regurgitación pulmonar y tricuspídea con un ventrículo derecho moderadamente dilatado y una aurícula derecha. El ventrículo izquierdo estaba ligeramente dilatado con una regurgitación mitral moderada. El cateterismo cardiaco derecho demostró presiones arteriales pulmonares de 74/30 mmHg con una presión venosa central de 28 mmHg. Se colocó un homotransplante pulmonar cuando el paciente tenía 57 años y se realizó una anuloplastia tricuspídea concomitante. A pesar de una presión venosa central más baja de 13 mmHg, el paciente seguía siendo readmitido varias veces por signos y síntomas de insuficiencia cardiaca derecha. La congestión venosa sistémica persistente finalmente dio lugar a una enfermedad renal en fase terminal para la que se inició una terapia de reemplazo renal a través de hemodiálisis intermitente. El caso se complicó por hemorragias gastrointestinales graves recurrentes, que requerían transfusiones de sangre frecuentes con hasta 60 unidades de glóbulos rojos por año. A pesar de esto, en combinación con la sustitución intravenosa de hierro, los niveles de hemoglobina variaron entre 5.3-8.8 g/dL. Debido a estos problemas de sangrado intratables, la anticoagulación oral con fenprocoumon se detuvo a la edad de 59 años.\nUna gastroscopia mostró una gastropatía erosiva con una mucosa difusa congestiva y friable. Como prevención de primera línea de las hemorragias gástricas recurrentes en el marco de la cirrosis, se inició el propranolol a una dosis de 5 mg por vía oral dos veces al día (el paciente no toleró una dosificación superior debido a la presión arterial baja). Además, se realizó una coagulación endoscópica de un angioma fúndico y un recorte de una lesión de Dieulafoy.\nSe creía que estas lesiones eran causadas por una gastropatía hipertensiva. Sin embargo, las hemorragias intractables persistieron.\nEl gradiente de presión venosa hepática se midió a 16 mmHg (27 mmHg-11 mmHg). Aunque hubo cierta reticencia debido al temor de empeorar la insuficiencia cardiaca derecha, se tomó la decisión de crear un TIPS. El procedimiento fue sin incidentes. Después de la colocación del TIPS, el gradiente de presión venosa hepática disminuyó a 4 mmHg (14 mmHg-10 mmHg). Por lo tanto, aunque el TIPS redujo considerablemente el gradiente venoso hepático, la presión portal se mantuvo alta debido a la elevada presión venosa central.\nDespués de la colocación del TIPS, el paciente desarrolló signos de encefalopatía hepática y se midieron niveles de amoniaco de 77 umol/L. Se inició el tratamiento con lactulosa oral y enemas, con poca mejora. En ese momento, se produjo otro episodio de sangrado gástrico.\nLa ecografía abdominal mostró buena permeabilidad del TIPS con flujo Doppler normal. Se detectó sangrado gástrico de una úlcera antral con endoscopia, a pesar de que la hiperemia gástrica disminuyó visualmente en comparación con la situación antes del TIPS. Se realizó una biopsia que mostró una mucosa foveolar edematosa, lo que sugiere isquemia de la mucosa. El sangrado fue demasiado difuso para una ligadura endoscópica adicional. No se encontró empeoramiento de la función hepática en los resultados de laboratorio, con el índice internacional normalizado 1.01 en este momento. La ecocardiografía no mostró cambios significativos en comparación con la situación antes de la colocación del TIPS. El ventrículo derecho permaneció moderadamente dilatado con una función longitudinal deficiente y una regurgitación tricuspídea severa persistente. Sin embargo, el estado general del paciente se deterioró y se desarrolló fiebre con consolidaciones pulmonares bilaterales.\nSe produjo una falla multiorgánica y, en ese momento, la familia del paciente decidió retirar el tratamiento. El paciente falleció finalmente 43 días después del procedimiento TIPS.\n\nMH - Resultado fatal\nMH - Mujer\nMH - Insuficiencia cardiaca/*complicaciones/fisiopatología\nMH - Encefalopatía hepática/etiología\nMH - Humanos\nMH - Hipertensión, Portal/etiología/fisiopatología/*cirugía\nMH - Cirrosis hepática/*complicaciones\nMH - Edad Media\nMH - Presión del portal\nMH - *Derivación portosistémica, intrahepática transyugular\nMH - Fracaso del tratamiento\n",
+        "gold_summary": "Una mujer de 60 años con antecedentes de estenosis congénita de la válvula pulmonar desarrolló insuficiencia cardíaca derecha, cirrosis hepática y enfermedad renal en fase terminal que requería terapia de reemplazo renal. La cirrosis hepática se complicó con hipertensión portal, lo que provocó hemorragias gastrointestinales intratables a pesar del tratamiento óptimo con betabloqueantes y la ligadura endoscópica de la banda. Debido al temor de que empeorara la insuficiencia cardíaca derecha, inicialmente se rechazó la colocación de una derivación intrahepática transyugular (TIPS). Sin embargo, como los problemas de hemorragia intratables persistieron y causaron grandes necesidades de transfusión, la TIPS se realizó finalmente como un procedimiento de rescate. Aunque la TIPS redujo con éxito el gradiente de presión venosa hepática de 16 mmHg a 4 mmHg, la presión portal se mantuvo alta a 14 mmHg debido a la persistencia de la insuficiencia cardíaca derecha con presión venosa central elevada. La encefalopatía hepática se desarrolló poco después de la colocación de la TIPS y culminó en una falla multiorgánica después de otro episodio de hemorragia gastrointestinal. En este punto, la familia del paciente decidió retirar la atención y el paciente falleció posteriormente.\n",
+        "synthetic_summary": {
+            "B1": "Esta es la historia de una mujer de 60 años con muchos problemas de salud. Desde niña tuvo un problema de la válvula del corazón. Con los años su corazón derecho dejó de funcionar bien. Por eso tuvo líquido en el vientre y en las piernas. También tuvo daño en el hígado (llamado cirrosis) y los riñones dejaron de funcionar, por lo que necesitaba diálisis.\n\nTenía hemorragias del estómago que no podían detenerse. Recibió muchas transfusiones de sangre. Los médicos probaron medicinas y tratamientos por endoscopia, pero las hemorragias siguieron.\n\nComo último intento, le hicieron un TIPS. Eso es poner un pequeño tubo dentro del hígado para bajar la presión en las venas del hígado. El tubo bajó la presión dentro del hígado, pero la presión en todo su cuerpo seguía alta porque su corazón derecho seguía muy enfermo.\n\nDespués del TIPS empezó a confundirse por problemas del hígado (encefalopatía hepática). Siguió sangrando y su salud empeoró. Tuvo fiebre y problemas en los pulmones y varios órganos empezaron a fallar. La familia decidió dejar de tratarla y ella murió 43 días después del procedimiento.\n\nEs una historia triste. Los médicos intentaron muchos tratamientos, pero no pudieron salvarla.",
+            "B2": "Summary (clear, kind, upper‑intermediate level)\n\nA 60‑year‑old woman with a long history of heart problems (including a narrow pulmonary valve from birth and later severe right‑sided heart failure) developed liver disease (cirrhosis) and kidney failure that needed dialysis. Because of the liver damage she had portal hypertension — high blood pressure in the veins that go into the liver — which caused repeated, hard‑to‑stop stomach and gut bleeding. Despite medicines to lower portal pressure (a beta‑blocker) and endoscopic treatments (procedures inside the stomach), the bleeding continued and she needed many blood transfusions.\n\nDoctors were worried that creating a TIPS (a transjugular intrahepatic portosystemic shunt — a small tube placed through the liver to lower portal pressure) might make her right heart failure worse. But because the bleeding was life‑threatening, they performed TIPS as a last‑rescue option. The procedure worked to lower the measured pressure difference in the liver (from 16 mmHg to 4 mmHg), but the overall portal pressure stayed high because her central venous pressure (the pressure returned to the heart) remained elevated from the bad right heart function.\n\nAfter TIPS she developed hepatic encephalopathy — a brain problem caused by the liver not removing toxins (her blood ammonia was high) — and had another major stomach bleed. Imaging showed the TIPS was open and working. A stomach biopsy suggested that the stomach lining had areas of poor blood supply (ischemia). Her heart scans did not show big new changes, but she got worse overall, developed fever and lung problems, and then multiorgan failure.\n\nGiven the poor outlook, the family chose to stop life‑support treatments, and she died 43 days after the TIPS procedure.\n\nKey points and explanations\n- Portal hypertension: high pressure in the liver’s blood vessels that can cause dangerous bleeding from the stomach or esophagus.  \n- TIPS: a tube placed inside the liver to lower that pressure; it can stop bleeding but may cause or worsen brain symptoms (encephalopathy) and can increase the load on a weak heart.  \n- In this case, TIPS lowered liver pressure measures but could not fix high portal pressure because the patient’s failing right heart kept central venous pressure high.  \n- Outcome: despite treatment, complications (encephalopathy, recurrent bleeding, infection, organ failure) led to death.\n\nThis case shows how complex decisions can be when severe liver disease and severe heart disease exist together: treatments that help one problem can make the other worse. The medical team tried several options, but the combined illnesses led to a poor outcome. My condolences to the patient’s family.",
+            "B3": "Resumen clínico (lectores universitarios)\n\nPaciente: mujer de 60 años con historia larga de cardiopatía congénita (estenosis pulmonar), arritmias (fibrilación y aleteo auricular tratadas con ablación del nódulo y marcapasos), insuficiencia cardíaca derecha progresiva y enfermedad renal crónica que evolucionó a insuficiencia renal terminal en hemodiálisis.\n\nProblema principal: cirrosis hepática por congestión venosa crónica (congestive hepatopathy) con hipertensión portal y hemorragias gastrointestinales recurrentes e intratables que requirieron transfusiones masivas.\n\nHallazgos relevantes\n- Laboratorio hepático: patrón colestático (ALP 388 U/L y GGT 291 U/L muy elevadas); ALT y AST solo ligeramente aumentadas. Albúmina baja (24 g/L). Bilirrubinas totales y directas, recuentos de plaquetas y leucocitos e INR estaban dentro de límites normales o apenas alterados, lo que sugiere función sintética hepática relativamente conservada a pesar de la congestión.\n- Hemodinámica: gradiente de presión venosa hepática (HVPG) de 16 mmHg antes del procedimiento; presión venosa central (PVC) crónicamente elevada por insuficiencia cardíaca derecha.\n- Clínica endoscópica: gastropatía congestiva difusa, lesión tipo Dieulafoy y úlceras antrales isquémicas; los sangrados fueron difusos y difíciles de controlar endoscópicamente.\n- Intervenciones previas: beta‑bloqueo (propranolol a baja dosis por hipotensión), múltiples tratamientos endoscópicos; anticoagulación oral suspendida por sangrados masivos.\n\nDecisión terapéutica y evolución\n- Se decidió implantar una derivación portosistémica intrahepática transyugular (TIPS) como última opción para reducir el riesgo hemorrágico. Riesgo teórico de empeoramiento de la insuficiencia cardíaca derecha motivó inicialmente reticencia.\n- Resultado hemodinámico: el TIPS redujo el HVPG de 16 a 4 mmHg, pero la presión portal absoluta se mantuvo elevada (≈14 mmHg) debido a la PVC alta persistente por la insuficiencia cardíaca derecha. Es decir, el gradiente hepático mejoró, pero la presión portal no se normalizó por el fallo cardíaco coexistente.\n- Complicaciones post‑procedimiento: el paciente desarrolló encefalopatía hepática (amonio 77 μmol/L) con respuesta clínica limitada a lactulosa y enemas. Persistió sangrado gástrico por úlceras antrales con cambios mucosos de tipo isquémico. Posteriormente se añadieron fiebre y consolidaciones pulmonares, progresión a fallo multiorgánico y, tras decisión familiar de retirar el soporte, falleció 43 días después del TIPS.\n\nInterpretación y lecciones clínicas\n- Este caso ilustra una forma de cirrosis secundaria a congestión venosa por insuficiencia cardíaca derecha, en la que la hipertensión portal tiene un componente prehepático/poshepático por PVC elevada. En tales pacientes, un TIPS puede reducir el gradiente portal pero no normalizar la presión portal si la presión venosa central sigue alta.\n- El TIPS conlleva riesgo de encefalopatía hepática y puede ofrecer beneficio limitado cuando la causa principal de la hipertensión portal es la insuficiencia cardíaca. Por ello, la selección de candidatos debe ser muy cuidadosa y multidisciplinaria (hepatología, cardiología y radiología intervencionista).\n- En pacientes similares, las alternativas o medidas complementarias a valorar incluyen optimización del estado cardíaco antes del TIPS, tratamiento dirigido de focos hemorrágicos localizados cuando sea posible, y planificación anticipada sobre riesgos de encefalopatía y manejo de infecciones nosocomiales.\n\nCierre\nSe trata de un caso complejo en el que la coexistencia de insuficiencia cardíaca derecha avanzada, hipertensión portal y sangrado digestivo masivo limitó las opciones terapéuticas y contribuyó a un desenlace fatal. La situación subraya la necesidad de evaluación individualizada y coordinación estrecha entre especialidades frente a decisiones invasivas como el TIPS. Mi más sentido pésame por el resultado adverso."
+        }
+    },
+    {
+        "article": "Una mujer tailandesa de 62 años presentó pérdida visual bilateral súbita y cefalea durante 5 días. Negó antecedentes de traumatismo craneal. Su historia clínica era significativa por presentar hipertensión mal controlada.\n\nLos signos vitales fueron normales, excepto por la presión arterial de 200/105 mmHg. La agudeza visual fue de no percepción de luz (NLP) con pupilas fijas en ambos ojos. La motilidad ocular de ambos ojos fue limitada en todas las direcciones. Ambas párpados fueron difíciles de abrir. Las medidas del exoftalmómetro de Hertel fueron de 16 mm en el ojo derecho y 14 mm en el ojo izquierdo. Había quemosis significativa y vasos de sacacorchos episclerales en ambos ojos. Ambas córneas mostraron un edema estromal leve y difuso sin infiltración. Las cámaras anteriores fueron profundas y tranquilas en ambos ojos. Las presiones intraoculares fueron de 45 mmHg y 48 mmHg en los ojos derecho e izquierdo, respectivamente. La gonioscopia reveló sangre en el canal de Schlemm en el ángulo nasal del ojo derecho. El examen del fondo de ojo mostró venas de la retina ligeramente dilatadas y tortuosas con discos ópticos de apariencia normal en ambos ojos. La relación taza-disco fue de 0.3 bilateralmente. La tomografía de coherencia óptica demostró un espesor normal de la mácula en cada ojo. No hubo ruido audible. Otros exámenes neurológicos fueron normales.\n\nLa resonancia magnética (MRI) con gadolinio del cerebro y las órbitas demostró la dilatación de las venas oftálmicas superiores bilaterales (SOVs) y un grado marcado de congestión orbital y periorbital bilateralmente. Sin embargo, no se observó ni compresión ni estiramiento de los nervios ópticos bilaterales. Es interesante destacar que la restricción de la difusión, con la correspondiente reducción del coeficiente de difusión aparente (ADC), en todo el segmento orbital de los nervios ópticos bilateralmente se reveló en la resonancia magnética ponderada en difusión (DWI). Esto es consistente con el PION bilateral. La angiografía por resonancia magnética (MRA) del cerebro y las órbitas reveló arterialización de los senos cavernosos bilaterales y de las SOVs.\n\nLa angiografía cerebral confirmó el diagnóstico de CCF durales bilaterales de drenaje anterior. La CCF dural derecha se alimentaba de las ramas durales de la ICA (tronco meningo-hipofisario derecho). La CCF dural izquierda se alimentaba de las ramas durales de la ECA (arteria meningo-hipofisaria izquierda y la arteria izquierda del foramen redondo y las ramas durales de la ICA (tronco meningo-hipofisario izquierdo). Cada lado de la CCF dural contribuía con flujo sanguíneo arterial a los SOV bilaterales (SOV contralateral a través de la comunicación inter-cavernosa). No se observó reflujo venoso cortical del flujo sanguíneo arterial. Basándose en estos hallazgos, se realizó una embolización transvenosa de la bobina. Los senos cavernosos bilaterales se embolizaron utilizando bobinas para ocluir los vasos de alimentación de las ramas durales de la ICA y la ECA. La angiografía cerebral inmediata posterior a la embolización mostró el cierre completo de las fístulas.\n\nTres meses después de la embolización, el examen oftálmico demostró una mejora progresiva de los signos oftálmicos antes mencionados; no obstante, la agudeza visual del paciente se mantuvo en NLP en ambos ojos.\n",
+        "gold_summary": "Reportamos el caso de una mujer de 62 años de edad con antecedentes de hipertensión arterial mal controlada que presentó pérdida visual bilateral súbita y cefalea durante 5 días. Negó antecedentes de traumatismo craneal. En el examen, sus agudezas visuales eran de no percepción de luz (NLP) con pupilas fijas en ambos ojos. La motilidad ocular de ambos ojos era limitada en todas las direcciones. Era difícil abrir ambos párpados. El examen del segmento anterior reveló quemosis bilateral y vasos del sacacorchos episclerales. La presión intraocular era de 45 y 48 mmHg en los ojos derecho e izquierdo, respectivamente. La gonioscopia reveló sangre en el canal de Schlemm en el ángulo nasal del ojo derecho. El examen del fondo de ojo mostró venas retinianas ligeramente dilatadas y tortuosas con discos ópticos de apariencia normal en ambos ojos. Las relaciones entre la copa y el disco eran de 0,3 bilateralmente. Otros exámenes neurológicos no presentaron anormalidades. La resonancia magnética demostró dilatación de las venas oftálmicas superiores bilaterales (SOV) y congestión orbital y periorbital bilateral marcada. Sin embargo, no hubo compresión o estiramiento de los nervios ópticos bilaterales. Se reveló una restricción de la difusión en la difusión ponderada por la difusión, con la correspondiente reducción del coeficiente de difusión aparente, en todo el segmento orbital bilateral de los nervios ópticos, consistente con PION bilateral. La angiografía por resonancia magnética reveló arterialización de los senos cavernosos bilaterales y las SOV. La angiografía cerebral confirmó el diagnóstico de CCF bilaterales de drenaje anterior. El tratamiento con embolización de bobina transvenosa fue exitoso. Tres meses después de la embolización, el examen oftálmico demostró una mejora progresiva de los signos oftálmicos antes mencionados; sin embargo, sus agudezas visuales permanecieron como NLP en ambos ojos.\n",
+        "synthetic_summary": {
+            "B1": "Había una mujer de 62 años que tenía la presión arterial alta y mal controlada. Un día empezó con dolor de cabeza y, en cinco días, dejó de ver con los dos ojos. No tuvo golpe en la cabeza.\n\nCuando la vieron en el hospital no veía nada en ninguno de los dos ojos. Sus pupilas no reaccionaban y los ojos casi no se podían mover. Tenía los párpados hinchados y costaba abrirlos. Los ojos estaban enrojecidos y con venas muy marcadas. La presión dentro de los ojos estaba muy alta. En uno de los ojos se encontró sangre en un canal del ángulo del ojo.\n\nLas partes que se miran dentro del ojo, como el disco del nervio óptico y la mácula, parecían normales en las pruebas. Pero en la resonancia magnética se vieron venas muy agrandadas detrás de los ojos y mucho hinchazón alrededor. También se vio que las señales del nervio que lleva la vista estaban dañadas por falta de riego. Esto significa que el nervio quedó herido por no recibir suficiente sangre. Los médicos llamaron a eso PION, que es un daño del nervio óptico por falta de sangre.\n\nLa causa fue una conexión anormal entre arterias y venas cerca de los ojos, llamada fístula carotídeo-cavernosa. Esa conexión hacía que llegara demasiada sangre a las venas de los ojos. Los médicos confirmaron esto con una angiografía, que es una prueba que mira los vasos.\n\nPara arreglarlo, los médicos metieron pequeñas bobinas por dentro de las venas para cerrar esas conexiones malas. Inmediatamente después, las pruebas mostraron que las fístulas se habían cerrado.\n\nTres meses después, la hinchazón y el enrojecimiento de los ojos mejoraron. Pero, aunque los ojos se veían mejor, la mujer no recuperó la visión y seguía sin poder ver nada con ninguno de los dos ojos.\n\nEn resumen: una fístula cerca del ojo causó hinchazón y daño al nervio de la vista. Los médicos la cerraron con un tratamiento que funcionó para parar el flujo malo, pero el daño al nervio ya era muy grande y la persona no recuperó la vista.",
+            "B2": "Resumen corto y claro (nivel B2, para lectores de secundaria)\n\nUna mujer tailandesa de 62 años con hipertensión arterial mal controlada acudió por una pérdida súbita de visión en ambos ojos y cefalea durante 5 días. No había sufrido traumatismo. En la consulta tenía presión arterial alta (200/105 mmHg). Su visión era “no percepción de luz” (NLP) en los dos ojos, es decir, no podía ver nada ni siquiera luz. Las pupilas estaban fijas, los movimientos oculares muy limitados y le costaba abrir los párpados.\n\nEn el examen de los ojos se vieron signos de congestión venosa: quemosis (hinchazón de la conjuntiva), vasos en “sacacorchos” (muy tortuosos) y leve edema de la córnea. La presión dentro de los ojos era muy alta (45 y 48 mmHg; valores normales están por debajo de 21 mmHg). Al mirar dentro del ojo, los vasos de la retina estaban algo dilatados y tortuosos, pero los discos ópticos parecían normales. Una tomografía (OCT) mostró máculas de grosor normal.\n\nLa resonancia magnética con contraste mostró venas oftálmicas superiores muy dilatadas y congestión marcada alrededor de las órbitas (la zona del ojo). En la resonancia de difusión se vio que toda la parte orbital de los nervios ópticos tenía “restricción de difusión” con reducción del ADC; esto indica lesión por falta de riego y es compatible con una neuropatía óptica isquémica posterior (PION). La angiografía por RM mostró “arterialización” de los senos cavernosos y de las venas oftálmicas, lo que sugería un flujo arterial anormal hacia las venas.\n\nLa angiografía cerebral confirmó la causa: fístulas carótido-cavernosas durales bilaterales (CCF) con drenaje hacia adelante. Una fístula carótido-cavernosa es una conexión anormal entre arterias y el seno cavernoso (una vena grande en la base del cráneo); eso pone mucha presión en las venas del ojo y produce los signos que se vieron. Cada fístula recibía sangre de ramas arteriales diferentes y ambas aportaban flujo a las venas oftálmicas. No había reflujo hacia las venas corticales del cerebro.\n\nSe trató realizando una embolización transvenosa con bobinas: mediante catéteres se colocaron bobinas dentro de los senos cavernosos para cerrar las fístulas. La angiografía inmediatamente después mostró cierre completo de las comunicaciones anormales. Tres meses tras el procedimiento, muchos signos en los ojos (hinchazón, congestión) habían mejorado, pero la visión no se recuperó y seguía siendo NLP en ambos ojos.\n\nComentarios prácticos y tono cuidadoso\n- El daño observado en la resonancia (PION) explica por qué la visión no volvió: hubo falta de riego y lesión del segmento orbital de los nervios ópticos, y ese daño suele ser irreversible.  \n- El tratamiento endovascular cerró la fístula y mejoró la congestión ocular, lo que fue positivo para la salud ocular general y para evitar más daño.  \n- En casos similares es importante controlar factores de riesgo (como la hipertensión) y buscar atención urgente ante cambios visuales repentinos. También puede necesitarse apoyo de rehabilitación visual si la pérdida es permanente.\n\nEste resumen describe los hallazgos y el tratamiento del caso de forma sencilla y respetuosa. Si quieres, puedo explicar con dibujos o comparar las estructuras implicadas para entender mejor cómo una fístula afecta al ojo.",
+            "B3": "Resumen clínico (nivel universitario, sensible y claro)\n\nPresentación y antecedentes\n- Paciente: mujer tailandesa de 62 años con hipertensión mal controlada.\n- Síntomas: pérdida visual súbita en ambos ojos y cefalea durante 5 días. Niega traumatismo craneal.\n- Signos vitales relevantes: presión arterial 200/105 mmHg.\n\nExploración oftalmológica (hallazgos anormales principales)\n- Agudeza visual: no percepción de luz (NLP) en ambos ojos — pérdida visual completa.\n- Pupilas fijas y motilidad ocular limitada en todas las direcciones; apertura palpebral dificultosa.\n- Quemosis (hinchazón de la conjuntiva) bilateral y vasos episclerales en “sacacorchos” (tortuosos).\n- Exoftalometría (Hertel): 16 mm OD, 14 mm OI (ligera protrusión derecha).\n- Presiones intraoculares muy elevadas: 45 mmHg (OD) y 48 mmHg (OI) — (normal ≈ 10–21 mmHg).\n- Gonioscopia: sangre en el canal de Schlemm en el ángulo nasal derecho (signo de hipertensión venosa ocular).\n- Fondo de ojo: venas retinianas levemente dilatadas/tortuosas; discos ópticos con aspecto normal (copa/disco 0,3 bilaterales).\n- Otros exámenes neurológicos normales.\n\nImágenes e interpretación (cómo se llegó al diagnóstico)\n- Resonancia magnética (RM) orbitarias con gadolinio: dilatación de las venas oftálmicas superiores bilaterales (SOV) y congestión orbital/periorbital marcada. No hubo compresión ni estiramiento visible de los nervios ópticos.\n- RM ponderada en difusión (DWI) con descenso del coeficiente de difusión aparente (ADC) en todo el segmento orbital de ambos nervios ópticos → compatible con neuropatía óptica isquémica posterior bilateral (PION), es decir, lesión por falta de riego en la porción posterior del nervio óptico.\n- Angio-RM: “arterialización” de los senos cavernosos bilaterales y de las SOVs (indica paso anormal de sangre arterial a las venas).\n- Angiografía cerebral: confirmó fístulas carotídeo-cavernosas (CCF) durales bilaterales con drenaje anterior. Las fístulas estaban alimentadas por ramas durales de la arteria carótida interna (ICA) y de la arteria carótida externa (ECA); había comunicación inter-cavernosa que permitía arterializar ambas SOVs. No se observó reflujo venoso cortical (lo que reduce, pero no elimina, otros riesgos neurológicos).\n\nDiagnóstico final\n- CCF durales bilaterales con drenaje anterior que causaron congestión venosa orbital intensa y elevación marcada de la presión intraocular, y PION bilateral que explica la ceguera aguda.\n\nTratamiento y evolución\n- Se realizó embolización transvenosa con bobinas de los senos cavernosos bilaterales para ocluir las ramas durales suministradoras (ICA y ECA). La angiografía inmediatamente posterior mostró cierre completo de las fístulas.\n- A los 3 meses: mejora progresiva de los signos externos oculares (quemosis, congestión, vascularización episcleral), pero la agudeza visual permaneció NLP en ambos ojos. Esto sugiere que la lesión isquémica del nervio óptico fue irreversible a pesar del cierre exitoso de las fístulas.\n\nImplicaciones clínicas y recomendaciones (qué significa y qué seguir)\n- Etiología y riesgo: las CCF durales pueden aparecer sin traumatismo y en pacientes con factores vasculares (como hipertensión). El drenaje venoso anómalo eleva la presión venosa orbital, aumentando la presión intraocular y el riesgo de isquemia del nervio óptico.\n- Importancia del diagnóstico precoz: cuanto antes se trate la fístula, mayor la probabilidad de prevenir daño isquémico irreversible. Sin embargo, si ya hay PION establecida, la recuperación visual puede no ser posible.\n- Seguimiento y manejo: control estricto de la presión arterial, control de la presión intraocular y vigilancia de complicaciones oculares y neurológicas. Evaluación para rehabilitación visual y apoyo psicosocial dada la ceguera bilateral persistente.\n- Consejos al equipo tratante: documentar función residual, ofrecer baja visión/rehabilitación, controlar factores de riesgo cardiovascular y planear seguimiento a largo plazo de la anatomía vascular mediante imágenes si hubiera síntomas nuevos.\n\nComentario empático final\nEste caso muestra cómo una fístula carotídeo-cavernosa dural puede producir una congestión orbital severa y daño isquémico del nervio óptico a pesar de un tratamiento endovascular exitoso. Lamentablemente, la lesión establecida en los nervios ópticos llevó a una ceguera permanente; sin embargo, el cierre de la fístula redujo la congestión y evitará probablemente nuevas complicaciones. Es importante ofrecer a la paciente apoyo multidisciplinario (cardiovascular, oftalmológico y de rehabilitación visual) y manejo riguroso de la hipertensión para prevenir futuras crisis."
+        }
+    },
+    {
+        "article": "Un paciente de 15 años de edad (altura = 161 cm; peso = 66 kg; superficie corporal = 1,70; grupo sanguíneo = B positivo) con cardiomiopatía dilatada fue derivado a la Universidad de Ankara con pérdida de conciencia y shock cardiogénico en julio de 2016. El apoyo de oxigenación de membrana extracorpórea venosa arterial se realizó aproximadamente 1 semana después. Su fracción de eyección ventricular izquierda fue del 22%. Ocho días después, el paciente recibió un implante de corazón artificial total SynCardia (50 ml; SynCardia Systems, Inc., Tucson, AZ, EE. UU.). En el día 131 postoperatorio después de la cirugía TAH, el paciente se quejó de pérdida de audición bilateral y fue derivado al departamento de oído, nariz y garganta.\n\nLos antecedentes médicos previos no revelaron evidencia de pérdida auditiva, antecedentes familiares de sordera o cualquier anomalía adicional en su niñez. Sus registros médicos no revelaron evidencia de meningitis. Sin embargo, había recibido amikacina (15 mg/kg), un antibiótico ototóxico, contra patógenos gramnegativos importantes durante su estancia en la unidad de cuidados intensivos. El paciente fue incluido en la lista de espera de trasplantes de corazón de alta urgencia y era móvil en el Freedom Driver portátil (SynCardia).\n\nEl examen otoscópico del paciente fue normal. La audiometría de tonos puros y la respuesta auditiva del tronco encefálico revelaron una pérdida auditiva profunda bilateral. La timpanometría mostró timpanogramas normales de tipo A bilaterales. Tanto la tomografía computarizada como la resonancia magnética confirmaron la morfología normal del laberinto y nervios cocleares intactos.\n\nFue examinado por un equipo multidisciplinario (cirugía cardiovascular, cuidados intensivos pediátricos, cardiología pediátrica, psiquiatría de consulta y enlace, fisioterapia y rehabilitación, enfermedades infecciosas y microbiología clínica, anestesiología, audiología y otorrinolaringología) para realizar un implante coclear. Después de analizar las posibles opciones con el paciente y sus padres, se decidió que se beneficiaría de un implante coclear debido a la pérdida auditiva y la reducción de la función cognitiva y la adaptación necesaria para el trasplante de corazón. Después de analizar su caso con el equipo multidisciplinario, se decidió un implante coclear del lado derecho (Nucleus CI24RE con Contour Advance Electrode; Cochlear, Macquarie University, Australia).\n\nEl paciente tomaba warfarina (10 mg/día), que se interrumpió tres días antes de la cirugía, y se inició la heparinización (dosis de carga de 50 U/kg y dosis de mantenimiento de 20 U/kg/h) cuando el tiempo de protrombina (cociente internacional normalizado [INR]) era inferior a 1,5. Dos horas antes de la cirugía, se interrumpió la heparinización. En el quirófano, se disponía de un dispositivo de reserva para un posible fallo del dispositivo TAH. El equipo de anestesia y el perfusionista controlaron de cerca los resultados del flujo para el TAH. El flujo sanguíneo no pulsátil afecta de forma negativa al control de los signos vitales, y la presión arterial no invasiva no fue suficiente en nuestro paciente. Bajo anestesia local, se realizó un cateterismo radial arterial invasivo. Además, se dejó la vena yugular interna izquierda en su lugar, lo que permitió el control de la presión venosa central y su uso como reemplazo de fluidos de gran volumen cuando fue necesario. Después de iniciar el control, se administraron con precaución 2 mg/kg de propofol, 1 mg/kg de bromuro de rocuronio y 1 µg/kg de fentanilo, y se intubió al paciente por vía oral. Se utilizó sevoflurano con una concentración alveolar mínima de 1 a 1,5 en oxígeno al 40 % para el mantenimiento. El óxido nítrico inhalado también estaba listo para usarse en caso de una posible crisis hipertensiva pulmonar.\n\nEl día 250 después del implante TAH, se realizó la cirugía de implante coclear con abordaje de ventana redonda sin complicaciones perioperatorias; el paciente tuvo una pérdida de sangre mínima (solo 50 ml). La duración de la operación fue de 120 minutos. El paciente fue extubado en el quirófano sin problemas circulatorios y respiratorios. La heparinización se inició a la hora 6 posoperatoria. Comenzamos con la warfarina el día 1 posoperatorio, y la heparinización se detuvo después de alcanzar un INR de 2.0. No se observaron complicaciones (infecciones, hematoma) en el seguimiento posoperatorio.\n\nEl implante coclear se activó en la semana 4 después de la operación. El equipo de audiología lo revisó 4 y 8 semanas después; mostró una mejora continua en su audición, con impedancias normales. Sus resultados de percepción del habla mejoraron significativamente 3 meses después del implante coclear.\n\nMH - Adolescente\nMH - Niño\nMH - *Implantación coclear\nMH - *Insuficiencia cardiaca/diagnóstico/etiología/cirugía\nMH - *Efectos adversos del trasplante de corazón\nMH - *Corazón, Artificial\nMH - Humanos\nMH - Hombre\nMH - Resultado del tratamiento\n",
+        "gold_summary": "Describimos el caso de un niño de 15 años con pérdida auditiva total bilateral postlingual tras la administración de medicamentos ototóxicos durante su estancia en la unidad de cuidados intensivos pediátricos. El paciente recibió el implante de corazón artificial total SynCardia (50 ml; SynCardia Systems, Inc., Tucson, AZ, EE. UU.) para la insuficiencia cardiaca biventricular en fase terminal como puente para el trasplante cardiaco. Durante su estancia en la lista de espera de trasplantes cardiacos urgentes, se sometió a una implantación coclear satisfactoria tras optimizar el estado de coagulación y hemostasis y una preparación anestésica adecuada.\n",
+        "synthetic_summary": {
+            "B1": "Un chico de 15 años tenía el corazón muy débil. Le pusieron un corazón artificial para ayudarle mientras esperaba un trasplante. Después de estar en la unidad de cuidados intensivos, dejó de oír en los dos oídos. Los médicos creyeron que fue por un antibiótico que puede dañar el oído.\n\nLas pruebas mostraron que la parte del oído y el nervio estaban bien, pero él tenía pérdida de audición profunda en los dos oídos. Un equipo de muchos médicos decidió ponerle un implante coclear en el oído derecho. Un implante coclear es un pequeño aparato que se coloca en la cabeza para devolver la sensación de sonido.\n\nAntes de la operación, los doctores cambiaron sus medicinas para la sangre con mucho cuidado. La cirugía fue corta y sin problemas. No hubo sangrado ni infección. El implante se activó cuatro semanas después. Con el tiempo, empezó a oír mejor y sus pruebas de habla mejoraron mucho a los tres meses.\n\nLos médicos cuidaron bien todos los pasos. El tratamiento ayudó al joven a recuperar parte de su audición y a prepararse mejor para su trasplante de corazón.",
+            "B2": "Summary:\n\nA 15-year-old boy with severe dilated cardiomyopathy was treated at a university center after losing consciousness and going into cardiogenic shock. He received extracorporeal membrane oxygenation (ECMO) for a week and, because his heart function was very poor (left ventricular ejection fraction 22%), he had a total artificial heart (TAH, a mechanical heart device) implanted eight days later as a bridge to transplant. About four months after the TAH surgery, he noticed sudden, severe hearing loss in both ears.\n\nTests showed profound bilateral sensorineural hearing loss (damage to the inner ear or hearing nerve), while ear anatomy and the cochlear nerves looked normal on CT and MRI. During his intensive care stay he had been given amikacin, an antibiotic that can be ototoxic (it can damage hearing), and this was the likely cause. A multidisciplinary team agreed that a cochlear implant (an electronic device that bypasses the damaged inner ear and stimulates the hearing nerve) would help him—both for communication and to support his care while waiting for a heart transplant. They chose a right-sided implant (Nucleus CI24RE with Contour Advance electrode).\n\nBecause he was taking warfarin (a blood thinner) for the TAH, the team carefully managed his anticoagulation: warfarin was stopped three days before surgery and he was switched to heparin (short-acting anticoagulant), which was paused two hours before the operation. The team used invasive blood-pressure and central venous monitoring during anesthesia to keep the TAH functioning safely. The cochlear implant surgery (round-window approach) was done about 250 days after the TAH implant without complications, with very little blood loss. He was extubated in the operating room and anticoagulation was restarted after surgery; warfarin was resumed on day 1 post-op and heparin stopped once the target INR was reached.\n\nThe implant was activated four weeks later. Follow-up audiology at 4 and 8 weeks showed improving hearing and normal device function, and his speech perception had improved significantly by three months. There were no infections, hematomas, or other complications. Overall, the case shows that, with careful planning and multidisciplinary care, a cochlear implant can be safely and successfully performed in a patient supported by a total artificial heart.",
+            "B3": "Resumen clínico (nivel universitario, lectura clara y empática)\n\nCaso\n- Paciente varón de 15 años con miocardiopatía dilatada e insuficiencia cardíaca biventricular terminal que requirió soporte con oxigenación por membrana extracorpórea y, después, implante de corazón artificial total (TAH SynCardia 50 ml) como puente al trasplante. La fracción de eyección del ventrículo izquierdo era del 22%.\n\nPresentación otológica\n- A los 131 días tras el implante del TAH el paciente refería pérdida auditiva bilateral. No había antecedentes previos de hipoacusia, meningitis ni sordera familiar. Durante su ingreso en la UCI se administró amikacina, un antibiótico con riesgo ototóxico.\n\nHallazgos objetivo\n- Examen otoscópico: normal.\n- Audiometría tonal y potenciales evocados auditivos del tronco cerebral (ABR): pérdida auditiva profunda bilateral (sensorioneural).\n- Timpanometría: curvas tipo A bilaterales (órganos medioauriculares normales).\n- TAC y resonancia magnética: morfología normal del laberinto y nervios cocleares intactos (anatomía favorable para implante coclear).\n- Conclusión clínica: pérdida auditiva postlingual profunda, muy probablemente asociada a ototoxicidad por aminoglucósido (amikacina).\n\nDecisión terapéutica\n- Un equipo multidisciplinario (cardiología, cirugía cardiovascular, cuidados intensivos pediátricos, anestesiología, infectología, ORL/audiología, rehabilitación, psiquiatría, perfusionista) evaluó riesgos y beneficios. Se optó por implante coclear unilateral derecho (Nucleus CI24RE con electrodo Contour Advance) para recuperar audición, mejorar función cognitiva y facilitar la adaptación al eventual trasplante cardíaco.\n\nManejo perioperatorio y anestésico (aspectos clave)\n- Anticoagulación: warfarina (10 mg/día) suspendida 3 días antes; puente con heparina (carga 50 U/kg, mantenimiento 20 U/kg/h) hasta INR < 1,5; heparina detenida 2 h antes de la cirugía; reiniciada 6 h posoperatorias y warfarina reintroducida el día 1 posoperatorio; heparina suspendida al alcanzar INR 2,0.\n- Monitoreo: presión arterial invasiva radial debido a flujo no pulsátil del TAH (la presión no invasiva fue insuficiente); control de presión venosa central mediante catéter yugular existente; perfusionista y equipo de anestesia supervisando flujo y dispositivo TAH; dispositivo de reserva disponible.\n- Anestesia: inducción y mantenimiento con dosis ajustadas de propofol, rocuronio, fentanilo y sevoflurano; óxido nítrico inhalado disponible para crisis hipertensiva pulmonar.\n- Procedimiento: implante por abordaje de ventana redonda sin complicaciones perioperatorias; tiempo quirúrgico 120 minutos; pérdida sanguínea mínima (50 ml). Extubado en quirófano sin problemas respiratorios o circulatorios.\n\nEvolución y resultados\n- Sin complicaciones posoperatorias (sin infección ni hematoma).\n- Activación del implante: semana 4 tras la cirugía.\n- Seguimiento audiológico a las semanas 4 y 8: impedancias normales y mejora progresiva de la audición.\n- Evaluación a los 3 meses: mejora marcada en percepción del habla.\n\nImplicaciones y enseñanzas clave\n- Es factible y seguro realizar implante coclear en pacientes con soporte circulatorio complejo (TAH) si se planifica y coordina cuidadosamente la anticoagulación, el control hemodinámico y el manejo anestésico.\n- La preservación de la anatomía coclear y de la vía auditiva en las pruebas de imagen favoreció el éxito del implante.\n- En pacientes que han recibido aminoglucósidos, debe sospecharse ototoxicidad si aparece disminución auditiva; la intervención temprana con implante coclear puede restaurar comunicación verbal y apoyar la rehabilitación global y la elegibilidad para trasplante.\n- Próximos pasos: rehabilitación audiológica continuada, seguimiento del TAH y del estado para trasplante cardiaco, y vigilancia de la anticoagulación.\n\nTono y enfoque\n- El tratamiento se diseñó teniendo en cuenta la seguridad del dispositivo cardíaco, la prevención de sangrado y trombosis, y el bienestar funcional y cognitivo del adolescente. El resultado funcional inicial fue favorable y supuso una mejora significativa en su comunicación y calidad de vida."
+        }
+    },
+    {
+        "article": "Se encontró a un hombre de 25 años de edad recostado por familiares después de una noche de fiesta, con vómitos, agresión y dolor localizado en la región glútea e inferior derecha. La evaluación inicial en el departamento de urgencias no reveló lesiones traumáticas; sin embargo, el empeoramiento de los síntomas llevó a una nueva evaluación al día siguiente. Los resultados de laboratorio revelaron un recuento sanguíneo completo sin alteraciones, niveles elevados de CPK sérica (42 527 IU/l), creatinina sérica (735 µmol/l), urea (44,3 mmol/l) y potasio (5,7 mmol/l). El análisis de orina reveló orina de color rojo-marrón sin glóbulos rojos, proteinuria (+1), glucosuria (+1) y WBC (9-10/hpf). Estos resultados confirmaron la RM y la IRA. La toxicología estableció la administración de 1796 µg/l de heroína (> 5 veces el nivel basal) sin detección de ninguna otra sustancia. Aunque inicialmente negó haber tomado medicamentos, después del análisis toxicológico, el paciente admitió que había administrado heroína una vez por vía intramuscular en la región glútea derecha la noche del incidente.\n\nUna tomografía computarizada demostró edema muscular glúteo y miositis localizada en la región glútea derecha. Al comenzar el tratamiento convencional con resucitación de fluidos intravenosos (IV), el tratamiento de la IRA fracasó, lo que hizo necesario el TRR con hemodiálisis debido a la progresión de la azotemia con un aumento de la creatinina sérica a 1052 µmol/l. La función renal mejoró tras el cese del TRR con una duración total de la estancia (LOS) de 9 días. El seguimiento posterior del paciente fue incompleto debido a la falta de asistencia.\n",
+        "gold_summary": "Este informe de caso describe a un hombre de 25 años que desarrolló una RM grave y lesión renal aguda (LRA) después de la administración intramuscular (IM) de heroína como usuario por primera vez. El uso de la heroína IM puede inducir niveles más altos de CPK debido a la toxicidad directa de los miocitos y el trauma mecánico. Los músculos glúteos altamente vascularizados con fibras tipo 1 en el sitio de la inyección probablemente exacerbaron la gravedad. Los factores adicionales incluyeron una menor densidad mitocondrial en los hombres y la exposición al alcohol. A pesar de la reanimación agresiva con líquidos, se requirió la terapia de reemplazo renal (RRT) y el paciente respondió bien a la hemodiálisis.\n",
+        "synthetic_summary": {
+            "B1": "Este cuento habla de un hombre de 25 años que se puso muy enfermo después de una noche de fiesta. Él recibió una sola inyección de heroína en el glúteo (la nalga). Al día siguiente tenía vómitos y mucho dolor en esa nalga.\n\nLa inyección dañó los músculos. Cuando los músculos se rompen, meten cosas en la sangre que pueden dañar los riñones. Sus análisis mostraron que tenía daño fuerte en los músculos y que los riñones no funcionaban bien. Los médicos le dieron líquidos por vena, pero sus riñones siguieron empeorando. Por eso necesitó hemodiálisis. La hemodiálisis es una máquina que limpia la sangre cuando los riñones no pueden hacerlo.\n\nDespués de la hemodiálisis y el tratamiento, sus riñones mejoraron. Estuvo en el hospital 9 días y salió después. No se sabe bien cómo siguió porque no volvió a las citas. Esto nos recuerda que inyectar drogas puede causar daño grave y que beber alcohol puede empeorar las cosas.",
+            "B2": "Resumen del caso (nivel escolar, B2)\n\nUn hombre de 25 años fue encontrado por su familia después de una noche de fiesta con vómitos, comportamiento agresivo y dolor en la nalga derecha. Al principio no se vieron heridas graves, pero al empeorar los síntomas volvió al hospital al día siguiente.\n\nQué se encontró\n- Tenía una prueba sanguínea con CPK muy alta (42 527 IU/L). La CPK es una enzima que sube cuando el músculo se destruye; niveles tan altos indican rabdomiólisis, es decir, daño muscular importante.  \n- La creatinina y la urea (marcadores de función renal) estaban muy elevadas: la creatinina llegó a 735 µmol/L y luego subió a 1052 µmol/L. Esto mostró una lesión renal aguda (insuficiencia renal súbita).  \n- La orina era de color rojo-marrón pero sin glóbulos rojos, lo que sugiere que la orina contenía productos del músculo dañado (mioglobina).  \n- La toxina detectada fue heroína en una concentración muy alta; el paciente finalmente admitió que había inyectado heroína por vía intramuscular en la nalga derecha esa noche (era su primer uso así).\n\nImágenes y tratamiento\n- Una tomografía mostró inflamación y edema del músculo glúteo derecho (miositis localizada).  \n- Comenzaron líquidos por vía intravenosa para intentar proteger los riñones, pero la función renal siguió empeorando. Por ello fue necesario aplicar terapia de reemplazo renal (hemodiálisis). Tras ese tratamiento la función renal mejoró y el paciente estuvo 9 días en el hospital. El seguimiento posterior no fue completo porque el paciente dejó de acudir a control.\n\nPor qué pudo pasar esto\n- La inyección intramuscular de heroína puede dañar el músculo de dos maneras: por la propia toxicidad de la sustancia sobre las células musculares y por el trauma mecánico de la aguja y del volumen inyectado.  \n- Los músculos glúteos, por su estructura y vascularización, pudieron favorecer una lesión más intensa en ese sitio.  \n- También se mencionan factores que pueden aumentar el riesgo, como el consumo de alcohol y diferencias biológicas entre hombres y mujeres.\n\nQué significa esto y qué sigue\n- La rabdomiólisis grave puede provocar fallo renal si los productos del músculo dañado llegan al riñón. El tratamiento urgente incluye líquidos y, si no es suficiente, diálisis para reemplazar la función renal temporalmente.  \n- Es importante el seguimiento médico para comprobar la recuperación completa del riñón y recibir apoyo para problemas relacionados con el consumo de drogas.\n\nTono final\nSucedió un daño muscular serio tras una inyección de heroína que terminó afectando los riñones. El tratamiento médico fue efectivo para recuperar la función renal en el hospital, pero el control ambulatorio fue incompleto. Si alguien tiene una situación parecida, debe buscar atención médica urgente y ayuda para el consumo de sustancias.",
+            "B3": "Resumen clínico (nivel lector universitario)\n\nPresentación y hallazgos principales\n- Hombre de 25 años fue encontrado somnoliento después de una noche de fiesta con vómitos, comportamiento agresivo y dolor localizado en la región glútea derecha.\n- La primera evaluación en urgencias no mostró signos de traumatismo externo. Al día siguiente empeoró y se repitió la valoración.\n- Hemograma dentro de límites normales; hallazgos anormales clave: CPK sérica muy elevada (42 527 IU/L), creatinina 735 µmol/L, urea 44,3 mmol/L y potasio 5,7 mmol/L.\n- Orina de color rojo‑marrón sin glóbulos rojos visibles, con proteinuria y glucosuria leves y leucocitos 9–10/campo: esto sugiere mioglobinuria (presencia de mioglobina en orina) secundaria a destrucción muscular, no sangrado urinario.\n- Tomografía mostró edema y miositis en el músculo glúteo derecho.\n\nDiagnóstico y causa probable\n- Se diagnosticó rabdomiólisis (destrucción aguda de músculo esquelético) con lesión renal aguda (LRA) secundaria.\n- La toxicología detectó una concentración elevada de heroína (1 796 µg/L) y el paciente, tras inicialmente negarlo, admitió haberse inyectado heroína intramuscularmente en la región glútea la noche previa. Fue su primer uso por esa vía.\n- La combinación de toxicidad directa sobre los miocitos, trauma mecánico por la inyección y factores locales (glúteo con gran vascularización y cierta composición de fibras musculares) probablemente aumentó la destrucción muscular. Otros factores contribuyentes mencionados fueron sexo masculino y consumo de alcohol.\n\nTratamiento y evolución\n- Se inició reanimación con líquidos IV (tratamiento estándar inicial para rabdomiólisis) pero la función renal no mejoró: la creatinina progresó hasta 1 052 µmol/L.\n- Fue necesario realizar terapia de reemplazo renal (TRR) mediante hemodiálisis. Tras el tratamiento renal la función renal mejoró.\n- Estancia hospitalaria total: 9 días. El seguimiento posterior fue incompleto por falta de asistencia.\n\nImplicaciones clínicas y recomendaciones prácticas\n- La inyección intramuscular de heroína puede provocar rabdomiólisis grave y LRA incluso en usuarios primerizos; por tanto, es importante sospecharlo si hay dolor local intenso, orina oscura y síntomas sistémicos tras consumo o inyección.\n- Signos de alarma que requieren valoración urgente: CPK muy elevada, hiperkalemia, oliguria/anuria, elevación rápida de creatinina o alteraciones ácido‑base.\n- Primeros pasos: hidratación IV agresiva, monitorización estrecha de electrolitos (especialmente potasio), diuresis y función renal; consultar precozmente a nefrología para valorar TRR si la clínica o los valores no responden.\n- También es importante abordar el consumo de sustancias: asesoramiento, programas de reducción de daños y seguimiento para evitar recurrencias y complicaciones a largo plazo.\n\nTono y contexto\n- El caso subraya que una conducta de consumo puntual puede tener consecuencias médicas graves y potencialmente reversibles con tratamiento oportuno. La atención médica temprana y el seguimiento son claves."
+        }
+    },
+    {
+        "article": "Una mujer de 63 años con antecedentes de obesidad e hipertensión arterial acudió a la sala de urgencias de un hospital de nivel secundario con un historial de siete días de fiebre, tos seca, hiposmia y mialgia. Al momento del ingreso, se encontraba alerta, con una frecuencia respiratoria de 22 ciclos por minuto, pulso de 90 latidos por minuto y saturación de oxígeno de 90 %. Los análisis de laboratorio revelaron linfopenia (1,55 x 109) y niveles elevados de proteína C reactiva (10,62 mg/dL). Se realizó una prueba de reacción en cadena de la polimerasa para COVID-19 a partir de un hisopado nasofaríngeo y de la garganta, que resultó positivo para el coronavirus del síndrome respiratorio agudo severo 2 (SARS-CoV-2).\n\nLa situación evolucionó rápidamente con fiebre, postración y empeoramiento de la disnea. La gasometría arterial reveló una insuficiencia respiratoria grave, mientras que la radiografía de tórax evidenció infiltrados pulmonares bilaterales. La paciente fue intubada y sometida a ventilación mecánica, pero su condición respiratoria continuó deteriorándose, a pesar de los mejores cuidados críticos, incluyendo ventilación en posición prona y bloqueo neuromuscular. Su examen de tomografía computarizada del tórax, tras la intubación, reveló extensas opacificaciones multifocales bilaterales en vidrio molido, sin signos de embolia pulmonar. Los ajustes iniciales del ventilador fueron: ventilación controlada por volumen con volumen corriente de 360 ml (6 ml/kg de peso corporal ideal), frecuencia respiratoria de 14 respiraciones por minuto, presión espiratoria positiva final (PEEP) de 14 cmH2O y complacencia estática de 44 cmH2O.\n\nEn el segundo día de internación, la gasometría arterial mostró pH de 7,34, presión parcial de dióxido de carbono (PaCO2) de 53 mmHg, presión parcial de oxígeno (PaO2) de 102 mmHg y bicarbonato (HCO3) de 29,7 mmol/L, con una proporción presión parcial de oxígeno/fracción inspirada de oxígeno (PaO2/FiO2) de 98. Ella cumplía los criterios para indicación de VV-ECMO y fue transferida a la unidad de terapia intensiva (UTI), que disponía de un programa establecido para VV-ECMO. El procedimiento fue realizado con seguridad, no habiendo ocurrido complicaciones. El análisis de la gasometría arterial 3 horas después del inicio de la VV-ECMO mostró pH de 7,386, PaCO2 de 43 mmHg, PaO2 de 94,3 mmHg y HCO3 de 25,4 mmol/L, sin cualquier variación abruta de la PaCO2. Tuvieron inicio la nutrición y la rehabilitación precoces tras la introducción de la VV-ECMO. En el 14º día de internación, la paciente desarrolló neumonía asociada al ventilador causada por Pseudomonas aeruginosa, siendo sometida a 7 días de antibioticoterapia con ceftazidima y vancomicina, con respuesta favorable. En el 20º día de internación, su radiografía del tórax y la complacencia mejoraron, y la paciente fue retirada de la VV-ECMO con éxito tras 455 horas de soporte, siendo traqueostomizada 7 días después. La paciente mantuvo buena función renal durante toda la internación.\n\nEn el día 34 de internación, luego de 7 días de destete de la sedación, con evolución positiva de su cuadro neurológico, ocurrió una crisis epiléptica generalizada limitada, que llevó a la investigación diagnóstica.\n\nInvestigación\nLos análisis de sangre de laboratorio revelaron una disminución de los niveles de proteína C reactiva (6,11 mg/dL), procalcitonina (0,07 ng/mL), fibrinógeno (307 ng/mL) y ferritina (2802 ng/mL), pero un aumento en los niveles de dímero D (18021 ng/mL) e interleucina 6 (10,4 pg/mL) en el día anterior al inicio de los síntomas. No se asoció ninguno de los fármacos administrados a la paciente con el SEPR, es decir, fármacos inmunosupresores, inmunomoduladores y quimioterápicos.\n\nSe realizó una resonancia magnética (RM) del cerebro y las imágenes de recuperación de inversión atenuada por fluidos (FLAIR) demostraron una hiperintensidad simétrica y confluente que afectaba a la sustancia blanca justa y subcortical, principalmente en las regiones occipital y parietal, pero también en la región frontal, temporal y cerebelosa izquierda. Los núcleos grises profundos se conservaron y no había presencia de ninguna área con restricción del contraste. Las imágenes ponderadas por susceptibilidad mostraron múltiples microhemorragias puntiformes que afectaban a la sustancia blanca superficial y profunda, pero que no afectaban al área con hiperintensidad en FLAIR. Las microhemorragias puntiformes involucraban predominantemente a la sustancia blanca justacortical y al cuerpo calloso (especialmente el codo y el esplenio). Además, había tres hemorragias subagudas de menos de 1 cm en las cápsulas externas, con hiperintensidad en T1.\n\nLa muestra de líquido cefalorraquídeo dio negativo para SARS-CoV-2 y los niveles de proteínas (31 mg/dL), glucosa (74 mg/dL) y lactato (1,89 mmol/L) se encontraban dentro de los parámetros normales.\n\nDesvelado\nLa paciente logró una recuperación casi total de los déficits neurológicos, a pesar de la miopatía de la enfermedad crítica, y fue dada de alta después de 44 días en el hospital. Se la derivó a un hospital secundario para su rehabilitación y prácticamente recuperó su estado mental previo.\n",
+        "gold_summary": "Una mujer de 63 años de edad acudió a la sala de urgencias con un historial de fiebre aguda, postración y disnea. Se le diagnosticó un caso grave de COVID-19 y síndrome de dificultad respiratoria aguda. A pesar de recibir atención médica intensiva, cumplía con los requisitos para someterse a una oxigenación por membrana extracorpórea. El día 34, luego de siete días de haber suspendido la sedación y de que su cuadro neurológico hubiera evolucionado de manera positiva, presentó una crisis tónico-clónica generalizada limitada, que no guardaba relación con un desequilibrio hidroelectrolítico o metabólico, lo que hizo necesario realizar una investigación diagnóstica. Los estudios de imágenes cerebrales revelaron un síndrome de encefalopatía posterior reversible.\n",
+        "synthetic_summary": {
+            "B1": "A 63-year-old woman got very sick with COVID-19. She had fever, cough, and trouble breathing. Doctors put a breathing tube in and used a special machine called ECMO. ECMO helps give oxygen to the blood when the lungs cannot.\n\nAfter many days, she woke and seemed to get better. Then she had a seizure, which is when the brain makes sudden, uncontrolled movements. Doctors did brain scans. The scans showed a problem called posterior reversible encephalopathy syndrome, or PRES. PRES means some parts of the brain get swollen and can cause seizures. The scans also showed a few very small bleeds, but the spinal fluid test did not show infection.\n\nThe doctors treated her and gave time to recover. She got better almost all the way and left the hospital after 44 days. She went to rehab and nearly returned to how she was before. This was a serious illness, but she improved a lot.",
+            "B2": "A 63-year-old woman with obesity and high blood pressure went to the emergency room after seven days of fever, dry cough, loss of smell, muscle pain and shortness of breath. Tests showed low lymphocytes (a type of white blood cell) and a high C‑reactive protein (CRP, a blood marker of inflammation). A PCR test was positive for SARS‑CoV‑2, the virus that causes COVID‑19.\n\nHer breathing got much worse and she developed severe lung failure (acute respiratory distress syndrome, or ARDS). She was put on a breathing tube (intubation) and a ventilator, but still did not get enough oxygen. On the second day her oxygenation was very poor (PaO2/FiO2 ratio 98), so she was started on venovenous extracorporeal membrane oxygenation (VV‑ECMO). ECMO is a machine that takes blood out of the body, adds oxygen and removes carbon dioxide, and then returns the blood — it is used when the lungs cannot work well enough by themselves. ECMO was started safely and she spent about 455 hours (almost 19 days) on it. During her ICU stay she also had early nutrition and physical rehabilitation. She developed a ventilator‑associated pneumonia due to Pseudomonas bacteria on day 14 and was treated with antibiotics and improved. Her kidneys worked well the whole time. She was taken off ECMO on day 20 and later had a tracheostomy (a small opening in the neck to help breathing) as part of recovery.\n\nOn day 34, after seven days without sedative drugs and after showing overall neurological improvement, she had a single generalized tonic‑clonic seizure (a convulsion affecting the whole body). Doctors checked blood tests, spinal fluid and did brain imaging to find the cause. Blood tests the day before showed that some inflammation markers had gone down (CRP, procalcitonin, fibrinogen, ferritin) but D‑dimer (a marker linked to blood clotting) and interleukin‑6 (IL‑6, an inflammatory molecule) were high. No medicines she had received were known to cause the brain syndrome identified.\n\nBrain MRI scans showed a pattern typical of posterior reversible encephalopathy syndrome (PRES). PRES is a condition where parts of the brain become swollen and can cause headaches, confusion, visual changes or seizures; it is often linked to severe illness, blood pressure problems, inflammation, or certain drugs. The MRI (FLAIR images) found symmetrical areas of swelling in the white matter, especially in the back of the brain (occipital and parietal lobes) and also in other regions. Another MRI sequence showed many tiny microbleeds (small spots of bleeding) in the white matter and in the corpus callosum. Spinal fluid tests were normal and did not show the virus.\n\nShe received supportive care, and her neurological state improved almost completely despite weakness from prolonged critical illness. She left the hospital on day 44 and was sent for rehabilitation; her mental status returned nearly to how it had been before illness.\n\nWhat this means and possible next steps\n- PRES is often reversible when the underlying problem is treated. In this case, diagnosis was made by MRI and by ruling out other causes.\n- Typical care includes controlling blood pressure if needed, treating infections or inflammation, preventing and treating seizures, and close monitoring with follow‑up imaging and rehabilitation.\n- The patient’s good recovery is encouraging and shows that even severe COVID‑19 cases with serious brain findings can improve with timely, supportive ICU care.\n\nIf you have questions about any term or part of the case, I can explain it more simply.",
+            "B3": "Resumen breve y empático\nUna mujer de 63 años con obesidad e hipertensión desarrolló COVID-19 grave con síndrome de distrés respiratorio agudo (SDRA). Requirió ventilación mecánica y soporte con oxigenación por membrana extracorpórea venovenosa (VV-ECMO). Tras una recuperación respiratoria progresiva y retirada de la sedación, presentó una crisis convulsiva generalizada; las imágenes cerebrales y las pruebas complementarias apoyaron el diagnóstico de encefalopatía posterior reversible (PRES). La paciente evolucionó favorablemente, recuperó casi por completo sus funciones neurológicas y fue dada de alta para rehabilitación.\n\nDatos clínicos y evolución\n- Presentación inicial: fiebre, tos seca, pérdida del olfato, mialgias y disnea tras 7 días de síntomas; saturación de oxígeno 90 % al ingreso. Laboratorio con linfopenia y proteína C reactiva elevada. PCR nasofaríngea positiva para SARS‑CoV‑2.  \n- Deterioro respiratorio progresivo con insuficiencia respiratoria y radiografía con infiltrados bilaterales → intubación y ventilación mecánica. A pesar de maniobras (prono, bloqueo neuromuscular) la oxigenación fue insuficiente (PaO2/FiO2 ≈ 98), por lo que se indicó VV‑ECMO.  \n- Soporte con VV‑ECMO realizado sin complicaciones; 455 horas de soporte (≈19 días). Durante la internación presentó neumonía asociada a ventilador por Pseudomonas aeruginosa tratada con ceftazidima y vancomicina con buena respuesta. Función renal conservada. Traqueostomía realizada 7 días después de retirar ECMO.  \n- Día 34 de internación, y 7 días después del destete de sedación, tuvo una crisis tónico‑clónica generalizada limitada, lo que motivó estudios neurológicos.\n\nInvestigaciones neurológicas y hallazgos\n- Resonancia magnética cerebral (FLAIR): hiperintensidad simétrica y confluente predominantemente en la sustancia blanca justa y subcortical de regiones occipitales y parietales, con afectación también en frontal, temporal y cerebelo izquierdo. Estos hallazgos son típicos de edema vasogénico en PRES.  \n- Secuencia de susceptibilidad: múltiples microhemorragias puntiformes en sustancia blanca superficial y profunda, afectando especialmente la sustancia blanca justacortical y el cuerpo calloso; además, tres hemorragias subagudas <1 cm en cápsulas externas (T1 hiperintenso).  \n- Líquido cefalorraquídeo: parámetros normales (proteínas, glucosa, lactato) y PCR para SARS‑CoV‑2 negativa.  \n- Laboratorio en el día previo a la crisis: descenso de PCR, procalcitonina, fibrinógeno y ferritina respecto a fases previas; aumento marcado de dímero D (18 021 ng/mL) e interleucina‑6 (10,4 pg/mL). No se habían administrado fármacos inmunosupresores, inmunomoduladores ni quimioterápicos asociados a PRES.\n\nInterpretación diagnóstica\n- Diagnóstico principal: PRES (síndrome de encefalopatía posterior reversible) manifestado por convulsión y por patrón típico de edema vasogénico en regiones posteriores en la RM.  \n- Hallazgos atípicos pero relevantes: microhemorragias y pequeñas hemorragias subagudas, que pueden acompañar a PRES en contextos de disfunción endotelial o coagulopatía.  \n- Factores de riesgo plausibles en este caso: COVID‑19 grave con respuesta inflamatoria y alteración de la coagulación, necesidad de VV‑ECMO y estancia prolongada en UCI. No se identificó causa medicamentosa directa.\n\nTratamiento y resultado\n- Manejo dirigido a soportar la función vital y controlar la convulsión; cuidados neuroprotectores y rehabilitación precoz.  \n- La paciente sufrió miopatía secundaria a enfermedad crítica pero alcanzó una recuperación neurológica casi completa. Fue dada de alta tras 44 días de hospitalización y remitida para rehabilitación, recuperando prácticamente su estado mental previo.\n\nImplicaciones y recomendaciones prácticas\n- En pacientes con COVID‑19 grave y estancia prolongada en UCI, nuevas manifestaciones neurológicas (especialmente convulsiones, alteración del estado mental o déficits visuales) deben investigarse con imagen cerebral (RM) y estudios básicos (laboratorio, LCR) para descartar PRES u otras complicaciones.  \n- PRES puede ser reversible si se identifica y trata a tiempo; sin embargo, puede coexistir con hemorragias microvascularizadas y coagulopatía, por lo que es importante monitorizar parámetros inflamatorios y de coagulación.  \n- La detección precoz y la rehabilitación son claves para una buena recuperación funcional.\n\nMensaje final empático\nEsta paciente afrontó una enfermedad muy grave y complicaciones importantes, pero gracias a una atención intensiva multidisciplinaria y evaluación neurológica oportuna logró recuperar su función neurológica en gran medida. La historia subraya la importancia de vigilar complicaciones neurológicas en COVID‑19 severo y de un abordaje integral que incluya imagen, control de la inflamación y rehabilitación."
+        }
+    },
+    {
+        "article": "Mujer de 65 años, originaria y residente de la Ciudad de México, con antecedente de infección por VIH de 20 años de diagnóstico con carga viral indetectable desde 2020 y con cuenta de CD4 de 1220 células por mililitro en febrero de 2022, hipotiroidismo de 29 años, cardiopatía isquémica de 9 años de diagnóstico, osteoporosis y dislipidemia, en tratamiento y bajo control médico.\n\nSu dermatosis problema se inició 10 años atrás, después de un cuadro de herpes zóster localizado en la extremidad inferior derecha y se complicó con una infección de tejidos blandos, referida como celulitis. Como secuela de este evento la paciente desarrolló úlcera, la cual ameritó corrección del defecto con 4 injertos cutáneos en diferentes tiempos quirúrgicos por cirugía plástica, con acompañamiento por parte de la clínica de heridas. Durante el seguimiento y a pesar de las medidas tomadas, no logró resolución completa y persistió con una úlcera asociada a dolor local, motivo de su envío a nuestro servicio.\n\nA la exploración física presentaba una dermatosis localizada en la extremidad inferior derecha, en la cara lateral del muslo, caracterizada por una neoformación aplanada sobre la que se asentaba una úlcera de 1.5 cm de diámetro, con fondo limpio, con costra sero-amarillenta, bordes sobreelevados, piel perilesional hiperpigmentada y queratósica, una cicatriz atrófica e hiperpigmentada. Se inició abordaje de la dermatosis mediante biopsia de piel, con reporte histopatológico de carcinoma verrugoso, por lo que se concluyó como úlcera de Marjolin asociada a carcinoma verrugoso en paciente portadora de VIH. Se canalizó al hospital de oncología para manejo con radioterapia.",
+        "gold_summary": "mujer de 65 años con el antecedente de ser portadora de infección por virus de inmunodeficiencia humana (VIH), que presentó un carcinoma verrugoso asociado a una úlcera de Marjolin secundaria a herpes zóster e infección de tejidos blandos en pierna derecha, con un periodo de latencia de 10 años desde el proceso infeccioso inicial hasta la confirmación histopatológica.",
+        "synthetic_summary": {
+            "B1": "Resumen simple y amable:\n\nUna mujer de 65 años de la Ciudad de México tenía varias enfermedades, entre ellas VIH que estaba bien controlado. Hace 10 años tuvo culebrilla (herpes zóster) en la pierna derecha y la zona se infectó. Quedó una llaga que no sanó. Le pusieron cuatro injertos de piel, pero la herida siguió dando problemas y le dolía.\n\nAl revisarla encontraron una lesión en el muslo derecho con una úlcera pequeña. Hicieron una biopsia (toman un pedacito para mirar al microscopio). El resultado mostró que la llaga se había convertido en un tipo de tumor llamado carcinoma verrugoso. Cuando una llaga vieja se transforma en cáncer se llama úlcera de Marjolin. \n\nLa paciente fue enviada al hospital de oncología para recibir radioterapia, que son rayos que ayudan a tratar el cáncer. Es una situación seria, pero ya la están atendiendo por especialistas.",
+            "B2": "Summary\n\nA 65-year-old woman from Mexico City, who has lived with HIV for 20 years and has been well controlled (undetectable viral load since 2020, CD4 count 1220 in 2022), developed a chronic skin problem on her right thigh. Ten years ago she had a shingles infection (herpes zoster) on the same leg that became complicated by a soft tissue infection (cellulitis). After that episode she developed a long‑standing ulcer (a nonhealing sore) that required four skin grafts and ongoing wound care, but the ulcer did not heal and caused local pain.\n\nOn exam doctors found a flattened new growth on the outside of her right thigh with a 1.5 cm ulcer in the center, raised edges, a clean base with a yellowish crust, and darkened, thickened skin around the sore. A skin biopsy (a small sample of tissue) showed verrucous carcinoma. This led to the diagnosis of a Marjolin ulcer — that is, a cancer that developed in a chronic wound or scar — associated with verrucous carcinoma (a slow‑growing, wart‑like form of squamous cell skin cancer).\n\nBecause the lesion is cancerous, the patient was referred to an oncology hospital for treatment with radiotherapy (radiation treatment). The key points are the long 10‑year delay between the original infection and the cancer, and that chronic, nonhealing ulcers can sometimes turn into cancer, so they need careful follow‑up and prompt treatment.",
+            "B3": "Resumen clínico (nivel universitario)\n\nPaciente: mujer de 65 años de la Ciudad de México.\n\nAntecedentes relevantes:\n- Infección por VIH desde hace 20 años; carga viral indetectable desde 2020 y recuento de CD4 de 1,220 células/mm3 (febrero 2022), es decir, control virológico y buena inmunidad en registros recientes.\n- Hipotiroidismo (29 años), cardiopatía isquémica (9 años), osteoporosis y dislipidemia, todas en tratamiento y control médico.\n\nHistoria de la lesión:\n- Hace 10 años sufrió herpes zóster localizado en la pierna derecha, complicándose con infección de partes blandas (celulitis).\n- Como secuela desarrolló una úlcera crónica en la cara lateral del muslo derecho que requirió cuatro injertos cutáneos en diferentes tiempos y seguimiento en clínica de heridas.\n- A pesar de los tratamientos la úlcera persistió y generó dolor local, por lo que fue remitida al servicio especializado.\n\nExploración física:\n- Neoformación aplanada en la cara lateral del muslo derecho sobre la que se asienta una úlcera de 1,5 cm de diámetro.\n- Fondo limpio con costra sero‑amarillenta, bordes sobreelevados, piel perilesional hiperpigmentada y queratósica, y cicatriz atrófica hiperpigmentada.\n\nDiagnóstico:\n- Biopsia cutánea con reporte histopatológico de carcinoma verrugoso.\n- Conclusión clínica: úlcera de Marjolin (malignización de una lesión crónica) asociada a carcinoma verrugoso en paciente portadora de VIH.\n\nInterpretación e implicaciones:\n- Una úlcera de Marjolin es la transformación maligna de una lesión crónica o cicatriz y suele aparecer tras procesos inflamatorios o traumáticos; la latencia de 10 años en este caso es compatible con ese patrón.\n- El carcinoma verrugoso es una variante bien diferenciada del carcinoma epidermoide (escamoso): tiende a crecer localmente y rara vez hace metástasis, pero puede ser destructivo en la zona afectada.\n- Aunque la paciente tiene VIH, sus registros recientes muestran buen control inmunológico, lo que es favorable para el manejo y pronóstico; no obstante, la historia de infección crónica fue el factor más relevante en la génesis de la lesión.\n\nPlan y siguientes pasos recomendados:\n- La paciente fue canalizada al hospital de oncología para manejo con radioterapia.\n- Es aconsejable un abordaje multidisciplinario: discusión en comité tumoral con cirugía oncológica y plastica, oncología radioterápica, medicina interna/infectología y clínica de heridas.\n- Considerar evaluación imagenológica local y ganglionar (ecografía o TC/RM) para determinar extensión y descartar compromiso profundo o adenopatías.\n- El tratamiento de elección para úlceras de Marjolin suele ser la escisión amplia con márgenes claros; la radioterapia puede usarse en determinados contextos, pero la decisión debe individualizarse según extensión, localización y comorbilidades.\n- Mantener control del dolor, cuidado local de la herida y seguimiento estrecho por riesgo de recurrencia.\n\nTono y perspectiva:\n- Se trata de una transformación maligna seria pero con opciones terapéuticas. El control virológico y el estado general de la paciente son datos favorables; una evaluación multidisciplinaria facilitará definir el mejor tratamiento y el seguimiento adecuado."
+        }
+    },
+    {
+        "article": "Una mujer de 90 años con hepatitis C y un historial de tabaquismo de 60 años proveniente de una zona rural presentó una hinchazón en la cara posteromedial del muslo izquierdo justo por encima de la rodilla. La hinchazón se notó por primera vez hace 3 años y aumentó gradualmente de tamaño durante este período. Ella sintió un leve malestar, pero niega cualquier síntoma asociado de dolor, picazón, secreción, fiebre o inmovilidad articular. Como provenía de una zona rural, también tenía un historial de exposición a animales.\nEn el examen físico, la hinchazón tenía una forma esférica de 14 × 10, era firme, fija y no sensible, con márgenes bien definidos en el aspecto posteromedial del muslo izquierdo, justo por encima de la rodilla. La piel que la recubría era pellizcable y mostraba venas prominentes, y la temperatura era comparable a la de la piel circundante.\nLa ecografía reveló una lesión quística grande con varios quistes pequeños en su interior, que medían 13,2 × 11 × 13,6 cm y un volumen de 1046 ml. Se originaba en la articulación de la rodilla izquierda y se extendía hasta la mitad del muslo. La ecografía Doppler en color no mostró vascularización en su interior. Se realizó una resonancia magnética que mostró una lesión quística grande (21 × 9,9 × 8,1 cm) con múltiples lesiones pequeñas dispersas, con extensión intramuscular e intermuscular que afectaban al aductor largo y al gracilis de manera medial y al bíceps femoral de manera posterior. Todas estas características eran indicativas de un quiste hidatídico. El diagnóstico se confirmó mediante una prueba de hemaglutinación para Echinococcus. La radiografía de tórax y la ecografía abdominal fueron normales.\nSe planificó la escisión quirúrgica de la tumefacción quística y se realizó una incisión en forma de S en la piel, seguida de una disección cuidadosa a través del tejido subcutáneo para acceder al quiste. La lesión estaba bien definida dentro de los planos intermuscular e intramuscular. Se realizó una disección meticulosa para aislar y extraer el quiste intacto, asegurando que no se derramara su contenido. Para minimizar el riesgo de contaminación, se irrigó a fondo el sitio quirúrgico con solución salina normal después de la escisión.\nLos hallazgos intraoperatorios revelaron una gran hinchazón quística intermuscular de 22 × 14 cm, que involucraba los compartimentos posterior y medial del muslo izquierdo. El quiste demostró extensión intramuscular hacia el aductor largo y el gracilis medialmente y hacia el bíceps femoral posteriormente, extendiéndose hasta la fosa poplítea. Cabe destacar que no había comunicación entre el quiste y la articulación de la rodilla. Una biopsia enviada al laboratorio confirmó aún más el diagnóstico. El examen histopatológico de la muestra extirpada reveló una pared quística fibrocondrogénica revestida por epitelio atenuado con infiltración inflamatoria. La presencia de material queratinoso focal caracterizó aún más la lesión. Estos hallazgos, junto con las características macroscópicas, favorecieron el diagnóstico de un quiste hidatídico. El curso postoperatorio fue sin complicaciones y el paciente fue dado de alta con una terapia antihelmíntica durante seis semanas. Se programaron visitas de seguimiento a la semana, tres semanas, seis semanas, nueve semanas y doce semanas. Durante estas visitas, el paciente no mostró signos de recurrencia o complicaciones.\n",
+        "gold_summary": "Una mujer de 90 años de edad, proveniente de una zona rural, presentó una hinchazón de crecimiento lento en el muslo posteromedial durante tres años. No tenía antecedentes de traumatismos ni síntomas sistémicos. El examen clínico reveló una masa firme y no dolorosa. Las imágenes sugieren una lesión quística, y la serología confirmó la infección por Echinococcus. Se realizó la extirpación quirúrgica, y la histopatología confirmó un quiste hidatídico. La paciente recibió un tratamiento posoperatorio de albendazol durante seis semanas. Su recuperación fue sin incidentes, sin recurrencia en el seguimiento.\n",
+        "synthetic_summary": {
+            "B1": "Una mujer de 90 años que vive en el campo tuvo una hinchazón en la parte de atrás y adentro del muslo izquierdo. La hinchazón creció despacio durante tres años. No le dolía y no tenía fiebre ni otros problemas. Las imágenes mostraron que era un gran saco lleno de líquido que venía de la rodilla y se metía entre los músculos. Un análisis de sangre dijo que había un parásito llamado Echinococcus. Los médicos quitaron el quiste con una operación y lo sacaron entero para que no se rompiera. El examen del tejido en el laboratorio confirmó que era un quiste hidatídico (un saco causado por ese parásito). Después de la operación, la paciente tomó un medicamento contra los parásitos durante seis semanas. Se recuperó bien y las revisiones no mostraron que el quiste volviera.",
+            "B2": "Resumen claro y amable:\n\nUna mujer de 90 años que vivía en zona rural notó durante tres años una hinchazón que fue creciendo lentamente en la parte trasera y medial del muslo izquierdo, justo por encima de la rodilla. Tenía un leve malestar pero sin dolor fuerte, fiebre, secreción ni problemas para mover la articulación. Por su historia, también había tenido contacto con animales, un dato importante en este caso.\n\nLas pruebas por imagen (ecografía y resonancia magnética) mostraron una gran lesión llena de líquido con muchas “pequeñas bolsas” dentro, que ocupaba espacio entre y dentro de varios músculos del muslo. Los resultados sugerían un quiste hidatídico, que es una bolsa formada por un parásito llamado Echinococcus (un tipo de gusano que puede contagiarse por animales). Un análisis de sangre específico (prueba de hemaglutinación) confirmó la infección. Radiografías del tórax y ecografía abdominal fueron normales, lo que indica que no había quistes visibles en pulmón o hígado.\n\nSe decidió operar y extraer la lesión. Los cirujanos hicieron una incisión, separaron cuidadosamente los planos musculares y sacaron el quiste entero sin romperlo (esto es importante para evitar que el parásito se disemine). Luego limpiaron la zona y enviaron tejido al laboratorio. El examen del tejido confirmó el diagnóstico de quiste hidatídico. La recuperación después de la cirugía fue buena; la paciente recibió albendazol (un medicamento antiparasitario) durante seis semanas y tuvo controles regulares en las semanas siguientes sin señales de recurrencia ni complicaciones.\n\nEn resumen: se trató de un quiste hidatídico grande en el muslo de una paciente mayor, confirmado por pruebas y tratado con cirugía cuidadosa y medicación antiparasitaria, con buena evolución.",
+            "B3": "Resumen clínico (nivel de lectura universitario)\n\nUna mujer de 90 años, procedente de zona rural con exposición a animales y antecedentes de hepatitis C y tabaquismo prolongado, consultó por una masa de crecimiento lento en la cara posteromedial del muslo izquierdo, detectada desde hace 3 años. La lesión era una tumoración esférica, firme, fija y no dolorosa, con piel intacta y venas superficiales prominentes.\n\nLa ecografía y la resonancia magnética mostraron una lesión predominantemente quística grande con múltiples “quistes hijos”, situada en planos intramuscular e intermuscular (afectando aductor largo, gracilis y bíceps femoral) y extendiéndose hasta la fosa poplítea; el Doppler no mostró vascularización. La serología por hemaglutinación fue positiva para Echinococcus, y las pruebas de extensión (radiografía de tórax y ecografía abdominal) no identificaron enfermedad en pulmón o hígado. Estos hallazgos apoyaron el diagnóstico de quiste hidatídico (hidatidosis) localizado en el muslo, una presentación poco frecuente.\n\nSe realizó resección quirúrgica cuidadosa mediante incisión en S y disección para extraer el quiste intacto —medida clave para evitar derrames que aumenten el riesgo de diseminación o reacción anafiláctica—; el espécimen medía alrededor de 22 × 14 cm y no tenía comunicación con la articulación de la rodilla. La histopatología confirmó pared quística con epitelio atenuado, infiltrado inflamatorio y material queratinoso, consistente con quiste hidatídico. El posoperatorio transcurrió sin complicaciones; recibió albendazol (terapia antihelmíntica) seis semanas y controles periódicos a 1, 3, 6, 9 y 12 semanas sin evidencia de recurrencia.\n\nImplicaciones y recomendaciones: la hidatidosis muscular es rara pero debe considerarse frente a masas quísticas en pacientes con exposición animal. El manejo combina cirugía (evitando abrir el quiste) y tratamiento farmacológico para reducir riesgo de recurrencia; se recomienda seguimiento a más largo plazo y evaluación serológica/imaginológica si aparecen nuevos síntomas."
+        }
+    },
+    {
+        "article": "Una paciente de 21 años de edad, soltera, con antecedentes de hipertensión y feocromocitoma metastásico, se presentó en nuestro hospital. Su cáncer se ha metastatizado en la vejiga, los huesos y los pulmones. También tiene un fuerte historial familiar de neoplasias, en particular de feocromocitoma. La paciente fue admitida debido a la hipertensión no controlada y los síntomas crónicos relacionados con su enfermedad.\n\nEn el ingreso (09/06/2024), la paciente era normotensa (PA: 104/66 mmHg), su frecuencia cardiaca era de aproximadamente 90 latidos por minuto, afebril a 36.9°C, y tenía una saturación de oxígeno de 99% en aire ambiente. El examen físico indicó un estado de desempeño del Grupo Cooperativo de Oncología del Este (ECOG) de 2, palidez consistente con anemia crónica, latido cardiaco regular sin murmullos o sonidos adicionales. El examen abdominal no fue notable, y no se observó edema o equimosis en las extremidades inferiores.\n\nLa paciente tiene antecedentes de hipertensión y paraganglioma, su medicación incluye (Doxazosin 2 mg, Labetalol 100 mg, Oxibutinina 5 mg, Aceite de parafina, Nifedipina 30 mg). Su historial quirúrgico incluye una adrenalectomía derecha a los diez años, y ha recibido varios tratamientos, incluidos análogos de somatostatina y radioterapia paliativa. El historial familiar revela una mutación familiar de la subunidad B de la deshidrogenasa del succinato (mutación SDBH) con un importante historial de tumores malignos endocrinos, incluidos feocromocitomas en su padre y hermana y cáncer de páncreas en su abuela.\n\nLas investigaciones de laboratorio, incluido el recuento sanguíneo completo, revelaron anemia significativa, con un nivel de hemoglobina de 7.5 g/dl. Había evidencia de hemólisis, como lo indican el alto recuento de reticulocitos, la bilirrubina indirecta y la lactato deshidrogenasa. La haptoglobina era baja. Los resultados de laboratorio se muestran en. El perfil de coagulación excluyó la coagulación intravascular diseminada (DIC), que muestra (PT: 15.6, PTT: 23.3, fibrinógeno: 489, dímero D: 0.63). La prueba de Coombs directa para excluir la anemia hemolítica autoinmune fue negativa. Los frotis de sangre periférica mostraron la presencia de esquistocitos, equinocitos y algunas células en forma de lágrima, además de trombocitopenia, todo lo cual apuntaba a la anemia hemolítica microangiopática (MAHA). Dado el contexto del cáncer metastásico, el paciente fue diagnosticado con anemia hemolítica microangiopática paraneoplásica en marzo/2024.\n\nEl paciente fue programado para el protocolo CVD (ciclofosfamida, vincristina y doxorrubicina), pero sin ciclofosfamida debido al efecto inductor de anemia de los agentes alquilantes. El paciente recibió un total de 5 ciclos. Como indicador de respuesta clínica, el paciente ya no experimentó anemia o trombocitopenia. Un nuevo frotis de sangre periférica reveló células normales, lo que sugiere una respuesta clínica al MAHA que coincide con la mejora de la neoplasia subyacente. Esto se alinea con la definición de MAHA como un síndrome paraneoplásico.\n\nLos medicamentos que se le suministran al paciente al momento del alta son: comprimidos de dexametasona de 2 mg, 4 mg por vía oral (PO) una vez al día (OD) durante 3 días, comprimidos de ondansetrón de 8 mg por vía oral (PO) una vez al día (OD) durante 3 días, comprimidos de metoclopramida de 10 mg por vía oral (PO) tres veces al día durante 3 días, calcio de 600 mg con vitamina D por vía oral (PO) una vez al día (OD) durante 1 día, comprimidos de labetalol de 100 mg por vía oral (PO) dos veces al día durante 1 día, comprimidos de doxazocina de 2 mg por vía oral (PO) dos veces al día durante 1 día, comprimidos de citalopram de 20 mg por vía oral (PO) durante 1 día, comprimidos de omeprazol de 20 mg, 40 mg por vía oral (PO) durante 1 día, comprimidos de paracetamol de 500 mg, 1000 mg por vía oral (PO) dos veces al día durante 1 día, cápsulas de aprepitant de 125 mg/80 mg, 1 cápsula por vía oral (PO) dos veces al día durante 3 días (con prescripción médica).\n\nEl paciente fue objeto de seguimiento el 01/07/2024, y su aspecto clínico era bueno y activo. El paciente se sometió a exámenes de laboratorio que incluían un recuento sanguíneo completo (WBC 6.59 10e3/ul, RBC 4.47 × 10^6/ul, HGB 13.2 g/dl, 40.0%, MCV 89.4 fL, PLT 41.5 10e3/ul), nitrógeno ureico en sangre 33.8 mg/dl, creatina cinasa-MB 36.1 u/l, creatinina sérica 0.97 mg/dl, cloruro 101.5 mmol/l, potasio 4.52 mmol/l, sodio 135 mmol/l.\n",
+        "gold_summary": "En este informe de caso, presentamos a una mujer soltera de 21 años con un fuerte historial familiar de neoplasia endocrina. Fue derivada a nuestro hospital para quimioterapia debido a un diagnóstico de feocromocitoma maligno, que había hecho metástasis en la vejiga urinaria, los huesos y los pulmones. Además, desarrolló anemia hemolítica microangiopática como un síndrome paraneoplásico.\n",
+        "synthetic_summary": {
+            "B1": "Esta es la historia de una mujer de 21 años con un tumor llamado feocromocitoma. El tumor se había extendido a la vejiga, los huesos y los pulmones. Muchas personas en su familia también han tenido tumores parecidos.\n\nEl tumor le causó una anemia especial. Esto quiere decir que sus glóbulos rojos se rompían dentro de vasos muy pequeños. Por eso estaba muy cansada y su sangre estaba baja. Los médicos hicieron pruebas y vieron que las células se rompían, pero que no era por una enfermedad del sistema que ataca la sangre.\n\nLe dieron quimioterapia para tratar el cáncer. Después de cinco ciclos de tratamiento, su sangre mejoró. Ya no tenía la anemia y el examen de sangre se veía mejor. Al salir del hospital le dieron medicinas para ayudar con los efectos del tratamiento. En el control posterior se veía activa y con la hemoglobina en un nivel normal.\n\nLos médicos piensan que la anemia fue causada por el cáncer. Al mejorar el cáncer, también mejoró la anemia. Esto es algo que puede pasar cuando un tumor causa problemas en otras partes del cuerpo.",
+            "B2": "Summary (B2 level, for readers aged ~11–17)\n\nThis report describes a 21-year-old woman with a rare and serious cancer called pheochromocytoma that had spread (metastasized) to her bladder, bones, and lungs. Pheochromocytoma is a tumor that starts in hormone-making cells of the adrenal glands. She also has a strong family history of similar tumors and a known inherited change (SDHB mutation) that raises the risk of these cancers.\n\nWhat happened\n- She was admitted because her cancer was causing ongoing problems and high blood pressure in the past. At admission her vital signs were stable.\n- Blood tests showed a severe drop in red blood cells (hemoglobin 7.5 g/dl) and signs that red blood cells were being destroyed inside small blood vessels. This condition is called microangiopathic hemolytic anemia (MAHA). MAHA is a type of anemia where red cells are broken into pieces as they pass through damaged tiny blood vessels. The blood smear (a slide of blood looked at under a microscope) showed broken red cells (schistocytes) and other abnormal cells. Tests ruled out autoimmune causes and widespread blood clotting (DIC).\n- Because her MAHA appeared together with advanced cancer, doctors diagnosed it as a paraneoplastic syndrome — a problem caused by the cancer but happening away from the tumor itself.\n\nTreatment and response\n- She was treated with a chemotherapy plan called CVD (vincristine and doxorubicin were used; cyclophosphamide was left out because it can worsen anemia). She received five cycles.\n- After treatment her anemia and the appearance of broken red cells improved, which suggests the MAHA got better as the cancer came under control.\n- On follow-up about a month later her hemoglobin was back to normal (13.2 g/dl). However, her platelet count was still low (41.5 × 10^3/µl), so some blood abnormalities persisted and need continued monitoring.\n\nOther notes\n- Discharge medicines included short courses of steroids and anti-nausea drugs, and her usual blood-pressure medicines.\n- The case shows how a cancer can cause serious blood problems (like MAHA) and that treating the underlying tumor can improve those problems. It also highlights the role of family genetics (SDHB mutation) in this patient’s illness.\n\nWhat comes next (typical steps)\n- Continued cancer treatment and close follow-up with blood tests to watch red cells and platelets.\n- Supportive care as needed (for example, blood transfusions if blood counts fall again).\n- Genetic counseling and family screening may be important because of the inherited SDHB change.\n\nThis summary aims to explain the case simply and calmly. If you have questions about any terms or want the information in Spanish, I can help with that.",
+            "B3": "Summary (college-level, empathetic)\n\nPatient and background\n- A 21‑year‑old woman with metastatic pheochromocytoma (spread to bladder, bones and lungs). She has a strong family history of endocrine cancers and a known familial SDHB mutation (pheochromocytomas in father and sister; pancreatic cancer in grandmother). She previously had a right adrenalectomy (age 10) and received somatostatin analogues and palliative radiotherapy.\n\nPresentation and examination\n- Admitted for uncontrolled hypertension and cancer‑related symptoms but on admission she was hemodynamically stable: blood pressure 104/66 mmHg, heart rate ~90/min, afebrile, oxygen saturation 99% on room air. Performance status was ECOG 2. Physical exam showed pallor consistent with chronic anemia; abdomen and lower limbs were unremarkable.\n\nKey laboratory and diagnostic findings\n- Severe anemia at presentation: hemoglobin 7.5 g/dL.\n- Evidence of hemolysis: high reticulocyte count, elevated indirect bilirubin and LDH, and low haptoglobin.\n- Peripheral blood smear: schistocytes (fragmented red cells), echinocytes, some teardrop cells, and thrombocytopenia — findings consistent with microangiopathic hemolytic anemia (MAHA).\n- Direct Coombs (direct antiglobulin) test was negative, arguing against autoimmune hemolysis.\n- Coagulation tests argued against disseminated intravascular coagulation (DIC) (PT 15.6 s, PTT 23.3 s, fibrinogen 489 mg/dL, D‑dimer 0.63).\n- Clinical impression: MAHA as a paraneoplastic syndrome related to her metastatic pheochromocytoma (diagnosed March 2024).\n\nTreatment course and response\n- She was treated with a modified CVD chemotherapy protocol (vincristine and doxorubicin were given; cyclophosphamide was omitted because of its anemia‑inducing effects). She completed five cycles.\n- Clinical response: the team reported resolution of anemia and normalization of the peripheral smear, which supports the interpretation that the MAHA was paraneoplastic and improved as the cancer was treated.\n\nFollow‑up (01/07/2024)\n- Clinically she appeared well and active.\n- Labs at follow‑up showed hemoglobin 13.2 g/dL and otherwise acceptable renal and electrolyte values. The platelet count was reported as 41.5 × 10^3/µL (marked thrombocytopenia), which contrasts with the statement that thrombocytopenia had resolved; this discrepancy warrants attention and close monitoring.\n\nMedications at discharge (summary)\n- Short steroid and antiemetic courses (dexamethasone, ondansetron, metoclopramide, aprepitant), ongoing blood‑pressure management (doxazosin, labetalol), supportive agents (calcium with vitamin D, paracetamol, omeprazole), and an SSRI (citalopram). (Exact dosages were used in the chart.)\n\nInterpretation and implications\n- MAHA in this case appears to be a paraneoplastic phenomenon linked to metastatic pheochromocytoma. Improvement of the hemolysis and anemia after systemic chemotherapy supports that the hematologic syndrome was driven by the cancer.\n- Persistent or recurrent thrombocytopenia at follow‑up (if confirmed) is concerning and should be investigated; causes could include ongoing marrow suppression, immune mechanisms, consumptive processes, or disease progression.\n- Management priorities going forward: continued oncologic treatment and surveillance of the cancer; regular CBC and hemolysis markers (LDH, bilirubin, haptoglobin, reticulocyte count); blood‑pressure control and symptomatic/supportive care; hematology input if the platelet count remains low or if hemolysis recurs; and genetic counseling/testing given the SDHB mutation and strong family history.\n\nEmpathetic note\n- This is a young patient facing advanced cancer and a serious paraneoplastic complication. The improvement in hemoglobin after cancer‑directed therapy is encouraging. Close multidisciplinary follow‑up (oncology, hematology, genetics, and supportive care) and clear communication with the patient and family about goals of care and next steps will be important."
+        }
+    }
+]
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@@ -0,0 +1,902 @@
+[
+    {
+        "article": "Información para el paciente\nUn hombre de 27 años y fumador estuvo involucrado en un accidente de tráfico; se cayó de su motocicleta sin casco. El hombre llevó la motocicleta al hospital e informó de un dolor de cabeza y heridas hemorrágicas en la frente.\n\nEl paciente no tiene antecedentes patológicos y trabaja en una zona rural.\n\nHallazgos clínicos\nTras su ingreso en urgencias, perdió el conocimiento y sufrió dos convulsiones. En la exploración física, la escala de coma de Glasgow fue de 6/15 (no abrió los ojos, se retiró al sentir dolor, no respondió verbalmente) con midriasis bilateral, dificultad hemodinámica y buena saturación. Se identificó una lesión craneal penetrante con una profusa hemorragia intracraneal.\n\nLínea de tiempo\nTras caerse de la motocicleta, el paciente volvió a montarse en ella e inmediatamente fue al hospital, quejándose de dolores de cabeza y de una herida en la frente por la que sangraba. Recibió tratamiento de urgencia para estabilizar sus funciones respiratorias y hemodinámicas. Ese mismo día, fue trasladado inconsciente a un centro mejor equipado, donde se le realizó un TAC y se sometió a una operación quirúrgica con éxito.\n\nEvaluación diagnóstica\nSu nivel de hemoglobina era de 6 g/dL y su grupo sanguíneo era O positivo. El hospital no tenía ni una unidad de cuidados intensivos ni un escáner. El único diagnóstico sugerido fue el de traumatismo agudo en la cabeza, complicado por hemorragia intracraneal que provocó shock y convulsiones. El pronóstico vital, basado en la presentación clínica, era malo.\n\nIntervención terapéutica\nUna intervención inicial consiste en un relleno intracraneal a través de la fractura craneal, seguido de un vendaje cefálico que ayuda a detener el sangrado. El tratamiento involucró la estabilización de la columna cervical, intubación orotraqueal con oxígeno a 6 L por minuto y la inserción de un catéter Foley. Se usaron dos puertos venosos periféricos para administrar NaCl 0.9 % 1000 CC, Geloplasma* 500 CC, Manitol 20 % 250 CC; Phenobarbital inj 40 mg/2 ml: 100 mg, luego Thiopental 250 mg: bolo de 100 mg × 2 debido a otras convulsiones; Amoxicillin + Clavulanic Acid injection 2 g; Gentamycin 160 mg intramuscularmente. Se realizó un suero antitetánico de 1500 IU y una transfusión de 450 CC de sangre.\n\nEl paciente fue trasladado inconsciente a un equipo en un hospital de primera categoría, sin intubación y en un estado hemodinámico estable.\n\nEl primer día después de la transferencia, el paciente evolucionó bien; estaba consciente y podía caminar, sin problemas neurológicos, hemodinámicos o respiratorios. La tomografía computarizada reveló un edema bifrontal agudo, una contusión hemorrágica del parénquima predominantemente en el lado derecho, una capa de hematoma subdural agudo (3 mm) en la región fronto-parieto-temporo-occipital izquierda, una hernia subfalcular izquierda de 5 mm, una compresión discreta del ventrículo lateral derecho, una hemorragia subaracnoidea superior bifrontal aguda, una fractura frontal deprimida con rotura osteomeníngea y una fractura de la tercera vértebra cervical con compresión de la médula espinal. El paciente se sometió a una operación exitosa en el hospital de primera categoría.\n\nSeguimiento y resultados\nEl período postoperatorio estuvo marcado por convulsiones, para las cuales se le administró anticonvulsivos al paciente, con un buen resultado.\n",
+        "gold_summary": "Un hombre de 27 años, fumador sin antecedentes patológicos, estuvo involucrado en un accidente de tráfico, al caerse de una motocicleta sin casco. En el ingreso al hospital de nuestro distrito rural, la escala de coma de Glasgow durante el examen físico fue de 6/15 con midriasis bilateral, distrés hemodinámico y buena saturación. Se identificó una lesión penetrante en la cabeza con profusa hemorragia intracraneal. Se usó el relleno intracraneal conocido en la neurocirugía de control de daños para taponar la hemorragia intracraneal grave y que es una maniobra neuroquirúrgica que salva vidas. El paciente fue trasladado inconsciente a un hospital de primera categoría, libre de intubación y en un estado hemodinámico estable. El período postoperatorio estuvo marcado por convulsiones, por lo que el paciente fue puesto en anticonvulsivos con un buen resultado.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre de 27 años se cayó de su moto sin casco y se lastimó la cabeza. Llegó al hospital con mucho dolor y sangrado. Tenía una herida grave en la cabeza y perdió el conocimiento. Lo llevaron a otro hospital donde le hicieron una operación para detener la sangre. Después, tuvo convulsiones, pero con medicinas mejoró mucho y pudo estar estable.",
+            "B2": "Un hombre de 27 años sufrió un accidente al caerse de su motocicleta sin casco y llegó al hospital con dolor de cabeza y una herida sangrante en la frente. Al ingresar, perdió el conocimiento y tuvo convulsiones; su nivel de conciencia era muy bajo y presentaba una lesión grave en la cabeza con hemorragia dentro del cráneo. Recibió tratamiento urgente para controlar el sangrado y estabilizar su estado, luego fue trasladado a un hospital mejor equipado. Allí, se le realizó una cirugía para tratar las fracturas y el daño cerebral. Después de la operación, tuvo convulsiones que se controlaron con medicamentos. Gracias a estos cuidados, el paciente mejoró y pudo recuperarse sin problemas neurológicos graves.",
+            "B3": "Un hombre de 27 años sufrió un accidente al caer de su motocicleta sin casco y presentó una lesión penetrante en la cabeza con hemorragia intracraneal grave. Al llegar al hospital rural, estaba inconsciente con una escala de coma de Glasgow de 6/15, midriasis bilateral y signos de inestabilidad hemodinámica. Se realizó un relleno intracraneal para controlar la hemorragia, una técnica neuroquirúrgica que ayuda a salvar vidas en casos graves. Posteriormente, fue trasladado a un hospital de mayor nivel, donde se confirmó mediante tomografía lesiones cerebrales múltiples, incluyendo edema, hematoma subdural y fracturas craneales y cervicales. Tras una cirugía exitosa, el paciente presentó convulsiones en el postoperatorio, las cuales fueron controladas con medicamentos anticonvulsivos. En consecuencia, su evolución fue favorable, recuperando la conciencia y la movilidad sin déficits neurológicos significativos. Este caso resalta la importancia de la intervención rápida y especializada en traumatismos craneales severos para mejorar el pronóstico."
+        }
+    },
+    {
+        "article": "La paciente era una madre de 54 años que provenía de una zona rural y que llegó al Hospital Especializado de Compresión de Nekemte con la queja de una masa en su vagina de 3 años de duración. Hace tres años, encontró una protuberancia de masa a través de su vagina, que gradualmente creció en tamaño con el tiempo. Había tenido dos bebés, el último hace 12 años. Ambos partos fueron en casa, ya que el centro de salud está demasiado lejos de su área de residencia, y fue asistida por una comadrona tradicional. Ella afirmó que todo había sido sin problemas. Inicialmente, hace tres años, hubo sangrado y una descarga ofensiva de la masa, pero eso se detuvo en el último año. Desarrolló laceraciones en la masa hace seis meses. Por esta razón, se divorció y se aisló de toda la vida social durante este largo período de tiempo. Ahora, su hermana mayor y otro familiar la trajeron al hospital específicamente por la laceración de la masa. No tenía ninguna otra enfermedad médica crónica conocida.\n\nHallazgo pertinente del PE\nSigno vital: PA = 100/60 mm hg, FC = 84 lpm, FR = 20 lpm, T° = 36.5°C, peso = 47 kg.\n\nGUS: hay una masa rosada en la vagina que se encuentra a unos 7 cm del anillo del himen.\n\nEl fondo uterino es la parte principal de la masa.\n\nHabía una laceración longitudinal de unos 5 cm en el lado derecho de la masa.\n\nNo hubo sangrado ni secreción de la masa ni del área de la laceración.\n\nLaboratorio\nCBC: hemoglobina = 12 g/dl, PLT = 285 mil, neutrófilos = 74%.\n\nAnálisis de orina: resultado normal.\n\nGrupo sanguíneo = A, RH = positivo.\n\nPrueba de VIH = negativa.\n\nHBSAg = negativo.\n\nEcografía: vejiga parcialmente llena visible en el abdomen, útero no visible en el abdomen. Por lo demás, no se observaron otros hallazgos pertinentes.\n\nRadiografía de tórax: radiografía de tórax normal.\n\nPor este motivo, se le diagnosticó una inversión uterina crónica. Se tomaron imágenes preoperatorias y postoperatorias, el fondo uterino era el punto principal de la masa que sobresalía completamente a través de la vagina y había una laceración crónica desarrollada en la superficie endometrial. Después de la operación, se observó un canal vaginal normal. Después de revisar las opciones de tratamiento con ella y su familia, se programó una cirugía y se realizó una histerectomía abdominal al día siguiente. Era una cirugía abdominal y era fácil introducir el útero en el abdomen. Como el tejido era redundante y distorsionado, es difícil identificar la referencia anatómica y los puntos de referencia quirúrgicos. Debido a esto, la cirugía fue difícil y hubo una lesión ureteral derecha transaccional intraoperatoria y se realizó una anastomosis de extremo a extremo. Se dio de alta el décimo día de la operación y se encontró que estaba mejorando. Se le dio una cita de seguimiento dos semanas después y cuando se evaluó se encontró que estaba bien.\n",
+        "gold_summary": "Una mujer de 54 años de edad acudió a nuestro hospital con la queja de una masa indolora en su vagina de 3 años de duración. Hace tres años, encontró una protuberancia de masa a través de su vagina, que gradualmente creció en tamaño con el tiempo. En el examen físico, el fondo uterino fue el punto principal de la masa y sobresalía 7 cm por debajo del anillo del himen. Como resultado, se le diagnosticó inversión uterina crónica y se le sometió a una histerectomía abdominal. Fue dada de alta en casa mejorada. Presentamos este caso debido a un factor no identificado que provocó la inversión uterina, la presentación tardía de la enfermedad y la dificultad en el tratamiento quirúrgico.\n",
+        "synthetic_summary": {
+            "B1": "Una mujer de 54 años tenía una bolita en su vagina desde hace tres años. Esa bolita era parte de su útero que salió hacia afuera. Los doctores hicieron una operación para quitar esa parte y ayudarla. Después de la cirugía, ella mejoró y está bien. Este caso fue especial porque la enfermedad apareció de forma rara y fue difícil de tratar.",
+            "B2": "Una mujer de 54 años llegó al hospital con una masa en la vagina que creció durante tres años. La masa era el fondo del útero que sobresalía, llamada inversión uterina crónica, una condición rara. Tenía una herida en la masa, pero no sangraba ni tenía secreción. La paciente no tenía otras enfermedades y sus análisis de sangre y orina fueron normales. Se decidió hacer una cirugía para quitar el útero, llamada histerectomía abdominal. La operación fue difícil porque el tejido estaba dañado y se lesionó un uréter, que se reparó en la cirugía. Después, la mujer mejoró y salió del hospital con seguimiento. Este caso muestra la importancia de tratar temprano para evitar problemas.",
+            "B3": "Una mujer de 54 años, procedente de una zona rural, acudió al hospital con una masa vaginal que había notado durante tres años y que había ido creciendo progresivamente. La paciente había tenido dos partos en casa sin complicaciones y presentó inicialmente sangrado y secreción maloliente, que cesaron hace un año. En el examen físico se observó que la masa, cuyo centro era el fondo uterino, sobresalía 7 cm por debajo del himen y presentaba una laceración crónica. Los estudios de laboratorio y radiografía no mostraron alteraciones significativas. El diagnóstico fue inversión uterina crónica, una condición en la que el útero se invierte y protruye hacia la vagina, aunque la causa exacta no fue identificada. Se realizó una histerectomía abdominal, procedimiento complicado por la distorsión anatómica, que causó una lesión en el uréter derecho, reparada durante la cirugía. La paciente evolucionó favorablemente y fue dada de alta con seguimiento posterior sin complicaciones. Este caso destaca la presentación tardía y la dificultad en el manejo quirúrgico de una inversión uterina crónica en un contexto rural con acceso limitado a servicios de salud."
+        }
+    },
+    {
+        "article": "Varón de 20 años, HIV negativo, con TB pulmonar y tratamiento irregular en 2020-2021. Se internó por síndrome de impregnación bacilar, dolor e impotencia funcional del hombro derecho. Presentaba mal estado general, adelgazado, hipotrofia muscular grave, lesiones tumorales frías fluctuantes fistulizadas en dorso, calota craneana y tórax anterior con secreción caseosa, sin presentar déficits motores ni sensitivos. El examen molecular rápido (GeneXpert Mtb/Rif) de secreción del tórax fue positivo para Mycobacterium tuberculosis, sensible a rifampicina (el antibiograma fenotípico mostró una cepa pansensible). La TC demostró consolidaciones pulmonares y árbol en brote, junto con el compromiso óseo de columna cervical, dorsal y lumbar con imágenes líticas y colecciones pre y paraespinales. En la RMN se observaron imágenes infiltrativas desde C4 a C6; D4 a D6, D9 a D12; fractura patológica de D6 y D10 e infiltración en L1, L2 y L3. Inició tratamiento anti-TB con esquema estándar de primera línea (isoniacida, rifampicina, pirazinamida, etambutol). Dada la extensa destrucción y el peligro de cuadriplejía/paraplejía por el compromiso cervical y/o dorsal, se indicó posición decúbito dorsal permanente, collar de Filadelfia, asistencia kinésica y conducta neuroquirúrgica en forma programada en los niveles cervicales, D6 y D10. Previo a la cirugía programada presentó un cuadro agudo de paraplejía con nivel sensitivo D8, con compromiso vesical. Se interpretó como nivel de compresión aguda en D6. Se indicó neurocirugía de urgencia con descompresión medular vía posterior con laminectomía dorsal 6 y parcialmente D5 y 7 y evacuación de una colección epidural. Fue recuperando la función motora y sensitiva en forma progresiva. Posteriormente se realizó la cirugía programada cervical vía anterior con corporectomía de C4, C5, C6 y C7 más artrodesis de C3 a D1 con reemplazo de cuerpo vertebral más injerto autólogo, placa y tornillos. En la TC de control se evidenció luxación posterior de D6 con compresión del canal espinal y deterioro neurológico por compresión medular. Se reconsideró la táctica quirúrgica debido a la inestabilidad mecánica y neurológica. Se realizó descompresión y alineación del nivel luxado con artrodesis posterior de los tres niveles espinales no adyacentes, cervical, dorsal 6 y dorsal 10 en un solo tiempo quirúrgico. Se fijó desde  C3 hasta D12 con tornillos poliaxiales y barra de transición cervicodorsal. En cada tiempo quirúrgico se evidenció evacuación espontánea de material caseoso, BAAR positivo, y se realizaron lavados profusos.  Presentó mejoría clínica, bacteriológica y resolución de las lesiones pulmonares. Recuperó movilidad con rehabilitación kinésica sumada al tratamiento específico (3 meses de primera fase e indicación de continuación con isoniacida y rifampicina hasta completar los 12 meses). Egresó caminando por sus propios medios, luego de una prolongada internación de 5 meses.",
+        "gold_summary": "Se presenta el caso de un varón de 20 años con espondilitis tuberculosa multinivel no contigua (cervical, dorsal 6, dorsal 10 y lumbar). Se trata de un paciente HIV negativo con tuberculosis diseminada con grave compromiso de su estado general y múltiples localizaciones de la enfermedad. Algunas tenían fistulas que secretaban caseum. El paciente presentó paraplejía aguda que requirió, teniendo en cuenta el nivel sensitivo a nivel dorsal 6, una primera cirugía urgente de descompresión por vía posterior. Luego se efectuó la cirugía programada. En primera instancia, la región cervical por vía anterior, con corporectomía, colocación de reemplazo de cuerpo vertebral más injerto autólogo y placa con tornillos. Posteriormente se evidenció luxación del nivel dorsal 6 hacia atrás comprimiendo la médula espinal y, dada la inestabilidad mecánica, se indicó un tercer tiempo quirúrgico por vía posterior que comprendió reducción, descompresión y fijación, resolviendo los tres niveles por vía posterior con barras y tornillos. El tratamiento quirúrgico, médico y kinésico de esta forma poco frecuente del mal de Pott fue exitoso, con recuperación de su estabilidad mecánica y progresiva recuperación de su estado neurológico.",
+        "synthetic_summary": {
+            "B1": "Un joven de 20 años tenía tuberculosis que afectaba sus huesos y pulmones. Tenía mucho dolor y dificultad para mover el hombro. La infección dañó varias partes de su columna y causó debilidad en sus piernas. Recibió medicinas, fisioterapia y varias cirugías para quitar la presión en su médula y arreglar sus huesos. Poco a poco mejoró y pudo caminar al salir del hospital.",
+            "B2": "Un joven de 20 años con tuberculosis pulmonar tuvo una infección grave que afectó varias vértebras de su columna, causando daño y pérdida de fuerza en sus piernas. Aunque no tenía VIH, su tuberculosis estaba muy avanzada y provocó heridas que secretaban material infectado. Cuando perdió movilidad en las piernas, le hicieron una cirugía urgente para aliviar la presión en la médula espinal. Después, le realizaron otras cirugías para estabilizar la columna y evitar más daños. Además, recibió tratamiento con medicamentos específicos contra la tuberculosis y rehabilitación física. Gracias a estas intervenciones, mejoró su estado general, recuperó fuerza y pudo caminar al salir del hospital después de cinco meses.",
+            "B3": "Un joven de 20 años con tuberculosis pulmonar, sin infección por VIH, presentó una forma grave y diseminada de tuberculosis ósea que afectó múltiples niveles de su columna vertebral, incluyendo regiones cervical, dorsal y lumbar. Su estado general estaba muy deteriorado, con pérdida muscular y lesiones tumorales que secretaban material caseoso, característico de la tuberculosis. Durante la hospitalización, desarrolló una paraplejía aguda causada por compresión medular en la región dorsal, lo que requirió una cirugía urgente para descomprimir la médula espinal. Posteriormente, se realizaron cirugías programadas para estabilizar la columna, que incluyeron la extracción de cuerpos vertebrales afectados y la colocación de injertos óseos y dispositivos de fijación. Sin embargo, se detectó una luxación en el nivel dorsal 6 que comprometía nuevamente la médula, por lo que se llevó a cabo una tercera intervención para corregir esta inestabilidad. Gracias a un tratamiento combinado con fármacos antituberculosos, cirugía y rehabilitación kinésica, el paciente logró una mejoría significativa, recuperando movilidad y estabilidad vertebral. Este caso ilustra la complejidad y gravedad del mal de Pott cuando afecta múltiples niveles vertebrales, así como la importancia de un manejo multidisciplinario para prevenir secuelas neurológicas graves."
+        }
+    },
+    {
+        "article": "Un hombre japonés de 23 años fue admitido en nuestro hospital debido al empeoramiento de la disnea de esfuerzo. Había mostrado dificultad para correr a los dos años y se le diagnosticó EDMD con una mutación genética de LMNA (Lamin A/C) en el exón 1 de leucina 102 a prolina. De acuerdo con las manifestaciones típicas de EDMD, sus codos, rodillas y tendones de Aquiles se habían contraído a los cinco años, y sus músculos cervicales posteriores se habían vuelto rígidos; sin embargo, continuó con su vida diaria habitual, aunque con una leve restricción de ejercicio. Su padre también había sido diagnosticado con EDMD y murió repentinamente a los 40 años.\n\nCuando el paciente tenía 19 años, fue admitido en un hospital por primera vez debido a una insuficiencia cardiaca congestiva. Los signos de insuficiencia de la RV, tales como edema de las piernas y congestión hepática, fueron prominentes, como lo indica el alto nivel de bilirrubina en sangre (2,5 mg/dL). La ecocardiografía mostró que la excursión sistólica del plano anular tricúspide (TAPSE) era de 5,7 mm, la velocidad de la RV de 5,1 cm/s y el cambio del área fraccional de la RV (RVFAC) del 19 %, lo que indica una marcada disfunción de la RV. Se introdujeron diuréticos de alta dosis además de carvedilol (10 mg/día) y enalapril (2,5 mg/día). A pesar de esos medicamentos, fue readmitido debido al empeoramiento de la insuficiencia de la RV.\n\nA los 22 años, se le implantó un desfibrilador cardioversor implantable (ICD) debido a su taquicardia ventricular no sostenida (VT) y a la historia familiar de muerte súbita cardiaca. En este momento, el cateterismo cardiaco derecho (RHC) mostró una presión de la cuña de la arteria pulmonar (PAWP) de 22 mmHg, presión auricular derecha (RAP) de 17 mmHg, e índice de trabajo de accidente cerebrovascular ventricular derecho (RVSWI) de 6.47, lo que sugiere una disfunción severa sostenida del RV. Como tal, el fallo del RV probablemente fue la principal condición patológica a lo largo de su curso clínico.\n\nTenía insuficiencia cardiaca sintomática con la clasificación III de la New York Heart Association con dosis máximas de medicación guiada por directrices, y su electrocardiograma mostraba un ritmo sinusal regular y bloqueo de rama izquierda con ancho QRS (150 ms). Su fracción de eyección del ventrículo izquierdo (LVEF) era ≤35 % en la ecocardiografía. Por lo tanto, se consideró que estaba indicado para CRT y se le actualizó a ICD a los 23 años.\n\nAl ingreso, su presión arterial era de 106/65 mmHg y su frecuencia cardíaca de 60 latidos/min con un ritmo regular. El examen físico reveló un tercer sonido cardíaco y un soplo pan sistólico (Levine II/VI) en la región apical. Los sonidos respiratorios eran claros, mientras que una vena yugular distendida y un edema de miembros inferiores eran evidentes. La radiografía de tórax indicó un aumento de la relación cardiotorácica (59%) sin congestión pulmonar.\n\nEl electrocardiograma mostró un ritmo biventricular debido a la TRC. La ecocardiografía reveló una ligera dilatación en ambos ventrículos (diámetro final diastólico del LV: 54 mm, diámetro del RV: 50 mm) con una reducción de la LVEF (30%). La función del RV también se redujo, como lo indican una reducción de la RVFAC (11%) y un bajo TAPSE (8 mm). Ambos ventrículos agrandados causaron una pérdida de sujeción y coaptación de las valvas que resultó en una regurgitación mitral moderada y una regurgitación tricuspídea severa. La vena cava inferior se dilató a 23 mm con una reducción de la fluctuación respiratoria.\n\nEn los hallazgos histológicos de los músculos cervicales posteriores realizados más tarde en la autopsia, se observó un aumento en la variación del tamaño de la fibra muscular con una infiltración moderada de tejido conectivo, lo que fue compatible con la EDMD. Los análisis de sangre revelaron péptido natriurético cerebral (BNP) 196.1 pg/mL, bilirrubina total 1.4 mg/dL, aspartato aminotransferasa (AST) 39 U/L, alanina aminotransferasa (ALT) 43 U/L, y gamma glutamil transpeptidasa (gamma-GTP) 451 U/L, lo que sugirió una disfunción hepática. Aunque las arterias coronarias estaban intactas en la angiografía, una biopsia endocárdica del VD reveló una hipertrofia cardiaca con un aumento de la magnitud del núcleo y el miocardio.\n\nLa microscopía electrónica demostró hallazgos típicos de la EDMD: un número reducido de miofibrillas, necrosis y la formación de pseudo- o verdaderas inclusiones. Dado que se descartaron otras cardiomiopatías secundarias mediante estos hallazgos clínicos e histológicos, diagnosticamos una cardiomiopatía relacionada con la EDMD.\n\n\nEl curso clínico del paciente. El cateterismo cardiaco derecho (RHC) en el día 11 mostró disfunción y congestión severa del LV/RV, y se iniciaron algunos inótropos. Aunque la hemodinámica del paciente mejoró, su función renal empeoró progresivamente en el día 38. Preocupados por el empeoramiento de su función renal debido a la disminución de la presión arterial, se iniciaron la dopamina y el soporte mecánico (IABP y CRRT), y la función renal y la hemodinámica del paciente mejoraron. Sin embargo, desarrolló insuficiencia hepática aguda junto con insuficiencia severa del RV indicada por los datos del RHC en el día 68. Aunque se introdujo ECMO veno-atrial en el día 71, la disfunción hepática y la DIC causaron diátesis hemorrágica sistémica, y el paciente falleció por fallo multiorgánico en el día 100. CRRT: terapia de reemplazo renal continua, DIC: coagulación intravascular diseminada, ECMO: oxigenación por membrana extracorpórea, IABP: bombeo de globo intraaórtico, LV: ventrículo izquierdo, RV: ventrículo derecho\n\nEl RHC en el día 11 mostró que el índice cardiaco (IC) era de 2,0 L/min/m2 (método de Fick), y la PAP era de 15 mmHg, lo que indicaba un subgrupo IV de Forrester. La presión arterial pulmonar (PAP) era de 29/12 (18) mmHg, y la RAP era de 15 mmHg. El RVSWI, uno de los parámetros hemodinámicos para la función del RV, se calculó con la siguiente fórmula: RVSWI (g·m/m2/latido)=[presión arterial pulmonar media (mPAP)-presión atrial derecha media (mRAP)]×índice de volumen de latido (SVI)×0.0136. Su RVSWI era de 1.36 g·m/m2/latido, lo que indicaba una disfunción severa del RV. Para compensar el síndrome de baja producción del paciente y la congestión, comenzamos una infusión continua de dobutamina (3.0 μg/kg/min) y añadimos milrinona (0.125 μg/kg/min) en el día 16.\n\n\nEn el día 32, los datos de RHC mejoraron, con un aumento del IC (2,48 L/min/m2), una reducción de la PAWP (13 mmHg) y un aumento de la RVSWI (2,8 g·m/m2/latido). Sin embargo, en el día 38, la función renal del paciente empeoró progresivamente, posiblemente debido a una presión venosa central alta (CVP) e hipotensión, ya que la presión arterial había sido de alrededor de 70/40 mmHg varios días antes del empeoramiento de la función renal. Para aumentar su presión arterial, se inició una infusión continua de dopamina (2,0 μg/kg/min); se redujo la milrinona y se interrumpieron el enalapril y la eplerenona. Además, se necesitaron temporalmente el bombeo de globo intraaórtico (IABP) y la terapia de reemplazo renal continuo (CRRT). A medida que la hemodinámica del paciente mejoró en respuesta al aumento de la saturación de oxígeno venoso mixto (SvO2, 70-80%) y el IC (3,0-3,5 L/min/m2), se retiraron el IABP y la CRRT en el día 45.\n\nSin embargo, el día 68, el IC volvió a disminuir a 1,25 l/min/m2 y la congestión pulmonar y la retención de fluidos del paciente se deterioraron; la PAWP era tan alta como la RAP, a 22 mmHg. Además, los niveles de bilirrubina en suero y las transaminasas hepáticas del paciente aumentaron drásticamente, lo que sugiere el desarrollo de insuficiencia hepática. El día 71, se inició la ECMO VA a través de una vena femoral a la arteria subclavia, pero debido a la diátesis hemorrágica sistémica acompañada por la coagulación intravascular diseminada (CID), el paciente falleció de insuficiencia multiorgánica el día 100.\n\nUna autopsia realizada con el consentimiento informado de la familia del paciente reveló un agrandamiento eferente en ambos ventrículos con un espesor de pared delgado. El examen histopatológico reveló que la hipertrofia miocárdica leve a moderada y la fibrosis severa eran evidentes en el RV y el LV. El peso del hígado aumentó significativamente a 2298 g, y se detectaron congestión hepática macroscópica y colestasis. En las imágenes microscópicas, el área de la vena porta apenas cambió, y se observó atrofia o pérdida de hepatocitos alrededor de las venas centrales, lo que indica un «hígado de shock». En los pulmones, se observó una hemorragia alveolar extensa, y se observó una colección de macrófagos que habían ingerido hemosiderina, lo que refleja una diátesis hemorrágica sistémica.\n\nMH - Adulto\nMH - Insuficiencia cardiaca/*etiología/fisiopatología/terapia\nMH - Humanos\nMH - Lamin tipo A/genética\nMH - Hombre\nMH - Distrofia muscular, Emery-Dreifuss/*complicaciones/diagnóstico/genética/terapia\nMH - Mutación\n",
+        "gold_summary": "Un hombre de 23 años tenía debilidad muscular progresiva y distrofia muscular de Emery-Dreifuss (EDMD) debido a una mutación de LMNA (lamina A/C). Insuficiencia cardiaca congestiva diagnosticada a los 19 años de edad. El tratamiento farmacológico máximo/resincronización cardiaca no logró mejorar la función cardiaca. Por lo tanto, fue hospitalizado debido a insuficiencia cardiaca. A pesar de la oxigenación por membrana extracorpórea, desarrolló una disfunción cardiaca derecha grave y falleció (fallo multiorgánico).\n",
+        "synthetic_summary": {
+            "B1": "Un joven de 23 años tenía una enfermedad llamada distrofia muscular de Emery-Dreifuss, que afecta los músculos y el corazón. Desde niño, tuvo problemas para moverse y luego su corazón comenzó a fallar. Aunque recibió medicinas y un aparato para ayudar al corazón, su salud empeoró. Finalmente, el corazón derecho dejó de funcionar bien y falleció.",
+            "B2": "Un joven de 23 años tenía distrofia muscular de Emery-Dreifuss, una enfermedad genética que afecta los músculos. Desde niño, presentó rigidez y contracturas musculares. A los 19 años, comenzó a tener problemas en el corazón, especialmente en el ventrículo derecho, que es una de sus cámaras. Los medicamentos y un dispositivo para sincronizar el latido no mejoraron su condición. A pesar de tratamientos avanzados, como la oxigenación por membrana extracorpórea (una máquina que ayuda a respirar), su corazón empeoró. Luego, sufrió insuficiencia hepática y renal, que son fallos en el hígado y los riñones. Finalmente, falleció por fallo multiorgánico. Este caso muestra la gravedad de esta enfermedad y la importancia de un seguimiento cuidadoso.",
+            "B3": "Un hombre japonés de 23 años con distrofia muscular de Emery-Dreifuss (EDMD), causada por una mutación en el gen LMNA, presentó insuficiencia cardiaca congestiva desde los 19 años. A pesar de recibir tratamiento farmacológico máximo y terapia de resincronización cardiaca, su función ventricular derecha se deterioró progresivamente, manifestando síntomas graves y signos evidentes de congestión. Durante la hospitalización, se detectó disfunción severa del ventrículo derecho junto con insuficiencia renal y hepática, lo que requirió soporte mecánico avanzado, incluyendo oxigenación por membrana extracorpórea (ECMO). Sin embargo, el paciente desarrolló coagulación intravascular diseminada y fallo multiorgánico, que finalmente condujeron a su fallecimiento. La autopsia reveló fibrosis cardiaca extensa, hipertrofia miocárdica y daño hepático por congestión, confirmando la gravedad de la cardiomiopatía asociada a EDMD. Este caso ilustra la complejidad y el pronóstico desfavorable de la insuficiencia cardiaca derecha en pacientes con EDMD, subrayando la necesidad urgente de estrategias terapéuticas más efectivas para esta condición."
+        }
+    },
+    {
+        "article": "Mujer de 65 años sin antecedentes patológicos destacables que en 2004 inició paroxismos lancinantes en los territorios V2 y V3 derechos, con desencadenantes clásicos, por lo que se le diagnosticó una neuralgia del trigémino derecho. En las resonancias magnéticas cerebrales hasta 2021 no se habían realizado las secuencias que permiten identificar si hay un cruce neurovascular. Desde el inicio, el control del dolor con carboxamidas fue difícil. En 2021 presentó exacerbación de los paroxismos previos que aparecieron en V1. La neuralgia se volvió refractaria, sin respuesta a las carboxamidas y la lamotrigina, y muy escasa al clonacepam, por lo que requirió perfusiones de fenitoína y/o lidocaína en las exacerbaciones graves. Simultáneamente inició paroxismos lancinantes en la parte posterior de la lengua y la pared lateral derecha de la orofaringe, que se exacerbaron con la deglución y que aumentaron progresivamente en intensidad y frecuencia. Se orientó como el inicio de una neuralgia del nervio glosofaríngeo derecho. Se repitió la resonancia magnética cerebral con secuencia CISS (del inglés, constructive interference in steady state), que mostró un contacto arterial significativo entre la arteria cerebelosa superior derecha y el origen del V par craneal derecho, y de la arteria cerebelosa anteroinferior con el origen de los pares craneales bajos derechos. Ante un caso de neuralgia del nervio trigémino y neuralgia del nervio glosofaríngeo clásicas, concomitantes y refractarias, se planteó una doble descompresión microvascular en un tiempo como mejor opción terapéutica.\n\nEn marzo de 2021 se realizó una craniectomía retrosigmoidea derecha con exposición de la cisterna perimesencefálica y las cisternas basales. Se procedió a la liberación del V par craneal, y se apreció un íntimo contacto con la arteria cerebelosa superior en su parte sensitiva y adelgazamiento en la zona de entrada de la raíz nerviosa. Se procedió a la colocación de teflón entre la arteria cerebelosa superior y el V par craneal en todo su trayecto. Posteriormente, se exploró la cisterna basal y se apreció loop vascular de la arteria cerebelosa anteroinferior en íntimo contacto con el IX par craneal, donde se colocó teflón y sellante dural encima. El postoperatorio cursó sin incidencias, con resolución completa de la neuralgia del nervio trigémino y reducción >50% de la intensidad de los paroxismos en el territorio glosofaríngeo. A los dos años continúa sin paroxismos trigeminales y presenta <1 paroxismo/mes de intensidad tolerable en el territorio glosofaríngeo desencadenado con la deglución. El tratamiento farmacológico continúa en pauta descendente sin que ello haya supuesto la reaparición de los paroxismos.",
+        "gold_summary": "Mujer de 65 años con NT derecho (inicialmente en V2-V3) desde 2004 con control regular con carboxamidas. Diecisiete años después empeoraron los paroxismos en V2-V3, aparecieron también en V1 y en el territorio del nervio glosofaríngeo derecho (oído derecho y fosa amigdalar al hablar y deglutir). La resonancia magnética cerebral mostró contacto arterial significativo entre arteria cerebelosa superior (ACS) con origen del V par craneal derecho y de la arteria cerebelosa antero-inferior (AICA) con el origen de pares craneales bajos derechos. Se realizó DMV de ambos pares craneales en un mismo tiempo quirúrgico mediante craniectomía retrosigmoidea, y se procedió a la liberación del V par craneal, en contacto íntimo con la ACS, y del IX par craneal en contacto con la AICA derecha, para lo que se puso teflón entre ellas. La paciente tuvo una resolución inmediata de los paroxismos trigeminales y una mejoría considerable en intensidad y frecuencia de los glosofaríngeos. A los 2 años de la intervención continúa la desescalada de tratamiento neuromodulador con buena respuesta.",
+        "synthetic_summary": {
+            "B1": "Una mujer de 65 años tenía dolores fuertes en la cara desde 2004. Con el tiempo, los dolores empeoraron y aparecieron en otras zonas, como la lengua y la garganta. Un estudio mostró que unas arterias tocaban nervios importantes en su cabeza. Los médicos hicieron una cirugía para separar las arterias de los nervios con un material especial. Después de la operación, los dolores mejoraron mucho y ella sigue bien dos años después.",
+            "B2": "Una mujer de 65 años tenía un dolor fuerte en la cara desde 2004. Este dolor fue causado por la neuralgia del nervio trigémino, que controla la sensibilidad de la cara. Con el tiempo, el dolor empeoró y apareció en la lengua y la garganta, indicando un problema en otro nervio llamado glosofaríngeo. Las imágenes del cerebro mostraron que unas arterias presionaban estos nervios. Se hizo una cirugía para separar las arterias de los nervios usando teflón, un material especial. Después de la operación, el dolor en la cara desapareció y el de la garganta mejoró mucho. Dos años después, la paciente tiene pocos episodios de dolor y reduce su medicación poco a poco.",
+            "B3": "Una mujer de 65 años presentó desde 2004 episodios de dolor intenso en el territorio del nervio trigémino derecho, inicialmente en las ramas V2 y V3, que se controlaban con dificultad mediante medicamentos. En 2021, el dolor empeoró y se extendió a la rama V1, además de aparecer nuevos episodios dolorosos en la lengua y la garganta, relacionados con el nervio glosofaríngeo derecho. Una resonancia magnética con secuencias especiales reveló que arterias cerebelosas estaban en contacto estrecho con los nervios afectados, lo que sugería una compresión vascular. Por ello, se realizó una cirugía de descompresión microvascular para liberar ambos nervios, colocando material de teflón para separar las arterias de los nervios. Tras la intervención, la paciente experimentó una desaparición completa del dolor trigeminal y una reducción significativa del dolor glosofaríngeo. Dos años después, mantiene un control adecuado del dolor con una reducción progresiva de la medicación, sin reaparición de los episodios intensos. Este caso muestra la efectividad de la cirugía en neuralgias craneales refractarias causadas por compresión vascular."
+        }
+    },
+    {
+        "article": "Hombre de 36 años, bisexual, en profilaxis antirretroviral de pre-exposición al HIV, sin antecedentes de viaje, que refirió haber asistido a un evento donde tuvo contactos con parejas ocasionales cuya identidad y antecedentes se desconocen. Diez días después comenzó con fiebre, odinofagia y dolor cervical por lo que consultó en varias oportunidades, hasta que a los siete días del inicio de los síntomas se internó por persistencia de los mismos a pesar del tratamiento antibiótico indicado. Al ingreso presentó exudado faríngeo, adenopatías cervicales bilaterales dolorosas y pápulas umbilicadas en escroto y pene y pústulas en cara de cinco días de evolución. Se realizó tomografía computarizada de cuello con contraste endovenoso que descartó colección, ecografía abdominal con leve hepatoesplenomegalia, e inició tratamiento empírico con ceftriaxona y azitromicina. Se tomaron muestras para cultivo, para serologías, y escarificación de dos lesiones de la cara que se enviaron al Laboratorio Nacional de Referencia, INEI-ANLIS Dr. Carlos G. Malbrán, para PCR de punto final para Orthopoxvirus, con resultado DETECTABLE, confirmando así el diagnóstico de viruela símica. La secuenciación arrojó un alto porcentaje de homología con secuencias del clado de África Occidental (MPV-ARG003-2022, Genbank_ID ON800897). Otros diagnósticos diferenciales fueron descartados. El paciente evolucionó con aparición de una úlcera en lengua y nuevas lesiones asincrónicas en glúteos, región perianal, inguinal derecha, umbilical, frontal, cuello, mano derecha y dorso de pie en un total de no más de 25. En el laboratorio se constató un aumento de transaminasas en 2.2 veces el valor normal, sin otros datos significativos.  Por persistencia del dolor cervical se solicitó nueva tomografía computarizada a los 14 días del inicio de los síntomas que evidenció adenomegalias con centro hipodenso de aspecto necrótico, que no requirieron drenaje quirúrgico. Al día 17 se realizó PCR en muestras de exudado de fauces y semen las que también resultaron positivas para virus de viruela símica. Se externó con franca mejoría clínica dos días después. El paciente dio su consentimiento informado escrito para la publicación de este informe de caso y las imágenes que lo acompañan.",
+        "gold_summary": "Se trata de un hombre joven, bisexual, en profilaxis antirretroviral de pre-exposición al HIV, cuya forma de presentación fue faringitis exudativa sin otra etiología documentada y adenopatías que evolucionaron a la necrosis, presencia de lesiones asincrónicas características en cara, cuello, abdomen, extremidades y genitales. El diagnóstico fue por detección de ADN viral por reacción en cadena de la polimerasa en lesiones de piel, exudado de fauces y semen. El compromiso faríngeo con presencia de exudado luego del descarte de otras infecciones, podría ser una rareza para la forma epidémica de la enfermedad. El hallazgo del virus en semen ya reportado en otras publicaciones no es suficiente aún para confirmar la vía sexual como forma de trasmisión.",
+        "synthetic_summary": {
+            "B1": "Un hombre joven tuvo fiebre, dolor de garganta y ganglios inflamados en el cuello. También apareció con pequeñas heridas en la piel del cuerpo y los genitales. Los médicos hicieron pruebas y encontraron un virus llamado viruela símica. El virus estaba en la saliva y en el semen. Poco a poco, el hombre mejoró con tratamiento, aunque tuvo algunas heridas nuevas. No se sabe con certeza cómo se contagió.",
+            "B2": "Un hombre de 36 años, bisexual y en prevención contra el VIH, tuvo fiebre y dolor de garganta. También presentó ganglios inflamados en el cuello y lesiones en la piel, como pápulas y pústulas. Se descartaron otras infecciones y confirmaron viruela símica, un virus detectado en lesiones, garganta y semen. La inflamación en el cuello empeoró, con áreas dañadas, pero no requirió cirugía. Aunque el virus apareció en el semen, no se sabe si se transmite por vía sexual. Después del tratamiento, mejoró y fue dado de alta. Este caso muestra que la viruela símica puede afectar la garganta y la piel de forma inusual.",
+            "B3": "Un hombre de 36 años, bisexual y en profilaxis antirretroviral para prevenir el VIH, presentó fiebre, dolor de garganta y dolor cervical tras un evento con contactos sexuales ocasionales. A pesar del tratamiento antibiótico, sus síntomas persistieron y desarrolló lesiones cutáneas características en varias zonas del cuerpo, incluyendo genitales y cara. Las pruebas confirmaron la presencia del virus de la viruela símica mediante PCR en muestras de piel, garganta y semen. Además, presentó adenopatías cervicales que evolucionaron a necrosis, detectadas por tomografía, sin requerir intervención quirúrgica. El compromiso faríngeo con exudado, tras descartar otras infecciones, es poco común en esta enfermedad. Aunque se detectó el virus en semen, esto no confirma que la transmisión sea exclusivamente sexual. El paciente mejoró clínicamente y fue dado de alta tras dos semanas. Este caso resalta la importancia de considerar la viruela símica en pacientes con síntomas faríngeos y lesiones cutáneas, especialmente en contextos de riesgo, y subraya la necesidad de seguir investigando las vías de transmisión del virus."
+        }
+    },
+    {
+        "article": "Paciente de sexo masculino de 23 años, natural de Itagüí - Colombia, antecedente familiar de muerte súbita de etiología no clara en abuelo a los 50 años, sin otros antecedentes familiares o personales de importancia. Venía en seguimiento externo por episodios sincopales a repetición con diagnóstico desde la infancia de disfunción del nodo sinusal sintomática por lo que se le implantó un marcapaso.\n\nDurante controles posteriores no hay reporte de deterioro de clase funcional hasta el año 2012 en Guayaquil-Ecuador. Durante su hospitalización se realiza el cambio de generador; en el primer mes postoperatorio presenta como complicación temprana una infección de bolsillo de marcapaso por lo que requirió el explante de la unidad generadora con posterior abandono de electrodo ventricular previamente implantado. Se realiza un nuevo implante de marcapaso en el lado contralateral sin complicaciones ni registro de nuevos eventos sincopales en los siguientes 10 años de seguimiento.\n\nSeis meses antes del ingreso presentaba deterioro de clase funcional NYHA III, sin otros síntomas y sin reportes de evaluaciones por servicio de electrofisiología desde el último implante de generador de marcapaso en 2012. Durante controles ambulatorios se reportó la suspensión del tratamiento con beta bloqueador debido a la pobre tolerancia.\n\nAl examen físico se encontró soplo sistólico en foco aórtico II/VI sin irradiación, no presentó signos de congestión central o periférica. Dentro de los laboratorios no se evidenció alteración en función renal, electrolítica ni del perfil hematológico. Se programó el marcapaso con evidencia de agotamiento de la batería de generador. Se realizó un ecocardiograma transtorácico donde se encontró hipertrofia concéntrica severa del septum interventricular a nivel medio ventricular, de 26 mm con gradiente intracavitario pico de 117 mmHg y movimiento sistólico anterior del velo mitral (SAM) el cual generaba una regurgitación mitral leve.\n\nFue evaluado por Heart Team, debido al score de riesgo de muerte súbita (16,8%) además de tener antecedentes familiares de muerte súbita considerando EUROSCORE II 0,67%; en cuanto a los electrodos abandonados previamente y la contraindicación de realización de resonancia magnética cardiaca, dado a la incompatibilidad del marcapaso, se realiza un estudio tomográfico y se consideró la realización de miectomía por sintomatología y variante documentada.\n\nFue programado para realización de miectomía medio ventricular por abordaje transapical con retiro de electrodos; se realizó la ventriculotomía izquierda en el ápex, con posterior resección del septum desde el parte medio ventricular hasta la base, con posterior retiro de electrodos adheridos a velo septal tricúspideo. No hubo complicaciones intraoperatorias y posteriormente se presentó disminución del gradiente intracavitario sin presencia del fenómeno SAM. Durante su estancia en Unidad de Cuidados Intensivos el paciente cursó con dos episodios documentados de taquicardia ventricular con inestabilidad hemodinámica por lo cual se le colocó un cardiodesfibrilador implantable (CDI) compatible con resonancia magnética (MRI) ST Jude sin presentar nuevos episodios de TV. El paciente cursó sin nuevas intercurrencias y se iniciaron los estudios ambulatorios de estudio genético debido a sus antecedente familiares.\n\nEl paciente presentó una evolución posoperatoria favorable luego del implante de CDI. En los estudios genéticos se encontró una variante, probablemente patogénica, en heterocigosis del FLNC, c 4636G>A consistente con miocardiopatía familiar hipertrófica tipo 26 autosómica dominante.\n\nActualmente, el paciente se encuentra en clase funcional I, sin arritmias evidenciadas en la telemetría y en tratamiento regular con Bisoprolol 5 mg. Se inició ampliación de estudio genético a familiares directos, sin embargo, debido al difícil acceso a servicios de salud su ejecución fue limitada.",
+        "gold_summary": "A continuación, se presenta el caso de un paciente sexo masculino de 23 años con diagnóstico de cardiomiopatía hipertrófica variante medio apical, en quien se documenta variante de la filamina C, ante la inadecuada respuesta y persistencia de sintomatología frente al manejo médico, se realizó el procedimiento de miectomía con abordaje transapical, con posterior mejoría de sintomatología clínica y obstrucción al tracto de salida.",
+        "synthetic_summary": {
+            "B1": "Un joven de 23 años tenía problemas en el corazón desde niño y usaba un marcapasos. Con el tiempo, su corazón se hizo más grueso y tuvo dificultad para que la sangre saliera bien. Le hicieron una operación para quitar parte del músculo grueso y mejoró mucho. También le pusieron un aparato para cuidar su ritmo del corazón. Ahora está bien y sigue con medicinas para cuidar su salud.",
+            "B2": "Un joven de 23 años con antecedentes familiares de muerte súbita tenía cardiomiopatía hipertrófica, una enfermedad del corazón que causa engrosamiento del músculo. A pesar de tener un marcapasos y tratamiento médico, presentaba síntomas graves y obstrucción en el corazón. Se le realizó una cirugía llamada miectomía para reducir el grosor del músculo y mejorar el flujo de sangre. Después, tuvo episodios de taquicardia ventricular, por lo que le implantaron un desfibrilador para prevenir problemas graves. Los estudios genéticos mostraron una variante en el gen FLNC, relacionada con su enfermedad. Actualmente, está estable, sin síntomas y con tratamiento, aunque el acceso a estudios para su familia ha sido difícil.",
+            "B3": "Un hombre de 23 años con antecedentes familiares de muerte súbita fue diagnosticado en la infancia con disfunción del nodo sinusal, lo que motivó la implantación de un marcapasos. Tras una infección del dispositivo y el reemplazo del generador, presentó deterioro funcional y síntomas persistentes a pesar del tratamiento médico. El ecocardiograma evidenció hipertrofia severa del septum interventricular con un gradiente intracavitario elevado y movimiento anómalo de la válvula mitral. Debido al alto riesgo de muerte súbita y la contraindicación para resonancia magnética, se optó por una miectomía medio ventricular vía transapical, retirando además electrodos antiguos. Posteriormente, el paciente desarrolló episodios de taquicardia ventricular que requirieron la implantación de un cardiodesfibrilador compatible con resonancia magnética. Los estudios genéticos identificaron una variante probablemente patogénica en el gen FLNC, asociada a miocardiopatía hipertrófica familiar. Actualmente, el paciente se encuentra estable en clase funcional I, sin arritmias y en tratamiento con bisoprolol, mientras se intenta ampliar el estudio genético a sus familiares directos, aunque con dificultades por el acceso limitado a servicios de salud."
+        }
+    },
+    {
+        "article": "Varón de 32 años, con antecedentes de infección por VIH en terapia anti-retroviral (carga viral indetectable y recuento de CD4 de 454 céls/mm3) y consumo de tabaco y drogas (marihuana, éxtasis y ketamina). Consultó en nuestra unidad de salud sexual por una historia de dos semanas de secreción uretral de aspecto mucoso con escaso ardor local, asociado a una úlcera eritematosa indurada en el surco balanoprepucial de 1,5 cm de diámetro, dolorosa y exudativa. Al examen físico presentaba una adenopatía inguinal izquierda de 2 cm, sensible a palpación, blanda, no adherida a planos profundos ni asociada a signos inflamatorios cutáneos. No presentaba fiebre ni otros síntomas asociados. En la anamnesis dirigida, refirió 20 parejas sexuales hombres en el último año, con relaciones sexuales orales y anales insertivas y receptivas, con uso ocasional de preservativo. No tenía antecedente de viajes fuera de Chile. Cuatro semanas antes del inicio de los síntomas, había tenido un contacto sexual de riesgo sin preservativo con una pareja contactada mediante una aplicación de telefonía móvil. Con el diagnóstico presuntivo de una sífilis primaria y uretritis en estudio, se tomaron muestras de sangre y secreción uretral para estudio microbiológico. Por la conducta sexual de alto riesgo, se tomó también un hisopado anorrectal para tinción de Gram y cultivo. De acuerdo con la norma vigente en Chile, se administraron tres dosis de 2,4 millones de UI de penicilina benzatina intramuscular separadas por una semana, además de 250 mg de ceftriaxona intramuscular y 1 g de azitromicina oral, ambas por una vez. El estudio de laboratorio confirmó el diagnóstico de sífilis, con un VDRL (Venereal disease research laboratory) reactivo con dilución de 1:2 y MHA-TP (Microhemagglutination assay for antibody to Treponema pallidum) reactivo. La tinción de Gram y los cultivos de secreción uretral (agar sangre y Thayer Martin) fueron negativos. La muestra anorrectal mostró escasos diplococos gramnegativos en la tinción de Gram, con desarrollo abundante de N. meningitidis y microbiota comensal en el cultivo corriente. La identificación bacteriana se realizó a través de espectrometría de masas MALDI-TOF MS. El paciente evolucionó favorablemente, sin secreción uretral y con regresión de la lesión ulcerada genital y la adenopatía inguinal a las dos semanas de seguimiento. Las tinciones de Gram y los cultivos de control de secreción uretral, faríngea y anorrectal resultaron negativos. Se citó al contacto sexual reciente para estudio y tratamiento. Sin embargo, éste se encontraba asintomático y los cultivos faríngeo, anorrectal y uretral realizados fueron negativos.",
+        "gold_summary": "Presentamos el caso de un HSH con infección por VIH, que consultó por un cuadro de uretritis y sifilis primaria, en el cual se aisló N. meningitidis en una muestra anorectal. Fue tratado en forma empírica con ceftriaxona y azitromicina, realizándose un cultivo de control post-tratamiento que fue negativo.",
+        "synthetic_summary": {
+            "B1": "Un hombre con VIH tuvo una herida roja y dolorosa en el pene y un poco de líquido en la orina. También tenía un bulto en la ingle. Los médicos pensaron que tenía sífilis, una enfermedad que se pasa con el contacto sexual. Le dieron medicinas para curar la infección. Después de dos semanas, la herida y el bulto desaparecieron y ya no tenía líquido. También encontraron una bacteria llamada N. meningitidis en una muestra, pero después del tratamiento no apareció más.",
+            "B2": "Un hombre de 32 años con VIH controlado consultó por secreción en el pene y una úlcera dolorosa. Tenía inflamación en la ingle y muchas parejas sexuales sin protección. Se sospechó sífilis primaria, una infección de transmisión sexual, y uretritis, inflamación de la uretra. Se hicieron análisis de sangre y cultivos para confirmar el diagnóstico. Encontraron sífilis y una bacteria llamada N. meningitidis en una muestra del ano. Recibió tratamiento con penicilina, ceftriaxona y azitromicina. Después de dos semanas, mejoró y los cultivos fueron negativos. Su pareja fue estudiada, pero no tenía infección. Este caso muestra la importancia de buscar y tratar infecciones en personas con conductas sexuales de riesgo.",
+            "B3": "Un hombre de 32 años con VIH controlado y antecedentes de consumo de drogas consultó por secreción uretral, úlcera dolorosa en el pene y adenopatía inguinal. Reportó múltiples parejas sexuales y prácticas de riesgo sin protección, lo que orientó hacia sífilis primaria y uretritis como diagnósticos iniciales. Se tomaron muestras para diagnóstico microbiológico y se inició tratamiento empírico con penicilina, ceftriaxona y azitromicina para cubrir posibles coinfecciones. Los análisis confirmaron sífilis, mientras que los cultivos uretrales resultaron negativos para patógenos comunes. No obstante, en la muestra anorrectal se aisló Neisseria meningitidis, una bacteria poco habitual en esta localización. Tras completar el tratamiento, el paciente mostró mejoría clínica significativa y las pruebas de control fueron negativas. Se realizó seguimiento del contacto sexual, quien no presentó infección ni síntomas, lo que refuerza la importancia del control epidemiológico. Este caso resalta la necesidad de considerar infecciones atípicas en pacientes con conductas sexuales de alto riesgo y la utilidad de un tratamiento amplio para cubrir posibles coinfecciones. Además, subraya la importancia del seguimiento y control de parejas sexuales para prevenir la transmisión."
+        }
+    },
+    {
+        "article": "Un paciente hispanoparlante de 63 años de edad se presentó en el hospital como una emergencia con inicio repentino de dificultad respiratoria severa, palpitaciones y sudoración profusa. Estaba en su estado habitual de salud y podía deambular con actividades independientes de la vida diaria hasta 30 minutos antes de su llegada a la sala de urgencias. Tenía un historial de 20 años de hipertensión, un historial de 15 años de diabetes mellitus, enfermedad de la arteria coronaria que requería la inserción de un stent de la arteria coronaria cinco años antes, un historial de diez años de insuficiencia cardiaca de la clase II de la New York Heart Association (NYHA) con una fracción de eyección reducida (EF) del 35 %, enfermedad renal crónica (CKD) en estadio 3B. Al ingresar en el hospital, sus medicamentos incluían carvedilol (25 mg dos veces al día), lisinopril (20 mg diario), espironolactona (25 mg diario), furosemida (20 mg diario), insulina glargina (20 unidades al acostarse), inyección de insulina lispro (7 unidades tres veces al día), atorvastatina (40 mg diario), y aspirina (81 mg diario), sin alergias a medicamentos conocidas.\n\nAl examen, su presión arterial era de 205/110 mmHg, su frecuencia respiratoria de 29 respiraciones/min, su frecuencia cardíaca de 118 latidos/min, la oximetría de pulso era de 82% (en aire ambiente) y su temperatura de 36.2°C. Su peso era de 72 kg y su estatura de 68 pulgadas, lo que resultó en un índice de masa corporal (IMC) de 24.13 kg/m2. Al examen físico, el paciente estaba en grave dificultad respiratoria, sudaba y no podía hablar con claridad. Su presión venosa yugular era elevada, como se muestra por la distensión de la vena yugular (3+). Al auscultar el tórax, se observaron crepitaciones bilaterales en todos los campos pulmonares. La auscultación cardíaca fue notable por un galope con una frecuencia regular y un murmullo sistólico 3/6 que se oía en la línea medioclavicular izquierda, al nivel del quinto espacio intercostal. El punto de impulso cardíaco máximo se desplazó hacia la izquierda (en la línea medioaxilar anterior) y no se observó distensión abdominal ni ascitis, con edema de los miembros inferiores (1+) hasta el nivel de la mitad de la pantorrilla.\n\nEl paciente fue trasladado a la zona de reanimación cardiopulmonar (RCP), donde se midieron los gases sanguíneos en el aire y se solicitaron pruebas de laboratorio. El paciente fue tratado con oxígeno al 100% utilizando una máscara no reanadora y se le colocó en posición de 90°, lo que produjo una mejora en la oximetría de pulso, que aumentó hasta el 90%. Un electrocardiograma (ECG) mostró taquicardia sinusal, depresión del ST del conductor lateral (de 1 mV), desviación del eje izquierdo e hipertrofia del ventrículo izquierdo. Se obtuvo una radiografía de tórax portátil que fue notable por una silueta cardiaca agrandada, señal de asta de ciervo de desviación venosa pulmonar del lóbulo superior (cefalización), y líneas B de Kerley, que indican edema intersticial.\n\nAunque se solicitaron pruebas de laboratorio, debido a que el paciente estaba gravemente enfermo y no se podía demorar el tratamiento, se inició un tratamiento inicial basado en los hallazgos clínicos, el historial clínico, el ECG, los gases arteriales en sangre y los hallazgos de rayos X. En vista de los hallazgos de las investigaciones iniciales y la ausencia de fiebre, se descartó la neumonía y se realizó un diagnóstico de edema pulmonar cardiogénico hipertensivo. Se inició un tratamiento intravenoso (IV) con nitroglicerina, comenzando a 30 mcg/min y aumentando en 15 mcg/min cada 3 minutos, con oximetría de pulso continua y monitoreo de los signos vitales cada 3 minutos. Después de 18 minutos, se tituló la nitroglicerina hasta 120 mcg/min y su presión arterial disminuyó a 148/82 mmHg, su presión arterial sistólica se redujo en un 29%, su presión arterial diastólica se redujo en un 25%, y su frecuencia cardíaca disminuyó a 87 latidos por minuto. Se hizo una rápida mejora clínica y el paciente pudo comunicarse con oraciones completas y pudo respirar sin el uso de músculos accesorios. La oximetría de pulso mostró una saturación de oxígeno >97%, y la suplementación de oxígeno continuó con el uso de una cánula nasal a 3 L/min y la medición de la oximetría de pulso del paciente fue >96%.\n\nDespués de 25 minutos, el paciente fue tratado con enalapril (2,5 mg IV) combinado con furosemida (20 mg IV). La nitroglicerina se redujo a una tasa de 10 mcg/min cada 5 minutos hasta que se interrumpió, seguido de una dosis oral de isosorbida dinitrato (30 mg). Después de la estabilización clínica completa, los resultados de los laboratorios mostraron un recuento de glóbulos blancos (WBC) de 11,43 × 109/uL, hemoglobina de 10,9 g/dl, hematocrito de 31,8%, plaquetas de 74 × 109/L, sodio de 144 mmol/L, potasio de 3,9 mmol/L, cloruro de 107 mmol/L, dióxido de carbono (CO2) de 25 mmol/L, nitrógeno ureico en sangre (BUN) de 27 mg/dL, creatinina de 1,4 mg/dL, péptido natriurético cerebral (BNP) de 3,452 pg/ml, y troponina I <0,05 ng/ml. Las mediciones de gases en sangre en aire incluyeron pH de 7,381, pCO2 de 44,8 mmHg, pO2 de 57 mmHg, HCO3 de 25,8 mmol/L, y saturación de oxígeno de 84%.\n\nSe evaluó al paciente para detectar la presencia de una posible embolia pulmonar (EP) subyacente, utilizando los criterios de estratificación de riesgo de EP de Wells, y se lo estratificó como de bajo riesgo, con una evaluación posterior con un nivel de dímero D de 340 ng/ml, que se interpretó como negativo. La evaluación para detectar hipertiroidismo mostró un valor normal de la medición ultrasensible del ensayo de la hormona estimulante de la tiroides en plasma (usTSH) de 2,56 μU/mL y tiroxina libre (T4) de 6,87 μU/mL.\n\nEl paciente fue admitido en la sala de hospital de medicina interna con un diagnóstico de edema pulmonar cardiogénico hipertensivo y fue dado de alta 48 horas después. Al momento del alta hospitalaria, su medicación incluía furosemida (40 mg diarios), carvedilol (12.5 mg dos veces al día), sacubitril/valsartan (24 mg/26 mg dos veces al día), espironolactona (25 mg diarios) e isosorbida mononitrato (60 mg diarios). El paciente fue sometido a seguimiento semanal por su cardiólogo, quien optimizó la terapia medicinal. No se registraron visitas a urgencias ni hospitalizaciones, al menos durante los siguientes 60 días.\n\nMH - Insuficiencia cardiaca/*complicaciones\nMH - Humanos\nMH - Hipertensión/*complicaciones\nMH - Infusiones, intravenosas\nMH - Hombre\nMH - Edad Media\nMH - Nitroglicerina/*administración y dosificación\nMH - Edema pulmonar/*terapia farmacológica/etiología\nMH - Insuficiencia respiratoria/*terapia farmacológica/etiología\nMH - Agentes vasodilatadores/*administración y dosificación\n",
+        "gold_summary": "Paciente: Hombre, 63 años\n\nDiagnóstico final: Edema pulmonar cardiovenoso hipertensivo\n\nSíntomas: falta de aire\n\nMedicación: —\n\nProcedimiento clínico: —\n\nEspecialidad: Medicina general e interna\n\nUn hombre hispano de 63 años con antecedentes de hipertensión, enfermedad de las arterias coronarias, insuficiencia cardiaca con una fracción de eyección reducida del 35 %, enfermedad renal crónica (ERC) y diabetes mellitus, se presentó como una emergencia con disnea aguda y grave. El paciente fue tratado inicialmente con 100 % de oxígeno suplementario y nitroglicerina intravenosa (IV) en dosis altas (30 mcg/min), que se ajustó cada 3 minutos, aumentando en 15 mcg/min hasta que se alcanzó una dosis de 120 mcg/min. Después de 18 minutos de terapia agresiva, la condición del paciente mejoró y ya no necesitaba ventilación mecánica.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre de 63 años llegó al hospital con mucha dificultad para respirar y sudoración. Tenía problemas del corazón, presión alta y diabetes. Le dieron oxígeno y un medicamento llamado nitroglicerina para ayudar su corazón. Después de un rato, empezó a sentirse mejor y pudo respirar mejor. Luego, siguió con medicinas para cuidar su corazón y estuvo bien en los días siguientes.",
+            "B2": "Un hombre de 63 años con hipertensión, diabetes y problemas del corazón llegó al hospital. Tenía dificultad grave para respirar y palpitaciones. Presentaba edema pulmonar cardiogénico, que es líquido acumulado en los pulmones por un mal bombeo del corazón. Lo trataron con oxígeno y nitroglicerina, un medicamento que baja la presión arterial. Después de unos minutos, su respiración mejoró mucho y pudo respirar sin ayuda. También recibió otros medicamentos para el corazón y los riñones. Fue hospitalizado dos días y luego dado de alta con seguimiento médico. No tuvo más problemas durante los siguientes dos meses.",
+            "B3": "Un hombre de 63 años con antecedentes de hipertensión, diabetes, enfermedad coronaria e insuficiencia cardíaca acudió a urgencias por dificultad respiratoria severa, palpitaciones y sudoración. A su llegada, presentó signos característicos de edema pulmonar cardiogénico hipertensivo, incluyendo presión arterial elevada, crepitaciones pulmonares y distensión venosa yugular. Se inició tratamiento inmediato con oxígeno al 100 % y nitroglicerina intravenosa, ajustando la dosis para reducir la presión arterial y mejorar la función cardíaca. En menos de 20 minutos, la saturación de oxígeno y la capacidad respiratoria mejoraron notablemente, permitiendo al paciente comunicarse con normalidad. Posteriormente, se administraron enalapril y furosemida para continuar el manejo farmacológico. Los estudios complementarios descartaron infecciones pulmonares y embolia pulmonar, confirmando el diagnóstico de edema pulmonar cardiogénico. Tras la estabilización clínica, el paciente fue ingresado en medicina interna y dado de alta en 48 horas con medicación optimizada para insuficiencia cardíaca e hipertensión. En el seguimiento posterior, no se registraron nuevas complicaciones ni hospitalizaciones, lo que indica un adecuado control clínico. Este caso subraya la importancia de un diagnóstico rápido y un tratamiento agresivo en pacientes con múltiples comorbilidades y edema pulmonar cardiogénico."
+        }
+    },
+    {
+        "article": "Historial clínico\nUn niño de 12 años se presentó en nuestro hospital con un mes de historia de sensación de cuerpo extraño y una masa conjuntival pedunculada carnosa que creció con el tiempo. No había historia de trauma o lesiones similares en el otro lado del cuerpo. Se descubrió una masa pedunculada carnosa rosácea de 15 mm de la conjuntiva palpebral derecha durante un examen oftalmológico. La agudeza visual estaba dentro de los límites normales. Se diagnosticó al niño como papiloma de células escamosas pedunculadas y se le realizó una biopsia excisional de la lesión.\n\nHallazgos macroscópicos y microscópicos\nRecibimos un fragmento de tejido blanco grisáceo, pequeño, firme, ovoide, fijado en formalina, de 1,5 x 1 cm, para su análisis patológico. En las secciones microscópicas se encontró una lesión poliopóidea hiperplásica con múltiples quistes globulares en la submucosa conjuntival, junto con una importante infiltración inflamatoria constituida por linfocitos, células plasmáticas y neutrófilos, así como enormes esporangios de paredes gruesas con numerosas endosporas. Las endosporas se liberaron después de que algunos de los esporangios maduros se rompieran. La rinosporidiosis conjuntival se diagnosticó histopatológicamente. No hubo recurrencia ni signo de rinosporidiosis en el ojo ni en ninguna otra área del cuerpo en el último examen del paciente, que fue 7 meses después de la escisión quirúrgica.\n",
+        "gold_summary": "Un niño de 12 años con una masa conjuntival pedunculada carnosa fue llevado al Centro Médico de la Universidad de Jimma con un historial de un mes de sensación de cuerpo extraño. Al paciente se le diagnosticó un papiloma pedunculado de células escamosas y se le realizó una biopsia excisional de la lesión. Se encontró que la masa era una lesión polipoide hiperplásica con numerosos quistes globulares dentro de la submucosa conjuntival, rodeados por un infiltrado inflamatorio pesado de linfocitos, células plasmáticas y neutrófilos, así como grandes esporas de paredes gruesas con numerosas endosporas en secciones microscópicas. Se diagnosticó histopatológicamente rinosporidiosis conjuntival.\n",
+        "synthetic_summary": {
+            "B1": "Un niño de 12 años tenía una masa rosa en el ojo que le causaba molestias. Los doctores pensaron que era un tipo de bulto llamado papiloma y le sacaron la masa para verla mejor. Al estudiar la masa, encontraron que tenía muchas células inflamadas y unas esporas especiales. La enfermedad se llama rinosporidiosis y no volvió a aparecer después de la operación. El niño está bien y su vista no se dañó.",
+            "B2": "Un niño de 12 años tenía una masa en el ojo derecho que le molestaba desde hace un mes. Los médicos pensaron que era un papiloma, un tumor benigno, y lo quitaron para analizarlo. Al estudiar el tejido, encontraron inflamación con muchas células del sistema inmunitario y estructuras llamadas esporangios con endosporas. Estas son características de una infección llamada rinosporidiosis, que afecta la conjuntiva, la membrana que cubre el ojo. Después de la cirugía, el niño no tuvo signos de que la infección volviera en siete meses. Por eso, el tratamiento fue exitoso y no hubo complicaciones.",
+            "B3": "Un niño de 12 años acudió al hospital con una masa carnosa pedunculada en la conjuntiva del ojo derecho, acompañada de sensación de cuerpo extraño durante un mes. La agudeza visual era normal y no había antecedentes de trauma. Inicialmente se diagnosticó un papiloma de células escamosas, por lo que se realizó una biopsia excisional. El análisis microscópico reveló una lesión polipoide con múltiples quistes en la submucosa conjuntival, junto a una inflamación intensa compuesta por linfocitos, células plasmáticas y neutrófilos. Además, se observaron grandes esporangios con paredes gruesas que contenían numerosas endosporas, características típicas de rinosporidiosis conjuntival, confirmando así el diagnóstico. No se detectaron signos de recurrencia ni afectación en otras áreas del cuerpo durante el seguimiento a los siete meses después de la cirugía. Este caso destaca la importancia de considerar infecciones poco comunes en lesiones conjuntivales pedunculadas para un diagnóstico y tratamiento adecuados."
+        }
+    },
+    {
+        "article": "Presentamos el caso clínico de un varón de quince años, sin antecedentes médicos ni intervenciones previas, que acude al servicio de urgencias de pediatría con clínica de vómitos y dolor abdominal epigástrico de cuatro días de evolución, manteniéndose afebril durante la evolución del cuadro.\n\nInicialmente fue manejado como gastroenteritis, pero ante la ausencia de mejoría, con persistencia del dolor abdominal de tipo cólico a nivel epigástrico y de los vómitos de aspecto bilioso, acude a urgencias para nueva valoración.\n\nA la exploración física el paciente presentaba aceptable estado general, se encontraba afebril, con signos leves de deshidratación. El abdomen se encontraba distendido, sin datos de peritonismo y con ruidos hidroaéreos disminuidos. La analítica no presentaba hallazgos significativos, realizándose una radiografía de abdomen con hallazgos sugestivos de obstrucción intestinal.\n\nDada la evolución se decide realizar una tomografía computarizada urgente, en la que se observó presencia de ascitis e importante dilatación de asas de intestino delgado, sugiriendo la interposición de un asa de intestino delgado en el inicio de la transcavidad de los epiplones, con cambio de calibre a nivel del hiato de Winslow.\n\nSe realizó intervención quirúrgica urgente, realizando inicialmente una laparoscopia exploradora. Se observaban asas de intestino delgado dilatadas, e íleon terminal, ciego y colon ascendente de calibre normal pero localizados en hipocondrio derecho, con el ciego muy móvil y sin presentar adherencias al espacio parietocólico derecho. Siguiendo proximalmente el íleon terminal, se observaron asas de intestino delgado de distinto calibre desde la profundidad de la teórica localización del hiato de Winslow. Se consiguió traccionar de ciego e íleon terminal hasta desplazarlos a fosa iliaca derecha, pero sin llegar a identificar correctamente el punto de cambio de calibre, ya que la interposición del borde inferior del hígado y la distensión de asas de intestino delgado dificultaban la técnica. Se intentó mejorar la visualización mediante punción percutánea de un asa dilatada para vaciar el gas, sin mejoría. Para asegurar la resolución del cuadro obstructivo se decidió realizar una laparotomía media supraumbilical. Al acceder a cavidad se evidenciaba el cambio de calibre en íleon, a unos 40 centímetros de la válvula ileocecal, con signos compatibles con herniación de un tramo de unos cinco centímetros de íleon a través de hiato de Winslow. En ambos extremos del asa herniada observamos la impronta congestiva del hiato sobre el asa (Fig. 3). Se identificó el hiato de Winslow, de calibre normal, por lo que no se realizó ninguna técnica preventiva para disminuir el riesgo de recidiva.\n\nDurante los primeros días del postoperatorio el paciente presentó un íleo paralítico, pudiendo retirar la sonda nasogástrica a los cinco días de la cirugía e iniciando tolerancia oral con buena respuesta. Simultáneamente desarrolló una colección pélvica que se manejó de forma conservadora con antibióticos, con buena evolución. Finalmente, el paciente fue dado de alta a los diez días de la intervención, con tránsito conservado, manteniéndose afebril y con buen estado general.\n\nActualmente el paciente está en seguimiento en consultas externas de cirugía pediátrica.",
+        "gold_summary": "Presentamos el caso clínico de un varón adolescente de 15 años sin antecedentes quirúrgicos previos, con clínica de dolor abdominal y vómitos, en el que la tomografía computarizada sugería un cuadro de obstrucción intestinal a causa de hernia interna a nivel del hiato de Winslow. Precisó de intervención quirúrgica mediante laparoscopia exploradora, reconvertida por mala visualización a laparotomía media supraumbilical, para reducción del asa de íleon herniada. Esta presentaba buen aspecto y no fue necesaria la resección intestinal. No se realizó ninguna técnica preventiva para disminuir el riesgo de recidiva. Postoperatoriamente, el paciente presentó una colección pélvica manejada de manera conservadora con antibióticos. Actualmente se encuentra en seguimiento en consultas externas de cirugía pediátrica.",
+        "synthetic_summary": {
+            "B1": "Un niño de 15 años tuvo dolor de barriga y vómitos por varios días. Los médicos hicieron una prueba y vieron que parte de su intestino estaba atrapada en un lugar raro dentro de su cuerpo. Lo operaron para sacar esa parte y estaba bien, sin daño. Después de la operación, tuvo una pequeña infección que mejoró con medicinas. Ahora el niño está bien y los doctores lo revisan para que siga sano.",
+            "B2": "Un chico de 15 años llegó al hospital con dolor en la parte superior del abdomen y vómitos durante cuatro días. No tenía fiebre, por eso pensaron que tenía gastroenteritis, una inflamación del estómago. Como no mejoró, le hicieron una tomografía, un examen que usa rayos X para ver el interior del cuerpo. Este examen mostró que tenía una obstrucción en el intestino delgado causada por una hernia en el hiato de Winslow, una abertura cerca del hígado. Fue necesario operarlo; empezaron con cirugía por laparoscopia, que usa pequeñas cámaras, pero tuvieron que hacer una abertura más grande para liberar el intestino atrapado. No fue necesario quitar ninguna parte del intestino. Después, tuvo una infección en la pelvis que trataron con antibióticos y mejoró. Ahora está bien y sigue en control médico para asegurar su recuperación.",
+            "B3": "Un adolescente de 15 años sin antecedentes médicos previos acudió con dolor abdominal y vómitos biliosos que persistieron durante cuatro días. Inicialmente tratado como gastroenteritis, la falta de mejoría y los hallazgos radiológicos sugirieron una obstrucción intestinal. La tomografía mostró dilatación de asas del intestino delgado y una posible hernia interna en el hiato de Winslow, un espacio anatómico detrás del hígado. Se realizó cirugía urgente, comenzando con laparoscopia que se convirtió en laparotomía para mejorar la visualización y reducir el asa intestinal herniada. No fue necesaria la resección del intestino ni se aplicaron técnicas para prevenir recurrencias. En el postoperatorio, el paciente presentó un íleo paralítico y una colección pélvica, esta última tratada con antibióticos de forma conservadora. Tras diez días, fue dado de alta en buen estado y sin fiebre. Actualmente, continúa en seguimiento en consultas externas de cirugía pediátrica para vigilar su recuperación y prevenir posibles complicaciones. Este caso destaca la importancia de considerar hernias internas en adolescentes con obstrucción intestinal y la necesidad de intervención quirúrgica oportuna para evitar daños mayores."
+        }
+    },
+    {
+        "article": "Un niño de 23 meses de edad con encefalopatía isquémica hipóxica al nacer, con buen potencial motor cerebral y desarrollo psicomotor normal. Tenía antecedentes personales de miocardiopatía restrictiva y fue incluido en un programa de trasplante cardiaco cuando tenía 16 meses de edad. También fue necesario implantarle un dispositivo de asistencia biventricular Berlin Heart externo. Para evitar eventos embólicos, se le administró un tratamiento antiplaquetario doble y anticoagulante. Cuando tenía 23 meses de edad, presentó desconexión y hemiparesia derecha. Una tomografía computarizada (TC) mostró una arteria cerebral media (ACM) izquierda hiperdensa, así como un infarto parietotemporal derecho crónico. Su análisis de sangre mostró: glóbulos rojos 4.16 × 106 µ/L; hemoglobina 11.4 g/gL; tiempo de tromboplastina parcial activada (TTPA) 93 segundos y relación internacional normalizada (INR) 1.08.\n\nEl tratamiento trombolítico intravenoso estaba contraindicado debido al doble tratamiento antiplaquetario y anticoagulante a la dosis completa con heparina, por lo que se realizó una trombectomía intraarterial. Aunque el paciente tenía 23 meses de edad, se encontraba en el tercer percentil de la curva de peso (10 kg). Bajo anestesia general, se perforó la arteria femoral derecha y se colocó una funda 4F de 11 cm de largo (Cordis, Irlanda). Se usó un catéter vertebral Radiofocus 4F (Glidecath de Terumo, Bélgica) para confirmar la oclusión del segmento M1 de la MCA izquierda. La arteria se recanalizó mediante trombectomía mecánica con un stentriever utilizando el catéter vertebral 4F como tutor, colocándolo en el segmento petroso de la arteria carótida. Se usó un dispositivo Trevo XP Pro Vue de 3 mm x 20 mm (Stryker, Países Bajos), con un microcatéter Rapid Transit recto (Codman Neurovascular, Reino Unido), abriendo la arteria en una sola pasada. Se retiró todo el sistema (catéter tutor, microcatéter y stentriever) simultáneamente. En la prueba de control, se detectó una disección iatrogénica de la arteria carótida interna izquierda, que no tuvo importancia clínica, ya que el hemisferio izquierdo se irrigaba a través de la arteria comunicante anterior.\n\nUn mes después, se realizó con éxito el trasplante de corazón. La única secuela neurológica a largo plazo que surgió como resultado del accidente cerebrovascular fue la espasticidad del miembro superior derecho.\n\nMH - Cardiomiopatía, Dilatada/complicaciones/cirugía\nMH - Cardiomiopatía, restrictiva/complicaciones/cirugía\nMH - Angiografía cerebral\nMH - Procedimientos/métodos endovasculares\nMH - Mujer\nMH - Estudios de seguimiento\nMH - Insuficiencia cardiaca/*complicaciones/tratamiento\nMH - Trasplante de corazón\nMH - *Dispositivos de asistencia cardíaca\nMH - Humanos\nMH - Infantil\nMH - Hombre\nMH - Arteria cerebral media/imágenes diagnósticas\nMH - Estudios Retrospectivos\nMH - Ictus/complicaciones/diagnóstico por imágenes/cirugía\nMH - Resultado del tratamiento\n",
+        "gold_summary": "Un niño de 16 meses de edad con cardiomiopatía restrictiva que fue incluido en una lista para un trasplante cardiaco. A los 20 meses de edad, requirió un implante de un dispositivo de asistencia biventricular externo (Berlin Heart) y tuvo un accidente cerebrovascular en el hemisferio izquierdo a los 23 meses. Se utilizó un enfoque intraarterial y produjo buenos resultados clínicos. Un mes después, se realizó con éxito un trasplante cardiaco.\n",
+        "synthetic_summary": {
+            "B1": "Un niño de casi dos años tenía un problema en su corazón y necesitaba un trasplante. Le pusieron un aparato para ayudar a su corazón a latir. Luego, tuvo un problema en el cerebro que le hizo perder fuerza en un brazo. Los médicos usaron un método especial para limpiar la arteria bloqueada y le ayudaron mucho. Un mes después, le dieron un nuevo corazón y mejoró bastante.",
+            "B2": "Un niño de 23 meses tenía una enfermedad del corazón llamada miocardiopatía restrictiva, que limita su función. Para ayudar su corazón, le pusieron un dispositivo externo llamado Berlin Heart. A esa edad, sufrió un accidente cerebrovascular, que ocurre cuando falta sangre en una parte del cerebro. No pudo recibir el tratamiento común porque tomaba medicinas para evitar coágulos. Por eso, le hicieron una trombectomía, que consiste en sacar el coágulo con un catéter. La arteria se abrió bien, aunque quedó una pequeña lesión sin problemas. Un mes después, recibió un trasplante de corazón exitoso. Solo quedó una rigidez en el brazo derecho como secuela del accidente.",
+            "B3": "Un niño de 23 meses con antecedentes de encefalopatía isquémica neonatal y cardiomiopatía restrictiva fue incluido en un programa de trasplante cardiaco, recibiendo un dispositivo de asistencia biventricular externo para soporte hemodinámico. A pesar de la anticoagulación y terapia antiplaquetaria, desarrolló un accidente cerebrovascular isquémico con hemiparesia derecha, contraindicado para tratamiento trombolítico. Se realizó una trombectomía mecánica intraarterial que permitió la recanalización de la arteria cerebral media izquierda en una única intervención, detectándose una disección arterial sin consecuencias clínicas graves debido al mantenimiento del flujo colateral cerebral. Un mes después, el paciente fue sometido con éxito a trasplante cardiaco, presentando como secuela neurológica persistente únicamente espasticidad en el miembro superior derecho. Este caso evidencia que la trombectomía mecánica puede constituir una estrategia terapéutica eficaz en pacientes pediátricos con alto riesgo y tratamientos complejos, facilitando el manejo exitoso del ictus isquémico y la posterior realización del trasplante cardiaco."
+        }
+    },
+    {
+        "article": "Una mujer de 23 años de edad se presentó al departamento de urgencias con pérdida de conciencia y exceso de secreciones orales 2 horas después de la ingestión de un veneno no especificado. No tenía movimientos corporales anormales, fiebre, diarrea, vómitos o sudoración. Inicialmente la habían llevado a un hospital primario cercano, donde fue tratada por posible intoxicación por OP con atropina y cimetidina durante 3 días, antes de ser trasladada al hospital Saint Peter. Después de un interrogatorio exhaustivo, se descubrió que la paciente había consumido unos 30 ml de 2,4-D en un intento de suicidio, precipitado por problemas financieros. No tenía antecedentes conocidos de enfermedad psiquiátrica, intentos de suicidio, episodios depresivos o abuso de sustancias. No se observaron trastornos cardíacos, renales o metabólicos previos.\n\nAl llegar al departamento de urgencias, la paciente estaba inconsciente. Sus constantes vitales eran PR 110/min, BP 120/70 mmHg, RR 21/min, y SPO2 96% en aire ambiente. Los resultados del examen físico fueron notables: un GCS de 6 sobre 15, pupilas dilatadas y reactivas, extremidades inferiores hipertónicas e hiperreflexivas, y reflejo plantar ascendente. Tras la investigación inicial, el recuento completo de células sanguíneas, la prueba de la función renal, la prueba de la función hepática, y la glucosa en sangre aleatoria fueron normales. Su electrocardiograma mostró taquicardia sinusal, mientras que la radiografía de tórax no fue notable. El análisis de gases en sangre arterial y el nivel sérico de la toxina no pudieron determinarse, ya que ninguno de los medios de prueba estaba disponible en el hospital.\n\nLa paciente fue trasladada a la unidad de cuidados intensivos (UCI), se le introdujo una sonda para proteger las vías respiratorias y se le inició inmediatamente una diuresis alcalina forzada. Su evolución en la UCI fue notable por el desarrollo de una insuficiencia renal (creatinina 3,1 ml/dL [intervalo de referencia 0,5-1,2 mg/dL], BUN 133 mg/dL [intervalo de referencia 16,6-48,5 mg/dL], análisis de orina 3+ hemoglobina y muchos glóbulos rojos), debido a una rabdomiolisis inducida por toxinas (nivel de creatina fosfocinasa de 1330 µg/L). Posteriormente, la paciente se volvió hipotensa y se le inició un tratamiento con vasopresores. La ecocardiografía y la ecografía abdominal no fueron significativas. A pesar de estos esfuerzos, falleció por colapso circulatorio el tercer día de estancia en la UCI.\n",
+        "gold_summary": "Aquí se informa sobre el caso de una joven granjera de la zona rural de Etiopía que fue internada en un hospital local tras perder el conocimiento y presentar exceso de secreciones orales 2 horas después de haber ingerido, de manera suicida, un agente tóxico desconocido. Originalmente, se la trató por intoxicación con organofosforados y luego se la trasladó al Hospital Saint Peter's en Addis Abeba para recibir atención médica más intensiva. Allí, se confirmó la ingesta de 2,4-D y se le brindó atención médica de apoyo, ventilación mecánica y diuresis alcalina forzada. A pesar de estas intervenciones, falleció varios días después.\n",
+        "synthetic_summary": {
+            "B1": "Una joven de 23 años tomó un veneno para intentar hacerse daño. Perdió el conocimiento y tenía mucha saliva. La llevaron a dos hospitales, donde le dieron medicinas y cuidados. Aunque trataron de ayudarla con máquinas y medicinas, su cuerpo se enfermó mucho y murió después de tres días.",
+            "B2": "Una mujer de 23 años perdió el conocimiento y tuvo exceso de saliva dos horas después de tomar un veneno para suicidarse. Al principio, la trataron pensando que era una intoxicación por organofosforados, pero luego se supo que había ingerido 2,4-D, un herbicida tóxico. Al llegar al hospital, estaba inconsciente y con reflejos anormales. Sus análisis de sangre y órganos fueron normales al inicio, pero luego desarrolló daño renal por destrucción muscular causada por el veneno. Recibió tratamiento en cuidados intensivos, incluyendo protección de las vías respiratorias y diuresis alcalina para eliminar el tóxico. Sin embargo, su condición empeoró con baja presión arterial y colapso circulatorio, y falleció al tercer día. Este caso muestra lo grave que puede ser la intoxicación con 2,4-D y la importancia de un diagnóstico rápido.",
+            "B3": "Una mujer de 23 años fue ingresada en urgencias tras perder el conocimiento y presentar secreciones orales abundantes, dos horas después de ingerir un veneno en un intento de suicidio. Inicialmente fue tratada como intoxicación por organofosforados, pero luego se confirmó que había consumido 2,4-D, un herbicida tóxico. Al llegar al hospital, estaba inconsciente con signos neurológicos graves y sin alteraciones en pruebas básicas. Fue trasladada a la unidad de cuidados intensivos, donde recibió ventilación mecánica y diuresis alcalina para eliminar la toxina. Sin embargo, desarrolló insuficiencia renal causada por daño muscular grave (rabdomiólisis) y presentó hipotensión que requirió vasopresores. A pesar del tratamiento, su estado empeoró hasta sufrir un colapso circulatorio que causó su fallecimiento al tercer día. Este caso refleja la gravedad de la intoxicación por 2,4-D y la dificultad para manejar sus complicaciones, subrayando la importancia de un diagnóstico rápido y un tratamiento especializado para mejorar el pronóstico."
+        }
+    },
+    {
+        "article": "Una paciente etíope de 35 años de edad se presentó en el departamento de urgencias del Colegio Médico del Hospital Yekatitit 12 con síntomas de falta de aire en reposo, ortopnea, disnea paroxística nocturna significativa, dolor torácico, tos productiva teñida de sangre y vómitos de materia ingerida (2-3 episodios por día) durante 2 semanas. Presentaba una hinchazón progresiva del cuerpo que comenzó en las extremidades inferiores y luego afectó a todo el cuerpo, fatigabilidad fácil, pérdida de apetito, fiebre intermitente de alto grado y sensación de ardor epigástrico durante la misma semana y con la misma duración. La paciente también experimentó una pérdida de peso y fatiga no especificadas durante los últimos 2 meses. Por lo demás, no tenía comorbilidades conocidas, ni comportamientos de riesgo, como fumar o beber alcohol, medicamentos o antecedentes familiares de neoplasia. Estaba casada, tenía cuatro hijos y no tenía antecedentes obstétricos negativos. Su ocupación era la agricultura y había vivido en una zona rural. Nunca había sido admitida por una queja similar.\n\nLa escala de coma de Glasgow (GCS) de la paciente fue de 15 sobre 15, y no había anormalidades de memoria, potencia o tono. La paciente estaba en grave dificultad respiratoria con saturación de oxígeno del 70% con aire atmosférico, frecuencia respiratoria de 30-35 latidos/minuto, y frecuencia del pulso de 120 por minuto. Tenía registros de fiebre de alto grado hasta el nivel de 39.5 0C y puede mantener su presión arterial. El examen de mama con ultrasonido y mamografía fue supuestamente normal. No se detectó linfadenopatía en áreas accesibles.\n\nEl examen del tórax reveló signos de derrame pleural que también se observaron en las imágenes y se analizaron. Una tomografía computarizada (TC) del tórax con contraste mostró derrame pericárdico y neumonía multifocal. La angiografía por TC mostró un defecto de llenado arterial pulmonar segmentario del lóbulo inferior en ambos lados, lo que sugiere embolia pulmonar y derrame pleural en ambos lados. Los frotis citológicos se informaron con láminas de células mesoteliales, neutrófilos y grupos dispersos de células grandes atípicas con nucleolos prominentes que sugieren derrame maligno. El análisis del líquido pleural mostró un líquido con predominio linfocítico con glucosa normal (82 mg/dl), proteínas (2,2 g/dl) y lactato deshidrogenasa (LDH) de 592 mg/dl.\n\nLa presión venosa yugular aumentó con los sonidos cardiacos apagados. La ecocardiografía mostró derrame pericárdico masivo con características de taponamiento cardiaco, fracción de eyección preservada (65%), y excursión sistólica del plano anular tricuspídeo (TAPSE) mayor a 18 mm. Un electrocardiograma (ECG) reveló solo taquicardia sinusal y desviación del eje. Se realizó una pericardiocentesis inmediata, se extrajo un drenaje de aproximadamente 250 ml de fluido hemorrágico y se aseguró la ventana pericárdica. La repetida ecocardiografía reveló una reducción del tamaño. El informe de citología del fluido pericárdico mostró numerosos linfocitos junto con células malignas atípicas que tenían prominentes nucleolos, lo que sugería un derrame maligno.\n\nEn el examen abdominal, mostró signos positivos de acumulación de fluidos sin órgano hinchable. La tomografía computarizada abdominal y pélvica mostró un aumento en el tamaño del hígado con múltiples lesiones hepáticas hipointensas que sugerían metástasis. Los órganos pélvicos, incluidos los ovarios y el útero, no presentaron lesiones identificadas. Se realizó una biopsia con aguja de la lesión hepática y los resultados revelaron un adenocarcinoma secundario.\n\nSe realizó un diagnóstico de insuficiencia cardíaca causada por una efusión pericárdica masiva maligna secundaria a un adenocarcinoma diseminado y un carcinoma de origen primario desconocido que afectaba al pulmón, la pleura, el pericardio y el tracto gastrointestinal. Se le diagnosticó a la paciente una trombosis venosa profunda extensa en la extremidad superior izquierda, una embolia pulmonar bilateral y segmentaria, posiblemente debido a la CUP diseminada. Los hallazgos también mostraron una neumonía multifocal superpuesta y una anemia leve de enfermedad crónica.\n\nEl recuento sanguíneo completo inicial reveló leucocitosis con un recuento de glóbulos blancos de 24 × 103 por ml, neutrófilos predominantes (91%), recuento de glóbulos rojos de 3.7 × 106 por µl, anemia normocítica leve (hemoglobina (Hgb) 11.2 mg/dl), volumen corpuscular medio (MCV) de 81.2 fl, y trombocitopenia severa (66 × 103/µl). Después del tratamiento antibiótico para neumonía, el recuento sanguíneo completo volvió a la normalidad (excepto para Hgb). Con niveles normales de bilirrubina, la aspartato aminotransferasa (AST) aumentó más de siete veces (263 U/L), mientras que la alanina transaminasa (ALT) aumentó más de nueve veces (332 U/L). Los electrolitos séricos (excepto para Na + con hiponatremia leve, 129 mEq/L) y las pruebas de función renal fueron normales. La albúmina era baja (2.12 g/dl). Los niveles de lactato deshidrogenasa (LDH) aumentaron casi dos veces desde el inicio (592 U/L). Los virus del virus de inmunodeficiencia humana, hepatitis B y hepatitis C no fueron reactivos. La sangre y el cultivo del líquido pleural no tuvieron crecimiento. Un antígeno carcinoembrionario (CEA) aumentó más de 400 veces (1000 µg/L) del inicio.\n\nLa paciente fue admitida en la sala general. Se realizó una ventana pericárdica y una inserción de un tubo torácico derecho con un cirujano cardiotorácico junto con un cardiólogo (ver la cantidad de aspirado antes). Se realizó una aspiración pleural terapéutica intermitente para el derrame pleural maligno. Una vez que la dosis de carga (60 mg) de frusemida produjo suficiente producción de orina, esta dosis se mantuvo tres veces (TID) al día. Esto se redujo y se dio de alta a la paciente con una dosis oral de 20 mg dos veces al día (BID). Se inició una dosis estándar de enoxaparina para el tromboembolismo pulmonar y la trombosis venosa profunda aguda extensa en la extremidad superior izquierda. Se administró enoxaparina por vía subcutánea 40 mg BID durante la hospitalización, que se cambió a 5 mg de warfarina oral diaria durante el alta debido a problemas financieros. La neumonía multifocal se trató con ceftazidima (1 g intravenoso TID) y vancomicina (1 g intravenoso BID) según el protocolo de tratamiento estándar nacional. El dolor se controló con un potente medicamento contra el dolor (morfina 5 mg intravenosa TID) y se redujo y suspendió. También estaba en la profilaxis de la úlcera. La paciente fue dada de alta de la sala médica con una mejora significativa después de 14 días de hospitalización y fue asignada a la unidad de oncología del hospital. Por lo tanto, para el cáncer de origen primario desconocido, se le dio un ciclo de quimioterapia (carboplatino/paclitaxel). Se perdió el seguimiento debido a problemas financieros, y la paciente murió en su casa cuatro meses después del alta.\n\nMH - Humanos\nMH - Mujer\nMH - *Insuficiencia cardiaca/etiología\nMH - Adulto\nMH - *Neoplasias, complicaciones/primaria desconocida",
+        "gold_summary": "Una mujer negra de 35 años se presentó con falta de aire en reposo, ortopnea, disnea paroxística nocturna, dolor torácico, tos productiva teñida de sangre y fiebre durante 2 semanas. También tenía hinchazón progresiva del cuerpo, fatigabilidad fácil, pérdida de apetito y dolor abdominal durante la misma semana. La imagen corporal reveló grandes derrames pleurales y pericárdicos, lesiones hepáticas metastásicas y defectos de llenado segmentarios y subsegmentarios vasculares pulmonares bilaterales. La citología de los fluidos pericardio y pleural sugieren derrame maligno. Las lesiones hepáticas y la biopsia con aguja indicaron adenocarcinoma de origen desconocido, y el nivel de antígeno carcinoembriónico también aumentó significativamente.\n",
+        "synthetic_summary": {
+            "B1": "Una mujer de 35 años tenía dificultad para respirar, tos con sangre y fiebre por dos semanas. Su cuerpo se hinchó y se cansaba fácil. Los médicos encontraron líquidos en su pecho y alrededor del corazón, y manchas en el hígado. Las pruebas mostraron que tenía un cáncer que se había extendido, pero no sabían de dónde empezó. La trataron en el hospital, pero la enfermedad era grave.",
+            "B2": "Una mujer de 35 años llegó al hospital con dificultad para respirar y dolor en el pecho. También tenía tos con sangre, fiebre y hinchazón en el cuerpo desde hacía dos semanas. Las pruebas mostraron líquido acumulado en el corazón y los pulmones, además de lesiones en el hígado. Estas lesiones indicaban un cáncer que se había extendido a otras partes del cuerpo. El análisis del líquido del corazón y los pulmones mostró células cancerosas. La biopsia confirmó un adenocarcinoma, un tipo de cáncer, pero no se pudo saber dónde comenzó. La paciente recibió tratamiento para la infección, el cáncer y los problemas del corazón y pulmones. Aunque mejoró al principio, falleció cuatro meses después por la enfermedad avanzada.",
+            "B3": "Una mujer etíope de 35 años acudió al hospital con dificultad respiratoria grave, tos con sangre, dolor torácico y fiebre persistente durante dos semanas, además de hinchazón progresiva y fatiga. Los estudios por imágenes revelaron derrames pleurales y pericárdicos extensos, lesiones hepáticas sospechosas de metástasis y signos de embolia pulmonar bilateral. El análisis del líquido pleural y pericárdico mostró células malignas, indicando derrames de origen canceroso. La biopsia hepática confirmó un adenocarcinoma metastásico, aunque no se identificó el tumor primario. La paciente también presentó trombosis venosa profunda y neumonía multifocal, complicaciones que se trataron con anticoagulantes y antibióticos. Se realizó una pericardiocentesis para aliviar el taponamiento cardíaco, y se inició quimioterapia con carboplatino y paclitaxel. A pesar de la intervención, la paciente falleció cuatro meses después del alta, debido a la progresión de un cáncer avanzado de origen desconocido que afectaba múltiples órganos. Este caso destaca la complejidad del diagnóstico y manejo de neoplasias metastásicas con presentación clínica grave y compromiso cardiopulmonar."
+        }
+    },
+    {
+        "article": "Paciente del sexo femenino de 17 años con diagnóstico de enfermedad de Graves con bocio difuso, la cual negó otros antecedentes de importancia.\n\nSu cuadro comenzó seis meses antes con pérdida de peso progresiva, episodios de ansiedad y agitación, temperaturas de 37.4 a 37.9 ºC, palpitaciones, dolor abdominal y diarrea intermitente. A los dos meses se agregó como síntoma el crecimiento de la cara anterior del cuello; al tercer mes presentó taquicardia de hasta 130 latidos por minuto. Al ser valorada por Endocrinología se le administró tiamazol de 15 mg cada 8 horas, el cual fue suspendido por cuadro de agranulocitosis. Por lo tanto, se le comenzó a administrar lugol y propanol de 20 mg cada 8 horas, sin respuesta adecuada. Por ende, se decidió aplicar una dosis terapéutica de yodo 131 (I-131) 10 mcU.\n\n\nExploración física\nA la exploración física, la paciente presentó como signos basales una presión arterial no invasiva (PANI) 137/75 mmHg, frecuencia cardiaca (FC) 105 lpm, frecuencia respiratoria (FR) 16 rpm, SpO2 95%, temperatura 37.4ºC. La paciente ingresó deambulando, con agitación leve, con actitud cooperadora; estaba hidratada y sin datos clínicos de vía aérea difícil, pero no se valoró movilidad de tráquea por crecimiento tiroideo de aproximadamente 7.5 x 7 x 10 cm). La superficie del cuello era regular y su movilidad tenía una adecuada extensión. A la auscultación cardiopulmonar no hubo ruidos agregados y la paciente tenía ruidos cardiacos aumentados en frecuencia; asimismo, abdomen blando, depresible, no doloroso, con peristalsis presente. Extremidades integras, sensibilidad con aumento de la percepción del calor, hiperhidrosis palmar, fuerza 5/5, y temblor fino.\n\nSe empleó la escala de Burch y Wartofsky y se obtuvieron 40 puntos con elevada probabilidad de tormenta tiroidea, por lo cual se decidió manejo con anestesia multimodal.\n\nEn la monitorización tipo 2 la paciente presentó signos vitales iniciales PANI 137/75 mmHg, frecuencia cardiaca 96 latidos por minuto, frecuencia respiratoria 16 respiraciones por minuto, 95% Spo2, monitoreo invasivo de tensión arterial.\n\nPor inducción endovenosa se le administraron a la paciente 2 mg de midazolam; 150 mcg de fentanilo; 5 mg de cisatracurio y 50 mg de propofol.\n\nEl abordaje de la vía aérea se hizo con videolaringoscopía Glide Scope con hoja hiperangular 3 sin complicaciones. La ventilación mecánica invasiva modo volumen presentó flujos bajos FIO2 (40%).\n\nSe llevó a cabo bloqueo cervical superficial bilateral ecoguiado con 4 mL de ropivacaina al 0.2% en cada lado (16 mg en total).\n\nPara el mantenimiento se empleó sevoflorano CAM 0.8, infusión de dexmedetomedina 0.7 a 0.4 mcg/kg/hora, infusión de lidocaína 25 mcg/kg/hora, concentración plasmática de fentanilo 0.001 mcg/mL.\n\nEn cuanto a los adyuvantes se empleó paracetamol 750 mg + parecoxib 40 mg + ketorolaco intravenoso 30 + sulfato de magnesio 1250 g en infusión para una hora. El balance de líquidos fue negativo. El tiempo anestésico fue de 215 minutos. En el transoperatorio, la paciente estuvo hemodinámicamente estable, con presión arterial media de 67 a 75 mmHg, que se considera adecuada para la perfusión de órganos.\n\nEn el postoperatorio la paciente presentó analgesia durante 12 horas. Rescate con 1 g de metamizol por razón necesaria, utilizando un solo rescate. Disfonía postoperatoria persistente, sin presencia de odinofagia.",
+        "gold_summary": "Adolescente de 17 años con enfermedad de Graves con manifestaciones clínicas descontroladas, la cual no respondió a tratamiento médico y se programó para tiroidectomia radical. Se obtuvieron 35 puntos en la Escala de Burch y Wartofsky. Se manejó con anestesia general y fueron disminuyendo los estímulos para control de vía aérea y regional a fin de disminuir los estímulos quirúrgicos. Se usaron medicamentos adyuvantes como sulfato de magnesio para la estabilidad transoperatoria.",
+        "synthetic_summary": {
+            "B1": "Una niña de 17 años tenía una enfermedad en la tiroides. Tenía pérdida de peso, nervios y su corazón latía rápido. Las medicinas no la ayudaron, por eso la operaron. En la cirugía, cuidaron su corazón y respiración con medicinas. Después, ella estuvo tranquila y sin mucho dolor.",
+            "B2": "Una joven de 17 años tenía enfermedad de Graves, que agranda la tiroides y causa síntomas. Ella perdió peso, sentía ansiedad y tenía palpitaciones, pero los medicamentos no funcionaron. Por eso, decidieron operarla para quitarle la tiroides. Durante la cirugía, usaron anestesia general para que no sintiera dolor ni se moviera. También cuidaron su respiración y le dieron medicinas para mantenerla estable. La operación duró más de tres horas y la paciente estuvo bien todo el tiempo. Después, tuvo un poco de dolor y dificultad para hablar, pero podía tragar sin problema. Este caso muestra lo importante que es cuidar bien a pacientes con problemas graves en la tiroides.",
+            "B3": "Una paciente de 17 años con enfermedad de Graves presentó síntomas graves como pérdida de peso, ansiedad, taquicardia y crecimiento del cuello debido a un bocio difuso, sin mejoría con tratamiento médico inicial. Debido a la falta de respuesta y complicaciones con medicamentos, se decidió realizar una tiroidectomía radical. Durante la cirugía, se aplicó anestesia general combinada con técnicas para reducir la estimulación de la vía aérea y bloqueo regional para controlar el dolor y la respuesta al estrés quirúrgico. Se emplearon fármacos adyuvantes, incluyendo sulfato de magnesio, para mantener la estabilidad hemodinámica. La paciente permaneció estable durante el procedimiento y experimentó analgesia prolongada en el postoperatorio, con solo un rescate analgésico necesario. No obstante, presentó disfonía persistente sin dolor al tragar. Este caso resalta la importancia de un manejo anestésico cuidadoso en pacientes con tormenta tiroidea y bocio voluminoso, buscando minimizar riesgos y optimizar la recuperación."
+        }
+    },
+    {
+        "article": "Una mujer de 30 años de edad, embarazada de 3, para 3, se presentó con disminución de la micción, dolor en el flanco izquierdo y fiebre durante 2 días después de una cesárea de emergencia por primera vez, indicada debido a la angustia materna y fetal secundaria al trabajo de parto prolongado y sangrado vaginal prolongado en el hospital Al-Thora, Ibb, Yemen. A pesar de los esfuerzos de reanimación, su recién nacido falleció después de 45 minutos. Durante la cesárea, se identificaron severas adherencias uterinas (ya que había lesiones de endometriosis y adherencias entre la pared posterior del útero y el colon sigmoide), y una pérdida de sangre estimada de 1500 cc, según el informe del ginecólogo. La paciente no recibió atención prenatal durante su embarazo. No es fumadora y negó condiciones médicas crónicas, abuso de drogas, intoxicación accidental o antecedentes quirúrgicos previos.\n\nEn el examen físico, el paciente se veía pálido, enfermo y febril durante la evaluación inicial, con una temperatura oral de 38 °C, pulso de 80 latidos por minuto y presión arterial de 95/70 mm Hg. El abdomen del paciente estaba levemente distendido, con sensibilidad moderada, principalmente en el cuadrante inferior izquierdo.\n\nLos datos de laboratorio fueron los siguientes: el recuento de glóbulos blancos (WBC) fue de 15,3 × 103/mL, con 90% de neutrófilos polimórficos (leucocitosis con predominio neutrofílico), la hemoglobina fue de 7,5 g/dL, el recuento de plaquetas fue de 200 × 103/µL, el nitrógeno ureico en sangre (BUN) fue de 23 mg/dl y la creatinina fue de 3,8 mg/dl. Otros análisis de sangre, como los de la función hepática y los de coagulación, estuvieron dentro de los rangos normales. La ecografía (US) mostró una hidronefrosis izquierda grave y un fluido libre moderado en la cavidad abdominal. Se realizó la aspiración de la punción abdominal y la creatinina en el punto fue de 52 mg/dL, lo que indica que el fluido era orina.\n\nLa paciente fue resucitada con glóbulos rojos concentrados y una amplia cobertura antibiótica. Después de esto, se le realizó una ureteroscopia urgente que mostró una oclusión total del uréter izquierdo. Se tomó la decisión de realizar una exploración quirúrgica, dada la inestabilidad hemodinámica, la falta de equipos de nefrostomía percutánea y la evidencia de contaminación intraabdominal. Durante la operación, se encontró fluido libre moderado en la cavidad abdominal. El uréter izquierdo fue aplastado y ligado con una sutura Vicryl (5 agujas) a unos 5 cm de su parte distal. Después de evacuar el fluido, se extirpó el segmento lesionado del uréter y se realizó una ureteroneocistostomía de forma refluyente tras distender la vejiga con solución salina a través del catéter. Además, diseccionamos el uréter, con cuidado, de los tejidos circundantes en dirección cefálica, espatulamos el extremo distal del uréter e insertamos un stent doble. Se implantó el uréter en la cúpula posterior de la vejiga urinaria con anastomosis sin tensión y se suturó con Vicryl 4-0 a través del uréter de espesor completo, luego la capa mucosa de la vejiga y la capa detrusora. Se insertó un drenaje Jackson-Pratt (JP) cerca de la anastomosis y se cerró la pared abdominal tras evaluar el contenido intraperitoneal.\n\n\nSeguimiento y resultado\nSe iniciaron líquidos transparentes el segundo día postoperatorio. La paciente tenía distensión abdominal leve, dolor y náuseas. El tercer día postoperatorio, tenía una distensión abdominal creciente y dejó de expulsar flatos. La ecografía abdominal mostró una gran cantidad de acumulación en la cavidad peritoneal. Los datos de laboratorio de sangre mostraron una leucocitosis (WBC de 22 × 103/mL con un cambio a la izquierda).\n\nUna tomografía computarizada (TC) del abdomen y la pelvis con contraste reveló una cantidad significativa de aire libre y líquido en todo el abdomen y la pelvis adyacente a la pared abdominal anterior. También se observaron múltiples localizaciones de gas libre en el mesenterio, con realce de contraste de múltiples bucles intestinales pequeños, sin evidencia de extravasación de contraste. Los hallazgos sugirieron una víscera perforada. Después de consultar al equipo de cirugía general, la paciente fue llevada inmediatamente al quirófano para una laparotomía exploratoria, que reveló una pequeña perforación en la parte rectosigmoidea con algo de derrame, peritonitis con edema del asa intestinal y alteración de la anastomosis ureteral. La complejidad de este caso nos obligó a realizar intervenciones en varias etapas de manera multidisciplinaria. En primer lugar, el ginecólogo realizó una histerectomía debido a endometritis (confirmada histopatológicamente), supuración severa y alteración de la sutura del útero. En segundo lugar, un urólogo realizó una derivación ureterocutánea del uréter izquierdo y se creó una urostomía en el lado izquierdo. Por último, el cirujano general realizó el procedimiento de colostomía después de reparar la lesión del colon y se creó una colostomía en el lado izquierdo. En el quinto día postoperatorio, se produjo retracción de la colostomía con infección de la herida y se observó comunicación entre la colostomía y la urostomía. Se decidió realizar una reexploración para reubicar la colostomía sigmoidea y se realizó una colostomía transversal derecha. Una semana después de la operación, la paciente experimentó una infección superficial de la pared abdominal complicada con dehiscencia de la herida e hipoalbuminemia (albúmina: 2 g/dL) que requirió tratamiento con varios desbridamientos, irrigación de la herida, antibióticos y terapia de apoyo. Los antibióticos recomendados fueron linezolid (600 mg IV cada 12 horas durante 7 días), luego cambiaron a ceftriaxona (1 g IV cada 12 horas durante 5 días) más metronidazol (500 mg IV cada 12 horas durante 5 días) y cambiaron a ciprofloxacina oral (500 mg cada 12 horas por vía oral durante 7 días). Gradualmente, reanudó su dieta normal y fue dada de alta 30 días después en condiciones estables. Requería atención domiciliaria para ayudarla con la colostomía, la ureterostomía y la deambulación.\n\nSeis meses después, se cerró la colostomía y se anastomosó el uréter mediante el procedimiento de colgajo de vejiga tabular de Boari (la vejiga se abrió en su superficie anterior y se volteó un colgajo de vejiga de espesor completo caudalmente y se tabularizó para anastomosis al segmento ureteral proximal después de la inserción de la endoprótesis doble J). Después de una recuperación postoperatoria sin incidentes, se dio de alta a la paciente el séptimo día postoperatorio. El seguimiento de un mes mediante ecografía y cistouretrografía miccional mostró un aspecto normal de la vejiga con capacidad vesical adecuada y un sistema del tracto urinario superior normal. Tres meses después, la ureteroscopia retrógrada mostró un calibre adecuado del uréter. Se hizo un seguimiento regular de la paciente con ecografía durante 3 meses durante un año. La paciente no tuvo síntomas irritativos o gastrointestinales en los 2 años de seguimiento.\n",
+        "gold_summary": "Una mujer de 30 años presentó disminución de la micción durante 2 días después de una cesárea. La ecografía mostró una hidronefrosis izquierda grave y un fluido abdominal libre moderado. Una ureteroscopia reveló una oclusión total del uréter izquierdo y, posteriormente, se realizó una ureteroneocistostomía. Dos días después, la paciente presentó complicaciones con distensión abdominal que requirieron una nueva exploración. La exploración reveló lesiones en el colon (recto-sigmoide), peritonitis, endometritis y alteración de la anastomosis ureteral. Se realizó una colostomía, reparación de lesiones en el colon, histerectomía y derivación ureterocutánea. La estancia hospitalaria de la paciente fue complicada, con retracción estomal que requirió revisión quirúrgica y dehiscencia de la herida, que se trató de forma conservadora. Después de 6 meses, se cerró la colostomía y se anastomosó el uréter mediante el procedimiento de colgajo de Boari.\n",
+        "synthetic_summary": {
+            "B1": "Una mujer de 30 años tuvo problemas para orinar y dolor después de una operación para sacar a su bebé. Los médicos encontraron que un tubo que lleva la orina estaba bloqueado y le hicieron una cirugía para arreglarlo. Luego tuvo dolor y el abdomen se le hinchó, por lo que hicieron otra operación. En esa cirugía, arreglaron partes del intestino y el útero. Después de varios cuidados, la mujer mejoró y volvió a la normalidad.",
+            "B2": "Una mujer de 30 años tuvo problemas para orinar y dolor tras una cesárea de emergencia. La ecografía mostró un riñón inflamado y líquido en el abdomen, que era orina. Los médicos encontraron que un conducto llamado uréter, que lleva la orina, estaba bloqueado y lo repararon con cirugía. Sin embargo, la paciente tuvo complicaciones como infección en el abdomen y daño en el colon y el útero. Por eso, le hicieron una colostomía, que es una abertura para evacuar heces, le quitaron el útero y crearon una nueva salida para la orina. Después de varios tratamientos y cirugías, cerraron la colostomía y repararon el uréter. La paciente mejoró y no tuvo problemas en dos años de seguimiento.",
+            "B3": "Una mujer de 30 años, tras una cesárea de emergencia por complicaciones en el parto, presentó disminución de la micción, dolor en el flanco izquierdo y fiebre. La ecografía reveló hidronefrosis severa y líquido libre en el abdomen, que resultó ser orina, indicando una lesión ureteral. Se realizó una ureteroneocistostomía para reparar el uréter afectado. Sin embargo, días después, la paciente desarrolló distensión abdominal y signos de infección, y una tomografía mostró aire libre en el abdomen, sugiriendo perforación intestinal. En la cirugía exploratoria se identificaron una perforación en el colon, peritonitis, endometritis y falla en la reparación del uréter. Se realizaron una colostomía, histerectomía y derivación ureterocutánea. La recuperación fue complicada por infección y dehiscencia de la herida, que se manejaron con antibióticos y cuidados locales. Seis meses después, se cerró la colostomía y se reconstruyó el uréter mediante un colgajo vesical. El seguimiento mostró una función urinaria y digestiva adecuada sin complicaciones a largo plazo. Este caso destaca la complejidad de las lesiones urinarias y abdominales postquirúrgicas y la necesidad de un manejo multidisciplinario cuidadoso."
+        }
+    },
+    {
+        "article": "Mujer de 43 años, con antecedente de hipertensión arterial con tratamiento con losartán, dos cesáreas y oclusión tubaria bilateral. Ingresó a nuestro hospital y refirió dolor de 24 horas de evolución, tipo cólico en hipogastrio e irradiación a fosa iliaca izquierda, además de náusea y vómito en dos ocasiones. Se agregaron evacuaciones semilíquidas en forma inicial y posteriormente cese en las evacuaciones y en la canalización de gases. A la exploración física, la paciente presentó dolor en el abdomen, así como distensión, especialmente hacia el flanco izquierdo. En el mesogastrio y el flanco izquierdo hubo la presencia de timpanismo. La peristalsis estaba presente, mínima, abolida en flanco izquierdo y mesogastrio. La irritación peritoneal estuvo ausente. Se colocó sonda nasogástrica, con gasto mínimo gástrico y sin mejoría en la sintomatología. Los estudios de laboratorio demostraron: 9700 leucocitos con un 87% de neutrófilos, creatinina de 0.7 mg/dL, urea de 22 mg/dL y proteína C reactiva de 5.0 mg/L. En la radiografía simple de abdomen presentó dilatación importante del lado izquierdo del colon, con niveles hidroaéreos. La tomografía muestra la dilatación del colon del lado izquierdo, con imagen que simula grano de café en el corte coronal.\n\nAnte estos hallazgos clínicos y de imagen, se decidió hacer laparotomía de urgencia ante la sospecha de la presencia de vólvulo de sigmoides o de síndrome adherencial complicado. Durante la cirugía se evidenció un ciego flexionado hacia adelante y a la izquierda, carente de fijación retroperitoneal. El punto de flexión fue producido por una banda de adherencia colocada sobre el colon ascendente. Se realizó liberación de la adherencia y se corroboró continuidad adecuada hacia el colon distal. No se evidenció la presencia de isquemia, necrosis o perforación del ciego. Se realizó apendicectomía con descompresión del ciego a través de base apendicular y posteriormente ligadura de esta. Se llevó a cabo cecopexia hacia pared de fosa iliaca derecha. Después de la cirugía, hubo mejoría clínica de la paciente, que tuvo evacuaciones presentes normales. La paciente siguió controles correctos en consulta externa de cirugía y se mantuvo asintomática.",
+        "gold_summary": "Mujer de 43 años que ingresó a un servicio de urgencias con datos de obstrucción intestinal. Se realizó tomografía simple de abdomen donde se identificó dilatación del colon e imagen que semejaba un grano de café invertido. Se hizo laparotomía exploradora y se identificó vólvulo cecal del tipo báscula, sin compromiso vascular. Se realizó desvolvulación, descompresión a través de apendicectomía, y cecopexia. Posterior a evento quirúrgico, la paciente se recuperó sin incidentes y fue dada de alta con controles adecuados por consulta externa.",
+        "synthetic_summary": {
+            "B1": "Una mujer de 43 años llegó al hospital con dolor fuerte en el abdomen y vómitos. Las imágenes mostraron que una parte del intestino estaba muy hinchada y torcida. Los médicos hicieron una operación para corregir el problema y quitar una parte pequeña del intestino llamada apéndice. Después de la cirugía, ella mejoró mucho y pudo ir a casa sin problemas. Ahora sigue revisándose con los doctores y está bien.",
+            "B2": "Una mujer de 43 años llegó al hospital con dolor abdominal, náuseas y vómitos. También tenía dificultad para evacuar y expulsar gases. En el examen, el abdomen estaba hinchado y doloroso, sobre todo en el lado izquierdo. Las imágenes mostraron que el colon estaba dilatado con una forma llamada “grano de café”, que indica una torsión del intestino llamada vólvulo. En la cirugía urgente, se encontró que el ciego, una parte del intestino, estaba doblado y atrapado por una banda de tejido. Se liberó esta banda, se descomprimió el intestino y se fijó para evitar que volviera a torcerse. La paciente mejoró después y no tuvo complicaciones.",
+            "B3": "Una mujer de 43 años con hipertensión y antecedentes quirúrgicos ingresó con dolor abdominal tipo cólico, náuseas, vómitos y cambios en sus evacuaciones. La exploración física mostró distensión y dolor en el abdomen, especialmente en el lado izquierdo, junto con signos de obstrucción intestinal. Los estudios de laboratorio indicaron inflamación leve y la radiografía reveló dilatación del colon izquierdo con niveles hidroaéreos. La tomografía confirmó la dilatación y mostró una imagen característica en forma de grano de café, sugerente de vólvulo. Ante estos hallazgos, se realizó una cirugía urgente donde se encontró un ciego desplazado y flexionado debido a una banda de adherencias, sin daño vascular ni necrosis. Se liberó la adherencia, se descomprimió el ciego mediante apendicectomía y se fijó el ciego a la pared abdominal (cecopexia). La paciente evolucionó favorablemente, recuperando la función intestinal normal y permaneció asintomática en controles posteriores. Este caso resalta la importancia de un diagnóstico rápido y tratamiento quirúrgico oportuno para evitar complicaciones graves en la obstrucción intestinal causada por vólvulo cecal."
+        }
+    },
+    {
+        "article": "Paciente de sexo femenino de 10 años, sin historia familiar de enfermedad tiroidea, portadora de bocio diagnosticado a los 9 años (ecografía tiroidea con sig nos compatibles de tiroiditis crónica) con presencia de anticuerpos antitiroideos positivos. Sin tratamiento al momento del ingreso hospitalario. Consultó por orina de aspecto espumoso de 5 días de evolución, asociado a dolor abdominal, vómitos profusos y diarrea. Evo lucionó con edema palpebral y de extremidades, disminución de la diuresis, decaimiento y fiebre de 38° C el día previo a su ingreso. Al momento de su eva luación en el servicio de urgencia destacó una pacien te con edema palpebral bilateral y pretibial, con bocio evidente (indoloro y sin nódulos palpables) y presen cia de soplo sistólico eyectivo en foco pulmonar IV/VI sin irradiación. Resto del examen sin alteraciones de significancia. Presión arterial 120/78 mmHg (percentil 95), temperatura 38,1°C, peso: 33.9 Kg, talla: 131,5 cm (p7), IMC 19,8 (p83).\n\nDentro de sus exámenes de admisión destacaron examen de orina completa con proteinuria +++, sin bacterias, sin nitritos, leucocitos 7 cel/uL (VN: 0-10 cel/uL), eritrocitos 4 cel/uL (VN: 0-15 cel/uL), índice proteinuria/creatininuria (IPC) 2 mg/mg, proteínas totales de 3.8 g/dL, hipoalbuminemia de 2,1 g/dL, hipercolesterolemia de 416 mg/dL, hipertrigliceridemia de 127 mg/dL y creatinina plasmática de 0,46 mg/dL (aclaramiento de creatinina calculado por fórmula de Schwartz: 125 ml/min/1,73 m2). Gases venosos, elec trolitos plasmáticos y hemograma dentro de rangos normales. En cuanto al estudio inmunológico destacó: inmunoglobulina A 181 mg/dL (VN 45-236), inmunoglobulina M 131 mg/dL (VN 52-242), inmunoglobulina G 208 (VN 608-1572) mg/dL, C3 125 mg/dL (VN 80-150), C4 37,3 mg/dL (VN 12-36). Ecografía renal normal. Se ingresó a la paciente con diagnóstico de SN y tiroiditis autoinmune.\n\nEn el contexto de SN se inició tratamiento con prednisona (60 mg/m2/día), con buena respuesta, logrando fundir edema y disminuir progresivamente la proteinuria hasta alcanzar rangos normales previo al egreso (IPC de egreso: 0.09, a los 6 días).\n\nDel punto de vista de función tiroidea su estudio mostró hormona tiroestimulante (TSH) 4,4 UI/ml (VN: 0,67-4,16 UI/ml), tiroxina (T4) libre 0,80 ng/ dL (VN: 0,86-1,4 ng/dL), anticuerpos antiperoxidasa (Anti Tpo) 120 U/ml (VN: 0-60 U/ml), anticuerpos antitiroglobulina (Anti-Tg) 82 U/ml (VN: 0-60 U/ ml), por lo que se inició terapia de sustitución con levotiroxina (25 mcg/día). La ecografía tiroidea descri bió tiroides de tamaño normal con leve aumento de vascularización difusa al Doppler, sin lesiones focales sólidas ni quísticas, siendo estos hallazgos sugerentes de tiroiditis. Resto del estudio (PCR para SARS CoV-2, anticuerpos anti citoplasma de neutrófilos, anticuer pos anti nucleares, anticuerpos anti DNA, anticuerpos anti estreptolisina O, anticuerpos anticardiolipinas, anticuerpos anti mieloperoxidasa y anticuerpos anti proteinasa 3) resultó negativo.\n\nA los 6 días de ingresada la paciente se encontraba en buenas condiciones, siendo dada de alta con prednisona (60 mg al día) y levotiroxina (25 ucg al día). En el seguimiento a los 12 meses la paciente se encontraba asintomática, con su patología tiroidea bajo control (TSH 1,11 UI/ml) con tratamiento de sustitución. No ha presentado recaídas del SN (examen de orina sin proteinuria y creatinina 0,44 mg/dL).",
+        "gold_summary": "Paciente de 10 años que se presenta con síndrome nefrótico y bocio. Se pesquisa antecedente de tiroiditis autoinmu ne e hipotiroidismo no tratado. Se inicia terapia corticoidal y hormonal de sustitución (levotiroxina), logrando buena respuesta clínica y de laboratorio.",
+        "synthetic_summary": {
+            "B1": "Una niña de 10 años tenía hinchazón en los ojos y piernas, y orina con espuma. También tenía un bulto en el cuello llamado bocio, por un problema en la tiroides. Los médicos le dieron medicinas para el riñón y para la tiroides. Con el tratamiento, mejoró mucho y después de un año estaba bien y sin síntomas.",
+            "B2": "Una niña de 10 años llegó al hospital con hinchazón, orina espumosa y dolor abdominal. Tenía bocio, que es un aumento de la glándula tiroides, y no recibía tratamiento para su tiroiditis autoinmune, una enfermedad que afecta la tiroides. Los análisis mostraron proteínas altas en la orina, baja albúmina en sangre y colesterol elevado, signos de síndrome nefrótico, que daña los riñones. Le dieron prednisona, un medicamento para reducir la inflamación, y levotiroxina para la tiroides. Después de seis días, mejoró mucho y pudo salir del hospital. Al año, seguía bien, sin síntomas ni problemas en los riñones, y con la tiroides controlada gracias al tratamiento.",
+            "B3": "Una niña de 10 años con bocio y tiroiditis autoinmune no tratada consultó por síntomas compatibles con síndrome nefrótico, incluyendo orina espumosa, edema y disminución de la diuresis. Al ingreso, se encontró proteinuria significativa, hipoalbuminemia y alteraciones lipídicas, junto con signos de hipotiroidismo y anticuerpos antitiroideos elevados. El diagnóstico fue síndrome nefrótico asociado a tiroiditis autoinmune. Se inició tratamiento con prednisona para controlar la proteinuria y levotiroxina para la función tiroidea, logrando rápida mejoría clínica y normalización de los parámetros urinarios. La ecografía tiroidea mostró signos compatibles con tiroiditis sin nódulos. Tras seis días de hospitalización, la paciente fue dada de alta en buenas condiciones y, al seguimiento de un año, permaneció asintomática, con función tiroidea estable y sin recaídas del síndrome nefrótico. Este caso resalta la importancia de evaluar la función tiroidea en pacientes pediátricos con síndrome nefrótico, ya que la coexistencia de enfermedades autoinmunes puede influir en el manejo y pronóstico. Por lo tanto, el control conjunto de ambas patologías fue clave para el éxito terapéutico."
+        }
+    },
+    {
+        "article": "La exploración neurológica exhaustiva puso de manifiesto una apariencia facial característica: mirada fija con los ojos muy abiertos, fruncimiento de la frente con una expresión de ceño fruncido (signo del procerus) y expresión fija de la parte inferior de la cara. La paciente presentaba hipocinesia-rigidez simétrica de predominio axial con postura retrocólica del tronco y el cuello. El examen de la deambulación reveló un patrón de la marcha del nivel superior caracterizado por una llamativa vacilación inicial que requería ayuda de objetos/personas cercanas. Una vez que comenzaba a caminar, los pasos mejoraban relativamente, pero volvía a aparecer una marcha inefectiva cuando intentaba girar. Exhibía zancadas cortas, congelación, base amplia de sustentación, desequilibrio, movimiento lento de los miembros inferiores, arrastre de los pies y pérdida de la fluidez normal del tronco y las extremidades. Los reflejos posturales estaban alterados. Asimismo, existía una dificultad grave para la bipedestación tras la sedestación y dificultad para darse la vuelta en la cama. Sin embargo, los signos frontales, como la rigidez paratónica, los reflejos de prensión, la incontinencia urinaria y las características de los déficits cognitivos frontales (por ejemplo, cambios disejecutivos y de personalidad e impulsividad) estaban ausentes, excepto por un estado apático progresivo. Los movimientos oculares sacádicos verticales estaban alterados, con amplitudes relativamente normales y movimientos sacádicos horizontales. Se evidenciaron sacadas de onda cuadrada y una oftalmoplejía supranuclear. La resonancia magnética del cerebro reveló atrofia del mesencéfalo, dilatación del acueducto de Silvio y del III ventrículo y atrofia de los lóbulos frontales, y los signos típicos del colibrí y de la gloria de la mañana. Finalmente, la paciente fue diagnosticada de una PSP probable.",
+        "gold_summary": "Mujer de 58 años sana que consultó por un trastorno de la marcha con caídas. La exploración neurológica mostró una apariencia facial característica (mirada fija, ojos muy abiertos, ceño fruncido y expresión fija hemifacial inferior), e hipocinesia-rigidez simétrica de predominio axial (postura retrocólica del tronco y el cuello). La exploración de la marcha reveló un trastorno de la marcha del nivel superior, caracterizado por una significativa vacilación inicial, que precisaba ayuda de objetos/personas cercanos. Al iniciar la marcha, los pasos mejoraban relativamente, pero reaparecía una deambulación inefectiva al girar. Presentaba zancadas cortas, congelación, base amplia de sustentación, desequilibrio, movimiento lento de las piernas, arrastre de los pies, y pérdida de la cadencia normal del tronco y las extremidades. Los reflejos posturales estaban alterados. La resonancia magnética cerebral desveló atrofia mesencefálica, dilatación de acueducto de Silvio y III ventrículo, atrofia frontal bilateral y el signo típico del colibrí. Finalmente, la paciente fue diagnosticada de una PSP probable.",
+        "synthetic_summary": {
+            "B1": "Una mujer de 58 años tenía problemas para caminar y se caía. Su cara parecía fija, con los ojos muy abiertos y ceño fruncido. Caminaba con pasos cortos, se detenía al girar y necesitaba ayuda para empezar a andar. Un estudio del cerebro mostró que algunas partes estaban más pequeñas de lo normal. Los médicos dijeron que tenía una enfermedad llamada PSP, que afecta el movimiento y el equilibrio.",
+            "B2": "Una mujer de 58 años consultó por problemas para caminar y caídas frecuentes. En la exploración, se observó una expresión facial fija con los ojos muy abiertos y ceño fruncido, junto con rigidez y movimiento lento del tronco y cuello. Su forma de caminar mostraba vacilación al comenzar, pasos cortos, dificultad para girar y pérdida del equilibrio. También tenía reflejos posturales alterados. La resonancia magnética mostró desgaste en partes del cerebro, como el mesencéfalo y los lóbulos frontales, además de cambios en los ventrículos cerebrales. Estos hallazgos, junto con los síntomas, llevaron al diagnóstico probable de parálisis supranuclear progresiva (PSP), una enfermedad que afecta el control del movimiento y el equilibrio. Por eso, es importante un seguimiento médico para manejar sus síntomas y evitar caídas.",
+            "B3": "Una mujer de 58 años consultó por dificultades para caminar y caídas frecuentes. En la evaluación neurológica se observó una expresión facial característica, con mirada fija, ojos muy abiertos y ceño fruncido, además de rigidez y lentitud en movimientos del tronco y cuello. Su forma de caminar mostraba vacilación al inicio, necesidad de apoyo, pasos cortos, congelación, desequilibrio y dificultad para girar, junto con reflejos posturales alterados. No se detectaron signos frontales típicos como cambios en la personalidad o incontinencia, salvo apatía progresiva. Los movimientos oculares verticales estaban afectados, evidenciando una parálisis supranuclear. La resonancia magnética reveló atrofia en el mesencéfalo y lóbulos frontales, dilatación ventricular y signos característicos como el del colibrí. Estos hallazgos indicaron un diagnóstico probable de parálisis supranuclear progresiva (PSP), una enfermedad neurodegenerativa que afecta el control motor y el equilibrio. Por lo tanto, se requiere seguimiento neurológico para manejar síntomas y evaluar posibles tratamientos."
+        }
+    },
+    {
+        "article": "Una mujer de 36 años, previamente sana, fue picada una vez por un insecto Hymenoptera desconocido, lo que le provocó hinchazón y eritema en la parte dorsal de la mano derecha. La fiebre punzante apareció en un plazo de 6 horas, a pesar de que el sitio de la picadura se volvió irreconocible gradualmente. Acudió a una clínica local donde le recetaron esteroides orales (prednisolona 20 mg/día) y antibióticos. Tres días después, acudió a nuestro departamento de urgencias por una fiebre intermitente. Presentaba una temperatura elevada (38,9°C), taquicardia e hipotensión (presión arterial 80/52 mmHg) en el momento de la clasificación. La electrocardiografía mostró fibrilación auricular con una frecuencia ventricular rápida de alrededor de 130 latidos por minuto y elevación difusa del ST. La radiografía de tórax mostró una relación cardiotorácica normal sin signos de infiltración o congestión. El hemograma no mostró eosinofilia, leucocitosis, leucopenia o desviación a la izquierda. La isoenzima MB de creatina cinasa (CK-MB) y la troponina cardíaca I se elevaron a 96,0 ng/mL y 8,0 ng/mL, respectivamente. La proteína C reactiva fue de 10,5 mg/L y la procalcitonina fue de 0,32 ng/mL. El NT-proBNP fue de 20 700 pg/mL. La ecocardiografía mostró una hipocinesia global del ventrículo izquierdo con una fracción de eyección del 30,6% y sin derrame pericárdico. El cateterismo cardíaco emergente no reveló lesiones de las arterias coronarias o vasospasmo. Se insertó un globo intraaórtico durante el procedimiento para el shock cardiogénico. La hipotensión progresó acompañada de taquicardia ventricular y fibrilación ventricular, y luego se produjo un paro cardíaco intrahospitalario. La reanimación cardiopulmonar manual no tuvo éxito durante 25 minutos y se usó el soporte cardiopulmonar percutáneo (PCPS, CAPIOX® Centrifugal Pump Controller SP-200, Terumo). La circulación espontánea se estableció 25 minutos después con una recuperación total de la conciencia.\n\nLa prueba rápida de antígeno de influenza (Directigen EZ Flu A+B; BD, Franklin Lakes, NJ, EE. UU.), los cultivos de esputo, los cultivos de sangre y los exámenes serológicos para los virus respiratorios recolectados al ingreso fueron negativos. En el día 2 del ingreso, los niveles séricos de CK-MB y troponina I alcanzaron un máximo de >303 ng/ml y >81 ng/ml, respectivamente. La ecocardiografía de seguimiento 24 horas después del inicio del PCPS mostró deterioro de la función ventricular izquierda, cierre persistente de las válvulas aórticas y trombos intracardiacos en la aurícula izquierda y el ventrículo izquierdo, aproximadamente 24 horas después del inicio del soporte mecánico. En el día 3, el shock progresó con falla multiorgánica. Se aplicó hemodiálisis venovenosa continua debido a la acidosis metabólica y oliguria. En el día 4, la función ventricular derecha también se deterioró gravemente y la actividad eléctrica del corazón desapareció gradualmente. El PCPS se cambió a soportes mecánicos bi-ventriculares a través de canalizaciones hacia la aurícula derecha, el tronco pulmonar, el ápex del ventrículo izquierdo y la aorta ascendente. Ambos sistemas se establecieron utilizando bombas de sangre centrífugas MEDTRONIC Affinity CP. Debido a la hemorragia pulmonar con consolidación bilateral severa de los pulmones, se usó un oxigenador de membrana para lograr una oxigenación adecuada. El flujo sanguíneo se estableció a 3.5 L/minuto, lo que podría mantener la presión arterial media en torno a 65 mmHg. Se realizó una biopsia endomiocárdica del ventrículo izquierdo y la patología reveló una inflamación significativa compuesta principalmente por linfocitos y algunos eosinófilos. El daño miocárdico con necrosis estuvo presente, pero no extenso. En términos de ajustes de ventilador, la presión de conducción y la presión de meseta se establecieron en torno a 15 y 30 cmH2O respectivamente para la protección pulmonar. Se usó la fibra broncoscopia repetidamente para eliminar los coágulos de sangre que obstruían las vías respiratorias principales. En el día 13 del ingreso, la actividad eléctrica del corazón del paciente permaneció ausente y ambas bombas de sangre se cambiaron a los sistemas de asistencia ventricular Levitronix Centri-Mag (Levitronix LLC, Waltham, MA, EE. UU.) para un mejor soporte. El paciente fue trasladado a un centro de trasplantes y se registró como candidato para un trasplante de corazón. En el día 14 se insertó otra cánula en la vena femoral común izquierda para aumentar el flujo de entrada del VAD derecho. Desde el día 14 hasta el día 48, el paciente sufrió episodios de sangrado masivo del mediastino y la vagina, infección de la herida esternal con formación de abscesos, infecciones por úlceras de presión y progresiva hiperbilirrubinemia. Su condición se estabilizó después de desbridamiento, hemostasia quirúrgica y uso de antibióticos fuertes. Se sometió a 5 cursos de intercambio de plasma terapéutico para evitar el rechazo mediado por anticuerpos y recibió un trasplante de corazón ortotópico el día 49. El estudio patológico del corazón del paciente mostró pancarditis de ambos ventrículos y ninguna alteración específica de las 3 arterias coronarias. La ECMO de VA se mantuvo hasta el día 58 para el apoyo postoperatorio del fallo cardiaco. La biopsia endomiocárdica repetida después del trasplante no mostró evidencia de rechazo celular o humoral. La paciente experimentó episodios de shock séptico bajo inmunosupresión y se sometió a una laparoscopia exploratoria y apendicectomía el día 93. La extubación se realizó el día 96 y se dio de alta el día 101. La paciente permaneció clínicamente estable en el seguimiento de 3 meses.\n\nMH - Adulto\nMH - Animales\nMH - Abejas\nMH - Picaduras y mordeduras/*complicaciones\nMH - Oxigenación por membrana extracorpórea\nMH - Mujer\nMH - Paro cardiaco/*etiología/tratamiento\nMH - Insuficiencia cardiaca/*etiología/terapia\nMH - *Trasplante de corazón\nMH - Dispositivos de asistencia cardiaca\nMH - Humanos\nMH - Hipersensibilidad/*diagnóstico\nMH - Miocarditis/*diagnóstico\nMH - Shock, Cardiogénico/*etiología/terapia\n",
+        "gold_summary": "Paciente: Mujer, 36 años\n\nDiagnóstico final: Shock cardiogénico • miocarditis\n\nSíntomas: Fiebre\n\nMedicación: —\n\nProcedimiento clínico: soporte circulatorio mecánico\n\nEspecialidad: Cirugía\n\n\nInforme del caso:\n\nReportamos el caso de una mujer de 36 años que desarrolló fiebre y shock cardiogénico 3 días después de una picadura de abeja. La angiografía cardíaca mostró arterias coronarias permeables y una función ventricular izquierda gravemente comprometida. Su hemodinámica permaneció inestable bajo una dosis alta de agentes inotrópicos y apoyo con un balón intraaórtico. El paro cardíaco intrahospitalario ocurrió 4 horas después del ingreso y recibió reanimación cardiopulmonar extracorpórea. Su oxigenación de membrana extracorpórea venosa periférica (VA ECMO) se cambió a dispositivos de asistencia ventricular bilateral (VAD) debido a una insuficiencia cardíaca derecha progresiva. El resultado de la biopsia endomiocárdica fue compatible con el cuadro de miocarditis por hipersensibilidad. Su corazón entró en paro persistente bajo apoyo circulatorio mecánico. Se sometió a un trasplante de corazón el día 49 del ingreso y permaneció clínicamente estable 6 meses después del alta.\n",
+        "synthetic_summary": {
+            "B1": "Una mujer de 36 años se enfermó después de que un insecto la picó en la mano. Tres días más tarde, tuvo fiebre y problemas graves en el corazón. Los médicos usaron máquinas para ayudar a su corazón a latir y luego le pusieron un corazón nuevo. Después de la operación, ella mejoró y estuvo estable al pasar el tiempo. Este caso muestra que una picadura puede causar problemas serios en el corazón.",
+            "B2": "Una mujer de 36 años sufrió una picadura de abeja que causó hinchazón y fiebre. Tres días después, desarrolló shock cardiogénico, una condición grave donde el corazón no puede bombear suficiente sangre. Los exámenes mostraron que sus arterias coronarias estaban normales, pero su corazón tenía una función muy baja. A pesar del tratamiento con medicamentos y dispositivos mecánicos para ayudar al corazón, sufrió un paro cardíaco. Fue necesario usar soporte mecánico avanzado y, finalmente, un trasplante de corazón. La biopsia reveló una inflamación del corazón llamada miocarditis por hipersensibilidad, causada probablemente por la picadura. Después del trasplante, la paciente mejoró y se mantuvo estable durante meses. Este caso muestra la gravedad que puede tener una reacción alérgica en el corazón.",
+            "B3": "Una mujer de 36 años, sin antecedentes médicos relevantes, desarrolló fiebre y shock cardiogénico tres días después de una picadura de abeja. A pesar del tratamiento con esteroides y antibióticos, presentó taquicardia, hipotensión y fibrilación auricular, acompañadas de elevación de marcadores cardíacos que indicaban daño miocárdico. La ecocardiografía reveló una función ventricular izquierda gravemente disminuida, mientras que el cateterismo descartó obstrucción coronaria. Tras un paro cardíaco intrahospitalario, se implementó soporte circulatorio mecánico mediante oxigenación por membrana extracorpórea (ECMO) y posteriormente dispositivos de asistencia ventricular bilateral debido a la progresión de la insuficiencia cardíaca. La biopsia endomiocárdica confirmó el diagnóstico de miocarditis por hipersensibilidad, una inflamación inmunomediada del músculo cardíaco. Debido a la falla cardíaca persistente, la paciente fue sometida a trasplante cardíaco en el día 49 de hospitalización. Posteriormente, presentó complicaciones infecciosas y hemorragias, pero logró estabilizarse y fue dada de alta con buena evolución clínica a los tres meses. Este caso subraya la gravedad de la miocarditis inducida por reacciones alérgicas a picaduras y la relevancia del soporte mecánico avanzado y trasplante en insuficiencia cardíaca severa."
+        }
+    },
+    {
+        "article": "Un hombre de 24 años con complicaciones cardiovasculares relacionadas con MFS fue admitido en nuestro departamento de medicina interna debido a 3 episodios consecutivos de insuficiencia cardiaca aguda descompensada con fracción de eyección reducida (ADHFrEF) de 2014 a 2017. Su historia médica restante incluye hipertensión arterial, dislipidemia, hipertiroidismo, shock anafiláctico debido a flecainida y hábito tabágico previo.\n\nEl diagnóstico de MFS se realizó en 2010, cuando se llevó a cabo la sustitución de la aorta ascendente y la válvula aórtica con prótesis mecánica debido a una disección aórtica aguda tipo A en presencia de antecedentes familiares (madre, padre y 3 hijos con MFS). Durante el período intraoperatorio, se produjo un síndrome coronario agudo inferior y se trató con cirugía de injerto de derivación de la arteria coronaria.\n\nEn mayo de 2014, se realizó la implantación de una prótesis mecánica de aorta descendente y arco aórtico debido a un aneurisma disecante crónico. El hematoma peri-aórtico y la isquemia medular complicaron la cirugía y causaron paraplejia de las extremidades inferiores, dolor y hipoestesia térmica, e incontinencia rectal. Después de 2 meses, durante su primera admisión por ADHFrEF, las pruebas de laboratorio fueron notables para N-terminal pro-BNP (NT-proBNP) de 12,000 pg/mL y el ecocardiograma transtorácico mostró una función de la prótesis normal, dilatación de todas las cámaras cardiacas (principalmente las izquierdas) con insuficiencia mitral y tricuspídea moderada, hipertrofia ventricular izquierda, acinesia de la pared inferior, discinesia septal e hipocinesia de las paredes restantes con reducción severa de la fracción de eyección ventricular izquierda (LVEF) −20%. Se le trató con diuréticos intravenosos y desfibrilador cardiaco interno (St. Jude Ellipse DR, modo DDD) sin terapia de resincronización cardiaca (criterios de electrocardiograma no cumplidos) y se le dio de alta con la máxima terapia médica (furosemida, carvedilol, ramipril, espironolactona, digoxina y amlodipina).\n\nEn agosto de 2017, se produjo un nuevo episodio de ADHFrEF. Los valores de laboratorio de admisión notables incluían NT-proBNP de 2719 pg/mL y midregional-proadrenomedullin (MR-proADM) de 1.61 nmol/L, mientras que el ecocardiograma transtorácico y transesofágico mostró un LVEF de 35%, función de prótesis normal, severa regurgitación tricuspídea, y ruptura de la valva anterior de la chorda tendineae con severa regurgitación mitral. Los pacientes fueron tratados con diuréticos intravenosos y digoxina y dados de alta con una terapia médica óptima (furosemida, carvedilol, ramipril, espironolactona, digoxina, y amlodipina).\n\nPor último, volvió a ser admitido en nuestro departamento de medicina interna en noviembre de 2017 debido a un tercer episodio de ADHFrEF y una acumulación de líquido mediastinal infectado secundaria a una corrección quirúrgica de insuficiencia valvular severa un mes antes con implantación de prótesis mecánica mitral (31 mm ST Jude) y anuloplastia tricúspide De Vega.\n\nEl examen físico reveló una presión arterial de 120/80 mm Hg, pulso de 82 bpm, frecuencia respiratoria de 26 apm, saturación de O2 de 87% en aire ambiente con posición ortopneica obligatoria, y un habitus marfanoide (peso de 147 kg, altura de 2.2 m). La evaluación cardiopulmonar reveló un segundo sonido cardíaco metálico, percusión opaca con reducción del frémito vocal táctil y crepitaciones en la base de los pulmones, disminución amplia de los sonidos respiratorios vesiculares, presencia de ascitis abundante e hinchazón de las piernas.\n\nLos valores de laboratorio notables incluyeron NT-proBNP de 10,132 pg/mL y MR-proADM de 2,36 nmoL/mL.\n\nEl análisis de gases arteriales reveló una hipoxemia grave con alcalosis respiratoria y metabólica (pH 7,56, pO2 46 mm Hg, pCO2 24,8 mm Hg, HCO3− 21,9 mm mol/L, gradiente alveolar-arterial 31 mm Hg). Aunque el electrocardiograma resaltó fibrilación auricular con frecuencia ventricular de 80 bpm, hipertrofia ventricular izquierda e isquemia subepicárdica infralateral, el ecocardiograma transtorácico mostró las mismas características que el anterior, excepto por una FEVI de 30 %, presencia de prótesis mecánicas mitrales con fuga paravalvular y gradiente medio de 9 mm Hg, e insuficiencia tricuspídea leve.\n\n\nEn la radiografía de tórax y en la tomografía computarizada de alta resolución se observa una congestión hilar con cardiomegalia, consolidación pulmonar en el lóbulo superior derecho y acumulación de líquido mediastínico infectado.\n\nEl paciente fue tratado con 250 mg de furosemida intravenosa por día, 100 mg de canrenona por día, 4,5 g de piperacilina/tazobactam cada 6 horas y 12 mg/kg de teicoplanina por día, y luego 12 mg/kg por día. El día 9, una vez alcanzada la estabilización hemodinámica, se agregó una dosis intermedia de sacubitril/valsartan de 49/51 mg por día a 3,125 mg de carvedilol por día, 100 mg de espironolactona por día, 250 mg de furosemida por día y 0,25 mg de digoxina por día.\n\nEn el seguimiento de 1 mes, sacubitril/valsartan se aumentó a 97/103 mg b.i.d. para la buena condición clínica del paciente, lo que permitió una reducción persistente y progresiva de los parámetros clínicos, de laboratorio (reducción de NT-proBNP e incremento de MR-proADM), de los parámetros ecocardiográficos (aumento del EFV final del ventrículo izquierdo (42 % vs 30 %), del diámetro final del ventrículo izquierdo, del diámetro diastólico final del ventrículo izquierdo, de la masa del ventrículo izquierdo y del índice de masa del ventrículo izquierdo) y una mejora de la calidad de vida sin nuevos episodios de ADHFrEF hasta el seguimiento de 9 meses (Fig. (Fig.1B1B y D; Tabla 1).1). Debido a la falta de un régimen de dosificación específico para sacubitril/valsartan en la miocardiopatía relacionada con la EM, utilizamos el esquema terapéutico recomendado.\n\nMH - Aminobutiratos/uso terapéutico\nMH - Antagonistas de los receptores de la angiotensina/*uso terapéutico\nMH - Compuestos de bifenilo\nMH - Combinaciones de fármacos\nMH - Insuficiencia cardiaca/*terapia farmacológica/*etiología\nMH - Humanos\nMH - Hombre\nMH - Síndrome de Marfan/*complicaciones\nMH - Tetrazoles/uso terapéutico\nMH - Resultado del tratamiento\nMH - Valsartán\nMH - Adultos jóvenes\n",
+        "gold_summary": "Preocupaciones de los pacientes:\nUn hombre de 24 años fue admitido en nuestro departamento de medicina interna debido a disnea, ascitis e hinchazón de las piernas. El análisis de gases en sangre arterial reveló una hipoxemia grave con alcalosis respiratoria y metabólica. La radiografía de tórax mostró una congestión hilar.\n\nDiagnósticos:\nInsuficiencia cardíaca aguda descompensada recurrente con fracción de eyección reducida a pesar de la terapia médica óptima en la cardiomiopatía relacionada con el síndrome de Marfan.\n\nIntervenciones y resultados:\nSe agregó sacubitril/valsartan a la terapia médica óptima después de la estabilización hemodinámica, lo que permitió una mejora clínica, de laboratorio y ecocardiográfica progresiva. El paciente mantuvo una supervivencia libre de insuficiencia cardiaca y una buena calidad de vida hasta el seguimiento de 9 meses.\n",
+        "synthetic_summary": {
+            "B1": "Un joven de 24 años con síndrome de Marfan tuvo problemas graves del corazón. Tenía dificultad para respirar, hinchazón en las piernas y líquido en el abdomen. Los médicos le dieron varios medicamentos y una nueva medicina llamada sacubitril/valsartan. Gracias a esto, su corazón mejoró y pudo vivir bien sin nuevos problemas durante nueve meses.",
+            "B2": "Un hombre de 24 años con síndrome de Marfan, que afecta el corazón y los vasos sanguíneos, sufrió tres episodios de insuficiencia cardíaca grave entre 2014 y 2017. A pesar de recibir tratamiento médico completo, su corazón funcionaba mal, con reducción en la capacidad de bombeo. En noviembre de 2017, ingresó con dificultad para respirar, hinchazón y líquido en el pecho. Se añadió un medicamento llamado sacubitril/valsartán tras estabilizarlo, lo que mejoró su estado clínico, los análisis de sangre y el funcionamiento del corazón. Después de nueve meses, el paciente mostró una mejor calidad de vida y no tuvo nuevos episodios de insuficiencia cardíaca. Este caso muestra que, aunque el síndrome de Marfan puede causar problemas graves, un tratamiento adecuado puede mejorar la salud y la supervivencia.",
+            "B3": "Un hombre de 24 años con síndrome de Marfan y antecedentes de múltiples cirugías aórticas ingresó por episodios recurrentes de insuficiencia cardíaca aguda con fracción de eyección reducida. A pesar del tratamiento médico óptimo y la implantación de prótesis mecánicas valvulares, desarrolló complicaciones como regurgitación valvular, paraplejia y acumulación de líquido mediastinal infectado. Durante su última hospitalización, presentó hipoxemia grave, congestión pulmonar y deterioro funcional cardíaco, lo que requirió estabilización intensiva. Tras la estabilización, se incorporó sacubitril/valsartán a la terapia habitual, logrando una mejoría significativa en parámetros clínicos, ecocardiográficos y bioquímicos, incluyendo aumento de la fracción de eyección y reducción de marcadores de insuficiencia cardíaca. En consecuencia, el paciente experimentó una mejora en su calidad de vida y permaneció libre de nuevas descompensaciones durante nueve meses de seguimiento. Este caso ilustra la complejidad del manejo de la cardiomiopatía asociada al síndrome de Marfan y sugiere que sacubitril/valsartán podría ser una opción terapéutica eficaz en insuficiencia cardíaca avanzada con fracción de eyección reducida en este contexto."
+        }
+    },
+    {
+        "article": "Paciente masculino de 41 años de edad quien ingresó en 2016 al servicio de urgencia con politraumatismo producto de accidente de tránsito; con trauma en miembros inferioA B res, en los rayos X se observa fractura de platillos tibiales izquierdos y fractura subtrocanteriana derecha, trauma toracoabdominal y trauma craneoencefálico leve.\nSe le practica osteosíntesis de fémur con clavo cefalomedular largo a foco cerrado corrigiendo la fractura subtrocanteriana y se le aplica tutor externo transarticular de rodilla como medida de control de daño local provisional; 15 días después se realiza osteosíntesis definitiva de su fractura de platillos tibiales. Evolución adecuada y satisfactoria de platillos tibiales.\nEntre 2016 y 2019 tuvo episodios esporádicos de dolor en cadera derecha que cedían fácilmente al manejo con antiinflamatorios y analgésicos sin limitar las actividades de la vida diaria y en la toma de rayos X se observaba fatiga de los bloqueos distales con dudas de la consolidación de la fractura.\nEn 2020 se incrementa el dolor en la cadera que no cede con el tratamiento médico y se acompaña de limitación funcional. En los rayos X de control se evidencia ruptura del clavo cefalomedular en su tercio proximal y no unión de la fractura subtrocantérica.\nEn Febrero de 2020 intento fallido de extracción de material de osteosíntesis (extrainstitucional), por lo que es remitido a nuestra institución. Se lleva a cirugía el 8 de Febrero, se realiza retiro de material de osteosíntesis, curetaje y toma de cultivo de foco de no unión. Cultivo positivo para Klebsiella pneumoniae recibiendo tratamiento con meropenem intravenoso por 10 días. Posteriormente se le realizó un lavado quirúrgico con drenaje de hematoma para el 20 de Febrero realizar nueva osteosíntesis con clavo cefalomedular + injerto óseo autólogo (tomado de ambas crestas iliacas) en foco de no unión.\nReactivación de la infección en Marzo de 2020, requiriendo nuevamente cirugía para lavados y desbridamiento quirúrgicos seriados (#5). Se aísla nueva bacteria Enterobacter que es manejada con vancomicina y meropenem. A f inales de Abril completa tratamiento médico y se le da salida en condiciones estables.\nEn Mayo de 2020 por persistencia de la infección se retira el material de osteosíntesis, se deja un clavo TENS endomedular recubierto de cemento con antibióticos (gentamicina).\nA finales de Mayo después de dos lavados quirúrgicos se retiró el clavo TENS, resección de bordes de fractura (hasta hueso sano) injerto óseo endomedular con un segmento de 10 cm de peroné no vascularizado (autólogo) y fijación de la fractura con una placa de soporte condíleo de fémur distal; colocación de sistema VAC y cierre definitivo de la herida en un segundo tiempo el 28 de Mayo de 2020. El paciente evolucionó adecuadamente, la herida quirúrgica cicatrizó por completo hasta el día de hoy con infección en remisión y evidencia radiológica de consolidación de la fractura, además paciente asintomático con función preservada de la extremidad.",
+        "gold_summary": "Masculino de 41 años de edad que sufre fractura subtrocantérica derecha producto de un accidente de tránsito que requirió manejo de osteosíntesis. Con posterior ruptura del clavo cefalomedular en su tercio proximal, no unión de la fractura e infecciones en sitio de la fractura. Fue tratado con múltiples lavados quirúrgicos, antibioticoterapia y un procedimiento ortopédico y quirúrgico poco convencional como el uso de una placa de soporte condíleo de fémur distal y un injerto óseo endomedular con un segmento de 10 cm de peroné no vascularizado. Paciente con evolución satisfactoria y favorable.",
+        "synthetic_summary": {
+            "B1": "Un hombre de 41 años tuvo un accidente y se rompió un hueso de la cadera. Le pusieron un clavo para arreglarlo, pero se rompió y el hueso no sanó bien. Además, tuvo una infección que necesitó varias cirugías y medicinas para curar. Le pusieron un injerto de hueso y una placa para ayudar a que el hueso se uniera. Ahora está bien, sin dolor y el hueso está sanando.",
+            "B2": "Un hombre de 41 años se fracturó la parte superior del fémur derecho en un accidente. Primero, le pusieron un clavo para unir el hueso, pero se rompió y la fractura no sanó bien. Además, tuvo infecciones en la zona de la fractura causadas por bacterias, que necesitaron varios antibióticos y cirugías para limpiar la herida. Finalmente, le hicieron una cirugía especial con un injerto de hueso, que es un pedazo de hueso tomado de otra parte del cuerpo, y una placa para sostener el hueso. Gracias a estos tratamientos, la fractura sanó, la infección desapareció y recuperó la función de su pierna sin dolor.",
+            "B3": "Un hombre de 41 años sufrió múltiples fracturas tras un accidente de tránsito, incluyendo una fractura subtrocantérica en la cadera derecha tratada inicialmente con un clavo cefalomedular. Sin embargo, presentó ruptura del clavo y pseudoartrosis, complicadas por infecciones causadas por Klebsiella pneumoniae y Enterobacter, lo que dificultó la consolidación ósea. Durante varios meses, se realizaron múltiples cirugías para retirar el material de osteosíntesis, desbridar la infección y administrar antibióticos dirigidos a los microorganismos identificados. Finalmente, se llevó a cabo un procedimiento reconstructivo complejo que incluyó la colocación de una placa de soporte en el fémur distal y un injerto óseo autólogo no vascularizado de peroné para estimular la consolidación. Gracias a este abordaje integral y multidisciplinario, la herida cicatrizó completamente, la infección se resolvió y la fractura mostró signos evidentes de consolidación ósea. En consecuencia, el paciente recuperó la función de la extremidad afectada sin dolor ni limitaciones funcionales. Este caso resalta la importancia de un tratamiento adaptado y coordinado ante complicaciones graves en fracturas infectadas."
+        }
+    },
+    {
+        "article": "Una adolescente de 17 años se presentó en nuestra clínica con una historia de dos meses de dolor torácico en el lado izquierdo y una historia de una semana de dolor en la espalda en el nivel de T7. El dolor torácico se acompañaba de palpitaciones y disnea que ocurrían de tres a cuatro días por semana. Una semana antes de la primera visita, las palpitaciones y la disnea se hicieron menos frecuentes, y desarrolló un dolor sordo diario intermitente en el lado izquierdo del pecho y la parte media de la espalda sin radiación, en la mayoría de los casos. El dolor ocurría tanto con el ejercicio como en reposo, y duraba horas, sin factores agravantes o atenuantes. Informó una intensidad del dolor de 2 a 6 en una escala de 10 puntos. La intensidad cambiaba durante un ataque, y el promedio era 4. Estaba sana por lo demás. No había limitación en la vida diaria. Visitó a un médico local un mes antes de visitar nuestra clínica. Los resultados de los exámenes electrocardiográficos y de laboratorio de Holter fueron normales. Su historial médico incluía migraña durante tres años. Sus medicamentos regulares eran lomerizina, loxoprofen y naratriptan para la prevención y el tratamiento agudo de la migraña. Su migraña estaba bien controlada, y rara vez experimentaba ataques. Negó trauma o cirugías previas. Negó síntomas sospechosos o antecedentes familiares de afecciones autoinmunes o inflamatorias.\n\nSu presión arterial era de 107/60 mmHg y su pulso de 62 latidos/min. Medía 162 cm de altura y pesaba 43 kg, con un índice de masa corporal de 16,4 kg/m2. No se escuchaba ningún murmullo ni arritmia en su examen cardiovascular. Los pulmones estaban limpios a la auscultación bilateral. La palpación del tórax provocó un dolor local no reproducible en las articulaciones inferiores esterno-costales; la maniobra de tracción del brazo horizontal y la maniobra del gallo cantando no provocaron dolor. No había sensibilidad en los músculos y huesos de la parte superior del cuerpo.\n\nLos hallazgos electrocardiográficos y de laboratorio, incluida la función tiroidea, fueron normales. El examen radiográfico torácico y torácico mostró el enderezamiento de la columna torácica superior y una pérdida de la curvatura cifótica normal. Las radiografías de las costillas inferiores no revelaron fractura ni neumotórax. Sospechamos un síndrome de la espalda recta, de acuerdo con los dos criterios diagnósticos diferentes propuestos por Davies et al. y DeLeon et al. La distancia entre la mitad del borde anterior de T8 y una línea vertical que conecta T4 a T12 fue de 0.91 cm. El diámetro anteroposterior fue de 74.0 cm, y el diámetro transversal fue de 243.2 cm. Le aconsejamos que comenzara y continuara la terapia quiropráctica para aumentar la cifosis torácica. Procedimos con una espera vigilante durante un mes en atención ambulatoria.\n\nDespués de esta primera visita, el dolor de pecho y de espalda se alivió gradualmente. Las palpitaciones y la disnea apenas se produjeron. Todos los síntomas desaparecieron en tres semanas. En la visita de seguimiento de un mes, se realizó una ecocardiografía, que reveló una regurgitación mitral trivial sin prolapso. Confirmamos el diagnóstico de síndrome de espalda recta. Reaseguramos a la paciente de que la enfermedad es benigna y le aconsejamos que continuara con la terapia quiropráctica. No ha tenido recaída de síntomas graves ni necesidad de visitar el hospital. Nunca volvió a visitar nuestra clínica en el año siguiente.\n",
+        "gold_summary": "Una adolescente de 17 años se presentó con su madre en nuestra clínica con un historial de dos meses de dolor en el pecho izquierdo y un historial de una semana de dolor en la parte media de la espalda. Diagnosticamos el síndrome de la columna vertebral basado en los hallazgos radiográficos del pecho y la columna vertebral y los síntomas de dolor en el pecho, palpitaciones y disnea. Tranquilizamos a la paciente de que la enfermedad era benigna y le aconsejamos que iniciara y continuara con la terapia quiropráctica. Todos los síntomas, incluido el dolor de espalda, desaparecieron en tres semanas.\n",
+        "synthetic_summary": {
+            "B1": "Una niña de 17 años tenía dolor en el pecho y en la espalda. Los doctores vieron que su columna estaba un poco recta y eso causaba el dolor. Le dijeron que no era grave y le dieron un tratamiento para mejorar la columna. Después de unas semanas, el dolor desapareció y se sintió mejor. Ahora está bien y sigue cuidando su espalda.",
+            "B2": "Una adolescente de 17 años tuvo dolor en el pecho izquierdo durante dos meses. También sentía dolor en la parte media de la espalda por una semana. Tenía palpitaciones y dificultad para respirar, pero estos síntomas mejoraron antes de la consulta. Los exámenes del corazón y la sangre fueron normales. Sin embargo, la radiografía mostró que su columna torácica estaba más recta de lo normal, causando el síndrome de la espalda recta. Este problema puede provocar dolor en el pecho y la espalda. Se le recomendó terapia quiropráctica para mejorar la curvatura de la columna. En tres semanas, sus síntomas desaparecieron y una ecocardiografía mostró solo un problema leve en la válvula mitral, sin gravedad. La paciente mejoró sin complicaciones y no volvió a tener síntomas.",
+            "B3": "Una adolescente de 17 años acudió a la clínica con dolor en el pecho izquierdo durante dos meses y dolor en la parte media de la espalda desde hace una semana, acompañado de palpitaciones y dificultad para respirar. Los exámenes iniciales, incluyendo electrocardiogramas y análisis de laboratorio, fueron normales. Sin embargo, las radiografías mostraron una pérdida de la curvatura normal de la columna torácica, lo que llevó a diagnosticar un síndrome de espalda recta, una condición benigna relacionada con la postura. Se recomendó terapia quiropráctica para mejorar la cifosis torácica y se realizó un seguimiento cuidadoso. Tras un mes, los síntomas mejoraron progresivamente y desaparecieron completamente en tres semanas. Una ecocardiografía posterior mostró una regurgitación mitral trivial sin complicaciones graves. La paciente fue tranquilizada sobre la naturaleza benigna de su condición y se le indicó continuar con la terapia. No presentó recaídas ni necesidad de atención médica adicional durante el año siguiente. Este caso resalta la importancia de considerar alteraciones posturales en adolescentes con dolor torácico y síntomas asociados, y el beneficio de un tratamiento conservador y seguimiento adecuado."
+        }
+    },
+    {
+        "article": "Una mujer de 59 años con urolitiasis bilateral recurrente se presentó con dolor en el flanco derecho, fiebre y fatiga. Se le había colocado un stent doble J derecho un año antes para una piedra pélvica sintomática, pero no se le dio seguimiento. Tenía insuficiencia cardíaca derecha, diabetes tipo 2 mal controlada y enfermedad renal crónica (nadir de creatinina: 18 mg/L).\nEstable clínicamente, tenía una escala de coma de Glasgow de 14/15 (respuesta verbal ligeramente alterada), fiebre (38,3 °C), sensibilidad en el flanco derecho y una producción de orina de 800 cc en 24 horas.\nLos resultados de laboratorio revelaron una lesión renal aguda, con un nivel de creatinina sérica de 107 mg/L (normal: 6-12 mg/L) y urea sanguínea de 3 g/L (normal: 0.15-0.45 g/L). Los marcadores inflamatorios estaban elevados, con un nivel de proteína C reactiva de 300 mg/L (normal: <5 mg/L) y un recuento de glóbulos blancos de 17,000/mm3 (normal: 4000-10,000/mm3). Además, el paciente exhibió anemia normocítica (hemoglobina: 7.6 g/dL; normal: 12-16 g/dL) e hipercalemia leve (potasio sérico: 5.4 mEq/L; normal: 3.5-5.1 mEq/L). El análisis de orina y el cultivo de orina fueron negativos para infección bacteriana.\nUna tomografía computarizada abdominal y pélvica sin contraste reveló una hidronefrosis del lado derecho, un stent de doble J calcificado en espiral en ambos extremos y una piedra en la pelvis derecha de 35 × 28 mm (588 UH). El riñón izquierdo está reducido en tamaño, con hidronefrosis y una piedra en la pelvis de 12 × 7 mm (531 UH).\n\nDebido a la obstructiva severa de la pielonefritis, en particular causada por la endoprótesis incrustada, se realizó una nefrostomía percutánea bilateral urgente, lo que produjo una importante mejora clínica y normalización de los marcadores inflamatorios y la función renal.\nTres días después, la paciente experimentó una convulsión generalizada asociada con disartria. Una tomografía computarizada urgente del cerebro mostró lesiones isquémicas en los lóbulos occipitales izquierdo y frontal derecho, lo que indicaba un accidente cerebrovascular embólico. Se le inició un tratamiento con enoxaparina (0,4 cc diarios) y Kardegic (160 mg diarios) para la prevención de accidentes cerebrovasculares.\nA pesar de la mejora neurológica, cuatro días después, la paciente desarrolló palidez mucocutánea progresiva, taquicardia (110 latidos por minuto), hipotensión (80/50 mmHg) y hematuria macroscópica por el catéter urinario. Los niveles de hemoglobina descendieron de 7,5 g/dL a 4,4 g/dL, lo que levantó sospechas de hemorragia activa. Se administró fluidoterapia, vasopresores intravenosos y transfusiones de sangre, estabilizando su estado para una exploración de angiografía por TAC con contraste.\nLa tomografía computarizada reveló una colección polar media heterogénea de 17 mm de espesor con extravasación de contraste en las fases arterial y portal, lo que indica una hemorragia activa de las arterias del polo superior y medio. También había coágulos intraluminales en la pelvis renal y la vejiga. Se hizo un diagnóstico de fístula arteriovenosa postnefrostomía, exacerbada por la terapia anticoagulante para el accidente cerebrovascular.\nSe realizó una arteriografía renal urgente a través del acceso a la arteria femoral derecha, utilizando un catéter de diagnóstico de calibre 5. La angiografía selectiva reveló una FAV en el polo inferior del riñón con drenaje venoso temprano hacia la vena cava inferior, junto con un pequeño pseudoaneurisma. La embolización superselectiva con microespirales de 3 mm y 5 mm logró ocluir con éxito la fístula, y se usaron partículas de Gelfoam para evitar el sangrado retrógrado. Una inyección final de contraste confirmó la oclusión completa de la fístula, restaurando la integridad arterial y deteniendo la hemorragia.\n\nDespués de la embolización, se vigiló de cerca al paciente en la UCI. La hemodinámica se mantuvo estable y se tomó la decisión colegiada de reintroducir la anticoagulación con monitorización del INR para controlar el accidente cerebrovascular isquémico mientras se equilibraba el riesgo de hemorragia. La hematuria se resolvió, la función renal se normalizó y la nefrostomía siguió siendo funcional.\nSe adoptó un enfoque multidisciplinario para el tratamiento definitivo. La primera etapa involucró la litotripsia endoscópica con láser del bucle inferior calcificado del stent de JJ, la inserción de un segundo stent de JJ en paralelo con el incrustado y la extracción de la nefrostomía, que se completó con éxito. La segunda etapa, programada seis semanas después, incluyó una ureteroscopia derecha flexible para liberar el bucle superior del stent de JJ calcificado, la fragmentación de la piedra pélvica derecha mediante litotripsia con láser y la extracción completa del stent incrustado. Lamentablemente, la salud del paciente se deterioró debido a múltiples factores, entre ellos, insuficiencia cardíaca, diabetes mal controlada, enfermedad renal crónica y un accidente cerebrovascular previo, lo que demoró la finalización de la segunda etapa del tratamiento planificado.\n",
+        "gold_summary": "Una mujer de 59 años con urolitiasis bilateral recurrente, insuficiencia cardiaca derecha, diabetes tipo 2 mal controlada y enfermedad renal crónica se presentó con dolor en el flanco derecho, fiebre y fatiga. Previamente se le había colocado un stent doble J derecho, pero se perdió su seguimiento. Una tomografía computarizada reveló una hidronefrosis, un stent calcificado y una piedra pélvica de 22 mm, lo que llevó a la realización de una nefrostomía percutánea. La paciente desarrolló un accidente cerebrovascular embólico tres días después y posteriormente presentó hematuria, hipotensión y anemia significativa. La angiografía por TC confirmó una FAV con sangrado activo, que se trató con éxito con embolización.\n",
+        "synthetic_summary": {
+            "B1": "Una mujer de 59 años tenía piedras en los riñones y un tubo llamado stent que se había calcificado. Ella sentía dolor, fiebre y cansancio. Los doctores le pusieron un drenaje para aliviar el riñón. Después, tuvo un problema en el cerebro llamado accidente cerebrovascular y sangró en el riñón. Los médicos usaron un tratamiento especial para detener el sangrado y mejorar su salud.",
+            "B2": "Una mujer de 59 años con piedras en ambos riñones y diabetes mal controlada llegó con dolor y fiebre. Tenía un stent, un tubo para ayudar al riñón derecho, pero no se le hizo seguimiento. Un examen mostró inflamación y una piedra grande en ese riñón, por eso le hicieron un drenaje urgente. Tres días después, sufrió un accidente cerebrovascular, que afecta el cerebro. Luego presentó sangrado en el riñón, anemia y presión baja. Un estudio confirmó una conexión anormal entre una arteria y una vena, causando la hemorragia. Se trató con una técnica para cerrar esa conexión y detener el sangrado. La paciente mejoró, aunque su salud seguía delicada por otras enfermedades.",
+            "B3": "Una mujer de 59 años con antecedentes de cálculos renales recurrentes, insuficiencia cardíaca derecha, diabetes mal controlada y enfermedad renal crónica acudió por dolor en el costado derecho, fiebre y cansancio. Tenía un stent doble J colocado un año antes sin seguimiento, y la tomografía mostró hidronefrosis, un stent calcificado y una piedra grande en el riñón derecho. Se realizó una nefrostomía percutánea urgente que mejoró su estado y función renal. Sin embargo, tres días después sufrió un accidente cerebrovascular embólico, por lo que inició tratamiento anticoagulante. Posteriormente presentó hemorragia activa con anemia grave y hematuria, detectándose una fístula arteriovenosa renal causada por la nefrostomía y agravada por la anticoagulación. La embolización superselectiva detuvo el sangrado con éxito. Tras la estabilización, se planificó un tratamiento escalonado para eliminar el stent calcificado y las piedras, aunque la recuperación se complicó por sus múltiples enfermedades crónicas y el accidente cerebrovascular. Este caso destaca la importancia del seguimiento en pacientes con stents y la necesidad de un manejo multidisciplinario ante complicaciones graves."
+        }
+    },
+    {
+        "article": "Un hombre de 52 años fue admitido en un hospital debido a palpitaciones repentinas y fatiga general. La electrocardiografía reveló taquicardia ventricular con una frecuencia cardíaca de 180 lpm. Su ritmo cardíaco volvió a un ritmo sinusal después de una cardioversión inmediata y luego fue derivado a nuestra institución para una investigación adicional. Su historial médico pasado incluía reconstrucción del tracto de salida del ventrículo derecho utilizando un injerto homólogo y cierre de un defecto septal ventricular para TOF, que se realizó 47 años antes. Sin embargo, se perdió su seguimiento posterior. Tras ser derivado a nuestra institución, su presión arterial era de 116/70 mmHg, frecuencia cardíaca de 80 lpm, y saturación de oxígeno del 99% (con aire ambiente). Al inspeccionar la pulsación de la vena yugular, se observaron claramente una onda prominente y un descenso profundo, que eran consistentes con el aumento de la presión de llenado del ventrículo derecho y la compensación del aumento de la contracción de la RA. Cabe destacar que la auscultación reveló un murmullo diastólico regurgitante agudo en el tercer espacio intercostal izquierdo, un primer sonido cardíaco ampliamente dividido (S1) y un segundo sonido cardíaco (S2), lo que indicaba un ventrículo derecho severamente dilatado debido a la liberación de PR libre y la presencia de una válvula pulmonar no funcional. Además, se auscultó un tercer sonido cardíaco (S3) en el cuarto borde paraesternal, que era consistente con un S3 derecho. El electrocardiograma reveló bloqueo completo del haz de rama derecha, con una duración de QRS de 200 lpm. La radiografía de tórax mostró cardiomegalia con dilatación de las arterias pulmonares bilaterales. La ecocardiografía transtorácica reveló una regresión completa de la válvula pulmonar, que resultó en PR libre y una dilatación prominente del ventrículo derecho. La evaluación volumétrica del ventrículo derecho se realizó utilizando una resonancia magnética cardíaca, que reveló un volumen final diastólico del ventrículo derecho de 428 ml (índice de volumen final diastólico del ventrículo derecho de 240 ml/m2), una fracción de eyección del ventrículo derecho del 36% y una fracción de eyección de PR del 74%. Además, la tomografía computarizada multidetector mostró claramente una regresión completa de la válvula pulmonar del injerto homólogo.\n\nEl paciente se sometió a un examen con catéter para investigar más a fondo su estado hemodinámico. Su forma de onda de presión RA fue particularmente notable, ya que consistía en una onda a prominente y un descenso y, que coincidían con el cuarto sonido cardiaco (S4) y S3 en un fonocardiograma, respectivamente. Además, se reveló que la presión arterial pulmonar final diastólica y la presión final diastólica del VD eran casi idénticas debido al PR libre. Por lo tanto, la evaluación clínica del «quinteto de sonidos cardiacos», que incluye un murmullo diastólico regurgitante agudo, un S1 ampliamente dividido, un S2 único y la presencia de un S3 y un S4 derechos, se confirmó mediante una evaluación hemodinámica y anatómica multimodal como insuficiencia cardiaca derecha grave concomitante con un VD significativamente dilatado debido a la regresión completa de la válvula pulmonar y el PR libre resultante.\n\nDespués del reemplazo de la válvula pulmonar, el «quinteto de sonidos del corazón» se resolvió por completo.\n\nMH - Insuficiencia cardiaca/*etiología\nMH - Murmullos cardiacos/*diagnóstico\nMH - *Sonidos del corazón\nMH - Humanos\nMH - Hombre\nMH - Edad Media\nMH - Insuficiencia de la válvula pulmonar/*complicaciones/diagnóstico\nMH - Taquicardia, ventricular/etiología\nMH - Tetralogía de Fallot/*cirugía\nMH - Disfunción ventricular, derecha/etiología\n",
+        "gold_summary": "Un hombre de 52 años fue derivado a nuestra institución para la evaluación de una taquicardia ventricular de inicio súbito. Su historia clínica incluía una reconstrucción del tracto de salida del ventrículo derecho a los 5 años de edad. La auscultación reveló un murmullo diastólico regurgitante agudo, un primer sonido cardiaco (S1) ampliamente dividido y un segundo sonido cardiaco (S2) único, lo que indicaba un ventrículo derecho severamente dilatado debido a una regurgitación pulmonar (RP) grave y la presencia de una válvula pulmonar no funcional. Además, el tercer sonido cardiaco (S3) y el cuarto sonido cardiaco (S4) del lado derecho estaban presentes, lo que era coherente con una presión de llenado del ventrículo derecho elevada y la presencia de un ventrículo derecho no conforme. Finalmente, el mencionado «quinteto de sonidos cardiacos» se confirmó mediante una evaluación multimodal como insuficiencia cardiaca del lado derecho con un ventrículo derecho concomitantemente severamente dilatado debido a la regresión completa de la válvula pulmonar y la consiguiente RP libre.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre de 52 años tuvo un problema en su corazón que hizo que latiera muy rápido. Cuando los doctores lo revisaron, vieron que una parte de su corazón estaba muy grande y no funcionaba bien porque una válvula no cerraba bien. Esto causaba que la sangre volviera hacia atrás. Después de cambiar la válvula, su corazón mejoró mucho. Los sonidos que escucharon en su corazón ayudaron a entender lo que pasaba.",
+            "B2": "Un hombre de 52 años llegó al hospital por palpitaciones y fatiga. Tenía antecedentes de cirugía en el corazón cuando era niño, pero no había recibido seguimiento. Los médicos encontraron que su ventrículo derecho, una de las cámaras del corazón, estaba muy dilatado porque la válvula pulmonar no funcionaba bien, causando que la sangre regresara al corazón (regurgitación pulmonar). Escucharon varios sonidos anormales en su corazón que indicaban problemas graves en el lado derecho. Las pruebas confirmaron que tenía insuficiencia cardíaca derecha por esta razón. Después de reemplazar la válvula pulmonar, los sonidos anormales desaparecieron y su condición mejoró. Este caso muestra la importancia de un seguimiento continuo tras cirugías cardíacas.",
+            "B3": "Un hombre de 52 años fue ingresado por taquicardia ventricular súbita y fatiga, con antecedentes de cirugía por tetralogía de Fallot en la infancia. La exploración física mostró un murmullo diastólico regurgitante agudo, un primer ruido cardíaco (S1) ampliamente dividido y un segundo ruido (S2) único, lo que sugería un ventrículo derecho severamente dilatado debido a regurgitación pulmonar grave y una válvula pulmonar no funcional. Además, se identificaron los sonidos cardíacos derechos S3 y S4, que se asocian con elevada presión de llenado ventricular y disfunción del ventrículo derecho. Los estudios de imagen y hemodinámicos confirmaron la ausencia completa de la válvula pulmonar y una insuficiencia cardíaca derecha significativa con dilatación ventricular marcada. Tras el reemplazo valvular pulmonar, desaparecieron los sonidos cardíacos anormales, evidenciando una mejoría clínica notable. Este caso destaca la importancia de una evaluación multimodal para diagnosticar y tratar complicaciones tardías en pacientes con cirugía previa de tetralogía de Fallot, especialmente cuando presentan arritmias y signos de insuficiencia cardíaca derecha."
+        }
+    },
+    {
+        "article": "Un hombre de 62 años con antecedentes médicos de cardiopatía no isquémica que derivó en insuficiencia cardíaca, en estado postoperatorio de un dispositivo de asistencia ventricular izquierdo, se sometió a un trasplante cardíaco ortotópico. Mientras se recuperaba en la UCI quirúrgica, desarrolló un empeoramiento de la distensión abdominal, sensibilidad y leucocitosis, lo que motivó la evaluación por el equipo de cirugía general 6 días después del trasplante. El paciente no había evacuado ni expulsado gases desde su cirugía y no había respondido a los enemas administrados ni a la metoclopramida oral por un presunto íleo posoperatorio. Se realizó una tomografía computarizada del abdomen y la pelvis, que reveló múltiples bucles intestinales dilatados con niveles de aire-líquido y un punto de transición en el intestino delgado proximal en el cuadrante superior izquierdo, lo que generó preocupación por una obstrucción. En función de estos hallazgos y del hecho de que el paciente no había sido sometido a cirugías abdominales previas, lo que hacía que la obstrucción intestinal fuera secundaria a las adherencias, se llevó al paciente al quirófano para una laparotomía exploratoria. En el quirófano, se encontró que el intestino estaba dilatado de forma difusa sin ninguna área de isquemia aparente. Se encontró que una porción del intestino delgado estaba adherida a la pared abdominal anterior en el cuadrante superior izquierdo. Tras una exploración adicional, se encontró que una línea motriz de LVAD retenida estaba tunelizada en la cavidad peritoneal, estrangulando un bucle de intestino delgado en el cuadrante superior izquierdo. La línea motriz se liberó de la pared abdominal y se retiró, y se liberó el bucle de intestino afectado. Se encontró que era viable después de unos minutos de reperfusión. Se examinó el intestino delgado en su totalidad, desde el ligamento de Trietz distalmente hasta el intestino ciego, y se encontró que estaba dilatado pero en general era normal. Se reparó una pequeña área de desgarro seroso en el punto de adhesión a la línea motriz, principalmente. Se devolvió el intestino a la cavidad abdominal y se cerró la fascia y la piel con suturas corrientes y grapas cutáneas.\n\nMH - *Eliminación de dispositivo\nMH - Migración de cuerpos extraños/*complicaciones\nMH - Insuficiencia cardiaca/*terapia\nMH - *Trasplante de corazón\nMH - Dispositivos de asistencia cardíaca/*efectos adversos\nMH - Humanos\nMH - Obstrucción intestinal/diagnóstico por imágenes/*etiología\nMH - Laparotomía\nMH - Hombre\nMH - Edad Media\nMH - Tomografía computarizada por rayos X\nMH - Estados Unidos\n",
+        "gold_summary": "Un hombre de 62 años con antecedentes de insuficiencia cardiaca inducida por cardiomiopatía no isquémica, post-puente de asistencia ventricular izquierda y trasplante cardiaco ortotópico, presentó distensión abdominal, dolor y leucocitosis seis días después del trasplante. La TAC de abdomen y pelvis reveló bucles intestinales dilatados, niveles de aire-líquido y un punto de transición en el intestino delgado proximal. Se diagnosticó al paciente una obstrucción intestinal y se le realizó una laparotomía exploratoria. Se encontró que tenía un conducto de LVAD intraabdominal retenido que estrangulaba un bucle de intestino delgado en el cuadrante superior izquierdo. Se retiró el conducto y se liberó la sección de intestino con el retorno de la perfusión.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre de 62 años tuvo una operación de corazón y luego tuvo dolor y hinchazón en la barriga. No podía hacer caca ni expulsar gases. Los doctores hicieron una foto especial y vieron que su intestino estaba muy hinchado y bloqueado. En la operación, encontraron un tubo que apretaba su intestino. Quitaron el tubo y el intestino volvió a funcionar bien. Ahora está mejor.",
+            "B2": "Un hombre de 62 años con insuficiencia cardíaca y trasplante de corazón presentó dolor y distensión abdominal seis días después de la cirugía. No había evacuado ni expulsado gases, y los tratamientos para un posible íleo no funcionaron. Una tomografía mostró que partes del intestino delgado estaban dilatadas y bloqueadas. En la cirugía, encontraron que un cable de un dispositivo cardíaco llamado LVAD estaba dentro del abdomen y apretaba el intestino, causando la obstrucción. Retiraron el cable y liberaron el intestino, que recuperó su función normal. El paciente no tenía daño intestinal grave, y se cerró la herida. Este caso muestra que dispositivos médicos pueden causar problemas inesperados que requieren atención rápida.",
+            "B3": "Un hombre de 62 años con insuficiencia cardíaca no isquémica, tras recibir un dispositivo de asistencia ventricular izquierdo y un trasplante cardíaco, presentó distensión abdominal, dolor y aumento de glóbulos blancos seis días después de la cirugía. No había evacuado ni expulsado gases, y no respondió a tratamientos para un posible íleo posoperatorio. Una tomografía mostró intestinos dilatados con un punto de obstrucción en el intestino delgado. Debido a la ausencia de cirugías abdominales previas, se descartaron adherencias como causa y se decidió realizar una cirugía exploratoria. Durante la operación, se encontró que una línea motriz del dispositivo de asistencia ventricular estaba dentro de la cavidad abdominal, atrapando y estrangulando un segmento del intestino delgado. Se retiró esta línea y se liberó el intestino, que recuperó su circulación normal tras la intervención. No se observaron áreas de daño irreversible en el intestino y se reparó una pequeña lesión en la pared intestinal. Este caso resalta la importancia de considerar complicaciones mecánicas relacionadas con dispositivos cardíacos en pacientes con síntomas abdominales tras trasplante."
+        }
+    },
+    {
+        "article": "Un paciente de 13 años de edad, del sexo masculino, fue admitido en el Hospital de Niños de Damasco tras notar una masa palpable agrandada en la región inguinal izquierda. Su historial médico no fue notable, excepto por una intervención quirúrgica en su columna vertebral 6 años atrás, debido a un accidente, que resultó en la pérdida de la función motora y la sensación en ambas extremidades inferiores.\n\nDebido al largo período que había pasado en la cama, el paciente desarrolló úlceras de decúbito en su pie izquierdo. El único hallazgo en el examen clínico fue una masa en el área inguinal izquierda, que era móvil en las estructuras profundas y también lo era la piel que la cubría. La masa no era sensible a la palpación y no se observaron signos de inflamación local.\n\nLos exámenes de laboratorio revelaron una ESR elevada (119 mm/h en la primera hora). Se solicitaron otros exámenes básicos de laboratorio, que incluían (recuento sanguíneo completo, pruebas de función hepática, electrolitos, urea, creatinina y LDH) y estaban dentro de los rangos normales para la edad. La realización de estos exámenes fue esencial para descartar enfermedades sistémicas. Dada la ausencia de hallazgos físicos indicativos de trastornos sistémicos o inmunodeficiencias, se consideró innecesario realizar exámenes adicionales como los de VIH o antiglobulina directa.\n\nLa tomografía computarizada del abdomen, el tórax y la pelvis mostró ganglios linfáticos agrandados por debajo del ligamento inguinal, el más grande de aproximadamente 3,5 por 2,4 cm. Otros órganos y ganglios estaban dentro de los límites normales.\n\nTodas las investigaciones mencionadas fueron esenciales para descartar otros diagnósticos de alto riesgo, como linfoma y leucemia. Sin embargo, no fueron suficientes para llegar al diagnóstico definitivo, por lo que se tomó la decisión de realizar una resección quirúrgica de los ganglios.\n\nPara confirmar los diagnósticos y descartar otras posibles diferencias que pudieran presentarse con ganglios linfáticos agrandados, se realizó la extirpación quirúrgica de todos estos ganglios agrandados bajo anestesia general y se enviaron biopsias para su estudio microscópico.\n\nLa biopsia mostró una arquitectura ganglionar hiperplásica con proliferación de histiocitos y células plasmáticas con proliferación vascular, lo que es compatible con el subtipo de enfermedad de Castleman de células plasmáticas.\n\nEl paciente fue dado de alta del hospital después de 14 días, tras comprobar que no había ganglios linfáticos agrandados. La única recomendación fue prednisolona oral. El paciente se sometió a un seguimiento mediante TAC de cuerpo entero cada tres meses. Durante cada visita al hospital, se realizó un examen clínico exhaustivo y pruebas de laboratorio (por ejemplo, análisis de sangre completo, VSG, proteína C reactiva, pruebas de función hepática, pruebas de función renal), además del TAC. Después de un período de seguimiento de 12 meses, el paciente no informó de nuevos síntomas o ganglios linfáticos agrandados. Además, no se observaron anomalías durante el examen clínico o en las pruebas de laboratorio.\n",
+        "gold_summary": "Reportamos un caso único de un niño de 13 años que presentó una masa palpable agrandada en la región inguinal izquierda sin ningún síntoma constitucional. La extirpación quirúrgica de esta masa fue esencial para descartar causas preocupantes. El examen patológico reveló cambios proliferativos consistentes con el tipo de célula plasmática de la enfermedad de Castleman, que es una de las formas más raras de la enfermedad en niños. Hasta donde sabemos, este caso es el primer caso reportado de enfermedad de Castleman unicéntrica (UCD) en el área inguinal. Durante un período de seguimiento de 12 meses, no se reportaron agrandamientos adicionales de los ganglios linfáticos u otros síntomas.\n",
+        "synthetic_summary": {
+            "B1": "Un niño de 13 años notó un bulto en la ingle izquierda. No tenía dolor ni fiebre, pero los médicos hicieron estudios para entender qué era. Le quitaron el bulto con una operación y descubrieron que tenía una enfermedad rara llamada Castleman, que afecta los ganglios. Después de un año, el niño está bien y no tiene más bultos ni síntomas.",
+            "B2": "Un niño de 13 años encontró una masa en la ingle izquierda sin dolor ni inflamación. Tenía parálisis en las piernas por un accidente, lo que causó heridas en el pie. Los análisis mostraron inflamación, pero no indicaron enfermedades graves. La tomografía mostró ganglios linfáticos agrandados, que son glándulas del sistema inmunitario, en la zona inguinal. Para saber qué era, se quitó la masa y se analizó en el laboratorio. El estudio reveló enfermedad de Castleman, una enfermedad rara que afecta los ganglios. Después de la cirugía, el niño recibió un medicamento llamado prednisolona y tuvo controles cada tres meses. Tras un año, no presentó nuevos síntomas ni ganglios inflamados, y su salud se mantuvo estable.",
+            "B3": "Un niño de 13 años fue ingresado tras notar una masa en la región inguinal izquierda, sin otros síntomas. Su historial incluía una lesión medular previa que causaba inmovilidad, lo que complicaba su estado general. Los análisis mostraron una inflamación elevada, pero sin alteraciones sistémicas. La tomografía reveló ganglios linfáticos aumentados de tamaño en la zona afectada, sin compromiso de otros órganos. Ante la sospecha de enfermedades graves como linfoma, se decidió extirpar quirúrgicamente los ganglios para un diagnóstico definitivo. El estudio microscópico confirmó la enfermedad de Castleman unicéntrica, subtipo de células plasmáticas, una condición rara en niños y especialmente inusual en la región inguinal. Tras la cirugía, el paciente recibió prednisolona y fue monitoreado con tomografías y análisis periódicos durante un año, sin evidenciar recurrencias ni nuevos síntomas. Este caso resalta la importancia de la biopsia para identificar esta enfermedad poco común y la necesidad de un seguimiento cuidadoso para prevenir complicaciones futuras."
+        }
+    },
+    {
+        "article": "Un hombre asiático de 55 años de edad, que había estado recibiendo tratamiento irregularmente (el paciente no cumplía con el tratamiento) para DCMP durante los últimos 6 meses, acudió con quejas de disnea al hacer ejercicio durante 1 semana y disminución de la producción de orina durante 2 días. El paciente aparentemente estaba bien hace 1 semana cuando empezó a desarrollar disnea, inicio insidioso, gradualmente progresiva, inicialmente de grado II de la New York Heart Association (NYHA) pero progresó a grado IV de la NYHA asociada con pesadez en el pecho. La historia de ortopnea y disnea nocturna paroxística estuvo presente. Esto estuvo asociado con tos con una cantidad moderada de expectoración espumosa, no purulenta. El paciente también se quejó de hinchazón de las extremidades inferiores bilaterales. No hubo historia de hinchazón periorbital, orina espumosa o hematuria. No hubo historia de palpitación, síncope, dolor de pecho o hemoptisis. El paciente también dio una historia de una sensación de hormigueo en ambas manos y pies durante 1 mes.\n\nEl paciente había tenido un episodio similar 6 meses atrás, por el que fue hospitalizado y tratado de manera conservadora como un caso de DCMP. Se le había practicado una cirugía de cataratas en ambos ojos 15 años atrás.\n\nEn el examen físico general, el paciente estaba consciente y orientado en cuanto al tiempo, el lugar y la persona, y afebril con una presión arterial de 90/60 mmHg en el brazo derecho en posición supina y una frecuencia de pulso de 110/min, que era de bajo volumen y todos los pulsos periféricos eran palpables. Presentaba taquipnea con una frecuencia respiratoria de 28/min y palidez. Tenía un edema de pedal B/L, que era de tipo lento con presión venosa yugular elevada (JVP). No se observó ictericia, cianosis, clubbing ni linfadenopatía. Mientras se medía la presión arterial, el paciente empezó a tener espasmos en la muñeca, lo que nos dio una pista para examinar más a fondo y revelar un signo de Chvostek positivo. El signo de Trousseau también fue positivo a los 10 segundos.\n\nEl examen del sistema cardiovascular reveló un latido apical localizado en el sexto espacio intercostal izquierdo, a 1 cm fuera de la línea medioclavicular, de carácter hiperdinámico. Se escucharon S1 y S2 con normalidad en todas las áreas.\n\nEl examen del sistema respiratorio reveló una reducción de la entrada de aire en las bases pulmonares bilaterales con crepitación fina al final de la inspiración bilateral. El examen del sistema nervioso abdominal y central no reveló nada de interés.\n\n\nInvestigaciones\n\nEn el momento del ingreso, el ECG mostró bloqueo completo de rama izquierda (B-R) con un intervalo QT prolongado. La hemoglobina era de 58 g/l (133-162) con un cuadro dimórfico. El volumen corpuscular medio era de 110 fL (80,0-100,0 fL), la hemoglobina corpuscular media era de 34 pg/mL (27,0-32,0 pg/mL), la concentración media de hemoglobina corpuscular era de 36,2 g/dL (32,0-35,0 g/dL). Otros análisis revelaron niveles séricos de vitamina B12 de 135 pg/mL (211-911 pg/mL). El nivel sérico de ácido fólico era de 5,40 ng/mL (>5,38 ng/mL). El nitrógeno ureico en sangre era de 53 mg/dL (10-50) con creatinina de 0,8 mg/dL (0,7-1,3). Los resultados de las pruebas de función hepática (LFT) estaban dentro de los límites normales. El perfil de calcio mostró 4,3 mg/dL de S.calcium (8,5-10,5), fosfato 7,1 mg/dL (2,5-4,5), 3,06 g/dL de S.albumin (3,5-5,5). En vista de la hipocalcemia e hiperfosfatemia, se realizó un estudio del nivel de hormona paratiroidea intacta, que resultó ser <0,23 ng/mL (14-72). El S.magnesium era de 2,0 mg/dL (1,7-2,2). El análisis de gases en sangre arterial (ABG) fue sugestivo de una acidosis metabólica leve. El perfil tiroideo y los niveles de IgAtTG estaban dentro de los límites normales. Los niveles de ferritina y ceruloplasmina séricos estaban dentro de los límites normales. El ultrasonido abdominal y torácico mostró derrame pleural bilateral en posición supina. La vena cava inferior (IVC) y las venas hepáticas eran prominentes. El reposo dentro de los límites normales. La radiografía de tórax mostró un aplanamiento de los ángulos costofrénicos bilaterales que sugería derrame pleural bilateral. La ecocardiografía reveló un ventrículo izquierdo dilatado (LV) con una fracción de eyección del ventrículo izquierdo del 15 %, que sugería DCMP con disfunción severa del LV. Se realizó un arteriograma coronario basal que fue normal. La TC sin contraste de la cabeza mostró calcificación simétrica bilateral (B/L) en el hemisferio cerebeloso B/L, ganglios basales B/L y calcificación cortical/subcortical en la región B/L fronto-parieto-occipital. El reposo dentro de los límites normales.\n\n\nTratamiento\n\nPara el CHF, se inició al paciente con dobutamina intravenosa a una dosis de 6 µg/kg y furosemida intravenosa 20 mg BD para la descongestión. Sin embargo, el paciente no mostró una mejora significativa con el tratamiento anterior. En vista de la hipocalcemia con hiperfosfatemia y bajos niveles de hormona paratiroidea, se consideró un diagnóstico de cardiomiopatía hipocalcemica con hipoparatiroidismo y se inició al paciente con inyección de gluconato de calcio 1 g (90 mg de calcio elemental) administrado por vía intravenosa seguido de infusión de gluconato de calcio en 500 ml de dextrosa al 5% a una velocidad de 37,5 mg/hora de calcio elemental. El paciente mostró una mejora significativa después de iniciar el gluconato de calcio. El paciente fue dado de alta en condiciones estables con comprimidos de calcio por vía oral 3 g/día junto con calcitriol 0,5 µg/día. También se inició con benzotiazida con triamtereno (25/50 mg) OD, ramipril 5 mg una vez al día y carvedilol 3,125 mg dos veces al día. Para la anemia megaloblástica, se administraron inyecciones de cianocobalamina según el protocolo.\n\n\nResultado y seguimiento\n\nAl cabo de tres meses, el paciente había mejorado notablemente.\n\nLas investigaciones mostraron S.calcium 7.7, S.phosphate 6.0 y albúmina 3.6. La hemoglobina fue de 10.1 g/dL. El eco mostró una mejora en la función del LV con una fracción de eyección del 25%. Se planificó una biopsia endomiocardial, pero el paciente se negó, por lo que no pudo realizarse.\n\nMH - Gluconato de calcio/administración y dosificación/uso terapéutico\nMH - Cardiomiopatía, Dilatada/*complicaciones/diagnóstico\nMH - Ecocardiografía/métodos\nMH - Insuficiencia cardiaca/terapia farmacológica/*etiología/fisiopatología\nMH - Humanos\nMH - Hipocalcemia/*complicaciones/diagnóstico/terapia farmacológica/fisiopatología\nMH - Hipoparatiroidismo/*complicaciones/terapia farmacológica\nMH - Hombre\nMH - Edad Media\nMH - Volumen de carrera\nMH - Resultado del tratamiento\nMH - Disfunción ventricular izquierda/diagnóstico por imágenes\n",
+        "gold_summary": "Presentamos el caso de un hombre asiático de 55 años que había tenido un caso conocido de miocardiopatía dilatada durante 6 meses, que se presentó con las principales quejas de falta de aire al hacer ejercicio y disminución de la producción de orina. En el examen físico general, se observaron características que sugerían una ICC. El signo de Chvostek y Trousseau fue positivo. El paciente tenía antecedentes de cirugía de cataratas en ambos ojos 15 años atrás. Otras investigaciones revelaron una hipocalcemia. La ecografía mostró una grave hipocinesia global del ventrículo izquierdo con una fracción de eyección del ventrículo izquierdo del 15%. Esta ICC fue refractaria al tratamiento convencional, aunque, con la suplementación de calcio, el paciente mejoró sintomáticamente. En el seguimiento después de 3 meses, se observó una mejora en los parámetros ecocardiográficos con una fracción de eyección que mejoró al 25%.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre de 55 años tenía problemas para respirar y orinar. Tenía una enfermedad del corazón llamada miocardiopatía dilatada. También tenía poco calcio en la sangre, lo que causaba otros signos en su cuerpo. El tratamiento con calcio ayudó mucho y su corazón mejoró después de tres meses. Ahora está mejor y sigue tomando su medicina.",
+            "B2": "Un hombre de 55 años con miocardiopatía dilatada, una enfermedad del músculo del corazón, tuvo dificultad para respirar al hacer ejercicio. También notó que orinaba menos de lo normal. En la revisión médica, se encontraron signos de insuficiencia cardíaca y síntomas de hipocalcemia, que es bajo calcio en la sangre. Los análisis mostraron niveles bajos de calcio y de hormona paratiroidea, indicando hipoparatiroidismo, una enfermedad que afecta el calcio. La ecocardiografía mostró que el ventrículo izquierdo del corazón funcionaba muy mal, con una fracción de eyección del 15%. El paciente no mejoró con el tratamiento común, pero al recibir calcio por vía intravenosa, su estado mejoró mucho. Después de tres meses, la función cardíaca subió al 25%, mostrando una recuperación parcial gracias al calcio y vitamina D.",
+            "B3": "Un hombre asiático de 55 años con miocardiopatía dilatada conocida presentó disnea de esfuerzo y oliguria, lo que motivó su consulta médica. En el examen físico se evidenciaron signos de insuficiencia cardíaca congestiva y manifestaciones neuromusculares positivas, como los signos de Chvostek y Trousseau, indicativos de hipocalcemia. Las pruebas de laboratorio mostraron hipocalcemia y niveles bajos de hormona paratiroidea, sugiriendo un cuadro de hipoparatiroidismo, mientras que la ecocardiografía reveló una fracción de eyección ventricular izquierda severamente reducida, del 15%. A pesar del tratamiento estándar para insuficiencia cardíaca, el paciente no presentó mejoría clínica hasta que se inició la administración intravenosa de gluconato de calcio, lo que produjo una recuperación significativa. Tres meses después, la función cardíaca mejoró con un aumento de la fracción de eyección al 25%, y los niveles de calcio se normalizaron parcialmente. Este caso resalta la importancia de identificar causas metabólicas reversibles, como el hipoparatiroidismo, en pacientes con miocardiopatía dilatada y síntomas refractarios, dado que el manejo adecuado puede modificar favorablemente el pronóstico."
+        }
+    },
+    {
+        "article": "Una mujer de 54 años de edad, libanesa, en hemodiálisis (HD) de mantenimiento tres veces por semana para glomeruloesclerosis segmentaria focal (GSF) fue admitida en el departamento de urgencias, luego de haber sido sometida a su HD programada la noche anterior, debido al inicio repentino de un dolor lumbar agudo en el lado izquierdo, náuseas y vómitos. El dolor había comenzado repentinamente cerca de 12 horas antes de su presentación y se agravó rápidamente. En una nota al margen, un hiperparatiroidismo secundario grave con calcificación cutánea vascular fue tratado con cinacalcet durante 3 años sin respuesta, lo que demandó una paratiroidectomía (hiperplasia de cuatro glándulas) 8 meses antes de su presentación actual. Cinco días antes de su presentación, fue admitida en el hospital debido a anemia grave y rectorragia. Su evaluación por ultrasonido renal mostró riñones bilaterales pequeños con parénquima delgado que contenía quistes de hasta 3 cm y calcificaciones vasculares sin hidronefrosis. Cuatro días antes de su presentación, la colonoscopia a través del íleo terminal reveló un pólipo de 7 mm en el colon descendente izquierdo, que fue removido por mucosectomía. La microscopía volvió como adenoma tubular sésil con displasia de bajo grado. La paciente negó fiebre o antecedentes de trauma. No hubo antecedentes previos de uso de antiplaquetarios. En la emergencia, su presión arterial y pulso fueron de 112/65 mmHg y 96 bpm, su temperatura fue de 36.8°C y presentaba abdomen levemente distendido, con dolor importante en el ángulo costovertebral izquierdo. Los hallazgos de laboratorio mostraron hemoglobina de 9.0 g/dL mientras que el hematocrito fue de 29.7%, recuento total de leucocitos 12.2 × 1000/microlitro, creatinina de 6.06 mg/dL, y nivel de proteína C reactiva de 6 mg/L. Además, el TP fue de 83% y el INR fue de 1.13. En el día de la presentación (es decir, 4 días después de la colonoscopia), se realizó una tomografía computarizada (TC) multifásica del tórax, abdomen y pelvis con y sin contraste intravenoso. El examen reveló un gran quiste y enormes hematomas intraparenquimatosos perirrenales izquierdos con una colección subcapsular de hasta 1,8 cm de espesor con colección hemática en todo el compartimiento renal que alcanzaba un diámetro de más de 9 × 4 cm, hidronefrosis izquierda y edema alrededor de la grasa en todo el flanco y calcificaciones en el hilo. Para la descompresión del sistema pélvico renal y drenaje, optamos por tratarla con inserción retrógrada de doble stent ureteral a la izquierda, que identificó un coágulo en la parte media del uréter izquierdo. Se realizaron cultivo de orina y citología y los resultados fueron negativos. Una simple radiografía del abdomen mostró el doble J en su lugar. La paciente permaneció hemodinámicamente estable, pero presentó una nueva caída en la hemoglobina (6.1 g/dL) la misma noche, lo que exigió una transfusión de una unidad de concentrado de eritrocitos leucodepleados para estabilización. Se tomó la decisión de explorar quirúrgicamente con diagnóstico presuntivo de hematoma perirrenal izquierdo subagudo y para excluir una malignidad subyacente. Se sometió a una sesión de HD sin heparina. En el tercer día, se sometió a una nefrectomía radical abierta a la izquierda con conservación de la glándula suprarrenal. Recibió 2 unidades más de concentrado de eritrocitos leucodepleados durante la intervención. El parénquima renal fue casi totalmente reemplazado por un hematoma que medía 9 × 9 × 7 cm y se extendía hasta la grasa perirrenal. Una pequeña masa papilar fue enviada por separado para análisis. La evaluación histopatológica detallada reveló un parénquima renal con lesiones de nefritis crónica mutilada por grandes áreas hemorrágicas que se extendían hasta la grasa perirrenal. Además, había una proliferación neoplásica de 2 mm, con arquitectura papilar cubierta por pequeñas células cúbicas atípicas y macrófagos espumosos en el eje, compatibles con adenoma papilar. Al día siguiente de la operación, la paciente fue sometida a HD y recibió un paquete de eritrocitos leucodepleados. El período postoperatorio fue sin intercorrerencias. El nivel de hemoglobina se mantuvo alrededor de 10 g/dL. La paciente se recuperó sin signos o síntomas de sangrado. La paciente permanece bien y asintomática y actualmente se encuentra en HD de mantenimiento regular.\n",
+        "gold_summary": "A continuación, se describe un caso inusual de una paciente con HD de 54 años de edad que presentó HPE pocos días después de una colonoscopia. La causa de la HPE fue la ruptura de un quiste de DRCA. Consideramos que la colonoscopia fue un factor desencadenante y planteamos hipótesis sobre su etiopatogenia. La paciente se sometió a una nefrectomía izquierda exitosa.\n",
+        "synthetic_summary": {
+            "B1": "Una mujer de 54 años que recibe diálisis tuvo un dolor fuerte en el lado izquierdo de la espalda y vómitos. Esto pasó pocos días después de un examen del colon. Los médicos encontraron un gran sangrado en su riñón izquierdo por un quiste roto. Ella fue operada para quitar ese riñón y se recuperó bien. Ahora sigue con su diálisis sin problemas.",
+            "B2": "Una mujer de 54 años que recibe hemodiálisis tuvo dolor fuerte en la espalda y vómitos. Esto ocurrió 12 horas después de su sesión habitual de diálisis, que limpia su sangre. Ella tenía una enfermedad grave en los riñones y una cirugía reciente por un problema hormonal. Cinco días antes, le quitaron un pólipo, que es un pequeño bulto, en el colon. En el hospital, tenía anemia y dolor en el lado izquierdo del cuerpo. La tomografía mostró un hematoma, que es sangre acumulada, alrededor del riñón izquierdo y un quiste roto. Le pusieron un stent, un tubo para aliviar la presión, pero luego fue necesaria una cirugía para quitar el riñón. El estudio del riñón mostró un tumor pequeño y benigno, que no es canceroso. La paciente se recuperó bien y sigue con su diálisis sin problemas.",
+            "B3": "Una mujer de 54 años en hemodiálisis por glomeruloesclerosis segmentaria focal presentó un dolor lumbar agudo izquierdo, náuseas y vómitos poco después de una colonoscopia. Su historial incluía hiperparatiroidismo secundario tratado quirúrgicamente y enfermedad renal crónica con quistes renales. La tomografía mostró un gran hematoma perirrenal izquierdo y un quiste roto, lo que causó compresión y sangrado. Se colocó un stent ureteral para aliviar la obstrucción, pero la paciente requirió transfusiones por caída de hemoglobina. Debido a la sospecha de malignidad y el hematoma, se realizó una nefrectomía radical izquierda. El estudio histológico reveló un adenoma papilar pequeño y extensa hemorragia renal. Tras la cirugía, la paciente se recuperó sin complicaciones y continúa en hemodiálisis. Este caso sugiere que la colonoscopia pudo haber desencadenado la ruptura del quiste renal, causando el hematoma perirrenal, un evento poco común en pacientes con enfermedad renal crónica avanzada. Por lo tanto, se destaca la importancia de evaluar riesgos en procedimientos invasivos en este grupo."
+        }
+    },
+    {
+        "article": "Se evaluó a una mujer de 30 años de edad con antecedentes de dos meses de dolor progresivo y disminución de la visión OD. Dos semanas antes del desarrollo de los síntomas oculares, la paciente comenzó a disminuir la prednisona como tratamiento para sus síntomas inflamatorios sistémicos. Los antecedentes médicos incluyen artritis inflamatoria, síntomas gastrointestinales que sugieren enfermedad intestinal inflamatoria y pérdida de peso de 20 libras antes de la presentación. Los detalles completos del caso de la paciente se informaron previamente y se resumen aquí junto con análisis adicionales de quimiocina y citoquina de fluido ocular.13\n\nEn el examen, las BCVAs fueron 20/40 OD y 20/20 OS, y las pupilas fueron 9 mm y akinéticas OD y 5 mm con una rápida reactividad a la luz OS. Las presiones intraoculares fueron 65 mmHg OD y 21 mmHg OS. El examen con lámpara de hendidura mostró precipitados queráticos granulomatosos pigmentados (KP) dentro de la córnea inferior, 3+ células de la cámara anterior, atrofia difusa del iris con pigmento en las zónulas, y ectropion uvea OD, y OS fue normal. La gonioscopia mostró 3+ células pigmentadas dentro del ángulo inferior OD. El examen del fondo fue normal en ambos ojos. Una paracentesis anterior diagnóstica fue positiva para ADN de VZV mediante pruebas de PCR, y las pruebas serológicas fueron positivas para anticuerpos IgG de VZV. Posteriormente, se le diagnosticó uveítis anterior hipertensiva asociada a VZV, lo que provocó el inicio de acetazolamida oral y timolol oftálmico, dorzolamida, y brimonidina para la hipertensión ocular, así como valaciclovir 1 g TID y acetato de prednisolona 1% cada 2 horas. El curso de la enfermedad de la paciente y otros detalles de su tratamiento se describieron previamente.13\n\nLa paciente fue diagnosticada con un accidente cerebrovascular (ACV), que se cree que se debe a una vasculopatía del SNC asociada al VVZ, y fue hospitalizada durante 2 semanas, durante las cuales sus síntomas oculares mejoraron gradualmente. Sin embargo, dos meses después de su ACV, desarrolló un empeoramiento del dolor y la visión en el ojo derecho, y su BCVA disminuyó a 20/100 con una PIO elevada de 39 mmHg OD. El examen reveló una inyección ciliar 1+ y 3+ células de la cámara anterior, y se cambió de prednisolona a difluprednato con una mejora mínima. Posteriormente, se sometió a un procedimiento de filtración de glaucoma con una derivación de Ahmed debido a su PIO elevada persistente a pesar de la máxima tolerancia de la terapia ocular hipertensiva. Se obtuvo una muestra de humor acuoso del ojo derecho durante la cirugía de filtración para un análisis de perfil de quimiocina/citoquina. Se estimaron los niveles de 22 citoquinas y quimioquinas, incluidos IFN-Y, IL-10, IL-12p70, IL-17A, IL-1B, IL-2, IL-5, IL-6, IL-8, TNF-a, IL-18, IL-1RA, IL-1a, IL-1a, IP-10, MCP-1, MIP-1a, MIP-1B, SDF-1a, IL-21, IL-22, IL-23 e IL-27, utilizando la técnica de inmunoensayo de perlas múltiplex. Se detectaron niveles de concentración de 7 citoquinas/quimioquinas, incluidos IL-6, IL-8, IL-18, MIP-1b, IP-10, MCP-1, e IL-1RA. La IL-1RA fue la citoquina más abundante (1000 pg/mL), mientras que IP-10 y MCP-1 fueron las segundas citoquinas más abundantes (150–200 pg/mL). Se detectaron niveles de 10–20 pg/mL de IL-18 y MCP-1b, pero a niveles mínimos en esta muestra de AqH. Se detectaron niveles de IL-6 e IL-8, pero se encontró que eran las citoquinas menos abundantes, cada una con niveles de <10 pg/mL.\n\n",
+        "gold_summary": "El caso 2 fue el de una mujer de 30 años con antecedentes de dos meses de dolor progresivo y disminución de la visión en el ojo derecho. Se le diagnosticó uveítis anterior hipertensiva tras una paracentesis diagnóstica de la cámara anterior. A pesar de la terapia exitosa para la uveítis anterior, su presión intraocular se mantuvo elevada y requirió un procedimiento de filtración de glaucoma. Se recolectó una muestra de fluido ocular en el momento de la cirugía para el análisis de perfiles de citoquinas/quimioquinas, y se detectaron niveles de 7 citoquinas/quimioquinas, entre ellas, IL-6, IL-8, IL-18, MIP-1B, IP-10, MCP-1 e IL-1RA, siendo IL-1RA la citoquina más abundante.\n",
+        "synthetic_summary": {
+            "B1": "Una mujer de 30 años tuvo dolor y visión baja en un ojo. Le encontraron inflamación y presión alta en ese ojo. Usó medicinas, pero la presión no bajó y tuvo que operarse. Durante la operación, se tomó un líquido del ojo para estudiar unas sustancias llamadas citoquinas. Encontraron varias citoquinas, siendo una llamada IL-1RA la que más había.",
+            "B2": "Una mujer de 30 años tuvo dolor y pérdida de visión en su ojo derecho durante dos meses. Le diagnosticaron uveítis anterior hipertensiva, que es inflamación del ojo con presión alta dentro de él. Aunque recibió tratamiento para la inflamación, la presión ocular siguió alta y necesitó cirugía para controlarla. Durante la operación, tomaron una muestra del líquido del ojo para analizar proteínas llamadas citoquinas y quimioquinas, que indican inflamación. Encontraron siete tipos de estas proteínas, siendo la IL-1RA la más abundante. Este análisis puede ayudar a entender mejor la enfermedad y mejorar el tratamiento en el futuro.",
+            "B3": "Una mujer de 30 años presentó dolor progresivo y pérdida de visión en el ojo derecho durante dos meses, tras reducir la prednisona usada para tratar síntomas inflamatorios sistémicos. Se le diagnosticó uveítis anterior hipertensiva asociada al virus varicela zóster (VZV), confirmada por PCR en fluido ocular. A pesar del tratamiento con medicamentos para reducir la presión intraocular y antivirales, su presión ocular permaneció elevada, requiriendo una cirugía de filtración de glaucoma. Durante esta intervención, se analizó el fluido ocular para identificar citoquinas y quimioquinas, sustancias que regulan la inflamación. Se detectaron siete de estas moléculas, destacando la IL-1RA como la más abundante, seguida por IP-10 y MCP-1. Estos hallazgos sugieren una respuesta inflamatoria compleja en el ojo afectado. Además, la paciente sufrió un accidente cerebrovascular probablemente relacionado con la vasculopatía causada por el VZV, complicando su cuadro clínico. En consecuencia, este caso resalta la importancia de monitorear la inflamación y la presión ocular en pacientes con uveítis por VZV, y la necesidad de intervenciones quirúrgicas cuando el tratamiento médico no es suficiente para controlar la presión intraocular."
+        }
+    },
+    {
+        "article": "Un varón negro de 2021 g de peso nació a las 35 semanas y tres días de edad gestacional estimada por repetición de cesárea debido a la preocupación por la disminución del movimiento fetal en el contexto de una puntuación de perfil biofísico baja (basada en el tono muscular, la frecuencia cardíaca, el movimiento, la respiración y el volumen de líquido amniótico). La historia materna fue notable por el rasgo de células falciformes, la edad materna avanzada y la obesidad. La historia del embarazo fue notable por oligohidramnios observados por ultrasonografía a las 31 semanas. La ecografía fetal también mostró distensión de la vejiga, hidroceles bilaterales, dilatación de la uretra y ascitis abdominal preocupantes por la obstrucción del tracto urinario inferior y la posible ruptura de la vejiga. La ruptura de membranas ocurrió al momento del parto.\n\nAl nacer, el bebé experimentó dificultad respiratoria y fue tratado con ventilación con presión positiva, oxígeno suplementario e intubación. Las puntuaciones de Apgar fueron de dos y siete a un minuto y cinco minutos de vida, respectivamente. El examen mostró hematomas sustanciales y oscurecimiento de la extremidad superior izquierda. El bebé fue trasladado a la unidad de cuidados intensivos neonatales para el tratamiento de la dificultad respiratoria y sospecha de obstrucción del tracto urinario inferior. En la evaluación realizada dentro de la hora posterior al nacimiento por especialistas en ortopedia y cirugía plástica, el tercio distal del antebrazo y la mano estaban cianóticos, y una gran ampolla y área circundante de descamación eran evidentes en el dorso de la mano. No se observó movimiento espontáneo de la extremidad superior izquierda, y no se provocó la retirada o respuesta a los estímulos. La ecografía Doppler mostró flujo arterial al nivel de la fosa antecubital, pero no se detectaron pulsos radiales o cubitales. Los hallazgos del examen físico fueron consistentes con NCS, probablemente debido a la compresión de la pared uterina debido a oligohidramnios durante el embarazo.\n\nDespués de aproximadamente 5 horas de exámenes en serie, así como una amplia discusión con los equipos de ortopedia, cirugía plástica, neonatología y anestesia pediátrica, así como con los padres del bebé, se tomó la decisión de realizar una fasciotomía descompresiva del antebrazo, la mano y el túnel carpiano para permitir el rescate de la extremidad. La fasciotomía se realizó aproximadamente 6 horas después del nacimiento. El bebé fue monitoreado de cerca durante los siguientes días. La apariencia de la extremidad superior izquierda mejoró gradualmente. Al tercer día de vida, el antebrazo y la mano habían mejorado notablemente en color y parecían bien vascularizados. Las señales Doppler estaban presentes en todo momento, desde la arteria braquial hasta cada dedo. Se permitió que las heridas de la fasciotomía se curaran por intención secundaria, y se aplicó una férula personalizada con la muñeca en posición neutra y los dedos extendidos. No hubo signos de infección o isquemia en curso. Las heridas se curaron bien a las seis semanas de edad. En la visita de seguimiento a los cuatro meses de edad, las heridas se curaron por completo. El paciente tenía un rango de movimiento pasivo completo de la muñeca y los dedos. Se observó que tenía una ligera flexión y extensión del dedo anular y meñique, pero por lo demás, un movimiento activo mínimo de la muñeca o la mano en este momento. Tenía un movimiento activo del hombro y el codo. El paciente continuará recibiendo terapia ocupacional, así como férulas y masaje de cicatrices para prevenir/minimizar las contracturas. Los equipos multidisciplinarios continuarán siguiendo su progreso y recuperación de cerca.\n",
+        "gold_summary": "Presentamos un caso de NCS diagnosticado y tratado en base a los hallazgos del examen físico. La ecografía fetal mostró distensión de la vejiga, hidroceles bilaterales, dilatación de la uretra y ascitis abdominal que preocupaban por la obstrucción del tracto urinario inferior y posible ruptura de la vejiga. Una hora después del nacimiento, el examen de la extremidad superior izquierda del lactante no mostró movimiento espontáneo, la mano y el antebrazo parecían oscuros y la mano tenía una gran ampolla con descamación. No se detectó pulso distal a la fosa antecubital mediante ecografía Doppler. Se diagnosticó al lactante con NCS y se le practicó una fasciotomía urgente. La apariencia clínica y la perfusión de la extremidad superior izquierda mejoraron gradualmente. A los cuatro meses de edad, las heridas se habían curado y el paciente tenía un rango de movimiento pasivo completo de la extremidad superior izquierda. La recuperación del movimiento activo está en curso.\n",
+        "synthetic_summary": {
+            "B1": "Un bebé nació un poco antes de tiempo y tuvo problemas para moverse en un brazo. Los doctores vieron que la mano estaba oscura y sin pulso, por eso hicieron una operación para ayudar. Poco a poco, el brazo mejoró y la sangre volvió a circular bien. A los cuatro meses, las heridas estaban curadas y el bebé podía mover un poco los dedos y el brazo. Los doctores seguirán ayudándolo con terapias para que mejore más.",
+            "B2": "Un bebé nació prematuro a las 35 semanas debido a problemas detectados en el embarazo, como poco líquido amniótico y signos de obstrucción en el tracto urinario. Al nacer, presentó dificultad para respirar y una mano y antebrazo izquierdos con color oscuro, sin movimiento ni pulso en la parte distal. Los médicos diagnosticaron un síndrome de compresión neonatal (NCS), causado probablemente por la presión en el útero. Se realizó una cirugía llamada fasciotomía para aliviar la presión en la extremidad. Después de varios días, la mano y el antebrazo mejoraron en color y circulación. A los cuatro meses, las heridas estaban sanadas y el bebé tenía buen movimiento pasivo, aunque el movimiento activo seguía en recuperación. Continuará con terapia para mejorar su función.",
+            "B3": "Un recién nacido prematuro de 35 semanas presentó signos prenatales de obstrucción urinaria y posible ruptura vesical, evidenciados por ecografía fetal que mostró distensión vesical, hidroceles y ascitis. Al nacer, el bebé presentó dificultad respiratoria y una extremidad superior izquierda con coloración oscura, ampolla y ausencia de movimiento, además de pulsos distales no detectables mediante Doppler, lo que condujo al diagnóstico de síndrome compartimental neonatal (NCS), probablemente secundario a compresión uterina asociada a oligohidramnios. Se realizó una fasciotomía descompresiva seis horas después del parto para preservar la viabilidad de la extremidad afectada. Tras el procedimiento, la perfusión y la apariencia de la mano y el antebrazo mejoraron progresivamente, confirmándose la recuperación vascular mediante Doppler. A los cuatro meses, las heridas estaban completamente cicatrizadas y el paciente exhibía rango de movimiento pasivo completo, aunque con limitación en el movimiento activo de muñeca y dedos, excepto en hombro y codo. El seguimiento multidisciplinario y la terapia ocupacional continuarán para optimizar la función y prevenir complicaciones como contracturas. Este caso resalta la importancia del diagnóstico temprano y tratamiento quirúrgico oportuno para preservar la funcionalidad en el NCS neonatal."
+        }
+    },
+    {
+        "article": "Una mujer de 38 años de edad fue admitida en la sala de cirugía en noviembre de 2022 con la principal queja de una hinchazón abdominal progresiva que se asoció con un dolor abdominal leve y una saciedad precoz durante cinco meses. No tenía síntomas sistémicos como pérdida de peso, estreñimiento, diarrea, deseo de alimentos salados, fatigabilidad fácil o dolor de cabeza.\nEn el examen, parecía estar bien alimentada, pero presentaba una gran distensión abdominal, un leve palidez, afebril y con un tinte de ictericia en la esclerótica.\nLa palpación abdominal reveló una gran masa intraabdominal, no dolorosa, que ocupaba todo el abdomen inferior y se extendía hacia el superior, sin signos de irritación peritoneal u organomegalia.\nLos análisis de sangre mostraron un recuento de glóbulos blancos (5,7 × 109/l), hemoglobina (9,8 g/dl), bilirrubina (103 mg/dl) con recuentos normales de plaquetas (393 × 109/l). Las enzimas hepáticas, AST (24,0 U/l), ALT (21,0 U/l), albúmina 42,7 g/l. Creatinina sérica (53 μmol/l) y ESR (80 mm/h). Todos los demás análisis de sangre fueron normales. Una ecografía abdominal reveló un complejo quiste abdominal, ambos riñones eran de tamaño normal y con una ecografía normal, el hígado parecía normal. La TC abdominal y pélvica de contraste, vistas axiales y coronales, demostraron un gran quiste suprarrenal de paredes delgadas (flechas azules) que medía aproximadamente 23,5 cm (AP) x 20,3 cm (T) x 32,2 cm (CC) con un volumen de 8 l. El gran quiste desplaza el riñón derecho (flechas rojas) inferomedial a través de la línea media y ejerce presión sobre el hígado, la vesícula biliar, el páncreas y los intestinos delgados. Se extiende hasta la fosa ilíaca derecha. Como había un tinte de esclerosis ictérica, pero la masa era separada del hígado, el páncreas, los conductos biliares y el riñón derecho. Dado el tamaño del quiste y sus efectos compresivos, se planificó una intervención quirúrgica. Se eligió un enfoque quirúrgico abierto.\n\nSe le practicó una laparotomía al paciente. Se le hizo una incisión abdominal en la línea media, bajo anestesia general, y tras abrir las capas de la pared abdominal, se identificó un enorme quiste retroperitoneal que ocupaba toda la cavidad abdominal.\n\nSe abrió el quiste para acceder al fluido que se aspiraba, como se demostró en la cistectomía que se realizó con éxito. Se aspiraron unos 8 l de fluido de color marrón de la masa. Se enviaron muestras de la pared quística y del fluido para su análisis histológico.\n\nLa paciente se recuperó sin incidentes y fue dada de alta el día 7 después de la operación. El seguimiento a los 6 y 12 meses no mostró recurrencia ni complicaciones. El examen citológico de la muestra informó la presencia de material amorfo, no hubo evidencia de malignidad. Los resultados histológicos indicaron que la pared quística contenía tejido suprarrenal sin atipia, había infiltración de la pared quística por células inflamatorias mononucleares. La superficie interna de la pared no estaba revestida por células específicas reconocibles. En cuanto a los hallazgos clínicos intraoperativos, donde el origen del quiste era incierto, los hallazgos fueron más sugerentes de un quiste gigante idiopático retroperitoneal.\n\n",
+        "gold_summary": "Una mujer de 38 años se presentó con distensión abdominal progresiva. Las imágenes revelaron un quiste retroperitoneal gigante. Debido a los recursos limitados, se realizó una laparotomía abierta y se extirpó completamente un quiste de 33 cm que contenía 8 l de líquido transparente. La histopatología confirmó un quiste retroperitoneal idiopático gigante.\n",
+        "synthetic_summary": {
+            "B1": "Una mujer de 38 años tenía la barriga muy hinchada y un poco de dolor. Los médicos encontraron un quiste muy grande dentro de su abdomen, que es una bolsa llena de líquido. Le hicieron una operación para sacar el quiste, que tenía 8 litros de líquido. Después, la mujer se recuperó bien y no volvió a tener problemas. El quiste no era peligroso ni un tumor.",
+            "B2": "Una mujer de 38 años tuvo hinchazón abdominal que aumentó durante cinco meses. También sentía dolor leve y llenura rápida al comer. En el examen, se encontró una masa grande en el abdomen y un poco de ictericia, que es color amarillo en los ojos. Las pruebas mostraron anemia leve y un quiste muy grande cerca de la glándula suprarrenal, que mide más de 30 cm. Este quiste presionaba otros órganos, por eso se decidió operar con cirugía abierta para quitarlo. Se sacaron 8 litros de líquido marrón del quiste y el análisis confirmó que no había cáncer. La paciente se recuperó bien y no tuvo problemas después de un año. El quiste fue considerado gigante y sin causa clara.",
+            "B3": "Una mujer de 38 años acudió por una hinchazón abdominal progresiva durante cinco meses, acompañada de dolor leve y sensación de llenura rápida. En la exploración se detectó una gran masa abdominal y un ligero tinte de ictericia, sin otros síntomas sistémicos. Los estudios de imagen mostraron un quiste retroperitoneal gigante de aproximadamente 33 cm, que desplazaba órganos vecinos sin afectarlos directamente. Debido al tamaño y la compresión que causaba, se decidió realizar una cirugía abierta para extirpar el quiste. Durante la operación, se aspiraron 8 litros de líquido marrón y se removió la masa sin complicaciones. El análisis histológico reveló tejido suprarrenal inflamado, sin signos de malignidad, y un origen idiopático del quiste. La paciente evolucionó favorablemente y no presentó recurrencias ni complicaciones en el seguimiento a un año. Este caso destaca la importancia de la intervención quirúrgica en quistes retroperitoneales grandes que causan síntomas por compresión, así como la necesidad de un diagnóstico histológico para descartar malignidad."
+        }
+    },
+    {
+        "article": "Un hombre de 71 años con diabetes y enfermedad de Chagas había perdido recientemente mucho peso (60 kg). La investigación clínica dio lugar a un diagnóstico de megaesófago asociado a una obstrucción significativa a nivel del cardias. Se realizó una dilatación esofágica con balón, recuperando con éxito el tránsito digestivo. Mientras tanto, durante la evaluación del riesgo quirúrgico, el paciente también presentó dolor torácico con el mínimo esfuerzo. La angiografía por tomografía computarizada coronaria realizada tres años antes mostró una enfermedad multivascular muy calcificada que afectaba a la arteria coronaria izquierda; en ese momento no se había realizado ninguna otra investigación. Esta vez, se lo derivó a nosotros para un cateterismo cardíaco.\nEl examen realizado el 16 de febrero de 2016 mostró: arteria coronaria derecha (RCA) con importante calcificación y una lesión del 50% en el tercio medio; arteria descendente posterior (PDA) y arteria posterolateral derecha (RPLA), con severa calcificación y lesiones del 80% y 70%, respectivamente; LM con 80% de lesiones calcificadas en el tercio distal; arteria descendente anterior izquierda (LAD) con significativa calcificación y 90% de lesión en el tercio medio; ramas diagonales (DG1 y DG2) con lesiones calcificadas del 70% y 80%, en el origen y en el tercio proximal, respectivamente; y arteria circunfleja izquierda (LCx) ocluida y calcificada, recibiendo colaterales grado II de múltiples orígenes. El volumen ventricular izquierdo y la contractilidad se conservaron.\n\nCon esta imagen angiográfica, una puntuación de riesgo de la Society of Thoracic Surgeons del 15,8 % para morbilidad o mortalidad, una puntuación EuroSCORE II del 4,67 %, y una debilidad significativa debido a una pérdida de peso importante y reciente, el equipo cardiaco decidió realizar una intervención coronaria percutánea (ICP) de la LM, LAD, DG1 y DG2 inicialmente y, en un segundo procedimiento después de 30 días, una ICP de las ramas de la RCA. En ambos procedimientos, también se indicó una RA debido a una calcificación significativa. No se abordaría la LCx, ya que angiográficamente el vaso no estaba tan gravemente afectado y también considerando la dificultad técnica de la recanalización, debido a la longitud del CTO y también a las paredes muy calcificadas (puntuación J-CTO 4). La LCx ya estaba recibiendo una circulación collateral de grado II.\nEl 19 de febrero de 2016, tras comenzar una terapia antiplaquetaria dual con aspirina y clopidogrel, el paciente se sometió a una angioplastia de la arteria descendente anterior, la arteria circunfleja y la arteria descendente derecha con una fresa de 1,5 mm, seguida de una predilatación con un balón de 3,0 mm x 20 mm a 14 atm y la implantación de stents liberadores de fármacos en la arteria descendente derecha y la arteria circunfleja, utilizando una técnica de mini-aplastamiento y un balón de contacto al final. Se realizó un balón de contacto en la bifurcación de la arteria descendente derecha/arteria circunfleja y, finalmente, se implantó el tercer stent liberador de fármacos desde el origen de la arteria descendente derecha para superponerse con el stent de la arteria descendente derecha. Se logró un éxito procedimental con un flujo TIMI de 3 y sin complicaciones clínicas o angiográficas.\nEl 22 de marzo de 2016, el paciente volvió para una PCI con un RotaWire PCI en el PDA y RPLA con una fresa de 1,5 mm, seguido por la implantación de dos DES de 2,75 mm x 20 mm y 2,75 mm x 16 mm a 12 atm en el PDA y RPLA, respectivamente, sin ninguna predilatación adicional. También observamos la presencia de una disección larga y severa en el tercio medio del RCA, sin duda causada por un manejo excesivo e intentos de remover la fresa, lo que causó una penetración profunda por el catéter guía 7F. Esta disección se corrigió rápidamente con la implantación de un tercer DES de 4,0 mm x 32 mm, y se obtuvo un flujo TIMI 3 final sin complicaciones clínicas o electrocardiográficas. Los dos sitios de punción femoral se ocluyeron con dispositivos AngioSeal 8F y 6F, respectivamente. El paciente permaneció en la unidad de cuidados intensivos durante 48 horas, la única anormalidad fue la elevación de CK-MB (el doble del valor de referencia). Fue dado de alta el día 3 en excelentes condiciones generales. El ecocardiograma de control mostró una contractilidad ventricular izquierda normal.\n",
+        "gold_summary": "Un hombre de 71 años con enfermedad de Chagas y angina estable en esfuerzo mínimo se sometió a una angiografía por tomografía computarizada y cineangiografía que reveló una enfermedad multivascular muy calcificada que afectaba a la arteria descendente anterior izquierda (LM). Debido al grado de calcificación, se decidió realizar una rotablation. La primera etapa de la intervención coronaria percutánea (ICP) con rotablation se realizó en la arteria descendente anterior izquierda (LM), la arteria descendente anterior izquierda y la segunda rama diagonal sin complicaciones. Casi 30 días después, volvió para una ICP de la arteria coronaria derecha (RCA). La estrategia propuesta fue la aterectomía rotativa en la arteria descendente anterior posterior (PDA) y la arteria posterolateral derecha (RPLA) con una fresa de 1,5 mm, seguida por la implantación de dos stents liberadores de fármacos (DES). A través del acceso a la arteria femoral derecha, la lesión de la RPLA se extirpó con éxito. Como no había signos de disección y se mantuvo el flujo TIMI 3, se reposicionó el RotaWire de 0,009″ para cruzar la lesión de la PDA y se realizó la extirpación de la lesión. Después de dos intentos, logramos cruzar la lesión con la fresa de 1,5 mm, sin embargo, se produjo el atrapamiento de la misma. El sistema se retiró hasta que el catéter guía penetró profundamente en la RCA, y se hicieron intentos para liberar el Rotablator moviéndolo hacia adelante y hacia atrás, pero la fresa ni siquiera giró. La arteria femoral contralateral se perforó y se insertó un catéter guía 6F JR, con el fin de mover un alambre guía y un pequeño globo de angioplastia tangencialmente a la fresa, pero sin éxito. Finalmente, avanzamos el alambre guía utilizando la técnica de «nudillo», aprovechando la torsión de la porción distal del alambre guía PT2, realizando una disección subintimal y reentrada, y pudimos cruzar fácilmente el globo, inflarlo y liberar la fresa atrapada. A través del sistema 6F, se implantaron dos DES programados y uno de rescate con éxito en la PDA, RPLA y RCA, obteniendo un flujo TIMI 3 final sin complicaciones.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre de 71 años tenía el corazón muy duro y con calcio. Le hicieron dos tratamientos para limpiar sus arterias. Usaron una máquina para quitar el calcio y pusieron tubos pequeños llamados stents. En el segundo tratamiento, la máquina tuvo un problema. Pero lo arreglaron con cuidado y todo salió bien. Al final, el hombre estuvo bien y su corazón funcionó normal.",
+            "B2": "Un hombre de 71 años con enfermedad de Chagas y dolor en el pecho fue diagnosticado con una enfermedad grave en las arterias del corazón, con muchas calcificaciones. Para tratarlo, se realizó una intervención llamada angioplastia con rotablación, que usa una fresa para eliminar las calcificaciones antes de colocar stents, que son pequeños tubos para mantener las arterias abiertas. La primera intervención fue exitosa en las arterias principales. Un mes después, se hizo una segunda intervención en otras arterias, donde la fresa se quedó atrapada. El equipo usó una técnica especial para liberar la fresa y luego colocaron los stents con éxito. El paciente tuvo buena recuperación y el corazón funcionaba normalmente tras el tratamiento.",
+            "B3": "Un hombre de 71 años con enfermedad de Chagas y diabetes presentó una pérdida de peso significativa y fue diagnosticado con megaesófago y obstrucción en el cardias. Durante la evaluación para cirugía, mostró dolor torácico al mínimo esfuerzo, y estudios previos revelaron enfermedad coronaria multivascular severamente calcificada. Se decidió realizar una intervención coronaria percutánea (ICP) en dos etapas, utilizando rotablation para tratar las lesiones calcificadas en las arterias principales. La primera intervención en la arteria descendente anterior y ramas diagonales fue exitosa y sin complicaciones. Un mes después, se realizó la segunda ICP en las ramas de la arteria coronaria derecha, donde se implantaron stents liberadores de fármacos tras la rotablation. Durante este procedimiento, se presentó una disección arterial que fue rápidamente corregida con un stent adicional. El paciente evolucionó favorablemente, sin complicaciones clínicas ni electrocardiográficas, y fue dado de alta en buen estado. El ecocardiograma de control mostró función ventricular izquierda normal. Este caso destaca la complejidad del manejo de enfermedad coronaria severa en pacientes con comorbilidades y la utilidad de técnicas avanzadas como la rotablation para mejorar el flujo coronario y la calidad de vida."
+        }
+    },
+    {
+        "article": "Una paciente de 29 años se presentó al departamento de urología con dolor intermittent en el flanco derecho durante un año y sensación de ardor urinaria ocasional sin hematuria; su estado general era estable. La paciente no mostró signos de tos, fatiga, pérdida de peso, no había tenido cirugías previas, pero había estado expuesta frecuentemente a ovejas. A pesar de los exámenes de laboratorio normales, el examen de anticuerpos de equinococos arrojó un resultado positivo. El ultrasonido abdominal posterior reveló una lesión quística grande en el riñón derecho, que medía aproximadamente 63 mm con paredes gruesas y sin flujo de doppler significativo. La tomografía computarizada con contraste, tanto en vista transversal como coronal, reveló una masa quística con septos en el lado lateral del riñón derecho, que presentaba una pared gruesa y regular que se intensificaba con el contraste. Esta lesión se clasificó como categoría 4 de Bosniak, con imágenes de tomografía computarizada en vista coronal que mostraban la participación del sistema colector y el contacto con el hígado. Se sospechó de HC en base a las evaluaciones clínicas y radiológicas. Los hallazgos de la radiografía de tórax no fueron significativos, sin evidencia de quistes pulmonares. Después de un régimen de tres meses de albendazol 400 mg administrado dos veces al día, la paciente se sometió a una intervención quirúrgica. Se realizó un procedimiento abierto a través de una incisión subcostal derecha de Kocher, lo que resultó en una nefrectomía derecha y una resección hepática parcial debido a las adherencias. El espécimen, que pesaba 372 g y medía 13 × 8 × 6 cm, mostró un gran quiste blanco con paredes delgadas que contenían una membrana desprendida, que afectaba los cálices renales y la pelvis. El diagnóstico final fue HC del riñón acompañado de pielonefritis crónica. Los exámenes de laboratorio posteriores al procedimiento mostraron resultados normales, con una producción urinaria estable y signos vitales. El catéter urinario se retiró después de 24 horas debido a una producción urinaria adecuada (2 L). El drenaje renal se retiró después de 3 días, con volúmenes de drenaje de 200 ml, 100 ml y ninguno en días consecutivos. La paciente volvió a sus actividades normales sin complicaciones.\n",
+        "gold_summary": "Se diagnosticó a una mujer de 29 años con dolor intermitente en el flanco derecho y ardor urinario un quiste hidatídico (HC) de categoría 4 de Bosniak, tras dar positivo en anticuerpos de equinococo. Las imágenes confirmaron el diagnóstico, lo que derivó en un tratamiento de tres meses con albendazol, seguido de una nefrectomía derecha y una resección hepática parcial. El análisis histopatológico confirmó un HC y una pielonefritis crónica. La paciente se recuperó sin incidentes y volvió a sus actividades normales.\n",
+        "synthetic_summary": {
+            "B1": "Una mujer de 29 años tuvo dolor en el lado derecho y ardor al orinar. Los médicos encontraron un quiste grande en su riñón, causado por un parásito llamado equinococo. Ella tomó medicina por tres meses y luego tuvo una operación para quitar el quiste y parte del hígado. Después, se recuperó bien y volvió a hacer su vida normal sin problemas.",
+            "B2": "Una mujer de 29 años tuvo dolor en el costado derecho y ardor al orinar durante un año. Sus análisis de sangre fueron normales, pero tenía anticuerpos contra equinococos, un parásito que causa quistes llamados hidatídicos. Las imágenes mostraron un quiste grande en su riñón derecho, clasificado como Bosniak 4, lo que indica riesgo. Después de tomar albendazol, un medicamento para el parásito, le hicieron una cirugía para quitar el riñón afectado y parte del hígado. El examen del quiste confirmó la infección y una inflamación crónica en el riñón. Tras la operación, la paciente se recuperó bien y pudo volver a su vida normal.",
+            "B3": "Una mujer de 29 años acudió al hospital por dolor intermitente en el costado derecho y ardor al orinar, sin sangre en la orina. Aunque sus análisis de laboratorio fueron normales, dio positivo en anticuerpos contra equinococos, parásitos que pueden causar quistes. Las imágenes por ultrasonido y tomografía mostraron un quiste grande en el riñón derecho, clasificado como categoría 4 de Bosniak, lo que indica un alto riesgo de malignidad o complicación. Tras un tratamiento con albendazol durante tres meses, se realizó una cirugía para extirpar el riñón afectado y parte del hígado debido a adherencias. El examen del tejido confirmó un quiste hidatídico, una infección parasitaria, junto con inflamación crónica del riñón. Después de la operación, la paciente tuvo una recuperación sin complicaciones, con función urinaria estable y retorno a sus actividades habituales. Este caso resalta la importancia de considerar infecciones parasitarias en pacientes con quistes renales y antecedentes de exposición a animales, así como la necesidad de un manejo combinado médico y quirúrgico para un tratamiento efectivo."
+        }
+    },
+    {
+        "article": "Una paciente de 46 años de edad fue admitida en nuestro hospital debido a opresión en el pecho y falta de aire que había durado más de un mes. Su historial médico incluía una tiroidectomía parcial, y no tenía antecedentes de tabaquismo o consumo de alcohol. Fue tratada con medicamentos regulares (comprimidos de liberación prolongada de succinato de metoprolol, comprimidos de sacubitril valsartán sodio, espironolactona, comprimidos de dapagliflozina) para la IC, pero la respuesta fue pobre. Durante el examen físico, la paciente estaba consciente y bien orientada. Su frecuencia cardíaca era de 68 latidos por minuto, la presión arterial era de 150/98 mm Hg, la frecuencia respiratoria era de 20 latidos por minuto. No había signos de sangrado o ictericia en la piel o membranas mucosas, y no se observó distensión de la vena yugular. La glándula tiroides no estaba agrandada. Los sonidos respiratorios eran gruesos en ambos pulmones, con roncus húmedos presentes en las bases pulmonares. La frecuencia cardíaca era de 68 lpm con un ritmo regular. El abdomen era suave, sin sensibilidad o sensibilidad de rebote, y el hígado y el bazo no eran palpables por debajo de la caja torácica. El signo de reflujo hepatoyugular fue negativo, pero había edema en ambas extremidades inferiores.\n\nLa paciente fue hospitalizada y se le realizaron los exámenes pertinentes. Los análisis bioquímicos mostraron una hormona estimulante de la tiroides (TSH) de 7,190 uIU/mL, triglicéridos de 0,81 mmol/L, colesterol de lipoproteínas de baja densidad (LDL-C) de 2,61 mmol/L, lipoproteína (a) de suero de 435 mg/L y NT-proBNP de 6245 pg/mL. Un examen de electrocardiograma (ECG) mostró bradicardia sinusal, anomalías de la onda T-U y duración del QRS de 90 ms. Un examen ecocardiográfico transtorácico posterior reveló un diámetro de la aurícula izquierda (LA) (anteroposterior) de 41 mm, un diámetro del ventrículo izquierdo (LVD) (anteroposterior) de 54 mm, un espesor del tabique interventricular en diástole (IVSD) de 9 mm, un espesor de la pared posterior del ventrículo izquierdo en la fase final de la diástole (LVPWd) de 9 mm, una fracción de eyección del ventrículo izquierdo (LVEF) del 28% (M-mode), una fracción de acortamiento (FS) del 13% y una presión de la arteria pulmonar de 29 mm Hg. No se observaron lesiones coronarias significativas en la angiografía coronaria computarizada (CCA). Se diagnosticó a la paciente con cardiomiopatía dilatada, insuficiencia cardiaca de clase III con LVEF reducida según la New York Heart Association (NYHA). En combinación con los parámetros, se puede observar que los volúmenes de la aurícula izquierda y el ventrículo izquierdo se reducen gradualmente, lo que indica que la función diastólica del ventrículo izquierdo está mejorando. El tratamiento con CCM revierte la remodelación miocárdica. Además, E/e′ refleja la presión de llenado ventricular izquierdo. El valor normal debe ser inferior a 8. Se puede observar que en este caso, E/e′ vuelve al valor normal tres meses después de la implantación de CCM. Estos dos puntos reflejan el papel de CCM en la mejora de la función diastólica miocárdica en el tratamiento de la insuficiencia cardiaca. En resumen, la paciente tenía las siguientes características: (1) LVEF mejoró pero se mantuvo tan bajo como el 30% después de la terapia óptima para la insuficiencia cardiaca; (2) opresión en el pecho y malestar con ligera actividad, grado de función cardiaca III; (3) ECG muestra QRS estrecho. Teniendo en cuenta el resultado positivo de la prueba preoperatoria de levosimendan, después de una discusión general y una comunicación completa con el paciente y su familia, se decidió realizar el tratamiento con CCM.\n\nEl procedimiento de implantación del CCM fue similar al de la implantación de un marcapasos tradicional. El paciente se colocó en posición supina, se desinfectó con una toalla y se perforó la vena subclavia izquierda dos veces bajo anestesia local, y se hizo la bolsa capsular después de insertar el alambre guía. Bajo la guía del alambre guía, se introdujeron dos vainas de desprendimiento, y se introdujeron dos cables de estimulación ventricular (Medtronic 3830-69) a través de la vaina, y se ajustó la posición de los cables a la superficie del tabique ventricular derecho con una distancia de 3 cm. Durante la operación, se probó el electrodo de campo cercano (RV), que mostró un umbral de estimulación de 0,5 V, una amplitud de la onda R detectada mayor de 10 mV, y una impedancia del cable de 1080 Ω; el electrodo de campo lejano (LS) mostró un umbral de estimulación de 0,5 V, una amplitud de la onda R detectada mayor de 15 mV, y una impedancia del cable de 900 Ω. Estas mediciones cumplieron los criterios para una implantación exitosa del electrodo. Ambos cables se anclaron de forma segura en el tabique ventricular derecho. Después de asegurarse de que no había estimulación diafragmática palpable con un pulso de estimulación de 10 V y una anchura de pulso de 0,4 ms, se conectaron los cables al generador de impulsos Optimizer Smart. Posteriormente, se ajustaron los impulsos de salida y se programaron y optimizaron los parámetros.\n\nLa monitorización del ECG postoperatorio inmediato indicó un suministro normal de impulsos CCM (Figura 1C). Observamos la respuesta de los pacientes al CCM al adherirnos a un protocolo de seguimiento estandarizado. Utilizando una amplia variedad de herramientas de evaluación, que incluían ultrasonografía Doppler cardiaca a color, análisis de sangre NT-ProBNP, pruebas de caminata de seis minutos (6MW) y el Cuestionario de Minnesota para Vivir con Insuficiencia Cardiaca (MLHFQ), evaluamos sistemáticamente el estado clínico de los pacientes. El paciente no experimentó opresión en el pecho ni falta de aire, y hubo una marcada mejora en la tolerancia al ejercicio y la calidad de vida.\n",
+        "gold_summary": "Presentamos a una paciente de 46 años que fue admitida en nuestro hospital debido a opresión torácica y falta de aire que duró más de un mes. La ecocardiografía reveló un diámetro del ventrículo izquierdo (anteroposterior) de 54 mm, el electrocardiograma mostró bradicardia sinusal y duración del QRS de 90 ms. La paciente no experimentó opresión torácica o falta de aire, y hubo una marcada mejora en la tolerancia al ejercicio y calidad de vida después de la implantación de la modulación de la contractilidad cardiaca.\n",
+        "synthetic_summary": {
+            "B1": "Una mujer de 46 años tenía dolor en el pecho y le costaba respirar por más de un mes. Su corazón no funcionaba bien y estaba cansada al hacer ejercicio. Le pusieron un aparato llamado CCM para ayudar a su corazón a latir mejor. Después del tratamiento, se sintió mucho mejor y pudo hacer más cosas sin dolor ni falta de aire.",
+            "B2": "Una mujer de 46 años llegó al hospital con opresión en el pecho y dificultad para respirar. Estos síntomas duraban más de un mes y afectaban su vida diaria. Tenía insuficiencia cardiaca, que significa que su corazón no bombeaba sangre bien. Su fracción de eyección, que mide la fuerza del corazón, era del 28%, un valor bajo. El electrocardiograma mostró un ritmo cardíaco lento, pero sin alteraciones graves en la señal eléctrica. A pesar del tratamiento con medicamentos, sus síntomas no mejoraron. Por eso, le implantaron un dispositivo llamado modulación de la contractilidad cardiaca (CCM), que ayuda a que el corazón funcione mejor. Después del procedimiento, la paciente dejó de sentir opresión y dificultad para respirar, y su calidad de vida mejoró mucho.",
+            "B3": "Una mujer de 46 años ingresó al hospital por opresión en el pecho y dificultad para respirar que persistieron más de un mes, a pesar del tratamiento para insuficiencia cardíaca. Su examen físico mostró signos de edema en las piernas y ruidos pulmonares anormales, mientras que pruebas complementarias indicaron una fracción de eyección del ventrículo izquierdo muy baja (28%) y niveles elevados de NT-proBNP, marcador de insuficiencia cardíaca. El electrocardiograma reveló bradicardia sinusal y un QRS estrecho, y la angiografía descartó enfermedad coronaria significativa. Se diagnosticó cardiomiopatía dilatada con insuficiencia cardíaca clase III. Debido a la respuesta insuficiente al tratamiento convencional, se decidió implantar un dispositivo de modulación de la contractilidad cardíaca (CCM), procedimiento similar a la colocación de un marcapasos, que mejoró la función diastólica y redujo la presión de llenado ventricular. Tras la implantación, la paciente mostró una notable mejoría clínica, con desaparición de la opresión torácica y la disnea, además de un aumento significativo en la tolerancia al ejercicio y calidad de vida. Este caso destaca el potencial de la CCM como opción terapéutica en insuficiencia cardíaca con fracción de eyección reducida y QRS estrecho."
+        }
+    },
+    {
+        "article": "Paciente de sexo femenino, 61 años, caucásica, casada, dos hijos, informó empeoramiento de los síntomas de la psoriasis tras el inicio de L-metilfolato 15 mg al día para tratamiento coadyuvante de la depresión. Informó depresión y psoriasis desde los 20 años. Desde los 41 años, la paciente no había tenido recidivas de las lesiones psoriáticas.\n\nPor su historial de depresiones, se le indicó carbonato de litio, pero no lo tomó debido a la psoriasis. En 2000, su cuadro depresivo mejoró con venlafaxina 225 mg al día. En 2016, debido a las oscilaciones de humor, se le agregó lamotrigina 100 mg al día y, para mejorar el sueño, se le sumó quetiapina 50 mg al día.\n\nEstas fueron las dosis actuales, con una mejora en la depresión, la calidad de vida y sin efectos adversos significativos.\n\nEn enero de 2019, se detectó polimorfismo en el gen MTHFR, con una mutación heterozigótica en C677T, y se le recetó a la paciente 15 mg diarios de L-metilfolato. Antes de que finalizara la primera semana de uso de L-metilfolato, aparecieron lesiones psoriáticas que no se habían manifestado en 20 años. Se informó lo ocurrido al psiquiatra, quien retiró la medicación y, 4 días después, las lesiones psoriáticas comenzaron a remitir, desapareciendo por completo al cabo de unas semanas. La paciente no volvió a registrar manifestaciones hasta principios de 2020.\n",
+        "gold_summary": "Paciente de sexo femenino, de 61 años, que había estado en remisión de psoriasis durante 20 años. Sufrió una recaída de psoriasis en forma de placa pocos días después de comenzar el tratamiento con L-metilfolato a una dosis diaria de 15 mg.\n",
+        "synthetic_summary": {
+            "B1": "Una mujer de 61 años tenía psoriasis, una enfermedad de la piel, pero no tuvo problemas por 20 años. Empezó a tomar un medicamento llamado L-metilfolato para la depresión. Después de unos días, la psoriasis volvió a aparecer. Cuando dejó de tomar ese medicamento, la piel mejoró y las manchas desaparecieron en unas semanas. Ahora está bien y sin problemas de psoriasis.",
+            "B2": "Una mujer de 61 años con psoriasis en remisión durante 20 años empezó a tomar L-metilfolato para tratar su depresión. Poco después de iniciar este medicamento, aparecieron lesiones de psoriasis que no tenía desde hace mucho tiempo. La paciente había mejorado su depresión con otros medicamentos y no presentaba problemas de piel. Al notar las lesiones, el psiquiatra suspendió el L-metilfolato, y en pocos días las lesiones comenzaron a desaparecer hasta desaparecer por completo en semanas. Este caso muestra que el L-metilfolato podría empeorar la psoriasis en algunas personas, por eso es importante vigilar la piel cuando se usa este tratamiento.",
+            "B3": "Una mujer de 61 años con antecedentes de psoriasis y depresión controlada desde hace décadas presentó una recaída tras iniciar L-metilfolato. Su depresión, manejada eficazmente con venlafaxina, lamotrigina y quetiapina, no había mostrado efectos adversos ni brotes de psoriasis en 20 años. En 2019, tras identificar una mutación en el gen MTHFR, se le prescribió L-metilfolato a 15 mg diarios para potenciar su tratamiento antidepresivo. Sin embargo, pocos días después de comenzar el suplemento, reaparecieron lesiones psoriáticas que no había experimentado en mucho tiempo. Al suspender el L-metilfolato, las lesiones mejoraron notablemente en cuatro días y desaparecieron completamente en semanas. Este caso sugiere que el L-metilfolato podría actuar como desencadenante de la psoriasis en pacientes con antecedentes de esta enfermedad. Por lo tanto, es fundamental que los médicos valoren cuidadosamente los riesgos y beneficios antes de indicar este tratamiento en personas con psoriasis previa. Además, se recomienda un seguimiento estrecho para detectar posibles reactivaciones."
+        }
+    },
+    {
+        "article": "Se diagnosticó osteoartritis bilateral de las articulaciones de la cadera en un paciente de 61 años de edad con tratamiento con esteroides para la artritis reumatoide y dolencias en la ingle bilateral. [9] Recibió una inyección intraarticular bilateral de ácido hialurónico y se presentó doce semanas después en nuestro departamento de urgencias con fiebre, un estado general reducido y un dolor cada vez más incapacitante. Las radiografías de la pelvis mostraron una destrucción progresiva y rápida de ambas articulaciones de la cadera con una osteólisis extensa, subluxación concomitante y un defecto óseo acetabular del lado izquierdo. La aspiración de la articulación mostró pus en ambas articulaciones de la cadera y se hizo el diagnóstico de artritis séptica bilateral progresiva rápida. Se realizó una resección bilateral de ambas cabezas femorales con desbridamiento de la articulación de la cadera y la implantación de espaciadores de PMMA cargados con antibióticos a través de un enfoque anterolateral mínimamente invasivo.\n\nSe inició un tratamiento antibiótico sistémico empírico con vancomicina y ampicilina por vía intravenosa. Se detectó E. coli en muestras de tejido de ambas articulaciones de la cadera y se adaptó el tratamiento antibiótico sistémico a meropenem por vía intravenosa. Se realizaron dos procedimientos quirúrgicos de seguimiento con intercambio de los espaciadores de PMMA cargados con antibiótico para controlar la infección debido al drenaje persistente.\n\nDoce semanas después de la resección de la cabeza femoral y el control exitoso de la infección, el paciente recibió una artroplastia total de cadera con el uso adicional de un revestimiento multicapa de plata (HyProtect®, Bio-Gate, Nürnberg, Alemania). Este revestimiento consiste en una capa de siloxano ultrafina directamente sobre la superficie del implante (10 a 30 nm), de la que se liberan iones de plata.\n\n12 semanas después de la resección de la cabeza femoral, se realizó una artroplastia total de cadera en el lado derecho con una copa estándar sin cemento (Allofit®, ZimmerBiomet, Varsovia, EE. UU.) y un vástago femoral sin cemento (Avenir®, ZimmerBiomet, Varsovia, EE. UU.) a través del enfoque anterolateral mínimamente invasivo previamente utilizado con este revestimiento multicapa de plata ultrafino. Tanto la superficie posterior de la copa como todo el eje femoral se revistieron con plata.\n\nLa cadera izquierda se trató 18 semanas después de la resección de la cabeza femoral con una jaula de refuerzo recubierta de plata (Burch-Schneider®, ZimmerBiomet, Varsovia, EE. UU.) para un defecto acetabular tipo IIB de Paprosky y una copa de polietileno cementada (Durasul®, ZimmerBiomet, Varsovia, EE. UU.). El vástago femoral sin cemento (Avenir®, ZimmerBiomet, Varsovia, EE. UU.) también se recubrió de plata en toda su parte intramedular. Esta intervención también se realizó mediante el enfoque anterolateral mínimamente invasivo utilizado previamente. El paciente se sometió a una terapia antibiótica sistémica durante un período de tratamiento total de 18 semanas después de la implantación del lado derecho. Se aplicó ertapenem 1 g por vía intravenosa durante este período de tiempo una vez al día, después de la descarga en un entorno ambulatorio. Esto permitió una cobertura antibiótica del lado derecho de 18 semanas y del lado izquierdo de 12 semanas de tratamiento antibiótico.\n\nSe recomendó el uso parcial de peso con 20 kg en el lado operado y el uso de muletas durante 6 semanas después de las intervenciones.\n\nLas heridas de ambos lados se curaron sin incidentes. El paciente fue visto regularmente para un seguimiento clínico y radiológico. Se logró el apoyo total del peso sin el uso de muletas 7 semanas después de la operación en ambos lados. No hubo signos de PIJ y no fue necesaria una cirugía de revisión adicional.\n\nEn un seguimiento final tres años después de la implantación de las prótesis recubiertas de plata, la paciente mostró un aspecto normal de la piel con mínimas cicatrices después de enfoques antero-laterales mínimamente invasivos en ambos lados sin signos de argiria. Hubo un excelente resultado funcional de ambas caderas con marcha normal y una puntuación WOMAC de 6 en ambos lados (dolor: 0, rigidez: 0, función física: 6). El recuento de leucocitos en sangre fue de 7,29/nl (referencia: 4,23-9,1) y el nivel de proteína C reactiva (PCR) fue de 12,4 mg/l (referencia: <5 mg/l). El nivel ligeramente elevado de PCR es atribuible a la artritis reumatoide subyacente de la paciente. Las radiografías revelaron componentes protésicos de cadera bien integrados y no sueltos en ambos lados tres años después de la implantación con una articulación correcta.\n",
+        "gold_summary": "Este informe de caso se refiere a un paciente de 61 años con destrucción rápida de ambas articulaciones de la cadera debido a una artritis séptica que se trató con éxito con una implantación por etapas de prótesis de cadera recubiertas con plata con un recubrimiento ultrafino multicapa de plata. En un seguimiento de tres años, no hubo signos de infección, se observó un buen estado de todos los componentes protésicos y el resultado funcional fue excelente.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre de 61 años tenía mucho dolor en las caderas por una infección grave. Los doctores le pusieron prótesis nuevas cubiertas con plata para ayudar a sanar y evitar más infecciones. Después de tres años, el hombre caminaba bien y no tenía dolor. Las radiografías mostraron que las prótesis estaban en buen lugar. La plata ayudó a que no volviera la infección.",
+            "B2": "Un paciente de 61 años con artritis reumatoide y osteoartritis en ambas caderas desarrolló una infección grave llamada artritis séptica. Esta infección causó dolor intenso y daño rápido en las articulaciones. Se realizó una cirugía para quitar las cabezas femorales infectadas y se colocaron espaciadores con antibióticos. Luego, se implantaron prótesis de cadera recubiertas con una capa muy fina de plata para evitar nuevas infecciones. El paciente recibió antibióticos durante varias semanas y pudo caminar sin muletas en poco tiempo. Tres años después, las radiografías mostraron que las prótesis estaban bien integradas y el paciente tenía una función normal sin dolor ni signos de infección.",
+            "B3": "Un paciente de 61 años con artritis reumatoide y osteoartritis bilateral de cadera desarrolló una artritis séptica que provocó rápida destrucción ósea en ambas articulaciones. Se realizó la extracción de las cabezas femorales infectadas y se colocaron espaciadores impregnados con antibióticos, seguidos de un tratamiento intravenoso dirigido tras identificar Escherichia coli como agente causal. Posteriormente, se implantaron prótesis totales de cadera recubiertas con una capa ultrafina de plata, diseñada para liberar iones antimicrobianos y prevenir nuevas infecciones, mediante un abordaje quirúrgico mínimamente invasivo. El paciente recibió un tratamiento antibiótico prolongado y recomendaciones para limitar la carga sobre las caderas durante la fase de recuperación. A los tres años, las prótesis mostraron una adecuada integración ósea sin signos de infección ni complicaciones, y el paciente recuperó una marcha funcional con cicatrices mínimas. Este caso evidencia la eficacia del recubrimiento de plata en prótesis articulares para controlar infecciones graves y lograr resultados funcionales satisfactorios en infecciones articulares complejas."
+        }
+    },
+    {
+        "article": "Una niña africana de raza negra, con 1000 g de peso, nacida a las 32 semanas de gestación, de madre viva, fue derivada a nuestra unidad de cuidados intensivos neonatales debido a múltiples anomalías congénitas y dificultad respiratoria moderada. La madre tiene 32 años y está en un matrimonio no consanguíneo. La madre no buscó atención médica hasta el inicio del tercer trimestre de embarazo, debido a un desprendimiento de placenta. El primer ultrasonido prenatal reveló oligohidramnios severos. No era diabética (la glucosa en sangre aleatoria fue de 5.1 mmol/L) y no recibió suplementos de ácido fólico durante el embarazo.\n\nAl ingreso, la bebé estaba alerta con características leves del síndrome de dificultad respiratoria. Presentaba múltiples rasgos dismórficos, entre ellos, microcefalia (circunferencia de la cabeza < 10%), occipucio prominente, orejas bajas, paladar hendido y labio derecho, micrognatia, contractura bilateral de los codos e inferiores más cortos.\n\n\nEl peso al nacer fue de 1000 g, la longitud del bebé fue de 40 cm y la circunferencia occipitofrontal fue de 30 cm.\n\nInvestigaciones\nLa radiografía esquelética mostró aplanamiento de las costillas, aplasia del fémur derecho e hipoplasia del fémur izquierdo. Los análisis de laboratorio incluyeron: hemograma completo, proteína C reactiva, creatinina, urea en sangre y electrolitos, todos dentro de los valores normales. La ecografía craneal fue normal, pero la ecocardiografía reveló un pequeño conducto arterioso permeable.\n\nDiagnóstico diferencial\nLa paciente presentaba aplasia femoral bilateral y facies inusuales. Estas características clínicas llevaron al diagnóstico de síndrome femoro-facial.\n\nLa similitud en la etiopatogénesis hace que el síndrome de regresión caudal sea el diagnóstico diferencial común. Ambos pueden ser causados por una hiperglucemia materna mal controlada. Sin embargo, los defectos faciales están ausentes en el síndrome de regresión caudal, la característica diagnóstica clave.\n\nLa hipoplasia femoral focal proximal y las anomalías craneofaciales suelen estar ausentes.\n\nEntre las condiciones que pueden provocar el labio leporino se incluye el síndrome de banda amniótica grave.\n\nTratamiento\nEl bebé recibió asistencia respiratoria y antibióticos empíricos. Participaron un cirujano ortopédico, un otorrinolaringólogo y un fisioterapeuta. Está previsto reparar quirúrgicamente el paladar hendido a los 6 meses de edad. La rehabilitación funcional está prevista antes de que el paciente comience a deambular. La cirugía de alargamiento de extremidades no se realiza actualmente en nuestro entorno.\n\nResultado y seguimiento\nEl paciente falleció a la edad de un mes por complicaciones de una sepsis neonatal grave de inicio tardío.\n",
+        "gold_summary": "Una niña africana de raza negra bantú de 1 día de vida fue admitida en la unidad neonatal debido a múltiples anomalías congénitas. La madre no buscó atención médica hasta el inicio del tercer trimestre, cuando tuvo un desprendimiento de placenta. La madre nunca recibió suplementos de ácido fólico prenatal. La niña tenía microcefalia, orejas bajas, paladar hendido derecho y labio, micrognatia, contractura y extremidades más cortas. Una radiografía esquelética mostró hipoplasia femoral. Presentamos este caso poco habitual y destacamos los retos en el diagnóstico y el tratamiento.\n",
+        "synthetic_summary": {
+            "B1": "Una niña nació con problemas en la cabeza y en sus piernas. Su mamá no fue al doctor hasta muy tarde en el embarazo y no tomó vitaminas. La niña tenía la cabeza pequeña, orejas bajas, y un labio y paladar partidos. Los huesos de sus piernas estaban débiles. Recibió ayuda para respirar y se planeó una cirugía, pero murió a un mes por una infección grave.",
+            "B2": "Una niña prematura de 32 semanas y 1000 gramos fue ingresada por varias malformaciones y dificultad para respirar. La madre no recibió atención médica hasta el tercer trimestre y no tomó ácido fólico. La bebé tenía microcefalia (cabeza pequeña), orejas bajas, paladar y labio hendidos, mandíbula pequeña y extremidades cortas con contracturas. Las radiografías mostraron falta de desarrollo en los huesos del muslo. Los análisis de sangre y el ultrasonido cerebral fueron normales, pero el corazón tenía un pequeño defecto. Se diagnosticó síndrome femoro-facial, que afecta los huesos de las piernas y la cara. Recibió apoyo respiratorio y antibióticos, y se planificó cirugía para el paladar. Lamentablemente, falleció a un mes por una infección grave. Este caso muestra la dificultad para tratar malformaciones complejas en recién nacidos.",
+            "B3": "Una recién nacida africana prematura de 32 semanas y bajo peso fue ingresada en cuidados intensivos debido a múltiples malformaciones congénitas y dificultad respiratoria moderada. La madre, sin control prenatal adecuado ni suplementación con ácido fólico, presentó desprendimiento placentario y oligohidramnios severo, factores que complicaron el embarazo. La bebé exhibía microcefalia, paladar hendido, labio leporino, micrognatia y contracturas en extremidades, además de hipoplasia y aplasia femoral evidenciadas en radiografías. Aunque la ecografía craneal resultó normal, se identificó un conducto arterioso permeable pequeño, lo que añadió complejidad al cuadro clínico. El diagnóstico principal fue síndrome femoro-facial, diferenciándose del síndrome de regresión caudal por la presencia de anomalías faciales características. La paciente recibió soporte respiratorio, tratamiento antibiótico y atención multidisciplinaria, con planes quirúrgicos para corregir el paladar hendido y rehabilitación funcional. No obstante, falleció a los 30 días debido a una sepsis neonatal grave, lo que subraya la dificultad en el manejo de neonatos con malformaciones múltiples, especialmente en entornos con recursos limitados para intervenciones quirúrgicas avanzadas."
+        }
+    },
+    {
+        "article": "Paciente de sexo masculino de 18 años, con diag nóstico clínico de Neurofibromatosis tipo 1 desde el primer año de vida. Entre sus antecedentes destaca que tiene educación completa, sus padres no son consan guíneos, y no tiene antecedentes familiares de manchas café con leche. Desde el punto de vista neurológico desarrolló durante la infancia retraso del desarrollo psicomotor fino y grueso, trastorno del lenguaje de predominio expresivo, con alteración fonológica y semántica del lenguaje, por lo que fue manejado con fonoaudiología en Escuela de Lenguaje, además de ki- nesioterapia y terapia ocupacional durante la infancia. Durante la adolescencia se le diagnosticó Trastorno por Déficit Atencional e Hiperactividad, que fue manejado con metilfenidato, manteniendo regular rendimiento escolar. Tuvo desarrollo puberal normal. Oftalmológi camente presentó nódulos de Lisch desde los 4 años de edad, euriblefaron y astigmatismo. Se mantuvo en control anual en Oftalmología y Neuropediatría. Su última Resonancia Magnética de cerebro fue realiza da 6 meses previo a la consulta en Dermatología, sin hallazgos patológicos y en la Resonancia Magnética de columna se evidenció discopatía L5-S1 y realce perifacetario en T11-T12 y T12-L1. A los 16 años se reali zó estudio genético que demostró deleción de exones 5-47 del gen NF1.\n\nA los 18 años consultó en servicio de Dermatología del Centro de Referencia en Salud Peñalolén Cordille ra Oriente por aparición de nueva mancha en muslo izquierdo de 1 año evolución, asintomática. Además, refirió aparición de nódulos en muñeca derecha, su praciliar derecho y cuero cabelludo, de unos meses de evolución, asintomáticos.\n\nAl examen físico destacaba presión arterial normal, macrocefalia (CC: 60 cm) y múltiples manchas café con leche generalizadas, efélides en axilas, y en zona supraciliar derecha, occipital y muñeca derecha nódulos subcutáneos ovalados de 0,5 cm, bien delimitados, móviles. En muslo izquierdo lateral pre sentaba placa de 25 mm algo rosada, con pérdida de anexos, y de consistencia blanda. Por último, en zona lumbar y pectoral, múltiples máculas rojo- azuladas pequeñas, de menos de 5 mm cada una, algu nas levemente deprimidas.\n\nSe realizó biopsia cutánea de máculas azuladas en pecho y de placa muslo, resultando ambas compatibles con NF. Se realizó una ecografía de nódulos supraciliar y occipital que resultó compatible con NF nodular subcutáneo.\n\nUsando la clasificación clínica de García-Martínez et al.1 se diagnosticó al paciente con NF superficial sub cutáneo nodular en zona supraciliar derecha, occipital y muñeca derecha, NF superficial cutáneo pseudoatró fico en muslo izquierdo lateral y NF superficial cutáneo rojo azulado en zona lumbar y pectoral.",
+        "gold_summary": "Paciente masculino de 18 años con diagnóstico desde la infancia de NF-1 que presenta múltiples nodulos ovalados en cara, zona occipital y muñeca, máculas rojo-azuladas en dorso y placa rosada atrófica en muslo. El estudio ecográfico de los nódulos fue compatible con neurofibromas y el estudio histopatológico de las lesiones de dorso y muslo compatibles con neurofibromas cutáneos.",
+        "synthetic_summary": {
+            "B1": "Un joven de 18 años tiene una enfermedad llamada neurofibromatosis desde pequeño. Tiene manchas café con leche en la piel y bultos suaves en la cara, la cabeza y la muñeca. También tiene manchas rojas y azules en la espalda y una mancha rosada en el muslo. Los médicos hicieron estudios y confirmaron que esos bultos y manchas son parte de su enfermedad. Él está bajo cuidado médico para controlar su salud.",
+            "B2": "Un joven de 18 años tiene neurofibromatosis tipo 1, una enfermedad que afecta la piel y los nervios. Aparecieron nuevas manchas café con leche y bultos blandos en su cara, cabeza y muñeca. También tenía una mancha rosada en el muslo y manchas rojo-azuladas en el pecho y la espalda. Los estudios con ecografía y biopsia mostraron que estas lesiones son neurofibromas, tumores benignos de los nervios. Aunque no le causan dolor, es importante controlar estas lesiones para evitar problemas. Desde niño recibe atención por dificultades en el desarrollo y el lenguaje. Actualmente, su estado general es bueno.",
+            "B3": "Un joven de 18 años con diagnóstico confirmado de Neurofibromatosis tipo 1 (NF-1) desde la infancia presenta múltiples lesiones cutáneas nuevas y preexistentes. A lo largo de su desarrollo, mostró retrasos psicomotores y del lenguaje, además de trastorno por déficit de atención e hiperactividad, para los cuales recibió tratamiento farmacológico y terapias específicas. En la evaluación dermatológica actual, se identificaron numerosas manchas café con leche, nódulos subcutáneos ovalados en la cara, occipucio y muñeca, junto con máculas rojo-azuladas pequeñas en regiones lumbar y pectoral, y una placa rosada con pérdida de anexos en el muslo izquierdo. Los estudios complementarios, que incluyeron biopsias y ecografías, confirmaron que estas lesiones corresponden a neurofibromas, tumores benignos característicos de la NF-1. Este caso ejemplifica la amplia variedad clínica de manifestaciones cutáneas en pacientes con NF-1 y resalta la necesidad de un seguimiento multidisciplinario para detectar nuevas lesiones y monitorear su evolución. Por lo tanto, se recomienda mantener controles dermatológicos y neurológicos periódicos para prevenir y manejar oportunamente posibles complicaciones asociadas."
+        }
+    },
+    {
+        "article": "Un hombre de 38 años de edad fue ingresado en el hospital por traumatismo torácico contundente. El paciente estaba generalmente sano y no tenía factores de riesgo de enfermedad coronaria. Fue golpeado en el pecho por un tornillo de alta velocidad que tenía aproximadamente 6 cm de diámetro mientras trabajaba en una fábrica. Voló aproximadamente 4 metros de distancia debido a la fuerza y presión del tornillo de alta velocidad. Perdió el conocimiento de inmediato, pero recuperó la conciencia varios minutos después. Fue trasladado inmediatamente a la sala de urgencias de un hospital local. Su puntaje en la escala de coma de Glasgow fue de 15. Se quejó de dolor torácico intenso y persistente, opresión y disnea. La tomografía computarizada del tórax mostró derrame pleural bilateral y fracturas de esternón y costillas. Por lo tanto, se insertó un tubo torácico durante varios días. Luego, fue dado de alta sin someterse a un electrocardiograma (ECG) u otros exámenes cardiovasculares.\n\nTres meses después del alta hospitalaria, durante un chequeo de seguimiento de rutina, todavía había presencia de derrame pleural con síntomas acompañantes de opresión en el pecho, falta de aire después de la actividad física, e incluso disnea por la noche, lo que motivó su ingreso en nuestro hospital. Sus constantes vitales durante el ingreso fueron las siguientes: frecuencia cardíaca regular de 98 latidos/min, presión arterial de 110/70 mmHg, y frecuencia respiratoria de 20 respiraciones/min. El examen físico mostró una pulsación carotídea y yugular normal. El movimiento respiratorio torácico bilateral y la actividad fueron normales, la fibrilación del lenguaje táctil del pulmón derecho disminuyó, la percusión del pulmón derecho presentó un sonido sordo, y los sonidos respiratorios disminuyeron. No hubo roncus ni estertores evidentes durante la auscultación pulmonar. No hubo murmullos en la auscultación cardíaca. Los exámenes del abdomen y las extremidades revelaron hallazgos normales. El primer ECG mostró evaluación ST e inversión de la onda T en las derivaciones I, aVL y V2-V5 y en el bloqueo de rama anterior izquierdo. La prueba de troponina-I fue negativa, y el nivel de NT-proBNP fue de 706 pg/ml (rango normal: 0-104 pg/ml), lo que sugiere un infarto de miocardio anterior antiguo. La ecocardiografía transtorácica mostró una aurícula izquierda de 26,4 mm, un ventrículo izquierdo de 51,8 mm, y una fracción de eyección ventricular izquierda (EF) del 32% (modo M). La pared anterior del LV e interventricular septum mostraron adelgazamiento a 6,6 mm, con un eco de movimiento notablemente reducido.\n\nAl examinar las arterias carótidas, intracraneales y de las extremidades inferiores del paciente, no se encontraron placas ateroscleróticas evidentes. Todos los hallazgos apoyaron el diagnóstico de infarto de miocardio antiguo (OMI), en lugar de arteriosclerosis. Sin embargo, el paciente era hemodinámicamente estable. Después de someterse a una terapia diurética, se le administraron bloqueadores beta, estatinas y estimulantes cardíacos, lo que alivió su malestar. La angiografía por tomografía computarizada coronaria mostró una estenosis moderada en la arteria LAD proximal. Para confirmar la estenosis y examinar el estado de la íntima coronaria, se realizó CAG 3 meses después del traumatismo torácico, que mostró un estrechamiento aproximado del 70% del lumen en la LAD proximal y el segmento coronario tenía una lesión curva. La arteria circunfleja izquierda (LCX) y la arteria coronaria derecha (RCA) eran normales. Los resultados de CAG confirmaron el diagnóstico de OMI, pero debido a la carga de costos, el paciente rechazó el examen IVUS. El paciente se sometió a una terapia conservadora y fue dado de alta del hospital varios días después.\n\nUn mes después, el 9 de diciembre de 2014, volvió al hospital para someterse a una intervención coronaria percutánea (ICP). Después de someterse a una terapia con fármacos, sus condiciones habían mejorado ligeramente. El examen físico y el ECG revelaron resultados casi normales. La ecocardiografía transtorácica mostró una mejora en la función sistólica del LV y EF del 45%. Se sometió a otra CAG 4 meses después del traumatismo torácico, que mostró una ligera mejora de la estenosis. Había aproximadamente un 60% de estrechamiento del lumen. Se realizó un IVUS y reveló que la gravedad de la lesión era del 55.9%, y la placa de bajo eco apareció antes de la formación de trombos después de la rotura subintimal. Completamos el examen sin más intervención porque solo se encontró un 55.9% de estrechamiento del lumen y el paciente tenía una hemodinámica estable sin evidencia de isquemia miocárdica constante. Se le recetó al paciente la medicación óptima, y su incomodidad se alivió gradualmente. El 17 de julio de 2018, 4 años después del traumatismo, la evaluación de seguimiento reveló que el paciente todavía experimentaba dificultad para respirar después de trabajar, pero se alivió poco después de descansar. El examen físico mostró los siguientes resultados: presión arterial de 114/80 mmHg, frecuencia cardíaca de 66 latidos/min, ausencia de anomalías obvias en la auscultación pulmonar y cardíaca; y ausencia de edema obvio en ambas extremidades inferiores. El ECG de seguimiento reveló los siguientes hallazgos: rS en las derivaciones V2-V4, inversión de la onda T en las derivaciones I, AVL y V2-V5 y bloqueo de rama izquierda. La ecocardiografía transtorácica mostró agrandamiento del ventrículo izquierdo con una aurícula izquierda de 39 mm, un ventrículo izquierdo de 54.7 mm y una EF del LV del 41% (Simpson's). También se observó adelgazamiento de la pared anterior del LV y del tabique interventricular, con la parte más delgada de 4.7 mm; el movimiento casi había desaparecido y el eco se había mejorado. Sin embargo, las arterias carótidas, intracraneales y de las extremidades inferiores seguían siendo normales. Además, descubrimos que los medicamentos recetados para tratar la insuficiencia cardíaca no se tomaron religiosamente después del alta; por lo tanto, recetamos 23.75 mg de metoprolol, 2.5 mg de benazepril y 20 mg de espironolactona para tomar una vez al día, y coenzima para tomar cada 10 horas.\n\nMH - Adulto\nMH - Errores de diagnóstico\nMH - Insuficiencia cardiaca/etiología\nMH - Humanos\nMH - Hombre\nMH - Infarto de miocardio/complicaciones/*etiología\nMH - Lesiones torácicas/*complicaciones\nMH - Tiempo hasta el tratamiento\nMH - Heridas, no penetrantes/complicaciones\n",
+        "gold_summary": "Preocupaciones de los pacientes:\nUn hombre de 38 años, previamente sano, fue admitido en nuestro hospital con una queja de disnea. Tenía un historial de haber sido golpeado en el pecho por un tornillo de alta velocidad mientras trabajaba en una fábrica 3 meses antes de ser admitido en el hospital.\n\nDiagnóstico:\nLuego de realizarse una angiografía coronaria y una ecocardiografía, finalmente se le diagnosticó un infarto de miocardio.\n\nIntervenciones:\nRecibió medicamentos optimizados, entre ellos, diuréticos, bloqueadores beta y estimulantes cardíacos.\n\nResultados:\nAl cabo de cuatro años de seguimiento, se le diagnosticó al paciente una insuficiencia cardíaca crónica con una fracción de eyección reducida.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre de 38 años recibió un fuerte golpe en el pecho con un tornillo mientras trabajaba. Tres meses después, tenía dificultad para respirar y dolor en el pecho. Los médicos descubrieron que había sufrido un daño en el corazón llamado infarto. Le dieron medicinas para ayudar a su corazón. Cuatro años después, sigue con problemas en el corazón, pero recibe tratamiento para sentirse mejor.",
+            "B2": "Un hombre de 38 años recibió un fuerte golpe en el pecho por un tornillo mientras trabajaba. Esto le causó fracturas y acumulación de líquido en el pulmón, llamada derrame pleural. Tres meses después, tuvo dificultad para respirar y dolor en el pecho. Las pruebas mostraron un infarto antiguo, que es daño en el corazón por falta de sangre. Aunque estaba estable, le dieron medicamentos para mejorar su corazón. La angiografía, un examen de las arterias, confirmó una obstrucción en una arteria del corazón. Con el tiempo, su corazón mejoró, pero cuatro años después desarrolló insuficiencia cardíaca, cuando el corazón no bombea bien. Le recetaron medicamentos para controlar su enfermedad y aliviar sus síntomas.",
+            "B3": "Un hombre de 38 años, sin antecedentes de enfermedad coronaria, sufrió un traumatismo torácico grave al ser golpeado en el pecho por un tornillo de alta velocidad en su trabajo. Inicialmente, presentó fracturas y derrame pleural, pero no se evaluó su corazón en ese momento. Tres meses después, acudió al hospital por dificultad para respirar y opresión en el pecho; los estudios revelaron signos de un infarto de miocardio antiguo y una función cardíaca disminuida. La angiografía coronaria mostró una estenosis significativa en la arteria coronaria izquierda, confirmando el diagnóstico. Recibió tratamiento con medicamentos como diuréticos y bloqueadores beta, mejorando su condición. Sin embargo, cuatro años después, persistió con insuficiencia cardíaca crónica y función ventricular reducida, atribuida a la lesión traumática inicial. No obstante, el paciente no siguió estrictamente la medicación prescrita, lo que pudo influir en la evolución. Este caso resalta la importancia de evaluar el daño cardíaco tras un trauma torácico severo y el seguimiento continuo para prevenir complicaciones a largo plazo."
+        }
+    },
+    {
+        "article": "La paciente era una recién nacida de 0 días de edad, de etnia Han, que nació a las 36 semanas de gestación de una mujer embarazada de 3, para 2, con un peso de 2650 g. Se le practicó una cesárea de urgencia debido a la angustia fetal, con puntuaciones de Apgar de 6 a 1 min y 5 min. Su grupo sanguíneo era O y RhD positivo. Al nacer, presentaba palidez, equimosis dispersas en múltiples áreas del cuerpo, sangrado de las mucosas e insuficiencia respiratoria, con un leve flujo de sangre hemorrágica también observado en los sitios de punción venosa. El análisis de gases en sangre de la arteria umbilical mostró un hematocrito de 0.08 y una hemoglobina de 23 g/L. La paciente requirió intubación endotraqueal y ventilación mecánica. Después de la transfusión de una suspensión de glóbulos rojos, los recuentos sanguíneos iniciales revelaron una trombocitopenia severa (recuento de plaquetas de 12 × 109/L), anemia (hemoglobina de 46 g/L) y leucopenia (recuento de leucocitos de 1.11 × 109/L).\n\nLa paciente fue ingresada en la unidad de cuidados intensivos neonatales a las 3 horas de vida para recibir tratamiento adicional. Durante la hospitalización, se le diagnosticó coagulación intravascular diseminada (CID), con tiempo de tromboplastina parcial activada (TTPA) de 73,10 segundos, tiempo de protrombina (TP) de 25,4 segundos, fibrinógeno (FIB) de 1,01 g/L, razón internacional normalizada (INR) de 2,26 y dímero D > 20 mg/L. Se le administró ventilación mecánica, corrección de la acidosis y transfusión de plasma fresco congelado. A pesar de múltiples transfusiones de glóbulos rojos y plaquetas, los niveles de hemoglobina y plaquetas permanecieron por debajo de lo normal (hemoglobina 106 g/L y plaquetas 11 × 109/L el día 3). También recibió tratamiento antiinfeccioso, cardiotónico, vasopresor y otro tratamiento sintomático. Un frotis periférico mostró áreas de tinción pálida agrandadas de glóbulos rojos, con una proporción de reticulocitos del 1,5% y un resultado negativo en la prueba directa de Coombs. No se realizó aspiración de médula ósea debido a su grave estado. No hubo evidencia clínica o de laboratorio de sepsis neonatal, y las pruebas para toxoplasma, rubéola, citomegalovirus y virus del herpes simple (TORCH); virus de hepatitis; y Treponema pallidum fueron negativas. El examen físico de admisión reveló un estado mental deficiente, disminución del tono muscular en las extremidades y reflejo pupilar lento a la luz. Todos los demás hallazgos fueron normales. El ultrasonido craneal y electroencefalograma de cabecera revelaron hemorragia intracraneal grave y bajo voltaje, respectivamente. Los hallazgos del ecocardiograma sugirieron un conducto arterioso patente, foramen oval permeable e hipertensión pulmonar. El ultrasonido abdominal indicó hemorragia gastrointestinal. A pesar de todos los esfuerzos, la paciente falleció el tercer día de vida debido a falla multiorgánica y hemorragia intracraneal masiva (la información detallada se puede encontrar en el Informe Suplementario).\n\nLos padres de la paciente no eran consanguíneos y ambos tenían talasemia. La madre, que compartía el mismo tipo de sangre que la paciente, tuvo una anemia leve durante el embarazo (nivel de hemoglobina de 97 g/L) y un historial de aborto inducido. Los exámenes prenatales no mostraron anomalías, ni tampoco hidrops fetal, y no recibió ninguna medicación durante el embarazo que pudiera provocar una enfermedad hemorrágica de inicio temprano en el recién nacido. La paciente también tenía un hermano de 1 año que gozaba de buena salud. Su abuelo tenía un historial de anemia leve (detalles desconocidos).\n\nSe obtuvo el consentimiento informado de los padres del paciente y se realizó un secuenciamiento de Sanger para descubrir la causa de la enfermedad. Se detectó una nueva mutación de MECOM de desplazamiento de marco heterocigótica [NM_001105078: c.157_158del (p.Met53Glyfs*2)] en el probando. Esta variante cambió el aminoácido 53 de metionina (codón ATG) a glicina (codón GGT), seguido de una terminación temprana. La mutación no se encontró en los padres o en el hermano mayor. La variante se clasificó como patogénica según las directrices del Colegio Americano de Genética Médica (ACMG) [14]. El algoritmo “AutoPVS1” brindó un fuerte apoyo para la interpretación de PVS1 de p.Met53Glyfs*2, lo que indica patogenicidad. La variante no se ha informado previamente en la Base de Datos de Mutación Genética Humana (HGMD) o en Clinvar. El análisis de conservación mostró que el residuo Met53 está altamente conservado en todas las especies de mamíferos (incluidos humanos, ratones, ratas, chimpancés y bovinos) utilizando Clustal Omega. Se generaron modelos de estructura de proteínas tridimensionales de las proteínas MECOM de tipo salvaje y mutantes utilizando SWISS-MODEL, lo que indica que la mutación de desplazamiento de marco causó una terminación temprana de la síntesis de aminoácidos, alterando significativamente la estructura de la proteína.\n",
+        "gold_summary": "Reportamos el caso de una neonata Han china de 0 días de vida que presentó trombocitopenia grave y hemorragia intracraneal, y que finalmente falleció por fallo multiorgánico e intracraneal el tercer día después del nacimiento. La secuenciación genética identificó una variante de cambio de marco heterocigótica, c.157_158del, dentro del gen MECOM. Esta variante condujo a una sustitución del 53.º aminoácido de metionina a glicina, terminando en el 54.º aminoácido. Una revisión exhaustiva de la literatura indicó que las mutaciones del gen MECOM incluían mutaciones sin sentido (68.3%), deleción (8.5%), sitio de empalme (8.5%), cambio de marco (7.3%) y sin sentido (7.3%). Las pacientes con mutaciones sin sentido frecuentemente presentaban sinostosis radiocubital, mientras que el fallo de la médula ósea se asociaba más comúnmente con los otros cuatro tipos de mutaciones.\n",
+        "synthetic_summary": {
+            "B1": "Una bebé nació con problemas graves en la sangre y sangraba mucho en la cabeza. Los médicos le hicieron pruebas y encontraron un cambio raro en un gen llamado MECOM. Este cambio causó que la proteína del cuerpo no funcionara bien. Aunque intentaron ayudarla, la bebé murió al tercer día. Este caso muestra que algunas mutaciones en el gen MECOM pueden causar problemas serios en la sangre y los huesos.",
+            "B2": "Una recién nacida de etnia Han tuvo problemas graves al nacer, como bajo número de plaquetas, que son células que ayudan a detener el sangrado. También presentó sangrado en el cerebro. A pesar de varios tratamientos, murió al tercer día por fallo de órganos y hemorragia. Se encontró una mutación nueva en el gen MECOM, que afecta una proteína importante para la médula ósea, donde se forman las células sanguíneas. Esta mutación cambió la estructura de la proteína, causando los problemas de la bebé. No se detectaron infecciones ni causas externas. El caso muestra que mutaciones en MECOM pueden causar fallos graves en recién nacidos.",
+            "B3": "Se describe el caso de una recién nacida de etnia Han que presentó trombocitopenia severa, anemia y hemorragia intracraneal grave desde el nacimiento, falleciendo a los tres días por fallo multiorgánico. La paciente nació a las 36 semanas por cesárea urgente debido a angustia fetal, con signos de sangrado y dificultad respiratoria que requirieron ventilación mecánica y múltiples transfusiones. Se diagnosticó coagulación intravascular diseminada, y a pesar del tratamiento intensivo, sus niveles de hemoglobina y plaquetas permanecieron bajos. No se detectaron infecciones ni causas externas, y el examen neurológico y cardiovascular mostró complicaciones graves. El análisis genético reveló una mutación heterocigótica de cambio de marco en el gen MECOM, que provocó una terminación prematura de la proteína, alterando su estructura. Esta variante no estaba presente en sus familiares y se clasificó como patogénica. Las mutaciones en MECOM están asociadas con fallos en la médula ósea y malformaciones óseas, lo que explica la gravedad del cuadro. Este caso subraya la importancia del diagnóstico genético temprano para comprender causas genéticas en neonatos con hemorragias graves y fallo hematológico, orientando posibles intervenciones futuras."
+        }
+    },
+    {
+        "article": "La paciente es una mujer de 74 años de edad, físicamente activa, que practica senderismo y equitación. Un mes después del tratamiento con inyección de cortisona de la tendinopatía insercional de Aquiles, sufrió una rotura total del tendón de Aquiles insercional al intentar dar un paso mientras montaba en bicicleta. Esta rotura se trató de forma conservadora con una bota de Walker durante 8 semanas. Después, mientras montaba a caballo, un intento de dar un paso provocó una nueva rotura total del tendón de Aquiles en la inserción. La rotura se trató quirúrgicamente con reinserción del tendón de Aquiles en el calcáneo, utilizando anclajes de sutura. Esto fue seguido por inmovilización en un yeso. Después de la operación, la paciente sufrió una infección profunda que no respondía a los antibióticos, signos de sepsis, y se indicó exploración quirúrgica. Durante la cirugía, se encontró que todo el tendón de Aquiles estaba gravemente afectado por la infección, más o menos destruido, y hubo que retirar el tendón de Aquiles distal de 7 cm (todo el tendón libre de Aquiles). Esto dejó una gran herida sin tejido tendinoso, y la piel se suturó sobre la herida. Después de este procedimiento, la inmovilización y el tratamiento con antibióticos de cloxacilina curaron la infección y la herida se curó adecuadamente. El pie se inmovilizó en un yeso durante las primeras 10 semanas, desde la máxima flexión plantar inicialmente, y luego la flexión plantar disminuyó gradualmente hasta alcanzar la posición neutra. Esto fue seguido por inmovilización en un yeso dorsal, evitando la extensión del tendón de Aquiles en flexión plantar, durante otros 3 meses. Se le dijo que aumentara gradualmente la carga al caminar, pero que evitara la extensión durante un total de 6 meses. Después de 6 meses se le ofreció reconstrucción quirúrgica con un injerto de flexor hallucis longus, pero como entonces tenía una función satisfactoria, decidió esperar y ver. Su función mejoró gradualmente, y un año después de la operación, cuando buscó ayuda por el dolor en el otro tendón de Aquiles, se notó la buena función en el lado operado. La exploración por ultrasonido mostró sorprendentemente un tendón que se parecía mucho a un tendón de Aquiles ligeramente tendinopático.\n",
+        "gold_summary": "Esta señora de 74 años padecía tendinopatía insercional de Aquiles. Después del tratamiento con una inyección local de cortisona, sufrió una rotura total del tendón de Aquiles insercional. Esta rotura se trató de forma conservadora y, después del tratamiento, el tendón de Aquiles volvió a romperse en la zona de inserción. La rotura se trató entonces con reinserción en la zona de inserción calcánea. Al poco tiempo del postoperatorio, la paciente sufrió una infección de herida quirúrgica profunda y sepsis. Debido al pobre efecto del tratamiento con antibióticos y a la destrucción total del tendón, se extirpó todo el tendón de Aquiles. Después de la extirpación, se inmovilizó en un yeso, seguido de movilización y aumento gradual de la carga. En un seguimiento de un año, la paciente caminaba sin cojera, podía levantar el talón hasta la mitad mientras estaba de pie sobre una pierna, había un tendón de Aquiles palpable y el escaneado por ultrasonido mostró una estructura muy similar a un tendón de Aquiles tendinopático y ligeramente engrosado. Había una regeneración evidente de todo el tendón de Aquiles y la función del tendón era sorprendentemente buena.\n",
+        "synthetic_summary": {
+            "B1": "Una señora de 74 años tuvo un problema en el tendón de Aquiles, que es un tejido que une el músculo al hueso del talón. Después de una inyección, el tendón se rompió dos veces. La segunda vez, la operaron y luego tuvo una infección grave. Por eso, le quitaron todo el tendón. Con el tiempo y cuidados, su pie mejoró mucho. Un año después, el tendón volvió a crecer y ella pudo caminar bien sin dolor.",
+            "B2": "Una mujer de 74 años tenía problemas en el tendón de Aquiles, que conecta el músculo con el talón. Recibió una inyección de cortisona para aliviar el dolor, pero poco después se rompió el tendón al andar en bicicleta. La primera rotura se trató con una bota especial para inmovilizar la pierna. Sin embargo, el tendón se volvió a romper mientras montaba a caballo. Esta segunda rotura requirió una operación, pero la paciente sufrió una infección grave que dañó todo el tendón. Por eso, fue necesario quitar el tendón dañado. Después de la cirugía, la pierna se inmovilizó con yeso y recibió antibióticos para curar la infección. Con el tiempo, la paciente mejoró y pudo caminar sin problemas. Un año después, el ultrasonido mostró que el tendón había crecido otra vez, aunque con algunas alteraciones.",
+            "B3": "Una mujer de 74 años, físicamente activa, sufrió una rotura completa del tendón de Aquiles tras recibir una inyección de cortisona para tratar una tendinopatía insercional. Inicialmente, la lesión se manejó con inmovilización, pero presentó una segunda rotura en la misma zona que requirió cirugía para la reinserción del tendón. Posteriormente, desarrolló una infección profunda que no respondió al tratamiento antibiótico, lo que provocó sepsis y destrucción del tendón, obligando a su extracción total. Después de la extirpación, se inmovilizó el pie durante varios meses y se administraron antibióticos, logrando controlar la infección y cicatrizar la herida. A pesar de la ausencia del tendón, la paciente mostró una mejoría progresiva en la función, y un año después caminaba sin cojera y podía realizar la elevación del talón. El ultrasonido reveló una estructura similar al tendón de Aquiles, aunque con cambios tendinopáticos, lo que sugiere una regeneración notable del tejido. Aunque se le ofreció una reconstrucción quirúrgica, la paciente decidió posponerla debido a su buena función actual. Este caso resalta la capacidad funcional que puede recuperarse incluso tras la pérdida total del tendón de Aquiles."
+        }
+    },
+    {
+        "article": "Una mujer de 47 años con antecedentes de CHB congénita se presentó con quejas de dolor en el cuello del lado izquierdo y dolor en el oído izquierdo. Aproximadamente 30 meses antes de la presentación, la paciente había notado una pequeña masa en el lado izquierdo de su cuello, que había aumentado gradualmente de tamaño. El dolor se localizó inicialmente en la región del cuello, pero se intensificó con el tiempo y se extendió al área del oído izquierdo.\nInicialmente, debido al dolor en el oído izquierdo, el paciente consultó a varios otorrinolaringólogos y fue tratado por un diagnóstico preliminar de otitis media. Sin embargo, a pesar de los tratamientos, el dolor persistió. Finalmente, un otorrinolaringólogo derivó al paciente para una ecografía, que reveló una masa en el lado izquierdo del cuello, lo que llevó a una derivación quirúrgica. Después de las evaluaciones iniciales, se solicitó una angiografía por TC, que reveló una masa de forma ovalada que medía 30 por 50 mm en la bifurcación de la arteria carótida izquierda, lo que sugiere un CBT tipo II de Shamblin.\n\nEvaluaciones cardiovasculares preoperatorias\nDada la historia del paciente de CHB congénita, se realizó una evaluación cardiovascular preoperatoria exhaustiva. Esto incluyó un electrocardiograma (ECG) de 12 derivaciones, que confirmó la presencia de CHB con un ritmo de escape ventricular estable. Se realizó una ecocardiografía transtorácica para evaluar la estructura y función cardiaca, revelando una función sistólica ventricular normal sin evidencia de anormalidades estructurales. Además, se obtuvo una consulta de cardiología para evaluar la aptitud del paciente para la cirugía y optimizar el manejo perioperatorio.\n\nConsideraciones anestésicas\nDebido a la CHB congénita del paciente y al potencial de inestabilidad hemodinámica durante la cirugía, se formuló un plan anestésico detallado. El paciente fue clasificado como estado físico III de la Sociedad Estadounidense de Anestesiología (ASA). Preoperativamente, se le colocó un marcapasos externo temporal para garantizar un control adecuado de la frecuencia cardíaca y se le insertó un catéter arterial para el monitoreo continuo de la presión arterial. La inducción de la anestesia se realizó utilizando una combinación de etomidato (0,3 mg/kg) y fentanilo (2 μg/kg) para minimizar las fluctuaciones hemodinámicas. El mantenimiento se logró con sevoflurano (1-2 %) y rocuronio (0,6 mg/kg) para la relajación muscular. Los parámetros hemodinámicos, incluida la frecuencia cardíaca, la presión arterial y la saturación de oxígeno, se controlaron de forma continua. Además, se le colocó un catéter venoso central para monitorear la presión venosa central y administrar medicamentos vasoactivos si fuera necesario. El equipo de anestesia mantuvo una comunicación estrecha con el equipo quirúrgico para abordar de forma inmediata cualquier cambio hemodinámico intraoperatorio.\n\nEnfoque quirúrgico\nEl paciente fue sometido a cirugía el 19 de mayo de 2024, después de la localización precisa de la TCC mediante angiografía por TC. El enfoque quirúrgico se eligió en base a la clasificación de Shamblin tipo II, que indica un encasamiento parcial de las arterias carótidas. Dada la proximidad del tumor a estructuras neurovasculares críticas, incluidos los nervios vago e hipogloso, se consideró que el enfoque quirúrgico abierto era el más apropiado para garantizar una resección completa y minimizar las complicaciones.\nTras la inducción de la anestesia general, se colocó al paciente en posición supina con el cuello extendido y rotado hacia la derecha. Se realizó una incisión oblicua paralela al músculo esternocleidomastoideo izquierdo, que se extendía desde la apófisis mastoidea hasta la escotadura esternal. Tras la incisión de la piel y la disección del platisma, se expuso con cuidado la vaina carotídea. Se identificaron la arteria carótida común y su bifurcación en las arterias carótidas internas y externas. Se observó el tumor, de 30 × 50 mm, en la bifurcación carotídea y se diseccionó con cuidado de los tejidos circundantes.\n\nManobras y precauciones específicas\n1.\nSe aplicaron pinzas vasculares temporales en las arterias carótidas internas y externas para controlar el flujo sanguíneo durante la disección del tumor. Esto minimizó el sangrado y proporcionó un campo quirúrgico despejado.\n2.\nSe utilizó neuromonitorización intraoperativa para evaluar la integridad de los nervios vago e hipogloso. La retroalimentación continua garantizó que las estructuras neurales se preservaran durante la disección.\n3.\nEl tumor se separó cuidadosamente de las arterias carótidas y las estructuras neurales circundantes, mediante una combinación de disección aguda y roma. Se logró la hemostasis mediante cauterización bipolar y pinzas quirúrgicas para minimizar el sangrado.\n4.\nEl marcapasos externo se monitoreó activamente durante todo el procedimiento para garantizar un ritmo cardíaco estable. El equipo de anestesia estaba preparado para administrar atropina o epinefrina si se producía una bradicardia o hipotensión significativas.\n2.5. Manejo postoperatorio\nTras asegurarse de que no había hemorragia activa y restablecer el flujo sanguíneo, se devolvieron los tejidos a su posición original y se cerró la herida en múltiples capas. Se aplicó un vendaje apropiado. La cirugía se completó sin complicaciones y con un sangrado mínimo en 2 h y 10 min. El paciente fue trasladado a la UCI vascular para una estrecha monitorización.\nDespués de la operación, se controló al paciente en la UCI durante 24 horas y, más tarde, se le trasladó a la planta general tras mejorar su estado clínico. El marcapasos externo se retiró el día 1 después de la operación, ya que el paciente mantenía un ritmo de escape ventricular estable. El paciente fue dado de alta en buenas condiciones generales el día 3 después de la operación, sin quejas específicas.\n2.6. Seguimiento y resultados a largo plazo\nEl examen histopatológico confirmó el diagnóstico definitivo de TCC en la paciente. Se realizaron evaluaciones de seguimiento a las 2 semanas, 1 mes, 6 meses y 1 año posteriores a la cirugía para evaluar los resultados quirúrgicos y cardíacos. En cada visita, la paciente se sometió a un ECG de 12 derivaciones para monitorear el CHB congénito, que permaneció sin cambios durante todo el período de seguimiento. Se repitió la ecocardiografía transtorácica a los 6 meses y un año, sin deterioro de la función cardíaca y con una función sistólica ventricular estable.\n\nPara evaluar el impacto de la extirpación del tumor en la función cardiaca, se realizó un análisis de la variabilidad de la frecuencia cardiaca (VFC) antes de la operación y a los 6 meses después de la misma. El análisis de la VFC antes de la operación demostró una reducción de la actividad parasimpática, probablemente debido a la compresión del nervio vago por el tumor. El análisis de la VFC después de la operación mostró una mejora significativa del tono parasimpático, lo que sugiere que la extirpación del tumor alivió la compresión del nervio vago y restauró la función autónoma normal.\nAsimismo, el paciente manifestó que el dolor en el cuello y en el oído había desaparecido por completo después de la cirugía, sin que se produjera una reaparición de los síntomas durante el período de seguimiento. Se realizaron estudios de imagen, que incluyeron ultrasonido Doppler y angiografía por TAC, a los 6 meses y al año, que no mostraron evidencia de reaparición del tumor o complicaciones vasculares.\n",
+        "gold_summary": "Describimos el caso de una mujer de 47 años con antecedentes de dolor en el cuello izquierdo y en el oído, acompañado por una masa en el cuello que había ido aumentando gradualmente durante 2,5 años. Después de las evaluaciones iniciales y de múltiples diagnósticos diferenciales, la angiografía por TC reveló una masa ovalada de 30 × 50 mm en la bifurcación carotídea izquierda, lo que confirmó un CCT tipo II de Shamblin. Las evaluaciones preoperatorias demostraron CHB congénita en el electrocardiograma y la ecocardiografía. La paciente se sometió a una resección completa del tumor con todas las precauciones necesarias, incluida la colocación temporal de un marcapasos y un cuidadoso seguimiento.\n",
+        "synthetic_summary": {
+            "B1": "Una mujer de 47 años tenía dolor en el cuello y en el oído izquierdo. También tenía una bolita en el cuello que creció poco a poco. Los doctores hicieron estudios y encontraron un tumor cerca de una arteria importante. La operaron con mucho cuidado y usaron un marcapasos para cuidar su corazón. Después de la cirugía, la mujer mejoró y el dolor desapareció.",
+            "B2": "Una mujer de 47 años tenía dolor en el cuello y oído izquierdo, con una masa que creció por 2 años y medio. Un examen especial llamado angiografía por tomografía mostró un tumor de 30 × 50 mm en una arteria importante del cuello. Este tumor se llama CBT tipo II. La paciente también tenía un problema del corazón desde su nacimiento, confirmado con un electrocardiograma y ecocardiografía, que son pruebas del corazón. Antes de la cirugía, le pusieron un marcapasos temporal para controlar su ritmo cardíaco. La operación fue cuidadosa para no dañar nervios ni vasos cercanos y lograron sacar el tumor sin problemas. Después, el dolor desapareció y no hubo señales de que el tumor regresara. El seguimiento mostró que su corazón funcionaba bien y que mejoró la función nerviosa afectada.",
+            "B3": "Una mujer de 47 años con bloqueo cardíaco completo (CHB) congénito presentó dolor progresivo en el cuello y oído izquierdo, junto con una masa creciente en el cuello durante 30 meses. Inicialmente tratada por otitis media sin mejoría, una ecografía y angiografía por tomografía computarizada (TC) identificaron un tumor carotídeo tipo II de Shamblin en la bifurcación de la arteria carótida izquierda. Antes de la cirugía, se realizó una evaluación cardiovascular completa que confirmó el CHB y una función cardíaca normal. Durante la operación, se usó un marcapasos externo temporal y neuromonitorización para proteger nervios importantes, logrando una resección completa del tumor sin complicaciones. En el postoperatorio, la paciente mostró una recuperación favorable, con desaparición del dolor y estabilidad cardíaca. El seguimiento a un año evidenció la ausencia de recurrencia tumoral y mejoría en la función del nervio vago, reflejada en una recuperación del tono parasimpático. Este caso destaca la importancia de un manejo multidisciplinario cuidadoso en pacientes con condiciones cardíacas congénitas sometidos a cirugía vascular compleja."
+        }
+    },
+    {
+        "article": "Una mujer de 19 años de edad acudió al servicio de urgencias de nuestro hospital con una queja principal de dos días de historia de cefalea, acompañada de náuseas recurrentes, vómitos y fiebre de un día. En el ingreso, su examen físico reveló una fiebre alta de 39.1°C, presión arterial elevada de 189/120 mmHg y una frecuencia cardíaca de 148 latidos por minuto. Los resultados de laboratorio indicaron un recuento de glóbulos blancos elevado de 14.77×10^9/L y un recuento de neutrófilos de 13.55×10^9/L, lo que sugiere una posible infección o respuesta inflamatoria. Se administró un tratamiento empírico inicial con antibióticos debido a la sospecha de infección, pero sus síntomas persistieron. Dados sus signos vitales anormales, marcadores inflamatorios elevados y falta de mejora de los síntomas, la paciente fue admitida para una evaluación diagnóstica adicional y transferida a la unidad de cuidados intensivos para una estrecha monitorización. Un año antes, la paciente había presentado síntomas similares y se le diagnosticó miocarditis en un hospital local en base a los hallazgos clínicos en ese momento. Durante esa hospitalización, también se le diagnosticó hipertensión y se le prescribieron medicamentos antihipertensivos. Sin embargo, después del alta, la paciente no se adhirió al tratamiento antihipertensivo prescrito y no controló regularmente su presión arterial. Además, es notable que su padre tenía antecedentes de muerte súbita inexplicable.\n\nPara investigar la etiología subyacente de los síntomas del paciente, se realizó una tomografía computarizada (TC) de tórax. De forma incidental, esta exploración reveló una masa suprarrenal izquierda con densidad de tejido blando, que medía 43 mm × 36 mm. No se observaron hallazgos patológicos en las exploraciones de TC de cabeza y tórax. El electrocardiograma demostró taquicardia sinusal con un intervalo PR acortado y ondas P altas y puntiagudas en las derivaciones II, III y aVF. La ecocardiografía transtorácica no reveló ninguna anomalía significativa.\n\nEn el segundo día de ingreso, el paciente mostró niveles crecientes de péptido natriurético cerebral (BNP) y troponina I (TnI). El cardiólogo diagnosticó provisionalmente al paciente con miocarditis de etiología incierta, basándose en la presentación clínica, los biomarcadores cardiacos elevados (BNP y TnI) y los hallazgos del electrocardiograma de apoyo. Se inició el tratamiento con metilprednisolona (0,25 g diarios) para abordar la posible inflamación miocárdica debida a la sospecha de miocarditis. Se administraron furosemida (20 mg cada 12 horas) y espironolactona (20 mg cada 12 horas) como diuréticos para controlar la retención de líquidos y reducir la carga de trabajo cardiaco. Se prescribió perindopril amlodipina (10 mg: 5 mg diarios) como inhibidor de la enzima convertidora de la angiotensina y bloqueador del canal del calcio para controlar la presión arterial y reducir la poscarga. Se usó tartrato de metoprolol (25 mg cada 12 horas) para controlar la frecuencia cardiaca y disminuir la demanda de oxígeno miocárdico, mientras que se administró esmolol (0,2 g/hora por infusión intravenosa), un bloqueador beta de acción corta, para controlar la frecuencia cardiaca aguda adicional debido a la taquicardia sinusal. Debido a la preocupación por una posible infección, se agregó moxifloxacina como terapia antibiótica empírica.\n\nDada la presentación del paciente con una masa suprarrenal e hipertensión, el endocrinólogo recomendó una evaluación de la relación aldosterona/renina, cortisol plasmático, catecolaminas plasmáticas y catecolaminas urinarias de 24 horas, junto con sus metabolitos. En posición supina, los niveles de catecolaminas plasmáticas y urinarias estaban marcadamente elevados (Tabla 1), incluyendo dopamina plasmática a 524,5 pmol/L, norepinefrina a 83975 pmol/L y epinefrina a 10579,3 pmol/L. Además, los niveles urinarios de 24 horas mostraron adrenalina libre a 4368,89 nmol/24 horas, norepinefrina libre superior a 12697,60 nmol/24 horas, normetaneprina a 8312 nmol/24 horas, metaneprinas a 4078 nmol/24 horas y ácido vanilmandélico a 58,1 mg/24 horas. Estos hallazgos apoyaron un diagnóstico clínico de feocromocitoma. En el quinto día posterior al ingreso, se interrumpió la terapia glucocorticoide y se sustituyó perindopril amlodipina con terazosin para un control más dirigido de la presión arterial.\n\nUna tomografía computarizada abdominal mejorada confirmó una masa suprarrenal izquierda, muy sugestiva de feocromocitoma. Además, después de obtener el consentimiento informado, se realizó una secuenciación del exoma completo, que reveló una mutación sin sentido heterocigótica, c.1900T > C: p. Cys634Arg, en el gen RET, que conduce a una sustitución de cisteína por arginina en el codón 634. Esta mutación levantó sospechas de un síndrome de neoplasia endocrina múltiple, lo que impulsó una evaluación adicional de las glándulas tiroides y paratiroides. La ecografía Doppler en color de la tiroides identificó una masa hipoecoica que medía 6 mm × 4 mm en el lóbulo tiroideo izquierdo, y se observó una leve elevación en los niveles de calcitonina. No se detectaron anormalidades significativas adicionales.\n\nA medida que la condición del paciente mejoró gradualmente, los niveles de cortisol en plasma y ACTH volvieron a la normalidad. El paciente fue dado de alta con una prescripción de tartrato de metoprolol (100 mg cada 12 horas) e hidrocloruro de ivabradina (5 mg cada 12 horas) para el tratamiento en el hogar. Tres meses después, después de lograr un estado clínico estable, el paciente se sometió a una resección del tumor suprarrenal izquierdo, que medía 50 mm × 40 mm × 30 mm. El análisis inmunohistoquímico confirmó una tinción positiva para Vim, CD56, Syn, CgA y NSE, con S-100 positivo en las células de Sertoli, mientras que CKpan, CD10, MART-1/Melan-A y Melan-A fueron negativos. El índice Ki67 fue del 1 %, lo que llevó a un diagnóstico definitivo de feocromocitoma suprarrenal. El paciente fue dado de alta sin más medicamentos y desde entonces se le ha dado seguimiento regular postoperatorio sin recurrencia de síntomas. Durante un seguimiento postoperatorio de 15 meses, el paciente exhibió hipercalcinotemia persistente leve con un tamaño de nódulo tiroideo estable, mientras que los niveles de PTH y calcio en suero mostraron un aumento progresivo (Tabla 2). Se realizó una gammagrafía paratiroidea adicional utilizando 99mTc-MIBI, y la conclusión fue un resultado negativo para el adenoma paratiroideo.\n",
+        "gold_summary": "Reportamos el caso de una mujer de 19 años que presentó feocromocitoma sin experimentar una crisis, a pesar de tener una masa suprarrenal significativa y someterse a un tratamiento glucocorticoide de alta dosis. Las pruebas genéticas revelaron una mutación de sentido erróneo heterocigótica en el gen RET (c.1900T > C: p. Cys634Arg), asociada con MEN2A. La evaluación endocrina adicional identificó un nódulo tiroideo con niveles de calcitonina levemente elevados, pero niveles normales de electrolitos y hormona paratiroidea. Durante un seguimiento postoperatorio de 15 meses, la paciente exhibió hipercalcitonemia persistente leve con tamaño de nódulo tiroideo estable, mientras que la PTH y los niveles de calcio sérico mostraron un aumento progresivo. Se realizó una gammagrafía paratiroidea adicional utilizando 99mTc-MIBI, que arrojó un resultado negativo para el adenoma paratiroideo.\n",
+        "synthetic_summary": {
+            "B1": "Una joven de 19 años tuvo dolor de cabeza, fiebre y vómitos. Le encontraron una masa en una glándula llamada suprarrenal, que produce hormonas. Los médicos descubrieron que tenía un tumor llamado feocromocitoma. También encontraron un cambio en un gen que puede causar problemas en otras glándulas. Después de una operación, la joven mejoró y sigue siendo revisada para cuidar su salud.",
+            "B2": "Una mujer de 19 años llegó al hospital con dolor de cabeza, vómitos y fiebre, además de presión arterial muy alta y taquicardia. Los análisis mostraron signos de infección y una masa en la glándula suprarrenal izquierda. Se sospechó una miocarditis (inflamación del corazón) y se inició tratamiento con medicamentos para controlar la presión y la frecuencia cardíaca. Las pruebas hormonales revelaron niveles muy altos de catecolaminas, lo que indicó un feocromocitoma, un tumor que produce hormonas. Se confirmó con una cirugía para quitar el tumor. Además, se encontró una mutación genética relacionada con un síndrome que afecta varias glándulas endocrinas. Tras la operación, la paciente mejoró y sigue en control médico para vigilar otros posibles problemas hormonales.",
+            "B3": "Una mujer de 19 años acudió al hospital con cefalea, náuseas, vómitos y fiebre, además de hipertensión severa y taquicardia. Los análisis mostraron una infección o inflamación, y se sospechó miocarditis, por lo que se inició tratamiento con glucocorticoides, diuréticos y control de la presión arterial. Sin embargo, una tomografía reveló una masa en la glándula suprarrenal, y los niveles elevados de catecolaminas confirmaron el diagnóstico de feocromocitoma, un tumor que produce hormonas que elevan la presión. Se identificó una mutación genética en el gen RET, vinculada al síndrome de neoplasia endocrina múltiple tipo 2A, lo que llevó a evaluar la tiroides, donde se encontró un pequeño nódulo con aumento leve de calcitonina. Tras estabilizar su estado, la paciente fue sometida a cirugía para extirpar el tumor suprarrenal, con confirmación patológica de feocromocitoma. En el seguimiento de 15 meses, persistió una ligera hipercalcitonemia y aumento progresivo de la hormona paratiroidea y calcio en sangre, aunque sin evidencia de adenoma paratiroideo. Este caso resalta la importancia de un diagnóstico integral y seguimiento en enfermedades endocrinas complejas."
+        }
+    },
+    {
+        "article": "Una refugiada etíope embarazada de 39 años (Gravida 3 Para 2+0) fue derivada a nuestro departamento de urgencias de medicina interna en el Hospital Universitario de Gadarif, Gadarif State, Sudán, con hinchazón generalizada progresiva, falta de aire y fatiga durante 6 semanas y una revisión sistémica sin importancia. La paciente fue admitida en el sitio de admisión de casos críticos y su historia, tomada con la ayuda de un intérprete de idiomas más tarde en la admisión, reveló un episodio remoto inicialmente no revelado de tres convulsiones tónico-clónicas generalizadas no provocadas hace 21 años que se trataron tradicionalmente. Sin embargo, no había antecedentes de traumatismo craneal o antecedentes familiares de convulsiones. El examen general de la paciente reveló un PWS del lado izquierdo que involucraba la división oftálmica del nervio trigémino. Sin embargo, este hallazgo se perdió inicialmente en la inspección pero luego fue confirmado por el cónyuge de la paciente para estar presente desde el nacimiento. La paciente también estaba muy pálida y tenía derrames pleurales bilaterales, hepatomegalia blanda e hinchazón bilateral de las extremidades inferiores.\n\nLas investigaciones iniciales revelaron un nivel de hemoglobina de 8,84 g/dl. Por lo tanto, se diagnosticó insuficiencia cardíaca debido a anemia y se trató a la paciente en consecuencia. Sin embargo, ocho días después de su ingreso, la paciente había desarrollado aproximadamente seis episodios de convulsiones tónico-clónicas focales a bilaterales que respondieron bien a la fenitoína, pero que dejaron a la paciente en un estado comatoso profundo con un GCS de tres. Fue posteriormente admitida en la unidad de cuidados intensivos (UCI) y se le insertó un tubo nasogástrico para ayudarla con su nutrición y administración de fármacos. Además, para evitar más convulsiones, se le inició un tratamiento con comprimidos de carbamazepina de 200 mg administrados a través del tubo nasogástrico.\n\nSe retrasó una tomografía computarizada (TC) sin contraste del cerebro para el día posterior a la estabilización, ya que solo había una máquina de tomografía computarizada en el estado de Gadarif y funcionaba de forma intermitente debido a la falta de un número suficiente de técnicos radiólogos. La tomografía computarizada reveló calcificaciones corticales en la parte posterior del área parietal izquierda, lo que planteó el diagnóstico diferencial de SWS. En consecuencia, se realizó un examen físico de repetición, que mostró la presencia de una lesión plana de color rojo púrpura en la frente y el ojo. Al interrogar al cónyuge, se confirmó la presencia de esta lesión y que no había cambiado desde el nacimiento, lo que nos ayudó a descartar el diagnóstico de una mancha salmón, ya que esta lesión no se desvaneció, por lo que se diagnosticó como PWS. Además, no tenía características de megalencefalia, síndrome de malformación capilar que por lo general incluye un gran tamaño de la cabeza o del cerebro, problemas en las articulaciones y malformaciones capilares en la piel. Tampoco tenía hipertrofia de extremidades, anomalías del drenaje linfático o excrecencias óseas o de tejidos blandos que sugieran el síndrome de Klippel-Trenaunay-Weber. Por lo tanto, en función de los hallazgos de la tomografía computarizada y la presentación típica, llegamos a la conclusión del diagnóstico de SWS.\n\nDos días después de ingresar en la UCI, la paciente experimentó un cambio fluctuante en su estado de conciencia y una nueva aparición de hemiparesia contralateral (contralateral al SPW), así como afasia y labilidad emocional. Desafortunadamente, cuatro días después de ingresar en la UCI, la paciente empezó a experimentar sangrado vaginal; por ello, se consultó al departamento de obstetricia y ginecología y se descubrió que la paciente tenía un embarazo no viable (28 semanas + 1 día) y se realizó una inducción sin incidentes. Durante el mismo período, la paciente se volvió combativa y poco cooperativa, lo que llevó a que se la inmovilizara físicamente. Tres días después, la paciente desarrolló nuevos ataques focales bilaterales que comenzaron como episodios mioclónicos faciales y, tras consultar con el departamento de neurología, se aumentó la dosis de carbamazepina de la paciente a 1000 mg diarios, lo que ayudó a prevenir la recurrencia de los ataques. Cabe mencionar que, en su segundo trimestre y antes de recibir el resultado de la tomografía computarizada, se exploró un diagnóstico de eclampsia, pero sus constantes lecturas de presión arterial con una presión sistólica superior a la normal de 139 la mayoría de los días y una presión diastólica con un máximo de 97 mmHg y un rango bajo de proteinuria, así como la ausencia de características sistémicas como deterioro renal o hepático, excluyeron este diagnóstico. Después de alcanzar el diagnóstico de SW, se puso en juego un enfoque multidisciplinario; por ello, se realizó una consulta oftalmológica para descartar glaucoma. Sin embargo, la paciente estaba muy irritable y era difícil realizar un examen de fondo de ojo. Además, la paciente fue trasladada a la sala de medicina interna tras la estabilización.\n",
+        "gold_summary": "Presentamos el caso de una refugiada de 39 años, no diabética y no hipertensa, que inicialmente presentó insuficiencia cardiaca debido a anemia, por lo que recibió transfusiones de sangre. Más adelante, al ingresar, desarrolló convulsiones múltiples focales bilaterales, irritabilidad severa, afasia y hemiplejía derecha, lo que motivó su ingreso a la UCI. Un examen y un historial médico repetidos revelaron una mancha de vino de Oporto ocular izquierda leve que inicialmente pasó desapercibida y un historial remoto de convulsiones no provocadas 20 años atrás. Las imágenes revelaron calcificaciones parietales y confirmaron el diagnóstico de SWS. Por lo tanto, se adoptó un enfoque multidisciplinario para comprender plenamente el diagnóstico de la paciente y determinar una estrategia de tratamiento, que incluyó consultas con los departamentos de neurología, oftalmología, otorrinolaringología y fisioterapia. Se logró un control exitoso de las convulsiones mediante la administración de fenitoína IV durante 3 días y el aumento gradual de la carbamazepina oral a 1 g diario a través de una sonda nasogástrica. Lamentablemente, debido a la falta de personal o recursos, no se pudieron realizar otras evaluaciones importantes para pacientes con SWS, como evaluaciones avanzadas de neuroimagen, psiquiátricas, de cirugía plástica y neurocirugía, así como revisiones dentales.\n",
+        "synthetic_summary": {
+            "B1": "Una mujer embarazada llegó al hospital con hinchazón y cansancio. También tenía dificultad para respirar y una mancha roja en la cara. Desde niña, ella tenía convulsiones. Los doctores dijeron que tenía síndrome de Sturge-Weber. Este problema afecta la piel y el cerebro. Le dieron medicinas para controlar las convulsiones y la cuidaron bien.",
+            "B2": "Una mujer refugiada de 39 años llegó al hospital con hinchazón, fatiga y dificultad para respirar. Tenía anemia grave y fue tratada por insuficiencia cardíaca. Luego, presentó convulsiones repetidas y perdió la conciencia, por lo que fue ingresada en cuidados intensivos. Una tomografía mostró calcificaciones en el cerebro, y al revisar su piel, se encontró una mancha roja en la frente que estaba desde su nacimiento. Esto llevó al diagnóstico de síndrome de Sturge-Weber, una enfermedad que afecta los vasos sanguíneos del cerebro y la piel. La paciente recibió medicamentos para controlar las convulsiones y se consultó a varios especialistas. Aunque mejoró, no se pudieron hacer algunos exámenes importantes por falta de recursos.",
+            "B3": "Una mujer refugiada de 39 años fue ingresada en un hospital en Sudán con hinchazón generalizada, dificultad para respirar y fatiga. Inicialmente se diagnosticó insuficiencia cardíaca causada por anemia, pero luego desarrolló convulsiones tónico-clónicas recurrentes que la llevaron a la unidad de cuidados intensivos. Tras una tomografía computarizada, se observaron calcificaciones cerebrales que, junto con la presencia de una mancha roja en la frente y el ojo izquierdo desde su nacimiento, permitieron diagnosticar el síndrome de Sturge-Weber (SWS), una enfermedad rara que afecta vasos sanguíneos y puede causar convulsiones y problemas neurológicos. La paciente presentó además hemiparesia, afasia y cambios en el estado de conciencia. Se descartó eclampsia como causa de sus síntomas durante el embarazo, que resultó no viable y fue inducido. El tratamiento incluyó fenitoína y un aumento progresivo de carbamazepina para controlar las convulsiones, y se implementó un abordaje multidisciplinario con neurología, oftalmología y otros especialistas. Sin embargo, la falta de recursos limitó la realización de estudios más avanzados y evaluaciones adicionales necesarias para el manejo completo del SWS."
+        }
+    },
+    {
+        "article": "Una paciente de 69 años se quejaba de una pérdida progresiva de la visión. Sus padres eran primos hermanos. Le habían diagnosticado retinitis pigmentosa 27 años antes. La paciente había fumado durante 15 años. Tenía antecedentes de hiperlipidemia e hipotiroidismo.\n\nTras una evaluación oftalmológica completa, se determinó que el paciente tenía una agudeza visual corregida (AVC) de contar los dedos a 5’ y 3’ en los ojos derecho e izquierdo, respectivamente. La retinoscopia mostró una refracción de –1.00 + 0.50×70 y –2.00 + 1.00×5 en los ojos derecho e izquierdo, respectivamente. El paciente tenía discos ópticos pálidos con una atrofia profunda extensa de la mácula central, hiperplasia del pigmento epitelial y otras áreas de atrofia multifocal en el ojo derecho. Además, el paciente tenía atrofia macular en el ojo izquierdo. En la imagen de autofluorescencia del fondo del ojo (FAF) del paciente, había evidencia de una hipoautofluorescencia central de la mácula, con una extensión centrífuga difusa desde su centro hasta su periferia.\n\nLa tomografía de coherencia óptica macular (OCT) determinó que el espesor macular promedio era de 191 µM y 193 µM en los ojos derecho e izquierdo, respectivamente. El volumen macular era de 6.9 mm3 y 7.0 mm3 en los ojos derecho e izquierdo, respectivamente. No se encontró edema macular, quistes o fluido subretinal en ninguno de los ojos.\n\nUna prueba de campo visual reveló que el paciente tenía desviaciones medias de –23.75 dB y –24.56 dB en los ojos derecho e izquierdo, respectivamente. Las desviaciones estándar de patrón fueron de +3.69 dB y +4.69 dB en los ojos derecho e izquierdo, respectivamente. Los resultados de un electrorretinograma de campo completo (ERG) mostraron una respuesta normal de bastones y una respuesta de conos disminuida, bilateralmente. Por estas razones, se realizó un diagnóstico clínico de enfermedad STGD1.\n\nSe encontró una variante patogénica homocigótica intrónica c.5714+5G>A del gen ABCA4 tras el análisis de secuenciación y eliminación/duplicación utilizando secuenciación de próxima generación (Invitae Corporation, San Francisco, California). Tenía seis variantes adicionales de significación incierta (VUS) en los genes CACNA1F, EYS, KCNV2, KLHL7, MKKS y USH2A.\n",
+        "gold_summary": "Una paciente de 69 años de edad se presentó en la clínica quejándose de una pérdida progresiva de la visión. La evaluación oftálmica fue notable para una mejor agudeza visual corregida de contar los dedos a 5' en el ojo derecho y 3' en el ojo izquierdo. Las imágenes revelaron una atrofia profunda y extensa de la mácula central, una hiperplasia del pigmento epitelial y otras áreas de atrofia multifocal en el ojo derecho. Además, las imágenes de autofluorescencia del fondo de la mácula mostraron una hipoautofluorescencia central con expansión bilateral a la periferia en ambos ojos. Un electrorretinograma de campo completo mostró una respuesta normal de los bastones, con una respuesta disminuida de los conos, bilateralmente. Las pruebas genéticas fueron positivas para una mutación inotrópica homocigótica en el gen ABCA4 de la variante c.5714+5G>A.\n",
+        "synthetic_summary": {
+            "B1": "Una mujer de 69 años tenía problemas para ver mejor con el tiempo. Sus ojos mostraban daño en una parte llamada mácula, que ayuda a ver bien. Las pruebas dijeron que algunas células de sus ojos no funcionaban bien. También encontraron un cambio en un gen que puede causar esta enfermedad en la vista. Los doctores la están cuidando para ayudarla.",
+            "B2": "Una mujer de 69 años tenía pérdida progresiva de la visión desde hace varios años. Su visión era muy baja y solo podía contar los dedos cerca de sus ojos. Las imágenes del fondo del ojo mostraron daño en la mácula, la parte central de la retina. Había áreas con desgaste y cambios en el color de la retina. La prueba eléctrica de la retina mostró que las células bastones funcionaban bien, pero las conos, que ayudan a ver colores y detalles, estaban dañadas. El análisis genético encontró una mutación en el gen ABCA4, que causa la enfermedad de Stargardt y afecta la visión central. Aunque no había inflamación ni líquido, el daño en la mácula explica su pérdida visual. Por eso, es importante hacer un seguimiento para controlar la enfermedad y buscar tratamientos.",
+            "B3": "Una mujer de 69 años consultó por pérdida progresiva de la visión, con antecedentes familiares consanguíneos y diagnóstico previo de retinitis pigmentosa. La evaluación oftalmológica mostró una agudeza visual muy reducida, con atrofia macular profunda y multifocal, además de hiperplasia del pigmento epitelial en el ojo derecho. Las imágenes de autofluorescencia revelaron una hipoautofluorescencia central que se extendía hacia la periferia en ambos ojos. La tomografía de coherencia óptica indicó un espesor macular disminuido sin signos de edema o líquido. El electrorretinograma evidenció una función normal de los bastones, pero una respuesta disminuida de los conos en ambos ojos. El análisis genético identificó una variante patogénica homocigótica en el gen ABCA4 (c.5714+5G>A), asociada con enfermedad de Stargardt tipo 1 (STGD1). Este caso resalta la importancia de combinar hallazgos clínicos, imagenológicos y genéticos para un diagnóstico preciso, lo que podría orientar futuros tratamientos o asesoramiento genético."
+        }
+    },
+    {
+        "article": "Un niño de 19 meses de edad fue admitido en el departamento de urgencias porque se cayó de la trona en la que comía. Esta caída ocurrió en un aparente bienestar, sin la presencia de signos o síntomas anticipados. Primero, se cayó sobre su glúteo y luego se golpeó la cabeza (occipucio) contra el suelo. Vomitó (tres episodios) y estaba muy irritable. Su frecuencia respiratoria y cardíaca eran >60 respiraciones y >150 latidos por minuto, mientras que la saturación de oxígeno era <80%. Tras el examen físico, el niño estaba hidratado y consciente, pero irritable. Más importante aún, observamos retracciones subcostal y, al auscultar, disminución de los sonidos respiratorios en la parte basal izquierda del tórax. El paciente fue ventilado con un balón de AMBU conectado a una fuente de oxígeno y monitorizado con un oxímetro de pulso. A pesar de nuestra intervención, la saturación de oxígeno cayó por debajo del 70% y cuanto más ventilábamos, más caía la saturación. La ecografía pulmonar mostró la ausencia de las típicas líneas A y la consolidación del pulmón, que se visualizó directamente como un parénquima sólido. Sobre la base del mal estado clínico, el paciente se sometió a intubación orotraqueal con un tubo endotraqueal con manguito. Después de que el bebé se estabilizó, se sometió a una tomografía computarizada (TC) de tórax que mostró una atelectasia completa del pulmón izquierdo con una interrupción del bronquio izquierdo principal a 12 cm de la bifurcación bronquial. Se sospechó un FBA ya que la madre también declaró que el bebé en los días anteriores había tenido un ataque de tos intenso y desapareció en 24 h sin ningún tratamiento. Por lo tanto, se realizó una broncoscopia rígida y se encontró y se eliminó rápidamente una almendra de 2 cm de diámetro en el bronquio izquierdo principal.\n\nEl paciente nunca había consumido antes almendras u otros frutos secos y, en esta ocasión, ingirió la almendra por accidente.\n\nEl bebé mostró una mejora clínica progresiva y, después de 24 horas, se le retiró la sonda y se le dio de alta de la unidad de cuidados intensivos para ser ingresado en la sala de pediatría general durante unos días, con una recuperación gradual y total de la función respiratoria.\n",
+        "gold_summary": "Describimos el caso de un niño de 19 meses que llegó a la sala de urgencias por un traumatismo en la cabeza. La evaluación clínica, sin embargo, reveló una dificultad respiratoria grave inexplicable que requería intubación traqueal. Después de nuestra evaluación, planteamos la hipótesis de que la dificultad respiratoria grave determinó un estado alterado de conciencia con el consiguiente traumatismo en la cabeza. Los hallazgos radiológicos levantaron la sospecha de aspiración de cuerpo extraño por la presencia de una atelectasia de todo el pulmón izquierdo. La tomografía computarizada mostró una interrupción abrupta del bronquio principal a 12 mm del casco. La siguiente broncoscopia identificó una amígdala de 2 cm.\n",
+        "synthetic_summary": {
+            "B1": "Un niño de 19 meses se cayó y se golpeó la cabeza. Tenía problemas para respirar y su oxígeno estaba bajo. Los médicos encontraron que tenía un fruto seco atorado en un pulmón. Lo sacaron con un tubo especial y el niño mejoró mucho. Después de unos días, pudo respirar bien y salió del hospital.",
+            "B2": "Un niño de 19 meses llegó al hospital tras caerse de la trona y golpearse la cabeza. Al principio parecía estar bien, pero vomitó varias veces y estaba muy irritable. Tenía dificultad para respirar y su oxígeno en sangre estaba muy bajo. Al examinarlo, notaron que su pulmón izquierdo no funcionaba bien. Una tomografía mostró que su bronquio izquierdo, una vía aérea del pulmón, estaba bloqueado. La madre recordó que el niño había tenido tos fuerte días antes. Al hacer una broncoscopia, que es mirar dentro de las vías respiratorias, encontraron y sacaron una almendra que el niño había tragado sin querer. Después de esto, el niño mejoró y pudo salir de la unidad de cuidados intensivos. Su respiración volvió a la normalidad con el tiempo.",
+            "B3": "Un niño de 19 meses fue llevado a urgencias tras una caída desde una trona, inicialmente sin síntomas graves, pero luego presentó vómitos e irritabilidad. A su llegada, mostró dificultad respiratoria severa con saturación de oxígeno críticamente baja y disminución de los sonidos respiratorios en el pulmón izquierdo. A pesar de la ventilación asistida, la oxigenación empeoró, por lo que se realizó una intubación orotraqueal para asegurar la vía aérea. La tomografía computarizada de tórax evidenció atelectasia completa del pulmón izquierdo y una interrupción en el bronquio principal, sugiriendo la presencia de un cuerpo extraño. La broncoscopia confirmó y permitió la extracción de una almendra de 2 cm alojada en el bronquio izquierdo. La madre recordó un episodio previo de tos intensa, probablemente relacionado con la aspiración accidental del alimento. Tras la extracción, el paciente mostró mejoría progresiva y fue trasladado a pediatría para continuar su recuperación. Este caso resalta la importancia de considerar la aspiración de cuerpos extraños en niños con dificultad respiratoria súbita, incluso cuando la causa inicial parezca diferente."
+        }
+    },
+    {
+        "article": "Una mujer nulípara de 35 años con antecedentes de infertilidad se presentó en la consulta externa. Informó de un antecedente de tres años de dolor sordo cíclico en el ombligo. El dolor se asoció a un nódulo umbilical que sangraba durante la menstruación. Cabe destacar que el dolor empeoraba durante la menstruación y se aliviaba con analgésicos. La paciente también informó de dismenorrea, menorragia y dispareunia. La paciente se había insertado un DIU de cobre 3 años antes y había estado usando Zinnia P (levonorgestrel y etinilestradiol) durante los últimos 3-4 meses para intentar aliviar el dolor. Su historial ginecológico previo no fue notable y tenía un ciclo menstrual regular. No había antecedentes médicos, quirúrgicos o sociales de importancia.\nAl examinarla, sus constantes vitales eran estables. Se observó una hinchazón hiperpigmentada (3 × 2 cm) en el ombligo al examinar el abdomen. La hinchazón era firme, inmóvil, no dolorosa, no reductible y no estaba ligada a estructuras subyacentes. Una resonancia magnética abdominal reveló una masa de mejora mal definida que medía 3 × 4 × 6 cm ubicada a lo largo de la pared abdominal anterior derecha y estaba conectada a un tracto sinusal que se extendía hacia la región suprapúbica, pero no se comunicaba con la cavidad peritoneal, hallazgos que sugieren endometriosis. El diagnóstico diferencial fue amplio, incluida una hernia umbilical, granuloma, cicatriz queloide, neoplasias malignas nodulares y anomalías embriológicas. Además, se observaron lesiones anexiales bilaterales, eran hiperintensas con áreas hipointensas focales y restricciones variables, la lesión del lado derecho medía 1,6 × 1,7 cm y la lesión del lado izquierdo medía 2,0 × 0,8 cm, hallazgos consistentes con endometriosis ovárica bilateral.\n\nSe programó al paciente para la extirpación quirúrgica del nódulo umbilical. La muestra se envió para un examen histopatológico. Los resultados revelaron una epidermis normal con glándulas endometriales dispersas y estroma dentro de la dermis. La fotomicroscopía resaltó la presencia de estroma endometrial y tejido graso subcutáneo. Esta morfología es consistente con la endometriosis. La recuperación postoperatoria de la paciente fue sin incidentes, y se la consideró apta para el alta el día 2 postoperatorio. Recibió asesoramiento sobre su fertilidad futura y la posibilidad de FIV, riesgo de recurrencia y se programó una visita de seguimiento en dos semanas. Se le inició con Dienogest, Visanne y un anticonceptivo oral combinado para el tratamiento de la endometriosis. Se la ha monitoreado clínicamente cada cuatro semanas, y no se han observado síntomas o signos de recurrencia local durante el período de seguimiento de 8 meses. Cabe destacar que, a pesar de que su condición permaneció estable después del tratamiento, no concibió en el transcurso del año siguiente.\n",
+        "gold_summary": "Presentamos el caso de una mujer nulípara de 35 años de edad del norte de Tanzania con un historial de infertilidad de 10 años. Al presentarse, la paciente informó de un historial de tres años de dolor cíclico asociado a una masa umbilical. Una resonancia magnética abdominal reveló una masa mal definida que se intensificaba y medía 3 × 4 × 6 cm, localizada a lo largo de la pared abdominal anterior derecha. La masa estaba conectada a un tracto sinusal que se extendía hacia la región suprapúbica, pero no mostraba comunicación con la cavidad peritoneal, lo que sugería endometriosis. Además, las lesiones anexiales bilaterales demostraron señales hiperintensas con áreas hipointensas focales y restricciones variables, consistentes con endometriomas ováricos bilaterales. La paciente se sometió a la extirpación de la masa umbilical y el examen histopatológico confirmó el diagnóstico de endometriosis umbilical primaria. A pesar de su condición estable después del tratamiento, no concibió durante el año siguiente.\n",
+        "synthetic_summary": {
+            "B1": "Una mujer de 35 años tenía dolor en el ombligo que empeoraba en su periodo. Tenía un bulto que sangraba durante la regla. Los médicos hicieron una imagen y vieron que tenía endometriosis, que es cuando un tejido parecido al de la regla crece fuera del útero. Le quitaron el bulto con cirugía y confirmó la enfermedad. Después del tratamiento, se sintió bien, pero no pudo quedar embarazada en un año.",
+            "B2": "Una mujer de 35 años tenía problemas para quedar embarazada y dolor en el ombligo. El bulto en su ombligo sangraba y dolía más durante la menstruación. La resonancia mostró una masa en la pared del abdomen y lesiones en los ovarios. Estos hallazgos indicaban endometriosis, que es cuando tejido parecido al del útero crece fuera de él. Le quitaron el bulto con cirugía y confirmaron que era endometriosis en el ombligo. Después, recibió tratamiento hormonal para controlar la enfermedad. Aunque mejoró y no tuvo nuevos síntomas por ocho meses, no pudo quedar embarazada en un año. Por eso, le recomendaron opciones para tratar su fertilidad en el futuro.",
+            "B3": "Una mujer de 35 años con infertilidad y dolor cíclico en el ombligo acudió a consulta, presentando un nódulo umbilical que sangraba durante la menstruación. La resonancia magnética mostró una masa en la pared abdominal derecha conectada a un tracto sinusal, sin comunicación con la cavidad peritoneal, lo que sugería endometriosis. Además, se detectaron lesiones en ambos ovarios compatibles con endometriomas. La paciente fue sometida a cirugía para extirpar el nódulo, y el análisis histopatológico confirmó endometriosis umbilical primaria. Tras la operación, recibió tratamiento hormonal y seguimiento regular, sin signos de recurrencia en ocho meses. Sin embargo, a pesar de la estabilidad clínica, no logró concebir en el año siguiente. Este caso destaca la importancia de considerar la endometriosis en pacientes con dolor umbilical cíclico y problemas de fertilidad, y la necesidad de un manejo integral que incluya cirugía, tratamiento médico y asesoramiento reproductivo."
+        }
+    },
+    {
+        "article": "Presentamos a un recién nacido de 15 minutos de edad, hijo de una madre para-cuatro que no recordaba su LNMP pero que afirmaba haber estado amenorreica durante los últimos nueve meses. Su madre había recibido atención prenatal en el centro de salud cercano dos veces y no había tenido incidentes. Sin embargo, no se le había realizado un ultrasonido obstétrico temprano. Por lo demás, no tiene antecedentes de enfermedades crónicas como diabetes mellitus e hipertensión. Durante su embarazo actual, no tuvo fiebre, dolor de cabeza o visión borrosa. Nunca había usado ninguna droga aparte de sulfato ferroso durante este embarazo. Sus hijos anteriores están todos sanos y vivos. A su llegada a nuestro hospital, tuvo una hemorragia vaginal de dos horas de duración. Posteriormente, fue admitida con un diagnóstico de embarazo de tercer trimestre más multigravida más hemorragia anteparto secundaria a desprendimiento de placenta más oligohidramnios severo más presentación de nalgas.\n\nEn el examen pélvico, tenía un sangrado vaginal activo. Se le realizó una ecografía obstétrica al llegar. En consecuencia, la edad gestacional era de 34 semanas, la placenta estaba en el fondo con un coágulo retroplacentario y el líquido amniótico había disminuido significativamente con un único bolsillo más profundo de 1,5 cm. El peso fetal estimado era de 2,4 kg y presentación de nalgas. Otras investigaciones de la madre son grupo sanguíneo AB+, VDRL=negativo, RBS=120 mg/dL, en CBC, glóbulos blancos=9000, hemoglobina=11 gm/dL, plaqueta=180,000 y neutrófilo=60%.\n\nTras obtener el consentimiento informado por escrito, se realizó una cesárea de urgencia por las indicaciones ya mencionadas para extraer un neonato vivo de 2,01 kg de peso con puntuaciones de 5 y 6 en las pruebas de Apgar en el primer y el quinto minuto, respectivamente.\n\nEl neonato no lloró y fue reanimado durante cinco minutos. Luego fue trasladado a la unidad de cuidados intensivos neonatales para recibir atención e investigaciones adicionales. Al llegar, el neonato estaba en dificultad respiratoria. Sus signos vitales eran de 160 latidos por minuto, 70 respiraciones por minuto, temperatura de 33,4 grados centígrados y saturación de oxígeno del 60%. La fontanela anterior del neonato medía 2 cm por 2 cm y tenía micrognatia y cuello corto. En el sistema respiratorio, había retracciones intercostales y subcostales, respiración trabajosa y gruñidos. En el examen precordial, se escucharon bien los sonidos s1 y s2, no había murmullo ni ritmo de galope. En el sistema musculoesquelético, había acortamiento bilateral de las extremidades superiores, la extremidad inferior derecha estaba normal en posición y estructura, la pierna izquierda giraba hacia adentro (flexión mediolateral) en la articulación de la rodilla y la estructura del pie era normal. En el examen neurológico, estaba letárgico, el tono era normotónico en la extremidad inferior derecha y el reflejo de Moro era difícil de evaluar. La investigación de laboratorio mostró grupo sanguíneo = A+, CRP = reactivo, WBC = 30,000, neutrófilos = 54%, linfocitos = 21.1%, HGB = 8 gm/dL y plaquetas = 150,000. Se realizó una radiografía que mostró un acortamiento extremo de las extremidades superiores. La extremidad inferior izquierda estaba internamente girada. La ecocardiografía fue normal. Con una evaluación de prematuro tardío (34-36 semanas por puntaje de Ballard) más bajo peso al nacer más apropiado para la edad gestacional más focomelia más asfixia perinatal más sepsis neonatal temprana, se manejó con apoyo de oxígeno, fluido de mantenimiento e antibióticos intravenosos. El neonato murió después de tres días de hospitalización.\n",
+        "gold_summary": "Presentamos a un neonato de 15 minutos de vida, hijo de una madre para-cuatro que no recordaba su LNMP pero que afirmaba estar amenorreica desde hacía nueve meses. El modo de parto fue por cesárea para extraer al neonato vivo, que pesaba 2,01 kg y tenía puntuaciones APGAR de 5 y 6 en el primer y quinto minutos, respectivamente. El neonato no lloró y fue reanimado durante cinco minutos. Después se lo trasladó a la unidad de cuidados intensivos neonatales para continuar con el tratamiento y las investigaciones. Sus signos vitales eran: pulso de 160 latidos por minuto, frecuencia respiratoria de 70 respiraciones por minuto, temperatura de 33,4 grados centígrados y saturación de oxígeno del 60%. La fontanela anterior del neonato medía 2 cm por 2 cm y tenía micrognatia y cuello corto. En el sistema respiratorio había retracciones intercostales y subcostales, respiración trabajosa y gruñidos. En el sistema musculoesquelético había acortamiento bilateral de la extremidad superior, la pierna derecha tenía una posición y estructura normales, la pierna izquierda giraba hacia adentro (se doblaba hacia la parte media) en la articulación de la rodilla y el pie tenía una estructura normal.\n",
+        "synthetic_summary": {
+            "B1": "Un bebé nació por cesárea porque su mamá tuvo problemas en el embarazo. El bebé pesó poco y no lloró al nacer, por eso lo ayudaron a respirar. Tenía dificultades para respirar y partes de sus brazos eran más cortas de lo normal. También una pierna estaba doblada hacia adentro. Lo cuidaron en un hospital, pero estaba muy débil.",
+            "B2": "Un recién nacido de 15 minutos llegó tras una cesárea urgente por problemas en el embarazo. Pesó 2,01 kg y tuvo bajas puntuaciones en la prueba de Apgar, que mide su estado al nacer. Fue reanimado y llevado a cuidados intensivos porque tenía dificultad para respirar y baja temperatura. Su saturación de oxígeno también era muy baja. Tenía la cabeza normal, pero la mandíbula era pequeña y el cuello corto. Además, sus brazos eran muy cortos y una pierna estaba girada hacia adentro, aunque el pie estaba normal. Los exámenes mostraron infección y anemia, una falta de glóbulos rojos. A pesar del tratamiento con oxígeno y antibióticos, el bebé falleció a los tres días. Este caso resalta la importancia del control prenatal temprano para detectar riesgos.",
+            "B3": "Se presentó un recién nacido de 15 minutos, hijo de una madre con embarazo complicado por desprendimiento placentario, oligohidramnios severo y presentación de nalgas. La cesárea de urgencia permitió extraer un bebé vivo, con peso de 2,01 kg y puntuaciones Apgar bajas que requirieron reanimación inmediata. Al ingreso a la unidad de cuidados intensivos neonatales, el neonato mostraba dificultad respiratoria, temperatura baja y saturación de oxígeno reducida. Se observaron características físicas como micrognatia (mandíbula pequeña) y cuello corto, además de acortamiento severo de las extremidades superiores y deformidad en la rodilla izquierda, mientras que la pierna derecha y el pie izquierdo eran normales. Los exámenes revelaron signos de infección, anemia y elevación de glóbulos blancos. Se diagnosticó prematuridad tardía, focomelia (malformación de las extremidades), asfixia perinatal y sepsis neonatal temprana. A pesar del tratamiento con oxígeno, líquidos y antibióticos, el neonato falleció tras tres días hospitalizado. Este caso resalta la importancia de un control prenatal adecuado y la vigilancia perinatal para detectar y manejar complicaciones graves que pueden afectar la supervivencia neonatal."
+        }
+    },
+    {
+        "article": "Mujer de 61 años con antecedente de carcinoma escamocelular de cuello uterino estadio FIGO IIB, diagnosticado en febrero de 2019, tratada en un hospital privado de cuarto nivel de atención, donde se ofrece cuidado ambulatorio y hospitalario para pacientes con condiciones complejas oncológicas y no oncológicas. Al momento del diagnóstico se realizó histerectomía radical con linfadenectomía pélvica, que descartó compromiso nodal. El tratamiento complementario de primera línea incluyó seis ciclos de quimioterapia con cisplatino, y braquiterapia y radioterapia, alcanzando una respuesta tumoral completa. En 2021, tras detectarse una recaída aislada en la región ilíaca, mediante tomografía, se administró cisplatino y 30 sesiones de radioterapia, logrando una nueva respuesta completa. En septiembre de 2022, una tomografía reveló otra recaída con compromiso del parametrio izquierdo, el uréter y la cadena ilíaca ipsilateral, por lo que se decidió primera línea para enfermedad recurrente con carboplatino, paclitaxel y pembrolizumab. Durante este régimen, la paciente presentó hipersensibilidad al platino en el quinto ciclo, gestionada con un protocolo de desensibilización, continuando con el pembrolizumab. En septiembre de 2023, ante la progresión en imágenes de una masa retroperitoneal única, debido a la falta de respuesta óptima, se inició gemcitabina, según guías de manejo, segunda línea de enfermedad recurrente, recibiendo una dosis acumulada de 8.544 mg/m2 hasta enero de 2024. Sin embargo, desarrolló síntomas de isquemia digital en manos, por lo que el tratamiento fue suspendido tras la segunda dosis del tercer ciclo, acumulando 11.744 mg/m2 de gemcitabina.\n\nEn febrero de 2024, la paciente ingresó al servicio de urgencias del mismo hospital donde era valorada de forma ambulatoria, remitida por oncología debido a progresión de los síntomas en sus extremidades. La paciente refería dolor lancinante y coloración azulada en dedos de manos; al examen físico se evidencia necrosis en el segundo dedo de la mano derecha, coloración ocre y fenómeno de Raynaud en los dedos de la mano izquierda. Las extremidades inferiores mostraban edema grado II en el miembro inferior izquierdo y pulsos presentes. Los estudios para autoinmunidad y vasculitis resultaron negativos, incluyendo anticuerpos anticitoplasma de neutrófilos (ANCAS), anticuerpos antinucleares (ANAS), anticuerpos antidesoxirribonucleicos (anti-DNA), cardiolipinas, prueba confirmatoria de anticoagulante lúpico, perfil de anticuerpos contra antígenos nucleares extraíbles (ENAS), anticuerpos contra proteinasa 3, anticuerpos antimieloperoxidasa y anticuerpos dirigidos contra la ADN topoisomerasa I (antiSCL). Además, el factor reumatoide y los niveles de complemento 3 (C3) y complemento 4 (C4) también fueron normales. Prueba serológica para sífilis (VDRL - Venereal Disease Research Laboratory) negativa, ecocardiograma transtorácico sin hallazgos de un foco cardioembólico.\n\nSe inició anticoagulación con heparina de bajo peso molecular, junto con ácido acetilsalicílico, estatina y un calcioantagonista. El equipo de cirugía de mano realizó amputación del segundo dedo de la mano derecha, confirmando necrosis por licuefacción en el estudio histopatológico.\n\nDurante el posoperatorio se agregó sildenafil al tratamiento, logrando una mejoría progresiva en los signos de isquemia de los dedos restantes. Durante la hospitalización, la paciente presenta complicación por sangrado vaginal masivo, requiriendo embolización de arterias uterinas.\n\nEl servicio de reumatología aplicó la escala de causalidad de Naranjo para determinar el papel de la gemcitabina en la vasculitis, con un puntaje de 8, lo que indicó que el medicamento probablemente provocó la necrosis.\n\nPosteriormente, a los 20 días de ingreso a hospitalización desarrolló deterioro neurológico, sin hallazgos significativos en la tomografía de cráneo. Evaluada por cuidados paliativos, su estado funcional se clasificó con un Barthel de 0/30, ECOG de 4 y Karnofsky de 10 %, con pronóstico de vida inferior a tres semanas según el Índice Pronóstico de Paciente (PPI: + 6 puntos). En consenso con la familia, se suspendieron estudios adicionales y se implementó un manejo paliativo integral. La paciente falleció tras el alta hospitalaria.",
+        "gold_summary": "Oaciente de 61 años tratada con gemcitabina (11.744 mg/m² acumulados) por enfermedad metastásica, en un hospital general de cuarto nivel, privado, no oncológico, donde venía siendo manejada de forma ambulatoria. Presentó necrosis distal del segundo dedo de la mano derecha, por lo que se suspendió el tratamiento y se requirió amputación de este dedo. Se realizó una búsqueda en Embase, Medline y Lilacs. Se buscaron estudios de reporte y series de casos sobre necrosis distal inducida por gemcitabina. Se extrajeron datos de dosis, diagnóstico y tratamiento.",
+        "synthetic_summary": {
+            "B1": "Una mujer de 61 años con cáncer recibió un medicamento llamado gemcitabina. Después de varias dosis, tuvo dolor y cambio de color en los dedos de las manos. Un dedo se dañó mucho y tuvieron que cortarlo. Los médicos pararon el medicamento y le dieron otros tratamientos para mejorar. Al final, su salud empeoró y recibió cuidados para estar tranquila.",
+            "B2": "Una mujer de 61 años con cáncer de cuello uterino recibió varios tratamientos, incluyendo gemcitabina para una recaída. Después de acumular una dosis alta de este medicamento, presentó dolor y cambio de color en los dedos de las manos, con necrosis (muerte del tejido) en uno de ellos. Se suspendió la gemcitabina y se amputó el dedo afectado. Los exámenes descartaron otras causas como enfermedades autoinmunes o infecciones. El equipo médico inició tratamientos para mejorar la circulación y controlar el daño. Sin embargo, la paciente empeoró, con problemas neurológicos y un estado general muy deteriorado. Finalmente, se decidió cuidar su bienestar con un manejo paliativo, y falleció poco después. Este caso sugiere que la gemcitabina pudo causar la necrosis en sus dedos.",
+            "B3": "Una mujer de 61 años con cáncer cervical avanzado recibió múltiples tratamientos, incluyendo cirugía, quimioterapia y radioterapia, logrando inicialmente respuestas completas. Tras varias recaídas, se le administró gemcitabina como segunda línea, acumulando una dosis considerable que posteriormente se asoció con isquemia digital y necrosis en un dedo de la mano. Esta complicación motivó la suspensión del fármaco y la amputación del dedo afectado, descartándose otras causas autoinmunes o vasculares mediante estudios complementarios. Durante la hospitalización, se implementó un tratamiento combinado con anticoagulantes, vasodilatadores y manejo quirúrgico, lo que permitió cierta mejoría en la circulación de los dedos restantes. No obstante, la paciente presentó complicaciones graves, como un sangrado vaginal masivo y deterioro neurológico, que condujeron a un enfoque paliativo integral. Finalmente, falleció poco después del alta hospitalaria. Este caso destaca la importancia de identificar efectos adversos poco frecuentes pero graves asociados a la gemcitabina, para ajustar el tratamiento y proporcionar un cuidado adecuado en pacientes con enfermedad avanzada."
+        }
+    },
+    {
+        "article": "Mujer de 53 años, con antecedente de AR de 15 años de diagnóstico en tratamiento con metotrexato, resto de antecedentes sin datos de importancia, la cual presentó cuadro clínico 8 meses antes (de acudir a nuestro servicio) con astenia y adinamia de forma progresiva, palidez de tegumentos, alzas térmicas no cuantificadas de predominio nocturno, pérdida de peso no intencionada de 15 kg en 6 meses aproximadamente, sin valoración ni seguimiento médico, a lo que se agregó 3 meses después disnea de grandes a medianos esfuerzos, y cuya sintomatología se agudizó 5 días antes (de acudir a nuestro servicio), aunada a sangrado de tubo digestivo alto (STDA), caracterizado por evacuaciones melénicas abundantes, 3 evacuaciones en 24 horas, hematemesis en 2 ocasiones, escasas, sin causa aparente. La paciente negó consumo de analgésicos no esteroideos (AINE) y tuvo aumento de volumen en la pierna izquierda, la cual le dolía y tenía la presencia de edema y eritema, con limitación a la movilidad, motivo por el cual acudió a (nuestro) Servicio de Urgencias.\n\nDurante su hospitalización con anemia severa sin repercusión hemodinámica, se transfundieron 3 concentrados eritrocitarios sin complicaciones aparentes. Después de su estabilización, se inició abordaje diagnóstico para síndrome consuntivo. Por el cuadro clínico de miembro inferior izquierdo se hizo US Doppler que evidenció trombosis venosa profunda. Se realizó ultrasonido de abdomen por probable hepatopatía por metotrexato, el cual reportó infartos esplénicos y hepáticos, así como presencia de cambios crónicos hepáticos. Se llevó a cabo endoscopía con evidencia de varices pequeñas, sin sangrado activo. Debido a la sospecha de neoplasia por los antecedentes y el cuadro clínico de la paciente, se llevó a cabo tomografía axial simple y contrastada de tórax y abdomen y se encontró hepatoesplenomegalia y múltiples conglomerados ganglionares axilares, mediastinales y paraaórticos que sugerían actividad infiltrativa. Esto se valoró por el Servicio de Cirugía General para la realización de biopsia de ganglio axilar derecho, donde se reportó proliferación neoplásica de células linfoides. Posteriormente se valoró por el Servicio de Hematología de la unidad, se solicitaron estudios de laboratorio (cuadro I) y se realizó aspirado de médula ósea en el que se evidenciaron células plasmáticas displásicas y células reticulares, por lo cual se concluyó que había la presencia de infiltración linfoplasmocitaria. Con los antecedentes, el cuadro clínico y los estudios complementarios se diagnosticó LNH estadio IV y la paciente fue enviada a hospital de tercer nivel para realización de inmunohistoquímica, estadificación e inicio de tratamiento. En tercer nivel se identificó linfoma difuso de células B con inmunofenotipo B CD20 con sobrecrecimiento de células dendríticas, y la paciente fue valorada para inicio de tratamiento con quimioterapia.",
+        "gold_summary": "Mujer de 55 años con antecedente de AR que ingresó a un servicio de medicina interna por sangrado de tubo digestivo; presentó datos clínicos de trombosis venosa profunda en miembro pélvico izquierdo y síndrome consuntivo en estudio. Durante su abordaje se identificó con infartos esplénicos y hepáticos, así como múltiples conglomerados ganglionares, por lo que se practicó biopsia de ganglio axilar que reportó proliferación neoplásica de células linfoides y aspirado de médula ósea con presencia de infiltración linfoplasmocitaria, con lo que se determinó diagnóstico de linfoma no Hodgkin estadio IV. La paciente fue enviada a un hospital de tercer nivel para inicio de tratamiento.",
+        "synthetic_summary": {
+            "B1": "Una mujer de 53 años tenía cansancio, palidez y pérdida de peso. También sangraba por la boca y tenía dolor y hinchazón en una pierna. Los médicos encontraron coágulos en la pierna y cambios en el hígado y el bazo. Después de hacer pruebas, descubrieron que tenía un tipo de cáncer llamado linfoma. La enviaron a otro hospital para empezar su tratamiento.",
+            "B2": "Una mujer de 53 años con artritis reumatoide presentó cansancio, pérdida de peso y sangrado digestivo. También tuvo dolor, hinchazón y enrojecimiento en la pierna izquierda, que resultó ser una trombosis venosa profunda (coágulo en la vena). Se encontraron daños en el bazo y el hígado, además de ganglios inflamados en varias partes del cuerpo. La biopsia de un ganglio mostró células anormales, y el examen de médula ósea confirmó infiltración de células cancerosas. Con estos hallazgos, se diagnosticó un linfoma no Hodgkin en etapa avanzada. Por eso, la paciente fue enviada a un hospital especializado para recibir tratamiento con quimioterapia.",
+            "B3": "Una mujer de 53 años con artritis reumatoide de larga evolución presentó síntomas progresivos como fatiga, pérdida de peso y palidez, acompañados de sangrado digestivo alto y dolor con edema en la pierna izquierda. Durante su ingreso hospitalario, se detectó anemia severa y trombosis venosa profunda en la pierna afectada. Estudios por imágenes revelaron infartos en el bazo y el hígado, además de múltiples ganglios linfáticos agrandados en distintas regiones del cuerpo. La biopsia de un ganglio axilar mostró proliferación anormal de células linfoides, y el aspirado de médula ósea confirmó infiltración linfoplasmocitaria. Estos hallazgos permitieron diagnosticar un linfoma no Hodgkin en estadio IV. Por lo tanto, la paciente fue remitida a un hospital especializado para realizar estudios adicionales, confirmar el tipo específico de linfoma y comenzar el tratamiento con quimioterapia. Este caso subraya la importancia de una evaluación exhaustiva ante síntomas sistémicos y complicaciones como trombosis y sangrado, especialmente en pacientes con enfermedades autoinmunes que reciben inmunosupresores."
+        }
+    },
+    {
+        "article": "Un hombre de 56 años se presentó en el departamento de urgencias de nuestro hospital debido a una falta de aire repentina y un episodio de síncope mientras caminaba dentro de su casa. Se sometió a una prostatectomía laparoscópica asistida por robot para el carcinoma de próstata, 5 días antes de su presentación en el departamento de urgencias. Su curso postoperatorio en el hospital fue sin incidentes. En el departamento de urgencias, su presión arterial era de 94/54 mmHg, frecuencia cardiaca de 121 latidos por minuto, frecuencia respiratoria de 20 respiraciones por minuto, no tenía fiebre y su saturación de oxígeno era de 92% con 6 L por minuto de oxígeno a través de una cánula nasal. El examen cardiaco reveló S1S2, regular, taquicardia, sin murmullos/galopes/ruidos respiratorios. El examen respiratorio reveló ruidos respiratorios vesiculares normales bilaterales. Se observó que tenía edema de extremidad inferior izquierdo asimétrico. El electrocardiograma (ECG) reveló taquicardia sinusal, sin cambios en la onda ST-T. La troponina estaba levemente elevada a 0.120 ng/mL (rango de referencia: 0 a 0.020). La angiografía por tomografía computarizada (CTA) del tórax mostró embolia pulmonar bilateral extensa, con una gran carga de coágulos en ambas arterias pulmonares principales, evidencia de insuficiencia ventricular derecha aguda. El examen dúplex venoso mostró trombosis venosa profunda izquierda aguda. El ecocardiograma mostró fracción de eyección ventricular izquierda normal del 60% al 65%, movimiento septal anormal y aplanamiento del tabique interventricular, presión sistólica ventricular derecha de 49.7 mmHg, ventrículo derecho moderadamente dilatado, función ventricular derecha disminuida, excursión sistólica tricuspídea de 12.1 mm (normal 15 a 20 mm). Como la mayoría de la carga de coágulos era distal, no se consideró susceptible de extracción quirúrgica, ya que la cirugía reciente era una contraindicación importante para la trombólisis. El paciente comenzó con un goteo de heparina e inhaló óxido nítrico a 20 ppm junto con 40 mg de sildenafil oral cada 8 horas. Al día siguiente, el paciente estaba hemodinámicamente estable y su óxido nítrico inhalado se redujo. Repetir el ecocardiograma 48 horas desde la presentación inicial mostró un tamaño y función del ventrículo derecho mejorados. Su presión sistólica ventricular derecha disminuyó a 22.4 mmHg y su excursión sistólica tricuspídea mejoró a 17.8 mm. Recomendamos que continuara con sildenafil durante el mes siguiente después del alta junto con anticoagulación oral con un plan de seguimiento como paciente ambulatorio. El paciente dio su consentimiento por escrito para el tratamiento durante su hospitalización. El paciente y sus familiares estaban bien informados sobre el plan de atención completo y estuvieron de acuerdo con el plan de atención.\n\nMH - Insuficiencia cardiaca/*terapia farmacológica/etiología\nMH - Humanos\nMH - Hombre\nMH - Edad Media\nMH - Inhibidores de la fosfodiesterasa 5/*uso terapéutico\nMH - Embolismo pulmonar/*complicaciones\nMH - Agentes vasodilatadores/*uso terapéutico\nMH - Disfunción ventricular, derecha/terapia/etiología\n",
+        "gold_summary": "Paciente: Hombre, 56 años\n\nDiagnóstico final: Insuficiencia cardíaca derecha por embolia pulmonar\n\nSíntomas: síncope\n\nMedicación: —\n\nProcedimiento clínico: —\n\nEspecialidad: Cardiología\n\nSe trata de un informe de caso en el que se utilizó sildenafil como agente de rescate para lograr una mejora en el tamaño y la función del ventrículo derecho en un caso de inicio agudo de embolia pulmonar masiva con insuficiencia aguda del ventrículo derecho en el escenario en el que la terapia trombolítica sistémica estaba contraindicada.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre de 56 años tuvo dificultad para respirar y se desmayó en su casa. Esto pasó después de una operación en la próstata. Los doctores encontraron coágulos en sus pulmones y una parte del corazón derecho estaba dañada. Le dieron un medicamento llamado sildenafil y oxígeno especial. Después, su corazón mejoró y pudo seguir su tratamiento en casa.",
+            "B2": "Un hombre de 56 años tuvo dificultad para respirar y un desmayo cinco días después de una cirugía de próstata. En urgencias, su presión arterial estaba baja y su corazón latía rápido. Tenía hinchazón en una pierna y problemas en el corazón derecho, detectados por imágenes y ecocardiograma. Se encontró que tenía coágulos en los pulmones, lo que causó insuficiencia del ventrículo derecho. No se pudo hacer cirugía para quitar los coágulos por su operación reciente. Recibió tratamiento con heparina, óxido nítrico inhalado y sildenafil, un medicamento que ayuda a relajar los vasos sanguíneos. Después de dos días, su corazón mejoró y se le recomendó continuar el tratamiento con sildenafil y anticoagulantes en casa para evitar más coágulos.",
+            "B3": "Un hombre de 56 años presentó falta de aire súbita y un episodio de síncope cinco días después de una prostatectomía laparoscópica. En urgencias, mostró taquicardia, hipotensión y saturación de oxígeno baja, además de edema en la pierna izquierda. Las pruebas revelaron una embolia pulmonar bilateral extensa con insuficiencia ventricular derecha aguda y trombosis venosa profunda en la pierna afectada. Debido a la reciente cirugía, la trombólisis no fue una opción viable. Por lo tanto, se inició tratamiento con heparina, óxido nítrico inhalado y sildenafil oral, un medicamento que relaja los vasos sanguíneos. Tras 48 horas, el paciente mejoró notablemente en la función y tamaño del ventrículo derecho, con estabilización hemodinámica. Se recomendó continuar con sildenafil y anticoagulación oral tras el alta para mantener la recuperación. Este caso destaca el uso exitoso de sildenafil como terapia alternativa en embolia pulmonar masiva cuando la trombólisis está contraindicada, mostrando una mejora significativa en la función cardíaca derecha y un manejo cuidadoso del paciente postoperatorio."
+        }
+    },
+    {
+        "article": "Presentamos el caso de un hombre de 78 años con antecedentes conocidos de fibrilación auricular crónica, cardiopatía hipertensiva y miocardiopatía no isquémica. Tenía una reducción global de la fracción de eyección del ventrículo izquierdo del 40-45 %, y su ecocardiograma no mostraba anomalías significativas. El paciente había sido seguido en la clínica de cardiología ambulatoria, donde fue tratado por insuficiencia cardiaca crónica en estadio C del Colegio Americano de Cardiología (ACC) con síntomas de clase III de la Asociación del Corazón de Nueva York (NYHA). A pesar de varios cambios en sus diuréticos e intentos de controlar su estado de líquidos, ganó 40 libras de peso en un período de 3 meses, con un aumento significativo de la falta de aire. A medida que su descompensación de la insuficiencia cardiaca progresó, fue hospitalizado durante 8 días y tratado con furosemida intravenosa (IV). Debido a su clasificación de la NYHA y su ingreso al hospital por exacerbación de la insuficiencia cardiaca, se indicó y se realizó un monitoreo hemodinámico invasivo con implantación de CardioMEMS. La implantación de su CardioMEMS se realizó en Grand Blanc, Michigan, a una altitud de 837 pies con una presión atmosférica de 731.2 el 9 de abril de 2019. Las mediciones hemodinámicas iniciales del cateterismo cardiaco mostraron una presión sistólica PA de 45 mmHg, presión diastólica PA de 16 mmHg y una presión PA media de 30 mmHg. La presión auricular derecha fue de 21 mmHg, presión ventricular derecha de 44/17 mmHg y la presión media de la cuña pulmonar fue de 24 mmHg. El procedimiento se completó sin complicaciones y el paciente fue dado de alta el mismo día.\n\nTras la implantación de CardioMEMS, el paciente permaneció estable durante 4 semanas sin empeoramiento de los síntomas de insuficiencia cardiaca. Cumplió con las lecturas diarias de CardioMEMS con una PA media que osciló entre 27 y 31 mmHg, y una presión diastólica de PA de 17 a 21 mmHg. Estos hallazgos hemodinámicos globales fueron estables en comparación con los del momento de la implantación.\n\nEl paciente viajó a Denver, Colorado, durante cuatro días a una altitud de 5280 pies con una presión atmosférica de 596.8 atm el 5 de mayo de 2019. Las grabaciones del primer día de su visita mostraron un aumento de la presión sistólica de 44 mmHg a 73 mmHg, un aumento de la presión media de 30 mmHg a 53 mmHg y un aumento de la presión diastólica de 20 mmHg a 40 mmHg. Al mismo tiempo, notó un aumento significativo de la falta de aire y la hinchazón de las extremidades inferiores. No buscó atención médica, sino que se contactó con su cardiólogo primario en Michigan. Su oxígeno nasal de referencia se incrementó de 1 litro a 2 litros y su dosis de furosemida se duplicó de 40 mg diarios a dos veces al día. Afortunadamente, este tratamiento mejoró los síntomas del paciente y evitó la admisión hospitalaria. Debido a que se evitó la admisión hospitalaria, no se dispuso de valores de laboratorio, imágenes de diagnóstico y signos vitales clínicos.\n\nDurante su estancia hospitalaria de 4 días, sus presiones invasivas se mantuvieron altas, pero disminuyeron lentamente y se estabilizaron con una PA sistólica de 72 mmHg, una PA media de 49 mmHg y una PA diastólica de 35 mmHg el día previo a su regreso a Michigan. El quinto día, volvió a Michigan y sus mediciones de presión invasiva se normalizaron rápidamente, con una presión PA media de 29 mmHg y una presión PA diastólica de 20 mmHg. Ha seguido estando bien mientras estuvo en Michigan con diuréticos de mantenimiento continuos y un control diario de las presiones PA con su dispositivo CardioMEMS.\n\nMH - Envejecido\nMH - *Altitud\nMH - Monitoreo de presión arterial, ambulatorio\nMH - *Insuficiencia cardiaca/diagnóstico/etiología\nMH - Hospitalización\nMH - Humanos\nMH - Hombre\nMH - Arteria Pulmonar\n",
+        "gold_summary": "Presentamos el caso de un hombre de 78 años con una exacerbación de la insuficiencia cardiaca mientras viajaba a gran altitud. Se detectó un aumento de sus presiones arteriales pulmonares (PA) mediante su dispositivo CardioMEMS implantado. La comprensión del cambio esperado en los registros de presión de la PA ayudó a identificar una verdadera exacerbación de la insuficiencia cardiaca en nuestro paciente. Esto llevó a un cambio rápido en la terapia médica, que en última instancia evitó la hospitalización.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre de 78 años con problemas del corazón tenía un aparato llamado CardioMEMS para medir la presión en sus pulmones. Cuando viajó a un lugar alto, su presión subió mucho y se sintió muy cansado y con falta de aire. Su doctor cambió su medicina y mejoró sin ir al hospital. El aparato ayudó a ver el problema a tiempo y cuidar mejor su salud.",
+            "B2": "Un hombre de 78 años con insuficiencia cardiaca tenía un dispositivo llamado CardioMEMS. Este aparato mide la presión en las arterias pulmonares, que son vasos del corazón. Al viajar a una ciudad en altura, su presión pulmonar subió mucho. Entonces, tuvo más dificultad para respirar y sus piernas se hincharon. Gracias al dispositivo, su doctor ajustó su tratamiento con diuréticos y oxígeno. Así, evitó la hospitalización. Cuando volvió a su ciudad, la presión volvió a la normalidad y mejoró. Este caso muestra que el monitoreo continuo ayuda a tratar a tiempo cambios en pacientes con insuficiencia cardiaca.",
+            "B3": "Un hombre de 78 años con insuficiencia cardiaca crónica y un dispositivo CardioMEMS implantado para monitorear la presión arterial pulmonar (PA) presentó una descompensación durante un viaje a Denver, a gran altitud. Antes del viaje, sus presiones pulmonares se mantenían estables, pero al llegar a 5280 pies, se observó un aumento significativo en las presiones sistólica, media y diastólica de la PA, acompañado de empeoramiento de la falta de aire y edema en las piernas. Sin embargo, el paciente no requirió hospitalización porque, tras comunicarse con su cardiólogo, se ajustó su tratamiento con oxígeno y diuréticos, lo que mejoró sus síntomas. Al regresar a menor altitud, sus presiones pulmonares volvieron a valores normales. Este caso muestra cómo el monitoreo continuo con CardioMEMS permitió detectar y manejar a tiempo una exacerbación real de insuficiencia cardiaca relacionada con el cambio de altitud, evitando complicaciones mayores. Además, resalta la importancia de adaptar el tratamiento en pacientes con insuficiencia cardiaca que viajan a altitudes elevadas, ya que la presión atmosférica puede influir en la función cardiopulmonar. Por lo tanto, el seguimiento remoto y la comunicación rápida con el equipo médico fueron claves para el buen manejo del paciente."
+        }
+    },
+    {
+        "article": "Un hombre de 55 años, previamente sano, fue derivado al servicio de urgencias por su médico de cabecera, quejándose de una fiebre de 3 semanas de evolución, tos productiva, disnea y sibilancias. Tenía un historial de 80 paquetes-año de consumo de tabaco y un historial familiar positivo de cáncer de pulmón. Había sido tratado por su médico de cabecera con un ciclo de amoxicilina oral y prednisona oral, pero sus síntomas empeoraron. Cuando llegó al servicio de urgencias, su recuento de glóbulos blancos era de 16,4 × 109/L (rango normal: 4,0-10,0 × 109/L), el recuento de neutrófilos de 13,8 × 109/L (rango normal: 2,0-7,0 × 109/L), la proteína C reactiva era de 118 mg/L (normal: 0-5 mg/L) y el sodio sérico era de 112 mmol/L (rango normal: 136-145 mmol/L). Otros marcadores bioquímicos estaban dentro de los límites normales. Una radiografía de tórax mostró consolidación del lóbulo medio e inferior derecho con derrame pleural moderado asociado. Fue admitido y tratado como neumonía adquirida en la comunidad y el estudio confirmó el diagnóstico de SIADH.\n\nEl paciente empeoró a pesar de la administración intravenosa de piperacilina-tazobactam y de claritromicina oral, con empeoramiento de la consolidación en la repetición de la radiografía de tórax. El paciente fue trasladado a la unidad de cuidados intensivos y, posteriormente, se le realizó una intubación y ventilación. Una tomografía computarizada (TC) de su tórax reveló una masa hilar derecha con afectación mediastinal y adenopatía hilar derecha con consolidación de espacio aéreo extenso superpuesta. Una biopsia realizada durante la broncoscopia reveló células pequeñas, histológicamente monótonas, con núcleos ovoides oscuros. No se observaron nucleolos, y varias figuras mitóticas estaban presentes. Las células tienen un citoplasma estrecho y mal definido. La inmunohistoquímica realizada en las células tumorales mostró negatividad a CD45, AE1/AE3, positividad a TTF1. También se observaron sinapsina mínima focal y positividad a cromogranina A. Este perfil inmunohistoquímico fue consistente con un diagnóstico de cáncer de pulmón de células pequeñas.\n\nLa estadificación completa, que consistió en una tomografía computarizada del cerebro y tórax-abdomen-pelvis, confirmó una enfermedad en estadio extenso con metástasis suprarrenales. El estado funcional ECOG de la paciente era deficiente debido a una combinación de SCLC y dificultad respiratoria que requería ventilación artificial. Como las tasas de respuesta con quimioterapia en SCLC son generalmente altas, se inició un tratamiento quimioterápico doble en forma de carboplatino y etopósido mientras la paciente estaba intubada en la UCI.\n\nEl paciente respondió bien al tratamiento y fue extubado y trasladado a la sala de ventilación no invasiva. Una nueva tomografía computarizada de tórax después de 1 ciclo mostró una buena respuesta parcial al tratamiento.\n\nEn el día 3 del ciclo 2 de quimioterapia, la paciente desarrolló dolor en la parte inferior de la espalda y debilidad bilateral en las extremidades inferiores. El examen identificó paresia motora bilateral en las extremidades inferiores (grado 3 del Consejo de Investigación Médica [MRC]) y paresia sensorial. El examen sensorial reveló ausencia de tacto ligero, pinchazo, coordinación y propiocepción en las extremidades inferiores. El día 3 de etopósido se retrasó como resultado de los nuevos hallazgos neurológicos.\n\nSe realizaron un TAC cerebral, resonancia magnética (RM) cerebral y resonancia magnética (RM) de la columna para investigar los nuevos hallazgos neurológicos. Todos los resultados radiológicos fueron normales, sin evidencia de metástasis intracerebrales, accidente cerebrovascular, mielitis o enfermedad leptomeníngea. Además, no hubo evidencia radiográfica obvia de compresión de la médula espinal, ya sea por compresión extrínseca por depósito metastásico óseo o depósitos intramedulares o leptomeníngeos.\n\nDos días después, un examen neurológico de seguimiento reveló tetraplejía, MRC grado 0 en las extremidades superiores e inferiores. Todos los reflejos tendinosos profundos estaban ausentes. Los músculos de la cabeza y el cuello, la cognición y el habla no se vieron afectados, y el examen de los nervios craneales fue normal.\n\nLos análisis de sangre de rutina, incluida la proteína C reactiva y la velocidad de sedimentación de eritrocitos, fueron normales. Los análisis de sangre específicos, incluidos los de vitamina B12 en suero, folato, serología del VIH, serología de la enfermedad de Lyme, serología del virus de Epstein-Barr, serología de Brucella, anticuerpos tiroideos, pruebas de función tiroidea, ANCA, ENA, ANA y electroforesis de proteínas séricas, fueron negativos o normales. Se enviaron anticuerpos para las pruebas de sangre Hu, Ri y Yo, y todos fueron negativos. En este momento, se sospechó un diagnóstico de polineuropatía simétrica ascendente aguda motora y sensorial y se realizó una punción lumbar. Los resultados del líquido cefalorraquídeo (LCR) revelaron una proteína total elevada de 3.32 g/L (normal 0.15–0.45), y otros parámetros fueron normales, con una repetición 3 días después que mostró resultados similares. La citología del LCR fue negativa para la malignidad y el cultivo del LCR también fue negativo.\n\nLa electromiografía fue consistente con una polineuropatía difusa predominantemente motora; los potenciales sensoriales se conservaron, pero fueron de pequeña amplitud. Las conducciones motoras mostraron características axonales/desmielinizantes mixtas, que no eran típicas del síndrome de Guillain-Barré.\n\nSe realizaron estudios de electromiografía y conducción nerviosa para investigar la polineuropatía motora y sensorial aguda del paciente. Los estudios de conducción nerviosa revelaron lo siguiente:\n\n•Nervios motores:\n◦Las amplitudes del potencial de acción muscular compuesto (CMAP) se redujeron notablemente en los nervios tibial y cubital de forma bilateral (tibial: 1,2 mV; normal > 4 mV; cubital: 0,8 mV; normal > 3 mV).\n◦Las velocidades de conducción motora (MCV) se desaceleraron en los nervios tibial y cubital (tibial: 30 m/s; normal > 40 m/s; cubital: 34 m/s; normal > 50 m/s), lo que es coherente con la desmielinización.\n◦Las latencias motoras distales se prolongaron, con un patrón mixto axonal y desmielinizante.\n•Nervios sensoriales:\n◦Las amplitudes del potencial de acción nerviosa sensorial (SNAP) se conservaron, pero fueron de poca amplitud en los nervios surales y medianos (sural: 4 μV; normal > 10 μV; mediano: 6 μV; normal > 15 μV).\n◦Las velocidades de conducción sensorial (VCS) se encontraban dentro de los límites normales.\nLos hallazgos electrofisiológicos revelaron una polineuropatía predominantemente motora con características axonales y desmielinizantes mixtas, atípicas para los síndromes paraneoplásicos clásicos, que generalmente son predominantemente sensoriales y se caracterizan por la ausencia de SNAP.\n\nMientras tanto, mientras estas investigaciones estaban en curso, se inició al paciente con dexametasona intravenosa y 0.4 g/kg/día de inmunoglobulina intravenosa sin ninguna mejora sintomática.\n\n3. Resultados y seguimiento\nA pesar de una importante respuesta oncológica inicial a la quimioterapia, el estado neurológico del paciente se deterioró rápidamente. Después de 1 ciclo de carboplatino y etopósido, las imágenes confirmaron una respuesta parcial con una reducción en el tamaño del tumor. Sin embargo, el inicio de una polineuropatía motora y sensorial grave y ascendente condujo a un compromiso respiratorio. Esta disociación entre las respuestas oncológicas y neurológicas destaca la naturaleza agresiva y refractaria del SNP, incluso cuando el tratamiento del cáncer es efectivo. Aunque la dexametasona intravenosa y la inmunoglobulina intravenosa se administraron rápidamente, no lograron mejorar los resultados neurológicos.\n\nSe llevaron a cabo largas y repetidas discusiones multidisciplinares con el paciente y su familia sobre la admisión en la unidad de cuidados intensivos para recibir apoyo ventilatorio. El paciente estaba bien informado y consciente de que era poco probable que sus síntomas neurológicos fueran reversibles y, por lo tanto, optó por el mejor tratamiento de apoyo. El paciente falleció 3 semanas después de los síntomas iniciales. La decisión del paciente de rechazar el apoyo ventilatorio invasivo en favor de los cuidados paliativos pone de relieve las consideraciones éticas que rodean la calidad de vida en los síndromes paraneoplásicos de progresión rápida.\n",
+        "gold_summary": "Preocupaciones del paciente: Un hombre de 55 años con un historial de 80 años fumando presenta al hospital con un historial de 3 semanas de fiebres, tos productiva, disnea y sibilancias. No tenía comorbilidades significativas.\n\nDiagnóstico: Extensas investigaciones radiológicas revelaron una gran masa en el hilum derecho que comprimía el bronquio inferior derecho con depósitos suprarrenales metastásicos. Las investigaciones bioquímicas confirmaron el síndrome de secreción inadecuada de la hormona antidiurética, y la histología identificó un CPCP.\n\nIntervenciones: A pesar de iniciar una quimioterapia combinada con carboplatino y etopósido, el paciente desarrolló parálisis motora progresiva y pérdida sensorial en el transcurso de 4 días, lo que derivó en un diagnóstico de polineuropatía motora y sensorial aguda paraneoplásica.\n\nResultados: Su estado empeoró rápidamente y falleció 14 días después de la aparición de los síntomas debido a una insuficiencia respiratoria, lo que pone de relieve la agresividad de los síndromes paraneoplásicos.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre de 55 años con tos y fiebre por tres semanas fue al hospital. Le encontraron un tumor en el pulmón y le dieron quimioterapia. Luego, empezó a perder fuerza en las piernas y brazos, y no podía sentir bien. Aunque el tumor mejoró, su cuerpo se puso muy débil y falleció poco tiempo después. Esto muestra que algunas enfermedades pueden ser muy graves y difíciles de tratar.",
+            "B2": "Un hombre de 55 años con un largo historial de fumar acudió al hospital con fiebre, tos y dificultad para respirar durante tres semanas. Las pruebas mostraron una masa en su pulmón derecho y metástasis en las glándulas suprarrenales, además de un síndrome llamado SIADH, que afecta el equilibrio de líquidos en el cuerpo. Fue diagnosticado con cáncer de pulmón de células pequeñas y comenzó quimioterapia. Sin embargo, desarrolló rápidamente debilidad y pérdida de sensibilidad en sus piernas, que empeoró hasta afectar sus brazos. Los estudios indicaron una polineuropatía, un daño en los nervios, relacionada con el cáncer. A pesar del tratamiento con esteroides e inmunoglobulinas, su condición neurológica empeoró y falleció pocas semanas después. Este caso muestra lo agresivos que pueden ser los efectos secundarios del cáncer, incluso cuando el tumor responde al tratamiento.",
+            "B3": "Un hombre de 55 años con antecedentes de tabaquismo prolongado consultó tras tres semanas de fiebre, tos y disnea progresiva. Las imágenes radiológicas revelaron una masa pulmonar derecha con metástasis en glándulas suprarrenales, y el análisis histopatológico confirmó un carcinoma pulmonar de células pequeñas. Se inició quimioterapia combinada, pero el paciente desarrolló rápidamente una polineuropatía motora y sensorial paraneoplásica, manifestada por parálisis progresiva y pérdida sensitiva en extremidades. A pesar del tratamiento con corticosteroides e inmunoglobulinas intravenosas, no se observó mejoría clínica, y su estado neurológico se deterioró hasta provocar insuficiencia respiratoria. Finalmente, el paciente decidió recibir cuidados paliativos y falleció semanas después. Este caso ilustra la agresividad y el rápido empeoramiento que pueden presentar los síndromes paraneoplásicos, incluso cuando el tumor responde inicialmente a la terapia oncológica. Además, resalta la importancia de considerar las decisiones éticas relacionadas con la calidad de vida en pacientes con complicaciones neurológicas graves asociadas al cáncer."
+        }
+    },
+    {
+        "article": "El paciente presentado firmó el Consentimiento Informado y se cumplieron los demás principios éticos, respetando la Resolución 466/12 del Consejo Nacional de Ética en Investigación. Este informe de caso fue aprobado por el Comité de Ética en Investigación de la Universidad Federal de São Paulo (UNIFESP), bajo el dictamen número 4.455.365.\n\nEl paciente, de 66 años de edad y sexo masculino, acudió a una consulta de otorrinolaringología por presentar disfagia tipo atragantamiento con sólidos y reflujo nasal de alimentos desde hacía un año. Había sufrido un accidente automovilístico 13 años atrás y era diabético. Se le realizó una videoendoscopia de la deglución (VED), en la que se observó, en la evaluación estructural, una protuberancia de la pared posterior de la hipofaringe con residuo salival sobre la lesión. En la evaluación funcional, tras la ingesta de alimentos sólidos, se observó una restricción de la retroflexión de la epiglotis, una limitación de la elevación de la laringe y un reflujo nasal de alimentos, con gran cantidad de residuo alimentario por encima de la lesión, en la pared posterior de la faringe. En la prueba de maniobras posturales, empeoró la disfagia al extender el cuello y mejoró la eliminación al flexionar la cabeza. Se le realizó una tomografía computarizada (TC) de la columna cervical, solicitada para evaluar la naturaleza de la lesión, que mostró la presencia de osteofitos cervicales anteriores entre las vértebras C3 y C6, el mayor de 12 milímetros (mm) de longitud, que estrechaba la columna aérea al nivel de la orofaringe e hipofaringe. Se descartaron otras causas de disfagia y se trató al paciente con terapia de deglución y omeprazol, dirigido al reflujo faringolaríngeo. Se realizaron 6 sesiones de terapia de deglución individualizada, con el objetivo de compensar el mecanismo de deglución ante un obstáculo mecánico en la región faríngea. Los principales aspectos trabajados fueron: modificación de la textura de la dieta, evitando alimentos sólidos y secos; maniobras posturales de deglución, probadas durante la VED, especialmente el chin tuck (“cabeza hacia abajo” o “flexión de la cabeza”), que aumenta el espacio de la válvula (“abre la válvula”) y mejora la presión de transferencia faríngea del alimento; y ejercicios de fortalecimiento de la lengua, para superar la barrera mecánica de la orofaringe durante la expulsión del alimento. Se recomendó, si fuera necesario, alternar la ingesta de alimentos sólidos con líquidos, ante la percepción de alimentos estancados en la faringe. Se le indicó que repitiera los ejercicios de lengua en el hogar, 2 a 3 veces al día. Después de las sesiones iniciales, el paciente presentó una respuesta satisfactoria, y se lo controló trimestralmente durante el primer año y semestralmente a partir del segundo año. Se lo derivó para una evaluación ortopédica para analizar la viabilidad quirúrgica, y se optó por un tratamiento conservador debido a la buena compensación con medidas clínicas. Sigue en seguimiento ambulatorio desde hace 2 años, y mantiene una deglución eficiente, sin incidencia de complicaciones relacionadas con la disfagia. Se optó por mantener reevaluaciones periódicas, al menos una vez al año, para detectar precozmente un posible nuevo desequilibrio de la homeostasis de la deglución relacionado con el deterioro gradual de las funciones en el contexto de la presbifagia o el surgimiento de un nuevo factor agresor.\n",
+        "gold_summary": "Se describió el caso de un paciente de 66 años con disfagia por atragantamiento con sólidos y reflujo nasal de alimentos desde hacía un año. La videoendoscopia de la deglución mostró una protuberancia en la pared posterior de la faringe y, al ofrecer alimentos sólidos, una restricción de la retroflexión de la epiglotis, reflujo nasal de alimentos y una gran cantidad de residuos de alimentos sobre la lesión. La tomografía computarizada de la columna cervical identificó la presencia de osteofitos cervicales anteriores entre las vértebras C3 y C6, el más grande con una longitud anteroposterior de 12 milímetros, que estrechaba la columna aérea a nivel de la orofaringe e hipofaringe. El paciente fue tratado adecuadamente con fonoterapia para la deglución.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre de 66 años tenía dificultad para tragar alimentos sólidos y parte de la comida le subía por la nariz. Los médicos vieron una protuberancia en su garganta que bloqueaba el paso de la comida. Un estudio mostró que unos huesos en su cuello estaban muy grandes y apretaban su garganta. Con ejercicios para tragar y cambios en su dieta, mejoró mucho y sigue bien con controles médicos.",
+            "B2": "Un hombre de 66 años tenía dificultad para tragar alimentos sólidos y reflujo nasal de comida. Al examinar su garganta con una cámara especial, se vio una protuberancia y problemas para mover la epiglotis, que ayuda a tragar. También había restos de comida acumulados en la garganta. Una tomografía mostró huesos extra en la columna cervical que estrechaban la vía aérea en la garganta. El tratamiento incluyó ejercicios para mejorar la deglución, cambios en la dieta y medicamentos para el reflujo. Después de varias sesiones, el paciente mejoró y no necesitó cirugía. Sigue en control médico para evitar que la dificultad para tragar empeore.",
+            "B3": "Un hombre de 66 años acudió por dificultad para tragar sólidos y reflujo nasal de alimentos durante un año. La evaluación mediante videoendoscopia de la deglución reveló una protuberancia en la pared posterior de la hipofaringe, con acumulación de saliva y residuos alimentarios, además de una restricción en el movimiento de la epiglotis y elevación laríngea, lo que causaba reflujo nasal. La tomografía computarizada mostró osteofitos (crecimientos óseos) en la columna cervical entre las vértebras C3 y C6, que comprimían la vía aérea en la orofaringe e hipofaringe. Se descartaron otras causas de disfagia y se inició tratamiento conservador con terapia de deglución, que incluyó modificaciones en la dieta, maniobras posturales para facilitar el paso del alimento y ejercicios para fortalecer la lengua. Tras seis sesiones, el paciente mejoró notablemente y se mantuvo bajo seguimiento regular durante dos años, sin complicaciones. Se consideró la opción quirúrgica, pero se optó por continuar con el tratamiento clínico debido a la buena respuesta. Las revisiones periódicas son importantes para detectar posibles cambios relacionados con el envejecimiento o nuevos factores que afecten la deglución."
+        }
+    },
+    {
+        "article": "Una paciente caucásica de 18 años de edad se presentó en nuestra clínica con quejas de múltiples bultos palpables en sus senos bilateralmente. En el examen físico, la paciente tenía múltiples lesiones pigmentadas lentigosas en su cara, cuerpo y esclerótica bilateralmente, nevos azules en su tronco y extremidades superiores y una cara redonda con forma de luna.\n\nTras la evaluación ultrasonográfica, se encontraron múltiples nódulos compactos (fibroadenomas) en ambos senos, siendo el más grande en el cuadrante superior externo del seno izquierdo, con un diámetro de 7,8 cm.\n\nEn 2018, se le había practicado una tiroidectomía total con el diagnóstico de adenoma folicular y la extirpación de un nódulo grande del seno izquierdo, debido a su gran tamaño y al dolor que causaba, con un informe de histopatología que sugería un fibroadenoma con estroma mixóide.\n\nSe realizó una biopsia por escisión de dos nódulos de la mama derecha con diagnóstico de fibroadenoma mixto, lo que respaldó nuestro diagnóstico de complejo de Carney.\n\nEn la resonancia magnética se encontraron múltiples fibroadenomas compactos en ambos senos, con alta intensidad de señal en las imágenes T2 y T2/FS, con tabiques internos sin restricción de difusión, compatibles con múltiples fibroadenomas mixoides.\n\nAdemás, había un par de ganglios linfáticos axilares y prominentes ganglios linfáticos mamarios internos bilaterales.\n\nAdemás, se observó una anomalía en la densidad de los tejidos blandos en el mediastino anterior, que medía 11 mm de espesor máximo, lo que sugería un timo prominente.\n\nTodos los hallazgos anteriores sugerían la posibilidad de un complejo de Carney. Se realizó una evaluación adicional en el laboratorio. Los análisis hormonales no mostraron anomalías en los niveles de testosterona, prolactina, PTH y DHEA-S.\n\nLuego se realizó un análisis genético que arrojó como resultado la mutación del gen PRHAR1A, heterocigótico para una variante sin sentido de significancia incierta en el exón 3 de este gen. Esta mutación nunca se había informado en la base de datos gnomAD.\n\nSe realizaron pruebas genéticas a los padres y se determinó que solo el padre era portador de la misma mutación genética.\n\nSe discutieron con la paciente varios planes de tratamiento conservadores, pero ninguno demostró proporcionar una solución/tratamiento definitivo. En el pasado se realizó la extirpación de los lóbulos grandes con alivio temporal de los síntomas de dolor de la paciente y las cirugías recurrentes estaban afectando su calidad de vida. La paciente también tuvo varias sesiones con la psicóloga de nuestra clínica y fue evaluada a fondo antes de decidir la solución final de una mastectomía bilateral.\n\nLa paciente se sometió a una mastectomía bilateral con conservación de la piel y colocación subcutánea de expansores de tejidos (suave, Motiva Flora®). La histopatología informó múltiples fibroadenomas mixóides en ambos senos, compatibles con el síndrome de Carney, con interrupción de la arquitectura normal del parénquima mamario. Las figuras muestran el fibroadenoma de forma macroscópica e histológica.\n\nEl cuidado de la herida fue mínimo, se le recomendó a la paciente usar un sujetador médico y visitas regulares a la clínica ambulatoria para seguimiento y rellenado adicional de los expansores de tejidos a intervalos regulares hasta que se alcanzó el tamaño deseado. Paciente antes y después de la mastectomía. Después de un año se realizó una segunda cirugía y los expansores se reemplazaron con implantes de silicona permanentes (suaves, Motiva Ergonomic®) submusculares, con los mismos requisitos mínimos de cuidado de la herida y colocación del sujetador.\n",
+        "gold_summary": "Una paciente de 18 años de edad se presentó en nuestra clínica con múltiples bultos palpables en sus senos bilateralmente. En el examen físico, la paciente también tenía múltiples lesiones pigmentadas lentigosas en su cara, cuerpo y esclerótica, nevos azules en su tronco y extremidades superiores y un rostro redondo con forma de luna. El diagnóstico del síndrome de Carney se decidió mediante imágenes, biopsias y análisis genético. La paciente se sometió a una mastectomía bilateral como plan de tratamiento profiláctico con colocación de expansores de tejidos.\n",
+        "synthetic_summary": {
+            "B1": "Una joven de 18 años tenía muchos bultos en sus dos senos. También tenía manchas oscuras en la piel y lunares azules en su cuerpo. Los médicos hicieron estudios y encontraron que tenía un problema llamado síndrome de Carney. Para ayudarla, le quitaron los senos y pusieron unos dispositivos para que la piel se estire. Después, le pusieron implantes para que todo se vea bien.",
+            "B2": "Una joven de 18 años llegó con varios bultos en ambos senos y manchas oscuras en la piel y ojos. Los estudios mostraron múltiples fibroadenomas, que son tumores benignos en los senos. También se sospechó el síndrome de Carney, una enfermedad rara, y se confirmó con una prueba genética. Ella ya había tenido una cirugía para quitar un tumor grande y doloroso, pero los bultos regresaron. Por eso, decidió hacerse una mastectomía bilateral, que es la extirpación de ambos senos, para evitar problemas futuros. Después, le colocaron expansores para preparar la piel y luego implantes de silicona. La paciente recibió seguimiento para cuidar las heridas y mejorar su recuperación.",
+            "B3": "Una paciente de 18 años acudió por múltiples bultos en ambos senos, acompañados de lesiones pigmentadas en la piel y nevos azules, además de una cara redonda característica. Los estudios por imagen y biopsias confirmaron la presencia de múltiples fibroadenomas mixoides, y el análisis genético identificó una mutación en el gen PRHAR1A, asociada al complejo de Carney, un síndrome poco común que afecta varios tejidos. A pesar de intentos con tratamientos conservadores y cirugías previas para aliviar el dolor, la recurrencia de los tumores afectaba significativamente su calidad de vida. Por ello, se decidió realizar una mastectomía bilateral con conservación de piel y colocación de expansores de tejido para la reconstrucción mamaria. El seguimiento incluyó cuidados mínimos de la herida y ajustes periódicos de los expansores hasta alcanzar el volumen deseado, seguido de una segunda cirugía para implantar prótesis permanentes de silicona. Este enfoque permitió controlar la enfermedad y mejorar el bienestar de la paciente, quien también recibió apoyo psicológico durante el proceso. En consecuencia, el manejo integral fue clave para abordar las complejidades del síndrome y sus manifestaciones clínicas."
+        }
+    },
+    {
+        "article": "Una adolescente femenino de 13 años sin antecedentes médico-quirúrgicos de interés acude a Urgencias por dolor e impotencia funcional en muñeca izquierda tras caída mientras patinaba. Diagnosticada de lesión en torus metafisaria con extensión fisaria de radio distal clasificada como lesión Peterson tipo I, es inmovilizada durante cuatro semanas con férula antebraquiopalmar. Dos semanas después de la retirada de la férula, acude nuevamente a Urgencias al sentir un crujido en la muñeca, sin sobreesfuerzo asociado e impotencia para movilizar el primer dedo de la mano izquierda. Clínicamente presenta déficit de extensión activa interfalángica, efecto tenodesis patológico, edema local y asimetría macroscópica a la comparación con la extremidad contralateral. Se estudia con resonancia magnética nuclear (RMN), identificando imagen de solución de continuidad del EPL. Con la paciente bajo anestesia general, se procede al tratamiento quirúrgico mediante transferencia tendinosa del extensor propio del índice (EPI) al remanente distal del EPL con sutura tipo Pulvertaft de monofilamento no absorbible. En el postoperatorio se inmovilizó la extremidad las cuatro primeras semanas.\n\nTras cuatro semanas, se autorizó movilidad evidenciando recuperación de extensión del primer dedo de la mano izquierda y cicatrices discretamente hipertróficas, sin dolor. El seguimiento a la sexta, duodécima semana y al año no reporta complicaciones, con una restitución completa de la función y una puntuación de 0 en la escala PRWE (Patient Rated Wrist Evaluation).",
+        "gold_summary": "Se presenta el caso de una paciente adolescente femenino que, tras tratamiento conservador con férula de una fractura fisaria Peterson tipo I en radio, sufre a las seis semanas déficit agudo de extensión del pulgar, diagnosticada mediante examen clínico radiológico de rotura espontánea del extensor pollicis longus. Es tratada por medio de transferencia del extensor propio del índice (EPI) con resultados satisfactorios y recuperación de su actividad habitual al mes postoperatorio.",
+        "synthetic_summary": {
+            "B1": "Una niña de 13 años se cayó mientras patinaba y se lastimó la muñeca. Tenía una fractura en un hueso del brazo y usó una férula por cuatro semanas. Después, tuvo dolor y no pudo mover el dedo pulgar. Los doctores vieron que un tendón estaba roto y la operaron para arreglarlo. Luego de un mes, pudo mover bien el dedo y no tuvo problemas.",
+            "B2": "Una niña de 13 años se cayó mientras patinaba y se fracturó la muñeca izquierda. Le pusieron una férula para inmovilizar la muñeca durante cuatro semanas. Dos semanas después de quitar la férula, sintió un crujido y no pudo mover el dedo pulgar. El examen y una resonancia, que es una imagen del cuerpo, mostraron que se rompió un tendón importante para mover el pulgar. La operaron para reparar el tendón usando otro tendón del dedo índice. Después de la cirugía, inmovilizaron la muñeca y, al mes, la niña recuperó el movimiento sin dolor. Un año después, no tuvo problemas y volvió a sus actividades normales.",
+            "B3": "Una adolescente de 13 años sufrió una fractura en la muñeca izquierda tras una caída mientras patinaba, diagnosticada como lesión Peterson tipo I en el radio distal, y fue tratada inicialmente con inmovilización mediante férula durante cuatro semanas. Dos semanas después de retirar la férula, presentó un crujido en la muñeca y dificultad para mover el pulgar, acompañado de edema y asimetría en la mano. La resonancia magnética confirmó la ruptura del tendón extensor largo del pulgar (EPL). Bajo anestesia general, se realizó una cirugía para transferir el tendón extensor propio del índice (EPI) al remanente del EPL, seguido de inmovilización por cuatro semanas. Tras este periodo, la paciente recuperó la movilidad completa del pulgar sin dolor, con cicatrices mínimas. El seguimiento a corto y largo plazo mostró una recuperación total de la función, sin complicaciones y con una puntuación de 0 en la escala PRWE, que mide la discapacidad de la muñeca. Este caso destaca la efectividad de la transferencia tendinosa en la reparación de rupturas espontáneas del EPL tras fracturas tratadas conservadoramente, permitiendo la recuperación funcional completa en adolescentes."
+        }
+    },
+    {
+        "article": "Se remitió a un hombre de 73 años para una SAVR para tratar la regurgitación valvular aórtica sintomática (AR). Dos años antes, había presentado múltiples lesiones exantématicas. Una biopsia de piel reveló infiltración de células plasmáticas, lo que motivó la derivación a un hematólogo. La tomografía computarizada reveló linfadenopatía sistémica y hepatoesplenomegalia. Una biopsia renal realizada por disfunción renal confirmó la amiloidosis AA; una biopsia de ganglios linfáticos mostró plasmocitosis interfolicular y un centro germinal hiperplásico, consistente con el subtipo plasmático de iMCD, apoyado por niveles elevados de IL-6 en plasma. Se administró al paciente TCZ intravenoso (640 mg cada 2 semanas), junto con prednisolona (10 mg diarios). La erupción cutánea y la linfadenopatía se resolvieron. La ecocardiografía reveló AR puro moderado y agrandamiento ventricular izquierdo. Dado que el paciente experimentó gradualmente disnea de esfuerzo con agrandamiento ventricular izquierdo progresivo, se consideró necesaria la SAVR.\n\nDebido al sangrado por hemorroides y a la hepatosplenomegalia, se consultó a un hepatólogo; se diagnosticó cirrosis hepática de Child-Pugh grado A y varices esofágicas. Se realizó una conferencia preoperatoria del equipo, en la que participaron un intensivista y un farmacéutico, en la que se revisaron los mecanismos de acción de TCZ, las posibles complicaciones y el tratamiento perioperatorio. La cirugía se realizó 26 días después de la última dosis de TCZ. Durante el período perioperatorio, se suspendió el tratamiento con TCZ, mientras que se continuó con los esteroides por vía oral o intravenosa. Las medidas preventivas para las infecciones del sitio quirúrgico (SSI) incluyeron la detección de portadores nasales de Staphylococcus aureus resistentes a la meticilina, la preparación antiséptica de la piel, la terapia antibiótica profiláctica y el control de la hiperglucemia. El cultivo nasal fue positivo para Staphylococcus coagulasa negativo. Se realizó el reemplazo de la válvula aórtica quirúrgica a través de una esternotomía media bajo circulación extracorpórea, con 65 minutos de tiempo de isquemia cardiaca y 128 minutos de tiempo de circulación extracorpórea. Se requirieron transfusiones de sangre, incluidos glóbulos rojos, plasma y plaquetas; el paciente fue extubado al día siguiente. Los hallazgos patológicos revelaron un espesamiento fibroso focal sin depósitos amiloides.\n\nLa herida quirúrgica no mostró signos de infección en el día 2 postoperatorio; se inició la terapia de presión negativa en la herida (NPWT) en la herida quirúrgica cerrada para evitar SSI. La terapia de presión negativa en la herida se interrumpió en el día 13 postoperatorio, sin aparente SSI. El paciente fue dado de alta en el día 17 postoperatorio sin ningún signo de infección.\n\nAunque los niveles de IL-6 aumentaron temporalmente los días 1 y 2 después de la operación, disminuyeron progresivamente hasta el día 24 después de la operación, y luego volvieron a aumentar al reanudarse el tratamiento con TCZ. Los niveles de proteína C reactiva (PCR) estaban ligeramente elevados, alcanzando un máximo de 0,56 mg/dL el día 2 después de la operación. Para el día 24 después de la operación, la PCR había aumentado a 1,06 mg/dL sin infección. Antes del aumento de la PCR, los niveles del factor de crecimiento endotelial vascular aumentaron el día 13 después de la operación.\n\nEl paciente no experimentó recurrencia de erupción cutánea o linfadenopatía durante el período perioperatorio. Los niveles de creatinina postoperatorios aumentaron temporalmente, pero volvieron a los niveles preoperatorios el día 24. Se reanudó el tratamiento con tocilizumab el día 30 postoperatorio tras confirmar la ausencia de infección, incluida la IFI.\n",
+        "gold_summary": "Un hombre de 73 años con enfermedad de Castleman, tratado con TCZ, se sometió a un reemplazo de la válvula aórtica por medio de esternotomía mediana para la regurgitación de la válvula aórtica con falta de aire al hacer ejercicio. Se implementaron medidas integrales para prevenir la infección del sitio quirúrgico junto con un examen minucioso durante el período perioperatorio. Tocilizumab se interrumpió 26 días antes de la cirugía y se reanudó 30 días después de la cirugía, durante los cuales los niveles de IL-6 en plasma disminuyeron. No hubo evidencia de infección o exacerbación de la enfermedad de Castleman. Los niveles del factor de crecimiento endotelial vascular aumentaron antes de un aumento en los niveles de proteína C reactiva después del alta hospitalaria y antes de la reanudación de TCZ.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre de 73 años tenía problemas en el corazón y en la piel. Le hicieron una operación para cambiar una válvula del corazón porque le costaba respirar. Durante la operación, cuidaron mucho que no se le infectara la herida. Dejó de tomar un medicamento llamado TCZ antes de la cirugía y lo volvió a tomar después. Todo salió bien y no tuvo infecciones ni empeoró su enfermedad.",
+            "B2": "Un hombre de 73 años con enfermedad de Castleman, que causa inflamación y problemas en órganos, necesitó un reemplazo de la válvula aórtica porque tenía dificultad para respirar y la válvula no funcionaba bien. Antes de la cirugía, se detuvo el tratamiento con tocilizumab (un medicamento que reduce la inflamación) para evitar infecciones. Durante y después de la operación, se tomaron muchas precauciones para prevenir infecciones en la herida. La cirugía fue exitosa y no hubo signos de infección ni empeoramiento de su enfermedad. El medicamento se volvió a dar 30 días después de la operación, cuando se confirmó que no había infecciones. Los análisis mostraron cambios en sustancias inflamatorias, pero el paciente se recuperó bien y fue dado de alta sin complicaciones.",
+            "B3": "Un hombre de 73 años con enfermedad de Castleman, caracterizada por inflamación linfática y amiloidosis, fue tratado con tocilizumab (TCZ) y esteroides para controlar sus síntomas. Debido a una regurgitación valvular aórtica moderada y progresiva que causaba dificultad para respirar, se decidió realizar un reemplazo quirúrgico de la válvula aórtica. El TCZ se suspendió 26 días antes de la cirugía para reducir riesgos, y se aplicaron estrictas medidas para prevenir infecciones en el sitio quirúrgico, incluyendo control de bacterias resistentes y cuidado de la herida con terapia de presión negativa. La operación se realizó sin complicaciones infecciosas y el paciente se recuperó adecuadamente, sin signos de infección ni empeoramiento de la enfermedad. Los niveles de IL-6, una proteína relacionada con la inflamación, aumentaron temporalmente tras la cirugía pero luego bajaron, y el TCZ se reanudó 30 días después al confirmar la ausencia de infección. Este caso muestra que, con un manejo cuidadoso, es posible realizar cirugías mayores en pacientes con enfermedad de Castleman tratados con TCZ sin aumentar el riesgo de complicaciones infecciosas."
+        }
+    },
+    {
+        "article": "Se trata de un paciente de sexo masculino de cuatro meses de edad, originario del centro de México y con dos hermanos hombres sanos. Durante el primer trimestre de gestación, su madre hipotiroidea consumió drogas. No obstante, el infante nació con peso y talla adecuados, fue alimentado con leche materna y recibió la vacuna del bacilo de Calmette-Guérin (BCG), sin desarrollo de cicatriz. La madre del paciente era prisionera en una cárcel y, junto con el bebé, compartían una celda insalubre con dos personas más.A los cuatro meses, el paciente fue valorado médicamente por un tumor doloroso en la región axilar izquierda. En la radiografía de tórax se observaron imágenes sugestivas de fracturas costales; se sospechó de maltrato infantil por parte de la madre, y el infante fue hospitalizado en un hospital pediátrico. Se determinó el peso (4.190 g) y la talla (58 cm) –por debajo del percentil tres–, saturación de oxígeno del 70 %, fiebre, tos, aumento de volumen en la región axilar izquierda, además de dolor, rubor y calor. En el cuadro hemático se encontró: hemoglobina de 8,8 g/dl (11,0 - 12,6), 29,3 × 109 leucocitos/L (6,0 - 17,5), 18,4 × 109 neutrófilos/L (1,0 - 8,5), 7,0 × 109 linfocitos/L (4,0 - 13,5), 3,5 × 109 monocitos/L, 459 × 109 plaquetas/L (150 - 350) y proteína C reactiva igual a 16 mg/L (< 3,0). En la primera tomografía toracoabdominal se observaron imágenes de un absceso en la región axilar izquierda, lesiones líticas en las costillas 3 a 6, neumonía apical izquierda, nódulos pulmonares en ambos pulmones y ganglios linfáticos cervicales y mediastinales incrementados de tamaño. En la biopsia del absceso axilar izquierdo se reportó miositis y paniculitis supurativa. Solo se hizo cultivo para bacterias del líquido broncoalveolar, el cual fue negativo, y la PCR para el complejo Mycobacterium tuberculosis fue negativa. Después de 41 días de hospitalización y de haber recibido dos esquemas de antimicrobianos –ceftriaxona-clindamicina y cefepima-vancomicina–, el paciente fue dado de alta.\n\nDos meses después, a los ocho meses de edad, reingresó al hospital por fiebre, irritabilidad y un absceso supurante en la escápula izquierda. En el cuadro hemático se encontró: hemoglobina de 10,8 g/dl (10,5 - 12), 21,2 × 109 leucocitos/L (6 - 17), 12,2 × 109 neutrófilos/L (1,5 - 8,5), 7,5 × 109 linfocitos/L (4 - 10,5), 1,2 × 109 monocitos/L (600), y 583 × 109 plaquetas/L (150 - 350); la prueba para la detección sérica de HIV fue negativa. En la tomografía de tórax se observó una consolidación apical izquierda, bronquiectasias, lesiones líticas en las costillas 2 a 7 y en las vértebras dorsales 2 a 7, además de una colección de líquido multiloculado; en el ultrasonido se encontró una fístula asociada con el absceso escapular. El paciente recibió piperacilina-tazobactam, que se sustituyó después por voriconazol al detectarse Aspergillus fumigatus en el cultivo de la muestra de secreción del absceso. Dada la recurrencia y la gravedad de la infección, se sospechó un error innato de la inmunidad. La prueba de dihidrorrodamina resultó sin producción de especies reactivas de oxígeno y la expresión de gp91phox en los neutrófilos fue nula, estableciéndose así el diagnóstico de enfermedad granulomatosa crónica ligada al cromosoma X. La variante patógena detectada por la secuenciación de nueva generación fue c.80_83del/Y (p.Val27Glyfs*33) en CYBB. La madre resultó portadora de la variante (c.80_83del/WT). No fue posible estudiar genéticamente a sus dos hermanos mayores, de sexo masculino, y aparentemente sanos. El paciente fue dado de alta después de 65 días de hospitalización y tratamiento con voriconazol por 28 días. Se inició profilaxis antibiótica diaria con trimetoprim-sulfametoxazol y profilaxis antifúngica con fluconazol dos veces a la semana. Dos meses después, al año de edad, el infante reingresó debido a una neumonía multifocal, por la cual requirió asistencia respiratoria mecánica. Se detectó el antígeno galactomanano en el suero y A. fumigatusen el cultivo del líquido del lavado broncoalveolar, por lo que se inició nuevamente tratamiento con voriconazol. El paciente sufrió una falla orgánica múltiple y falleció un mes después de su ingreso.\n",
+        "gold_summary": "Se presenta el caso de un infante con enfermedad granulomatosa crónica y aspergilosis invasiva. Se trata de un lactante de sexo masculino de cuatro meses de edad, de madre hipotiroidea y con quien convive en la celda de la cárcel. El infante presentó tumores en la región axilar izquierda y la radiografía de tórax sugirió fracturas costales; fue hospitalizado ante la sospecha de maltrato infantil. En la tomografía de tórax se observó un absceso axilar, osteólisis de costillas, neumonía y nódulos pulmonares; el paciente recibió antibióticos de amplio espectro y fue dado de alta. A los ocho meses, reingresó por fiebre y extensión del absceso purulento hacia la región escapular izquierda; en la tomografía se observaron imágenes de empeoramiento de la condición. Se aisló Aspergillus fumigatus de la secreción del absceso y se diagnosticó aspergilosis invasiva; se inició tratamiento con voriconazol por 28 días. Mediante la prueba de dihidrorrodamina, se diagnosticó enfermedad granulomatosa crónica causada por la variante patógena c.80_83del/Y del gen CYBB, portada por la madre (c.80_83del/WT). A los 12 meses, el paciente reingresó nuevamente por aspergilosis invasiva, resistente al tratamiento, con desenlace fatal.",
+        "synthetic_summary": {
+            "B1": "Un bebé de cuatro meses tuvo un bulto doloroso en la axila y problemas en los huesos y pulmones. Los doctores pensaron que podía estar lastimado, pero luego encontraron una infección grave con un hongo llamado Aspergillus. Descubrieron que tenía una enfermedad que hace que su cuerpo no luche bien contra las infecciones. Aunque recibió medicinas, su salud empeoró y murió a los 12 meses. Su mamá tiene la misma enfermedad, pero no está enferma.",
+            "B2": "Un bebé de cuatro meses tuvo un tumor doloroso en la axila izquierda y fracturas en las costillas. Al principio, se pensó que era maltrato, pero las pruebas mostraron una infección grave con abscesos (acumulación de pus) y neumonía (infección en los pulmones). Recibió antibióticos y salió del hospital. A los ocho meses regresó con fiebre y un absceso más grande. Se encontró un hongo llamado Aspergillus fumigatus, que causó una infección llamada aspergilosis invasiva. También se diagnosticó una enfermedad llamada granulomatosa crónica, que afecta el sistema inmunitario y fue causada por un problema genético heredado de su madre. A pesar del tratamiento con medicamentos antifúngicos, el bebé volvió a enfermar a los 12 meses y falleció por la infección grave y daño en varios órganos.",
+            "B3": "Se reporta el caso de un lactante masculino de cuatro meses con enfermedad granulomatosa crónica (EGC), una condición genética que afecta la capacidad del sistema inmunitario para combatir infecciones. El niño, cuya madre era hipotiroidea y estaba en prisión, presentó inicialmente un absceso axilar y fracturas costales, lo que llevó a sospechar maltrato infantil. Sin embargo, estudios posteriores revelaron infecciones pulmonares y lesiones óseas, y se aisló Aspergillus fumigatus, un hongo que causó aspergilosis invasiva. La prueba de dihidrorrodamina confirmó la EGC ligada al cromosoma X, identificando una mutación en el gen CYBB, heredada de su madre. A pesar del tratamiento con antifúngicos y antibióticos, el paciente sufrió recurrencias graves y finalmente falleció a los 12 meses debido a una falla orgánica múltiple. Este caso destaca la importancia de considerar errores innatos de la inmunidad en lactantes con infecciones recurrentes y complicadas, especialmente cuando la respuesta a tratamientos convencionales es insuficiente. Por lo tanto, el diagnóstico temprano y la profilaxis adecuada son cruciales para mejorar el pronóstico en pacientes con EGC."
+        }
+    },
+    {
+        "article": "Se trata de un hombre de 66 años de edad que vive en la ciudad de Juan Bautista Alberdi de la provincia de Buenos Aires, con antecedentes de hipertensión arterial y trastorno obsesivo compulsivo. Su medicación habitual incluía amlodipina, quetiapina, venlafaxina y ácido valproico. Consultó por presentar fiebre de 39ºC de cuatro días de evolución sin síntomas asociados y se internó para estudio en sala general. Al examen de ingreso se constató un paciente lúcido, sin foco motor, sin trastorno sensitivo ni rigidez de nuca (escala de coma de Glasgow (GCS) 15/15). El resto del examen físico y el laboratorio general no presentaron particularidades. Los cultivos de sangre y orina resultaron negativos, y la tomografía computarizada de encéfalo, tórax, abdomen y pelvis no mostró afecciones. A las 24 horas agregó episodios de desorientación témporo-espacial que alternaban con otros de somnolencia (GCS 13/15). Al examen físico se constató temblor grueso distal en los cuatro miembros. El examen del LCR informó: líquido incoloro, límpido, y aspecto post centrifugado también límpido. Recuento de leucocitos 310/mm3 (mononucleares 54%, polimorfonucleares 46%), hematíes < de 1000/mm3, proteínas 0.76 g/l, glucosa 54 mg/dl (glucemia 120 mg/dl), y ácido láctico 21 mg/dl. Se inició tratamiento empírico con aciclovir 10 mg/kg endovenoso cada 8 horas. Se solicitaron en LCR: PCR para virus de herpes simple (VHS) y para virus de encefalopatía equina del oeste (VEEO) que resultaron no reactivas. Sin embargo, la IgM (ELISA) para EEO resultó positiva en suero y en LCR a los diez días. La RMN de encéfalo evidenció aumento en la intensidad en secuencias FLAIR y T2 a nivel de la región dorsal del tronco encefálico (tanto protuberancial, como también bulbar y mesencefálico), ambos pedúnculos cerebrales y ganglios de la base, con afectación bilateral y ligero predominio ganglio basal derecho. También se observaron múltiples imágenes focales hiperintensas en la sustancia blanca de ambos hemisferios cerebrales. El paciente evolucionó con deterioro del sensorio (GCS 8/15), sin protección de la vía aérea, por lo que ingresó a UTI. Requirió intubación y ventilación mecánica, con utilización de sedación y analgesia. Al ingreso a UTI presentaba: estado ácido-base (EAB) arterial: pH 7.11, pCO2 136 mmHg, pO2 75 mmHg, bicarbonato 43 mEq/l, exceso de base 11 mEq/l, saturación 88% (Con FIO2 21%), ácido láctico 11.5 mg/dl. Se inició la ventilación mecánica con un volumen minuto respiratorio (VMR) de 9.8 litros (volumen tidal 490 ml que corresponde a 6 ml/kg de peso teórico, frecuencia respiratoria 20 por minuto, presión positiva al final de espiración (PEEP) 5 cmH2 O, fracción inspirada de oxígeno 30%) se extrajo sangre para EAB arterial: pH 7.40, pCO2 41 mmHg, pO2 65 mmHg, bicarbonato 28 mEq/l, exceso de base 0 mEq/l, saturación 93%, PAFI 216. Evolucionó sin fiebre, estable hemodinámicamente, con adecuada oxigenación y ritmo diurético. Al suspender sedantes presentó GCS de 3 puntos sobre 10 (correspondiente con evaluación ocular 1 y motor 2 puntos), con rigidez generalizada y reflejos osteotendinosos adecuados, con movimientos rítmicos linguales y peribucales. El electroencefalograma de 12 canales no evidenció descargas patológicas. Al décimo día de inicio de los síntomas presentó apertura ocular y menor rigidez, pero no toleraba la modalidad respiratoria espontánea por hipoventilación e hipercapnia que lo llevaron a hipoxemia transitoria. En el EAB arterial presentó: pH 7.31, pCO2 70 mmHg, pO2 76 mmHg, bicarbonato 35 mEq/l, exceso de base 8 mEq/l bajo asistencia ventilatoria en modalidad espontánea de presión soporte de 5 cmH2 O, frecuencia respiratoria 6 por minuto, PEEP 5 cmH2 O y volumen tidal entre 120-150 ml. Los siguientes días el paciente se conectó, respondiendo órdenes simples y complejas, y movilizó simétricamente los miembros con cierta debilidad. Por intolerancia a las pruebas ventilatorias espontáneas fue traqueostomizado. En la evaluación funcional respiratoria presentaba presión inspiratoria máxima menor a -40 cm de H2 O, presión espiratoria máxima mayor a 80 cm de H2 O, pero continuaba con hipercapnia en la prueba ventilatoria espontánea, por lo que requirió soporte ventilatorio con modalidad controlada. Se realizó ecocardiograma transtorácico que informó cavidades derechas normales, sin signos de hipertensión pulmonar. En la nueva RMN de encéfalo se evidenció disminución de las áreas hiperintensas en secuencias FLAIR y T2 visibles previamente.\n\nEl enfermo evolucionó con requerimiento de menor soporte ventilatorio en forma progresiva al momento del desarrollo de este informe.",
+        "gold_summary": "Presentamos el caso de un varón de 66 años de edad oriundo de la ciudad Juan Bautista Alberdi de la provincia de Buenos Aires con antecedentes de hipertensión arterial y trastorno obsesivo compulsivo. Consultó por fiebre súbita de cuatro días de evolución, con desarrollo de encefalopatía durante su internación. La punción lumbar mostró un líquido cefalorraquídeo cristalino, aunque inflamatorio de predominio mononuclear. La RMN de encéfalo informó hiperintensidad en secuencias FLAIR y T2 en el dorso del tronco encefálico. Ingresó a terapia intensiva por deterioro neurológico y acidosis respiratoria grave, requiriendo asistencia ventilatoria mecánica. Luego de 10 días presentó mejoría neurológica, sin déficit motor pero con hipoventilación alveolar que dificultaron el destete del respirador.",
+        "synthetic_summary": {
+            "B1": "Un hombre de 66 años tuvo fiebre alta por cuatro días. Luego, se puso confundido y muy dormido. Los médicos vieron que su cerebro estaba inflamado. Estuvo en cuidados intensivos y usó una máquina para respirar. Después de diez días, mejoró y pudo moverse bien. Pero aún le cuesta respirar sin ayuda.",
+            "B2": "Un hombre de 66 años con hipertensión y trastorno obsesivo tuvo fiebre alta durante cuatro días. Al llegar al hospital, estaba alerta, pero luego se volvió confundido y somnoliento. El análisis del líquido cefalorraquídeo, que protege el cerebro, mostró inflamación. La resonancia magnética reveló daño en el tronco encefálico, parte vital del cerebro. Fue llevado a cuidados intensivos por empeoramiento neurológico y problemas graves para respirar. Necesitó un respirador mecánico para ayudar a respirar. Después de diez días, mejoró su estado mental y movilidad, pero aún tenía dificultad para respirar sin ayuda. Este caso muestra la importancia de un diagnóstico rápido y tratamiento adecuado en infecciones del sistema nervioso que afectan la respiración.",
+            "B3": "Un hombre de 66 años con antecedentes de hipertensión y trastorno obsesivo compulsivo presentó fiebre alta durante cuatro días sin otros síntomas asociados. Inicialmente permaneció lúcido, pero posteriormente desarrolló desorientación, somnolencia y temblor en las extremidades, lo que indicó deterioro neurológico. El análisis del líquido cefalorraquídeo evidenció inflamación, mientras que la resonancia magnética mostró alteraciones en el tronco encefálico y ganglios basales, sugiriendo una infección central. Se inició tratamiento empírico con aciclovir, aunque las pruebas confirmaron infección por virus de encefalitis equina del oeste. La condición neurológica del paciente empeoró, requiriendo ingreso a cuidados intensivos y ventilación mecánica debido a acidosis respiratoria severa. Tras diez días, mejoró el nivel de conciencia y la movilidad, pero persistió hipoventilación que dificultó la retirada del soporte ventilatorio. La evolución fue favorable, con reducción progresiva de las lesiones cerebrales en imágenes posteriores y disminución del soporte respiratorio. Este caso resalta la importancia de considerar infecciones virales poco comunes en pacientes con fiebre y alteración neurológica, así como la necesidad de cuidados intensivos para manejar complicaciones respiratorias graves."
+        }
+    },
+    {
+        "article": "Mujer de 27 años de edad oriunda del interior de la Provincia de Buenos Aires sin antecedentes personales o familiares de relevancia, consultó por sangrado vaginal. El estudio colposcópico evidenció formación polipoide que protruía por el orificio cervical externo (OCE). Se arribó clínicamente al diagnóstico de mioma nascens y se tomó una muestra de biopsia para su evaluación. Ante el diagnóstico patológico de sarcoma, se instauró quimioterapia, con el fin de reducir la masa lesional. Una vez lograda la reducción del tamaño, se decidió derivarla a nuestra institución para realizar tratamiento quirúrgico. Se recibió una pieza de histerectomía total con anexos, f ijada en formol al 10%. Cuerpo de 5 × 5 × 3.2 cm, cuello de 3.5 × 3 × 2 cm, ambas trompas de 4.5 × 0.7 cm y ovarios de 4 × 2.5 × 2.5 cm. A la apertura de la pieza, se observó a nivel de la unión cérvico-ístmica una formación polipoide pediculada de 8.5 cm de diámetro, que emergía hacia el canal endocervical y se exteriorizaba por el OCE. La superficie externa era parda, lobulada, con sectores rojizos. Al corte, se observaba blanquecina, blanda, con sectores de aspecto gelatinoso y formaciones quísticas de hasta 0,6 cm de dimensión máxima. Luego del procesamiento de rutina, se efectuaron secciones histológicas y se colorearon con hematoxilina-eosina (H-E), las cuales evidenciaron sectores celulares alternados por áreas laxas, mixoides junto a glándulas ístmico-endometriales típicas. La proliferación, predominantemente fusocelular atípica se disponía en nidos, constituidos por células de amplio citoplasma eosinófilo y núcleos excéntricos con cromatina homogénea, algunos pleomórficos. Se apreciaron estriaciones citoplasmáticas transversales en dichas células. El estroma era ampliamente mixoide y ricamente vascularizado. Se destacaban focalmente áreas celulares densamente condensadas inmediatas y próximas al revestimiento epitelial intacto, pero separadas de él, por una fina capa de estroma laxo. Esto se conoce como cambium layer o capa cambial. Se realizaron técnicas de inmunohistoquímica para desmina, actina músculo específico (AME) y miogenina (MYF4), las cuales resultaron positivas, mientras que la actina músculo liso fue negativa. Esta inmunomarcación permitió comprobar la estirpe muscular estriada y en última instancia arribar al diagnóstico, junto al cuadro morfológico, de RMS embrionario. Asimismo, la presencia de rabdomioblastos agrupados constituyendo la capa cambial a nivel subepitelial resultó fundamental y necesario para tipificar al RMS embrionario como botrioide, independientemente de la presentación macroscópica en forma de racimos polipoides.",
+        "gold_summary": "Presentamos el caso de una mujer de 27 años que consultó por sangrado vaginal y en quien se evidenció en la colposcopia, una lesión polipoide blanquecina que se exteriorizaba a través del orificio cervical externo. El estudio histológico reveló sectores celulares alternados por áreas laxas, mixoides, junto a glándulas ístmico-endometriales típicas. La proliferación fusocelular atípica, se disponía en nidos, constituidos por células de amplio citoplasma eosinófilo con estriaciones citoplasmáticas transversales y núcleos excéntricos con cromatina homogénea. Se exhibían áreas de células densamente condensadas inmediatas y próximas al revestimiento epitelial intacto, pero separadas de él, por una fina capa de estroma laxo (capa cambial). El perfil de inmunomarcación resultó positivo para desmina, actina músculo específico y miogenina, y negativo para actina músculo liso. Se realizó diagnóstico de rabdomiosarcoma embrionario botroide de cuerpo uterino.",
+        "synthetic_summary": {
+            "B1": "Una mujer de 27 años tuvo sangrado en la parte baja de su cuerpo. Los doctores encontraron un bulto que salía del cuello del útero. Al estudiar el bulto, vieron que tenía células raras que crecían mucho. Con pruebas especiales, supieron que era un tipo de tumor llamado rabdomiosarcoma. Ella recibió tratamiento para reducir el bulto y luego le hicieron una operación para quitarlo.",
+            "B2": "Una mujer de 27 años consultó por sangrado vaginal y se encontró una masa que salía del cuello del útero. Al analizarla, los médicos vieron células anormales con características de músculo estriado, confirmadas por pruebas especiales. La masa tenía una capa llamada cambial, que es típica de un tipo raro de tumor llamado rabdomiosarcoma embrionario botrioide. Este tumor es maligno y se originó en el útero. Primero se trató con quimioterapia para reducirlo y luego se realizó una cirugía para extirparlo. Este caso muestra la importancia de estudiar bien las lesiones para dar un diagnóstico correcto y planear el mejor tratamiento.",
+            "B3": "Una mujer de 27 años consultó por sangrado vaginal y se detectó una masa polipoide que sobresalía por el orificio cervical externo. Inicialmente se sospechó un mioma, pero la biopsia reveló un sarcoma, por lo que se inició quimioterapia para reducir el tumor. Tras la disminución del tamaño, se realizó una histerectomía total con anexos. El análisis macroscópico mostró una formación polipoide en la unión cérvico-ístmica, con áreas blanquecinas, gelatinosas y quísticas. El estudio histológico evidenció una proliferación celular fusocelular atípica con células que presentaban estriaciones citoplasmáticas y núcleos excéntricos, junto a una capa cambial, que es una zona de células densamente agrupadas bajo el epitelio. La inmunohistoquímica confirmó la presencia de marcadores de músculo estriado, como desmina, actina músculo específico y miogenina, descartando músculo liso. Estos hallazgos permitieron diagnosticar un rabdomiosarcoma embrionario botroide, un tumor maligno raro que afecta el cuerpo uterino. Este diagnóstico es clave para definir el tratamiento y pronóstico, que incluye cirugía y quimioterapia."
+        }
+    },
+    {
+        "article": "Un hombre de 53 años de edad, que inició diálisis por disfunción renal en etapa terminal debido a nefropatía diabética o nefroesclerosis en nuestro departamento de nefrología 10 años antes, se sometió a una ecocardiografía de seguimiento anual para estenosis valvular aórtica progresiva (AVS) y regurgitación moderada con fracción de eyección ventricular izquierda (LVEF) normal. Un año antes, se observaron calcificaciones que sugerían MAC en el anillo mitral posterior, que no se habían visto dos años antes. En el último seguimiento, la ecocardiografía reveló una masa redonda de superficie lisa de 22 × 17 mm con alta ecogenicidad en el área circundante y un brillo interno ligeramente disminuido en el anillo mitral posterior del lado auricular izquierdo. El paciente no tenía síntomas significativos ni hallazgos físicos, excepto un soplo sistólico.\n\nLa ecocardiografía también reveló una VS moderada con un flujo de pico valvular transaórtico de 3,76 m/s y una regurgitación valvular aórtica moderada. Se observó una regurgitación mitral leve pero no estenosis. El patrón de velocidad de flujo de entrada del VI mostró un patrón pseudo-normal con un agrandamiento de la aurícula izquierda de 47 mm de diámetro. La ecocardiografía en serie durante dos años reveló un agrandamiento del VI y una disminución de la FEVI. El diámetro final diastólico/final sistólico del VI y la FEVI fueron de 50/33 mm y 64 %, respectivamente, hace dos años; 57/41 mm y 52 % hace un año; y 59/47 mm y 42 % en el último seguimiento.\n\nTeniendo en cuenta el estado de la hemodiálisis, predijimos la progresión a una AVS casi severa, con empeoramiento de la disfunción sistólica del LV, que se convertiría en una indicación para el reemplazo de la válvula aórtica (AVR) en un futuro cercano.\n\nLa tomografía computarizada (TC) reveló una masa de alta densidad sin realce de contraste. La resonancia magnética (MRI) mostró una masa bien definida de alta intensidad en el centro, con un borde hipointenso en la imagen T1 y una señal desprovista en T2. Se excluyeron los neoplasmas, incluidos los mixomas y los fibroelastomas papilares, en función de sus características de imagen. Los hallazgos de laboratorio no indicaron infección, y no se sospechó de vegetación con endocarditis infecciosa. Teniendo en cuenta la disfunción renal en etapa terminal en la hemodiálisis y los hallazgos de imagen, se sospechó CCMA. El rápido agrandamiento de la masa generó preocupación sobre una potencial embolia. En consecuencia, la masa se resecó con AVR.\n\nLa incisión del atrio izquierdo reveló una masa por debajo del endocardio auricular en el anillo de la válvula mitral (P1-2); se observaron sustancias cremosas en la incisión de la masa, lo que sugiere CCMA. Después de la extirpación y desbridamiento del tejido, el sitio de la incisión se suturó con prolina. Se realizó el reemplazo de la válvula aórtica utilizando una válvula SJM de 21 mm. La retirada del bypass cardiopulmonar fue relativamente suave. Al momento del alta, se prescribió warfarina y aspirina, junto con bisoprolol para la fibrilación auricular paroxística después de la cirugía.\n\nNo se observaron eventos embólicos antes o después de la cirugía.\n\nEl examen histopatológico reveló calcificaciones granulares y nodulares dispersas, que consistían principalmente en infiltración de células inflamatorias y proliferación vascular de neutrófilos, linfocitos, células espumosas, macrófagos tisulares y células plasmáticas, con osificación parcial compatible con CICM. La biopsia miocárdica LV para descartar cardiomiopatía secundaria y la válvula aórtica resecada mostraron células inflamatorias similares a las observadas en CICM. Por lo tanto, se diagnosticó CICM en base a la disminución del movimiento de la pared y la fibrosis miocárdica, con infiltración de células inflamatorias > 14 mm2, células T CD3 positivas > 7/mm2 y negatividad de tenascina C (4C8).7 Sin embargo, no se pudo determinar la causa de CICM.\n\nLa ecocardiografía 6 meses después de la resección no mostró recurrencia del tumor (ver material complementario en línea), ni progresión de la regurgitación mitral, función normal de la válvula aórtica protésica y ninguna mejora de la FEVI (41 %)\n\n",
+        "gold_summary": "Un hombre de 52 años con insuficiencia renal en fase terminal que requería hemodiálisis se sometió a una ecocardiografía anual de seguimiento para detectar una disfunción valvular aórtica. La ecocardiografía reveló una masa circular bien definida de 22 × 17 mm en el anillo de la valva mitral posterior que no se había detectado 2 años antes. En función de las características de la imagen, se sospechó que la masa era un CCMA. Se había agrandado rápidamente y suponía un riesgo potencial de embolia; por lo tanto, se extirpó al mismo tiempo que la sustitución de la válvula aórtica. Aunque se sospechó un CCMA en función de los hallazgos intraoperativos, el diagnóstico histopatológico fue un CAT. Tras el análisis histológico de la muestra de miocardio del ventrículo izquierdo y la válvula aórtica extirpada, se observó una infiltración de células inflamatorias crónicas; por lo tanto, se diagnosticó una cardiomiopatía inflamatoria crónica.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre con problemas graves en sus riñones necesitaba un tratamiento especial llamado diálisis. En un examen del corazón, los doctores encontraron una masa redonda en una parte del corazón llamada válvula mitral. Esta masa creció rápido y podía causar problemas, por eso la quitaron junto con otra válvula que estaba dañada. Al estudiar la masa, vieron que había inflamación en el corazón. Después de la cirugía, el hombre mejoró y no hubo problemas nuevos.",
+            "B2": "Un hombre de 53 años con insuficiencia renal avanzada en hemodiálisis fue controlado por problemas en sus válvulas del corazón. En una ecocardiografía anual, se detectó una masa nueva de 22 × 17 mm en el anillo mitral, que había crecido rápido y podía causar embolias. Se decidió extirparla junto con el reemplazo de la válvula aórtica. Las imágenes sugirieron que la masa era un depósito calcificado llamado CCMA, pero el examen del tejido mostró que era un tumor llamado CAT. Además, se encontró inflamación crónica en el músculo del corazón, diagnosticándose una cardiomiopatía inflamatoria crónica. Después de la cirugía, el paciente no tuvo complicaciones ni regreso del tumor, aunque la función del corazón no mejoró.",
+            "B3": "Un hombre de 53 años con insuficiencia renal terminal en hemodiálisis presentó una masa de 22 × 17 mm en el anillo mitral posterior, detectada mediante ecocardiografía anual, que no estaba presente dos años antes. La masa mostró rápido crecimiento y se sospechó una calcificación caseosa del anillo mitral (CCMA), una lesión que puede aumentar el riesgo de embolias. Debido a esta preocupación, se decidió extirpar la masa junto con el reemplazo de la válvula aórtica, ya que el paciente también tenía estenosis valvular aórtica progresiva y disfunción ventricular izquierda. El examen histopatológico reveló calcificaciones con infiltración de células inflamatorias, lo que llevó al diagnóstico de una cardiomiopatía inflamatoria crónica, descartando tumores como mixomas. Tras la cirugía, no hubo eventos embólicos ni recurrencia de la masa en el seguimiento a seis meses, aunque la función ventricular izquierda no mejoró. Este caso destaca la importancia de un diagnóstico preciso mediante imágenes y análisis histológicos para guiar el tratamiento en pacientes con enfermedades renales avanzadas y complicaciones cardíacas complejas."
+        }
+    },
+    {
+        "article": "Paciente masculino de 28 años, sin antecedentes de importancia, acude a consulta de dermatología con un cuadro cutáneo de 48 horas de evolución caracterizado por dos placas eritematosas con ampollas centrales más ulceración superficial localizadas en cara flexora de brazo y antebrazo derecho equidistantes del pliegue del codo, acompañadas de una sensación de ardor y prurito en el lugar de las lesiones. No presentó síntomas sistémicos ni se automedicó. Como antecedente refiere que se encontraba de vacaciones en la región costera de Ecuador al momento de aparecer las lesiones. Se realizó una biopsia incisional que reportó epidermis con acantosis, paraqueratosis y espongiosis, neutrófilos en estrato córneo e infiltrado linfocitario perivascular en dermis superficial, media y profunda. Por las características clínicas, el antecedente de viaje a una región tropical y los hallazgos histológicos se diagnosticó como dermatitis por Paederus. Se indicó tratamiento con antihistamínicos, esteroides tópicos y compresas frías. Después de 8 días de tratamiento, las lesiones remitieron dejando una hiperpigmentación postinflamatoria.",
+        "gold_summary": "Se comunica el caso de un paciente masculino de 28 años, que acude a consulta de dermatología con cuadro de 48 horas de evolución de dos placas eritematosas con ampollas centrales más ulceración superficial localizadas en cara flexora de brazo y antebrazo derecho, acompañadas de una sensación de ardor y prurito en el lugar de las lesiones, sin síntomas acompañantes. Como antecedente refiere que se encontraba de vacaciones en la región costera de Ecuador al momento de aparecer las lesiones. Se realizó una biopsia incisional y por las características clínicas y el antecedente de viaje a una región tropical se diagnosticó como dermatitis por Paederus y se indicó tratamiento con antihistamínicos, esteroides tópicos y compresas frías. Después de 8 días de tratamiento, las lesiones remitieron dejando una hiperpigmentación postinflamatoria.",
+        "synthetic_summary": {
+            "B1": "Un hombre de 28 años tuvo en su brazo dos manchas rojas con ampollas y un poco de herida. Le dolían y picaban. Estaba de vacaciones en un lugar tropical cuando le salieron. Los doctores hicieron una prueba de piel y dijeron que era una irritación por un insecto llamado Paederus. Le dieron medicinas y después de 8 días, las heridas mejoraron, pero quedó una mancha oscura en la piel.",
+            "B2": "Un hombre de 28 años fue al dermatólogo por dos manchas rojas en su brazo derecho. Las manchas tenían ampollas y una pequeña herida, y aparecieron hace dos días. Él sentía ardor y picazón en esas zonas. Estaba de vacaciones en la costa de Ecuador cuando comenzaron los síntomas. El médico tomó una muestra de piel para analizarla, llamada biopsia, que mostró inflamación. El diagnóstico fue dermatitis por Paederus, una reacción causada por un insecto tropical. Le dieron medicamentos para la picazón, cremas con esteroides y compresas frías. Después de ocho días, las heridas mejoraron, pero quedó una mancha oscura en la piel. Este caso muestra la importancia de conocer enfermedades en viajes a lugares cálidos.",
+            "B3": "Un hombre de 28 años, sin antecedentes médicos relevantes, consultó por la aparición de dos placas eritematosas con ampollas y ulceración superficial en el brazo y antebrazo derecho, desarrolladas en un lapso de 48 horas y acompañadas de ardor y prurito. Durante sus vacaciones en la costa de Ecuador, surgieron estas lesiones cutáneas sin que presentara síntomas sistémicos ni se automedicara. La biopsia cutánea reveló cambios inflamatorios caracterizados por acantosis (engrosamiento de la epidermis) y un infiltrado inflamatorio celular. Considerando la presentación clínica, el antecedente de exposición en zona tropical y los hallazgos histopatológicos, se estableció el diagnóstico de dermatitis por Paederus, una reacción irritativa causada por el contacto con un insecto que libera una toxina vesicante. El tratamiento incluyó antihistamínicos, corticosteroides tópicos y aplicación de compresas frías para controlar la inflamación y el prurito. Después de ocho días de terapia, las lesiones mostraron mejoría significativa, aunque persistió una hiperpigmentación residual secundaria a la inflamación previa. Este caso subraya la relevancia de considerar factores ambientales y antecedentes de viaje en el diagnóstico diferencial de lesiones cutáneas, además de demostrar que un manejo oportuno puede prevenir complicaciones mayores."
+        }
+    },
+    {
+        "article": "Un hombre de 35 años de edad, herido en un accidente de tráfico, fue trasladado a nuestro hospital, que está equipado con un ER híbrido. Había sufrido una lesión potencialmente mortal, con su pierna derecha acortada y girada. Los signos vitales del paciente a su llegada fueron los siguientes: frecuencia respiratoria de 24 respiraciones/min, saturación de oxígeno del 99 % con 12 L de administración de oxígeno, frecuencia cardiaca de 143 latidos/min, presión arterial de 80/40 mmHg, y puntuación de Glasgow Coma Scale de E4V4M6. Intentamos realizar un TAC y resucitar al paciente. El TAC reveló un hemotórax izquierdo, ensanchamiento del mediastino, y fractura pélvica. Como la presión arterial del paciente cayó rápidamente antes del TAC, se administraron procedimientos de salvamento, como intubación de emergencia, preperitoneal pelvic packing, y transfusión masiva, con un cuidadoso control de la presión arterial en el ER híbrido. Después de la estabilización de los signos vitales con estos procedimientos, el TAC con contraste reveló una fractura de BTAI de grado IV que se extendía hacia la cavidad torácica izquierda. La embolización arterial transcatéter (TAE) para la fractura pélvica y la fijación esquelética externa de la fractura del fémur derecho se realizaron primero, ya que el radiólogo y el cirujano cardiovascular, que realizan TEVAR en nuestro centro médico, no estaban disponibles en ese momento. Posteriormente, se realizó TEVAR utilizando un injerto de stent (GORE C-TAG 26 × 150 mm; WL Gore & Associates, Flagstaff, Arizona, EE. UU.) en el ER híbrido sin transferir al paciente. Se desplegó un injerto de stent justo distal de la arteria carótida común izquierda (zona II) y el extremo distal del injerto de stent se posicionó en el nivel de Th 8. Decidimos sacrificar LSCA ya que el flujo sanguíneo de la arteria vertebral izquierda fue suficiente según lo evaluado por angiografía. El paciente no tuvo síntomas que sugirieran isquemia después de TEVER. Durante la cirugía, se administraron 50 unidades/kg (3000 unidades) de heparina. El paciente fue trasladado a un hospital de rehabilitación el día 41 postoperatorio.\n",
+        "gold_summary": "Un hombre de 35 años de edad sufrió múltiples lesiones tras un accidente de tráfico y fue trasladado a nuestro hospital en estado de shock. La tomografía computarizada reveló una fractura de TAI de grado IV que se extendía hasta la cavidad torácica y una fractura pélvica. Poco tiempo después de realizar un relleno pélvico preperitoneal y una embolización arterial transcatéter para la fractura pélvica, se realizó un TEVAR en el quirófano híbrido sin trasladar al paciente. El paciente fue trasladado a un hospital de rehabilitación el día 41 después de la operación.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre de 35 años tuvo un accidente y llegó al hospital muy grave. Tenía huesos rotos en la pierna y la pelvis, y una herida en una arteria del pecho. Los médicos usaron máquinas para ver sus heridas y le hicieron varias operaciones para salvarlo. Después de 41 días, pudo ir a otro hospital para seguir su recuperación.",
+            "B2": "Un hombre de 35 años sufrió un accidente de tráfico con lesiones graves, incluyendo una fractura pélvica y una lesión en la arteria torácica. Al llegar al hospital, estaba en estado de shock con presión arterial baja y frecuencia cardíaca alta. Se realizaron varios procedimientos para estabilizarlo, como transfusiones, intubación y control de la fractura pélvica. Luego, se llevó a cabo una cirugía llamada TEVAR para reparar la arteria dañada, sin mover al paciente del quirófano híbrido. La arteria vertebral izquierda tenía buen flujo, por eso se decidió cerrar otra arteria sin problemas. Después de la operación, el paciente mejoró y fue enviado a rehabilitación 41 días más tarde.",
+            "B3": "Un hombre de 35 años sufrió un accidente de tráfico que le causó lesiones graves, incluyendo una fractura pélvica y una lesión traumática aórtica (BTAI) de grado IV que se extendía hacia la cavidad torácica. Al llegar al hospital, presentó signos vitales inestables que requirieron intubación de emergencia, control de hemorragias mediante relleno pélvico preperitoneal y transfusión masiva. Tras estabilizarlo, se realizó una embolización arterial para controlar la fractura pélvica y se fijó externamente la fractura del fémur derecho. Posteriormente, se llevó a cabo una reparación endovascular de la aorta (TEVAR) en el quirófano híbrido, evitando el traslado del paciente, y se decidió sacrificar la arteria subclavia izquierda tras confirmar un flujo sanguíneo adecuado por la arteria vertebral. Durante la cirugía se administró heparina para prevenir coágulos. El paciente evolucionó sin signos de isquemia y fue dado de alta para rehabilitación el día 41 postoperatorio. Este caso muestra la importancia de un manejo multidisciplinario y el uso de tecnología avanzada para tratar lesiones complejas en situaciones críticas."
+        }
+    },
+    {
+        "article": "Hombre de 31 años con antecedentes de consumo de alcohol, tabaco, cocaína inhalada, tuberculosis pulmonar tratada, nefrectomía izquierda y esplenectomía post-traumática. Consultó al servicio de urgencias por cuadro de una semana de evolución que inició inmediatamente posterior a la aplicación intramuscular de penicilina por contacto sexual con pareja con sífilis, caracterizado por dolor en región glútea derecha que irradiaba hasta pie, con posterior aparición de dermatosis purpúrica relacionada con sitio de inyección, siendo una lesión tipo placa configurada en forma anular, con bordes irregulares y distribución racemosa que medía 15 centímetros (cm), con piel sana en su interior. También presentaba una pequeña escara escrotal y una extensa lesión plantar derecha de aspecto livedoide desde la zona talar hasta la punta de los dedos que no respetaba margen estricto. Se realizó ecografía del glúteo mayor, que mostró pérdida del patrón fibrilar heterogéneo, aumento del espesor del mismo a nivel de su tercio medio de aspecto edematoso, además de edema del tejido celular subcutáneo (TCS); en región plantar homolateral y en escroto edema de TCS. En el laboratorio presentó leucocitosis de 13.7 × 109/L, proteína C reactiva de 3.2 mg/dL (normal hasta 0.5 mg/dL), que se interpretaron como reactantes de fase aguda, también aumento de transaminasas con aspartato aminotransferasa de 175 UI/L (normal hasta 32), alanino aminotransferasa de 245 UI/L (normal hasta 33), creatina kinasa con un valor de 2741 UI/L (normal hasta 170) y lactato deshidrogenasa de 2499 UI/L (normal hasta 250) representando compromiso muscular. Se realizaron serologías completas para sífilis, con venereal disease research laboratory (VDRL y anticuerpos treponémicos), virus de la inmunodeficiencia humana (HIV) hepatitis B, hepatitis C, con resultados negativos. La cronología, las manifestaciones clínicas y la posterior biopsia, respaldaron el diagnóstico de síndrome de Nicolau, para lo cual se inició anticoagulación con enoxaparina 1 mg/ kg c/12 hs vía subcutánea, cilostazol 100 mg cada 12 horas y tramadol, por 10 días. Se realizó biopsia de piel de glúteo que evidenció necrosis epidérmica y extensión a epitelio folicular, con formación de ampolla secundaria a reepitelización, sin vasculitis ni trombosis vascular, vinculable a embolia cutis medicamentosa en fase aguda, hubo franca mejoría con descenso de valores de transaminasas, con aspartato aminotransferasa de 39 UI/L, alanino aminotransferasa de 77 UI/L y creatin kinasa de 167 UI/L.  No se solicitó perfil inmunológico, basados en que nuestro diagnóstico presuntivo inicial no justificaba la búsqueda de otras etiologías. Se otorgó alta con cilostazol y analgésicos, control ambulatorio a los 3 meses con mejoría del dolor y de las lesiones, quedando en glúteo derecho cicatriz discrómica con presencia de descamación fina y en pie derecho cicatriz discrómica con zonas de descamación gruesas en región de apoyo tarso metatarsiano asociado a mínimas lesiones livedoides en planta del mismo pie.",
+        "gold_summary": "Se reporta el caso de un hombre de 31 años que presenta este síndrome luego de la aplicación de penicilina benzatínica intramuscular. La biopsia apoyó el diagnóstico. Recibió tratamiento con enoxaparina y cilostazol con posterior mejoría.",
+        "synthetic_summary": {
+            "B1": "Un hombre de 31 años tuvo dolor y una mancha grande en la piel después de recibir una inyección de penicilina. La piel se dañó, pero no hubo infección. Los médicos hicieron una biopsia y vieron que la piel estaba lastimada por la medicina. Lo trataron con medicinas para mejorar la sangre y el dolor. Después, el hombre mejoró y las heridas sanaron con cicatrices pequeñas.",
+            "B2": "Un hombre de 31 años con antecedentes de consumo de drogas y cirugías tuvo dolor en la nalga derecha. Apareció una lesión grande en la piel tras recibir una inyección de penicilina. La lesión tenía bordes irregulares y piel sana en el centro. También tenía heridas en el escroto y el pie derecho. Los exámenes mostraron inflamación, daño en los músculos y aumento de glóbulos blancos, pero no había infecciones como sífilis. La biopsia de piel mostró muerte del tejido sin inflamación en los vasos, indicando síndrome de Nicolau, una complicación rara por la inyección. Se trató con anticoagulantes y analgésicos, mejorando las lesiones y el dolor. Al alta, quedó una cicatriz leve y la recuperación fue progresiva.",
+            "B3": "Un hombre de 31 años con antecedentes de consumo de sustancias y cirugías previas consultó por dolor intenso en la región glútea derecha tras recibir una inyección intramuscular de penicilina por contacto con sífilis. Presentó una lesión cutánea purpúrica y livedoide en el glúteo, escroto y planta del pie derecho, acompañada de inflamación muscular y subcutánea evidenciada por ecografía. Los análisis mostraron inflamación sistémica y daño muscular, aunque las pruebas para sífilis y otras infecciones fueron negativas. La biopsia cutánea reveló necrosis epidérmica sin vasculitis ni trombosis, confirmando el diagnóstico de síndrome de Nicolau, una embolia cutánea inducida por la inyección. Se inició tratamiento con anticoagulantes y analgésicos, logrando mejoría clínica y bioquímica significativa. Al alta, el paciente presentó cicatrices con descamación en las zonas afectadas, y en el seguimiento a los tres meses persistieron lesiones mínimas y mejoría del dolor. Este caso destaca la importancia de reconocer esta rara complicación tras la administración intramuscular de medicamentos para evitar daños mayores y guiar un manejo adecuado."
+        }
+    },
+    {
+        "article": "Un varón de cuatro días de edad, nacido a las 39 semanas y 4 días de gestación, acude a un servicio de urgencias con un empeoramiento de la dificultad respiratoria y el estridor, que se ve agravado por la alimentación y la posición supina.\n\nNació de una madre de 31 años con serología significativa para una prueba de Coomb positiva indirecta, con un parto vaginal sin complicaciones y puntuaciones de APGAR de ocho y nueve en el primer y quinto minuto, respectivamente. Su peso al nacer fue de 3050 g. La ecografía fetal mostró preocupación por un foco intracardíaco, con un embarazo sin complicaciones. El curso de enfermería fue significativo solo por una prueba de audición bilateral fallida y un ecocardiograma normal. El bebé fue dado de alta en el día dos de vida. Se observó que tenía congestión nasal en el momento de la descarga. Se instruyó a la familia para que le aspirara la nariz y usara gotas salinas según fuera necesario.\n\nEn el día cuatro de vida, la madre del lactante notó estridor asociado con dificultad para alimentarse y el pediatra lo derivó al servicio de urgencias. El examen en el servicio de urgencias es significativo para el estridor inspiratorio agudo con tirones traqueales y retracciones subcostal. Además, se observa que tiene pectus excavatum. El estridor y el aumento del trabajo respiratorio mejoran con la posición prona o lateral. La evaluación de laboratorio es significativa para la acidosis respiratoria en el gas sanguíneo venoso [pH 7.18 y CO2 73 mmHg (9,732 Pa)] y el análisis de orina que revela bacterias moderadas y 11-20 glóbulos blancos sin la presencia de nitrito urinario o esterasa leucocitaria. Un recuento sanguíneo completo es tranquilizador. Se le coloca una cánula nasal de alto flujo y se inicia con ampicilina y gentamicina después de obtener cultivos de sangre.\n\nSe le aumentó la presión positiva continua en la vía aérea (CPAP) y se lo trasladó a una unidad de cuidados intensivos neonatales de nivel III para continuar con el tratamiento y la evaluación de otorrinolaringología. Se le introdujo un tubo nasogástrico por las dos fosas nasales sin dificultad. La laringoscopia flexible mostró una cuerda vocal izquierda inmóvil y cavidades nasales estrechas con edema de los cornetes nasales, aritenoides bilaterales y cuerdas vocales. La broncoscopia no reveló ninguna otra anormalidad. El examen físico posterior se caracterizó por rasgos dismórficos sutiles, que incluían orejas de implantación baja, retromicrognatia, microftalmia y clinodactilia de los dedos de los pies. Se interrumpió el tratamiento antibiótico empírico tras un examen infeccioso tranquilizador. Se consultó a un equipo multidisciplinario.\n\nEl paciente finalmente requirió intubación a las dos semanas de vida debido al empeoramiento del fallo respiratorio. Se administraron ciprofloxacina nasal y dexametasona para el edema de las vías respiratorias superiores. Una resonancia magnética del cerebro, cuello y tórax mostró un curso normal de los nervios laríngeos recurrentes. La evaluación genética incluyó un análisis de microarreglo cromosómico normal (CMA). La prueba adicional del panel genético fue positiva para la variante patogénica en el gen CHD7, consistente con el síndrome CHARGE. En este caso, el VFP se atribuyó a la asociación conocida con el síndrome CHARGE. La evaluación continua reveló otras características consistentes con el síndrome CHARGE, incluidos colobomas bilaterales, glaucoma, pérdida auditiva confirmada y anomalías genitales.\n\nLa repetición de la broncoscopia en el día 42 de vida demostró una mejora en el edema laríngeo general, pero continuó con un edema leve de las cuerdas vocales bilaterales. El paciente fue extubado después de la broncoscopia en el marco de un edema de las vías respiratorias mejorado. Sin embargo, fue re-intubado el día 46 de vida debido al empeoramiento de la insuficiencia respiratoria. La repetición de la laringoscopia ese día mostró un edema continuado. En este momento, el paciente ya había recibido múltiples ciclos cortos de Dexamethasone en un intento de disminuir el edema de las vías respiratorias. Debido a la necesidad de re-intubación, fue tratado con Tobramycin tópico y Dexamethasone aplicado directamente a las cuerdas vocales mediante laringoscopia directa durante cinco días. Después de este tratamiento, fue extubado con éxito a los dos meses de edad y se le colocó un tubo de gastrostomía a los tres meses.\n\nEn el momento de la colocación del tubo de gastrotomía, se le realizó una broncoscopia y una microlaringoscopia adicionales que demostraron que la cuerda vocal izquierda afectada originalmente era totalmente móvil, pero que mostraba una nueva inmovilidad de la cuerda derecha; la etiología de esto no está clara. Ambas cuerdas vocales seguían estando ligeramente edematosas, pero habían mejorado mucho desde la evaluación anterior. El paciente fue dado de alta en aire ambiente a los cuatro meses de edad y continúa siendo seguido de cerca por el otorrinolaringólogo. En la laringoscopia ambulatoria de repetición a los cuatro meses de edad, ambas cuerdas aparecían móviles con un edema de las vías respiratorias continuado.\n\n",
+        "gold_summary": "Un bebé de cuatro días de edad, a término, varón, nacido por parto vaginal sin complicaciones, con un curso de enfermería significativo para la falta de audición, se presentó en un departamento de emergencias (DE) con dificultad respiratoria y estridor en aumento. Fue trasladado a una unidad de cuidados intensivos neonatales (UCIN) de nivel III para una evaluación posterior y se le practicó una intubación debido a la hipercarbia progresiva. La laringoscopia reveló una parálisis unilateral de las cuerdas vocales (PCV) del lado izquierdo. Se le sometió a una evaluación posterior que incluyó un cerebro, cuello y tórax normales en una resonancia magnética. Se consultó a genética por la preocupación de los rasgos dismórficos en el examen físico. Después de las pruebas del panel de genes, la PCV se atribuyó a la asociación conocida con el síndrome CHARGE. Se observó un edema de las vías respiratorias en la laringoscopia que impidió la extubación hasta los dos meses de edad. Se identificaron otras características del síndrome CHARGE, incluidos los colobomas, el glaucoma, la pérdida auditiva neurosensorial y las anomalías genitales. Se le dio de alta con aire ambiente y después de la colocación de un tubo de gastrostomía con seguimiento de otorrinolaringología.\n",
+        "synthetic_summary": {
+            "B1": "Un bebé de cuatro días tenía problemas para respirar y un ruido raro al respirar llamado estridor. Fue llevado al hospital y le hicieron pruebas que mostraron que una cuerda vocal no se movía bien. También descubrieron que tenía un síndrome llamado CHARGE, que causa varios problemas de salud. El bebé recibió tratamiento y mejoró poco a poco. Después de dos meses, pudo respirar mejor y salió del hospital con cuidados especiales.",
+            "B2": "Un bebé de cuatro días, nacido sin problemas, llegó al hospital con dificultad para respirar. Tenía un sonido agudo al inhalar llamado estridor, que empeoraba al alimentarse o estar boca arriba. En el hospital, vieron que una de sus cuerdas vocales no se movía, lo que dificultaba su respiración. Además, tenía rasgos físicos poco comunes, por eso hicieron pruebas genéticas. Estas pruebas confirmaron que tenía síndrome CHARGE, una enfermedad que afecta ojos, oídos y órganos genitales. El bebé necesitó un tubo para respirar durante dos meses y luego pudo hacerlo solo. También le pusieron un tubo para alimentarse directo al estómago y sigue siendo revisado por especialistas.",
+            "B3": "Un recién nacido de cuatro días, nacido a término por parto vaginal sin complicaciones, acudió a urgencias por dificultad respiratoria y estridor que empeoraban con la alimentación y la posición supina. En la evaluación inicial, se detectó estridor inspiratorio, acidosis respiratoria y signos de infección urinaria, por lo que se inició tratamiento antibiótico y soporte respiratorio con CPAP. La laringoscopia reveló parálisis unilateral de la cuerda vocal izquierda y edema en las vías respiratorias superiores, mientras que la broncoscopia no mostró otras anomalías. Además, se identificaron rasgos dismórficos y, tras una evaluación genética, se confirmó el diagnóstico de síndrome CHARGE, una condición que afecta múltiples órganos y explica la parálisis vocal. Durante su evolución, el paciente requirió intubación prolongada y tratamiento con corticosteroides y antibióticos tópicos para reducir el edema laríngeo. Finalmente, fue extubado con éxito y se le colocó un tubo de gastrostomía para alimentación. Fue dado de alta con seguimiento cercano por otorrinolaringología, presentando mejoría en la movilidad de las cuerdas vocales y control del edema respiratorio. Este caso destaca la importancia de una evaluación multidisciplinaria en neonatos con síntomas respiratorios y características dismórficas."
+        }
+    },
+    {
+        "article": "Mujer de 17 años oriunda de Tucumán, acudió a la consulta por cuadro de vías aéreas superiores y hemoptisis leve. La tomografía computarizada de tórax informó, en lóbulo superior derecho, una imagen redondeada de paredes regulares y lisas de 25x24x24 mm, rodeado de un tenue halo periférico en vidrio esmerilado. No se observaba realce ante la administración de contraste endovenoso. Se sugirió un posible quiste broncogénico, por lo que se realizó una RMN de tórax que informó imagen redondeada de paredes regulares y lisas que alcanzó un diámetro anteroposterior de 25 x 24 x 24.5 mm con intensidad de señal líquida. Debido a la localización central de la lesión, se realizó una lobectomía superior derecha videoasistida. Dado que el estudio anatomopatológico intraoperatorio fue indeterminado, se complementó la resección pulmonar con un vaciamiento ganglionar mediastínico. La anatomía patológica definitiva informó neumocitoma esclerosante de 2 x 1.7 cm. La inmunomarcación fue positiva para TTF1, CK, CK7 y napsina.",
+        "gold_summary": "Describimos aquí el caso de una paciente de 17 años con diagnóstico de neumocitoma esclerosante con presentación infrecuente.",
+        "synthetic_summary": {
+            "B1": "Una joven de 17 años tenía tos y un poco de sangre al toser. Le hicieron una radiografía especial y vieron una bolita en el pulmón derecho. Los médicos pensaron que era un quiste y le sacaron esa parte del pulmón. Al revisar bien, encontraron que era un tumor llamado neumocitoma esclerosante, que es raro. Ahora está en tratamiento y bajo cuidado.",
+            "B2": "Una joven de 17 años consultó por tos con sangre leve y síntomas respiratorios. La tomografía mostró una lesión redonda en el pulmón derecho, sin cambios con contraste, lo que sugirió un quiste broncogénico, una bolsa anormal con líquido. La resonancia confirmó que la lesión contenía líquido en su interior. Por la ubicación, se decidió extirpar la parte superior del pulmón derecho con cirugía asistida por video. Durante la operación, no se pudo identificar el tipo exacto de lesión, por eso se retiraron ganglios cercanos para análisis. El estudio final reveló un neumocitoma esclerosante, un tumor pulmonar raro y benigno. Los análisis mostraron que las células tenían marcadores específicos que confirmaron el diagnóstico.",
+            "B3": "Una joven de 17 años consultó por síntomas respiratorios y hemoptisis leve. La tomografía mostró una lesión redondeada con bordes lisos en el lóbulo superior derecho del pulmón, sin realce tras contraste, lo que sugirió inicialmente un quiste broncogénico. La resonancia magnética confirmó una imagen con características líquidas y tamaño similar. Debido a la ubicación central de la lesión, se decidió realizar una lobectomía videoasistida y un vaciamiento ganglionar mediastínico, ya que el diagnóstico intraoperatorio no fue concluyente. El estudio anatomopatológico final identificó un neumocitoma esclerosante, un tumor pulmonar poco común, con marcadores inmunohistoquímicos positivos para TTF1, CK, CK7 y napsina. Este caso resalta la importancia de considerar diagnósticos poco frecuentes en lesiones pulmonares en jóvenes y la necesidad de un manejo quirúrgico cuidadoso para obtener un diagnóstico definitivo y tratamiento adecuado. Por lo tanto, el seguimiento y evaluación continua serán clave para asegurar un buen pronóstico."
+        }
+    },
+    {
+        "article": "Una mujer asiática de 28 años fue admitida en el hospital para el tratamiento de «una masa pélvica durante 10 meses» el 11 de noviembre de 2018. La paciente solía tener menstruación regular, volumen menstrual moderado, dismenorrea y un G1P0L0A1. Examen ginecológico: la parte posterior del útero tenía aproximadamente 8 cm de diámetro con poca actividad y sensibilidad, pero no se observaron otras anomalías. La paciente no tenía una causa obvia de dolor abdominal durante los primeros 10 meses previos al ingreso. El examen de ultrasonido reveló una masa heterogénea en la parte superior derecha del útero con un diámetro de aproximadamente 4 cm, un nódulo del epiplón mayor con un diámetro de aproximadamente 2 cm y un nivel de CA125 sérico de 416 mU/mL. Se diagnosticó como «endometriosis, masas pélvicas inflamatorias». Se administró una terapia de rehidratación antiinfecciosa y se dio de alta a la paciente con alivio del dolor. Dos semanas después del alta, el nivel de CA125 sérico de la paciente disminuyó a 106 mU/mL y volvió a la normalidad después de 6 semanas. Sin embargo, la masa pélvica aumentó gradualmente. El reexamen de la ecografía pélvica realizada mostró una masa ecoica mixta de 7.7 cm x 7.4 cm x 8.2 cm en el lado derecho del útero con un límite claro, eco puntiforme fino en el quiste y derrame abdominal y pélvico. La ecografía de contraste mostró que la pared del quiste de la masa pélvica estaba significativamente mejorada, se sospechaba malignidad y se recomendó un tratamiento quirúrgico. El 14 de noviembre de 2018, la paciente se sometió a liberación de adherencias pélvicas e intestinales transabdominales, omento, ovarios bilaterales, peritoneo multipunto y múltiples adenomiosis y histerectomía. Durante la operación, se aspiraron aproximadamente 600 ml de ascitis hemorrágica. Tras la exploración, se observó una masa de color rojo grisáceo con un diámetro de aproximadamente 8 cm en la superficie del epiplón mayor, que era suave y se asemejaba a carne podrida. Se encontraron depósitos de celulosa marrón difusos en la superficie del útero, ovarios bilaterales, pared abdominal, tracto intestinal, surco lateral del recto y pared anterior del recto. Las lesiones no se eliminaron por completo y algunas áreas se electrocoagularon. El examen patológico de la muestra resecada mostró endometriosis del tejido retiniano con vasodilatación, ampollas, infiltración linfocítica difusa y focal, folículos ováricos císticos bilaterales, fibrosis peritoneal dentro de la necrosis del tejido adiposo, proliferación de fibroblastos, aumento de la infiltración de células espumosas y adenomiosis uterina. La patología de ascitis mostró muchos glóbulos rojos, un pequeño número de linfocitos y neutrófilos y ninguna célula tumoral. Después de la operación, la paciente se recuperó sin problemas y se trató con agonista de la hormona liberadora de gonadotropina (GnRH-α). Se inició leuprorelina una vez al mes durante 6 meses, seguido de dienogest oral (DNG) durante 3 años, después de lo cual se interrumpió la medicación durante 3 meses. La paciente concibió de forma natural y tuvo un embarazo normal. Se dio a luz a un bebé de 3300 g por vía vaginal a las 39 semanas + 3 días de gestación. Tanto la madre como el bebé estaban sanos, sin recurrencia ni reacciones adversas durante el seguimiento.\n\nMH - Humanos\nMH - Mujer\nMH - *Endometriosis/complicaciones/terapia\nMH - Adulto",
+        "gold_summary": "Preocupaciones de la paciente: Una mujer de 28 años de edad vino a nuestro hospital para recibir tratamiento debido al descubrimiento de una masa pélvica 10 meses antes. Después de la admisión, la paciente se sometió a tratamiento quirúrgico y fue dada de alta en 1 semana. Recibió tratamiento médico durante 3 años después del alta. Después de la retirada de la medicación, la paciente quedó embarazada y dio a luz a un niño sin recurrencia durante el seguimiento.\n\nDiagnósticos: Los diagnósticos iniciales al ingreso fueron «¿masa pelviana inflamatoria?» y «¿endometriosis?». Después de 10 meses, la paciente volvió a ser internada en el hospital debido a un aumento gradual de la masa, y se le diagnosticó endometriosis.\n\nIntervenciones: El paciente fue tratado con terapia antiinfecciosa de rehidratación por primera vez, y el paciente fue tratado quirúrgicamente por segunda vez, seguido de agonista de la hormona liberadora de gonadotropina (GnRH-α) y tratamiento con dienogest (DNG) después de la cirugía.\n\nResultados: Después de 6 ciclos de tratamiento con GnRH-α y 3 años de tratamiento con DNG, un hijo nació con éxito tras la interrupción de la medicación y, hasta ahora, no se han producido reacciones adversas ni recurrencias durante el período de seguimiento.\n",
+        "synthetic_summary": {
+            "B1": "Una mujer de 28 años tenía una masa en la parte baja de su barriga desde hace 10 meses. Los doctores le hicieron una operación para quitarla y luego le dieron medicinas por tres años. Después de dejar las medicinas, pudo tener un bebé sano sin problemas. La masa era por una enfermedad llamada endometriosis, que causa dolor y bultos en el útero. Ella se recuperó bien y está sana.",
+            "B2": "Una mujer de 28 años tuvo una masa en la pelvis durante 10 meses con dolor leve. Su menstruación era regular, pero al llegar al hospital encontraron una masa en el útero. También tenía un nivel alto de CA125, una proteína que indica inflamación o enfermedad. Primero recibió medicamentos, pero la masa creció y parecía peligrosa, por eso la operaron. Durante la cirugía encontraron tejido inflamado y endometriosis, que es tejido del útero fuera de su lugar. Después, recibió tratamiento hormonal por tres años para evitar que la enfermedad volviera. Finalmente, pudo quedar embarazada y tuvo un bebé sano sin problemas. Su recuperación fue buena y no tuvo complicaciones.",
+            "B3": "Una mujer de 28 años fue hospitalizada por una masa pélvica presente durante 10 meses, inicialmente diagnosticada como posible endometriosis o inflamación. Al ingreso, se detectó una masa en el útero y un nivel elevado de CA125, marcador asociado a procesos inflamatorios o malignos. Tras un tratamiento inicial con antibióticos y rehidratación, el nivel de CA125 volvió a la normalidad, pero la masa creció, lo que llevó a una intervención quirúrgica para extirpar adherencias y tejido afectado. Durante la operación se encontraron lesiones extensas y ascitis hemorrágica, y el análisis patológico confirmó endometriosis con inflamación y fibrosis. Posteriormente, la paciente recibió terapia hormonal con agonistas de GnRH y dienogest durante varios años. Tras la suspensión del tratamiento, logró un embarazo natural y dio a luz sin complicaciones. Durante el seguimiento, no se observaron recurrencias ni efectos adversos, lo que sugiere que el manejo combinado quirúrgico y médico fue efectivo para controlar la enfermedad y preservar la fertilidad. Este caso resalta la importancia de un diagnóstico cuidadoso y un tratamiento integral en pacientes jóvenes con masas pélvicas sospechosas."
+        }
+    },
+    {
+        "article": "Presentamos una paciente de 76 años de edad, que es traída al servicio de urgencias por bajo nivel de conciencia con tendencia al sueño.\n\nComo antecedentes médicos de interés destaca una enfermedad pulmonar intersticial difusa, dislipemia e hipertensión arterial.\n\nA la exploración física el paciente se encuentra estuporosa, arreactiva, con atonía de las 4 extremidades y desviación conjugada de la mirada hacia la derecha, sin fiebre y con una leve sequedad en piel y mucosas. La analítica sanguínea no muestra alteraciones significativas.\n\nEl paciente es valorado por el servicio de neurología que considera la realización de una TC cerebral urgente ante la sospecha de patología intracraneal de evolución aguda. Las pruebas de imagen ponen de manifiesto la presencia de numerosas burbujas aéreas que se disponen en los surcos cerebrales, cuerpo calloso y ambos tálamos así como áreas hipodensas cortico-subcorticales de distribución parcheada en hemisferio cerebeloso izquierdo y parietooccipitales bilaterales, todo ello compatible con isquemia cerebral subaguda secundaria a embolismo gaseoso.\n\nAnte los antecedentes personales de enfermedad pulmonar intersticial difusa se decide también realizar una placa de tórax en proyección anteroposterior y una TC torácica que objetivan un neumotórax apical izquierdo y aire ectópico en mediastino superior.\n\nSe decide el ingreso en la Unidad de Ictus del centro para control estrecho de constantes, sin embargo, la paciente presenta una evolución tórpida con el fallecimiento el segundo día de ingreso debido a fracaso multiorgánico.",
+        "gold_summary": "Paciente de 76 años con una enfermedad pulmonar intersticial difusa preexistente, que experimentó un ictus masivo debido a un neumomediastino espontáneo. Su presentación incluyó confusión, convulsiones y debilidad motora. Las pruebas de imagen revelaron burbujas de aire en los surcos cerebrales y áreas hipodensas en el cerebelo y parietooccipitales. Además, se observó neumotórax y aire en el mediastino superior en las radiografías de tórax y la tomografía torácica. A pesar de las medidas terapéuticas como el oxígeno hiperbárico, la paciente lamentablemente falleció debido al fallo multiorgánico.",
+        "synthetic_summary": {
+            "B1": "Una mujer de 76 años llegó al hospital muy dormida y con problemas para moverse. Tenía una enfermedad en los pulmones y presión alta. Las pruebas mostraron que había burbujas de aire en su cerebro y aire fuera del pulmón. Esto causó un daño en su cerebro. Aunque la cuidaron mucho, ella murió después de dos días por problemas en varios órganos.",
+            "B2": "Una mujer de 76 años con enfermedad pulmonar crónica llegó al hospital muy somnolienta. Estaba adormecida, sin responder y con debilidad en brazos y piernas. Las imágenes del cerebro mostraron burbujas de aire que bloquearon vasos sanguíneos, causando daño por falta de sangre. También se encontró aire fuera del pulmón (neumotórax) y en la zona central del pecho (mediastino). La paciente fue ingresada para vigilancia, pero su estado empeoró. Finalmente, falleció por fallo de varios órganos. Este caso muestra que problemas pulmonares pueden causar daños graves en el cerebro por aire en la sangre.",
+            "B3": "Una mujer de 76 años con enfermedad pulmonar intersticial difusa fue ingresada por bajo nivel de conciencia y tendencia al sueño. En la exploración, se encontró estupor, falta de respuesta y desviación ocular, sin fiebre ni alteraciones en análisis sanguíneos. La tomografía cerebral mostró múltiples burbujas de aire en áreas clave del cerebro, junto con lesiones compatibles con isquemia causada por embolismo gaseoso. Debido a sus antecedentes pulmonares, se realizó una radiografía y tomografía de tórax que revelaron un neumotórax apical izquierdo y aire en el mediastino superior. La paciente fue ingresada en la Unidad de Ictus para monitorización, pero su estado empeoró rápidamente, falleciendo al segundo día por fallo multiorgánico. Este caso resalta la gravedad de las complicaciones pulmonares que pueden desencadenar embolismos gaseosos cerebrales y la dificultad para su manejo clínico."
+        }
+    },
+    {
+        "article": "Un hombre de 24 años de edad, de etnia persa, presentó una queja principal de mal olor bucal después de un período de recuperación de la enfermedad leve por coronavirus 2019 (COVID-19), que quería resolver lo antes posible. Su dentista notó pérdida ósea y sangrado al explorar el área interproximal de los dientes número 18 y 19 clínicamente. Se realizó un escalamiento y un aplanamiento radicular, y se ordenaron radiografías periapicales y panorámicas para la evaluación del paciente. Sin embargo, el paciente se negó a tomar radiografías. La halitosis del paciente disminuyó después de 1 semana de tratamiento. Después de 2 meses, el paciente volvió a su dentista con la queja principal de sensibilidad al frío en sus incisivos mandibulares. El dentista realizó una prueba de vitalidad, y los dientes eran vitales excepto los números 23 y 24. El dentista tomó una radiografía periapical, y una lesión radiolucente en la mandíbula anterior era evidente.\n\nEn la radiografía panorámica, se evidenció una lesión radiolúcida lítica grande y bien definida con bordes festoneados que se extendían desde el diente número 31 en el lado derecho hasta el ramus ascendente izquierdo. Un estudio posterior de tomografía computarizada de haz cónico (TCFC) reveló una lesión lítica multilocular grande, con un margen relativamente distinto, que causó adelgazamiento y perforación de los cortexes bucales y linguales y signos de festoneado.\n\nTras el examen, se remitió al paciente a un cirujano oral y maxilofacial. En la entrevista médica, el paciente explicó su prolapso de la válvula mitral; antecedentes de episodios recurrentes de otitis desde el primer año de vida; antecedentes de septicemia de origen desconocido cuando tenía un año de edad, tras episodios de diarrea y vómitos; antecedentes de uso de broncodilatadores para la alergia estacional; antecedentes de uso de levotiroxina, cabergolina, acetato de desmopresina (DDAVP) en spray y gel de testosterona durante 4 años tras el diagnóstico de síndrome de silla turca vacía, tras poliúria y polidipsia; y, por último, antecedentes de infección reciente por COVID-19 (3 meses antes). Su historia familiar reveló tiroiditis de Hashimoto en su familia materna; su abuelo, su madre y sus tres tías padecían este tipo de hipotiroidismo. El historial quirúrgico previo del paciente incluía una reparación de una hernia inguinal 10 años antes sin complicaciones. Además, el paciente era obeso, con un índice de masa corporal (IMC) de 34,5.\n\nEn el examen clínico, los hallazgos extraorales e intraorales no fueron relevantes. Los exámenes de laboratorio, incluido el recuento sanguíneo completo (CBC), fueron normales, excepto por un aumento en la velocidad de sedimentación globular (ESR) y los niveles de proteína C reactiva (CRP). Se realizó una biopsia incisional en la mandíbula anterior y la muestra se envió al departamento de patología oral y maxilofacial de la Universidad de Ciencias Médicas Shahid Beheshti. Las secciones mostraron una infiltración difusa de grandes células de tinción pálida, como los histiocitos, con eosinófilos dentados y numerosos en el fondo fibroso. Un examen de inmunohistoquímica (IHC) reveló un positivo disperso para el grupo de diferenciación 1a (CD-1a) (+ +), un positivo fuerte para Langerin (CD-207) (+ + +), y más del 50% positivo para S-100.\n\nDe acuerdo con los datos clínicos, radiológicos e histopatológicos, se llegó al diagnóstico de LCH. Los diagnósticos diferenciales fueron osteomielitis, granuloma eosinófilo y metástasis ósea. Sin embargo, debido a las pruebas de laboratorio, los datos radiológicos y el historial clínico, se confirmó el diagnóstico de LCH. Por lo tanto, para un examen más a fondo, el paciente fue derivado al departamento de medicina nuclear para una tomografía por emisión de positrones con fluor-2-desoxiglucosa y una tomografía computarizada (FDG PET/CT), que reveló lesiones líticas hipermetabólicas en la mandíbula, el parietal derecho, el frontal izquierdo y el esfenoidal izquierdo, y opacidad hipermetabólica en el seno etmoidal izquierdo. Además, se observó una actividad metabólica aumentada en la región sellar, hidrocefalia comunicante y amígdalas palatinas hipermetabólicas prominentes. Además, se evidenció una actividad metabólica heterogénea aumentada en las tibias y fémures bilaterales.\n\nUna resonancia magnética del cerebro reveló una notable ampliación de la intensidad del material del líquido cefalorraquídeo (LCR) que contiene la silla turca. La adenohipófisis apareció como una capa delgada en la base de la silla turca agrandada, y se observaron cambios homogéneos e inflamatorios en las células aéreas mastoideas izquierdas. Se observó la extensión de la inflamación hacia el oído medio izquierdo (es de destacar que el paciente había sufrido de otitis durante muchos años). De acuerdo con la implicación multifocal de la enfermedad y su pronóstico cuestionable, el paciente fue derivado al departamento de oncología para quimioterapia sistémica. Pruebas posteriores revelaron mutaciones en el oncogen BRAF y no se detectaron mutaciones en KRAS y NRAS. El oncólogo eligió un régimen de denosumab, vinblastina, etopósido, 6-mercaptopurina, metotrexato y pegfilgrastim; sin embargo, el seguimiento no fue posible ya que el paciente falleció tras un accidente.\n",
+        "gold_summary": "Un paciente de 24 años de edad, de etnia persa, se presentó con una queja principal de halitosis tras recuperarse de la enfermedad por coronavirus 2019 en el consultorio de su dentista general. Los exámenes intraorales y extraorales no revelaron ningún problema específico. En la sesión de seguimiento tras el tratamiento periodontal de fase I, la sensibilidad de los dientes al estímulo frío era evidente, y las radiografías revelaron una gran lesión intraósea lítica en la mandíbula. Una biopsia incisional reveló células de Langerhans y una reacción positiva a Langerina y al grupo de diferenciación 1a, por lo que se le diagnosticó histiocitosis de células de Langerhans. Después de realizar una tomografía por emisión de positrones con fluoro-2-desoxiglucosa y una tomografía computarizada, una resonancia magnética y una tomografía computarizada de haz cónico, debido a la implicación generalizada de la enfermedad, el paciente fue derivado a un oncólogo. En última instancia, se descubrió que los problemas de salud infantil del paciente, incluidos los problemas endocrinos, probablemente fueron causados por una histiocitosis de células de Langerhans no diagnosticada. El oncólogo eligió un régimen de denosumab, vinblastina, etopósido, 6-mercaptopurina, metotrexato y pegfilgrastim. El seguimiento no fue posible ya que el paciente falleció tras un accidente.\n",
+        "synthetic_summary": {
+            "B1": "Un joven de 24 años tuvo mal olor en la boca después de recuperarse de COVID-19. Su dentista encontró problemas en los huesos de la mandíbula y le hizo un tratamiento. Más tarde, se descubrió una lesión grande en su mandíbula. Los médicos hicieron pruebas y encontraron una enfermedad llamada histiocitosis de células de Langerhans, que afecta los huesos y otros órganos. El paciente recibió tratamiento, pero murió en un accidente.",
+            "B2": "Un hombre de 24 años consultó por mal olor en la boca después de recuperarse del COVID-19. Su dentista notó pérdida de hueso y sangrado entre dos dientes, y tras un tratamiento, la halitosis mejoró. Sin embargo, dos meses después, el paciente tuvo sensibilidad dental y se descubrió una lesión grande en la mandíbula mediante radiografías. Una biopsia confirmó que tenía histiocitosis de células de Langerhans, una enfermedad que afecta los huesos y otros órganos. Estudios adicionales mostraron que la enfermedad estaba en varias partes del cuerpo, por eso fue enviado a oncología para quimioterapia. El paciente tenía antecedentes de problemas de salud desde niño, posiblemente relacionados con esta enfermedad. Lamentablemente, no se pudo hacer un seguimiento porque falleció en un accidente.",
+            "B3": "Un hombre de 24 años presentó mal olor bucal tras recuperarse de COVID-19, y su dentista detectó pérdida ósea y sangrado entre dos molares. Aunque inicialmente mejoró con tratamiento periodontal, luego desarrolló sensibilidad dental y se descubrió una lesión ósea grande en la mandíbula mediante radiografías. Una biopsia mostró células características de la histiocitosis de células de Langerhans (LCH), una enfermedad rara que afecta huesos y tejidos. Estudios de imagen adicionales revelaron que la enfermedad estaba extendida a varios huesos del cráneo y extremidades, así como inflamación en el cerebro y oído medio, vinculada a antecedentes de otitis recurrente y problemas endocrinos desde la infancia. Debido a la afectación múltiple, el paciente fue derivado a oncología para recibir quimioterapia con varios fármacos. Se identificó una mutación en el gen BRAF, relacionada con la enfermedad. Lamentablemente, no se pudo realizar seguimiento porque el paciente falleció en un accidente. Este caso destaca la importancia de considerar la LCH en pacientes jóvenes con síntomas óseos y antecedentes médicos complejos, ya que su diagnóstico temprano puede influir en el tratamiento y pronóstico."
+        }
+    },
+    {
+        "article": "La paciente es una mujer de 66 años de edad que goza de buena salud. A mediados de la década de 1980, recibió varias sesiones de tratamiento con rayos grenz en el cuero cabelludo para aliviar el picor asociado con la psoriasis del cuero cabelludo. Con un tratamiento regular de aproximadamente una sesión al mes durante un período de 5 años, que se complementó de vez en cuando con alquitrán de hulla, ácido salicílico y prednisona, logró cierto alivio de su enfermedad. Con el tiempo, su cabello se adelgazó; la piel en toda el área del cuero cabelludo se volvió sensible al dolor y se produjo cicatrización. Los tratamientos con rayos grenz se habían administrado en una clínica privada; no se disponía de detalles del tratamiento, como la dosis única y acumulada. No había sufrido radiodermitis.\n\nEn un período muy breve en 2020, unos 35 años después de que cesara el tratamiento de radiación, aparecieron numerosos BCC y queratosis actínicas premalignas (AK) en su cuero cabelludo. Se inició un régimen de tratamiento de extirpación quirúrgica de BCC verificado por histología preoperatoria y crioterapia de AK por evaluación del médico. La terapia fotodinámica o los tratamientos tópicos no eran aplicables debido a la sensibilidad al dolor y las secuelas de la cirugía. De 2020 a 2022, recibió varios tratamientos de criocirugía y curetaje y un total de 13 extirpaciones quirúrgicas de BCC por cirugía de Mohs. Se estima que su número total de extirpaciones a lo largo del tiempo es de unos 30. Los BCC recalcitrantes y de novo en el cuero cabelludo cada vez más dañado, obviamente, son un desafío eterno; por lo tanto, los cirujanos plásticos y los dermatólogos buscaban otra modalidad de tratamiento con un mejor índice terapéutico.\n\nEn septiembre de 2022, aparecieron nuevos CCB confirmados histológicamente en el cuero cabelludo. La exploración por ultrasonido (DermaScan C, Cortex Technology ApS, Aalborg, Dinamarca) mostró tumores ecolucidos de 0,5-1,3 mm de espesor en ambos sitios analizados histológicamente, así como en algunas lesiones adicionales que pudieron identificarse en base al examen clínico y dermatoscópico. La paciente, tras ser informada, dio su consentimiento por escrito para el tratamiento con HIFU, con o sin biopsia de pretratamiento de las lesiones sospechosas.\n\nSe delinearon las lesiones elegibles para el tratamiento con un rotulador impermeable, incluyendo un margen perilesional de 2 mm. Se mapeó cada lesión seleccionada en una lámina transparente para ayudar a determinar la ubicación precisa en el seguimiento. Se usó el ultrasonido de 20 MHz para confirmar la profundidad de las lesiones identificadas al inicio y en las visitas de seguimiento posteriores. Debido al estado del cuero cabelludo conocido por ser sensible al dolor, se administró anestesia local (lidocaína 25 mg/ml + adrenalina 5 mg/ml, Amgros I/S, Copenhagen, Dinamarca) a todas las lesiones 10-15 minutos antes del tratamiento.\n\nLas lesiones fueron tratadas con HIFU utilizando la sonda de 1.3 mm; ajustes de 150 ms/dosis y energía acústica de 0.9 J/dosis. Se aplicaron 20-200 dosis a las lesiones, dependiendo de la extensión de la lesión. Las lesiones tratadas se curaron de forma espontánea sin complicaciones o necesidad de tratamiento especial. Se programaron visitas de seguimiento cada 3-6 meses para controlar la tasa de curación/recaída, tolerancia local y lesiones nuevas no identificadas anteriormente.\n\nDurante los 15 meses posteriores a la limpieza inicial con HIFU, se trataron con HIFU un total de 10 lesiones que, de acuerdo con las rutinas, hubieran requerido una biopsia seguida de una cirugía de escisión, en sesiones de unos 30 minutos. Las lesiones se curaron en unos pocos días sin complicaciones ni necesidad de intervención. Se observó una limpieza total en 7 de 8 lesiones de BCC tratadas y en ambas lesiones de AK. La única lesión recurrente de BCC de pequeño tamaño se observó después de 15 meses entre las primeras seis lesiones tratadas; la lesión se volvió a tratar con HIFU. Ejemplos de lesiones curadas 15 meses después del tratamiento con HIFU; el tumor con recurrencia.\n",
+        "gold_summary": "Una mujer de 66 años que en la década de 1980 había recibido varios tratamientos de rayos gamma en el cuero cabelludo desarrolló múltiples carcinomas basocelulares en la zona. Se le habían realizado más de 30 cirugías de escisión, incluida la cirugía de Mohs, en el pasado, con muchas complicaciones locales, pero, no obstante, los cánceres recurrentes. Los tratamientos con HIFU aplicados a ocho carcinomas basocelulares y dos lesiones precancerosas dieron como resultado una limpieza completa en el control a los 12 meses, pero una recurrencia después de 15 meses.\n",
+        "synthetic_summary": {
+            "B1": "Una mujer de 66 años tuvo problemas en su cuero cabelludo por un tratamiento con rayos hace muchos años. Aparecieron muchos bultos que eran cáncer de piel. Ella tuvo muchas cirugías para quitar esos bultos, pero algunos volvieron. Luego, le trataron con una máquina especial llamada HIFU, que usa calor para curar sin cortar. Después de un año, casi todos los bultos se curaron, pero uno volvió y lo trataron otra vez.",
+            "B2": "Una mujer de 66 años recibió en los años 80 tratamientos con rayos en el cuero cabelludo para la psoriasis, lo que causó adelgazamiento y cicatrización de la piel. Treinta y cinco años después, aparecieron muchos carcinomas basocelulares (cáncer de piel) y lesiones precancerosas. Se realizaron más de 30 cirugías para eliminarlos, pero los tumores seguían apareciendo. En 2022, se usó un nuevo tratamiento llamado HIFU, que usa ultrasonido para destruir las lesiones sin cirugía. Después de 15 meses, siete de ocho cánceres y dos lesiones precancerosas desaparecieron sin complicaciones. Solo una lesión pequeña volvió a aparecer y se trató de nuevo con éxito. Este método parece una buena opción para casos difíciles.",
+            "B3": "Una mujer de 66 años, que en los años 80 recibió tratamientos con rayos grenz en el cuero cabelludo para psoriasis, desarrolló décadas después múltiples carcinomas basocelulares (BCC) y queratosis actínicas (AK), lesiones premalignas. A pesar de más de 30 cirugías, incluyendo cirugía de Mohs, y tratamientos con crioterapia, las lesiones persistían y el cuero cabelludo estaba sensible y cicatrizado. En 2022 se empleó ultrasonido para evaluar las lesiones y se inició tratamiento con ultrasonido focalizado de alta intensidad (HIFU), que permite destruir tumores mediante calor sin cirugía. Se aplicó anestesia local y se trataron 10 lesiones en sesiones breves. La mayoría de las lesiones curaron espontáneamente sin complicaciones y se observó una limpieza completa en 7 de 8 BCC y en ambas AK durante un seguimiento de 15 meses. Solo una lesión pequeña recurrió y fue tratada nuevamente con éxito. Este caso muestra que el HIFU puede ser una opción efectiva y menos invasiva para tratar BCC resistentes en un cuero cabelludo dañado y sensible, aunque se requiere seguimiento para detectar recurrencias. Por lo tanto, esta técnica podría ofrecer un mejor balance entre eficacia y tolerancia en pacientes con múltiples lesiones difíciles de manejar."
+        }
+    },
+    {
+        "article": "Se realizó un trasplante cardíaco ortotópico a una niña de 12 años con insuficiencia cardíaca en fase terminal debido a una miocardiopatía restrictiva. Durante la operación, se presentó una disfunción primaria grave del injerto, que requirió el uso de oxigenación por membrana extracorpórea venosa arterial. La función cardíaca se recuperó completamente después de 4 días, y su período postoperatorio se complicó por una insuficiencia renal aguda transitoria y un bloqueo auriculoventricular completo que duró >3 semanas después de la operación. Para evitar la disincronía del ventrículo izquierdo y el posible daño de la derivación del ventrículo derecho debido a las biopsias endomiocárdicas de vigilancia de rechazo múltiple, se indicó un marcapasos biventricular transvenoso que utiliza un marcapasos del ventrículo izquierdo aislado a través de la vena coronaria.\n\nBajo anestesia local y sedación suave, se cortó la vena cefálica izquierda y se introdujo un catéter guía en la vena subclavia y se colocó en el seno coronario inicialmente para realizar un venograma cardiaco. Se implantó un electrodo de estimulación endocárdica de elución de esteroides unipolar con mecanismo de fijación activa (Attain StarFix® 4195, Medtronic, Minneapolis, MN) en la rama de la vena interventricular anterior. Las medidas en el momento del implante fueron las siguientes: umbral 2 V a 0,4 ms, onda R 6 mV e impedancia 300 Ω a 4,8 mA. Se implantó un segundo electrodo de estimulación endocárdica de elución de esteroides bipolar con fijación activa (2088T®, St. Jude Medical, Minneapolis, MN) en la aurícula derecha.\n\nAmbos cables se aseguraron y se conectaron a un marcapasos adaptable a la frecuencia (Accent DR®, St. Jude Medical, Minneapolis, MN) que se colocó en una bolsa muscular infraclavicular izquierda y se programó a VDD. Las mediciones de los cables electrofisiológicos fueron estables después del implante: umbral ventricular 1.5 V a 0.7 ms, onda R 4.5 mV, onda P 4.3 mV (bipolar), impedancia ventricular 260 Ω y vida útil estimada de la batería de 5 años.\n\nEl electrocardiograma posterior al implante mostró complejos de morfología de bloqueo de rama derecha, y la evaluación ecocardiográfica mostró ausencia de disincronías auriculoventriculares, interventriculares e intraventriculares. En el seguimiento a 5 años, el paciente permaneció en Clase Funcional I con el mismo sistema de estimulación y conservó la función ventricular.\n\nMH - Bloqueo auriculoventricular/etiología/*terapia\nMH - Niño\nMH - Sinus coronario\nMH - Mujer\nMH - Insuficiencia cardiaca/cirugía\nMH - Trasplante de corazón/*efectos adversos\nMH - Ventrículos del corazón\nMH - Humanos\nMH - *Marcapasos, artificial\nMH - Disfunción/complicaciones/tratamiento del injerto primario\n",
+        "gold_summary": "Se sometió a un trasplante de corazón ortotópico a un niño de 12 años con insuficiencia cardiaca en fase terminal debido a una miocardiopatía restrictiva. La disfunción primaria del injerto precisó oxigenación con membrana extracorpórea venosa arterial. La función cardiaca se normalizó, pero el bloqueo auriculoventricular completo persistió después de 3 semanas. Se realizó un marcapaso bicameral con marcapaso transvenoso del ventrículo izquierdo a través del seno coronario. Tras 5 años de seguimiento, el paciente se encuentra estable con el mismo sistema de marcapaso y con la función ventricular preservada.\n",
+        "synthetic_summary": {
+            "B1": "Una niña de 12 años recibió un trasplante de corazón porque su corazón estaba muy enfermo. Durante la operación, su nuevo corazón tuvo problemas y usaron una máquina para ayudar a que el corazón funcionara. Después, le pusieron un marcapasos especial para ayudar a que su corazón latiera bien. Cinco años después, la niña está bien y su corazón funciona correctamente con el marcapasos.",
+            "B2": "Una niña de 12 años con insuficiencia cardíaca grave recibió un trasplante de corazón. Durante la operación, el nuevo corazón tuvo problemas y usaron una máquina que oxigena la sangre. Después de cuatro días, su corazón mejoró, pero apareció un bloqueo en la señal eléctrica que duró más de tres semanas. Para tratarlo, le pusieron un marcapasos que estimula ambos ventrículos, con un cable en una vena llamada seno coronario. Cinco años después, la niña está estable, con buen funcionamiento del corazón y sin problemas con el marcapasos. Este caso muestra que, aunque hubo complicaciones, el tratamiento fue exitoso a largo plazo.",
+            "B3": "Una niña de 12 años con insuficiencia cardíaca terminal por miocardiopatía restrictiva recibió un trasplante cardíaco ortotópico. Durante la cirugía, presentó una disfunción grave del injerto que requirió oxigenación por membrana extracorpórea, logrando recuperación completa en cuatro días. Sin embargo, desarrolló un bloqueo auriculoventricular completo que persistió más de tres semanas y una insuficiencia renal aguda transitoria. Para prevenir problemas de sincronía ventricular y daños por biopsias frecuentes, se implantó un marcapasos biventricular transvenoso con un electrodo en el ventrículo izquierdo a través del seno coronario. El procedimiento se realizó bajo sedación leve y anestesia local, y las mediciones eléctricas del marcapasos fueron estables. Tras cinco años de seguimiento, la paciente mantiene una función ventricular preservada y se encuentra en clase funcional I, sin disincronías cardíacas. Este caso muestra que el uso de marcapasos biventriculares transvenosos puede ser una opción efectiva y segura para manejar bloqueos auriculoventriculares prolongados tras trasplante cardíaco en niños, mejorando la calidad de vida y la función cardíaca a largo plazo."
+        }
+    },
+    {
+        "article": "Una paciente de 20 años de edad se presentó con distensión abdominal progresiva asociada con calambres abdominales, incapacidad para expulsar flatos y heces, así como vómitos frecuentes de materia ingerida y biliar de un día de duración. El día anterior, dio a luz por cesárea por una indicación de bradicardia fetal severa. También tenía preeclampsia sin signos de gravedad y desnutrición de inicio en la edad adulta con un índice de masa corporal (IMC) de 16,5 kg/M2. No tenía antecedentes de cirugía abdominal previa. Negó cualquier queja similar en el pasado o antecedentes de cambio de hábitos intestinales o estreñimiento con paso de heces sanguinolentas. No tenía ninguna enfermedad médica crónica conocida.\n\nEn el examen físico, la paciente se veía enferma y con dolor. Su presión arterial era de 90/70 mmHg, su pulso oscilaba entre 116 y 120 latidos por minuto, y su frecuencia respiratoria era de 22 a 24 respiraciones por minuto. No se registró fiebre. Su abdomen estaba muy distendido y simétrico, con visibles movimientos intestinales peristálticos. Había una difusa sensibilidad directa en todo su abdomen, más en el cuadrante inferior derecho. Había un signo positivo de acumulación de fluido intraperitoneal con opacidad cambiante. Había una herida quirúrgica suprapúbica bien aproximada con un vendaje limpio. El examen rectal digital no mostró nada destacable. Tenía una herida superficial lineal de 3 cm de largo, orientada verticalmente, en su labio mayor izquierdo, que el equipo de obstetricia pensó inicialmente que era una quemadura de yodo en la piel.\n\nSe le introdujo un catéter y se le resucitó con dos bolsas de solución salina normal y produjo 200 ml de orina en una hora. Se le introdujo una sonda nasogástrica (NGT) pero no hubo una salida significativa. Se le realizó un hemograma completo y una radiografía abdominal simple. Su recuento de glóbulos blancos era de 1780 células/µl con predominio de neutrófilos del 88 %, hemoglobina de 12,7 mg/dl y un recuento de plaquetas de 78 x 103/ µl. Su prueba de función renal era normal y sus enzimas hepáticas estaban ligeramente elevadas por encima del rango normal pero no fue significativo. Su radiografía abdominal simple muestra múltiples niveles de aire-líquido ubicados centralmente con un bucle intestinal grande dilatado ubicado periféricamente y blanqueamiento del espacio pélvico que indica una acumulación de líquido. No se solicitó una tomografía computarizada abdominal (CT) porque trabajamos en un entorno con recursos limitados y para pacientes con obstrucción intestinal, solicitamos una tomografía computarizada cuando existe la posibilidad de un diagnóstico alternativo o cuando se sospecha una obstrucción tumoral.\n\nTras obtener el consentimiento informado por escrito, se exploró a la paciente bajo anestesia general con un diagnóstico de abdomen agudo secundario a obstrucción intestinal mixta secundaria a vólvulo del intestino delgado. El hallazgo intraoperatorio fue un íleon distal que rodeaba el ciego y el colon ascendente proximal, ambos móviles y no adheridos a la pared abdominal posterolateral derecha. Tanto el íleon como el ciego, así como el colon ascendente, eran viables. La punta del apéndice estaba enredada con el nudo ileal y estaba gangrenoso. El intestino delgado proximal y el intestino grueso distal estaban muy distendidos, pero en su ubicación normal. Había unos cuatro litros de líquido intraperitoneal seroso.\n\nDurante la operación, la paciente se mantuvo hipotensa (80/50 mmHg) desde que se le indujo la anestesia y se le administró un vasopresor. Debido a la inestabilidad de la paciente y a la viabilidad de los intestinos afectados por el nudo, se procedió a una hemicolectomía derecha. Se realizó una descompresión proximal y distal de los intestinos delgado y grueso distendidos, respectivamente. Se fijó el ciego y el colon ascendente a la pared abdominal posterolateral derecha con suturas seromusculares interrumpidas con hilo no absorbible (Silk 2-0).\n\nDespués del procedimiento, se le retiró la intubación y se le dio alimentación por vía oral (NPO) durante 24 horas y se le administró un fluido de mantenimiento con reposición de la pérdida. A pesar de la reanimación con fluidos y el apoyo con vasopresores, ella se encontraba persistentemente hipotensa, por lo que se le administró un tratamiento antibiótico doble con ceftriaxona 1 g, IV, BID y metronidazol 500 mg, IV, TID, en vista de un posible shock séptico de origen genitourinario. Su estado empeoró gradualmente y, tras una nueva evaluación el primer día postoperatorio, la herida superficial en su vulva se había extendido hacia la zona suprapúbica con signos clínicos de gangrena de Fournier. Por ello, revisamos su tratamiento antibiótico a meropenem 1 g, IV, BID, vancomicina 1 g, IV, BID y metronidazol 500 mg, IV, TID. Después de obtener el consentimiento informado por escrito, se la volvió a llevar al quirófano para un desbridamiento radical de la gangrena de Fournier y, posteriormente, se la trasladó a la unidad de cuidados intensivos quirúrgicos (ICU) intubada debido a un shock séptico persistente y un retraso en la recuperación de la anestesia. Lamentablemente, falleció con fallo multiorgánico debido a un shock séptico refractario en su segundo día postoperatorio, después de la exploración inicial.\n",
+        "gold_summary": "Presentamos un caso de nudos ileocecales en una paciente posparto con distensión abdominal, vómitos y ausencia de heces y flatos. La radiografía abdominal simple reveló bucles intestinales dilatados con múltiples niveles de aire y fluidos. Se realizó una laparotomía exploratoria con hallazgo intraoperatorio de nudos ileocecales con intestino viable, ciego móvil y colon ascendente y punta gangrenosa del apéndice. Deshicimos el nudo y realizamos una apendectomía. Debido a la inestabilidad intraoperatoria de los signos vitales de la paciente, se aplazó la hemicolectomía derecha y se fijaron el ciego y el colon ascendente a la pared abdominal posterolateral derecha.\n",
+        "synthetic_summary": {
+            "B1": "Una joven tuvo dolor y su barriga muy hinchada después de tener un bebé. No podía ir al baño ni sacar gases y vomitaba mucho. Los doctores vieron que su intestino estaba torcido y con problemas. La operaron para arreglarlo, pero luego se enfermó más y tuvo una infección grave. Aunque intentaron ayudarla, no pudo mejorar y falleció.",
+            "B2": "Una joven de 20 años, recién operada por cesárea, llegó con dolor y distensión abdominal. No podía expulsar gases ni heces y tenía vómitos frecuentes. La radiografía mostró intestinos dilatados con niveles de aire y líquido, señal clara de obstrucción intestinal. En la cirugía, encontraron un nudo en el intestino cerca del ciego y colon, con el apéndice inflamado y sin sangre. Deshicieron el nudo y quitaron el apéndice enfermo. Como la paciente estaba inestable, no hicieron cirugía mayor, sino fijaron partes del intestino para evitar movimientos. Después, la paciente desarrolló una infección grave llamada gangrena de Fournier y falleció por shock séptico y fallo de órganos. Este caso muestra la importancia de un diagnóstico y tratamiento rápido tras el parto.",
+            "B3": "Una mujer de 20 años, recién dada a luz por cesárea, presentó distensión abdominal progresiva, dolor, vómitos y ausencia de evacuación. Su examen mostró abdomen distendido con sensibilidad y signos de acumulación de líquido en el abdomen. La radiografía evidenció dilatación intestinal con niveles de aire y líquido. Durante la cirugía, se encontró un nudo formado por el íleon alrededor del ciego y colon ascendente, con la punta del apéndice gangrenosa. Aunque los intestinos eran viables, la paciente se mantuvo inestable, por lo que se realizó una hemicolectomía derecha y se fijaron el ciego y el colon a la pared abdominal para evitar recurrencias. Posteriormente, desarrolló una infección grave llamada gangrena de Fournier, que requirió desbridamiento quirúrgico y tratamiento antibiótico intensivo. A pesar de las intervenciones, la paciente sufrió un shock séptico refractario que llevó a un fallo multiorgánico y su fallecimiento. Este caso resalta la complejidad de manejar complicaciones posparto con obstrucción intestinal y la importancia de un diagnóstico y tratamiento oportunos para evitar desenlaces fatales."
+        }
+    },
+    {
+        "article": "Un hombre de 38 años se presentó en el hospital con opresión en el pecho y falta de aire. Tres años antes, había experimentado síntomas similares después de la actividad y recibió tratamiento en nuestro hospital. La ecocardiografía ambulatoria indicó una masa de eco del corazón izquierdo que sugería un mixoma, lo que llevó a su ingreso para una evaluación adicional. El examen físico reveló pigmentación de las orejas del paciente caracterizada por múltiples puntos pequeños de color café y negro. La tomografía computarizada abdominal (TC) mostró múltiples hígados y pequeños quistes en el riñón izquierdo. Las pruebas genéticas identificaron mutaciones en los genes TTN y PRKAR1A. El diagnóstico de CNC se confirmó mediante examen clínico, imágenes y pruebas genéticas. Después del tratamiento sintomático, la condición del paciente mejoró; sin embargo, rechazó la intervención quirúrgica. El 20 de septiembre de 2023, el paciente se presentó en nuestro hospital con opresión en el pecho y falta de aire exacerbadas. Informó dificultad para permanecer acostado boca arriba y necesidad de sentarse erguido para respirar. El examen físico reveló distensión de la vena yugular, desplazamiento hacia la izquierda y hacia abajo del límite del corazón, ritmo cardíaco irregular en la auscultación y un murmullo de la válvula mitral de intensidad 2/6-3/6 en el cuarto espacio intercostal a lo largo del margen izquierdo del esternón. Se escucharon estertores húmedos en ambos campos pulmonares medio e inferior. La palpación reveló un hígado firme que se extendía tres dedos por debajo del proceso xifoides y dos dedos por debajo de la caja torácica, junto con un edema de pitting leve en ambas extremidades inferiores. Las imágenes ecocardiográficas indicaron un agrandamiento global del corazón, dilatación del seno aórtico y arteria pulmonar, regurgitación mitral pequeña a moderada y una masa ecógena irregular que medía 54 mm × 43 mm en la cámara izquierda unida al tabique auricular. La fracción de eyección del ventrículo izquierdo (FEVI) fue del 23,1 %, con acortamiento fraccional (FS) del 10,9 %. La electrocardiografía demostró fibrilación auricular (frecuencia ventricular promedio, 150 latidos/min) y ondas Q anormales en las derivaciones V1-V3. Basándose en la historia del paciente, el diagnóstico incluyó DCM y CNC con mixoma cardíaco. Dada la presencia de insuficiencia cardíaca en etapa terminal y mixoma cardíaco concurrente, el paciente fue hospitalizado y se consideró el trasplante de corazón como una opción terapéutica viable para abordar ambas afecciones simultáneamente. Un corazón de donante adecuado estuvo disponible para su trasplante inmediato el 1 de octubre de 2024.\n\n\nProcedimiento quirúrgico\n\nLa piel y los tejidos subcutáneos se incisionaron cuidadosamente capa por capa a través de una esternotomía media. El esternón se abrió longitudinalmente y se controló el sangrado mediante electrocoagulación y cera ósea. La exploración extracardíaca reveló un agrandamiento global del corazón, más prominente en el ventrículo izquierdo. El corazón mostró una disminución de la fuerza contráctil. La aorta y la arteria pulmonar principal (AP) se diseccionaron desde la región supravalvular. Algunos tejidos se conservaron para suturarlos posteriormente, mientras que la mayor parte de la aurícula derecha enferma, la aurícula izquierda (AL), el ventrículo derecho y el ventrículo izquierdo se extirparon. La resección reveló una masa mucoide de color blanco grisáceo. Los tejidos de la aurícula izquierda del donante y del receptor se suturaron utilizando hilos Prolene 3/0 dobles continuos. La anastomosis se inspeccionó meticulosamente varias veces y no se observó sangrado significativo. De forma similar, la anastomosis término-terminal de la aorta ascendente del donante y la arteria pulmonar del receptor se realizó utilizando suturas Prolene 5/0 continuas, y una inspección cuidadosa no reveló sangrado.\n\nAdemás, la LA del donante y la PA del receptor se cerraron de forma segura utilizando suturas Prolene 5/0 dobles y continuas. Los tejidos de la vena cava inferior tanto del donante como del receptor se suturaron de forma similar con suturas Prolene 5/0, y se realizaron varias inspecciones para confirmar que no había presencia de sangrado significativo. El lado izquierdo del corazón se desinfló y, a medida que comenzó el recalentamiento, se restableció la oxigenación, se soltó la aorta ascendente y el corazón volvió espontáneamente al ritmo sinusal. Se aplicó sutura continua con Prolene 5/0 tanto a la vena cava superior del donante como del receptor y se inspeccionó de forma diligente para garantizar la ausencia de sangrado significativo. Después de la interrupción exitosa de la circulación asistida, se descanuló la cavidad venosa. Se recogieron muestras de tejido del corazón izquierdo y de la materia gris del paciente para un examen histopatológico, y se confirmó el diagnóstico de DCM y mixoma cardiaco.\n\n\nManejo postoperatorio\n\nEl primer día después del trasplante de corazón, el paciente produjo 1200 ml de orina. Los exámenes de laboratorio revelaron un nivel de troponina T hipersensible de 796.70 ng/L y un nivel de NT-proBNP de 10798 pg/ml. El recuento completo de sangre mostró un recuento de glóbulos blancos de 17.15 × 109/L, sin anomalías significativas en otros resultados de exámenes. El ecocardiógrafo mostró un EFV del 65 %, FS del 35 %, un espesor de la pared ventricular normal y ecogenicidad, y no se observaron anomalías discernibles en la morfología y estructura de la válvula. Después del trasplante de corazón, se administró una terapia hormonal intravenosa de succinato sódico de metilprednisolona (0.25 g) para mejorar la inmunidad, y se proporcionó un tratamiento intravenoso antiinfeccioso con cefoperazona y sulbactam sódico (2 g). El paciente recibió una solución nutriente y tiopronina en el primer día después de la cirugía. En el día tres postoperatorio, se reemplazó el succinato sódico de metilprednisolona con acetato de prednisona oral (25 mg). Se administraron cápsulas de micofenolato de mofetilo (0.5 g) por vía oral para minimizar el rechazo del corazón, y se administró acetato de carpofénico intravenoso (50 mg) para prevenir infecciones fúngicas. La producción de orina del paciente fue de 2000 ml, con niveles de troponina T hipersensible de 390 ng/L, niveles de NT-proBNP de 7877 pg/ml, y un recuento de leucocitos de 12.15 × 109/L. En el día siete postoperatorio, se introdujeron cápsulas de tacrolimus a una dosis oral de (1 mg) para minimizar el rechazo del paciente al corazón del donante, con un cuidadoso monitoreo de las concentraciones sanguíneas. Subsiguientemente, la dosis oral de acetato de prednisona se redujo gradualmente a (10 mg) mientras se ajustaba la concentración sanguínea de tacrolimus a 10.90 ng/L. La recuperación del paciente mejoró. El 20 de octubre de 2023, la ecocardiografía de seguimiento (Fig. 6) no mostró anomalías, con niveles de troponina T de 85 ng/L, NT-proBNP de 210 pg/ml, y todos los demás resultados de exámenes dentro de los rangos normales. El paciente exhibió una excelente recuperación postoperatoria y fue dado de alta. Las visitas regulares de seguimiento a nuestro departamento después del alta mostraron que el paciente permanece en buen estado.\n\nMH - Humanos\nMH - *Cardiomiopatía, Dilatada/cirugía/etiología/diagnóstico/diagnóstico por imágenes\nMH - Hombre\nMH - *Complejo de Carney/genética/diagnóstico/cirugía/complicaciones\nMH - Adulto\nMH - *Trasplante de corazón\nMH - *Mixoma/complicaciones/cirugía/diagnóstico por imágenes/diagnóstico/genética\nMH - *Insuficiencia cardiaca/etiología/diagnóstico/cirugía\nMH - *Neoplasias cardiacas/cirugía/complicaciones/diagnóstico por imágenes/diagnóstico/genética\nMH - Resultado del tratamiento\nMH - Subunidad/genética de la proteína quinasa Rlalpha dependiente de AMP cíclico\n",
+        "gold_summary": "Aquí, reportamos un caso de insuficiencia cardiaca debido al síndrome de Carney que resultó en mixoma cardiaco combinado con cardiomiopatía dilatada. Un hombre de 35 años de edad fue admitido en el hospital hace tres años debido a opresión torácica repentina y falta de aire. La ecocardiografía indicó mixoma, y una combinación de cribado genético y examen físico confirmó el síndrome de Carney con mixoma cardiaco. Después del tratamiento sintomático, fue dado de alta. Las intervenciones quirúrgicas no fueron consideradas en ese momento. Sin embargo, la opresión torácica y los síntomas de falta de aire del paciente empeoraron, y volvió al hospital. Se confirmó una función cardiaca de grado IV de la New York Heart Association, y la ecocardiografía indicó la presencia de cardiomiopatía dilatada acompañada de mixoma cardiaco. En última instancia, la insuficiencia cardiaca del paciente fue tratada con éxito con un trasplante cardiaco.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre de 35 años tenía problemas en el corazón que le causaban dolor en el pecho y dificultad para respirar. Los médicos encontraron un bulto llamado mixoma en su corazón y una enfermedad llamada síndrome de Carney. Con el tiempo, su corazón se hizo más débil y grande. Para ayudarlo, le hicieron un trasplante de corazón, y después de la operación, se recuperó muy bien. Ahora está sano y sigue en control con los doctores.",
+            "B2": "Un hombre de 38 años sentía opresión en el pecho y dificultad para respirar. Tres años antes, le detectaron un mixoma cardíaco, un tumor benigno en el corazón. También le diagnosticaron síndrome de Carney, una enfermedad genética que causa tumores y manchas en la piel. Aunque mejoró con tratamiento, no quiso operarse. Después, sus síntomas empeoraron y le diagnosticaron insuficiencia cardíaca grave con cardiomiopatía dilatada, que es cuando el corazón se agranda y no bombea bien. Le hicieron un trasplante de corazón para tratar estas enfermedades. Tras la operación, su función cardíaca mejoró mucho y se recuperó sin problemas. Ahora sigue controles médicos y está estable.",
+            "B3": "Un hombre de 38 años con síndrome de Carney, una enfermedad genética rara que causa tumores en el corazón, presentó opresión en el pecho y dificultad para respirar. Inicialmente, se detectó un mixoma cardíaco, un tumor benigno, y se confirmó el diagnóstico mediante pruebas genéticas y clínicas. A pesar del tratamiento sintomático, el paciente rechazó la cirugía y su condición empeoró, desarrollando insuficiencia cardíaca avanzada y cardiomiopatía dilatada, que afecta la capacidad del corazón para bombear sangre. La ecocardiografía mostró un corazón agrandado con una masa tumoral significativa y función ventricular gravemente reducida. Debido a la gravedad de su estado, se optó por un trasplante de corazón, que se realizó con éxito. El procedimiento quirúrgico incluyó la extirpación del corazón enfermo y la implantación del órgano donante, con cuidados postoperatorios que evitaron el rechazo y las infecciones. Tras la cirugía, el paciente mostró una recuperación notable, con mejoría en la función cardíaca y sin complicaciones importantes. Este caso destaca la importancia del diagnóstico temprano y el manejo adecuado del síndrome de Carney con mixoma cardíaco y cardiomiopatía dilatada, donde el trasplante cardíaco puede ser una opción vital en etapas avanzadas."
+        }
+    },
+    {
+        "article": "Un paciente de 52 años de edad con un diagnóstico inicial de arteria pulmonar fue admitido en el departamento de cardiología para una evaluación médica y una decisión sobre el tratamiento posterior. El paciente tenía un historial de neumotórax espontáneo del lado derecho, tratado con toracocentesis y drenaje por vacío 35 años antes. El paciente sentía una disnea creciente al hacer ejercicio. También se quejaba de signos de insuficiencia ventricular derecha y cianosis. Cuatro años antes, el paciente fue hospitalizado tres veces por fibrilación auricular paroxística que se convirtió en ritmo sinusal por cardioversión eléctrica, además de que el examen electrocardiográfico era normal.\n\nEn ese mismo año, la angiografía coronaria indicó arterias coronarias normales. La ecocardiografía reveló una hipertensión pulmonar leve con una presión sistólica calculada en el ventrículo derecho de 36 mmHg sin dilatación de ese ventrículo.\n\nEn los años siguientes, se observó insuficiencia cardiaca progresiva con aumento de la presión arterial pulmonar en la ecocardiografía. Se realizó angio-CT en dos ocasiones y se excluyó la hipertensión pulmonar tromboembólica crónica en cada ocasión. La tomografía computarizada de alta resolución excluyó la patología pulmonar intersticial. La espirometría fue normal. La detección de enfermedades autoinmunes y la infección por VIH fue negativa.\n\n\nLínea de tiempo: historia, curso de la enfermedad, diagnóstico y tratamiento\n\n1976  neumotórax derecho\n2007 Hospitalizado tres veces por fibrilación auricular e insuficiencia cardiaca. Se le realizaron ecocardiografías, cardioversiones y coronografías. En cada ocasión, fue dado de alta de los servicios con diagnósticos de fibrilación auricular, insuficiencia cardiaca e insuficiencia cardiaca de clase II de la NYHA.\n2010-2011: Aumento de la falta de aire y síntomas de insuficiencia cardiaca. El paciente fue hospitalizado tres veces. Se detectaron características indirectas de hipertensión pulmonar en ecocardiografía. Se realizó tres veces un examen de tórax por TAC; se excluyó la embolia pulmonar o la hipertensión arterial pulmonar tromboembólica crónica (2 x angio-TAC) o la fibrosis pulmonar (tomografía computarizada de alta resolución).\nSe estableció el diagnóstico de hipertensión pulmonar, clase III de la OMS.\nDEC-2011 Admisión a la clínica de cardiología – ecocardiografía (TTE, TEE), prueba de caminata de 6 minutos, NT-proBNP, cateterización cardiaca derecha, prueba de vasoreactividad pulmonar.\nSe estableció el diagnóstico de hipertensión pulmonar arterial irreversible.\nSe ha iniciado el tratamiento con iloprost y sildenafil\nEn enero de 2012, visita de control: mejora en la clase de la OMS, disminución de la concentración de NT-proBNP e incremento de la distancia en la prueba de 6 minutos.\nMAY-2012. Control RHC. La SaO2 de las muestras de sangre obtenidas durante el RHC de la arteria del lóbulo superior del pulmón derecho fue del 87 %.\nEl diagnóstico angiográfico de las arterias pulmonares reveló fístulas de HAP entre las arterias subclavianas y el lóbulo superior del pulmón derecho.\nJUN 2012  angiografía por TC de las arterias sistémicas reveló la presencia adicional de fístulas arteriales bronquiales en el lóbulo superior de las arterias del pulmón derecho\nIII-2013 Embolización de fístulas\nVI-2013. Muerte como resultado del empeoramiento de la insuficiencia cardiaca, combinado con neumonía.\n\n\n\nEn el ingreso a nuestra clínica, la clase funcional del paciente fue evaluada como OMS III. En el examen físico, el segundo sonido cardiaco (S2) fue acentuado con S2 dividido ensanchado. Además, la auscultación cardiaca indicó un murmullo holosistólico de regurgitación tricuspídea. La auscultación del tórax no mostró un murmullo vascular. La cianosis periférica y central fue marcada. Se examinaron la hepatomegalia, el edema periférico y las venas varicosas bilateralmente.\n\nLa SaO2 obtenida por el método de oximetría de pulso se redujo al 88 %. La electrocardiografía reveló fibrilación auricular, desviación del eje derecho y onda T negativa en las derivaciones precordiales v1-v3. Las pruebas adicionales fueron las siguientes: concentración de NT-proBNP - 3383 pg/ml, distancia de la prueba de caminata de seis minutos - 373 m con 7/10 puntos en la escala de disnea de Borg.\n\nLa ecocardiografía mostró características de hipertensión pulmonar grave: agrandamiento del ventrículo derecho a 44 mm (cuatro cámaras), con función deprimida del TAPSE del ventrículo derecho de 9 mm, agrandamiento del área de la aurícula derecha a 40 cm2, regurgitación tricuspídea grave (++++), aumento del PSVR calculado a 112 mmHg, acortamiento del tiempo de aceleración de la arteria pulmonar a 60 ms y derrame pericárdico leve. No hubo defecto en el tabique interventricular. La ecocardiografía transesofágica tampoco mostró un defecto en el tabique auricular, lo que se confirmó más tarde con angio-TAC.\n\n\nLa SaO2 de la sangre obtenida de la arteria radial se redujo al 87,8%. Se realizó un cateterismo cardiaco derecho. La SaO2 de las muestras de sangre obtenidas durante el RHC de la vena cava superior, la vena cava inferior, la aurícula derecha, el tronco pulmonar, la arteria del lóbulo medio del pulmón derecho y la arteria pulmonar izquierda ascendieron respectivamente a: 64,8%; 77,4%; 73,2%; 70,2%; 69,3%; 71,2% y no indicaron la presencia de un shunt de izquierda a derecha.\n\nLas mediciones hemodinámicas mostraron una hipertensión pulmonar precapilar grave, irreversible en las pruebas de vasoreactividad con óxido nítrico inhalado (80 ppm) y una combinación de sildenafil oral (50 mg) y óxido nítrico inhalado (80 ppm).\n\nEn base a todos los datos clínicos y los resultados de la RHC, se estableció un diagnóstico de hipertensión pulmonar idiopática irreversible.\n\nSe inició el tratamiento con iloprost inhalado (Ventavis) 6 × 5 µg y sildenafil (Revatio) por vía oral 3 × 20 mg. Además, se administraron digoxina (0,1 mg diarios), warfarina (INR rango: 2-3), furosemida (40 mg por vía oral diarios) y espironolactona (100 mg diarios).\n\nUn mes después se realizó un seguimiento no invasivo. El paciente manifestó una mejoría en la capacidad física, clase II según la OMS, concentración de NT-proBNP: 1014 pg/ml. Distancia en la prueba de caminata de seis minutos: 471 m.\n\nCinco meses después se realizó una evaluación invasiva. La RHC mostró valores de PAP más elevados que en las mediciones iniciales [75,4/51,8 (59,7) mm Hg] y PVR (13,4 WU) (Tabla 22 – control RHC).\n\nLa saturación de oxígeno de las muestras de sangre obtenidas durante la RHC de la arteria lobular superior del pulmón derecho fue elevada y ascendió al 89.7%.\n\nEn la angiografía pulmonar se detectó la reducción del trazo vascular periférico típico de la hipertensión arterial pulmonar y la falta de contraste de la arteria del lóbulo superior derecho. Además, se encontró evidencia de flujo sanguíneo retrógrado visible como un contraste negativo en la arteria pulmonar derecha. Después, se realizó una arteriografía de la arteria subclavia derecha y se detectó una enorme malformación vascular que se comunicaba con la arteria del lóbulo superior derecho.\n\nLa angio-TC de las arterias sistémicas confirmó la presencia de las fístulas previamente descritas y reveló la presencia adicional de fístulas de la arteria bronquial en el lóbulo superior de las arterias del pulmón derecho.\n\nSe realizó embolización selectiva de las fístulas (mezcla al 50% de Lipiodol y pegamento monomérico de n-butil-2-cianoacrilato). La embolización no produjo ningún cambio clínico en el estado del paciente.\n\nMH - Fístula arterio-arterial/*complicaciones\nMH - *Cateterización cardiaca\nMH - Angiografía por tomografía computarizada\nMH - Hipertensión pulmonar primaria familiar/*diagnóstico/terapia farmacológica\nMH - Resultado fatal\nMH - Insuficiencia cardiaca/fisiopatología\nMH - Humanos",
+        "gold_summary": "Un paciente caucásico de 52 años de edad con hipertensión pulmonar (HP) confirmada por ecocardiografía fue admitido en el departamento de cardiología debido a disnea de esfuerzo y signos de insuficiencia ventricular derecha. La exploración rutinaria para detectar causas de HP secundaria fue negativa. El cateterismo cardiaco derecho (CCR) confirmó una HP arterial de alto grado [presión arterial pulmonar media (PAPm); 50,6 mmHg, presión de enclavamiento pulmonar (PWP); 11,3 mmHg, resistencia vascular pulmonar (PVR); 11,9 unidades de Wood (UW)] irreversible en la prueba con óxido nítrico inhalado. La saturación de oxígeno (SaO2) de las muestras de sangre obtenidas durante el primer CCR osciló entre 69,3 y 73,2%. Se diagnosticó hipertensión arterial pulmonar idiopática. Se inició el tratamiento con iloprost inhalado y sildenafil.\n\nEl control RHC, realizado 5 meses después, mostró valores de mPAP (59,7 mmHg) y PVR (13,4 WU) más altos en comparación con la medición inicial. El SaO2 de sangre obtenida durante el RHC de la arteria del lóbulo superior del pulmón derecho fue elevado y ascendió al 89,7 %.\n\nLuego se realizó una arteriografía pulmonar. Se encontró falta de contraste en la arteria del lóbulo superior derecho con evidencia de flujo sanguíneo retrógrado visible como contraste negativo en la arteria pulmonar derecha. Después, una arteriografía de la arteria subclavia derecha detectó una enorme malformación vascular que se comunicaba con la arteria del lóbulo superior derecho. Después, un angiograma por tomografía computarizada (angio-CT) reveló adicionalmente el agrandamiento de las arterias bronquiales que se originaban en las fístulas hacia la arteria pulmonar del lóbulo superior derecho.\n\nA pesar del tratamiento farmacológico intensivo, que incluyó la terapia de la hipertensión pulmonar y la embolización percutánea de las fístulas, el estado del paciente siguió deteriorándose. Falleció tres meses después de la embolización debido a una insuficiencia cardiaca grave complicada por neumonía.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre de 52 años tenía dificultad para respirar. Su corazón derecho no funcionaba bien. Los médicos vieron que tenía presión alta en las arterias del pulmón. Le dieron medicinas, pero su salud empeoró. Encontraron vasos raros en su pulmón derecho y trataron de cerrarlos. No mejoró y murió por problemas del corazón y una infección.",
+            "B2": "Un hombre de 52 años con hipertensión pulmonar (presión alta en las arterias del pulmón) tenía dificultad para respirar y signos de insuficiencia del lado derecho del corazón. Tras varias pruebas, se confirmó que su hipertensión pulmonar era grave y no reversible. Se inició un tratamiento con medicamentos para mejorar la circulación pulmonar. Sin embargo, cinco meses después, una nueva prueba mostró que su presión pulmonar había aumentado y se descubrió una malformación en las arterias del pulmón derecho. Se intentó tratar esta malformación con un procedimiento llamado embolización, pero no mejoró su condición. Lamentablemente, el paciente murió tres meses después debido a una insuficiencia cardiaca grave y una infección pulmonar. Este caso muestra lo difícil que puede ser tratar algunas formas de hipertensión pulmonar.",
+            "B3": "Un hombre de 52 años con hipertensión pulmonar (HP) presentó dificultad para respirar y signos de insuficiencia ventricular derecha. Tras descartar causas secundarias, el cateterismo cardiaco confirmó una HP arterial grave e irreversible. Inicialmente, la saturación de oxígeno en sangre fue baja, pero cinco meses después aumentó en la arteria del lóbulo superior derecho. La angiografía reveló una malformación vascular con fístulas entre arterias sistémicas y pulmonares en ese mismo lóbulo. A pesar del tratamiento con iloprost y sildenafil, y la embolización de las fístulas, la función cardiaca empeoró. El paciente falleció tres meses después debido a insuficiencia cardiaca y neumonía. Este caso resalta la complejidad de la HP idiopática cuando se asocia a malformaciones vasculares, lo que dificulta el manejo y empeora el pronóstico, incluso con terapias avanzadas."
+        }
+    },
+    {
+        "article": "Paciente de 73 años, diagnosticada de enfermedad pulmonar obstructiva crónica (EPOC), hipertensión arterial (HTA), trastorno bipolar, ansiedad, depresión, hipotiroidismo y artritis reumatoide, condiciones para las cuales tiene prescrito el tratamiento reflejado en el Anexo I.\n\nRealiza una llamada telefónica a la farmacia comunitaria para solicitar información sobre una nueva medicación prescrita para el tratamiento de una infección de orina y un déficit de vitamina D, diagnosticados tras la realización de una analítica completa en el servicio de urgencias de un hospital privado.\n\nLa paciente es totalmente dependiente y no sale de casa, siendo su cuidadora la persona que siempre va a retirar su medicación y elabora los pastilleros semanales.\n\nLos fármacos prescritos para el tratamiento de la infección de orina fueron cefuroxima 250 mg (1 comprimido cada 12 horas durante 5 días) y butilescopolamina 10 mg (1 comprimido en la mañana si presentaba molestias).\n\nPara el déficit de vitamina D se le prescribió colecalciferol 50.000 U.I. (1 cápsula una vez al mes durante dos meses) y colecalciferol 25.000 UI (1 cápsula una vez al mes tras finalizar el envase de 50.000 U.I.).\n\nESTUDIO Y EVALUACIÓN\nSe lleva a cabo el servicio de dispensación (SD) sin incidencias, siguiendo la metodología expuesta en la Guía práctica para los Servicios Profesionales Farmacéuticos Asistenciales en la Farmacia Comunitaria. Posteriormente, la paciente contacta con la farmacia comunitaria, preocupada porque la nueva medicación le ha generado confusión, ya que ella tomaba unas cápsulas naranjas para su déficit de vitamina D prescritas por su médico de Atención Primaria hace unos meses y en la parte del informe de urgencias en la que figura el tratamiento venía reflejado una medicación nueva para ese mismo problema de salud. Además, coincidió con que su cuidadora habitual ya no podrá trabajar más con ella y no la podrá ayudar con su medicación. Por ello, se le propone a la paciente el servicio de Revisión del Uso del Medicamento (RUM) con el objetivo de evaluar el grado de conocimiento que tienen la paciente con respecto a sus patologías y su tratamiento, a la par que poder resolver posibles errores en la administración de los distintos fármacos que forman parte del mismo. Se le explica en qué consiste todo el procedimiento y decide aceptar.\n\nTras esto, se procedió a citar a la cuidadora en la farmacia con la tarjeta sanitaria de la paciente, su bolsa de medicación para hacer una revisión exhaustiva de su botiquín y el último informe de urgencias con el objetivo de recopilar toda la información necesaria para realizar el servicio asistencial vía telefónica. Durante la llamada con la paciente, se procede a cumplimentar el formulario RUM, el cual se volcó posteriormente en la plataforma SEFAC e_XPERT ®. Además, para poder evaluar correctamente todo el tratamiento farmacológico, se emplearon herramientas como el CIMA (donde se consultaron las fichas técnicas de los medicamentos) y el BotPlus (donde se consultaron las posibles interacciones farmacológicas).\n\nINTERVENCIÓN\nTras la primera toma de contacto a través de la entrevista telefónica y hacer revisión del botiquín, se pudo detectar que la paciente y su cuidadora no estaban haciendo una gestión apropiada de la medicación. Tras la revisión de su botiquín, se hallaron envases caducados y con anotaciones erróneas sobre su uso, blísteres con comprimidos partidos que no deberían de estarlo y acúmulo de varios envases de un mismo fármaco. Al tratarse de una paciente dependiente, polimedicada y con problemas para gestionar correctamente su tratamiento antes y durante la ausencia de su cuidadora habitual se decidió con el fin de garantizar la seguridad farmacoterapéutica y mejorar la adherencia al tratamiento derivar al servicio de sistema personalizado de dosificación (SPD). A través de la plataforma de SEFAC e_XPERT ® se procedió a redactar un informe de derivación a su médico de Atención Primaria (MAP) del Sistema Nacional de Salud (SNS) (ver Anexo II), donde se detallaba la inclusión de la paciente en el servicio de Revisión del Uso de la Medicación y su posterior derivación al servicio de SPD. Además, quedaron recogidas las siguientes propuestas de intervención:\n\nRevisión de la pauta posológica de tramadol 50 mg de liberación retardada por la existencia de un posible error en la prescripción.\n\nRevisión del tratamiento prescrito para el déficit de vitamina D por la existencia de una duplicidad terapéutica.\n\nCambio del absorbente de incontinencia de tipo pants a elástico alegando la situación de dependencia de la paciente y las dificultades para realizar una correcta colocación por parte de la cuidadora al pasar encamada la mayor parte del tiempo. Se aportaron los Códigos Nacionales (CN) correspondientes.\n\nRevisión del tratamiento para la EPOC por dificultades de empleo del inhalador y falta de adherencia terapéutica.\n\nRESULTADOS\nDurante la cita médica, la médico de atención primaria recibe el informe de derivación entregado a la cuidadora donde, además, se solicita contacto con la farmacia comunitaria para poder iniciar de forma correcta el servicio de SPD. Tras hablar con ella vía telefónica, se realizaron los siguientes cambios en su tratamiento:\n\nDéficit de vitamina D: anulación de calcifediol y sustitución por colecalciferol prescrito en el Servicio de Urgencias.\n\nArtritis reumatoide: modificación de pauta de tramadol de liberación prolongada a 1-0-1 y empleo de paracetamol 1000 mg 1-1-1 si precisa.\n\nIncontinencia urinaria: sustitución de absorbente tipo pants por elástico.\n\nEPOC: no se realizó un cambio de tratamiento. La médico de atención primaria consideró oportuno llevar a cabo una supervisión diaria por parte de la cuidadora en cada una de las tomas del inhalador.",
+        "gold_summary": "Paciente 73 años, dependiente, polimedicada y pluripatológica contacta telefónicamente con la farmacia comunitaria para solicitar información sobre un tratamiento de nueva prescripción para una infección de orina y un déficit de vitamina D. La dispensación de la medicación a su cuidadora deriva en mayores dudas a la paciente, por lo que se le ofrece el servicio de revisión del uso del medicamento (RUM). Durante la prestación del servicio se detectan varias incidencias en su tratamiento, por lo que se decide realizar un informe de derivación al médico de atención primaria para una revisión completa del tratamiento y poder así derivar a la paciente al servicio de Sistema Personalizado de Dosificación (SPD) con el fin de garantizar la seguridad farmacoterapéutica de la paciente y mejorar su adherencia al tratamiento.",
+        "synthetic_summary": {
+            "B1": "Una mujer de 73 años pidió ayuda para sus medicinas. Tenía dudas sobre nuevos medicamentos y vitamina D. La farmacia revisó sus pastillas y encontró errores. Hablaron con su doctor para cambiar algunas medicinas. Así, ella podrá tomar todo bien y estar segura.",
+            "B2": "Una mujer de 73 años, con varias enfermedades y que depende de su cuidadora para tomar medicamentos, pidió ayuda en la farmacia sobre un nuevo tratamiento para una infección de orina y falta de vitamina D. La paciente estaba confundida porque tenía medicamentos similares antes y su cuidadora ya no podía ayudarla. Por eso, la farmacia revisó todos sus medicamentos y encontró errores, como pastillas vencidas y dosis mal anotadas. Se informó al médico para que revisara el tratamiento y se propuso un sistema personalizado para organizar mejor las medicinas. Así, se busca que la paciente tome sus medicamentos de forma segura y correcta, mejorando su salud y evitando problemas.",
+            "B3": "Una paciente de 73 años, con múltiples enfermedades y dependiente, solicitó información en la farmacia sobre un nuevo tratamiento para una infección urinaria y déficit de vitamina D. La confusión surgió porque ya tomaba otro suplemento para la vitamina D y su cuidadora habitual dejó de asistirla. Se ofreció un servicio de revisión del uso del medicamento (RUM) para evaluar su conocimiento y corregir errores en la administración. Durante la revisión, se encontraron medicamentos caducados, dosis incorrectas y duplicidades, lo que llevó a derivarla al sistema personalizado de dosificación (SPD) para mejorar la seguridad y adherencia. Se informó al médico de atención primaria, quien ajustó el tratamiento, eliminando duplicidades y modificando dosis, además de cambiar el tipo de absorbente para la incontinencia y supervisar el uso del inhalador para la EPOC. Este enfoque integral permitió optimizar el manejo farmacológico y garantizar un seguimiento adecuado, adaptado a las necesidades de la paciente y su situación de dependencia."
+        }
+    },
+    {
+        "article": "Nuestra paciente era una mujer japonesa de 83 años con insuficiencia cardiaca crónica (fracción de eyección: aproximadamente 30 %) que inició un tratamiento con empagliflozina 10 mg diarios unos 8 meses antes de su ingreso. Nunca se le había diagnosticado diabetes mellitus (HbA1c 5.9 % antes de iniciar el tratamiento con empagliflozina). Unos 6 meses antes de su ingreso, su tratamiento se cambió a dapagliflozina 5 mg. Sus diuréticos y otros medicamentos cardiacos no se ajustaron durante ese tiempo. Dos semanas antes de su ingreso, tropezó y cayó, sufriendo fracturas vertebrales y de costillas. La paciente se debilitó significativamente por el dolor de las fracturas, lo que le causó dificultad para caminar y anorexia. Solo podía comer el 50-70 % de su ingesta dietética habitual. Esto empeoró en la semana siguiente, cuando también desarrolló náuseas y vómitos y redujo aún más su ingesta de alimentos a solo el 10-20 % de la cantidad habitual. Durante este período, continuó tomando dapagliflozina. Fue ingresada en el hospital.\nAl ingreso, la paciente estaba consciente con una temperatura corporal de 37.4°C, presión arterial de 124/68 mmHg, frecuencia cardiaca de 91 bpm y saturación de oxígeno de 98% en aire ambiente. Los análisis de sangre revelaron un nivel de glucosa en sangre de 124 mg/dL, pH de 7.3, concentración de HCO3– de 14 mmol/L, exceso de base de -10 mEq/L, brecha aniónica de 20 mEq/L y concentración de b-hidroxibutirato de 5150 umol/L (Tabla 1). Estos hallazgos fueron consistentes con el diagnóstico de cetoacidosis normoglucémica. La paciente no tenía antecedentes de consumo de alcohol, tabaquismo o uso de drogas.\nSe descartaron otras causas de acidosis con alto déficit aniónico. Su nivel de péptido C era coherente con los niveles de glucosa en sangre en el ingreso, lo que indicaba que tenía una secreción de insulina adecuada; por lo tanto, no se inició la administración de insulina. Se interrumpió el uso de inhibidores de SGLT2 y la paciente se trató inicialmente con solución salina isotónica y una infusión de mantenimiento de aproximadamente 170 g de glucosa diarios.\nA pesar de no haber iniciado la insulina, su pH (7.418), concentración de HCO3– (20.7 mmol/L) y brecha aniónica (13.3 mEq/L) mejoraron al día siguiente de su ingreso. Se inició la dieta Carb 60, pero se continuaron las infusiones intravenosas de glucosa porque la ingesta de alimentos de la paciente era escasa. La cantidad de infusión de glucosa administrada se ajustó según su ingesta de alimentos. En el cuarto día de hospitalización, las cetonas urinarias desaparecieron.\nLa infusión de glucosa se interrumpió el día 12 de la hospitalización, una vez que el paciente pudo comer comidas completas. Aunque el nivel de glucosa en sangre del paciente estaba dentro del rango normal, la excreción de glucosa en la orina fue de 3+ (>500 mg/dL) durante 8 días después de la última dosis de dapagliflozina.\nAl ingreso, la paciente no podía caminar debido al dolor de la fractura, la fatiga general y el síndrome de desuso, pero después de la rehabilitación pudo hacerlo de forma independiente. Fue dada de alta el día 19 de hospitalización, tras someterse a rehabilitación.\nLos inhibidores de SGLT2 no se reiniciaron.\n\nMH - Humanos\nMH - Mujer\nMH - *Insuficiencia cardiaca/inducida químicamente\nMH - *Inhibidores del transportador de glucosa y sodio 2/efectos adversos\nMH - Edad 80 años y más\nMH - Cetosis/químicamente inducida\nMH - glucósidos/efectos adversos\nMH - Cetoacidosis diabética/inducida químicamente\n",
+        "gold_summary": "A continuación, describimos un caso de cetoacidosis en una mujer japonesa de 83 años sin diabetes a la que se le administraron inhibidores de SGLT2 para la insuficiencia cardiaca (fracción de eyección: aproximadamente 30 %). Dos semanas antes de su ingreso, había sufrido una fractura vertebral y una fractura de costilla debido a una caída, a la que siguió una anorexia, pero continuó tomando inhibidores de SGLT2. En el momento del ingreso, los resultados de los análisis de sangre revelaron un nivel de glucosa en sangre de 124 mg/dL, un nivel de hemoglobina A1C del 5,9 %, un pH de 7,329, una concentración de HCO₃⁻ de 14,3 mmol/L y una concentración de β-hidroxibutirato de 5150 μmol/L, lo que condujo a un diagnóstico de cetoacidosis euglucémica. El nivel de péptido C de la paciente coincidía con los niveles de glucosa en sangre en el momento del ingreso, lo que indicaba que tenía una secreción de insulina adecuada. La paciente fue tratada únicamente con administración de glucosa sin insulina y fue dada de alta tras la interrupción del inhibidor de SGLT2.\n",
+        "synthetic_summary": {
+            "B1": "Una mujer de 83 años con problemas del corazón tomó un medicamento para su enfermedad. Se cayó y se lastimó, lo que le causó mucho dolor y dejó de comer bien. Aunque no tenía diabetes, su cuerpo hizo algo llamado cetoacidosis, que es un problema con la energía. En el hospital, la cuidaron con líquidos y azúcar, y mejoró sin usar insulina. Luego pudo caminar y salir del hospital.",
+            "B2": "Una mujer japonesa de 83 años con insuficiencia cardíaca tomó medicamentos llamados inhibidores de SGLT2 para tratar su corazón, aunque no tenía diabetes. Después de una caída, sufrió fracturas y dejó de comer bien, pero siguió tomando estos medicamentos. Al ingresar al hospital, sus análisis mostraron niveles normales de azúcar en sangre, pero tenía una acidosis llamada cetoacidosis euglucémica, que es un problema grave con ácidos en la sangre. Su cuerpo producía insulina normalmente, por eso no recibió insulina, solo glucosa por vía intravenosa y se suspendió el medicamento. Con tratamiento y rehabilitación, mejoró y pudo caminar de nuevo. Los inhibidores de SGLT2 no se volvieron a usar para evitar riesgos.",
+            "B3": "Una mujer japonesa de 83 años con insuficiencia cardiaca y sin diabetes desarrolló cetoacidosis normoglucémica tras sufrir fracturas que le causaron anorexia y debilidad, mientras continuaba con inhibidores de SGLT2 para su tratamiento cardiaco. Al ingresar al hospital, sus análisis mostraron niveles normales de glucosa, acidosis metabólica y elevación de β-hidroxibutirato, confirmando el diagnóstico. La secreción de insulina era adecuada, por lo que no se administró insulina; solo se suspendió el inhibidor de SGLT2 y se inició tratamiento con glucosa intravenosa y líquidos. Su condición mejoró rápidamente, con normalización del pH y desaparición de cetonas en orina en pocos días. Aunque la glucosa en sangre permaneció normal, la excreción urinaria de glucosa continuó elevada después de suspender el fármaco. La paciente pudo caminar tras rehabilitación y fue dada de alta sin reiniciar el inhibidor de SGLT2. Este caso resalta la importancia de vigilar la cetoacidosis en pacientes con insuficiencia cardiaca que reciben estos medicamentos, incluso sin diabetes, especialmente ante situaciones de estrés o ingesta reducida."
+        }
+    },
+    {
+        "article": "Una recién nacida fue evaluada en la sala de neonatos poco tiempo después del parto debido a la presencia de extensas lesiones similares a cicatrices en sus flancos y muslos superiores. La bebé, nacida de una madre asiática de 28 años a las 39 semanas de gestación, formaba parte de un embarazo gemelar espontáneo. Su madre, que ya había tenido cinco hijos, había tenido un aborto espontáneo en el primer trimestre durante su segundo embarazo.\n\nLos padres eran primos hermanos y no habían tenido problemas de salud en sus tres hijos vivos. La ecografía a las 13 semanas confirmó un embarazo bicorial y diacítico y la ausencia de actividad cardíaca en uno de los gemelos. Las ecografías posteriores mostraron un feto que se desarrollaba con normalidad junto a un gemelo no viable.\n\nDurante el embarazo, la madre no informó sobre el uso de medicamentos o síntomas como fiebre y erupción cutánea. Dio negativo para estreptococo del grupo B y fue admitida en el departamento de urgencias obstétricas con dolores de parto. La niña fue entregada por vía vaginal, pesando 2,83 kg, y fue vigorosa al nacer. A la placenta se le unió un remanente fetal no viable comprimido que medía 6 × 2 cm. La placenta pesaba 460 g y parecía normal al examen.\n\nLa niña presentaba lesiones cutáneas extensas e irregulares, que se caracterizaban por un aspecto estrellado en ambos flancos, que se extendían lateralmente sobre la zona glútea y el muslo superior. Las lesiones eran simétricas en ambos flancos. No obstante, las lesiones en los muslos eran notablemente más leves en el lado izquierdo. Sus constantes vitales eran estables y no presentaba otras anomalías externas. El examen clínico de sus sistemas respiratorio, cardiovascular, gastrointestinal y neurológico reveló resultados normales, y no se observaron otras anomalías cutáneas, incluida la ausencia de lesiones ampollosas.\n\nDada la naturaleza simétrica de las anomalías cutáneas y el contexto de embarazo de mellizos con FP, se realizó un diagnóstico de aplasia cutis congénita grupo V. Los exámenes de laboratorio, que incluían hemograma completo, electrolitos y pruebas de función renal e hepática, arrojaron resultados normales. Los exámenes de detección de toxoplasmosis, rubéola, citomegalovirus, herpes simple y VIH (TORCH) arrojaron resultados negativos. La ecografía del cerebro, abdomen y corazón no reveló anomalías.\n\nDado que las lesiones se curaron en el útero, solo se prescribieron emolientes locales. Después de 48 horas de observación, el bebé fue dado de alta en su casa, con derivaciones a clínicas de dermatología pediátrica y cirugía plástica. En el seguimiento de 2 semanas, no se observaron cambios en las lesiones de la piel ni nuevos síntomas. Su análisis de microarreglo cromosómico fue reportado como normal.\n",
+        "gold_summary": "Informamos sobre un neonato al que se le diagnosticó ACC de grupo G-V asociado con fetus papyraceus de un embarazo gemelar di-coriónico y di-amniótico. Nacida de una madre asiática de 28 años, esta niña presentaba lesiones extensas, cicatrizadas, similares a las cicatrices en sus flancos y muslos superiores. Estas lesiones eran consistentes con la distribución en forma de «H» comúnmente descrita en ACC ligada a fetus papyraceus. A pesar de las manifestaciones dermatológicas significativas, la niña no mostró otras anormalidades externas o implicación sistémica, y las evaluaciones exhaustivas, incluidos los ultrasonidos y el microarray cromosómico, fueron normales.\n",
+        "synthetic_summary": {
+            "B1": "Una bebé nació con marcas en la piel que parecían cicatrices en sus costados y muslos. Estas marcas se deben a un problema llamado aplasia cutis, que ocurre cuando la piel no se forma bien en el embarazo. La niña estaba sana y no tenía otros problemas en su cuerpo. Los médicos revisaron su cuerpo y todo estaba normal. Ella recibió un tratamiento suave para cuidar su piel y está bien.",
+            "B2": "Una recién nacida presentó cicatrices en la piel en los lados del cuerpo y muslos. Estas lesiones, con forma de «H» y simétricas, son típicas de aplasia cutis congénita grupo V, una condición donde un gemelo no viable afecta al otro durante el embarazo. La bebé nació sana y sin otros problemas de salud. Las pruebas médicas, como ecografías y análisis de sangre, no mostraron anomalías. Las lesiones se curaron dentro del útero, por eso solo se aplicaron cremas para hidratar la piel. Después de dos semanas, las cicatrices no cambiaron. La niña sigue bajo control en dermatología y cirugía plástica para vigilar su evolución.",
+            "B3": "Se presentó el caso de una recién nacida con lesiones cutáneas extensas en forma de cicatrices en ambos flancos y muslos superiores, nacida de un embarazo gemelar donde uno de los fetos no era viable. Estas lesiones, simétricas y con un patrón en “H”, fueron diagnosticadas como aplasia cutis congénita (ACC) grupo V, una condición relacionada con la presencia del fetus papyraceus, que es un feto muerto y comprimido en embarazos múltiples. A pesar de la apariencia notable de la piel, la bebé no mostró otras anomalías físicas ni problemas en sus órganos, confirmados mediante ecografías y análisis cromosómicos normales. Los exámenes para infecciones comunes en el embarazo resultaron negativos, y sus signos vitales se mantuvieron estables. El tratamiento consistió en cuidados locales con emolientes para favorecer la cicatrización, sin necesidad de intervenciones más invasivas. Después de 48 horas de observación, la niña fue dada de alta y seguida en consultas especializadas, sin que se observaran cambios adversos en las lesiones ni nuevos síntomas en las semanas posteriores. Este caso destaca la importancia de reconocer la ACC grupo V en contextos de embarazo gemelar con fetus papyraceus, ya que puede presentarse con lesiones cutáneas significativas pero sin afectación sistémica."
+        }
+    },
+    {
+        "article": "Información para el paciente\nUn hombre de 44 años de edad fue ingresado en nuestro hospital con quejas principales de neumaturia y cistitis repetida. El paciente también tenía antecedentes de hipotiroidismo.\n\nLa tomografía computarizada con contraste mejorado reveló múltiples divertículos del colon sigmoide, y el límite entre el divertículo y la vejiga no estaba claro. La endoscopia gastrointestinal inferior reveló una fístula en el colon rectosigmoide aproximadamente a 15 cm del borde anal. La cistoscopia reveló una fístula en la pared posterior izquierda de la vejiga. Se diagnosticó una fístula vesicovaginal y se planificó una cirugía laparoscópica. Los hallazgos intraoperatorios revelaron una inflamación severa alrededor de la fístula vesicovaginal, y también se habían formado adhesiones severas entre el íleon y la vejiga. El íleon y la vejiga eran difíciles de exfoliar debido a las adhesiones severas. Por lo tanto, decidimos realizar una resección intestinal combinada. El colon rectosigmoide, incluida la fístula, se movilizó y se resecó. La fístula vesical se seccionó y se cerró con una sutura de púas sin nudos (V-LocTM 180, Covidien, Mansfield). La anastomosis sigmoide-rectal se reconstruyó utilizando la técnica de doble grapado. La resección parcial del íleon se reconstruyó con una anastomosis funcional de extremo a extremo (FEEA). Además de la presencia de una anastomosis de 2 sitios, había una inflamación severa en el área circundante, y considerando el riesgo de fuga anastomótica, se creó una ileostomía de derivación 30 cm proximal a la anastomosis ileo-ileal.\n\nLos procedimientos quirúrgicos incluyeron resección anterior alta laparoscópica, resección parcial del intestino delgado, cistectomía parcial y derivación en forma de asa. La operación duró 236 minutos y la pérdida de sangre fue de 50 ml. El curso postoperatorio fue sin incidentes y el cierre de la ileostomía se planificó 1 mes después de la cirugía inicial. Con ayuda laparoscópica, se eliminaron las adherencias entre el omento y la pared abdominal alrededor del estoma. Se realizó una movilización completa alrededor del estoma y el intestino se sacó hacia afuera. El íleon se reconstruyó utilizando FEEA. El procedimiento quirúrgico implicó el cierre de la ileostomía asistida por laparoscopia. La operación duró 100 minutos y la pérdida de sangre fue de 30 ml.\n\nHallazgos clínicos\nAl día siguiente de la cirugía, se produjo un shock sintomático debido a la presión arterial baja (<80 mm Hg) y la taquicardia. Los análisis de sangre mostraron que la hemoglobina disminuyó de 15.3 antes de la cirugía a 8.6 g/dL después de la cirugía.\n\nEvaluación diagnóstica\nLa tomografía computarizada abdominal (TC) reveló una gran cantidad de fluido de alta densidad en la cavidad abdominal. El diagnóstico fue sangrado posoperatorio y shock hemorrágico. Se insertó un catéter venoso central y se administraron 8 unidades de glóbulos rojos y 8 unidades de plasma fresco congelado para estabilizar los signos vitales. Los signos vitales se estabilizaron y no se observó progresión de la anemia después de eso. Aunque se logró la hemostasia, la distensión abdominal severa y los altos niveles de respuesta inflamatoria (proteína C reactiva [CRP] a 42.9 mg/dL y recuento de glóbulos blancos [WBC] de 18,500/uL) persistieron 7 días después de la cirugía.\n\nLa TC con contraste reveló que el hematoma intraabdominal se localizaba en el abdomen inferior izquierdo y derecho, y se consideró posible el drenaje percutáneo. En el día 8 posoperatorio, se insertaron tubos de drenaje de 18 Fr en el abdomen inferior izquierdo y derecho a través de una punción guiada por TC, y se drenó una gran cantidad de sangre antigua. Después del drenaje, la reacción inflamatoria y la distensión abdominal causadas por la infección del hematoma residual mejoraron (CRP a 1,9 mg/dL y WBC de 5000/μL). No se observó progresión de la anemia. En el día 14 posoperatorio, el drenaje en el abdomen inferior derecho cambió de sangre antigua a jugo intestinal. Una angiografía de drenaje reveló fuga anastomótica tardía en el sitio de cierre de la ileostomía. No hubo signos de peritonitis con buen drenaje, pero el drenaje fue de aproximadamente 100 a 200 ml, y el flato del drenaje continuó. No se observó disminución del drenaje durante los siguientes 14 días.\n\nIntervención terapéutica\nAunque se consideró la posibilidad de una nueva operación, se esperaban adhesiones intraabdominales severas debido a la historia de cirugías anteriores, sangrado postoperatorio y fuga anastomótica. Por lo tanto, se consideró que la nueva operación era un procedimiento de alto riesgo. La tomografía computarizada con contraste mostró que un hematoma organizado permanecía en el mesenterio del intestino delgado y el íleon en el lado distal de 10 cm de la anastomosis estaba comprimido cerca del hematoma restante. Teniendo en cuenta la estenosis del íleon en el lado anal de la anastomosis debido a un hematoma residual como la causa de fuga anastomótica, se intentó la dilatación radioscópica del área de estenosis a través del drenaje en el día 24 postoperatorio. Se colocó un introductor de funda Cordis BRITE TIP® (8 Fr × 23 cm) en la fístula donde ocurrió la fuga anastomótica después del drenaje angiográfico. Se usó un hilo radioscópico GT (0.016 pulgadas, 180 cm, 90°) (Terumo, Tokio, Japón) y un microcatéter Renegade HI-FLO (135 × 20 cm) (Boston Scientific, Tokio, Japón) para alcanzar el íleon terminal. Usando el catéter Selecon MP II (6 Fr, 80 cm, φ20 mm) (Terumo), se identificó el área de estenosis en el íleon debido a la compresión del hematoma donde el globo no podía pasar.\n\nSe realizó dilatación con globo fluoroscópica en la estenosis del íleo utilizando un globo guiado por alambre CRE PRO GI (180 cm, 15-18 mm) (Boston Scientific), inflado a 16,5 mm de diámetro a 4,5 atm durante 3 minutos.\n\nSeguimiento y resultados\nDesde el día posterior a la dilatación con globo, la cantidad de drenaje disminuyó notablemente, y se observaron flatos y defecaciones desde el ano. Una semana después de la dilatación con globo, el drenaje fue casi nulo, y se determinó que la fuga anastomótica se había resuelto. El drenaje se eliminó gradualmente. La ingesta oral fue buena, y tuvo movimientos intestinales regulares. Fue dado de alta el día 45 posterior a la operación. Desde entonces, no se ha informado de ninguna recurrencia de la estenosis o fuga anastomótica.\n",
+        "gold_summary": "Preocupaciones del paciente: Presentamos el caso de un hombre de 44 años con fuga anastomótica tardía después del cierre de la ileostomía, causada por la compresión de un hematoma intraabdominal que se curó rápidamente después de la dilatación fluoroscópica con globo del área de la estenosis intestinal.\n\nDiagnósticos: Se produjo sangrado postoperatorio y shock hemorrágico el día 1 postoperatorio tras el cierre de la ileostomía. Los signos vitales se estabilizaron tras la transfusión de sangre, y se realizó con éxito un drenaje guiado por tomografía computarizada para reducir el volumen del hematoma. Sin embargo, el hematoma residual comprimió el íleon en el lado anal de la anastomosis, lo que provocó una fuga anastomótica tardía.\n\nIntervenciones/resultados: Se realizó con éxito la dilatación con balón fluoroscópico del área estenótica a través del drenaje y la fuga anastomótica se curó rápidamente.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre de 44 años tuvo una operación en el intestino y la vejiga. Después, sufrió una hemorragia y se formó un coágulo grande en su abdomen. Este coágulo apretó una parte del intestino y causó una fuga. Los médicos usaron un globo especial para abrir esa parte apretada. Después del tratamiento, la fuga se curó y el hombre mejoró mucho.",
+            "B2": "Un hombre de 44 años tuvo una cirugía para reparar una fístula entre el colon y la vejiga. Después del cierre de una ileostomía (una abertura temporal en el intestino), sufrió sangrado y shock, pero se estabilizó con transfusiones y drenaje de un hematoma (acumulación de sangre). Sin embargo, el hematoma restante presionó el intestino delgado, causando una estenosis (estrechamiento) y una fuga en la zona de la anastomosis (unión quirúrgica). Para tratarlo, se realizó una dilatación con un globo especial guiado por imágenes, lo que abrió el estrechamiento. Después de este procedimiento, la fuga se cerró rápidamente, el drenaje disminuyó y el paciente mejoró, siendo dado de alta sin complicaciones posteriores.",
+            "B3": "Un hombre de 44 años ingresó con neumaturia y cistitis recurrente, diagnosticándose una fístula entre el colon sigmoide y la vejiga. Se realizó una cirugía laparoscópica que incluyó resección intestinal y cierre de la fístula, seguida de una ileostomía de derivación para prevenir complicaciones. Tras el cierre de la ileostomía, el paciente presentó shock hemorrágico por sangrado postoperatorio, que se controló con transfusiones y drenaje guiado por tomografía. Sin embargo, un hematoma residual comprimió el íleon cerca de la anastomosis, causando una fuga tardía. Debido al alto riesgo quirúrgico para una nueva operación, se optó por una dilatación con globo guiada por fluoroscopia a través del drenaje, logrando aliviar la estenosis intestinal. Esta intervención permitió la rápida resolución de la fuga anastomótica, con disminución del drenaje y recuperación de la función intestinal. El paciente fue dado de alta sin recurrencias, lo que sugiere que la dilatación con globo puede ser una alternativa efectiva y menos invasiva para tratar fugas anastomóticas causadas por estenosis secundaria a hematomas postoperatorios."
+        }
+    },
+    {
+        "article": "Paciente femenino de 23 años, ASA I, acude al Centro de Salud de la Universidad Peruana de Ciencias Aplicadas (CUS-UPC) para colocarle un implante en la zona edéntula de la pieza 1.6. Durante la evaluación, la paciente refiere que hace unos meses se le fracturó la primera molar superior derecha y, como consecuencia, le realizaron la exodoncia atraumática de dicha pieza dentaria.\n\nTras la inspección clínica, se observó la ausencia de la pieza dentaria 1.6, fenotipo gingival delgado y disminución en altura de reborde edéntulo Seibert tipo II 13. Tomográficamente, se registraron medidas de la altura del reborde óseo residual en relación con el piso del seno maxilar (6 mm) y el ancho de la cresta ósea a nivel cervical (11,20 mm), medio (11,80 mm) y apical (12,40 mm), con lo que se identifica la presencia de un seno maxilar ovoide, según Nie et al. Se realizó la planificación quirúrgica para la realización de una elevación del seno maxilar con abordaje transcrestal y la colocación de un implante dental de 4,8 x 8 mm.\n\nSe inició el procedimiento quirúrgico, que consistió en lo siguiente:\n\n• Asepsia y antisepsia\n\n• Técnica anestesia infiltrativa por vestibular y palatino de la zona edéntula 1.6 utilizando 2 cartuchos de lidocaína al 2% con epinefrina 1:80.000.\n\n• Incisión supracrestal en la zona edéntula 1.6 e incisiones sulculares en mesial de la pieza dentaria 1.7 y en distal de la pieza dentaria 1.5.\n\n• Decolado del colgajo a espesor parcial y, luego, se procedió a probar la guía quirúrgica para realizar la secuencia de fresado hasta una longitud de 6 mm, dejando 1 mm de distancia al piso del seno maxilar, el cual fue comprobado con los calibradores de profundidad, según el diámetro de la fresa que se utilizó durante la osteotomía. La secuencia de fresado se realizó hasta la fresa 3,5 mm de diámetro y luego se procedió a realizar el levantamiento de 2 mm del seno maxilar con la técnica de abordaje transcrestal mediante el uso de un osteótomo, hasta llegar a una longitud de 8 mm.\n\n• Colocación del implante φ 4,8 x 8 mm (Bone Level tapered, Straumann®) y tornillo de cierre, ambos con un torque de inserción de 20 N.\n\n• Sutura con puntos interrumpidos con ácido poliglicólico 5/0 y lavado de la zona quirúrgica con suero fisiológico al 0,09%.\n\n• Radiografía posquirúrgica del implante en zona edéntula 1.6.\n\n• Indicación de tomar amoxicilina de 500 mg + ácido clavulánico 125 mg cada 8 horas durante 7 días, ketorolaco de 10 mg cada 8 horas por 3 días, cetirizina de 10 mg cada 24 horas por 3 días y clorhexidina al 0,12%, 2 veces al día, por 10 días. Entre las indicaciones posquirúrgicas se le indicó a la paciente reposo absoluto, sin esfuerzo físico, dieta blanda, no sonarse la nariz, no succionar líquidos por dos semanas, no sumergir la cabeza en agua, tampoco estornudar o toser con la boca abierta, mantener la cabeza elevada y aplicarse compresas de hielo durante las primeras 4 horas.\n\nSe realizó un control posquirúrgico a los 7 días, el cual evidenció tejidos blandos en proceso de cicatrización, por lo que se procedió al retiro de puntos y lavado con suero fisiológico al 0,9%, y se realizó una tomografía de control que evidenció la elevación de seno maxilar, con 2,83 mm aproximadamente. Asimismo, se realizaron controles posquirúrgicos a los 35 y 56 días, en los cueles se hallaron tejidos blandos en completo proceso de cicatrización.",
+        "gold_summary": "Se realizó un levantamiento de seno maxilar sin injerto óseo en una paciente de sexo femenino de 23 años que requería la colocación de un implante dental en la zona edéntula de la pieza 16. La evaluación clínica y tomográfica permitieron planificar y realizar la elevación de seno maxilar mediante el abordaje transcrestal y sin la necesidad de injerto óseo. El reborde residual de 6 mm permitió la colocación de un implante dental simultáneo. Luego de 6 meses de seguimiento tomográfico, antes de la carga protésica, se consiguió una altura ósea vertical de 8,83 mm, lo que dio como resultado una ganancia ósea vertical de 2,83 mm. Adicionalmente, se observa una adecuada integración del implante dental sin complicaciones posoperatorias.",
+        "synthetic_summary": {
+            "B1": "Una joven de 23 años necesitaba un diente nuevo porque se le rompió uno. Los doctores revisaron su boca y vieron que faltaba hueso donde iba el diente. Hicieron una cirugía para levantar el suelo del seno maxilar, que es un espacio en la cara, y pusieron un implante. Después de la operación, la zona sanó bien y el implante quedó firme sin problemas.",
+            "B2": "Una mujer de 23 años necesitaba un implante dental por un molar faltante. Los exámenes mostraron que había suficiente hueso, pero el seno maxilar estaba muy cerca. Por eso, se hizo una cirugía para levantar el seno maxilar, que es una cavidad cerca de los dientes. Usaron una técnica especial llamada abordaje transcrestal, sin poner injerto óseo. Durante la misma operación, colocaron el implante dental. Después de seis meses, las imágenes mostraron que el hueso creció 2,83 mm. Esto permitió que el implante estuviera bien integrado y estable. La paciente se recuperó sin problemas y los tejidos cicatrizaron correctamente.",
+            "B3": "Una paciente de 23 años acudió para la colocación de un implante dental en la zona donde se había extraído la primera molar superior derecha. La evaluación clínica mostró un reborde óseo residual de 6 mm y un fenotipo gingival delgado, mientras que la tomografía confirmó las medidas óseas y la forma del seno maxilar. Se planificó una elevación del seno maxilar mediante abordaje transcrestal, sin necesidad de injerto óseo, para permitir la colocación simultánea de un implante de 4,8 x 8 mm. El procedimiento incluyó anestesia local, fresado cuidadoso para evitar perforar el seno, elevación de 2 mm del piso sin complicaciones y la inserción del implante con un torque adecuado. El postoperatorio fue controlado con medicación antibiótica, analgésicos y cuidados específicos para evitar presión en el seno maxilar. A los 7 días se observó una cicatrización favorable y la tomografía de control mostró una ganancia ósea vertical de aproximadamente 2,83 mm. En los controles posteriores, la paciente presentó tejidos blandos bien cicatrizados y una correcta integración del implante, lo que indica un resultado exitoso sin complicaciones. Por lo tanto, esta técnica demostró ser efectiva para la rehabilitación ósea y la colocación segura del implante."
+        }
+    },
+    {
+        "article": "Una paciente de 42 años de edad fue remitida a nuestro centro terciario de cáncer con antecedentes de seroma recurrente del seno izquierdo. La paciente se había sometido a una extracción bilateral de implantes mamarios con una capsulotomía parcial 11 meses antes de su primera visita a nuestro centro. La paciente no presentaba ninguna comorbilidad notable y tenía antecedentes de aumento bilateral de senos con implantes mamarios en el plano submuscular en 2003, a la edad de 21 años. No se pudo localizar ninguna información sobre el tipo de implantes que había recibido originalmente. La paciente volvió a consultar al mismo cirujano en 2008, quejándose de seroma bilateral, para someterse a un primer reemplazo bilateral de implantes mamarios con implantes mamarios anatómicos texturados de 425 cc (Sebbin LSA TF 425). En 2013, se sometió a un segundo procedimiento de reemplazo de implantes para aumentar el tamaño con implantes mamarios de 480 cc del mismo fabricante (Sebbin LSA TF 480). En 2017, la paciente volvió para una revisión en la que se quejaba de dolor y aumento del volumen del seno bilateralmente. En ese momento, se le realizó una exploración por ultrasonido que identificó efusiones periprostéticas bilaterales sin linfadenopatía o masas palpables en las regiones mamarias. Las efusiones se drenaron sin análisis, pero reaparecieron a lo largo de los años, cuando la paciente buscó ayuda del mismo cirujano y se sometió a un tercer procedimiento de revisión en 2022, con un reemplazo bilateral de implantes mamarios y una toma de muestras de la cápsula anterior. El cirujano envió dos especímenes desde el lado derecho (9 x 1 cm y 3 x 3 cm) y uno desde el lado izquierdo (2 x 1 cm). El informe histopatológico del espécimen encontró «material proteico amorfo celular acellular» en el lado derecho y «tejido fibroso escleroso con inflamación de linfocitos-monocitos, que requiere correlación con la presentación clínica» en el lado izquierdo. A pesar de la extracción, el seroma reapareció en el lado izquierdo, y se envió para pruebas citopatológicas que identificaron «una población de células pleomórficas atípicas irregulares con contornos irregulares que sugieren un proceso linfoproliferativo con CD30+ elementos» para los que se recomendaron pruebas diagnósticas adicionales. Por esta razón, la paciente buscó tratamiento en nuestra institución, donde el caso fue gestionado por un equipo multidisciplinario (MDT) que incluía a un cirujano plástico, un hematopatólogo, un hematólogo, un oncólogo, un radioterapeuta, un oncólogo quirúrgico y un radiólogo de mama. El espécimen histopatológico original de la toma de la cápsula se revisó por un hematopatólogo de nuestro centro de referencia, que identificó células CD30+ grandes y escasas atípicas con contornos irregulares que se consideraron compatibles con el diagnóstico de BIA-ALCL. Las células presentaron el siguiente fenotipo: CD30+, CD3-, CD7-, CD5-, CD4-, CD8-, Granzima B+/-, TIA1-, ALK1-, PAX5-, CD79a-, CD68-, CD15-/+. La paciente recibió una exploración por ultrasonido con aspiración por aguja fina y citopatología de la efusión recurrente que confirmó un proceso CD30+ linfoproliferativo atípico con captación de 18F-FDG (fluorodeoxiglucosa) (SUV máx. 1,8). No se pudieron localizar otras áreas de captación en todos los demás segmentos corporales explorados. La paciente también recibió una exploración por resonancia magnética de ambos senos con medio de contraste para completar la estadificación preoperativa, confirmando el seroma del lado izquierdo. Los portaobjetos del espécimen de la cirugía anterior se revisaron por el hematopatólogo que consideró los hallazgos suficientes para identificar BIA-ALCL con infiltración temprana de la cápsula periprostética (pT2 según el sistema de estadificación MD Anderson-TNM). Tres semanas después de la visita inicial, la paciente se sometió a cirugía radical con capsulotomía en bloque que contenía solo 150 cc de efusión serosa sin implante. El contenido líquido se envió para cultivo y citopatología, mientras que el espécimen sólido se envió para examen histopatológico. Además, la paciente se sometió a biopsia de ganglio linfático centinela de 2 ganglios axilares identificados preoperativamente a través de linfografía segmentaria. Los ganglios linfáticos presentaron una linfadenopatía silicona-asociada reactiva crónica sin signos de linfadenopatía metastásica. El informe histopatológico de la cápsula reveló agregados celulares infiltrantes en la cápsula periprostética, pero márgenes de resección claros y sin signos de infiltración más allá de la cápsula. Como tal, la paciente recibió un estadio IC (pT3pN0M0). El curso postoperatorio fue sin incidentes, y no se consideraron necesarios más tratamientos adyuvantes por el MDT. La paciente continuó su estricto protocolo de seguimiento, con PET/CT de 6, 12 y 18 meses posteriores a la cirugía que no mostró signos de recurrencia de enfermedad local o distante. Como está, la paciente continúa sus visitas de seguimiento y exploraciones, con supervivencia libre de enfermedad más allá de 18 meses.\n",
+        "gold_summary": "Describimos el caso de una mujer de 42 años con antecedentes de aumento de senos bilateral con fines cosméticos 21 años antes, que desarrolló seroma recurrente del lado izquierdo. Buscó ayuda de su primer cirujano, quien realizó 2 procedimientos de intercambio de implantes mamarios, colocando dispositivos texturados y, finalmente, una extracción bilateral de implantes mamarios en el transcurso de dos décadas. La paciente no recibió capsulectomías en los intercambios de implantes anteriores y recibió una muestra de la cápsula anterior en el último procedimiento, donde se diagnosticó BIA-ALCL en el lado izquierdo. Fue derivada a un centro de cáncer terciario donde el examen preoperatorio confirmó la presencia de enfermedad residual local. Después de la gestión del equipo multidisciplinario, se sometió a una revisión de capsulectomía en bloque del lado izquierdo sin necesidad de tratamientos adicionales. El curso postoperatorio fue sin incidentes y sin signos de recurrencias locales a los 18 meses de seguimiento.\n",
+        "synthetic_summary": {
+            "B1": "Una mujer de 42 años tuvo problemas con sus implantes de seno que le causaban líquido acumulado. Cambió sus implantes varias veces y luego se los quitó. Al revisar una muestra, los médicos encontraron un tipo raro de enfermedad llamada BIA-ALCL. Fue tratada en un hospital especial con una operación para quitar la parte afectada. Después de la cirugía, está bien y no ha tenido problemas en más de un año.",
+            "B2": "Una mujer de 42 años tuvo líquido acumulado (seroma) en su seno izquierdo tras varios cambios de implantes mamarios. Aunque le quitaron los implantes, el líquido volvió a aparecer. Al analizar una muestra de tejido, encontraron un cáncer raro llamado BIA-ALCL, que se relaciona con implantes mamarios. En un hospital especializado, confirmaron que el cáncer estaba solo en la cápsula que rodea el implante. Le hicieron una cirugía para quitar toda la cápsula afectada y no necesitó más tratamientos. Después de 18 meses, no hay señales de que el cáncer haya regresado. Ella sigue en control médico para asegurarse de que todo esté bien.",
+            "B3": "Una mujer de 42 años con antecedentes de aumento mamario bilateral desde los 21 años presentó un seroma recurrente en el seno izquierdo. A lo largo de casi dos décadas, se sometió a varios reemplazos de implantes texturados y, finalmente, a la extracción bilateral de implantes sin capsulectomía completa. En el último procedimiento, se detectó un linfoma anaplásico de células grandes asociado a implantes mamarios (BIA-ALCL) en la cápsula del lado izquierdo. Tras su derivación a un centro especializado, un equipo multidisciplinario confirmó la enfermedad residual local mediante estudios de imagen y análisis histopatológicos. La paciente fue tratada con una capsulectomía en bloque radical sin necesidad de quimioterapia ni radioterapia. El postoperatorio transcurrió sin complicaciones y los controles con tomografía por emisión de positrones y resonancia magnética no mostraron recurrencia a los 18 meses. Este caso resalta la importancia de un diagnóstico precoz y un manejo integral en pacientes con seromas persistentes tras implantes mamarios, ya que el tratamiento quirúrgico adecuado puede lograr una supervivencia libre de enfermedad sin tratamientos adicionales."
+        }
+    },
+    {
+        "article": "Se trata de un paciente de 50 años que se presentó con una queja de dolor e hinchazón de la lengua de tres días de duración. Asociado a esto, tenía dolor al tragar, dificultad para abrir la boca, falta de aire y babeo. Asimismo, tenía fiebre alta y un tipo de dolor de cabeza global. Por lo demás, no tenía traumatismo en la lengua, ni procedimientos dentales u orales recientes, ni antecedentes de tabaquismo ni de enfermedad médica crónica como diabetes mellitus, enfermedad cardiaca e hipertensión. Históricamente, había tenido un dolor dental agudo en los últimos seis meses antes de su queja actual. Había masticado khat desde su niñez y tenía una mala higiene oral.\n\nEn el examen físico, se veía muy enfermo y sus signos vitales eran: presión arterial 115 por 70 mmHg, pulso 120 latidos por minuto, frecuencia respiratoria 20, temperatura 39 grados centígrados y saturación de oxígeno 92% de oxígeno. En el examen HEENT, había una hinchazón significativa de la lengua en el área anterolateral izquierdo, fluctuante a la palpación, y tenía un borde eritematoso. Hay múltiples caries en las áreas maxilares y mandibulares. No hubo hallazgos pertinentes en los sistemas restantes.\n\nTras obtener el consentimiento informado, el paciente fue trasladado al quirófano con el diagnóstico de absceso lingual. Posteriormente, se realizó la incisión y el drenaje bajo anestesia general, y se drenaron unos 30 ml de pus espeso. La bolsa se lavó con solución salina normal y peróxido de hidrógeno al 2 %. El paciente fue trasladado a la sala de cirugía con signos vitales estables y había tomado ceftriaxona 1 g por vía intravenosa dos veces al día y metronidazol 500 mg por vía intravenosa tres veces al día durante dos días. Fue dado de alta después de dos días de estancia en el hospital con mejoría y Augmentin 625 mg por vía oral tres veces al día durante cinco días.\n",
+        "gold_summary": "Se trata de un paciente de 50 años que se presentó con una queja de dolor e hinchazón de la lengua de tres días de duración. Asociado a esto, tenía dolor al tragar, dificultad para abrir la boca, falta de aire y babeo. Asimismo, tenía fiebre alta y un tipo de dolor de cabeza global. En el examen físico, había una hinchazón significativa de la lengua en el área anterolateral izquierda, fluctuante a la palpación, y tenía un borde eritematoso. Después de que se tomó el consentimiento informado, el paciente fue trasladado al quirófano con el diagnóstico de absceso de la lengua. Posteriormente, se hizo una incisión y drenaje bajo anestesia general, y se drenaron unos 30 ml de pus espeso. El bolsillo se lavó con solución salina normal y peróxido de hidrógeno al 2%. El paciente fue trasladado a la sala de cirugía con signos vitales estables y había estado tomando antibióticos. Fue dado de alta después de dos días de estancia en el hospital.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre de 50 años tenía dolor e hinchazón en la lengua desde hacía tres días. También le dolía tragar, tenía dificultad para abrir la boca y fiebre alta. Los médicos vieron que su lengua estaba muy hinchada y con pus. Le hicieron una pequeña operación para sacar el pus y le dieron medicinas para la infección. Después de dos días en el hospital, mejoró y pudo irse a su casa.",
+            "B2": "Un hombre de 50 años llegó con dolor e hinchazón en la lengua desde hacía tres días. También tenía dificultad para tragar, abrir la boca y falta de aire, además de fiebre alta y dolor de cabeza. En el examen, se observó una gran hinchazón en el lado izquierdo de la lengua, con enrojecimiento y líquido al tocarla. Los médicos diagnosticaron un absceso, que es una acumulación de pus por infección. El paciente fue operado bajo anestesia general para abrir y drenar el pus, limpiando la zona con soluciones especiales. Recibió antibióticos por vía intravenosa y mejoró en dos días. Luego continuó con antibióticos orales en casa y fue dado de alta. Este caso muestra la importancia de tratar rápido las infecciones para evitar problemas graves.",
+            "B3": "Un hombre de 50 años acudió al hospital presentando dolor e inflamación en la lengua desde hacía tres días, junto con dificultad para tragar y abrir la boca. Además, refería disnea y sialorrea, acompañadas de fiebre alta y cefalea generalizada. En la exploración física se evidenció una tumefacción notable en el lado izquierdo de la lengua, con una zona blanda y eritematosa al tacto. No había antecedentes de traumatismos ni enfermedades crónicas, aunque el paciente mostraba mala higiene oral y episodios recientes de dolor dental. Se diagnosticó un absceso lingual, por lo que se realizó una incisión y drenaje bajo anestesia general, extrayendo aproximadamente 30 ml de pus purulento. La cavidad se irrigó con solución salina y peróxido de hidrógeno al 2%, y el paciente recibió tratamiento antibiótico intravenoso durante su hospitalización. Su estado clínico mejoró progresivamente, y tras dos días fue dado de alta con indicaciones para continuar la terapia antibiótica por vía oral. Este caso subraya la importancia de un diagnóstico precoz y un manejo adecuado para prevenir complicaciones severas en infecciones linguales."
+        }
+    },
+    {
+        "article": "Hombre de 73 años de edad de origen latinoamericano, con antecedente de madre con diagnóstico de demencia tipo Alzheimer con panel genético negativo; hermano con diagnóstico de ELA; hermana con diagnóstico de enfermedad de Parkinson. La sintomatología progresiva comenzó desde el año 2016 y se caracterizó por síntomas progresivos de hiposmia, hipoacusia, estreñimiento e insomnio, los cuales ameritaron valoración por otorrinolaringología y audiología, sin conclusión diagnóstica. En el año 2020 los familiares notaron que el paciente presentaba problemas en la memoria episódica, olvidos de objetos de la vida cotidiana, problemas de ganancias en su negocio (de comercio). Estos síntomas fueron progresivos hasta que el paciente empezó a tener limitación en las tareas diarias, como al manejar y al cambiar las velocidades, además de al salir de su casa. A finales de ese año el paciente comenzó a presentar debilidad muscular distal, manifestada al abrir botellas, cepillarse los dientes, lo cual progresó de forma insidiosa, no fluctuante, sin predominio de horario.\n\nEn enero de 2021 el paciente comenzó con alteraciones de la marcha, las cuales condicionaron caídas frecuentes hasta más de 6 veces a la semana, esto debido a inestabilidad postural. El paciente acudió a valoración en mayo. Se le hizo test de MoCA de 16 puntos con alteraciones en la fluidez del lenguaje y repetición de oraciones; en la abstracción, recuerdo diferido y problemas visuoespaciales y disejecutivos. El test de Luria dio positivo. El paciente presentó facie hipomímica, emitió con hipofonía, entrecortado y lento, y presentó reflejo nauseoso disminuido, rigidez generalizada de predominio izquierdo, hipotrofia generalizada, bradicinesia de predominio izquierdo, fuerza 4/5 generalizada, reflejos de estiramientos musculares 3/4, reflejos abdominocutáneos abolidos, signos de Hoffmann y Trömner presentes de forma bilateral, respuesta plantar extensora bilateral, fasciculaciones en extremidades inferiores evocadas al tacto, marcha con pasos cortos, congelamiento de la marcha al giro, pull test positivo (inestabilidad postural). Se manejó con levodopa carbidopa a una dosis gradual. Al seguimiento a los 3 meses el paciente había presentado nula mejoría en cuanto a los síntomas parkinsónicos, aumento de la debilidad muscular y persistieron los datos de motoneurona inferior y superior. Con estos hallazgos se realizó resonancia magnética (RM) del encéfalo. La velocidad de neuroconducción (VCN) presentó neuropatía axonal motora de miembros torácicos en relación con atrofia y neuroconducción sensitiva sin alteraciones. La electromiografía (EMG) presentó datos de denervación activa (aumento de actividad insercional, potenciales de fibrilación, fasciculación) y reinervación crónica (potenciales de acción de la unidad motora polifásicos, y bajo reclutamiento a la contracción máxima) en los 5 segmentos corporales, lo cual es compatible con enfermedad de motoneurona.\n\n\nLa EMG mostró un aumento de actividad insercional en músculos deltoides, bíceps, tríceps, extensor digital común bilateral y músculos linguales de forma bilateral. Se observaron abundantes potenciales de fibrilación y predominó la fasciculación en los músculos de los miembros torácicos. Durante la contracción, se observó una activación del potencial de acción de la unidad motora (PAUM) de forma polifásica y de gran amplitud. Y a máxima contracción se observó una disminución del reclutamiento en la mayoría de los músculos evaluados.\n\nEl paciente perdió seguimiento un año. Al vover a valoración se encontraba con postración en cama, afásico, aumento de los datos de parkinsonismo y síndrome de motoneurona. Se decidió realizar panel genético que resultó negativo para C9ORF72, así como para 143 genes más involucrados en enfermedades neuromusculares y neurodegenerativas, incluidos los genes VCP, MAT3, asociados a ELA, NOTCH3, asociado a demencia frontotemporal, sin alteraciones. Se reportó resultado de variante patogénica para el gen POLG: C.2209G>C, p.(Gly737Arg), relacionado con síndrome de depleción mitocondrial autosómico dominante y recesivo. Se realizó sesión de asesoramiento genético y el paciente fue informado. En mayo de 2022, el paciente presentaba disfagia y acudió en silla de ruedas, por lo que fue enviado a que se le practicara una gastrostomía.",
+        "gold_summary": "Presentamos un caso de origen latinoamericano que inicialmente se manifestó con síntomas sistémicos de más de 6 años de evolución, con posteriores alteraciones cognitivas. Después presentó alteraciones de la marcha y síntomas motores sugestivos de parkinsonismo con datos atípicos y datos de enfermedad de motoneurona. Se hicieron estudios de extensión que confirmaron hallazgos compatibles con afectación en motoneurona superior e inferior. Observamos mutación en gen POLG, relacionada con síndrome de depleción mitocondrial.",
+        "synthetic_summary": {
+            "B1": "Un hombre de 73 años empezó con problemas para oler, oír y dormir. Luego tuvo olvidos y dificultad para hacer tareas diarias. También perdió fuerza en sus manos y se cayó muchas veces al caminar. Los doctores encontraron que tenía problemas en las neuronas que controlan los músculos. Además, descubrieron un cambio en un gen llamado POLG, que puede afectar la energía de las células. Su estado fue empeorando con el tiempo.",
+            "B2": "Un hombre de 73 años comenzó hace más de seis años con pérdida del olfato, audición baja, estreñimiento e insomnio. Luego, presentó problemas de memoria y dificultad para realizar tareas diarias. Más tarde, tuvo debilidad muscular y problemas para caminar, con caídas frecuentes. Los exámenes mostraron signos de enfermedad de motoneurona, que afecta las células nerviosas que controlan los músculos, y síntomas similares al Parkinson. Se encontró una mutación en el gen POLG, que puede causar problemas en las mitocondrias, las partes de las células que producen energía. A pesar del tratamiento con levodopa, no mejoró y su estado empeoró hasta necesitar una gastrostomía para alimentarse. Este caso muestra una enfermedad compleja con síntomas neurológicos variados.",
+            "B3": "Un hombre de 73 años presentó desde 2016 síntomas progresivos como anosmia, hipoacusia, estreñimiento e insomnio, seguidos de deterioro cognitivo y dificultades funcionales. En 2021, desarrolló alteraciones de la marcha con caídas frecuentes, rigidez, bradicinesia, debilidad muscular, reflejos anormales y fasciculaciones, sugiriendo compromiso motor. Estudios neurofisiológicos evidenciaron afectación de motoneuronas superiores e inferiores, compatibles con enfermedad de motoneurona. La resonancia magnética y análisis genéticos descartaron mutaciones comunes, pero identificaron una variante patogénica en el gen POLG, relacionada con un síndrome de depleción mitocondrial. A pesar del tratamiento con levodopa, no se observó mejoría en los síntomas parkinsonianos y la debilidad muscular progresó. Un año después, el paciente presentó afasia, mayor discapacidad motora y disfagia, que requirieron gastrostomía para soporte nutricional. Este caso ilustra una enfermedad neurodegenerativa compleja con manifestaciones atípicas de parkinsonismo y motoneuronopatía, vinculada a una mutación genética poco frecuente, lo que resalta la importancia de estudios genéticos en cuadros neurológicos progresivos y atípicos."
+        }
+    },
+    {
+        "article": "Mujer de 33 años, previamente sana, presentó disnea progresiva, fiebre alta, sudores nocturnos y pérdida de peso en diciembre de 2017. Después de un mes de evolución, fue ingresada en un hospital general con insuficiencia respiratoria aguda y shock séptico con infiltrados alveolares difusos, ictericia, hemoptisis y petequias en las extremidades inferiores. Fue intubada y necesitó soporte hemodinámico. Se detectó un soplo sistólico mitral a la ausculta del precordio. Había leucocitosis acentuada con desviación a la izquierda, plaquetopenia, disfunción hepática y renal asociada a proteinuria subnefrótica y consumo de complemento. El resultado de los anticuerpos antinucleares fue de 1/80, a pesar de los niveles normales de anti-DNA de doble cadena, anti-SM y anti-PR3. Después de la administración de ceftriaxona, mejoró clínicamente. Fiebre amarilla, dengue, chikungunya, leptospirosis, VIH y hepatitis virales fueron descartados. Las hemoculturas fueron positivas para Haemophilus spp. en las seis muestras recolectadas. El ecocardiograma transtorácico (ETT) demostró una masa ecogénica amorfa con superficie irregular y algunos elementos móviles que envolvían ambos folletos de la válvula mitral, midiendo 20x17 mm en el folleto anterior y 19 mm en su mayor diámetro en los folletos posteriores, resultando en regurgitación grave por flail mitral y perforación. La resonancia magnética mostró pequeños abscesos esplénicos, tratados de manera conservadora. Un aneurisma micótico no complicado de la arteria cerebral media izquierda fue tratado por embolización percutánea. Treinta días después de la hospitalización, se sometió a un reemplazo de la válvula mitral con éxito por una prótesis valvular biológica de tamaño 29 mm y después de una extensa resección del tumor. Se evidenció regurgitación aórtica moderada debido a lesión de la fibrosa intervalvar mitroaórtica y retracción de la cúspide no coronaria, tratada de manera conservadora. El examen patológico confirmó la presencia de un mixoma valvular mitral infectado. La paciente completó 28 días de ceftriaxona y gentamicina, recibiendo el alta hospitalaria asintomática. En el seguimiento de un año, no hubo evidencia de recurrencia y se constató solamente regurgitación aórtica leve. Los mixomas infectados presentan mayor riesgo de eventos embólicos, aunque las manifestaciones clínicas son indistinguibles de tumores no infectados.2 El presente caso parece ser el sexto de mixoma valvular mitral infectado relatado en la literatura, llenando criterios definitivos para el diagnóstico, y el tercero causado por un microorganismo del grupo HACEK.3 - 8 De los 64 mixomas valvulares mitrales publicados de 2006 a 2012, los síntomas eran cardiovasculares en 36,7%; 9,5 a 21,6% de los mixomas de la válvula mitral fueron sometidos al cambio de válvula y el tiempo del diagnóstico hasta la cirugía varió de algunas horas a 42 días.2 , 9 La mortalidad operatoria y general fue relatada como siendo, respectivamente, 2,6 a 3% y 5,1 a 21%.2 , 10 En la presente serie, la mayoría de los pacientes presentó insuficiencia cardiaca sintomática, fueron sometidos al cambio de válvula mitral y todos presentaron buenos resultados en el seguimiento.\n",
+        "gold_summary": "Una mujer de 33 años de edad, con antecedentes de fiebre y disnea de unos pocos días de evolución, fue hospitalizada con un síndrome lupoide, con hemocultivos positivos para Haemophilus spp. El ecocardiograma reveló una masa gigante que involucraba ambas valvas mitrales, con una severa regurgitación mitral que requería un reemplazo valvular mitral biológico. La microscopía reveló un mixoma infectado y la paciente fue dada de alta asintomática tras finalizar la terapia con antibióticos. Ella tuvo un buen seguimiento.\n",
+        "synthetic_summary": {
+            "B1": "Una mujer de 33 años tuvo fiebre, dificultad para respirar y perdió peso. En el hospital, los médicos encontraron una masa en su corazón que dañaba una válvula llamada mitral. Ella recibió antibióticos y después le pusieron una válvula nueva. La masa era un tumor llamado mixoma infectado. Después del tratamiento, la mujer mejoró mucho y se sintió bien.",
+            "B2": "Una mujer de 33 años llegó al hospital con dificultad para respirar y fiebre alta. También había perdido peso sin razón aparente. Tenía una infección grave causada por bacterias llamadas Haemophilus. La infección afectó la válvula mitral, que controla el flujo de sangre en el corazón. Un ecocardiograma, que es un examen del corazón con ultrasonido, mostró una masa grande en esa válvula. Esta masa causaba una fuga grave de sangre. Por eso, la paciente necesitó un reemplazo de la válvula mitral con una prótesis biológica. El examen confirmó que la masa era un mixoma infectado, un tumor raro en la válvula. Recibió antibióticos durante 28 días y mejoró sin síntomas. Un año después, estaba bien, con solo una leve fuga en otra válvula. Este caso es muy raro y muestra la importancia de un diagnóstico y tratamiento rápidos para evitar problemas graves.",
+            "B3": "Una mujer de 33 años, sin antecedentes previos, presentó síntomas progresivos como dificultad para respirar, fiebre alta y pérdida de peso, que evolucionaron a insuficiencia respiratoria y shock séptico. En el hospital, se detectó una masa en la válvula mitral mediante ecocardiograma, que causaba una regurgitación grave y daño valvular. Los hemocultivos confirmaron infección por Haemophilus spp., un microorganismo del grupo HACEK, y se diagnosticó un mixoma valvular mitral infectado, un tumor cardíaco raro y grave. La paciente recibió tratamiento antibiótico con ceftriaxona y gentamicina, además de un reemplazo quirúrgico exitoso de la válvula mitral. También se trataron complicaciones como abscesos esplénicos y un aneurisma cerebral micótico. Tras completar el tratamiento, la paciente fue dada de alta sin síntomas y, en un seguimiento de un año, no se observaron recurrencias, solo una leve regurgitación aórtica. Este caso destaca la importancia de un diagnóstico temprano y manejo integral para evitar complicaciones graves en mixomas infectados, que aunque son poco comunes, presentan alto riesgo de eventos embólicos y requieren tratamiento quirúrgico y antibiótico."
+        }
+    },
+    {
+        "article": "Mujer de 71 años, que fue atendida en urgencias del Hospital de Mataró (Barcelona, España) el 9 de septiembre de 2020 con debilidad progresiva, por lo que se decidió su ingreso en neurología. Como antecedentes patológicos destacaban hipertensión arterial, temblor esencial, artrosis y trastorno de ansiedad leve, en tratamiento con gabapentina, sertralina y tramadol. La paciente había consultado a su médico de cabecera el 1 de septiembre de 2020 por dolor abdominal, junto con diarrea leve que duró 24 horas. Al día siguiente comenzó a sentirse débil y, a lo largo de los días siguientes, apareció disnea y disfagia, por lo que se sospechó laringitis y se le recetó prednisona. El 8 de septiembre de 2020 fue visitada nuevamente por su médico de cabecera por empeoramiento global de la debilidad; presentaba, además, disartria, disfagia y ptosis bilateral, por lo que fue derivada a urgencias del hospital.\n\nA su llegada no presentaba fiebre, la presión arterial y la frecuencia cardíaca eran normales, y la exploración física era normal, a excepción de taquipnea moderada. El examen neurológico mostró ptosis palpebral bilateral, parálisis facial bilateral, midriasis bilateral arreactiva a la luz y a la acomodación, oftalmoparesia bilateral tanto para la suprainfraversión como para la mirada horizontal bilateral, tetraparesia moderada en las extremidades (3/5), y disfonía y disfagia graves. Ella estaba consciente y el contenido del lenguaje era normal, al igual que los reflejos miotáticos, la sensibilidad y la coordinación. Las maniobras de fatigabilidad no fueron concluyentes y se realizó la prueba del hielo, que resultó positiva, mejorando –transitoriamente– la ptosis.\n\nLa reacción en cadena de la polimerasa (PCR) para el SARS-CoV-2 fue repetidamente negativa (en su ambulatorio y en el hospital). La gasometría arterial mostró hipoxemia: 75, con SO2 al 95%, y el resto de las exploraciones realizadas en urgencias resultaron normales (radiografía de tórax, análisis de sangre de rutina, electrocardiograma).\n\nSe inició tratamiento de soporte con oxígeno, sueroterapia, nutrición por sonda nasogástrica y medidas encaminadas a la prevención de complicaciones. El cuadro se estabilizó el tercer día del ingreso en planta, sin requerir soporte ventilatorio avanzado, y comenzó una mejoría lenta a partir del octavo día, iniciando tolerancia a la dieta adaptada de disfagia. Durante la primera semana presentaba hipotensión arterial, que fue corrigiéndose con la sueroterapia. A partir de la segunda semana, pudo iniciar rehabilitación física, con buena evolución, por lo que fue trasladada a un centro específico de rehabilitación al 19.º día, y entonces fue capaz de deambular con ayuda bilateral. En la visita de control en consultas externas de neurología seis semanas después, la paciente estaba completamente recuperada.",
+        "gold_summary": "Describimos el caso confirmado de botulismo alimentario en una paciente atendida en nuestro hospital en septiembre de 2020. La instauración en pocos días de una afectación bilateral de pares craneales, incluyendo disfagia, disnea y disartria, junto con midriasis y tetraparesia graves, precedida de diarrea, constituyó la presentación clínica en el primer caso; mientras que en su familiar cursó con síntomas inespecíficos y transitorios. Constatamos disautonomía consistente en hipotensión arterial. Teniendo en cuenta la situación pandémica en aquel momento, se descartó repetidamente la infección por SARS-CoV-2 antes de plantear alternativas diagnósticas. La neurotoxina B de C. botulinum fue detectada en las heces de la paciente, confirmando el diagnóstico de botulismo, que relacionamos con la ingesta de una conserva casera de alubias. Se completó el diagnóstico diferencial del cuadro descartando otras posibles etiologías.",
+        "synthetic_summary": {
+            "B1": "Una mujer de 71 años se enfermó después de comer unas alubias en conserva. Tenía mucha debilidad, dificultad para hablar y tragar, y sus ojos no respondían bien a la luz. Los médicos buscaron y no encontraron coronavirus. Luego, dijeron que tenía botulismo, una enfermedad causada por una toxina que puede venir de alimentos en mal estado. Con tratamiento y cuidado, ella mejoró y pudo caminar otra vez.",
+            "B2": "Una mujer de 71 años llegó al hospital con debilidad progresiva y dificultad para tragar. También tenía problemas para respirar y antes sufrió diarrea leve con dolor abdominal. En la revisión, tenía parálisis en varios nervios de la cara y pupilas dilatadas que no reaccionaban a la luz. Además, mostraba debilidad en brazos y piernas, y dificultad para hablar. Se descartaron infecciones como COVID-19 y otras causas comunes. Finalmente, se confirmó botulismo, una intoxicación causada por una toxina bacteriana, relacionada con comer conservas caseras. Recibió oxígeno y alimentación por sonda, mejorando poco a poco. Después de seis semanas de rehabilitación, se recuperó completamente. Este caso muestra la importancia de pensar en botulismo ante síntomas neurológicos graves y alimentos caseros.",
+            "B3": "Una mujer de 71 años ingresó en un hospital tras presentar debilidad progresiva, dificultad para tragar y respirar, así como caída de los párpados y problemas en el habla. Estos síntomas aparecieron después de un episodio de diarrea leve y dolor abdominal. En la exploración neurológica se observaron parálisis facial, debilidad en las extremidades y pupilas dilatadas que no respondían a la luz. Se descartó infección por COVID-19 y otras causas comunes. La paciente recibió tratamiento de soporte, incluyendo oxígeno y nutrición por sonda, y mejoró lentamente tras una semana, iniciando rehabilitación física. Se confirmó el diagnóstico de botulismo alimentario al detectar la neurotoxina de Clostridium botulinum en sus heces, relacionada con el consumo de una conserva casera. Durante su evolución, presentó hipotensión que se corrigió con líquidos intravenosos. Se completó el diagnóstico descartando otras enfermedades. Seis semanas después, la paciente había recuperado completamente su movilidad y funciones. Este caso destaca la importancia de considerar botulismo en cuadros neurológicos agudos tras síntomas digestivos, especialmente cuando se descartan infecciones virales prevalentes."
+        }
+    },
+    {
+        "article": "Un hombre de 52 años presentó pérdida de agudeza visual en su ojo derecho (OD) dos días después de una inyección intravenosa no complicada de ranibizumab con una aguja de 30 G. Su historial médico incluía PE, miopía alta y vitrectomía pars plana en el OD debido a desprendimiento de retina. Recibía tratamiento mensual con ranibizumab debido a neovascularización coroidea secundaria a estrías angioides, con 78 inyecciones previas en el OD. En el momento de la presentación, su BCVA era de 6/18 y la presión intraocular (IOP) era de 3 mmHg. El examen con lámpara de hendidura del segmento anterior no mostró nada de particular. El examen de fondo de ojo y los escaneos OCT revelaron pliegues corio-retinianos posteriores. En conjunto, la baja presión intraocular y los hallazgos del fondo de ojo llevaron al diagnóstico de hipotensión maculopatía. Se prescribió dexametasona tópica y atropina para mejorar la función del cuerpo ciliar. La IOP se normalizó en tres días con recuperación de la agudeza visual y resolución de los pliegues corio-retinianos. Cuatro meses después, se realizó una nueva inyección intravenosa anti-VEGF en el cuadrante inferolateral y el paciente informó disminución de la agudeza visual en el día siguiente a la inyección. La BCVA era contar los dedos y la IOP era de 2 mmHg. Los pliegues corio-retinianos en el polo posterior estaban presentes, incluso más prominentemente esta vez. El examen con lámpara de hendidura reveló una herida abierta en la esclerótica en el sitio de la inyección. La herida se suturó con monofilamento 10-0 y se prescribió dexametasona tópica y atropina. El paciente se recuperó bien y presentó una BCVA de 6/12 y una IOP de 12 mmHg.\n",
+        "gold_summary": "Un hombre de 52 años se quejó de pérdida de visión en el ojo derecho (OD) dos días después de un IVI anti-VEGF sin complicaciones para el tratamiento de la neovascularización coroidea secundaria a estrías angioides. Su historial médico incluía PE, miopía patológica y una vitrectomía pars plana (PPV) previa debido a un desprendimiento de retina. La agudeza visual mejor corregida (BCVA) en el OD disminuyó de 6/12 a 6/18 después del IVI. La presión intraocular (IOP) era de 3 mmHg y se observaron pliegues corio-retinianos en el polo posterior. Se prescribió dexametasona tópica y atropina, y se observó una recuperación completa después de tres días. Cuatro meses después, el paciente desarrolló un nuevo episodio de pérdida de visión después de otro IVI. Su BCVA era contar los dedos, la IOP era de 2 mmHg, y se observaron pliegues corio-retinianos más evidentes. Esta vez, una herida escleral abierta en el sitio de inyección era evidente y fue necesaria una sutura escleral. Una vez más, el paciente se recuperó bien.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre de 52 años perdió visión en su ojo derecho después de una inyección para tratar su ojo. Tenía problemas en ese ojo por una cirugía y una enfermedad. Su presión en el ojo estaba baja y se vieron arrugas en la parte de atrás del ojo. Le dieron un medicamento en gotas y mejoró en tres días. Más tarde, tuvo otro problema tras otra inyección y le cosieron una herida en el ojo. Luego, volvió a mejorar.",
+            "B2": "Un hombre de 52 años perdió la visión en su ojo derecho dos días después de una inyección para tratar la retina, que es la parte del ojo que recibe la luz. Tenía miopía alta, que es dificultad para ver de lejos, y había tenido una cirugía por desprendimiento de retina antes. Su visión empeoró y la presión dentro del ojo bajó mucho, causando pliegues en la retina. Le dieron gotas para subir la presión y mejorar la función del ojo, y mejoró en tres días. Cuatro meses después, tras otra inyección, volvió a perder visión y la presión bajó aún más. Esta vez encontraron una herida abierta en el lugar de la inyección, que cerraron con puntos. Después del tratamiento, su visión y presión ocular mejoraron otra vez.",
+            "B3": "Un hombre de 52 años con antecedentes de miopía alta, vitrectomía previa y neovascularización coroidea secundaria a estrías angioides presentó pérdida de visión en su ojo derecho tras una inyección intravenosa de ranibizumab. Dos días después del procedimiento, su agudeza visual disminuyó y la presión intraocular fue muy baja, acompañada de pliegues corio-retinianos, lo que llevó al diagnóstico de hipotensión maculopatía. Se trató con dexametasona tópica y atropina, logrando normalizar la presión y recuperar la visión en tres días. Sin embargo, cuatro meses más tarde, tras una nueva inyección, sufrió otra caída de la agudeza visual y presión intraocular aún más baja, con pliegues corio-retinianos más marcados. En esta ocasión, se detectó una herida abierta en la esclerótica en el sitio de la inyección, que requirió sutura. Tras el tratamiento, el paciente mejoró notablemente su visión y presión ocular. Este caso destaca la importancia de vigilar complicaciones como la hipotensión ocular y lesiones escleral postinyección, para actuar rápidamente y evitar daños permanentes."
+        }
+    },
+    {
+        "article": "Una mujer de 82 años acudió al servicio de urgencias por dolor abdominal, diarrea, confusión y deterioro de su estado general de varios días de evolución. Entre sus antecedentes médicos destacaban hipertensión arterial tratada e hipotiroidismo en tratamiento sustitutivo. No se recogieron antecedentes quirúrgicos ni hábitos tóxicos de interés. A la exploración física, la frecuencia cardíaca era de 84 lpm, tensión arterial de 105/82 mmHg, temperatura de 38 °C y saturación de oxígeno de 95% en aire ambiente. Las mucosas estaban secas y el abdomen era difusamente doloroso a la palpación sin masas palpables ni reacción peritoneal. La analítica realizada mostró una hemoglobina de 13.1 g/dL, proteína C reactiva a 122.9 mg/L sin leucocitosis (8.9 × 10^9/L), hiponatremia (130 mmol/L), hipopotasemia (2.9 mmol/L), pruebas de función renal, hepáticas, lipasa y enzimas cardiacas normales. El frotis para SARSCoV-2 fue negativo. La orina era maloliente con presencia de nitritos positivos, hematíes (+++) y leucocitos (+) por lo que se envió la muestra para cultivo microbiológico. Ante estos hallazgos se inició antibioticoterapia probabilista con ceftriaxona ante la sospecha de una posible infección urinaria y se decidió realizar una tomografía tóraco-abdomino-pélvica para descartar la presencia de un foco infeccioso profundo. Este examen reveló la presencia de signos de broncopatía crónica y una neumatosis vesical parietal a nivel abdominal compatible con una cistitis enfisematosa. El cultivo de orina reveló la presencia de Escherichia coli (> 100 000 UFC/m) sensible a la antibioticoterapia prescrita empíricamente y los hemocultivos fueron positivos al mismo germen. Se decidió el ingreso de la paciente en servicio de medicina interna y se continuó el tratamiento antibiótico durante 7 días con una evolución favorable desde el punto de vista clínico y analítico, permitiendo el alta hospitalaria.",
+        "gold_summary": "Una mujer de 82 años con antecedentes de hipertensión arterial e hipotiroidismo acudió al servicio de urgencias por dolor abdominal, diarrea, confusión y deterioro de su estado general de varios días de evolución. A su admisión, la paciente se encontraba febril y la analítica mostró una elevación de la proteína C reactiva sin leucocitosis (8.9 × 10^9/L). En ese contexto se realizó exudado nasofaríngeo para SARS-CoV-2 que fue negativo. Con estos resultados, la sospecha inicial era la de un cuadro infeccioso de origen digestivo. La muestra de orina era maloliente con presencia de leucocitos y nitritos enviándose a cultivo microbiológico. Se inició tratamiento antibiótico empírico con una cefalosporina de tercera generación ante la sospecha de une posible infección urinaria. Se decidió la realización de una tomografía tóraco-abdomino-pélvica con el objetivo de evaluar la presencia de otros focos infecciosos en una paciente de edad avanzada. Este estudio mostró una cistitis enfisematosa, una enfermedad poco frecuente en una paciente sin ninguno de los factores de riesgo clásicos para esta entidad. Los cultivos de orina y sangre fueron positivos para Escherichia coli sensible al antibiótico empírico por lo que se continuó para completar 7 días de tratamiento. La evolución clínica fue favorable.",
+        "synthetic_summary": {
+            "B1": "Una mujer de 82 años llegó al hospital con dolor de barriga, diarrea y confusión. Tenía fiebre y su orina olía mal, con señales de infección. Los médicos hicieron una prueba y encontraron una infección rara en la vejiga llamada cistitis enfisematosa. Le dieron un antibiótico que funcionó bien. Después de una semana, la mujer mejoró y pudo salir del hospital.",
+            "B2": "Una mujer de 82 años llegó al hospital con dolor abdominal, diarrea y confusión durante varios días. Tenía fiebre y signos de inflamación en la sangre, pero no aumentaron sus glóbulos blancos. La prueba para COVID-19 fue negativa. La orina tenía mal olor y mostraba infección, por eso comenzaron un antibiótico mientras esperaban el resultado del cultivo. Una tomografía mostró una infección rara en la vejiga llamada cistitis enfisematosa, que produce gas en la pared. Los cultivos confirmaron que la bacteria Escherichia coli causaba la infección y respondía al antibiótico. La paciente recibió tratamiento por siete días y mejoró, por eso pudo salir del hospital sin problemas.",
+            "B3": "Una mujer de 82 años con hipertensión e hipotiroidismo acudió a urgencias por dolor abdominal, diarrea, confusión y deterioro general. Presentaba fiebre y análisis con proteína C reactiva elevada, pero sin aumento de glóbulos blancos. Se descartó infección por SARS-CoV-2. La orina maloliente con leucocitos y nitritos positivos sugirió infección urinaria, por lo que se inició tratamiento con ceftriaxona. La tomografía reveló una cistitis enfisematosa, una infección rara caracterizada por la presencia de gas en la pared de la vejiga, sin factores de riesgo habituales en esta paciente. Los cultivos de orina y sangre confirmaron infección por Escherichia coli sensible al antibiótico. La paciente fue ingresada y recibió tratamiento durante siete días, con mejoría clínica y analítica, lo que permitió su alta hospitalaria. Este caso destaca la importancia de considerar infecciones urinarias graves en pacientes mayores, incluso sin factores de riesgo clásicos, y la utilidad de estudios de imagen para identificar complicaciones."
+        }
+    },
+    {
+        "article": "Varón nacido a las 38 semanas de gestación y sin controles obstétricos prenatales, producto de un parto eutócico sin complicaciones con un peso de 2.678 g y Apgar 7 y 8 al minuto y a los cinco minutos de vida, respectivamente; derivado por sospecha de enterocolitis necrotizante a los siete días de vida. Al nacimiento, en su hospital de origen, se descartaron malformaciones congénitas externas y se colocó una sonda orogástrica para verificar la permeabilidad esofágica, obteniendo 200 mL de líquido amniótico. Posteriormente inició alimentación vía oral pero debido a succión débil y vómitos biliosos fue ingresado en la unidad de cuidados intensivos neonatales. A las 4 horas de vida se realizó radiografía abdominal observando una imagen de doble burbuja atípica, por lo cual realizaron un control radiológico 48 horas después identificando gas intestinal aparentemente distal, y presentó meconiorrexis a las 50 horas de vida. Dos días después reinició la alimentación oral, tras lo cual presentó nuevamente vómitos de aspecto biliar y distensión abdominal que mejoró con el ayuno y sonda orogástrica; por lo cual se sospechó enterocolitis necrotizante indicándose dieta absoluta, nutrición parenteral total y antibioterapia con ampicilina y amikacina. A los siete días de vida y debido a la persistencia de los síntomas pese al tratamiento instaurado, fue derivado a nuestro centro. A su llegada presentaba distensión abdominal, sin ruidos intestinales ni signos de irritación peritoneal, por lo que se realizó tránsito intestinal sin progresión distal y colon por enema con hallazgo de microcolon, todo ello sugestivo de atresia intestinal yeyunoileal. Tras la realización de los estudios de imagen y con la sospecha de atresia intestinal se realizó una laparotomía exploradora mediante abordaje supraumbilical transverso, observando adherencias hepatoileales, una hernia interna a través de un defecto mesentérico con incarceración de un asa yeyunal y atresia yeyunoileal tipo IV. Se identificaron dos sitios de atresia a 56 cm del ángulo de Treitz y a 36 cm de la válvula ileocecal, con un segmento interatrésico de 10 cm con meconio intraluminal y cambios de coloración con aspecto violáceo pero sin perforación; la diferencia de diámetros intestinales proximal a distal tenía una relación 3:1. Se decidió disecar el mesenterio y resecar el asa ciega (10 cm) para realizar una anastomosis término-oblicua yeyunoileal, corroborando la permeabilidad distal con sonda intraluminal y administración de solución fisiológica hasta que presentó evacuación rectal. El reporte de histopatología confirmó una atresia yeyunoileal tipo IV con enteritis crónica leve. El paciente evolucionó favorablemente y al 5º día postoperatorio inició alimentación oral con adecuada tolerancia progresiva y descenso paulatino de la nutrición parenteral total con retirada al 8º día postoperatorio. Al 6° día de la intervención presentó deposiciones espontáneas y a los 20 días de vida fue dado de alta sin complicaciones. Doce meses después el paciente continúa asintomático con adecuada ganancia ponderal y tolerancia a la alimentación complementaria con deposiciones diarias de características normales.",
+        "gold_summary": "Recién nacido de sexo masculino, nacido a término, derivado por vómitos, evacuaciones escasas y distensión abdominal. A los 8 días de vida y tras excluir diversas causas de distensión abdominal se sometió a laparotomía exploradora, identificando una hernia transmesentérica y dos sitios de atresia intestinal. Se realizó resección del segmento atrésico y anastomosis primaria, con buena evolución.",
+        "synthetic_summary": {
+            "B1": "Un bebé nació sin problemas pero empezó a vomitar y tener la barriga hinchada. Los doctores le hicieron estudios y encontraron que su intestino tenía dos partes bloqueadas. Le hicieron una operación para quitar esas partes y unir el intestino. Después de la cirugía, el bebé mejoró mucho y pudo comer bien. Ahora está sano y crece feliz.",
+            "B2": "Un bebé nacido a término presentó vómitos con bilis, distensión abdominal y pocas evacuaciones. Al principio, se sospechó una infección intestinal grave llamada enterocolitis necrotizante, pero los síntomas no mejoraron con el tratamiento. Las radiografías mostraron problemas en el intestino, y se realizó una cirugía para explorar el abdomen. Durante la operación, se encontró una hernia interna y dos áreas donde el intestino estaba bloqueado (atresia intestinal). Se quitó la parte dañada y se unieron los extremos sanos del intestino. Después de la cirugía, el bebé mejoró, comenzó a alimentarse bien y fue dado de alta sin complicaciones. Un año después, sigue sano y crece adecuadamente.",
+            "B3": "Un recién nacido a término, sin controles prenatales, presentó desde sus primeros días vómitos biliosos, succión débil y distensión abdominal. Inicialmente se sospechó enterocolitis necrotizante, pero ante la persistencia de síntomas se realizaron estudios que sugirieron atresia intestinal yeyunoileal, una obstrucción congénita del intestino delgado. Durante la cirugía se encontró una hernia interna con encarcelamiento de un asa intestinal y dos sitios de atresia, que fueron corregidos mediante resección y anastomosis. El diagnóstico se confirmó por histopatología, que mostró atresia tipo IV con inflamación leve. Tras la intervención, el paciente mejoró progresivamente, toleró la alimentación oral y fue dado de alta sin complicaciones. Un año después, el niño continúa asintomático, con crecimiento adecuado y buena digestión. Este caso resalta la importancia de un diagnóstico oportuno y tratamiento quirúrgico en atresias intestinales para evitar complicaciones severas y asegurar un buen pronóstico."
+        }
+    },
+    {
+        "article": "Se remitió a un hombre de 86 años para que se le implantara una válvula aórtica transfemoral.\n\nLa historia significativa incluyó el hecho de fumar 40 cajetillas al año (hasta fines de la década de 1980) y la fibrilación auricular paroxística que requería anticoagulación con Coumadin desde 1999, seguida poco después por la implantación de un marcapasos ventricular debido a bradicardia. Fue admitido por síncope en mayo de 2011 y se le diagnosticó una estenosis aórtica calcificada severa. Era eupneico y no mostraba signos de insuficiencia cardiaca o retención de líquidos. La ecocardiografía transtorácica reveló una estenosis aórtica severa (gradiente medio: 58 mmHg, área de la válvula aórtica: 0,4 cm2) con hipertrofia ventricular izquierda, fracción de eyección ventricular izquierda deteriorada (29%), acinesia inferior apical y obstrucción septal subvalvular (septum: 18 mm) con dilatación biauricular e hipertensión pulmonar con dilatación de la vena cava.\n\nLa angiografía coronaria mostró una estenosis del 75% de la arteria descendente anterior izquierda. El examen de eco-Doppler encontró vasos normales en el cuello. Se agregó aspirina 80 mg diariamente a su tratamiento; el paciente fue programado para un reemplazo de la válvula aórtica, pero no llegó hasta agosto, cuando fue readmitido en urgencias por disnea aguda y confusión. Había ganado 6 kg de peso, con edemas en las piernas y signos clínicos de derrame pleural. En ese momento, su SpO2 era del 92% y la proteína B-natriurética estaba elevada a 2336 pg·mL−1 (normal < 100 pg·mL−1).\n\nTras la terapia diurética y la eliminación de 850 ml de derrame pleural, se realizó una valvuloplastia de balón percutáneo aórtico de emergencia (Cristal Balloon, 23 mm) e inmediatamente después se le implantó un stent de metal desnudo (Biotronik-Pro-Kinetic 2.74 × 10.0) en la arteria descendente anterior izquierda. El gradiente medio transvalvular disminuyó de 59 a 38 mmHg. Se observaron algunas torsades de pointe el día 6 después de la intervención, que desaparecieron cuando la frecuencia más baja del marcapasos se aceleró a 80 latidos/min. Su estado mejoró drásticamente y se le dio el alta con furosemida, aldactazina y clopidogrel. Tras una revisión cuidadosa del expediente del paciente por parte del equipo cardiaco, se consideró que el riesgo de una cirugía valvular era demasiado alto (Euroscore logístico: 51%), y se propuso al paciente un implante de válvula aórtica transfemoral.\n\nLas notas de las enfermeras mencionan la hiperventilación nocturna y las crisis de ansiedad. El paciente era semiautónomo y vivía con su hija.\n\nLa implantación de la válvula aórtica transfemoral se programó para octubre de 2011. En el ingreso, 2 días antes del procedimiento, el paciente se describió como «ansioso e hiperventilante»; su peso era de 67 kg para una altura de 168 cm; el volumen espiratorio forzado en 1 s (FEV1) era de 1,1 L (50% del valor previsto) y la capacidad vital forzada de 1,7 L (55%); la presión arterial sistémica era de 120/60 mmHg; la concentración de hemoglobina era de 167 g·L−1; la creatinina era de 12,7 g·L−1; la tasa de filtración glomerular se calculó en 54 ml·min−1·m−2; el potasio era de 3,7 mEq·L−1; el sodio era de 141 mEq·L−1; el bicarbonato era de 22 mEq·L−1; y la proteína B natriurética era de 2.073 pg·mL−1. La ecografía describió un área de superficie de la válvula aórtica de 0,5 cm2 con un gradiente aórtico medio de 55 mmHg y acinesia inferoapical en el ventrículo izquierdo. La fracción de eyección se midió en 27% por el método Simpson biplano con regurgitación mitral moderada con dilatación biauricular y se estimó la presión pulmonar sistólica en >69 mmHg. La radiografía de tórax no mostró derrame pleural significativo. El paciente era totalmente dependiente del marcapasos.\n\nDos horas antes de la intervención, el paciente recibió 1 g de acetaminofeno por vía oral. Al llegar al quirófano, el paciente, plenamente consciente, presentaba respiración de Cheyne-Stokes periódica; cada ciclo duraba unos 85 s, con apneas de entre 15 y 20 s y grandes oscilaciones de la SpO2 entre el 88 % y el 99 %. Se le colocó dos catéteres intravenosos periféricos y uno arterial. El trazado arterial también mostraba oscilaciones de 85 s y una presión sistólica de 130 a 150 mmHg. Se le aplicó una máscara facial de oxígeno al 40 % con ventilación no invasiva; la SpO2 alcanzó un rango más estable (92 %-99 %). Diez minutos después, los análisis de gases en sangre mostraron un pH de 7,39, Pao2 de 108 mmHg, Paco2 de 40 mmHg, SaO2 del 97 %, y oscilaciones de lactato de 1,2 mEq·L−1. Se instaló una línea de muestreo capnógrafo dentro de la máscara facial para monitorizar la frecuencia respiratoria (Carescape Monitor B650, GE Healthcare, Helsinki, Finlandia). La monitorización también incluía un ECG de 12 derivaciones, oximetría de pulso, y oximetría cerebral regional (rSO2) mediante espectroscopia infrarroja cercana en el frente (INVOS, Somanetics). La capnografía reveló que las oscilaciones de la presión arterial eran sincrónicas con el ritmo de la respiración y que la presión disminuía durante los períodos apneicos e hipopneicos y aumentaba durante la hiperventilación; la rSO2 seguía el mismo patrón, a pesar de que la SpO2 del dedo permanecía a un nivel constante de 99 %. Se inició una infusión de propofol a una concentración objetivo de 0,2 µg·mL−1; se administraron 2,5 µg de sufentanilo antes de que los operadores infiltraran cada ingle con 200 mg de mepivacaína; el paciente se quedó dormido pero se mantuvo despierto al menor contacto con su cara o cuando su nombre se susurraba al oído; se administraron otros 2,5 µg de sufentanilo antes de la dilatación femoral de la arteria, un procedimiento requerido antes del reemplazo de la válvula. Los ciclos de ventilación se desaceleraron a un máximo de 120 s con 24 s de apneas centrales. Cuando la angiografía y los catéteres operativos estaban en su lugar en la aorta ascendente y se introdujo un marcapasos temporal en el ventrículo derecho, se indujo un ritmo rápido de 200 latidos/min para permitir una nueva dilatación de la válvula calcificada. Este procedimiento duró <25 s, durante el cual el paciente permaneció consciente y continuó respirando de la forma habitual, el ritmo se indujo justo después del final de un período apneico. Se preparó una válvula de 26 mm (SAPIEN, Edwards Lifesciences) y se introdujo en el orificio aórtico. Se dio una señal a los operadores una vez que la respiración se reanudó al final de un período apneico; se inició un ritmo ventricular rápido que llevó a la asistolia a una presión arterial media de 45 mmHg, y la válvula se expandió con balón y la angiografía confirmó la ausencia de fuga paravalvular. El balón se desinfló justo antes de que se detuviera el ritmo rápido, y el corazón volvió a latir a 80 latidos/min bajo la estimulación del marcapasos implantado. La secuencia completa se filmó; duró 31 s, durante los cuales el paciente siguió respirando regularmente (8 veces durante la detención circulatoria, es decir, una tasa de 16 veces por minuto) y no se despertó. Las expulsiones de sangre se reanudaron inmediatamente después de la deflación del balón, con una presión sistólica de 80 mmHg. Después de unas respiraciones profundas, la respiración se hizo regular; no se produjeron nuevos períodos apneicos ni oscilaciones de la presión arterial o rSO2. La hipertensión sistémica se desarrolló rápidamente, culminando después de 1 min a 190 mmHg y se controló con 40 mg de urapidil intravenoso durante los siguientes 15 min. La ecografía transtorácica midió el área valvular a 1,6 cm2 y el gradiente transvalvular máximo a 15 mmHg. La estimación de la presión arterial pulmonar mediante ecografía transtorácica mostró un gradiente sistólico de la presión ventricular derecha-aurícula derecha de 69 mmHg 1 día antes del procedimiento y 45 mmHg 2 días después. Un mes después, era de 28 mmHg. La evolución posterior no tuvo incidentes, y el paciente fue dado de alta 72 h después sin haber vuelto a la respiración periódica.\n\nMH - Edad 80 años y más\nMH - Cirugía de la válvula aórtica\nMH - *Estenosis/cirugía de la válvula aórtica\nMH - *Respiración de Cheyne-Stokes\nMH - Ecocardiografía\nMH - *Insuficiencia cardiaca\nMH - *Implantación de prótesis valvulares cardíacas\nMH - Hemodinámica\nMH - Humanos\nMH - Hombre\nMH - Resultado del tratamiento\n",
+        "gold_summary": "Se remitió a un hombre de 86 años para la implantación de una válvula aórtica transfemoral. La ecocardiografía transtorácica reveló una estenosis grave (gradiente medio: 58 mmHg, área de la válvula aórtica: 0,4 cm2), y después de una discusión multidisciplinaria, se consideró que el riesgo de la cirugía era demasiado alto (Euroscore logístico: 51%), y se propuso al paciente para la implantación de una válvula aórtica transfemoral (TAVI). Al llegar al quirófano, se observó que el paciente, completamente consciente, tenía respiración de Cheyne-Stokes (CSB), que persistió después de la administración de oxígeno al 40%. El procedimiento TAVI fue exitoso, y el patrón CSB se interrumpió en 8 s.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre de 86 años tenía un problema en su corazón llamado estenosis aórtica, que hace difícil que la sangre salga bien. Su operación era muy riesgosa, así que los doctores le pusieron una válvula nueva sin abrir el pecho. Antes de la operación, respiraba de una forma rara llamada Cheyne-Stokes, que es cuando la respiración cambia mucho. Después de poner la válvula, su respiración volvió a la normalidad y la operación fue un éxito.",
+            "B2": "Un hombre de 86 años con estenosis aórtica grave fue considerado de alto riesgo para cirugía tradicional, por lo que se propuso implantarle una válvula aórtica transfemoral (TAVI). Al llegar al quirófano, el paciente estaba consciente y presentaba respiración de Cheyne-Stokes, un patrón irregular con pausas y oscilaciones en la respiración. Se le administró oxígeno, pero la respiración anormal persistió. Durante el procedimiento TAVI, que fue exitoso, la respiración de Cheyne-Stokes se interrumpió rápidamente. Después de la intervención, la función cardíaca mejoró y no se observaron nuevos episodios de respiración irregular. El paciente fue dado de alta sin complicaciones. Este caso muestra que el TAVI puede ser una opción segura para pacientes con alto riesgo quirúrgico y problemas respiratorios asociados.",
+            "B3": "Un hombre de 86 años con estenosis aórtica severa y múltiples comorbilidades, como fibrilación auricular y enfermedad coronaria, fue considerado de alto riesgo para cirugía convencional, por lo que se planificó un implante de válvula aórtica transfemoral (TAVI). Antes del procedimiento, se identificó un patrón respiratorio anormal denominado respiración de Cheyne-Stokes, caracterizado por ciclos alternantes de hiperventilación y apnea, que persistió incluso con oxígeno suplementario. Durante el TAVI, realizado bajo sedación consciente, el paciente mantuvo este patrón respiratorio, aunque se interrumpió brevemente tras la implantación de la válvula. El procedimiento resultó exitoso, evidenciándose una mejoría significativa en la función valvular sin complicaciones respiratorias posteriores. La desaparición del patrón de Cheyne-Stokes después de la intervención sugiere una mejora hemodinámica sustancial. Este caso resalta la viabilidad del TAVI en pacientes ancianos con alto riesgo quirúrgico y la importancia de monitorear patrones respiratorios complejos, que reflejan la gravedad de la insuficiencia cardiaca y pueden mejorar tras el tratamiento."
+        }
+    },
+    {
+        "article": "Una mujer árabe tunecina de 62 años, diagnosticada con la enfermedad de Von Hippel-Lindau en 2021, presentó varias manifestaciones relacionadas con la enfermedad. Tenía antecedentes de múltiples cirugías, principalmente por tumores renales, suprarrenales y pancreáticos, con hallazgos incidentales de masas ováricas.\n\nLa paciente no presentaba síntomas desde el punto de vista ginecológico, pero se quejaba principalmente de dolores de cabeza antes de someterse a una cirugía cerebral. No tenía antecedentes familiares o psicosociales significativos.\n\nSu historial quirúrgico incluye\n2021: Un tumor no operable (6 cm) del saco endolinfático del hueso petroso izquierdo, tratado con radioterapia.\n\n2021: Adrenalectomía izquierda por un feocromocitoma de 6 cm. El examen patológico reveló un feocromocitoma.\n\n2021: Nefrectomía izquierda por un tumor renal izquierdo roto. La microscopía mostró un carcinoma renal multifocal de células claras de grado nuclear 2.\n\n2022: Duodenopancreatectomía cefálica por una masa en el páncreas. El examen histológico confirmó tres cistadenomas serosos y dos tumores neuroendocrinos bien diferenciados.\n\nEn enero de 2021, durante la vigilancia posoperatoria con una tomografía computarizada (TC) abdominal-pélvica, se descubrió incidentalmente una masa anexial izquierda sólida de 4 cm, lo que levantó sospechas de malignidad. La masa se confirmó mediante ultrasonido transvaginal e IRM pélvica, clasificada como Sistema de Reporte y Datos Ováricos-Anexiales (O-RADS) 5 (alta sospecha de malignidad).\n\nExamen ginecológico e historial quirúrgico\nExamen físico: No se detectó masa abdominal-pélvica.\n\nExamen con espéculo: cuello uterino sano.\n\nSe observaron cicatrices quirúrgicas de una nefrectomía izquierda y una duodenopancreatectomía cefálica anteriores.\n\nUna reunión multidisciplinaria del personal concluyó que era necesaria la cirugía. Se realizó una laparotomía a través de una incisión en la línea media por debajo del ombligo, que reveló una masa quística sólida bien definida en el anexo izquierdo. No había ascitis ni signos de carcinomatosis peritoneal, y el anexo derecho parecía normal, sin signos macroscópicos de malignidad observados intraoperatoriamente, incluida la ausencia de vegetaciones exocísticas.\n\nSe realizó una citología junto con una anexectomía izquierda y la muestra se envió para un examen de sección congelada. Los resultados no fueron concluyentes, lo que planteó la posibilidad de tumores de margen o específicos del síndrome de Von Hippel-Lindau. Teniendo en cuenta el estado posmenopáusico de la paciente, se realizó una anexectomía derecha y una histerectomía total.\n\nEl examen histológico posterior reveló cistadenomas papilares de células claras bilaterales de las trompas de Falopio y el ligamento ancho, característicos de la enfermedad de Von Hippel-Lindau (0,5 cm en el lado derecho y 4 cm en el lado izquierdo). Los tumores consistían en papilas densamente compactadas con núcleos fibrosos, cubiertos por un epitelio monocapa.\n\nEl período postoperatorio inmediato transcurrió sin incidentes y, en el seguimiento de 1 mes, no se detectaron anomalías. Desde entonces, se ha hecho un seguimiento al paciente cada 4 meses con ecografías pélvicas normales. Durante estos 2 años de seguimiento, no han surgido complicaciones, pero el paciente fue readmitido recientemente en el departamento de neurocirugía por la recurrencia de un tumor cerebral.\n",
+        "gold_summary": "Una mujer blanca norteafricana de 62 años de edad, diagnosticada con la enfermedad de Von Hippel-Lindau en 2021, presentó múltiples manifestaciones, entre ellas, un tumor del hueso petroso izquierdo, feocromocitoma izquierdo, carcinoma de células renales izquierdo, riñón derecho con múltiples quistes y masas pancreáticas. Se sometió a varios tratamientos, entre ellos, radioterapia, adrenalectomía, nefrectomía y duodenopancreatectomía cefálica. Los exámenes de ultrasonografía y resonancia magnética revelaron una masa quística sólida en la región anexial izquierda. La laparoscopia identificó tumores quísticos en la mesosalpinx derecha e izquierda. Después de una histerectomía con anexectomía bilateral, el examen histológico reveló cistadenomas papilares de células claras bilaterales de la mesosalpinx y el ligamento ancho, compatibles con la enfermedad de Von Hippel-Lindau.\n",
+        "synthetic_summary": {
+            "B1": "Una mujer de 62 años tiene una enfermedad llamada Von Hippel-Lindau que causa tumores en varias partes del cuerpo. Ella tuvo tumores en el riñón, el páncreas y el hueso, y recibió varias cirugías. Se encontró una masa en la zona de los ovarios que parecía peligrosa. Le hicieron una operación para quitar esa masa y parte del útero. Los exámenes mostraron que los tumores estaban relacionados con su enfermedad. Después de la cirugía, está bien y sigue en control médico.",
+            "B2": "Una mujer de 62 años con enfermedad de Von Hippel-Lindau tenía varios tumores en órganos como riñones y páncreas. En 2021, detectaron una masa sospechosa cerca del ovario izquierdo, aunque no tenía síntomas. Por eso, decidieron hacer una cirugía para quitar esa masa. Durante la operación, encontraron tumores también en las trompas de Falopio y en el ligamento ancho. Los análisis mostraron que eran cistadenomas papilares de células claras, un tipo de tumor relacionado con su enfermedad. Después de la cirugía, la paciente estuvo bien y no tuvo problemas en los controles. Sin embargo, volvió a aparecer un tumor cerebral, por eso sigue en vigilancia médica constante.",
+            "B3": "Una mujer tunecina de 62 años con diagnóstico previo de enfermedad de Von Hippel-Lindau en 2021 presentó múltiples tumores en riñones, páncreas y glándulas suprarrenales, tratados mediante cirugía y radioterapia. Durante el seguimiento, se identificó una masa sólida en el anexo ovárico izquierdo, sospechosa de malignidad, confirmada por ultrasonido y resonancia magnética. A pesar de la ausencia de síntomas ginecológicos y masas palpables, se decidió realizar laparotomía, encontrando una masa quística sólida sin evidencia de diseminación tumoral. La biopsia intraoperatoria resultó inconclusa, por lo que se completó con histerectomía y anexectomía bilateral debido al estado posmenopáusico de la paciente. El análisis histológico confirmó la presencia de cistadenomas papilares de células claras en ambas trompas de Falopio y el ligamento ancho, lesiones típicas de esta enfermedad genética. La paciente evolucionó sin complicaciones inmediatas y, tras dos años de seguimiento con ecografías pélvicas normales, no se observaron recurrencias ginecológicas. No obstante, fue readmitida por recurrencia de un tumor cerebral, lo que refleja la naturaleza multisistémica y compleja de esta patología."
+        }
+    },
+    {
+        "article": "Una mujer embarazada de 31 años que había sido sometida a una cesárea fue derivada a la unidad de ultrasonido de nuestro departamento para un examen de ultrasonido morfológico de segundo trimestre. La paciente no tenía antecedentes familiares destacables y no había tomado medicamentos ni había estado expuesta a teratógenos durante el primer trimestre del embarazo. Los exámenes serológicos para diversas enfermedades infecciosas fueron negativos y un examen de ultrasonido previo a las 14 semanas fue normal. El triple examen para anomalías fetales también fue negativo a las 16 semanas.\n\nDurante la ecografía de la semana 20, se observó un feto masculino con una edad sonográfica compuesta de 20 semanas y 2 días que presentaba un edema significativo de las extremidades inferiores y líquido amniótico normal. Se recomendó un examen de seguimiento en 2 semanas, junto con pruebas de TORCH y pruebas de Coombs indirectas.\n\nSin embargo, se observó nuevamente edema subcutáneo en ambas extremidades inferiores durante la ecografía morfológica de la semana 23, lo que sugiere un posible diagnóstico de EM. Debido al linfedema persistente en las extremidades inferiores, se realizó una amniocentesis.\n\nLos exámenes posteriores revelaron que el cariotipo masculino era normal (46, XY), y el análisis molecular para el síndrome de Noonan fue negativo. Se realizó la secuenciación de nucleótidos del líquido amniótico con la secuenciación Illumina de 150 bases. Se aplicó el sistema de bioinformática (North-Oehler Aligarh, GATX) mientras se verificaba adicionalmente la existencia de deleciones/duplicaciones/CNV (Copy Number Variations) en el gen FLT4. El análisis identificó una mutación c.3116C>A p. (Ala1039Asp), que es una variante patogénica no conocida en el gen FLT4, lo que confirma el diagnóstico de linfedema hereditario tipo 1A – enfermedad de Milroy. El análisis de sangre materno confirmó la mutación materna y se realizó el asesoramiento genético.\n\nLa cesárea se realizó a las 38 semanas y 6 días de gestación y nació un neonato de sexo masculino que pesaba 3850 g y medía 46 cm con una puntuación de Apgar de 9/10. Después del parto se reconoció un edema en la extremidad inferior. El examen histopatológico de la placenta, el cordón umbilical y el saco amniótico no mostró signos de corioamnionitis u otra patología.\n",
+        "gold_summary": "Presentamos un informe de caso de una primera mutación descrita de un feto masculino diagnosticado prenatalmente con síndrome de Milroy a través de amniocentesis. El feto tenía edema bilateral de miembros inferiores, y las pruebas genéticas confirmaron el diagnóstico de síndrome de Milroy. La paciente fue monitoreada de cerca durante todo el embarazo, y después del parto, el lactante fue tratado con terapias apropiadas, incluyendo prendas de compresión y drenaje linfático manual. Los padres recibieron asesoramiento y apoyo apropiados.\n",
+        "synthetic_summary": {
+            "B1": "Una mujer embarazada fue revisada con ultrasonido y se vio que su bebé tenía hinchazón en las piernas. Se hicieron pruebas y encontraron un cambio en un gen que causa el síndrome de Milroy, una enfermedad que afecta el líquido en el cuerpo. La mamá y el bebé recibieron ayuda y cuidados especiales. El bebé nació sano y con apoyo para mejorar su salud.",
+            "B2": "Una mujer embarazada fue evaluada con ultrasonido en la semana 20 y se detectó edema en las piernas del feto, un signo anormal que se confirmó en la semana 23. Se realizaron pruebas genéticas que encontraron una mutación en el gen FLT4, lo que indicó que el bebé tenía síndrome de Milroy, una enfermedad hereditaria que causa linfedema (hinchazón por problemas en los vasos linfáticos). La madre también tenía esta mutación. El bebé nació por cesárea a término con buen estado general, pero con edema en una pierna. Después del nacimiento, recibió tratamientos para controlar la hinchazón, y los padres recibieron asesoramiento genético para entender la condición. El seguimiento durante el embarazo fue cuidadoso para asegurar la salud del bebé.",
+            "B3": "Una mujer embarazada fue evaluada mediante ecografías durante el segundo trimestre, donde se detectó edema en las extremidades inferiores del feto, lo que sugirió un problema linfático. Los análisis genéticos realizados a partir del líquido amniótico identificaron una mutación en el gen FLT4, confirmando el diagnóstico de síndrome de Milroy, una forma hereditaria de linfedema. La madre también portaba esta mutación, por lo que recibió asesoramiento genético. El embarazo continuó bajo vigilancia cuidadosa y el bebé nació por cesárea a término, presentando edema en las piernas desde el nacimiento. No se encontraron otras complicaciones placentarias ni infecciones. Tras el parto, el recién nacido fue tratado con medidas específicas para el linfedema, como prendas de compresión y drenaje linfático manual. Este caso destaca la importancia de la detección prenatal y el manejo multidisciplinario para mejorar el pronóstico en enfermedades genéticas raras que afectan el sistema linfático."
+        }
+    },
+    {
+        "article": "Un paciente de 50 años con antecedentes médicos conocidos de diabetes mellitus (DM) e hipertensión (HTN), que se manejaba de manera irregular, se presentó en nuestro hospital en la ciudad de Sana’a, Yemen, el 25 de mayo de 2022, a las 5:30 p. m. El paciente fue derivado a otro hospital y manifestó un dolor abdominal agudo que había durado una semana antes del ingreso. El dolor se localizaba en la región epigástrica, de inicio repentino, empeoramiento progresivo y radiación hacia la espalda. Además, el paciente experimentó distensión abdominal generalizada, náuseas, vómitos y fatiga significativa. También se informó un historial de melena y vómitos relacionados con los alimentos durante el mes pasado. Dos días antes del ingreso, el paciente había recibido una transfusión de sangre de 2 unidades. No había antecedentes de cirugías previas ni antecedentes familiares de neoplasias.\n\nAl examinar al paciente, se constató que estaba consciente y alerta, pero que presentaba un aspecto pálido. La presión arterial era de 90/60 mmHg y el pulso de 120 latidos por minuto. Se observó distensión abdominal generalizada, particularmente prominente en la región supraumbilical con desplazamiento hacia abajo del ombligo. Se constató una leve sensibilidad en la zona epigástrica, junto con sonidos intestinales positivos, el examen rectal digital reveló un tono normal del esfínter anal y no se detectó ninguna masa palpable.\n\nLos exámenes hematológicos y bioquímicos revelaron anemia microcítica hipocrómica con un nivel de hemoglobina de 6 g/dL (rango normal: 12-15.5 g/dL), un recuento de glóbulos blancos de 16,000 (rango normal: 4-10,000), y un recuento de plaquetas de 303. El nivel de nitrógeno ureico en sangre fue de 7 mg/dL (rango normal: 10-20 mg/dL), la creatinina fue de 0.49 mg/dL (rango normal: 0.7-1.5% / dL), el índice internacional normalizado fue de 1.34 (rango normal: 0.62-1.3), el tiempo de protrombina (PT) fue de 16.9, el tiempo de tromboplastina parcial (PTT) fue de 30, el calcio fue de 8.0 mg/dL (rango normal: 8.5-10.1 mg / dL) y el ácido láctico fue de 1.9 mmol/L (rango normal: 0.5-2.2% / L). Los niveles de enzimas hepáticas y amilasa estuvieron dentro de los límites normales.\n\nSe realizaron estudios de diagnóstico por imágenes, que incluyeron una radiografía de tórax y una ecografía abdominal. La radiografía de tórax no reveló aire subdiafragmático, pero se observó una elevación en el diafragma izquierdo. La ecografía abdominal demostró la presencia de una acumulación de líquido intraabdominal. Posteriormente, se realizó una angiografía por TC abdominal, que reveló un hematoma de aproximadamente 14,3 × 8,8 cm en la región paraumbilical. En el interior del hematoma, se identificó un aneurisma arterial de 3,4 × 2,2 cm conectado a la arteria gastroduodenal, acompañado de cambios edematosos circundantes. Estos hallazgos sugieren la presencia de un aneurisma trombosado grande en la arteria gastroduodenal. Además, se observó la evisceración del diafragma izquierdo, que contiene el bazo y parte del estómago, junto con una acumulación de líquido intraperitoneal leve a moderada. No se detectó evidencia de un aneurisma aórtico.\n\nPara estabilizar al paciente, se inició la reanimación con 1000 ml de lactato de Ringer y se transfundieron tres unidades de sangre fresca. Se obtuvo el consentimiento informado para la intervención de alto riesgo y el paciente fue llevado inmediatamente al quirófano. Bajo anestesia general, en posición supina y con estricta adhesión a las técnicas asépticas, se realizó una incisión de laparotomía en la línea media. Cuando se abrió el peritoneo, se evacuó aproximadamente 2000 ml de sangre, revelando una masa pulsátil ocluida en el duodeno. Se logró una exposición adecuada utilizando un retractor auto-reforzado. La flexión del hígado y el colon transverso se movilizaron inferiormente desde la cabeza del páncreas y se eliminó la sangre coagulada del intestino delgado. Se realizó una disección meticulosa sobre el gran aneurisma ocluido pulsátil en la arteria gastroduodenal abriendo el ligamento gastrohepático. La movilización del píloro y el duodeno lejos de la cabeza del páncreas expuso una fístula que conectaba el duodeno y el aneurisma, sin contenido digestivo. Después de la heparinización, se realizó un pinzamiento proximal y distal de la arteria gastroduodenal. Posteriormente, se abrió el pseudoaneurisma y se evacuó una cantidad significativa de trombo. Se realizó una aneurismorrafía utilizando suturas de prolina 7.0. La perforación en la primera parte del duodeno se reparó en dos capas y se insertó una sonda nasogástrica más allá de la perforación. Se logró una irrigación exhaustiva con solución salina normal y una hemostasia meticulosa. Se colocó un drenaje abdominal y se cerró la incisión abdominal en capas. El paciente fue trasladado a la unidad de cuidados intensivos (UCI) para una estrecha monitorización y observación.\n\nDurante el período postoperatorio, el drenaje abdominal recolectó aproximadamente 100 ml de fluido seroso, que se eliminó el tercer día después de la operación. La recuperación de la paciente progresó sin complicaciones. Diez días después de la cirugía, la paciente fue dada de alta en condiciones favorables. Se programaron citas de seguimiento en el departamento ambulatorio y se mantuvo una comunicación regular por teléfono, con la condición de la paciente reportada como satisfactoria.\n",
+        "gold_summary": "Un hombre de 50 años se presentó con dolor abdominal agudo, anemia y signos de inestabilidad hemodinámica. Las imágenes de diagnóstico, incluida la CTA, revelaron un aneurisma de la arteria gastroduodenal grande y trombosado con evidencia de ruptura. El paciente se sometió a exploración y reparación quirúrgica abierta para abordar tanto el aneurisma como la perforación duodenal. La recuperación del paciente fue satisfactoria y fue dado de alta en condiciones estables.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre de 50 años tenía dolor fuerte en la barriga y estaba muy cansado. Los doctores encontraron una bolsa grande y peligrosa en una arteria cerca del estómago, que estaba rota. Él tuvo una operación para arreglar la bolsa y un agujero en el estómago. Después de la cirugía, se recuperó bien y pudo salir del hospital sin problemas.",
+            "B2": "Un hombre de 50 años con diabetes e hipertensión mal controladas llegó al hospital con dolor fuerte en el abdomen. Tenía anemia y presión arterial baja, lo que indicaba un problema grave. Las pruebas mostraron un aneurisma grande, que es una dilatación en una arteria, con coágulos y ruptura en la arteria gastroduodenal. Además, tenía una perforación en el duodeno, que es la primera parte del intestino delgado. Fue operado de urgencia para reparar el aneurisma y cerrar la perforación. Durante la cirugía, se retiró la sangre acumulada y se arreglaron las lesiones. Después, el paciente mejoró sin complicaciones y salió del hospital diez días después. Se programaron controles para asegurar que su recuperación siga bien.",
+            "B3": "Un hombre de 50 años con diabetes e hipertensión mal controladas llegó al hospital con dolor abdominal intenso, distensión y síntomas de sangrado digestivo. Los estudios por imágenes mostraron un hematoma grande y un aneurisma trombosado en la arteria gastroduodenal, además de una hernia diafragmática que contenía el bazo y parte del estómago. Debido a la gravedad, se realizó una cirugía urgente para evacuar la hemorragia, reparar el aneurisma y cerrar una perforación en el duodeno. Durante la operación, se retiró el coágulo y se suturó cuidadosamente la arteria afectada y el duodeno. El paciente recibió soporte con líquidos y transfusiones sanguíneas, y fue monitoreado en la unidad de cuidados intensivos. La evolución postoperatoria fue favorable, sin complicaciones, y fue dado de alta diez días después en buen estado. Este caso resalta la importancia de un diagnóstico rápido y un tratamiento quirúrgico oportuno para aneurismas viscerales complicados, especialmente en pacientes con factores de riesgo como diabetes e hipertensión."
+        }
+    },
+    {
+        "article": "Una mujer de 60 años fue admitida en el departamento de nefrología con dolor epigástrico, hematemesis y edema en la pierna. La presión arterial era de 90/50 mmHg, dentro del rango normal para esta paciente.\nLos resultados de laboratorio fueron notables para las enzimas hepáticas alteradas con un patrón colestático: los niveles de alanina amino transferasa (ALT) y aspartato amino transferasa (AST) fueron ligeramente elevados a 28 U/L y 61 U/L, respectivamente, mientras que los niveles de fosfatasa alcalina (388 U/L) y gamma glutamiltransferasa (291 U/L) fueron muy elevados. Los niveles de albúmina en suero fueron de 24 g/L y el índice internacional normalizado fue normal a 1.02.\nOtros resultados de laboratorio, incluidos la bilirrubina total (0,32 mg/dL), la bilirrubina directa (0,26 mg/dL), el recuento total de plaquetas (176 000 plaquetas por microlitro) y el recuento de glóbulos blancos (8400 células por microlitro), se encontraban dentro de los valores normales.\nEl paciente tenía un extenso historial de enfermedades cardiacas y renales. A los 11 años, se le diagnosticó estenosis congénita de la válvula pulmonar, por lo que se le practicó una valvulotomía. Más adelante, desarrolló fibrilación auricular y aleteo auricular, que no toleró bien y para los que se intentó, sin éxito, la ablación del aleteo. Como el paciente seguía teniendo síntomas, se le practicó una ablación del nódulo auriculoventricular con colocación de un marcapasos.\nSe inició anticoagulación oral con fenprocoumon debido a una puntuación CHA2DS2-Vasc de 3 (mujer, insuficiencia cardiaca y enfermedad vascular periférica). A la edad de 55 años, se desarrolló una insuficiencia cardiaca derecha manifiesta y la paciente continuó luchando con ascitis y edemas periféricos que requerían múltiples ingresos hospitalarios. Además, también desarrolló un problema de efusiones pleurales transudativas recurrentes de etiología poco clara.\nLa ecocardiografía en ese momento mostró una severa regurgitación pulmonar y tricuspídea con un ventrículo derecho moderadamente dilatado y una aurícula derecha. El ventrículo izquierdo estaba ligeramente dilatado con una regurgitación mitral moderada. El cateterismo cardiaco derecho demostró presiones arteriales pulmonares de 74/30 mmHg con una presión venosa central de 28 mmHg. Se colocó un homotransplante pulmonar cuando el paciente tenía 57 años y se realizó una anuloplastia tricuspídea concomitante. A pesar de una presión venosa central más baja de 13 mmHg, el paciente seguía siendo readmitido varias veces por signos y síntomas de insuficiencia cardiaca derecha. La congestión venosa sistémica persistente finalmente dio lugar a una enfermedad renal en fase terminal para la que se inició una terapia de reemplazo renal a través de hemodiálisis intermitente. El caso se complicó por hemorragias gastrointestinales graves recurrentes, que requerían transfusiones de sangre frecuentes con hasta 60 unidades de glóbulos rojos por año. A pesar de esto, en combinación con la sustitución intravenosa de hierro, los niveles de hemoglobina variaron entre 5.3-8.8 g/dL. Debido a estos problemas de sangrado intratables, la anticoagulación oral con fenprocoumon se detuvo a la edad de 59 años.\nUna gastroscopia mostró una gastropatía erosiva con una mucosa difusa congestiva y friable. Como prevención de primera línea de las hemorragias gástricas recurrentes en el marco de la cirrosis, se inició el propranolol a una dosis de 5 mg por vía oral dos veces al día (el paciente no toleró una dosificación superior debido a la presión arterial baja). Además, se realizó una coagulación endoscópica de un angioma fúndico y un recorte de una lesión de Dieulafoy.\nSe creía que estas lesiones eran causadas por una gastropatía hipertensiva. Sin embargo, las hemorragias intractables persistieron.\nEl gradiente de presión venosa hepática se midió a 16 mmHg (27 mmHg-11 mmHg). Aunque hubo cierta reticencia debido al temor de empeorar la insuficiencia cardiaca derecha, se tomó la decisión de crear un TIPS. El procedimiento fue sin incidentes. Después de la colocación del TIPS, el gradiente de presión venosa hepática disminuyó a 4 mmHg (14 mmHg-10 mmHg). Por lo tanto, aunque el TIPS redujo considerablemente el gradiente venoso hepático, la presión portal se mantuvo alta debido a la elevada presión venosa central.\nDespués de la colocación del TIPS, el paciente desarrolló signos de encefalopatía hepática y se midieron niveles de amoniaco de 77 umol/L. Se inició el tratamiento con lactulosa oral y enemas, con poca mejora. En ese momento, se produjo otro episodio de sangrado gástrico.\nLa ecografía abdominal mostró buena permeabilidad del TIPS con flujo Doppler normal. Se detectó sangrado gástrico de una úlcera antral con endoscopia, a pesar de que la hiperemia gástrica disminuyó visualmente en comparación con la situación antes del TIPS. Se realizó una biopsia que mostró una mucosa foveolar edematosa, lo que sugiere isquemia de la mucosa. El sangrado fue demasiado difuso para una ligadura endoscópica adicional. No se encontró empeoramiento de la función hepática en los resultados de laboratorio, con el índice internacional normalizado 1.01 en este momento. La ecocardiografía no mostró cambios significativos en comparación con la situación antes de la colocación del TIPS. El ventrículo derecho permaneció moderadamente dilatado con una función longitudinal deficiente y una regurgitación tricuspídea severa persistente. Sin embargo, el estado general del paciente se deterioró y se desarrolló fiebre con consolidaciones pulmonares bilaterales.\nSe produjo una falla multiorgánica y, en ese momento, la familia del paciente decidió retirar el tratamiento. El paciente falleció finalmente 43 días después del procedimiento TIPS.\n\nMH - Resultado fatal\nMH - Mujer\nMH - Insuficiencia cardiaca/*complicaciones/fisiopatología\nMH - Encefalopatía hepática/etiología\nMH - Humanos\nMH - Hipertensión, Portal/etiología/fisiopatología/*cirugía\nMH - Cirrosis hepática/*complicaciones\nMH - Edad Media\nMH - Presión del portal\nMH - *Derivación portosistémica, intrahepática transyugular\nMH - Fracaso del tratamiento\n",
+        "gold_summary": "Una mujer de 60 años con antecedentes de estenosis congénita de la válvula pulmonar desarrolló insuficiencia cardíaca derecha, cirrosis hepática y enfermedad renal en fase terminal que requería terapia de reemplazo renal. La cirrosis hepática se complicó con hipertensión portal, lo que provocó hemorragias gastrointestinales intratables a pesar del tratamiento óptimo con betabloqueantes y la ligadura endoscópica de la banda. Debido al temor de que empeorara la insuficiencia cardíaca derecha, inicialmente se rechazó la colocación de una derivación intrahepática transyugular (TIPS). Sin embargo, como los problemas de hemorragia intratables persistieron y causaron grandes necesidades de transfusión, la TIPS se realizó finalmente como un procedimiento de rescate. Aunque la TIPS redujo con éxito el gradiente de presión venosa hepática de 16 mmHg a 4 mmHg, la presión portal se mantuvo alta a 14 mmHg debido a la persistencia de la insuficiencia cardíaca derecha con presión venosa central elevada. La encefalopatía hepática se desarrolló poco después de la colocación de la TIPS y culminó en una falla multiorgánica después de otro episodio de hemorragia gastrointestinal. En este punto, la familia del paciente decidió retirar la atención y el paciente falleció posteriormente.\n",
+        "synthetic_summary": {
+            "B1": "Una mujer de 60 años tenía problemas en el corazón, el hígado y los riñones. Su hígado estaba dañado y tenía sangrados en el estómago que no paraban. Le pusieron un tubo especial llamado TIPS para ayudar a bajar la presión en el hígado. Aunque esto ayudó, siguió teniendo problemas y se enfermó más. Al final, su familia decidió dejar el tratamiento y ella falleció.",
+            "B2": "Una mujer de 60 años tenía problemas del corazón desde niña. Desarrolló insuficiencia cardíaca derecha, cirrosis hepática (daño grave en el hígado) y enfermedad renal grave. La cirrosis causó hipertensión portal, que es presión alta en las venas del hígado. Esto provocó sangrados en el estómago difíciles de controlar, aunque usaron medicamentos y procedimientos endoscópicos. Por miedo a empeorar su corazón, dudaron en hacer una derivación llamada TIPS, que baja la presión en el hígado. Finalmente, hicieron la TIPS, pero la presión en la vena central siguió alta por la insuficiencia cardíaca. Después, la paciente tuvo encefalopatía hepática (problemas cerebrales por el hígado) y otro sangrado, causando falla de varios órganos. La familia decidió retirar el tratamiento y la paciente falleció.",
+            "B3": "Una mujer de 60 años con estenosis congénita de la válvula pulmonar y múltiples complicaciones cardíacas desarrolló insuficiencia cardíaca derecha, cirrosis hepática e insuficiencia renal terminal que requirió hemodiálisis. La cirrosis se complicó con hipertensión portal, provocando hemorragias gastrointestinales recurrentes difíciles de controlar a pesar de tratamientos con betabloqueantes y procedimientos endoscópicos. Inicialmente, se descartó la colocación de una derivación portosistémica intrahepática transyugular (TIPS) debido al riesgo de empeorar la insuficiencia cardíaca. Sin embargo, ante la persistencia del sangrado y la necesidad frecuente de transfusiones, se decidió realizar la TIPS como medida de rescate. El procedimiento logró reducir el gradiente de presión venosa hepática, aunque la presión portal permaneció elevada debido a la insuficiencia cardíaca derecha persistente. Posteriormente, la paciente desarrolló encefalopatía hepática y sufrió un nuevo episodio hemorrágico, seguido de falla multiorgánica. Ante el deterioro progresivo, la familia optó por retirar el soporte terapéutico, y la paciente falleció 43 días después del procedimiento. Este caso evidencia la complejidad del manejo de la hipertensión portal en pacientes con insuficiencia cardíaca avanzada y las limitaciones terapéuticas en estos escenarios."
+        }
+    },
+    {
+        "article": "Una mujer tailandesa de 62 años presentó pérdida visual bilateral súbita y cefalea durante 5 días. Negó antecedentes de traumatismo craneal. Su historia clínica era significativa por presentar hipertensión mal controlada.\n\nLos signos vitales fueron normales, excepto por la presión arterial de 200/105 mmHg. La agudeza visual fue de no percepción de luz (NLP) con pupilas fijas en ambos ojos. La motilidad ocular de ambos ojos fue limitada en todas las direcciones. Ambas párpados fueron difíciles de abrir. Las medidas del exoftalmómetro de Hertel fueron de 16 mm en el ojo derecho y 14 mm en el ojo izquierdo. Había quemosis significativa y vasos de sacacorchos episclerales en ambos ojos. Ambas córneas mostraron un edema estromal leve y difuso sin infiltración. Las cámaras anteriores fueron profundas y tranquilas en ambos ojos. Las presiones intraoculares fueron de 45 mmHg y 48 mmHg en los ojos derecho e izquierdo, respectivamente. La gonioscopia reveló sangre en el canal de Schlemm en el ángulo nasal del ojo derecho. El examen del fondo de ojo mostró venas de la retina ligeramente dilatadas y tortuosas con discos ópticos de apariencia normal en ambos ojos. La relación taza-disco fue de 0.3 bilateralmente. La tomografía de coherencia óptica demostró un espesor normal de la mácula en cada ojo. No hubo ruido audible. Otros exámenes neurológicos fueron normales.\n\nLa resonancia magnética (MRI) con gadolinio del cerebro y las órbitas demostró la dilatación de las venas oftálmicas superiores bilaterales (SOVs) y un grado marcado de congestión orbital y periorbital bilateralmente. Sin embargo, no se observó ni compresión ni estiramiento de los nervios ópticos bilaterales. Es interesante destacar que la restricción de la difusión, con la correspondiente reducción del coeficiente de difusión aparente (ADC), en todo el segmento orbital de los nervios ópticos bilateralmente se reveló en la resonancia magnética ponderada en difusión (DWI). Esto es consistente con el PION bilateral. La angiografía por resonancia magnética (MRA) del cerebro y las órbitas reveló arterialización de los senos cavernosos bilaterales y de las SOVs.\n\nLa angiografía cerebral confirmó el diagnóstico de CCF durales bilaterales de drenaje anterior. La CCF dural derecha se alimentaba de las ramas durales de la ICA (tronco meningo-hipofisario derecho). La CCF dural izquierda se alimentaba de las ramas durales de la ECA (arteria meningo-hipofisaria izquierda y la arteria izquierda del foramen redondo y las ramas durales de la ICA (tronco meningo-hipofisario izquierdo). Cada lado de la CCF dural contribuía con flujo sanguíneo arterial a los SOV bilaterales (SOV contralateral a través de la comunicación inter-cavernosa). No se observó reflujo venoso cortical del flujo sanguíneo arterial. Basándose en estos hallazgos, se realizó una embolización transvenosa de la bobina. Los senos cavernosos bilaterales se embolizaron utilizando bobinas para ocluir los vasos de alimentación de las ramas durales de la ICA y la ECA. La angiografía cerebral inmediata posterior a la embolización mostró el cierre completo de las fístulas.\n\nTres meses después de la embolización, el examen oftálmico demostró una mejora progresiva de los signos oftálmicos antes mencionados; no obstante, la agudeza visual del paciente se mantuvo en NLP en ambos ojos.\n",
+        "gold_summary": "Reportamos el caso de una mujer de 62 años de edad con antecedentes de hipertensión arterial mal controlada que presentó pérdida visual bilateral súbita y cefalea durante 5 días. Negó antecedentes de traumatismo craneal. En el examen, sus agudezas visuales eran de no percepción de luz (NLP) con pupilas fijas en ambos ojos. La motilidad ocular de ambos ojos era limitada en todas las direcciones. Era difícil abrir ambos párpados. El examen del segmento anterior reveló quemosis bilateral y vasos del sacacorchos episclerales. La presión intraocular era de 45 y 48 mmHg en los ojos derecho e izquierdo, respectivamente. La gonioscopia reveló sangre en el canal de Schlemm en el ángulo nasal del ojo derecho. El examen del fondo de ojo mostró venas retinianas ligeramente dilatadas y tortuosas con discos ópticos de apariencia normal en ambos ojos. Las relaciones entre la copa y el disco eran de 0,3 bilateralmente. Otros exámenes neurológicos no presentaron anormalidades. La resonancia magnética demostró dilatación de las venas oftálmicas superiores bilaterales (SOV) y congestión orbital y periorbital bilateral marcada. Sin embargo, no hubo compresión o estiramiento de los nervios ópticos bilaterales. Se reveló una restricción de la difusión en la difusión ponderada por la difusión, con la correspondiente reducción del coeficiente de difusión aparente, en todo el segmento orbital bilateral de los nervios ópticos, consistente con PION bilateral. La angiografía por resonancia magnética reveló arterialización de los senos cavernosos bilaterales y las SOV. La angiografía cerebral confirmó el diagnóstico de CCF bilaterales de drenaje anterior. El tratamiento con embolización de bobina transvenosa fue exitoso. Tres meses después de la embolización, el examen oftálmico demostró una mejora progresiva de los signos oftálmicos antes mencionados; sin embargo, sus agudezas visuales permanecieron como NLP en ambos ojos.\n",
+        "synthetic_summary": {
+            "B1": "Una mujer de 62 años tuvo pérdida de la vista en ambos ojos y dolor de cabeza por cinco días. Tenía la presión alta sin control. Los médicos vieron que sus ojos estaban inflamados y con mucha presión dentro. Un estudio mostró que las venas cerca de sus ojos estaban muy hinchadas. Le hicieron un tratamiento para cerrar unas venas que estaban mal y mejoraron los signos, pero no recuperó la vista.",
+            "B2": "Una mujer de 62 años con presión alta mal controlada perdió la visión en ambos ojos de forma súbita. También tuvo dolor de cabeza durante cinco días. Al examinarla, no podía ver nada y sus pupilas no respondían a la luz. Sus ojos estaban inflamados, con vasos sanguíneos anormales y presión ocular muy alta. La resonancia mostró venas dilatadas y congestión alrededor de los ojos, sin daño directo a los nervios ópticos. Sin embargo, había daño en los nervios que transmiten la visión (PION bilateral). Se confirmó que tenía fístulas carotídeo-cavernosas, conexiones anormales entre arterias y venas del cerebro. La trataron con embolización para cerrar estas conexiones. Tres meses después, mejoraron los signos en los ojos, pero la pérdida de visión siguió.",
+            "B3": "Una mujer de 62 años con hipertensión mal controlada presentó pérdida visual súbita en ambos ojos y cefalea durante cinco días, sin antecedentes de traumatismo. Al examen, no percibía luz y tenía pupilas fijas, con movilidad ocular limitada y dificultad para abrir los párpados. Se observaron signos inflamatorios en la superficie ocular, presión intraocular elevada y sangre en el canal de Schlemm. La resonancia magnética mostró venas oftálmicas superiores dilatadas y congestión orbital, sin daño directo a los nervios ópticos, aunque se detectó un tipo de lesión llamada neuropatía isquémica del nervio óptico posterior (PION) en ambos ojos. La angiografía cerebral confirmó fístulas carotídeo-cavernosas (CCF) bilaterales, que son conexiones anormales entre arterias y venas en la base del cráneo. Se realizó una embolización transvenosa para cerrar estas fístulas, logrando su oclusión completa. Tres meses después, los signos inflamatorios mejoraron, pero la pérdida visual persistió sin recuperación. Este caso resalta la importancia de un diagnóstico rápido y tratamiento adecuado para evitar daños irreversibles en la visión."
+        }
+    },
+    {
+        "article": "Un paciente de 15 años de edad (altura = 161 cm; peso = 66 kg; superficie corporal = 1,70; grupo sanguíneo = B positivo) con cardiomiopatía dilatada fue derivado a la Universidad de Ankara con pérdida de conciencia y shock cardiogénico en julio de 2016. El apoyo de oxigenación de membrana extracorpórea venosa arterial se realizó aproximadamente 1 semana después. Su fracción de eyección ventricular izquierda fue del 22%. Ocho días después, el paciente recibió un implante de corazón artificial total SynCardia (50 ml; SynCardia Systems, Inc., Tucson, AZ, EE. UU.). En el día 131 postoperatorio después de la cirugía TAH, el paciente se quejó de pérdida de audición bilateral y fue derivado al departamento de oído, nariz y garganta.\n\nLos antecedentes médicos previos no revelaron evidencia de pérdida auditiva, antecedentes familiares de sordera o cualquier anomalía adicional en su niñez. Sus registros médicos no revelaron evidencia de meningitis. Sin embargo, había recibido amikacina (15 mg/kg), un antibiótico ototóxico, contra patógenos gramnegativos importantes durante su estancia en la unidad de cuidados intensivos. El paciente fue incluido en la lista de espera de trasplantes de corazón de alta urgencia y era móvil en el Freedom Driver portátil (SynCardia).\n\nEl examen otoscópico del paciente fue normal. La audiometría de tonos puros y la respuesta auditiva del tronco encefálico revelaron una pérdida auditiva profunda bilateral. La timpanometría mostró timpanogramas normales de tipo A bilaterales. Tanto la tomografía computarizada como la resonancia magnética confirmaron la morfología normal del laberinto y nervios cocleares intactos.\n\nFue examinado por un equipo multidisciplinario (cirugía cardiovascular, cuidados intensivos pediátricos, cardiología pediátrica, psiquiatría de consulta y enlace, fisioterapia y rehabilitación, enfermedades infecciosas y microbiología clínica, anestesiología, audiología y otorrinolaringología) para realizar un implante coclear. Después de analizar las posibles opciones con el paciente y sus padres, se decidió que se beneficiaría de un implante coclear debido a la pérdida auditiva y la reducción de la función cognitiva y la adaptación necesaria para el trasplante de corazón. Después de analizar su caso con el equipo multidisciplinario, se decidió un implante coclear del lado derecho (Nucleus CI24RE con Contour Advance Electrode; Cochlear, Macquarie University, Australia).\n\nEl paciente tomaba warfarina (10 mg/día), que se interrumpió tres días antes de la cirugía, y se inició la heparinización (dosis de carga de 50 U/kg y dosis de mantenimiento de 20 U/kg/h) cuando el tiempo de protrombina (cociente internacional normalizado [INR]) era inferior a 1,5. Dos horas antes de la cirugía, se interrumpió la heparinización. En el quirófano, se disponía de un dispositivo de reserva para un posible fallo del dispositivo TAH. El equipo de anestesia y el perfusionista controlaron de cerca los resultados del flujo para el TAH. El flujo sanguíneo no pulsátil afecta de forma negativa al control de los signos vitales, y la presión arterial no invasiva no fue suficiente en nuestro paciente. Bajo anestesia local, se realizó un cateterismo radial arterial invasivo. Además, se dejó la vena yugular interna izquierda en su lugar, lo que permitió el control de la presión venosa central y su uso como reemplazo de fluidos de gran volumen cuando fue necesario. Después de iniciar el control, se administraron con precaución 2 mg/kg de propofol, 1 mg/kg de bromuro de rocuronio y 1 µg/kg de fentanilo, y se intubió al paciente por vía oral. Se utilizó sevoflurano con una concentración alveolar mínima de 1 a 1,5 en oxígeno al 40 % para el mantenimiento. El óxido nítrico inhalado también estaba listo para usarse en caso de una posible crisis hipertensiva pulmonar.\n\nEl día 250 después del implante TAH, se realizó la cirugía de implante coclear con abordaje de ventana redonda sin complicaciones perioperatorias; el paciente tuvo una pérdida de sangre mínima (solo 50 ml). La duración de la operación fue de 120 minutos. El paciente fue extubado en el quirófano sin problemas circulatorios y respiratorios. La heparinización se inició a la hora 6 posoperatoria. Comenzamos con la warfarina el día 1 posoperatorio, y la heparinización se detuvo después de alcanzar un INR de 2.0. No se observaron complicaciones (infecciones, hematoma) en el seguimiento posoperatorio.\n\nEl implante coclear se activó en la semana 4 después de la operación. El equipo de audiología lo revisó 4 y 8 semanas después; mostró una mejora continua en su audición, con impedancias normales. Sus resultados de percepción del habla mejoraron significativamente 3 meses después del implante coclear.\n\nMH - Adolescente\nMH - Niño\nMH - *Implantación coclear\nMH - *Insuficiencia cardiaca/diagnóstico/etiología/cirugía\nMH - *Efectos adversos del trasplante de corazón\nMH - *Corazón, Artificial\nMH - Humanos\nMH - Hombre\nMH - Resultado del tratamiento\n",
+        "gold_summary": "Describimos el caso de un niño de 15 años con pérdida auditiva total bilateral postlingual tras la administración de medicamentos ototóxicos durante su estancia en la unidad de cuidados intensivos pediátricos. El paciente recibió el implante de corazón artificial total SynCardia (50 ml; SynCardia Systems, Inc., Tucson, AZ, EE. UU.) para la insuficiencia cardiaca biventricular en fase terminal como puente para el trasplante cardiaco. Durante su estancia en la lista de espera de trasplantes cardiacos urgentes, se sometió a una implantación coclear satisfactoria tras optimizar el estado de coagulación y hemostasis y una preparación anestésica adecuada.\n",
+        "synthetic_summary": {
+            "B1": "Un niño de 15 años tuvo problemas graves en su corazón y usó un corazón artificial. Durante su tratamiento, perdió la audición en los dos oídos por un medicamento. Los doctores le pusieron un implante coclear, que es un aparato para ayudar a oír. La operación fue segura y después el niño pudo escuchar mejor poco a poco.",
+            "B2": "Un adolescente de 15 años con insuficiencia cardiaca grave recibió un corazón artificial total. Este dispositivo ayuda a mantener su vida mientras espera un trasplante de corazón. Durante su tratamiento, tomó un antibiótico llamado amikacina, que puede dañar el oído y causó pérdida auditiva profunda en ambos oídos. Se confirmó que sus oídos y nervios auditivos estaban normales antes de decidir implantarle un implante coclear, un dispositivo que mejora la audición. La cirugía se realizó con cuidado, controlando su coagulación y estado general, y no tuvo complicaciones. Después de activar el implante, el paciente mejoró mucho en la audición y en la comprensión del habla. Esto mejora su calidad de vida mientras espera el trasplante.",
+            "B3": "Un adolescente de 15 años con cardiomiopatía dilatada avanzada recibió un corazón artificial total SynCardia como puente para un trasplante cardíaco. Durante su estancia en la unidad de cuidados intensivos, se le administró amikacina, un antibiótico aminoglucósido conocido por su ototoxicidad, lo que provocó una pérdida auditiva profunda bilateral. Los estudios audiológicos confirmaron que las estructuras cocleares permanecían intactas, descartando otras etiologías para la hipoacusia. Debido a esta pérdida auditiva y a la necesidad de preservar su función cognitiva para el trasplante, se optó por la colocación de un implante coclear. La cirugía se realizó sin complicaciones, tras una cuidadosa gestión del tratamiento anticoagulante y monitorización hemodinámica, considerando el soporte del corazón artificial. En los meses posteriores, el implante coclear mejoró significativamente la audición y la percepción del habla del paciente. Este caso evidencia la relevancia de un abordaje multidisciplinario en pacientes con dispositivos cardíacos complejos y complicaciones secundarias, facilitando una mejor calidad de vida mientras esperan el trasplante."
+        }
+    },
+    {
+        "article": "Se encontró a un hombre de 25 años de edad recostado por familiares después de una noche de fiesta, con vómitos, agresión y dolor localizado en la región glútea e inferior derecha. La evaluación inicial en el departamento de urgencias no reveló lesiones traumáticas; sin embargo, el empeoramiento de los síntomas llevó a una nueva evaluación al día siguiente. Los resultados de laboratorio revelaron un recuento sanguíneo completo sin alteraciones, niveles elevados de CPK sérica (42 527 IU/l), creatinina sérica (735 µmol/l), urea (44,3 mmol/l) y potasio (5,7 mmol/l). El análisis de orina reveló orina de color rojo-marrón sin glóbulos rojos, proteinuria (+1), glucosuria (+1) y WBC (9-10/hpf). Estos resultados confirmaron la RM y la IRA. La toxicología estableció la administración de 1796 µg/l de heroína (> 5 veces el nivel basal) sin detección de ninguna otra sustancia. Aunque inicialmente negó haber tomado medicamentos, después del análisis toxicológico, el paciente admitió que había administrado heroína una vez por vía intramuscular en la región glútea derecha la noche del incidente.\n\nUna tomografía computarizada demostró edema muscular glúteo y miositis localizada en la región glútea derecha. Al comenzar el tratamiento convencional con resucitación de fluidos intravenosos (IV), el tratamiento de la IRA fracasó, lo que hizo necesario el TRR con hemodiálisis debido a la progresión de la azotemia con un aumento de la creatinina sérica a 1052 µmol/l. La función renal mejoró tras el cese del TRR con una duración total de la estancia (LOS) de 9 días. El seguimiento posterior del paciente fue incompleto debido a la falta de asistencia.\n",
+        "gold_summary": "Este informe de caso describe a un hombre de 25 años que desarrolló una RM grave y lesión renal aguda (LRA) después de la administración intramuscular (IM) de heroína como usuario por primera vez. El uso de la heroína IM puede inducir niveles más altos de CPK debido a la toxicidad directa de los miocitos y el trauma mecánico. Los músculos glúteos altamente vascularizados con fibras tipo 1 en el sitio de la inyección probablemente exacerbaron la gravedad. Los factores adicionales incluyeron una menor densidad mitocondrial en los hombres y la exposición al alcohol. A pesar de la reanimación agresiva con líquidos, se requirió la terapia de reemplazo renal (RRT) y el paciente respondió bien a la hemodiálisis.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre de 25 años se sintió mal después de usar heroína en el glúteo una vez. Tuvo dolor, vómitos y problemas en los músculos y los riñones. Los médicos le dieron líquidos y tratamiento para ayudar a sus riñones, pero necesitó una máquina para limpiar su sangre. Después de varios días, mejoró y salió del hospital. Es importante cuidar el cuerpo y no usar drogas peligrosas.",
+            "B2": "Un hombre de 25 años llegó con vómitos, agresividad y dolor en el glúteo derecho. Los análisis mostraron daño muscular grave, con niveles altos de CPK, una enzima que indica lesión en músculos. También tenía problemas en los riñones, confirmando una lesión renal aguda. Encontraron heroína en su sangre, aunque al principio negó usarla. Luego admitió haberse inyectado la droga en el glúteo derecho. La tomografía mostró inflamación en el músculo de esa zona. Recibió líquidos por vía intravenosa, pero su función renal empeoró y necesitó diálisis para limpiar su sangre. Después del tratamiento, mejoró y estuvo nueve días en el hospital. Este caso muestra que inyectar heroína puede causar daño muscular y renal grave, por eso requiere seguimiento médico.",
+            "B3": "Un hombre de 25 años fue encontrado tras una noche de fiesta con vómitos, agresividad y dolor en la región glútea derecha. Inicialmente no se detectaron lesiones traumáticas, pero al empeorar sus síntomas se realizaron análisis que mostraron elevación marcada de la creatina fosfoquinasa (CPK), creatinina y potasio, indicando daño muscular severo y lesión renal aguda. El paciente admitió después haber usado heroína por vía intramuscular en el glúteo derecho, lo que explicó la toxicidad muscular observada. La tomografía evidenció inflamación y daño local en el músculo glúteo. A pesar del tratamiento con líquidos intravenosos, la función renal empeoró, requiriendo hemodiálisis para reemplazo renal. Tras nueve días de hospitalización, la función renal mejoró y se suspendió la diálisis; sin embargo, el seguimiento fue limitado por la falta de asistencia del paciente. Este caso resalta que la inyección intramuscular de heroína puede causar daño muscular grave y complicaciones renales, lo que requiere atención médica inmediata y tratamiento intensivo."
+        }
+    },
+    {
+        "article": "Una mujer de 63 años con antecedentes de obesidad e hipertensión arterial acudió a la sala de urgencias de un hospital de nivel secundario con un historial de siete días de fiebre, tos seca, hiposmia y mialgia. Al momento del ingreso, se encontraba alerta, con una frecuencia respiratoria de 22 ciclos por minuto, pulso de 90 latidos por minuto y saturación de oxígeno de 90 %. Los análisis de laboratorio revelaron linfopenia (1,55 x 109) y niveles elevados de proteína C reactiva (10,62 mg/dL). Se realizó una prueba de reacción en cadena de la polimerasa para COVID-19 a partir de un hisopado nasofaríngeo y de la garganta, que resultó positivo para el coronavirus del síndrome respiratorio agudo severo 2 (SARS-CoV-2).\n\nLa situación evolucionó rápidamente con fiebre, postración y empeoramiento de la disnea. La gasometría arterial reveló una insuficiencia respiratoria grave, mientras que la radiografía de tórax evidenció infiltrados pulmonares bilaterales. La paciente fue intubada y sometida a ventilación mecánica, pero su condición respiratoria continuó deteriorándose, a pesar de los mejores cuidados críticos, incluyendo ventilación en posición prona y bloqueo neuromuscular. Su examen de tomografía computarizada del tórax, tras la intubación, reveló extensas opacificaciones multifocales bilaterales en vidrio molido, sin signos de embolia pulmonar. Los ajustes iniciales del ventilador fueron: ventilación controlada por volumen con volumen corriente de 360 ml (6 ml/kg de peso corporal ideal), frecuencia respiratoria de 14 respiraciones por minuto, presión espiratoria positiva final (PEEP) de 14 cmH2O y complacencia estática de 44 cmH2O.\n\nEn el segundo día de internación, la gasometría arterial mostró pH de 7,34, presión parcial de dióxido de carbono (PaCO2) de 53 mmHg, presión parcial de oxígeno (PaO2) de 102 mmHg y bicarbonato (HCO3) de 29,7 mmol/L, con una proporción presión parcial de oxígeno/fracción inspirada de oxígeno (PaO2/FiO2) de 98. Ella cumplía los criterios para indicación de VV-ECMO y fue transferida a la unidad de terapia intensiva (UTI), que disponía de un programa establecido para VV-ECMO. El procedimiento fue realizado con seguridad, no habiendo ocurrido complicaciones. El análisis de la gasometría arterial 3 horas después del inicio de la VV-ECMO mostró pH de 7,386, PaCO2 de 43 mmHg, PaO2 de 94,3 mmHg y HCO3 de 25,4 mmol/L, sin cualquier variación abruta de la PaCO2. Tuvieron inicio la nutrición y la rehabilitación precoces tras la introducción de la VV-ECMO. En el 14º día de internación, la paciente desarrolló neumonía asociada al ventilador causada por Pseudomonas aeruginosa, siendo sometida a 7 días de antibioticoterapia con ceftazidima y vancomicina, con respuesta favorable. En el 20º día de internación, su radiografía del tórax y la complacencia mejoraron, y la paciente fue retirada de la VV-ECMO con éxito tras 455 horas de soporte, siendo traqueostomizada 7 días después. La paciente mantuvo buena función renal durante toda la internación.\n\nEn el día 34 de internación, luego de 7 días de destete de la sedación, con evolución positiva de su cuadro neurológico, ocurrió una crisis epiléptica generalizada limitada, que llevó a la investigación diagnóstica.\n\nInvestigación\nLos análisis de sangre de laboratorio revelaron una disminución de los niveles de proteína C reactiva (6,11 mg/dL), procalcitonina (0,07 ng/mL), fibrinógeno (307 ng/mL) y ferritina (2802 ng/mL), pero un aumento en los niveles de dímero D (18021 ng/mL) e interleucina 6 (10,4 pg/mL) en el día anterior al inicio de los síntomas. No se asoció ninguno de los fármacos administrados a la paciente con el SEPR, es decir, fármacos inmunosupresores, inmunomoduladores y quimioterápicos.\n\nSe realizó una resonancia magnética (RM) del cerebro y las imágenes de recuperación de inversión atenuada por fluidos (FLAIR) demostraron una hiperintensidad simétrica y confluente que afectaba a la sustancia blanca justa y subcortical, principalmente en las regiones occipital y parietal, pero también en la región frontal, temporal y cerebelosa izquierda. Los núcleos grises profundos se conservaron y no había presencia de ninguna área con restricción del contraste. Las imágenes ponderadas por susceptibilidad mostraron múltiples microhemorragias puntiformes que afectaban a la sustancia blanca superficial y profunda, pero que no afectaban al área con hiperintensidad en FLAIR. Las microhemorragias puntiformes involucraban predominantemente a la sustancia blanca justacortical y al cuerpo calloso (especialmente el codo y el esplenio). Además, había tres hemorragias subagudas de menos de 1 cm en las cápsulas externas, con hiperintensidad en T1.\n\nLa muestra de líquido cefalorraquídeo dio negativo para SARS-CoV-2 y los niveles de proteínas (31 mg/dL), glucosa (74 mg/dL) y lactato (1,89 mmol/L) se encontraban dentro de los parámetros normales.\n\nDesvelado\nLa paciente logró una recuperación casi total de los déficits neurológicos, a pesar de la miopatía de la enfermedad crítica, y fue dada de alta después de 44 días en el hospital. Se la derivó a un hospital secundario para su rehabilitación y prácticamente recuperó su estado mental previo.\n",
+        "gold_summary": "Una mujer de 63 años de edad acudió a la sala de urgencias con un historial de fiebre aguda, postración y disnea. Se le diagnosticó un caso grave de COVID-19 y síndrome de dificultad respiratoria aguda. A pesar de recibir atención médica intensiva, cumplía con los requisitos para someterse a una oxigenación por membrana extracorpórea. El día 34, luego de siete días de haber suspendido la sedación y de que su cuadro neurológico hubiera evolucionado de manera positiva, presentó una crisis tónico-clónica generalizada limitada, que no guardaba relación con un desequilibrio hidroelectrolítico o metabólico, lo que hizo necesario realizar una investigación diagnóstica. Los estudios de imágenes cerebrales revelaron un síndrome de encefalopatía posterior reversible.\n",
+        "synthetic_summary": {
+            "B1": "Una mujer de 63 años llegó al hospital con fiebre y tos. Tenía COVID-19 grave y necesitó una máquina para respirar. Luego mejoró, pero tuvo convulsiones. Los médicos encontraron un problema en su cerebro que se puede curar. Al final, la mujer se recuperó casi por completo y volvió a casa.",
+            "B2": "Una mujer de 63 años con obesidad e hipertensión llegó al hospital con fiebre y tos seca. Tenía dificultad para respirar y fue diagnosticada con COVID-19 grave y daño pulmonar severo. Necesitó ventilación mecánica y un tratamiento especial llamado oxigenación por membrana extracorpórea. Después de mejorar, al día 34 tuvo una crisis epiléptica, sin problemas metabólicos. Las imágenes del cerebro mostraron un síndrome reversible que afecta la parte posterior del cerebro. Este síndrome puede mejorar con tratamiento adecuado. La paciente recibió atención y casi recuperó su estado mental antes de ir a rehabilitación.",
+            "B3": "Una mujer de 63 años con antecedentes de obesidad e hipertensión ingresó con fiebre, tos seca y dificultad respiratoria, diagnosticándose COVID-19 grave con síndrome de dificultad respiratoria aguda. A pesar de la ventilación mecánica avanzada, su función respiratoria empeoró, por lo que se indicó oxigenación por membrana extracorpórea venovenosa (VV-ECMO), procedimiento que se realizó sin complicaciones. Durante la hospitalización, desarrolló neumonía asociada al ventilador, la cual fue tratada con antibióticos, y mostró mejoría progresiva que permitió retirar la VV-ECMO. Sin embargo, al día 34, tras suspender la sedación y con evolución neurológica favorable, presentó una crisis epiléptica generalizada. La resonancia magnética cerebral reveló alteraciones compatibles con síndrome de encefalopatía posterior reversible, caracterizado por lesiones en sustancia blanca y microhemorragias. El análisis del líquido cefalorraquídeo no evidenció infección viral ni alteraciones significativas. Finalmente, la paciente recuperó casi por completo sus funciones neurológicas y fue dada de alta para continuar rehabilitación, demostrando una evolución positiva tras un cuadro crítico complejo. Este caso subraya la importancia de vigilar complicaciones neurológicas tardías en pacientes con COVID-19 grave."
+        }
+    },
+    {
+        "article": "Mujer de 65 años, originaria y residente de la Ciudad de México, con antecedente de infección por VIH de 20 años de diagnóstico con carga viral indetectable desde 2020 y con cuenta de CD4 de 1220 células por mililitro en febrero de 2022, hipotiroidismo de 29 años, cardiopatía isquémica de 9 años de diagnóstico, osteoporosis y dislipidemia, en tratamiento y bajo control médico.\n\nSu dermatosis problema se inició 10 años atrás, después de un cuadro de herpes zóster localizado en la extremidad inferior derecha y se complicó con una infección de tejidos blandos, referida como celulitis. Como secuela de este evento la paciente desarrolló úlcera, la cual ameritó corrección del defecto con 4 injertos cutáneos en diferentes tiempos quirúrgicos por cirugía plástica, con acompañamiento por parte de la clínica de heridas. Durante el seguimiento y a pesar de las medidas tomadas, no logró resolución completa y persistió con una úlcera asociada a dolor local, motivo de su envío a nuestro servicio.\n\nA la exploración física presentaba una dermatosis localizada en la extremidad inferior derecha, en la cara lateral del muslo, caracterizada por una neoformación aplanada sobre la que se asentaba una úlcera de 1.5 cm de diámetro, con fondo limpio, con costra sero-amarillenta, bordes sobreelevados, piel perilesional hiperpigmentada y queratósica, una cicatriz atrófica e hiperpigmentada. Se inició abordaje de la dermatosis mediante biopsia de piel, con reporte histopatológico de carcinoma verrugoso, por lo que se concluyó como úlcera de Marjolin asociada a carcinoma verrugoso en paciente portadora de VIH. Se canalizó al hospital de oncología para manejo con radioterapia.",
+        "gold_summary": "mujer de 65 años con el antecedente de ser portadora de infección por virus de inmunodeficiencia humana (VIH), que presentó un carcinoma verrugoso asociado a una úlcera de Marjolin secundaria a herpes zóster e infección de tejidos blandos en pierna derecha, con un periodo de latencia de 10 años desde el proceso infeccioso inicial hasta la confirmación histopatológica.",
+        "synthetic_summary": {
+            "B1": "Una mujer de 65 años tuvo una infección en la pierna derecha hace 10 años. Esa infección dejó una herida que no sanó bien y se convirtió en una úlcera. Los médicos hicieron una prueba y encontraron un tipo de cáncer llamado carcinoma verrugoso. Ella tiene VIH, pero está controlado. Ahora recibe tratamiento con radioterapia para mejorar su salud.",
+            "B2": "Una mujer de 65 años con VIH controlado tenía una úlcera en la pierna derecha desde hace 10 años. La úlcera comenzó después de un herpes zóster, una infección viral, que se complicó con una infección bacteriana. A pesar de varios injertos de piel y tratamientos, la herida no sanó y causaba dolor. Al examinarla, se vio una lesión con bordes elevados y piel oscura alrededor. La biopsia mostró que era una úlcera de Marjolin, una herida crónica que puede volverse cancerosa. Además, estaba asociada a un carcinoma verrugoso, un tipo de cáncer de piel. Por eso, la paciente fue enviada a un hospital para radioterapia y tratar el cáncer. Este caso destaca la importancia de cuidar heridas que no sanan bien.",
+            "B3": "Una mujer de 65 años con infección por VIH controlada desde hace varios años presentó una úlcera crónica en la pierna derecha, que se originó tras un herpes zóster complicado con infección de tejidos blandos hace una década. A pesar de múltiples injertos cutáneos y seguimiento médico, la lesión no sanó completamente y persistió con dolor local. La exploración mostró una úlcera con bordes elevados y piel circundante alterada, lo que llevó a realizar una biopsia. El estudio histopatológico confirmó la presencia de un carcinoma verrugoso, un tipo de cáncer de piel, asociado a una úlcera de Marjolin, que es una lesión maligna que puede desarrollarse en heridas crónicas o cicatrices. Esta complicación en una paciente con VIH resalta la importancia de un seguimiento cuidadoso de lesiones cutáneas crónicas. En consecuencia, la paciente fue referida a oncología para recibir tratamiento con radioterapia, buscando controlar la enfermedad y mejorar su calidad de vida. Este caso muestra cómo infecciones previas y heridas persistentes pueden evolucionar a procesos malignos, especialmente en personas con condiciones inmunológicas especiales."
+        }
+    },
+    {
+        "article": "Una mujer de 90 años con hepatitis C y un historial de tabaquismo de 60 años proveniente de una zona rural presentó una hinchazón en la cara posteromedial del muslo izquierdo justo por encima de la rodilla. La hinchazón se notó por primera vez hace 3 años y aumentó gradualmente de tamaño durante este período. Ella sintió un leve malestar, pero niega cualquier síntoma asociado de dolor, picazón, secreción, fiebre o inmovilidad articular. Como provenía de una zona rural, también tenía un historial de exposición a animales.\nEn el examen físico, la hinchazón tenía una forma esférica de 14 × 10, era firme, fija y no sensible, con márgenes bien definidos en el aspecto posteromedial del muslo izquierdo, justo por encima de la rodilla. La piel que la recubría era pellizcable y mostraba venas prominentes, y la temperatura era comparable a la de la piel circundante.\nLa ecografía reveló una lesión quística grande con varios quistes pequeños en su interior, que medían 13,2 × 11 × 13,6 cm y un volumen de 1046 ml. Se originaba en la articulación de la rodilla izquierda y se extendía hasta la mitad del muslo. La ecografía Doppler en color no mostró vascularización en su interior. Se realizó una resonancia magnética que mostró una lesión quística grande (21 × 9,9 × 8,1 cm) con múltiples lesiones pequeñas dispersas, con extensión intramuscular e intermuscular que afectaban al aductor largo y al gracilis de manera medial y al bíceps femoral de manera posterior. Todas estas características eran indicativas de un quiste hidatídico. El diagnóstico se confirmó mediante una prueba de hemaglutinación para Echinococcus. La radiografía de tórax y la ecografía abdominal fueron normales.\nSe planificó la escisión quirúrgica de la tumefacción quística y se realizó una incisión en forma de S en la piel, seguida de una disección cuidadosa a través del tejido subcutáneo para acceder al quiste. La lesión estaba bien definida dentro de los planos intermuscular e intramuscular. Se realizó una disección meticulosa para aislar y extraer el quiste intacto, asegurando que no se derramara su contenido. Para minimizar el riesgo de contaminación, se irrigó a fondo el sitio quirúrgico con solución salina normal después de la escisión.\nLos hallazgos intraoperatorios revelaron una gran hinchazón quística intermuscular de 22 × 14 cm, que involucraba los compartimentos posterior y medial del muslo izquierdo. El quiste demostró extensión intramuscular hacia el aductor largo y el gracilis medialmente y hacia el bíceps femoral posteriormente, extendiéndose hasta la fosa poplítea. Cabe destacar que no había comunicación entre el quiste y la articulación de la rodilla. Una biopsia enviada al laboratorio confirmó aún más el diagnóstico. El examen histopatológico de la muestra extirpada reveló una pared quística fibrocondrogénica revestida por epitelio atenuado con infiltración inflamatoria. La presencia de material queratinoso focal caracterizó aún más la lesión. Estos hallazgos, junto con las características macroscópicas, favorecieron el diagnóstico de un quiste hidatídico. El curso postoperatorio fue sin complicaciones y el paciente fue dado de alta con una terapia antihelmíntica durante seis semanas. Se programaron visitas de seguimiento a la semana, tres semanas, seis semanas, nueve semanas y doce semanas. Durante estas visitas, el paciente no mostró signos de recurrencia o complicaciones.\n",
+        "gold_summary": "Una mujer de 90 años de edad, proveniente de una zona rural, presentó una hinchazón de crecimiento lento en el muslo posteromedial durante tres años. No tenía antecedentes de traumatismos ni síntomas sistémicos. El examen clínico reveló una masa firme y no dolorosa. Las imágenes sugieren una lesión quística, y la serología confirmó la infección por Echinococcus. Se realizó la extirpación quirúrgica, y la histopatología confirmó un quiste hidatídico. La paciente recibió un tratamiento posoperatorio de albendazol durante seis semanas. Su recuperación fue sin incidentes, sin recurrencia en el seguimiento.\n",
+        "synthetic_summary": {
+            "B1": "Una mujer de 90 años tenía una hinchazón en el muslo que creció poco a poco durante tres años. La hinchazón no dolía ni causaba otros problemas. Los médicos hicieron estudios y encontraron un quiste causado por un parásito llamado Echinococcus. Le quitaron el quiste con una operación y luego tomó medicinas para curarse. La mujer mejoró bien y no tuvo problemas después.",
+            "B2": "Una mujer de 90 años de una zona rural tenía una hinchazón en el muslo izquierdo. La hinchazón creció lentamente durante tres años y no le causaba dolor. Al examinarla, se encontró una masa firme que no dolía al tocarla. Las imágenes por ecografía y resonancia mostraron un quiste con varias partes pequeñas dentro. La prueba de sangre confirmó que era un quiste hidatídico, una infección causada por un parásito llamado Echinococcus. La mujer fue operada para quitar el quiste sin romperlo y evitar infecciones. Después, recibió medicamentos para eliminar el parásito. La recuperación fue buena y no hubo problemas ni regreso del quiste en las revisiones.",
+            "B3": "Una mujer de 90 años, con antecedentes de hepatitis C y exposición a animales en zona rural, presentó una hinchazón creciente durante tres años en la parte posterior interna del muslo izquierdo, sin dolor ni otros síntomas asociados. La exploración física mostró una masa firme, fija y sin sensibilidad, mientras que la ecografía y resonancia magnética revelaron una lesión quística grande con múltiples quistes pequeños, compatible con un quiste hidatídico, confirmado por pruebas serológicas. La cirugía consistió en la extirpación cuidadosa del quiste sin romperlo, evitando la contaminación, y el análisis histopatológico confirmó el diagnóstico. No se encontró comunicación con la articulación de la rodilla ni afectación de órganos torácicos o abdominales. El postoperatorio transcurrió sin complicaciones, y la paciente recibió tratamiento antihelmíntico durante seis semanas. En el seguimiento, no se observaron signos de recurrencia ni complicaciones, lo que indica un buen pronóstico tras la intervención. Este caso resalta la importancia de considerar infecciones parasitarias en masas quísticas en pacientes con exposición rural, y la necesidad de un manejo quirúrgico cuidadoso para evitar complicaciones."
+        }
+    },
+    {
+        "article": "Una paciente de 21 años de edad, soltera, con antecedentes de hipertensión y feocromocitoma metastásico, se presentó en nuestro hospital. Su cáncer se ha metastatizado en la vejiga, los huesos y los pulmones. También tiene un fuerte historial familiar de neoplasias, en particular de feocromocitoma. La paciente fue admitida debido a la hipertensión no controlada y los síntomas crónicos relacionados con su enfermedad.\n\nEn el ingreso (09/06/2024), la paciente era normotensa (PA: 104/66 mmHg), su frecuencia cardiaca era de aproximadamente 90 latidos por minuto, afebril a 36.9°C, y tenía una saturación de oxígeno de 99% en aire ambiente. El examen físico indicó un estado de desempeño del Grupo Cooperativo de Oncología del Este (ECOG) de 2, palidez consistente con anemia crónica, latido cardiaco regular sin murmullos o sonidos adicionales. El examen abdominal no fue notable, y no se observó edema o equimosis en las extremidades inferiores.\n\nLa paciente tiene antecedentes de hipertensión y paraganglioma, su medicación incluye (Doxazosin 2 mg, Labetalol 100 mg, Oxibutinina 5 mg, Aceite de parafina, Nifedipina 30 mg). Su historial quirúrgico incluye una adrenalectomía derecha a los diez años, y ha recibido varios tratamientos, incluidos análogos de somatostatina y radioterapia paliativa. El historial familiar revela una mutación familiar de la subunidad B de la deshidrogenasa del succinato (mutación SDBH) con un importante historial de tumores malignos endocrinos, incluidos feocromocitomas en su padre y hermana y cáncer de páncreas en su abuela.\n\nLas investigaciones de laboratorio, incluido el recuento sanguíneo completo, revelaron anemia significativa, con un nivel de hemoglobina de 7.5 g/dl. Había evidencia de hemólisis, como lo indican el alto recuento de reticulocitos, la bilirrubina indirecta y la lactato deshidrogenasa. La haptoglobina era baja. Los resultados de laboratorio se muestran en. El perfil de coagulación excluyó la coagulación intravascular diseminada (DIC), que muestra (PT: 15.6, PTT: 23.3, fibrinógeno: 489, dímero D: 0.63). La prueba de Coombs directa para excluir la anemia hemolítica autoinmune fue negativa. Los frotis de sangre periférica mostraron la presencia de esquistocitos, equinocitos y algunas células en forma de lágrima, además de trombocitopenia, todo lo cual apuntaba a la anemia hemolítica microangiopática (MAHA). Dado el contexto del cáncer metastásico, el paciente fue diagnosticado con anemia hemolítica microangiopática paraneoplásica en marzo/2024.\n\nEl paciente fue programado para el protocolo CVD (ciclofosfamida, vincristina y doxorrubicina), pero sin ciclofosfamida debido al efecto inductor de anemia de los agentes alquilantes. El paciente recibió un total de 5 ciclos. Como indicador de respuesta clínica, el paciente ya no experimentó anemia o trombocitopenia. Un nuevo frotis de sangre periférica reveló células normales, lo que sugiere una respuesta clínica al MAHA que coincide con la mejora de la neoplasia subyacente. Esto se alinea con la definición de MAHA como un síndrome paraneoplásico.\n\nLos medicamentos que se le suministran al paciente al momento del alta son: comprimidos de dexametasona de 2 mg, 4 mg por vía oral (PO) una vez al día (OD) durante 3 días, comprimidos de ondansetrón de 8 mg por vía oral (PO) una vez al día (OD) durante 3 días, comprimidos de metoclopramida de 10 mg por vía oral (PO) tres veces al día durante 3 días, calcio de 600 mg con vitamina D por vía oral (PO) una vez al día (OD) durante 1 día, comprimidos de labetalol de 100 mg por vía oral (PO) dos veces al día durante 1 día, comprimidos de doxazocina de 2 mg por vía oral (PO) dos veces al día durante 1 día, comprimidos de citalopram de 20 mg por vía oral (PO) durante 1 día, comprimidos de omeprazol de 20 mg, 40 mg por vía oral (PO) durante 1 día, comprimidos de paracetamol de 500 mg, 1000 mg por vía oral (PO) dos veces al día durante 1 día, cápsulas de aprepitant de 125 mg/80 mg, 1 cápsula por vía oral (PO) dos veces al día durante 3 días (con prescripción médica).\n\nEl paciente fue objeto de seguimiento el 01/07/2024, y su aspecto clínico era bueno y activo. El paciente se sometió a exámenes de laboratorio que incluían un recuento sanguíneo completo (WBC 6.59 10e3/ul, RBC 4.47 × 10^6/ul, HGB 13.2 g/dl, 40.0%, MCV 89.4 fL, PLT 41.5 10e3/ul), nitrógeno ureico en sangre 33.8 mg/dl, creatina cinasa-MB 36.1 u/l, creatinina sérica 0.97 mg/dl, cloruro 101.5 mmol/l, potasio 4.52 mmol/l, sodio 135 mmol/l.\n",
+        "gold_summary": "En este informe de caso, presentamos a una mujer soltera de 21 años con un fuerte historial familiar de neoplasia endocrina. Fue derivada a nuestro hospital para quimioterapia debido a un diagnóstico de feocromocitoma maligno, que había hecho metástasis en la vejiga urinaria, los huesos y los pulmones. Además, desarrolló anemia hemolítica microangiopática como un síndrome paraneoplásico.\n",
+        "synthetic_summary": {
+            "B1": "Una joven de 21 años tiene un tipo de cáncer llamado feocromocitoma que se ha extendido a varios órganos. También tiene anemia, que es cuando hay pocas células rojas en la sangre. Su anemia fue causada por su cáncer y mejoró con el tratamiento. Ahora está mejor y sus exámenes de sangre están normales.",
+            "B2": "Una mujer de 21 años con antecedentes familiares de tumores endocrinos llegó al hospital por un cáncer llamado feocromocitoma, que se había extendido a su vejiga, huesos y pulmones. Tenía anemia grave causada por la destrucción de sus glóbulos rojos, llamada anemia hemolítica microangiopática, que está relacionada con su cáncer. Recibió un tratamiento de quimioterapia que mejoró su anemia y la cantidad de plaquetas en su sangre. Al alta, estaba estable y activa, con análisis de sangre normales. Este caso muestra cómo un cáncer puede causar problemas en la sangre y cómo el tratamiento adecuado puede ayudar a mejorar la salud del paciente. Es importante seguir controlando su estado para evitar complicaciones.",
+            "B3": "Una mujer de 21 años con antecedentes familiares de tumores endocrinos y feocromocitoma metastásico en vejiga, huesos y pulmones, ingresó por hipertensión no controlada y síntomas crónicos. Presentaba anemia grave con signos de destrucción de glóbulos rojos, confirmando anemia hemolítica microangiopática (MAHA) como síndrome paraneoplásico asociado a su cáncer. Se le administró un tratamiento quimioterapéutico adaptado, excluyendo agentes que pudieran empeorar la anemia, con buena respuesta clínica evidenciada por la normalización de su sangre y mejoría del estado general. Durante el seguimiento, mostró estabilidad clínica y parámetros sanguíneos mejorados, lo que indica control tanto de la neoplasia como de la anemia. Este caso resalta la importancia de reconocer la MAHA en pacientes con cáncer avanzado para ajustar el tratamiento y mejorar el pronóstico. Por lo tanto, el manejo integrado de la enfermedad tumoral y sus complicaciones hematológicas es fundamental para optimizar la calidad de vida y la evolución del paciente."
+        }
+    }
+]
\ No newline at end of file
diff --git a/generating_data/raw_file/es_synthetic_error.json b/generating_data/raw_file/es_synthetic_error.json
new file mode 100644
index 0000000000000000000000000000000000000000..47d73d9bd43eaea25866ba7688a7b0142e5debe6
--- /dev/null
+++ b/generating_data/raw_file/es_synthetic_error.json
@@ -0,0 +1,902 @@
+[
+    {
+        "article": "Información para el paciente\nUn hombre de 27 años y fumador estuvo involucrado en un accidente de tráfico; se cayó de su motocicleta sin casco. El hombre llevó la motocicleta al hospital e informó de un dolor de cabeza y heridas hemorrágicas en la frente.\n\nEl paciente no tiene antecedentes patológicos y trabaja en una zona rural.\n\nHallazgos clínicos\nTras su ingreso en urgencias, perdió el conocimiento y sufrió dos convulsiones. En la exploración física, la escala de coma de Glasgow fue de 6/15 (no abrió los ojos, se retiró al sentir dolor, no respondió verbalmente) con midriasis bilateral, dificultad hemodinámica y buena saturación. Se identificó una lesión craneal penetrante con una profusa hemorragia intracraneal.\n\nLínea de tiempo\nTras caerse de la motocicleta, el paciente volvió a montarse en ella e inmediatamente fue al hospital, quejándose de dolores de cabeza y de una herida en la frente por la que sangraba. Recibió tratamiento de urgencia para estabilizar sus funciones respiratorias y hemodinámicas. Ese mismo día, fue trasladado inconsciente a un centro mejor equipado, donde se le realizó un TAC y se sometió a una operación quirúrgica con éxito.\n\nEvaluación diagnóstica\nSu nivel de hemoglobina era de 6 g/dL y su grupo sanguíneo era O positivo. El hospital no tenía ni una unidad de cuidados intensivos ni un escáner. El único diagnóstico sugerido fue el de traumatismo agudo en la cabeza, complicado por hemorragia intracraneal que provocó shock y convulsiones. El pronóstico vital, basado en la presentación clínica, era malo.\n\nIntervención terapéutica\nUna intervención inicial consiste en un relleno intracraneal a través de la fractura craneal, seguido de un vendaje cefálico que ayuda a detener el sangrado. El tratamiento involucró la estabilización de la columna cervical, intubación orotraqueal con oxígeno a 6 L por minuto y la inserción de un catéter Foley. Se usaron dos puertos venosos periféricos para administrar NaCl 0.9 % 1000 CC, Geloplasma* 500 CC, Manitol 20 % 250 CC; Phenobarbital inj 40 mg/2 ml: 100 mg, luego Thiopental 250 mg: bolo de 100 mg × 2 debido a otras convulsiones; Amoxicillin + Clavulanic Acid injection 2 g; Gentamycin 160 mg intramuscularmente. Se realizó un suero antitetánico de 1500 IU y una transfusión de 450 CC de sangre.\n\nEl paciente fue trasladado inconsciente a un equipo en un hospital de primera categoría, sin intubación y en un estado hemodinámico estable.\n\nEl primer día después de la transferencia, el paciente evolucionó bien; estaba consciente y podía caminar, sin problemas neurológicos, hemodinámicos o respiratorios. La tomografía computarizada reveló un edema bifrontal agudo, una contusión hemorrágica del parénquima predominantemente en el lado derecho, una capa de hematoma subdural agudo (3 mm) en la región fronto-parieto-temporo-occipital izquierda, una hernia subfalcular izquierda de 5 mm, una compresión discreta del ventrículo lateral derecho, una hemorragia subaracnoidea superior bifrontal aguda, una fractura frontal deprimida con rotura osteomeníngea y una fractura de la tercera vértebra cervical con compresión de la médula espinal. El paciente se sometió a una operación exitosa en el hospital de primera categoría.\n\nSeguimiento y resultados\nEl período postoperatorio estuvo marcado por convulsiones, para las cuales se le administró anticonvulsivos al paciente, con un buen resultado.\n",
+        "gold_summary": "Un hombre de 27 años, fumador sin antecedentes patológicos, estuvo involucrado en un accidente de tráfico, al caerse de una motocicleta sin casco. En el ingreso al hospital de nuestro distrito rural, la escala de coma de Glasgow durante el examen físico fue de 6/15 con midriasis bilateral, distrés hemodinámico y buena saturación. Se identificó una lesión penetrante en la cabeza con profusa hemorragia intracraneal. Se usó el relleno intracraneal conocido en la neurocirugía de control de daños para taponar la hemorragia intracraneal grave y que es una maniobra neuroquirúrgica que salva vidas. El paciente fue trasladado inconsciente a un hospital de primera categoría, libre de intubación y en un estado hemodinámico estable. El período postoperatorio estuvo marcado por convulsiones, por lo que el paciente fue puesto en anticonvulsivos con un buen resultado.\n",
+        "synthetic_summary": {
+            "B1": "A man fell off his motorcycle and hurt his head. He did not wear a helmet. \n\nAt the first hospital, he was very sleepy and had a bad head wound. He was bleeding inside his head. \n\nDoctors put a special bandage inside his head to stop the bleeding. \n\nThen, they took him to a bigger hospital. He was still sleepy but his body was okay. \n\nAfter surgery, he had some shaking fits. The doctors gave him medicine to help. He got better.",
+            "B2": "**What Happened:**  \nA 27-year-old man who smokes had a motorcycle accident. He was not wearing a helmet and fell, hurting his head badly. When he arrived at the first hospital in a rural area, doctors found that he was in a deep coma. His Glasgow Coma Scale score was 6 out of 15, which means he was very unresponsive. He also had both pupils enlarged (called bilateral mydriasis), signs of serious blood flow problems (hemodynamic distress), but his oxygen levels were okay. Doctors saw a deep wound in his head with heavy bleeding inside his skull.\n\n**How They Treated Him:**  \nTo stop the bleeding inside his skull, surgeons used a special method called intracranial packing. This means they carefully filled the wound inside the skull to control the bleeding. This is a life-saving brain surgery technique. After this, the patient was moved while unconscious to a bigger hospital with better equipment. He was stable in terms of blood flow and breathing and did not need a breathing tube (intubation).\n\n**What Happened After Surgery:**  \nAfter the operation, the patient had seizures (convulsions). To control these, doctors gave him medicine called anticonvulsants. This treatment worked well, and he improved.\n\n**Summary:**  \nThis young man had a serious head injury from a motorcycle crash without a helmet. Quick brain surgery to stop bleeding saved his life. Even though he had seizures afterward, medicine helped him recover well. This case shows how important fast and proper treatment is for severe head injuries.",
+            "B3": "**Background**  \nA 27-year-old man who smokes and has no prior medical conditions was involved in a traffic accident after falling from a motorcycle without wearing a helmet. He initially presented at a rural district hospital with a penetrating head injury and significant intracranial bleeding.\n\n**Key Findings**  \nUpon arrival, his Glasgow Coma Scale (GCS) score was 6 out of 15, indicating severe impairment of consciousness: he did not open his eyes, withdrew from painful stimuli, and was nonverbal. He exhibited bilateral pupil dilation (midriasis), hemodynamic distress (unstable blood circulation), but maintained adequate oxygen saturation. A penetrating cranial wound with profuse intracranial hemorrhage was identified. Laboratory tests showed severe anemia with a hemoglobin level of 6 g/dL. Imaging was not available at this facility.\n\n**Clinical Interpretation and Initial Management**  \nGiven the severity of the intracranial bleeding, a neurocritical procedure known as intracranial packing (a damage control neurosurgical technique) was performed to tamponade (stop) the hemorrhage and stabilize the patient’s condition. Supportive measures included cervical spine stabilization, airway management with orotracheal intubation, intravenous fluids, anticonvulsants to control seizures, antibiotics to prevent infection, and blood transfusion. Despite the critical condition, the patient was transferred unconscious but hemodynamically stable and without intubation to a tertiary care hospital equipped for advanced neuroimaging and surgery.\n\n**Further Diagnostic Findings and Surgical Intervention**  \nAt the tertiary center, a computed tomography (CT) scan revealed multiple severe brain injuries: acute bifrontal brain swelling (edema), a hemorrhagic contusion predominantly on the right side, a thin acute subdural hematoma on the left side, a 5 mm left subfalcine herniation (displacement of brain tissue), mild compression of the right lateral ventricle, acute bifrontal subarachnoid hemorrhage, a depressed frontal bone fracture with osteomeningeal disruption (fracture involving bone and meninges), and a cervical spine fracture at the third vertebra causing spinal cord compression. The patient underwent successful neurosurgical intervention to address these injuries.\n\n**Postoperative Course and Outcome**  \nThe postoperative period was complicated by seizures, which were effectively managed with anticonvulsant medications. The patient’s neurological, respiratory, and hemodynamic status improved, and he regained consciousness and mobility without significant deficits.\n\n**Summary**  \nThis case illustrates the critical importance of prompt neurocritical care in severe traumatic brain injury, especially in resource-limited settings. The use of intracranial packing as an emergency damage control technique, followed by transfer to a specialized center for definitive surgical management, contributed to a favorable outcome despite the initial poor neurological status. Ongoing seizure control and multidisciplinary care remain essential components of recovery."
+        }
+    },
+    {
+        "article": "La paciente era una madre de 54 años que provenía de una zona rural y que llegó al Hospital Especializado de Compresión de Nekemte con la queja de una masa en su vagina de 3 años de duración. Hace tres años, encontró una protuberancia de masa a través de su vagina, que gradualmente creció en tamaño con el tiempo. Había tenido dos bebés, el último hace 12 años. Ambos partos fueron en casa, ya que el centro de salud está demasiado lejos de su área de residencia, y fue asistida por una comadrona tradicional. Ella afirmó que todo había sido sin problemas. Inicialmente, hace tres años, hubo sangrado y una descarga ofensiva de la masa, pero eso se detuvo en el último año. Desarrolló laceraciones en la masa hace seis meses. Por esta razón, se divorció y se aisló de toda la vida social durante este largo período de tiempo. Ahora, su hermana mayor y otro familiar la trajeron al hospital específicamente por la laceración de la masa. No tenía ninguna otra enfermedad médica crónica conocida.\n\nHallazgo pertinente del PE\nSigno vital: PA = 100/60 mm hg, FC = 84 lpm, FR = 20 lpm, T° = 36.5°C, peso = 47 kg.\n\nGUS: hay una masa rosada en la vagina que se encuentra a unos 7 cm del anillo del himen.\n\nEl fondo uterino es la parte principal de la masa.\n\nHabía una laceración longitudinal de unos 5 cm en el lado derecho de la masa.\n\nNo hubo sangrado ni secreción de la masa ni del área de la laceración.\n\nLaboratorio\nCBC: hemoglobina = 12 g/dl, PLT = 285 mil, neutrófilos = 74%.\n\nAnálisis de orina: resultado normal.\n\nGrupo sanguíneo = A, RH = positivo.\n\nPrueba de VIH = negativa.\n\nHBSAg = negativo.\n\nEcografía: vejiga parcialmente llena visible en el abdomen, útero no visible en el abdomen. Por lo demás, no se observaron otros hallazgos pertinentes.\n\nRadiografía de tórax: radiografía de tórax normal.\n\nPor este motivo, se le diagnosticó una inversión uterina crónica. Se tomaron imágenes preoperatorias y postoperatorias, el fondo uterino era el punto principal de la masa que sobresalía completamente a través de la vagina y había una laceración crónica desarrollada en la superficie endometrial. Después de la operación, se observó un canal vaginal normal. Después de revisar las opciones de tratamiento con ella y su familia, se programó una cirugía y se realizó una histerectomía abdominal al día siguiente. Era una cirugía abdominal y era fácil introducir el útero en el abdomen. Como el tejido era redundante y distorsionado, es difícil identificar la referencia anatómica y los puntos de referencia quirúrgicos. Debido a esto, la cirugía fue difícil y hubo una lesión ureteral derecha transaccional intraoperatoria y se realizó una anastomosis de extremo a extremo. Se dio de alta el décimo día de la operación y se encontró que estaba mejorando. Se le dio una cita de seguimiento dos semanas después y cuando se evaluó se encontró que estaba bien.\n",
+        "gold_summary": "Una mujer de 54 años de edad acudió a nuestro hospital con la queja de una masa indolora en su vagina de 3 años de duración. Hace tres años, encontró una protuberancia de masa a través de su vagina, que gradualmente creció en tamaño con el tiempo. En el examen físico, el fondo uterino fue el punto principal de la masa y sobresalía 7 cm por debajo del anillo del himen. Como resultado, se le diagnosticó inversión uterina crónica y se le sometió a una histerectomía abdominal. Fue dada de alta en casa mejorada. Presentamos este caso debido a un factor no identificado que provocó la inversión uterina, la presentación tardía de la enfermedad y la dificultad en el tratamiento quirúrgico.\n",
+        "synthetic_summary": {
+            "B1": "A lady had a bump inside her that grew for three years. The bump was soft and did not hurt. The doctors found that part inside her was turned the wrong way. They did a big operation to help her. After the operation, she got better and went home. The doctors wanted to share this story because it was a hard problem to fix.",
+            "B2": "**What Happened**\n\nA 54-year-old woman came to the hospital because she had a lump in her vagina for three years. This lump slowly got bigger over time. She did not feel pain from it. When doctors examined her, they found that the top part of her uterus (called the uterine fundus) was the main part of the lump. This part was sticking out about 7 centimeters below the opening of the vagina.\n\n**What It Means**\n\nThe doctors diagnosed her with a condition called chronic uterine inversion. This means that the uterus had turned inside out and pushed down into the vagina. This is a rare and serious problem that can be hard to treat, especially when it is found late.\n\n**What They Did**\n\nTo fix the problem, the doctors performed surgery called an abdominal hysterectomy. This surgery removes the uterus through an opening in the belly. The surgery was difficult because the tissues were damaged and the usual landmarks inside the body were hard to see. During the operation, a nearby tube called the right ureter (which carries urine from the kidney to the bladder) was accidentally injured but was repaired right away.\n\n**Outcome**\n\nThe woman stayed in the hospital for ten days after surgery and showed improvement. She was sent home and later checked again, where she was found to be doing well.\n\n**Why This Case Is Important**\n\nThis case is important because the cause of the uterine inversion was not clear. Also, the woman came for treatment very late, which made the surgery more difficult. It shows how important it is to seek medical help early and how complex some gynecological problems can be.",
+            "B3": "**Background**  \nA 54-year-old woman from a rural area presented to a specialized hospital with a three-year history of a painless vaginal mass. She first noticed a protruding lump through her vagina that gradually increased in size over time. Her obstetric history included two home births assisted by a traditional birth attendant, with no reported complications. Initially, the mass was associated with bleeding and foul-smelling discharge, which ceased during the last year. Six months prior to presentation, the mass developed a longitudinal laceration. The patient experienced social isolation and marital separation due to this condition. She had no known chronic medical illnesses.\n\n**Key Findings**  \nOn physical examination, vital signs were stable: blood pressure 100/60 mm Hg, heart rate 84 beats per minute, respiratory rate 20 breaths per minute, temperature 36.5°C, and weight 47 kg. Gynecological examination revealed a pink vaginal mass located approximately 7 cm below the hymenal ring. The uterine fundus constituted the main component of the mass, which protruded entirely through the vagina. A 5 cm longitudinal laceration was present on the right side of the mass, without active bleeding or discharge. Laboratory tests showed normal hemoglobin (12 g/dL), platelet count (285,000/µL), and neutrophil percentage (74%). Urinalysis was normal. Serologic tests were negative for HIV and hepatitis B surface antigen. Ultrasound imaging showed a partially filled bladder but did not visualize the uterus in the abdomen. Chest X-ray was normal.\n\n**Clinical Interpretation**  \nThe diagnosis was chronic uterine inversion, a rare condition in which the uterine fundus turns inside out and protrudes through the vagina. This diagnosis was supported by the clinical finding that the uterine fundus formed the main part of the vaginal mass. The chronicity of the inversion and the presence of a laceration on the endometrial surface complicated the clinical picture. The etiology of the inversion in this case was unclear, as there was no recent childbirth or identifiable precipitating factor. The delay in seeking medical care contributed to the advanced presentation and complexity of treatment.\n\n**Next Steps and Treatment**  \nAfter discussing treatment options with the patient and her family, an abdominal hysterectomy was scheduled and performed the following day. During surgery, the uterus was easily repositioned into the abdominal cavity; however, distorted and redundant tissue made anatomical landmarks difficult to identify. This complexity led to an intraoperative injury of the right ureter (the tube connecting the kidney to the bladder), which was repaired by end-to-end anastomosis (surgical reconnection). The patient’s postoperative course was uneventful, and she was discharged on the tenth day with clinical improvement. Follow-up two weeks later confirmed satisfactory recovery.\n\n**Summary**  \nThis case highlights a rare presentation of chronic uterine inversion in a middle-aged woman with a delayed diagnosis and challenging surgical management. The absence of a clear precipitating event, prolonged duration of the condition, and anatomical distortion contributed to the complexity of care. The successful surgical outcome underscores the importance of timely intervention and multidisciplinary management in such unusual gynecological cases."
+        }
+    },
+    {
+        "article": "Varón de 20 años, HIV negativo, con TB pulmonar y tratamiento irregular en 2020-2021. Se internó por síndrome de impregnación bacilar, dolor e impotencia funcional del hombro derecho. Presentaba mal estado general, adelgazado, hipotrofia muscular grave, lesiones tumorales frías fluctuantes fistulizadas en dorso, calota craneana y tórax anterior con secreción caseosa, sin presentar déficits motores ni sensitivos. El examen molecular rápido (GeneXpert Mtb/Rif) de secreción del tórax fue positivo para Mycobacterium tuberculosis, sensible a rifampicina (el antibiograma fenotípico mostró una cepa pansensible). La TC demostró consolidaciones pulmonares y árbol en brote, junto con el compromiso óseo de columna cervical, dorsal y lumbar con imágenes líticas y colecciones pre y paraespinales. En la RMN se observaron imágenes infiltrativas desde C4 a C6; D4 a D6, D9 a D12; fractura patológica de D6 y D10 e infiltración en L1, L2 y L3. Inició tratamiento anti-TB con esquema estándar de primera línea (isoniacida, rifampicina, pirazinamida, etambutol). Dada la extensa destrucción y el peligro de cuadriplejía/paraplejía por el compromiso cervical y/o dorsal, se indicó posición decúbito dorsal permanente, collar de Filadelfia, asistencia kinésica y conducta neuroquirúrgica en forma programada en los niveles cervicales, D6 y D10. Previo a la cirugía programada presentó un cuadro agudo de paraplejía con nivel sensitivo D8, con compromiso vesical. Se interpretó como nivel de compresión aguda en D6. Se indicó neurocirugía de urgencia con descompresión medular vía posterior con laminectomía dorsal 6 y parcialmente D5 y 7 y evacuación de una colección epidural. Fue recuperando la función motora y sensitiva en forma progresiva. Posteriormente se realizó la cirugía programada cervical vía anterior con corporectomía de C4, C5, C6 y C7 más artrodesis de C3 a D1 con reemplazo de cuerpo vertebral más injerto autólogo, placa y tornillos. En la TC de control se evidenció luxación posterior de D6 con compresión del canal espinal y deterioro neurológico por compresión medular. Se reconsideró la táctica quirúrgica debido a la inestabilidad mecánica y neurológica. Se realizó descompresión y alineación del nivel luxado con artrodesis posterior de los tres niveles espinales no adyacentes, cervical, dorsal 6 y dorsal 10 en un solo tiempo quirúrgico. Se fijó desde  C3 hasta D12 con tornillos poliaxiales y barra de transición cervicodorsal. En cada tiempo quirúrgico se evidenció evacuación espontánea de material caseoso, BAAR positivo, y se realizaron lavados profusos.  Presentó mejoría clínica, bacteriológica y resolución de las lesiones pulmonares. Recuperó movilidad con rehabilitación kinésica sumada al tratamiento específico (3 meses de primera fase e indicación de continuación con isoniacida y rifampicina hasta completar los 12 meses). Egresó caminando por sus propios medios, luego de una prolongada internación de 5 meses.",
+        "gold_summary": "Se presenta el caso de un varón de 20 años con espondilitis tuberculosa multinivel no contigua (cervical, dorsal 6, dorsal 10 y lumbar). Se trata de un paciente HIV negativo con tuberculosis diseminada con grave compromiso de su estado general y múltiples localizaciones de la enfermedad. Algunas tenían fistulas que secretaban caseum. El paciente presentó paraplejía aguda que requirió, teniendo en cuenta el nivel sensitivo a nivel dorsal 6, una primera cirugía urgente de descompresión por vía posterior. Luego se efectuó la cirugía programada. En primera instancia, la región cervical por vía anterior, con corporectomía, colocación de reemplazo de cuerpo vertebral más injerto autólogo y placa con tornillos. Posteriormente se evidenció luxación del nivel dorsal 6 hacia atrás comprimiendo la médula espinal y, dada la inestabilidad mecánica, se indicó un tercer tiempo quirúrgico por vía posterior que comprendió reducción, descompresión y fijación, resolviendo los tres niveles por vía posterior con barras y tornillos. El tratamiento quirúrgico, médico y kinésico de esta forma poco frecuente del mal de Pott fue exitoso, con recuperación de su estabilidad mecánica y progresiva recuperación de su estado neurológico.",
+        "synthetic_summary": {
+            "B1": "A young man was very sick with a bad bone infection in his back and neck. This made his body weak and he could not move his legs well. \n\nDoctors did three surgeries to help him. They fixed his bones and took away the bad parts. \n\nAfter the surgeries and special medicine, he got stronger. He could move better and walk again. The doctors helped him get well step by step.",
+            "B2": "**What Happened to the Patient**  \nA 20-year-old man had a serious infection called tuberculosis (TB) that affected many parts of his spine. This type of TB is called \"tuberculous spondylitis,\" which means the infection damaged several bones in his neck (cervical), upper back (dorsal), and lower back (lumbar). He did not have HIV, but his TB was very severe and spread to different areas. Some infected spots had fistulas, which are openings that let out a thick, cheese-like fluid called caseum.\n\n**The Problem and Surgeries**  \nThe patient suddenly became unable to move his legs (paraplegia) because the infection pressed on his spinal cord around the middle of his back (dorsal level 6). This urgent problem needed quick surgery to relieve the pressure from the back of his spine. After this emergency surgery, doctors planned more operations. First, they operated on his neck from the front, removing damaged vertebrae (bones in the spine) and replacing them with a bone graft from his own body plus metal plates and screws to hold everything together.\n\nLater, doctors found that one of the vertebrae in his upper back (dorsal 6) had slipped backward, pressing again on his spinal cord. Because this caused instability in his spine, he needed a third surgery from the back. This operation fixed the slipped bone, relieved pressure, and stabilized three different spine areas using metal rods and screws.\n\n**Treatment and Recovery**  \nAlong with surgery, the patient received strong medicine to fight TB and physical therapy to help him regain strength and movement. This combined treatment worked well. He gradually recovered his nerve function and spine stability. After about five months in the hospital, he was able to walk on his own again.\n\n**What This Means**  \nThis case shows how serious and complicated spinal TB can be, especially when it affects multiple parts of the spine and causes sudden paralysis. Careful surgery, medicine, and rehabilitation can help patients recover even from severe cases like this one.",
+            "B3": "**Background**  \nThis report describes a 20-year-old man diagnosed with multifocal, non-contiguous tuberculous spondylitis (also known as Pott’s disease) affecting multiple spinal levels: cervical (neck), dorsal (mid-back at levels 6 and 10), and lumbar regions. The patient was HIV-negative but had disseminated tuberculosis with severe general health deterioration and widespread involvement of bone and soft tissue. Some lesions had developed fistulas—abnormal passages—that discharged caseous material (a cheese-like necrotic substance characteristic of tuberculosis).\n\n**Key Findings**  \n- The patient presented with acute paraplegia (loss of motor and sensory function in the lower limbs) corresponding to a sensory level at dorsal vertebra 6 (D6), indicating spinal cord compression at this site.  \n- Initial urgent neurosurgical intervention involved posterior decompression via laminectomy (removal of the vertebral arch) at D6 and adjacent levels, with evacuation of an epidural abscess containing acid-fast bacilli (Mycobacterium tuberculosis).  \n- Subsequently, a planned anterior cervical surgery was performed, including corporectomy (removal of vertebral bodies C4 to C7), placement of vertebral body replacements, autologous bone grafting, and stabilization with plates and screws to restore cervical spine integrity.  \n- Postoperative imaging revealed posterior dislocation (luxation) at D6 causing renewed spinal cord compression and neurological decline. Due to mechanical instability, a third surgery was undertaken via a posterior approach to realign, decompress, and stabilize the spine. This involved fixation from cervical level C3 through thoracic level D12 using polyaxial screws and transitional rods, addressing all affected spinal segments in a single procedure.  \n- Throughout surgical interventions, caseous material was consistently evacuated, and extensive irrigation was performed to reduce infection burden.\n\n**Clinical Interpretation**  \nThis case exemplifies a severe and uncommon presentation of Pott’s disease with multiple non-adjacent spinal involvements leading to mechanical instability and acute neurological compromise. The combination of disseminated tuberculosis, extensive bone destruction, and epidural abscess formation necessitated a multidisciplinary approach including urgent and staged neurosurgical decompression and stabilization, alongside prolonged anti-tuberculosis chemotherapy and rehabilitative physiotherapy. The patient’s HIV-negative status and pansensitive bacterial strain (sensitive to all first-line drugs) likely contributed to favorable microbiological response.\n\n**Next Steps and Outcome**  \nFollowing a prolonged five-month hospitalization, the patient demonstrated progressive neurological recovery and regained independent ambulation. The treatment plan included an initial intensive phase of four-drug anti-tuberculosis therapy for three months, followed by continuation with isoniazid and rifampicin to complete a total of twelve months of therapy. Rehabilitation through physical therapy was integral to restoring function and mobility. This comprehensive medical and surgical management successfully restored spinal stability and improved neurological status in a complex case of advanced spinal tuberculosis."
+        }
+    },
+    {
+        "article": "Un hombre japonés de 23 años fue admitido en nuestro hospital debido al empeoramiento de la disnea de esfuerzo. Había mostrado dificultad para correr a los dos años y se le diagnosticó EDMD con una mutación genética de LMNA (Lamin A/C) en el exón 1 de leucina 102 a prolina. De acuerdo con las manifestaciones típicas de EDMD, sus codos, rodillas y tendones de Aquiles se habían contraído a los cinco años, y sus músculos cervicales posteriores se habían vuelto rígidos; sin embargo, continuó con su vida diaria habitual, aunque con una leve restricción de ejercicio. Su padre también había sido diagnosticado con EDMD y murió repentinamente a los 40 años.\n\nCuando el paciente tenía 19 años, fue admitido en un hospital por primera vez debido a una insuficiencia cardiaca congestiva. Los signos de insuficiencia de la RV, tales como edema de las piernas y congestión hepática, fueron prominentes, como lo indica el alto nivel de bilirrubina en sangre (2,5 mg/dL). La ecocardiografía mostró que la excursión sistólica del plano anular tricúspide (TAPSE) era de 5,7 mm, la velocidad de la RV de 5,1 cm/s y el cambio del área fraccional de la RV (RVFAC) del 19 %, lo que indica una marcada disfunción de la RV. Se introdujeron diuréticos de alta dosis además de carvedilol (10 mg/día) y enalapril (2,5 mg/día). A pesar de esos medicamentos, fue readmitido debido al empeoramiento de la insuficiencia de la RV.\n\nA los 22 años, se le implantó un desfibrilador cardioversor implantable (ICD) debido a su taquicardia ventricular no sostenida (VT) y a la historia familiar de muerte súbita cardiaca. En este momento, el cateterismo cardiaco derecho (RHC) mostró una presión de la cuña de la arteria pulmonar (PAWP) de 22 mmHg, presión auricular derecha (RAP) de 17 mmHg, e índice de trabajo de accidente cerebrovascular ventricular derecho (RVSWI) de 6.47, lo que sugiere una disfunción severa sostenida del RV. Como tal, el fallo del RV probablemente fue la principal condición patológica a lo largo de su curso clínico.\n\nTenía insuficiencia cardiaca sintomática con la clasificación III de la New York Heart Association con dosis máximas de medicación guiada por directrices, y su electrocardiograma mostraba un ritmo sinusal regular y bloqueo de rama izquierda con ancho QRS (150 ms). Su fracción de eyección del ventrículo izquierdo (LVEF) era ≤35 % en la ecocardiografía. Por lo tanto, se consideró que estaba indicado para CRT y se le actualizó a ICD a los 23 años.\n\nAl ingreso, su presión arterial era de 106/65 mmHg y su frecuencia cardíaca de 60 latidos/min con un ritmo regular. El examen físico reveló un tercer sonido cardíaco y un soplo pan sistólico (Levine II/VI) en la región apical. Los sonidos respiratorios eran claros, mientras que una vena yugular distendida y un edema de miembros inferiores eran evidentes. La radiografía de tórax indicó un aumento de la relación cardiotorácica (59%) sin congestión pulmonar.\n\nEl electrocardiograma mostró un ritmo biventricular debido a la TRC. La ecocardiografía reveló una ligera dilatación en ambos ventrículos (diámetro final diastólico del LV: 54 mm, diámetro del RV: 50 mm) con una reducción de la LVEF (30%). La función del RV también se redujo, como lo indican una reducción de la RVFAC (11%) y un bajo TAPSE (8 mm). Ambos ventrículos agrandados causaron una pérdida de sujeción y coaptación de las valvas que resultó en una regurgitación mitral moderada y una regurgitación tricuspídea severa. La vena cava inferior se dilató a 23 mm con una reducción de la fluctuación respiratoria.\n\nEn los hallazgos histológicos de los músculos cervicales posteriores realizados más tarde en la autopsia, se observó un aumento en la variación del tamaño de la fibra muscular con una infiltración moderada de tejido conectivo, lo que fue compatible con la EDMD. Los análisis de sangre revelaron péptido natriurético cerebral (BNP) 196.1 pg/mL, bilirrubina total 1.4 mg/dL, aspartato aminotransferasa (AST) 39 U/L, alanina aminotransferasa (ALT) 43 U/L, y gamma glutamil transpeptidasa (gamma-GTP) 451 U/L, lo que sugirió una disfunción hepática. Aunque las arterias coronarias estaban intactas en la angiografía, una biopsia endocárdica del VD reveló una hipertrofia cardiaca con un aumento de la magnitud del núcleo y el miocardio.\n\nLa microscopía electrónica demostró hallazgos típicos de la EDMD: un número reducido de miofibrillas, necrosis y la formación de pseudo- o verdaderas inclusiones. Dado que se descartaron otras cardiomiopatías secundarias mediante estos hallazgos clínicos e histológicos, diagnosticamos una cardiomiopatía relacionada con la EDMD.\n\n\nEl curso clínico del paciente. El cateterismo cardiaco derecho (RHC) en el día 11 mostró disfunción y congestión severa del LV/RV, y se iniciaron algunos inótropos. Aunque la hemodinámica del paciente mejoró, su función renal empeoró progresivamente en el día 38. Preocupados por el empeoramiento de su función renal debido a la disminución de la presión arterial, se iniciaron la dopamina y el soporte mecánico (IABP y CRRT), y la función renal y la hemodinámica del paciente mejoraron. Sin embargo, desarrolló insuficiencia hepática aguda junto con insuficiencia severa del RV indicada por los datos del RHC en el día 68. Aunque se introdujo ECMO veno-atrial en el día 71, la disfunción hepática y la DIC causaron diátesis hemorrágica sistémica, y el paciente falleció por fallo multiorgánico en el día 100. CRRT: terapia de reemplazo renal continua, DIC: coagulación intravascular diseminada, ECMO: oxigenación por membrana extracorpórea, IABP: bombeo de globo intraaórtico, LV: ventrículo izquierdo, RV: ventrículo derecho\n\nEl RHC en el día 11 mostró que el índice cardiaco (IC) era de 2,0 L/min/m2 (método de Fick), y la PAP era de 15 mmHg, lo que indicaba un subgrupo IV de Forrester. La presión arterial pulmonar (PAP) era de 29/12 (18) mmHg, y la RAP era de 15 mmHg. El RVSWI, uno de los parámetros hemodinámicos para la función del RV, se calculó con la siguiente fórmula: RVSWI (g·m/m2/latido)=[presión arterial pulmonar media (mPAP)-presión atrial derecha media (mRAP)]×índice de volumen de latido (SVI)×0.0136. Su RVSWI era de 1.36 g·m/m2/latido, lo que indicaba una disfunción severa del RV. Para compensar el síndrome de baja producción del paciente y la congestión, comenzamos una infusión continua de dobutamina (3.0 μg/kg/min) y añadimos milrinona (0.125 μg/kg/min) en el día 16.\n\n\nEn el día 32, los datos de RHC mejoraron, con un aumento del IC (2,48 L/min/m2), una reducción de la PAWP (13 mmHg) y un aumento de la RVSWI (2,8 g·m/m2/latido). Sin embargo, en el día 38, la función renal del paciente empeoró progresivamente, posiblemente debido a una presión venosa central alta (CVP) e hipotensión, ya que la presión arterial había sido de alrededor de 70/40 mmHg varios días antes del empeoramiento de la función renal. Para aumentar su presión arterial, se inició una infusión continua de dopamina (2,0 μg/kg/min); se redujo la milrinona y se interrumpieron el enalapril y la eplerenona. Además, se necesitaron temporalmente el bombeo de globo intraaórtico (IABP) y la terapia de reemplazo renal continuo (CRRT). A medida que la hemodinámica del paciente mejoró en respuesta al aumento de la saturación de oxígeno venoso mixto (SvO2, 70-80%) y el IC (3,0-3,5 L/min/m2), se retiraron el IABP y la CRRT en el día 45.\n\nSin embargo, el día 68, el IC volvió a disminuir a 1,25 l/min/m2 y la congestión pulmonar y la retención de fluidos del paciente se deterioraron; la PAWP era tan alta como la RAP, a 22 mmHg. Además, los niveles de bilirrubina en suero y las transaminasas hepáticas del paciente aumentaron drásticamente, lo que sugiere el desarrollo de insuficiencia hepática. El día 71, se inició la ECMO VA a través de una vena femoral a la arteria subclavia, pero debido a la diátesis hemorrágica sistémica acompañada por la coagulación intravascular diseminada (CID), el paciente falleció de insuficiencia multiorgánica el día 100.\n\nUna autopsia realizada con el consentimiento informado de la familia del paciente reveló un agrandamiento eferente en ambos ventrículos con un espesor de pared delgado. El examen histopatológico reveló que la hipertrofia miocárdica leve a moderada y la fibrosis severa eran evidentes en el RV y el LV. El peso del hígado aumentó significativamente a 2298 g, y se detectaron congestión hepática macroscópica y colestasis. En las imágenes microscópicas, el área de la vena porta apenas cambió, y se observó atrofia o pérdida de hepatocitos alrededor de las venas centrales, lo que indica un «hígado de shock». En los pulmones, se observó una hemorragia alveolar extensa, y se observó una colección de macrófagos que habían ingerido hemosiderina, lo que refleja una diátesis hemorrágica sistémica.\n\nMH - Adulto\nMH - Insuficiencia cardiaca/*etiología/fisiopatología/terapia\nMH - Humanos\nMH - Lamin tipo A/genética\nMH - Hombre\nMH - Distrofia muscular, Emery-Dreifuss/*complicaciones/diagnóstico/genética/terapia\nMH - Mutación\n",
+        "gold_summary": "Un hombre de 23 años tenía debilidad muscular progresiva y distrofia muscular de Emery-Dreifuss (EDMD) debido a una mutación de LMNA (lamina A/C). Insuficiencia cardiaca congestiva diagnosticada a los 19 años de edad. El tratamiento farmacológico máximo/resincronización cardiaca no logró mejorar la función cardiaca. Por lo tanto, fue hospitalizado debido a insuficiencia cardiaca. A pesar de la oxigenación por membrana extracorpórea, desarrolló una disfunción cardiaca derecha grave y falleció (fallo multiorgánico).\n",
+        "synthetic_summary": {
+            "B1": "A young man had weak muscles that got worse. He had a sickness called EDMD. His heart did not work well when he was 19. Medicine and special heart help did not make him better. He went to the hospital because his heart was very sick. Even with strong help, his heart stopped working right. He passed away because his body was very tired.",
+            "B2": "**What Happened to the Patient**\n\nA 23-year-old man had a muscle disease called Emery-Dreifuss muscular dystrophy (EDMD). This disease was caused by a change, or mutation, in a gene called LMNA, which affects proteins important for muscle cells. Because of this, his muscles became weaker over time.\n\nWhen he was 19 years old, he was diagnosed with heart failure. Heart failure means the heart cannot pump blood well enough to meet the body’s needs. He was given the strongest medicines and a special treatment called cardiac resynchronization therapy (CRT). CRT helps the heart’s chambers beat in a better rhythm. But even with these treatments, his heart function did not improve.\n\n**What the Doctors Did**\n\nHe was admitted to the hospital because his heart failure got worse. The right side of his heart, which pumps blood to the lungs, was severely damaged and not working well. The doctors tried a machine called extracorporeal membrane oxygenation (ECMO). ECMO helps by taking over the work of the heart and lungs temporarily.\n\n**What It Means**\n\nDespite all treatments, the right side of his heart failed badly. This caused other organs in his body to stop working, a condition called multiple organ failure. Sadly, he passed away because his heart and other organs could not recover.\n\nThis case shows how EDMD can cause serious heart problems that are hard to treat, especially when the right side of the heart is affected.",
+            "B3": "**Background**  \nA 23-year-old Japanese man was diagnosed with Emery-Dreifuss muscular dystrophy (EDMD), a genetic disorder characterized by progressive muscle weakness and contractures, caused by a mutation in the LMNA gene (lamin A/C) affecting exon 1 (leucine 102 to proline). His symptoms began in early childhood with difficulty running at age two and joint contractures by age five. His father also had EDMD and died suddenly at age 40, indicating a familial pattern. At 19 years old, he developed congestive heart failure primarily due to severe right ventricular (RV) dysfunction.\n\n**Key Clinical Findings**  \n- Initial presentation included signs of right heart failure such as leg edema and liver congestion, with elevated bilirubin (2.5 mg/dL).  \n- Echocardiography revealed marked RV dysfunction: tricuspid annular plane systolic excursion (TAPSE) of 5.7 mm, RV fractional area change (RVFAC) of 19%, and low RV systolic velocity.  \n- Despite high-dose diuretics and medications including carvedilol and enalapril, his heart failure worsened, requiring hospital readmission.  \n- At age 22, he received an implantable cardioverter-defibrillator (ICD) due to non-sustained ventricular tachycardia and family history of sudden cardiac death. Right heart catheterization showed elevated pulmonary artery wedge pressure (22 mmHg), right atrial pressure (17 mmHg), and severely reduced RV stroke work index (RVSWI), confirming sustained severe RV failure.  \n- At 23, with symptomatic heart failure classified as New York Heart Association (NYHA) class III and left ventricular ejection fraction (LVEF) ≤35%, he underwent cardiac resynchronization therapy (CRT) upgrade to his ICD.  \n- On admission, physical examination revealed a third heart sound, pansystolic murmur, jugular venous distension, and lower limb edema. Chest X-ray showed cardiomegaly without pulmonary congestion.  \n- Electrocardiogram demonstrated biventricular pacing rhythm post-CRT. Echocardiography showed mild biventricular dilation (LV end-diastolic diameter 54 mm, RV diameter 50 mm), reduced LVEF (30%), severely impaired RV function (RVFAC 11%, TAPSE 8 mm), and significant mitral and tricuspid valve regurgitation due to ventricular enlargement.  \n- Laboratory tests indicated hepatic dysfunction (elevated bilirubin, AST, ALT, gamma-GTP) and elevated brain natriuretic peptide (BNP 196.1 pg/mL). Coronary angiography was normal.  \n- Endomyocardial biopsy of the RV revealed cardiomyocyte hypertrophy with nuclear enlargement and myocardial changes consistent with EDMD, including reduced myofibrils, necrosis, and characteristic nuclear inclusions on electron microscopy. Other secondary cardiomyopathies were excluded.\n\n**Clinical Course and Management**  \n- Right heart catheterization on hospital day 11 confirmed severe biventricular dysfunction and congestion (cardiac index 2.0 L/min/m², pulmonary artery pressure 29/12 mmHg, right atrial pressure 15 mmHg, RVSWI 1.36 g·m/m²/beat).  \n- Inotropic support with dobutamine and milrinone was initiated, leading to temporary hemodynamic improvement by day 32 (cardiac index 2.48 L/min/m², reduced pulmonary wedge pressure, increased RVSWI).  \n- By day 38, renal function deteriorated, likely due to hypotension and elevated central venous pressure. Dopamine infusion was started, milrinone dose reduced, and renin-angiotensin system inhibitors discontinued. Mechanical circulatory support with intra-aortic balloon pump (IABP) and continuous renal replacement therapy (CRRT) were implemented, resulting in improved hemodynamics and renal function by day 45.  \n- On day 68, cardiac output declined again (cardiac index 1.25 L/min/m²), with worsening pulmonary congestion and fluid retention. Pulmonary wedge pressure and right atrial pressure both elevated to 22 mmHg. Liver enzymes and bilirubin rose sharply, indicating acute hepatic failure.  \n- Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) was initiated on day 71 due to severe RV failure and multiorgan dysfunction. Despite this, systemic hemorrhagic diathesis caused by disseminated intravascular coagulation (DIC) developed. The patient died from multiorgan failure on day 100.\n\n**Autopsy Findings**  \n- Both ventricles were enlarged with thin walls. Histology showed mild to moderate myocardial hypertrophy and severe fibrosis in the RV and left ventricle (LV).  \n- The liver was markedly enlarged (2298 g) with macroscopic congestion and cholestasis. Microscopic examination revealed central vein hepatocyte loss and atrophy consistent with “shock liver” due to circulatory failure.  \n- Lungs showed extensive alveolar hemorrhage and hemosiderin-laden macrophages, reflecting systemic hemorrhagic diathesis.\n\n**Clinical Interpretation**  \nThis patient’s course exemplifies the severe cardiac complications of EDMD caused by LMNA mutation, particularly progressive right ventricular failure refractory to maximal medical therapy and device intervention. The combination of biventricular dysfunction, valvular regurgitation secondary to ventricular dilation, and hepatic and renal dysfunction due to congestion and low cardiac output culminated in multiorgan failure. Histopathological and ultrastructural findings confirmed the diagnosis of EDMD-related cardiomyopathy and excluded other secondary causes.\n\n**Next Steps and Considerations**  \n- Early recognition of EDMD-associated cardiomyopathy and close monitoring of RV function are critical, given the propensity for severe RV failure.  \n- Advanced therapies such as mechanical circulatory support may provide temporary stabilization but may not prevent progression to multiorgan failure in severe cases.  \n- Genetic counseling and family screening are important due to the hereditary nature and risk of sudden cardiac death.  \n- Future research into targeted therapies for LMNA-related cardiomyopathies is needed to improve outcomes.\n\nIn summary, this case highlights the devastating cardiac manifestations of EDMD with LMNA mutation, emphasizing the challenges in managing severe right heart failure and the importance of comprehensive multidisciplinary care."
+        }
+    },
+    {
+        "article": "Mujer de 65 años sin antecedentes patológicos destacables que en 2004 inició paroxismos lancinantes en los territorios V2 y V3 derechos, con desencadenantes clásicos, por lo que se le diagnosticó una neuralgia del trigémino derecho. En las resonancias magnéticas cerebrales hasta 2021 no se habían realizado las secuencias que permiten identificar si hay un cruce neurovascular. Desde el inicio, el control del dolor con carboxamidas fue difícil. En 2021 presentó exacerbación de los paroxismos previos que aparecieron en V1. La neuralgia se volvió refractaria, sin respuesta a las carboxamidas y la lamotrigina, y muy escasa al clonacepam, por lo que requirió perfusiones de fenitoína y/o lidocaína en las exacerbaciones graves. Simultáneamente inició paroxismos lancinantes en la parte posterior de la lengua y la pared lateral derecha de la orofaringe, que se exacerbaron con la deglución y que aumentaron progresivamente en intensidad y frecuencia. Se orientó como el inicio de una neuralgia del nervio glosofaríngeo derecho. Se repitió la resonancia magnética cerebral con secuencia CISS (del inglés, constructive interference in steady state), que mostró un contacto arterial significativo entre la arteria cerebelosa superior derecha y el origen del V par craneal derecho, y de la arteria cerebelosa anteroinferior con el origen de los pares craneales bajos derechos. Ante un caso de neuralgia del nervio trigémino y neuralgia del nervio glosofaríngeo clásicas, concomitantes y refractarias, se planteó una doble descompresión microvascular en un tiempo como mejor opción terapéutica.\n\nEn marzo de 2021 se realizó una craniectomía retrosigmoidea derecha con exposición de la cisterna perimesencefálica y las cisternas basales. Se procedió a la liberación del V par craneal, y se apreció un íntimo contacto con la arteria cerebelosa superior en su parte sensitiva y adelgazamiento en la zona de entrada de la raíz nerviosa. Se procedió a la colocación de teflón entre la arteria cerebelosa superior y el V par craneal en todo su trayecto. Posteriormente, se exploró la cisterna basal y se apreció loop vascular de la arteria cerebelosa anteroinferior en íntimo contacto con el IX par craneal, donde se colocó teflón y sellante dural encima. El postoperatorio cursó sin incidencias, con resolución completa de la neuralgia del nervio trigémino y reducción >50% de la intensidad de los paroxismos en el territorio glosofaríngeo. A los dos años continúa sin paroxismos trigeminales y presenta <1 paroxismo/mes de intensidad tolerable en el territorio glosofaríngeo desencadenado con la deglución. El tratamiento farmacológico continúa en pauta descendente sin que ello haya supuesto la reaparición de los paroxismos.",
+        "gold_summary": "Mujer de 65 años con NT derecho (inicialmente en V2-V3) desde 2004 con control regular con carboxamidas. Diecisiete años después empeoraron los paroxismos en V2-V3, aparecieron también en V1 y en el territorio del nervio glosofaríngeo derecho (oído derecho y fosa amigdalar al hablar y deglutir). La resonancia magnética cerebral mostró contacto arterial significativo entre arteria cerebelosa superior (ACS) con origen del V par craneal derecho y de la arteria cerebelosa antero-inferior (AICA) con el origen de pares craneales bajos derechos. Se realizó DMV de ambos pares craneales en un mismo tiempo quirúrgico mediante craniectomía retrosigmoidea, y se procedió a la liberación del V par craneal, en contacto íntimo con la ACS, y del IX par craneal en contacto con la AICA derecha, para lo que se puso teflón entre ellas. La paciente tuvo una resolución inmediata de los paroxismos trigeminales y una mejoría considerable en intensidad y frecuencia de los glosofaríngeos. A los 2 años de la intervención continúa la desescalada de tratamiento neuromodulador con buena respuesta.",
+        "synthetic_summary": {
+            "B1": "A lady who is 65 years old had sharp pain on the right side of her face since 2004. The pain got worse after many years. She also had pain in her right ear and throat when she talked or swallowed.\n\nDoctors took pictures of her brain. They saw that some blood vessels were touching important nerves.\n\nShe had a surgery to gently move the blood vessels away from the nerves. The doctors put soft pads between them.\n\nAfter the surgery, her face pain went away right away. The ear and throat pain got much better.\n\nTwo years later, she is still doing well and needs less medicine.",
+            "B2": "**What Happened to the Patient?**  \nA 65-year-old woman had a condition called trigeminal neuralgia on the right side of her face since 2004. Trigeminal neuralgia causes sudden, sharp pain in parts of the face. At first, the pain was in two areas called V2 and V3. She was treated with medicines called carboxamides, which helped control the pain for many years.\n\n**How Did Her Condition Change?**  \nSeventeen years later, her pain got worse and spread to another area called V1. She also started having sharp pains in parts of her throat and ear on the right side. This new pain was caused by a problem with another nerve called the glossopharyngeal nerve, which affects the throat and tongue.\n\n**What Did the MRI Show?**  \nA special brain scan called an MRI found that two arteries (blood vessels) were pressing on the nerves causing the pain. One artery, called the superior cerebellar artery, was touching the trigeminal nerve. Another artery, called the anterior inferior cerebellar artery, was pressing on the glossopharyngeal nerve.\n\n**What Treatment Did She Receive?**  \nDoctors performed a surgery called microvascular decompression. This means they carefully moved the arteries away from the nerves to stop the pressure. They placed a small piece of soft material called Teflon between the arteries and nerves to keep them apart. The surgery was done through a small opening in the skull behind the ear.\n\n**What Were the Results?**  \nAfter surgery, the woman’s trigeminal nerve pain stopped right away. The pain in her throat and ear also got much better. Two years later, she still has very little pain and is reducing her medicines without problems.\n\n**Why Is This Important?**  \nThis case shows that when blood vessels press on nerves, it can cause severe pain. Surgery to separate the vessels from the nerves can help people who do not get better with medicines. It can improve their quality of life and reduce the need for strong drugs.",
+            "B3": "**Background**  \nA 65-year-old woman had been diagnosed in 2004 with right-sided trigeminal neuralgia (TN), initially affecting the V2 and V3 branches of the trigeminal nerve. Her pain was characterized by sudden, severe episodes triggered by typical stimuli. Over the years, she was managed with carbamazepine (a carboxamide anticonvulsant), but pain control remained challenging. Seventeen years later, in 2021, her symptoms worsened: the painful paroxysms intensified in the original V2-V3 areas, extended to the V1 territory, and new lancinating pain appeared in the right glossopharyngeal nerve (cranial nerve IX) distribution, involving the right ear and tonsillar fossa, especially during speaking and swallowing.\n\n**Key Findings**  \nA brain MRI with constructive interference in steady state (CISS) sequences revealed significant neurovascular contact: the right superior cerebellar artery (SCA) was closely compressing the root entry zone of the right trigeminal nerve (cranial nerve V), and the right anterior inferior cerebellar artery (AICA) was in intimate contact with the lower cranial nerves, including the glossopharyngeal nerve (cranial nerve IX). This neurovascular compression is a recognized cause of classical neuralgias affecting these cranial nerves.\n\n**Clinical Interpretation**  \nThe patient exhibited classical, concomitant, and medically refractory neuralgia of both the trigeminal and glossopharyngeal nerves. Pharmacological treatments, including carbamazepine, lamotrigine, and clonazepam, were insufficient, and she required intravenous infusions of phenytoin and lidocaine during severe exacerbations. The neurovascular compression identified by MRI suggested that microvascular decompression (MVD) surgery could be the most effective therapeutic option.\n\n**Next Steps and Outcome**  \nIn March 2021, the patient underwent a right retrosigmoid craniectomy to expose the perimesencephalic and basal cisterns. During surgery, the trigeminal nerve was found to be compressed and thinned at its root entry zone by the superior cerebellar artery. A Teflon pad was placed between the artery and nerve to relieve the compression. Similarly, the glossopharyngeal nerve was decompressed by inserting Teflon between it and the anterior inferior cerebellar artery, with additional dural sealant applied.\n\nPostoperatively, the patient experienced immediate and complete resolution of trigeminal neuralgia symptoms and a greater than 50% reduction in the intensity and frequency of glossopharyngeal neuralgia paroxysms. Two years after surgery, she remains free of trigeminal pain and has fewer than one mild glossopharyngeal pain episode per month, typically triggered by swallowing. Her neuromodulatory medications are being gradually reduced without recurrence of symptoms.\n\n**Summary**  \nThis case illustrates the successful use of simultaneous microvascular decompression of both the trigeminal and glossopharyngeal nerves to treat refractory, classical neuralgias caused by neurovascular compression. The procedure provided durable pain relief and allowed significant reduction of pharmacological treatment over a two-year follow-up period."
+        }
+    },
+    {
+        "article": "Hombre de 36 años, bisexual, en profilaxis antirretroviral de pre-exposición al HIV, sin antecedentes de viaje, que refirió haber asistido a un evento donde tuvo contactos con parejas ocasionales cuya identidad y antecedentes se desconocen. Diez días después comenzó con fiebre, odinofagia y dolor cervical por lo que consultó en varias oportunidades, hasta que a los siete días del inicio de los síntomas se internó por persistencia de los mismos a pesar del tratamiento antibiótico indicado. Al ingreso presentó exudado faríngeo, adenopatías cervicales bilaterales dolorosas y pápulas umbilicadas en escroto y pene y pústulas en cara de cinco días de evolución. Se realizó tomografía computarizada de cuello con contraste endovenoso que descartó colección, ecografía abdominal con leve hepatoesplenomegalia, e inició tratamiento empírico con ceftriaxona y azitromicina. Se tomaron muestras para cultivo, para serologías, y escarificación de dos lesiones de la cara que se enviaron al Laboratorio Nacional de Referencia, INEI-ANLIS Dr. Carlos G. Malbrán, para PCR de punto final para Orthopoxvirus, con resultado DETECTABLE, confirmando así el diagnóstico de viruela símica. La secuenciación arrojó un alto porcentaje de homología con secuencias del clado de África Occidental (MPV-ARG003-2022, Genbank_ID ON800897). Otros diagnósticos diferenciales fueron descartados. El paciente evolucionó con aparición de una úlcera en lengua y nuevas lesiones asincrónicas en glúteos, región perianal, inguinal derecha, umbilical, frontal, cuello, mano derecha y dorso de pie en un total de no más de 25. En el laboratorio se constató un aumento de transaminasas en 2.2 veces el valor normal, sin otros datos significativos.  Por persistencia del dolor cervical se solicitó nueva tomografía computarizada a los 14 días del inicio de los síntomas que evidenció adenomegalias con centro hipodenso de aspecto necrótico, que no requirieron drenaje quirúrgico. Al día 17 se realizó PCR en muestras de exudado de fauces y semen las que también resultaron positivas para virus de viruela símica. Se externó con franca mejoría clínica dos días después. El paciente dio su consentimiento informado escrito para la publicación de este informe de caso y las imágenes que lo acompañan.",
+        "gold_summary": "Se trata de un hombre joven, bisexual, en profilaxis antirretroviral de pre-exposición al HIV, cuya forma de presentación fue faringitis exudativa sin otra etiología documentada y adenopatías que evolucionaron a la necrosis, presencia de lesiones asincrónicas características en cara, cuello, abdomen, extremidades y genitales. El diagnóstico fue por detección de ADN viral por reacción en cadena de la polimerasa en lesiones de piel, exudado de fauces y semen. El compromiso faríngeo con presencia de exudado luego del descarte de otras infecciones, podría ser una rareza para la forma epidémica de la enfermedad. El hallazgo del virus en semen ya reportado en otras publicaciones no es suficiente aún para confirmar la vía sexual como forma de trasmisión.",
+        "synthetic_summary": {
+            "B1": "A young man got sick with a sore throat and bumps on his skin. The bumps were on his face, neck, belly, arms, and private parts. Doctors found a virus in his skin, throat, and body fluid. This virus made him feel bad. The sore throat with white stuff was not from other germs. The virus was also found in his body fluid, but we don’t know if it spreads that way. The man got better with care.",
+            "B2": "**Who Was Affected and What Happened**  \nThis report is about a young man, 36 years old, who is bisexual and takes medicine to prevent HIV infection before exposure. He got sick with a sore throat that had white patches (called exudate) and swollen, painful lymph nodes in his neck. These symptoms got worse and turned into tissue damage (necrosis). He also developed skin sores that appeared at different times on his face, neck, belly, arms, legs, and private areas.\n\n**How They Found Out What It Was**  \nDoctors tested samples from his skin sores, throat, and semen using a special lab test called PCR. PCR looks for the virus’s DNA, which is the virus’s genetic material. This test confirmed he had monkeypox virus. Finding the virus in his throat with white patches is unusual for monkeypox during this outbreak. Also, the virus was found in his semen, but scientists are still not sure if monkeypox spreads through sexual contact.\n\n**What This Means**  \nThis case shows that monkeypox can cause a sore throat with white patches and serious neck swelling, which is not common. It also raises questions about how the virus spreads, especially since it was found in semen. More research is needed to understand if sexual transmission is a main way the virus spreads.",
+            "B3": "**Background**  \nA 36-year-old bisexual man, who was taking pre-exposure antiretroviral prophylaxis against HIV and had no recent travel history, attended a social event where he had sexual contact with multiple casual partners of unknown health status. Ten days later, he developed fever, sore throat (odynophagia), and neck pain. Despite multiple medical consultations and antibiotic treatment, his symptoms persisted, leading to hospital admission seven days after symptom onset.\n\n**Key Findings**  \nUpon admission, the patient exhibited a pharyngeal exudate (a visible coating or discharge in the throat), painful bilateral cervical lymphadenopathy (swollen lymph nodes on both sides of the neck), umbilicated papules on the scrotum and penis, and pustular skin lesions on the face that had been evolving for five days. Imaging studies included a contrast-enhanced computed tomography (CT) scan of the neck, which ruled out abscess formation, and an abdominal ultrasound revealing mild enlargement of the liver and spleen (hepatoesplenomegaly). Empirical antibiotic therapy with ceftriaxone and azithromycin was initiated.\n\nSamples were collected for bacterial cultures, serological tests, and PCR (polymerase chain reaction) testing for Orthopoxvirus from skin lesion scrapings. The PCR test returned positive for Orthopoxvirus DNA, confirming the diagnosis of monkeypox (viruela símica). Viral genome sequencing showed a high degree of similarity to the West African clade of monkeypox virus (MPV-ARG003-2022, Genbank_ID ON800897). Other potential diagnoses were excluded.\n\nDuring hospitalization, the patient developed an ulcer on the tongue and new asynchronous (occurring at different times) skin lesions on the buttocks, perianal area, right groin, umbilical region, forehead, neck, right hand, and the dorsum of the foot, totaling fewer than 25 lesions. Laboratory tests revealed elevated liver transaminases at 2.2 times the upper limit of normal, without other significant abnormalities.\n\nDue to persistent neck pain, a follow-up CT scan at 14 days post-symptom onset showed enlarged lymph nodes with central areas of necrosis (tissue death), which did not require surgical drainage. On day 17, PCR testing of throat swabs and semen samples also detected monkeypox virus DNA. The patient’s clinical condition improved significantly, and he was discharged two days later.\n\n**Clinical Interpretation**  \nThis case illustrates a young bisexual man on HIV pre-exposure prophylaxis presenting primarily with exudative pharyngitis and cervical lymphadenopathy that progressed to necrosis, alongside characteristic asynchronous cutaneous lesions distributed across the face, neck, abdomen, extremities, and genitalia. The diagnosis was confirmed by detection of monkeypox viral DNA via PCR in skin lesions, throat exudate, and semen.\n\nThe presence of pharyngeal involvement with exudate, after excluding other infectious causes, may represent an uncommon manifestation in the current monkeypox epidemic. Although monkeypox virus DNA was found in semen—consistent with previous reports—this finding alone does not definitively establish sexual transmission as a primary route of infection.\n\n**Next Steps**  \nContinued clinical monitoring for resolution of lesions and symptoms is essential. Further research is needed to clarify the role of pharyngeal involvement in monkeypox and to determine the significance of viral presence in semen regarding transmission dynamics. Patient education on infection control and follow-up testing may be warranted to prevent further spread. The patient provided informed consent for publication of this case and associated images."
+        }
+    },
+    {
+        "article": "Paciente de sexo masculino de 23 años, natural de Itagüí - Colombia, antecedente familiar de muerte súbita de etiología no clara en abuelo a los 50 años, sin otros antecedentes familiares o personales de importancia. Venía en seguimiento externo por episodios sincopales a repetición con diagnóstico desde la infancia de disfunción del nodo sinusal sintomática por lo que se le implantó un marcapaso.\n\nDurante controles posteriores no hay reporte de deterioro de clase funcional hasta el año 2012 en Guayaquil-Ecuador. Durante su hospitalización se realiza el cambio de generador; en el primer mes postoperatorio presenta como complicación temprana una infección de bolsillo de marcapaso por lo que requirió el explante de la unidad generadora con posterior abandono de electrodo ventricular previamente implantado. Se realiza un nuevo implante de marcapaso en el lado contralateral sin complicaciones ni registro de nuevos eventos sincopales en los siguientes 10 años de seguimiento.\n\nSeis meses antes del ingreso presentaba deterioro de clase funcional NYHA III, sin otros síntomas y sin reportes de evaluaciones por servicio de electrofisiología desde el último implante de generador de marcapaso en 2012. Durante controles ambulatorios se reportó la suspensión del tratamiento con beta bloqueador debido a la pobre tolerancia.\n\nAl examen físico se encontró soplo sistólico en foco aórtico II/VI sin irradiación, no presentó signos de congestión central o periférica. Dentro de los laboratorios no se evidenció alteración en función renal, electrolítica ni del perfil hematológico. Se programó el marcapaso con evidencia de agotamiento de la batería de generador. Se realizó un ecocardiograma transtorácico donde se encontró hipertrofia concéntrica severa del septum interventricular a nivel medio ventricular, de 26 mm con gradiente intracavitario pico de 117 mmHg y movimiento sistólico anterior del velo mitral (SAM) el cual generaba una regurgitación mitral leve.\n\nFue evaluado por Heart Team, debido al score de riesgo de muerte súbita (16,8%) además de tener antecedentes familiares de muerte súbita considerando EUROSCORE II 0,67%; en cuanto a los electrodos abandonados previamente y la contraindicación de realización de resonancia magnética cardiaca, dado a la incompatibilidad del marcapaso, se realiza un estudio tomográfico y se consideró la realización de miectomía por sintomatología y variante documentada.\n\nFue programado para realización de miectomía medio ventricular por abordaje transapical con retiro de electrodos; se realizó la ventriculotomía izquierda en el ápex, con posterior resección del septum desde el parte medio ventricular hasta la base, con posterior retiro de electrodos adheridos a velo septal tricúspideo. No hubo complicaciones intraoperatorias y posteriormente se presentó disminución del gradiente intracavitario sin presencia del fenómeno SAM. Durante su estancia en Unidad de Cuidados Intensivos el paciente cursó con dos episodios documentados de taquicardia ventricular con inestabilidad hemodinámica por lo cual se le colocó un cardiodesfibrilador implantable (CDI) compatible con resonancia magnética (MRI) ST Jude sin presentar nuevos episodios de TV. El paciente cursó sin nuevas intercurrencias y se iniciaron los estudios ambulatorios de estudio genético debido a sus antecedente familiares.\n\nEl paciente presentó una evolución posoperatoria favorable luego del implante de CDI. En los estudios genéticos se encontró una variante, probablemente patogénica, en heterocigosis del FLNC, c 4636G>A consistente con miocardiopatía familiar hipertrófica tipo 26 autosómica dominante.\n\nActualmente, el paciente se encuentra en clase funcional I, sin arritmias evidenciadas en la telemetría y en tratamiento regular con Bisoprolol 5 mg. Se inició ampliación de estudio genético a familiares directos, sin embargo, debido al difícil acceso a servicios de salud su ejecución fue limitada.",
+        "gold_summary": "A continuación, se presenta el caso de un paciente sexo masculino de 23 años con diagnóstico de cardiomiopatía hipertrófica variante medio apical, en quien se documenta variante de la filamina C, ante la inadecuada respuesta y persistencia de sintomatología frente al manejo médico, se realizó el procedimiento de miectomía con abordaje transapical, con posterior mejoría de sintomatología clínica y obstrucción al tracto de salida.",
+        "synthetic_summary": {
+            "B1": "There is a young man who is 23 years old. His heart muscle is very thick in the middle part. This made it hard for his heart to work well. \n\nDoctors gave him medicine, but he still felt sick. So, they did a small surgery to help his heart. After the surgery, he felt better and his heart worked easier.",
+            "B2": "**What Happened to the Patient?**\n\nThis is the story of a 23-year-old man diagnosed with a heart condition called hypertrophic cardiomyopathy. This means the muscle in the middle and tip of his heart was too thick. Because of this, his heart had trouble pumping blood properly.\n\n**What Did the Doctors Do?**\n\nThe usual medicines did not help him enough, and he still had symptoms. So, the doctors decided to perform a surgery called a myectomy. In this surgery, they removed some of the thickened heart muscle through the tip of the heart (this is called a transapical approach). This helped reduce the blockage in his heart and made it easier for blood to flow.\n\n**What Was the Result?**\n\nAfter the surgery, the patient felt better and his heart worked more smoothly. This procedure improved his symptoms and helped open up the path for blood to leave the heart.",
+            "B3": "**Background**  \nThis case involves a 23-year-old man from Itagüí, Colombia, with a family history notable for sudden unexplained death in his grandfather at age 50. Since childhood, he experienced recurrent episodes of syncope (fainting) attributed to symptomatic sinus node dysfunction, for which a pacemaker was implanted. Over the years, he underwent pacemaker generator replacements and management of complications, including a pocket infection requiring removal and contralateral reimplantation. For about a decade, he remained free of syncope episodes.\n\nApproximately six months before his most recent hospital admission, the patient’s functional status deteriorated to New York Heart Association (NYHA) Class III, indicating marked limitation of physical activity due to symptoms. He had discontinued beta-blocker therapy because of poor tolerance. Physical examination revealed a mild systolic murmur at the aortic area without signs of heart failure. Laboratory tests showed no abnormalities in kidney function, electrolytes, or blood counts. Pacemaker interrogation revealed battery depletion.\n\n**Key Findings**  \nA transthoracic echocardiogram demonstrated severe concentric hypertrophy of the mid-ventricular septum measuring 26 mm, with a significant intracavitary pressure gradient of 117 mmHg. There was also systolic anterior motion (SAM) of the mitral valve leaflet causing mild mitral regurgitation. Due to the presence of abandoned pacemaker leads and contraindications for cardiac magnetic resonance imaging (MRI), a computed tomography (CT) scan was performed for further evaluation.\n\nThe patient’s calculated risk of sudden cardiac death was high (16.8%), compounded by his family history. The Heart Team decided on surgical intervention given his symptomatic status and documented mid-ventricular hypertrophic cardiomyopathy variant.\n\n**Clinical Interpretation**  \nThe diagnosis is hypertrophic cardiomyopathy (HCM), specifically the mid-apical variant, characterized by thickening of the heart muscle in the mid-portion of the left ventricle. This hypertrophy caused obstruction to blood flow and contributed to his symptoms. Genetic testing identified a likely pathogenic heterozygous variant in the FLNC gene (filamin C), which is associated with familial hypertrophic cardiomyopathy type 26, inherited in an autosomal dominant pattern.\n\n**Treatment and Outcome**  \nThe patient underwent a transapical mid-ventricular myectomy—a surgical procedure to remove the thickened septal muscle via an incision at the apex of the heart. During surgery, abandoned pacemaker leads attached to the septal leaflet of the tricuspid valve were also removed. The procedure successfully reduced the intracavitary gradient and eliminated the SAM phenomenon.\n\nPostoperatively, the patient experienced two episodes of hemodynamically unstable ventricular tachycardia (a dangerous rapid heart rhythm), prompting implantation of a magnetic resonance imaging-compatible implantable cardioverter defibrillator (ICD). Following ICD placement, no further arrhythmias were recorded. The patient’s functional status improved to NYHA Class I, indicating no limitation of physical activity.\n\n**Next Steps**  \nGenetic studies have been extended to first-degree relatives to identify other potentially affected family members, although access to genetic services remains limited. The patient continues on regular medical therapy with bisoprolol 5 mg daily and is monitored closely with telemetry, showing no arrhythmias to date.\n\n**Summary**  \nIn summary, this young man with familial hypertrophic cardiomyopathy of the mid-apical variant and a pathogenic FLNC gene mutation underwent successful surgical myectomy after inadequate response to medical management. Postoperative improvement in symptoms and obstruction was achieved, and prophylactic ICD implantation addressed his arrhythmic risk. Ongoing genetic evaluation of his family aims to improve early detection and management of this inherited condition."
+        }
+    },
+    {
+        "article": "Varón de 32 años, con antecedentes de infección por VIH en terapia anti-retroviral (carga viral indetectable y recuento de CD4 de 454 céls/mm3) y consumo de tabaco y drogas (marihuana, éxtasis y ketamina). Consultó en nuestra unidad de salud sexual por una historia de dos semanas de secreción uretral de aspecto mucoso con escaso ardor local, asociado a una úlcera eritematosa indurada en el surco balanoprepucial de 1,5 cm de diámetro, dolorosa y exudativa. Al examen físico presentaba una adenopatía inguinal izquierda de 2 cm, sensible a palpación, blanda, no adherida a planos profundos ni asociada a signos inflamatorios cutáneos. No presentaba fiebre ni otros síntomas asociados. En la anamnesis dirigida, refirió 20 parejas sexuales hombres en el último año, con relaciones sexuales orales y anales insertivas y receptivas, con uso ocasional de preservativo. No tenía antecedente de viajes fuera de Chile. Cuatro semanas antes del inicio de los síntomas, había tenido un contacto sexual de riesgo sin preservativo con una pareja contactada mediante una aplicación de telefonía móvil. Con el diagnóstico presuntivo de una sífilis primaria y uretritis en estudio, se tomaron muestras de sangre y secreción uretral para estudio microbiológico. Por la conducta sexual de alto riesgo, se tomó también un hisopado anorrectal para tinción de Gram y cultivo. De acuerdo con la norma vigente en Chile, se administraron tres dosis de 2,4 millones de UI de penicilina benzatina intramuscular separadas por una semana, además de 250 mg de ceftriaxona intramuscular y 1 g de azitromicina oral, ambas por una vez. El estudio de laboratorio confirmó el diagnóstico de sífilis, con un VDRL (Venereal disease research laboratory) reactivo con dilución de 1:2 y MHA-TP (Microhemagglutination assay for antibody to Treponema pallidum) reactivo. La tinción de Gram y los cultivos de secreción uretral (agar sangre y Thayer Martin) fueron negativos. La muestra anorrectal mostró escasos diplococos gramnegativos en la tinción de Gram, con desarrollo abundante de N. meningitidis y microbiota comensal en el cultivo corriente. La identificación bacteriana se realizó a través de espectrometría de masas MALDI-TOF MS. El paciente evolucionó favorablemente, sin secreción uretral y con regresión de la lesión ulcerada genital y la adenopatía inguinal a las dos semanas de seguimiento. Las tinciones de Gram y los cultivos de control de secreción uretral, faríngea y anorrectal resultaron negativos. Se citó al contacto sexual reciente para estudio y tratamiento. Sin embargo, éste se encontraba asintomático y los cultivos faríngeo, anorrectal y uretral realizados fueron negativos.",
+        "gold_summary": "Presentamos el caso de un HSH con infección por VIH, que consultó por un cuadro de uretritis y sifilis primaria, en el cual se aisló N. meningitidis en una muestra anorectal. Fue tratado en forma empírica con ceftriaxona y azitromicina, realizándose un cultivo de control post-tratamiento que fue negativo.",
+        "synthetic_summary": {
+            "B1": "A man with a virus called HIV felt sick in his private parts. He had a sore and some pain. Doctors gave him medicine to help him get better. They checked him again after the medicine. The tests showed he was all better.",
+            "B2": "**What Happened:**  \nA 32-year-old man who has HIV and takes medicine for it went to a sexual health clinic. He had symptoms of urethritis, which means inflammation or infection of the tube that carries urine out of the body. He also had a sore on his penis that looked like a primary syphilis ulcer. Syphilis is a sexually transmitted infection caused by bacteria.\n\n**What They Found:**  \nTests showed he had syphilis. They also took a sample from his anus and found a type of bacteria called *Neisseria meningitidis*. This bacteria usually lives in the nose and throat but can sometimes be found in other places. The doctors tested his urine and throat samples too, but those were negative for infection.\n\n**How They Treated Him:**  \nThe doctors gave him antibiotics called ceftriaxone and azithromycin to treat the infections. After treatment, follow-up tests showed no signs of infection, and his symptoms got better.\n\n**What This Means:**  \nThis case shows that people with HIV and risky sexual behaviors can have more than one infection at the same time. It is important to test for different bacteria and treat them properly. The presence of *Neisseria meningitidis* in the anus is unusual but can happen. Early diagnosis and treatment help patients recover and prevent spreading infections to others.",
+            "B3": "Background  \nA 32-year-old man who has sex with men (MSM) and is living with HIV—well-controlled on antiretroviral therapy with an undetectable viral load and a CD4 count of 454 cells/mm³—presented with a two-week history of mucous urethral discharge accompanied by mild local burning. He also had a painful, indurated (firm) erythematous ulcer measuring 1.5 cm located in the balanopreputial sulcus (the groove between the glans and foreskin of the penis). Physical examination revealed a tender, soft, 2 cm left inguinal lymph node that was not fixed to deeper tissues and showed no overlying skin inflammation. The patient denied fever or other systemic symptoms. His sexual history included 20 male partners in the past year, engaging in oral and anal sex (both insertive and receptive) with occasional condom use. He reported a recent high-risk sexual encounter without condom use four weeks prior, with a partner met through a mobile application. He had no history of travel outside Chile.\n\nKey Findings  \nBased on the clinical presentation, primary syphilis and urethritis were suspected. Blood and urethral discharge samples were collected for microbiological testing, and due to his high-risk sexual behavior, an anorectal swab was also obtained for Gram staining and culture. Laboratory results confirmed syphilis with reactive VDRL (Venereal Disease Research Laboratory) at a dilution of 1:2 and reactive MHA-TP (Microhemagglutination assay for antibodies to Treponema pallidum). Gram stain and cultures of urethral secretions were negative for common pathogens. The anorectal sample showed few gram-negative diplococci on Gram stain, and culture grew abundant Neisseria meningitidis along with normal commensal flora. Bacterial identification was performed using MALDI-TOF mass spectrometry, a precise technique for microbial identification.\n\nClinical Interpretation  \nThe patient was empirically treated according to Chilean guidelines with three weekly intramuscular doses of 2.4 million units of benzathine penicillin for syphilis, a single intramuscular dose of 250 mg ceftriaxone, and a single oral dose of 1 g azithromycin targeting potential urethritis pathogens. Following treatment, the patient showed clinical improvement with resolution of urethral discharge, healing of the genital ulcer, and regression of the inguinal lymphadenopathy within two weeks. Follow-up Gram stains and cultures from urethral, pharyngeal, and anorectal sites were negative. The recent sexual contact was also evaluated and treated, although he remained asymptomatic and had negative cultures from pharyngeal, anorectal, and urethral sites.\n\nNext Steps  \nThis case highlights the importance of considering Neisseria meningitidis as a potential colonizer or pathogen in anorectal samples from MSM with urethritis and syphilis, especially in the context of high-risk sexual behavior and HIV infection. Continued surveillance and appropriate microbiological testing are essential for accurate diagnosis and effective treatment. Sexual partners should be promptly evaluated and treated to prevent reinfection and further transmission."
+        }
+    },
+    {
+        "article": "Un paciente hispanoparlante de 63 años de edad se presentó en el hospital como una emergencia con inicio repentino de dificultad respiratoria severa, palpitaciones y sudoración profusa. Estaba en su estado habitual de salud y podía deambular con actividades independientes de la vida diaria hasta 30 minutos antes de su llegada a la sala de urgencias. Tenía un historial de 20 años de hipertensión, un historial de 15 años de diabetes mellitus, enfermedad de la arteria coronaria que requería la inserción de un stent de la arteria coronaria cinco años antes, un historial de diez años de insuficiencia cardiaca de la clase II de la New York Heart Association (NYHA) con una fracción de eyección reducida (EF) del 35 %, enfermedad renal crónica (CKD) en estadio 3B. Al ingresar en el hospital, sus medicamentos incluían carvedilol (25 mg dos veces al día), lisinopril (20 mg diario), espironolactona (25 mg diario), furosemida (20 mg diario), insulina glargina (20 unidades al acostarse), inyección de insulina lispro (7 unidades tres veces al día), atorvastatina (40 mg diario), y aspirina (81 mg diario), sin alergias a medicamentos conocidas.\n\nAl examen, su presión arterial era de 205/110 mmHg, su frecuencia respiratoria de 29 respiraciones/min, su frecuencia cardíaca de 118 latidos/min, la oximetría de pulso era de 82% (en aire ambiente) y su temperatura de 36.2°C. Su peso era de 72 kg y su estatura de 68 pulgadas, lo que resultó en un índice de masa corporal (IMC) de 24.13 kg/m2. Al examen físico, el paciente estaba en grave dificultad respiratoria, sudaba y no podía hablar con claridad. Su presión venosa yugular era elevada, como se muestra por la distensión de la vena yugular (3+). Al auscultar el tórax, se observaron crepitaciones bilaterales en todos los campos pulmonares. La auscultación cardíaca fue notable por un galope con una frecuencia regular y un murmullo sistólico 3/6 que se oía en la línea medioclavicular izquierda, al nivel del quinto espacio intercostal. El punto de impulso cardíaco máximo se desplazó hacia la izquierda (en la línea medioaxilar anterior) y no se observó distensión abdominal ni ascitis, con edema de los miembros inferiores (1+) hasta el nivel de la mitad de la pantorrilla.\n\nEl paciente fue trasladado a la zona de reanimación cardiopulmonar (RCP), donde se midieron los gases sanguíneos en el aire y se solicitaron pruebas de laboratorio. El paciente fue tratado con oxígeno al 100% utilizando una máscara no reanadora y se le colocó en posición de 90°, lo que produjo una mejora en la oximetría de pulso, que aumentó hasta el 90%. Un electrocardiograma (ECG) mostró taquicardia sinusal, depresión del ST del conductor lateral (de 1 mV), desviación del eje izquierdo e hipertrofia del ventrículo izquierdo. Se obtuvo una radiografía de tórax portátil que fue notable por una silueta cardiaca agrandada, señal de asta de ciervo de desviación venosa pulmonar del lóbulo superior (cefalización), y líneas B de Kerley, que indican edema intersticial.\n\nAunque se solicitaron pruebas de laboratorio, debido a que el paciente estaba gravemente enfermo y no se podía demorar el tratamiento, se inició un tratamiento inicial basado en los hallazgos clínicos, el historial clínico, el ECG, los gases arteriales en sangre y los hallazgos de rayos X. En vista de los hallazgos de las investigaciones iniciales y la ausencia de fiebre, se descartó la neumonía y se realizó un diagnóstico de edema pulmonar cardiogénico hipertensivo. Se inició un tratamiento intravenoso (IV) con nitroglicerina, comenzando a 30 mcg/min y aumentando en 15 mcg/min cada 3 minutos, con oximetría de pulso continua y monitoreo de los signos vitales cada 3 minutos. Después de 18 minutos, se tituló la nitroglicerina hasta 120 mcg/min y su presión arterial disminuyó a 148/82 mmHg, su presión arterial sistólica se redujo en un 29%, su presión arterial diastólica se redujo en un 25%, y su frecuencia cardíaca disminuyó a 87 latidos por minuto. Se hizo una rápida mejora clínica y el paciente pudo comunicarse con oraciones completas y pudo respirar sin el uso de músculos accesorios. La oximetría de pulso mostró una saturación de oxígeno >97%, y la suplementación de oxígeno continuó con el uso de una cánula nasal a 3 L/min y la medición de la oximetría de pulso del paciente fue >96%.\n\nDespués de 25 minutos, el paciente fue tratado con enalapril (2,5 mg IV) combinado con furosemida (20 mg IV). La nitroglicerina se redujo a una tasa de 10 mcg/min cada 5 minutos hasta que se interrumpió, seguido de una dosis oral de isosorbida dinitrato (30 mg). Después de la estabilización clínica completa, los resultados de los laboratorios mostraron un recuento de glóbulos blancos (WBC) de 11,43 × 109/uL, hemoglobina de 10,9 g/dl, hematocrito de 31,8%, plaquetas de 74 × 109/L, sodio de 144 mmol/L, potasio de 3,9 mmol/L, cloruro de 107 mmol/L, dióxido de carbono (CO2) de 25 mmol/L, nitrógeno ureico en sangre (BUN) de 27 mg/dL, creatinina de 1,4 mg/dL, péptido natriurético cerebral (BNP) de 3,452 pg/ml, y troponina I <0,05 ng/ml. Las mediciones de gases en sangre en aire incluyeron pH de 7,381, pCO2 de 44,8 mmHg, pO2 de 57 mmHg, HCO3 de 25,8 mmol/L, y saturación de oxígeno de 84%.\n\nSe evaluó al paciente para detectar la presencia de una posible embolia pulmonar (EP) subyacente, utilizando los criterios de estratificación de riesgo de EP de Wells, y se lo estratificó como de bajo riesgo, con una evaluación posterior con un nivel de dímero D de 340 ng/ml, que se interpretó como negativo. La evaluación para detectar hipertiroidismo mostró un valor normal de la medición ultrasensible del ensayo de la hormona estimulante de la tiroides en plasma (usTSH) de 2,56 μU/mL y tiroxina libre (T4) de 6,87 μU/mL.\n\nEl paciente fue admitido en la sala de hospital de medicina interna con un diagnóstico de edema pulmonar cardiogénico hipertensivo y fue dado de alta 48 horas después. Al momento del alta hospitalaria, su medicación incluía furosemida (40 mg diarios), carvedilol (12.5 mg dos veces al día), sacubitril/valsartan (24 mg/26 mg dos veces al día), espironolactona (25 mg diarios) e isosorbida mononitrato (60 mg diarios). El paciente fue sometido a seguimiento semanal por su cardiólogo, quien optimizó la terapia medicinal. No se registraron visitas a urgencias ni hospitalizaciones, al menos durante los siguientes 60 días.\n\nMH - Insuficiencia cardiaca/*complicaciones\nMH - Humanos\nMH - Hipertensión/*complicaciones\nMH - Infusiones, intravenosas\nMH - Hombre\nMH - Edad Media\nMH - Nitroglicerina/*administración y dosificación\nMH - Edema pulmonar/*terapia farmacológica/etiología\nMH - Insuficiencia respiratoria/*terapia farmacológica/etiología\nMH - Agentes vasodilatadores/*administración y dosificación\n",
+        "gold_summary": "Paciente: Hombre, 63 años\n\nDiagnóstico final: Edema pulmonar cardiovenoso hipertensivo\n\nSíntomas: falta de aire\n\nMedicación: —\n\nProcedimiento clínico: —\n\nEspecialidad: Medicina general e interna\n\nUn hombre hispano de 63 años con antecedentes de hipertensión, enfermedad de las arterias coronarias, insuficiencia cardiaca con una fracción de eyección reducida del 35 %, enfermedad renal crónica (ERC) y diabetes mellitus, se presentó como una emergencia con disnea aguda y grave. El paciente fue tratado inicialmente con 100 % de oxígeno suplementario y nitroglicerina intravenosa (IV) en dosis altas (30 mcg/min), que se ajustó cada 3 minutos, aumentando en 15 mcg/min hasta que se alcanzó una dosis de 120 mcg/min. Después de 18 minutos de terapia agresiva, la condición del paciente mejoró y ya no necesitaba ventilación mecánica.\n",
+        "synthetic_summary": {
+            "B1": "A man, 63 years old, had trouble breathing very badly. He felt very sick and came to the hospital fast.\n\nThe doctors gave him special air to help him breathe. They also gave him medicine through a tiny tube in his arm.\n\nThe medicine helped his heart and made him feel better soon. After a little while, he could breathe easier and talk again.",
+            "B2": "**Patient Overview**  \nA 63-year-old Hispanic man came to the hospital suddenly having a hard time breathing. He had a history of high blood pressure, heart artery disease, heart failure with a weak heart pump (his heart’s ejection fraction was 35%, which means his heart was pumping less blood than normal), chronic kidney disease, and diabetes.\n\n**What Happened**  \nBefore arriving at the hospital, he was able to do daily activities but then quickly developed severe shortness of breath, fast heartbeat, and heavy sweating. When doctors examined him, they found his blood pressure was very high, his breathing was fast, and his oxygen levels were low. His heart and lungs showed signs of stress and fluid buildup.\n\n**How They Treated Him**  \nDoctors gave him oxygen at 100% to help him breathe better. They also started a medicine called nitroglycerin through an IV (a tube in his vein). Nitroglycerin helps open blood vessels and lower blood pressure. They began with a low dose and increased it every few minutes until they reached a higher dose. After about 18 minutes, his breathing and heart rate improved a lot, and he no longer needed a breathing machine.\n\n**What This Means**  \nThe patient was diagnosed with heart-related lung swelling, called cardiogenic pulmonary edema, caused by his high blood pressure and heart failure. Quick treatment with oxygen and nitroglycerin helped reduce the fluid in his lungs and improved his condition. After stabilizing, he was given other medicines to support his heart and kidneys. He stayed in the hospital for two days and then went home with follow-up care. This case shows how important fast treatment is for severe heart and lung problems.",
+            "B3": "**Background**  \nA 63-year-old Hispanic man with a complex medical history presented to the hospital as an emergency case due to sudden, severe shortness of breath (dyspnea), palpitations, and profuse sweating. His past medical conditions included longstanding hypertension (20 years), coronary artery disease treated with a stent five years prior, type 2 diabetes mellitus (15 years), chronic kidney disease stage 3B, and chronic heart failure classified as New York Heart Association (NYHA) class II with a reduced left ventricular ejection fraction (LVEF) of 35%. Prior to this acute episode, he was independent in daily activities and ambulatory.\n\n**Key Findings on Presentation**  \nUpon arrival, the patient exhibited markedly elevated blood pressure (205/110 mmHg), rapid breathing (29 breaths per minute), and a fast heart rate (118 beats per minute). His oxygen saturation was critically low at 82% on room air. Physical examination revealed severe respiratory distress with inability to speak clearly, elevated jugular venous pressure indicating increased central venous pressure, bilateral crackles throughout the lungs consistent with pulmonary edema, a third heart sound (gallop rhythm), and a systolic murmur (grade 3/6) heard at the left midclavicular line. The point of maximal cardiac impulse was displaced laterally, suggesting cardiac enlargement. Mild lower extremity edema was also noted.\n\nElectrocardiogram (ECG) showed sinus tachycardia, left ventricular hypertrophy, left axis deviation, and ST segment depression in lateral leads. Chest X-ray demonstrated an enlarged cardiac silhouette, pulmonary venous congestion (cephalization), and Kerley B lines indicative of interstitial pulmonary edema. Arterial blood gases confirmed hypoxemia with a partial pressure of oxygen (pO2) of 57 mmHg and oxygen saturation of 84%.\n\n**Clinical Interpretation**  \nThe clinical picture and diagnostic tests led to a diagnosis of hypertensive cardiogenic pulmonary edema, a condition where elevated blood pressure and impaired heart function cause fluid accumulation in the lungs. Infectious causes such as pneumonia were ruled out due to absence of fever and clinical signs. The patient’s acute respiratory failure was attributed to worsening heart failure exacerbated by uncontrolled hypertension.\n\n**Treatment and Response**  \nImmediate management included administration of 100% oxygen via a non-rebreather mask and positioning the patient upright at 90 degrees to improve breathing. Intravenous nitroglycerin was initiated at 30 micrograms per minute and titrated upward by 15 micrograms every three minutes to a maximum of 120 micrograms per minute. This vasodilator therapy effectively reduced preload and afterload, leading to a rapid decrease in blood pressure (to 148/82 mmHg) and heart rate (to 87 beats per minute). Within 18 minutes, the patient’s respiratory distress markedly improved, allowing him to speak in full sentences and breathe without accessory muscle use. Oxygen saturation increased to over 97%, and supplemental oxygen was then maintained via nasal cannula at 3 liters per minute.\n\nSubsequently, intravenous enalapril (an angiotensin-converting enzyme inhibitor) and furosemide (a loop diuretic) were administered to further reduce cardiac workload and remove excess fluid. Nitroglycerin infusion was gradually tapered and replaced with oral isosorbide dinitrate. Laboratory tests after stabilization showed elevated brain natriuretic peptide (BNP) levels consistent with heart failure, mild anemia, and stable renal function. Troponin levels were normal, indicating no acute myocardial injury. Evaluation for pulmonary embolism and thyroid dysfunction was negative.\n\n**Next Steps and Outcome**  \nThe patient was admitted to the internal medicine ward with a diagnosis of hypertensive cardiogenic pulmonary edema. His medication regimen was optimized before discharge 48 hours later, including increased doses of diuretics, beta-blockers, angiotensin receptor-neprilysin inhibitors (sacubitril/valsartan), mineralocorticoid receptor antagonists (spironolactone), and long-acting nitrates. Follow-up care with cardiology was arranged on a weekly basis to monitor and adjust therapy. During the subsequent 60 days, the patient remained stable without further emergency visits or hospitalizations.\n\n---\n\nThis case illustrates the critical importance of rapid recognition and aggressive management of hypertensive cardiogenic pulmonary edema in patients with advanced heart failure and multiple comorbidities. Early use of intravenous vasodilators and oxygen therapy can quickly reverse respiratory failure and improve clinical outcomes."
+        }
+    },
+    {
+        "article": "Historial clínico\nUn niño de 12 años se presentó en nuestro hospital con un mes de historia de sensación de cuerpo extraño y una masa conjuntival pedunculada carnosa que creció con el tiempo. No había historia de trauma o lesiones similares en el otro lado del cuerpo. Se descubrió una masa pedunculada carnosa rosácea de 15 mm de la conjuntiva palpebral derecha durante un examen oftalmológico. La agudeza visual estaba dentro de los límites normales. Se diagnosticó al niño como papiloma de células escamosas pedunculadas y se le realizó una biopsia excisional de la lesión.\n\nHallazgos macroscópicos y microscópicos\nRecibimos un fragmento de tejido blanco grisáceo, pequeño, firme, ovoide, fijado en formalina, de 1,5 x 1 cm, para su análisis patológico. En las secciones microscópicas se encontró una lesión poliopóidea hiperplásica con múltiples quistes globulares en la submucosa conjuntival, junto con una importante infiltración inflamatoria constituida por linfocitos, células plasmáticas y neutrófilos, así como enormes esporangios de paredes gruesas con numerosas endosporas. Las endosporas se liberaron después de que algunos de los esporangios maduros se rompieran. La rinosporidiosis conjuntival se diagnosticó histopatológicamente. No hubo recurrencia ni signo de rinosporidiosis en el ojo ni en ninguna otra área del cuerpo en el último examen del paciente, que fue 7 meses después de la escisión quirúrgica.\n",
+        "gold_summary": "Un niño de 12 años con una masa conjuntival pedunculada carnosa fue llevado al Centro Médico de la Universidad de Jimma con un historial de un mes de sensación de cuerpo extraño. Al paciente se le diagnosticó un papiloma pedunculado de células escamosas y se le realizó una biopsia excisional de la lesión. Se encontró que la masa era una lesión polipoide hiperplásica con numerosos quistes globulares dentro de la submucosa conjuntival, rodeados por un infiltrado inflamatorio pesado de linfocitos, células plasmáticas y neutrófilos, así como grandes esporas de paredes gruesas con numerosas endosporas en secciones microscópicas. Se diagnosticó histopatológicamente rinosporidiosis conjuntival.\n",
+        "synthetic_summary": {
+            "B1": "A 12-year-old boy had a bump in his eye. It felt like something was there for one month.\n\nDoctors took out the bump to look at it closely. They found tiny parts inside that showed an infection.\n\nThe boy got better after the bump was taken out. The doctors will keep checking to make sure he stays well.",
+            "B2": "**What Happened:**  \nA 12-year-old boy went to the hospital because he felt like something was stuck in his eye for about a month. Doctors found a pink, soft lump growing on the inside of his right eyelid. His vision was normal. At first, they thought it was a type of growth called a \"pedunculated squamous papilloma,\" which means a small, finger-like bump made of skin cells.\n\n**What They Did:**  \nThe doctors removed the lump completely and sent it to the lab for testing. A biopsy, which is when a small piece of tissue is taken for closer study under a microscope, was done to understand what the lump really was.\n\n**What They Found:**  \nUnder the microscope, the lump was not just a simple growth. It was a polyp-like lesion, meaning it looked like a small bump with many tiny cysts (small fluid-filled sacs) inside the tissue beneath the eye’s surface. There were many immune cells around it, such as lymphocytes, plasma cells, and neutrophils—these cells help fight infections. The key finding was the presence of large thick-walled sporangia, which are structures that hold spores. Spores are tiny particles that some organisms use to reproduce. These sporangia contained many endospores, which are spores inside the sporangia. This showed that the lump was caused by an infection called conjunctival rhinosporidiosis, which is a rare disease caused by a microorganism that infects the eye’s lining.\n\n**What It Means:**  \nThe boy’s eye lump was actually an infection, not just a harmless growth. After the lump was removed, the boy was checked again 7 months later. There were no signs that the infection came back or spread to other parts of his body. This means the treatment worked well.",
+            "B3": "Background  \nA 12-year-old boy presented with a one-month history of a sensation of a foreign body in his right eye, accompanied by a progressively enlarging, fleshy, pedunculated (stalk-like) conjunctival mass. There was no history of trauma or similar lesions elsewhere. Visual acuity was normal. Initially, the lesion was clinically diagnosed as a pedunculated squamous cell papilloma, and an excisional biopsy was performed to remove the mass.\n\nKey Findings  \nGross examination revealed a small, firm, oval-shaped tissue fragment measuring 1.5 x 1 cm. Microscopic analysis showed a hyperplastic polypoid lesion characterized by multiple globular cysts located within the submucosal layer of the conjunctiva. The lesion was accompanied by a dense inflammatory infiltrate composed of lymphocytes, plasma cells, and neutrophils. Notably, numerous large thick-walled sporangia (structures containing spores) were observed, each containing many endospores. Some mature sporangia had ruptured, releasing these endospores. These histopathological features confirmed the diagnosis of conjunctival rhinosporidiosis, a chronic granulomatous infection caused by the aquatic protist Rhinosporidium seeberi.\n\nClinical Interpretation  \nAlthough initially suspected to be a squamous papilloma, the lesion was identified as rhinosporidiosis based on its distinctive microscopic appearance. This infection is rare and typically presents as polypoid masses on mucous membranes, including the conjunctiva. The inflammatory response and presence of sporangia with endospores are hallmark features. The patient showed no signs of recurrence or spread to other body areas during follow-up seven months after surgical excision.\n\nNext Steps  \nContinued clinical monitoring is recommended to detect any potential recurrence early. Given the localized nature of the lesion and successful complete excision, prognosis is favorable. Patient education about avoiding exposure to stagnant water sources, which are implicated in the transmission of Rhinosporidium seeberi, may help prevent reinfection."
+        }
+    },
+    {
+        "article": "Presentamos el caso clínico de un varón de quince años, sin antecedentes médicos ni intervenciones previas, que acude al servicio de urgencias de pediatría con clínica de vómitos y dolor abdominal epigástrico de cuatro días de evolución, manteniéndose afebril durante la evolución del cuadro.\n\nInicialmente fue manejado como gastroenteritis, pero ante la ausencia de mejoría, con persistencia del dolor abdominal de tipo cólico a nivel epigástrico y de los vómitos de aspecto bilioso, acude a urgencias para nueva valoración.\n\nA la exploración física el paciente presentaba aceptable estado general, se encontraba afebril, con signos leves de deshidratación. El abdomen se encontraba distendido, sin datos de peritonismo y con ruidos hidroaéreos disminuidos. La analítica no presentaba hallazgos significativos, realizándose una radiografía de abdomen con hallazgos sugestivos de obstrucción intestinal.\n\nDada la evolución se decide realizar una tomografía computarizada urgente, en la que se observó presencia de ascitis e importante dilatación de asas de intestino delgado, sugiriendo la interposición de un asa de intestino delgado en el inicio de la transcavidad de los epiplones, con cambio de calibre a nivel del hiato de Winslow.\n\nSe realizó intervención quirúrgica urgente, realizando inicialmente una laparoscopia exploradora. Se observaban asas de intestino delgado dilatadas, e íleon terminal, ciego y colon ascendente de calibre normal pero localizados en hipocondrio derecho, con el ciego muy móvil y sin presentar adherencias al espacio parietocólico derecho. Siguiendo proximalmente el íleon terminal, se observaron asas de intestino delgado de distinto calibre desde la profundidad de la teórica localización del hiato de Winslow. Se consiguió traccionar de ciego e íleon terminal hasta desplazarlos a fosa iliaca derecha, pero sin llegar a identificar correctamente el punto de cambio de calibre, ya que la interposición del borde inferior del hígado y la distensión de asas de intestino delgado dificultaban la técnica. Se intentó mejorar la visualización mediante punción percutánea de un asa dilatada para vaciar el gas, sin mejoría. Para asegurar la resolución del cuadro obstructivo se decidió realizar una laparotomía media supraumbilical. Al acceder a cavidad se evidenciaba el cambio de calibre en íleon, a unos 40 centímetros de la válvula ileocecal, con signos compatibles con herniación de un tramo de unos cinco centímetros de íleon a través de hiato de Winslow. En ambos extremos del asa herniada observamos la impronta congestiva del hiato sobre el asa (Fig. 3). Se identificó el hiato de Winslow, de calibre normal, por lo que no se realizó ninguna técnica preventiva para disminuir el riesgo de recidiva.\n\nDurante los primeros días del postoperatorio el paciente presentó un íleo paralítico, pudiendo retirar la sonda nasogástrica a los cinco días de la cirugía e iniciando tolerancia oral con buena respuesta. Simultáneamente desarrolló una colección pélvica que se manejó de forma conservadora con antibióticos, con buena evolución. Finalmente, el paciente fue dado de alta a los diez días de la intervención, con tránsito conservado, manteniéndose afebril y con buen estado general.\n\nActualmente el paciente está en seguimiento en consultas externas de cirugía pediátrica.",
+        "gold_summary": "Presentamos el caso clínico de un varón adolescente de 15 años sin antecedentes quirúrgicos previos, con clínica de dolor abdominal y vómitos, en el que la tomografía computarizada sugería un cuadro de obstrucción intestinal a causa de hernia interna a nivel del hiato de Winslow. Precisó de intervención quirúrgica mediante laparoscopia exploradora, reconvertida por mala visualización a laparotomía media supraumbilical, para reducción del asa de íleon herniada. Esta presentaba buen aspecto y no fue necesaria la resección intestinal. No se realizó ninguna técnica preventiva para disminuir el riesgo de recidiva. Postoperatoriamente, el paciente presentó una colección pélvica manejada de manera conservadora con antibióticos. Actualmente se encuentra en seguimiento en consultas externas de cirugía pediátrica.",
+        "synthetic_summary": {
+            "B1": "A boy, 15 years old, had belly pain and throwing up. Doctors found a part of his tummy was stuck inside. He needed an operation to fix it. The stuck part looked okay, so they did not need to take it out. After the operation, he had a little problem but got medicine and felt better. Now, the doctors are checking on him to make sure he stays well.",
+            "B2": "**What Happened:**  \nA 15-year-old boy came to the hospital with stomach pain and vomiting. Scans showed that part of his small intestine was stuck in a rare internal hernia near an area called the \"hiatus of Winslow.\" This caused a blockage in his intestines.\n\n**What Doctors Did:**  \nDoctors first tried to fix the problem using a small camera and tools through tiny cuts (called laparoscopy). But because they couldn’t see well enough, they made a larger cut in his belly (called laparotomy) to fix the hernia. They carefully moved the stuck part of the intestine back to its normal place. The intestine looked healthy, so they did not need to remove any part of it. They also did not do anything extra to stop the hernia from happening again.\n\n**After Surgery:**  \nAfter the operation, the boy had some trouble with his intestines moving normally, but this improved after a few days. He also developed a small collection of fluid in his pelvis, which was treated successfully with antibiotics. He recovered well and was sent home 10 days later.\n\n**Current Status:**  \nThe boy is now being checked regularly by pediatric surgeons to make sure he continues to heal well.",
+            "B3": "**Background**  \nThis case involves a 15-year-old male adolescent with no prior surgical history who presented with abdominal pain and vomiting. Initial evaluation raised suspicion of intestinal obstruction caused by an internal hernia through the foramen of Winslow (also known as the epiploic foramen), a rare anatomical passage connecting the greater and lesser sacs of the abdomen.\n\n**Key Findings**  \nComputed tomography (CT) imaging revealed signs consistent with small bowel obstruction, specifically showing dilated loops of small intestine and ascites, with evidence suggesting that a segment of ileum (the final portion of the small intestine) had herniated through the foramen of Winslow. The patient’s clinical presentation included persistent colicky epigastric pain and bilious vomiting, but he remained afebrile and showed only mild dehydration.\n\n**Clinical Intervention**  \nAn urgent surgical approach was undertaken, beginning with exploratory laparoscopy. During this procedure, dilated small bowel loops were observed, and the cecum and terminal ileum were found abnormally positioned in the right upper abdomen but without adhesions. Due to limited visualization caused by bowel distension and anatomical constraints, the surgery was converted to an open laparotomy via a supraumbilical midline incision. This allowed direct identification of the herniated ileal segment approximately 40 centimeters from the ileocecal valve. The herniated bowel appeared viable, showing congestion at the edges where it was compressed by the foramen, but no intestinal resection was necessary. The foramen of Winslow was of normal size, and no additional surgical procedures were performed to prevent recurrence.\n\n**Postoperative Course and Follow-Up**  \nIn the immediate postoperative period, the patient developed a paralytic ileus (temporary cessation of bowel motility), which resolved by the fifth day, allowing removal of the nasogastric tube and initiation of oral intake. Additionally, he developed a pelvic fluid collection that was successfully managed conservatively with antibiotic therapy. The patient’s condition improved steadily, and he was discharged ten days after surgery in good general health, afebrile, and with normal bowel function. He continues to be monitored in pediatric surgery outpatient clinics.\n\n**Summary**  \nThis case illustrates a rare cause of small bowel obstruction due to internal herniation through the foramen of Winslow in an adolescent without prior abdominal surgery. Prompt imaging and surgical intervention allowed successful reduction of the hernia without bowel resection. Conservative management of postoperative complications resulted in favorable recovery. Ongoing follow-up is essential to monitor for potential recurrence or late complications."
+        }
+    },
+    {
+        "article": "Un niño de 23 meses de edad con encefalopatía isquémica hipóxica al nacer, con buen potencial motor cerebral y desarrollo psicomotor normal. Tenía antecedentes personales de miocardiopatía restrictiva y fue incluido en un programa de trasplante cardiaco cuando tenía 16 meses de edad. También fue necesario implantarle un dispositivo de asistencia biventricular Berlin Heart externo. Para evitar eventos embólicos, se le administró un tratamiento antiplaquetario doble y anticoagulante. Cuando tenía 23 meses de edad, presentó desconexión y hemiparesia derecha. Una tomografía computarizada (TC) mostró una arteria cerebral media (ACM) izquierda hiperdensa, así como un infarto parietotemporal derecho crónico. Su análisis de sangre mostró: glóbulos rojos 4.16 × 106 µ/L; hemoglobina 11.4 g/gL; tiempo de tromboplastina parcial activada (TTPA) 93 segundos y relación internacional normalizada (INR) 1.08.\n\nEl tratamiento trombolítico intravenoso estaba contraindicado debido al doble tratamiento antiplaquetario y anticoagulante a la dosis completa con heparina, por lo que se realizó una trombectomía intraarterial. Aunque el paciente tenía 23 meses de edad, se encontraba en el tercer percentil de la curva de peso (10 kg). Bajo anestesia general, se perforó la arteria femoral derecha y se colocó una funda 4F de 11 cm de largo (Cordis, Irlanda). Se usó un catéter vertebral Radiofocus 4F (Glidecath de Terumo, Bélgica) para confirmar la oclusión del segmento M1 de la MCA izquierda. La arteria se recanalizó mediante trombectomía mecánica con un stentriever utilizando el catéter vertebral 4F como tutor, colocándolo en el segmento petroso de la arteria carótida. Se usó un dispositivo Trevo XP Pro Vue de 3 mm x 20 mm (Stryker, Países Bajos), con un microcatéter Rapid Transit recto (Codman Neurovascular, Reino Unido), abriendo la arteria en una sola pasada. Se retiró todo el sistema (catéter tutor, microcatéter y stentriever) simultáneamente. En la prueba de control, se detectó una disección iatrogénica de la arteria carótida interna izquierda, que no tuvo importancia clínica, ya que el hemisferio izquierdo se irrigaba a través de la arteria comunicante anterior.\n\nUn mes después, se realizó con éxito el trasplante de corazón. La única secuela neurológica a largo plazo que surgió como resultado del accidente cerebrovascular fue la espasticidad del miembro superior derecho.\n\nMH - Cardiomiopatía, Dilatada/complicaciones/cirugía\nMH - Cardiomiopatía, restrictiva/complicaciones/cirugía\nMH - Angiografía cerebral\nMH - Procedimientos/métodos endovasculares\nMH - Mujer\nMH - Estudios de seguimiento\nMH - Insuficiencia cardiaca/*complicaciones/tratamiento\nMH - Trasplante de corazón\nMH - *Dispositivos de asistencia cardíaca\nMH - Humanos\nMH - Infantil\nMH - Hombre\nMH - Arteria cerebral media/imágenes diagnósticas\nMH - Estudios Retrospectivos\nMH - Ictus/complicaciones/diagnóstico por imágenes/cirugía\nMH - Resultado del tratamiento\n",
+        "gold_summary": "Un niño de 16 meses de edad con cardiomiopatía restrictiva que fue incluido en una lista para un trasplante cardiaco. A los 20 meses de edad, requirió un implante de un dispositivo de asistencia biventricular externo (Berlin Heart) y tuvo un accidente cerebrovascular en el hemisferio izquierdo a los 23 meses. Se utilizó un enfoque intraarterial y produjo buenos resultados clínicos. Un mes después, se realizó con éxito un trasplante cardiaco.\n",
+        "synthetic_summary": {
+            "B1": "Un niño muy pequeño tenía un corazón que no trabajaba bien. Los doctores dijeron que necesitaba un nuevo corazón. \n\nLe pusieron una máquina para ayudar su corazón a trabajar. Un día, su cabeza se puso un poco mal. \n\nLos doctores usaron una forma especial para ayudar a que la sangre volviera a moverse bien en su cabeza. Después, el niño se sintió mejor. \n\nUn mes después, los doctores le pusieron un corazón nuevo. Ahora, el niño está más fuerte.",
+            "B2": "**What Happened to the Child?**  \nA boy who was 16 months old had a heart problem called restrictive cardiomyopathy. This means his heart was stiff and could not pump blood well. Because of this, doctors put him on a waiting list for a heart transplant.\n\n**Medical Treatment Before the Stroke**  \nWhen he was 20 months old, he needed a special machine called a Berlin Heart. This machine helps the heart pump blood when it is too weak. It is placed outside the body and supports both sides of the heart.\n\n**The Stroke and How It Was Treated**  \nAt 23 months old, the boy had a stroke in the left side of his brain. A stroke happens when blood flow to part of the brain is blocked, causing brain cells to be damaged. Because he was already taking blood-thinning medicines, doctors could not use the usual clot-busting medicine. Instead, they used a method called intraarterial thrombectomy. This means they inserted a tiny tube into an artery and removed the blood clot directly from the blocked brain artery. This treatment worked well and helped restore blood flow.\n\n**What Happened Afterward**  \nOne month after the stroke treatment, the boy successfully received a new heart through a transplant surgery. The only lasting problem from the stroke was some stiffness and weakness in his right arm.\n\n**Why This Is Important**  \nThis case shows that even very young children with serious heart problems can be treated for strokes using advanced methods. It also highlights how careful planning and treatment can lead to good outcomes, including successful heart transplants.",
+            "B3": "Background  \nA male toddler, initially diagnosed with restrictive cardiomyopathy at 16 months of age, was placed on a heart transplant waiting list due to progressive cardiac insufficiency. At 20 months, he required implantation of an external biventricular assist device (Berlin Heart) to support his heart function. His medical history also included hypoxic-ischemic encephalopathy at birth, although his neurodevelopment was normal prior to these events.\n\nKey Findings  \nAt 23 months, the child experienced an acute ischemic stroke affecting the left middle cerebral artery (MCA) territory, resulting in right-sided hemiparesis and decreased responsiveness. Brain imaging revealed a hyperdense left MCA and evidence of a chronic right parietotemporal infarct. Laboratory tests showed mild anemia and prolonged activated partial thromboplastin time (aPTT), with an international normalized ratio (INR) within normal limits. Due to ongoing full-dose anticoagulation and dual antiplatelet therapy, intravenous thrombolysis was contraindicated.\n\nClinical Intervention  \nGiven these constraints, an intraarterial mechanical thrombectomy was performed under general anesthesia. Access was obtained via the right femoral artery, and a 4F vertebral catheter was used to confirm occlusion of the left MCA M1 segment. Recanalization was achieved in a single pass using a 3 mm x 20 mm Trevo XP Pro Vue stent retriever, with simultaneous removal of the catheter system. A minor iatrogenic dissection of the left internal carotid artery was detected but was clinically insignificant because collateral circulation via the anterior communicating artery maintained adequate cerebral perfusion.\n\nClinical Outcome and Follow-Up  \nOne month following the thrombectomy, the patient underwent a successful heart transplant. The only lasting neurological deficit from the stroke was spasticity affecting the right upper limb. Overall, the intraarterial thrombectomy approach in this very young child with complex cardiac pathology and anticoagulation requirements resulted in favorable neurological and cardiac outcomes.\n\nNext Steps  \nContinued multidisciplinary follow-up is essential to monitor cardiac graft function, manage neurological sequelae such as spasticity, and optimize rehabilitation to support motor recovery. This case highlights the feasibility and efficacy of mechanical thrombectomy in pediatric patients with contraindications to thrombolytic therapy."
+        }
+    },
+    {
+        "article": "Una mujer de 23 años de edad se presentó al departamento de urgencias con pérdida de conciencia y exceso de secreciones orales 2 horas después de la ingestión de un veneno no especificado. No tenía movimientos corporales anormales, fiebre, diarrea, vómitos o sudoración. Inicialmente la habían llevado a un hospital primario cercano, donde fue tratada por posible intoxicación por OP con atropina y cimetidina durante 3 días, antes de ser trasladada al hospital Saint Peter. Después de un interrogatorio exhaustivo, se descubrió que la paciente había consumido unos 30 ml de 2,4-D en un intento de suicidio, precipitado por problemas financieros. No tenía antecedentes conocidos de enfermedad psiquiátrica, intentos de suicidio, episodios depresivos o abuso de sustancias. No se observaron trastornos cardíacos, renales o metabólicos previos.\n\nAl llegar al departamento de urgencias, la paciente estaba inconsciente. Sus constantes vitales eran PR 110/min, BP 120/70 mmHg, RR 21/min, y SPO2 96% en aire ambiente. Los resultados del examen físico fueron notables: un GCS de 6 sobre 15, pupilas dilatadas y reactivas, extremidades inferiores hipertónicas e hiperreflexivas, y reflejo plantar ascendente. Tras la investigación inicial, el recuento completo de células sanguíneas, la prueba de la función renal, la prueba de la función hepática, y la glucosa en sangre aleatoria fueron normales. Su electrocardiograma mostró taquicardia sinusal, mientras que la radiografía de tórax no fue notable. El análisis de gases en sangre arterial y el nivel sérico de la toxina no pudieron determinarse, ya que ninguno de los medios de prueba estaba disponible en el hospital.\n\nLa paciente fue trasladada a la unidad de cuidados intensivos (UCI), se le introdujo una sonda para proteger las vías respiratorias y se le inició inmediatamente una diuresis alcalina forzada. Su evolución en la UCI fue notable por el desarrollo de una insuficiencia renal (creatinina 3,1 ml/dL [intervalo de referencia 0,5-1,2 mg/dL], BUN 133 mg/dL [intervalo de referencia 16,6-48,5 mg/dL], análisis de orina 3+ hemoglobina y muchos glóbulos rojos), debido a una rabdomiolisis inducida por toxinas (nivel de creatina fosfocinasa de 1330 µg/L). Posteriormente, la paciente se volvió hipotensa y se le inició un tratamiento con vasopresores. La ecocardiografía y la ecografía abdominal no fueron significativas. A pesar de estos esfuerzos, falleció por colapso circulatorio el tercer día de estancia en la UCI.\n",
+        "gold_summary": "Aquí se informa sobre el caso de una joven granjera de la zona rural de Etiopía que fue internada en un hospital local tras perder el conocimiento y presentar exceso de secreciones orales 2 horas después de haber ingerido, de manera suicida, un agente tóxico desconocido. Originalmente, se la trató por intoxicación con organofosforados y luego se la trasladó al Hospital Saint Peter's en Addis Abeba para recibir atención médica más intensiva. Allí, se confirmó la ingesta de 2,4-D y se le brindó atención médica de apoyo, ventilación mecánica y diuresis alcalina forzada. A pesar de estas intervenciones, falleció varios días después.\n",
+        "synthetic_summary": {
+            "B1": "A young woman drank a bad poison on purpose. She felt very sick and could not wake up. \n\nDoctors gave her special care to help her breathe and clean her body. They tried very hard to make her better. \n\nBut she got very sick and passed away after a few days. The doctors were very sorry.",
+            "B2": "**What Happened to the Patient**  \nA 23-year-old woman from a rural area in Ethiopia was taken to a local hospital after she lost consciousness and had too much saliva two hours after swallowing a poison. At first, doctors thought she had been poisoned by a common type of pesticide called organophosphates. She was treated for that but later sent to a bigger hospital in Addis Ababa for more care.\n\n**What They Found Out**  \nAt the bigger hospital, doctors learned she had actually swallowed a chemical called 2,4-D, which is a type of weed killer. She had taken it on purpose to try to harm herself because of money problems. The doctors gave her treatments to help her body get rid of the poison. This included helping her breathe with a machine and using a special method called forced alkaline diuresis, which helps flush out toxins through urine.\n\n**What Happened Next**  \nEven with these treatments, her condition got worse. She developed kidney failure and muscle damage caused by the poison. Her blood pressure dropped, and she needed medicine to support her heart and circulation. Sadly, despite all the care, she died a few days later because her body’s circulation collapsed.\n\n**What This Means**  \nThis case shows how dangerous 2,4-D poisoning can be. Even with quick and strong medical help, it can cause serious damage to the body and can be fatal. It also highlights the importance of mental health support, especially for people facing tough life problems.",
+            "B3": "Background  \nA 23-year-old woman from a rural area in Ethiopia was admitted to a local hospital after losing consciousness and exhibiting excessive oral secretions approximately two hours following the intentional ingestion of an unknown toxic substance. Initially, she was treated for suspected organophosphate poisoning with atropine and cimetidine for three days before being transferred to Saint Peter’s Hospital in Addis Ababa for more advanced care.  \n\nKey Findings  \nUpon detailed evaluation at Saint Peter’s Hospital, it was confirmed that the patient had ingested approximately 30 ml of 2,4-Dichlorophenoxyacetic acid (2,4-D), a herbicide, in a suicide attempt triggered by financial difficulties. At admission, she was unconscious with a Glasgow Coma Scale (GCS) score of 6/15, dilated but reactive pupils, increased muscle tone and reflexes in the lower limbs, and an upward plantar reflex. Vital signs showed a heart rate of 110 beats per minute, blood pressure of 120/70 mmHg, respiratory rate of 21 breaths per minute, and oxygen saturation of 96% on room air. Laboratory tests including complete blood count, kidney and liver function tests, and random blood glucose were within normal limits initially. Electrocardiogram revealed sinus tachycardia, and chest X-ray was unremarkable. Unfortunately, arterial blood gas analysis and serum toxin levels were unavailable.  \n\nClinical Interpretation  \nThe patient was admitted to the intensive care unit (ICU), where airway protection was established via intubation, and forced alkaline diuresis was initiated to enhance toxin elimination. During her ICU stay, she developed acute kidney injury evidenced by elevated creatinine (3.1 mg/dL) and blood urea nitrogen (133 mg/dL), along with hematuria and numerous red blood cells in urine analysis. These findings were attributed to rhabdomyolysis (muscle breakdown) induced by the toxin, as indicated by a high creatine phosphokinase level (1330 µg/L). Subsequently, she became hypotensive and required vasopressor support. Cardiac and abdominal ultrasounds showed no significant abnormalities. Despite aggressive supportive care, she succumbed to circulatory collapse on the third day of ICU admission.  \n\nNext Steps and Considerations  \nThis case highlights the severe toxicity associated with 2,4-D herbicide ingestion, which can lead to rapid neurological deterioration, muscle breakdown, kidney failure, and cardiovascular collapse. Early recognition and aggressive supportive management, including airway protection and forced alkaline diuresis, are critical but may not prevent fatal outcomes in severe poisoning. Limited availability of specific diagnostic tests and antidotes in resource-constrained settings poses additional challenges. Mental health evaluation and preventive strategies addressing underlying psychosocial stressors are essential to reduce the risk of such suicide attempts."
+        }
+    },
+    {
+        "article": "Una paciente etíope de 35 años de edad se presentó en el departamento de urgencias del Colegio Médico del Hospital Yekatitit 12 con síntomas de falta de aire en reposo, ortopnea, disnea paroxística nocturna significativa, dolor torácico, tos productiva teñida de sangre y vómitos de materia ingerida (2-3 episodios por día) durante 2 semanas. Presentaba una hinchazón progresiva del cuerpo que comenzó en las extremidades inferiores y luego afectó a todo el cuerpo, fatigabilidad fácil, pérdida de apetito, fiebre intermitente de alto grado y sensación de ardor epigástrico durante la misma semana y con la misma duración. La paciente también experimentó una pérdida de peso y fatiga no especificadas durante los últimos 2 meses. Por lo demás, no tenía comorbilidades conocidas, ni comportamientos de riesgo, como fumar o beber alcohol, medicamentos o antecedentes familiares de neoplasia. Estaba casada, tenía cuatro hijos y no tenía antecedentes obstétricos negativos. Su ocupación era la agricultura y había vivido en una zona rural. Nunca había sido admitida por una queja similar.\n\nLa escala de coma de Glasgow (GCS) de la paciente fue de 15 sobre 15, y no había anormalidades de memoria, potencia o tono. La paciente estaba en grave dificultad respiratoria con saturación de oxígeno del 70% con aire atmosférico, frecuencia respiratoria de 30-35 latidos/minuto, y frecuencia del pulso de 120 por minuto. Tenía registros de fiebre de alto grado hasta el nivel de 39.5 0C y puede mantener su presión arterial. El examen de mama con ultrasonido y mamografía fue supuestamente normal. No se detectó linfadenopatía en áreas accesibles.\n\nEl examen del tórax reveló signos de derrame pleural que también se observaron en las imágenes y se analizaron. Una tomografía computarizada (TC) del tórax con contraste mostró derrame pericárdico y neumonía multifocal. La angiografía por TC mostró un defecto de llenado arterial pulmonar segmentario del lóbulo inferior en ambos lados, lo que sugiere embolia pulmonar y derrame pleural en ambos lados. Los frotis citológicos se informaron con láminas de células mesoteliales, neutrófilos y grupos dispersos de células grandes atípicas con nucleolos prominentes que sugieren derrame maligno. El análisis del líquido pleural mostró un líquido con predominio linfocítico con glucosa normal (82 mg/dl), proteínas (2,2 g/dl) y lactato deshidrogenasa (LDH) de 592 mg/dl.\n\nLa presión venosa yugular aumentó con los sonidos cardiacos apagados. La ecocardiografía mostró derrame pericárdico masivo con características de taponamiento cardiaco, fracción de eyección preservada (65%), y excursión sistólica del plano anular tricuspídeo (TAPSE) mayor a 18 mm. Un electrocardiograma (ECG) reveló solo taquicardia sinusal y desviación del eje. Se realizó una pericardiocentesis inmediata, se extrajo un drenaje de aproximadamente 250 ml de fluido hemorrágico y se aseguró la ventana pericárdica. La repetida ecocardiografía reveló una reducción del tamaño. El informe de citología del fluido pericárdico mostró numerosos linfocitos junto con células malignas atípicas que tenían prominentes nucleolos, lo que sugería un derrame maligno.\n\nEn el examen abdominal, mostró signos positivos de acumulación de fluidos sin órgano hinchable. La tomografía computarizada abdominal y pélvica mostró un aumento en el tamaño del hígado con múltiples lesiones hepáticas hipointensas que sugerían metástasis. Los órganos pélvicos, incluidos los ovarios y el útero, no presentaron lesiones identificadas. Se realizó una biopsia con aguja de la lesión hepática y los resultados revelaron un adenocarcinoma secundario.\n\nSe realizó un diagnóstico de insuficiencia cardíaca causada por una efusión pericárdica masiva maligna secundaria a un adenocarcinoma diseminado y un carcinoma de origen primario desconocido que afectaba al pulmón, la pleura, el pericardio y el tracto gastrointestinal. Se le diagnosticó a la paciente una trombosis venosa profunda extensa en la extremidad superior izquierda, una embolia pulmonar bilateral y segmentaria, posiblemente debido a la CUP diseminada. Los hallazgos también mostraron una neumonía multifocal superpuesta y una anemia leve de enfermedad crónica.\n\nEl recuento sanguíneo completo inicial reveló leucocitosis con un recuento de glóbulos blancos de 24 × 103 por ml, neutrófilos predominantes (91%), recuento de glóbulos rojos de 3.7 × 106 por µl, anemia normocítica leve (hemoglobina (Hgb) 11.2 mg/dl), volumen corpuscular medio (MCV) de 81.2 fl, y trombocitopenia severa (66 × 103/µl). Después del tratamiento antibiótico para neumonía, el recuento sanguíneo completo volvió a la normalidad (excepto para Hgb). Con niveles normales de bilirrubina, la aspartato aminotransferasa (AST) aumentó más de siete veces (263 U/L), mientras que la alanina transaminasa (ALT) aumentó más de nueve veces (332 U/L). Los electrolitos séricos (excepto para Na + con hiponatremia leve, 129 mEq/L) y las pruebas de función renal fueron normales. La albúmina era baja (2.12 g/dl). Los niveles de lactato deshidrogenasa (LDH) aumentaron casi dos veces desde el inicio (592 U/L). Los virus del virus de inmunodeficiencia humana, hepatitis B y hepatitis C no fueron reactivos. La sangre y el cultivo del líquido pleural no tuvieron crecimiento. Un antígeno carcinoembrionario (CEA) aumentó más de 400 veces (1000 µg/L) del inicio.\n\nLa paciente fue admitida en la sala general. Se realizó una ventana pericárdica y una inserción de un tubo torácico derecho con un cirujano cardiotorácico junto con un cardiólogo (ver la cantidad de aspirado antes). Se realizó una aspiración pleural terapéutica intermitente para el derrame pleural maligno. Una vez que la dosis de carga (60 mg) de frusemida produjo suficiente producción de orina, esta dosis se mantuvo tres veces (TID) al día. Esto se redujo y se dio de alta a la paciente con una dosis oral de 20 mg dos veces al día (BID). Se inició una dosis estándar de enoxaparina para el tromboembolismo pulmonar y la trombosis venosa profunda aguda extensa en la extremidad superior izquierda. Se administró enoxaparina por vía subcutánea 40 mg BID durante la hospitalización, que se cambió a 5 mg de warfarina oral diaria durante el alta debido a problemas financieros. La neumonía multifocal se trató con ceftazidima (1 g intravenoso TID) y vancomicina (1 g intravenoso BID) según el protocolo de tratamiento estándar nacional. El dolor se controló con un potente medicamento contra el dolor (morfina 5 mg intravenosa TID) y se redujo y suspendió. También estaba en la profilaxis de la úlcera. La paciente fue dada de alta de la sala médica con una mejora significativa después de 14 días de hospitalización y fue asignada a la unidad de oncología del hospital. Por lo tanto, para el cáncer de origen primario desconocido, se le dio un ciclo de quimioterapia (carboplatino/paclitaxel). Se perdió el seguimiento debido a problemas financieros, y la paciente murió en su casa cuatro meses después del alta.\n\nMH - Humanos\nMH - Mujer\nMH - *Insuficiencia cardiaca/etiología\nMH - Adulto\nMH - *Neoplasias, complicaciones/primaria desconocida",
+        "gold_summary": "Una mujer negra de 35 años se presentó con falta de aire en reposo, ortopnea, disnea paroxística nocturna, dolor torácico, tos productiva teñida de sangre y fiebre durante 2 semanas. También tenía hinchazón progresiva del cuerpo, fatigabilidad fácil, pérdida de apetito y dolor abdominal durante la misma semana. La imagen corporal reveló grandes derrames pleurales y pericárdicos, lesiones hepáticas metastásicas y defectos de llenado segmentarios y subsegmentarios vasculares pulmonares bilaterales. La citología de los fluidos pericardio y pleural sugieren derrame maligno. Las lesiones hepáticas y la biopsia con aguja indicaron adenocarcinoma de origen desconocido, y el nivel de antígeno carcinoembriónico también aumentó significativamente.\n",
+        "synthetic_summary": {
+            "B1": "A lady felt very tired and had trouble breathing. She had pain in her chest and cough with blood. Her body got swollen and she had fever too.\n\nDoctors took pictures of her chest and belly. They saw extra fluid around her heart and lungs. They found spots in her liver that were not normal.\n\nThe fluid had bad cells, which told the doctors she had a kind of cancer. The cancer started in a place they could not find. The lady needed help to feel better.",
+            "B2": "**What Happened to the Patient?**\n\nA 35-year-old woman came to the hospital because she had trouble breathing even when resting. She also had chest pain, a cough with blood, fever, and swelling all over her body. These problems had lasted for about two weeks. She felt very tired, lost her appetite, and had stomach pain during this time.\n\n**What Did the Doctors Find?**\n\nDoctors took pictures of her chest and abdomen. They found large amounts of fluid around her lungs and heart. They also saw spots on her liver that looked like cancer had spread there. Blood flow in her lungs was partly blocked, which can cause serious breathing problems.\n\nWhen doctors tested the fluid around her heart and lungs, they found cancer cells. A small tissue sample (called a biopsy) from her liver showed she had a type of cancer called adenocarcinoma. This cancer had spread but doctors did not know where it started. A blood test showed very high levels of a marker called carcinoembryonic antigen, which often rises in cancer.\n\n**What Does This Mean?**\n\nThe woman had cancer that had spread to many parts of her body, including her lungs, liver, and the lining around her heart and lungs. This caused fluid buildup and made it hard for her to breathe. The exact place where the cancer began was unknown, which sometimes happens and is called cancer of unknown primary origin. This condition is serious and needs careful treatment.",
+            "B3": "**Background**  \nA 35-year-old Ethiopian woman presented with a two-week history of severe respiratory symptoms including shortness of breath at rest, difficulty breathing when lying flat (orthopnea), sudden nighttime breathlessness (paroxysmal nocturnal dyspnea), chest pain, productive cough with blood, and fever. She also experienced progressive swelling starting in her lower limbs and spreading throughout her body, easy fatigue, loss of appetite, and upper abdominal burning pain during the same period. Additionally, she reported unintentional weight loss and generalized fatigue over the previous two months. She had no known prior illnesses, risk factors such as smoking or alcohol use, medication use, or family history of cancer. Her occupation was farming in a rural area, and she had no previous similar hospital admissions.\n\n**Key Findings**  \nClinical examination revealed severe respiratory distress with low oxygen saturation (70% on room air), rapid breathing (30–35 breaths per minute), and a fast heart rate (120 beats per minute). She had a high fever (up to 39.5°C) but stable blood pressure. Chest imaging identified large bilateral pleural effusions (fluid around the lungs) and a massive pericardial effusion (fluid around the heart). Computed tomography (CT) scans showed multifocal pneumonia, segmental and subsegmental pulmonary arterial filling defects on both sides consistent with pulmonary embolism (blood clots in the lungs), and multiple hypointense lesions in an enlarged liver suggestive of metastases. No abnormalities were found in pelvic organs.\n\nAnalysis of fluid samples from both the pericardial and pleural spaces revealed malignant cells with prominent nucleoli, indicating cancerous effusions. A liver biopsy confirmed the presence of adenocarcinoma (a type of glandular cancer). Blood tests showed elevated white blood cells with neutrophil predominance, mild normocytic anemia, severe thrombocytopenia (low platelets), elevated liver enzymes (AST and ALT), low albumin, and a markedly increased carcinoembryonic antigen (CEA) level, a tumor marker often elevated in adenocarcinomas. Tests for HIV and hepatitis viruses were negative, and cultures of blood and pleural fluid showed no infection.\n\n**Clinical Interpretation**  \nThe patient was diagnosed with heart failure secondary to a massive malignant pericardial effusion caused by widely disseminated adenocarcinoma of unknown primary origin (CUP). The cancer involved the lungs, pleura, pericardium, liver, and gastrointestinal tract. She also had extensive deep vein thrombosis in her left upper limb and bilateral segmental pulmonary embolism, likely related to the hypercoagulable state induced by her malignancy. Concurrent multifocal pneumonia and mild anemia of chronic disease were also present.\n\n**Next Steps and Management**  \nThe patient underwent urgent pericardiocentesis (drainage of pericardial fluid) and a pericardial window procedure to relieve cardiac tamponade (compression of the heart by fluid). A chest tube was inserted to manage the pleural effusions, with intermittent therapeutic drainage. She received intravenous antibiotics (ceftazidime and vancomycin) for pneumonia and anticoagulation therapy initially with enoxaparin and later switched to warfarin due to financial constraints. Diuretics were administered to manage fluid overload, and pain was controlled with intravenous morphine. After 14 days of hospitalization, she showed significant clinical improvement and was discharged with plans for oncology follow-up. She received one cycle of chemotherapy with carboplatin and paclitaxel targeting the cancer of unknown primary. Unfortunately, due to financial difficulties, she was lost to follow-up and passed away at home four months after discharge.\n\n---\n\nThis case illustrates the complexity of diagnosing and managing advanced malignancy presenting with cardiac and pulmonary complications, emphasizing the challenges faced in resource-limited settings."
+        }
+    },
+    {
+        "article": "Paciente del sexo femenino de 17 años con diagnóstico de enfermedad de Graves con bocio difuso, la cual negó otros antecedentes de importancia.\n\nSu cuadro comenzó seis meses antes con pérdida de peso progresiva, episodios de ansiedad y agitación, temperaturas de 37.4 a 37.9 ºC, palpitaciones, dolor abdominal y diarrea intermitente. A los dos meses se agregó como síntoma el crecimiento de la cara anterior del cuello; al tercer mes presentó taquicardia de hasta 130 latidos por minuto. Al ser valorada por Endocrinología se le administró tiamazol de 15 mg cada 8 horas, el cual fue suspendido por cuadro de agranulocitosis. Por lo tanto, se le comenzó a administrar lugol y propanol de 20 mg cada 8 horas, sin respuesta adecuada. Por ende, se decidió aplicar una dosis terapéutica de yodo 131 (I-131) 10 mcU.\n\n\nExploración física\nA la exploración física, la paciente presentó como signos basales una presión arterial no invasiva (PANI) 137/75 mmHg, frecuencia cardiaca (FC) 105 lpm, frecuencia respiratoria (FR) 16 rpm, SpO2 95%, temperatura 37.4ºC. La paciente ingresó deambulando, con agitación leve, con actitud cooperadora; estaba hidratada y sin datos clínicos de vía aérea difícil, pero no se valoró movilidad de tráquea por crecimiento tiroideo de aproximadamente 7.5 x 7 x 10 cm). La superficie del cuello era regular y su movilidad tenía una adecuada extensión. A la auscultación cardiopulmonar no hubo ruidos agregados y la paciente tenía ruidos cardiacos aumentados en frecuencia; asimismo, abdomen blando, depresible, no doloroso, con peristalsis presente. Extremidades integras, sensibilidad con aumento de la percepción del calor, hiperhidrosis palmar, fuerza 5/5, y temblor fino.\n\nSe empleó la escala de Burch y Wartofsky y se obtuvieron 40 puntos con elevada probabilidad de tormenta tiroidea, por lo cual se decidió manejo con anestesia multimodal.\n\nEn la monitorización tipo 2 la paciente presentó signos vitales iniciales PANI 137/75 mmHg, frecuencia cardiaca 96 latidos por minuto, frecuencia respiratoria 16 respiraciones por minuto, 95% Spo2, monitoreo invasivo de tensión arterial.\n\nPor inducción endovenosa se le administraron a la paciente 2 mg de midazolam; 150 mcg de fentanilo; 5 mg de cisatracurio y 50 mg de propofol.\n\nEl abordaje de la vía aérea se hizo con videolaringoscopía Glide Scope con hoja hiperangular 3 sin complicaciones. La ventilación mecánica invasiva modo volumen presentó flujos bajos FIO2 (40%).\n\nSe llevó a cabo bloqueo cervical superficial bilateral ecoguiado con 4 mL de ropivacaina al 0.2% en cada lado (16 mg en total).\n\nPara el mantenimiento se empleó sevoflorano CAM 0.8, infusión de dexmedetomedina 0.7 a 0.4 mcg/kg/hora, infusión de lidocaína 25 mcg/kg/hora, concentración plasmática de fentanilo 0.001 mcg/mL.\n\nEn cuanto a los adyuvantes se empleó paracetamol 750 mg + parecoxib 40 mg + ketorolaco intravenoso 30 + sulfato de magnesio 1250 g en infusión para una hora. El balance de líquidos fue negativo. El tiempo anestésico fue de 215 minutos. En el transoperatorio, la paciente estuvo hemodinámicamente estable, con presión arterial media de 67 a 75 mmHg, que se considera adecuada para la perfusión de órganos.\n\nEn el postoperatorio la paciente presentó analgesia durante 12 horas. Rescate con 1 g de metamizol por razón necesaria, utilizando un solo rescate. Disfonía postoperatoria persistente, sin presencia de odinofagia.",
+        "gold_summary": "Adolescente de 17 años con enfermedad de Graves con manifestaciones clínicas descontroladas, la cual no respondió a tratamiento médico y se programó para tiroidectomia radical. Se obtuvieron 35 puntos en la Escala de Burch y Wartofsky. Se manejó con anestesia general y fueron disminuyendo los estímulos para control de vía aérea y regional a fin de disminuir los estímulos quirúrgicos. Se usaron medicamentos adyuvantes como sulfato de magnesio para la estabilidad transoperatoria.",
+        "synthetic_summary": {
+            "B1": "A girl, 17 years old, was very sick with her thyroid.  \nHer medicine did not help her get better.  \n\nDoctors gave her special sleep medicine for surgery.  \nThey helped her breathe and kept her calm during surgery.  \n\nThey used extra medicine to keep her body steady.  \nThis helped her feel safe and well during the operation.",
+            "B2": "**Patient Background and Condition**  \nThis is about a 17-year-old girl who has Graves' disease. Graves' disease is a condition where the thyroid gland, a small organ in the neck, makes too much thyroid hormone. This caused her symptoms like weight loss, fast heartbeat, anxiety, and a swollen neck. Her symptoms were not controlled well by medicines, so doctors planned to remove her thyroid gland through surgery.\n\n**What the Doctors Did**  \nBefore surgery, doctors checked her condition using a scoring system called the Burch and Wartofsky scale. She scored 35 points, showing a high risk of a serious thyroid problem called a thyroid storm. To keep her safe during surgery, doctors gave her general anesthesia, which makes her unconscious and pain-free. They also used special techniques to protect her airway and reduce the body’s stress response during the operation.\n\n**Medications Used During Surgery**  \nThe medical team gave her extra medicines like magnesium sulfate. This medicine helps keep her heart and blood pressure stable while the surgery is happening. Using these medicines and careful anesthesia helped the doctors manage her condition safely during the operation.\n\n**Summary**  \nIn short, this young patient had a serious thyroid problem that did not get better with medicine. She needed surgery to remove her thyroid. The doctors prepared carefully to keep her safe by using anesthesia and special medicines to control her body's reactions during the operation.",
+            "B3": "Background  \nA 17-year-old female patient was diagnosed with Graves’ disease, characterized by diffuse thyroid enlargement (goiter). Her symptoms began six months prior and included progressive weight loss, episodes of anxiety and agitation, low-grade fever (37.4 to 37.9 ºC), palpitations, abdominal pain, and intermittent diarrhea. Two months into her illness, she developed noticeable anterior neck swelling, and by the third month, she exhibited a rapid heart rate (tachycardia) reaching 130 beats per minute. Initial treatment with thiamazole (an antithyroid medication) was discontinued due to agranulocytosis (a dangerous drop in white blood cells). Subsequent therapy with Lugol’s iodine and propranolol was ineffective, leading to the decision to administer a therapeutic dose of radioactive iodine (I-131).\n\nKey Findings  \nOn physical examination, the patient was mildly agitated but cooperative, with stable vital signs: blood pressure 137/75 mmHg, heart rate 105 bpm, respiratory rate 16 breaths per minute, oxygen saturation 95%, and temperature 37.4ºC. The thyroid gland was significantly enlarged (approximately 7.5 x 7 x 10 cm), causing anterior neck swelling but without airway obstruction signs. Cardiopulmonary auscultation revealed increased heart sounds consistent with tachycardia; the abdomen was soft and non-tender. Neurologically, she exhibited fine tremors, increased heat sensitivity, and excessive sweating of the palms. Using the Burch and Wartofsky scoring system—a tool to assess the likelihood of thyroid storm (a life-threatening exacerbation of hyperthyroidism)—she scored 40 points, indicating a high probability of thyroid storm.\n\nClinical Interpretation  \nDue to the severity and poor response to medical treatment, the patient was scheduled for a radical thyroidectomy (surgical removal of the thyroid gland). Anesthesia management involved general anesthesia with careful reduction of airway and surgical stimuli to minimize physiological stress. Airway control was achieved via videolaryngoscopy without complications. Bilateral superficial cervical nerve blocks using ultrasound guidance and ropivacaine (a local anesthetic) were performed to provide regional anesthesia and reduce surgical stimulation. The anesthetic regimen included sevoflurane inhalation, intravenous infusions of dexmedetomidine (a sedative), lidocaine, and fentanyl (an opioid), along with adjuvant medications such as magnesium sulfate to promote intraoperative hemodynamic stability. Throughout the 215-minute procedure, the patient remained hemodynamically stable, with adequate organ perfusion.\n\nNext Steps  \nPostoperatively, the patient experienced effective pain relief lasting 12 hours, requiring only a single dose of rescue analgesic (metamizol). She developed persistent postoperative hoarseness (dysphonia) without throat pain (odinophagia), which will require monitoring and possibly further evaluation to assess vocal cord function. Continued multidisciplinary care including endocrinology, anesthesiology, and otolaryngology is essential to manage her recovery and address any complications related to thyroidectomy and Graves’ disease."
+        }
+    },
+    {
+        "article": "Una mujer de 30 años de edad, embarazada de 3, para 3, se presentó con disminución de la micción, dolor en el flanco izquierdo y fiebre durante 2 días después de una cesárea de emergencia por primera vez, indicada debido a la angustia materna y fetal secundaria al trabajo de parto prolongado y sangrado vaginal prolongado en el hospital Al-Thora, Ibb, Yemen. A pesar de los esfuerzos de reanimación, su recién nacido falleció después de 45 minutos. Durante la cesárea, se identificaron severas adherencias uterinas (ya que había lesiones de endometriosis y adherencias entre la pared posterior del útero y el colon sigmoide), y una pérdida de sangre estimada de 1500 cc, según el informe del ginecólogo. La paciente no recibió atención prenatal durante su embarazo. No es fumadora y negó condiciones médicas crónicas, abuso de drogas, intoxicación accidental o antecedentes quirúrgicos previos.\n\nEn el examen físico, el paciente se veía pálido, enfermo y febril durante la evaluación inicial, con una temperatura oral de 38 °C, pulso de 80 latidos por minuto y presión arterial de 95/70 mm Hg. El abdomen del paciente estaba levemente distendido, con sensibilidad moderada, principalmente en el cuadrante inferior izquierdo.\n\nLos datos de laboratorio fueron los siguientes: el recuento de glóbulos blancos (WBC) fue de 15,3 × 103/mL, con 90% de neutrófilos polimórficos (leucocitosis con predominio neutrofílico), la hemoglobina fue de 7,5 g/dL, el recuento de plaquetas fue de 200 × 103/µL, el nitrógeno ureico en sangre (BUN) fue de 23 mg/dl y la creatinina fue de 3,8 mg/dl. Otros análisis de sangre, como los de la función hepática y los de coagulación, estuvieron dentro de los rangos normales. La ecografía (US) mostró una hidronefrosis izquierda grave y un fluido libre moderado en la cavidad abdominal. Se realizó la aspiración de la punción abdominal y la creatinina en el punto fue de 52 mg/dL, lo que indica que el fluido era orina.\n\nLa paciente fue resucitada con glóbulos rojos concentrados y una amplia cobertura antibiótica. Después de esto, se le realizó una ureteroscopia urgente que mostró una oclusión total del uréter izquierdo. Se tomó la decisión de realizar una exploración quirúrgica, dada la inestabilidad hemodinámica, la falta de equipos de nefrostomía percutánea y la evidencia de contaminación intraabdominal. Durante la operación, se encontró fluido libre moderado en la cavidad abdominal. El uréter izquierdo fue aplastado y ligado con una sutura Vicryl (5 agujas) a unos 5 cm de su parte distal. Después de evacuar el fluido, se extirpó el segmento lesionado del uréter y se realizó una ureteroneocistostomía de forma refluyente tras distender la vejiga con solución salina a través del catéter. Además, diseccionamos el uréter, con cuidado, de los tejidos circundantes en dirección cefálica, espatulamos el extremo distal del uréter e insertamos un stent doble. Se implantó el uréter en la cúpula posterior de la vejiga urinaria con anastomosis sin tensión y se suturó con Vicryl 4-0 a través del uréter de espesor completo, luego la capa mucosa de la vejiga y la capa detrusora. Se insertó un drenaje Jackson-Pratt (JP) cerca de la anastomosis y se cerró la pared abdominal tras evaluar el contenido intraperitoneal.\n\n\nSeguimiento y resultado\nSe iniciaron líquidos transparentes el segundo día postoperatorio. La paciente tenía distensión abdominal leve, dolor y náuseas. El tercer día postoperatorio, tenía una distensión abdominal creciente y dejó de expulsar flatos. La ecografía abdominal mostró una gran cantidad de acumulación en la cavidad peritoneal. Los datos de laboratorio de sangre mostraron una leucocitosis (WBC de 22 × 103/mL con un cambio a la izquierda).\n\nUna tomografía computarizada (TC) del abdomen y la pelvis con contraste reveló una cantidad significativa de aire libre y líquido en todo el abdomen y la pelvis adyacente a la pared abdominal anterior. También se observaron múltiples localizaciones de gas libre en el mesenterio, con realce de contraste de múltiples bucles intestinales pequeños, sin evidencia de extravasación de contraste. Los hallazgos sugirieron una víscera perforada. Después de consultar al equipo de cirugía general, la paciente fue llevada inmediatamente al quirófano para una laparotomía exploratoria, que reveló una pequeña perforación en la parte rectosigmoidea con algo de derrame, peritonitis con edema del asa intestinal y alteración de la anastomosis ureteral. La complejidad de este caso nos obligó a realizar intervenciones en varias etapas de manera multidisciplinaria. En primer lugar, el ginecólogo realizó una histerectomía debido a endometritis (confirmada histopatológicamente), supuración severa y alteración de la sutura del útero. En segundo lugar, un urólogo realizó una derivación ureterocutánea del uréter izquierdo y se creó una urostomía en el lado izquierdo. Por último, el cirujano general realizó el procedimiento de colostomía después de reparar la lesión del colon y se creó una colostomía en el lado izquierdo. En el quinto día postoperatorio, se produjo retracción de la colostomía con infección de la herida y se observó comunicación entre la colostomía y la urostomía. Se decidió realizar una reexploración para reubicar la colostomía sigmoidea y se realizó una colostomía transversal derecha. Una semana después de la operación, la paciente experimentó una infección superficial de la pared abdominal complicada con dehiscencia de la herida e hipoalbuminemia (albúmina: 2 g/dL) que requirió tratamiento con varios desbridamientos, irrigación de la herida, antibióticos y terapia de apoyo. Los antibióticos recomendados fueron linezolid (600 mg IV cada 12 horas durante 7 días), luego cambiaron a ceftriaxona (1 g IV cada 12 horas durante 5 días) más metronidazol (500 mg IV cada 12 horas durante 5 días) y cambiaron a ciprofloxacina oral (500 mg cada 12 horas por vía oral durante 7 días). Gradualmente, reanudó su dieta normal y fue dada de alta 30 días después en condiciones estables. Requería atención domiciliaria para ayudarla con la colostomía, la ureterostomía y la deambulación.\n\nSeis meses después, se cerró la colostomía y se anastomosó el uréter mediante el procedimiento de colgajo de vejiga tabular de Boari (la vejiga se abrió en su superficie anterior y se volteó un colgajo de vejiga de espesor completo caudalmente y se tabularizó para anastomosis al segmento ureteral proximal después de la inserción de la endoprótesis doble J). Después de una recuperación postoperatoria sin incidentes, se dio de alta a la paciente el séptimo día postoperatorio. El seguimiento de un mes mediante ecografía y cistouretrografía miccional mostró un aspecto normal de la vejiga con capacidad vesical adecuada y un sistema del tracto urinario superior normal. Tres meses después, la ureteroscopia retrógrada mostró un calibre adecuado del uréter. Se hizo un seguimiento regular de la paciente con ecografía durante 3 meses durante un año. La paciente no tuvo síntomas irritativos o gastrointestinales en los 2 años de seguimiento.\n",
+        "gold_summary": "Una mujer de 30 años presentó disminución de la micción durante 2 días después de una cesárea. La ecografía mostró una hidronefrosis izquierda grave y un fluido abdominal libre moderado. Una ureteroscopia reveló una oclusión total del uréter izquierdo y, posteriormente, se realizó una ureteroneocistostomía. Dos días después, la paciente presentó complicaciones con distensión abdominal que requirieron una nueva exploración. La exploración reveló lesiones en el colon (recto-sigmoide), peritonitis, endometritis y alteración de la anastomosis ureteral. Se realizó una colostomía, reparación de lesiones en el colon, histerectomía y derivación ureterocutánea. La estancia hospitalaria de la paciente fue complicada, con retracción estomal que requirió revisión quirúrgica y dehiscencia de la herida, que se trató de forma conservadora. Después de 6 meses, se cerró la colostomía y se anastomosó el uréter mediante el procedimiento de colgajo de Boari.\n",
+        "synthetic_summary": {
+            "B1": "A lady had a baby by surgery. After that, she had trouble peeing. The doctor saw her tummy had extra fluid and a blocked tube from her kidney. They fixed the blocked tube with surgery.\n\nA few days later, her tummy got bigger and hurt. The doctors found problems in her tummy and some parts were sick. They did more surgeries to help her and fixed the sick parts.\n\nShe stayed in the hospital for a long time. After many days, the doctors helped her tummy and tubes work better again. She got better and went home.",
+            "B2": "**What Happened to the Patient?**  \nA 30-year-old woman had trouble urinating for two days after having a cesarean section (a surgery to deliver a baby). An ultrasound showed that her left kidney was swollen because urine was blocked, and there was some fluid inside her belly. A special camera test called ureteroscopy found that her left ureter—the tube that carries urine from the kidney to the bladder—was completely blocked. To fix this, doctors performed surgery called ureteroneocystostomy, which means they connected the ureter to the bladder in a new way.\n\n**What Complications Occurred?**  \nTwo days after the surgery, the woman’s belly became swollen and painful. Doctors did another surgery and found several problems: a small hole in her colon (part of the large intestine), inflammation of the lining of her abdomen (called peritonitis), infection of the uterus lining (endometritis), and issues with the new ureter connection. To treat these, surgeons removed her uterus (hysterectomy), repaired the colon, created a colostomy (an opening in the abdomen to let stool exit), and made a new opening for urine to leave the body (ureterocutaneous diversion).\n\n**How Did the Recovery Go?**  \nHer hospital stay was difficult. The colostomy started to pull back and got infected, so she needed another surgery to fix it. She also had a wound that opened up but was treated without more surgery. After six months, doctors closed the colostomy and repaired the ureter again using a technique called the Boari flap, which uses part of the bladder to rebuild the ureter. After this, she recovered well with normal bladder and kidney function. Over two years of follow-up, she had no major problems with urination or digestion.\n\n**What Does This Mean?**  \nThis case shows how serious complications can happen after cesarean surgery, especially when organs like the ureter and colon are injured. It also highlights the importance of careful surgery and follow-up care to fix these problems and help the patient recover fully.",
+            "B3": "**Background**  \nA 30-year-old woman, three pregnancies and three births, presented with reduced urine output and left flank pain accompanied by fever two days after an emergency cesarean section. The cesarean was performed due to prolonged labor complicated by maternal and fetal distress and significant vaginal bleeding; unfortunately, the newborn died shortly after delivery. During surgery, severe uterine adhesions related to endometriosis and adhesions between the uterus and sigmoid colon were noted. The patient had no prenatal care, no chronic illnesses, and no prior surgeries.\n\n**Key Findings**  \nPostoperatively, ultrasound imaging revealed severe left-sided hydronephrosis (swelling of the kidney due to urine buildup) and moderate free fluid in the abdominal cavity. Analysis of the abdominal fluid confirmed it was urine, indicating urinary leakage. Ureteroscopy demonstrated a complete obstruction of the left ureter. Given the patient’s hemodynamic instability and lack of percutaneous nephrostomy equipment, surgical exploration was undertaken. Intraoperatively, the left ureter was found crushed and ligated near its distal end. The damaged ureteral segment was excised, and a ureteroneocystostomy (surgical reimplantation of the ureter into the bladder) was performed with insertion of a double-J stent to maintain patency.\n\nTwo days after surgery, the patient developed increasing abdominal distension and ceased passing gas, with laboratory tests showing elevated white blood cells indicative of infection. A contrast-enhanced CT scan revealed free air and fluid throughout the abdomen and pelvis, suggesting bowel perforation. Emergency exploratory laparotomy identified a small perforation in the rectosigmoid colon, peritonitis (inflammation of the abdominal lining), endometritis (uterine infection), and disruption of the ureteral anastomosis.\n\n**Clinical Interpretation**  \nThe patient’s postoperative course was complicated by multiple severe intra-abdominal infections and organ injuries. The bowel perforation and peritonitis necessitated surgical repair and creation of a colostomy (diversion of the colon to an abdominal opening). The uterine infection and suture disruption required a hysterectomy (removal of the uterus). The ureteral anastomosis failure led to the creation of a left-sided ureterocutaneous diversion (bringing the ureter to the skin surface) and a urostomy for urinary drainage.\n\nSubsequently, the patient experienced stoma retraction with wound infection and communication between the colostomy and urostomy sites, requiring reoperation to relocate the colostomy. She also developed wound dehiscence (opening of the surgical wound) and hypoalbuminemia (low blood protein levels), which were managed with repeated wound care, antibiotics, and supportive therapy.\n\n**Next Steps and Outcome**  \nAfter a prolonged hospital stay of 30 days with multidisciplinary care, the patient was discharged in stable condition with home care support for her stomas and mobility. Six months later, the colostomy was closed, and the ureter was reconstructed using a Boari flap procedure—a technique where a flap of bladder tissue is tubularized and connected to the proximal ureter after stent placement. Postoperative recovery was uneventful.\n\nFollow-up imaging, including ultrasound and voiding cystourethrography, demonstrated normal bladder capacity and upper urinary tract anatomy. Ureteroscopy three months later confirmed a well-calibrated ureter. Over two years of follow-up, the patient remained free of urinary or gastrointestinal symptoms, indicating successful long-term recovery."
+        }
+    },
+    {
+        "article": "Mujer de 43 años, con antecedente de hipertensión arterial con tratamiento con losartán, dos cesáreas y oclusión tubaria bilateral. Ingresó a nuestro hospital y refirió dolor de 24 horas de evolución, tipo cólico en hipogastrio e irradiación a fosa iliaca izquierda, además de náusea y vómito en dos ocasiones. Se agregaron evacuaciones semilíquidas en forma inicial y posteriormente cese en las evacuaciones y en la canalización de gases. A la exploración física, la paciente presentó dolor en el abdomen, así como distensión, especialmente hacia el flanco izquierdo. En el mesogastrio y el flanco izquierdo hubo la presencia de timpanismo. La peristalsis estaba presente, mínima, abolida en flanco izquierdo y mesogastrio. La irritación peritoneal estuvo ausente. Se colocó sonda nasogástrica, con gasto mínimo gástrico y sin mejoría en la sintomatología. Los estudios de laboratorio demostraron: 9700 leucocitos con un 87% de neutrófilos, creatinina de 0.7 mg/dL, urea de 22 mg/dL y proteína C reactiva de 5.0 mg/L. En la radiografía simple de abdomen presentó dilatación importante del lado izquierdo del colon, con niveles hidroaéreos. La tomografía muestra la dilatación del colon del lado izquierdo, con imagen que simula grano de café en el corte coronal.\n\nAnte estos hallazgos clínicos y de imagen, se decidió hacer laparotomía de urgencia ante la sospecha de la presencia de vólvulo de sigmoides o de síndrome adherencial complicado. Durante la cirugía se evidenció un ciego flexionado hacia adelante y a la izquierda, carente de fijación retroperitoneal. El punto de flexión fue producido por una banda de adherencia colocada sobre el colon ascendente. Se realizó liberación de la adherencia y se corroboró continuidad adecuada hacia el colon distal. No se evidenció la presencia de isquemia, necrosis o perforación del ciego. Se realizó apendicectomía con descompresión del ciego a través de base apendicular y posteriormente ligadura de esta. Se llevó a cabo cecopexia hacia pared de fosa iliaca derecha. Después de la cirugía, hubo mejoría clínica de la paciente, que tuvo evacuaciones presentes normales. La paciente siguió controles correctos en consulta externa de cirugía y se mantuvo asintomática.",
+        "gold_summary": "Mujer de 43 años que ingresó a un servicio de urgencias con datos de obstrucción intestinal. Se realizó tomografía simple de abdomen donde se identificó dilatación del colon e imagen que semejaba un grano de café invertido. Se hizo laparotomía exploradora y se identificó vólvulo cecal del tipo báscula, sin compromiso vascular. Se realizó desvolvulación, descompresión a través de apendicectomía, y cecopexia. Posterior a evento quirúrgico, la paciente se recuperó sin incidentes y fue dada de alta con controles adecuados por consulta externa.",
+        "synthetic_summary": {
+            "B1": "A lady felt very sick with a tummy ache. The doctors took pictures of her belly. They saw a part of her tummy was very big and twisted.\n\nThe doctors did a big tummy surgery. They fixed the twisted part. They also took out a small part called the appendix. After the surgery, the lady felt better.\n\nShe went home and the doctors checked on her. She stayed healthy and happy.",
+            "B2": "**What Happened:**  \nA 43-year-old woman came to the emergency room with signs of a blocked intestine. A CT scan (a special type of X-ray that shows detailed pictures inside the body) showed that part of her large intestine, called the colon, was swollen. The scan also showed a shape that looked like an upside-down coffee bean, which can mean a twist in the intestine.\n\n**What the Doctors Found:**  \nDuring surgery, doctors found that a part of her colon called the cecum had twisted. This type of twist is called a \"bascula\" volvulus, which means the cecum flipped like a seesaw. Luckily, the blood flow was not cut off, so the tissue was still healthy.\n\n**What They Did:**  \nThe doctors untwisted the cecum to fix the blockage. They also removed the appendix (called an appendectomy) to help decompress, or relieve pressure, in the cecum. Then, they attached the cecum to the abdominal wall (a procedure called cecopexy) to keep it from twisting again.\n\n**How She Recovered:**  \nAfter the surgery, the woman got better without any problems. She was able to have normal bowel movements and was sent home with follow-up visits to make sure she stayed healthy.",
+            "B3": "**Background:**  \nA 43-year-old woman with a history of hypertension treated with losartan, two previous cesarean sections, and bilateral tubal ligation presented to the emergency department. She reported 24 hours of colicky lower abdominal pain radiating to the left iliac fossa, accompanied by nausea and two episodes of vomiting. Initially, she experienced semi-liquid bowel movements, which then ceased along with the passage of gas. Physical examination revealed abdominal tenderness and distension, especially on the left side, with tympanism (a hollow drum-like sound) in the mesogastric and left flank regions. Bowel sounds were minimal and absent in some areas, but there was no sign of peritoneal irritation (no inflammation of the abdominal lining).\n\n**Key Findings:**  \nLaboratory tests showed a white blood cell count of 9,700 with 87% neutrophils (indicating a possible infection or inflammation), normal kidney function (creatinine 0.7 mg/dL, urea 22 mg/dL), and mildly elevated C-reactive protein (5.0 mg/L, a marker of inflammation). Abdominal X-rays demonstrated significant dilation of the left colon with air-fluid levels, suggesting bowel obstruction. A computed tomography (CT) scan confirmed left-sided colonic dilation and revealed an inverted “coffee bean” sign on coronal images, a classic indicator of volvulus (twisting of the bowel).\n\n**Clinical Interpretation:**  \nGiven the clinical presentation and imaging findings, an urgent exploratory laparotomy (surgical opening of the abdomen) was performed with suspicion of sigmoid volvulus or complicated adhesive syndrome. During surgery, the cecum (the beginning of the large intestine) was found twisted forward and to the left, lacking normal retroperitoneal fixation (meaning it was abnormally mobile). The twist was caused by an adhesive band over the ascending colon. There was no evidence of compromised blood flow, tissue death, or perforation. The surgical team released the adhesion, confirmed normal bowel continuity, performed an appendectomy to decompress the cecum via the appendiceal base, and secured the cecum to the right iliac fossa wall (cecopexy) to prevent recurrence.\n\n**Next Steps and Outcome:**  \nFollowing surgery, the patient’s symptoms improved significantly. She resumed normal bowel movements and was discharged with appropriate outpatient surgical follow-up. Throughout subsequent visits, she remained asymptomatic, indicating a successful resolution of the cecal volvulus without complications."
+        }
+    },
+    {
+        "article": "Paciente de sexo femenino de 10 años, sin historia familiar de enfermedad tiroidea, portadora de bocio diagnosticado a los 9 años (ecografía tiroidea con sig nos compatibles de tiroiditis crónica) con presencia de anticuerpos antitiroideos positivos. Sin tratamiento al momento del ingreso hospitalario. Consultó por orina de aspecto espumoso de 5 días de evolución, asociado a dolor abdominal, vómitos profusos y diarrea. Evo lucionó con edema palpebral y de extremidades, disminución de la diuresis, decaimiento y fiebre de 38° C el día previo a su ingreso. Al momento de su eva luación en el servicio de urgencia destacó una pacien te con edema palpebral bilateral y pretibial, con bocio evidente (indoloro y sin nódulos palpables) y presen cia de soplo sistólico eyectivo en foco pulmonar IV/VI sin irradiación. Resto del examen sin alteraciones de significancia. Presión arterial 120/78 mmHg (percentil 95), temperatura 38,1°C, peso: 33.9 Kg, talla: 131,5 cm (p7), IMC 19,8 (p83).\n\nDentro de sus exámenes de admisión destacaron examen de orina completa con proteinuria +++, sin bacterias, sin nitritos, leucocitos 7 cel/uL (VN: 0-10 cel/uL), eritrocitos 4 cel/uL (VN: 0-15 cel/uL), índice proteinuria/creatininuria (IPC) 2 mg/mg, proteínas totales de 3.8 g/dL, hipoalbuminemia de 2,1 g/dL, hipercolesterolemia de 416 mg/dL, hipertrigliceridemia de 127 mg/dL y creatinina plasmática de 0,46 mg/dL (aclaramiento de creatinina calculado por fórmula de Schwartz: 125 ml/min/1,73 m2). Gases venosos, elec trolitos plasmáticos y hemograma dentro de rangos normales. En cuanto al estudio inmunológico destacó: inmunoglobulina A 181 mg/dL (VN 45-236), inmunoglobulina M 131 mg/dL (VN 52-242), inmunoglobulina G 208 (VN 608-1572) mg/dL, C3 125 mg/dL (VN 80-150), C4 37,3 mg/dL (VN 12-36). Ecografía renal normal. Se ingresó a la paciente con diagnóstico de SN y tiroiditis autoinmune.\n\nEn el contexto de SN se inició tratamiento con prednisona (60 mg/m2/día), con buena respuesta, logrando fundir edema y disminuir progresivamente la proteinuria hasta alcanzar rangos normales previo al egreso (IPC de egreso: 0.09, a los 6 días).\n\nDel punto de vista de función tiroidea su estudio mostró hormona tiroestimulante (TSH) 4,4 UI/ml (VN: 0,67-4,16 UI/ml), tiroxina (T4) libre 0,80 ng/ dL (VN: 0,86-1,4 ng/dL), anticuerpos antiperoxidasa (Anti Tpo) 120 U/ml (VN: 0-60 U/ml), anticuerpos antitiroglobulina (Anti-Tg) 82 U/ml (VN: 0-60 U/ ml), por lo que se inició terapia de sustitución con levotiroxina (25 mcg/día). La ecografía tiroidea descri bió tiroides de tamaño normal con leve aumento de vascularización difusa al Doppler, sin lesiones focales sólidas ni quísticas, siendo estos hallazgos sugerentes de tiroiditis. Resto del estudio (PCR para SARS CoV-2, anticuerpos anti citoplasma de neutrófilos, anticuer pos anti nucleares, anticuerpos anti DNA, anticuerpos anti estreptolisina O, anticuerpos anticardiolipinas, anticuerpos anti mieloperoxidasa y anticuerpos anti proteinasa 3) resultó negativo.\n\nA los 6 días de ingresada la paciente se encontraba en buenas condiciones, siendo dada de alta con prednisona (60 mg al día) y levotiroxina (25 ucg al día). En el seguimiento a los 12 meses la paciente se encontraba asintomática, con su patología tiroidea bajo control (TSH 1,11 UI/ml) con tratamiento de sustitución. No ha presentado recaídas del SN (examen de orina sin proteinuria y creatinina 0,44 mg/dL).",
+        "gold_summary": "Paciente de 10 años que se presenta con síndrome nefrótico y bocio. Se pesquisa antecedente de tiroiditis autoinmu ne e hipotiroidismo no tratado. Se inicia terapia corticoidal y hormonal de sustitución (levotiroxina), logrando buena respuesta clínica y de laboratorio.",
+        "synthetic_summary": {
+            "B1": "A girl who is 10 years old was feeling sick. She had swelling and a big bump on her neck. Her body was not working well because her thyroid was tired. \n\nThe doctor gave her medicine to help her body and her neck. The medicine helped her feel better and get strong again.",
+            "B2": "**What Happened to the Patient?**  \nA 10-year-old girl came to the hospital with swelling caused by a kidney problem called nephrotic syndrome. She also had a swollen thyroid gland, known as a goiter. Doctors found out she had an autoimmune thyroid disease, which means her immune system was attacking her thyroid. This caused her thyroid to work less than normal, a condition called hypothyroidism. Before coming to the hospital, she had not received any treatment for this.\n\n**How Did the Doctors Treat Her?**  \nThe doctors started two treatments. First, they gave her corticosteroids, a type of medicine that helps reduce swelling and inflammation in the kidneys. Second, they gave her levothyroxine, a hormone medicine that replaces the missing thyroid hormone. This helped her thyroid work better.\n\n**What Was the Result?**  \nThe treatments worked well. Her swelling went down, and tests showed her kidney and thyroid problems improved. After 12 months, she felt fine, her thyroid was under control, and her kidney function was normal. She did not have any relapses of the kidney problem.  \n\nThis case shows how important it is to treat both kidney and thyroid problems together when they happen at the same time.",
+            "B3": "**Background:**  \nA 10-year-old girl with no family history of thyroid disease was diagnosed at age 9 with a goiter and chronic autoimmune thyroiditis, confirmed by thyroid ultrasound and positive thyroid autoantibodies. She had not received treatment for her thyroid condition prior to hospital admission. She presented with a five-day history of foamy urine, abdominal pain, frequent vomiting, and diarrhea. Subsequently, she developed swelling of the eyelids and limbs, reduced urine output, fatigue, and fever (38°C) one day before admission.\n\n**Key Findings:**  \nOn examination, the patient had bilateral eyelid and pretibial edema, a visibly enlarged but painless goiter without palpable nodules, and a systolic ejection murmur heard at the pulmonary area (grade IV/VI). Vital signs showed elevated blood pressure at the 95th percentile (120/78 mmHg) and mild fever (38.1°C). Her weight was 33.9 kg, height 131.5 cm (7th percentile), and body mass index (BMI) 19.8 (83rd percentile).\n\nLaboratory tests revealed significant proteinuria (+++), with a protein-to-creatinine ratio of 2 mg/mg, hypoalbuminemia (2.1 g/dL), elevated total cholesterol (416 mg/dL) and triglycerides (127 mg/dL), and normal kidney function (creatinine 0.46 mg/dL; estimated glomerular filtration rate 125 ml/min/1.73 m²). Urinalysis showed no infection. Immunological studies indicated low IgG levels (208 mg/dL), normal IgA and IgM, and normal complement levels (C3 and C4). Thyroid function tests showed mildly elevated thyroid-stimulating hormone (TSH 4.4 UI/ml), low free thyroxine (T4 0.80 ng/dL), and elevated thyroid autoantibodies (anti-thyroid peroxidase 120 U/ml and anti-thyroglobulin 82 U/ml). Thyroid ultrasound demonstrated a normal-sized gland with diffuse increased blood flow, consistent with thyroiditis. Additional autoimmune and infectious markers were negative.\n\n**Clinical Interpretation:**  \nThe patient was diagnosed with nephrotic syndrome (a kidney disorder causing protein loss in urine and edema) in the context of untreated autoimmune thyroiditis and hypothyroidism. The nephrotic syndrome explained her edema, proteinuria, and lipid abnormalities. The thyroiditis accounted for her goiter and abnormal thyroid function tests.\n\n**Next Steps and Outcome:**  \nTreatment was initiated with high-dose corticosteroids (prednisone 60 mg/m²/day) to control the nephrotic syndrome, resulting in resolution of edema and normalization of proteinuria within six days. Levothyroxine replacement therapy (25 mcg/day) was started to address hypothyroidism. The patient’s clinical condition improved steadily, and she was discharged on both medications.\n\nAt 12-month follow-up, she remained asymptomatic with well-controlled thyroid function (TSH 1.11 UI/ml) on levothyroxine and no relapse of nephrotic syndrome, as evidenced by normal urine tests and stable kidney function.\n\n---\n\nThis case illustrates the coexistence of autoimmune thyroiditis with nephrotic syndrome in a pediatric patient, highlighting the importance of comprehensive evaluation and combined hormonal and immunosuppressive therapy for optimal outcomes."
+        }
+    },
+    {
+        "article": "La exploración neurológica exhaustiva puso de manifiesto una apariencia facial característica: mirada fija con los ojos muy abiertos, fruncimiento de la frente con una expresión de ceño fruncido (signo del procerus) y expresión fija de la parte inferior de la cara. La paciente presentaba hipocinesia-rigidez simétrica de predominio axial con postura retrocólica del tronco y el cuello. El examen de la deambulación reveló un patrón de la marcha del nivel superior caracterizado por una llamativa vacilación inicial que requería ayuda de objetos/personas cercanas. Una vez que comenzaba a caminar, los pasos mejoraban relativamente, pero volvía a aparecer una marcha inefectiva cuando intentaba girar. Exhibía zancadas cortas, congelación, base amplia de sustentación, desequilibrio, movimiento lento de los miembros inferiores, arrastre de los pies y pérdida de la fluidez normal del tronco y las extremidades. Los reflejos posturales estaban alterados. Asimismo, existía una dificultad grave para la bipedestación tras la sedestación y dificultad para darse la vuelta en la cama. Sin embargo, los signos frontales, como la rigidez paratónica, los reflejos de prensión, la incontinencia urinaria y las características de los déficits cognitivos frontales (por ejemplo, cambios disejecutivos y de personalidad e impulsividad) estaban ausentes, excepto por un estado apático progresivo. Los movimientos oculares sacádicos verticales estaban alterados, con amplitudes relativamente normales y movimientos sacádicos horizontales. Se evidenciaron sacadas de onda cuadrada y una oftalmoplejía supranuclear. La resonancia magnética del cerebro reveló atrofia del mesencéfalo, dilatación del acueducto de Silvio y del III ventrículo y atrofia de los lóbulos frontales, y los signos típicos del colibrí y de la gloria de la mañana. Finalmente, la paciente fue diagnosticada de una PSP probable.",
+        "gold_summary": "Mujer de 58 años sana que consultó por un trastorno de la marcha con caídas. La exploración neurológica mostró una apariencia facial característica (mirada fija, ojos muy abiertos, ceño fruncido y expresión fija hemifacial inferior), e hipocinesia-rigidez simétrica de predominio axial (postura retrocólica del tronco y el cuello). La exploración de la marcha reveló un trastorno de la marcha del nivel superior, caracterizado por una significativa vacilación inicial, que precisaba ayuda de objetos/personas cercanos. Al iniciar la marcha, los pasos mejoraban relativamente, pero reaparecía una deambulación inefectiva al girar. Presentaba zancadas cortas, congelación, base amplia de sustentación, desequilibrio, movimiento lento de las piernas, arrastre de los pies, y pérdida de la cadencia normal del tronco y las extremidades. Los reflejos posturales estaban alterados. La resonancia magnética cerebral desveló atrofia mesencefálica, dilatación de acueducto de Silvio y III ventrículo, atrofia frontal bilateral y el signo típico del colibrí. Finalmente, la paciente fue diagnosticada de una PSP probable.",
+        "synthetic_summary": {
+            "B1": "A lady, 58 years old, had trouble walking and fell down.  \n\nHer face looked special. Her eyes were wide open and her forehead was wrinkled. Her face did not move much.  \n\nShe stood and walked in a strange way. She needed help to start walking. Her steps were small and slow. She sometimes got stuck and had trouble turning.  \n\nHer legs moved slowly, and she dragged her feet. She wobbled and lost balance.  \n\nA brain picture showed some parts were smaller than normal.  \n\nThe doctors said she has a sickness called PSP. It makes walking and moving hard.",
+            "B2": "**What They Found**\n\nA 58-year-old woman, who was healthy before, came to the doctor because she had trouble walking and was falling. When the doctors examined her, they noticed her face looked very specific: her eyes were wide open and fixed, her forehead was wrinkled as if frowning, and the lower part of her face looked stiff. She also had stiffness and slow movements, especially in the middle part of her body like her neck and trunk, which made her stand with her body leaning backward.\n\nWhen she tried to walk, she hesitated a lot at first and needed help from nearby objects or people. After starting to walk, her steps got a bit better, but when she tried to turn around, her walking became unsteady again. She took short steps, sometimes froze while walking, had a wide stance to keep balance, and dragged her feet. Her legs moved slowly, and the normal smooth movement of her body and arms was lost. Her balance reflexes, which help keep her steady, were also not working properly.\n\n**What It Means**\n\nA brain scan called an MRI showed that parts of her brain were shrinking. This included the midbrain (a part that helps control movement), the fluid spaces inside her brain were larger than normal, and both sides of the front part of her brain were smaller. The scan also showed a special pattern called the \"hummingbird sign,\" which doctors use to help identify certain brain diseases.\n\nBased on all these signs—her facial expression, walking problems, and brain scan—the doctors diagnosed her with probable Progressive Supranuclear Palsy (PSP). PSP is a rare brain disorder that affects movement, balance, and eye movements. It causes stiffness, slow movement, and difficulty walking and turning, which matches what this patient experienced.",
+            "B3": "**Background**  \nA previously healthy 58-year-old woman sought medical evaluation due to difficulties with walking and recurrent falls. Her neurological examination revealed distinctive facial features and motor symptoms suggestive of a neurodegenerative disorder.\n\n**Key Findings**  \n- **Facial Appearance:** The patient exhibited a characteristic fixed gaze with widely opened eyes, a furrowed brow (notably the procerus sign, indicating persistent forehead wrinkling), and a fixed expression in the lower half of the face.  \n- **Motor Symptoms:** She demonstrated symmetrical hypokinesia (reduced movement) and rigidity predominantly affecting the axial muscles, resulting in a retrocollis posture—an abnormal backward bending of the trunk and neck.  \n- **Gait Abnormalities:** Her walking pattern was consistent with a higher-level gait disorder. Initially, she showed marked hesitation requiring support from nearby objects or people. Once walking commenced, step length improved somewhat, but ineffective gait recurred during turning maneuvers. Additional features included short steps, freezing episodes (temporary inability to move), a broad base of support, imbalance, slow leg movements, foot dragging, and loss of normal fluidity in trunk and limb movements. Postural reflexes were impaired, contributing to her instability.  \n- **Other Neurological Signs:** Although she had severe difficulty standing up from a seated position and turning in bed, frontal lobe signs such as paratonic rigidity (variable muscle tone), grasp reflexes, urinary incontinence, and cognitive deficits typical of frontal lobe dysfunction (executive dysfunction, personality changes, impulsivity) were absent, except for a progressively apathetic state. Vertical saccadic eye movements were impaired, with relatively preserved amplitude and horizontal saccades; square wave jerks and supranuclear ophthalmoplegia (eye movement paralysis due to brainstem dysfunction) were also observed.  \n- **Neuroimaging:** Brain MRI revealed midbrain (mesencephalon) atrophy, enlargement of the cerebral aqueduct (aqueduct of Sylvius) and third ventricle, bilateral frontal lobe atrophy, and characteristic radiological signs known as the “hummingbird sign” and “morning glory sign,” which are indicative of progressive supranuclear palsy (PSP).\n\n**Clinical Interpretation**  \nThe combination of symmetrical axial rigidity, distinctive facial expression, higher-level gait disturbance with freezing and postural instability, vertical gaze palsy, and specific MRI findings strongly supports a diagnosis of probable progressive supranuclear palsy. PSP is a rare neurodegenerative condition characterized by tau protein accumulation leading to motor and cognitive impairments.\n\n**Next Steps**  \nManagement should focus on symptomatic treatment and supportive care, including physical therapy to address gait and balance difficulties, and monitoring for progression of motor and cognitive symptoms. Referral to a movement disorders specialist is recommended for comprehensive evaluation and to discuss potential inclusion in clinical trials or advanced therapies."
+        }
+    },
+    {
+        "article": "Una mujer de 36 años, previamente sana, fue picada una vez por un insecto Hymenoptera desconocido, lo que le provocó hinchazón y eritema en la parte dorsal de la mano derecha. La fiebre punzante apareció en un plazo de 6 horas, a pesar de que el sitio de la picadura se volvió irreconocible gradualmente. Acudió a una clínica local donde le recetaron esteroides orales (prednisolona 20 mg/día) y antibióticos. Tres días después, acudió a nuestro departamento de urgencias por una fiebre intermitente. Presentaba una temperatura elevada (38,9°C), taquicardia e hipotensión (presión arterial 80/52 mmHg) en el momento de la clasificación. La electrocardiografía mostró fibrilación auricular con una frecuencia ventricular rápida de alrededor de 130 latidos por minuto y elevación difusa del ST. La radiografía de tórax mostró una relación cardiotorácica normal sin signos de infiltración o congestión. El hemograma no mostró eosinofilia, leucocitosis, leucopenia o desviación a la izquierda. La isoenzima MB de creatina cinasa (CK-MB) y la troponina cardíaca I se elevaron a 96,0 ng/mL y 8,0 ng/mL, respectivamente. La proteína C reactiva fue de 10,5 mg/L y la procalcitonina fue de 0,32 ng/mL. El NT-proBNP fue de 20 700 pg/mL. La ecocardiografía mostró una hipocinesia global del ventrículo izquierdo con una fracción de eyección del 30,6% y sin derrame pericárdico. El cateterismo cardíaco emergente no reveló lesiones de las arterias coronarias o vasospasmo. Se insertó un globo intraaórtico durante el procedimiento para el shock cardiogénico. La hipotensión progresó acompañada de taquicardia ventricular y fibrilación ventricular, y luego se produjo un paro cardíaco intrahospitalario. La reanimación cardiopulmonar manual no tuvo éxito durante 25 minutos y se usó el soporte cardiopulmonar percutáneo (PCPS, CAPIOX® Centrifugal Pump Controller SP-200, Terumo). La circulación espontánea se estableció 25 minutos después con una recuperación total de la conciencia.\n\nLa prueba rápida de antígeno de influenza (Directigen EZ Flu A+B; BD, Franklin Lakes, NJ, EE. UU.), los cultivos de esputo, los cultivos de sangre y los exámenes serológicos para los virus respiratorios recolectados al ingreso fueron negativos. En el día 2 del ingreso, los niveles séricos de CK-MB y troponina I alcanzaron un máximo de >303 ng/ml y >81 ng/ml, respectivamente. La ecocardiografía de seguimiento 24 horas después del inicio del PCPS mostró deterioro de la función ventricular izquierda, cierre persistente de las válvulas aórticas y trombos intracardiacos en la aurícula izquierda y el ventrículo izquierdo, aproximadamente 24 horas después del inicio del soporte mecánico. En el día 3, el shock progresó con falla multiorgánica. Se aplicó hemodiálisis venovenosa continua debido a la acidosis metabólica y oliguria. En el día 4, la función ventricular derecha también se deterioró gravemente y la actividad eléctrica del corazón desapareció gradualmente. El PCPS se cambió a soportes mecánicos bi-ventriculares a través de canalizaciones hacia la aurícula derecha, el tronco pulmonar, el ápex del ventrículo izquierdo y la aorta ascendente. Ambos sistemas se establecieron utilizando bombas de sangre centrífugas MEDTRONIC Affinity CP. Debido a la hemorragia pulmonar con consolidación bilateral severa de los pulmones, se usó un oxigenador de membrana para lograr una oxigenación adecuada. El flujo sanguíneo se estableció a 3.5 L/minuto, lo que podría mantener la presión arterial media en torno a 65 mmHg. Se realizó una biopsia endomiocárdica del ventrículo izquierdo y la patología reveló una inflamación significativa compuesta principalmente por linfocitos y algunos eosinófilos. El daño miocárdico con necrosis estuvo presente, pero no extenso. En términos de ajustes de ventilador, la presión de conducción y la presión de meseta se establecieron en torno a 15 y 30 cmH2O respectivamente para la protección pulmonar. Se usó la fibra broncoscopia repetidamente para eliminar los coágulos de sangre que obstruían las vías respiratorias principales. En el día 13 del ingreso, la actividad eléctrica del corazón del paciente permaneció ausente y ambas bombas de sangre se cambiaron a los sistemas de asistencia ventricular Levitronix Centri-Mag (Levitronix LLC, Waltham, MA, EE. UU.) para un mejor soporte. El paciente fue trasladado a un centro de trasplantes y se registró como candidato para un trasplante de corazón. En el día 14 se insertó otra cánula en la vena femoral común izquierda para aumentar el flujo de entrada del VAD derecho. Desde el día 14 hasta el día 48, el paciente sufrió episodios de sangrado masivo del mediastino y la vagina, infección de la herida esternal con formación de abscesos, infecciones por úlceras de presión y progresiva hiperbilirrubinemia. Su condición se estabilizó después de desbridamiento, hemostasia quirúrgica y uso de antibióticos fuertes. Se sometió a 5 cursos de intercambio de plasma terapéutico para evitar el rechazo mediado por anticuerpos y recibió un trasplante de corazón ortotópico el día 49. El estudio patológico del corazón del paciente mostró pancarditis de ambos ventrículos y ninguna alteración específica de las 3 arterias coronarias. La ECMO de VA se mantuvo hasta el día 58 para el apoyo postoperatorio del fallo cardiaco. La biopsia endomiocárdica repetida después del trasplante no mostró evidencia de rechazo celular o humoral. La paciente experimentó episodios de shock séptico bajo inmunosupresión y se sometió a una laparoscopia exploratoria y apendicectomía el día 93. La extubación se realizó el día 96 y se dio de alta el día 101. La paciente permaneció clínicamente estable en el seguimiento de 3 meses.\n\nMH - Adulto\nMH - Animales\nMH - Abejas\nMH - Picaduras y mordeduras/*complicaciones\nMH - Oxigenación por membrana extracorpórea\nMH - Mujer\nMH - Paro cardiaco/*etiología/tratamiento\nMH - Insuficiencia cardiaca/*etiología/terapia\nMH - *Trasplante de corazón\nMH - Dispositivos de asistencia cardiaca\nMH - Humanos\nMH - Hipersensibilidad/*diagnóstico\nMH - Miocarditis/*diagnóstico\nMH - Shock, Cardiogénico/*etiología/terapia\n",
+        "gold_summary": "Paciente: Mujer, 36 años\n\nDiagnóstico final: Shock cardiogénico • miocarditis\n\nSíntomas: Fiebre\n\nMedicación: —\n\nProcedimiento clínico: soporte circulatorio mecánico\n\nEspecialidad: Cirugía\n\n\nInforme del caso:\n\nReportamos el caso de una mujer de 36 años que desarrolló fiebre y shock cardiogénico 3 días después de una picadura de abeja. La angiografía cardíaca mostró arterias coronarias permeables y una función ventricular izquierda gravemente comprometida. Su hemodinámica permaneció inestable bajo una dosis alta de agentes inotrópicos y apoyo con un balón intraaórtico. El paro cardíaco intrahospitalario ocurrió 4 horas después del ingreso y recibió reanimación cardiopulmonar extracorpórea. Su oxigenación de membrana extracorpórea venosa periférica (VA ECMO) se cambió a dispositivos de asistencia ventricular bilateral (VAD) debido a una insuficiencia cardíaca derecha progresiva. El resultado de la biopsia endomiocárdica fue compatible con el cuadro de miocarditis por hipersensibilidad. Su corazón entró en paro persistente bajo apoyo circulatorio mecánico. Se sometió a un trasplante de corazón el día 49 del ingreso y permaneció clínicamente estable 6 meses después del alta.\n",
+        "synthetic_summary": {
+            "B1": "A lady got a bee sting on her hand. After three days, she felt very sick and had a fever. Her heart was very weak and could not work well. Doctors helped her with special machines to keep her heart and body working. Her heart stopped, but they helped her start it again. She needed a new heart to get better. After the new heart, she felt much better and stayed healthy.",
+            "B2": "**What Happened to the Patient**\n\nA 36-year-old woman, who was healthy before, got a bee sting on her right hand. Within a few hours, she developed swelling and redness where she was stung. Three days later, she had a fever and her condition worsened quickly. She went to the hospital with a very fast heartbeat, low blood pressure, and signs of heart problems.\n\n**What the Doctors Found**\n\nTests showed that her heart’s left ventricle (the main pumping chamber) was very weak and not working well. Her heart arteries were clear, so the problem was not a blocked artery. She went into shock, which means her heart could not pump enough blood to her body. She even had a cardiac arrest, where her heart stopped beating properly.\n\nDoctors used machines to help her heart and lungs work. First, they used a balloon pump to support her heart, but it wasn’t enough. Then, they used a special machine called ECMO (extracorporeal membrane oxygenation), which takes over the work of the heart and lungs. Later, they switched to devices called ventricular assist devices (VADs) to help both sides of her heart.\n\nA biopsy, which is when a small piece of heart tissue is taken for testing, showed she had myocarditis. Myocarditis is an inflammation of the heart muscle, often caused by an allergic reaction or infection. In her case, it was likely due to a hypersensitivity reaction to the bee sting.\n\n**What This Means**\n\nHer heart stopped working despite all the support from machines. Because of this, she needed a heart transplant. The transplant was done 49 days after she was admitted to the hospital. After the surgery, she recovered well and was stable six months later.\n\n**Summary**\n\nThis case shows how a bee sting can sometimes cause a serious allergic reaction leading to inflammation of the heart muscle (myocarditis). This can cause heart failure and shock, needing advanced treatments like heart support machines and even a heart transplant. Early medical care and specialized support are crucial in such rare but life-threatening cases.",
+            "B3": "**Background**  \nA previously healthy 36-year-old woman experienced a single sting from an unidentified Hymenoptera insect (a group that includes bees and wasps). Within six hours, she developed fever, swelling, and redness on the back of her right hand at the sting site, which gradually became unrecognizable. Despite initial treatment with oral steroids and antibiotics at a local clinic, she presented three days later with intermittent fever, elevated heart rate, low blood pressure, and signs of severe cardiac distress.\n\n**Key Findings**  \n- On admission, she had a high fever (38.9°C), tachycardia, hypotension (80/52 mmHg), and atrial fibrillation with a rapid ventricular response (~130 bpm).  \n- Electrocardiogram showed diffuse ST elevation; chest X-ray was normal.  \n- Blood tests revealed elevated cardiac enzymes: CK-MB at 96.0 ng/mL and troponin I at 8.0 ng/mL, indicating myocardial injury. Inflammatory markers were mildly elevated (CRP 10.5 mg/L, procalcitonin 0.32 ng/mL). NT-proBNP was markedly elevated at 20,700 pg/mL, reflecting heart failure.  \n- Echocardiography demonstrated global hypokinesia (reduced movement) of the left ventricle with a severely reduced ejection fraction (30.6%), without pericardial effusion.  \n- Emergent cardiac catheterization showed no coronary artery blockages or vasospasm.  \n- Despite intra-aortic balloon pump support and high-dose inotropes, her hemodynamic status deteriorated, culminating in ventricular tachycardia, ventricular fibrillation, and in-hospital cardiac arrest.  \n- After 25 minutes of unsuccessful manual resuscitation, extracorporeal cardiopulmonary resuscitation (ECPR) with percutaneous cardiopulmonary support (PCPS) was initiated, restoring spontaneous circulation and consciousness.  \n- Follow-up showed worsening cardiac enzyme levels (>303 ng/mL CK-MB, >81 ng/mL troponin I) and progressive left ventricular dysfunction with intracardiac thrombi.  \n- Multiorgan failure ensued, requiring continuous venovenous hemodialysis for metabolic acidosis and oliguria. Right ventricular function also deteriorated, leading to loss of cardiac electrical activity.  \n- Mechanical circulatory support was escalated to biventricular assist devices (VADs) with membrane oxygenation due to severe pulmonary hemorrhage and bilateral lung consolidation.  \n- Endomyocardial biopsy revealed significant myocardial inflammation predominantly composed of lymphocytes and some eosinophils, consistent with hypersensitivity myocarditis. Myocardial necrosis was present but limited.  \n- The patient experienced multiple complications including massive bleeding, sternal wound infection with abscess formation, pressure ulcer infections, and progressive liver dysfunction. These were managed with surgical debridement, hemostasis, and broad-spectrum antibiotics.  \n- Five courses of therapeutic plasma exchange were performed to prevent antibody-mediated rejection in preparation for heart transplantation.  \n- On hospital day 49, she underwent orthotopic heart transplantation. Pathology of the explanted heart confirmed pancarditis (inflammation of all heart layers) without coronary artery abnormalities.  \n- Post-transplant, she required continued venoarterial extracorporeal membrane oxygenation (VA ECMO) for cardiac support until day 58. Subsequent biopsies showed no evidence of cellular or humoral rejection.  \n- She experienced septic shock episodes under immunosuppression, necessitating exploratory laparoscopy and appendectomy on day 93.  \n- Extubation occurred on day 96, and she was discharged on day 101. At three months follow-up, she remained clinically stable.\n\n**Clinical Interpretation**  \nThis case illustrates a rare but severe hypersensitivity myocarditis triggered by an insect sting, leading to fulminant cardiogenic shock and cardiac arrest. The absence of coronary artery disease and the biopsy findings support an immune-mediated myocardial inflammation rather than ischemic injury. Despite maximal medical and mechanical support, including intra-aortic balloon pump, extracorporeal membrane oxygenation, and biventricular assist devices, the patient’s heart function deteriorated irreversibly, necessitating heart transplantation. The successful transplantation and stabilization highlight the importance of advanced mechanical circulatory support and immunomodulatory therapies in managing fulminant myocarditis.\n\n**Next Steps**  \n- Continued close monitoring for transplant rejection and infection under immunosuppression.  \n- Rehabilitation to recover physical function post-hospitalization.  \n- Long-term cardiology follow-up to assess graft function and manage immunosuppressive therapy.  \n- Patient education regarding avoidance of insect stings and early recognition of hypersensitivity reactions."
+        }
+    },
+    {
+        "article": "Un hombre de 24 años con complicaciones cardiovasculares relacionadas con MFS fue admitido en nuestro departamento de medicina interna debido a 3 episodios consecutivos de insuficiencia cardiaca aguda descompensada con fracción de eyección reducida (ADHFrEF) de 2014 a 2017. Su historia médica restante incluye hipertensión arterial, dislipidemia, hipertiroidismo, shock anafiláctico debido a flecainida y hábito tabágico previo.\n\nEl diagnóstico de MFS se realizó en 2010, cuando se llevó a cabo la sustitución de la aorta ascendente y la válvula aórtica con prótesis mecánica debido a una disección aórtica aguda tipo A en presencia de antecedentes familiares (madre, padre y 3 hijos con MFS). Durante el período intraoperatorio, se produjo un síndrome coronario agudo inferior y se trató con cirugía de injerto de derivación de la arteria coronaria.\n\nEn mayo de 2014, se realizó la implantación de una prótesis mecánica de aorta descendente y arco aórtico debido a un aneurisma disecante crónico. El hematoma peri-aórtico y la isquemia medular complicaron la cirugía y causaron paraplejia de las extremidades inferiores, dolor y hipoestesia térmica, e incontinencia rectal. Después de 2 meses, durante su primera admisión por ADHFrEF, las pruebas de laboratorio fueron notables para N-terminal pro-BNP (NT-proBNP) de 12,000 pg/mL y el ecocardiograma transtorácico mostró una función de la prótesis normal, dilatación de todas las cámaras cardiacas (principalmente las izquierdas) con insuficiencia mitral y tricuspídea moderada, hipertrofia ventricular izquierda, acinesia de la pared inferior, discinesia septal e hipocinesia de las paredes restantes con reducción severa de la fracción de eyección ventricular izquierda (LVEF) −20%. Se le trató con diuréticos intravenosos y desfibrilador cardiaco interno (St. Jude Ellipse DR, modo DDD) sin terapia de resincronización cardiaca (criterios de electrocardiograma no cumplidos) y se le dio de alta con la máxima terapia médica (furosemida, carvedilol, ramipril, espironolactona, digoxina y amlodipina).\n\nEn agosto de 2017, se produjo un nuevo episodio de ADHFrEF. Los valores de laboratorio de admisión notables incluían NT-proBNP de 2719 pg/mL y midregional-proadrenomedullin (MR-proADM) de 1.61 nmol/L, mientras que el ecocardiograma transtorácico y transesofágico mostró un LVEF de 35%, función de prótesis normal, severa regurgitación tricuspídea, y ruptura de la valva anterior de la chorda tendineae con severa regurgitación mitral. Los pacientes fueron tratados con diuréticos intravenosos y digoxina y dados de alta con una terapia médica óptima (furosemida, carvedilol, ramipril, espironolactona, digoxina, y amlodipina).\n\nPor último, volvió a ser admitido en nuestro departamento de medicina interna en noviembre de 2017 debido a un tercer episodio de ADHFrEF y una acumulación de líquido mediastinal infectado secundaria a una corrección quirúrgica de insuficiencia valvular severa un mes antes con implantación de prótesis mecánica mitral (31 mm ST Jude) y anuloplastia tricúspide De Vega.\n\nEl examen físico reveló una presión arterial de 120/80 mm Hg, pulso de 82 bpm, frecuencia respiratoria de 26 apm, saturación de O2 de 87% en aire ambiente con posición ortopneica obligatoria, y un habitus marfanoide (peso de 147 kg, altura de 2.2 m). La evaluación cardiopulmonar reveló un segundo sonido cardíaco metálico, percusión opaca con reducción del frémito vocal táctil y crepitaciones en la base de los pulmones, disminución amplia de los sonidos respiratorios vesiculares, presencia de ascitis abundante e hinchazón de las piernas.\n\nLos valores de laboratorio notables incluyeron NT-proBNP de 10,132 pg/mL y MR-proADM de 2,36 nmoL/mL.\n\nEl análisis de gases arteriales reveló una hipoxemia grave con alcalosis respiratoria y metabólica (pH 7,56, pO2 46 mm Hg, pCO2 24,8 mm Hg, HCO3− 21,9 mm mol/L, gradiente alveolar-arterial 31 mm Hg). Aunque el electrocardiograma resaltó fibrilación auricular con frecuencia ventricular de 80 bpm, hipertrofia ventricular izquierda e isquemia subepicárdica infralateral, el ecocardiograma transtorácico mostró las mismas características que el anterior, excepto por una FEVI de 30 %, presencia de prótesis mecánicas mitrales con fuga paravalvular y gradiente medio de 9 mm Hg, e insuficiencia tricuspídea leve.\n\n\nEn la radiografía de tórax y en la tomografía computarizada de alta resolución se observa una congestión hilar con cardiomegalia, consolidación pulmonar en el lóbulo superior derecho y acumulación de líquido mediastínico infectado.\n\nEl paciente fue tratado con 250 mg de furosemida intravenosa por día, 100 mg de canrenona por día, 4,5 g de piperacilina/tazobactam cada 6 horas y 12 mg/kg de teicoplanina por día, y luego 12 mg/kg por día. El día 9, una vez alcanzada la estabilización hemodinámica, se agregó una dosis intermedia de sacubitril/valsartan de 49/51 mg por día a 3,125 mg de carvedilol por día, 100 mg de espironolactona por día, 250 mg de furosemida por día y 0,25 mg de digoxina por día.\n\nEn el seguimiento de 1 mes, sacubitril/valsartan se aumentó a 97/103 mg b.i.d. para la buena condición clínica del paciente, lo que permitió una reducción persistente y progresiva de los parámetros clínicos, de laboratorio (reducción de NT-proBNP e incremento de MR-proADM), de los parámetros ecocardiográficos (aumento del EFV final del ventrículo izquierdo (42 % vs 30 %), del diámetro final del ventrículo izquierdo, del diámetro diastólico final del ventrículo izquierdo, de la masa del ventrículo izquierdo y del índice de masa del ventrículo izquierdo) y una mejora de la calidad de vida sin nuevos episodios de ADHFrEF hasta el seguimiento de 9 meses (Fig. (Fig.1B1B y D; Tabla 1).1). Debido a la falta de un régimen de dosificación específico para sacubitril/valsartan en la miocardiopatía relacionada con la EM, utilizamos el esquema terapéutico recomendado.\n\nMH - Aminobutiratos/uso terapéutico\nMH - Antagonistas de los receptores de la angiotensina/*uso terapéutico\nMH - Compuestos de bifenilo\nMH - Combinaciones de fármacos\nMH - Insuficiencia cardiaca/*terapia farmacológica/*etiología\nMH - Humanos\nMH - Hombre\nMH - Síndrome de Marfan/*complicaciones\nMH - Tetrazoles/uso terapéutico\nMH - Resultado del tratamiento\nMH - Valsartán\nMH - Adultos jóvenes\n",
+        "gold_summary": "Preocupaciones de los pacientes:\nUn hombre de 24 años fue admitido en nuestro departamento de medicina interna debido a disnea, ascitis e hinchazón de las piernas. El análisis de gases en sangre arterial reveló una hipoxemia grave con alcalosis respiratoria y metabólica. La radiografía de tórax mostró una congestión hilar.\n\nDiagnósticos:\nInsuficiencia cardíaca aguda descompensada recurrente con fracción de eyección reducida a pesar de la terapia médica óptima en la cardiomiopatía relacionada con el síndrome de Marfan.\n\nIntervenciones y resultados:\nSe agregó sacubitril/valsartan a la terapia médica óptima después de la estabilización hemodinámica, lo que permitió una mejora clínica, de laboratorio y ecocardiográfica progresiva. El paciente mantuvo una supervivencia libre de insuficiencia cardiaca y una buena calidad de vida hasta el seguimiento de 9 meses.\n",
+        "synthetic_summary": {
+            "B1": "A man felt very tired and had trouble breathing. His legs and belly were swollen. The doctors found his heart was very weak.\n\nThey gave him special medicine to help his heart. After the medicine, he started feeling better. He stayed healthy and happy for many months.",
+            "B2": "**What Happened to the Patient**  \nA 24-year-old man with Marfan syndrome, a genetic condition affecting connective tissues, was admitted to the hospital because he had trouble breathing, swelling in his legs, and fluid buildup in his abdomen (called ascites). Blood tests showed he had low oxygen levels and an imbalance in his blood’s acid-base balance. A chest X-ray revealed fluid congestion near the center of his lungs.\n\n**What the Doctors Found**  \nHe was diagnosed with repeated episodes of acute heart failure. This means his heart was not pumping blood well, and the amount of blood the left side of his heart could pump (called the ejection fraction) was very low. This happened even though he was already receiving the best available heart medicines. His heart problems were related to Marfan syndrome, which can cause the heart and blood vessels to weaken.\n\n**How They Treated Him and What Happened Next**  \nAfter stabilizing his condition, doctors added a new medicine called sacubitril/valsartan to his treatment. This drug helps the heart work better by relaxing blood vessels and reducing harmful hormones. Over the next several months, the patient showed steady improvement. Tests showed his heart was pumping more effectively, and his symptoms got better. He stayed free from further heart failure episodes and had a better quality of life for at least nine months after starting the new medicine.",
+            "B3": "**Background**  \nA 24-year-old man with a known diagnosis of Marfan syndrome (MFS) and multiple cardiovascular complications was admitted to the internal medicine department presenting with worsening shortness of breath (dyspnea), abdominal fluid accumulation (ascites), and leg swelling. His medical history included repeated episodes of acute decompensated heart failure with reduced left ventricular ejection fraction (ADHFrEF) despite receiving optimal medical therapy. Previous interventions included multiple aortic surgeries and valve replacements due to aortic dissection and aneurysms, complicated by paraplegia and other sequelae.  \n\n**Key Findings**  \nOn admission, arterial blood gas analysis revealed severe hypoxemia (low oxygen levels in the blood) accompanied by both respiratory and metabolic alkalosis. Chest X-ray demonstrated hilar congestion, indicating fluid overload and pulmonary vascular congestion. Echocardiographic evaluation showed persistent left ventricular systolic dysfunction with reduced ejection fraction (around 30-35%), mechanical valve prostheses with paravalvular leakage, and varying degrees of valvular regurgitation. Laboratory tests showed markedly elevated N-terminal pro-B-type natriuretic peptide (NT-proBNP), a biomarker indicating heart failure severity, and elevated midregional proadrenomedullin (MR-proADM), reflecting disease severity and prognosis.  \n\n**Clinical Interpretation**  \nThe patient suffered from recurrent acute decompensated heart failure episodes due to cardiomyopathy associated with Marfan syndrome, characterized by progressive left ventricular dysfunction and valvular insufficiencies despite maximal conventional medical treatment. The complexity of his condition was compounded by prior surgical interventions and complications such as paraplegia and mediastinal infection. The persistent elevation of heart failure biomarkers and echocardiographic findings underscored the severity and refractory nature of his cardiac dysfunction.  \n\n**Interventions and Outcomes**  \nFollowing hemodynamic stabilization, sacubitril/valsartan—a combination drug that inhibits neprilysin and blocks angiotensin II receptors, thereby improving heart failure outcomes—was introduced into his treatment regimen alongside existing medications including beta-blockers, diuretics, mineralocorticoid receptor antagonists, and digoxin. Over the subsequent months, the patient exhibited progressive clinical improvement, evidenced by reduced symptoms, decreased NT-proBNP levels, and improved echocardiographic parameters such as increased left ventricular ejection fraction (from 30% to 42%) and favorable changes in ventricular dimensions and mass. Importantly, he maintained a good quality of life without further episodes of acute heart failure during a nine-month follow-up period.  \n\n**Next Steps**  \nGiven the lack of established dosing guidelines for sacubitril/valsartan in Marfan syndrome-related cardiomyopathy, the therapeutic approach followed recommended heart failure protocols. Continued close monitoring of cardiac function, biomarker levels, and clinical status is essential. Further research is warranted to define optimal management strategies for heart failure in patients with connective tissue disorders like Marfan syndrome."
+        }
+    },
+    {
+        "article": "Paciente masculino de 41 años de edad quien ingresó en 2016 al servicio de urgencia con politraumatismo producto de accidente de tránsito; con trauma en miembros inferioA B res, en los rayos X se observa fractura de platillos tibiales izquierdos y fractura subtrocanteriana derecha, trauma toracoabdominal y trauma craneoencefálico leve.\nSe le practica osteosíntesis de fémur con clavo cefalomedular largo a foco cerrado corrigiendo la fractura subtrocanteriana y se le aplica tutor externo transarticular de rodilla como medida de control de daño local provisional; 15 días después se realiza osteosíntesis definitiva de su fractura de platillos tibiales. Evolución adecuada y satisfactoria de platillos tibiales.\nEntre 2016 y 2019 tuvo episodios esporádicos de dolor en cadera derecha que cedían fácilmente al manejo con antiinflamatorios y analgésicos sin limitar las actividades de la vida diaria y en la toma de rayos X se observaba fatiga de los bloqueos distales con dudas de la consolidación de la fractura.\nEn 2020 se incrementa el dolor en la cadera que no cede con el tratamiento médico y se acompaña de limitación funcional. En los rayos X de control se evidencia ruptura del clavo cefalomedular en su tercio proximal y no unión de la fractura subtrocantérica.\nEn Febrero de 2020 intento fallido de extracción de material de osteosíntesis (extrainstitucional), por lo que es remitido a nuestra institución. Se lleva a cirugía el 8 de Febrero, se realiza retiro de material de osteosíntesis, curetaje y toma de cultivo de foco de no unión. Cultivo positivo para Klebsiella pneumoniae recibiendo tratamiento con meropenem intravenoso por 10 días. Posteriormente se le realizó un lavado quirúrgico con drenaje de hematoma para el 20 de Febrero realizar nueva osteosíntesis con clavo cefalomedular + injerto óseo autólogo (tomado de ambas crestas iliacas) en foco de no unión.\nReactivación de la infección en Marzo de 2020, requiriendo nuevamente cirugía para lavados y desbridamiento quirúrgicos seriados (#5). Se aísla nueva bacteria Enterobacter que es manejada con vancomicina y meropenem. A f inales de Abril completa tratamiento médico y se le da salida en condiciones estables.\nEn Mayo de 2020 por persistencia de la infección se retira el material de osteosíntesis, se deja un clavo TENS endomedular recubierto de cemento con antibióticos (gentamicina).\nA finales de Mayo después de dos lavados quirúrgicos se retiró el clavo TENS, resección de bordes de fractura (hasta hueso sano) injerto óseo endomedular con un segmento de 10 cm de peroné no vascularizado (autólogo) y fijación de la fractura con una placa de soporte condíleo de fémur distal; colocación de sistema VAC y cierre definitivo de la herida en un segundo tiempo el 28 de Mayo de 2020. El paciente evolucionó adecuadamente, la herida quirúrgica cicatrizó por completo hasta el día de hoy con infección en remisión y evidencia radiológica de consolidación de la fractura, además paciente asintomático con función preservada de la extremidad.",
+        "gold_summary": "Masculino de 41 años de edad que sufre fractura subtrocantérica derecha producto de un accidente de tránsito que requirió manejo de osteosíntesis. Con posterior ruptura del clavo cefalomedular en su tercio proximal, no unión de la fractura e infecciones en sitio de la fractura. Fue tratado con múltiples lavados quirúrgicos, antibioticoterapia y un procedimiento ortopédico y quirúrgico poco convencional como el uso de una placa de soporte condíleo de fémur distal y un injerto óseo endomedular con un segmento de 10 cm de peroné no vascularizado. Paciente con evolución satisfactoria y favorable.",
+        "synthetic_summary": {
+            "B1": "A man hurt his right thigh bone in a car crash. Doctors put a special metal stick inside to help the bone heal.\n\nThe metal stick broke, and the bone did not heal well. The place got infected, so doctors cleaned it many times and gave medicine.\n\nThey used a special plate and a bone piece from his leg to help fix the bone. Now, he is feeling better and his bone is healing well.",
+            "B2": "**What Happened to the Patient**  \nA 41-year-old man was in a serious car accident that broke a bone in his right thigh called the subtrochanteric femur. This type of fracture is near the top of the thigh bone, close to the hip. To fix the break, doctors used a metal rod called a cephalomedullary nail, which is inserted inside the bone to hold it together.\n\n**Complications After Surgery**  \nLater, the metal rod broke near the top, and the bone did not heal properly. This is called a \"non-union,\" meaning the broken parts did not join back together. The area also got infected, which made healing harder.\n\n**How Doctors Treated the Problem**  \nThe patient had several surgeries to clean out the infection and remove damaged tissue. He was given strong antibiotics to fight the bacteria causing the infection. Because the usual treatment was not enough, doctors used a special approach: they placed a metal plate to support the lower part of the thigh bone near the knee (called a condylar support plate). They also used a bone graft, which means they took a 10-centimeter piece of bone from his own lower leg (the fibula) and put it inside the thigh bone to help it heal. This graft was \"non-vascularized,\" meaning it did not have its own blood supply but still helped the bone grow.\n\n**Outcome**  \nAfter these treatments, the patient healed well. The infection went away, the bone joined together properly, and he regained good use of his leg. This case shows how complex bone injuries with infection can be treated successfully using surgery and antibiotics.",
+            "B3": "**Background**  \nA 41-year-old male patient sustained a right subtrochanteric femur fracture as a result of a motor vehicle accident. Initial management involved osteosynthesis (surgical fixation of the bone) using a long cephalomedullary nail to stabilize the fracture.\n\n**Key Findings**  \nFollowing initial treatment, the patient experienced mechanical failure characterized by a fracture of the cephalomedullary nail at its proximal third and non-union (failure of the bone ends to heal together) of the subtrochanteric fracture. Additionally, the patient developed infections at the fracture site caused by bacteria including Klebsiella pneumoniae and later Enterobacter species. These infections complicated the healing process and required intensive management.\n\n**Clinical Interpretation**  \nThe patient underwent multiple surgical interventions including repeated surgical washouts (lavages) and debridements (removal of infected tissue), combined with targeted intravenous antibiotic therapy to control the infections. Due to persistent infection and non-union, a complex orthopedic procedure was performed involving removal of the initial fixation hardware, placement of a temporary antibiotic-impregnated intramedullary nail (TENS nail), and ultimately reconstruction using a 10-centimeter segment of non-vascularized autologous fibula bone graft (taken from the patient’s own fibula) placed inside the bone canal (endomedullary). This graft was stabilized with a distal femoral condylar support plate, an unconventional but effective method to achieve mechanical stability and promote bone healing.\n\n**Next Steps and Outcome**  \nFollowing these interventions, the patient’s surgical wound healed completely without further signs of infection. Radiological imaging confirmed successful consolidation of the fracture. The patient remains asymptomatic with preserved function of the affected limb, indicating a favorable clinical outcome after a challenging course of treatment."
+        }
+    },
+    {
+        "article": "Una adolescente de 17 años se presentó en nuestra clínica con una historia de dos meses de dolor torácico en el lado izquierdo y una historia de una semana de dolor en la espalda en el nivel de T7. El dolor torácico se acompañaba de palpitaciones y disnea que ocurrían de tres a cuatro días por semana. Una semana antes de la primera visita, las palpitaciones y la disnea se hicieron menos frecuentes, y desarrolló un dolor sordo diario intermitente en el lado izquierdo del pecho y la parte media de la espalda sin radiación, en la mayoría de los casos. El dolor ocurría tanto con el ejercicio como en reposo, y duraba horas, sin factores agravantes o atenuantes. Informó una intensidad del dolor de 2 a 6 en una escala de 10 puntos. La intensidad cambiaba durante un ataque, y el promedio era 4. Estaba sana por lo demás. No había limitación en la vida diaria. Visitó a un médico local un mes antes de visitar nuestra clínica. Los resultados de los exámenes electrocardiográficos y de laboratorio de Holter fueron normales. Su historial médico incluía migraña durante tres años. Sus medicamentos regulares eran lomerizina, loxoprofen y naratriptan para la prevención y el tratamiento agudo de la migraña. Su migraña estaba bien controlada, y rara vez experimentaba ataques. Negó trauma o cirugías previas. Negó síntomas sospechosos o antecedentes familiares de afecciones autoinmunes o inflamatorias.\n\nSu presión arterial era de 107/60 mmHg y su pulso de 62 latidos/min. Medía 162 cm de altura y pesaba 43 kg, con un índice de masa corporal de 16,4 kg/m2. No se escuchaba ningún murmullo ni arritmia en su examen cardiovascular. Los pulmones estaban limpios a la auscultación bilateral. La palpación del tórax provocó un dolor local no reproducible en las articulaciones inferiores esterno-costales; la maniobra de tracción del brazo horizontal y la maniobra del gallo cantando no provocaron dolor. No había sensibilidad en los músculos y huesos de la parte superior del cuerpo.\n\nLos hallazgos electrocardiográficos y de laboratorio, incluida la función tiroidea, fueron normales. El examen radiográfico torácico y torácico mostró el enderezamiento de la columna torácica superior y una pérdida de la curvatura cifótica normal. Las radiografías de las costillas inferiores no revelaron fractura ni neumotórax. Sospechamos un síndrome de la espalda recta, de acuerdo con los dos criterios diagnósticos diferentes propuestos por Davies et al. y DeLeon et al. La distancia entre la mitad del borde anterior de T8 y una línea vertical que conecta T4 a T12 fue de 0.91 cm. El diámetro anteroposterior fue de 74.0 cm, y el diámetro transversal fue de 243.2 cm. Le aconsejamos que comenzara y continuara la terapia quiropráctica para aumentar la cifosis torácica. Procedimos con una espera vigilante durante un mes en atención ambulatoria.\n\nDespués de esta primera visita, el dolor de pecho y de espalda se alivió gradualmente. Las palpitaciones y la disnea apenas se produjeron. Todos los síntomas desaparecieron en tres semanas. En la visita de seguimiento de un mes, se realizó una ecocardiografía, que reveló una regurgitación mitral trivial sin prolapso. Confirmamos el diagnóstico de síndrome de espalda recta. Reaseguramos a la paciente de que la enfermedad es benigna y le aconsejamos que continuara con la terapia quiropráctica. No ha tenido recaída de síntomas graves ni necesidad de visitar el hospital. Nunca volvió a visitar nuestra clínica en el año siguiente.\n",
+        "gold_summary": "Una adolescente de 17 años se presentó con su madre en nuestra clínica con un historial de dos meses de dolor en el pecho izquierdo y un historial de una semana de dolor en la parte media de la espalda. Diagnosticamos el síndrome de la columna vertebral basado en los hallazgos radiográficos del pecho y la columna vertebral y los síntomas de dolor en el pecho, palpitaciones y disnea. Tranquilizamos a la paciente de que la enfermedad era benigna y le aconsejamos que iniciara y continuara con la terapia quiropráctica. Todos los síntomas, incluido el dolor de espalda, desaparecieron en tres semanas.\n",
+        "synthetic_summary": {
+            "B1": "A 17-year-old girl had pain in her chest and back. We looked at her chest and back with pictures. We found her back was a little different. We told her the pain was not from something bad. We helped her with gentle care for her back. After three weeks, all her pain went away. She felt much better and was happy.",
+            "B2": "**What Happened:**  \nA 17-year-old girl came to the clinic with two months of pain on the left side of her chest and one week of pain in the middle of her back. She also felt her heart beating fast sometimes and had trouble breathing.\n\n**What the Doctors Found:**  \nAfter doing X-rays of her chest and spine, the doctors found that her upper back had lost its normal curve. This condition is called \"straight back syndrome,\" where the spine is straighter than usual. This can cause chest pain and other symptoms like palpitations (feeling your heart beat) and shortness of breath.\n\n**What They Did:**  \nThe doctors told her that this condition is not dangerous (benign). They suggested she start and keep doing chiropractic therapy, which is a treatment where specialists help improve spine alignment.\n\n**What Happened Next:**  \nWithin three weeks, all her symptoms, including chest and back pain, went away. She felt better and did not need to come back to the clinic for this problem again.",
+            "B3": "Background  \nA 17-year-old female adolescent presented with a two-month history of left-sided chest pain and a one-week history of mid-back pain at the level of the seventh thoracic vertebra (T7). The chest pain was accompanied by episodes of palpitations (awareness of heartbeats) and shortness of breath occurring three to four times per week. Prior to her first clinic visit, these palpitations and breathing difficulties became less frequent, but she developed a dull, intermittent daily pain in the left chest and mid-back area. The pain occurred both during exercise and at rest, lasting for hours without clear triggers or relieving factors. Pain intensity varied between 2 and 6 on a 10-point scale, averaging around 4. She had no other health issues limiting daily activities and had a history of well-controlled migraine treated with lomerizine, loxoprofen, and naratriptan.\n\nKey Findings  \nPhysical examination revealed normal vital signs, including blood pressure of 107/60 mmHg and pulse rate of 62 beats per minute. Cardiovascular and lung examinations were unremarkable, with no murmurs, arrhythmias, or abnormal lung sounds. Palpation of the chest wall elicited localized pain over the lower sternocostal joints but was not reproducible with arm movement maneuvers. Laboratory tests, including thyroid function, and electrocardiogram (ECG) were normal. Chest and spinal radiographs demonstrated a straightening of the upper thoracic spine with loss of the normal kyphotic (outward) curvature. Measurements indicated a reduced distance between vertebral landmarks consistent with a diagnosis of “straight back syndrome,” a condition characterized by decreased thoracic spinal curvature. No rib fractures or lung abnormalities were identified. Echocardiography performed at follow-up showed trivial mitral valve regurgitation without prolapse, which was clinically insignificant.\n\nClinical Interpretation  \nThe patient’s symptoms of chest and back pain, palpitations, and shortness of breath were attributed to straight back syndrome, a benign musculoskeletal condition caused by the loss of normal thoracic spinal curvature. This syndrome can mimic cardiac symptoms but generally does not involve structural heart disease. The diagnosis was supported by radiographic evidence and the absence of significant cardiac abnormalities. The patient was reassured about the benign nature of her condition.\n\nNext Steps  \nThe patient was advised to begin and maintain chiropractic therapy aimed at restoring normal thoracic kyphosis. During a one-month period of outpatient observation, her symptoms gradually resolved, with complete disappearance of chest and back pain, palpitations, and dyspnea within three weeks. She was encouraged to continue chiropractic treatment to prevent recurrence. Over the following year, she experienced no relapse of symptoms and did not require further hospital visits."
+        }
+    },
+    {
+        "article": "Una mujer de 59 años con urolitiasis bilateral recurrente se presentó con dolor en el flanco derecho, fiebre y fatiga. Se le había colocado un stent doble J derecho un año antes para una piedra pélvica sintomática, pero no se le dio seguimiento. Tenía insuficiencia cardíaca derecha, diabetes tipo 2 mal controlada y enfermedad renal crónica (nadir de creatinina: 18 mg/L).\nEstable clínicamente, tenía una escala de coma de Glasgow de 14/15 (respuesta verbal ligeramente alterada), fiebre (38,3 °C), sensibilidad en el flanco derecho y una producción de orina de 800 cc en 24 horas.\nLos resultados de laboratorio revelaron una lesión renal aguda, con un nivel de creatinina sérica de 107 mg/L (normal: 6-12 mg/L) y urea sanguínea de 3 g/L (normal: 0.15-0.45 g/L). Los marcadores inflamatorios estaban elevados, con un nivel de proteína C reactiva de 300 mg/L (normal: <5 mg/L) y un recuento de glóbulos blancos de 17,000/mm3 (normal: 4000-10,000/mm3). Además, el paciente exhibió anemia normocítica (hemoglobina: 7.6 g/dL; normal: 12-16 g/dL) e hipercalemia leve (potasio sérico: 5.4 mEq/L; normal: 3.5-5.1 mEq/L). El análisis de orina y el cultivo de orina fueron negativos para infección bacteriana.\nUna tomografía computarizada abdominal y pélvica sin contraste reveló una hidronefrosis del lado derecho, un stent de doble J calcificado en espiral en ambos extremos y una piedra en la pelvis derecha de 35 × 28 mm (588 UH). El riñón izquierdo está reducido en tamaño, con hidronefrosis y una piedra en la pelvis de 12 × 7 mm (531 UH).\n\nDebido a la obstructiva severa de la pielonefritis, en particular causada por la endoprótesis incrustada, se realizó una nefrostomía percutánea bilateral urgente, lo que produjo una importante mejora clínica y normalización de los marcadores inflamatorios y la función renal.\nTres días después, la paciente experimentó una convulsión generalizada asociada con disartria. Una tomografía computarizada urgente del cerebro mostró lesiones isquémicas en los lóbulos occipitales izquierdo y frontal derecho, lo que indicaba un accidente cerebrovascular embólico. Se le inició un tratamiento con enoxaparina (0,4 cc diarios) y Kardegic (160 mg diarios) para la prevención de accidentes cerebrovasculares.\nA pesar de la mejora neurológica, cuatro días después, la paciente desarrolló palidez mucocutánea progresiva, taquicardia (110 latidos por minuto), hipotensión (80/50 mmHg) y hematuria macroscópica por el catéter urinario. Los niveles de hemoglobina descendieron de 7,5 g/dL a 4,4 g/dL, lo que levantó sospechas de hemorragia activa. Se administró fluidoterapia, vasopresores intravenosos y transfusiones de sangre, estabilizando su estado para una exploración de angiografía por TAC con contraste.\nLa tomografía computarizada reveló una colección polar media heterogénea de 17 mm de espesor con extravasación de contraste en las fases arterial y portal, lo que indica una hemorragia activa de las arterias del polo superior y medio. También había coágulos intraluminales en la pelvis renal y la vejiga. Se hizo un diagnóstico de fístula arteriovenosa postnefrostomía, exacerbada por la terapia anticoagulante para el accidente cerebrovascular.\nSe realizó una arteriografía renal urgente a través del acceso a la arteria femoral derecha, utilizando un catéter de diagnóstico de calibre 5. La angiografía selectiva reveló una FAV en el polo inferior del riñón con drenaje venoso temprano hacia la vena cava inferior, junto con un pequeño pseudoaneurisma. La embolización superselectiva con microespirales de 3 mm y 5 mm logró ocluir con éxito la fístula, y se usaron partículas de Gelfoam para evitar el sangrado retrógrado. Una inyección final de contraste confirmó la oclusión completa de la fístula, restaurando la integridad arterial y deteniendo la hemorragia.\n\nDespués de la embolización, se vigiló de cerca al paciente en la UCI. La hemodinámica se mantuvo estable y se tomó la decisión colegiada de reintroducir la anticoagulación con monitorización del INR para controlar el accidente cerebrovascular isquémico mientras se equilibraba el riesgo de hemorragia. La hematuria se resolvió, la función renal se normalizó y la nefrostomía siguió siendo funcional.\nSe adoptó un enfoque multidisciplinario para el tratamiento definitivo. La primera etapa involucró la litotripsia endoscópica con láser del bucle inferior calcificado del stent de JJ, la inserción de un segundo stent de JJ en paralelo con el incrustado y la extracción de la nefrostomía, que se completó con éxito. La segunda etapa, programada seis semanas después, incluyó una ureteroscopia derecha flexible para liberar el bucle superior del stent de JJ calcificado, la fragmentación de la piedra pélvica derecha mediante litotripsia con láser y la extracción completa del stent incrustado. Lamentablemente, la salud del paciente se deterioró debido a múltiples factores, entre ellos, insuficiencia cardíaca, diabetes mal controlada, enfermedad renal crónica y un accidente cerebrovascular previo, lo que demoró la finalización de la segunda etapa del tratamiento planificado.\n",
+        "gold_summary": "Una mujer de 59 años con urolitiasis bilateral recurrente, insuficiencia cardiaca derecha, diabetes tipo 2 mal controlada y enfermedad renal crónica se presentó con dolor en el flanco derecho, fiebre y fatiga. Previamente se le había colocado un stent doble J derecho, pero se perdió su seguimiento. Una tomografía computarizada reveló una hidronefrosis, un stent calcificado y una piedra pélvica de 22 mm, lo que llevó a la realización de una nefrostomía percutánea. La paciente desarrolló un accidente cerebrovascular embólico tres días después y posteriormente presentó hematuria, hipotensión y anemia significativa. La angiografía por TC confirmó una FAV con sangrado activo, que se trató con éxito con embolización.\n",
+        "synthetic_summary": {
+            "B1": "A lady was feeling pain and fever. She had a tube in her body to help her pee. The tube got stuck and caused a big problem. Doctors put a small tube in her back to help her pee better. After that, she had a problem with her brain and felt very weak. She also started to bleed a lot inside. The doctors found the bleeding and fixed it with a special treatment. Now she is getting better.",
+            "B2": "**What Happened to the Patient**\n\nA 59-year-old woman had repeated kidney stones on both sides. She also had heart failure on the right side, poorly controlled type 2 diabetes, and chronic kidney disease. She came to the hospital with pain on her right side, fever, and feeling very tired. A year before, she had a special tube called a \"double J stent\" placed in her right kidney to help with a kidney stone, but she did not get follow-up care.\n\n**What the Doctors Found**\n\nA CT scan (a detailed X-ray) showed swelling in her right kidney because urine was blocked. The stent in her kidney had hardened with calcium, and there was a large stone about 22 mm in size. To help drain her kidneys, doctors placed tubes directly into both kidneys, called percutaneous nephrostomies.\n\n**Complications and Treatment**\n\nThree days later, she had a stroke caused by a blood clot blocking blood flow to her brain. She was treated with blood thinners to prevent more strokes. Soon after, she developed blood in her urine, low blood pressure, and severe anemia (low red blood cells). A special CT scan with contrast dye showed an abnormal connection between an artery and a vein in her kidney, called an arteriovenous fistula (AVF), which was causing active bleeding.\n\nDoctors performed an angiography, a test that looks at blood vessels, and confirmed the AVF. They treated it by blocking the abnormal blood vessels using tiny coils in a procedure called embolization. This stopped the bleeding successfully.\n\n**Summary**\n\nThis patient had complex kidney problems with stones and a stent that caused blockage and infection. After treatment to drain her kidneys, she had a stroke and then bleeding from a rare complication called an arteriovenous fistula. Thanks to quick imaging and treatment, the bleeding was stopped, and her condition improved.",
+            "B3": "Background  \nA 59-year-old woman with a history of recurrent bilateral kidney stones (urolithiasis), right-sided heart failure, poorly controlled type 2 diabetes, and chronic kidney disease presented with right flank pain, fever, and fatigue. One year earlier, she had a right double-J ureteral stent placed for a symptomatic pelvic kidney stone, but she did not receive follow-up care.\n\nKey Findings  \nOn presentation, imaging with non-contrast computed tomography (CT) showed right-sided hydronephrosis (swelling of the kidney due to urine buildup), a calcified double-J stent with spiral calcifications at both ends, and a large right pelvic kidney stone measuring approximately 35 × 28 mm. The left kidney was small, with hydronephrosis and a smaller stone. Laboratory tests revealed acute kidney injury with severely elevated serum creatinine and urea levels, high inflammatory markers (C-reactive protein and white blood cell count), normocytic anemia, and mild hyperkalemia. Urine cultures were negative for bacterial infection.\n\nClinical Interpretation and Course  \nDue to severe obstructive pyelonephritis (kidney infection caused by blockage) related to the embedded stent, urgent bilateral percutaneous nephrostomies (catheter drainage directly from the kidneys) were performed, resulting in significant clinical improvement and normalization of inflammatory markers and kidney function. However, three days later, the patient experienced a generalized seizure and speech difficulties. Brain CT revealed ischemic strokes in the left occipital and right frontal lobes, consistent with embolic cerebrovascular events. She was started on anticoagulation therapy with enoxaparin and aspirin to prevent further strokes.\n\nFour days after the stroke, the patient developed progressive mucocutaneous pallor, rapid heart rate (tachycardia), low blood pressure (hypotension), and visible blood in the urine (macroscopic hematuria) from the urinary catheter. Her hemoglobin dropped sharply from 7.5 g/dL to 4.4 g/dL, indicating active bleeding. After stabilization with fluids, vasopressors, and blood transfusions, a contrast-enhanced CT angiography revealed an active arterial hemorrhage from the middle and upper poles of the right kidney, along with intraluminal clots in the renal pelvis and bladder. This bleeding was attributed to an arteriovenous fistula (an abnormal connection between an artery and a vein) that developed after the nephrostomy procedure and was worsened by anticoagulation therapy.\n\nNext Steps and Outcome  \nUrgent renal angiography confirmed the presence of a fistula in the lower pole of the right kidney with early venous drainage and a small pseudoaneurysm. Superselective embolization using microcoils and Gelfoam particles successfully occluded the fistula, stopping the bleeding and restoring arterial integrity. The patient was closely monitored in the intensive care unit, with careful reintroduction of anticoagulation to balance stroke prevention and bleeding risk. Hematuria resolved, kidney function normalized, and nephrostomy catheters remained functional.\n\nA multidisciplinary treatment plan was implemented. The first stage involved endoscopic laser lithotripsy to fragment the calcified lower loop of the stent, insertion of a second parallel double-J stent, and removal of the nephrostomy. The second stage, planned six weeks later, included flexible ureteroscopy to free the calcified upper loop of the stent, laser fragmentation of the right pelvic stone, and complete removal of the embedded stent. Unfortunately, the patient’s overall health deteriorated due to her underlying heart failure, poorly controlled diabetes, chronic kidney disease, and prior stroke, delaying completion of the second treatment stage."
+        }
+    },
+    {
+        "article": "Un hombre de 52 años fue admitido en un hospital debido a palpitaciones repentinas y fatiga general. La electrocardiografía reveló taquicardia ventricular con una frecuencia cardíaca de 180 lpm. Su ritmo cardíaco volvió a un ritmo sinusal después de una cardioversión inmediata y luego fue derivado a nuestra institución para una investigación adicional. Su historial médico pasado incluía reconstrucción del tracto de salida del ventrículo derecho utilizando un injerto homólogo y cierre de un defecto septal ventricular para TOF, que se realizó 47 años antes. Sin embargo, se perdió su seguimiento posterior. Tras ser derivado a nuestra institución, su presión arterial era de 116/70 mmHg, frecuencia cardíaca de 80 lpm, y saturación de oxígeno del 99% (con aire ambiente). Al inspeccionar la pulsación de la vena yugular, se observaron claramente una onda prominente y un descenso profundo, que eran consistentes con el aumento de la presión de llenado del ventrículo derecho y la compensación del aumento de la contracción de la RA. Cabe destacar que la auscultación reveló un murmullo diastólico regurgitante agudo en el tercer espacio intercostal izquierdo, un primer sonido cardíaco ampliamente dividido (S1) y un segundo sonido cardíaco (S2), lo que indicaba un ventrículo derecho severamente dilatado debido a la liberación de PR libre y la presencia de una válvula pulmonar no funcional. Además, se auscultó un tercer sonido cardíaco (S3) en el cuarto borde paraesternal, que era consistente con un S3 derecho. El electrocardiograma reveló bloqueo completo del haz de rama derecha, con una duración de QRS de 200 lpm. La radiografía de tórax mostró cardiomegalia con dilatación de las arterias pulmonares bilaterales. La ecocardiografía transtorácica reveló una regresión completa de la válvula pulmonar, que resultó en PR libre y una dilatación prominente del ventrículo derecho. La evaluación volumétrica del ventrículo derecho se realizó utilizando una resonancia magnética cardíaca, que reveló un volumen final diastólico del ventrículo derecho de 428 ml (índice de volumen final diastólico del ventrículo derecho de 240 ml/m2), una fracción de eyección del ventrículo derecho del 36% y una fracción de eyección de PR del 74%. Además, la tomografía computarizada multidetector mostró claramente una regresión completa de la válvula pulmonar del injerto homólogo.\n\nEl paciente se sometió a un examen con catéter para investigar más a fondo su estado hemodinámico. Su forma de onda de presión RA fue particularmente notable, ya que consistía en una onda a prominente y un descenso y, que coincidían con el cuarto sonido cardiaco (S4) y S3 en un fonocardiograma, respectivamente. Además, se reveló que la presión arterial pulmonar final diastólica y la presión final diastólica del VD eran casi idénticas debido al PR libre. Por lo tanto, la evaluación clínica del «quinteto de sonidos cardiacos», que incluye un murmullo diastólico regurgitante agudo, un S1 ampliamente dividido, un S2 único y la presencia de un S3 y un S4 derechos, se confirmó mediante una evaluación hemodinámica y anatómica multimodal como insuficiencia cardiaca derecha grave concomitante con un VD significativamente dilatado debido a la regresión completa de la válvula pulmonar y el PR libre resultante.\n\nDespués del reemplazo de la válvula pulmonar, el «quinteto de sonidos del corazón» se resolvió por completo.\n\nMH - Insuficiencia cardiaca/*etiología\nMH - Murmullos cardiacos/*diagnóstico\nMH - *Sonidos del corazón\nMH - Humanos\nMH - Hombre\nMH - Edad Media\nMH - Insuficiencia de la válvula pulmonar/*complicaciones/diagnóstico\nMH - Taquicardia, ventricular/etiología\nMH - Tetralogía de Fallot/*cirugía\nMH - Disfunción ventricular, derecha/etiología\n",
+        "gold_summary": "Un hombre de 52 años fue derivado a nuestra institución para la evaluación de una taquicardia ventricular de inicio súbito. Su historia clínica incluía una reconstrucción del tracto de salida del ventrículo derecho a los 5 años de edad. La auscultación reveló un murmullo diastólico regurgitante agudo, un primer sonido cardiaco (S1) ampliamente dividido y un segundo sonido cardiaco (S2) único, lo que indicaba un ventrículo derecho severamente dilatado debido a una regurgitación pulmonar (RP) grave y la presencia de una válvula pulmonar no funcional. Además, el tercer sonido cardiaco (S3) y el cuarto sonido cardiaco (S4) del lado derecho estaban presentes, lo que era coherente con una presión de llenado del ventrículo derecho elevada y la presencia de un ventrículo derecho no conforme. Finalmente, el mencionado «quinteto de sonidos cardiacos» se confirmó mediante una evaluación multimodal como insuficiencia cardiaca del lado derecho con un ventrículo derecho concomitantemente severamente dilatado debido a la regresión completa de la válvula pulmonar y la consiguiente RP libre.\n",
+        "synthetic_summary": {
+            "B1": "A man had a fast, strong heartbeat that started suddenly. When the doctor listened to his heart, they heard some special sounds. These sounds showed his right side of the heart was very big and not working well. This happened because a heart valve was not working and letting blood go the wrong way. The doctors checked carefully and found his right heart was very tired and stretched out.",
+            "B2": "**What Happened to the Patient**  \nA 52-year-old man came to the hospital because he suddenly had a very fast heartbeat called ventricular tachycardia. When he was 5 years old, he had surgery to fix a problem in the right side of his heart. This history was important for understanding his current condition.\n\n**What the Doctors Heard and Found**  \nWhen the doctors listened to his heart with a stethoscope, they heard unusual sounds. These included a loud whooshing noise during the heart’s resting phase (called a diastolic murmur), and some extra heart sounds named S3 and S4 on the right side. These sounds showed that his right ventricle—the heart chamber that pumps blood to the lungs—was very stretched out and not working well. This happened because his pulmonary valve, which controls blood flow from the right ventricle to the lungs, was not working and letting blood flow backward. This backward flow is called pulmonary regurgitation.\n\n**What This Means**  \nThe doctors used different tests to confirm that the man had right-sided heart failure. This means the right ventricle was too weak and enlarged because the valve was completely damaged and blood was leaking back freely. The combination of the five specific heart sounds they heard helped them understand how serious his condition was.\n\n**Summary**  \nIn short, the man’s old heart surgery and the failure of his pulmonary valve caused his right heart to become very enlarged and weak. This led to heart failure on the right side and caused the unusual heart sounds the doctors detected.",
+            "B3": "**Background**  \nA 52-year-old man was referred to our institution for evaluation following a sudden onset of ventricular tachycardia, a rapid heart rhythm originating from the lower chambers of the heart. His medical history was significant for surgical reconstruction of the right ventricular outflow tract (RVOT) performed at age 5, as part of treatment for tetralogy of Fallot (a congenital heart defect). This prior surgery involved using a homograft (a donor valve graft) to reconstruct the pulmonary valve area.\n\n**Key Findings**  \nOn physical examination, auscultation (listening with a stethoscope) revealed a distinctive combination of heart sounds and murmurs, collectively described as a “quintet of cardiac sounds”:  \n- A sharp, diastolic regurgitant murmur indicating severe pulmonary regurgitation (PR), meaning blood was flowing backward through the pulmonary valve.  \n- A widely split first heart sound (S1), reflecting abnormal timing of valve closures due to right ventricular dilation.  \n- A single second heart sound (S2), consistent with a nonfunctional pulmonary valve.  \n- The presence of both a third heart sound (S3) and a fourth heart sound (S4) on the right side of the chest, which are abnormal sounds associated with increased filling pressures and reduced compliance (stiffness) of the right ventricle.\n\nThese auscultatory findings suggested a severely dilated right ventricle with significant volume overload caused by free pulmonary regurgitation due to complete degeneration (regression) of the pulmonary valve homograft.\n\n**Clinical Interpretation**  \nMultimodal diagnostic evaluation—including echocardiography, cardiac magnetic resonance imaging, and invasive hemodynamic catheterization—confirmed the clinical impression. The right ventricle was markedly enlarged and dysfunctional, with elevated filling pressures and free pulmonary regurgitation resulting from complete failure of the pulmonary valve graft. This constellation of findings explained the patient’s right-sided heart failure and arrhythmia.\n\n**Next Steps**  \nThe patient underwent pulmonary valve replacement surgery. Following this intervention, the abnormal “quintet” of heart sounds resolved completely, indicating restoration of more normal right ventricular function and valve competence. This case highlights the long-term complications that can arise decades after congenital heart surgery and underscores the importance of ongoing surveillance in such patients."
+        }
+    },
+    {
+        "article": "Un hombre de 62 años con antecedentes médicos de cardiopatía no isquémica que derivó en insuficiencia cardíaca, en estado postoperatorio de un dispositivo de asistencia ventricular izquierdo, se sometió a un trasplante cardíaco ortotópico. Mientras se recuperaba en la UCI quirúrgica, desarrolló un empeoramiento de la distensión abdominal, sensibilidad y leucocitosis, lo que motivó la evaluación por el equipo de cirugía general 6 días después del trasplante. El paciente no había evacuado ni expulsado gases desde su cirugía y no había respondido a los enemas administrados ni a la metoclopramida oral por un presunto íleo posoperatorio. Se realizó una tomografía computarizada del abdomen y la pelvis, que reveló múltiples bucles intestinales dilatados con niveles de aire-líquido y un punto de transición en el intestino delgado proximal en el cuadrante superior izquierdo, lo que generó preocupación por una obstrucción. En función de estos hallazgos y del hecho de que el paciente no había sido sometido a cirugías abdominales previas, lo que hacía que la obstrucción intestinal fuera secundaria a las adherencias, se llevó al paciente al quirófano para una laparotomía exploratoria. En el quirófano, se encontró que el intestino estaba dilatado de forma difusa sin ninguna área de isquemia aparente. Se encontró que una porción del intestino delgado estaba adherida a la pared abdominal anterior en el cuadrante superior izquierdo. Tras una exploración adicional, se encontró que una línea motriz de LVAD retenida estaba tunelizada en la cavidad peritoneal, estrangulando un bucle de intestino delgado en el cuadrante superior izquierdo. La línea motriz se liberó de la pared abdominal y se retiró, y se liberó el bucle de intestino afectado. Se encontró que era viable después de unos minutos de reperfusión. Se examinó el intestino delgado en su totalidad, desde el ligamento de Trietz distalmente hasta el intestino ciego, y se encontró que estaba dilatado pero en general era normal. Se reparó una pequeña área de desgarro seroso en el punto de adhesión a la línea motriz, principalmente. Se devolvió el intestino a la cavidad abdominal y se cerró la fascia y la piel con suturas corrientes y grapas cutáneas.\n\nMH - *Eliminación de dispositivo\nMH - Migración de cuerpos extraños/*complicaciones\nMH - Insuficiencia cardiaca/*terapia\nMH - *Trasplante de corazón\nMH - Dispositivos de asistencia cardíaca/*efectos adversos\nMH - Humanos\nMH - Obstrucción intestinal/diagnóstico por imágenes/*etiología\nMH - Laparotomía\nMH - Hombre\nMH - Edad Media\nMH - Tomografía computarizada por rayos X\nMH - Estados Unidos\n",
+        "gold_summary": "Un hombre de 62 años con antecedentes de insuficiencia cardiaca inducida por cardiomiopatía no isquémica, post-puente de asistencia ventricular izquierda y trasplante cardiaco ortotópico, presentó distensión abdominal, dolor y leucocitosis seis días después del trasplante. La TAC de abdomen y pelvis reveló bucles intestinales dilatados, niveles de aire-líquido y un punto de transición en el intestino delgado proximal. Se diagnosticó al paciente una obstrucción intestinal y se le realizó una laparotomía exploratoria. Se encontró que tenía un conducto de LVAD intraabdominal retenido que estrangulaba un bucle de intestino delgado en el cuadrante superior izquierdo. Se retiró el conducto y se liberó la sección de intestino con el retorno de la perfusión.\n",
+        "synthetic_summary": {
+            "B1": "A man had a new heart put inside him. After the surgery, his tummy got big and hurt. The doctors took pictures and saw his tummy was blocked. \n\nThey did a surgery to look inside. They found a tube that was squeezing his tummy. The doctors took the tube out and helped his tummy feel better.",
+            "B2": "**What Happened to the Patient**  \nA 62-year-old man had serious heart problems caused by a condition called non-ischemic cardiomyopathy, which means his heart muscle was weak for reasons other than blocked arteries. He had a special device called a left ventricular assist device (LVAD) to help his heart pump blood. Later, he received a heart transplant to replace his damaged heart.\n\n**New Symptoms After Surgery**  \nSix days after the heart transplant, the man developed a swollen belly, pain, and a high number of white blood cells (leukocytosis), which usually means infection or inflammation. He also couldn’t pass gas or have a bowel movement, which suggested a problem with his intestines.\n\n**Tests and Diagnosis**  \nDoctors did a CT scan, a type of detailed X-ray, of his abdomen and pelvis. The scan showed that parts of his small intestine were swollen and filled with air and fluid. There was a specific spot where the intestine seemed blocked. This led doctors to think he had an intestinal obstruction, meaning something was stopping food and gas from moving through his intestines.\n\n**What the Surgery Found**  \nThe patient had surgery to look inside his abdomen. They found that a cable from his old LVAD device had moved inside his belly and was squeezing a loop of his small intestine. This squeezing blocked the intestine and caused the swelling and pain. The doctors carefully removed the cable and freed the intestine. After a few minutes, blood flow returned to the intestine, showing it was still healthy.\n\n**What This Means**  \nThis case shows that devices like LVADs can sometimes cause unexpected problems after surgery. In this man’s case, a leftover part of the device caused a blockage in his intestines. Quick diagnosis and surgery helped fix the problem before the intestine was permanently damaged.",
+            "B3": "Background  \nA 62-year-old man with a history of non-ischemic cardiomyopathy leading to heart failure underwent implantation of a left ventricular assist device (LVAD) as a bridge to an orthotopic heart transplant. Six days after the transplant surgery, while recovering in the surgical intensive care unit, he developed worsening abdominal distension, tenderness, and an elevated white blood cell count (leukocytosis). Notably, he had not passed stool or gas since the operation and had not responded to enemas or oral metoclopramide, raising suspicion for postoperative ileus (a temporary lack of intestinal movement).\n\nKey Findings  \nA computed tomography (CT) scan of the abdomen and pelvis demonstrated multiple dilated loops of small intestine with air-fluid levels and a clear transition point in the proximal small bowel located in the left upper quadrant. These imaging findings suggested a mechanical small bowel obstruction rather than a simple ileus. Given that the patient had no prior abdominal surgeries (which commonly cause adhesions leading to obstruction), the surgical team proceeded with an exploratory laparotomy.\n\nClinical Interpretation  \nDuring surgery, the small intestine was diffusely dilated but showed no signs of ischemia (lack of blood flow). A segment of small bowel was found adherent to the anterior abdominal wall in the left upper quadrant. Further exploration revealed that a retained driveline (a cable) from the previously implanted LVAD had migrated into the peritoneal cavity and was strangulating a loop of small intestine at that site. The driveline was carefully freed from the abdominal wall and removed, and the affected intestinal loop was released. After a few minutes of reperfusion (restoration of blood flow), the bowel appeared viable. The entire small intestine was inspected from the distal duodenum (ligament of Treitz) to the cecum; although dilated, it was otherwise normal. A small serosal tear (a superficial tear of the intestinal lining) at the adhesion site was repaired primarily. The intestines were returned to the abdominal cavity, and the abdominal wall was closed.\n\nNext Steps  \nThe patient’s intestinal obstruction was successfully resolved by removing the retained LVAD driveline causing mechanical strangulation. This case highlights a rare but serious complication of cardiac assist devices involving migration of device components into the abdominal cavity, leading to bowel obstruction. Close postoperative monitoring and prompt imaging are essential in transplant patients presenting with abdominal symptoms to identify such complications early. Surgical exploration remains the definitive treatment when mechanical obstruction is suspected."
+        }
+    },
+    {
+        "article": "Un paciente de 13 años de edad, del sexo masculino, fue admitido en el Hospital de Niños de Damasco tras notar una masa palpable agrandada en la región inguinal izquierda. Su historial médico no fue notable, excepto por una intervención quirúrgica en su columna vertebral 6 años atrás, debido a un accidente, que resultó en la pérdida de la función motora y la sensación en ambas extremidades inferiores.\n\nDebido al largo período que había pasado en la cama, el paciente desarrolló úlceras de decúbito en su pie izquierdo. El único hallazgo en el examen clínico fue una masa en el área inguinal izquierda, que era móvil en las estructuras profundas y también lo era la piel que la cubría. La masa no era sensible a la palpación y no se observaron signos de inflamación local.\n\nLos exámenes de laboratorio revelaron una ESR elevada (119 mm/h en la primera hora). Se solicitaron otros exámenes básicos de laboratorio, que incluían (recuento sanguíneo completo, pruebas de función hepática, electrolitos, urea, creatinina y LDH) y estaban dentro de los rangos normales para la edad. La realización de estos exámenes fue esencial para descartar enfermedades sistémicas. Dada la ausencia de hallazgos físicos indicativos de trastornos sistémicos o inmunodeficiencias, se consideró innecesario realizar exámenes adicionales como los de VIH o antiglobulina directa.\n\nLa tomografía computarizada del abdomen, el tórax y la pelvis mostró ganglios linfáticos agrandados por debajo del ligamento inguinal, el más grande de aproximadamente 3,5 por 2,4 cm. Otros órganos y ganglios estaban dentro de los límites normales.\n\nTodas las investigaciones mencionadas fueron esenciales para descartar otros diagnósticos de alto riesgo, como linfoma y leucemia. Sin embargo, no fueron suficientes para llegar al diagnóstico definitivo, por lo que se tomó la decisión de realizar una resección quirúrgica de los ganglios.\n\nPara confirmar los diagnósticos y descartar otras posibles diferencias que pudieran presentarse con ganglios linfáticos agrandados, se realizó la extirpación quirúrgica de todos estos ganglios agrandados bajo anestesia general y se enviaron biopsias para su estudio microscópico.\n\nLa biopsia mostró una arquitectura ganglionar hiperplásica con proliferación de histiocitos y células plasmáticas con proliferación vascular, lo que es compatible con el subtipo de enfermedad de Castleman de células plasmáticas.\n\nEl paciente fue dado de alta del hospital después de 14 días, tras comprobar que no había ganglios linfáticos agrandados. La única recomendación fue prednisolona oral. El paciente se sometió a un seguimiento mediante TAC de cuerpo entero cada tres meses. Durante cada visita al hospital, se realizó un examen clínico exhaustivo y pruebas de laboratorio (por ejemplo, análisis de sangre completo, VSG, proteína C reactiva, pruebas de función hepática, pruebas de función renal), además del TAC. Después de un período de seguimiento de 12 meses, el paciente no informó de nuevos síntomas o ganglios linfáticos agrandados. Además, no se observaron anomalías durante el examen clínico o en las pruebas de laboratorio.\n",
+        "gold_summary": "Reportamos un caso único de un niño de 13 años que presentó una masa palpable agrandada en la región inguinal izquierda sin ningún síntoma constitucional. La extirpación quirúrgica de esta masa fue esencial para descartar causas preocupantes. El examen patológico reveló cambios proliferativos consistentes con el tipo de célula plasmática de la enfermedad de Castleman, que es una de las formas más raras de la enfermedad en niños. Hasta donde sabemos, este caso es el primer caso reportado de enfermedad de Castleman unicéntrica (UCD) en el área inguinal. Durante un período de seguimiento de 12 meses, no se reportaron agrandamientos adicionales de los ganglios linfáticos u otros síntomas.\n",
+        "synthetic_summary": {
+            "B1": "A boy had a bump on his left groin. The bump did not hurt him. \n\nDoctors took out the bump to see what it was. It was a very rare kind of lump. \n\nAfter one year, the boy was feeling good. No new bumps grew.",
+            "B2": "**A Rare Case of Castleman Disease in a 13-Year-Old Boy**\n\nA 13-year-old boy noticed a lump in his left groin area. He did not have other common symptoms like fever or weight loss. Doctors removed the lump through surgery to find out what was causing it and to rule out serious illnesses.\n\nWhen the lump was studied under a microscope, it showed signs of a rare condition called Castleman disease. This disease causes certain immune cells, called plasma cells, to grow too much in lymph nodes. Lymph nodes are small organs that help fight infections. Castleman disease is very uncommon in children, and this is the first known case found in the groin area.\n\nAfter the surgery, the boy was closely checked for a year. He had regular scans and blood tests to make sure no new lumps appeared and that he stayed healthy. During this time, he did not develop any new symptoms or swollen lymph nodes.\n\nThis case helps doctors understand more about rare diseases like Castleman disease in children and shows how important surgery and careful follow-up are for diagnosis and treatment.",
+            "B3": "Background  \nThis report describes a unique case involving a 13-year-old boy who developed a palpable, enlarged mass in his left inguinal (groin) region without any accompanying systemic symptoms such as fever, weight loss, or night sweats. His medical history was notable only for a prior spinal surgery following an accident, which resulted in paralysis and sensory loss in both lower limbs.\n\nKey Findings  \nClinical examination identified a mobile, non-tender mass in the left inguinal area without signs of local inflammation. Laboratory tests showed a markedly elevated erythrocyte sedimentation rate (ESR) of 119 mm/hour, indicating inflammation, while other blood parameters—including complete blood count, liver and kidney function tests, electrolytes, and lactate dehydrogenase (LDH)—were within normal limits. Imaging studies using computed tomography (CT) scans of the abdomen, chest, and pelvis revealed enlarged lymph nodes below the inguinal ligament, the largest measuring approximately 3.5 by 2.4 cm. No abnormalities were found in other organs or lymph node regions.\n\nClinical Interpretation  \nGiven the presence of enlarged lymph nodes and elevated inflammatory markers, serious conditions such as lymphoma or leukemia were considered and subsequently ruled out through diagnostic workup. Definitive diagnosis required surgical removal and biopsy of the affected lymph nodes. Histopathological analysis demonstrated hyperplastic lymph node architecture characterized by proliferation of histiocytes (immune cells) and plasma cells (antibody-producing cells), along with increased vascularity. These findings are consistent with the plasma cell subtype of Castleman disease, a rare lymphoproliferative disorder. Notably, this represents the first reported case of unicentric Castleman disease (UCD)—meaning localized to a single lymph node region—occurring in the inguinal area in a pediatric patient.\n\nNext Steps and Follow-Up  \nThe patient was discharged after 14 days with a prescription for oral prednisolone (a corticosteroid) and underwent regular follow-up every three months. Follow-up assessments included whole-body CT scans, thorough physical examinations, and laboratory tests monitoring inflammatory markers and organ function. Over a 12-month period, no new lymph node enlargements or symptoms emerged, and all clinical and laboratory evaluations remained normal, indicating stable remission.\n\nSummary  \nThis case highlights the importance of surgical biopsy in diagnosing unexplained lymphadenopathy in children and expands the clinical spectrum of unicentric Castleman disease by documenting its occurrence in the inguinal region. The patient’s favorable outcome after surgical excision and medical management underscores the potential for effective control of this rare condition with appropriate intervention and monitoring."
+        }
+    },
+    {
+        "article": "Un hombre asiático de 55 años de edad, que había estado recibiendo tratamiento irregularmente (el paciente no cumplía con el tratamiento) para DCMP durante los últimos 6 meses, acudió con quejas de disnea al hacer ejercicio durante 1 semana y disminución de la producción de orina durante 2 días. El paciente aparentemente estaba bien hace 1 semana cuando empezó a desarrollar disnea, inicio insidioso, gradualmente progresiva, inicialmente de grado II de la New York Heart Association (NYHA) pero progresó a grado IV de la NYHA asociada con pesadez en el pecho. La historia de ortopnea y disnea nocturna paroxística estuvo presente. Esto estuvo asociado con tos con una cantidad moderada de expectoración espumosa, no purulenta. El paciente también se quejó de hinchazón de las extremidades inferiores bilaterales. No hubo historia de hinchazón periorbital, orina espumosa o hematuria. No hubo historia de palpitación, síncope, dolor de pecho o hemoptisis. El paciente también dio una historia de una sensación de hormigueo en ambas manos y pies durante 1 mes.\n\nEl paciente había tenido un episodio similar 6 meses atrás, por el que fue hospitalizado y tratado de manera conservadora como un caso de DCMP. Se le había practicado una cirugía de cataratas en ambos ojos 15 años atrás.\n\nEn el examen físico general, el paciente estaba consciente y orientado en cuanto al tiempo, el lugar y la persona, y afebril con una presión arterial de 90/60 mmHg en el brazo derecho en posición supina y una frecuencia de pulso de 110/min, que era de bajo volumen y todos los pulsos periféricos eran palpables. Presentaba taquipnea con una frecuencia respiratoria de 28/min y palidez. Tenía un edema de pedal B/L, que era de tipo lento con presión venosa yugular elevada (JVP). No se observó ictericia, cianosis, clubbing ni linfadenopatía. Mientras se medía la presión arterial, el paciente empezó a tener espasmos en la muñeca, lo que nos dio una pista para examinar más a fondo y revelar un signo de Chvostek positivo. El signo de Trousseau también fue positivo a los 10 segundos.\n\nEl examen del sistema cardiovascular reveló un latido apical localizado en el sexto espacio intercostal izquierdo, a 1 cm fuera de la línea medioclavicular, de carácter hiperdinámico. Se escucharon S1 y S2 con normalidad en todas las áreas.\n\nEl examen del sistema respiratorio reveló una reducción de la entrada de aire en las bases pulmonares bilaterales con crepitación fina al final de la inspiración bilateral. El examen del sistema nervioso abdominal y central no reveló nada de interés.\n\n\nInvestigaciones\n\nEn el momento del ingreso, el ECG mostró bloqueo completo de rama izquierda (B-R) con un intervalo QT prolongado. La hemoglobina era de 58 g/l (133-162) con un cuadro dimórfico. El volumen corpuscular medio era de 110 fL (80,0-100,0 fL), la hemoglobina corpuscular media era de 34 pg/mL (27,0-32,0 pg/mL), la concentración media de hemoglobina corpuscular era de 36,2 g/dL (32,0-35,0 g/dL). Otros análisis revelaron niveles séricos de vitamina B12 de 135 pg/mL (211-911 pg/mL). El nivel sérico de ácido fólico era de 5,40 ng/mL (>5,38 ng/mL). El nitrógeno ureico en sangre era de 53 mg/dL (10-50) con creatinina de 0,8 mg/dL (0,7-1,3). Los resultados de las pruebas de función hepática (LFT) estaban dentro de los límites normales. El perfil de calcio mostró 4,3 mg/dL de S.calcium (8,5-10,5), fosfato 7,1 mg/dL (2,5-4,5), 3,06 g/dL de S.albumin (3,5-5,5). En vista de la hipocalcemia e hiperfosfatemia, se realizó un estudio del nivel de hormona paratiroidea intacta, que resultó ser <0,23 ng/mL (14-72). El S.magnesium era de 2,0 mg/dL (1,7-2,2). El análisis de gases en sangre arterial (ABG) fue sugestivo de una acidosis metabólica leve. El perfil tiroideo y los niveles de IgAtTG estaban dentro de los límites normales. Los niveles de ferritina y ceruloplasmina séricos estaban dentro de los límites normales. El ultrasonido abdominal y torácico mostró derrame pleural bilateral en posición supina. La vena cava inferior (IVC) y las venas hepáticas eran prominentes. El reposo dentro de los límites normales. La radiografía de tórax mostró un aplanamiento de los ángulos costofrénicos bilaterales que sugería derrame pleural bilateral. La ecocardiografía reveló un ventrículo izquierdo dilatado (LV) con una fracción de eyección del ventrículo izquierdo del 15 %, que sugería DCMP con disfunción severa del LV. Se realizó un arteriograma coronario basal que fue normal. La TC sin contraste de la cabeza mostró calcificación simétrica bilateral (B/L) en el hemisferio cerebeloso B/L, ganglios basales B/L y calcificación cortical/subcortical en la región B/L fronto-parieto-occipital. El reposo dentro de los límites normales.\n\n\nTratamiento\n\nPara el CHF, se inició al paciente con dobutamina intravenosa a una dosis de 6 µg/kg y furosemida intravenosa 20 mg BD para la descongestión. Sin embargo, el paciente no mostró una mejora significativa con el tratamiento anterior. En vista de la hipocalcemia con hiperfosfatemia y bajos niveles de hormona paratiroidea, se consideró un diagnóstico de cardiomiopatía hipocalcemica con hipoparatiroidismo y se inició al paciente con inyección de gluconato de calcio 1 g (90 mg de calcio elemental) administrado por vía intravenosa seguido de infusión de gluconato de calcio en 500 ml de dextrosa al 5% a una velocidad de 37,5 mg/hora de calcio elemental. El paciente mostró una mejora significativa después de iniciar el gluconato de calcio. El paciente fue dado de alta en condiciones estables con comprimidos de calcio por vía oral 3 g/día junto con calcitriol 0,5 µg/día. También se inició con benzotiazida con triamtereno (25/50 mg) OD, ramipril 5 mg una vez al día y carvedilol 3,125 mg dos veces al día. Para la anemia megaloblástica, se administraron inyecciones de cianocobalamina según el protocolo.\n\n\nResultado y seguimiento\n\nAl cabo de tres meses, el paciente había mejorado notablemente.\n\nLas investigaciones mostraron S.calcium 7.7, S.phosphate 6.0 y albúmina 3.6. La hemoglobina fue de 10.1 g/dL. El eco mostró una mejora en la función del LV con una fracción de eyección del 25%. Se planificó una biopsia endomiocardial, pero el paciente se negó, por lo que no pudo realizarse.\n\nMH - Gluconato de calcio/administración y dosificación/uso terapéutico\nMH - Cardiomiopatía, Dilatada/*complicaciones/diagnóstico\nMH - Ecocardiografía/métodos\nMH - Insuficiencia cardiaca/terapia farmacológica/*etiología/fisiopatología\nMH - Humanos\nMH - Hipocalcemia/*complicaciones/diagnóstico/terapia farmacológica/fisiopatología\nMH - Hipoparatiroidismo/*complicaciones/terapia farmacológica\nMH - Hombre\nMH - Edad Media\nMH - Volumen de carrera\nMH - Resultado del tratamiento\nMH - Disfunción ventricular izquierda/diagnóstico por imágenes\n",
+        "gold_summary": "Presentamos el caso de un hombre asiático de 55 años que había tenido un caso conocido de miocardiopatía dilatada durante 6 meses, que se presentó con las principales quejas de falta de aire al hacer ejercicio y disminución de la producción de orina. En el examen físico general, se observaron características que sugerían una ICC. El signo de Chvostek y Trousseau fue positivo. El paciente tenía antecedentes de cirugía de cataratas en ambos ojos 15 años atrás. Otras investigaciones revelaron una hipocalcemia. La ecografía mostró una grave hipocinesia global del ventrículo izquierdo con una fracción de eyección del ventrículo izquierdo del 15%. Esta ICC fue refractaria al tratamiento convencional, aunque, con la suplementación de calcio, el paciente mejoró sintomáticamente. En el seguimiento después de 3 meses, se observó una mejora en los parámetros ecocardiográficos con una fracción de eyección que mejoró al 25%.\n",
+        "synthetic_summary": {
+            "B1": "There was a man who felt very tired and had trouble breathing when he played. His body was not making enough pee. The doctor found his heart was very weak. The doctor saw signs that his body did not have enough calcium. The man had surgery on his eyes a long time ago. The doctor gave him special medicine with calcium. After some time, the man started to feel better and his heart worked a little better too.",
+            "B2": "**What Happened to the Patient**\n\nA 55-year-old Asian man had a heart condition called dilated cardiomyopathy, which means his heart’s left ventricle was enlarged and weak. He had been diagnosed with this condition for about six months. He came to the hospital because he was having trouble breathing during exercise and was producing less urine than usual.\n\n**What the Doctors Found**\n\nDuring the physical exam, the doctors noticed signs of heart failure, which means the heart was not pumping blood well. Two special signs called Chvostek and Trousseau were positive. These signs suggest low calcium levels in the body. The patient also had a history of cataract surgery in both eyes 15 years ago.\n\nBlood tests showed that his calcium levels were very low (a condition called hypocalcemia). An ultrasound of his heart showed that the left ventricle was not moving well and had a very low ejection fraction of 15%. The ejection fraction tells us how much blood the heart pumps out with each beat; normal is usually above 50%.\n\n**How They Treated Him**\n\nThe patient’s heart failure did not get better with usual treatments. Because of his low calcium and other signs, doctors gave him calcium supplements through an IV (a needle in the vein). After starting calcium treatment, his symptoms improved noticeably.\n\n**What Happened Next**\n\nThree months later, the patient was doing much better. His heart’s ejection fraction improved to 25%, showing his heart was pumping more effectively. This case shows that low calcium levels can cause or worsen heart problems, and treating the calcium deficiency can help improve heart function.",
+            "B3": "**Background**  \nA 55-year-old Asian man with a known diagnosis of dilated cardiomyopathy (DCMP) for six months presented with progressive shortness of breath during exertion and decreased urine output. His symptoms had worsened over the past week, progressing from moderate to severe heart failure symptoms, including orthopnea (difficulty breathing when lying flat), paroxysmal nocturnal dyspnea (sudden nighttime breathlessness), chest heaviness, productive cough with frothy sputum, and bilateral lower limb swelling. He also reported tingling sensations in both hands and feet for one month. The patient had a history of bilateral cataract surgery 15 years prior and had been non-compliant with his DCMP treatment.\n\n**Key Findings**  \nOn physical examination, signs consistent with congestive heart failure (CHF) were evident, including elevated jugular venous pressure and bilateral pedal edema. Notably, the patient exhibited a positive Chvostek sign (facial muscle twitching upon tapping, indicative of low calcium) and a positive Trousseau sign (carpopedal spasm induced by blood pressure cuff inflation), both suggestive of hypocalcemia. Cardiovascular examination revealed a hyperdynamic apical impulse displaced laterally, while respiratory exam showed decreased breath sounds and fine crackles at both lung bases, consistent with pulmonary congestion.\n\nLaboratory investigations revealed severe hypocalcemia (serum calcium 4.3 mg/dL; normal 8.5–10.5 mg/dL), hyperphosphatemia (serum phosphate 7.1 mg/dL; normal 2.5–4.5 mg/dL), and markedly low intact parathyroid hormone (PTH) levels (<0.23 ng/mL; normal 14–72 ng/mL), confirming hypoparathyroidism as the underlying cause of the hypocalcemia. The patient also had macrocytic anemia with low vitamin B12 levels. Electrocardiogram showed a complete left bundle branch block and prolonged QT interval, both associated with hypocalcemia. Echocardiography demonstrated a severely dilated left ventricle with global hypokinesia and a markedly reduced ejection fraction of 15%, consistent with severe DCMP. Imaging studies revealed bilateral pleural effusions and symmetrical brain calcifications in the cerebellum and basal ganglia, which are characteristic findings in chronic hypoparathyroidism.\n\n**Clinical Interpretation**  \nThis patient’s presentation reflects a rare but significant cause of dilated cardiomyopathy secondary to chronic hypocalcemia caused by hypoparathyroidism. The hypocalcemia likely contributed to the severe left ventricular dysfunction and refractory congestive heart failure that did not respond adequately to standard heart failure therapies. The positive Chvostek and Trousseau signs, along with biochemical evidence of hypocalcemia and suppressed PTH, were critical diagnostic clues. The presence of brain calcifications further supports the chronicity of hypoparathyroidism.\n\n**Treatment and Outcome**  \nInitial management with intravenous dobutamine and diuretics aimed at relieving heart failure symptoms was insufficient. Upon recognition of hypocalcemia and hypoparathyroidism, intravenous calcium gluconate supplementation was initiated, followed by continuous calcium infusion and oral calcium and calcitriol (active vitamin D) therapy. This targeted treatment led to significant symptomatic improvement and partial recovery of left ventricular function, with the ejection fraction improving from 15% to 25% over three months. Additional management included correction of vitamin B12 deficiency and standard heart failure medications such as ramipril, carvedilol, and diuretics.\n\n**Next Steps and Follow-Up**  \nThe patient was discharged in stable condition with ongoing oral calcium and calcitriol supplementation and heart failure medications. Follow-up after three months showed improved biochemical parameters (serum calcium 7.7 mg/dL, phosphate 6.0 mg/dL) and partial recovery of cardiac function. Although an endomyocardial biopsy was planned to further characterize the cardiomyopathy, the patient declined the procedure. Continued monitoring of calcium levels, cardiac function, and anemia is essential to optimize long-term outcomes.\n\n---\n\nThis case highlights the importance of considering metabolic causes such as hypoparathyroidism-induced hypocalcemia in patients with dilated cardiomyopathy and refractory heart failure, as appropriate correction can lead to significant clinical improvement."
+        }
+    },
+    {
+        "article": "Una mujer de 54 años de edad, libanesa, en hemodiálisis (HD) de mantenimiento tres veces por semana para glomeruloesclerosis segmentaria focal (GSF) fue admitida en el departamento de urgencias, luego de haber sido sometida a su HD programada la noche anterior, debido al inicio repentino de un dolor lumbar agudo en el lado izquierdo, náuseas y vómitos. El dolor había comenzado repentinamente cerca de 12 horas antes de su presentación y se agravó rápidamente. En una nota al margen, un hiperparatiroidismo secundario grave con calcificación cutánea vascular fue tratado con cinacalcet durante 3 años sin respuesta, lo que demandó una paratiroidectomía (hiperplasia de cuatro glándulas) 8 meses antes de su presentación actual. Cinco días antes de su presentación, fue admitida en el hospital debido a anemia grave y rectorragia. Su evaluación por ultrasonido renal mostró riñones bilaterales pequeños con parénquima delgado que contenía quistes de hasta 3 cm y calcificaciones vasculares sin hidronefrosis. Cuatro días antes de su presentación, la colonoscopia a través del íleo terminal reveló un pólipo de 7 mm en el colon descendente izquierdo, que fue removido por mucosectomía. La microscopía volvió como adenoma tubular sésil con displasia de bajo grado. La paciente negó fiebre o antecedentes de trauma. No hubo antecedentes previos de uso de antiplaquetarios. En la emergencia, su presión arterial y pulso fueron de 112/65 mmHg y 96 bpm, su temperatura fue de 36.8°C y presentaba abdomen levemente distendido, con dolor importante en el ángulo costovertebral izquierdo. Los hallazgos de laboratorio mostraron hemoglobina de 9.0 g/dL mientras que el hematocrito fue de 29.7%, recuento total de leucocitos 12.2 × 1000/microlitro, creatinina de 6.06 mg/dL, y nivel de proteína C reactiva de 6 mg/L. Además, el TP fue de 83% y el INR fue de 1.13. En el día de la presentación (es decir, 4 días después de la colonoscopia), se realizó una tomografía computarizada (TC) multifásica del tórax, abdomen y pelvis con y sin contraste intravenoso. El examen reveló un gran quiste y enormes hematomas intraparenquimatosos perirrenales izquierdos con una colección subcapsular de hasta 1,8 cm de espesor con colección hemática en todo el compartimiento renal que alcanzaba un diámetro de más de 9 × 4 cm, hidronefrosis izquierda y edema alrededor de la grasa en todo el flanco y calcificaciones en el hilo. Para la descompresión del sistema pélvico renal y drenaje, optamos por tratarla con inserción retrógrada de doble stent ureteral a la izquierda, que identificó un coágulo en la parte media del uréter izquierdo. Se realizaron cultivo de orina y citología y los resultados fueron negativos. Una simple radiografía del abdomen mostró el doble J en su lugar. La paciente permaneció hemodinámicamente estable, pero presentó una nueva caída en la hemoglobina (6.1 g/dL) la misma noche, lo que exigió una transfusión de una unidad de concentrado de eritrocitos leucodepleados para estabilización. Se tomó la decisión de explorar quirúrgicamente con diagnóstico presuntivo de hematoma perirrenal izquierdo subagudo y para excluir una malignidad subyacente. Se sometió a una sesión de HD sin heparina. En el tercer día, se sometió a una nefrectomía radical abierta a la izquierda con conservación de la glándula suprarrenal. Recibió 2 unidades más de concentrado de eritrocitos leucodepleados durante la intervención. El parénquima renal fue casi totalmente reemplazado por un hematoma que medía 9 × 9 × 7 cm y se extendía hasta la grasa perirrenal. Una pequeña masa papilar fue enviada por separado para análisis. La evaluación histopatológica detallada reveló un parénquima renal con lesiones de nefritis crónica mutilada por grandes áreas hemorrágicas que se extendían hasta la grasa perirrenal. Además, había una proliferación neoplásica de 2 mm, con arquitectura papilar cubierta por pequeñas células cúbicas atípicas y macrófagos espumosos en el eje, compatibles con adenoma papilar. Al día siguiente de la operación, la paciente fue sometida a HD y recibió un paquete de eritrocitos leucodepleados. El período postoperatorio fue sin intercorrerencias. El nivel de hemoglobina se mantuvo alrededor de 10 g/dL. La paciente se recuperó sin signos o síntomas de sangrado. La paciente permanece bien y asintomática y actualmente se encuentra en HD de mantenimiento regular.\n",
+        "gold_summary": "A continuación, se describe un caso inusual de una paciente con HD de 54 años de edad que presentó HPE pocos días después de una colonoscopia. La causa de la HPE fue la ruptura de un quiste de DRCA. Consideramos que la colonoscopia fue un factor desencadenante y planteamos hipótesis sobre su etiopatogenia. La paciente se sometió a una nefrectomía izquierda exitosa.\n",
+        "synthetic_summary": {
+            "B1": "A lady who gets kidney cleaning had a big problem. She had pain and bleeding near her left kidney. This happened a few days after a doctor looked inside her tummy with a camera. \n\nA small bubble near her kidney broke and made the pain. The lady had an operation to take out her left kidney. She got better after the surgery.",
+            "B2": "**What Happened:**  \nA 54-year-old woman who regularly receives hemodialysis (a treatment that cleans the blood when kidneys don’t work well) suddenly developed severe pain in her left lower back, along with nausea and vomiting. This happened just a few days after she had a colonoscopy, which is a test where doctors look inside the large intestine with a camera.\n\n**What They Found:**  \nDoctors discovered that she had a large blood collection (called a hematoma) around her left kidney. This was caused by the breaking (rupture) of a cyst, which is a fluid-filled sac in the kidney. The cyst was related to her kidney disease. The bleeding and swelling around the kidney were serious enough that she needed surgery to remove the entire left kidney. During surgery, they also found a small non-cancerous tumor called a papillary adenoma.\n\n**What It Means:**  \nThe doctors think that the colonoscopy might have triggered the cyst to break and cause the bleeding. This is a rare and unusual complication. After surgery, the woman recovered well and continues her regular dialysis treatments without problems.\n\n**Summary:**  \nThis case shows that people on dialysis with kidney cysts might have rare risks after procedures like colonoscopy. Careful monitoring is important. The woman’s kidney was successfully removed, and she is doing well now.",
+            "B3": "Background  \nThis report details an unusual case involving a 54-year-old woman undergoing maintenance hemodialysis (HD) for focal segmental glomerulosclerosis, who developed a spontaneous hemorrhage around her left kidney (perirenal hemorrhage) shortly after a colonoscopy procedure. Her medical history included severe secondary hyperparathyroidism treated unsuccessfully with medication, leading to surgical removal of her parathyroid glands eight months prior.\n\nKey Findings  \nWithin days following the colonoscopy, the patient experienced sudden, severe left-sided lower back pain accompanied by nausea and vomiting. Imaging studies revealed a large cyst in her left kidney that had ruptured, causing extensive bleeding into the kidney tissue and surrounding areas. Additional findings included left-sided hydronephrosis (swelling of the kidney due to urine buildup) and vascular calcifications. Laboratory tests showed anemia and elevated inflammatory markers. Despite initial stabilization and insertion of a ureteral stent to relieve urinary obstruction, her hemoglobin levels dropped further, necessitating blood transfusions.\n\nClinical Interpretation  \nThe spontaneous rupture of the renal cyst was identified as the cause of the hemorrhage. The temporal relationship between the colonoscopy and the hemorrhage suggests that the colonoscopy may have acted as a triggering event, possibly through increased intra-abdominal pressure or vascular stress. Histopathological examination after surgical removal of the left kidney confirmed chronic kidney inflammation with extensive hemorrhage and identified a small benign papillary adenoma (a non-cancerous tumor) within the renal tissue.\n\nNext Steps and Outcome  \nGiven the severity of the hemorrhage and to exclude underlying malignancy, the patient underwent a successful open radical nephrectomy (complete removal of the left kidney) while preserving the adrenal gland. Postoperative recovery was uneventful, with stabilization of hemoglobin levels and no further bleeding episodes. The patient continues on regular maintenance hemodialysis and remains asymptomatic.\n\nSummary  \nThis case highlights a rare but serious complication—spontaneous perirenal hemorrhage due to rupture of a cyst in a dialysis patient—potentially precipitated by a recent colonoscopy. It underscores the importance of careful monitoring for acute abdominal or flank pain in patients with chronic kidney disease undergoing invasive procedures. Surgical intervention can be lifesaving and diagnostic in such complex scenarios."
+        }
+    },
+    {
+        "article": "Se evaluó a una mujer de 30 años de edad con antecedentes de dos meses de dolor progresivo y disminución de la visión OD. Dos semanas antes del desarrollo de los síntomas oculares, la paciente comenzó a disminuir la prednisona como tratamiento para sus síntomas inflamatorios sistémicos. Los antecedentes médicos incluyen artritis inflamatoria, síntomas gastrointestinales que sugieren enfermedad intestinal inflamatoria y pérdida de peso de 20 libras antes de la presentación. Los detalles completos del caso de la paciente se informaron previamente y se resumen aquí junto con análisis adicionales de quimiocina y citoquina de fluido ocular.13\n\nEn el examen, las BCVAs fueron 20/40 OD y 20/20 OS, y las pupilas fueron 9 mm y akinéticas OD y 5 mm con una rápida reactividad a la luz OS. Las presiones intraoculares fueron 65 mmHg OD y 21 mmHg OS. El examen con lámpara de hendidura mostró precipitados queráticos granulomatosos pigmentados (KP) dentro de la córnea inferior, 3+ células de la cámara anterior, atrofia difusa del iris con pigmento en las zónulas, y ectropion uvea OD, y OS fue normal. La gonioscopia mostró 3+ células pigmentadas dentro del ángulo inferior OD. El examen del fondo fue normal en ambos ojos. Una paracentesis anterior diagnóstica fue positiva para ADN de VZV mediante pruebas de PCR, y las pruebas serológicas fueron positivas para anticuerpos IgG de VZV. Posteriormente, se le diagnosticó uveítis anterior hipertensiva asociada a VZV, lo que provocó el inicio de acetazolamida oral y timolol oftálmico, dorzolamida, y brimonidina para la hipertensión ocular, así como valaciclovir 1 g TID y acetato de prednisolona 1% cada 2 horas. El curso de la enfermedad de la paciente y otros detalles de su tratamiento se describieron previamente.13\n\nLa paciente fue diagnosticada con un accidente cerebrovascular (ACV), que se cree que se debe a una vasculopatía del SNC asociada al VVZ, y fue hospitalizada durante 2 semanas, durante las cuales sus síntomas oculares mejoraron gradualmente. Sin embargo, dos meses después de su ACV, desarrolló un empeoramiento del dolor y la visión en el ojo derecho, y su BCVA disminuyó a 20/100 con una PIO elevada de 39 mmHg OD. El examen reveló una inyección ciliar 1+ y 3+ células de la cámara anterior, y se cambió de prednisolona a difluprednato con una mejora mínima. Posteriormente, se sometió a un procedimiento de filtración de glaucoma con una derivación de Ahmed debido a su PIO elevada persistente a pesar de la máxima tolerancia de la terapia ocular hipertensiva. Se obtuvo una muestra de humor acuoso del ojo derecho durante la cirugía de filtración para un análisis de perfil de quimiocina/citoquina. Se estimaron los niveles de 22 citoquinas y quimioquinas, incluidos IFN-Y, IL-10, IL-12p70, IL-17A, IL-1B, IL-2, IL-5, IL-6, IL-8, TNF-a, IL-18, IL-1RA, IL-1a, IL-1a, IP-10, MCP-1, MIP-1a, MIP-1B, SDF-1a, IL-21, IL-22, IL-23 e IL-27, utilizando la técnica de inmunoensayo de perlas múltiplex. Se detectaron niveles de concentración de 7 citoquinas/quimioquinas, incluidos IL-6, IL-8, IL-18, MIP-1b, IP-10, MCP-1, e IL-1RA. La IL-1RA fue la citoquina más abundante (1000 pg/mL), mientras que IP-10 y MCP-1 fueron las segundas citoquinas más abundantes (150–200 pg/mL). Se detectaron niveles de 10–20 pg/mL de IL-18 y MCP-1b, pero a niveles mínimos en esta muestra de AqH. Se detectaron niveles de IL-6 e IL-8, pero se encontró que eran las citoquinas menos abundantes, cada una con niveles de <10 pg/mL.\n\n",
+        "gold_summary": "El caso 2 fue el de una mujer de 30 años con antecedentes de dos meses de dolor progresivo y disminución de la visión en el ojo derecho. Se le diagnosticó uveítis anterior hipertensiva tras una paracentesis diagnóstica de la cámara anterior. A pesar de la terapia exitosa para la uveítis anterior, su presión intraocular se mantuvo elevada y requirió un procedimiento de filtración de glaucoma. Se recolectó una muestra de fluido ocular en el momento de la cirugía para el análisis de perfiles de citoquinas/quimioquinas, y se detectaron niveles de 7 citoquinas/quimioquinas, entre ellas, IL-6, IL-8, IL-18, MIP-1B, IP-10, MCP-1 e IL-1RA, siendo IL-1RA la citoquina más abundante.\n",
+        "synthetic_summary": {
+            "B1": "A lady had pain and her eye got blurry. Doctors found her eye was very sore inside. They gave her medicine to help. But her eye pressure stayed high. So, she had a small surgery to help her eye. During the surgery, doctors took some eye juice to check. They found some tiny helpers that show how her eye was feeling. One helper was the most in her eye juice. The lady is getting care to help her eye feel better.",
+            "B2": "**What Happened to the Patient**  \nA 30-year-old woman had been feeling increasing pain and losing vision in her right eye for two months. Doctors found she had a condition called hypertensive anterior uveitis. This means there was inflammation (swelling and irritation) in the front part of her eye, along with high pressure inside the eye. To confirm this, they took a small sample of fluid from her eye—a procedure called a paracentesis—and tested it.\n\n**Treatment and Challenges**  \nEven though the treatment helped reduce the inflammation, the pressure inside her eye stayed too high. High eye pressure can damage the eye and cause glaucoma, which can lead to vision loss. Because of this, she needed surgery called glaucoma filtration to help lower the pressure.\n\n**What the Tests Showed**  \nDuring the surgery, doctors collected some eye fluid to study certain proteins called cytokines and chemokines. These proteins are important because they help control inflammation and immune responses in the body. The test found seven different cytokines and chemokines in her eye fluid. The most common one was IL-1RA, which helps reduce inflammation. Others found included IL-6, IL-8, IL-18, MIP-1B, IP-10, and MCP-1. Knowing which proteins are present helps doctors understand the inflammation happening inside the eye and may guide future treatments.",
+            "B3": "**Background**  \nA 30-year-old woman presented with a two-month history of progressively worsening pain and decreased vision in her right eye. Her medical history included inflammatory arthritis, gastrointestinal symptoms suggestive of inflammatory bowel disease, and significant weight loss prior to presentation. Two weeks before her ocular symptoms began, she had started tapering off prednisone, which she had been using to manage systemic inflammatory symptoms.\n\n**Key Findings**  \nOn examination, her best-corrected visual acuity (BCVA) was 20/40 in the right eye and 20/20 in the left eye. The right pupil was dilated (9 mm) and non-reactive, while the left pupil was normal. Intraocular pressure (IOP) was markedly elevated in the right eye at 65 mmHg (normal range approximately 10-21 mmHg) and normal in the left eye. Slit-lamp examination revealed granulomatous pigmented keratic precipitates (inflammatory deposits on the cornea), significant inflammation in the anterior chamber (3+ cells), diffuse iris atrophy with pigment dispersion, and ectropion uveae (an abnormality of the iris margin) in the right eye. The left eye appeared normal. Gonioscopy showed pigmented inflammatory cells in the angle of the right eye. Fundus examination was normal in both eyes.\n\nA diagnostic anterior chamber paracentesis (sampling of aqueous humor) tested positive for varicella-zoster virus (VZV) DNA by polymerase chain reaction (PCR), and serology confirmed VZV IgG antibodies, establishing a diagnosis of VZV-associated hypertensive anterior uveitis (inflammation of the front part of the eye with elevated eye pressure).\n\nDespite initiation of antiviral therapy (oral valacyclovir) and multiple ocular hypotensive agents (acetazolamide, timolol, dorzolamide, brimonidine), her intraocular pressure remained elevated. She was treated with topical corticosteroids (prednisolone acetate initially, later switched to difluprednate) with minimal improvement in inflammation and pressure control.\n\nTwo months after suffering a stroke attributed to central nervous system vasculopathy related to VZV, her right eye symptoms worsened, with BCVA declining to 20/100 and IOP rising to 39 mmHg. Due to persistent elevated IOP despite maximal medical therapy, she underwent glaucoma filtration surgery with an Ahmed valve implant.\n\n**Clinical Interpretation**  \nDuring the glaucoma surgery, aqueous humor was collected for detailed analysis of inflammatory mediators, specifically a panel of 22 cytokines and chemokines (signaling proteins involved in immune responses). Seven of these mediators were detected at measurable levels: interleukin (IL)-6, IL-8, IL-18, macrophage inflammatory protein-1 beta (MIP-1β), interferon gamma-induced protein 10 (IP-10), monocyte chemoattractant protein-1 (MCP-1), and IL-1 receptor antagonist (IL-1RA).\n\nAmong these, IL-1RA was the most abundant cytokine, present at approximately 1000 pg/mL. IP-10 and MCP-1 were the next most prevalent, each at 150–200 pg/mL. IL-18 and MIP-1β were detected at lower concentrations (10–20 pg/mL), while IL-6 and IL-8 were present at minimal levels (<10 pg/mL).\n\nThe elevated IL-1RA suggests a significant anti-inflammatory response within the eye, potentially reflecting the immune system’s attempt to counterbalance ongoing inflammation caused by VZV infection. The presence of chemokines such as IP-10 and MCP-1 indicates recruitment of immune cells to the ocular tissues, consistent with active inflammation.\n\n**Next Steps**  \nManagement of VZV-associated hypertensive anterior uveitis requires ongoing antiviral therapy combined with careful control of intraocular pressure to prevent optic nerve damage and vision loss. The patient’s need for glaucoma filtration surgery underscores the severity of ocular hypertension in this condition. Monitoring cytokine profiles in aqueous humor may provide insights into disease activity and therapeutic response, potentially guiding personalized treatment strategies in complex cases of viral uveitis with secondary glaucoma."
+        }
+    },
+    {
+        "article": "Un varón negro de 2021 g de peso nació a las 35 semanas y tres días de edad gestacional estimada por repetición de cesárea debido a la preocupación por la disminución del movimiento fetal en el contexto de una puntuación de perfil biofísico baja (basada en el tono muscular, la frecuencia cardíaca, el movimiento, la respiración y el volumen de líquido amniótico). La historia materna fue notable por el rasgo de células falciformes, la edad materna avanzada y la obesidad. La historia del embarazo fue notable por oligohidramnios observados por ultrasonografía a las 31 semanas. La ecografía fetal también mostró distensión de la vejiga, hidroceles bilaterales, dilatación de la uretra y ascitis abdominal preocupantes por la obstrucción del tracto urinario inferior y la posible ruptura de la vejiga. La ruptura de membranas ocurrió al momento del parto.\n\nAl nacer, el bebé experimentó dificultad respiratoria y fue tratado con ventilación con presión positiva, oxígeno suplementario e intubación. Las puntuaciones de Apgar fueron de dos y siete a un minuto y cinco minutos de vida, respectivamente. El examen mostró hematomas sustanciales y oscurecimiento de la extremidad superior izquierda. El bebé fue trasladado a la unidad de cuidados intensivos neonatales para el tratamiento de la dificultad respiratoria y sospecha de obstrucción del tracto urinario inferior. En la evaluación realizada dentro de la hora posterior al nacimiento por especialistas en ortopedia y cirugía plástica, el tercio distal del antebrazo y la mano estaban cianóticos, y una gran ampolla y área circundante de descamación eran evidentes en el dorso de la mano. No se observó movimiento espontáneo de la extremidad superior izquierda, y no se provocó la retirada o respuesta a los estímulos. La ecografía Doppler mostró flujo arterial al nivel de la fosa antecubital, pero no se detectaron pulsos radiales o cubitales. Los hallazgos del examen físico fueron consistentes con NCS, probablemente debido a la compresión de la pared uterina debido a oligohidramnios durante el embarazo.\n\nDespués de aproximadamente 5 horas de exámenes en serie, así como una amplia discusión con los equipos de ortopedia, cirugía plástica, neonatología y anestesia pediátrica, así como con los padres del bebé, se tomó la decisión de realizar una fasciotomía descompresiva del antebrazo, la mano y el túnel carpiano para permitir el rescate de la extremidad. La fasciotomía se realizó aproximadamente 6 horas después del nacimiento. El bebé fue monitoreado de cerca durante los siguientes días. La apariencia de la extremidad superior izquierda mejoró gradualmente. Al tercer día de vida, el antebrazo y la mano habían mejorado notablemente en color y parecían bien vascularizados. Las señales Doppler estaban presentes en todo momento, desde la arteria braquial hasta cada dedo. Se permitió que las heridas de la fasciotomía se curaran por intención secundaria, y se aplicó una férula personalizada con la muñeca en posición neutra y los dedos extendidos. No hubo signos de infección o isquemia en curso. Las heridas se curaron bien a las seis semanas de edad. En la visita de seguimiento a los cuatro meses de edad, las heridas se curaron por completo. El paciente tenía un rango de movimiento pasivo completo de la muñeca y los dedos. Se observó que tenía una ligera flexión y extensión del dedo anular y meñique, pero por lo demás, un movimiento activo mínimo de la muñeca o la mano en este momento. Tenía un movimiento activo del hombro y el codo. El paciente continuará recibiendo terapia ocupacional, así como férulas y masaje de cicatrices para prevenir/minimizar las contracturas. Los equipos multidisciplinarios continuarán siguiendo su progreso y recuperación de cerca.\n",
+        "gold_summary": "Presentamos un caso de NCS diagnosticado y tratado en base a los hallazgos del examen físico. La ecografía fetal mostró distensión de la vejiga, hidroceles bilaterales, dilatación de la uretra y ascitis abdominal que preocupaban por la obstrucción del tracto urinario inferior y posible ruptura de la vejiga. Una hora después del nacimiento, el examen de la extremidad superior izquierda del lactante no mostró movimiento espontáneo, la mano y el antebrazo parecían oscuros y la mano tenía una gran ampolla con descamación. No se detectó pulso distal a la fosa antecubital mediante ecografía Doppler. Se diagnosticó al lactante con NCS y se le practicó una fasciotomía urgente. La apariencia clínica y la perfusión de la extremidad superior izquierda mejoraron gradualmente. A los cuatro meses de edad, las heridas se habían curado y el paciente tenía un rango de movimiento pasivo completo de la extremidad superior izquierda. La recuperación del movimiento activo está en curso.\n",
+        "synthetic_summary": {
+            "B1": "A baby was born with a hurt arm. The arm looked dark and had a big blister. The baby could not move the arm. Doctors did a special cut to help the arm feel better. After some time, the arm started to look better. The baby’s arm healed and could move a little bit. The doctors will keep helping the baby get stronger.",
+            "B2": "**What They Found Before Birth**  \nBefore the baby was born, doctors used ultrasound (a test that uses sound waves to see inside the body) and found some problems. The baby’s bladder was swollen, there was extra fluid around both testicles (called hydroceles), the tube that carries urine out (urethra) was widened, and there was fluid in the belly (ascites). These signs suggested that the baby’s urinary tract was blocked and the bladder might have burst.\n\n**What Happened After Birth**  \nOne hour after birth, doctors checked the baby’s left arm and hand. They noticed the arm and hand looked dark and had a big blister with peeling skin. The baby could not move that arm on its own. Using a Doppler ultrasound (which checks blood flow), they found no pulse below the elbow crease. These signs showed the baby had a condition called neonatal compartment syndrome (NCS). NCS happens when pressure builds up inside the muscles, cutting off blood flow and causing damage.\n\n**How They Treated It**  \nTo save the arm, doctors quickly performed a surgery called a fasciotomy. This surgery cuts open the tight tissue around the muscles to relieve pressure and restore blood flow. After the surgery, the baby’s arm gradually looked better and blood flow improved.\n\n**Recovery and Follow-Up**  \nBy four months old, the baby’s surgical wounds had healed well. The baby could move the arm passively, meaning someone else could move it for them fully. Active movement, where the baby moves the arm by themselves, was still improving. The baby could move the shoulder and elbow but had limited movement in the wrist and fingers. The medical team will keep helping with therapy and special splints to improve movement and prevent stiffness.\n\n**Summary**  \nThis case shows how doctors used tests and physical exams to find and treat a serious arm problem in a newborn. Early surgery helped save the arm, and ongoing care is helping the baby regain movement.",
+            "B3": "**Background**  \nThis case involves a newborn male infant born prematurely at 35 weeks and 3 days gestation, weighing 2021 grams. The pregnancy was complicated by maternal factors including sickle cell trait, advanced maternal age, and obesity. Prenatal ultrasound revealed oligohydramnios (low amniotic fluid), bladder distension, bilateral hydroceles (fluid accumulation around the testes), urethral dilation, and abdominal ascites, raising concerns about lower urinary tract obstruction and possible bladder rupture. Due to decreased fetal movements and a low biophysical profile score, delivery was performed by repeat cesarean section. At birth, the infant exhibited respiratory distress requiring ventilatory support.\n\n**Key Findings**  \nWithin one hour after birth, physical examination of the infant’s left upper limb revealed significant abnormalities: the distal third of the forearm and hand appeared cyanotic (bluish discoloration indicating poor oxygenation), a large blister with surrounding skin peeling was present on the dorsum of the hand, and there was no spontaneous movement or response to stimuli in that limb. Doppler ultrasound detected arterial blood flow only up to the antecubital fossa (the front of the elbow), with absent radial and ulnar pulses distally. These findings were consistent with neonatal compartment syndrome (NCS), a condition characterized by increased pressure within muscle compartments leading to compromised circulation and tissue damage. The suspected cause was in utero compression of the limb due to oligohydramnios.\n\n**Clinical Interpretation**  \nThe diagnosis of NCS was established based on clinical signs and Doppler imaging. Given the severity of ischemia and risk of permanent damage, an urgent decompressive fasciotomy (surgical release of the muscle compartments) of the forearm, hand, and carpal tunnel was performed approximately six hours after birth. Postoperatively, the limb’s color and perfusion gradually improved, with Doppler signals restored from the brachial artery down to the fingers. The fasciotomy wounds were managed by secondary intention healing and immobilized with a custom splint maintaining the wrist in a neutral position and fingers extended. No infection or ongoing ischemia was observed.\n\n**Next Steps and Follow-Up**  \nAt four months of age, the fasciotomy wounds had fully healed. The infant demonstrated full passive range of motion in the wrist and fingers, with some limited active movement—specifically slight flexion and extension of the ring and little fingers, but minimal active wrist or hand movement. Active movement of the shoulder and elbow was preserved. The patient continues to receive multidisciplinary care including occupational therapy, splinting, and scar massage aimed at preventing contractures and promoting functional recovery. Ongoing monitoring by orthopedic, plastic surgery, neonatology, and rehabilitation teams will guide further management and support the infant’s neurological and musculoskeletal development."
+        }
+    },
+    {
+        "article": "Una mujer de 38 años de edad fue admitida en la sala de cirugía en noviembre de 2022 con la principal queja de una hinchazón abdominal progresiva que se asoció con un dolor abdominal leve y una saciedad precoz durante cinco meses. No tenía síntomas sistémicos como pérdida de peso, estreñimiento, diarrea, deseo de alimentos salados, fatigabilidad fácil o dolor de cabeza.\nEn el examen, parecía estar bien alimentada, pero presentaba una gran distensión abdominal, un leve palidez, afebril y con un tinte de ictericia en la esclerótica.\nLa palpación abdominal reveló una gran masa intraabdominal, no dolorosa, que ocupaba todo el abdomen inferior y se extendía hacia el superior, sin signos de irritación peritoneal u organomegalia.\nLos análisis de sangre mostraron un recuento de glóbulos blancos (5,7 × 109/l), hemoglobina (9,8 g/dl), bilirrubina (103 mg/dl) con recuentos normales de plaquetas (393 × 109/l). Las enzimas hepáticas, AST (24,0 U/l), ALT (21,0 U/l), albúmina 42,7 g/l. Creatinina sérica (53 μmol/l) y ESR (80 mm/h). Todos los demás análisis de sangre fueron normales. Una ecografía abdominal reveló un complejo quiste abdominal, ambos riñones eran de tamaño normal y con una ecografía normal, el hígado parecía normal. La TC abdominal y pélvica de contraste, vistas axiales y coronales, demostraron un gran quiste suprarrenal de paredes delgadas (flechas azules) que medía aproximadamente 23,5 cm (AP) x 20,3 cm (T) x 32,2 cm (CC) con un volumen de 8 l. El gran quiste desplaza el riñón derecho (flechas rojas) inferomedial a través de la línea media y ejerce presión sobre el hígado, la vesícula biliar, el páncreas y los intestinos delgados. Se extiende hasta la fosa ilíaca derecha. Como había un tinte de esclerosis ictérica, pero la masa era separada del hígado, el páncreas, los conductos biliares y el riñón derecho. Dado el tamaño del quiste y sus efectos compresivos, se planificó una intervención quirúrgica. Se eligió un enfoque quirúrgico abierto.\n\nSe le practicó una laparotomía al paciente. Se le hizo una incisión abdominal en la línea media, bajo anestesia general, y tras abrir las capas de la pared abdominal, se identificó un enorme quiste retroperitoneal que ocupaba toda la cavidad abdominal.\n\nSe abrió el quiste para acceder al fluido que se aspiraba, como se demostró en la cistectomía que se realizó con éxito. Se aspiraron unos 8 l de fluido de color marrón de la masa. Se enviaron muestras de la pared quística y del fluido para su análisis histológico.\n\nLa paciente se recuperó sin incidentes y fue dada de alta el día 7 después de la operación. El seguimiento a los 6 y 12 meses no mostró recurrencia ni complicaciones. El examen citológico de la muestra informó la presencia de material amorfo, no hubo evidencia de malignidad. Los resultados histológicos indicaron que la pared quística contenía tejido suprarrenal sin atipia, había infiltración de la pared quística por células inflamatorias mononucleares. La superficie interna de la pared no estaba revestida por células específicas reconocibles. En cuanto a los hallazgos clínicos intraoperativos, donde el origen del quiste era incierto, los hallazgos fueron más sugerentes de un quiste gigante idiopático retroperitoneal.\n\n",
+        "gold_summary": "Una mujer de 38 años se presentó con distensión abdominal progresiva. Las imágenes revelaron un quiste retroperitoneal gigante. Debido a los recursos limitados, se realizó una laparotomía abierta y se extirpó completamente un quiste de 33 cm que contenía 8 l de líquido transparente. La histopatología confirmó un quiste retroperitoneal idiopático gigante.\n",
+        "synthetic_summary": {
+            "B1": "A lady had a big tummy that grew bigger. Doctors found a big sack inside her tummy. They did a big cut to take the sack out. The sack was very big and had lots of clear water inside. The doctors said the sack was not from anything bad. She got better after the doctors helped her.",
+            "B2": "**What Happened to the Patient**  \nA 38-year-old woman had a growing belly swelling that lasted for five months. Doctors used imaging tests and found a very large cyst in the retroperitoneal area. This area is the space in the back of the abdomen, behind the organs.\n\n**What the Doctors Did**  \nBecause of limited medical resources, the doctors decided to do an open surgery called a laparotomy. This means they made a large cut in her belly to reach the cyst. They removed the whole cyst, which was about 33 centimeters wide and held 8 liters of clear fluid. That is a very big cyst.\n\n**What the Tests Showed**  \nAfter surgery, the doctors studied the cyst tissue under a microscope. They found it was an idiopathic cyst, which means the cause is unknown. It was a giant retroperitoneal cyst, but it was not cancerous or caused by infection.\n\n**What This Means**  \nThe woman recovered well after surgery and had no problems during follow-up visits. Removing the cyst helped relieve her symptoms and prevented future complications. This case shows how doctors can treat large cysts even when resources are limited.",
+            "B3": "**Background**  \nA 38-year-old woman experienced progressive abdominal swelling over five months, accompanied by mild abdominal pain and early satiety (feeling full quickly). She did not report systemic symptoms such as weight loss, changes in bowel habits, fatigue, or headaches. On examination, she appeared well-nourished but had significant abdominal distension, mild pallor, and a yellowish discoloration of the sclera (the white part of the eyes), indicating jaundice. A large, non-tender mass was palpable throughout the lower and upper abdomen without signs of peritoneal irritation or enlargement of other organs.\n\n**Key Findings**  \nLaboratory tests showed mild anemia (hemoglobin 9.8 g/dL), elevated bilirubin (103 mg/dL), normal white blood cell and platelet counts, normal liver enzymes (AST 24 U/L, ALT 21 U/L), normal albumin and kidney function, and an elevated erythrocyte sedimentation rate (ESR 80 mm/h), suggesting inflammation. Abdominal ultrasound revealed a complex cystic mass, with normal kidneys and liver appearance. Contrast-enhanced CT scans identified a very large (approximately 23.5 x 20.3 x 32.2 cm) thin-walled cyst located in the retroperitoneal space above the right kidney. This cyst displaced the right kidney medially and inferiorly and compressed adjacent organs including the liver, gallbladder, pancreas, and small intestines. Despite the patient’s jaundice, the cyst was separate from the liver, pancreas, bile ducts, and kidney.\n\n**Clinical Interpretation**  \nGiven the cyst’s enormous size (about 8 liters in volume) and its compressive effects on surrounding structures, surgical removal was indicated. An open laparotomy was performed, revealing a giant retroperitoneal cyst occupying the entire abdominal cavity. Approximately 8 liters of brown fluid were aspirated from the cyst. Samples of the cyst wall and fluid were sent for histological and cytological analysis. Cytology showed amorphous material without malignant cells. Histology demonstrated adrenal tissue within the cyst wall without cellular atypia, with infiltration by mononuclear inflammatory cells. The inner surface of the cyst wall lacked a recognizable epithelial lining. These findings, along with intraoperative observations, suggested the diagnosis of a giant idiopathic retroperitoneal cyst—meaning a large cyst of unknown origin located behind the peritoneum (the lining of the abdominal cavity).\n\n**Next Steps**  \nThe patient’s postoperative recovery was uneventful, and she was discharged on the seventh day after surgery. Follow-up evaluations at six and twelve months showed no recurrence of the cyst or complications. Continued monitoring is recommended to detect any potential future issues, although the benign nature of the cyst and complete surgical removal suggest a favorable prognosis."
+        }
+    },
+    {
+        "article": "Un hombre de 71 años con diabetes y enfermedad de Chagas había perdido recientemente mucho peso (60 kg). La investigación clínica dio lugar a un diagnóstico de megaesófago asociado a una obstrucción significativa a nivel del cardias. Se realizó una dilatación esofágica con balón, recuperando con éxito el tránsito digestivo. Mientras tanto, durante la evaluación del riesgo quirúrgico, el paciente también presentó dolor torácico con el mínimo esfuerzo. La angiografía por tomografía computarizada coronaria realizada tres años antes mostró una enfermedad multivascular muy calcificada que afectaba a la arteria coronaria izquierda; en ese momento no se había realizado ninguna otra investigación. Esta vez, se lo derivó a nosotros para un cateterismo cardíaco.\nEl examen realizado el 16 de febrero de 2016 mostró: arteria coronaria derecha (RCA) con importante calcificación y una lesión del 50% en el tercio medio; arteria descendente posterior (PDA) y arteria posterolateral derecha (RPLA), con severa calcificación y lesiones del 80% y 70%, respectivamente; LM con 80% de lesiones calcificadas en el tercio distal; arteria descendente anterior izquierda (LAD) con significativa calcificación y 90% de lesión en el tercio medio; ramas diagonales (DG1 y DG2) con lesiones calcificadas del 70% y 80%, en el origen y en el tercio proximal, respectivamente; y arteria circunfleja izquierda (LCx) ocluida y calcificada, recibiendo colaterales grado II de múltiples orígenes. El volumen ventricular izquierdo y la contractilidad se conservaron.\n\nCon esta imagen angiográfica, una puntuación de riesgo de la Society of Thoracic Surgeons del 15,8 % para morbilidad o mortalidad, una puntuación EuroSCORE II del 4,67 %, y una debilidad significativa debido a una pérdida de peso importante y reciente, el equipo cardiaco decidió realizar una intervención coronaria percutánea (ICP) de la LM, LAD, DG1 y DG2 inicialmente y, en un segundo procedimiento después de 30 días, una ICP de las ramas de la RCA. En ambos procedimientos, también se indicó una RA debido a una calcificación significativa. No se abordaría la LCx, ya que angiográficamente el vaso no estaba tan gravemente afectado y también considerando la dificultad técnica de la recanalización, debido a la longitud del CTO y también a las paredes muy calcificadas (puntuación J-CTO 4). La LCx ya estaba recibiendo una circulación collateral de grado II.\nEl 19 de febrero de 2016, tras comenzar una terapia antiplaquetaria dual con aspirina y clopidogrel, el paciente se sometió a una angioplastia de la arteria descendente anterior, la arteria circunfleja y la arteria descendente derecha con una fresa de 1,5 mm, seguida de una predilatación con un balón de 3,0 mm x 20 mm a 14 atm y la implantación de stents liberadores de fármacos en la arteria descendente derecha y la arteria circunfleja, utilizando una técnica de mini-aplastamiento y un balón de contacto al final. Se realizó un balón de contacto en la bifurcación de la arteria descendente derecha/arteria circunfleja y, finalmente, se implantó el tercer stent liberador de fármacos desde el origen de la arteria descendente derecha para superponerse con el stent de la arteria descendente derecha. Se logró un éxito procedimental con un flujo TIMI de 3 y sin complicaciones clínicas o angiográficas.\nEl 22 de marzo de 2016, el paciente volvió para una PCI con un RotaWire PCI en el PDA y RPLA con una fresa de 1,5 mm, seguido por la implantación de dos DES de 2,75 mm x 20 mm y 2,75 mm x 16 mm a 12 atm en el PDA y RPLA, respectivamente, sin ninguna predilatación adicional. También observamos la presencia de una disección larga y severa en el tercio medio del RCA, sin duda causada por un manejo excesivo e intentos de remover la fresa, lo que causó una penetración profunda por el catéter guía 7F. Esta disección se corrigió rápidamente con la implantación de un tercer DES de 4,0 mm x 32 mm, y se obtuvo un flujo TIMI 3 final sin complicaciones clínicas o electrocardiográficas. Los dos sitios de punción femoral se ocluyeron con dispositivos AngioSeal 8F y 6F, respectivamente. El paciente permaneció en la unidad de cuidados intensivos durante 48 horas, la única anormalidad fue la elevación de CK-MB (el doble del valor de referencia). Fue dado de alta el día 3 en excelentes condiciones generales. El ecocardiograma de control mostró una contractilidad ventricular izquierda normal.\n",
+        "gold_summary": "Un hombre de 71 años con enfermedad de Chagas y angina estable en esfuerzo mínimo se sometió a una angiografía por tomografía computarizada y cineangiografía que reveló una enfermedad multivascular muy calcificada que afectaba a la arteria descendente anterior izquierda (LM). Debido al grado de calcificación, se decidió realizar una rotablation. La primera etapa de la intervención coronaria percutánea (ICP) con rotablation se realizó en la arteria descendente anterior izquierda (LM), la arteria descendente anterior izquierda y la segunda rama diagonal sin complicaciones. Casi 30 días después, volvió para una ICP de la arteria coronaria derecha (RCA). La estrategia propuesta fue la aterectomía rotativa en la arteria descendente anterior posterior (PDA) y la arteria posterolateral derecha (RPLA) con una fresa de 1,5 mm, seguida por la implantación de dos stents liberadores de fármacos (DES). A través del acceso a la arteria femoral derecha, la lesión de la RPLA se extirpó con éxito. Como no había signos de disección y se mantuvo el flujo TIMI 3, se reposicionó el RotaWire de 0,009″ para cruzar la lesión de la PDA y se realizó la extirpación de la lesión. Después de dos intentos, logramos cruzar la lesión con la fresa de 1,5 mm, sin embargo, se produjo el atrapamiento de la misma. El sistema se retiró hasta que el catéter guía penetró profundamente en la RCA, y se hicieron intentos para liberar el Rotablator moviéndolo hacia adelante y hacia atrás, pero la fresa ni siquiera giró. La arteria femoral contralateral se perforó y se insertó un catéter guía 6F JR, con el fin de mover un alambre guía y un pequeño globo de angioplastia tangencialmente a la fresa, pero sin éxito. Finalmente, avanzamos el alambre guía utilizando la técnica de «nudillo», aprovechando la torsión de la porción distal del alambre guía PT2, realizando una disección subintimal y reentrada, y pudimos cruzar fácilmente el globo, inflarlo y liberar la fresa atrapada. A través del sistema 6F, se implantaron dos DES programados y uno de rescate con éxito en la PDA, RPLA y RCA, obteniendo un flujo TIMI 3 final sin complicaciones.\n",
+        "synthetic_summary": {
+            "B1": "A man who is 71 years old had very hard and narrow heart tubes. Doctors used a tiny drill to help open them. \n\nFirst, they fixed the left side tubes without problems. Then, after about one month, they fixed the right side tubes too. \n\nSometimes, the tiny drill got stuck. The doctors worked carefully to free it. They used small wires and balloons to help. \n\nIn the end, the tubes were open and blood could flow well. The man felt better and had no problems.",
+            "B2": "**What They Found**  \nA 71-year-old man with Chagas disease—a condition caused by a parasite affecting the heart—and chest pain during light activity had serious blockages in several heart arteries. These arteries were very hardened by calcium deposits, especially in the left main artery, which is a major blood vessel supplying the heart. Because of this heavy calcification, doctors decided to use a special procedure called rotablation. Rotablation uses a tiny rotating drill to remove the hard calcium from inside the arteries, helping to open them up.\n\n**What They Did**  \nThe treatment was done in two main steps. First, doctors performed rotablation and placed drug-releasing stents (small tubes that keep arteries open) in the left main artery and nearby branches. This went smoothly without problems. About a month later, the patient returned for the second part of the treatment focused on the right coronary artery. Again, rotablation was used on two branches, followed by placing two drug-releasing stents.  \n\nDuring this second procedure, the rotating drill got stuck inside one artery branch. The medical team tried several ways to free it, including using wires and small balloons to carefully move the drill. After some effort, they used a special wire technique called the \"knuckle\" method, which allowed them to safely cross the blockage and release the stuck drill. Then, they successfully placed the planned stents in the affected arteries.\n\n**What It Means**  \nThis case shows how doctors can treat very hardened and blocked heart arteries using advanced tools like rotablation and drug-releasing stents. Even when complications happen—like the drill getting stuck—skilled techniques can fix the problem without harm. The final result was good blood flow through the arteries and no complications, helping the patient’s heart work better.",
+            "B3": "**Background**  \nA 71-year-old man with a history of Chagas disease and stable angina on minimal exertion underwent coronary imaging that revealed severe, multivessel coronary artery disease characterized by extensive calcification, particularly affecting the left main coronary artery (LM) and its branches. Given the heavy calcification, the medical team planned a staged percutaneous coronary intervention (PCI) incorporating rotational atherectomy (rotablation) to modify the calcified plaques and facilitate stent placement.\n\n**Key Findings and Procedures**  \n- **First Stage PCI:** The initial procedure targeted the left main artery, the left anterior descending artery (LAD), and the second diagonal branch (DG2). Rotablation was successfully performed without complications, followed by drug-eluting stent (DES) implantation, restoring adequate blood flow.\n\n- **Second Stage PCI (Approximately 30 Days Later):** The patient returned for intervention on the right coronary artery (RCA) system. The strategy involved rotational atherectomy of the posterior descending artery (PDA) and the right posterolateral artery (RPLA) using a 1.5 mm burr, followed by implantation of two DES. The RPLA lesion was successfully treated via right femoral artery access, maintaining TIMI grade 3 flow (normal blood flow) without evidence of arterial dissection.\n\n- After repositioning the Rotawire guidewire, attempts were made to cross the PDA lesion with the 1.5 mm burr. Although the lesion was crossed after two attempts, the burr became entrapped within the artery. During attempts to withdraw the system, the guiding catheter deeply engaged the RCA, complicating retrieval.\n\n- Multiple maneuvers to free the burr were attempted, including advancing a guidewire and a small angioplasty balloon tangentially to the burr via contralateral femoral artery access, but these efforts were unsuccessful.\n\n- Ultimately, the team employed a “knuckle wire” technique, which involves creating a looped guidewire tip to safely dissect the subintimal space (the layer beneath the inner lining of the artery) and reenter the true lumen beyond the obstruction. This allowed successful passage of the balloon, inflation to release the entrapped burr, and safe retrieval.\n\n- Following burr release, two planned DES and one rescue DES were implanted successfully in the PDA, RPLA, and RCA, achieving final TIMI 3 flow without clinical or electrocardiographic complications.\n\n**Clinical Interpretation**  \nThis case illustrates the complexity of managing heavily calcified multivessel coronary artery disease in an elderly patient with Chagas disease. Rotational atherectomy was essential to modify the calcified plaques and enable effective stent deployment. The entrapment of the rotablation burr is a recognized but rare complication requiring advanced interventional techniques for resolution. The use of the knuckle wire technique for subintimal dissection and reentry was critical in safely retrieving the device and completing the procedure successfully.\n\n**Next Steps and Prognosis**  \nThe patient tolerated both procedures well, with restoration of normal coronary blood flow and no immediate complications. Continued dual antiplatelet therapy and close clinical follow-up are necessary to monitor for restenosis or other adverse events. The successful management of this complex case highlights the importance of careful procedural planning and the availability of advanced interventional strategies in treating severe calcified coronary artery disease."
+        }
+    },
+    {
+        "article": "Una paciente de 29 años se presentó al departamento de urología con dolor intermittent en el flanco derecho durante un año y sensación de ardor urinaria ocasional sin hematuria; su estado general era estable. La paciente no mostró signos de tos, fatiga, pérdida de peso, no había tenido cirugías previas, pero había estado expuesta frecuentemente a ovejas. A pesar de los exámenes de laboratorio normales, el examen de anticuerpos de equinococos arrojó un resultado positivo. El ultrasonido abdominal posterior reveló una lesión quística grande en el riñón derecho, que medía aproximadamente 63 mm con paredes gruesas y sin flujo de doppler significativo. La tomografía computarizada con contraste, tanto en vista transversal como coronal, reveló una masa quística con septos en el lado lateral del riñón derecho, que presentaba una pared gruesa y regular que se intensificaba con el contraste. Esta lesión se clasificó como categoría 4 de Bosniak, con imágenes de tomografía computarizada en vista coronal que mostraban la participación del sistema colector y el contacto con el hígado. Se sospechó de HC en base a las evaluaciones clínicas y radiológicas. Los hallazgos de la radiografía de tórax no fueron significativos, sin evidencia de quistes pulmonares. Después de un régimen de tres meses de albendazol 400 mg administrado dos veces al día, la paciente se sometió a una intervención quirúrgica. Se realizó un procedimiento abierto a través de una incisión subcostal derecha de Kocher, lo que resultó en una nefrectomía derecha y una resección hepática parcial debido a las adherencias. El espécimen, que pesaba 372 g y medía 13 × 8 × 6 cm, mostró un gran quiste blanco con paredes delgadas que contenían una membrana desprendida, que afectaba los cálices renales y la pelvis. El diagnóstico final fue HC del riñón acompañado de pielonefritis crónica. Los exámenes de laboratorio posteriores al procedimiento mostraron resultados normales, con una producción urinaria estable y signos vitales. El catéter urinario se retiró después de 24 horas debido a una producción urinaria adecuada (2 L). El drenaje renal se retiró después de 3 días, con volúmenes de drenaje de 200 ml, 100 ml y ninguno en días consecutivos. La paciente volvió a sus actividades normales sin complicaciones.\n",
+        "gold_summary": "Se diagnosticó a una mujer de 29 años con dolor intermitente en el flanco derecho y ardor urinario un quiste hidatídico (HC) de categoría 4 de Bosniak, tras dar positivo en anticuerpos de equinococo. Las imágenes confirmaron el diagnóstico, lo que derivó en un tratamiento de tres meses con albendazol, seguido de una nefrectomía derecha y una resección hepática parcial. El análisis histopatológico confirmó un HC y una pielonefritis crónica. La paciente se recuperó sin incidentes y volvió a sus actividades normales.\n",
+        "synthetic_summary": {
+            "B1": "A lady had pain on her right side and a burning feeling when she peed. Doctors found a big sack in her right kidney. They gave her medicine for three months to help. Then, they did surgery to take out the sick kidney and part of her liver. After the surgery, she felt better and went back to her normal life.",
+            "B2": "**What They Found**  \nA 29-year-old woman had pain on her right side and a burning feeling when urinating. Tests showed she had a hydatid cyst in her right kidney. A hydatid cyst is a fluid-filled sac caused by a parasite called Echinococcus. Blood tests found antibodies, which are proteins the body makes to fight this parasite. Scans of her kidney showed a large cyst with thick walls, which doctors classified as Bosniak category 4. This means the cyst looked suspicious and could be harmful.\n\n**What They Did**  \nThe woman took a medicine called albendazole for three months. Albendazole helps kill the parasite causing the cyst. After the medicine, she had surgery to remove her right kidney (called a nephrectomy) and part of her liver because the cyst was stuck to it. The removed tissue showed the cyst and signs of long-term kidney infection, called chronic pyelonephritis.\n\n**What It Means**  \nThe surgery and medicine worked well. After the operation, the woman recovered without problems. Her urine and vital signs were normal, and she was able to return to her regular activities. This case shows how doctors can treat a dangerous kidney cyst caused by parasites using medicine and surgery.",
+            "B3": "Background  \nA 29-year-old woman presented with intermittent pain in her right flank and occasional burning during urination, but no blood in her urine. She was otherwise stable, with no history of surgery or systemic symptoms like cough, fatigue, or weight loss. Notably, she had frequent exposure to sheep, which is relevant because sheep can carry Echinococcus parasites. Laboratory tests were normal except for a positive antibody test for Echinococcus, indicating exposure to the parasite that causes hydatid disease.\n\nKey Findings  \nImaging studies revealed a large cystic lesion measuring approximately 63 mm in the right kidney. Ultrasound showed thick walls without significant blood flow, while contrast-enhanced computed tomography (CT) demonstrated a cystic mass with internal septations and a thick, regularly enhancing wall. This lesion was classified as Bosniak category 4, which suggests a high risk of malignancy or complex cystic disease. The CT also showed involvement of the kidney’s collecting system and contact with the liver. Chest X-rays were unremarkable, showing no lung cysts.  \n\nClinical Interpretation  \nBased on the clinical presentation, positive serology, and imaging characteristics, the diagnosis of a hydatid cyst (HC) in the right kidney was made. Hydatid cysts are caused by infection with the larval stage of Echinococcus tapeworms. The presence of a Bosniak category 4 cyst raised concerns for a complex cystic lesion requiring surgical intervention. Chronic inflammation of the kidney’s pelvis and calyces (chronic pyelonephritis) was also identified on pathological examination.\n\nNext Steps and Outcome  \nThe patient underwent a three-month course of albendazole, an antiparasitic medication, at 400 mg twice daily to reduce the risk of parasite spread during surgery. Subsequently, she had an open right nephrectomy (removal of the right kidney) through a subcostal Kocher incision, along with partial liver resection due to adhesions between the cyst and the liver. The surgical specimen weighed 372 grams and measured 13 × 8 × 6 cm, revealing a large white cyst with thin walls and detached membranes affecting the renal collecting system. Histopathology confirmed the diagnosis of hydatid cyst and chronic pyelonephritis.  \n\nPostoperative recovery was uneventful. Urine output remained stable, allowing removal of the urinary catheter after 24 hours and renal drainage tubes after three days. The patient experienced no complications and returned to her normal daily activities."
+        }
+    },
+    {
+        "article": "Una paciente de 46 años de edad fue admitida en nuestro hospital debido a opresión en el pecho y falta de aire que había durado más de un mes. Su historial médico incluía una tiroidectomía parcial, y no tenía antecedentes de tabaquismo o consumo de alcohol. Fue tratada con medicamentos regulares (comprimidos de liberación prolongada de succinato de metoprolol, comprimidos de sacubitril valsartán sodio, espironolactona, comprimidos de dapagliflozina) para la IC, pero la respuesta fue pobre. Durante el examen físico, la paciente estaba consciente y bien orientada. Su frecuencia cardíaca era de 68 latidos por minuto, la presión arterial era de 150/98 mm Hg, la frecuencia respiratoria era de 20 latidos por minuto. No había signos de sangrado o ictericia en la piel o membranas mucosas, y no se observó distensión de la vena yugular. La glándula tiroides no estaba agrandada. Los sonidos respiratorios eran gruesos en ambos pulmones, con roncus húmedos presentes en las bases pulmonares. La frecuencia cardíaca era de 68 lpm con un ritmo regular. El abdomen era suave, sin sensibilidad o sensibilidad de rebote, y el hígado y el bazo no eran palpables por debajo de la caja torácica. El signo de reflujo hepatoyugular fue negativo, pero había edema en ambas extremidades inferiores.\n\nLa paciente fue hospitalizada y se le realizaron los exámenes pertinentes. Los análisis bioquímicos mostraron una hormona estimulante de la tiroides (TSH) de 7,190 uIU/mL, triglicéridos de 0,81 mmol/L, colesterol de lipoproteínas de baja densidad (LDL-C) de 2,61 mmol/L, lipoproteína (a) de suero de 435 mg/L y NT-proBNP de 6245 pg/mL. Un examen de electrocardiograma (ECG) mostró bradicardia sinusal, anomalías de la onda T-U y duración del QRS de 90 ms. Un examen ecocardiográfico transtorácico posterior reveló un diámetro de la aurícula izquierda (LA) (anteroposterior) de 41 mm, un diámetro del ventrículo izquierdo (LVD) (anteroposterior) de 54 mm, un espesor del tabique interventricular en diástole (IVSD) de 9 mm, un espesor de la pared posterior del ventrículo izquierdo en la fase final de la diástole (LVPWd) de 9 mm, una fracción de eyección del ventrículo izquierdo (LVEF) del 28% (M-mode), una fracción de acortamiento (FS) del 13% y una presión de la arteria pulmonar de 29 mm Hg. No se observaron lesiones coronarias significativas en la angiografía coronaria computarizada (CCA). Se diagnosticó a la paciente con cardiomiopatía dilatada, insuficiencia cardiaca de clase III con LVEF reducida según la New York Heart Association (NYHA). En combinación con los parámetros, se puede observar que los volúmenes de la aurícula izquierda y el ventrículo izquierdo se reducen gradualmente, lo que indica que la función diastólica del ventrículo izquierdo está mejorando. El tratamiento con CCM revierte la remodelación miocárdica. Además, E/e′ refleja la presión de llenado ventricular izquierdo. El valor normal debe ser inferior a 8. Se puede observar que en este caso, E/e′ vuelve al valor normal tres meses después de la implantación de CCM. Estos dos puntos reflejan el papel de CCM en la mejora de la función diastólica miocárdica en el tratamiento de la insuficiencia cardiaca. En resumen, la paciente tenía las siguientes características: (1) LVEF mejoró pero se mantuvo tan bajo como el 30% después de la terapia óptima para la insuficiencia cardiaca; (2) opresión en el pecho y malestar con ligera actividad, grado de función cardiaca III; (3) ECG muestra QRS estrecho. Teniendo en cuenta el resultado positivo de la prueba preoperatoria de levosimendan, después de una discusión general y una comunicación completa con el paciente y su familia, se decidió realizar el tratamiento con CCM.\n\nEl procedimiento de implantación del CCM fue similar al de la implantación de un marcapasos tradicional. El paciente se colocó en posición supina, se desinfectó con una toalla y se perforó la vena subclavia izquierda dos veces bajo anestesia local, y se hizo la bolsa capsular después de insertar el alambre guía. Bajo la guía del alambre guía, se introdujeron dos vainas de desprendimiento, y se introdujeron dos cables de estimulación ventricular (Medtronic 3830-69) a través de la vaina, y se ajustó la posición de los cables a la superficie del tabique ventricular derecho con una distancia de 3 cm. Durante la operación, se probó el electrodo de campo cercano (RV), que mostró un umbral de estimulación de 0,5 V, una amplitud de la onda R detectada mayor de 10 mV, y una impedancia del cable de 1080 Ω; el electrodo de campo lejano (LS) mostró un umbral de estimulación de 0,5 V, una amplitud de la onda R detectada mayor de 15 mV, y una impedancia del cable de 900 Ω. Estas mediciones cumplieron los criterios para una implantación exitosa del electrodo. Ambos cables se anclaron de forma segura en el tabique ventricular derecho. Después de asegurarse de que no había estimulación diafragmática palpable con un pulso de estimulación de 10 V y una anchura de pulso de 0,4 ms, se conectaron los cables al generador de impulsos Optimizer Smart. Posteriormente, se ajustaron los impulsos de salida y se programaron y optimizaron los parámetros.\n\nLa monitorización del ECG postoperatorio inmediato indicó un suministro normal de impulsos CCM (Figura 1C). Observamos la respuesta de los pacientes al CCM al adherirnos a un protocolo de seguimiento estandarizado. Utilizando una amplia variedad de herramientas de evaluación, que incluían ultrasonografía Doppler cardiaca a color, análisis de sangre NT-ProBNP, pruebas de caminata de seis minutos (6MW) y el Cuestionario de Minnesota para Vivir con Insuficiencia Cardiaca (MLHFQ), evaluamos sistemáticamente el estado clínico de los pacientes. El paciente no experimentó opresión en el pecho ni falta de aire, y hubo una marcada mejora en la tolerancia al ejercicio y la calidad de vida.\n",
+        "gold_summary": "Presentamos a una paciente de 46 años que fue admitida en nuestro hospital debido a opresión torácica y falta de aire que duró más de un mes. La ecocardiografía reveló un diámetro del ventrículo izquierdo (anteroposterior) de 54 mm, el electrocardiograma mostró bradicardia sinusal y duración del QRS de 90 ms. La paciente no experimentó opresión torácica o falta de aire, y hubo una marcada mejora en la tolerancia al ejercicio y calidad de vida después de la implantación de la modulación de la contractilidad cardiaca.\n",
+        "synthetic_summary": {
+            "B1": "A lady felt tightness in her chest and had trouble breathing for a long time. The doctors checked her heart and found it was not working well. After a small machine was put in her chest, she felt much better. She could play and move without feeling tired or sick.",
+            "B2": "**What Happened to the Patient**  \nA 46-year-old woman came to the hospital because she had chest tightness and trouble breathing for over a month. Tests showed that her left heart ventricle—the main pumping chamber—was larger than normal. Her heart’s electrical activity showed a slower heartbeat and normal timing of the heart’s electrical signals.\n\n**What Treatment She Received**  \nDoctors used a special device called cardiac contractility modulation (CCM). This device sends electrical signals to the heart to help it pump better. The device was put in through a procedure similar to getting a pacemaker.\n\n**What Changed After Treatment**  \nAfter getting the CCM device, the woman no longer felt chest tightness or shortness of breath. She could exercise more easily, and her overall quality of life improved a lot. This shows that CCM can help people with heart problems feel better and have stronger heart function.",
+            "B3": "**Background**  \nA 46-year-old woman was admitted to the hospital with chest tightness and shortness of breath that had persisted for over one month. Her medical history included a partial thyroidectomy, and she had no history of smoking or alcohol use. Despite receiving standard medications for heart failure—including metoprolol succinate, sacubitril-valsartan, spironolactone, and dapagliflozin—her symptoms and cardiac function showed limited improvement.\n\n**Key Findings**  \nInitial diagnostic tests revealed the following:  \n- Transthoracic echocardiography showed an enlarged left ventricle with an anteroposterior diameter of 54 mm and a severely reduced left ventricular ejection fraction (LVEF) of 28%, indicating significant impairment of the heart’s pumping ability.  \n- Electrocardiogram (ECG) demonstrated sinus bradycardia (slow heart rate) with a narrow QRS complex duration of 90 milliseconds, suggesting normal electrical conduction through the ventricles.  \n- Laboratory tests showed elevated thyroid-stimulating hormone (TSH) at 7.19 uIU/mL and a markedly increased NT-proBNP level of 6245 pg/mL, consistent with heart failure.  \n- Coronary computed tomography angiography excluded significant coronary artery disease.  \n- Clinical examination noted bilateral lower limb edema and lung crackles, consistent with fluid overload due to heart failure.\n\n**Clinical Interpretation**  \nThe patient was diagnosed with dilated cardiomyopathy and New York Heart Association (NYHA) class III heart failure with reduced ejection fraction. Despite optimized medical therapy, her LVEF remained low (~30%), and she continued to experience symptoms with minimal exertion. The narrow QRS complex excluded the typical indication for cardiac resynchronization therapy (CRT). Given a positive response to a preoperative levosimendan test (a drug that temporarily improves heart muscle contraction), the medical team decided to proceed with cardiac contractility modulation (CCM) therapy. CCM is a device-based treatment designed to enhance the strength of heart muscle contractions in patients with heart failure who do not qualify for CRT.\n\n**Treatment and Outcome**  \nThe CCM device was implanted via a procedure similar to pacemaker insertion, with leads positioned on the right ventricular septum. Postoperative monitoring confirmed appropriate device function and electrical parameters within normal limits. Over a standardized follow-up period, the patient underwent comprehensive evaluations including echocardiography, NT-proBNP blood tests, six-minute walk tests, and quality-of-life questionnaires. Following CCM implantation, the patient experienced complete resolution of chest tightness and shortness of breath. Additionally, there was a significant improvement in exercise tolerance and overall quality of life.\n\n**Next Steps**  \nContinued monitoring of cardiac function and symptomatology will be essential to assess long-term benefits of CCM therapy. This case highlights CCM as a promising therapeutic option for patients with dilated cardiomyopathy and heart failure with reduced ejection fraction who remain symptomatic despite optimal medical treatment and have a narrow QRS complex."
+        }
+    },
+    {
+        "article": "Paciente de sexo femenino, 61 años, caucásica, casada, dos hijos, informó empeoramiento de los síntomas de la psoriasis tras el inicio de L-metilfolato 15 mg al día para tratamiento coadyuvante de la depresión. Informó depresión y psoriasis desde los 20 años. Desde los 41 años, la paciente no había tenido recidivas de las lesiones psoriáticas.\n\nPor su historial de depresiones, se le indicó carbonato de litio, pero no lo tomó debido a la psoriasis. En 2000, su cuadro depresivo mejoró con venlafaxina 225 mg al día. En 2016, debido a las oscilaciones de humor, se le agregó lamotrigina 100 mg al día y, para mejorar el sueño, se le sumó quetiapina 50 mg al día.\n\nEstas fueron las dosis actuales, con una mejora en la depresión, la calidad de vida y sin efectos adversos significativos.\n\nEn enero de 2019, se detectó polimorfismo en el gen MTHFR, con una mutación heterozigótica en C677T, y se le recetó a la paciente 15 mg diarios de L-metilfolato. Antes de que finalizara la primera semana de uso de L-metilfolato, aparecieron lesiones psoriáticas que no se habían manifestado en 20 años. Se informó lo ocurrido al psiquiatra, quien retiró la medicación y, 4 días después, las lesiones psoriáticas comenzaron a remitir, desapareciendo por completo al cabo de unas semanas. La paciente no volvió a registrar manifestaciones hasta principios de 2020.\n",
+        "gold_summary": "Paciente de sexo femenino, de 61 años, que había estado en remisión de psoriasis durante 20 años. Sufrió una recaída de psoriasis en forma de placa pocos días después de comenzar el tratamiento con L-metilfolato a una dosis diaria de 15 mg.\n",
+        "synthetic_summary": {
+            "B1": "A lady, 61 years old, felt better from her skin problem for 20 years. When she took a new medicine, her skin problem came back after a few days.",
+            "B2": "**What Happened:**  \nA 61-year-old woman had psoriasis, which is a skin condition that causes red, scaly patches. She had been free of these patches for 20 years. However, after she started taking a medicine called L-methylfolate (15 mg daily) to help with her depression, the psoriasis came back within a few days.\n\n**What This Means:**  \nL-methylfolate is a form of folate, a vitamin important for brain function. In this case, it seemed to trigger the return of her psoriasis. When she stopped taking the medicine, her skin got better and the psoriasis disappeared after a few weeks. This shows that some treatments for depression might affect other health conditions, like psoriasis, and doctors need to watch for this.",
+            "B3": "Background  \nA 61-year-old Caucasian woman with a longstanding history of both depression and psoriasis since her twenties had maintained complete remission of psoriatic lesions for 20 years prior to the recent event. Her depression had been managed with various medications over the years, including venlafaxine, lamotrigine, and quetiapine, which improved her mood and quality of life without significant side effects. In January 2019, genetic testing revealed a heterozygous C677T polymorphism in the MTHFR gene, a mutation that can affect folate metabolism. Based on this finding, she was prescribed L-methylfolate at 15 mg daily as an adjunct treatment for her depression.\n\nKey Findings  \nWithin the first week of starting L-methylfolate, the patient developed new psoriatic plaques, marking a relapse after two decades without skin manifestations. This temporal association suggested a potential link between L-methylfolate administration and psoriasis reactivation. Upon notification, her psychiatrist discontinued the L-methylfolate. Subsequently, the psoriatic lesions began to resolve within four days and completely disappeared over the following weeks. No further psoriasis flares were reported until early 2020.\n\nClinical Interpretation  \nThis case illustrates a probable adverse reaction where L-methylfolate, used to support antidepressant therapy in a patient with an MTHFR gene variant, may have triggered a psoriasis relapse. The mechanism could involve immune modulation or altered folate metabolism influencing skin cell proliferation and inflammation. Given the patient’s long remission and the close timing of lesion appearance after starting L-methylfolate, causality is strongly suggested.\n\nNext Steps  \nClinicians should be aware of the potential for L-methylfolate to exacerbate or reactivate psoriasis in susceptible individuals, especially those with a history of the disease. Careful monitoring is advised when initiating folate supplementation in patients with psoriasis. Alternative strategies for managing depression in such patients should be considered to avoid triggering dermatological complications. Further research is warranted to clarify the relationship between folate metabolism and psoriasis pathogenesis."
+        }
+    },
+    {
+        "article": "Se diagnosticó osteoartritis bilateral de las articulaciones de la cadera en un paciente de 61 años de edad con tratamiento con esteroides para la artritis reumatoide y dolencias en la ingle bilateral. [9] Recibió una inyección intraarticular bilateral de ácido hialurónico y se presentó doce semanas después en nuestro departamento de urgencias con fiebre, un estado general reducido y un dolor cada vez más incapacitante. Las radiografías de la pelvis mostraron una destrucción progresiva y rápida de ambas articulaciones de la cadera con una osteólisis extensa, subluxación concomitante y un defecto óseo acetabular del lado izquierdo. La aspiración de la articulación mostró pus en ambas articulaciones de la cadera y se hizo el diagnóstico de artritis séptica bilateral progresiva rápida. Se realizó una resección bilateral de ambas cabezas femorales con desbridamiento de la articulación de la cadera y la implantación de espaciadores de PMMA cargados con antibióticos a través de un enfoque anterolateral mínimamente invasivo.\n\nSe inició un tratamiento antibiótico sistémico empírico con vancomicina y ampicilina por vía intravenosa. Se detectó E. coli en muestras de tejido de ambas articulaciones de la cadera y se adaptó el tratamiento antibiótico sistémico a meropenem por vía intravenosa. Se realizaron dos procedimientos quirúrgicos de seguimiento con intercambio de los espaciadores de PMMA cargados con antibiótico para controlar la infección debido al drenaje persistente.\n\nDoce semanas después de la resección de la cabeza femoral y el control exitoso de la infección, el paciente recibió una artroplastia total de cadera con el uso adicional de un revestimiento multicapa de plata (HyProtect®, Bio-Gate, Nürnberg, Alemania). Este revestimiento consiste en una capa de siloxano ultrafina directamente sobre la superficie del implante (10 a 30 nm), de la que se liberan iones de plata.\n\n12 semanas después de la resección de la cabeza femoral, se realizó una artroplastia total de cadera en el lado derecho con una copa estándar sin cemento (Allofit®, ZimmerBiomet, Varsovia, EE. UU.) y un vástago femoral sin cemento (Avenir®, ZimmerBiomet, Varsovia, EE. UU.) a través del enfoque anterolateral mínimamente invasivo previamente utilizado con este revestimiento multicapa de plata ultrafino. Tanto la superficie posterior de la copa como todo el eje femoral se revistieron con plata.\n\nLa cadera izquierda se trató 18 semanas después de la resección de la cabeza femoral con una jaula de refuerzo recubierta de plata (Burch-Schneider®, ZimmerBiomet, Varsovia, EE. UU.) para un defecto acetabular tipo IIB de Paprosky y una copa de polietileno cementada (Durasul®, ZimmerBiomet, Varsovia, EE. UU.). El vástago femoral sin cemento (Avenir®, ZimmerBiomet, Varsovia, EE. UU.) también se recubrió de plata en toda su parte intramedular. Esta intervención también se realizó mediante el enfoque anterolateral mínimamente invasivo utilizado previamente. El paciente se sometió a una terapia antibiótica sistémica durante un período de tratamiento total de 18 semanas después de la implantación del lado derecho. Se aplicó ertapenem 1 g por vía intravenosa durante este período de tiempo una vez al día, después de la descarga en un entorno ambulatorio. Esto permitió una cobertura antibiótica del lado derecho de 18 semanas y del lado izquierdo de 12 semanas de tratamiento antibiótico.\n\nSe recomendó el uso parcial de peso con 20 kg en el lado operado y el uso de muletas durante 6 semanas después de las intervenciones.\n\nLas heridas de ambos lados se curaron sin incidentes. El paciente fue visto regularmente para un seguimiento clínico y radiológico. Se logró el apoyo total del peso sin el uso de muletas 7 semanas después de la operación en ambos lados. No hubo signos de PIJ y no fue necesaria una cirugía de revisión adicional.\n\nEn un seguimiento final tres años después de la implantación de las prótesis recubiertas de plata, la paciente mostró un aspecto normal de la piel con mínimas cicatrices después de enfoques antero-laterales mínimamente invasivos en ambos lados sin signos de argiria. Hubo un excelente resultado funcional de ambas caderas con marcha normal y una puntuación WOMAC de 6 en ambos lados (dolor: 0, rigidez: 0, función física: 6). El recuento de leucocitos en sangre fue de 7,29/nl (referencia: 4,23-9,1) y el nivel de proteína C reactiva (PCR) fue de 12,4 mg/l (referencia: <5 mg/l). El nivel ligeramente elevado de PCR es atribuible a la artritis reumatoide subyacente de la paciente. Las radiografías revelaron componentes protésicos de cadera bien integrados y no sueltos en ambos lados tres años después de la implantación con una articulación correcta.\n",
+        "gold_summary": "Este informe de caso se refiere a un paciente de 61 años con destrucción rápida de ambas articulaciones de la cadera debido a una artritis séptica que se trató con éxito con una implantación por etapas de prótesis de cadera recubiertas con plata con un recubrimiento ultrafino multicapa de plata. En un seguimiento de tres años, no hubo signos de infección, se observó un buen estado de todos los componentes protésicos y el resultado funcional fue excelente.\n",
+        "synthetic_summary": {
+            "B1": "A man had very bad pain in both his hip joints. The doctor fixed his hips with special new parts covered in silver. After three years, he felt much better. His hips worked well and there was no sickness.",
+            "B2": "**What Happened to the Patient**  \nA 61-year-old patient had a fast and serious infection in both hip joints called septic arthritis. This infection caused quick damage and destruction of the hip joints. Septic arthritis means the joints were infected with bacteria, causing pain and swelling.\n\n**How Doctors Treated It**  \nThe doctors removed the damaged parts of the hips and cleaned the infection. Then, they put in special hip implants in stages. These implants had a very thin silver coating. Silver can help stop infections because it kills bacteria.\n\nThe patient also took strong antibiotics through the veins to fight the infection. After the infection was under control, the doctors replaced the temporary implants with permanent ones, also coated with silver.\n\n**What Happened After Treatment**  \nThree years later, the patient was doing very well. There were no signs of infection coming back. The hip implants were stable and working properly. The patient could walk normally and had very little pain or stiffness.\n\n**Why This Is Important**  \nThis case shows that using silver-coated hip implants, along with antibiotics and careful surgery, can help treat serious hip infections successfully. It also shows that patients can recover well and keep their hip function after such infections.",
+            "B3": "Background  \nThis case report describes a 61-year-old patient with rapidly progressing destruction of both hip joints caused by bilateral septic arthritis (a severe joint infection). The patient had a history of rheumatoid arthritis treated with steroids and presented with worsening bilateral groin pain, fever, and general decline. Initial imaging revealed extensive bone loss and joint damage in both hips, and joint fluid aspiration confirmed the presence of pus, establishing the diagnosis of rapidly progressive septic arthritis.\n\nKey Findings and Treatment  \nThe patient underwent a staged surgical approach beginning with bilateral removal of the femoral heads (the ball portion of the hip joint) and thorough cleaning (debridement) of the infected joints. Antibiotic-loaded polymethylmethacrylate (PMMA) spacers were implanted using a minimally invasive anterolateral surgical approach. Empirical intravenous antibiotics (vancomycin and ampicillin) were started but later adjusted to meropenem after cultures identified Escherichia coli bacteria in both hip joint tissues. Due to persistent drainage, two additional surgeries were performed to exchange the antibiotic spacers and control the infection.\n\nAfter twelve weeks of successful infection control, the patient received total hip replacements. The implants were coated with a novel ultrathin multilayer silver coating (HyProtect®), which releases silver ions known for their antimicrobial properties. The right hip was replaced first using a cementless cup and femoral stem, both coated with silver. Six weeks later, the left hip was reconstructed using a silver-coated reinforcement cage and cemented polyethylene cup to address a significant acetabular bone defect, along with a silver-coated cementless femoral stem. Both surgeries used the same minimally invasive anterolateral approach.\n\nThe patient continued systemic antibiotic therapy for a total of 18 weeks post-implantation, including outpatient intravenous ertapenem once daily. Partial weight-bearing with crutches was recommended for six weeks after surgery. Both surgical wounds healed without complications.\n\nClinical Interpretation and Outcomes  \nAt regular clinical and radiological follow-ups, the patient achieved full weight-bearing without crutches seven weeks after surgery on both sides. There were no signs of periprosthetic joint infection (infection around the implants), and no revision surgeries were required. Three years after implantation, the patient exhibited excellent functional outcomes with normal walking ability and minimal hip pain or stiffness, as reflected by a low WOMAC score (a standardized measure of hip function). Blood tests showed normal white blood cell counts and a slightly elevated C-reactive protein level attributed to underlying rheumatoid arthritis rather than infection. Radiographs demonstrated well-integrated, stable hip prostheses without loosening or joint abnormalities. The patient’s skin appeared normal without discoloration (no argyria, a rare silver-related skin condition).\n\nNext Steps and Implications  \nThis case illustrates that staged bilateral hip replacement using silver-coated implants combined with prolonged targeted antibiotic therapy can successfully treat severe bilateral septic arthritis with rapid joint destruction. The ultrathin multilayer silver coating provided effective antimicrobial protection without adverse skin effects over a three-year period. Such an approach may offer a valuable option for managing complex joint infections, especially in patients with compromised immune systems or extensive bone damage. Continued monitoring is essential to detect any late complications, but the long-term results in this patient are highly encouraging."
+        }
+    },
+    {
+        "article": "Una niña africana de raza negra, con 1000 g de peso, nacida a las 32 semanas de gestación, de madre viva, fue derivada a nuestra unidad de cuidados intensivos neonatales debido a múltiples anomalías congénitas y dificultad respiratoria moderada. La madre tiene 32 años y está en un matrimonio no consanguíneo. La madre no buscó atención médica hasta el inicio del tercer trimestre de embarazo, debido a un desprendimiento de placenta. El primer ultrasonido prenatal reveló oligohidramnios severos. No era diabética (la glucosa en sangre aleatoria fue de 5.1 mmol/L) y no recibió suplementos de ácido fólico durante el embarazo.\n\nAl ingreso, la bebé estaba alerta con características leves del síndrome de dificultad respiratoria. Presentaba múltiples rasgos dismórficos, entre ellos, microcefalia (circunferencia de la cabeza < 10%), occipucio prominente, orejas bajas, paladar hendido y labio derecho, micrognatia, contractura bilateral de los codos e inferiores más cortos.\n\n\nEl peso al nacer fue de 1000 g, la longitud del bebé fue de 40 cm y la circunferencia occipitofrontal fue de 30 cm.\n\nInvestigaciones\nLa radiografía esquelética mostró aplanamiento de las costillas, aplasia del fémur derecho e hipoplasia del fémur izquierdo. Los análisis de laboratorio incluyeron: hemograma completo, proteína C reactiva, creatinina, urea en sangre y electrolitos, todos dentro de los valores normales. La ecografía craneal fue normal, pero la ecocardiografía reveló un pequeño conducto arterioso permeable.\n\nDiagnóstico diferencial\nLa paciente presentaba aplasia femoral bilateral y facies inusuales. Estas características clínicas llevaron al diagnóstico de síndrome femoro-facial.\n\nLa similitud en la etiopatogénesis hace que el síndrome de regresión caudal sea el diagnóstico diferencial común. Ambos pueden ser causados por una hiperglucemia materna mal controlada. Sin embargo, los defectos faciales están ausentes en el síndrome de regresión caudal, la característica diagnóstica clave.\n\nLa hipoplasia femoral focal proximal y las anomalías craneofaciales suelen estar ausentes.\n\nEntre las condiciones que pueden provocar el labio leporino se incluye el síndrome de banda amniótica grave.\n\nTratamiento\nEl bebé recibió asistencia respiratoria y antibióticos empíricos. Participaron un cirujano ortopédico, un otorrinolaringólogo y un fisioterapeuta. Está previsto reparar quirúrgicamente el paladar hendido a los 6 meses de edad. La rehabilitación funcional está prevista antes de que el paciente comience a deambular. La cirugía de alargamiento de extremidades no se realiza actualmente en nuestro entorno.\n\nResultado y seguimiento\nEl paciente falleció a la edad de un mes por complicaciones de una sepsis neonatal grave de inicio tardío.\n",
+        "gold_summary": "Una niña africana de raza negra bantú de 1 día de vida fue admitida en la unidad neonatal debido a múltiples anomalías congénitas. La madre no buscó atención médica hasta el inicio del tercer trimestre, cuando tuvo un desprendimiento de placenta. La madre nunca recibió suplementos de ácido fólico prenatal. La niña tenía microcefalia, orejas bajas, paladar hendido derecho y labio, micrognatia, contractura y extremidades más cortas. Una radiografía esquelética mostró hipoplasia femoral. Presentamos este caso poco habitual y destacamos los retos en el diagnóstico y el tratamiento.\n",
+        "synthetic_summary": {
+            "B1": "A baby girl was born with some parts of her body different. Her head was very small. Her ears were low. Her mouth had a split on one side. Her chin was small. Her arms and legs were shorter and stiff.\n\nHer mom did not go to the doctor much when she was pregnant. The baby’s leg bones were not fully grown.\n\nThe doctors helped the baby breathe and planned to fix her mouth later. This case was special and hard to take care of.",
+            "B2": "**A Baby Girl with Multiple Birth Defects**\n\nA newborn baby girl from Africa was admitted to the neonatal intensive care unit just one day after birth. She had several birth defects, which are problems present from birth. Her mother did not get medical care until late in pregnancy, after a serious problem called placenta detachment. The mother also did not take folic acid supplements, which help prevent some birth defects.\n\n**What They Found**\n\nThe baby had a small head (called microcephaly), low-set ears, a split in the roof of her mouth on the right side (called a cleft palate), a cleft lip, a small lower jaw (micrognathia), stiff joints, and shorter arms and legs. An X-ray showed that the bones in her thighs were underdeveloped, a condition called femoral hypoplasia.\n\n**Why This Case Is Important**\n\nThis case is unusual because of the combination of facial and limb problems. It shows how hard it can be to diagnose and treat babies with many birth defects, especially when prenatal care is limited. The doctors worked with different specialists to help the baby, but sadly, she passed away at one month old due to a severe infection.\n\nThis case helps us understand the importance of early prenatal care and folic acid supplements to reduce the risk of birth defects.",
+            "B3": "**Background**  \nA newborn African Bantu girl, one day old and weighing 1000 grams, was admitted to the neonatal intensive care unit due to multiple congenital abnormalities. The mother, aged 32 and in a non-consanguineous marriage, did not seek prenatal care until the third trimester, when she experienced placental abruption. Notably, she did not receive folic acid supplementation during pregnancy. The pregnancy was complicated by severe oligohydramnios (low amniotic fluid volume). The infant was born prematurely at 32 weeks gestation.\n\n**Key Findings**  \nOn examination, the infant exhibited several dysmorphic features including microcephaly (head circumference below the 10th percentile), low-set ears, a right-sided cleft lip and palate, micrognathia (small lower jaw), bilateral elbow contractures, and shortened lower limbs. The baby showed mild respiratory distress consistent with neonatal respiratory distress syndrome. Birth measurements included a length of 40 cm and an occipitofrontal head circumference of 30 cm.\n\nRadiographic imaging revealed skeletal abnormalities characterized by flattening of the ribs, aplasia (complete absence) of the right femur, and hypoplasia (underdevelopment) of the left femur. Laboratory tests including complete blood count, C-reactive protein, kidney function markers, and electrolytes were within normal limits. Cranial ultrasound was normal, but echocardiography identified a small patent ductus arteriosus (a persistent fetal blood vessel).\n\n**Clinical Interpretation**  \nThe combination of bilateral femoral aplasia and distinctive facial anomalies led to the diagnosis of femoral-facial syndrome, a rare congenital disorder. This syndrome shares some etiological features with caudal regression syndrome, which is often linked to poorly controlled maternal hyperglycemia; however, caudal regression syndrome typically lacks the facial abnormalities seen here. Other differential diagnoses considered included amniotic band syndrome, which can cause cleft lip but does not explain the femoral defects.\n\n**Treatment and Management**  \nThe infant received respiratory support and empirical antibiotic therapy. A multidisciplinary team involving orthopedic surgery, otolaryngology, and physiotherapy was engaged. Surgical repair of the cleft palate was planned for six months of age, and functional rehabilitation was scheduled before the child would begin walking. Limb lengthening surgery was not available in the treating facility.\n\n**Outcome and Follow-Up**  \nDespite medical interventions, the infant died at one month of age due to complications from late-onset severe neonatal sepsis.\n\n**Summary**  \nThis case highlights the diagnostic and therapeutic challenges posed by femoral-facial syndrome in a premature infant with multiple congenital anomalies and limited prenatal care. It underscores the importance of early prenatal monitoring and multidisciplinary management in complex congenital disorders."
+        }
+    },
+    {
+        "article": "Paciente de sexo masculino de 18 años, con diag nóstico clínico de Neurofibromatosis tipo 1 desde el primer año de vida. Entre sus antecedentes destaca que tiene educación completa, sus padres no son consan guíneos, y no tiene antecedentes familiares de manchas café con leche. Desde el punto de vista neurológico desarrolló durante la infancia retraso del desarrollo psicomotor fino y grueso, trastorno del lenguaje de predominio expresivo, con alteración fonológica y semántica del lenguaje, por lo que fue manejado con fonoaudiología en Escuela de Lenguaje, además de ki- nesioterapia y terapia ocupacional durante la infancia. Durante la adolescencia se le diagnosticó Trastorno por Déficit Atencional e Hiperactividad, que fue manejado con metilfenidato, manteniendo regular rendimiento escolar. Tuvo desarrollo puberal normal. Oftalmológi camente presentó nódulos de Lisch desde los 4 años de edad, euriblefaron y astigmatismo. Se mantuvo en control anual en Oftalmología y Neuropediatría. Su última Resonancia Magnética de cerebro fue realiza da 6 meses previo a la consulta en Dermatología, sin hallazgos patológicos y en la Resonancia Magnética de columna se evidenció discopatía L5-S1 y realce perifacetario en T11-T12 y T12-L1. A los 16 años se reali zó estudio genético que demostró deleción de exones 5-47 del gen NF1.\n\nA los 18 años consultó en servicio de Dermatología del Centro de Referencia en Salud Peñalolén Cordille ra Oriente por aparición de nueva mancha en muslo izquierdo de 1 año evolución, asintomática. Además, refirió aparición de nódulos en muñeca derecha, su praciliar derecho y cuero cabelludo, de unos meses de evolución, asintomáticos.\n\nAl examen físico destacaba presión arterial normal, macrocefalia (CC: 60 cm) y múltiples manchas café con leche generalizadas, efélides en axilas, y en zona supraciliar derecha, occipital y muñeca derecha nódulos subcutáneos ovalados de 0,5 cm, bien delimitados, móviles. En muslo izquierdo lateral pre sentaba placa de 25 mm algo rosada, con pérdida de anexos, y de consistencia blanda. Por último, en zona lumbar y pectoral, múltiples máculas rojo- azuladas pequeñas, de menos de 5 mm cada una, algu nas levemente deprimidas.\n\nSe realizó biopsia cutánea de máculas azuladas en pecho y de placa muslo, resultando ambas compatibles con NF. Se realizó una ecografía de nódulos supraciliar y occipital que resultó compatible con NF nodular subcutáneo.\n\nUsando la clasificación clínica de García-Martínez et al.1 se diagnosticó al paciente con NF superficial sub cutáneo nodular en zona supraciliar derecha, occipital y muñeca derecha, NF superficial cutáneo pseudoatró fico en muslo izquierdo lateral y NF superficial cutáneo rojo azulado en zona lumbar y pectoral.",
+        "gold_summary": "Paciente masculino de 18 años con diagnóstico desde la infancia de NF-1 que presenta múltiples nodulos ovalados en cara, zona occipital y muñeca, máculas rojo-azuladas en dorso y placa rosada atrófica en muslo. El estudio ecográfico de los nódulos fue compatible con neurofibromas y el estudio histopatológico de las lesiones de dorso y muslo compatibles con neurofibromas cutáneos.",
+        "synthetic_summary": {
+            "B1": "A boy has a condition since he was little. He has small bumps on his face and arm. He also has red and blue spots on his back. He has a soft pink patch on his leg. The doctor checked and said these are not harmful bumps on his skin.",
+            "B2": "**Patient Background**  \nThis is about an 18-year-old boy who has had Neurofibromatosis type 1 (NF-1) since he was a baby. NF-1 is a genetic condition that causes tumors called neurofibromas to grow on nerves and skin. He has had learning and attention difficulties, and some eye problems related to NF-1.  \n\n**What They Found**  \nAt 18, he noticed new lumps on his right wrist, eyebrow area, and scalp. He also had a pink patch on his left thigh and small blue-red spots on his back and chest. These lumps were soft, oval, and could move under the skin.  \n\n**Tests and Results**  \nDoctors used ultrasound (a test that uses sound waves to look under the skin) on the lumps and found they matched neurofibromas, which are benign tumors made of nerve tissue. They also took small tissue samples (biopsies) from the pink patch and blue-red spots. The lab tests confirmed these were also neurofibromas in the skin.  \n\n**What It Means**  \nThis boy has different types of neurofibromas on his skin and under it. Some are nodules (small lumps), some are flat patches that look different in color or texture. These findings fit with his NF-1 diagnosis and help doctors understand how the disease is affecting his skin now. Regular check-ups will be important to watch for any changes.",
+            "B3": "**Background**  \nThe patient is an 18-year-old male with a clinical diagnosis of Neurofibromatosis type 1 (NF1) established during infancy. His medical history includes developmental delays in fine and gross motor skills, expressive language disorder with phonological and semantic impairments, and attention deficit hyperactivity disorder (ADHD) managed with methylphenidate. He has macrocephaly and ophthalmologic findings consistent with NF1, such as Lisch nodules. Genetic testing at age 16 confirmed a deletion in exons 5-47 of the NF1 gene. Previous brain MRI was normal, while spinal MRI showed degenerative changes at L5-S1 and facet joint enhancement in the thoracolumbar region.\n\n**Key Findings**  \nAt 18 years old, the patient presented with new dermatological findings:  \n- Multiple well-defined, oval, subcutaneous nodules approximately 0.5 cm in size located on the right supraciliary (above the eyebrow), occipital scalp, and right wrist areas. These nodules were asymptomatic and mobile.  \n- A 25 mm soft, slightly pink plaque with loss of skin appendages on the lateral left thigh.  \n- Numerous small (less than 5 mm), red-blue macules scattered on the lumbar and pectoral regions, some with slight depression.\n\n**Diagnostic Studies**  \n- Ultrasound imaging of the nodules on the supraciliary and occipital regions showed features consistent with subcutaneous neurofibromas.  \n- Skin biopsies of the red-blue macules on the chest and the plaque on the thigh revealed histopathological findings compatible with cutaneous neurofibromas.\n\n**Clinical Interpretation**  \nThe patient exhibits multiple types of neurofibromas associated with NF1:  \n- Nodular subcutaneous neurofibromas on the face (supraciliary), occipital scalp, and wrist.  \n- Superficial cutaneous neurofibroma with a pseudoatrophic (appearing atrophic but not truly so) plaque on the lateral thigh.  \n- Superficial cutaneous neurofibromas presenting as red-blue macules on the lumbar and pectoral areas.\n\nThese findings align with the clinical classification of NF1-related skin manifestations described by García-Martínez et al., indicating a complex presentation of superficial and subcutaneous neurofibromas in this patient.\n\n**Next Steps**  \nContinued multidisciplinary follow-up is recommended, including dermatology, neurology, and ophthalmology, to monitor for progression or new lesions. Management should focus on symptomatic relief and surveillance for potential complications of NF1, such as malignant transformation or neurological involvement. Genetic counseling may also be beneficial given the confirmed NF1 gene deletion."
+        }
+    },
+    {
+        "article": "Un hombre de 38 años de edad fue ingresado en el hospital por traumatismo torácico contundente. El paciente estaba generalmente sano y no tenía factores de riesgo de enfermedad coronaria. Fue golpeado en el pecho por un tornillo de alta velocidad que tenía aproximadamente 6 cm de diámetro mientras trabajaba en una fábrica. Voló aproximadamente 4 metros de distancia debido a la fuerza y presión del tornillo de alta velocidad. Perdió el conocimiento de inmediato, pero recuperó la conciencia varios minutos después. Fue trasladado inmediatamente a la sala de urgencias de un hospital local. Su puntaje en la escala de coma de Glasgow fue de 15. Se quejó de dolor torácico intenso y persistente, opresión y disnea. La tomografía computarizada del tórax mostró derrame pleural bilateral y fracturas de esternón y costillas. Por lo tanto, se insertó un tubo torácico durante varios días. Luego, fue dado de alta sin someterse a un electrocardiograma (ECG) u otros exámenes cardiovasculares.\n\nTres meses después del alta hospitalaria, durante un chequeo de seguimiento de rutina, todavía había presencia de derrame pleural con síntomas acompañantes de opresión en el pecho, falta de aire después de la actividad física, e incluso disnea por la noche, lo que motivó su ingreso en nuestro hospital. Sus constantes vitales durante el ingreso fueron las siguientes: frecuencia cardíaca regular de 98 latidos/min, presión arterial de 110/70 mmHg, y frecuencia respiratoria de 20 respiraciones/min. El examen físico mostró una pulsación carotídea y yugular normal. El movimiento respiratorio torácico bilateral y la actividad fueron normales, la fibrilación del lenguaje táctil del pulmón derecho disminuyó, la percusión del pulmón derecho presentó un sonido sordo, y los sonidos respiratorios disminuyeron. No hubo roncus ni estertores evidentes durante la auscultación pulmonar. No hubo murmullos en la auscultación cardíaca. Los exámenes del abdomen y las extremidades revelaron hallazgos normales. El primer ECG mostró evaluación ST e inversión de la onda T en las derivaciones I, aVL y V2-V5 y en el bloqueo de rama anterior izquierdo. La prueba de troponina-I fue negativa, y el nivel de NT-proBNP fue de 706 pg/ml (rango normal: 0-104 pg/ml), lo que sugiere un infarto de miocardio anterior antiguo. La ecocardiografía transtorácica mostró una aurícula izquierda de 26,4 mm, un ventrículo izquierdo de 51,8 mm, y una fracción de eyección ventricular izquierda (EF) del 32% (modo M). La pared anterior del LV e interventricular septum mostraron adelgazamiento a 6,6 mm, con un eco de movimiento notablemente reducido.\n\nAl examinar las arterias carótidas, intracraneales y de las extremidades inferiores del paciente, no se encontraron placas ateroscleróticas evidentes. Todos los hallazgos apoyaron el diagnóstico de infarto de miocardio antiguo (OMI), en lugar de arteriosclerosis. Sin embargo, el paciente era hemodinámicamente estable. Después de someterse a una terapia diurética, se le administraron bloqueadores beta, estatinas y estimulantes cardíacos, lo que alivió su malestar. La angiografía por tomografía computarizada coronaria mostró una estenosis moderada en la arteria LAD proximal. Para confirmar la estenosis y examinar el estado de la íntima coronaria, se realizó CAG 3 meses después del traumatismo torácico, que mostró un estrechamiento aproximado del 70% del lumen en la LAD proximal y el segmento coronario tenía una lesión curva. La arteria circunfleja izquierda (LCX) y la arteria coronaria derecha (RCA) eran normales. Los resultados de CAG confirmaron el diagnóstico de OMI, pero debido a la carga de costos, el paciente rechazó el examen IVUS. El paciente se sometió a una terapia conservadora y fue dado de alta del hospital varios días después.\n\nUn mes después, el 9 de diciembre de 2014, volvió al hospital para someterse a una intervención coronaria percutánea (ICP). Después de someterse a una terapia con fármacos, sus condiciones habían mejorado ligeramente. El examen físico y el ECG revelaron resultados casi normales. La ecocardiografía transtorácica mostró una mejora en la función sistólica del LV y EF del 45%. Se sometió a otra CAG 4 meses después del traumatismo torácico, que mostró una ligera mejora de la estenosis. Había aproximadamente un 60% de estrechamiento del lumen. Se realizó un IVUS y reveló que la gravedad de la lesión era del 55.9%, y la placa de bajo eco apareció antes de la formación de trombos después de la rotura subintimal. Completamos el examen sin más intervención porque solo se encontró un 55.9% de estrechamiento del lumen y el paciente tenía una hemodinámica estable sin evidencia de isquemia miocárdica constante. Se le recetó al paciente la medicación óptima, y su incomodidad se alivió gradualmente. El 17 de julio de 2018, 4 años después del traumatismo, la evaluación de seguimiento reveló que el paciente todavía experimentaba dificultad para respirar después de trabajar, pero se alivió poco después de descansar. El examen físico mostró los siguientes resultados: presión arterial de 114/80 mmHg, frecuencia cardíaca de 66 latidos/min, ausencia de anomalías obvias en la auscultación pulmonar y cardíaca; y ausencia de edema obvio en ambas extremidades inferiores. El ECG de seguimiento reveló los siguientes hallazgos: rS en las derivaciones V2-V4, inversión de la onda T en las derivaciones I, AVL y V2-V5 y bloqueo de rama izquierda. La ecocardiografía transtorácica mostró agrandamiento del ventrículo izquierdo con una aurícula izquierda de 39 mm, un ventrículo izquierdo de 54.7 mm y una EF del LV del 41% (Simpson's). También se observó adelgazamiento de la pared anterior del LV y del tabique interventricular, con la parte más delgada de 4.7 mm; el movimiento casi había desaparecido y el eco se había mejorado. Sin embargo, las arterias carótidas, intracraneales y de las extremidades inferiores seguían siendo normales. Además, descubrimos que los medicamentos recetados para tratar la insuficiencia cardíaca no se tomaron religiosamente después del alta; por lo tanto, recetamos 23.75 mg de metoprolol, 2.5 mg de benazepril y 20 mg de espironolactona para tomar una vez al día, y coenzima para tomar cada 10 horas.\n\nMH - Adulto\nMH - Errores de diagnóstico\nMH - Insuficiencia cardiaca/etiología\nMH - Humanos\nMH - Hombre\nMH - Infarto de miocardio/complicaciones/*etiología\nMH - Lesiones torácicas/*complicaciones\nMH - Tiempo hasta el tratamiento\nMH - Heridas, no penetrantes/complicaciones\n",
+        "gold_summary": "Preocupaciones de los pacientes:\nUn hombre de 38 años, previamente sano, fue admitido en nuestro hospital con una queja de disnea. Tenía un historial de haber sido golpeado en el pecho por un tornillo de alta velocidad mientras trabajaba en una fábrica 3 meses antes de ser admitido en el hospital.\n\nDiagnóstico:\nLuego de realizarse una angiografía coronaria y una ecocardiografía, finalmente se le diagnosticó un infarto de miocardio.\n\nIntervenciones:\nRecibió medicamentos optimizados, entre ellos, diuréticos, bloqueadores beta y estimulantes cardíacos.\n\nResultados:\nAl cabo de cuatro años de seguimiento, se le diagnosticó al paciente una insuficiencia cardíaca crónica con una fracción de eyección reducida.\n",
+        "synthetic_summary": {
+            "B1": "A man got hurt when a big screw hit his chest. He had trouble breathing after that. Doctors looked inside his heart with special pictures. They found his heart was hurt. The man took medicine to help his heart work better. After a long time, his heart was still not strong. The doctors said he has a heart problem that needs care.",
+            "B2": "**What Happened to the Patient**  \nA 38-year-old man, who was healthy before, got hit hard in the chest by a fast-moving screw while working in a factory. This injury happened three months before he came to the hospital with trouble breathing.\n\n**What the Doctors Found**  \nAfter doing special heart tests called an angiography (which looks at the heart’s blood vessels) and an echocardiogram (an ultrasound that shows how the heart is working), doctors found that he had a heart attack. A heart attack happens when blood flow to part of the heart is blocked, causing damage to the heart muscle.\n\n**How They Treated Him**  \nThe doctors gave him medicines to help his heart work better. These included diuretics (which help remove extra fluid), beta-blockers (which slow the heart rate and lower blood pressure), and drugs that help the heart pump stronger.\n\n**What Happened Over Time**  \nFour years later, the man was diagnosed with chronic heart failure. This means his heart was not pumping blood as well as it should. The tests showed his heart’s pumping ability was reduced, which can cause symptoms like tiredness and difficulty breathing.\n\n**Summary**  \nThis case shows how a serious chest injury can lead to heart damage and long-term heart problems. Early diagnosis and treatment are important, but sometimes heart function can still decline over time.",
+            "B3": "**Background:**  \nA 38-year-old man with no prior health issues experienced a severe blunt chest trauma when struck by a high-speed screw approximately 6 cm in diameter at his workplace. The impact caused him to lose consciousness briefly and resulted in multiple chest injuries, including bilateral pleural effusions and fractures of the sternum and ribs. Initially, he was treated with chest tube drainage and discharged without cardiovascular evaluation.\n\n**Key Findings:**  \nThree months after the injury, the patient presented with persistent chest discomfort, exertional shortness of breath, and nocturnal dyspnea. Physical examination revealed diminished breath sounds and dullness on percussion over the right lung, but no cardiac murmurs. Electrocardiogram (ECG) showed ST segment changes and T wave inversions in leads I, aVL, and V2-V5, along with a left anterior fascicular block. Cardiac biomarkers were negative for acute injury, but NT-proBNP was elevated, suggesting cardiac stress. Transthoracic echocardiography demonstrated left ventricular (LV) systolic dysfunction with an ejection fraction (EF) of 32%, thinning of the anterior LV wall and interventricular septum, and markedly reduced wall motion. Coronary angiography revealed approximately 70% stenosis in the proximal left anterior descending (LAD) artery with a curved lesion, while other coronary arteries were normal. No evidence of atherosclerosis was found in carotid, intracranial, or peripheral arteries.\n\n**Clinical Interpretation:**  \nThe clinical picture and imaging studies supported a diagnosis of an old anterior myocardial infarction (heart attack) secondary to blunt chest trauma rather than traditional atherosclerotic coronary artery disease. The trauma likely caused coronary artery injury leading to ischemic damage and subsequent chronic heart failure with reduced ejection fraction. Despite the significant coronary narrowing, the patient remained hemodynamically stable.\n\n**Interventions and Follow-Up:**  \nThe patient was managed conservatively with optimized medical therapy including diuretics, beta-blockers, statins, and cardiac stimulants. Percutaneous coronary intervention (PCI) was performed one month later, resulting in symptomatic improvement and partial recovery of LV function (EF improved to 45%). Follow-up angiography and intravascular ultrasound (IVUS) showed some reduction in stenosis severity and stable plaque characteristics without evidence of ongoing ischemia, so no further invasive procedures were undertaken. Over a four-year follow-up period, the patient continued to experience exertional dyspnea but remained stable on medical therapy. Echocardiography at that time showed persistent LV enlargement and systolic dysfunction (EF 41%), consistent with chronic heart failure. Medication adherence was noted to be suboptimal, prompting adjustments in his pharmacological regimen.\n\n**Next Steps:**  \nContinued close monitoring of cardiac function and symptoms is essential. Strict adherence to prescribed heart failure medications—including beta-blockers, ACE inhibitors, and aldosterone antagonists—is critical to managing his chronic condition and improving quality of life. Regular follow-up with echocardiography and clinical assessment will help detect any progression and guide further treatment decisions."
+        }
+    },
+    {
+        "article": "La paciente era una recién nacida de 0 días de edad, de etnia Han, que nació a las 36 semanas de gestación de una mujer embarazada de 3, para 2, con un peso de 2650 g. Se le practicó una cesárea de urgencia debido a la angustia fetal, con puntuaciones de Apgar de 6 a 1 min y 5 min. Su grupo sanguíneo era O y RhD positivo. Al nacer, presentaba palidez, equimosis dispersas en múltiples áreas del cuerpo, sangrado de las mucosas e insuficiencia respiratoria, con un leve flujo de sangre hemorrágica también observado en los sitios de punción venosa. El análisis de gases en sangre de la arteria umbilical mostró un hematocrito de 0.08 y una hemoglobina de 23 g/L. La paciente requirió intubación endotraqueal y ventilación mecánica. Después de la transfusión de una suspensión de glóbulos rojos, los recuentos sanguíneos iniciales revelaron una trombocitopenia severa (recuento de plaquetas de 12 × 109/L), anemia (hemoglobina de 46 g/L) y leucopenia (recuento de leucocitos de 1.11 × 109/L).\n\nLa paciente fue ingresada en la unidad de cuidados intensivos neonatales a las 3 horas de vida para recibir tratamiento adicional. Durante la hospitalización, se le diagnosticó coagulación intravascular diseminada (CID), con tiempo de tromboplastina parcial activada (TTPA) de 73,10 segundos, tiempo de protrombina (TP) de 25,4 segundos, fibrinógeno (FIB) de 1,01 g/L, razón internacional normalizada (INR) de 2,26 y dímero D > 20 mg/L. Se le administró ventilación mecánica, corrección de la acidosis y transfusión de plasma fresco congelado. A pesar de múltiples transfusiones de glóbulos rojos y plaquetas, los niveles de hemoglobina y plaquetas permanecieron por debajo de lo normal (hemoglobina 106 g/L y plaquetas 11 × 109/L el día 3). También recibió tratamiento antiinfeccioso, cardiotónico, vasopresor y otro tratamiento sintomático. Un frotis periférico mostró áreas de tinción pálida agrandadas de glóbulos rojos, con una proporción de reticulocitos del 1,5% y un resultado negativo en la prueba directa de Coombs. No se realizó aspiración de médula ósea debido a su grave estado. No hubo evidencia clínica o de laboratorio de sepsis neonatal, y las pruebas para toxoplasma, rubéola, citomegalovirus y virus del herpes simple (TORCH); virus de hepatitis; y Treponema pallidum fueron negativas. El examen físico de admisión reveló un estado mental deficiente, disminución del tono muscular en las extremidades y reflejo pupilar lento a la luz. Todos los demás hallazgos fueron normales. El ultrasonido craneal y electroencefalograma de cabecera revelaron hemorragia intracraneal grave y bajo voltaje, respectivamente. Los hallazgos del ecocardiograma sugirieron un conducto arterioso patente, foramen oval permeable e hipertensión pulmonar. El ultrasonido abdominal indicó hemorragia gastrointestinal. A pesar de todos los esfuerzos, la paciente falleció el tercer día de vida debido a falla multiorgánica y hemorragia intracraneal masiva (la información detallada se puede encontrar en el Informe Suplementario).\n\nLos padres de la paciente no eran consanguíneos y ambos tenían talasemia. La madre, que compartía el mismo tipo de sangre que la paciente, tuvo una anemia leve durante el embarazo (nivel de hemoglobina de 97 g/L) y un historial de aborto inducido. Los exámenes prenatales no mostraron anomalías, ni tampoco hidrops fetal, y no recibió ninguna medicación durante el embarazo que pudiera provocar una enfermedad hemorrágica de inicio temprano en el recién nacido. La paciente también tenía un hermano de 1 año que gozaba de buena salud. Su abuelo tenía un historial de anemia leve (detalles desconocidos).\n\nSe obtuvo el consentimiento informado de los padres del paciente y se realizó un secuenciamiento de Sanger para descubrir la causa de la enfermedad. Se detectó una nueva mutación de MECOM de desplazamiento de marco heterocigótica [NM_001105078: c.157_158del (p.Met53Glyfs*2)] en el probando. Esta variante cambió el aminoácido 53 de metionina (codón ATG) a glicina (codón GGT), seguido de una terminación temprana. La mutación no se encontró en los padres o en el hermano mayor. La variante se clasificó como patogénica según las directrices del Colegio Americano de Genética Médica (ACMG) [14]. El algoritmo “AutoPVS1” brindó un fuerte apoyo para la interpretación de PVS1 de p.Met53Glyfs*2, lo que indica patogenicidad. La variante no se ha informado previamente en la Base de Datos de Mutación Genética Humana (HGMD) o en Clinvar. El análisis de conservación mostró que el residuo Met53 está altamente conservado en todas las especies de mamíferos (incluidos humanos, ratones, ratas, chimpancés y bovinos) utilizando Clustal Omega. Se generaron modelos de estructura de proteínas tridimensionales de las proteínas MECOM de tipo salvaje y mutantes utilizando SWISS-MODEL, lo que indica que la mutación de desplazamiento de marco causó una terminación temprana de la síntesis de aminoácidos, alterando significativamente la estructura de la proteína.\n",
+        "gold_summary": "Reportamos el caso de una neonata Han china de 0 días de vida que presentó trombocitopenia grave y hemorragia intracraneal, y que finalmente falleció por fallo multiorgánico e intracraneal el tercer día después del nacimiento. La secuenciación genética identificó una variante de cambio de marco heterocigótica, c.157_158del, dentro del gen MECOM. Esta variante condujo a una sustitución del 53.º aminoácido de metionina a glicina, terminando en el 54.º aminoácido. Una revisión exhaustiva de la literatura indicó que las mutaciones del gen MECOM incluían mutaciones sin sentido (68.3%), deleción (8.5%), sitio de empalme (8.5%), cambio de marco (7.3%) y sin sentido (7.3%). Las pacientes con mutaciones sin sentido frecuentemente presentaban sinostosis radiocubital, mientras que el fallo de la médula ósea se asociaba más comúnmente con los otros cuatro tipos de mutaciones.\n",
+        "synthetic_summary": {
+            "B1": "A baby girl was born very sick. She had very bad bleeding in her head. She got very weak and could not get better. The doctors found a tiny change in her body that made her sick. This change was in a special part called MECOM. Some other children with changes like this have different problems too. The doctors learned a lot to help others in the future.",
+            "B2": "**What Happened to the Baby**  \nThis report is about a newborn baby girl from the Han ethnic group in China. She was born with very low platelet counts, a condition called severe thrombocytopenia. Platelets are tiny cells in the blood that help stop bleeding. Sadly, she also had bleeding inside her brain (intracranial hemorrhage). Despite medical care, she passed away on her third day of life due to multiple organ failure and brain bleeding.\n\n**What the Genetic Test Found**  \nDoctors did a genetic test called sequencing to find out why she was so sick. They found a change in a gene called MECOM. Genes are like instructions for the body, and the MECOM gene helps make proteins important for blood cell development. The change was a \"frameshift mutation,\" which means the gene’s instructions got shifted and messed up. Specifically, the 53rd building block of the protein (called an amino acid, methionine) was changed to another one (glycine), and then the protein chain stopped too early at the 54th amino acid. This early stop likely caused the protein to not work properly.\n\n**What This Means in a Bigger Picture**  \nScientists have studied many mutations in the MECOM gene before. Most of these mutations (about 68%) are called \"nonsense mutations,\" which also cause the protein to stop early. Other types include deletions (pieces missing), splice site mutations (errors in how the gene is read), and frameshift mutations like in this baby. Patients with nonsense mutations often have a condition called radioulnar synostosis, where two bones in the arm are fused together. However, problems with bone marrow failure, which affects blood cell production, are more common with the other types of mutations, including frameshift mutations.\n\n**Summary**  \nIn short, this baby had a rare and serious genetic mutation in the MECOM gene that caused her blood cells to not develop properly. This led to severe bleeding and organ failure soon after birth. Understanding these mutations helps doctors learn more about blood diseases and may guide future treatments.",
+            "B3": "**Background**  \nThis report describes a newborn female infant of Han Chinese ethnicity who was born at 36 weeks gestation and presented immediately after birth with severe thrombocytopenia (a critically low platelet count) and intracranial hemorrhage (bleeding within the brain). Despite intensive medical interventions, she died on the third day of life due to multiorgan failure and massive intracranial bleeding. Genetic analysis through Sanger sequencing revealed a previously unreported heterozygous frameshift mutation in the MECOM gene, specifically a deletion of two nucleotides (c.157_158del). This mutation altered the 53rd amino acid from methionine to glycine and caused premature termination at the 54th amino acid, significantly disrupting the protein’s structure.\n\n**Key Findings**  \n- The identified MECOM mutation is a frameshift variant leading to early protein truncation, which likely impairs normal protein function.  \n- This mutation was not present in the patient’s parents or healthy older sibling, indicating it arose de novo (newly in the patient).  \n- Conservation analysis showed that the methionine at position 53 is highly conserved across mammalian species, underscoring its biological importance.  \n- Structural modeling predicted that this frameshift mutation drastically alters the three-dimensional conformation of the MECOM protein.  \n- A comprehensive literature review of MECOM mutations revealed that:  \n  - Nonsense mutations (which introduce premature stop codons) account for approximately 68.3% of reported cases.  \n  - Other mutation types include deletions (8.5%), splice-site mutations (8.5%), frameshift mutations (7.3%), and missense mutations (7.3%).  \n- Clinically, patients with nonsense mutations frequently exhibit radioulnar synostosis (fusion of the radius and ulna bones in the forearm), whereas bone marrow failure—a critical reduction in blood cell production—is more commonly associated with the other four mutation types, including frameshift mutations like the one identified in this case.\n\n**Clinical Interpretation**  \nThe patient’s severe thrombocytopenia, intracranial hemorrhage, and rapid progression to multiorgan failure are consistent with bone marrow failure syndromes linked to MECOM mutations. The frameshift mutation identified likely disrupted MECOM protein function, contributing to defective hematopoiesis (blood cell formation), coagulation abnormalities, and bleeding complications observed in this neonate. The absence of familial inheritance suggests a spontaneous mutation event. This case expands the spectrum of known pathogenic MECOM variants and highlights the critical role of this gene in early hematopoietic development and vascular integrity.\n\n**Next Steps**  \n- Further research is warranted to better understand the molecular mechanisms by which MECOM frameshift mutations cause bone marrow failure and hemorrhagic complications.  \n- Genetic counseling should be offered to the family to discuss the implications of a de novo MECOM mutation and the low recurrence risk for future pregnancies.  \n- Clinicians should consider MECOM gene analysis in neonates presenting with unexplained severe thrombocytopenia and bleeding, especially when accompanied by bone marrow failure signs.  \n- Development of targeted therapies or early interventions for MECOM-related hematologic disorders remains an important future goal."
+        }
+    },
+    {
+        "article": "La paciente es una mujer de 74 años de edad, físicamente activa, que practica senderismo y equitación. Un mes después del tratamiento con inyección de cortisona de la tendinopatía insercional de Aquiles, sufrió una rotura total del tendón de Aquiles insercional al intentar dar un paso mientras montaba en bicicleta. Esta rotura se trató de forma conservadora con una bota de Walker durante 8 semanas. Después, mientras montaba a caballo, un intento de dar un paso provocó una nueva rotura total del tendón de Aquiles en la inserción. La rotura se trató quirúrgicamente con reinserción del tendón de Aquiles en el calcáneo, utilizando anclajes de sutura. Esto fue seguido por inmovilización en un yeso. Después de la operación, la paciente sufrió una infección profunda que no respondía a los antibióticos, signos de sepsis, y se indicó exploración quirúrgica. Durante la cirugía, se encontró que todo el tendón de Aquiles estaba gravemente afectado por la infección, más o menos destruido, y hubo que retirar el tendón de Aquiles distal de 7 cm (todo el tendón libre de Aquiles). Esto dejó una gran herida sin tejido tendinoso, y la piel se suturó sobre la herida. Después de este procedimiento, la inmovilización y el tratamiento con antibióticos de cloxacilina curaron la infección y la herida se curó adecuadamente. El pie se inmovilizó en un yeso durante las primeras 10 semanas, desde la máxima flexión plantar inicialmente, y luego la flexión plantar disminuyó gradualmente hasta alcanzar la posición neutra. Esto fue seguido por inmovilización en un yeso dorsal, evitando la extensión del tendón de Aquiles en flexión plantar, durante otros 3 meses. Se le dijo que aumentara gradualmente la carga al caminar, pero que evitara la extensión durante un total de 6 meses. Después de 6 meses se le ofreció reconstrucción quirúrgica con un injerto de flexor hallucis longus, pero como entonces tenía una función satisfactoria, decidió esperar y ver. Su función mejoró gradualmente, y un año después de la operación, cuando buscó ayuda por el dolor en el otro tendón de Aquiles, se notó la buena función en el lado operado. La exploración por ultrasonido mostró sorprendentemente un tendón que se parecía mucho a un tendón de Aquiles ligeramente tendinopático.\n",
+        "gold_summary": "Esta señora de 74 años padecía tendinopatía insercional de Aquiles. Después del tratamiento con una inyección local de cortisona, sufrió una rotura total del tendón de Aquiles insercional. Esta rotura se trató de forma conservadora y, después del tratamiento, el tendón de Aquiles volvió a romperse en la zona de inserción. La rotura se trató entonces con reinserción en la zona de inserción calcánea. Al poco tiempo del postoperatorio, la paciente sufrió una infección de herida quirúrgica profunda y sepsis. Debido al pobre efecto del tratamiento con antibióticos y a la destrucción total del tendón, se extirpó todo el tendón de Aquiles. Después de la extirpación, se inmovilizó en un yeso, seguido de movilización y aumento gradual de la carga. En un seguimiento de un año, la paciente caminaba sin cojera, podía levantar el talón hasta la mitad mientras estaba de pie sobre una pierna, había un tendón de Aquiles palpable y el escaneado por ultrasonido mostró una estructura muy similar a un tendón de Aquiles tendinopático y ligeramente engrosado. Había una regeneración evidente de todo el tendón de Aquiles y la función del tendón era sorprendentemente buena.\n",
+        "synthetic_summary": {
+            "B1": "A lady who is 74 years old had a hurt in her heel tendon. She got a shot to help it, but then the tendon broke. The tendon broke again later. \n\nShe had an operation to fix it. After the operation, she got a big infection. The doctors had to take out the whole tendon. \n\nShe wore a cast to keep her foot still. Slowly, she started to move and walk more. \n\nOne year later, she could walk well and stand on one foot. Her heel tendon grew back a lot. It worked very well again.",
+            "B2": "**What Happened to the Patient**\n\nA 74-year-old woman had a problem called insertional Achilles tendinopathy. This means the tendon that connects her calf muscle to her heel bone was damaged where it attaches. She got a cortisone injection, which is a medicine shot to reduce swelling and pain. But after this treatment, her Achilles tendon completely tore near the heel.\n\nAt first, doctors treated the tear without surgery by using a special walking boot. However, the tendon tore again in the same place. This time, she had surgery to reattach the tendon to her heel bone using stitches and anchors.\n\n**Complications and Treatment**\n\nSoon after the surgery, she developed a deep infection in the wound. The infection was serious and caused sepsis, which is when the body has a strong reaction to infection. Antibiotics didn’t work well, so doctors had to do another surgery. They found that the entire Achilles tendon was badly damaged by the infection and had to remove 7 centimeters of it. This left a big open wound, which was closed by sewing the skin over it.\n\nAfter this, she wore a cast to keep her foot still and took antibiotics to fight the infection. The wound healed well, and she stayed in casts for several months. At first, her foot was kept in a pointed position to protect the area, then slowly moved to a normal position. She was told to start walking carefully but avoid stretching the tendon for six months.\n\n**Recovery and Outcome**\n\nOne year later, she was able to walk without limping and could lift her heel halfway while standing on one leg. Doctors could feel a tendon in her heel area, and an ultrasound scan showed a structure that looked like a slightly thickened Achilles tendon. This means her body had grown new tendon tissue even though the original tendon was removed.\n\nHer tendon function was surprisingly good, showing that the Achilles tendon can regenerate and work well after being completely removed and treated carefully.",
+            "B3": "**Background**  \nThe patient is a 74-year-old physically active woman who initially suffered from insertional Achilles tendinopathy, a condition characterized by pain and degeneration at the point where the Achilles tendon attaches to the heel bone (calcaneus). She received a local corticosteroid injection as treatment.\n\n**Key Findings**  \nShortly after the injection, she experienced a complete rupture of the insertional Achilles tendon while attempting to step during cycling. This first rupture was managed conservatively with immobilization using a Walker boot for eight weeks. However, upon returning to horseback riding, a second complete rupture occurred at the same insertion site. This time, surgical repair was performed by reattaching the tendon to the calcaneus using suture anchors, followed by immobilization in a cast.\n\nSoon after surgery, the patient developed a deep surgical wound infection accompanied by signs of sepsis (a severe systemic infection). Antibiotic therapy was ineffective, necessitating surgical exploration. During this procedure, the entire free portion of the Achilles tendon (approximately 7 cm) was found to be severely infected and largely destroyed, requiring complete removal (extirpation) of the distal Achilles tendon. The resulting large wound was closed by suturing the skin over the defect.\n\nPostoperatively, the patient underwent immobilization in a cast initially positioned in maximum plantar flexion (to reduce tension on the tendon area), which was gradually adjusted to a neutral foot position over 10 weeks. This was followed by dorsal casting to prevent tendon extension for an additional three months. Weight-bearing was increased gradually, but active extension of the tendon was restricted for a total of six months.\n\n**Clinical Interpretation**  \nDespite the complete removal of the Achilles tendon, the patient’s function improved progressively without immediate reconstructive surgery. At one-year follow-up, she was able to walk without limping and could perform a partial heel raise while standing on one leg. Palpation revealed a structure consistent with an Achilles tendon, and ultrasound imaging showed a tendon-like formation that was slightly thickened and exhibited features of mild tendinopathy (degenerative changes). This indicated remarkable regeneration of the entire Achilles tendon and unexpectedly good functional recovery.\n\n**Next Steps**  \nAlthough surgical reconstruction using a flexor hallucis longus tendon graft (a tendon transfer procedure) was offered at six months postoperatively, the patient chose to defer this intervention due to satisfactory functional status. Continued monitoring and conservative management remain appropriate unless function deteriorates or symptoms worsen."
+        }
+    },
+    {
+        "article": "Una mujer de 47 años con antecedentes de CHB congénita se presentó con quejas de dolor en el cuello del lado izquierdo y dolor en el oído izquierdo. Aproximadamente 30 meses antes de la presentación, la paciente había notado una pequeña masa en el lado izquierdo de su cuello, que había aumentado gradualmente de tamaño. El dolor se localizó inicialmente en la región del cuello, pero se intensificó con el tiempo y se extendió al área del oído izquierdo.\nInicialmente, debido al dolor en el oído izquierdo, el paciente consultó a varios otorrinolaringólogos y fue tratado por un diagnóstico preliminar de otitis media. Sin embargo, a pesar de los tratamientos, el dolor persistió. Finalmente, un otorrinolaringólogo derivó al paciente para una ecografía, que reveló una masa en el lado izquierdo del cuello, lo que llevó a una derivación quirúrgica. Después de las evaluaciones iniciales, se solicitó una angiografía por TC, que reveló una masa de forma ovalada que medía 30 por 50 mm en la bifurcación de la arteria carótida izquierda, lo que sugiere un CBT tipo II de Shamblin.\n\nEvaluaciones cardiovasculares preoperatorias\nDada la historia del paciente de CHB congénita, se realizó una evaluación cardiovascular preoperatoria exhaustiva. Esto incluyó un electrocardiograma (ECG) de 12 derivaciones, que confirmó la presencia de CHB con un ritmo de escape ventricular estable. Se realizó una ecocardiografía transtorácica para evaluar la estructura y función cardiaca, revelando una función sistólica ventricular normal sin evidencia de anormalidades estructurales. Además, se obtuvo una consulta de cardiología para evaluar la aptitud del paciente para la cirugía y optimizar el manejo perioperatorio.\n\nConsideraciones anestésicas\nDebido a la CHB congénita del paciente y al potencial de inestabilidad hemodinámica durante la cirugía, se formuló un plan anestésico detallado. El paciente fue clasificado como estado físico III de la Sociedad Estadounidense de Anestesiología (ASA). Preoperativamente, se le colocó un marcapasos externo temporal para garantizar un control adecuado de la frecuencia cardíaca y se le insertó un catéter arterial para el monitoreo continuo de la presión arterial. La inducción de la anestesia se realizó utilizando una combinación de etomidato (0,3 mg/kg) y fentanilo (2 μg/kg) para minimizar las fluctuaciones hemodinámicas. El mantenimiento se logró con sevoflurano (1-2 %) y rocuronio (0,6 mg/kg) para la relajación muscular. Los parámetros hemodinámicos, incluida la frecuencia cardíaca, la presión arterial y la saturación de oxígeno, se controlaron de forma continua. Además, se le colocó un catéter venoso central para monitorear la presión venosa central y administrar medicamentos vasoactivos si fuera necesario. El equipo de anestesia mantuvo una comunicación estrecha con el equipo quirúrgico para abordar de forma inmediata cualquier cambio hemodinámico intraoperatorio.\n\nEnfoque quirúrgico\nEl paciente fue sometido a cirugía el 19 de mayo de 2024, después de la localización precisa de la TCC mediante angiografía por TC. El enfoque quirúrgico se eligió en base a la clasificación de Shamblin tipo II, que indica un encasamiento parcial de las arterias carótidas. Dada la proximidad del tumor a estructuras neurovasculares críticas, incluidos los nervios vago e hipogloso, se consideró que el enfoque quirúrgico abierto era el más apropiado para garantizar una resección completa y minimizar las complicaciones.\nTras la inducción de la anestesia general, se colocó al paciente en posición supina con el cuello extendido y rotado hacia la derecha. Se realizó una incisión oblicua paralela al músculo esternocleidomastoideo izquierdo, que se extendía desde la apófisis mastoidea hasta la escotadura esternal. Tras la incisión de la piel y la disección del platisma, se expuso con cuidado la vaina carotídea. Se identificaron la arteria carótida común y su bifurcación en las arterias carótidas internas y externas. Se observó el tumor, de 30 × 50 mm, en la bifurcación carotídea y se diseccionó con cuidado de los tejidos circundantes.\n\nManobras y precauciones específicas\n1.\nSe aplicaron pinzas vasculares temporales en las arterias carótidas internas y externas para controlar el flujo sanguíneo durante la disección del tumor. Esto minimizó el sangrado y proporcionó un campo quirúrgico despejado.\n2.\nSe utilizó neuromonitorización intraoperativa para evaluar la integridad de los nervios vago e hipogloso. La retroalimentación continua garantizó que las estructuras neurales se preservaran durante la disección.\n3.\nEl tumor se separó cuidadosamente de las arterias carótidas y las estructuras neurales circundantes, mediante una combinación de disección aguda y roma. Se logró la hemostasis mediante cauterización bipolar y pinzas quirúrgicas para minimizar el sangrado.\n4.\nEl marcapasos externo se monitoreó activamente durante todo el procedimiento para garantizar un ritmo cardíaco estable. El equipo de anestesia estaba preparado para administrar atropina o epinefrina si se producía una bradicardia o hipotensión significativas.\n2.5. Manejo postoperatorio\nTras asegurarse de que no había hemorragia activa y restablecer el flujo sanguíneo, se devolvieron los tejidos a su posición original y se cerró la herida en múltiples capas. Se aplicó un vendaje apropiado. La cirugía se completó sin complicaciones y con un sangrado mínimo en 2 h y 10 min. El paciente fue trasladado a la UCI vascular para una estrecha monitorización.\nDespués de la operación, se controló al paciente en la UCI durante 24 horas y, más tarde, se le trasladó a la planta general tras mejorar su estado clínico. El marcapasos externo se retiró el día 1 después de la operación, ya que el paciente mantenía un ritmo de escape ventricular estable. El paciente fue dado de alta en buenas condiciones generales el día 3 después de la operación, sin quejas específicas.\n2.6. Seguimiento y resultados a largo plazo\nEl examen histopatológico confirmó el diagnóstico definitivo de TCC en la paciente. Se realizaron evaluaciones de seguimiento a las 2 semanas, 1 mes, 6 meses y 1 año posteriores a la cirugía para evaluar los resultados quirúrgicos y cardíacos. En cada visita, la paciente se sometió a un ECG de 12 derivaciones para monitorear el CHB congénito, que permaneció sin cambios durante todo el período de seguimiento. Se repitió la ecocardiografía transtorácica a los 6 meses y un año, sin deterioro de la función cardíaca y con una función sistólica ventricular estable.\n\nPara evaluar el impacto de la extirpación del tumor en la función cardiaca, se realizó un análisis de la variabilidad de la frecuencia cardiaca (VFC) antes de la operación y a los 6 meses después de la misma. El análisis de la VFC antes de la operación demostró una reducción de la actividad parasimpática, probablemente debido a la compresión del nervio vago por el tumor. El análisis de la VFC después de la operación mostró una mejora significativa del tono parasimpático, lo que sugiere que la extirpación del tumor alivió la compresión del nervio vago y restauró la función autónoma normal.\nAsimismo, el paciente manifestó que el dolor en el cuello y en el oído había desaparecido por completo después de la cirugía, sin que se produjera una reaparición de los síntomas durante el período de seguimiento. Se realizaron estudios de imagen, que incluyeron ultrasonido Doppler y angiografía por TAC, a los 6 meses y al año, que no mostraron evidencia de reaparición del tumor o complicaciones vasculares.\n",
+        "gold_summary": "Describimos el caso de una mujer de 47 años con antecedentes de dolor en el cuello izquierdo y en el oído, acompañado por una masa en el cuello que había ido aumentando gradualmente durante 2,5 años. Después de las evaluaciones iniciales y de múltiples diagnósticos diferenciales, la angiografía por TC reveló una masa ovalada de 30 × 50 mm en la bifurcación carotídea izquierda, lo que confirmó un CCT tipo II de Shamblin. Las evaluaciones preoperatorias demostraron CHB congénita en el electrocardiograma y la ecocardiografía. La paciente se sometió a una resección completa del tumor con todas las precauciones necesarias, incluida la colocación temporal de un marcapasos y un cuidadoso seguimiento.\n",
+        "synthetic_summary": {
+            "B1": "A lady had a bump on her neck for a long time. It made her neck and ear hurt. Doctors looked inside her neck with special pictures. They found a lump near her neck’s big blood tubes.\n\nShe has a heart condition since she was born. Doctors checked her heart carefully before the operation. They gave her a special helper for her heart during surgery.\n\nThe doctors took out the lump carefully. They watched her heart and body closely. After the operation, she felt better and the pain went away.",
+            "B2": "**What Happened to the Patient**  \nA 47-year-old woman had pain on the left side of her neck and in her left ear. She also noticed a small lump in her neck that slowly grew bigger over about two and a half years. Doctors did many tests to find out what was causing her symptoms. A special scan called a CT angiography showed a tumor about 3 by 5 centimeters in size at a place where the main artery in her neck splits into two branches. This tumor was identified as a type II carotid body tumor (CBT), which means it partly surrounded these important arteries.\n\n**Heart Condition and Preparation for Surgery**  \nBefore surgery, doctors found that the woman had a congenital complete heart block (CHB). This is a condition where the heart’s electrical signals are blocked, causing a slow heartbeat. They confirmed this with an electrocardiogram (ECG), which records the heart’s electrical activity, and an echocardiogram, which uses ultrasound to look at the heart’s structure and function. Because of her heart condition, the medical team prepared carefully for surgery. They placed a temporary pacemaker to control her heart rate during the operation and monitored her blood pressure closely.\n\n**Surgery and Care During the Operation**  \nThe surgery aimed to remove the tumor completely while protecting nearby nerves and blood vessels. The doctors made an incision on the left side of her neck to reach the tumor. They used clamps on the arteries to control bleeding and special monitoring to make sure important nerves stayed safe. The pacemaker was watched closely to keep her heart beating steadily. The surgery lasted a little over two hours and went smoothly without major problems.\n\n**Recovery and Follow-Up**  \nAfter surgery, the woman was watched carefully in the intensive care unit for a day. Her temporary pacemaker was removed the next day because her heart rhythm remained stable. She left the hospital three days after surgery feeling well, with no pain in her neck or ear. Tests done over the next year showed no return of the tumor and no problems with her heart. Importantly, removing the tumor helped improve the function of her vagus nerve, which controls many automatic body functions, including heart rate. This was shown by tests measuring heart rate variability before and after surgery.\n\n**Summary**  \nThis case shows how a slow-growing tumor in the neck can cause pain and affect nearby nerves and blood vessels. Careful diagnosis and planning are essential, especially when the patient has a heart condition like CHB. With proper surgical techniques and monitoring, the tumor was safely removed, leading to pain relief and improved nerve function without harming the patient’s heart.",
+            "B3": "**Background**  \nA 47-year-old woman with a history of congenital complete heart block (CHB) presented with progressive left-sided neck pain and left ear pain. Approximately 30 months prior, she had noticed a small mass on the left side of her neck that gradually increased in size. Initial symptoms were localized neck pain that later intensified and radiated to the left ear. Despite multiple consultations and treatment for presumed middle ear infection (otitis media), her pain persisted. Subsequent ultrasound imaging identified a neck mass, prompting further evaluation.\n\n**Key Findings**  \nComputed tomography (CT) angiography revealed an oval-shaped mass measuring 30 × 50 mm located at the bifurcation of the left carotid artery. This finding was consistent with a Shamblin type II carotid body tumor (CBT), indicating partial encasement of the carotid arteries. Preoperative cardiovascular assessment confirmed the presence of congenital CHB with a stable ventricular escape rhythm on a 12-lead electrocardiogram (ECG). Transthoracic echocardiography showed normal ventricular systolic function without structural abnormalities. A cardiology consultation was obtained to optimize perioperative management.\n\n**Clinical Interpretation and Management**  \nGiven the patient’s CHB and the tumor’s proximity to critical neurovascular structures—including the vagus and hypoglossal nerves—an open surgical approach was selected to ensure complete tumor resection while minimizing complications. Anesthetic management included preoperative placement of a temporary external pacemaker and arterial line for continuous hemodynamic monitoring. Induction and maintenance of anesthesia were carefully tailored to avoid hemodynamic instability. Intraoperative neuromonitoring was employed to preserve nerve function. Temporary vascular clamps controlled blood flow during tumor dissection, and meticulous surgical technique achieved complete tumor removal with minimal bleeding.\n\n**Postoperative Course and Follow-up**  \nThe surgery lasted approximately two hours and ten minutes without complications. The patient was monitored in a vascular intensive care unit postoperatively, with the temporary pacemaker removed on postoperative day one after confirming stable cardiac rhythm. She was discharged in good condition on postoperative day three without residual symptoms. Histopathology confirmed the diagnosis of carotid body tumor.\n\nLong-term follow-up at intervals up to one year included serial ECGs, echocardiography, and imaging studies (Doppler ultrasound and CT angiography), all showing stable cardiac function and no tumor recurrence. Heart rate variability analysis demonstrated preoperative parasympathetic dysfunction likely caused by vagus nerve compression from the tumor, which improved significantly after tumor removal. The patient reported complete resolution of neck and ear pain, with no symptom recurrence during follow-up.\n\n**Next Steps**  \nContinued periodic cardiovascular and imaging surveillance is recommended to monitor for potential tumor recurrence and to assess cardiac function given the underlying congenital CHB. The multidisciplinary approach combining careful preoperative cardiac evaluation, tailored anesthetic management, and precise surgical technique contributed to a favorable outcome in this complex case."
+        }
+    },
+    {
+        "article": "Una mujer de 19 años de edad acudió al servicio de urgencias de nuestro hospital con una queja principal de dos días de historia de cefalea, acompañada de náuseas recurrentes, vómitos y fiebre de un día. En el ingreso, su examen físico reveló una fiebre alta de 39.1°C, presión arterial elevada de 189/120 mmHg y una frecuencia cardíaca de 148 latidos por minuto. Los resultados de laboratorio indicaron un recuento de glóbulos blancos elevado de 14.77×10^9/L y un recuento de neutrófilos de 13.55×10^9/L, lo que sugiere una posible infección o respuesta inflamatoria. Se administró un tratamiento empírico inicial con antibióticos debido a la sospecha de infección, pero sus síntomas persistieron. Dados sus signos vitales anormales, marcadores inflamatorios elevados y falta de mejora de los síntomas, la paciente fue admitida para una evaluación diagnóstica adicional y transferida a la unidad de cuidados intensivos para una estrecha monitorización. Un año antes, la paciente había presentado síntomas similares y se le diagnosticó miocarditis en un hospital local en base a los hallazgos clínicos en ese momento. Durante esa hospitalización, también se le diagnosticó hipertensión y se le prescribieron medicamentos antihipertensivos. Sin embargo, después del alta, la paciente no se adhirió al tratamiento antihipertensivo prescrito y no controló regularmente su presión arterial. Además, es notable que su padre tenía antecedentes de muerte súbita inexplicable.\n\nPara investigar la etiología subyacente de los síntomas del paciente, se realizó una tomografía computarizada (TC) de tórax. De forma incidental, esta exploración reveló una masa suprarrenal izquierda con densidad de tejido blando, que medía 43 mm × 36 mm. No se observaron hallazgos patológicos en las exploraciones de TC de cabeza y tórax. El electrocardiograma demostró taquicardia sinusal con un intervalo PR acortado y ondas P altas y puntiagudas en las derivaciones II, III y aVF. La ecocardiografía transtorácica no reveló ninguna anomalía significativa.\n\nEn el segundo día de ingreso, el paciente mostró niveles crecientes de péptido natriurético cerebral (BNP) y troponina I (TnI). El cardiólogo diagnosticó provisionalmente al paciente con miocarditis de etiología incierta, basándose en la presentación clínica, los biomarcadores cardiacos elevados (BNP y TnI) y los hallazgos del electrocardiograma de apoyo. Se inició el tratamiento con metilprednisolona (0,25 g diarios) para abordar la posible inflamación miocárdica debida a la sospecha de miocarditis. Se administraron furosemida (20 mg cada 12 horas) y espironolactona (20 mg cada 12 horas) como diuréticos para controlar la retención de líquidos y reducir la carga de trabajo cardiaco. Se prescribió perindopril amlodipina (10 mg: 5 mg diarios) como inhibidor de la enzima convertidora de la angiotensina y bloqueador del canal del calcio para controlar la presión arterial y reducir la poscarga. Se usó tartrato de metoprolol (25 mg cada 12 horas) para controlar la frecuencia cardiaca y disminuir la demanda de oxígeno miocárdico, mientras que se administró esmolol (0,2 g/hora por infusión intravenosa), un bloqueador beta de acción corta, para controlar la frecuencia cardiaca aguda adicional debido a la taquicardia sinusal. Debido a la preocupación por una posible infección, se agregó moxifloxacina como terapia antibiótica empírica.\n\nDada la presentación del paciente con una masa suprarrenal e hipertensión, el endocrinólogo recomendó una evaluación de la relación aldosterona/renina, cortisol plasmático, catecolaminas plasmáticas y catecolaminas urinarias de 24 horas, junto con sus metabolitos. En posición supina, los niveles de catecolaminas plasmáticas y urinarias estaban marcadamente elevados (Tabla 1), incluyendo dopamina plasmática a 524,5 pmol/L, norepinefrina a 83975 pmol/L y epinefrina a 10579,3 pmol/L. Además, los niveles urinarios de 24 horas mostraron adrenalina libre a 4368,89 nmol/24 horas, norepinefrina libre superior a 12697,60 nmol/24 horas, normetaneprina a 8312 nmol/24 horas, metaneprinas a 4078 nmol/24 horas y ácido vanilmandélico a 58,1 mg/24 horas. Estos hallazgos apoyaron un diagnóstico clínico de feocromocitoma. En el quinto día posterior al ingreso, se interrumpió la terapia glucocorticoide y se sustituyó perindopril amlodipina con terazosin para un control más dirigido de la presión arterial.\n\nUna tomografía computarizada abdominal mejorada confirmó una masa suprarrenal izquierda, muy sugestiva de feocromocitoma. Además, después de obtener el consentimiento informado, se realizó una secuenciación del exoma completo, que reveló una mutación sin sentido heterocigótica, c.1900T > C: p. Cys634Arg, en el gen RET, que conduce a una sustitución de cisteína por arginina en el codón 634. Esta mutación levantó sospechas de un síndrome de neoplasia endocrina múltiple, lo que impulsó una evaluación adicional de las glándulas tiroides y paratiroides. La ecografía Doppler en color de la tiroides identificó una masa hipoecoica que medía 6 mm × 4 mm en el lóbulo tiroideo izquierdo, y se observó una leve elevación en los niveles de calcitonina. No se detectaron anormalidades significativas adicionales.\n\nA medida que la condición del paciente mejoró gradualmente, los niveles de cortisol en plasma y ACTH volvieron a la normalidad. El paciente fue dado de alta con una prescripción de tartrato de metoprolol (100 mg cada 12 horas) e hidrocloruro de ivabradina (5 mg cada 12 horas) para el tratamiento en el hogar. Tres meses después, después de lograr un estado clínico estable, el paciente se sometió a una resección del tumor suprarrenal izquierdo, que medía 50 mm × 40 mm × 30 mm. El análisis inmunohistoquímico confirmó una tinción positiva para Vim, CD56, Syn, CgA y NSE, con S-100 positivo en las células de Sertoli, mientras que CKpan, CD10, MART-1/Melan-A y Melan-A fueron negativos. El índice Ki67 fue del 1 %, lo que llevó a un diagnóstico definitivo de feocromocitoma suprarrenal. El paciente fue dado de alta sin más medicamentos y desde entonces se le ha dado seguimiento regular postoperatorio sin recurrencia de síntomas. Durante un seguimiento postoperatorio de 15 meses, el paciente exhibió hipercalcinotemia persistente leve con un tamaño de nódulo tiroideo estable, mientras que los niveles de PTH y calcio en suero mostraron un aumento progresivo (Tabla 2). Se realizó una gammagrafía paratiroidea adicional utilizando 99mTc-MIBI, y la conclusión fue un resultado negativo para el adenoma paratiroideo.\n",
+        "gold_summary": "Reportamos el caso de una mujer de 19 años que presentó feocromocitoma sin experimentar una crisis, a pesar de tener una masa suprarrenal significativa y someterse a un tratamiento glucocorticoide de alta dosis. Las pruebas genéticas revelaron una mutación de sentido erróneo heterocigótica en el gen RET (c.1900T > C: p. Cys634Arg), asociada con MEN2A. La evaluación endocrina adicional identificó un nódulo tiroideo con niveles de calcitonina levemente elevados, pero niveles normales de electrolitos y hormona paratiroidea. Durante un seguimiento postoperatorio de 15 meses, la paciente exhibió hipercalcitonemia persistente leve con tamaño de nódulo tiroideo estable, mientras que la PTH y los niveles de calcio sérico mostraron un aumento progresivo. Se realizó una gammagrafía paratiroidea adicional utilizando 99mTc-MIBI, que arrojó un resultado negativo para el adenoma paratiroideo.\n",
+        "synthetic_summary": {
+            "B1": "A young woman was very sick with a big lump in her body. Doctors found a tiny change in her genes that can cause some health problems. They saw a small bump in her neck and some blood tests were a little different. After the lump was taken out, she felt better. The doctors keep checking her to make sure she stays healthy.",
+            "B2": "**What Happened to the Patient**\n\nA 19-year-old woman had a large tumor on her adrenal gland, called a pheochromocytoma. This tumor can cause serious problems by making the body release too many stress hormones. Surprisingly, she did not have a sudden crisis, even though the tumor was big and she was treated with strong steroid medicine.\n\n**What the Tests Showed**\n\nGenetic testing found a change (mutation) in a gene called RET. This mutation is linked to a condition called MEN2A, which can cause tumors in different hormone-producing glands. Further tests showed she had a small lump in her thyroid gland and slightly high levels of a hormone called calcitonin, which can be a sign of thyroid problems. However, her blood minerals and parathyroid hormone levels were normal at first.\n\n**What Happened After Treatment**\n\nAfter surgery to remove the adrenal tumor, doctors followed her for 15 months. During this time, her calcitonin levels stayed a little high, but the thyroid lump did not grow. Meanwhile, her parathyroid hormone and blood calcium levels slowly increased. Another scan was done to check for parathyroid tumors, but it did not find any.\n\n**What This Means**\n\nThis case shows how a genetic mutation can cause hormone-related tumors without obvious early symptoms. Careful monitoring is important because other gland problems may develop later. The patient is being watched closely to catch any new issues early and manage them properly.",
+            "B3": "**Background**  \nThis report describes a 19-year-old woman diagnosed with a pheochromocytoma—a tumor of the adrenal gland that typically secretes excess catecholamines (stress hormones)—who did not experience a hypertensive crisis despite having a sizable adrenal mass and receiving high-dose glucocorticoid therapy. Genetic testing identified a heterozygous missense mutation in the RET gene (c.1900T > C: p.Cys634Arg), a mutation known to be associated with Multiple Endocrine Neoplasia type 2A (MEN2A), a hereditary syndrome characterized by tumors in multiple endocrine glands.\n\n**Key Findings**  \n- The patient’s adrenal tumor was confirmed as a pheochromocytoma through imaging and immunohistochemical analysis after surgical removal.  \n- Additional endocrine evaluation revealed a small thyroid nodule accompanied by mildly elevated serum calcitonin levels, a marker often elevated in medullary thyroid carcinoma, which is commonly associated with MEN2A.  \n- Despite these findings, the patient’s serum electrolytes and parathyroid hormone (PTH) levels were initially within normal ranges.  \n- Over a 15-month postoperative follow-up, the patient continued to exhibit mild hypercalcitoninemia (elevated calcitonin) with a stable thyroid nodule size. However, both PTH and serum calcium levels showed a progressive increase, suggesting evolving parathyroid involvement.  \n- A parathyroid scan using 99mTc-MIBI imaging was performed to evaluate for parathyroid adenoma (a benign tumor that can cause hyperparathyroidism), but the result was negative.\n\n**Clinical Interpretation**  \nThis case illustrates a pheochromocytoma presentation without the typical hypertensive crisis, even under glucocorticoid treatment, which can sometimes exacerbate catecholamine secretion. The identification of the RET gene mutation confirms the diagnosis of MEN2A syndrome, which predisposes patients to pheochromocytomas, medullary thyroid carcinoma, and parathyroid abnormalities. The presence of a thyroid nodule with elevated calcitonin supports early medullary thyroid involvement, while the progressive rise in PTH and calcium levels during follow-up raises concern for developing parathyroid pathology, despite negative imaging findings at this stage.\n\n**Next Steps**  \nContinued close monitoring of thyroid and parathyroid function is essential, including periodic imaging and biochemical assessments, to detect any progression toward medullary thyroid carcinoma or hyperparathyroidism. Early identification and management of these endocrine tumors are critical to improving long-term outcomes in patients with MEN2A. Genetic counseling and family screening are also recommended given the hereditary nature of the RET mutation."
+        }
+    },
+    {
+        "article": "Una refugiada etíope embarazada de 39 años (Gravida 3 Para 2+0) fue derivada a nuestro departamento de urgencias de medicina interna en el Hospital Universitario de Gadarif, Gadarif State, Sudán, con hinchazón generalizada progresiva, falta de aire y fatiga durante 6 semanas y una revisión sistémica sin importancia. La paciente fue admitida en el sitio de admisión de casos críticos y su historia, tomada con la ayuda de un intérprete de idiomas más tarde en la admisión, reveló un episodio remoto inicialmente no revelado de tres convulsiones tónico-clónicas generalizadas no provocadas hace 21 años que se trataron tradicionalmente. Sin embargo, no había antecedentes de traumatismo craneal o antecedentes familiares de convulsiones. El examen general de la paciente reveló un PWS del lado izquierdo que involucraba la división oftálmica del nervio trigémino. Sin embargo, este hallazgo se perdió inicialmente en la inspección pero luego fue confirmado por el cónyuge de la paciente para estar presente desde el nacimiento. La paciente también estaba muy pálida y tenía derrames pleurales bilaterales, hepatomegalia blanda e hinchazón bilateral de las extremidades inferiores.\n\nLas investigaciones iniciales revelaron un nivel de hemoglobina de 8,84 g/dl. Por lo tanto, se diagnosticó insuficiencia cardíaca debido a anemia y se trató a la paciente en consecuencia. Sin embargo, ocho días después de su ingreso, la paciente había desarrollado aproximadamente seis episodios de convulsiones tónico-clónicas focales a bilaterales que respondieron bien a la fenitoína, pero que dejaron a la paciente en un estado comatoso profundo con un GCS de tres. Fue posteriormente admitida en la unidad de cuidados intensivos (UCI) y se le insertó un tubo nasogástrico para ayudarla con su nutrición y administración de fármacos. Además, para evitar más convulsiones, se le inició un tratamiento con comprimidos de carbamazepina de 200 mg administrados a través del tubo nasogástrico.\n\nSe retrasó una tomografía computarizada (TC) sin contraste del cerebro para el día posterior a la estabilización, ya que solo había una máquina de tomografía computarizada en el estado de Gadarif y funcionaba de forma intermitente debido a la falta de un número suficiente de técnicos radiólogos. La tomografía computarizada reveló calcificaciones corticales en la parte posterior del área parietal izquierda, lo que planteó el diagnóstico diferencial de SWS. En consecuencia, se realizó un examen físico de repetición, que mostró la presencia de una lesión plana de color rojo púrpura en la frente y el ojo. Al interrogar al cónyuge, se confirmó la presencia de esta lesión y que no había cambiado desde el nacimiento, lo que nos ayudó a descartar el diagnóstico de una mancha salmón, ya que esta lesión no se desvaneció, por lo que se diagnosticó como PWS. Además, no tenía características de megalencefalia, síndrome de malformación capilar que por lo general incluye un gran tamaño de la cabeza o del cerebro, problemas en las articulaciones y malformaciones capilares en la piel. Tampoco tenía hipertrofia de extremidades, anomalías del drenaje linfático o excrecencias óseas o de tejidos blandos que sugieran el síndrome de Klippel-Trenaunay-Weber. Por lo tanto, en función de los hallazgos de la tomografía computarizada y la presentación típica, llegamos a la conclusión del diagnóstico de SWS.\n\nDos días después de ingresar en la UCI, la paciente experimentó un cambio fluctuante en su estado de conciencia y una nueva aparición de hemiparesia contralateral (contralateral al SPW), así como afasia y labilidad emocional. Desafortunadamente, cuatro días después de ingresar en la UCI, la paciente empezó a experimentar sangrado vaginal; por ello, se consultó al departamento de obstetricia y ginecología y se descubrió que la paciente tenía un embarazo no viable (28 semanas + 1 día) y se realizó una inducción sin incidentes. Durante el mismo período, la paciente se volvió combativa y poco cooperativa, lo que llevó a que se la inmovilizara físicamente. Tres días después, la paciente desarrolló nuevos ataques focales bilaterales que comenzaron como episodios mioclónicos faciales y, tras consultar con el departamento de neurología, se aumentó la dosis de carbamazepina de la paciente a 1000 mg diarios, lo que ayudó a prevenir la recurrencia de los ataques. Cabe mencionar que, en su segundo trimestre y antes de recibir el resultado de la tomografía computarizada, se exploró un diagnóstico de eclampsia, pero sus constantes lecturas de presión arterial con una presión sistólica superior a la normal de 139 la mayoría de los días y una presión diastólica con un máximo de 97 mmHg y un rango bajo de proteinuria, así como la ausencia de características sistémicas como deterioro renal o hepático, excluyeron este diagnóstico. Después de alcanzar el diagnóstico de SW, se puso en juego un enfoque multidisciplinario; por ello, se realizó una consulta oftalmológica para descartar glaucoma. Sin embargo, la paciente estaba muy irritable y era difícil realizar un examen de fondo de ojo. Además, la paciente fue trasladada a la sala de medicina interna tras la estabilización.\n",
+        "gold_summary": "Presentamos el caso de una refugiada de 39 años, no diabética y no hipertensa, que inicialmente presentó insuficiencia cardiaca debido a anemia, por lo que recibió transfusiones de sangre. Más adelante, al ingresar, desarrolló convulsiones múltiples focales bilaterales, irritabilidad severa, afasia y hemiplejía derecha, lo que motivó su ingreso a la UCI. Un examen y un historial médico repetidos revelaron una mancha de vino de Oporto ocular izquierda leve que inicialmente pasó desapercibida y un historial remoto de convulsiones no provocadas 20 años atrás. Las imágenes revelaron calcificaciones parietales y confirmaron el diagnóstico de SWS. Por lo tanto, se adoptó un enfoque multidisciplinario para comprender plenamente el diagnóstico de la paciente y determinar una estrategia de tratamiento, que incluyó consultas con los departamentos de neurología, oftalmología, otorrinolaringología y fisioterapia. Se logró un control exitoso de las convulsiones mediante la administración de fenitoína IV durante 3 días y el aumento gradual de la carbamazepina oral a 1 g diario a través de una sonda nasogástrica. Lamentablemente, debido a la falta de personal o recursos, no se pudieron realizar otras evaluaciones importantes para pacientes con SWS, como evaluaciones avanzadas de neuroimagen, psiquiátricas, de cirugía plástica y neurocirugía, así como revisiones dentales.\n",
+        "synthetic_summary": {
+            "B1": "A lady was very tired and had trouble breathing. She also had swelling and felt weak.\n\nDoctors found she had a red mark on her face since she was born. She had seizures, which are like strong shakes.\n\nThey took pictures of her head and saw some spots inside. This helped doctors know what was wrong.\n\nThe doctors gave her medicine to stop the seizures. They asked many helpers to take care of her.\n\nSome tests could not be done because there were not enough helpers or tools. But the doctors did their best to help her feel better.",
+            "B2": "**Patient Background and Initial Problems**  \nThis is the story of a 39-year-old pregnant woman who came to the hospital feeling very tired, short of breath, and swollen all over. At first, doctors found she had heart failure caused by anemia. Anemia means her blood didn’t have enough healthy red blood cells to carry oxygen. She was given blood transfusions to help.  \n\n**New Symptoms and Tests**  \nSoon after, she started having several seizures. Seizures are sudden bursts of electrical activity in the brain that can cause shaking or loss of consciousness. She also became very irritable, had trouble speaking (called aphasia), and weakness on one side of her body (hemiplegia). Because of these serious problems, she was moved to the intensive care unit (ICU) for close monitoring.  \n\nDoctors then noticed a special birthmark on her left eye area called a port-wine stain. This is a flat, red-purple mark caused by extra blood vessels under the skin. It had been there since birth but was missed at first. She also had a history of seizures 20 years ago. A brain scan showed calcium deposits in part of her brain, which helped doctors diagnose her with Sturge-Weber Syndrome (SWS).  \n\n**What is Sturge-Weber Syndrome?**  \nSWS is a rare condition where abnormal blood vessels affect the skin, brain, and sometimes the eyes. This can cause seizures, weakness, and other problems.  \n\n**Treatment and Care**  \nTo control her seizures, doctors gave her medicines called phenytoin (through an IV for 3 days) and carbamazepine (given by a feeding tube, gradually increased to 1000 mg per day). These medicines helped reduce her seizures.  \n\nBecause SWS can affect many parts of the body, a team of specialists worked together to care for her. This included neurologists (brain doctors), eye doctors, ear-nose-throat specialists, and physical therapists.  \n\n**Challenges and Limitations**  \nUnfortunately, the hospital did not have enough staff or equipment to do some important tests and treatments. For example, advanced brain imaging, psychiatric evaluations, plastic surgery, brain surgery, and dental check-ups were not possible.  \n\n**Summary**  \nThis patient’s case shows how Sturge-Weber Syndrome can cause serious health issues like seizures and weakness. Early recognition of the birthmark and brain changes helped doctors make the diagnosis. Treating her seizures and involving different specialists was important for her care, even though some resources were limited.",
+            "B3": "**Background**  \nThis case involves a 39-year-old Ethiopian refugee woman with no history of diabetes or hypertension. She initially presented with symptoms of heart failure attributed to anemia and received blood transfusions accordingly. Her medical history, obtained later with interpreter assistance, revealed a remote episode of unprovoked generalized tonic-clonic seizures approximately 20 years prior, which had been treated traditionally and not medically documented.\n\n**Key Findings**  \nDuring her hospital stay, the patient developed multiple bilateral focal seizures, severe irritability, expressive language impairment (aphasia), and right-sided hemiplegia (paralysis). These neurological deteriorations necessitated admission to the intensive care unit (ICU). A repeated physical examination uncovered a subtle port-wine stain (PWS)—a flat, reddish-purple vascular birthmark—on the left ocular region, which had been overlooked initially. Imaging studies, specifically a non-contrast brain computed tomography (CT) scan, revealed cortical calcifications in the left parietal lobe. These findings, combined with the clinical presentation, supported the diagnosis of Sturge-Weber syndrome (SWS), a rare neurocutaneous disorder characterized by facial vascular malformations, neurological symptoms, and leptomeningeal angiomas.\n\n**Clinical Interpretation**  \nThe presence of the PWS in the ophthalmic division of the trigeminal nerve distribution, the history of seizures, and the characteristic cortical calcifications on imaging are hallmark features of SWS. The patient’s neurological decline, including new-onset hemiplegia and aphasia, reflects the progressive cerebral involvement typical of this syndrome. The initial misrecognition of the PWS delayed the diagnosis. The seizures were managed successfully with intravenous phenytoin for three days, followed by gradual escalation of oral carbamazepine to 1000 mg daily administered via a nasogastric tube, which helped control seizure recurrence.\n\n**Next Steps and Management Approach**  \nA multidisciplinary strategy was implemented to address the complex manifestations of SWS. Consultations were arranged with neurology, ophthalmology, otolaryngology, and physiotherapy departments to provide comprehensive care. Unfortunately, due to limited resources and personnel, advanced neuroimaging modalities, psychiatric evaluations, plastic surgery assessments, neurosurgical consultations, and dental examinations—important components in the management of SWS—could not be performed. Continued monitoring and supportive care remain essential, with emphasis on seizure control, neurological rehabilitation, and surveillance for potential complications such as glaucoma and developmental delays.\n\n---\n\nThis case underscores the importance of thorough clinical examination and history-taking, especially in patients with subtle congenital signs, to facilitate early diagnosis of rare syndromes like Sturge-Weber. It also highlights challenges in resource-limited settings that may impact the extent of diagnostic and therapeutic interventions."
+        }
+    },
+    {
+        "article": "Una paciente de 69 años se quejaba de una pérdida progresiva de la visión. Sus padres eran primos hermanos. Le habían diagnosticado retinitis pigmentosa 27 años antes. La paciente había fumado durante 15 años. Tenía antecedentes de hiperlipidemia e hipotiroidismo.\n\nTras una evaluación oftalmológica completa, se determinó que el paciente tenía una agudeza visual corregida (AVC) de contar los dedos a 5’ y 3’ en los ojos derecho e izquierdo, respectivamente. La retinoscopia mostró una refracción de –1.00 + 0.50×70 y –2.00 + 1.00×5 en los ojos derecho e izquierdo, respectivamente. El paciente tenía discos ópticos pálidos con una atrofia profunda extensa de la mácula central, hiperplasia del pigmento epitelial y otras áreas de atrofia multifocal en el ojo derecho. Además, el paciente tenía atrofia macular en el ojo izquierdo. En la imagen de autofluorescencia del fondo del ojo (FAF) del paciente, había evidencia de una hipoautofluorescencia central de la mácula, con una extensión centrífuga difusa desde su centro hasta su periferia.\n\nLa tomografía de coherencia óptica macular (OCT) determinó que el espesor macular promedio era de 191 µM y 193 µM en los ojos derecho e izquierdo, respectivamente. El volumen macular era de 6.9 mm3 y 7.0 mm3 en los ojos derecho e izquierdo, respectivamente. No se encontró edema macular, quistes o fluido subretinal en ninguno de los ojos.\n\nUna prueba de campo visual reveló que el paciente tenía desviaciones medias de –23.75 dB y –24.56 dB en los ojos derecho e izquierdo, respectivamente. Las desviaciones estándar de patrón fueron de +3.69 dB y +4.69 dB en los ojos derecho e izquierdo, respectivamente. Los resultados de un electrorretinograma de campo completo (ERG) mostraron una respuesta normal de bastones y una respuesta de conos disminuida, bilateralmente. Por estas razones, se realizó un diagnóstico clínico de enfermedad STGD1.\n\nSe encontró una variante patogénica homocigótica intrónica c.5714+5G>A del gen ABCA4 tras el análisis de secuenciación y eliminación/duplicación utilizando secuenciación de próxima generación (Invitae Corporation, San Francisco, California). Tenía seis variantes adicionales de significación incierta (VUS) en los genes CACNA1F, EYS, KCNV2, KLHL7, MKKS y USH2A.\n",
+        "gold_summary": "Una paciente de 69 años de edad se presentó en la clínica quejándose de una pérdida progresiva de la visión. La evaluación oftálmica fue notable para una mejor agudeza visual corregida de contar los dedos a 5' en el ojo derecho y 3' en el ojo izquierdo. Las imágenes revelaron una atrofia profunda y extensa de la mácula central, una hiperplasia del pigmento epitelial y otras áreas de atrofia multifocal en el ojo derecho. Además, las imágenes de autofluorescencia del fondo de la mácula mostraron una hipoautofluorescencia central con expansión bilateral a la periferia en ambos ojos. Un electrorretinograma de campo completo mostró una respuesta normal de los bastones, con una respuesta disminuida de los conos, bilateralmente. Las pruebas genéticas fueron positivas para una mutación inotrópica homocigótica en el gen ABCA4 de la variante c.5714+5G>A.\n",
+        "synthetic_summary": {
+            "B1": "A lady who is 69 years old had trouble seeing. Her eyes were very weak. Doctors looked inside her eyes and saw some parts were very thin and not working well. Tests showed some parts of her eyes worked okay, but others did not work well. They found a tiny change in her body that made her eyes weak.",
+            "B2": "**Patient's Vision Problems**\n\nA 69-year-old woman came to the eye clinic because her vision was getting worse over time. When tested, she could only see well enough to count fingers at 5 feet with her right eye and 3 feet with her left eye. This shows her vision was very poor.\n\n**What the Eye Tests Showed**\n\nImages of her eyes revealed serious damage in the central part of the retina called the macula. The macula helps us see fine details. She had areas where the tissue was thinning or dying (called atrophy) and changes in the pigment cells that support the retina. Both eyes showed these problems, but the right eye had more widespread damage.\n\nAnother test called autofluorescence imaging showed that the center of her macula was less bright than normal, which means the cells there were not healthy. This dim area spread from the center toward the edges in both eyes.\n\n**How Her Retina Was Working**\n\nAn electrorretinogram (ERG), which measures how well the light-sensing cells in the eye work, showed that her rod cells (which help us see in dim light) were working normally. However, her cone cells (which help us see color and fine details) were not working well in both eyes.\n\n**Genetic Findings**\n\nGenetic testing found that she has a specific mutation in a gene called ABCA4. This gene is important for the health of the retina. The mutation she has is called c.5714+5G>A and is present in both copies of the gene (this is called homozygous). This mutation is known to cause a disease called Stargardt disease, which leads to progressive vision loss.\n\n**What This Means**\n\nThe combination of her symptoms, eye test results, and genetic mutation confirms that she has Stargardt disease. This condition causes damage to the macula and leads to worsening vision over time. Understanding her genetic mutation helps doctors confirm the diagnosis and may guide future treatments.",
+            "B3": "Background  \nA 69-year-old female patient presented with a history of progressively worsening vision loss. She had been diagnosed with retinitis pigmentosa 27 years earlier and had additional medical conditions including hyperlipidemia and hypothyroidism. Her parents were first cousins, indicating consanguinity, which can increase the risk of inherited genetic disorders. She also had a 15-year history of smoking.\n\nKey Findings  \nOphthalmologic examination revealed severely reduced corrected visual acuity, measured as the ability to count fingers at 5 feet in the right eye and 3 feet in the left eye. Retinoscopy showed mild myopic refractive errors with astigmatism in both eyes. Fundus examination demonstrated pale optic discs and extensive, deep atrophy of the central macula in the right eye, accompanied by hyperplasia (increased growth) of the retinal pigment epithelium and multifocal atrophic areas. The left eye also exhibited macular atrophy. Autofluorescence imaging of the retina showed central hypoautofluorescence (reduced natural fluorescence indicating tissue loss or dysfunction) in the macula, with a diffuse centrifugal spread toward the peripheral retina in both eyes.\n\nOptical coherence tomography (OCT) measured average macular thickness of approximately 191 µm in the right eye and 193 µm in the left eye, with macular volumes of 6.9 mm³ and 7.0 mm³, respectively. No macular edema, cysts, or subretinal fluid were detected. Visual field testing revealed significant mean deviations of –23.75 dB (right eye) and –24.56 dB (left eye), indicating severe visual field loss. Pattern standard deviations were elevated, suggesting irregularity in the visual field defects.\n\nFull-field electroretinography (ERG) demonstrated normal rod photoreceptor (responsible for low-light vision) function but bilaterally reduced cone photoreceptor (responsible for color and central vision) responses. These findings supported a clinical diagnosis of Stargardt disease type 1 (STGD1), a hereditary macular dystrophy.\n\nClinical Interpretation  \nGenetic testing using next-generation sequencing identified a homozygous intronic pathogenic variant c.5714+5G>A in the ABCA4 gene, which is known to cause STGD1 by disrupting normal gene splicing and protein function. Additionally, six variants of uncertain significance (VUS) were detected in other retinal disease-associated genes (CACNA1F, EYS, KCNV2, KLHL7, MKKS, and USH2A), but their clinical relevance remains unclear.\n\nNext Steps  \nGiven the confirmed genetic diagnosis of STGD1, management should focus on supportive care, including low vision rehabilitation and monitoring for potential complications. Genetic counseling is recommended to discuss inheritance patterns, prognosis, and implications for family members. Further research or clinical trials may be considered for emerging therapies targeting ABCA4-related retinal degeneration. Regular ophthalmologic follow-up is essential to assess disease progression and address any new ocular findings."
+        }
+    },
+    {
+        "article": "Un niño de 19 meses de edad fue admitido en el departamento de urgencias porque se cayó de la trona en la que comía. Esta caída ocurrió en un aparente bienestar, sin la presencia de signos o síntomas anticipados. Primero, se cayó sobre su glúteo y luego se golpeó la cabeza (occipucio) contra el suelo. Vomitó (tres episodios) y estaba muy irritable. Su frecuencia respiratoria y cardíaca eran >60 respiraciones y >150 latidos por minuto, mientras que la saturación de oxígeno era <80%. Tras el examen físico, el niño estaba hidratado y consciente, pero irritable. Más importante aún, observamos retracciones subcostal y, al auscultar, disminución de los sonidos respiratorios en la parte basal izquierda del tórax. El paciente fue ventilado con un balón de AMBU conectado a una fuente de oxígeno y monitorizado con un oxímetro de pulso. A pesar de nuestra intervención, la saturación de oxígeno cayó por debajo del 70% y cuanto más ventilábamos, más caía la saturación. La ecografía pulmonar mostró la ausencia de las típicas líneas A y la consolidación del pulmón, que se visualizó directamente como un parénquima sólido. Sobre la base del mal estado clínico, el paciente se sometió a intubación orotraqueal con un tubo endotraqueal con manguito. Después de que el bebé se estabilizó, se sometió a una tomografía computarizada (TC) de tórax que mostró una atelectasia completa del pulmón izquierdo con una interrupción del bronquio izquierdo principal a 12 cm de la bifurcación bronquial. Se sospechó un FBA ya que la madre también declaró que el bebé en los días anteriores había tenido un ataque de tos intenso y desapareció en 24 h sin ningún tratamiento. Por lo tanto, se realizó una broncoscopia rígida y se encontró y se eliminó rápidamente una almendra de 2 cm de diámetro en el bronquio izquierdo principal.\n\nEl paciente nunca había consumido antes almendras u otros frutos secos y, en esta ocasión, ingirió la almendra por accidente.\n\nEl bebé mostró una mejora clínica progresiva y, después de 24 horas, se le retiró la sonda y se le dio de alta de la unidad de cuidados intensivos para ser ingresado en la sala de pediatría general durante unos días, con una recuperación gradual y total de la función respiratoria.\n",
+        "gold_summary": "Describimos el caso de un niño de 19 meses que llegó a la sala de urgencias por un traumatismo en la cabeza. La evaluación clínica, sin embargo, reveló una dificultad respiratoria grave inexplicable que requería intubación traqueal. Después de nuestra evaluación, planteamos la hipótesis de que la dificultad respiratoria grave determinó un estado alterado de conciencia con el consiguiente traumatismo en la cabeza. Los hallazgos radiológicos levantaron la sospecha de aspiración de cuerpo extraño por la presencia de una atelectasia de todo el pulmón izquierdo. La tomografía computarizada mostró una interrupción abrupta del bronquio principal a 12 mm del casco. La siguiente broncoscopia identificó una amígdala de 2 cm.\n",
+        "synthetic_summary": {
+            "B1": "A little boy fell and hurt his head. But he had trouble breathing too. \n\nThe doctors found that his left lung was not working well. They saw something blocking his breathing tube. \n\nThey used a tiny camera and found a big almond stuck inside. The doctors took it out carefully. \n\nAfter that, the boy felt better and could breathe well again.",
+            "B2": "**What Happened:**  \nA 19-month-old boy was brought to the emergency room after hitting his head in a fall. At first, it seemed like a simple injury. But doctors noticed he was having serious trouble breathing, which was not expected from just a fall.\n\n**What They Found:**  \nThe boy’s breathing was very fast and his oxygen levels were low. Tests showed that his left lung was not working properly because it had collapsed (this is called atelectasis). A special scan (CT scan) showed that the main airway to his left lung was blocked about 12 millimeters from where the airway splits. Doctors thought something was stuck in his airway.\n\n**What They Did:**  \nUsing a procedure called bronchoscopy, where a thin tube with a camera is inserted into the airways, doctors found and removed a 2-centimeter almond stuck in his left main bronchus (the airway to the lung). The boy had accidentally swallowed the almond, which caused the breathing problems and then led to the fall and head injury.\n\n**What It Means:**  \nThis case shows how a foreign object stuck in the airway can cause serious breathing problems in young children. Sometimes, these problems can lead to other injuries, like a fall. Quick diagnosis and removal of the object helped the boy recover fully.",
+            "B3": "**Background**  \nThis report concerns a 19-month-old boy who was brought to the emergency department following a head injury sustained from a fall out of his high chair. Although the initial concern was trauma, the clinical evaluation revealed severe respiratory distress that could not be explained solely by the fall.  \n\n**Key Findings**  \nUpon examination, the child exhibited signs of respiratory compromise, including a rapid breathing rate (>60 breaths per minute), elevated heart rate (>150 beats per minute), and dangerously low oxygen saturation (<80%). Physical assessment showed decreased breath sounds in the lower left lung area and subcostal retractions (inward movement of the lower chest during inhalation), indicating respiratory difficulty. Lung ultrasound demonstrated absence of normal air patterns (A-lines) and showed lung consolidation, suggesting solidification of lung tissue. Despite oxygen support and ventilation, the child’s oxygen levels continued to decline, necessitating endotracheal intubation for airway protection and ventilation.  \n\nA chest computed tomography (CT) scan revealed complete collapse (atelectasis) of the left lung and an abrupt interruption of the left main bronchus approximately 12 millimeters from the bifurcation (where the airway splits). These imaging findings raised suspicion of a foreign body aspiration (FBA). The mother reported that the child had experienced a severe coughing episode days earlier that resolved spontaneously, supporting this hypothesis.  \n\nSubsequent rigid bronchoscopy confirmed the presence of a 2-centimeter almond lodged in the left main bronchus, which was promptly removed. Notably, the child had no prior history of consuming nuts, indicating accidental ingestion.  \n\n**Clinical Interpretation**  \nThe severe respiratory distress likely caused a decreased level of consciousness, which in turn led to the head trauma from the fall. The foreign body aspiration caused obstruction of the left main bronchus, resulting in complete lung collapse and respiratory failure. This explains the child’s critical condition upon arrival.  \n\n**Next Steps and Outcome**  \nFollowing removal of the almond and stabilization, the child showed progressive clinical improvement. After 24 hours, the breathing tube was removed, and he was transferred from the intensive care unit to the general pediatric ward. Over the subsequent days, he made a full recovery of respiratory function without further complications.  \n\nThis case highlights the importance of considering foreign body aspiration in young children presenting with unexplained respiratory distress, even when initial presentation suggests trauma. Prompt imaging and bronchoscopic intervention can be lifesaving."
+        }
+    },
+    {
+        "article": "Una mujer nulípara de 35 años con antecedentes de infertilidad se presentó en la consulta externa. Informó de un antecedente de tres años de dolor sordo cíclico en el ombligo. El dolor se asoció a un nódulo umbilical que sangraba durante la menstruación. Cabe destacar que el dolor empeoraba durante la menstruación y se aliviaba con analgésicos. La paciente también informó de dismenorrea, menorragia y dispareunia. La paciente se había insertado un DIU de cobre 3 años antes y había estado usando Zinnia P (levonorgestrel y etinilestradiol) durante los últimos 3-4 meses para intentar aliviar el dolor. Su historial ginecológico previo no fue notable y tenía un ciclo menstrual regular. No había antecedentes médicos, quirúrgicos o sociales de importancia.\nAl examinarla, sus constantes vitales eran estables. Se observó una hinchazón hiperpigmentada (3 × 2 cm) en el ombligo al examinar el abdomen. La hinchazón era firme, inmóvil, no dolorosa, no reductible y no estaba ligada a estructuras subyacentes. Una resonancia magnética abdominal reveló una masa de mejora mal definida que medía 3 × 4 × 6 cm ubicada a lo largo de la pared abdominal anterior derecha y estaba conectada a un tracto sinusal que se extendía hacia la región suprapúbica, pero no se comunicaba con la cavidad peritoneal, hallazgos que sugieren endometriosis. El diagnóstico diferencial fue amplio, incluida una hernia umbilical, granuloma, cicatriz queloide, neoplasias malignas nodulares y anomalías embriológicas. Además, se observaron lesiones anexiales bilaterales, eran hiperintensas con áreas hipointensas focales y restricciones variables, la lesión del lado derecho medía 1,6 × 1,7 cm y la lesión del lado izquierdo medía 2,0 × 0,8 cm, hallazgos consistentes con endometriosis ovárica bilateral.\n\nSe programó al paciente para la extirpación quirúrgica del nódulo umbilical. La muestra se envió para un examen histopatológico. Los resultados revelaron una epidermis normal con glándulas endometriales dispersas y estroma dentro de la dermis. La fotomicroscopía resaltó la presencia de estroma endometrial y tejido graso subcutáneo. Esta morfología es consistente con la endometriosis. La recuperación postoperatoria de la paciente fue sin incidentes, y se la consideró apta para el alta el día 2 postoperatorio. Recibió asesoramiento sobre su fertilidad futura y la posibilidad de FIV, riesgo de recurrencia y se programó una visita de seguimiento en dos semanas. Se le inició con Dienogest, Visanne y un anticonceptivo oral combinado para el tratamiento de la endometriosis. Se la ha monitoreado clínicamente cada cuatro semanas, y no se han observado síntomas o signos de recurrencia local durante el período de seguimiento de 8 meses. Cabe destacar que, a pesar de que su condición permaneció estable después del tratamiento, no concibió en el transcurso del año siguiente.\n",
+        "gold_summary": "Presentamos el caso de una mujer nulípara de 35 años de edad del norte de Tanzania con un historial de infertilidad de 10 años. Al presentarse, la paciente informó de un historial de tres años de dolor cíclico asociado a una masa umbilical. Una resonancia magnética abdominal reveló una masa mal definida que se intensificaba y medía 3 × 4 × 6 cm, localizada a lo largo de la pared abdominal anterior derecha. La masa estaba conectada a un tracto sinusal que se extendía hacia la región suprapúbica, pero no mostraba comunicación con la cavidad peritoneal, lo que sugería endometriosis. Además, las lesiones anexiales bilaterales demostraron señales hiperintensas con áreas hipointensas focales y restricciones variables, consistentes con endometriomas ováricos bilaterales. La paciente se sometió a la extirpación de la masa umbilical y el examen histopatológico confirmó el diagnóstico de endometriosis umbilical primaria. A pesar de su condición estable después del tratamiento, no concibió durante el año siguiente.\n",
+        "synthetic_summary": {
+            "B1": "A lady had a pain in her belly button for three years. The pain came and went with her monthly time. She had a small bump there that sometimes bled.\n\nDoctors took pictures and found a lump inside her belly wall. They thought it was a kind of tissue that should be inside her tummy but was outside.\n\nThe bump was taken out by doctors. Tests showed it was this special tissue. After the medicine and surgery, she felt better but did not have a baby yet.",
+            "B2": "**Case Summary: A Woman with Umbilical Endometriosis and Infertility**\n\nA 35-year-old woman who had never been pregnant came to the doctor because she had been unable to have children for 10 years. She also had a painful lump near her belly button that hurt in a cycle, getting worse during her periods. \n\n**What They Found**\n\nAn MRI scan showed a lump about 3 by 4 by 6 centimeters on the right side of her lower belly wall. This lump was connected to a small tract (a narrow channel) that went toward the area above her pubic bone but did not connect to the inside of her abdomen. These findings suggested she had endometriosis. Endometriosis is a condition where tissue similar to the lining inside the uterus grows outside it, causing pain and other problems. The scan also showed abnormal areas on both of her ovaries, called endometriomas, which are cysts related to endometriosis.\n\n**What They Did**\n\nThe doctors surgically removed the lump near her belly button. They tested the tissue by looking at it under a microscope—a process called a biopsy, where a small piece of tissue is examined to find out what it is. The test confirmed that the lump was caused by endometriosis in the belly button area, which is rare.\n\n**What It Means**\n\nAfter surgery and treatment, the woman’s condition was stable, and she did not have new symptoms for at least eight months. However, she still did not become pregnant during the following year. This case shows how endometriosis can cause pain and infertility, and how surgery plus medication can help manage the condition, although pregnancy may still be difficult.",
+            "B3": "Background  \nThis case involves a 35-year-old woman from northern Tanzania who has never given birth (nulliparous) and has experienced infertility for 10 years. She presented with a three-year history of cyclic, dull pain centered around the navel, accompanied by a firm, hyperpigmented umbilical mass that bled during menstruation. Her menstrual history included painful periods (dysmenorrhea), heavy bleeding (menorrhagia), and painful intercourse (dyspareunia). She had a copper intrauterine device (IUD) inserted three years prior and had recently used combined oral contraceptives containing levonorgestrel and ethinylestradiol to manage her symptoms. Her menstrual cycles were regular, and there were no significant medical, surgical, or social histories.\n\nKey Findings  \nImaging with abdominal magnetic resonance imaging (MRI) revealed a poorly defined mass measuring 3 × 4 × 6 cm along the right anterior abdominal wall. This mass was connected to a sinus tract extending toward the suprapubic region but did not communicate with the peritoneal cavity. These features suggested the presence of endometriosis (growth of endometrial tissue outside the uterus). Additionally, bilateral ovarian lesions were identified, showing hyperintense signals with focal hypointense areas and variable diffusion restrictions, consistent with bilateral ovarian endometriomas (cysts formed by endometriosis in the ovaries).\n\nClinical Interpretation  \nThe patient underwent surgical excision of the umbilical mass. Histopathological examination of the tissue confirmed primary umbilical endometriosis, characterized by normal epidermis with scattered endometrial glands and stroma (connective tissue) within the dermis. Postoperative recovery was uneventful, and the patient was discharged on the second day after surgery. She received counseling regarding her fertility prospects, including the option of in vitro fertilization (IVF), and was informed about the risk of disease recurrence. Medical management was initiated with dienogest (a progestin used to treat endometriosis), Visanne (a brand name for dienogest), and combined oral contraceptives to suppress endometriosis activity. Follow-up visits every four weeks over eight months showed no signs of local recurrence.\n\nNext Steps  \nDespite stable disease control following surgery and medical therapy, the patient did not conceive within the subsequent year. Continued monitoring and fertility support, including assisted reproductive technologies, remain important considerations given her history of infertility and endometriosis. Further evaluation and multidisciplinary management may be necessary to optimize her reproductive outcomes."
+        }
+    },
+    {
+        "article": "Presentamos a un recién nacido de 15 minutos de edad, hijo de una madre para-cuatro que no recordaba su LNMP pero que afirmaba haber estado amenorreica durante los últimos nueve meses. Su madre había recibido atención prenatal en el centro de salud cercano dos veces y no había tenido incidentes. Sin embargo, no se le había realizado un ultrasonido obstétrico temprano. Por lo demás, no tiene antecedentes de enfermedades crónicas como diabetes mellitus e hipertensión. Durante su embarazo actual, no tuvo fiebre, dolor de cabeza o visión borrosa. Nunca había usado ninguna droga aparte de sulfato ferroso durante este embarazo. Sus hijos anteriores están todos sanos y vivos. A su llegada a nuestro hospital, tuvo una hemorragia vaginal de dos horas de duración. Posteriormente, fue admitida con un diagnóstico de embarazo de tercer trimestre más multigravida más hemorragia anteparto secundaria a desprendimiento de placenta más oligohidramnios severo más presentación de nalgas.\n\nEn el examen pélvico, tenía un sangrado vaginal activo. Se le realizó una ecografía obstétrica al llegar. En consecuencia, la edad gestacional era de 34 semanas, la placenta estaba en el fondo con un coágulo retroplacentario y el líquido amniótico había disminuido significativamente con un único bolsillo más profundo de 1,5 cm. El peso fetal estimado era de 2,4 kg y presentación de nalgas. Otras investigaciones de la madre son grupo sanguíneo AB+, VDRL=negativo, RBS=120 mg/dL, en CBC, glóbulos blancos=9000, hemoglobina=11 gm/dL, plaqueta=180,000 y neutrófilo=60%.\n\nTras obtener el consentimiento informado por escrito, se realizó una cesárea de urgencia por las indicaciones ya mencionadas para extraer un neonato vivo de 2,01 kg de peso con puntuaciones de 5 y 6 en las pruebas de Apgar en el primer y el quinto minuto, respectivamente.\n\nEl neonato no lloró y fue reanimado durante cinco minutos. Luego fue trasladado a la unidad de cuidados intensivos neonatales para recibir atención e investigaciones adicionales. Al llegar, el neonato estaba en dificultad respiratoria. Sus signos vitales eran de 160 latidos por minuto, 70 respiraciones por minuto, temperatura de 33,4 grados centígrados y saturación de oxígeno del 60%. La fontanela anterior del neonato medía 2 cm por 2 cm y tenía micrognatia y cuello corto. En el sistema respiratorio, había retracciones intercostales y subcostales, respiración trabajosa y gruñidos. En el examen precordial, se escucharon bien los sonidos s1 y s2, no había murmullo ni ritmo de galope. En el sistema musculoesquelético, había acortamiento bilateral de las extremidades superiores, la extremidad inferior derecha estaba normal en posición y estructura, la pierna izquierda giraba hacia adentro (flexión mediolateral) en la articulación de la rodilla y la estructura del pie era normal. En el examen neurológico, estaba letárgico, el tono era normotónico en la extremidad inferior derecha y el reflejo de Moro era difícil de evaluar. La investigación de laboratorio mostró grupo sanguíneo = A+, CRP = reactivo, WBC = 30,000, neutrófilos = 54%, linfocitos = 21.1%, HGB = 8 gm/dL y plaquetas = 150,000. Se realizó una radiografía que mostró un acortamiento extremo de las extremidades superiores. La extremidad inferior izquierda estaba internamente girada. La ecocardiografía fue normal. Con una evaluación de prematuro tardío (34-36 semanas por puntaje de Ballard) más bajo peso al nacer más apropiado para la edad gestacional más focomelia más asfixia perinatal más sepsis neonatal temprana, se manejó con apoyo de oxígeno, fluido de mantenimiento e antibióticos intravenosos. El neonato murió después de tres días de hospitalización.\n",
+        "gold_summary": "Presentamos a un neonato de 15 minutos de vida, hijo de una madre para-cuatro que no recordaba su LNMP pero que afirmaba estar amenorreica desde hacía nueve meses. El modo de parto fue por cesárea para extraer al neonato vivo, que pesaba 2,01 kg y tenía puntuaciones APGAR de 5 y 6 en el primer y quinto minutos, respectivamente. El neonato no lloró y fue reanimado durante cinco minutos. Después se lo trasladó a la unidad de cuidados intensivos neonatales para continuar con el tratamiento y las investigaciones. Sus signos vitales eran: pulso de 160 latidos por minuto, frecuencia respiratoria de 70 respiraciones por minuto, temperatura de 33,4 grados centígrados y saturación de oxígeno del 60%. La fontanela anterior del neonato medía 2 cm por 2 cm y tenía micrognatia y cuello corto. En el sistema respiratorio había retracciones intercostales y subcostales, respiración trabajosa y gruñidos. En el sistema musculoesquelético había acortamiento bilateral de la extremidad superior, la pierna derecha tenía una posición y estructura normales, la pierna izquierda giraba hacia adentro (se doblaba hacia la parte media) en la articulación de la rodilla y el pie tenía una estructura normal.\n",
+        "synthetic_summary": {
+            "B1": "A baby was born by a special surgery. The baby was very small and did not cry at first. The doctors helped the baby breathe for five minutes.\n\nThe baby went to a special room to get more help. The baby’s heart beat fast and breathing was hard. The baby’s body was cold and needed more air.\n\nThe baby’s head was soft and the neck was short. The baby’s arms were shorter than usual. One leg was normal, but the other leg turned inward. The feet looked normal.",
+            "B2": "**What Happened at Birth**\n\nA baby boy was born by cesarean section after 34 weeks of pregnancy. He weighed 2.01 kilograms (about 4.4 pounds). Right after birth, his Apgar scores were 5 and 6 at one and five minutes. (Apgar scores are quick tests that check how well a baby is doing after birth, with higher numbers meaning better health.) The baby did not cry at first and needed help to start breathing. He was resuscitated for five minutes and then taken to the neonatal intensive care unit (NICU) for special care.\n\n**Health Condition After Birth**\n\nIn the NICU, the baby had a fast heartbeat (160 beats per minute) and was breathing very quickly (70 breaths per minute). His body temperature was low at 33.4°C (normal is about 36.5–37.5°C), and his oxygen level was low at 60% (normal is above 90%). The soft spot on his head (called the anterior fontanelle) measured 2 cm by 2 cm. He had a small lower jaw (micrognathia) and a short neck.\n\n**Breathing and Muscle Issues**\n\nThe baby showed signs of breathing difficulty, such as pulling in the skin between and below his ribs (called intercostal and subcostal retractions), working hard to breathe, and making grunting sounds. His arms were unusually short on both sides. His right leg looked normal, but his left leg was turned inward at the knee joint. His left foot looked normal.\n\n**Summary**\n\nThis newborn had several serious health problems, including trouble breathing, unusual limb development, and low oxygen levels. He needed urgent medical care in the NICU to try to support his breathing and overall health.",
+            "B3": "**Background**  \nA newborn infant, only 15 minutes old, was delivered by emergency cesarean section due to complications during the third trimester of pregnancy. The mother, a para-four (having had four previous pregnancies), was uncertain of her last menstrual period but reported amenorrhea (absence of menstruation) for nine months. The pregnancy was complicated by severe oligohydramnios (low amniotic fluid), placental abruption (premature separation of the placenta), and breech presentation. The infant weighed 2.01 kilograms at birth and had Apgar scores of 5 and 6 at one and five minutes, respectively. The newborn did not cry spontaneously and required five minutes of resuscitation before being transferred to the neonatal intensive care unit (NICU) for further management and evaluation.\n\n**Key Findings**  \nUpon admission to the NICU, the newborn exhibited significant respiratory distress characterized by a rapid heart rate of 160 beats per minute, a high respiratory rate of 70 breaths per minute, low body temperature (33.4°C), and critically low oxygen saturation at 60%. Physical examination revealed an anterior fontanelle (soft spot on the head) measuring 2 cm by 2 cm, micrognathia (an abnormally small lower jaw), and a short neck. Respiratory signs included intercostal and subcostal retractions (inward movements of the muscles between and below the ribs), labored breathing, and grunting sounds, indicating difficulty in breathing.\n\nMusculoskeletal abnormalities were prominent: there was bilateral shortening of the upper limbs, while the right lower limb appeared normal in both position and structure. The left lower limb was internally rotated at the knee joint (flexion mediolateral), although the foot maintained a normal structure. Neurologically, the infant was lethargic with normal muscle tone in the right lower limb; however, the Moro reflex (a startle reflex) was difficult to assess.\n\n**Clinical Interpretation**  \nThe newborn’s presentation is consistent with a late preterm infant (gestational age estimated between 34 and 36 weeks) complicated by multiple serious conditions: low birth weight appropriate for gestational age, phocomelia (severe shortening of the limbs), perinatal asphyxia (oxygen deprivation around the time of birth), and early-onset neonatal sepsis (a systemic infection). The respiratory distress and musculoskeletal abnormalities suggest significant congenital and perinatal challenges. Laboratory findings supported infection and anemia, with elevated white blood cell count and reactive C-reactive protein, hemoglobin of 8 g/dL, and moderate thrombocytopenia (low platelet count).\n\n**Next Steps**  \nThe infant was managed with supportive oxygen therapy, intravenous fluids, and antibiotics to address sepsis. Despite these interventions, the newborn’s condition deteriorated, and the infant died after three days of hospitalization. This case highlights the critical importance of early prenatal care, including ultrasound evaluation, and the challenges posed by severe obstetric complications and congenital anomalies in neonatal outcomes."
+        }
+    },
+    {
+        "article": "Mujer de 61 años con antecedente de carcinoma escamocelular de cuello uterino estadio FIGO IIB, diagnosticado en febrero de 2019, tratada en un hospital privado de cuarto nivel de atención, donde se ofrece cuidado ambulatorio y hospitalario para pacientes con condiciones complejas oncológicas y no oncológicas. Al momento del diagnóstico se realizó histerectomía radical con linfadenectomía pélvica, que descartó compromiso nodal. El tratamiento complementario de primera línea incluyó seis ciclos de quimioterapia con cisplatino, y braquiterapia y radioterapia, alcanzando una respuesta tumoral completa. En 2021, tras detectarse una recaída aislada en la región ilíaca, mediante tomografía, se administró cisplatino y 30 sesiones de radioterapia, logrando una nueva respuesta completa. En septiembre de 2022, una tomografía reveló otra recaída con compromiso del parametrio izquierdo, el uréter y la cadena ilíaca ipsilateral, por lo que se decidió primera línea para enfermedad recurrente con carboplatino, paclitaxel y pembrolizumab. Durante este régimen, la paciente presentó hipersensibilidad al platino en el quinto ciclo, gestionada con un protocolo de desensibilización, continuando con el pembrolizumab. En septiembre de 2023, ante la progresión en imágenes de una masa retroperitoneal única, debido a la falta de respuesta óptima, se inició gemcitabina, según guías de manejo, segunda línea de enfermedad recurrente, recibiendo una dosis acumulada de 8.544 mg/m2 hasta enero de 2024. Sin embargo, desarrolló síntomas de isquemia digital en manos, por lo que el tratamiento fue suspendido tras la segunda dosis del tercer ciclo, acumulando 11.744 mg/m2 de gemcitabina.\n\nEn febrero de 2024, la paciente ingresó al servicio de urgencias del mismo hospital donde era valorada de forma ambulatoria, remitida por oncología debido a progresión de los síntomas en sus extremidades. La paciente refería dolor lancinante y coloración azulada en dedos de manos; al examen físico se evidencia necrosis en el segundo dedo de la mano derecha, coloración ocre y fenómeno de Raynaud en los dedos de la mano izquierda. Las extremidades inferiores mostraban edema grado II en el miembro inferior izquierdo y pulsos presentes. Los estudios para autoinmunidad y vasculitis resultaron negativos, incluyendo anticuerpos anticitoplasma de neutrófilos (ANCAS), anticuerpos antinucleares (ANAS), anticuerpos antidesoxirribonucleicos (anti-DNA), cardiolipinas, prueba confirmatoria de anticoagulante lúpico, perfil de anticuerpos contra antígenos nucleares extraíbles (ENAS), anticuerpos contra proteinasa 3, anticuerpos antimieloperoxidasa y anticuerpos dirigidos contra la ADN topoisomerasa I (antiSCL). Además, el factor reumatoide y los niveles de complemento 3 (C3) y complemento 4 (C4) también fueron normales. Prueba serológica para sífilis (VDRL - Venereal Disease Research Laboratory) negativa, ecocardiograma transtorácico sin hallazgos de un foco cardioembólico.\n\nSe inició anticoagulación con heparina de bajo peso molecular, junto con ácido acetilsalicílico, estatina y un calcioantagonista. El equipo de cirugía de mano realizó amputación del segundo dedo de la mano derecha, confirmando necrosis por licuefacción en el estudio histopatológico.\n\nDurante el posoperatorio se agregó sildenafil al tratamiento, logrando una mejoría progresiva en los signos de isquemia de los dedos restantes. Durante la hospitalización, la paciente presenta complicación por sangrado vaginal masivo, requiriendo embolización de arterias uterinas.\n\nEl servicio de reumatología aplicó la escala de causalidad de Naranjo para determinar el papel de la gemcitabina en la vasculitis, con un puntaje de 8, lo que indicó que el medicamento probablemente provocó la necrosis.\n\nPosteriormente, a los 20 días de ingreso a hospitalización desarrolló deterioro neurológico, sin hallazgos significativos en la tomografía de cráneo. Evaluada por cuidados paliativos, su estado funcional se clasificó con un Barthel de 0/30, ECOG de 4 y Karnofsky de 10 %, con pronóstico de vida inferior a tres semanas según el Índice Pronóstico de Paciente (PPI: + 6 puntos). En consenso con la familia, se suspendieron estudios adicionales y se implementó un manejo paliativo integral. La paciente falleció tras el alta hospitalaria.",
+        "gold_summary": "Oaciente de 61 años tratada con gemcitabina (11.744 mg/m² acumulados) por enfermedad metastásica, en un hospital general de cuarto nivel, privado, no oncológico, donde venía siendo manejada de forma ambulatoria. Presentó necrosis distal del segundo dedo de la mano derecha, por lo que se suspendió el tratamiento y se requirió amputación de este dedo. Se realizó una búsqueda en Embase, Medline y Lilacs. Se buscaron estudios de reporte y series de casos sobre necrosis distal inducida por gemcitabina. Se extrajeron datos de dosis, diagnóstico y tratamiento.",
+        "synthetic_summary": {
+            "B1": "A lady was very sick and took strong medicine. The medicine made her finger hurt and turn bad. The doctors had to take off her finger to help her feel better. They looked for stories about this problem to learn more.",
+            "B2": "**Patient Background and Treatment**\n\nA 61-year-old woman was being treated with a cancer drug called gemcitabine. This medicine was given because her cancer had spread to other parts of her body. She received a total dose of 11,744 mg per square meter of her body size. She was cared for at a private hospital that handles complex medical cases but is not specialized only in cancer.\n\n**What Happened**\n\nDuring her treatment, she developed a serious problem in her right hand. The tip of her second finger (the index finger) started to die, a condition called necrosis. Because of this, doctors stopped the gemcitabine treatment and had to remove (amputate) that finger to prevent the problem from getting worse.\n\n**Research and Findings**\n\nDoctors looked through medical research databases to find other cases where gemcitabine caused similar finger tissue death. They searched for reports and case studies to understand how often this happens, what doses are involved, and how it can be treated.\n\n**Summary**\n\nThis case shows that gemcitabine, while used to fight cancer, can sometimes cause serious side effects like tissue death in fingers. Recognizing these symptoms early is important so doctors can stop the medicine and take action to protect the patient’s health.",
+            "B3": "**Background**  \nA 61-year-old woman with metastatic cancer was receiving gemcitabine chemotherapy at a cumulative dose of 11,744 mg/m². She was being treated on an outpatient basis at a private, fourth-level general hospital without a specialized oncology department.\n\n**Key Clinical Findings**  \nDuring treatment, the patient developed distal necrosis of the second finger on her right hand. This severe tissue damage necessitated discontinuation of gemcitabine and surgical amputation of the affected finger. Diagnostic evaluations excluded autoimmune and vasculitic causes, and other potential contributors such as infectious or cardioembolic sources were ruled out.\n\n**Clinical Interpretation**  \nThe temporal relationship between gemcitabine administration and the onset of digital necrosis, supported by a Naranjo causality score of 8, strongly suggests that gemcitabine was the probable cause of this adverse vascular event. This case highlights a rare but serious complication of gemcitabine therapy involving ischemic necrosis of peripheral digits.\n\n**Literature Review**  \nA comprehensive search was conducted in medical databases including Embase, Medline, and Lilacs to identify case reports and series documenting gemcitabine-induced distal necrosis. Relevant data were extracted regarding cumulative doses, clinical presentation, and management strategies.\n\n**Next Steps and Recommendations**  \nClinicians should maintain vigilance for signs of digital ischemia in patients receiving gemcitabine, especially at higher cumulative doses. Early recognition and prompt discontinuation of the drug are critical to prevent progression to irreversible tissue damage. Multidisciplinary management, including surgical intervention and supportive therapies, may be required to address complications. Further research is needed to better understand the pathophysiology and optimal treatment of gemcitabine-associated vascular toxicity."
+        }
+    },
+    {
+        "article": "Mujer de 53 años, con antecedente de AR de 15 años de diagnóstico en tratamiento con metotrexato, resto de antecedentes sin datos de importancia, la cual presentó cuadro clínico 8 meses antes (de acudir a nuestro servicio) con astenia y adinamia de forma progresiva, palidez de tegumentos, alzas térmicas no cuantificadas de predominio nocturno, pérdida de peso no intencionada de 15 kg en 6 meses aproximadamente, sin valoración ni seguimiento médico, a lo que se agregó 3 meses después disnea de grandes a medianos esfuerzos, y cuya sintomatología se agudizó 5 días antes (de acudir a nuestro servicio), aunada a sangrado de tubo digestivo alto (STDA), caracterizado por evacuaciones melénicas abundantes, 3 evacuaciones en 24 horas, hematemesis en 2 ocasiones, escasas, sin causa aparente. La paciente negó consumo de analgésicos no esteroideos (AINE) y tuvo aumento de volumen en la pierna izquierda, la cual le dolía y tenía la presencia de edema y eritema, con limitación a la movilidad, motivo por el cual acudió a (nuestro) Servicio de Urgencias.\n\nDurante su hospitalización con anemia severa sin repercusión hemodinámica, se transfundieron 3 concentrados eritrocitarios sin complicaciones aparentes. Después de su estabilización, se inició abordaje diagnóstico para síndrome consuntivo. Por el cuadro clínico de miembro inferior izquierdo se hizo US Doppler que evidenció trombosis venosa profunda. Se realizó ultrasonido de abdomen por probable hepatopatía por metotrexato, el cual reportó infartos esplénicos y hepáticos, así como presencia de cambios crónicos hepáticos. Se llevó a cabo endoscopía con evidencia de varices pequeñas, sin sangrado activo. Debido a la sospecha de neoplasia por los antecedentes y el cuadro clínico de la paciente, se llevó a cabo tomografía axial simple y contrastada de tórax y abdomen y se encontró hepatoesplenomegalia y múltiples conglomerados ganglionares axilares, mediastinales y paraaórticos que sugerían actividad infiltrativa. Esto se valoró por el Servicio de Cirugía General para la realización de biopsia de ganglio axilar derecho, donde se reportó proliferación neoplásica de células linfoides. Posteriormente se valoró por el Servicio de Hematología de la unidad, se solicitaron estudios de laboratorio (cuadro I) y se realizó aspirado de médula ósea en el que se evidenciaron células plasmáticas displásicas y células reticulares, por lo cual se concluyó que había la presencia de infiltración linfoplasmocitaria. Con los antecedentes, el cuadro clínico y los estudios complementarios se diagnosticó LNH estadio IV y la paciente fue enviada a hospital de tercer nivel para realización de inmunohistoquímica, estadificación e inicio de tratamiento. En tercer nivel se identificó linfoma difuso de células B con inmunofenotipo B CD20 con sobrecrecimiento de células dendríticas, y la paciente fue valorada para inicio de tratamiento con quimioterapia.",
+        "gold_summary": "Mujer de 55 años con antecedente de AR que ingresó a un servicio de medicina interna por sangrado de tubo digestivo; presentó datos clínicos de trombosis venosa profunda en miembro pélvico izquierdo y síndrome consuntivo en estudio. Durante su abordaje se identificó con infartos esplénicos y hepáticos, así como múltiples conglomerados ganglionares, por lo que se practicó biopsia de ganglio axilar que reportó proliferación neoplásica de células linfoides y aspirado de médula ósea con presencia de infiltración linfoplasmocitaria, con lo que se determinó diagnóstico de linfoma no Hodgkin estadio IV. La paciente fue enviada a un hospital de tercer nivel para inicio de tratamiento.",
+        "synthetic_summary": {
+            "B1": "A lady who is 55 years old felt very tired and sick. She had bleeding inside her tummy. Her left leg was swollen and hurt. Doctors found a big problem with her blood in her leg.\n\nThey did many tests and found some parts inside her body were not working well. They took a tiny piece from her body to look at it closely. They found some bad cells that made her sick.\n\nThe doctors said she has a kind of sickness called lymphoma. She went to a special hospital to get medicine to help her feel better.",
+            "B2": "**What Happened to the Patient**\n\nA 55-year-old woman with a history of rheumatoid arthritis (a disease that causes joint inflammation) came to the hospital because she was bleeding from her digestive tract. She also showed signs of a blood clot in a vein of her left leg and had symptoms like extreme tiredness and weight loss, which doctors call a \"consumption syndrome.\"\n\n**What the Doctors Found**\n\nDuring her tests, doctors discovered she had small areas of tissue death (called infarcts) in her spleen and liver. They also found many swollen lymph nodes, which are small glands that help fight infections. To learn more, they took a biopsy, which means removing a small piece of a lymph node from her armpit to look at under a microscope. This showed an abnormal growth of certain immune cells called lymphoid cells. They also took a sample from her bone marrow (the soft tissue inside bones that makes blood cells) and found that it was invaded by unusual immune cells.\n\n**What It Means**\n\nAll these findings led doctors to diagnose her with stage IV non-Hodgkin lymphoma. This is a type of cancer that starts in the lymphatic system, which is part of the body's defense system. Stage IV means the cancer has spread to many parts of the body. Because of this, she was sent to a specialized hospital to get more tests and begin treatment, which usually involves chemotherapy to fight the cancer cells.",
+            "B3": "Background  \nA 53-year-old woman with a 15-year history of rheumatoid arthritis (RA) treated with methotrexate presented with a progressively worsening clinical picture over eight months. Her symptoms included increasing fatigue and weakness, pale skin, intermittent low-grade fevers mainly at night, and an unintentional weight loss of approximately 15 kilograms over six months. Three months into this course, she developed shortness of breath on moderate to heavy exertion. Five days before hospital admission, her symptoms worsened, accompanied by upper gastrointestinal bleeding characterized by multiple black, tarry stools (melena) and two episodes of vomiting blood (hematemesis). She denied use of nonsteroidal anti-inflammatory drugs (NSAIDs). Additionally, she experienced swelling, pain, redness, and limited movement in her left leg.\n\nKey Findings  \nUpon hospital admission, the patient was found to have severe anemia requiring transfusion of three units of red blood cells without complications. Diagnostic evaluation for a wasting syndrome (syndrome consuntivo) was initiated. Doppler ultrasound of the left lower limb revealed deep vein thrombosis (DVT). Abdominal ultrasound, performed due to concern for liver disease related to methotrexate use, showed multiple infarctions (areas of tissue death due to lack of blood supply) in the spleen and liver, along with chronic liver changes. Upper endoscopy identified small esophageal varices without active bleeding. Computed tomography (CT) scans of the chest and abdomen demonstrated enlargement of the liver and spleen (hepatoesplenomegaly) and multiple enlarged lymph node clusters in the axillary (armpit), mediastinal (central chest), and para-aortic (near the aorta) regions, suggestive of infiltrative disease.\n\nA biopsy of a right axillary lymph node revealed neoplastic proliferation of lymphoid cells. Bone marrow aspiration showed infiltration by abnormal plasma cells and reticular cells, indicating lymphoplasmacytic infiltration. These findings, combined with the clinical presentation and imaging, led to a diagnosis of stage IV non-Hodgkin lymphoma (NHL).\n\nClinical Interpretation  \nThe patient’s longstanding RA and immunosuppressive therapy likely contributed to the development of an aggressive lymphoid malignancy. The presence of deep vein thrombosis, multiple organ infarctions, and widespread lymphadenopathy reflect extensive disease involvement. Stage IV NHL indicates disseminated lymphoma with bone marrow involvement, requiring prompt specialized treatment.\n\nNext Steps  \nThe patient was referred to a tertiary care center for further immunohistochemical studies to precisely classify the lymphoma subtype. At the specialized center, the diagnosis was refined to diffuse large B-cell lymphoma (DLBCL) with CD20-positive immunophenotype and dendritic cell proliferation. She was evaluated for initiation of chemotherapy tailored to this aggressive lymphoma subtype. Close monitoring and multidisciplinary management are essential to address both the malignancy and associated complications such as thrombosis and organ infarctions."
+        }
+    },
+    {
+        "article": "Un hombre de 56 años se presentó en el departamento de urgencias de nuestro hospital debido a una falta de aire repentina y un episodio de síncope mientras caminaba dentro de su casa. Se sometió a una prostatectomía laparoscópica asistida por robot para el carcinoma de próstata, 5 días antes de su presentación en el departamento de urgencias. Su curso postoperatorio en el hospital fue sin incidentes. En el departamento de urgencias, su presión arterial era de 94/54 mmHg, frecuencia cardiaca de 121 latidos por minuto, frecuencia respiratoria de 20 respiraciones por minuto, no tenía fiebre y su saturación de oxígeno era de 92% con 6 L por minuto de oxígeno a través de una cánula nasal. El examen cardiaco reveló S1S2, regular, taquicardia, sin murmullos/galopes/ruidos respiratorios. El examen respiratorio reveló ruidos respiratorios vesiculares normales bilaterales. Se observó que tenía edema de extremidad inferior izquierdo asimétrico. El electrocardiograma (ECG) reveló taquicardia sinusal, sin cambios en la onda ST-T. La troponina estaba levemente elevada a 0.120 ng/mL (rango de referencia: 0 a 0.020). La angiografía por tomografía computarizada (CTA) del tórax mostró embolia pulmonar bilateral extensa, con una gran carga de coágulos en ambas arterias pulmonares principales, evidencia de insuficiencia ventricular derecha aguda. El examen dúplex venoso mostró trombosis venosa profunda izquierda aguda. El ecocardiograma mostró fracción de eyección ventricular izquierda normal del 60% al 65%, movimiento septal anormal y aplanamiento del tabique interventricular, presión sistólica ventricular derecha de 49.7 mmHg, ventrículo derecho moderadamente dilatado, función ventricular derecha disminuida, excursión sistólica tricuspídea de 12.1 mm (normal 15 a 20 mm). Como la mayoría de la carga de coágulos era distal, no se consideró susceptible de extracción quirúrgica, ya que la cirugía reciente era una contraindicación importante para la trombólisis. El paciente comenzó con un goteo de heparina e inhaló óxido nítrico a 20 ppm junto con 40 mg de sildenafil oral cada 8 horas. Al día siguiente, el paciente estaba hemodinámicamente estable y su óxido nítrico inhalado se redujo. Repetir el ecocardiograma 48 horas desde la presentación inicial mostró un tamaño y función del ventrículo derecho mejorados. Su presión sistólica ventricular derecha disminuyó a 22.4 mmHg y su excursión sistólica tricuspídea mejoró a 17.8 mm. Recomendamos que continuara con sildenafil durante el mes siguiente después del alta junto con anticoagulación oral con un plan de seguimiento como paciente ambulatorio. El paciente dio su consentimiento por escrito para el tratamiento durante su hospitalización. El paciente y sus familiares estaban bien informados sobre el plan de atención completo y estuvieron de acuerdo con el plan de atención.\n\nMH - Insuficiencia cardiaca/*terapia farmacológica/etiología\nMH - Humanos\nMH - Hombre\nMH - Edad Media\nMH - Inhibidores de la fosfodiesterasa 5/*uso terapéutico\nMH - Embolismo pulmonar/*complicaciones\nMH - Agentes vasodilatadores/*uso terapéutico\nMH - Disfunción ventricular, derecha/terapia/etiología\n",
+        "gold_summary": "Paciente: Hombre, 56 años\n\nDiagnóstico final: Insuficiencia cardíaca derecha por embolia pulmonar\n\nSíntomas: síncope\n\nMedicación: —\n\nProcedimiento clínico: —\n\nEspecialidad: Cardiología\n\nSe trata de un informe de caso en el que se utilizó sildenafil como agente de rescate para lograr una mejora en el tamaño y la función del ventrículo derecho en un caso de inicio agudo de embolia pulmonar masiva con insuficiencia aguda del ventrículo derecho en el escenario en el que la terapia trombolítica sistémica estaba contraindicada.\n",
+        "synthetic_summary": {
+            "B1": "A man felt very tired and faint while walking. He had a problem with his heart because some blood clots blocked his lungs. The doctors gave him special medicine to help his heart work better. After the medicine, his heart got stronger and he started to feel better. The doctors will keep helping him so he stays healthy.",
+            "B2": "**What Happened to the Patient**  \nA 56-year-old man suddenly had trouble breathing and fainted while walking at home. He had surgery to remove his prostate because of cancer just five days before. After surgery, he seemed fine until these new problems started.\n\n**What the Doctors Found**  \nAt the hospital, tests showed he had a large blood clot blocking both of his main lung arteries. This condition is called a pulmonary embolism. Because of the clot, the right side of his heart was struggling and not working well. He also had swelling in his left leg, which was caused by a deep vein blood clot.\n\n**How They Treated Him**  \nThe usual treatment to break up clots with strong medicine was not safe because he had just had surgery. Instead, doctors gave him a medicine called sildenafil (often used for other heart and lung problems) and a gas called nitric oxide to help his heart and lungs work better. They also gave him blood thinners to prevent more clots.\n\n**What This Means**  \nUsing sildenafil helped improve the size and function of the right side of his heart. This case shows that sildenafil can be a helpful treatment when usual clot-busting medicines can’t be used. The patient got better and was planned to continue sildenafil and blood thinners after leaving the hospital.\n\n**Summary**  \nThis man had a serious lung clot that hurt his heart. Because surgery made some treatments risky, doctors used sildenafil to help his heart recover. This approach worked well and improved his heart function.",
+            "B3": "**Background**  \nA 56-year-old man presented to the emergency department with sudden shortness of breath and a fainting episode (syncope) while walking at home. Notably, he had undergone a robot-assisted laparoscopic prostatectomy for prostate cancer five days prior, with an initially uneventful postoperative course. Upon arrival, his vital signs showed low blood pressure (94/54 mmHg), rapid heart rate (121 beats per minute), normal respiratory rate (20 breaths per minute), and reduced oxygen saturation (92%) despite supplemental oxygen. Physical examination revealed an irregular swelling (edema) in his left lower limb.  \n\n**Key Findings**  \n- Electrocardiogram (ECG) demonstrated sinus tachycardia without ischemic changes.  \n- Troponin levels were mildly elevated (0.120 ng/mL; normal <0.020 ng/mL), indicating some cardiac stress or injury.  \n- Computed tomography angiography (CTA) of the chest revealed extensive bilateral pulmonary embolism (blood clots in both main pulmonary arteries) causing acute right ventricular (RV) failure.  \n- Venous duplex ultrasound confirmed acute deep vein thrombosis (DVT) in the left leg.  \n- Echocardiogram showed normal left ventricular function (ejection fraction 60–65%) but abnormal septal motion and flattening of the interventricular septum, signs of right ventricular strain. The right ventricle was moderately enlarged with reduced function, elevated right ventricular systolic pressure (49.7 mmHg), and decreased tricuspid annular plane systolic excursion (TAPSE) of 12.1 mm (normal range 15–20 mm), indicating impaired RV contraction.  \n\n**Clinical Interpretation**  \nThis patient developed acute right heart failure secondary to a massive pulmonary embolism shortly after surgery. Due to the recent prostatectomy, systemic thrombolysis (clot-dissolving therapy) was contraindicated because of bleeding risk. Surgical removal of clots was also deemed unsuitable because most clots were located distally in the pulmonary arteries.  \n\n**Treatment and Outcome**  \nThe patient was started on intravenous heparin for anticoagulation, inhaled nitric oxide (a pulmonary vasodilator) at 20 parts per million to reduce pulmonary artery pressure, and oral sildenafil (a phosphodiesterase-5 inhibitor that dilates blood vessels) at 40 mg every eight hours as a rescue therapy to improve right ventricular function. After one day, hemodynamic stability improved, allowing reduction of inhaled nitric oxide. A repeat echocardiogram 48 hours later showed significant improvement in right ventricular size and function: systolic pressure decreased to 22.4 mmHg, and TAPSE improved to 17.8 mm.  \n\n**Next Steps**  \nThe patient was discharged with a plan to continue sildenafil for one month alongside oral anticoagulation. Close outpatient follow-up was arranged to monitor cardiac function and manage anticoagulation therapy. The patient and his family were fully informed and consented to the treatment plan.  \n\n**Summary**  \nThis case illustrates the successful use of sildenafil as an adjunctive therapy to improve right ventricular function in acute massive pulmonary embolism complicated by right heart failure, particularly when thrombolytic therapy is contraindicated due to recent surgery. The combined approach with anticoagulation and pulmonary vasodilators contributed to clinical stabilization and cardiac recovery."
+        }
+    },
+    {
+        "article": "Presentamos el caso de un hombre de 78 años con antecedentes conocidos de fibrilación auricular crónica, cardiopatía hipertensiva y miocardiopatía no isquémica. Tenía una reducción global de la fracción de eyección del ventrículo izquierdo del 40-45 %, y su ecocardiograma no mostraba anomalías significativas. El paciente había sido seguido en la clínica de cardiología ambulatoria, donde fue tratado por insuficiencia cardiaca crónica en estadio C del Colegio Americano de Cardiología (ACC) con síntomas de clase III de la Asociación del Corazón de Nueva York (NYHA). A pesar de varios cambios en sus diuréticos e intentos de controlar su estado de líquidos, ganó 40 libras de peso en un período de 3 meses, con un aumento significativo de la falta de aire. A medida que su descompensación de la insuficiencia cardiaca progresó, fue hospitalizado durante 8 días y tratado con furosemida intravenosa (IV). Debido a su clasificación de la NYHA y su ingreso al hospital por exacerbación de la insuficiencia cardiaca, se indicó y se realizó un monitoreo hemodinámico invasivo con implantación de CardioMEMS. La implantación de su CardioMEMS se realizó en Grand Blanc, Michigan, a una altitud de 837 pies con una presión atmosférica de 731.2 el 9 de abril de 2019. Las mediciones hemodinámicas iniciales del cateterismo cardiaco mostraron una presión sistólica PA de 45 mmHg, presión diastólica PA de 16 mmHg y una presión PA media de 30 mmHg. La presión auricular derecha fue de 21 mmHg, presión ventricular derecha de 44/17 mmHg y la presión media de la cuña pulmonar fue de 24 mmHg. El procedimiento se completó sin complicaciones y el paciente fue dado de alta el mismo día.\n\nTras la implantación de CardioMEMS, el paciente permaneció estable durante 4 semanas sin empeoramiento de los síntomas de insuficiencia cardiaca. Cumplió con las lecturas diarias de CardioMEMS con una PA media que osciló entre 27 y 31 mmHg, y una presión diastólica de PA de 17 a 21 mmHg. Estos hallazgos hemodinámicos globales fueron estables en comparación con los del momento de la implantación.\n\nEl paciente viajó a Denver, Colorado, durante cuatro días a una altitud de 5280 pies con una presión atmosférica de 596.8 atm el 5 de mayo de 2019. Las grabaciones del primer día de su visita mostraron un aumento de la presión sistólica de 44 mmHg a 73 mmHg, un aumento de la presión media de 30 mmHg a 53 mmHg y un aumento de la presión diastólica de 20 mmHg a 40 mmHg. Al mismo tiempo, notó un aumento significativo de la falta de aire y la hinchazón de las extremidades inferiores. No buscó atención médica, sino que se contactó con su cardiólogo primario en Michigan. Su oxígeno nasal de referencia se incrementó de 1 litro a 2 litros y su dosis de furosemida se duplicó de 40 mg diarios a dos veces al día. Afortunadamente, este tratamiento mejoró los síntomas del paciente y evitó la admisión hospitalaria. Debido a que se evitó la admisión hospitalaria, no se dispuso de valores de laboratorio, imágenes de diagnóstico y signos vitales clínicos.\n\nDurante su estancia hospitalaria de 4 días, sus presiones invasivas se mantuvieron altas, pero disminuyeron lentamente y se estabilizaron con una PA sistólica de 72 mmHg, una PA media de 49 mmHg y una PA diastólica de 35 mmHg el día previo a su regreso a Michigan. El quinto día, volvió a Michigan y sus mediciones de presión invasiva se normalizaron rápidamente, con una presión PA media de 29 mmHg y una presión PA diastólica de 20 mmHg. Ha seguido estando bien mientras estuvo en Michigan con diuréticos de mantenimiento continuos y un control diario de las presiones PA con su dispositivo CardioMEMS.\n\nMH - Envejecido\nMH - *Altitud\nMH - Monitoreo de presión arterial, ambulatorio\nMH - *Insuficiencia cardiaca/diagnóstico/etiología\nMH - Hospitalización\nMH - Humanos\nMH - Hombre\nMH - Arteria Pulmonar\n",
+        "gold_summary": "Presentamos el caso de un hombre de 78 años con una exacerbación de la insuficiencia cardiaca mientras viajaba a gran altitud. Se detectó un aumento de sus presiones arteriales pulmonares (PA) mediante su dispositivo CardioMEMS implantado. La comprensión del cambio esperado en los registros de presión de la PA ayudó a identificar una verdadera exacerbación de la insuficiencia cardiaca en nuestro paciente. Esto llevó a un cambio rápido en la terapia médica, que en última instancia evitó la hospitalización.\n",
+        "synthetic_summary": {
+            "B1": "There was a man who was 78 years old. He had a heart problem. \n\nHe went to a place high up on a mountain. His heart had to work harder there. \n\nA small machine inside him showed his heart was having trouble. \n\nThe doctor saw this and gave him new medicine. \n\nThe medicine helped him feel better. He did not have to go to the hospital.",
+            "B2": "**What Happened:**  \nA 78-year-old man with heart failure traveled to a high-altitude place. He had a special device called CardioMEMS implanted in his chest. This device measures the pressure in the blood vessels of the lungs, called pulmonary artery pressure. When he went to a higher altitude, the device showed his lung blood pressure went up a lot.\n\n**What This Means:**  \nNormally, going to high places can raise lung blood pressure a bit. But in this man’s case, the increase was much bigger than expected. This showed that his heart failure was getting worse. Because doctors understood these pressure changes, they quickly changed his medicine.\n\n**What They Did:**  \nHis doctor increased his oxygen and medicine to help remove extra fluid from his body. This treatment helped him feel better and stopped him from needing to go to the hospital.\n\n**Why It’s Important:**  \nThis case shows how using a device like CardioMEMS can help monitor heart failure closely, especially when patients face challenges like traveling to high altitudes. It helps doctors catch problems early and treat them before they become emergencies.",
+            "B3": "Background  \nThis case involves a 78-year-old man with a history of chronic atrial fibrillation, hypertensive heart disease, and non-ischemic cardiomyopathy. His left ventricular ejection fraction—a measure of heart pumping efficiency—was reduced to 40-45%. He had been managed for chronic heart failure classified as stage C by the American College of Cardiology (ACC) and symptomatic at New York Heart Association (NYHA) class III. Despite outpatient treatment, including adjustments in diuretics to manage fluid overload, he experienced significant weight gain and worsening shortness of breath, culminating in an 8-day hospitalization where he received intravenous diuretics.\n\nKey Findings  \nGiven his advanced heart failure and recent hospitalization, a CardioMEMS device—a small implant that continuously monitors pulmonary artery (PA) pressures—was implanted to enable close hemodynamic monitoring. Initial invasive measurements at implantation showed elevated pulmonary artery pressures consistent with his heart failure status but were stable. Over the next four weeks, daily CardioMEMS readings remained stable, with mean PA pressures between 27 and 31 mmHg.\n\nThe patient then traveled to Denver, Colorado, at an altitude of 5,280 feet, where atmospheric pressure is lower. On the first day at this higher altitude, CardioMEMS recorded a marked increase in pulmonary artery pressures: systolic PA pressure rose from 44 mmHg to 73 mmHg, mean PA pressure from 30 mmHg to 53 mmHg, and diastolic PA pressure from 20 mmHg to 40 mmHg. Clinically, he developed significantly worsened shortness of breath and swelling in his legs. Without seeking immediate hospital care, he contacted his cardiologist remotely. His oxygen supplementation was increased, and his oral diuretic dose was doubled, which improved his symptoms and prevented hospitalization.\n\nDuring his hospital stay in Denver, invasive pressures remained elevated but gradually decreased. Upon returning to Michigan, his pulmonary artery pressures rapidly normalized to near baseline values. He continued stable outpatient management with maintenance diuretics and daily CardioMEMS monitoring.\n\nClinical Interpretation  \nThis case highlights the impact of high altitude on pulmonary artery pressures in a patient with advanced heart failure. The CardioMEMS device provided real-time, objective data that distinguished between expected physiological changes due to altitude and a true exacerbation of heart failure. Recognizing the abnormal rise in PA pressures enabled timely adjustment of medical therapy, preventing further clinical deterioration and hospitalization.\n\nNext Steps  \nContinued close monitoring with CardioMEMS is essential for this patient to detect early signs of decompensation. Patients with heart failure traveling to high altitudes should be counseled about potential risks, and clinicians should be aware of how altitude-related changes in pulmonary pressures may mimic or exacerbate heart failure symptoms. Prompt communication and adjustment of therapies based on hemodynamic data can improve outcomes and reduce hospital admissions."
+        }
+    },
+    {
+        "article": "Un hombre de 55 años, previamente sano, fue derivado al servicio de urgencias por su médico de cabecera, quejándose de una fiebre de 3 semanas de evolución, tos productiva, disnea y sibilancias. Tenía un historial de 80 paquetes-año de consumo de tabaco y un historial familiar positivo de cáncer de pulmón. Había sido tratado por su médico de cabecera con un ciclo de amoxicilina oral y prednisona oral, pero sus síntomas empeoraron. Cuando llegó al servicio de urgencias, su recuento de glóbulos blancos era de 16,4 × 109/L (rango normal: 4,0-10,0 × 109/L), el recuento de neutrófilos de 13,8 × 109/L (rango normal: 2,0-7,0 × 109/L), la proteína C reactiva era de 118 mg/L (normal: 0-5 mg/L) y el sodio sérico era de 112 mmol/L (rango normal: 136-145 mmol/L). Otros marcadores bioquímicos estaban dentro de los límites normales. Una radiografía de tórax mostró consolidación del lóbulo medio e inferior derecho con derrame pleural moderado asociado. Fue admitido y tratado como neumonía adquirida en la comunidad y el estudio confirmó el diagnóstico de SIADH.\n\nEl paciente empeoró a pesar de la administración intravenosa de piperacilina-tazobactam y de claritromicina oral, con empeoramiento de la consolidación en la repetición de la radiografía de tórax. El paciente fue trasladado a la unidad de cuidados intensivos y, posteriormente, se le realizó una intubación y ventilación. Una tomografía computarizada (TC) de su tórax reveló una masa hilar derecha con afectación mediastinal y adenopatía hilar derecha con consolidación de espacio aéreo extenso superpuesta. Una biopsia realizada durante la broncoscopia reveló células pequeñas, histológicamente monótonas, con núcleos ovoides oscuros. No se observaron nucleolos, y varias figuras mitóticas estaban presentes. Las células tienen un citoplasma estrecho y mal definido. La inmunohistoquímica realizada en las células tumorales mostró negatividad a CD45, AE1/AE3, positividad a TTF1. También se observaron sinapsina mínima focal y positividad a cromogranina A. Este perfil inmunohistoquímico fue consistente con un diagnóstico de cáncer de pulmón de células pequeñas.\n\nLa estadificación completa, que consistió en una tomografía computarizada del cerebro y tórax-abdomen-pelvis, confirmó una enfermedad en estadio extenso con metástasis suprarrenales. El estado funcional ECOG de la paciente era deficiente debido a una combinación de SCLC y dificultad respiratoria que requería ventilación artificial. Como las tasas de respuesta con quimioterapia en SCLC son generalmente altas, se inició un tratamiento quimioterápico doble en forma de carboplatino y etopósido mientras la paciente estaba intubada en la UCI.\n\nEl paciente respondió bien al tratamiento y fue extubado y trasladado a la sala de ventilación no invasiva. Una nueva tomografía computarizada de tórax después de 1 ciclo mostró una buena respuesta parcial al tratamiento.\n\nEn el día 3 del ciclo 2 de quimioterapia, la paciente desarrolló dolor en la parte inferior de la espalda y debilidad bilateral en las extremidades inferiores. El examen identificó paresia motora bilateral en las extremidades inferiores (grado 3 del Consejo de Investigación Médica [MRC]) y paresia sensorial. El examen sensorial reveló ausencia de tacto ligero, pinchazo, coordinación y propiocepción en las extremidades inferiores. El día 3 de etopósido se retrasó como resultado de los nuevos hallazgos neurológicos.\n\nSe realizaron un TAC cerebral, resonancia magnética (RM) cerebral y resonancia magnética (RM) de la columna para investigar los nuevos hallazgos neurológicos. Todos los resultados radiológicos fueron normales, sin evidencia de metástasis intracerebrales, accidente cerebrovascular, mielitis o enfermedad leptomeníngea. Además, no hubo evidencia radiográfica obvia de compresión de la médula espinal, ya sea por compresión extrínseca por depósito metastásico óseo o depósitos intramedulares o leptomeníngeos.\n\nDos días después, un examen neurológico de seguimiento reveló tetraplejía, MRC grado 0 en las extremidades superiores e inferiores. Todos los reflejos tendinosos profundos estaban ausentes. Los músculos de la cabeza y el cuello, la cognición y el habla no se vieron afectados, y el examen de los nervios craneales fue normal.\n\nLos análisis de sangre de rutina, incluida la proteína C reactiva y la velocidad de sedimentación de eritrocitos, fueron normales. Los análisis de sangre específicos, incluidos los de vitamina B12 en suero, folato, serología del VIH, serología de la enfermedad de Lyme, serología del virus de Epstein-Barr, serología de Brucella, anticuerpos tiroideos, pruebas de función tiroidea, ANCA, ENA, ANA y electroforesis de proteínas séricas, fueron negativos o normales. Se enviaron anticuerpos para las pruebas de sangre Hu, Ri y Yo, y todos fueron negativos. En este momento, se sospechó un diagnóstico de polineuropatía simétrica ascendente aguda motora y sensorial y se realizó una punción lumbar. Los resultados del líquido cefalorraquídeo (LCR) revelaron una proteína total elevada de 3.32 g/L (normal 0.15–0.45), y otros parámetros fueron normales, con una repetición 3 días después que mostró resultados similares. La citología del LCR fue negativa para la malignidad y el cultivo del LCR también fue negativo.\n\nLa electromiografía fue consistente con una polineuropatía difusa predominantemente motora; los potenciales sensoriales se conservaron, pero fueron de pequeña amplitud. Las conducciones motoras mostraron características axonales/desmielinizantes mixtas, que no eran típicas del síndrome de Guillain-Barré.\n\nSe realizaron estudios de electromiografía y conducción nerviosa para investigar la polineuropatía motora y sensorial aguda del paciente. Los estudios de conducción nerviosa revelaron lo siguiente:\n\n•Nervios motores:\n◦Las amplitudes del potencial de acción muscular compuesto (CMAP) se redujeron notablemente en los nervios tibial y cubital de forma bilateral (tibial: 1,2 mV; normal > 4 mV; cubital: 0,8 mV; normal > 3 mV).\n◦Las velocidades de conducción motora (MCV) se desaceleraron en los nervios tibial y cubital (tibial: 30 m/s; normal > 40 m/s; cubital: 34 m/s; normal > 50 m/s), lo que es coherente con la desmielinización.\n◦Las latencias motoras distales se prolongaron, con un patrón mixto axonal y desmielinizante.\n•Nervios sensoriales:\n◦Las amplitudes del potencial de acción nerviosa sensorial (SNAP) se conservaron, pero fueron de poca amplitud en los nervios surales y medianos (sural: 4 μV; normal > 10 μV; mediano: 6 μV; normal > 15 μV).\n◦Las velocidades de conducción sensorial (VCS) se encontraban dentro de los límites normales.\nLos hallazgos electrofisiológicos revelaron una polineuropatía predominantemente motora con características axonales y desmielinizantes mixtas, atípicas para los síndromes paraneoplásicos clásicos, que generalmente son predominantemente sensoriales y se caracterizan por la ausencia de SNAP.\n\nMientras tanto, mientras estas investigaciones estaban en curso, se inició al paciente con dexametasona intravenosa y 0.4 g/kg/día de inmunoglobulina intravenosa sin ninguna mejora sintomática.\n\n3. Resultados y seguimiento\nA pesar de una importante respuesta oncológica inicial a la quimioterapia, el estado neurológico del paciente se deterioró rápidamente. Después de 1 ciclo de carboplatino y etopósido, las imágenes confirmaron una respuesta parcial con una reducción en el tamaño del tumor. Sin embargo, el inicio de una polineuropatía motora y sensorial grave y ascendente condujo a un compromiso respiratorio. Esta disociación entre las respuestas oncológicas y neurológicas destaca la naturaleza agresiva y refractaria del SNP, incluso cuando el tratamiento del cáncer es efectivo. Aunque la dexametasona intravenosa y la inmunoglobulina intravenosa se administraron rápidamente, no lograron mejorar los resultados neurológicos.\n\nSe llevaron a cabo largas y repetidas discusiones multidisciplinares con el paciente y su familia sobre la admisión en la unidad de cuidados intensivos para recibir apoyo ventilatorio. El paciente estaba bien informado y consciente de que era poco probable que sus síntomas neurológicos fueran reversibles y, por lo tanto, optó por el mejor tratamiento de apoyo. El paciente falleció 3 semanas después de los síntomas iniciales. La decisión del paciente de rechazar el apoyo ventilatorio invasivo en favor de los cuidados paliativos pone de relieve las consideraciones éticas que rodean la calidad de vida en los síndromes paraneoplásicos de progresión rápida.\n",
+        "gold_summary": "Preocupaciones del paciente: Un hombre de 55 años con un historial de 80 años fumando presenta al hospital con un historial de 3 semanas de fiebres, tos productiva, disnea y sibilancias. No tenía comorbilidades significativas.\n\nDiagnóstico: Extensas investigaciones radiológicas revelaron una gran masa en el hilum derecho que comprimía el bronquio inferior derecho con depósitos suprarrenales metastásicos. Las investigaciones bioquímicas confirmaron el síndrome de secreción inadecuada de la hormona antidiurética, y la histología identificó un CPCP.\n\nIntervenciones: A pesar de iniciar una quimioterapia combinada con carboplatino y etopósido, el paciente desarrolló parálisis motora progresiva y pérdida sensorial en el transcurso de 4 días, lo que derivó en un diagnóstico de polineuropatía motora y sensorial aguda paraneoplásica.\n\nResultados: Su estado empeoró rápidamente y falleció 14 días después de la aparición de los síntomas debido a una insuficiencia respiratoria, lo que pone de relieve la agresividad de los síndromes paraneoplásicos.\n",
+        "synthetic_summary": {
+            "B1": "A man was very sick with cough and fever for many days. Doctors found a big lump in his chest. He had a kind of cancer that made him very weak.\n\nThe man got medicine to fight the cancer. But his body stopped moving and feeling in some parts. He got very tired and could not breathe well.\n\nEven with help, the man got worse and passed away. This shows some sickness can be very strong and fast.",
+            "B2": "**What Happened to the Patient?**  \nA 55-year-old man who had smoked a lot for many years came to the hospital. He had been feeling sick for three weeks with fever, coughing up mucus, trouble breathing, and wheezing. Before this, he was mostly healthy.\n\n**What Did the Doctors Find?**  \nScans showed a large tumor in his right lung near the main airway. The cancer had spread to his adrenal glands, which are small organs above the kidneys. Blood tests showed he had a condition called SIADH, where the body makes too much of a hormone that controls water balance. A biopsy, which means taking a small piece of tissue to look at under a microscope, confirmed he had small cell lung cancer—a fast-growing type of lung cancer.\n\n**What Treatment Did He Get?**  \nHe started chemotherapy with two drugs called carboplatin and etoposide. However, within four days, he began losing movement and feeling in his legs and arms. Doctors diagnosed him with a rare nerve problem called paraneoplastic motor and sensory polyneuropathy. This means his immune system, reacting to the cancer, was attacking his nerves, causing weakness and numbness.\n\n**What Was the Outcome?**  \nDespite treatment, his condition got worse quickly. He developed severe breathing problems and passed away about two weeks after the nerve symptoms began. This case shows how aggressive and dangerous nerve problems linked to cancer can be, even when the cancer treatment initially works.",
+            "B3": "**Background**  \nA 55-year-old man with a significant smoking history of 80 pack-years, but no prior major health issues, presented to the hospital after three weeks of persistent fever, productive cough, shortness of breath, and wheezing. His family history was notable for lung cancer. Initial outpatient treatment with oral amoxicillin and prednisone failed to improve his symptoms.\n\n**Key Findings**  \nUpon hospital admission, laboratory tests revealed elevated white blood cell and neutrophil counts, a markedly raised C-reactive protein (118 mg/L), and severe hyponatremia (serum sodium 112 mmol/L). Chest X-ray showed consolidation in the right middle and lower lung lobes with moderate pleural effusion. These findings led to a diagnosis of community-acquired pneumonia complicated by the syndrome of inappropriate antidiuretic hormone secretion (SIADH).\n\nDespite broad-spectrum intravenous antibiotics (piperacillin-tazobactam) and oral clarithromycin, the patient’s respiratory status deteriorated, necessitating intensive care admission with intubation and mechanical ventilation. A chest CT scan identified a large right hilar mass compressing the lower right bronchus, extensive airspace consolidation, mediastinal involvement, and right hilar lymphadenopathy. Biopsy via bronchoscopy revealed small, monotonous cells with features consistent with small-cell lung cancer (SCLC), confirmed by immunohistochemical markers positive for TTF1 and chromogranin A, and negative for CD45 and AE1/AE3.\n\nStaging imaging demonstrated extensive-stage disease with adrenal metastases. Despite poor functional status (ECOG performance status compromised by respiratory failure), chemotherapy with carboplatin and etoposide was initiated while the patient remained ventilated.\n\n**Clinical Course and Neurological Complications**  \nThe patient initially responded well oncologically, with partial tumor regression after one chemotherapy cycle. However, on the third day of the second cycle, he developed rapidly progressive neurological symptoms: bilateral lower limb weakness and sensory loss, progressing within days to tetraplegia (complete paralysis of all four limbs) with absent deep tendon reflexes. Cranial nerve function, cognition, and speech remained intact.\n\nExtensive neuroimaging (brain and spinal MRI and CT) showed no evidence of brain metastases, stroke, spinal cord compression, leptomeningeal disease, or myelitis. Blood tests for infectious, autoimmune, and paraneoplastic antibodies (including Hu, Ri, and Yo) were negative. Cerebrospinal fluid analysis revealed elevated protein without malignant cells or infection. Electrophysiological studies demonstrated a predominantly motor polyneuropathy with mixed axonal and demyelinating features, atypical for classic paraneoplastic syndromes, which usually present with sensory neuropathy.\n\nA diagnosis of acute, symmetrical, ascending motor and sensory polyneuropathy of paraneoplastic origin was made. Treatment with intravenous dexamethasone and immunoglobulin was initiated promptly but failed to halt neurological decline.\n\n**Outcomes and Interpretation**  \nDespite effective chemotherapy reducing tumor burden, the patient’s neurological condition worsened rapidly, leading to respiratory failure secondary to neuromuscular compromise. This dissociation between tumor response and neurological deterioration highlights the aggressive and refractory nature of paraneoplastic neuropathies associated with SCLC.\n\nFollowing multidisciplinary discussions, the patient, fully informed of the poor prognosis and low likelihood of neurological recovery, elected to forgo invasive ventilatory support in favor of palliative care. He died three weeks after the onset of neurological symptoms.\n\n**Next Steps and Clinical Implications**  \nThis case underscores the importance of early recognition of paraneoplastic neurological syndromes in patients with SCLC, especially when neurological symptoms progress rapidly despite oncological treatment. It also highlights the challenges in managing such syndromes, given their poor response to immunotherapy and the ethical considerations regarding quality of life and intensive care support. Multidisciplinary communication and patient-centered decision-making remain critical in guiding care for these complex cases."
+        }
+    },
+    {
+        "article": "El paciente presentado firmó el Consentimiento Informado y se cumplieron los demás principios éticos, respetando la Resolución 466/12 del Consejo Nacional de Ética en Investigación. Este informe de caso fue aprobado por el Comité de Ética en Investigación de la Universidad Federal de São Paulo (UNIFESP), bajo el dictamen número 4.455.365.\n\nEl paciente, de 66 años de edad y sexo masculino, acudió a una consulta de otorrinolaringología por presentar disfagia tipo atragantamiento con sólidos y reflujo nasal de alimentos desde hacía un año. Había sufrido un accidente automovilístico 13 años atrás y era diabético. Se le realizó una videoendoscopia de la deglución (VED), en la que se observó, en la evaluación estructural, una protuberancia de la pared posterior de la hipofaringe con residuo salival sobre la lesión. En la evaluación funcional, tras la ingesta de alimentos sólidos, se observó una restricción de la retroflexión de la epiglotis, una limitación de la elevación de la laringe y un reflujo nasal de alimentos, con gran cantidad de residuo alimentario por encima de la lesión, en la pared posterior de la faringe. En la prueba de maniobras posturales, empeoró la disfagia al extender el cuello y mejoró la eliminación al flexionar la cabeza. Se le realizó una tomografía computarizada (TC) de la columna cervical, solicitada para evaluar la naturaleza de la lesión, que mostró la presencia de osteofitos cervicales anteriores entre las vértebras C3 y C6, el mayor de 12 milímetros (mm) de longitud, que estrechaba la columna aérea al nivel de la orofaringe e hipofaringe. Se descartaron otras causas de disfagia y se trató al paciente con terapia de deglución y omeprazol, dirigido al reflujo faringolaríngeo. Se realizaron 6 sesiones de terapia de deglución individualizada, con el objetivo de compensar el mecanismo de deglución ante un obstáculo mecánico en la región faríngea. Los principales aspectos trabajados fueron: modificación de la textura de la dieta, evitando alimentos sólidos y secos; maniobras posturales de deglución, probadas durante la VED, especialmente el chin tuck (“cabeza hacia abajo” o “flexión de la cabeza”), que aumenta el espacio de la válvula (“abre la válvula”) y mejora la presión de transferencia faríngea del alimento; y ejercicios de fortalecimiento de la lengua, para superar la barrera mecánica de la orofaringe durante la expulsión del alimento. Se recomendó, si fuera necesario, alternar la ingesta de alimentos sólidos con líquidos, ante la percepción de alimentos estancados en la faringe. Se le indicó que repitiera los ejercicios de lengua en el hogar, 2 a 3 veces al día. Después de las sesiones iniciales, el paciente presentó una respuesta satisfactoria, y se lo controló trimestralmente durante el primer año y semestralmente a partir del segundo año. Se lo derivó para una evaluación ortopédica para analizar la viabilidad quirúrgica, y se optó por un tratamiento conservador debido a la buena compensación con medidas clínicas. Sigue en seguimiento ambulatorio desde hace 2 años, y mantiene una deglución eficiente, sin incidencia de complicaciones relacionadas con la disfagia. Se optó por mantener reevaluaciones periódicas, al menos una vez al año, para detectar precozmente un posible nuevo desequilibrio de la homeostasis de la deglución relacionado con el deterioro gradual de las funciones en el contexto de la presbifagia o el surgimiento de un nuevo factor agresor.\n",
+        "gold_summary": "Se describió el caso de un paciente de 66 años con disfagia por atragantamiento con sólidos y reflujo nasal de alimentos desde hacía un año. La videoendoscopia de la deglución mostró una protuberancia en la pared posterior de la faringe y, al ofrecer alimentos sólidos, una restricción de la retroflexión de la epiglotis, reflujo nasal de alimentos y una gran cantidad de residuos de alimentos sobre la lesión. La tomografía computarizada de la columna cervical identificó la presencia de osteofitos cervicales anteriores entre las vértebras C3 y C6, el más grande con una longitud anteroposterior de 12 milímetros, que estrechaba la columna aérea a nivel de la orofaringe e hipofaringe. El paciente fue tratado adecuadamente con fonoterapia para la deglución.\n",
+        "synthetic_summary": {
+            "B1": "A man had trouble swallowing food for one year. Food sometimes went up his nose. Doctors saw a bump in his throat. The bump made it hard to swallow well. They found some bone bumps in his neck pressing on his throat. The man did special swallowing exercises. These helped him eat better and feel okay.",
+            "B2": "**What They Found**  \nA 66-year-old man had trouble swallowing solid foods and sometimes food went up into his nose. Doctors used a special camera test called videoendoscopy to look at his throat while he swallowed. They saw a bump on the back wall of his throat and noticed that a flap called the epiglottis, which normally helps protect the airway when swallowing, was not moving properly. Food was getting stuck and even going up into his nose.  \n\nA CT scan, which is a detailed X-ray, showed that the man had bone spurs (called osteophytes) on the front part of his neck bones between the third and sixth vertebrae. The largest bone spur was about 12 millimeters long and was pressing on the airway in his throat, making it harder to swallow.  \n\n**What It Means**  \nThe bone spurs were causing a mechanical blockage in his throat, leading to swallowing problems and food going the wrong way. This condition can make eating difficult and uncomfortable.  \n\n**How They Helped**  \nThe doctors treated him with swallowing therapy, also called phonotherapy. This therapy included exercises to strengthen his tongue and special swallowing techniques to help food pass safely. They also changed his diet to avoid hard, dry foods and taught him to tilt his head down when swallowing, which made swallowing easier.  \n\nAfter treatment, the man’s swallowing improved a lot. He continues to be checked regularly to make sure his swallowing stays good and to catch any new problems early. Surgery was considered but not needed because the therapy worked well.",
+            "B3": "Background  \nThis report describes a 66-year-old male patient who experienced difficulty swallowing (dysphagia) characterized by choking on solid foods and nasal regurgitation of food over the course of one year. His medical history included a motor vehicle accident 13 years prior and diabetes mellitus.\n\nKey Findings  \nA videoendoscopic evaluation of swallowing revealed a prominent protrusion on the posterior wall of the hypopharynx (the lower part of the throat), accompanied by salivary residue above the lesion. Functionally, after ingestion of solid food, there was limited backward bending (retroflexion) of the epiglottis (a flap that prevents food from entering the airway), restricted elevation of the larynx, nasal reflux of food, and significant food residue accumulating above the lesion on the posterior pharyngeal wall. Postural swallowing maneuvers demonstrated that extending the neck worsened the dysphagia, while flexing the head improved food clearance.\n\nA computed tomography (CT) scan of the cervical spine identified anterior cervical osteophytes (bony growths) between vertebrae C3 and C6, with the largest measuring 12 millimeters in length. These osteophytes compressed the airway at the levels of the oropharynx and hypopharynx, creating a mechanical obstruction contributing to the swallowing difficulties. Other potential causes of dysphagia were excluded.\n\nClinical Interpretation  \nThe patient’s dysphagia was primarily caused by mechanical obstruction from cervical osteophytes impinging on the pharyngeal airway. The impaired epiglottic retroflexion and laryngeal elevation further compromised safe swallowing, leading to nasal reflux and food residue accumulation.\n\nNext Steps and Treatment  \nThe patient underwent individualized swallowing therapy (phonotherapy) consisting of six sessions aimed at compensating for the mechanical barrier. Treatment strategies included modifying food texture to avoid solid and dry foods, implementing postural swallowing techniques—particularly the chin tuck maneuver (head flexion), which increases the space in the pharyngeal valve and improves food transfer pressure—and tongue strengthening exercises to facilitate food propulsion past the obstruction. Patients were advised to alternate solids with liquids if food stasis was perceived and to perform tongue exercises at home two to three times daily.\n\nThe patient showed a satisfactory clinical response to therapy. Follow-up was conducted quarterly during the first year and biannually thereafter. An orthopedic evaluation considered surgical options but ultimately favored conservative management due to effective symptom control with clinical measures. After two years of outpatient follow-up, the patient maintained efficient swallowing without complications related to dysphagia. Annual reevaluations were recommended to monitor for potential deterioration of swallowing function due to aging (presbyphagia) or new pathological factors."
+        }
+    },
+    {
+        "article": "Una paciente caucásica de 18 años de edad se presentó en nuestra clínica con quejas de múltiples bultos palpables en sus senos bilateralmente. En el examen físico, la paciente tenía múltiples lesiones pigmentadas lentigosas en su cara, cuerpo y esclerótica bilateralmente, nevos azules en su tronco y extremidades superiores y una cara redonda con forma de luna.\n\nTras la evaluación ultrasonográfica, se encontraron múltiples nódulos compactos (fibroadenomas) en ambos senos, siendo el más grande en el cuadrante superior externo del seno izquierdo, con un diámetro de 7,8 cm.\n\nEn 2018, se le había practicado una tiroidectomía total con el diagnóstico de adenoma folicular y la extirpación de un nódulo grande del seno izquierdo, debido a su gran tamaño y al dolor que causaba, con un informe de histopatología que sugería un fibroadenoma con estroma mixóide.\n\nSe realizó una biopsia por escisión de dos nódulos de la mama derecha con diagnóstico de fibroadenoma mixto, lo que respaldó nuestro diagnóstico de complejo de Carney.\n\nEn la resonancia magnética se encontraron múltiples fibroadenomas compactos en ambos senos, con alta intensidad de señal en las imágenes T2 y T2/FS, con tabiques internos sin restricción de difusión, compatibles con múltiples fibroadenomas mixoides.\n\nAdemás, había un par de ganglios linfáticos axilares y prominentes ganglios linfáticos mamarios internos bilaterales.\n\nAdemás, se observó una anomalía en la densidad de los tejidos blandos en el mediastino anterior, que medía 11 mm de espesor máximo, lo que sugería un timo prominente.\n\nTodos los hallazgos anteriores sugerían la posibilidad de un complejo de Carney. Se realizó una evaluación adicional en el laboratorio. Los análisis hormonales no mostraron anomalías en los niveles de testosterona, prolactina, PTH y DHEA-S.\n\nLuego se realizó un análisis genético que arrojó como resultado la mutación del gen PRHAR1A, heterocigótico para una variante sin sentido de significancia incierta en el exón 3 de este gen. Esta mutación nunca se había informado en la base de datos gnomAD.\n\nSe realizaron pruebas genéticas a los padres y se determinó que solo el padre era portador de la misma mutación genética.\n\nSe discutieron con la paciente varios planes de tratamiento conservadores, pero ninguno demostró proporcionar una solución/tratamiento definitivo. En el pasado se realizó la extirpación de los lóbulos grandes con alivio temporal de los síntomas de dolor de la paciente y las cirugías recurrentes estaban afectando su calidad de vida. La paciente también tuvo varias sesiones con la psicóloga de nuestra clínica y fue evaluada a fondo antes de decidir la solución final de una mastectomía bilateral.\n\nLa paciente se sometió a una mastectomía bilateral con conservación de la piel y colocación subcutánea de expansores de tejidos (suave, Motiva Flora®). La histopatología informó múltiples fibroadenomas mixóides en ambos senos, compatibles con el síndrome de Carney, con interrupción de la arquitectura normal del parénquima mamario. Las figuras muestran el fibroadenoma de forma macroscópica e histológica.\n\nEl cuidado de la herida fue mínimo, se le recomendó a la paciente usar un sujetador médico y visitas regulares a la clínica ambulatoria para seguimiento y rellenado adicional de los expansores de tejidos a intervalos regulares hasta que se alcanzó el tamaño deseado. Paciente antes y después de la mastectomía. Después de un año se realizó una segunda cirugía y los expansores se reemplazaron con implantes de silicona permanentes (suaves, Motiva Ergonomic®) submusculares, con los mismos requisitos mínimos de cuidado de la herida y colocación del sujetador.\n",
+        "gold_summary": "Una paciente de 18 años de edad se presentó en nuestra clínica con múltiples bultos palpables en sus senos bilateralmente. En el examen físico, la paciente también tenía múltiples lesiones pigmentadas lentigosas en su cara, cuerpo y esclerótica, nevos azules en su tronco y extremidades superiores y un rostro redondo con forma de luna. El diagnóstico del síndrome de Carney se decidió mediante imágenes, biopsias y análisis genético. La paciente se sometió a una mastectomía bilateral como plan de tratamiento profiláctico con colocación de expansores de tejidos.\n",
+        "synthetic_summary": {
+            "B1": "A young girl had many lumps in her breasts. She also had spots on her face and body. Doctors did tests and found a special sickness called Carney syndrome. To help her, they gently took away her breast lumps and used soft bags to help her body look nice.",
+            "B2": "**What They Found**  \nAn 18-year-old patient came to the clinic because she felt many lumps in both of her breasts. When doctors examined her, they also saw several dark spots on her face, body, and the white part of her eyes. She had blue-colored moles on her trunk and arms, and her face was round, shaped like a moon. These signs made doctors suspect a rare condition called Carney complex.\n\n**How They Confirmed the Diagnosis**  \nTo be sure, doctors used imaging tests like ultrasound and MRI to look at the lumps in her breasts. They also took small tissue samples, called biopsies, from some lumps to study under a microscope. Genetic testing showed a change in a gene called PRKAR1A, which is linked to Carney complex. This gene change was also found in her father.\n\n**What It Means**  \nCarney complex is a condition that causes multiple benign (non-cancerous) tumors, like fibroadenomas, which are lumps made of gland and connective tissue in the breast. These lumps can grow large and cause pain or discomfort. Because the lumps kept coming back and affected her quality of life, doctors and the patient decided on a preventive treatment.\n\n**Treatment and Care**  \nThe patient had both breasts removed in a surgery called bilateral mastectomy. During this surgery, doctors kept the skin and placed special devices called tissue expanders under the skin. These expanders help stretch the skin to prepare for breast implants later. After healing and regular check-ups, she had a second surgery to replace the expanders with permanent silicone implants. This plan helped manage her symptoms and improved her quality of life.",
+            "B3": "**Background**  \nAn 18-year-old Caucasian woman presented with multiple palpable lumps in both breasts. On physical examination, she exhibited several lentiginous pigmented lesions (small, flat, brownish spots) on her face, body, and both scleras (the white part of the eyes), as well as blue nevi (benign blue-colored skin moles) on her trunk and upper limbs. Her facial features included a characteristic round, “moon-shaped” face. These clinical signs raised suspicion for Carney complex, a rare genetic syndrome involving multiple tumors and pigmented skin lesions.\n\n**Key Findings**  \n- **Breast Imaging and Biopsy:** Ultrasound and magnetic resonance imaging (MRI) revealed multiple compact fibroadenomas (benign breast tumors) in both breasts, with the largest measuring 7.8 cm in the upper outer quadrant of the left breast. MRI showed these lesions as high-intensity signals on T2-weighted images with internal septations but no diffusion restriction, consistent with myxoid (gelatinous) fibroadenomas.  \n- **Histopathology:** Surgical biopsies confirmed the presence of mixed fibroadenomas in both breasts, supporting the diagnosis of Carney complex.  \n- **Additional Findings:** Enlarged axillary and internal mammary lymph nodes were noted, along with an anterior mediastinal soft tissue density measuring 11 mm, suggestive of a prominent thymus gland.  \n- **Laboratory and Genetic Testing:** Hormonal studies showed normal levels of testosterone, prolactin, parathyroid hormone (PTH), and dehydroepiandrosterone sulfate (DHEA-S). Genetic analysis identified a heterozygous nonsense mutation of uncertain significance in exon 3 of the PRKAR1A gene, a mutation not previously reported in population databases. Parental testing revealed that the patient’s father carried the same mutation.\n\n**Clinical Interpretation**  \nThe constellation of clinical features, imaging, histopathological findings, and genetic results confirmed the diagnosis of Carney complex. This syndrome is characterized by multiple benign tumors, pigmented skin lesions, and endocrine abnormalities, often caused by mutations in the PRKAR1A gene. The patient’s recurrent large fibroadenomas caused pain and significantly affected her quality of life. Conservative treatments, including repeated surgical excisions of large lobules, provided only temporary relief.\n\n**Next Steps and Treatment**  \nAfter thorough psychological evaluation and discussion of treatment options, the patient elected to undergo bilateral skin-sparing mastectomy with placement of subcutaneous tissue expanders (soft Motiva Flora® expanders) as a prophylactic measure to manage her extensive fibroadenomas and improve quality of life. Histopathology of the removed breast tissue confirmed multiple myxoid fibroadenomas disrupting normal breast architecture, consistent with Carney complex. Postoperative care involved minimal wound management, use of a medical bra, and regular outpatient visits for gradual tissue expander inflation until the desired breast size was achieved. One year later, a second surgery replaced the expanders with permanent submuscular silicone implants (Motiva Ergonomic®), maintaining similar postoperative care protocols.\n\nThis comprehensive approach addressed both the physical and psychological impacts of the disease, providing a definitive treatment to prevent recurrence of painful fibroadenomas and improve the patient’s well-being."
+        }
+    },
+    {
+        "article": "Una adolescente femenino de 13 años sin antecedentes médico-quirúrgicos de interés acude a Urgencias por dolor e impotencia funcional en muñeca izquierda tras caída mientras patinaba. Diagnosticada de lesión en torus metafisaria con extensión fisaria de radio distal clasificada como lesión Peterson tipo I, es inmovilizada durante cuatro semanas con férula antebraquiopalmar. Dos semanas después de la retirada de la férula, acude nuevamente a Urgencias al sentir un crujido en la muñeca, sin sobreesfuerzo asociado e impotencia para movilizar el primer dedo de la mano izquierda. Clínicamente presenta déficit de extensión activa interfalángica, efecto tenodesis patológico, edema local y asimetría macroscópica a la comparación con la extremidad contralateral. Se estudia con resonancia magnética nuclear (RMN), identificando imagen de solución de continuidad del EPL. Con la paciente bajo anestesia general, se procede al tratamiento quirúrgico mediante transferencia tendinosa del extensor propio del índice (EPI) al remanente distal del EPL con sutura tipo Pulvertaft de monofilamento no absorbible. En el postoperatorio se inmovilizó la extremidad las cuatro primeras semanas.\n\nTras cuatro semanas, se autorizó movilidad evidenciando recuperación de extensión del primer dedo de la mano izquierda y cicatrices discretamente hipertróficas, sin dolor. El seguimiento a la sexta, duodécima semana y al año no reporta complicaciones, con una restitución completa de la función y una puntuación de 0 en la escala PRWE (Patient Rated Wrist Evaluation).",
+        "gold_summary": "Se presenta el caso de una paciente adolescente femenino que, tras tratamiento conservador con férula de una fractura fisaria Peterson tipo I en radio, sufre a las seis semanas déficit agudo de extensión del pulgar, diagnosticada mediante examen clínico radiológico de rotura espontánea del extensor pollicis longus. Es tratada por medio de transferencia del extensor propio del índice (EPI) con resultados satisfactorios y recuperación de su actividad habitual al mes postoperatorio.",
+        "synthetic_summary": {
+            "B1": "A 13-year-old girl hurt her wrist when she fell. She wore a special brace to help her wrist heal. After six weeks, she could not move her thumb well. The doctors found a small tear in a thumb muscle. They fixed it with a small surgery using a finger muscle. One month after, she could move her thumb again and felt better.",
+            "B2": "**What Happened:**  \nA 13-year-old girl hurt her left wrist when she fell while skating. She was diagnosed with a type of wrist fracture called a Peterson type I fracture. This means a small break near the growth plate of one of the wrist bones. Doctors treated her by putting her wrist in a splint for four weeks to help it heal.\n\n**New Problem:**  \nTwo weeks after removing the splint, she felt a crack in her wrist and couldn’t move her thumb properly. Doctors found that a tendon called the extensor pollicis longus (EPL), which helps straighten the thumb, had suddenly torn. This was confirmed using an MRI, a special scan that shows soft tissues like tendons.\n\n**How They Fixed It:**  \nTo fix the torn tendon, surgeons took another tendon from her index finger called the extensor proprius indicis (EPI). They moved this tendon to replace the damaged EPL tendon. This surgery helped restore the thumb’s movement.\n\n**Recovery:**  \nAfter surgery, her wrist was kept still for four weeks. Then, she started moving her thumb again. Over the next few months, she healed well without pain or problems. One year later, she had full use of her thumb and wrist, showing a complete recovery.\n\n**Summary:**  \nThis case shows that a wrist fracture can sometimes cause a tendon tear later on. Using a tendon transfer surgery can successfully restore thumb movement and help patients return to normal activities.",
+            "B3": "**Background:**  \nA 13-year-old female adolescent with no significant prior medical or surgical history initially presented to the emergency department after a fall while skating, experiencing pain and functional impairment in her left wrist. She was diagnosed with a distal radius metaphyseal torus fracture extending into the growth plate (physis), classified as a Peterson type I lesion. The injury was managed conservatively with immobilization using a forearm-palmar splint for four weeks.\n\n**Key Findings:**  \nTwo weeks after removal of the splint, the patient returned to the emergency department reporting a sudden cracking sensation in the wrist without any new trauma or overexertion. She exhibited an inability to actively extend the thumb’s interphalangeal joint, accompanied by local swelling and visible asymmetry compared to the opposite hand. Clinical examination revealed a pathological tenodesis effect (an abnormal tendon tension pattern), indicating dysfunction of the extensor pollicis longus (EPL) tendon. Magnetic resonance imaging (MRI) confirmed a complete rupture (discontinuity) of the EPL tendon.\n\n**Clinical Interpretation:**  \nThe patient developed an acute spontaneous rupture of the EPL tendon six weeks after the initial fracture, a known but uncommon complication following distal radius fractures. This rupture resulted in loss of active thumb extension, significantly impairing hand function.\n\n**Treatment and Outcome:**  \nUnder general anesthesia, surgical intervention was performed involving a tendon transfer procedure. The extensor indicis proprius (EIP) tendon, which normally extends the index finger, was rerouted and sutured to the distal remnant of the ruptured EPL tendon using a Pulvertaft weave technique with non-absorbable monofilament sutures. Postoperatively, the limb was immobilized for four weeks.\n\nAfter immobilization, gradual mobilization was allowed, and by one month post-surgery, the patient demonstrated restored active extension of the thumb without pain. Follow-up evaluations at six weeks, twelve weeks, and one year showed complete functional recovery, no complications, and a Patient Rated Wrist Evaluation (PRWE) score of zero, indicating no residual disability.\n\n**Next Steps:**  \nContinued monitoring is recommended to ensure long-term tendon function and to detect any late complications. This case highlights the importance of recognizing delayed EPL tendon rupture after distal radius fractures and the effectiveness of EIP tendon transfer in restoring thumb extension and hand function in adolescent patients."
+        }
+    },
+    {
+        "article": "Se remitió a un hombre de 73 años para una SAVR para tratar la regurgitación valvular aórtica sintomática (AR). Dos años antes, había presentado múltiples lesiones exantématicas. Una biopsia de piel reveló infiltración de células plasmáticas, lo que motivó la derivación a un hematólogo. La tomografía computarizada reveló linfadenopatía sistémica y hepatoesplenomegalia. Una biopsia renal realizada por disfunción renal confirmó la amiloidosis AA; una biopsia de ganglios linfáticos mostró plasmocitosis interfolicular y un centro germinal hiperplásico, consistente con el subtipo plasmático de iMCD, apoyado por niveles elevados de IL-6 en plasma. Se administró al paciente TCZ intravenoso (640 mg cada 2 semanas), junto con prednisolona (10 mg diarios). La erupción cutánea y la linfadenopatía se resolvieron. La ecocardiografía reveló AR puro moderado y agrandamiento ventricular izquierdo. Dado que el paciente experimentó gradualmente disnea de esfuerzo con agrandamiento ventricular izquierdo progresivo, se consideró necesaria la SAVR.\n\nDebido al sangrado por hemorroides y a la hepatosplenomegalia, se consultó a un hepatólogo; se diagnosticó cirrosis hepática de Child-Pugh grado A y varices esofágicas. Se realizó una conferencia preoperatoria del equipo, en la que participaron un intensivista y un farmacéutico, en la que se revisaron los mecanismos de acción de TCZ, las posibles complicaciones y el tratamiento perioperatorio. La cirugía se realizó 26 días después de la última dosis de TCZ. Durante el período perioperatorio, se suspendió el tratamiento con TCZ, mientras que se continuó con los esteroides por vía oral o intravenosa. Las medidas preventivas para las infecciones del sitio quirúrgico (SSI) incluyeron la detección de portadores nasales de Staphylococcus aureus resistentes a la meticilina, la preparación antiséptica de la piel, la terapia antibiótica profiláctica y el control de la hiperglucemia. El cultivo nasal fue positivo para Staphylococcus coagulasa negativo. Se realizó el reemplazo de la válvula aórtica quirúrgica a través de una esternotomía media bajo circulación extracorpórea, con 65 minutos de tiempo de isquemia cardiaca y 128 minutos de tiempo de circulación extracorpórea. Se requirieron transfusiones de sangre, incluidos glóbulos rojos, plasma y plaquetas; el paciente fue extubado al día siguiente. Los hallazgos patológicos revelaron un espesamiento fibroso focal sin depósitos amiloides.\n\nLa herida quirúrgica no mostró signos de infección en el día 2 postoperatorio; se inició la terapia de presión negativa en la herida (NPWT) en la herida quirúrgica cerrada para evitar SSI. La terapia de presión negativa en la herida se interrumpió en el día 13 postoperatorio, sin aparente SSI. El paciente fue dado de alta en el día 17 postoperatorio sin ningún signo de infección.\n\nAunque los niveles de IL-6 aumentaron temporalmente los días 1 y 2 después de la operación, disminuyeron progresivamente hasta el día 24 después de la operación, y luego volvieron a aumentar al reanudarse el tratamiento con TCZ. Los niveles de proteína C reactiva (PCR) estaban ligeramente elevados, alcanzando un máximo de 0,56 mg/dL el día 2 después de la operación. Para el día 24 después de la operación, la PCR había aumentado a 1,06 mg/dL sin infección. Antes del aumento de la PCR, los niveles del factor de crecimiento endotelial vascular aumentaron el día 13 después de la operación.\n\nEl paciente no experimentó recurrencia de erupción cutánea o linfadenopatía durante el período perioperatorio. Los niveles de creatinina postoperatorios aumentaron temporalmente, pero volvieron a los niveles preoperatorios el día 24. Se reanudó el tratamiento con tocilizumab el día 30 postoperatorio tras confirmar la ausencia de infección, incluida la IFI.\n",
+        "gold_summary": "Un hombre de 73 años con enfermedad de Castleman, tratado con TCZ, se sometió a un reemplazo de la válvula aórtica por medio de esternotomía mediana para la regurgitación de la válvula aórtica con falta de aire al hacer ejercicio. Se implementaron medidas integrales para prevenir la infección del sitio quirúrgico junto con un examen minucioso durante el período perioperatorio. Tocilizumab se interrumpió 26 días antes de la cirugía y se reanudó 30 días después de la cirugía, durante los cuales los niveles de IL-6 en plasma disminuyeron. No hubo evidencia de infección o exacerbación de la enfermedad de Castleman. Los niveles del factor de crecimiento endotelial vascular aumentaron antes de un aumento en los niveles de proteína C reactiva después del alta hospitalaria y antes de la reanudación de TCZ.\n",
+        "synthetic_summary": {
+            "B1": "A man, 73 years old, had a sick heart valve. He needed a new valve to help him breathe better. \n\nDoctors stopped his medicine called TCZ before the surgery. They worked hard to keep him safe from germs. \n\nThe man had the valve fixed with a big surgery on his chest. After the surgery, he got his medicine again. \n\nHe did not get sick or feel worse. The doctors watched his blood to make sure he was okay. \n\nHe got better and went home without any problems.",
+            "B2": "**What Happened to the Patient**  \nA 73-year-old man had a heart problem called aortic valve regurgitation, which means his heart valve was leaking. This caused him to feel short of breath when he exercised. He also had a rare disease called Castleman disease, which affects the immune system and causes swollen lymph nodes and other symptoms. To treat his heart problem, doctors planned a surgery to replace his faulty valve.\n\n**Treatment Before and During Surgery**  \nBefore surgery, the man was taking a medicine called tocilizumab (TCZ), which helps control Castleman disease by lowering inflammation. The doctors stopped this medicine 26 days before the surgery to reduce risks. They carefully checked for infections and took many steps to prevent infection at the surgery site. During surgery, they replaced his heart valve through an operation called a median sternotomy, which means they opened the chest through the breastbone.\n\n**After Surgery and Recovery**  \nAfter the surgery, the man’s medicine was restarted 30 days later once doctors confirmed he had no infections. Blood tests showed that levels of IL-6, a substance related to inflammation, went down after stopping TCZ and then went back up when the medicine was restarted. Another blood marker called C-reactive protein (CRP), which can show inflammation or infection, rose slightly but without any signs of infection. The patient did not have any return of Castleman disease symptoms like skin rash or swollen lymph nodes. His kidney function went back to normal after a temporary change.\n\n**What This Means**  \nThis case shows that it is possible to safely stop and restart tocilizumab around the time of major heart surgery in a patient with Castleman disease. Careful infection prevention and monitoring are very important. The patient recovered well without infection or worsening of his disease.",
+            "B3": "Background  \nA 73-year-old man diagnosed with idiopathic multicentric Castleman disease (iMCD), specifically the plasma cell subtype characterized by elevated interleukin-6 (IL-6) levels, was undergoing treatment with tocilizumab (TCZ), an IL-6 receptor inhibitor. He presented with symptomatic moderate aortic valve regurgitation (AR) and progressive left ventricular enlargement causing exertional dyspnea, necessitating surgical aortic valve replacement (SAVR) via median sternotomy.\n\nKey Clinical History and Findings  \nTwo years prior, the patient developed multiple skin rashes. Skin biopsy revealed plasma cell infiltration, prompting hematology referral. Imaging showed systemic lymphadenopathy and hepatosplenomegaly. Renal biopsy confirmed AA amyloidosis (a condition involving abnormal protein deposits), and lymph node biopsy demonstrated interfollicular plasmacytosis and germinal center hyperplasia consistent with iMCD. Treatment with intravenous TCZ (640 mg biweekly) plus daily prednisolone (10 mg) led to resolution of skin lesions and lymphadenopathy. Echocardiography identified moderate pure AR and left ventricular enlargement. Additionally, hepatology evaluation diagnosed compensated cirrhosis (Child-Pugh A) with esophageal varices.\n\nPerioperative Management  \nGiven the patient’s complex condition, a multidisciplinary team—including intensivists and pharmacists—conducted a preoperative conference to review TCZ’s mechanism, potential complications, and perioperative management. TCZ was discontinued 26 days before surgery, while corticosteroids were maintained orally or intravenously. Infection prevention strategies included screening for methicillin-resistant Staphylococcus aureus nasal carriage (which was negative; only coagulase-negative Staphylococcus was detected), antiseptic skin preparation, prophylactic antibiotics, and glycemic control.\n\nSurgical Procedure and Outcomes  \nThe SAVR was performed under cardiopulmonary bypass with 65 minutes of cardiac ischemia and 128 minutes of extracorporeal circulation. Blood product transfusions were required. The patient was extubated the following day. Pathology of the excised valve showed focal fibrous thickening without amyloid deposits. Postoperative wound care included negative pressure wound therapy (NPWT) initiated on postoperative day 2 to prevent surgical site infection (SSI), discontinued on day 13 without signs of infection. The patient was discharged on postoperative day 17 with no evidence of SSI.\n\nLaboratory and Clinical Course Post-Surgery  \nPlasma IL-6 levels transiently increased on postoperative days 1 and 2 but gradually declined by day 24, prior to resuming TCZ therapy on day 30. C-reactive protein (CRP), a marker of inflammation, peaked modestly at 0.56 mg/dL on day 2 and rose to 1.06 mg/dL by day 24 without clinical infection. Notably, vascular endothelial growth factor (VEGF) levels increased on day 13, preceding the CRP rise. Renal function, assessed by creatinine, showed a temporary postoperative increase but returned to baseline by day 24. Throughout the perioperative period, there was no recurrence of skin rash or lymphadenopathy.\n\nClinical Interpretation  \nThis case demonstrates that careful perioperative management, including temporary cessation of TCZ and continuation of corticosteroids, combined with comprehensive infection prevention measures, can enable safe cardiac surgery in patients with iMCD receiving immunomodulatory therapy. The transient postoperative increases in IL-6 and VEGF without infection suggest inflammatory responses related to surgery and disease activity rather than infectious complications. Resumption of TCZ after confirming absence of infection was well tolerated, with no disease exacerbation.\n\nNext Steps and Recommendations  \nContinued close monitoring of inflammatory markers (IL-6, CRP, VEGF) and clinical signs is essential in the postoperative period for patients with iMCD undergoing major surgery. Multidisciplinary coordination is critical to balance immunosuppression and infection risk. This case supports the feasibility of elective cardiac surgery with appropriate perioperative planning in patients treated with TCZ for Castleman disease."
+        }
+    },
+    {
+        "article": "Se trata de un paciente de sexo masculino de cuatro meses de edad, originario del centro de México y con dos hermanos hombres sanos. Durante el primer trimestre de gestación, su madre hipotiroidea consumió drogas. No obstante, el infante nació con peso y talla adecuados, fue alimentado con leche materna y recibió la vacuna del bacilo de Calmette-Guérin (BCG), sin desarrollo de cicatriz. La madre del paciente era prisionera en una cárcel y, junto con el bebé, compartían una celda insalubre con dos personas más.A los cuatro meses, el paciente fue valorado médicamente por un tumor doloroso en la región axilar izquierda. En la radiografía de tórax se observaron imágenes sugestivas de fracturas costales; se sospechó de maltrato infantil por parte de la madre, y el infante fue hospitalizado en un hospital pediátrico. Se determinó el peso (4.190 g) y la talla (58 cm) –por debajo del percentil tres–, saturación de oxígeno del 70 %, fiebre, tos, aumento de volumen en la región axilar izquierda, además de dolor, rubor y calor. En el cuadro hemático se encontró: hemoglobina de 8,8 g/dl (11,0 - 12,6), 29,3 × 109 leucocitos/L (6,0 - 17,5), 18,4 × 109 neutrófilos/L (1,0 - 8,5), 7,0 × 109 linfocitos/L (4,0 - 13,5), 3,5 × 109 monocitos/L, 459 × 109 plaquetas/L (150 - 350) y proteína C reactiva igual a 16 mg/L (< 3,0). En la primera tomografía toracoabdominal se observaron imágenes de un absceso en la región axilar izquierda, lesiones líticas en las costillas 3 a 6, neumonía apical izquierda, nódulos pulmonares en ambos pulmones y ganglios linfáticos cervicales y mediastinales incrementados de tamaño. En la biopsia del absceso axilar izquierdo se reportó miositis y paniculitis supurativa. Solo se hizo cultivo para bacterias del líquido broncoalveolar, el cual fue negativo, y la PCR para el complejo Mycobacterium tuberculosis fue negativa. Después de 41 días de hospitalización y de haber recibido dos esquemas de antimicrobianos –ceftriaxona-clindamicina y cefepima-vancomicina–, el paciente fue dado de alta.\n\nDos meses después, a los ocho meses de edad, reingresó al hospital por fiebre, irritabilidad y un absceso supurante en la escápula izquierda. En el cuadro hemático se encontró: hemoglobina de 10,8 g/dl (10,5 - 12), 21,2 × 109 leucocitos/L (6 - 17), 12,2 × 109 neutrófilos/L (1,5 - 8,5), 7,5 × 109 linfocitos/L (4 - 10,5), 1,2 × 109 monocitos/L (600), y 583 × 109 plaquetas/L (150 - 350); la prueba para la detección sérica de HIV fue negativa. En la tomografía de tórax se observó una consolidación apical izquierda, bronquiectasias, lesiones líticas en las costillas 2 a 7 y en las vértebras dorsales 2 a 7, además de una colección de líquido multiloculado; en el ultrasonido se encontró una fístula asociada con el absceso escapular. El paciente recibió piperacilina-tazobactam, que se sustituyó después por voriconazol al detectarse Aspergillus fumigatus en el cultivo de la muestra de secreción del absceso. Dada la recurrencia y la gravedad de la infección, se sospechó un error innato de la inmunidad. La prueba de dihidrorrodamina resultó sin producción de especies reactivas de oxígeno y la expresión de gp91phox en los neutrófilos fue nula, estableciéndose así el diagnóstico de enfermedad granulomatosa crónica ligada al cromosoma X. La variante patógena detectada por la secuenciación de nueva generación fue c.80_83del/Y (p.Val27Glyfs*33) en CYBB. La madre resultó portadora de la variante (c.80_83del/WT). No fue posible estudiar genéticamente a sus dos hermanos mayores, de sexo masculino, y aparentemente sanos. El paciente fue dado de alta después de 65 días de hospitalización y tratamiento con voriconazol por 28 días. Se inició profilaxis antibiótica diaria con trimetoprim-sulfametoxazol y profilaxis antifúngica con fluconazol dos veces a la semana. Dos meses después, al año de edad, el infante reingresó debido a una neumonía multifocal, por la cual requirió asistencia respiratoria mecánica. Se detectó el antígeno galactomanano en el suero y A. fumigatusen el cultivo del líquido del lavado broncoalveolar, por lo que se inició nuevamente tratamiento con voriconazol. El paciente sufrió una falla orgánica múltiple y falleció un mes después de su ingreso.\n",
+        "gold_summary": "Se presenta el caso de un infante con enfermedad granulomatosa crónica y aspergilosis invasiva. Se trata de un lactante de sexo masculino de cuatro meses de edad, de madre hipotiroidea y con quien convive en la celda de la cárcel. El infante presentó tumores en la región axilar izquierda y la radiografía de tórax sugirió fracturas costales; fue hospitalizado ante la sospecha de maltrato infantil. En la tomografía de tórax se observó un absceso axilar, osteólisis de costillas, neumonía y nódulos pulmonares; el paciente recibió antibióticos de amplio espectro y fue dado de alta. A los ocho meses, reingresó por fiebre y extensión del absceso purulento hacia la región escapular izquierda; en la tomografía se observaron imágenes de empeoramiento de la condición. Se aisló Aspergillus fumigatus de la secreción del absceso y se diagnosticó aspergilosis invasiva; se inició tratamiento con voriconazol por 28 días. Mediante la prueba de dihidrorrodamina, se diagnosticó enfermedad granulomatosa crónica causada por la variante patógena c.80_83del/Y del gen CYBB, portada por la madre (c.80_83del/WT). A los 12 meses, el paciente reingresó nuevamente por aspergilosis invasiva, resistente al tratamiento, con desenlace fatal.",
+        "synthetic_summary": {
+            "B1": "A baby boy was very sick. He had a big sore under his arm and a cough. Doctors found he had broken ribs and a bad lung infection.\n\nThe baby got medicine and stayed in the hospital. Later, he got sick again with a bad sore on his back. Doctors found a tiny bug called fungus in the sore. They gave him special medicine.\n\nThe doctors found out his body had trouble fighting germs. His mom also had a tiny change in her body that caused this. The baby got very sick many times and could not get better. He passed away when he was one year old.",
+            "B2": "**Case Summary: A Baby with a Rare Immune Disease and Fungal Infection**\n\nThis is the story of a baby boy from central Mexico who had a serious health problem called chronic granulomatous disease (CGD). CGD is a rare condition where the immune system, which normally fights infections, does not work properly. Because of this, the baby got a dangerous fungal infection called invasive aspergillosis, caused by a fungus named Aspergillus fumigatus.\n\n**What Happened at First**\n\nThe baby was four months old when he was first taken to the hospital. He had a painful lump under his left arm and a chest X-ray showed possible broken ribs. Doctors were worried about child abuse, so they admitted him to the hospital. Scans showed an abscess (a painful collection of pus) near his left armpit, damage to some ribs, pneumonia (lung infection), and small lumps in his lungs. He was treated with strong antibiotics and sent home after more than a month.\n\n**The Infection Returns and Gets Worse**\n\nAt eight months old, the baby came back to the hospital with fever and a larger pus-filled abscess near his shoulder blade. Scans showed the infection had spread and damaged more bones in his ribs and spine. Tests on the pus found the fungus Aspergillus fumigatus. This confirmed he had invasive aspergillosis, a serious fungal infection. Doctors started treating him with an antifungal medicine called voriconazole.\n\n**Finding the Cause: A Genetic Immune Problem**\n\nBecause the infection kept coming back and was very severe, doctors suspected a problem with his immune system. A special test called the dihydrorhodamine test showed his immune cells could not produce reactive oxygen species—chemicals needed to kill germs. This confirmed he had chronic granulomatous disease. Genetic testing found a mutation (a change) in a gene called CYBB, which causes the disease. His mother carried the same gene change but did not have symptoms.\n\n**Final Outcome**\n\nAt one year old, the baby was hospitalized again with a severe lung infection caused by the same fungus. Despite treatment, his condition worsened, leading to multiple organ failure. Sadly, he passed away one month after this last hospital stay.\n\n**What This Means**\n\nThis case shows how chronic granulomatous disease can cause serious infections that are hard to treat. Early diagnosis is important so doctors can give the right medicines and protect patients from dangerous germs. It also highlights the role of genetics in some immune system problems.",
+            "B3": "**Background**  \nThis case involves a male infant from central Mexico, born to a mother with hypothyroidism who was incarcerated and living in an unsanitary prison cell with the infant. The infant was four months old when first evaluated due to a painful swelling in the left armpit (axillary region). Initial chest X-rays suggested rib fractures, raising concerns about possible child abuse. The infant was hospitalized for further evaluation and treatment.\n\n**Key Findings**  \n- At four months, imaging revealed an abscess in the left axilla, bone destruction (osteolytic lesions) in ribs 3 to 6, pneumonia in the upper left lung, pulmonary nodules in both lungs, and enlarged lymph nodes in the neck and mediastinum (central chest area).  \n- Laboratory tests showed anemia (hemoglobin 8.8 g/dL), elevated white blood cell count with neutrophilia, increased platelets, and elevated C-reactive protein, indicating inflammation and infection.  \n- Biopsy of the axillary abscess showed muscle and fat tissue inflammation with pus formation (miositis and paniculitis supurativa).  \n- Cultures for bacteria and PCR testing for Mycobacterium tuberculosis were negative.  \n- The infant received broad-spectrum antibiotics (ceftriaxone-clindamycin and cefepime-vancomycin) and was discharged after 41 days.\n\n- At eight months, the infant was readmitted with fever, irritability, and a spreading purulent abscess near the left shoulder blade (scapula).  \n- Imaging showed worsening lung consolidation, bronchiectasis (permanent airway dilation), new osteolytic lesions in ribs 2 to 7 and vertebrae 2 to 7, and a multiloculated fluid collection with an associated fistula.  \n- Blood tests indicated persistent inflammation; HIV testing was negative.  \n- Culture of the abscess secretion isolated Aspergillus fumigatus, a fungus causing invasive aspergillosis. Treatment was switched to voriconazole, an antifungal medication.  \n\n- Due to recurrent severe infections, an innate immune defect was suspected.  \n- A dihydrorhodamine (DHR) test, which measures neutrophil production of reactive oxygen species critical for killing pathogens, was abnormal, showing no reactive oxygen species production.  \n- Flow cytometry revealed absent expression of gp91^phox, a protein essential for neutrophil function.  \n- Genetic sequencing identified a pathogenic mutation (c.80_83del/Y, causing a frameshift and premature stop codon) in the CYBB gene, confirming X-linked chronic granulomatous disease (CGD).  \n- The mother was found to be a carrier of this mutation (heterozygous for c.80_83del). Genetic testing of the two older brothers was not performed.\n\n- After 65 days of hospitalization and 28 days of voriconazole treatment, the infant was discharged with daily antibiotic prophylaxis (trimethoprim-sulfamethoxazole) and twice-weekly antifungal prophylaxis (fluconazole).\n\n- At one year of age, the infant was readmitted with multifocal pneumonia requiring mechanical ventilation.  \n- Serum galactomannan antigen testing and bronchoalveolar lavage cultures again confirmed invasive Aspergillus fumigatus infection.  \n- Despite resuming voriconazole treatment, the infant developed multiple organ failure and died one month later.\n\n**Clinical Interpretation**  \nThis infant’s presentation of recurrent severe infections, including invasive aspergillosis and osteomyelitis (bone infection), combined with the absence of neutrophil oxidative burst activity and the identified CYBB gene mutation, confirms a diagnosis of X-linked chronic granulomatous disease. CGD is a primary immunodeficiency characterized by defective neutrophil function leading to impaired killing of certain bacteria and fungi, predisposing patients to life-threatening infections. The presence of Aspergillus fumigatus infections is typical in CGD patients. The initial suspicion of child abuse was reconsidered in light of the underlying immunodeficiency and infection-related bone lesions.\n\n**Next Steps and Management**  \n- The patient was managed with prolonged antifungal therapy and antibiotic prophylaxis to prevent recurrent infections.  \n- Genetic counseling was provided to the family, given the X-linked inheritance pattern and maternal carrier status.  \n- Unfortunately, despite aggressive treatment, the infant succumbed to invasive fungal infection complicated by multiple organ failure.  \n- Early diagnosis of CGD is critical to initiate prophylactic therapies and consider curative options such as hematopoietic stem cell transplantation.  \n- Family members, especially male siblings, should be evaluated for carrier status or disease to enable early intervention."
+        }
+    },
+    {
+        "article": "Se trata de un hombre de 66 años de edad que vive en la ciudad de Juan Bautista Alberdi de la provincia de Buenos Aires, con antecedentes de hipertensión arterial y trastorno obsesivo compulsivo. Su medicación habitual incluía amlodipina, quetiapina, venlafaxina y ácido valproico. Consultó por presentar fiebre de 39ºC de cuatro días de evolución sin síntomas asociados y se internó para estudio en sala general. Al examen de ingreso se constató un paciente lúcido, sin foco motor, sin trastorno sensitivo ni rigidez de nuca (escala de coma de Glasgow (GCS) 15/15). El resto del examen físico y el laboratorio general no presentaron particularidades. Los cultivos de sangre y orina resultaron negativos, y la tomografía computarizada de encéfalo, tórax, abdomen y pelvis no mostró afecciones. A las 24 horas agregó episodios de desorientación témporo-espacial que alternaban con otros de somnolencia (GCS 13/15). Al examen físico se constató temblor grueso distal en los cuatro miembros. El examen del LCR informó: líquido incoloro, límpido, y aspecto post centrifugado también límpido. Recuento de leucocitos 310/mm3 (mononucleares 54%, polimorfonucleares 46%), hematíes < de 1000/mm3, proteínas 0.76 g/l, glucosa 54 mg/dl (glucemia 120 mg/dl), y ácido láctico 21 mg/dl. Se inició tratamiento empírico con aciclovir 10 mg/kg endovenoso cada 8 horas. Se solicitaron en LCR: PCR para virus de herpes simple (VHS) y para virus de encefalopatía equina del oeste (VEEO) que resultaron no reactivas. Sin embargo, la IgM (ELISA) para EEO resultó positiva en suero y en LCR a los diez días. La RMN de encéfalo evidenció aumento en la intensidad en secuencias FLAIR y T2 a nivel de la región dorsal del tronco encefálico (tanto protuberancial, como también bulbar y mesencefálico), ambos pedúnculos cerebrales y ganglios de la base, con afectación bilateral y ligero predominio ganglio basal derecho. También se observaron múltiples imágenes focales hiperintensas en la sustancia blanca de ambos hemisferios cerebrales. El paciente evolucionó con deterioro del sensorio (GCS 8/15), sin protección de la vía aérea, por lo que ingresó a UTI. Requirió intubación y ventilación mecánica, con utilización de sedación y analgesia. Al ingreso a UTI presentaba: estado ácido-base (EAB) arterial: pH 7.11, pCO2 136 mmHg, pO2 75 mmHg, bicarbonato 43 mEq/l, exceso de base 11 mEq/l, saturación 88% (Con FIO2 21%), ácido láctico 11.5 mg/dl. Se inició la ventilación mecánica con un volumen minuto respiratorio (VMR) de 9.8 litros (volumen tidal 490 ml que corresponde a 6 ml/kg de peso teórico, frecuencia respiratoria 20 por minuto, presión positiva al final de espiración (PEEP) 5 cmH2 O, fracción inspirada de oxígeno 30%) se extrajo sangre para EAB arterial: pH 7.40, pCO2 41 mmHg, pO2 65 mmHg, bicarbonato 28 mEq/l, exceso de base 0 mEq/l, saturación 93%, PAFI 216. Evolucionó sin fiebre, estable hemodinámicamente, con adecuada oxigenación y ritmo diurético. Al suspender sedantes presentó GCS de 3 puntos sobre 10 (correspondiente con evaluación ocular 1 y motor 2 puntos), con rigidez generalizada y reflejos osteotendinosos adecuados, con movimientos rítmicos linguales y peribucales. El electroencefalograma de 12 canales no evidenció descargas patológicas. Al décimo día de inicio de los síntomas presentó apertura ocular y menor rigidez, pero no toleraba la modalidad respiratoria espontánea por hipoventilación e hipercapnia que lo llevaron a hipoxemia transitoria. En el EAB arterial presentó: pH 7.31, pCO2 70 mmHg, pO2 76 mmHg, bicarbonato 35 mEq/l, exceso de base 8 mEq/l bajo asistencia ventilatoria en modalidad espontánea de presión soporte de 5 cmH2 O, frecuencia respiratoria 6 por minuto, PEEP 5 cmH2 O y volumen tidal entre 120-150 ml. Los siguientes días el paciente se conectó, respondiendo órdenes simples y complejas, y movilizó simétricamente los miembros con cierta debilidad. Por intolerancia a las pruebas ventilatorias espontáneas fue traqueostomizado. En la evaluación funcional respiratoria presentaba presión inspiratoria máxima menor a -40 cm de H2 O, presión espiratoria máxima mayor a 80 cm de H2 O, pero continuaba con hipercapnia en la prueba ventilatoria espontánea, por lo que requirió soporte ventilatorio con modalidad controlada. Se realizó ecocardiograma transtorácico que informó cavidades derechas normales, sin signos de hipertensión pulmonar. En la nueva RMN de encéfalo se evidenció disminución de las áreas hiperintensas en secuencias FLAIR y T2 visibles previamente.\n\nEl enfermo evolucionó con requerimiento de menor soporte ventilatorio en forma progresiva al momento del desarrollo de este informe.",
+        "gold_summary": "Presentamos el caso de un varón de 66 años de edad oriundo de la ciudad Juan Bautista Alberdi de la provincia de Buenos Aires con antecedentes de hipertensión arterial y trastorno obsesivo compulsivo. Consultó por fiebre súbita de cuatro días de evolución, con desarrollo de encefalopatía durante su internación. La punción lumbar mostró un líquido cefalorraquídeo cristalino, aunque inflamatorio de predominio mononuclear. La RMN de encéfalo informó hiperintensidad en secuencias FLAIR y T2 en el dorso del tronco encefálico. Ingresó a terapia intensiva por deterioro neurológico y acidosis respiratoria grave, requiriendo asistencia ventilatoria mecánica. Luego de 10 días presentó mejoría neurológica, sin déficit motor pero con hipoventilación alveolar que dificultaron el destete del respirador.",
+        "synthetic_summary": {
+            "B1": "There was a man who felt very sick with a fever. He got very sleepy and confused. The doctors took some fluid from his back to check. His brain pictures showed some changes. He needed help to breathe with a machine. After many days, he started to feel a little better. He could move his arms and legs. But he still needed help to breathe well. The doctors took good care of him.",
+            "B2": "**Patient Background and Symptoms**  \nThis is a 66-year-old man from Juan Bautista Alberdi, Buenos Aires. He has high blood pressure and obsessive-compulsive disorder. He came to the hospital with a sudden fever lasting four days. While in the hospital, he developed encephalopathy, which means his brain was not working properly.\n\n**Tests and Findings**  \nA lumbar puncture, where fluid around the brain and spine is collected, showed clear fluid but with signs of inflammation, mostly from certain immune cells called mononuclear cells. An MRI scan of his brain showed unusual bright areas in parts of his brainstem, which is the lower part of the brain that controls many vital functions.\n\n**Hospital Course and Treatment**  \nHis condition got worse, and he was moved to the intensive care unit because his brain function declined and he developed severe breathing problems caused by his lungs not removing carbon dioxide properly (called respiratory acidosis). He needed a machine to help him breathe. After about 10 days, he started to improve neurologically. He did not have muscle weakness, but he still had trouble breathing deeply on his own. This made it hard to take him off the breathing machine.\n\n**What This Means**  \nThis case shows how a brain infection or inflammation can cause serious problems with thinking and breathing. Even when brain function improves, breathing issues can continue and require ongoing support. Doctors must carefully monitor both brain and lung function in such patients.",
+            "B3": "Background  \nThis case involves a 66-year-old man from Juan Bautista Alberdi, Buenos Aires province, with a medical history of hypertension and obsessive-compulsive disorder. His regular medications included amlodipine, quetiapine, venlafaxine, and valproic acid. He initially presented with a sudden onset of high fever (39ºC) lasting four days, without other associated symptoms, and was admitted for evaluation.\n\nKey Findings  \nDuring hospitalization, the patient developed encephalopathy characterized by fluctuating episodes of temporal-spatial disorientation and somnolence. Neurological examination revealed a coarse distal tremor in all four limbs. Initial cerebrospinal fluid (CSF) analysis showed a clear, colorless fluid with an inflammatory profile predominantly of mononuclear cells (54%) and a significant leukocyte count (310/mm³), normal glucose relative to blood glucose, mildly elevated protein, and low lactate levels. Polymerase chain reaction (PCR) tests for herpes simplex virus and western equine encephalitis virus in CSF were negative; however, enzyme-linked immunosorbent assay (ELISA) detected positive IgM antibodies against eastern equine encephalitis virus (EEEV) in both serum and CSF ten days after symptom onset. Brain magnetic resonance imaging (MRI) demonstrated increased signal intensity on FLAIR and T2 sequences in the dorsal brainstem (including the pons, medulla, and midbrain), bilateral cerebral peduncles, and basal ganglia with a slight right-sided predominance, along with multiple hyperintense focal lesions in the white matter of both cerebral hemispheres.\n\nClinical Interpretation  \nThe patient’s neurological status deteriorated to a Glasgow Coma Scale (GCS) score of 8/15, with loss of airway protection, necessitating admission to the intensive care unit (ICU), endotracheal intubation, and mechanical ventilation. Arterial blood gas analysis revealed severe respiratory acidosis with hypercapnia (elevated carbon dioxide levels) and hypoxemia (reduced oxygen levels). Ventilatory support was carefully adjusted, resulting in improved acid-base balance and oxygenation. Sedation withdrawal revealed a low GCS score (3/10) with generalized rigidity and preserved tendon reflexes, accompanied by rhythmic tongue and perioral movements. Electroencephalography showed no pathological discharges. After ten days, the patient exhibited partial neurological recovery with eye opening and reduced rigidity but continued to experience alveolar hypoventilation (inadequate ventilation at the lung level) and hypercapnia, complicating weaning from mechanical ventilation. Functional respiratory testing indicated adequate inspiratory and expiratory muscle strength but persistent hypoventilation during spontaneous breathing trials, leading to the decision to perform a tracheostomy. Follow-up brain MRI showed a reduction in previously noted hyperintense lesions.\n\nNext Steps  \nThe patient’s clinical course demonstrated gradual neurological improvement and a progressive decrease in ventilatory support requirements. Continued respiratory rehabilitation and monitoring are essential to facilitate successful weaning from mechanical ventilation. Ongoing neurological assessment and supportive care remain critical, given the severity of encephalitis caused by eastern equine encephalitis virus, a rare but serious infection affecting the central nervous system."
+        }
+    },
+    {
+        "article": "Mujer de 27 años de edad oriunda del interior de la Provincia de Buenos Aires sin antecedentes personales o familiares de relevancia, consultó por sangrado vaginal. El estudio colposcópico evidenció formación polipoide que protruía por el orificio cervical externo (OCE). Se arribó clínicamente al diagnóstico de mioma nascens y se tomó una muestra de biopsia para su evaluación. Ante el diagnóstico patológico de sarcoma, se instauró quimioterapia, con el fin de reducir la masa lesional. Una vez lograda la reducción del tamaño, se decidió derivarla a nuestra institución para realizar tratamiento quirúrgico. Se recibió una pieza de histerectomía total con anexos, f ijada en formol al 10%. Cuerpo de 5 × 5 × 3.2 cm, cuello de 3.5 × 3 × 2 cm, ambas trompas de 4.5 × 0.7 cm y ovarios de 4 × 2.5 × 2.5 cm. A la apertura de la pieza, se observó a nivel de la unión cérvico-ístmica una formación polipoide pediculada de 8.5 cm de diámetro, que emergía hacia el canal endocervical y se exteriorizaba por el OCE. La superficie externa era parda, lobulada, con sectores rojizos. Al corte, se observaba blanquecina, blanda, con sectores de aspecto gelatinoso y formaciones quísticas de hasta 0,6 cm de dimensión máxima. Luego del procesamiento de rutina, se efectuaron secciones histológicas y se colorearon con hematoxilina-eosina (H-E), las cuales evidenciaron sectores celulares alternados por áreas laxas, mixoides junto a glándulas ístmico-endometriales típicas. La proliferación, predominantemente fusocelular atípica se disponía en nidos, constituidos por células de amplio citoplasma eosinófilo y núcleos excéntricos con cromatina homogénea, algunos pleomórficos. Se apreciaron estriaciones citoplasmáticas transversales en dichas células. El estroma era ampliamente mixoide y ricamente vascularizado. Se destacaban focalmente áreas celulares densamente condensadas inmediatas y próximas al revestimiento epitelial intacto, pero separadas de él, por una fina capa de estroma laxo. Esto se conoce como cambium layer o capa cambial. Se realizaron técnicas de inmunohistoquímica para desmina, actina músculo específico (AME) y miogenina (MYF4), las cuales resultaron positivas, mientras que la actina músculo liso fue negativa. Esta inmunomarcación permitió comprobar la estirpe muscular estriada y en última instancia arribar al diagnóstico, junto al cuadro morfológico, de RMS embrionario. Asimismo, la presencia de rabdomioblastos agrupados constituyendo la capa cambial a nivel subepitelial resultó fundamental y necesario para tipificar al RMS embrionario como botrioide, independientemente de la presentación macroscópica en forma de racimos polipoides.",
+        "gold_summary": "Presentamos el caso de una mujer de 27 años que consultó por sangrado vaginal y en quien se evidenció en la colposcopia, una lesión polipoide blanquecina que se exteriorizaba a través del orificio cervical externo. El estudio histológico reveló sectores celulares alternados por áreas laxas, mixoides, junto a glándulas ístmico-endometriales típicas. La proliferación fusocelular atípica, se disponía en nidos, constituidos por células de amplio citoplasma eosinófilo con estriaciones citoplasmáticas transversales y núcleos excéntricos con cromatina homogénea. Se exhibían áreas de células densamente condensadas inmediatas y próximas al revestimiento epitelial intacto, pero separadas de él, por una fina capa de estroma laxo (capa cambial). El perfil de inmunomarcación resultó positivo para desmina, actina músculo específico y miogenina, y negativo para actina músculo liso. Se realizó diagnóstico de rabdomiosarcoma embrionario botroide de cuerpo uterino.",
+        "synthetic_summary": {
+            "B1": "A young woman had some bleeding. Doctors found a small, soft lump in her body. They looked at it very closely with a microscope. The lump had special muscle cells inside. These cells helped the doctors know what it was. The doctors said it was a kind of muscle lump called embryonal rhabdomyosarcoma. They will help her feel better.",
+            "B2": "**What Happened:**  \nA 27-year-old woman went to the doctor because she had vaginal bleeding. During the exam, doctors found a white, polyp-like growth sticking out from the opening of her cervix (the lower part of the uterus). A polyp is a small lump of tissue that can grow in places like the cervix.\n\n**What They Found:**  \nThe doctors took a small tissue sample (called a biopsy) to look at under a microscope. They saw that the tissue had unusual cells mixed with normal gland cells from the uterus. The unusual cells were shaped like spindles and grouped in clusters. These cells had certain features, like pinkish cytoplasm (the cell’s body) with tiny stripes and nuclei (the cell’s control center) that looked different from normal.\n\nNear the surface lining of the cervix, they noticed a special layer of tightly packed cells separated by a thin layer of loose tissue. This layer is called the \"cambium layer\" and is important in identifying certain tumors.\n\n**How They Confirmed the Diagnosis:**  \nThe doctors used special tests called immunohistochemistry. These tests check for proteins that help identify what type of cells are present. The tumor cells tested positive for proteins called desmin, specific muscle actin, and myogenin. They tested negative for smooth muscle actin. This pattern showed that the tumor came from skeletal muscle cells, not smooth muscle.\n\n**What It Means:**  \nAll these findings led to the diagnosis of a rare type of cancer called embryonal botryoid rhabdomyosarcoma. This is a cancer that starts in immature muscle cells and often forms grape-like clusters (botryoid means \"like a bunch of grapes\"). It happened in the uterus of this young woman.\n\nThis diagnosis is important because it guides the treatment, which usually includes chemotherapy to shrink the tumor and surgery to remove it.",
+            "B3": "**Background**  \nA 27-year-old woman from the interior region of Buenos Aires Province, with no significant personal or family medical history, sought medical attention due to vaginal bleeding. During colposcopic examination, a polypoid (polyp-like) lesion was observed protruding through the external cervical os (the opening of the cervix). Initially suspected to be a myoma nascens (a type of benign fibroid tumor), a biopsy was taken for further evaluation.\n\n**Key Findings**  \nHistological analysis of the biopsy revealed a complex tissue pattern characterized by alternating cellular areas and loose, myxoid (gelatinous) regions, alongside typical isthmic-endometrial glands (glands from the region between the cervix and uterine body). The predominant cell population was atypical spindle-shaped (fusocellular) cells arranged in nests. These cells exhibited abundant eosinophilic cytoplasm (pink-staining under microscope), transverse cytoplasmic striations (indicative of muscle differentiation), and eccentric nuclei with uniform chromatin.  \n\nNotably, there were focal areas of densely packed cells located immediately beneath the intact epithelial lining but separated from it by a thin layer of loose connective tissue (stroma). This arrangement is known as the \"cambium layer,\" a characteristic feature in certain tumors.  \n\nImmunohistochemical staining—a technique that uses antibodies to detect specific proteins—showed positive results for desmin, specific muscle actin (actina músculo específico), and myogenin (MYF4), all markers indicative of striated muscle differentiation. Conversely, staining was negative for smooth muscle actin, helping to exclude smooth muscle tumors.\n\n**Clinical Interpretation**  \nCombining the microscopic features with the immunohistochemical profile, the diagnosis was established as embryonal rhabdomyosarcoma (RMS) of the uterine body, specifically the botryoid subtype. The presence of the cambium layer composed of clustered rhabdomyoblasts (immature muscle cells) beneath the epithelium was critical for this classification, regardless of the lesion’s polypoid gross appearance.\n\n**Next Steps**  \nFollowing the pathological diagnosis, the patient underwent chemotherapy aimed at reducing the tumor mass. After achieving significant reduction, she was referred for surgical treatment, which involved total hysterectomy with removal of adnexal structures (fallopian tubes and ovaries). The surgical specimen confirmed the presence of the described tumor at the cervico-isthmic junction, consistent with the initial diagnosis.\n\nThis case highlights the importance of thorough histopathological and immunohistochemical evaluation in young women presenting with unusual cervical masses and vaginal bleeding, to accurately diagnose rare malignant tumors such as botryoid embryonal rhabdomyosarcoma and guide appropriate multimodal treatment."
+        }
+    },
+    {
+        "article": "Un hombre de 53 años de edad, que inició diálisis por disfunción renal en etapa terminal debido a nefropatía diabética o nefroesclerosis en nuestro departamento de nefrología 10 años antes, se sometió a una ecocardiografía de seguimiento anual para estenosis valvular aórtica progresiva (AVS) y regurgitación moderada con fracción de eyección ventricular izquierda (LVEF) normal. Un año antes, se observaron calcificaciones que sugerían MAC en el anillo mitral posterior, que no se habían visto dos años antes. En el último seguimiento, la ecocardiografía reveló una masa redonda de superficie lisa de 22 × 17 mm con alta ecogenicidad en el área circundante y un brillo interno ligeramente disminuido en el anillo mitral posterior del lado auricular izquierdo. El paciente no tenía síntomas significativos ni hallazgos físicos, excepto un soplo sistólico.\n\nLa ecocardiografía también reveló una VS moderada con un flujo de pico valvular transaórtico de 3,76 m/s y una regurgitación valvular aórtica moderada. Se observó una regurgitación mitral leve pero no estenosis. El patrón de velocidad de flujo de entrada del VI mostró un patrón pseudo-normal con un agrandamiento de la aurícula izquierda de 47 mm de diámetro. La ecocardiografía en serie durante dos años reveló un agrandamiento del VI y una disminución de la FEVI. El diámetro final diastólico/final sistólico del VI y la FEVI fueron de 50/33 mm y 64 %, respectivamente, hace dos años; 57/41 mm y 52 % hace un año; y 59/47 mm y 42 % en el último seguimiento.\n\nTeniendo en cuenta el estado de la hemodiálisis, predijimos la progresión a una AVS casi severa, con empeoramiento de la disfunción sistólica del LV, que se convertiría en una indicación para el reemplazo de la válvula aórtica (AVR) en un futuro cercano.\n\nLa tomografía computarizada (TC) reveló una masa de alta densidad sin realce de contraste. La resonancia magnética (MRI) mostró una masa bien definida de alta intensidad en el centro, con un borde hipointenso en la imagen T1 y una señal desprovista en T2. Se excluyeron los neoplasmas, incluidos los mixomas y los fibroelastomas papilares, en función de sus características de imagen. Los hallazgos de laboratorio no indicaron infección, y no se sospechó de vegetación con endocarditis infecciosa. Teniendo en cuenta la disfunción renal en etapa terminal en la hemodiálisis y los hallazgos de imagen, se sospechó CCMA. El rápido agrandamiento de la masa generó preocupación sobre una potencial embolia. En consecuencia, la masa se resecó con AVR.\n\nLa incisión del atrio izquierdo reveló una masa por debajo del endocardio auricular en el anillo de la válvula mitral (P1-2); se observaron sustancias cremosas en la incisión de la masa, lo que sugiere CCMA. Después de la extirpación y desbridamiento del tejido, el sitio de la incisión se suturó con prolina. Se realizó el reemplazo de la válvula aórtica utilizando una válvula SJM de 21 mm. La retirada del bypass cardiopulmonar fue relativamente suave. Al momento del alta, se prescribió warfarina y aspirina, junto con bisoprolol para la fibrilación auricular paroxística después de la cirugía.\n\nNo se observaron eventos embólicos antes o después de la cirugía.\n\nEl examen histopatológico reveló calcificaciones granulares y nodulares dispersas, que consistían principalmente en infiltración de células inflamatorias y proliferación vascular de neutrófilos, linfocitos, células espumosas, macrófagos tisulares y células plasmáticas, con osificación parcial compatible con CICM. La biopsia miocárdica LV para descartar cardiomiopatía secundaria y la válvula aórtica resecada mostraron células inflamatorias similares a las observadas en CICM. Por lo tanto, se diagnosticó CICM en base a la disminución del movimiento de la pared y la fibrosis miocárdica, con infiltración de células inflamatorias > 14 mm2, células T CD3 positivas > 7/mm2 y negatividad de tenascina C (4C8).7 Sin embargo, no se pudo determinar la causa de CICM.\n\nLa ecocardiografía 6 meses después de la resección no mostró recurrencia del tumor (ver material complementario en línea), ni progresión de la regurgitación mitral, función normal de la válvula aórtica protésica y ninguna mejora de la FEVI (41 %)\n\n",
+        "gold_summary": "Un hombre de 52 años con insuficiencia renal en fase terminal que requería hemodiálisis se sometió a una ecocardiografía anual de seguimiento para detectar una disfunción valvular aórtica. La ecocardiografía reveló una masa circular bien definida de 22 × 17 mm en el anillo de la valva mitral posterior que no se había detectado 2 años antes. En función de las características de la imagen, se sospechó que la masa era un CCMA. Se había agrandado rápidamente y suponía un riesgo potencial de embolia; por lo tanto, se extirpó al mismo tiempo que la sustitución de la válvula aórtica. Aunque se sospechó un CCMA en función de los hallazgos intraoperativos, el diagnóstico histopatológico fue un CAT. Tras el análisis histológico de la muestra de miocardio del ventrículo izquierdo y la válvula aórtica extirpada, se observó una infiltración de células inflamatorias crónicas; por lo tanto, se diagnosticó una cardiomiopatía inflamatoria crónica.\n",
+        "synthetic_summary": {
+            "B1": "A man had very sick kidneys and needed a machine to help him. Doctors checked his heart every year. They found a small round lump on his heart valve. The lump was new and getting bigger.\n\nThe lump could cause problems, so doctors took it out. They also fixed his heart valve. After looking at the lump and heart tissue, doctors found some sick cells inside. This meant the man had a long-lasting heart sickness.\n\nThe doctors helped him feel better by fixing his heart.",
+            "B2": "**What They Found**  \nA 52-year-old man with severe kidney failure was getting regular heart ultrasounds to check his heart valves. During one test, doctors found a round lump about 22 by 17 millimeters in size on the ring of his mitral valve, which is a valve that controls blood flow in the heart. This lump was not there two years earlier. Based on the images, doctors thought it might be a caseous calcification of the mitral annulus (CCMA). CCMA is a rare condition where calcium builds up and forms a soft, cheese-like mass in the heart valve ring.\n\n**What It Means**  \nThe lump was growing quickly and could cause serious problems like an embolism, which is when something blocks blood flow in the body. Because of this risk, doctors decided to remove the lump during surgery while also replacing the patient’s aortic valve, another heart valve that was not working well.\n\n**What They Learned After Surgery**  \nEven though the lump looked like CCMA during surgery, the detailed lab tests on the tissue showed it was actually a calcified amorphous tumor (CAT). This is a rare, non-cancerous growth made of calcium and other materials. Further tests on the heart muscle and the removed aortic valve showed many chronic inflammatory cells—these are immune cells that indicate long-term inflammation. Because of this, doctors diagnosed the patient with chronic inflammatory cardiomyopathy, a condition where the heart muscle is inflamed over a long time.\n\n**Summary**  \nIn short, a man with kidney failure had a growing lump on his heart valve. It looked like one condition but turned out to be a rare tumor linked to long-lasting heart inflammation. The lump was safely removed, and the faulty valve was replaced to help his heart work better.",
+            "B3": "**Background**  \nA 52-year-old man with end-stage renal disease (ESRD) requiring hemodialysis underwent annual echocardiographic monitoring due to progressive aortic valve dysfunction. His renal failure was secondary to diabetic nephropathy or nephrosclerosis, and he had a history of aortic valve stenosis and moderate regurgitation with preserved left ventricular ejection fraction (LVEF) at baseline.\n\n**Key Findings**  \nDuring the latest echocardiogram, a newly identified, well-defined, round mass measuring 22 × 17 mm was detected on the posterior mitral valve annulus. This mass was absent in imaging studies performed two years earlier. The mass exhibited high echogenicity with a smooth surface and slightly reduced internal brightness, raising suspicion for caseous calcification of the mitral annulus (CCMA), a rare form of mitral annular calcification characterized by a toothpaste-like consistency. The mass had enlarged rapidly, creating concern for potential embolic complications.\n\nAdditional echocardiographic findings included moderate aortic valve stenosis with a peak transaortic flow velocity of 3.76 m/s, moderate aortic regurgitation, mild mitral regurgitation without stenosis, and a pseudo-normal diastolic filling pattern of the left ventricle (LV). Serial echocardiograms over two years showed progressive LV enlargement and declining systolic function, with LVEF decreasing from 64% to 42%.\n\nComputed tomography (CT) revealed a high-density mass without contrast enhancement, while cardiac magnetic resonance imaging (MRI) showed a well-circumscribed lesion with high central intensity and hypointense borders on T1-weighted images and signal void on T2-weighted images. These imaging characteristics helped exclude cardiac tumors such as myxomas and papillary fibroelastomas. Laboratory tests showed no signs of infection, and infective endocarditis was ruled out.\n\n**Clinical Interpretation**  \nGiven the patient’s ESRD on hemodialysis and imaging features, CCMA was the leading diagnosis. However, the rapid growth of the mass and risk of embolism warranted surgical intervention. The patient underwent surgical excision of the mass combined with aortic valve replacement (AVR).\n\nIntraoperative findings revealed a mass beneath the left atrial endocardium at the posterior mitral annulus (segments P1-2) containing a creamy substance consistent with CCMA. After mass removal and debridement, the mitral annulus was repaired, and the aortic valve was replaced with a 21 mm mechanical prosthesis. Postoperative recovery was uneventful, with anticoagulation and rate control medications initiated due to paroxysmal atrial fibrillation.\n\nUnexpectedly, histopathological examination of the excised mass demonstrated granular and nodular calcifications with extensive infiltration of chronic inflammatory cells, including neutrophils, lymphocytes, foam cells, macrophages, and plasma cells, along with partial bone formation (ossification). These findings were consistent with chronic inflammatory calcific cardiomyopathy (CICM), a diagnosis further supported by myocardial biopsy of the left ventricle and analysis of the excised aortic valve, both showing similar inflammatory cell infiltration. Immunohistochemical markers confirmed chronic inflammatory involvement with T-cell predominance and absence of tenascin C expression. The exact etiology of the CICM remained undetermined.\n\n**Next Steps and Follow-Up**  \nSix months post-surgery, echocardiography showed no recurrence of the mass, stable mild mitral regurgitation, normal function of the prosthetic aortic valve, and persistent reduced LVEF at 41%. No embolic events occurred before or after surgery.\n\nThe case highlights the diagnostic challenge in differentiating CCMA from other cardiac masses and underscores the importance of histopathological evaluation in cases with atypical features. It also illustrates the potential coexistence of chronic inflammatory cardiomyopathy in patients with ESRD and valvular calcifications. Continued cardiac monitoring and management of systolic dysfunction remain essential in this patient’s care."
+        }
+    },
+    {
+        "article": "Paciente masculino de 28 años, sin antecedentes de importancia, acude a consulta de dermatología con un cuadro cutáneo de 48 horas de evolución caracterizado por dos placas eritematosas con ampollas centrales más ulceración superficial localizadas en cara flexora de brazo y antebrazo derecho equidistantes del pliegue del codo, acompañadas de una sensación de ardor y prurito en el lugar de las lesiones. No presentó síntomas sistémicos ni se automedicó. Como antecedente refiere que se encontraba de vacaciones en la región costera de Ecuador al momento de aparecer las lesiones. Se realizó una biopsia incisional que reportó epidermis con acantosis, paraqueratosis y espongiosis, neutrófilos en estrato córneo e infiltrado linfocitario perivascular en dermis superficial, media y profunda. Por las características clínicas, el antecedente de viaje a una región tropical y los hallazgos histológicos se diagnosticó como dermatitis por Paederus. Se indicó tratamiento con antihistamínicos, esteroides tópicos y compresas frías. Después de 8 días de tratamiento, las lesiones remitieron dejando una hiperpigmentación postinflamatoria.",
+        "gold_summary": "Se comunica el caso de un paciente masculino de 28 años, que acude a consulta de dermatología con cuadro de 48 horas de evolución de dos placas eritematosas con ampollas centrales más ulceración superficial localizadas en cara flexora de brazo y antebrazo derecho, acompañadas de una sensación de ardor y prurito en el lugar de las lesiones, sin síntomas acompañantes. Como antecedente refiere que se encontraba de vacaciones en la región costera de Ecuador al momento de aparecer las lesiones. Se realizó una biopsia incisional y por las características clínicas y el antecedente de viaje a una región tropical se diagnosticó como dermatitis por Paederus y se indicó tratamiento con antihistamínicos, esteroides tópicos y compresas frías. Después de 8 días de tratamiento, las lesiones remitieron dejando una hiperpigmentación postinflamatoria.",
+        "synthetic_summary": {
+            "B1": "A man had red, sore spots on his arm. The spots had little blisters and hurt a bit. He felt itchy and burning there. \n\nHe got these spots while on a trip to a warm place. The doctor looked closely and said it was a skin problem from a bug. \n\nThe doctor gave him medicine and cold cloths to help. After some days, the spots got better but left some dark marks.",
+            "B2": "**What Happened:**  \nA 28-year-old man went to a skin doctor because he had two red patches on his right arm and forearm. These patches had blisters in the middle and some shallow sores. He felt burning and itching where the patches were. This had started just two days before he saw the doctor. He did not have any other symptoms and had not taken any medicine on his own. He said the patches appeared while he was on vacation in a coastal area of Ecuador, which is a tropical place.\n\n**What the Doctors Did:**  \nThe doctor took a small piece of skin from one of the patches to look at it under a microscope. This is called a biopsy. The skin sample showed certain changes that matched a condition called Paederus dermatitis. This is a skin irritation caused by contact with a small insect called Paederus, common in tropical areas.\n\n**Treatment and Outcome:**  \nThe doctor treated him with antihistamines (medicine that helps reduce itching), steroid creams (to reduce inflammation), and cold compresses (to soothe the skin). After eight days, the patches got better, but the skin where the patches were became darker than the surrounding skin. This darkening is called post-inflammatory hyperpigmentation and usually fades over time.\n\n**Summary:**  \nThis man’s skin problem was caused by an insect bite during his trip to a tropical area. With proper treatment, his skin improved quickly, though some temporary dark spots remained.",
+            "B3": "**Background:**  \nA 28-year-old man with no significant past medical history presented to a dermatology clinic with a skin condition that had developed over 48 hours. He exhibited two red (erythematous) plaques on the inner (flexor) surfaces of his right arm and forearm. Each plaque featured a central blister (vesicle) and superficial ulceration. The affected areas were equidistant from the elbow crease. The patient reported burning and itching sensations localized to the lesions but denied any systemic symptoms such as fever or malaise. He had not used any medications on his own. Notably, the lesions appeared while he was vacationing in a coastal region of Ecuador, a tropical environment.\n\n**Key Findings:**  \nA skin biopsy was performed, revealing several microscopic changes: thickening of the epidermis (acanthosis), retention of nuclei in the outer skin layer (parakeratosis), fluid accumulation between skin cells (spongiosis), presence of neutrophils (a type of white blood cell) in the outermost skin layer (stratum corneum), and a lymphocytic (another type of white blood cell) infiltrate surrounding blood vessels in the superficial, middle, and deep layers of the dermis (the skin’s inner layer).\n\n**Clinical Interpretation:**  \nBased on the clinical presentation, histological findings, and the patient’s recent travel to a tropical area, the diagnosis was established as Paederus dermatitis. This condition results from contact with Paederus beetles, which release an irritant toxin causing characteristic skin inflammation.\n\n**Next Steps:**  \nTreatment was initiated with oral antihistamines to reduce itching, topical corticosteroids to decrease inflammation, and cold compresses to soothe the affected skin. After eight days of therapy, the lesions resolved, leaving behind postinflammatory hyperpigmentation—areas of darker skin where the inflammation had occurred. The patient’s symptoms improved without complications."
+        }
+    },
+    {
+        "article": "Un hombre de 35 años de edad, herido en un accidente de tráfico, fue trasladado a nuestro hospital, que está equipado con un ER híbrido. Había sufrido una lesión potencialmente mortal, con su pierna derecha acortada y girada. Los signos vitales del paciente a su llegada fueron los siguientes: frecuencia respiratoria de 24 respiraciones/min, saturación de oxígeno del 99 % con 12 L de administración de oxígeno, frecuencia cardiaca de 143 latidos/min, presión arterial de 80/40 mmHg, y puntuación de Glasgow Coma Scale de E4V4M6. Intentamos realizar un TAC y resucitar al paciente. El TAC reveló un hemotórax izquierdo, ensanchamiento del mediastino, y fractura pélvica. Como la presión arterial del paciente cayó rápidamente antes del TAC, se administraron procedimientos de salvamento, como intubación de emergencia, preperitoneal pelvic packing, y transfusión masiva, con un cuidadoso control de la presión arterial en el ER híbrido. Después de la estabilización de los signos vitales con estos procedimientos, el TAC con contraste reveló una fractura de BTAI de grado IV que se extendía hacia la cavidad torácica izquierda. La embolización arterial transcatéter (TAE) para la fractura pélvica y la fijación esquelética externa de la fractura del fémur derecho se realizaron primero, ya que el radiólogo y el cirujano cardiovascular, que realizan TEVAR en nuestro centro médico, no estaban disponibles en ese momento. Posteriormente, se realizó TEVAR utilizando un injerto de stent (GORE C-TAG 26 × 150 mm; WL Gore & Associates, Flagstaff, Arizona, EE. UU.) en el ER híbrido sin transferir al paciente. Se desplegó un injerto de stent justo distal de la arteria carótida común izquierda (zona II) y el extremo distal del injerto de stent se posicionó en el nivel de Th 8. Decidimos sacrificar LSCA ya que el flujo sanguíneo de la arteria vertebral izquierda fue suficiente según lo evaluado por angiografía. El paciente no tuvo síntomas que sugirieran isquemia después de TEVER. Durante la cirugía, se administraron 50 unidades/kg (3000 unidades) de heparina. El paciente fue trasladado a un hospital de rehabilitación el día 41 postoperatorio.\n",
+        "gold_summary": "Un hombre de 35 años de edad sufrió múltiples lesiones tras un accidente de tráfico y fue trasladado a nuestro hospital en estado de shock. La tomografía computarizada reveló una fractura de TAI de grado IV que se extendía hasta la cavidad torácica y una fractura pélvica. Poco tiempo después de realizar un relleno pélvico preperitoneal y una embolización arterial transcatéter para la fractura pélvica, se realizó un TEVAR en el quirófano híbrido sin trasladar al paciente. El paciente fue trasladado a un hospital de rehabilitación el día 41 después de la operación.\n",
+        "synthetic_summary": {
+            "B1": "A man got hurt in a car crash. He had bad hurts in his chest and hip. Doctors helped him in the hospital. They fixed his hurts with special tools. After many days, he felt better. Then, he went to a place to get more help to get strong.",
+            "B2": "**What Happened to the Patient**  \nA 35-year-old man was hurt badly in a car accident and brought to the hospital in shock. Shock means his body was not getting enough blood flow. A special scan called a CT scan showed he had a serious tear in a large artery near his chest (called a grade IV traumatic aortic injury) and a broken pelvis.\n\n**How Doctors Treated Him**  \nFirst, doctors did a procedure to stop bleeding in his pelvis by packing the area and blocking certain blood vessels using a method called embolization. Then, without moving him to another room, they fixed the artery tear using a surgery called TEVAR. TEVAR stands for Thoracic Endovascular Aortic Repair, which means they placed a small tube called a stent inside the artery to keep it open and stop the bleeding.\n\n**What Happened After Treatment**  \nThe man stayed in the hospital to recover and was later sent to a rehabilitation hospital 41 days after the surgery. Rehabilitation is where patients get help to regain strength and heal after serious injuries.",
+            "B3": "**Background**  \nA 35-year-old man sustained multiple severe injuries in a traffic accident and was brought to our hospital in a state of shock. Upon arrival, his vital signs indicated respiratory distress, low blood pressure, and a rapid heart rate. He also exhibited a shortened and rotated right leg, suggesting significant trauma.\n\n**Key Findings**  \nInitial computed tomography (CT) scans revealed several critical injuries:  \n- A grade IV blunt thoracic aortic injury (BTAI), which extended into the left thoracic cavity.  \n- A pelvic fracture accompanied by a left-sided hemothorax (blood accumulation in the chest).  \n- Mediastinal widening, indicating possible vascular injury or bleeding.\n\nDue to rapid deterioration in blood pressure before the CT, emergency interventions were initiated, including intubation, preperitoneal pelvic packing (a surgical technique to control pelvic bleeding), and massive blood transfusion. After stabilizing the patient’s vital signs, contrast-enhanced CT confirmed the extent of the aortic injury.\n\n**Clinical Interpretation**  \nGiven the severity of the injuries, a staged approach was taken:  \n1. Transcatheter arterial embolization (TAE) was performed to control bleeding from the pelvic fracture.  \n2. External skeletal fixation was applied to stabilize the fractured right femur.  \n3. Thoracic endovascular aortic repair (TEVAR) was then conducted in the hybrid emergency room without transferring the patient. This procedure involved placing a stent graft (GORE C-TAG 26 × 150 mm) just distal to the left common carotid artery (zone II) and extending to the level of the eighth thoracic vertebra.  \n4. The left subclavian artery (LSCA) was intentionally sacrificed during the procedure because angiography demonstrated sufficient blood flow through the left vertebral artery, minimizing the risk of ischemia. The patient exhibited no signs of ischemic complications post-TEVAR.  \n5. During surgery, anticoagulation was managed with heparin at a dose of 50 units/kg (total 3000 units).\n\n**Next Steps**  \nFollowing successful stabilization and repair, the patient’s recovery progressed without major complications. He was transferred to a rehabilitation hospital on postoperative day 41 to continue recovery and functional restoration. This case highlights the importance of rapid multidisciplinary intervention and the utility of hybrid emergency rooms in managing complex trauma without patient transfer."
+        }
+    },
+    {
+        "article": "Hombre de 31 años con antecedentes de consumo de alcohol, tabaco, cocaína inhalada, tuberculosis pulmonar tratada, nefrectomía izquierda y esplenectomía post-traumática. Consultó al servicio de urgencias por cuadro de una semana de evolución que inició inmediatamente posterior a la aplicación intramuscular de penicilina por contacto sexual con pareja con sífilis, caracterizado por dolor en región glútea derecha que irradiaba hasta pie, con posterior aparición de dermatosis purpúrica relacionada con sitio de inyección, siendo una lesión tipo placa configurada en forma anular, con bordes irregulares y distribución racemosa que medía 15 centímetros (cm), con piel sana en su interior. También presentaba una pequeña escara escrotal y una extensa lesión plantar derecha de aspecto livedoide desde la zona talar hasta la punta de los dedos que no respetaba margen estricto. Se realizó ecografía del glúteo mayor, que mostró pérdida del patrón fibrilar heterogéneo, aumento del espesor del mismo a nivel de su tercio medio de aspecto edematoso, además de edema del tejido celular subcutáneo (TCS); en región plantar homolateral y en escroto edema de TCS. En el laboratorio presentó leucocitosis de 13.7 × 109/L, proteína C reactiva de 3.2 mg/dL (normal hasta 0.5 mg/dL), que se interpretaron como reactantes de fase aguda, también aumento de transaminasas con aspartato aminotransferasa de 175 UI/L (normal hasta 32), alanino aminotransferasa de 245 UI/L (normal hasta 33), creatina kinasa con un valor de 2741 UI/L (normal hasta 170) y lactato deshidrogenasa de 2499 UI/L (normal hasta 250) representando compromiso muscular. Se realizaron serologías completas para sífilis, con venereal disease research laboratory (VDRL y anticuerpos treponémicos), virus de la inmunodeficiencia humana (HIV) hepatitis B, hepatitis C, con resultados negativos. La cronología, las manifestaciones clínicas y la posterior biopsia, respaldaron el diagnóstico de síndrome de Nicolau, para lo cual se inició anticoagulación con enoxaparina 1 mg/ kg c/12 hs vía subcutánea, cilostazol 100 mg cada 12 horas y tramadol, por 10 días. Se realizó biopsia de piel de glúteo que evidenció necrosis epidérmica y extensión a epitelio folicular, con formación de ampolla secundaria a reepitelización, sin vasculitis ni trombosis vascular, vinculable a embolia cutis medicamentosa en fase aguda, hubo franca mejoría con descenso de valores de transaminasas, con aspartato aminotransferasa de 39 UI/L, alanino aminotransferasa de 77 UI/L y creatin kinasa de 167 UI/L.  No se solicitó perfil inmunológico, basados en que nuestro diagnóstico presuntivo inicial no justificaba la búsqueda de otras etiologías. Se otorgó alta con cilostazol y analgésicos, control ambulatorio a los 3 meses con mejoría del dolor y de las lesiones, quedando en glúteo derecho cicatriz discrómica con presencia de descamación fina y en pie derecho cicatriz discrómica con zonas de descamación gruesas en región de apoyo tarso metatarsiano asociado a mínimas lesiones livedoides en planta del mismo pie.",
+        "gold_summary": "Se reporta el caso de un hombre de 31 años que presenta este síndrome luego de la aplicación de penicilina benzatínica intramuscular. La biopsia apoyó el diagnóstico. Recibió tratamiento con enoxaparina y cilostazol con posterior mejoría.",
+        "synthetic_summary": {
+            "B1": "A man got a medicine shot in his bottom. After that, his skin got hurt and sore. The doctor took a tiny piece of his skin to look at it. The doctor gave him medicine to help him feel better. After some time, he started to get better.",
+            "B2": "**What Happened:**  \nA 31-year-old man developed a rare condition called Nicolau syndrome after receiving an injection of penicillin, an antibiotic, into his muscle. This syndrome can cause skin damage and pain near the injection site.\n\n**What They Found:**  \nA small piece of skin tissue (called a biopsy) was taken and showed damage to the skin layers but no signs of blood vessel inflammation or clots. This helped doctors confirm the diagnosis of Nicolau syndrome.\n\n**How They Treated It:**  \nThe man was treated with medicines to prevent blood clots (enoxaparin) and to improve blood flow (cilostazol). After treatment, his symptoms and skin lesions got better.\n\n**What It Means:**  \nNicolau syndrome is a serious but rare reaction to certain injections. Early diagnosis and treatment can help improve recovery and reduce complications.",
+            "B3": "**Background:**  \nA 31-year-old man with a history of alcohol and tobacco use, inhaled cocaine consumption, treated pulmonary tuberculosis, left kidney removal (nephrectomy), and traumatic spleen removal (splenectomy) presented to the emergency department. His symptoms began one week after receiving an intramuscular injection of benzathine penicillin, administered due to sexual contact with a partner diagnosed with syphilis.\n\n**Key Findings:**  \nThe patient initially experienced pain in the right gluteal (buttock) region radiating down to the foot. Subsequently, he developed a purpuric (purple-colored) skin rash at the injection site, characterized by a 15-centimeter annular (ring-shaped) plaque with irregular edges and a racemose (cluster-like) distribution, with healthy skin in the center. Additional lesions included a small scrotal eschar (dead tissue) and an extensive livedoid (mottled) lesion on the right sole extending from the heel to the toes without a clear margin.\n\nUltrasound imaging of the right gluteus maximus muscle revealed loss of normal fibrous pattern, heterogeneous texture, increased thickness with edema (swelling), and subcutaneous tissue swelling. Similar subcutaneous edema was noted on the right sole and scrotum.\n\nLaboratory tests showed elevated white blood cell count (leukocytosis of 13.7 × 10^9/L) and increased C-reactive protein (3.2 mg/dL; normal <0.5 mg/dL), indicating an acute inflammatory response. Liver enzymes were markedly elevated: aspartate aminotransferase (AST) at 175 IU/L (normal up to 32 IU/L) and alanine aminotransferase (ALT) at 245 IU/L (normal up to 33 IU/L). Muscle damage markers were also high, with creatine kinase (CK) at 2741 IU/L (normal up to 170 IU/L) and lactate dehydrogenase (LDH) at 2499 IU/L (normal up to 250 IU/L). Serological tests for syphilis (including VDRL and treponemal antibodies), HIV, hepatitis B, and hepatitis C were all negative.\n\nA skin biopsy from the gluteal lesion demonstrated epidermal necrosis extending to the hair follicle epithelium, with secondary blister formation due to re-epithelialization. Importantly, there was no evidence of vasculitis (blood vessel inflammation) or vascular thrombosis (clotting). These findings were consistent with acute-phase cutaneous embolism caused by medication (embolía cutis medicamentosa).\n\n**Clinical Interpretation:**  \nThe clinical presentation, timing after penicillin injection, imaging, laboratory findings, and biopsy results supported a diagnosis of Nicolau syndrome. This rare complication involves tissue necrosis and embolic phenomena following intramuscular drug administration.\n\n**Treatment and Outcome:**  \nThe patient was treated with subcutaneous enoxaparin (a blood thinner) at 1 mg/kg every 12 hours, cilostazol (a medication that improves blood flow) 100 mg every 12 hours, and tramadol for pain control over 10 days. Following treatment, there was significant clinical improvement, including normalization of liver enzymes (AST decreased to 39 IU/L, ALT to 77 IU/L) and muscle enzymes (CK reduced to 167 IU/L).\n\nNo immunological profile testing was performed, as the initial diagnosis did not suggest alternative causes. The patient was discharged with cilostazol and analgesics and followed up three months later. At that time, pain and skin lesions had improved substantially. Residual findings included a discolored scar with fine peeling on the right gluteus and a similar scar with thicker peeling and minimal livedoid lesions on the right sole.\n\n**Next Steps:**  \nContinued outpatient monitoring is recommended to assess long-term healing and manage any residual skin changes or discomfort. Awareness of Nicolau syndrome as a potential complication of intramuscular injections is important for early diagnosis and treatment to prevent severe tissue damage."
+        }
+    },
+    {
+        "article": "Un varón de cuatro días de edad, nacido a las 39 semanas y 4 días de gestación, acude a un servicio de urgencias con un empeoramiento de la dificultad respiratoria y el estridor, que se ve agravado por la alimentación y la posición supina.\n\nNació de una madre de 31 años con serología significativa para una prueba de Coomb positiva indirecta, con un parto vaginal sin complicaciones y puntuaciones de APGAR de ocho y nueve en el primer y quinto minuto, respectivamente. Su peso al nacer fue de 3050 g. La ecografía fetal mostró preocupación por un foco intracardíaco, con un embarazo sin complicaciones. El curso de enfermería fue significativo solo por una prueba de audición bilateral fallida y un ecocardiograma normal. El bebé fue dado de alta en el día dos de vida. Se observó que tenía congestión nasal en el momento de la descarga. Se instruyó a la familia para que le aspirara la nariz y usara gotas salinas según fuera necesario.\n\nEn el día cuatro de vida, la madre del lactante notó estridor asociado con dificultad para alimentarse y el pediatra lo derivó al servicio de urgencias. El examen en el servicio de urgencias es significativo para el estridor inspiratorio agudo con tirones traqueales y retracciones subcostal. Además, se observa que tiene pectus excavatum. El estridor y el aumento del trabajo respiratorio mejoran con la posición prona o lateral. La evaluación de laboratorio es significativa para la acidosis respiratoria en el gas sanguíneo venoso [pH 7.18 y CO2 73 mmHg (9,732 Pa)] y el análisis de orina que revela bacterias moderadas y 11-20 glóbulos blancos sin la presencia de nitrito urinario o esterasa leucocitaria. Un recuento sanguíneo completo es tranquilizador. Se le coloca una cánula nasal de alto flujo y se inicia con ampicilina y gentamicina después de obtener cultivos de sangre.\n\nSe le aumentó la presión positiva continua en la vía aérea (CPAP) y se lo trasladó a una unidad de cuidados intensivos neonatales de nivel III para continuar con el tratamiento y la evaluación de otorrinolaringología. Se le introdujo un tubo nasogástrico por las dos fosas nasales sin dificultad. La laringoscopia flexible mostró una cuerda vocal izquierda inmóvil y cavidades nasales estrechas con edema de los cornetes nasales, aritenoides bilaterales y cuerdas vocales. La broncoscopia no reveló ninguna otra anormalidad. El examen físico posterior se caracterizó por rasgos dismórficos sutiles, que incluían orejas de implantación baja, retromicrognatia, microftalmia y clinodactilia de los dedos de los pies. Se interrumpió el tratamiento antibiótico empírico tras un examen infeccioso tranquilizador. Se consultó a un equipo multidisciplinario.\n\nEl paciente finalmente requirió intubación a las dos semanas de vida debido al empeoramiento del fallo respiratorio. Se administraron ciprofloxacina nasal y dexametasona para el edema de las vías respiratorias superiores. Una resonancia magnética del cerebro, cuello y tórax mostró un curso normal de los nervios laríngeos recurrentes. La evaluación genética incluyó un análisis de microarreglo cromosómico normal (CMA). La prueba adicional del panel genético fue positiva para la variante patogénica en el gen CHD7, consistente con el síndrome CHARGE. En este caso, el VFP se atribuyó a la asociación conocida con el síndrome CHARGE. La evaluación continua reveló otras características consistentes con el síndrome CHARGE, incluidos colobomas bilaterales, glaucoma, pérdida auditiva confirmada y anomalías genitales.\n\nLa repetición de la broncoscopia en el día 42 de vida demostró una mejora en el edema laríngeo general, pero continuó con un edema leve de las cuerdas vocales bilaterales. El paciente fue extubado después de la broncoscopia en el marco de un edema de las vías respiratorias mejorado. Sin embargo, fue re-intubado el día 46 de vida debido al empeoramiento de la insuficiencia respiratoria. La repetición de la laringoscopia ese día mostró un edema continuado. En este momento, el paciente ya había recibido múltiples ciclos cortos de Dexamethasone en un intento de disminuir el edema de las vías respiratorias. Debido a la necesidad de re-intubación, fue tratado con Tobramycin tópico y Dexamethasone aplicado directamente a las cuerdas vocales mediante laringoscopia directa durante cinco días. Después de este tratamiento, fue extubado con éxito a los dos meses de edad y se le colocó un tubo de gastrostomía a los tres meses.\n\nEn el momento de la colocación del tubo de gastrotomía, se le realizó una broncoscopia y una microlaringoscopia adicionales que demostraron que la cuerda vocal izquierda afectada originalmente era totalmente móvil, pero que mostraba una nueva inmovilidad de la cuerda derecha; la etiología de esto no está clara. Ambas cuerdas vocales seguían estando ligeramente edematosas, pero habían mejorado mucho desde la evaluación anterior. El paciente fue dado de alta en aire ambiente a los cuatro meses de edad y continúa siendo seguido de cerca por el otorrinolaringólogo. En la laringoscopia ambulatoria de repetición a los cuatro meses de edad, ambas cuerdas aparecían móviles con un edema de las vías respiratorias continuado.\n\n",
+        "gold_summary": "Un bebé de cuatro días de edad, a término, varón, nacido por parto vaginal sin complicaciones, con un curso de enfermería significativo para la falta de audición, se presentó en un departamento de emergencias (DE) con dificultad respiratoria y estridor en aumento. Fue trasladado a una unidad de cuidados intensivos neonatales (UCIN) de nivel III para una evaluación posterior y se le practicó una intubación debido a la hipercarbia progresiva. La laringoscopia reveló una parálisis unilateral de las cuerdas vocales (PCV) del lado izquierdo. Se le sometió a una evaluación posterior que incluyó un cerebro, cuello y tórax normales en una resonancia magnética. Se consultó a genética por la preocupación de los rasgos dismórficos en el examen físico. Después de las pruebas del panel de genes, la PCV se atribuyó a la asociación conocida con el síndrome CHARGE. Se observó un edema de las vías respiratorias en la laringoscopia que impidió la extubación hasta los dos meses de edad. Se identificaron otras características del síndrome CHARGE, incluidos los colobomas, el glaucoma, la pérdida auditiva neurosensorial y las anomalías genitales. Se le dio de alta con aire ambiente y después de la colocación de un tubo de gastrostomía con seguimiento de otorrinolaringología.\n",
+        "synthetic_summary": {
+            "B1": "A baby boy was born healthy and came to the hospital because he had trouble breathing. The doctors saw that one of his voice cords did not move. They did special pictures and tests to learn more.\n\nThe baby has a condition called CHARGE syndrome. This can make breathing hard and cause other problems with eyes, ears, and body. The doctors helped him breathe with a tube for some time.\n\nAfter some medicine and care, the baby got better. He went home with a special feeding tube and will see doctors to help him grow strong.",
+            "B2": "**What Happened to the Baby?**\n\nA baby boy, four days old and born full-term through a normal vaginal delivery, went to the emergency room because he was having more trouble breathing and making a noisy sound called stridor. Stridor happens when air has trouble passing through the throat or windpipe. The baby also had hearing problems noticed earlier.\n\n**What Did the Doctors Find?**\n\nThe baby was moved to a special intensive care unit for newborns. He needed help breathing with a tube because his body wasn’t getting rid of carbon dioxide properly, which can be dangerous. When doctors looked at his vocal cords using a camera (a test called laryngoscopy), they found that one vocal cord on the left side was paralyzed, meaning it couldn’t move.\n\nThey did an MRI scan of his brain, neck, and chest, which looked normal. Because the baby had some unusual physical features, doctors checked his genes. Genetic testing showed he had a condition called CHARGE syndrome. This syndrome can cause many problems, including vocal cord paralysis.\n\n**What Does CHARGE Syndrome Mean?**\n\nCHARGE syndrome is a condition that affects many parts of the body. In this baby, it caused the vocal cord paralysis and other issues like eye problems (colobomas and glaucoma), hearing loss, and genital abnormalities.\n\n**How Was the Baby Treated?**\n\nThe baby had swelling (edema) in his airway, which made it hard to remove the breathing tube until he was two months old. After treatment, including medicine to reduce swelling and special care, he was able to breathe on his own. A feeding tube was placed to help him eat safely. He was sent home breathing normal air but continues to be monitored by ear, nose, and throat specialists.\n\n**Summary**\n\nThis baby’s breathing problems were caused by a paralyzed vocal cord linked to CHARGE syndrome. Thanks to careful medical care and ongoing monitoring, he improved and was able to leave the hospital safely.",
+            "B3": "**Background**  \nA full-term male infant, born vaginally without complications and weighing 3050 grams, initially showed a normal neonatal course except for bilateral hearing loss detected on screening. At four days old, he presented to the emergency department with worsening respiratory difficulty and inspiratory stridor (a high-pitched breathing sound), which was aggravated by feeding and lying on his back. Physical examination revealed inspiratory stridor with tracheal tugging, subcostal retractions, and pectus excavatum (a sunken chest deformity). His respiratory distress improved when positioned prone or on his side. Laboratory tests showed respiratory acidosis with elevated carbon dioxide levels and moderate bacteriuria without signs of urinary tract infection. Initial treatment included nasal high-flow oxygen and empiric antibiotics.\n\n**Key Findings**  \n- Flexible laryngoscopy identified left vocal cord paralysis (VCP) and swelling (edema) of nasal and laryngeal structures, including the nasal turbinates and arytenoids. Bronchoscopy revealed no additional abnormalities.  \n- Subtle dysmorphic features were noted on physical exam: low-set ears, a small and receding lower jaw (retromicrognathia), abnormally small eyes (microphthalmia), and curved toes (clinodactyly).  \n- Despite initial antibiotic treatment, infection was ruled out, and antibiotics were discontinued.  \n- The infant’s respiratory status worsened, requiring intubation at two weeks of age. Treatment for airway edema included systemic corticosteroids (dexamethasone) and topical antibiotics.  \n- MRI of the brain, neck, and chest showed normal anatomy of the recurrent laryngeal nerves, which control vocal cord movement.  \n- Genetic testing with chromosomal microarray was normal, but a targeted gene panel identified a pathogenic variant in the CHD7 gene, confirming a diagnosis of CHARGE syndrome—a genetic disorder characterized by multiple congenital anomalies.  \n- Additional features consistent with CHARGE syndrome included bilateral colobomas (defects in eye structure), glaucoma, sensorineural hearing loss, and genital abnormalities.  \n- Repeated laryngoscopies showed persistent but improving airway edema and fluctuating vocal cord mobility. The left vocal cord initially paralyzed became mobile, but a new paralysis developed on the right side for unclear reasons.\n\n**Clinical Interpretation**  \nThe infant’s unilateral vocal cord paralysis was attributed to CHARGE syndrome, a condition known to affect cranial nerve function and cause airway abnormalities. The airway edema complicated respiratory management and delayed extubation until two months of age. The fluctuating vocal cord mobility underscores the complexity of airway involvement in CHARGE syndrome. The presence of multiple characteristic anomalies supported the genetic diagnosis and guided multidisciplinary care.\n\n**Next Steps**  \n- The patient was successfully extubated after targeted treatment of airway edema and subsequently required gastrostomy tube placement for feeding support.  \n- He was discharged breathing ambient air at four months of age with ongoing otolaryngology follow-up.  \n- Continued monitoring of airway status and vocal cord function is essential, given the dynamic nature of his airway edema and vocal cord mobility.  \n- Multidisciplinary care including genetics, ophthalmology, audiology, and endocrinology is important to address the full spectrum of CHARGE syndrome manifestations."
+        }
+    },
+    {
+        "article": "Mujer de 17 años oriunda de Tucumán, acudió a la consulta por cuadro de vías aéreas superiores y hemoptisis leve. La tomografía computarizada de tórax informó, en lóbulo superior derecho, una imagen redondeada de paredes regulares y lisas de 25x24x24 mm, rodeado de un tenue halo periférico en vidrio esmerilado. No se observaba realce ante la administración de contraste endovenoso. Se sugirió un posible quiste broncogénico, por lo que se realizó una RMN de tórax que informó imagen redondeada de paredes regulares y lisas que alcanzó un diámetro anteroposterior de 25 x 24 x 24.5 mm con intensidad de señal líquida. Debido a la localización central de la lesión, se realizó una lobectomía superior derecha videoasistida. Dado que el estudio anatomopatológico intraoperatorio fue indeterminado, se complementó la resección pulmonar con un vaciamiento ganglionar mediastínico. La anatomía patológica definitiva informó neumocitoma esclerosante de 2 x 1.7 cm. La inmunomarcación fue positiva para TTF1, CK, CK7 y napsina.",
+        "gold_summary": "Describimos aquí el caso de una paciente de 17 años con diagnóstico de neumocitoma esclerosante con presentación infrecuente.",
+        "synthetic_summary": {
+            "B1": "A girl who is 17 years old had a small lump in her lung. The lump was not common. Doctors helped her feel better.",
+            "B2": "**What Happened:**  \nA 17-year-old girl from Tucumán went to the doctor because she had mild coughing up of blood and symptoms like a cold. A special chest scan called a CT scan showed a round, smooth-edged spot about 2.5 cm wide in her right upper lung. This spot looked like it might be a bronchogenic cyst, which is a fluid-filled sac that can form in the lungs.\n\n**What the Doctors Did:**  \nTo learn more, doctors did another scan called an MRI, which also showed a round, smooth spot with liquid inside. Because the spot was in a tricky place in the lung, the doctors decided to remove the upper part of her right lung using a small camera and tools (a surgery called video-assisted lobectomy). During the surgery, they checked the tissue but couldn’t tell exactly what it was, so they also removed nearby lymph nodes to be safe.\n\n**What They Found:**  \nAfter careful testing, the final diagnosis was a sclerosing pneumocytoma. This is a rare type of lung tumor made up of certain lung cells. Special tests showed the tumor cells had markers called TTF1, CK, CK7, and napsin, which help doctors identify this tumor.\n\n**What It Means:**  \nSclerosing pneumocytoma is an uncommon lung tumor that usually grows slowly and can be treated by surgery. Finding it in a young person like this girl is unusual. The surgery to remove the tumor and nearby lymph nodes was important to make sure the tumor was completely taken out and to check if it had spread.",
+            "B3": "**Background:**  \nA 17-year-old woman from Tucumán presented with symptoms involving the upper respiratory tract and mild hemoptysis (coughing up small amounts of blood). Initial imaging with chest computed tomography (CT) revealed a well-defined, round lesion measuring approximately 25 x 24 x 24 mm in the right upper lung lobe. This lesion had smooth walls and was surrounded by a faint ground-glass opacity (a hazy area on imaging that suggests partial filling of air spaces). There was no enhancement of the lesion after intravenous contrast administration, which suggested a non-vascular nature. Given these features, a bronchogenic cyst (a congenital cystic lesion of the lung) was initially suspected.\n\n**Key Findings:**  \nFurther evaluation with magnetic resonance imaging (MRI) confirmed the presence of a round lesion with smooth walls and liquid-like signal intensity, consistent with a cystic or fluid-containing structure. Due to the lesion’s central location within the lung, a video-assisted thoracoscopic surgery (VATS) was performed to remove the right upper lobe (lobectomy). During surgery, an intraoperative pathological examination was inconclusive, prompting an extended procedure that included mediastinal lymph node dissection to assess for potential spread.\n\nThe final pathological analysis identified the lesion as a sclerosing pneumocytoma (also known as sclerosing hemangioma), measuring 2 x 1.7 cm. Immunohistochemical staining showed positivity for thyroid transcription factor-1 (TTF-1), cytokeratin (CK), CK7, and napsin A, markers that support the diagnosis of this rare benign lung tumor originating from pneumocytes (lung cells).\n\n**Clinical Interpretation:**  \nSclerosing pneumocytoma is an uncommon benign tumor of the lung that typically affects middle-aged women and is rarely seen in adolescents. Its presentation with mild hemoptysis and the imaging characteristics in this young patient were unusual, making preoperative diagnosis challenging. The lesion’s smooth, cyst-like appearance and lack of contrast enhancement initially suggested a benign cystic lesion rather than a tumor. Definitive diagnosis required surgical resection and detailed pathological examination.\n\n**Next Steps:**  \nFollowing complete surgical removal of the lesion and mediastinal lymph node sampling, the prognosis is generally excellent, as sclerosing pneumocytoma is benign with very low risk of recurrence or metastasis. Continued clinical follow-up with periodic imaging is recommended to monitor for any signs of recurrence, although this is rare. This case highlights the importance of considering sclerosing pneumocytoma in the differential diagnosis of solitary pulmonary nodules, even in young patients with atypical presentations."
+        }
+    },
+    {
+        "article": "Una mujer asiática de 28 años fue admitida en el hospital para el tratamiento de «una masa pélvica durante 10 meses» el 11 de noviembre de 2018. La paciente solía tener menstruación regular, volumen menstrual moderado, dismenorrea y un G1P0L0A1. Examen ginecológico: la parte posterior del útero tenía aproximadamente 8 cm de diámetro con poca actividad y sensibilidad, pero no se observaron otras anomalías. La paciente no tenía una causa obvia de dolor abdominal durante los primeros 10 meses previos al ingreso. El examen de ultrasonido reveló una masa heterogénea en la parte superior derecha del útero con un diámetro de aproximadamente 4 cm, un nódulo del epiplón mayor con un diámetro de aproximadamente 2 cm y un nivel de CA125 sérico de 416 mU/mL. Se diagnosticó como «endometriosis, masas pélvicas inflamatorias». Se administró una terapia de rehidratación antiinfecciosa y se dio de alta a la paciente con alivio del dolor. Dos semanas después del alta, el nivel de CA125 sérico de la paciente disminuyó a 106 mU/mL y volvió a la normalidad después de 6 semanas. Sin embargo, la masa pélvica aumentó gradualmente. El reexamen de la ecografía pélvica realizada mostró una masa ecoica mixta de 7.7 cm x 7.4 cm x 8.2 cm en el lado derecho del útero con un límite claro, eco puntiforme fino en el quiste y derrame abdominal y pélvico. La ecografía de contraste mostró que la pared del quiste de la masa pélvica estaba significativamente mejorada, se sospechaba malignidad y se recomendó un tratamiento quirúrgico. El 14 de noviembre de 2018, la paciente se sometió a liberación de adherencias pélvicas e intestinales transabdominales, omento, ovarios bilaterales, peritoneo multipunto y múltiples adenomiosis y histerectomía. Durante la operación, se aspiraron aproximadamente 600 ml de ascitis hemorrágica. Tras la exploración, se observó una masa de color rojo grisáceo con un diámetro de aproximadamente 8 cm en la superficie del epiplón mayor, que era suave y se asemejaba a carne podrida. Se encontraron depósitos de celulosa marrón difusos en la superficie del útero, ovarios bilaterales, pared abdominal, tracto intestinal, surco lateral del recto y pared anterior del recto. Las lesiones no se eliminaron por completo y algunas áreas se electrocoagularon. El examen patológico de la muestra resecada mostró endometriosis del tejido retiniano con vasodilatación, ampollas, infiltración linfocítica difusa y focal, folículos ováricos císticos bilaterales, fibrosis peritoneal dentro de la necrosis del tejido adiposo, proliferación de fibroblastos, aumento de la infiltración de células espumosas y adenomiosis uterina. La patología de ascitis mostró muchos glóbulos rojos, un pequeño número de linfocitos y neutrófilos y ninguna célula tumoral. Después de la operación, la paciente se recuperó sin problemas y se trató con agonista de la hormona liberadora de gonadotropina (GnRH-α). Se inició leuprorelina una vez al mes durante 6 meses, seguido de dienogest oral (DNG) durante 3 años, después de lo cual se interrumpió la medicación durante 3 meses. La paciente concibió de forma natural y tuvo un embarazo normal. Se dio a luz a un bebé de 3300 g por vía vaginal a las 39 semanas + 3 días de gestación. Tanto la madre como el bebé estaban sanos, sin recurrencia ni reacciones adversas durante el seguimiento.\n\nMH - Humanos\nMH - Mujer\nMH - *Endometriosis/complicaciones/terapia\nMH - Adulto",
+        "gold_summary": "Preocupaciones de la paciente: Una mujer de 28 años de edad vino a nuestro hospital para recibir tratamiento debido al descubrimiento de una masa pélvica 10 meses antes. Después de la admisión, la paciente se sometió a tratamiento quirúrgico y fue dada de alta en 1 semana. Recibió tratamiento médico durante 3 años después del alta. Después de la retirada de la medicación, la paciente quedó embarazada y dio a luz a un niño sin recurrencia durante el seguimiento.\n\nDiagnósticos: Los diagnósticos iniciales al ingreso fueron «¿masa pelviana inflamatoria?» y «¿endometriosis?». Después de 10 meses, la paciente volvió a ser internada en el hospital debido a un aumento gradual de la masa, y se le diagnosticó endometriosis.\n\nIntervenciones: El paciente fue tratado con terapia antiinfecciosa de rehidratación por primera vez, y el paciente fue tratado quirúrgicamente por segunda vez, seguido de agonista de la hormona liberadora de gonadotropina (GnRH-α) y tratamiento con dienogest (DNG) después de la cirugía.\n\nResultados: Después de 6 ciclos de tratamiento con GnRH-α y 3 años de tratamiento con DNG, un hijo nació con éxito tras la interrupción de la medicación y, hasta ahora, no se han producido reacciones adversas ni recurrencias durante el período de seguimiento.\n",
+        "synthetic_summary": {
+            "B1": "A lady had a bump inside her tummy for a long time. The doctors helped her with a surgery to make her feel better.\n\nAfter the surgery, she took medicine for a long time. Then, she stopped the medicine and had a baby boy.\n\nBoth the lady and the baby are healthy and happy now. The bump did not come back.",
+            "B2": "**What Happened to the Patient?**  \nA 28-year-old woman went to the hospital because she had a lump in her pelvic area for 10 months. The doctors first thought it might be inflammation or a condition called endometriosis. Endometriosis happens when tissue similar to the lining inside the uterus grows outside it, which can cause pain and lumps.\n\n**What Did the Doctors Do?**  \nAt first, she received treatment to fight infection and help her body heal. But the lump kept growing, so she had surgery to remove it and other affected tissues. After the surgery, she took special hormone medicines for several years. One medicine was called a GnRH agonist, which lowers certain hormone levels to help stop the disease. Later, she took another medicine called dienogest to keep the condition under control.\n\n**What Was the Outcome?**  \nAfter finishing the medicines, the woman was able to get pregnant naturally. She had a healthy baby boy and no signs of the disease came back during the follow-up time. Both mother and baby stayed healthy without any problems.\n\n**Why Is This Important?**  \nThis case shows that with surgery and hormone treatments, women with endometriosis and pelvic masses can recover well. It also shows that pregnancy is possible after treatment, which is encouraging for patients with this condition.",
+            "B3": "**Background**  \nA 28-year-old Asian woman was admitted to the hospital after being diagnosed with a pelvic mass that had been present for 10 months. Initially, she experienced regular menstrual cycles with moderate flow and dysmenorrhea (painful menstruation). Her obstetric history included one pregnancy without live births. At admission, gynecological examination revealed an approximately 8 cm diameter mass on the posterior uterus with limited mobility and mild tenderness. Ultrasound imaging identified a heterogeneous mass about 4 cm in size on the upper right uterus, a 2 cm nodule on the greater omentum (a fatty apron-like structure in the abdomen), and an elevated serum CA125 level of 416 mU/mL, a marker often increased in endometriosis and certain malignancies. The initial diagnosis considered inflammatory pelvic masses and endometriosis.\n\n**Key Findings**  \nFollowing initial anti-infective rehydration therapy, the patient’s pain improved and she was discharged. Serum CA125 levels decreased to 106 mU/mL two weeks post-discharge and normalized by six weeks. However, the pelvic mass progressively enlarged. Repeat pelvic ultrasound showed a mixed echogenic mass measuring approximately 7.7 x 7.4 x 8.2 cm on the right side of the uterus, with clear borders, fine punctate echoes within the cyst, and evidence of abdominal and pelvic fluid accumulation (ascites). Contrast-enhanced ultrasound suggested significant enhancement of the cyst wall, raising suspicion for malignancy and prompting surgical intervention.\n\nDuring surgery, approximately 600 ml of hemorrhagic ascitic fluid was aspirated. A reddish-gray, soft mass about 8 cm in diameter was found on the surface of the greater omentum, resembling necrotic tissue. Diffuse brownish deposits consistent with endometriotic lesions were observed on the uterus, both ovaries, abdominal wall, intestinal tract, and rectal areas. Complete removal of lesions was not feasible; some areas were treated with electrocoagulation. Histopathological examination confirmed endometriosis involving the omental tissue, characterized by blood vessel dilation, blister formation, diffuse and focal lymphocytic infiltration, bilateral ovarian cystic follicles, peritoneal fibrosis with adipose tissue necrosis, fibroblast proliferation, increased foam cell infiltration, and uterine adenomyosis (presence of endometrial tissue within the uterine muscle). Cytology of ascitic fluid revealed numerous red blood cells, few lymphocytes and neutrophils, and no malignant cells.\n\n**Clinical Interpretation**  \nThe patient’s pelvic mass was ultimately diagnosed as endometriosis with extensive involvement of pelvic and abdominal structures, complicated by hemorrhagic ascites. The elevated CA125 initially suggested possible malignancy but normalized after treatment, consistent with endometriosis rather than cancer. Surgical removal of accessible lesions combined with postoperative medical therapy aimed to suppress residual disease and prevent recurrence.\n\n**Interventions and Treatment**  \nPostoperatively, the patient received monthly injections of a gonadotropin-releasing hormone agonist (GnRH-α), specifically leuprorelin, for six months to induce a hypoestrogenic state that inhibits endometrial tissue growth. This was followed by three years of oral dienogest (DNG), a progestin effective in managing endometriosis by reducing inflammation and lesion size. After discontinuing medication for three months, the patient conceived naturally.\n\n**Outcomes and Follow-Up**  \nThe patient experienced a normal pregnancy and delivered a healthy infant weighing 3300 grams vaginally at 39 weeks and 3 days gestation. Throughout the follow-up period, there were no signs of disease recurrence or adverse effects related to treatment. Both mother and child remained in good health.\n\n---\n\nThis case illustrates the complex presentation and management of extensive endometriosis with pelvic masses and hemorrhagic ascites. It highlights the importance of combining surgical and long-term medical therapies to achieve symptom control, preserve fertility, and prevent recurrence."
+        }
+    },
+    {
+        "article": "Presentamos una paciente de 76 años de edad, que es traída al servicio de urgencias por bajo nivel de conciencia con tendencia al sueño.\n\nComo antecedentes médicos de interés destaca una enfermedad pulmonar intersticial difusa, dislipemia e hipertensión arterial.\n\nA la exploración física el paciente se encuentra estuporosa, arreactiva, con atonía de las 4 extremidades y desviación conjugada de la mirada hacia la derecha, sin fiebre y con una leve sequedad en piel y mucosas. La analítica sanguínea no muestra alteraciones significativas.\n\nEl paciente es valorado por el servicio de neurología que considera la realización de una TC cerebral urgente ante la sospecha de patología intracraneal de evolución aguda. Las pruebas de imagen ponen de manifiesto la presencia de numerosas burbujas aéreas que se disponen en los surcos cerebrales, cuerpo calloso y ambos tálamos así como áreas hipodensas cortico-subcorticales de distribución parcheada en hemisferio cerebeloso izquierdo y parietooccipitales bilaterales, todo ello compatible con isquemia cerebral subaguda secundaria a embolismo gaseoso.\n\nAnte los antecedentes personales de enfermedad pulmonar intersticial difusa se decide también realizar una placa de tórax en proyección anteroposterior y una TC torácica que objetivan un neumotórax apical izquierdo y aire ectópico en mediastino superior.\n\nSe decide el ingreso en la Unidad de Ictus del centro para control estrecho de constantes, sin embargo, la paciente presenta una evolución tórpida con el fallecimiento el segundo día de ingreso debido a fracaso multiorgánico.",
+        "gold_summary": "Paciente de 76 años con una enfermedad pulmonar intersticial difusa preexistente, que experimentó un ictus masivo debido a un neumomediastino espontáneo. Su presentación incluyó confusión, convulsiones y debilidad motora. Las pruebas de imagen revelaron burbujas de aire en los surcos cerebrales y áreas hipodensas en el cerebelo y parietooccipitales. Además, se observó neumotórax y aire en el mediastino superior en las radiografías de tórax y la tomografía torácica. A pesar de las medidas terapéuticas como el oxígeno hiperbárico, la paciente lamentablemente falleció debido al fallo multiorgánico.",
+        "synthetic_summary": {
+            "B1": "A lady who was 76 years old felt very sleepy and confused. She had a problem with her lungs before. Doctors found tiny air bubbles in her brain. She also had air where it should not be in her chest. The doctors tried to help her, but she became very sick and died.",
+            "B2": "**What Happened to the Patient**\n\nA 76-year-old woman with a lung disease called interstitial lung disease came to the emergency room because she was very sleepy and had a low level of consciousness. She also had other health problems like high blood pressure and high cholesterol.\n\n**What the Doctors Found**\n\nWhen the doctors examined her, she was almost unresponsive and had weak muscles in all her arms and legs. Her eyes were looking to one side, but she did not have a fever. Blood tests were normal. Brain scans showed many tiny air bubbles inside her brain, which is not normal. These bubbles were found in different parts of the brain, including areas that looked damaged because of low blood flow. This damage was caused by air bubbles blocking blood vessels, a condition called cerebral air embolism.\n\nBecause of her lung disease, the doctors also took chest X-rays and a CT scan of her chest. These tests showed a collapsed part of her left lung (called pneumothorax) and air trapped in the space in the middle of her chest (called pneumomediastinum).\n\n**What This Means**\n\nThe air bubbles in her brain came from the air escaping her damaged lung and traveling through her blood vessels to her brain. This caused a serious type of stroke. The doctors treated her with oxygen therapy, but her condition got worse. Sadly, she died two days later because several of her organs stopped working.\n\n**Summary**\n\nThis case shows how lung problems can sometimes cause air to enter the bloodstream and block blood flow to the brain. This is very dangerous and can lead to severe brain damage and death.",
+            "B3": "**Background**  \nA 76-year-old woman with a history of diffuse interstitial lung disease, dyslipidemia, and hypertension was brought to the emergency department due to decreased consciousness and a tendency to sleep excessively. Her medical background is significant for chronic lung pathology, which likely contributed to her acute presentation.\n\n**Key Findings**  \nOn physical examination, the patient was stuporous (severely reduced responsiveness), unreactive to stimuli, exhibited muscle weakness (atonia) in all four limbs, and had conjugate gaze deviation to the right. She was afebrile but showed mild dryness of the skin and mucous membranes. Blood tests did not reveal any significant abnormalities.\n\nUrgent brain computed tomography (CT) was performed due to suspicion of an acute intracranial event. Imaging demonstrated multiple air bubbles located in the cerebral sulci (grooves on the brain surface), the corpus callosum (a major brain structure connecting the two hemispheres), and both thalami (deep brain nuclei). Additionally, there were patchy hypodense (less dense) areas in the left cerebellar hemisphere and bilateral parieto-occipital regions, consistent with subacute cerebral ischemia (areas of reduced blood flow) secondary to cerebral air embolism (air bubbles obstructing blood vessels).\n\nGiven the patient’s underlying interstitial lung disease, chest imaging was also conducted. Chest X-ray and thoracic CT scan revealed a left apical pneumothorax (air in the pleural space at the lung apex) and ectopic air in the superior mediastinum (the central compartment of the thoracic cavity), indicating spontaneous pneumomediastinum (air leakage into the mediastinal space).\n\n**Clinical Interpretation**  \nThe patient suffered a massive ischemic stroke caused by cerebral air embolism originating from spontaneous pneumomediastinum and pneumothorax, likely related to her preexisting diffuse interstitial lung disease. The presence of air bubbles within cerebral vessels led to widespread brain ischemia, manifesting as decreased consciousness, motor weakness, and gaze abnormalities. Despite supportive care, including admission to the stroke unit for close monitoring, the patient’s condition deteriorated rapidly.\n\n**Next Steps and Outcome**  \nAlthough hyperbaric oxygen therapy (a treatment that uses high-pressure oxygen to reduce air emboli) was considered, the patient’s clinical course was unfavorable. She developed multiorgan failure and died on the second day of hospitalization. This case highlights the severe neurological and systemic consequences of spontaneous air embolism in patients with underlying lung disease."
+        }
+    },
+    {
+        "article": "Un hombre de 24 años de edad, de etnia persa, presentó una queja principal de mal olor bucal después de un período de recuperación de la enfermedad leve por coronavirus 2019 (COVID-19), que quería resolver lo antes posible. Su dentista notó pérdida ósea y sangrado al explorar el área interproximal de los dientes número 18 y 19 clínicamente. Se realizó un escalamiento y un aplanamiento radicular, y se ordenaron radiografías periapicales y panorámicas para la evaluación del paciente. Sin embargo, el paciente se negó a tomar radiografías. La halitosis del paciente disminuyó después de 1 semana de tratamiento. Después de 2 meses, el paciente volvió a su dentista con la queja principal de sensibilidad al frío en sus incisivos mandibulares. El dentista realizó una prueba de vitalidad, y los dientes eran vitales excepto los números 23 y 24. El dentista tomó una radiografía periapical, y una lesión radiolucente en la mandíbula anterior era evidente.\n\nEn la radiografía panorámica, se evidenció una lesión radiolúcida lítica grande y bien definida con bordes festoneados que se extendían desde el diente número 31 en el lado derecho hasta el ramus ascendente izquierdo. Un estudio posterior de tomografía computarizada de haz cónico (TCFC) reveló una lesión lítica multilocular grande, con un margen relativamente distinto, que causó adelgazamiento y perforación de los cortexes bucales y linguales y signos de festoneado.\n\nTras el examen, se remitió al paciente a un cirujano oral y maxilofacial. En la entrevista médica, el paciente explicó su prolapso de la válvula mitral; antecedentes de episodios recurrentes de otitis desde el primer año de vida; antecedentes de septicemia de origen desconocido cuando tenía un año de edad, tras episodios de diarrea y vómitos; antecedentes de uso de broncodilatadores para la alergia estacional; antecedentes de uso de levotiroxina, cabergolina, acetato de desmopresina (DDAVP) en spray y gel de testosterona durante 4 años tras el diagnóstico de síndrome de silla turca vacía, tras poliúria y polidipsia; y, por último, antecedentes de infección reciente por COVID-19 (3 meses antes). Su historia familiar reveló tiroiditis de Hashimoto en su familia materna; su abuelo, su madre y sus tres tías padecían este tipo de hipotiroidismo. El historial quirúrgico previo del paciente incluía una reparación de una hernia inguinal 10 años antes sin complicaciones. Además, el paciente era obeso, con un índice de masa corporal (IMC) de 34,5.\n\nEn el examen clínico, los hallazgos extraorales e intraorales no fueron relevantes. Los exámenes de laboratorio, incluido el recuento sanguíneo completo (CBC), fueron normales, excepto por un aumento en la velocidad de sedimentación globular (ESR) y los niveles de proteína C reactiva (CRP). Se realizó una biopsia incisional en la mandíbula anterior y la muestra se envió al departamento de patología oral y maxilofacial de la Universidad de Ciencias Médicas Shahid Beheshti. Las secciones mostraron una infiltración difusa de grandes células de tinción pálida, como los histiocitos, con eosinófilos dentados y numerosos en el fondo fibroso. Un examen de inmunohistoquímica (IHC) reveló un positivo disperso para el grupo de diferenciación 1a (CD-1a) (+ +), un positivo fuerte para Langerin (CD-207) (+ + +), y más del 50% positivo para S-100.\n\nDe acuerdo con los datos clínicos, radiológicos e histopatológicos, se llegó al diagnóstico de LCH. Los diagnósticos diferenciales fueron osteomielitis, granuloma eosinófilo y metástasis ósea. Sin embargo, debido a las pruebas de laboratorio, los datos radiológicos y el historial clínico, se confirmó el diagnóstico de LCH. Por lo tanto, para un examen más a fondo, el paciente fue derivado al departamento de medicina nuclear para una tomografía por emisión de positrones con fluor-2-desoxiglucosa y una tomografía computarizada (FDG PET/CT), que reveló lesiones líticas hipermetabólicas en la mandíbula, el parietal derecho, el frontal izquierdo y el esfenoidal izquierdo, y opacidad hipermetabólica en el seno etmoidal izquierdo. Además, se observó una actividad metabólica aumentada en la región sellar, hidrocefalia comunicante y amígdalas palatinas hipermetabólicas prominentes. Además, se evidenció una actividad metabólica heterogénea aumentada en las tibias y fémures bilaterales.\n\nUna resonancia magnética del cerebro reveló una notable ampliación de la intensidad del material del líquido cefalorraquídeo (LCR) que contiene la silla turca. La adenohipófisis apareció como una capa delgada en la base de la silla turca agrandada, y se observaron cambios homogéneos e inflamatorios en las células aéreas mastoideas izquierdas. Se observó la extensión de la inflamación hacia el oído medio izquierdo (es de destacar que el paciente había sufrido de otitis durante muchos años). De acuerdo con la implicación multifocal de la enfermedad y su pronóstico cuestionable, el paciente fue derivado al departamento de oncología para quimioterapia sistémica. Pruebas posteriores revelaron mutaciones en el oncogen BRAF y no se detectaron mutaciones en KRAS y NRAS. El oncólogo eligió un régimen de denosumab, vinblastina, etopósido, 6-mercaptopurina, metotrexato y pegfilgrastim; sin embargo, el seguimiento no fue posible ya que el paciente falleció tras un accidente.\n",
+        "gold_summary": "Un paciente de 24 años de edad, de etnia persa, se presentó con una queja principal de halitosis tras recuperarse de la enfermedad por coronavirus 2019 en el consultorio de su dentista general. Los exámenes intraorales y extraorales no revelaron ningún problema específico. En la sesión de seguimiento tras el tratamiento periodontal de fase I, la sensibilidad de los dientes al estímulo frío era evidente, y las radiografías revelaron una gran lesión intraósea lítica en la mandíbula. Una biopsia incisional reveló células de Langerhans y una reacción positiva a Langerina y al grupo de diferenciación 1a, por lo que se le diagnosticó histiocitosis de células de Langerhans. Después de realizar una tomografía por emisión de positrones con fluoro-2-desoxiglucosa y una tomografía computarizada, una resonancia magnética y una tomografía computarizada de haz cónico, debido a la implicación generalizada de la enfermedad, el paciente fue derivado a un oncólogo. En última instancia, se descubrió que los problemas de salud infantil del paciente, incluidos los problemas endocrinos, probablemente fueron causados por una histiocitosis de células de Langerhans no diagnosticada. El oncólogo eligió un régimen de denosumab, vinblastina, etopósido, 6-mercaptopurina, metotrexato y pegfilgrastim. El seguimiento no fue posible ya que el paciente falleció tras un accidente.\n",
+        "synthetic_summary": {
+            "B1": "A young man had bad breath after he got better from a sickness. The dentist looked at his mouth but did not see a clear problem. Later, the man’s teeth felt cold and hurt. The dentist took pictures and found a big problem in his jaw bone.\n\nThe doctors took a small piece from the jaw to look at it. They found special cells that told them the man had a rare sickness called Langerhans disease. The sickness was in many parts of his body.\n\nThe doctors sent him to a special doctor for medicine. They gave him strong medicine to help. Sadly, the man died after an accident and could not be checked again.",
+            "B2": "**What Happened to the Patient?**  \nA 24-year-old man from Persia went to his dentist because he had bad breath after recovering from COVID-19. At first, the dentist didn’t find any clear problems in his mouth. But later, the patient felt his teeth were sensitive to cold. X-rays showed a large area of bone loss inside his lower jaw.\n\n**What Did the Tests Show?**  \nThe dentist took a small tissue sample (called a biopsy) from the jaw. Under the microscope, doctors found special immune cells called Langerhans cells. These cells tested positive for certain markers, which helped doctors diagnose a rare disease called Langerhans Cell Histiocytosis (LCH). This disease causes these immune cells to build up and damage bones and other tissues.\n\n**How Serious Was the Disease?**  \nFurther scans, including PET/CT and MRI, showed that the disease affected many parts of the patient’s body, including his skull bones and brain area. This explained some of his past health problems as a child, like hormone issues and ear infections, which were likely caused by undiagnosed LCH.\n\n**What Treatment Was Given?**  \nBecause the disease was widespread, the patient was sent to a cancer specialist (oncologist) for treatment. The doctor chose a combination of medicines, including denosumab and chemotherapy drugs, to try to control the disease.\n\n**What Happened Next?**  \nUnfortunately, the patient died in an accident before doctors could see how well the treatment worked.\n\n**Summary**  \nThis case shows how Langerhans Cell Histiocytosis can cause serious health problems that may be hard to diagnose at first. It also highlights the importance of thorough testing when unusual symptoms like bone lesions and tooth sensitivity appear after illnesses like COVID-19.",
+            "B3": "**Background**  \nA 24-year-old Persian man initially sought dental care due to persistent bad breath (halitosis) following recovery from a mild COVID-19 infection. His dentist observed bone loss and bleeding between two molars and performed periodontal treatment. Although initial oral and extraoral examinations showed no significant abnormalities, the patient later developed sensitivity to cold in his lower front teeth. Subsequent dental imaging revealed a large destructive (lytic) lesion within the jawbone.\n\n**Key Findings**  \n- Radiographic studies, including panoramic X-rays and cone-beam computed tomography (CBCT), identified a well-defined, multilocular lytic lesion extending across the lower jaw with cortical bone thinning and perforation.  \n- An incisional biopsy of the lesion demonstrated infiltration by pale-staining large cells consistent with Langerhans cells, accompanied by numerous eosinophils (a type of white blood cell). Immunohistochemical testing was strongly positive for Langerin (CD-207) and CD1a markers, confirming the presence of Langerhans cells. Over 50% of cells also expressed S-100 protein.  \n- Differential diagnoses considered included osteomyelitis (bone infection), eosinophilic granuloma, and bone metastases; however, clinical, radiological, and laboratory data supported a diagnosis of Langerhans Cell Histiocytosis (LCH).  \n- Further systemic evaluation with fluorodeoxyglucose positron emission tomography/computed tomography (FDG PET/CT) revealed multiple hypermetabolic (active) lytic lesions in the jaw, several skull bones (parietal, frontal, sphenoid), and the left ethmoidal sinus. Increased metabolic activity was also noted in the pituitary region, bilateral thigh and shin bones, and enlarged palatine tonsils.  \n- Brain magnetic resonance imaging (MRI) showed enlargement and inflammatory changes in the pituitary region (sella turcica), consistent with the patient’s known history of pituitary dysfunction (empty sella syndrome), as well as chronic mastoid and middle ear inflammation correlating with his longstanding history of recurrent ear infections (otitis).  \n- Laboratory tests were largely normal except for elevated inflammatory markers (erythrocyte sedimentation rate and C-reactive protein).  \n\n**Clinical Interpretation**  \nThe diagnosis of multisystem Langerhans Cell Histiocytosis was established, explaining the patient’s diverse clinical history including childhood endocrine abnormalities, recurrent infections, and recent jaw lesions. LCH is a rare disorder characterized by clonal proliferation of Langerhans cells, which can infiltrate bone and various organs, causing destructive lesions and systemic symptoms. The presence of BRAF oncogene mutations further supported the diagnosis and informed treatment options.  \n\n**Next Steps**  \nDue to the multifocal involvement and uncertain prognosis, the patient was referred to oncology for systemic chemotherapy. The treatment regimen selected included denosumab (a bone resorption inhibitor), vinblastine, etoposide, 6-mercaptopurine, methotrexate, and pegfilgrastim (a growth factor to support white blood cell counts). Unfortunately, follow-up was not possible as the patient died in an unrelated accident shortly after treatment initiation.  \n\nThis case highlights the importance of considering Langerhans Cell Histiocytosis in young adults presenting with unexplained bone lesions and systemic symptoms, especially when accompanied by a history of endocrine dysfunction and recurrent infections. Early diagnosis and multidisciplinary management are critical for optimizing outcomes in this complex disease."
+        }
+    },
+    {
+        "article": "La paciente es una mujer de 66 años de edad que goza de buena salud. A mediados de la década de 1980, recibió varias sesiones de tratamiento con rayos grenz en el cuero cabelludo para aliviar el picor asociado con la psoriasis del cuero cabelludo. Con un tratamiento regular de aproximadamente una sesión al mes durante un período de 5 años, que se complementó de vez en cuando con alquitrán de hulla, ácido salicílico y prednisona, logró cierto alivio de su enfermedad. Con el tiempo, su cabello se adelgazó; la piel en toda el área del cuero cabelludo se volvió sensible al dolor y se produjo cicatrización. Los tratamientos con rayos grenz se habían administrado en una clínica privada; no se disponía de detalles del tratamiento, como la dosis única y acumulada. No había sufrido radiodermitis.\n\nEn un período muy breve en 2020, unos 35 años después de que cesara el tratamiento de radiación, aparecieron numerosos BCC y queratosis actínicas premalignas (AK) en su cuero cabelludo. Se inició un régimen de tratamiento de extirpación quirúrgica de BCC verificado por histología preoperatoria y crioterapia de AK por evaluación del médico. La terapia fotodinámica o los tratamientos tópicos no eran aplicables debido a la sensibilidad al dolor y las secuelas de la cirugía. De 2020 a 2022, recibió varios tratamientos de criocirugía y curetaje y un total de 13 extirpaciones quirúrgicas de BCC por cirugía de Mohs. Se estima que su número total de extirpaciones a lo largo del tiempo es de unos 30. Los BCC recalcitrantes y de novo en el cuero cabelludo cada vez más dañado, obviamente, son un desafío eterno; por lo tanto, los cirujanos plásticos y los dermatólogos buscaban otra modalidad de tratamiento con un mejor índice terapéutico.\n\nEn septiembre de 2022, aparecieron nuevos CCB confirmados histológicamente en el cuero cabelludo. La exploración por ultrasonido (DermaScan C, Cortex Technology ApS, Aalborg, Dinamarca) mostró tumores ecolucidos de 0,5-1,3 mm de espesor en ambos sitios analizados histológicamente, así como en algunas lesiones adicionales que pudieron identificarse en base al examen clínico y dermatoscópico. La paciente, tras ser informada, dio su consentimiento por escrito para el tratamiento con HIFU, con o sin biopsia de pretratamiento de las lesiones sospechosas.\n\nSe delinearon las lesiones elegibles para el tratamiento con un rotulador impermeable, incluyendo un margen perilesional de 2 mm. Se mapeó cada lesión seleccionada en una lámina transparente para ayudar a determinar la ubicación precisa en el seguimiento. Se usó el ultrasonido de 20 MHz para confirmar la profundidad de las lesiones identificadas al inicio y en las visitas de seguimiento posteriores. Debido al estado del cuero cabelludo conocido por ser sensible al dolor, se administró anestesia local (lidocaína 25 mg/ml + adrenalina 5 mg/ml, Amgros I/S, Copenhagen, Dinamarca) a todas las lesiones 10-15 minutos antes del tratamiento.\n\nLas lesiones fueron tratadas con HIFU utilizando la sonda de 1.3 mm; ajustes de 150 ms/dosis y energía acústica de 0.9 J/dosis. Se aplicaron 20-200 dosis a las lesiones, dependiendo de la extensión de la lesión. Las lesiones tratadas se curaron de forma espontánea sin complicaciones o necesidad de tratamiento especial. Se programaron visitas de seguimiento cada 3-6 meses para controlar la tasa de curación/recaída, tolerancia local y lesiones nuevas no identificadas anteriormente.\n\nDurante los 15 meses posteriores a la limpieza inicial con HIFU, se trataron con HIFU un total de 10 lesiones que, de acuerdo con las rutinas, hubieran requerido una biopsia seguida de una cirugía de escisión, en sesiones de unos 30 minutos. Las lesiones se curaron en unos pocos días sin complicaciones ni necesidad de intervención. Se observó una limpieza total en 7 de 8 lesiones de BCC tratadas y en ambas lesiones de AK. La única lesión recurrente de BCC de pequeño tamaño se observó después de 15 meses entre las primeras seis lesiones tratadas; la lesión se volvió a tratar con HIFU. Ejemplos de lesiones curadas 15 meses después del tratamiento con HIFU; el tumor con recurrencia.\n",
+        "gold_summary": "Una mujer de 66 años que en la década de 1980 había recibido varios tratamientos de rayos gamma en el cuero cabelludo desarrolló múltiples carcinomas basocelulares en la zona. Se le habían realizado más de 30 cirugías de escisión, incluida la cirugía de Mohs, en el pasado, con muchas complicaciones locales, pero, no obstante, los cánceres recurrentes. Los tratamientos con HIFU aplicados a ocho carcinomas basocelulares y dos lesiones precancerosas dieron como resultado una limpieza completa en el control a los 12 meses, pero una recurrencia después de 15 meses.\n",
+        "synthetic_summary": {
+            "B1": "A lady who is 66 years old had special light treatments on her head many years ago. After that, she got some small skin bumps that were not good. She had many surgeries to take them away. The bumps kept coming back.\n\nDoctors used a new kind of treatment with sound waves on ten bumps. After one year, most bumps were gone. One bump came back after a little more time. The new treatment helped her a lot.",
+            "B2": "**What Happened Before**\n\nA 66-year-old woman had a history of scalp treatments in the 1980s using special rays called gamma rays. These were meant to help with her scalp psoriasis, a skin condition that causes itching and scaling. Over time, her scalp skin became thin, sensitive, and scarred. About 35 years after these treatments stopped, she developed many small skin cancers called basal cell carcinomas (BCC) and some early warning signs of cancer called actinic keratoses (AK) on her scalp.\n\n**Past Treatments and Challenges**\n\nShe had more than 30 surgeries to remove these skin cancers, including a precise method called Mohs surgery, which removes cancer layer by layer. Despite many surgeries, new cancers kept coming back. The skin damage and pain made some usual treatments like light therapy or creams impossible.\n\n**New Treatment with HIFU**\n\nDoctors tried a newer treatment called High-Intensity Focused Ultrasound (HIFU). This method uses focused sound waves to destroy tumors without cutting the skin. They treated eight BCC tumors and two AK lesions with HIFU. Before treatment, they used ultrasound imaging to measure the size and depth of the tumors. Local numbing medicine was given to reduce pain during the procedure.\n\n**Results After HIFU**\n\nThe treated areas healed on their own without problems. After 12 months, seven out of eight BCC tumors and both AK lesions were completely gone. However, one small BCC tumor came back after 15 months but was treated again with HIFU. The treatment sessions lasted about 30 minutes each.\n\n**What This Means**\n\nHIFU showed promise as a less painful option to treat skin cancers on damaged scalp skin, especially when surgery is difficult. It helped clear most tumors with few side effects. Still, some tumors may come back, so regular check-ups are important. This treatment could be a useful alternative for patients with repeated skin cancers and sensitive skin.",
+            "B3": "**Background**  \nA 66-year-old woman, previously in good health, underwent multiple sessions of grenz ray therapy (a form of superficial radiation) to her scalp during the mid-1980s to relieve itching caused by scalp psoriasis. This treatment, administered approximately once a month over five years and occasionally combined with coal tar, salicylic acid, and prednisone, provided symptomatic relief. Over time, the patient experienced scalp skin thinning, increased pain sensitivity, and scarring. Details about the radiation dose were unavailable, and she did not develop radiation-induced skin inflammation (radiodermatitis).\n\nApproximately 35 years after cessation of radiation therapy, in 2020, the patient developed numerous basal cell carcinomas (BCCs)—a common form of skin cancer—and premalignant actinic keratoses (AKs) on her scalp. She underwent extensive treatment including over 30 surgical excisions, among them 13 Mohs micrographic surgeries (a precise technique to remove skin cancers), as well as cryotherapy and curettage for AKs. Despite these interventions, recurrent and new BCCs continued to arise on her increasingly damaged scalp, posing a significant therapeutic challenge. Due to pain sensitivity and prior surgical sequelae, topical or photodynamic therapies were unsuitable.\n\n**Key Findings**  \nIn September 2022, new histologically confirmed BCCs appeared on the scalp. Ultrasound imaging identified tumors measuring 0.5 to 1.3 mm in thickness, including lesions not previously biopsied but clinically and dermatoscopically suspicious. After informed consent, the patient was treated with high-intensity focused ultrasound (HIFU), a non-invasive technique that uses focused sound waves to ablate tissue. Lesions were carefully mapped and marked with a 2 mm margin; local anesthesia was administered to minimize pain.\n\nHIFU treatment parameters included a 1.3 mm probe, 150 milliseconds per dose, and acoustic energy of 0.9 joules per dose, with 20 to 200 doses applied depending on lesion size. Treated lesions healed spontaneously without complications or need for additional care. Follow-up visits every 3 to 6 months monitored healing, recurrence, and emergence of new lesions.\n\nOver 15 months, 10 lesions that would have otherwise required biopsy and surgical excision were treated with HIFU in approximately 30-minute sessions. Seven of eight BCCs and both AKs showed complete clearance at 12 months. One small BCC recurred after 15 months and was successfully re-treated with HIFU.\n\n**Clinical Interpretation**  \nThis case illustrates the long-term risk of multiple BCCs developing decades after scalp radiation therapy. Conventional surgical management, including Mohs surgery, was extensive but insufficient to prevent recurrence and was associated with local complications and pain sensitivity. HIFU emerged as a promising alternative treatment modality, offering effective tumor clearance with minimal invasiveness and rapid healing in a patient with a highly sensitive and scarred scalp.\n\nThe high rate of lesion clearance and favorable tolerability suggest HIFU may be a valuable option for managing recurrent or new BCCs and premalignant lesions in patients with compromised scalp skin where surgery or topical therapies are limited.\n\n**Next Steps**  \nContinued monitoring is essential to detect any further recurrences or new lesions. Additional studies are warranted to evaluate the long-term efficacy and safety of HIFU in treating BCCs, particularly in patients with prior radiation exposure and complex clinical histories. Multidisciplinary collaboration among dermatologists, plastic surgeons, and oncologists will be important to optimize individualized treatment strategies for such challenging cases."
+        }
+    },
+    {
+        "article": "Se realizó un trasplante cardíaco ortotópico a una niña de 12 años con insuficiencia cardíaca en fase terminal debido a una miocardiopatía restrictiva. Durante la operación, se presentó una disfunción primaria grave del injerto, que requirió el uso de oxigenación por membrana extracorpórea venosa arterial. La función cardíaca se recuperó completamente después de 4 días, y su período postoperatorio se complicó por una insuficiencia renal aguda transitoria y un bloqueo auriculoventricular completo que duró >3 semanas después de la operación. Para evitar la disincronía del ventrículo izquierdo y el posible daño de la derivación del ventrículo derecho debido a las biopsias endomiocárdicas de vigilancia de rechazo múltiple, se indicó un marcapasos biventricular transvenoso que utiliza un marcapasos del ventrículo izquierdo aislado a través de la vena coronaria.\n\nBajo anestesia local y sedación suave, se cortó la vena cefálica izquierda y se introdujo un catéter guía en la vena subclavia y se colocó en el seno coronario inicialmente para realizar un venograma cardiaco. Se implantó un electrodo de estimulación endocárdica de elución de esteroides unipolar con mecanismo de fijación activa (Attain StarFix® 4195, Medtronic, Minneapolis, MN) en la rama de la vena interventricular anterior. Las medidas en el momento del implante fueron las siguientes: umbral 2 V a 0,4 ms, onda R 6 mV e impedancia 300 Ω a 4,8 mA. Se implantó un segundo electrodo de estimulación endocárdica de elución de esteroides bipolar con fijación activa (2088T®, St. Jude Medical, Minneapolis, MN) en la aurícula derecha.\n\nAmbos cables se aseguraron y se conectaron a un marcapasos adaptable a la frecuencia (Accent DR®, St. Jude Medical, Minneapolis, MN) que se colocó en una bolsa muscular infraclavicular izquierda y se programó a VDD. Las mediciones de los cables electrofisiológicos fueron estables después del implante: umbral ventricular 1.5 V a 0.7 ms, onda R 4.5 mV, onda P 4.3 mV (bipolar), impedancia ventricular 260 Ω y vida útil estimada de la batería de 5 años.\n\nEl electrocardiograma posterior al implante mostró complejos de morfología de bloqueo de rama derecha, y la evaluación ecocardiográfica mostró ausencia de disincronías auriculoventriculares, interventriculares e intraventriculares. En el seguimiento a 5 años, el paciente permaneció en Clase Funcional I con el mismo sistema de estimulación y conservó la función ventricular.\n\nMH - Bloqueo auriculoventricular/etiología/*terapia\nMH - Niño\nMH - Sinus coronario\nMH - Mujer\nMH - Insuficiencia cardiaca/cirugía\nMH - Trasplante de corazón/*efectos adversos\nMH - Ventrículos del corazón\nMH - Humanos\nMH - *Marcapasos, artificial\nMH - Disfunción/complicaciones/tratamiento del injerto primario\n",
+        "gold_summary": "Se sometió a un trasplante de corazón ortotópico a un niño de 12 años con insuficiencia cardiaca en fase terminal debido a una miocardiopatía restrictiva. La disfunción primaria del injerto precisó oxigenación con membrana extracorpórea venosa arterial. La función cardiaca se normalizó, pero el bloqueo auriculoventricular completo persistió después de 3 semanas. Se realizó un marcapaso bicameral con marcapaso transvenoso del ventrículo izquierdo a través del seno coronario. Tras 5 años de seguimiento, el paciente se encuentra estable con el mismo sistema de marcapaso y con la función ventricular preservada.\n",
+        "synthetic_summary": {
+            "B1": "A 12-year-old child got a new heart because the old one was very sick. After surgery, the new heart had trouble working at first. Doctors helped the heart with a special machine. \n\nThe heart got better, but the child’s heartbeat was still slow. So, doctors put in a small machine called a pacemaker to help the heart beat right. \n\nFive years later, the child is doing well. The pacemaker is still helping, and the heart works fine.",
+            "B2": "**Heart Transplant and Recovery in a 12-Year-Old Girl**\n\nA 12-year-old girl with very serious heart failure caused by a condition called restrictive cardiomyopathy (where the heart walls are stiff) received a heart transplant. During the surgery, her new heart did not work well at first, so doctors used a machine called extracorporeal membrane oxygenation (ECMO). This machine helps by pumping and adding oxygen to the blood outside the body, giving the heart time to heal. After four days, her heart started working normally again.\n\n**Complications and Pacemaker Treatment**\n\nAfter the transplant, she had some problems. One was acute kidney failure, which got better over time. Another was a complete atrioventricular (AV) block, meaning the electrical signals between the upper and lower parts of her heart were blocked for more than three weeks. To fix this, doctors implanted a special pacemaker. A pacemaker is a small device that helps control the heartbeat by sending electrical signals.\n\nThis pacemaker was placed using a less invasive method through veins, including the coronary sinus (a large vein on the heart). It helped coordinate the left and right sides of her heart to beat properly and avoid damage from repeated heart tissue tests (biopsies). The device worked well and was programmed to adjust the heart rate as needed.\n\n**Long-Term Outcome**\n\nFive years after the pacemaker was implanted, the girl remained healthy and active (Class I functional status, meaning no symptoms during normal activity). Her heart function stayed good, and the pacemaker system continued to work effectively without complications.\n\n**What This Means**\n\nThis case shows that even with serious complications after a heart transplant, careful treatment with advanced devices like a biventricular pacemaker can help patients recover and live well long-term. It also highlights the importance of monitoring and managing heart rhythm problems after transplant surgery.",
+            "B3": "**Background**  \nA 12-year-old girl with end-stage heart failure caused by restrictive cardiomyopathy underwent an orthotopic heart transplant (replacement of the diseased heart with a donor heart in the same anatomical position). During the surgery, she developed severe primary graft dysfunction, a serious complication where the transplanted heart initially fails to function properly. This required the use of veno-arterial extracorporeal membrane oxygenation (ECMO), a life-support technique that temporarily takes over the heart and lung function. After four days, her cardiac function fully recovered.\n\n**Key Findings**  \nDespite recovery of heart function, the patient experienced a complete atrioventricular (AV) block—a condition where the electrical signals between the heart’s upper chambers (atria) and lower chambers (ventricles) are completely interrupted—that persisted for more than three weeks postoperatively. Additionally, she had transient acute kidney injury during her postoperative course.\n\nTo prevent left ventricular dyssynchrony (a harmful lack of coordinated contraction in the left ventricle) and avoid potential damage to the right ventricle caused by repeated endomyocardial biopsies (tissue samples taken from the heart muscle to monitor for rejection), a biventricular transvenous pacemaker was implanted. This device included a lead placed in the left ventricle via the coronary sinus (a vein collecting blood from the heart muscle), which is an uncommon but effective approach in this context.\n\nThe implantation procedure involved accessing the left cephalic vein under local anesthesia and mild sedation. A steroid-eluting, unipolar active fixation lead (Attain StarFix® 4195) was positioned in the anterior interventricular vein branch for left ventricular pacing. Electrical measurements at implantation showed a pacing threshold of 2 volts at 0.4 milliseconds, an R wave amplitude of 6 millivolts, and impedance of 300 ohms at 4.8 milliamperes, indicating good lead function. A second bipolar steroid-eluting active fixation lead (2088T®) was placed in the right atrium.\n\nBoth leads were secured and connected to a rate-adaptive dual-chamber pacemaker (Accent DR®), implanted in a subclavicular muscle pocket on the left side and programmed to VDD mode (ventricular pacing with atrial sensing). Post-implantation electrophysiological parameters remained stable, with a ventricular pacing threshold of 1.5 volts at 0.7 milliseconds, R wave amplitude of 4.5 millivolts, P wave amplitude of 4.3 millivolts (bipolar), ventricular lead impedance of 260 ohms, and an estimated battery life of five years.\n\nElectrocardiogram after implantation showed complexes with right bundle branch block morphology, consistent with left ventricular pacing. Echocardiographic evaluation confirmed the absence of atrioventricular, interventricular, or intraventricular dyssynchrony, indicating effective synchronized heart contractions.\n\n**Clinical Interpretation**  \nThis case demonstrates successful management of persistent complete AV block following heart transplantation complicated by primary graft dysfunction. The use of a biventricular pacing system with a transvenous left ventricular lead via the coronary sinus effectively restored synchronized ventricular contraction, avoiding the risks associated with right ventricular lead placement and repeated biopsies. The stable electrical parameters and preserved ventricular function over five years highlight the long-term efficacy and safety of this approach in pediatric heart transplant patients.\n\n**Next Steps**  \nContinued long-term follow-up is essential to monitor pacemaker function, battery longevity, and cardiac performance. Regular assessments should include device interrogation, echocardiography to detect any emerging dyssynchrony or dysfunction, and surveillance for transplant rejection as clinically indicated. This case supports considering biventricular pacing with coronary sinus lead placement in similar pediatric patients with post-transplant conduction disturbances."
+        }
+    },
+    {
+        "article": "Una paciente de 20 años de edad se presentó con distensión abdominal progresiva asociada con calambres abdominales, incapacidad para expulsar flatos y heces, así como vómitos frecuentes de materia ingerida y biliar de un día de duración. El día anterior, dio a luz por cesárea por una indicación de bradicardia fetal severa. También tenía preeclampsia sin signos de gravedad y desnutrición de inicio en la edad adulta con un índice de masa corporal (IMC) de 16,5 kg/M2. No tenía antecedentes de cirugía abdominal previa. Negó cualquier queja similar en el pasado o antecedentes de cambio de hábitos intestinales o estreñimiento con paso de heces sanguinolentas. No tenía ninguna enfermedad médica crónica conocida.\n\nEn el examen físico, la paciente se veía enferma y con dolor. Su presión arterial era de 90/70 mmHg, su pulso oscilaba entre 116 y 120 latidos por minuto, y su frecuencia respiratoria era de 22 a 24 respiraciones por minuto. No se registró fiebre. Su abdomen estaba muy distendido y simétrico, con visibles movimientos intestinales peristálticos. Había una difusa sensibilidad directa en todo su abdomen, más en el cuadrante inferior derecho. Había un signo positivo de acumulación de fluido intraperitoneal con opacidad cambiante. Había una herida quirúrgica suprapúbica bien aproximada con un vendaje limpio. El examen rectal digital no mostró nada destacable. Tenía una herida superficial lineal de 3 cm de largo, orientada verticalmente, en su labio mayor izquierdo, que el equipo de obstetricia pensó inicialmente que era una quemadura de yodo en la piel.\n\nSe le introdujo un catéter y se le resucitó con dos bolsas de solución salina normal y produjo 200 ml de orina en una hora. Se le introdujo una sonda nasogástrica (NGT) pero no hubo una salida significativa. Se le realizó un hemograma completo y una radiografía abdominal simple. Su recuento de glóbulos blancos era de 1780 células/µl con predominio de neutrófilos del 88 %, hemoglobina de 12,7 mg/dl y un recuento de plaquetas de 78 x 103/ µl. Su prueba de función renal era normal y sus enzimas hepáticas estaban ligeramente elevadas por encima del rango normal pero no fue significativo. Su radiografía abdominal simple muestra múltiples niveles de aire-líquido ubicados centralmente con un bucle intestinal grande dilatado ubicado periféricamente y blanqueamiento del espacio pélvico que indica una acumulación de líquido. No se solicitó una tomografía computarizada abdominal (CT) porque trabajamos en un entorno con recursos limitados y para pacientes con obstrucción intestinal, solicitamos una tomografía computarizada cuando existe la posibilidad de un diagnóstico alternativo o cuando se sospecha una obstrucción tumoral.\n\nTras obtener el consentimiento informado por escrito, se exploró a la paciente bajo anestesia general con un diagnóstico de abdomen agudo secundario a obstrucción intestinal mixta secundaria a vólvulo del intestino delgado. El hallazgo intraoperatorio fue un íleon distal que rodeaba el ciego y el colon ascendente proximal, ambos móviles y no adheridos a la pared abdominal posterolateral derecha. Tanto el íleon como el ciego, así como el colon ascendente, eran viables. La punta del apéndice estaba enredada con el nudo ileal y estaba gangrenoso. El intestino delgado proximal y el intestino grueso distal estaban muy distendidos, pero en su ubicación normal. Había unos cuatro litros de líquido intraperitoneal seroso.\n\nDurante la operación, la paciente se mantuvo hipotensa (80/50 mmHg) desde que se le indujo la anestesia y se le administró un vasopresor. Debido a la inestabilidad de la paciente y a la viabilidad de los intestinos afectados por el nudo, se procedió a una hemicolectomía derecha. Se realizó una descompresión proximal y distal de los intestinos delgado y grueso distendidos, respectivamente. Se fijó el ciego y el colon ascendente a la pared abdominal posterolateral derecha con suturas seromusculares interrumpidas con hilo no absorbible (Silk 2-0).\n\nDespués del procedimiento, se le retiró la intubación y se le dio alimentación por vía oral (NPO) durante 24 horas y se le administró un fluido de mantenimiento con reposición de la pérdida. A pesar de la reanimación con fluidos y el apoyo con vasopresores, ella se encontraba persistentemente hipotensa, por lo que se le administró un tratamiento antibiótico doble con ceftriaxona 1 g, IV, BID y metronidazol 500 mg, IV, TID, en vista de un posible shock séptico de origen genitourinario. Su estado empeoró gradualmente y, tras una nueva evaluación el primer día postoperatorio, la herida superficial en su vulva se había extendido hacia la zona suprapúbica con signos clínicos de gangrena de Fournier. Por ello, revisamos su tratamiento antibiótico a meropenem 1 g, IV, BID, vancomicina 1 g, IV, BID y metronidazol 500 mg, IV, TID. Después de obtener el consentimiento informado por escrito, se la volvió a llevar al quirófano para un desbridamiento radical de la gangrena de Fournier y, posteriormente, se la trasladó a la unidad de cuidados intensivos quirúrgicos (ICU) intubada debido a un shock séptico persistente y un retraso en la recuperación de la anestesia. Lamentablemente, falleció con fallo multiorgánico debido a un shock séptico refractario en su segundo día postoperatorio, después de la exploración inicial.\n",
+        "gold_summary": "Presentamos un caso de nudos ileocecales en una paciente posparto con distensión abdominal, vómitos y ausencia de heces y flatos. La radiografía abdominal simple reveló bucles intestinales dilatados con múltiples niveles de aire y fluidos. Se realizó una laparotomía exploratoria con hallazgo intraoperatorio de nudos ileocecales con intestino viable, ciego móvil y colon ascendente y punta gangrenosa del apéndice. Deshicimos el nudo y realizamos una apendectomía. Debido a la inestabilidad intraoperatoria de los signos vitales de la paciente, se aplazó la hemicolectomía derecha y se fijaron el ciego y el colon ascendente a la pared abdominal posterolateral derecha.\n",
+        "synthetic_summary": {
+            "B1": "A lady had a big tummy and felt sick. She could not poop or pass gas. The doctors took a picture and saw her tummy was very full inside.\n\nThe doctors did a big surgery to look inside. They found some parts of her tummy tied in a knot. They fixed the knot and took out a sick part called the appendix.\n\nThe lady's body was very weak during the surgery. The doctors put some parts in a safe place to help her heal.",
+            "B2": "**What Happened to the Patient**  \nA 20-year-old woman who had just given birth by cesarean section came to the hospital with a swollen belly, stomach cramps, vomiting, and no bowel movements or gas passing. These symptoms suggested her intestines were blocked.\n\n**What the Doctors Found**  \nAn X-ray showed her intestines were swollen and filled with air and fluid, which means something was blocking the normal flow inside her intestines. During surgery, doctors found that parts of her small intestine and the beginning of her large intestine (called the ileocecal area) were twisted into knots. This twisting can cut off blood flow and cause serious problems.\n\n**What the Doctors Did**  \nThe doctors carefully untwisted the knotted intestines. They also found that the tip of her appendix (a small tube attached to the large intestine) was dead or gangrenous, so they removed it in a surgery called an appendectomy. Because the patient’s vital signs (like blood pressure and heart rate) were unstable during surgery, the doctors decided not to remove part of her colon at that time. Instead, they fixed the mobile parts of her intestines to the abdominal wall to prevent future twisting.\n\n**What This Means**  \nThis case shows how dangerous intestinal knots can be, especially after childbirth. Quick surgery to untwist the intestines and remove dead tissue is crucial. However, the patient’s unstable condition made the surgery more complicated. Fixing the intestines in place helped reduce the risk of the problem happening again.",
+            "B3": "Background  \nThis case involves a 20-year-old woman who developed progressive abdominal distension, cramping pain, vomiting, and an inability to pass gas or stool shortly after a cesarean delivery. Her clinical presentation and imaging suggested an acute intestinal obstruction. She had no prior abdominal surgeries or chronic illnesses but was noted to have adult-onset malnutrition and preeclampsia without severe features.\n\nKey Findings  \n- Physical examination revealed a markedly distended and tender abdomen with signs of fluid accumulation in the peritoneal cavity.  \n- Laboratory tests showed leukopenia (low white blood cell count) with neutrophil predominance, mild thrombocytopenia (low platelet count), normal kidney function, and slightly elevated liver enzymes.  \n- Abdominal X-ray demonstrated multiple central air-fluid levels and a large dilated bowel loop peripherally, consistent with bowel obstruction and intraperitoneal fluid.  \n- Intraoperative exploration identified ileocecal knots—twisting of the distal ileum around the cecum and ascending colon—which were viable (alive) except for the gangrenous (dead) tip of the appendix. The cecum and ascending colon were mobile and not adherent to the abdominal wall. Approximately four liters of serous fluid were present in the abdominal cavity.\n\nClinical Interpretation  \nThe patient’s symptoms and imaging were consistent with a mixed-type small bowel obstruction caused by ileocecal knotting, a rare but serious condition where loops of intestine twist around each other, potentially compromising blood flow. The viability of the intestines indicated that immediate resection was not necessary except for the gangrenous appendix, which was removed. Due to the patient’s unstable vital signs during surgery, the planned right hemicolectomy (removal of the right colon) was postponed. Instead, the surgical team untwisted the knot, performed an appendectomy, and fixed the cecum and ascending colon to the posterior abdominal wall to prevent recurrence.\n\nNext Steps  \nPostoperatively, the patient required intensive fluid resuscitation and vasopressor support due to persistent low blood pressure. Despite broad-spectrum antibiotics and surgical intervention, she developed Fournier’s gangrene (a severe soft tissue infection) extending from a vulvar wound to the suprapubic area, necessitating radical surgical debridement. She was transferred to the intensive care unit but ultimately succumbed to refractory septic shock and multiorgan failure on the second postoperative day.\n\nSummary  \nThis case highlights the complexity of managing ileocecal knotting in a postpartum patient complicated by malnutrition and preeclampsia. Early recognition and surgical intervention are critical, but patient instability and subsequent infectious complications can significantly worsen prognosis."
+        }
+    },
+    {
+        "article": "Un hombre de 38 años se presentó en el hospital con opresión en el pecho y falta de aire. Tres años antes, había experimentado síntomas similares después de la actividad y recibió tratamiento en nuestro hospital. La ecocardiografía ambulatoria indicó una masa de eco del corazón izquierdo que sugería un mixoma, lo que llevó a su ingreso para una evaluación adicional. El examen físico reveló pigmentación de las orejas del paciente caracterizada por múltiples puntos pequeños de color café y negro. La tomografía computarizada abdominal (TC) mostró múltiples hígados y pequeños quistes en el riñón izquierdo. Las pruebas genéticas identificaron mutaciones en los genes TTN y PRKAR1A. El diagnóstico de CNC se confirmó mediante examen clínico, imágenes y pruebas genéticas. Después del tratamiento sintomático, la condición del paciente mejoró; sin embargo, rechazó la intervención quirúrgica. El 20 de septiembre de 2023, el paciente se presentó en nuestro hospital con opresión en el pecho y falta de aire exacerbadas. Informó dificultad para permanecer acostado boca arriba y necesidad de sentarse erguido para respirar. El examen físico reveló distensión de la vena yugular, desplazamiento hacia la izquierda y hacia abajo del límite del corazón, ritmo cardíaco irregular en la auscultación y un murmullo de la válvula mitral de intensidad 2/6-3/6 en el cuarto espacio intercostal a lo largo del margen izquierdo del esternón. Se escucharon estertores húmedos en ambos campos pulmonares medio e inferior. La palpación reveló un hígado firme que se extendía tres dedos por debajo del proceso xifoides y dos dedos por debajo de la caja torácica, junto con un edema de pitting leve en ambas extremidades inferiores. Las imágenes ecocardiográficas indicaron un agrandamiento global del corazón, dilatación del seno aórtico y arteria pulmonar, regurgitación mitral pequeña a moderada y una masa ecógena irregular que medía 54 mm × 43 mm en la cámara izquierda unida al tabique auricular. La fracción de eyección del ventrículo izquierdo (FEVI) fue del 23,1 %, con acortamiento fraccional (FS) del 10,9 %. La electrocardiografía demostró fibrilación auricular (frecuencia ventricular promedio, 150 latidos/min) y ondas Q anormales en las derivaciones V1-V3. Basándose en la historia del paciente, el diagnóstico incluyó DCM y CNC con mixoma cardíaco. Dada la presencia de insuficiencia cardíaca en etapa terminal y mixoma cardíaco concurrente, el paciente fue hospitalizado y se consideró el trasplante de corazón como una opción terapéutica viable para abordar ambas afecciones simultáneamente. Un corazón de donante adecuado estuvo disponible para su trasplante inmediato el 1 de octubre de 2024.\n\n\nProcedimiento quirúrgico\n\nLa piel y los tejidos subcutáneos se incisionaron cuidadosamente capa por capa a través de una esternotomía media. El esternón se abrió longitudinalmente y se controló el sangrado mediante electrocoagulación y cera ósea. La exploración extracardíaca reveló un agrandamiento global del corazón, más prominente en el ventrículo izquierdo. El corazón mostró una disminución de la fuerza contráctil. La aorta y la arteria pulmonar principal (AP) se diseccionaron desde la región supravalvular. Algunos tejidos se conservaron para suturarlos posteriormente, mientras que la mayor parte de la aurícula derecha enferma, la aurícula izquierda (AL), el ventrículo derecho y el ventrículo izquierdo se extirparon. La resección reveló una masa mucoide de color blanco grisáceo. Los tejidos de la aurícula izquierda del donante y del receptor se suturaron utilizando hilos Prolene 3/0 dobles continuos. La anastomosis se inspeccionó meticulosamente varias veces y no se observó sangrado significativo. De forma similar, la anastomosis término-terminal de la aorta ascendente del donante y la arteria pulmonar del receptor se realizó utilizando suturas Prolene 5/0 continuas, y una inspección cuidadosa no reveló sangrado.\n\nAdemás, la LA del donante y la PA del receptor se cerraron de forma segura utilizando suturas Prolene 5/0 dobles y continuas. Los tejidos de la vena cava inferior tanto del donante como del receptor se suturaron de forma similar con suturas Prolene 5/0, y se realizaron varias inspecciones para confirmar que no había presencia de sangrado significativo. El lado izquierdo del corazón se desinfló y, a medida que comenzó el recalentamiento, se restableció la oxigenación, se soltó la aorta ascendente y el corazón volvió espontáneamente al ritmo sinusal. Se aplicó sutura continua con Prolene 5/0 tanto a la vena cava superior del donante como del receptor y se inspeccionó de forma diligente para garantizar la ausencia de sangrado significativo. Después de la interrupción exitosa de la circulación asistida, se descanuló la cavidad venosa. Se recogieron muestras de tejido del corazón izquierdo y de la materia gris del paciente para un examen histopatológico, y se confirmó el diagnóstico de DCM y mixoma cardiaco.\n\n\nManejo postoperatorio\n\nEl primer día después del trasplante de corazón, el paciente produjo 1200 ml de orina. Los exámenes de laboratorio revelaron un nivel de troponina T hipersensible de 796.70 ng/L y un nivel de NT-proBNP de 10798 pg/ml. El recuento completo de sangre mostró un recuento de glóbulos blancos de 17.15 × 109/L, sin anomalías significativas en otros resultados de exámenes. El ecocardiógrafo mostró un EFV del 65 %, FS del 35 %, un espesor de la pared ventricular normal y ecogenicidad, y no se observaron anomalías discernibles en la morfología y estructura de la válvula. Después del trasplante de corazón, se administró una terapia hormonal intravenosa de succinato sódico de metilprednisolona (0.25 g) para mejorar la inmunidad, y se proporcionó un tratamiento intravenoso antiinfeccioso con cefoperazona y sulbactam sódico (2 g). El paciente recibió una solución nutriente y tiopronina en el primer día después de la cirugía. En el día tres postoperatorio, se reemplazó el succinato sódico de metilprednisolona con acetato de prednisona oral (25 mg). Se administraron cápsulas de micofenolato de mofetilo (0.5 g) por vía oral para minimizar el rechazo del corazón, y se administró acetato de carpofénico intravenoso (50 mg) para prevenir infecciones fúngicas. La producción de orina del paciente fue de 2000 ml, con niveles de troponina T hipersensible de 390 ng/L, niveles de NT-proBNP de 7877 pg/ml, y un recuento de leucocitos de 12.15 × 109/L. En el día siete postoperatorio, se introdujeron cápsulas de tacrolimus a una dosis oral de (1 mg) para minimizar el rechazo del paciente al corazón del donante, con un cuidadoso monitoreo de las concentraciones sanguíneas. Subsiguientemente, la dosis oral de acetato de prednisona se redujo gradualmente a (10 mg) mientras se ajustaba la concentración sanguínea de tacrolimus a 10.90 ng/L. La recuperación del paciente mejoró. El 20 de octubre de 2023, la ecocardiografía de seguimiento (Fig. 6) no mostró anomalías, con niveles de troponina T de 85 ng/L, NT-proBNP de 210 pg/ml, y todos los demás resultados de exámenes dentro de los rangos normales. El paciente exhibió una excelente recuperación postoperatoria y fue dado de alta. Las visitas regulares de seguimiento a nuestro departamento después del alta mostraron que el paciente permanece en buen estado.\n\nMH - Humanos\nMH - *Cardiomiopatía, Dilatada/cirugía/etiología/diagnóstico/diagnóstico por imágenes\nMH - Hombre\nMH - *Complejo de Carney/genética/diagnóstico/cirugía/complicaciones\nMH - Adulto\nMH - *Trasplante de corazón\nMH - *Mixoma/complicaciones/cirugía/diagnóstico por imágenes/diagnóstico/genética\nMH - *Insuficiencia cardiaca/etiología/diagnóstico/cirugía\nMH - *Neoplasias cardiacas/cirugía/complicaciones/diagnóstico por imágenes/diagnóstico/genética\nMH - Resultado del tratamiento\nMH - Subunidad/genética de la proteína quinasa Rlalpha dependiente de AMP cíclico\n",
+        "gold_summary": "Aquí, reportamos un caso de insuficiencia cardiaca debido al síndrome de Carney que resultó en mixoma cardiaco combinado con cardiomiopatía dilatada. Un hombre de 35 años de edad fue admitido en el hospital hace tres años debido a opresión torácica repentina y falta de aire. La ecocardiografía indicó mixoma, y una combinación de cribado genético y examen físico confirmó el síndrome de Carney con mixoma cardiaco. Después del tratamiento sintomático, fue dado de alta. Las intervenciones quirúrgicas no fueron consideradas en ese momento. Sin embargo, la opresión torácica y los síntomas de falta de aire del paciente empeoraron, y volvió al hospital. Se confirmó una función cardiaca de grado IV de la New York Heart Association, y la ecocardiografía indicó la presencia de cardiomiopatía dilatada acompañada de mixoma cardiaco. En última instancia, la insuficiencia cardiaca del paciente fue tratada con éxito con un trasplante cardiaco.\n",
+        "synthetic_summary": {
+            "B1": "A man had a big problem with his heart. His heart was very tired and not working well. He had a lump inside his heart. This made it hard for him to breathe and his chest hurt.\n\nDoctors found out he had a special sickness called Carney syndrome. They gave him medicine to help him feel better. But later, he felt worse again.\n\nHis heart was very weak, and the lump was still there. The doctors gave him a new heart from a kind donor. After the new heart, he started to feel much better.",
+            "B2": "**What Happened to the Patient**\n\nThis report talks about a 35-year-old man who had serious heart problems caused by a condition called Carney syndrome. Carney syndrome is a rare disorder that can cause tumors, like a mixoma, which is a type of growth inside the heart. Three years ago, the man went to the hospital because he suddenly felt chest tightness and had trouble breathing. An ultrasound of his heart (called an echocardiogram) showed he had a mixoma. Doctors also did genetic tests and a physical exam, which confirmed he had Carney syndrome along with the heart tumor.\n\n**How the Condition Changed**\n\nAt first, the man was treated to help with his symptoms and sent home without surgery. But over time, his chest tightness and breathing problems got worse. When he returned to the hospital, tests showed his heart was very weak and enlarged—a condition called dilated cardiomyopathy, where the heart muscle stretches and cannot pump blood well. The mixoma was still present, making his heart problems more serious. His heart failure was classified as stage IV, meaning it was very severe.\n\n**How He Was Treated**\n\nBecause of the severe heart failure and the tumor, doctors decided the best treatment was a heart transplant. This means replacing his damaged heart with a healthy one from a donor. The transplant surgery was successful, and after careful monitoring and medication to prevent rejection and infection, the patient recovered well. This case shows how Carney syndrome can cause serious heart problems and that a heart transplant can be a life-saving option when other treatments are not enough.",
+            "B3": "**Background**  \nThis report describes the case of a 38-year-old man diagnosed with Carney Complex (CNC), a rare genetic disorder characterized by multiple tumors and skin pigmentation abnormalities, who developed severe heart failure due to a combination of a cardiac myxoma (a benign heart tumor) and dilated cardiomyopathy (DCM, a condition where the heart muscle weakens and enlarges). The patient initially presented three years prior with chest tightness and shortness of breath. At that time, echocardiography revealed a mass in the left heart chamber consistent with a myxoma. Physical examination showed characteristic skin pigmentation on his ears, and abdominal CT scans identified multiple liver lesions and small kidney cysts. Genetic testing confirmed mutations in the TTN and PRKAR1A genes, establishing the diagnosis of CNC.\n\n**Key Findings**  \n- Initial symptoms included chest discomfort and dyspnea (shortness of breath).  \n- Echocardiography detected a left atrial cardiac myxoma.  \n- Physical signs included multiple small brown and black pigmented spots on the ears.  \n- Imaging revealed liver nodules and renal cysts.  \n- Genetic analysis identified pathogenic mutations in TTN (associated with cardiomyopathy) and PRKAR1A (linked to CNC).  \n- The patient initially received symptomatic treatment and declined surgical intervention.\n\nThree years later, the patient returned with worsening chest tightness and severe shortness of breath, now unable to lie flat and requiring an upright position to breathe comfortably. Physical examination revealed signs of advanced heart failure: jugular vein distension, displaced cardiac borders, irregular heart rhythm with a mitral valve murmur, lung crackles, an enlarged and firm liver, and mild leg swelling. Echocardiography showed global cardiac enlargement, dilation of the aortic root and pulmonary artery, moderate mitral valve regurgitation, and a large irregular myxoma measuring 54 mm by 43 mm attached to the atrial septum. The left ventricular ejection fraction (LVEF), a measure of heart pumping efficiency, was severely reduced to 23.1%, indicating advanced systolic dysfunction. Electrocardiography revealed atrial fibrillation with a rapid ventricular rate and abnormal Q waves in the anterior leads, consistent with myocardial damage.\n\n**Clinical Interpretation**  \nThe patient’s clinical picture was consistent with end-stage heart failure due to dilated cardiomyopathy complicated by a large cardiac myxoma, both manifestations of Carney Complex. The combination of a large intracardiac tumor and severely impaired heart function presented a complex therapeutic challenge. Given the severity of heart failure (New York Heart Association Class IV) and the presence of the myxoma, heart transplantation was considered the most effective treatment option to simultaneously address both conditions.\n\n**Surgical Procedure and Postoperative Course**  \nThe patient underwent a successful orthotopic heart transplant via median sternotomy. The diseased heart, including the large myxoma, was completely excised. The donor heart was carefully anastomosed to the recipient’s great vessels and atrial tissues with meticulous attention to hemostasis. Histopathological examination of the explanted heart confirmed dilated cardiomyopathy and the presence of a myxoma.\n\nPostoperatively, the patient’s cardiac function improved markedly, with echocardiography showing a normalized ejection fraction of 65% and no structural abnormalities. Immunosuppressive therapy was initiated promptly to prevent graft rejection, including corticosteroids, mycophenolate mofetil, and tacrolimus, alongside prophylactic antibiotics and antifungals. Laboratory markers of cardiac injury and heart failure (troponin T and NT-proBNP) decreased progressively. The patient’s recovery was uneventful, and he was discharged in stable condition with normal cardiac function. Follow-up visits confirmed sustained clinical improvement and graft function.\n\n**Next Steps**  \nContinued regular follow-up is essential to monitor for potential transplant rejection, infection, or recurrence of CNC manifestations. Long-term management includes adherence to immunosuppressive therapy and surveillance for other systemic complications of Carney Complex. Genetic counseling may be recommended for the patient and family members due to the hereditary nature of the syndrome.\n\n---\n\nThis case highlights the complexity of managing cardiac manifestations of Carney Complex, particularly when complicated by dilated cardiomyopathy and large intracardiac tumors. Heart transplantation can be a life-saving intervention in end-stage heart failure when conventional surgical options are not feasible or declined."
+        }
+    },
+    {
+        "article": "Un paciente de 52 años de edad con un diagnóstico inicial de arteria pulmonar fue admitido en el departamento de cardiología para una evaluación médica y una decisión sobre el tratamiento posterior. El paciente tenía un historial de neumotórax espontáneo del lado derecho, tratado con toracocentesis y drenaje por vacío 35 años antes. El paciente sentía una disnea creciente al hacer ejercicio. También se quejaba de signos de insuficiencia ventricular derecha y cianosis. Cuatro años antes, el paciente fue hospitalizado tres veces por fibrilación auricular paroxística que se convirtió en ritmo sinusal por cardioversión eléctrica, además de que el examen electrocardiográfico era normal.\n\nEn ese mismo año, la angiografía coronaria indicó arterias coronarias normales. La ecocardiografía reveló una hipertensión pulmonar leve con una presión sistólica calculada en el ventrículo derecho de 36 mmHg sin dilatación de ese ventrículo.\n\nEn los años siguientes, se observó insuficiencia cardiaca progresiva con aumento de la presión arterial pulmonar en la ecocardiografía. Se realizó angio-CT en dos ocasiones y se excluyó la hipertensión pulmonar tromboembólica crónica en cada ocasión. La tomografía computarizada de alta resolución excluyó la patología pulmonar intersticial. La espirometría fue normal. La detección de enfermedades autoinmunes y la infección por VIH fue negativa.\n\n\nLínea de tiempo: historia, curso de la enfermedad, diagnóstico y tratamiento\n\n1976  neumotórax derecho\n2007 Hospitalizado tres veces por fibrilación auricular e insuficiencia cardiaca. Se le realizaron ecocardiografías, cardioversiones y coronografías. En cada ocasión, fue dado de alta de los servicios con diagnósticos de fibrilación auricular, insuficiencia cardiaca e insuficiencia cardiaca de clase II de la NYHA.\n2010-2011: Aumento de la falta de aire y síntomas de insuficiencia cardiaca. El paciente fue hospitalizado tres veces. Se detectaron características indirectas de hipertensión pulmonar en ecocardiografía. Se realizó tres veces un examen de tórax por TAC; se excluyó la embolia pulmonar o la hipertensión arterial pulmonar tromboembólica crónica (2 x angio-TAC) o la fibrosis pulmonar (tomografía computarizada de alta resolución).\nSe estableció el diagnóstico de hipertensión pulmonar, clase III de la OMS.\nDEC-2011 Admisión a la clínica de cardiología – ecocardiografía (TTE, TEE), prueba de caminata de 6 minutos, NT-proBNP, cateterización cardiaca derecha, prueba de vasoreactividad pulmonar.\nSe estableció el diagnóstico de hipertensión pulmonar arterial irreversible.\nSe ha iniciado el tratamiento con iloprost y sildenafil\nEn enero de 2012, visita de control: mejora en la clase de la OMS, disminución de la concentración de NT-proBNP e incremento de la distancia en la prueba de 6 minutos.\nMAY-2012. Control RHC. La SaO2 de las muestras de sangre obtenidas durante el RHC de la arteria del lóbulo superior del pulmón derecho fue del 87 %.\nEl diagnóstico angiográfico de las arterias pulmonares reveló fístulas de HAP entre las arterias subclavianas y el lóbulo superior del pulmón derecho.\nJUN 2012  angiografía por TC de las arterias sistémicas reveló la presencia adicional de fístulas arteriales bronquiales en el lóbulo superior de las arterias del pulmón derecho\nIII-2013 Embolización de fístulas\nVI-2013. Muerte como resultado del empeoramiento de la insuficiencia cardiaca, combinado con neumonía.\n\n\n\nEn el ingreso a nuestra clínica, la clase funcional del paciente fue evaluada como OMS III. En el examen físico, el segundo sonido cardiaco (S2) fue acentuado con S2 dividido ensanchado. Además, la auscultación cardiaca indicó un murmullo holosistólico de regurgitación tricuspídea. La auscultación del tórax no mostró un murmullo vascular. La cianosis periférica y central fue marcada. Se examinaron la hepatomegalia, el edema periférico y las venas varicosas bilateralmente.\n\nLa SaO2 obtenida por el método de oximetría de pulso se redujo al 88 %. La electrocardiografía reveló fibrilación auricular, desviación del eje derecho y onda T negativa en las derivaciones precordiales v1-v3. Las pruebas adicionales fueron las siguientes: concentración de NT-proBNP - 3383 pg/ml, distancia de la prueba de caminata de seis minutos - 373 m con 7/10 puntos en la escala de disnea de Borg.\n\nLa ecocardiografía mostró características de hipertensión pulmonar grave: agrandamiento del ventrículo derecho a 44 mm (cuatro cámaras), con función deprimida del TAPSE del ventrículo derecho de 9 mm, agrandamiento del área de la aurícula derecha a 40 cm2, regurgitación tricuspídea grave (++++), aumento del PSVR calculado a 112 mmHg, acortamiento del tiempo de aceleración de la arteria pulmonar a 60 ms y derrame pericárdico leve. No hubo defecto en el tabique interventricular. La ecocardiografía transesofágica tampoco mostró un defecto en el tabique auricular, lo que se confirmó más tarde con angio-TAC.\n\n\nLa SaO2 de la sangre obtenida de la arteria radial se redujo al 87,8%. Se realizó un cateterismo cardiaco derecho. La SaO2 de las muestras de sangre obtenidas durante el RHC de la vena cava superior, la vena cava inferior, la aurícula derecha, el tronco pulmonar, la arteria del lóbulo medio del pulmón derecho y la arteria pulmonar izquierda ascendieron respectivamente a: 64,8%; 77,4%; 73,2%; 70,2%; 69,3%; 71,2% y no indicaron la presencia de un shunt de izquierda a derecha.\n\nLas mediciones hemodinámicas mostraron una hipertensión pulmonar precapilar grave, irreversible en las pruebas de vasoreactividad con óxido nítrico inhalado (80 ppm) y una combinación de sildenafil oral (50 mg) y óxido nítrico inhalado (80 ppm).\n\nEn base a todos los datos clínicos y los resultados de la RHC, se estableció un diagnóstico de hipertensión pulmonar idiopática irreversible.\n\nSe inició el tratamiento con iloprost inhalado (Ventavis) 6 × 5 µg y sildenafil (Revatio) por vía oral 3 × 20 mg. Además, se administraron digoxina (0,1 mg diarios), warfarina (INR rango: 2-3), furosemida (40 mg por vía oral diarios) y espironolactona (100 mg diarios).\n\nUn mes después se realizó un seguimiento no invasivo. El paciente manifestó una mejoría en la capacidad física, clase II según la OMS, concentración de NT-proBNP: 1014 pg/ml. Distancia en la prueba de caminata de seis minutos: 471 m.\n\nCinco meses después se realizó una evaluación invasiva. La RHC mostró valores de PAP más elevados que en las mediciones iniciales [75,4/51,8 (59,7) mm Hg] y PVR (13,4 WU) (Tabla 22 – control RHC).\n\nLa saturación de oxígeno de las muestras de sangre obtenidas durante la RHC de la arteria lobular superior del pulmón derecho fue elevada y ascendió al 89.7%.\n\nEn la angiografía pulmonar se detectó la reducción del trazo vascular periférico típico de la hipertensión arterial pulmonar y la falta de contraste de la arteria del lóbulo superior derecho. Además, se encontró evidencia de flujo sanguíneo retrógrado visible como un contraste negativo en la arteria pulmonar derecha. Después, se realizó una arteriografía de la arteria subclavia derecha y se detectó una enorme malformación vascular que se comunicaba con la arteria del lóbulo superior derecho.\n\nLa angio-TC de las arterias sistémicas confirmó la presencia de las fístulas previamente descritas y reveló la presencia adicional de fístulas de la arteria bronquial en el lóbulo superior de las arterias del pulmón derecho.\n\nSe realizó embolización selectiva de las fístulas (mezcla al 50% de Lipiodol y pegamento monomérico de n-butil-2-cianoacrilato). La embolización no produjo ningún cambio clínico en el estado del paciente.\n\nMH - Fístula arterio-arterial/*complicaciones\nMH - *Cateterización cardiaca\nMH - Angiografía por tomografía computarizada\nMH - Hipertensión pulmonar primaria familiar/*diagnóstico/terapia farmacológica\nMH - Resultado fatal\nMH - Insuficiencia cardiaca/fisiopatología\nMH - Humanos",
+        "gold_summary": "Un paciente caucásico de 52 años de edad con hipertensión pulmonar (HP) confirmada por ecocardiografía fue admitido en el departamento de cardiología debido a disnea de esfuerzo y signos de insuficiencia ventricular derecha. La exploración rutinaria para detectar causas de HP secundaria fue negativa. El cateterismo cardiaco derecho (CCR) confirmó una HP arterial de alto grado [presión arterial pulmonar media (PAPm); 50,6 mmHg, presión de enclavamiento pulmonar (PWP); 11,3 mmHg, resistencia vascular pulmonar (PVR); 11,9 unidades de Wood (UW)] irreversible en la prueba con óxido nítrico inhalado. La saturación de oxígeno (SaO2) de las muestras de sangre obtenidas durante el primer CCR osciló entre 69,3 y 73,2%. Se diagnosticó hipertensión arterial pulmonar idiopática. Se inició el tratamiento con iloprost inhalado y sildenafil.\n\nEl control RHC, realizado 5 meses después, mostró valores de mPAP (59,7 mmHg) y PVR (13,4 WU) más altos en comparación con la medición inicial. El SaO2 de sangre obtenida durante el RHC de la arteria del lóbulo superior del pulmón derecho fue elevado y ascendió al 89,7 %.\n\nLuego se realizó una arteriografía pulmonar. Se encontró falta de contraste en la arteria del lóbulo superior derecho con evidencia de flujo sanguíneo retrógrado visible como contraste negativo en la arteria pulmonar derecha. Después, una arteriografía de la arteria subclavia derecha detectó una enorme malformación vascular que se comunicaba con la arteria del lóbulo superior derecho. Después, un angiograma por tomografía computarizada (angio-CT) reveló adicionalmente el agrandamiento de las arterias bronquiales que se originaban en las fístulas hacia la arteria pulmonar del lóbulo superior derecho.\n\nA pesar del tratamiento farmacológico intensivo, que incluyó la terapia de la hipertensión pulmonar y la embolización percutánea de las fístulas, el estado del paciente siguió deteriorándose. Falleció tres meses después de la embolización debido a una insuficiencia cardiaca grave complicada por neumonía.\n",
+        "synthetic_summary": {
+            "B1": "A man, 52 years old, had trouble breathing. His heart was not working well. Doctors found high pressure in his lungs.\n\nThey gave him medicine to help his lungs and heart. But his sickness got worse.\n\nDoctors found a big problem with blood vessels in his lungs. They tried to fix it with a special treatment.\n\nEven with help, the man got very sick and passed away.",
+            "B2": "**What They Found**\n\nA 52-year-old man had a serious lung problem called pulmonary hypertension (PH), which means high blood pressure in the lungs. This made it hard for his heart to pump blood and caused symptoms like shortness of breath and heart failure signs. Tests showed his lung blood pressure was very high and did not get better with usual treatments. Doctors found no common causes for his condition, so they diagnosed him with idiopathic pulmonary arterial hypertension—meaning the cause was unknown.\n\n**Further Testing and Discoveries**\n\nFive months after starting treatment with medicines called iloprost (inhaled) and sildenafil (oral), his lung blood pressure actually got worse. When doctors took pictures of his lung arteries using special X-rays (arteriography and CT angiography), they found abnormal blood vessel connections called fistulas. These fistulas were large, unusual links between arteries supplying blood to his right upper lung. Such connections can cause blood to flow the wrong way and worsen his condition.\n\n**Treatment and Outcome**\n\nDoctors tried to fix the fistulas by blocking them through a procedure called embolization, where materials are used to close off abnormal vessels. Unfortunately, this did not improve his health. Despite intensive medical treatment and the procedure, his heart failure got worse. He passed away three months later due to severe heart failure complicated by pneumonia.\n\n**What This Means**\n\nThis case shows how pulmonary hypertension can sometimes be caused by rare blood vessel problems in the lungs. Even with advanced treatments, these cases can be very serious and hard to manage. It highlights the importance of thorough testing to find hidden causes and the challenges doctors face in treating complex heart and lung diseases.",
+            "B3": "**Background**  \nA 52-year-old Caucasian man was admitted to the cardiology department due to progressive shortness of breath during exertion and clinical signs of right ventricular heart failure. Initial echocardiography confirmed pulmonary hypertension (PH). The patient’s medical history included spontaneous right-sided pneumothorax 35 years earlier and recurrent episodes of paroxysmal atrial fibrillation. Routine investigations to identify secondary causes of pulmonary hypertension—including tests for thromboembolic disease, interstitial lung disease, autoimmune disorders, and HIV infection—were all negative.\n\n**Key Findings**  \nRight heart catheterization (RHC) demonstrated severe precapillary pulmonary arterial hypertension with a mean pulmonary artery pressure (mPAP) of 50.6 mmHg, pulmonary wedge pressure (PWP) of 11.3 mmHg, and elevated pulmonary vascular resistance (PVR) of 11.9 Wood units (WU). The condition was irreversible, as shown by a lack of response to inhaled nitric oxide during vasoreactivity testing. Oxygen saturation (SaO2) in blood samples taken during the initial RHC ranged between 69.3% and 73.2%, consistent with significant hypoxemia. Based on these findings, a diagnosis of idiopathic pulmonary arterial hypertension was established.\n\nAfter initiating targeted pharmacological therapy with inhaled iloprost and oral sildenafil, the patient was re-evaluated five months later. Follow-up RHC revealed worsening hemodynamics, with an increased mPAP of 59.7 mmHg and PVR of 13.4 WU. Notably, SaO2 measured in the right upper lobe pulmonary artery increased to 89.7%, an unexpected finding suggesting abnormal vascular communication.\n\nSubsequent pulmonary arteriography identified absence of contrast filling in the right upper lobe pulmonary artery and evidence of retrograde blood flow (visible as negative contrast) in the right pulmonary artery. Further angiography of the right subclavian artery uncovered a large vascular malformation connecting systemic arteries to the pulmonary artery of the right upper lobe. Computed tomography angiography (angio-CT) confirmed these findings and additionally revealed enlarged bronchial arteries forming fistulous connections to the pulmonary artery in the same region.\n\n**Clinical Interpretation**  \nThe patient’s pulmonary hypertension was complicated by the presence of multiple systemic-to-pulmonary arterial fistulas (abnormal direct connections between systemic arteries—such as subclavian and bronchial arteries—and pulmonary arteries). These vascular malformations likely contributed to abnormal blood flow patterns, increased oxygen saturation in pulmonary artery samples, and progressive right heart failure. Despite aggressive medical therapy for pulmonary arterial hypertension, the fistulas represented a significant pathological factor exacerbating the patient’s condition.\n\n**Next Steps and Outcome**  \nSelective percutaneous embolization of the identified arterial fistulas was performed using a mixture of Lipiodol and n-butyl-2-cyanoacrylate glue to occlude the abnormal vessels. Unfortunately, this intervention did not result in clinical improvement. The patient’s condition continued to deteriorate, culminating in death three months after embolization due to severe right heart failure complicated by pneumonia.\n\nThis case underscores the importance of thorough vascular imaging in patients with pulmonary hypertension who exhibit atypical hemodynamic or oxygenation findings, as underlying vascular malformations such as systemic-to-pulmonary arterial fistulas can significantly impact prognosis and therapeutic strategies."
+        }
+    },
+    {
+        "article": "Paciente de 73 años, diagnosticada de enfermedad pulmonar obstructiva crónica (EPOC), hipertensión arterial (HTA), trastorno bipolar, ansiedad, depresión, hipotiroidismo y artritis reumatoide, condiciones para las cuales tiene prescrito el tratamiento reflejado en el Anexo I.\n\nRealiza una llamada telefónica a la farmacia comunitaria para solicitar información sobre una nueva medicación prescrita para el tratamiento de una infección de orina y un déficit de vitamina D, diagnosticados tras la realización de una analítica completa en el servicio de urgencias de un hospital privado.\n\nLa paciente es totalmente dependiente y no sale de casa, siendo su cuidadora la persona que siempre va a retirar su medicación y elabora los pastilleros semanales.\n\nLos fármacos prescritos para el tratamiento de la infección de orina fueron cefuroxima 250 mg (1 comprimido cada 12 horas durante 5 días) y butilescopolamina 10 mg (1 comprimido en la mañana si presentaba molestias).\n\nPara el déficit de vitamina D se le prescribió colecalciferol 50.000 U.I. (1 cápsula una vez al mes durante dos meses) y colecalciferol 25.000 UI (1 cápsula una vez al mes tras finalizar el envase de 50.000 U.I.).\n\nESTUDIO Y EVALUACIÓN\nSe lleva a cabo el servicio de dispensación (SD) sin incidencias, siguiendo la metodología expuesta en la Guía práctica para los Servicios Profesionales Farmacéuticos Asistenciales en la Farmacia Comunitaria. Posteriormente, la paciente contacta con la farmacia comunitaria, preocupada porque la nueva medicación le ha generado confusión, ya que ella tomaba unas cápsulas naranjas para su déficit de vitamina D prescritas por su médico de Atención Primaria hace unos meses y en la parte del informe de urgencias en la que figura el tratamiento venía reflejado una medicación nueva para ese mismo problema de salud. Además, coincidió con que su cuidadora habitual ya no podrá trabajar más con ella y no la podrá ayudar con su medicación. Por ello, se le propone a la paciente el servicio de Revisión del Uso del Medicamento (RUM) con el objetivo de evaluar el grado de conocimiento que tienen la paciente con respecto a sus patologías y su tratamiento, a la par que poder resolver posibles errores en la administración de los distintos fármacos que forman parte del mismo. Se le explica en qué consiste todo el procedimiento y decide aceptar.\n\nTras esto, se procedió a citar a la cuidadora en la farmacia con la tarjeta sanitaria de la paciente, su bolsa de medicación para hacer una revisión exhaustiva de su botiquín y el último informe de urgencias con el objetivo de recopilar toda la información necesaria para realizar el servicio asistencial vía telefónica. Durante la llamada con la paciente, se procede a cumplimentar el formulario RUM, el cual se volcó posteriormente en la plataforma SEFAC e_XPERT ®. Además, para poder evaluar correctamente todo el tratamiento farmacológico, se emplearon herramientas como el CIMA (donde se consultaron las fichas técnicas de los medicamentos) y el BotPlus (donde se consultaron las posibles interacciones farmacológicas).\n\nINTERVENCIÓN\nTras la primera toma de contacto a través de la entrevista telefónica y hacer revisión del botiquín, se pudo detectar que la paciente y su cuidadora no estaban haciendo una gestión apropiada de la medicación. Tras la revisión de su botiquín, se hallaron envases caducados y con anotaciones erróneas sobre su uso, blísteres con comprimidos partidos que no deberían de estarlo y acúmulo de varios envases de un mismo fármaco. Al tratarse de una paciente dependiente, polimedicada y con problemas para gestionar correctamente su tratamiento antes y durante la ausencia de su cuidadora habitual se decidió con el fin de garantizar la seguridad farmacoterapéutica y mejorar la adherencia al tratamiento derivar al servicio de sistema personalizado de dosificación (SPD). A través de la plataforma de SEFAC e_XPERT ® se procedió a redactar un informe de derivación a su médico de Atención Primaria (MAP) del Sistema Nacional de Salud (SNS) (ver Anexo II), donde se detallaba la inclusión de la paciente en el servicio de Revisión del Uso de la Medicación y su posterior derivación al servicio de SPD. Además, quedaron recogidas las siguientes propuestas de intervención:\n\nRevisión de la pauta posológica de tramadol 50 mg de liberación retardada por la existencia de un posible error en la prescripción.\n\nRevisión del tratamiento prescrito para el déficit de vitamina D por la existencia de una duplicidad terapéutica.\n\nCambio del absorbente de incontinencia de tipo pants a elástico alegando la situación de dependencia de la paciente y las dificultades para realizar una correcta colocación por parte de la cuidadora al pasar encamada la mayor parte del tiempo. Se aportaron los Códigos Nacionales (CN) correspondientes.\n\nRevisión del tratamiento para la EPOC por dificultades de empleo del inhalador y falta de adherencia terapéutica.\n\nRESULTADOS\nDurante la cita médica, la médico de atención primaria recibe el informe de derivación entregado a la cuidadora donde, además, se solicita contacto con la farmacia comunitaria para poder iniciar de forma correcta el servicio de SPD. Tras hablar con ella vía telefónica, se realizaron los siguientes cambios en su tratamiento:\n\nDéficit de vitamina D: anulación de calcifediol y sustitución por colecalciferol prescrito en el Servicio de Urgencias.\n\nArtritis reumatoide: modificación de pauta de tramadol de liberación prolongada a 1-0-1 y empleo de paracetamol 1000 mg 1-1-1 si precisa.\n\nIncontinencia urinaria: sustitución de absorbente tipo pants por elástico.\n\nEPOC: no se realizó un cambio de tratamiento. La médico de atención primaria consideró oportuno llevar a cabo una supervisión diaria por parte de la cuidadora en cada una de las tomas del inhalador.",
+        "gold_summary": "Paciente 73 años, dependiente, polimedicada y pluripatológica contacta telefónicamente con la farmacia comunitaria para solicitar información sobre un tratamiento de nueva prescripción para una infección de orina y un déficit de vitamina D. La dispensación de la medicación a su cuidadora deriva en mayores dudas a la paciente, por lo que se le ofrece el servicio de revisión del uso del medicamento (RUM). Durante la prestación del servicio se detectan varias incidencias en su tratamiento, por lo que se decide realizar un informe de derivación al médico de atención primaria para una revisión completa del tratamiento y poder así derivar a la paciente al servicio de Sistema Personalizado de Dosificación (SPD) con el fin de garantizar la seguridad farmacoterapéutica de la paciente y mejorar su adherencia al tratamiento.",
+        "synthetic_summary": {
+            "B1": "A 73-year-old lady who needs help with her medicines called the pharmacy. She was confused about new medicine for a pee infection and vitamin D. The pharmacy helped her by checking all her medicines carefully. They found some problems and told her doctor. The doctor will help make her medicine easier and safer to take every day.",
+            "B2": "**Patient Background and Concern**  \nA 73-year-old woman who depends on others for care and takes many medicines called her local pharmacy. She wanted to understand new medicines prescribed for a urinary tract infection and low vitamin D levels. Her caregiver usually picks up her medicines and helps organize them.\n\n**What Happened at the Pharmacy**  \nWhen the pharmacy gave the new medicines to the caregiver, the patient became confused. She was still taking older vitamin D capsules prescribed earlier and saw different instructions from the hospital report. Also, her usual caregiver could no longer help her with her medicines. Because of this, the pharmacy offered a special service called a Medication Use Review (RUM). This service checks how well the patient understands her health problems and medicines and looks for any mistakes in how she takes them. The patient agreed to this review.\n\n**Findings from the Review**  \nThe pharmacy team met with the caregiver and reviewed all the patient’s medicines and medical reports. They found several problems: expired medicines, wrong notes about how to take them, broken pills that should not be broken, and multiple packages of the same medicine. Since the patient depends on others and has many health issues, the pharmacy suggested using a Personalized Dosage System (SPD). This system organizes medicines into daily doses to make taking them safer and easier.\n\n**Next Steps and Doctor’s Role**  \nThe pharmacy wrote a detailed report for the patient’s primary care doctor. The report explained the medication review and recommended using the SPD service. It also suggested checking some medicines for possible errors and adjusting treatments, like changing vitamin D medicine to avoid duplicates and switching incontinence supplies to better suit the patient’s needs.\n\n**Outcome**  \nThe doctor reviewed the report and made changes to the patient’s treatment. For example, they stopped one vitamin D medicine and kept the one from the hospital, adjusted pain medicine doses, and changed the incontinence product. For her lung disease, the doctor decided no medicine changes were needed but asked the caregiver to help watch how she uses her inhaler every day.\n\n**What This Means**  \nThis case shows how important it is to carefully review medicines for older patients who take many drugs and rely on caregivers. By working together, the pharmacy and doctor helped make the patient’s treatment safer and easier to follow. The Personalized Dosage System will help prevent mistakes and improve her health.",
+            "B3": "Background  \nA 73-year-old woman with multiple chronic conditions—including chronic obstructive pulmonary disease (COPD), hypertension, bipolar disorder, anxiety, depression, hypothyroidism, and rheumatoid arthritis—is fully dependent on a caregiver for daily activities and medication management. Recently, she was diagnosed with a urinary tract infection and vitamin D deficiency during an emergency hospital visit. New medications were prescribed for these conditions, which her caregiver collected from the community pharmacy.\n\nKey Findings  \nAfter dispensing the new medications—cefuroxime and butylscopolamine for the infection, and high-dose colecalciferol (vitamin D) supplements—the patient contacted the pharmacy expressing confusion. She was uncertain because she had previously been taking a different vitamin D capsule prescribed by her primary care physician, and the emergency report listed a new vitamin D treatment. Additionally, her usual caregiver was no longer able to assist with medication management, increasing her concerns.  \n\nThe pharmacy offered a comprehensive Medication Use Review (MUR) service to assess the patient’s understanding of her illnesses and treatments, identify administration errors, and clarify any doubts. With the patient’s consent, the caregiver was invited to the pharmacy to review the patient’s medication supplies and recent hospital report. A detailed telephone interview was conducted to complete the MUR documentation, utilizing clinical databases to verify medication information and potential drug interactions.\n\nClinical Interpretation  \nThe review revealed significant issues in medication management: expired medications, incorrect usage notes, broken tablets that should not have been split, and multiple redundant packages of the same drug. Given the patient’s dependency, complex medication regimen, and recent loss of caregiver support, these findings indicated a high risk for medication errors and poor adherence.  \n\nConsequently, the pharmacy prepared a referral report for the patient’s primary care physician recommending a full treatment reassessment and enrollment in a Personalized Dosage System (PDS) service to improve medication safety and adherence. Specific recommendations included:  \n- Re-evaluating the dosing schedule of prolonged-release tramadol due to a suspected prescribing error.  \n- Reviewing vitamin D therapy to resolve duplicate treatments.  \n- Changing the type of incontinence absorbent from pants to elastic, considering the patient’s bedridden status and caregiver’s difficulties with application.  \n- Assessing COPD treatment adherence and inhaler technique.\n\nNext Steps  \nThe primary care physician received the referral and coordinated with the pharmacy to initiate the PDS service. Treatment adjustments were made as follows:  \n- Vitamin D deficiency: discontinuation of calcifediol and continuation of colecalciferol as prescribed in the emergency setting.  \n- Rheumatoid arthritis pain management: modification of tramadol dosing and addition of paracetamol as needed.  \n- Urinary incontinence: replacement of absorbent pants with elastic type.  \n- COPD: no medication changes, but daily supervision of inhaler use by the caregiver was implemented.\n\nThis multidisciplinary approach aimed to enhance the patient’s medication safety, simplify her regimen, and support adherence in the context of her complex health status and caregiving challenges."
+        }
+    },
+    {
+        "article": "Nuestra paciente era una mujer japonesa de 83 años con insuficiencia cardiaca crónica (fracción de eyección: aproximadamente 30 %) que inició un tratamiento con empagliflozina 10 mg diarios unos 8 meses antes de su ingreso. Nunca se le había diagnosticado diabetes mellitus (HbA1c 5.9 % antes de iniciar el tratamiento con empagliflozina). Unos 6 meses antes de su ingreso, su tratamiento se cambió a dapagliflozina 5 mg. Sus diuréticos y otros medicamentos cardiacos no se ajustaron durante ese tiempo. Dos semanas antes de su ingreso, tropezó y cayó, sufriendo fracturas vertebrales y de costillas. La paciente se debilitó significativamente por el dolor de las fracturas, lo que le causó dificultad para caminar y anorexia. Solo podía comer el 50-70 % de su ingesta dietética habitual. Esto empeoró en la semana siguiente, cuando también desarrolló náuseas y vómitos y redujo aún más su ingesta de alimentos a solo el 10-20 % de la cantidad habitual. Durante este período, continuó tomando dapagliflozina. Fue ingresada en el hospital.\nAl ingreso, la paciente estaba consciente con una temperatura corporal de 37.4°C, presión arterial de 124/68 mmHg, frecuencia cardiaca de 91 bpm y saturación de oxígeno de 98% en aire ambiente. Los análisis de sangre revelaron un nivel de glucosa en sangre de 124 mg/dL, pH de 7.3, concentración de HCO3– de 14 mmol/L, exceso de base de -10 mEq/L, brecha aniónica de 20 mEq/L y concentración de b-hidroxibutirato de 5150 umol/L (Tabla 1). Estos hallazgos fueron consistentes con el diagnóstico de cetoacidosis normoglucémica. La paciente no tenía antecedentes de consumo de alcohol, tabaquismo o uso de drogas.\nSe descartaron otras causas de acidosis con alto déficit aniónico. Su nivel de péptido C era coherente con los niveles de glucosa en sangre en el ingreso, lo que indicaba que tenía una secreción de insulina adecuada; por lo tanto, no se inició la administración de insulina. Se interrumpió el uso de inhibidores de SGLT2 y la paciente se trató inicialmente con solución salina isotónica y una infusión de mantenimiento de aproximadamente 170 g de glucosa diarios.\nA pesar de no haber iniciado la insulina, su pH (7.418), concentración de HCO3– (20.7 mmol/L) y brecha aniónica (13.3 mEq/L) mejoraron al día siguiente de su ingreso. Se inició la dieta Carb 60, pero se continuaron las infusiones intravenosas de glucosa porque la ingesta de alimentos de la paciente era escasa. La cantidad de infusión de glucosa administrada se ajustó según su ingesta de alimentos. En el cuarto día de hospitalización, las cetonas urinarias desaparecieron.\nLa infusión de glucosa se interrumpió el día 12 de la hospitalización, una vez que el paciente pudo comer comidas completas. Aunque el nivel de glucosa en sangre del paciente estaba dentro del rango normal, la excreción de glucosa en la orina fue de 3+ (>500 mg/dL) durante 8 días después de la última dosis de dapagliflozina.\nAl ingreso, la paciente no podía caminar debido al dolor de la fractura, la fatiga general y el síndrome de desuso, pero después de la rehabilitación pudo hacerlo de forma independiente. Fue dada de alta el día 19 de hospitalización, tras someterse a rehabilitación.\nLos inhibidores de SGLT2 no se reiniciaron.\n\nMH - Humanos\nMH - Mujer\nMH - *Insuficiencia cardiaca/inducida químicamente\nMH - *Inhibidores del transportador de glucosa y sodio 2/efectos adversos\nMH - Edad 80 años y más\nMH - Cetosis/químicamente inducida\nMH - glucósidos/efectos adversos\nMH - Cetoacidosis diabética/inducida químicamente\n",
+        "gold_summary": "A continuación, describimos un caso de cetoacidosis en una mujer japonesa de 83 años sin diabetes a la que se le administraron inhibidores de SGLT2 para la insuficiencia cardiaca (fracción de eyección: aproximadamente 30 %). Dos semanas antes de su ingreso, había sufrido una fractura vertebral y una fractura de costilla debido a una caída, a la que siguió una anorexia, pero continuó tomando inhibidores de SGLT2. En el momento del ingreso, los resultados de los análisis de sangre revelaron un nivel de glucosa en sangre de 124 mg/dL, un nivel de hemoglobina A1C del 5,9 %, un pH de 7,329, una concentración de HCO₃⁻ de 14,3 mmol/L y una concentración de β-hidroxibutirato de 5150 μmol/L, lo que condujo a un diagnóstico de cetoacidosis euglucémica. El nivel de péptido C de la paciente coincidía con los niveles de glucosa en sangre en el momento del ingreso, lo que indicaba que tenía una secreción de insulina adecuada. La paciente fue tratada únicamente con administración de glucosa sin insulina y fue dada de alta tras la interrupción del inhibidor de SGLT2.\n",
+        "synthetic_summary": {
+            "B1": "There was an old lady who was very sick with her heart. She fell and hurt her back and ribs. After that, she did not want to eat much food. She kept taking her medicine for her heart.\n\nWhen she went to the hospital, the doctors found she had a problem with her body that made her feel very tired and sick. But her sugar was not too high. The doctors gave her sugar water to help her feel better. They stopped her heart medicine for a while.\n\nAfter some days, she got stronger and could eat more food. She did not need the medicine again. Then she went home feeling better.",
+            "B2": "**What Happened to the Patient**  \nAn 83-year-old Japanese woman who did not have diabetes was taking a type of medicine called an SGLT2 inhibitor. This medicine helps with heart failure, a condition where the heart does not pump blood well. About two weeks before going to the hospital, she fell and broke some bones in her spine and ribs. Because of the pain, she ate much less food than usual but kept taking the SGLT2 inhibitor medicine.\n\n**What the Doctors Found**  \nWhen she arrived at the hospital, blood tests showed her blood sugar was normal at 124 mg/dL, and her long-term blood sugar level (called hemoglobin A1C) was 5.9%, which is also normal. However, other tests showed she had a condition called ketoacidosis. Ketoacidosis happens when the body produces too many acids called ketones, which can be dangerous. Usually, ketoacidosis happens with very high blood sugar, but in her case, the blood sugar was normal. This is called euglycemic ketoacidosis. Her insulin levels were normal, meaning her body was still making enough insulin.\n\n**How They Treated Her**  \nThe doctors stopped the SGLT2 inhibitor medicine and gave her glucose (a type of sugar) through an IV to help her body recover. They did not give her insulin because her insulin levels were okay. After treatment, her condition improved, and she was able to leave the hospital safely.\n\n**What This Means**  \nThis case shows that people taking SGLT2 inhibitors can develop ketoacidosis even if their blood sugar is normal, especially if they eat very little or are sick. It is important for doctors and patients to watch for this condition and stop the medicine if needed.",
+            "B3": "**Background**  \nThis report describes an 83-year-old Japanese woman with chronic heart failure characterized by a reduced left ventricular ejection fraction of approximately 30%. Although she had no prior diagnosis of diabetes mellitus (her hemoglobin A1c was 5.9% before treatment), she was prescribed sodium-glucose cotransporter 2 (SGLT2) inhibitors—initially empagliflozin and later dapagliflozin—to manage her heart failure. Two weeks before hospital admission, she sustained vertebral and rib fractures after a fall, which led to significant pain, reduced mobility, and anorexia (loss of appetite). Despite her worsening nutritional intake, she continued taking the SGLT2 inhibitor.\n\n**Key Findings at Admission**  \nUpon hospital admission, the patient was conscious and hemodynamically stable with a body temperature of 37.4°C, blood pressure of 124/68 mmHg, heart rate of 91 beats per minute, and oxygen saturation of 98% on room air. Laboratory tests revealed:  \n- Blood glucose level of 124 mg/dL (within normal range)  \n- Hemoglobin A1c of 5.9% (indicating no chronic hyperglycemia)  \n- Arterial blood pH of 7.329 (mild acidemia)  \n- Serum bicarbonate (HCO3–) concentration of 14.3 mmol/L (reduced, indicating metabolic acidosis)  \n- Elevated anion gap (20 mEq/L), consistent with high anion gap metabolic acidosis  \n- β-hydroxybutyrate level of 5150 μmol/L, indicating significant ketosis  \n- C-peptide levels appropriate for her blood glucose, suggesting preserved endogenous insulin secretion  \n\nThese findings supported a diagnosis of euglycemic diabetic ketoacidosis (DKA), a form of ketoacidosis occurring with normal or near-normal blood glucose levels, which is a recognized adverse effect of SGLT2 inhibitors.\n\n**Clinical Interpretation**  \nThe patient’s ketoacidosis was likely precipitated by the combination of reduced oral intake due to anorexia and ongoing SGLT2 inhibitor therapy. The preserved insulin secretion indicated that insulin deficiency was not the primary cause, differentiating this case from classic type 1 diabetic ketoacidosis. Other causes of high anion gap metabolic acidosis were excluded. The continuation of SGLT2 inhibitors during a period of catabolic stress and poor nutrition likely contributed to the development of ketoacidosis despite normal glucose levels.\n\n**Treatment and Outcome**  \nManagement involved immediate discontinuation of the SGLT2 inhibitor and administration of isotonic saline along with intravenous glucose infusion (approximately 170 grams per day) to reverse ketosis and correct metabolic acidosis. Insulin therapy was not initiated due to adequate endogenous insulin secretion and controlled blood glucose levels. The patient’s acid-base status improved by the next day, with normalization of pH and bicarbonate levels and reduction of the anion gap. Oral intake was gradually reintroduced with a carbohydrate-controlled diet, and intravenous glucose was adjusted accordingly. Urinary ketones resolved by hospital day four. Glucose infusions were stopped on day 12 once the patient resumed full oral nutrition. Notably, glucosuria (glucose in urine) persisted for eight days after stopping dapagliflozin, reflecting the drug’s prolonged renal effects.\n\nAlthough initially unable to walk due to fracture pain, fatigue, and disuse syndrome, the patient regained independent ambulation through rehabilitation and was discharged on hospital day 19. SGLT2 inhibitors were not restarted.\n\n**Next Steps and Considerations**  \nThis case highlights the risk of euglycemic ketoacidosis in elderly patients treated with SGLT2 inhibitors, especially during periods of reduced oral intake or physiological stress such as fractures. Clinicians should monitor for signs of ketoacidosis even when blood glucose levels are normal and consider temporary discontinuation of SGLT2 inhibitors in such contexts. Patient education regarding the risks of continuing these medications during illness or poor nutrition is essential to prevent similar adverse events."
+        }
+    },
+    {
+        "article": "Una recién nacida fue evaluada en la sala de neonatos poco tiempo después del parto debido a la presencia de extensas lesiones similares a cicatrices en sus flancos y muslos superiores. La bebé, nacida de una madre asiática de 28 años a las 39 semanas de gestación, formaba parte de un embarazo gemelar espontáneo. Su madre, que ya había tenido cinco hijos, había tenido un aborto espontáneo en el primer trimestre durante su segundo embarazo.\n\nLos padres eran primos hermanos y no habían tenido problemas de salud en sus tres hijos vivos. La ecografía a las 13 semanas confirmó un embarazo bicorial y diacítico y la ausencia de actividad cardíaca en uno de los gemelos. Las ecografías posteriores mostraron un feto que se desarrollaba con normalidad junto a un gemelo no viable.\n\nDurante el embarazo, la madre no informó sobre el uso de medicamentos o síntomas como fiebre y erupción cutánea. Dio negativo para estreptococo del grupo B y fue admitida en el departamento de urgencias obstétricas con dolores de parto. La niña fue entregada por vía vaginal, pesando 2,83 kg, y fue vigorosa al nacer. A la placenta se le unió un remanente fetal no viable comprimido que medía 6 × 2 cm. La placenta pesaba 460 g y parecía normal al examen.\n\nLa niña presentaba lesiones cutáneas extensas e irregulares, que se caracterizaban por un aspecto estrellado en ambos flancos, que se extendían lateralmente sobre la zona glútea y el muslo superior. Las lesiones eran simétricas en ambos flancos. No obstante, las lesiones en los muslos eran notablemente más leves en el lado izquierdo. Sus constantes vitales eran estables y no presentaba otras anomalías externas. El examen clínico de sus sistemas respiratorio, cardiovascular, gastrointestinal y neurológico reveló resultados normales, y no se observaron otras anomalías cutáneas, incluida la ausencia de lesiones ampollosas.\n\nDada la naturaleza simétrica de las anomalías cutáneas y el contexto de embarazo de mellizos con FP, se realizó un diagnóstico de aplasia cutis congénita grupo V. Los exámenes de laboratorio, que incluían hemograma completo, electrolitos y pruebas de función renal e hepática, arrojaron resultados normales. Los exámenes de detección de toxoplasmosis, rubéola, citomegalovirus, herpes simple y VIH (TORCH) arrojaron resultados negativos. La ecografía del cerebro, abdomen y corazón no reveló anomalías.\n\nDado que las lesiones se curaron en el útero, solo se prescribieron emolientes locales. Después de 48 horas de observación, el bebé fue dado de alta en su casa, con derivaciones a clínicas de dermatología pediátrica y cirugía plástica. En el seguimiento de 2 semanas, no se observaron cambios en las lesiones de la piel ni nuevos síntomas. Su análisis de microarreglo cromosómico fue reportado como normal.\n",
+        "gold_summary": "Informamos sobre un neonato al que se le diagnosticó ACC de grupo G-V asociado con fetus papyraceus de un embarazo gemelar di-coriónico y di-amniótico. Nacida de una madre asiática de 28 años, esta niña presentaba lesiones extensas, cicatrizadas, similares a las cicatrices en sus flancos y muslos superiores. Estas lesiones eran consistentes con la distribución en forma de «H» comúnmente descrita en ACC ligada a fetus papyraceus. A pesar de las manifestaciones dermatológicas significativas, la niña no mostró otras anormalidades externas o implicación sistémica, y las evaluaciones exhaustivas, incluidos los ultrasonidos y el microarray cromosómico, fueron normales.\n",
+        "synthetic_summary": {
+            "B1": "A baby girl was born with special marks on her skin. The marks looked like scars on her sides and legs.\n\nShe was born with a twin, but the other twin did not grow. The marks are from that.\n\nThe baby is healthy and strong. Doctors checked her body and it is all okay.\n\nShe will be cared for gently, and the marks will be watched.",
+            "B2": "**What They Found**  \nA newborn baby girl was diagnosed with a skin condition called aplasia cutis congenita (ACC) group V. This means she was born with areas on her skin that did not develop properly, leaving scar-like marks. These marks appeared on her sides (flanks) and upper thighs. The pattern of the marks looked like the letter \"H,\" which is common in this type of ACC linked to a condition called fetus papyraceus. Fetus papyraceus happens when one twin in a twin pregnancy dies early and becomes flattened, like a small paper-thin fetus.\n\n**What It Means**  \nEven though the baby had these noticeable skin scars, she did not have any other visible problems or health issues. Doctors checked her body thoroughly, including her brain, heart, and abdomen with ultrasound scans, and tested her chromosomes with a special test called a microarray. All these tests came back normal, showing no other problems. This means the skin condition was isolated and did not affect her overall health.",
+            "B3": "Background  \nThis report describes a newborn female diagnosed with group V congenital aplasia cutis (ACC), a rare condition characterized by localized absence of skin, associated with fetus papyraceus (a compressed, nonviable twin) in a dichorionic diamniotic twin pregnancy. The infant was born to a 28-year-old Asian mother following a spontaneous twin pregnancy complicated by the demise of one twin early in gestation.\n\nKey Findings  \nAt birth, the newborn exhibited extensive, scar-like skin lesions symmetrically distributed on both flanks and upper thighs. These lesions displayed a characteristic “H”-shaped pattern, which is commonly observed in ACC linked to fetus papyraceus. The lesions on the left thigh were notably less severe than those on the right. Despite the significant dermatological findings, the infant’s vital signs were stable, and no other external anomalies were present. Comprehensive clinical examinations of the respiratory, cardiovascular, gastrointestinal, and neurological systems revealed normal function. Importantly, no blistering or other skin abnormalities were detected.\n\nLaboratory investigations, including complete blood count, electrolyte panels, and renal and hepatic function tests, were within normal limits. Screening for congenital infections—specifically toxoplasmosis, rubella, cytomegalovirus, herpes simplex virus, and HIV (the TORCH panel)—yielded negative results. Ultrasound imaging of the brain, abdomen, and heart showed no abnormalities. Genetic analysis via chromosomal microarray was also normal.\n\nClinical Interpretation  \nThe symmetrical, scar-like skin lesions in the context of a twin pregnancy complicated by fetus papyraceus support the diagnosis of group V congenital aplasia cutis. This form of ACC is thought to result from vascular disruptions related to the demise of one twin, leading to localized skin loss in the surviving twin. The absence of systemic involvement and normal laboratory and imaging studies indicate that the condition was confined to the skin without affecting other organ systems.\n\nNext Steps  \nSince the skin lesions had already undergone in utero healing, treatment was limited to the application of topical emollients to maintain skin integrity. After 48 hours of observation without complications, the infant was discharged home with referrals to pediatric dermatology and plastic surgery specialists for ongoing management. At a two-week follow-up, the skin lesions remained stable without progression or new symptoms. Continued monitoring is advised to assess long-term skin healing and to address any potential functional or cosmetic concerns."
+        }
+    },
+    {
+        "article": "Información para el paciente\nUn hombre de 44 años de edad fue ingresado en nuestro hospital con quejas principales de neumaturia y cistitis repetida. El paciente también tenía antecedentes de hipotiroidismo.\n\nLa tomografía computarizada con contraste mejorado reveló múltiples divertículos del colon sigmoide, y el límite entre el divertículo y la vejiga no estaba claro. La endoscopia gastrointestinal inferior reveló una fístula en el colon rectosigmoide aproximadamente a 15 cm del borde anal. La cistoscopia reveló una fístula en la pared posterior izquierda de la vejiga. Se diagnosticó una fístula vesicovaginal y se planificó una cirugía laparoscópica. Los hallazgos intraoperatorios revelaron una inflamación severa alrededor de la fístula vesicovaginal, y también se habían formado adhesiones severas entre el íleon y la vejiga. El íleon y la vejiga eran difíciles de exfoliar debido a las adhesiones severas. Por lo tanto, decidimos realizar una resección intestinal combinada. El colon rectosigmoide, incluida la fístula, se movilizó y se resecó. La fístula vesical se seccionó y se cerró con una sutura de púas sin nudos (V-LocTM 180, Covidien, Mansfield). La anastomosis sigmoide-rectal se reconstruyó utilizando la técnica de doble grapado. La resección parcial del íleon se reconstruyó con una anastomosis funcional de extremo a extremo (FEEA). Además de la presencia de una anastomosis de 2 sitios, había una inflamación severa en el área circundante, y considerando el riesgo de fuga anastomótica, se creó una ileostomía de derivación 30 cm proximal a la anastomosis ileo-ileal.\n\nLos procedimientos quirúrgicos incluyeron resección anterior alta laparoscópica, resección parcial del intestino delgado, cistectomía parcial y derivación en forma de asa. La operación duró 236 minutos y la pérdida de sangre fue de 50 ml. El curso postoperatorio fue sin incidentes y el cierre de la ileostomía se planificó 1 mes después de la cirugía inicial. Con ayuda laparoscópica, se eliminaron las adherencias entre el omento y la pared abdominal alrededor del estoma. Se realizó una movilización completa alrededor del estoma y el intestino se sacó hacia afuera. El íleon se reconstruyó utilizando FEEA. El procedimiento quirúrgico implicó el cierre de la ileostomía asistida por laparoscopia. La operación duró 100 minutos y la pérdida de sangre fue de 30 ml.\n\nHallazgos clínicos\nAl día siguiente de la cirugía, se produjo un shock sintomático debido a la presión arterial baja (<80 mm Hg) y la taquicardia. Los análisis de sangre mostraron que la hemoglobina disminuyó de 15.3 antes de la cirugía a 8.6 g/dL después de la cirugía.\n\nEvaluación diagnóstica\nLa tomografía computarizada abdominal (TC) reveló una gran cantidad de fluido de alta densidad en la cavidad abdominal. El diagnóstico fue sangrado posoperatorio y shock hemorrágico. Se insertó un catéter venoso central y se administraron 8 unidades de glóbulos rojos y 8 unidades de plasma fresco congelado para estabilizar los signos vitales. Los signos vitales se estabilizaron y no se observó progresión de la anemia después de eso. Aunque se logró la hemostasia, la distensión abdominal severa y los altos niveles de respuesta inflamatoria (proteína C reactiva [CRP] a 42.9 mg/dL y recuento de glóbulos blancos [WBC] de 18,500/uL) persistieron 7 días después de la cirugía.\n\nLa TC con contraste reveló que el hematoma intraabdominal se localizaba en el abdomen inferior izquierdo y derecho, y se consideró posible el drenaje percutáneo. En el día 8 posoperatorio, se insertaron tubos de drenaje de 18 Fr en el abdomen inferior izquierdo y derecho a través de una punción guiada por TC, y se drenó una gran cantidad de sangre antigua. Después del drenaje, la reacción inflamatoria y la distensión abdominal causadas por la infección del hematoma residual mejoraron (CRP a 1,9 mg/dL y WBC de 5000/μL). No se observó progresión de la anemia. En el día 14 posoperatorio, el drenaje en el abdomen inferior derecho cambió de sangre antigua a jugo intestinal. Una angiografía de drenaje reveló fuga anastomótica tardía en el sitio de cierre de la ileostomía. No hubo signos de peritonitis con buen drenaje, pero el drenaje fue de aproximadamente 100 a 200 ml, y el flato del drenaje continuó. No se observó disminución del drenaje durante los siguientes 14 días.\n\nIntervención terapéutica\nAunque se consideró la posibilidad de una nueva operación, se esperaban adhesiones intraabdominales severas debido a la historia de cirugías anteriores, sangrado postoperatorio y fuga anastomótica. Por lo tanto, se consideró que la nueva operación era un procedimiento de alto riesgo. La tomografía computarizada con contraste mostró que un hematoma organizado permanecía en el mesenterio del intestino delgado y el íleon en el lado distal de 10 cm de la anastomosis estaba comprimido cerca del hematoma restante. Teniendo en cuenta la estenosis del íleon en el lado anal de la anastomosis debido a un hematoma residual como la causa de fuga anastomótica, se intentó la dilatación radioscópica del área de estenosis a través del drenaje en el día 24 postoperatorio. Se colocó un introductor de funda Cordis BRITE TIP® (8 Fr × 23 cm) en la fístula donde ocurrió la fuga anastomótica después del drenaje angiográfico. Se usó un hilo radioscópico GT (0.016 pulgadas, 180 cm, 90°) (Terumo, Tokio, Japón) y un microcatéter Renegade HI-FLO (135 × 20 cm) (Boston Scientific, Tokio, Japón) para alcanzar el íleon terminal. Usando el catéter Selecon MP II (6 Fr, 80 cm, φ20 mm) (Terumo), se identificó el área de estenosis en el íleon debido a la compresión del hematoma donde el globo no podía pasar.\n\nSe realizó dilatación con globo fluoroscópica en la estenosis del íleo utilizando un globo guiado por alambre CRE PRO GI (180 cm, 15-18 mm) (Boston Scientific), inflado a 16,5 mm de diámetro a 4,5 atm durante 3 minutos.\n\nSeguimiento y resultados\nDesde el día posterior a la dilatación con globo, la cantidad de drenaje disminuyó notablemente, y se observaron flatos y defecaciones desde el ano. Una semana después de la dilatación con globo, el drenaje fue casi nulo, y se determinó que la fuga anastomótica se había resuelto. El drenaje se eliminó gradualmente. La ingesta oral fue buena, y tuvo movimientos intestinales regulares. Fue dado de alta el día 45 posterior a la operación. Desde entonces, no se ha informado de ninguna recurrencia de la estenosis o fuga anastomótica.\n",
+        "gold_summary": "Preocupaciones del paciente: Presentamos el caso de un hombre de 44 años con fuga anastomótica tardía después del cierre de la ileostomía, causada por la compresión de un hematoma intraabdominal que se curó rápidamente después de la dilatación fluoroscópica con globo del área de la estenosis intestinal.\n\nDiagnósticos: Se produjo sangrado postoperatorio y shock hemorrágico el día 1 postoperatorio tras el cierre de la ileostomía. Los signos vitales se estabilizaron tras la transfusión de sangre, y se realizó con éxito un drenaje guiado por tomografía computarizada para reducir el volumen del hematoma. Sin embargo, el hematoma residual comprimió el íleon en el lado anal de la anastomosis, lo que provocó una fuga anastomótica tardía.\n\nIntervenciones/resultados: Se realizó con éxito la dilatación con balón fluoroscópico del área estenótica a través del drenaje y la fuga anastomótica se curó rápidamente.\n",
+        "synthetic_summary": {
+            "B1": "A man had a problem after his tummy surgery. He had some bleeding and felt very weak. Doctors gave him blood to help him feel better.\n\nLater, a small bump inside his tummy pressed on his tummy tube. This made a little hole that caused trouble.\n\nDoctors used a tiny balloon to open the tight spot. After that, the hole got better fast.\n\nThe man felt good and healed well.",
+            "B2": "**What Happened to the Patient**  \nA 44-year-old man had surgery to close an ileostomy, which is when part of the small intestine (called the ileum) is brought out through the belly to let waste leave the body. After the surgery, he developed a late leak where the intestines were joined back together. This leak was caused by pressure from a blood clot (called a hematoma) inside his abdomen pressing on the intestine and narrowing it.\n\n**What the Doctors Found**  \nOn the first day after surgery, the patient had heavy bleeding and went into shock, which means his blood pressure dropped dangerously low. He needed blood transfusions to stabilize him. Doctors used a CT scan (a special type of X-ray) to find and drain the blood clot inside his belly. Even after draining most of it, some clot remained and pressed on his ileum near the surgical join, causing the intestine to narrow (called stenosis). This narrowing led to a leak at the join, allowing intestinal fluid to escape.\n\n**How They Fixed It**  \nInstead of doing another risky surgery, doctors used a less invasive method called balloon dilation. They inserted a small balloon through the drainage tube into the narrowed part of the intestine. Then, using X-ray guidance, they inflated the balloon to widen the narrow area. This procedure quickly healed the leak. Afterward, the drainage decreased, and the patient was able to have normal bowel movements. He recovered well and was discharged about six weeks after the initial surgery, with no return of the leak or narrowing.",
+            "B3": "**Background**  \nA 44-year-old man with a history of hypothyroidism was admitted to the hospital presenting with pneumaturia (air in the urine) and recurrent cystitis (bladder infections). Imaging studies revealed multiple diverticula (small pouches) in the sigmoid colon and an unclear boundary between the colon and bladder, leading to the diagnosis of a vesicocolic fistula (an abnormal connection between the colon and bladder). He underwent complex laparoscopic surgery involving resection of the affected colon segment, partial small intestine removal, partial cystectomy (bladder removal), and creation of a diverting ileostomy (temporary intestinal opening).\n\n**Key Findings**  \nOn the first day after ileostomy closure surgery, the patient developed hemorrhagic shock due to postoperative bleeding, evidenced by a significant drop in hemoglobin and low blood pressure with rapid heart rate. Computed tomography (CT) scans showed a large intra-abdominal hematoma (collection of blood). After blood transfusions and CT-guided drainage of the hematoma, the patient’s vital signs stabilized. However, persistent inflammation and abdominal distension remained. Subsequent imaging revealed that a residual organized hematoma compressed the ileum (part of the small intestine) near the anastomosis (surgical connection) site, causing a late anastomotic leak. This leak was identified by the presence of intestinal fluid draining through the abdominal drain.\n\n**Clinical Interpretation**  \nThe late anastomotic leak was attributed to stenosis (narrowing) of the ileum caused by compression from the residual hematoma. Due to the patient’s history of multiple surgeries, postoperative bleeding, and adhesions (scar tissue), a repeat surgical intervention was considered high risk. Therefore, a minimally invasive approach was chosen.\n\n**Therapeutic Intervention and Outcome**  \nOn postoperative day 24, fluoroscopic balloon dilation was performed through the existing drainage tract to widen the stenotic segment of the ileum. Using specialized catheters and guidewires, the narrowed area was identified and dilated with a balloon inflated to 16.5 mm diameter under fluoroscopic guidance. Following this procedure, the volume of abdominal drainage decreased markedly, and the patient resumed normal intestinal function, including passing gas and stool per anus. Within one week, the anastomotic leak resolved completely, allowing gradual removal of the drains. The patient tolerated oral intake well and had regular bowel movements. He was discharged on postoperative day 45 without recurrence of stenosis or leakage.\n\n**Next Steps**  \nContinued outpatient monitoring is essential to detect any potential recurrence of intestinal narrowing or leakage. This case highlights the effectiveness of fluoroscopic balloon dilation as a less invasive alternative to surgery for managing late anastomotic leaks caused by mechanical compression from residual hematomas."
+        }
+    },
+    {
+        "article": "Paciente femenino de 23 años, ASA I, acude al Centro de Salud de la Universidad Peruana de Ciencias Aplicadas (CUS-UPC) para colocarle un implante en la zona edéntula de la pieza 1.6. Durante la evaluación, la paciente refiere que hace unos meses se le fracturó la primera molar superior derecha y, como consecuencia, le realizaron la exodoncia atraumática de dicha pieza dentaria.\n\nTras la inspección clínica, se observó la ausencia de la pieza dentaria 1.6, fenotipo gingival delgado y disminución en altura de reborde edéntulo Seibert tipo II 13. Tomográficamente, se registraron medidas de la altura del reborde óseo residual en relación con el piso del seno maxilar (6 mm) y el ancho de la cresta ósea a nivel cervical (11,20 mm), medio (11,80 mm) y apical (12,40 mm), con lo que se identifica la presencia de un seno maxilar ovoide, según Nie et al. Se realizó la planificación quirúrgica para la realización de una elevación del seno maxilar con abordaje transcrestal y la colocación de un implante dental de 4,8 x 8 mm.\n\nSe inició el procedimiento quirúrgico, que consistió en lo siguiente:\n\n• Asepsia y antisepsia\n\n• Técnica anestesia infiltrativa por vestibular y palatino de la zona edéntula 1.6 utilizando 2 cartuchos de lidocaína al 2% con epinefrina 1:80.000.\n\n• Incisión supracrestal en la zona edéntula 1.6 e incisiones sulculares en mesial de la pieza dentaria 1.7 y en distal de la pieza dentaria 1.5.\n\n• Decolado del colgajo a espesor parcial y, luego, se procedió a probar la guía quirúrgica para realizar la secuencia de fresado hasta una longitud de 6 mm, dejando 1 mm de distancia al piso del seno maxilar, el cual fue comprobado con los calibradores de profundidad, según el diámetro de la fresa que se utilizó durante la osteotomía. La secuencia de fresado se realizó hasta la fresa 3,5 mm de diámetro y luego se procedió a realizar el levantamiento de 2 mm del seno maxilar con la técnica de abordaje transcrestal mediante el uso de un osteótomo, hasta llegar a una longitud de 8 mm.\n\n• Colocación del implante φ 4,8 x 8 mm (Bone Level tapered, Straumann®) y tornillo de cierre, ambos con un torque de inserción de 20 N.\n\n• Sutura con puntos interrumpidos con ácido poliglicólico 5/0 y lavado de la zona quirúrgica con suero fisiológico al 0,09%.\n\n• Radiografía posquirúrgica del implante en zona edéntula 1.6.\n\n• Indicación de tomar amoxicilina de 500 mg + ácido clavulánico 125 mg cada 8 horas durante 7 días, ketorolaco de 10 mg cada 8 horas por 3 días, cetirizina de 10 mg cada 24 horas por 3 días y clorhexidina al 0,12%, 2 veces al día, por 10 días. Entre las indicaciones posquirúrgicas se le indicó a la paciente reposo absoluto, sin esfuerzo físico, dieta blanda, no sonarse la nariz, no succionar líquidos por dos semanas, no sumergir la cabeza en agua, tampoco estornudar o toser con la boca abierta, mantener la cabeza elevada y aplicarse compresas de hielo durante las primeras 4 horas.\n\nSe realizó un control posquirúrgico a los 7 días, el cual evidenció tejidos blandos en proceso de cicatrización, por lo que se procedió al retiro de puntos y lavado con suero fisiológico al 0,9%, y se realizó una tomografía de control que evidenció la elevación de seno maxilar, con 2,83 mm aproximadamente. Asimismo, se realizaron controles posquirúrgicos a los 35 y 56 días, en los cueles se hallaron tejidos blandos en completo proceso de cicatrización.",
+        "gold_summary": "Se realizó un levantamiento de seno maxilar sin injerto óseo en una paciente de sexo femenino de 23 años que requería la colocación de un implante dental en la zona edéntula de la pieza 16. La evaluación clínica y tomográfica permitieron planificar y realizar la elevación de seno maxilar mediante el abordaje transcrestal y sin la necesidad de injerto óseo. El reborde residual de 6 mm permitió la colocación de un implante dental simultáneo. Luego de 6 meses de seguimiento tomográfico, antes de la carga protésica, se consiguió una altura ósea vertical de 8,83 mm, lo que dio como resultado una ganancia ósea vertical de 2,83 mm. Adicionalmente, se observa una adecuada integración del implante dental sin complicaciones posoperatorias.",
+        "synthetic_summary": {
+            "B1": "A young woman needed a new tooth in her mouth. The doctor helped by making space inside her cheek bone. They put a new tooth part there without using extra bone. After some months, the new tooth part fit very well. The woman healed nicely and felt good.",
+            "B2": "**What They Did**  \nA 23-year-old woman needed a dental implant where her upper right first molar (tooth 16) was missing. To prepare for the implant, doctors performed a procedure called a maxillary sinus lift. This means they gently lifted the sinus membrane above the upper jaw to create more space for the implant. They did this without adding any bone graft material, which is sometimes used to help bone grow.\n\n**How They Planned and Performed the Procedure**  \nUsing clinical exams and special 3D X-rays (called tomography), the doctors measured the bone height. They found there was 6 millimeters of bone left, which was enough to place the implant right after lifting the sinus. The sinus lift was done through the top of the jawbone (transcrestal approach), carefully raising the sinus membrane by about 2 millimeters. Then, they placed a dental implant that was 4.8 mm wide and 8 mm long.\n\n**What They Found After 6 Months**  \nSix months later, before putting on the final tooth, they took another 3D X-ray. It showed that the bone height had increased to about 8.83 millimeters. This means the procedure helped the bone grow by nearly 3 millimeters vertically. The implant was well integrated, meaning it was stable and healthy, and there were no problems after surgery.\n\n**What This Means**  \nThis case shows that a sinus lift without bone grafts can work well when there is enough existing bone. It allows placing the implant at the same time and helps new bone grow to support the implant. The patient healed well and can now have a strong, lasting dental implant.",
+            "B3": "**Background**  \nA 23-year-old healthy female patient (ASA I classification) presented for dental implant placement in the edentulous area corresponding to tooth 1.6 (upper right first molar). The tooth had been atraumatically extracted several months prior due to a fracture. Clinical examination revealed a thin gingival phenotype and a Seibert type II ridge defect characterized by reduced vertical height of the alveolar ridge. Cone-beam computed tomography (CBCT) showed a residual bone height of 6 mm from the alveolar crest to the floor of the maxillary sinus and adequate bone width (approximately 11–12 mm). The maxillary sinus was identified as ovoid in shape.\n\n**Key Findings and Surgical Planning**  \nGiven the limited residual bone height, a transcrestal maxillary sinus lift without bone grafting was planned to increase vertical bone height and allow simultaneous placement of a dental implant measuring 4.8 mm in diameter by 8 mm in length. The transcrestal approach involved osteotomy preparation up to 6 mm depth, maintaining a 1 mm safety margin from the sinus floor, followed by a controlled 2 mm sinus membrane elevation using an osteotome.\n\n**Surgical Procedure**  \nUnder local anesthesia with lidocaine and epinephrine, a supracrestal incision was made in the edentulous area with sulcular incisions adjacent to neighboring teeth. A partial-thickness flap was raised, and the osteotomy sequence was performed with increasing drill diameters up to 3.5 mm. The sinus membrane was gently elevated transcrestally by 2 mm. The implant was then placed at 8 mm depth with an insertion torque of 20 Ncm, followed by closure with interrupted sutures using 5/0 polyglycolic acid. Postoperative care included antibiotics (amoxicillin/clavulanic acid), analgesics (ketorolac), antihistamines (cetirizine), and chlorhexidine mouthwash, along with strict instructions to avoid nasal pressure, physical exertion, and other activities that could compromise sinus healing.\n\n**Clinical Interpretation and Follow-Up**  \nAt the 7-day postoperative visit, soft tissues showed normal healing, and sutures were removed. A control CBCT scan confirmed a vertical bone gain of approximately 2.83 mm in the sinus lift area, increasing the total bone height to 8.83 mm. Subsequent follow-ups at 35 and 56 days demonstrated complete soft tissue healing without complications. The implant exhibited proper osseointegration (bone integration) with no signs of infection or failure.\n\n**Next Steps**  \nAfter a 6-month healing period confirmed by tomographic imaging, the implant site achieved sufficient vertical bone height for prosthetic loading (placement of the dental crown). The successful transcrestal sinus lift without grafting allowed simultaneous implant placement, reducing treatment time and morbidity. Continued monitoring will ensure long-term implant stability and function."
+        }
+    },
+    {
+        "article": "Una paciente de 42 años de edad fue remitida a nuestro centro terciario de cáncer con antecedentes de seroma recurrente del seno izquierdo. La paciente se había sometido a una extracción bilateral de implantes mamarios con una capsulotomía parcial 11 meses antes de su primera visita a nuestro centro. La paciente no presentaba ninguna comorbilidad notable y tenía antecedentes de aumento bilateral de senos con implantes mamarios en el plano submuscular en 2003, a la edad de 21 años. No se pudo localizar ninguna información sobre el tipo de implantes que había recibido originalmente. La paciente volvió a consultar al mismo cirujano en 2008, quejándose de seroma bilateral, para someterse a un primer reemplazo bilateral de implantes mamarios con implantes mamarios anatómicos texturados de 425 cc (Sebbin LSA TF 425). En 2013, se sometió a un segundo procedimiento de reemplazo de implantes para aumentar el tamaño con implantes mamarios de 480 cc del mismo fabricante (Sebbin LSA TF 480). En 2017, la paciente volvió para una revisión en la que se quejaba de dolor y aumento del volumen del seno bilateralmente. En ese momento, se le realizó una exploración por ultrasonido que identificó efusiones periprostéticas bilaterales sin linfadenopatía o masas palpables en las regiones mamarias. Las efusiones se drenaron sin análisis, pero reaparecieron a lo largo de los años, cuando la paciente buscó ayuda del mismo cirujano y se sometió a un tercer procedimiento de revisión en 2022, con un reemplazo bilateral de implantes mamarios y una toma de muestras de la cápsula anterior. El cirujano envió dos especímenes desde el lado derecho (9 x 1 cm y 3 x 3 cm) y uno desde el lado izquierdo (2 x 1 cm). El informe histopatológico del espécimen encontró «material proteico amorfo celular acellular» en el lado derecho y «tejido fibroso escleroso con inflamación de linfocitos-monocitos, que requiere correlación con la presentación clínica» en el lado izquierdo. A pesar de la extracción, el seroma reapareció en el lado izquierdo, y se envió para pruebas citopatológicas que identificaron «una población de células pleomórficas atípicas irregulares con contornos irregulares que sugieren un proceso linfoproliferativo con CD30+ elementos» para los que se recomendaron pruebas diagnósticas adicionales. Por esta razón, la paciente buscó tratamiento en nuestra institución, donde el caso fue gestionado por un equipo multidisciplinario (MDT) que incluía a un cirujano plástico, un hematopatólogo, un hematólogo, un oncólogo, un radioterapeuta, un oncólogo quirúrgico y un radiólogo de mama. El espécimen histopatológico original de la toma de la cápsula se revisó por un hematopatólogo de nuestro centro de referencia, que identificó células CD30+ grandes y escasas atípicas con contornos irregulares que se consideraron compatibles con el diagnóstico de BIA-ALCL. Las células presentaron el siguiente fenotipo: CD30+, CD3-, CD7-, CD5-, CD4-, CD8-, Granzima B+/-, TIA1-, ALK1-, PAX5-, CD79a-, CD68-, CD15-/+. La paciente recibió una exploración por ultrasonido con aspiración por aguja fina y citopatología de la efusión recurrente que confirmó un proceso CD30+ linfoproliferativo atípico con captación de 18F-FDG (fluorodeoxiglucosa) (SUV máx. 1,8). No se pudieron localizar otras áreas de captación en todos los demás segmentos corporales explorados. La paciente también recibió una exploración por resonancia magnética de ambos senos con medio de contraste para completar la estadificación preoperativa, confirmando el seroma del lado izquierdo. Los portaobjetos del espécimen de la cirugía anterior se revisaron por el hematopatólogo que consideró los hallazgos suficientes para identificar BIA-ALCL con infiltración temprana de la cápsula periprostética (pT2 según el sistema de estadificación MD Anderson-TNM). Tres semanas después de la visita inicial, la paciente se sometió a cirugía radical con capsulotomía en bloque que contenía solo 150 cc de efusión serosa sin implante. El contenido líquido se envió para cultivo y citopatología, mientras que el espécimen sólido se envió para examen histopatológico. Además, la paciente se sometió a biopsia de ganglio linfático centinela de 2 ganglios axilares identificados preoperativamente a través de linfografía segmentaria. Los ganglios linfáticos presentaron una linfadenopatía silicona-asociada reactiva crónica sin signos de linfadenopatía metastásica. El informe histopatológico de la cápsula reveló agregados celulares infiltrantes en la cápsula periprostética, pero márgenes de resección claros y sin signos de infiltración más allá de la cápsula. Como tal, la paciente recibió un estadio IC (pT3pN0M0). El curso postoperatorio fue sin incidentes, y no se consideraron necesarios más tratamientos adyuvantes por el MDT. La paciente continuó su estricto protocolo de seguimiento, con PET/CT de 6, 12 y 18 meses posteriores a la cirugía que no mostró signos de recurrencia de enfermedad local o distante. Como está, la paciente continúa sus visitas de seguimiento y exploraciones, con supervivencia libre de enfermedad más allá de 18 meses.\n",
+        "gold_summary": "Describimos el caso de una mujer de 42 años con antecedentes de aumento de senos bilateral con fines cosméticos 21 años antes, que desarrolló seroma recurrente del lado izquierdo. Buscó ayuda de su primer cirujano, quien realizó 2 procedimientos de intercambio de implantes mamarios, colocando dispositivos texturados y, finalmente, una extracción bilateral de implantes mamarios en el transcurso de dos décadas. La paciente no recibió capsulectomías en los intercambios de implantes anteriores y recibió una muestra de la cápsula anterior en el último procedimiento, donde se diagnosticó BIA-ALCL en el lado izquierdo. Fue derivada a un centro de cáncer terciario donde el examen preoperatorio confirmó la presencia de enfermedad residual local. Después de la gestión del equipo multidisciplinario, se sometió a una revisión de capsulectomía en bloque del lado izquierdo sin necesidad de tratamientos adicionales. El curso postoperatorio fue sin incidentes y sin signos de recurrencias locales a los 18 meses de seguimiento.\n",
+        "synthetic_summary": {
+            "B1": "A lady had breast implants many years ago. She had some swelling on her left side. The doctor changed her implants two times. Then, the doctor took out both implants. \n\nThe doctor found some unusual cells on the left side. The lady went to a special cancer center. They checked carefully and found some leftover cells. \n\nThe doctors did a surgery to take out the problem. The lady got better and did not need more medicine. After 18 months, she is doing well and feels good.",
+            "B2": "**What Happened to the Patient**\n\nA 42-year-old woman had breast implants placed for cosmetic reasons when she was 21 years old. Over the years, she developed a problem called a seroma, which is a buildup of fluid, on her left breast. She went back to her original surgeon several times. The surgeon replaced her implants twice and finally removed both implants after nearly 20 years. During the last surgery, a small piece of the tissue capsule (the scar tissue that forms around an implant) was taken for testing.\n\n**What the Tests Showed**\n\nThe tests on the capsule tissue found a rare type of cancer called Breast Implant-Associated Anaplastic Large Cell Lymphoma (BIA-ALCL). This cancer starts in the immune cells near the implant. The patient was sent to a special cancer center for more tests. These tests confirmed that the cancer was still present but only in the tissue around the implant, without spreading elsewhere.\n\n**How the Patient Was Treated**\n\nA team of doctors from different specialties worked together to plan her treatment. She had surgery to remove the entire capsule and any remaining fluid on the left side. No implants were left in her body. The surgery went well, and no additional treatments like chemotherapy or radiation were needed.\n\n**What This Means**\n\nThe patient recovered without problems and has been closely monitored for 18 months. So far, there are no signs that the cancer has come back. This case shows how important it is to check for BIA-ALCL when patients have persistent fluid buildup around breast implants. Early diagnosis and complete removal of the affected tissue can lead to a good outcome.",
+            "B3": "Background  \nThis report concerns a 42-year-old woman who underwent bilateral breast augmentation for cosmetic reasons at age 21. Over the following two decades, she experienced recurrent fluid accumulation (seroma) on the left breast. Initially, she consulted her original surgeon, who performed two implant replacement surgeries using textured implants but did not remove the surrounding scar tissue capsule (capsulectomy) during those procedures. Eventually, the patient underwent bilateral removal of breast implants approximately 11 months before presenting to a tertiary cancer center.\n\nKey Findings  \nDuring the last implant removal surgery, a tissue sample from the capsule surrounding the left breast implant was taken. Histopathological examination revealed Breast Implant-Associated Anaplastic Large Cell Lymphoma (BIA-ALCL), a rare type of lymphoma linked to textured breast implants. Further evaluation at the cancer center confirmed residual localized disease on the left side through imaging and cytopathology, including identification of atypical CD30-positive lymphoid cells characteristic of BIA-ALCL. No evidence of spread to lymph nodes or distant sites was found. The disease was staged as pT3pN0M0 (stage IC) according to the MD Anderson TNM system, indicating tumor infiltration confined to the capsule without nodal or distant metastasis.\n\nClinical Interpretation  \nThe diagnosis of BIA-ALCL was established after recurrent seroma prompted investigation. The absence of prior capsulectomy during implant exchanges likely contributed to disease persistence. Multidisciplinary evaluation involving plastic surgery, hematopathology, hematology, oncology, radiotherapy, surgical oncology, and breast radiology specialists guided management. The patient underwent a radical en bloc capsulectomy (complete removal of the capsule and surrounding tissue) on the left side, which yielded clear surgical margins and no evidence of disease beyond the capsule. Sentinel lymph node biopsy showed reactive changes related to silicone but no lymphoma involvement.\n\nNext Steps and Outcome  \nPostoperative recovery was uneventful, and given the localized nature of the lymphoma with complete surgical excision, no additional adjuvant therapy was recommended. The patient has been closely monitored with periodic PET/CT scans at 6, 12, and 18 months post-surgery, all showing no signs of local recurrence or distant disease. She remains disease-free beyond 18 months following surgery and continues regular follow-up evaluations to ensure ongoing remission."
+        }
+    },
+    {
+        "article": "Se trata de un paciente de 50 años que se presentó con una queja de dolor e hinchazón de la lengua de tres días de duración. Asociado a esto, tenía dolor al tragar, dificultad para abrir la boca, falta de aire y babeo. Asimismo, tenía fiebre alta y un tipo de dolor de cabeza global. Por lo demás, no tenía traumatismo en la lengua, ni procedimientos dentales u orales recientes, ni antecedentes de tabaquismo ni de enfermedad médica crónica como diabetes mellitus, enfermedad cardiaca e hipertensión. Históricamente, había tenido un dolor dental agudo en los últimos seis meses antes de su queja actual. Había masticado khat desde su niñez y tenía una mala higiene oral.\n\nEn el examen físico, se veía muy enfermo y sus signos vitales eran: presión arterial 115 por 70 mmHg, pulso 120 latidos por minuto, frecuencia respiratoria 20, temperatura 39 grados centígrados y saturación de oxígeno 92% de oxígeno. En el examen HEENT, había una hinchazón significativa de la lengua en el área anterolateral izquierdo, fluctuante a la palpación, y tenía un borde eritematoso. Hay múltiples caries en las áreas maxilares y mandibulares. No hubo hallazgos pertinentes en los sistemas restantes.\n\nTras obtener el consentimiento informado, el paciente fue trasladado al quirófano con el diagnóstico de absceso lingual. Posteriormente, se realizó la incisión y el drenaje bajo anestesia general, y se drenaron unos 30 ml de pus espeso. La bolsa se lavó con solución salina normal y peróxido de hidrógeno al 2 %. El paciente fue trasladado a la sala de cirugía con signos vitales estables y había tomado ceftriaxona 1 g por vía intravenosa dos veces al día y metronidazol 500 mg por vía intravenosa tres veces al día durante dos días. Fue dado de alta después de dos días de estancia en el hospital con mejoría y Augmentin 625 mg por vía oral tres veces al día durante cinco días.\n",
+        "gold_summary": "Se trata de un paciente de 50 años que se presentó con una queja de dolor e hinchazón de la lengua de tres días de duración. Asociado a esto, tenía dolor al tragar, dificultad para abrir la boca, falta de aire y babeo. Asimismo, tenía fiebre alta y un tipo de dolor de cabeza global. En el examen físico, había una hinchazón significativa de la lengua en el área anterolateral izquierda, fluctuante a la palpación, y tenía un borde eritematoso. Después de que se tomó el consentimiento informado, el paciente fue trasladado al quirófano con el diagnóstico de absceso de la lengua. Posteriormente, se hizo una incisión y drenaje bajo anestesia general, y se drenaron unos 30 ml de pus espeso. El bolsillo se lavó con solución salina normal y peróxido de hidrógeno al 2%. El paciente fue trasladado a la sala de cirugía con signos vitales estables y había estado tomando antibióticos. Fue dado de alta después de dos días de estancia en el hospital.\n",
+        "synthetic_summary": {
+            "B1": "A man had a big sore and swelling on his tongue. It hurt to swallow and open his mouth. He also had trouble breathing and drooled. He had a fever and a headache.\n\nThe doctor saw his tongue was very swollen and red. The man went to the hospital to get help. The doctor made a small cut to let out the bad stuff inside. They cleaned his tongue carefully.\n\nThe man took medicine to help him get better. After two days, he felt better and went home.",
+            "B2": "**What Happened to the Patient**\n\nA 50-year-old man came to the hospital because his tongue was painful and swollen for three days. He also had trouble swallowing, opening his mouth, and was drooling. He felt short of breath, had a high fever, and a headache all over his head.\n\n**What the Doctors Found**\n\nWhen the doctors examined him, they saw a big swelling on the left side of his tongue. The swelling felt soft and had a red edge. The man looked very sick and had a fast heartbeat and a fever.\n\n**What the Doctors Did**\n\nThe doctors decided he had a tongue abscess. An abscess is a pocket of pus, which is a thick fluid made of dead cells and bacteria. They took his permission and took him to surgery. While he was asleep under general anesthesia (which means he was fully unconscious), they made a small cut in his tongue to drain about 30 milliliters of thick pus. Then, they cleaned the area with saltwater and a mild hydrogen peroxide solution to kill germs.\n\n**After Treatment**\n\nAfter the surgery, the man was given strong antibiotics through an IV to fight the infection. His vital signs became stable, meaning his heart rate, breathing, and temperature improved. He stayed in the hospital for two days and then was sent home with more antibiotics to take by mouth. His condition got better after the treatment.",
+            "B3": "Background  \nA 50-year-old man presented with a three-day history of tongue pain and swelling. His symptoms also included difficulty swallowing (odynophagia), trouble opening his mouth (trismus), shortness of breath, excessive drooling, high fever, and a diffuse headache. He had no recent oral trauma, dental procedures, or chronic medical conditions such as diabetes, heart disease, or hypertension. However, he had experienced acute dental pain in the preceding six months and had a history of chewing khat since childhood, along with poor oral hygiene.\n\nKey Findings  \nOn physical examination, the patient appeared acutely ill. Vital signs showed a blood pressure of 115/70 mmHg, a rapid pulse of 120 beats per minute, a respiratory rate of 20 breaths per minute, a fever of 39°C, and oxygen saturation of 92%. Examination of the head, eyes, ears, nose, and throat (HEENT) revealed significant swelling on the anterolateral left side of the tongue. The area was fluctuant to touch, indicating fluid collection, and had a red (erythematous) border. Multiple dental caries were observed in both the upper (maxillary) and lower (mandibular) teeth. No other systemic abnormalities were noted.\n\nClinical Interpretation  \nThe presentation and examination findings were consistent with a lingual abscess, a localized collection of pus within the tongue tissue. Given the severity of symptoms and risk of airway compromise, prompt surgical intervention was necessary.\n\nNext Steps  \nAfter obtaining informed consent, the patient was taken to the operating room for incision and drainage under general anesthesia. Approximately 30 milliliters of thick pus were evacuated from the abscess cavity. The area was thoroughly irrigated with normal saline and 2% hydrogen peroxide to reduce bacterial load. Postoperatively, the patient was monitored in the surgical ward with stable vital signs. He received intravenous antibiotics—ceftriaxone 1 gram twice daily and metronidazole 500 milligrams three times daily—for two days. Following clinical improvement, he was discharged after a two-day hospital stay with a prescription for oral Augmentin (amoxicillin-clavulanate) 625 milligrams three times daily for five days to complete the antibiotic course."
+        }
+    },
+    {
+        "article": "Hombre de 73 años de edad de origen latinoamericano, con antecedente de madre con diagnóstico de demencia tipo Alzheimer con panel genético negativo; hermano con diagnóstico de ELA; hermana con diagnóstico de enfermedad de Parkinson. La sintomatología progresiva comenzó desde el año 2016 y se caracterizó por síntomas progresivos de hiposmia, hipoacusia, estreñimiento e insomnio, los cuales ameritaron valoración por otorrinolaringología y audiología, sin conclusión diagnóstica. En el año 2020 los familiares notaron que el paciente presentaba problemas en la memoria episódica, olvidos de objetos de la vida cotidiana, problemas de ganancias en su negocio (de comercio). Estos síntomas fueron progresivos hasta que el paciente empezó a tener limitación en las tareas diarias, como al manejar y al cambiar las velocidades, además de al salir de su casa. A finales de ese año el paciente comenzó a presentar debilidad muscular distal, manifestada al abrir botellas, cepillarse los dientes, lo cual progresó de forma insidiosa, no fluctuante, sin predominio de horario.\n\nEn enero de 2021 el paciente comenzó con alteraciones de la marcha, las cuales condicionaron caídas frecuentes hasta más de 6 veces a la semana, esto debido a inestabilidad postural. El paciente acudió a valoración en mayo. Se le hizo test de MoCA de 16 puntos con alteraciones en la fluidez del lenguaje y repetición de oraciones; en la abstracción, recuerdo diferido y problemas visuoespaciales y disejecutivos. El test de Luria dio positivo. El paciente presentó facie hipomímica, emitió con hipofonía, entrecortado y lento, y presentó reflejo nauseoso disminuido, rigidez generalizada de predominio izquierdo, hipotrofia generalizada, bradicinesia de predominio izquierdo, fuerza 4/5 generalizada, reflejos de estiramientos musculares 3/4, reflejos abdominocutáneos abolidos, signos de Hoffmann y Trömner presentes de forma bilateral, respuesta plantar extensora bilateral, fasciculaciones en extremidades inferiores evocadas al tacto, marcha con pasos cortos, congelamiento de la marcha al giro, pull test positivo (inestabilidad postural). Se manejó con levodopa carbidopa a una dosis gradual. Al seguimiento a los 3 meses el paciente había presentado nula mejoría en cuanto a los síntomas parkinsónicos, aumento de la debilidad muscular y persistieron los datos de motoneurona inferior y superior. Con estos hallazgos se realizó resonancia magnética (RM) del encéfalo. La velocidad de neuroconducción (VCN) presentó neuropatía axonal motora de miembros torácicos en relación con atrofia y neuroconducción sensitiva sin alteraciones. La electromiografía (EMG) presentó datos de denervación activa (aumento de actividad insercional, potenciales de fibrilación, fasciculación) y reinervación crónica (potenciales de acción de la unidad motora polifásicos, y bajo reclutamiento a la contracción máxima) en los 5 segmentos corporales, lo cual es compatible con enfermedad de motoneurona.\n\n\nLa EMG mostró un aumento de actividad insercional en músculos deltoides, bíceps, tríceps, extensor digital común bilateral y músculos linguales de forma bilateral. Se observaron abundantes potenciales de fibrilación y predominó la fasciculación en los músculos de los miembros torácicos. Durante la contracción, se observó una activación del potencial de acción de la unidad motora (PAUM) de forma polifásica y de gran amplitud. Y a máxima contracción se observó una disminución del reclutamiento en la mayoría de los músculos evaluados.\n\nEl paciente perdió seguimiento un año. Al vover a valoración se encontraba con postración en cama, afásico, aumento de los datos de parkinsonismo y síndrome de motoneurona. Se decidió realizar panel genético que resultó negativo para C9ORF72, así como para 143 genes más involucrados en enfermedades neuromusculares y neurodegenerativas, incluidos los genes VCP, MAT3, asociados a ELA, NOTCH3, asociado a demencia frontotemporal, sin alteraciones. Se reportó resultado de variante patogénica para el gen POLG: C.2209G>C, p.(Gly737Arg), relacionado con síndrome de depleción mitocondrial autosómico dominante y recesivo. Se realizó sesión de asesoramiento genético y el paciente fue informado. En mayo de 2022, el paciente presentaba disfagia y acudió en silla de ruedas, por lo que fue enviado a que se le practicara una gastrostomía.",
+        "gold_summary": "Presentamos un caso de origen latinoamericano que inicialmente se manifestó con síntomas sistémicos de más de 6 años de evolución, con posteriores alteraciones cognitivas. Después presentó alteraciones de la marcha y síntomas motores sugestivos de parkinsonismo con datos atípicos y datos de enfermedad de motoneurona. Se hicieron estudios de extensión que confirmaron hallazgos compatibles con afectación en motoneurona superior e inferior. Observamos mutación en gen POLG, relacionada con síndrome de depleción mitocondrial.",
+        "synthetic_summary": {
+            "B1": "There was a man who started feeling sick many years ago. He had trouble walking and moving his body. Doctors found that some parts inside his body were not working well. They also found a change in his body that can be passed from family. The doctors are helping him feel better.",
+            "B2": "**What Happened to the Patient**\n\nThis is the story of a 73-year-old man from Latin America who had health problems for over six years. At first, he had general symptoms like trouble smelling, hearing loss, constipation, and trouble sleeping. Later, he began having memory problems and difficulty with everyday tasks like driving and handling money. Over time, he also showed signs of muscle weakness and problems with walking, including frequent falls.\n\n**What the Doctors Found**\n\nDoctors noticed symptoms similar to Parkinson’s disease, such as slow movements, stiff muscles, and trouble with balance. However, some signs were unusual. Tests showed problems with both the upper and lower motor neurons. Motor neurons are nerve cells that control muscle movement. Problems in these neurons can cause muscle weakness and loss of coordination.\n\nFurther tests, including nerve and muscle studies, confirmed damage to these motor neurons. Genetic testing found a change (mutation) in a gene called POLG. This gene is important for how mitochondria work. Mitochondria are parts of cells that produce energy. The mutation is linked to a condition called mitochondrial depletion syndrome, which affects energy production in cells and can cause muscle and nerve problems.\n\n**What This Means**\n\nThis patient’s case shows how complex neurological diseases can be. His symptoms combined features of Parkinson’s disease and motor neuron disease, which is rare. The discovery of the POLG gene mutation helps explain his condition and may guide future care. Understanding such genetic causes is important for diagnosing and managing similar diseases.",
+            "B3": "Background  \nThis case involves a 73-year-old Latino man with a family history notable for neurodegenerative diseases, including Alzheimer’s dementia in his mother, amyotrophic lateral sclerosis (ALS) in his brother, and Parkinson’s disease in his sister. His symptoms began progressively in 2016 with systemic signs such as reduced sense of smell (hyposmia), hearing loss (hypoacusis), constipation, and insomnia. These early symptoms prompted evaluations by ear, nose, and throat specialists and audiologists but did not yield a definitive diagnosis. By 2020, the patient developed cognitive difficulties, including episodic memory loss and forgetfulness affecting daily life and business activities. Subsequently, he experienced increasing difficulty performing routine tasks such as driving and mobility outside his home. Toward the end of 2020, distal muscle weakness emerged, impairing fine motor skills like opening bottles and brushing teeth, progressing steadily without fluctuations.\n\nKey Findings  \nIn early 2021, the patient developed gait disturbances characterized by frequent falls due to postural instability. Cognitive testing using the Montreal Cognitive Assessment (MoCA) scored 16/30, revealing impairments in language fluency, sentence repetition, abstract thinking, delayed recall, visuospatial skills, and executive function. Neurological examination showed reduced facial expression (hypomimia), low and slow speech volume (hypophonia), diminished gag reflex, generalized rigidity predominantly on the left side, muscle wasting (hypotrophy), slowed movements (bradykinesia), mild generalized weakness (4/5 strength), hyperactive deep tendon reflexes, absent abdominal reflexes, bilateral positive Hoffmann and Trömner signs (indicative of upper motor neuron involvement), bilateral extensor plantar responses, and fasciculations (muscle twitches) in the lower limbs. His gait was marked by short steps, freezing during turns, and a positive pull test indicating postural instability.  \n\nElectrophysiological studies revealed motor axonal neuropathy in the upper limbs with preserved sensory conduction. Electromyography (EMG) demonstrated active denervation (increased insertional activity, fibrillation potentials, fasciculations) and chronic reinnervation (large, polyphasic motor unit potentials with reduced recruitment) across five body segments, consistent with combined upper and lower motor neuron disease. These findings supported a diagnosis of motor neuron disease, overlapping with atypical parkinsonism features.  \n\nClinical Interpretation  \nThe patient’s clinical presentation and diagnostic studies indicate a complex neurodegenerative syndrome involving both upper and lower motor neurons, alongside atypical parkinsonism and cognitive decline. The presence of combined motor neuron signs and parkinsonian features, along with progressive cognitive impairment, suggests an overlap of neurodegenerative processes rather than a classical isolated disorder. Genetic testing identified a pathogenic variant in the POLG gene (c.2209G>C, p.Gly737Arg), which is associated with mitochondrial DNA depletion syndromes inherited in autosomal dominant or recessive patterns. This mutation may contribute to the multisystem neurodegenerative phenotype observed. Notably, extensive genetic panels for other neuromuscular and neurodegenerative disorders, including C9ORF72 and genes linked to frontotemporal dementia and ALS, were negative.  \n\nNext Steps  \nThe patient’s condition progressed to severe disability, including aphasia (loss of speech) and wheelchair dependence, with worsening parkinsonism and motor neuron disease signs. Due to swallowing difficulties (dysphagia), a gastrostomy tube was placed to ensure adequate nutrition. Genetic counseling was provided to the patient and family to explain the implications of the POLG mutation. Ongoing multidisciplinary management focusing on symptom control, supportive care, and monitoring for complications is essential. Further research may clarify the role of POLG mutations in adult-onset neurodegenerative syndromes with overlapping motor neuron and parkinsonian features."
+        }
+    },
+    {
+        "article": "Mujer de 33 años, previamente sana, presentó disnea progresiva, fiebre alta, sudores nocturnos y pérdida de peso en diciembre de 2017. Después de un mes de evolución, fue ingresada en un hospital general con insuficiencia respiratoria aguda y shock séptico con infiltrados alveolares difusos, ictericia, hemoptisis y petequias en las extremidades inferiores. Fue intubada y necesitó soporte hemodinámico. Se detectó un soplo sistólico mitral a la ausculta del precordio. Había leucocitosis acentuada con desviación a la izquierda, plaquetopenia, disfunción hepática y renal asociada a proteinuria subnefrótica y consumo de complemento. El resultado de los anticuerpos antinucleares fue de 1/80, a pesar de los niveles normales de anti-DNA de doble cadena, anti-SM y anti-PR3. Después de la administración de ceftriaxona, mejoró clínicamente. Fiebre amarilla, dengue, chikungunya, leptospirosis, VIH y hepatitis virales fueron descartados. Las hemoculturas fueron positivas para Haemophilus spp. en las seis muestras recolectadas. El ecocardiograma transtorácico (ETT) demostró una masa ecogénica amorfa con superficie irregular y algunos elementos móviles que envolvían ambos folletos de la válvula mitral, midiendo 20x17 mm en el folleto anterior y 19 mm en su mayor diámetro en los folletos posteriores, resultando en regurgitación grave por flail mitral y perforación. La resonancia magnética mostró pequeños abscesos esplénicos, tratados de manera conservadora. Un aneurisma micótico no complicado de la arteria cerebral media izquierda fue tratado por embolización percutánea. Treinta días después de la hospitalización, se sometió a un reemplazo de la válvula mitral con éxito por una prótesis valvular biológica de tamaño 29 mm y después de una extensa resección del tumor. Se evidenció regurgitación aórtica moderada debido a lesión de la fibrosa intervalvar mitroaórtica y retracción de la cúspide no coronaria, tratada de manera conservadora. El examen patológico confirmó la presencia de un mixoma valvular mitral infectado. La paciente completó 28 días de ceftriaxona y gentamicina, recibiendo el alta hospitalaria asintomática. En el seguimiento de un año, no hubo evidencia de recurrencia y se constató solamente regurgitación aórtica leve. Los mixomas infectados presentan mayor riesgo de eventos embólicos, aunque las manifestaciones clínicas son indistinguibles de tumores no infectados.2 El presente caso parece ser el sexto de mixoma valvular mitral infectado relatado en la literatura, llenando criterios definitivos para el diagnóstico, y el tercero causado por un microorganismo del grupo HACEK.3 - 8 De los 64 mixomas valvulares mitrales publicados de 2006 a 2012, los síntomas eran cardiovasculares en 36,7%; 9,5 a 21,6% de los mixomas de la válvula mitral fueron sometidos al cambio de válvula y el tiempo del diagnóstico hasta la cirugía varió de algunas horas a 42 días.2 , 9 La mortalidad operatoria y general fue relatada como siendo, respectivamente, 2,6 a 3% y 5,1 a 21%.2 , 10 En la presente serie, la mayoría de los pacientes presentó insuficiencia cardiaca sintomática, fueron sometidos al cambio de válvula mitral y todos presentaron buenos resultados en el seguimiento.\n",
+        "gold_summary": "Una mujer de 33 años de edad, con antecedentes de fiebre y disnea de unos pocos días de evolución, fue hospitalizada con un síndrome lupoide, con hemocultivos positivos para Haemophilus spp. El ecocardiograma reveló una masa gigante que involucraba ambas valvas mitrales, con una severa regurgitación mitral que requería un reemplazo valvular mitral biológico. La microscopía reveló un mixoma infectado y la paciente fue dada de alta asintomática tras finalizar la terapia con antibióticos. Ella tuvo un buen seguimiento.\n",
+        "synthetic_summary": {
+            "B1": "A lady who was 33 years old felt very sick. She had fever and trouble breathing. Doctors found a big lump in her heart valve. The lump made her heart not work well. She had a new heart valve put in. The lump was not safe because it had germs. The lady took medicine to get better. After the medicine, she felt good and went home. She stayed healthy after that.",
+            "B2": "**What Happened to the Patient**  \nA 33-year-old woman who was previously healthy started having trouble breathing and a fever that lasted a few days. She went to the hospital and was found to have a condition that looked like lupus, an illness where the immune system attacks the body. Blood tests showed she had an infection caused by a type of bacteria called Haemophilus.\n\n**What the Doctors Found**  \nAn ultrasound of her heart (called an echocardiogram) showed a large, unusual growth on her mitral valve. The mitral valve is a part of the heart that helps control blood flow. This growth caused the valve to leak badly, which made her heart work harder. Because of this, she needed surgery to replace the damaged valve with a new, biological one.\n\n**What the Tests Showed**  \nWhen the doctors looked at the removed growth under a microscope, they found it was a mixoma. A mixoma is a rare, non-cancerous tumor made of heart tissue. In this case, the tumor was infected by bacteria.\n\n**How She Was Treated and What Happened Next**  \nAfter surgery, she received antibiotics to fight the infection. She recovered well and left the hospital without symptoms. Doctors followed her for a year and she stayed healthy with no signs of the tumor coming back.\n\n**Why This Case Is Important**  \nInfected mixomas on the mitral valve are very rare. This case helps doctors learn more about how to find and treat this unusual problem. Early diagnosis and surgery, along with antibiotics, can lead to a good outcome.",
+            "B3": "**Background**  \nA 33-year-old previously healthy woman developed progressive shortness of breath, high fever, night sweats, and weight loss over several weeks. She was admitted to the hospital with acute respiratory failure and septic shock. Clinical examination revealed a mitral systolic murmur, and laboratory tests showed marked white blood cell elevation, low platelets, liver and kidney dysfunction, proteinuria, and complement consumption. Blood cultures grew Haemophilus species, a member of the HACEK group of bacteria known to cause endocarditis. Infectious diseases such as yellow fever, dengue, chikungunya, leptospirosis, HIV, and viral hepatitis were excluded.\n\n**Key Findings**  \nA transthoracic echocardiogram identified a large, irregular, mobile mass involving both leaflets of the mitral valve, measuring approximately 20 mm in size, causing severe mitral regurgitation due to leaflet flail and perforation. Magnetic resonance imaging revealed small splenic abscesses and a mycotic (infectious) aneurysm in the left middle cerebral artery, which was treated by percutaneous embolization. Thirty days after admission, the patient underwent successful mitral valve replacement with a 29 mm biological prosthesis and extensive tumor resection. Moderate aortic regurgitation was noted due to involvement of the mitroaortic fibrous area but was managed conservatively.\n\n**Clinical Interpretation**  \nPathological examination confirmed the diagnosis of an infected mitral valve myxoma (a benign cardiac tumor). This case represents a rare instance of a mitral valve myxoma complicated by infection with Haemophilus spp., fulfilling definitive diagnostic criteria. Infected myxomas carry a higher risk of embolic events compared to non-infected tumors, although their clinical presentation is similar. The patient completed a 28-day course of ceftriaxone and gentamicin antibiotics and was discharged without symptoms. One-year follow-up showed no tumor recurrence and only mild residual aortic valve leakage.\n\n**Next Steps**  \nContinued clinical and echocardiographic monitoring is recommended to detect any recurrence or progression of valve dysfunction. Early surgical intervention combined with targeted antibiotic therapy is critical in managing infected cardiac myxomas to reduce morbidity and mortality. This case adds to the limited literature on infected mitral valve myxomas, particularly those caused by HACEK organisms, and highlights the importance of multidisciplinary care in complex infective endocarditis cases."
+        }
+    },
+    {
+        "article": "Mujer de 71 años, que fue atendida en urgencias del Hospital de Mataró (Barcelona, España) el 9 de septiembre de 2020 con debilidad progresiva, por lo que se decidió su ingreso en neurología. Como antecedentes patológicos destacaban hipertensión arterial, temblor esencial, artrosis y trastorno de ansiedad leve, en tratamiento con gabapentina, sertralina y tramadol. La paciente había consultado a su médico de cabecera el 1 de septiembre de 2020 por dolor abdominal, junto con diarrea leve que duró 24 horas. Al día siguiente comenzó a sentirse débil y, a lo largo de los días siguientes, apareció disnea y disfagia, por lo que se sospechó laringitis y se le recetó prednisona. El 8 de septiembre de 2020 fue visitada nuevamente por su médico de cabecera por empeoramiento global de la debilidad; presentaba, además, disartria, disfagia y ptosis bilateral, por lo que fue derivada a urgencias del hospital.\n\nA su llegada no presentaba fiebre, la presión arterial y la frecuencia cardíaca eran normales, y la exploración física era normal, a excepción de taquipnea moderada. El examen neurológico mostró ptosis palpebral bilateral, parálisis facial bilateral, midriasis bilateral arreactiva a la luz y a la acomodación, oftalmoparesia bilateral tanto para la suprainfraversión como para la mirada horizontal bilateral, tetraparesia moderada en las extremidades (3/5), y disfonía y disfagia graves. Ella estaba consciente y el contenido del lenguaje era normal, al igual que los reflejos miotáticos, la sensibilidad y la coordinación. Las maniobras de fatigabilidad no fueron concluyentes y se realizó la prueba del hielo, que resultó positiva, mejorando –transitoriamente– la ptosis.\n\nLa reacción en cadena de la polimerasa (PCR) para el SARS-CoV-2 fue repetidamente negativa (en su ambulatorio y en el hospital). La gasometría arterial mostró hipoxemia: 75, con SO2 al 95%, y el resto de las exploraciones realizadas en urgencias resultaron normales (radiografía de tórax, análisis de sangre de rutina, electrocardiograma).\n\nSe inició tratamiento de soporte con oxígeno, sueroterapia, nutrición por sonda nasogástrica y medidas encaminadas a la prevención de complicaciones. El cuadro se estabilizó el tercer día del ingreso en planta, sin requerir soporte ventilatorio avanzado, y comenzó una mejoría lenta a partir del octavo día, iniciando tolerancia a la dieta adaptada de disfagia. Durante la primera semana presentaba hipotensión arterial, que fue corrigiéndose con la sueroterapia. A partir de la segunda semana, pudo iniciar rehabilitación física, con buena evolución, por lo que fue trasladada a un centro específico de rehabilitación al 19.º día, y entonces fue capaz de deambular con ayuda bilateral. En la visita de control en consultas externas de neurología seis semanas después, la paciente estaba completamente recuperada.",
+        "gold_summary": "Describimos el caso confirmado de botulismo alimentario en una paciente atendida en nuestro hospital en septiembre de 2020. La instauración en pocos días de una afectación bilateral de pares craneales, incluyendo disfagia, disnea y disartria, junto con midriasis y tetraparesia graves, precedida de diarrea, constituyó la presentación clínica en el primer caso; mientras que en su familiar cursó con síntomas inespecíficos y transitorios. Constatamos disautonomía consistente en hipotensión arterial. Teniendo en cuenta la situación pandémica en aquel momento, se descartó repetidamente la infección por SARS-CoV-2 antes de plantear alternativas diagnósticas. La neurotoxina B de C. botulinum fue detectada en las heces de la paciente, confirmando el diagnóstico de botulismo, que relacionamos con la ingesta de una conserva casera de alubias. Se completó el diagnóstico diferencial del cuadro descartando otras posibles etiologías.",
+        "synthetic_summary": {
+            "B1": "A lady got very weak and had trouble talking and swallowing. She also had trouble breathing and her eyes were not working well. She had eaten some homemade beans before feeling sick.\n\nDoctors found a tiny bug made her sick. They gave her care and she got better slowly. Her family was checked too, but they felt only a little sick. The doctors made sure it was not a virus before finding the bug.",
+            "B2": "**What Happened to the Patient**  \nA 71-year-old woman came to the hospital with increasing weakness. Before this, she had stomach pain and mild diarrhea for one day. Soon after, she began having trouble breathing, swallowing, and speaking clearly. She also developed drooping eyelids and weakness in her arms and legs. These symptoms appeared quickly over a few days.\n\n**What the Doctors Found**  \nDoctors noticed she had problems with many nerves in her face and eyes. She had trouble moving her eyes, her pupils did not react to light, and she had weak muscles in all four limbs. She also had low blood pressure. Tests for COVID-19 were done several times and were all negative. Other tests like chest X-rays and blood work were normal.\n\n**How They Diagnosed Botulism**  \nThe doctors suspected botulism, a rare illness caused by a toxin from bacteria called *Clostridium botulinum*. This toxin can cause muscle weakness and nerve problems. They found the toxin in her stool (poop), confirming the diagnosis. The illness was linked to eating homemade canned beans.\n\n**Treatment and Outcome**  \nShe received supportive care, including oxygen and feeding through a tube. After a few days, her condition stopped getting worse and slowly improved. She started physical therapy and was able to walk with help after about three weeks. Six weeks later, she had fully recovered.\n\n**Why This Case Is Important**  \nThis case shows how botulism can cause serious nerve and muscle problems quickly. It also highlights the need to rule out other diseases, like COVID-19, before making the diagnosis. Eating homemade canned food can sometimes cause botulism if not prepared safely.",
+            "B3": "**Background**  \nIn September 2020, a 71-year-old woman was admitted to a hospital in Barcelona with rapidly progressing neurological symptoms. Her initial complaints included bilateral cranial nerve involvement manifesting as difficulty swallowing (dysphagia), breathing difficulty (dyspnea), and speech impairment (dysarthria), accompanied by severe pupil dilation unresponsive to light (bilateral mydriasis) and moderate weakness affecting all four limbs (tetraparesis). These symptoms developed shortly after a brief episode of diarrhea. Given the ongoing COVID-19 pandemic, repeated tests for SARS-CoV-2 infection were performed and consistently returned negative results.\n\n**Key Findings**  \n- Clinical presentation included bilateral cranial nerve palsies, severe dysphagia, dyspnea, dysarthria, bilateral mydriasis unresponsive to light and accommodation, and moderate tetraparesis.  \n- Autonomic dysfunction was evident, particularly hypotension (low blood pressure).  \n- Neurological examination showed preserved consciousness, normal language content, intact reflexes, sensation, and coordination. The ice pack test transiently improved eyelid drooping (ptosis), supporting a neuromuscular transmission disorder.  \n- Laboratory and imaging studies, including chest X-ray, routine blood tests, arterial blood gas analysis (which showed low oxygen levels), and electrocardiogram, were largely unremarkable aside from hypoxemia.  \n- Polymerase chain reaction (PCR) tests for SARS-CoV-2 were repeatedly negative.  \n- Detection of Clostridium botulinum neurotoxin type B in the patient’s stool confirmed the diagnosis of foodborne botulism.  \n- The source was identified as consumption of a homemade canned bean product.  \n- Differential diagnosis excluded other potential causes of the neurological syndrome.\n\n**Clinical Interpretation**  \nThis case represents a confirmed instance of foodborne botulism characterized by rapid onset of bilateral cranial nerve dysfunction and generalized muscle weakness following gastrointestinal symptoms. The presence of autonomic disturbances such as hypotension aligns with the known effects of botulinum neurotoxin on the autonomic nervous system. The negative SARS-CoV-2 tests were crucial to exclude COVID-19-related neurological complications during the pandemic. The positive ice pack test and the detection of botulinum toxin in stool samples provided definitive evidence supporting the diagnosis.\n\n**Next Steps**  \nThe patient received supportive care including oxygen therapy, intravenous fluids, and nutritional support via a nasogastric tube. She was monitored closely for respiratory compromise and autonomic instability. Over the course of hospitalization, her condition stabilized by day three without requiring advanced ventilatory support. Gradual neurological improvement began around day eight, allowing initiation of a dysphagia-adapted diet and physical rehabilitation by the second week. After 19 days, she was transferred to a specialized rehabilitation center and was able to walk with bilateral assistance. At a six-week follow-up, the patient had fully recovered. This case underscores the importance of early recognition and comprehensive management of botulism, as well as thorough exclusion of other diagnoses in similar clinical presentations."
+        }
+    },
+    {
+        "article": "Un hombre de 52 años presentó pérdida de agudeza visual en su ojo derecho (OD) dos días después de una inyección intravenosa no complicada de ranibizumab con una aguja de 30 G. Su historial médico incluía PE, miopía alta y vitrectomía pars plana en el OD debido a desprendimiento de retina. Recibía tratamiento mensual con ranibizumab debido a neovascularización coroidea secundaria a estrías angioides, con 78 inyecciones previas en el OD. En el momento de la presentación, su BCVA era de 6/18 y la presión intraocular (IOP) era de 3 mmHg. El examen con lámpara de hendidura del segmento anterior no mostró nada de particular. El examen de fondo de ojo y los escaneos OCT revelaron pliegues corio-retinianos posteriores. En conjunto, la baja presión intraocular y los hallazgos del fondo de ojo llevaron al diagnóstico de hipotensión maculopatía. Se prescribió dexametasona tópica y atropina para mejorar la función del cuerpo ciliar. La IOP se normalizó en tres días con recuperación de la agudeza visual y resolución de los pliegues corio-retinianos. Cuatro meses después, se realizó una nueva inyección intravenosa anti-VEGF en el cuadrante inferolateral y el paciente informó disminución de la agudeza visual en el día siguiente a la inyección. La BCVA era contar los dedos y la IOP era de 2 mmHg. Los pliegues corio-retinianos en el polo posterior estaban presentes, incluso más prominentemente esta vez. El examen con lámpara de hendidura reveló una herida abierta en la esclerótica en el sitio de la inyección. La herida se suturó con monofilamento 10-0 y se prescribió dexametasona tópica y atropina. El paciente se recuperó bien y presentó una BCVA de 6/12 y una IOP de 12 mmHg.\n",
+        "gold_summary": "Un hombre de 52 años se quejó de pérdida de visión en el ojo derecho (OD) dos días después de un IVI anti-VEGF sin complicaciones para el tratamiento de la neovascularización coroidea secundaria a estrías angioides. Su historial médico incluía PE, miopía patológica y una vitrectomía pars plana (PPV) previa debido a un desprendimiento de retina. La agudeza visual mejor corregida (BCVA) en el OD disminuyó de 6/12 a 6/18 después del IVI. La presión intraocular (IOP) era de 3 mmHg y se observaron pliegues corio-retinianos en el polo posterior. Se prescribió dexametasona tópica y atropina, y se observó una recuperación completa después de tres días. Cuatro meses después, el paciente desarrolló un nuevo episodio de pérdida de visión después de otro IVI. Su BCVA era contar los dedos, la IOP era de 2 mmHg, y se observaron pliegues corio-retinianos más evidentes. Esta vez, una herida escleral abierta en el sitio de inyección era evidente y fue necesaria una sutura escleral. Una vez más, el paciente se recuperó bien.\n",
+        "synthetic_summary": {
+            "B1": "A man had trouble seeing with his right eye. This happened two days after a special eye medicine was given. \n\nHis eye was hurt before and needed surgery. After the medicine, his eye pressure was very low. The doctor gave him eye drops to help. After three days, his eye got better.\n\nFour months later, the man had trouble seeing again after the same medicine. This time, the doctor found a small cut in his eye. The doctor fixed the cut with stitches. The man got better again.",
+            "B2": "**What Happened to the Patient**\n\nA 52-year-old man lost some vision in his right eye two days after getting a special medicine injection called anti-VEGF. This medicine helps treat new, unwanted blood vessels growing under the retina, which can cause vision problems. He had a history of serious eye issues, including very strong nearsightedness and surgery to fix a detached retina.\n\n**First Episode**\n\nAfter the first injection, his sharpness of vision dropped from 6/12 to 6/18 (this means he saw less clearly). The pressure inside his eye was very low (3 mmHg; normal is around 10-21 mmHg). Doctors found folds in the back part of his eye, called chorio-retinal folds. These folds happen when the eye pressure is too low, causing the layers in the eye to wrinkle. He was given eye drops with dexamethasone (a steroid to reduce inflammation) and atropine (to help the eye’s muscles). After three days, his eye pressure and vision returned to normal.\n\n**Second Episode**\n\nFour months later, after another injection, he lost even more vision—he could only count fingers. His eye pressure was even lower at 2 mmHg, and the folds in his eye were worse. This time, doctors found an open wound in the white part of his eye (the sclera) where the injection was given. They had to sew this wound closed with very fine stitches. After treatment with the same eye drops, he recovered well again, with vision improving to 6/12 and normal eye pressure.\n\n**What This Means**\n\nThis case shows that low eye pressure after injections can cause vision problems and changes inside the eye. Sometimes, the injection can cause a small wound that lets fluid leak out, lowering the pressure. Treating with medicine and fixing any wounds helps the eye heal and vision improve. It’s important for doctors to watch for these problems after injections to keep patients’ eyes healthy.",
+            "B3": "**Background**  \nA 52-year-old man with a history of preeclampsia (PE), high myopia (severe nearsightedness), and prior pars plana vitrectomy (PPV) in his right eye (OD) due to retinal detachment, was undergoing monthly intravitreal injections (IVI) of ranibizumab, an anti-vascular endothelial growth factor (anti-VEGF) therapy. This treatment was for choroidal neovascularization secondary to angioid streaks, and he had previously received 78 injections in the affected eye.\n\n**Key Findings – First Episode**  \nTwo days after an uncomplicated IVI, the patient experienced decreased visual acuity in the right eye. His best-corrected visual acuity (BCVA) dropped from 6/12 to 6/18. Intraocular pressure (IOP) was markedly low at 3 mmHg (normal range approximately 10–21 mmHg). Anterior segment examination with slit-lamp microscopy showed no abnormalities. Fundus examination and optical coherence tomography (OCT) scans revealed posterior chorioretinal folds—wrinkles in the layers of the retina and choroid. These findings, combined with the low IOP, led to a diagnosis of hypotony maculopathy, a condition where low eye pressure causes structural changes and visual impairment.\n\n**Clinical Management and Outcome – First Episode**  \nThe patient was treated with topical dexamethasone (a corticosteroid to reduce inflammation) and atropine (to relax the ciliary body and improve aqueous humor production). Within three days, his IOP normalized, visual acuity improved, and the chorioretinal folds resolved.\n\n**Key Findings – Second Episode**  \nFour months later, following another anti-VEGF IVI administered in the inferolateral quadrant of the eye, the patient again reported vision loss the day after injection. This time, BCVA had deteriorated severely to the ability to count fingers only, and IOP was even lower at 2 mmHg. Posterior chorioretinal folds were more prominent. Slit-lamp examination revealed an open scleral wound at the injection site, indicating a full-thickness scleral defect causing persistent hypotony.\n\n**Clinical Management and Outcome – Second Episode**  \nThe scleral wound was surgically repaired with a 10-0 monofilament suture. The patient was again treated with topical dexamethasone and atropine. Following this intervention, the patient’s IOP returned to normal levels (12 mmHg), and visual acuity improved to 6/12, indicating a good recovery.\n\n**Clinical Interpretation**  \nThis case illustrates hypotony maculopathy as a rare but significant complication following intravitreal anti-VEGF injections, particularly in eyes with prior vitrectomy and high myopia, which may predispose to scleral thinning and wound leakage. The initial hypotony was transient and resolved with medical therapy, but the second episode was due to an open scleral wound requiring surgical closure. Prompt recognition and treatment of hypotony maculopathy are essential to prevent permanent visual loss.\n\n**Next Steps and Recommendations**  \n- Careful monitoring of IOP and retinal morphology after intravitreal injections, especially in patients with risk factors such as prior vitrectomy and high myopia.  \n- Immediate evaluation for scleral wound integrity if hypotony and vision loss occur post-injection.  \n- Consideration of surgical repair for persistent scleral leaks to restore normal eye pressure and prevent maculopathy.  \n- Continued use of anti-inflammatory and cycloplegic agents to support ciliary body function and reduce inflammation during recovery."
+        }
+    },
+    {
+        "article": "Una mujer de 82 años acudió al servicio de urgencias por dolor abdominal, diarrea, confusión y deterioro de su estado general de varios días de evolución. Entre sus antecedentes médicos destacaban hipertensión arterial tratada e hipotiroidismo en tratamiento sustitutivo. No se recogieron antecedentes quirúrgicos ni hábitos tóxicos de interés. A la exploración física, la frecuencia cardíaca era de 84 lpm, tensión arterial de 105/82 mmHg, temperatura de 38 °C y saturación de oxígeno de 95% en aire ambiente. Las mucosas estaban secas y el abdomen era difusamente doloroso a la palpación sin masas palpables ni reacción peritoneal. La analítica realizada mostró una hemoglobina de 13.1 g/dL, proteína C reactiva a 122.9 mg/L sin leucocitosis (8.9 × 10^9/L), hiponatremia (130 mmol/L), hipopotasemia (2.9 mmol/L), pruebas de función renal, hepáticas, lipasa y enzimas cardiacas normales. El frotis para SARSCoV-2 fue negativo. La orina era maloliente con presencia de nitritos positivos, hematíes (+++) y leucocitos (+) por lo que se envió la muestra para cultivo microbiológico. Ante estos hallazgos se inició antibioticoterapia probabilista con ceftriaxona ante la sospecha de una posible infección urinaria y se decidió realizar una tomografía tóraco-abdomino-pélvica para descartar la presencia de un foco infeccioso profundo. Este examen reveló la presencia de signos de broncopatía crónica y una neumatosis vesical parietal a nivel abdominal compatible con una cistitis enfisematosa. El cultivo de orina reveló la presencia de Escherichia coli (> 100 000 UFC/m) sensible a la antibioticoterapia prescrita empíricamente y los hemocultivos fueron positivos al mismo germen. Se decidió el ingreso de la paciente en servicio de medicina interna y se continuó el tratamiento antibiótico durante 7 días con una evolución favorable desde el punto de vista clínico y analítico, permitiendo el alta hospitalaria.",
+        "gold_summary": "Una mujer de 82 años con antecedentes de hipertensión arterial e hipotiroidismo acudió al servicio de urgencias por dolor abdominal, diarrea, confusión y deterioro de su estado general de varios días de evolución. A su admisión, la paciente se encontraba febril y la analítica mostró una elevación de la proteína C reactiva sin leucocitosis (8.9 × 10^9/L). En ese contexto se realizó exudado nasofaríngeo para SARS-CoV-2 que fue negativo. Con estos resultados, la sospecha inicial era la de un cuadro infeccioso de origen digestivo. La muestra de orina era maloliente con presencia de leucocitos y nitritos enviándose a cultivo microbiológico. Se inició tratamiento antibiótico empírico con una cefalosporina de tercera generación ante la sospecha de une posible infección urinaria. Se decidió la realización de una tomografía tóraco-abdomino-pélvica con el objetivo de evaluar la presencia de otros focos infecciosos en una paciente de edad avanzada. Este estudio mostró una cistitis enfisematosa, una enfermedad poco frecuente en una paciente sin ninguno de los factores de riesgo clásicos para esta entidad. Los cultivos de orina y sangre fueron positivos para Escherichia coli sensible al antibiótico empírico por lo que se continuó para completar 7 días de tratamiento. La evolución clínica fue favorable.",
+        "synthetic_summary": {
+            "B1": "An old lady felt sick with tummy pain and diarrhea. She was confused and not feeling well for many days.\n\nThe doctor checked her and gave her medicine to fight germs. They did a special picture to see inside her tummy.\n\nThey found a small problem in her bladder. The medicine helped her get better after a week.",
+            "B2": "**What Happened to the Patient**  \nAn 82-year-old woman went to the emergency room because she had belly pain, diarrhea, confusion, and was feeling very weak for several days. She had a history of high blood pressure and low thyroid hormone levels, but no surgeries or harmful habits. When the doctors checked her, she had a fever and some signs of infection in her blood tests. They tested her for COVID-19, which was negative.\n\n**What the Doctors Found**  \nThe doctors noticed her urine smelled bad and had signs of infection, like white blood cells and chemicals called nitrites. They sent her urine for testing and started her on antibiotics right away, thinking she might have a urinary tract infection. To be sure, they did a CT scan, which is a special X-ray that looks inside the body. The scan showed she had a rare kind of bladder infection called emphysematous cystitis. This means there was gas in the bladder wall caused by bacteria.\n\n**What the Tests Showed**  \nThe urine and blood tests grew a bacteria called Escherichia coli, which is a common cause of infections. This bacteria was sensitive to the antibiotic she was already taking, so the doctors continued the treatment for seven days.\n\n**What It Means**  \nEven though this bladder infection is rare and usually happens in people with certain risk factors, this patient did not have those. Thanks to the quick diagnosis and treatment, she got better and was able to leave the hospital. This case shows how important it is to check carefully for infections in older patients who feel very sick.",
+            "B3": "Background  \nAn 82-year-old woman with a medical history of hypertension and hypothyroidism presented to the emergency department with several days of abdominal pain, diarrhea, confusion, and general deterioration. On admission, she was febrile, and laboratory tests revealed elevated C-reactive protein (CRP), an inflammatory marker, without an increase in white blood cell count (leukocytosis). A nasopharyngeal swab for SARS-CoV-2 was negative. Initial clinical suspicion focused on an infectious process of digestive origin.\n\nKey Findings  \nUrine analysis showed a foul odor, presence of leukocytes (white blood cells), and positive nitrites, suggesting a urinary tract infection. A urine sample was sent for microbiological culture. Empirical antibiotic treatment was started with a third-generation cephalosporin (ceftriaxone) due to the suspicion of urinary infection. Given the patient’s advanced age and clinical presentation, a thoraco-abdominopelvic computed tomography (CT) scan was performed to identify any deep infectious foci. The CT scan revealed emphysematous cystitis, a rare form of bladder infection characterized by gas within the bladder wall. This diagnosis was notable because the patient lacked the classical risk factors typically associated with this condition.\n\nClinical Interpretation  \nBoth urine and blood cultures grew Escherichia coli, a common bacterial pathogen, which was sensitive to the empirically prescribed antibiotic. This confirmed the diagnosis of a systemic urinary tract infection complicated by emphysematous cystitis. The absence of classical risk factors in this elderly patient highlights the importance of thorough imaging and microbiological evaluation in atypical presentations.\n\nNext Steps  \nThe patient was admitted to the internal medicine service and continued on the same antibiotic regimen to complete a seven-day course. Her clinical and laboratory parameters improved favorably, allowing for hospital discharge. This case underscores the need for prompt recognition and treatment of emphysematous cystitis, especially in elderly patients presenting with nonspecific symptoms and systemic infection signs."
+        }
+    },
+    {
+        "article": "Varón nacido a las 38 semanas de gestación y sin controles obstétricos prenatales, producto de un parto eutócico sin complicaciones con un peso de 2.678 g y Apgar 7 y 8 al minuto y a los cinco minutos de vida, respectivamente; derivado por sospecha de enterocolitis necrotizante a los siete días de vida. Al nacimiento, en su hospital de origen, se descartaron malformaciones congénitas externas y se colocó una sonda orogástrica para verificar la permeabilidad esofágica, obteniendo 200 mL de líquido amniótico. Posteriormente inició alimentación vía oral pero debido a succión débil y vómitos biliosos fue ingresado en la unidad de cuidados intensivos neonatales. A las 4 horas de vida se realizó radiografía abdominal observando una imagen de doble burbuja atípica, por lo cual realizaron un control radiológico 48 horas después identificando gas intestinal aparentemente distal, y presentó meconiorrexis a las 50 horas de vida. Dos días después reinició la alimentación oral, tras lo cual presentó nuevamente vómitos de aspecto biliar y distensión abdominal que mejoró con el ayuno y sonda orogástrica; por lo cual se sospechó enterocolitis necrotizante indicándose dieta absoluta, nutrición parenteral total y antibioterapia con ampicilina y amikacina. A los siete días de vida y debido a la persistencia de los síntomas pese al tratamiento instaurado, fue derivado a nuestro centro. A su llegada presentaba distensión abdominal, sin ruidos intestinales ni signos de irritación peritoneal, por lo que se realizó tránsito intestinal sin progresión distal y colon por enema con hallazgo de microcolon, todo ello sugestivo de atresia intestinal yeyunoileal. Tras la realización de los estudios de imagen y con la sospecha de atresia intestinal se realizó una laparotomía exploradora mediante abordaje supraumbilical transverso, observando adherencias hepatoileales, una hernia interna a través de un defecto mesentérico con incarceración de un asa yeyunal y atresia yeyunoileal tipo IV. Se identificaron dos sitios de atresia a 56 cm del ángulo de Treitz y a 36 cm de la válvula ileocecal, con un segmento interatrésico de 10 cm con meconio intraluminal y cambios de coloración con aspecto violáceo pero sin perforación; la diferencia de diámetros intestinales proximal a distal tenía una relación 3:1. Se decidió disecar el mesenterio y resecar el asa ciega (10 cm) para realizar una anastomosis término-oblicua yeyunoileal, corroborando la permeabilidad distal con sonda intraluminal y administración de solución fisiológica hasta que presentó evacuación rectal. El reporte de histopatología confirmó una atresia yeyunoileal tipo IV con enteritis crónica leve. El paciente evolucionó favorablemente y al 5º día postoperatorio inició alimentación oral con adecuada tolerancia progresiva y descenso paulatino de la nutrición parenteral total con retirada al 8º día postoperatorio. Al 6° día de la intervención presentó deposiciones espontáneas y a los 20 días de vida fue dado de alta sin complicaciones. Doce meses después el paciente continúa asintomático con adecuada ganancia ponderal y tolerancia a la alimentación complementaria con deposiciones diarias de características normales.",
+        "gold_summary": "Recién nacido de sexo masculino, nacido a término, derivado por vómitos, evacuaciones escasas y distensión abdominal. A los 8 días de vida y tras excluir diversas causas de distensión abdominal se sometió a laparotomía exploradora, identificando una hernia transmesentérica y dos sitios de atresia intestinal. Se realizó resección del segmento atrésico y anastomosis primaria, con buena evolución.",
+        "synthetic_summary": {
+            "B1": "A baby boy was born healthy. He had a tummy that was big and hard. He threw up and did not poop much.\n\nDoctors looked inside his tummy with surgery. They found a small hole and two blockages in his tummy tubes.\n\nThey fixed the blockages and closed the hole. The baby got better and is doing well now.",
+            "B2": "**What Happened:**  \nA baby boy was born at full term but started having problems like vomiting, fewer bowel movements, and a swollen belly. These symptoms made doctors worried about his intestines.\n\n**What the Doctors Did:**  \nWhen the baby was 8 days old, after checking for different causes of his belly swelling, the doctors performed surgery called a laparotomy. This means they opened his belly to look inside. They found a hernia, which is when part of the intestine pushes through a weak spot, and two places where the intestine was blocked or missing a part. This blockage is called intestinal atresia.\n\n**How They Fixed It:**  \nThe doctors removed the blocked parts of the intestine and connected the healthy ends together. This connection is called an anastomosis. After the surgery, the baby got better and recovered well.\n\n**What It Means:**  \nIntestinal atresia is a serious condition where parts of the intestine don’t form properly, causing blockages. Surgery is needed to fix it so food can pass through normally. This baby’s case shows that with timely surgery, babies with this condition can recover and grow healthy.",
+            "B3": "**Background:**  \nA full-term male newborn, delivered without prenatal obstetric care, initially presented with bilious vomiting, abdominal distension, and reduced bowel movements within the first week of life. Despite initial management for suspected necrotizing enterocolitis, symptoms persisted, prompting further evaluation.\n\n**Key Findings:**  \nAt eight days old, after excluding other causes of abdominal distension, imaging studies suggested intestinal obstruction characterized by a microcolon and absence of distal gas progression. During exploratory surgery (laparotomy), a transmesenteric hernia (an internal hernia through a defect in the intestinal mesentery) was discovered, along with two separate sites of jejunoileal atresia (complete blockage of the small intestine at two locations). The affected intestinal segments showed significant diameter discrepancy and localized inflammation but no perforation.\n\n**Clinical Interpretation:**  \nThe presence of multiple jejunoileal atresias (type IV) combined with an internal hernia explained the newborn’s symptoms of vomiting and abdominal distension. Surgical resection of the atretic (blocked) bowel segments and primary anastomosis (reconnection of healthy bowel ends) was performed to restore intestinal continuity. Histopathology confirmed mild chronic inflammation without additional pathology.\n\n**Next Steps and Outcome:**  \nPostoperatively, the infant demonstrated progressive tolerance to oral feeding, gradual discontinuation of parenteral nutrition, and normal bowel movements by the sixth day after surgery. The patient was discharged at 20 days of life without complications. Follow-up at twelve months showed normal growth, adequate nutritional intake, and regular bowel function, indicating a favorable long-term prognosis."
+        }
+    },
+    {
+        "article": "Se remitió a un hombre de 86 años para que se le implantara una válvula aórtica transfemoral.\n\nLa historia significativa incluyó el hecho de fumar 40 cajetillas al año (hasta fines de la década de 1980) y la fibrilación auricular paroxística que requería anticoagulación con Coumadin desde 1999, seguida poco después por la implantación de un marcapasos ventricular debido a bradicardia. Fue admitido por síncope en mayo de 2011 y se le diagnosticó una estenosis aórtica calcificada severa. Era eupneico y no mostraba signos de insuficiencia cardiaca o retención de líquidos. La ecocardiografía transtorácica reveló una estenosis aórtica severa (gradiente medio: 58 mmHg, área de la válvula aórtica: 0,4 cm2) con hipertrofia ventricular izquierda, fracción de eyección ventricular izquierda deteriorada (29%), acinesia inferior apical y obstrucción septal subvalvular (septum: 18 mm) con dilatación biauricular e hipertensión pulmonar con dilatación de la vena cava.\n\nLa angiografía coronaria mostró una estenosis del 75% de la arteria descendente anterior izquierda. El examen de eco-Doppler encontró vasos normales en el cuello. Se agregó aspirina 80 mg diariamente a su tratamiento; el paciente fue programado para un reemplazo de la válvula aórtica, pero no llegó hasta agosto, cuando fue readmitido en urgencias por disnea aguda y confusión. Había ganado 6 kg de peso, con edemas en las piernas y signos clínicos de derrame pleural. En ese momento, su SpO2 era del 92% y la proteína B-natriurética estaba elevada a 2336 pg·mL−1 (normal < 100 pg·mL−1).\n\nTras la terapia diurética y la eliminación de 850 ml de derrame pleural, se realizó una valvuloplastia de balón percutáneo aórtico de emergencia (Cristal Balloon, 23 mm) e inmediatamente después se le implantó un stent de metal desnudo (Biotronik-Pro-Kinetic 2.74 × 10.0) en la arteria descendente anterior izquierda. El gradiente medio transvalvular disminuyó de 59 a 38 mmHg. Se observaron algunas torsades de pointe el día 6 después de la intervención, que desaparecieron cuando la frecuencia más baja del marcapasos se aceleró a 80 latidos/min. Su estado mejoró drásticamente y se le dio el alta con furosemida, aldactazina y clopidogrel. Tras una revisión cuidadosa del expediente del paciente por parte del equipo cardiaco, se consideró que el riesgo de una cirugía valvular era demasiado alto (Euroscore logístico: 51%), y se propuso al paciente un implante de válvula aórtica transfemoral.\n\nLas notas de las enfermeras mencionan la hiperventilación nocturna y las crisis de ansiedad. El paciente era semiautónomo y vivía con su hija.\n\nLa implantación de la válvula aórtica transfemoral se programó para octubre de 2011. En el ingreso, 2 días antes del procedimiento, el paciente se describió como «ansioso e hiperventilante»; su peso era de 67 kg para una altura de 168 cm; el volumen espiratorio forzado en 1 s (FEV1) era de 1,1 L (50% del valor previsto) y la capacidad vital forzada de 1,7 L (55%); la presión arterial sistémica era de 120/60 mmHg; la concentración de hemoglobina era de 167 g·L−1; la creatinina era de 12,7 g·L−1; la tasa de filtración glomerular se calculó en 54 ml·min−1·m−2; el potasio era de 3,7 mEq·L−1; el sodio era de 141 mEq·L−1; el bicarbonato era de 22 mEq·L−1; y la proteína B natriurética era de 2.073 pg·mL−1. La ecografía describió un área de superficie de la válvula aórtica de 0,5 cm2 con un gradiente aórtico medio de 55 mmHg y acinesia inferoapical en el ventrículo izquierdo. La fracción de eyección se midió en 27% por el método Simpson biplano con regurgitación mitral moderada con dilatación biauricular y se estimó la presión pulmonar sistólica en >69 mmHg. La radiografía de tórax no mostró derrame pleural significativo. El paciente era totalmente dependiente del marcapasos.\n\nDos horas antes de la intervención, el paciente recibió 1 g de acetaminofeno por vía oral. Al llegar al quirófano, el paciente, plenamente consciente, presentaba respiración de Cheyne-Stokes periódica; cada ciclo duraba unos 85 s, con apneas de entre 15 y 20 s y grandes oscilaciones de la SpO2 entre el 88 % y el 99 %. Se le colocó dos catéteres intravenosos periféricos y uno arterial. El trazado arterial también mostraba oscilaciones de 85 s y una presión sistólica de 130 a 150 mmHg. Se le aplicó una máscara facial de oxígeno al 40 % con ventilación no invasiva; la SpO2 alcanzó un rango más estable (92 %-99 %). Diez minutos después, los análisis de gases en sangre mostraron un pH de 7,39, Pao2 de 108 mmHg, Paco2 de 40 mmHg, SaO2 del 97 %, y oscilaciones de lactato de 1,2 mEq·L−1. Se instaló una línea de muestreo capnógrafo dentro de la máscara facial para monitorizar la frecuencia respiratoria (Carescape Monitor B650, GE Healthcare, Helsinki, Finlandia). La monitorización también incluía un ECG de 12 derivaciones, oximetría de pulso, y oximetría cerebral regional (rSO2) mediante espectroscopia infrarroja cercana en el frente (INVOS, Somanetics). La capnografía reveló que las oscilaciones de la presión arterial eran sincrónicas con el ritmo de la respiración y que la presión disminuía durante los períodos apneicos e hipopneicos y aumentaba durante la hiperventilación; la rSO2 seguía el mismo patrón, a pesar de que la SpO2 del dedo permanecía a un nivel constante de 99 %. Se inició una infusión de propofol a una concentración objetivo de 0,2 µg·mL−1; se administraron 2,5 µg de sufentanilo antes de que los operadores infiltraran cada ingle con 200 mg de mepivacaína; el paciente se quedó dormido pero se mantuvo despierto al menor contacto con su cara o cuando su nombre se susurraba al oído; se administraron otros 2,5 µg de sufentanilo antes de la dilatación femoral de la arteria, un procedimiento requerido antes del reemplazo de la válvula. Los ciclos de ventilación se desaceleraron a un máximo de 120 s con 24 s de apneas centrales. Cuando la angiografía y los catéteres operativos estaban en su lugar en la aorta ascendente y se introdujo un marcapasos temporal en el ventrículo derecho, se indujo un ritmo rápido de 200 latidos/min para permitir una nueva dilatación de la válvula calcificada. Este procedimiento duró <25 s, durante el cual el paciente permaneció consciente y continuó respirando de la forma habitual, el ritmo se indujo justo después del final de un período apneico. Se preparó una válvula de 26 mm (SAPIEN, Edwards Lifesciences) y se introdujo en el orificio aórtico. Se dio una señal a los operadores una vez que la respiración se reanudó al final de un período apneico; se inició un ritmo ventricular rápido que llevó a la asistolia a una presión arterial media de 45 mmHg, y la válvula se expandió con balón y la angiografía confirmó la ausencia de fuga paravalvular. El balón se desinfló justo antes de que se detuviera el ritmo rápido, y el corazón volvió a latir a 80 latidos/min bajo la estimulación del marcapasos implantado. La secuencia completa se filmó; duró 31 s, durante los cuales el paciente siguió respirando regularmente (8 veces durante la detención circulatoria, es decir, una tasa de 16 veces por minuto) y no se despertó. Las expulsiones de sangre se reanudaron inmediatamente después de la deflación del balón, con una presión sistólica de 80 mmHg. Después de unas respiraciones profundas, la respiración se hizo regular; no se produjeron nuevos períodos apneicos ni oscilaciones de la presión arterial o rSO2. La hipertensión sistémica se desarrolló rápidamente, culminando después de 1 min a 190 mmHg y se controló con 40 mg de urapidil intravenoso durante los siguientes 15 min. La ecografía transtorácica midió el área valvular a 1,6 cm2 y el gradiente transvalvular máximo a 15 mmHg. La estimación de la presión arterial pulmonar mediante ecografía transtorácica mostró un gradiente sistólico de la presión ventricular derecha-aurícula derecha de 69 mmHg 1 día antes del procedimiento y 45 mmHg 2 días después. Un mes después, era de 28 mmHg. La evolución posterior no tuvo incidentes, y el paciente fue dado de alta 72 h después sin haber vuelto a la respiración periódica.\n\nMH - Edad 80 años y más\nMH - Cirugía de la válvula aórtica\nMH - *Estenosis/cirugía de la válvula aórtica\nMH - *Respiración de Cheyne-Stokes\nMH - Ecocardiografía\nMH - *Insuficiencia cardiaca\nMH - *Implantación de prótesis valvulares cardíacas\nMH - Hemodinámica\nMH - Humanos\nMH - Hombre\nMH - Resultado del tratamiento\n",
+        "gold_summary": "Se remitió a un hombre de 86 años para la implantación de una válvula aórtica transfemoral. La ecocardiografía transtorácica reveló una estenosis grave (gradiente medio: 58 mmHg, área de la válvula aórtica: 0,4 cm2), y después de una discusión multidisciplinaria, se consideró que el riesgo de la cirugía era demasiado alto (Euroscore logístico: 51%), y se propuso al paciente para la implantación de una válvula aórtica transfemoral (TAVI). Al llegar al quirófano, se observó que el paciente, completamente consciente, tenía respiración de Cheyne-Stokes (CSB), que persistió después de la administración de oxígeno al 40%. El procedimiento TAVI fue exitoso, y el patrón CSB se interrumpió en 8 s.\n",
+        "synthetic_summary": {
+            "B1": "There was an old man who needed a new heart valve. His heart valve was very tight and hard to open. Doctors said a big surgery was too risky for him. \n\nSo, they chose a smaller, safer way to put in a new valve. When he came to the hospital, he was awake but his breathing was uneven. \n\nThe doctors gave him some oxygen. Then, they put in the new valve carefully. After the new valve was in, his breathing got better very fast. The new valve helped him feel better.",
+            "B2": "**What They Found**  \nAn 86-year-old man needed a new aortic valve because his current valve was very narrow, a condition called severe aortic stenosis. This was shown by an ultrasound of his heart (called a transthoracic echocardiogram), which measured how tight the valve was and how much blood could flow through it. Because surgery was very risky for him, doctors decided to use a less invasive method called transfemoral aortic valve implantation (TAVI). This means they replaced the valve by threading a new valve through a blood vessel in his leg.\n\n**What Happened During the Procedure**  \nWhen the patient arrived in the operating room, he was fully awake but showed a special breathing pattern called Cheyne-Stokes breathing. This means his breathing went through cycles of fast breathing followed by pauses. Even after giving him oxygen, this breathing pattern continued. The doctors carefully performed the TAVI procedure while monitoring his breathing and heart closely.\n\n**What It Means**  \nThe TAVI procedure was successful. Interestingly, the abnormal breathing pattern stopped shortly after the valve was replaced. This shows that fixing the heart valve helped improve his breathing problems. The patient recovered well and was able to leave the hospital a few days later without the breathing issues returning. This case highlights how treating heart valve problems can also help with related breathing difficulties.",
+            "B3": "**Background**  \nAn 86-year-old man was referred for transfemoral aortic valve implantation due to severe calcific aortic stenosis. His medical history included heavy smoking, paroxysmal atrial fibrillation requiring long-term anticoagulation, ventricular pacemaker implantation for bradycardia, and prior diagnosis of severe aortic stenosis with left ventricular dysfunction. Echocardiography showed a critically narrowed aortic valve with a mean gradient of 58 mmHg and valve area of 0.4 cm², alongside left ventricular hypertrophy, reduced ejection fraction (29%), regional wall motion abnormalities, and pulmonary hypertension. Coronary angiography revealed a 75% stenosis in the left anterior descending artery. Due to high surgical risk (logistic EuroSCORE of 51%), the multidisciplinary heart team recommended transcatheter aortic valve implantation (TAVI) as a less invasive alternative.\n\n**Key Findings at Procedure Admission**  \nOn admission two days before the procedure, the patient exhibited anxiety and hyperventilation. Pulmonary function tests showed moderate obstruction (FEV1 50% predicted). Vital signs and laboratory tests indicated stable but compromised cardiac and renal function. Echocardiography confirmed severe aortic stenosis with an aortic valve area of 0.5 cm², a mean gradient of 55 mmHg, severely reduced left ventricular ejection fraction (27%), moderate mitral regurgitation, and elevated pulmonary artery pressures (>69 mmHg). The patient was fully dependent on his ventricular pacemaker.\n\nImmediately prior to the procedure, the patient was fully conscious but demonstrated Cheyne-Stokes breathing (CSB), characterized by periodic cycles of hyperventilation alternating with central apneas lasting 15–20 seconds, with large fluctuations in oxygen saturation (SpO2 ranging from 88% to 99%). Administration of 40% oxygen via a facial mask stabilized oxygen saturation but did not abolish the CSB pattern.\n\n**Clinical Interpretation**  \nCheyne-Stokes breathing is a form of central sleep apnea commonly associated with advanced heart failure and impaired cardiac output. It reflects instability in the respiratory control system and can lead to oscillations in blood oxygenation and cerebral oxygen delivery. In this patient, the presence of CSB indicated significant cardiopulmonary compromise but did not preclude proceeding with the TAVI procedure.\n\n**Procedure and Outcome**  \nThe TAVI procedure was performed under monitored anesthesia care with sedation using propofol and sufentanil, combined with local anesthesia. During valve deployment, rapid ventricular pacing was induced to facilitate balloon expansion of the calcified valve. Remarkably, the patient remained conscious and continued breathing regularly throughout the brief circulatory arrest period. Following valve implantation, echocardiography confirmed a significant improvement in valve area (1.6 cm²) and a reduction in transvalvular gradient (maximum 15 mmHg). Pulmonary artery pressures decreased progressively over the following days.\n\nImportantly, the Cheyne-Stokes breathing pattern ceased abruptly within seconds after valve implantation and did not recur during the postoperative period. The patient’s respiratory pattern normalized, and he was discharged three days later without further episodes of periodic breathing.\n\n**Next Steps and Clinical Significance**  \nThis case illustrates that TAVI can be successfully performed in elderly patients with severe aortic stenosis complicated by Cheyne-Stokes respiration and advanced heart failure. The resolution of CSB following valve replacement suggests that improving cardiac function and hemodynamics can stabilize respiratory control mechanisms. Continuous monitoring of respiratory patterns and cerebral oxygenation during TAVI may provide valuable insights into patient status and procedural safety. Postoperative follow-up should include assessment of cardiac function and respiratory stability to optimize long-term outcomes."
+        }
+    },
+    {
+        "article": "Una mujer árabe tunecina de 62 años, diagnosticada con la enfermedad de Von Hippel-Lindau en 2021, presentó varias manifestaciones relacionadas con la enfermedad. Tenía antecedentes de múltiples cirugías, principalmente por tumores renales, suprarrenales y pancreáticos, con hallazgos incidentales de masas ováricas.\n\nLa paciente no presentaba síntomas desde el punto de vista ginecológico, pero se quejaba principalmente de dolores de cabeza antes de someterse a una cirugía cerebral. No tenía antecedentes familiares o psicosociales significativos.\n\nSu historial quirúrgico incluye\n2021: Un tumor no operable (6 cm) del saco endolinfático del hueso petroso izquierdo, tratado con radioterapia.\n\n2021: Adrenalectomía izquierda por un feocromocitoma de 6 cm. El examen patológico reveló un feocromocitoma.\n\n2021: Nefrectomía izquierda por un tumor renal izquierdo roto. La microscopía mostró un carcinoma renal multifocal de células claras de grado nuclear 2.\n\n2022: Duodenopancreatectomía cefálica por una masa en el páncreas. El examen histológico confirmó tres cistadenomas serosos y dos tumores neuroendocrinos bien diferenciados.\n\nEn enero de 2021, durante la vigilancia posoperatoria con una tomografía computarizada (TC) abdominal-pélvica, se descubrió incidentalmente una masa anexial izquierda sólida de 4 cm, lo que levantó sospechas de malignidad. La masa se confirmó mediante ultrasonido transvaginal e IRM pélvica, clasificada como Sistema de Reporte y Datos Ováricos-Anexiales (O-RADS) 5 (alta sospecha de malignidad).\n\nExamen ginecológico e historial quirúrgico\nExamen físico: No se detectó masa abdominal-pélvica.\n\nExamen con espéculo: cuello uterino sano.\n\nSe observaron cicatrices quirúrgicas de una nefrectomía izquierda y una duodenopancreatectomía cefálica anteriores.\n\nUna reunión multidisciplinaria del personal concluyó que era necesaria la cirugía. Se realizó una laparotomía a través de una incisión en la línea media por debajo del ombligo, que reveló una masa quística sólida bien definida en el anexo izquierdo. No había ascitis ni signos de carcinomatosis peritoneal, y el anexo derecho parecía normal, sin signos macroscópicos de malignidad observados intraoperatoriamente, incluida la ausencia de vegetaciones exocísticas.\n\nSe realizó una citología junto con una anexectomía izquierda y la muestra se envió para un examen de sección congelada. Los resultados no fueron concluyentes, lo que planteó la posibilidad de tumores de margen o específicos del síndrome de Von Hippel-Lindau. Teniendo en cuenta el estado posmenopáusico de la paciente, se realizó una anexectomía derecha y una histerectomía total.\n\nEl examen histológico posterior reveló cistadenomas papilares de células claras bilaterales de las trompas de Falopio y el ligamento ancho, característicos de la enfermedad de Von Hippel-Lindau (0,5 cm en el lado derecho y 4 cm en el lado izquierdo). Los tumores consistían en papilas densamente compactadas con núcleos fibrosos, cubiertos por un epitelio monocapa.\n\nEl período postoperatorio inmediato transcurrió sin incidentes y, en el seguimiento de 1 mes, no se detectaron anomalías. Desde entonces, se ha hecho un seguimiento al paciente cada 4 meses con ecografías pélvicas normales. Durante estos 2 años de seguimiento, no han surgido complicaciones, pero el paciente fue readmitido recientemente en el departamento de neurocirugía por la recurrencia de un tumor cerebral.\n",
+        "gold_summary": "Una mujer blanca norteafricana de 62 años de edad, diagnosticada con la enfermedad de Von Hippel-Lindau en 2021, presentó múltiples manifestaciones, entre ellas, un tumor del hueso petroso izquierdo, feocromocitoma izquierdo, carcinoma de células renales izquierdo, riñón derecho con múltiples quistes y masas pancreáticas. Se sometió a varios tratamientos, entre ellos, radioterapia, adrenalectomía, nefrectomía y duodenopancreatectomía cefálica. Los exámenes de ultrasonografía y resonancia magnética revelaron una masa quística sólida en la región anexial izquierda. La laparoscopia identificó tumores quísticos en la mesosalpinx derecha e izquierda. Después de una histerectomía con anexectomía bilateral, el examen histológico reveló cistadenomas papilares de células claras bilaterales de la mesosalpinx y el ligamento ancho, compatibles con la enfermedad de Von Hippel-Lindau.\n",
+        "synthetic_summary": {
+            "B1": "A lady who is 62 years old had a sickness called Von Hippel-Lindau. This sickness made her have lumps in different parts of her body. She had many surgeries to help her feel better.\n\nDoctors found a lump near her tummy. They did a big surgery to take out some parts inside. The lumps were not harmful but needed to be checked.\n\nAfter the surgery, she got better and the doctors keep watching her to help her stay healthy.",
+            "B2": "**What Happened to the Patient**\n\nA 62-year-old woman from North Africa was diagnosed in 2021 with Von Hippel-Lindau disease. This is a rare genetic condition that causes tumors to grow in different parts of the body. She had several health problems related to this disease, including tumors in her brain bone, adrenal gland, left kidney, and pancreas. She had many treatments like radiation therapy and surgeries to remove some of these tumors.\n\n**What They Found in Her Pelvic Area**\n\nDuring check-ups, doctors found a solid cystic mass (a lump with both solid and fluid parts) near her left ovary using ultrasound and MRI scans. To learn more, they did surgery to look inside her abdomen. They found cystic tumors on both sides near her fallopian tubes and a ligament called the mesosalpinx, which supports the tubes.\n\n**What the Tests Showed**\n\nAfter removing her uterus and both ovaries and fallopian tubes, the lab examined the tissue. They found special tumors called clear cell papillary cystadenomas. These are a type of benign (non-cancerous) tumor made of clear cells arranged in finger-like shapes called papillae. These tumors are known to be linked to Von Hippel-Lindau disease.\n\n**What This Means**\n\nThe discovery of these tumors in her reproductive organs is part of how Von Hippel-Lindau disease can affect the body. The surgery went well, and follow-up tests showed no new problems in the pelvic area. However, she still needs regular check-ups because the disease can cause tumors to come back or appear in other places, like her brain.",
+            "B3": "Background  \nA 62-year-old North African woman was diagnosed with Von Hippel-Lindau (VHL) disease in 2021. VHL is a hereditary condition characterized by the development of multiple tumors and cysts in various organs. Since diagnosis, she has exhibited several manifestations of the disease affecting different anatomical sites.\n\nKey Findings  \nHer medical history includes:  \n- A 6 cm tumor in the left petrous bone (part of the temporal bone near the ear), treated with radiotherapy.  \n- A 6 cm left adrenal gland tumor identified as a pheochromocytoma (a rare tumor of adrenal gland tissue).  \n- A ruptured left kidney tumor, pathologically confirmed as multifocal clear cell renal cell carcinoma (a type of kidney cancer).  \n- Multiple pancreatic masses, including three serous cystadenomas (benign cystic tumors) and two well-differentiated neuroendocrine tumors, treated by a pancreaticoduodenectomy (surgical removal of the pancreas head and duodenum).\n\nDuring postoperative surveillance in January 2021, imaging studies—abdominal-pelvic computed tomography (CT), transvaginal ultrasound, and pelvic magnetic resonance imaging (MRI)—detected a 4 cm solid-cystic mass in the left adnexal region (area adjacent to the uterus, including the ovaries and fallopian tubes). This lesion was classified as O-RADS 5, indicating a high suspicion for malignancy.\n\nClinical Interpretation  \nPhysical and gynecological examinations revealed no palpable abdominal or pelvic masses, and the cervix appeared healthy. Surgical scars from previous kidney and pancreatic surgeries were noted. A multidisciplinary team recommended surgical intervention.\n\nDuring laparotomy (open abdominal surgery), a well-defined solid-cystic mass was found in the left adnexa. No ascites (fluid accumulation) or peritoneal carcinomatosis (widespread abdominal cancer) was observed. The right adnexa appeared normal macroscopically. Intraoperative frozen section analysis of the left adnexal mass was inconclusive, raising the possibility of tumors associated with VHL syndrome.\n\nGiven the patient’s postmenopausal status and the uncertain diagnosis, surgeons performed a total hysterectomy (removal of the uterus) and bilateral salpingo-oophorectomy (removal of both fallopian tubes and ovaries).\n\nHistopathological examination revealed bilateral clear cell papillary cystadenomas located in the fallopian tubes’ mesosalpinx (the tissue supporting the tubes) and the broad ligament (a peritoneal fold supporting the uterus and adnexa). These tumors consisted of densely packed papillae lined by a single layer of epithelial cells with clear cytoplasm, features characteristic of VHL-associated lesions.\n\nNext Steps  \nThe patient’s immediate postoperative course was uneventful. At one-month follow-up, no abnormalities were detected. She has since undergone regular pelvic ultrasound examinations every four months, all of which have remained normal over a two-year period. However, she was recently readmitted to neurosurgery for recurrence of a brain tumor, indicating ongoing disease activity in the central nervous system.\n\nSummary  \nThis case illustrates the multisystem involvement of Von Hippel-Lindau disease, including rare bilateral clear cell papillary cystadenomas of the fallopian tubes and broad ligament. Surgical management was guided by imaging, intraoperative findings, and histopathology, emphasizing the importance of multidisciplinary care and vigilant long-term surveillance in patients with VHL syndrome."
+        }
+    },
+    {
+        "article": "Una mujer embarazada de 31 años que había sido sometida a una cesárea fue derivada a la unidad de ultrasonido de nuestro departamento para un examen de ultrasonido morfológico de segundo trimestre. La paciente no tenía antecedentes familiares destacables y no había tomado medicamentos ni había estado expuesta a teratógenos durante el primer trimestre del embarazo. Los exámenes serológicos para diversas enfermedades infecciosas fueron negativos y un examen de ultrasonido previo a las 14 semanas fue normal. El triple examen para anomalías fetales también fue negativo a las 16 semanas.\n\nDurante la ecografía de la semana 20, se observó un feto masculino con una edad sonográfica compuesta de 20 semanas y 2 días que presentaba un edema significativo de las extremidades inferiores y líquido amniótico normal. Se recomendó un examen de seguimiento en 2 semanas, junto con pruebas de TORCH y pruebas de Coombs indirectas.\n\nSin embargo, se observó nuevamente edema subcutáneo en ambas extremidades inferiores durante la ecografía morfológica de la semana 23, lo que sugiere un posible diagnóstico de EM. Debido al linfedema persistente en las extremidades inferiores, se realizó una amniocentesis.\n\nLos exámenes posteriores revelaron que el cariotipo masculino era normal (46, XY), y el análisis molecular para el síndrome de Noonan fue negativo. Se realizó la secuenciación de nucleótidos del líquido amniótico con la secuenciación Illumina de 150 bases. Se aplicó el sistema de bioinformática (North-Oehler Aligarh, GATX) mientras se verificaba adicionalmente la existencia de deleciones/duplicaciones/CNV (Copy Number Variations) en el gen FLT4. El análisis identificó una mutación c.3116C>A p. (Ala1039Asp), que es una variante patogénica no conocida en el gen FLT4, lo que confirma el diagnóstico de linfedema hereditario tipo 1A – enfermedad de Milroy. El análisis de sangre materno confirmó la mutación materna y se realizó el asesoramiento genético.\n\nLa cesárea se realizó a las 38 semanas y 6 días de gestación y nació un neonato de sexo masculino que pesaba 3850 g y medía 46 cm con una puntuación de Apgar de 9/10. Después del parto se reconoció un edema en la extremidad inferior. El examen histopatológico de la placenta, el cordón umbilical y el saco amniótico no mostró signos de corioamnionitis u otra patología.\n",
+        "gold_summary": "Presentamos un informe de caso de una primera mutación descrita de un feto masculino diagnosticado prenatalmente con síndrome de Milroy a través de amniocentesis. El feto tenía edema bilateral de miembros inferiores, y las pruebas genéticas confirmaron el diagnóstico de síndrome de Milroy. La paciente fue monitoreada de cerca durante todo el embarazo, y después del parto, el lactante fue tratado con terapias apropiadas, incluyendo prendas de compresión y drenaje linfático manual. Los padres recibieron asesoramiento y apoyo apropiados.\n",
+        "synthetic_summary": {
+            "B1": "A baby boy had swelling in his legs before he was born. Doctors did special tests and found out why. The baby was watched carefully while still in the mommy's tummy. After he was born, the doctors helped him feel better with special care. The mommy and daddy got help and answers too.",
+            "B2": "**What They Found Before Birth**  \nDoctors studied a pregnant woman whose unborn baby showed swelling (called edema) in both lower legs during an ultrasound. To learn more, they took a small sample of the fluid around the baby (called amniocentesis) to test the baby’s genes. The tests found a new change, or mutation, in a gene called FLT4. This mutation caused a condition called Milroy syndrome, which is a type of inherited lymphedema. Lymphedema means that fluid builds up in the body because the lymphatic system, which helps drain fluid, does not work properly.\n\n**What This Means**  \nMilroy syndrome causes swelling, especially in the legs, starting before birth. Knowing this helped doctors watch the pregnancy carefully and prepare for the baby’s needs after birth. The baby was born healthy but with swelling in the legs.\n\n**After Birth Care and Support**  \nAfter the baby was born, doctors treated the swelling with special methods like compression garments (tight clothing that helps push fluid out) and manual lymphatic drainage (a gentle massage to move fluid). The parents also received genetic counseling, which means they got information and support about the condition and what it might mean for their family.\n\nThis case shows how genetic testing before birth can help diagnose rare conditions early. It also highlights the importance of careful care and support for both the baby and the family.",
+            "B3": "**Background**  \nThis case report describes a pregnant 31-year-old woman whose male fetus was diagnosed prenatally with Milroy disease, a hereditary form of primary lymphedema (chronic swelling caused by lymphatic system malformation). The pregnancy was otherwise unremarkable, with no family history of genetic disorders, no exposure to harmful substances during the first trimester, and normal early ultrasounds and serological tests. Initial screening for fetal anomalies was negative.\n\n**Key Findings**  \nAt 20 weeks and 2 days gestation, ultrasound revealed significant bilateral swelling (edema) of the fetus’s lower limbs, despite normal amniotic fluid levels. Follow-up ultrasound at 23 weeks confirmed persistent subcutaneous edema in both lower extremities. Given the ongoing lymphedema, amniocentesis was performed for genetic analysis. Standard chromosomal testing showed a normal male karyotype (46, XY), and molecular testing for Noonan syndrome was negative. Advanced genetic sequencing of amniotic fluid identified a previously undescribed pathogenic mutation (c.3116C>A p.(Ala1039Asp)) in the FLT4 gene, which encodes a receptor important for lymphatic development. This mutation confirmed the diagnosis of hereditary lymphedema type 1A, known as Milroy disease. Maternal blood testing revealed that the mother also carried the same mutation, prompting genetic counseling for the family.\n\n**Clinical Interpretation**  \nMilroy disease is a rare genetic disorder characterized by congenital lymphedema, typically affecting the lower limbs due to defective lymphatic vessel formation. The prenatal detection of limb edema combined with molecular confirmation of an FLT4 mutation allowed for early diagnosis and informed management. The absence of other fetal anomalies and normal placental pathology supported the isolated nature of this condition.\n\n**Next Steps and Outcome**  \nThe pregnancy was closely monitored, and delivery was by cesarean section at 38 weeks and 6 days gestation. The newborn male weighed 3850 grams, measured 46 cm, and had excellent Apgar scores (9/10), indicating good immediate health. Postnatally, the infant exhibited lower limb edema consistent with the prenatal findings. Appropriate therapeutic interventions, including compression garments and manual lymphatic drainage, were initiated to manage the lymphedema. The parents received comprehensive genetic counseling and support to understand the condition, its inheritance, and implications for future pregnancies.\n\nThis case highlights the value of detailed prenatal ultrasound combined with advanced genetic testing in diagnosing rare hereditary conditions like Milroy disease, enabling early intervention and family planning guidance."
+        }
+    },
+    {
+        "article": "Un paciente de 50 años con antecedentes médicos conocidos de diabetes mellitus (DM) e hipertensión (HTN), que se manejaba de manera irregular, se presentó en nuestro hospital en la ciudad de Sana’a, Yemen, el 25 de mayo de 2022, a las 5:30 p. m. El paciente fue derivado a otro hospital y manifestó un dolor abdominal agudo que había durado una semana antes del ingreso. El dolor se localizaba en la región epigástrica, de inicio repentino, empeoramiento progresivo y radiación hacia la espalda. Además, el paciente experimentó distensión abdominal generalizada, náuseas, vómitos y fatiga significativa. También se informó un historial de melena y vómitos relacionados con los alimentos durante el mes pasado. Dos días antes del ingreso, el paciente había recibido una transfusión de sangre de 2 unidades. No había antecedentes de cirugías previas ni antecedentes familiares de neoplasias.\n\nAl examinar al paciente, se constató que estaba consciente y alerta, pero que presentaba un aspecto pálido. La presión arterial era de 90/60 mmHg y el pulso de 120 latidos por minuto. Se observó distensión abdominal generalizada, particularmente prominente en la región supraumbilical con desplazamiento hacia abajo del ombligo. Se constató una leve sensibilidad en la zona epigástrica, junto con sonidos intestinales positivos, el examen rectal digital reveló un tono normal del esfínter anal y no se detectó ninguna masa palpable.\n\nLos exámenes hematológicos y bioquímicos revelaron anemia microcítica hipocrómica con un nivel de hemoglobina de 6 g/dL (rango normal: 12-15.5 g/dL), un recuento de glóbulos blancos de 16,000 (rango normal: 4-10,000), y un recuento de plaquetas de 303. El nivel de nitrógeno ureico en sangre fue de 7 mg/dL (rango normal: 10-20 mg/dL), la creatinina fue de 0.49 mg/dL (rango normal: 0.7-1.5% / dL), el índice internacional normalizado fue de 1.34 (rango normal: 0.62-1.3), el tiempo de protrombina (PT) fue de 16.9, el tiempo de tromboplastina parcial (PTT) fue de 30, el calcio fue de 8.0 mg/dL (rango normal: 8.5-10.1 mg / dL) y el ácido láctico fue de 1.9 mmol/L (rango normal: 0.5-2.2% / L). Los niveles de enzimas hepáticas y amilasa estuvieron dentro de los límites normales.\n\nSe realizaron estudios de diagnóstico por imágenes, que incluyeron una radiografía de tórax y una ecografía abdominal. La radiografía de tórax no reveló aire subdiafragmático, pero se observó una elevación en el diafragma izquierdo. La ecografía abdominal demostró la presencia de una acumulación de líquido intraabdominal. Posteriormente, se realizó una angiografía por TC abdominal, que reveló un hematoma de aproximadamente 14,3 × 8,8 cm en la región paraumbilical. En el interior del hematoma, se identificó un aneurisma arterial de 3,4 × 2,2 cm conectado a la arteria gastroduodenal, acompañado de cambios edematosos circundantes. Estos hallazgos sugieren la presencia de un aneurisma trombosado grande en la arteria gastroduodenal. Además, se observó la evisceración del diafragma izquierdo, que contiene el bazo y parte del estómago, junto con una acumulación de líquido intraperitoneal leve a moderada. No se detectó evidencia de un aneurisma aórtico.\n\nPara estabilizar al paciente, se inició la reanimación con 1000 ml de lactato de Ringer y se transfundieron tres unidades de sangre fresca. Se obtuvo el consentimiento informado para la intervención de alto riesgo y el paciente fue llevado inmediatamente al quirófano. Bajo anestesia general, en posición supina y con estricta adhesión a las técnicas asépticas, se realizó una incisión de laparotomía en la línea media. Cuando se abrió el peritoneo, se evacuó aproximadamente 2000 ml de sangre, revelando una masa pulsátil ocluida en el duodeno. Se logró una exposición adecuada utilizando un retractor auto-reforzado. La flexión del hígado y el colon transverso se movilizaron inferiormente desde la cabeza del páncreas y se eliminó la sangre coagulada del intestino delgado. Se realizó una disección meticulosa sobre el gran aneurisma ocluido pulsátil en la arteria gastroduodenal abriendo el ligamento gastrohepático. La movilización del píloro y el duodeno lejos de la cabeza del páncreas expuso una fístula que conectaba el duodeno y el aneurisma, sin contenido digestivo. Después de la heparinización, se realizó un pinzamiento proximal y distal de la arteria gastroduodenal. Posteriormente, se abrió el pseudoaneurisma y se evacuó una cantidad significativa de trombo. Se realizó una aneurismorrafía utilizando suturas de prolina 7.0. La perforación en la primera parte del duodeno se reparó en dos capas y se insertó una sonda nasogástrica más allá de la perforación. Se logró una irrigación exhaustiva con solución salina normal y una hemostasia meticulosa. Se colocó un drenaje abdominal y se cerró la incisión abdominal en capas. El paciente fue trasladado a la unidad de cuidados intensivos (UCI) para una estrecha monitorización y observación.\n\nDurante el período postoperatorio, el drenaje abdominal recolectó aproximadamente 100 ml de fluido seroso, que se eliminó el tercer día después de la operación. La recuperación de la paciente progresó sin complicaciones. Diez días después de la cirugía, la paciente fue dada de alta en condiciones favorables. Se programaron citas de seguimiento en el departamento ambulatorio y se mantuvo una comunicación regular por teléfono, con la condición de la paciente reportada como satisfactoria.\n",
+        "gold_summary": "Un hombre de 50 años se presentó con dolor abdominal agudo, anemia y signos de inestabilidad hemodinámica. Las imágenes de diagnóstico, incluida la CTA, revelaron un aneurisma de la arteria gastroduodenal grande y trombosado con evidencia de ruptura. El paciente se sometió a exploración y reparación quirúrgica abierta para abordar tanto el aneurisma como la perforación duodenal. La recuperación del paciente fue satisfactoria y fue dado de alta en condiciones estables.\n",
+        "synthetic_summary": {
+            "B1": "A man had a big tummy ache and felt very weak. Doctors found a big bump in a blood tube near his tummy. The bump was hurting him inside. \n\nThe doctors did a big operation to fix the bump and a hole in his tummy. After the operation, he got better and went home feeling okay.",
+            "B2": "**What Happened to the Patient**  \nA 50-year-old man came to the hospital with sudden, severe belly pain. He also had anemia, which means he had fewer red blood cells than normal, making him feel weak and tired. His blood pressure was low, and his heart was beating fast, showing signs that his body was under stress.\n\n**What the Doctors Found**  \nDoctors used special imaging tests, including a CT angiography (a scan that looks at blood vessels), and found a large bulge called an aneurysm in an artery near his stomach and small intestine. This aneurysm had a blood clot inside it and had started to leak or rupture, which is dangerous because it can cause internal bleeding.\n\n**What the Treatment Was**  \nThe patient had surgery to open his abdomen and fix the problem. During the operation, doctors removed the blood clot and repaired the damaged artery. They also fixed a hole in the first part of his small intestine (the duodenum) that was connected to the aneurysm. After surgery, he was closely monitored in the intensive care unit.\n\n**How the Patient Did Afterwards**  \nThe patient recovered well without any major problems. After about ten days, he was healthy enough to leave the hospital. Doctors planned follow-up visits to keep checking on him and make sure he stayed well.",
+            "B3": "Background  \nA 50-year-old man with a history of poorly controlled diabetes mellitus and hypertension presented with acute abdominal pain lasting one week. His symptoms included severe epigastric pain radiating to the back, generalized abdominal distension, nausea, vomiting, fatigue, and a recent history of gastrointestinal bleeding (melena and vomiting related to food). He was hemodynamically unstable on admission, showing low blood pressure and a rapid pulse, along with pallor indicating anemia.\n\nKey Findings  \nLaboratory tests revealed severe microcytic hypochromic anemia (hemoglobin 6 g/dL), elevated white blood cell count (16,000/µL), and normal liver enzymes and amylase. Imaging studies included chest X-ray, abdominal ultrasound, and abdominal CT angiography (CTA). The CTA identified a large (approximately 14.3 × 8.8 cm) hematoma near the umbilical region containing a 3.4 × 2.2 cm thrombosed aneurysm of the gastroduodenal artery. Surrounding tissue showed edema, and there was mild to moderate intraperitoneal fluid accumulation. The left diaphragm was herniated, containing the spleen and part of the stomach. No aortic aneurysm was detected.\n\nClinical Interpretation  \nThe patient was diagnosed with a large, thrombosed gastroduodenal artery aneurysm complicated by rupture and a duodenal perforation with an associated fistula between the aneurysm and the duodenum. These findings explained his abdominal pain, anemia from bleeding, and hemodynamic instability. The presence of the aneurysm and duodenal perforation represented a surgical emergency requiring prompt intervention.\n\nNext Steps  \nAfter initial stabilization with intravenous fluids and blood transfusions, the patient underwent emergency open laparotomy. Approximately 2000 mL of intra-abdominal blood was evacuated. Surgical exploration revealed the thrombosed aneurysm and a fistula connecting it to the first part of the duodenum. The aneurysm was carefully dissected, clamped proximally and distally, opened, and evacuated of thrombus. The aneurysm was repaired using prolene sutures (aneurismorrhaphy). The duodenal perforation was repaired in two layers, and a nasogastric tube was placed beyond the repair site. The abdomen was irrigated, hemostasis achieved, and a drain placed before closure. Postoperatively, the patient was monitored in the intensive care unit. His recovery was uneventful, with minimal serous drainage that resolved by day three. He was discharged in stable condition ten days after surgery and scheduled for outpatient follow-up, with ongoing communication confirming satisfactory recovery."
+        }
+    },
+    {
+        "article": "Una mujer de 60 años fue admitida en el departamento de nefrología con dolor epigástrico, hematemesis y edema en la pierna. La presión arterial era de 90/50 mmHg, dentro del rango normal para esta paciente.\nLos resultados de laboratorio fueron notables para las enzimas hepáticas alteradas con un patrón colestático: los niveles de alanina amino transferasa (ALT) y aspartato amino transferasa (AST) fueron ligeramente elevados a 28 U/L y 61 U/L, respectivamente, mientras que los niveles de fosfatasa alcalina (388 U/L) y gamma glutamiltransferasa (291 U/L) fueron muy elevados. Los niveles de albúmina en suero fueron de 24 g/L y el índice internacional normalizado fue normal a 1.02.\nOtros resultados de laboratorio, incluidos la bilirrubina total (0,32 mg/dL), la bilirrubina directa (0,26 mg/dL), el recuento total de plaquetas (176 000 plaquetas por microlitro) y el recuento de glóbulos blancos (8400 células por microlitro), se encontraban dentro de los valores normales.\nEl paciente tenía un extenso historial de enfermedades cardiacas y renales. A los 11 años, se le diagnosticó estenosis congénita de la válvula pulmonar, por lo que se le practicó una valvulotomía. Más adelante, desarrolló fibrilación auricular y aleteo auricular, que no toleró bien y para los que se intentó, sin éxito, la ablación del aleteo. Como el paciente seguía teniendo síntomas, se le practicó una ablación del nódulo auriculoventricular con colocación de un marcapasos.\nSe inició anticoagulación oral con fenprocoumon debido a una puntuación CHA2DS2-Vasc de 3 (mujer, insuficiencia cardiaca y enfermedad vascular periférica). A la edad de 55 años, se desarrolló una insuficiencia cardiaca derecha manifiesta y la paciente continuó luchando con ascitis y edemas periféricos que requerían múltiples ingresos hospitalarios. Además, también desarrolló un problema de efusiones pleurales transudativas recurrentes de etiología poco clara.\nLa ecocardiografía en ese momento mostró una severa regurgitación pulmonar y tricuspídea con un ventrículo derecho moderadamente dilatado y una aurícula derecha. El ventrículo izquierdo estaba ligeramente dilatado con una regurgitación mitral moderada. El cateterismo cardiaco derecho demostró presiones arteriales pulmonares de 74/30 mmHg con una presión venosa central de 28 mmHg. Se colocó un homotransplante pulmonar cuando el paciente tenía 57 años y se realizó una anuloplastia tricuspídea concomitante. A pesar de una presión venosa central más baja de 13 mmHg, el paciente seguía siendo readmitido varias veces por signos y síntomas de insuficiencia cardiaca derecha. La congestión venosa sistémica persistente finalmente dio lugar a una enfermedad renal en fase terminal para la que se inició una terapia de reemplazo renal a través de hemodiálisis intermitente. El caso se complicó por hemorragias gastrointestinales graves recurrentes, que requerían transfusiones de sangre frecuentes con hasta 60 unidades de glóbulos rojos por año. A pesar de esto, en combinación con la sustitución intravenosa de hierro, los niveles de hemoglobina variaron entre 5.3-8.8 g/dL. Debido a estos problemas de sangrado intratables, la anticoagulación oral con fenprocoumon se detuvo a la edad de 59 años.\nUna gastroscopia mostró una gastropatía erosiva con una mucosa difusa congestiva y friable. Como prevención de primera línea de las hemorragias gástricas recurrentes en el marco de la cirrosis, se inició el propranolol a una dosis de 5 mg por vía oral dos veces al día (el paciente no toleró una dosificación superior debido a la presión arterial baja). Además, se realizó una coagulación endoscópica de un angioma fúndico y un recorte de una lesión de Dieulafoy.\nSe creía que estas lesiones eran causadas por una gastropatía hipertensiva. Sin embargo, las hemorragias intractables persistieron.\nEl gradiente de presión venosa hepática se midió a 16 mmHg (27 mmHg-11 mmHg). Aunque hubo cierta reticencia debido al temor de empeorar la insuficiencia cardiaca derecha, se tomó la decisión de crear un TIPS. El procedimiento fue sin incidentes. Después de la colocación del TIPS, el gradiente de presión venosa hepática disminuyó a 4 mmHg (14 mmHg-10 mmHg). Por lo tanto, aunque el TIPS redujo considerablemente el gradiente venoso hepático, la presión portal se mantuvo alta debido a la elevada presión venosa central.\nDespués de la colocación del TIPS, el paciente desarrolló signos de encefalopatía hepática y se midieron niveles de amoniaco de 77 umol/L. Se inició el tratamiento con lactulosa oral y enemas, con poca mejora. En ese momento, se produjo otro episodio de sangrado gástrico.\nLa ecografía abdominal mostró buena permeabilidad del TIPS con flujo Doppler normal. Se detectó sangrado gástrico de una úlcera antral con endoscopia, a pesar de que la hiperemia gástrica disminuyó visualmente en comparación con la situación antes del TIPS. Se realizó una biopsia que mostró una mucosa foveolar edematosa, lo que sugiere isquemia de la mucosa. El sangrado fue demasiado difuso para una ligadura endoscópica adicional. No se encontró empeoramiento de la función hepática en los resultados de laboratorio, con el índice internacional normalizado 1.01 en este momento. La ecocardiografía no mostró cambios significativos en comparación con la situación antes de la colocación del TIPS. El ventrículo derecho permaneció moderadamente dilatado con una función longitudinal deficiente y una regurgitación tricuspídea severa persistente. Sin embargo, el estado general del paciente se deterioró y se desarrolló fiebre con consolidaciones pulmonares bilaterales.\nSe produjo una falla multiorgánica y, en ese momento, la familia del paciente decidió retirar el tratamiento. El paciente falleció finalmente 43 días después del procedimiento TIPS.\n\nMH - Resultado fatal\nMH - Mujer\nMH - Insuficiencia cardiaca/*complicaciones/fisiopatología\nMH - Encefalopatía hepática/etiología\nMH - Humanos\nMH - Hipertensión, Portal/etiología/fisiopatología/*cirugía\nMH - Cirrosis hepática/*complicaciones\nMH - Edad Media\nMH - Presión del portal\nMH - *Derivación portosistémica, intrahepática transyugular\nMH - Fracaso del tratamiento\n",
+        "gold_summary": "Una mujer de 60 años con antecedentes de estenosis congénita de la válvula pulmonar desarrolló insuficiencia cardíaca derecha, cirrosis hepática y enfermedad renal en fase terminal que requería terapia de reemplazo renal. La cirrosis hepática se complicó con hipertensión portal, lo que provocó hemorragias gastrointestinales intratables a pesar del tratamiento óptimo con betabloqueantes y la ligadura endoscópica de la banda. Debido al temor de que empeorara la insuficiencia cardíaca derecha, inicialmente se rechazó la colocación de una derivación intrahepática transyugular (TIPS). Sin embargo, como los problemas de hemorragia intratables persistieron y causaron grandes necesidades de transfusión, la TIPS se realizó finalmente como un procedimiento de rescate. Aunque la TIPS redujo con éxito el gradiente de presión venosa hepática de 16 mmHg a 4 mmHg, la presión portal se mantuvo alta a 14 mmHg debido a la persistencia de la insuficiencia cardíaca derecha con presión venosa central elevada. La encefalopatía hepática se desarrolló poco después de la colocación de la TIPS y culminó en una falla multiorgánica después de otro episodio de hemorragia gastrointestinal. En este punto, la familia del paciente decidió retirar la atención y el paciente falleció posteriormente.\n",
+        "synthetic_summary": {
+            "B1": "There was a lady who was 60 years old. She had a sick heart and sick liver. Her liver made her bleed in her tummy. The doctors tried many ways to stop the bleeding. \n\nThey put a special tube in her liver to help. The tube helped a little, but she still had problems. After that, she got very sick. Her family chose to stop the medicine. The lady passed away. \n\nThe doctors tried their best to help her feel better.",
+            "B2": "**What Happened to the Patient**\n\nA 60-year-old woman had a history of heart problems from birth, including a narrow pulmonary valve. Over time, she developed right-sided heart failure, liver scarring called cirrhosis, and severe kidney disease that needed dialysis (a treatment that cleans the blood when kidneys fail). Her liver disease caused high blood pressure in the veins of the liver, known as portal hypertension. This led to serious stomach and intestinal bleeding that was hard to stop, even with medicines called beta-blockers and special procedures to tie off bleeding vessels.\n\n**What Doctors Tried**\n\nAt first, doctors did not want to place a special tube called a TIPS (transjugular intrahepatic portosystemic shunt) because they worried it might make her heart failure worse. A TIPS is a small tunnel created inside the liver to reduce high pressure in the liver veins and help control bleeding. But because her bleeding kept happening and she needed many blood transfusions, they decided to do the TIPS as a last option.\n\n**What Happened After the TIPS**\n\nThe TIPS successfully lowered the pressure difference inside her liver veins from 16 mmHg to 4 mmHg. However, the overall pressure in her liver’s blood vessels stayed high at 14 mmHg because her heart failure was still causing high pressure in the veins near the heart. Soon after the TIPS, she developed a brain condition called hepatic encephalopathy, which happens when the liver cannot remove toxins properly, affecting brain function.\n\n**Final Outcome**\n\nAfter another episode of stomach bleeding, her condition worsened, leading to failure of multiple organs. At this point, her family chose to stop medical treatments, and she passed away 43 days after the TIPS procedure.\n\n**Summary**\n\nThis case shows how complex it can be to treat liver and heart problems when they happen together. Even though the TIPS helped reduce liver vein pressure, the ongoing heart failure made it hard to control the disease. Unfortunately, the patient’s condition became too severe to recover.",
+            "B3": "**Background**  \nA 60-year-old woman with a history of congenital pulmonary valve stenosis developed progressive right-sided heart failure, liver cirrhosis, and end-stage renal disease requiring intermittent hemodialysis. Her cardiac history included multiple interventions, such as pulmonary valve valvulotomy in childhood, atrial arrhythmias managed unsuccessfully with ablation, atrioventricular node ablation with pacemaker implantation, and later pulmonary and tricuspid valve regurgitation leading to right ventricular dilation. Despite a pulmonary homograft and tricuspid annuloplasty, she experienced persistent systemic venous congestion contributing to her liver and kidney disease.\n\n**Key Findings**  \nThe patient’s liver cirrhosis was complicated by portal hypertension, evidenced by a hepatic venous pressure gradient of 16 mmHg (normal <5 mmHg), which led to recurrent and severe gastrointestinal bleeding. Endoscopic evaluation revealed gastropathy with congestive mucosal changes and vascular lesions such as a Dieulafoy lesion and a fundic angioma, treated with coagulation and band ligation. Despite optimal medical therapy including beta-blockers (propranolol) and endoscopic interventions, bleeding persisted, causing severe anemia and frequent blood transfusions (up to 60 units of red blood cells per year). Anticoagulation was discontinued due to bleeding risks.\n\nBecause of concerns that transjugular intrahepatic portosystemic shunt (TIPS) placement might worsen her right heart failure, the procedure was initially deferred. However, ongoing intractable bleeding necessitated TIPS as a salvage therapy. Post-TIPS, the hepatic venous pressure gradient decreased substantially from 16 mmHg to 4 mmHg, indicating effective decompression of portal hypertension. Nevertheless, portal pressure remained elevated at 14 mmHg due to persistently high central venous pressure from right heart failure.\n\nFollowing TIPS placement, the patient developed hepatic encephalopathy, confirmed by elevated blood ammonia levels (77 µmol/L), which responded poorly to standard treatments such as lactulose. Another episode of gastric bleeding occurred despite reduced mucosal hyperemia. Biopsy of the gastric mucosa showed foveolar edema suggestive of ischemia. Liver function tests remained stable, and echocardiography showed no significant changes in cardiac status, with persistent right ventricular dilation and severe tricuspid regurgitation.\n\n**Clinical Interpretation**  \nThis case illustrates the complex interplay between advanced right heart failure and secondary liver cirrhosis with portal hypertension. The elevated central venous pressure from right heart failure contributed to persistent portal hypertension and congestive gastropathy, complicating management of gastrointestinal bleeding. Although TIPS effectively reduced the hepatic venous pressure gradient, it did not normalize portal pressures due to ongoing cardiac dysfunction. The development of hepatic encephalopathy after TIPS reflects the known risk of shunting portal blood away from hepatic metabolism. Ultimately, the patient’s condition deteriorated with multiorgan failure, including recurrent bleeding and pulmonary complications.\n\n**Next Steps and Outcome**  \nGiven the refractory nature of her bleeding and progressive organ failure, the patient’s family elected to withdraw life-sustaining treatments. The patient died 43 days after TIPS placement. This case underscores the challenges in managing portal hypertension and bleeding in patients with concomitant severe right heart failure, highlighting the need for careful multidisciplinary evaluation when considering invasive procedures like TIPS in this population."
+        }
+    },
+    {
+        "article": "Una mujer tailandesa de 62 años presentó pérdida visual bilateral súbita y cefalea durante 5 días. Negó antecedentes de traumatismo craneal. Su historia clínica era significativa por presentar hipertensión mal controlada.\n\nLos signos vitales fueron normales, excepto por la presión arterial de 200/105 mmHg. La agudeza visual fue de no percepción de luz (NLP) con pupilas fijas en ambos ojos. La motilidad ocular de ambos ojos fue limitada en todas las direcciones. Ambas párpados fueron difíciles de abrir. Las medidas del exoftalmómetro de Hertel fueron de 16 mm en el ojo derecho y 14 mm en el ojo izquierdo. Había quemosis significativa y vasos de sacacorchos episclerales en ambos ojos. Ambas córneas mostraron un edema estromal leve y difuso sin infiltración. Las cámaras anteriores fueron profundas y tranquilas en ambos ojos. Las presiones intraoculares fueron de 45 mmHg y 48 mmHg en los ojos derecho e izquierdo, respectivamente. La gonioscopia reveló sangre en el canal de Schlemm en el ángulo nasal del ojo derecho. El examen del fondo de ojo mostró venas de la retina ligeramente dilatadas y tortuosas con discos ópticos de apariencia normal en ambos ojos. La relación taza-disco fue de 0.3 bilateralmente. La tomografía de coherencia óptica demostró un espesor normal de la mácula en cada ojo. No hubo ruido audible. Otros exámenes neurológicos fueron normales.\n\nLa resonancia magnética (MRI) con gadolinio del cerebro y las órbitas demostró la dilatación de las venas oftálmicas superiores bilaterales (SOVs) y un grado marcado de congestión orbital y periorbital bilateralmente. Sin embargo, no se observó ni compresión ni estiramiento de los nervios ópticos bilaterales. Es interesante destacar que la restricción de la difusión, con la correspondiente reducción del coeficiente de difusión aparente (ADC), en todo el segmento orbital de los nervios ópticos bilateralmente se reveló en la resonancia magnética ponderada en difusión (DWI). Esto es consistente con el PION bilateral. La angiografía por resonancia magnética (MRA) del cerebro y las órbitas reveló arterialización de los senos cavernosos bilaterales y de las SOVs.\n\nLa angiografía cerebral confirmó el diagnóstico de CCF durales bilaterales de drenaje anterior. La CCF dural derecha se alimentaba de las ramas durales de la ICA (tronco meningo-hipofisario derecho). La CCF dural izquierda se alimentaba de las ramas durales de la ECA (arteria meningo-hipofisaria izquierda y la arteria izquierda del foramen redondo y las ramas durales de la ICA (tronco meningo-hipofisario izquierdo). Cada lado de la CCF dural contribuía con flujo sanguíneo arterial a los SOV bilaterales (SOV contralateral a través de la comunicación inter-cavernosa). No se observó reflujo venoso cortical del flujo sanguíneo arterial. Basándose en estos hallazgos, se realizó una embolización transvenosa de la bobina. Los senos cavernosos bilaterales se embolizaron utilizando bobinas para ocluir los vasos de alimentación de las ramas durales de la ICA y la ECA. La angiografía cerebral inmediata posterior a la embolización mostró el cierre completo de las fístulas.\n\nTres meses después de la embolización, el examen oftálmico demostró una mejora progresiva de los signos oftálmicos antes mencionados; no obstante, la agudeza visual del paciente se mantuvo en NLP en ambos ojos.\n",
+        "gold_summary": "Reportamos el caso de una mujer de 62 años de edad con antecedentes de hipertensión arterial mal controlada que presentó pérdida visual bilateral súbita y cefalea durante 5 días. Negó antecedentes de traumatismo craneal. En el examen, sus agudezas visuales eran de no percepción de luz (NLP) con pupilas fijas en ambos ojos. La motilidad ocular de ambos ojos era limitada en todas las direcciones. Era difícil abrir ambos párpados. El examen del segmento anterior reveló quemosis bilateral y vasos del sacacorchos episclerales. La presión intraocular era de 45 y 48 mmHg en los ojos derecho e izquierdo, respectivamente. La gonioscopia reveló sangre en el canal de Schlemm en el ángulo nasal del ojo derecho. El examen del fondo de ojo mostró venas retinianas ligeramente dilatadas y tortuosas con discos ópticos de apariencia normal en ambos ojos. Las relaciones entre la copa y el disco eran de 0,3 bilateralmente. Otros exámenes neurológicos no presentaron anormalidades. La resonancia magnética demostró dilatación de las venas oftálmicas superiores bilaterales (SOV) y congestión orbital y periorbital bilateral marcada. Sin embargo, no hubo compresión o estiramiento de los nervios ópticos bilaterales. Se reveló una restricción de la difusión en la difusión ponderada por la difusión, con la correspondiente reducción del coeficiente de difusión aparente, en todo el segmento orbital bilateral de los nervios ópticos, consistente con PION bilateral. La angiografía por resonancia magnética reveló arterialización de los senos cavernosos bilaterales y las SOV. La angiografía cerebral confirmó el diagnóstico de CCF bilaterales de drenaje anterior. El tratamiento con embolización de bobina transvenosa fue exitoso. Tres meses después de la embolización, el examen oftálmico demostró una mejora progresiva de los signos oftálmicos antes mencionados; sin embargo, sus agudezas visuales permanecieron como NLP en ambos ojos.\n",
+        "synthetic_summary": {
+            "B1": "A lady had a big headache and could not see with her eyes. Her eyes were very hard to open. The doctor saw her eyes were swollen and red. Her eye pressure was very high.\n\nThe doctor took pictures of her brain and eyes. They saw some big, swollen veins. The nerves in her eyes were hurt. The doctor fixed the problem with a special treatment.\n\nAfter three months, her eyes looked better, but she still could not see. The doctor will keep helping her.",
+            "B2": "**What Happened to the Patient**\n\nA 62-year-old woman from Thailand suddenly lost vision in both eyes and had a headache for five days. She did not have any recent head injuries but had high blood pressure that was not well controlled.\n\n**What the Doctors Found**\n\nWhen the doctors examined her, she could not see any light in either eye. Her pupils did not react to light, and she had trouble moving her eyes in any direction. It was also hard to open her eyelids. The front parts of her eyes showed swelling and unusual blood vessels. The pressure inside her eyes was very high—much higher than normal. A special eye test showed blood in a drainage channel of one eye. The back of her eyes looked mostly normal except for some swollen veins.\n\nBrain scans (MRI) showed that the veins near her eyes were swollen and there was swelling around the eye sockets. The nerves that carry vision from the eyes to the brain did not look squished or stretched. However, another MRI test showed signs of damage to these nerves caused by low blood flow, called posterior ischemic optic neuropathy (PION), affecting both eyes. Additional imaging showed abnormal blood flow in certain brain veins called the cavernous sinuses and the veins near the eyes.\n\n**What Was Causing the Problem**\n\nFurther tests confirmed she had two abnormal connections between arteries and veins near her brain, called bilateral dural carotid-cavernous fistulas (CCFs). These connections caused blood to flow the wrong way, leading to the swelling and high eye pressure.\n\n**How They Treated It**\n\nDoctors treated her by blocking these abnormal blood vessels using tiny coils inserted through the veins. This procedure successfully closed the abnormal connections.\n\n**What Happened After Treatment**\n\nThree months later, many of the eye swelling signs improved. Unfortunately, her vision did not get better and she remained unable to see light in both eyes.\n\n**Summary**\n\nThis case shows how abnormal blood vessel connections near the brain can cause sudden vision loss and eye swelling. Even with successful treatment to fix the blood flow, damage to the optic nerves can cause permanent vision loss. Controlling high blood pressure and early diagnosis are important to prevent serious problems like this.",
+            "B3": "**Background**  \nA 62-year-old Thai woman with a history of poorly controlled hypertension experienced sudden, bilateral vision loss and headache lasting five days. She denied any history of head trauma. Her vital signs were normal except for severe hypertension, with a blood pressure of 200/105 mmHg.\n\n**Key Findings**  \n- **Ocular Examination:**  \n  - Visual acuity was no light perception (NLP) in both eyes, with fixed pupils.  \n  - Eye movement was limited in all directions bilaterally.  \n  - Both eyelids were difficult to open.  \n  - Significant conjunctival swelling (chemosis) and twisted episcleral vessels (described as “corkscrew” vessels) were present in both eyes.  \n  - Mild, diffuse corneal stromal edema was noted without infiltration.  \n  - Anterior chambers of both eyes were deep and quiet.  \n  - Intraocular pressures were markedly elevated at 45 mmHg (right eye) and 48 mmHg (left eye).  \n  - Gonioscopy revealed blood in the Schlemm’s canal at the nasal angle of the right eye.  \n  - Fundus examination showed slightly dilated and tortuous retinal veins with normal-appearing optic discs and a cup-to-disc ratio of 0.3 bilaterally.  \n  - Optical coherence tomography (OCT) showed normal macular thickness in both eyes.  \n  - Neurological examination was otherwise normal.\n\n- **Imaging Studies:**  \n  - Magnetic resonance imaging (MRI) with gadolinium contrast demonstrated bilateral dilation of the superior ophthalmic veins (SOVs) and marked orbital and periorbital congestion on both sides. There was no evidence of compression or stretching of the optic nerves.  \n  - Diffusion-weighted imaging (DWI) MRI revealed restricted diffusion along the entire orbital segment of both optic nerves, with a corresponding decrease in the apparent diffusion coefficient (ADC), consistent with bilateral posterior ischemic optic neuropathy (PION).  \n  - Magnetic resonance angiography (MRA) showed arterialization (abnormal arterial blood flow) of the bilateral cavernous sinuses and SOVs.  \n  - Cerebral angiography confirmed bilateral dural carotid-cavernous fistulas (CCFs) with anterior drainage. The right-sided fistula was supplied by dural branches of the internal carotid artery (ICA), specifically the right meningo-hypophyseal trunk. The left-sided fistula received blood from dural branches of both the external carotid artery (ECA) and ICA. Both fistulas contributed arterial blood flow to the bilateral SOVs, including contralateral flow via intercavernous communications. No cortical venous reflux was observed.\n\n**Clinical Interpretation**  \nThe patient’s sudden bilateral vision loss and ocular findings were caused by bilateral dural carotid-cavernous fistulas leading to venous congestion and elevated intraocular pressure. The restricted diffusion in the optic nerves indicated ischemic injury consistent with bilateral posterior ischemic optic neuropathy (PION), explaining the irreversible vision loss despite the absence of direct optic nerve compression. The elevated intraocular pressures and vascular abnormalities contributed to the ocular signs such as chemosis, corkscrew episcleral vessels, and corneal edema.\n\n**Next Steps and Outcome**  \nThe patient underwent successful transvenous coil embolization of the bilateral cavernous sinuses to occlude the fistulas and their feeding vessels. Immediate post-procedure angiography confirmed complete closure of the fistulas. Three months after embolization, ocular signs such as chemosis and vascular congestion showed progressive improvement. However, the patient’s visual acuity remained at no light perception in both eyes, indicating permanent bilateral vision loss.\n\n---\n\nThis case highlights the importance of recognizing dural carotid-cavernous fistulas as a cause of sudden bilateral vision loss and orbital congestion, especially in patients with vascular risk factors like hypertension. Early diagnosis and intervention can resolve vascular abnormalities but may not reverse ischemic optic nerve damage once established."
+        }
+    },
+    {
+        "article": "Un paciente de 15 años de edad (altura = 161 cm; peso = 66 kg; superficie corporal = 1,70; grupo sanguíneo = B positivo) con cardiomiopatía dilatada fue derivado a la Universidad de Ankara con pérdida de conciencia y shock cardiogénico en julio de 2016. El apoyo de oxigenación de membrana extracorpórea venosa arterial se realizó aproximadamente 1 semana después. Su fracción de eyección ventricular izquierda fue del 22%. Ocho días después, el paciente recibió un implante de corazón artificial total SynCardia (50 ml; SynCardia Systems, Inc., Tucson, AZ, EE. UU.). En el día 131 postoperatorio después de la cirugía TAH, el paciente se quejó de pérdida de audición bilateral y fue derivado al departamento de oído, nariz y garganta.\n\nLos antecedentes médicos previos no revelaron evidencia de pérdida auditiva, antecedentes familiares de sordera o cualquier anomalía adicional en su niñez. Sus registros médicos no revelaron evidencia de meningitis. Sin embargo, había recibido amikacina (15 mg/kg), un antibiótico ototóxico, contra patógenos gramnegativos importantes durante su estancia en la unidad de cuidados intensivos. El paciente fue incluido en la lista de espera de trasplantes de corazón de alta urgencia y era móvil en el Freedom Driver portátil (SynCardia).\n\nEl examen otoscópico del paciente fue normal. La audiometría de tonos puros y la respuesta auditiva del tronco encefálico revelaron una pérdida auditiva profunda bilateral. La timpanometría mostró timpanogramas normales de tipo A bilaterales. Tanto la tomografía computarizada como la resonancia magnética confirmaron la morfología normal del laberinto y nervios cocleares intactos.\n\nFue examinado por un equipo multidisciplinario (cirugía cardiovascular, cuidados intensivos pediátricos, cardiología pediátrica, psiquiatría de consulta y enlace, fisioterapia y rehabilitación, enfermedades infecciosas y microbiología clínica, anestesiología, audiología y otorrinolaringología) para realizar un implante coclear. Después de analizar las posibles opciones con el paciente y sus padres, se decidió que se beneficiaría de un implante coclear debido a la pérdida auditiva y la reducción de la función cognitiva y la adaptación necesaria para el trasplante de corazón. Después de analizar su caso con el equipo multidisciplinario, se decidió un implante coclear del lado derecho (Nucleus CI24RE con Contour Advance Electrode; Cochlear, Macquarie University, Australia).\n\nEl paciente tomaba warfarina (10 mg/día), que se interrumpió tres días antes de la cirugía, y se inició la heparinización (dosis de carga de 50 U/kg y dosis de mantenimiento de 20 U/kg/h) cuando el tiempo de protrombina (cociente internacional normalizado [INR]) era inferior a 1,5. Dos horas antes de la cirugía, se interrumpió la heparinización. En el quirófano, se disponía de un dispositivo de reserva para un posible fallo del dispositivo TAH. El equipo de anestesia y el perfusionista controlaron de cerca los resultados del flujo para el TAH. El flujo sanguíneo no pulsátil afecta de forma negativa al control de los signos vitales, y la presión arterial no invasiva no fue suficiente en nuestro paciente. Bajo anestesia local, se realizó un cateterismo radial arterial invasivo. Además, se dejó la vena yugular interna izquierda en su lugar, lo que permitió el control de la presión venosa central y su uso como reemplazo de fluidos de gran volumen cuando fue necesario. Después de iniciar el control, se administraron con precaución 2 mg/kg de propofol, 1 mg/kg de bromuro de rocuronio y 1 µg/kg de fentanilo, y se intubió al paciente por vía oral. Se utilizó sevoflurano con una concentración alveolar mínima de 1 a 1,5 en oxígeno al 40 % para el mantenimiento. El óxido nítrico inhalado también estaba listo para usarse en caso de una posible crisis hipertensiva pulmonar.\n\nEl día 250 después del implante TAH, se realizó la cirugía de implante coclear con abordaje de ventana redonda sin complicaciones perioperatorias; el paciente tuvo una pérdida de sangre mínima (solo 50 ml). La duración de la operación fue de 120 minutos. El paciente fue extubado en el quirófano sin problemas circulatorios y respiratorios. La heparinización se inició a la hora 6 posoperatoria. Comenzamos con la warfarina el día 1 posoperatorio, y la heparinización se detuvo después de alcanzar un INR de 2.0. No se observaron complicaciones (infecciones, hematoma) en el seguimiento posoperatorio.\n\nEl implante coclear se activó en la semana 4 después de la operación. El equipo de audiología lo revisó 4 y 8 semanas después; mostró una mejora continua en su audición, con impedancias normales. Sus resultados de percepción del habla mejoraron significativamente 3 meses después del implante coclear.\n\nMH - Adolescente\nMH - Niño\nMH - *Implantación coclear\nMH - *Insuficiencia cardiaca/diagnóstico/etiología/cirugía\nMH - *Efectos adversos del trasplante de corazón\nMH - *Corazón, Artificial\nMH - Humanos\nMH - Hombre\nMH - Resultado del tratamiento\n",
+        "gold_summary": "Describimos el caso de un niño de 15 años con pérdida auditiva total bilateral postlingual tras la administración de medicamentos ototóxicos durante su estancia en la unidad de cuidados intensivos pediátricos. El paciente recibió el implante de corazón artificial total SynCardia (50 ml; SynCardia Systems, Inc., Tucson, AZ, EE. UU.) para la insuficiencia cardiaca biventricular en fase terminal como puente para el trasplante cardiaco. Durante su estancia en la lista de espera de trasplantes cardiacos urgentes, se sometió a una implantación coclear satisfactoria tras optimizar el estado de coagulación y hemostasis y una preparación anestésica adecuada.\n",
+        "synthetic_summary": {
+            "B1": "A boy, 15 years old, got very sick with his heart. He needed a special machine to help his heart work. While he was in the hospital, he lost his hearing in both ears. \n\nDoctors helped him by putting a tiny device in his ear. This device helps him hear sounds again. The surgery went well, and he is getting better.",
+            "B2": "**What Happened to the Patient**  \nA 15-year-old boy had severe heart failure and needed a total artificial heart implanted to keep him alive while waiting for a heart transplant. During his time in the hospital, he was given a medicine called amikacin, which can sometimes harm the ears and cause hearing loss. After some time, he developed total hearing loss in both ears.\n\n**How Doctors Helped**  \nDoctors checked his ears and hearing carefully. Tests showed he had deep hearing loss, but his ear structures looked normal. Because he needed to communicate and prepare for his future heart transplant, the medical team decided to give him a cochlear implant. A cochlear implant is a small device placed inside the ear that helps people hear by sending signals directly to the hearing nerve.\n\n**The Surgery and Recovery**  \nBefore surgery, doctors made sure his blood could clot properly to avoid bleeding problems. The operation went well without complications, and he lost very little blood. After surgery, his hearing device was turned on four weeks later. Over the next few months, his hearing and ability to understand speech improved a lot.\n\n**What This Means**  \nThis case shows that even patients with serious heart problems and artificial hearts can safely have cochlear implants. With careful preparation and teamwork among different specialists, hearing can be restored, which helps patients communicate and improves their quality of life.",
+            "B3": "Background  \nThis report details the case of a 15-year-old male patient with end-stage biventricular heart failure who underwent implantation of a total artificial heart (TAH) device (SynCardia 50 ml) as a bridge to cardiac transplantation. During his prolonged stay in the pediatric intensive care unit (ICU), he received amikacin, an antibiotic known for its ototoxic (ear-damaging) potential. Subsequently, the patient developed profound bilateral postlingual (after language acquisition) hearing loss.\n\nKey Findings  \n- The patient’s initial cardiac condition necessitated TAH implantation due to severely reduced left ventricular ejection fraction (22%).  \n- Approximately four months after TAH implantation, he reported bilateral hearing loss.  \n- Audiological assessments, including pure tone audiometry and brainstem auditory evoked responses, confirmed profound bilateral sensorineural hearing loss.  \n- Middle ear function was normal, and imaging studies (CT and MRI) showed intact cochlear nerves and normal inner ear anatomy, ruling out structural causes.  \n- No prior history of hearing impairment, meningitis, or familial deafness was identified.  \n- The hearing loss was attributed primarily to ototoxicity from amikacin administered during ICU care.  \n\nClinical Interpretation  \nThe patient’s profound bilateral hearing loss developed in the context of critical illness and exposure to ototoxic medication. Given the severity of his hearing impairment and its impact on cognitive function and communication—factors crucial for successful heart transplantation and rehabilitation—a multidisciplinary team evaluated the benefits and risks of cochlear implantation. The team included specialists in cardiovascular surgery, pediatric cardiology, infectious diseases, anesthesiology, audiology, otolaryngology, psychiatry, and rehabilitation.\n\nAfter careful coagulation management—temporarily discontinuing warfarin and transitioning to heparin to optimize bleeding risk—and meticulous anesthetic planning considering the non-pulsatile blood flow from the TAH, the patient underwent a right-sided cochlear implant (Nucleus CI24RE with Contour Advance Electrode). The surgery was performed without complications, minimal blood loss, and stable hemodynamics. Postoperative recovery was uneventful, with anticoagulation safely resumed.\n\nNext Steps and Outcomes  \n- The cochlear implant was activated four weeks post-surgery.  \n- Follow-up audiological evaluations at one and two months demonstrated continuous improvement in auditory function and normal device impedance.  \n- Speech perception scores improved significantly by three months after implantation, indicating successful auditory rehabilitation.  \n- The patient remained on the urgent heart transplant waiting list, benefiting from improved communication and cognitive function facilitated by the cochlear implant.  \n\nThis case highlights the importance of multidisciplinary care in managing complex patients with advanced cardiac devices who develop secondary complications such as ototoxic hearing loss. Cochlear implantation can be safely and effectively performed in patients supported by a total artificial heart, improving quality of life and transplant readiness."
+        }
+    },
+    {
+        "article": "Se encontró a un hombre de 25 años de edad recostado por familiares después de una noche de fiesta, con vómitos, agresión y dolor localizado en la región glútea e inferior derecha. La evaluación inicial en el departamento de urgencias no reveló lesiones traumáticas; sin embargo, el empeoramiento de los síntomas llevó a una nueva evaluación al día siguiente. Los resultados de laboratorio revelaron un recuento sanguíneo completo sin alteraciones, niveles elevados de CPK sérica (42 527 IU/l), creatinina sérica (735 µmol/l), urea (44,3 mmol/l) y potasio (5,7 mmol/l). El análisis de orina reveló orina de color rojo-marrón sin glóbulos rojos, proteinuria (+1), glucosuria (+1) y WBC (9-10/hpf). Estos resultados confirmaron la RM y la IRA. La toxicología estableció la administración de 1796 µg/l de heroína (> 5 veces el nivel basal) sin detección de ninguna otra sustancia. Aunque inicialmente negó haber tomado medicamentos, después del análisis toxicológico, el paciente admitió que había administrado heroína una vez por vía intramuscular en la región glútea derecha la noche del incidente.\n\nUna tomografía computarizada demostró edema muscular glúteo y miositis localizada en la región glútea derecha. Al comenzar el tratamiento convencional con resucitación de fluidos intravenosos (IV), el tratamiento de la IRA fracasó, lo que hizo necesario el TRR con hemodiálisis debido a la progresión de la azotemia con un aumento de la creatinina sérica a 1052 µmol/l. La función renal mejoró tras el cese del TRR con una duración total de la estancia (LOS) de 9 días. El seguimiento posterior del paciente fue incompleto debido a la falta de asistencia.\n",
+        "gold_summary": "Este informe de caso describe a un hombre de 25 años que desarrolló una RM grave y lesión renal aguda (LRA) después de la administración intramuscular (IM) de heroína como usuario por primera vez. El uso de la heroína IM puede inducir niveles más altos de CPK debido a la toxicidad directa de los miocitos y el trauma mecánico. Los músculos glúteos altamente vascularizados con fibras tipo 1 en el sitio de la inyección probablemente exacerbaron la gravedad. Los factores adicionales incluyeron una menor densidad mitocondrial en los hombres y la exposición al alcohol. A pesar de la reanimación agresiva con líquidos, se requirió la terapia de reemplazo renal (RRT) y el paciente respondió bien a la hemodiálisis.\n",
+        "synthetic_summary": {
+            "B1": "A man used a strong drug in his bottom muscle. This made his muscles very hurt and sick. His kidneys, which clean the blood, also got very sick. \n\nDoctors gave him lots of water and special care. He needed a machine to help his kidneys work. After some time, he started to feel better.",
+            "B2": "**What Happened to the Patient**  \nThis report talks about a 25-year-old man who got very sick after injecting heroin into his buttock muscle for the first time. Heroin is a strong drug, and injecting it into a muscle can harm muscle cells directly and cause injury from the needle itself. This damage made his muscle tissue break down badly, a condition called rhabdomyolysis (RM).  \n\n**Why the Muscle and Kidneys Were Affected**  \nThe buttock muscles have many blood vessels and special muscle fibers, which may have made the damage worse. Also, men usually have fewer mitochondria—tiny parts inside cells that produce energy—which might have made his muscles more vulnerable. Drinking alcohol before or during drug use can also increase the risk of muscle and kidney problems.  \n\n**What Happened to His Kidneys**  \nBecause of the muscle damage, harmful substances leaked into his blood and caused his kidneys to stop working well. This is called acute kidney injury (AKI). Even though doctors gave him fluids through an IV to help, his kidneys got worse, and he needed a treatment called hemodialysis. Hemodialysis is a way to clean the blood when the kidneys can’t do it.  \n\n**Outcome**  \nAfter the dialysis treatment, his kidney function improved, and he stayed in the hospital for nine days. Unfortunately, he did not continue with follow-up care after leaving the hospital.  \n\n**What This Means**  \nInjecting heroin into muscles can cause serious muscle and kidney damage, especially in people who use it for the first time. Early treatment is very important, but sometimes kidney support like dialysis is needed. This case shows how dangerous heroin injections can be and why medical help should be sought quickly.",
+            "B3": "**Background**  \nThis case report involves a 25-year-old man who developed severe rhabdomyolysis (RM)—a condition characterized by the breakdown of muscle tissue—and acute kidney injury (AKI) following his first intramuscular (IM) use of heroin. The patient initially presented after a night of partying with symptoms including vomiting, aggression, and localized pain in the right lower gluteal region. Initial emergency evaluation showed no trauma, but worsening symptoms prompted further investigation.\n\n**Key Findings**  \nLaboratory tests revealed markedly elevated serum creatine phosphokinase (CPK) levels at 42,527 IU/L, indicating extensive muscle damage. Kidney function markers were significantly impaired, with serum creatinine at 735 µmol/L, urea at 44.3 mmol/L, and potassium at 5.7 mmol/L, confirming acute kidney injury. Urinalysis showed red-brown urine without red blood cells, mild proteinuria and glucosuria, and increased white blood cells, consistent with muscle breakdown and renal involvement. Toxicology confirmed a high serum heroin concentration (1796 µg/L), more than five times the baseline level, with no other substances detected. The patient initially denied drug use but later admitted to a single IM heroin injection in the right gluteal area on the night of symptom onset.\n\nImaging via computed tomography (CT) demonstrated localized muscle edema and myositis (muscle inflammation) in the right gluteal region, correlating with the injection site.\n\n**Clinical Interpretation**  \nIntramuscular heroin administration can cause direct toxicity to muscle cells (myocytes) and mechanical trauma, leading to elevated CPK levels and severe rhabdomyolysis. The gluteal muscles, being highly vascularized and rich in type 1 muscle fibers (which are more susceptible to injury), likely contributed to the severity of muscle damage in this case. Additional factors that may have exacerbated the condition include the patient’s male sex, associated with lower mitochondrial density in muscle tissue, and concurrent alcohol exposure, which can potentiate muscle injury.\n\nDespite aggressive intravenous fluid resuscitation aimed at preventing kidney damage, the patient’s renal function deteriorated, necessitating renal replacement therapy (RRT) via hemodialysis. Following this intervention, kidney function improved, and the patient was discharged after a nine-day hospital stay.\n\n**Next Steps**  \nThe patient’s follow-up was incomplete due to lack of attendance, highlighting the importance of continued monitoring after severe rhabdomyolysis and AKI, especially in cases related to substance use. Future care should focus on renal function surveillance, counseling on substance abuse risks, and prevention of recurrent muscle injury. This case underscores the potential for severe muscle and kidney complications following intramuscular heroin use, even in first-time users, and the need for prompt recognition and treatment."
+        }
+    },
+    {
+        "article": "Una mujer de 63 años con antecedentes de obesidad e hipertensión arterial acudió a la sala de urgencias de un hospital de nivel secundario con un historial de siete días de fiebre, tos seca, hiposmia y mialgia. Al momento del ingreso, se encontraba alerta, con una frecuencia respiratoria de 22 ciclos por minuto, pulso de 90 latidos por minuto y saturación de oxígeno de 90 %. Los análisis de laboratorio revelaron linfopenia (1,55 x 109) y niveles elevados de proteína C reactiva (10,62 mg/dL). Se realizó una prueba de reacción en cadena de la polimerasa para COVID-19 a partir de un hisopado nasofaríngeo y de la garganta, que resultó positivo para el coronavirus del síndrome respiratorio agudo severo 2 (SARS-CoV-2).\n\nLa situación evolucionó rápidamente con fiebre, postración y empeoramiento de la disnea. La gasometría arterial reveló una insuficiencia respiratoria grave, mientras que la radiografía de tórax evidenció infiltrados pulmonares bilaterales. La paciente fue intubada y sometida a ventilación mecánica, pero su condición respiratoria continuó deteriorándose, a pesar de los mejores cuidados críticos, incluyendo ventilación en posición prona y bloqueo neuromuscular. Su examen de tomografía computarizada del tórax, tras la intubación, reveló extensas opacificaciones multifocales bilaterales en vidrio molido, sin signos de embolia pulmonar. Los ajustes iniciales del ventilador fueron: ventilación controlada por volumen con volumen corriente de 360 ml (6 ml/kg de peso corporal ideal), frecuencia respiratoria de 14 respiraciones por minuto, presión espiratoria positiva final (PEEP) de 14 cmH2O y complacencia estática de 44 cmH2O.\n\nEn el segundo día de internación, la gasometría arterial mostró pH de 7,34, presión parcial de dióxido de carbono (PaCO2) de 53 mmHg, presión parcial de oxígeno (PaO2) de 102 mmHg y bicarbonato (HCO3) de 29,7 mmol/L, con una proporción presión parcial de oxígeno/fracción inspirada de oxígeno (PaO2/FiO2) de 98. Ella cumplía los criterios para indicación de VV-ECMO y fue transferida a la unidad de terapia intensiva (UTI), que disponía de un programa establecido para VV-ECMO. El procedimiento fue realizado con seguridad, no habiendo ocurrido complicaciones. El análisis de la gasometría arterial 3 horas después del inicio de la VV-ECMO mostró pH de 7,386, PaCO2 de 43 mmHg, PaO2 de 94,3 mmHg y HCO3 de 25,4 mmol/L, sin cualquier variación abruta de la PaCO2. Tuvieron inicio la nutrición y la rehabilitación precoces tras la introducción de la VV-ECMO. En el 14º día de internación, la paciente desarrolló neumonía asociada al ventilador causada por Pseudomonas aeruginosa, siendo sometida a 7 días de antibioticoterapia con ceftazidima y vancomicina, con respuesta favorable. En el 20º día de internación, su radiografía del tórax y la complacencia mejoraron, y la paciente fue retirada de la VV-ECMO con éxito tras 455 horas de soporte, siendo traqueostomizada 7 días después. La paciente mantuvo buena función renal durante toda la internación.\n\nEn el día 34 de internación, luego de 7 días de destete de la sedación, con evolución positiva de su cuadro neurológico, ocurrió una crisis epiléptica generalizada limitada, que llevó a la investigación diagnóstica.\n\nInvestigación\nLos análisis de sangre de laboratorio revelaron una disminución de los niveles de proteína C reactiva (6,11 mg/dL), procalcitonina (0,07 ng/mL), fibrinógeno (307 ng/mL) y ferritina (2802 ng/mL), pero un aumento en los niveles de dímero D (18021 ng/mL) e interleucina 6 (10,4 pg/mL) en el día anterior al inicio de los síntomas. No se asoció ninguno de los fármacos administrados a la paciente con el SEPR, es decir, fármacos inmunosupresores, inmunomoduladores y quimioterápicos.\n\nSe realizó una resonancia magnética (RM) del cerebro y las imágenes de recuperación de inversión atenuada por fluidos (FLAIR) demostraron una hiperintensidad simétrica y confluente que afectaba a la sustancia blanca justa y subcortical, principalmente en las regiones occipital y parietal, pero también en la región frontal, temporal y cerebelosa izquierda. Los núcleos grises profundos se conservaron y no había presencia de ninguna área con restricción del contraste. Las imágenes ponderadas por susceptibilidad mostraron múltiples microhemorragias puntiformes que afectaban a la sustancia blanca superficial y profunda, pero que no afectaban al área con hiperintensidad en FLAIR. Las microhemorragias puntiformes involucraban predominantemente a la sustancia blanca justacortical y al cuerpo calloso (especialmente el codo y el esplenio). Además, había tres hemorragias subagudas de menos de 1 cm en las cápsulas externas, con hiperintensidad en T1.\n\nLa muestra de líquido cefalorraquídeo dio negativo para SARS-CoV-2 y los niveles de proteínas (31 mg/dL), glucosa (74 mg/dL) y lactato (1,89 mmol/L) se encontraban dentro de los parámetros normales.\n\nDesvelado\nLa paciente logró una recuperación casi total de los déficits neurológicos, a pesar de la miopatía de la enfermedad crítica, y fue dada de alta después de 44 días en el hospital. Se la derivó a un hospital secundario para su rehabilitación y prácticamente recuperó su estado mental previo.\n",
+        "gold_summary": "Una mujer de 63 años de edad acudió a la sala de urgencias con un historial de fiebre aguda, postración y disnea. Se le diagnosticó un caso grave de COVID-19 y síndrome de dificultad respiratoria aguda. A pesar de recibir atención médica intensiva, cumplía con los requisitos para someterse a una oxigenación por membrana extracorpórea. El día 34, luego de siete días de haber suspendido la sedación y de que su cuadro neurológico hubiera evolucionado de manera positiva, presentó una crisis tónico-clónica generalizada limitada, que no guardaba relación con un desequilibrio hidroelectrolítico o metabólico, lo que hizo necesario realizar una investigación diagnóstica. Los estudios de imágenes cerebrales revelaron un síndrome de encefalopatía posterior reversible.\n",
+        "synthetic_summary": {
+            "B1": "A 63-year-old woman felt very sick with fever and trouble breathing. Doctors found she had a bad lung sickness called COVID-19. She needed special help to breathe with a machine.\n\nAfter many days, she started to feel better. But one day, she had a big seizure. The doctors checked her brain with pictures. They found a problem that can get better with time. The doctors helped her and she got better again.",
+            "B2": "**What Happened to the Patient**  \nA 63-year-old woman went to the emergency room with a high fever, extreme tiredness, and trouble breathing. Doctors found she had a severe case of COVID-19, which caused serious lung problems called acute respiratory distress syndrome. Even with strong medical care, her lungs were not working well enough, so she needed a special treatment called extracorporeal membrane oxygenation (ECMO). This machine helps oxygenate the blood outside the body when the lungs can’t do it properly.\n\n**What Happened Later**  \nAfter 34 days in the hospital and seven days without sedation (medicine that keeps patients calm or asleep), her brain condition seemed to be improving. But then she had a type of seizure called a tonic-clonic seizure, which causes stiffening and jerking movements. This seizure was not caused by common problems like imbalances in body fluids or chemicals, so doctors did more tests to find out why.\n\n**What the Tests Showed**  \nBrain scans revealed a condition called posterior reversible encephalopathy syndrome (PRES). This means parts of the brain, especially in the back areas, were swollen but could get better with treatment. PRES can cause seizures and other neurological symptoms but is often reversible if treated properly.\n\n**What This Means**  \nThis case shows that severe COVID-19 can lead to serious brain problems like PRES, even after the main lung issues start to improve. Doctors need to watch for these complications to provide the right care. The patient eventually recovered most of her brain functions and was able to leave the hospital after 44 days.",
+            "B3": "Background  \nA 63-year-old woman with a history of obesity and hypertension presented to the emergency department after seven days of acute fever, dry cough, loss of smell (hyposmia), muscle pain (myalgia), and progressive shortness of breath (dyspnea). Initial evaluation confirmed severe COVID-19 infection complicated by acute respiratory distress syndrome (ARDS). Despite intensive medical management, including mechanical ventilation with lung-protective settings and prone positioning, her respiratory function deteriorated, necessitating initiation of venovenous extracorporeal membrane oxygenation (VV-ECMO) on hospital day two.\n\nKey Findings  \nAfter 34 days of hospitalization and following seven days of sedation withdrawal with neurological improvement, the patient experienced a generalized tonic-clonic seizure. This event was not attributable to electrolyte imbalances or metabolic disturbances, prompting further diagnostic evaluation. Brain magnetic resonance imaging (MRI) with fluid-attenuated inversion recovery (FLAIR) sequences demonstrated symmetrical, confluent hyperintensities predominantly affecting the subcortical and juxtacortical white matter in the occipital and parietal lobes, as well as involvement of frontal, temporal, and left cerebellar regions. Susceptibility-weighted imaging revealed multiple small microhemorrhages in superficial and deep white matter, especially in the juxtacortical areas and corpus callosum, without contrast restriction or involvement of deep gray matter. Cerebrospinal fluid analysis was unremarkable and negative for SARS-CoV-2.\n\nClinical Interpretation  \nThese imaging findings are consistent with posterior reversible encephalopathy syndrome (PRES), a neurological disorder characterized by reversible vasogenic edema predominantly affecting the posterior cerebral regions. PRES can occur in critically ill patients and may be triggered by severe systemic inflammation, endothelial dysfunction, or fluctuations in blood pressure, all of which are common in severe COVID-19 cases requiring advanced respiratory support such as VV-ECMO. The absence of metabolic or infectious causes for the seizure and the typical MRI pattern support this diagnosis.\n\nNext Steps  \nThe patient underwent early nutritional and rehabilitative interventions during VV-ECMO support. Following treatment of a ventilator-associated pneumonia and gradual respiratory improvement, she was successfully weaned off VV-ECMO after 19 days of support. After the neurological event, she received appropriate seizure management and continued rehabilitation. Ultimately, she achieved near-complete recovery of neurological function despite critical illness myopathy and was discharged after 44 days of hospitalization with referral for continued rehabilitation. This case underscores the importance of vigilant neurological monitoring and timely imaging in critically ill COVID-19 patients, especially those undergoing advanced life support therapies."
+        }
+    },
+    {
+        "article": "Mujer de 65 años, originaria y residente de la Ciudad de México, con antecedente de infección por VIH de 20 años de diagnóstico con carga viral indetectable desde 2020 y con cuenta de CD4 de 1220 células por mililitro en febrero de 2022, hipotiroidismo de 29 años, cardiopatía isquémica de 9 años de diagnóstico, osteoporosis y dislipidemia, en tratamiento y bajo control médico.\n\nSu dermatosis problema se inició 10 años atrás, después de un cuadro de herpes zóster localizado en la extremidad inferior derecha y se complicó con una infección de tejidos blandos, referida como celulitis. Como secuela de este evento la paciente desarrolló úlcera, la cual ameritó corrección del defecto con 4 injertos cutáneos en diferentes tiempos quirúrgicos por cirugía plástica, con acompañamiento por parte de la clínica de heridas. Durante el seguimiento y a pesar de las medidas tomadas, no logró resolución completa y persistió con una úlcera asociada a dolor local, motivo de su envío a nuestro servicio.\n\nA la exploración física presentaba una dermatosis localizada en la extremidad inferior derecha, en la cara lateral del muslo, caracterizada por una neoformación aplanada sobre la que se asentaba una úlcera de 1.5 cm de diámetro, con fondo limpio, con costra sero-amarillenta, bordes sobreelevados, piel perilesional hiperpigmentada y queratósica, una cicatriz atrófica e hiperpigmentada. Se inició abordaje de la dermatosis mediante biopsia de piel, con reporte histopatológico de carcinoma verrugoso, por lo que se concluyó como úlcera de Marjolin asociada a carcinoma verrugoso en paciente portadora de VIH. Se canalizó al hospital de oncología para manejo con radioterapia.",
+        "gold_summary": "mujer de 65 años con el antecedente de ser portadora de infección por virus de inmunodeficiencia humana (VIH), que presentó un carcinoma verrugoso asociado a una úlcera de Marjolin secundaria a herpes zóster e infección de tejidos blandos en pierna derecha, con un periodo de latencia de 10 años desde el proceso infeccioso inicial hasta la confirmación histopatológica.",
+        "synthetic_summary": {
+            "B1": "A lady is 65 years old. She had a sickness in her leg a long time ago. \n\nAfter many years, a sore on her leg did not heal. The doctors found a kind of bump that needs special care. \n\nShe is getting help from the doctors now.",
+            "B2": "**What Happened to the Patient**\n\nA 65-year-old woman who has lived with HIV (a virus that attacks the immune system) for 20 years developed a special kind of skin cancer called verrucous carcinoma. This cancer grew in an area on her right leg where she had a long-lasting sore called a Marjolin ulcer. The ulcer appeared after she had shingles (also known as herpes zoster) and a soft tissue infection in the same leg.\n\n**How It Developed**\n\nThe sore started about 10 years ago after the shingles infection. Despite treatment, the ulcer did not heal completely and stayed painful. Doctors took a small piece of the sore (a biopsy) to look at the cells under a microscope. This test confirmed the presence of verrucous carcinoma, a slow-growing type of skin cancer.\n\n**What This Means**\n\nThe cancer developed from a long-lasting wound caused by infection and inflammation. This kind of cancer linked to old wounds is called a Marjolin ulcer. Because the patient has HIV, her immune system might have been weaker, which can affect healing and increase cancer risk. She was referred to a cancer hospital to receive radiation therapy, a treatment that uses high-energy rays to kill cancer cells.",
+            "B3": "Background  \nA 65-year-old woman from Mexico City with a 20-year history of HIV infection, well controlled since 2020 with an undetectable viral load and a robust CD4 count of 1220 cells/mm³ as of early 2022. Her medical history also includes longstanding hypothyroidism (29 years), ischemic heart disease (9 years), osteoporosis, and dyslipidemia, all under medical management.\n\nKey Findings  \nThe patient developed a skin condition on her right lower limb that began 10 years ago following a localized herpes zoster (shingles) infection complicated by soft tissue infection diagnosed as cellulitis. This event led to a chronic ulcer at the site, which required four separate skin graft surgeries performed by plastic surgery and ongoing wound care. Despite these interventions, the ulcer persisted, causing local pain and prompting further evaluation.\n\nOn physical examination, there was a lesion on the lateral aspect of the right thigh characterized by a flat new growth (neoformation) with an overlying 1.5 cm ulcer. The ulcer had a clean base with a yellowish crust, raised edges, surrounding hyperpigmented and thickened (keratotic) skin, and an atrophic, hyperpigmented scar nearby.\n\nA skin biopsy was performed, and histopathological analysis confirmed the diagnosis of verrucous carcinoma—a slow-growing, wart-like form of squamous cell carcinoma—arising in association with a Marjolin ulcer. A Marjolin ulcer is a malignant transformation occurring in a chronic wound or scar, in this case secondary to the prior herpes zoster and soft tissue infection.\n\nClinical Interpretation  \nThis case illustrates a rare but serious complication in a patient with HIV: the development of a verrucous carcinoma within a chronic ulcer (Marjolin ulcer) that evolved over a decade following an initial infectious insult. The latency period of 10 years between the initial herpes zoster and cellulitis and the malignant transformation is consistent with known patterns of Marjolin ulcers developing in chronic wounds.\n\nNext Steps  \nThe patient was referred to an oncology hospital for management with radiotherapy, which is appropriate for verrucous carcinoma in this context. Continued multidisciplinary care, including infectious disease, dermatology, oncology, and wound care specialists, will be essential to optimize outcomes."
+        }
+    },
+    {
+        "article": "Una mujer de 90 años con hepatitis C y un historial de tabaquismo de 60 años proveniente de una zona rural presentó una hinchazón en la cara posteromedial del muslo izquierdo justo por encima de la rodilla. La hinchazón se notó por primera vez hace 3 años y aumentó gradualmente de tamaño durante este período. Ella sintió un leve malestar, pero niega cualquier síntoma asociado de dolor, picazón, secreción, fiebre o inmovilidad articular. Como provenía de una zona rural, también tenía un historial de exposición a animales.\nEn el examen físico, la hinchazón tenía una forma esférica de 14 × 10, era firme, fija y no sensible, con márgenes bien definidos en el aspecto posteromedial del muslo izquierdo, justo por encima de la rodilla. La piel que la recubría era pellizcable y mostraba venas prominentes, y la temperatura era comparable a la de la piel circundante.\nLa ecografía reveló una lesión quística grande con varios quistes pequeños en su interior, que medían 13,2 × 11 × 13,6 cm y un volumen de 1046 ml. Se originaba en la articulación de la rodilla izquierda y se extendía hasta la mitad del muslo. La ecografía Doppler en color no mostró vascularización en su interior. Se realizó una resonancia magnética que mostró una lesión quística grande (21 × 9,9 × 8,1 cm) con múltiples lesiones pequeñas dispersas, con extensión intramuscular e intermuscular que afectaban al aductor largo y al gracilis de manera medial y al bíceps femoral de manera posterior. Todas estas características eran indicativas de un quiste hidatídico. El diagnóstico se confirmó mediante una prueba de hemaglutinación para Echinococcus. La radiografía de tórax y la ecografía abdominal fueron normales.\nSe planificó la escisión quirúrgica de la tumefacción quística y se realizó una incisión en forma de S en la piel, seguida de una disección cuidadosa a través del tejido subcutáneo para acceder al quiste. La lesión estaba bien definida dentro de los planos intermuscular e intramuscular. Se realizó una disección meticulosa para aislar y extraer el quiste intacto, asegurando que no se derramara su contenido. Para minimizar el riesgo de contaminación, se irrigó a fondo el sitio quirúrgico con solución salina normal después de la escisión.\nLos hallazgos intraoperatorios revelaron una gran hinchazón quística intermuscular de 22 × 14 cm, que involucraba los compartimentos posterior y medial del muslo izquierdo. El quiste demostró extensión intramuscular hacia el aductor largo y el gracilis medialmente y hacia el bíceps femoral posteriormente, extendiéndose hasta la fosa poplítea. Cabe destacar que no había comunicación entre el quiste y la articulación de la rodilla. Una biopsia enviada al laboratorio confirmó aún más el diagnóstico. El examen histopatológico de la muestra extirpada reveló una pared quística fibrocondrogénica revestida por epitelio atenuado con infiltración inflamatoria. La presencia de material queratinoso focal caracterizó aún más la lesión. Estos hallazgos, junto con las características macroscópicas, favorecieron el diagnóstico de un quiste hidatídico. El curso postoperatorio fue sin complicaciones y el paciente fue dado de alta con una terapia antihelmíntica durante seis semanas. Se programaron visitas de seguimiento a la semana, tres semanas, seis semanas, nueve semanas y doce semanas. Durante estas visitas, el paciente no mostró signos de recurrencia o complicaciones.\n",
+        "gold_summary": "Una mujer de 90 años de edad, proveniente de una zona rural, presentó una hinchazón de crecimiento lento en el muslo posteromedial durante tres años. No tenía antecedentes de traumatismos ni síntomas sistémicos. El examen clínico reveló una masa firme y no dolorosa. Las imágenes sugieren una lesión quística, y la serología confirmó la infección por Echinococcus. Se realizó la extirpación quirúrgica, y la histopatología confirmó un quiste hidatídico. La paciente recibió un tratamiento posoperatorio de albendazol durante seis semanas. Su recuperación fue sin incidentes, sin recurrencia en el seguimiento.\n",
+        "synthetic_summary": {
+            "B1": "A very old lady had a bump on her leg. The bump grew slowly for three years. It did not hurt her.\n\nDoctors took pictures and found a big bubble inside her leg. They did a test and found tiny germs called Echinococcus.\n\nThe doctors took out the bubble with surgery. The lady took medicine for six weeks. She got better and felt well.",
+            "B2": "**What Happened:**  \nA 90-year-old woman from a rural area noticed a slow-growing swelling on the inside back part of her left thigh, just above the knee. This swelling had been there for three years. She did not have any injuries or other general symptoms like fever or pain.\n\n**What the Doctors Found:**  \nWhen the doctors examined her, they felt a firm lump that did not hurt. Imaging tests, like ultrasound and MRI, showed that the lump was a large cyst—a sac filled with fluid and smaller cysts inside. Blood tests confirmed she was infected with a parasite called *Echinococcus*, which causes a condition known as a hydatid cyst.\n\n**What They Did:**  \nThe doctors carefully removed the cyst through surgery, making sure not to spill its contents to avoid spreading the infection. Lab tests on the removed tissue confirmed it was a hydatid cyst. After surgery, she took a medicine called albendazole for six weeks to kill any remaining parasites.\n\n**Outcome:**  \nThe woman recovered well without any problems. Follow-up visits showed no signs that the cyst had come back or caused complications.",
+            "B3": "Background  \nA 90-year-old woman from a rural area, with a history of hepatitis C and long-term tobacco use, noticed a gradually enlarging swelling on the inner back side of her left thigh, just above the knee. This swelling had been present for three years and caused only mild discomfort without pain, itching, discharge, fever, or joint immobility. She also had a history of exposure to animals due to her rural environment.\n\nKey Findings  \nPhysical examination identified a well-defined, firm, fixed, and non-tender spherical mass measuring approximately 14 × 10 cm in the posteromedial aspect of the left thigh. The overlying skin was pinchable with prominent veins and normal temperature. Ultrasound imaging revealed a large cystic lesion containing multiple smaller cysts, measuring about 13 × 11 × 14 cm, originating near the left knee joint and extending up the thigh. Color Doppler ultrasound showed no blood flow within the lesion. Magnetic resonance imaging (MRI) confirmed a large cystic mass (21 × 9.9 × 8.1 cm) with multiple small cystic components extending within and between muscles, specifically involving the adductor longus, gracilis medially, and biceps femoris posteriorly. These imaging features were suggestive of a hydatid cyst, an infection caused by the parasite Echinococcus. This diagnosis was confirmed by a positive hemagglutination test for Echinococcus antibodies. Chest X-ray and abdominal ultrasound showed no additional involvement.\n\nClinical Interpretation  \nThe lesion was diagnosed as a hydatid cyst, a parasitic cystic infection that can involve soft tissues. The absence of communication between the cyst and the knee joint was noted during surgery. Histopathological examination of the excised tissue revealed a fibrocartilaginous cyst wall lined by attenuated epithelium with inflammatory infiltration and focal keratinous material, consistent with a hydatid cyst. The cyst was carefully removed intact through a surgical incision to prevent spillage and contamination, with thorough irrigation of the surgical site afterward.\n\nNext Steps and Outcome  \nPostoperatively, the patient was treated with albendazole, an anti-parasitic medication, for six weeks to reduce the risk of recurrence. Follow-up visits at one, three, six, nine, and twelve weeks showed no signs of cyst recurrence or complications. The patient’s recovery was uneventful, and she was discharged in stable condition.\n\nSummary  \nIn summary, this elderly woman’s slowly growing thigh mass was diagnosed as a hydatid cyst caused by Echinococcus infection, confirmed by imaging, serology, and histopathology. Surgical excision combined with postoperative anti-parasitic therapy resulted in a successful outcome without recurrence during follow-up."
+        }
+    },
+    {
+        "article": "Una paciente de 21 años de edad, soltera, con antecedentes de hipertensión y feocromocitoma metastásico, se presentó en nuestro hospital. Su cáncer se ha metastatizado en la vejiga, los huesos y los pulmones. También tiene un fuerte historial familiar de neoplasias, en particular de feocromocitoma. La paciente fue admitida debido a la hipertensión no controlada y los síntomas crónicos relacionados con su enfermedad.\n\nEn el ingreso (09/06/2024), la paciente era normotensa (PA: 104/66 mmHg), su frecuencia cardiaca era de aproximadamente 90 latidos por minuto, afebril a 36.9°C, y tenía una saturación de oxígeno de 99% en aire ambiente. El examen físico indicó un estado de desempeño del Grupo Cooperativo de Oncología del Este (ECOG) de 2, palidez consistente con anemia crónica, latido cardiaco regular sin murmullos o sonidos adicionales. El examen abdominal no fue notable, y no se observó edema o equimosis en las extremidades inferiores.\n\nLa paciente tiene antecedentes de hipertensión y paraganglioma, su medicación incluye (Doxazosin 2 mg, Labetalol 100 mg, Oxibutinina 5 mg, Aceite de parafina, Nifedipina 30 mg). Su historial quirúrgico incluye una adrenalectomía derecha a los diez años, y ha recibido varios tratamientos, incluidos análogos de somatostatina y radioterapia paliativa. El historial familiar revela una mutación familiar de la subunidad B de la deshidrogenasa del succinato (mutación SDBH) con un importante historial de tumores malignos endocrinos, incluidos feocromocitomas en su padre y hermana y cáncer de páncreas en su abuela.\n\nLas investigaciones de laboratorio, incluido el recuento sanguíneo completo, revelaron anemia significativa, con un nivel de hemoglobina de 7.5 g/dl. Había evidencia de hemólisis, como lo indican el alto recuento de reticulocitos, la bilirrubina indirecta y la lactato deshidrogenasa. La haptoglobina era baja. Los resultados de laboratorio se muestran en. El perfil de coagulación excluyó la coagulación intravascular diseminada (DIC), que muestra (PT: 15.6, PTT: 23.3, fibrinógeno: 489, dímero D: 0.63). La prueba de Coombs directa para excluir la anemia hemolítica autoinmune fue negativa. Los frotis de sangre periférica mostraron la presencia de esquistocitos, equinocitos y algunas células en forma de lágrima, además de trombocitopenia, todo lo cual apuntaba a la anemia hemolítica microangiopática (MAHA). Dado el contexto del cáncer metastásico, el paciente fue diagnosticado con anemia hemolítica microangiopática paraneoplásica en marzo/2024.\n\nEl paciente fue programado para el protocolo CVD (ciclofosfamida, vincristina y doxorrubicina), pero sin ciclofosfamida debido al efecto inductor de anemia de los agentes alquilantes. El paciente recibió un total de 5 ciclos. Como indicador de respuesta clínica, el paciente ya no experimentó anemia o trombocitopenia. Un nuevo frotis de sangre periférica reveló células normales, lo que sugiere una respuesta clínica al MAHA que coincide con la mejora de la neoplasia subyacente. Esto se alinea con la definición de MAHA como un síndrome paraneoplásico.\n\nLos medicamentos que se le suministran al paciente al momento del alta son: comprimidos de dexametasona de 2 mg, 4 mg por vía oral (PO) una vez al día (OD) durante 3 días, comprimidos de ondansetrón de 8 mg por vía oral (PO) una vez al día (OD) durante 3 días, comprimidos de metoclopramida de 10 mg por vía oral (PO) tres veces al día durante 3 días, calcio de 600 mg con vitamina D por vía oral (PO) una vez al día (OD) durante 1 día, comprimidos de labetalol de 100 mg por vía oral (PO) dos veces al día durante 1 día, comprimidos de doxazocina de 2 mg por vía oral (PO) dos veces al día durante 1 día, comprimidos de citalopram de 20 mg por vía oral (PO) durante 1 día, comprimidos de omeprazol de 20 mg, 40 mg por vía oral (PO) durante 1 día, comprimidos de paracetamol de 500 mg, 1000 mg por vía oral (PO) dos veces al día durante 1 día, cápsulas de aprepitant de 125 mg/80 mg, 1 cápsula por vía oral (PO) dos veces al día durante 3 días (con prescripción médica).\n\nEl paciente fue objeto de seguimiento el 01/07/2024, y su aspecto clínico era bueno y activo. El paciente se sometió a exámenes de laboratorio que incluían un recuento sanguíneo completo (WBC 6.59 10e3/ul, RBC 4.47 × 10^6/ul, HGB 13.2 g/dl, 40.0%, MCV 89.4 fL, PLT 41.5 10e3/ul), nitrógeno ureico en sangre 33.8 mg/dl, creatina cinasa-MB 36.1 u/l, creatinina sérica 0.97 mg/dl, cloruro 101.5 mmol/l, potasio 4.52 mmol/l, sodio 135 mmol/l.\n",
+        "gold_summary": "En este informe de caso, presentamos a una mujer soltera de 21 años con un fuerte historial familiar de neoplasia endocrina. Fue derivada a nuestro hospital para quimioterapia debido a un diagnóstico de feocromocitoma maligno, que había hecho metástasis en la vejiga urinaria, los huesos y los pulmones. Además, desarrolló anemia hemolítica microangiopática como un síndrome paraneoplásico.\n",
+        "synthetic_summary": {
+            "B1": "A young woman, 21 years old, was very sick with cancer. The cancer spread to her bladder, bones, and lungs. She also had a kind of sickness that made her blood weak. Doctors gave her medicine to help her get better.",
+            "B2": "**What They Found**  \nThis is the story of a 21-year-old woman who has a family history of certain types of tumors called endocrine neoplasias. She was diagnosed with a rare cancer called malignant pheochromocytoma. This cancer had spread, or metastasized, to her bladder, bones, and lungs. Because of this, she needed chemotherapy treatment at the hospital.\n\n**What It Means**  \nAlong with her cancer, she developed a condition called microangiopathic hemolytic anemia. This is a type of anemia where the body’s small blood vessels cause damage to red blood cells, making them break apart early. This anemia happened as a paraneoplastic syndrome, which means it was caused by the cancer but not directly by the tumor itself. Treating her cancer helped improve this anemia.",
+            "B3": "Background  \nThis case involves a 21-year-old unmarried woman with a significant family history of endocrine tumors, including pheochromocytomas (tumors of the adrenal gland that produce excess hormones). She was referred to the hospital for chemotherapy following a diagnosis of malignant pheochromocytoma that had metastasized (spread) to multiple sites, including the urinary bladder, bones, and lungs.\n\nKey Findings  \nUpon admission, the patient exhibited controlled blood pressure and a stable heart rate, but laboratory tests revealed severe anemia characterized by low hemoglobin levels (7.5 g/dL) and signs of hemolysis (destruction of red blood cells). Specific findings included elevated reticulocyte counts (immature red blood cells), increased indirect bilirubin, elevated lactate dehydrogenase, and low haptoglobin. Blood smear analysis showed fragmented red blood cells (schistocytes), spiky cells (echinocytes), tear-drop shaped cells, and a reduced platelet count (thrombocytopenia). Coagulation studies ruled out disseminated intravascular coagulation, and autoimmune causes of hemolytic anemia were excluded by a negative direct Coombs test. These results supported a diagnosis of microangiopathic hemolytic anemia (MAHA), a condition where small blood vessels cause mechanical destruction of red blood cells.\n\nClinical Interpretation  \nThe MAHA was identified as a paraneoplastic syndrome—an indirect effect of the underlying metastatic cancer rather than a direct invasion of blood vessels. The patient’s cancer was associated with a familial mutation in the succinate dehydrogenase subunit B gene (SDHB), which predisposes to malignant endocrine tumors. The patient underwent chemotherapy with vincristine and doxorubicin (excluding cyclophosphamide to avoid worsening anemia) over five cycles. Following treatment, her anemia and thrombocytopenia resolved, and blood smears normalized, indicating a positive clinical response correlating with improvement in the underlying cancer.\n\nNext Steps  \nAt discharge, the patient was prescribed a regimen including dexamethasone (a corticosteroid), antiemetics (ondansetron, metoclopramide, aprepitant) to manage chemotherapy side effects, antihypertensives (labetalol, doxazosin), and supportive medications such as calcium with vitamin D and omeprazole. Follow-up laboratory tests one month later showed normalized hemoglobin and red blood cell counts, though platelet counts remained low, warranting continued monitoring. The patient’s clinical condition was stable and active at follow-up.\n\nIn summary, this case highlights the development of microangiopathic hemolytic anemia as a paraneoplastic complication in a young woman with metastatic pheochromocytoma linked to a hereditary SDHB mutation. The patient’s hematologic abnormalities improved with targeted chemotherapy addressing the underlying malignancy."
+        }
+    }
+]
\ No newline at end of file
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new file mode 100644
index 0000000000000000000000000000000000000000..f8a25c319e4cf58fb0ac8c8d679d70d3742e3af6
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@@ -0,0 +1,902 @@
+[
+    {
+        "article": "Une femme de 80 ans, qui était évaluée pour une perte de poids involontaire importante, a été admise au service des urgences en raison de vomissements et de l'apparition soudaine de douleurs aiguës dans sa cuisse droite. Les douleurs étaient constantes et s'aggravaient avec le mouvement. L'examen clinique a révélé un point très sensible dans la région médiale proximale de sa cuisse droite. Il n'y avait aucune indication de traumatisme.\n\nLa patiente a été envoyée pour une radiographie de la hanche droite afin d'examiner une éventuelle fracture pathologique. Aucune fracture ou désalignement n'a été observé, et elle a été admise au service d'orthopédie pour la gestion de la douleur et la mobilisation. Elle a été renvoyée le jour suivant malgré une douleur persistante et des vomissements. Le troisième jour, la patiente a été réadmise au service des urgences avec les mêmes symptômes. Elle était apyrexique, mais en raison de marqueurs d'infection légèrement élevés, de leucocytes à 13,5 × 109/L (fourchette de référence 4,1–9,8 × 109/L) et de CRP à 60 mg/L (< 5 mg/L), une radiographie thoracique a été réalisée, révélant des consolidations confluentes basales dans le poumon droit, soulevant des soupçons d'infiltration pneumonique. La patiente a été transférée au service médical pour observation. Les antibiotiques n'ont pas été initiés en raison de symptômes respiratoires minimes.\n\nLe quatrième jour, l'état de la femme s'est détérioré, avec une tachycardie (rythme cardiaque de 119 bpm), une fréquence respiratoire de 28 respirations par minute (plage normale : 12-16), et une fièvre de 38,1 °C. Son taux de CRP a également augmenté de 50 à 250 mg/L. La pipéracilline-tazobactam a été initiée par voie intraveineuse à une dose ajustée au poids de 2 g x 4, et elle a été envoyée pour une tomodensitométrie du thorax/abdomen/pelvis en raison d'une suspicion de septicémie d'origine abdominale. La tomodensitométrie a révélé une boucle intestinale emprisonnée qui dépassait le canal obturateur droit et une dilatation intestinale pré-obstructive, compatible avec une hernie obturatrice aiguë irréductible. Le chirurgien de garde a été rapidement consulté, et la patiente a été programmée pour une chirurgie d'urgence.\n\nPendant la laparoscopie sous anesthésie générale, une petite boucle intestinale emprisonnée a été découverte dans le canal obturateur, ce qui correspond aux résultats de la tomodensitométrie. L'intestin a été réduit avec précaution, sans signe de nécrose ou de perforation. Après la réduction de la hernie, la patiente a présenté une hypotension, avec une tension artérielle de 98/37 mmHg. L'analyse des gaz artériels intraopérative a montré un pH de 7,22 (7,36-7,44), une PCO2 (a) de 7,0 (4,7-6,0 kPa), une PO2 (a) de 15,0 (> 8,7 kPa), un HCO3 de 19 (22-26 mmol/L), un excès de base de -6,6 (1,9-4,5 mmol/L), un Cl de 104 (98-107 mmol/L), et un lactate de 1,0 (0,4-1,3 mmol/L), ce qui correspond à une acidose respiratoire et métabolique mixte. L'hypercapnie était présumée être causée par l'absorption périopérative de gaz CO2 insufflé du péritoine dans le réseau capillaire. Une perfusion de norépinéphrine a été initiée à 0,04 mcg/kg/min, et la ventilation minute a été augmentée pour corriger l'acidose. Le segment de l'intestin grêle réduit a été réévalué et a été considéré comme encore viable, sans besoin de résection. Le défaut de hernie a été fermé avec des sutures primaires en utilisant une suture barbelée non absorbable, sans noeud (V-Loc) pour minimiser le temps de chirurgie en raison de la détérioration de l'état du patient.\n\nLa patiente a été extubée immédiatement après l'opération et a été observée dans l'unité de soins intensifs jusqu'au jour suivant. Les vasopresseurs et un tube nasogastrique de décompression ont été retirés le premier jour postopératoire. Elle a ensuite été transférée dans le service de chirurgie. La fonction intestinale a repris le deuxième jour postopératoire. Les antibiotiques ont été arrêtés le troisième jour postopératoire. Le même jour, elle a également été transférée dans le service de médecine pour une évaluation plus approfondie de sa perte de poids.",
+        "gold_summary": "Une femme de 80 ans ayant des antécédents de perte de poids involontaire s'est présentée au service des urgences en raison de douleurs aiguës dans la cuisse droite, de nausées et de vomissements. À l'examen, la patiente a présenté une sensibilité à la palpation dans la partie proximale et médiale de la cuisse droite. La tomographie par ordinateur abdominale a révélé une boucle de l'intestin grêle saillie dans le canal obturateur droit, compatible avec une hernie obturatrice incarnée. Une laparoscopie d'urgence a été réalisée, révélant que le segment de l'intestin grêle affecté était viable après réduction de la hernie. En raison du développement d'une acidose respiratoire et d'une hypotension, le défaut obturateur a été principalement suturé pour réduire le temps d'opération. La patiente a bien récupéré et a été transférée au service médical pour une évaluation plus approfondie de sa perte de poids.\n",
+        "synthetic_summary": {
+            "B1": "Une dame de 80 ans avait très mal à la cuisse droite. Elle avait aussi mal au ventre et vomissait. Les docteurs ont fait une photo spéciale de son ventre. Ils ont vu que un petit bout de son ventre était coincé dans un trou. \n\nIls ont fait une petite opération pour remettre ce bout à sa place. Après, elle a eu un peu de mal à respirer et son cœur battait vite. Les docteurs ont vite réparé le trou pour que ça aille mieux. \n\nLa dame a bien guéri. Ensuite, elle est allée voir d’autres docteurs pour comprendre pourquoi elle avait perdu du poids.",
+            "B2": "Une femme de 80 ans, qui avait perdu beaucoup de poids sans raison, est venue aux urgences parce qu’elle avait très mal à la cuisse droite, des nausées et des vomissements. Lors de l’examen, les médecins ont trouvé une zone très sensible à toucher sur le haut et l’intérieur de sa cuisse droite.\n\nPour comprendre ce qui se passait, ils ont fait un scanner (une sorte d’image détaillée à l’intérieur du corps). Ce scanner a montré qu’une partie de son intestin grêle était coincée dans un petit passage osseux appelé le canal obturateur, ce qui correspond à une hernie obturatrice. Une hernie, c’est quand un organe pousse à travers un trou ou un passage où il ne devrait pas être.\n\nLa patiente a donc subi une opération appelée laparoscopie, où les chirurgiens utilisent une petite caméra pour réparer la hernie. Ils ont réussi à remettre l’intestin à sa place, et celui-ci était encore en bonne santé, sans être abîmé.\n\nPendant l’opération, la patiente a eu des problèmes avec sa respiration et sa tension artérielle qui est devenue trop basse. Pour que l’opération soit plus rapide et moins risquée, les chirurgiens ont fermé le trou de la hernie avec des points de suture simples.\n\nAprès l’opération, la patiente s’est bien remise. Elle a été surveillée en soins intensifs puis transférée dans un service médical pour continuer à chercher la cause de sa perte de poids.",
+            "B3": "Contexte  \nUne femme de 80 ans, présentant une perte de poids involontaire importante, a été admise aux urgences pour des vomissements associés à une douleur aiguë, constante et localisée dans la partie proximale médiale de la cuisse droite, sans antécédent traumatique. Initialement, une radiographie de la hanche droite n’a montré ni fracture ni anomalie osseuse. Malgré une prise en charge symptomatique, ses douleurs et vomissements ont persisté, conduisant à plusieurs réadmissions. Une radiographie thoracique a révélé des signes d’infiltration pulmonaire, mais sans traitement antibiotique immédiat en raison de symptômes respiratoires minimes. Le quatrième jour, l’état général s’est aggravé avec fièvre, tachycardie, augmentation marquée de la CRP et suspicion de septicémie, justifiant une tomodensitométrie (TDM) thoraco-abdomino-pelvienne.\n\nPrincipales Observations  \nLa TDM a mis en évidence une hernie obturatrice aiguë irréductible, caractérisée par une boucle intestinale emprisonnée dans le canal obturateur droit, avec une dilatation intestinale pré-obstructive. Une intervention chirurgicale d’urgence par laparoscopie a été réalisée. L’exploration a confirmé la présence de l’intestin grêle incarcéré sans signes de nécrose ni de perforation. Après réduction de la hernie, la patiente a présenté une hypotension et une acidose respiratoire et métabolique mixte, probablement liée à l’absorption peropératoire de CO2 insufflé dans la cavité péritonéale. Une prise en charge hémodynamique par norépinéphrine et une adaptation de la ventilation ont permis de corriger ces troubles. Le défaut herniaire a été fermé par une suture primaire rapide avec un fil barbelé non résorbable afin de limiter la durée opératoire compte tenu de la dégradation de l’état clinique.\n\nInterprétation Clinique  \nCette présentation illustre une hernie obturatrice aiguë, une cause rare mais grave de douleur inguinale ou de cuisse chez la personne âgée, souvent difficile à diagnostiquer en raison de symptômes peu spécifiques. L’absence de traumatisme et la localisation précise de la douleur, associées à une obstruction intestinale sur imagerie, ont orienté vers ce diagnostic. La prise en charge chirurgicale rapide est essentielle pour éviter la nécrose intestinale. La survenue d’une acidose mixte et d’une hypotension en peropératoire souligne l’importance d’une surveillance anesthésique attentive et d’une gestion adaptée des complications métaboliques.\n\nProchaines Étapes  \nAprès une récupération postopératoire favorable, la patiente a été transférée en unité de soins intensifs pour surveillance rapprochée, puis en service de chirurgie. La reprise de la fonction intestinale a été rapide, et les antibiotiques ont été arrêtés au troisième jour postopératoire. Elle a ensuite été orientée vers le service médical pour une évaluation approfondie de sa perte de poids initiale, afin d’en identifier la cause sous-jacente et d’adapter la prise en charge globale. Cette démarche vise à prévenir d’autres complications et à améliorer son pronostic général."
+        }
+    },
+    {
+        "article": "Février 2020, un homme de 36 ans sans antécédents médicaux significatifs a présenté une masse pénos-scrotale gauche datant de 5 ans. Il n'a pas de symptômes du tractus urinaire inférieur. Il n'a pas d'antécédents de traumatisme ou d'infections et a nié toute histoire de perte de poids, d'anorexie ou de fièvre. À l'examen, il y a une surface lisse, une lésion kystique tendre d'environ 20 mm * 20 mm attachée au côté gauche de l'urètre bulbaire à la jonction pénos-scrotale, elle était profonde sans aucune traction de la peau et n'était pas liée au cordon spermatique gauche et elle était partiellement mobile.\n\nL'échographie Doppler a montré une masse hypoéchogène bien définie mesurant 2,7 * 3,1 * 2,0 cm avec une vascularisation significativement accrue à gauche de la jonction péno-scrotale. L'imagerie par résonance magnétique du bassin a révélé une masse dans le côté inféro-latéral gauche de la base du pénis avec un plan de graisse clair, qui est isointense aux testicules dans l'imagerie pondérée en T2, l'imagerie pondérée en T1 et l'imagerie pondérée en diffusion et elle était reliée au canal déférent, aucune lymphadénopathie n'a été notée. Les taux d'alpha-foetoprotéine et de bêta-gonadotrophine humaine étaient tous dans la plage normale. Compte tenu des résultats de l'examen et de la douleur ressentie par le patient, il a été décidé de procéder à l'ablation chirurgicale de la masse à des fins diagnostiques et thérapeutiques. Au cours de l'opération, une masse a été vue dans le côté postéro-latéral gauche du scrotum et elle a été complètement réséquée et envoyée pour l'histopathologie.\n\nL'histopathologie de la masse a montré un tumeur à cellules fusiformes disposées en faisceaux interlacés, les cellules ont des noyaux vésiculaires fusiformes à chromatine uniformément dispersée et des nucléoles peu visibles. La tumeur a montré une activité mitotique élevée atteignant 3/champ de haute puissance. L'analyse immunohistochimique était cohérente avec un sarcome synovial, révélant un TLE-1, CD99, lymphome à cellules B 2 (BLC2), cytokératine focale et antigène membranaire épithélial focal (EMA) positifs. Le matériel a été envoyé pour une hybridation in situ par fluorescence (FISH) et a révélé un réarrangement du gène SS18 à 18q11.2, qui a été observé dans les sarcomes synoviales. Les marges de la masse étaient difficiles à évaluer par histopathologie, car l'échantillon avait des marges fragmentées.\n\nLe patient s'est présenté à la clinique après 2 semaines et, après avoir reçu le rapport d'histopathologie, une ré-excision avec une marge plus large a été discutée avec le patient et il a accepté. Une tomographie par émission de positrons - tomographie par ordinateur (PET/CT) a été réalisée pour la tête et le cou, la poitrine, l'abdomen, le pelvis et les structures musculo-squelettiques. Seul un nodule thyroïdien de 29 * 27 mm dans le pôle inférieur du lobe thyroïdien gauche avec un hypermétabolisme modéré à des valeurs d'absorption standardisées (SUV) de 4,9. L'échographie thyroïdienne a montré un nodule solide isoéchogène bien défini dans le pôle inférieur du lobe thyroïdien gauche sans foyers échogènes. Le rapport d'imagerie et de données du système de thyroïde (TIRADS) était TR3.\n\nUne deuxième résection a été réalisée 3 semaines après la première. L'échantillon entier a été résectionné des deux cordes bilatéralement, ce qui a été approfondi jusqu'à atteindre le corps spongieux, qui a été rasé en haut jusqu'à l'urètre. L'échantillon a été envoyé pour une histopathologie. La masse résectionnée mesurait 6,0 × 6,0 × 3,0 cm et était négative pour toute pathologie. Le patient a ensuite été placé sous surveillance active et après 16 mois de surveillance active, il a été trouvé porteur de lésions métastatiques dans le sixième segment du foie et le corps vertébral L1. L'équipe d'oncologie a commencé un régime de chimiothérapie d'ifosfamide et de doxorubicine pendant 6 cycles sans amélioration de la lésion du foie. Une résection chirurgicale a été réalisée pour les cinquième et sixième sections du foie avec cholécystectomie. Le patient a ensuite développé une nouvelle lésion pulmonaire et a commencé un traitement par pazopanib et une radiothérapie stéréotaxique du corps. Le patient a ensuite été soumis à une surveillance pendant 6 mois, puis a développé de nouvelles lésions du foie et des poumons, puis un régime de chimiothérapie de gemcitabine et de docétaxel pour 3 cycles et a progressé, puis a commencé 2 cycles de dacarbazine et a progressé, puis 2 cycles de pembrolizumab et a progressé. Le patient a ensuite été transféré en soins palliatifs et a cessé de suivre le traitement.\n",
+        "gold_summary": "Un homme de 36 ans a présenté une masse péno-scrotale tendre pendant 5 ans. Le patient a subi une résection chirurgicale de la masse. L'histopathologie a révélé une tumeur à cellules fusiformes organisées en faisceaux entrelacés. L'analyse immunohistochimique a révélé un TLE-1, CD99, lymphome à cellules B 2 (BLC2), cytokératine focale et antigène membranaire épithélial focal (EMA) positifs. Dans notre cas, le patient a été agressivement traité avec deux résections chirurgicales et a malgré tout progressé et a métastasé et a continué à progresser même après différents régimes de chimiothérapie.\n",
+        "synthetic_summary": {
+            "B1": "Un homme avait une grosse boule douce depuis longtemps. Les docteurs ont enlevé cette boule avec une opération. Ils ont regardé la boule au microscope et ont vu que c’était une maladie avec des cellules qui ne sont pas normales. \n\nMême après deux opérations et plusieurs traitements, la maladie est restée et a commencé à aller dans d’autres parties du corps. Les docteurs ont essayé beaucoup de médicaments, mais la maladie a continué à grandir.",
+            "B2": "### Ce qu'ils ont trouvé\n\nUn homme de 36 ans avait une grosseur douloureuse au niveau du pénis et du scrotum depuis 5 ans. Les médecins ont décidé d’enlever cette masse par chirurgie pour savoir ce que c’était. En regardant la masse au microscope, ils ont vu qu’elle était composée de cellules allongées (appelées cellules fusiformes) organisées en faisceaux. Des tests spéciaux ont montré que cette masse était un sarcome synovial, un type rare de tumeur cancéreuse.\n\n### Ce que cela signifie\n\nMalgré deux opérations pour enlever la tumeur, le cancer a continué à se propager dans d’autres parties du corps, comme le foie et les poumons. Le patient a aussi reçu plusieurs traitements de chimiothérapie, mais la maladie a continué à évoluer. Finalement, il a dû arrêter les traitements actifs et passer en soins palliatifs, qui visent à soulager les symptômes.\n\n### En résumé\n\nCette histoire montre qu’un sarcome synovial peut être difficile à traiter, même avec des opérations et des médicaments puissants. C’est une tumeur rare qui peut se propager rapidement et nécessite une surveillance attentive.",
+            "B3": "Résumé détaillé et structuré :\n\n**Contexte**  \nUn homme de 36 ans, sans antécédents médicaux notables, a consulté pour une masse indolore et tendre située à la jonction péno-scrotale gauche, présente depuis environ cinq ans. Il ne présentait aucun symptôme urinaire, ni antécédent de traumatisme ou d’infection, et aucun signe général tel que perte de poids ou fièvre. L’examen clinique a révélé une lésion kystique profonde, partiellement mobile, attachée au côté gauche de l’urètre bulbaire, sans adhérence à la peau ni au cordon spermatique.\n\n**Principales observations**  \nL’échographie Doppler a montré une masse hypoéchogène bien délimitée, d’environ 2,7 × 3,1 × 2,0 cm, avec une vascularisation accrue. L’IRM pelvienne a confirmé la présence d’une masse isointense aux testicules, localisée au côté inféro-latéral gauche de la base du pénis, en contact avec le canal déférent, sans atteinte ganglionnaire. Les marqueurs tumoraux sériques (alpha-foetoprotéine et bêta-hCG) étaient normaux.\n\nUne intervention chirurgicale a été réalisée pour retirer la masse à des fins diagnostiques et thérapeutiques. L’analyse histopathologique a montré une tumeur composée de cellules fusiformes organisées en faisceaux entrelacés, avec une activité mitotique élevée (3 mitoses par champ de haute puissance). L’immunohistochimie a révélé une expression positive de TLE-1, CD99, BCL2, cytokératine focale et antigène membranaire épithélial (EMA), caractéristiques d’un sarcome synovial. La confirmation moléculaire par hybridation in situ en fluorescence (FISH) a mis en évidence un réarrangement du gène SS18, typique de cette tumeur. Les marges chirurgicales étaient fragmentées, rendant leur évaluation difficile.\n\nAprès deux semaines, une réexcision avec marges plus larges a été proposée et acceptée par le patient. Un PET/CT a révélé un nodule thyroïdien modérément hypermétabolique, classé TR3 au TIRADS, sans autre localisation suspecte. La deuxième chirurgie a consisté en une résection étendue jusqu’au corps spongieux et à l’urètre, avec un prélèvement complet des tissus concernés. L’analyse histologique n’a montré aucune tumeur résiduelle.\n\n**Interprétation clinique**  \nMalgré une prise en charge chirurgicale agressive avec deux résections complètes, le patient a développé, après 16 mois de surveillance, des métastases hépatiques et vertébrales. Le traitement systémique par chimiothérapie (ifosfamide et doxorubicine) n’a pas permis de contrôler la progression hépatique. Une résection hépatique a été réalisée, suivie d’une apparition de lésions pulmonaires traitées par pazopanib (un inhibiteur de tyrosine kinase) et radiothérapie stéréotaxique. La maladie a continué à évoluer avec l’apparition de nouvelles métastases hépatiques et pulmonaires, malgré plusieurs lignes de chimiothérapie (gemcitabine-docétaxel, dacarbazine) et immunothérapie (pembrolizumab). Finalement, le patient a été orienté vers des soins palliatifs.\n\n**Prochaines étapes**  \nCe cas illustre la nature agressive et récidivante du sarcome synovial, même après un traitement chirurgical complet et des protocoles chimiothérapeutiques multiples. La surveillance régulière et multidisciplinaire est essentielle. Le pronostic reste réservé en cas de métastases, soulignant la nécessité de nouvelles approches thérapeutiques pour ce type de tumeur rare."
+        }
+    },
+    {
+        "article": "Une Chinoise de 30 ans a présenté une masse ovarienne gauche lors d'un examen physique de routine. Elle était asymptomatique et n'avait pas d'antécédents médicaux de tumeurs cérébrales ou de troubles neurologiques. La patiente souffrait d'ovaires polykystiques à l'âge de 19 ans sans aucun traitement. Les taux sériques de CEA, CA125 et CA19-9 étaient dans les limites normales.\n\nUne IRM a révélé une lésion hypointense pondérée en T1 et hyperintense pondérée en T2 mesurant 6,3 × 4,8 cm dans la région adnexale gauche, avec un nodule de fixation mural à signal légèrement inférieur. En outre, l'image pondérée en diffusion (DWI) a montré un signal isointense des nodules muraux. Par conséquent, il a été considéré comme une tumeur bénigne ou limite.\n\nLa patiente a subi une résection laparoscopique de l'ovaire gauche et de la trompe de Fallope. Au cours des 12 mois de suivi, elle a subi des examens d'échographie pelvienne et abdominale tous les trois mois, et aucune anomalie n'a été détectée. Elle est restée en bonne condition après la chirurgie sans chimiothérapie.\n\nConstatations pathologiques\nL'examen macroscopique a révélé une masse kystique de 5 × 3,5 × 1 cm dans l'ovaire gauche. Deux nodules muraux de 0,8 cm et 1,2 cm de diamètre ont été observés, de couleur rouge-gris et de texture molle. L'examen histologique a révélé un nodule bien défini sous faible grossissement. Les composants du tératome comprenaient l'épiderme, des appendices cutanés étaient visibles dans le nodule mural environnant et le tissu de la paroi du kyste. Sous fort grossissement, il a révélé des cellules gliales désordonnées et des ganglions proliférant dans le nodule mural. Des ganglions anormaux ont été agrégés, avec un noyau de grande taille et irrégulier, qui présentait également des nucléoles évidents, et des cellules binucléées ont été observées. Les figures mitotiques ont été difficilement identifiées.\n\nImmunohistochimiquement, les cellules gliales étaient positives pour GFAP et Olig2. Les cellules ganglionnaires étaient positives pour Neu-N, CgA, Nestin et CR. En outre, les cellules ganglionnaires exprimaient CD34 et mettaient en évidence les cellules tumorales ramifiées. Une faible expression de NSE et une expression de P53 de type sauvage ont été observées dans certaines cellules tumorales. En outre, les cellules tumorales étaient négatives pour IDH1 et BRAF V600E. L'indice Ki67 était d'environ 5 %. Sur la base de ces résultats, un diagnostic de gangliogliome résultant d'un tératome kystique mature ovarien a été établi.\n",
+        "gold_summary": "La patiente, une femme de 30 ans sans antécédents médicaux de tumeurs cérébrales ou de troubles neurologiques, a présenté une masse kystique dans l'ovaire gauche, accompagnée de deux nodules muraux. D'un point de vue histologique, le nodule mural du tératome présentait une combinaison de cellules ganglionnaires et gliales néoplasiques. Notamment, les cellules ganglionnaires présentaient une binucléation et une distribution focale, avec la présence occasionnelle de corps de Nissl. Immunohistochimiquement, GFAP et Olig2 étaient positifs dans les cellules gliales, la chromogranine A (CgA), Nestin, CD34, Neu-N et Calretinin (CR) étaient positifs dans les cellules ganglionnaires. Les cellules tumorales présentaient un faible indice Ki67, une expression de P53 de type sauvage et étaient négatives pour IDH1 et BRAF V600E. La patiente a subi une résection laparoscopique de l'ovaire gauche et de la trompe de Fallope et elle était en bonne condition à 12 mois de suivi.\n",
+        "synthetic_summary": {
+            "B1": "Une dame avait une petite boule dans son ventre. Cette boule venait d’un petit sac dans son corps appelé l’ovaire. \n\nLes docteurs ont enlevé cette boule avec une petite opération. Après, la dame allait bien et n’avait plus de problème. \n\nDans la boule, il y avait des petites cellules différentes, mais elles n’étaient pas méchantes. Tout est bien passé et la dame est restée en bonne santé.",
+            "B2": "Une femme chinoise de 30 ans a découvert une masse dans son ovaire gauche lors d’un examen médical de routine. Elle n’avait aucun symptôme ni antécédent de tumeur au cerveau ou de problème neurologique. Cette masse était un kyste avec deux petites excroissances appelées nodules sur sa paroi.\n\nQuand les médecins ont examiné ces nodules au microscope, ils ont vu qu’ils contenaient deux types de cellules : des cellules gliales et des cellules ganglionnaires. Les cellules gliales sont des cellules qui soutiennent les neurones dans le cerveau, et les cellules ganglionnaires sont des cellules nerveuses. Certaines cellules ganglionnaires avaient deux noyaux, ce qui est inhabituel, et on a aussi vu des petites structures appelées corps de Nissl, typiques des neurones.\n\nPour mieux comprendre la nature de ces cellules, les médecins ont utilisé des tests spéciaux appelés immunohistochimie. Ces tests montrent quels types de protéines les cellules fabriquent. Les cellules gliales étaient positives pour des protéines nommées GFAP et Olig2, tandis que les cellules ganglionnaires montraient des protéines comme la chromogranine A, Nestin, CD34, Neu-N et Calrétinine. Ces résultats ont aidé à confirmer que la masse était un gangliogliome, une tumeur rare composée de ces deux types de cellules nerveuses, qui s’est développée à partir d’un tératome kystique mature de l’ovaire (un type de tumeur ovarienne contenant différents tissus).\n\nLa patiente a subi une chirurgie par laparoscopie pour enlever l’ovaire gauche et la trompe de Fallope. Après 12 mois de suivi avec des échographies régulières, elle allait bien et aucune nouvelle anomalie n’a été détectée. Aucun traitement supplémentaire comme la chimiothérapie n’a été nécessaire.",
+            "B3": "Résumé détaillé et structuré pour un public adulte non spécialiste\n\nContexte  \nUne femme chinoise de 30 ans, sans antécédents de tumeurs cérébrales ni troubles neurologiques, a découvert lors d’un examen médical de routine une masse kystique au niveau de son ovaire gauche. Elle avait des antécédents d’ovaires polykystiques à l’âge de 19 ans, non traités. Les marqueurs tumoraux sanguins classiques (CEA, CA125, CA19-9) étaient normaux. Une imagerie par résonance magnétique (IRM) a montré une lésion de 6,3 × 4,8 cm dans la région de l’ovaire gauche, avec des caractéristiques suggérant une tumeur bénigne ou à potentiel limité de malignité.\n\nPrincipales observations  \nLa patiente a subi une intervention chirurgicale par laparoscopie pour retirer l’ovaire gauche et la trompe de Fallope. L’examen macroscopique a révélé une masse kystique de 5 × 3,5 × 1 cm comportant deux nodules muraux rouges-gris, mous, mesurant 0,8 cm et 1,2 cm. L’analyse histologique a montré que ces nodules contenaient des éléments typiques d’un tératome mature (une tumeur composée de différents types de tissus, ici notamment de l’épiderme et des annexes cutanées), mais aussi une prolifération anormale de cellules gliales (cellules du système nerveux) et de cellules ganglionnaires (neurones). Ces cellules ganglionnaires présentaient des caractéristiques atypiques, comme la présence de deux noyaux (binucléation) et des noyaux volumineux et irréguliers. Les figures de division cellulaire (mitoses) étaient rares.\n\nL’étude immunohistochimique, qui utilise des marqueurs spécifiques pour identifier les types cellulaires, a confirmé la nature nerveuse de la tumeur : les cellules gliales exprimaient GFAP et Olig2, tandis que les cellules ganglionnaires étaient positives pour Neu-N, chromogranine A (CgA), Nestin, calrétinine (CR) et CD34. Certaines cellules tumorales montraient une faible activité de prolifération (indice Ki67 d’environ 5 %) et une expression normale de la protéine P53, sans mutation des gènes IDH1 et BRAF V600E, ce qui est rassurant quant à l’agressivité tumorale. Ces caractéristiques ont permis de diagnostiquer un gangliogliome, une tumeur rare composée de cellules nerveuses gliales et ganglionnaires, développée à partir d’un tératome kystique mature de l’ovaire.\n\nInterprétation clinique  \nCe cas illustre une tumeur ovarienne très rare, où un gangliogliome s’est formé à l’intérieur d’un tératome mature. Le gangliogliome est habituellement une tumeur du système nerveux central, mais ici il est survenu dans un tissu ovarien. La faible activité proliférative et l’absence de mutations génétiques associées à des formes plus agressives suggèrent un pronostic favorable.\n\nProchaines étapes  \nAprès la chirurgie, la patiente a été suivie régulièrement par échographie pelvienne et abdominale tous les trois mois pendant un an. Aucun signe de récidive ou de complication n’a été détecté, et elle est restée en bonne santé sans avoir nécessité de traitement complémentaire comme la chimiothérapie. Un suivi prolongé reste cependant recommandé pour surveiller toute éventuelle récidive."
+        }
+    },
+    {
+        "article": "Femme de 76 ans, de nationalité paraguayenne, résidant à Buenos Aires, sans antécédents de voyages récents, ayant des antécédents de sténose aortique et d’hypertension artérielle, traitement habituel : bisoprolol. Elle a commencé à présenter des symptômes 5 jours avant son admission, avec une fièvre, une toux avec expectoration mucopurulente et une dyspnée qui a progressé jusqu’à la classe fonctionnelle III-IV, des douleurs abdominales et des céphalées. Elle a été traitée en ambulatoire 48 heures avant son admission avec de l’amoxicilline-acide clavulanique ; un test SARS-CoV-2, un virus de la grippe A et B et un virus respiratoire syncytial ont été effectués par réaction en chaîne de la polymérase, qui s’est avéré négatif. Elle a consulté l’hôpital pour une dyspnée de classe fonctionnelle IV, des nausées et des douleurs abdominales, une tomographie axiale assistée par ordinateur (TAC) a été réalisée, qui a mis en évidence un infiltrat interstitiel bilatéral. Admise à l’unité de soins intensifs le 30 mars 2023, avec un choc septique secondaire à un foyer respiratoire, une fièvre de 38 °C, 120 battements par minute et une acidose, les scores de gravité SOFA (Sepsis Related Organ Failures Assesment) ont totalisé 7 points et APACHE II (Acute Physiology and Cronic Health Classification System II) 21 points. Une réanimation a été initiée avec des fluides, des analyses cliniques ont été effectuées, qui ont mis en évidence une hématocrite élevée, une hémoconcentration, une leucocytose et une insuffisance rénale aiguë, des échantillons ont été prélevés pour des hémocultures, des cultures d’urine et des cultures respiratoires. Des échantillons ont été envoyés au laboratoire de virologie sanguine pour les virus dengue et CHIKV. Une échocardiographie a été réalisée en mode point of care ultrasound (POCUS) qui a mis en évidence une sténose aortique modérée, avec une vitesse de pointe de 3,4 m/seconde, une fonction systolique du ventricule gauche préservée, sans altération de la mobilité segmentaire, sans signe d’insuffisance cardiaque aiguë, aucune végétation n’a été observée sur les valves par cette approche. Un traitement a été initié avec des antibiotiques à large spectre : ceftriaxone et vancomycine. Elle a évolué avec une progression des insuffisances respiratoires, hémodynamiques et rénales. Elle a nécessité une ventilation mécanique, des vasopresseurs à haute dose, une perfusion de furosémide pour oligurie, un choc réfractaire, et elle est décédée le 31 mars 2023. Les cultures bactériologiques de sang, d’urine et de sécrétions trachéales ont conclu sans développement bactérien, réaction en chaîne de la polymérase en temps réel et antigène NS1 non détectable pour virus dengue, et réaction en chaîne de la polymérase en temps réel pour CHIKV détectable dans le sérum.\n",
+        "gold_summary": "C'est le cas d'une femme de 76 ans, ayant des antécédents d'hypertension artérielle et de sténose aortique, admise en soins intensifs pour un choc septique avec foyer respiratoire, avec un modèle de pneumonie interstitielle, une évolution torpide et un décès dans les 24 heures suivant l'admission. Le résultat détectable du virus Chikungunya par réaction en chaîne de la polymérase en temps réel a été reçu post mortem.\n",
+        "synthetic_summary": {
+            "B1": "Une dame de 76 ans était très malade. Elle avait de la fièvre et du mal à respirer. \n\nElle est allée à l’hôpital. Les docteurs ont trouvé un gros problème dans ses poumons. \n\nIls ont cherché un virus et ont trouvé un virus appelé Chikungunya. \n\nMalheureusement, elle est morte très vite après être arrivée à l’hôpital. \n\nLes docteurs ont fait tout leur possible pour l’aider.",
+            "B2": "Cas d’une femme de 76 ans avec des problèmes de santé connus, comme l’hypertension artérielle (pression élevée) et une sténose aortique (rétrécissement d’une valve du cœur). Elle a été admise aux soins intensifs car elle avait une infection grave qui a provoqué un choc septique, c’est-à-dire que son corps réagissait très fort à une infection, ce qui a affecté ses poumons avec une pneumonie interstitielle (inflammation dans les tissus autour des alvéoles pulmonaires). Malgré les soins, son état s’est rapidement aggravé et elle est décédée moins de 24 heures après son arrivée à l’hôpital. Après son décès, les médecins ont découvert la présence du virus Chikungunya dans son sang grâce à un test appelé réaction en chaîne de la polymérase (PCR), qui sert à détecter le matériel génétique du virus. Cela signifie que cette infection virale a probablement joué un rôle important dans sa maladie grave.",
+            "B3": "Résumé détaillé et structuré pour un public adulte non spécialiste\n\nContexte  \nIl s’agit d’une femme de 76 ans, originaire du Paraguay et vivant à Buenos Aires, présentant des antécédents médicaux importants, notamment une sténose aortique (rétrécissement de la valve aortique du cœur) et une hypertension artérielle. Elle était sous traitement par bisoprolol. Cinq jours avant son admission à l’hôpital, elle a développé une fièvre, une toux avec expectoration mucopurulente (crachats contenant du mucus et du pus), une difficulté respiratoire progressive (dyspnée), des douleurs abdominales et des maux de tête. Un traitement antibiotique ambulatoire par amoxicilline-acide clavulanique avait été prescrit, sans amélioration. Les tests virologiques initiaux pour le SARS-CoV-2, la grippe A et B, ainsi que le virus respiratoire syncytial étaient négatifs.\n\nPrincipales observations  \nÀ son admission, la patiente présentait une dyspnée sévère (classe fonctionnelle IV), des nausées, des douleurs abdominales et une fièvre à 38 °C. Une tomodensitométrie thoracique a révélé un infiltrat interstitiel bilatéral, signe d’une pneumonie touchant les deux poumons. Elle a été admise en unité de soins intensifs pour un choc septique (une défaillance circulatoire grave liée à une infection) d’origine respiratoire. Les scores de gravité étaient élevés (SOFA à 7 points, APACHE II à 21 points), témoignant d’une maladie sévère. Les analyses sanguines montraient une hémoconcentration (augmentation de la concentration des cellules sanguines), une leucocytose (augmentation des globules blancs) et une insuffisance rénale aiguë. Une échocardiographie réalisée au lit du patient confirmait une sténose aortique modérée sans signes d’insuffisance cardiaque aiguë ni d’infection valvulaire. Des prélèvements pour cultures bactériennes (sang, urine, sécrétions respiratoires) et pour recherche virale (dengue et chikungunya) ont été effectués.\n\nInterprétation clinique  \nMalgré une prise en charge intensive comprenant des antibiotiques à large spectre (ceftriaxone et vancomycine), une réanimation hémodynamique, une ventilation mécanique et un traitement diurétique, l’état de la patiente s’est rapidement aggravé avec une défaillance multiviscérale (respiratoire, circulatoire et rénale). Elle a développé un choc réfractaire, c’est-à-dire un état de défaillance circulatoire résistant aux traitements, et est décédée moins de 24 heures après son admission. Les cultures bactériennes sont restées négatives, excluant une infection bactérienne détectable. En revanche, la réaction en chaîne de la polymérase en temps réel (PCR) a détecté la présence du virus chikungunya dans le sérum, tandis que les tests pour le virus de la dengue étaient négatifs.\n\nProchaines étapes et conclusion  \nCe cas illustre une forme sévère et rapidement fatale d’infection par le virus chikungunya, qui peut se manifester par un syndrome de choc septique avec atteinte pulmonaire interstitielle et défaillance multiviscérale, même en l’absence de co-infection bactérienne détectable. Il souligne l’importance de considérer les infections virales tropicales émergentes dans le diagnostic différentiel des syndromes septiques, surtout dans les régions où ces virus sont endémiques ou en cas de mobilité internationale. La détection post mortem du virus chikungunya suggère que cette infection a été le facteur déclenchant principal de la dégradation clinique. Une vigilance accrue et une prise en charge adaptée sont nécessaires pour améliorer le pronostic dans de tels cas."
+        }
+    },
+    {
+        "article": "Il s’agit d’un garçon de 16 ans qui, dans les mois précédant la consultation, souffre occasionnellement de paralysies du sommeil, quelques minutes après le début de la sieste postprandiale, qui lui causent beaucoup d’anxiété, principale raison pour laquelle il se rend à la consultation. Ces paralysies du sommeil sont parfois accompagnées d’hallucinations hypnopompiques (qu’il attribue à des rêves ou au fait de ne pas être complètement éveillé). Il a un horaire de sommeil nocturne d’environ sept heures, plus deux heures de sieste qui lui procurent beaucoup de repos. Il a de bonnes performances scolaires. Lorsqu’il a fait une anamnèse ciblée, il a déclaré qu’après avoir souffert de ces paralysies du sommeil pendant des mois, il a eu des épisodes de secousses des bras et des jambes, surtout quand il riait, qui l’ont presque fait tomber (il pensait que cela arrivait à tout le monde). Par la suite, ces symptômes ont été rejoints par environ trois réveils nocturnes de courte durée, avec une réconciliation immédiate et occasionnelle, et des attaques de sommeil le matin, qu’il relie aux cours de mathématiques (le professeur est très ennuyeux). Après la suspicion clinique, nous avons demandé un test de latences multiples du sommeil et une étude polysomnographique nocturne, qui sont concluants avec le diagnostic de narcolepsie (latence de sommeil très courte, latence de sommeil REM avancée, sommeil quelque peu fragmenté, moyenne dans le test de latences multiples du sommeil de 2,1 minutes et présence de quatre REM au début du sommeil). Étant donné que ces épisodes de somnolence lui arrivent tous les jours à la même heure, nous lui avons prescrit une sieste matinale brève qui, au début, l’a beaucoup rafraîchi et il a déclaré pouvoir continuer ses activités scolaires. Par la suite, nous avons ajouté modafinil à la même heure (200 mg). Nous lui avons recommandé la venlafaxine pour les cataplexies ou même un traitement à l’oxybate de sodium (ce dernier refuse de le prendre à cause de l’inconfort de la deuxième dose, et la venlafaxine refuse également à cause de la peur des effets secondaires). Nous avons convenu qu’il se conformerait à une bonne hygiène du sommeil, prendrait le modafinil et continuerait les siestes programmées (la sieste du soir qu’il faisait déjà et la sieste du matin). Et, s’il empire, nous ajouterons d’autres traitements. Il se porte bien avec cette routine, ne ressent pas beaucoup de fragmentation du sommeil nocturne (un ou deux réveils très brefs après lesquels il se rendort sans problème) ; en fait, il se réveille reposé, les cataplexies sont occasionnelles et ne le gênent pas dans son quotidien, et les crises de sommeil sont très contrôlées. Il se sent mieux et sans grandes limitations dans sa vie quotidienne (bon rendement scolaire, il ne boit pas d’alcool, mais cela ne l’affecte pas non plus, car il n’a jamais bu, il a des horaires de sommeil réguliers et fait de l’activité physique régulière).\n",
+        "gold_summary": "Homme de 16 ans consultant après avoir consulté différents spécialistes en raison de paralysies du sommeil pendant les siestes, qui lui causaient de la peur et occasionnellement la chute d'objets de ses mains (diagnostiquées comme possibles myoclonies). Dans l'anamnèse, nous avons été surpris par la présence de paralysies du sommeil immédiatement après le début des siestes et, dans l'anamnèse dirigée, ces mouvements brusques provoqués par des émotions étaient compatibles avec des cataplexies, nous avons donc réalisé une étude polysomnographique nocturne et un test de latences multiples du sommeil. Avec l'évolution, des hallucinations hypnopomphiques et un sommeil fragmenté nocturne sont apparus, ainsi qu'une somnolence diurne occasionnelle (la tétrade symptomatologique typique de la narcolepsie avec cataplexie de type 1 a été complétée).\n",
+        "synthetic_summary": {
+            "B1": "Il y a un garçon de 16 ans. Parfois, quand il fait une sieste, il ne peut pas bouger. Ça lui fait un peu peur.\n\nParfois, ses bras et ses jambes bougent tout seuls quand il rit. Ça peut le faire tomber.\n\nLe docteur a fait des examens pour comprendre. Le garçon a un problème qui s’appelle narcolepsie.\n\nIl dort mal la nuit et il est très fatigué le jour. Le docteur lui a donné des siestes et un médicament.\n\nMaintenant, il va mieux. Il peut continuer l’école et jouer sans trop de soucis.",
+            "B2": "Un garçon de 16 ans est venu consulter parce qu’il avait souvent des paralysies du sommeil pendant ses siestes. Ces paralysies, c’est quand on ne peut pas bouger en s’endormant ou en se réveillant, ce qui lui faisait peur. Parfois, il laissait tomber des objets à cause de secousses dans ses mains, appelées myoclonies, qui sont des mouvements brusques involontaires.\n\nLors de l’entretien, on a remarqué que ces paralysies arrivaient juste après le début de ses siestes. Il avait aussi des mouvements soudains quand il riait, ce qui correspond à des cataplexies. Les cataplexies sont des pertes temporaires de force dans certains muscles, souvent déclenchées par des émotions fortes.\n\nPour mieux comprendre ses symptômes, les médecins ont fait deux examens du sommeil : une étude polysomnographique la nuit et un test de latences multiples du sommeil. Ces tests ont montré qu’il avait un sommeil fragmenté, des hallucinations en s’endormant ou en se réveillant (appelées hallucinations hypnopompiques), et une somnolence pendant la journée.\n\nTous ces signes ensemble forment ce qu’on appelle la narcolepsie de type 1 avec cataplexie. C’est une maladie du sommeil où la personne s’endort trop facilement et a des épisodes de faiblesse musculaire liés aux émotions. Grâce au diagnostic, il a pu commencer un traitement adapté pour mieux gérer ses symptômes.",
+            "B3": "Résumé destiné à un public non spécialiste\n\nContexte  \nUn garçon de 16 ans a consulté après avoir souffert pendant plusieurs mois de paralysies du sommeil survenant quelques minutes après le début de ses siestes postprandiales (après le repas). Ces épisodes provoquaient chez lui une grande anxiété. Par ailleurs, il rapportait parfois des hallucinations au réveil (hallucinations hypnopompiques), qu’il attribuait à des rêves ou à un état de semi-éveil. Il avait un rythme de sommeil nocturne d’environ sept heures, complété par deux heures de sieste, ce qui lui assurait un bon repos. Ses résultats scolaires étaient bons.\n\nPrincipales observations  \nAu cours de l’anamnèse approfondie, le patient a décrit des secousses soudaines des bras et des jambes, surtout lors d’épisodes de rire, qui le faisaient presque tomber. Ces mouvements brusques, initialement considérés comme des myoclonies (contractions musculaires involontaires), ont été réinterprétés comme des cataplexies, c’est-à-dire des pertes soudaines de tonus musculaire déclenchées par des émotions. Par la suite, il a présenté des réveils nocturnes brefs et occasionnels ainsi que des épisodes de somnolence matinale, notamment en classe de mathématiques.\n\nInterprétation clinique  \nDevant ce tableau associant paralysies du sommeil, hallucinations hypnopompiques, cataplexies et somnolence diurne, les médecins ont suspecté une narcolepsie de type 1. Cette maladie neurologique se caractérise par une somnolence excessive durant la journée et des troubles spécifiques du sommeil paradoxal (REM). Les examens complémentaires réalisés — une polysomnographie nocturne et un test de latences multiples du sommeil — ont confirmé ce diagnostic. Ces tests ont montré une latence très courte avant l’endormissement, une apparition précoce du sommeil paradoxal, un sommeil nocturne fragmenté, ainsi qu’une moyenne de latence de sommeil diurne très basse (2,1 minutes) avec plusieurs épisodes de sommeil paradoxal au début du sommeil.\n\nProchaines étapes et prise en charge  \nPour gérer ses symptômes, une sieste matinale courte a été prescrite, ce qui a amélioré sa vigilance et sa capacité à suivre ses cours. Un traitement médicamenteux par modafinil (200 mg) a été ajouté pour lutter contre la somnolence diurne. Des options thérapeutiques pour les cataplexies, comme la venlafaxine ou l’oxybate de sodium, ont été proposées, mais le patient a refusé ces traitements en raison de la crainte des effets secondaires ou de l’inconfort lié à la prise. Il a été conseillé de maintenir une bonne hygiène du sommeil et de continuer les siestes programmées. Actuellement, il se sent bien, avec un sommeil nocturne peu fragmenté, des cataplexies occasionnelles sans impact majeur sur sa vie quotidienne, et une somnolence diurne bien contrôlée. Son rendement scolaire reste bon, il ne consomme pas d’alcool, suit des horaires réguliers de sommeil et pratique une activité physique régulière.\n\nEn résumé, ce cas illustre une narcolepsie de type 1 chez un adolescent, diagnostiquée grâce à une évaluation clinique précise et des examens spécialisés, avec une prise en charge adaptée combinant hygiène du sommeil, siestes programmées et traitement médicamenteux."
+        }
+    },
+    {
+        "article": "Un nouveau-né de 3050 g à terme est né après une grossesse sans complication d'une femme primipare de 20 ans à 39 semaines de grossesse. La grossesse était sans complication. L'accouchement n'a pas été prolongé avec un accouchement vaginal spontané sans incident. Les scores d'Apgar étaient de 8 et 9 à 1 min et 5 min, respectivement, avec un score de grimace normal de 2. Son Apgar est resté à 9 à 10 et 20 minutes. Il était alerte avec un bon cri, une couleur rose, une fréquence cardiaque de 134 et une fréquence respiratoire de 56. Il a reçu de la vitamine K à la naissance. Il s'est présenté à notre hôpital avec un refus de téter pendant trois jours à l'âge de 29 jours. La famille a également déclaré qu'il avait eu des vomissements intermittents depuis la naissance. Sinon, il n'y avait pas d'antécédents de diathèse hémorragique, de fièvre, de raideur du cou ou de convulsions. À la présentation, il avait une fontanelle antérieure bombée. Moro était incomplet ; la succion n'a pas été soutenue mais un bon tonus musculaire a été noté dans toutes les extrémités. Son compte sanguin complet (CBC) et son profil de coagulation étaient normaux. L'IRM du cerveau a montré une convexité cérébrale bilatérale T1WI et T2WI hyperintense mesurant 2 cm avec une extension supracerebrale et péraciduculaire. En outre, l'obliteration du quatrième ventricule et la dilatation du troisième ventricule et du ventricule latéral ont également été notées. Sous anesthésie générale, le patient a été placé en position ventrale en utilisant une incision cutanée médiane, une craniostomie bilatérale a été réalisée. Après l'ouverture de la dure-mère dans une incision cruciforme, une membrane épaisse et bien définie ; avec du sang hémolysé sombre est sorti sous pression. En chirurgie, le patient a eu un arrêt cardiaque pour lequel un cycle de réanimation cardiopulmonaire (RCP) a été effectué et un retour de la circulation spontanée a été obtenu. Après cela, la peau a été fermée, un drain sous-dural a été placé et le patient a été extubé et transféré à l'unité de soins intensifs (USI). Le scanner CT de contrôle effectué le 3e jour postopératoire a montré une évacuation complète de l'hématome et une amélioration de l'hydrocéphalie. Le patient a été libéré le 7e jour postopératoire. Le premier mois de suivi postopératoire a été sans incident avec des jalons de développement normaux atteints pour son âge.\n",
+        "gold_summary": "Un nouveau-né de sexe masculin âgé de vingt-neuf jours a présenté un échec de la succion pendant trois jours associé à des vomissements. L'imagerie a montré un hématome sous-dural chronique bilatéral postérieur et une hydrocéphalie obstructive. Une craniostomie bilatérale et une évacuation de l'hématome ont été effectuées, ce qui a donné un excellent résultat.\n",
+        "synthetic_summary": {
+            "B1": "Un petit bébé de 29 jours avait du mal à boire son lait. Il vomissait aussi souvent. Les docteurs ont fait une photo de sa tête. Ils ont vu du sang qui appuyait sur son cerveau. Ils ont fait une petite opération pour enlever ce sang. Après, le bébé allait beaucoup mieux. Il a bien grandi et joué comme les autres enfants.",
+            "B2": "Un bébé garçon de 29 jours avait du mal à téter depuis trois jours et vomissait parfois. Une image médicale (IRM) a montré qu’il avait un hématome sous-dural chronique, c’est-à-dire une accumulation de sang entre le cerveau et sa membrane, des deux côtés à l’arrière de la tête. Cette accumulation bloquait aussi la circulation normale du liquide dans son cerveau, provoquant une hydrocéphalie, c’est-à-dire un gonflement des ventricules cérébraux. Pour le soigner, les médecins ont fait une opération appelée craniostomie bilatérale, où ils ont ouvert le crâne de chaque côté pour enlever le sang accumulé. Après cette intervention, le bébé s’est bien rétabli et a pu être libéré de l’hôpital avec un bon développement.",
+            "B3": "Résumé détaillé destiné à un adulte éduqué non-médecin\n\n**Contexte**  \nUn nouveau-né de sexe masculin, né à terme à 39 semaines de grossesse avec un poids de 3050 grammes, a présenté un développement initial sans complication. La grossesse et l’accouchement vaginal spontané se sont déroulés normalement, avec des scores d’Apgar (évaluation rapide de l’état du nouveau-né) de 8 à 1 minute et 9 à 5 minutes, indiquant une bonne adaptation à la vie extra-utérine. À la naissance, le bébé était alerte, avec une bonne coloration de la peau, une fréquence cardiaque et respiratoire normales, et il a reçu la vitamine K pour prévenir les saignements.\n\n**Principales observations**  \nÀ l’âge de 29 jours, le nourrisson a été amené à l’hôpital en raison d’un refus de téter persistant depuis trois jours, accompagné de vomissements intermittents depuis la naissance. Aucun antécédent de troubles hémorragiques, de fièvre, de raideur de la nuque ou de convulsions n’a été rapporté. À l’examen, une fontanelle antérieure (zone molle sur le crâne du bébé) bombée a été observée, signe possible d’augmentation de la pression intracrânienne. Les réflexes étaient partiellement altérés (réflexe de Moro incomplet, succion non soutenue), mais le tonus musculaire restait bon. Les analyses sanguines, incluant la numération formule sanguine et le bilan de coagulation, étaient normales.\n\nL’imagerie par résonance magnétique (IRM) cérébrale a révélé la présence d’un hématome sous-dural chronique bilatéral (accumulation de sang entre le cerveau et la membrane qui le recouvre) mesurant environ 2 cm, avec extension vers les espaces autour du cerveau. De plus, une hydrocéphalie obstructive a été détectée, caractérisée par une dilatation des ventricules cérébraux (espaces remplis de liquide) due à une obstruction du quatrième ventricule.\n\n**Interprétation clinique**  \nL’hématome sous-dural chronique a provoqué une augmentation de la pression intracrânienne, expliquant les symptômes de refus de téter, les vomissements et la fontanelle bombée. L’hydrocéphalie obstructive, conséquence de cette accumulation de sang, nécessitait une intervention chirurgicale pour éviter des dommages cérébraux supplémentaires.\n\n**Prochaines étapes et évolution**  \nLe nouveau-né a subi une intervention chirurgicale sous anesthésie générale, consistant en une craniostomie bilatérale (ouverture des os du crâne) et une évacuation de l’hématome. Lors de l’opération, une membrane épaisse contenant du sang hémolysé (sang dégradé) a été retirée sous pression. Une complication cardiaque a surgi en cours d’intervention, nécessitant une réanimation cardio-pulmonaire, qui a permis un retour à la circulation spontanée. Un drain sous-dural a été placé pour évacuer les liquides résiduels.\n\nLe suivi post-opératoire a été favorable : un scanner cérébral réalisé trois jours après l’opération a montré une évacuation complète de l’hématome et une amélioration de l’hydrocéphalie. Le bébé a été libéré de l’hôpital au septième jour post-opératoire. Un suivi d’un mois a confirmé une évolution sans complication, avec un développement psychomoteur adapté à son âge.\n\n**Conclusion**  \nCe cas illustre qu’un hématome sous-dural chronique chez un nouveau-né, même s’il peut entraîner des symptômes inquiétants tels que le refus de téter et des vomissements, peut être efficacement traité par chirurgie. Une prise en charge rapide et adaptée permet une récupération complète avec un bon pronostic neurologique."
+        }
+    },
+    {
+        "article": "Une femme enceinte de 32 ans atteinte du syndrome de Holt-Oram a été adressée à notre établissement pour une échographie d'anatomie de routine du deuxième trimestre. Elle avait des antécédents familiaux positifs du syndrome de Holt-Oram impliquant sa mère et sa sœur. Chez tous les membres de la famille concernés, la seule preuve clinique du syndrome concerne les défauts des membres supérieurs, avec une malformation de l'os carpien et une agenèse du pouce. L'échographie a rapporté une aplasie bilatérale des rayons, un ulna légèrement incurvé et une torsion bilatérale de la main avec quatre rayons digitaux. Une augmentation significative de l'oreillette droite sans régurgitation tricuspide a également été détectée. La patiente a refusé l'amniocentèse et a décidé de poursuivre la grossesse. Au moment de l'échographie de suivi à 30 semaines, l'élargissement de l'oreillette droite a été confirmé sans insuffisance tricuspide ou autres malformations cardiaques. La patiente a subi une césarienne d'urgence à 40 semaines de gestation en raison d'une bradycardie fœtale pendant le travail. Un nourrisson de sexe masculin a été livré avec un poids de naissance de 3 110 g et un score d'APGAR de 9 et 9 à 1′ et 5′ min. L'évaluation postnatale a confirmé la grave hypoplasie des rayons, un ulna légèrement incurvé et une agenèse du premier rayon. L'échocardiographie néonatale a constaté un élargissement de l'oreillette droite et a également constaté un défaut atrial et deux petits défects du septum ventriculaire non détectés prénatalement. L'analyse génétique a également été réalisée et une mutation TBX5 a été détectée.\n",
+        "gold_summary": "Nous présentons le cas d'une femme enceinte de 32 ans atteinte du syndrome de Holt-Oram, qui a été adressée à notre établissement pour une échographie d'anatomie de routine au deuxième trimestre. L'échographie a révélé une aplasie bilatérale du radius, un ulna légèrement incurvé et une main tordue bilatérale avec quatre rayons digitaux. Une augmentation significative de l'oreillette droite sans régurgitation tricuspidienne a également été détectée. La patiente a refusé l'amniocentèse et l'évaluation postnatale a confirmé le diagnostic du syndrome de Holt-Oram.\n",
+        "synthetic_summary": {
+            "B1": "Une maman avait un bébé dans son ventre. Les docteurs ont regardé son bébé avec une machine spéciale. Ils ont vu que les mains du bébé étaient un peu différentes. Le bébé avait moins de doigts et ses bras étaient un peu tordus. Le cœur du bébé avait une partie un peu plus grande que d’habitude. La maman a choisi de ne pas faire un autre test. Après la naissance, les docteurs ont confirmé que le bébé avait ce problème. Tout va bien, et les docteurs vont bien s’occuper du bébé.",
+            "B2": "Cas d'une femme enceinte avec le syndrome de Holt-Oram\n\nUne femme de 32 ans, enceinte, a passé une échographie au deuxième trimestre de sa grossesse. Elle a une maladie appelée syndrome de Holt-Oram, qui affecte surtout les bras et les mains. Dans sa famille, sa mère et sa sœur ont aussi cette maladie. \n\nCe qu’ils ont trouvé pendant l’échographie\n\nL’échographie a montré que certains os de ses avant-bras, appelés radius, étaient absents des deux côtés. L’ulna, un autre os de l’avant-bras, était un peu courbé. Ses mains étaient tordues et avaient seulement quatre doigts au lieu de cinq. Ils ont aussi vu que la partie droite du cœur, appelée oreillette droite, était plus grande que la normale, mais sans problème de valve.\n\nCe que cela signifie pour la grossesse\n\nLa femme a choisi de ne pas faire un test appelé amniocentèse, qui consiste à prélever un peu de liquide autour du bébé pour chercher des problèmes génétiques. Après la naissance, le bébé a été examiné et a montré les mêmes malformations des bras et des mains. Une échographie du cœur du bébé a révélé des défauts supplémentaires non vus avant la naissance. Une analyse génétique a confirmé une mutation dans un gène appelé TBX5, responsable du syndrome de Holt-Oram.\n\nEn résumé, ce cas montre comment le syndrome de Holt-Oram peut affecter les membres supérieurs et le cœur, et l’importance du suivi médical pendant la grossesse.",
+            "B3": "Résumé détaillé et structuré :\n\n**Contexte**  \nUne femme enceinte de 32 ans, porteuse du syndrome de Holt-Oram, a été suivie dans notre établissement. Ce syndrome, présent dans sa famille (sa mère et sa sœur en sont également atteintes), se manifeste habituellement par des malformations des membres supérieurs, notamment des anomalies des os du carpe et une absence du pouce.\n\n**Principales observations prénatales**  \nLors de l’échographie d’anatomie réalisée au deuxième trimestre, plusieurs anomalies ont été détectées : une aplasie bilatérale des rayons (absence des os radiaux dans les avant-bras), un ulna légèrement incurvé et une torsion bilatérale des mains avec seulement quatre doigts visibles. Par ailleurs, une dilatation importante de l’oreillette droite du cœur a été observée, sans signe de régurgitation de la valve tricuspide (pas de reflux sanguin anormal). La patiente a choisi de ne pas réaliser d’amniocentèse (prélèvement de liquide amniotique pour analyse génétique).\n\n**Suivi et naissance**  \nÀ 30 semaines de grossesse, l’élargissement de l’oreillette droite a été confirmé sans apparition d’autres malformations cardiaques. La patiente a accouché par césarienne d’urgence à 40 semaines en raison d’une bradycardie fœtale (ralentissement du rythme cardiaque du bébé) pendant le travail. Le nouveau-né, un garçon pesant 3 110 grammes, présentait un score d’APGAR élevé (9/10 à 1 et 5 minutes), indiquant une bonne adaptation à la naissance.\n\n**Évaluation postnatale**  \nL’examen du nourrisson a confirmé les anomalies des membres supérieurs : hypoplasie sévère des rayons, ulna incurvé et absence du premier rayon (pouce). L’échocardiographie néonatale a révélé une dilatation de l’oreillette droite, un défaut du septum atrial (trou entre les deux oreillettes) ainsi que deux petits défauts du septum ventriculaire (trous entre les ventricules), ces derniers n’ayant pas été détectés avant la naissance. Une analyse génétique a identifié une mutation du gène TBX5, responsable du syndrome de Holt-Oram.\n\n**Interprétation clinique**  \nCe cas illustre la variabilité des manifestations du syndrome de Holt-Oram, qui associe des malformations osseuses des membres supérieurs à des anomalies cardiaques, parfois difficiles à détecter prénatalement. La mutation du gène TBX5 confirme le diagnostic génétique.\n\n**Prochaines étapes**  \nUn suivi cardiologique et orthopédique est nécessaire pour le nouveau-né afin de gérer les malformations cardiaques et des membres. La famille a été informée des implications génétiques et des possibilités de prise en charge adaptées."
+        }
+    },
+    {
+        "article": "Une femme de 20 ans a été suivie depuis l'âge de huit ans pour une NS idiopathique inaugurée par une thrombose veineuse cérébrale étendue à la veine jugulaire droite avec une embolie pulmonaire massive. La patiente n'a eu aucune séquelle. Elle n'avait pas d'autre antécédent médical ou chirurgical. Il n'a pas été rapporté d'antécédent familial de thrombose. La patiente n'a pas eu de biopsie car elle n'avait pas d'insuffisance rénale ni d'hématurie brute, ni d'hypertension à la première présentation ; en outre, elle n'avait pas d'autre signe rénal évocateur d'un syndrome néphrotique secondaire. Elle a été mise en conséquence sous traitement anticoagulant (antagoniste de la vitamine K par voie orale) et sous traitement corticoïde oral avec une bonne évolution. Par la suite, la patiente a reçu plusieurs cures de corticoïdes à haute dose pour des rechutes de NS dépendantes des stéroïdes. Elle a donc été mise sous mycophenolate mofetil (MMF) comme traitement de fond pour éviter les corticoïdes et assurer une croissance normale. Une évaluation exhaustive de la thrombophilie a été réalisée et n'a pas montré d'anomalie. Le taux d'homocystéine, le taux de fibrinogène sanguin, la protéine C, la protéine S, l'antithrombine III, la mutation du facteur V Leiden, la mutation JAK-2, les cryoglobulines, les anticorps anti-cardiolipine, le lupus anticoagulant et les anticorps anti-bêta-1-glycoprotéine étaient normaux. Le traitement anticoagulant a été arrêté après neuf ans. L'évolution a été émaillée par la survenue de plusieurs rechutes de sa maladie contrôlées par un traitement corticoïde oral. La rémission de la NS a été notée depuis 2017, le MMF a donc été progressivement arrêté en 2019 et la patiente est restée asymptomatique et sans aucune rechute.\n\nUn an plus tard, le patient est venu à notre service des urgences pour une douleur abdominale diffuse aiguë intense sans irradiation particulière associée à des vomissements postprandiaux et un œdème des membres inférieurs bilatéral depuis les six dernières heures. L'examen physique a révélé une sensibilité épigastrique intense avec des signes vitaux normaux (pression artérielle de 120/70 mm Hg, fréquence cardiaque de 83 bpm et saturation en oxygène à 100 % sur l'air ambiant). Le patient était apyrétique avec une conscience normale. Le reste de l'examen physique était sans objet. L'analyse d'urine avec labstix a révélé une protéinurie. Les résultats de l'analyse de gaz sanguins ont montré une acidose métabolique avec compensation respiratoire. D'autres tests de laboratoire ont révélé une hypoalbuminémie, une hypercholestérolémie, un temps de prothrombine à 90 %, des taux élevés de D-dimères, de lactate déshydrogénase et de créatine phosphokinase ainsi qu'un syndrome inflammatoire biologique avec une CRP de 37 mg/L et une leucocytose à 26,4 x 103/µL. Les fonctions rénales et hépatiques étaient normales.\n\nLe patient a été hospitalisé dans une unité de soins intensifs avec une surveillance étroite des signes vitaux et l'initiation de mesures de réanimation. Une échographie abdominale a été réalisée d'urgence, montrant un épanchement intra-abdominal de faible à modérée abondance. Un scanner abdominal a révélé une thrombose aiguë de l'artère mésentérique supérieure avec une ischémie mésentérique aiguë. Le patient a été immédiatement dirigé vers la salle d'opération. L'exploration intra-opératoire a confirmé une ischémie mésentérique avec une nécrose étendue de presque la totalité de l'intestin grêle, rendant leurs résections incompatibles avec la vie, comme le montre la figure 3. Le patient est mort après 48 heures.\n",
+        "gold_summary": "Nous présentons le cas d'une femme de 20 ans ayant une histoire de 12 ans de NS idiopathique révélée par une thrombose veineuse cérébrale étendue avec embolie pulmonaire traitée par une thérapie anticoagulante et une thérapie orale par corticostéroïdes suivie par du mycophenolate mofetil (MMF). L'évaluation de la thrombophilie n'a pas montré d'anomalies. L'évolution a été marquée par la survenue de plusieurs rechutes de NS contrôlées par une thérapie orale par corticostéroïdes jusqu'en 2017. Par la suite, la patiente n'a pas présenté de rechute de sa maladie. Le traitement anticoagulant et le MMF ont été arrêtés. Un an plus tard, la patiente a présenté une douleur abdominale aiguë diffuse sévère associée à des vomissements postprandiaux et un oedème des membres inférieurs bilatéraux. Les résultats de laboratoire ont confirmé une rechute de NS. Une tomodensitométrie abdominale a révélé une thrombose aiguë de l'artère mésentérique supérieure avec une ischémie mésentérique aiguë. L'exploration intraopératoire a montré une ischémie mésentérique avec une nécrose étendue de l'intestin grêle rendant leurs résections incompatibles avec la vie. La patiente est morte après 48 heures.\n",
+        "synthetic_summary": {
+            "B1": "Il y avait une jeune fille malade depuis longtemps. Son corps avait eu un gros problème avec le sang qui ne circulait pas bien dans sa tête. Elle a pris des médicaments pour aider son sang et pour la soigner. Parfois, elle était encore un peu malade, mais les médicaments l’aidaient.\n\nUn jour, elle a eu très mal au ventre. Elle vomissait et ses jambes étaient un peu gonflées. Les docteurs ont fait des examens et ont vu que le sang ne passait plus bien dans une partie de son ventre. Ils ont essayé de l’aider avec une opération, mais son ventre était trop malade. Elle est partie au ciel après deux jours.\n\nC’est une histoire triste. Les docteurs ont tout fait pour la soigner.",
+            "B2": "Cas d’une jeune femme de 20 ans suivie depuis ses 8 ans pour un syndrome néphrotique (NS) idiopathique, c’est-à-dire une maladie des reins sans cause connue. Au début, elle avait eu une thrombose, qui est un caillot de sang, dans une veine du cerveau, ainsi qu’une embolie pulmonaire, un caillot dans les poumons. Elle a été traitée avec des médicaments qui empêchent la formation de caillots (anticoagulants) et des corticoïdes, des médicaments qui réduisent l’inflammation. Plus tard, pour éviter les effets secondaires des corticoïdes, elle a reçu un autre médicament appelé mycophénolate mofétil (MMF).\n\nPendant plusieurs années, elle a eu des rechutes de son syndrome néphrotique, mais elles étaient contrôlées par les traitements. Tous les tests pour chercher une cause de sa tendance à faire des caillots étaient normaux. En 2017, sa maladie s’est calmée, et les traitements ont été arrêtés progressivement. \n\nUn an après l’arrêt des médicaments, elle est venue aux urgences avec une forte douleur au ventre, des vomissements et un gonflement des jambes. Les analyses ont montré que son syndrome néphrotique était revenu. Une tomodensitométrie, un examen d’imagerie, a révélé une thrombose aiguë dans une artère importante qui alimente l’intestin (artère mésentérique supérieure). Cette obstruction a provoqué une ischémie, c’est-à-dire un manque de sang, qui a causé la mort d’une grande partie de son intestin grêle.\n\nMalheureusement, lors de l’opération, les médecins ont constaté que la nécrose de l’intestin était trop étendue pour être réparée. La patiente est décédée 48 heures plus tard. Ce cas montre que même après une longue période sans symptômes, des complications graves peuvent survenir chez les patients avec un syndrome néphrotique.",
+            "B3": "Résumé détaillé et structuré\n\nContexte  \nNous rapportons le cas d’une femme de 20 ans suivie depuis l’âge de 8 ans pour un syndrome néphrotique (NS) idiopathique, initialement révélé par une thrombose veineuse cérébrale étendue à la veine jugulaire droite, compliquée d’une embolie pulmonaire massive. Ce tableau a nécessité un traitement anticoagulant oral par antagonistes de la vitamine K et une corticothérapie orale, avec une bonne évolution initiale. La patiente n’avait pas d’antécédents familiaux de thrombose ni d’autres pathologies associées. Une évaluation exhaustive de la thrombophilie (recherche d’anomalies des facteurs de coagulation, mutations génétiques, anticorps antiphospholipides, etc.) n’a révélé aucune anomalie. Au fil des années, plusieurs rechutes de NS dépendantes des stéroïdes ont conduit à l’instauration d’un traitement immunosuppresseur par mycophénolate mofétil (MMF) pour limiter l’exposition aux corticoïdes et préserver la croissance. Après une rémission prolongée débutant en 2017, le MMF a été arrêté en 2019, et la patiente est restée asymptomatique sans rechute.\n\nPrincipales observations  \nUn an après l’arrêt du traitement, la patiente s’est présentée aux urgences pour une douleur abdominale aiguë diffuse, intense, associée à des vomissements après les repas et un œdème bilatéral des membres inférieurs. L’examen clinique a montré une sensibilité épigastrique marquée avec des signes vitaux stables et absence de fièvre. Les analyses urinaires ont mis en évidence une protéinurie, signe d’une rechute du syndrome néphrotique. Les bilans sanguins ont révélé une acidose métabolique compensée, une hypoalbuminémie, une hypercholestérolémie, une élévation des D-dimères, de la lactate déshydrogénase, de la créatine phosphokinase, ainsi qu’un syndrome inflammatoire biologique avec une CRP élevée et une leucocytose importante. Les fonctions rénales et hépatiques étaient normales.\n\nInterprétation clinique  \nL’imagerie abdominale par échographie a montré un épanchement intra-abdominal modéré, tandis que la tomodensitométrie a confirmé une thrombose aiguë de l’artère mésentérique supérieure, responsable d’une ischémie mésentérique aiguë. Cette complication vasculaire grave est une urgence chirurgicale. L’exploration opératoire a révélé une nécrose étendue de presque tout l’intestin grêle, rendant impossible une résection viable compatible avec la survie.\n\nProchaines étapes et conclusion  \nMalgré une prise en charge rapide en soins intensifs et une intervention chirurgicale, la patiente est décédée 48 heures après son admission. Ce cas illustre la gravité des complications thromboemboliques chez une jeune patiente avec un syndrome néphrotique idiopathique, même après une longue période de rémission et l’arrêt du traitement anticoagulant. Il souligne l’importance d’une surveillance attentive et d’une prise en charge multidisciplinaire dans ces situations à haut risque."
+        }
+    },
+    {
+        "article": "Un Chinois de 38 ans a été admis à notre hôpital pendant plus de deux ans avec une protéinurie modérée accompagnée d'une hématurie microscopique lors d'un examen de laboratoire. Le patient était asymptomatique. Il n'y avait pas d'antécédents d'autres maladies, et aucun membre de la famille du patient n'avait de maladies rénales ou auto-immunes. Il n'y avait pas d'antécédents de consommation de médicaments ou de plantes médicinales chinoises. À l'admission, sa tension artérielle était de 151/81 mmHg, et l'examen physique n'a révélé aucun signe spécifique de hyperlipidémie, tel que l'opacité cornéenne ou les xanthomes. Au moment de la présentation, il avait une protéinurie (0,94 g/24 h) et une hématurie, mais pas de leucocyturie. Son taux de filtration glomérulaire estimé (eGFR) était de 84 ml/min par 1,73 m2. Les taux de cholestérol total et de triglycérides étaient de 205 mg/dL et de 115 mg/dL, respectivement. Les indicateurs immunologiques, tels que les taux de C3, C4 et IgA sériques, étaient normaux. Les autres paramètres de laboratoire sont décrits dans le tableau 1. L'analyse par immunofluorescence a montré une forte coloration pour les IgA, C3 et ApoE, mais une coloration négative pour les IgG, IgM, C1q et C4. En outre, l'immunofluorescence double a montré que KM55 et IgA étaient tous deux colorés positivement dans la région mésangulaire. La biopsie rénale a révélé une dilatation marquée des capillaires remplis de substances thrombotiques et une prolifération mésangulaire. Environ 12 % de la fibrose interstitielle avec atrophie tubulaire a également été observée. Les substances thrombotiques ont été colorées positivement pour le Soudan III et ApoE. L'examen au microscope électronique a révélé un dépôt de granules lipidiques dans la lumière capillaire glomérulaire dilatée, une hyperplasie mésangulaire et un dépôt électronique dense dans la région mésangulaire. Ces caractéristiques pathologiques étaient compatibles avec celles de la LGP avec IgAN.\n\nL'analyse du gène ApoE a révélé une transition hétérozygote C→T dans l'exon 3, qui a modifié l'acide aminé en position 25 de l'arginine à la cystéine (mutation de Kyoto). Le génotypage familial a montré que cette mutation a été transmise du père à sa fille. L'ApoE sérique était de 14,4 mg/dL déterminé par immuno-essai enzymatique (LOT : 20210702, JianCheng Bioengineering Institute). Combiné avec les résultats ci-dessus, le patient a été diagnostiqué avec LPG accompagné d'IgAN.\n\nAprès la biopsie rénale, le patient a été suivi en consultation externe à l'hôpital de Daping. Le taux de lipides plasmatiques et la TFGe étaient dans les limites normales pendant 18 mois, même sans médicaments hypolipidémiants. La protéinurie s'est améliorée (fluctuant à + ~ ± ; rapport albumine urinaire/créatinine de 186,06 mg/g Cr à 111,72 mg/g Cr) après l'administration de 10 mg d'énalapril par jour. En outre, nous avons suivi sa fille et ses taux de protéines urinaires sont restés négatifs.\n",
+        "gold_summary": "Un homme de 38 ans a été admis à notre hôpital en raison de protéinurie et d'hématurie, qui ont été découvertes lors d'un examen urinaire. La fonction rénale et les taux de lipides et de lipoprotéines dans le sang étaient normaux. Après biopsie rénale, le patient a été diagnostiqué comme ayant une LPG avec IgAN. L'analyse du gène ApoE a montré une transition hétérozygote C→T dans l'exon 3, entraînant un changement du 25e acide aminé de l'arginine à la cystéine (mutation de Kyoto). L'analyse génétique de la famille a montré que cette mutation a été héritée de son père et transmise à sa fille. L'ApoE sérique était de 14,4 mg/dL. Combinée aux résultats ci-dessus, le patient a été diagnostiqué comme ayant une LPG accompagnée d'IgAN. Après 18 mois de traitement par enalapril sans thérapie hypolipidémiant, la fonction rénale et les taux de lipides dans le sang étaient stables et les taux de protéines dans l'urine ont été significativement améliorés.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 38 ans est venu à l'hôpital.  \nIl avait un peu de protéines et du sang dans son pipi.  \n\nSon corps marchait bien. Son sang était normal.  \nLes médecins ont regardé un petit bout de son rein.  \n\nIls ont trouvé un problème spécial appelé LPG avec IgAN.  \nCe problème vient d'un petit changement dans un gène.  \n\nCe changement vient de son papa et il peut passer à sa fille.  \nLe monsieur a pris un médicament doux pour aider ses reins.  \n\nAprès un moment, il allait mieux. Son pipi était plus propre.  \nTout cela montre que les médecins peuvent aider même quand c’est compliqué.",
+            "B2": "### Ce qu'ils ont trouvé chez le patient\n\nUn homme de 38 ans a été suivi pendant plus de deux ans parce qu’il avait des protéines et du sang dans ses urines, découverts lors d’un examen médical. Malgré cela, il ne présentait pas de symptômes et ses reins fonctionnaient normalement. Ses taux de cholestérol et de graisses dans le sang étaient aussi normaux. Pour comprendre ce qui se passait, les médecins ont fait une biopsie rénale, c’est-à-dire qu’ils ont prélevé un petit morceau de son rein pour l’examiner.\n\n### Ce que cela signifie\n\nL’analyse de la biopsie a montré qu’il avait une maladie appelée LPG (lipoprotéine glomérulaire) associée à une autre maladie rénale appelée IgAN (néphropathie à IgA). Ces maladies affectent les petits filtres dans les reins. En plus, ils ont étudié un gène appelé ApoE et ont découvert une mutation particulière, appelée mutation de Kyoto, qui change une partie de la protéine fabriquée par ce gène. Cette mutation a été héritée de son père et transmise à sa fille. Le taux de la protéine ApoE dans son sang était mesuré à 14,4 mg/dL.\n\n### Le suivi et le traitement\n\nAprès le diagnostic, le patient a été traité avec un médicament appelé énalapril, qui aide à protéger les reins. Pendant 18 mois, sans prendre de médicaments pour réduire les graisses dans le sang, sa fonction rénale est restée stable et la quantité de protéines dans ses urines a beaucoup diminué. Sa fille, qui porte aussi la mutation, n’a pas montré de signes de maladie dans ses analyses d’urine.\n\n### En résumé\n\nCe cas montre qu’une mutation génétique peut causer une maladie rénale rare. Grâce à un diagnostic précis et un traitement adapté, la fonction des reins du patient a été protégée et son état s’est amélioré. Cela souligne l’importance de surveiller les membres de la famille quand une mutation génétique est détectée.",
+            "B3": "Résumé détaillé et structuré\n\nContexte  \nUn homme chinois de 38 ans a été suivi pendant plus de deux ans en raison d’une protéinurie modérée associée à une hématurie microscopique détectée lors d’examens de laboratoire. Il était asymptomatique, sans antécédents personnels ou familiaux de maladies rénales ou auto-immunes, et ne prenait aucun médicament ni plante médicinale. À l’admission, sa tension artérielle était légèrement élevée (151/81 mmHg), mais l’examen physique ne révélait aucun signe clinique d’hyperlipidémie, comme des opacités cornéennes ou des xanthomes.\n\nPrincipales observations  \nLes analyses biologiques initiales ont montré une protéinurie de 0,94 g/24 h et une hématurie sans leucocyturie. La fonction rénale, évaluée par le taux de filtration glomérulaire estimé (eGFR), était normale à 84 ml/min/1,73 m². Les taux de cholestérol total (205 mg/dL) et de triglycérides (115 mg/dL) étaient dans les limites normales. Les marqueurs immunologiques, notamment les compléments C3 et C4 ainsi que les immunoglobulines A (IgA), étaient également normaux. L’immunofluorescence sur biopsie rénale a révélé une forte présence d’IgA, de C3 et d’apolipoprotéine E (ApoE) dans la région mésangiale des glomérules, tandis que les autres immunoglobulines et compléments étaient absents. La double immunofluorescence a confirmé la co-localisation de KM55 (un anticorps spécifique des IgA anormales) et des IgA dans cette région.\n\nL’examen histologique a montré une dilatation marquée des capillaires glomérulaires remplis de thrombi lipidiques, une prolifération mésangiale et environ 12 % de fibrose interstitielle avec atrophie tubulaire. Les thrombi étaient positifs à la coloration au Soudan III, indiquant la présence de lipides, et à l’ApoE. L’analyse au microscope électronique a confirmé la présence de dépôts lipidiques dans la lumière capillaire dilatée, une hyperplasie mésangiale et des dépôts denses dans la zone mésangiale. Ces caractéristiques sont compatibles avec une lipodystrophie glomérulaire lipoprotéique (LPG) associée à une néphropathie à IgA (IgAN).\n\nInterprétation clinique  \nL’analyse génétique a identifié une mutation hétérozygote C→T dans l’exon 3 du gène ApoE, provoquant un changement de l’acide aminé 25 de l’arginine à la cystéine, connue sous le nom de mutation de Kyoto. Cette mutation a été héritée du père du patient et transmise à sa fille, qui ne présentait pas de protéinurie. Le taux sérique d’ApoE était mesuré à 14,4 mg/dL. L’ensemble des données cliniques, histologiques et génétiques a conduit au diagnostic de LPG associée à une IgAN.\n\nProchaines étapes et évolution  \nAprès la confirmation diagnostique, le patient a été suivi en consultation externe sans traitement hypolipidémiant. Sous traitement par inhibiteur de l’enzyme de conversion (énalapril 10 mg/jour), la fonction rénale et les taux lipidiques plasmatiques sont restés stables pendant 18 mois. La protéinurie s’est nettement améliorée, avec une réduction du rapport albumine urinaire/créatinine de 186,06 mg/g à 111,72 mg/g. La fille du patient, porteuse de la mutation, n’a pas développé de protéinurie au cours du suivi.\n\nEn résumé, ce cas illustre une forme rare de maladie rénale caractérisée par une accumulation lipoprotéique glomérulaire associée à une néphropathie à IgA, liée à une mutation génétique spécifique de l’ApoE. Le suivi prolongé montre une évolution stable sous traitement conservateur, soulignant l’importance d’un diagnostic précis et d’une prise en charge adaptée."
+        }
+    },
+    {
+        "article": "Chef des plaintes\nUne femme enceinte de 35 ans a été admise pour des douleurs abdominales 3 heures avant son admission.\n\nHistorique de la maladie actuelle\nElle est initialement venue à la sage-femme avec des douleurs de travail qui étaient de plus en plus fréquentes la veille de son admission. Après une observation de nuit, elle a ressenti des douleurs de travail de plus en plus fréquentes et plus fortes jusqu'à ce qu'elle ressente un inconfort abdominal, aucun mouvement fœtal n'a été ressenti et le rythme cardiaque fœtal était difficile à trouver par la sage-femme. Plus tard, elle a été dirigée vers l'hôpital Otto Iskandar Dinata en raison de la suspicion de mort fœtale intra-utérine. Après un entretien approfondi, elle a obtenu l'eau de la médecine à base de plantes bouillie que sa voisine lui a donnée, qui lui a suggéré de boire l'eau à base de plantes extraite pour l'aider lorsque le travail commencerait, ce qui est censé aider à améliorer le déroulement du travail. Elle a dit que l'eau était faite d'eau bouillie de rumput Fatimah de sa voisine. Pendant l'admission à l'hôpital, elle s'est plainte d'un inconfort abdominal qui ressemblait à une crampe musculaire et à une déchirure.\n\nHistorique personnel et historique familial\nSon antécédent obstétrical indiquait qu'elle était G2P1A0, sa dernière menstruation avait eu lieu le 31 septembre 2022, et l'âge gestationnel actuel était de 41 semaines. Il n'y avait eu aucune complication lors de sa précédente grossesse ; la sage-femme locale avait assisté son accouchement, et le bébé pesait 2600 grammes. Elle était mariée depuis l'âge de 21 ans avec son mari actuel, qui avait huit ans de plus qu'elle. Durant sa grossesse, elle avait eu un contrôle de routine avec la sage-femme tous les mois. Il n'y avait pas de antécédents familiaux pertinents.\n\nExamen physique\nLa tension artérielle de la patiente était de 80/60 mmHg, la fréquence cardiaque de 128 bpm, la fréquence respiratoire de 20 fois par minute, la taille du corps de 152 cm, le poids corporel de 58 kg, et avant la grossesse son poids corporel était de 58 kg. L'examen obstétrique a révélé que son abdomen était raide et tendu, la contraction était difficile d'accès, le son cardiaque fœtal était négatif, aucun signe d'anneau de faisceau, et la hauteur du fond était de 32 cm. De VT, la membrane était positive, et l'ouverture du col était de 3 cm.\n\nDiagnostic final\nLe diagnostic final de ce cas était G2P1A0 parturient aterm phase latente ; abdomen aigu en raison de la suspicion de décollement placentaire ; et décès foetal intra-utérin.\n\nTraitement\nUne laparotomie exploratoire a été décidée en raison de la douleur abdominale aiguë. Au cours de l'intervention, il n'y avait aucun signe de vie de la part du bébé, le bébé était une fille, son poids était de 2350 grammes et sa longueur était de 44 cm. L'opérateur a également constaté que le placenta était situé à l'extérieur et que son utérus était déjà rompu, environ 15-18 cm. L'opérateur a décidé de pratiquer une hystérectomie subtotale sur la patiente en raison du contexte éloigné et d'une transfusion sanguine non disponible, il est donc risqué de pratiquer une hystérotomie.\n\nRésultat et suivi\nLe bébé ne pouvait pas être sauvé en raison d'une mortinaissance. Son diagnostic final était rupture utérine spontanée > 15 cm en P2A0 post-terme ; mortinaissance. Plus tard, elle a été hospitalisée pendant quelques jours, puis son état s'est amélioré. La patiente était triste du résultat de la naissance, mais reconnaissante au médecin parce que l'équipe a pu la sauver. Elle a dit qu'elle serait plus prudente quant à ce qu'elle consomme, en particulier la médecine traditionnelle.\n",
+        "gold_summary": "Une femme enceinte de 35 ans a été envoyée à l'hôpital en raison de douleurs abdominales 3 heures avant son admission, en raison d'une suspicion de mort fœtale intra-utérine. Elle a bu l'eau aux herbes extraite pour l'aider à accoucher, qui était faite d'eau bouillie avec du rumput Fatimah de chez sa voisine. Elle a ensuite été diagnostiquée avec une phase latente de l'aterme parturient G2P1A0 ; abdomen aigu en raison d'une suspicion de décollement du placenta dd/ rupture de l'utérus ; et mort fœtale intra-utérine. Une laparotomie exploratoire a été décidée en raison de douleurs abdominales aiguës, et pendant la procédure, l'opérateur a décidé de faire une hystérectomie subtotale sur la patiente. L'opérateur a constaté que son utérus était déjà rompu, environ 15-18 cm et que le placenta était situé à l'extérieur de l'utérus.\n",
+        "synthetic_summary": {
+            "B1": "Une maman avait très mal au ventre. Elle attendait un bébé. \n\nLe bébé ne bougeait plus. La maman avait bu une eau spéciale donnée par sa voisine. \n\nÀ l’hôpital, les docteurs ont vu que le ventre de la maman était très dur. Le bébé était triste, il ne vivait plus dans le ventre. \n\nLes docteurs ont fait une opération pour aider la maman. Ils ont trouvé que le ventre de la maman était cassé. \n\nIls ont fait tout pour que la maman aille mieux. La maman était triste, mais elle est en sécurité maintenant.",
+            "B2": "Une femme enceinte de 35 ans est venue à l’hôpital parce qu’elle avait très mal au ventre depuis trois heures. Elle avait aussi arrêté de sentir les mouvements de son bébé, et la sage-femme ne pouvait pas entendre le cœur du bébé. Avant cela, elle avait bu une infusion à base d’une plante appelée rumput Fatimah, donnée par sa voisine, pour aider à faciliter le travail.\n\nÀ l’hôpital, les médecins ont découvert que le bébé était mort dans l’utérus. Ils ont aussi suspecté que le placenta, qui nourrit le bébé, s’était détaché ou que l’utérus s’était déchiré, ce qui cause une douleur très forte au ventre. Pour comprendre ce qui se passait, ils ont fait une opération appelée laparotomie exploratoire, qui consiste à ouvrir le ventre pour examiner l’intérieur.\n\nPendant l’opération, ils ont confirmé que l’utérus était déchiré sur une grande longueur (15 à 18 cm) et que le placenta était sorti de sa place normale. Le bébé, une fille, pesait 2350 grammes mais ne vivait plus. À cause de la gravité de la situation, les médecins ont dû enlever une partie de l’utérus (hystérectomie subtotale) pour sauver la vie de la maman.\n\nAprès l’opération, la femme s’est remise petit à petit. Elle était triste de la perte de son bébé, mais elle était aussi reconnaissante envers l’équipe médicale qui l’avait sauvée. Elle a dit qu’elle ferait plus attention à ce qu’elle boit ou prend pendant sa grossesse, surtout les remèdes à base de plantes.",
+            "B3": "Résumé détaillé et structuré\n\nContexte  \nUne femme enceinte de 35 ans, à terme (41 semaines de grossesse), a été admise à l’hôpital après avoir ressenti des douleurs abdominales aiguës survenues trois heures avant son admission. Elle avait initialement consulté une sage-femme pour des contractions de travail de plus en plus fréquentes la veille, mais au cours de la nuit, elle a ressenti un inconfort abdominal croissant, l’absence de mouvements fœtaux et une difficulté à détecter le rythme cardiaque du bébé, ce qui a conduit à la suspicion d’une mort fœtale intra-utérine. Par ailleurs, elle avait consommé une infusion à base de plantes (rumput Fatimah) recommandée par sa voisine pour faciliter le travail.\n\nPrincipales observations  \nÀ l’examen, la patiente présentait une tension artérielle basse (80/60 mmHg), une fréquence cardiaque élevée (128 bpm) et un abdomen tendu et raide. L’examen obstétrical a confirmé l’absence de rythme cardiaque fœtal, une ouverture cervicale de 3 cm, et une hauteur utérine de 32 cm. L’état clinique évoquait un abdomen aigu, avec suspicion de décollement placentaire ou rupture utérine. La patiente était en phase latente du travail, avec un antécédent obstétrical de deuxième grossesse, un accouchement précédent sans complication.\n\nInterprétation clinique  \nDevant la douleur abdominale aiguë et les signes cliniques, une laparotomie exploratoire a été réalisée. Au cours de l’intervention, il a été constaté que le fœtus était décédé, pesant 2350 grammes et mesurant 44 cm. L’opérateur a découvert une rupture utérine importante, estimée entre 15 et 18 cm, ainsi qu’un placenta situé en dehors de l’utérus, confirmant la gravité de la situation. En raison de l’état avancé de la rupture et de l’absence de possibilité de transfusion sanguine, une hystérectomie subtotale (ablation partielle de l’utérus) a été pratiquée pour préserver la vie de la patiente.\n\nProchaines étapes et suivi  \nLa patiente a été hospitalisée plusieurs jours après l’intervention, son état s’est progressivement amélioré. Bien qu’attristée par la perte de son enfant, elle a exprimé sa gratitude envers l’équipe médicale pour avoir sauvé sa vie. Elle a également indiqué qu’elle serait désormais plus prudente quant à la consommation de médecines traditionnelles pendant la grossesse. Ce cas souligne l’importance d’une surveillance médicale rigoureuse et la prudence face à l’usage de remèdes non contrôlés en période périnatale."
+        }
+    },
+    {
+        "article": "Une primigravide de 19 ans, à 35 semaines de gestation, sans antécédents médicaux ou familiaux, sans consanguinité, a été adressée pour évaluation d'une masse pelvienne fœtale découverte lors d'une échographie du troisième trimestre. À l'admission, les signes vitaux étaient dans les limites normales et les échographies fœtales antérieures étaient également dans la norme.\n\nLa patiente a été hospitalisée pour un examen de la malformation fœtale. L'échographie obstétrique transabdominale a montré un fœtus unique en position longitudinale, une présentation cul-de-sac complète et des données biométriques et un poids fœtal adéquats pour l'âge gestationnel. Les résultats anatomiques comprenaient une tête fœtale avec hypotélorisme et microphthalmie ; un abdomen fœtal avec une image hypogénique circulaire de 58 × 59 × 69 mm aux contours irréguliers et un volume de 124 centimètres cubes localisé postérieur à la vessie, sans absorption de doppler couleur ; un système urinaire fœtal non compromis, avec une impression diagnostique d'hydrométrorcolpos fœtal. L'imagerie par résonance magnétique fœtale complémentaire a confirmé la présence d'hypotélorisme, de microphthalmie et, dans le bassin fœtal, d'une lésion kystique de 74 × 64 × 52 mm de taille significative et de morphologie ronde s'étendant du bassin à l'abdomen, de haute intensité de signal en T2 et faible en T1, sans septations ou composants solides à l'intérieur. Elle a provoqué un déplacement antérieur de la vessie et un déplacement postérieur du rectum. Une petite formation sacculaire a été observée dans la partie supérieure, suggérant la présence de liquide dans l'utérus, compatible avec l'impression diagnostique d'hydrométrorcolpos fœtal.\n\nPendant l'hospitalisation, la patiente a eu une activité utérine prématurée ; l'infection a été écartée avec un hémogramme complet, une protéine C réactive et une analyse d'urine normale. Une maturation pulmonaire prématurée tardive a été instituée. La progression du travail prématuré et une présentation par le siège complète ont nécessité une césarienne immédiate à 36 semaines pour accoucher d'un seul fœtus avec un liquide amniotique normal, une nouveau-née de sexe féminin pesant 2 550 g, un APGAR de 2, 0, 0 à une, cinq et dix minutes, respectivement. La réanimation néonatale n'a pas été efficace, le résultat étant la mort périnatale.\n\nL'examen post mortem a révélé des oreilles basses, une micrognathie, un large pont nasal et une anoftalmie bilatérale ; le cou et la poitrine avaient une apparence normale ; l'abdomen était gonflé ; il y avait des syndactylie dans les membres supérieurs et inférieurs ; les organes génitaux externes féminins avaient un hymen imperforé. L'examen interne du crâne et des sections du cerveau n'a révélé aucune preuve de malformations graves ou de lésions focales. Le thorax, le cœur, les poumons et le diaphragme étaient normaux. L'abdomen, le foie, la rate, les reins et la vessie avaient une morphologie normale. L'utérus et le vagin avaient une apparence kystique et étaient nettement dilatés par le contenu de matériel jaunâtre associé à l'atrésie vaginale. Ces résultats ont confirmé un diagnostic définitif de FS.\n",
+        "gold_summary": "Une primigravide de 19 ans, enceinte de 35 semaines, présentant une hydrométrorrhée associée à un hypotélorisme et une microphtalmie. Une césarienne a été pratiquée en raison d'un travail de siège et d'une mort périnatale. L'autopsie a confirmé une hydrométrorrhée secondaire à une atrésie vaginale et un hymen imperforé, associés à un cryptophthalmos, des syndactylie, des malformations nasales et auriculaires, confirmant le diagnostic du syndrome de Fraser.\n",
+        "synthetic_summary": {
+            "B1": "Une maman attend un bébé. Le bébé avait un problème dans son ventre. Son petit ventre était rempli de liquide.\n\nLe bébé avait aussi des petits yeux et des petites oreilles différentes. La maman a dû faire une opération pour aider le bébé à naître.\n\nMalheureusement, le bébé n’a pas pu vivre. Les docteurs ont regardé le bébé après. Ils ont vu que le bébé avait un petit passage fermé dans son ventre.\n\nC’est pour cela que le bébé avait du liquide. Le bébé avait aussi des petits doigts collés. C’est un problème qu’on appelle le syndrome de Fraser.",
+            "B2": "Une jeune femme de 19 ans, enceinte de 35 semaines pour la première fois, a été suivie car une masse anormale a été trouvée chez son bébé lors d’une échographie. Cette masse était liée à un problème appelé hydrométrorcolpos, c’est-à-dire une accumulation de liquide dans l’utérus et le vagin du fœtus, causée par une fermeture anormale du vagin (atrésie vaginale) et un hymen qui ne s’ouvre pas (imperforé). \n\nLe bébé présentait aussi des traits particuliers : les yeux étaient très petits (microphtalmie) ou absents (cryptophtalmie), les yeux étaient rapprochés (hypotélorisme), et il y avait des doigts fusionnés (syndactylie). D’autres malformations concernaient le nez et les oreilles. \n\nÀ cause d’un travail prématuré et d’une position du bébé en siège, une césarienne a été réalisée à 36 semaines. Malheureusement, le bébé est décédé peu après la naissance malgré les efforts pour le réanimer. L’autopsie a confirmé toutes ces anomalies et a permis de poser le diagnostic du syndrome de Fraser, une maladie rare qui cause plusieurs malformations congénitales.",
+            "B3": "Résumé détaillé et structuré pour un public non spécialiste\n\n**Contexte**  \nUne jeune femme de 19 ans, enceinte pour la première fois et à 35 semaines de grossesse, a été prise en charge après la découverte lors d’une échographie d’une masse anormale au niveau du pelvis (bassin) du fœtus. Aucun antécédent médical ou familial particulier n’était signalé, et les examens prénataux précédents étaient normaux.\n\n**Principales observations**  \nL’échographie a révélé un fœtus unique avec des mesures normales pour son âge gestationnel, mais présentant plusieurs anomalies : un espacement anormalement réduit entre les yeux (hypotélorisme), des yeux très petits (microphthalmie), et une masse kystique située derrière la vessie, correspondant à une accumulation de liquide dans l’utérus et le vagin fœtaux (hydrométrorcolpos). L’IRM fœtale a confirmé ces anomalies, montrant une masse kystique importante dans le bassin et l’abdomen, déformant les organes voisins, ainsi qu’une accumulation de liquide dans l’utérus, compatible avec une obstruction au niveau vaginal.\n\nPendant l’hospitalisation, la patiente a présenté un travail prématuré avec une présentation du fœtus par le siège (fesses en premier). Une césarienne a été réalisée à 36 semaines. La naissance a donné lieu à un nouveau-né féminin de poids normal mais avec un score d’Apgar très faible (indicateur de vitalité à la naissance), et malgré les efforts de réanimation, le nouveau-né est décédé peu après la naissance.\n\nL’examen post mortem a mis en évidence plusieurs malformations : absence des yeux (anoftalmie bilatérale), malformations du visage (pont nasal large, micrognathie), oreilles basses, fusion des doigts et orteils (syndactylie), et des organes génitaux externes féminins avec un hymen imperforé. L’utérus et le vagin étaient dilatés et remplis de liquide, confirmant une obstruction vaginale (atrésie vaginale). Les autres organes internes, y compris le cerveau, le cœur et les poumons, étaient normaux.\n\n**Interprétation clinique**  \nL’ensemble des anomalies observées, notamment les malformations oculaires, faciales, des membres et des organes génitaux, ainsi que l’hydrométrorcolpos due à une obstruction vaginale, correspondent au syndrome de Fraser. Ce syndrome génétique rare se caractérise par des malformations congénitales multiples affectant principalement les yeux, les voies génitales et les membres.\n\n**Prochaines étapes**  \nCe diagnostic souligne l’importance d’un suivi prénatal approfondi en cas de détection de masses pelviennes fœtales et d’anomalies morphologiques. Il permet également d’orienter le conseil génétique pour les parents, en vue d’évaluer le risque de récidive dans les grossesses futures. La prise en charge néonatale et chirurgicale dépendra de la sévérité des malformations et de la viabilité du nouveau-né."
+        }
+    },
+    {
+        "article": "Une femme de 67 ans atteinte d'une cardiomyopathie dilatée, diagnostiquée il y a 10 ans avec une fraction d'éjection ventriculaire gauche (FEVG) de 35 % (intervalle de référence : 50 % - 70 %) et une MR modérée, a été adressée pour dyspnée de classe II et III de la New York Heart Association (NYHA). Elle ne présentait pas de facteurs de risque cardiovasculaires significatifs ou d'autres comorbidités qui auraient pu affecter la stratégie de traitement. Ses symptômes persistaient malgré un traitement médical optimal avec 10 mg de carvedilol, 2,5 mg d'énalapril, 25 mg de spironolactone, 30 mg d'azosémide et 3,75 mg de tolvaptan par jour. À l'examen physique, la patiente mesurait 160 cm, pesait 57 kg, avait une tension artérielle de 123/71 mmHg et une fréquence cardiaque de 100/min. L'examen cardiaque a révélé un murmure d'éjection systolique de grade II/VI de Levine au troisième espace intercostal gauche et un oedème modéré des membres inférieurs.\n\nLes taux de peptide natriurétique de type B en ambulatoire allaient de 150 à 250 pg/mL (intervalle normal : < 125 pg/mL). L’échocardiographie transthoracique a révélé un diamètre de fin de diastole du ventricule gauche de 70 mm (intervalle normal : 35-52 mm), une fraction d’éjection du ventricule gauche de 31 %, et une MR fonctionnelle sévère entre les crêtes A2 et P2, caractérisée par une fraction régurgitante de 59 % (seuil pour une MR sévère : 50 %) et une surface effective de l’orifice régurgitant de 0,27 cm2 (seuil pour une MR sévère : 0,20 cm2). L’échocardiographie transœsophagienne (TEE) a confirmé un rétrécissement significatif de la veine contractée > 11 mm (seuil pour une MR sévère : 7 mm). Malgré un score de la Society of Thoracic Surgeons faible (1,89 %), notre équipe multidisciplinaire a choisi le M-TEER en utilisant deux dispositifs MitraClip de deuxième génération en raison du dysfonctionnement du ventricule gauche, de l’étiologie fonctionnelle de la MR et de la préférence du patient pour une mobilisation précoce.\n\nLa réparation transcathéter de la valve mitrale bord à bord a été réalisée sous anesthésie générale. Au cours de la préparation du clip, une légère résistance a été constatée lorsque l'introduction du clip glissait sur le clip. Bien que le clip ait semblé fonctionner normalement lors des contrôles, l'introduction n'a pas été inspectée de manière approfondie. Le clip a ensuite été avancé dans le système sans difficulté. Après la ponction transeptale et l'avancement vers la position de chevauchement, le clip a été positionné sur la valve mitrale sans problème. Cependant, lorsque le levier de verrouillage a été déverrouillé pour ouverture dans la LA, le clip a montré un mouvement limité et ne s'est pas ouvert au-delà de 30°.\n\nLes premières tentatives de fermeture et de récupération du clip ont échoué en raison de la résistance du positionneur de bras. Pour résoudre le problème, nous avons ramené le positionneur de bras à la position neutre et tiré la poignée de verrouillage vers l'arrière d'environ 5 mm. Nous avons ensuite légèrement tourné le positionneur de bras dans le sens de la fermeture, puis dans le sens de l'ouverture. Lorsque cette manœuvre a échoué, nous avons répété le processus en tournant davantage le positionneur de bras dans le sens de la fermeture, ce qui a engendré une résistance mécanique sans précédent. Au cours de la rotation suivante dans le sens de l'ouverture, le clip s'est soudainement ouvert à 180° et s'est détaché du système de distribution de clips (CDS), restant connecté uniquement par la ligne de préhension dans sa position par défaut.\n\nSous TEE et guidage fluoroscopique, nous avons effectué le retrait direct du clip. Bien que les pinces aient été temporairement déplacées vers le bas lors du détachement, elles sont revenues à leur position relevée lors d'une traction contrôlée vers le cathéter guide orientable (SGC). La position de la pince a été maintenue pour assurer une connexion sécurisée. En utilisant une traction douce et régulière sur le CDS, le clip a été progressivement guidé vers le SGC. Le clip s'est inversé au cours de ce processus et est partiellement entré dans le SGC, permettant un retrait sécurisé de l'ensemble du système dans l'oreillette droite. L'échocardiographie transœsophagienne a révélé un défaut septal auriculaire de 2 à 3 mm, mais aucune autre complication mécanique n'a été observée avec une hémodynamique stable. Le CDS et le SGC ont été récupérés par une incision fémorale. Une inspection minutieuse du système récupéré a révélé une déchirure de l'introducteur qui n'était pas visible lors de la préparation initiale.\n\nÀ la suite de la récupération du système, deux dispositifs MitraClip NT ont été implantés avec succès en utilisant de nouveaux CDS et SGC, ce qui a entraîné une MR résiduelle modérée. Les rayons X et TEE ont confirmé qu'aucun composant du dispositif n'était resté chez le patient.\n\nLa patiente a été déchargée le jour 4 sans complications. Au cours du suivi ambulatoire, la pharmacothérapie a été optimisée : le traitement par bêta-bloquant a été changé de carvedilol 10 mg à bisoprolol 3,75 mg quotidien, qui a ensuite été augmenté à 5 mg. L'inhibiteur de l'enzyme de conversion de l'angiotensine a été changé d'énalapril 2,5 mg à perindopril 4 mg quotidien, et a ensuite été remplacé par sacubitril/valsartan 200 mg quotidien. L'empagliflozine 10 mg quotidien a été ajoutée au régime après son approbation réglementaire. Ses symptômes s'étaient améliorés à la classe NYHA I et sont restés stables pendant 4,5 ans.\n",
+        "gold_summary": "Une femme de 67 ans atteinte de cardiomyopathie dilatée a subi une M-TEER pour une MR fonctionnelle sévère. Bien que la résistance ait été constatée lors de la préparation initiale et du chargement de l'appareil, les tests fonctionnels limités sont apparus normaux et la procédure a été poursuivie. Au cours de la manipulation du clip dans l'oreillette gauche, la résistance mécanique dans le bras de positionnement a conduit à un détachement inattendu du MitraClip, relié uniquement par la ligne de préhension. Grâce à une traction soigneuse sous guidage échocardiographique et fluoroscopique, nous avons récupéré le clip par voie percutanée avec succès. La procédure a été complétée avec de nouveaux systèmes MitraClip, obtenant une MR résiduelle modérée. Les symptômes de la patiente sont passés de New York Heart Association Classes II et III à I, avec une amélioration soutenue pendant 4,5 ans de suivi.\n",
+        "synthetic_summary": {
+            "B1": "Une dame avait un cœur un peu fatigué. Elle avait une valve du cœur qui laissait passer trop de sang. \n\nLes docteurs ont mis un petit clip pour aider la valve à mieux marcher. Au début, le clip a eu un petit problème. Il s’est un peu détaché. \n\nLes docteurs ont bien regardé avec des images et ont doucement retiré le clip cassé. Puis, ils ont mis un nouveau clip. \n\nAprès, la dame a eu moins de mal à respirer et elle s’est sentie mieux longtemps.",
+            "B2": "Une femme de 67 ans souffrait d'une cardiomyopathie dilatée, c’est-à-dire que son cœur était élargi et battait moins bien. Elle avait aussi une fuite importante de la valve mitrale, appelée régurgitation mitrale (MR), qui empêchait le sang de circuler normalement. Pour traiter cela, les médecins ont décidé de faire une réparation de la valve mitrale sans chirurgie ouverte, en utilisant un dispositif appelé MitraClip.\n\nAu début de la procédure, ils ont senti une résistance quand ils préparaient et chargeaient le clip, mais les tests semblaient normaux, alors ils ont continué. Pendant qu’ils manipulaient le clip dans l’oreillette gauche du cœur, une partie du dispositif s’est détachée de façon inattendue, restant seulement attachée par un fil de maintien. Grâce à une surveillance par échographie et rayons X, ils ont réussi à retirer le clip cassé avec précaution, sans causer de problème grave.\n\nEnsuite, ils ont utilisé un nouveau système MitraClip pour terminer la réparation. Après cela, la fuite de la valve mitrale était réduite à un niveau modéré. La patiente a vu ses symptômes s’améliorer : elle est passée d’une difficulté à respirer modérée à une absence presque totale de symptômes. Cette amélioration est restée stable pendant plus de 4 ans.",
+            "B3": "Résumé détaillé et structuré pour un public non spécialiste mais informé :\n\n**Contexte**  \nUne femme de 67 ans souffrant d’une cardiomyopathie dilatée (une maladie du muscle cardiaque qui entraîne un agrandissement et une diminution de la fonction du ventricule gauche) a été prise en charge pour une régurgitation mitrale (MR) fonctionnelle sévère. Cette régurgitation correspond à un reflux anormal du sang à travers la valve mitrale, aggravant son insuffisance cardiaque malgré un traitement médical optimal. Ses symptômes correspondaient à une dyspnée modérée à sévère (classes II et III selon la classification de la New York Heart Association).\n\n**Principales observations**  \nLors de la procédure de réparation transcathéter de la valve mitrale par MitraClip (une technique mini-invasive visant à réduire la fuite valvulaire en pinçant les feuillets de la valve), une résistance mécanique a été détectée lors de la préparation et de l’introduction du dispositif. Initialement, les tests fonctionnels du clip semblaient normaux, ce qui a conduit à poursuivre l’intervention. Cependant, lors de la manipulation du clip dans l’oreillette gauche, une résistance inhabituelle dans le bras de positionnement a provoqué un détachement accidentel du clip du système de distribution. Le clip est alors resté suspendu uniquement par la ligne de préhension, risquant une complication grave.\n\n**Interprétation clinique**  \nCe détachement inattendu a nécessité une manœuvre délicate de récupération percutanée (sans chirurgie ouverte), réalisée sous guidage échocardiographique transœsophagien et fluoroscopique (techniques d’imagerie permettant de visualiser précisément le cœur et le dispositif en temps réel). Grâce à une traction contrôlée et progressive, le clip a pu être retiré en toute sécurité par la voie veineuse, évitant ainsi une intervention chirurgicale plus invasive. L’inspection du matériel retiré a révélé une déchirure de l’introducteur (partie du système d’introduction du clip), non détectée initialement, à l’origine probable de la résistance et du dysfonctionnement.\n\n**Prochaines étapes et suivi**  \nAprès cette complication, la procédure a été reprise avec de nouveaux dispositifs MitraClip, permettant une réduction satisfaisante de la régurgitation mitrale à un niveau modéré. La patiente a été libérée sans complication majeure et a bénéficié d’une optimisation de son traitement médical, incluant des modifications de ses médicaments pour améliorer la fonction cardiaque. Son état clinique s’est nettement amélioré, avec une réduction des symptômes à la classe NYHA I (symptômes minimes ou absents), et cette amélioration est restée stable pendant plus de 4 ans et demi.\n\n**Conclusion**  \nCette expérience souligne l’importance d’une vigilance accrue lors de la préparation et de la manipulation des dispositifs MitraClip, car une résistance mécanique peut masquer un défaut matériel pouvant entraîner un détachement du clip. Une récupération percutanée réussie est possible grâce à une coordination multidisciplinaire et un guidage d’imagerie précis, permettant de poursuivre la prise en charge avec succès et d’améliorer durablement la qualité de vie du patient."
+        }
+    },
+    {
+        "article": "Femme de 65 ans, native et originaire de Mérida, au Venezuela, ayant une antécédent chirurgical d'appendicectomie ouverte, qui présente une maladie actuelle de 4 mois d'évolution caractérisée par une douleur abdominale d'apparition insidieuse, d'intensité modérée, lancinante, initialement généralisée, mais localisée dans la fosse iliaque droite après 3 mois, ce qui l'a amenée à consulter un médecin, qui lui a indiqué un traitement médical, avec une amélioration partielle du tableau. Étant donné que la symptomatologie persiste et qu'une masse palpable apparaît dans la fosse iliaque droite, elle se rend au service de gastroentérologie de notre établissement, où une coloscopie est réalisée, qui révèle une tumeur sous-épithéliale dans la région cecale.\n\nElle présente également une altération du schéma de défécation, alternant périodes de constipation et diarrhées, des élévations de température d'apparition récente (15 jours) et une intolérance à la voie orale (solides), raison pour laquelle elle a été adressée au service de chirurgie générale.\n\nL’examen physique a révélé un état clinique stable, une absence de fièvre, une hydratation adéquate, une bonne coloration cutanée et muqueuse ; à l’examen abdominal, un abdomen plat, des bruits hydroaéreux présents, un abdomen mou, dépressible, une masse palpable dans la fosse iliaque droite de 5 × 5 cm, mobile, douloureuse à la palpation et sans signe d’irritation péritonéale ; au toucher rectal, un anus sans altérations, un sphincter avec une tonicité conservée, une ampoule rectale aux parois lisses, sans tuméfaction palpable, et avec peu de selles molles à l’intérieur ; un examen gynécologique sans altérations ; le reste de l’examen physique, sans altérations.\n\nUne tomographie par ordinateur à double contraste (oral et intraveineux) est demandée, dans laquelle on observe une perte de la configuration habituelle dans la région iléo-cécale avec une augmentation importante du volume du côlon, et on observe l'incursion de l'iléon dans le côlon droit sur une longue distance allant du côlon transverse à l'angle splénique, où on observe une formation sacculaire remplie de contraste oral. Au cours de la phase artérielle, la région cæcale ne montre aucun changement de densité et les trajets vasculaires sont visibles dans tout l'intérieur du côlon, accompagnés de tissu adipeux, mais il existe un double renforcement dans la région de l'angle splénique du côlon transverse. On conclut que les résultats suggèrent une intussusception intestinale secondaire à une tumeur.\n\nAu vu des résultats de l’examen tomographique et de l’examen physique, la patiente a été emmenée au bloc opératoire, où on a constaté la présence d’un petit liquide jaunâtre libre dans la cavité abdominale. Une intussusception iléo-colique a été observée jusqu’à l’angle hépatique du côlon transverse. En réduisant l’intussusception, on a observé une tumeur de 10 cm dans la valve iléo-cécale et de 10 cm dans l’intestin grêle, qui envahit la séreuse, qui est indurée et qui compromet la lumière intestinale, et de multiples adénopathies de tailles variées (non > 2 cm) dans le mésentère du côlon droit, sans évidence de lésions dans le foie. On a effectué la manœuvre de Cattell-Braasch, une hémicolectomie droite jusqu’à l’émergence de l’artère colique droite, la fermeture du moignon du côlon transverse et la confection d’une anastomose iléo-transverse latérale, le lavage et le drainage de la cavité, et la fermeture par plans de la cavité abdominale. L’acte chirurgical s’est achevé sans complications et la patiente a eu une évolution clinique favorable. Au bout de 48 heures de postopératoire, elle a commencé à prendre des aliments par voie orale. Elle a été renvoyée à la maison cinq jours après l’opération, le drain a été retiré au bout de 10 jours et la patiente a été suivie par le service de chirurgie générale, sans évènements dans son évolution.\n\nL’échantillon étudié a révélé une lésion néoplasique caractérisée par la prolifération de structures tubulaires revêtues d’un revêtement endothélial présentant un cytoplasme éosinophile, des noyaux vésiculaires sans nucléole, des vacuoles intracytoplasmiques présentant des lumières endothéliales, quelques érythrocytes et des mitoses isolées (trois sur 40 champs de haute puissance). Cette zone présente une augmentation du tissu conjonctif fibreux. On observe à la périphérie un infiltrat inflammatoire polymorphonuclearnéutrophile et lymphocytaire important avec des zones de nécrose, des détritus cellulaires et des érythrocytes extravasés. Des colorations spéciales au PAS (acide périodique-Schiff) et au trichrome de Gomori ont révélé la présence de tissu conjonctif fibreux autour des zones de lésion néoplasique décrites ; les coupes de l’intestin grêle revêtu de muqueuse ne présentent pas de modifications significatives, tout comme le mésentère. Les résultats de l’examen de l’intestin grêle sont compatibles avec une HÉ de malignité intermédiaire.\n",
+        "gold_summary": "Femme de 65 ans se présentant avec des douleurs abdominales chroniques. Une tomographie par ordinateur a été réalisée et une incursion de l'iléon dans le côlon droit a été observée. Elle a été emmenée au bloc opératoire où on a découvert une intussusception intestinale iléo-colique due à une tumeur de l'intestin grêle, avec un résultat anatomopathologique d'hémangio-endothéliome épithélioïde.\n",
+        "synthetic_summary": {
+            "B1": "Une dame de 65 ans avait mal au ventre depuis longtemps. \n\nLes docteurs ont fait une grande photo de son ventre. Ils ont vu que une partie de son intestin était rentrée dans une autre. \n\nElle est allée à l’hôpital pour une opération. Les docteurs ont trouvé une grosse boule dans son intestin. \n\nIls ont enlevé cette boule pour qu’elle aille mieux. Après, elle a commencé à se sentir mieux.",
+            "B2": "Femme de 65 ans avec des douleurs au ventre depuis plusieurs mois. Un examen spécial appelé tomographie a montré que l’intestin grêle s’était glissé dans le côlon droit, ce qui s’appelle une intussusception. Lors de l’opération, les médecins ont trouvé une grosse tumeur dans l’intestin grêle qui causait ce problème. Après analyse au microscope, cette tumeur a été identifiée comme un hémangio-endothéliome épithélioïde, un type de tumeur qui vient des cellules des vaisseaux sanguins et qui a un comportement entre bénin et malin. La patiente a bien récupéré après l’opération.",
+            "B3": "Résumé détaillé et structuré pour un public non spécialiste\n\nContexte  \nUne femme de 65 ans, originaire du Venezuela, a consulté pour des douleurs abdominales évoluant depuis quatre mois. Ces douleurs, initialement diffuses, se sont localisées dans la partie inférieure droite de l’abdomen. Elle présentait également des troubles du transit intestinal alternant constipation et diarrhée, une fièvre récente et une difficulté à tolérer les aliments solides. Une masse palpable a été détectée dans la fosse iliaque droite (zone située en bas à droite de l’abdomen).\n\nPrincipales observations  \nUne coloscopie a révélé une tumeur sous la muqueuse du côlon cæcal (première partie du côlon). Une tomodensitométrie (scanner) avec injection de produit de contraste a montré que l’iléon (dernière partie de l’intestin grêle) s’était introduit dans le côlon droit sur une longue distance, formant une invagination intestinale appelée intussusception. Cette situation est souvent causée par une masse tumorale qui agit comme un point d’ancrage. Au bloc opératoire, une intussusception iléo-colique a été confirmée, s’étendant jusqu’à l’angle hépatique du côlon transverse. Une tumeur de 10 cm a été trouvée au niveau de la valve iléo-cæcale et de l’intestin grêle, envahissant la couche externe de l’intestin (séreuse) et obstruant partiellement la lumière intestinale. Plusieurs ganglions lymphatiques élargis ont été observés dans la région mésentérique (zone de fixation de l’intestin).\n\nInterprétation clinique  \nLa tumeur responsable de l’intussusception a été retirée chirurgicalement par une hémicolectomie droite (ablation de la partie droite du côlon) avec rétablissement de la continuité intestinale par une anastomose entre l’iléon et le côlon transverse. L’analyse anatomopathologique a identifié la lésion comme un hémangio-endothéliome épithélioïde, une tumeur rare d’origine vasculaire présentant une malignité intermédiaire, caractérisée par la prolifération de cellules endothéliales atypiques formant des structures tubulaires. Cette tumeur peut provoquer une inflammation locale et une nécrose (mort cellulaire).\n\nProchaines étapes  \nAprès une évolution postopératoire favorable, la patiente a repris une alimentation orale normale et a été suivie en consultation sans complication. La prise en charge ultérieure dépendra de l’évaluation oncologique pour déterminer la nécessité éventuelle d’un traitement complémentaire. Un suivi régulier est indispensable pour surveiller toute récidive ou complication liée à cette tumeur rare."
+        }
+    },
+    {
+        "article": "Un garçon est né par césarienne d'urgence en raison d'une détresse fœtale à 40 semaines de grossesse. La mère avait 33 ans et était enceinte de 1 enfant et de 1 enfant en voie de naissance. Ni les parents ni le frère n'avaient des antécédents familiaux d'anomalies congénitales, de maladies liées à l'aorte ou de mort subite. D'après les résultats de l'échographie prénatale à la fin du deuxième trimestre, la longueur du fémur du fœtus était de 1 à 3 semaines plus longue que la longueur supposée de l'âge gestationnel réel. L'échocardiographie fœtale a montré une cardiomégalie avec un rapport de circonférence cardiaque-thoracique fœtale de 0,5 ou plus en fonction de la durée de vie du bébé. En outre, la taille du foramen ovale était plus grande que la normale et une constriction aortique gauche a été observée à côté du bassin de l'artère sous-clavière. En outre, aucune autre anomalie n'a été constatée lors de l'échographie prénatale.\n\nÀ la naissance, le poids était de 3560 g (75e percentile), la longueur de 56,5 cm (au-dessus du 90e percentile), et le tour de tête de 36 cm (au-dessus du 90e percentile). Les scores d'Apgar à 1 et 5 minutes étaient de 4 et 6 points, respectivement. Dans la salle d'accouchement, la patiente ne respirait pas spontanément et avait une bradycardie et une cyanose. Après avoir été admise à l'unité de soins intensifs néonatals, diverses malformations musculo-squelettiques ont été confirmées par examen physique. Une arachnodactylie sévère et une camptodactylie ont été observées dans les deux mains et les deux pieds, et la plante des pieds était plate. Les articulations du coude et du genou n'étaient pas complètement étendues. Le visage avait une hypoplasie malaire avec un aspect facial sénile. L'œil était profondément enfoncé avec une fissure palpebrale oblique vers le bas, et l'oreille avec un cartilage hypoplasique était mal positionnée et froissée. La patiente présentait une bouche tombante, une suture coronale proéminente et une brachycephalie. Un murmure systolique de grade V/VI a été entendu à la fois à la limite sternale supérieure et à la limite sternale inférieure gauche avec un parasternal de grade III. L'échocardiographie a montré une mauvaise contractilité cardiaque, une hypertension pulmonaire sévère, un sinus aortique dilaté (20,2 mm) (Z-score ; 8,08 par Boston, 6,37 par Detroit, ou 5,97 par Halifax), et une dysfonction valvulaire intracardiaque multiple avec prolapsus valvulaire (régurgitation aortique modérée, régurgitation mitrale sévère, régurgitation tricuspide modérée, et régurgitation valvulaire pulmonaire modérée). Les résultats de l'examen ophtalmologique ont montré une ectopie lentis dans les deux yeux ainsi qu'une subluxation du cristallin. Une hernie hépatique a été confirmée par une radiographie abdominale et une échographie. Le score systémique de la manifestation musculo-squelettique était de 11 points, selon les critères de Gand (critères diagnostiques internationaux pour la MFS).\n\nPour le diagnostic génétique, le séquençage de Sanger et la réaction en chaîne de la polymérase ont été effectués sur la séquence nucléotidique comme référence pour le gène FBN1. En conséquence, une mutation dans laquelle G, la première base du 32e intron sous la forme d'une mutation hétérogène, a été remplacée par T (c.3964 + 1G > T). Cela a été confirmé comme la variante pathogène probable sur la base de la directive ACMG/AMP de 2015. L'emplacement de la mutation a été inclus dans le site précédemment connu sous le nom de région néonatale de MFS (exons 24-32). Le patient a pu être diagnostiqué avec MFS néonatale avec une nouvelle mutation du gène FBN1 dans les 2 semaines de la vie.\n\nLe premier jour de la vie, une cyanose différentielle a été constatée, indiquant une hypoxémie réfractaire malgré un apport en oxygène supérieur à 60 % et des signes d'un faible débit cardiaque. La patiente a été prise en charge médicalement pour améliorer le faible débit cardiaque en fonction de la régurgitation mitrale sévère et de la régurgitation aortique. La réduction de la postcharge, y compris l'infusion continue de milrinone, la sédation complète avec l'infusion continue de fentanyl et l'utilisation de diurétiques ont été tentées pour améliorer l'oligurie et l'insuffisance cardiaque. Malgré la prise en charge médicale, la patiente a présenté une insuffisance respiratoire, une insuffisance cardiaque et une hypertension pulmonaire sévère nécessitant une ventilation mécanique invasive continue. La régurgitation aortique, la régurgitation mitrale, l'hypertension pulmonaire et la contractilité cardiaque se sont aggravées. Après plusieurs consultations avec la famille et le personnel médical de la patiente au sujet du plan de traitement, les soins palliatifs ont été poursuivis au lieu d'un traitement chirurgical. En conséquence, la congestion hépatique et pulmonaire accompagnée d'une hémorragie pulmonaire a progressé également. Elle a finalement progressé vers un syndrome de défaillance multiviscérale et la patiente est morte 32 jours après la naissance.\n\nMH - Anomalies/complications cardiovasculaires\nMH - Système cardiovasculaire/pathologie",
+        "gold_summary": "Inquiétudes des patients:\nUn nouveau-né atteint de MFS néonatale et d'une atteinte cardiaque sévère. Il présentait diverses caractéristiques cliniques sévères telles que l'arachnodactylie, la camptodactylie, la contracture des articulations du coude et du genou, un aspect facial sénile et une dépression profonde avec fissure palpérale inclinée vers le bas, un cartilage d'oreille hypoplasique, une bouche affaissée, une brachycephalie et une ectopie du cristallin.\n\nDiagnosis:\nL'analyse génétique a révélé une nouvelle mutation au nucléotide 3964 (c.3964 + 1 G > T) dans l'intron 32 du gène fibrillin-1. Cette mutation est identifiée dans la région dite néonatale de l'exon 24 à 32 de la fibrilline-1, comme indiqué précédemment.\n\nInterventions:\nLe patient a été traité médicalement pour améliorer la faible débit cardiaque en fonction de la régurgitation mitrale sévère et de la régurgitation aortique. La réduction de la précharge, la sédation complète et l'utilisation de diurétiques ont été tentées pour améliorer l'oligurie et l'insuffisance cardiaque.\n\nRésultats:\nMalgré la prise en charge médicale, la régurgitation aortique, la régurgitation mitrale, l'hypertension pulmonaire et la contractilité cardiaque se sont aggravées. Le traitement chirurgical est essentiel pour prolonger la vie du patient, cependant, les considérations relatives à la progression grave de la maladie font que les familles décident de poursuivre les soins palliatifs au lieu du traitement chirurgical. Quelques mois après la naissance, il a présenté une régurgitation aortique, une régurgitation mitrale et une insuffisance cardiaque congestive rapidement progressives, qui ont conduit à la mort.\n",
+        "synthetic_summary": {
+            "B1": "Un bébé est né avec un cœur très malade. Ses mains et ses pieds étaient très différents, avec des doigts longs et pliés. Son visage avait une forme spéciale, un peu triste.\n\nLes docteurs ont cherché pourquoi. Ils ont trouvé un petit changement dans un gène, une partie très importante pour le corps.\n\nIls ont donné des médicaments pour aider son cœur à mieux travailler. Mais le cœur est resté très faible.\n\nLes docteurs et la famille ont décidé de le soigner doucement, sans opération. Le bébé est parti au ciel après un mois. Les docteurs étaient très tristes, mais ils ont fait de leur mieux pour lui.",
+            "B2": "**Ce qu'ils ont trouvé chez le bébé**  \nUn garçon est né avec une forme grave d'une maladie appelée syndrome de Marfan néonatal (MFS). Cette maladie affecte le tissu conjonctif, qui aide à soutenir le corps. Le bébé avait plusieurs signes visibles : des doigts très longs et pliés (arachnodactylie et camptodactylie), des articulations du coude et du genou qui ne pouvaient pas bien s’étendre, un visage avec des traits âgés, des yeux enfoncés avec une paupière inclinée vers le bas, des oreilles mal formées, une bouche tombante et une tête un peu plus large que la normale. Ses yeux présentaient aussi un problème appelé ectopie lentis, où le cristallin est déplacé.\n\n**Ce que cela signifie au niveau génétique**  \nLes médecins ont fait un test génétique et ont trouvé une nouvelle mutation dans le gène FBN1, qui fabrique une protéine importante appelée fibrilline-1. Cette mutation se trouve dans une partie du gène connue pour causer des formes sévères de MFS chez les nouveau-nés. Cette découverte a confirmé le diagnostic de MFS néonatal.\n\n**Comment ils ont essayé de l’aider**  \nLe bébé avait un cœur très faible avec plusieurs problèmes : des valves cardiaques qui fuyaient (régurgitations mitrale et aortique), une pression élevée dans les poumons (hypertension pulmonaire) et une mauvaise contraction du cœur. Pour l’aider, les médecins ont donné des médicaments pour améliorer le fonctionnement du cœur, réduire la charge de travail du cœur, calmer le bébé et augmenter la production d’urine. Malgré ces traitements, son état cardiaque s’est détérioré.\n\n**Ce qui s’est passé ensuite**  \nÀ cause de la gravité de la maladie, une opération chirurgicale aurait été nécessaire pour prolonger sa vie. Cependant, la famille et l’équipe médicale ont décidé de ne pas faire de chirurgie et de se concentrer sur des soins palliatifs, c’est-à-dire des soins pour soulager la souffrance. Malheureusement, le bébé a développé une insuffisance cardiaque grave, une défaillance de plusieurs organes et est décédé 32 jours après sa naissance.\n\n**En résumé**  \nCe cas montre une forme très sévère du syndrome de Marfan chez un nouveau-né, liée à une mutation génétique rare. Malgré les traitements médicaux, la maladie a rapidement progressé, soulignant la difficulté à gérer cette forme grave de MFS chez les bébés.",
+            "B3": "Résumé détaillé et structuré pour un public adulte non spécialiste\n\n**Contexte**  \nUn nouveau-né a été diagnostiqué avec un syndrome de Marfan (MFS) néonatal, une forme sévère et précoce de cette maladie génétique affectant le tissu conjonctif. Ce garçon est né par césarienne d’urgence à terme, suite à une souffrance fœtale. Aucun antécédent familial d’anomalies congénitales ou de maladies cardiovasculaires graves n’était connu. L’échographie prénatale avait déjà révélé une cardiomégalie (augmentation du volume cardiaque) et des anomalies vasculaires, notamment une constriction aortique gauche.\n\n**Principales observations cliniques**  \nÀ la naissance, le bébé présentait un poids et une taille supérieurs à la moyenne, mais des difficultés respiratoires avec bradycardie (ralentissement du rythme cardiaque) et cyanose (coloration bleutée de la peau) ont été notées. L’examen physique a mis en évidence plusieurs malformations musculo-squelettiques caractéristiques :  \n- Arachnodactylie sévère (doigts anormalement longs et fins) et camptodactylie (doigts en flexion permanente) aux mains et aux pieds.  \n- Raideur partielle des articulations du coude et du genou.  \n- Visage atypique avec hypoplasie malaire (sous-développement des pommettes), aspect « sénile », yeux enfoncés avec fissures palpébrales obliques vers le bas, oreilles malformées et mal positionnées, bouche tombante, brachycéphalie (tête large et courte).  \n- Un souffle cardiaque important a été entendu, indiquant des anomalies valvulaires sévères.\n\nL’échocardiographie a confirmé une dysfonction cardiaque grave :  \n- Dilatation importante du sinus aortique (une partie de l’aorte proche du cœur).  \n- Prolapsus (affaissement) et régurgitations sévères des valves cardiaques (aortique, mitrale, tricuspide et pulmonaire).  \n- Hypertension pulmonaire sévère et mauvaise contractilité du cœur.\n\nUn examen ophtalmologique a révélé une ectopie lentis, c’est-à-dire un déplacement anormal du cristallin dans les deux yeux. Par ailleurs, une hernie hépatique a été détectée.\n\nLe score musculo-squelettique selon les critères internationaux de Gand était élevé (11 points), confirmant la sévérité des manifestations.\n\n**Diagnostic génétique**  \nL’analyse génétique a identifié une mutation nouvelle et pathogène dans le gène FBN1, responsable de la production de fibrilline-1, une protéine essentielle du tissu conjonctif. Cette mutation (c.3964 + 1G > T) se situe dans une région du gène associée aux formes néonatales sévères du syndrome de Marfan (exons 24 à 32). Ce diagnostic a été établi dans les deux premières semaines de vie.\n\n**Interventions et évolution**  \nDès le premier jour, le nouveau-né présentait une hypoxémie réfractaire (manque d’oxygène dans le sang malgré un apport élevé en oxygène) et un faible débit cardiaque. La prise en charge médicale a consisté en :  \n- Réduction de la postcharge (la résistance contre laquelle le cœur doit pomper) par l’infusion continue de milrinone, un médicament améliorant la contractilité cardiaque.  \n- Sédation profonde avec fentanyl pour diminuer le stress cardiaque.  \n- Utilisation de diurétiques pour améliorer la fonction rénale et réduire la surcharge liquidienne.\n\nMalgré ces mesures, l’état cardiaque s’est rapidement détérioré avec aggravation des régurgitations valvulaires, de l’hypertension pulmonaire et de la fonction cardiaque. La ventilation mécanique invasive a été nécessaire pour soutenir la respiration.\n\nAprès plusieurs discussions entre l’équipe médicale et la famille, il a été décidé de privilégier les soins palliatifs plutôt qu’un traitement chirurgical, compte tenu de la gravité et de la progression rapide de la maladie.\n\n**Résultats et pronostic**  \nLa maladie a évolué vers une insuffisance cardiaque congestive sévère, une congestion hépatique et pulmonaire, ainsi qu’une hémorragie pulmonaire. Le nouveau-né a développé un syndrome de défaillance multiviscérale (dysfonctionnement simultané de plusieurs organes) et est décédé à l’âge de 32 jours.\n\n**Conclusion**  \nCe cas illustre la forme néonatale sévère du syndrome de Marfan, caractérisée par une mutation spécifique du gène FBN1 et une atteinte multisystémique majeure, notamment cardiaque, musculo-squelettique et oculaire. Malgré une prise en charge médicale intensive, le pronostic reste très réservé, soulignant l’importance d’un diagnostic précoce et d’une communication claire avec les familles pour orienter les décisions thérapeutiques."
+        }
+    },
+    {
+        "article": "La patiente était une Chinoise de 75 ans, une agricultrice de la ville de Yongzhou, dans la province du Hunan, en Chine. Deux mois auparavant, la patiente présentait des symptômes de vertiges, de manque d'appétit, de sommeil médiocre et de faiblesse des membres sans cause évidente. La patiente a progressivement empiré et a été diagnostiquée avec une gastrite atrophique chronique avec positivité Helicobacter pylori (Hp), une hypoproteinémie et une IDA. En outre, une hypertrophie de l'oreillette gauche et une dysfonction diastolique du ventricule gauche ont été diagnostiquées par échocardiographie.\n\nLes résultats des tests sanguins de routine étaient les suivants : un nombre de globules rouges (RBC) de 1,84 × 1012/L, un taux d’hématocrite de 13 %, un nombre de plaquettes de 500 × 109/L, un taux d’hémoglobine de 35 g/L (valeur critique), un volume corpusculaire moyen de 70,7 fL, un taux de protéines totales de 44,6 g/L, un taux d’éosinophiles de 5,3 %, un taux de sédimentation érythrocytaire de 25 mm/h, un taux d’immunoglobuline (Ig)E de 1282,2 IU/ml, un taux de fer sérique de 3,85 μmol/L et un résultat positif au test de sang occulte dans les selles. L’examen cytomorphologique de la moelle osseuse a révélé une prolifération active des granulocytes, des mégacaryocytes et des cellules myéloïdes. Un examen par cytométrie de flux n’a pas indiqué les immunophénotypes anormaux indicatifs d’une leucémie aiguë, d’un MDS, d’un lymphome ou de tumeurs myéloïdes. L’endoscopie gastro-intestinale a montré la présence de nématodes vivants dans la partie descendante du duodénum du patient. La patiente a été traitée avec des globules rouges à faible teneur en leucocytes pour corriger une anémie sévère et l’antihelminthique albendazole. Après le traitement, son taux d’hémoglobine a été confirmé à 77 g/L. Au cours des visites de suivi, la patiente a été traitée avec succès avec un antihelminthique et son anémie a été guérie.\n\nExamens d'imagerie et morphologiques\nPour exclure une maladie gastro-intestinale, le patient a subi une endoscopie gastro-intestinale. Des nématodes vivants ont été découverts se nourrissant de la muqueuse de la partie descendante du duodénum du patient. Des œufs d'ankylostomes ont été trouvés dans les selles par flottation en saumure saturée. Par conséquent, le patient a finalement été diagnostiqué avec une IDA sévère causée par une infection par ankylostomes.",
+        "gold_summary": "Une Chinoise de 75 ans qui présentait des vertiges, un manque d’appétit, des troubles du sommeil et une faiblesse des membres a été diagnostiquée avec une gastrite atrophique chronique et a été testée positive pour Helicobacter pylori, une anémie ferriprive avec une concentration en hémoglobine de 35 g/L et une hypertrophie de l’oreillette gauche. Cependant, après un traitement symptomatique, la patiente ne s’est pas améliorée. Une endoscopie gastro-intestinale supérieure a révélé la présence de nématodes vivants dans la partie descendante du duodénum de la patiente. Un examen fécal par flottation en saumure saturée a révélé des œufs d’ankylostomes. Une vérification supplémentaire par un test de réaction en chaîne de la polymérase par transcription inverse semi-nested a confirmé que l’espèce d’ankylostomes était Necator americanus. L’albendazole a été utilisé pour un traitement antihelminthique. Au cours des visites de suivi, nous avons constaté que le traitement antihelminthique était efficace et que son anémie avait été guérie.\n",
+        "synthetic_summary": {
+            "B1": "Une dame de 75 ans se sentait très fatiguée et avait mal au ventre. Elle avait aussi du mal à manger et à bien dormir. Le docteur a trouvé qu’elle avait un problème dans son ventre et qu’elle manquait beaucoup de sang.\n\nLe docteur a regardé dans son ventre avec une petite caméra. Il a vu des petits vers vivants qui faisaient du mal. Ces vers prenaient le sang de la dame.\n\nLe docteur lui a donné un médicament pour tuer les vers. Après ça, la dame a commencé à aller mieux. Elle a retrouvé du sang et elle n’était plus fatiguée. Tout va mieux maintenant.",
+            "B2": "Une femme chinoise de 75 ans avait plusieurs problèmes : elle se sentait étourdie, n’avait pas d’appétit, dormait mal et avait des muscles faibles. Les médecins ont d’abord découvert qu’elle avait une inflammation chronique de l’estomac appelée gastrite atrophique, et une infection par une bactérie nommée Helicobacter pylori. Elle souffrait aussi d’une anémie ferriprive, c’est-à-dire un manque de fer qui rend le sang faible, avec un taux très bas d’hémoglobine (une protéine qui transporte l’oxygène dans le sang). Son cœur montrait aussi des signes de stress avec une partie appelée oreillette gauche qui était plus grosse que la normale.\n\nMalgré un traitement pour ses symptômes, son état ne s’améliorait pas. Les médecins ont alors fait une endoscopie, c’est-à-dire qu’ils ont utilisé une caméra pour regarder à l’intérieur de son tube digestif. Ils ont trouvé des vers vivants, appelés nématodes, dans une partie de l’intestin appelée le duodénum. En analysant ses selles, ils ont aussi trouvé des œufs de ces vers, appelés ankylostomes. Un test spécial a confirmé que ces vers étaient de l’espèce Necator americanus.\n\nPour soigner cette infection, la patiente a reçu un médicament appelé albendazole, qui tue ces vers. Après ce traitement, son anémie s’est améliorée et elle a retrouvé la santé lors des visites de contrôle. Ce cas montre que des infections par des parasites peuvent causer une anémie sévère, et qu’un bon diagnostic est important pour donner le bon traitement.",
+            "B3": "Contexte  \nUne femme chinoise de 75 ans, agricultrice dans la province du Hunan, a présenté pendant deux mois des symptômes progressifs comprenant des vertiges, une perte d’appétit, des troubles du sommeil et une faiblesse des membres, sans cause évidente. Elle a été initialement diagnostiquée avec une gastrite atrophique chronique associée à une infection par Helicobacter pylori, une anémie ferriprive sévère (concentration en hémoglobine de 35 g/L), une hypoprotéinémie, ainsi qu’une hypertrophie de l’oreillette gauche et une dysfonction diastolique du ventricule gauche.\n\nPrincipales Observations  \nLes analyses sanguines ont montré une anémie très sévère avec un nombre de globules rouges très bas (1,84 × 10^12/L), un taux d’hématocrite de 13 %, un volume corpusculaire moyen réduit (70,7 fL), un taux de protéines totales abaissé (44,6 g/L), ainsi qu’une élévation notable des immunoglobulines E (1282,2 IU/ml). Le test de sang occulte dans les selles était positif, suggérant une perte de sang digestive. L’examen de la moelle osseuse a révélé une prolifération active des cellules myéloïdes sans signe de leucémie ou autre maladie hématologique maligne.  \n\nUne endoscopie digestive haute a mis en évidence la présence de nématodes vivants dans la partie descendante du duodénum, confirmant une infection parasitaire. L’analyse des selles par flottation en saumure saturée a identifié des œufs d’ankylostomes. Une analyse moléculaire par PCR a précisé que l’espèce en cause était Necator americanus, un ver parasite responsable d’infections intestinales pouvant entraîner une anémie ferriprive sévère par saignement chronique.\n\nInterprétation Clinique  \nL’anémie sévère de la patiente était principalement due à une infection par ankylostomes provoquant une perte sanguine digestive chronique, aggravée par la gastrite atrophique et l’infection à Helicobacter pylori. Le diagnostic initial d’anémie ferriprive a été complété par la découverte de ce parasite, ce qui a modifié la prise en charge thérapeutique.\n\nProchaines Étapes  \nLa patiente a reçu une transfusion de globules rouges à faible teneur en leucocytes pour corriger son anémie critique, ainsi qu’un traitement antihelminthique à base d’albendazole. Lors des visites de suivi, le traitement a été efficace : les nématodes ont été éliminés et le taux d’hémoglobine est remonté à 77 g/L, avec une guérison complète de l’anémie. Ce cas souligne l’importance de rechercher une cause parasitaire chez les patients présentant une anémie ferriprive sévère, surtout dans les zones où les infections par ankylostomes sont endémiques."
+        }
+    },
+    {
+        "article": "Un nourrisson de 5 mois a été admis au service d'urgence pédiatrique avec des antécédents de toux et d'obstruction nasale depuis trois jours. Son état général s'était détérioré au cours des 24 heures précédentes, avec de la fièvre, des efforts respiratoires, une perte d'appétit et des vomissements après les repas.\n\nIl s'agissait d'un nourrisson en bonne santé, ayant eu une grossesse à faible risque, avec des soins prénataux tardifs (3e trimestre), une échographie obstétrique normale (à 26 semaines de gestation), mais sans échographie morphologique. Il est né par voie vaginale, à terme, avec un poids adéquat pour l'âge gestationnel, sans complications.\n\nL'examen physique à l'admission a révélé un patient apyrétique (36,8 °C), tachycardique (158 bpm), tachypneique (50 bpm), avec hypoxémie (SpO2 92 %). L'auscultation pulmonaire a révélé une réduction des bruits respiratoires sur le côté gauche de l'hémithorax et la présence de râles fins, de ronflements et de respiration sifflante bilatérale diffuse. Une coryza hyaline et une détresse respiratoire ont été observées, avec une rétraction intercostale, sous-costale et sternale modérée à sévère. L'auscultation cardiaque a révélé des bruits cardiaques étouffés. Il y a eu une amélioration de la saturation en oxygène (98 %) et de l'effort respiratoire avec l'administration d'oxygène par un cathéter nasal.\n\nLe patient a été diagnostiqué avec une AVB et admis au service pédiatrique en raison de la nécessité d'oxygène supplémentaire et d'un effort respiratoire modéré à sévère. Des tests de laboratoire et d'imagerie ont été demandés.\n\nLe virus respiratoire syncytial a été détecté sur un écouvillon nasopharyngé. La formule leucocytaire était normale (8 000/μL), avec une prédominance de lymphocytes (72 % = 5 760/μL) et la présence de lymphocytes réactifs (2 % = 160/μL), en plus d'une thrombocytose modérée (487 000/μL). La protéine C-réactive (CRP) était normale (5,8 mg/L ; valeur de référence : moins de 10 mg/dL). La radiographie thoracique a montré un élargissement du contour cardiaque.\n\nEn raison des résultats radiographiques, une investigation cardiaque a été réalisée, qui a révélé des taux de troponine de 86,5 pg/mL (valeur de référence : jusqu'à 19,8 pg/mL) et de créatine phosphokinase-MB (CKMB) de 18 U/L (valeur de référence : jusqu'à 16U/L). L'électrocardiogramme a montré une altération de la repolarisation ventriculaire gauche. L'échocardiogramme a montré une masse hétérogène, mesurant 52 × 38 mm, sur la paroi latérale du ventricule gauche, avec des zones de calcification, préservant l'écoulement et le reflux du ventricule gauche.\n\nL'angiographie par TDM du thorax a montré une grande masse cardiaque intramurale dans le ventricule gauche avec une restriction significative du volume ventriculaire et une extension extra-cardiaque, de petits foyers de calcification centrale et un petit épanchement péricardique.\n\nL'IRM cardiaque a montré une masse dans le ventricule gauche, mesurant 5,5 × 5,3 cm, mobile avec le cycle cardiaque, s'étendant jusqu'à l'artère pulmonaire et dans le médiastin. Un effet de masse important a été noté dans le ventricule gauche, avec une réduction de la cavité ventriculaire, altérant modérément sa fonction globale (fraction d'éjection ventriculaire gauche [EF] = 46 %). Les images pondérées en T2 ont montré un hypersignal myocardique modéré et une absorption de contraste nettement retardée (> 10 minutes).\n\nL'extension extra-cardiaque de la lésion et l'épanchement péricardique suggéraient un comportement agressif. Cependant, la caractérisation du site et des tissus, c'est-à-dire les foyers de calcification et l'amélioration nettement ralentie, suggéraient des composants fibrotiques. Par conséquent, les hypothèses suggérées par les tests d'imagerie étaient le rhabdomyosarcome et le fibrome cardiaque.\n\nUn Holter a été effectué et a montré un bloc de branche droit complet et des extrasystoles supraventriculaires isolées. Une IRM abdominale totale et une échographie transfontanellaire ont été effectuées, en raison de la possibilité d'un rhabdomyosarcome cardiaque, les deux étant normaux.\n\nLe patient a subi une cathétérisation cardiaque pour biopsie, et des fragments ont été envoyés pour analyse histopathologique et immunohistochimique. La biopsie étant peu concluante, il a été décidé de commencer un traitement par sirolimus hors indication.\n\nPendant l'utilisation de sirolimus, des échocardiogrammes périodiques ont été réalisés, en plus des tests de laboratoire hebdomadaires, y compris la numération sanguine, la CRP, la dose de sirolimus sérique, la fonction rénale, la fonction hépatique et le profil lipidique. Pendant cette période, la dose de sirolimus sérique a été maintenue dans la plage thérapeutique, entre 5 et 10 ng/mL, sans modification des autres tests de laboratoire.\n\nL'échocardiogramme de la deuxième semaine d'utilisation du sirolimus a identifié un épanchement péricardique important, provoquant un dysfonctionnement du ventricule droit (VD), et une péricardiocentèse a été réalisée, drainant 48 ml de liquide séro-sanguinolent.\n\nAprès trois semaines d'utilisation de sirolimus, une IRM de contrôle a été réalisée et il n'y a pas eu de changements significatifs dans la taille ou les caractéristiques de la masse tumorale, par conséquent l'utilisation hors indication de sirolimus a été interrompue.\n\nUne nouvelle cathétérisation cardiaque avec biopsie a été réalisée. Deux fragments de tissus ont été envoyés pour analyse anatomopathologique, le plus grand mesurant 1,5 cm de longueur et 0,1 cm de diamètre. Cette fois, l'analyse histopathologique a été concluante pour un fibrome cardiaque.\n\nLa masse était une tumeur histologiquement bénigne, mais avec un comportement agressif en raison de sa taille, de son emplacement et de son infiltration dans le myocarde. La patiente a nécessité une hospitalisation prolongée, avec l'utilisation de médicaments vasoactifs en raison d'un compromis hémodynamique. La tumeur n'a pas répondu à l'utilisation hors indication de sirolimus, nécessitant une polypharmacie cardiologique, de multiples hospitalisations en raison d'une décompensation cardiaque, et la patiente a développé une insuffisance cardiaque congestive de classe fonctionnelle 3 (ICC), atteignant une EF de 35 %.\n\nEn raison de l'aggravation progressive de la EF et, par conséquent, de la classe fonctionnelle de l'ICC, il a été décidé d'inclure le patient dans la liste de transplantation cardiaque, car la résection de la tumeur était impossible en raison de son infiltration dans la paroi myocardique du ventricule gauche.\n\nSix mois après le diagnostic, la patiente a subi une transplantation cardiaque dans le même hôpital où le diagnostic a été posé, avec un bon déroulement postopératoire. L'anatomie et les résultats histopathologiques de l'échantillon chirurgical ont confirmé le diagnostic de fibrome cardiaque.",
+        "gold_summary": "Un nourrisson de 5 mois a été admis au service d'urgence pédiatrique avec une bronchiolite virale aiguë nécessitant une hospitalisation. Il présentait un virus respiratoire syncytial détectable dans un écouvillon oropharyngé, un test sanguin avec lymphocytose et une radiographie thoracique a révélé une cardiomégalie. Des tests cardiaques supplémentaires ont été effectués, détectant une élévation des biomarqueurs cardiaques, un électrocardiogramme avec une altération de la repolarisation ventriculaire gauche et une échocardiographie avec une masse hétérogène dans le ventricule gauche, avec des zones de calcification. Une angiotomographie thoracique suggérait un rhabdomyosarcome ou un fibrome cardiaque et une résonance magnétique a montré une masse, avec des caractéristiques suggérant un fibrome. Le diagnostic final a été fait après deux cathétérismes cardiaques pour biopsie de la lésion, confirmant un fibrome cardiaque par examen anatomo-pathologique. Le patient ayant une dysfonction systolique modérée à sévère, il a été soumis à une transplantation cardiaque.\n",
+        "synthetic_summary": {
+            "B1": "Un bébé de 5 mois est allé à l'hôpital parce qu'il avait du mal à respirer. Il avait un gros rhume avec une toux et un nez bouché.\n\nLes docteurs ont fait des examens et ont trouvé un gros bouton dans son cœur. Ce bouton était comme une boule dure avec des parties calcifiées.\n\nIls ont fait plusieurs tests pour comprendre ce que c'était. Après deux examens où ils ont pris un petit morceau du bouton, ils ont su que c'était un fibrome. C'est une boule qui n'est pas un cancer, mais qui peut être dangereuse parce qu'elle est grande.\n\nLe bébé avait du mal à faire battre son cœur normalement. Alors, les docteurs ont décidé de lui donner un nouveau cœur. Après l'opération, il allait mieux.",
+            "B2": "Un bébé de 5 mois est arrivé aux urgences avec une infection virale des voies respiratoires, appelée bronchiolite, qui a nécessité son hospitalisation. Les médecins ont trouvé un virus appelé virus respiratoire syncytial dans un prélèvement nasal. Une prise de sang a montré une augmentation de certains globules blancs (lymphocytes), et une radiographie du thorax a révélé que son cœur était plus gros que la normale.\n\nPour mieux comprendre ce problème cardiaque, plusieurs examens ont été faits. Des analyses ont montré que des substances dans le sang, liées au cœur, étaient élevées, ce qui peut indiquer un stress ou une blessure du muscle cardiaque. L’électrocardiogramme, qui mesure l’activité électrique du cœur, montrait des anomalies dans une partie du cœur appelée ventricule gauche. Une échographie du cœur a découvert une grosse masse, c’est-à-dire une tumeur, avec des zones calcifiées, à l’intérieur du ventricule gauche.\n\nD’autres examens d’imagerie, comme une angiotomodensitométrie et une résonance magnétique, ont aidé à mieux voir cette masse. Les images suggéraient que la tumeur pouvait être soit un rhabdomyosarcome (un cancer du muscle cardiaque), soit un fibrome cardiaque (une tumeur bénigne faite de tissu fibreux). Pour confirmer le diagnostic, les médecins ont réalisé deux biopsies, c’est-à-dire qu’ils ont prélevé un petit morceau de la masse pour l’étudier au microscope. L’analyse a montré qu’il s’agissait d’un fibrome cardiaque, une tumeur non cancéreuse.\n\nMalheureusement, cette tumeur était assez grande et située dans une partie importante du cœur, ce qui a causé une mauvaise fonction du muscle cardiaque. Le bébé a développé une insuffisance cardiaque modérée à sévère, ce qui signifie que son cœur ne pompait pas le sang correctement. Comme la tumeur ne pouvait pas être enlevée par chirurgie, les médecins ont décidé de placer le bébé sur la liste pour une transplantation cardiaque.\n\nSix mois après le diagnostic, le bébé a reçu un nouveau cœur grâce à une transplantation, qui s’est bien passée. L’étude du cœur enlevé a confirmé le diagnostic de fibrome cardiaque. Ce cas montre qu’une tumeur bénigne du cœur peut être très grave à cause de sa taille et de son emplacement, et que parfois la transplantation est la meilleure solution.",
+            "B3": "Résumé détaillé et structuré\n\nContexte  \nUn nourrisson de 5 mois, initialement en bonne santé, a été admis aux urgences pédiatriques pour une bronchiolite virale aiguë, caractérisée par une toux, une obstruction nasale, une détresse respiratoire et une fièvre évoluant depuis plusieurs jours. Le virus respiratoire syncytial a été identifié comme agent infectieux. Lors de l’examen initial, une hypoxémie modérée et une tachypnée ont été constatées, nécessitant une oxygénothérapie.\n\nPrincipales observations  \nOutre les signes respiratoires, la radiographie thoracique a révélé une cardiomégalie (augmentation du volume cardiaque), ce qui a motivé la réalisation d’examens cardiaques complémentaires. Ces investigations ont montré :  \n- Une élévation des biomarqueurs cardiaques, notamment la troponine et la créatine phosphokinase-MB, suggérant une atteinte myocardique.  \n- Un électrocardiogramme avec altération de la repolarisation du ventricule gauche, indiquant une anomalie électrique cardiaque.  \n- Une échocardiographie a mis en évidence une masse hétérogène de grande taille (environ 5 cm) localisée sur la paroi latérale du ventricule gauche, avec des zones de calcification, sans obstruction du flux sanguin.  \n- Une angiotomodensitométrie thoracique a confirmé la présence d’une masse intramurale avec extension extra-cardiaque et un petit épanchement péricardique.  \n- Une imagerie par résonance magnétique cardiaque a précisé la taille, la mobilité et l’extension de la masse, ainsi que des caractéristiques tissulaires compatibles avec un fibrome cardiaque, bien que le diagnostic différentiel incluait un rhabdomyosarcome (tumeur maligne).\n\nUne surveillance électrocardiographique prolongée a révélé un bloc de branche droit complet et des extrasystoles supraventriculaires isolées. Des examens complémentaires à la recherche d’extensions tumorales (IRM abdominale, échographie transfontanellaire) étaient normaux.\n\nInterprétation clinique  \nLa nature de la masse cardiaque a été confirmée après deux procédures de cathétérisme cardiaque avec biopsie. La première biopsie était peu concluante, ce qui a conduit à un traitement expérimental par sirolimus, sans amélioration notable. La seconde biopsie a confirmé le diagnostic de fibrome cardiaque, une tumeur bénigne mais localement agressive, infiltrant le myocarde et altérant la fonction ventriculaire gauche (fraction d’éjection réduite à 35 %). Cette infiltration a provoqué une insuffisance cardiaque congestive sévère, nécessitant une prise en charge médicale complexe et des hospitalisations répétées.\n\nProchaines étapes  \nEn raison de l’aggravation progressive de la fonction cardiaque et de l’impossibilité de réséquer la tumeur chirurgicalement, le nourrisson a été inscrit sur la liste de transplantation cardiaque. Six mois après le diagnostic initial, il a bénéficié d’une transplantation cardiaque avec un bon résultat postopératoire. L’analyse anatomopathologique de la pièce opératoire a confirmé le diagnostic de fibrome cardiaque.\n\nCe cas illustre la complexité du diagnostic et de la prise en charge des masses cardiaques chez le nourrisson, ainsi que l’importance d’une évaluation multidisciplinaire et d’un suivi rigoureux pour adapter le traitement en fonction de l’évolution clinique et des résultats des examens complémentaires."
+        }
+    },
+    {
+        "article": "Patient de 15 mois, sexe féminin, première fille de parents en bonne santé, non consanguins. Sa grossesse a été contrôlée et s'est déroulée sans complications. Elle est née par accouchement vaginal à 40 semaines de gestation, avec un poids de 2635 grammes (percentile 2), une taille de 48 cm (percentile 8) et un périmètre crânien de 33 cm (percentile 5), selon les courbes d'Alarcón et Pittaluga4 avec un score d'APGAR de 9-10.\n\nElle a évolué avec un développement psychomoteur normal et n’a pas eu de maladies intercurrentes. À l’âge de 4 mois, un souffle cardiaque a été ausculté lors d’un contrôle pédiatrique, et elle a été référée en cardiologie. Un échocardiogramme a révélé une sténose des branches pulmonaires, ce qui, ajouté à la découverte d’un front proéminent lors de l’examen physique, a motivé son orientation vers la génétique clinique.\n\nL'évaluation génétique a révélé des caractéristiques telles qu'une implantation antérieure des cheveux élevée, des sourcils droits, des yeux enfoncés, des pavillons auriculaires proéminents, un pont nasal bas, un profil nasal convexe avec une pointe bulbeuse, une columelle courte et un menton pointu. En outre, un souffle systolique a été détecté au niveau du poumon lors de l'auscultation. Aucune altération de l'abdomen, des organes génitaux ou des extrémités n'a été observée.\n\nDes examens complémentaires ont été réalisés en raison du soupçon de SALG. Les radiographies de la colonne vertébrale ont révélé des vertèbres D4 et D6 avec une tendance morphologique en papillon et une ossification incomplète de l'arc postérieur de L5. Les radiographies des extrémités et du bassin, ainsi que les échographies abdominales et rénales, n'ont pas révélé d'anomalies. Les analyses des paramètres hormonaux, biochimiques, de la fonction hépatique et rénale n'ont révélé qu'une légère élévation de la LDH.\n\nL’hypothèse diagnostique principale a été confirmée par un panel commercial pour les anomalies cardiaques congénitales et l’hétérotaxie, qui comprenait les deux gènes associés à SALG (JAG1 et NOTCH2), permettant l’étude des variantes ponctuelles et des variantes du nombre de copies (CNV) des gènes analysés, un aspect important pour la pathologie étudiée. Cette analyse a identifié une microdélétion pathogénique hétérozygote couvrant la totalité de la séquence codante du gène JAG1 , ainsi que trois variantes hétérozygotes de signification incertaine dans les gènes DNAH11, NME8 et NEK8 (associés à la dyskinésie ciliaire primaire et à la néphronoptisis, toutes deux héréditaires autosomiques récessives).\n\nÉtant donné qu'une délétion complète du gène JAG1 a été identifiée et compte tenu des rapports de gènes contiguës associés à des pathologies qui pourraient nécessiter des interventions supplémentaires chez la patiente, il a été décidé de procéder à une étude plus approfondie au moyen d'un caryotype moléculaire (Affymetrix CytoScan 750K). L'array a confirmé la présence d'une microdélétion pathogénique, arr[GRCh37] 20p12.2(10414643_10792802)x1, d'environ 378 kb, qui comprenait 5 gènes : MKKS, SLX4IP, JAG1, MIR6870, LINC01752. Cela a confirmé moléculairement le SALG en raison de la délétion complète du gène JAG1.\n\nLa patiente remplissait trois des sept critères cliniques pour le diagnostic de SALG, avec une sténose des branches des artères pulmonaires, des vertèbres thoraciques en forme de papillon et des caractéristiques faciales typiques, y compris des yeux enfoncés, un bout du nez bulbeux et un menton pointu. Les contrôles ultérieurs n'ont pas révélé de modifications des tests de la fonction hépatique ou rénale, d'anomalies ophtalmologiques ou de xantomes. Son développement neurologique est conforme à son âge.\n\nIl a été suggéré aux parents de procéder à une étude du caryotype moléculaire pour déterminer la possibilité d’être porteur de CNV, ce qui les exposerait à un risque de récurrence de 50 % pour un autre enfant. Cependant, pour des raisons économiques, cette étude n’a pas été réalisée.\n\n",
+        "gold_summary": "Patient de sexe féminin, qui a été diagnostiquée avec un souffle cardiaque à l'âge de 4 mois. L'échocardiographie a révélé une sténose des branches pulmonaires, ce qui, avec le front proéminent observé à l'examen physique, a motivé son orientation vers la génétique clinique. En raison du soupçon de SALG, des études complémentaires ont été réalisées, qui ont révélé des vertèbres en papillon et un panel génétique qui a identifié une délétion pathogénique en hétérozygotie, couvrant toute la séquence codante du gène JAG1. Pour exclure une délétion plus étendue, un caryotype moléculaire a été réalisé, confirmant une microdélétion pathogénique sur le chromosome 20 de 378 kb (arr[GRCh37] 20p12.2(10414643_10792802)x1).\n",
+        "synthetic_summary": {
+            "B1": "Il y a une petite fille qui a eu un bruit spécial au cœur quand elle avait 4 mois. Les docteurs ont regardé son cœur avec une machine. Ils ont vu que le chemin du sang vers les poumons était un peu serré.\n\nLes docteurs ont aussi vu que ses os du dos étaient un peu différents. Ils ont fait un test pour regarder ses gènes, qui sont comme des petites instructions dans le corps. Ce test a montré qu’il manquait un petit morceau important dans ses gènes.\n\nPour être sûrs, ils ont fait un autre test plus grand. Ce test a confirmé qu’un petit morceau sur un de ses chromosomes était absent. Cela explique pourquoi elle a ces petits problèmes. Les docteurs vont bien s’occuper d’elle.",
+            "B2": "### Ce qu’ils ont trouvé chez la patiente\n\nUne petite fille de 15 mois a été suivie après la découverte d’un souffle au cœur à 4 mois. Un examen spécial du cœur, appelé échocardiogramme, a montré que certaines artères pulmonaires étaient rétrécies (on appelle cela une sténose). Lors de l’examen physique, les médecins ont aussi remarqué que son front était un peu plus saillant que la normale. Ces signes ont conduit les médecins à demander des tests génétiques pour mieux comprendre ce qui se passait.\n\n### Ce que cela signifie\n\nLes examens complémentaires ont montré que certaines vertèbres dans son dos avaient une forme particulière appelée « vertèbres en papillon ». Ensuite, un test génétique appelé « panel génétique » a révélé qu’elle avait une délétion, c’est-à-dire une partie manquante, dans un gène important nommé JAG1. Ce gène joue un rôle dans le développement de plusieurs organes, y compris le cœur. Pour vérifier si cette délétion était plus grande, un autre test appelé caryotype moléculaire a été fait. Ce test a confirmé qu’une petite partie du chromosome 20, qui contient le gène JAG1 et quelques autres gènes, manquait chez cette enfant.\n\n### Conclusion\n\nCette délétion génétique explique les problèmes cardiaques et les signes physiques observés. Ce diagnostic correspond à une maladie appelée syndrome d’Alagille (SALG), qui peut affecter plusieurs parties du corps. La patiente est suivie régulièrement pour surveiller son développement et sa santé. Les médecins ont aussi proposé d’étudier les parents pour voir s’ils portent cette délétion, car cela pourrait influencer le risque pour d’autres enfants, mais cette étude n’a pas été réalisée pour des raisons financières.",
+            "B3": "Résumé détaillé et structuré pour un public non spécialiste\n\nContexte  \nIl s’agit d’une fillette de 15 mois, née sans complication majeure, avec un développement psychomoteur normal jusqu’à présent. À l’âge de 4 mois, un souffle cardiaque a été détecté lors d’un examen pédiatrique de routine, ce qui a conduit à une consultation en cardiologie.\n\nPrincipales observations  \nL’échocardiogramme a révélé une sténose (rétrécissement) des branches des artères pulmonaires. Par ailleurs, l’examen clinique a mis en évidence un front proéminent ainsi que des traits faciaux caractéristiques, notamment des yeux enfoncés, un nez avec une pointe bulbeuse et un menton pointu. Ces signes ont orienté les médecins vers une évaluation génétique. Des radiographies ont montré des vertèbres thoraciques en forme de papillon, une anomalie osseuse spécifique. Les autres examens (échographies abdominales et rénales, analyses sanguines) étaient globalement normaux, à l’exception d’une légère augmentation de la lactate déshydrogénase (LDH), une enzyme pouvant refléter une activité cellulaire accrue ou une lésion tissulaire.\n\nInterprétation clinique  \nLe diagnostic principal suspecté était le syndrome Alagille (SALG), une maladie génétique rare caractérisée par des anomalies cardiaques, osseuses et des traits faciaux spécifiques. Un test génétique ciblé a identifié une microdélétion pathogénique en hétérozygotie (c’est-à-dire affectant une seule copie du gène) qui supprime entièrement la séquence codante du gène JAG1, connu pour être responsable du SALG. Pour préciser l’étendue de cette délétion, un caryotype moléculaire (analyse chromosomique fine) a été réalisé, confirmant la présence d’une microdélétion d’environ 378 kilobases sur le chromosome 20, englobant cinq gènes dont JAG1. Cette découverte confirme de manière moléculaire le diagnostic de SALG chez cette patiente.\n\nProchaines étapes  \nLa patiente remplit trois des sept critères cliniques habituellement utilisés pour diagnostiquer le SALG : la sténose des artères pulmonaires, les vertèbres en papillon et les caractéristiques faciales typiques. Son développement neurologique est normal à ce jour, et aucun autre signe associé (comme des anomalies hépatiques, rénales ou oculaires) n’a été détecté jusqu’à présent. Il a été recommandé aux parents de réaliser un caryotype moléculaire afin de déterminer s’ils sont porteurs de cette microdélétion, ce qui pourrait entraîner un risque de transmission de 50 % à un autre enfant. Toutefois, cette étude n’a pas été effectuée pour des raisons financières.\n\nEn résumé, cette jeune patiente présente un syndrome Alagille confirmé génétiquement, avec des manifestations cardiaques, osseuses et faciales caractéristiques, nécessitant un suivi multidisciplinaire pour surveiller l’apparition éventuelle d’autres complications liées à cette maladie génétique."
+        }
+    },
+    {
+        "article": "Une femme de 82 ans atteinte de diabète de type 2 et d'insuffisance rénale chronique a été admise à l'hôpital avec un antécédent de 7 jours de fièvre, de délire et de dyspnée. Elle avait subi une prothèse valvulaire aortique (prothèse valvulaire sans suture de Perceval) 18 mois auparavant en raison d'une sténose aortique. La période post-opératoire immédiate a été compliquée par un épisode de fibrillation auriculaire paroxystique, un épanchement pleural gauche transudatif et une oligoanurie rénale. Elle n'a présenté aucune infection compliquée et l'incision de la sternotomie médiane s'est normalement refermée. Entre 1 et 14 mois après une chirurgie aortique, elle a été admise à l'hôpital cinq fois en raison d'une insuffisance cardiaque sévère inexpliquée et d'un épisode de fibrillation auriculaire paroxystique. Elle n'a présenté aucune fièvre ou autre signe d'infection et n'a reçu aucun traitement antibiotique. Un échocardiogramme transoesophagien réalisé 3 mois après la chirurgie a montré une prothèse valvulaire aortique sans altération. Au cours de l'examen physique, sa température était de 39 °C, elle était confuse et tachypneique. Un murmure de la fonction cardiaque de 3/6 a été observé en position aortique et une crépitation pulmonaire basale a été observée. Elle présentait des ulcères de pression non infectés de grade II au niveau des talons et de la région sacrococcygienne. Les tests de laboratoire ont montré un nombre normal de cellules sanguines, une créatinine sérique de 2,14 mg/dL et une augmentation de la protéine C-réactive (13 mg/dL) et une hyperglycémie (628 mg/dL). Une radiographie thoracique a montré un épanchement pleural gauche et un oedème pulmonaire interstitiel bilatéral. Deux ensembles de bouteilles de culture sanguine aérobie et anaérobie ont été prélevés à l'admission, et une ceftriaxone empirique (2 mg/dL) et une levofloxacine ajustée à la fonction rénale (250 mg/dL) ont été démarrées. Après 26 à 80 heures d'incubation dans le système BACTEC FX (Becton, Dickinson and Company), les quatre bouteilles de culture sanguine étaient positives. La coloration Gram a montré des bacilles Gram positifs coryneformes avec des formes ramifiées occasionnelles. Après incubation sur de l'agar CNA et de l'agar chocolat, les colonies étaient inférieures à 2 mm, luisantes et jaunes. Les colonies pénétraient dans l'agar lors d'une incubation ultérieure. Le 5e jour d'admission, des cultures sanguines ont été obtenues à nouveau, et le même organisme a été cultivé dans 1 des 4 bouteilles. Les isolats ont été initialement identifiés par une matrice-assistée par laser-ionisation-temps de vol (MALDI-TOF MS, Bruker Daltonics) comme C. cellulans. Par la suite, l'identification a été confirmée par API Coryne strip (bioMérieux ; code numéro 7572767), qui était une « excellente identification » pour C. cellulans avec une fiabilité de 99,9 %, et par séquençage de l'ARN 16S (en utilisant l'outil d'analyse de séquence BLAST de la base de données GenBank), montrant une similitude de 100 % avec C. cellulans et 99,8 % avec C. funkei. Les tests de susceptibilité antimicrobienne ont été effectués en utilisant un panneau de microdilution microtitre MICroSTREP plus 6 (MicroScan Walk Away, Beckman Coulter). Après les critères d'Eucast pour Corynebacterium, l'isolate était sensible ou probablement sensible (pour les antibiotiques sans critères d'Eucast, mais avec une faible MIC) à l'amoxicilline-clavulanate (MIC = 2 mg/L), à la daptomycine (MIC = 0,5 mg/L), à la levofloxacin (MIC = 2 mg/L), à la linezolid (MIC≤1 mg/L), à la tétracycline (MIC = 0,5 mg/L), au trimethoprim-sulfamethoxazole (MIC = 0,006 mg/L) et à la vancomycine (MIC = 0,5 mg/L), et résistante ou probablement résistante à l'amikacine (MIC = 32 mg/L), à la cefotaxime (MIC> 2 mg/L), à la ciprofloxacine (MIC> 2 mg/L), à la clindamycine (MIC> 2 mg/L), à l'érythromycine (MIC = 1 mg/L), à la gentamycine (MIC = 4 mg/L), à l'imipenem (MIC = 4 mg/L), au meropenem (MIC = 8 mg/L) et à la rifampicine (MIC = 1 mg/L). Les MICs de l'amoxicilline-clavulanate, de la cefotaxime, du meropenem, du trimethoprim-sulfamethoxazole et de la vancomycine ont également été déterminés par Etest® (bioMérieux) en utilisant de l'agar Mueller-Hinton plus 5 % de sang, et des résultats similaires ont été trouvés.\n\nLe 7e jour, un échocardiogramme transthoracique n’a pas révélé de modifications. Le traitement a été changé pour de l’amoxicilline-clavulanate (1 g trois fois par jour, par voie intraveineuse), et de nouvelles cultures sanguines obtenues 24 heures plus tard étaient négatives. Un échocardiogramme transoesophagien réalisé le 9e jour de l’hospitalisation a révélé une végétation échogène et mobile de 6 × 9 mm sur la valve aortique prothétique fixée à la commissure entre la cuspide coronaire droite et la cuspide non coronaire. La fonction de la valve prothétique était par ailleurs normale. Le 11e jour, l’amoxicilline-clavulanate a été changé pour de la vancomycine ajustée à la fonction rénale (750 mg par jour) plus du linézolide (600 mg deux fois par jour, par voie intraveineuse). Le remplacement chirurgical a été considéré comme inapproprié chez cette patiente en raison de la comorbidité, de l’âge avancé, de la mobilité limitée et du rejet de la famille. Dans les jours suivants, elle a développé une anémie sévère, un état confusionnel aigu et une insuffisance cardiaque réfractaire. La prise de décision en fin de vie a été mise en œuvre, en donnant la priorité au contrôle des symptômes, et le traitement antibiotique a été changé en amoxicilline-clavulanate le 22e jour de l’admission. Le 28e jour, elle a été transférée dans un autre hôpital pour des soins palliatifs, et elle est morte 7 jours plus tard à cause d’une septicémie et d’une insuffisance cardiaque sévère. Une autopsie n’a pas été réalisée.",
+        "gold_summary": "Une femme de 82 ans avec une valve prothétique aortique a été admise à l'hôpital avec de la fièvre et une insuffisance cardiaque. Des examens complémentaires ont révélé le diagnostic d'endocardite infectieuse à C. cellulans (IE). La souche a été identifiée par MALDI-TOF MS, API Coryne et séquençage de l'ARNr 16S. La patiente a été jugée non opérable et est morte malgré la thérapie antibiotique 35 jours après son admission.\n",
+        "synthetic_summary": {
+            "B1": "Une dame de 82 ans avait un petit cœur avec une pièce spéciale. Elle est venue à l’hôpital parce qu’elle avait de la fièvre et que son cœur ne marchait pas bien. Les docteurs ont trouvé une petite bête qui faisait du mal à son cœur. Ils ont donné des médicaments pour la combattre. Mais la dame était trop fatiguée et elle est partie au ciel après un mois. Les docteurs ont tout fait pour l’aider.",
+            "B2": "Une femme de 82 ans, qui avait une valve cardiaque artificielle, est arrivée à l’hôpital avec de la fièvre et des problèmes au cœur. Après plusieurs examens, les médecins ont découvert qu’elle avait une infection grave appelée endocardite infectieuse, causée par une bactérie nommée Corynebacterium cellulans. Pour identifier cette bactérie, ils ont utilisé différentes méthodes scientifiques, comme le MALDI-TOF MS (une technique qui analyse les protéines), un test appelé API Coryne, et une analyse de l’ARN, qui est une sorte d’empreinte génétique. À cause de son âge, de ses autres maladies et de son état général, les médecins ont décidé qu’elle ne pouvait pas subir une opération pour réparer sa valve. Malgré le traitement avec des antibiotiques, son état s’est aggravé et elle est décédée 35 jours après son arrivée à l’hôpital.",
+            "B3": "Résumé détaillé destiné à un public non médical mais instruit\n\nContexte  \nUne femme de 82 ans, souffrant de diabète de type 2 et d’insuffisance rénale chronique, avait reçu une valve aortique artificielle (prothèse valvulaire sans suture de Perceval) 18 mois avant son hospitalisation, en raison d’un rétrécissement de la valve aortique (sténose). Depuis l’opération, elle avait présenté plusieurs épisodes d’insuffisance cardiaque sévère inexpliquée et de fibrillation auriculaire paroxystique (troubles du rythme cardiaque), sans signes évidents d’infection.\n\nPrincipales observations  \nElle a été admise à l’hôpital avec une fièvre élevée (39 °C), un état de confusion mentale (délire) et une difficulté à respirer (dyspnée). L’examen physique a révélé un souffle cardiaque au niveau de la valve aortique, des crépitements dans les poumons, ainsi que des ulcères de pression non infectés. Les analyses sanguines ont montré une inflammation importante (protéine C-réactive élevée), une hyperglycémie sévère et une fonction rénale altérée. Une radiographie thoracique a mis en évidence un épanchement pleural (accumulation de liquide autour des poumons) et un œdème pulmonaire.\n\nDes prélèvements sanguins ont été réalisés, et après plusieurs jours d’incubation, une bactérie appelée Corynebacterium cellulans a été isolée. Cette identification a été confirmée par plusieurs méthodes de laboratoire, dont la spectrométrie de masse (MALDI-TOF MS), un test biochimique spécifique (API Coryne) et le séquençage génétique de l’ARN ribosomal 16S, qui a montré une correspondance quasi parfaite avec cette espèce bactérienne. Les tests de sensibilité aux antibiotiques ont indiqué que la bactérie était sensible à certains traitements, notamment l’amoxicilline-clavulanate, la vancomycine et le linézolide, mais résistante à d’autres.\n\nUn examen échographique approfondi du cœur (échocardiographie transoesophagienne) a révélé la présence d’une végétation (amas bactérien) mobile de 6 × 9 mm fixée sur la valve aortique prothétique, confirmant le diagnostic d’endocardite infectieuse, c’est-à-dire une infection de la valve cardiaque artificielle.\n\nInterprétation clinique  \nLe diagnostic d’endocardite infectieuse à Corynebacterium cellulans sur prothèse valvulaire aortique a été établi. En raison de l’âge avancé de la patiente, de ses multiples comorbidités, de sa mobilité réduite et du refus de la famille, une intervention chirurgicale pour remplacer la valve infectée n’a pas été envisagée. Le traitement antibiotique a été adapté en fonction des résultats de sensibilité, mais la patiente a rapidement développé des complications graves, notamment une anémie sévère, une confusion accrue et une insuffisance cardiaque réfractaire.\n\nProchaines étapes et issue  \nFace à la détérioration clinique, une décision de soins palliatifs a été prise, visant à soulager les symptômes plutôt qu’à poursuivre un traitement curatif agressif. La patiente a été transférée dans un établissement spécialisé pour ces soins et est décédée 35 jours après son admission, des suites d’une septicémie (infection généralisée) et d’une insuffisance cardiaque sévère. Aucun examen post-mortem n’a été réalisé.\n\nCe cas illustre la difficulté de prise en charge des infections sur prothèse valvulaire chez des patients âgés avec de nombreuses comorbidités, ainsi que l’importance d’une identification précise de l’agent infectieux pour guider le traitement antibiotique."
+        }
+    },
+    {
+        "article": "Patient et observation\nInformations relatives au patient: il s´agissait d´un patient âgé de 67 ans, sans antécédents pathologiques qui a consulté pour une gêne à la déglutition avec une dysphonie et une altération de l´état général.\n\nRésultats cliniques: l'examen clinique initial trouvait un patient conscient avec un score de Glasgow à 15/15, apyrétique, une tension artérielle de 12/07 cmHg, une saturation en oxygène de 100%, une fréquence cardiaque à 80/min, des conjonctives normocolorées avec la présence d´une volumineuse masse au niveau du cavum. Il n´y avait pas d´hépatomégalie ni de splénomégalie, les aires ganglionnaires étaient libres, le reste de l'examen somatique était normal.\n\nChronologie: le patient présentait depuis 6 mois une gêne à la déglutition avec une dysphonie, le tableau clinique s´est aggravé par l´installation d´une dysphagie aux solides avec une altération de l´état général (amaigrissement chiffré à 15kg/6 mois).\n\nDémarche diagnostique: la TDM cervico-thoraco-abdomino-pelvienne a objectivé une masse nasopharyngée de 70 mm x 40 mm étendue sur 60 mm. Le bilan biologique du patient était normal (la numération de formule sanguine, le bilan rénal et hépatique, la lacticodéshydrogénase et les sérologies VIH VHC VHB). L´étude histologique et immunohistochimique de la biopsie nasopharyngée était en faveur de LNH folliculaire B grade 1,2 CD20+; CD19+; CD79a+; CD10+ sur 2 lectures dans deux laboratoires différents. La biopsie ostéomédullaire était normale ainsi que le bilan préthérapeutique.\n\nIntervention thérapeutique: le patient a reçu 4 cures RCHOP 21 (rituximab 375mg/m2 en intraveineux (iv), cyclophosphamide 750 mg/m2 iv, oncovin 2 mg iv, prednisolone 100 mg par voie orale, et doxorubicine 50 mg/m2 (iv) sans réponse puis 3 cures RDHAOX (rituximab 375 mg/m2 en intraveineux (iv) à J1, aracytine haute dose 2 g/m2 x 2 iv à J2, dexamethasone 40 mg de J1 à J4, et oxalipatine 100 mg/m2 à J1) sans réponse clinique.\n\nSuivi et résultats des interventions thérapeutiques: la persistance et l´augmentation de la masse nasopharyngée a conduit à la réalisation de la trachéotomie, la biopsie de la masse nasopharyngée a objectivé la disparition de l´infiltration lymphoïde B avec présence des dépôts amyloïdes AL type kappa.\n\nL´immunoélectrophorèse des protéines plasmatiques a mis en évidence la présence de l´immunoglobuline M kappa, le dosage des chaines légères n´a pas été réalisé par manque de moyens, le myélogramme et une deuxième biopsie ostéomédullaire étaient normaux, la TEP scan a objectivé un processus nasopharyngé hypermétabolique sans autres anomalies, l´évaluation cardiaque (ECG, peptides natriurétiques, troponine, echocoeur) et rénale étaient sans particularités, le malade est actuellement sous protocole bortezomib, prednisone et bendamustine avec bonne évolution clinique après première cure.",
+        "gold_summary": "Nous rapportons le cas d´un patient âgé de 67 ans sans ATCDs pathologiques particuliers ayant présenté une altération de l´état général avec une dysphonie et dysphagie d´aggravation progressive avec une volumineuse masse du cavum dont la biopsie était en faveur d´un lymphome non hodgkinien folliculaire B grade 1 et 2. La tomodensitométrie (TDM) cervico-thoraco-abdomino-pelvienne a objectivé une masse nasopharyngée de 70 mm x 40 mm étendue sur 60 mm. La biopsie ostéomédullaire était normale ainsi que le bilan préthérapeutique. Le malade a reçu 4 cures de protocole Rituximab plus CHOP (cyclophosphamide, adriamycine, prednisone et oncovin) sans réponse puis 3 cures Rituximab plus DHAOX (dexamethasone, aracytine haute dose, et oxalipatine) avec persistance de la masse. La biopsie de cette dernière a objectivé la disparition de l´infiltration lymphoïde B avec présence des dépôts amyloïdes AL. L´immunoélectrophorèse des protéines plasmatiques a mis en évidence la présence de l´immunoglobuline M. La tomographie par émission de positons (TEP) scan a objectivé un processus nasopharyngé hypermétabolique. Le malade est actuellement sous protocole bortezomib, prednisone et bendamustine.",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 67 ans avait mal pour avaler et sa voix changeait. Il avait une grosse boule dans la gorge. Les docteurs ont regardé avec des machines et ont trouvé cette boule. Ils ont pris un petit bout pour voir ce que c’était. \n\nIls ont donné des médicaments pour essayer de faire partir la boule, mais ça n’a pas marché. La boule est restée là. Ensuite, ils ont trouvé un autre problème avec des petits morceaux qui s’appellent amyloïdes. \n\nMaintenant, le monsieur prend d’autres médicaments. Il va un peu mieux. Les docteurs continuent de bien s’occuper de lui.",
+            "B2": "Cas d’un homme de 67 ans avec des difficultés à avaler et à parler\n\nUn homme de 67 ans, sans problème de santé connu avant, a commencé à avoir des difficultés pour avaler et une voix enrouée. Ces symptômes ont empiré sur six mois, avec une perte de poids importante. Lors de l’examen, les médecins ont trouvé une grosse masse dans la partie haute de sa gorge, appelée cavum.\n\nCe qu’ils ont découvert\n\nUne tomodensitométrie (un type de scanner) a montré que cette masse mesurait environ 7 cm sur 4 cm et s’étendait sur 6 cm. Une biopsie, c’est-à-dire un prélèvement d’un petit morceau de cette masse, a révélé qu’il s’agissait d’un lymphome non hodgkinien folliculaire de type B, un cancer des cellules du système immunitaire. D’autres examens, comme une biopsie de la moelle osseuse, étaient normaux.\n\nLes traitements essayés\n\nLe patient a d’abord reçu quatre cycles d’un traitement appelé R-CHOP, qui combine plusieurs médicaments contre le cancer, mais cela n’a pas fonctionné. Ensuite, il a eu trois cycles d’un autre traitement appelé R-DHAOX, toujours sans amélioration. La masse est restée présente et a même augmenté.\n\nCe qu’ils ont fait ensuite\n\nUne nouvelle biopsie de la masse a montré que les cellules cancéreuses avaient disparu, mais qu’il y avait maintenant des dépôts d’une substance appelée amyloïde AL, qui peut s’accumuler anormalement dans les tissus. Des analyses sanguines ont détecté une immunoglobuline M, une protéine liée au système immunitaire. Un autre examen appelé TEP scan a confirmé que la masse dans la gorge était toujours active.\n\nTraitement actuel et évolution\n\nLe patient reçoit maintenant un nouveau traitement avec des médicaments nommés bortezomib, prednisone et bendamustine. Après la première cure, son état s’est amélioré. Les médecins continuent de le suivre pour surveiller sa santé.",
+            "B3": "Résumé détaillé et structuré\n\nContexte  \nNous présentons le cas d’un homme de 67 ans, sans antécédents médicaux notables, qui a consulté pour une gêne progressive à la déglutition accompagnée d’une dysphonie (modification de la voix) et d’une altération générale de son état de santé. Ces symptômes s’étaient aggravés sur six mois, avec notamment une perte de poids importante de 15 kg.\n\nPrincipales observations cliniques et diagnostiques  \nL’examen clinique a révélé une masse volumineuse au niveau du cavum (la partie supérieure du pharynx derrière le nez), sans autres anomalies notables. Une tomodensitométrie (TDM) cervico-thoraco-abdomino-pelvienne a confirmé la présence d’une masse nasopharyngée mesurant 70 mm sur 40 mm et s’étendant sur 60 mm. Les analyses biologiques, incluant la numération sanguine, les fonctions rénale et hépatique, ainsi que les sérologies virales, étaient normales. La biopsie de la masse a montré un lymphome non hodgkinien (LNH) folliculaire B de grade 1 et 2, caractérisé par la présence de marqueurs CD20+, CD19+, CD79a+ et CD10+. La biopsie de la moelle osseuse était normale, tout comme le bilan préthérapeutique.\n\nInterventions thérapeutiques et évolution  \nLe patient a d’abord reçu quatre cycles de chimiothérapie selon le protocole R-CHOP (rituximab, cyclophosphamide, doxorubicine, vincristine et prednisone), sans réponse clinique. Une deuxième ligne de traitement comprenant trois cycles de chimiothérapie R-DHAOX (rituximab, dexaméthasone, aracytine à haute dose et oxaliplatine) a également été inefficace, la masse nasopharyngée persistant et augmentant de volume. Une trachéotomie a été réalisée pour assurer la respiration. Une nouvelle biopsie de la masse a révélé la disparition des cellules lymphoïdes B, mais la présence de dépôts amyloïdes de type AL (amyloïdose liée à une accumulation anormale de protéines) de type kappa.\n\nExamens complémentaires et prise en charge actuelle  \nL’immunoélectrophorèse des protéines plasmatiques a détecté une immunoglobuline M de type kappa, suggérant une production anormale de cette protéine. Le myélogramme et une deuxième biopsie de la moelle osseuse sont restés normaux. La tomographie par émission de positons (TEP-scan) a montré une activité métabolique élevée uniquement au niveau de la masse nasopharyngée, sans autre localisation suspecte. Les évaluations cardiaque et rénale n’ont révélé aucune anomalie. Le patient est actuellement traité par un protocole associant bortezomib (un inhibiteur du protéasome), prednisone et bendamustine, avec une amélioration clinique notable après la première cure.\n\nInterprétation clinique  \nCe cas illustre une présentation rare d’un lymphome non hodgkinien folliculaire du nasopharynx, initialement réfractaire aux traitements standards, évoluant vers une amyloïdose locale. La détection d’une immunoglobuline monoclonale et la persistance d’une masse hypermétabolique ont orienté vers une prise en charge adaptée par des agents ciblant les cellules malignes et les dépôts amyloïdes.\n\nProchaines étapes  \nLa surveillance clinique et radiologique sera essentielle pour évaluer la réponse au traitement actuel et détecter toute récidive ou complication. Un suivi multidisciplinaire impliquant oncologues, hématologues et spécialistes ORL est recommandé pour optimiser la prise en charge."
+        }
+    },
+    {
+        "article": "Un homme africain de 53 ans ayant des antécédents médicaux d'hypertension diagnostiquée à la mi-vingtaine, d'ICS systolique et de cardiomyopathie non ischémique a présenté une aggravation de la dyspnée d'effort, un œdème des membres inférieurs, une dyspnée nocturne paroxystique et une orthopnée pendant environ une semaine. Le patient prenait six médicaments antihypertenseurs en ambulatoire, dont la clonidine, l'hydralazine, le mononitrate d'isosorbide, le valsartan et la furosémide. Malgré le respect des médicaments, il a été admis fréquemment pour des exacerbations de l'ICS. Il a nié avoir consommé du tabac, de la drogue ou de l'alcool. Bien qu'il ait été diagnostiqué d'hypertension à un jeune âge, le patient ne se rappelait pas avoir subi des tests supplémentaires pour des causes secondaires de l'HTN au moment du diagnostic. Il se rappelait un diagnostic d'hypokaliémie chronique, qui avait été attribué à l'utilisation de la furosémide, et il s'était vu prescrire des suppléments de potassium par intermittence dans le passé. Il a nié toute antécédent familial connu de PA ou d'HTN non contrôlée. Les signes vitaux ont révélé une tension artérielle de 163/103 mm Hg, une fréquence cardiaque de 74 battements par minute, une fréquence respiratoire de 17 et une saturation en oxygène de 95 % sur une canule nasale de 3 L. Les résultats pertinents de l'examen physique comprenaient une distension veineuse jugulaire, un œdème pitting bilatéral des membres inférieurs, des râles bilatéraux et un galop S3 proéminent.\n\n\nEnquêtes\n\nL'ECG ne révélait aucune modification ischémique aiguë, un rythme sinusal avec un bloc de branche gauche chronique. Les troponines étaient négatives à trois reprises consécutives. La radiographie thoracique révélait une congestion vasculaire pulmonaire bilatérale. L'échocardiographie transthoracique révélait une hypertrophie ventriculaire gauche modérée et une dilatation avec une hypokinésie globale et une fraction d'éjection de 10 % à 15 %. Aucune anomalie valvulaire n'a été notée. L'IRM cardiaque révélait des zones de fibrose myocardique probablement liées à une hypertrophie, atypique pour une maladie ischémique et atypique pour un infarctus antérieur ou une amyloïdose. Les études de laboratoire révélaient un potassium sérique de 2,6 mmol/L et un bicarbonate de 34 mmol/L. Une PA était suspectée, et des tests complémentaires ont révélé un taux plasmatique d'aldostérone élevé de 154 ng/dL (normal inférieur à 39,2 ng/dL), une activité rénine plasmatique (AR) diminuée de moins de 2,1 ng/mL/heure et un rapport de concentration plasmatique d'aldostérone/AR plasmatique (PAC/PRA) de 73,3 (ng/dL)/(ng/mL/heure).\n\nLes résultats d’un test de suppression de la dexaméthasone pendant la nuit, d’un test de la fonction thyroïdienne et des métanéphrines plasmatiques et urinaires étaient normaux. Un test de suppression de la dexaméthasone par surcharge saline orale n’a pas été effectué par crainte d’exacerber son œdème pulmonaire et son insuffisance cardiaque. La TDM de l’abdomen et du bassin avec injection de produit de contraste a montré un adénome de la glande surrénale gauche bien défini et homogène de 1,2 × 2,4 cm. L’échantillonnage ultérieur de la veine surrénale a confirmé une PA unilatérale avec latéralisation vers la glande surrénale gauche (tableau 1). Le rapport cortisol de la veine surrénale inférieure à cortisol de la veine cave inférieure pour les veines surrénales gauche et droite était supérieur à 3, ce qui correspond à une canulation réussie de la veine surrénale. Le rapport aldostérone de la veine surrénale à cortisol de la veine surrénale était de 14,8 et 2,2, respectivement. Un rapport de latéralisation supérieur à 4 est compatible avec une maladie unilatérale, tandis qu’un rapport de latéralisation inférieur à 3 est compatible avec une maladie bilatérale. Le rapport de latéralisation du patient de gauche à droite était de 6,7, ce qui correspond à une maladie unilatérale. Le patient a commencé un traitement par spironolactone avec une amélioration de sa tension artérielle et de son hypokaliémie et a été référé pour une adrénalectomie gauche.",
+        "gold_summary": "Un homme africain de 53 ans ayant des antécédents de 25 ans d’hypertension artérielle non contrôlée et d’insuffisance cardiaque systolique a présenté une exacerbation aiguë d’insuffisance cardiaque congestive. Il a été trouvé qu’il souffrait d’hypokaliémie sévère, des tests supplémentaires ont donc été effectués et l’aldostéronisme primaire a été confirmé. La tomographie par ordinateur a montré un adénome homogène bien défini de 1,2 × 2,4 cm de la glande surrénale gauche. L’échantillonnage de la veine surrénale a confirmé un aldostéronisme primaire unilatéral avec latéralisation vers la glande surrénale gauche. Le patient a commencé à prendre de la spironolactone et a été référé à une chirurgie pour une adrénalectomie gauche laparoscopique.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur avait le cœur fatigué et une tension trop haute depuis longtemps. Il avait aussi un problème avec un petit bouton sur une glande près de son ventre. Ce bouton faisait que son corps gardait trop de sel et perdait du potassium, ce qui le rendait très malade.\n\nLes docteurs ont donné un médicament pour l’aider. Ils ont aussi prévu une petite opération pour enlever ce bouton. Cela va l’aider à se sentir mieux et à avoir un cœur plus fort.",
+            "B2": "### Ce qu'ils ont trouvé chez le patient\n\nUn homme de 53 ans souffrait depuis 25 ans d’hypertension artérielle (c’est quand la pression du sang est trop élevée) et d’insuffisance cardiaque, ce qui signifie que son cœur ne pompait pas bien le sang. Récemment, ses symptômes se sont aggravés, avec plus de difficultés à respirer et des gonflements aux jambes. Les médecins ont découvert qu’il avait un faible taux de potassium dans le sang, ce qui peut causer des problèmes sérieux.\n\n### Ce que cela signifie\n\nAprès plusieurs tests, ils ont confirmé qu’il avait une maladie appelée aldostéronisme primaire. C’est quand une glande dans le corps, appelée la glande surrénale, produit trop d’aldostérone, une hormone qui fait augmenter la pression artérielle et fait perdre du potassium. Une tomographie (un type d’image médicale) a montré une petite tumeur bénigne (un adénome) sur la glande surrénale gauche.\n\n### Le traitement proposé\n\nPour savoir si la tumeur était bien la cause du problème, les médecins ont prélevé du sang directement dans les veines des glandes surrénales. Cela a confirmé que la glande gauche était responsable. Le patient a alors commencé un médicament appelé spironolactone, qui bloque l’effet de l’aldostérone et aide à faire baisser la pression artérielle et à augmenter le potassium. Ensuite, il a été orienté vers une opération pour enlever la glande surrénale gauche par chirurgie laparoscopique, une technique peu invasive.",
+            "B3": "Résumé détaillé et structuré\n\nContexte  \nUn homme africain de 53 ans, avec un historique médical notable d’hypertension artérielle (HTA) diagnostiquée vers l’âge de 25 ans, d’insuffisance cardiaque systolique chronique (ICS) et de cardiomyopathie non ischémique, a présenté une aggravation récente de symptômes d’insuffisance cardiaque congestive. Ces symptômes comprenaient une dyspnée à l’effort, un œdème des membres inférieurs, une dyspnée nocturne paroxystique et une orthopnée, évoluant depuis environ une semaine. Malgré un traitement antihypertenseur intensif comportant six médicaments, dont la clonidine, l’hydralazine, le mononitrate d’isosorbide, le valsartan et la furosémide, le patient avait des hospitalisations fréquentes pour exacerbations de son insuffisance cardiaque. Il ne rapportait pas de consommation de tabac, d’alcool ou de drogues, et ne connaissait pas d’antécédents familiaux d’hypertension non contrôlée.\n\nPrincipales observations cliniques et paracliniques  \nÀ l’examen, la tension artérielle était élevée (163/103 mm Hg), avec une fréquence cardiaque normale (74 bpm), une saturation en oxygène légèrement diminuée sous oxygène nasal, et des signes d’insuffisance cardiaque congestive : distension veineuse jugulaire, œdème bilatéral des jambes, râles pulmonaires bilatéraux et galop S3. L’électrocardiogramme montrait un rythme sinusal avec un bloc de branche gauche chronique, sans signe d’ischémie aiguë. Les troponines étaient négatives. La radiographie thoracique confirmait une congestion vasculaire pulmonaire. L’échocardiographie révélait une hypertrophie ventriculaire gauche modérée, une dilatation cardiaque avec hypokinésie globale et une fraction d’éjection très basse (10-15 %), sans anomalie valvulaire. L’IRM cardiaque montrait des zones de fibrose myocardique atypiques, non compatibles avec une maladie ischémique classique ou une amyloïdose.\n\nLes analyses biologiques mettaient en évidence une hypokaliémie sévère (potassium à 2,6 mmol/L) et une alcalose métabolique (bicarbonate à 34 mmol/L). Devant cette hypokaliémie persistante, un aldostéronisme primaire (PA) a été suspecté. Les dosages plasmatiques ont confirmé un taux élevé d’aldostérone (154 ng/dL, valeur normale < 39,2 ng/dL), une activité rénine plasmatique très basse (< 2,1 ng/mL/h) et un rapport aldostérone/rénine plasmatique très élevé (73,3), ce qui est caractéristique d’un aldostéronisme primaire.\n\nLes examens complémentaires, incluant un test de suppression à la dexaméthasone, des bilans thyroïdiens et des dosages de métanéphrines plasmatiques et urinaires, étaient normaux, éliminant d’autres causes endocriniennes. Une imagerie abdominale par tomodensitométrie avec injection a révélé un adénome surrénalien gauche bien délimité et homogène de 1,2 × 2,4 cm. L’échantillonnage sélectif des veines surrénales a confirmé la sécrétion unilatérale excessive d’aldostérone par la glande gauche, avec un rapport de latéralisation de 6,7 (valeur > 4 indiquant une maladie unilatérale).\n\nInterprétation clinique  \nCe patient souffrait d’un aldostéronisme primaire unilatéral dû à un adénome surrénalien gauche, responsable d’une hypertension artérielle sévère et résistante, d’une hypokaliémie chronique et probablement contributive à sa cardiomyopathie et à son insuffisance cardiaque systolique. La confirmation par échantillonnage veineux surrénalien a permis de distinguer une forme unilatérale, susceptible d’être traitée chirurgicalement, d’une forme bilatérale qui serait traitée médicalement.\n\nProchaines étapes  \nLe patient a été mis sous spironolactone, un antagoniste des récepteurs de l’aldostérone, ce qui a amélioré sa tension artérielle et corrigé son hypokaliémie. Il a ensuite été orienté vers une chirurgie d’adrénalectomie laparoscopique gauche, visant à retirer l’adénome responsable de la sécrétion excessive d’aldostérone et ainsi potentiellement améliorer son contrôle tensionnel et sa fonction cardiaque."
+        }
+    },
+    {
+        "article": "Une femme de 57 ans ayant suivi pendant 8 ans un traitement de cardiomyopathie dilatée idiopathique a présenté une aggravation de la classe fonctionnelle et des hospitalisations récurrentes pour insuffisance cardiaque. La classe fonctionnelle de la New York Heart Association était de 4 et l'Interagency Registry for Mechanically Assisted Circulatory Support était de 5. Elle avait été traitée avec une thérapie médicale guidée par les directives à des doses maximales tolérées, notamment avec de l'énalapril 10 mg b.i.d., du métoprolol 50 mg b.i.d., de la spironolactone 25 mg, de la furosémide 40 mg b.i.d. et de la digoxine 0,125 mg par jour, pendant au moins 5 ans. Les comorbidités comprenaient le tabagisme actif et l'obésité morbide (indice de masse corporelle de 37 kg/m2). Elle était principalement limitée par la fatigue d'effort et la dyspnée, malgré une euvolemie principalement non dépendante de doses élevées de diurétiques. L'électrocardiogramme de repos (ECG) a montré un rythme sinusal à une fréquence de 70 bpm et une durée de QRS de 80 ms. La fraction d'éjection ventriculaire gauche était de 23 %, avec un ventricule gauche dilaté (diamètre de fin de diastole de 6,7 cm) et une hypokinésie diffuse. Un test d'effort cardiopulmonaire (CPET) a démontré une capacité d'exercice sévèrement diminuée, avec une consommation maximale d'oxygène (VO2 de pointe) de 12 ml/kg/min (ou 16,46 ml/kg/min lorsque corrigée pour la masse corporelle maigre), ainsi que d'autres variables indiquant un pronostic défavorable d'insuffisance cardiaque, y compris la ventilation minute/production de dioxyde de carbone (VE/VCO2) de 42 et la respiration périodique. À la deuxième minute de l'exercice, à une fréquence cardiaque de 131 bpm, la patiente a développé une LBBB avec un élargissement du QRS à 200 ms. Cette constatation a persisté dans la phase de récupération. Il convient de noter que la réponse pressorostatique a également été observée pendant le CPET. Une échocardiographie d'effort a ensuite démontré une dyssynchronie intraventriculaire et interventriculaire induite par l'exercice, avec un retard électromécanique du début du QRS à l'onde S de plus de 65 ms et une différence entre les intervalles pré-éjection gauche et droite de plus de 40 ms, respectivement.\n\nLa patiente n’étant pas considérée comme éligible à une transplantation cardiaque, compte tenu de ses comorbidités actives, il a été décidé de lui implanter un CRT (Etrinsa 8 HF‐T, Biotronik, Berlin, Allemagne) pour tenter de corriger l’EI‐LBBB. L’imagerie par résonance magnétique cardiaque réalisée avant l’insertion du CRT n’a montré qu’une petite zone d’amélioration tardive du gadolinium au niveau du septum basilaire mésocardique, mais aucun motif suggérant une étiologie spécifique autre qu’une cardiomyopathie dilatée non ischémique n’a été noté. Initialement, la stimulation biventriculaire a été réglée à une fréquence cardiaque minimale de 75 bpm avec un retard atrioventriculaire de 105‐80 ms, et l’ECG a montré une durée de QRS de 145 ms.\n\nAprès l'implantation du CRT, l'état du patient s'est amélioré et il a été classé dans la catégorie II de la New York Heart Association. Il n'y a pas eu de récidive d'hospitalisation pour insuffisance cardiaque. Le traitement médical a été relativement inchangé après le CRT, à l'exception de l'introduction de l'amiodarone en raison d'arythmies ventriculaires et du changement de metoprolol à carvedilol et de l'introduction de l'hydralazine, tous deux pour améliorer la gestion de l'hypertension, car les niveaux de pression artérielle ont augmenté et la tolérance aux médicaments s'est améliorée après le CRT. L'interrogation du stimulateur cardiaque a montré une stimulation auriculaire à 94 % et une stimulation biventriculaire à 100 %. Quelques mois plus tard, un CPET répété à 6 et 12 mois a démontré une amélioration significative et soutenue de la capacité d'exercice. La stimulation biventriculaire a eu lieu à 100 % du temps d'exercice, et la respiration périodique était absente lors des deux examens. Une remodélisation cardiaque inverse et une amélioration de la fraction d'éjection ont également été observées.",
+        "gold_summary": "Une femme de 57 ans atteinte de cardiomyopathie dilatée idiopathique (fraction d'éjection de 23 %) a présenté une insuffisance cardiaque de classe IV selon la New York Heart Association et des hospitalisations récurrentes. Au cours de l'évaluation de la transplantation cardiaque, un nouveau début de bloc de branche gauche intermittent a été observé lors du test d'effort cardiopulmonaire. La CRT a été implantée et un taux de resynchronisation de 97 % a été atteint. Au cours du suivi de 12 mois, les paramètres d'exercice cliniques et pronostiques se sont améliorés.\n",
+        "synthetic_summary": {
+            "B1": "Une dame avait un cœur qui ne marchait pas bien. Elle se fatiguait beaucoup et avait du mal à respirer. \n\nLes docteurs ont mis une petite machine dans son cœur. Cette machine aide le cœur à battre mieux. \n\nAprès, elle allait mieux. Elle pouvait faire plus de choses sans se sentir fatiguée. Le cœur de la dame est devenu plus fort.",
+            "B2": "Une femme de 57 ans souffrait d'une maladie du cœur appelée cardiomyopathie dilatée, ce qui signifie que son muscle cardiaque était affaibli et élargi. Sa capacité à pomper le sang était très faible, avec une fraction d'éjection de 23 % (normalement, elle devrait être autour de 55-70 %). Elle avait aussi des symptômes graves d’insuffisance cardiaque, ce qui la limitait beaucoup dans ses activités quotidiennes.\n\nLors d’un test d’effort, qui sert à voir comment le cœur fonctionne pendant l’exercice, les médecins ont découvert qu’elle développait un problème électrique appelé bloc de branche gauche (c’est un retard dans la transmission du signal électrique dans le cœur). Ce problème n’était pas toujours présent, mais il apparaissait quand elle faisait de l’exercice, ce qui pouvait aggraver son insuffisance cardiaque.\n\nComme elle ne pouvait pas recevoir une greffe de cœur à cause d’autres problèmes de santé, les médecins ont décidé de lui poser un appareil appelé resynchroniseur cardiaque (CRT). Cet appareil aide à coordonner les battements du cœur en envoyant des impulsions électriques pour que les deux ventricules battent ensemble de façon plus efficace.\n\nAprès l’implantation du CRT, sa condition s’est nettement améliorée. Elle a pu faire plus d’exercice, ses symptômes ont diminué, et elle n’a plus été hospitalisée pour son insuffisance cardiaque. Le suivi sur 12 mois a montré que son cœur fonctionnait mieux, avec une meilleure capacité à pomper le sang et une meilleure coordination des battements. En résumé, le CRT a permis de stabiliser sa maladie et d’améliorer sa qualité de vie.",
+            "B3": "Résumé détaillé et structuré\n\nContexte  \nUne femme de 57 ans souffrant depuis huit ans d’une cardiomyopathie dilatée idiopathique, caractérisée par une fraction d’éjection ventriculaire gauche très basse (23 %) et un ventricule gauche dilaté, présentait une insuffisance cardiaque sévère, classée IV selon la New York Heart Association. Malgré un traitement médical optimal et à doses maximales tolérées, incluant des inhibiteurs de l’enzyme de conversion, bêta-bloquants, diurétiques et digoxine, elle subissait des hospitalisations répétées pour décompensation cardiaque. Ses comorbidités comprenaient un tabagisme actif et une obésité morbide (IMC de 37 kg/m²). Elle était limitée principalement par une fatigue à l’effort et une dyspnée, avec une capacité d’exercice très réduite démontrée par un test d’effort cardiopulmonaire (CPET).\n\nPrincipales observations  \nLors du CPET, la patiente a développé un bloc de branche gauche (LBBB) intermittent induit par l’exercice, avec un allongement marqué de la durée du complexe QRS (passant à 200 ms), persistant en phase de récupération. Une échocardiographie d’effort a confirmé une dyssynchronie électromécanique intraventriculaire et interventriculaire liée à ce bloc, suggérant un retard dans la contraction coordonnée des ventricules. L’imagerie par résonance magnétique cardiaque n’a révélé qu’une petite zone de fibrose mésocardique sans signe d’ischémie, confirmant l’origine non ischémique de la cardiomyopathie. La patiente n’était pas candidate à la transplantation cardiaque en raison de ses comorbidités.\n\nIntervention et suivi  \nUn stimulateur cardiaque de resynchronisation (CRT) a été implanté afin de corriger cette dyssynchronie induite par l’exercice. La programmation initiale a permis une stimulation biventriculaire efficace, avec une réduction de la durée du QRS à 145 ms. Après l’implantation, l’état clinique s’est nettement amélioré, avec un passage à la classe II de la NYHA et l’absence de nouvelles hospitalisations pour insuffisance cardiaque. Le traitement médical a été ajusté, notamment par l’introduction d’amiodarone pour des arythmies ventriculaires et le remplacement du métoprolol par du carvedilol, ainsi que l’ajout d’hydralazine pour mieux contrôler l’hypertension, rendue possible par une meilleure tolérance post-CRT. Le stimulateur a assuré une stimulation auriculaire à 94 % et biventriculaire à 100 %.\n\nProchaines étapes et résultats  \nLes tests d’effort répétés à 6 et 12 mois ont montré une amélioration significative et durable de la capacité d’exercice, avec une disparition de la respiration périodique et une stimulation biventriculaire maintenue à 100 % pendant l’effort. Par ailleurs, une remodélisation cardiaque inverse a été observée, avec une amélioration de la fraction d’éjection ventriculaire gauche, témoignant d’un bénéfice structurel et fonctionnel durable du CRT dans ce contexte d’insuffisance cardiaque avancée associée à un bloc de branche gauche induit par l’exercice."
+        }
+    },
+    {
+        "article": "Patient de dix mois, sexe féminin, hospitalisée à l'HCPA depuis neuf mois, a séjourné en unité de soins intensifs néonatale (UTIN) pendant quatre mois pour une recherche génétique, nécessitant une ventilation mécanique invasive (VMI) pour la stabilité du cadre respiratoire. Au cours de l'hospitalisation, elle a eu besoin d'une trachéotomie (TQT) et d'une VMI pour une utilisation à domicile. Pour cela, la patiente a été adaptée à l'UTIN au ventilateur mécanique Trilogy 100 (Philips Respironics, États-Unis), mode ventilatoire avec pression contrôlée, pression inspiratoire (IPAP) de 25 cmH2O, pression expiratoire (EPAP) de 6 cmH2O, fréquence respiratoire (FR) de 22 irpm, sensibilité auto-track et temps inspiratoire de 0,8 seconde.\n\nAprès son adaptation, il a été libéré dans l'unité de soins intensifs pédiatriques, où il était cliniquement stable, sans besoin d'oxygénothérapie, en attendant la libération judiciaire pour soins à domicile. Cependant, au neuvième mois d'hospitalisation, il a commencé à avoir de la fièvre et une hypoxémie (saturation partielle en oxygène (SpO2): 90%), nécessitant l'administration d'oxygène (2 L/min) et le transfert sur un lit d'isolement, où il a effectué le test de réaction en chaîne de la polymérase (PCR) pour COVID-19, dont le résultat a été positif.\n\nL’équipe de physiothérapie de l’unité, afin de prévenir la dispersion d’aérosols, a installé un circuit d’aspiration fermé, bien que peu efficace, car l’enfant était actif et déconnectait fréquemment le circuit de VMI. Elle a également inséré un filtre à haute efficacité de particules d’air (HEPA) à la sortie du respirateur, suivi d’un filtre échangeur de chaleur et d’humidité (HME) près de la TCT. Elle a utilisé un filtre échangeur de chaleur et d’humidité (HMEF) dans le réanimateur manuel pour la réalisation de techniques de décongestion bronchique et un filtre HEPA à la sortie de l’air comprimé, afin de réduire la dispersion d’aérosol pendant l’aspiration des voies aériennes.\n\nLa radiographie thoracique initiale ne révélait aucune anomalie. La gazométrie veineuse a indiqué une acidose respiratoire (pH = 7,27 ; pCO2 = 69,9 ; HCO3 = 31,7), nécessitant des ajustements des paramètres ventilatoires (IPAP = 28 cmH2O ; EPAP = 5 cmH2O ; FR = 25 irpm), et l'utilisation d'oxygénothérapie (1 L/min). Sept jours après le début des symptômes, une nouvelle radiographie thoracique a été réalisée, révélant la présence d'un infiltrat péri-hilar et une apparente consolidation dans le lobe moyen.\n\nPendant les séances de kinésithérapie, des techniques manuelles ont été utilisées pour maintenir l'expansion pulmonaire et promouvoir l'hygiène bronchique. Les techniques les plus utilisées étaient : la compression/décompression, l'expiration lente prolongée (ELPr), l'hyperinsufflation manuelle (HM) avec sac auto-gonflable et le bag squeezing. Afin de maintenir la patiente active et prévenir la régression du tableau moteur, l'encadrement familial a maintenu la stimulation motrice quotidienne.\n\n19 jours après le début des symptômes de COVID-19, la patiente a été autorisée à quitter l'hôpital, cliniquement stable, avec un résultat négatif au test SARS-CoV-2, une gazométrie sans modification et un retour aux paramètres ventilatoires utilisés avant l'infection. Quelques jours avant la sortie, l'enquête génétique a été menée à bien, confirmant le syndrome d'Ondine. Malgré une hospitalisation prolongée (300 jours), la patiente contrôlait sa tête, pouvait s'asseoir sans soutien, roulait et saisissait et atteignait des objets sans difficulté. En outre, l'évaluation fonctionnelle au moyen de l'échelle d'état fonctionnel (FSS-Brésil) a indiqué un degré modéré de dysfonctionnement (12 points), et les soins de physiothérapie motrice et respiratoire ont été poursuivis à domicile.\n",
+        "gold_summary": "sexe féminin, 10 mois, avec une maladie chronique préexistante, hospitalisée depuis la naissance, utilisant une ventilation mécanique par trachéotomie, a évolué avec une hypoxémie, nécessitant une oxygénothérapie et une augmentation des paramètres ventilatoires, confirmant la COVID-19. Des techniques de désobstruction bronchique et de maintien de l'expansion pulmonaire ont été réalisées. En outre, l'enfant a acquis, pendant l'hospitalisation, le contrôle de la tête, la position assise sans soutien, le roulement et la portée des objets et, pendant l'infection par le coronavirus, des instructions ont été données à la famille pour le maintien des repères moteurs acquis.\n",
+        "synthetic_summary": {
+            "B1": "Il y a une petite fille de 10 mois. Elle est restée longtemps à l’hôpital. Elle avait besoin d’un petit tuyau pour l’aider à bien respirer.\n\nUn jour, elle est tombée malade avec un virus qui s’appelle le coronavirus. Elle avait du mal à bien respirer. Les docteurs lui ont donné un peu plus d’air pour l’aider.\n\nLes docteurs ont aussi fait des petits massages pour aider ses poumons à être plus forts. La famille a aidé la petite fille à bouger tous les jours.\n\nPendant son séjour, la petite fille a appris à tenir sa tête, à s’asseoir toute seule, à se retourner et à attraper des choses. Les grandes personnes ont continué à l’aider même après qu’elle soit sortie de l’hôpital.",
+            "B2": "Fille de 10 mois avec une maladie chronique, hospitalisée depuis sa naissance, elle utilisait un ventilateur mécanique via une trachéotomie pour l’aider à respirer. Pendant son séjour, elle a développé une baisse de l’oxygène dans le sang (hypoxémie), ce qui a nécessité de lui donner de l’oxygène supplémentaire et d’augmenter les réglages du ventilateur. Un test a confirmé qu’elle avait la COVID-19.\n\nPour l’aider à mieux respirer, les médecins ont utilisé des techniques spéciales pour nettoyer ses poumons et garder ses poumons bien ouverts. Pendant son hospitalisation, elle a aussi appris à mieux contrôler sa tête, à s’asseoir sans aide, à se retourner et à attraper des objets. Pendant sa maladie, la famille a reçu des conseils pour continuer à soutenir ses progrès moteurs à la maison.",
+            "B3": "Résumé destiné à un adulte non spécialiste\n\n**Contexte**  \nUne fillette de dix mois, atteinte d’une maladie chronique rare appelée syndrome d’Ondine, a été hospitalisée depuis sa naissance. Elle nécessitait une ventilation mécanique invasive via une trachéotomie (une ouverture chirurgicale dans la trachée pour aider à respirer). Après plusieurs mois en unité de soins intensifs néonatale, elle était stable sur un ventilateur mécanique adapté à domicile.\n\n**Principales observations**  \nAu neuvième mois d’hospitalisation, la patiente a présenté une fièvre et une baisse de la saturation en oxygène (hypoxémie), ce qui a conduit à la réalisation d’un test PCR qui a confirmé une infection par le virus SARS-CoV-2 (COVID-19). Elle a alors reçu de l’oxygène supplémentaire et ses paramètres de ventilation ont été ajustés pour améliorer sa respiration. Les radiographies thoraciques ont montré une évolution vers une inflammation pulmonaire avec des infiltrats et une consolidation, signes typiques d’une infection respiratoire.\n\nPour limiter la dispersion du virus dans l’air, l’équipe de physiothérapie a mis en place un circuit d’aspiration fermé et des filtres spécifiques sur le ventilateur et les équipements utilisés lors des soins respiratoires. Des techniques manuelles de kinésithérapie respiratoire ont été appliquées pour favoriser le nettoyage des voies aériennes et maintenir l’expansion des poumons. Ces techniques comprenaient notamment des compressions thoraciques, des expirations lentes prolongées, et des hyperinsufflations manuelles.\n\n**Interprétation clinique**  \nMalgré la gravité potentielle de la COVID-19 chez un nourrisson dépendant d’une ventilation mécanique, la patiente est restée stable grâce à une prise en charge adaptée, incluant des ajustements ventilatoires et des soins de kinésithérapie respiratoire. La stimulation motrice quotidienne, assurée par la famille, a permis à l’enfant de progresser sur le plan moteur malgré la longue hospitalisation.\n\n**Prochaines étapes**  \nAprès 19 jours d’infection, la fillette a été déclarée guérie avec un test négatif au SARS-CoV-2, un retour aux paramètres ventilatoires initiaux et une stabilité clinique. Elle avait acquis des capacités motrices importantes, telles que le contrôle de la tête, la position assise sans soutien, le roulé-boulé et la préhension d’objets. Un suivi kinésithérapique continu, à la fois respiratoire et moteur, a été mis en place à domicile pour soutenir son développement et sa qualité de vie."
+        }
+    },
+    {
+        "article": "Une femme japonaise de 35 ans, pesant 42,7 kg (poids sec, 41,1 kg avant la grossesse), et mesurant 147 cm a été opérée par césarienne. Elle souffrait d'une insuffisance rénale due à une glomérulonéphrite chronique. Avant de devenir enceinte, elle avait été soumise à une hémodialyse trois fois par semaine. L'accès à l'hémodialyse (fistule artério-veineuse) se trouvait dans son bras supérieur gauche. Les symptômes et le déroulement du traitement jusqu'à la césarienne sont décrits dans le tableau 1. Lorsque la grossesse a été identifiée, elle a reçu une hémodialyse cinq fois par semaine. Bien qu'elle n'ait pas présenté de symptômes avant la grossesse, elle a déclaré avoir souffert d'une dyspnée à 12 semaines de gestation et a ensuite développé une toux sévère. L'échocardiographie transthoracique (TTE) a montré une fraction d'éjection ventriculaire gauche (FEVG) de 40 % et une hypertension pulmonaire modérée. Après l'hospitalisation, l'hémodialyse a été augmentée à six fois par semaine pour prévenir une insuffisance cardiaque. La FEVG a été améliorée à près de 50 % et les symptômes ont également été améliorés, de sorte que le plan était de reporter l'accouchement aussi longtemps que possible. Cependant, elle a de nouveau développé une toux et une dyspnée à 22 semaines de gestation.\n\nLa radiographie thoracique a montré une congestion importante. La TTE a montré une EFV de 20 %, une régurgitation mitrale modérée à modérée et une dilatation ventriculaire gauche. Elle a donc été admise à l'unité de soins intensifs (USI). La saturation en oxygène percutanée (SpO2) était de 92 % en air ambiant, de sorte que l'oxygène supplémentaire a été fourni à 1 l/minute par canule nasale. Après l'administration d'oxygène, la SpO2 était de 98 %. En outre, le volume d'eau a été éliminé par ultrafiltration extracorporelle. Bien que l'état respiratoire et la fonction cardiaque se soient légèrement améliorés avec les soins intensifs, une conférence clinique d'obstétriciens, de pédiatres, d'urologues, de cardiologues et d'anesthésiologistes a décidé qu'une césarienne devait être pratiquée à 24 semaines 0 jours de gestation. L'anticoagulant utilisé pour la dialyse a été changé de l'héparine au nafamostat mesylate (nafamostat) à 23 semaines de gestation pour la césarienne. Les tests sanguins ont montré une hémoglobine de 10,1 g/dl et des plaquettes de 12,1 × 104/μl. Le temps de prothrombine international normalisé était de 0,85 et le temps de thromboplastine partielle activée était de 25,6 secondes.\n\nLorsque la patiente est arrivée dans la salle d'opération, deux lignes veineuses périphériques intraveineuses ont été insérées avec une canule de calibre 22 et une canule de calibre 18 dans l'avant-bras droit pour une réanimation par fluides. Une ligne artérielle a été insérée par l'artère radiale droite avec une canule de calibre 22. Des lignes veineuses centrales ont été insérées par l'artère jugulaire. Nous avons inséré les lignes veineuses centrales en utilisant l'échographie tout en surveillant attentivement la pression artérielle. L'échographie a montré que l'artère jugulaire était claire et nous avons vérifié que la position légère de Trendelenburg ne modifiait pas la dynamique circulatoire. Dans l'ensemble, la procédure a été menée à bien sans changements significatifs dans l'hémodynamique. Des agents anesthésiques épidurales et rachidiens ont été administrés dans la position latérale droite aux espaces intervertébraux L3-L4 et Th10-Th11, respectivement. Après une infiltration locale de 1 % de mepivacaïne, une ligne épidurale a été insérée avec une aiguille Tuohy de calibre 18. L'espace épidural a été confirmé en utilisant la méthode conventionnelle de perte de résistance. Après un test d'aspiration, un résultat négatif a été obtenu, une dose d'essai de 1 % de mepivacaïne (3 ml) a été administrée par le biais du cathéter. La ponction lombaire a été réalisée avec succès et 5 mg de bupivacaïne hyperbare à 0,5 % et 10 μg de fentanyl ont été administrés par voie intrathécale avec une aiguille épidurale Quincke de calibre 25. Le montant et le type d'agents anesthésiques ont été décidés par les anesthésiologistes et les chirurgiens. L'administration continue de la phénylephrine a été immédiatement commencée à 1 mg/heure pour éviter une hypotension due à l'anesthésie. Cinq millilitres de 0,25 % de ropivacaïne ont été administrés par le biais du cathéter épidural.\n\nAprès confirmation du blocus sensoriel au niveau Th4, l'opération a été commencée. Avant l'accouchement, 0,1 mg de nitroglycérine a été administré pour détendre l'utérus. Le nouveau-né a été livré 4 minutes après le début de la césarienne. Les pressions artérielles veineuse centrale et périphérique ont été maintenues pendant la césarienne. La patiente n'a signalé aucune nausée, douleur ou dyspnée intraopérative. Après l'accouchement, 600 mg d'acétaminophène ont été administrés. Une fois l'opération terminée sans complications, 2 mg de morphine ont été administrés via le cathéter péridural, qui a ensuite été retiré. Les temps d'opération et d'anesthésie étaient respectivement de 49 minutes et 88 minutes. Les volumes de perfusion totale et de perte de sang étaient respectivement de 1050 ml et 1029 ml. Après l'opération, la patiente a été transférée à l'unité de soins intensifs et une hémodialyse a été effectuée. Elle a été transférée au service de gynécologie le jour postopératoire (POD) 5 et a été libérée le POD 10. La fonction cardiaque s'est améliorée après la césarienne. Au moment de la rédaction du présent rapport, la mère et l'enfant allaient bien.",
+        "gold_summary": "Nous avons rencontré un cas dans lequel une césarienne a été réalisée en utilisant une anesthésie rachidienne et épidurale combinée pour une femme enceinte souffrant d'insuffisance rénale et cardiaque chronique. La femme japonaise de 35 ans avait été soumise à une hémodialyse pendant plusieurs années. Les symptômes d'insuffisance cardiaque apparus pendant la grossesse se sont initialement améliorés avec des traitements tels que l'augmentation de l'hémodialyse, mais ont réapparu. Elle a été admise à l'unité de soins intensifs. Le plan initial était de livrer le bébé après quelques semaines, mais la progression de l'insuffisance cardiaque est devenue une préoccupation. Après une conférence clinique entre le personnel, une césarienne avec anesthésie rachidienne et épidurale combinée a été programmée pour 24 semaines, 0 jours de gestation. L'anticoagulant pour dialyse a également été changé de l'héparine au nafamostat en préparation pour la césarienne. La surveillance a été commencée avec des pressions veineuses centrales et radiales avant l'induction de l'anesthésie. Une anesthésie rachidienne et épidurale combinée a été induite et la césarienne a été complétée sans complications. La chirurgie a été initiée sous administration continue de phényléphrine, qui était destinée à éviter l'hypotension due à l'anesthésie. L'état hémodynamique et respiratoire du patient est resté stable après l'opération. Après la césarienne, la morphine a été administrée par voie épidurale et le cathéter épidural a été retiré.\n",
+        "synthetic_summary": {
+            "B1": "Une maman était très malade avec son cœur et ses reins. Elle attendait un bébé. \n\nLe bébé est venu au monde grâce à une opération appelée césarienne. \n\nPour ne pas faire mal à la maman, les docteurs ont donné un médicament spécial pour qu’elle ne sente rien. \n\nTout s’est bien passé. La maman et le bébé vont bien maintenant.",
+            "B2": "Cas d’une césarienne chez une femme enceinte avec des problèmes rénaux et cardiaques\n\nUne femme japonaise de 35 ans souffrait d’une maladie des reins qui l’obligeait à faire une hémodialyse, c’est-à-dire un traitement qui filtre le sang quand les reins ne fonctionnent plus bien. Pendant sa grossesse, elle a aussi eu des problèmes au cœur, comme une insuffisance cardiaque, qui ont causé des difficultés à respirer et une toux sévère.\n\nAu début, son état s’est amélioré grâce à l’augmentation des séances d’hémodialyse, mais ses symptômes sont revenus et elle a dû être hospitalisée en soins intensifs. Les médecins ont décidé qu’il était nécessaire de faire une césarienne à 24 semaines de grossesse pour protéger sa santé et celle du bébé.\n\nPour l’opération, ils ont utilisé une anesthésie combinée : une anesthésie rachidienne (injection dans le dos pour bloquer la douleur) et une anesthésie épidurale (injection dans un espace proche de la moelle épinière). Avant l’anesthésie, ils ont installé des dispositifs pour surveiller sa tension artérielle et son cœur de près.\n\nPendant la césarienne, un médicament appelé phényléphrine a été donné en continu pour éviter que sa tension ne baisse à cause de l’anesthésie. L’opération s’est bien passée, sans complications, et la maman est restée stable au niveau du cœur et de la respiration. Après la naissance, elle a reçu de la morphine par voie épidurale pour soulager la douleur, puis le cathéter a été retiré.\n\nLa maman a été surveillée en soins intensifs après la césarienne et a continué son traitement d’hémodialyse. Sa fonction cardiaque s’est améliorée, et elle a pu quitter l’hôpital en bonne santé, tout comme son bébé. Ce cas montre l’importance d’une surveillance attentive et d’une collaboration entre différents spécialistes pour gérer une grossesse compliquée par des maladies graves.",
+            "B3": "Résumé détaillé et structuré\n\nContexte  \nNous rapportons le cas d’une femme japonaise de 35 ans, atteinte d’une insuffisance rénale chronique secondaire à une glomérulonéphrite, traitée par hémodialyse régulière avant et pendant sa grossesse. Cette patiente, de faible poids et petite taille, a développé au cours de sa grossesse une insuffisance cardiaque avec une fonction ventriculaire gauche altérée et une hypertension pulmonaire modérée, nécessitant une augmentation progressive de la fréquence des séances d’hémodialyse. Malgré une amélioration initiale, ses symptômes cardiaques se sont aggravés à 22 semaines de gestation, avec une diminution significative de la fraction d’éjection ventriculaire gauche (FEVG) à 20 %, une régurgitation mitrale modérée et une dilatation ventriculaire gauche, conduisant à son admission en unité de soins intensifs.\n\nPrincipales observations  \nFace à la dégradation de son état cardiorespiratoire, une décision multidisciplinaire impliquant obstétriciens, pédiatres, urologues, cardiologues et anesthésiologistes a été prise pour programmer une césarienne à 24 semaines de gestation afin de préserver la santé maternelle et fœtale. En préparation à cette intervention, l’anticoagulant utilisé pour la dialyse a été modifié, passant de l’héparine au nafamostat mélysate, afin de réduire les risques hémorragiques. La patiente a été placée sous surveillance hémodynamique rigoureuse, avec la pose de lignes veineuses périphériques, d’une ligne artérielle radiale et d’une ligne veineuse centrale jugulaire, toutes réalisées sous guidage échographique pour minimiser les complications. L’anesthésie a été réalisée par une technique combinée rachidienne et épidurale, avec administration de bupivacaïne hyperbare et fentanyl intrathécaux, ainsi que de ropivacaïne par voie épidurale. Une perfusion continue de phényléphrine a été initiée pour prévenir l’hypotension induite par l’anesthésie.\n\nInterprétation clinique  \nLa césarienne s’est déroulée sans complications majeures, avec une stabilité hémodynamique et respiratoire maintenue tout au long de l’intervention. Le nouveau-né a été délivré rapidement, quatre minutes après le début de la chirurgie. La gestion anesthésique a permis d’éviter les épisodes d’hypotension et de dyspnée, et la douleur postopératoire a été efficacement contrôlée par la morphine administrée par voie épidurale avant le retrait du cathéter. Les volumes de perfusion et les pertes sanguines ont été bien équilibrés. Après l’opération, la patiente a été transférée en soins intensifs pour poursuivre l’hémodialyse et la surveillance, puis au service de gynécologie, avec une amélioration progressive de sa fonction cardiaque. Au moment du rapport, la mère et l’enfant étaient en bonne santé.\n\nProchaines étapes  \nCe cas illustre l’importance d’une prise en charge multidisciplinaire et d’une anesthésie adaptée chez une femme enceinte présentant une insuffisance rénale chronique sous dialyse et une insuffisance cardiaque sévère. La coordination entre les équipes médicales, la modification prudente des anticoagulants, la surveillance hémodynamique avancée et l’utilisation d’une anesthésie combinée ont permis une césarienne sécurisée à un stade précoce de la grossesse. Un suivi cardiaque et néphrologique continu reste essentiel pour optimiser la santé maternelle et le développement de l’enfant à long terme."
+        }
+    },
+    {
+        "article": "Une femme de 34 ans sans antécédents médicaux ou chirurgicaux a été présentée au service des urgences avec un historique de cinq jours de fatigue, d'intolérance à la chaleur, de transpiration et de palpitations qui s'aggravaient progressivement. Ses symptômes n'avaient pas de variation diurne. La patiente a décrit une fatigue et des palpitations présentes avec une intensité plus modérée au cours des deux dernières années, mais qui n'a jamais été suffisamment gênante pour qu'elle cherche une attention médicale. Après un interrogatoire plus approfondi, la patiente a déclaré avoir perdu cinq kilos de poids involontaire au cours des cinq derniers mois. Elle n'a pas signalé de diarrhée, de symptômes respiratoires ou de douleurs thoraciques. Ses menstruations étaient régulières. La patiente a arrêté de fumer trois mois avant sa présentation et n'a jamais consommé d'alcool. La patiente a nié toute consommation excessive de caféine dans son alimentation.\n\nUn examen physique a révélé une euthermie (36,6 °C), une tachycardie avec une fréquence cardiaque (FC) allant jusqu'à 120 battements par minute (BPM), une tension artérielle élevée (140/100 mmHg), une fréquence respiratoire de 20 respirations par minute, une saturation en oxygène de 99 % en air ambiant et un indice de masse corporelle (IMC) de 23,5 kg/m2. Un examen plus approfondi a révélé un goitre diffus, de fins tremblements bilatéraux sur les mains tendues, une proptose bilatérale, un retard et une rétraction des paupières bilatérales, plus marqués du côté droit. Un électrocardiogramme a montré une tachycardie sinusale (TS) sans changements ischémiques ou signes d'hypertension chronique. Une radiographie thoracique et un échocardiogramme transthoracique au lit n'ont révélé aucune pathologie. Un profil sanguin complet et des tests de la fonction rénale et hépatique n'ont pas révélé de pathologie.\n\nDe nouvelles analyses sanguines ont révélé une thyrotoxicose avec suppression totale de l'hormone stimulant la thyroïde (TSH) (<0,01 mUI/L, plage normale : 0,3-4,2), avec une augmentation de la T3 (17,8 pmol/L, plage normale : 3,7-6,4) et de la T4 (52,5 pmol/L, plage normale : 11-23,3). Son anticorps anti-récepteur de la TSH (TRAB) était positif (16,5 IU/L, seuil de 1,75 IU/L), confirmant ainsi un diagnostic de maladie de Basedow (GBD). La patiente a été informée de la maladie de Basedow et des effets et effets secondaires (en particulier l'agranulocytose) du CBZ. Elle a ensuite commencé à prendre du CBZ 20 mg une fois par jour (OD) et du propranolol 80 mg à libération prolongée (SR) OD avec un suivi ambulatoire pour une répétition du TFT et un ajustement supplémentaire de la dose. Cependant, après quatre semaines, la patiente a revisité le service des urgences avec une histoire de trois jours de palpitations associées à une gêne thoracique et des vertiges. L'examen physique a révélé un ST (HR 137 BPM) et un examen thyroïdien similaire à sa visite initiale. Un panel TFT répété a montré TSH <0,01, T3 : 17,5, et T4 : 64,1. Elle a nié le non-respect du traitement. Le CBZ a été augmenté à 20 mg deux fois par jour (BD), et le propranolol 80 mg SR a été poursuivi. La patiente a été vue à la clinique endocrinienne après deux semaines. Elle s'est toujours plainte de palpitations et d'intolérance à la chaleur ; cependant, le ST s'est stabilisé.\n\nDeux semaines après la visite en clinique, la patiente s'est rendue aux urgences pour la troisième fois avec des palpitations gênantes depuis un jour. L'examen a révélé un ST (HR140 BPM), et son IMC était passé à 24,5 kg/m2. Les TFT ont montré une hyperthyroïdie persistante (TSH <0,01, T3 : 12,1, T4 : 54,1). La patiente a été admise et a reçu du CBZ 20 mg trois fois par jour (TD) et du propranolol 160 mg SR OD sous surveillance. Ses TFT ont été répétés cinq jours plus tard, montrant une hyperthyroïdie persistante avec seulement une amélioration marginale de la T4 (39 pmol/L). La possibilité d'une non-observance du traitement a été discutée lors d'une entrevue détaillée avec la patiente. La patiente a insisté sur le respect strict du traitement. Elle était gênée par des symptômes persistants, sans stress ou dépression sous-jacents, et voulait que les symptômes soient traités. Elle avait pris du poids et avait une réduction de son nombre absolu de neutrophiles, ce qui suggérait une observance du traitement.\n\nEn outre, son TRAB a été réduit de 16,5 à 6,9. Elle a été libérée (sous CBZ 20 mg par voie orale et propranolol 160 mg par voie orale) avec un plan de suivi rapproché.\n\nLors de la visite de suivi après quatre semaines, elle restait hyperthyroïdienne (TSH : 0,01, T3 : 11,1, T4 : 43,9) avec un rythme cardiaque normal. La patiente a été invitée à apporter des bouteilles vides de son médicament pour vérifier son respect du traitement, ce qui a renforcé la possibilité de prendre les médicaments comme prescrit. La malabsorption a été écartée avec un dépistage négatif de la maladie cœliaque (anticorps anti-transglutaminase tissulaire négatifs) et des taux normaux de cyanocobalamine et d'albumine. La GD résistante à la CBZ a été considérée à ce stade et a été transférée à 100 mg de PTU par voie orale, avec 160 mg de propranolol SR OD et 20 mg de prednisolone par jour pendant deux mois avec un régime de réduction progressive. À la visite de suivi de quatre semaines, elle n'avait pas constaté d'amélioration de ses TFT (TSH : <0,01, T3 : 11,3, T4 : 40,1). Après une autre visite de suivi de quatre semaines, ses stéroïdes ont été arrêtés et la dose de PTU a été augmentée à 150 mg par voie orale, en raison de TFT persistants dérangés (TSH : <0,01, T3 : 12, T4 : 40,4). La patiente a eu une réponse partielle à la dose augmentée de PTU avec des TFT répétés après un mois, indiquant TSH <0,01, T3 : 7, T4 : 25,5. La tendance des TFT de la patiente depuis le diagnostic jusqu'à la dernière visite de suivi est représentée graphiquement.\n\nÉtant donné la réponse partielle aux doses croissantes de PTU, la patiente a été référée à l'équipe chirurgicale pour un traitement définitif par thyroïdectomie, évitant ainsi les éventuelles complications hépatotoxiques et hématologiques des doses plus élevées de PTU à long terme. La patiente a bien toléré la thyroïdectomie totale sans aucune complication. Son dernier profil thyroïdien était normal (TSH 3,42) avec une lévothyroxine de substitution à 75 mcg par jour.\n",
+        "gold_summary": "Une femme de 34 ans a présenté une fatigue, une intolérance à la chaleur, une transpiration et des palpitations qui s'aggravaient progressivement depuis 5 jours. Elle a été diagnostiquée avec une GD sur la base de ses tests de fonction thyroïdienne (TFT) et a commencé à prendre du CBZ et du propranolol. Malgré le fait qu'elle ait respecté les doses de CBZ de 20 mg une fois par jour puis deux fois par jour, ses TFT sont restés inchangés pendant 4 mois. Cependant, la patiente a de nouveau consulté les urgences en raison d'une thyrotoxicose persistante et de TFT inchangés. Sa dose a finalement été augmentée à 20 mg trois fois par jour, et l'administration sous surveillance n'a pas amélioré ses TFT. La patiente a finalement été transférée à PTU 150 mg trois fois par jour avec des stéroïdes, avec une amélioration minimale. La patiente a finalement subi une thyroïdectomie pour éviter l'utilisation à long terme de PTU.\n",
+        "synthetic_summary": {
+            "B1": "Une dame se sentait très fatiguée et avait chaud tout le temps. Son cœur battait très vite. \n\nLe docteur a dit qu’elle avait un problème avec une petite partie dans son cou qui fait des choses importantes pour le corps. \n\nElle a pris des médicaments, mais ça n’a pas beaucoup aidé. Elle est allée plusieurs fois chez le docteur parce qu’elle se sentait toujours mal. \n\nFinalement, les docteurs ont enlevé cette petite partie du cou avec une opération. Après, elle allait mieux et se sentait plus calme.",
+            "B2": "Une femme de 34 ans a commencé à se sentir très fatiguée, à avoir chaud facilement, à transpirer beaucoup et à avoir des palpitations pendant cinq jours. Ces symptômes ont empiré avec le temps. Après des analyses, les médecins ont découvert qu’elle avait une maladie appelée maladie de Basedow. Cette maladie fait que la glande thyroïde produit trop d’hormones, ce qui explique ses symptômes.\n\nPour la soigner, elle a commencé un traitement avec un médicament appelé carbimazole (CBZ) et un autre appelé propranolol, qui aide à calmer le cœur. Malgré cela, ses analyses de sang montraient toujours un excès d’hormones thyroïdiennes pendant plusieurs mois, même quand elle prenait bien ses médicaments. Ses symptômes sont restés présents, et elle a dû revenir plusieurs fois aux urgences.\n\nLes médecins ont augmenté la dose de CBZ, mais cela n’a pas beaucoup aidé. Ensuite, ils ont changé son traitement pour un autre médicament, le propylthiouracile (PTU), associé à des stéroïdes, qui sont des médicaments pour réduire l’inflammation. Cette nouvelle combinaison a un peu amélioré ses résultats, mais pas complètement.\n\nFinalement, pour éviter les risques liés à la prise prolongée de médicaments puissants, les médecins ont décidé de lui enlever toute la thyroïde par une opération appelée thyroïdectomie. Après cette chirurgie, elle a bien récupéré et a commencé un traitement de remplacement avec une hormone appelée lévothyroxine, qui aide à garder son corps en équilibre. Ses analyses sont alors redevenues normales.",
+            "B3": "Résumé détaillé et structuré pour un public adulte non spécialiste\n\n**Contexte**  \nUne femme de 34 ans, sans antécédents médicaux particuliers, s’est présentée aux urgences avec des symptômes progressifs sur cinq jours : fatigue importante, intolérance à la chaleur, transpiration excessive et palpitations cardiaques. Ces signes s’inscrivaient dans un contexte de fatigue et de palpitations modérées depuis deux ans, sans consultation médicale préalable. Elle avait également perdu 5 kg involontairement sur les cinq derniers mois. Aucun autre symptôme digestif, respiratoire ou thoracique n’était rapporté. Ses règles étaient régulières, elle avait arrêté de fumer récemment et ne consommait ni alcool ni caféine en excès.\n\n**Principales observations cliniques et paracliniques**  \nL’examen physique a révélé une tachycardie (fréquence cardiaque jusqu’à 120 battements par minute), une tension artérielle élevée (140/100 mmHg), un goitre diffus (augmentation homogène de la taille de la thyroïde), des tremblements fins aux mains, une proptose (exophtalmie) bilatérale et des anomalies palpébrales caractéristiques (retrait et retard des paupières). L’électrocardiogramme confirmait une tachycardie sinusale sans signes d’ischémie. Les radiographies thoraciques et l’échocardiogramme étaient normaux. Les analyses sanguines initiales montraient une thyrotoxicose : suppression complète de l’hormone stimulant la thyroïde (TSH), augmentation marquée des hormones thyroïdiennes T3 et T4, et présence d’anticorps anti-récepteur de la TSH (TRAB) positifs, confirmant le diagnostic de maladie de Basedow (ou maladie de Graves-Basedow), une maladie auto-immune responsable d’une hyperactivité thyroïdienne.\n\n**Interprétation clinique et évolution thérapeutique**  \nLa patiente a été informée de sa maladie et des risques liés au traitement par carbimazole (CBZ), notamment l’agranulocytose (diminution sévère des globules blancs). Elle a débuté un traitement par CBZ à faible dose (20 mg une fois par jour) associé à un bêta-bloquant (propranolol) pour contrôler les symptômes cardiaques. Malgré une augmentation progressive des doses de CBZ jusqu’à 20 mg trois fois par jour sur plusieurs semaines, ses symptômes et ses analyses thyroïdiennes sont restés pathologiques, avec une thyrotoxicose persistante et une fréquence cardiaque élevée. La surveillance stricte du traitement a été confirmée, excluant une mauvaise observance ou une malabsorption digestive. La persistance de l’hyperthyroïdie malgré un traitement bien suivi a conduit à considérer une résistance au carbimazole.\n\nUn changement de traitement a été effectué, avec introduction du propylthiouracile (PTU) à doses croissantes, associé à une courte corticothérapie pour tenter de réduire l’inflammation thyroïdienne. Cette stratégie a apporté une amélioration partielle, mais la thyrotoxicose persistait.\n\n**Prochaines étapes et prise en charge définitive**  \nDevant la résistance au traitement médical et pour éviter les complications liées à l’utilisation prolongée de fortes doses de PTU (notamment des effets toxiques sur le foie et le sang), la patiente a été orientée vers une intervention chirurgicale. Une thyroïdectomie totale (ablation complète de la thyroïde) a été réalisée sans complication. Après l’opération, la patiente a reçu un traitement substitutif par lévothyroxine (hormone thyroïdienne de synthèse) à dose adaptée, permettant un retour à un profil thyroïdien normal.\n\n**Conclusion**  \nCe cas illustre une forme de maladie de Basedow résistante au traitement antithyroïdien classique, nécessitant une prise en charge progressive et multidisciplinaire, incluant une surveillance attentive, des ajustements thérapeutiques et, en dernier recours, une intervention chirurgicale pour contrôler durablement l’hyperthyroïdie et prévenir les complications."
+        }
+    },
+    {
+        "article": "Une Japonaise de 71 ans ayant des antécédents de diabète de type 1, d’insuffisance rénale en phase terminale, de blocus auriculo-ventriculaire complet et d’infarctus antérieur du myocarde a été admise au service de gastroentérologie de notre hôpital pour évaluation et traitement d’une perte de conscience aiguë secondaire à une hypoglycémie. Au moment de son admission, elle portait un stimulateur cardiaque permanent et était en dialyse trois fois par semaine. Le service d’orthopédie a été contacté pour évaluer un gonflement, une chaleur et une rougeur de sa main gauche dus à une morsure au bout de son majeur gauche auto-infligée lors d’un épisode de démence. Un traitement standard par céfazoline intraveineuse (1 g par jour) a été prescrit pour traiter une suspicion de cellulite. L’infection n’a pas répondu et a progressé malgré deux jours complets de traitement antibiotique. Une culture bactérienne de la lésion a révélé une bactérie résistante à la méthicilline (MRSA). Après un examen physique, la patiente a présenté les quatre signes cardinaux de la tendinite du fléchisseur de Kanavel. Une perfusion de vancomycine (valeur minimale, 15-20 µg/mL) a été initiée pour traiter l’infection à MRSA, ainsi qu’un débridement de la plaie et une amputation partielle de l’articulation interphalangienne distale. Une décompression du nerf médian a été réalisée pour soulager la pression résultant d’un abcès purulent. Bien que la rougeur et le gonflement aient persisté après cette procédure, la progression de l’infection a semblé quelque peu réduite. Bien que le traitement antibiotique par vancomycine ait été poursuivi, la patiente s’est soudainement plainte de douleurs abdominales, de sang brun foncé dans les selles indiquant une hémorragie gastro-intestinale, et a développé des signes compatibles avec un choc systémique. Sa tension artérielle systolique initiale était de 60 mmHg, ce qui a réagi à l’administration aiguë de vasopresseurs. Les données de laboratoire comprenaient un nombre élevé de globules blancs (9890/mm3), ainsi qu’une augmentation des taux sériques de protéine C réactive (CRP ; 259,7 mg/L) et de créatinine (421,7 µmol/L) et une réduction des taux de sodium (132 mEq/L), de glucose sanguin (2,6 mmol/L) et d’hémoglobine (8,2 g/dL). Les résultats d’une tomographie par ordinateur (CT) ont abouti à un diagnostic d’ischémie mésentérique non occlusive ; une résection intestinale d’urgence a été effectuée. Des tubes d’alimentation ont été initiés et poursuivis pendant une semaine. La norépinephrine a été ajoutée à son traitement pour maintenir la tension artérielle à des niveaux nécessaires pour soutenir la perfusion des organes avec une pression artérielle moyenne cible de 70.\n\nPendant son séjour à l'hôpital, la patiente a été exposée au SARS-CoV-2 après avoir été en contact étroit prolongé avec une personne infectée pendant une dialyse. Son prélèvement nasal a été positif pour le COVID-19 en utilisant un test d'amplification isotherme induite par boucle. Quatre jours après le test positif, elle a développé des signes de pneumonie aiguë. Les résultats d'une radiographie thoracique et d'une tomodensitométrie ont confirmé ce diagnostic et ont révélé une consolidation des poumons ainsi que des épanchements pleuraux bilatéraux. Un traitement antiviral avec favipiravir (200 mg par voie orale deux fois par jour) a été initié et la patiente a été transférée à l'unité de soins intensifs. Cela était conforme aux recommandations au moment de l'administration. La patiente était hypervolémique avec une demande d'oxygène accrue. Une hémodiafiltration continue a été effectuée pour éviter une surcharge liquidienne.\n\nImmédiatement avant l’exposition au COVID-19, la patiente a développé des signes cliniques de fasciite nécrosante. L’infection s’était étendue au fascia et à la musculature environnante de sa main gauche. Bien qu’une amputation d’urgence de la main ait été jugée nécessaire, la patiente a développé un choc septique et a eu besoin d’une respiration artificielle en raison d’une augmentation soudaine de la demande en oxygène. L’oxygène à haut débit a été administré en continu par le tube endotrachéal, et son traitement antiviral a été changé pour du remdesivir (100 mg intraveineux une fois par jour) avec de l’hydrocortisone intraveineuse (200 mg/dose). Le remdesivir était encore en phase d’utilisation compassionnelle à ce moment-là. Alors qu’elle suivait un traitement pour des événements aigus potentiellement mortels, l’infection a progressé pour inclure les phalanges du troisième doigt gauche, avec une nécrose osseuse visible sur la radiographie. La vancomycine (500 mg) a été prescrite pour gérer l’ostéomyélite et prévenir sa propagation. La patiente a ensuite développé un syndrome de détresse respiratoire aiguë (ARDS). Bien que l’infection COVID-19 de la patiente ait été contrôlée après deux semaines, elle a développé une coagulation intravasculaire disséminée (DIC; score >4) qui a peut-être accéléré la croissance bactérienne. L’héparine étant contre-indiquée dans ce cas, l’ART-123, une forme recombinante et soluble de thrombomoduline alpha, a été administrée par voie intraveineuse (12 800 U une fois par jour pendant 3 jours) pour dissoudre les caillots systémiques. L’infection a progressé pour inclure la nécrose de l’ensemble du troisième doigt ainsi que la peau, le fascia et la musculature jusqu’à l’articulation radio-carpienne avec des signes d’invasion progressive dans l’avant-bras. Malheureusement, les restrictions et les fermetures d’hôpitaux liées à la COVID ont empêché tout traitement chirurgical supplémentaire à ce moment-là.\n\nLe patient a finalement récupéré de COVID-19. Deux semaines après le diagnostic initial, le patient a été sevré de la ventilation mécanique et le tube endotrachéal a été retiré. Deux semaines après l'extubation, le patient a terminé le traitement pour COVID-19 et a eu un test négatif pour l'antigène SARS-CoV-2. Une amputation majeure au tiers distal de l'avant-bras a ensuite été réalisée. Les tissus ont été débridés et lavés complètement pendant la procédure et tous les tissus infectés ont été enlevés. Étant donné que le site de l'amputation était proximal à sa sonde d'hémodialyse, son remplacement a été discuté avec des chirurgiens vasculaires et des néphrologues. La procédure a révélé une calcification importante des artères de son avant-bras gauche avec tortuosité et éventuelles occlusions, tant proximales que distales à la sonde. Le bruit et le frisson détectés dans la sonde ont également suggéré la possibilité d'un syndrome ischémique hypoperfusif distal. Une couverture adéquate du lambeau de peau a été obtenue et la souche a été fermée ; une étude radiographique de suivi n'a révélé aucune complication. La souche a semblé guérir bien, un mois plus tard, la patiente a succombé à un choc septique et à un arrêt cardiopulmonaire.\n",
+        "gold_summary": "Une femme de 71 ans a présenté une infection non contrôlée suite à une blessure auto-infligée au moyen de son index gauche. Une culture bactérienne de la lésion a révélé la présence de Staphylococcus aureus résistant à la méthicilline (MRSA). L'infection n'a pas pu être contrôlée par des antibiotiques ou des interventions supplémentaires, y compris un débridement et une amputation mineure. Elle a contracté une COVID-19 sévère à l'hôpital, ce qui a limité les options de traitement disponibles. Dans une tentative de contrôle de l'infection, la patiente a finalement subi une amputation majeure de l'avant-bras gauche distal. En se rétablissant de la procédure, la patiente a succombé à un choc septique et à un arrêt cardiopulmonaire.\n",
+        "synthetic_summary": {
+            "B1": "Une dame de 71 ans s’est fait très mal à la main gauche. Une vilaine bactérie est entrée dans sa blessure. Les médicaments n’ont pas réussi à la faire partir.\n\nElle est tombée très malade avec un gros rhume appelé COVID-19. Cela a rendu son traitement plus difficile. Les docteurs ont dû couper une grande partie de son bras pour arrêter la maladie.\n\nMême après l’opération, elle est restée très malade. Son cœur et sa respiration se sont arrêtés. Les docteurs ont fait tout leur possible pour l’aider.",
+            "B2": "Une femme de 71 ans s’est blessée toute seule au bout de son doigt gauche. Cette blessure s’est infectée à cause d’une bactérie appelée Staphylococcus aureus résistante à certains antibiotiques (on l’appelle MRSA). Malgré plusieurs traitements avec des antibiotiques, un nettoyage de la plaie (débridement) et même une petite amputation du doigt, l’infection n’a pas disparu.\n\nPendant son séjour à l’hôpital, elle a aussi attrapé une forme grave de COVID-19. Cette maladie a compliqué son état et a limité les traitements possibles pour son infection. L’infection a continué à s’étendre, touchant les muscles et les os de sa main.\n\nPour essayer de stopper l’infection, les médecins ont dû amputer une grande partie de son avant-bras gauche. Après cette opération, elle a d’abord commencé à se rétablir. Malheureusement, elle a ensuite souffert d’un choc septique, une réaction grave du corps à l’infection, qui a provoqué un arrêt du cœur et des poumons, et elle est décédée.",
+            "B3": "Résumé détaillé et structuré\n\nContexte  \nUne femme japonaise de 71 ans, présentant plusieurs antécédents médicaux graves dont un diabète de type 1, une insuffisance rénale terminale nécessitant une dialyse, un bloc auriculo-ventriculaire complet traité par stimulateur cardiaque, et un antécédent d’infarctus du myocarde, a été hospitalisée suite à une perte de conscience liée à une hypoglycémie. Par la suite, elle a développé une infection sévère à la main gauche, consécutive à une morsure auto-infligée lors d’un épisode de démence.\n\nPrincipales observations  \nInitialement suspectée de cellulite, la lésion infectieuse de la main gauche a révélé la présence d’un Staphylococcus aureus résistant à la méthicilline (MRSA) après culture bactérienne. Malgré un traitement antibiotique intraveineux par céfazoline puis vancomycine, ainsi que des interventions chirurgicales comprenant un débridement et une amputation partielle de la phalange distale, l’infection a progressé. La patiente a développé une fasciite nécrosante, une infection grave touchant le fascia (tissu conjonctif entourant les muscles) et les muscles adjacents, nécessitant une amputation d’urgence de la main. \n\nParallèlement, la patiente a contracté une infection sévère à SARS-CoV-2 (COVID-19) lors de sa dialyse, évoluant vers une pneumonie aiguë et un syndrome de détresse respiratoire aiguë (ARDS). Le traitement antiviral a été adapté au fil du temps, incluant favipiravir puis remdesivir, associé à une corticothérapie par hydrocortisone. La COVID-19 a limité les possibilités chirurgicales et a aggravé l’état général, notamment par le développement d’une coagulation intravasculaire disséminée (DIC), un trouble de la coagulation favorisant la formation de caillots sanguins dans les petits vaisseaux, ce qui a pu accélérer la progression de l’infection bactérienne.\n\nInterprétation clinique  \nL’infection à MRSA, initialement localisée, s’est étendue rapidement malgré un traitement antibiotique adapté et des interventions chirurgicales répétées. La survenue concomitante d’une infection sévère à COVID-19 a compliqué la prise en charge, en limitant les options chirurgicales et en aggravant l’état immunitaire et circulatoire de la patiente. La fasciite nécrosante a progressé jusqu’à l’atteinte osseuse (ostéomyélite) et à la nécrose extensive des tissus mous de l’avant-bras gauche. La présence de calcifications artérielles et de troubles vasculaires a également contribué à une mauvaise perfusion locale, compliquant la cicatrisation.\n\nProchaines étapes et issue  \nAprès stabilisation de la COVID-19 et sevrage de la ventilation mécanique, une amputation majeure au tiers distal de l’avant-bras gauche a été réalisée, avec débridement complet des tissus infectés. La prise en charge post-opératoire a été adaptée en concertation multidisciplinaire, notamment en raison de la proximité de la fistule d’hémodialyse. Malgré une cicatrisation initialement satisfaisante, la patiente a finalement succombé à un choc septique et à un arrêt cardiopulmonaire un mois après l’amputation.\n\nCe cas illustre la complexité de la prise en charge des infections sévères chez un patient polymorbide, aggravée par une infection concomitante à COVID-19, et souligne l’importance d’une intervention rapide et multidisciplinaire dans les infections nécrosantes à germes résistants."
+        }
+    },
+    {
+        "article": "C’est le cas d’une femme de 36 ans de la région d’Oromia, zone d’Arsi occidentale, qui présentait une toux, une dysphonie et un ronflement depuis 6 mois, ainsi qu’une perte de poids importante mais non quantifiée, une fatigue et une fièvre modérée et intermittente, pour lesquels elle avait consulté différents établissements de santé sans amélioration notable de ses symptômes. Elle souffrait de diabète depuis 5 ans et prenait de la metformine 500 mg deux fois par jour avec un contrôle glycémique médiocre. Les résultats de l’examen physique à la présentation, y compris l’examen de la gorge, étaient anodins. Le taux de sucre dans le sang au hasard était de 300 mg/dl au moment de la présentation (élevé). La laryngoscopie a révélé une tumeur irrégulière sur le tiers antérieur du cordon vocal bilatéralement, impliquant la commissure antérieure. Le résultat de la biopsie a révélé des granulés actinomycosiques avec formation d’abcès. La patiente a ensuite été traitée par pénicilline G (pendant 1 mois), avec la résolution de ses symptômes au cours du suivi, puis par amoxicilline pendant les 6 mois suivants, qui a été arrêtée lorsqu’elle a été complètement rétablie de ses symptômes et que la masse a été éliminée lors du suivi laryngoscopique.\n\nLors de l'enquête, la formule sanguine complète, le taux de sédimentation érythrocytaire, les tests de la fonction rénale et les tests de la fonction hépatique étaient tous dans les limites normales. Les tests sérologiques pour le virus de l'immunodéficience humaine (VIH), l'antigène de surface de l'hépatite B (HbsAg) et l'ARN du virus de l'hépatite C (ARN HCV) ont révélé des résultats négatifs. Son taux de sucre dans le sang au hasard était de 300 mg/dl, ce qui est élevé, et son contrôle glycémique était également médiocre sur le tableau de suivi.\n\nSon examen d'oto-rhino-laryngologie était sans particularité, mais une laryngoscopie souple a révélé une masse irrégulière dans le tiers antérieur du cordon vocal des deux côtés, avec une atteinte de la commissure antérieure.\n",
+        "gold_summary": "Il s'agissait d'une femme de 36 ans de la région d'Oromia, dans la zone d'Arsi occidentale, qui présentait une toux, une dysphonie et un ronflement depuis 6 mois, ainsi qu'une perte de poids importante mais non quantifiée, une fatigue et une fièvre modérée et intermittente, pour laquelle elle avait consulté plusieurs établissements de santé sans amélioration notable de ses symptômes. Elle souffrait de diabète depuis 5 ans et prenait de la metformine 500 mg deux fois par jour avec un contrôle glycémique médiocre. Les résultats de l'examen physique à la présentation, y compris l'examen de la gorge, étaient anodins. Le taux de sucre dans le sang au hasard était de 300 mg/dl au moment de la présentation (élevé). La laryngoscopie a révélé une tumeur irrégulière sur le tiers antérieur du cordon vocal bilatéralement, impliquant la commissure antérieure. Le résultat de la biopsie a révélé des granulés actinomycosiques avec formation d'abcès. La patiente a ensuite commencé à prendre de la pénicilline G, et ses symptômes ont disparu au cours du suivi, puis elle a pris de l'amoxicilline pendant les 6 mois suivants, qui a été arrêtée lorsqu'elle a complètement récupéré de ses symptômes et que la masse a été éliminée lors du suivi laryngoscopique.\n",
+        "synthetic_summary": {
+            "B1": "Il y avait une dame qui toussait beaucoup depuis longtemps. Elle avait aussi mal à la gorge et elle était très fatiguée.\n\nSon sucre dans le sang était trop haut. C’est pour ça qu’elle avait besoin de médicaments.\n\nLe docteur a regardé sa gorge avec une petite caméra. Il a vu une boule qui ne devait pas être là.\n\nElle a pris des médicaments très forts. Petit à petit, elle est devenue mieux. La boule est partie et elle n’a plus eu mal.",
+            "B2": "Cas d’une femme de 36 ans avec des symptômes persistants\n\nUne femme de 36 ans vivant dans la région d’Oromia avait une toux, une voix enrouée (dysphonie) et un ronflement depuis six mois. Elle avait aussi perdu beaucoup de poids sans pouvoir dire combien, se sentait très fatiguée et avait de la fièvre qui revenait par moments. Malgré plusieurs visites chez des médecins, ses symptômes ne s’amélioraient pas. Elle souffrait de diabète depuis cinq ans et prenait un médicament appelé metformine, mais son taux de sucre dans le sang restait élevé.\n\nCe qu’ils ont découvert\n\nLors de son examen médical, rien d’anormal n’a été trouvé en regardant sa gorge. Cependant, une analyse spéciale appelée laryngoscopie, qui permet de voir l’intérieur de la gorge et des cordes vocales, a montré une tumeur irrégulière sur la partie avant des deux cordes vocales. Une biopsie, c’est-à-dire un prélèvement d’un petit morceau de cette tumeur pour l’examiner au microscope, a révélé qu’il s’agissait d’une infection appelée actinomycose. Cette infection provoquait des petits amas de bactéries (granulés) et des abcès, qui sont des poches de pus.\n\nLe traitement et le suivi\n\nLa patiente a reçu un traitement avec un antibiotique appelé pénicilline G pendant un mois. Ses symptômes ont alors commencé à disparaître. Ensuite, elle a pris un autre antibiotique, l’amoxicilline, pendant six mois. Après ce traitement long, elle a complètement récupéré, et la masse dans sa gorge avait disparu lors d’un nouvel examen. Ce cas montre l’importance de bien diagnostiquer une tumeur pour éviter une mauvaise interprétation et de suivre un traitement adapté, surtout chez une personne diabétique dont le système immunitaire est plus fragile.",
+            "B3": "Résumé détaillé et structuré :\n\nContexte  \nUne femme de 36 ans, originaire de la région d’Oromia (zone d’Arsi occidentale), a consulté pour une toux persistante, une dysphonie (modification de la voix) et un ronflement évoluant depuis six mois. Ces symptômes s’accompagnaient d’une perte de poids importante mais non quantifiée, d’une fatigue généralisée et d’une fièvre modérée, intermittente. Malgré plusieurs consultations dans différents établissements de santé, aucun traitement n’avait permis d’améliorer son état. Par ailleurs, elle était diabétique depuis cinq ans, traitée par metformine 500 mg deux fois par jour, avec un contrôle glycémique insuffisant.\n\nPrincipales observations  \nÀ l’examen clinique initial, y compris l’inspection de la gorge, aucun signe particulier n’a été relevé. Cependant, le taux de glucose sanguin mesuré de manière aléatoire était élevé, à 300 mg/dl. Une laryngoscopie souple a mis en évidence une masse tumorale irrégulière située sur le tiers antérieur des cordes vocales des deux côtés, avec une atteinte de la commissure antérieure (zone de jonction entre les deux cordes vocales). La biopsie de cette lésion a révélé la présence de granulomes actinomycosiques, caractérisés par des amas bactériens formant des abcès.\n\nPar ailleurs, les analyses sanguines complémentaires, comprenant la formule sanguine complète, la vitesse de sédimentation érythrocytaire, ainsi que les tests de fonction rénale et hépatique, étaient normales. Les sérologies pour le VIH, l’hépatite B (antigène HbsAg) et l’hépatite C (ARN viral) étaient négatives.\n\nInterprétation clinique  \nLe diagnostic posé était une actinomycose laryngée, une infection bactérienne chronique rare qui peut simuler une tumeur maligne. Cette pathologie est favorisée par un terrain immunodéprimé, ici probablement lié au diabète mal contrôlé.\n\nProchaines étapes et traitement  \nLa patiente a été traitée initialement par pénicilline G pendant un mois, ce qui a permis une régression progressive des symptômes. Un traitement d’entretien par amoxicilline a ensuite été poursuivi pendant six mois. Le suivi laryngoscopique a montré la disparition complète de la masse tumorale, et la patiente a retrouvé un état clinique normal, justifiant l’arrêt du traitement antibiotique.\n\nEn résumé, ce cas illustre l’importance d’envisager une infection actinomycotique dans le diagnostic différentiel d’une masse laryngée, notamment chez un patient diabétique, et souligne l’efficacité d’un traitement antibiotique prolongé adapté."
+        }
+    },
+    {
+        "article": "Nous présentons un nouveau-né âgé de cinq jours admis à l'unité de soins intensifs néonatals avec une plainte d'absence de l'orifice anal. Le bébé n'a pas passé de méconium pendant 48 heures depuis la naissance et plus tard, les familles ont remarqué que le méconium passait par l'orifice urétral avec l'urine. Après une évaluation plus approfondie, ils ont constaté qu'il n'y avait pas de l'ouverture anale en dehors d'une légère fosse sur la zone qui était supposée être une ouverture anale. En outre, le nouveau-né avait un gonflement abdominal qui a progressivement augmenté depuis la naissance. Sinon, le nouveau-né n'avait pas de fièvre, une décoloration jaunâtre de la peau et des yeux, des vomissements et des mouvements corporels anormaux.\n\nLe bébé est né d'une mère para-quatre de 32 ans qui ne se souvient pas de sa dernière période menstruelle normale mais qui prétend être aménorrhéique depuis neuf mois. La mère a bénéficié de soins prénataux au centre de santé voisin et tout s'est bien passé. Elle a accouché au centre de santé voisin par accouchement vaginal spontané après avoir travaillé pendant 14 heures et le poids de naissance était de 3,2 kg. Le nouveau-né a pleuré immédiatement après la naissance avec des scores APGAR de 7 et 10 à la 1re et à la 10e minutes, respectivement. La mère n'a pas de maladies chroniques comme l'hypertension et le diabète sucré. Ses enfants précédents sont tous en bonne santé et vivants.\n\nL'examen physique a révélé une apparence générale alerte et des signes vitaux suivants : pouls = 152 battements par minute, respiration = 46 respirations par minute, température = 36 °C et saturation en oxygène veineux = 97 % dans l'air ambiant. L'examen de la tête a révélé une circonférence de 42 cm et une fontanelle antérieure de 2 cm. Les résultats physiques positifs pertinents ont été observés dans l'abdomen et le système génito-urinaire. L'abdomen était très distendu et il n'y avait pas d'ouverture anale autre qu'une fossette sur la région sacrococcygienne. L'examen du système génito-urinaire a révélé des organes génitaux externes féminins à l'inspection, avec des grandes lèvres bien développées et aucune fusion. Cependant, à la palpation, les petites lèvres étaient entièrement fusionnées à la base du clitoris et il n'y avait pas de vagin. Le phallus mesurait environ 0,8 cm avec une ouverture centrale par laquelle des selles liquides s'écoulait en pleurant. L'ouverture urétrale est une voie commune pour les voies urinaires, génitales et rectales. Il n'y a pas de gonades palpables dans les plis labio-scrotal et dans la région inguinale.\n\nDes tests de laboratoire et des images ont été réalisés pour explorer les résultats. Le compte total de globules blancs = 20 000, neutrophiles = 53 %, lymphocytes = 23 %, globules rouges = 5*106, hémoglobine = 15 g/dl, plaquettes = 272*103, le groupe sanguin était A+, et la glycémie aléatoire était de 120 g/dl. Une radiographie abdominale a été réalisée et elle a montré l'absence d'ombre d'air dans le gros intestin distal. L'échographie abdomino-pelvienne a été réalisée pour révéler les structures de Müller et l'état de l'intestin distal. Cependant, elle a seulement montré un rein surnuméraire unilatéral (côté gauche), un se trouvant dans la fosse rénale et l'autre se trouvant caudale sur le muscle psoas gauche, ayant tous deux des capsules distinctes et un apport sanguin avec un seul rein normal contralatéral. L'échographie n'a pas commenté les structures de Müller en raison de la vessie effondrée étant incapable de visualiser les structures.\n\nLa patiente a été admise avec un diagnostic de terme + Poids normal à la naissance + Approprié pour l'âge gestationnel + Anomalie du cloaque + Genitalia ambiguë + Rein surnuméraire + Sepsis néonatal précoce. Le nouveau-né a été géré avec des fluides de maintien calculés et des antibiotiques intraveineux, ampicillin 150 mg/kg/dose Iv deux fois par jour (BID) et gentamicine 3 mg/kg/dose iv quotidiennement. Le deuxième jour de l'admission, le bébé a été référé à l'hôpital spécialisé Black Lion pour une meilleure évaluation et gestion.\n",
+        "gold_summary": "Nous présentons un nouveau-né de cinq jours admis à l'unité de soins intensifs néonatals avec une plainte d'absence de l'orifice anal. Le bébé n'avait pas passé de méconium dans les 48 heures suivant l'accouchement, mais les familles ont ensuite réalisé que le méconium avait traversé l'orifice urétral avec l'urine. L'enfant est né d'une femme para-quatre de 32 ans qui prétend avoir été aménorrhéique au cours des neuf derniers mois, mais ne se souvenait pas de ses dernières règles régulières. À l'examen physique, l'abdomen était grossièrement distendu, et il n'y avait pas d'ouverture anale autre qu'une fossette sur la région sacrococcygienne, et les organes génitaux externes semblent féminins à l'inspection avec des grandes lèvres bien développées et aucune fusion.\n",
+        "synthetic_summary": {
+            "B1": "Il y a un bébé de cinq jours. Ce bébé n’a pas de petit trou pour faire caca. Au début, il n’a pas fait de caca. Puis, la famille a vu que le caca sortait avec la pipi. Le ventre du bébé est tout rond et un peu gros. Le bébé a des parties du corps comme une fille dehors. Mais il manque un petit trou pour faire caca. Tout cela fait que le bébé doit aller à l’hôpital pour être soigné.",
+            "B2": "Présentation du cas  \nNous parlons d’un bébé de cinq jours qui a été amené à l’unité de soins intensifs pour nouveau-nés parce qu’il n’avait pas d’ouverture anale visible. Normalement, les bébés évacuent une première selle appelée méconium dans les premières 48 heures après la naissance. Ici, le bébé n’avait pas fait cela, mais sa famille a remarqué plus tard que le méconium sortait avec l’urine, par un orifice urétral.\n\nCe qu’ils ont observé à la naissance  \nLe bébé est né d’une maman de 32 ans qui avait déjà eu quatre enfants. Elle disait ne pas avoir eu ses règles depuis environ neuf mois, mais ne se souvenait pas précisément de la date de ses dernières règles normales. Le bébé est né par voie naturelle, pesant 3,2 kg, et a bien réagi à la naissance.\n\nCe qu’ils ont trouvé à l’examen  \nÀ l’examen, le ventre du bébé était très gonflé. Il n’y avait pas de vrai trou anal, seulement une petite fossette à l’endroit où devrait se trouver l’anus. Les organes génitaux externes semblaient féminins : on voyait bien les grandes lèvres, sans fusion. Cependant, en touchant, les petites lèvres étaient soudées à la base du clitoris, et il n’y avait pas de vagin visible. Le phallus (petit organe) mesurait environ 0,8 cm et avait une ouverture par laquelle des selles liquides sortaient quand le bébé pleurait. L’urètre, qui sert normalement à faire sortir l’urine, était une voie commune pour l’urine, les selles et les sécrétions génitales.  \n\nConclusion  \nCe bébé présente une malformation appelée anomalie du cloaque, où les voies urinaires, génitales et digestives ne sont pas séparées normalement. Cette situation nécessite une prise en charge médicale spécialisée pour éviter des complications graves.",
+            "B3": "Résumé détaillé et structuré pour un public adulte non spécialiste\n\nContexte  \nNous rapportons le cas d’un nouveau-né âgé de cinq jours, admis en unité de soins intensifs néonatals en raison de l’absence apparente de l’orifice anal. Depuis la naissance, le bébé n’avait pas éliminé le méconium (les premières selles du nouveau-né) pendant 48 heures, ce qui a alerté la famille. Par la suite, ils ont observé que le méconium passait anormalement par l’orifice urétral, mélangé à l’urine.\n\nPrincipales observations cliniques  \nLe bébé est issu d’une mère de 32 ans, ayant déjà eu quatre enfants en bonne santé, et qui rapporte une absence de règles (aménorrhée) depuis environ neuf mois, sans pouvoir préciser la date de ses dernières règles normales. La grossesse a été suivie sans complication apparente, et l’accouchement s’est déroulé par voie basse après un travail de 14 heures. Le nouveau-né pesait 3,2 kg à la naissance et avait des scores APGAR (évaluation rapide de l’état du nouveau-né) de 7 à la première minute et 10 à la dixième minute, indiquant une bonne adaptation initiale.\n\nÀ l’examen physique, l’enfant était alerte, avec des signes vitaux normaux pour son âge (pouls rapide à 152 battements par minute, respiration à 46 par minute, température normale à 36 °C, et bonne saturation en oxygène). L’abdomen était très distendu, témoignant d’une accumulation anormale de gaz ou de liquide. L’anus était absent, remplacé par une simple fossette dans la région sacrococcygienne (au bas du dos). Les organes génitaux externes présentaient une apparence féminine : de grandes lèvres bien formées sans fusion apparente. Toutefois, à la palpation, les petites lèvres étaient fusionnées à la base du clitoris, et il n’y avait pas de vagin visible. Le phallus mesurait environ 0,8 cm et comportait une ouverture centrale par laquelle s’écoulaient des selles liquides lors des pleurs. L’orifice urétral était unique et commun aux voies urinaires, génitales et digestives. Aucune gonade (ovaire ou testicule) n’était palpable dans les plis labio-scrotaux ni dans la région inguinale.\n\nExamens complémentaires  \nLes analyses sanguines ont montré une augmentation des globules blancs (20 000/mm³), suggérant une infection, avec une formule leucocytaire normale. Le groupe sanguin était A+, et la glycémie était normale. La radiographie abdominale a révélé l’absence d’air dans la partie terminale du gros intestin, ce qui est compatible avec une obstruction ou une anomalie anatomique. L’échographie abdomino-pelvienne a mis en évidence un rein surnuméraire (un rein supplémentaire) du côté gauche, avec deux reins distincts et vascularisés, mais n’a pas permis de visualiser clairement les structures génitales internes en raison de la vessie effondrée.\n\nInterprétation clinique  \nLe diagnostic principal retenu est celui d’une anomalie cloacale, une malformation congénitale rare où les voies urinaires, génitales et digestives se rejoignent en un seul orifice. Cette anomalie s’accompagne d’une ambiguïté génitale, rendant difficile la détermination du sexe biologique, et d’une malformation rénale associée (rein surnuméraire). Le nouveau-né présente également un sepsis néonatal précoce, une infection grave du nouveau-né nécessitant une prise en charge urgente.\n\nPrise en charge et prochaines étapes  \nLe bébé a été traité initialement par des perfusions pour maintenir son hydratation et par une antibiothérapie intraveineuse combinant l’ampicilline et la gentamicine pour lutter contre l’infection. En raison de la complexité de son état, il a été transféré au deuxième jour d’hospitalisation dans un centre spécialisé (hôpital Black Lion) pour une évaluation plus approfondie et une prise en charge multidisciplinaire adaptée, incluant probablement une intervention chirurgicale et un suivi endocrinologique et urologique.\n\nCe cas illustre l’importance d’une reconnaissance précoce des malformations congénitales complexes et la nécessité d’une prise en charge spécialisée pour optimiser le pronostic du nouveau-né."
+        }
+    },
+    {
+        "article": "Ce patient était un homme blanc de 73 ans, hypertendu, qui a été admis en unité de soins intensifs avec une insuffisance respiratoire aiguë due à la COVID-19. Peu après son admission, il a été intubé orotrachéalement et placé en position couchée sur le dos pour améliorer l'hypoxie due au syndrome respiratoire aigu sévère (SRAS). Au troisième jour de son admission, il a développé une oligurie, une azotémie et une surcharge de volume. Le service de néphrologie a été activé pour effectuer un accès veineux profond pour la TSR. Le patient ne pouvait pas être placé en position couchée sur le dos en raison d'une hypoxémie importante. Un cathéter de dialyse de longue durée a été inséré dans la veine poplitée gauche. Il a été soumis à une hémodialyse intermittente conventionnelle quotidienne pendant 8 jours. Le flux sanguin pendant les séances est resté entre 300 et 400 ml/min. En raison de la gravité du tableau clinique, le patient a fini par décéder des suites d'une insuffisance respiratoire au 11e jour. Ce rapport de cas décrit une situation difficile pour obtenir un accès vasculaire en traitant des patients atteints de COVID-19 en position couchée sur le dos. Aspects techniques La veine poplitée gauche a été évaluée par ultrasons. Nous avons utilisé des coupes transversales et longitudinales pour éviter toute valve, en faisant attention à ne pas blesser le nerf tibial superficiel ou l'artère poplitée, la structure la plus profonde de la fosse poplitée. La veine poplitée a été perforée avec une aiguille 18GA x 7 cm, et un guide-fil de 0,035 pouces a été inséré sans aucune résistance. Une incision a été faite dans la peau au-dessus du fil, la veine a été dilatée et le permcath de 50 cm a été inséré par le néphrologue interventionnel, à l'aide d'un introducteur divisible 16F. Le brassard a été suturé sur le tissu sous-cutané. Les voies artérielle et veineuse ont été testées et salinisées avec succès. Une hémodialyse intermittente conventionnelle a été initiée sans difficulté.\n",
+        "gold_summary": "Le patient était un homme de 73 ans qui était venu initialement dans notre service avec une insuffisance respiratoire aiguë secondaire à la COVID-19. Peu après son admission, il a été intubé orotrachéalement et mis en position couchée pour améliorer l'hypoxie due au syndrome respiratoire aigu sévère (SARS). Au troisième jour de son admission, il a développé une lésion rénale aiguë oligurique et une surcharge de volume. Le service de néphrologie a été sollicité pour effectuer un accès veineux profond pour une thérapie de remplacement rénal (TRS). Le patient ne pouvait pas être mis en position couchée en raison d'une hypoxémie importante. Un Permcath de 50 cm (MAHURKARTM, Covidien, Massachusetts, États-Unis) a été inséré dans la veine poplitée gauche.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 73 ans était très malade à cause d’un virus. Il avait du mal à bien respirer. Les médecins l’ont aidé avec un tuyau pour qu’il puisse mieux respirer.\n\nAprès quelques jours, ses reins ne fonctionnaient plus bien. Il fallait l’aider à nettoyer son sang. Mais il ne pouvait pas rester allongé sur le dos.\n\nAlors, les médecins ont mis un petit tuyau spécial dans une veine derrière son genou. Ce tuyau a aidé à nettoyer son sang.",
+            "B2": "Ce qu'ils ont observé  \nUn homme de 73 ans est arrivé à l'hôpital avec des difficultés graves pour respirer à cause de la COVID-19. Très vite, il a dû être intubé, c’est-à-dire qu’un tube a été placé dans sa gorge pour l’aider à respirer. Il était couché sur le dos pour améliorer l’oxygène dans son sang.\n\nCe qui s'est passé ensuite  \nAu troisième jour, ses reins ont commencé à mal fonctionner. Il produisait très peu d’urine (on appelle cela une oligurie) et avait trop de liquide dans le corps. Les médecins spécialistes des reins, appelés néphrologues, ont été appelés pour l’aider. Ils devaient mettre en place un accès veineux profond, c’est-à-dire un tube spécial dans une grosse veine, pour faire une thérapie de remplacement rénal. Cette thérapie sert à filtrer le sang quand les reins ne fonctionnent plus bien.\n\nLe défi technique  \nLe problème était que le patient ne pouvait pas être couché sur le dos à cause de son manque d’oxygène. Alors, les médecins ont choisi une veine située derrière le genou, appelée veine poplitée, pour insérer le cathéter (le tube). Ils ont utilisé une échographie, une technique avec des ultrasons, pour bien voir la veine et éviter d’abîmer les nerfs ou les artères proches. Le cathéter de 50 cm a été placé avec soin par un spécialiste.\n\nCe que cela signifie  \nCette situation montre qu’il est possible de mettre un accès veineux profond dans la veine poplitée quand les patients atteints de COVID-19 ne peuvent pas être couchés sur le dos. Cela aide à faire la dialyse, un traitement qui remplace la fonction des reins, même dans des cas très compliqués. Malheureusement, malgré ces soins, le patient est décédé à cause de la gravité de sa maladie respiratoire.",
+            "B3": "Résumé détaillé et structuré\n\nContexte  \nUn homme blanc de 73 ans, souffrant d’hypertension artérielle, a été admis en unité de soins intensifs pour une insuffisance respiratoire aiguë liée à une infection par le virus SARS-CoV-2 (COVID-19). Rapidement après son admission, il a été intubé orotrachéalement et placé en décubitus dorsal (couché sur le dos) afin d’améliorer son hypoxie (manque d’oxygène dans le sang) due au syndrome respiratoire aigu sévère (SRAS).\n\nPrincipales observations  \nAu troisième jour d’hospitalisation, le patient a présenté une insuffisance rénale aiguë caractérisée par une oligurie (diminution de la production d’urine), une azotémie (accumulation de déchets azotés dans le sang) et une surcharge volémique (excès de liquide dans l’organisme). Ces complications ont conduit à la nécessité d’une thérapie de remplacement rénal (TRR), une forme de dialyse destinée à remplacer temporairement la fonction rénale défaillante. Cependant, en raison de son hypoxémie sévère, il était impossible de le repositionner en décubitus dorsal, ce qui compliquait l’accès vasculaire habituel pour la dialyse.\n\nIntervention technique  \nPour contourner cette difficulté, l’équipe de néphrologie a réalisé un accès veineux profond en insérant un cathéter de dialyse de longue durée (Permcath de 50 cm) dans la veine poplitée gauche, située derrière le genou. Cette procédure a été guidée par échographie afin d’éviter les structures anatomiques sensibles telles que le nerf tibial superficiel et l’artère poplitée. L’aiguille utilisée (18 gauge, 7 cm) a permis une ponction précise, suivie de l’introduction d’un guide-fil sans résistance. Après une incision cutanée, la veine a été dilatée et le cathéter inséré à l’aide d’un introducteur divisible de calibre 16 French. Le cathéter a été fixé solidement au tissu sous-cutané par suture. Les voies artérielle et veineuse du cathéter ont été testées et rincées avec succès, permettant le démarrage sans complication d’une hémodialyse intermittente conventionnelle quotidienne, avec un débit sanguin maintenu entre 300 et 400 ml/min.\n\nÉvolution clinique et conclusion  \nMalgré ces mesures, la gravité de l’atteinte respiratoire a conduit au décès du patient au onzième jour d’hospitalisation. Ce cas illustre la complexité et les défis techniques rencontrés pour établir un accès vasculaire chez des patients atteints de COVID-19 en hypoxémie sévère, notamment lorsque la position couchée sur le dos n’est pas possible. L’utilisation de la veine poplitée comme site alternatif d’accès pour la dialyse peut constituer une solution viable dans ce contexte clinique difficile."
+        }
+    },
+    {
+        "article": "Homme, fils d'une mère de 28 ans au moment de la naissance et d'un père de 34 ans. Pas de consanguinité, pas d'antécédents familiaux, né de deuxième grossesse, contrôlée, de cours normal. Sérologies : toxoplasme, virus de l'immunodéficience humaine et HBsAg négatifs, et rubéole immunitaire. Dépistage combiné du premier trimestre à risque faible. Échographies prénatales normales. Pas de contact ou d'ingestion connue de toxiques et/ou de tératogènes. Accouchement eutopique à 40 semaines. Apgar : 9/10. Poids à la naissance : 3 780 g (p50-90, graphiques Fenton). Longueur : 52 cm (p50-90). Périmètre crânien : 37 cm (p90). Examen néonatal décrit comme normal. Dépistages néonataux métabolique et auditif sans altérations.\n\nIl était suivi par une neuropédiatre pour retard psychomoteur dans son évolution : marche autonome à 18 mois et retard de langage. Il a suivi un programme de prise en charge précoce à partir de la deuxième année de vie, avec des soutiens scolaires (audition et langage + pédagogie thérapeutique) dès le début de l'école maternelle et une adaptation du programme scolaire dès l'école primaire. Quotient intellectuel à 6 ans : 68. Il suit actuellement une formation fonctionnelle. Autres problèmes de santé : exotropie alternante décompensée en attente de chirurgie, obésité suivie par une endocrinologie infantile et diagnostic de bêtalasémie mineure.\n\nÉvalué lors d'une consultation en génétique clinique à l'âge de 8,5 ans : poids, 45 kg (p95 ; écart-type, DS) = 1,75 ; taille, 138 cm (p77 ; DS) = 0,77 ; indice de masse corporelle, 23,63 (p96 ; DS) = 1,85 ; et périmètre crânien, 57 cm (p99 ; DS) = 3,05). Phénotype avec macro-céphalie, obésité troncale avec adipomastie, front large et large, yeux enfoncés, nez bulbeux, pavillons auriculaires décollés légèrement non dysplasiques, menton effilé, uvula courte et large, voix nasale, phalanges distales des mains effilées, pieds plats laxés et pénis enfoui dans la graisse pré-pubienne.\n\nÉtude génétique. Array SNP/CNV 750K (plateforme GeneChipÒ System 3000, AffymetrixÒ, Cyto-Scan Assay P/N 703038 Rev.5. Analyse avec le programme Chromosome Analysis Suite, AffymetrixÒ v.3.3): une délétion de 586 kb est détectée dans la bande cytologique Xq21.1 arr[GRCh37]Xq21.1(79564583_80150138)x0. La délétion inclut un seul gène avec pathologie connue associée, BRWD3. Un array est ensuite réalisé sur la mère et la sœur, asymptomatiques, toutes deux porteuses de la délétion identifiée chez le patient, non présente chez la grand-mère maternelle.\n",
+        "gold_summary": "Homme sans antécédents familiaux ou périnataux d'intérêt avec un trouble du développement neurologique : retard psychomoteur, retard de langage et déficience cognitive, macro-céphalie (p > 99) et obésité. Phénotype avec dysmorphie faciale : front large, yeux enfoncés, nez bulbeux, oreilles décollées et menton pointu. Array d'hybridation génomique comparée avec délétion de 586 ko dans Xq21.1, qui inclut un seul gène associé à la pathologie, BRWD3. Une étude a ensuite été réalisée sur la mère et la sœur, asymptomatiques, et toutes deux porteuses de la délétion.\n",
+        "synthetic_summary": {
+            "B1": "Il y a un garçon qui a du mal à marcher et à parler. Sa tête est un peu plus grande que celle des autres enfants. Il est aussi un peu gros.\n\nSon visage est un peu différent : son front est large, ses yeux sont un peu enfoncés, son nez est un peu rond, ses oreilles sont un peu décollées et son menton est pointu.\n\nLes docteurs ont regardé ses gènes. Ils ont trouvé un petit morceau qui manque dans un gène important. Sa maman et sa sœur ont aussi ce petit morceau qui manque, mais elles vont bien.",
+            "B2": "### Ce qu'ils ont trouvé chez ce garçon\n\nCe garçon n’a pas d’antécédents familiaux ou problèmes à la naissance. Cependant, il a eu des difficultés à grandir normalement : il a marché tard (à 18 mois), a eu un retard pour parler, et a une intelligence un peu plus faible que la moyenne. Il est aussi obèse et a une tête plus grande que la normale (ce qu’on appelle une macro-céphalie). Son visage présente des traits particuliers : un front large, des yeux un peu enfoncés, un nez rond et gros, des oreilles décollées, et un menton pointu.\n\n### Ce que cela signifie\n\nLes médecins ont fait un test spécial pour chercher des changements dans ses gènes. Ils ont découvert qu’il manque une petite partie d’un chromosome X, précisément une région appelée Xq21.1. Cette partie contient un seul gène important nommé BRWD3, qui est lié à des troubles du développement. Ce gène manquant peut expliquer ses difficultés.\n\n### Ce qu’ils ont vérifié ensuite\n\nPour mieux comprendre, ils ont aussi testé sa mère et sa sœur. Ces deux femmes ont la même absence de cette partie du chromosome, mais elles ne montrent pas de symptômes. Cela peut arriver car les filles ont deux chromosomes X, donc l’autre peut compenser. Cette découverte aide à comprendre la cause de ses problèmes et à mieux suivre sa santé.",
+            "B3": "Résumé destiné à un public adulte non spécialiste\n\nContexte  \nIl s’agit d’un garçon sans antécédents familiaux ou complications à la naissance, suivi depuis l’enfance pour des troubles du développement neurologique. Son évolution a été marquée par un retard psychomoteur (marche autonome à 18 mois), un retard du langage et une déficience intellectuelle modérée (quotient intellectuel de 68 à 6 ans). Il présente également une macro-céphalie (périmètre crânien supérieur au 99e percentile) et une obésité importante, avec un excès de graisse au niveau du tronc. Sur le plan clinique, son visage montre plusieurs caractéristiques particulières : un front large, des yeux enfoncés, un nez arrondi (bulbeux), des oreilles légèrement décollées et un menton pointu.\n\nPrincipales observations génétiques  \nUne analyse génétique approfondie a révélé une délétion (perte) d’une petite région d’ADN de 586 kilobases sur le chromosome X, précisément dans la région Xq21.1. Cette délétion affecte un seul gène connu pour être impliqué dans des troubles similaires, appelé BRWD3. Afin de mieux comprendre l’origine de cette anomalie, des tests ont été réalisés chez la mère et la sœur du patient, qui ne présentent aucun symptôme, mais qui sont toutes deux porteuses de la même délétion. Cette observation suggère une transmission familiale avec une expression variable des symptômes.\n\nInterprétation clinique  \nLe tableau clinique du patient, associant retard du développement, déficience intellectuelle, macro-céphalie et obésité, ainsi que les caractéristiques faciales particulières, est cohérent avec l’impact de la délétion du gène BRWD3. Ce gène joue un rôle important dans le développement neurologique. La présence de la délétion chez des membres asymptomatiques de la famille souligne la complexité de l’expression clinique, qui peut varier d’un individu à l’autre.\n\nProchaines étapes  \nUn suivi multidisciplinaire est recommandé pour accompagner le développement cognitif, moteur et social du patient, ainsi que pour gérer les autres problèmes de santé associés, comme l’obésité et les troubles oculaires. La prise en charge génétique familiale permet d’informer sur les risques de transmission et d’adapter le conseil génétique. Des investigations complémentaires pourraient être envisagées pour mieux comprendre les mécanismes impliqués et optimiser le suivi médical."
+        }
+    },
+    {
+        "article": "Un patient de 86 ans s'est présenté aux urgences pour un priapisme non douloureux de 3 semaines. Notre patient, un ancien agent de nettoyage, n'a connu qu'un accident ischémique transitoire. Il n'a pas d'antécédents chirurgicaux. L'examen physique a révélé un pénis semi-erect non douloureux avec une légère déviation latérale et un gland lisse. Aucune lésion pénienne superficielle n'a été observée. Le patient a déclaré avoir perdu des érections normales il y a près de 20 ans. Tous les signes cliniques étaient en faveur d'un priapisme non ischémique. Le patient était un ancien fumeur et a également déclaré avoir des symptômes respiratoires supérieurs modérés. Les résultats des analyses de laboratoire et des analyses d'urine étaient remarquables ; par conséquent, la décision a été de poursuivre les investigations en ambulatoire en utilisant une échographie pénienne et une tomodensitométrie thoracoabdominale (CT) à la recherche d'une tumeur maligne.\n\nUne échographie Doppler du pénis a été réalisée, révélant des nodules hypoéchogènes circonscrits infiltrant l'albugée du corps caverneux, avec une prédominance à la base et du côté droit. Aucune anomalie n'a été détectée dans le corps spongieux. Un indice résistif normal avec une vitesse artérielle pénienne normale a été mesuré, en faveur d'une situation non ischémique.\n\nLa TDM thoraco-abdominale a révélé une masse au niveau du hilum gauche du poumon entourant les structures broncho-vasculaires. Plusieurs nodules bilatéraux et micronodules ont été observés. Les plus grands étaient situés à l'apex droit et à la base droite du poumon. Des ganglions lymphatiques médiastinaux élargis ont également été observés à la station paratrachéale inférieure. Le foie a également été affecté par plusieurs lésions ; la plus grande était située au segment 7, qui mesurait 96 mm. Des lésions de la glande surrénale gauche et du pancréas ont été notées. Enfin, deux lésions ostéolytiques ont été observées sur la première côte gauche et sur le processus transverse de la cinquième vertèbre lombaire (L5). Le patient a été référé au spécialiste du cancer du poumon pour de nouvelles investigations. Une biopsie pulmonaire a été réalisée, confirmant un adénocarcinome du poumon. L'analyse moléculaire des cellules a montré une variante pGly12Cys (G12C) du gène KRAS. PDL-1 a également été noté comme positif.\n\nAprès une discussion multidisciplinaire, la décision a été prise pour la patiente de poursuivre une chimiothérapie à quatre cycles et une immunothérapie par le cisplatine, le pemetrexed et le pembrolizumab. La patiente a mal toléré le premier cycle de chimiothérapie et a développé une pancytopénie fébrile. La décision a été prise d'arrêter la chimiothérapie et de poursuivre l'immunothérapie par le pembrolizumab.\n\nEn ce qui concerne les lésions du pénis, le patient ne ressentant aucune douleur, une surveillance a été adoptée.\n",
+        "gold_summary": "Nous rapportons le cas d'un patient de 86 ans qui a présenté un priapisme non douloureux de 3 semaines. Une échographie Doppler du pénis et une tomodensitométrie thoracique et abdominale ont été effectuées, révélant une masse pulmonaire hilaire gauche ainsi que des lésions dans le foie, les glandes surrénales, le pancréas, les structures osseuses et le pénis. Les métastases péniennes sont associées à un mauvais pronostic en raison des fréquentes lésions malignes disséminées dans d'autres sites.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 86 ans avait un problème avec son corps qui restait un peu dur sans faire mal. Les docteurs ont regardé avec des machines spéciales. Ils ont trouvé un gros mal dans ses poumons et aussi dans d’autres parties de son corps comme le foie et les os. Ce mal peut être très sérieux car il est dans plusieurs endroits. Les docteurs vont l’aider avec des médicaments pour essayer de le soigner.",
+            "B2": "Cas d’un homme de 86 ans avec un priapisme non douloureux\n\nUn homme de 86 ans est venu aux urgences parce que son pénis restait partiellement en érection depuis trois semaines, sans douleur. Ce phénomène s’appelle un priapisme. Il avait perdu ses érections normales depuis environ 20 ans. L’examen a montré que son pénis était semi-erect avec une légère courbure, mais sans blessure visible.\n\nCe qu’ils ont découvert grâce aux examens\n\nUne échographie spéciale (Doppler) du pénis a montré des petites masses dans une partie du pénis appelée le corps caverneux. Une autre analyse par scanner (tomodensitométrie) a révélé une grosse tumeur dans le poumon gauche, ainsi que plusieurs petites tumeurs dans le foie, les glandes surrénales, le pancréas, et des os. Ces tumeurs sont des métastases, c’est-à-dire que le cancer s’est propagé à plusieurs endroits du corps. Une biopsie du poumon a confirmé qu’il s’agissait d’un adénocarcinome, un type de cancer du poumon.\n\nCe que cela signifie pour le patient\n\nLa présence de métastases dans le pénis et d’autres organes montre que le cancer est avancé. Cela rend le pronostic plus sérieux. Le patient a commencé un traitement combinant chimiothérapie et immunothérapie, mais il a eu des effets secondaires importants. La chimiothérapie a été arrêtée, et seul le traitement par immunothérapie a continué. Comme le priapisme ne lui causait pas de douleur, les médecins ont choisi de simplement surveiller cette situation.\n\nEn résumé, ce cas montre comment un cancer du poumon peut se propager à des endroits rares comme le pénis, ce qui complique le traitement et le pronostic.",
+            "B3": "Résumé détaillé et structuré :\n\nContexte  \nUn homme de 86 ans s’est présenté aux urgences avec un priapisme (érection prolongée) non douloureux, persistant depuis trois semaines. Ce patient, ancien agent de nettoyage, avait des antécédents limités à un accident ischémique transitoire et ne rapportait aucune chirurgie antérieure. Il avait perdu ses érections normales depuis environ vingt ans. L’examen clinique a montré un pénis semi-érect, non douloureux, avec une légère déviation latérale et un gland lisse, sans lésion cutanée visible. Les signes cliniques suggéraient un priapisme non ischémique. Le patient était un ancien fumeur et présentait des symptômes respiratoires modérés.\n\nPrincipales observations  \nDes examens complémentaires ont été réalisés en ambulatoire. L’échographie Doppler pénienne a montré des nodules hypoéchogènes (zones plus sombres à l’échographie) infiltrant l’albuginée (membrane entourant les corps caverneux du pénis), surtout à la base et à droite, sans anomalie du corps spongieux. Les flux sanguins pénien étaient normaux, confirmant l’absence d’ischémie.  \nLa tomodensitométrie (TDM) thoraco-abdominale a révélé une masse au niveau du hile pulmonaire gauche, entourant les structures broncho-vasculaires, ainsi que plusieurs nodules pulmonaires bilatéraux. Des ganglions lymphatiques médiastinaux élargis ont été observés. Par ailleurs, plusieurs lésions hépatiques, une atteinte de la glande surrénale gauche, du pancréas et des lésions osseuses (sur la première côte gauche et la cinquième vertèbre lombaire) ont été identifiées. Ces images étaient compatibles avec des métastases multiples.  \nUne biopsie pulmonaire a confirmé un adénocarcinome pulmonaire, avec une mutation spécifique du gène KRAS (pGly12Cys) et une expression positive de PDL-1, ce qui oriente vers des options thérapeutiques ciblées.\n\nInterprétation clinique  \nLe priapisme non douloureux chez ce patient s’explique par une infiltration métastatique du pénis, une localisation rare mais grave de la dissémination tumorale. La présence simultanée de multiples métastases viscérales et osseuses témoigne d’un cancer pulmonaire avancé avec un pronostic défavorable. La mutation KRAS et la positivité de PDL-1 permettent d’envisager une immunothérapie.  \n\nProchaines étapes  \nAprès discussion multidisciplinaire, une chimiothérapie combinée à une immunothérapie (cisplatine, pemetrexed et pembrolizumab) a été initiée. Cependant, le patient a mal toléré la chimiothérapie, développant une pancytopénie fébrile (baisse sévère des cellules sanguines avec fièvre), conduisant à l’arrêt de la chimiothérapie et la poursuite exclusive de l’immunothérapie. Concernant les lésions péniennes, en l’absence de douleur, une surveillance a été privilégiée sans intervention immédiate.  \n\nEn résumé, ce cas illustre une présentation rare de métastases péniennes révélant un cancer pulmonaire avancé, soulignant l’importance d’une évaluation complète devant un priapisme non ischémique chez un patient âgé."
+        }
+    },
+    {
+        "article": "Une femme enceinte de 22 ans, gravida 5, para 1, ayant fait trois fausses couches à la 5e semaine de grossesse, a été admise au service d'endocrinologie pour évaluation d'une hypokaliémie sévère détectée lors d'un test de grossesse au service de gynécologie. 16 ans auparavant, à l'âge de 6 ans, elle avait commencé à avoir des crampes après avoir pleuré ou avoir perdu son sang-froid, sans étourdissements, convulsions ou autres symptômes. Les tests de laboratoire ont révélé une hypokaliémie (données manquantes), et les symptômes ont été soulagés après supplémentation en potassium. Par la suite, elle a connu des crampes récurrentes après avoir pleuré, avoir perdu son sang-froid ou être fatiguée. Les symptômes ont été soulagés sans aucun traitement et n'ont eu aucun effet sur sa vie quotidienne ; par conséquent, elle n'a pas porté attention à ces symptômes. Deux jours avant son admission, elle a subi un test de laboratoire pour la grossesse. Son résultat de test sanguin a révélé des troubles électrolytiques sévères : son taux de potassium sérique était de 2,42 mmol/L et son taux de magnésium était de 0,65 mmol/L, mais elle n'avait aucun symptôme. Après supplémentation en chlorure de potassium par voie intraveineuse et orale au service des urgences, la patiente a été admise au service d'endocrinologie pour enquête sur l'hypokaliémie.\n\nAu moment de la présentation, la patiente ne transpirait pas, ne vomissait pas, n'avait pas de diarrhée, ni d'anorexie. Elle a nié avoir abusé de laxatifs ou de diurétiques, avoir une hypokaliémie ou des crampes chez d'autres membres de la famille. L'examen physique a révélé une taille de 149 cm, un poids de 46,3 kg et une tension artérielle de 97/71 mmHg. Il n'y avait aucun signe positif à l'examen physique, à l'exception du signe de Trousseau. Des examens de laboratoire détaillés ont été effectués pour un diagnostic et un traitement ultérieurs. L'analyse de laboratoire a révélé une hypokaliémie, une alcalose métabolique, une perte de potassium rénale, une hypomagnésémie, une hypocalciurie, une hyperréninémie et un hyperaldostéronisme avec une tension artérielle normale, ce qui a indiqué un diagnostic clinique de GS. Le diagnostic a été confirmé lorsqu'une mutation hétérozygote c.1077C>G (p.Asn359Lys) et c.965-1_976delGCGGACATTTTTGinsACCGAAAATTTT dans SLC12A3 a été identifiée par séquençage de l'exome entier. Après que les niveaux d'électrolytes ont été maintenus dans une plage relativement optimale, le traitement intraveineux a été changé en supplémentation orale.\n",
+        "gold_summary": "La patiente ne présentait aucun symptôme spécifique, mais souffrait d'hypokaliémie, d'alcalose métabolique, d'hypomagnésémie, d'hypocalciurie, d'hyperréninémie, d'hyperaldostéronisme et avait une tension artérielle normale. L'ensemble de ces symptômes indiquait le diagnostic clinique du syndrome de Gitelman, qui a été confirmé par une analyse génétique. De nombreux médicaments ont des données de sécurité limitées en début de grossesse, et des taux optimaux de potassium et de magnésium sont nécessaires pour une grossesse réussie.\n",
+        "synthetic_summary": {
+            "B1": "La dame avait un problème avec ses petits sels dans le corps. Ces petits sels sont très importants pour que le corps marche bien. \n\nElle n’avait pas mal, mais son corps avait besoin d’aide pour avoir assez de ces petits sels. Les docteurs ont trouvé que c’était un problème spécial appelé syndrome de Gitelman. \n\nPour que le bébé grandisse bien, il faut que la maman ait assez de ces petits sels. Les docteurs vont l’aider à rester en bonne santé pendant la grossesse.",
+            "B2": "Ce qu’ils ont trouvé  \nLa patiente ne montrait pas de symptômes évidents, mais ses analyses sanguines ont révélé plusieurs problèmes : un faible taux de potassium (hypokaliémie), un déséquilibre dans l’acidité du sang (alcalose métabolique), un faible taux de magnésium (hypomagnésémie), moins de calcium dans les urines (hypocalciurie), ainsi qu’une augmentation de certaines hormones rénales (hyperréninémie et hyperaldostéronisme). Sa tension artérielle était normale malgré ces anomalies.\n\nCe que cela signifie  \nCes résultats ont conduit les médecins à diagnostiquer un syndrome de Gitelman. Ce syndrome est une maladie génétique qui affecte les reins et cause ces déséquilibres d’électrolytes. Le diagnostic a été confirmé grâce à un test génétique qui a trouvé des mutations dans un gène appelé SLC12A3.\n\nPourquoi c’est important pendant la grossesse  \nPendant la grossesse, il est très important d’avoir des niveaux corrects de potassium et de magnésium pour la santé de la mère et du bébé. De plus, beaucoup de médicaments ne sont pas toujours sûrs au début de la grossesse. C’est pourquoi les médecins ont ajusté le traitement pour maintenir ces niveaux d’électrolytes dans une bonne plage, en utilisant des suppléments adaptés.",
+            "B3": "Résumé détaillé et structuré pour un public adulte non spécialiste\n\n**Contexte**  \nUne femme enceinte de 22 ans, avec un historique de plusieurs grossesses (gravida 5, para 1) et trois fausses couches précoces, a été hospitalisée en endocrinologie après la découverte d’un faible taux de potassium dans le sang (hypokaliémie) lors d’un test de grossesse. Depuis l’enfance, elle souffrait de crampes musculaires récurrentes, souvent déclenchées par des émotions fortes ou la fatigue, mais ces symptômes n’avaient jamais été investigués ni traités sérieusement.\n\n**Principales observations**  \nÀ son admission, la patiente ne présentait pas de symptômes aigus tels que sueurs, vomissements ou diarrhée, et elle n’avait pas d’antécédents familiaux similaires. Son examen physique était globalement normal, à l’exception d’un signe de Trousseau positif (un signe clinique indiquant une hypocalcémie ou un déséquilibre électrolytique). Les analyses sanguines ont montré plusieurs anomalies : un taux très bas de potassium (hypokaliémie), un déséquilibre du pH sanguin avec une alcalose métabolique (augmentation du pH), un faible taux de magnésium (hypomagnésémie), une faible excrétion urinaire de calcium (hypocalciurie), ainsi qu’une augmentation des hormones rénales rénine et aldostérone (hyperréninémie et hyperaldostéronisme). Malgré ces anomalies, sa tension artérielle restait normale.\n\n**Interprétation clinique**  \nL’ensemble de ces résultats orientait vers un diagnostic clinique de syndrome de Gitelman, une maladie génétique rare qui affecte les reins et perturbe l’équilibre des électrolytes. Ce diagnostic a été confirmé par une analyse génétique qui a identifié des mutations spécifiques dans le gène SLC12A3, responsable de cette pathologie. Le syndrome de Gitelman entraîne une perte excessive de potassium et de magnésium par les reins, ce qui peut provoquer des crampes musculaires et d’autres complications, notamment pendant la grossesse.\n\n**Prochaines étapes**  \nLe traitement a consisté à corriger les déséquilibres électrolytiques par une supplémentation en potassium et magnésium, d’abord par voie intraveineuse puis par voie orale une fois les taux stabilisés. Il est important de maintenir des niveaux optimaux de ces minéraux pour assurer une grossesse saine, car de nombreux médicaments ne sont pas sûrs en début de grossesse et les déséquilibres électrolytiques peuvent compromettre le développement fœtal. Un suivi médical régulier est donc essentiel pour adapter le traitement et prévenir les complications.\n\n---\n\nCe résumé met en lumière l’importance d’une évaluation approfondie des symptômes apparemment bénins, surtout chez une femme enceinte, afin d’identifier des troubles rares mais potentiellement graves comme le syndrome de Gitelman."
+        }
+    },
+    {
+        "article": "Présentation et traitement initial\n\nUne femme de 67 ans s'est présentée à l'Institut de cardiologie de Varsovie, en Pologne, en juin 2016, avec un antécédent de trois semaines d'insuffisance cardiaque croissante. La patiente présentait des symptômes de la classe fonctionnelle IV de la New York Heart Association (NYHA) qui comprenaient une dyspnée, une faiblesse et une prise de poids. La patiente avait des antécédents d'insuffisance cardiaque chronique due à une cardiomyopathie dilatée. Elle avait une fraction d'éjection ventriculaire gauche (FEVG) de 25 % et une régurgitation mitrale sévère. En 2015, elle a été diagnostiquée avec une fibrillation auriculaire paroxystique et une hypothyroïdie. Elle avait été précédemment traitée avec le système d'annuloplastie percutanée Mitralign (Mitralign Inc., Tewksbury MA, USA) pour la régurgitation mitrale. Elle avait également été précédemment traitée avec un dispositif de thérapie de resynchronisation cardiaque (CRT-D). Cependant, elle a souffert d'un œdème pulmonaire récurrent avec des épisodes d'hypertension pulmonaire et a nécessité une intubation et une ventilation. La patiente a été admise à la clinique de thérapie cardiaque intensive pour un traitement médical immédiat. Un IABP avec accès par cathéter par artère fémorale a été utilisé initialement. À ce stade, parce qu'elle souffrait d'hypertension pulmonaire sévère, cela a été considéré comme une contre-indication pour une transplantation cardiaque. Au cours des 115 jours de séjour à l'hôpital, la patiente a souffert d'immobilité associée à la mise en place du cathéter IABP.\n\nEn décembre 2016, après plusieurs tentatives infructueuses pour retirer le cathéter IABP de l'artère fémorale, il a été décidé de changer l'accès IABP de l'artère fémorale vers l'artère iliaque externe. Après avoir réinstallé le cathéter IABP, l'objectif était de combiner une gestion pharmacologique optimale avec une rééducation physique active et passive.\n\nUne approche en quatre étapes utilisant l'artère iliaque externe pour le placement du cathéter IABP\n\nUne technique innovante a été récemment développée dans notre établissement pour répondre aux problèmes résultant du placement à long terme d'un IABP fémoral. La patiente a été informée de cette nouvelle procédure et a signé un consentement éclairé écrit pour ce traitement. L'artère iliaque externe gauche a été utilisée pour l'insertion du cathéter IABP et comprenait un conduit prothétique Gelsoft de 8 mm de diamètre (Vascutek, Inchinnan, Écosse, Royaume-Uni). Une greffe de Dacron biseautée de 8 mm a été anastomosée bout à bout à l'artère avec une suture en polypropylène 5-0. Le cathéter a été retiré sous-cutanément de l'espace rétropéritonéal gauche vers le quadrant inférieur droit de l'abdomen. Aucune complication n'est survenue pendant la procédure.\n\nLa procédure mise au point dans notre établissement comprenait quatre étapes principales. La première étape a commencé par une incision longitudinale du quadrant inférieur gauche depuis l’arcade costale inférieure jusqu’à la partie supérieure du ligament inguinal. La peau, le tissu sous-cutané et les muscles ont été incisés jusqu’à la membrane péritonéale pour exposer l’artère iliaque externe. À l’aide de rétracteurs, les organes intra-abdominaux ont été déplacés vers le médiastin pour exposer les artères iliaques. Une anastomose latérale a été réalisée entre l’artère iliaque externe et le greffon prothétique. La deuxième étape de la procédure a comporté une incision de 1 cm dans le côté droit de l’abdomen, à 5-6 cm de l’ombilic et 2 cm en dessous. Un tunnel a été créé dans le plan sous-cutané du côté droit de l’abdomen vers le côté gauche. La troisième étape de la procédure a consisté à faire avancer la partie proximale du cathéter de l’IABP du côté droit de l’abdomen à travers le tunnel sous-cutané vers le côté gauche. Le cathéter a été placé dans l’aorte thoracique descendante à travers le greffon prothétique, l’artère iliaque et l’aorte. Le cathéter a été noué et scellé au niveau du site de connexion avec le greffon à l’aide d’une suture prolène 2-0. La quatrième étape de la procédure a consisté à fermer la plaie rétropéritonéale. L’utilisation du conduit vasculaire a permis de retirer relativement facilement l’IABP d’une petite incision dans le quadrant inférieur gauche de l’abdomen, qui a été fermée à l’aide de deux points de suture.\n\n\nRésultats et suivi des patients\n\nAprès la procédure IABP, le patient a été autorisé à s'asseoir, à se tenir debout et à marcher avec assistance et aucune complication neurologique ne s'est produite. Il n'y a eu aucun épisode de septicémie lié au site d'insertion. Après la procédure IABP transiliaque, le patient a présenté une réduction des taux sériques de créatinine et de bilirubine totale. Le patient n'a pas eu d'ischémie des membres pendant la contre-pulsation IABP. Les améliorations constatées pendant la physiothérapie comprenaient la marche sur 290 mètres pendant un test de marche de six minutes. Le patient a connu une amélioration significative de la fonction cardiaque avec une réduction de l'hypertension pulmonaire et de la résistance vasculaire pulmonaire. 195 jours après le changement de l'accès IABP, le patient a subi une transplantation cardiaque réussie.",
+        "gold_summary": "Patient : Femme, 67 ans\n\nDiagnostic final : Insuffisance cardiaque\n\nSymptômes : douleur thoracique • dyspnée • faible tolérance à l'exercice\n\nMédication : —\n\nProcédure clinique : insertion intra-articulaire d'une pompe à ballonnet - nouvelle technique\n\nSpécialité : chirurgie cardiaque\n\nRapport de cas:\nUne femme de 67 ans se présentait avec des antécédents d'insuffisance cardiaque. Elle avait des symptômes de classe fonctionnelle IV de la New York Heart Association (NYHA). La patiente avait des antécédents d'insuffisance cardiaque chronique due à une cardiomyopathie dilatée avec une fraction d'éjection ventriculaire gauche de 25 %, une régurgitation mitrale sévère, une fibrillation auriculaire paroxystique et une hypothyroïdie. Un traitement pharmacologique immédiat a été initié et un cathéter IABP a été initialement inséré en utilisant l'accès par l'artère fémorale. Au cours des 115 jours de traitement hospitalier, plusieurs tentatives infructueuses ont été faites pour retirer le cathéter IABP. En raison de l'immobilité prolongée du patient, l'accès du cathéter IABP a été changé de l'artère fémorale à l'artère iliaque externe. Un greffon prothétique en Dacron et un canal sous-cutané ont été utilisés. Une pharmacothérapie optimale a été initiée et la patiente a subi une rééducation et une mobilisation avec une amélioration significative de la fonction cardiaque. 195 jours après le changement de l'accès du cathéter IABP, la patiente a subi une transplantation cardiaque réussie.\n",
+        "synthetic_summary": {
+            "B1": "Il y avait une dame très malade de son cœur. Son cœur ne marchait pas bien. Elle avait beaucoup de mal à respirer et à bouger.\n\nLes docteurs ont mis un petit tuyau spécial pour aider son cœur. Au début, ils l'ont mis dans une grosse veine de sa jambe. Mais ça ne marchait pas bien longtemps.\n\nAlors, les docteurs ont changé le tuyau et l'ont mis dans un autre endroit, près du ventre. Cela a aidé la dame à bouger un peu et à se sentir mieux.\n\nAprès, elle a pu avoir un nouveau cœur. Maintenant, elle va mieux et peut faire plus de choses. Les docteurs ont bien pris soin d'elle.",
+            "B2": "Présentation du cas  \nUne femme de 67 ans souffrait d’une insuffisance cardiaque grave. Cela signifie que son cœur ne pompait pas assez bien le sang. Elle avait des difficultés à respirer, une grande fatigue et ne pouvait presque plus faire d’efforts. Son cœur était affaibli à cause d’une maladie appelée cardiomyopathie dilatée, qui rend le muscle cardiaque plus faible. Elle avait aussi des problèmes avec une valve du cœur (la valve mitrale) qui ne se fermait pas bien, ainsi qu’un rythme cardiaque irrégulier (fibrillation auriculaire) et une thyroïde moins active (hypothyroïdie).\n\nTraitement initial et complications  \nPour l’aider, les médecins ont mis en place un petit appareil appelé pompe à ballonnet intra-aortique (IABP). Cet appareil aide le cœur à mieux fonctionner en facilitant la circulation du sang. Au début, ils ont inséré ce dispositif par une artère située dans la cuisse (artère fémorale). Mais après plusieurs mois, ils n’ont pas réussi à retirer ce cathéter à cause de complications. De plus, la patiente est restée très immobilisée, ce qui n’était pas bon pour sa santé.\n\nNouvelle technique pour améliorer la situation  \nPour résoudre ce problème, les médecins ont décidé de changer la manière d’insérer la pompe. Cette fois, ils ont utilisé une autre artère plus haute dans le corps, appelée artère iliaque externe, située près de l’abdomen. Ils ont placé un petit tube artificiel (greffon en Dacron) pour connecter la pompe à cette artère. Le cathéter a été passé sous la peau d’un côté à l’autre de l’abdomen pour éviter les complications. Cette technique a permis à la patiente de se lever, de marcher avec de l’aide et de faire de la rééducation sans problème.\n\nRésultats et évolution  \nGrâce à cette nouvelle méthode, la fonction de son cœur s’est améliorée, et sa pression dans les poumons a diminué. Elle a pu marcher presque 300 mètres lors d’un test de six minutes, ce qui montre une meilleure capacité physique. Après environ six mois avec ce nouveau système, la patiente a pu recevoir une greffe de cœur avec succès. Cette approche innovante a donc aidé à stabiliser sa santé en attendant la transplantation.",
+            "B3": "Résumé détaillé et structuré\n\nContexte  \nUne femme de 67 ans, présentant une insuffisance cardiaque chronique liée à une cardiomyopathie dilatée, a été admise en juin 2016 à l’Institut de cardiologie de Varsovie (Pologne) avec une aggravation progressive de son insuffisance cardiaque sur trois semaines. Elle était classée en stade IV selon la New York Heart Association (NYHA), témoignant d’une dyspnée sévère, d’une faiblesse importante et d’une prise de poids. Ses antécédents comprenaient une fraction d’éjection ventriculaire gauche (FEVG) très réduite à 25 %, une régurgitation mitrale sévère, une fibrillation auriculaire paroxystique et une hypothyroïdie. Elle avait déjà bénéficié d’un traitement percutané par annuloplastie mitrale et d’une thérapie de resynchronisation cardiaque avec défibrillateur implantable (CRT-D). Malgré ces traitements, elle a présenté des épisodes récurrents d’œdème pulmonaire et d’hypertension pulmonaire sévère, nécessitant une intubation et une ventilation mécanique.\n\nPrincipales observations  \nÀ son admission, un cathéter de pompe à ballonnet intra-aortique (IABP) a été placé par voie fémorale pour soutenir la fonction cardiaque. Cependant, après 115 jours d’hospitalisation, plusieurs tentatives de retrait du cathéter IABP ont échoué, et la patiente a souffert d’immobilité prolongée liée à la présence du cathéter fémoral. En raison de l’hypertension pulmonaire sévère, la transplantation cardiaque était initialement contre-indiquée. Pour permettre une meilleure mobilisation et réduire les complications liées à l’immobilisation, l’équipe médicale a décidé de changer le site d’accès du cathéter IABP de l’artère fémorale à l’artère iliaque externe.\n\nIntervention innovante  \nUne technique chirurgicale innovante a été développée pour ce changement d’accès. Elle comportait quatre étapes principales :  \n1. Une incision longitudinale dans le quadrant inférieur gauche de l’abdomen a permis d’exposer l’artère iliaque externe. Un greffon prothétique en Dacron de 8 mm a été anastomosé bout à bout à cette artère.  \n2. Une petite incision a été réalisée dans le quadrant inférieur droit de l’abdomen, à environ 5-6 cm de l’ombilic, pour créer un tunnel sous-cutané reliant les deux côtés de l’abdomen.  \n3. Le cathéter IABP a été introduit à travers ce tunnel, puis inséré via le greffon prothétique dans l’aorte thoracique descendante. Le cathéter a été fixé et scellé au niveau de la connexion avec le greffon.  \n4. La plaie rétropéritonéale a été refermée. Cette approche a permis un retrait ultérieur du cathéter par une petite incision, minimisant ainsi les risques.\n\nRésultats et suivi  \nAprès le repositionnement du cathéter IABP par voie iliaque externe, la patiente a pu s’asseoir, se tenir debout et marcher avec assistance, sans complications neurologiques ni infections liées au site d’insertion. Les paramètres biologiques se sont améliorés, notamment une diminution des taux de créatinine et de bilirubine totale. Aucun signe d’ischémie des membres n’a été observé durant la contre-pulsation. La rééducation physique a permis une progression notable, avec une distance de marche de 290 mètres lors d’un test de marche de six minutes. Sur le plan cardiaque, une amélioration significative a été constatée, avec une réduction de l’hypertension pulmonaire et de la résistance vasculaire pulmonaire. Enfin, 195 jours après le changement d’accès du cathéter IABP, la patiente a bénéficié d’une transplantation cardiaque réussie.\n\nConclusion  \nCe cas illustre l’efficacité et la sécurité d’une nouvelle technique d’accès iliaque externe pour l’insertion prolongée d’un cathéter IABP chez une patiente en insuffisance cardiaque avancée. Cette approche a permis une meilleure mobilisation, une amélioration clinique notable et a servi de pont vers une transplantation cardiaque."
+        }
+    },
+    {
+        "article": "Patient féminine caucasienne de 73 ans qui a consulté pour un trouble mammaire avec une anomalie rose de la peau du sein droit il y a environ 30 jours. La mammographie bilatérale 5 mois avant la consultation a montré des anomalies bénignes (rapport d'imagerie mammaire et système de données - BI-RADS™ 2). La patiente avait des antécédents de carcinome canalaire invasif du sein droit G3 sans type spécial, qui avait été traité par résection segmentaire et dissection des ganglions axillaires de niveaux I et II en décembre 2011. Au moment de la chirurgie, on a observé une tumeur de 3,0 cm et trois ganglions axillaires métastatiques (3/10). L'immunohistochimie a révélé que la tumeur était positive pour le récepteur des œstrogènes (90%), positive pour le récepteur de la progestérone (2%), négative pour HER-2, positive pour Ki-67 (60%) et du sous-type luminaire B. La thérapie adjuvante de la patiente comprenait six cycles de doxorubicine, cyclophosphamide et paclitaxel, suivis d'une radiothérapie (25 séances avec une dose de 50 Gy au sein droit et à la fossa supraclaviculaire, plus une dose de 10 Gy). La patiente suit actuellement un traitement endocrinologique avec le létrozole (6 ans de traitement). Au cours de l'examen physique, elle a présenté deux lésions roses au sein droit, dont une érythémateuse légère et presque imperceptible au niveau de la jonction quadrante supérieure (JQS) et une autre lésion violacée plus intense au niveau de la jonction quadrante inférieure (JQI) mesurant 0,5 cm.\n\nUne biopsie incisionnelle de la lésion a été réalisée au JQI, qui a révélé une lésion vasculaire atypique en coloration hématoxyline-éosine. Une étude immuno-histochimique complémentaire de l'angiosarcome a été suggérée pour compléter le diagnostic. Après le résultat de cette étude, la patiente a été soumise à une résection des deux lésions cutanées. Le rapport pathologique anatomique de l'échantillon résectionné a montré un angiosarcome bien différencié (G1), une néoplasie caractérisée par des anastomoses vasculaires alignées par des cellules endothéliales atypiques caractérisées par la présence d'hyperchromatisme et d'anisocaryose et, dans certains cas, contenant des érythrocytes, organisées dans le modèle de croissance infiltrée, pénétrant le parenchyme mammaire et le derme au JQI, mesurant 1,9x1,4 cm, et au JQI, constituant une néoplasie limitée au derme, mesurant 1,1x0,5 cm. L'examen immuno-histochimique a révélé une positivité pour l'expression du groupe de différenciation 31 (CD31) et de l'oncogène C-MYC, confirmant la malignité secondaire à la radiothérapie. La tomographie par ordinateur du thorax et de l'abdomen et la scintigraphie osseuse n'ont pas montré de signes de métastases à distance. La patiente a subi une mastectomie simple du côté droit, sans reconstruction, comme traitement complémentaire. Le rapport final histopathologique a montré un angiosarcome bien différencié (G1) et trois foyers microscopiques ont été trouvés dans le parenchyme mammaire, dont le plus grand mesurait 2 mm. Deux ans après la chirurgie, la patiente n'a pas développé de récidive.\n",
+        "gold_summary": "Nous rapportons le cas d'une femme de 73 ans ayant des antécédents de traitement conservateur d'un cancer du sein droit, présentant une modification rose discrète de la peau du sein homolatéral. La mammographie a montré un résultat compatible avec des modifications bénignes (BI-RADS 2). L'hématoxyline-éosine a montré une lésion vasculaire atypique et a suggéré une immunohistochimie pour une élucidation diagnostique. La patiente a subi une résection de la lésion et l'histologie a montré un angiosarcome radiogénique. Une mastectomie simple a ensuite été réalisée. L'immunohistochimie a montré une positivité pour les antigènes CD31 et CD34, et l'amplification de l'oncogène C-MYC a confirmé le diagnostic d'un angiosarcome induit par une radiothérapie mammaire. Le retard dans le diagnostic constitue un problème important. Étant donné que les modifications initiales de la peau de l'angiosarcome radiogénique sont subtiles et peuvent être confondues avec d'autres affections cutanées bénignes, telles que les télangiectasies, nous soulignons dans ce rapport les aspects cliniques, afin de mettre en garde contre la possibilité d'un angiosarcome du sein chez les patients ayant des antécédents de radiothérapie adjuvante pour le traitement du cancer du sein. La patiente est restée asymptomatique 16 mois après la chirurgie.\n",
+        "synthetic_summary": {
+            "B1": "Une dame de 73 ans avait un petit changement rose sur sa peau du sein droit. Ce changement était très léger et facile à ne pas voir. Avant, elle avait eu un traitement pour un gros problème au même sein.\n\nLes docteurs ont pris un petit bout de peau pour regarder de près. Ils ont trouvé un petit problème dans les vaisseaux du sang. Ce problème est venu à cause d’un traitement qu’elle avait eu avant.\n\nPour aider la dame, les docteurs ont enlevé la partie malade du sein. Après, ils ont enlevé tout le sein droit pour être sûrs que tout allait bien.\n\nCe problème sur la peau peut être difficile à voir. Parfois, il ressemble à des petites taches qui ne font pas peur. C’est pourquoi les docteurs veulent bien regarder quand une personne a eu un traitement avant.\n\nMaintenant, la dame va bien et n’a plus de problème. Les docteurs continuent à bien la surveiller.",
+            "B2": "Cas d’une femme de 73 ans avec un cancer du sein traité auparavant\n\nUne femme de 73 ans avait déjà eu un cancer du sein droit, traité en 2011 par une opération partielle et une radiothérapie (rayons pour tuer les cellules cancéreuses). Cinq mois avant sa nouvelle consultation, une mammographie (radiographie du sein) montrait des anomalies bénignes, c’est-à-dire sans gravité.\n\nCe qu’ils ont trouvé récemment\n\nLa patiente a remarqué une légère coloration rose sur la peau de son sein droit. Lors de l’examen, deux petites taches roses ont été observées. Une biopsie, c’est-à-dire un prélèvement d’un petit morceau de peau, a été faite sur l’une des lésions. L’analyse au microscope a montré des cellules anormales dans des vaisseaux sanguins, ce qui a suggéré un angiosarcome. L’angiosarcome est un type rare de cancer qui se forme dans les cellules des vaisseaux sanguins.\n\nCe que cela signifie\n\nL’angiosarcome découvert est lié à la radiothérapie reçue plusieurs années auparavant. Pour confirmer ce diagnostic, des tests spéciaux ont montré la présence de certaines protéines (CD31, C-MYC) caractéristiques de ce cancer. La patiente a ensuite subi une ablation complète du sein droit (mastectomie simple) pour enlever toutes les cellules malades.\n\nPourquoi c’est important\n\nL’angiosarcome après radiothérapie est difficile à détecter au début, car il ressemble à des problèmes de peau bénins comme de simples rougeurs. Ce cas montre qu’il faut être vigilant chez les patients ayant eu une radiothérapie du sein, même longtemps après, pour ne pas rater ce type de cancer rare. Deux ans après l’opération, la patiente n’a pas eu de récidive, ce qui est un bon signe.",
+            "B3": "Résumé détaillé et structuré\n\nContexte  \nNous présentons le cas d’une femme caucasienne de 73 ans, ayant des antécédents de cancer du sein droit traité par chirurgie conservatrice et radiothérapie il y a plus de dix ans. La patiente a consulté pour une modification cutanée récente, discrètement rosée, sur le sein droit, apparue environ un mois avant la consultation. Une mammographie réalisée cinq mois auparavant avait montré uniquement des anomalies bénignes (classification BI-RADS 2).\n\nPrincipales observations  \nÀ l’examen clinique, deux lésions cutanées distinctes ont été identifiées sur le sein droit : une lésion légèrement érythémateuse et quasi imperceptible dans le quadrant supérieur, et une autre lésion violacée plus visible dans le quadrant inférieur, mesurant environ 0,5 cm. Une biopsie incisionnelle de la lésion du quadrant inférieur a révélé une lésion vasculaire atypique à l’hématoxyline-éosine, ce qui a motivé la réalisation d’une étude immunohistochimique complémentaire. Cette dernière a montré une expression positive des marqueurs CD31 et de l’oncogène C-MYC, confirmant la nature maligne de la lésion et son caractère secondaire à une radiothérapie antérieure. Le diagnostic final était un angiosarcome mammaire bien différencié (grade 1), une tumeur rare et agressive d’origine vasculaire, infiltrant à la fois le derme et le parenchyme mammaire.\n\nInterprétation clinique  \nL’angiosarcome radiogénique du sein est une complication tardive rare mais grave de la radiothérapie adjuvante pour cancer du sein. Son diagnostic est souvent retardé en raison de l’aspect clinique initial très subtil, pouvant être confondu avec des lésions cutanées bénignes telles que les télangiectasies. L’immunohistochimie, notamment la positivité pour CD31 et l’amplification de C-MYC, est essentielle pour confirmer le diagnostic. Dans ce cas, l’angiosarcome s’est manifesté plus de dix ans après le traitement initial, soulignant la nécessité d’une surveillance attentive des modifications cutanées chez les patientes irradiées.\n\nProchaines étapes  \nAprès confirmation du diagnostic, la patiente a subi une résection chirurgicale des lésions cutanées, suivie d’une mastectomie simple sans reconstruction. L’examen histopathologique post-opératoire a confirmé la présence de foyers microscopiques d’angiosarcome dans le parenchyme mammaire. Les examens d’imagerie complémentaires n’ont pas révélé de métastases à distance. Deux ans après la chirurgie, la patiente reste sans signe de récidive ni de métastase, ce qui est un résultat favorable compte tenu de la nature agressive de cette tumeur.\n\nConclusion  \nCe cas illustre l’importance d’une vigilance accrue face à toute modification cutanée nouvelle chez une patiente ayant reçu une radiothérapie mammaire, même plusieurs années auparavant. La reconnaissance précoce de l’angiosarcome radiogénique permet une prise en charge chirurgicale rapide, améliorant ainsi le pronostic. Nous recommandons aux cliniciens de considérer ce diagnostic dans le suivi à long terme des patientes traitées pour cancer du sein."
+        }
+    },
+    {
+        "article": "Homme de 40 ans, admis aux urgences pour douleurs thoraciques. Ses antécédents comprenaient un surpoids, une stéatose hépatique non alcoolique, un syndrome d'apnée du sommeil sans besoin de pression positive continue des voies respiratoires et une coronaropathie chez son grand-père. Les symptômes ont débuté 6 jours avant la consultation, sous forme de douleurs thoraciques de classe fonctionnelle II (1000 mètres), intensité 5/10, brûlantes, non irradiées, d'une durée de 15 à 20 minutes, qui s'amélioraient avec le repos et sans association de dyspnée, palpitations ou transpiration. Des épisodes similaires ont été répétés les jours suivants avant la consultation, dans la même classe fonctionnelle, 2 heures avant l'admission, débutant la douleur dans la classe fonctionnelle IV, postprandial, d'intensité 8/10, associée à une dyspnée, ce qui a conduit le patient à consulter.À l'admission, les signes vitaux suivants ont été observés : TA 150/80 mmHg, FC 85 LPM, FR 16 RPM, saturation 98 % (0,21), non fébrile. Douleur thoracique résiduelle d'intensité 4/10, sans signes d'insuffisance cardiaque. Un électrocardiogramme a été réalisé, où des ondes T négatives, symétriques, ont été visualisées dans les dérivations précordiales et supradesnivel de ST de < 1 mm avec des ondes T bifasic en V3, sans ondes Q et bonne progression de R dans les précordiales (non observé dans l'électrocardiogramme préalable). Laboratoire : Hto 43 %, Cr 0,8 mg/dl, troponine ultrasensible de 132 pg/ml avec élévation ultérieure à 172 pg/ml. On a interprété infarctus aigu du myocarde sans élévation du ST, TIMI score de 3 points, GRACE score 66 points. On a administré une charge d'aspirine, des statines de haute intensité et une anticoagulation avec de l'héparine de faible poids moléculaire. Il a commencé un traitement avec de la nitroglycérine intraveineuse, avec une amélioration de la douleur. Un nouvel électrocardiogramme a été réalisé, où des ondes T négatives ont été visualisées dans les précordiales, mais persistance du supradesnivel avec une onde T bifasic en V2-V3. L'échocardiogramme a mis en évidence une bonne fonction ventriculaire et une hypokinésie antéroseptal, basale et médiale. L'angiographie a mis en évidence des lésions graves dans le tiers proximal, moyen de l'artère descendante antérieure et une lésion grave dans le tiers moyen de la première diagonale, ce qui a conduit à la pose de trois stents libérant des médicaments dans ces lésions. Un nouvel électrocardiogramme a été réalisé après la pose des stents, où l'absence de changements a été observée. Le patient a été libéré sans complications.\n",
+        "gold_summary": "Il s’agit d’un homme de 40 ans sans antécédents cardiovasculaires, qui a été admis à notre centre pour des douleurs précordiales. L’électrocardiogramme a révélé un schéma typique, déjà décrit, connu sous le nom de syndrome de Wellens de type 1 ou A, caractérisé par un supradesnivel du ST < 1 mm et une onde T biphasique dans la dérivation V3. On a diagnostiqué un infarctus aigu du myocarde sans élévation du ST, TIMI 3 et GRACE score 66 points. Ce schéma électrocardiographique est à haut risque, au-delà des scores stratifiants, étant donné qu’il est corrélé à une lésion grave de l’artère descendante antérieure au niveau proximal et nécessite une intervention percutanée sans délai. La coronarographie a révélé 3 lésions graves : tiers proximal et moyen de l’artère descendante antérieure et première diagonale.\n",
+        "synthetic_summary": {
+            "B1": "Un homme de 40 ans avait mal au cœur. Ce mal est un signe que son cœur est un peu malade. Les docteurs ont fait un dessin spécial du cœur appelé électrocardiogramme. Ce dessin montrait un problème important. Ce problème peut faire très mal au cœur si on ne soigne pas vite. Les docteurs ont regardé dans ses petites routes du cœur avec une caméra spéciale. Ils ont vu trois endroits très bouchés. Ils ont mis de petits tuyaux pour aider le cœur à mieux marcher. Maintenant, il va mieux et il est en sécurité.",
+            "B2": "### Ce qu'ils ont trouvé chez le patient\n\nUn homme de 40 ans est venu à l'hôpital parce qu'il avait des douleurs dans la poitrine. Son électrocardiogramme, qui est un examen pour voir l'activité électrique du cœur, montrait un signe spécial appelé syndrome de Wellens de type 1. Cela signifie qu'il y avait un petit changement dans les ondes du cœur, notamment une onde T en deux phases dans une zone appelée V3. Ce signe est important car il montre un problème grave dans une artère du cœur.\n\n### Ce que cela signifie\n\nLe patient avait un infarctus du myocarde sans élévation du segment ST, ce qui veut dire qu'il y avait un début d'attaque cardiaque sans certains signes classiques sur l'électrocardiogramme. Les scores TIMI et GRACE, qui aident à mesurer le risque, étaient modérés, mais le signe du syndrome de Wellens indique un risque élevé. Cela signifie que l'artère descendante antérieure, une grosse artère qui nourrit le cœur, était gravement bouchée.\n\n### Ce qu'ils ont fait ensuite\n\nPour confirmer le problème, les médecins ont fait une coronarographie, un examen qui montre les artères du cœur. Ils ont trouvé trois endroits où les artères étaient très bouchées. Pour traiter cela, ils ont posé trois stents, qui sont de petits tubes métalliques qui maintiennent les artères ouvertes. Après cette intervention, le patient s'est amélioré et a pu sortir de l'hôpital sans problème.\n\n### En résumé\n\nCe cas montre l'importance de reconnaître le syndrome de Wellens sur un électrocardiogramme. Même si les autres tests ne paraissent pas très graves, ce signe indique une obstruction importante dans une artère du cœur qui doit être traitée rapidement pour éviter une crise cardiaque sévère.",
+            "B3": "Contexte  \nUn homme de 40 ans, sans antécédents cardiovasculaires majeurs, a été admis aux urgences pour des douleurs thoraciques récurrentes, évoluant depuis six jours. Ces douleurs, initialement modérées et soulagées par le repos, sont devenues plus intenses et associées à une gêne respiratoire, ce qui a motivé la consultation.  \n\nPrincipales Observations  \nÀ l’admission, l’électrocardiogramme (ECG) a montré des anomalies caractéristiques, notamment un léger sus-décalage du segment ST inférieur à 1 mm et une onde T biphasique dans la dérivation V3, signes typiques du syndrome de Wellens de type 1 (ou type A). Par ailleurs, la troponine ultrasensible, un marqueur de lésion cardiaque, était élevée et en augmentation, confirmant un infarctus aigu du myocarde sans élévation persistante du segment ST. Les scores cliniques TIMI (3 points) et GRACE (66 points) ont indiqué un risque modéré.  \n\nInterprétation Clinique  \nLe syndrome de Wellens est un motif électrocardiographique à haut risque, révélateur d’une atteinte sévère de l’artère coronaire descendante antérieure proximale, qui peut entraîner un infarctus majeur s’il n’est pas traité rapidement. Ce risque élevé dépasse souvent les prédictions des scores cliniques classiques.  \n\nProchaines Étapes  \nUne coronarographie a été réalisée en urgence, mettant en évidence trois lésions coronariennes sévères : dans les tiers proximal et moyen de l’artère descendante antérieure ainsi que dans la première branche diagonale. Ces lésions ont été traitées par la pose de trois stents à libération médicamenteuse. Après cette intervention, le patient a présenté une amélioration clinique significative et a pu être libéré sans complications.  \n\nRésumé  \nCe cas illustre l’importance de reconnaître le syndrome de Wellens à l’ECG, un signe précoce d’une obstruction critique de l’artère coronaire descendante antérieure, nécessitant une prise en charge rapide par angioplastie. Malgré un risque modéré selon les scores usuels, ce syndrome impose une intervention urgente pour prévenir un infarctus étendu."
+        }
+    },
+    {
+        "article": "Un patient iranien de 38 ans s'est présenté au service des urgences de l'hôpital de Kowsar, à Semnan, le 2 octobre 2021, avec pour principaux symptômes une douleur abdominale sévère et un œdème des membres inférieurs. La douleur, qui provenait de la région ombilicale et se répandait dans tout l'abdomen, a motivé la visite. Les signes vitaux ont été enregistrés comme suit : tension artérielle (TA) = 130/90 mmHg, fréquence cardiaque (FC) = 80 bpm, et température (T) = 37 °C. L'examen abdominal a révélé des bruits intestinaux normaux, une légère sensibilité dans la région inguinale, et des bruits tympaniques. Il a également été noté qu'il souffrait d'une SBS congénitale avec une longueur totale mesurée de l'intestin grêle d'environ 185 cm, significativement plus courte que la normale, et une absence de l'épiploon.\n\nLe 10 août 2021, la patiente a subi une hémicolectomie droite et une iléostomie en raison de douleurs abdominales associées à un diagnostic d'obstruction intestinale. Par la suite, le 21 septembre 2021, la patiente a subi une colostomie et a été hospitalisée pendant 6 jours (dont 3 jours en unité de soins intensifs [USI]). Après la sortie, la patiente a présenté des douleurs abdominales et un œdème, avec une escalade des symptômes le 1er octobre 2021. Des nausées ont été signalées lors de l'admission, mais sans vomissements, et il n'y a pas eu de plaintes liées à la miction. En raison de douleurs postprandiales et d'un mauvais appétit, la prise alimentaire de la patiente a été compromise. Aucune fièvre, aucun frisson, ni aucune dyspnée n'ont été signalés. Un œdème des membres inférieurs a été constaté (2+), sans clubbing ou cyanose observée. Les autres signes vitaux étaient dans les limites normales (pouls 82 battements/minute, tension artérielle 110/70 mmHg, fréquence respiratoire 18 respirations/minute, température 37 °C). La sensibilité abdominale a entravé un examen complet en raison de douleurs sévères. L'examen de la tête, du cou et de la poitrine n'a révélé aucune constatation spécifique.\n\nLe compte sanguin complet a indiqué une leucocytose (hémoglobine 11,7 g/dL, nombre de globules blancs 19,23 × 103/µL, plaquettes 406 × 103/µL, RBC 4,30 × 106/µL, et hématocrite [HTC] 34,3%), tandis que l'analyse des gaz du sang artériel a montré une alcalose métabolique (pH 7,56, pression partielle d'oxygène [PO2] 204,5 mmHg, pression partielle de dioxyde de carbone [PCO2] 31,9 mmHg, excès de base [BE] 7,0 mmol/L, et bicarbonate [HCO3] 29,1 mmol/L).\n\nRadiographies abdominales et thoraciques d’un homme de 38 ans atteint du syndrome congénital de l’intestin court et d’absence de l’omentum. Radiographie abdominale couchée démontrant des boucles intestinales dilatées et l’absence de l’omentum, sans preuve de niveaux air-fluide. La radiographie thoracique ne montrait pas non plus de signes d’anomalies significatives, confirmant les résultats cardiopulmonaires normaux. La radiographie abdominale debout révélait des signes de distension gazeuse et de boucles compatibles avec le diagnostic du patient.\n\nUne tomographie par ordinateur (CT) à contraste amélioré de l'abdomen et du bassin a été recommandée. La sécrétion fécale des sutures du patient a soulevé des préoccupations concernant une péritonite postopératoire due à une fuite anastomotique, ce qui a nécessité une intervention chirurgicale immédiate. Le patient a subi une laparotomie d'urgence, un drainage et une jéjunostomie à double baril.\n\nLa récupération du patient s'est déroulée sans incident, avec une prise orale de liquides clairs autorisée le jour postopératoire 2 et une prise de liquides complète autorisée le jour postopératoire 4.\n\nPour l'absence congénitale d'omentum et le syndrome du petit intestin, les options de traitement comprennent un soutien nutritionnel, tel que la nutrition parentérale ou entérale totale. Les cas graves peuvent nécessiter une intervention chirurgicale pour allonger le reste de l'intestin ou effectuer une transplantation intestinale. Les stratégies pour le syndrome du petit intestin résultant de l'absence congénitale d'omentum peuvent impliquer un soutien nutritionnel, ainsi que l'amélioration de l'expression des protéines de transport (telles que les cotransporteurs Na+/glucose, les échangeurs Na+/H+) pour faciliter l'adaptation intestinale. Les interventions humaines comprennent le traitement par glutamine et par hormone de croissance ou l'administration de peptides glucagon-like, bien que des études multicentres soient nécessaires pour obtenir des preuves concluantes.\n",
+        "gold_summary": "Ce rapport de cas présente une convergence unique de ces conditions rares chez un homme iranien de 38 ans ayant des antécédents d'obstruction intestinale nécessitant une hémicolectomie droite et une iléostomie. Il s'est ensuite présenté au service des urgences en présentant une douleur abdominale intense et un gonflement de ses membres inférieurs. Les examens de laboratoire ont révélé une augmentation du nombre de globules blancs et une alcalose métabolique. Au cours de l'exploration chirurgicale provoquée par sa présentation aiguë, l'absence congénitale de l'omentum et le syndrome du petit intestin ont été confirmés. Une jéjunostomie a été réalisée, mais malheureusement, cette intervention a entraîné une malabsorption sévère et une cachexie ultérieure. Ce cas met en lumière la rare occurrence de fuite anastomotique et de péritonite ultérieure suite à une hémicolectomie droite et une iléostomie chez un patient présentant les conditions combinées d'intestin court congénital et d'absence congénitale de l'omentum.\n",
+        "synthetic_summary": {
+            "B1": "Un homme avait très mal au ventre. Ses jambes étaient un peu gonflées. Son ventre était spécial car son intestin était plus court que d’habitude. Il avait aussi un morceau du ventre qui manquait. Les docteurs ont fait une opération pour l’aider. Après, il a eu encore des problèmes et a dû être opéré une autre fois. Les docteurs ont pris soin de lui pour qu’il puisse manger et boire doucement. C’est un cas très rare et les docteurs apprennent beaucoup pour mieux aider d’autres personnes.",
+            "B2": "**Résumé simplifié pour un élève de 14 ans :**\n\nCe cas parle d’un homme de 38 ans qui avait deux problèmes rares : un intestin très court dès la naissance (ce qui signifie que son intestin est beaucoup plus petit que la normale) et l’absence d’une partie du ventre appelée l’épiploon (une sorte de tissu qui protège les organes). Il avait déjà eu une opération où on lui a enlevé une partie de son gros intestin (hémicolectomie droite) et où on a fait une ouverture pour évacuer les selles (iléostomie).\n\nPlus tard, il est venu aux urgences parce qu’il avait très mal au ventre et ses jambes étaient enflées. Les examens ont montré qu’il avait beaucoup de globules blancs, ce qui indique une infection, et un problème dans son sang appelé alcalose métabolique (c’est un déséquilibre chimique dans le corps). Les médecins ont fait une nouvelle opération et ont confirmé qu’il manquait bien l’épiploon et que son intestin était très court.\n\nIls ont fait une autre intervention appelée jéjunostomie, qui consiste à créer une nouvelle ouverture dans une partie de l’intestin pour l’aider à mieux digérer. Malheureusement, cette opération a causé des difficultés graves pour absorber les aliments, ce qui a affaibli le patient.\n\nCe cas est important parce qu’il montre qu’il est rare d’avoir à la fois un intestin très court et l’absence d’épiploon, et que cela peut compliquer les opérations et entraîner des infections graves comme une fuite au niveau des sutures et une inflammation du ventre (péritonite). Pour ces patients, il faut souvent un soutien spécial pour la nutrition, parfois avec des solutions nutritives directement dans le sang, et dans certains cas, d’autres opérations ou même une transplantation d’intestin peuvent être nécessaires.",
+            "B3": "Résumé détaillé et structuré\n\nContexte  \nCe rapport décrit le cas d’un homme iranien de 38 ans présentant une association rare de deux anomalies congénitales : le syndrome de l’intestin court (SIC), caractérisé par une longueur anormalement courte de l’intestin grêle (environ 185 cm au lieu de la normale), et l’absence congénitale de l’épiploon (omentum), une structure graisseuse abdominale jouant un rôle protecteur. Le patient avait des antécédents récents d’obstruction intestinale ayant nécessité une hémicolectomie droite (ablation d’une partie du côlon) et une iléostomie (dérivation de l’intestin grêle vers la peau).\n\nPrincipales observations  \nLe patient s’est présenté aux urgences avec une douleur abdominale intense, localisée initialement autour du nombril puis diffuse, accompagnée d’un œdème (gonflement) des membres inférieurs. Les signes vitaux étaient globalement stables, mais l’examen abdominal était limité par la douleur. Les analyses sanguines ont montré une leucocytose (augmentation du nombre de globules blancs à 19,23 × 10^3/µL), signe d’inflammation ou d’infection, ainsi qu’une alcalose métabolique (pH sanguin élevé à 7,56), indiquant un déséquilibre acido-basique. Les radiographies ont révélé une distension des anses intestinales sans signe clair d’obstruction complète, tandis que la tomodensitométrie (CT) a suggéré une fuite anastomotique (fuite au niveau de la jonction chirurgicale intestinale), responsable d’une péritonite postopératoire (inflammation du péritoine, la membrane qui tapisse la cavité abdominale).\n\nIntervention et évolution  \nFace à cette complication grave, une laparotomie d’urgence a été réalisée, avec drainage de la péritonite et mise en place d’une jéjunostomie à double baril (création d’une ouverture chirurgicale dans le jéjunum, une partie de l’intestin grêle). La récupération postopératoire s’est déroulée sans incident majeur, avec reprise progressive de l’alimentation orale. Toutefois, la combinaison du syndrome de l’intestin court et de l’absence d’épiploon a conduit à une malabsorption sévère, exposant le patient à un risque important de dénutrition et de cachexie (perte de poids et de masse musculaire).\n\nInterprétation clinique  \nCe cas illustre la complexité de la prise en charge d’un patient présentant simultanément un syndrome de l’intestin court congénital et une absence congénitale d’épiploon, deux conditions rares qui compliquent la fonction digestive et la protection abdominale. La survenue d’une fuite anastomotique et d’une péritonite postopératoire après une hémicolectomie droite et une iléostomie souligne la fragilité de ces patients et la nécessité d’une surveillance étroite. Le syndrome de l’intestin court impose un soutien nutritionnel intensif, souvent par nutrition parentérale (intraveineuse) ou entérale (par sonde), et peut nécessiter des interventions chirurgicales complémentaires pour améliorer l’absorption intestinale.\n\nProchaines étapes et perspectives thérapeutiques  \nLe traitement à long terme du syndrome de l’intestin court associé à l’absence d’épiploon repose sur un soutien nutritionnel adapté et des stratégies visant à favoriser l’adaptation intestinale. Des approches pharmacologiques, telles que l’administration de glutamine, d’hormone de croissance ou de peptides glucagon-like (qui stimulent la croissance et la fonction intestinale), sont en cours d’évaluation mais nécessitent des études supplémentaires pour confirmer leur efficacité. Dans les cas sévères, des interventions chirurgicales visant à allonger l’intestin ou une transplantation intestinale peuvent être envisagées. Ce cas souligne l’importance d’une prise en charge multidisciplinaire pour optimiser le pronostic de ces patients présentant des anomalies congénitales rares et complexes."
+        }
+    },
+    {
+        "article": "Un homme de 20 ans travaillant comme fermier, sans antécédents médicaux et chirurgicaux, a été admis au service des urgences se plaignant de douleurs coliques sévères dans la région du flanc droit, irradiant la région environnante et l'aine. La douleur est associée à une fièvre élevée et à des vomissements récurrents. Il a signalé une hématurie indolore, une fièvre et des symptômes pseudo-grippaux 2 semaines avant son admission à l'hôpital. La fièvre et les symptômes pseudo-grippaux avaient été traités avec l'utilisation d'une analgésie. Il n'avait pas d'antécédents de maladie des calculs urinaires ou d'infections des voies urinaires. L'examen physique a révélé une sensibilité dans l'aine droite et une sensibilité positive de l'angle costovértebral droit, sinon, il était normal. Un test complet de numération sanguine, une analyse d'urine, une analyse des selles et une échographie abdominale ont été effectués. L'analyse de laboratoire a révélé une leucocytose modérée de 20 000/mm3 (intervalle normal : 4,5-11 × 103/mm3), une neutrophilie relative et une lymphopénie relative. La créatinine sérique était normale. L'analyse d'urine a révélé une hématurie +3 et des cristaux d'oxalate de calcium. L'analyse des selles a révélé la présence d'Entamoeba histolytica, sans œufs ou vers détectés, et le reste de l'analyse des selles était normal. L'échographie abdominale a révélé une structure cylindrique hyperechoïque de 6 mm de diamètre et de 6 cm de longueur dans la partie distale de l'uretère droit impliquant la jonction urétéro-vésicale (JUV) associée à une hydronéphrose droite minimale et une légère augmentation de l'échogénicité du rein droit. Il n'y a pas de calcul rénal définitif ; sinon, les deux reins sont normaux en taille, site et forme. L'imagerie Doppler n'a pas été réalisée.\n\nIl a été hospitalisé au service d'urologie ; un traitement conservateur a été initialement suivi. Une tomodensitométrie de contraste a été réalisée, qui a montré une structure tubulaire de 6 cm (un corps étranger) située à l'urètre distal environ 2,5 cm à l'intérieur de la vessie. La structure montre une densité de tissu mou dans la paroi et une densité de fluide dans la partie intérieure, ce qui provoque une hydrourénéphrose du côté droit minimale. Une image axiale au niveau de la partie distale de l'urètre droit montre un urètre dilaté et un défaut de remplissage arrondi représentant le parasite obstructeur. Image axiale de la tomodensitométrie au niveau de la jonction vésico-urétérale à 10 minutes de retard, montrant le parasite qui passe partiellement à travers la jonction vésico-urétérale. Sinon, le rein droit est normal en taille, écho-texture et épaisseur corticale, sans calculs ni masses. Il n'y a aucune preuve d'une fistule entre les voies gastro-intestinale et urinaire.\n\nUne urétéroscopie a été réalisée à l'hôpital. Au cours de l'intervention, une structure ressemblant à de la cire de 6 mm a été découverte dans le tiers distal de l'uretère droit, accompagnée d'une quantité importante de pus. En outre, une projection ressemblant à un polype a été observée dans la vue de l'urétéroscope. L'objet extrait mesurait 6 cm de longueur, avait une coloration brune, n'était pas une structure mobile et présentait une consistance élastique serrée. Pour faciliter le drainage du pus, un double J (stent urétéral) a été inséré. Par la suite, l'échantillon mort a été soumis à un examen pathologique, qui l'a identifié comme étant A lumbricoides. La patiente a reçu un comprimé d'albendazole de 400 mg une fois par jour pendant 3 jours et a connu une récupération sans incident.\n",
+        "gold_summary": "Dans ce rapport, nous présentons le cas d'un homme de 20 ans qui est arrivé aux urgences avec de graves douleurs au flanc droit, une forte fièvre et des vomissements récurrents. Des évaluations diagnostiques ont été menées, y compris un test de numération sanguine complète, une analyse d'urine, une analyse des selles, une échographie abdominale et un scanner. Le diagnostic final était A lumbricoides trouvé dans la partie distale de l'uretère. Une procédure d'urétéroscopie a confirmé le diagnostic et a extrait le ver, qui mesurait 6 cm de longueur, avait une couleur brune et présentait une consistance élastique serrée.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 20 ans avait très mal sur le côté droit du ventre. Il avait aussi de la fièvre et il vomissait souvent. Les docteurs ont fait des examens avec des prises de sang, de l’urine, et des images du ventre.\n\nIls ont trouvé un petit ver dans un tuyau qui va du ventre à la vessie. Ce ver était long et brun. Les docteurs ont fait une petite opération pour le sortir. Après, le monsieur a pris des médicaments et il est allé mieux.",
+            "B2": "**Ce qu'ils ont trouvé**  \nUn jeune homme de 20 ans est venu aux urgences parce qu’il avait très mal au côté droit du ventre, de la fièvre élevée et des vomissements répétés. Il avait aussi remarqué du sang dans ses urines quelques semaines avant. Les médecins ont fait plusieurs examens : une prise de sang, une analyse d’urine, une analyse des selles, une échographie du ventre et un scanner.\n\n**Ce que cela signifie**  \nLes examens ont montré qu’il y avait un ver appelé *Ascaris lumbricoides* coincé dans une partie de son uretère, qui est un petit tube qui transporte l’urine du rein à la vessie. Ce ver mesurait 6 centimètres de long, était brun et avait une texture élastique. Ce parasite a causé une infection et une obstruction, ce qui expliquait la douleur et la fièvre.\n\n**Comment ils ont traité le problème**  \nLes médecins ont utilisé un petit tube avec une caméra, appelé urétéroscope, pour aller chercher le ver dans l’uretère. Ils ont aussi mis un petit drain pour aider à évacuer le pus et ont donné un médicament antiparasitaire nommé albendazole pendant trois jours. Après cela, le patient s’est bien rétabli sans problème.  \n\nCe cas est rare car ce type de ver se trouve habituellement dans l’intestin, pas dans les voies urinaires. Cela montre l’importance de bien chercher la cause quand une douleur au flanc est sévère et ne s’explique pas facilement.",
+            "B3": "Résumé détaillé et structuré :\n\nContexte  \nUn homme de 20 ans, sans antécédents médicaux notables, travaillant comme fermier, a été admis aux urgences pour des douleurs coliques sévères localisées au flanc droit, irradiant vers l’aine, accompagnées d’une fièvre élevée et de vomissements répétés. Deux semaines avant son admission, il avait présenté une hématurie (présence de sang dans les urines) indolore, une fièvre et des symptômes pseudo-grippaux, traités uniquement par des analgésiques. Il n’avait pas d’antécédents de calculs urinaires ni d’infections des voies urinaires.\n\nPrincipales observations  \nL’examen physique a révélé une sensibilité marquée au niveau de l’aine droite et une douleur à la percussion de l’angle costovértebral droit, signe souvent associé à une atteinte rénale. Les analyses de laboratoire ont montré une leucocytose modérée (20 000/mm3), une neutrophilie relative et une lymphopénie relative, témoignant d’une réaction inflammatoire. La créatinine sérique était normale, indiquant une fonction rénale préservée. L’analyse d’urine a mis en évidence une hématurie importante (+3) et la présence de cristaux d’oxalate de calcium. L’analyse des selles a révélé la présence d’Entamoeba histolytica, un parasite intestinal, sans détection d’œufs ou de vers. L’échographie abdominale a montré une structure cylindrique hyperechoïque de 6 mm de diamètre et 6 cm de longueur dans la partie distale de l’uretère droit, au niveau de la jonction urétéro-vésicale, associée à une hydronéphrose (dilatation du bassinet rénal) droite légère et une augmentation modérée de l’échogénicité du rein droit, sans calcul rénal visible.\n\nInterprétation clinique  \nUne tomodensitométrie (scanner) avec injection de contraste a confirmé la présence d’une structure tubulaire de 6 cm située dans l’uretère distal, partiellement à l’intérieur de la vessie, provoquant une obstruction et une hydronéphrose modérée. Cette structure présentait une densité de tissu mou dans sa paroi et une densité liquidienne en son centre, compatible avec un corps étranger parasitaire. L’urétéroscopie a permis d’explorer directement l’uretère et de découvrir une formation ressemblant à de la cire, de 6 mm de diamètre, accompagnée de pus abondant et d’une projection polypoïde. L’extraction de cet objet a révélé un ver brun de 6 cm de long, non mobile, à consistance élastique serrée. L’examen anatomopathologique a identifié ce corps étranger comme étant Ascaris lumbricoides, un parasite intestinal rarement responsable d’une migration vers les voies urinaires.\n\nProchaines étapes et prise en charge  \nLe patient a été traité par insertion d’un stent urétéral double J pour faciliter le drainage du pus et soulager l’obstruction. Un traitement antiparasitaire par albendazole (400 mg par jour pendant 3 jours) a été administré. L’évolution clinique a été favorable, avec une récupération complète sans complications. Ce cas illustre une forme rare de migration d’Ascaris lumbricoides vers l’uretère, provoquant une obstruction urétérale, une infection et une inflammation sévère nécessitant une prise en charge combinée endoscopique et médicamenteuse."
+        }
+    },
+    {
+        "article": "Une patiente de 27 ans a présenté une rougeur, des démangeaisons et des brûlures de l’œil droit quatre heures après avoir reçu sa troisième dose totale de vaccin de rappel à ARN messager contre la COVID-19. Elle a utilisé des larmes artificielles, mais ses symptômes sont restés inchangés le jour suivant, ce qui l’a incitée à consulter un ophtalmologue. Elle a nié une photophobie, une vision floue, une vision double, une sensation de corps étranger, une épiphorie, des éclairs de lumière ou des corps flottants. Il n’y a pas eu d’épisodes similaires antérieurs avec le même vaccin avant les deux doses. L’œil gauche était asymptomatique et non affecté. Les antécédents médicaux de la patiente étaient importants pour l’astigmatisme myopique des deux yeux, la conjonctivite allergique bilatérale, la rhinite allergique, la maladie de Crohn et l’asthme intermittent modéré.\n\nL'examen ophtalmologique a révélé une acuité visuelle corrigée de 20/20 bilatéralement. Les pressions intraoculaires mesurées étaient de 15 mmHg dans l'œil droit et de 16 mmHg dans l'œil gauche. La conjonctive droite avait une injection 2+ qui blanchissait avec des gouttes de phényléphrine. Il n'y avait pas d'injection sclérale, pas de sensibilité sclérale, et pas d'irritation physique adjacente à la zone de l'épisclérite (par exemple, pas de trichiasis). La chambre antérieure de l'œil droit paraissait profonde et calme. L'épisclérite associée a été décrite. Le reste de l'examen clinique des segments antérieur et postérieur était sans importance. La patiente a continué à utiliser des larmes artificielles et a commencé à prendre de l'ibuprofène 200 mg trois fois par jour pendant une semaine. La patiente a respecté et toléré le régime décrit et une semaine plus tard, tous les symptômes oculaires et signes ont disparu.\n\nLa patiente était satisfaite des soins qu'elle a reçus. Elle était soulagée que ses symptômes aient disparu et que sa vision finale n'ait pas été affectée. Elle prévoit de vérifier auprès de son rhumatologue avant les prochaines doses de vaccin de rappel COVID-19. Le consentement éclairé écrit a été obtenu de la patiente pour publication et pour l'utilisation des données et des images.\n",
+        "gold_summary": "Une femme de 27 ans a présenté un œil rouge, des démangeaisons et des brûlures d'un jour. La patiente a déclaré avoir développé ces symptômes dans les 3 à 4 heures suivant la vaccination. Ses antécédents médicaux étaient pertinents pour la maladie de Crohn. L'examen ophtalmologique a révélé une injection conjonctivale droite 2+ qui blanchissait avec des gouttes de phényléphrine. Sinon, son examen ophtalmologique était sans importance. La patiente a commencé à utiliser des larmes artificielles et de l'ibuprofène 200 mg trois fois par jour pendant une semaine. Après une semaine, tous les symptômes ont disparu et l'examen ophtalmologique est revenu à la ligne de base.\n",
+        "synthetic_summary": {
+            "B1": "Une femme a eu un œil rouge et qui gratte.  \nCela est arrivé après qu'elle a reçu un vaccin.  \n\nLe docteur a regardé son œil.  \nIl était un peu rouge, mais pas très grave.  \n\nElle a pris des gouttes pour les yeux et un médicament doux.  \nAprès une semaine, son œil allait bien.  \n\nElle était contente et son œil voyait bien.",
+            "B2": "Une jeune femme de 27 ans a eu l’œil droit rouge, qui la démangeait et la brûlait, environ 4 heures après avoir reçu sa troisième dose de vaccin contre la COVID-19. Elle n’avait jamais eu ces symptômes après ses premières doses. Elle n’a pas eu de problèmes de vision ou d’autres sensations bizarres dans l’œil. Ses antécédents médicaux incluent une maladie appelée Crohn, de l’asthme et des allergies.\n\nQuand le médecin a examiné son œil, il a vu que la partie blanche de l’œil droit était rouge, mais cette rougeur s’est atténuée avec un médicament en gouttes. Son examen de la vue était normal, et il n’y avait pas d’autres signes de blessure ou d’infection. Le médecin a diagnostiqué une épisclérite, c’est une inflammation légère de la couche juste sous la surface de l’œil, qui peut causer rougeur et gêne.\n\nPour soigner cela, elle a continué à mettre des larmes artificielles, c’est-à-dire des gouttes qui humidifient l’œil, et a pris un médicament contre la douleur et l’inflammation appelé ibuprofène, trois fois par jour pendant une semaine. Après ce traitement, ses symptômes ont complètement disparu et son œil est redevenu normal.\n\nLa patiente était contente car sa vision n’a pas été affectée et elle se sent mieux. Elle a prévu de parler avec son médecin spécialiste avant de recevoir d’autres rappels du vaccin COVID-19.",
+            "B3": "Résumé destiné à un public adulte non spécialiste\n\nContexte  \nUne femme de 27 ans a développé une rougeur, des démangeaisons et une sensation de brûlure à l’œil droit environ quatre heures après avoir reçu sa troisième dose de vaccin à ARN messager contre la COVID-19. Ces symptômes sont apparus rapidement après la vaccination et ont persisté malgré l’utilisation de larmes artificielles. La patiente ne présentait pas de troubles visuels tels que vision floue ou double, ni d’autres signes oculaires inquiétants. Ses antécédents médicaux comprenaient notamment la maladie de Crohn, un astigmatisme myopique, une conjonctivite allergique bilatérale, une rhinite allergique et un asthme intermittent modéré.\n\nPrincipales observations  \nL’examen ophtalmologique a montré une acuité visuelle normale corrigée (20/20) dans les deux yeux. La pression à l’intérieur de l’œil était également normale. L’œil droit présentait une rougeur modérée de la conjonctive (la membrane qui recouvre la partie blanche de l’œil), qui s’atténuait après instillation de gouttes de phényléphrine (un médicament qui réduit la rougeur en contractant les vaisseaux sanguins). Il n’y avait pas d’inflammation de la sclère (la partie blanche de l’œil) ni d’autres signes d’irritation ou de blessure. La chambre antérieure de l’œil (espace entre la cornée et l’iris) était calme et profonde, sans signe d’inflammation. L’ensemble des autres structures oculaires examinées était normal. Le diagnostic retenu était une épisclérite, une inflammation bénigne et localisée de la couche superficielle de la sclère.\n\nInterprétation clinique  \nL’épisclérite est une inflammation généralement bénigne qui peut provoquer rougeur et gêne oculaire, souvent sans compromettre la vision. Dans ce cas, elle est survenue rapidement après la vaccination, suggérant une réaction inflammatoire locale. L’absence de signes plus graves et la normalité des examens complémentaires ont permis d’écarter d’autres causes plus sévères.\n\nPrise en charge et évolution  \nLa patiente a poursuivi l’utilisation de larmes artificielles pour apaiser l’œil et a commencé un traitement anti-inflammatoire léger à base d’ibuprofène (200 mg trois fois par jour) pendant une semaine. Ce traitement a été bien toléré et a permis une disparition complète des symptômes et une normalisation de l’examen ophtalmologique au bout de sept jours. La patiente a exprimé sa satisfaction quant à la prise en charge et le résultat, et prévoit de consulter son rhumatologue avant toute future dose de vaccin de rappel afin d’évaluer les risques éventuels.\n\nConclusion  \nCe cas illustre une épisclérite transitoire survenue peu après une vaccination contre la COVID-19, qui a répondu favorablement à un traitement symptomatique simple. Il souligne l’importance d’un suivi médical adapté en cas d’effets secondaires oculaires post-vaccinaux, tout en rassurant sur le pronostic généralement bon de cette complication."
+        }
+    },
+    {
+        "article": "Nous décrivons une femme de 25 ans chez qui on a diagnostiqué une AD depuis l'enfance et une apparition ultérieure de vitiligo lentement progressif à l'âge de 16 ans. Au début de l'examen, la patiente présentait une xérose cutanée diffuse, des papules excoriées et des plaques sur le dos, et des lésions érythémateuses lichénifiées sur les membres supérieurs et le dos des mains avec un indice de gravité et de surface de l'eczéma (EASI) de 18. La patiente a rapporté des démangeaisons intenses (échelle de numérotation des démangeaisons [NRS] = 10). Des macules achromiques confluentes évoquant un vitiligo étaient également présentes sur les coudes et sur le visage, principalement dans la région des paupières, bilatéralement. La patiente présentait également de multiples macules achromiques de forme irrégulière sur le cou, le tronc et le dos des mains, et des manifestations hypopigmentées initiales dans la région axillaire gauche et le genou gauche avec un indice de gravité et de surface de l'eczéma (VASI) de 0,45. Les deux affections cutanées ont eu un impact sur sa qualité de vie, ce qui a entraîné un indice de qualité de vie dermatologique (DLQI) de 17.\n\nLes traitements antérieurs pour la DA comprenaient des corticostéroïdes topiques et systémiques, des inhibiteurs topiques de la calcineurine, des antihistaminiques et un court traitement par cyclosporine, qui a été abandonné en raison d'une intolérance. Les traitements antérieurs pour le vitiligo comprenaient un traitement à court terme par des corticostéroïdes topiques et systémiques au début de la maladie et, pendant les 2 premières années, sans résultats. Par la suite, le tacrolimus, un inhibiteur topique de la calcineurine, a été utilisé pendant plusieurs années suivant un régime d'entretien pulsé proactif après une période d'induction initiale, donnant des bénéfices thérapeutiques minimes. Des antioxydants et des produits à base de vitamines ont également été utilisés comme traitements adjuvants. Pour des raisons logistiques, le patient a refusé la photothérapie.\n\nÉtant donné la coexistence de la DA et du vitiligo, et compte tenu des avantages potentiels supplémentaires, une thérapie systémique avec 15 mg d'upadacitinib par jour a été initiée après des évaluations médicales et de laboratoire pour exclure la grossesse et d'autres contre-indications. Sur la base de l'indication approuvée de l'upadacitinib pour la DA, nous avons opté pour un début de traitement en vue d'atteindre la dose efficace la plus faible.\n\nUne amélioration progressive de la DA a été observée après les premières semaines de traitement avec une rémission clinique à la semaine 16 (EASI 0 ; NRS 0) associée à une amélioration de la qualité de vie (DLQI 0). Dans le même temps, une nette amélioration du vitiligo a été observée avec une repigmentation complète des zones acromiques du cou, du tronc, du dos des mains et des coudes (Fig. 1b), et une repigmentation partielle mais significative des patches acromiques de la région des paupières (Fig. 2b) (VASI = 0.25). Une rémission presque complète du vitiligo a été obtenue à la semaine 28 de traitement et a été maintenue jusqu'à 1 an de suivi, sans effets secondaires, à l'exception d'une légère aggravation de l'acné, facilement contrôlée par des traitements topiques.\n",
+        "gold_summary": "Nous décrivons une femme de 25 ans chez qui on a diagnostiqué une AD depuis l'enfance et une apparition ultérieure de vitiligo lentement progressif à l'âge de 16 ans. Une thérapie systémique avec l'inhibiteur de JAK1 upadacitinib 15 mg par jour a été commencée, après une évaluation médicale et de laboratoire pour exclure une grossesse et d'autres contre-indications. Une amélioration progressive de l'AD a été observée après les premières semaines de traitement avec une rémission clinique à la semaine 16. Dans le même temps, une nette amélioration du vitiligo a été observée avec une rémission presque complète atteinte à la semaine 28 de traitement.\n",
+        "synthetic_summary": {
+            "B1": "Il y a une dame qui avait la peau qui grattait beaucoup depuis qu'elle était petite. Elle avait aussi des taches blanches sur sa peau qui sont venues quand elle avait 16 ans.\n\nLes docteurs lui ont donné un médicament spécial à prendre chaque jour. Ce médicament a aidé sa peau à aller beaucoup mieux. Au bout de quelques semaines, ses démangeaisons ont disparu.\n\nAprès un peu plus de six mois, les taches blanches sur sa peau ont presque toutes disparu aussi. Elle se sentait beaucoup mieux et n’avait presque plus de problèmes de peau.",
+            "B2": "Une jeune femme de 25 ans souffrait depuis son enfance d'une dermatite atopique (AD), une maladie de la peau qui cause des démangeaisons et des plaques rouges. À 16 ans, elle a aussi développé un vitiligo, une maladie où la peau perd sa couleur normale par endroits. Pour traiter ces deux problèmes, les médecins lui ont donné un médicament appelé upadacitinib, qui agit sur certaines protéines du corps pour réduire l’inflammation. Avant de commencer ce traitement, ils ont vérifié qu’elle ne soit pas enceinte et qu’elle n’ait pas d’autres problèmes de santé.\n\nAprès quelques semaines, sa dermatite s’est beaucoup améliorée, et au bout de 16 semaines, ses symptômes avaient presque disparu. En même temps, son vitiligo a aussi commencé à s’améliorer, avec un retour de la couleur de la peau sur plusieurs zones. Après 28 semaines, la plupart des taches blanches du vitiligo avaient presque complètement disparu. Ce bon résultat a duré pendant un an, avec seulement un léger problème d’acné, facile à soigner. Ce traitement a donc aidé cette patiente à mieux vivre avec ses maladies de peau.",
+            "B3": "Résumé détaillé et structuré :\n\nContexte  \nNous présentons le cas d’une femme de 25 ans souffrant d’une dermatite atopique (DA) diagnostiquée depuis l’enfance, associée à un vitiligo d’apparition progressive à partir de l’âge de 16 ans. Lors de l’examen initial, la patiente présentait une xérose cutanée diffuse, des lésions eczémateuses lichénifiées et excoriées sur le dos et les membres supérieurs, avec un indice de gravité et de surface de l’eczéma (EASI) de 18, traduisant une forme modérée à sévère de DA. Elle rapportait également des démangeaisons intenses (échelle NRS = 10). Par ailleurs, des macules achromiques confluentes, caractéristiques du vitiligo, étaient visibles sur le visage (notamment les paupières), les coudes, le cou, le tronc et le dos des mains, avec un indice de gravité et de surface du vitiligo (VASI) de 0,45. Ces deux affections cutanées impactaient significativement la qualité de vie de la patiente (DLQI = 17).\n\nPrincipales Observations  \nLes traitements antérieurs pour la DA comprenaient des corticostéroïdes topiques et systémiques, des inhibiteurs topiques de la calcineurine, des antihistaminiques et un court traitement par cyclosporine, interrompu pour intolérance. Pour le vitiligo, des corticostéroïdes topiques et systémiques avaient été utilisés sans succès, suivis d’un traitement prolongé par tacrolimus topique avec des bénéfices minimes. La patiente avait également essayé des antioxydants et des vitamines, mais avait refusé la photothérapie pour des raisons logistiques.\n\nInterprétation Clinique  \nCompte tenu de la coexistence de la DA et du vitiligo, et des bénéfices potentiels d’une thérapie ciblée, un traitement systémique par upadacitinib (inhibiteur sélectif de la Janus kinase 1, JAK1) à la dose de 15 mg par jour a été initié après exclusion d’une grossesse et d’autres contre-indications. Ce choix thérapeutique visait à utiliser la dose efficace la plus faible, conformément aux indications approuvées pour la DA.\n\nProchaines Étapes et Résultats  \nUne amélioration progressive de la DA a été observée dès les premières semaines, avec une rémission clinique complète à la semaine 16 (EASI 0, NRS 0), accompagnée d’une amélioration totale de la qualité de vie (DLQI 0). Parallèlement, une amélioration significative du vitiligo a été notée, avec une repigmentation complète des zones achromiques du cou, du tronc, du dos des mains et des coudes, ainsi qu’une repigmentation partielle mais notable des paupières (VASI réduit à 0,25). À la semaine 28, la patiente présentait une rémission quasi complète du vitiligo, maintenue jusqu’à un an de suivi. Le traitement a été bien toléré, avec pour seul effet secondaire une légère aggravation de l’acné, contrôlée par des soins topiques.\n\nEn résumé, ce cas illustre l’efficacité de l’upadacitinib dans le traitement simultané de la dermatite atopique modérée à sévère et du vitiligo associé, avec une amélioration clinique durable et un profil de tolérance favorable."
+        }
+    },
+    {
+        "article": "Patient et observation\nInformations relatives au patient (présentation du patient): il s'agit d'un jeune homme de 28 ans célibataire sans enfant, militaire en activité. Présente depuis 5 semaines, des douleurs abdominales d'installation progressive plus marquées à l'épigastre et l'hypochondre droite, suivi peu de temps après par une fièvre non chiffrée, des frissons, sueurs profuses dans un contexte d'anorexie et d'amaigrissement chiffré à 6kgs. Notons que le patient n'est pas alcoolo-tabagique, vacciné au BCG ne présentant aucun autre antécédent personnel ou familial contributif.\n\nRésultats cliniques: à l'admission, l'examen physique a retrouvé le patient dans un état général altéré, asthénique avec un amaigrissement chiffré à 6kgs sur un mois. Un syndrome inflammatoire à réponse systémique clinique était présent avec comme éléments: une fièvre à 39,1°C, une tachycardie (124 battements/min), une polypnée (22 cycles/min). L'examen pulmonaire et l'exploration des aires ganglionnaires superficielles étaient sans particularité. Au niveau abdominal, une sensibilité modérée à l'hypochondre droite avec une hépatomégalie a été retrouvée.\n\nChronologie: remonte à février 2022 par l'installation d'une douleur abdominale diffuse avec trouble du transite à type de diarrhée-constipation, le tout dans un contexte de conservation de l'état général avec fébricule à prédominance nocturne. Un traitement syntagmatique a été instauré sans succès. L'évolution est marquée par la persistance de la fébricule associée à une anorexie et un amaigrissement progressif chiffré à 12kgs sur trois mois. Devant ce trouble du transit avec fièvre inexpliquée et la dégradation de l'état général le patient sera admis aux urgences pour meilleure investigation.\n\nDémarche diagnostique: dès son admission, des bilans ont été réalisés rapportant un syndrome infectieux biologique une hyperleucocytose (17800 élts/mm3) à prédominance neutrophile (14000 élts/mm3) et une protéine C-réactive élevée à 323 mg/L.\n\nFace à sa douleur abdominale, la lipasémie et la troponine réalisées sont revenues normales respectivement 38 UI/L (VN: <3 78 UI/L) et 4 ng/L (VN: 2 à 16 ng/L). Le bilan hépatique stable avec des ALAT (Alanine amino-transférase) à 22 UI/L (VN: < 40UI/L), des ASAT (Aspartate amino-transférase) à 17 UI/L (VN: < 35UI/L), des GGT (Gamma glutamyl transférase) à 42 UI/L (VN: < 50UI/L), PAL (Phosphatases alcalines) à 115 UI/L (VN: 40- 150 UI/L) et une bilirubinémie normale. La fonction hépatique était normale avec un taux de prothrombine à 78% et une albuminémie à 39 g/L. L'ionogramme sanguin ainsi que la fonction rénale sont revenus normaux. La radiographie du thorax et l'échographie abdominale réalisés sans particularité.\n\nAvec une procalcitonine positive à 4,1ng/L, un bilan infectieux à la recherche du foyer infectieux a été initié entre autres un examen cytobactériologique des urines et des hémocultures lors des pics fébriles à 39°C qui sont tous deux revenus négatifs. Les sérologies hépatites virales B, C et VIH, ainsi que la sérologie de la syphilis réalisée en hospitalisation étaient toutes négatives. La lactate déshydrogénase (LDH) et la béta-2 microglobuline étaient normales respectivement 231 UI/L et 2,28 mg/L. Le GeneXpert à la recherche du Mycobactérium sur ces pièces biopsiques était négatif. Le quantiféron était revenu négatif. La recherche du Mycobactérium sur les expectorations matinales de 3 jours consécutifs était négative.\n\nSur le plan morphologique, un scanner thoraco-abdomino-pelvien a montré au niveau de l'étage abdominal, un foie augmenté de taille (flèche hépatique à 17cm), siège de multiples lésions hypodenses tissulaire, arrondies bien limitées, non rehaussées après injection du produit de contraste dont les plus volumineuses siègent au segment I (21 x 16mm) et au segment V (36 x 27mm). Au niveau des étages thoracique et pelvien, aucune lésion suspecte n'a été mise en évidence. Des premières biopsies hépatiques obtenues par ponction écho-guidée ont révélées à l'examen histologique des lésions hépatiques fibro-inflammatoires subaiguës, sans indice histologique de spécificité ou de malignité.\n\nUne IRM hépatique à la suite du scanner a objectivé un foie dysmorphique, siège de lésions en signal hétérogène T2 entourée d'une paroi en hypersignal T2, rehaussée en périphérie après injection du produit de contraste dont les plus volumineuses siègent au segment I (20 x 22mm) et au segment V (33 x 31mm). Aucune adénopathie profonde n'avait été objectivée, aussi bien au scanner qu'à l'IRM. Une cœlioscopie diagnostique réalisée sur les nodules hépatiques, l'examen histologique a retrouvé des granulomes épithélioides et gigantocellulaires de taille variable avec nécrose caséeuse en faveur d'une tuberculose hépatique.\n\nIntervention thérapeutique: le patient a été mis sous traitement antituberculeux selon le protocole standard pendant mois à savoir: Phase 1: quadrithérapie (Isoniazide + Rifampicine + Pyrazinamide + Ethambutol) en une seule prise orale chaque matin à jeun pendant 2 mois. Phase 2: bithérapie (Isoniazide + Rifampicine) en une seule prise orale chaque matin à jeun pendant 4 mois\n\nSuivi et résultats des interventions thérapeutiques: dès les premiers jours du traitement, une bonne réponse a été obtenue avec disparition du syndrome inflammatoire à réponse systémique tant sur le plan clinique que biologique. Au bout de trois mois de traitement, un scanner hépatique de contrôle a montré une diminution du nombre et du volume des lésions hépatiques.",
+        "gold_summary": "Ce cas clinique rapporté chez un jeune marocain, se présentant dans un tableau de colique hépatique évoluant depuis un mois associé à des signes frustres d'imprégnation tuberculeuse. Des lésions nodulaires hépatiques non spécifiques ont été révélées au scanner et à l'imagerie par résonance magnétique (IRM) hépatique. Le diagnostic de tuberculose hépatique focale a été confirmé après analyse anatomopathologique sur biopsies des nodules hépatiques obtenues au décours d'une cœlioscopie. Après début du traitement anti bacillaire bien conduit, une bonne amélioration clinico-biologique a été obtenue.",
+        "synthetic_summary": {
+            "B1": "Il y a un jeune homme qui avait mal au ventre depuis longtemps. Il avait aussi de la fièvre et il perdait du poids. \n\nLe docteur a fait des images de son ventre. Il a vu des petites bosses dans son foie. \n\nLe docteur a pris un petit bout de ces bosses pour regarder de près. Il a trouvé une maladie appelée tuberculose. \n\nLe jeune homme a pris des médicaments pour guérir. Très vite, il a commencé à aller mieux.",
+            "B2": "Cas d’un jeune homme de 28 ans avec des douleurs au ventre et de la fièvre\n\nCe jeune homme, militaire, a commencé à avoir des douleurs dans le ventre, surtout en haut à droite, depuis environ un mois. Il avait aussi de la fièvre, des sueurs, une perte d’appétit et il a maigri de plusieurs kilos. À l’hôpital, les médecins ont remarqué qu’il était fatigué, avait de la fièvre élevée et son ventre était sensible au toucher.\n\nCe qu’ils ont trouvé grâce aux examens\n\nLes analyses de sang ont montré une forte infection, mais les tests pour des maladies comme l’hépatite ou le VIH étaient négatifs. Une radiographie du thorax et une échographie du ventre n’ont rien montré de spécial. Par contre, un scanner et une IRM du foie ont révélé plusieurs petites lésions (zones anormales) dans le foie. Pour comprendre ce que c’était, les médecins ont fait une biopsie, c’est-à-dire qu’ils ont prélevé un petit morceau de tissu du foie. L’analyse a montré des signes de tuberculose, une infection causée par une bactérie qui peut toucher plusieurs organes.\n\nLe traitement et l’évolution\n\nLe patient a commencé un traitement spécial contre la tuberculose, avec plusieurs médicaments pendant six mois. Très vite, il s’est senti mieux, la fièvre est partie et les analyses sanguines sont redevenues normales. Après trois mois, les images du foie montraient que les lésions avaient diminué.\n\nEn résumé\n\nCe cas montre qu’une tuberculose peut parfois toucher le foie et provoquer des douleurs et de la fièvre. Grâce aux examens précis et à la biopsie, les médecins ont pu poser le bon diagnostic et soigner efficacement ce jeune homme.",
+            "B3": "Résumé détaillé et structuré pour un public adulte non spécialiste\n\n**Contexte**  \nUn homme marocain de 28 ans, militaire en activité, sans antécédents médicaux notables, a présenté depuis environ cinq semaines des douleurs abdominales progressives localisées principalement à l’épigastre (partie haute de l’abdomen) et à l’hypochondre droit (région sous les côtes à droite). Ces douleurs ont été accompagnées rapidement d’une fièvre élevée, de frissons, de sueurs abondantes, d’une perte d’appétit (anorexie) et d’une perte de poids importante de 6 kg en un mois. Son état général s’est détérioré, avec une fatigue marquée et une inflammation systémique confirmée par la fièvre, une accélération du rythme cardiaque (tachycardie) et une respiration rapide (polypnée). L’examen clinique a révélé une hépatomégalie (augmentation du volume du foie) sensible à la palpation.\n\n**Principales observations**  \nLes examens biologiques ont montré un syndrome inflammatoire important avec une hyperleucocytose (augmentation des globules blancs) à prédominance neutrophile et une protéine C-réactive très élevée, témoignant d’une inflammation active. Les tests hépatiques et la fonction rénale étaient normaux, ainsi que les examens radiologiques standards (radiographie thoracique, échographie abdominale). La recherche d’infections courantes, y compris les hépatites virales, le VIH, la syphilis, ainsi que la recherche de bactéries dans le sang et les urines, était négative. De même, les tests spécifiques à la tuberculose (GeneXpert, quantiféron, recherche de bacilles dans les expectorations) étaient négatifs.\n\nUn scanner thoraco-abdomino-pelvien a révélé un foie augmenté de taille avec plusieurs lésions nodulaires hypodenses (zones plus sombres) bien délimitées, sans rehaussement après injection de produit de contraste, situées principalement dans les segments I et V du foie. L’IRM hépatique a confirmé ces lésions, montrant des zones hétérogènes avec une paroi périphérique rehaussée. Aucune adénopathie (ganglion lymphatique anormal) profonde n’a été détectée. Les premières biopsies hépatiques guidées par échographie ont montré des lésions fibro-inflammatoires sans signe de cancer ni d’infection spécifique.\n\nLa confirmation diagnostique a été obtenue par une cœlioscopie (intervention chirurgicale mini-invasive permettant de visualiser et prélever des tissus dans l’abdomen) ciblant les nodules hépatiques. L’examen histologique a mis en évidence des granulomes épithélioïdes et gigantocellulaires avec nécrose caséeuse, caractéristiques typiques de la tuberculose hépatique focale.\n\n**Interprétation clinique**  \nCe cas illustre une tuberculose hépatique focale, une forme rare de tuberculose extra-pulmonaire qui peut se manifester par des douleurs abdominales, une fièvre prolongée et une altération de l’état général. Le diagnostic est souvent difficile car les examens biologiques et radiologiques sont peu spécifiques, et les tests classiques de recherche de bacilles tuberculeux peuvent être négatifs. La confirmation repose sur l’analyse histologique des lésions hépatiques, mettant en évidence les granulomes avec nécrose caséeuse, signe pathognomonique de la tuberculose.\n\n**Prochaines étapes et suivi thérapeutique**  \nLe patient a été traité selon le protocole standard antituberculeux, comprenant une phase initiale de quatre médicaments (Isoniazide, Rifampicine, Pyrazinamide, Ethambutol) pendant deux mois, suivie d’une phase d’entretien de deux médicaments (Isoniazide et Rifampicine) pendant quatre mois, le tout administré par voie orale à jeun. Dès les premiers jours de traitement, une amélioration clinique et biologique rapide a été observée, avec disparition des signes inflammatoires systémiques. Au bout de trois mois, un scanner de contrôle a montré une réduction significative du nombre et de la taille des lésions hépatiques, témoignant de l’efficacité du traitement.\n\n**Conclusion**  \nCette observation souligne l’importance de considérer la tuberculose hépatique dans le diagnostic différentiel des lésions nodulaires hépatiques chez un patient présentant un syndrome inflammatoire prolongé et une altération de l’état général, même en l’absence de signes pulmonaires ou de tests microbiologiques positifs. La biopsie hépatique et l’examen histologique restent essentiels pour confirmer le diagnostic et permettre une prise en charge adaptée, qui conduit généralement à une guérison complète sous traitement antituberculeux."
+        }
+    },
+    {
+        "article": "Le patient était un Japonais de 59 ans ayant une histoire de diabète de type 1 de 28 ans. Il visitait notre hôpital tous les mois pour la gestion du diabète avec une thérapie intensive utilisant des injections d'insuline à doses multiples. Sa taille et son poids étaient de 168 cm et 52 kg (indice de masse corporelle : 18,4 kg/m2), respectivement. Il a présenté une sécrétion d'insuline déplétée (le niveau de C-peptide sérique était inférieur à la limite de détection), de sorte que ses taux de glycémie fluctuaient sévèrement, et son taux d'hémoglobine A1c (HbA1c) était d'environ 9,0 % malgré une thérapie intensive d'insuline. Il avait été diagnostiqué avec une régurgitation aortique sévère asymptomatique chronique (grade III) 16 ans avant la présentation actuelle, mais avait refusé un suivi pour la régurgitation aortique. Il n'avait jamais subi d'opération chirurgicale ni l'implantation de dispositifs prothétiques.\n\nHuit jours après sa visite régulière à l'hôpital, il a consulté une clinique d'urgence se plaignant de difficultés respiratoires et avait une fièvre supérieure à 38℃. Jusqu'à ce jour, il n'avait pas remarqué de fièvre, de frissons, de faiblesse ou d'autres symptômes. Sa tension artérielle et son pouls étaient de 192/82 mmHg et 118/min, respectivement. Il présentait une orthopnée et sa saturation en oxygène (SpO2) était de 80%. Il a été transporté au service des urgences de notre hôpital. Un examen physique a révélé un murmure systolique de Levine 3/6, bien que son murmure cardiaque n'ait pas été vérifié lors des visites régulières à l'hôpital. Aucune constatation physique suggérant une IE, telle que les nœuds d'Osler, les lésions de Janeway ou les pétéchies conjonctivales, n'a été reconnue. Son nombre de globules blancs (WBC) a été nettement augmenté à 20 800 /μL, et sa protéine C-réactive (CRP) a été élevée à 6,06 mg/dL. La créatine phosphokinase MB sérique était dans la plage normale, à 6,0 IU/L, et la troponine T était négative. La radiographie thoracique a montré une congestion pulmonaire avec un élargissement cardiaque (rapport cardiothoracique : 55%). L'électrocardiographie a révélé une élévation du ST sur V1-V4, mais l'échocardiographie d'urgence n'a révélé aucune dysfonction de la contractilité cardiaque. Il a été diagnostiqué avec une insuffisance cardiaque aiguë due à une maladie valvulaire, et un traitement par ventilation positive non invasive et nitrates a été initié.\n\nAprès admission à l'hôpital, un examen détaillé par échocardiographie transthoracique a montré une grave régurgitation aortique, une grave régurgitation mitrale et une végétation mobile sur la valve mitrale. L'échocardiographie transœsophagienne a révélé une végétation mobile de 16,5 × 6 mm sur la valve mitrale antérieure et une végétation non mobile de 11,2 × 5 mm sur la cuspide non coronaire de la valve aortique. Ces résultats ont soulevé de fortes suspicions de NVP. Dans ce cas, la tomographie par ordinateur (CT) et l'imagerie par résonance magnétique n'ont révélé aucun infarctus cérébral ou hémorragie, bien qu'une végétation mobile ait été détectée.\n\nEn examinant l'évolution clinique jusqu'à l'hospitalisation, nous avons noté que lors de la visite quatre mois avant l'admission, son nombre de globules blancs était légèrement élevé. Le mois suivant, son taux d'albumine (Alb) était tombé à 3,0 g/dL, et son taux d'hémoglobine (Hb) avait diminué progressivement au cours des 2 mois précédant l'admission. Au cours de cette période, il avait perdu 4 kg. Une oesophagogastroduodénoscopie et une tomodensitométrie du corps entier ont été effectuées, mais aucune anomalie n'a été détectée. Un mois plus tard, il avait regagné un peu de poids, et les résultats de laboratoire étaient presque normaux, à l'exception d'un taux de CRP légèrement élevé (0,54 mg/dL). À la dernière visite (8 jours avant l'admission), son nombre de globules blancs était de nouveau monté à 9 300 /μL, tandis que ses taux d'hémoglobine et d'albumine étaient de nouveau tombés à 13,1 g/dL et 3,0 g/dL, respectivement. En outre, son taux de CRP était passé à 4,18 mg/dL. À ce moment-là, sa tension artérielle diastolique avait manifesté une baisse évidente. Jusqu'à présent, il n'avait pas connu de fièvre ou de symptômes autres que la perte de poids. Nous avons soupçonné des maladies d'origine infectieuse et/ou maligne et avons initié des examens complets pour identifier la source de ses résultats cliniques.\n\nAprès le début du traitement de l'insuffisance cardiaque, ses symptômes cliniques ont rapidement diminué et sa stabilité hémodynamique a été maintenue pendant les six premières heures. Il a initialement reçu une antibiothérapie empirique intraveineuse consistant en 12 g/jour d'ampicilline sulbactam (ABPC/S) et 120 mg/jour de gentamycine (GM). Trois ensembles de cultures sanguines ont été obtenus à l'admission, et tous étaient positifs pour S. warneri [concentration inhibitrice minimale (CIM) à ABPC/S ≤8 μg/mL ; CIM à GM ≤1 μg/mL ; CIM à cefazolin (CEZ) ≤2 μg/mL]. Ainsi, l'IE causée par cet organisme a été diagnostiquée.\n\nSelon la directive clinique établie par la Japanese Circulation Society, la chirurgie d'urgence est généralement recommandée pour l'insuffisance cardiaque de NYHA III à IV ou la chirurgie urgente pour la végétation mobile de l'EVE dépassant 10 mm et le dysfonctionnement sévère de la valve. Dans ce cas, cependant, son insuffisance cardiaque a été améliorée avec succès. Sur la base de la directive, le risque d'embolie a été considéré comme ayant été réduit par l'administration d'une antibiothérapie appropriée. En outre, le patient avait un diabète de type 1, et son contrôle glycémique était si mauvais que nous craignions que la chirurgie à double valve ne soit une procédure à haut risque. Par conséquent, nous avons planifié une chirurgie élective après un contrôle suffisant de l'infection et du diabète.\n\nEn fonction des résultats de la culture sanguine, le régime antibiotique a été changé pour 6 g/jour de CEZ. Un examen dentaire détaillé n'a révélé aucune anomalie, telle que la parodontite. Après quatre semaines de traitement antibiotique, il a subi une intervention chirurgicale. Sa valve aortique s'est avérée bicuspide, et les anneaux aortiques et mitraux étaient intacts sans formation d'abcès. De grandes végétations ont été exentérées, et les valves aortiques et mitrales ont été remplacées par des valves mécaniques. Il n'a pas eu de complications postopératoires et a été renvoyé à la maison le 22e jour après l'opération sans embolie apparente. Il n'a pas eu de récidive depuis plus de deux ans après l'opération.",
+        "gold_summary": "Un homme de 59 ans atteint de diabète de type 1 a présenté une insuffisance cardiaque. L'échocardiographie a montré de grandes végétations sur les valves mitrale et aortique. La culture bactérienne sanguine était positive pour Staphylococcus warneri, un membre de la famille des staphylocoques coagulase-négatifs (CoNS). Il a été diagnostiqué avec une endocardite valvulaire native (NVE) induite par les bactéries résidentes et a finalement subi un double remplacement valvulaire. Rétrospectivement, de légères anomalies des données de laboratoire et une perte de poids débutant quatre mois auparavant ont peut-être été des signes de NVE. Il n'avait pas d'antécédents de thérapies immunosuppressives ou d'implantation de dispositifs médicaux.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 59 ans était très malade du cœur. Son cœur avait des petites choses qui ne vont pas sur les portes du cœur. Ces petites choses venaient de petites bêtes dans son sang. Le docteur a donné des médicaments pour tuer ces bêtes. Après, il a fait une opération pour changer deux portes du cœur. Avant d’être très malade, il avait perdu du poids et ses analyses montraient que quelque chose n’allait pas. Il n’avait pas d’autres maladies ni d’appareils dans son corps. Maintenant, il va mieux.",
+            "B2": "**Résumé adapté pour un adolescent de 14 ans :**\n\nUn homme japonais de 59 ans, qui avait un diabète de type 1 depuis longtemps, est tombé malade avec un problème sérieux au cœur appelé insuffisance cardiaque. Cela signifie que son cœur ne pompait pas le sang correctement. Des examens spéciaux, appelés échocardiographies, ont montré qu'il y avait de grosses \"végétations\" sur deux valves importantes de son cœur (les valves mitrale et aortique). Ces végétations sont comme des amas de bactéries et de cellules qui s'accrochent aux valves.\n\nDes analyses de son sang ont révélé la présence d’une bactérie appelée Staphylococcus warneri. Cette bactérie fait partie d’un groupe appelé staphylocoques coagulase-négatifs, qui vivent normalement sur la peau mais peuvent parfois causer des infections graves. Les médecins ont donc diagnostiqué une infection des valves du cœur, appelée endocardite valvulaire native (NVE), qui n’était pas liée à une opération ou à un appareil médical implanté.\n\nEn regardant en arrière, ils ont remarqué que cet homme avait perdu du poids et avait des résultats de laboratoire légèrement anormaux plusieurs mois avant que ses symptômes graves n’apparaissent. Ces signes auraient pu indiquer que l’infection commençait déjà. Finalement, il a dû subir une opération pour remplacer les deux valves malades par des valves mécaniques. Après l’opération, il s’est bien rétabli et n’a plus eu de problème depuis plus de deux ans.\n\nCe cas montre que même des bactéries qui vivent normalement sur la peau peuvent causer des infections graves du cœur, surtout chez des personnes avec des problèmes comme le diabète. Il est important de surveiller les signes subtils pour agir rapidement.",
+            "B3": "Résumé détaillé et structuré\n\nContexte  \nUn homme japonais de 59 ans, souffrant depuis 28 ans d’un diabète de type 1 mal contrôlé malgré une insulinothérapie intensive, a présenté une insuffisance cardiaque aiguë. Il avait une régurgitation aortique sévère chronique asymptomatique diagnostiquée 16 ans auparavant, mais sans suivi régulier ni intervention chirurgicale. Son indice de masse corporelle était faible (18,4 kg/m²), et il présentait une sécrétion d’insuline quasi nulle, entraînant des fluctuations importantes de sa glycémie.\n\nPrincipales observations  \nÀ son admission en urgence, le patient souffrait de difficultés respiratoires, d’une fièvre élevée (>38 °C), d’une saturation en oxygène basse (80 %) et d’une hypertension artérielle avec tachycardie. L’examen physique a révélé un souffle cardiaque systolique, sans signes périphériques classiques d’endocardite infectieuse (tels que nodules d’Osler, lésions de Janeway ou pétéchies). Les analyses sanguines montraient une leucocytose importante (20 800/μL) et une élévation marquée de la protéine C-réactive (6,06 mg/dL), témoignant d’une inflammation aiguë. La radiographie thoracique indiquait une congestion pulmonaire et une cardiomégalie, tandis que l’électrocardiogramme montrait une élévation du segment ST sans anomalie de la contractilité cardiaque à l’échocardiographie.\n\nUne échocardiographie transthoracique puis transœsophagienne a mis en évidence une régurgitation sévère des valves aortique et mitrale, ainsi que de grandes végétations mobiles sur la valve mitrale (16,5 × 6 mm) et la valve aortique (11,2 × 5 mm). Ces images étaient fortement évocatrices d’une endocardite valvulaire native (NVE). Les cultures sanguines réalisées à l’admission ont isolé Staphylococcus warneri, un staphylocoque coagulase-négatif, confirmant l’infection bactérienne.\n\nUne analyse rétrospective des données cliniques a montré que, dès quatre mois avant l’admission, le patient présentait une légère augmentation des globules blancs, une baisse progressive de l’albumine et de l’hémoglobine, ainsi qu’une perte de poids de 4 kg, sans autres symptômes ni anomalies détectées lors d’examens complémentaires. Ces signes précurseurs non spécifiques suggéraient une infection chronique évolutive.\n\nInterprétation clinique  \nLe diagnostic d’endocardite valvulaire native à Staphylococcus warneri a été posé chez un patient sans antécédent d’immunosuppression ni d’implantation de dispositifs médicaux, ce qui est rare car ces bactéries sont généralement associées aux infections nosocomiales ou liées aux prothèses. La présence de végétations volumineuses sur les valves, associée à une insuffisance cardiaque aiguë, justifiait habituellement une intervention chirurgicale urgente. Cependant, compte tenu de l’amélioration clinique sous traitement antibiotique adapté et du risque élevé lié à son diabète mal contrôlé, une chirurgie élective a été programmée.\n\nProchaines étapes  \nAprès quatre semaines d’antibiothérapie ciblée, le patient a subi un double remplacement valvulaire aortique et mitral. L’examen peropératoire a confirmé une valve aortique bicuspide sans abcès, avec exérèse complète des végétations. La convalescence a été favorable, sans complications ni embolies, et le patient est resté sans récidive d’endocardite plus de deux ans après l’intervention.\n\nCe cas souligne l’importance de surveiller attentivement les signes biologiques subtils et les pertes de poids inexpliquées chez les patients à risque, afin de détecter précocement une endocardite, même en l’absence de symptômes classiques ou d’antécédents d’immunodépression ou de dispositifs implantés."
+        }
+    },
+    {
+        "article": "Il s’agit d’un patient de 8 mois né d’une mère para 3. La mère avait un suivi ANC, mais il était irrégulier, et il était dans un centre de santé rural avec une mauvaise installation où elle ne pouvait pas obtenir d’échographie obstétricale. L’accouchement a eu lieu à la maison avec une sage-femme traditionnelle. Après l’accouchement, les parents ont remarqué un gonflement sur la partie occipitale de la tête. Il a progressivement augmenté de taille pour atteindre la taille actuelle. Les parents sont allés au centre de santé, où ils ont été dirigés vers l’hôpital principal, qui les a ensuite dirigés vers notre centre. Le gonflement n’avait pas de décharge, et le patient n’avait pas de fièvre, de vomissements, de difficultés à téter, de pleurs aigus, de mouvements corporels anormaux ou de léthargie. Après l’examen du patient, il y avait un gonflement de 40 cm sur 35 cm, transilluminant la lumière, masse occipitale tendre, sur la zone des sinus frontaux. Il y avait un défaut osseux palpable à la base du sac. Les fontanelles antérieure et postérieure n’étaient pas ouvertes. Le bébé était joueur, alerte, bougeant toutes les extrémités, suçant bien, et avait des signes vitaux stables. Le patient a ensuite été examiné avec un CBC, un groupe sanguin, des tests de fonction rénale et hépatique qui étaient dans la plage normale, et une IRM du cerveau a révélé un énorme sac occipital hypointense et hyperintense T2 avec de multiples flux vides montrant le torcula, le sinus sagittal supérieur et le sinus transverse, et une partie du lobe occipital droit du cerveau avec un défaut osseux à la base du sac. Après avoir obtenu un consentement écrit informé, le patient a été placé sur la table d’opération avec la tête suspendue au-delà du bord de la table d’opération sur le côté de la machine d’anesthésie, avec un anesthésiste tenant la tête et le sac suspendu au-delà de la table, et a été intubé avec la première tentative. Après intubation, le patient a été placé en position couchée sur le côté avec l’aide d’une étrière Mayfield. Les cheveux ont été rasés et nettoyés avec de l’eau et du savon, et un assistant tenant la masse avec une main gantée stérile, la peau a ensuite été nettoyée et drapée. Initialement, nous avons fait une incision cutanée transversale, drainée le LCR, et le sac s’est effondré. Puis, le tissu cérébral dysplasique a été réséqué, et le sinus veineux, la tumeur, le torcula et d’autres tissus cérébraux viables ont été réduits doucement au crâne. La dure-mère a été disséquée, taillée, taillée et fermée comme une primaire étanche. Nous n’avons pas recommandé une cranioplastie dans un cas d’encéphalocèle occipital géant avec un risque élevé d’hydrocéphalie postopératoire ; par conséquent, nous n’avons pas fermé le défaut osseux. Après cela, la peau a été taillée et fermée en deux couches. Après l’opération, le patient est resté dans le service de neurochirurgie pendant sept jours sans hydrocéphalie et sans déficit neurologique. Le patient est ensuite suivi dans une clinique externe toutes les deux semaines sans complications chirurgicales ou neurologiques.\n",
+        "gold_summary": "Il s'agit d'un cas d'un nourrisson de 8 mois né d'une mère qui n'avait pas bénéficié de soins anténataux réguliers. Après que le bébé ait présenté une masse postérieure de la tête progressivement croissante, qui est cystique, transilluminante, tendre et de 40 cm x 35 cm, l'imagerie a démontré un petit tissu cérébral principalement partie du lobe occipital droit avec la majeure partie du sac occupé par le liquide cérébrospinal. La réparation a été effectuée et le tissu cérébral dysplasique a été résectionné, puis le tissu cérébral sain et les sinus durales ont été réduits au crâne, puis le patient est resté à l'hôpital et a été suivi de près pour l'hydrocéphalie pendant sept jours et a été renvoyé sans hydrocéphalie et sans déficit neurologique.\n",
+        "synthetic_summary": {
+            "B1": "Un bébé de 8 mois avait un gros bouton mou sur sa tête. Ce bouton était rempli d’eau et un peu mou. Le docteur a regardé avec une machine spéciale. Il a vu que dans ce bouton, il y avait un peu de cerveau et beaucoup d’eau.\n\nLe docteur a fait une opération pour enlever la partie qui ne va pas. Il a remis doucement le reste du cerveau à sa place. Après l’opération, le bébé est resté à l’hôpital pour être sûr qu’il allait bien. Le bébé est rentré à la maison sans problème. Il bouge bien et est en bonne santé.",
+            "B2": "Voici un résumé simple et clair pour un élève de 14 ans :\n\nCe cas parle d’un bébé de 8 mois dont la maman n’a pas eu de suivi médical régulier pendant la grossesse. Après la naissance, les parents ont remarqué un gros gonflement à l’arrière de la tête du bébé. Ce gonflement était rempli de liquide, doux au toucher, et mesurait environ 40 cm sur 35 cm. Une analyse avec une machine spéciale (IRM) a montré que ce sac contenait surtout du liquide cérébral, mais aussi une petite partie du cerveau, surtout dans la zone appelée le lobe occipital droit.\n\nLes médecins ont fait une opération pour enlever le tissu cérébral qui n’était pas normal et remettre doucement le reste du cerveau et des veines importantes à leur place dans le crâne. Ils ont fermé la peau sans réparer l’os à cause des risques. Après l’opération, le bébé est resté à l’hôpital pendant une semaine. Pendant ce temps, les médecins ont vérifié qu’il n’y avait pas de problème avec l’accumulation de liquide dans le cerveau (appelée hydrocéphalie). Le bébé est sorti de l’hôpital en bonne santé, sans problème neurologique, et il est suivi régulièrement pour s’assurer que tout va bien.",
+            "B3": "Résumé détaillé et structuré pour un public non médical éduqué\n\nContexte  \nIl s’agit d’un nourrisson de 8 mois, né d’une mère ayant bénéficié d’un suivi prénatal irrégulier dans un centre rural dépourvu d’échographie obstétricale. L’accouchement s’est déroulé à domicile avec l’aide d’une sage-femme traditionnelle. Peu après la naissance, les parents ont observé un gonflement important à l’arrière de la tête de l’enfant, qui a progressivement augmenté de taille.\n\nPrincipales observations  \nÀ l’examen clinique, une masse occipitale (à l’arrière du crâne) de grande taille (40 cm sur 35 cm), molle, sensible au toucher, et laissant passer la lumière (transilluminante) a été constatée. Un défaut osseux palpable était présent à la base de cette masse. Le bébé ne présentait aucun signe d’infection, de troubles neurologiques ou de difficultés d’alimentation, et ses fontanelles (espaces mous entre les os du crâne) étaient fermées. Les analyses sanguines et les fonctions rénales et hépatiques étaient normales. L’imagerie par résonance magnétique (IRM) a révélé que la masse contenait principalement du liquide cérébrospinal, avec une petite portion de tissu cérébral dysplasique (anormal) provenant du lobe occipital droit, ainsi que des structures veineuses importantes (sinus veineux) impliquées dans le drainage sanguin du cerveau.\n\nInterprétation clinique  \nLe diagnostic principal est une encéphalocèle occipitale géante, une malformation congénitale caractérisée par une protrusion de tissu cérébral et de liquide à travers un défaut osseux du crâne. La présence de tissu cérébral dysplasique et de sinus veineux dans le sac rend la prise en charge chirurgicale délicate, notamment en raison du risque de complications telles que l’hydrocéphalie (accumulation excessive de liquide dans le cerveau) après l’opération.\n\nProchaines étapes et prise en charge  \nAprès obtention du consentement éclairé des parents, une intervention chirurgicale a été réalisée sous anesthésie générale. Le patient a été positionné de manière à permettre une manipulation sécurisée de la masse. La chirurgie a consisté à drainer le liquide cérébrospinal contenu dans le sac, à réséquer (retirer) le tissu cérébral dysplasique non fonctionnel, puis à repositionner délicatement le tissu cérébral sain et les sinus veineux dans le crâne. La dure-mère (membrane protectrice du cerveau) a été soigneusement refermée de manière étanche. En raison du risque élevé d’hydrocéphalie postopératoire, le défaut osseux n’a pas été fermé par une cranioplastie (reconstruction osseuse). La peau a été refermée en deux couches. Le patient est resté hospitalisé en neurochirurgie pendant sept jours, période durant laquelle aucun signe d’hydrocéphalie ni de déficit neurologique n’a été observé. Par la suite, il a été suivi régulièrement en consultation externe toutes les deux semaines, sans complications chirurgicales ni neurologiques.\n\nConclusion  \nCe cas illustre la prise en charge réussie d’une encéphalocèle occipitale géante chez un nourrisson, malgré un suivi prénatal limité et une présentation tardive. La chirurgie a permis de retirer le tissu cérébral anormal tout en préservant les structures vitales, avec un bon résultat neurologique à court terme. Un suivi attentif reste essentiel pour détecter toute complication ultérieure."
+        }
+    },
+    {
+        "article": "Cet homme de 53 ans a présenté initialement une gêne thoracique aiguë comme symptôme isolé. Il était auparavant un non-fumeur actif, en forme et en bonne santé, sans antécédents médicaux ni familiaux.\n\nLors de l'examen, il avait des bruits cardiaques normaux sans murmures. Sa pression veineuse jugulaire n'était pas élevée. Sa poitrine était claire et il n'y avait pas d'œdème de la cheville.\n\nSa tension artérielle était de 98/78 mm Hg et son rythme cardiaque de 62 battements par minute. Sa saturation en oxygène était de 100 % en air ambiant et son rythme respiratoire de 16 respirations par minute. Il était apyrexial avec une température de 37,1 °C.\n\n\nEnquêtes\n\nL'ECG a montré une hypertrophie ventriculaire gauche et des inversions de l'onde T généralisées. Les taux sériques de troponine cardiaque de haute sensibilité (hs-cTnI) sont passés de 28 ng/L (0 heure) à 77 ng/L (6 heures) (limite supérieure de référence pour cet essai : 34 ng/L). Il a été traité par une double antiagrégation plaquettaire pour un diagnostic de travail d'infarctus du myocarde sans élévation du segment ST.\n\nL'angiographie coronarienne CT a montré une plaque calcifiée dans deux artères coronaires. L'angiographie conventionnelle n'a confirmé aucune limitation du flux. L'échocardiographie transthoracique a montré une HVI modérée avec une obstruction significative du tractus de sortie. Il y avait une légère insuffisance systolique avec une akinésie localisée de la paroi inférieure. Une IRM cardiaque a été demandée en tant qu'investigation ambulatoire.\n\nUn mois plus tard, le patient a été réadmis avec de nouveaux malaises thoraciques. Quatre jours de télémétrie n’ont révélé aucune dysrythmie au cours de ces épisodes de malaise. L’ECG n’a montré aucune modification dynamique. Il y avait une augmentation statique de faible niveau de hs-cTnI à 37 ng/L, 30 ng/L et 33 ng/L, respectivement, prise quotidiennement en raison de multiples épisodes intermittents de douleurs thoraciques sur plusieurs jours. Le taux de protéine C réactive était inférieur à 3 mg/L et il était apyremique.\n\nL'IRM cardiaque a montré une hypertrophie ventriculaire gauche concentrique, une zone d'oedème inféro-latéral probable et un schéma inhabituel d'amélioration tardive du gadolinium (LGE) principalement endocardique avec une amélioration de la paroi médiane du septum et une amélioration sous-endocardique diffuse. Il avait des volumes de LV normaux et une fraction d'éjection (61%), mais une masse élevée à 221 g (101 g/m2) compatible avec une hypertrophie. Comme sa tension artérielle restait normale, nous étions réticents à attribuer l'hypertrophie ventriculaire gauche à une cardiopathie hypertensive.\n\n\nDiagnostic différentiel\n\nEn raison de la nature inhabituelle de l'affaire, elle a été discutée lors de la réunion de l'équipe multidisciplinaire régionale. L'IRM ne semblait pas être classique, ni de myocardite, ni d'amyloïde, mais le résultat de la réunion avait suggéré de dépister une cardiomyopathie amyloïde et une maladie d'Anderson-Fabry.\n\nLe taux d'alpha galactosidase était normal, ce qui excluait effectivement la maladie de Fabry.\n\nLa chaîne légère libre de sérum (SF) a montré une augmentation de la SF Kappa à 253,20 mg/L (plage de référence : 3,3-19,4) avec une normale de la SF Lambda 9,6 mg/L (plage de référence : 5,7-26,3). Le rapport kappa/lambda était de 26,375 (plage de référence : 0,26-1,65).\n\nL'aspirat de moelle osseuse a montré des particules largement masquées par des dépôts extracellulaires protéiniques bleus, nuageux et amorphes. Ces dépôts étaient teintés en rose saumon par la coloration au rouge Congo. Lorsqu'ils ont été visualisés au microscope à lumière polarisée, ils ont présenté une biréfringence verte caractéristique, compatible avec une accumulation d'amyloïdes. Il y avait un léger excès de cellules plasmatiques, insuffisant pour diagnostiquer une dyscrasie plasmatique.\n\nLa coloration de l'aspirat de la bourse graisseuse au rouge Congo n'a pas fourni de preuves convaincantes de la présence de dépôts amyloïdes.\n\nUne tomodensitométrie de l'abdomen et du bassin ne révélait rien d'autre qui puisse expliquer son amyloïdose. Les tests de dépistage de l'hépatite B, de l'hépatite C et du VIH étaient négatifs. L'électrophorèse du sérum ne révélait aucune bande monoclonale anormale et les immunoglobulines étaient normales.\n\n\nTraitement\n\nLe patient a été référé au National Amyloidosis Centre à Londres où le diagnostic a été confirmé. Sur leur recommandation, l'équipe d'hématologie locale a supervisé l'administration de chimiothérapie pour l'amylose primaire AL avec implication cardiaque. Il a reçu un cycle de 21 jours de VCD (bortezomib, cyclophosphamide et dexaméthasone).\n\nDes médicaments de soutien supplémentaires ont été fournis, notamment la doxycycline, l'aciclovir et l'allopurinol pour les 2 premiers cycles de chimiothérapie.\n\n\nRésultat et suivi\n\nLe suivi à 1 an du diagnostic a montré que le patient restait stable, que sa douleur thoracique avait complètement disparu et qu'il ne présentait toujours aucun symptôme d'insuffisance cardiaque.\n\nCependant, lorsque la pandémie de COVID-19 a frappé le pays, ses cliniciens du Centre national d'amylose ont arrêté sa chimiothérapie, compte tenu de ses bons progrès avec le traitement et des risques associés de COVID-19.\n\nDeux mois plus tard, il a présenté un autre épisode de douleurs thoraciques et une augmentation modérée de la hs-cTnI. Sa chimiothérapie a donc été réintroduite et ses douleurs thoraciques ont ensuite disparu.",
+        "gold_summary": "Un homme de 53 ans s'est présenté à un hôpital général de district avec des douleurs thoraciques, des modifications de l'ECG et une légère augmentation de la troponine cardiaque de haute sensibilité. Il n'y avait aucun symptôme d'insuffisance cardiaque. L'angiographie coronarienne par TDM a révélé une maladie calcifiante modérée et l'angiographie conventionnelle n'a confirmé aucune limitation du flux. L'échocardiographie a montré une hypertrophie ventriculaire gauche (HVG). Sa tension artérielle est restée normale tout au long de son admission. Le centre tertiaire a qualifié cela d'événement de « rupture de plaque », mais l'HVG est restée inexpliquée. L'IRM cardiaque a montré un modèle inhabituel de rehaussement tardif du gadolinium, qui n'était pas classique de l'amyloïde. Cependant, une augmentation de la chaîne légère kappa libre sérique ainsi que le dépôt d'amyloïde sur son aspirât de moelle osseuse ont confirmé le diagnostic d'amyloïdose primaire AL avec implication cardiaque. Le patient a ensuite suivi une chimiothérapie et est resté stable à 1 an de suivi.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 53 ans avait mal au cœur. Les docteurs ont fait des examens. Son cœur était un peu plus gros que d’habitude. Son cœur ne battait pas trop vite et sa tension était normale.\n\nLes docteurs ont cherché pourquoi son cœur était gros. Ils ont trouvé des petites choses bizarres dans son sang et dans un petit bout de son os. Ces choses s’appellent amyloïde. C’est une sorte de poussière qui ne doit pas être là.\n\nLe monsieur a pris des médicaments très forts pour enlever cette poussière. Après un an, il allait mieux. Il n’avait plus mal au cœur et il était stable. Les docteurs continuent de bien s’occuper de lui.",
+            "B2": "Un homme de 53 ans est venu à l’hôpital à cause de douleurs au niveau de la poitrine. Son électrocardiogramme (ECG), qui enregistre l’activité électrique du cœur, montrait des signes anormaux. De plus, un test sanguin a révélé une légère augmentation d’une protéine appelée troponine, qui indique souvent un problème au cœur. Malgré ces signes, il n’avait pas de symptômes d’insuffisance cardiaque, c’est-à-dire que son cœur fonctionnait encore assez bien.\n\nPour mieux comprendre ce qui se passait, les médecins ont fait plusieurs examens. Une angiographie par scanner a montré des plaques calcifiées dans ses artères coronaires, mais sans bloquer le flux du sang. Une échographie du cœur a révélé que la paroi du ventricule gauche, la partie principale du cœur qui pompe le sang, était plus épaisse que la normale. Sa tension artérielle est restée normale pendant tout le temps.\n\nUne IRM cardiaque, un examen qui donne des images précises du cœur, a montré un motif inhabituel qui ne correspondait pas aux maladies cardiaques classiques, comme l’amylose (une maladie où des protéines anormales s’accumulent dans les tissus). Cependant, des analyses sanguines ont trouvé une augmentation d’une protéine appelée chaîne légère kappa libre. En plus, un prélèvement de moelle osseuse a montré des dépôts d’amyloïde, confirmant que le patient avait une amyloïdose primaire AL, une maladie où des protéines anormales s’accumulent dans le cœur et peuvent le rendre malade.\n\nLe patient a alors reçu une chimiothérapie, un traitement pour combattre cette maladie. Un an après, il allait bien, ses douleurs avaient disparu et son cœur fonctionnait toujours correctement. Ce cas montre l’importance de faire plusieurs examens pour trouver la vraie cause d’un problème cardiaque quand les signes ne sont pas habituels.",
+            "B3": "Résumé détaillé et structuré pour un public adulte non spécialiste\n\n**Contexte**  \nUn homme de 53 ans, auparavant en bonne santé sans antécédents médicaux ni familiaux notables, s’est présenté à l’hôpital avec une douleur thoracique aiguë isolée. À l’examen clinique, ses paramètres vitaux étaient stables, sans signes d’insuffisance cardiaque ni anomalies respiratoires. Son électrocardiogramme (ECG) a révélé une hypertrophie ventriculaire gauche (HVG) et des anomalies de l’onde T, tandis que les taux de troponine cardiaque de haute sensibilité, un marqueur de lésion cardiaque, étaient légèrement élevés.\n\n**Principales observations**  \n- L’angiographie coronarienne par scanner a montré des plaques calcifiées dans deux artères coronaires, sans obstruction significative confirmée par l’angiographie conventionnelle.  \n- L’échocardiographie a confirmé une hypertrophie modérée du ventricule gauche avec une obstruction importante du tractus de sortie, mais la fonction systolique était légèrement altérée localement.  \n- Une IRM cardiaque a mis en évidence une hypertrophie concentrique du ventricule gauche, une zone probable d’œdème (inflammation) dans la paroi inféro-latérale, ainsi qu’un schéma atypique de rehaussement tardif du gadolinium (un agent de contraste), principalement dans la couche interne du muscle cardiaque.  \n- La tension artérielle du patient est restée normale, ce qui rend improbable une cause hypertensive pour l’hypertrophie.\n\n**Interprétation clinique et diagnostic différentiel**  \nFace à ces résultats inhabituels, une réunion multidisciplinaire a été organisée. L’IRM ne correspondait pas aux images typiques de myocardite (inflammation du muscle cardiaque) ni d’amyloïdose cardiaque classique. Un dépistage a été réalisé pour la maladie d’Anderson-Fabry (une maladie génétique rare) et la cardiomyopathie amyloïde. Le test enzymatique a exclu la maladie de Fabry.  \n\nCependant, une analyse sanguine a montré une augmentation très marquée des chaînes légères kappa libres, protéines anormales produites par certaines cellules immunitaires. L’aspiration de moelle osseuse a révélé des dépôts extracellulaires compatibles avec de l’amyloïde, une protéine anormale qui peut s’accumuler dans les tissus. Ces dépôts ont été confirmés par une coloration spécifique (rouge Congo) et une biréfringence caractéristique au microscope polarisant.  \n\nCes éléments ont permis de poser le diagnostic d’amyloïdose primaire de type AL (impliquant des chaînes légères d’immunoglobulines) avec atteinte cardiaque, malgré l’absence de signes classiques d’une maladie plasmatique sévère.\n\n**Traitement**  \nLe patient a été adressé à un centre spécialisé en amyloïdose où le diagnostic a été confirmé. Il a reçu une chimiothérapie adaptée, combinant bortezomib, cyclophosphamide et dexaméthasone, visant à réduire la production des protéines amyloïdes. Un traitement de soutien incluant des antibiotiques et des médicaments antiviraux et anti-inflammatoires a également été administré.  \n\n**Résultats et suivi**  \nUn an après le diagnostic, le patient était stable, sans douleur thoracique ni signes d’insuffisance cardiaque. Pendant la pandémie de COVID-19, la chimiothérapie a été temporairement arrêtée en raison de son bon état et des risques infectieux. Cependant, à la reprise de douleurs thoraciques et d’une nouvelle élévation modérée de la troponine, le traitement a été réintroduit, ce qui a permis la disparition des symptômes.\n\n---\n\nCe cas illustre la complexité du diagnostic d’amyloïdose cardiaque, une maladie rare où des protéines anormales s’accumulent dans le cœur, provoquant une hypertrophie et des symptômes parfois trompeurs. Une prise en charge spécialisée et un suivi rigoureux sont essentiels pour stabiliser la maladie et améliorer la qualité de vie du patient."
+        }
+    },
+    {
+        "article": "Une femme de 58 ans s'est présentée au service des urgences avec un antécédent de dyspnée qui s'aggravait depuis 6 mois. Au cours des 10 jours précédents, ses symptômes s'étaient gravement aggravés, accompagnés d'un léger inconfort thoracique et d'un gonflement des jambes bilatérales. Ses antécédents médicaux comprenaient l'asthme et l'hypertension. À son arrivée, elle a été trouvée hypoxémique avec une saturation en oxygène de 74 %, qui est passée à 94 % avec 5 litres d'oxygène supplémentaire. L'examen physique a révélé des crépitations inspiratoires bilatérales et un œdème pitting dans les membres inférieurs.\n\nLes examens de laboratoire ont révélé un taux élevé de NT-proBNP (peptide natriurétique cérébral) de 2110 ng/mL (intervalle <125 ng/mL) et des taux normaux de troponine. L'angiographie thoracique par tomodensitométrie (CT) a révélé des infiltrats modérés bilatéraux de verre dépoli, un tronc de l'artère pulmonaire (PA) élargi et une dilatation de l'oreillette droite (RA) et du ventricule droit (RV) sans preuve d'embolie pulmonaire. L'échocardiographie transthoracique (TTE) a montré une fraction d'éjection ventriculaire gauche (LVEF) de 75 % à 80 %, une dilatation modérée de la RA et de la RV, un aplati systolique et diastolique du septum intervéculaire, une fonction systolique réduite du RV et une pression systolique de la PA estimée de 55 à 60 mm Hg. Aucun shunt intracardiaque n'a été identifié par Doppler couleur ou injection de contraste saline agitée.\n\nLe patient a été initié à la furosémide intraveineuse. La cathétérisation cardiaque droite (RHC) a été réalisée le jour suivant, tandis que le patient recevait 3 litres d'oxygène supplémentaire par canule nasale. La procédure a confirmé la PH, avec une pression artérielle pulmonaire moyenne (mPAP) de 41 mm Hg et un débit cardiaque élevé de 8,46 L/min par la méthode de Fick. Un test de vasoreactivité utilisant le protocole standard d'adénosine a confirmé que le patient n'était pas vasoreactif, indiquant que la thérapie par inhibiteur des canaux calciques ne serait pas bénéfique. Les autres investigations, y compris la numération globulaire complète, l'hormone stimulant la thyroïde, le dépistage du VIH, le dépistage des anticorps antinucléaires, le facteur rhumatoïde et les taux de thiamine, n'ont pas été remarquables. Les études d'imagerie, y compris l'angiographie par CT du thorax et de l'abdomen et l'échographie Doppler du foie, ont exclu les shunts systémiques, les malformations artério-veineuses pulmonaires et la splénomégalie. Au moment de la sortie, l'hypoxémie du patient avait été résolue par la diurèse.\n\nL'évaluation en consultation externe comprenait un test de la fonction pulmonaire qui a montré un léger défaut ventilatoire obstructif. L'étude du sommeil et l'étude de la ventilation-perfusion n'ont pas été remarquées. Comme la RHC a démontré une pression d'occlusion de l'artère pulmonaire (pression de coin) de 11 mmHg (<15 mmHg) et un gradient transpulmonaire élevé de 26 mmHg (>12 mmHg), le PH de groupe II dû à une maladie cardiaque gauche a été exclu. On lui a prescrit un inhalateur corticostéroïde et on a continué à lui administrer de la furosémide par voie orale (20 mg par jour). La thérapie spécifique à l'hypertension pulmonaire n'a pas été initiée, étant donné que son PH a été classé dans le groupe III, attribué à une maladie pulmonaire obstructive. Au cours des rendez-vous de suivi, la patiente a signalé une amélioration initiale de sa dyspnée perçue, qui s'est ensuite stabilisée. Elle est restée systématiquement dans la catégorie intermédiaire à faible risque selon l'outil d'évaluation du risque à 4 niveaux pour le suivi de l'hypertension pulmonaire.\n\nDeux ans plus tard, elle est revenue avec une dyspnée et un gonflement des jambes qui s'aggravaient après avoir arrêté la furosémide. Une nouvelle angiographie pulmonaire par TDM a révélé des résultats similaires à ceux de l'imagerie initiale, mais a également identifié une veine pulmonaire gauche anormale qui se drainait dans le tronc brachio-céphalque gauche. Une révision rétrospective de son premier scanner a confirmé l'anomalie manquée. L'EEFT a montré une EFV de 60 %, une dilatation modérée de l'AR et de la RV, une fonction systolique réduite de la RV et une pression systolique artérielle pulmonaire estimée de 50 à 55 mmHg. Contrairement à la première RHC, l'évaluation du shunt a cette fois-ci démontré une augmentation de 6 % de la saturation en oxygène entre la veine cave supérieure (VCS) et l'AR, confirmant un shunt gauche-droit. Cette divergence était due à la mesure de la saturation de la VCS obtenue de manière appropriée au-dessus du drainage de la veine cave supérieure, guidée par la connaissance de la PAPVR issue des résultats de la TDM. La fraction de shunt (Qp/Qs) a été calculée à 1,52. En conséquence, son PH a été reclassé dans le groupe I en raison d'une cardiopathie congénitale de l'adulte.\n\nLa patiente a reçu un traitement par diurétiques intraveineux. En raison de son PH modéré et de sa classification à risque intermédiaire-faible basée sur l'outil d'évaluation du risque en 4 catégories (OMS-FC III, NT-proBNP 81 pg/mL, et une distance de marche de 460 m en 6 minutes), une thérapie spécifique à la PH n'a pas été conseillée. Elle a refusé des évaluations complémentaires, y compris une imagerie par résonance magnétique cardiaque (IRM) et une orientation vers un centre de cardiologie congénitale adulte, préférant poursuivre une surveillance ambulatoire étroite.\n",
+        "gold_summary": "Nous rapportons le cas d'une femme de 58 ans qui a présenté initialement une dyspnée progressive et a été diagnostiquée avec une hypertension pulmonaire de groupe III attribuée à une maladie pulmonaire obstructive. Deux ans plus tard, elle est revenue avec des symptômes similaires après avoir arrêté la thérapie diurétique. Une évaluation plus approfondie a révélé une anomalie antérieurement non détectée de la veine pulmonaire gauche drainant dans la veine innominata gauche.\n",
+        "synthetic_summary": {
+            "B1": "Une dame avait du mal à bien respirer depuis longtemps. Les docteurs ont d'abord pensé que c’était à cause de ses poumons. \n\nAprès deux ans, elle est revenue avec les mêmes problèmes. Cette fois, les docteurs ont trouvé un petit tuyau du cœur qui n’était pas normal. \n\nCe tuyau faisait que le sang ne circulait pas bien. Les docteurs vont continuer à l’aider doucement.",
+            "B2": "Cas d'une femme de 58 ans avec essoufflement progressif\n\nUne femme de 58 ans a d'abord consulté pour un essoufflement qui s'aggravait depuis plusieurs mois. Les médecins ont pensé qu'elle avait une hypertension pulmonaire (c’est une pression trop élevée dans les artères des poumons) liée à une maladie pulmonaire obstructive, c’est-à-dire un problème qui gêne la respiration.\n\nCe qu’ils ont découvert plus tard\n\nDeux ans après, elle est revenue avec les mêmes symptômes, surtout après avoir arrêté un médicament appelé diurétique, qui aide à éliminer l’eau en excès dans le corps. Cette fois, les examens ont montré une anomalie qu’on n’avait pas vue avant : une veine pulmonaire gauche qui se vidait dans une mauvaise veine, appelée veine innominée gauche. Cette malformation a provoqué un mélange anormal du sang, ce qui a contribué à son hypertension pulmonaire.\n\nCe que cela signifie\n\nAu début, son problème respiratoire était attribué à une maladie pulmonaire, mais en réalité, elle avait aussi une malformation cardiaque congénitale (présente depuis la naissance) qui causait son hypertension pulmonaire. Cette découverte a changé la façon dont les médecins comprenaient sa maladie et son traitement.",
+            "B3": "Résumé détaillé et structuré\n\nContexte  \nUne femme de 58 ans s’est présentée aux urgences avec une dyspnée progressive sur six mois, aggravée depuis dix jours, accompagnée d’un léger inconfort thoracique et d’un œdème bilatéral des jambes. Ses antécédents médicaux incluaient de l’asthme et de l’hypertension artérielle. À l’admission, elle était hypoxémique avec une saturation en oxygène à 74 %, améliorée à 94 % sous oxygène. L’examen clinique a révélé des crépitations pulmonaires bilatérales et un œdème des membres inférieurs.\n\nPrincipales observations  \nLes analyses sanguines ont montré un taux élevé de NT-proBNP (2110 ng/mL), indiquant une surcharge cardiaque, tandis que la troponine était normale. L’angiographie thoracique par tomodensitométrie (CT) a mis en évidence des infiltrats en verre dépoli bilatéraux, une dilatation du tronc de l’artère pulmonaire, ainsi qu’une dilatation modérée de l’oreillette droite (RA) et du ventricule droit (RV), sans embolie pulmonaire. L’échocardiographie transthoracique (ETT) a confirmé une fonction ventriculaire gauche préservée (fraction d’éjection 75-80 %), une dilatation modérée du RA et du RV, un aplatissement du septum interventriculaire, une fonction systolique réduite du RV et une pression artérielle pulmonaire systolique élevée (55-60 mmHg). Aucun shunt intracardiaque n’a été détecté à l’échographie Doppler couleur ni par injection de contraste.\n\nUne cathétérisation cardiaque droite (RHC) a confirmé une hypertension pulmonaire (pression artérielle pulmonaire moyenne de 41 mmHg) avec un débit cardiaque élevé. Le test de vasoréactivité à l’adénosine était négatif, excluant l’efficacité des inhibiteurs calciques. Les examens complémentaires (bilan sanguin, dépistage infectieux et auto-immun, imagerie abdominale et hépatique) n’ont pas révélé d’autres causes. Les tests fonctionnels pulmonaires ont montré un léger trouble obstructif. L’hypertension pulmonaire a été classée en groupe III, liée à une maladie pulmonaire obstructive, et traitée par diurétiques et corticostéroïdes inhalés, sans traitement spécifique de l’hypertension pulmonaire.\n\nInterprétation clinique  \nDeux ans plus tard, après arrêt de la furosémide, la patiente a présenté une récidive des symptômes. Une nouvelle angiographie thoracique a révélé une anomalie vasculaire congénitale jusque-là méconnue : une veine pulmonaire gauche drainant anormalement dans le tronc brachio-céphalique gauche (veine innominata). La révision des images initiales a confirmé que cette malformation avait été manquée. L’échocardiographie a montré une fonction ventriculaire gauche légèrement réduite (fraction d’éjection 60 %), une dilatation modérée du RA et du RV, une fonction systolique droite altérée et une pression artérielle pulmonaire élevée. La cathétérisation cardiaque a cette fois détecté un shunt gauche-droite confirmé par une augmentation de la saturation en oxygène entre la veine cave supérieure et l’oreillette droite, avec un ratio de flux pulmonaire sur flux systémique (Qp/Qs) de 1,52. Ces résultats ont conduit à reclasser l’hypertension pulmonaire en groupe I, liée à une cardiopathie congénitale adulte.\n\nProchaines étapes  \nLa patiente a été traitée par diurétiques intraveineux. En raison de la sévérité modérée de son hypertension pulmonaire et de son risque intermédiaire-faible, aucun traitement spécifique de l’hypertension pulmonaire n’a été initié. Malgré la recommandation d’examens complémentaires, notamment une imagerie cardiaque par résonance magnétique et une consultation en cardiologie congénitale, la patiente a préféré poursuivre un suivi ambulatoire rapproché.\n\nEn résumé, ce cas illustre l’importance d’une évaluation approfondie et répétée en cas d’hypertension pulmonaire, notamment pour détecter des anomalies vasculaires congénitales pouvant être initialement méconnues et modifier la classification et la prise en charge thérapeutique."
+        }
+    },
+    {
+        "article": "Il s’agit d’un homme de 27 ans, originaire et résident de Mexico, dont les parents et trois frères sont apparemment en bonne santé. Il a reçu le vaccin BCG à la naissance, mais a présenté une réaction indésirable deux mois plus tard, avec une adénite aux deux aisselles et un défaut de cicatrisation au site d’injection du vaccin ; il a été amélioré par l’administration de rifampicine pendant huit mois, mais a conservé une cicatrice chéloïde. À neuf mois, il a développé une candidose buccale et dans la région de la couche. Bien que les deux aient régressé sous traitement, ils ont récidivé. La candidose buccale persiste à ce jour et affecte sa langue et ses gencives. À l’âge de sept ans, il a présenté une teigne du cuir chevelu, qui a été améliorée par un traitement non spécifié. Depuis l’âge de 10 ans, il a présenté une rosacée du visage, initialement avec des papules et un érythème de la peau des joues et du nez, et actuellement avec des changements chroniques. À l’âge de 15 ans, il a présenté une onychomycose, a reçu de multiples traitements antifongiques, sans amélioration et avec persistance à ce jour. Il a présenté une rosacée oculaire depuis l’enfance et souffre également d’asthme et de rhinite allergique.\n\nLes tests cutanés ont été positifs pour les acariens, les épithéliums animaux et le pollen. Des stéroïdes topiques et des bronchodilatateurs inhalés ont été administrés. En raison de la nature chronique de la candidose, une altération du système immunitaire a été considérée, une infection par le VIH a été écartée et le patient a été informé qu'il souffrait d'une maladie granulomateuse chronique (la base du diagnostic n'est pas connue). À 26 ans, il a présenté de la fièvre, une perte de poids, une asthénie, une adynamie, une hyporésie, une toux, une hémoptysie, une dyspnée et un abcès fessier. Au service des urgences, le patient était en mauvais état général, avec une malnutrition, une pâleur de la peau et des muqueuses, une détresse respiratoire, une saturation en oxygène de 87 %, une rosacée au visage, à la langue et aux muqueuses orales avec des plaques blanches, un érythème des gencives, une cicatrice de vaccination BCG de 5 cm de diamètre, une hypoventilation pulmonaire et une onychomycose des mains et des pieds.\n\nL’examen thoracique a révélé une image de pleurésie droite et de pneumonie multifocale. L’échographie du fessier a révélé un abcès profond. Les résultats de laboratoire ont révélé une anémie, une leucocytose avec neutrophilie et une élévation de la protéine C réactive. Le test de dihydrorhodamine était normal, ce qui a exclu le diagnostic précédent de maladie granulomateuse chronique. La culture de l’échantillon prélevé dans la cavité buccale et l’hémoculture ont révélé une croissance de Candida albicans ; la culture de l’expectoration a révélé une croissance de C. albicans et de C. krusei ; la culture du liquide broncho-alvéolaire était négative.\n\nLe patient a été traité par vancomycine pour l'abcès, ce qui a entraîné une amélioration. Le patient a reçu de la ceftriaxone, de la clarithromycine et du fluconazole, mais la fièvre a persisté. Une biopsie pleurale a été pratiquée, au cours de laquelle M. tuberculosis a été détecté par PCR. La phase intensive du schéma antituberculeux, ou antifimique, a été initiée avec de l'isoniazide, de la rifampicine, de la pyrazinamide et de l'étambutol, avec une amélioration adéquate. Au cours de cette hospitalisation, il a également développé un zona qui a disparu après 10 jours de valaciclovir. Actuellement, le patient termine son traitement antituberculeux.En réévaluant le cas, en raison des antécédents d'infection par le bacille de Calmette-Guérin, de tuberculose, de zona, de candidose mucocutané et de rosacée, le diagnostic a été orienté vers une augmentation de la fonction de STAT1 (figure 4). Un panel de gènes d'erreurs innées de l'immunité a été demandé par séquençage de nouvelle génération, et la variante pathogénique c.961A>G (p.Arg321Gly) a été trouvée dans le gène STAT1, associée à une augmentation de la fonction de STAT1. Ses parents et ses trois frères ne portent pas la mutation (WT/WT) du gène STAT1.\n",
+        "gold_summary": "Ce rapport concerne un patient qui a présenté une augmentation de la fonction du facteur STAT1 au cours de sa première année de vie. Il a maintenant 27 ans et a présenté une infection par le bacille de Calmette-Guérin et Mycobacterium tuberculosis, une candidose mucocutané chronique, une teigne de la tête (tinea capitis) et une rosacée faciale et oculaire. Une infection par le VIH a été écartée. Des manifestations cliniques ont fait suspecter une immunodéficience congénitale, en particulier une augmentation de la fonction ou de l'activité du STAT1. Le diagnostic a été confirmé par le séquençage de plusieurs gènes associés à des immunodéficiences congénitales. La variante pathogénique c.961A>G (p.Arg321Gly) du gène STAT1, précédemment rapportée comme une mutation augmentant la fonction, a été trouvée chez ce patient.\n",
+        "synthetic_summary": {
+            "B1": "Il y a un monsieur qui est malade depuis qu’il est bébé. Son corps a du mal à se défendre contre certains microbes. Il a eu plusieurs infections, comme des boutons sur la tête, des plaques rouges sur le visage, et des champignons dans la bouche. \n\nLes docteurs ont fait beaucoup de tests. Ils ont trouvé que son corps a un petit problème dans un gène appelé STAT1. Ce problème fait que son corps ne peut pas bien se battre contre les microbes. \n\nMaintenant, il reçoit des soins pour l’aider à aller mieux. Les docteurs surveillent bien sa santé pour qu’il soit plus fort.",
+            "B2": "**Ce qu’ils ont découvert chez le patient**\n\nCe résumé parle d’un homme de 27 ans qui a eu plusieurs problèmes de santé depuis tout petit. Il a eu une réaction grave au vaccin BCG, qui protège contre la tuberculose, avec des infections aux aisselles et une mauvaise cicatrisation. Ensuite, il a eu des infections à champignons dans la bouche et sur la peau, qui sont revenues plusieurs fois malgré les traitements. Il a aussi eu des problèmes de peau comme la teigne (une infection du cuir chevelu) et la rosacée (rougeurs sur le visage et les yeux). Il a souffert d’asthme et d’allergies aussi.\n\n**Ce que cela signifie**\n\nLes médecins ont pensé que son système immunitaire ne fonctionnait pas bien, car il avait beaucoup d’infections qui duraient longtemps. Ils ont vérifié qu’il n’avait pas le VIH, une maladie qui affaiblit aussi le système immunitaire. Plus tard, ils ont découvert qu’il avait une maladie génétique rare liée au gène STAT1. Ce gène aide normalement le corps à combattre les infections, mais chez lui, il fonctionne trop fort (on parle d’« augmentation de la fonction »). Cette anomalie cause des infections répétées et des problèmes inflammatoires.\n\n**Comment ils ont confirmé le diagnostic**\n\nPour être sûrs, les médecins ont fait un test spécial appelé séquençage génétique. Ce test regarde les gènes liés aux maladies du système immunitaire. Ils ont trouvé une mutation précise dans le gène STAT1, appelée c.961A>G (p.Arg321Gly), qui est connue pour rendre ce gène trop actif. Cette mutation n’était pas présente chez ses parents ni chez ses frères, ce qui signifie qu’elle est apparue chez lui seul.\n\n**Résumé final**\n\nEn résumé, cet homme a une maladie génétique rare qui fait que son système immunitaire ne fonctionne pas normalement. Cela explique ses infections à répétition, notamment la tuberculose, les infections à champignons et les problèmes de peau. Grâce à la découverte de cette mutation dans le gène STAT1, les médecins peuvent mieux comprendre sa maladie et adapter son traitement.",
+            "B3": "Résumé détaillé et structuré\n\nContexte  \nCe rapport décrit le cas d’un homme de 27 ans présentant une augmentation de la fonction du facteur de transcription STAT1, une protéine impliquée dans la régulation de la réponse immunitaire. Dès sa première année de vie, ce patient a manifesté des infections récurrentes et chroniques, notamment une réaction anormale au vaccin BCG (utilisé contre la tuberculose), avec une adénite (inflammation des ganglions lymphatiques) et un défaut de cicatrisation. Il a également souffert d’une candidose mucocutanée persistante (infection fongique affectant la bouche et la peau), d’une teigne du cuir chevelu (infection fongique), ainsi que d’une rosacée chronique touchant le visage et les yeux.\n\nPrincipales observations  \nAu cours de son évolution clinique, le patient a présenté plusieurs infections sévères, dont une tuberculose active confirmée par PCR sur biopsie pleurale, ainsi qu’un zona. Les examens ont exclu une infection par le VIH. Les analyses immunologiques initiales avaient suggéré une maladie granulomateuse chronique, mais ce diagnostic a été écarté grâce à un test fonctionnel normal (test de dihydrorhodamine). Les cultures ont révélé la présence de Candida albicans et Candida krusei dans plusieurs prélèvements. Le patient a reçu des traitements antifongiques, antibiotiques et antituberculeux adaptés, avec une amélioration progressive.\n\nInterprétation clinique  \nDevant le tableau clinique associant des infections mycobactériennes, fongiques mucocutanées persistantes, et des manifestations inflammatoires chroniques (rosacée), une immunodéficience congénitale liée à une hyperactivation de STAT1 a été suspectée. Cette hypothèse a été confirmée par un séquençage génétique ciblé, qui a identifié une mutation pathogénique spécifique (c.961A>G, p.Arg321Gly) dans le gène STAT1. Cette variante est connue pour augmenter la fonction de STAT1, entraînant une dysrégulation immunitaire qui favorise les infections chroniques et les troubles inflammatoires observés chez ce patient. Les membres de sa famille proche ne portent pas cette mutation, suggérant une mutation de novo (apparue spontanément).\n\nProchaines étapes  \nLe patient poursuit actuellement son traitement antituberculeux et bénéficie d’une prise en charge adaptée à son immunodéficience. La reconnaissance de cette mutation permet d’orienter la surveillance clinique, d’adapter les traitements antimicrobiens et d’envisager un suivi spécialisé en immunologie. Ce cas illustre l’importance de considérer des causes génétiques rares dans les infections chroniques et récurrentes, notamment lorsque les diagnostics classiques sont exclus. Une prise en charge multidisciplinaire est essentielle pour optimiser la qualité de vie et prévenir les complications."
+        }
+    },
+    {
+        "article": "La patiente est une fille de 6 ans issue d'une famille d'agriculteurs dans une région non haute altitude. Elle a présenté une cyanose modérée des lèvres à la naissance et a été initialement diagnostiquée comme souffrant d'une cardiopathie congénitale. En raison de la cyanose progressive et de la dyspnée, la patiente a été amenée à notre clinique externe pour un diagnostic et un traitement ultérieurs. Elle a connu une croissance et un développement normaux sans retards physiques ou intellectuels importants. La famille a déclaré qu'elle était sujette à des pneumonies et qu'elle toussait fréquemment depuis sa naissance. L'examen physique a révélé des bruits cardiaques importants, des doigts clubbés et une cyanose des lèvres. L'électrocardiographie a montré un rythme sinusal avec une hypertrophie biventriculaire et une déviation de l'axe droit. L'échocardiographie transthoracique a révélé une hypertrophie importante des deux ventricules et de l'oreillette gauche, avec un écho absent entre la paroi gauche de l'aorte ascendante et la paroi droite de la principale artère pulmonaire (MPA), qui mesurait environ 18 mm. Il y avait un segment étroit dans l'isthme de l'arc aortique, mesurant environ 4 mm, et une interruption de l'arc aortique distale à l'artère sous-clavière gauche (LSA). L'artère pulmonaire droite (RPA) est issue de l'aorte ascendante, tandis que l'artère pulmonaire gauche (LPA) provient du tronc pulmonaire. Entre l'aorte descendante et l'artère pulmonaire gauche, il y avait un PDA proéminent d'un diamètre d'environ 6 mm. Les septes atrio-ventriculaires et ventriculaires étaient intacts, la fonction valvulaire était normale, et les origines des artères coronaires étaient normales. L'hypertension pulmonaire était de 50 mm Hg. La patiente n'a pas pris de traitement antihypertensif pulmonaire avant la chirurgie. Par la suite, la patiente a subi une angiographie par CT, qui a confirmé les résultats de l'échocardiographie. La reconstruction en 3 dimensions a clairement montré un APW de type I, un IAA de type A et un PDA. Quatre branches artérielles ont également été visualisées, à savoir l'artère carotide commune droite (RCCA), l'artère carotide commune gauche (LCCA), l'artère sous-clavière droite anormale (ARSA), et l'artère sous-clavière gauche, qui toutes sont issues de l'extrémité proximale de l'arc aortique interrompu.\n\nSur la base de l'historique médical du patient et des examens, un diagnostic définitif de syndrome de Berry a été établi, et une intervention chirurgicale a été indiquée. La famille du patient a demandé une intervention chirurgicale. Une approche standard de mi-sternotomie a été réalisée, révélant de nombreux vaisseaux collatéraux de l'artère pulmonaire principale. Au cours de la réparation de l'arc aortique interrompu, une arrêt circulatoire hypothermique conventionnelle profonde et une perfusion cérébrale sélective ont été utilisées. Tout d'abord, le canal artériel a été disséqué distalement et ligaturé, suivi d'une excision du tissu du canal. L'arc aortique et l'aorte descendante ont été soigneusement mobilisés, et une anastomose end-to-side a été réalisée entre l'aorte descendante et l'arc aortique. La paroi antérieure a été renforcée à l'aide d'un patch péricardique. Après la correction de l'IAA, le RPA a été déconnecté. L'APW a été observée, et le défaut était situé à environ 1 cm de l'annulus de la valve aortique. L'origine des artères coronaires était normale. Le long du bord de l'APW, l'aorte et le MPA ont été séparés, tandis que le RPA a été anastomosé en bout-à-bout au MPA. Un patch péricardique bovin a été utilisé, et l'incision dans l'aorte a été fermée avec des sutures prolène 6-0 de manière continue. L'échocardiographie transœsophagienne intraopérative a confirmé un flux continu à travers l'arc aortique et aucune dérivation entre le MPA et l'aorte. Le patient a reçu un traitement supplémentaire en unité de soins intensifs post-opératoire et a été transféré dans une salle de soins ordinaires après 5 jours. L'hypertension pulmonaire a été réduite à 26 mm Hg après la chirurgie et aucun médicament contre l'hypertension pulmonaire n'a été nécessaire. Le patient n'a pas eu besoin de soutien hémodynamique après la chirurgie. Une évaluation réussie a été réalisée, et le patient a été renvoyé 7 jours plus tard.\n",
+        "gold_summary": "Inquiétudes des patients : Dans cet article, nous rapportons le cas d'une fille de 6 ans atteinte du syndrome de Berry qui présentait des symptômes ischémiques et hypoxiques importants.\n\nDiagnostics : Sur la base des antécédents médicaux du patient et des examens, un diagnostic définitif du syndrome de Berry a été établi.\n\nInterventions : Elle a subi un traitement chirurgical en 1 étape et a été déchargée avec succès. Le processus chirurgical visait à préserver le potentiel de croissance de l'aorte et des artères pulmonaires tout en assurant un écoulement ventriculaire gauche non obstrué et la continuité de l'arc aortique, en évitant toute dérivation entre les principales artères pulmonaires.\n\nRésultats : L'échocardiographie transœsophagienne intraopératoire a confirmé un flux continu à travers l'arc aortique et l'absence de dérivation entre le MPA et l'aorte.\n",
+        "synthetic_summary": {
+            "B1": "Il y a une petite fille de 6 ans. Elle avait un problème avec son cœur depuis qu'elle est née. Ses lèvres étaient un peu bleues.\n\nLes docteurs ont fait beaucoup de tests. Ils ont trouvé un problème spécial appelé syndrome de Berry.\n\nLes docteurs ont fait une opération pour aider son cœur. Ils ont réparé les tuyaux du cœur pour que le sang puisse bien passer.\n\nAprès l'opération, tout allait bien. Le sang circulait bien dans son cœur. La petite fille a pu rentrer chez elle, toute contente et en bonne santé.",
+            "B2": "**Ce qu’ils ont découvert chez la patiente**  \nCet article parle d’une fille de 6 ans qui souffrait d’un problème cardiaque rare appelé syndrome de Berry. Ce syndrome provoquait chez elle des difficultés à respirer et un manque d’oxygène dans le sang, ce qui expliquait la couleur bleutée de ses lèvres (cyanose) et sa fatigue.\n\n**Comment ils ont confirmé le diagnostic**  \nLes médecins ont utilisé plusieurs examens, comme une échographie du cœur et un scanner, pour bien comprendre son cœur et ses gros vaisseaux. Ils ont vu que certaines artères importantes étaient mal formées ou interrompues, ce qui empêchait le sang de circuler normalement.\n\n**Le traitement réalisé**  \nPour réparer ces problèmes, la patiente a subi une opération chirurgicale complexe. Les chirurgiens ont reconnecté les artères principales du cœur et ont réparé les parties abîmées en utilisant des tissus spéciaux. Leur but était de permettre au cœur et aux artères de grandir normalement et d’assurer un bon passage du sang sans fuite ni obstruction.\n\n**Les résultats après l’opération**  \nPendant l’opération, une échographie a montré que le sang circulait bien dans les artères réparées, sans fuite entre elles. Après la chirurgie, la pression dans les poumons de la patiente a diminué, elle n’a plus eu besoin de médicaments pour cela, et elle a pu quitter l’hôpital en bonne santé quelques jours plus tard.\n\nEn résumé, grâce à un diagnostic précis et une opération bien faite, cette jeune fille a pu être soignée efficacement pour un problème cardiaque grave.",
+            "B3": "Résumé détaillé et structuré du cas clinique\n\nContexte  \nNous présentons le cas d’une fille de 6 ans issue d’une famille d’agriculteurs, présentant depuis la naissance une cyanose modérée des lèvres et une dyspnée progressive. Initialement suspectée d’une cardiopathie congénitale, elle a également souffert de pneumonies fréquentes et d’une toux chronique. Son développement physique et intellectuel était par ailleurs normal. L’examen clinique a révélé des signes cardiaques importants, notamment des doigts clubbés (une déformation des extrémités des doigts liée à une hypoxie chronique) et une cyanose persistante.\n\nPrincipales observations diagnostiques  \nLes examens complémentaires ont montré un rythme cardiaque sinusal avec hypertrophie des deux ventricules et déviation de l’axe droit à l’électrocardiogramme. L’échocardiographie transthoracique a mis en évidence une hypertrophie marquée des ventricules et de l’oreillette gauche, une interruption de l’arc aortique distal à l’artère sous-clavière gauche, un pont vasculaire anormal entre l’aorte ascendante et l’artère pulmonaire principale (appelé communication aorto-pulmonaire ou APW), ainsi qu’un canal artériel persistant (PDA). L’artère pulmonaire droite provenait directement de l’aorte ascendante, tandis que l’artère pulmonaire gauche émanait du tronc pulmonaire. L’hypertension pulmonaire était modérée, évaluée à 50 mm Hg. Une angiographie par tomodensitométrie a confirmé ces anomalies et a permis une reconstruction tridimensionnelle précise, identifiant un APW de type I, une interruption de l’arc aortique (IAA) de type A, et un PDA. Quatre branches artérielles principales étaient visualisées, dont une artère sous-clavière droite anormale.\n\nInterprétation clinique  \nL’ensemble des données cliniques et radiologiques a permis d’établir un diagnostic définitif de syndrome de Berry, une malformation cardiaque congénitale rare caractérisée par la combinaison d’une communication aorto-pulmonaire, d’une interruption de l’arc aortique et d’un canal artériel persistant. Cette pathologie entraîne une hypoxie chronique et une surcharge cardiaque, expliquant la cyanose et les symptômes respiratoires de la patiente.\n\nIntervention chirurgicale  \nUne intervention chirurgicale en une seule étape a été réalisée via une sternotomie médiane. La procédure a inclus la ligature et l’excision du canal artériel, la mobilisation et la reconstruction de l’arc aortique interrompu par une anastomose entre l’aorte descendante et l’arc aortique, renforcée par un patch péricardique. L’artère pulmonaire droite a été déconnectée de l’aorte et rattachée en bout-à-bout au tronc pulmonaire. La communication aorto-pulmonaire a été fermée à l’aide d’un patch péricardique bovin. La chirurgie a été réalisée sous arrêt circulatoire hypothermique profond avec perfusion cérébrale sélective pour protéger le cerveau.\n\nRésultats postopératoires  \nL’échocardiographie transœsophagienne réalisée en peropératoire a confirmé un flux sanguin continu et non obstrué à travers l’arc aortique, sans dérivation entre l’aorte et l’artère pulmonaire principale. La patiente a été prise en charge en unité de soins intensifs, puis transférée en service conventionnel après cinq jours. L’hypertension pulmonaire a diminué à 26 mm Hg sans nécessité de traitement médicamenteux spécifique. Aucun soutien hémodynamique n’a été requis après la chirurgie. La patiente a été jugée stable et a pu quitter l’hôpital une semaine après l’intervention.\n\nProchaines étapes  \nUn suivi cardiologique régulier est recommandé pour surveiller la croissance et la fonction des structures cardiaques réparées, ainsi que pour détecter toute complication tardive. Cette prise en charge vise à assurer une qualité de vie optimale et un développement normal à long terme."
+        }
+    },
+    {
+        "article": "En décembre 2020, un homme de 43 ans ayant des antécédents d'hépatite B de 9 ans a subi une échographie lors d'un examen médical de routine à l'hôpital populaire de Ruian, qui a révélé plusieurs lésions hypoéchogènes dans son foie.\n\nLes tests de laboratoire ont montré une légère élévation des taux d'alpha-foetoprotéine (AFP) (AFP : 32,9 ng/ml), tandis que les autres marqueurs tumoraux tels que les antigènes glucidiques 19-9, 125 et 153, et l'antigène carcino-embryonnaire étaient dans les limites normales. Les lésions apparaissaient comme de faible densité avec des marges peu claires sur l'imagerie par tomographie par ordinateur (CT) et présentaient une intensification centripète de la phase artérielle à la phase portale sur l'imagerie par tomographie par ordinateur à contraste dynamique. Les tailles des lésions variaient, la plus grande étant une lésion de forme irrégulière mesurant 4,1 × 4,3 cm de diamètre.\n\nEn ce qui concerne l'imagerie par résonance magnétique (IRM) à contraste dynamique, la plus grande lésion a présenté une amélioration périphérique immédiate en forme d'anneau, suivie d'une amélioration continue progressive et d'une cicatrice d'amélioration centrale. Pendant ce temps, les lésions plus petites ont présenté une amélioration en forme d'anneau avec une amélioration centripète progressive pendant les phases veineuse portale et retardée. Pour un examen plus approfondi, le patient a été envoyé à l'hôpital Huashan de Shanghai le 30 décembre 2020.\n\nLe patient a rapidement subi une tomographie par émission de positrons (TEP) avec [18F]-FDG, qui n’a révélé aucune absorption évidente. Cependant, la TEP avec [11C] acétate a indiqué une faible absorption uniquement pour la plus grande lésion située dans le lobe VII (valeur de l’absorption standard maximale [VASmax] = 4,21, rapport tumeur-arrière-plan [RTAB] = 1,45), tandis que les autres plus petites n’ont pas montré d’absorption. Fait intéressant, la TEP avec [68Ga] Ga-FAPI-04 a non seulement montré une forte absorption élevée pour la plus grande lésion (VASmax = 1,94, RTAB = 3,08), mais aussi pour les plus petites lésions intrahépatiques (VASmax = 1,47, RTAB = 2,33).\n\nSur la base des examens existants, un diagnostic préliminaire de carcinome hépatocellulaire (CHC) a été établi. Le patient a ensuite bénéficié d'une hépatectomie partielle en 6 jours, et le diagnostic a été confirmé par une analyse pathologique. La plus grande lésion située dans le segment VII a été identifiée comme un CHC solitaire, tandis que les autres lésions plus petites ont été diagnostiquées comme des hémangioendothéliomes épithéliaux hépatiques (HEHE).\n\nMicroscopiquement, de plus petites lésions sont apparues sous forme de nids et de cordes de cellules endothéliales épithélioïdes, avec des lumières intracytoplasmiques réparties dans tout le stroma myxo-hyalinique. La coloration CD31 et ERG1 était fortement positive, confirmant le diagnostic de lésion hépatique de type HEHE (Fig. 4A-E). La lésion hépatique du segment VII a présenté une positivité pour Hep1 en immunohistochimie, confirmant le diagnostic de HCC.\n\nLe patient a été libéré le jour postopératoire 9 et aucune récidive n'a été détectée lors de son suivi jusqu'à présent.\n",
+        "gold_summary": "Nous présentons un cas de carcinome hépatocellulaire synchrone (CHC) et de HEHE chez un patient chinois de 43 ans. Des lésions hépatiques hypoéchogènes multiples ont été décrites, mais aucun résultat d'imagerie spécifique n'a été détecté sur une tomographie par ordinateur (CT) ou une imagerie par résonance magnétique (MRI) améliorée par contraste. Le patient a ensuite subi une TEP/CT avec [18F]-FDG, une TEP/CT avec acétate [11C] et une TEP/CT avec [68Ga]Ga-FAPI-04. Les lésions de HEHE n'ont pas présenté de prise sur les images TEP/CT avec 18F-FDG et 11C-acétate, mais ont présenté une visualisation claire dans la TEP/CT avec [68Ga]Ga-FAPI-04. La plus grande lésion située dans le segment VII a finalement été diagnostiquée comme CHC, tandis que les autres plus petites ont été diagnostiquées comme HEHE, ce qui a été confirmé par une coloration immunohistochimique pour CD31. À notre connaissance, seuls 2 cas ont été rapportés dans la littérature mondiale, et le premier cas a utilisé à la fois l'acétate [11C] et le [68Ga]Ga-FAPI-04 TEP/CT au lieu du 18F-FDG TEP/CT.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 43 ans avait des petits problèmes dans son foie. Les docteurs ont fait des images pour regarder dedans. Ils ont vu plusieurs petites taches.\n\nIls ont utilisé des machines spéciales pour mieux voir ces taches. Une machine montrait bien la grosse tache, mais pas les petites. Une autre machine montrait toutes les taches très bien.\n\nAprès, les docteurs ont enlevé la grosse tache avec une opération. Ils ont regardé les taches au microscope. La grosse tache était un type de maladie du foie. Les petites taches étaient un autre type, moins dangereux.\n\nLe monsieur va bien maintenant. C’est une histoire très rare que les docteurs ont racontée.",
+            "B2": "### Ce qu'ils ont trouvé\n\nUn homme de 43 ans, qui avait une hépatite B depuis plusieurs années, a découvert plusieurs petites zones anormales dans son foie lors d’un examen médical. Ces zones ne se voyaient pas clairement avec les examens habituels comme la tomographie par ordinateur (CT) ou l’imagerie par résonance magnétique (IRM) avec injection de produit de contraste.\n\nPour mieux comprendre, les médecins ont utilisé différents types de tomographies par émission de positrons (TEP). La TEP avec un produit appelé [18F]-FDG, souvent utilisée pour détecter des cancers, n’a rien montré d’important. Ensuite, une TEP avec un autre produit, l’acétate [11C], a détecté faiblement la plus grande lésion, mais pas les plus petites. Enfin, une TEP avec un produit spécial nommé [68Ga]Ga-FAPI-04 a montré clairement toutes les lésions, grandes et petites.\n\n### Ce que cela signifie\n\nAprès une opération pour enlever une partie du foie, les médecins ont analysé les tissus. Ils ont découvert que la plus grande lésion était un carcinome hépatocellulaire (CHC), c’est-à-dire un cancer du foie courant. Les autres petites lésions étaient des hémangioendothéliomes épithéliaux hépatiques (HEHE), une tumeur rare qui vient des cellules des vaisseaux sanguins dans le foie.\n\nPour confirmer ces diagnostics, ils ont utilisé une technique appelée coloration immunohistochimique, qui permet de repérer certaines protéines spécifiques dans les cellules. Cette analyse a confirmé la nature différente des lésions.\n\n### Pourquoi ce cas est important\n\nCe cas est très rare car il montre la présence en même temps de deux types de tumeurs différentes dans le foie. De plus, c’est la première fois qu’on utilise à la fois la TEP avec acétate [11C] et la TEP avec [68Ga]Ga-FAPI-04 pour détecter ces lésions, alors que la TEP classique avec [18F]-FDG n’était pas efficace. Cela peut aider les médecins à mieux diagnostiquer ce genre de cas à l’avenir.\n\nLe patient a bien récupéré après l’opération et, jusqu’à maintenant, aucune nouvelle tumeur n’a été détectée.",
+            "B3": "Résumé détaillé et structuré pour un public adulte non spécialiste\n\n**Contexte**  \nUn homme chinois de 43 ans, suivi depuis neuf ans pour une hépatite B, a découvert lors d’un examen médical de routine plusieurs lésions inhabituelles dans son foie. Ces anomalies ont été détectées initialement par échographie, puis explorées par des techniques d’imagerie plus avancées, afin de déterminer leur nature exacte.\n\n**Principales observations**  \nLes examens d’imagerie ont montré plusieurs lésions hépatiques hypoéchogènes (zones moins denses à l’échographie) de tailles variables, dont la plus grande mesurait environ 4 cm. Ces lésions présentaient des caractéristiques particulières à la tomodensitométrie (scanner) et à l’imagerie par résonance magnétique (IRM) avec injection de produit de contraste, notamment une prise de contraste progressive et des formes en anneau, mais sans spécificité suffisante pour un diagnostic clair.\n\nLes analyses sanguines ont révélé une légère augmentation de l’alpha-foetoprotéine (AFP), un marqueur souvent associé au cancer du foie, tandis que d’autres marqueurs tumoraux étaient normaux.\n\nPour mieux caractériser ces lésions, le patient a subi plusieurs examens par tomographie par émission de positons (TEP) utilisant différents traceurs radioactifs : le [18F]-FDG, l’acétate [11C] et le [68Ga]Ga-FAPI-04. La TEP avec [18F]-FDG, souvent utilisée pour détecter les cancers, n’a pas montré d’absorption significative. La TEP avec acétate [11C] a révélé une faible absorption uniquement dans la plus grande lésion, tandis que la TEP avec [68Ga]Ga-FAPI-04 a mis en évidence une forte absorption non seulement dans la plus grande lésion, mais aussi dans les plus petites.\n\nAprès résection partielle du foie, l’analyse microscopique a confirmé que la plus grande lésion était un carcinome hépatocellulaire (CHC), un type fréquent de cancer du foie. Les autres lésions plus petites ont été identifiées comme des hémangioendothéliomes épithéliaux hépatiques (HEHE), une tumeur vasculaire rare. Ce diagnostic a été confirmé par des techniques d’immunohistochimie, notamment la coloration positive pour CD31 et ERG1, qui sont des marqueurs des cellules endothéliales (cellules tapissant les vaisseaux sanguins).\n\n**Interprétation clinique**  \nCe cas illustre la coexistence rare et simultanée de deux types de lésions hépatiques : un carcinome hépatocellulaire et plusieurs hémangioendothéliomes épithéliaux. La difficulté diagnostique a été accentuée par le fait que les techniques d’imagerie classiques et la TEP avec [18F]-FDG n’ont pas détecté toutes les lésions. En revanche, la TEP avec [68Ga]Ga-FAPI-04 s’est révélée particulièrement sensible pour visualiser ces lésions vasculaires rares, ce qui pourrait représenter un progrès important dans le diagnostic de ce type de tumeurs.\n\nÀ notre connaissance, seuls deux cas similaires ont été rapportés dans la littérature mondiale, et ce cas est le premier à utiliser simultanément la TEP avec acétate [11C] et avec [68Ga]Ga-FAPI-04 pour différencier ces lésions.\n\n**Prochaines étapes et suivi**  \nLe patient a été opéré avec succès, la partie du foie contenant les lésions a été retirée, et il a été libéré neuf jours après l’intervention. Jusqu’à présent, aucun signe de récidive n’a été observé lors du suivi post-opératoire.\n\nCe cas souligne l’importance d’utiliser plusieurs techniques d’imagerie complémentaires pour diagnostiquer précisément des lésions hépatiques complexes et rares, ce qui permet d’adapter au mieux la prise en charge thérapeutique."
+        }
+    },
+    {
+        "article": "Un homme de 65 ans a présenté une enflure et une déformation boutonnière du doigt médian droit six mois après un accident de moto survenu le 1er janvier 2023. Au début, il a géré la blessure avec des analgésiques et n'a pas consulté un médecin. Après six mois de symptômes persistants, y compris une incapacité à étendre complètement le doigt et un œdème visible, il a demandé un traitement.\n\nConstatations cliniques\nL'inspection de la main droite a révélé la présence d'une déformation avec oedème. L'amplitude active du mouvement (ROM) était altérée dans l'articulation PIP du troisième doigt de la main droite. L'amplitude active du mouvement (ROM) de l'articulation PIP du troisième doigt de la main droite était de 45 à 110 degrés. L'amplitude passive du mouvement (ROM) de l'articulation PIP du troisième doigt de la main droite était normale.\n\nÉvaluation diagnostique\nNous avons effectué une radiographie de la main droite AP/Lateral qui a montré qu'il n'y avait aucune anomalie osseuse et nous avons diagnostiqué une déformation des tissus mous due à une blessure centrale par glissement.\n\nTechnique chirurgicale\nUne reconstruction du défaut de glissement central utilisant le côté ulnaire du tendon flexor digitorum superficiel a été réalisée. Sous anesthésie, le patient a été positionné en décubitus dorsal avec un garrot appliqué au bras supérieur. Une incision médiolatérale a été pratiquée sur le côté ulnaire de la phalange médiane droite, centrée sur l'articulation PIP. L'incision s'est étendue dorsalement de manière oblique. Une incision transversale a été pratiquée sur le pli de flexion de l'articulation MCP, juste proximal à la poulie A1. La procédure implique l'identification et la protection du faisceau neurovasculaire digital ulnaire, l'exposition du glissement central et du tendon extenseur à l'articulation PIPJ, les lambeaux dorsaux de pleine épaisseur sont élevés. Le tissu cicatriciel et le tissu pseudo-tendineux sont identifiés et excisés. Le glissement central ne peut pas être réparé en premier, donc le glissement ulnaire du tendon FDS est utilisé pour la reconstruction. Le faisceau neurovasculaire ulnaire est mobilisé pour visualiser l'insertion périostale de la poulie A3.\n\nLe tendon extenseur est mobilisé et tenolysé, suivi d'une incision de la capsule dorsale de l'articulation PIP et de l'ablation du tissu interposé. L'insertion périostée de la poulie A3 est incisée longitudinalement, et la capsule palmaire de l'articulation PIP est incisée longitudinalement. Le slip ulnaire du tendon FDS est identifié et une suture monofilament non résorbable 2-0 est placée autour de lui. Une incision transversale est faite au pli de flexion de l'articulation MCP, proximal à la poulie A1, révélant la gaine du tendon fléchisseur. La gaine du tendon et la poulie A1 sont incisées longitudinalement. Le tendon FDS est identifié. Le slip ulnaire du tendon FDS est isolé et tranché pour libérer le slip ulnaire, en évitant l'enchevêtrement ou la capture du slip radial. La suture 2-0 qui a été placée autour du slip ulnaire au niveau de l'articulation PIP est utilisée pour libérer le slip distal du tendon FDS et délivrer le slip ulnaire du tendon FDS distalement.\n\nUne perceuse de 2,8 mm est utilisée pour créer un tunnel osseux verticalement orienté dorsal à volar. Un élévateur est placé entre le tendon du flexor digitorum profundus, la plaque volar et l'aspect volar de la base de la phalange médiane, protégeant les structures anatomiques volar. Le tendon FDS passe à travers le tunnel tout en maintenant l'articulation PIP en extension et en position réduite. Le tendon FDS passe à travers la section proximale intacte du tendon central et du tendon extenseur. Un tisserand de tendon complète un tissage de Pulvertaft, confirmant la tension appropriée avec l'articulation PIPJ en position réduite, en pleine extension. Une suture non absorbable 3-0 sécurise le tissage de Pulvertaft. Les marges de la reconstruction de la capsule et du tunnel central sont approximées à travers l'articulation PIP, et les adhérences sont libérées et les bandes latérales mobilisées.\n\nLa posture générale, la stabilité et le mouvement avec la tenodèse sont évalués. Toutes les incisions sont abondamment irriguées. Le garrot est dégonflé et l'hémostase est obtenue. Le remplissage capillaire de tous les doigts est évalué. La peau est fermée à l'aide de points de suture horizontaux. Un pansement stérile est appliqué avec une attelle d'extension de l'articulation PIP appropriée pour permettre un mouvement précoce de l'articulation DIP et de l'articulation MCP.\n\nSuivi et résultats\nLe premier suivi a été effectué 4 jours plus tard pour le traitement de la plaie. Le patient a reçu du méloxicam oral à 7,5 mg deux fois par jour et de la doxycycline à 100 mg deux fois par jour pendant 3 jours. Le deuxième suivi a été effectué 3 jours plus tard pour le traitement de la plaie. Après 2 semaines, nous avons enlevé la plaque arrière, retiré la suture externe et commencé l'exercice de ROM active et passive. Après 3 semaines, la plaie a été guérie et nous avons constaté que la ROM de l'articulation PIP était de 0 à 90 degrés. Et après un mois, le patient est venu avec une ROM active et passive de l'articulation PIP de 0 à 100 degrés, et un résultat fonctionnel amélioré. Après 7 semaines de réadaptation physique, les patients sont déjà de retour au travail avec une ROM active et passive de l'articulation PIP de 0 à 110 degrés. La fonction de la main droite du patient est évaluée avec le score DASH, qui s'améliore significativement de 50 à 4,2.\n",
+        "gold_summary": "Un patient de 65 ans a présenté un gonflement et une déformation boutonnière du troisième doigt de la main droite. Le patient était tombé précédemment d'une moto et son pouce droit avait été écrasé par une moto six mois auparavant. Après l'incident, le pouce droit du patient ne pouvait plus être complètement étendu. La main droite du patient a présenté un oedème avec flexion de l'articulation interphalangienne (PIP) et hyperextension de l'articulation interphalangienne distale (DIP). L'amplitude de mouvement (ROM) du pouce droit était de 45 à 110 degrés. La radiographie de la main droite AP/oblique ne montrait aucune ossification de la déformation. Le patient a subi une reconstruction du défaut de glissement central en utilisant le côté ulnaire partiel du tendon superficiel du flexor digitorum. Une attelle de prolongation du pouce droit a été appliquée pendant 2 semaines. L'exercice actif et passif de l'amplitude de mouvement du pouce droit a commencé 2 semaines après l'attelle de prolongation du pouce droit. L'amplitude de mouvement du pouce droit (0 à 90 degrés) a été significativement améliorée 1 mois après l'intervention chirurgicale. L'amplitude de mouvement du pouce droit a été rétablie à la normale 2 mois après l'intervention chirurgicale. La fonction de la main droite du patient a été évaluée avec le score DASH, qui s'est amélioré significativement de 50 à 4,2.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 65 ans s’est fait mal au doigt de la main droite. Son doigt était tout gonflé et ne pouvait pas bien bouger. Il ne pouvait pas tendre son doigt comme avant.\n\nLe docteur a regardé son doigt avec une photo spéciale. Il a vu que les os allaient bien. Mais les tissus autour du doigt étaient cassés.\n\nLe docteur a fait une petite opération pour réparer le doigt. Il a utilisé une partie d’un tendon pour aider à remettre le doigt droit.\n\nAprès l’opération, le monsieur a porté une attelle pour tenir son doigt droit. Puis, il a commencé à bouger doucement son doigt.\n\nPetit à petit, son doigt a mieux bougé. Après deux mois, il pouvait bouger son doigt normalement. Sa main allait beaucoup mieux et il pouvait faire ses activités.",
+            "B2": "Un homme de 65 ans a eu un accident de moto qui a blessé son doigt du milieu de la main droite. Six mois après, son doigt était gonflé et déformé, avec une difficulté à l’étendre complètement. Cette déformation s’appelle une « boutonnière », où l’articulation du milieu du doigt (appelée PIP) est pliée, tandis que l’extrémité du doigt est trop tendue.\n\nÀ l’examen, le mouvement actif de cette articulation PIP allait de 45 à 110 degrés, ce qui est limité. Une radiographie a montré que les os étaient normaux, mais que les tissus mous autour du tendon extenseur du doigt étaient abîmés à cause de la blessure.\n\nPour réparer cela, les médecins ont fait une opération pour reconstruire le tendon endommagé. Ils ont utilisé une partie d’un autre tendon appelé « tendon fléchisseur superficiel » pour remplacer la partie cassée. Après l’opération, une attelle a été mise pour garder le doigt en extension pendant deux semaines.\n\nDeux semaines plus tard, le patient a commencé des exercices pour bouger son doigt activement et passivement, c’est-à-dire en bougeant lui-même et en aidant son doigt à bouger. Un mois après la chirurgie, le mouvement du doigt s’était beaucoup amélioré, allant de 0 à 90 degrés. Après environ deux mois, le mouvement était presque normal, entre 0 et 110 degrés.\n\nEnfin, la fonction de la main a été mesurée avec un test appelé score DASH, qui évalue la capacité à utiliser la main. Ce score est passé de 50 (beaucoup de difficulté) à 4,2 (presque normal), montrant une très bonne récupération. En résumé, grâce à la chirurgie et à la rééducation, le patient a retrouvé un bon mouvement et une bonne fonction de son doigt blessé.",
+            "B3": "Résumé détaillé et structuré destiné à un adulte éduqué non-médecin\n\nContexte  \nUn homme de 65 ans a présenté une enflure et une déformation dite « boutonnière » du troisième doigt (doigt médian) de la main droite, survenue six mois après un accident de moto. Lors de cet accident, son doigt avait été écrasé, entraînant une incapacité à l’étendre complètement. Initialement, il n’avait pas consulté de médecin et avait seulement pris des analgésiques. Après six mois de symptômes persistants, notamment une incapacité à redresser complètement le doigt et un œdème visible, il a recherché un traitement médical.\n\nPrincipales observations cliniques  \nL’examen de la main droite a révélé un œdème associé à une déformation caractéristique avec flexion de l’articulation interphalangienne proximale (PIP) du troisième doigt et hyperextension de l’articulation interphalangienne distale (DIP). L’amplitude active de mouvement (capacité du patient à bouger son doigt lui-même) de l’articulation PIP était limitée, allant de 45 à 110 degrés, tandis que l’amplitude passive (mouvement réalisé par un examinateur) était normale. Une radiographie de la main droite n’a montré aucune anomalie osseuse, excluant une fracture ou autre lésion osseuse.\n\nInterprétation clinique  \nLe diagnostic retenu était une déformation des tissus mous liée à une lésion du glissement central du tendon extenseur du doigt, responsable de la déformation boutonnière. Cette lésion empêche le redressement complet de l’articulation PIP.\n\nTechnique chirurgicale  \nLe patient a subi une intervention chirurgicale visant à reconstruire le tendon extenseur central défectueux. Cette reconstruction a utilisé une partie spécifique (le slip ulnaire) du tendon fléchisseur superficiel des doigts (flexor digitorum superficialis, FDS) pour remplacer la portion endommagée. L’opération a été réalisée sous anesthésie avec un garrot au bras. Une incision a été pratiquée sur le côté ulnaire (côté interne) de la phalange moyenne du troisième doigt, centrée sur l’articulation PIP. Le chirurgien a soigneusement isolé et protégé les nerfs et vaisseaux sanguins digitaux, retiré le tissu cicatriciel et les tissus anormaux, puis mobilisé le tendon extenseur. Une gaine et une poulie tendineuse ont été incisées pour libérer le tendon fléchisseur superficiel, dont une portion a été détachée et tissée (technique de Pulvertaft) pour reconstruire le tendon extenseur central. Un tunnel osseux a été créé dans la phalange moyenne pour faire passer ce tendon de substitution, permettant ainsi de restaurer la fonction d’extension de l’articulation PIP. La stabilité et la tension du nouveau tendon ont été vérifiées avant la fermeture des incisions. Une attelle d’extension a été appliquée pour immobiliser l’articulation PIP en position étendue, tout en permettant un mouvement précoce des autres articulations du doigt.\n\nSuivi et résultats  \nLe patient a été revu quatre jours après l’opération pour le soin de la plaie, puis à nouveau trois jours plus tard. Il a reçu un traitement médicamenteux comprenant un anti-inflammatoire (méloxicam) et un antibiotique (doxycycline) pendant trois jours. Deux semaines après l’opération, l’attelle a été retirée et des exercices actifs et passifs de mobilisation de l’articulation PIP ont été commencés. Après trois semaines, la plaie était cicatrisée et l’amplitude de mouvement de l’articulation PIP s’était améliorée, atteignant 0 à 90 degrés. Un mois après l’intervention, la mobilité active et passive de l’articulation PIP était de 0 à 100 degrés, avec une amélioration fonctionnelle notable. Après sept semaines de rééducation, le patient avait retrouvé une amplitude de mouvement normale de 0 à 110 degrés et avait repris son activité professionnelle. L’évaluation fonctionnelle de la main droite par le score DASH (Disabilities of the Arm, Shoulder and Hand, un questionnaire mesurant la capacité fonctionnelle) a montré une amélioration majeure, passant de 50 (indiquant une incapacité importante) à 4,2 (quasi absence de handicap).\n\nConclusion  \nCette reconstruction chirurgicale du tendon extenseur central à l’aide d’un segment du tendon fléchisseur superficiel a permis de restaurer efficacement la fonction et la mobilité du doigt affecté, avec une récupération fonctionnelle quasi complète et un retour rapide aux activités quotidiennes."
+        }
+    },
+    {
+        "article": "Une femme de 26 ans a été référée par un neurologue pour une perte de vision progressive, séquentielle et bilatérale et une vision floue survenues au cours d'un mois à partir de l'œil droit et plus prononcées dans cet œil, sans mouvements oculaires douloureux. Elle avait des antécédents médicaux de syndrome cliniquement isolé impliquant la moelle épinière. Ses symptômes sensoriels avaient débuté 7 ans avant la présentation, impliquant son pied gauche et se déplaçant sur une période de plusieurs semaines pour atteindre un niveau distal à la taille. Son imagerie par résonance magnétique (IRM) du cerveau et de la moelle épinière avait révélé une lésion dans la région infratentorielle et une autre dans la moelle épinière thoracique. Les IRM de suivi ont identifié de nouvelles lésions d'amélioration temporellement distinctes aux niveaux C4, C6-C7, T2 et T7-T8. Des examens complémentaires ont révélé des résultats négatifs pour les anticorps anti-aquaporine-4 et anti-protéine des oligodendrocytes myéliniques (MOG). Elle ne recevait aucune médication au moment de la présentation et son historique de tabagisme et de consommation d'alcool était insignifiant. Ses antécédents familiaux étaient insignifiants pour les causes héréditaires de la perte de vision, y compris la LHON.\n\nL'examen neuro-ophtalmologique a révélé une acuité visuelle corrigée (AV) de 20/100 OD et 20/30-2 OS. Son AV a progressivement amélioré lors des visites de suivi. Les plaques de couleur Ishihara ont révélé qu'elle était capable de lire seulement 1 sur 17 plaques de couleur dans l'œil droit et 14 sur 17 plaques de couleur dans l'œil gauche. Il n'y avait pas de défaut pupillaire afférent relatif. La tomographie en cohérence optique (OCT) a révélé une épaisseur moyenne de la couche de fibres nerveuses rétiniennes de 83 microns OD et 93 microns OS avec un léger amincissement temporel. L'examen du fond d'œil dilaté a révélé une pâleur des deux nerfs optiques avec un rapport de la coupole au disque de 0,2.\n\nLe diagnostic différentiel pour ses symptômes visuels comprenait des neuropathies optiques bilatérales, telles que la neurite optique ou la LHON. Les carences nutritionnelles ont été exclues en raison du nombre normal de globules rouges, de B12, de folate. Elle a ensuite pris 1 250 mg de prednisone par voie orale par jour pendant 3 jours, suivis de 60 mg et d'une réduction progressive de 10 mg tous les 5 jours ; toutefois, lors de la visite de suivi, elle n'a signalé aucune amélioration de ses symptômes. Des examens complémentaires ont révélé des hyperintensités T2 modérées du côté droit du chiasma optique et trois nouvelles lésions de la substance blanche cérébrale (splenium ; 2 lésions de la substance blanche pariétale péri-ventriculaire gauche) sur l'IRM. Les résultats de l'IRM et les bandes oligoclonales détectées par ponction lombaire ont confirmé le diagnostic de la sclérose en plaque. Au cours des visites de suivi ultérieures, son test de champ visuel Humphrey a révélé des scotomes centraux bilatéraux dans les deux yeux. La nature lentement progressive, l'implication séquentielle des yeux, les scotomes centraux symétriques, les symptômes non sensibles aux stéroïdes et les hyperintensités du chiasma optique détectées par IRM étaient suggestives de la LHON. L'examen du fond d'œil dilaté a révélé une pâleur temporelle. Les tests génétiques pour les trois mutations primaires ont été négatifs ; toutefois, elle était hétérozygote pour la variante c.152A>G du gène DNAJC30 associée à la sclérose en plaque latérale. Elle a également été testée positive pour la variante c.1239C>T dans le gène UQCRC1 avec un modèle d'héritage autosomique dominant. Elle a été diagnostiquée avec le syndrome de Harding et a commencé à prendre 300 mg d'idébénone par voie orale par TDS quotidiennement, ce qui a conduit à une amélioration de ses symptômes. Son AV a progressivement amélioré au fil des visites annuelles de suivi (son dernier AV corrigé était de 20/40-2 OD et 20/20-2 OS) et les métriques et examens OCT sont restés stables avec une pâleur temporelle bilatérale. Les champs visuels et les OCT 4 ans après le suivi sont présentés.\n",
+        "gold_summary": "Nous présentons une femme de 26 ans avec une perte visuelle progressive, séquentielle, indolore, bilatérale qui ne répond pas aux stéroïdes, et deux épisodes distincts de troubles neurologiques temporaires évoquant une démyélinisation du système nerveux central. Des investigations approfondies, y compris des tests sérologiques, ont exclu d'autres causes, y compris une neuromyélite optique négative et des anticorps anti-protéine oligodendrocytaire de myéline (MOG) et des carences nutritionnelles. L'IRM a détecté des zones de démyélinisation dans la moelle épinière et le cerveau (zones infratentoriales et périventriculaires). Après une analyse génétique révélant une mutation c.152A>G (p.Tyr51Cys) au niveau du gène DNAJC30, une LHON a été suggérée. Elle a été traitée par idébenone et son acuité visuelle a été résolue à 4 ans de suivi.\n",
+        "synthetic_summary": {
+            "B1": "Une jeune femme avait de plus en plus de mal à voir avec ses deux yeux. Ça a commencé par un œil, puis l’autre. Ça ne faisait pas mal. \n\nLes docteurs ont fait beaucoup de tests pour comprendre pourquoi. Ils ont regardé son cerveau et sa moelle. Ils ont vu des zones un peu abîmées. \n\nIls ont aussi cherché si elle avait des maladies dans le sang, mais rien n’a montré. \n\nIls ont trouvé un petit changement dans ses gènes. C’est pour ça qu’elle avait du mal à voir. \n\nLes docteurs lui ont donné un médicament spécial. Avec ce médicament, elle a peu à peu mieux vu. \n\nAprès plusieurs années, sa vue s’est bien améliorée. Les docteurs sont contents car elle va mieux.",
+            "B2": "### Ce qu'ils ont trouvé\n\nUne jeune femme de 26 ans a perdu progressivement la vue dans ses deux yeux, surtout dans le droit, sans douleur. Elle avait déjà eu des problèmes nerveux dans la moelle épinière plusieurs années avant. Des examens ont montré des zones abîmées dans son cerveau et sa moelle épinière, ce qui indique une maladie qui détruit la gaine protectrice des nerfs, appelée démyélinisation. Les médecins ont cherché d’autres causes, comme des infections ou des carences en vitamines, mais rien n’a été trouvé.\n\n### Ce que cela signifie\n\nLes tests ont montré que ce n’était pas une maladie appelée neuromyélite optique ni une autre maladie liée aux anticorps. L’IRM a montré des lésions dans des zones spécifiques du cerveau et de la moelle épinière. Une analyse génétique a révélé une mutation dans un gène appelé DNAJC30, ce qui a orienté vers un diagnostic de LHON, une maladie génétique qui cause une perte de vision due à un problème dans les cellules des nerfs optiques.\n\n### Le traitement et l’évolution\n\nElle a reçu un médicament nommé idébenone, qui aide à protéger les cellules nerveuses. Après quatre ans de suivi, sa vision s’est nettement améliorée. Ce cas montre qu’une perte de vision progressive et sans douleur peut être liée à des maladies génétiques même si d’autres troubles nerveux sont présents. Un diagnostic précis et un traitement adapté peuvent améliorer les symptômes.",
+            "B3": "Résumé détaillé et structuré\n\nContexte  \nUne femme de 26 ans a présenté une perte progressive et séquentielle de la vision, touchant d’abord l’œil droit puis l’œil gauche, sans douleur lors des mouvements oculaires. Ses antécédents comprenaient un syndrome cliniquement isolé avec des symptômes sensoriels liés à des lésions démyélinisantes de la moelle épinière, identifiées par imagerie par résonance magnétique (IRM). Au moment de la consultation, elle ne prenait aucun traitement et n’avait pas d’antécédents familiaux significatifs de maladies héréditaires de la vision, notamment la neuropathie optique héréditaire de Leber (LHON).\n\nPrincipales observations  \nL’examen neuro-ophtalmologique a montré une acuité visuelle corrigée sévèrement réduite à l’œil droit (20/100) et modérément diminuée à l’œil gauche (20/30-2), avec une altération importante de la perception des couleurs à l’œil droit. La tomographie en cohérence optique (OCT) a révélé un amincissement léger mais notable de la couche des fibres nerveuses rétiniennes, plus marqué à droite. L’examen du fond d’œil a mis en évidence une pâleur bilatérale des nerfs optiques, signe d’atrophie. L’IRM cérébrale a montré des lésions démyélinisantes dans plusieurs régions, notamment le chiasma optique droit et la substance blanche périventriculaire, ainsi que dans la moelle épinière. Les examens biologiques ont exclu la présence d’anticorps anti-aquaporine-4 et anti-MOG, ainsi que des carences nutritionnelles pouvant expliquer la neuropathie optique.\n\nInterprétation clinique  \nLe tableau clinique et radiologique évoquait initialement une sclérose en plaques (SEP), confirmée par la présence de bandes oligoclonales dans le liquide céphalorachidien. Cependant, la perte visuelle progressive, bilatérale, avec scotomes centraux symétriques et absence de réponse aux corticostéroïdes, ainsi que les anomalies du chiasma optique à l’IRM, suggéraient également une neuropathie optique héréditaire de Leber (LHON). Les tests génétiques ont exclu les trois mutations primaires classiques de la LHON, mais ont identifié une variante hétérozygote c.152A>G dans le gène DNAJC30, récemment associée à une forme de LHON. Une autre mutation dans le gène UQCRC1, à transmission autosomique dominante, a aussi été détectée. Ces résultats ont conduit au diagnostic de syndrome de Harding, une forme combinée de SEP et de LHON.\n\nProchaines étapes et évolution  \nLa patiente a été traitée par idébenone, un médicament antioxydant utilisé dans la LHON, à la dose de 300 mg trois fois par jour. Ce traitement a permis une amélioration progressive de son acuité visuelle sur une période de quatre ans, avec une stabilisation des paramètres OCT et une persistance d’une pâleur temporelle bilatérale des nerfs optiques. Les champs visuels ont montré une amélioration partielle des scotomes centraux. Ce cas illustre l’importance d’une évaluation multidisciplinaire approfondie, incluant l’imagerie, la biologie et la génétique, pour différencier les neuropathies optiques démyélinisantes des neuropathies héréditaires et adapter le traitement en conséquence."
+        }
+    },
+    {
+        "article": "Nous décrivons le cas d'un patient de 18 ans atteint de DMD et en fauteuil roulant depuis l'âge de 11 ans, qui a toujours été suivi par une équipe multidisciplinaire au sein de notre établissement. Depuis l'âge de 6 ans, il a été traité par un médicament oral avec du déflazacort. Au cours de ces années, le patient a été régulièrement suivi par des pneumologues utilisant la spirométrie et par des neurologues qui ont surveillé l'évolution de la maladie neuromusculaire en termes de fonction thoraco‐abdominale et de scoliose. La capacité vitale forcée (CVF), le volume expiratoire forcé en 1 s (VEF1) et le débit expiratoire de pointe (PEF) étaient respectivement de 60 %, 70 % et 70 % des valeurs prévues (CVF, 2,24 l ; VEF1, 2,09 l ; PEF, 4,07 l). Le patient a également subi une cathétérisation cardiaque droite pour surveiller les résistances vasculaires pulmonaires avec des valeurs témoins dans la plage normale. Lorsqu'il a progressivement développé une cardiomyopathie dilatée en 2016, à l'âge de 14 ans, il a subi une implantation de LVAD HeartWare, en raison d'une insuffisance cardiaque réfractaire aiguë. L'option de transplantation cardiaque n'a pas été envisagée par les chirurgiens cardiaques pédiatriques, (i) en raison de l'urgence dans laquelle se trouvait le patient et (ii) en raison du scepticisme commun à l'égard de la transplantation cardiaque chez ces patients atteints de DMD. Le sevrage de la ventilation mécanique s'est produit de manière routinière, et aucune complication postopératoire n'a été rencontrée.\n\nAu cours des 47 mois suivants, le patient a été régulièrement suivi, et nous n'avons rapporté qu'une infection du site de sortie, traitée par antibiotiques et toilette chirurgicale, 30 mois après l'implantation du LVAD. Le débridement de la ligne de commande consistait en une incision de la peau suivant le trajet du câble, une extériorisation du câble plus proximalement, un nettoyage du trajet fistuleux et une nouvelle suture de la peau. Bien que la récupération ait été excellente, étant donné que la sortie de la ligne de commande était très proche de la plaie sternale, le patient a été suffisamment stressé psychologiquement pour demander spontanément une solution radicale au problème. La CVF, la VEMS et le PEF étaient respectivement de 1,66 l, 1,62 l et 4,41 l. Compte tenu des bonnes conditions générales du patient et de sa motivation personnelle, notre équipe multidisciplinaire a commencé à envisager une transplantation cardiaque comme option. Ainsi, le 12 février 2020, à l'âge de 18 ans, le patient a subi une transplantation cardiaque sans complications postopératoires. Le sevrage de la ventilation mécanique a eu lieu comme d'habitude une fois de plus. Le premier jour post-transplantation, il a été possible d'extuber le patient. La sortie de l'unité de soins intensifs a été possible le troisième jour postopératoire. En ce qui concerne la mobilisation, dans notre unité, les patients sont suivis par une équipe spécialisée de physiothérapeutes. Le patient a été formé par eux dès les premiers jours ; et dès qu'il a été transféré de l'unité de soins intensifs au service, la mobilisation a été commencée dès que possible. En ce qui concerne la stabilisation sternale, comme nous le faisons habituellement, nous avons suggéré d'utiliser une bande sternale en tissu. La mobilisation en fauteuil roulant a été possible le cinquième jour postopératoire. La durée totale de l'hospitalisation était de 3 semaines, le temps nécessaire pour effectuer les trois biopsies canoniques pour l'évaluation de tout rejet myocardique. Une thérapie immunosuppressive standard à trois agents a été administrée (cyclosporine, mycophenolate mofetil et stéroïdes). Au bout de 3 mois, la CVF, la VEMS et le PEF étaient inchangés par rapport à la période pré-transplantation.",
+        "gold_summary": "Nous décrivons le cas d'un patient de 18 ans, atteint de DMD et en fauteuil roulant depuis l'âge de 11 ans. Il a progressivement développé une cardiomyopathie dilatée et, en 2016, à l'âge de 14 ans, il a subi une implantation de LVAD HeartWare, en tant que traitement de destination, sans complications postopératoires. Il a été suivi pendant 47 mois consécutifs ; et 30 mois après l'implantation de LVAD, il a développé une infection du site de sortie, traitée par antibiotiques et toilette chirurgicale. À la suite de cet événement, sur la base des bonnes conditions générales du patient et de sa volonté, nous avons commencé à envisager la transplantation cardiaque comme option. Avant que le patient ne soit inscrit, il a subi un examen approfondi, et nous avons trouvé des valeurs plus élevées de capacité vitale forcée, de volume expiratoire forcé en 1 s, et de débit expiratoire de pointe, par rapport aux valeurs prévues des patients DMD du même âge. Le patient n'a ni scoliose ni besoin de ventilation mécanique non invasive, et enfin, il a toujours été traité avec des stéroïdes avec une fonction thoraco-abdominale stable au fil des ans. Conformément à ces considérations, le patient a été inscrit pour une transplantation cardiaque. Le 12 février 2020, à l'âge de 18 ans, le patient a subi une transplantation cardiaque sans complications postopératoires. La transplantation cardiaque n'est pas considérée comme une option valable pour les patients DMD, en raison du manque de disponibilité des donneurs et de la nature systémique de la maladie DMD. Considérant que ce patient avait déjà connu une complication liée au LVAD et qu'il avait une meilleure condition générale que ses pairs DMD, nous l'avons inscrit pour une transplantation cardiaque. Nous décrivons le cas d'un patient DMD qui a subi une transplantation cardiaque réussie après 47 mois d'assistance LVAD HeartWare. Le suivi de trois mois est sans incident.\n",
+        "synthetic_summary": {
+            "B1": "Il y a un garçon de 18 ans qui est en fauteuil roulant depuis qu’il a 11 ans. Son cœur est devenu très fatigué quand il avait 14 ans. Alors, les médecins lui ont mis une petite machine pour aider son cœur à battre. Cette machine a bien marché pendant presque 4 ans.\n\nUn jour, il a eu une petite infection. Les docteurs ont donné des médicaments et ont nettoyé la blessure. Après ça, le garçon voulait un autre traitement pour aller mieux. Les médecins ont décidé de lui donner un nouveau cœur.\n\nLe 12 février 2020, ils ont fait une opération pour lui mettre un nouveau cœur. Tout s’est bien passé. Le garçon a bien récupéré et il va bien trois mois après l’opération. Les docteurs sont contents car c’est rare que ça marche aussi bien.",
+            "B2": "Cas d’un jeune patient atteint de dystrophie musculaire de Duchenne (DMD)\n\nNous parlons ici d’un garçon de 18 ans qui souffre de dystrophie musculaire de Duchenne, une maladie qui affaiblit ses muscles. Il est en fauteuil roulant depuis l’âge de 11 ans. À 14 ans, son cœur a commencé à s’affaiblir sérieusement, ce qui a nécessité la pose d’un appareil appelé LVAD. Ce dispositif aide le cœur à pomper le sang quand il ne peut plus le faire seul.\n\nPendant presque 4 ans, il a été suivi régulièrement. Trente mois après la pose de cet appareil, il a eu une infection autour du câble de sortie, mais cela a été soigné avec des antibiotiques et une petite opération. Malgré cela, le patient souhaitait une solution plus durable.\n\nAprès plusieurs examens, les médecins ont constaté que ses poumons fonctionnaient mieux que ceux d’autres patients atteints de la même maladie. Il n’avait pas de scoliose (courbure de la colonne) ni besoin d’aide pour respirer. Son état général était donc assez bon.\n\nGrâce à cela et à sa motivation, l’équipe médicale a décidé de lui proposer une transplantation cardiaque, c’est-à-dire de remplacer son cœur malade par un cœur sain. Cette opération est rare chez les patients atteints de DMD, car la maladie touche tout le corps et il y a peu de cœurs disponibles.\n\nLe 12 février 2020, à 18 ans, il a subi la transplantation sans problème majeur. Après l’opération, il a été rapidement sevré de la ventilation artificielle et a pu commencer sa rééducation avec des kinésithérapeutes. Trois mois plus tard, son état était stable, sans rejet du nouveau cœur et avec une fonction pulmonaire similaire à avant la transplantation.\n\nCe cas montre qu’une transplantation cardiaque peut être une option possible pour certains patients atteints de DMD, surtout s’ils sont en bonne condition générale et bien suivis.",
+            "B3": "Résumé détaillé et structuré :\n\nContexte  \nNous présentons le cas d’un patient de 18 ans atteint de dystrophie musculaire de Duchenne (DMD), une maladie neuromusculaire progressive, qui est en fauteuil roulant depuis l’âge de 11 ans. Suivi depuis l’enfance par une équipe multidisciplinaire, il a reçu un traitement continu par déflazacort (un corticostéroïde) depuis l’âge de 6 ans. Sa fonction respiratoire a été régulièrement évaluée par spirométrie, montrant une capacité vitale forcée (CVF), un volume expiratoire maximal en 1 seconde (VEF1) et un débit expiratoire de pointe (PEF) respectivement autour de 60-70 % des valeurs attendues pour son âge. Il n’a jamais présenté de scoliose ni nécessité de ventilation mécanique non invasive.\n\nPrincipales observations  \nÀ 14 ans, le patient a développé une cardiomyopathie dilatée, une complication cardiaque grave fréquente dans la DMD, conduisant à une insuffisance cardiaque aiguë réfractaire. En raison de l’urgence et du scepticisme habituel concernant la transplantation cardiaque chez les patients DMD, une implantation d’un dispositif d’assistance ventriculaire gauche (LVAD HeartWare) a été réalisée comme traitement de destination. L’intervention s’est déroulée sans complications postopératoires majeures. Pendant les 47 mois suivants, le patient a été suivi régulièrement. Trente mois après l’implantation du LVAD, il a présenté une infection au niveau du site de sortie du câble du dispositif, traitée efficacement par antibiotiques et débridement chirurgical.\n\nInterprétation clinique  \nSuite à cette complication et compte tenu de l’état général relativement bon du patient, ainsi que de sa motivation personnelle, l’équipe multidisciplinaire a envisagé la transplantation cardiaque comme option thérapeutique. Avant l’inscription sur liste, un bilan complet a révélé que ses paramètres respiratoires (CVF, VEF1, PEF) étaient supérieurs à ceux habituellement observés chez des patients DMD du même âge. De plus, il ne présentait pas de scoliose ni de besoin en ventilation mécanique non invasive, et sa fonction thoraco-abdominale était stable, ce qui est favorable pour une transplantation. Ces éléments ont conduit à son inscription sur liste de transplantation.\n\nProchaines étapes et résultats  \nLe 12 février 2020, à 18 ans, le patient a subi une transplantation cardiaque sans complications postopératoires. Le sevrage de la ventilation mécanique a été rapide, avec extubation dès le premier jour post-opératoire et sortie de l’unité de soins intensifs au troisième jour. La mobilisation a été initiée précocement avec l’aide de physiothérapeutes spécialisés, et le patient a pu utiliser son fauteuil roulant dès le cinquième jour. La durée totale d’hospitalisation a été de trois semaines, incluant la surveillance par biopsies cardiaques pour détecter tout rejet. Une immunosuppression standard à trois agents a été mise en place. Au terme d’un suivi de trois mois, la fonction respiratoire est restée stable par rapport à la période pré-transplantation, et aucun incident n’a été rapporté.\n\nConclusion  \nLa transplantation cardiaque est rarement envisagée chez les patients atteints de DMD en raison de la nature systémique de la maladie et des difficultés liées à la disponibilité des donneurs. Cependant, ce cas illustre qu’avec une sélection rigoureuse basée sur l’état général, la fonction respiratoire et la motivation du patient, la transplantation cardiaque peut être une option viable et réussie après une période prolongée d’assistance ventriculaire mécanique. Ce suivi favorable à court terme ouvre la voie à une réflexion plus large sur la prise en charge cardiaque avancée chez certains patients DMD."
+        }
+    },
+    {
+        "article": "M. S. était un patient de 88 ans, retraité, ouvrier du bâtiment, veuf, vivant seul dans un appartement au premier étage avec des escaliers. Il n’avait qu’une fille, sa principale personne de soutien. Il n’avait pas de services d’aide à domicile avant son hospitalisation.\n\nSon historique clinique était marqué par des arthrites répétées décrites comme de la goutte, une insuffisance cardiaque sur une sténose aortique serrée qui a ensuite bénéficié d'une TAVI, une insuffisance rénale chronique modérée (clairance 45 ml/min/1,73 m2), un stenting bi-fémoral aorto-bi-fémoral, une hypertension artérielle, un accident ischémique transitoire, un tremblement essentiel et une thrombose veineuse du droit. Il n'avait pas de mauvaises habitudes ou d'allergies.\n\nLe 7 novembre, ce patient a été admis au service des urgences pour décompensation cardio-rénale consécutive à une pneumopathie. Le patient s'est rétabli avec un traitement antibiotique associé à un traitement diurétique. Après cinq jours, il a été transféré dans une unité gériatrique pour une évaluation gériatrique standardisée et pour une rééducation en raison d'un déconditionnement physique.\n\nLes premiers prélèvements sanguins du 13 novembre ont révélé un taux de calcium de 2,55 mmol/L, corrigé à 2,84 mmol/L. Il y avait une dénutrition sévère avec une dose d'albumine mesurée à 28,3 mmol/L. Une PTH a été augmentée à 94 ng/L et une 25-hydroxy-vitamine D effondrée à 15 nmol/L. Cliniquement, il ne présentait aucun signe clinique évocateur d'hypercalcémie. La radiographie thoracique ne révélait aucune anomalie. En décembre, compte tenu du soupçon d'hyperparathyroïdie secondaire due à une hypovitaminose D et non conforme aux recommandations standard, une échographie parathyroïdienne n'a révélé aucun nodule suspect. Une supplémentation en cholécalciférol a été introduite. En outre, une gestion nutritionnelle a été initiée. M. S présentait en même temps une arthrite douloureuse des genoux avec épanchement articulaire associé à un syndrome inflammatoire biologique. Une chondrocalcinose était suspectée mais le taux d'acide urique était élevé à 478 µmol/L. Une ponction a été réalisée : 920 cellules nucléées par mm3 et des cristaux d'urate sodique ont été trouvés dans le liquide articulaire. Le traitement par la colchicine et ensuite l'ajout d'allopurinol ont amélioré les symptômes. L'état cardiaque et les améliorations physiques ont permis au patient de rentrer chez lui le 2 janvier.\n\nMalheureusement, une nouvelle décompensation cardiaque a nécessité une nouvelle hospitalisation le 23 janvier. Au cours de cette hospitalisation ultérieure, les taux de calcium sanguin sont restés légèrement élevés (2,64 mmol/L) et la PTH a été significativement augmentée (191 ng/L) malgré la supplémentation en vitamine D. En mars, un échantillon d’urine de 24 heures a été collecté pour la mesure de la calciurie, qui a révélé une diminution de la concentration de calcium urinaire de 1,23 mmol/L. L’excrétion fractionnée du calcium était de 1,2 %. En raison de ces résultats inhabituels, une scintigraphie parathyroïdienne MIBI n’a révélé aucune anomalie en faveur d’un adénome ou d’une hyperplasie parathyroïdienne. En avril, une analyse génétique pour détecter la mutation inhibitrice du gène CASR codant pour le récepteur sensible au calcium (gène 3q21.1) a révélé une variante pathogène classée comme FHH de type 1 selon les directives ACMG. La famille du patient a été informée et un dépistage génétique a été organisé pour éviter des tests supplémentaires inutiles. Le patient a finalement pu rentrer chez lui. Le patient et sa famille ont donné leur consentement éclairé pour ce rapport de cas. L’approbation éthique n’a pas été requise pour ce manuscrit. Consentement pour publication de la fille du patient obtenu.",
+        "gold_summary": "Nous rapportons le diagnostic de FHH chez un patient polypathologique de 88 ans présentant une hypercalcémie découverte lors d'un contrôle pour décompensation cardiaque. Malgré une présentation clinique confuse avec des symptômes de goutte, y compris des épisodes répétés d'arthrite du genou, une hypercalcémie persistante a conduit à des investigations complémentaires. Les tests biologiques ont exclu un hyperparathyroïdisme primaire ou hyperparathyroïdisme lié à une tumeur maligne, confirmant le diagnostic de FHH par la détection d'une mutation inhibitrice dans le gène du récepteur sensible au calcium.\n",
+        "synthetic_summary": {
+            "B1": "Il y avait un monsieur très âgé qui avait un os de la cuisse un peu malade. Il avait aussi un cœur qui travaillait difficilement. Un jour, les docteurs ont vu que son corps avait trop de calcium, une chose qui aide nos os mais qui doit être juste. \n\nLes docteurs ont fait beaucoup de tests. Ils ont cherché pourquoi il avait trop de calcium. Ils ont trouvé que c’était à cause d’un petit problème dans ses gènes, comme un dessin dans son corps qui est un peu différent. Ce problème s’appelle FHH. Ce n’est pas dangereux, mais ça fait que son corps garde plus de calcium que d’habitude.\n\nLes docteurs ont expliqué tout ça à sa famille pour qu’ils comprennent bien. Le monsieur a pu rentrer chez lui, et tout le monde était content de savoir ce qui se passait.",
+            "B2": "**Ce qu’ils ont découvert**  \nUn homme de 88 ans, avec plusieurs problèmes de santé, a été hospitalisé à cause de problèmes cardiaques. Lors des examens, les médecins ont trouvé un taux de calcium un peu trop élevé dans son sang, ce qui peut être un signe de maladie. En même temps, il avait des douleurs aux genoux liées à la goutte, une maladie qui cause des inflammations et des douleurs dans les articulations.\n\n**Ce que cela signifie**  \nPour comprendre pourquoi son calcium était élevé, les médecins ont fait plusieurs tests. Ils ont d’abord vérifié s’il avait une maladie appelée hyperparathyroïdie, qui fait produire trop d’hormones parathyroïdiennes et augmente le calcium dans le sang. Mais ces tests n’ont pas montré cette maladie ni de tumeur. Ensuite, ils ont cherché une cause génétique en analysant un gène important pour contrôler le calcium dans le corps. Ils ont trouvé une mutation, c’est-à-dire un changement dans ce gène, qui explique pourquoi le calcium reste élevé. Cette maladie génétique s’appelle la « FHH » (hypercalcémie familiale bénigne), qui est une condition où le corps garde un taux de calcium un peu élevé, mais sans danger grave.\n\n**Conclusion**  \nCe cas montre que même chez une personne âgée avec plusieurs maladies, il est important de bien chercher la cause d’un taux de calcium élevé. La découverte de la mutation génétique a permis d’éviter des traitements inutiles et d’informer la famille. Cela aide à mieux comprendre la santé du patient et à mieux le soigner.",
+            "B3": "Résumé détaillé et structuré :\n\n**Contexte**  \nM. S., un homme de 88 ans avec de multiples antécédents médicaux complexes, dont une insuffisance cardiaque sur sténose aortique traitée par TAVI, une insuffisance rénale chronique modérée, une hypertension artérielle, et des épisodes répétés d’arthrite attribués à la goutte, a été hospitalisé pour une décompensation cardio-rénale liée à une pneumopathie. Son état général s’est amélioré sous traitement, mais une hypercalcémie persistante a été détectée lors des bilans sanguins.\n\n**Principales observations**  \nAu cours de son hospitalisation, M. S. présentait une hypercalcémie modérée (calcium corrigé jusqu’à 2,84 mmol/L) associée à une augmentation de la parathormone (PTH) et une carence sévère en vitamine D. L’hypercalcémie n’était pas accompagnée de signes cliniques évidents. Les investigations radiologiques et scintigraphiques n’ont pas révélé d’adénome ou d’hyperplasie parathyroïdienne. Par ailleurs, la ponction articulaire a confirmé la présence de cristaux d’urate sodique, expliquant les épisodes d’arthrite. Malgré une supplémentation en vitamine D et un traitement adapté de la goutte, la PTH restait élevée et la calciurie faible, ce qui est atypique pour un hyperparathyroïdisme primaire.\n\n**Interprétation clinique**  \nFace à cette constellation de résultats biologiques et cliniques, une hypercalcémie familiale bénigne (FHH) a été suspectée. Cette pathologie génétique rare se caractérise par une hypercalcémie modérée, une PTH élevée ou normale, et une faible excrétion urinaire de calcium, sans complications majeures. L’analyse génétique a confirmé la présence d’une mutation pathogène du gène CASR, codant pour le récepteur sensible au calcium, validant ainsi le diagnostic de FHH de type 1 selon les recommandations internationales.\n\n**Prochaines étapes**  \nLe diagnostic de FHH a permis d’éviter des investigations invasives ou des traitements inappropriés pour une hyperparathyroïdie primaire. La famille a été informée et un dépistage génétique a été proposé pour identifier d’éventuels autres membres porteurs de la mutation. Le patient a pu retourner à son domicile avec un suivi adapté, sans nécessité de traitement spécifique pour l’hypercalcémie. Ce cas illustre l’importance d’une évaluation approfondie des causes d’hypercalcémie, notamment chez les patients âgés polypathologiques, afin de poser un diagnostic précis et d’optimiser la prise en charge."
+        }
+    },
+    {
+        "article": "Une femme de 65 ans présentant une dyspnée a été admise dans un hôpital local et a été hospitalisée pour insuffisance cardiaque et pneumonie en octobre 2017. Une immunoélectrophorèse urinaire a révélé la présence de la protéine Bence Jones de type λ. Une analyse de l'urine immunoélectrophorèse a révélé une hématurie de 1,29 g/grammes de créatinine urinaire et < 1 globule rouge/champ de haute puissance. Les facteurs de complément du sérum 3 et 4 étaient normaux. Les anticorps antinucléaires, le facteur rhumatoïde et les anticorps cytoplasmiques antineutrophiles étaient négatifs. Son analyse d'urine a révélé une protéinurie de 1,29 g/grammes de créatinine urinaire et < 1 globule rouge/champ de haute puissance. La tomodensitométrie a révélé des épanchements pleuraux bilatéraux et des infiltrations pulmonaires indiquant une pneumonie dans les deux poumons. L'échocardiographie après admission a révélé les résultats suivants : diamètre de fin de diastole du ventricule gauche, 41,8 mm ; diamètre de fin de systole du ventricule gauche, 28,7 mm ; fraction d'éjection, 59,6 % ; épaisseur du septum interventriculaire, 14,8 mm ; épaisseur de la paroi postérieure du ventricule gauche, 14,5 mm ; rapport E/A, 1,14 ; et E/e' 14,75. L'épaississement étendu du ventricule gauche et du septum interventriculaire et la dysfonction diastolique (restrictive) ont été observés, et ces anomalies étaient compatibles avec une amyloïdose cardiaque. Après admission, elle a commencé un traitement avec des antimicrobiens, de la dobutamine, et une dialyse continue par hémodialyse (CHDF). Les paramètres de la CHDF étaient les suivants : débit sanguin de 60-80 ml/min, débit de dialysat de 100-300 ml/h, et débit de filtration de 100-300 ml/h. Son état général s'est stabilisé progressivement, et elle a été transférée à une hémodialyse intermittente (HD). La HD a été réalisée pendant 4 h avec un débit sanguin de 100-120 ml/min, en utilisant un dialyseur en polyéthersulfone (PES-15Eαeco, Nipro Corporation, Osaka, Japon). Cependant, elle a développé une thrombocytopénie, et des anticorps anti-héparine-facteur plaquettaire 4 (PF4) sont devenus positifs (1,1 U/mL ; valeur négative inférieure à 0,9 U/mL) le 14e jour après admission. Nous avons arrêté l'héparine en raison d'une suspicion de thrombocytopénie induite par l'héparine (TIH), et avons administré un régime de dialyse continue et un argatroban. En outre, elle a développé une hypotension intradialytique (IDH). Dans ces circonstances, il était difficile de poursuivre la HD, et nous avons donc changé la RRT en PD. Un cathéter de PD a été inséré sous anesthésie locale le 16e jour après admission. À partir du 2e jour postopératoire, une PD ambulatoire continue a été initiée, et nous avons ajusté le régime de PD en fonction du volume de la patiente. Le régime de PD a finalement été fixé à une dialyse péritonéale automatisée utilisant 4 L de tampon neutralisé à 1,35 % de glucose par dialyse péritonéale (Midpeliq 135L, Terumo Corporation, Tokyo, Japon) et une solution de 1 L de 7,5 % d'icodextrine par dialyse péritonéale (Nicopeliq, Terumo Corporation, Tokyo, Japon) par jour. L'élimination de fluide par la PD était d'environ 500 ml/jour, et nous avons pu gérer le volume de la patiente avec succès grâce à ce régime. Le volume d'urine était d'environ 1000 ml/jour avec l'administration de 160 mg/jour de furosémide, 50 mg/jour de spironolactone, et 15 mg/jour de tolvaptan, et n'a pas changé pendant l'hospitalisation, indiquant une bonne fonction rénale résiduelle. Elle a été renvoyée à la maison le 44e jour après admission. Les niveaux de BNP et de NT-proBNP étaient améliorés à 195,1 pg/mL et 12 922,0 pg/mL à la décharge, respectivement. Depuis lors, elle a été suivie en tant que patient externe, et elle continue la PD pendant 2 ans sans aucun symptôme ou complication grave. Elle a une bonne qualité de vie et aime voyager autour du Japon. Les résultats de l'échocardiographie après décharge étaient comme suit : diamètre de fin de diastole du ventricule gauche, 42,9 mm ; diamètre de fin de systole du ventricule gauche, 31,0 mm ; fraction d'éjection, 54,1 % ; épaisseur du septum interventriculaire, 16,4 mm ; épaisseur de la paroi postérieure du ventricule gauche, 11,4 mm ; rapport E/A, 0,71 ; et E/e' 8,57. Ces résultats étaient similaires à ceux pendant l'hospitalisation, bien que la dysfonction diastolique ait été légèrement améliorée.",
+        "gold_summary": "Une femme de 65 ans a été hospitalisée pour insuffisance cardiaque et pneumonie dans un hôpital voisin. Elle avait été précédemment diagnostiquée comme souffrant d'amylose à chaînes légères (AL) et traitée par mélphalan plus dexaméthasone (Mel-Dex) et lenalidomide plus dexaméthasone (Len-Dex). Elle a commencé un traitement comprenant des antimicrobiens et des diurétiques, mais sa fonction rénale s'est progressivement détériorée, et elle a été transférée dans notre hôpital pour des soins néphrologiques. Elle a été traitée par des antimicrobiens, de la noradrénaline, de la dobutamine et une hémodiafiltration continue. Son état général s'est progressivement stabilisé, et elle a été transférée à une hémodialyse intermittente (HD). Cependant, la HD a été interrompue en raison d'une hypotension intradialytique et du développement d'une thrombocytopénie induite par l'héparine. Son traitement de remplacement rénal a été transféré à une dialyse péritonéale (DP), ce qui a permis un bon contrôle du volume et une fonction cardiaque stable. Elle a été libérée et est toujours en bonne condition, sans complications graves et avec un pronostic considérablement meilleur que prévu.\n",
+        "synthetic_summary": {
+            "B1": "Une dame de 65 ans était très malade. Son cœur et ses poumons ne marchaient pas bien. Elle a été soignée à l’hôpital avec des médicaments et des machines pour l’aider à respirer et à nettoyer son sang.\n\nAu début, on a utilisé une machine spéciale pour l’aider, mais elle a eu des problèmes avec cette machine. Alors, les médecins ont changé de méthode. Ils ont mis un petit tuyau dans son ventre pour faire un autre type de soin.\n\nAvec ce nouveau soin, elle a commencé à aller mieux. Son cœur est resté stable et elle n’a pas eu de gros problèmes. Après un moment, elle est rentrée chez elle. Maintenant, elle va bien et peut faire des choses qu’elle aime, comme voyager.",
+            "B2": "Une femme de 65 ans a été hospitalisée à cause de problèmes au cœur (insuffisance cardiaque) et d’une infection des poumons (pneumonie). Elle souffrait déjà d’une maladie appelée amylose à chaînes légères, où des protéines anormales s’accumulent dans certains organes, ce qui peut les abîmer. Elle avait reçu des traitements pour cette maladie auparavant.\n\nÀ son arrivée, elle a reçu des médicaments pour combattre l’infection et aider son cœur. Mais ses reins ont commencé à mal fonctionner, ce qui a nécessité des soins spécialisés. Elle a d’abord été traitée avec une méthode appelée hémodiafiltration continue, qui aide à nettoyer le sang quand les reins ne fonctionnent plus bien.\n\nEnsuite, elle est passée à une hémodialyse intermittente, une autre technique pour filtrer le sang. Cependant, cette méthode a causé des problèmes : sa tension artérielle baissait trop pendant la dialyse, et elle a développé une baisse du nombre de plaquettes dans le sang à cause d’un médicament appelé héparine. Cela a obligé les médecins à arrêter cette dialyse.\n\nPour continuer à l’aider, ils ont choisi une autre technique appelée dialyse péritonéale. Cette méthode utilise la membrane à l’intérieur de l’abdomen pour filtrer le sang, ce qui est plus doux pour le corps. Grâce à cette dialyse, ils ont pu bien contrôler le volume de liquide dans son corps et maintenir une fonction cardiaque stable.\n\nAprès son hospitalisation, la patiente a pu rentrer chez elle. Depuis plus de deux ans, elle continue la dialyse péritonéale sans complications graves. Elle se sent bien, a une bonne qualité de vie, et peut même voyager. Son cœur fonctionne toujours de manière stable, ce qui est une très bonne nouvelle pour son pronostic.",
+            "B3": "Résumé destiné à un public adulte non spécialiste, structuré et clair :\n\n**Contexte**  \nUne femme de 65 ans, déjà suivie pour une amylose à chaînes légères (une maladie où des protéines anormales s’accumulent dans les tissus), a été hospitalisée initialement pour une insuffisance cardiaque et une pneumonie. Elle avait reçu des traitements spécifiques contre son amylose, incluant des médicaments comme le mélphalan, la dexaméthasone et le lénalidomide. Sa fonction rénale s’est progressivement détériorée, nécessitant une prise en charge spécialisée en néphrologie.\n\n**Principales observations cliniques et traitements**  \nÀ son transfert dans un hôpital spécialisé, elle a reçu des antimicrobiens, des médicaments pour soutenir son cœur (dobutamine, noradrénaline) et une dialyse continue par hémodiafiltration pour remplacer la fonction rénale défaillante. Son état s’est amélioré, ce qui a permis de passer à une hémodialyse intermittente (traitement par filtration du sang plusieurs fois par semaine).\n\nCependant, la patiente a rapidement présenté une hypotension lors des séances d’hémodialyse (baisse importante de la pression artérielle) ainsi qu’une thrombocytopénie (diminution du nombre de plaquettes sanguines), liée à une réaction immunitaire contre l’héparine, un médicament anticoagulant utilisé durant la dialyse. Cette complication a conduit à l’arrêt de l’héparine et à l’abandon de l’hémodialyse classique.\n\nPour poursuivre le traitement rénal, une dialyse péritonéale (DP) a été mise en place. Cette méthode utilise la membrane du péritoine (une fine couche à l’intérieur de l’abdomen) pour filtrer le sang, ce qui est moins agressif sur la pression artérielle. La patiente a ainsi bénéficié d’une dialyse péritonéale automatisée adaptée à son volume corporel, permettant un contrôle efficace des liquides et une bonne fonction rénale résiduelle.\n\n**Interprétation clinique**  \nL’amylose cardiaque a été confirmée par des examens d’imagerie montrant un épaississement des parois du cœur et une altération de la fonction diastolique (capacité du cœur à se remplir). Malgré cette atteinte, la dialyse péritonéale a permis de stabiliser la fonction cardiaque et d’éviter les complications liées à l’hémodialyse classique.\n\n**Prochaines étapes et évolution**  \nLa patiente a pu quitter l’hôpital en bon état après 44 jours et continue la dialyse péritonéale à domicile depuis plus de deux ans, sans complications majeures. Sa qualité de vie est bonne, elle reste active et apprécie voyager. Les examens cardiaques réalisés après sa sortie montrent une légère amélioration de la fonction diastolique, confirmant la stabilité de son état.\n\n**Conclusion**  \nCe cas illustre l’importance d’adapter le traitement de remplacement rénal chez les patients présentant une amylose cardiaque et des complications liées à l’hémodialyse. La dialyse péritonéale s’est révélée une alternative efficace et bien tolérée, permettant une meilleure qualité de vie et un pronostic amélioré."
+        }
+    },
+    {
+        "article": "Un homme de 60 ans s'est effondré dans la salle de sauna d'un hôtel capsule, un établissement d'hébergement économique doté de petits dortoirs, où il résidait depuis deux ans. Le patient a déclaré avoir eu pendant une semaine un manque d'appétit, une diarrhée et une fièvre modérée, accompagnés d'une dyspnée qui s'aggravait progressivement au cours des trois jours précédant son admission. Son historique médical et ses médicaments étaient inconnus en raison d'un manque de contacts familiaux et d'une dyspnée sévère qui a empêché de recueillir des antécédents détaillés.\n\nLors de son admission, le patient présentait une tachycardie, une tachypnée et une hypoxémie. Ses signes vitaux étaient les suivants : tension artérielle 128/85 mmHg, fréquence cardiaque 120 battements par minute, fréquence respiratoire 40 respirations par minute, saturation en oxygène 88 % sur un masque non respiratoire de 15 L, et température corporelle 37,8 °C, correspondant à une fièvre modérée. L'examen physique a révélé une respiration rapide et peu profonde utilisant les muscles respiratoires accessoires. Son score sur l'échelle de Glasgow était E4V5M6.\n\nLes premiers résultats de laboratoire ont révélé une acidose métabolique sévère avec compensation respiratoire, comme en témoigne une analyse des gaz du sang artériel indiquant un pH de 7,067, une pression partielle de dioxyde de carbone (pCO₂) de 63,1 mmHg, une pression partielle d'oxygène (pO₂) de 126 mmHg, un bicarbonate (HCO₃⁻) de 17,3 mmol/L et un lactate de 11 mmol/L. Les résultats de laboratoire ont également indiqué une dysfonction rénale sévère avec une urée sanguine (BUN) de 147,2 mg/dL et une créatinine de 8,82 mg/dL. L'aspartate aminotransférase (AST) était élevée à 268 U/L et l'alanine aminotransférase (ALT) à 108 U/L, ainsi que la lactate déshydrogénase (LDH) à 1910 U/L et la créatine kinase (CK) à 1552 U/L. Une inflammation marquée était évidente, avec un nombre de globules blancs (WBC) de 64 × 10⁹/L et un taux de protéine C-réactive (CRP) de 17,13 mg/dL. La patiente avait également une thrombocytopénie, avec un nombre de plaquettes (PLT) de 8,6 × 10⁹/L (voir Tableau 1 pour les résultats de laboratoire complets). Les tests pour le VIH, COVID-19, et l'antigène urinaire de la légionnelle étaient négatifs. Une tomodensitométrie thoracique a révélé des consolidations bilatérales avec des lésions cavitaires, principalement dans le poumon gauche.\n\nDes échantillons d'expectorations obtenus par lavage bronchoalvéolaire ont révélé à la fois des cocci Gram-positifs et des bâtonnets Gram-négatifs. Le patient a été diagnostiqué comme souffrant d'une pneumonie sévère et d'un abcès pulmonaire causé par une infection polymicrobienne. Il a été intubé lors de son admission en USI. Des antibiotiques empiriques, dont la vancomycine, la pipéracilline-tazobactam et l'azithromycine, ont été initiés. De l'hydrocortisone à 200 mg/jour a également été administrée. Le rapport initial PaO₂/FiO₂ était de 110 lors de la ventilation mécanique, ce qui correspond à un ARDS modéré. En raison de l'aggravation de l'hypoxie, un blocus neuromusculaire a été initié et poursuivi pendant 48 heures, et une position couchée a été initiée. En raison de l'aggravation de la dysfonction rénale, une thérapie de remplacement rénal a été initiée. Une stratégie d'hypercapnie permissive a permis un pH aussi bas que 7,15.\n\nAu troisième jour, son rapport PaO₂/FiO₂ avait rapidement diminué à 65, ce qui témoignait d'une nouvelle détérioration. Une thérapie par l'oxyde nitrique inhalé a été initiée, mais elle n'a pas entraîné d'amélioration significative. Par conséquent, une oxygénation extracorporelle à membrane (OEC) a été initiée le soir du troisième jour.\n\nLes cultures d'expectorations n'ont donné que des résultats pour Moraxella catarrhalis, ce qui était en contradiction avec la première coloration de Gram, ce qui suggère une infection polymicrobienne. Les résultats de la culture étaient en contradiction avec les résultats de la première coloration de Gram. Compte tenu de cette contradiction et du fait que le patient résidait dans un hôtel capsule, la tuberculose a été suspectée comme cause sous-jacente de sa pneumonie réfractaire et de son SDRA. Au quatrième jour de l'admission, les bacilles acido-résistants étaient fortement positifs (>10 bacilles acido-résistants par champ d'huile), et la réaction en chaîne de la polymérase a détecté Mycobacterium tuberculosis, confirmant le diagnostic de tuberculose pulmonaire. Un traitement anti-tuberculeux avec isoniazide, rifampicine, pyrazinamide et éthambutol a été initié. 1 g de méthylprednisolone a été administré pendant trois jours pour traiter le SDRA associé à la tuberculose. Une bronchoscopie quotidienne a été effectuée pour gérer l'expectoration.\n\nEntre les jours 9 et 11, l'état clinique du patient s'est amélioré, comme en témoigne la résolution radiographique des infiltrats pulmonaires et une augmentation de la compliance respiratoire à 40 ml/cmH₂O, permettant un sevrage réussi de la MV-ECMO. Par la suite, une trachéotomie a été réalisée cinq jours plus tard pour faciliter un soutien ventilatoire prolongé.\n\nDeux jours après la trachéotomie, une lésion hépatique induite par les médicaments a nécessité l'ajustement de la thérapie anti-TB à l'étambutol, la streptomycine et la lévofloxacine. La cyclosérine a été ajoutée trois jours plus tard. Le patient est resté dépendant d'un ventilateur et a été transféré dans un hôpital spécialisé dans la tuberculose 29 jours après son admission. Étant donné que de nombreux professionnels de santé ont été exposés à la tuberculose avant sa confirmation, un programme de dépistage de l'exposition a été mis en place. Il comprenait une évaluation médicale, une radiographie thoracique et un test de libération d'interféron gamma sans identifier de cas de tuberculose active ou latente parmi le personnel.\n",
+        "gold_summary": "Nous rapportons le cas d'un homme de 60 ans qui a développé une insuffisance respiratoire sévère après s'être effondré dans une sauna. Initialement diagnostiqué avec une pneumonie communautaire sévère et un syndrome de détresse respiratoire aiguë (SDRA), son état s'est détérioré malgré un traitement standard, nécessitant une oxygénation extracorporelle à membrane (OECV) veino-veineuse. Les tests de bacilles acido-résistants ont confirmé une tuberculose pulmonaire (TB) au jour 4, ce qui a entraîné l'initiation d'une thérapie anti-TB. Après une amélioration clinique, le patient a été sevré avec succès de l'OECV et transféré dans un hôpital spécialisé en TB pour des soins continus.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 60 ans est tombé dans un sauna. Il avait du mal à respirer très fort. Les docteurs ont d'abord pensé qu'il avait une grosse infection aux poumons. Ils lui ont donné des médicaments et de l'oxygène. Mais il allait encore plus mal.\n\nAprès quelques jours, les docteurs ont trouvé que c'était une maladie appelée tuberculose. C'est une maladie qui peut rendre les poumons très malades. Ils ont commencé un traitement spécial pour ça. Peu à peu, le monsieur a commencé à aller mieux.\n\nIl a pu arrêter l'oxygène spécial. Puis, il est allé dans un autre hôpital pour continuer ses soins. Les docteurs ont bien pris soin de lui.",
+            "B2": "Cas d’un homme de 60 ans avec une grave maladie des poumons\n\nUn homme de 60 ans s’est effondré dans un sauna et a été amené à l’hôpital. Il avait de la fièvre, de la diarrhée, et des difficultés à respirer qui s’aggravaient depuis plusieurs jours. À son arrivée, il avait une respiration très rapide, un cœur qui battait vite, et un manque d’oxygène dans le sang. Les examens ont montré qu’il avait une infection grave des poumons appelée pneumonie, avec aussi un syndrome de détresse respiratoire aiguë (SDRA). Cela signifie que ses poumons ne pouvaient plus bien apporter de l’oxygène à son corps.\n\nLes médecins ont commencé un traitement avec plusieurs antibiotiques et ont aidé sa respiration avec un ventilateur. Comme son état ne s’améliorait pas, ils ont utilisé une machine spéciale appelée oxygénation extracorporelle à membrane (OEC), qui remplace temporairement le travail des poumons pour apporter de l’oxygène au sang.\n\nAu quatrième jour, des tests ont montré que l’homme avait une tuberculose pulmonaire, une infection bactérienne qui peut être très grave si elle n’est pas traitée. Les médecins ont alors commencé un traitement spécifique contre la tuberculose. Après plusieurs jours, son état s’est amélioré, il a pu être sevré de la machine OEC, et transféré dans un hôpital spécialisé pour continuer ses soins.\n\nCe cas montre que la tuberculose peut parfois causer des infections pulmonaires très sévères, difficiles à diagnostiquer au début. Un traitement rapide et adapté est essentiel pour aider le patient à guérir.",
+            "B3": "Résumé détaillé et structuré pour un public adulte non spécialiste\n\nContexte  \nUn homme de 60 ans, résidant depuis deux ans dans un hôtel capsule (un type d’hébergement économique avec de petits dortoirs), s’est effondré dans la salle de sauna de l’établissement. Il présentait depuis une semaine des symptômes digestifs (manque d’appétit, diarrhée), une fièvre modérée et une dyspnée (difficulté à respirer) qui s’aggravait depuis trois jours. Son historique médical était inconnu, car il n’avait pas de contacts familiaux et son état respiratoire sévère empêchait de recueillir des informations détaillées.\n\nPrincipales observations cliniques et résultats  \nÀ son admission, le patient avait une fréquence cardiaque élevée (tachycardie), une respiration rapide (tachypnée) et une faible saturation en oxygène malgré un apport important d’oxygène. Sa température corporelle indiquait une fièvre modérée. L’examen physique montrait une respiration rapide et superficielle utilisant les muscles accessoires, signe d’un effort respiratoire important. Son état neurologique était globalement conservé.\n\nLes analyses sanguines ont révélé une acidose métabolique sévère (un déséquilibre acido-basique), une hypoxémie (manque d’oxygène dans le sang), une insuffisance rénale grave, ainsi qu’une élévation marquée des enzymes hépatiques et musculaires, témoignant d’une atteinte multi-organique. Une importante inflammation était présente, avec un nombre très élevé de globules blancs et une protéine C-réactive élevée. Le patient souffrait également d’une thrombocytopénie (diminution du nombre de plaquettes sanguines). Les tests pour le VIH, le COVID-19 et la légionellose étaient négatifs. L’imagerie thoracique (scanner) montrait des lésions pulmonaires bilatérales avec des zones de consolidation et des cavités, surtout dans le poumon gauche.\n\nLes prélèvements pulmonaires ont mis en évidence une infection polymicrobienne (plusieurs types de bactéries), ce qui a conduit au diagnostic initial de pneumonie sévère avec abcès pulmonaire. Le patient a été intubé et placé en unité de soins intensifs. Un traitement antibiotique large a été débuté, associé à des corticostéroïdes. Malgré ces mesures, son état respiratoire s’est rapidement aggravé, avec un syndrome de détresse respiratoire aiguë (SDRA) modéré à sévère nécessitant une ventilation mécanique avancée, un blocage neuromusculaire et une position couchée spécifique pour améliorer l’oxygénation. Sa fonction rénale s’est également détériorée, nécessitant une dialyse.\n\nInterprétation clinique  \nAu troisième jour, la détérioration respiratoire s’est poursuivie, avec une hypoxie sévère résistante aux traitements classiques, ce qui a conduit à la mise en place d’une oxygénation extracorporelle à membrane (OECM), une technique de suppléance respiratoire extracorporelle. Les cultures pulmonaires ont finalement isolé Moraxella catarrhalis, mais ce résultat ne correspondait pas à la diversité bactérienne initialement observée. Compte tenu de cette discordance et du contexte de vie en hôtel capsule, la tuberculose pulmonaire a été suspectée.\n\nAu quatrième jour, la confirmation est venue de la détection de bacilles acido-résistants dans les prélèvements pulmonaires et de la réaction en chaîne par polymérase (PCR) identifiant Mycobacterium tuberculosis. Le diagnostic de tuberculose pulmonaire a ainsi été établi. Un traitement spécifique anti-tuberculeux combinant plusieurs médicaments a été initié, ainsi qu’une corticothérapie à haute dose pour traiter le SDRA associé à la tuberculose. Une bronchoscopie quotidienne a été réalisée pour faciliter l’élimination des sécrétions pulmonaires.\n\nProchaines étapes et évolution  \nEntre les jours 9 et 11, l’état clinique du patient s’est nettement amélioré, avec une résolution visible des lésions pulmonaires à l’imagerie et une meilleure compliance (souplesse) pulmonaire, permettant le sevrage réussi de l’OECM. Une trachéotomie a été réalisée pour faciliter la ventilation prolongée. Cependant, une toxicité hépatique liée aux médicaments anti-tuberculeux a nécessité l’ajustement du traitement. Le patient est resté dépendant de la ventilation mécanique et a été transféré dans un centre spécialisé dans la prise en charge de la tuberculose 29 jours après son admission initiale.\n\nUn dépistage systématique des professionnels de santé exposés avant la confirmation du diagnostic a été mis en place, incluant examens médicaux, radiographies thoraciques et tests immunologiques, sans détection de cas de tuberculose active ou latente parmi le personnel.\n\nEn résumé, ce cas illustre une tuberculose pulmonaire sévère compliquée d’un SDRA réfractaire nécessitant une oxygénation extracorporelle, diagnostiquée tardivement en raison d’une présentation initiale atypique et d’une infection polymicrobienne concomitante. La prise en charge a combiné des traitements anti-infectieux, respiratoires et de soutien multi-organique, avec une évolution favorable sous traitement adapté."
+        }
+    },
+    {
+        "article": "Un garçon de 4 ans, chez qui on avait diagnostiqué une dilatation pyélo-calicielle droite prénatalement, a présenté de multiples microcystes hyperechogènes dans le groupe caliceal supérieur droit après la naissance. Les consultations régulières n'ont révélé aucune anomalie physique, mais les ultrasons de suivi ont indiqué un élargissement progressif de trois kystes polaires supérieurs.\n\nÀ la naissance, une échographie rénale a révélé une dilatation modérée du système calycéal supérieur et de multiples microcystes hyperechoïques dans le rein supérieur droit. Le rein gauche a présenté une légère dilatation des cavités pyélo-calycéales (7 mm de diamètre antéro-postérieur).\n\nÀ 2 mois, l'enfant a développé une infection fébrile des voies urinaires (IVU). L'échographie a montré le rein droit mesurant 58 mm, avec une lésion kystique de 24 mm et une formation hypèrechoïque (18 × 8 mm), qui était mobile. Le rein gauche mesurait 54 mm, avec une dilatation calycée globale modérée (10 mm de diamètre antéro-postérieur). Une cystourétrographie de miction à 5 mois a confirmé un reflux vésico-urétéral bilatéral (RVU), grade 2. La scintigraphie rénale DMSA a montré une fonction rénale symétrique sans cicatrisation. Un traitement antiseptique urinaire prophylactique a été démarré avec un suivi clinique et radiologique régulier.\n\nÀ 7 mois, une uro-CT a identifié des kystes corticaux simples, dont le plus grand mesurait 37 mm, et a révélé des cavités urétéro-pyélo-calciques bilatérales finement délimitées. À 11 mois, le rein droit mesurait 75 mm, avec trois kystes (39 × 29 × 25 mm, 17 × 14 × 11 mm, et 10 × 6 × 5 mm). Le rein gauche est resté normal, et aucune infection urinaire récurrente n'a été observée, ce qui a permis l'arrêt des antibiotiques prophylactiques à 1,5 ans.\n\nÀ 2 ans, le rein droit mesurait 100 mm, avec deux kystes polaires supérieurs (60 × 50 × 53 mm et 15 × 12 × 2 mm). Le rein gauche restait normal. À 3,5 ans, une échographie de suivi a montré un kyste polaire supérieur exophytique mesurant 70 × 47 mm, avec des parois minces et des septations incomplètes. Le rein gauche restait normal.\n\nUne aspiration de kyste percutanée guidée par tomodensitométrie a donné un fluide séreux. L'analyse cytologique a confirmé un fluide paucicellulaire dépourvu de caractéristiques anaplasiques. Cependant, l'échographie post-aspiration a révélé un kyste dans le sinus polaire supérieur du rein droit (81 × 78 × 64 mm). À la lumière de ces résultats, une intervention chirurgicale a été recommandée.\n\nUne néphrectomie droite haute a été réalisée par voie ouverte, par incision antérolatérale lombaire. L'examen anatomo-pathologique a révélé que l'échantillon de la néphrectomie hémi était occupé par un kyste de consistance scléreuse, de couleur blanchâtre. Ce kyste était recouvert par une demi-lune de tissu rénal de 0,6 cm d'épaisseur. L'examen en coupe séquentielle de la paroi de ce kyste a révélé un deuxième kyste dont la lumière était remplie d'une substance pâteuse de couleur blanc jaunâtre. Le kyste plus grand avait une surface interne tapissée d'un épithélium multicouche, souvent de type transitionnel et de type squameux kératinisé. Le reste de la paroi du kyste était composé de tissu fibreux riche en cellules musculaires lisses. Le plus petit kyste présentait des caractéristiques d'un kyste dermoïde, dont la lumière était remplie de kératine et de cellules squameuses desquamées. Sa paroi était tapissée d'un épithélium épidermique et contenait des follicules pileux et des glandes sébacées. On a observé autour de ces kystes des tissus conjonctifs et adipeux contenant un autre kyste tapissé d'épithélium squameux et des tubules entourés concentriquement par du tissu conjonctif cellulaire ressemblant à une dysplasie rénale. En outre, le tissu rénal identifié macroscopiquement ne présentait aucune lésion.\n\nLe suivi postopératoire sur trois ans n'a révélé aucune infection urinaire. La surveillance par ultrasons a démontré un rein droit réduit à 50 mm et un rein gauche normal, sans lésions kystiques ou solides et sans dilatation des cavités excrétoires.\n",
+        "gold_summary": "Nous rapportons le cas d'un garçon de 4 ans chez qui on a diagnostiqué une dilatation pyélo-calicielle droite in utero, confirmée après la naissance comme étant une MCDK. Les ultrasons de suivi ont révélé une croissance rapide de trois kystes du pôle supérieur, atteignant 8 cm. Une néphrectomie du pôle supérieur droit a été réalisée, et l'histopathologie a révélé un kyste dermoïde rénal dans le cadre d'une dysplasie rénale multicystique segmentaire.\n",
+        "synthetic_summary": {
+            "B1": "Un petit garçon avait un gros ballon d'eau dans son rein droit. Ce ballon est devenu plus grand avec le temps. Les docteurs ont enlevé cette partie du rein pour que le garçon aille mieux. Ils ont regardé le ballon et ont vu qu’il était fait de petites choses spéciales, mais ce n’était pas dangereux. Maintenant, le garçon va bien.",
+            "B2": "Cas d’un garçon de 4 ans avec un problème rénal détecté avant sa naissance. On avait vu que la partie supérieure du rein droit était un peu dilatée, c’est-à-dire élargie. Après sa naissance, des échographies ont montré plusieurs petits kystes (des sortes de petites poches remplies de liquide) dans cette même zone. Ces kystes ont grossi rapidement, jusqu’à atteindre environ 8 centimètres.\n\nPour éviter des complications, les médecins ont décidé d’enlever la partie supérieure du rein droit. En analysant ce tissu en laboratoire, ils ont découvert que ces kystes étaient en fait des kystes dermoïdes. Ce sont des kystes particuliers qui contiennent des cellules de la peau, comme des follicules pileux (petits sacs où poussent les poils) et des glandes. Cette situation faisait partie d’une maladie appelée dysplasie rénale multicystique segmentaire, ce qui signifie que certaines parties du rein se sont mal formées avec plusieurs kystes.\n\nAprès l’opération, le garçon a été suivi pendant trois ans sans nouvelle infection urinaire ni problème au rein restant, qui est resté normal. Ce cas montre l’importance de surveiller les kystes rénaux chez les enfants pour décider du meilleur traitement.",
+            "B3": "Résumé détaillé et structuré\n\nContexte  \nUn garçon de 4 ans a été suivi dès la période prénatale pour une dilatation pyélo-calicielle droite, c’est-à-dire une dilatation des cavités rénales supérieures du rein droit. Après la naissance, des examens échographiques ont montré la présence de multiples microkystes hyperechogènes dans la partie supérieure de ce rein. Au fil du temps, ces kystes ont grossi progressivement, sans anomalies physiques associées ni infections urinaires répétées après un traitement prophylactique initial.\n\nPrincipales observations  \nLes échographies successives ont révélé une augmentation notable de la taille de trois kystes localisés au pôle supérieur du rein droit, atteignant jusqu’à 8 centimètres. Une tomodensitométrie a confirmé la présence de ces formations kystiques simples, tandis que le rein gauche est resté normal sans dilatation ni kystes. Une aspiration percutanée du liquide contenu dans un kyste a montré un fluide clair sans cellules anormales, mais le kyste s’est reconstitué rapidement. En raison de cette évolution, une intervention chirurgicale a été décidée.\n\nInterprétation clinique  \nLa néphrectomie partielle du pôle supérieur droit a permis l’examen anatomopathologique approfondi. Celui-ci a mis en évidence un kyste dermoïde rénal, une formation bénigne rare caractérisée par la présence d’un épithélium épidermique avec des structures annexielles telles que des follicules pileux et des glandes sébacées, ainsi qu’un autre kyste tapissé d’un épithélium transitionnel et squameux kératinisé. Ces kystes étaient entourés de tissu conjonctif et adipeux présentant des signes de dysplasie rénale segmentaire, c’est-à-dire une anomalie du développement du rein avec formation de kystes. Le tissu rénal adjacent ne montrait pas de lésions malignes.\n\nProchaines étapes et suivi  \nLe suivi clinique et radiologique sur trois ans après la chirurgie n’a révélé aucune récidive de kystes ni infection urinaire. Le rein droit réséqué est réduit en taille, tandis que le rein gauche reste normal sans signes de dilatation ou de kystes. Cette prise en charge a donc permis un contrôle efficace de la pathologie, évitant des complications infectieuses ou fonctionnelles ultérieures.\n\nEn résumé, ce cas illustre une forme rare de dysplasie rénale multicystique segmentaire associée à un kyste dermoïde, diagnostiquée dès la période prénatale, avec une évolution progressive nécessitant une intervention chirurgicale partielle et un suivi à long terme favorable."
+        }
+    },
+    {
+        "article": "Un homme syrien de 61 ans ayant des antécédents d’alcoolisme et de tabagisme lourd a été présenté au service de dermatologie avec des plaintes de lésions pigmentées prurigineuses sans télangiectasies, desquamation ou atrophie sur le côté droit de son tronc et de sa cuisse droite. Le patient a nié avoir été exposé antérieurement à des produits chimiques ou solvants, et il n’y avait pas de antécédents familiaux de cancers de la peau, de maladies de la peau ou de conditions systémiques pertinentes. Ces lésions étaient persistantes depuis 3 ans, et le patient avait précédemment reçu une crème topique à 0,1 % d’hydrocortisone par un dermatologue local pour soulager les démangeaisons ; le patient utilisait la crème par intermittence et seulement lorsque les démangeaisons étaient sévères. À l’examen clinique, des plaques hyperpigmentées étaient visibles sur le côté droit de son tronc et la surface latérale de sa cuisse droite, sans autres caractéristiques cliniques. Les tests sanguins du patient étaient dans les limites normales, à l’exception d’une légère augmentation du nombre de globules blancs. Compte tenu des caractéristiques non spécifiques, une biopsie de la peau a été réalisée pour une évaluation plus approfondie, et l’examen histopathologique de la biopsie a révélé une épiderme hyperkératosique parakeratosique avec une légère spongiose. Le derme papillaire était modérément infiltré par des lymphocytes atypiques avec un léger dépôt de mélanophages. L’infiltration lymphocytaire était située en grappes et en distribution basilaire linéaire le long de la jonction dermo-épidermique. L’immunochimie des lymphocytes atypiques était CD3+, CD8+, CD4−, CD20−. Une tomographie par ordinateur (CT) du thorax et de l’abdomen a été réalisée, mais n’a donné que des résultats normaux sans lymphadénopathie ou organomégalie. Le patient a été diagnostiqué comme étant atteint d’un HPMF au stade précoce et a été ensuite référé à un hôpital spécialisé pour recevoir le traitement. Notre patient a subi une thérapie par psoralène et lumière ultraviolette A (PUVA), avec 8-méthoxypsoralène oral deux fois par semaine, et a été prescrit une crème topique à 0,1 % de bétaméthasone dipropionate. Après 12 semaines de traitement, les démangeaisons ont été soulagées, et l’hyperpigmentation a régressé, mais n’a pas disparu. Le pronostic à long terme du patient est excellent, et il a été conseillé de lui appliquer une crème hydratante et d’éviter l’exposition au soleil, et il est évalué tous les 6 mois pour détecter toute rechute ou nouvelle lésion sur d’autres parties du corps.\n\n",
+        "gold_summary": "Un Syrien de 61 ans s'est présenté à la clinique de dermatologie se plaignant d'une lésion prurigineuse pigmentée persistante sur le côté droit du tronc et de la cuisse droite. L'examen histologique de la biopsie cutanée a montré une épiderme parakeratosique hyperkératosique avec une spongiose et un dépôt de mélanophages. L'immunohistochimie a montré CD3+, CD4-, CD8+ et CD20-, et notre patient a été diagnostiqué avec une mycose fongoïde hyperpigmentée, et a été ensuite traité avec du psoralène et une thérapie aux ultraviolets A. Une très bonne amélioration a été notée, et le pronostic était excellent.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 61 ans avait une tache qui gratte sur son corps. Cette tache était là depuis longtemps. Le docteur a pris un petit bout de peau pour regarder de près. Il a trouvé des choses spéciales qui expliquent pourquoi ça gratte. Le monsieur a reçu un traitement avec une lumière spéciale et une crème. Après le traitement, la tache a beaucoup moins gêné et le monsieur va bien. Le docteur va continuer à vérifier pour que tout reste bien.",
+            "B2": "Un homme syrien de 61 ans est venu consulter en dermatologie à cause de taches foncées qui démangeaient sur le côté droit de son torse et de sa cuisse. Ces taches étaient présentes depuis trois ans. Pour mieux comprendre ce problème, les médecins ont prélevé un petit morceau de peau (c’est ce qu’on appelle une biopsie) et l’ont examiné au microscope. Ils ont vu que la couche supérieure de la peau était épaissie et qu’il y avait des cellules spéciales appelées lymphocytes anormaux regroupés sous la peau. Ces cellules avaient des marqueurs particuliers (CD3+, CD8+, CD4−, CD20−) qui ont aidé à poser le diagnostic.\n\nLe diagnostic était une maladie appelée mycose fongoïde hyperpigmentée. C’est un type rare de cancer de la peau qui peut provoquer des taches sombres et des démangeaisons. Pour le traiter, le patient a reçu un médicament appelé psoralène, associé à une lumière spéciale ultraviolette A (PUVA), ainsi qu’une crème à base de cortisone pour calmer les démangeaisons. Après trois mois de traitement, les démangeaisons ont beaucoup diminué et les taches ont commencé à s’estomper, même si elles n’ont pas complètement disparu. Le médecin a expliqué que le pronostic, c’est-à-dire les chances de bien aller à long terme, était très bon. Le patient doit continuer à hydrater sa peau, éviter le soleil et revenir tous les six mois pour vérifier que la maladie ne revient pas.",
+            "B3": "Résumé détaillé destiné à un adulte éduqué non-médecin\n\nContexte  \nUn homme syrien de 61 ans, avec des antécédents importants d’alcoolisme et de tabagisme, a consulté en dermatologie pour des lésions pigmentées qui démangeaient, situées sur le côté droit de son tronc et de sa cuisse droite. Ces lésions étaient présentes depuis environ trois ans et ne présentaient pas d’autres signes visibles comme des vaisseaux dilatés (télangiectasies), une desquamation (peau qui pèle) ou une atrophie (amincissement de la peau). Le patient n’avait pas d’exposition connue à des produits chimiques ni d’antécédents familiaux de maladies cutanées ou de cancers de la peau. Il avait utilisé de manière intermittente une crème à base d’hydrocortisone pour soulager les démangeaisons.\n\nPrincipales observations  \nÀ l’examen clinique, des plaques foncées (hyperpigmentées) étaient visibles sur le tronc et la cuisse droite, sans autres anomalies. Les analyses sanguines étaient normales, sauf une légère augmentation du nombre de globules blancs, ce qui peut indiquer une inflammation. Une biopsie cutanée a été réalisée pour mieux comprendre la nature des lésions. L’analyse au microscope a montré une peau avec un épaississement de la couche cornée (hyperkératose) et une présence anormale de cellules dans cette couche (parakératose), ainsi qu’une légère inflammation entre les cellules de l’épiderme (spongiose). Dans la couche sous-jacente (derme papillaire), on a observé un infiltrat modéré de lymphocytes atypiques (un type de globules blancs impliqués dans la défense immunitaire) regroupés et alignés le long de la jonction entre l’épiderme et le derme. Ces lymphocytes exprimaient certains marqueurs spécifiques (CD3+, CD8+, CD4−, CD20−), ce qui est caractéristique d’une forme particulière de lymphome cutané.\n\nInterprétation clinique  \nSur la base des résultats cliniques et histologiques, le diagnostic retenu était celui d’une mycose fongoïde hyperpigmentée (MFH), une forme rare et précoce de lymphome cutané à cellules T, qui se manifeste par des lésions pigmentées prurigineuses. Une imagerie par scanner (tomodensitométrie) du thorax et de l’abdomen n’a pas montré d’extension de la maladie à d’autres organes ou ganglions lymphatiques, ce qui est un bon signe pour le pronostic.\n\nProchaines étapes et traitement  \nLe patient a été orienté vers un centre spécialisé où il a reçu un traitement combiné associant du psoralène (un médicament sensibilisant la peau à la lumière) et une photothérapie par rayons ultraviolets A (PUVA), ainsi qu’une crème corticoïde topique à base de bétaméthasone. Après 12 semaines, les démangeaisons ont nettement diminué et l’hyperpigmentation a régressé, bien qu’elle ne soit pas complètement disparue. Le pronostic à long terme est considéré comme excellent. Le patient a reçu des conseils pour appliquer régulièrement une crème hydratante, éviter l’exposition excessive au soleil et se faire suivre tous les six mois afin de détecter rapidement toute récidive ou apparition de nouvelles lésions."
+        }
+    },
+    {
+        "article": "Nous présentons le cas d'un homme de 82 ans ayant un diagnostic confirmé par biopsie endoscopique d'un adénocarcinome du côlon ascendant. Les études de stadification préopératoire n'ont pas révélé de signes de maladie à distance et il avait un CEA de 2,8 ng/mL. Une hémicolectomie droite laparoscopique a été réalisée et il a eu un bon postopératoire. L'anatomie pathologique a rapporté un adénocarcinome modérément différencié de stade 1, T1 N0, qui n'a pas nécessité de traitement adjuvant.\n\nAu cours du suivi oncologique, une image d'aspect nodulaire en chaîne iliaque primitive gauche mesurant 22 mm sur son axe mineur a été identifiée par tomographie. En raison de cette découverte, une TEP-TDM avec 18F-FDG a été réalisée, qui a mis en évidence une lésion ovoïde, unique, au niveau rétropéritonéal, adjacente à la bifurcation aortique d'environ 34 mm de diamètre major avec un faible renforcement après administration de contraste iodé.\n\nCette image s’est avérée hypermétabolique (SUV : 6,7). Aucune autre image liée à la pathologie étudiée n’a été trouvée. Compte tenu des antécédents du patient, une biopsie percutanée guidée par imagerie a été programmée sous anesthésie locale. La procédure a été bien tolérée et n’a été associée à aucune complication. Cette étude a démontré que la découverte était un schwannome. Après un an de suivi, une augmentation de la taille de la lésion biopsiée a été constatée (44 mm de diamètre maximum), sans manifestations cliniques. En revanche, il n’y a eu aucune preuve de progression de la maladie oncologique.\n",
+        "gold_summary": "Nous présentons le cas d'un patient de 82 ans, récemment diagnostiqué d'un adénocarcinome du côlon modérément différencié et d'un nodule hypermétabolique périaortique comme découverte fortuite.\n\nRésultats : la biopsie percutanée du nodule périaortique a confirmé le diagnostic de schwannome. Au cours de l'année de suivi, la croissance du schwannome a été démontrée. Il n'y a pas de signe de progression de sa maladie oncologique.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 82 ans avait un petit cancer dans son gros ventre. Les docteurs ont enlevé ce petit cancer avec une opération. \n\nAprès, ils ont trouvé une petite boule près d’un gros tuyau dans son ventre. Ils ont fait un petit examen pour regarder cette boule. \n\nLa boule n’était pas un nouveau cancer, c’était une autre chose qui s’appelle un schwannome. Cette boule a un peu grandi en un an, mais le monsieur va bien. Son cancer ne revient pas.",
+            "B2": "Cas d’un homme de 82 ans avec un cancer du côlon\n\nUn homme de 82 ans a été diagnostiqué avec un cancer du côlon, appelé adénocarcinome, qui est un type de tumeur qui vient des cellules de la muqueuse du côlon. Ce cancer était à un stade précoce (stade 1), ce qui signifie qu’il n’avait pas encore touché les ganglions lymphatiques ni d’autres parties du corps. Il a subi une opération pour enlever la partie malade du côlon, et la récupération s’est bien passée. Aucun traitement supplémentaire n’a été nécessaire.\n\nDécouverte d’une autre masse près de l’aorte\n\nLors des contrôles après l’opération, les médecins ont trouvé une petite masse (ou nodule) près de l’aorte, une grosse artère dans le ventre. Cette masse mesurait environ 3 centimètres et était active sur une imagerie spéciale appelée TEP-TDM, qui montre les zones où les cellules consomment beaucoup d’énergie. Pour savoir ce que c’était, ils ont fait une biopsie, c’est-à-dire qu’ils ont prélevé un petit morceau de cette masse avec une aiguille, sous anesthésie locale.\n\nCe qu’ils ont découvert\n\nL’analyse de la biopsie a montré que cette masse était un schwannome. Un schwannome est une tumeur bénigne, ce qui veut dire qu’elle n’est pas cancéreuse. Elle vient des cellules qui entourent les nerfs. Pendant un an, les médecins ont suivi cette masse et ont vu qu’elle avait grossi un peu, mais le patient n’avait pas de symptômes. En même temps, il n’y avait aucun signe que son cancer du côlon s’était aggravé ou étendu.\n\nEn résumé, cet homme a eu un cancer du côlon traité avec succès, et une autre masse bénigne a été découverte et surveillée sans problème majeur.",
+            "B3": "Contexte  \nNous rapportons le cas d’un homme de 82 ans récemment diagnostiqué d’un adénocarcinome modérément différencié du côlon ascendant, de stade précoce (T1 N0), traité par hémicolectomie droite laparoscopique sans nécessité de traitement complémentaire. Lors du suivi oncologique, une masse nodulaire hypermétabolique a été découverte de manière fortuite au niveau rétropéritonéal, près de la bifurcation aortique.\n\nPrincipales Observations  \nLa tomographie par émission de positons couplée à la tomodensitométrie (TEP-TDM) a montré une lésion ovoïde unique, de 34 mm de diamètre, avec un métabolisme élevé (SUV 6,7), sans autre anomalie suspecte. Une biopsie percutanée guidée par imagerie a été réalisée sans complication, confirmant que cette masse correspondait à un schwannome, une tumeur bénigne des gaines nerveuses.\n\nInterprétation Clinique  \nAu cours d’un suivi d’un an, le schwannome a augmenté de taille, passant à 44 mm, mais sans provoquer de symptômes cliniques ni de signes de progression de l’adénocarcinome colique. Cette évolution suggère que la masse nodulaire est une lésion bénigne indépendante, sans impact sur la maladie cancéreuse initiale.\n\nProchaines Étapes  \nLa surveillance régulière reste indiquée pour suivre l’évolution du schwannome, en l’absence de manifestations cliniques ou de progression tumorale. Ce cas illustre l’importance d’une évaluation approfondie des masses nodulaires découvertes lors du suivi oncologique afin d’éviter des traitements inutiles."
+        }
+    },
+    {
+        "article": "Un homme de 71 ans hospitalisé dans un autre hôpital pour insuffisance cardiaque, ayant déjà été admis plusieurs fois pour insuffisance cardiaque, a été transféré dans notre hôpital pour une évaluation et un traitement plus poussés de son insuffisance cardiaque réfractaire. Bien qu'il ait été soupçonné d'avoir une amyloïdose cardiaque dans l'hôpital précédent, un diagnostic n'a pas été établi.\n\nÀ son admission à notre hôpital, il a reçu des médicaments oraux, dont de nombreux types de diurétiques, mais il avait toujours une dyspnée avec une classe fonctionnelle IV de la NYHA. Sa tension artérielle était de 106/70 mmHg, et le troisième son de cœur était audible au sommet. Des veines jugulaires congestionnées ont été observées, mais aucun œdème périphérique n’a été trouvé. La radiographie thoracique a montré un rapport cardiothoracique élevé de 61 % avec un épanchement pleural bilatéral. Les résultats électrocardiographiques étaient une fréquence cardiaque de 65/min avec une fibrillation auriculaire, un retard de conduction intra-ventriculaire et une déviation de l’axe gauche. L’échocardiographie transthoracique a révélé une hypertrophie diffuse du ventricule gauche (VG) avec une augmentation de l’épaisseur de la paroi de 12 mm, un mouvement de la paroi du VG hypokinétique modéré (fraction d’éjection = 43 %), une augmentation de l’épaisseur de la paroi du ventricule droit de 7 mm avec une fonction systolique du VD réduite et une dilatation biatriale. L’échocardiographie par spectrométrie de diffusion a montré un modèle de contraction longitudinale « apical sparing ». Il avait des résultats anormaux aux tests de laboratoire, avec un taux élevé de peptide natriurétique cérébral (BNP) (1 186 pg/mL) et un taux élevé de troponine T cardiaque de haute sensibilité (0,057 ng/mL). La scintigraphie au pyrophosphate de 99mTechnetium (99mTc-PYP) a révélé une prise cardiaque de grade 3 sur l’imagerie de fusion SPECT/CT. La protéine de Bence-Jones n’était pas détectable, et le rapport de la chaîne légère libre κ/λ était normal. Plus tard, nous avons effectué une biopsie endomyocardique et une analyse génétique, et nous avons finalement posé un diagnostic de ATTRwt.\n\nEn ce qui concerne la gestion de l'insuffisance cardiaque, nous avons essayé de contrôler son insuffisance cardiaque avec une oxygénothérapie et une prise en charge médicale, y compris une injection intraveineuse de furosémide, mais il avait toujours une dyspnée avec une fatigue générale persistante, et son taux de bilirubine a augmenté. La cathétérisation cardiaque droite (RHC) a montré une pression de coin artérielle pulmonaire élevée et une hypertension pulmonaire et un faible indice cardiaque de 1,37 L/min/m2 (thermodilution) avec une pression moyenne auriculaire droite de 8 mmHg.\n\nSur la base de ces résultats, nous avons commencé une perfusion de dobutamine à 2 μg/kg/min pour son faible débit cardiaque. Ses symptômes ont considérablement amélioré avec l'amélioration des taux de créatinine et de bilirubine. Six jours plus tard, nous avons administré du pimobendan afin de réduire progressivement la perfusion de dobutamine. Au cours du traitement, il était fondamentalement stable, à l'exception d'une détérioration temporaire de l'insuffisance cardiaque due à la grippe. Après un mois de traitement médical et de rééducation cardiaque en hospitalisation, la perfusion de dobutamine a été arrêtée et le RHC a montré une amélioration spectaculaire de son état hémodynamique. Depuis sa sortie de l'hôpital, son état est resté stable sans détérioration de l'insuffisance cardiaque ou des arythmies pendant six mois.",
+        "gold_summary": "Nous avons traité un homme de 71 ans souffrant d'insuffisance cardiaque réfractaire due à l'ATTRwt. Il devait être dépendant d'une perfusion de dobutamine. Nous avons administré du pimobendan et avons réussi à améliorer ses symptômes et son état hémodynamique pour permettre sa sortie de l'hôpital. Une enquête rétrospective supplémentaire a révélé qu'il y avait huit patients atteints d'amyloïdose ATTR auxquels on avait administré du pimobendan. Bien que tous les patients au moment de l'administration du pimobendan étaient de classe III ou IV de la NYHA avec une hospitalisation répétée pour insuffisance cardiaque, le pimobendan semblait être efficace pour améliorer les symptômes et permettre aux patients d'être sortis et de recevoir des soins médicaux ambulatoires. En outre, en se concentrant sur les changements dans certains biomarqueurs, nous avons constaté que les valeurs du peptide natriurétique cérébral et du taux de filtration glomérulaire estimé s'étaient améliorées après l'administration du pimobendan chez 5 patients consécutifs pour lesquels les données étaient disponibles sans traitement supplémentaire (p = 0,018 et 0,051, respectivement).\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 71 ans avait un cœur très fatigué. Il avait du mal à respirer et se sentait très fatigué. Les docteurs lui ont donné un médicament spécial appelé pimobendan. Ce médicament l’a beaucoup aidé. Il a pu sortir de l’hôpital et se sentir mieux.\n\nD’autres personnes avec un cœur fatigué ont aussi pris ce médicament. Ça les a aidées à se sentir mieux aussi. Les docteurs ont vu que leur cœur et leur corps allaient un peu mieux après. C’est un médicament qui peut aider quand le cœur est très fatigué.",
+            "B2": "### Ce qu'ils ont fait et observé\n\nUn homme de 71 ans souffrait d'une forme grave d'insuffisance cardiaque causée par une maladie appelée ATTRwt, qui est une accumulation anormale de protéines dans le cœur. Cette maladie rend le cœur moins capable de pomper le sang. Au début, il avait besoin d'un médicament appelé dobutamine, administré par perfusion, pour aider son cœur à fonctionner. \n\nLes médecins lui ont donné un autre médicament, le pimobendan, qui aide le cœur à mieux se contracter et à se détendre. Grâce à ce traitement, ses symptômes se sont améliorés, son cœur a mieux fonctionné, et il a pu quitter l'hôpital.\n\n### Ce qu'ils ont découvert en regardant d'autres patients\n\nEn regardant en arrière, les médecins ont trouvé huit autres patients atteints de la même maladie ATTR qui avaient aussi reçu du pimobendan. Tous ces patients étaient très malades, avec des difficultés importantes à respirer et des hospitalisations fréquentes. Pourtant, le pimobendan a aidé à améliorer leurs symptômes. Cela leur a permis de sortir de l’hôpital et de continuer leurs soins à la maison.\n\n### Ce que cela signifie\n\nLes médecins ont aussi mesuré certains marqueurs dans le sang, comme le peptide natriurétique cérébral (BNP), qui indique la gravité de l'insuffisance cardiaque, et la fonction des reins. Chez cinq patients, ces marqueurs se sont améliorés après le traitement au pimobendan, sans autre changement de traitement. Cela suggère que ce médicament pourrait être utile pour aider les patients atteints d’ATTRwt à mieux vivre avec leur maladie.\n\n### Conclusion simple\n\nLe pimobendan semble être un médicament prometteur pour aider les personnes souffrant d’une forme grave d’insuffisance cardiaque liée à l’ATTRwt. Il peut améliorer leurs symptômes et leur qualité de vie, en réduisant la nécessité d’hospitalisations fréquentes. Cependant, il faut encore plus d’études pour confirmer ces résultats.",
+            "B3": "Résumé détaillé et structuré\n\nContexte  \nNous avons pris en charge un homme de 71 ans présentant une insuffisance cardiaque réfractaire, c’est-à-dire résistante aux traitements habituels. Ce patient avait déjà été hospitalisé à plusieurs reprises pour cette pathologie. Une suspicion d’amyloïdose cardiaque avait été évoquée auparavant, mais aucun diagnostic précis n’avait été établi. L’amyloïdose ATTRwt (amyloïdose à transthyrétine de type sauvage) est une maladie caractérisée par le dépôt anormal de protéines transthyrétine dans le cœur, entraînant une altération progressive de sa fonction.\n\nPrincipales observations  \nÀ son admission dans notre établissement, malgré un traitement médicamenteux comprenant plusieurs diurétiques oraux, le patient présentait une dyspnée sévère (essoufflement) classée en stade IV selon la classification de la NYHA, indiquant une limitation importante des activités quotidiennes. L’examen clinique montrait une tension artérielle basse (106/70 mmHg), un troisième bruit cardiaque audible, des veines jugulaires congestionnées, mais sans œdème périphérique. L’imagerie thoracique révélait une cardiomégalie (cœur élargi) avec un épanchement pleural bilatéral. L’électrocardiogramme montrait une fibrillation auriculaire, un retard de conduction intra-ventriculaire et une déviation de l’axe gauche. L’échocardiographie mettait en évidence une hypertrophie diffuse du ventricule gauche (paroi épaissie à 12 mm), une fonction systolique modérément réduite (fraction d’éjection à 43 %), une hypertrophie du ventricule droit avec fonction réduite, ainsi qu’une dilatation des deux oreillettes. Un modèle spécifique de contraction appelé « apical sparing » était observé, caractéristique de l’amyloïdose cardiaque. Les analyses sanguines montraient des taux élevés de peptide natriurétique cérébral (BNP), un marqueur d’insuffisance cardiaque, et de troponine T cardiaque de haute sensibilité, signe de lésion myocardique. La scintigraphie au pyrophosphate de technétium-99m (99mTc-PYP) confirmait une prise cardiaque importante (grade 3), compatible avec une amyloïdose ATTR. Les tests pour une amyloïdose de type AL (protéine de Bence-Jones et rapport κ/λ) étaient négatifs. La biopsie cardiaque et l’analyse génétique ont permis de confirmer le diagnostic d’ATTRwt.\n\nInterprétation clinique  \nLe patient présentait une insuffisance cardiaque avancée avec un faible débit cardiaque et une hypertension pulmonaire, confirmés par cathétérisme cardiaque droit. Malgré un traitement médical intensif, incluant oxygénothérapie et diurétiques intraveineux, ses symptômes persistaient. Une perfusion continue de dobutamine, un médicament stimulant la contraction cardiaque, a été initiée, entraînant une amélioration notable des symptômes et des paramètres biologiques (créatinine et bilirubine). Afin de réduire progressivement la dobutamine, du pimobendan, un médicament inotrope et vasodilatateur, a été introduit. Ce traitement a permis de stabiliser le patient, malgré une aggravation temporaire liée à une infection grippale. Après un mois de prise en charge médicale et de rééducation cardiaque, la dobutamine a pu être arrêtée, et le cathétérisme a montré une nette amélioration hémodynamique. Le patient est resté stable sans aggravation de son insuffisance cardiaque ni d’arythmies pendant six mois après sa sortie.\n\nProchaines étapes et observations complémentaires  \nUne analyse rétrospective portant sur huit patients atteints d’amyloïdose ATTR traités par pimobendan a été réalisée. Tous ces patients étaient en stade III ou IV de la NYHA et avaient des hospitalisations répétées pour insuffisance cardiaque. Le pimobendan semblait efficace pour améliorer les symptômes, permettant la sortie hospitalière et la poursuite des soins en ambulatoire. De plus, chez cinq patients pour lesquels des données biomarqueurs étaient disponibles, on a observé une amélioration significative du peptide natriurétique cérébral (BNP) et une tendance à l’amélioration du débit de filtration glomérulaire estimé (une mesure de la fonction rénale) après l’introduction du pimobendan, sans autres traitements concomitants (p = 0,018 et 0,051 respectivement).\n\nEn résumé, cette étude suggère que le pimobendan pourrait représenter une option thérapeutique bénéfique pour les patients atteints d’amyloïdose cardiaque ATTRwt avec insuffisance cardiaque avancée, en améliorant les symptômes, la fonction cardiaque et la qualité de vie, tout en permettant une réduction progressive des traitements inotropes plus invasifs."
+        }
+    },
+    {
+        "article": "Femme de 76 ans, ayant des antécédents d'hypertension artérielle il y a 14 ans, en traitement avec candésartan, sans autre élément d'intérêt. Elle s'est présentée aux urgences, avec des antécédents d'AVC de 48 heures d'évolution, des signes cliniques de dysarthrie et d'hémiplégie droite qui ont disparu en quelques heures et ont récidivé 24 heures plus tard. À son arrivée aux urgences, avec 5 heures d'évolution. L'examen physique a révélé des signes vitaux normaux, somnolence, désorientation dans le temps et l'espace, regard préférentiel vers la gauche, hémianopsie homonyme droite, force musculaire 0 sur 5 dans l'hémicorps droit sur l'échelle de Daniels ; hyperréflexie dans les membres inférieurs 3/4 et hyporéflexie dans le membre supérieur droit 1/4, réponse plantaire extensora bilatérale, sans autre élément. Une tomographie par ordinateur (CT) cérébrale urgente a été réalisée immédiatement, qui a mis en évidence une image hyperdense extra-axiale en relation avec la face latérale gauche de la médulla oblongue qui s'étend jusqu'au pont, avec de multiples densités à ce niveau. L'étude urgente a été complétée par une angiotomographie cérébrale qui a mis en évidence une dolichocéphalie basilaire de 5,09 mm de diamètre et une anévrisme fusiforme au niveau de l'artère vertébrale gauche, d'environ 20 x 9 mm, partiellement oblitéré avec thrombus mural et calcifié, avec un passage adéquat du contraste. L'imagerie par résonance magnétique cérébrale dans les heures qui ont suivi a révélé une restriction de la diffusion dans le territoire de l'artère choroïde antérieure gauche et dans le territoire basilaire de la protubérance.\n",
+        "gold_summary": "Une femme de 76 ans a été admise aux urgences pour un accident vasculaire cérébral ischémique qui a touché le territoire de l'artère cérébrale antérieure gauche et basilaire. Les examens d'imagerie ont révélé une dolichocéphalie basilaire associée à un anévrisme fusiforme avec thrombus intra-anévrisme dans l'artère vertébrale gauche. Les deux anomalies anatomiques sont associées à un accident vasculaire cérébral ischémique.\n",
+        "synthetic_summary": {
+            "B1": "Une dame de 76 ans est venue à l’hôpital parce qu’elle avait eu un problème avec son cerveau. Son cerveau avait un petit souci qui l’a fait tomber malade. \n\nLes médecins ont regardé dans sa tête avec des machines spéciales. Ils ont vu que des petits tuyaux dans sa tête étaient un peu abîmés. Cela a causé le problème dans son cerveau. \n\nLes docteurs vont l’aider pour qu’elle aille mieux.",
+            "B2": "Une femme de 76 ans est venue aux urgences parce qu’elle avait des signes d’accident vasculaire cérébral, c’est-à-dire un problème dans le cerveau causé par un manque de sang. Elle avait des difficultés à parler et une paralysie d’un côté de son corps, qui sont apparues, ont disparu, puis sont revenues. \n\nLes médecins ont fait plusieurs examens d’imagerie, comme un scanner et une IRM, pour voir ce qui se passait dans son cerveau. Ils ont découvert deux anomalies importantes : d’abord, une dolichocéphalie basilaire, c’est-à-dire que l’artère principale à la base du cerveau est plus longue et plus large que la normale. Ensuite, ils ont trouvé un anévrisme fusiforme dans une autre artère du cerveau, ce qui signifie qu’une partie de cette artère est gonflée et contient un caillot de sang à l’intérieur.\n\nCes deux problèmes ont causé une réduction du flux sanguin dans certaines zones du cerveau, ce qui a provoqué l’accident vasculaire cérébral. En résumé, ces anomalies dans les vaisseaux sanguins ont empêché le sang d’arriver normalement au cerveau, ce qui a causé les symptômes de la patiente.",
+            "B3": "Résumé détaillé et structuré pour un public adulte non spécialiste\n\n**Contexte**  \nUne femme de 76 ans, avec des antécédents d’hypertension artérielle traitée depuis 14 ans, s’est présentée aux urgences suite à un accident vasculaire cérébral (AVC) survenu il y a 48 heures. Elle avait initialement présenté des troubles de la parole (dysarthrie) et une paralysie partielle du côté droit du corps (hémiplégie), qui avaient disparu temporairement avant de réapparaître 24 heures plus tard. Lors de son admission, cinq heures après la récidive, elle était somnolente, désorientée dans le temps et l’espace, avec un regard dévié vers la gauche, une perte de la vision dans la moitié droite du champ visuel (hémianopsie homonyme droite) et une paralysie complète du côté droit (force musculaire nulle).\n\n**Principales observations**  \nL’examen neurologique a également montré des réflexes anormaux : une hyperactivité des réflexes dans les jambes et une diminution dans le bras droit, ainsi qu’une réponse plantaire anormale des deux côtés. Une tomodensitométrie (scanner) cérébrale urgente a révélé une image anormale dense en dehors du tissu cérébral normal, localisée sur la face latérale gauche du bulbe rachidien (médulla oblongata) et s’étendant jusqu’au pont, avec plusieurs zones de densité variable. Une angio-CT cérébrale a mis en évidence deux anomalies importantes : une dolichocéphalie basilaire (une dilatation anormale de l’artère basilaire, ici mesurée à 5,09 mm de diamètre) et un anévrisme fusiforme (une dilatation en forme de fuseau) de l’artère vertébrale gauche, mesurant environ 20 x 9 mm, partiellement obstrué par un caillot (thrombus mural) et calcifié, mais avec un passage suffisant du contraste injecté. L’imagerie par résonance magnétique (IRM) cérébrale réalisée peu après a confirmé la présence d’une zone d’ischémie (manque d’apport sanguin) dans le territoire de l’artère choroïde antérieure gauche ainsi que dans la région desservie par l’artère basilaire au niveau du pont.\n\n**Interprétation clinique**  \nCes résultats indiquent que la patiente a subi un AVC ischémique affectant plusieurs territoires cérébraux, en lien avec des anomalies vasculaires complexes : une dilatation anormale de l’artère basilaire (dolichocéphalie) et un anévrisme fusiforme de l’artère vertébrale gauche, avec présence d’un thrombus. Ces anomalies vasculaires sont des facteurs de risque importants d’AVC, car elles peuvent entraîner une obstruction partielle du flux sanguin ou la formation de caillots qui bloquent la circulation cérébrale.\n\n**Prochaines étapes**  \nLa prise en charge de cette patiente doit inclure une surveillance neurologique étroite, un traitement adapté pour prévenir la formation de nouveaux caillots, et une évaluation spécialisée pour déterminer la nécessité éventuelle d’une intervention chirurgicale ou endovasculaire sur l’anévrisme. Un suivi régulier par imagerie sera également nécessaire pour surveiller l’évolution des anomalies vasculaires identifiées."
+        }
+    },
+    {
+        "article": "Une femme de 31 ans de la République du Zimbabwe s'est présentée au service des urgences de notre hôpital avec une fièvre de 3 jours, des douleurs thoraciques, des vomissements et une diarrhée. La patiente n'avait pas d'antécédents médicaux de pneumonie, de maladies contagieuses ou de contacts malades connus et a nié l'utilisation de tabac ou d'alcool. De plus, elle n'avait pas d'antécédents d'hospitalisation. Au Zimbabwe, un sous-groupe de la population consomme habituellement de l'argile rouge, et la patiente faisait partie de ce groupe. En raison de l'indisponibilité de l'argile rouge, elle a eu recours à la consommation de terre de jardin une fois tous les deux mois, avec son ingestion la plus récente survenue six jours avant la présentation. Elle a développé une fièvre avec une température maximale de 38,8 ° C accompagnée de frissons, de toux non productive et de douleurs thoraciques du côté droit exacerbées par la respiration 3 jours après l'ingestion du sol. Elle a connu quatre épisodes de vomissements de liquide jaune-vert et une diarrhée sévère, avec des selles jaunes aqueuses survenant 3 à 6 fois par heure à son apogée. La patiente s'est auto-administrée de l'ibuprofène, mais ses symptômes ont persisté, ce qui a conduit à son renvoi à notre hôpital en raison de l'aggravation de la diarrhée et de la fatigue.\nL'examen physique du patient a révélé les signes vitaux suivants : température corporelle de 38 °C, tension artérielle de 100/60 mmHg, fréquence cardiaque de 83 battements/min, fréquence respiratoire de 18 respirations/min, et saturation en oxygène de 99 % en air ambiant. L'auscultation a révélé des bruits respiratoires bruyants bilatéraux. Les résultats de laboratoire ont indiqué un nombre de globules blancs de 28,65 × 109/L, avec des neutrophiles à 25,95 × 109/L et un pourcentage de neutrophiles de 90,6 %. La protéine C-réactive était élevée à 198,76 mg/L. En outre, le D-dimère (22,62 mg/L), la créatinine (276,0 μmol/L), l'azote uréique (14,27 mmol/L), la bilirubine totale (61,0 μmol/L), la bilirubine directe (18,3 μmol/L) et la bilirubine indirecte (42,7 μmol/L) étaient élevés. La tomographie par ordinateur thoracique (CT) a révélé deux lésions suspectes dans le lobe inférieur gauche, avec une cavitation observée dans la plus grande lésion.\nUne thérapie empirique avec de la pipéracline-tazobactam et de la moxifloxacine a été initiée. Pour identifier l'agent pathogène responsable, une bronchoscopie a été réalisée et une culture du liquide de lavage broncho-alvéolaire (BALF) a identifié P. aeruginosa et un test de sensibilité antimicrobienne a démontré que l'isolement de P. aeruginosa était pan-sensible à la cefoperazone-sulbactam, à la lévofloxacine, à la ceftazidime, à la ceftazidime-avibactam, au meropenem, à la pipéracline-tazobactam, à la ciprofloxacine, à la cefepime, à l'aztréonam et à l'imipénem. Une culture fécale a simultanément indiqué une infection avec P. aeruginosa, tandis qu'une culture microbienne sanguine et urinaire n'a montré aucune anomalie significative. Par conséquent, le régime antibactérien a été ajusté à la pipéracline-tazobactam et à la ciprofloxacine sur la base des résultats de sensibilité. Des traitements symptomatiques, y compris une inhibition de l'acidité, une protection gastrique, une protection hépatique, des agents antidiarrhéiques et une régulation de la flore intestinale, ont été administrés, ce qui a entraîné une amélioration significative des symptômes gastro-intestinaux.\n\nAprès 3 jours de traitement, la fièvre, les vomissements et la diarrhée de la patiente ont disparu, ne laissant qu'une toux modérée. Une nouvelle tomographie effectuée 11 jours plus tard a montré un élargissement et une fusion des lésions dans le lobe inférieur gauche avec un petit épanchement pleural du côté gauche. Malgré ces résultats radiologiques, les marqueurs d'infection de la patiente s'étaient considérablement améliorés, ce qui a conduit à sa sortie avec des instructions pour poursuivre la thérapie par moxifloxacine en ambulatoire. Un mois plus tard, une nouvelle tomographie a démontré une réduction significative des lésions du lobe inférieur gauche, et la patiente est restée asymptomatique.\n",
+        "gold_summary": "Nous présentons le cas d'une patiente de 31 ans en bonne santé, enseignante au collège, qui a développé une CAP due à P. aeruginosa après avoir ingéré de la terre de jardin pendant trois jours consécutifs. La patiente a été admise avec des symptômes incluant de la fièvre, des douleurs thoraciques, des vomissements et une diarrhée. La tomographie par ordinateur (CT) thoracique a révélé deux lésions suspectes dans le lobe inférieur gauche, dont une lésion présentant une cavitation. La culture microbiologique du liquide de lavage broncho-alvéolaire (BALF) et des selles a confirmé la présence d'une infection à P. aeruginosa. Les tests de sensibilité antimicrobienne ultérieurs ont révélé que l'isolement de P. aeruginosa était pan-sensible. Après 13 jours de traitement antimicrobien ciblé, les symptômes et les marqueurs de laboratoire de la patiente ont considérablement amélioré. Une tomographie par ordinateur de suivi un mois plus tard a démontré une résolution substantielle des lésions du lobe inférieur gauche, et la patiente est restée asymptomatique.\n",
+        "synthetic_summary": {
+            "B1": "Une dame a mangé de la terre du jardin. Après, elle a eu de la fièvre et mal à la poitrine. Elle a aussi beaucoup vomi et eu la diarrhée.\n\nLe docteur a fait une photo spéciale de ses poumons. Il a vu des petits trous dans un côté. Ils ont trouvé des microbes dans sa gorge et dans son ventre.\n\nLe docteur lui a donné des médicaments pour tuer les microbes. Après plusieurs jours, elle allait beaucoup mieux. Un mois plus tard, ses poumons étaient presque guéris. Elle n’avait plus mal ni de fièvre.",
+            "B2": "Cas d'une femme de 31 ans avec une infection pulmonaire rare\n\nUne femme de 31 ans, enseignante, est tombée malade après avoir mangé de la terre de jardin pendant trois jours. Elle a eu de la fièvre, des douleurs dans la poitrine, des vomissements et une diarrhée. Ces symptômes ont duré plusieurs jours et l'ont amenée à consulter à l'hôpital.\n\nCe qu'ils ont trouvé\n\nUne radiographie spéciale appelée tomodensitométrie (CT) a montré deux zones anormales dans son poumon gauche, dont une avec un trou appelé cavitation. Pour comprendre ce qui causait l'infection, les médecins ont prélevé un liquide dans ses poumons et ont aussi analysé ses selles. Ils ont découvert une bactérie appelée Pseudomonas aeruginosa, qui est connue pour causer des infections, mais qui est rare chez des personnes en bonne santé.\n\nCe que cela signifie\n\nLes tests ont montré que cette bactérie pouvait être tuée par plusieurs antibiotiques. La patiente a donc reçu un traitement ciblé avec des médicaments adaptés. Après 13 jours, ses symptômes ont beaucoup diminué et les analyses de sang sont revenues presque normales. Un mois plus tard, une nouvelle radiographie a montré que les lésions dans son poumon avaient beaucoup régressé. Elle n’avait plus de symptômes et se sentait bien.\n\nEn résumé, cette patiente a eu une infection pulmonaire causée par une bactérie rare, probablement liée à la consommation de terre. Grâce à un bon diagnostic et un traitement adapté, elle a pu guérir complètement.",
+            "B3": "Résumé détaillé et structuré pour un public non médical éduqué\n\nContexte  \nUne femme de 31 ans, originaire du Zimbabwe, s’est présentée aux urgences avec une fièvre persistante depuis trois jours, accompagnée de douleurs thoraciques, de vomissements et de diarrhée sévère. Elle n’avait pas d’antécédents médicaux particuliers ni d’exposition connue à des maladies infectieuses. Cependant, elle consommait occasionnellement de la terre, une pratique culturelle locale, et avait ingéré de la terre de jardin six jours avant l’apparition des symptômes.\n\nPrincipales observations  \nÀ son admission, la patiente présentait une fièvre modérée (38 °C), une pression artérielle basse normale (100/60 mmHg), une fréquence cardiaque et respiratoire normales, ainsi qu’une bonne saturation en oxygène. L’examen pulmonaire a révélé des bruits respiratoires anormaux des deux côtés. Les analyses sanguines ont montré une forte augmentation des globules blancs, notamment des neutrophiles, ainsi qu’une élévation importante de la protéine C-réactive, un marqueur d’inflammation. D’autres tests ont mis en évidence une altération de la fonction rénale (créatinine élevée), une augmentation des produits de dégradation du sang (D-dimères) et une élévation des taux de bilirubine, suggérant une atteinte hépatique ou biliaire. Une tomodensitométrie (scanner) thoracique a détecté deux lésions suspectes dans le lobe inférieur gauche du poumon, dont une avec une cavité, signe d’une infection pulmonaire sévère.\n\nInterprétation clinique  \nUne infection pulmonaire grave, appelée pneumonie acquise en communauté (PAC), a été suspectée. Une bronchoscopie a permis de prélever un échantillon de liquide des voies respiratoires profondes (liquide de lavage broncho-alvéolaire). La culture de ce liquide ainsi que celle des selles ont confirmé la présence de la bactérie Pseudomonas aeruginosa, un micro-organisme opportuniste souvent résistant aux antibiotiques. Heureusement, dans ce cas, la bactérie était sensible à plusieurs antibiotiques, ce qui a permis d’adapter le traitement. La patiente a reçu initialement une association d’antibiotiques à large spectre, puis un traitement ciblé à base de pipéracilline-tazobactam et de ciprofloxacine, en fonction des résultats de sensibilité. Parallèlement, elle a bénéficié de soins symptomatiques pour protéger son estomac, son foie et réguler ses troubles digestifs.\n\nProchaines étapes et évolution  \nAprès trois jours de traitement, la fièvre, les vomissements et la diarrhée ont disparu, ne laissant qu’une toux modérée. Un scanner réalisé onze jours plus tard a montré une aggravation radiologique avec une extension des lésions pulmonaires et un petit épanchement pleural, mais les marqueurs biologiques d’infection s’étaient nettement améliorés. La patiente a donc pu être sortie de l’hôpital avec une prescription d’antibiotiques oraux à poursuivre en ambulatoire. Un contrôle un mois plus tard a révélé une réduction significative des lésions pulmonaires et l’absence de symptômes, témoignant d’une guérison complète.\n\nEn résumé, ce cas illustre une pneumonie grave à Pseudomonas aeruginosa survenue après ingestion de terre contaminée, traitée avec succès grâce à une prise en charge rapide, un diagnostic précis et un traitement antibiotique adapté."
+        }
+    },
+    {
+        "article": "Un garçon de 15 ans a été présenté à notre clinique avec la plainte principale d'hypertrichose focale des cheveux blancs depuis 4 mois. Il avait des antécédents de vitiligo depuis l'âge de 10 ans. La lésion de vitiligo était située sur son cou droit et traitée avec une pommade topique de tacrolimus à 0,1 % environ deux fois par jour et une thérapie au laser excimer de 308 nm (500 mJ/cm2) et au laser CO2 fractionné (25 W, largeur d'impulsion 2 ms, pas 1,3 mm) toutes les 2 semaines au cours des dernières années, et il a remarqué les cheveux blancs anormaux il y a 4 mois. Les cheveux blancs anormaux sur la lésion de vitiligo poussent plus vite que les cheveux normaux sur d'autres parties du cou. Il a nié avoir jamais utilisé une autre pommade dans cette région. Après avoir arrêté le tacrolimus pendant un demi-mois, les cheveux blancs sur son cou droit ont cessé de pousser. Au suivi de 2 mois, aucune nouvelle croissance de cheveux blancs n'a été observée. Pendant cette période, le patient a continué à recevoir la thérapie au laser excimer de 308 nm et au laser CO2 fractionné toutes les 2 semaines. Nous proposons que l'hypertrichose focale ait été induite par le tacrolimus.\n",
+        "gold_summary": "Nous présentons un garçon de 15 ans avec une hypertrichose focale des cheveux blancs depuis 4 mois, après un traitement par tacrolimus topique 0,1 % pommade. Il a nié avoir jamais utilisé une autre pommade dans cette région. Après avoir arrêté le tacrolimus pendant un demi-mois, l'hypertrichose focale s'est améliorée.\n",
+        "synthetic_summary": {
+            "B1": "Un garçon avait des cheveux blancs qui poussaient beaucoup sur son cou. Il avait une crème spéciale pour sa peau. Quand il a arrêté la crème, les cheveux blancs ont arrêté de pousser vite. Maintenant, ça va mieux.",
+            "B2": "Un garçon de 15 ans avait une tache de vitiligo, c’est-à-dire une zone de peau où la couleur a disparu, sur son cou droit depuis plusieurs années. Pour soigner cette zone, il utilisait une pommade appelée tacrolimus et recevait aussi des traitements au laser. Depuis 4 mois, il a remarqué que des cheveux blancs poussaient plus vite et en plus grande quantité sur cette zone. Quand il a arrêté d’utiliser la pommade tacrolimus pendant environ deux semaines, cette croissance anormale de cheveux blancs s’est arrêtée. Deux mois plus tard, aucun nouveau cheveu blanc n’était apparu. Cela suggère que la pommade tacrolimus a probablement causé cette pousse rapide et locale de cheveux blancs, appelée hypertrichose focale.",
+            "B3": "Contexte  \nUn garçon de 15 ans, suivi pour un vitiligo localisé sur le cou droit depuis l’âge de 10 ans, a été traité pendant plusieurs années par une pommade topique de tacrolimus à 0,1 % appliquée deux fois par jour, ainsi que par des séances régulières de laser excimer (308 nm) et de laser CO2 fractionné.  \n\nPrincipales Observations  \nDepuis quatre mois, il a développé une hypertrichose focale, c’est-à-dire une croissance excessive et localisée de cheveux blancs sur la zone atteinte par le vitiligo. Ces cheveux blancs poussaient plus rapidement que les cheveux normaux situés ailleurs sur son cou. Le patient a nié l’utilisation d’autres traitements topiques dans cette région.  \n\nInterprétation Clinique  \nAprès l’arrêt du tacrolimus pendant environ deux semaines, la croissance anormale des cheveux blancs s’est arrêtée. Lors du suivi à deux mois, aucune nouvelle repousse excessive n’a été observée, bien que le patient ait continué les traitements au laser. Ces éléments suggèrent que l’hypertrichose focale était probablement induite par l’application du tacrolimus.  \n\nProchaines Étapes  \nIl est recommandé de surveiller l’évolution de la zone traitée sans tacrolimus et d’évaluer l’efficacité et la tolérance des autres modalités thérapeutiques, notamment les lasers, afin de gérer au mieux le vitiligo tout en évitant les effets secondaires indésirables comme l’hypertrichose."
+        }
+    },
+    {
+        "article": "Une femme afro-américaine de 48 ans ayant des antécédents médicaux importants pour une hypertension essentielle non contrôlée s'est présentée au service des urgences avec une plainte principale de palpitations. Elle a également signalé une fatigue associée et un essoufflement. Au cours du mois dernier, elle a décrit une sensation intermittente de battements cardiaques irréguliers sans déclencheurs spécifiques. Ses symptômes ont progressé vers une gêne thoracique du côté gauche avec des picotements associés au membre supérieur gauche. En outre, elle a signalé des taches noires dans sa vision, ainsi qu'une dysphagie principalement aux solides, qui s'était également aggravée au cours des dernières semaines. Elle n'avait pas d'antécédents de symptômes similaires dans le passé. Elle ne prenait aucun médicament.\n\nLors de l'admission, les signes vitaux étaient significatifs pour une tension artérielle de 166/92 mmHg et une fréquence cardiaque de 109 battements/minute. Un examen physique était significatif pour une pâleur conjonctivale, sans preuve de glossite ou de koilonychia. Au service des urgences, un panel métabolique complet était normal, y compris une créatinine sérique de 0,56 mg/dL [0,60-1,20 mg/dL]. Un électrocardiogramme a montré une tachycardie sinusale avec complexes ventriculaires prématurés occasionnels. Les troponines étaient dans les limites normales. L'hémoglobine à l'admission était de 5,7 g/dL [11,9-15,1 g/dL] avec un volume corpusculaire moyen de 65,3 fL [80,0-96,0 fL]. La ferritine était de 3,1 ng/mL [11,0-306,8 ng/mL]. Le test immunochimique fécal (FIT) était négatif. Après un interrogatoire plus approfondi, la patiente a déclaré qu'elle avait encore ses règles, mais n'a pas décrit de ménorragie. Elle a nié avoir eu des hématèmesis, des hématochèses ou des mélénas. Elle a reçu 2 unités de globules rouges en poche au service des urgences et a commencé à recevoir des perfusions de complexes de fer déxtran par voie intraveineuse à 1400 mg.\n\nLa patiente était incapable de s'asseoir pour un esophagogramme afin d'évaluer une dysphagie secondaire à des nausées et des vomissements en essayant de boire l'agent de contraste. La gastroentérologie a été consultée, et la patiente a subi une endoscopie œsophagopancréatique (EOPC) et une coloscopie le jour 6 de son hospitalisation. Les résultats de la coloscopie étaient dans les limites normales. L'EOPC a révélé quelques sténoses intrinsèques dans l'œsophage supérieur, dont la plus étroite mesurait 9 millimètres. Des biopsies ont été obtenues à partir de l'œsophage proximal et distal avec des pinces à froid pour un soupçon d'œsophagite éosinophile par opposition au syndrome de Plummer-Vinson, en fonction de l'apparence macroscopique. Un examen pathologique de l'œsophage a montré une muqueuse uniquement squameuse, avec une inflammation chronique modérée. Aucune éosinophilie n'a été observée. Compte tenu des résultats cliniques, de laboratoire et endoscopiques, un diagnostic de syndrome de Plummer-Vinson a été posé. Sa dysphagie s'est améliorée au cours des 9 jours suivants à l'hôpital après des perfusions de fer et des transfusions sanguines, et elle a pu tolérer un régime alimentaire normal en mangeant lentement avec de petites bouchées.\n\nElle a subi un examen cardiaque pour évaluer les palpitations, y compris un échocardiogramme, qui a révélé une fraction d'éjection de 30 à 34 %, avec une hypokinésie globale et sans pathologie valvulaire ou hypertension pulmonaire. Un test de stress nucléaire a été négatif pour l'ischémie myocardique. Un nouveau diagnostic d'insuffisance cardiaque congestive avec fraction d'éjection réduite a été fait. La cardiologie a été consultée et elle a commencé un traitement par carvedilol, lisinopril, spironolactone et hydralazine. Elle a reçu un gilet de sauvetage à l'hôpital lors de la sortie.\n\nEnviron 6 mois après sa sortie, un appel téléphonique de suivi a été fait à la patiente. Elle a déclaré qu'elle avait respecté tous ses médicaments et que sa dysphagie avait été résolue. Au moment de l'appel téléphonique, elle tolérait une alimentation normale sans aucune restriction alimentaire.",
+        "gold_summary": "Patient : Femme, 48 ans\n\nDiagnostic final : syndrome de Plummer-Vinson\n\nSymptômes : douleur thoracique • fatigue • palpitation\n\nMédication : —\n\nProcédure clinique : oesophagogastroduodénoscopie (EGD) • coloscopie\n\nSpécialité : Médecine générale et interne\n\nNous présentons le cas d'une femme afro-américaine de 48 ans souffrant d'anémie symptomatique et d'une insuffisance cardiaque congestive secondaire à l'hypertension, qui présentait les symptômes classiques de la PVS.\n",
+        "synthetic_summary": {
+            "B1": "Il y a une dame de 48 ans qui se sentait très fatiguée. Son cœur battait très vite et elle avait mal à la poitrine. Elle avait aussi du mal à avaler sa nourriture.\n\nLes docteurs ont fait des examens pour comprendre pourquoi elle avait ces problèmes. Ils ont trouvé qu'elle avait un manque de fer dans son corps. Ce manque rendait son cœur fatigué et sa gorge un peu serrée.\n\nIls lui ont donné du fer et des médicaments pour aider son cœur. Après un moment, elle a commencé à se sentir mieux. Elle pouvait manger normalement et son cœur allait mieux.\n\nLes docteurs ont pris bien soin d'elle pour qu'elle guérisse doucement. Tout va mieux maintenant.",
+            "B2": "Cas d’une femme de 48 ans avec syndrome de Plummer-Vinson\n\nUne femme afro-américaine de 48 ans est venue aux urgences parce qu’elle avait des palpitations, une fatigue importante et des difficultés à avaler, surtout les aliments solides. Elle avait aussi des douleurs dans la poitrine du côté gauche et des picotements dans le bras gauche. Ces symptômes sont apparus progressivement sur un mois.\n\nLors de son arrivée, sa tension artérielle était élevée et son cœur battait rapidement. Les analyses ont montré qu’elle avait une anémie sévère, c’est-à-dire un manque important de globules rouges, avec un faible taux de fer dans le sang. Pour comprendre la cause de son problème, les médecins ont fait une endoscopie, qui consiste à regarder l’intérieur de l’œsophage avec une petite caméra. Ils ont trouvé des rétrécissements dans la partie haute de son œsophage. Les biopsies, c’est-à-dire des petits prélèvements de tissu, ont montré une inflammation, mais pas d’autres maladies comme l’œsophagite éosinophile. Ces résultats ont permis de poser le diagnostic de syndrome de Plummer-Vinson, une maladie rare liée à une carence en fer qui provoque des difficultés à avaler.\n\nElle a reçu des transfusions de sang et des perfusions de fer pour corriger son anémie. Après neuf jours, ses difficultés à avaler se sont améliorées et elle a pu manger normalement en prenant de petites bouchées.\n\nEn plus, un examen du cœur a révélé qu’elle avait une insuffisance cardiaque, ce qui signifie que son cœur ne pompait pas le sang aussi bien qu’il devrait. Un traitement spécifique a été commencé pour cette maladie cardiaque.\n\nSix mois plus tard, lors d’un suivi par téléphone, la patiente a dit qu’elle suivait bien son traitement et que ses problèmes pour avaler avaient disparu. Elle mangeait normalement sans difficulté.\n\nEn résumé, ce cas montre comment une carence en fer peut causer des symptômes importants comme des difficultés à avaler et une anémie sévère, et comment un traitement adapté peut améliorer la qualité de vie.",
+            "B3": "Résumé détaillé pour un public non médical éduqué\n\nContexte  \nUne femme afro-américaine de 48 ans, avec une hypertension artérielle essentielle mal contrôlée, s’est présentée aux urgences en raison de palpitations cardiaques, de fatigue et d’essoufflement. Elle rapportait également une gêne thoracique du côté gauche accompagnée de picotements dans le bras gauche, ainsi que des troubles visuels (apparition de taches noires) et une difficulté à avaler principalement les aliments solides, qui s’aggravaient depuis plusieurs semaines. Elle ne prenait aucun traitement au moment de sa consultation.\n\nPrincipales observations  \nÀ son admission, sa tension artérielle était élevée (166/92 mmHg) et sa fréquence cardiaque rapide (109 battements par minute). L’examen physique a révélé une pâleur des conjonctives, signe d’anémie, sans autres anomalies visibles. Les analyses sanguines ont montré une anémie sévère avec un taux d’hémoglobine très bas (5,7 g/dL, alors que la normale est autour de 12-15 g/dL) et un volume moyen des globules rouges diminué, indiquant une anémie ferriprive (due à un manque de fer). La ferritine, qui reflète les réserves en fer, était également très basse. Un test de recherche de sang occulte dans les selles était négatif, et la patiente n’a pas rapporté de saignements digestifs visibles. Elle a reçu des transfusions sanguines et un traitement par perfusion intraveineuse de fer.\n\nPour explorer la dysphagie, une endoscopie œsophagienne et une coloscopie ont été réalisées. La coloscopie était normale. L’endoscopie a montré plusieurs rétrécissements (sténoses) dans la partie supérieure de l’œsophage, avec une zone la plus étroite mesurant 9 millimètres. Des biopsies ont été prélevées pour exclure une inflammation spécifique appelée œsophagite éosinophile. L’analyse histologique a révélé une inflammation chronique modérée sans infiltration éosinophile. Ces résultats, associés à l’anémie ferriprive et aux symptômes, ont conduit au diagnostic de syndrome de Plummer-Vinson (PVS), une maladie rare caractérisée par une triade : anémie ferriprive, dysphagie et sténoses œsophagiennes.\n\nPar ailleurs, un examen cardiaque a montré une insuffisance cardiaque congestive avec une fraction d’éjection (mesure de la fonction de pompage du cœur) réduite à 30-34 %, sans signes d’ischémie (manque d’apport sanguin au muscle cardiaque). Un traitement médical adapté a été instauré (bêta-bloquant, inhibiteur de l’enzyme de conversion, diurétique et vasodilatateur).\n\nInterprétation clinique  \nLe syndrome de Plummer-Vinson est une cause rare de dysphagie liée à une anémie ferriprive sévère. Dans ce cas, l’anémie non traitée a probablement contribué à la fatigue, aux palpitations et à la détérioration de la fonction cardiaque. Le traitement par supplémentation en fer et transfusions a permis une amélioration progressive de la dysphagie et des symptômes généraux. L’insuffisance cardiaque a été prise en charge de manière spécifique.\n\nProchaines étapes  \nLa patiente a été suivie à distance six mois après sa sortie. Elle rapportait une bonne observance des traitements prescrits, une résolution complète de la dysphagie et une alimentation normale sans restriction. Ce suivi souligne l’importance d’un diagnostic précoce et d’un traitement adapté du syndrome de Plummer-Vinson et de ses complications associées, notamment cardiaques."
+        }
+    },
+    {
+        "article": "La patiente était une femme de 81 ans ayant des antécédents médicaux d’hypertension et d’hyperlipidémie. La patiente a été amenée à notre hôpital avec une hémiplégie droite sévère et une aphasie totale, et la note de l’échelle des accidents vasculaires cérébraux des National Institutes of Health (NIHSS) était de 16 à l’admission. Le dernier point de contrôle connu (LKW) était de 12 heures. Dans notre établissement, nous suivons un protocole d’imagerie basé sur le temps pour les cas d’AVC aigus : les cas dans les 4,5 heures suivant le début sont soumis à une CTA en premier, tandis que les cas au-delà de 4,5 heures sont évalués en premier avec une IRM. L’IRM a révélé un infarctus cérébral dans la région de l’artère cérébrale moyenne gauche, et le score de l’Alberta Stroke Program Early CT Score (DWI ASPECTS) était de 7. L’ARM a révélé une occlusion du segment M2 gauche. Cependant, les résultats de la radiographie thoracique ont indiqué une anomalie possible dans l’arc aortique, ce qui nous a conduit à effectuer une CTA supplémentaire pour évaluer la voie d’accès à la thrombectomie. La CTA a révélé une RAA avec une ramification en miroir. La patiente n’a pas reçu d’activateur de plasminogène de tissu recombinant par voie intraveineuse. Bien que les preuves soutenant la MT dans de tels scénarios soient limitées, nous avons soigneusement évalué l’état de la patiente en fonction de plusieurs facteurs : le score modifié de Rankin (mRS) avant l’AVC était de 0, le DWI ASPECTS était de 7, et la présentation était un AVC réveillant avec un DWI-FLAIR non conforme, ce qui suggère que le temps réel depuis le début de l’AVC pourrait ne pas être aussi long que le LKW l’indique. En outre, la patiente présentait des symptômes sévères avec un NIHSS de 16. Sur la base de ces facteurs, nous avons jugé que la MT était appropriée, car elle offrait une chance d’améliorer le résultat de la patiente.\n\nNous avons choisi le système de guidage habituel. Une gaine de 9 Fr a été insérée dans l'artère fémorale commune droite. Un fil-guide (Radifocus ; Terumo, Tokyo, Japon) et un cathéter JB2 de 6 Fr (Medikit, Tokyo, Japon) ont été avancés à l'aide d'un cathéter guide à ballon OPTIMO de 9 Fr (Tokai Medical Products, Aichi, Japon).\n\nLe cathéter guide a été avancé de l'aorte abdominale au milieu de la colonne vertébrale vers l'aorte thoracique du côté droit de la colonne vertébrale et a été facilement placé dans l'artère carotide interne gauche de la manière habituelle en se référant à l'ACP. L'angiographie de l'artère carotide interne gauche a révélé une occlusion du tronc inférieur gauche M2. La thrombolyse dans la réperfusion de l'infarctus cérébral 2B a été réalisée en utilisant Trevo NXT 3 × 32 mm (Stryker, Fremont, CA, USA) et Catalyst 6 (Stryker) après 3 passes. Le temps de la ponction à la recanalisation était de 61 minutes (10 minutes, de la ponction au placement du cathéter guide dans l'artère carotide interne gauche ; 51 minutes, du placement du cathéter guide à la recanalisation). La TDM post-procédurale a révélé une petite hémorragie sous-arachnoïdienne.\n\nLa fibrillation auriculaire n'a pas été détectée, et une TDM de contraste de l'ensemble du corps a été réalisée pour rechercher davantage la source de l'embolie. Une thrombose veineuse profonde (TVP) et une embolie pulmonaire (EP) ont été observées dans la veine fémorale profonde droite et dans les deux artères pulmonaires, respectivement. L'échocardiographie transœsophagienne a démontré un foramen ovale patent (FOP). Malgré les anticorps antinucléaires et la coagulabilité examinés à l'aide de tests sanguins, ceux-ci n'étaient pas la cause de l'infarctus cérébral. La pathogenèse de l'infarctus cérébral a été déterminée comme étant une embolie paradoxale, et l'apixaban a été administré après que la TVP et l'EP aient été révélées. Le thrombus dans la veine fémorale et l'artère pulmonaire a presque disparu, et l'infarctus cérébral n'a pas récidivé. L'hémiplégie droite et l'aphasie ont persisté, et à la sortie, le score mRS était de 5.\n",
+        "gold_summary": "Une femme de 81 ans a présenté une hémiplégie droite sévère et une aphasie. La note de l'échelle des accidents vasculaires cérébraux des National Institutes of Health était de 16, l'imagerie par résonance magnétique a révélé une valeur de 7 sur l'échelle de l'Alberta Stroke Program Early CT, et l'angiographie par résonance magnétique a révélé une occlusion de la M2 gauche. L'angiographie par résonance magnétique a révélé un arc aortique droit avec des branches en miroir. La thrombectomie mécanique a été réalisée en utilisant le système habituel, et une recanalisation efficace a été obtenue avec un stent retriever et un cathéter d'aspiration après 3 passes. L'angiographie par résonance magnétique a révélé une embolie pulmonaire et une thrombose veineuse profonde (TVP) dans la veine fémorale profonde droite, et l'échocardiographie transœsophagienne a révélé un foramen ovale patent. L'électrocardiographie n'a pas révélé de fibrillation auriculaire, et les autres examens n'ont pas révélé d'autre cause ; par conséquent, un embolisme cérébral paradoxal a été diagnostiqué. Après un traitement anticoagulant, aucune récidive d'infarctus, d'embolie pulmonaire ou de TVP n'a été observée. Une hémiplégie droite sévère et une aphasie totale ne se sont pas améliorées, et la patiente a été sortie le jour 37 après admission avec une note de 5 sur l'échelle de Rankin modifiée.\n",
+        "synthetic_summary": {
+            "B1": "Une dame de 81 ans est tombée très malade. Elle ne pouvait plus bouger son bras et sa jambe droits. Elle ne pouvait plus parler non plus.\n\nLes médecins ont fait des images de sa tête. Ils ont vu que le sang ne passait plus bien dans une partie de son cerveau. Ils ont aussi vu que son cœur avait un petit trou.\n\nLes docteurs ont fait une opération pour enlever un caillot dans son cerveau. Après, elle a pris des médicaments pour que ça n’arrive plus.\n\nElle est restée à l’hôpital un moment. Elle ne pouvait pas encore bouger son côté droit ni parler quand elle est rentrée chez elle. Les médecins vont continuer à l’aider.",
+            "B2": "**Ce qu’ils ont trouvé chez la patiente**  \nUne femme de 81 ans est arrivée à l’hôpital avec une paralysie sévère du côté droit de son corps (appelée hémiplégie) et une incapacité totale à parler (aphasie). Son état était grave, avec un score de 16 sur une échelle utilisée pour mesurer la gravité des accidents vasculaires cérébraux (AVC). Une IRM a montré une zone endommagée dans une partie du cerveau appelée artère cérébrale moyenne gauche, avec un score de 7 sur une autre échelle qui évalue l’étendue de l’infarctus. Une autre imagerie a révélé que cette artère était bloquée dans une zone appelée segment M2 gauche. De plus, ils ont découvert que l’arc de l’aorte (une grosse artère du cœur) avait une forme particulière appelée « arc aortique droit avec branches en miroir ».\n\n**Ce qu’ils ont fait et pourquoi**  \nLes médecins ont décidé de réaliser une thrombectomie mécanique, c’est-à-dire qu’ils ont utilisé des outils spéciaux pour enlever le caillot qui bloquait l’artère du cerveau. Ils ont utilisé un stent retriever (un petit filet pour attraper le caillot) et un cathéter d’aspiration (un tube pour aspirer le caillot). Après trois tentatives, ils ont réussi à débloquer l’artère. Pendant les examens, ils ont aussi trouvé une embolie pulmonaire (un caillot dans les poumons) et une thrombose veineuse profonde (un caillot dans une grosse veine de la jambe droite). Une échographie spéciale du cœur a montré un foramen ovale patent, c’est une petite ouverture anormale entre deux parties du cœur qui peut laisser passer des caillots vers le cerveau.\n\n**Ce que cela signifie pour la patiente**  \nIls n’ont pas trouvé de fibrillation auriculaire (un rythme cardiaque irrégulier qui peut causer des caillots) ni d’autres causes pour l’AVC. Ils ont donc conclu que l’AVC était dû à un « embolisme paradoxal », c’est-à-dire qu’un caillot est passé de la circulation veineuse vers la circulation artérielle à travers cette ouverture du cœur, puis a bloqué une artère du cerveau. La patiente a reçu un traitement anticoagulant (médicaments qui empêchent la formation de nouveaux caillots). Après ce traitement, les caillots dans la jambe et les poumons ont presque disparu, et elle n’a pas eu de nouvel AVC. Cependant, la paralysie et l’incapacité à parler sont restées sévères. Elle est sortie de l’hôpital après 37 jours avec un score de 5 sur l’échelle de Rankin modifiée, ce qui signifie qu’elle avait besoin d’aide importante pour ses activités quotidiennes.",
+            "B3": "Résumé détaillé et structuré pour un public adulte non spécialiste\n\n**Contexte**  \nUne femme de 81 ans, avec des antécédents d’hypertension artérielle et d’hyperlipidémie (taux élevé de lipides dans le sang), a été admise à l’hôpital présentant une hémiplégie droite sévère (paralysie d’un côté du corps) et une aphasie totale (incapacité à parler ou comprendre le langage). À son admission, son score NIHSS (National Institutes of Health Stroke Scale), qui évalue la gravité de l’accident vasculaire cérébral (AVC), était de 16, indiquant un AVC sévère. Le dernier moment où elle était connue sans symptômes (Last Known Well, LKW) remontait à 12 heures.\n\n**Principales observations**  \n- L’imagerie par résonance magnétique (IRM) a montré un infarctus cérébral dans le territoire de l’artère cérébrale moyenne gauche, avec un score DWI ASPECTS de 7, ce qui indique une atteinte modérée du cerveau.  \n- L’angiographie par résonance magnétique (ARM) a révélé une occlusion du segment M2 gauche de l’artère cérébrale moyenne.  \n- Une anomalie anatomique rare a été détectée : un arc aortique droit avec une ramification en miroir, ce qui a nécessité une évaluation spécifique par angiographie par tomodensitométrie (CTA) pour planifier la procédure.  \n- La patiente n’a pas reçu de traitement thrombolytique intraveineux (activateur de plasminogène tissulaire recombinant) en raison du délai depuis le début des symptômes.  \n- Malgré cela, la thrombectomie mécanique (MT), une intervention visant à retirer le caillot, a été réalisée avec succès en utilisant un stent retriever (Trevo NXT) et un cathéter d’aspiration (Catalyst 6) après trois tentatives, permettant une recanalisation efficace en 61 minutes.  \n- Une petite hémorragie sous-arachnoïdienne (saignement dans l’espace autour du cerveau) a été détectée après la procédure, sans complication majeure.  \n- Des examens complémentaires ont révélé l’absence de fibrillation auriculaire (rythme cardiaque irrégulier souvent responsable d’AVC).  \n- Une thrombose veineuse profonde (TVP) a été identifiée dans la veine fémorale profonde droite, ainsi qu’une embolie pulmonaire (obstruction des artères pulmonaires par un caillot).  \n- L’échocardiographie transœsophagienne a mis en évidence un foramen ovale patent (FOP), une communication anormale entre les deux oreillettes du cœur, pouvant permettre le passage de caillots veineux vers la circulation artérielle cérébrale (embolie paradoxale).  \n- Aucun autre facteur de risque ou cause (comme des troubles de la coagulation ou des anticorps spécifiques) n’a été identifié.\n\n**Interprétation clinique**  \nLe diagnostic principal est celui d’un infarctus cérébral causé par une embolie paradoxale, c’est-à-dire un caillot provenant des veines profondes (TVP) qui a traversé le FOP pour atteindre le cerveau. La thrombectomie mécanique a été jugée appropriée malgré le délai prolongé, en raison de la sévérité des symptômes, du bon état fonctionnel antérieur de la patiente (score mRS de 0 avant l’AVC) et de signes suggérant que le temps réel depuis le début de l’AVC était probablement plus court que le LKW indiqué.\n\n**Prochaines étapes et évolution**  \n- La patiente a été traitée par anticoagulants (apixaban) pour prévenir la formation de nouveaux caillots.  \n- Après traitement, la thrombose veineuse et l’embolie pulmonaire ont presque disparu, et aucune récidive d’AVC n’a été observée.  \n- Cependant, les déficits neurologiques sévères (hémiplégie droite et aphasie totale) sont restés présents.  \n- À sa sortie, 37 jours après l’admission, la patiente avait un score modifié de Rankin (mRS) de 5, indiquant une dépendance sévère pour les activités quotidiennes.\n\n**Conclusion**  \nCe cas illustre la complexité du diagnostic et du traitement d’un AVC sévère chez une patiente âgée présentant une anatomie vasculaire atypique et une embolie paradoxale. La prise en charge rapide et adaptée, incluant une thrombectomie mécanique malgré un délai prolongé, a permis d’éviter une aggravation fatale, bien que des séquelles importantes persistent."
+        }
+    },
+    {
+        "article": "Un homme de 37 ans s'est présenté à notre établissement de troisième niveau pour une uvéite en janvier 2020, suite à une référence pour une évaluation vitréorétinienne plus approfondie. Ses symptômes étaient des éclairs et des photoréactions, principalement dans l'œil droit. Il avait été diagnostiqué auparavant avec une probable BRCSCR bilatérale à l'été 2016. Les évaluations de laboratoire initiales, y compris le compte sanguin complet, le bilan métabolique complet, l'hémoglobine A1c et les études du fer, étaient toutes normales. Les évaluations de laboratoire pour les étiologies infectieuses, y compris les tests QuantiFERON-TB Gold (QFT), le réactif plasmatique rapide (RPR) et l'absorption des anticorps fluorescents (FTA-ABS), étaient toutes négatives ou non réactives. L'imagerie par résonance magnétique du cerveau en septembre 2016 était normale. En novembre 2016, le patient a été traité par corticostéroïde topique et bevacizumab intravitréen dans l'œil droit (OD), ainsi que 60 mg de prednisone orale quotidienne. En décembre 2016, il a commencé un traitement immunomodulateur (IMT) avec la cyclosporine et le méthotrexate, qui ont tous deux été arrêtés en 2017 en raison d'un manque d'efficacité possible. Le patient a ensuite commencé un traitement par adalimumab, au cours duquel ses symptômes (éclairs et corps flottants) se sont améliorés. Après environ 1 an de traitement, l'adalimumab a été arrêté en raison de la réduction des taux de fer sérique début 2019. En octobre 2019, il a reçu une injection intravitréenne de fluocinolone acétonide de 0,18 mg dans l'œil droit, mais n'a constaté aucune amélioration ultérieure des symptômes visuels.\n\nLors de l'examen initial en janvier 2020, le patient a noté un inconfort oculaire modéré (OD > OS), une vision trouble (OD > OS) et des corps flottants (OU). L'acuité visuelle était de 20/20 OU. Lors de l'évaluation initiale, l'examen des systèmes était négatif du point de vue systémique. Les pressions intraoculaires étaient de 13 mm Hg OD et 12 mm Hg OS. L'examen du segment antérieur était remarquable pour une éruption bilatérale de grade 1+, avec une cataracte sous-capsulaire postérieure modérée OD, mais était par ailleurs sans particularité. L'examen du fond d'œil dilaté était remarquable pour un œdème du disque optique (OD > OS) et des lésions choriorétinales hypopigmentées ovoïdes péripapillaires et périphériques (OU). L'œil droit présentait également une atrophie temporale péripapillaire, des cellules vitreuses 1+, des modifications pigmentaires du pigment rétinien maculaire et une petite hémorragie rétinienne dans la périphérie du quadrant supérotemporal. La tomographie par cohérence optique dans le domaine spectral (SD-OCT) a montré une élévation du disque optique dans le liquide intrarétinien péripapillaire avec une membrane épirétinienne modérée (ERM) OD > OS. L'angiographie à la fluorescéine grand angle (FA) (OPTOS Plc, Dunfermline, Royaume-Uni) a montré un média trouble, une fuite du disque et une coloration péripapillaire OD, et une fuite optique diffuse avec une coloration segmentaire modérée des veinules le long de l'arcade temporale inférieure OS. Il y avait une hyperfluorescence de plusieurs lésions dans la région péripapillaire et le long de l'arcade temporale inférieure sans aucun signe de fuite OU.\n\nDeux semaines plus tard, l'électrorétinographie de champ complet (ffERG) a montré une dysfonction rétinienne globale modérée à modérée, avec des régions géographiques claires de dépression maculaire (OD > OS). Les temps de clignotement implicites de 30 Hz ont révélé un retard significatif dans les deux yeux (OS > OD). Le potentiel évoqué visuel a montré un retard relativement symétrique pour les petits et les grands stimuli, suggérant une dysfonction modérée du nerf optique. Les champs visuels de Goldmann (GVF) et les champs visuels de Humphrey (HVF) ont montré un élargissement du point aveugle OD et un point aveugle normal sans constriction généralisée OS. Les évaluations de laboratoire n'étaient remarquables que pour la positivité de l'antigène leucocytaire humain (HLA) A29. Les résultats des tests de l'enzyme de conversion de l'angiotensine, de la lysozyme et du QFT répété étaient tous dans les limites normales.\n\nLors de la visite de suivi d'un mois en février 2020, le patient a noté une acuité visuelle stable, une certaine amélioration des corps flottants dans les deux yeux et une opacité persistante principalement dans l'OD. L'acuité visuelle est restée de 20/20 OU. La pression intraoculaire était de 15 mm Hg OD et 8 mm Hg OS. L'examen du segment antérieur a été remarquable pour un éclat OU de 1+. L'examen du fond d'œil dilaté a été remarquable pour 0,5+ cellules et 0,5+ opacité du vitré OU. Les résultats de l'examen global du pôle postérieur étaient stables. Les résultats de l'OCT SD et de la FA grand angle étaient relativement inchangés depuis la première visite. La coréoangiographie en indocyanine verte grand angle (ICG) a montré un médium clair, de multiples taches hypocyanescentes dans le pôle postérieur et la périphérie médiane dans la phase intermédiaire, et des taches hypocyanescentes ont disparu dans la phase tardive OU. L'autofluorescence du fond d'œil a montré une hypofluorescence autour du disque optique et de la rétine.\n\nLe patient a été diagnostiqué avec un BSCR sur la base de la positivité HLA-A29, de l’aspect typique du fond d’œil et de l’évaluation négative pour d’autres étiologies auto-immunes et infectieuses. Étant donné la maladie active du patient, comme en témoigne l’œdème du disque optique associé à des cellules vitreuses dans les deux yeux, ainsi que les résultats très suggestifs de la FA et de l’ICG, le patient a commencé un traitement par infliximab à une dose de 7,5 mg/kg par mois. Il a également reçu 3 jours de méthylprednisolone par voie intraveineuse (IV) à une dose de 1000 mg/jour, suivis d’un traitement par voie orale de prednisone.\n\nLe patient ne s'est pas présenté à la visite de suivi avant avril 2021 et a reçu huit cycles de 7,5 mg/kg d'infliximab en perfusion avec 1000 mg de prednisone pendant 3 jours au cours de cette période. La vision était réduite à 20/40 OD en raison de la formation de cataracte sous-capsulaire postérieure (PSC) et était de 20/20 OS. Aucune cellule AC et aucune éruption n'étaient présentes dans les deux yeux. Le vitré était trouble en OD en raison de la formation de cataracte. Le disque optique SD-OCT ne présentait pas de changements significatifs. Sur la FA, le média était flou au centre OD en raison de la formation de cataracte. La coloration partielle du disque optique était présente dans l'OU. Il n'y avait pas de coloration vasculaire rétinienne et de fuite capillaire dans l'OU. La coloration des lésions choroïdiennes péripapillaires dans les cadres précoce et tardif de la FA restait la même dans l'OU. Quatre mois plus tard, le patient a reçu quatre cycles supplémentaires d'infusions IFX en plus d'un jour de 1000 mg de méthylprednisolone. La vision a diminué à 20/70 OD en raison de la progression de la PSC et était de 20/20 OS. L'examen ophtalmologique, les résultats SD-OCT et FA sont restés inchangés. L'ICG a été effectué et les taches hypocyanescentes ont montré une nette amélioration avec quelques taches hypocyanescentes au pôle postérieur (OS>OD) dans les deux yeux sur ICG. Les tests électrophysiologiques, y compris ffERG, mfERG et VEP et les tests du champ visuel, y compris GVF et HVF, sont restés inchangés depuis la visite initiale. Bien qu'il y ait eu une amélioration significative des résultats oculaires à l'examen et à la fois dans la FA et dans l'ICG, le mycophenolate mofetil 2000 mg quotidien a été ajouté à son traitement en raison de la présence d'oedème du disque optique et il restait quelques taches hypocyanescentes au pôle postérieur dans l'ICG.\n",
+        "gold_summary": "Un homme de 37 ans s'est présenté à notre service d'uvéites tertiaires avec un inconfort oculaire bilatéral, une vision trouble et des corps flottants. L'examen oculaire a révélé une vitrite, un œdème du disque optique et des lésions choriorétinales hypopigmentées ovoïdes, visibles sur la choroangiographie au vert indocyanine sous forme de multiples taches hypocyanescentes dans la phase intermédiaire. L'électrorétinographie à champ complet et le potentiel évoqué visuel ont montré une dysfonction rétinienne globale et une dysfonction du nerf optique. Les évaluations de laboratoire n'ont révélé que la positivité de l'antigène leucocytaire humain (HLA)-A29. Le patient a été diagnostiqué comme souffrant d'une RCBS et a commencé un traitement par prednisone orale et a finalement été traité par infliximab.\n",
+        "synthetic_summary": {
+            "B1": "Un homme de 37 ans avait mal aux yeux et voyait flou. Il voyait aussi des petites taches qui bougent dans ses yeux. Le docteur a regardé ses yeux et a vu qu’ils étaient un peu gonflés et qu’il y avait des taches bizarres. Des tests ont montré que ses yeux ne fonctionnaient pas très bien. Le docteur a trouvé un signe spécial dans son sang. Il a dit que l’homme avait une maladie des yeux appelée RCBS. Pour l’aider, il a donné des médicaments pour calmer ses yeux et pour que ça aille mieux.",
+            "B2": "Un homme de 37 ans est venu consulter pour des douleurs aux deux yeux, une vision un peu floue et des petites taches qui bougent dans son champ de vision. Lors de l’examen, les médecins ont trouvé une inflammation dans le vitré (la partie claire à l’intérieur de l’œil), un gonflement du disque optique (la zone où le nerf optique sort de l’œil) et des taches claires en forme d’œuf sur la rétine, la couche sensible à la lumière au fond de l’œil. Une technique spéciale appelée choroangiographie au vert d’indocyanine a montré plusieurs taches sombres dans ces zones, ce qui indique un problème dans la couche appelée choroïde.\n\nDes tests électriques ont mesuré le fonctionnement de la rétine et du nerf optique. Ils ont montré que la rétine ne fonctionnait pas bien partout et que le nerf optique était aussi affecté. Les analyses de sang n’ont rien montré d’anormal, sauf la présence d’un marqueur appelé HLA-A29, qui est souvent lié à une maladie appelée rétinite à points blancs ou syndrome de Birdshot (RCBS). Ce diagnostic a été confirmé par l’aspect des yeux et les résultats des examens.\n\nPour traiter cette maladie, le patient a commencé par prendre des corticoïdes par voie orale (la prednisone) pour calmer l’inflammation. Ensuite, il a reçu un médicament appelé infliximab, qui agit sur le système immunitaire pour réduire l’inflammation plus efficacement. Ce traitement vise à protéger la vision et à limiter les dégâts dans les yeux causés par cette maladie.",
+            "B3": "Résumé détaillé et structuré pour un public non spécialiste :\n\n**Contexte**  \nUn homme de 37 ans a consulté dans un centre spécialisé en uvéite (inflammation de l’œil) pour des symptômes oculaires bilatéraux, comprenant un inconfort, une vision trouble et la présence de corps flottants (petites taches ou filaments qui dérivent dans le champ visuel). Il avait déjà été suivi pour une suspicion de choriorétinite bilatérale liée à la présence de l’antigène HLA-A29, un marqueur génétique associé à une maladie inflammatoire rare appelée syndrome de Birdshot (ou choriorétinite à Birdshot).\n\n**Principales observations cliniques et examens**  \nL’examen ophtalmologique a montré une inflammation du vitré (vitrite), un œdème (gonflement) du disque optique (zone où le nerf optique entre dans l’œil) et des lésions ovales hypopigmentées (zones plus claires) sur la choroïde et la rétine. Ces lésions étaient visibles sur une imagerie spécifique appelée coréoangiographie au vert d’indocyanine, qui a révélé de multiples taches hypocyanescentes (zones où le colorant ne s’accumule pas) au stade intermédiaire de l’examen.  \n\nDes tests électrophysiologiques, notamment l’électrorétinographie à champ complet (ffERG) et le potentiel évoqué visuel (VEP), ont mis en évidence une dysfonction globale de la rétine et une atteinte modérée du nerf optique, confirmant que la maladie affectait à la fois la rétine et la transmission nerveuse visuelle.\n\nLes analyses de laboratoire n’ont révélé aucune infection ou autre cause auto-immune, à l’exception de la présence de l’antigène HLA-A29, fortement associé au syndrome de Birdshot.\n\n**Interprétation clinique**  \nSur la base des signes cliniques, des résultats d’imagerie et de l’analyse génétique, le diagnostic de choriorétinite à Birdshot (BSCR) a été confirmé. Cette maladie inflammatoire chronique affecte principalement la choroïde et la rétine, entraînant des troubles visuels progressifs si elle n’est pas traitée.\n\n**Prise en charge et évolution**  \nLe patient a débuté un traitement par corticostéroïdes oraux (prednisone) pour réduire l’inflammation. En raison de la persistance et de l’activité de la maladie, un traitement immunosuppresseur par infliximab (un anticorps monoclonal ciblant l’inflammation) a été instauré. Ce traitement a permis une amélioration des symptômes et une stabilisation des lésions oculaires, bien que la formation de cataracte (opacification du cristallin) ait progressivement réduit la vision dans l’œil droit.\n\n**Prochaines étapes**  \nLe suivi régulier est essentiel pour surveiller l’activité inflammatoire, ajuster le traitement immunosuppresseur et prévenir les complications visuelles. Des examens complémentaires, tels que l’imagerie par tomographie et l’électrophysiologie, continueront à guider la prise en charge. Un traitement additionnel par mycophénolate mofétil a été ajouté pour contrôler l’œdème du disque optique persistant.\n\n---\n\nCe résumé met en lumière l’importance d’un diagnostic précis et d’une prise en charge adaptée dans une maladie rare et complexe comme la choriorétinite à Birdshot, afin de préserver la fonction visuelle du patient."
+        }
+    },
+    {
+        "article": "Une fille est née à 34 semaines de grossesse avec un poids de naissance de 2 820 g. Un traitement complet de corticostéroïdes prénataux avait été administré et l'imagerie prénatale de routine a montré des polyhydramnios et un fœtus de grande taille pour la date. La mère avait des antécédents de diabète gestationnel et de pré-éclampsie.\n\nL'enfant est né par césarienne en bonne condition avec des scores APGAR de 61, 95 et 1 010, mais en raison de difficultés respiratoires, elle a reçu un surfactant par administration moins invasive 25 minutes après la naissance. Elle a ensuite été transférée à l'unité de soins intensifs néonataux sous ventilation assistée continue à 40 % d'oxygène. 4 heures après la naissance, en raison de difficultés respiratoires persistantes et d'une augmentation des besoins en oxygène jusqu'à 60 %, elle a été intubée et ventilée mécaniquement. Une radiographie thoracique a révélé des preuves d'une éventuelle éventration bilatérale des diaphragmes. Un examen échographique du diaphragme a confirmé ce soupçon. Un échocardiogramme (ECHO) effectué à ce moment-là a révélé une hypoplasie modérée de l'isthme, mais un ECHO répété a démontré un cœur normal sur le plan structurel. Après avoir subi un essai de respiration spontanée et une période d'évaluation non invasive de l'activité électrique du diaphragme, elle a été extubée avec succès après 36 heures de soutien ventilatoire invasif. En outre, elle n'a pas eu besoin d'un soutien respiratoire non invasif après extubation et elle a continué à se ventiler par l'air jusqu'à la sortie. Comme elle n'a pas eu besoin de périodes prolongées de soutien respiratoire invasif, elle n'a pas été considérée comme une candidate à une intervention chirurgicale dans la période néonatale aiguë.\n\nPendant sa période néonatale, elle a présenté une hypoglycémie à l'admission à l'unité néonatale avec une glycémie de 0,4 mmol/L et a nécessité une concentration maximale de glucose de 20 %. Elle a ensuite été diagnostiquée comme ayant un hyperinsulinisme et a commencé à recevoir du diazoxide. Elle avait une mauvaise alimentation malgré une vidéofluroscopie et un examen ORL normaux et a ensuite eu besoin d'une aide alimentaire par sonde nasogastrique. Au cours de l'évaluation neurologique, elle a présenté une hypotonie centrale avec des réflexes vifs et a été notée pour avoir de nombreux naevus mélanocytaires sur la face latérale des deux bras avec des taches supplémentaires sur le sacrum. L'examen histopathologique d'une biopsie par ponction a démontré des résultats compatibles avec une mélanocytose cutanée. Elle est née avec deux dents néonatales qui ont été enlevées après la naissance, mais elle a ensuite développé deux lésions fibreuses sur la crête alvéolaire antérieure qui étaient pédiculées et mobiles, elles ont ensuite été enlevées à 1 mois. Une enquête neurologique approfondie a été réalisée et a révélé une imagerie par résonance magnétique cérébrale normale, avec une électromyographie des membres supérieurs et inférieurs et des études de conduction nerveuse normales. Compte tenu du diagnostic différentiel de l'atrophie musculaire spinale, une analyse d'immunohistochimie a été réalisée, qui a donné des résultats normaux. Une évaluation ophtalmologique et une échographie rénale ont été réalisées, elles étaient normales. Les tests génétiques postnataux ont révélé une mutation du gène KMT2D, associée au syndrome de Kabuki.\n\nElle a été renvoyée chez elle le 64e jour après la naissance avec un soutien alimentaire nasogastrique et a continué à prendre des médicaments diazodix. Elle continue de recevoir une aide importante de la part d'ergothérapeutes, de logopèdes et d'équipes de physiothérapie.\n\nImagerie et mesures\nLa zone thoracique radiographique thoracique (CRTA) mesurée après extubation (trois jours après la naissance) était de 1 654 mm2, équivalant à celle d'un nourrisson à terme avec hernie diaphragmatique congénitale sévère. L'imagerie par ultrasons (USS) a montré une éventration diaphragmatique focale avec bombement du dôme du foie dans les hémithorax droit et gauche. Un essai de respiration spontanée (SBT) a été effectué avant l'exubation et l'électromyographie du diaphragme a été mesurée pendant cette période. L'amplitude moyenne de l'activité électrique diaphragmatique était de 2,47 μV, similaire en magnitude à celle des nourrissons ventilés du même âge gestationnel avec diaphragmes intacts. Elle a réussi le SBT et l'extubation ultérieure.\n\nLes parents ont donné leur consentement écrit éclairé pour ce rapport et l'approbation éthique a été donnée pour la mesure de l'EMG du diaphragme pendant la SBT avant l'extubation (référence REC : 20/SW/0,062).\n",
+        "gold_summary": "Une fille née à 34 semaines de gestation a nécessité une intubation et une ventilation à la naissance. L'imagerie radiographique thoracique a révélé une densité bilatérale à la base des deux champs pulmonaires avec des hémi-diaphragmes surélevés. L'imagerie par ultrasons a montré une éventration diaphragmatique focale avec bombement du dôme du foie dans les hémithorax droit et gauche. L'évaluation de l'activité électrique du diaphragme lors d'un essai de respiration spontanée a révélé une amplitude moyenne cohérente avec celle des nourrissons ventilés du même âge gestationnel avec des diaphragmes intacts. Elle a donc été extubée avec succès. La surface thoracique mesurée après extubation était de 1 654 mm2, équivalant à celle d'un nourrisson à terme présentant une hernie diaphragmatique congénitale sévère. L'activité électrique du diaphragme étant normale, cela suggère que le remplacement du tissu musculaire diaphragmatique par des bandes fibreuses était probablement seulement partiel, et explique pourquoi l'extubation a été réussie. Elle présentait d'autres anomalies au cours de la période néonatale, notamment une mélanocytose cutanée, une hypotonie centrale, un hyperinsulinisme et une mauvaise alimentation. L'enfant a fait l'objet d'une enquête approfondie qui a révélé une mutation du gène KMT2D associée au syndrome de Kabuki.\n",
+        "synthetic_summary": {
+            "B1": "Une petite fille est née un peu avant le temps prévu. Elle avait du mal à bien respirer. Les médecins ont regardé ses poumons avec des images. Ils ont vu que ses muscles sous les poumons étaient un peu différents. Mais ses muscles pouvaient quand même bien bouger. \n\nLa petite fille a pu respirer toute seule après un moment. Elle avait aussi des taches sur la peau et avait du mal à manger. Les docteurs ont fait beaucoup de tests. Ils ont trouvé qu’elle a un petit problème dans ses gènes appelé syndrome de Kabuki. \n\nElle est suivie par des médecins et des spécialistes pour l’aider à grandir. Tout le monde prend bien soin d’elle.",
+            "B2": "**Résumé adapté pour un adolescent de 14 ans :**\n\nUne fille est née un peu avant terme, à 34 semaines de grossesse. Dès la naissance, elle a eu des difficultés à respirer, alors les médecins ont dû l’aider avec un tube pour la ventilation. Des radios et des échographies ont montré que ses deux diaphragmes (les muscles qui aident à respirer sous les poumons) étaient un peu anormaux : ils étaient surélevés et une partie du foie poussait vers la poitrine. Cela s’appelle une éventration diaphragmatique, ce qui signifie que le muscle du diaphragme est remplacé en partie par du tissu fibreux, moins souple.\n\nPour vérifier si son diaphragme fonctionnait bien malgré cela, les médecins ont mesuré l’activité électrique de ce muscle pendant qu’elle essayait de respirer seule. Ils ont trouvé que cette activité était normale, comme chez d’autres bébés du même âge avec un diaphragme sain. Grâce à cela, ils ont pu retirer le tube de ventilation avec succès.\n\nLa taille de sa cage thoracique était similaire à celle d’un bébé né à terme avec une grave hernie diaphragmatique, une autre maladie du diaphragme. Mais ici, comme son diaphragme gardait une bonne activité, cela explique pourquoi elle a pu respirer sans tube assez rapidement.\n\nPendant son séjour à l’hôpital, elle a aussi eu d’autres problèmes : une peau avec des taches spéciales appelées mélanocytose, un tonus musculaire faible (hypotonie), un excès d’insuline qui fait baisser le sucre dans le sang (hyperinsulinisme), et des difficultés à s’alimenter. Après plusieurs examens, les médecins ont découvert qu’elle avait une mutation dans un gène appelé KMT2D. Cette mutation est liée à une maladie rare nommée syndrome de Kabuki, qui peut expliquer plusieurs de ses symptômes.\n\nEn résumé, malgré des problèmes au diaphragme, la fonction musculaire était assez bonne pour qu’elle puisse respirer seule rapidement. Ses autres troubles ont été étudiés et liés à un syndrome génétique. Elle reçoit maintenant des soins adaptés pour l’aider à grandir et se développer.",
+            "B3": "Résumé détaillé et structuré\n\nContexte  \nUne fille est née prématurément à 34 semaines de gestation, avec un poids de naissance de 2 820 g. Sa mère avait des antécédents de diabète gestationnel et de pré-éclampsie. Malgré un traitement prénatal complet par corticostéroïdes, l’enfant a présenté des difficultés respiratoires dès la naissance, nécessitant une intubation et une ventilation mécanique.\n\nPrincipales observations  \nL’imagerie radiographique thoracique initiale a montré une densité anormale bilatérale à la base des deux poumons, associée à une élévation des deux hémidiaphragmes. Une échographie diaphragmatique a confirmé la présence d’une éventration focale des deux diaphragmes, caractérisée par un bombement du dôme hépatique dans les cavités thoraciques droite et gauche. Cette anomalie traduit un déplacement partiel du tissu musculaire diaphragmatique par des bandes fibreuses.\n\nAvant l’extubation, une évaluation fonctionnelle a été réalisée : un essai de respiration spontanée (SBT) accompagné d’une mesure de l’activité électrique du diaphragme (électromyographie diaphragmatique). L’amplitude moyenne de cette activité était de 2,47 μV, valeur comparable à celle observée chez des nourrissons prématurés ventilés du même âge gestationnel mais présentant un diaphragme intact. Cette normalité fonctionnelle a permis une extubation réussie après 36 heures de ventilation invasive, sans nécessité de soutien respiratoire non invasif par la suite.\n\nLa surface thoracique radiographique mesurée trois jours après l’extubation était de 1 654 mm², une valeur similaire à celle d’un nourrisson à terme atteint d’une hernie diaphragmatique congénitale sévère. Cette mesure souligne l’importance de l’éventration diaphragmatique, bien que la fonction diaphragmatique ait été préservée partiellement.\n\nPar ailleurs, l’enfant a présenté plusieurs autres anomalies cliniques au cours de sa période néonatale : une hypoglycémie sévère due à un hyperinsulinisme, une hypotonie centrale (diminution du tonus musculaire liée au système nerveux central), une mauvaise alimentation nécessitant une nutrition par sonde nasogastrique, ainsi que des lésions cutanées multiples compatibles avec une mélanocytose (accumulation de cellules pigmentées). Deux dents néonatales ont été retirées peu après la naissance, suivies de l’ablation de lésions fibreuses pédiculées au niveau de la crête alvéolaire.\n\nUne investigation neurologique approfondie, incluant une imagerie par résonance magnétique cérébrale normale, une électromyographie et des études de conduction nerveuse normales, ainsi qu’une analyse immunohistochimique excluant une atrophie musculaire spinale, a été réalisée. Les examens ophtalmologiques et rénaux étaient également normaux.\n\nLes tests génétiques postnataux ont identifié une mutation du gène KMT2D, confirmant le diagnostic du syndrome de Kabuki, une maladie génétique rare associée à des anomalies multisystémiques.\n\nInterprétation clinique  \nLa présence d’une éventration diaphragmatique bilatérale focale avec maintien d’une activité électrique diaphragmatique normale suggère que le remplacement musculaire par du tissu fibreux était partiel, ce qui a permis une fonction respiratoire suffisante pour une extubation précoce réussie. Cette observation est importante car elle indique que, malgré une anomalie anatomique significative, la fonction diaphragmatique peut être préservée, évitant ainsi une intervention chirurgicale néonatale urgente.\n\nLes autres manifestations cliniques, notamment l’hyperinsulinisme, l’hypotonie centrale et la mélanocytose cutanée, ainsi que la mutation génétique identifiée, s’inscrivent dans le cadre du syndrome de Kabuki, qui explique la complexité du tableau clinique.\n\nProchaines étapes  \nL’enfant a été sortie de l’hôpital à 64 jours de vie, avec un soutien nutritionnel par sonde nasogastrique et un traitement médicamenteux par diazoxide pour contrôler l’hyperinsulinisme. Elle bénéficie d’un suivi pluridisciplinaire comprenant ergothérapie, orthophonie et physiothérapie pour accompagner son développement moteur et fonctionnel.\n\nCe cas souligne l’importance d’une évaluation fonctionnelle précise du diaphragme chez les nouveau-nés présentant des anomalies anatomiques, afin d’adapter au mieux la prise en charge respiratoire. Le diagnostic génétique permet également d’orienter le suivi et la prise en charge globale de l’enfant."
+        }
+    },
+    {
+        "article": "Patient de sexe masculin de 59 ans ayant des antécédents d'hémochromatose, d'accident ischémique transitoire et de glaucome. Il avait des antécédents familiaux de décès de deux oncles paternels à l'âge de 60 ans, suite à une maladie neurologique non spécifiée. Il présentait une histoire familiale de dysarthrie et de parésie faciale d'apparition soudaine, avec une amélioration en quelques jours. Après une semaine, il a présenté des mouvements involontaires du membre supérieur gauche (MSE), associés à une dysarthrie, une anomie légère (difficulté à nommer des personnes et des objets) et une dyscalculie (difficulté de calcul). Il ne présentait pas de fièvre ou d'autres symptômes. L'examen neurologique ne révélait pas de modification significative des fonctions nerveuses supérieures, avec une dysarthrie légère, une parésie faciale centrale droite, des mouvements myocloniques du MSE et une hémiface gauche. L'IRM-CE a montré une modification en T2 et en diffusion (DWI) dans le caudé droit et le putamen droit, sans implication du striatum contralatéral. En raison de la persistance de l'aggravation, il a répété l'IRM-CE cinq jours plus tard, ce qui a révélé une hyper-signe supplémentaire en diffusion du cortex fronto-pariéto-cingulaire médiale. L'enquête menée pour identifier les causes auto-immunes, infectieuses et paranéoplasiques a été négative. Le LCR présentait une augmentation de la protéine tau et de la protéine 14.3.3 normale. L'EEG a révélé une activité lente pariétale droite et frontotemporale bilatérale. Au cours des deux semaines suivantes, la dysarthrie s'est aggravée et une ataxie de la marche a fait son apparition. La possibilité d'une encéphalite auto-immune a été évoquée, et le patient a reçu une méthylprednisolone par voie intraveineuse (1 g pendant cinq jours), sans amélioration. Au cours des mois suivants, la détérioration neurologique s'est poursuivie, avec une évolution vers l'artérite (incapacité de la parole) et la dysphagie, l'hémiplégie gauche, l'incontinence urinaire et une détérioration cognitive avec altération de la mémoire récente, désorientation temporelle et dysfonction exécutive. Une nouvelle IRM-CE a été réalisée, qui a montré une restriction de la diffusion des ganglions de la base bilatérale et de multiples zones corticales, principalement le cortex frontal et pariétal. L'EEG a révélé une activité périodique de complexes de pointe-onde généralisée avec réactivité à la stimulation. Le patient est décédé quatre mois après le début de la maladie. L'analyse génétique effectuée par la suite a été positive pour la mutation c.598G > A (E200K).\n",
+        "gold_summary": "Nous présentons le cas d'un patient de 59 ans ayant présenté une parésie faciale centrale et une dysarthrie, suivies de myoclonies du côté gauche. L'IRM cérébrale initiale a montré une hyperintensité en T2 et une diffusion dans le caudé et le putamen droits et un liquide céphalorachidien hyperprotéinorachique. Les examens pour des causes auto-immunes, infectieuses et paranéoplasiques ont été négatifs. Au cours des mois suivants, il a progressivement présenté une hémiplégie gauche, une dysphagie, une incontinence urinaire et un mutisme acinétique. L'IRM cérébrale a montré une évolution vers une restriction de la diffusion des ganglions de la base bilatéralement et de multiples zones corticales ; l'électroencéphalographie a montré une activité périodique et une protéine Tau élevée dans le liquide céphalorachidien. L'analyse génétique a révélé une mutation c.598G > A. Le décès est survenu après quatre mois de maladie.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 59 ans a eu des problèmes pour parler et bouger un côté de son visage. Puis, son bras gauche bougeait tout seul. \n\nLes médecins ont fait des images de son cerveau. Ils ont vu des choses qui ne vont pas bien. Ils ont cherché si c’était une maladie avec des microbes ou autre, mais rien n’a été trouvé. \n\nAvec le temps, il a eu de plus en plus de difficultés. Il ne pouvait presque plus parler, ni marcher bien. Son corps ne répondait plus comme avant. \n\nLes images du cerveau ont montré que plusieurs parties étaient malades. Les médecins ont aussi fait des tests dans son cerveau qui ont montré des signes de maladie. \n\nAprès, ils ont trouvé un petit changement dans ses gènes. Ce monsieur est mort quatre mois après que la maladie a commencé. \n\nC’est une maladie très grave qui rend le corps et le cerveau très malades.",
+            "B2": "Cas d’un homme de 59 ans avec des problèmes neurologiques graves\n\nCe patient de 59 ans a d’abord eu une faiblesse au visage d’un côté (appelée parésie faciale centrale) et des difficultés à parler clairement (dysarthrie). Ensuite, il a eu des mouvements involontaires rapides (myoclonies) du bras gauche.\n\nCe qu’ils ont trouvé au début\n\nUne IRM du cerveau a montré des zones anormales dans deux parties du cerveau appelées le caudé et le putamen, situées du côté droit. Le liquide autour du cerveau (liquide céphalorachidien) contenait plus de protéines que la normale. Ils ont cherché si une infection, une maladie auto-immune ou un cancer pouvait expliquer ces symptômes, mais tous les tests étaient négatifs.\n\nCe qui s’est passé ensuite\n\nAu fil des mois, son état s’est aggravé. Il a perdu la force dans tout le côté gauche du corps (hémiplégie), a eu du mal à avaler (dysphagie), a perdu le contrôle de sa vessie (incontinence urinaire) et a fini par ne plus pouvoir parler du tout (mutisme acinétique).\n\nNouvelles analyses\n\nUne nouvelle IRM a montré que les zones anormales s’étaient étendues, touchant les deux côtés des ganglions de la base (zones profondes du cerveau) et plusieurs régions du cortex, la partie externe du cerveau. Un examen appelé électroencéphalographie (EEG), qui mesure l’activité électrique du cerveau, a montré des motifs anormaux périodiques. De plus, une protéine appelée Tau, liée à la mort des cellules nerveuses, était élevée dans le liquide cérébral.\n\nDiagnostic génétique\n\nUne analyse génétique a découvert une mutation spécifique nommée c.598G > A (E200K). Cette mutation est connue pour causer une maladie neurologique grave.\n\nConclusion\n\nMalheureusement, la maladie a évolué rapidement et le patient est décédé quatre mois après le début des symptômes. Ce cas montre l’importance de combiner les examens cliniques, l’imagerie, les analyses du liquide cérébral et la génétique pour comprendre certaines maladies du cerveau.",
+            "B3": "Résumé détaillé et structuré pour un public non spécialiste\n\n**Contexte**  \nIl s’agit d’un homme de 59 ans avec des antécédents médicaux comprenant une hémochromatose (accumulation excessive de fer dans l’organisme), un accident ischémique transitoire (un mini-AVC) et un glaucome. Sa famille présentait des cas de maladies neurologiques non précisées, notamment chez deux oncles décédés vers 60 ans. Le patient a développé progressivement des troubles neurologiques débutant par une faiblesse faciale centrale (parésie faciale) et des difficultés d’élocution (dysarthrie), suivies de mouvements involontaires (myoclonies) du bras gauche.\n\n**Principales observations**  \n- L’imagerie cérébrale par résonance magnétique (IRM) initiale a montré des anomalies dans des zones profondes du cerveau appelées noyaux gris centraux (caudé et putamen droits), visibles sur des séquences spécifiques (hyperintensité en T2 et diffusion).  \n- Le liquide céphalorachidien (LCR), qui entoure le cerveau et la moelle épinière, présentait une augmentation de protéines, signe d’une atteinte neurologique, avec une élévation de la protéine Tau, un marqueur de dégénérescence neuronale.  \n- Les investigations pour exclure des causes auto-immunes, infectieuses ou liées à un cancer (paranéoplasiques) ont été négatives.  \n- Au fil des semaines et des mois, les symptômes ont évolué vers une paralysie complète du côté gauche du corps (hémiplégie), des difficultés à avaler (dysphagie), une perte du contrôle de la vessie (incontinence urinaire) et un mutisme acinétique (incapacité à parler malgré la conscience).  \n- Les examens d’imagerie ultérieurs ont montré une extension des lésions, avec une atteinte bilatérale des noyaux gris centraux et de nombreuses zones corticales (parties externes du cerveau), notamment dans les régions frontales et pariétales.  \n- L’électroencéphalogramme (EEG), qui mesure l’activité électrique cérébrale, a révélé des anomalies périodiques caractéristiques.  \n- L’évolution clinique rapide et les résultats des examens ont conduit à suspecter une maladie neurodégénérative grave.\n\n**Interprétation clinique**  \nLe tableau clinique, l’imagerie et les analyses biologiques sont compatibles avec une encéphalopathie prionique, une maladie neurodégénérative rare et rapidement progressive. La confirmation est venue de l’analyse génétique qui a identifié une mutation spécifique (c.598G > A, aussi appelée E200K) connue pour être associée à une forme héréditaire de cette maladie.\n\n**Prochaines étapes et pronostic**  \nMalheureusement, malgré les investigations et un traitement immunosuppresseur initial (corticothérapie par méthylprednisolone), la maladie a rapidement progressé, conduisant au décès du patient quatre mois après le début des symptômes. Ce cas illustre la difficulté de diagnostic précoce des encéphalopathies prioniques héréditaires et la nécessité d’une prise en charge multidisciplinaire rapide."
+        }
+    },
+    {
+        "article": "Il s’agit d’un cas d’un homme de 23 ans ayant des antécédents médicaux sans particularité, qui a été référé pour une dyspnée inexpliquée. Avant sa maladie actuelle, il était en bonne santé et n’avait aucune difficulté à effectuer ses activités quotidiennes. Ses deux parents avaient le diabète, et son grand-père est décédé d’une crise cardiaque à l’âge de 74 ans. En outre, après avoir examiné de plus près les antécédents familiaux, nous avons découvert que l’oncle du patient avait des antécédents d’acromégalie.\n\nL’état du patient a commencé deux semaines avant son admission lorsqu’il a commencé à se plaindre de fièvre, de congestion nasale et de rhinorrhée. Trois jours plus tard, il a commencé à se plaindre de vomissements, de diarrhée et de douleurs abdominales. Après avoir été admis au service de médecine interne, nous avons été consultés pour des palpitations, une dyspnée et une orthopnée prononcées.\n\nPendant l'examen, sa température était légèrement élevée à 37,9 °C, sa tension artérielle était de 150/90 mmHg, sa fréquence cardiaque de 110/min et sa fréquence respiratoire de 22/min. L'auscultation a révélé de fines crépitations pulmonaires basales avec des ronflements expiratoires modérés bilatéraux. En outre, un souffle diastolique précoce a été détecté. Ses veines du cou étaient congestionnées, mais ne pulsaient pas, et il n'y avait pas d'œdème des membres inférieurs ou d'ascite.\n\nLes résultats de laboratoire étaient remarquables pour un niveau élevé de peptide natriurétique cérébral (BNP) (340 pg/mL). Les résultats complémentaires comprenaient un épanchement pleural bilatéral modéré et une cardiomégalie observée sur la radiographie thoracique. L'ECG a révélé une tachycardie sinusale avec des ondes T inversées dans les dérivations V3 et V4. L'échocardiographie transthoracique (TTE) a montré un ventricule gauche (VG) modérément dilaté et hypertrophié, une fonction systolique du VG légèrement altérée avec une fraction d'éjection de 48 % en mode M, une fonction diastolique altérée, une régurgitation mitrale modérée et une régurgitation aortique sévère. La racine aortique était nettement dilatée, avec des diamètres de 3,2 cm à l'annulus, 4,9 cm au sinus de Valsalva et 7,5 cm à la jonction sino-tubulaire (JST).\n\nEn conséquence, une aortographie a été réalisée, confirmant les mesures échocardiographiques des diamètres de la racine aortique. En outre, elle a révélé une dilatation de l'aorte ascendante d'un diamètre de 10 cm et de l'aorte descendante d'un diamètre de 2,5 cm. Le patient a commencé à prendre les médicaments suivants : Furosémide (20 mg toutes les 8 heures), Ramipril (1,25 mg une fois par jour) et Empagliflozin (10 mg une fois par jour). En 10 jours, le patient a connu une légère amélioration des symptômes, en particulier de la dyspnée, et a déclaré avoir mieux dormi. Une radiographie thoracique de suivi a montré une résolution partielle de l'épanchement pleural.\n\nAu début, nous avons considéré une maladie du tissu conjonctif comme le syndrome de Marfan ou d'Ehlers-Danlos. Cependant, le patient manquait les caractéristiques physiques typiques et les signes associés de ces conditions. En outre, son test de fonction pulmonaire était normal, ce qui serait probablement anormal dans un trouble multisystémique du tissu conjonctif. Les résultats de laboratoire ont montré des taux normaux de VS et de protéine C-réactive, ce qui réduit la probabilité d'une vascularite comme cause de la dilatation de la racine aortique. Le panel auto-immun, y compris les tests ANA et RF, était également négatif.\n\nL’acromégalie a ensuite été considérée comme la cause potentielle de l’hypertrophie de la LV et de la dilatation de la racine aortique, en particulier compte tenu des antécédents familiaux de la maladie. Par conséquent, le taux de facteur de croissance analogue à l’insuline 1 (IGF-1) a été mesuré et était élevé (320 ng/ml), et le taux de GH est resté supérieur à la normale (1,1 ng/ml) après un test de tolérance au glucose par voie orale confirmant le diagnostic d’acromégalie. Une image IRM du cerveau pondérée en T2 a montré une masse hyperintense de 7 × 4 mm dans la selle turcique, compatible avec un microadénome hypophysaire.\n\nPar la suite, la décision de procéder à l'opération a été prise après avoir obtenu le consentement du patient. Après une angiographie coronarienne normale, le patient a subi une procédure de remplacement de greffe composite, impliquant la valve aortique, la racine aortique et l'aorte ascendante (procédure de Bentall). Une valve mécanique a été utilisée, et le patient a commencé à prendre de la warfarine à une dose quotidienne de 3 mg, avec une surveillance étroite pour atteindre un taux de coagulation cible de 2 à 3.\n\nÀ la suite d'une consultation avec l'endocrinologue, le patient a commencé à recevoir des injections mensuelles d'acétate d'octréotide. Un plan de suivi complet a été établi, qui comprenait le contrôle du fonctionnement de la valve, l'évaluation de la fonction LV, la vérification de la conformité au traitement et la vérification des valeurs d'IGF-1 et d'INR. Mis à part une légère dyspnée d'effort, il est resté asymptomatique pendant 8 semaines après l'opération. Au cours de cette période, les échocardiogrammes de suivi ont montré que la valve aortique remplacée fonctionnait normalement sans aucune fuite ou dysfonctionnement. La racine aortique et l'aorte ascendante étaient également stables, sans aucun signe de dilatation, d'anévrisme ou d'autres complications. Il n'y a pas eu de progression de son hypertrophie LV non plus. Son niveau d'IGF-1 le plus récent était de 290 ng/ml, ce qui est légèrement inférieur au premier, et il a été maintenu sous Octreotide sans effets indésirables significatifs.\n",
+        "gold_summary": "Ce rapport présente le cas d'un homme de 23 ans sans antécédents médicaux significatifs, qui a présenté une dyspnée sévère après une infection thoracique. Il manquait des caractéristiques physiques distinctes de troubles génétiques ou endocriniens, mais son oncle souffrait d'acromégalie. L'échocardiographie a révélé une hypertrophie ventriculaire gauche et une dilatation massive de la racine aortique. L'augmentation du facteur de croissance analogue à l'insuline 1 (IGF-1) a confirmé le diagnostic d'acromégalie. Le patient a subi une procédure de Bentall, et son acromégalie a été gérée avec de l'octréotide et des suivis réguliers.\n",
+        "synthetic_summary": {
+            "B1": "Il y a un jeune homme de 23 ans. Il avait du mal à bien respirer après être tombé malade. Son cœur était un peu plus gros que d’habitude. Une partie de son gros vaisseau du cœur était aussi très grande. \n\nLes docteurs ont fait des tests. Ils ont trouvé qu’il avait une maladie qui fait grandir trop certaines parties du corps. Cette maladie vient de sa famille. \n\nPour l’aider, les docteurs ont fait une opération pour réparer son cœur. Il prend aussi des médicaments pour que ça aille mieux. Maintenant, il va mieux et les docteurs le surveillent souvent.",
+            "B2": "Cas d’un jeune homme de 23 ans avec des difficultés à respirer après une infection. Avant cela, il était en bonne santé et n’avait pas de problèmes médicaux connus. Son oncle avait une maladie appelée acromégalie, qui provoque une production trop élevée d’une hormone de croissance.\n\nLors de son examen, les médecins ont trouvé que son cœur était agrandi et que la partie principale de son aorte (le gros vaisseau qui sort du cœur) était très dilatée, ce qui peut être dangereux. Une échographie du cœur a montré que le muscle du ventricule gauche (la chambre qui pompe le sang vers le corps) était épaissi et que la valve aortique ne fonctionnait pas bien.\n\nPour comprendre la cause, ils ont mesuré un facteur de croissance appelé IGF-1, qui était élevé. Cela a confirmé que le patient avait une acromégalie. Une IRM du cerveau a montré une petite tumeur dans une glande appelée hypophyse, responsable de cette maladie.\n\nLe patient a subi une opération appelée procédure de Bentall, qui remplace la valve aortique et la partie dilatée de l’aorte. Après l’opération, il a commencé un traitement avec un médicament nommé octréotide, qui aide à contrôler la production d’hormones. Il est suivi régulièrement pour vérifier le fonctionnement de sa valve, la taille de son cœur et ses niveaux d’hormones.\n\nHuit semaines après l’opération, le patient allait mieux, avec une bonne fonction cardiaque et une diminution des symptômes. Son traitement continue sans effets secondaires importants. Ce cas montre l’importance de rechercher des causes hormonales quand un jeune présente des problèmes cardiaques graves.",
+            "B3": "Résumé détaillé et structuré du cas clinique\n\nContexte  \nCe rapport décrit le cas d’un homme de 23 ans, auparavant en bonne santé, qui a été admis pour une dyspnée (difficulté à respirer) progressive survenue après une infection respiratoire aiguë. Aucun antécédent médical personnel notable n’était rapporté, mais une histoire familiale importante a été relevée, notamment un oncle atteint d’acromégalie (une maladie endocrinienne caractérisée par une production excessive d’hormone de croissance).\n\nPrincipales observations cliniques et paracliniques  \nLe patient présentait une fièvre légère, une hypertension artérielle modérée (150/90 mmHg), une tachycardie (110 battements par minute) et des signes d’insuffisance cardiaque, notamment des crépitements pulmonaires et un souffle diastolique précoce à l’auscultation. L’examen ne montrait pas d’œdème périphérique ni d’autres signes d’insuffisance veineuse.  \n\nLes analyses sanguines ont révélé un taux élevé de peptide natriurétique cérébral (BNP), un marqueur de stress cardiaque. La radiographie thoracique a montré une cardiomégalie (augmentation de la taille du cœur) et un épanchement pleural bilatéral modéré. L’électrocardiogramme (ECG) indiquait une tachycardie sinusale avec des anomalies de la repolarisation.  \n\nL’échocardiographie transthoracique a mis en évidence une dilatation modérée et une hypertrophie du ventricule gauche, une fonction systolique légèrement altérée (fraction d’éjection à 48 %), une régurgitation mitrale modérée et une régurgitation aortique sévère. La racine aortique était massivement dilatée, avec des diamètres allant jusqu’à 7,5 cm à la jonction sino-tubulaire. Une aortographie a confirmé ces mesures et a révélé une dilatation importante de l’aorte ascendante (10 cm de diamètre).  \n\nDiagnostic différentiel et confirmation  \nInitialement, des maladies du tissu conjonctif telles que le syndrome de Marfan ou d’Ehlers-Danlos ont été envisagées, mais l’absence de signes physiques caractéristiques et des tests pulmonaires normaux ont rendu ces diagnostics improbables. Les marqueurs inflammatoires et auto-immuns étaient normaux, excluant une vascularite.  \n\nCompte tenu des antécédents familiaux, une acromégalie a été suspectée. Le dosage du facteur de croissance analogue à l’insuline 1 (IGF-1) était élevé, et la persistance d’un taux élevé d’hormone de croissance (GH) après un test de tolérance au glucose a confirmé ce diagnostic. L’IRM cérébrale a montré un microadénome hypophysaire compatible avec une tumeur sécrétante de GH.  \n\nTraitement et suivi  \nLe patient a été traité initialement par des médicaments diurétiques, un inhibiteur de l’enzyme de conversion (Ramipril) et un inhibiteur du SGLT2 (Empagliflozin), ce qui a amélioré ses symptômes. Après confirmation du diagnostic, il a subi une intervention chirurgicale majeure (procédure de Bentall) consistant en un remplacement composite de la valve aortique, de la racine aortique et de l’aorte ascendante, avec implantation d’une valve mécanique. Un traitement anticoagulant par warfarine a été instauré pour prévenir les complications thromboemboliques.  \n\nParallèlement, un traitement endocrinien par injections mensuelles d’acétate d’octréotide, un analogue de la somatostatine, a été débuté pour contrôler la sécrétion hormonale liée à l’acromégalie.  \n\nAu suivi à huit semaines, le patient présentait une amélioration clinique notable avec une fonction valvulaire normale, une stabilité de la racine aortique et de l’aorte ascendante, et une absence de progression de l’hypertrophie ventriculaire gauche. Le taux d’IGF-1 était en diminution, témoignant d’un bon contrôle de la maladie endocrinienne, sans effets secondaires significatifs liés au traitement.  \n\nConclusion  \nCe cas illustre l’importance de considérer l’acromégalie comme cause possible d’une dilatation massive de la racine aortique et d’une hypertrophie ventriculaire gauche, surtout en présence d’antécédents familiaux évocateurs. Une prise en charge multidisciplinaire combinant chirurgie cardiaque et traitement endocrinien permet une amélioration clinique et un contrôle efficace de la maladie sous-jacente. Un suivi régulier est essentiel pour surveiller la fonction cardiaque, la conformité au traitement et l’évolution de l’acromégalie."
+        }
+    },
+    {
+        "article": "Une fillette de 2 ans a été admise aux urgences avec une fièvre élevée de 5 jours, une toux et un gonflement bilatéral des paupières. Avant le début de cette maladie, elle souffrait d'un œdème et d'un furoncle au niveau de la peau du visage, au niveau du périné. Elle était auparavant en bonne santé.\n\nL'examen physique a révélé une fille très malade avec un œdème périorbitaire et facial, une fièvre élevée, une fréquence respiratoire accrue, une SpO2 diminuée et des crépitations thoraciques.\n\nUn examen oculaire a révélé un gonflement autour des yeux des deux côtés. Les deux globes ont montré une proptose axiale. Les examens ont également montré une injection, une décharge purulente dans les deux yeux avec des pupilles à réaction lente, une conjonctivite chimique sévère et une ophtalmoplegie externe affectant les troisième, quatrième et sixième nerfs crâniens.\n\nLe rapport de disque vertical de l'œil droit était de 0,3, tandis que celui de l'œil gauche était de 0,4. Il n'y avait aucune preuve de congestion des veines rétiniennes ou d'œdème du disque.\n\nLes examens de laboratoire ont révélé une numération leucocytaire significativement élevée (32 000 cellules/mm3), une faible hémoglobine (5,5 mg/dL) et une protéine C-réactive élevée (112 mg/L). La culture sanguine était négative.\n\nLa tomographie par ordinateur orbitale a révélé un épaississement important des tissus mous périorbitaux bilatéraux et un oedème sous-cutané facial. En outre, la tomographie par ordinateur avec contraste du thorax a révélé de multiples lésions cavitaires situées périphériquement dans les poumons bilatéraux (embolies septiques) et un pneumothorax modéré bilatéral associé avec des zones de consolidation avec bronchogramme aérien dans le poumon inférieur gauche.\n\nLe patient a été admis à l'unité de soins intensifs pédiatriques et un traitement a été initié avec de la ceftriaxone intraveineuse (IV) à 500 mg toutes les 12 heures, de la clindamycine IV à 100 mg toutes les 8 heures, des gouttes oculaires Voltaren toutes les 8 heures, des gouttes oculaires Lomefloxacin toutes les 12 heures après une dose de charge initiale d'une goutte toutes les 5 minutes pendant 25 minutes, de la pommade au chloramphénicol pour la nuit et du sirop d'ibuprofène oral toutes les 8 heures. Des tubes thoraciques bilatéraux ont été insérés pour la décompression du pneumothorax.\n\nSon nombre de globules blancs est revenu à la normale et sa radiographie thoracique s'est considérablement améliorée. Elle a quitté l'hôpital après 15 jours avec une antibiothérapie orale (co_amoxiclav syrup 400mg) à prendre pendant une semaine.\n",
+        "gold_summary": "Une fillette de 2 ans a présenté une fièvre élevée, une toux et un gonflement des paupières bilatérales pendant 5 jours, précédés d'un œdème et d'un furoncle de la peau du visage péranasal. L'examen a révélé une proptose axiale bilatérale et une cellulite orbitale et thoracique bilatérale, une embolie pulmonaire septique et un pneumothorax bilatéral.\n",
+        "synthetic_summary": {
+            "B1": "Une petite fille de 2 ans avait de la fièvre et une grosseur autour des yeux. Elle toussait aussi depuis plusieurs jours.\n\nAvant, elle avait une grosse boule sur la peau de son visage. Son corps était très fatigué.\n\nLes docteurs ont vu que ses yeux étaient très gonflés. Ses poumons avaient aussi des problèmes.\n\nElle est allée à l’hôpital pour se soigner. Les docteurs lui ont donné des médicaments pour l’aider à guérir.\n\nAprès un moment, elle est devenue mieux et a pu rentrer chez elle.",
+            "B2": "Une fillette de 2 ans est arrivée à l'hôpital avec une forte fièvre, une toux et un gonflement des paupières des deux yeux qui duraient depuis cinq jours. Avant cela, elle avait un gonflement et un furoncle (une grosseur douloureuse avec du pus) sur la peau de son visage près du nez. Lors de l'examen, les médecins ont remarqué que ses yeux étaient poussés vers l'avant (ce qu'on appelle une proptose) des deux côtés, ainsi qu’un gonflement important autour des yeux et du visage.\n\nDes examens plus poussés ont montré qu’elle avait une infection grave autour des yeux (appelée cellulite orbitale) et dans la poitrine. Dans ses poumons, il y avait des zones infectées avec des caillots de sang infectés (embolie septique) et de l’air s’était accumulé dans la poitrine des deux côtés (pneumothorax), ce qui peut rendre la respiration difficile.\n\nElle a été soignée avec des antibiotiques puissants et des soins pour les yeux, ainsi qu’une intervention pour enlever l’air dans la poitrine. Après deux semaines de traitement, son état s’est beaucoup amélioré et elle a pu quitter l’hôpital avec des médicaments à prendre à la maison.",
+            "B3": "Contexte  \nUne fillette de 2 ans, auparavant en bonne santé, a été admise aux urgences après cinq jours de fièvre élevée, de toux et d’un gonflement marqué des paupières des deux yeux. Avant l’apparition de ces symptômes, elle présentait un œdème et un furoncle au niveau de la peau du visage, près du périnée.\n\nPrincipales Observations  \nL’examen clinique a montré un état général très altéré, avec un œdème important autour des yeux et du visage, une fréquence respiratoire accélérée, une saturation en oxygène diminuée et des crépitations à l’auscultation pulmonaire. L’examen oculaire a révélé un gonflement périorbitaire bilatéral, une proptose axiale (déplacement vers l’avant des globes oculaires) des deux yeux, une conjonctivite sévère avec sécrétions purulentes, une réaction pupillaire lente et une paralysie des nerfs crâniens responsables des mouvements oculaires (nerfs III, IV et VI). Le fond d’œil ne montrait pas de signes d’œdème du nerf optique ni de congestion veineuse.\n\nLes analyses sanguines ont mis en évidence une forte augmentation des globules blancs (32 000/mm³), une anémie sévère (hémoglobine à 5,5 g/dL) et une inflammation importante (protéine C-réactive à 112 mg/L). Les cultures sanguines sont restées négatives.\n\nL’imagerie par tomodensitométrie (TDM) orbitale a confirmé un épaississement important des tissus mous autour des yeux et un œdème sous-cutané du visage. La TDM thoracique avec injection a révélé la présence de multiples lésions cavitaires périphériques dans les deux poumons, compatibles avec des embolies septiques (petits caillots infectés), ainsi qu’un pneumothorax modéré bilatéral (présence d’air dans la cavité pleurale) et des zones de consolidation pulmonaire avec bronchogramme aérien dans le lobe inférieur gauche.\n\nInterprétation Clinique  \nLe tableau clinique et radiologique correspond à une cellulite orbitale bilatérale sévère compliquée d’une embolie pulmonaire septique et d’un pneumothorax bilatéral. La paralysie des nerfs oculomoteurs traduit une atteinte neurologique locale liée à l’infection. L’anémie et la forte réaction inflammatoire témoignent de la gravité de l’infection.\n\nProchaines Étapes  \nLa patiente a été admise en unité de soins intensifs pédiatriques. Un traitement antibiotique intraveineux combinant ceftriaxone et clindamycine a été instauré, accompagné de soins oculaires locaux (gouttes et pommade antibiotiques, anti-inflammatoires). Un drainage par tubes thoraciques bilatéraux a été réalisé pour traiter le pneumothorax. Après une amélioration clinique et biologique, la fillette est sortie de l’hôpital au bout de 15 jours avec une antibiothérapie orale à poursuivre une semaine. Le suivi a montré une résolution progressive des symptômes et une récupération satisfaisante."
+        }
+    },
+    {
+        "article": "Nous présentons le cas d'un Marocain blanc de 38 ans, sans facteurs de risque cardiovasculaire et ayant des antécédents de cécité bilatérale inexpliquée, qui s'est présenté au service des urgences avec un œdème chronique des membres et une dyspnée progressive.\n\nL'évaluation initiale a révélé un patient hémodynamiquement stable avec une tension artérielle normale de 105/76 mmHg, une fréquence cardiaque de 45 battements par minute et une saturation en oxygène de 93 % en air ambiant. L'examen physique a révélé une distension de la veine jugulaire externe, un œdème des jambes étendu et une ascite. L'auscultation cardiopulmonaire a révélé un murmure holosystolique 4/6 au foyer mitral avec des crépitations diffuses bilatérales symétriques. L'examen ophtalmologique a révélé une acuité visuelle réduite à la perception de la lumière.\n\nUn électrocardiogramme a montré une bradycardie sinusale avec une fréquence cardiaque de 45 battements par minute et un bloc de branche droit complet. La radiographie thoracique a révélé une cardiomégalie et une congestion périhiliale. Le taux de peptide natriurétique de type B était de 1230 pg/ml (pour une plage normale inférieure à 300 pg/ml), le taux de créatinine était de 9,6 mg/l (pour une plage normale comprise entre 6 et 12,5 mg/l), le taux d'albumine était légèrement bas à 36 g/l (pour une plage normale supérieure à 39 g/l), et il y avait une haute sensibilité de la troponine à 294 ng/l (pour une plage normale inférieure à 35 ng/l). Les autres résultats des tests de laboratoire étaient normaux, en particulier les taux de ferritine, de TSH et d'électrolyte.\n\nL'échocardiographie transthoracique (TTE) a montré un ventricule gauche dilaté (diamètre diastolique de base à la fin de 60 mm) avec une fraction d'éjection sévèrement réduite à 15 % (biplan Simpson), une régurgitation mitrale modérée et un thrombus apical mesurant 19 mm × 18 mm. Le ventricule droit était sévèrement dilaté (diamètre diastolique de base à la fin de 51 mm), avec une dysfonction systolique (excursion systolique du plan annulaire tricuspide (TAPSE) de 12 mm et onde S' du ventricule droit sur doppler tissulaire (S'VD) de 5 cm/s) et une régurgitation tricuspide sévère. La veine cave inférieure (VCI) était pléthorique avec un diamètre maximal de 37 mm.\n\nL’histoire détaillée a révélé que depuis ses 20 ans, le patient avait des problèmes de marche, une perte auditive et une anosmie et que sa cécité avait commencé avec une vision nocturne altérée, mais il n’avait jamais été évalué par un ophtalmologue avant cette présentation. Les examens neurologiques ont révélé une amyotrophie bilatérale des jambes avec une ataxie bilatérale. Un examen ophtalmologique a été effectué pour explorer sa cécité et a révélé une rétinite pigmentaire. L’image clinique du patient associant une cardiomyopathie dilatée aux signes neurologiques spécifiques était fortement suggestive de la maladie de Refsum. Nous avons effectué un dosage des concentrations plasmatiques d’acide phytique, qui a révélé un taux remarquablement élevé de 324 μmol/l, confirmant la maladie de Refsum. Initialement, le patient a été mis sous furosémide intraveineuse, qui a ensuite soulagé ses symptômes d’insuffisance cardiaque. Il a ensuite reçu un traitement par furosémide oral [40 mg deux fois par jour (b.i.d)], des inhibiteurs de l’enzyme de conversion de l’angiotensine (ramipril 2,5 mg b.i.d), de la spironolactone (25 mg une fois par jour (o.d)) et un inhibiteur de SGLT2 (empagliflozine 10 mg o.d.). Les bêta-bloquants n’ont pas été administrés en raison d’une bradycardie sinusale. En outre, le patient a reçu des antagonistes de la vitamine K pour le thrombus ventriculaire gauche.\n\nEn ce qui concerne le traitement spécifique de la maladie de Refsum, le patient a été conseillé de suivre un régime alimentaire restreint conçu pour éliminer les aliments contenant du phytol, avec un apport quotidien en acide phytanique inférieur à 10 mg. Cela impliquait d'éviter la consommation de viande ou de graisses provenant d'animaux ruminants (tels que l'agneau et le bœuf) et de produits de boulangerie contenant des graisses animales, ainsi que de produits laitiers tels que le beurre et le fromage.\n\nLe patient a récupéré et son état a été stabilisé avec des symptômes de l'insuffisance cardiaque chronique de classe NYHA 2 ; il a donc été renvoyé à domicile sous traitement médical pour insuffisance cardiaque, antagonistes de la vitamine K (VKA) et régime hyphatico-acide.",
+        "gold_summary": "Nous rapportons le cas d'un Marocain blanc de 38 ans admis dans notre service pour un épisode d'insuffisance cardiaque aiguë décompensée. L'échocardiographie transthoracique a révélé une cardiomyopathie dilatée avec une fraction d'éjection réduite à 15 %. Une évaluation plus approfondie a révélé des caractéristiques différentes de la maladie de Refsum. Un taux plasmatique élevé d'acide phytanique a confirmé le diagnostic. Les manifestations cardiaques sont fréquentes dans le cours tardif de la maladie de Refsum chez l'adulte et comprennent une cardiomyopathie, des anomalies électriques et une mort cardiaque subite. En outre, les arythmies restent l'une des principales causes de décès chez ces patients.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 38 ans avait un gros problème avec son cœur. Son cœur ne battait pas bien fort. \n\nLes docteurs ont fait des examens et ont trouvé une maladie appelée maladie de Refsum. Cette maladie peut rendre le cœur très fatigué. \n\nCette maladie peut aussi causer des problèmes avec le rythme du cœur. C’est pour ça que le cœur peut parfois s’arrêter. \n\nLes docteurs ont donné des médicaments pour aider son cœur à mieux marcher. Ils ont aussi conseillé de manger certains aliments pour aider le corps. \n\nLe monsieur va mieux maintenant et il doit continuer ses soins pour rester en bonne santé.",
+            "B2": "Cas d’un homme de 38 ans avec une maladie rare appelée maladie de Refsum\n\nNous racontons l’histoire d’un homme de 38 ans venu à l’hôpital avec des problèmes graves au cœur. Une échographie du cœur a montré que sa pompe cardiaque, appelée ventricule gauche, était très faible, avec seulement 15 % de force pour envoyer le sang. Cela s’appelle une cardiomyopathie dilatée.\n\nEn cherchant la cause, les médecins ont découvert que cet homme avait aussi des signes d’une maladie rare appelée maladie de Refsum. Cette maladie provoque une accumulation dans le corps d’une substance appelée acide phytanique. Un test sanguin a montré que son taux d’acide phytanique était très élevé, ce qui a confirmé le diagnostic.\n\nLa maladie de Refsum peut causer des problèmes cardiaques, surtout chez les adultes qui en souffrent depuis longtemps. Ces problèmes incluent une faiblesse du cœur, des troubles du rythme cardiaque (c’est-à-dire que le cœur bat trop vite, trop lentement ou de façon irrégulière) et un risque de mort subite.\n\nChez ces patients, les troubles du rythme sont une cause importante de décès. C’est pourquoi il est essentiel de diagnostiquer cette maladie tôt et de commencer un traitement adapté, qui comprend un régime alimentaire spécial pour réduire l’acide phytanique et des médicaments pour protéger le cœur.",
+            "B3": "### Contexte  \nNous présentons le cas d’un homme marocain de 38 ans, sans antécédents cardiovasculaires connus, qui s’est présenté aux urgences avec un œdème chronique des membres inférieurs et une dyspnée progressive. Il avait également des antécédents de cécité bilatérale inexpliquée depuis plusieurs années, associée à des troubles neurologiques tels que des difficultés de marche, une perte auditive et une anosmie (perte de l’odorat).\n\n### Principales observations  \nL’examen clinique a montré un patient stable sur le plan hémodynamique mais avec une bradycardie (fréquence cardiaque à 45 battements par minute), une distension des veines jugulaires, un œdème étendu des jambes et une ascite. L’auscultation cardiaque a révélé un souffle holosystolique important au niveau mitral, et des crépitements pulmonaires diffus. L’électrocardiogramme a confirmé une bradycardie sinusale avec un bloc de branche droit complet. La radiographie thoracique a montré une cardiomégalie et une congestion pulmonaire.\n\nLes analyses biologiques ont mis en évidence un taux élevé de peptide natriurétique de type B (BNP), un marqueur d’insuffisance cardiaque, ainsi qu’une élévation significative de la troponine, signe d’atteinte myocardique. L’échocardiographie transthoracique a révélé une cardiomyopathie dilatée sévère avec une fraction d’éjection du ventricule gauche très basse (15 %), une dilatation et dysfonction du ventricule droit, une régurgitation mitrale modérée, une régurgitation tricuspide sévère, et la présence d’un thrombus (caillot) dans l’apex du ventricule gauche.\n\nL’examen neurologique a confirmé une amyotrophie (fonte musculaire) des jambes et une ataxie (trouble de la coordination). L’évaluation ophtalmologique a diagnostiqué une rétinite pigmentaire, une maladie dégénérative de la rétine responsable de la cécité nocturne et progressive.\n\n### Interprétation clinique  \nL’association d’une cardiomyopathie dilatée sévère, de troubles neurologiques spécifiques et d’une rétinite pigmentaire a orienté vers la maladie de Refsum, une maladie métabolique rare caractérisée par une accumulation d’acide phytanique dans l’organisme. La confirmation diagnostique a été obtenue par la mesure d’un taux plasmatique très élevé d’acide phytanique.\n\nLes manifestations cardiaques, bien que rares, sont reconnues dans les formes tardives de la maladie de Refsum chez l’adulte. Elles incluent une cardiomyopathie dilatée, des anomalies électriques du cœur telles que des troubles du rythme, et un risque accru de mort subite. Les arythmies cardiaques représentent une cause majeure de mortalité chez ces patients.\n\n### Prochaines étapes et prise en charge  \nLe patient a été traité initialement par des diurétiques intraveineux pour soulager les symptômes d’insuffisance cardiaque, puis par un traitement médical standard comprenant des inhibiteurs de l’enzyme de conversion de l’angiotensine, de la spironolactone et un inhibiteur de SGLT2. Les bêta-bloquants ont été évités en raison de la bradycardie. Un traitement anticoagulant par antagonistes de la vitamine K a été instauré pour prévenir les complications du thrombus ventriculaire.\n\nUn régime alimentaire strict a été prescrit, visant à réduire l’apport en acide phytanique en évitant les aliments riches en phytol, notamment les viandes et graisses d’animaux ruminants (agneau, bœuf), les produits laitiers et certains produits de boulangerie. Ce régime est essentiel pour limiter la progression de la maladie.\n\nAprès stabilisation, le patient a été renvoyé à domicile avec un suivi cardiologique et neurologique, sous traitement médical pour son insuffisance cardiaque et régime hyposodé et pauvre en acide phytanique.\n\n---\n\nCe cas illustre l’importance de considérer une maladie métabolique rare comme la maladie de Refsum devant une cardiomyopathie dilatée associée à des signes neurologiques et ophtalmologiques spécifiques, afin d’adapter la prise en charge et améliorer le pronostic."
+        }
+    },
+    {
+        "article": "En novembre 2019, un garçon âgé de 12 ans a été admis à l'hôpital pour enfants de Wuxi pour des vertiges intermittents, des maux de tête pendant plus d'un mois et une marche instable pendant une demi-mois. Il est à noter que le patient avait une toux modérée une semaine avant le début et qu'elle s'est résolue spontanément sans intervention. En outre, le garçon n'avait pas reçu de vaccinations depuis l'âge de 6 ans. Certains tests neurologiques, tels que le test d'Oppenheim, le signe de Brudzinski, le signe de Kernig et le signe de Babinski, ont donné des résultats négatifs, tandis que le test de marche en tandem et le test de doigt à nez ont donné des résultats positifs, en particulier dans la main droite. En outre, un spectre de maladies démyélinisantes du système nerveux central, tels que les anticorps contre l'aquaporine-4, la glycoprotéine oligodendrocytaire de myéline et la protéine acide fibrillaire gliale, était négatif. Les tests suivants pertinents pour l'encéphalite anti-NMDAR ont révélé que les récepteurs AMPA1/2 et GABABR dans le LCR étaient négatifs, mais que le tétramère NMDA IgG était positif avec un titre de 1:32. L'IRM du cerveau a révélé des signaux aberrants dans les deux hémisphères cérébelleux, indiquant une atrophie cérébelleuse significative. Finalement, le garçon a été diagnostiqué comme ayant une encéphalite anti-NMDAR. La détection de certains marqueurs tumoraux, notamment l'alpha-foetoprotéine, l'antigène carcino-embryonnaire, l'antigène glucidique (CA) 125 et le CA 19-9, a été effectuée pour exclure la possibilité de tumeurs, et tous étaient négatifs. Ce patient a ensuite été traité par une thérapie par impulsions de sodium succinate de méthylprednisolone (20 mg/kg, 3 jours) et a ensuite changé en comprimés de prednisolone (40 mg, po, qd). Finalement, les symptômes du garçon ont été soulagés et il a été sorti de l'hôpital. Les visites de suivi en janvier et en mai 2020 ont révélé que cet enfant était en bonne santé sans symptômes notables. Cependant, l'enfant a été réadmis à l'hôpital en août 2020 avec une dysgraphie pendant 6 jours. Les résultats de l'examen neurologique étaient comparables à la dernière fois, avec le test du doigt à nez restant positif, mais le Tandem Gait était négatif. Le titre de l'IgG NMDAR était de 1:10 dans le sérum et de 1:3.2 dans le LCR, et l'imagerie IRM a révélé une aggravation des lésions dans les hémisphères cérébelleux. En outre, le test de bande oligoclonale d'IgG dans le LCR a été effectué, et le résultat était positif. L'IgG anti-NMDAR combinée aux résultats d'imagerie a conduit au diagnostic d'encéphalite anti-NMDAR récurrente. Un protocole thérapeutique similaire a été appliqué, et le garçon a été renvoyé après l'amélioration de ses symptômes. Les visites de suivi ultérieures ont révélé que les symptômes du garçon avaient été atténués dans une certaine mesure, mais il y a eu une récidive. En outre, sa mémoire et ses capacités d'apprentissage étaient quelque peu altérées.\n\nLe séquençage du transcriptome du LCR a été effectué dans les deux épisodes pour aider à interpréter davantage l'étiologie de ce cas. Avant l'examen, le consentement éclairé a été obtenu auprès du garçon et de ses parents. En résumé, l'ARN total du LCR a été extrait à l'aide du kit RNeasy Micro (Qiagen) en suivant les instructions du fabricant, à partir duquel l'ARN ribosomique hôte a été retiré avant la construction de la bibliothèque de séquençage. La bibliothèque a ensuite été construite à l'aide du kit Trio RNA-seq (Nugen), et le séquençage méta-transcriptomique a été effectué sur la plateforme Illumina hiseq X-ten comme décrit précédemment. Les lectures brutes résultantes ont d'abord été ajustées pour supprimer celles de faible qualité et les adaptateurs à l'aide du logiciel Trimmomatic, et les lectures d'origine humaine ont été supprimées à l'aide du script interne. Les lectures propres générées ont ensuite été appliquées directement à l'analyse par blast contre la base de données nr dans NCBI pour analyser la composition taxonomique à l'aide de BLAST + 2.12.0. Après cela, les lectures d'intérêt ont été cartographiées aux séquences de référence pour résoudre la couverture à l'aide de bowie2, et ensuite assemblées de novo à l'aide du programme Megahit sous les paramètres par défaut. Les contigs assemblés ont ensuite été utilisés comme requêtes pour l'analyse par blast afin de confirmer leur statut taxonomique. En outre, le programme MEGA a été utilisé pour aligner et construire un arbre de probabilité maximale pour la relation phylogénétique avec d'autres souches de référence.\n\nPour le séquençage du premier épisode, il y avait 37 013 105 paires de lectures générées au total, dont la majorité était attribuée à l'Homo sapiens comme prévu. Sur la base de l'analyse de lecture par blast, celles qui appartenaient probablement aux eucaryotes, aux bactéries et aux virus représentaient respectivement 70,54 %, 17,04 % et 7,61 % des lectures non humaines. En outre, des résultats similaires ont été obtenus à partir de l'analyse de blast utilisant des contigs assemblés comme requêtes. Parmi ces lectures provenant d'agents exogènes présumés, un total de 2 459 peut être cartographié au hRSV de type B (souche SE01A-0135-V02) avec une couverture de 98,5 % de sa séquence génomique (numéro d'accès MZ516143). En particulier, la plupart des lectures étaient concentrées sur l'emplacement des gènes NS1, NS2 et L. La RT-PCR et le séquençage sanger ont été utilisés pour combler les lacunes des contigs assemblés et confirmer les séquences génomiques. Enfin, avec un total de 15 184 bases, la séquence de l'ensemble du génome a été récupérée, à l'exception d'une partie de la région 3' UTR. En outre, elle avait été déposée dans le Genbank (numéro d'accès ON630422). Sur la base de l'analyse de la séquence, la séquence génomique acquise partageait 99,69 % d'identité nucléotidique avec SE01A-0135-V02. Par la suite, en utilisant l'arbre ML basé sur le gène G, la relation phylogénétique de la souche Wuxi avec d'autres génotypes du groupe hRSV B a été démêlée. Les résultats ont indiqué que cette souche était groupée avec SE01A-0135-V02 dans B6, le génotype hRSV le plus répandu dans le groupe B dans le monde. Les autres lectures ont été dispersées dans d'autres groupes taxonomiques avec un faible nombre de lectures ou de contigs assemblés courts. La deuxième séquence a abouti à 34 609 924 paires de lectures, et à l'exception des lectures provenant d'êtres humains, aucune lecture associée à des agents n'a été confirmée comme étant pertinente pour les conditions de maladie humaine. En raison de l'absence de tests d'anticorps ou d'antigènes du hRSV au moment de l'apparition, nous avons effectué le test de l'IgG hRSV dans le sérum après le séquençage du LCR en utilisant le kit ELISA hRSV-IgG (SHUANGYING BIOLOGICAL), et le résultat a été positif.",
+        "gold_summary": "L'enfant a présenté une ataxie et des récepteurs anti-NMDA positifs dans le liquide céphalorachidien, diagnostiqués comme une encéphalite à récepteurs anti-NMDA en association avec des images IRM crâniales. Après une thérapie par impulsions hormonales à haute dose et des médicaments, la maladie s'est améliorée et il a été renvoyé. Cependant, une rechute a eu lieu presque un an plus tard, et l'imagerie IRM crâniale a montré une atrophie cérébelleuse progressive. Une souche hRSV du groupe B a été détectée dans son liquide céphalorachidien, et la séquence du génome entier a été récupérée en utilisant le séquençage du transcriptome.\n",
+        "synthetic_summary": {
+            "B1": "Un garçon avait du mal à marcher et avait mal à la tête. Les docteurs ont trouvé un problème dans son cerveau. Ils ont donné des médicaments pour l’aider. Il est devenu mieux et est rentré chez lui.\n\nMais presque un an plus tard, il est redevenu malade. Son cerveau avait un peu changé. Les docteurs ont trouvé un petit virus dans son liquide du cerveau. Ils ont étudié ce virus pour mieux comprendre. Les docteurs continuent de s’occuper bien de lui.",
+            "B2": "**Ce qu'ils ont trouvé chez l'enfant**\n\nUn garçon de 12 ans a eu des problèmes d'équilibre et de coordination, appelés ataxie. Les médecins ont découvert dans son liquide céphalorachidien (le liquide autour du cerveau et de la moelle épinière) des anticorps contre les récepteurs NMDA. Ces anticorps peuvent attaquer le cerveau et causent une maladie appelée encéphalite anti-NMDA, qui provoque des troubles neurologiques. Une IRM du cerveau a montré des signes d’atrophie, c’est-à-dire que certaines parties du cerveau, notamment le cervelet, ont diminué de taille.\n\n**Ce que cela signifie et comment ils ont traité l’enfant**\n\nLe garçon a reçu un traitement avec des médicaments appelés corticostéroïdes à haute dose, qui réduisent l’inflammation. Ses symptômes se sont améliorés, et il a pu quitter l’hôpital. Mais presque un an plus tard, il a eu une rechute, avec des difficultés à écrire (dysgraphie) et une aggravation des lésions cérébrales visibles à l’IRM.\n\n**Ce qu’ils ont découvert grâce à des analyses avancées**\n\nLes médecins ont analysé le liquide céphalorachidien en détail grâce à une technique appelée séquençage du transcriptome. Cette méthode permet d’identifier les virus ou autres agents présents. Ils ont trouvé un virus appelé hRSV (virus respiratoire syncytial) de type B dans le liquide. Ce virus est souvent responsable d’infections respiratoires, mais ici, il pourrait être lié à l’encéphalite de l’enfant. Ils ont même pu reconstituer presque tout le génome de ce virus à partir du liquide.\n\n**Conclusion**\n\nCe cas montre qu’une infection par le virus hRSV pourrait être associée à une encéphalite anti-NMDA chez cet enfant. Le traitement par corticostéroïdes a aidé, mais la maladie peut revenir et causer des problèmes neurologiques persistants. Cette découverte est importante pour mieux comprendre comment certaines infections peuvent déclencher des maladies du cerveau.",
+            "B3": "Résumé détaillé et structuré pour un public non médical éduqué :\n\n**Contexte**  \nUn garçon de 12 ans a été hospitalisé en novembre 2019 pour des symptômes neurologiques progressifs, notamment des vertiges intermittents, des maux de tête persistants et une démarche instable. Les examens cliniques ont révélé des troubles de la coordination motrice, en particulier une ataxie (difficulté à coordonner les mouvements) affectant la main droite. Les tests neurologiques spécifiques ont exclu plusieurs autres maladies démyélinisantes (affectant la gaine protectrice des nerfs), mais ont mis en évidence la présence d’anticorps dirigés contre les récepteurs NMDA (N-méthyl-D-aspartate) dans le liquide céphalorachidien (LCR), confirmant le diagnostic d’encéphalite anti-NMDAR, une inflammation auto-immune du cerveau.\n\n**Principales observations**  \nL’imagerie par résonance magnétique (IRM) cérébrale a montré des anomalies dans les deux hémisphères du cervelet, avec une atrophie cérébelleuse significative (réduction du volume du cervelet). Aucun signe de tumeur n’a été détecté grâce à des marqueurs tumoraux négatifs. Le patient a été traité par une corticothérapie à haute dose (médicaments anti-inflammatoires puissants) avec une amélioration notable des symptômes, ce qui a permis sa sortie de l’hôpital. Lors des suivis en début et milieu d’année 2020, il était en bonne santé apparente.\n\nCependant, en août 2020, le garçon a présenté une rechute caractérisée par une dysgraphie (difficulté à écrire) et une aggravation des lésions cérébelleuses à l’IRM. Le titre des anticorps anti-NMDAR dans le sang et le LCR restait positif, confirmant une récidive de l’encéphalite. Un test de bande oligoclonale d’IgG dans le LCR, indiquant une inflammation chronique du système nerveux central, était également positif. Malgré un nouveau traitement similaire, des altérations persistantes de la mémoire et des capacités d’apprentissage ont été notées.\n\n**Interprétation clinique et investigations complémentaires**  \nPour mieux comprendre l’origine de cette maladie auto-immune et sa récidive, une analyse approfondie du transcriptome (ensemble des ARN exprimés) du LCR a été réalisée lors des deux épisodes. Cette analyse a permis d’identifier la présence d’une infection par le virus respiratoire syncytial humain (hRSV) de type B dans le LCR lors du premier épisode. Le génome complet de ce virus a été séquencé, confirmant son identité et son appartenance au génotype B6, un des plus répandus mondialement. Aucune autre infection virale ou bactérienne significative n’a été détectée. Lors du second épisode, aucune trace virale n’a été retrouvée dans le LCR, mais un test sanguin a confirmé une exposition antérieure au hRSV.\n\n**Prochaines étapes et conclusion**  \nCe cas illustre une encéphalite anti-NMDAR associée à une infection par le virus respiratoire syncytial, suggérant que ce virus pourrait jouer un rôle déclencheur ou aggravant dans cette maladie auto-immune neurologique. Le suivi clinique et neurologique à long terme est essentiel, car des rechutes et des séquelles cognitives peuvent survenir malgré un traitement adapté. Cette observation souligne l’importance d’une investigation approfondie des agents infectieux dans les encéphalites auto-immunes, notamment par des techniques avancées comme le séquençage du transcriptome du liquide céphalorachidien."
+        }
+    },
+    {
+        "article": "Une femme de huit ans d'origine indienne du sud a été présentée au service des urgences pour évaluation de maux de tête. Elle avait des maux de tête depuis plusieurs jours, qui ont été gérés avec de l'acétaminophène à la maison. Elle a nié des antécédents de vision floue, de vertiges, d'apnée du sommeil, de syncope et de traumatisme crânien. Il n'y avait pas d'antécédents de maux de gorge, d'infection cutanée, de vomissements et de diarrhée récents. Dans le passé, elle avait des maux de tête de nature similaire de manière intermittente pendant environ un an. Il n'y avait pas d'antécédents d'aggravation des maux de tête avec la lumière ou le son. La production d'urine était normale et il n'y avait pas d'antécédents de gonflement des pieds ou de l'abdomen ou de gonflement du visage. Il n'y avait pas d'autres problèmes médicaux passés importants connus, y compris une maladie cardiaque congénitale. Il n'y avait pas d'antécédents d'administration d'agents stimulant l'érythropoïétine ou de voyages récents en haute altitude. Elle est née à terme sans complications périnatales. Les antécédents familiaux étaient importants pour la consanguinité parentale, qui étaient les premiers cousins. Il n'y avait pas d'antécédents familiaux de migraines et d'érythrocytose.\n\nLors de l'examen, les signes vitaux ont montré un enfant apyrétique avec une fréquence cardiaque de 90 battements par minute, une fréquence respiratoire de 18 par minute et une pression artérielle manuelle de 190/100 mm Hg, qui est restée élevée de manière persistante lors des examens répétés. Sa saturation en oxygène était de 90 à 92 %, mais n'a pas nécessité de supplémentation en oxygène. La taille était au 75e centile et le poids au 55e centile. L'examen physique n'a été remarquable que pour le strabisme. Il n'y avait pas de poches pétéchiales, d'ascite ou d'œdème pédial. Elle a continué à avoir des maux de tête. Une tomographie par ordinateur non contrôlée du cerveau n'a pas révélé de signes d'hémorragie, d'infarctus ou de thrombose. L'hypertension a été gérée avec de l'hydralazine et du labetalol intraveineux. Elle a été admise pour une évaluation supplémentaire de l'hypertension. Les tests de la fonction rénale ont montré une urée sanguine de 14 mg/dL et une créatinine sérique de 1,6 mg/dL. L'albumine sérique était de 3,1 g/dL. Les autres électrolytes étaient normaux. Le compte sanguin complet a montré une hémoglobine de 17 g/dL, un hématocrite de 51 %, un nombre de globules blancs de 7,2 × 109/L et un nombre de plaquettes de 247 × 109/L (normal : 150-300 × 109/L). La saturation en fer était de 18 % (normal : 20-55 %), le fer était de 45 µg/dL (35-150 µg/dL), la transferrine était de 176 mg/dL (200-360 mg/dL), la capacité totale de liaison du fer (TIBC) était de 246 µg/dL (225-430 µg/dL), et la ferritine était de 98 ng/mL. Les taux de vitamine B12 et de folate étaient normaux. La biopsie de la moelle osseuse n'a pas été obtenue. L'analyse d'urine a montré une protéinurie de 4+ sans hématurie microscopique. Le rapport protéine/créatinine dans l'urine était de 14,6. Il y avait une hypercholestérolémie. Les compléments en fer étaient normaux. Les anticorps antinucléaires, antineutrophiles cytoplasmiques, anti-membranes basales glomérulaires et anti-ADN double brin étaient négatifs. Le panel de l'hépatite, le virus de l'immunodéficience humaine et le test de la tuberculine étaient tous négatifs. La fonction thyroïdienne, les catécholamines sériques, l'activité de la rénine plasmatique et la sécrétion de l'aldostérone étaient normales. L'étude duplex de l'artère rénale n'a révélé aucune sténose de l'artère rénale. La radiographie thoracique n'a révélé aucune preuve de consolidation, de pneumothorax ou d'épanchement. L'échographie abdominale était normale. Les swacnb nasopharyngés pour les virus respiratoires étaient négatifs. Sa saturation en oxygène est restée faible pendant quelques jours. L'échocardiogramme a montré des preuves d'hypertrophie ventriculaire gauche modérée, mais aucune autre anomalie. Le traitement consistait en une hydratation intraveineuse et l'initiation d'agents antihypertensifs, amlodipine et labetalol. Les pressions artérielles se sont stabilisées, mais la polycytémie était persistante (hémoglobine 15-16 g/dL). L'écho-cardiogramme a montré des preuves d'hypertrophie ventriculaire gauche modérée, mais aucune autre anomalie. Le traitement consistait en une hydratation intraveineuse et l'initiation d'agents antihypertensifs, amlodipine et labetalol. Les pressions artérielles étaient stables, mais la polycytémie était persistante (hémoglobine 15-16 g/dL). L'écho-cardiogramme a montré des preuves d'hypertrophie ventriculaire gauche modérée, mais aucune autre anomalie. Le traitement consistait en une hydratation intraveineuse et l'initiation d'agents antihypertensifs, amlodipine et labetalol. Les pressions artérielles étaient stables, mais la polycytémie était persistante (hémoglobine 15-16 g/dL). L'écho-cardiogramme a montré des preuves d'hypertrophie ventriculaire gauche modérée, mais aucune autre anomalie. Le traitement consistait en une hydratation intraveineuse et l'initiation d'agents antihypertensifs, amlodipine et labetalol. Les pressions artérielles étaient stables, mais la polycytémie était persistante (hémoglobine 15-16 g/dL).\n\nLa créatinine sérique a augmenté au cours des jours suivants pour atteindre 1,8 mg/dL (taux de filtration glomérulaire estimé de 32 ml/1,73 m2/min) par Schwartz. La concentration de parathyroïde intacte dans le sérum était de 217 pg/mL (normal : 12-88 pg/mL). La protéinurie néphrotique persistait, mais le rapport entre la protéine et la créatinine dans les urines a diminué pour atteindre des valeurs allant de 5 à 7 après l'ajout de lisinopril. Une biopsie rénale percutanée réalisée une semaine après la présentation initiale a montré des preuves de FSGS avec une atrophie tubulaire sévère et une fibrose interstitielle. Il y avait un effacement partiel du processus unguéal. Les tests génétiques pour la FSGS ont montré des mutations hétérozygotes dans ACTN4, INF2 et KANK1 et une mutation homozygote dans NUP93 par séquençage de nouvelle génération. En raison de mutations génétiques héréditaires et de la probabilité de résistance aux stéroïdes, elle n'a pas été traitée avec des stéroïdes ou des agents immunosuppresseurs. L'hypertension a été gérée avec lisinopril, amlodipine et labetalol avec une stabilisation de la pression artérielle. Un agent antiplaquettaire a été ajouté. La thérapie par fer a été initiée pour une anémie ferriprive modérée (IDA). Sa saturation en oxygène est revenue à la normale au moment de la sortie et la polycytémie a été résolue sans la nécessité d'une phlébotomie. Elle a ensuite progressé vers une maladie rénale en phase terminale dix mois après la présentation initiale et a été initialement traitée par hémodialyse chronique suivie d'une dialyse péritonéale. Elle a reçu un rein de donneur décédé quatre mois après avoir été en dialyse sans qu'il y ait eu de récurrence de FSGS lors de son dernier suivi deux mois après la transplantation. Sa maintenance immunosuppression consistait en tacrolimus, mycophenolate et prednisone.\n",
+        "gold_summary": "Nous décrivons ici une fille de 8 ans atteinte d'érythrocytose associée à une néphropathie et à une insuffisance rénale chronique avancée. L'érythrocytose a été découverte lors de l'évaluation pour une urgence hypertensive. Elle avait également une protéinurie de type néphrotique sans oedème. L'hémoglobine sérique et l'hématocrite étaient de 17 g/dL et de 51 %, respectivement, malgré une hydratation. Le test de la fonction rénale a montré un taux de filtration glomérulaire estimé de 30 ml/min/1,73 m2. Il y avait une anémie légère par carence en fer avec une saturation en fer sérique de 18 %. Le taux d'EPO sérique était normal. L'EPO urinaire n'a pas été mesuré. La biopsie rénale a montré des preuves de glomérulosclérose segmentaire focale. Les tests génétiques pour la néphropathie à IgA ont montré des mutations dans les gènes des podocytes : NUP93, INF2, KANK1 et ACTN4. L'analyse de la séquence des gènes associés à l'érythrocytose n'a montré aucune variante dans aucun de ces gènes. Dix mois plus tard, elle a eu besoin d'une dialyse chronique et, par la suite, d'une transplantation rénale 14 mois après la présentation initiale.\n",
+        "synthetic_summary": {
+            "B1": "Il y a une petite fille de 8 ans qui avait très mal à la tête. Son cœur battait vite et sa tension était très haute. Son corps avait trop de sang épais, ce qui n’est pas normal.\n\nSes reins, qui aident à nettoyer le corps, ne fonctionnaient pas bien. Les docteurs ont fait beaucoup de tests pour comprendre. Ils ont trouvé que ses reins étaient abîmés.\n\nIls ont aussi regardé ses gènes, qui sont comme des petits livres dans le corps. Ces livres avaient des pages un peu cassées, ce qui explique pourquoi elle est malade.\n\nLa petite fille a dû aller à l’hôpital pour recevoir des soins spéciaux. Après un moment, elle a eu besoin d’une machine pour l’aider à nettoyer son sang. Puis, elle a reçu un nouveau rein pour aller mieux.\n\nLes docteurs prennent bien soin d’elle pour qu’elle soit en bonne santé.",
+            "B2": "Une fille de 8 ans a été hospitalisée à cause de maux de tête et d’une tension artérielle très élevée. Lors des examens, les médecins ont découvert qu’elle avait une érythrocytose, c’est-à-dire un nombre trop élevé de globules rouges dans le sang. En même temps, elle présentait une maladie des reins appelée néphropathie, avec une perte importante de protéines dans les urines (protéinurie) mais sans gonflement du corps.\n\nLes analyses ont montré que ses reins fonctionnaient mal, avec un taux de filtration glomérulaire très bas, ce qui signifie que ses reins ne nettoyaient pas bien le sang. Elle avait aussi une légère anémie due à un manque de fer, malgré un taux normal d’érythropoïétine (EPO), une hormone qui aide à fabriquer les globules rouges. Une biopsie, c’est-à-dire un prélèvement d’un petit morceau de rein, a révélé une forme spécifique de maladie rénale appelée glomérulosclérose segmentaire focale (FSGS), qui endommage les filtres des reins.\n\nDes tests génétiques ont montré qu’elle avait des mutations dans plusieurs gènes importants pour les cellules des reins, appelées podocytes (NUP93, INF2, KANK1 et ACTN4). Ces mutations expliquent probablement sa maladie rénale. Par contre, aucune mutation liée directement à l’érythrocytose n’a été trouvée.\n\nMalgré les traitements pour contrôler sa tension artérielle et protéger ses reins, sa maladie a progressé. Dix mois après son hospitalisation, elle a dû commencer une dialyse, un traitement qui remplace temporairement la fonction des reins. Quatorze mois après, elle a reçu une greffe de rein. Depuis la transplantation, elle est suivie régulièrement et ne présente pas de récidive de sa maladie rénale.",
+            "B3": "Résumé détaillé et structuré\n\nContexte  \nNous rapportons le cas d’une fille de 8 ans d’origine sud-indienne, admise en urgence pour des maux de tête persistants et une hypertension artérielle sévère. Lors de son évaluation, une érythrocytose (augmentation anormale du nombre de globules rouges) a été découverte, associée à une protéinurie de type néphrotique (présence importante de protéines dans les urines sans œdème) et une insuffisance rénale chronique avancée.\n\nPrincipales observations  \nÀ l’admission, la patiente présentait une pression artérielle très élevée (190/100 mm Hg) et une saturation en oxygène légèrement diminuée (90-92 %) sans besoin d’oxygène supplémentaire. L’hémoglobine était élevée à 17 g/dL avec un hématocrite à 51 %, indiquant une polyglobulie persistante malgré une hydratation adéquate. Les analyses sanguines ont révélé une fonction rénale altérée, avec une créatinine sérique augmentée (1,6 puis 1,8 mg/dL) et un taux de filtration glomérulaire estimé à environ 30 ml/min/1,73 m², témoignant d’une insuffisance rénale modérée à sévère. Par ailleurs, une anémie modérée par carence en fer a été identifiée, avec une saturation en fer sérique basse (18 %), mais le taux d’érythropoïétine (EPO), hormone stimulant la production de globules rouges, était normal. Une protéinurie importante (rapport protéine/créatinine urinaire jusqu’à 14,6) était présente sans hématurie.\n\nL’imagerie cérébrale était normale, excluant une cause neurologique aiguë des maux de tête. L’échocardiogramme a montré une hypertrophie ventriculaire gauche modérée, conséquence probable de l’hypertension chronique. Les examens complémentaires, incluant des tests immunologiques et infectieux, étaient négatifs. L’étude des artères rénales n’a pas révélé de sténose, et l’échographie abdominale était normale.\n\nUne biopsie rénale a été réalisée une semaine après l’admission, montrant une glomérulosclérose segmentaire focale (FSGS), caractérisée par une atteinte partielle des glomérules rénaux, accompagnée d’une atrophie tubulaire sévère et d’une fibrose interstitielle, signes d’une maladie rénale chronique avancée. L’analyse génétique a identifié plusieurs mutations hétérozygotes dans des gènes codant pour des protéines des podocytes (cellules spécialisées du glomérule) : ACTN4, INF2, KANK1, ainsi qu’une mutation homozygote dans NUP93. Ces anomalies génétiques expliquent la résistance probable aux traitements immunosuppresseurs classiques.\n\nInterprétation clinique  \nCette patiente présente une forme génétique complexe de néphropathie chronique avec FSGS associée à une érythrocytose non expliquée par une production excessive d’EPO. L’absence de mutations dans les gènes connus de l’érythrocytose suggère que la polyglobulie est secondaire à la maladie rénale. La protéinurie néphrotique sans œdème et l’hypertension sévère sont des manifestations classiques de la FSGS avancée. La présence de mutations multiples dans les gènes des podocytes confirme une origine héréditaire et oriente vers une faible probabilité de réponse aux corticostéroïdes ou autres immunosuppresseurs.\n\nProchaines étapes et évolution  \nLe traitement initial a consisté en une gestion rigoureuse de l’hypertension artérielle par plusieurs antihypertenseurs (lisinopril, amlodipine, labetalol) et une hydratation intraveineuse. Une thérapie par fer a été instaurée pour corriger l’anémie ferriprive. La saturation en oxygène est revenue à la normale, et la polycythémie a disparu sans recours à la phlébotomie. Malgré ces mesures, la fonction rénale a continué à se détériorer, conduisant à une insuffisance rénale terminale dix mois après le diagnostic initial. La patiente a alors été mise en dialyse chronique, d’abord hémodialyse puis dialyse péritonéale, avant de recevoir une transplantation rénale quatre mois plus tard. Le suivi post-transplantation a montré l’absence de récidive de la FSGS sous traitement immunosuppresseur standard (tacrolimus, mycophénolate, prednisone).\n\nCe cas illustre la complexité des néphropathies génétiques associées à des anomalies hématologiques et souligne l’importance d’un diagnostic précis, incluant la génétique, pour orienter la prise en charge et le pronostic."
+        }
+    },
+    {
+        "article": "Le patient, un homme de 61 ans, a été diagnostiqué avec une pancréatite aiguë neuf mois avant son admission et a reçu un traitement conservateur. Après sa sortie, il a éprouvé de manière intermittente une distension et une douleur abdominale supérieure, et une tomographie par ordinateur (CT) abdominale a montré la formation d'une pseudo-cyste pancréatique. Quatre jours avant son admission, le patient a développé une dyspnée sévère avec douleur thoracique et toux, suffisamment sévère pour l'empêcher de rester allongé. L'examen physique a indiqué un essoufflement, des sons respiratoires diminués bilatéraux, une tachycardie, et aucune anomalie abdominale. Le patient avait une longue histoire de consommation d'alcool et de tabac et de multiples interventions chirurgicales antérieures, y compris une chirurgie de fixation lombaire et une ablation de lipome de la paroi abdominale.\n\nLes tests de laboratoire ont montré une légère augmentation du marqueur tumoral du sérum, l’antigène du cancer 125, à 98,25 U/mL (intervalle normal 0–35 U/mL) et de l’amylase urinaire à 333 U/L (intervalle normal 32–641 U/L). L’imagerie (CT) a révélé une épanchement pleural bilatéral massif et la formation d’une pseudo-kystée pancréatique.\n\nDiagnostic et interventions\nLors de l'admission, une ponction thoracique a été effectuée, la culture bactérienne du liquide pleural était négative, aucune cellule tumorale n'a été trouvée, mais le niveau de l'antigène du cancer 125 dans le liquide pleural était significativement élevé à 1859 U/mL (intervalle normal 0-35 U/mL). Les niveaux d'amylase dans le liquide pleural étaient de 53 844 U/L à gauche et de 1365 U/L à droite. Le sixième jour, un diagnostic de PPF a été confirmé, et une ERCP a été effectuée avec la mise en place d'un conduit naso-pancréatique de 7Fr pour drainer la pseudo-cyste pancréatique.\n\nImmédiatement après l'admission, une ponction thoracique a été réalisée, drainant une grande quantité de liquide pleural teinté de sang pâle, ainsi qu'un soutien nutritionnel parentéral et un traitement par somatostatine, aidant progressivement le patient à effectuer des exercices de fonction pulmonaire. Le septième jour, un examen ERCP a révélé une communication entre le pseudocyste pancréatique et la cavité pleurale. Au cours de la canulation du canal pancréatique, le guide-fil a pu pénétrer dans le pseudocyste, de sorte qu'un canal naso-pancréatique de 7 Fr a été placé pour le drainage. La culture du liquide pancréatique du canal naso-pancréatique a révélé la présence d'Enterococcus faecium et de Klebsiella pneumoniae, mais le patient n'a pas développé de fièvre, et le nombre de globules blancs et de protéines C-réactives était normal, mais des antibiotiques ont été administrés. Le neuvième jour, aucun liquide n'a été drainé des drains thoraciques bilatéraux, et une autre ERCP a été réalisée. Le canal naso-pancréatique a été sectionné à la papille duodénale, laissant la partie interne comme stent du canal pancréatique.\n\nRésultats\nLe patient a reçu un total de 13 jours de traitement hospitalier, au cours duquel 4180 mL de liquide pleural a été drainé du côté gauche, 2470 mL du côté droit et 495 mL du conduit naso-pancréatique. Six mois après la sortie, le conduit naso-pancréatique restant a été enlevé. Il n’y a pas eu de récidive au cours d’un suivi de 5 ans, et l’état général du patient était bon\n",
+        "gold_summary": "Inquiétudes du patient : Un homme de 61 ans ayant des antécédents de consommation d'alcool et de tabac a présenté une dyspnée sévère, des douleurs thoraciques et une toux. Il avait été diagnostiqué avec une pancréatite aiguë 9 mois auparavant et avait éprouvé de manière intermittente des douleurs et une distension abdominale supérieures après le traitement.\n\nDiagnoses : PPF.\n\nInterventions : Le patient a subi un drain thoracique, un drain du conduit pancréato-nasal et un stent du conduit pancréatique, ainsi qu'une nutrition parentérale et une thérapie par la somatostatine.\n\nRésultats : Le traitement a entraîné la résolution de l'épanchement pleural et du pseudocyste. La patiente n'a pas eu de récidive au cours d'une période de suivi de 5 ans.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 61 ans avait mal au ventre et du mal à respirer. Il toussait beaucoup et avait mal à la poitrine.\n\nLes docteurs ont trouvé un gros sac d’eau près de ses poumons. Ce sac venait d’un problème dans son ventre.\n\nIls ont mis des petits tuyaux pour faire sortir l’eau. Ils ont aussi donné des médicaments et de la nourriture spéciale.\n\nAprès le traitement, le monsieur allait beaucoup mieux. Il n’a plus eu ce problème pendant longtemps.",
+            "B2": "**Ce qu'il s'est passé avec le patient**  \nUn homme de 61 ans, qui avait déjà eu une inflammation du pancréas (appelée pancréatite aiguë) neuf mois plus tôt, a commencé à avoir des difficultés à respirer, des douleurs dans la poitrine et une toux. Avant cela, il avait aussi ressenti des douleurs et un gonflement dans le haut du ventre. Il avait un passé de consommation d’alcool et de tabac.\n\n**Ce qu'ils ont découvert**  \nLes médecins ont trouvé qu'il avait une accumulation de liquide autour de ses poumons (appelée épanchement pleural) et une sorte de poche remplie de liquide près du pancréas, appelée pseudo-kyste pancréatique. En analysant le liquide autour des poumons, ils ont vu des niveaux très élevés d’une protéine liée au cancer (l’antigène CA 125), mais sans cellules cancéreuses. Ils ont aussi confirmé que le liquide venait du pancréas, ce qui a permis de poser le diagnostic de fistule pancréatico-pleurale (PPF), c’est-à-dire un passage anormal entre le pancréas et la cavité autour des poumons.\n\n**Comment ils ont traité le patient**  \nPour soigner ce problème, ils ont d’abord drainé le liquide autour des poumons avec des tubes. Ensuite, ils ont placé un petit tube (appelé drain naso-pancréatique) dans le canal du pancréas pour faire sortir le liquide du pseudo-kyste. Le patient a aussi reçu une nutrition spéciale par voie veineuse et un médicament appelé somatostatine, qui aide à réduire la production de liquide par le pancréas. Des antibiotiques ont été donnés pour prévenir les infections, même si le patient n’avait pas de fièvre.\n\n**Les résultats**  \nAprès 13 jours à l’hôpital, beaucoup de liquide avait été retiré, et le patient a pu récupérer progressivement. Six mois plus tard, le drain a été enlevé. Pendant les cinq années qui ont suivi, il n’y a pas eu de retour du problème, et le patient est resté en bonne santé.  \n\nEn résumé, grâce à un traitement bien adapté, cette complication rare de la pancréatite a été guérie sans récidive.",
+            "B3": "Résumé détaillé et structuré pour un public adulte non spécialiste\n\n**Contexte**  \nUn homme de 61 ans, avec des antécédents importants de consommation d’alcool et de tabac, a été initialement diagnostiqué avec une pancréatite aiguë il y a neuf mois. Après un traitement conservateur, il a continué à ressentir de façon intermittente une distension et des douleurs dans la partie supérieure de l’abdomen. Une tomodensitométrie (CT) abdominale a révélé la formation d’une pseudo-kyste pancréatique, une cavité remplie de liquide résultant d’une inflammation du pancréas. Quatre jours avant son admission à l’hôpital, il a développé une dyspnée sévère (difficulté à respirer), accompagnée de douleurs thoraciques et d’une toux, au point de ne plus pouvoir rester allongé.\n\n**Principales observations**  \nÀ l’examen clinique, le patient présentait un essoufflement marqué, des bruits respiratoires diminués des deux côtés du thorax, une accélération du rythme cardiaque (tachycardie) et aucun signe d’anomalie abdominale. Les analyses sanguines ont montré une légère augmentation du marqueur tumoral CA 125 et une élévation modérée de l’amylase urinaire, enzyme liée au pancréas. L’imagerie a confirmé la présence d’un épanchement pleural massif bilatéral (accumulation anormale de liquide dans les deux cavités pleurales entourant les poumons) ainsi que la pseudo-kyste pancréatique.\n\nLors de l’admission, une ponction thoracique a permis de prélever du liquide pleural. La culture bactérienne était négative et aucune cellule tumorale n’a été détectée, mais le taux de CA 125 dans ce liquide était très élevé, tout comme celui de l’amylase, particulièrement à gauche. Ces résultats ont orienté vers un diagnostic de fistule pancréatico-pleurale (PPF), une communication anormale entre le pancréas et la cavité pleurale, permettant au liquide pancréatique de s’accumuler dans le thorax.\n\n**Interventions cliniques**  \nLe patient a bénéficié d’un drainage thoracique bilatéral pour évacuer le liquide pleural, d’une nutrition parentérale (alimentation par voie veineuse) et d’un traitement par somatostatine, une hormone qui réduit la sécrétion pancréatique, favorisant la cicatrisation. Une cholangiopancréatographie rétrograde endoscopique (ERCP), examen permettant d’explorer et de traiter les voies biliaires et pancréatiques, a été réalisée. Elle a confirmé la communication entre le pseudo-kyste et la cavité pleurale. Un drain naso-pancréatique (un tube inséré par le nez jusqu’au pancréas) a été placé pour permettre le drainage du pseudo-kyste. La culture du liquide pancréatique a révélé la présence de bactéries (Enterococcus faecium et Klebsiella pneumoniae), mais sans signes d’infection active, bien que des antibiotiques aient été administrés par précaution.\n\nAprès neuf jours, le drain naso-pancréatique a été transformé en stent interne, un dispositif maintenant le canal pancréatique ouvert pour faciliter le drainage naturel. Le drainage thoracique a progressivement cessé, indiquant une amélioration.\n\n**Résultats et suivi**  \nAu total, plus de 6 litres de liquide pleural ont été drainés, ainsi que près de 0,5 litre par le drain pancréatique. Le patient est resté hospitalisé 13 jours, avec une amélioration progressive de sa fonction pulmonaire. Six mois après sa sortie, le stent pancréatique a été retiré sans complication. Aucun épisode de récidive n’a été observé lors d’un suivi de cinq ans, et l’état général du patient est resté satisfaisant.\n\n**Interprétation clinique**  \nCette prise en charge combinant drainage thoracique, drainage endoscopique du pseudo-kyste et traitement médical a permis la guérison complète d’une fistule pancréatico-pleurale, une complication rare mais grave de la pancréatite aiguë. Le suivi prolongé sans récidive souligne l’efficacité de cette approche multidisciplinaire.\n\n**Prochaines étapes**  \nLa surveillance régulière du patient reste essentielle pour détecter toute complication tardive. Une gestion prudente des facteurs de risque, notamment l’abstinence alcoolique, est recommandée pour prévenir une nouvelle pancréatite."
+        }
+    },
+    {
+        "article": "Une femme de 65 ans a été admise avec un antécédent de myalgie, de faiblesse généralisée et de douleurs thoraciques non spécifiques intermittentes datant d'un mois.\n\nElle avait souffert d'un accident vasculaire cérébral deux ans auparavant, qui avait limité sa mobilité et pour lequel elle résidait dans une maison de retraite. Elle avait également connu un infarctus du myocarde sans élévation du segment ST (NSTEMI), avec intervention coronarienne percutanée sur l'artère descendante antérieure gauche cinq mois avant son admission actuelle. Ses autres antécédents comprenaient une maladie rénale chronique (MRC), une dyslipidémie, une hypertension résistante, une épilepsie, une insuffisance cardiaque, un diabète sucré de type 2 et un asthme. Elle était non-fumeuse et n'avait pas d'antécédents d'abus d'alcool.\n\nLes médicaments qu'elle prenait avant son admission comprenaient de nombreux médicaments anti-hypertensifs, de l'aspirine, du ticagrelor et de l'insuline. On lui a également prescrit de l'atorvastatine 80 mg, qu'elle prenait depuis près de deux décennies, bien que la dose ait été augmentée de 20 mg deux ans auparavant.\n\nLors de l'examen, elle avait une force globalement réduite, plus prononcée du côté droit, qui était le côté affecté par son accident vasculaire cérébral antérieur, et une sensibilité musculaire généralisée. Le reste de l'examen clinique était globalement insignifiant, avec un examen cardiovasculaire normal et aucune autre preuve d'un processus rhumatologique sous-jacent tel qu'une éruption cutanée ou un gonflement articulaire.\n\nLa découverte la plus notable issue de ses premières analyses en laboratoire fut un taux de troponine T cardiaque de haute sensibilité (hs-cTnT) nettement élevé de 3794 ng/l (normal < 12 ng/l), sans changement dynamique significatif entre les tests en série, et dont on a noté qu'il avait été relevé à un niveau similaire plusieurs mois auparavant suite à son NSTEMI. Une créatine kinase (CK) a ensuite été contrôlée, dont on a également constaté qu'elle était significativement élevée à 9416 U/l (normal 25-200 IU/l).\n\nSon ECG ne montrait aucune modification aiguë, et son échocardiogramme transthoracique (TTE) révélait une hypertrophie ventriculaire gauche (LVH), mais une fraction d'éjection ventriculaire gauche normale sans anomalies du mouvement de la paroi régionale, une fonction ventriculaire droite normale et aucune pathologie valvulaire significative.\n\nAu début, on ignorait si son CK représentait des dommages au muscle cardiaque ou squelettique. La signification de l'augmentation de hs-cTnT était également incertaine. On pensait que le syndrome coronarien aigu avait été exclu, car ses symptômes initiaux étaient incompatibles avec cela, il n'y avait pas de changements ECG ou TTE aigus, et les niveaux de hs-cTnT étaient relativement statiques. Le diagnostic différentiel était considéré comme étant entre la myocardite chronique, avec la faiblesse étant due à une myosite coexistante ou à un déconditionnement, et la myositis sans implication cardiaque et avec une fausse élévation de hs-cTnT.\n\nD’autres tests ont été demandés pour différencier ces deux possibilités. Une troponine cardiaque de haute sensibilité (hs-cTnI) a été réalisée et n’a été que légèrement élevée à 55 ng/l. Une hs-cTnT appariée prise au même moment est restée significativement élevée à 4532 ng/l. Une IRM cardiaque n’a montré aucune infiltration cardiaque ou inflammation. Une amélioration tardive du gadolinium dans une zone focale probablement due à son NSTEMI antérieur a été observée.\n\nSur la base des investigations ci-dessus, il a été estimé que les lésions cardiaques aiguës significatives avaient été exclues. La myosite avec fausse élévation de hs-cTnT était désormais considérée comme le diagnostic le plus probable et un avis de rhumatologie a été demandé. Ils ont conseillé un certain nombre de tests d'anticorps. Parmi ceux-ci, les anticorps anti-HMG-CoA réductase étaient positifs et les anticorps anti-PM/SCL75 étaient faiblement positifs. Les autres tests complémentaires recommandés à ce moment-là, y compris les tests ANA, ANCA et hépatite B/C, étaient négatifs, et une TDM du thorax, de l'abdomen et du bassin ne révélait aucune preuve de malignité sous-jacente. La constatation initiale d'une TSH élevée signifiait qu'une hypothyroïdie contribuant à la myosite devait être envisagée. Cependant, le fT4 s'est avéré normal, indiquant que le patient souffrait d'une hypothyroïdie infraclinique et excluant cette dernière comme facteur contributif significatif.\n\nUne IRM bilatérale des cuisses a également été conseillée, qui a révélé un changement de signal diffus élevé dans tous les muscles de la cuisse avec un œdème environnant correspondant à une myosite généralisée.\n\nSur la base des résultats cliniques, IRM et anticorps, un diagnostic de NMI induit par les statines a été posé. Pour confirmation, une biopsie musculaire du quadriceps a été réalisée. Les résultats n'étaient pas disponibles avant la sortie, mais lorsqu'ils ont été examinés, ils ont montré des changements compatibles avec la NMI.\n\nÀ la suite du diagnostic, l'atorvastatine a été arrêtée et la patiente a commencé à prendre de la prednisolone 40 mg OD. Cependant, elle a eu une réponse modeste, avec une réduction de ses taux de CK, mais peu de changement de ses symptômes. Par conséquent, après deux semaines de traitement par stéroïdes, elle a commencé à prendre une dose croissante de mycophenolate, à partir de 250 mg BD et d'immunoglobuline intraveineuse 2 g/kg sur cinq jours, parallèlement à un traitement IV de 500 mg de méthylprednisolone OD pendant trois jours, suivi d'une dose accrue de prednisolone orale à 60 mg OD. Il en a résulté une amélioration progressive des symptômes et une réduction continue de ses taux de CK. Sa cTnT a également diminué, mais est restée significativement élevée au-dessus de sa valeur initiale, même après plusieurs mois de traitement. Elle a été renvoyée chez elle avec du mycophenolate (1 g BD au moment du renvoi) et une dose de sevrage de prednisolone (30 mg OD au moment du renvoi). Elle devait être suivie par l'équipe de rhumatologie, mais malheureusement, elle n'a pas assisté à ses rendez-vous cliniques programmés.\n",
+        "gold_summary": "Nous présentons ici le cas d'une femme de 65 ans sous atorvastatine à long terme qui a présenté une faiblesse généralisée, des douleurs thoraciques non spécifiques et une troponine T cardiaque élevée de manière persistante. Après enquête, une lésion myocardique aiguë a été exclue et un diagnostic de myopathie nécrosante immuno-médiée induite par les statines (IMNM) a été posé. La patiente a présenté une amélioration après l'arrêt de l'atorvastatine et l'instauration d'une thérapie immunosuppressive avec mycophenolate, immunoglobuline intraveineuse et stéroïdes.\n",
+        "synthetic_summary": {
+            "B1": "Une dame de 65 ans se sentait très faible et avait mal à la poitrine. Elle prenait un médicament pour son cœur depuis longtemps. Les docteurs ont fait beaucoup de tests. Ils ont vu que son cœur allait bien. Mais ses muscles étaient malades à cause du médicament. Ils ont arrêté ce médicament. Puis, ils lui ont donné d’autres médicaments pour aider ses muscles à guérir. Peu à peu, elle a commencé à aller mieux.",
+            "B2": "Cas d’une femme de 65 ans avec faiblesse et douleurs thoraciques\n\nUne femme de 65 ans, qui prenait depuis longtemps un médicament appelé atorvastatine pour son cholestérol, a ressenti une faiblesse générale dans ses muscles et des douleurs au niveau de la poitrine. Les analyses ont montré que sa troponine T cardiaque, une substance qui peut indiquer un problème au cœur, était très élevée. Cependant, les examens ont exclu une maladie cardiaque aiguë.\n\nCe qu’ils ont découvert\n\nAprès plusieurs tests, les médecins ont conclu que la patiente souffrait d’une myopathie nécrosante immuno-médiée (IMNM). C’est une maladie rare où le système immunitaire attaque les muscles, causant leur destruction. Cette maladie était probablement causée par l’atorvastatine, le médicament qu’elle prenait. Une IRM des cuisses et une biopsie musculaire ont confirmé ce diagnostic.\n\nCe qu’ils ont fait et ce que cela signifie\n\nLes médecins ont arrêté l’atorvastatine et ont commencé un traitement pour calmer le système immunitaire. Ce traitement comprenait des stéroïdes (prednisolone), un médicament appelé mycophenolate et des immunoglobulines par perfusion. La patiente a montré une amélioration progressive de sa force musculaire et une baisse des marqueurs de destruction musculaire dans le sang. Ce cas montre qu’il est important de reconnaître que certains médicaments peuvent provoquer des maladies musculaires graves, mais qu’un traitement adapté peut aider à améliorer les symptômes.",
+            "B3": "Résumé détaillé et structuré pour un public adulte non spécialiste\n\nContexte  \nUne femme de 65 ans, avec de multiples antécédents médicaux dont un infarctus du myocarde récent traité par intervention coronarienne, une maladie rénale chronique, un diabète de type 2 et une hypertension résistante, a été admise pour une faiblesse musculaire généralisée, des douleurs thoraciques intermittentes non spécifiques et des douleurs musculaires (myalgies) évoluant depuis un mois. Elle prenait notamment de l’atorvastatine à forte dose depuis près de vingt ans, un médicament destiné à réduire le cholestérol.\n\nPrincipales observations  \nÀ l’examen clinique, la patiente présentait une faiblesse musculaire diffuse, plus marquée du côté droit, correspondant à son ancien accident vasculaire cérébral, ainsi qu’une sensibilité musculaire généralisée. Les examens cardiaques initiaux (ECG et échocardiographie) ne montraient pas de signes d’atteinte cardiaque aiguë. Cependant, les analyses sanguines révélaient une élévation très importante de la troponine T cardiaque (un marqueur habituellement associé à une atteinte du muscle cardiaque) ainsi qu’une augmentation très élevée de la créatine kinase (CK), un marqueur de lésion musculaire, sans variation significative dans le temps. Une troponine I cardiaque, un autre marqueur plus spécifique, était seulement légèrement élevée. Une IRM cardiaque n’a pas montré d’inflammation ni d’atteinte myocardique active, ce qui a permis d’exclure une lésion cardiaque aiguë.\n\nDes examens complémentaires ont mis en évidence la présence d’anticorps spécifiques, notamment des anticorps anti-HMG-CoA réductase, associés à une forme particulière de myopathie inflammatoire appelée myopathie nécrosante immuno-médiée (NMI) induite par les statines. Une IRM des muscles des cuisses a confirmé une inflammation musculaire diffuse compatible avec une myosite (inflammation des muscles). Une biopsie musculaire a confirmé ce diagnostic.\n\nInterprétation clinique  \nLe tableau clinique, biologique et radiologique a conduit au diagnostic d’une myopathie nécrosante immuno-médiée liée à la prise prolongée d’atorvastatine. Cette maladie auto-immune provoque une inflammation musculaire sévère et une destruction des fibres musculaires, expliquant la faiblesse et les douleurs musculaires. L’élévation persistante de la troponine T, malgré l’absence d’atteinte cardiaque aiguë, s’explique par une libération de ce marqueur par les muscles squelettiques atteints, ce qui peut induire une fausse impression d’atteinte cardiaque.\n\nProchaines étapes et traitement  \nL’atorvastatine a été arrêtée immédiatement. La patiente a été traitée par une association de corticostéroïdes (prednisolone), d’immunosuppresseurs (mycophenolate) et d’immunoglobulines intraveineuses, visant à réduire l’inflammation musculaire et à moduler la réponse immunitaire. Cette prise en charge a entraîné une amélioration progressive des symptômes et une diminution des marqueurs musculaires dans le sang. Toutefois, la troponine T est restée élevée au-dessus des valeurs normales, ce qui reflète la persistance d’une atteinte musculaire chronique. La patiente devait bénéficier d’un suivi spécialisé en rhumatologie, mais elle n’a pas assisté aux consultations programmées.\n\nEn résumé, ce cas illustre une complication rare mais grave de la prise prolongée de statines, nécessitant un diagnostic précis pour éviter une confusion avec une maladie cardiaque aiguë et permettre une prise en charge adaptée par immunosuppression."
+        }
+    },
+    {
+        "article": "Une patiente de 17 ans a été envoyée du service de pédiatrie au service de médecine buccale de l’hôpital Hasan Sadikin avec des plaintes de douleurs buccales, de sécheresse des lèvres et de difficultés à avaler. Cette condition a rendu difficile pour la patiente de manger et de boire, ce qui a entraîné une faiblesse et une débilité de la condition physique de la patiente. L’ulcère est présent depuis 3 jours, ne s’est pas amélioré et a tendance à saigner. Cependant, le saignement a cessé depuis la veille. Le service de pédiatrie a administré Kenalog en Orabase® en réponse à la condition orale de cette patiente.\n\nLe patient s'est plaint de douleurs corporelles, d'éruptions cutanées et de perte de cheveux il y a deux mois. Cette condition a été examinée à l'hôpital Kebon Jati, et le diagnostic de SLE a été confirmé. Il y a environ deux semaines, le patient s'est plaint de la même condition et a finalement décidé d'être traité à l'hôpital Hasan Sadikin. Des examens complets et multidisciplinaires ont établi qu'en plus du SLE, le patient a également été diagnostiqué avec une hépatosplénomégalie, au cours de la troisième semaine d'hospitalisation. L'élargissement du foie et de la rate a été constaté lors d'une tomographie par ordinateur abdominale.\n\nPendant cette période de deux semaines, le patient a suivi un régime médicamenteux diversifié administré par le service de pédiatrie, qui comprend le levofloxacin, l'amikacin, l'ampicillin-sulbactam et l'ethambutol pour les antibiotiques. Le fluconazole a été administré par voie intraveineuse. Des anti-inflammatoires stéroïdiens ont été administrés par voie intraveineuse, le méthylprednisolone et l'acétonide de triamcinolone par voie topique. L'oméprazole et le carbonate de calcium ont été administrés comme antiacides et inhibiteurs de la pompe à protons. Des compléments alimentaires tels que la vitamine D et le curcuma ainsi que du paracétamol ont également été administrés.\n\nL’examen extraoral a révélé une conjonctive anémique, une sécheresse et une exfoliation des lèvres qui tendent à saigner, ainsi que des croûtes hémorragiques séreuses et sanguinolentes. L’examen intraoral a révélé des lésions couvrant presque toutes les régions de la muqueuse buccale. Des ulcérations multiples sur la muqueuse labiale supérieure et inférieure. Une ulcération douloureuse sur la muqueuse buccale gauche mesurant 5 × 6 mm avec bord érythémateux. Un érythème palatal central a été observé sur le palais dur. Une pseudomembrane de candidose a également été observée sur le dos de la langue, accompagnée d’un allongement des papilles.\n\nGestion des cas\nNaCl 0,9 % a été administré et utilisé pour effectuer plusieurs instructions liées à l'état buccal de la patiente. Le nettoyage des dents à l'aide d'une gaze humidifiée au sérum physiologique était la chose la plus importante, car pendant les deux semaines d'hospitalisation, la patiente a négligé son hygiène buccale. Des croûtes hémorragiques sur les lèvres et la muqueuse labiale ont également été soignées à l'aide d'une gaze humidifiée (NaCl 0,9 %) aussi souvent que possible. Cela a été fait cinq fois par jour, dans le but d'humidifier les lèvres et d'enlever les croûtes.\n\nL'état de multiples ulcérations étendues sur la muqueuse labiale supérieure et inférieure, un mélange d'onguent stéroïdien topique, a été administré à la patiente. Un mélange contenant 0,5 mg de dexaméthasone mélangé à 2,5 mg de lanoline et à de la gelée de pétrole a été prescrit à la patiente pour l'utiliser trois fois par jour, après application d'un pansement salin. Compte tenu des autres ulcérations, dont une sur la muqueuse buccale gauche et d'autres ulcères difficiles à atteindre à la main, 0,025 % d'acide hyaluronique a été administré pour soulager l'inflammation localement.\n\nLors de la deuxième visite, le 22 novembre 2022, on a constaté que l'état général de la cavité buccale du patient s'était amélioré. La langue du patient présentait toujours une plaque blanchâtre, qui a finalement été traitée par une suspension orale de Nystatin®, mais a dû être arrêtée après 2 jours d'administration en raison de l'état d'hépatosplénomégalie. La pommade a été arrêtée et remplacée par de la gelée de pétrole. Les autres médicaments ont été poursuivis jusqu'à la prochaine évaluation, pendant les 6 jours suivants. Le 28 novembre 2022, le patient ne s'est plaint d'aucun problème de cavité buccale, mais il y avait toujours une présence clinique de chéilite exfoliative, de langue recouverte et d'ulcère dans la muqueuse buccale gauche, qui avait disparu.\n\nLe patient a été renvoyé à la maison 2 jours plus tard et a continué les soins ambulatoires. La dernière visite a eu lieu le 16 décembre 2022. Le patient n'avait aucune plainte, pouvait suivre les instructions d'hygiène buccale et a conseillé au patient d'extraire les racines des dents de lait 55 et 65.\n",
+        "gold_summary": "Une patiente de 17 ans a été référée par le service de pédiatrie avec des ulcères de la bouche accompagnés de lèvres sèches et une tendance à saigner. La lésion la plus préoccupante était située sur la muqueuse buccale gauche, une ulcération unique mesurant 5x6 mm. De multiples ulcérations se sont répandues sur la muqueuse labiale supérieure et inférieure, avec des croûtes hémorragiques sur les lèvres. Une ulcération douloureuse peut entraîner des difficultés à ouvrir la bouche et une altération de la fonction alimentaire et de la fonction de boire. Un érythème central a été observé sur le palais. Une candidose pseudomembraneuse a également été observée sur la langue de la patiente. L’hépatosplénomégalie a été confirmée par une tomodensitométrie, avec des valeurs enzymatiques de SGPT (386 U/L) et SGOT (504 U/L).\n\nGestion des cas\nL’administration de 0,9 % de NaCl a été indiquée au patient pour maintenir l’hygiène buccale et aider à hydrater les lèvres afin d’éliminer les croûtes hémorragiques. Administration de 0,025 % de solution buccale d’acide hyaluronique et de pommade stéroïde topique pour les conditions ulcérées et inflammatoires. Des ajustements de médicaments ont été faits en fonction des tests de laboratoire et l’état clinique du patient s’est amélioré.\n",
+        "synthetic_summary": {
+            "B1": "Une jeune fille avait mal dans la bouche. Ses lèvres étaient très sèches et parfois saignaient. Elle avait aussi une petite plaie qui faisait très mal dans la bouche. Cela la gênait pour manger et boire.\n\nLe docteur a aidé en nettoyant bien sa bouche avec de l’eau spéciale. Il a mis une crème douce pour soigner les plaies. Petit à petit, la bouche de la fille allait mieux. Elle pouvait manger et boire sans trop de douleur. Le docteur a continué à la soigner avec attention jusqu’à ce qu’elle aille mieux.",
+            "B2": "Résumé pour un élève de 14 ans :\n\nUne jeune fille de 17 ans avait de grosses plaies douloureuses dans la bouche, surtout sur la joue gauche, mesurant environ 5 millimètres sur 6. Elle avait aussi plusieurs autres plaies sur les lèvres, qui étaient sèches et parfois saignaient. Ces blessures rendaient difficile pour elle d’ouvrir la bouche, de manger et de boire normalement. Sur le toit de sa bouche, on a vu une zone rouge irritée. Sa langue avait aussi une sorte de couche blanche appelée candidose, qui est une infection due à un champignon. En plus, ses médecins ont découvert que son foie et sa rate étaient plus gros que la normale, ce qui a été confirmé par un scanner.\n\nPour soigner tout ça, les médecins ont utilisé une solution saline (du NaCl à 0,9 %) pour nettoyer sa bouche et hydrater ses lèvres afin d’enlever les croûtes qui saignaient. Ils lui ont aussi donné une pommade spéciale avec des médicaments stéroïdes pour calmer l’inflammation et aider les plaies à guérir. Une autre solution, contenant de l’acide hyaluronique, a été appliquée pour réduire la douleur et l’inflammation dans la bouche. Les médecins ont aussi ajusté ses médicaments en fonction des résultats des analyses. Grâce à ces soins, son état s’est amélioré avec le temps.",
+            "B3": "Résumé détaillé et structuré pour un public non médical éduqué\n\n**Contexte**  \nUne jeune patiente de 17 ans, déjà diagnostiquée avec un lupus érythémateux systémique (SLE), a été adressée du service de pédiatrie au service de médecine buccale en raison de douleurs importantes dans la bouche, de sécheresse des lèvres, de saignements et de difficultés à avaler. Ces symptômes ont fortement perturbé son alimentation et sa capacité à boire, entraînant une fatigue générale. Par ailleurs, une hépatosplénomégalie (augmentation du volume du foie et de la rate) a été détectée par scanner abdominal, accompagnée d’une élévation marquée des enzymes hépatiques SGPT et SGOT, témoignant d’une atteinte hépatique.\n\n**Principales observations cliniques**  \nL’examen buccal a révélé plusieurs lésions :  \n- Une ulcération douloureuse unique de 5 × 6 mm sur la muqueuse buccale gauche, avec un bord rougeâtre (érythémateux).  \n- De multiples ulcérations étendues sur la muqueuse labiale supérieure et inférieure, accompagnées de croûtes hémorragiques sur les lèvres, provoquant une sécheresse et une tendance au saignement.  \n- Un érythème (rougeur) central sur le palais dur.  \n- Une candidose pseudomembraneuse (infection fongique caractérisée par un dépôt blanchâtre) sur le dos de la langue, avec un allongement des papilles linguales.  \nCes lésions ont causé une gêne importante, notamment des difficultés à ouvrir la bouche et à s’alimenter normalement.\n\n**Interprétation clinique et prise en charge**  \nLa gestion a reposé sur plusieurs mesures :  \n- Une hygiène buccale rigoureuse a été instaurée, avec des nettoyages fréquents à l’aide de compresses imbibées de solution saline (NaCl 0,9 %) pour hydrater les lèvres, éliminer les croûtes et nettoyer les dents, car la patiente avait négligé ces soins pendant son hospitalisation.  \n- Un traitement local combinant une pommade stéroïdienne topique (contenant de la dexaméthasone) et une solution d’acide hyaluronique à 0,025 % a été appliqué pour réduire l’inflammation et favoriser la cicatrisation des ulcérations.  \n- Une suspension antifongique orale (Nystatin®) a été initialement utilisée pour traiter la candidose, mais a été arrêtée en raison de la complication hépatique.  \n- Le traitement médicamenteux systémique a été adapté en fonction des résultats biologiques et de l’évolution clinique, incluant des antibiotiques, des anti-inflammatoires stéroïdiens et des compléments nutritionnels.\n\n**Évolution et suivi**  \nAprès deux semaines de soins, l’état buccal s’est nettement amélioré : les ulcérations ont diminué, la douleur a régressé et la patiente a pu reprendre une alimentation plus normale. La candidose a été contrôlée, bien que des signes résiduels de chéilite exfoliative (desquamation des lèvres) et de langue recouverte subsistaient. La patiente a été autorisée à poursuivre les soins à domicile, avec des recommandations strictes d’hygiène buccale. Lors de la dernière visite, elle ne présentait plus de symptômes et avait bien intégré les consignes. Une extraction des racines des dents de lait a été conseillée pour prévenir d’éventuelles complications dentaires.\n\n**Conclusion**  \nCette prise en charge multidisciplinaire a permis d’améliorer significativement les lésions buccales sévères liées au lupus, tout en tenant compte des complications hépatiques associées. L’hygiène buccale adaptée, le traitement local anti-inflammatoire et antifongique, ainsi que le suivi médical rigoureux ont été essentiels pour la récupération fonctionnelle et le confort de la patiente."
+        }
+    },
+    {
+        "article": "Une fillette âgée d’un an a été adressée à notre hôpital avec un antécédent de 3 mois de diarrhée et de perte de poids. Elle était nourrie au sein et à l’aide de lait maternisé. À 6 mois, elle a commencé à manger du riz et du soja. À 8 mois, elle a commencé à manger du lait de vache et du blé. À 9 mois, elle a développé des vomissements, une diarrhée et une anorexie. Son diagnostic initial était une gastro-entérite infectieuse et un syndrome post-entérite. Un mois avant son admission à notre hôpital, elle a été admise à l’hôpital précédent parce que ses symptômes ne s’étaient pas améliorés en deux mois et que sa perte de poids progressait. Au cours des 2 mois précédant son admission, son régime alimentaire était illimité. Bien que ses vomissements aient été améliorés après quelques jours de jeûne, la prise orale de diètes élémentaires, de lait maternisé ou de porridge de riz a entraîné des diarrhées répétées. À son admission à notre hôpital, son examen physique a révélé ce qui suit : taille, 69,0 cm (écart-type [ES] : 2,2) ; poids, 6641 g (ES : 2,8) ; 999 g de moins que le poids mesuré 3 mois auparavant ; température corporelle, 37,1 °C ; fréquence cardiaque, 96 battements par minute ; et tension artérielle, 88/50 mmHg. Les résultats de ses tests sanguins étaient les suivants : nombre de globules blancs, 16 900/mL (ES : 7 000-15 000) ; pourcentage d’éosinophiles, 2,0 % (ES : < 5,6) ; hémoglobine, 9,9 g/dL (ES : 13,7-16,8) ; et nombre de plaquettes, 679 × 103 cellules/mL. Les résultats de ses tests de laboratoire étaient les suivants : protéines totales, 6,4 g/dL (ES : 6,8-8,1) ; albumine, 3,9 g/dL (ES : 4,1-5,1) ; aspartate aminotransférase, 35 IU/L (ES : 20-45) ; alanine aminotransférase, 17 IU/L (ES : 4-24) ; azote uréique sanguin, 7,4 mg/dL (ES : 8-20) ; protéine C-réactive, 0,47 mg/dL (ES : < 0,03) ; sodium, 135 mEq/L (ES : 137-147) ; potassium, 3,6 mEq/L (ES : 3,6-5,2) ; bicarbonate, 19,1 mmol/L (ES : 21,0-27,0) ; et acide lactique, 21 mg/dL (ES : 4-16) ; à ce moment, un nombre suffisant de calories, d’acides aminés et de graisses était administré par voie intraveineuse. Le taux d’IgE était de 1028 IU/mL (ES : < 30) et les tests radioallergosorbent étaient positifs pour le lait (63,7 UA/mL classe 5), la caséine (9,8 UA/mL classe 3), l’alpha-lactalbumine (51,6 UA/mL classe 5), le blanc d’œuf (58,8 UA/mL classe 5), le jaune d’œuf (10,8 UA/mL classe 3), l’ovomucoïde (13,2 UA/mL classe 3), le blé (14,5 UA/mL classe 3) et le soja (1,3 UA/mL classe 2). Les tests de piqûre cutanée n’ont pas été effectués pour confirmer les résultats des tests d’IgE spécifiques. Les taux d’Ig (IgG, 954 [NR 357-989] et IgM, 89 [NR 29-190]) et les ratios de sous-ensemble de lymphocytes étaient normaux. Les tests d’adénovirus fécaux, de rotavirus et de norovirus étaient négatifs.\n\nDes examens d'imagerie et d'endoscopie ont été réalisés pour déterminer la cause de la diarrhée prolongée. La tomodensitométrie abdominale et les examens par ultrasons n'ont révélé aucune anomalie dans l'intestin grêle ; l'intestin grêle était dilaté mais aucun épaississement de la paroi n'a été observé, ce qui suggère une entérite non spécifique. Une endoscopie digestive haute n'a révélé aucune anomalie macroscopique de l'œsophage au duodénum. Cependant, l'histopathologie de la muqueuse duodénale a révélé la perte de la structure villositaire muqueuse, une hyperplasie des cryptes, une apoptose des cryptes et une infiltration de lymphocytes et d'éosinophiles (<20 éos/hpf) dans la lamina propria, avec des abcès cryptes partiellement formés. Une coloscopie totale n'a révélé aucune anomalie macroscopique ; cependant, l'histopathologie de la muqueuse colique a révélé une érosion des muqueuses ; une cryptite avec une diminution des cellules caliciformes, une fibrose, des cellules plasmatiques et des lymphocytes ; et une infiltration de certains éosinophiles (<20 éos/hpf) dans la lamina propria. Ces résultats étaient similaires aux résultats de la muqueuse duodénale.\n\nL’auto-immunité intestinale et la maladie intestinale inflammatoire (MII) étaient suspectées ; des tests complémentaires ont donc été effectués. L’antigène de 75 kDa lié à l’auto-immunité intestinale et les anticorps anti-villosités étaient absents et aucune variante pathogène significative n’a été trouvée dans 25 gènes (couverts par l’assurance publique au Japon) liés aux MII monogéniques et à l’immunodéficience, polyendocrinopathie, syndrome lié à l’X de l’intestin (IPEX). L’EGID a été considérée dans le diagnostic différentiel, mais un diagnostic de FPE a finalement été suspecté sur la base des caractéristiques de la muqueuse intestinale, telles que l’atrophie des villosités de la muqueuse intestinale, l’hyperplasie des cryptes, l’infiltration d’éosinophiles en dessous des critères diagnostiques de l’EGID (<20 eos/hpf), et l’infiltration de lymphocytes. Le nombre d’éosinophiles dans le sang périphérique n’était pas élevé non plus. Une MII non IgE-GIFA atypique (7) a été suspectée (positive pour les IgE spécifiques) (7). Sa diarrhée a disparu après un traitement par prednisolone (PSL) (1 mg/kg) et l’élimination complète du lait maternisé, du lait de vache et des œufs de poule de son alimentation. Aucune rechute n’a eu lieu, même après l’arrêt du PSL un mois plus tard. Les effets indésirables dus au traitement à long terme par PSL, tels que l’hypertension, ne se sont pas produits. Cinq mois après l’arrêt du PSL oral et l’élimination complète du lait maternisé, du lait de vache et des œufs de poule de son alimentation, l’histopathologie du duodénum a révélé une structure villositaire normale et une disposition des conduits bien différenciée. Trois mois après la deuxième EGD, elle a recommencé à manger des œufs de poule sans éprouver de symptômes gastro-intestinaux tels que diarrhée et vomissements ; cependant, trois mois plus tard, ses symptômes, y compris les douleurs abdominales et la diarrhée, ont réapparu en quelques jours après la reprise de la consommation de lait de vache. Sur la base des résultats susmentionnés, la FPE a été diagnostiquée, et le lait de vache était soupçonné d’être la source de l’allergie. À 2 ans et 3 mois, sa taille était passée à 81,5 cm (SD −1,4) et son poids à 11,4 kg (SD +0,33) sans éprouver de symptômes gastro-intestinaux.\n",
+        "gold_summary": "Nous décrivons le cas d’une fille de 1 an atteinte d’une entéropathie induite par les protéines alimentaires (EIP) qui était difficile à diagnostiquer. Elle a été adressée à notre hôpital avec un historique de 3 mois de diarrhée, de vomissements et de perte de poids. Bien que sa diarrhée ait diminué après quelques jours de jeûne, la prise orale de régimes alimentaires élémentaires, de lait maternisé ou de porridge de riz a entraîné des rechutes répétées. Le taux d’IgE sérique était de 1028 IU/mL, et les tests radioallergosorbents étaient positifs pour le lait, la caséine, l’alpha-lactalbumine et d’autres allergènes. Une histopathologie de la muqueuse duodénale a révélé une perte de la structure villose de la muqueuse, une hyperplasie des cryptes, une apoptose des cryptes et une infiltration de lymphocytes et d’éosinophiles (<20 éos/hpf) dans la lamina propria. Après un traitement par prednisolone (PSL) et l’élimination complète du lait de vache et des œufs de poule de son régime alimentaire, la diarrhée de la patiente a disparu. Cinq mois après l’arrêt du PSL oral et l’élimination complète du lait de vache et des œufs de poule, le duodénum présentait une structure villose muqueuse normale et des conduits bien différenciés. Aucune anomalie n’a été observée lors d’une nouvelle exposition aux œufs ; toutefois, la diarrhée a réapparu après la nouvelle exposition au lait de vache.\n",
+        "synthetic_summary": {
+            "B1": "Une petite fille avait mal au ventre et faisait souvent caca mou. Elle perdait du poids et ne se sentait pas bien. Quand elle mangeait du lait ou des œufs, son ventre faisait encore plus mal. \n\nLes docteurs ont trouvé que son ventre était un peu malade à l’intérieur. Ils lui ont donné un médicament doux et ont enlevé le lait et les œufs de sa nourriture. \n\nAprès ça, elle a été mieux. Elle a pu manger des œufs sans problème, mais le lait lui faisait encore mal au ventre. Maintenant, elle va bien et grandit doucement.",
+            "B2": "**Ce qu’ils ont trouvé chez la petite fille**\n\nUne fillette d’un an avait depuis trois mois une diarrhée, des vomissements et elle perdait du poids. Quand elle ne mangeait rien pendant quelques jours, ses symptômes s’amélioraient. Mais dès qu’elle reprenait certains aliments comme le lait maternisé, le porridge de riz ou des régimes spéciaux, la diarrhée revenait. \n\nLes médecins ont fait des analyses de son sang et ont trouvé un taux très élevé d’IgE, une protéine liée aux allergies. Ils ont aussi détecté qu’elle était allergique à plusieurs aliments, notamment au lait de vache et à des protéines du lait comme la caséine et l’alpha-lactalbumine.\n\nUne biopsie, c’est-à-dire un petit prélèvement de tissu de son intestin, a montré que la muqueuse de son intestin grêle était abîmée : les villosités (petites structures qui aident à absorber les nutriments) étaient détruites, et il y avait une inflammation avec des cellules immunitaires appelées lymphocytes et éosinophiles.\n\n**Ce que cela signifie et comment elle a été soignée**\n\nLes médecins ont pensé qu’elle avait une entéropathie induite par les protéines alimentaires (EIP), une maladie où l’intestin réagit mal à certaines protéines des aliments. Pour la soigner, ils ont donné un médicament anti-inflammatoire appelé prednisolone et ont complètement retiré le lait de vache et les œufs de son alimentation.\n\nAprès ce traitement, sa diarrhée a disparu. Cinq mois après avoir arrêté le médicament et toujours sans manger de lait ni d’œufs, son intestin était revenu à la normale, selon une nouvelle biopsie. Elle a pu recommencer à manger des œufs sans problème, mais quand elle a repris le lait de vache, la diarrhée est revenue rapidement.\n\n**En résumé**\n\nCette petite fille souffrait d’une allergie grave au lait de vache qui provoquait une inflammation de son intestin et des troubles digestifs importants. Grâce à un traitement adapté et à l’élimination des aliments responsables, elle a pu guérir et grandir normalement. Ce cas montre l’importance de bien diagnostiquer les allergies alimentaires qui peuvent toucher l’intestin chez les jeunes enfants.",
+            "B3": "Résumé détaillé et structuré :\n\nContexte  \nNous rapportons le cas d’une fillette d’un an présentant une entéropathie induite par les protéines alimentaires (EIP), une maladie rare et difficile à diagnostiquer, caractérisée par une inflammation chronique de l’intestin liée à une réaction immunitaire aux protéines alimentaires. La patiente avait un antécédent de trois mois de diarrhée persistante, de vomissements et de perte de poids importante malgré une alimentation variée incluant lait maternel, lait maternisé, riz, soja, lait de vache et blé.\n\nPrincipales observations  \nÀ son admission, la fillette montrait une dénutrition sévère avec une perte de près d’un kilogramme en trois mois. Les analyses sanguines révélaient une anémie modérée, une légère augmentation des globules blancs, un taux élevé d’IgE sériques (1028 IU/mL, bien au-dessus de la normale), et des tests allergologiques positifs pour plusieurs allergènes alimentaires, notamment le lait de vache, la caséine, l’alpha-lactalbumine, ainsi que les œufs, le blé et le soja. Les examens d’imagerie abdominale étaient peu spécifiques, montrant un intestin grêle dilaté sans épaississement de la paroi. L’endoscopie digestive haute ne montrait pas d’anomalies visibles, mais l’analyse histologique de la muqueuse duodénale révélait une atrophie villositaire (perte de la structure normale des villosités intestinales), une hyperplasie des cryptes (augmentation du nombre de cellules dans les glandes intestinales), une apoptose (mort cellulaire programmée) des cryptes, ainsi qu’une infiltration modérée de lymphocytes et d’éosinophiles (moins de 20 éosinophiles par champ à fort grossissement) dans la lamina propria (tissu sous-jacent à l’épithélium intestinal). La coloscopie et l’histologie colique montraient des signes inflammatoires similaires, sans anomalies macroscopiques. Les investigations complémentaires excluaient une maladie inflammatoire chronique de l’intestin (MICI) et une maladie auto-immune intestinale, ainsi que des immunodéficiences génétiques.\n\nInterprétation clinique  \nLe diagnostic final retenu était une entéropathie protéino-induite (EIP), une forme d’allergie alimentaire non IgE-médiée ou atypique, caractérisée par une inflammation intestinale chronique provoquée par une réaction immunitaire aux protéines alimentaires, en particulier celles du lait de vache. La présence d’IgE spécifiques élevées suggérait une composante allergique mixte. La disparition des symptômes après un traitement par corticostéroïdes oraux (prednisolone à 1 mg/kg) et l’élimination stricte du lait de vache, du lait maternisé et des œufs de poule confirmait ce diagnostic. L’absence de rechute après arrêt du traitement et la normalisation de la structure villositaire duodénale cinq mois plus tard témoignaient de la réversibilité de la maladie sous traitement adapté. La réintroduction des œufs n’a pas provoqué de symptômes, tandis que la réexposition au lait de vache a rapidement déclenché une récidive de diarrhée et de douleurs abdominales, confirmant le rôle du lait comme allergène principal.\n\nProchaines étapes  \nLe suivi de la patiente a montré une amélioration significative de sa croissance et de son état général, avec un poids et une taille dans les normes sans symptômes gastro-intestinaux à l’âge de 2 ans et 3 mois, sous régime d’élimination du lait de vache. Ce cas illustre l’importance d’envisager une entéropathie protéino-induite dans les diarrhées chroniques de l’enfant, surtout en présence d’allergies alimentaires multiples, et souligne la nécessité d’une prise en charge combinant exclusion alimentaire et traitement anti-inflammatoire pour éviter les complications nutritionnelles et favoriser la récupération intestinale."
+        }
+    },
+    {
+        "article": "Un homme de 63 ans a été admis à notre service d'urgence avec des antécédents d'hématurie fréquente. L'examen physique n'a révélé aucun problème et son taux de créatinine sérique était normal, avec une créatinine sérique de 1,2 mg/dL. Une tomographie par ordinateur (CT) a révélé une croissance vésicale infiltrative étendue, principalement sur la paroi latérale droite et la voûte, avec une hydrourénonefrose gauche modérée et une insuffisance rénale droite due à une obstruction haute pression du côté gauche. Une tomographie par ordinateur (CT) a été programmée pour une cystoscopie diagnostique avec biopsie transurétrale. Cependant, il s'est présenté à l'urgence avant la date prévue d'admission avec une instabilité hémodynamique, une distension abdominale et une difficulté respiratoire, pour laquelle une assistance ventilatoire et inotrope était nécessaire. Son panel biochimique a montré une créatinine élevée (20 mg/dL), une hyperkaliémie (9 mEq/L) et une hyponatrémie (128 mEq/L), et sa gazométrie a montré une acidose métabolique sévère (pH 7,1). Après avoir interrogé les soignants du patient, un historique d'oligurie avec distension abdominale progressive au cours des 2 derniers jours a été obtenu, pour lequel il avait été soumis à une ponction de fluide « ascitique » dans un centre externe. Des mesures anti-hyperkaliémiques ont été initiées. Une échographie au chevet a montré une hydrourénonefrose gauche avec une hydrourénonefrose droite sévère et un fluide libre dans l'abdomen. Compte tenu de l'instabilité hémodynamique et de l'absence de dialyse dans nos installations, il a été décidé de procéder à une néphrostomie d'urgence au chevet, insérée dans le rein gauche fonctionnant seul. Sous guidage par ultrasons, une néphrostomie percutanée (NPC) a été insérée au chevet et l'état général du patient s'est amélioré. Il y a eu une diurèse initiale avec une chute du taux de créatinine à un nadir de 2 mg/dL. En raison des taux élevés de créatinine, la tomographie a été répétée après 4 jours de ponction de fluide et, à notre grande surprise, nous avons remarqué que la pointe du cathéter en forme de queue de cochon se trouvait dans l'espace péréphrénique gauche agissant comme un drain percutané avec résolution complète du fluide libre dans l'abdomen. La chronologie des événements d'une créatinine sérique initialement extrêmement élevée qui avait diminué de manière spectaculaire après le drainage du fluide extravasé, s'est ajustée à un tableau clinique de pseudo insuffisance rénale due à l'absorption d'urine extravasée. Nous avons émis l'hypothèse que la source de l'urine extravasée était très probablement une rupture du fornix rénal en raison d'une obstruction haute pression du côté gauche. Compte tenu de la créatinine sérique encore élevée et de la sortie graduellement décroissante du cathéter en forme de queue de cochon, un NPC a été inséré dans le système de collecte sous guidage fluoroscopique, suivi d'une normalisation de sa créatinine. Un néfrogramme par CT avec cystogram a été réalisé dans la suite et a montré une obstruction urétérale distale gauche et une vessie petite et intacte, excluant une perforation de la vessie. Une biopsie par cystoscopie de la croissance de la vessie a confirmé qu'il s'agissait d'un carcinome épidermoïde invasif musculaire. Nous avons expliqué le diagnostic et le pronostic au patient et avons effectué une laparotomie exploratoire 2 semaines après la biopsie. Au cours de l'opération, une réaction démoplastique dense a été observée autour de la vessie, qui a été rétrécie et collée aux parois latérales pelviennes et à l'os pubien. En raison de la nature inopérable de la maladie, le plan de cystectomie radicale a été abandonné et une dérivation palliative du conduit iléal a été réalisée sous guidage fluoroscopique, suivie d'une normalisation de sa créatinine. Le patient a bien récupéré après l'opération et a été libéré 5 jours plus tard. Cependant, il a développé de multiples métastases thoraciques au cours des mois suivants et son état général s'est détérioré de façon constante, ce qui a entraîné sa mort 3 mois après l'opération en raison d'une cachexie.\n",
+        "gold_summary": "Nous rapportons un cas de carcinome de la vessie qui a présenté des caractéristiques similaires à une insuffisance rénale aiguë, et qui s'est révélé plus tard être une pseudo-insuffisance rénale due à un écoulement urinaire intrapéritonéal d'une rupture du fornix rénal. Le patient a été traité en urgence avec un drainage percutané suivi d'une néphrostomie percutanée, ce qui a conduit à une normalisation de la créatinine. La cystoscopie a révélé une croissance de la vessie dans une vessie intacte de faible capacité, confirmée par biopsie comme étant un carcinome épidermoïde invasif musculaire. En raison de la nature avancée de sa malignité, il a été soumis à une dérivation de l'intestin grêle palliative, mais a ensuite développé des métastases thoraciques et a fini par succomber à la maladie.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur avait un gros problème avec sa vessie. Son corps faisait comme s’il avait un gros souci aux reins, mais ce n’était pas vrai. En fait, de l’urine fuyait à l’intérieur de son ventre à cause d’un petit trou dans un rein.\n\nLes docteurs ont aidé le monsieur en mettant un petit tuyau pour faire sortir l’urine. Ça a beaucoup aidé son corps à aller mieux.\n\nIls ont regardé sa vessie avec une petite caméra et ont vu une grosseur. Cette grosseur était un type de maladie grave.\n\nLe monsieur a eu une opération pour l’aider, mais la maladie était très forte. Après, il est devenu très malade et il est parti au ciel. Les docteurs ont fait tout leur possible pour le soigner.",
+            "B2": "Cas d’un homme de 63 ans avec un cancer de la vessie compliqué\n\nUn homme de 63 ans est venu à l’hôpital avec du sang dans les urines. Les examens ont montré une grosseur dans sa vessie, mais ses reins semblaient fonctionner normalement au début. Cependant, il est revenu en urgence avec de graves problèmes : son abdomen était gonflé, il avait du mal à respirer, et ses reins ne fonctionnaient presque plus. \n\nCe qu’ils ont découvert\n\nUne échographie a montré que ses reins étaient très enflés à cause d’un blocage, et qu’il y avait du liquide libre dans son ventre. En fait, de l’urine s’était échappée à cause d’une rupture dans une partie du rein appelée le fornix. Cette fuite d’urine dans l’abdomen a donné l’impression que ses reins étaient en très mauvais état, alors qu’en réalité, c’était une « pseudo-insuffisance rénale » causée par l’absorption de cette urine.\n\nComment ils l’ont soigné\n\nPour l’aider, les médecins ont placé un petit tube appelé néphrostomie dans son rein pour drainer l’urine bloquée. Cela a rapidement amélioré son état et fait baisser le taux de créatinine, une substance qui montre si les reins fonctionnent bien. Plus tard, une biopsie (prélèvement d’un petit morceau de tissu) de la vessie a confirmé qu’il avait un cancer appelé carcinome épidermoïde invasif musculaire.\n\nLe suivi et le pronostic\n\nLe cancer était trop avancé pour être enlevé par chirurgie. Les médecins ont donc fait une opération pour créer une dérivation, c’est-à-dire un nouveau chemin pour que l’urine puisse sortir du corps. Malgré cela, le cancer s’est propagé aux poumons quelques mois plus tard, et le patient est malheureusement décédé trois mois après l’opération à cause de la maladie.\n\nEn résumé, ce cas montre qu’un cancer de la vessie peut causer des problèmes graves aux reins, parfois difficiles à distinguer d’une vraie insuffisance rénale. Un traitement rapide avec drainage peut améliorer la situation, mais le pronostic dépend de la gravité du cancer.",
+            "B3": "Résumé détaillé et structuré\n\nContexte  \nNous présentons le cas d’un homme de 63 ans atteint d’un carcinome de la vessie, qui s’est initialement manifesté par des symptômes évoquant une insuffisance rénale aiguë. Cette présentation inhabituelle a compliqué le diagnostic et la prise en charge initiale.\n\nPrincipales observations  \nLe patient a été admis avec des antécédents d’hématurie (présence de sang dans les urines) fréquente, sans anomalie à l’examen physique ni altération initiale de la fonction rénale (créatinine à 1,2 mg/dL). Une tomodensitométrie (scanner) a montré une masse infiltrante importante au niveau de la vessie, associée à une dilatation des voies urinaires supérieures (hydrourétéro-néphrose) surtout du côté gauche, causée par une obstruction urétérale. Avant la cystoscopie diagnostique programmée, le patient s’est présenté en urgence dans un état critique avec instabilité hémodynamique, distension abdominale et insuffisance respiratoire, nécessitant une assistance ventilatoire et des médicaments pour soutenir la circulation. Les analyses sanguines ont révélé une insuffisance rénale sévère (créatinine à 20 mg/dL), une hyperkaliémie (taux élevé de potassium), une hyponatrémie (faible taux de sodium) et une acidose métabolique grave.\n\nUne échographie a confirmé une obstruction sévère des deux reins et la présence de liquide libre dans l’abdomen. Devant l’urgence et l’absence de dialyse disponible, une néphrostomie percutanée (drainage direct du rein) a été réalisée en urgence sur le rein gauche, seul rein fonctionnel. Cette intervention a permis une amélioration rapide de l’état général, une reprise de la production d’urine et une baisse significative de la créatinine. Une nouvelle imagerie a révélé que le drain avait également permis d’évacuer le liquide accumulé dans l’espace péréphrénique (autour du rein), ce qui a conduit à la résolution complète du liquide libre abdominal. Ce tableau correspondait à une pseudo-insuffisance rénale causée par l’absorption d’urine extravasée dans l’abdomen, probablement due à une rupture du fornix rénal (petite zone du rein) liée à l’obstruction urétérale.\n\nUne seconde néphrostomie a été placée sous contrôle radiologique dans le système collecteur rénal, ce qui a permis la normalisation complète de la fonction rénale. La cystoscopie a confirmé la présence d’une tumeur dans une vessie de faible capacité mais intacte, et la biopsie a identifié un carcinome épidermoïde invasif musculaire. Lors d’une laparotomie exploratrice réalisée deux semaines plus tard, la tumeur était inopérable en raison d’une réaction tissulaire dense et d’adhérences pelviennes. Une dérivation palliative par conduit iléal (création d’un passage urinaire à partir de l’intestin grêle) a été effectuée, avec une bonne récupération postopératoire.\n\nInterprétation clinique  \nCe cas illustre une présentation rare d’un cancer de la vessie avancé, compliqué par une obstruction urétérale bilatérale et une rupture rénale entraînant un écoulement d’urine dans l’abdomen, responsable d’une pseudo-insuffisance rénale sévère. Le diagnostic a nécessité une prise en charge multidisciplinaire urgente combinant drainage rénal, imagerie répétée, endoscopie et chirurgie. La nature agressive du carcinome épidermoïde et l’extension locale ont limité les options thérapeutiques curatives.\n\nProchaines étapes  \nMalgré la dérivation palliative et la stabilisation initiale, le patient a développé des métastases thoraciques dans les mois suivants, avec une dégradation progressive de son état général. Il est décédé trois mois après l’intervention chirurgicale, en raison d’une cachexie (dénutrition sévère liée à la maladie cancéreuse). Ce cas souligne l’importance d’un diagnostic précoce des tumeurs vésicales et la vigilance face aux complications obstructives pouvant simuler une insuffisance rénale aiguë."
+        }
+    },
+    {
+        "article": "La patiente, une femme de 56 ans, a été admise pour « 10 jours de ptosis du côté droit et 1 jour de ptosis du côté gauche ». Il y a 10 jours, la patiente n’avait pas de ptosis du côté droit évident et aucune restriction de mouvement du côté gauche, accompagnée de douleurs pariétales et occipitales, pas de nausées, pas de vomissements, pas de vertiges, pas de marche instable, pas de sensation de coton dans les pieds, pas de mots prononcés, pas de suffocation ou de toux en buvant de l’eau. La patiente a été traitée à l’extérieur de l’hôpital et a présenté des examens pertinents pour considérer le diagnostic d’« anévrisme cérébral ». Il y a 1 jour, la ptosis du côté droit de la patiente s’est aggravée, elle a donc été envoyée au service de neurochirurgie de notre hôpital. Antécédents médicaux : pas d’antécédents d’hypertension, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies 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vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de\n",
+        "gold_summary": "Une patiente de 56 ans a été admise à l'hôpital pour « 10 jours de chute de l'œil droit et 1 jour d'aggravation ». Après admission, l'examen physique a révélé que la patiente souffrait d'une scoliose sévère. La reconstruction 3D et le scanner CT amélioré des vaisseaux de la tête ont montré que les anévrismes de l'artère carotide interne droite C6 avaient été découpés sous anesthésie générale. Après l'opération, la patiente avait une pression artérielle élevée, avec un grand nombre de crachats en mousse rose attirés par le cathéter de la trachée, et les poumons étaient disséminés avec des râles humides lors de l'auscultation. Après le traitement de l'insuffisance cardiaque, la patiente est retournée à l'unité de soins intensifs par le cathéter de la trachée. Huit heures plus tard, le cathéter de la trachée a été retiré et la patiente a été libérée du ventilateur. Les symptômes ont été soulagés le cinquième jour après l'opération.\n",
+        "synthetic_summary": {
+            "B1": "Une dame avait un problème avec son œil qui tombait. Elle est venue à l'hôpital pour se faire soigner.\n\nLes docteurs ont regardé dans sa tête avec une machine spéciale. Ils ont trouvé un petit problème dans un vaisseau.\n\nIls ont fait une opération pour réparer ce problème. Après, la dame a eu un peu de mal à respirer.\n\nLes docteurs l'ont aidée à mieux respirer avec un petit tuyau. Après quelques heures, ils ont enlevé ce tuyau.\n\nPeu à peu, la dame s'est sentie mieux. Cinq jours après, elle allait beaucoup mieux.",
+            "B2": "Présentation du cas  \nUne femme de 56 ans est venue à l’hôpital parce que son paupière droite tombait depuis 10 jours, et cela s’est aggravé depuis un jour. Lors de son arrivée, les médecins ont aussi remarqué qu’elle avait une scoliose, c’est-à-dire une courbure importante de la colonne vertébrale.\n\nCe qu’ils ont découvert  \nDes examens spéciaux, comme un scanner en 3D des vaisseaux sanguins de sa tête, ont montré qu’elle avait un anévrisme sur une artère importante du côté droit du cerveau. Un anévrisme est une sorte de « ballon » qui se forme sur une artère et qui peut être dangereux s’il éclate.\n\nLe traitement et l’évolution  \nLa patiente a subi une opération sous anesthésie générale pour réparer cet anévrisme. Après l’opération, elle a eu une pression artérielle élevée et des difficultés respiratoires. Les médecins ont utilisé un tube dans sa trachée pour l’aider à respirer et ont constaté que ses poumons présentaient des signes d’infection ou de liquide, ce qui a nécessité un traitement pour une insuffisance cardiaque, c’est-à-dire quand le cœur ne pompe pas assez bien le sang. Huit heures après, le tube a été retiré et elle a pu respirer seule. Cinq jours après l’opération, ses symptômes s’étaient beaucoup améliorés.\n\nEn résumé  \nCette patiente a été prise en charge rapidement pour un anévrisme cérébral qui causait une chute de paupière. Grâce à une opération et des soins intensifs, elle a pu se rétablir progressivement.",
+            "B3": "Résumé détaillé et structuré :\n\nContexte  \nUne femme de 56 ans a été hospitalisée en raison d’un ptosis (chute de la paupière) du côté droit évoluant depuis dix jours, avec une aggravation récente survenue depuis un jour, ainsi qu’un ptosis débutant du côté gauche. Initialement, elle ne présentait pas de troubles moteurs ni de symptômes neurologiques associés tels que nausées, vomissements, vertiges ou troubles de l’équilibre. Aucun antécédent médical notable, notamment d’hypertension ou de maladies vasculaires, n’a été rapporté.\n\nPrincipales observations  \nÀ l’admission, l’examen physique a mis en évidence une scoliose sévère. Des examens d’imagerie, incluant une reconstruction 3D et un scanner tomodensitométrique (CT) avec injection de produit de contraste des vaisseaux cérébraux, ont révélé la présence d’un anévrisme au niveau de l’artère carotide interne droite, segment C6. La patiente a été prise en charge chirurgicalement sous anesthésie générale pour la découpe (traitement) de cet anévrisme.\n\nInterprétation clinique  \nSuite à l’intervention, la patiente a présenté une hypertension artérielle ainsi que des expectorations abondantes de mousse rose, évacuées par un cathéter trachéal, signes évocateurs d’une insuffisance cardiaque aiguë avec œdème pulmonaire. L’auscultation pulmonaire a révélé des râles humides diffus, confirmant une atteinte pulmonaire. Une prise en charge adaptée de l’insuffisance cardiaque a été mise en place, incluant la ventilation assistée via le cathéter trachéal en unité de soins intensifs.\n\nProchaines étapes et évolution  \nHuit heures après la stabilisation, le cathéter trachéal a été retiré et la patiente a pu être sevrée du ventilateur. Les symptômes neurologiques, notamment le ptosis, se sont améliorés progressivement, avec un soulagement notable dès le cinquième jour post-opératoire. La surveillance clinique et cardiopulmonaire a été maintenue pour prévenir toute complication ultérieure.\n\nCe cas illustre l’importance d’une prise en charge multidisciplinaire rapide devant un ptosis progressif associé à un anévrisme cérébral, ainsi que la vigilance nécessaire face aux complications cardiorespiratoires post-chirurgicales."
+        }
+    },
+    {
+        "article": "Femme de 69 ans, ayant des antécédents d'hypertension, de diabète sucré insulinodépendant, de céphalées chroniques et de tabagisme. Elle a rapporté une semaine plus tôt des maux de tête, des troubles de la conscience et des vomissements. L'examen en salle d'urgence a révélé un coma (échelle de coma de Glasgow à 5), une raideur de la nuque et une absence de réflexe pupillaire.\n\nLa tomographie par ordinateur (CT) a montré une HSA diffuse, une hémorragie intra-ventriculaire légère et une hydrocéphalie. L'angiographie par tomographie par ordinateur a montré un anévrisme de l'artère carotide interne supraclinoïde à droite. Une fois admise dans l'unité de soins intensifs (USI), elle a reçu un traitement avec ventilation mécanique invasive, acide tranexamique, nimodipine et VPA entérale (400 mg, trois fois par jour). Un drainage lombaire externe et une embolisation endovasculaire de l'anévrisme ont été effectués, sans preuve de vasospasme angiographique. La tomographie par ordinateur initiale a montré une hydrocéphalie, et un drainage ventriculaire externe a été effectué.\n\nEn guise de complication initiale, la patiente a développé une dysfonction neurocardiogénique, avec un électrocardiogramme montrant des modifications diffuses de la repolarisation et une troponine élevée (716 ng/mL). L'échocardiographie transthoracique a montré une dysfonction systolique (fraction d'éjection du ventricule gauche de 35 %) et des anomalies régionales de la contractilité parietale, qui ont été interprétées comme une cardiomyopathie de stress. Pendant son séjour en unité de soins intensifs, malgré le retrait de la sédation, la patiente est restée dans le coma (échelle de coma de Glasgow à 5 au sixième jour). Les tomographies ultérieures ont été négatives pour une hydrocéphalie, des lésions ischémiques ou d'autres complications.\n\nLes fonctions hépatique, rénale et thyroïdienne étaient normales, et elle ne présentait pas de troubles hydroélectrolytiques. Aucune complication extraneurologique n'a été trouvée. Le drainage ventriculaire externe a été retiré avec des cultures stériles. Le Doppler transcrânien était négatif pour le vasospasme et a montré un taux de pulsatilité normal. L'IRM n'a pas détecté d'anomalies. L'EEG standard a exclu les modèles ictal, mais a montré un modèle de DPG à prédominance frontale, caractérisé par un modèle de décharge périodique continue, une morphologie triphasée et une absence de fluctuation spontanée, comme on le voit dans les dysfonctions cérébrales toxiques et/ou métaboliques. (4) Compte tenu de ces résultats, la dose de VPA était de 65,3 µg/mL (plage thérapeutique de 50 - 100 µg/mL), et la dose d'ammoniac était de 160,2 µg/mL (plage normale de 18,7 - 86,0 µg/mL). Il n'y avait pas de défaillance hépatique ou de saignement gastro-intestinal. L'administration de VPA a ensuite été arrêtée, et un traitement pour hyperammonémie avec lactulose et une diète restreinte en protéines a été initié. Le taux d'ammoniac a diminué progressivement jusqu'à la normalisation (81,7 µg/mL), ce qui a été corrélé à une amélioration neurologique, comme en témoigne la réponse au commandement le jour 12.\n\nLes EEG suivants ont progressivement amélioré jusqu'à la normale. La patiente a eu besoin d'une trachéotomie pour retirer la ventilation mécanique et a présenté une fistule trachéo-œsophagienne comme complication. Elle a fini par décéder 85 jours après son admission.\n",
+        "gold_summary": "Nous rapportons le cas d'un patient ayant présenté une hémorragie sous-arachnoïdienne et ayant reçu une prophylaxie anticonvulsivante avec du valproate, qui a connu une aggravation neurologique associée à des taux plasmatiques élevés d'ammoniac et des décharges périodiques sur l'électroencéphalogramme, sans autre cause identifiable. L'arrêt du traitement par l'acide valproïque et la normalisation des taux plasmatiques d'ammoniac ont entraîné une amélioration du tableau neurologique et électroencéphalographique.\n",
+        "synthetic_summary": {
+            "B1": "Une dame est tombée très malade avec un gros mal de tête. Les docteurs lui ont donné un médicament pour l’aider. Mais ce médicament a rendu son cerveau un peu fatigué. \n\nLes docteurs ont arrêté ce médicament. Après, elle a commencé à aller un peu mieux. Son cerveau a pu se reposer et devenir plus fort.",
+            "B2": "Voici un résumé adapté pour un adolescent de 14 ans en classe de biologie :\n\n**Ce qu'ils ont observé**  \nUne femme de 69 ans a eu une hémorragie sous-arachnoïdienne, c’est-à-dire un saignement autour du cerveau. Pour éviter des crises d’épilepsie, les médecins lui ont donné un médicament appelé valproate. Ce médicament peut parfois provoquer une augmentation d’une substance dans le sang appelée ammoniac, qui peut être toxique pour le cerveau.\n\n**Ce qui s’est passé**  \nAprès le traitement, la patiente a eu une aggravation de son état neurologique : elle était plus confuse et ne répondait pas bien. Des examens ont montré que son taux d’ammoniac dans le sang était très élevé et que son cerveau montrait des signaux anormaux sur l’électroencéphalogramme (EEG), un test qui enregistre l’activité électrique du cerveau.\n\n**Ce que cela signifie**  \nLes médecins ont arrêté le valproate et ont commencé un traitement pour faire baisser l’ammoniac dans son corps. Peu à peu, son état neurologique s’est amélioré, et les signaux anormaux sur l’EEG ont disparu. Cela montre que l’augmentation de l’ammoniac causée par le valproate a probablement aggravé son état cérébral.\n\nEn résumé, ce cas montre qu’un médicament utilisé pour prévenir les crises peut parfois causer des problèmes graves en augmentant l’ammoniac, et qu’il est important de surveiller cela pour ajuster le traitement.",
+            "B3": "Résumé destiné à un public adulte non spécialiste\n\nContexte  \nNous présentons le cas d’une femme de 69 ans ayant subi une hémorragie sous-arachnoïdienne (saignement autour du cerveau) due à la rupture d’un anévrisme cérébral. Elle a été traitée en soins intensifs, notamment par un médicament anticonvulsivant appelé valproate de sodium (VPA), pour prévenir les crises d’épilepsie.\n\nPrincipales observations  \nPeu après le début du traitement, la patiente est restée dans un coma profond malgré l’absence de complications évidentes telles que des lésions cérébrales supplémentaires ou une infection. Des examens électroencéphalographiques (EEG) ont montré des anomalies caractéristiques de dysfonction cérébrale, avec des décharges électriques périodiques. Par ailleurs, des analyses sanguines ont révélé une élévation importante du taux d’ammoniac, une substance normalement éliminée par le foie, sans signe de défaillance hépatique ni autre cause évidente d’augmentation.\n\nInterprétation clinique  \nL’association d’un taux élevé d’ammoniac et des anomalies EEG a suggéré que le valproate de sodium était responsable d’une toxicité neurologique, aggravant l’état de la patiente. Cette toxicité est connue pour provoquer une accumulation d’ammoniac dans le sang, ce qui peut perturber le fonctionnement cérébral.\n\nProchaines étapes et évolution  \nL’arrêt du valproate a été décidé, accompagné d’un traitement visant à réduire l’ammoniac sanguin (lactulose et régime pauvre en protéines). Progressivement, le taux d’ammoniac est revenu à la normale, ce qui a coïncidé avec une amélioration de l’état neurologique et une normalisation des tracés EEG. Malgré ces mesures, la patiente a présenté d’autres complications graves et est décédée environ trois mois après son admission.\n\nConclusion  \nCe cas illustre qu’en cas d’hémorragie cérébrale traitée par valproate, une aggravation neurologique inexpliquée peut être liée à une hyperammoniémie induite par le médicament. La reconnaissance rapide de cette complication et l’arrêt du traitement sont essentiels pour améliorer le pronostic neurologique."
+        }
+    },
+    {
+        "article": "Un homme de 48 ans a été transféré dans notre hôpital depuis un établissement psychiatrique pour somnolence, ataxie cérébelleuse et dysarthrie de trois jours. Il n'avait pas eu de fièvre au cours du mois précédent. Il a déclaré avoir sniffé de l'escitalopram et du clonazépam dans les jours précédents, ainsi que du disulfirame par voie intranasale (1 à 2 g par jour avec une dose maximale de 10 g par jour dans les 48 heures précédentes) au cours des deux derniers mois à des fins récréatives.\n\nIl avait des antécédents de tension artérielle élevée non traitée et de schizophrénie paranoïde, qui avaient entraîné trois hospitalisations pour exacerbation en raison de l'absence de traitement. Il prenait de l'olanzapine 10 mg/8 heures et du paliperidone 100 mg par voie intramusculaire mensuelle pour la schizophrénie, ainsi que du clonazépam 0,5 mg/24 heures et de l'escitalopram 15 mg/24 heures. Il était également sous traitement par disulfiram 250 mg par voie orale par jour pour son alcoolisme chronique, malgré un mode de consommation actif.\n\nLors de l'arrivée aux urgences, la fréquence respiratoire était de 20 respirations/minute, la saturation en oxygène dans l'air ambiant était de 98 %, la fréquence cardiaque de 85 battements/minute, la pression artérielle de 177/100 mmHg et la température de 36,2 °C. Le patient était stupéfié et désorienté, avec une échelle de coma de Glasgow de 13/15. L'examen cardiovasculaire, respiratoire et abdominal était anodin. L'examen neurologique a mis en évidence des pupilles myotiques hyporéactives, un clignement abondant, une dysarthrie marquée et une démarche instable. Il n'y avait aucun signe clinique d'hypertension intracrânienne ou d'irritation méningée.\n\nL'analyse sanguine a révélé une acidose métabolique hyperchlorémique (pH : 7,28 ; bicarbonate réel : 16,4 mmol/L), une polyglobulie et une macrocytose. La fonction rénale et le profil hépatique étaient normaux. Aucune autre constatation d'intérêt n'a été trouvée. L'étude toxicologique a été négative pour l'éthanol, le méthanol et l'éthylène glycol. Le dépistage des toxines dans l'urine par immunodosage a été positif pour les benzodiazépines. La tomographie par ordinateur a révélé des hypodensités symétriques légères non spécifiques des noyaux pâles et des bras postérieurs des capsules internes, une atrophie cérébrale et des infarctus lacunaires chroniques.\n\nSoupçonnant que l’encéphalopathie du patient était liée à une intoxication médicamenteuse (probablement par des benzodiazépines), sans pouvoir exclure d’autres possibilités diagnostiques, il a été admis en salle d’hospitalisation. Cette première hypothèse reposait sur le fait qu’il s’agissait d’un syndrome hypnotique-sédatif chez un patient ayant déclaré avoir consommé des benzodiazépines et ayant présenté un résultat positif à un examen qualitatif des urines.\n\nLes taux plasmatiques de diazepam, de nordiazepam et de clonazépam ont été demandés, tous dans la plage thérapeutique ou infrathérapeutique (72 ng/mL, 412 ng/mL et négatif, respectivement). Un électroencéphalogramme a montré une activité lente diffuse, sans altérations focales ou épileptiformes. L'examen du liquide céphalorachidien a montré une hyperprotéinorachie légère et tous les tests microbiologiques ont été négatifs.\n\nL’interrogatoire du patient était difficile, car les informations fournies étaient souvent contradictoires. L’explication selon laquelle les taux de clonazépam étaient négatifs était que l’on ne pouvait pas garantir que le patient avait réellement pris du clonazépam. Sur la base de ces taux plasmatiques, il était très probable qu’il ne l’avait pas fait. D’autre part, le fait que les taux plasmatiques de diazepam et de nordiazepam étaient positifs était cohérent avec les informations fournies par le patient. Rétrospectivement, des ampoules de diazepam ont été trouvées chez le patient. Les taux plasmatiques dans la fourchette thérapeutique n’excluent pas la possibilité d’effets indésirables, mais rendent leur gravité et l’évolution clinique suivie par le patient moins probables. Les benzodiazépines ont probablement contribué au tableau, mais la causalité ne pouvait pas être attribuée en fonction de ces taux plasmatiques.\n\nD’autre part, l’acidémie hyperchlorémique avec des taux normaux de lactate dans le contexte clinique de ce patient nous a conduit à envisager un trouble métabolique, en particulier une acidémie organique, un trouble de la bêta-oxydation des acides gras ou un trouble du cycle de l’urée. L’étude systématique dans le plasma et l’urine des acides gras, acylcarnitines, acylglycines et carnitine était négative. En outre, les taux d’ammonium étaient normaux et une hypoglycémie hypocétotique n’a pas été retrouvée. L’acidémie s’est résolue en moins de 24 heures sans mesures spécifiques, ce qui rend très peu probable l’hypothèse d’un trouble métabolique. En outre, lors de la stabilisation initiale, le patient avait reçu une sédation intensive avec du NaCl à 0,9 %, ce qui aurait pu contribuer à l’acidémie.\n\nAu cours des 24 heures qui ont suivi, il a présenté une diminution progressive du niveau de conscience, avec un développement d'une insuffisance respiratoire rapidement progressive nécessitant une intubation endotrachéale et une ventilation mécanique, et un transfert vers l'unité de soins intensifs.\n\nL'examen respiratoire et la radiographie thoracique suggéraient une pneumonie par aspiration bronchique, et il a été traité en conséquence. Une IRM cérébrale a été réalisée pour rechercher l'étiologie de l'encéphalopathie. Elle a révélé un signal hyperintense hétérogène bilatéral et étendu dans les deux globes palléaux, le bras postérieur de la capsule interne et le putamen, sur les images FLAIR et T2. La séquence T1 renforcée a montré une hypointensité dans ces régions.\n\nSur la base de ces résultats, l'affaire a été réorientée vers une encéphalopathie induite par le disulfirame, étant donné que le schéma radiologique avait été décrit précédemment dans la littérature dans d'autres cas d'intoxication par le disulfirame, ainsi que dans des cas d'intoxication par le monoxyde de carbone (mais ce n'était pas le scénario clinique). Le diagnostic d'encéphalopathie par disulfirame a été fait par des critères d'exclusion. Selon l'algorithme de Naranjo et al [5], avec un score de 4 sur 10, il a été considéré possible d'attribuer la causalité au disulfirame dans ce cas. À son tour, les cas publiés d'encéphalopathie par disulfirame présentent d'importantes similitudes avec ce cas. Cependant, il n'y a pas de cas décrits de disulfirame inhalé, car ce n'est pas une voie d'administration approuvée. Malheureusement, il n'a pas été possible de mesurer les niveaux plasmatiques de disulfirame.\n\nAu cours des deux semaines suivantes, l'état respiratoire du patient s'est progressivement amélioré jusqu'à ce qu'il puisse être extubé. Après le retrait de la sédation, l'examen neurologique a révélé des difficultés de supination, un tremblement intentionnel et une dysmétrie de la manœuvre doigt-nez, ainsi qu'une faiblesse proximale des membres supérieurs et inférieurs. Par la suite, le patient a présenté une amélioration neurologique. La limitation de la motilité oculaire et la faiblesse ont disparu en quelques jours, mais un léger tremblement et une légère dysmétrie ont persisté. En raison de la myopathie du patient en état critique, la marche n'a pu être explorée avant deux semaines, moment où une résolution complète de l'ataxie a été observée.\n\nLe patient a été renvoyé avec un léger tremblement intentionnel résiduel. L'IRM cérébrale de contrôle à deux mois a montré une évolution des zones symétriques d'œdème cytotoxique vers une nécrose.\n",
+        "gold_summary": "Un patient de 48 ans souffrant d'alcoolisme chronique qui a déclaré avoir inhalé une dose très élevée de disulfiram sans avoir consommé d'alcool en même temps a développé une encéphalopathie aiguë avec une insuffisance respiratoire rapidement progressive. L'imagerie cérébrale a révélé une atteinte bilatérale symétrique étendue des deux noyaux gris centraux, un signe caractéristique de cette intoxication. La récupération neurologique a été lente. Deux mois après l'intoxication, le patient présentait un léger tremblement intentionnel résiduel et une IRM a montré une évolution des zones symétriques d'œdème cytotoxique vers la nécrose.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 48 ans a eu un gros problème au cerveau. Il a pris un médicament d’une façon très dangereuse. Ce médicament a fait que son cerveau a eu mal et il a eu du mal à respirer.\n\nLe docteur a fait une photo spéciale de son cerveau. Cette photo a montré que deux parties du cerveau étaient très malades. C’est un signe que le médicament l’a beaucoup embêté.\n\nLe monsieur a guéri doucement, mais il avait encore un petit tremblement après deux mois. Une autre photo a montré que son cerveau avait encore des traces de ce problème. Les docteurs ont aidé le monsieur à aller mieux.",
+            "B2": "**Ce qu’ils ont trouvé :**  \nUn homme de 48 ans, qui avait un problème d’alcool et prenait un médicament appelé disulfirame pour l’aider à arrêter, a inhalé une grande quantité de ce médicament. Il n’avait pas bu d’alcool en même temps. Peu après, il est devenu très somnolent, avait des difficultés à parler clairement et à marcher droit. Son cerveau a été touché, ce qui a causé une maladie grave appelée encéphalopathie, accompagnée d’un problème respiratoire qui s’est rapidement aggravé.\n\n**Ce que cela signifie :**  \nLes examens d’imagerie de son cerveau ont montré des lésions spécifiques dans des zones précises appelées noyaux gris centraux, ce qui est typique d’une intoxication au disulfirame. Même si le patient a reçu des soins, sa récupération a été lente. Deux mois plus tard, il avait encore un léger tremblement quand il bougeait volontairement la main, et une nouvelle imagerie a montré que certaines zones du cerveau avaient évolué vers une destruction des cellules (nécrose).\n\n**En résumé :**  \nInhaler une grande quantité de disulfirame peut provoquer une grave atteinte du cerveau avec des symptômes sérieux. La guérison peut prendre du temps, et des séquelles comme un tremblement peuvent persister. Cette situation est rare, surtout par inhalation, car ce médicament est normalement pris par voie orale.",
+            "B3": "Résumé détaillé destiné à un adulte éduqué non-médecin\n\nContexte  \nUn homme de 48 ans, souffrant d’alcoolisme chronique et de schizophrénie paranoïde, a été admis en urgence pour une somnolence importante, des troubles de la coordination (ataxie cérébelleuse) et des difficultés d’élocution (dysarthrie) apparus sur trois jours. Il avait récemment inhalé (sniffé) plusieurs médicaments, dont du disulfirame à des doses très élevées, ainsi que de l’escitalopram et du clonazépam, dans un contexte d’usage récréatif. Son traitement habituel comprenait notamment des antipsychotiques et du disulfirame oral prescrit pour son alcoolisme, malgré une consommation d’alcool toujours active.\n\nPrincipales observations cliniques et paracliniques  \nÀ son arrivée, le patient était désorienté et somnolent, avec une pression artérielle élevée mais sans fièvre ni signes d’infection initiale. L’examen neurologique montrait des pupilles contractées peu réactives, une dysarthrie marquée et une démarche instable, sans signe d’hypertension intracrânienne ni d’irritation des méninges. Les analyses sanguines révélaient une acidose métabolique hyperchlorémique (un déséquilibre du pH sanguin), une augmentation du nombre de globules rouges (polyglobulie) et une macrocytose (globules rouges de grande taille), mais la fonction rénale et hépatique était normale. Les tests toxicologiques ont confirmé la présence de benzodiazépines, mais les taux plasmatiques de ces médicaments étaient dans les limites thérapeutiques ou inférieures, ce qui ne permettait pas d’expliquer totalement la gravité des symptômes. L’électroencéphalogramme montrait une activité cérébrale ralentie, sans foyer épileptique, et le liquide céphalorachidien ne révélait pas d’infection.\n\nÉvolution clinique et investigations complémentaires  \nLe patient a rapidement présenté une aggravation de son état de conscience, avec une insuffisance respiratoire nécessitant une intubation et une ventilation mécanique. Une pneumonie par aspiration a été diagnostiquée et traitée. L’imagerie cérébrale par IRM a montré des lésions bilatérales symétriques étendues dans les noyaux gris centraux (globes palléaux, putamen, capsules internes), caractérisées par un œdème cytotoxique visible sur certaines séquences spécifiques. Ces anomalies radiologiques sont typiques d’une encéphalopathie toxique.\n\nInterprétation clinique  \nAprès exclusion d’autres causes métaboliques, infectieuses ou toxiques, le diagnostic a été orienté vers une encéphalopathie induite par le disulfirame, un médicament utilisé pour traiter l’alcoolisme mais ici inhalé à forte dose, une voie d’administration non autorisée et peu documentée. Ce diagnostic repose sur la concordance entre les antécédents de consommation, les résultats d’imagerie caractéristiques et l’absence d’autres explications. Le score de causalité selon l’algorithme de Naranjo a indiqué une probabilité possible d’imputabilité au disulfirame.\n\nProchaines étapes et pronostic  \nAu cours des deux semaines suivantes, l’état respiratoire du patient s’est amélioré, permettant le sevrage de la ventilation mécanique. Sur le plan neurologique, une amélioration progressive a été observée, bien que des troubles moteurs résiduels tels qu’un tremblement intentionnel et une légère dysmétrie (difficulté à coordonner les mouvements fins) aient persisté. Deux mois après l’intoxication, l’IRM de contrôle a montré une évolution des lésions initiales d’œdème vers une nécrose (mort cellulaire) dans les zones affectées. Le patient a été renvoyé avec un léger tremblement résiduel, témoignant d’une récupération partielle mais incomplète.\n\nEn résumé, ce cas illustre une encéphalopathie grave causée par une intoxication au disulfirame inhalé, caractérisée par des lésions cérébrales bilatérales symétriques et une récupération neurologique lente avec séquelles persistantes."
+        }
+    },
+    {
+        "article": "Homme de 64 ans, sans antécédents pathologiques, qui vivait avec des animaux de compagnie (chiens). Il a consulté pour une céphalée holocraniale, une hémianopsie homonyme droite d'une semaine d'évolution associée à un épisode de crise convulsive tonique clonique généralisée, sans fièvre. Une TDM du cerveau a été réalisée, qui a mis en évidence une lésion au niveau cortico-sous-cortical frontal, accompagnée d'un œdème. Par la suite, une IRM du cerveau a été réalisée, dont le coefficient de diffusion a révélé une lésion hétérogène avec restriction dans cette séquence et corrélation dans ADC, avec un halo hypointense périphérique associé à un vaste œdème vasogénique qui a généré un effet de masse avec un effondrement partiel du ventricule latéral droit et du corps calleux et une déviation non significative de la ligne médiane vers la gauche, qui mesure 67x36x26 mm. Une excision complète d'une lésion encapsulée avec contenu purulent a été réalisée par accès transcortical, en commençant une thérapie antibiotique avec meropenem/vancomycin jusqu'à l'isolement en culture d'A. aphrophilus, en complétant le traitement avec ceftriaxone pendant 21 jours. Au cours de son séjour à l'hôpital, une échographie de l'abdomen total, du fond de l'œil et une échocardiographie transœsophagienne ont été réalisées, sans preuve d'autres sites d'infection. Il a évolué favorablement, ce qui a permis sa sortie de l'hôpital.\n",
+        "gold_summary": "Il s’agit d’un patient de 64 ans, sans antécédents significatifs, qui a été admis aux urgences pour un cas de céphalée, d’hémianopsie d’une semaine d’évolution et de crises toniques cloniques, et qui a ensuite été diagnostiqué d’un abcès cérébral dû à A. aphrophilus après des études d’imagerie et une culture de lésion cérébrale.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 64 ans avait très mal à la tête. Il ne voyait pas bien d’un côté de ses yeux. Il a eu une grosse crise où son corps bougeait tout seul. Les docteurs ont fait des photos de sa tête. Ils ont trouvé une boule avec du pus dedans. Ils ont enlevé cette boule et donné des médicaments pour tuer les microbes. Le monsieur a bien guéri et est rentré chez lui.",
+            "B2": "Voici un résumé adapté pour un élève de 14 ans en classe de biologie :\n\n**Ce qu’ils ont trouvé**  \nUn homme de 64 ans, en bonne santé avant, est venu à l’hôpital parce qu’il avait mal à la tête partout, ne voyait plus bien d’un côté de son champ de vision depuis une semaine, et avait eu une crise d’épilepsie. Les médecins ont fait des examens du cerveau avec des images spéciales (scanner et IRM). Ils ont vu une grosse boule avec du liquide et un gonflement autour dans une partie de son cerveau.\n\n**Ce que cela signifie**  \nCette boule était un abcès cérébral, c’est-à-dire une infection avec du pus dans le cerveau. Pour savoir quel microbe causait l’infection, ils ont enlevé cette boule en chirurgie et ont analysé le liquide. Ils ont trouvé une bactérie appelée *Aggregatibacter aphrophilus*. C’est une bactérie qui peut venir de la bouche ou des animaux.\n\n**Le traitement et le résultat**  \nLe patient a reçu des antibiotiques puissants pendant plusieurs semaines pour tuer la bactérie. Les médecins ont aussi vérifié s’il y avait d’autres infections dans son corps, mais ils n’en ont pas trouvé. Grâce au traitement, il s’est bien rétabli et a pu quitter l’hôpital.\n\nEn résumé, cet homme avait une infection rare dans le cerveau qui a causé des symptômes sérieux, mais grâce à la chirurgie et aux antibiotiques, il a guéri.",
+            "B3": "Contexte  \nUn homme de 64 ans, sans antécédents médicaux notables, vivant avec des chiens comme animaux de compagnie, a consulté pour des symptômes neurologiques récents comprenant une céphalée généralisée, une perte de vision dans la moitié droite du champ visuel (hémianopsie homonyme droite) évoluant depuis une semaine, ainsi qu’un épisode de crise convulsive tonico-clonique généralisée. Il ne présentait pas de fièvre.\n\nPrincipales observations  \nUne tomodensitométrie (TDM) cérébrale initiale a révélé une lésion cortico-sous-corticale frontale accompagnée d’un œdème. Une imagerie par résonance magnétique (IRM) a ensuite montré que cette lésion était hétérogène avec une restriction de diffusion, entourée d’un halo hypointense, et associée à un important œdème vasogénique provoquant un effet de masse. Cette masse mesurait environ 67 x 36 x 26 mm et entraînait un effondrement partiel du ventricule latéral droit et du corps calleux, ainsi qu’une légère déviation de la ligne médiane vers la gauche.\n\nInterprétation clinique  \nLe tableau clinique et les examens d’imagerie ont conduit à la suspicion d’un abcès cérébral. Une intervention chirurgicale par voie transcorticale a permis l’excision complète d’une lésion encapsulée contenant du pus. L’analyse microbiologique a isolé la bactérie Aggregatibacter aphrophilus, un germe peu fréquent mais connu pour causer des infections cérébrales. Le patient a reçu un traitement antibiotique initial par méropénem et vancomycine, adapté ensuite à la ceftriaxone pendant 21 jours en fonction des résultats de culture.\n\nProchaines étapes et évolution  \nDes examens complémentaires, notamment une échographie abdominale, un fond d’œil et une échocardiographie transœsophagienne, n’ont pas révélé d’autres foyers infectieux. L’évolution clinique a été favorable sous traitement, permettant la sortie de l’hôpital sans complications supplémentaires.\n\nRésumé  \nCe cas illustre un abcès cérébral chez un patient sans facteurs de risque apparents, diagnostiqué grâce à l’imagerie cérébrale et confirmé par la culture bactérienne. La prise en charge combinant chirurgie et antibiothérapie ciblée a permis une évolution positive."
+        }
+    },
+    {
+        "article": "Il s’agit d’une patiente de 34 ans dont la maladie dure depuis quatre semaines. Deux mois auparavant, elle avait accouché par césarienne à la 37e semaine de grossesse et avait présenté des saignements persistants de la plaie opératoire. Dans ses antécédents personnels, elle a nié avoir présenté des antécédents de saignements pendant l’enfance ou l’adolescence. Trois ans auparavant, elle avait donné naissance à son premier enfant (également par césarienne), qui est mort à cause d’une chromosomopathie (selon la patiente). En outre, elle a déclaré être allergique au tramadol.\n\nLe tableau clinique a débuté par une lombalgie due à une lithiase rénale bilatérale. Par la suite, il a réussi à expulser un calcul et a ensuite présenté une hématurie pendant trois jours, pour laquelle il a reçu de l’acide tranexamique toutes les 12 heures. Trois semaines plus tard, il a présenté une douleur dans la région inférieure de la cuisse gauche qui a augmenté en intensité, avec un durcissement de la zone. En raison de la persistance des symptômes, on lui a prescrit du diclofenac par voie intramusculaire, qui a provoqué une ecchymose et un saignement dans la région des fesses et qui persiste malgré la compression avec des compresses.\n\nLa patiente a subi une échographie Doppler qui a révélé une thrombose veineuse profonde du membre inférieur gauche et s’est rendue à l’hôpital local avec ces résultats. Elle a été traitée par anticoagulant sous-cutané à l’énoxaparine 30 mg/24 h, ainsi que par de la morphine pour la gestion de la douleur et a été hospitalisée. Le jour suivant, elle a présenté une épigastralgie, une vision trouble, une fréquence cardiaque de 117 battements/min, une tension artérielle de 113/85 mmHg et une saturation de 93 %. Il a été décidé de suspendre l’énoxaparine. L’hémogramme a révélé une hémoglobine de 6,4 g/dl, ce qui représentait une différence de 4 g/dl par rapport au résultat un jour avant son admission, qui était de 10,4 g/dl. En conséquence, deux paquets globulaires ont été transfusés. En raison de la suspicion de vascularite, elle a été traitée par méthylprednisolone et a été référée à notre hôpital pour une étude plus approfondie.\n\nL'examen physique à l'admission a révélé une pâleur sévère, une écailleuse étendue sur la cuisse et la face latérale du genou gauche, ainsi qu'un hématome sur la cuisse droite. L'hémogramme a révélé une anémie modérée (Hb = 9,8 g/dl), normocytaire et normocromatique. L'examen biochimique a révélé des valeurs de glucose de 160 mg/dl. Les enzymes hépatiques AST et ALT étaient respectivement de 52 U/L et 86 U/L. Le profil de coagulation a montré une prolongation du temps de thromboplastine partielle activée (TTPa) de 91,2 s. Les autres composants de l'hémogramme, biochimique, électrolytique, hépatique et de coagulation étaient normaux. L'échographie des tissus mous de la région fessière droite a révélé une collection au niveau du tissu cellulaire sous-cutané (TCSC) et un œdème jusqu'au tiers supérieur de la cuisse. L'échographie Doppler du membre inférieur gauche a montré une bonne fluximétrie sans signe de thrombose dans la veine fémorale commune, superficielle et profonde.\n\nUn traitement symptomatique a été initié et une hémoculture et une uréoculture ont été demandées, qui ont été négatives. Les taux d'anticorps antinucléaires (ANA), de complément C3 et C4 et de ferritine étaient dans la plage de référence.\n\nDevant la suspicion d'hémophilie acquise, des études ont été demandées pour confirmation, où une correction partielle du TTPa a été trouvée dans le test de mélange. Le facteur VIII a été mesuré, son activité étant diminuée (<1,0 U/dl) et la présence d'un inhibiteur du facteur VIII a été démontrée : 8,64 unités Bethesda/ml. Ce qui a permis de confirmer le diagnostic d'hémophilie acquise, qui a été lié au post-partum par le début des symptômes.\n\nLa prednisone a été initiée à 50 mg po au petit déjeuner et 10 mg po au déjeuner, la cyclophosphamide à 50 mg 2 comprimés po q 24 h et le complexe coagulant anti-inhibiteur hémophilique (FEIBA). Cinq jours plus tard, ce dernier a été arrêté en raison de douleurs thoraciques oppressives, de dyspnée et de nausées (éventuelle réaction indésirable au médicament), et a été remplacé par le facteur VII recombinant activé (NovoSeven).\n\nL’évolution clinique de la patiente a été favorable, avec une diminution de l’ecchymose et l’absence de tout autre symptôme, et elle a pu quitter l’hôpital.\n",
+        "gold_summary": "Une patiente de 34 ans se présente avec des douleurs lombaires, une hématurie et un hématome dans la région fessière droite, sans antécédent de saignement. En raison de l'étendue des manifestations hémorragiques, elle est transférée au service des urgences. Les examens auxiliaires du profil de coagulation, le test de mélange et la mesure des titres d'inhibiteurs du facteur VIII ont confirmé le diagnostic.\n",
+        "synthetic_summary": {
+            "B1": "Une dame a eu mal au dos et des bleus sur ses fesses. Elle n’avait jamais eu de saignement avant. Les docteurs ont fait des tests pour comprendre. Ils ont trouvé un problème avec son sang qui fait qu’elle saigne plus facilement.",
+            "B2": "Une femme de 34 ans a commencé à avoir des douleurs dans le bas du dos, du sang dans les urines et un gros bleu sur la fesse droite. Elle n’avait jamais eu de problèmes de saignement avant. Comme ses saignements étaient importants, elle a été envoyée aux urgences pour des examens. Ces tests ont montré qu’elle avait un problème avec un facteur de coagulation appelé facteur VIII, ce qui a permis de diagnostiquer une maladie rare appelée hémophilie acquise. Cette maladie empêche le sang de bien coaguler, ce qui cause des saignements importants.",
+            "B3": "Résumé détaillé destiné à un public non spécialiste\n\nContexte  \nUne femme de 34 ans, récemment accouchée par césarienne il y a deux mois, a présenté plusieurs symptômes inquiétants sur une période de quatre semaines. Initialement, elle souffrait de douleurs lombaires liées à des calculs rénaux, puis a eu du sang dans les urines (hématurie). Par la suite, elle a développé une douleur et un durcissement au niveau de la cuisse gauche, suivis d’un hématome (bleu) important dans la région de la fesse droite, qui ne s’est pas résorbé malgré les soins locaux.\n\nPrincipales observations  \nÀ l’hôpital, une échographie Doppler a révélé une thrombose veineuse profonde (caillot sanguin dans une veine) du membre inférieur gauche. Elle a reçu un traitement anticoagulant, mais a rapidement présenté une baisse importante de son taux d’hémoglobine (indiquant une anémie due à une perte de sang), une douleur abdominale et des troubles visuels. L’anticoagulant a été arrêté. L’examen physique a montré une pâleur importante, des ecchymoses étendues et un hématome. Des analyses sanguines ont révélé une coagulation anormale, avec un allongement marqué du temps de thromboplastine partielle activée (TTPa), ce qui indique un problème dans la cascade de coagulation.\n\nInterprétation clinique  \nDevant ces signes, une suspicion d’hémophilie acquise a été émise. L’hémophilie acquise est une maladie rare dans laquelle le corps produit des anticorps qui inhibent le facteur VIII, une protéine essentielle à la coagulation normale du sang. Cette pathologie peut survenir après une grossesse (post-partum) et se manifeste par des saignements inhabituels et difficiles à contrôler. Les tests spécifiques ont confirmé la présence d’un inhibiteur du facteur VIII et une activité très faible de ce facteur, établissant ainsi le diagnostic.\n\nProchaines étapes et traitement  \nLa patiente a été traitée par des médicaments immunosuppresseurs (prednisone et cyclophosphamide) pour réduire la production des anticorps inhibiteurs, ainsi que par des agents de substitution pour contrôler les saignements (complexe coagulant anti-inhibiteur hémophilique, puis facteur VII recombinant activé en raison d’effets secondaires). L’évolution a été favorable, avec une réduction progressive des ecchymoses et une amélioration clinique, permettant sa sortie de l’hôpital.\n\nEn résumé, cette patiente a développé une forme rare d’hémophilie acquise après son accouchement, responsable de saignements importants et inhabituels, diagnostiquée grâce à des tests spécifiques de coagulation et traitée efficacement par une combinaison de médicaments immunosuppresseurs et de facteurs de coagulation."
+        }
+    },
+    {
+        "article": "Un patient de 70 ans ayant des antécédents médicaux importants pour l’hépatite C, traité par une thérapie par interféron trois ans auparavant, et une hypertrophie de la prostate. Malgré des résultats virologiques négatifs persistants lors du suivi, le patient a été référé à notre service en raison d’une suspicion de carcinome hépatocellulaire (CHC). Notamment, le mode de vie du patient inclut la consommation quotidienne de 300 à 500 ml de whisky sans antécédents de tabagisme. Les tests sanguins étaient négatifs pour l’antigène HB et positifs pour les anticorps du VHC. La fonction hépatique était de grade A avec une classification de 5 points de Child-Pugh, et les dommages au foie étaient également de grade A. Le score ALBI était de -2,43, ALBI grade 2a, et ICG R15 19,1 %. Les marqueurs tumoraux étaient normaux avec CEA 2,5 ng/ml, mais AFP élevée 1984 ng/ml et CA19-9 3135 U/ml.\n\nTomographie par ordinateur (CT) avec contraste : une masse multinodulaire fusionnée d'une longueur maximale de 91 mm couvrant le segment postérieur et le lobe caudé a été observée. Le CHC a été détecté par une coloration foncée dans la phase précoce et par un lavage dans la phase d'équilibre. La limite de la branche primaire de la veine porte droite était masquée. Un hémangiome a été observé au S5 du foie et un petit kyste a été observé au S6 du foie.\n\nStratégie de traitement initial : Le diagnostic de CHC était cT3N0M0, cStage III. Il n'y avait pas de frontière avec la première branche de la veine porte, et la résection du lobe caudé droit du foie était considérée comme une résection radicale. Cependant, la limite de résection était de 44 % sur la base d'une ICG R15 résiduelle du foie de 40 % [4], et la résection a été jugée impossible en raison de la mauvaise fonction résiduelle du foie.\n\nThérapie ciblée : Le traitement initial consistait en une thérapie ciblée avec un agent ciblé moléculairement (lenvatinib, 8 mg) et une embolisation artérielle transcathéter (TAE). Une tomographie par ordinateur réalisée 4 semaines après le début du traitement a montré que la tumeur avait augmenté d'environ 120 % pour atteindre une longueur maximale de 110 mm. Nous avons changé pour une combinaison de thérapie ciblée atezolizumab (1200 mg) et bevacizumab (1000 mg), qui s'est avérée utile dans les cas négatifs au lenvatinib. Aucun événement indésirable n'est survenu avec les deux thérapies ciblées. Une tomographie par ordinateur réalisée après quatre cycles d'atézolizumab plus bevacizumab a montré que la tumeur avait rétréci à un diamètre maximal de 60 mm, l'effet de contraste avait disparu et la masse avait une absorption généralement faible.\n\nLes marqueurs tumoraux ont été normalisés à 3,4 ng/ml AFP et 18 U/ml CA19-9.\n\nConstatations chirurgicales : lobectomie post-hépatique. La perte de sang était de 293 ml. 6 h 23 min.\n\nConstatations histopathologiques : grossièrement, la tumeur était blanc jaunâtre avec d'autres fusions nodales. Histologiquement, la plupart des tumeurs étaient nécrotiques, et il n'y avait aucune preuve de HCC actif résiduel. La formation de granulome épithélioïde a été observée dans la région environnante, ce qui a été considéré comme un changement post-traitement.\n\nSure-après l'opération : La patiente ne présentait aucun signe de défaillance hépatique post-opératoire ; cependant, la TDM réalisée le jour 7 post-opératoire a révélé la formation d'un abcès du tronc. Un drainage percutané a rapidement soulagé l'inflammation, et la patiente a quitté l'hôpital le jour 22 post-opératoire sans que le drain n'ait été retiré. Le drain a été retiré le jour 38 post-opératoire. La patiente est actuellement en vie 16 mois après l'opération sans récidive. Il n'y a pas de traitement recommandé après résection, et aucun traitement supplémentaire n'a été fourni.\n",
+        "gold_summary": "Le patient, un homme d'une soixantaine d'années, a développé un CHC de 11,5 cm (T3N0M0 stade III) dans la zone hépatique postérieure après avoir été virologiquement négatif pour l'hépatite C. La tumeur était proche de la branche de la veine porte droite, rendant le lobe du foie non résécable en raison d'une mauvaise fonction hépatique. Après l'agrandissement de la tumeur, il a été traité avec atezolizumab et bevacizumab. Après 5 cycles, la tumeur a considérablement rétréci, permettant une résection complète avec élimination du segment postérieur. L'opération a révélé des tumeurs principalement nécrotiques sans cellules cancéreuses actives restantes.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur avait une grosse boule dans son foie. Cette boule était trop grande et près d’un gros tuyau du foie. Son foie ne pouvait pas être enlevé tout de suite parce qu’il ne fonctionnait pas bien. \n\nAlors, il a pris des médicaments spéciaux. Ces médicaments ont aidé la boule à devenir plus petite. Après ça, les docteurs ont pu enlever la partie du foie avec la boule. \n\nQuand ils ont regardé la boule enlevée, ils ont vu qu’il n’y avait plus de vilaines cellules dedans. Le monsieur va mieux maintenant.",
+            "B2": "Résumé simple pour un élève de 14 ans :\n\nUn homme d’environ 70 ans avait un gros cancer du foie appelé carcinome hépatocellulaire (CHC). Ce cancer mesurait environ 11,5 cm et se trouvait dans une partie importante du foie, près d’une grosse veine. Son foie ne fonctionnait pas très bien, donc les médecins ne pouvaient pas enlever la tumeur directement par chirurgie au début.\n\nLa tumeur a grossi malgré un premier traitement. Alors, les médecins ont utilisé un nouveau traitement avec deux médicaments, atezolizumab et bevacizumab, qui ciblent spécifiquement les cellules cancéreuses. Après cinq cycles de ce traitement, la tumeur a beaucoup diminué de taille.\n\nGrâce à cette réduction, les médecins ont pu faire une opération pour enlever la partie du foie où se trouvait la tumeur. Lorsqu’ils ont examiné la tumeur en détail après l’opération, ils ont vu que la plupart des cellules cancéreuses étaient mortes et qu’il ne restait plus de cancer actif.\n\nEn résumé, grâce à ce traitement spécial, la tumeur a rétréci suffisamment pour que la chirurgie soit possible et efficace.",
+            "B3": "Résumé détaillé et structuré pour un lecteur non spécialiste\n\n**Contexte**  \nUn homme de 70 ans, avec des antécédents d’hépatite C traitée et une hypertrophie de la prostate, a été suivi pour une suspicion de carcinome hépatocellulaire (CHC), un cancer du foie. Malgré une guérison virologique de l’hépatite C, il présentait une masse tumorale importante dans le foie. Son mode de vie comprenait une consommation quotidienne modérée d’alcool. Les analyses sanguines montraient une fonction hépatique relativement préservée, mais des marqueurs tumoraux (AFP et CA19-9) très élevés, suggérant une activité tumorale importante.\n\n**Principales observations**  \nL’imagerie par tomodensitométrie (CT) a révélé une masse tumorale volumineuse (jusqu’à 91 mm initialement) dans la partie postérieure et le lobe caudé du foie, avec des caractéristiques typiques du CHC. La tumeur était proche de la branche principale de la veine porte droite, ce qui compliquait la possibilité d’une chirurgie. Le diagnostic retenu était un CHC de stade III (T3N0M0). La fonction hépatique résiduelle après résection prévue était insuffisante, rendant la chirurgie initialement impossible.\n\n**Intervention thérapeutique**  \nLe patient a d’abord reçu un traitement ciblé par lenvatinib et une embolisation artérielle, mais la tumeur a continué de croître (jusqu’à 110 mm). Le traitement a été modifié en une association d’atezolizumab (un immunothérapie) et bevacizumab (un anti-angiogénique). Après quatre cycles de cette combinaison, la tumeur a nettement diminué de taille (60 mm), avec disparition des signes d’activité tumorale à l’imagerie et normalisation des marqueurs sanguins.\n\n**Résultats chirurgicaux et histopathologiques**  \nLa chirurgie a pu être réalisée, consistant en une résection du lobe postérieur du foie. L’intervention s’est déroulée sans complication majeure immédiate, avec une perte sanguine modérée. L’analyse microscopique de la pièce opératoire a montré que la majorité de la tumeur était nécrotique (tissu mort) et qu’aucune cellule cancéreuse active n’était détectée, indiquant une réponse complète au traitement. Des modifications inflammatoires compatibles avec un effet post-thérapeutique ont été observées.\n\n**Suivi post-opératoire et pronostic**  \nAprès l’opération, le patient n’a pas présenté d’insuffisance hépatique. Une complication infectieuse locale (abcès) a été rapidement prise en charge par drainage. Le patient a quitté l’hôpital en bon état et le drain a été retiré sans problème. Seize mois après la chirurgie, il est toujours en vie sans signe de récidive tumorale. Aucun traitement complémentaire n’a été nécessaire.\n\n**Conclusion**  \nCe cas illustre qu’une tumeur hépatique initialement non résécable, en raison de sa taille et de la fonction hépatique limitée, peut devenir opérable après une réponse significative à une immunothérapie combinée ciblée. Cette stratégie a permis une résection complète et une réponse histologique complète, offrant un pronostic favorable à moyen terme."
+        }
+    },
+    {
+        "article": "Un homme de 39 ans s'est présenté dans un centre de soins tertiaires après avoir tenté de se pendre une heure auparavant. Selon le rapport du SMU, il a été trouvé sur le sol en train de tousser du sang à côté d'un arbre avec une corde de suspension. À la présentation, il était alerte et orienté. Il a rapporté avoir des difficultés à projeter sa voix, mais a nié avoir une dyspnée. L'examen physique a révélé une marque de ligature le long du cou antérieur au niveau du cartilage thyroïde. La saillie thyroïdienne pouvait être palpée, mais d'autres repères cervicaux étaient masqués par un emphysème sous-cutané.\n\nL'angiographie par TDM a révélé des lésions de l'intima avec thrombus (AAST grades III-V) des carotides communes bilatérales, de la carotide externe gauche et des artères vertébrales bilatérales. Une fracture de la vertèbre C4 a été constatée. Il y avait un emphysème sous-cutané étendu avec pneumomédiastinum. En y regardant de plus près, les muscles du bandeau infra-hyoïdien étaient rompus, avec une distension de l'os hyoïde et de l'épiglotte en supériorité et du cartilage thyroïde en infériorité. L'IRM a démontré une déchirure partielle du ligament nuchal, nécessitant une immobilisation continue de la colonne vertébrale.\n\nLe service OTO-HNS a été consulté pour évaluer les voies respiratoires du patient. La laryngoscopie souple a révélé des cordes mobiles bilatérales avec un léger oedème laryngé. L'épiglotte semblait être détachée du cartilage laryngé et la muqueuse des plis aryépiglottiques/fausses cordes était perturbée.\n\nPeu après l'évaluation initiale par l'OTO-HNS, le patient a été emmené en salle d'opération pour une intubation nasotrachéale consciente contrôlée. Il était stable du point de vue des voies respiratoires et, en raison de l'étendue de ses lacérations de la muqueuse laryngée, nous avons estimé que la meilleure option était de le transférer en salle d'opération pour une prise en charge définitive des voies respiratoires sous visualisation directe la nuit de son arrivée. Le deuxième jour de l'hospitalisation, le patient a subi une trachéotomie, une laryngoscopie, une oesophagoscopie et une réparation de la lésion hyolaryngée. Après avoir soulevé les lambeaux, un petit défaut a été constaté au-dessus de la pointe thyroïdienne dans la couche d'investissement du fascia cervical profond qui, lorsqu'il a été ouvert, a révélé un grand défaut des tissus mous s'étendant dans les voies respiratoires supraglótiques. Les muscles sterno-hyoïdien, thyro-hyoïdien et omo-hyoïdien avaient rompu 1 à 2 cm en dessous de leur insertion sur le hyoïde. La membrane thyro-hyoïdienne était complètement détruite, tout comme la muqueuse des fausses cordes et des plis aryépiglottiques. L'épiglotte a été détachée du cartilage thyroïde et a été déviée vers le haut par le hyoïde en raison des forces non opposées de la musculature supra-hyoïdienne.\n\nEn raison de lésions concomitantes de la colonne cervicale, le cou devait rester dans une position neutre. Une pince Allis a été utilisée pour rétracter l'hyoïde inférieure et une seule pince pour tirer le larynx/trachée vers le haut. La muqueuse laryngée a été réparée en premier avec une suture interrompue 4-0 en vicryl. Pour maintenir la tension hors de la plaie, une thyrohyoïdeopexie modifiée avec épiglotopexie a été réalisée. Une aiguille de calibre 20 a été passée à travers le cartilage thyroïde antérieur sous visualisation avec un bronchoscope flexible pour assurer une distance adéquate au-dessus de la commissure antérieure avant de passer la suture médiane. Du côté des voies respiratoires, la suture a ensuite été passée à travers le pétale de l'épiglotte. Le bras inférieur de quatre sutures supplémentaires 2-0 en vicryl a été passé à travers l'ala thyroïde supérieure (2 sutures de chaque côté). Le bras supérieur de chaque suture a ensuite été passé autour de l'hyoïde. Ces sutures de tension ont été sécurisées, en maintenant les hyoïdes et les cartilages thyroïdes en étroite proximité. Les extrémités rompues de la musculature de la ceinture ont été réapproximées, des drains de Penrose ont été placés et l'incision a été fermée en plusieurs couches.\n\nLe patient a eu une sonde de gastrostomie. Il a commencé à recevoir de l'héparine pour un thrombus carotidien et a continué une semaine de traitement intraveineux par Unasyn. Le premier changement de trachéotomie a été effectué le jour postopératoire (POD) 7 une fois que la résolution de l'œdème des voies respiratoires a été confirmée avec une laryngoscopie souple. Une étude de déglutition vidéo le jour postopératoire (POD) 14 a révélé une dysphagie oropharyngée modérée ou modérée qui a été minimisée avec des stratégies de déglutition. Il a été décannulé le jour postopératoire (POD) 17 et a été renvoyé le jour suivant.\n\nAu moment du suivi, le patient ne portait plus de collier cervical. Il tolérait une alimentation normale. Sa voix était légèrement enrouée, considérée comme un grade un pour la rugosité sur l'échelle GRBAS (grade, rugueux, respiratoire, asthénie, tension), mais il était capable de communiquer sans limitation. La laryngoscopie a démontré un larynx bien guéri avec des cordes vocales mobiles, un raccourcissement des plis aryépiglottiques gauches et un déplacement inférieur de l'épiglotte. La CTA du cou de suivi pour évaluer sa blessure carotidienne a démontré la résolution de l'air cervical avec une voie aérienne ouverte/intacte.\n",
+        "gold_summary": "Nous rapportons le cas d'un homme de 39 ans admis en unité de soins intensifs après une tentative de strangulation. Alerté et cliniquement stable, ses principaux symptômes étaient la douleur et des changements de voix. Son examen externe était remarquable seulement pour une marque de ligature cervicale et un emphysème sous-cutané à la palpation. L'imagerie par tomodensitométrie a révélé une rupture des muscles du col de l'hyoid et un déplacement de l'hyoid et de l'épiglotte vers le haut. Une laryngoscopie souple ultérieure par l'équipe d'Otorhinolaryngologie-Chirurgie de la Tête et du Cou (OTO-HNS) a révélé une avulsion de l'épiglotte du cartilage thyroïde et une rupture des plis aryépiglottiques/fausse corde muqueuse, entraînant une plaie ouverte dans les tissus mous du cou antérieur. La voie aérienne a été sécurisée en salle d'opération par intubation nasotrachéale fibreoptique. Une trachéotomie a été réalisée. L'exploration du cou a révélé une section des muscles du col antérieur et de la membrane thyro-hyoïde. La plaie a été réparée en couches par une thyro-hyoïdeopexie modifiée. Au mois suivant, le patient a été décanulé avec succès et tolérait une alimentation normale.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur a eu un gros accident au cou. Il avait mal et sa voix avait changé. \n\nLe docteur a vu une marque sur son cou et un gonflement sous la peau. \n\nDes images ont montré que des muscles et des parties du cou étaient cassés et déplacés. \n\nLe docteur a regardé dans sa gorge avec une petite caméra. Il a vu que des morceaux étaient cassés et ouverts. \n\nPour l’aider à bien respirer, le docteur a mis un petit tuyau dans son nez jusqu’à sa gorge. \n\nAprès, il a fait une petite ouverture dans son cou pour l’aider à respirer mieux. \n\nLe docteur a réparé les muscles et les parties cassées doucement. \n\nAprès un mois, le monsieur allait mieux. Il pouvait manger et parler presque normalement.",
+            "B2": "Cas d’un homme de 39 ans après une tentative de strangulation\n\nUn homme de 39 ans a été amené à l’hôpital après avoir essayé de se pendre. À son arrivée, il était conscient et stable, mais avait mal au cou et sa voix avait changé. En examinant son cou, les médecins ont vu une marque laissée par la corde et ont senti un gonflement sous la peau dû à de l’air qui s’était infiltré.\n\nDes examens d’imagerie ont montré que certains muscles autour d’un petit os du cou appelé l’os hyoïde étaient déchirés. Cet os et une partie appelée l’épiglotte, qui aide à protéger les voies respiratoires, avaient été déplacés vers le haut. Une caméra flexible a permis de voir que l’épiglotte s’était détachée d’un cartilage important du larynx, et que la muqueuse à l’intérieur du cou était déchirée, créant une blessure ouverte.\n\nPour protéger ses voies respiratoires, les médecins ont placé un tube dans sa trachée par le nez, sous contrôle visuel. Ensuite, ils ont fait une trachéotomie, c’est-à-dire une ouverture dans la trachée pour l’aider à respirer. Lors de l’opération, ils ont découvert que plusieurs muscles du cou et une membrane appelée membrane thyro-hyoïdienne étaient coupés. Ils ont réparé ces blessures en recousant les tissus en plusieurs couches et en fixant l’os hyoïde au cartilage pour stabiliser la zone.\n\nAprès un mois, le patient a pu retirer la trachéotomie et a repris une alimentation normale. Sa voix était légèrement enrouée, mais il pouvait parler normalement. Cette prise en charge rapide et précise a permis une bonne récupération malgré la gravité des blessures.",
+            "B3": "Résumé détaillé et structuré pour un public non spécialiste\n\nContexte  \nUn homme de 39 ans a été admis en soins intensifs après une tentative de pendaison. Il avait été retrouvé conscient, capable de répondre, mais toussant du sang. À l’examen, une marque de ligature était visible sur la partie avant du cou, accompagnée d’un emphysème sous-cutané (présence d’air sous la peau) qui masquait certains repères anatomiques. Il se plaignait d’une voix altérée sans difficulté respiratoire apparente.\n\nPrincipales observations  \nLes examens d’imagerie par tomodensitométrie (TDM) ont montré des lésions graves des artères carotides et vertébrales, ainsi qu’une fracture de la quatrième vertèbre cervicale. Un emphysème sous-cutané étendu et un pneumomédiastin (air dans la cavité médiastinale) étaient également présents. Les muscles situés sous l’os hyoïde (un petit os du cou) étaient rompus, provoquant un déplacement vers le haut de l’os hyoïde et de l’épiglotte (structure cartilagineuse qui protège les voies respiratoires pendant la déglutition). Une IRM a révélé une déchirure partielle du ligament nuchal, imposant une immobilisation stricte de la colonne cervicale.\n\nL’examen endoscopique des voies respiratoires par l’équipe ORL a montré que les cordes vocales bougeaient encore, mais avec un léger œdème. L’épiglotte était détachée du cartilage thyroïde, et la muqueuse des plis aryépiglottiques et des fausses cordes vocales était déchirée, créant une plaie ouverte dans les tissus mous du cou.\n\nIntervention et prise en charge  \nPour sécuriser les voies respiratoires, une intubation nasotrachéale sous contrôle visuel a été réalisée en salle d’opération. Le lendemain, une trachéotomie (ouverture chirurgicale dans la trachée) a été effectuée, accompagnée d’une exploration approfondie du cou. Cette intervention a confirmé la rupture des muscles sterno-hyoïdien, thyro-hyoïdien et omo-hyoïdien, ainsi que la destruction complète de la membrane thyro-hyoïdienne et de la muqueuse des fausses cordes et plis aryépiglottiques. L’épiglotte était déviée vers le haut en raison de la perte de soutien musculaire.\n\nLa réparation chirurgicale a consisté en une suture minutieuse des tissus muqueux et musculaires, associée à une thyro-hyoïdeopexie modifiée (technique visant à rapprocher et stabiliser l’os hyoïde et le cartilage thyroïde) et une épiglotopexie (fixation de l’épiglotte). Cette intervention a permis de restaurer l’intégrité des structures laryngées tout en maintenant la colonne cervicale en position neutre, indispensable à cause des lésions vertébrales.\n\nSuivi et évolution  \nLe patient a reçu un traitement anticoagulant pour prévenir les complications liées aux thromboses artérielles, ainsi qu’une antibiothérapie intraveineuse. Une sonde de gastrostomie a été posée pour assurer la nutrition. La première révision de la trachéotomie a eu lieu au septième jour postopératoire, après confirmation de la réduction de l’œdème. Une évaluation de la déglutition a montré une dysphagie modérée, qui a été améliorée par des exercices et stratégies spécifiques. Le patient a été décanulé au dix-septième jour et a pu reprendre une alimentation normale.\n\nAu suivi, il ne portait plus de collier cervical, sa voix était légèrement enrouée mais fonctionnelle, et l’examen endoscopique montrait un larynx bien cicatrisé avec des cordes vocales mobiles. L’imagerie de contrôle a confirmé la résolution de l’air sous-cutané et la conservation d’une voie aérienne ouverte.\n\nConclusion  \nCe cas illustre la complexité des lésions cervicales après une tentative de pendaison, impliquant à la fois des atteintes vasculaires, osseuses, musculaires et muqueuses. La prise en charge multidisciplinaire, combinant imagerie avancée, intervention chirurgicale précise et suivi fonctionnel, a permis une récupération satisfaisante des fonctions respiratoires et vocales du patient."
+        }
+    },
+    {
+        "article": "Le patient était un garçon de 16 ans qui a été référé à notre hôpital en juillet 2022 en raison d'une insuffisance cardiaque sévère.\n\nÀ l'âge de 13 ans, il a été diagnostiqué d'une dystrophie musculaire de Becker portant la mutation causale dans le gène DMD (chrX:32841413-32862977, mutation hétérozygote) et le gène DSC2 (chr18:28659938, mutation hétérozygote). Il avait des antécédents de dyspnée légère et de détresse thoracique à l'effort et a reçu un traitement pour une dysfonction cardiaque ; cependant, la fonction cardiaque s'est détériorée et il a été référé à notre hôpital pour la première fois. L'examen physique lors de sa première consultation a révélé une taille de 173 cm, un poids de 78 kg, une tension artérielle de 110/90 mmHg, une fréquence cardiaque de 76 battements/minute, une fréquence respiratoire de 20 battements/minute, une température corporelle de 36,5 °C et une SpO2 de 100 % en air ambiant. Il n'y avait pas de dilatation de la veine jugulaire au niveau du cou. Ses sons d'auscultation cardiaque et pulmonaire étaient normaux. Son abdomen était plat. Il y avait un léger oedème au niveau du pied et de la cheville. Le patient ne présentait pas de lésions des omoplates ou de lordose. Une pseudo-hypertrophie des muscles gastrocnémiens bilatéraux a été observée. Le signe de Gower était négatif. Les tests de laboratoire ont montré que le taux de prohormone N-terminal du peptide natriurétique cérébral (NT-proBNP) était de 471,55 pg/ml, l'hémoglobine myocardique était de 272,61 ng/ml, la créatine kinase (CK) était de 5 493 U/L, la créatine kinase-MB (CK-MB) était de 115 U/L, la créatine kinase-MM (CK-MM) était de 5 378U/L. L'alanine aminotransférase (ALT) était de 138 U/L, l'aspartate aminotransférase (AST) était de 92 U/L, la lactate déshydrogénase (LDH) était de 393U/L. L'échocardiographie transthoracique a montré une fraction d'éjection ventriculaire gauche de 19 %, une dilatation de l'oreillette gauche, du ventricule gauche et de l'oreillette droite, une insuffisance mitrale modérée, une insuffisance ventriculaire systolique sévère, une diminution de la fonction diastolique du cœur entier. L'IRM des jambes a révélé des changements de dystrophie musculaire dans les cuisses bilatérales. Les traitements médicamenteux ont été commencés, y compris le sacubitril-valsartan, le carvedilol, l'ivabradine, le tolvaptan, la trimétazidine et ajustés en fonction des directives de traitement de l'insuffisance cardiaque dans les 3 prochaines années de suivi. La valeur de la LVEF lors de l'écho-cardiographie transthoracique a fluctué à 30-35 %.\n\nLe premier jour de cette consultation, le patient a présenté une détérioration de la douleur thoracique, des palpitations et un essoufflement au repos indiquant une insuffisance cardiaque progressive. Il a été envoyé à notre hôpital à 21 heures. À l'examen physique, tension artérielle de 106/63 mmHg, fréquence cardiaque de 120 battements/minute irréguliers, fréquence respiratoire de 20 battements/minute, température corporelle de 37℃ et SpO2 de 97 % en air ambiant. Un examen thoracique a révélé des crépitations humides dans les deux poumons. Ses bruits cardiaques étaient intacts mais irréguliers, et aucun murmure cardiaque n'a été observé. Sa force musculaire était de 5/5. Les tests de laboratoire ont montré les résultats suivants : numération des globules blancs, 10,56 × 109/L avec neutrophiles 60,5 % ; hémoglobine, 144 g/L ; numération plaquettaire, 177 × 109/L. La fonction de coagulation était légèrement anormale, comme suit : temps de prothrombine (PT), 14,8 s ; temps de thromboplastine partielle activée (APTT), 27,1 s ; D-Dimer, 0,27 mg/L. L'examen biochimique a montré une teneur en potassium de 3,9 mmol/L, une créatinine de 67µmol/L. Son taux total de bilirubine était normal, mais ses taux d'enzymes hépatiques étaient légèrement élevés, comme suit : ALT, 109 U/L ; AST, 87 U/L ; LDH, 376U/L. NT-proBNP était nettement élevé à 9 171pg/ml. Le niveau de cTnT était de 0,107 ng/ml. Les niveaux d'électrolytes étaient normaux. L'électrocardiogramme a montré une fibrillation auriculaire avec une fréquence ventriculaire rapide et un bloc cardiaque intra-ventriculaire.\n\nÀ 22 heures le premier jour, la détresse thoracique s'aggravait. 150 mg d'amiodaron par injection intraveineuse ont échoué à la cardioversion. La fréquence ventriculaire était de 120 bpm. Puis, 450 mg d'amiodaron ont été utilisés pour le contrôle de la fréquence et du rythme par goutte à goutte intraveineuse continue (6ug/Kg/min). Au même moment, nous avons fourni une perfusion continue de peptide natriurétique cérébral humain recombinant pour améliorer la fonction cardiaque clinique. Le moniteur ECG a montré une fibrillation auriculaire avec une fréquence ventriculaire de 90 bpm.\n\nÀ 13 heures le deuxième jour, la patiente est devenue pâle, a commencé à transpirer et a eu une orthopnée. La tension artérielle de la patiente a chuté à 75/50 mmHg, la fréquence cardiaque était de 74 bpm. L'amiodarone et la natriurèse cérébrale humaine recombinante ont donc été arrêtés et une perfusion intraveineuse de dopamine et de dobutamine a été administrée. Tous les médicaments oraux ont été arrêtés au même moment. L'ECG a montré un rythme sinusal normal de 84 bpm et un bloc auriculo-ventriculaire de deuxième degré. L'échocardiographie d'urgence au chevet de la patiente a montré une dilatation du cœur entier avec une fonction systolique réduite du ventricule gauche et droit (FEVG 25%), une hypertension artérielle pulmonaire modérée, un épanchement péricardique infime. L'examen physique a montré une tension artérielle de 89/60 mmHg, une fréquence cardiaque de 74 bpm régulièrement et une SpO2 de 99 % sous 3 L/minute d'oxygène. Des taches de peau étaient visibles sur les deux membres inférieurs. Le volume d'urine le deuxième jour était de 1000 ml.\n\nLe troisième jour, l'échographie abdominale a révélé des calculs biliaires et une cholécystite. Le meropénem (0,5 g q12h ivgtt) a été utilisé empiriquement pour contrôler l'infection. Le volume d'urine a diminué à 400 ml.\n\nLe 4e jour, le patient s'est plaint d'un soulagement de la gêne thoracique. Les tests de laboratoire ont montré les résultats suivants : ALT, 7 391 U/L ; AST, 5 671 U/L ; LDH, 8 089U/L ; CK, 2 875pg/ml, CK-MM, 28 522U/L ; CK-MB, 229U/L ; azote uréique, 29.8mmol/L ; acide urique, 859µmol/L ; créatinine, 305 µmol/L ; eGRF, < 30 ml/min/1.73m2 ; plaquette,104 × 109/L ; PTs, 29.3 s ; APTT, 29.9 s ; Fibrinogen, 163 mg/dl ; D-Dimer > 40 mg/L. Il a été envoyé en ICU pour un traitement supplémentaire.\n\nNous avons fourni un traitement de remplacement rénal continu au chevet du patient. Des administrations d'isoglycyrrhizate, de glutathion réduit et de phosphatidylcholine polyénique ont été administrées pour protéger la fonction hépatique. De la dopamine et de la dobutamine (1,3ug/kg/min) ont été administrées pour maintenir la tension artérielle et renforcer la contraction cardiaque. Des examens de laboratoire ont été effectués pour surveiller les paramètres associés du patient. Fonction de coagulation : le PT était de 22 s. Le D-dimère était supérieur à 40 mg/L. Les fonctions hépatiques étaient comme suit : taux total de bilirubine de 75,5 µmol/L, ALT de 5 060 U/L, AST de 1 952 U/L, LDH de 8 089U/L. Fonction rénale : azote uréique sanguin de 23,8 mmol/L, acide urique de 604 µmol/L, créatinine de 322 µmol/L, et eGRF de 23 ml/min/1,73m2. NT-proBNP était de 5701 pg/ml, CK était de 11476U/L, CK-MM de 11308U/L, CK-MB de 168U/L. L'ECG a montré un rythme sinusal normal de 62 bpm, un bloc cardiaque intra-ventriculaire, une hypertrophie de l'oreillette gauche et une déviation de l'axe gauche.\n\nÀ 22 heures, le 5e jour, la dopamine a été arrêtée. La tension artérielle a fluctué entre 90 et 112/50 et 70 mmHg. Nous avons administré du sacubitril-valsartan oral à 25 mg bid et de la trimétazidine orale à 35 mg bid le 10 juillet. L'ivabradine (5 mg bid p.o.) et le tolvaptan (10 mg qd p.o.) ont été administrés le 10e jour en raison d'une hémodynamique stable, d'une amélioration de la fonction rénale et d'une augmentation du volume quotidien d'urine. La dobutamine a été arrêtée le 11e jour. L'héparine de faible poids moléculaire a été démarrée le 12e jour.\n\nLe 15e jour, un réexamen des examens de laboratoire a suggéré une amélioration significative de la fonction hépatique. L'alanine aminotransférase était tombée à 255 U/L, l'aspartate aminotransférase à 35U/L. La quantité quotidienne de transfusion était de 2 106 ml avec une production quotidienne d'urine de 1 125 ml. Par conséquent, la polyen phosphatidylcholine a été arrêtée. Les cathéters d'hémodialyse ont été enlevés.",
+        "gold_summary": "Nous présentons le cas d’un garçon de 16 ans admis pour insuffisance cardiaque et fibrillation auriculaire. Il a été diagnostiqué comme souffrant d’une dystrophie musculaire de Becker et les tests génétiques ont révélé des mutations concomitantes dans les gènes DMD, ABCB4 et DSC2. L’amiodarone a été prescrit pour contrôler la fibrillation auriculaire paroxystique par voie intraveineuse. Cependant, les taux d’enzymes hépatiques étaient fortement élevés, ainsi que le choc cardiaque, l’insuffisance rénale et les troubles de la coagulation. Après une thérapie de remplacement rénal continue au chevet du patient, la fonction hépatique et l’état clinique du patient se sont rétablis.\n",
+        "synthetic_summary": {
+            "B1": "Il y a un garçon de 16 ans qui avait un cœur très fatigué. Son cœur battait très vite et pas bien. \n\nIl avait aussi un problème avec ses muscles. Des docteurs ont donné un médicament pour aider son cœur. Mais ce médicament a rendu son foie malade. \n\nLe garçon est devenu très fatigué et son corps ne marchait plus bien. Les docteurs ont aidé son corps avec une machine spéciale pour nettoyer son sang. \n\nPetit à petit, il a commencé à aller mieux. Son foie et son cœur ont retrouvé un peu de force. Les docteurs continuent de bien s’occuper de lui.",
+            "B2": "Cas d’un garçon de 16 ans avec une maladie musculaire et des problèmes de cœur\n\nCe garçon de 16 ans souffrait d’une maladie appelée dystrophie musculaire de Becker. Cette maladie affecte les muscles et est causée par des changements dans certains gènes, notamment le gène DMD. Il avait aussi des mutations dans d’autres gènes liés au cœur. Depuis ses 13 ans, il avait des difficultés à respirer et des douleurs dans la poitrine quand il faisait des efforts.\n\nCe qu’ils ont découvert à l’hôpital\n\nLorsqu’il est arrivé à l’hôpital, son cœur ne fonctionnait plus bien. Il avait une insuffisance cardiaque sévère, ce qui signifie que son cœur ne pompait pas assez de sang. Il avait aussi une fibrillation auriculaire, un problème où le cœur bat de façon irrégulière et rapide. Les médecins ont essayé de contrôler ce rythme avec un médicament appelé amiodarone, donné par perfusion.\n\nLes complications graves\n\nMalheureusement, son état s’est aggravé : ses enzymes du foie étaient très élevées, ce qui montre que son foie était en souffrance. En plus, il a eu un choc cardiaque (son cœur ne pompait plus assez de sang pour le corps), une insuffisance rénale (ses reins ne fonctionnaient plus bien) et des problèmes de coagulation du sang, ce qui peut causer des saignements ou des caillots.\n\nLe traitement et l’évolution\n\nPour l’aider, les médecins ont utilisé une thérapie appelée remplacement rénal continu. C’est une machine qui fait le travail des reins quand ils ne fonctionnent plus. Ils ont aussi donné des médicaments pour protéger son foie et soutenir son cœur. Peu à peu, grâce à ces soins, la fonction de son foie s’est améliorée et son état général s’est stabilisé.\n\nEn résumé\n\nCe cas montre qu’une maladie musculaire peut aussi causer de graves problèmes au cœur et aux autres organes. Un suivi médical attentif et des traitements adaptés sont essentiels pour aider ces patients à se rétablir.",
+            "B3": "Résumé détaillé et structuré pour un public non-médecin éduqué\n\n**Contexte**  \nNous rapportons le cas d’un garçon de 16 ans atteint d’une dystrophie musculaire de Becker, une maladie génétique affectant les muscles, diagnostiquée à l’âge de 13 ans. Cette maladie est liée à une mutation dans le gène DMD, responsable de la production de la dystrophine, une protéine essentielle au fonctionnement musculaire. Le patient présentait également une mutation dans le gène DSC2, impliqué dans la structure du muscle cardiaque. Il avait des antécédents de difficultés respiratoires légères à l’effort et une détérioration progressive de la fonction cardiaque, conduisant à une insuffisance cardiaque sévère.\n\n**Principales observations cliniques**  \nLors de son admission en juillet 2022, le patient souffrait d’une insuffisance cardiaque avancée avec une fraction d’éjection du ventricule gauche très basse (19 %), indiquant une capacité réduite du cœur à pomper le sang. Il présentait une fibrillation auriculaire, un trouble du rythme cardiaque caractérisé par des battements irréguliers et rapides, provoquant des palpitations, une douleur thoracique et un essoufflement même au repos. L’échocardiographie montrait une dilatation des différentes cavités cardiaques et une insuffisance mitrale modérée. Les analyses sanguines révélaient une élévation marquée des marqueurs cardiaques et musculaires (créatine kinase, NT-proBNP), témoignant d’une souffrance musculaire et cardiaque importante.\n\nAu cours de l’hospitalisation, le patient a développé une aggravation rapide de son état, avec une douleur thoracique plus intense, une hypotension (baisse de la tension artérielle), une insuffisance rénale aiguë (diminution de la fonction des reins) et des troubles de la coagulation sanguine. Les enzymes hépatiques (ALT, AST, LDH) étaient fortement élevées, indiquant une atteinte hépatique sévère. L’électrocardiogramme a confirmé la fibrillation auriculaire avec une fréquence ventriculaire rapide et un bloc cardiaque intra-ventriculaire.\n\n**Interprétation clinique**  \nLe traitement initial par amiodarone, un médicament antiarythmique administré par voie intraveineuse pour contrôler la fibrillation auriculaire, n’a pas permis de restaurer un rythme cardiaque normal. L’état hémodynamique du patient s’est détérioré, nécessitant l’arrêt de ce traitement et la mise en place d’une assistance médicamenteuse par dopamine et dobutamine pour soutenir la fonction cardiaque et la pression artérielle. Une thérapie de remplacement rénal continu a été instaurée en raison de l’insuffisance rénale aiguë. Parallèlement, un traitement antibiotique a été administré pour une cholécystite (inflammation de la vésicule biliaire) détectée lors d’une échographie abdominale.\n\nMalgré la gravité initiale, la prise en charge intensive a permis une amélioration progressive de la fonction hépatique, rénale et cardiaque. Les médicaments ont été ajustés pour stabiliser la fonction cardiaque, incluant des traitements oraux comme le sacubitril-valsartan, la trimétazidine, l’ivabradine et le tolvaptan. La coagulation sanguine a été surveillée et traitée avec de l’héparine de faible poids moléculaire pour prévenir les complications thromboemboliques.\n\n**Prochaines étapes et suivi**  \nAprès plusieurs jours en unité de soins intensifs, le patient a montré une amélioration clinique significative avec une réduction des enzymes hépatiques et une meilleure fonction rénale. Le volume urinaire a augmenté, témoignant d’une récupération rénale. Les cathéters d’hémodialyse ont été retirés, et les traitements ont été adaptés pour maintenir la stabilité hémodynamique et cardiaque. Un suivi régulier est nécessaire pour surveiller l’évolution de la dystrophie musculaire, la fonction cardiaque et les complications associées, afin d’ajuster les traitements et prévenir de nouvelles dégradations.\n\n**Conclusion**  \nCe cas illustre la complexité de la prise en charge d’un adolescent atteint de dystrophie musculaire de Becker avec insuffisance cardiaque sévère et complications multiples, notamment une fibrillation auriculaire résistante au traitement initial, une atteinte hépatique et rénale aiguë. La mise en œuvre rapide d’une thérapie de remplacement rénal continue et l’adaptation des traitements médicamenteux ont permis une amélioration notable de son état clinique."
+        }
+    },
+    {
+        "article": "Informations du patient: il s´agit de Mr RL, âgé de 27 ans, soudeur de profession, célibataire, de bas niveau socioéconomique et sans antécédent pathologique particulier.\n\nRésultats cliniques: le patient était confus (Glasgow Coma Scale (GCS) 13/15-ème), agité pupilles en mydriase, avait des tremblements avec tachypnée et tachycardie, une hyperréfléxie associée à des myoclonies spontanées plus marquées au niveau des membres inférieurs avec une hypersudation et des frissons.\n\nChronologie: l´histoire de maladie remonte à une semaine avant sa consultation chez un médecin neurologue en secteur libéral, par l´installation des propos de persécution, des propos de négation de filiation, une bizarrerie de comportement et des attitudes hallucinatoires puis le tableau s´est compliqué par une agitation psychomotrice et un diagnostic initial d´un accès psychotique aigu a été retenu, et le patient a été mis sous halopéridone 5 mg par jour.\n\nDeux mois après, l´évolution a été marquée par une mauvaise observance thérapeutique avec persistance de la symptomatologie psychotique associée à des symptômes négatifs tel que la perte de plaisir, l´isolement et l´abolition avec un sommeil perturbé, motivant le malade à refaire une consultation chez le même médecin traitant qui lui a ajouté de la paroxétine 20 mg par jour et l´amitriptyline 25 mg par jour.\n\nQuelques heures (6 à 8h) après la prise des deux antidépresseurs, le malade présentait une perte de conscience et agitation psychomotrice motivant son hospitalisation aux unités des soins intensifs.\n\nDémarche diagnostique: le malade a bénéficié d´un bilan biologique complet, objectivant une perturbation des électrolytes avec une acidose métabolique et un taux de créatine phosphokinase (CPK) à 100 UL/L, l'examen cytobactériologique des urines (ECBU), l'étude du liquide céphalorachidien et les hémocultures se sont avérés négatifs. La concentration plasmatique de la C-reactive protein (CRP) et la numération formule sanguine étaient normales.\n\nL´électrocardiogramme (ECG) a objectivé une arythmie cardiaque par fibrillation auriculaire, et la radiographie thoracique et l'imagerie par résonance magnétique (IRM) cérébrale étaient sans particularités. Le diagnostic de syndrome sérotoninergique a été retenu après avoir éliminé une étiologie infectieuse, métabolique ou neurologique.\n\nIntervention thérapeutique: le patient a été mis sous ventilation mécanique, gavage 500cc/8H, réhydratation par eau plate 500cc/8H, ration de base SG 5% + 2g Nacl + 2g Kcl +1g ca 2+ / 8h , et SS 0,9% 500cc/4H, sédation par midazolam 8mg/H, IPP 40mg /j, avec un anticoagulant à visée préventive et insuline selon dextro.\n\nSuivi et résultats: l´état clinique hémodynamique et neurologique du patient s´est stabilisé après 24h, ensuite il a été transféré au service de psychiatrie où le médecin traitant a trouvé un patient calme sur le plan moteur, bien orienté dans le temps et l´espace, ayant eu un délire mystico religieux et de persécution, certaines réponses déplacées, un jugement perturbé sans présence d´un syndrome dépressif ni maniaque ou confusionnel. L´évolution de la symptomatologie psychiatrique a été marquée par une bonne amélioration avec un bon retour à l´état pré morbide, stabilisée sous neuroleptique atypique type olanzapine avec une posologie initiale de 5 mg par jour.",
+        "gold_summary": "Nous rapportons le cas clinique d´un patient qui a présenté un état de confusion avec une agitation psychomotrice et une hyperréfléxie et des myoclonies spontanées suite à la prise simultanée de la paroxétine et l´amitriptyline. Le diagnostic de syndrome sérotoninergique a été retenu après avoir éliminé les autres éventuels diagnostics, nécessitant une hospitalisation en unité de soins intensifs.",
+        "synthetic_summary": {
+            "B1": "Un monsieur a pris deux médicaments en même temps. Après, il est devenu très confus et agité. Son corps bougeait tout seul et vite. Les docteurs ont trouvé que c’était à cause des médicaments. Ils l’ont aidé à l’hôpital pour qu’il aille mieux. Maintenant, il va mieux grâce aux soins.",
+            "B2": "Cas d’un jeune homme de 27 ans avec un problème sérieux après la prise de deux médicaments.\n\nCe qu’ils ont observé : Ce patient, qui travaille comme soudeur, est devenu confus et très agité. Il avait aussi des réflexes très vifs et des secousses musculaires involontaires, surtout dans les jambes. Ces symptômes sont apparus quelques heures après avoir commencé à prendre deux antidépresseurs en même temps : la paroxétine et l’amitriptyline.\n\nCe que cela signifie : Les médecins ont cherché à comprendre ce qui causait ces signes. Ils ont fait plusieurs examens pour éliminer des infections, des problèmes du cœur ou du cerveau. Finalement, ils ont conclu que le patient souffrait d’un syndrome sérotoninergique. C’est une réaction grave qui peut arriver quand il y a trop de sérotonine, une substance chimique du cerveau, à cause de certains médicaments.\n\nComment ils ont aidé le patient : Il a été hospitalisé en soins intensifs pour recevoir un traitement adapté, comme une assistance respiratoire et des médicaments pour calmer son corps. Après 24 heures, son état s’est amélioré. Puis, il a été transféré en psychiatrie où il a reçu un autre médicament pour stabiliser son état mental. Progressivement, il est revenu à son état normal.\n\nEn résumé, ce cas montre qu’il faut faire très attention quand on combine certains médicaments, car cela peut provoquer des réactions graves comme le syndrome sérotoninergique.",
+            "B3": "Résumé détaillé et structuré pour un public non médical éduqué\n\nContexte  \nNous présentons le cas de Monsieur RL, un homme de 27 ans, soudeur de profession, sans antécédents médicaux connus. Il a initialement consulté pour des troubles psychiatriques débutant par des idées de persécution, des hallucinations et des comportements inhabituels, conduisant à un diagnostic d’accès psychotique aigu. Son traitement initial comprenait un neuroleptique, l’halopéridone.\n\nPrincipales observations  \nAprès deux mois, malgré un traitement ajusté par l’ajout de deux antidépresseurs, la paroxétine et l’amitriptyline, le patient a rapidement développé une perte de conscience et une agitation importante, nécessitant une hospitalisation en soins intensifs. À son admission, il présentait une confusion, une agitation psychomotrice, des pupilles dilatées, des tremblements, une respiration rapide (tachypnée), un rythme cardiaque accéléré (tachycardie), des réflexes exagérés (hyperréflexie), ainsi que des contractions musculaires involontaires (myoclonies), surtout au niveau des jambes, accompagnées de sueurs abondantes et de frissons.\n\nInterprétation clinique  \nUn bilan complet a été réalisé : les analyses sanguines ont montré un déséquilibre des électrolytes et une acidose métabolique (un excès d’acidité dans le sang), mais aucune infection ni inflammation n’a été détectée. L’électrocardiogramme a révélé une fibrillation auriculaire (un trouble du rythme cardiaque), tandis que l’imagerie cérébrale était normale. Après avoir exclu les causes infectieuses, métaboliques et neurologiques, le diagnostic retenu était un syndrome sérotoninergique. Ce syndrome est une réaction grave liée à un excès de sérotonine dans le système nerveux, souvent provoquée par la prise simultanée de plusieurs médicaments augmentant la sérotonine, comme ici la paroxétine et l’amitriptyline.\n\nProchaines étapes et évolution  \nLe patient a été pris en charge en unité de soins intensifs avec une ventilation mécanique, une hydratation adaptée et une sédation pour contrôler son agitation. Après stabilisation de son état neurologique et hémodynamique, il a été transféré en psychiatrie. Là, il était calme, bien orienté, avec des troubles psychiatriques résiduels mais sans dépression ni confusion. Sous traitement par olanzapine, un neuroleptique atypique, son état psychiatrique s’est nettement amélioré, avec un retour progressif à son état antérieur.\n\nEn résumé, ce cas illustre l’importance de reconnaître rapidement le syndrome sérotoninergique, une complication potentiellement grave liée à l’association de certains antidépresseurs, afin d’adapter la prise en charge et d’éviter des conséquences sévères."
+        }
+    },
+    {
+        "article": "Un patient de 26 ans a été admis à notre hôpital avec des antécédents de jaunisse récurrente de la peau et des urines depuis plus d'un an. Le 1er juin 2022, le patient a présenté une jaunisse et des urines jaunes, sans déclencheur évident. Un examen échographique a révélé la présence de plusieurs calculs dans les voies biliaires communes et intrahépatiques, avec une légère dilatation des voies biliaires intrahépatiques (diamètre : 0,32 cm, référence : ≤ 0,2 cm) et des voies biliaires communes (diamètre : 1,04 cm, référence : 0,6-0,8 cm). Ces résultats ont confirmé l'impression initiale de jaunisse obstructive. Le 15 juin 2022, le patient a subi une cholédocholithotomie laparoscopique, une cholécystectomie et une lithotomie cholédoque. Cependant, il n'y a eu aucune amélioration de la fonction hépatique ni des symptômes de jaunisse après la chirurgie au cours de l'année écoulée. Afin de rechercher une assistance médicale supplémentaire, le patient a été admis à notre hôpital avec un ictère d'origine inconnue le 12 août 2023. Le patient a nié une histoire de tabagisme, d'abus d'alcool et d'utilisation à long terme de médicaments nocifs pour le foie, y compris des suppléments à base de plantes et des compléments alimentaires.\n\nL’examen physique a révélé la présence d’un jaunissement généralisé de la peau et de la sclère, ainsi qu’une rate palpable de 2 doigts sous la cage thoracique. En outre, l’indice de masse corporelle du sujet a été enregistré à 17,4 kg/m².\n\nLes résultats des examens de laboratoire vitaux ont été présentés dans le tableau 1. En outre, les anticorps antinucléaires (ANA) 1:100, les anticorps antineutrophiles cytoplasmiques (p-ANCA) positifs, le profil d'anticorps des maladies auto-immunes du foie étaient tous négatifs ; l'hépatite A à E, le virus d'Epstein-Barr, le cytomégalovirus, le virus Coxsackie, le virus de l'herpès zoster, le treponema pallidum et le virus de l'immunodéficience humaine étaient tous négatifs.\n\nLa cholangiopancréatographie par résonance magnétique (MRCP) a révélé l’existence d’un canal biliaire intrahépatique gauche et d’un canal biliaire commun dilatés, en l’absence de vésicule biliaire, d’une splénomégalie et de nombreux ganglions lymphatiques élargis dans la région hilaire. L’examen histologique du foie a révélé que la structure des lobules hépatiques et du réseau capillaire des voies biliaires n’était pas clairement discernable. Certains capillaires biliaires présentaient une dilatation, accompagnée de la formation d’un thrombus biliaire. Il existait également une fibrose de pontage des voies porteuses vers la veine centrale. La disparition des voies biliaires a été observée dans 10 des 12 voies porteuses. Ce phénomène est le plus souvent attribué au syndrome de la voie biliaire effacée (VBDS). Le score simplifié de Scheuer indiquait un grade 2 et un stade 3 à 4. Le séquençage de l’exome entier a révélé la présence d’une mutation hétérozygote dans PKLR (NM_000298.5:c.119G > A) et UGT1A1 (NM_000463.2:c.3275T > G).\n\nÀ la lumière des preuves susmentionnées, un diagnostic révisé a été rendu comme étant un VBDS avec PLKR et UGT1A1 mutation, cirrhose cholestatique. Une dose de 1000 mg/j d’acide ursodexycholique (UDCA) et 8 mg/j de méthylprednisolone a été administrée afin d’améliorer la cholestase et l’inflammation hépatique.\n\nAu fil du temps, une imagerie par résonance magnétique (IRM) à contraste amélioré, réalisée le 10 septembre 2023, a révélé la présence de calculs dans le canal biliaire commun, malgré l'absence de fièvre, de douleurs abdominales ou d'autres symptômes. La patiente a refusé de faire retirer les calculs du canal biliaire commun. Le 25 octobre 2023, un examen MRCP a révélé des changements dynamiques. Le système biliaire a présenté une sténose en bandes et un aspect d'arbre élagué, ce qui était cohérent avec l'aspect de la cholangite sclérosante observé par imagerie. Une nouvelle coloscopie a été réalisée avec une préparation intestinale adéquate, en respectant les directives pour les patients présentant des lésions muqueuses présumées, qui a révélé la présence d'une UC impliquant l'iléon terminal et le hémicolon droit. Ce résultat était cohérent avec les manifestations coloscopiques de la PSC-UC. En outre, la PSC-UC est un sous-type unique de UC, ce qui rend difficile l'application des critères de classification de Montréal pour décrire la topographie de la maladie. Par conséquent, le diagnostic a été révisé à PSC-UC avec des mutations PLKR et UGT1A1, cholédocholithiase.\n\nLe 25 novembre 2023, une cholangiopancréatographie rétrograde transduodénoscopique (ERCP) et une sphinctérotomie endoscopique (EST) ont été réalisées. Une pierre noire irrégulière de 4 mm × 5 mm et un grand nombre de pierres sédimentaires ont été enlevées avec succès en utilisant une dilatation papillaire duodénale endoscopique (EPBD). Après la résolution de l’obstruction, un régime à long terme de 1000 mg/d UDCA en association avec 10 mg/d d’acide obéticholique (OCA) a été prescrit pour améliorer la cholestase. En outre, 8 g/d de colestyramine a été prescrit pour faciliter l’adsorption des acides biliaires en excès, tandis que 1,2 g/d de rifaximine a été administré pour prévenir une infection des voies biliaires. En outre, étant donné que la UC du patient était limitée à l’iléon terminal et au droit hémicolon, il y avait peu de selles mucopurulentes et sanglantes, ainsi que de diarrhée. Les comprimés de mésalazine (2 g par jour) ont été administrés dans le but d’améliorer l’inflammation du côlon. Le 30 juillet 2024, la fonction hépatique du patient était la suivante : TB/DB 33/25,9 μmol/L, phosphatase alcaline (ALP)/GGT 183/112 U/L, IgG 17,19 g/L. L’état du patient est resté stable.\n",
+        "gold_summary": "Inquiétudes du patient : Un patient de sexe masculin âgé de 26 ans se plaint d'une histoire de peau et d'urine jaunes récurrentes depuis plus d'un an.\n\nDiagnostics : Après imagerie par cholangiopancréatographie par résonance magnétique dynamique, manifestation coloscopique, biopsie du foie et séquençage de l'exome entier, le patient a finalement été diagnostiqué avec une CSP - colite ulcéreuse avec mutation PLKR et UGT1A1.\n\nInterventions : Après résolution de l'obstruction, un régime à long terme de 1000 mg/j d'acide ursodexycholique en association avec 10 mg/j d'acide obéticholique pour améliorer la cholestase, 8 g/j de cholestyramine pour faciliter l'adsorption des acides biliaires en excès et 1,2 g/j de rifaximine pour prévenir l'infection des voies biliaires ont été prescrits.\n\nRésultats : Les paramètres biochimiques du foie du patient se sont considérablement améliorés. Son état est stable et il n'a pas subi de transplantation de foie à ce jour.\n",
+        "synthetic_summary": {
+            "B1": "Il y a un monsieur qui avait la peau et la pipi jaunes depuis longtemps. \n\nLes docteurs ont fait beaucoup de tests pour comprendre pourquoi. Ils ont trouvé que son foie ne marchait pas bien à cause de petits problèmes dedans.\n\nIls lui ont donné des médicaments pour aider son foie à mieux travailler et pour éviter les infections. \n\nMaintenant, il va mieux et il est en bonne santé. Les docteurs continuent de bien s’occuper de lui.",
+            "B2": "Histoire du patient  \nUn jeune homme de 26 ans a eu plusieurs épisodes de jaunisse, c’est-à-dire un jaunissement de la peau et des urines, pendant plus d’un an. Cela l’a beaucoup inquiété car les symptômes revenaient sans raison claire.\n\nCe qu’ils ont découvert  \nDes examens d’imagerie ont montré que ses voies biliaires, qui transportent la bile dans le foie, étaient dilatées et contenaient des calculs (petits cailloux). Une biopsie du foie, qui consiste à prélever un petit morceau de tissu pour l’analyser, a révélé une maladie appelée syndrome de la voie biliaire effacée (VBDS). Ce syndrome signifie que certaines petites voies biliaires ont disparu, ce qui cause des problèmes pour évacuer la bile. De plus, des analyses génétiques ont trouvé des mutations dans deux gènes, PKLR et UGT1A1, qui peuvent affecter le fonctionnement du foie. Une coloscopie, un examen du gros intestin, a montré une colite ulcéreuse (UC), une inflammation chronique du côlon, associée à une maladie appelée cholangite sclérosante primitive (PSC), qui touche aussi les voies biliaires.\n\nTraitements donnés  \nAprès avoir enlevé les calculs dans les voies biliaires grâce à une intervention endoscopique, le patient a reçu plusieurs médicaments :  \n- L’acide ursodésoxycholique (UDCA) et l’acide obéticholique (OCA) pour aider à réduire l’accumulation de bile dans le foie (cholestase).  \n- La cholestyramine pour absorber les acides biliaires en excès et éviter qu’ils ne causent des problèmes.  \n- La rifaximine pour prévenir les infections des voies biliaires.  \n- La mésalazine pour calmer l’inflammation du côlon liée à la colite ulcéreuse.\n\nÉvolution et état actuel  \nGrâce à ces traitements, les analyses du foie se sont nettement améliorées. Le patient est stable, sans aggravation de la maladie, et n’a pas eu besoin de greffe du foie jusqu’à présent. Ce suivi montre l’importance d’un diagnostic précis et d’un traitement adapté pour gérer des maladies complexes du foie et du système digestif.",
+            "B3": "Résumé détaillé et structuré pour un public adulte non spécialiste\n\nContexte  \nUn homme de 26 ans a consulté pour des épisodes récurrents de jaunisse (coloration jaune de la peau et des urines) depuis plus d’un an. Initialement, des calculs biliaires ont été détectés et retirés chirurgicalement, mais les symptômes et la fonction hépatique ne se sont pas améliorés. Le patient ne présentait pas d’antécédents de tabagisme, d’alcoolisme ou de prise prolongée de médicaments hépatotoxiques.\n\nPrincipales observations  \nÀ l’examen clinique, le patient présentait un ictère généralisé et une rate légèrement augmentée de volume. Son indice de masse corporelle était faible (17,4 kg/m²). Les analyses sanguines excluaient les hépatites virales, les infections virales courantes et les maladies auto-immunes du foie. L’imagerie par résonance magnétique (MRCP) a montré une dilatation des voies biliaires intrahépatiques et du canal biliaire commun, l’absence de vésicule biliaire, une splénomégalie (augmentation de la rate) et des ganglions lymphatiques élargis au niveau du hile hépatique. La biopsie hépatique a révélé une disparition quasi totale des voies biliaires dans la majorité des espaces porte, un phénomène caractéristique du syndrome de la voie biliaire effacée (VBDS), ainsi qu’une fibrose avancée (cicatrisation du foie) correspondant à une cirrhose cholestatique. Le séquençage génétique a identifié des mutations hétérozygotes dans les gènes PKLR et UGT1A1, impliqués respectivement dans le métabolisme énergétique et la conjugaison de la bilirubine.\n\nInterprétation clinique  \nLe diagnostic final a été révisé en une cholangite sclérosante primitive (CSP) associée à une colite ulcéreuse (CU), avec mutations génétiques PKLR et UGT1A1, compliquée de cholédocholithiase (calculs dans le canal biliaire commun) et de cirrhose cholestatique. La CSP est une maladie inflammatoire chronique des voies biliaires qui peut évoluer vers une destruction progressive des canaux biliaires, tandis que la CU est une maladie inflammatoire chronique de l’intestin. Cette association est connue sous le nom de PSC-UC, un sous-type particulier de colite ulcéreuse.\n\nProchaines étapes et traitement  \nAprès extraction endoscopique des calculs biliaires, le patient a reçu un traitement médicamenteux combiné :  \n- Acide ursodésoxycholique (1000 mg/j) et acide obéticholique (10 mg/j) pour améliorer la cholestase (réduction de l’accumulation de bile dans le foie).  \n- Cholestyramine (8 g/j) pour adsorber les acides biliaires en excès et limiter leur toxicité.  \n- Rifaximine (1,2 g/j) pour prévenir les infections des voies biliaires.  \n- Mésalazine (2 g/j) pour contrôler l’inflammation intestinale liée à la colite ulcéreuse.\n\nRésultats  \nAu suivi le 30 juillet 2024, la fonction hépatique du patient montrait une amélioration notable des paramètres biochimiques, avec une bilirubine totale et directe diminuée, une réduction des enzymes hépatiques (phosphatase alcaline et GGT) et une stabilisation de l’état clinique. Le patient n’a pas nécessité de transplantation hépatique à ce jour et son état reste stable sous traitement."
+        }
+    },
+    {
+        "article": "Le cas d'une femme de 43 ans, ayant des antécédents de cancer du sein, diagnostiqué avant la ménopause, est décrit. La patiente a présenté des symptômes gastro-intestinaux non spécifiques, tels que la plénitude postprandiale, l'augmentation du périmètre abdominal, des douleurs abdominales intermittentes, avec prédominance dans le méogastre, qui ont évolué pendant 12 mois. Par la suite, une dyspnée modérée a été ajoutée. La patiente s'est présentée à un médecin de premier contact, qui a établi le protocole d'étude et lui a demandé une échographie de l'abdomen et du bassin, qui a mis en évidence une tumeur qui couvrait l'ensemble de la cavité abdominale, et a complété l'étude par une tomographie par ordinateur avec contraste du thorax, de l'abdomen et du bassin, qui a montré une tumeur de 27,5 x 12,7 x 28,2 cm, hétérogène, à prédominance liquide, avec présence de septa.\n\nLes marqueurs tumoraux ont présenté Ca 125 à 84,16, ACE 10,07, AFP 1,83, B-HGC 0,1. La numération formule sanguine a montré des tests de fonction hépatique et des temps de coagulation dans les paramètres normaux. La patiente a été envoyée au Service des tumeurs gynécologiques de l’Hôpital d’oncologie du Centre médical national Siglo XXI, où nous avons proposé une laparotomie avec étude transopératoire. L’intervention chirurgicale a été effectuée et une salpingo-ovariectomie gauche a été réalisée et envoyée pour étude transopératoire.\n\nL'intervention chirurgicale a révélé une mucinose, avec un taux de carcinomatose de 16 points, avec des implants de mucine dans toute l'étendue du péritoine pariétal, la capsule de Gleason et la rate, ainsi qu'une tumeur ovarienne gauche rompue.\n\nL’ovaire gauche de 3450 g, mesurant 28 x 27 x 14 cm, a été reçu en étude transopératoire avec une capsule rompue, une surface interne multiloculaire avec un contenu mucineux et une zone kystique de 7 x 6,5 cm a été identifiée avec un contenu sébacé et des poils. Aux coupes histologiques, on a observé un tissu ectodermique composé d’épithélium squameux et de follicules pileux, ainsi qu’un tissu endodermique composé d’épithélium de type intestinal, qui dans plusieurs coupes a présenté une atypie marquée avec une disposition architecturale complexe jusqu’à ce que l’on trouve des cellules en anneau de sceau, correspondant à un adénocarcinome. Aucun élément immature n’a été identifié dans l’échantillon de la tumeur.\n\nLa chirurgie de stade et de réduction de la tumeur de l'ovaire a été poursuivie, avec une hystérectomie totale + salpingo-ovariectomie bilatérale + péritonectomie + appendicectomie. Des résultats positifs ont été obtenus en termes d'activité tumorale, et une cholécystectomie et une splénectomie ont été décidées. Une chimiothérapie hyperthermique intra-opératoire a été ajoutée avec 45 mg de cisplatine dans 1000 ml de solution saline physiologique à 0,9 % à 40 °C, et une réduction de la tumeur optimale a été obtenue, qui a été classée comme stade IIIC. Des implants de la tumeur (adénocarcinome) ont également été observés dans l'omentum, la capsule hépatique et la capsule splénique dans le rapport histopathologique.\n\nLa patiente a été envoyée au service d'oncologie médicale et a été considérée comme candidate à un traitement adjuvant par carboplatine et paclitaxel en six cycles, qui s'est terminé sans incident. Elle a actuellement de bons résultats oncologiques, avec une période sans maladie de sept mois ; elle est suivie par le service des tumeurs gynécologiques.\n",
+        "gold_summary": "Femme de 43 ans, atteinte d'un tératome mature malin à cellules en anneau de sceau. Une citoréduction primaire optimale a été réalisée ; hystérectomie totale, salpingo-ovariectomie bilatérale, péritonectomie, appendicectomie, cholécystectomie et splénectomie, ainsi qu'une chimiothérapie hyperthermique intra-opératoire (HIPEC).\n",
+        "synthetic_summary": {
+            "B1": "Une dame de 43 ans avait une grosse boule dans son ventre. Les docteurs ont enlevé cette boule avec une grande opération. Ils ont aussi enlevé quelques parties du corps pour que la dame aille mieux. Après, elle a reçu un médicament chaud pour aider à guérir. Maintenant, elle va un peu mieux.",
+            "B2": "Cas d’une femme de 43 ans avec un type rare de tumeur appelée tératome mature malin, qui contient des cellules spéciales nommées « cellules en anneau de sceau ». Cette tumeur se trouvait dans son ovaire gauche et avait aussi envahi d’autres parties de l’abdomen.\n\nPour la traiter, les médecins ont fait une opération importante pour enlever autant de tumeur que possible. Ils ont retiré l’utérus, les deux ovaires, une partie de la membrane qui recouvre l’abdomen (péritoine), l’appendice, la vésicule biliaire et la rate. Pendant l’opération, ils ont aussi appliqué une chimiothérapie spéciale chauffée directement dans le ventre, appelée chimiothérapie hyperthermique intra-opératoire (HIPEC), pour tuer les cellules cancéreuses restantes.\n\nAprès cette opération et le traitement, la patiente a reçu six cycles de chimiothérapie par médicaments pour aider à prévenir le retour du cancer. Sept mois après, elle va bien et n’a pas de signes de maladie. Les médecins continuent de la suivre pour surveiller sa santé.",
+            "B3": "Résumé détaillé destiné à un public adulte non spécialiste\n\nContexte  \nUne femme de 43 ans, avec des antécédents de cancer du sein avant la ménopause, a présenté pendant un an des symptômes digestifs non spécifiques, notamment une sensation de plénitude après les repas, une augmentation du tour de taille et des douleurs abdominales intermittentes localisées principalement dans la région centrale de l’abdomen. Par la suite, elle a développé une difficulté modérée à respirer (dyspnée). Ces signes ont conduit à des examens d’imagerie qui ont révélé une volumineuse masse tumorale occupant la quasi-totalité de la cavité abdominale.\n\nPrincipales observations  \nL’échographie et la tomodensitométrie (scanner) ont montré une tumeur de grande taille (environ 27,5 x 12,7 x 28,2 cm), présentant une composition majoritairement liquide avec des cloisons internes (septa). Les marqueurs tumoraux sanguins ont révélé une élévation modérée du CA 125, un marqueur souvent associé aux tumeurs ovariennes, tandis que d’autres marqueurs étaient dans les limites normales. Les analyses sanguines générales, y compris la fonction hépatique et la coagulation, étaient normales.\n\nUne intervention chirurgicale majeure a été réalisée, comprenant l’ablation de l’ovaire gauche affecté, qui pesait 3,45 kg et mesurait 28 x 27 x 14 cm. L’examen macroscopique a montré une tumeur rompue avec un contenu mucineux (gélatineux) et des zones kystiques contenant du matériel sébacé et des poils. L’analyse microscopique a révélé un tératome mature, c’est-à-dire une tumeur composée de différents types de tissus normalement présents dans l’embryon, notamment des tissus ectodermiques (épithélium squameux, follicules pileux) et endodermiques (épithélium intestinal). Certaines zones présentaient des anomalies cellulaires importantes, avec une architecture complexe et la présence de cellules en anneau de sceau, caractéristiques d’un adénocarcinome (cancer glandulaire). Aucun tissu immature (plus agressif) n’a été détecté.\n\nL’extension de la maladie était importante, avec des implants tumoraux disséminés sur le péritoine (membrane tapissant la cavité abdominale), la capsule entourant le foie (capsule hépatique), la rate (capsule splénique) et l’omentum (tissu graisseux abdominal). Un score de carcinomatose péritonéale de 16 a été attribué, indiquant une atteinte étendue.\n\nInterprétation clinique  \nLe diagnostic principal est celui d’un tératome mature malin avec transformation maligne en adénocarcinome à cellules en anneau de sceau, une forme rare et agressive. Le stade de la maladie a été classé IIIC, correspondant à une extension importante dans la cavité abdominale mais sans métastases à distance.\n\nProchaines étapes et prise en charge  \nUne chirurgie de cytoréduction optimale a été réalisée, visant à retirer la totalité visible de la tumeur. Cette intervention comprenait une hystérectomie totale (ablation de l’utérus), une salpingo-ovariectomie bilatérale (ablation des deux ovaires et trompes), une péritonectomie (ablation du péritoine affecté), une appendicectomie (ablation de l’appendice), une cholécystectomie (ablation de la vésicule biliaire) et une splénectomie (ablation de la rate). En complément, une chimiothérapie hyperthermique intra-opératoire (HIPEC) a été administrée, consistant en une perfusion de cisplatine chauffé directement dans la cavité abdominale pour détruire les cellules tumorales résiduelles.\n\nAprès la chirurgie, la patiente a reçu un traitement adjuvant par chimiothérapie systémique associant carboplatine et paclitaxel, sur six cycles, sans complications majeures. Le suivi oncologique à sept mois montre une absence de récidive, témoignant d’une bonne réponse initiale au traitement.\n\nConclusion  \nCe cas illustre la complexité et la gravité d’un tératome mature malin avec transformation carcinomateuse, nécessitant une prise en charge multidisciplinaire combinant chirurgie étendue et chimiothérapie ciblée. La surveillance régulière reste essentielle pour détecter une éventuelle récidive."
+        }
+    },
+    {
+        "article": "Femme de 60 ans, ancienne fumeuse, en surpoids et atteinte de polyarthrite rhumatoïde, traitée par méthotrexate et golimumab. Antécédent d'exérèse en bloc d'une tumeur pelvienne, avec résection du rectum, reconstruction par anastomose colorectale et sacrectomie distale au niveau de la quatrième vertèbre sacrée (S4). L'anatomie pathologique correspondait à une formation kystique multiloculaire de 22 x 8,5 cm. Les coupes histologiques ont révélé une paroi de tissu fibreux avec revêtement épithélial squameux ou pseudo-stratifié, et des infiltrats lympho-histiocytaires, des vaisseaux sanguins ectasiques et des structures glandulaires occasionnelles avec des modifications de type réactif. Ces résultats étaient compatibles avec un tératome kystique mature. Deux ans après l'exérèse, elle a présenté des symptômes au niveau sacré. Des tomodensitogrammes et des examens IRM ont été demandés, qui ont révélé, au niveau des dernières vertèbres sacrées, la présence d'une formation de parties molles hétérogènes d'environ 60 mm de diamètre, associée à une raréfaction des plans graisseux et à un liquide adjacente peu abondant. Une biopsie par aiguille fine a été réalisée, dont le résultat a confirmé la récidive d'un tératome mature. Après la stadification, qui n'a pas révélé de maladie systémique, elle a été évaluée par un comité multidisciplinaire de tumeurs et une conduite chirurgicale en bloc a été indiquée. Une approche postérieure a été réalisée en résécant la cicatrice pré-existante, une section partielle des muscles fessiers et pyramidaux, une section sacrée au niveau S2-S3, en respectant les deux racines S3, une libération de l'espace pré-sacré et une exérèse de la pièce. La patiente a évolué favorablement dans la période post-opératoire. L'examen anatomo-pathologique macroscopique a révélé une formation tumorale de 7,8 x 6 x 4,5 cm adhérente à l'os sacré. Au moment de la coupe, elle était principalement solide, de consistance hétérogène avec des secteurs d'aspect friable, des zones kystiques avec du liquide et du gel et des foyers de calcification. Les coupes histologiques ont montré l'atteinte osseuse par des structures glandulaires néoplasiques avec un pléomorphisme nucléaire modéré, la formation de structures micropapillaires, la production de mucine et des zones de nécrose. Dans certaines zones kystiques périphériques, on a reconnu un épithélium cilié colonnaire mature. Les marges chirurgicales de résection étaient libres de toute atteinte néoplasique. Les techniques d'immunomarquage ont été positives pour CK20, calretinine, p53 et, de manière focale, pour CDX2, et négatives pour CK7, WT-1, PAX8 et CA125. Ces résultats étaient compatibles avec une récidive de tératome mature avec transformation somatique maligne vers un adénocarcinome de type colorectal. Une vidéocolonoscopie normale a été réalisée, confirmant ainsi le diagnostic de transformation maligne de tératome sacré. Elle est restée sous contrôle multidisciplinaire. Après 24 mois sans maladie, elle a présenté une détérioration de l'état général et une augmentation rapide de CA 19.9, ce qui a conduit à une PET/CT qui a révélé de multiples images hyper-capteurs au niveau viscéral, des tissus mous et des os compatibles avec un secondaire. En raison de la détérioration fonctionnelle rapide, elle n'a pas pu recevoir un traitement systémique et est décédée deux mois plus tard.\n",
+        "gold_summary": "Le cas d'une femme de 60 ans ayant des antécédents de résection en bloc d'une tumeur pelviane présacrée dont l'anatomie pathologique a rapporté un tératome mature a été présenté. Après 2 ans, elle s'est présentée pour une douleur sacro-coccygienne. Les études d'imagerie ont révélé une tumeur de 6 cm avec une atteinte osseuse des dernières vertèbres sacrées. Une biopsie avec aiguille épaisse a été réalisée et a rapporté une récidive de tératome mature. Après cette stadification qui n'a pas mis en évidence de maladie systémique, elle a été évaluée par un comité multidisciplinaire et une conduite chirurgicale a été indiquée. Une résection en bloc a été réalisée avec une sacrectomie distale au niveau de S3 et des muscles environnants. L'étude anatomopathologique a rapporté la présence d'un tératome mature avec une transformation maligne, avec un composant d'adénocarcinome de type colorectal. Les marges de résection étaient exemptes de tumeur. Après une nouvelle évaluation multidisciplinaire, une stratégie de contrôle a été décidée. Elle est restée exempte de maladie pendant 24 mois, à partir desquels elle a présenté une détérioration générale associée à la progression de la maladie, et est morte 2 mois plus tard.\n",
+        "synthetic_summary": {
+            "B1": "Il y avait une dame de 60 ans. Elle avait une grosse boule près du bas du dos. Les docteurs l'ont enlevée avec une opération. Cette boule s'appelait un tératome, c'est une sorte de grosse boule pas dangereuse au début.\n\nDeux ans plus tard, la dame avait mal au bas du dos. Les docteurs ont fait des images et ont vu que la boule était revenue. Ils ont fait une autre opération pour l'enlever encore une fois.\n\nAprès l'opération, ils ont trouvé que la boule avait changé et était devenue un peu méchante. Mais ils ont réussi à tout enlever. La dame est restée bien pendant deux ans.\n\nPuis, elle est devenue très malade et est partie au ciel deux mois après. Les docteurs ont tout fait pour l'aider.",
+            "B2": "**Résumé adapté pour un adolescent de 14 ans**\n\nCette histoire parle d’une femme de 60 ans qui avait une grosse tumeur appelée tératome mature dans la région du bassin, près des os du bas du dos. Un tératome mature est une tumeur qui contient différents types de tissus, comme des cellules de peau ou des glandes, mais qui est normalement bénigne (pas cancéreuse). Elle avait déjà subi une opération importante pour enlever cette tumeur.\n\nDeux ans plus tard, elle a commencé à avoir des douleurs dans le bas du dos, près du coccyx. Des examens d’imagerie, comme des scanners et des IRM, ont montré qu’une nouvelle masse d’environ 6 centimètres s’était formée près des os sacrés (les os à la base de la colonne vertébrale). Une biopsie, c’est-à-dire un prélèvement d’un petit morceau de la tumeur, a confirmé que le tératome était revenu.\n\nLes médecins ont décidé de refaire une opération pour enlever cette nouvelle tumeur. Pendant l’opération, ils ont enlevé une partie des os sacrés et des muscles autour. Après l’analyse de la tumeur en laboratoire, ils ont découvert que cette fois, le tératome avait changé et s’était transformé en un cancer appelé adénocarcinome, qui ressemble à un cancer du côlon (le gros intestin). Heureusement, les bords de la tumeur enlevée étaient propres, ce qui veut dire que tout le cancer visible avait été retiré.\n\nAprès l’opération, la femme a été suivie régulièrement. Elle est restée en bonne santé sans signe de maladie pendant deux ans. Puis, son état s’est rapidement détérioré et des examens ont montré que le cancer s’était étendu à d’autres parties du corps. Malheureusement, elle n’a pas pu recevoir de traitement à cause de sa santé fragile et elle est décédée deux mois plus tard.\n\n**Ce qu’il faut retenir** : Un tératome mature est une tumeur souvent bénigne, mais dans ce cas, elle est revenue et s’est transformée en un cancer plus agressif. Le suivi médical est très important pour détecter ces changements à temps.",
+            "B3": "Résumé détaillé et structuré\n\nContexte  \nIl s’agit du cas d’une femme de 60 ans, ancienne fumeuse et en surpoids, souffrant de polyarthrite rhumatoïde traitée par méthotrexate et golimumab. Elle avait un antécédent chirurgical important : une exérèse en bloc d’une tumeur pelvienne présacrée, réalisée deux ans auparavant, comprenant la résection du rectum, une anastomose colorectale et une sacrectomie distale au niveau de la quatrième vertèbre sacrée (S4). L’analyse anatomopathologique initiale avait confirmé un tératome kystique mature, une tumeur bénigne composée de différents types de tissus, avec une paroi fibreuse et un revêtement épithélial varié.\n\nPrincipales observations  \nDeux ans après cette intervention, la patiente a présenté des douleurs au niveau sacro-coccygien. Les examens d’imagerie par tomodensitométrie (TDM) et imagerie par résonance magnétique (IRM) ont révélé une masse hétérogène d’environ 6 cm au niveau des dernières vertèbres sacrées, avec une atteinte osseuse locale. Une biopsie par aiguille fine a confirmé la récidive du tératome mature. La stadification n’a pas montré de maladie systémique à distance. Un comité multidisciplinaire a alors recommandé une nouvelle intervention chirurgicale en bloc, comprenant une sacrectomie partielle au niveau des vertèbres S2-S3, avec résection des muscles environnants.\n\nInterprétation clinique  \nL’examen anatomopathologique de la pièce opératoire a révélé une tumeur de 7,8 x 6 x 4,5 cm adhérente à l’os sacré, présentant des zones solides, kystiques et calcifiées. Histologiquement, la tumeur montrait une transformation maligne avec la présence d’un adénocarcinome de type colorectal, caractérisé par des structures glandulaires néoplasiques, un pléomorphisme nucléaire modéré, des formations micropapillaires, une production de mucine et des zones de nécrose. Des techniques d’immunomarquage ont confirmé ce diagnostic, avec des marqueurs positifs pour CK20, calrétinine, p53 et focaux pour CDX2, et négatifs pour CK7, WT-1, PAX8 et CA125. Les marges chirurgicales étaient exemptes de cellules tumorales, indiquant une résection complète. Une vidéocolonoscopie normale a permis d’exclure une origine colique primaire, confirmant ainsi la transformation maligne du tératome sacré.\n\nProchaines étapes et évolution  \nAprès la chirurgie, la patiente est restée sous surveillance multidisciplinaire. Elle est restée sans signe de maladie pendant 24 mois. Cependant, elle a ensuite présenté une détérioration rapide de son état général, accompagnée d’une élévation marquée du marqueur tumoral CA 19-9. Une tomographie par émission de positons (PET/CT) a révélé de multiples lésions secondaires au niveau viscéral, des tissus mous et osseux, témoignant d’une dissémination métastatique. En raison de la dégradation rapide de son état fonctionnel, elle n’a pas pu bénéficier d’un traitement systémique et est décédée deux mois plus tard.\n\nCe cas illustre la rare possibilité de transformation maligne d’un tératome mature présacré en adénocarcinome de type colorectal, soulignant l’importance d’une prise en charge multidisciplinaire rigoureuse et d’un suivi prolongé."
+        }
+    },
+    {
+        "article": "Les dossiers médicaux des patients atteints de myotonie congénitale, étudiés et suivis au sein du service de neurologie pédiatrique d’un hôpital de troisième niveau entre 2015 et 2020, ont été examinés. Les critères d’inclusion étaient un diagnostic clinique (myotonie, phénomène de réchauffement, patron électromyographique caractéristique et/ou antécédents familiaux) et/ou un diagnostic moléculaire (mutation dans le gène CLCN1). Les signes et symptômes cliniques, ainsi que les résultats des examens complémentaires et la mutation génétique trouvée, ont été recueillis au moyen d’un examen du dossier médical. Les variables démographiques (âge et sexe), l’évolution de la maladie (âge de début, symptômes et signes, temps écoulé jusqu’au diagnostic et évolution clinique), les antécédents familiaux et l’évaluation de la réponse au traitement ont été recueillis.\n\nCinq cas ont été identifiés avec un diagnostic clinique de myotonie congénitale (trois avec la maladie de Becker et deux avec la maladie de Thomsen). L'incidence par rapport au nombre de naissances est estimée à 1:15 000 nouveau-nés pour les cas avec le phénotype Becker et 1:21 000 nouveau-nés pour les phénotypes Thomsen.\n\nLa plupart de nos patients étaient des femmes, et le seul homme a commencé avant l'âge de six ans. La clinique initiale comprenait une myotonie des membres inférieurs chez quatre des cinq patients et des membres supérieurs également chez tous sauf un. L'âge au début variait de 22 mois à 12 ans, avec une médiane de 6 ans. Le diagnostic génétique a été effectué dans tous les cas environ deux ans après le début, et la famille d'une patiente a refusé de le faire. Tous ont présenté une aggravation par le froid, mais le phénomène de réchauffement, seulement ceux qui avaient le phénotype de Becker.\n\nLes patients atteints de myotonie congénitale récessive ont présenté une certaine progression. En ce qui concerne les antécédents familiaux, il convient de noter que les patientes 2 et 3 étaient sœurs, sans que les parents ne présentent aucun symptôme, et que la mère de la patiente 1 présentait des symptômes modérés et douteux au froid. La patiente qui a refusé l'étude avait des antécédents de myotonie du côté maternel.\n\nLes analyses sanguines n’ont révélé aucune augmentation de la créatine kinase chez aucun des patients. L’électromyogramme était pathologique chez tous les patients, sauf chez le premier patient âgé de 2,8/12 ans. Par la suite, le test n’a pas été répété car il n’était plus considéré comme nécessaire.\n\nLe traitement le plus utilisé initialement était l'oxcarbazépine (chez les patients atteints de la forme récessive), avec une bonne réponse en général. Dans le cas 2, il a perdu de l'efficacité avec le temps et le mexiletine a été initié. Le patient 4 a commencé à prendre plusieurs médicaments sans succès en raison d'une perte d'efficacité ou d'effets secondaires. Le patient 5 a refusé le traitement en raison d'une clinique légère.\n\nLe patient 1 présentait une mutation probablement pathogène non décrite précédemment (CLCN1 : c.824T>C), héritée de sa mère. Les cas 1 à 3 présentaient un phénotype Becker avec des mutations en hétérozygotie composée, et les cas 4 et 5 présentaient un phénotype Thomsen. Le cas 5 a refusé l'étude génétique.\n",
+        "gold_summary": "Les dossiers médicaux des patients atteints de myotonie congénitale, étudiés et suivis au sein du service de neurologie pédiatrique d'un hôpital de troisième niveau entre 2015 et 2020, ont été examinés. Les variables démographiques (âge et sexe), l'évolution de la maladie (âge de début, symptômes et signes, délai de diagnostic et évolution clinique), les antécédents familiaux et l'évaluation de la réponse au traitement ont été collectés. Cinq cas ont été identifiés avec un diagnostic clinique de myotonie congénitale (trois avec la maladie de Becker et deux avec la maladie de Thomsen). L'incidence par rapport au nombre de naissances a été estimée à 1:15 000 nouveau-nés pour les cas avec le phénotype Becker et à 1:21 000 nouveau-nés pour les phénotypes Thomsen. Nous avons trouvé une mutation probablement pathogénique non décrite précédemment (CLCN1 : c.824T>C).\n",
+        "synthetic_summary": {
+            "B1": "Il y a des enfants qui ont des muscles un peu raides. Cela s’appelle la myotonie congénitale. \n\nLes docteurs ont regardé cinq enfants qui ont cette raideur. Trois enfants ont un type appelé Becker. Deux enfants ont un autre type appelé Thomsen. \n\nCette maladie arrive très rarement. C’est comme si un bébé sur beaucoup de bébés avait cette raideur. \n\nLes docteurs ont aussi trouvé un petit changement dans un gène. Ce changement peut expliquer pourquoi les muscles sont raides. \n\nLes enfants peuvent être aidés par des médicaments. Les docteurs apprennent à mieux les soigner. \n\nTout va bien, il faut juste être patient et gentil avec les muscles.",
+            "B2": "Étude sur la myotonie congénitale chez des enfants\n\nCe qu’ils ont fait :  \nLes médecins ont étudié les dossiers de cinq enfants atteints de myotonie congénitale, une maladie rare qui rend les muscles raides et difficiles à bouger. Ces enfants ont été suivis dans un service de neurologie pédiatrique entre 2015 et 2020. Ils ont regardé leur âge, leur sexe, quand les symptômes ont commencé, comment la maladie a évolué, leurs antécédents familiaux, et comment ils ont répondu aux traitements.\n\nCe qu’ils ont trouvé :  \nParmi ces cinq enfants, trois avaient une forme appelée maladie de Becker et deux avaient une autre forme appelée maladie de Thomsen. Ces formes sont liées à des mutations dans un gène appelé CLCN1, qui contrôle le fonctionnement des muscles. Ils ont estimé que la maladie de Becker touche environ 1 bébé sur 15 000, et la maladie de Thomsen environ 1 sur 21 000 naissances.  \n\nUne mutation nouvelle, jamais décrite avant, a été découverte chez un des enfants. Cette mutation pourrait expliquer certains symptômes.  \n\nCe que cela signifie :  \nLa myotonie congénitale est rare mais peut commencer dès la petite enfance. Les symptômes peuvent varier selon la forme de la maladie. Connaître les mutations génétiques aide à mieux comprendre la maladie et à choisir les traitements adaptés. Cette étude montre aussi que la maladie peut être héritée même si les parents ne présentent pas toujours de symptômes visibles.",
+            "B3": "Résumé détaillé sur la myotonie congénitale étudiée dans un service de neurologie pédiatrique\n\nContexte  \nEntre 2015 et 2020, les dossiers médicaux de patients atteints de myotonie congénitale ont été analysés dans un hôpital de troisième niveau, au sein du service de neurologie pédiatrique. La myotonie congénitale est une maladie neuromusculaire caractérisée par une difficulté à relâcher les muscles après leur contraction, liée à des mutations génétiques, notamment dans le gène CLCN1. Le diagnostic reposait sur des critères cliniques (présence de myotonie, phénomène de réchauffement, électromyogramme spécifique, antécédents familiaux) et/ou sur une confirmation moléculaire par identification d’une mutation génétique.\n\nPrincipales observations  \nCinq patients ont été identifiés avec un diagnostic clinique de myotonie congénitale : trois présentaient la forme dite de Becker (forme récessive) et deux la forme de Thomsen (forme dominante). L’incidence estimée était d’environ 1 cas pour 15 000 naissances pour la forme de Becker, et 1 cas pour 21 000 naissances pour la forme de Thomsen. La majorité des patients étaient des filles, avec un seul garçon ayant débuté les symptômes avant l’âge de six ans. L’apparition des premiers signes variait entre 22 mois et 12 ans, avec une médiane à 6 ans. Les symptômes initiaux concernaient principalement la myotonie des membres inférieurs, puis des membres supérieurs chez la plupart des patients. Tous les patients ont présenté une aggravation des symptômes par le froid, mais le phénomène de réchauffement (amélioration temporaire de la raideur musculaire après exercice) n’était observé que chez ceux atteints de la forme de Becker.\n\nSur le plan génétique, tous les patients ont bénéficié d’un diagnostic moléculaire environ deux ans après le début des symptômes, sauf une patiente dont la famille a refusé l’analyse. Une mutation nouvelle, probablement pathogène, jamais décrite auparavant (mutation CLCN1 : c.824T>C), a été identifiée chez un patient et héritée de sa mère. Les trois patients avec la forme de Becker présentaient des mutations en hétérozygotie composée (deux mutations différentes sur les deux copies du gène), tandis que les deux patients avec la forme de Thomsen présentaient une mutation dominante.  \n\nLes antécédents familiaux étaient variables : deux sœurs étaient atteintes sans que les parents ne présentent de symptômes, tandis que la mère d’une autre patiente avait des signes modérés aggravés par le froid. Aucun patient ne présentait d’élévation des enzymes musculaires (créatine kinase) dans le sang. L’électromyogramme, examen mesurant l’activité électrique des muscles, était anormal chez tous les patients sauf un, chez qui il n’a pas été répété après un premier test normal.\n\nConcernant le traitement, l’oxcarbazépine, un médicament anticonvulsivant, a été utilisé initialement chez les patients atteints de la forme récessive avec une bonne efficacité générale. Cependant, chez un patient, son efficacité a diminué avec le temps, nécessitant un changement pour la mexilétine, un autre traitement. Un autre patient a essayé plusieurs médicaments sans succès en raison d’effets secondaires ou de perte d’efficacité, tandis qu’un dernier patient a refusé tout traitement en raison de symptômes légers.\n\nInterprétation clinique  \nCette étude confirme la variabilité clinique et génétique de la myotonie congénitale, avec des formes récessives et dominantes présentant des profils différents en termes d’âge d’apparition, de symptômes et de réponse au traitement. L’identification d’une nouvelle mutation pathogène élargit la connaissance génétique de cette maladie. Le retard moyen de diagnostic d’environ deux ans souligne l’importance d’une reconnaissance précoce des signes cliniques et d’un suivi adapté.\n\nProchaines étapes  \nUn suivi longitudinal des patients est nécessaire pour mieux comprendre l’évolution naturelle de la maladie et l’efficacité à long terme des traitements. La sensibilisation des familles et des professionnels de santé à la diversité des manifestations cliniques pourrait améliorer le diagnostic précoce. Enfin, la recherche génétique doit se poursuivre pour identifier d’autres mutations et mieux personnaliser la prise en charge thérapeutique."
+        }
+    },
+    {
+        "article": "Homme de 68 ans, hypertension artérielle, maladie pulmonaire obstructive chronique et tabagisme actif, consulté aux urgences le 01/02/23 pour perte d'acuité visuelle progressive (3 mois d'évolution) associée à une hémiplégie brachio-crurale gauche, exacerbée les jours précédant la consultation.\n\nUn NIHSS de 5 points a été observé, avec une dysarthrie et une parésie minimale du côté gauche, une tension artérielle de 160/80 mm Hg, une fréquence cardiaque de 75 lpm et une oxymétrie de pouls de 94 % (FiO2 environnementale). Une angio-CT a révélé une sténose sévère de l'ACI droite et une IRM a mis en évidence des infarctus aigus dans l'hémisphère cérébral droit.\n\nL’écho Doppler a confirmé une sténose sévère (VPS 356 cm/s) de l’ACI droite. Après avoir été évalué minutieusement, confirmant une sténose carotidienne droite sévère symptomatique associée à une lésion morphologiquement haute (qui rend la CEA techniquement difficile) et un risque chirurgical élevé, nous avons décidé de procéder à un traitement endovasculaire par TCAR.\n\nLe 8 février 2003, sous anesthésie générale et héparinisation systémique (100 UI/kg d'héparine non fractionnée, pour un temps d'activation de la coagulation (ACT) > 250 s), la dissection de l'ACC et de la VYI a été réalisée. Une fois la fistule carotidio-jugulaire créée, l'ACC a été clampée, ce qui a entraîné une inversion dynamique du flux.\n\nAprès avoir traversé la lésion (avec la micro-guide-wire) et canalisé l’ACI distale, un stent carotidien (Casper® Mirovention, Terumo) de 8 × 30 mm a été déployé. Étant donné que la lésion était sévère et distale, un phénomène de migration proximale (vers l’ACC) s’est produit pendant le déploiement, nécessitant l’installation d’un deuxième stent (7 × 30 mm) pour traiter la lésion de manière satisfaisante.\n\nL'angiographie a montré une amélioration immédiate du lumen de l'ACI et une expansion adéquate des stents. L'ACC a été débloquée (rétablissement du flux cérébral antérograde), les éléments endovasculaires ont été retirés et l'incision a été fermée comme décrit précédemment.\n\nLe patient a récupéré de manière satisfaisante, n’a présenté aucune complication et a été libéré le deuxième jour postopératoire avec un double traitement antiplaquettaire.\n\nAu cours du suivi, il n'a présenté aucun événement neurologique et l'écho-doppler de contrôle (3, 6 et 12 mois) a montré que le stent était perméable et ne présentait aucun signe de ré-sténose.\n",
+        "gold_summary": "Homme de 68 ans souffrant d'hypertension et de maladie pulmonaire obstructive chronique, ayant développé un accident vasculaire cérébral secondaire à une sténose sévère de l'artère carotide interne droite. Une TCAR a été décidée en raison de sa localisation et du risque chirurgical. Au cours de la procédure, une fistule temporaire a été créée entre l'artère carotide et la veine jugulaire ipsilatérale pour inverser le flux et protéger le cerveau, permettant le déploiement sécurisé du stent. Le patient s'est rétabli sans complications et reste asymptomatique un an après le suivi.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 68 ans avait un gros problème dans une grosse artère du cou. Cette artère était très bouchée. Cela faisait qu’il avait du mal à voir et à bouger un peu son bras et sa jambe.\n\nLes docteurs ont fait une petite opération pour aider le sang à mieux passer. Ils ont mis un petit tuyau spécial dans l’artère. Pour protéger son cerveau, ils ont changé le sens du sang pendant l’opération.\n\nAprès, le monsieur a bien guéri. Il va bien et il n’a plus de problème un an après. Les docteurs sont contents.",
+            "B2": "**Ce qu’ils ont trouvé**  \nUn homme de 68 ans, qui avait de l’hypertension (pression artérielle élevée), une maladie des poumons et qui fumait, a perdu progressivement la vue d’un œil pendant trois mois. Il avait aussi une faiblesse d’un côté du corps. Des examens ont montré qu’une grosse artère du cou, appelée artère carotide interne droite, était très rétrécie. Ce rétrécissement avait causé un petit accident vasculaire cérébral (AVC) dans son cerveau.\n\n**Ce qu’ils ont fait**  \nLes médecins ont décidé de traiter ce problème en utilisant une technique appelée TCAR (traitement endovasculaire par voie transcervicale). Cette méthode consiste à passer par une petite ouverture dans le cou pour placer un petit tube métallique appelé stent dans l’artère rétrécie. Pour protéger le cerveau pendant l’opération, ils ont temporairement changé le sens du flux sanguin en créant un passage entre l’artère carotide et une veine proche. Cela empêche les caillots de remonter vers le cerveau.\n\nPendant l’intervention, ils ont posé un premier stent, mais comme la zone était très étroite et difficile, ils ont dû mettre un deuxième stent pour bien ouvrir l’artère. L’opération s’est bien passée sans problème.\n\n**Ce que cela signifie**  \nLe patient s’est bien remis, sans complication, et il a pu sortir de l’hôpital rapidement. Un suivi régulier pendant un an a montré que les stents restaient ouverts et qu’il n’y avait pas de nouveau rétrécissement. Cette technique a donc permis de traiter efficacement son problème vasculaire et d’éviter d’autres accidents cérébraux.",
+            "B3": "Résumé détaillé et structuré pour un public non spécialiste\n\nContexte  \nUn homme de 68 ans, présentant des antécédents d’hypertension artérielle, de maladie pulmonaire obstructive chronique (une maladie respiratoire chronique) et un tabagisme actif, a consulté aux urgences pour une perte progressive de la vision sur trois mois, associée à une faiblesse musculaire affectant le bras et la jambe gauches (hémiplégie brachio-crurale), aggravée dans les jours précédant la consultation.\n\nPrincipales observations  \nL’examen neurologique a révélé un score NIHSS (échelle d’évaluation de la gravité d’un accident vasculaire cérébral) de 5, avec une difficulté à articuler les mots (dysarthrie) et une faiblesse légère du côté gauche. Les constantes vitales étaient stables, avec une tension artérielle à 160/80 mm Hg et une saturation en oxygène normale.  \nLes examens d’imagerie ont montré une sténose sévère (rétrécissement important) de l’artère carotide interne droite, confirmée par un angio-CT et un écho-Doppler avec une vitesse de pointe systolique très élevée (356 cm/s), signe d’un rétrécissement critique. Une IRM cérébrale a mis en évidence des infarctus aigus (zones de tissu cérébral endommagé par un manque d’oxygène) dans l’hémisphère droit du cerveau, expliquant les symptômes neurologiques.\n\nInterprétation clinique  \nLa sténose carotidienne droite était responsable d’un accident vasculaire cérébral ischémique (causé par une obstruction de la circulation sanguine). La localisation haute de la lésion et le risque élevé lié à une chirurgie classique (endarterectomie carotidienne) ont conduit à choisir une approche endovasculaire innovante appelée TCAR (TransCarotid Artery Revascularization). Cette technique consiste à traiter la sténose par l’intérieur du vaisseau, en créant temporairement une fistule (connexion) entre l’artère carotide et la veine jugulaire du même côté pour inverser le flux sanguin et ainsi protéger le cerveau des emboles (caillots ou débris) lors du déploiement du stent.\n\nDéroulement de la procédure  \nSous anesthésie générale et anticoagulation contrôlée, les chirurgiens ont réalisé la dissection des vaisseaux concernés, créé la fistule carotido-jugulaire, puis clampé l’artère carotide commune pour inverser le flux sanguin. Un premier stent carotidien de 8 × 30 mm a été déployé, mais en raison de la sévérité et de la localisation distale de la lésion, une migration proximale du stent s’est produite, nécessitant la pose d’un second stent de 7 × 30 mm pour assurer une couverture complète et une bonne expansion. L’angiographie a confirmé l’amélioration immédiate du calibre de l’artère carotide interne. La fistule a été fermée, le flux sanguin cérébral normal rétabli, et la procédure terminée sans incident.\n\nÉvolution et suivi  \nLe patient a récupéré sans complication, a été libéré dès le deuxième jour postopératoire sous traitement antiplaquettaire double (médicaments pour prévenir la formation de caillots). Lors du suivi à 3, 6 et 12 mois, il est resté asymptomatique, sans nouvel événement neurologique, et les contrôles échographiques ont montré une perméabilité durable des stents, sans signe de rétrécissement.\n\nConclusion  \nCette prise en charge par TCAR a permis de traiter efficacement une sténose carotidienne sévère à haut risque chirurgical, avec une protection cérébrale optimale et une récupération favorable sur un an, illustrant une alternative sûre et efficace à la chirurgie classique dans des cas complexes."
+        }
+    },
+    {
+        "article": "Un patient de 72 ans s'est présenté avec des douleurs thoraciques irradiant vers son bras gauche et une dyspnée progressive au cours des dernières semaines. Il avait des antécédents de thrombose veineuse profonde du membre inférieur et d'hypertension artérielle contrôlée. Il n'y avait pas d'autres comorbidités pertinentes.\n\nL’examen physique a révélé un bon état général du patient, sans signe d’insuffisance cardiaque, une tension artérielle de 156/101 mmHg et une fréquence cardiaque de 73 bpm. L’eupnée était présente et la saturation en oxygène artériel était de 93 %. La fonction rénale était altérée, avec une créatinine sérique de 115 μmol/L et un taux de filtration glomérulaire estimé de 54 mL/min/1,73 m², la troponine T de haute sensibilité était légèrement élevée à 29 ng/L et le NT-proBNP significativement augmenté à 5463 ng/L. L’ECG a révélé un flutter auriculaire nouvellement diagnostiqué, avec un rythme cardiaque irrégulier de 93 bpm, ainsi que des troubles de la repolarisation antérieure et inférieure (inversion de l’onde T dans les dérivations II, III, aVF, V1-V4). Le score CHA2DS2-VASc était de 4 points.\n\n\nL’échocardiographie transthoracique a montré une fonction d’éjection ventriculaire gauche normale (LVEF 55%), une fonction ventriculaire droite légèrement altérée (TAPSE 18 mm), et une augmentation de la pression artérielle pulmonaire (sPAP 47 mm Hg). Un test de stress vélocipédique a été effectué et a montré une baisse significative de la pression artérielle de 138/74 mm Hg au repos à 118/76 mm Hg à 67% de la fréquence cardiaque maximale prévue par âge.\n\nSur la base de ces résultats, une maladie coronarienne pertinente était attendue, probablement avec une maladie de l'artère principale gauche (sur la base de la chute de la pression artérielle lors du test de stress).\n\nLa PE était un diagnostic différentiel possible (Wells Score de 4,5 points prévoyait un risque modéré avec une probabilité de PE de 16,2 %). L'anticoagulation était déjà indiquée en raison du flutter auriculaire.\n\nLe flutter auriculaire nouvellement documenté a été considéré comme associé à la maladie sous-jacente. Il n'y avait aucun signe d'anomalies neurologiques.\n\n\nEnquêtes\n\nL’angiographie coronarienne a révélé une maladie coronarienne à deux vaisseaux suivie d’une intervention coronarienne percutanée ad hoc avec revascularisation complète. La cathétérisation cardiaque droite, réalisée en raison de la légère augmentation de la pression artérielle pré-capillaire et post-capillaire, a révélé une pression artérielle moyenne élevée (mPAP) de 38 mmHg d’origine pré-capillaire et post-capillaire. L’angiographie pulmonaire a montré une occlusion thrombo-embolique de l’artère pulmonaire sous-segmentale du lobe inférieur droit. L’analyse des gaz du sang artériel a montré une alcalose respiratoire, partiellement compensée métaboliquement (pH 7,49, pCO23,4 kPa, pO211,7 kPa, HCO319,5 mmol/L, excès de base −3,8 mmol/L).\n\n\nTraitement\n\nLe patient a ensuite été admis à l'unité de soins coronariens (CCU) où une double antiagrégation plaquettaire (DAPT) avec aspirine et clopidogrel, ainsi qu'une anticoagulation orale avec apixaban ont été démarrés.\n\nLa surveillance hémodynamique à la CCU était acceptable avec une tension artérielle de 140/100 mmHg, une fréquence cardiaque de 85 bpm, une fréquence respiratoire de 17/min et un taux de SO2 de 94 % dans l'air ambiant. La TDM du thorax le jour suivant a confirmé la présence d'une EP avec des EP étendues, bilatérales, centrales et périphériques. Ces résultats étaient plus avancés que ceux de l'angiographie pulmonaire de la veille. Dans une évaluation ultérieure, le seul changement supplémentaire était un nouveau diagnostic de bloc de branche droit (BBR) et un changement de l'axe cardiaque sur l'ECG. La patiente ne ressentait toujours aucune gêne ni signe d'instabilité cardiopulmonaire et l'examen des gaz du sang artériel était inchangé.\n\nAu cours d'une chute après mobilisation indépendante sur le CCU, le patient a développé un arrêt circulatoire avec activité électrique sans pouls (PEA). Une réanimation cardiopulmonaire immédiate a été commencée. Au cours de la réanimation, une cathétérisation cardiaque droite a été effectuée, qui a montré un thrombus occlusif dans l'artère pulmonaire droite et s'est avérée impossible à mobiliser par des techniques interventionnelles.\n\n\nRésultat et suivi\n\nAprès 45 minutes de réanimation mécanique, le patient a développé une ligne plate sur l'ECG. Compte tenu des résultats récents de l'angiographie pulmonaire et de la réanimation mécanique déjà longue et infructueuse, la reprise de la circulation spontanée était très improbable et les efforts de réanimation ont été arrêtés, ce qui a entraîné la mort du patient.",
+        "gold_summary": "Nous présentons le cas d'un homme de 72 ans atteint d'un thromboembolisme pulmonaire aigu sous-massif. L'indice de gravité de l'embolie pulmonaire et la stratification du risque clinique commune recommandaient une anticoagulation systémique et un déroulement clinique sans complications était prévu. Une stratégie de reperfusion primaire n'était pas indiquée par les directives actuelles. Sous anticoagulation établie, le patient a été trouvé en arrêt cardiaque immédiatement après la mobilisation du lit le lendemain matin. La cathétérisation cardiaque droite sous réanimation en cours a révélé une obstruction complète de l'artère pulmonaire droite par un gros thrombus. L'intervention dirigée par cathéter pour contourner le thrombus avec des fils-guides interventionnels a échoué. En fin de compte, le patient est mort d'une insuffisance cardiaque droite aiguë.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 72 ans avait un gros caillot dans ses poumons. Ce caillot empêchait le sang de bien passer. Les docteurs lui ont donné des médicaments pour aider le sang à circuler. \n\nMais un jour, quand il s’est levé, son cœur s’est arrêté. Les docteurs ont essayé de l’aider, mais le caillot était trop gros. Ils n’ont pas réussi à le faire partir. \n\nLe monsieur est très malade à cause de ce caillot. Les docteurs ont fait tout leur possible pour l’aider.",
+            "B2": "Cas d’un homme de 72 ans avec une embolie pulmonaire grave\n\nNous racontons l’histoire d’un homme de 72 ans qui avait une embolie pulmonaire aiguë, c’est-à-dire un caillot de sang bloquant une artère dans ses poumons. Cette situation est très sérieuse car elle empêche le sang de circuler normalement et peut fatiguer le cœur.\n\nAu début, les médecins ont évalué la gravité de son problème. Selon les règles habituelles, il devait recevoir un traitement par anticoagulants, des médicaments qui empêchent la formation de nouveaux caillots. Ils pensaient que ce traitement suffirait et que le patient n’aurait pas de complications graves.\n\nCependant, le lendemain matin, juste après s’être levé de son lit, l’homme a eu un arrêt cardiaque, c’est-à-dire que son cœur a cessé de battre correctement. Pendant la réanimation, les médecins ont fait une cathétérisation cardiaque droite, une procédure où l’on insère un petit tube dans le cœur pour voir ce qui se passe. Ils ont découvert que l’artère pulmonaire droite était complètement bloquée par un gros caillot.\n\nIls ont essayé d’enlever ce caillot avec des outils spéciaux, mais cela n’a pas fonctionné. Malheureusement, malgré tous les efforts, le cœur droit du patient n’a pas pu continuer à fonctionner, et il est décédé à cause d’une insuffisance cardiaque aiguë.\n\nCe cas montre que même avec un traitement adapté, une embolie pulmonaire peut évoluer rapidement et devenir mortelle. Il est important de surveiller de près ces patients et d’agir vite en cas de signes d’aggravation.",
+            "B3": "Résumé détaillé et structuré pour un public non spécialiste\n\nContexte  \nUn homme de 72 ans s’est présenté avec des douleurs thoraciques irradiant vers le bras gauche et une difficulté progressive à respirer. Ses antécédents médicaux comprenaient une thrombose veineuse profonde (un caillot sanguin dans une veine profonde) et une hypertension artérielle bien contrôlée. À l’admission, il ne montrait pas de signes évidents d’insuffisance cardiaque, mais son électrocardiogramme (ECG) a révélé un flutter auriculaire (un trouble du rythme cardiaque) nouvellement diagnostiqué, ainsi que des anomalies électriques suggérant une atteinte cardiaque. Ses analyses sanguines ont montré une légère élévation de la troponine (marqueur de souffrance cardiaque) et une forte augmentation du NT-proBNP (indicateur de stress cardiaque). L’échocardiographie a montré une fonction normale du ventricule gauche mais une fonction légèrement altérée du ventricule droit, avec une pression artérielle pulmonaire élevée.\n\nPrincipales observations  \nUn test d’effort a mis en évidence une baisse anormale de la pression artérielle, suggérant une maladie coronarienne significative. L’angiographie coronarienne a confirmé une maladie des artères coronaires à deux vaisseaux, traitée par une intervention percutanée avec revascularisation complète. Par ailleurs, une cathétérisation cardiaque droite a révélé une hypertension pulmonaire d’origine mixte (pré- et post-capillaire). L’angiographie pulmonaire a identifié une occlusion thrombo-embolique (caillot) dans une artère pulmonaire sous-segmentaire du lobe inférieur droit. Une embolie pulmonaire (obstruction des artères pulmonaires par des caillots) était donc confirmée. Le patient a été traité par une double antiagrégation plaquettaire (aspirine et clopidogrel) et une anticoagulation orale (apixaban).\n\nInterprétation clinique  \nMalgré un traitement anticoagulant adapté, le patient a présenté le lendemain un arrêt circulatoire (arrêt cardiaque) lors d’une mobilisation. Une réanimation a été immédiatement initiée, et une nouvelle cathétérisation cardiaque droite réalisée en cours de réanimation a montré une obstruction complète de l’artère pulmonaire droite par un gros thrombus. Les tentatives d’éliminer ce caillot par intervention guidée par cathéter ont échoué. L’évolution a été rapidement fatale, avec une insuffisance cardiaque droite aiguë (incapacité brutale du cœur droit à pomper le sang vers les poumons), conduisant au décès du patient après 45 minutes de réanimation.\n\nProchaines étapes et enseignements  \nCe cas illustre la gravité potentielle d’une embolie pulmonaire aiguë sous-massive, même lorsque la prise en charge initiale par anticoagulation est conforme aux recommandations. La survenue brutale d’un arrêt cardiaque lié à une obstruction complète de l’artère pulmonaire souligne la nécessité d’une surveillance étroite et d’une prise en charge rapide en cas d’aggravation. Les interventions interventionnelles pour retirer le thrombus peuvent être techniquement difficiles et ne garantissent pas toujours le succès. Ce cas rappelle l’importance d’une évaluation multidisciplinaire et d’une adaptation rapide du traitement en fonction de l’évolution clinique."
+        }
+    },
+    {
+        "article": "Un patient de 25 ans a consulté pour une consultation neurochirurgicale concernant sa santé. Ses antécédents comprenaient une chute dans une piscine pendant les vacances deux semaines auparavant. La chute avait entraîné une fracture de la colonne cervicale. Le patient a subi une intervention chirurgicale pendant ses vacances. Une stabilisation postérieure de la colonne cervicale a été réalisée. Le patient portait un collier cervical et la plaie chirurgicale n’avait pas encore cicatrisé, les sutures n’ayant pas encore été enlevées. Le patient ne présentait aucune parésie et pouvait se déplacer seul. Il n’avait pas de documentation médicale détaillée ni de rapports d’examen préopératoire et postopératoire. Au moment de la sortie, on lui a donné une imagerie post-opératoire de la colonne cervicale incomplète sous la forme de quelques vieilles radiographies qui montraient certaines vues, mais sans images numériques. Le résumé de la sortie ne contenait pas la description détaillée du traitement fourni, notamment les détails de l’instrumentation utilisée. Le personnel de l’hôpital ou les opérateurs ne pouvaient pas être contactés parce qu’ils ne répondaient pas au téléphone ou aux e-mails et aux SMS. Nous avons décidé qu’une nouvelle imagerie post-opératoire de la colonne cervicale devait être obtenue. Elle a révélé une fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et\n",
+        "gold_summary": "Nous présentons un cas de fracture atypique du couteau du bourreau causée par une chute en avant dans une piscine et un choc contre le fond de la piscine. Le patient avait subi une opération dans un autre établissement, où une stabilisation postérieure des articulations C2-C3 avait été réalisée. En raison de la présence de vis dans les espaces articulaires C1-C2, le patient ne pouvait pas effectuer de mouvements de rotation de la tête. Une stabilisation antérieure pour prévenir une luxation de C2 contre C3 n'avait pas non plus été réalisée, et une stabilité rachidienne appropriée n'avait pas été assurée. Notre décision de réopérer a été motivée, entre autres facteurs, par notre intention de restaurer les mouvements de rotation de la tête. La chirurgie de révision a été réalisée à partir d'une approche antérieure et postérieure. Après la chirurgie, le patient a pu tourner la tête tout en maintenant la stabilité de la colonne cervicale. Le cas présenté ici représente non seulement un exemple unique de fracture atypique du couteau du bourreau, mais met également en évidence une technique de fixation qui a fourni la stabilité nécessaire pour une fusion réussie. La méthode utilisée a restauré le mouvement de rotation fonctionnel de la tête, préservant ainsi la qualité de vie du patient, ce qui est d'une importance primordiale compte tenu de l'âge du patient.\n",
+        "synthetic_summary": {
+            "B1": "Un jeune homme est tombé dans une piscine. Il s’est fait très mal au cou. Des docteurs ont mis des petits morceaux pour tenir son cou bien droit. Mais il ne pouvait pas tourner sa tête. Alors, d’autres docteurs ont fait une nouvelle opération. Ils ont réparé son cou pour qu’il puisse tourner la tête sans douleur. Maintenant, il va mieux et peut bouger sa tête comme avant. C’est très important pour lui.",
+            "B2": "Voici un résumé adapté pour un élève de 14 ans en biologie :\n\n**Ce qu’ils ont découvert**  \nUn jeune homme de 25 ans est tombé dans une piscine et s’est blessé au cou, plus précisément à la colonne cervicale, qui est la partie haute de la colonne vertébrale dans le cou. Il a eu une fracture compliquée au niveau de la deuxième vertèbre cervicale (appelée C2). Il a été opéré dans un autre hôpital où les chirurgiens ont fixé les vertèbres C2 et C3 par l’arrière du cou avec des vis pour stabiliser la colonne.\n\n**Ce qui posait problème**  \nMalheureusement, les vis ont été placées de manière à bloquer les mouvements de rotation de la tête, car elles touchaient les articulations entre les vertèbres C1 et C2, qui permettent de tourner la tête. De plus, la fixation n’a pas empêché une mauvaise position entre C2 et C3, ce qui aurait pu causer des problèmes de stabilité.\n\n**Ce qu’ils ont fait ensuite**  \nLes médecins ont décidé de refaire une opération pour corriger cela. Cette nouvelle chirurgie a été faite en combinant deux approches : par l’avant et par l’arrière du cou. Grâce à cette intervention, ils ont pu stabiliser correctement la colonne cervicale tout en permettant au patient de tourner la tête normalement.\n\n**Pourquoi c’est important**  \nCe cas est spécial car il montre une fracture rare et une technique chirurgicale qui a réussi à stabiliser la colonne tout en gardant la mobilité de la tête. Cela est très important pour la qualité de vie du patient, surtout qu’il est jeune et a besoin de pouvoir bouger sa tête facilement au quotidien.",
+            "B3": "**Contexte**  \nUn patient de 25 ans a été pris en charge suite à une chute dans une piscine ayant provoqué une fracture complexe de la colonne cervicale, notamment au niveau de la deuxième vertèbre cervicale (C2). Initialement, il avait subi une intervention chirurgicale dans un autre établissement, avec une stabilisation postérieure des vertèbres C2 et C3. Cependant, les documents médicaux fournis étaient incomplets, et l’imagerie post-opératoire initiale montrait un positionnement inapproprié des vis, notamment au niveau de C2, où elles s’étendaient dans l’espace articulaire entre C1 et C2, limitant ainsi la mobilité de la tête.\n\n**Principales Observations**  \n- Fracture atypique du col de C2, incluant une fracture du pars interarticularis (partie de l’arc osseux de la vertèbre) gauche, une dislocation entre C2 et C3, ainsi qu’un déplacement antérieur d’une partie du corps vertébral de C2.  \n- Stabilisation postérieure initiale réalisée, mais avec un mauvais positionnement des vis au niveau de C2, entraînant une fixation excessive de l’articulation C1-C2.  \n- Absence de stabilisation antérieure visant à prévenir la luxation entre C2 et C3, ce qui a compromis la stabilité globale de la colonne cervicale.  \n- Le patient ne présentait pas de déficit moteur et pouvait se déplacer, mais sa mobilité de rotation de la tête était sévèrement limitée.\n\n**Interprétation Clinique**  \nLe cas illustre une fracture complexe et atypique de la colonne cervicale, souvent appelée « fracture du couteau du bourreau », caractérisée par des lésions multiples sur C2 et une instabilité rachidienne importante. La fixation initiale, bien que partiellement correcte au niveau de C3, a été insuffisante et mal positionnée à C2, entraînant une limitation fonctionnelle majeure. La fixation inappropriée dans l’espace articulaire C1-C2 a bloqué la rotation normale de la tête, affectant significativement la qualité de vie du patient, particulièrement à son jeune âge.\n\n**Prochaines Étapes et Prise en Charge**  \nUne réintervention chirurgicale a été décidée afin de corriger la fixation et restaurer la mobilité fonctionnelle. Cette chirurgie de révision a combiné une approche antérieure et postérieure pour :  \n- Retirer ou repositionner les vis mal placées afin de libérer l’articulation C1-C2 et permettre la rotation de la tête.  \n- Réaliser une stabilisation antérieure complémentaire pour prévenir la luxation entre C2 et C3 et assurer une stabilité rachidienne optimale.  \n- Garantir une fusion osseuse solide entre C2 et C3, tout en préservant la fonction articulaire essentielle.\n\nAprès cette intervention, le patient a retrouvé la capacité de tourner la tête tout en maintenant une stabilité cervicale adéquate. Ce cas met en lumière non seulement la complexité des fractures atypiques du col de C2, mais aussi l’importance d’une technique chirurgicale adaptée qui équilibre la stabilité mécanique et la préservation des mouvements fonctionnels. La réussite de cette prise en charge est cruciale pour maintenir la qualité de vie chez un patient jeune, en lui permettant de conserver une mobilité normale de la tête tout en protégeant la colonne cervicale."
+        }
+    },
+    {
+        "article": "Une femme de 29 ans, enceinte de 29 semaines, ayant eu 3 accouchements vaginaux spontanés et dont le dernier enfant avait été livré par césarienne suite à une induction de travail infructueuse 4 ans avant la grossesse en cours, est venue pour un suivi de l'ANC à un âge gestationnel de 32 semaines depuis son LNMP.\n\nAprès avoir examiné les antécédents médicaux, il a été découvert que tous ses enfants étaient en bonne santé, qu'ils allaient bien à l'école et qu'ils n'avaient pas d'antécédents connus de troubles génétiques ou convulsifs. Elle a été examinée au laboratoire de recherche sur les maladies vénériennes (VDRL), à l'antigène de surface de l'hépatite B (HBSag) et à l'analyse d'urine, qui ont tous été négatifs. Toutes les lignées cellulaires du CBC étaient normales, son groupe sanguin était A et son Rh était positif, selon le compte sanguin complet (CBC), le groupe sanguin et le Rh. Une échographie obstétrique a également été réalisée, montrant une échographie anatomique normale de toutes les parties du corps du fœtus, à l'exception du cœur. Une évaluation détaillée de l'échocardiographie fœtale a été réalisée avec les résultats suivants : les deux oreillettes ont une taille comparable et un situs normal. Les deux valves atrioventriculaires et semilunaire sont normalement positionnées avec ouverture et fermeture normales. Les deux ventricules sont comparables en taille et contractilité ; en 2D et en couleur, le ventricule gauche forme le sommet du cœur sans aucun défaut du septum ventriculaire. Mais sur les muscles papillaires du ventricule gauche, il y avait deux masses échogènes circonscrites, rondes, mesurant 18,2 mm par 8,3 mm et 13,5 mm par 8,3 mm. Après évaluation du tractus de sortie, les deux LVOT (ventricule gauche) et RVOT (ventricule droit) ont une anatomie et une fonction normales en utilisant l'évaluation par ultrasons 2D et CF. Selon les résultats de l'écho fœtal, un diagnostic de rhabdomyome cardiaque a été posé. Étant donné qu'il existe un risque élevé de sclérose tubéreuse dans le rhabdomyome cardiaque, une neurosonographie détaillée et d'autres examens systématiques ont été effectués pour rechercher d'autres signes de sclérose tubéreuse. Malgré la recherche d'autres signes de sclérose tubéreuse, aucun autre signe n'a été trouvé autre que la tumeur. Elle a eu un suivi régulier ANC de 32 semaines de gestation à 39 semaines sans aucune complication.\n\nÀ 39 semaines de grossesse plus 1 jour, elle a subi une césarienne pour l'indication d'une grossesse à terme plus une demande de césarienne répétée, avec un résultat de 3200 grammes pour la fille avec un score APGAR de 10 et 10 à la 1re et 5e minutes. La mère et le nouveau-né ont eu une période postopératoire sans problème et ont été libérés le troisième jour.\n\nAprès la naissance, le nouveau-né a été évalué les 1er, 7e et 30e jours pour toute régression ou augmentation de la masse, toute apparition de lésions cutanées ou de convulsions. Tous les résultats des examens physiques étaient normaux, et la taille de la masse était similaire à l'évaluation antepartum.\n\nAu septième mois, l'enfant a été évaluée à nouveau et, après interrogatoire, l'enfant avait un développement excellent pour son groupe d'âge. L'enfant a été examinée pour un retard de développement neurologique et elle grandissait de manière appropriée pour son âge. Une étude d'écholocographie par un cardiologue pédiatrique a révélé des masses hyperechoiques bien circonscrites sur les deux muscles papillaires du ventricule gauche, mesurant chacun 21,8 mm sur 9,2 mm et 14,7 mm sur 8,5 mm et ne créant aucune obstruction de l'écoulement vers le ventricule gauche.\n\nUne histoire familiale a été obtenue, et un examen physique avec mesures anthropométriques a été effectué pour évaluer son état de développement lors de son évaluation de première année. L'enfant se développait normalement, comme les autres enfants de son âge. À l'exception du cœur, tous les systèmes examinés étaient remarquables. Une étude d'échocardiographie a révélé des masses hyperechoiques bien circonscrites sur les deux muscles papillaires du ventricule gauche, sans augmentation de taille et sans obstruction de l'écoulement vers le ventricule gauche.\n",
+        "gold_summary": "Nous rapportons un cas isolé de masse intra-cardiaque fœtale asymptomatique (rhabdomyome) découverte à 32 semaines de gestation et suivie en ambulatoire jusqu'à 39 semaines et un jour, date à laquelle une césarienne a été pratiquée. Après l'accouchement, l'enfant a été évalué au 1er jour, au 7e jour, au 30e jour, au 7e mois et au 12e mois. Après un examen, la croissance anthropométrique et neurocomportementale de l'enfant était saine. À l'exception de la tumeur, qui n'a ni augmenté ni diminué de taille, aucun des critères de diagnostic cliniques du complexe de sclérose tubéreuse n'a été rencontré chez cet enfant jusqu'à l'âge d'un an.\n",
+        "synthetic_summary": {
+            "B1": "Un bébé avait une petite boule dans son cœur avant de naître. Les docteurs ont regardé cette boule plusieurs fois pendant la grossesse. \n\nAprès la naissance, ils ont aussi regardé le bébé souvent. Le bébé grandit bien et est en bonne santé. La petite boule dans le cœur ne change pas de taille. \n\nLe bébé n’a pas d’autres problèmes. Tout va bien pour lui jusqu’à un an.",
+            "B2": "Cas d’une tumeur au cœur chez un bébé avant la naissance\n\nUne femme enceinte de 29 semaines a passé une échographie qui a montré une masse dans le cœur de son bébé. Cette masse, appelée rhabdomyome, est une tumeur bénigne (non cancéreuse) qui peut apparaître dans le muscle du cœur. Les médecins ont suivi la maman et le bébé de près jusqu’à la naissance, qui a eu lieu par césarienne à 39 semaines.\n\nCe qu’ils ont observé après la naissance\n\nLe bébé a été examiné plusieurs fois : au 1er, 7e, 30e jour, puis à 7 et 12 mois. La tumeur est restée de la même taille et n’a pas causé de problème pour le cœur ou la santé générale de l’enfant. Le développement du bébé, c’est-à-dire sa croissance et ses capacités neurologiques (comme bouger et apprendre), était normal.\n\nCe que cela signifie\n\nLe rhabdomyome peut être lié à une maladie appelée sclérose tubéreuse, qui cause des problèmes dans plusieurs organes. Mais dans ce cas, aucun autre signe de cette maladie n’a été trouvé chez l’enfant jusqu’à un an. Cela veut dire que, pour l’instant, la tumeur ne semble pas causer de complications graves. Les médecins continuent de surveiller l’enfant pour s’assurer que tout reste normal.",
+            "B3": "Résumé détaillé et structuré :\n\nContexte  \nNous présentons le cas d’une femme enceinte de 29 semaines, dont la grossesse était suivie régulièrement. Lors d’une échographie obstétricale de routine à 32 semaines, une masse cardiaque fœtale a été détectée. Cette patiente avait un historique obstétrical comprenant trois accouchements vaginaux spontanés et une césarienne quatre ans auparavant. Aucun antécédent familial ou personnel de troubles génétiques ou convulsifs n’était rapporté.\n\nPrincipales observations  \nL’échocardiographie fœtale a révélé deux masses bien délimitées, échogènes (c’est-à-dire visibles en échographie) sur les muscles papillaires du ventricule gauche, mesurant environ 18 x 8 mm et 13 x 8 mm. Ces masses n’entraînaient aucune obstruction du flux sanguin ni anomalie fonctionnelle du cœur. Les autres organes et systèmes du fœtus étaient normaux, et les analyses maternelles (tests infectieux, groupe sanguin, etc.) ne montraient aucune anomalie. En raison de la nature des masses, un diagnostic de rhabdomyome cardiaque fœtal a été posé. Ce type de tumeur bénigne du muscle cardiaque est fréquemment associé à la sclérose tubéreuse, une maladie génétique caractérisée par la formation de tumeurs bénignes dans plusieurs organes. Par conséquent, des examens complémentaires, notamment une neurosonographie, ont été réalisés pour rechercher d’autres signes de sclérose tubéreuse, sans résultat positif.\n\nInterprétation clinique  \nLe suivi prénatal s’est poursuivi sans complication jusqu’à 39 semaines et un jour, où une césarienne programmée a été réalisée. La naissance s’est déroulée normalement, avec un nouveau-né en bonne santé, pesant 3200 grammes et présentant un score APGAR optimal (10/10 aux 1re et 5e minutes). Après la naissance, l’enfant a été suivi régulièrement aux 1er, 7e, 30e jours, puis à 7 et 12 mois. Les masses cardiaques ont été surveillées par échocardiographie pédiatrique, montrant une légère augmentation de taille (jusqu’à environ 22 x 9 mm et 15 x 8 mm) mais sans obstruction ni impact fonctionnel. Aucun signe clinique de sclérose tubéreuse (comme des lésions cutanées, des convulsions ou un retard de développement neurologique) n’a été observé. Le développement neurocomportemental et la croissance physique de l’enfant étaient normaux et adaptés à son âge.\n\nProchaines étapes  \nCe cas illustre l’importance d’un suivi échocardiographique et clinique rigoureux des rhabdomyomes cardiaques fœtaux, en particulier pour exclure ou détecter précocement une sclérose tubéreuse. Bien que cette maladie puisse s’accompagner de complications sévères, l’absence d’autres signes cliniques jusqu’à l’âge d’un an est rassurante. La surveillance pédiatrique doit se poursuivre pour détecter toute évolution tardive. Ce suivi multidisciplinaire permet d’assurer une prise en charge adaptée et un pronostic favorable pour l’enfant."
+        }
+    },
+    {
+        "article": "Un garçon de terme avec un poids à la naissance de 3 kg a été livré par césarienne en raison de la détresse fœtale. Il a pleuré immédiatement après la naissance. Des soins de routine ont été donnés et à 10 minutes de vie, il a été remarqué qu'il avait une faible lecture de SpO2 (saturation en oxygène) de 75-80%. Ainsi, il a été mis sous oxygène par boîte de tête à 5 L/min. Il a eu de bons efforts respiratoires avec une tachypnée modérée. Comme il continuait d'avoir une faible SpO2 même après un essai à la fois de 5 L/min d'oxygène de la boîte de tête et de PEEP (pression expiratoire positive) du réanimateur en pièce T avec 6 cm d'eau avec FiO2 (fraction d'oxygène inspirée) à 100%, il a été intubé et a commencé une ventilation à pression positive. Le bébé a été transféré à l'unité de soins intensifs néonatals pour une gestion ultérieure.\n\nMême après ventilation mécanique en mode synchronisée intermittent obligatoire (SIMV) avec des pressions stabilisatrices maximales de PEEP 6 cm et une pression de pointe de 20 cm d'eau et une sédation adéquate, la SpO2 maximale atteinte était de 80 %. Il avait une cyanose et des signes de mauvaise perfusion (tachycardie et temps de remplissage capillaire prolongé). Le bébé a donc été mis sous soutien inotrope après un bolus de solution saline normale. Les différentiels initiaux considérés étaient le choc septique, le pneumothorax, les malformations pulmonaires et la cyanose cardiaque. Une culture sanguine a été effectuée et le bébé a été mis sous antibiotiques de première ligne. La radiographie thoracique a montré une ombre cardiaque normale et des champs pulmonaires normaux. Un échocardiogramme a été effectué qui a exclu une hypertension pulmonaire persistante et une maladie cardiaque structurelle.\n\nLes gaz sanguins artériels réalisés après 1 h de ventilation (à 2 h de vie) ont montré un pH de 7,5, paCO2 de 19,1 mmHg, paO2 de 199 mmHg, lactate de 4 mmol/L, bicarbonate de 18,1 mmol/L et un excès de base de −3,6. Comme il y avait une hyperoxémie inexpliquée malgré une faible SpO2 et une cyanose persistante, une méthémoglobinémie a été suspectée, ce qui a été confirmé par un niveau élevé de metHb (méthémoglobine) (7,6 %). Les valeurs de gaz sanguins en série ont montré une hyperoxémie et des niveaux élevés de metHb. Il a reçu une dose unique de 3 mg de bleu de méthylène par voie intraveineuse et a commencé à prendre de l'acide ascorbique oral à 300 mg une fois par jour. Ses paramètres ventilatoires ont été progressivement sevré et il a été extubé après 16 h à l'air ambiant. Les inotropes ont également été réduits et arrêtés en 24 h. Comme sa culture sanguine n'avait pas de croissance, les antibiotiques ont été arrêtés après 2 jours. À partir du jour 2 de la vie, il a maintenu une saturation de 75 à 85 % en air ambiant.\n\nIl n'y avait pas de données pertinentes sur les antécédents périnataux et familiaux. Le taux de glucose-6-phosphate déshydrogénase et l'électrophorèse de l'hémoglobine étaient également normaux. Depuis le jour 3, il recevait des aliments orogastriques et était par ailleurs stable, à l'exception d'une cyanose persistante. Après l'envoi d'un test génétique (exome clinique), il a été renvoyé à la maison le jour 9, tout en recevant des aliments par voie orale, car il restait stable, à l'exception d'une cyanose et d'une faible lecture de SpO2 (80-85 %) en air ambiant avec un paO2 normal.\n\nAprès la décharge, le bébé a été suivi régulièrement et à 2 mois de vie, sa saturation en air ambiant était de 88 à 90 % et à 4 mois, sa SpO2 était > 92 % en air ambiant sans cyanose. L'exome clinique a montré une mutation dans la chaîne gamma de l'hémoglobine fœtale - substitution d'acides aminés de la tyrosine par l'histidine au codon 63 (p.His63Tyr) en raison d'une mutation de sens erroné dans le gène HBG2 (chr11:g.5275647G>A). Une fois que nous avons reçu le résultat du test génétique, l'acide ascorbique oral a été arrêté et les parents ont été conseillés sur l'excellent pronostic de cette maladie rare. À 5 mois de vie, il était bien, acyanotique et son niveau de metHb était normal.\n",
+        "gold_summary": "Nous rapportons un nouveau-né présenté avec cyanose et désaturation dès la naissance, qui a ensuite été trouvé métémoglobinémique et a commencé un traitement. L'évaluation génétique a révélé une mutation dans la chaîne gamma de l'hémoglobine fœtale (HbF) provoquant une hémoglobine anormale. Les mutations physiologiquement significatives dans les gènes de la gamma-globine provoquent des symptômes chez le fœtus et le nouveau-né qui disparaissent progressivement au cours des premiers mois de la vie.\n",
+        "synthetic_summary": {
+            "B1": "Un bébé est né avec une couleur un peu bleue. Il avait du mal à bien respirer. Les docteurs ont trouvé que son sang avait un problème spécial. Ce problème vient d’un petit changement dans une partie du sang appelée hémoglobine. Ce changement fait que le bébé a moins d’oxygène dans son corps. \n\nAvec des médicaments et du temps, le bébé est devenu de plus en plus fort. Après quelques mois, il a commencé à aller mieux tout seul. Ce problème disparaît souvent quand les bébés grandissent un peu. Les docteurs ont dit aux parents que tout allait bien maintenant.",
+            "B2": "Un bébé est né avec une couleur bleutée de la peau (cyanose) et un faible taux d’oxygène dans le sang (désaturation). Après des examens, on a découvert qu’il avait un problème appelé méthémoglobinémie. Cela signifie que son sang contenait une forme d’hémoglobine (la protéine qui transporte l’oxygène) qui ne fonctionnait pas bien. \n\nUn test génétique a montré que ce bébé avait une mutation dans une partie spéciale de l’hémoglobine appelée chaîne gamma, qui est présente surtout chez les bébés avant la naissance (hémoglobine fœtale). Cette mutation rend l’hémoglobine anormale et cause les symptômes observés. \n\nHeureusement, ce problème disparaît généralement tout seul en quelques mois, car l’hémoglobine normale remplace peu à peu l’hémoglobine fœtale. Le bébé a reçu un traitement pour aider son sang à mieux transporter l’oxygène et s’est amélioré avec le temps. Les médecins ont expliqué aux parents que cette maladie rare a un très bon pronostic.",
+            "B3": "Résumé détaillé pour un public non spécialiste\n\nContexte  \nUn nouveau-né à terme, pesant 3 kg, est né par césarienne en raison d’une souffrance fœtale. Dès la naissance, il a présenté une cyanose (coloration bleutée de la peau liée à un manque d’oxygène) et une saturation en oxygène (SpO2) anormalement basse, autour de 75-80 %, malgré une bonne respiration initiale. Malgré plusieurs interventions, dont l’oxygénothérapie, l’intubation et la ventilation mécanique, sa saturation restait faible et il montrait des signes de mauvaise perfusion sanguine.\n\nPrincipales observations  \nLes examens initiaux ont exclu des causes fréquentes telles que le choc septique, un pneumothorax (présence d’air dans la cavité pleurale), des malformations pulmonaires ou des maladies cardiaques congénitales. Les gaz du sang ont révélé une hyperoxémie (taux élevé d’oxygène dans le sang artériel) paradoxale malgré la faible saturation mesurée, ce qui a conduit à suspecter une méthémoglobinémie. Cette maladie est caractérisée par une augmentation de la méthémoglobine, une forme anormale d’hémoglobine incapable de transporter efficacement l’oxygène. Ce diagnostic a été confirmé par un taux élevé de méthémoglobine (7,6 %). Le bébé a reçu un traitement par bleu de méthylène intraveineux, suivi d’une supplémentation orale en acide ascorbique (vitamine C), ce qui a permis une amélioration progressive de sa saturation et une extubation réussie.\n\nInterprétation clinique  \nL’analyse génétique a identifié une mutation dans le gène HBG2, responsable de la chaîne gamma de l’hémoglobine fœtale (HbF). Cette mutation entraîne la substitution d’un acide aminé (tyrosine remplacée par histidine) dans la molécule d’hémoglobine, provoquant la formation d’une hémoglobine anormale qui favorise la méthémoglobinémie. Ce type de mutation est rare mais physiologiquement significative, car elle affecte principalement les nouveau-nés et les fœtus, chez qui l’hémoglobine gamma est prédominante. Les symptômes, notamment la cyanose et la désaturation, tendent à disparaître progressivement dans les premiers mois de la vie, au fur et à mesure que l’hémoglobine fœtale est remplacée par l’hémoglobine adulte.\n\nProchaines étapes et pronostic  \nAprès stabilisation, le bébé a été suivi régulièrement. Sa saturation en oxygène s’est améliorée avec le temps, atteignant plus de 92 % à quatre mois sans cyanose. Le traitement par acide ascorbique a été arrêté une fois le diagnostic confirmé. Les parents ont été informés de l’excellent pronostic de cette maladie rare, qui ne nécessite généralement pas de traitement à long terme. À cinq mois, l’enfant était en bonne santé, sans cyanose, avec un taux normal de méthémoglobine.\n\nEn résumé, ce cas illustre une forme rare de méthémoglobinémie congénitale liée à une mutation de l’hémoglobine fœtale, responsable d’une cyanose néonatale persistante mais transitoire, avec un bon pronostic à moyen terme."
+        }
+    },
+    {
+        "article": "Homme de 35 ans ayant des antécédents de rupture totale du ligament croisé antérieur il y a 10 ans. Il a suivi un traitement conservateur avec immobilisation pendant quatre semaines, puis une physiothérapie pendant six mois avec une amélioration partielle des symptômes. À la fin du traitement conservateur, il a effectué des activités de la vie quotidienne sans limitation apparente jusqu'à un mois avant la nouvelle évaluation, avec une douleur de 6/10 sur l'échelle EVA du genou et une sensation d'instabilité en descendant les escaliers et un œdème intermittent, sans nouveau mécanisme de blessure. L'examen physique a révélé une douleur à la palpation sur la ligne articulaire latérale et la surface antérieure du genou ; arcs de mobilité du genou avec flexion active de 85° et flexion passive de 100°, extension complète. Force par groupes musculaires du genou 5/5 avec douleur référée à la face antérieure du genou. Les manœuvres spéciales pour évaluer cliniquement l'articulation du genou ont révélé : élévation antérieure, Lachman, Lelli : positive ; McMurray, Steinman et Apley latéral et médial : positive. Une résonance magnétique simple du genou droit a été demandée, elle a révélé : absence de LCA, arthrose grade III-IV du compartiment fémoro-tibial médial, arthrose grade II du compartiment fémoro-tibial latéral, amincissement de la corne postérieure et du corps du ménisque latéral avec une partie résiduelle minimale, déchirure horizontale de la corne postérieure et du corps du ménisque médial, oedème du ligament croisé postérieur (LCP) avec changement de la dégénérescence mucoïde. Des mesures radiographiques ont été prises pour l'intercondylé et l'angle alpha, en coupe axiale et sagittale, respectivement. Il a été décidé de procéder à une arthroscopie du genou. Avant la procédure chirurgicale et sous anesthésie générale, le test de pivot shift a été effectué, qui s'est révélé positif avec un degré III. Une arthroscopie a été effectuée, révélant : déchirure fermée et invétérée complète du LCA, pincement du LCP, rupture du corne postérieur et du corps du ménisque latéral, rupture chronique invétérée et extrudée du ménisque médial, pincement fémoro-tibial antérieur, corps libres intra-articulaires, lésion condrale de 1 cm2 sur le condyle fémoral latéral dans la zone de charge, arthrose grade IV du compartiment fémoro-tibial médial, synovite sous-quadricipitale. 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déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchir\nEn raison du degré d'arthrose, il a été décidé de ne pas effectuer de tunnels du LCA pour éviter de futures complications lors de la chirurgie définitive d'arthroplastie du genou. Après la chirurgie, l'utilisation d'un mobilisateur passif du genou de 0° d'extension à 100° de flexion ainsi que la marche assistée par des béquilles ont été indiqués.\nLe jour suivant l'opération, le patient a quitté l'hôpital sans complications et a commencé une physiothérapie pour renforcer et stabiliser les muscles. Au cours des visites de suivi à trois, six et neuf mois, le patient a déclaré ne présenter aucun symptôme, pouvoir effectuer ses activités quotidiennes sans aucune restriction et pratiquer des activités sportives à faible impact sans aucune entrave.\n",
+        "gold_summary": "Nous présentons le cas d'un patient de 35 ans avec rupture du LCA involuée de 10 ans. Avec une gestion conservatrice initiale qui évolue vers une instabilité du genou et une douleur dans la ligne articulaire médiale et latérale, ainsi qu'une augmentation du volume et une limitation fonctionnelle. Après des études diagnostiques, il est décidé de procéder à une arthroscopie diagnostique-thérapeutique et un suivi étroit est poursuivi pour la pathologie associée.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur a eu mal au genou il y a longtemps. Son genou était cassé à l'intérieur. Au début, il a pris soin de son genou sans opération. Mais après, son genou faisait encore mal et bougeait mal. Le docteur a regardé dedans avec une petite caméra. Puis, il a aidé le genou à guérir. Maintenant, le monsieur va mieux et peut bouger sans douleur.",
+            "B2": "Cas d’un homme de 35 ans avec une rupture du ligament croisé antérieur (LCA) datant de 10 ans. Au début, il a suivi un traitement sans chirurgie, avec immobilisation et rééducation. Cela a amélioré un peu ses symptômes, mais il a ensuite ressenti une douleur au genou, surtout sur les côtés, et une sensation d’instabilité, notamment en descendant les escaliers. Son genou gonflait parfois et il avait du mal à plier complètement la jambe.\n\nDes examens, dont une IRM (une sorte de photo détaillée de l’intérieur du genou), ont montré que le ligament croisé antérieur était complètement déchiré. Il y avait aussi des signes d’arthrose, c’est-à-dire que le cartilage du genou s’était usé, surtout à l’intérieur du genou. De plus, les ménisques, qui sont des sortes de coussins dans le genou, étaient abîmés et déchirés.\n\nPour mieux comprendre et traiter ces problèmes, les médecins ont réalisé une arthroscopie. C’est une opération où ils regardent à l’intérieur du genou avec une petite caméra. Ils ont confirmé la déchirure complète du ligament, les lésions des ménisques, l’usure du cartilage et une inflammation de la membrane qui entoure le genou.\n\nÀ cause de l’arthrose avancée, ils ont décidé de ne pas reconstruire le ligament tout de suite, car cela pourrait compliquer une future opération pour remplacer le genou (arthroplastie). Après l’opération, le patient a commencé une rééducation pour renforcer ses muscles et améliorer la stabilité de son genou.\n\nLors des contrôles à 3, 6 et 9 mois, il n’avait plus de douleur ni d’instabilité. Il pouvait faire ses activités normales sans problème et pratiquer des sports doux. Ce suivi montre que l’arthroscopie et la rééducation ont bien aidé à gérer sa douleur et à améliorer sa qualité de vie malgré la blessure ancienne.",
+            "B3": "Résumé détaillé et structuré pour un public non-médecin éduqué\n\nContexte  \nUn homme de 35 ans présente une rupture complète du ligament croisé antérieur (LCA) de son genou droit datant de dix ans. Initialement, il a suivi un traitement sans chirurgie, comprenant une immobilisation puis une rééducation, ce qui avait permis une amélioration partielle. Cependant, un mois avant la nouvelle consultation, il a ressenti une douleur modérée (6 sur 10) et une sensation d’instabilité en descendant les escaliers, accompagnées d’un gonflement intermittent, sans qu’un nouvel accident ne soit survenu.\n\nPrincipales observations  \nL’examen clinique a montré une douleur localisée sur les côtés et à l’avant du genou, une limitation de la flexion active (85°) et passive (100°), avec une extension complète. La force musculaire était conservée mais douloureuse à certains mouvements. Plusieurs tests spécifiques du genou, destinés à évaluer la stabilité et l’intégrité des structures ligamentaires et méniscales, se sont révélés positifs, indiquant une instabilité importante et des lésions associées. L’imagerie par résonance magnétique a confirmé l’absence du LCA, des signes avancés d’arthrose (usure du cartilage) dans les compartiments internes et externes du genou, ainsi que des déchirures des ménisques médial et latéral, et des modifications du ligament croisé postérieur (LCP). L’arthroscopie (examen visuel interne du genou) a confirmé ces lésions, révélant une rupture complète et ancienne du LCA, des déchirures méniscales chroniques, des corps libres dans l’articulation, une lésion du cartilage sur le condyle fémoral latéral, une arthrose sévère du compartiment médial, et une inflammation de la membrane synoviale.\n\nInterprétation clinique  \nLa rupture ancienne du LCA associée à une arthrose avancée et à des lésions méniscales chroniques explique les symptômes d’instabilité, de douleur et de limitation fonctionnelle. En raison du degré élevé d’arthrose, il a été décidé de ne pas reconstruire le LCA par chirurgie ligamentaire classique, afin d’éviter des complications lors d’une éventuelle future arthroplastie (remplacement articulaire) du genou.\n\nProchaines étapes  \nLe patient a bénéficié d’une arthroscopie pour traiter certaines lésions et améliorer les symptômes. Après l’intervention, une mobilisation passive du genou (avec un appareil limitant les mouvements entre 0° et 100° de flexion) et une marche assistée par béquilles ont été prescrites. Une rééducation a été mise en place pour renforcer les muscles et stabiliser l’articulation. Lors des suivis à trois, six et neuf mois, le patient a rapporté une disparition des douleurs et de l’instabilité, une reprise complète des activités quotidiennes sans restriction, ainsi que la possibilité de pratiquer des sports à faible impact sans gêne.\n\nEn résumé, ce cas illustre la prise en charge d’une rupture ancienne du ligament croisé antérieur compliquée d’arthrose sévère et de lésions méniscales, où la chirurgie arthroscopique et la rééducation ont permis d’améliorer significativement la qualité de vie du patient malgré l’absence de reconstruction ligamentaire."
+        }
+    },
+    {
+        "article": "Notre patient est un homme hispanique de 37 ans en bonne santé qui a subi une rupture simultanée de ses tendons rotuliens bilatéraux après avoir sauté en tentant de faire un « panier de lay-up » en jouant au basket-ball. Les antécédents pertinents comprennent une reconstruction du ligament croisé antérieur (LCA) du genou droit en utilisant un autogreffe de tendon patellaire osseux ipsilatéral (BPTB) en 2002. Le patient était incapable de marcher et s’est présenté à notre clinique en fauteuil roulant. Le patient était incapable d’effectuer une élévation de la jambe droite et avait un défaut sensible au pôle inférieur de la patella bilatéralement. Les radiographies en plan ont démontré une patella alta bilatérale et les études d’IRM ont démontré des ruptures du tendon patellaire proximal bilatéral. La recommandation pour une réparation chirurgicale aiguë simultanée des deux genoux a été donnée au patient.\n\nTechnique opératoire\nL'examen intraopératoire a révélé une importante enflure des deux genoux, avec une extension et une flexion complètes à 140 degrés bilatéralement. Il y avait un défaut palpable et une patella alta bilatérale associée à une rupture du tendon rotulien.\n\nLe genou a été abordé par l'approche standard antérieure médiane. L'étendue de la déchirure a été élucidée, impliquant à la fois le réticulum médial et latéral. Un hématome a été évacué, et les tissus profonds et sous-cutanés ont été irrigués. Des sutures de traction ont été placées dans le tendon quadriceps pour aider à mobiliser la rotule distalement. Le tendon patellaire proximal et le moignon distal du tendon patellaire ont été élucidés.\n\nDeux ancrages de suture bio-composites SwiveLock de 4,75 mm (système d'implant SpeedBridge avec aiguille Scorpion-Multifire, Arthrex, Inc., n° AR-2600SBS-8) ont été placés dans le pôle inférieur de la rotule à l'origine du tendon rotulien. Une suture de verrouillage de Krackow a été réalisée avec chacun des ancrages de suture SwiveLock avec une suture de traction. Cette dernière a été amenée vers le haut et vers le bas du tendon rotulien dans une configuration de suture de verrouillage. Le genou a été placé en flexion à 30 degrés et la longueur du tendon rotulien a été fixée à 4,5 cm. Comme le patient ne disposait pas d'un tendon rotulien contra-latéral intact pour servir de base à la longueur du tendon rotulien, 4,5 cm a été choisi car il s'agit d'une longueur de tendon rotulien moyenne chez les hommes, récemment décrite dans la littérature. Une fluoroscopie intraopératoire en C-arm a été utilisée pour confirmer la hauteur du tendon rotulien. Cette dernière a été vérifiée par un double contrôle en tentant d'obtenir un indice de Caton-Deschamps d'environ 1:1. Les nœuds ont ensuite été noués à partir de la configuration de suture de verrouillage dans la réparation supérieure vers les ancrages de suture dans la rotule.\n\nLes mêmes ancrages avaient des sutures #2 FiberTape (Arthrex, Inc) chargées. Elles étaient croisées dans une configuration de pont de suture et placées dans des ancrages SwiveLock séparés dans le tubercule tibial avec le genou à 30 degrés de flexion. Le paratenon restant et les tissus mous ont été imbriqués pour aider à renforcer la réparation. Le rétaintec médiale et latérale ont ensuite été réparés avec une suture #2 FiberWire de verrouillage (Arthrex, Inc). Après une irrigation approfondie des tissus profonds et sous-cutanés, une fermeture standard en couches a ensuite été réalisée.\n\nLe genou gauche a été traité ensuite de la même manière. À la fin de cette procédure, chaque genou était capable d'obtenir une flexion de 0 à 30 degrés sans aucune tension excessive sur les réparations.\n\nSuivi des patients\nLe patient a été maintenu en position non portante, à l’exception des transferts, pendant 6 semaines après l’opération. Les deux genoux étaient initialement bloqués en pleine extension avec une attelle. Deux jours après l’opération, le patient a commencé une thérapie physique avec une machine de mouvement passif continu, augmentant d’environ 15° par semaine. Après 6 semaines, le patient a commencé à supporter tout son poids avec des attelles bloquées en extension avec un déambulateur. Son ROM était d’environ 0-110° sur les deux jambes, et il pouvait effectuer des élévations de la jambe droite sans difficulté.\n\nÀ 10 mois, il a démontré une force quadriceps de 5/5, une extension de -10° et une flexion de 140° bilatéralement. Le score IKDC (Knee Documentation Committee) était de 57 bilatéralement.\n\nÀ 12 mois, le patient avait un alignement normal avec une force quadriceps symétrique bilatérale. Sa ROM restait à −10 degrés d'extension passive non corrigée et 140 degrés de flexion bilatérale. Le score IKDC du genou droit et gauche du patient s'est amélioré à 69 et 72, respectivement. Son score Lysholm enregistré à 12 mois pour son genou droit et gauche était de 94 et 99, respectivement.\n",
+        "gold_summary": "Nous décrivons le cas d'un homme de 37 ans qui a présenté une rupture bilatérale simultanée du tendon rotulien sans aucun facteur de risque associé. En outre, il s'agit de la première utilisation rapportée de la technique de suture-pont avec des ancrages de suture rotuliens et tibiaux pour réparer une rupture bilatérale proximale du tendon rotulien. Au suivi à 12 mois, le patient avait un alignement normal, aucune épanchement et une force quadriceps symétrique.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 37 ans s’est fait très mal aux deux genoux en même temps. Ses tendons, qui aident à bouger ses jambes, se sont cassés. Les docteurs ont réparé ses tendons avec une méthode spéciale. Un an après, ses genoux allaient bien. Il pouvait bouger ses jambes normalement et sans douleur.",
+            "B2": "Cas d’un homme de 37 ans avec rupture des deux tendons rotuliens\n\nNous racontons ici l’histoire d’un homme de 37 ans en bonne santé qui s’est cassé en même temps les deux tendons rotuliens. Ces tendons relient la rotule (l’os devant le genou) au tibia (l’os de la jambe). Cette blessure est rare, surtout sans cause évidente.\n\nUne nouvelle méthode de réparation\n\nLes médecins ont utilisé une technique spéciale appelée « suture-pont ». Cela consiste à fixer les tendons avec des petits ancrages, un côté sur la rotule et l’autre sur le tibia, pour bien les recoller. C’est la première fois que cette méthode est décrite pour ce type de blessure des deux genoux en même temps.\n\nRésultats après un an\n\nUn an après l’opération, le patient avait un bon alignement des genoux, sans gonflement ni douleur. Il avait retrouvé une force normale dans ses muscles du devant de la cuisse (quadriceps) des deux côtés. Cela montre que la réparation a bien fonctionné et que le patient a pu récupérer sa mobilité.",
+            "B3": "Résumé destiné à un public adulte non spécialiste\n\nContexte  \nNous rapportons le cas d’un homme de 37 ans, en bonne santé générale, qui a subi simultanément une rupture des deux tendons rotuliens (les tendons situés juste en dessous de la rotule, essentiels pour l’extension du genou) sans facteur de risque apparent. Ce type de blessure bilatérale est extrêmement rare, surtout chez une personne sans antécédents médicaux majeurs.\n\nPrincipales observations et intervention chirurgicale  \nLe patient ne pouvait plus marcher ni lever la jambe droite, et présentait une position anormalement haute des rotules (patella alta) confirmée par radiographies et IRM, indiquant une rupture proximale des tendons rotuliens des deux genoux. Une réparation chirurgicale simultanée des deux tendons a été réalisée.\n\nLa technique opératoire utilisée était innovante : des ancrages de suture bio-composites ont été placés à la base des rotules et au niveau des tubercules tibiaux (parties osseuses du genou), permettant de fixer solidement les tendons en utilisant une configuration appelée « suture-pont ». Cette méthode assure une réparation stable en répartissant les forces sur plusieurs points d’ancrage. La longueur du tendon a été ajustée à une mesure moyenne connue chez les hommes, car le tendon intact du côté opposé n’était pas disponible pour référence. La réparation a été renforcée par la suture des tissus mous environnants. Les deux genoux ont été traités de manière identique.\n\nSuivi et résultats cliniques  \nAprès l’opération, le patient a été immobilisé en extension pendant 6 semaines, avec une rééducation progressive débutée dès le deuxième jour grâce à un appareil de mouvement passif. À 6 semaines, il a pu commencer à supporter son poids avec des attelles. À 10 mois, la force musculaire du quadriceps était maximale (5/5), avec une amplitude de mouvement du genou allant de -10° en extension (légère limitation) à 140° en flexion, et un score fonctionnel modéré (IKDC 57). À 12 mois, l’alignement des genoux était normal, la force musculaire symétrique, et la mobilité maintenue. Les scores fonctionnels se sont améliorés (IKDC 69-72, score Lysholm 94-99), témoignant d’une excellente récupération.\n\nInterprétation clinique  \nCe cas illustre une rupture bilatérale simultanée du tendon rotulien chez un patient sans facteurs de risque, traitée avec succès par une technique chirurgicale innovante utilisant des ancrages de suture en configuration « pont ». Cette méthode a permis une réparation solide et une récupération fonctionnelle satisfaisante à un an, avec un retour à une force musculaire normale et une bonne mobilité.\n\nProchaines étapes  \nLe suivi à plus long terme permettra de confirmer la durabilité de cette réparation et la récupération fonctionnelle complète. Cette technique pourrait représenter une option efficace pour des cas similaires de ruptures bilatérales du tendon rotulien."
+        }
+    },
+    {
+        "article": "Patient de 4 ans, sexe masculin, ayant des antécédents d'impétigo nasal deux semaines avant son admission (traité avec mupirocine topique et céfadroxil oral ; dose, durée et adhérence au traitement inconnus), sans autres antécédents morbides, qui a présenté une hématurie macroscopique glomérulaire associée à un œdème des membres inférieurs de 5 jours d'évolution, auxquels s'ajoutent les douze dernières heures avant la consultation, céphalée, nausées et vomissements. Il s'est rendu au service d'urgence (SU) en état convulsif, après 20 minutes de convulsion tonique-clonique généralisée.\n\nLors de son admission au SU, le patient était apyrétique, avec une pression artérielle non évaluable, un état de conscience quantitatif associé à une hypertonie généralisée et un œdème pré-palpébral et pré-tibial. L'intubation endotrachéale a été décidée et le phénobarbital (10 mg/kg) a été administré pour gérer le statut convulsif.\n\nLors de l'examen physique en unité de soins intensifs (USI), la tension artérielle était de 134/94 mmHg (PAM 110 mmHg) (p95 pour le patient 108/66 mmHg, p95+12 120/78 mmHg).\n\nLes paramètres de laboratoire initiaux comprenaient : urine complète avec hématurie (> 100 érythrocytes par champ), protéinurie 3+ et leucocyturie 10-25 par champ, créatinémie 0,3 mg/dL, anémie avec hématocrite (HTO) 21 %, hémoglobine (Hb) 7 g/dL, avec volume corpusculaire moyen (VCM) et concentration d'hémoglobine corpusculaire moyenne (CHCM) normaux, leucocytose de 23 900 cellules/mm3, thrombocytose de 756 000/mm3, sans élévation des réactifs de phase aiguë, hypocomplémentémie avec niveau de complément C3 à 25 mg/dL (valeur normale, VN : 80-150 mg/dL) et C4 normal. Le test rapide d'antigène pour Streptococcus beta-hémolytique groupe A (Streptococcus pyogenes) dans la gorge a été positif et l'Antiestreptolisine O (ASO) a été (+). La tomographie par ordinateur du cerveau sans contraste n'a pas montré de changements aigus. L'échographie rénale a conclu une néphromégalie bilatérale avec augmentation de l'échogénicité corticale et diminution de la différenciation corticomédullaire.\n\nLe patient a été diagnostiqué avec un syndrome néphrétique par GNAPE compliqué d'urgence hypertensive - état convulsif.\n\nAu cours des 24 premières heures de son séjour en USI, le patient a eu besoin d'une ventilation mécanique (VM) et d'une thérapie anticonvulsivante avec du phénobarbital. Il a évolué sans crise épileptique, avec un électroencéphalogramme (EEG) normal (au lendemain de son admission) et une étude du liquide céphalorachidien normale. Une thérapie antibiotique a été initiée pour éradiquer Streptococcus pyogenes avec du cefotaxime et une thérapie diurétique avec du furosémide.\n\nLe jour suivant, il a présenté une détérioration de la fonction rénale avec une augmentation de la créatinine à 0,99 mg/dL, une hypertension artérielle et une protéinurie de 24 heures de 36,6 mg/m2/h, sans oligurie. Il a commencé un traitement antihypertenseur avec amlodipine et labetalol intraveineux, avec un bon contrôle initial.\n\nÉtant donné l'évolution favorable, l'extubation a été réalisée au bout de 48 heures, et elle a été bien tolérée du point de vue ventilatoire. Néanmoins, après 24 heures d'extubation, le patient a vu sa conscience s'aggraver, avec une ouverture oculaire et un retrait des membres uniquement en réponse à une stimulation douloureuse et une faible réponse verbale (échelle de coma de Glasgow 8), et a développé une tension artérielle > p95+12 malgré une thérapie par labetalol en perfusion continue (jusqu'à 3 mg/kg/h), amlodipine (10 mg/jour) et furosémide, nécessitant à nouveau une VM et une perfusion de nitroprussiate de sodium (jusqu'à 3 mcg/kg/min), dans le but de réduire progressivement la tension artérielle (25 % par jour) pour prévenir des dommages neurologiques secondaires. Étant donné la présence de symptomatologie neurologique aiguë associée à l'hypertension artérielle chez un patient souffrant de glomérulonéphrite, le diagnostic de PRES a été suspecté, et a été confirmé par une IRM du cerveau (jour 5), qui a montré une augmentation du signal sous-cortical dans la région occipitale bilatérale et symétrique, sans restriction de la diffusion, compatible avec un oedème vasogénique (PRES). L'évaluation ophtalmologique était normale, et un nouvel EEG a révélé des épisodes occasionnels de dépression de tension généralisée.\n\nL'énalapril a été ajouté au traitement. Finalement, après 10 jours de sevrage pharmacologique lent, la tension artérielle a été normalisée. L'IRM de contrôle (jour 12) a révélé une régression des résultats précédents. L'extubation a été réussie après 5 jours.\n\nPendant son séjour à l’unité de soins intensifs, la concentration d’hémoglobine a chuté à 5 g/dL, avec un volume corpusculaire moyen et une concentration d’hémoglobine corpusculaire moyenne normaux, sans plaquétopénie, ce qui a fait suspecter une anémie hémolytique en raison d’un test de Coombs direct positif et d’une hémoglobinurie. Deux transfusions de globules rouges ont été nécessaires. Il a été décidé de commencer un traitement stéroïdien avec du méthylprednisolone (1 mg/kg/j) pendant 72 heures. Le coprocultures était négatif, tout comme l’antigène urinaire pour Streptococcus pneumoniae. Une sérologie pour virus Epstein-Barr et Parvovirus B19, un profil d’antigènes nucléaires extractibles (ENA), des anticorps anti-cytoplasme des neutrophiles (ANCA), des anticorps anti-ADN, des anticorps anti-B2 glycoprotéine 1, des anticorps anti-cardiolipines et un anticoagulant lupique, qui ont tous été négatifs. Toutes les cultures étaient négatives (cultures sanguines, urinaires, aspirats endotrachéaux et pharyngés). Seul ANA (anticorps antinucléaires) positif 1/160 a été noté.\n\nL’état du patient s’est amélioré, avec une tension artérielle plus basse, un taux de complément plus élevé et une urine sans protéinurie ni hématurie. Le test de Coombs direct est resté positif au neuvième jour de l’hospitalisation.\n\nLe patient a quitté l'hôpital le 31e jour, normotendu, sans anémie, avec une fonction rénale préservée, sans protéinurie ni hématurie, avec une normalisation des taux de C3 et asymptomatique du point de vue neurologique. Il a été libéré avec un traitement pharmacologique avec prednisone, amlodipine, enalapril et acide folique. Le patient n'a pas présenté de récidive et est resté asymptomatique 6 mois après la sortie.\n",
+        "gold_summary": "Patient de 4 ans, avec des antécédents de 5 jours d'hématurie et d'œdème, auxquels s'ajoutaient des céphalées, des nausées et des vomissements, a présenté un état convulsif et une crise hypertensive. Les résultats de laboratoire ont révélé une hypocomplémentémie C3 et des titres élevés d'anti-estréptolysine O, ce qui a été interprété comme une GNAPE. Il a évolué vers une encéphalopathie, ce qui a fait suspecter un PRES secondaire à une crise hypertensive, ce qui a finalement été confirmé par une IRM du cerveau. Il a également présenté une anémie hémolytique auto-immune, avec une hémoglobine allant jusqu'à 5 g/dL. Son traitement a été basé sur une thérapie antihypertensive, des mesures de neuroprotection et un traitement stéroïdien. Il a quitté l'hôpital 31 jours après son admission, asymptomatique 6 mois après sa sortie.\n",
+        "synthetic_summary": {
+            "B1": "Un petit garçon de 4 ans était très malade. Il avait du sang dans son pipi et ses jambes étaient gonflées. Il avait aussi mal à la tête, avait envie de vomir et se sentait très fatigué.\n\nUn jour, il a fait une grosse crise où il a bougé tout son corps sans contrôle. Les docteurs l'ont aidé à se calmer et à respirer avec une machine.\n\nIls ont fait beaucoup de tests. Ils ont trouvé que son corps avait un problème avec ses reins. Ses reins ne marchaient pas bien. Son cerveau aussi avait un peu de mal à cause de la pression dans son corps.\n\nLe garçon était très fatigué et avait besoin de médicaments pour son cœur et ses reins. Il a aussi reçu des médicaments pour aider son sang.\n\nAprès beaucoup de soins, il est devenu de mieux en mieux. Au bout d’un mois, il est rentré à la maison. Six mois plus tard, il allait très bien, sans douleur ni problème. Les docteurs étaient contents.",
+            "B2": "**Résumé adapté pour un adolescent de 14 ans**\n\nUn garçon de 4 ans est arrivé à l’hôpital avec plusieurs problèmes : il avait du sang dans les urines depuis 5 jours, des gonflements aux jambes, et depuis peu, des maux de tête, des nausées et des vomissements. Il a ensuite fait une crise de convulsions (des mouvements incontrôlés du corps) à cause d’une forte hypertension (pression artérielle très élevée).\n\nLes examens ont montré que ses reins étaient touchés par une maladie appelée glomérulonéphrite aiguë post-infectieuse (GNAPE). Cette maladie survient souvent après une infection, ici une infection à streptocoque (une bactérie), et provoque une inflammation des petits filtres des reins. On a aussi découvert que son système immunitaire utilisait beaucoup une protéine appelée complément C3, qui était très basse dans son sang.\n\nPendant son séjour, il a développé une complication au cerveau appelée PRES (encéphalopathie postérieure réversible), qui est un gonflement temporaire du cerveau causé par l’hypertension. Cette complication a été confirmée grâce à une IRM (un examen d’imagerie). En plus, il a eu une anémie hémolytique auto-immune, ce qui veut dire que son corps détruisait ses propres globules rouges, provoquant une baisse importante de son taux d’hémoglobine (la protéine qui transporte l’oxygène dans le sang).\n\nPour le soigner, les médecins ont utilisé des médicaments pour faire baisser sa tension artérielle, des médicaments pour protéger son cerveau, et des corticoïdes (des médicaments anti-inflammatoires puissants) pour contrôler l’anémie. Après environ un mois d’hospitalisation, il est sorti de l’hôpital en bonne santé, sans symptômes, avec ses reins et son cerveau bien remis. Six mois plus tard, il allait toujours bien, sans retour de la maladie.",
+            "B3": "Résumé détaillé et structuré pour un public non spécialiste mais instruit\n\nContexte  \nUn garçon de 4 ans, sans antécédents médicaux majeurs, a présenté une hématurie visible (sang dans les urines) et un œdème des jambes depuis cinq jours, précédés deux semaines plus tôt d’une infection cutanée nasale (impétigo) traitée localement et par antibiotiques oraux. Dans les heures précédant son admission, il a développé des maux de tête, des nausées et des vomissements, puis a fait une crise convulsive généralisée.\n\nPrincipales observations  \nÀ l’arrivée aux urgences, l’enfant était inconscient avec une rigidité musculaire généralisée et un œdème au visage et aux jambes. Sa tension artérielle n’a pas pu être mesurée immédiatement, mais elle était élevée en unité de soins intensifs (134/94 mmHg, au-dessus du 95e percentile pour son âge). Les analyses urinaires ont montré une hématurie importante, une protéinurie (présence de protéines dans les urines) et une inflammation locale. Les examens sanguins ont révélé une anémie sévère (hémoglobine à 7 g/dL), une leucocytose (augmentation des globules blancs), une thrombocytose (augmentation des plaquettes) et une hypocomplémentémie marquée (faible taux de complément C3, protéine du système immunitaire), tandis que le complément C4 était normal. Un test rapide a confirmé la présence d’une infection par Streptococcus pyogenes (bactérie responsable d’infections streptococciques). L’imagerie cérébrale initiale (scanner) était normale, mais une échographie rénale a montré une augmentation du volume des reins et des modifications de leur structure.\n\nInterprétation clinique  \nLe diagnostic principal était une glomérulonéphrite aiguë post-infectieuse (GNAPE), une inflammation des glomérules rénaux survenant après une infection streptococcique, responsable du syndrome néphrétique (hématurie, œdème, hypertension). L’enfant a présenté une complication grave : une urgence hypertensive avec état convulsif nécessitant une ventilation mécanique et un traitement anticonvulsivant. Malgré un traitement initial, il a développé une encéphalopathie hypertensive caractérisée par une altération de la conscience et une pression artérielle très élevée, réfractaire aux traitements classiques. Une IRM cérébrale a confirmé le diagnostic de PRES (encéphalopathie réversible postérieure), une complication neurologique liée à l’hypertension sévère, caractérisée par un œdème vasogénique dans les régions occipitales du cerveau.\n\nPar ailleurs, une anémie hémolytique auto-immune a été diagnostiquée, confirmée par un test de Coombs direct positif et la présence d’hémoglobinurie (perte d’hémoglobine dans les urines), nécessitant des transfusions sanguines et un traitement par corticostéroïdes.\n\nProchaines étapes et évolution  \nLe traitement a combiné une prise en charge antihypertensive intensive (amlodipine, labetalol, nitroprussiate de sodium, puis ajout d’énalapril), une neuroprotection par contrôle strict de la pression artérielle, une antibiothérapie ciblée contre Streptococcus pyogenes, des diurétiques pour gérer l’œdème, ainsi qu’une corticothérapie pour l’anémie auto-immune. L’état neurologique s’est progressivement amélioré, avec une normalisation de la conscience et une régression des anomalies à l’IRM cérébrale. La fonction rénale s’est stabilisée, l’anémie a été corrigée, et les marqueurs immunologiques (complément C3) sont revenus à la normale. Le patient a été extubé avec succès et est sorti de l’hôpital au 31e jour, en bon état général, sans signes neurologiques ni récurrence de la maladie. Six mois après sa sortie, il restait asymptomatique sous traitement médicamenteux adapté.\n\nCe cas illustre la complexité et la gravité potentielle d’une glomérulonéphrite post-infectieuse chez l’enfant, notamment lorsqu’elle s’accompagne d’une hypertension sévère et de complications neurologiques telles que le PRES, ainsi que d’une anémie hémolytique auto-immune, nécessitant une prise en charge multidisciplinaire intensive."
+        }
+    },
+    {
+        "article": "Un homme de 56 ans ayant des antécédents d’hypertension diagnostiquée à 46 ans était bien géré avec 40 mg de telmisartan et 5 mg d’amlodipine. Le patient consommait occasionnellement de l’alcool et ne fumait pas.\n\nUne TTE de 2011 a révélé une AR modérée dirigée vers l’AML, avec une vena contracta de 2,5 mm, une largeur de jet de 6,5 mm et un diamètre du tractus de sortie ventriculaire gauche (LVOT) de 29 mm. Le diamètre de l’aorte ascendante était de 38 mm. Une régurgitation mitrale modérée a également été observée, sans preuve de perforation ou de végétation.\n\nSix mois avant son admission, la patiente a ressenti une douleur dans la huitième dent supérieure gauche et des saignements récurrents lors du brossage. Durant les 3 mois précédant son admission, la patiente a eu des fièvres intermittentes supérieures à 40 °C sans essoufflement. N’ayant constaté aucune amélioration, la patiente s’est présentée à notre hôpital en avril 2016, a été admise le jour même pour une évaluation et un traitement complémentaires, et a été diagnostiquée avec une fièvre d’origine inconnue (FUO).\n\nLors de l’admission, la taille, le poids et l’indice de masse corporelle du patient étaient respectivement de 179 cm, 79,2 kg et 24,7 kg/m². Il était conscient et avait une température de 37,2°C, une tension artérielle de 124/77 mmHg, une fréquence cardiaque de 90 b.p.m. et une saturation en oxygène de 95 % (air ambiant). L’auscultation a révélé des bruits respiratoires clairs et un murmure systolique à la quatrième frontière sternale gauche, sans murmure diastolique. Il n’y avait pas de rougeurs cutanées, d’œdème, de lymphadénopathie pathologique ou de résultats neurologiques ou fondoscopiques anormaux.\n\nUn électrocardiogramme à 12 dérivations a montré un rythme sinusal normal avec une fréquence cardiaque de 82 b.p.m. et un axe normal. La radiographie thoracique a révélé un rapport cardiothoracique de 51 % sans congestion pulmonaire ou épanchement pleural. Les scanners de tomographie par ordinateur à contraste amélioré du thorax au bassin n’ont révélé aucune anomalie, source d’infection, lésion néoplasique ou source d’embolie. La scintigraphie au gallium réalisée pour étudier la fièvre de cause inconnue n’a révélé aucune accumulation anormale.\n\nBien que les lésions néoplasiques, la maladie du collagène et les maladies infectieuses aient été considérées comme des causes possibles de fièvre, ces résultats ont exclu les maladies néoplasiques et du collagène. Les cultures sanguines des jours 1 à 4 de l'hospitalisation (deux ensembles chacune) étaient positives pour S. oralis. La consultation avec le service de chirurgie dentaire et buccale a révélé une carie dans la huitième dent supérieure gauche, qui a nécessité un traitement et a été diagnostiquée comme une source possible de bactériémie.\n\nCes résultats suggéraient une IE, ce qui a entraîné une consultation en cardiologie. L’ECR a révélé les résultats suivants : fraction d’éjection ventriculaire gauche (FEVG) de 62 %, diamètre diastolique/systolique du ventricule gauche de 58/42 mm, diamètre de l’aorte ascendante de 38 mm, régurgitation mitrale modérée, régurgitation tricuspidale triviale (RT) et gradient de pression RT de 20 mmHg. L’AR, conforme aux résultats de 2011, avait dévié vers l’arrière, en collision avec l’AML. Une évaluation semi-quantitative a révélé un diamètre de la voie de sortie du ventricule gauche de 29 mm, une veine contractée de 4,2 mm et une largeur du jet de 6,5 mm, indiquant une AR modérée. Une végétation de 7,7 mm a été détectée au site de l’impact de l’AR sur l’AML, provoquant une perforation et un reflux.\n\nUn TEE le jour 5 de l'hospitalisation a confirmé des résultats similaires à ceux du TTE, montrant l'AR migrant empiétant sur l'AML avec végétation et perforation. Le TEE a également révélé une flexion partielle de la cuspide aortique droite (RCC) et un prolapsus, mais aucune végétation de la valve aortique (AV). Sur la base des critères de Duke, un diagnostic définitif d'IE a été établi. Aucune anomalie n'a été trouvée dans les examens du fond d'œil ou dermatologiques.\n\nLe traitement comprenait 8 g/jour d’AMPC (2 g q6) et 160 mg/jour de GM (80 mg q12). La patiente a présenté une défervescence, n’a pas eu de problèmes hémodynamiques et était dans un état stable sans insuffisance cardiaque ou symptômes neurologiques.\n\nLe septième jour, une IRM du cerveau a révélé de multiples signaux faibles dans les hémisphères cérébraux bilatéraux, le pons, les ganglions basaux bilatéraux, le thalamus gauche et le lobe frontal gauche sur l'image pondérée en fonction de la susceptibilité, qui étaient considérés comme étant dus à une hémorragie post-infarctus causée par un embolisme lié à l'IE.\n\nEn raison d'un dysfonctionnement valvulaire important, le traitement antibiotique a été poursuivi et une intervention chirurgicale a été planifiée pour le jour 19. Environ 7 mm de végétation ont été enlevés de l'AML au site du jet AR, suivis d'une réparation de la valve mitrale (résection de la végétation A2, patch péricardique autologue, Physio II, 32 mm) et d'une annuloplastie tricuspide (TAP) (procédure de De Vega). Une flexion partielle du RCC a été observée sans aucune végétation AV. Pour remédier à la RA résiduelle et prévenir une IE récurrente, une valvuloplastie aortique et un remplacement de l'aorte ascendante (annuloplastie CV-9 22 mm, triples 24 mm) ont été effectués simultanément. La patiente n'a présenté aucune complication postopératoire apparente. L'AMPC et le GM ont été administrés pendant 42 et 17 jours, respectivement. La patiente a été déchargée sans aucun résultat anormal.\n\nLe TTE à 6 mois postopératoirement n'a montré aucune récidive d'IE et aucune dysfonction de la valve mitrale. La patiente est restée stable pendant 3 ans et 10 mois postopératoirement.\n",
+        "gold_summary": "En 2011, un homme de 56 ans a présenté une AR modérée vers la LMA, révélée par un échocardiogramme transthoracique. En 2016, 3 mois avant son admission, le patient avait présenté des fièvres intermittentes de plus de 40 °C, qui ne s'amélioraient pas, et a été référé à notre hôpital. Un examen détaillé a révélé une végétation sur la LMA où la valve aortique était déplacée, et le site était perforé. L'AR était modérée. Les cultures sanguines étaient positives pour Streptococcus oralis. À partir de ces résultats, un diagnostic définitif d'endocardite infectieuse (EI) a été fait. Le patient a eu un infarctus cérébral et a subi une chirurgie semi-d'urgence.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 56 ans avait un petit problème avec son cœur. En 2011, on a vu que son cœur laissait un peu le sang revenir en arrière.\n\nEn 2016, il avait souvent de la fièvre très forte. Il est allé à l’hôpital pour comprendre pourquoi.\n\nLes docteurs ont trouvé une petite boule sur une partie de son cœur. Cette boule venait d’une infection.\n\nIls ont aussi trouvé des microbes dans son sang. C’est pour ça qu’il avait de la fièvre.\n\nLe monsieur a eu un petit problème au cerveau à cause de ça.\n\nLes docteurs l’ont aidé avec des médicaments et une opération au cœur.\n\nAprès, il est allé mieux et il est resté en bonne santé.",
+            "B2": "Voici un résumé clair et adapté pour un adolescent de 14 ans :\n\n**Ce qu’ils ont trouvé :**  \nUn homme de 56 ans avait déjà un problème au cœur appelé régurgitation aortique (AR), ce qui signifie que la valve aortique ne se ferme pas bien et laisse du sang refluer. En 2016, il a commencé à avoir des fièvres très élevées pendant plusieurs mois, sans que cela s’améliore. Lorsqu’il est venu à l’hôpital, les médecins ont découvert une petite masse appelée végétation sur une autre valve du cœur, la valve mitrale, à l’endroit où le sang qui reflue frappait cette valve. Cette végétation a causé un trou (perforation) dans la valve.\n\n**Ce que cela signifie :**  \nLes analyses de sang ont montré la présence d’une bactérie appelée Streptococcus oralis, qui vient souvent de la bouche. Cela a permis de diagnostiquer une infection grave du cœur appelée endocardite infectieuse (EI). Cette infection a provoqué un petit accident vasculaire cérébral, car des morceaux de la végétation se sont détachés et ont bloqué des vaisseaux dans le cerveau.\n\n**Le traitement et le suivi :**  \nLe patient a reçu des antibiotiques puissants pour combattre l’infection. Comme la valve était abîmée, il a dû subir une opération pour réparer les valves du cœur et remplacer une partie de l’aorte, la grosse artère qui sort du cœur. Après la chirurgie et le traitement, il s’est bien remis et n’a plus eu de problème au cœur pendant plusieurs années.  \n\nCe cas montre l’importance de traiter rapidement les infections du cœur, surtout quand des bactéries de la bouche peuvent passer dans le sang et attaquer les valves cardiaques.",
+            "B3": "Résumé détaillé et structuré pour un public non spécialiste\n\n**Contexte**  \nUn homme de 56 ans, suivi pour une hypertension bien contrôlée, avait déjà présenté en 2011 une régurgitation aortique (RA) modérée, c’est-à-dire un reflux sanguin anormal au niveau de la valve aortique, dirigé vers la valve mitrale antérieure (LMA). Cette anomalie valvulaire avait été détectée par échocardiographie transthoracique (TTE).\n\n**Principales observations en 2016**  \nTrois mois avant son admission en 2016, le patient a souffert de fièvres intermittentes élevées (supérieures à 40 °C) sans amélioration, associées à des douleurs dentaires et des saignements lors du brossage. À son admission, les examens cliniques et d’imagerie ont confirmé la persistance d’une RA modérée, avec une particularité : une végétation (amas de bactéries et de cellules inflammatoires) de 7,7 mm a été identifiée sur la valve mitrale antérieure, précisément à l’endroit où le jet de régurgitation aortique impactait la valve. Cette végétation avait provoqué une perforation de la valve, aggravant le reflux.\n\nLes analyses microbiologiques ont révélé la présence de Streptococcus oralis dans les cultures sanguines, une bactérie commune dans la bouche, ce qui a orienté vers une endocardite infectieuse (EI), une infection grave des valves cardiaques. Cette infection était probablement liée à la carie dentaire identifiée sur la huitième dent supérieure gauche.\n\n**Interprétation clinique**  \nLe diagnostic définitif d’endocardite infectieuse a été établi selon les critères reconnus (critères de Duke). L’infection a entraîné des complications, notamment un infarctus cérébral embolique, c’est-à-dire une obstruction des vaisseaux sanguins du cerveau par des fragments infectieux détachés de la végétation.\n\n**Traitement et évolution**  \nLe patient a reçu un traitement antibiotique intensif combinant de l’amoxicilline et de la gentamicine. En raison de la gravité des lésions valvulaires et du risque de complications, une intervention chirurgicale a été réalisée environ 19 jours après l’admission. Cette chirurgie comprenait l’ablation de la végétation, la réparation de la valve mitrale (avec un patch de péricarde autologue), une annuloplastie tricuspide pour renforcer la valve tricuspide, ainsi qu’une valvuloplastie aortique et un remplacement de l’aorte ascendante pour corriger la régurgitation aortique résiduelle et prévenir une récidive d’infection.\n\nLa convalescence postopératoire a été favorable, sans complication apparente. Le patient a poursuivi les antibiotiques pendant plusieurs semaines et, lors du suivi à six mois, aucune récidive d’endocardite ni dysfonction valvulaire n’a été détectée. Il est resté stable et en bonne santé pendant près de quatre ans après l’intervention.\n\n**Prochaines étapes**  \nCe cas illustre l’importance d’une prise en charge rapide et complète de l’endocardite infectieuse, notamment chez les patients présentant des anomalies valvulaires préexistantes. La surveillance régulière, le traitement des infections dentaires et une intervention chirurgicale adaptée sont essentielles pour prévenir les complications graves et assurer une bonne qualité de vie à long terme."
+        }
+    },
+    {
+        "article": "Garçon de 11 ans présentant une céphalée occipitale et frontale bilatérale associée à des vomissements de 12 heures d'évolution après une chute banale sur la région sacro-coccygienne. Antécédent de SM dû à une mutation de type missense en hétérozygotie dans le gène FBN1 c.2243G>A.\n\nL'examen neurologique et l'examen par appareil étaient normaux, sauf en ce qui concerne l'habitude marfanoïde. Une analyse générale et une radiographie sacro-coccygienne ont été effectuées, sans anomalies. La céphalée s'est améliorée, jusqu'à disparaître en décubitus, mais elle réapparaissait en se levant et ne tolérait pas la position debout, raison pour laquelle elle a été admise.\n\nPendant l'admission, il a présenté une faible réponse à l'analgésie. Une tomographie axiale assistée par ordinateur (TAC) crânienne a été réalisée, qui a montré une augmentation de la densité des sinus transverses, probablement liée à un flux veineux lent. En raison du soupçon de SHI en relation avec une éventuelle fistule de LCR, une résonance magnétique (RM) crâniomédullaire a été demandée. La RM a montré une légère descente amygdale (5 mm) et un décollement de la dure-mère avec des collections liquides à l'extérieur de la dure-mère au niveau dorsal et lombo-sacré, compatible avec une fistule de LCR ; en outre, des kystes périneuraux de Tarlov ont été visualisés au niveau sacré. Cette image n'était pas compatible avec une ectasie dure, et le patient ne disposait pas de neuro-imagerie préalable.\n\nLe patient a été traité par hyperhydratation, analgésiques mineurs (dexkétoprofène et métamizole), hydrocortisone intraveineuse à la dose initiale de 8 mg/kg/jour, caféine par voie orale à la dose de 2,5 mg/kg/jour, et repos au lit en position de Trendelenburg. Cinq jours plus tard, le patient a commencé une mobilisation progressive, présentant une évolution favorable, avec une amélioration de la céphalée et tolérant la position debout. Il a pu quitter l'hôpital 12 jours plus tard.\n\nAprès quatre mois asymptomatiques, la clinique réapparut en même temps que le début de l'activité sportive à l'école. L'IRM de contrôle a montré la disparition de la collection dorsale avec persistance de collections sacrées. Il a de nouveau reçu le même schéma de traitement conservateur que lors de l'admission précédente.\n\nL’IRM de contrôle un an après a montré la résolution des collections sous-duraux ou extra-duraux dans le canal rachidien et a identifié comme nouvelle découverte une fine image d’hydromélie dorsale moyenne. Deux ans après la première admission, il a consulté de nouveau pour des céphalées orthostatiques, une IRM a été réalisée et a constaté une ré-fistulisation au niveau de L5-S1. Compte tenu de la récidive, un traitement par patch hématique épidural (PHE) lombaire (L4-L5) a été décidé par le service d’anesthésiologie. Un an après sa réalisation, et trois ans depuis le début de la clinique, le patient reste asymptomatique.\n",
+        "gold_summary": "Nous rapportons le cas d'un garçon de 11 ans avec céphalées orthostatiques et vomissements depuis 12 heures après une chute sur la région sacro-coccygienne ; antécédent de syndrome de Marfan. L'IRM crânio-médullaire a montré des collections liquides extra-durales au niveau dorsal et lombo-sacré compatibles avec une fistule de LCR. L'évolution a été favorable après traitement, mais deux nouveaux épisodes sont survenus pendant le suivi, ce qui a conduit à l'application d'un patch hématico-épidural deux ans après le début.\n",
+        "synthetic_summary": {
+            "B1": "Il y a un garçon de 11 ans. Il a eu mal à la tête et vomi après une petite chute. Son mal de tête changeait quand il se levait ou s’allongeait. \n\nLe docteur a fait des images de sa tête et de son dos. Ils ont vu un peu d’eau où il ne faut pas. C’est pour ça qu’il avait mal. \n\nLe garçon a pris des médicaments et il a beaucoup reposé. Après, il allait mieux. Mais parfois, il avait encore mal. Alors, les docteurs ont fait un petit soin spécial pour l’aider. \n\nMaintenant, il va bien et il n’a plus mal. Les docteurs sont contents.",
+            "B2": "Cas d’un garçon de 11 ans avec des maux de tête et des vomissements après une chute\n\nUn garçon de 11 ans est venu à l’hôpital parce qu’il avait mal à la tête, surtout quand il se levait, et il vomissait depuis environ 12 heures. Cela est arrivé après qu’il soit tombé sur le bas de son dos (la région sacro-coccygienne). Il a aussi un problème génétique appelé syndrome de Marfan, qui affecte ses tissus.\n\nCe qu’ils ont trouvé avec les examens\n\nLes médecins ont fait plusieurs examens. Une IRM, qui est une sorte de scanner très précis, a montré qu’il y avait du liquide qui s’était échappé autour de la moelle épinière, dans le dos et le bas du dos. Ce liquide venait d’une petite fuite appelée fistule du liquide céphalorachidien (LCR), qui est le liquide qui protège normalement le cerveau et la moelle épinière.\n\nLe traitement et ce qui s’est passé ensuite\n\nLe garçon a reçu des médicaments pour la douleur, des soins pour augmenter le liquide dans son corps, et il a dû rester au lit dans une position spéciale pour aider à guérir la fuite. Après quelques jours, il allait mieux et pouvait se lever sans douleur. Cependant, au cours des mois suivants, les symptômes sont revenus deux fois. Finalement, deux ans après le début de ses problèmes, les médecins ont décidé de faire un traitement appelé patch hématico-épidural. Ce traitement consiste à injecter du sang dans la zone autour de la moelle épinière pour boucher la fuite. Un an après ce traitement, le garçon n’a plus eu de symptômes et se porte bien.",
+            "B3": "Résumé détaillé et structuré\n\nContexte  \nUn garçon de 11 ans, porteur d’un syndrome de Marfan lié à une mutation génétique du gène FBN1, a présenté des céphalées bilatérales (à l’arrière et au front de la tête) associées à des vomissements, survenues 12 heures après une chute apparemment bénigne sur la région sacro-coccygienne (bas du dos). Initialement, l’examen neurologique était normal à l’exception d’un aspect marfanoïde (caractéristiques physiques typiques du syndrome de Marfan). Les examens radiologiques standards n’ont révélé aucune anomalie. La céphalée s’améliorait en position couchée mais réapparaissait dès que le patient se mettait debout, ce qui a motivé son hospitalisation.\n\nPrincipales observations  \nLors de l’admission, la douleur était peu soulagée par les analgésiques classiques. Une tomodensitométrie (TDM) cérébrale a montré une augmentation de la densité des sinus transverses, suggérant un ralentissement du flux veineux. Une suspicion de syndrome d’hypotension intracrânienne (SHI) secondaire à une fistule de liquide céphalorachidien (LCR) a conduit à la réalisation d’une imagerie par résonance magnétique (IRM) crânio-médullaire. Cette IRM a révélé :  \n- Une légère descente des amygdales cérébelleuses (5 mm), signe de pression intracrânienne basse.  \n- Un décollement de la dure-mère (membrane entourant le cerveau et la moelle épinière) avec des collections de liquide en dehors de celle-ci au niveau dorsal et lombo-sacré, compatible avec une fistule de LCR.  \n- La présence de kystes périneuraux de Tarlov au niveau sacré.  \nCes images n’étaient pas compatibles avec une ectasie dure (dilatation anormale de la dure-mère), et aucune imagerie antérieure n’était disponible pour comparaison.\n\nInterprétation clinique  \nLe diagnostic principal retenu était celui d’une fistule de LCR responsable d’un syndrome d’hypotension intracrânienne, expliquant les céphalées orthostatiques (qui s’aggravent en position debout) et les vomissements. Le syndrome de Marfan, connu pour fragiliser les tissus conjonctifs, peut favoriser la survenue de telles fistules.\n\nProchaines étapes et évolution  \nLe traitement initial a été conservateur, comprenant :  \n- Hyperhydratation pour augmenter le volume de liquide dans le corps.  \n- Analgésiques mineurs (dexkétoprofène, métamizole).  \n- Hydrocortisone intraveineuse (8 mg/kg/jour).  \n- Caféine orale (2,5 mg/kg/jour), connue pour ses effets sur la pression intracrânienne.  \n- Repos strict au lit en position de Trendelenburg (tête plus basse que les pieds) pour favoriser la fermeture de la fistule.  \n\nAprès cinq jours, le patient a pu se mobiliser progressivement avec amélioration des symptômes, et a quitté l’hôpital au bout de 12 jours.  \n\nCependant, quatre mois plus tard, les symptômes sont réapparus avec la reprise d’activités sportives. L’IRM de contrôle a montré la disparition de la collection dorsale mais la persistance de collections au niveau sacré. Le même traitement conservateur a été réappliqué avec succès.  \n\nUn an après, l’IRM a montré la résolution complète des collections sous-durales et extra-durales, mais a révélé une fine hydromélie dorsale moyenne (accumulation anormale de liquide dans la moelle épinière).  \n\nDeux ans après la première hospitalisation, le patient a de nouveau présenté des céphalées orthostatiques. L’IRM a confirmé une récidive de la fistule au niveau lombaire (L5-S1). En raison de cette récidive, un traitement par patch hématique épidural lombaire (injection de sang autologue dans l’espace épidural pour colmater la fuite) a été réalisé.  \n\nUn an après ce traitement, soit trois ans après le début des symptômes, le patient est resté asymptomatique.\n\nConclusion  \nCe cas illustre la complexité du diagnostic et du traitement du syndrome d’hypotension intracrânienne chez un enfant porteur d’un syndrome de Marfan, avec une fistule de liquide céphalorachidien confirmée par IRM. Le traitement conservateur peut être efficace, mais la récidive impose parfois des interventions plus spécifiques comme le patch hématique épidural. Le suivi prolongé est essentiel pour surveiller l’évolution et prévenir les complications."
+        }
+    },
+    {
+        "article": "Un homme de 54 ans ayant des antécédents de syndrome de Wolff-Parkinson-White ayant entraîné un arrêt cardiaque dans la vingtaine a ensuite développé une cardiomyopathie non ischémique (New York Heart Association, classe IV, avec une fraction d'éjection de 15 %). Il a été admis pour insuffisance cardiaque et a suivi un traitement complexe en unité de soins cardiaques avec retrait de l'AICD/pacemaker en raison d'une endocardite et anticoagulation avec Coumadin pour thrombus auriculaire droit/fibrillation auriculaire. Il a été renvoyé, mais a dû être réadmis à plusieurs reprises pour insuffisance cardiaque, nécessitant finalement une oxygénation extracorporelle par membrane veino-artérielle par l'artère fémorale droite et la veine fémorale gauche en tant que réanimation cardiopulmonaire électronique en janvier 2020 et restera sous ECMO pendant 5 semaines. Il a subi une implantation de LVAD en utilisant les sites de canulation du ventricule gauche et de l'aorte ascendante 16 jours après la canulation ECMO et une trachéotomie ultérieure en février pour une insuffisance respiratoire persistante.\n\nDeux jours avant le retrait des canules ECMO, le patient a subi une amputation guillotine de l’extrémité inférieure droite en raison d’une gangrène sèche due à une dissection iliaque et à une embolisation distale. Cinq jours plus tard, le jour 25 après le LVAD, on a constaté une fuite de selles au niveau du site de sortie de la ligne de perfusion. L’équipe de chirurgie cardiothoracique a emmené le patient en salle d’opération et a procédé à une exploration limitée, constatant une blessure intestinale due à la ligne de perfusion. La blessure a été réparée avec une suture interrompue en soie et la ligne de perfusion a été laissée intacte. Trois jours après cette réparation, l’équipe de chirurgie des soins aigus a été consultée en raison d’une nouvelle fuite de selles au niveau du site de sortie de la ligne de perfusion. Le patient a été déclaré sévèrement septique. Il a été mis sous antibiotiques et emmené en salle d’opération pour une laparotomie exploratoire formelle et on a constaté que la ligne de perfusion LVAD traversait la cavité abdominale du quadrant supérieur droit au flanc gauche. La ligne de perfusion avait blessé le côlon transverse distal et la réparation antérieure avait fui. Il y avait une abondance de liquide fécal et de nombreux abcès intra-abdominaux qui ont été drainés. En raison de la septicémie du patient, le côlon a été agrafé proximal et distal au segment blessé et l’échantillon a été enlevé. Le patient a été laissé en discontinuité et un pansement abdominal temporaire a été placé pour une deuxième opération prévue. Il est revenu à l’unité de soins intensifs où il a reçu des antibiotiques, une ventilation mécanique et des vasopresseurs.\n\nTrois jours plus tard, lors de la deuxième opération prévue, l’abdomen paraissait propre. En raison de la nécessité du LVAD, la ligne de transmission ne pouvait pas être déconnectée. La première priorité était de mobiliser la ligne de transmission hors du péritoine. L’abdomen du patient a été ouvert du côté gauche de manière transversale pour permettre à la ligne de transmission de se rendre au milieu. Le péritoine a été enlevé du côté droit de l’abdomen du patient pour développer un plan rétro-rectal dans le but de repositionner la ligne de transmission à l’emplacement extra-péritonéal prévu. Une incision transversale plus petite a été faite du côté droit pour que la ligne de transmission se trouve dans ce plan rétro-rectal, loin de la ligne médiane. Ainsi, la ligne de transmission a été retirée avec succès du péritoine sans déconnexion. Une hémicolectomie droite a été réalisée, mais en raison de la ligne de transmission sortant près du quadrant inférieur droit, une iléostomie terminale a été réalisée dans le quadrant inférieur gauche. Sa fascie a été fermée et des sutures de rétention ont été placées en raison du mauvais état nutritionnel du patient et du degré de septicémie abdominale. Le patient s’est bien rétabli après l’opération et a pu reprendre une nutrition entérale le jour 3 post-opératoire, répondant à ses besoins caloriques le jour 7 post-opératoire. Il a subi une révision de son amputation guillotine 15 jours après sa dernière opération abdominale.\n\nL’évolution du patient a été compliquée par un abcès intra-abdominal nécessitant un drainage par radiologie interventionnelle 3 semaines après sa dernière chirurgie abdominale ainsi qu’un traitement antibiotique IV prolongé pour des organismes résistants, y compris VRE. Le patient a terminé son traitement antibiotique et a eu ses drains retirés. Au moment de ce rapport, le patient reste hospitalisé, tolère une nutrition entérale, est déconnecté de la ventilation mécanique et suit une thérapie physique.",
+        "gold_summary": "Un homme de 54 ans ayant des antécédents de syndrome de Wolff-Parkinson-White ayant entraîné de multiples réadmissions pour insuffisance cardiaque a finalement eu besoin d’un dispositif d’assistance ventriculaire gauche (LVAD). Plusieurs semaines plus tard, on a découvert qu’il y avait des selles qui s’écoulaient du site de la ligne de commande. Le patient a été emmené en salle d’opération pour une exploration limitée par l’équipe de chirurgie cardiothoracique et une blessure intestinale a été identifiée et réparée. Trois jours après cette réparation, des selles s’écoulaient à nouveau du site de la ligne de commande, ce qui a nécessité une nouvelle exploration par l’équipe de chirurgie d’urgence. En intra-opératoire, la réparation antérieure s’est avérée être une fuite et de multiples abcès intra-abdominaux ont été découverts. Le côlon transverse a été réséqué et laissé en discontinuité. Au cours d’une deuxième opération prévue, la ligne de commande LVAD a été relocalisée pour être extra-péritonéale et une colostomie a été formée.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur avait un gros problème au cœur. Il avait un appareil pour aider son cœur à battre. \n\nUn jour, il y a eu un trou dans son ventre. Des choses qui viennent de son ventre sont sorties par un petit trou près de l’appareil. \n\nLes docteurs ont fait une petite opération pour réparer. Mais ça a recommencé à couler. \n\nAlors, ils ont fait une grande opération. Ils ont enlevé une partie du ventre qui faisait mal. Ils ont aussi changé la place de l’appareil pour qu’il ne fasse plus de mal. \n\nAprès, le monsieur a commencé à aller un peu mieux. Les docteurs l’aident beaucoup pour qu’il guérisse.",
+            "B2": "Un homme de 54 ans avait un problème cardiaque sérieux appelé syndrome de Wolff-Parkinson-White, qui a causé plusieurs arrêts du cœur et une insuffisance cardiaque grave. Pour l’aider, les médecins ont installé un appareil appelé LVAD, qui aide le cœur à pomper le sang.\n\nQuelques semaines après cette opération, des selles (c’est-à-dire des matières fécales) ont commencé à sortir par un endroit où passait une ligne de l’appareil. Cela montrait qu’il y avait une blessure dans son intestin. Les chirurgiens ont fait une première opération pour réparer cette blessure.\n\nCependant, trois jours plus tard, les selles ont recommencé à fuir. Une nouvelle opération a révélé que la première réparation avait échoué. Ils ont aussi trouvé beaucoup d’infections et d’abcès dans le ventre du patient. Les médecins ont dû enlever une partie du côlon (le gros intestin) malade et ont laissé le ventre ouvert temporairement pour mieux soigner.\n\nLors d’une deuxième opération, ils ont déplacé la ligne de l’appareil LVAD pour qu’elle ne traverse plus la cavité abdominale, afin d’éviter d’autres blessures. Ils ont aussi fait une colostomie, c’est-à-dire qu’ils ont créé une ouverture sur le ventre pour que les selles puissent sortir ailleurs, le temps que l’intestin guérisse.\n\nAprès ces interventions, le patient a reçu des antibiotiques et des soins intensifs. Il a finalement pu commencer à manger par son estomac et a commencé une rééducation. Malgré des complications, il s’est bien remis et continue son traitement à l’hôpital.",
+            "B3": "Résumé détaillé et structuré\n\nContexte  \nUn homme de 54 ans, présentant un antécédent de syndrome de Wolff-Parkinson-White ayant provoqué un arrêt cardiaque dans sa jeunesse, a développé une cardiomyopathie non ischémique sévère avec une fraction d’éjection très basse (15 %). Après plusieurs hospitalisations pour insuffisance cardiaque avancée, il a nécessité la mise en place d’un dispositif d’assistance ventriculaire gauche (LVAD) pour soutenir sa fonction cardiaque.\n\nPrincipales observations  \nQuelques semaines après l’implantation du LVAD, une fuite de selles a été observée au niveau du site de sortie de la ligne de perfusion du dispositif. Une première intervention chirurgicale limitée a révélé une blessure intestinale liée à la ligne de perfusion, qui a été réparée sans retirer la ligne. Cependant, trois jours plus tard, la fuite de selles est réapparue, accompagnée d’un état septique sévère. Une laparotomie exploratoire a montré que la ligne de perfusion traversait la cavité abdominale, ayant perforé le côlon transverse distal. La réparation initiale avait cédé, et de multiples abcès intra-abdominaux ainsi qu’une contamination fécale importante étaient présents. Le segment colique lésé a été réséqué, avec exclusion proximale et distale du côlon (discontinuité), et un pansement abdominal temporaire a été posé en vue d’une deuxième intervention.\n\nInterprétation clinique  \nLa complication majeure était une perforation colique causée par la ligne de perfusion du LVAD, entraînant une péritonite fécale et une septicémie sévère. La nécessité de maintenir le LVAD fonctionnel a compliqué la prise en charge chirurgicale, notamment pour le repositionnement de la ligne de transmission afin d’éviter une nouvelle contamination intra-abdominale. La discontinuité colique a été choisie pour limiter la contamination et permettre une meilleure gestion de l’infection.\n\nProchaines étapes  \nLors de la deuxième intervention, la ligne de transmission du LVAD a été déplacée hors du péritoine, dans un plan rétro-rectal extra-péritonéal, sans déconnexion du dispositif. Une hémicolectomie droite a été réalisée, suivie d’une iléostomie terminale pour assurer une sortie des selles éloignée du site de sortie de la ligne de transmission. La fermeture abdominale a été renforcée par des sutures de rétention en raison du risque élevé lié à l’état nutritionnel et infectieux du patient. Après cette opération, le patient a bien récupéré, a repris une nutrition entérale adéquate et a pu être sevré de la ventilation mécanique. Sa prise en charge a été compliquée par un abcès intra-abdominal secondaire, drainé par radiologie interventionnelle, et par une infection à germes résistants nécessitant un traitement antibiotique prolongé. Au moment du rapport, le patient est stable, hors ventilation, nourri par voie entérale et suit une rééducation physique."
+        }
+    },
+    {
+        "article": "Adolescent de 14 ans, auparavant en bonne santé, qui a consulté au Service des urgences primaires d'Osorno pour une toux irritative prédominante nocturne de 11 jours d'évolution. Traitement symptomatique indiqué, avec une évolution vers une dyspnée et une orthopnée. Il s'est rendu au Service des urgences de l'Hôpital de base d'Osorno (HBO), où il a été observé une insuffisance respiratoire sévère, une intolérance à la position couchée et une douleur abdominale. Il a été admis à l'unité de soins intensifs pédiatriques (UCIP), tachycardique, hypertendu, polypneique, saturant 96 % avec FiO2 35 %, rosé, hydraté et bien perfusé, avec des jugulaires plates, des adénopathies supraclaviculaires bilatérales de petite taille. Le thorax sans rétraction des parties molles, maintenu en position genou-poignet, avait un murmure pulmonaire diminué dans les deux bases, et l'auscultation cardiaque avait des sons étouffés, sans souffle. L'abdomen peu dépressible et sensible dans les deux hypocondres, des viscères de taille douteuse et des extrémités sans lésions. La radiographie thoracique a montré une masse médiastinale supérieure et une atélétose du lobe moyen droit associée à un épanchement pleural ipsilatéral. Aucune TDM avec contraste n'a été réalisée pour contre-indication anesthésique, comme indiqué dans le résumé du transfert de l'HBO. Il a été transféré en urgence à l'unité de soins intensifs pédiatriques (UCIP HBV), souffrant d'un syndrome de compression médiastinale, avec suspicion clinique de lymphome non hodgkinien. Il a été évalué par les équipes d'hémato-oncologie infantile, de chirurgie infantile, de soins intensifs pédiatriques, d'imagerie, de radiothérapie et, en raison du risque vital immédiat associé au diagnostic, il a été décidé d'offrir un traitement cytoréducteur, avec 6 mg/m2 de dexaméthasone et 100 mg/m2 de cyclophosphamide par jour pendant 5 jours, en plus d'une prophylaxie du syndrome de lyse tumorale (allopurinol 10 mg/kg/jour toutes les 8 heures), d'une surhydratation (3 000 ml/m2) et d'un traitement de l'insuffisance respiratoire. Physiopathologiquement, les masses médiastiniques rivalisent pour un espace avec des structures d'importance vitale. La pression intrathoracique négative, qui est la somme des forces anatomiques (y compris le tonus de la musculature intercostale) et physiologiques (respiration), tire effectivement la tumeur vers l'avant. La gravité exerce une force opposée, tirant la tumeur vers l'arrière sur des structures vulnérables, comme l'arbre trachéo-bronchique et le cœur droit (oreillette droite et artère pulmonaire). L'anesthésie, le bloc neuromusculaire et la ventilation à pression positive, pourraient exercer des effets profonds sur cet équilibre, tout comme l'effet net des pressions sur la tumeur, lorsque le patient adopte différentes positions. Ce qui permet de prévoir les changements d'effet d'anesthésie et de développer des stratégies pour prévenir et inverser l'effondrement cardiorespiratoire. Le patient a évolué vers un syndrome de lyse tumorale 24 heures après son admission, associé à une insuffisance rénale, avec une uricémie (14,6 mg/dl), LDH (2 177 U/L), un profil lipidique normal (cholestérol total, dans la plage normale élevée, HDL cholestérol dans la limite normale inférieure, triglycérides 159 mg/dl), fibrinogène 498 mg/dl et dimère D 1,61 ug/ml, phosphémie 8,8 mg/dL et créatinémie 0,82 mg/dL. Il a reçu de la rasburicase pour traiter le syndrome de lyse tumorale (0,2 mg/kg/jour), en suspendant l'allopurinol et en continuant la citoréduction avec dexaméthasone à la moitié de la dose initiale (3 mg/m2 par jour), sans cyclophosphamide.\n\nUne évaluation néphrologique a été réalisée, confirmant une insuffisance rénale secondaire à un syndrome de lyse tumorale, sans urgence diététique et tendance à l'hypertension, avec une créatininémie de 1,54 mg/dL, une phosphémie de 11 mg/dL, sans hypernatrémie. Elle a continué avec une hyperhydratation, un diurétique (furosémide) et un antihypertensif (amlodipine). Du point de vue respiratoire, elle a présenté une demande d'oxygène, avec une FIO2 de 35 % par masque de Venturi, l'apport étant suspendu le troisième jour de l'admission. Elle a évolué avec des épisodes d'agitation psychomotrice, associés au diagnostic en cours, qui ont été traités conformément au protocole institutionnel d'agitation psychomotrice, avec un soutien psychologique et psychiatrique, avec une évolution satisfaisante. Au troisième jour de l'admission et du traitement, une TDM thoracique, abdominale et pelvienne a été réalisée avec contraste, avec une augmentation de la taille du thymus, d'aspect homogène, probablement dans le contexte d'un processus lymphoprolifératif et de résultats suggérant une thrombose pulmonaire droite, avec une thrombose de la veine jugulaire gauche, un épanchement pleural bilatéral étendu associé à des atelectases dans les deux bases, avec des signes de néphropathie médicale bilatérale. Une anticoagulation a été indiquée avec de l'enoxaparine (1 mg/kg de dose, toutes les 12 heures) pendant vingt jours. Puis une TDM thoracique de contrôle a montré la résolution de la thrombose.Au quatrième jour de l'admission et du traitement, une étude diagnostique et d'extension a été réalisée, qui comprenait, entre autres, un profil biochimique complet, y compris un profil lipidique, une hyperplasie granulopoïétique de la moelle osseuse (myélogramme), une cytométrie de flux (moelle osseuse) dans laquelle aucune cellule prédominante clonale ou immunophénotype néoplasique n'a été observée, une cytométrie de flux dans le sang périphérique négatif pour les cellules néoplasiques, un cytologique de liquide pleural négatif pour les cellules néoplasiques, une cytométrie de flux de liquide pleural sans preuve de néoplasie hématologique. Elle a été présentée au comité oncologique pédiatrique, soulignant qu'il n'a pas été possible de prélever une biopsie de la tumeur étant donné que la masse médiastinale a disparu avec le traitement cytoréducteur, en assumant le diagnostic de lymphome lymphoblastique en raison du tableau clinique et de la réponse au traitement, selon le protocole PINDA 0516. Ce protocole prévoit une induction IA de huit doses de Lasp E. coli de 10 000 UI/m2. Après avoir reçu sept doses de L-asp et une dose cumulative de quatre-vingt-dix-mille unités internationales plus glucocorticoïdes (prednisone), elle a présenté un tableau de déclin, des vomissements, des douleurs abdominales et une déshydratation légère. Une suspicion de pancréatite a été suspectée, qui a été écartée par des valeurs normales d'amylase/lipase et des tests hépatiques normaux. À ce moment, elle avait un électrolyte plasmatique avec une hyponatrémie de 126 mOsm/kg, une hypertriglycéridémie de 1 115 mg/dL et un cholestérol total de 435 mg/dL). En raison de la persistance de l'hyponatrémie malgré un traitement de remplacement adéquat, elle a été évaluée par la néphrologie infantile, soulignant l'absence de modifications neurologiques, la normotension, les résultats d'osmolalité plasmatique 272 mOsm/kg et d'osmolalité urinaire 510 mOsm/kg, les deux valeurs normales. Avec l'hyponatrémie et l'hypertriglycéridémie, une suspicion de RAM de pseudo-hyponatrémie secondaire à une hypertriglycéridémie associée à L-asp a été évoquée. Elle a été évaluée par gastroentérologie et endocrinologie, indiquant un régime faible en sucres raffinés et riche en fibres, des fibrates (ciprofibrate 100 mg par voie orale par jour) et des oméga 3 (4 g par voie orale par jour), jusqu'à atteindre des valeurs de triglycérides de 300 mg/dL. Deux semaines plus tard, les triglycérides avaient une valeur de 79 mg/dL. Le ciprofibrate et les oméga 3 ont été suspendus, indiquant une utilisation prophylactique associée à un traitement corticoïde et L-asp. Elle a terminé douze doses de L-asp avec une dose cumulative de cent quatre-vingt-quatre mille unités internationales correspondant au protocole d'induction. La suspicion de RAM a été soumise à une évaluation de la causalité, avec l'algorithme de Karch et Lasagna modifié par l'OMS5, qui a abouti à une RAM « définitive » pour la combinaison L-asp et Prednisone\n",
+        "gold_summary": "Le tableau clinique d'un adolescent qui a présenté une pseudo-hyponatrémie et une hypertriglycéridémie au cours du traitement par lymphome non hodgkinien lymphoblastique (LNH) a été décrit. Une suspicion de réaction indésirable aux médicaments (RAM) a été évaluée selon l'algorithme de causalité modifié (Karch et Lasagna), ce qui a conduit à une RAM « définitive » pour l'association L-asp et corticoïdes. Il a été traité avec un régime hypogras et des médicaments modifiant les lipides. L-asp et prednisone n'ont pas été suspendus en raison de la fin de l'indication, conformément au protocole. L'hypertriglycéridémie a été récupérée sans complications après 14 jours de traitement.\n",
+        "synthetic_summary": {
+            "B1": "Un garçon malade a eu un problème avec son sang pendant son traitement. Ce problème venait des médicaments qu'il prenait. Les docteurs ont donné des médicaments et une nourriture spéciale pour l’aider. Il a continué ses médicaments importants pour guérir. Après deux semaines, il allait mieux et son sang est redevenu normal.",
+            "B2": "**Ce qu'ils ont observé chez l'adolescent**  \nUn garçon de 14 ans, traité pour un type de cancer appelé lymphome non hodgkinien lymphoblastique, a développé deux problèmes pendant son traitement : une fausse baisse du sodium dans le sang (appelée pseudo-hyponatrémie) et un taux très élevé de graisses dans le sang (hypertriglycéridémie). Ces troubles sont liés aux médicaments qu’il recevait, notamment la L-asparaginase (L-asp) et les corticoïdes (comme la prednisone).\n\n**Ce que cela signifie**  \nLes médecins ont utilisé une méthode spéciale pour vérifier si ces problèmes venaient bien des médicaments. Ils ont confirmé que c’était une réaction indésirable « définitive » due à la combinaison de L-asp et de corticoïdes. Pour traiter l’hypertriglycéridémie, ils ont donné un régime pauvre en graisses et des médicaments qui aident à réduire les lipides dans le sang.\n\n**Le suivi et l’évolution**  \nMalgré ces effets secondaires, les médicaments contre le cancer n’ont pas été arrêtés car le traitement devait être terminé selon le protocole médical. Après environ deux semaines de traitement pour les graisses élevées, le taux de triglycérides est revenu à la normale sans complications. Cela montre que même si certains médicaments peuvent causer des effets secondaires, ils peuvent être gérés efficacement avec un suivi adapté.",
+            "B3": "Résumé détaillé et structuré\n\nContexte  \nUn adolescent de 14 ans, auparavant en bonne santé, a été hospitalisé pour un lymphome lymphoblastique non hodgkinien (LNH) avec une masse médiastinale causant un syndrome de compression. Le traitement initial comprenait une chimiothérapie cytoréductrice à base de dexaméthasone et cyclophosphamide, suivi du protocole d’induction avec L-asparaginase (L-asp) et prednisone. Pendant son hospitalisation, il a présenté plusieurs complications, notamment un syndrome de lyse tumorale, une thrombose veineuse, une insuffisance rénale, ainsi qu’une hypertriglycéridémie et une pseudo-hyponatrémie.\n\nPrincipales observations  \nAu cours du traitement, après plusieurs doses de L-asp et de glucocorticoïdes, le patient a développé une hyponatrémie persistante (sodium plasmatique à 126 mOsm/kg) associée à une hypertriglycéridémie importante (jusqu’à 1 115 mg/dL) et un cholestérol total élevé (435 mg/dL). L’évaluation néphrologique a exclu une cause neurologique ou une altération de l’osmolalité plasmatique et urinaire, suggérant que l’hyponatrémie était une pseudo-hyponatrémie secondaire à l’hypertriglycéridémie induite par le traitement. Le patient a reçu un régime pauvre en sucres raffinés et riche en fibres, ainsi que des médicaments hypolipémiants (ciprofibrate et oméga-3), permettant une normalisation progressive des triglycérides en deux semaines. L-asp et prednisone n’ont pas été interrompus, car ils étaient indispensables à la poursuite du protocole thérapeutique.\n\nInterprétation clinique  \nL’association entre L-asparaginase et glucocorticoïdes est reconnue pour induire des perturbations métaboliques, notamment une hypertriglycéridémie pouvant entraîner une pseudo-hyponatrémie. L’évaluation de la réaction indésirable aux médicaments (RAM) selon l’algorithme modifié de Karch et Lasagna a conclu à une RAM « définitive » liée à cette association thérapeutique. La prise en charge a été adaptée pour contrôler les anomalies lipidiques sans compromettre le traitement oncologique, ce qui a permis une résolution complète sans complications.\n\nProchaines étapes  \nLe patient a terminé le protocole d’induction avec un total de douze doses de L-asparaginase et une corticothérapie associée. La surveillance clinique et biologique a été maintenue pour prévenir toute récidive de troubles métaboliques. Cette observation souligne l’importance d’une prise en charge multidisciplinaire et d’une vigilance accrue face aux effets secondaires métaboliques des traitements anticancéreux chez l’enfant et l’adolescent."
+        }
+    },
+    {
+        "article": "Femme de 34 ans. Antécédent de tumeur bénigne de la glande salivaire sous-maxillaire droite et de multiples fibroadénomes mammaires. Fumeuse modérée. Elle a consulté pour diplopie soudaine, altération de la coordination du membre supérieur droit, bradylalie et anomies isolées. À l'admission, l'examen neurologique a révélé une amélioration avec un examen normal. La tension artérielle et la glycémie étaient normales. Une IRM du cerveau a été réalisée, qui a révélé une image restrictive en séquence de diffusion au niveau de l'hippocampe gauche. L'admission à l'unité de soins cérébraux a été décidée pour la surveillance, les tests de dépistage et le traitement. Les résultats des analyses générales de laboratoire, de la vitesse de sédimentation des érythrocytes, de la protéine C réactive, de la sous-unité bêta de l'hCG, du VIH, du VDRL, du collagénogramme et de l'analyse toxicologique des urines étaient normaux. Les thrombophilies acquises et génétiques étaient négatives. L'angiotomographie des vaisseaux intra- et extra-crâniens, d'origine embryonnaire fœtale de l'artère cérébrale postérieure gauche, sans autre résultat important, a été réalisée. La télémétrie de 72 heures n'a pas révélé d'arythmie cardiaque. Considérant un éventuel embolus paradoxal, une échographie Doppler veineuse des quatre membres sans thrombose, une échographie transcrânienne Doppler avec contraste, avec passage spontané de bulles « rideau » dans les deux artères sylviennes et un échocardiogramme transthoracique avec contraste (ETT-c) a été réalisée, qui a indiqué un court-circuit droite-gauche avec passage modéré spontané avant le deuxième battement cardiaque. Il a été interprété comme un AVC associé à une FOP probable et un traitement a été initié avec double antiagrégation et statines. Au cours de la procédure préalable à la fermeture de la FOP, une échographie intracardiaque a été réalisée, sans preuve de communication interauriculaire ou de court-circuit intracardiaque droite-gauche. Il a été décidé de compléter l'évaluation avec une angiographie pulmonaire intra- et extra-crânienne, qui a révélé une MAV dans le segment postérieur du lobe pulmonaire inférieur droit. L'angiographie pulmonaire numérique a confirmé une MAV à haut débit. Une angiographie pulmonaire a été réalisée, avec occlusion complète du vaisseau par un dispositif endovasculaire, préservant les artères normales. Au cours du suivi, une évaluation clinique, gynécologique, oncologique et rhumatologique a été réalisée sans résultats pertinents. La patiente ne remplissait aucun des critères de Curaçao pour la télangiectasie hémorragique héréditaire (syndrome de Rendu-Osler-Weber), c'est-à-dire épistaxis récurrente, télangiectasies cutanées/muqueuses et atteinte viscérale multiple, ni n'avait d'antécédent de maladie chez un parent au premier degré. Il a également été décidé de procéder à un examen génétique avec un panel de télangiectasie hémorragique héréditaire (gènes : ACVRL1, ENG, EPHB4, GDF2, RASA1 et SMAD4), avec résultat négatif. La découverte a été interprétée comme une MAVP sporadique. La patiente est actuellement stable sur le plan clinique et neurologique. Le consentement éclairé de la patiente a été obtenu, autorisant la publication, la reproduction et la diffusion du cas clinique.\n",
+        "gold_summary": "Nous présentons le cas d’une femme de 34 ans ayant un AVC ischémique talamique gauche. Un passage de bulles « en rideau » dans les artères cérébrales a été détecté par Doppler transcrânien. L’échographie intracardiaque n’a pas révélé de foramen ovale perméable, ce qui a conduit à la réalisation d’une angiotomographie pulmonaire, qui a confirmé la présence d’une MAVP. La patiente a bénéficié d’un traitement endovasculaire réussi.\n",
+        "synthetic_summary": {
+            "B1": "Une dame de 34 ans a eu un problème dans son cerveau. Ce problème a fait que son corps ne bougeait pas bien. Les docteurs ont cherché d’où venait ce problème. Ils ont trouvé un petit passage dans ses poumons qui ne devait pas être là. Les docteurs ont réparé ce passage avec un soin spécial. Maintenant, elle va mieux et se sent bien.",
+            "B2": "Voici un résumé simple et clair pour un élève de 14 ans :\n\nUne femme de 34 ans a eu un accident vasculaire cérébral (AVC) à cause d’un problème dans une petite partie de son cerveau appelée le thalamus. Les médecins ont fait plusieurs examens pour comprendre pourquoi. Ils ont trouvé des bulles d’air qui passaient dans ses vaisseaux sanguins du cerveau, ce qui peut causer des caillots. Mais ils n’ont pas trouvé de trou dans son cœur, ce qui est souvent une cause de ce genre de problème.\n\nAlors, ils ont cherché ailleurs et ont découvert une malformation dans un vaisseau sanguin de ses poumons, appelée malformation artério-veineuse pulmonaire (MAVP). C’est une sorte de connexion anormale entre une artère et une veine qui peut laisser passer des caillots vers le cerveau.\n\nPour soigner cela, les médecins ont fait une intervention appelée traitement endovasculaire. Ils ont bouché cette malformation en passant par les vaisseaux sanguins, sans ouvrir la poitrine. Grâce à ce traitement, la patiente va bien maintenant.",
+            "B3": "Résumé détaillé et structuré\n\nContexte  \nNous rapportons le cas d’une femme de 34 ans, présentant des antécédents de tumeur bénigne de la glande salivaire sous-maxillaire droite et de multiples fibroadénomes mammaires. Fumeuse modérée, elle a consulté en raison d’une diplopie soudaine (vision double), d’une altération de la coordination du membre supérieur droit, d’une bradylalie (ralentissement de la parole) et d’anomalies isolées du langage. À son admission, l’examen neurologique était revenu à la normale, avec une tension artérielle et une glycémie normales.\n\nPrincipales observations  \nL’IRM cérébrale a montré une lésion restrictive en séquence de diffusion au niveau de l’hippocampe gauche, compatible avec un accident vasculaire cérébral (AVC) ischémique. Les analyses biologiques générales, incluant marqueurs inflammatoires, sérologies infectieuses, et tests de thrombophilie, étaient normales ou négatives. L’angiotomographie cérébrale a révélé une variante anatomique sans anomalie significative. La surveillance cardiaque n’a pas détecté d’arythmie.\n\nUne échographie Doppler transcrânienne avec contraste a mis en évidence un passage spontané de bulles « en rideau » dans les artères cérébrales, suggérant un court-circuit droite-gauche. Cependant, l’échographie intracardiaque réalisée avant une éventuelle fermeture du foramen ovale perméable (FOP) n’a pas confirmé la présence d’une communication interauriculaire ni de court-circuit intracardiaque. En complément, une angiographie pulmonaire a révélé une malformation artérioveineuse pulmonaire (MAVP) à haut débit dans le segment postérieur du lobe pulmonaire inférieur droit.\n\nInterprétation clinique  \nL’AVC ischémique a été attribué à un embolisme paradoxal secondaire à cette MAVP, qui permettait le passage direct de sang veineux vers la circulation artérielle sans filtration pulmonaire. L’absence de critères cliniques et génétiques pour la télangiectasie hémorragique héréditaire (syndrome de Rendu-Osler-Weber) a conduit à considérer la MAVP comme sporadique.\n\nProchaines étapes et suivi  \nLa patiente a bénéficié d’un traitement endovasculaire par occlusion complète de la MAVP, préservant les artères normales. Les évaluations cliniques complémentaires, gynécologiques, oncologiques et rhumatologiques n’ont pas révélé d’autres pathologies associées. La patiente est actuellement stable sur le plan neurologique et clinique. Son consentement éclairé a été obtenu pour la publication de ce cas."
+        }
+    }
+]
\ No newline at end of file
diff --git a/generating_data/score/es_syntheticV3_aggregate_metrics.json b/generating_data/score/es_syntheticV3_aggregate_metrics.json
new file mode 100644
index 0000000000000000000000000000000000000000..ed5aff9c0eecd848ab3fb5a9802d0e4192fc9d6b
--- /dev/null
+++ b/generating_data/score/es_syntheticV3_aggregate_metrics.json
@@ -0,0 +1,60 @@
+{
+  "config": {
+    "weights": {
+      "w_rouge": 0.5,
+      "w_bert": 0.5
+    },
+    "quantiles": {
+      "worst_q": 0.33,
+      "best_q": 0.67,
+      "good_q": 0.5
+    },
+    "thresholds": {
+      "B1": {
+        "worst_thr": 0.447808442930168,
+        "best_thr": 0.4685943565892835,
+        "good_thr": 0.4590858975817874
+      },
+      "B2": {
+        "worst_thr": 0.5084380281022721,
+        "best_thr": 0.5420982254271056,
+        "good_thr": 0.5206064335573108
+      },
+      "B3": {
+        "worst_thr": 0.5019653275501893,
+        "best_thr": 0.5440850403537373,
+        "good_thr": 0.524079490930252
+      }
+    }
+  },
+  "B1": {
+    "ROUGE-L-Sum": 0.1873410503259442,
+    "BERTScore_F": 0.7296109676361084,
+    "combined_mean": 0.45847600898102625,
+    "count": 100,
+    "best_rate": 0.33,
+    "good_rate": 0.34,
+    "worst_rate": 0.33,
+    "is_good_rate": 0.5
+  },
+  "B2": {
+    "ROUGE-L-Sum": 0.2698462206061245,
+    "BERTScore_F": 0.7795004910230636,
+    "combined_mean": 0.5246733558145941,
+    "count": 100,
+    "best_rate": 0.33,
+    "good_rate": 0.34,
+    "worst_rate": 0.33,
+    "is_good_rate": 0.5
+  },
+  "B3": {
+    "ROUGE-L-Sum": 0.2509233585026421,
+    "BERTScore_F": 0.7980521380901336,
+    "combined_mean": 0.5244877482963879,
+    "count": 100,
+    "best_rate": 0.33,
+    "good_rate": 0.34,
+    "worst_rate": 0.33,
+    "is_good_rate": 0.5
+  }
+}
\ No newline at end of file
diff --git a/generating_data/score/es_syntheticV3_scored.json b/generating_data/score/es_syntheticV3_scored.json
new file mode 100644
index 0000000000000000000000000000000000000000..0669e9f5f8c426c1c53369a84f7b3b9bb52fc24e
--- /dev/null
+++ b/generating_data/score/es_syntheticV3_scored.json
@@ -0,0 +1,4202 @@
+[
+  {
+    "id": 0,
+    "gold_summary": "Un hombre de 27 años, fumador sin antecedentes patológicos, estuvo involucrado en un accidente de tráfico, al caerse de una motocicleta sin casco. En el ingreso al hospital de nuestro distrito rural, la escala de coma de Glasgow durante el examen físico fue de 6/15 con midriasis bilateral, distrés hemodinámico y buena saturación. Se identificó una lesión penetrante en la cabeza con profusa hemorragia intracraneal. Se usó el relleno intracraneal conocido en la neurocirugía de control de daños para taponar la hemorragia intracraneal grave y que es una maniobra neuroquirúrgica que salva vidas. El paciente fue trasladado inconsciente a un hospital de primera categoría, libre de intubación y en un estado hemodinámico estable. El período postoperatorio estuvo marcado por convulsiones, por lo que el paciente fue puesto en anticonvulsivos con un buen resultado.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Un hombre se cayó de su moto y se lastimó la cabeza. No llevaba casco y se hizo una herida que sangraba mucho. Cuando llegó al hospital, estaba muy dormido y no podía hablar ni abrir los ojos. \n\nLos doctores pusieron algo para parar la sangre dentro de su cabeza. Luego lo llevaron a otro hospital donde lo cuidaron mejor. Después de la operación, tuvo algunos temblores, pero le dieron medicina y se mejoró.",
+        "score": {
+          "ROUGE-L-Sum": 0.16814159292035397,
+          "BERTScore_F": 0.7161517143249512
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.4421466536226526
+        }
+      },
+      "B2": {
+        "text": "**Lo que pasó con el paciente**  \nUn hombre de 27 años que fuma tuvo un accidente al caerse de su motocicleta sin usar casco. Cuando llegó al hospital en una zona rural, estaba muy grave. No respondía bien, tenía las pupilas dilatadas en ambos ojos y sangraba mucho dentro de su cabeza por una herida penetrante.\n\n**Qué hicieron los médicos**  \nPara detener la hemorragia dentro de su cráneo, los médicos usaron una técnica llamada relleno intracraneal. Esto significa que colocaron un material especial para tapar la herida y controlar el sangrado, lo cual es una cirugía que puede salvar vidas en casos graves. Luego, lo trasladaron a un hospital mejor equipado, donde estaba inconsciente pero estable en cuanto a su circulación y respiración.\n\n**Qué pasó después de la operación**  \nDespués de la cirugía, el paciente tuvo convulsiones, que son movimientos involuntarios causados por problemas en el cerebro. Por eso, le dieron medicamentos llamados anticonvulsivos para controlar estas convulsiones. Gracias a este tratamiento, el paciente mejoró y tuvo una buena recuperación.",
+        "score": {
+          "ROUGE-L-Sum": 0.3053892215568862,
+          "BERTScore_F": 0.7984228134155273
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5519060174862067
+        }
+      },
+      "B3": {
+        "text": "Resumen detallado para público general universitario\n\nContexto  \nUn hombre de 27 años, fumador y sin antecedentes médicos previos, sufrió un accidente de tráfico al caerse de una motocicleta sin usar casco. Tras la caída, presentó dolor de cabeza y una herida sangrante en la frente, por lo que acudió al hospital local en una zona rural.\n\nHallazgos clínicos y evaluación inicial  \nAl llegar al hospital, el paciente perdió el conocimiento y tuvo dos convulsiones. La evaluación neurológica mostró una escala de coma de Glasgow de 6 sobre 15, lo que indica un estado de coma profundo (no abría los ojos, respondía solo con movimientos para evitar el dolor y no hablaba). Además, presentaba midriasis bilateral (dilatación anormal de ambas pupilas), dificultad para mantener la presión arterial (distrés hemodinámico) y buena saturación de oxígeno. Se detectó una lesión penetrante en el cráneo con una hemorragia intracraneal abundante, lo que significa que la sangre estaba acumulándose dentro del cerebro debido a la lesión.\n\nIntervención inicial y traslado  \nEn el hospital rural, donde no había unidad de cuidados intensivos ni tomografía computarizada (TAC), se aplicó un tratamiento de emergencia para controlar el sangrado intracraneal mediante una técnica quirúrgica llamada relleno intracraneal, que consiste en taponar la fractura del cráneo para detener la hemorragia y estabilizar al paciente. Además, se estabilizó la columna cervical, se realizó intubación orotraqueal para asegurar la respiración, se administraron líquidos intravenosos, medicamentos anticonvulsivos para controlar las convulsiones, antibióticos para prevenir infecciones y una transfusión sanguínea debido a la anemia severa (hemoglobina de 6 g/dL). Posteriormente, el paciente fue trasladado inconsciente pero hemodinámicamente estable a un hospital de mayor nivel con mejores recursos.\n\nDiagnóstico y tratamiento avanzado  \nEn el hospital de referencia, se realizó una tomografía computarizada que reveló múltiples lesiones cerebrales graves: edema cerebral (hinchazón del cerebro) en ambas áreas frontales, contusión hemorrágica (moretón con sangrado) en el tejido cerebral del lado derecho, un hematoma subdural agudo (acumulación de sangre entre el cerebro y la membrana que lo cubre) en el lado izquierdo, una hernia subfalcular (desplazamiento del cerebro hacia un lado), compresión ventricular leve, hemorragia subaracnoidea (sangrado en el espacio que rodea el cerebro), fractura deprimida del hueso frontal con ruptura de las membranas que cubren el cerebro, y fractura de la tercera vértebra cervical con compresión de la médula espinal. El paciente fue sometido a una cirugía exitosa para tratar estas lesiones.\n\nEvolución y seguimiento  \nDurante el postoperatorio, el paciente presentó convulsiones que fueron controladas con medicamentos anticonvulsivos, logrando una buena respuesta clínica. Al día siguiente de la cirugía, el paciente estaba consciente, podía caminar y no mostraba problemas neurológicos, respiratorios ni circulatorios.\n\nInterpretación clínica  \nEste caso ilustra la gravedad de los traumatismos craneoencefálicos penetrantes y la importancia de una intervención rápida y adecuada, incluso en entornos con recursos limitados. La técnica de relleno intracraneal utilizada inicialmente fue fundamental para controlar la hemorragia y estabilizar al paciente antes del traslado. La atención especializada posterior y el manejo multidisciplinario permitieron una recuperación favorable a pesar de las múltiples lesiones cerebrales y de la médula espinal.\n\nPróximos pasos  \nSe recomienda continuar con el seguimiento neurológico y rehabilitación para evaluar y tratar posibles secuelas a largo plazo, así como mantener el control de las convulsiones con medicación adecuada. Además, es fundamental promover el uso de casco y medidas de seguridad vial para prevenir este tipo de accidentes.",
+        "score": {
+          "ROUGE-L-Sum": 0.23938223938223938,
+          "BERTScore_F": 0.8202024698257446
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.529792354603992
+        }
+      }
+    }
+  },
+  {
+    "id": 1,
+    "gold_summary": "Una mujer de 54 años de edad acudió a nuestro hospital con la queja de una masa indolora en su vagina de 3 años de duración. Hace tres años, encontró una protuberancia de masa a través de su vagina, que gradualmente creció en tamaño con el tiempo. En el examen físico, el fondo uterino fue el punto principal de la masa y sobresalía 7 cm por debajo del anillo del himen. Como resultado, se le diagnosticó inversión uterina crónica y se le sometió a una histerectomía abdominal. Fue dada de alta en casa mejorada. Presentamos este caso debido a un factor no identificado que provocó la inversión uterina, la presentación tardía de la enfermedad y la dificultad en el tratamiento quirúrgico.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Había una señora que tenía una bolita en su cuerpo. Esa bolita estaba en un lugar muy especial dentro de ella. La bolita creció poco a poco durante mucho tiempo. Los doctores vieron que esa bolita era parte de un órgano que estaba fuera de su lugar. Ella tuvo que ir al hospital para que los doctores la ayudaran con una operación. Después de la operación, la señora se sintió mejor y pudo ir a su casa. Los doctores contaron esta historia para que otros puedan aprender.",
+        "score": {
+          "ROUGE-L-Sum": 0.16521739130434784,
+          "BERTScore_F": 0.7476157546043396
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.45641657295434374
+        }
+      },
+      "B2": {
+        "text": "**Lo que le Pasó a la Paciente**  \nUna mujer de 54 años notó hace tres años una masa o bulto que salía de su vagina. Esta masa fue creciendo poco a poco y no le causaba dolor. Al principio, tuvo sangrado y mal olor, pero eso paró hace un año. También se lastimó la masa hace seis meses, lo que la hizo sentirse mal y alejarse de su familia y amigos.\n\n**Qué Encontraron los Médicos**  \nCuando la examinaron, vieron que la masa era parte del útero que había salido hacia afuera por la vagina. Esto se llama inversión uterina crónica, que es cuando el útero se da vuelta y sale fuera del cuerpo. Había una herida larga en la masa, pero no estaba sangrando en ese momento. Los exámenes de sangre y orina estaban normales, y no tenía infecciones como VIH o hepatitis.\n\n**Cómo la Ayudaron**  \nLos médicos decidieron hacer una cirugía para quitar el útero, llamada histerectomía abdominal. La operación fue complicada porque el tejido estaba muy cambiado y era difícil saber dónde estaban las partes normales. Durante la cirugía, se lastimó un conducto que lleva la orina desde el riñón a la vejiga, pero lo repararon en el mismo momento. Después de la operación, la paciente mejoró y pudo volver a casa. En el control dos semanas después, estaba bien y sin problemas.\n\n**Por Qué es Importante Este Caso**  \nEste caso es especial porque la inversión uterina es rara y no se sabe exactamente qué la causó en esta mujer. Además, ella llegó al hospital muy tarde, cuando la situación ya era difícil de tratar. La cirugía fue complicada, pero al final tuvo un buen resultado. Esto muestra la importancia de buscar ayuda médica a tiempo cuando se tiene una masa o bulto en el cuerpo.",
+        "score": {
+          "ROUGE-L-Sum": 0.2370689655172414,
+          "BERTScore_F": 0.7791949510574341
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.5081319582873377
+        }
+      },
+      "B3": {
+        "text": "Resumen para Público General Educado\n\nContexto  \nUna mujer de 54 años, originaria de una zona rural, acudió al hospital tras presentar durante tres años una masa que sobresalía por su vagina. Esta masa fue creciendo lentamente y, en sus primeros años, estuvo acompañada de sangrado y secreción con mal olor, aunque estos síntomas desaparecieron en el último año. La paciente había tenido dos partos en casa, asistida por una comadrona tradicional, sin complicaciones aparentes. Debido a la masa y a una herida (laceración) que apareció en ella hace seis meses, la paciente sufrió aislamiento social y divorcio. Finalmente, fue llevada al hospital por familiares para recibir atención médica.\n\nHallazgos Clínicos  \nAl examen físico, se encontró una masa de color rosado ubicada aproximadamente a 7 centímetros del borde del himen (la membrana que rodea la entrada de la vagina). La parte principal de esta masa correspondía al fondo uterino, que es la parte superior del útero. En la masa había una herida longitudinal de unos 5 centímetros, pero no se observó sangrado ni secreción en ese momento. Los signos vitales de la paciente estaban dentro de rangos normales y los análisis de sangre y orina no mostraron alteraciones significativas. La ecografía abdominal no logró visualizar el útero en su posición habitual, lo que apoyó el diagnóstico.\n\nDiagnóstico e Interpretación Clínica  \nSe diagnosticó a la paciente con inversión uterina crónica, una condición poco común en la que el útero se voltea hacia adentro y puede protruir a través de la vagina. En este caso, la inversión era completa y prolongada, lo que causó la formación de la masa visible y la laceración en su superficie. La causa exacta que originó esta inversión uterina no pudo ser identificada, lo que hace este caso especialmente relevante.\n\nTratamiento y Evolución  \nDespués de discutir las opciones con la paciente y su familia, se decidió realizar una histerectomía abdominal, que consiste en la extirpación quirúrgica del útero a través del abdomen. Durante la cirugía, se encontró que el tejido estaba muy distorsionado y redundante, lo que dificultó la identificación de las estructuras anatómicas normales. Esto llevó a una complicación quirúrgica: una lesión en el uréter derecho (el conducto que conecta el riñón con la vejiga), que fue reparada mediante una anastomosis (unión quirúrgica) de extremo a extremo. La paciente fue dada de alta diez días después de la operación, con mejoría clínica, y en el control posterior mostró una recuperación satisfactoria, con un canal vaginal normal.\n\nImportancia del Caso  \nEste caso destaca la presentación tardía y poco común de una inversión uterina crónica en una mujer rural, así como las dificultades quirúrgicas asociadas a esta condición. La ausencia de atención médica temprana y la falta de acceso a centros de salud contribuyeron a la evolución prolongada y compleja del caso. La experiencia subraya la necesidad de mejorar el acceso a servicios médicos y la educación sanitaria en áreas rurales para prevenir complicaciones graves.",
+        "score": {
+          "ROUGE-L-Sum": 0.21676300578034682,
+          "BERTScore_F": 0.8029177784919739
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.5098403921361604
+        }
+      }
+    }
+  },
+  {
+    "id": 2,
+    "gold_summary": "Se presenta el caso de un varón de 20 años con espondilitis tuberculosa multinivel no contigua (cervical, dorsal 6, dorsal 10 y lumbar). Se trata de un paciente HIV negativo con tuberculosis diseminada con grave compromiso de su estado general y múltiples localizaciones de la enfermedad. Algunas tenían fistulas que secretaban caseum. El paciente presentó paraplejía aguda que requirió, teniendo en cuenta el nivel sensitivo a nivel dorsal 6, una primera cirugía urgente de descompresión por vía posterior. Luego se efectuó la cirugía programada. En primera instancia, la región cervical por vía anterior, con corporectomía, colocación de reemplazo de cuerpo vertebral más injerto autólogo y placa con tornillos. Posteriormente se evidenció luxación del nivel dorsal 6 hacia atrás comprimiendo la médula espinal y, dada la inestabilidad mecánica, se indicó un tercer tiempo quirúrgico por vía posterior que comprendió reducción, descompresión y fijación, resolviendo los tres niveles por vía posterior con barras y tornillos. El tratamiento quirúrgico, médico y kinésico de esta forma poco frecuente del mal de Pott fue exitoso, con recuperación de su estabilidad mecánica y progresiva recuperación de su estado neurológico.",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Había un joven de 20 años muy enfermo con un hueso del cuello y la espalda roto por una infección. Esta infección era muy fuerte y estaba en muchos lugares de su cuerpo. A veces, de sus heridas salía una cosa blanda y fea. \n\nUn día, el joven no pudo mover sus piernas. Los doctores hicieron una operación rápida para ayudar a su espalda y que pudiera sentir y mover mejor. Después, le hicieron otra operación para arreglar los huesos del cuello con partes nuevas y tornillos. \n\nLuego, vieron que un hueso de su espalda estaba fuera de lugar y apretaba la parte que mueve y siente el cuerpo. Entonces, hicieron otra operación para poner todo en su lugar con barras y tornillos. \n\nCon medicinas, ejercicios y las operaciones, el joven mejoró mucho. Ahora puede caminar y está más fuerte. Los doctores están contentos porque él está mejor.",
+        "score": {
+          "ROUGE-L-Sum": 0.18085106382978722,
+          "BERTScore_F": 0.745992124080658
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.4634215939552226
+        }
+      },
+      "B2": {
+        "text": "**Caso de Tuberculosis en la Columna Vertebral**\n\nEste es el caso de un joven de 20 años que tenía tuberculosis, una infección causada por una bacteria llamada Mycobacterium tuberculosis. Aunque no tenía VIH, la infección estaba muy extendida y afectaba varias partes de su columna vertebral: el cuello (cervical), la parte media de la espalda (dorsal) y la zona baja (lumbar). Algunas áreas tenían heridas abiertas que soltaban una sustancia llamada caseum, que es un material parecido a queso que se forma por la infección.\n\n**Problemas y Tratamiento Inicial**\n\nEl paciente sufrió una pérdida súbita de movimiento y sensibilidad en las piernas, llamada paraplejía, debido a que la médula espinal estaba comprimida en la zona dorsal 6 (parte media de la espalda). Por eso, tuvo que someterse a una cirugía urgente para aliviar la presión en la médula, llamada descompresión, realizada por la parte trasera de la columna.\n\nDespués, se hizo una cirugía programada en el cuello, por la parte delantera, donde se removieron varios cuerpos vertebrales dañados (corporectomía). Para reemplazarlos, se usaron injertos, que son partes de hueso tomadas del propio paciente, junto con placas y tornillos para estabilizar la columna.\n\n**Complicación y Cirugía Final**\n\nMás adelante, se descubrió que una vértebra en la zona dorsal 6 se había desplazado hacia atrás, presionando otra vez la médula espinal y causando inestabilidad en la columna. Por esta razón, se realizó una tercera cirugía por la parte trasera para corregir el desplazamiento, aliviar la presión y fijar la columna con barras y tornillos desde el cuello hasta la parte media de la espalda.\n\n**Resultado**\n\nCon el tratamiento combinado de medicamentos para la tuberculosis, cirugías y rehabilitación física, el paciente mejoró mucho. Recuperó la estabilidad de su columna y la función de sus piernas, pudiendo caminar por sí mismo después de una larga hospitalización de cinco meses. Este caso muestra cómo, aunque la tuberculosis en la columna puede ser grave y complicada, un tratamiento adecuado puede llevar a una buena recuperación.",
+        "score": {
+          "ROUGE-L-Sum": 0.26850258175559377,
+          "BERTScore_F": 0.7944828271865845
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.5314927044710891
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe describe el caso de un joven de 20 años, sin infección por VIH, que presentó tuberculosis pulmonar y ósea diseminada, con afectación de múltiples niveles de la columna vertebral (cervical, dorsal y lumbar) en forma no contigua. El paciente tenía un estado general muy deteriorado, con pérdida de peso, atrofia muscular severa y lesiones tumorales en la piel que secretaban material caseoso (una sustancia similar a queso, típica de la tuberculosis). Estas lesiones estaban fistulizadas, es decir, comunicadas con el exterior, en regiones como el dorso, el cráneo y el tórax anterior.\n\n**Hallazgos Clave**  \n- Confirmación microbiológica de Mycobacterium tuberculosis sensible a rifampicina y otros antibióticos habituales.  \n- Imágenes de tomografía computarizada y resonancia magnética que mostraron consolidaciones pulmonares, lesiones óseas líticas (áreas de destrucción ósea) en varios niveles vertebrales y colecciones (acumulaciones de líquido o pus) pre y paraespinales.  \n- Fracturas patológicas en las vértebras dorsales D6 y D10, con infiltración tumoral desde C4 a C6, D4 a D6, D9 a D12 y L1 a L3.  \n- Episodio agudo de paraplejía (pérdida de movimiento y sensibilidad en las piernas) con nivel sensitivo en D8 y compromiso vesical, atribuible a compresión medular aguda en D6.\n\n**Interpretación Clínica**  \nEl paciente presentó una forma grave y poco común de tuberculosis ósea conocida como mal de Pott, con afectación de múltiples niveles vertebrales no contiguos. La destrucción ósea extensa y la presencia de colecciones pusieron en riesgo la integridad neurológica, con riesgo de parálisis permanente. La paraplejía aguda requirió una intervención quirúrgica urgente para descomprimir la médula espinal mediante laminectomía (extirpación de parte de la vértebra) y evacuación de la colección epidural. Posteriormente, se realizó una cirugía programada en la región cervical por vía anterior, que incluyó la extracción de varios cuerpos vertebrales afectados (corporectomía), reconstrucción con injerto óseo autólogo y fijación con placa y tornillos. Sin embargo, se detectó una luxación posterior en D6 que comprimía nuevamente la médula, causando inestabilidad mecánica y deterioro neurológico. Esto motivó una tercera cirugía por vía posterior para reducir la luxación, descomprimir la médula y fijar los niveles cervical y dorsales afectados con tornillos y barras, estabilizando la columna desde C3 hasta D12.\n\n**Próximos Pasos y Evolución**  \nEl tratamiento combinado, que incluyó terapia antituberculosa estándar de primera línea durante al menos 12 meses, intervenciones quirúrgicas escalonadas y rehabilitación kinésica intensiva, permitió la recuperación progresiva de la función motora y sensitiva del paciente. Además, se logró la resolución de las lesiones pulmonares y la estabilidad mecánica de la columna vertebral. Tras una prolongada hospitalización de cinco meses, el paciente egresó caminando por sus propios medios, evidenciando una evolución favorable en un caso complejo y de alta gravedad.",
+        "score": {
+          "ROUGE-L-Sum": 0.27586206896551724,
+          "BERTScore_F": 0.7858632206916809
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.5308626448285991
+        }
+      }
+    }
+  },
+  {
+    "id": 3,
+    "gold_summary": "Un hombre de 23 años tenía debilidad muscular progresiva y distrofia muscular de Emery-Dreifuss (EDMD) debido a una mutación de LMNA (lamina A/C). Insuficiencia cardiaca congestiva diagnosticada a los 19 años de edad. El tratamiento farmacológico máximo/resincronización cardiaca no logró mejorar la función cardiaca. Por lo tanto, fue hospitalizado debido a insuficiencia cardiaca. A pesar de la oxigenación por membrana extracorpórea, desarrolló una disfunción cardiaca derecha grave y falleció (fallo multiorgánico).\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Había un hombre joven con músculos muy débiles. Tenía una enfermedad que hace que los músculos se pongan muy rígidos y duros. Su corazón también se puso muy cansado y no podía trabajar bien. Los doctores le dieron medicinas y una máquina para ayudar su corazón. Pero su corazón se puso peor y se enfermó mucho. Al final, su cuerpo no pudo seguir y él murió.",
+        "score": {
+          "ROUGE-L-Sum": 0.15853658536585363,
+          "BERTScore_F": 0.7072277069091797
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.43288214613751663
+        }
+      },
+      "B2": {
+        "text": "**Lo que le pasaba al paciente:**  \nUn joven japonés de 23 años tenía una enfermedad llamada distrofia muscular de Emery-Dreifuss (EDMD). Esta enfermedad afecta los músculos y está causada por un cambio en un gen llamado LMNA, que produce una proteína importante para las células. Desde pequeño, él tenía problemas para moverse bien y sus músculos se ponían rígidos. A los 19 años, comenzó a tener problemas graves en su corazón, especialmente en la parte derecha, lo que causaba insuficiencia cardiaca, es decir, que el corazón no podía bombear sangre correctamente.\n\n**Tratamientos y evolución:**  \nEl paciente recibió varios medicamentos para mejorar su corazón y un dispositivo llamado desfibrilador para prevenir ritmos cardiacos peligrosos. Más tarde, le pusieron un tratamiento llamado terapia de resincronización cardiaca, que ayuda a que las partes del corazón trabajen juntas mejor. Sin embargo, ninguno de estos tratamientos logró mejorar suficientemente la función de su corazón.\n\n**Lo que ocurrió en el hospital:**  \nFue ingresado en el hospital por empeoramiento de su insuficiencia cardiaca. Los médicos usaron máquinas especiales para ayudar a su corazón y a sus órganos, como la oxigenación por membrana extracorpórea (ECMO), que es un sistema que ayuda a oxigenar la sangre cuando el corazón y los pulmones no funcionan bien. A pesar de estos esfuerzos, su corazón derecho siguió fallando gravemente, lo que provocó que otros órganos también dejaran de funcionar, y lamentablemente falleció.\n\n**Qué significa este caso:**  \nEste caso muestra cómo la distrofia muscular de Emery-Dreifuss puede afectar no solo los músculos, sino también el corazón, causando insuficiencia cardiaca severa que es difícil de tratar. La mutación genética en LMNA juega un papel importante en esta enfermedad. Aunque existen tratamientos avanzados, en algunos casos la enfermedad puede progresar y causar complicaciones graves que llevan a la muerte.",
+        "score": {
+          "ROUGE-L-Sum": 0.22911694510739858,
+          "BERTScore_F": 0.7612161636352539
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.49516655437132623
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe presenta el caso de un hombre japonés de 23 años con distrofia muscular de Emery-Dreifuss (EDMD), una enfermedad genética causada por una mutación en el gen LMNA que codifica la proteína lamina A/C. Esta mutación específica (leucina 102 a prolina en el exón 1) provocó debilidad muscular progresiva desde la infancia, contracturas articulares y rigidez muscular, manifestaciones típicas de esta enfermedad. Además, existía un antecedente familiar importante, ya que su padre también padeció EDMD y falleció súbitamente a los 40 años.\n\n**Hallazgos Clave**  \nA los 19 años, el paciente desarrolló insuficiencia cardíaca congestiva, principalmente por disfunción severa del ventrículo derecho (RV), evidenciada por síntomas como edema en las piernas y congestión hepática, así como por estudios ecocardiográficos y cateterismo cardíaco que mostraron una función ventricular deteriorada. A pesar de recibir tratamiento farmacológico intensivo con diuréticos, betabloqueantes y inhibidores de la enzima convertidora de angiotensina, la función cardíaca no mejoró. A los 22 años se le implantó un desfibrilador cardioversor implantable (ICD) debido a episodios de taquicardia ventricular y riesgo de muerte súbita.\n\nCuando la insuficiencia cardíaca progresó a una etapa avanzada (clasificación funcional III de la New York Heart Association), se le realizó una terapia de resincronización cardíaca (CRT) para mejorar la función del corazón. Sin embargo, al ingreso hospitalario a los 23 años, persistían signos de insuficiencia cardíaca derecha grave, con dilatación de ambos ventrículos, reducción significativa de la fracción de eyección del ventrículo izquierdo (LVEF 30%) y disfunción severa del ventrículo derecho, acompañada de insuficiencia valvular mitral y tricuspídea.\n\nDurante su hospitalización, el paciente presentó empeoramiento progresivo de la función renal y hepática, complicaciones que reflejaban la insuficiencia multiorgánica secundaria a la falla cardíaca avanzada. Se implementaron tratamientos de soporte hemodinámico, incluyendo infusiones de medicamentos inotrópicos, bombeo de globo intraaórtico (IABP), terapia de reemplazo renal continua (CRRT) y finalmente oxigenación por membrana extracorpórea (ECMO) veno-arterial. A pesar de estas intervenciones, desarrolló coagulación intravascular diseminada (CID) y una diátesis hemorrágica sistémica, que culminaron en su fallecimiento por fallo multiorgánico al día 100 de hospitalización.\n\n**Interpretación Clínica**  \nEste caso ilustra la evolución grave y progresiva de la insuficiencia cardíaca en un paciente con EDMD causada por una mutación en LMNA, destacando la predominancia de la disfunción del ventrículo derecho como factor principal en su deterioro clínico. La resistencia a los tratamientos convencionales y avanzados, como la terapia farmacológica máxima, resincronización cardíaca y soporte mecánico, refleja la complejidad y severidad de la cardiomiopatía asociada a esta enfermedad genética. Los hallazgos histopatológicos post mortem confirmaron la presencia de hipertrofia miocárdica, fibrosis severa en ambos ventrículos y daño hepático compatible con congestión crónica y “hígado de shock”.\n\n**Próximos Pasos y Consideraciones**  \nEste caso subraya la necesidad de un diagnóstico temprano y un seguimiento riguroso en pacientes con EDMD, especialmente aquellos con mutaciones en LMNA, dado el alto riesgo de insuficiencia cardíaca progresiva y muerte súbita. La identificación de disfunción ventricular derecha precoz podría orientar intervenciones más agresivas o la consideración temprana de trasplante cardíaco. Además, se requiere investigación continua para desarrollar terapias específicas que puedan modificar el curso de la cardiomiopatía en EDMD y mejorar la supervivencia y calidad de vida de estos pacientes.",
+        "score": {
+          "ROUGE-L-Sum": 0.16223776223776223,
+          "BERTScore_F": 0.8112456798553467
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.48674172104655444
+        }
+      }
+    }
+  },
+  {
+    "id": 4,
+    "gold_summary": "Mujer de 65 años con NT derecho (inicialmente en V2-V3) desde 2004 con control regular con carboxamidas. Diecisiete años después empeoraron los paroxismos en V2-V3, aparecieron también en V1 y en el territorio del nervio glosofaríngeo derecho (oído derecho y fosa amigdalar al hablar y deglutir). La resonancia magnética cerebral mostró contacto arterial significativo entre arteria cerebelosa superior (ACS) con origen del V par craneal derecho y de la arteria cerebelosa antero-inferior (AICA) con el origen de pares craneales bajos derechos. Se realizó DMV de ambos pares craneales en un mismo tiempo quirúrgico mediante craniectomía retrosigmoidea, y se procedió a la liberación del V par craneal, en contacto íntimo con la ACS, y del IX par craneal en contacto con la AICA derecha, para lo que se puso teflón entre ellas. La paciente tuvo una resolución inmediata de los paroxismos trigeminales y una mejoría considerable en intensidad y frecuencia de los glosofaríngeos. A los 2 años de la intervención continúa la desescalada de tratamiento neuromodulador con buena respuesta.",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Había una señora de 65 años que tenía dolor fuerte en la cara desde hace mucho tiempo. El dolor estaba en un lado de su cara y a veces se hacía más fuerte. También empezó a dolerle la garganta y el oído cuando comía o hablaba.\n\nLos doctores le hicieron una foto especial de su cabeza. Vieron que unas partes de su cuerpo, que son como tubitos, estaban tocando nervios que causaban el dolor.\n\nEntonces, los doctores hicieron una operación para poner un pedacito suave entre los tubitos y los nervios. Esto ayudó mucho a que el dolor se fuera.\n\nDespués de la operación, la señora se sintió mucho mejor. El dolor casi no volvió y pudo tomar menos medicina. Está feliz y tranquila.",
+        "score": {
+          "ROUGE-L-Sum": 0.2030769230769231,
+          "BERTScore_F": 0.7409898638725281
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.4720333934747256
+        }
+      },
+      "B2": {
+        "text": "**Lo que le Pasó a la Paciente**  \nUna mujer de 65 años tuvo un dolor muy fuerte y repentino en la cara desde 2004. Este dolor afectaba principalmente dos zonas de su cara, llamadas V2 y V3, que son partes del nervio trigémino, un nervio que ayuda a sentir la cara. A pesar de tomar medicamentos llamados carboxamidas para controlar el dolor, este empeoró después de muchos años. Además, el dolor apareció en otra zona llamada V1 y también en el área de la garganta y oído derecho, que están conectados con otro nervio llamado glosofaríngeo.\n\n**Lo que Encontraron en las Pruebas**  \nSe le hizo una resonancia magnética especial que mostró que dos arterias (vasos sanguíneos) estaban presionando los nervios afectados. Una arteria llamada cerebelosa superior estaba tocando el nervio trigémino, y otra llamada cerebelosa antero-inferior estaba en contacto con el nervio glosofaríngeo. Esta presión puede causar los dolores intensos que ella sentía.\n\n**Qué Hicieron para Ayudarla**  \nLos médicos realizaron una cirugía llamada descompresión microvascular. En esta operación, hicieron una pequeña apertura en el cráneo para llegar a los nervios y separar las arterias que los estaban presionando. Para evitar que las arterias volvieran a tocar los nervios, colocaron un material llamado teflón entre ellos.\n\n**Resultados Después de la Cirugía**  \nDespués de la operación, el dolor en la cara (del nervio trigémino) desapareció completamente. El dolor en la garganta y oído (del nervio glosofaríngeo) mejoró mucho, con menos intensidad y frecuencia. Dos años después, la paciente sigue mejor, con muy pocos episodios de dolor que puede controlar fácilmente y ha podido reducir los medicamentos que tomaba.\n\n**En Resumen**  \nEsta paciente tenía dolores fuertes causados por arterias que presionaban nervios en su cabeza. La cirugía para separar esas arterias de los nervios fue exitosa y mejoró mucho su calidad de vida.",
+        "score": {
+          "ROUGE-L-Sum": 0.2829827915869981,
+          "BERTScore_F": 0.7746610641479492
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.5288219278674736
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe trata de una mujer de 65 años que desde 2004 presentaba episodios de dolor intenso y punzante en las ramas V2 y V3 del nervio trigémino derecho (que corresponden a zonas de la cara como el maxilar y la mandíbula). Estos episodios, conocidos como neuralgia del trigémino, inicialmente se controlaban con medicamentos llamados carboxamidas. Sin embargo, diecisiete años después, el dolor empeoró, extendiéndose también a la rama V1 (zona de la frente) y aparecieron nuevos episodios dolorosos en el territorio del nervio glosofaríngeo derecho, afectando áreas como el oído y la parte lateral de la garganta, especialmente al hablar y tragar.\n\n**Hallazgos Clave**  \nUna resonancia magnética cerebral con una técnica especial (secuencia CISS) reveló que dos arterias cerebrales —la arteria cerebelosa superior (ACS) y la arteria cerebelosa anteroinferior (AICA)— estaban en contacto directo y presionando los orígenes de los nervios afectados: la ACS sobre el nervio trigémino derecho y la AICA sobre los nervios craneales inferiores, incluido el nervio glosofaríngeo derecho.\n\n**Interpretación Clínica**  \nEsta compresión vascular es una causa conocida de neuralgias craneales, ya que la presión constante puede irritar los nervios y provocar los episodios de dolor intenso. En este caso, la paciente presentaba neuralgia del trigémino y neuralgia del glosofaríngeo simultáneamente, ambas resistentes al tratamiento farmacológico habitual.\n\n**Próximos Pasos y Tratamiento**  \nSe decidió realizar una cirugía llamada descompresión microvascular (DMV) en un solo procedimiento, mediante una craniectomía retrosigmoidea (una apertura quirúrgica en la parte posterior del cráneo). Durante la intervención, se liberaron ambos nervios de la presión arterial colocando pequeñas almohadillas de teflón entre las arterias y los nervios para evitar el contacto directo.  \n\n**Resultados y Seguimiento**  \nLa paciente experimentó una resolución inmediata de los episodios dolorosos relacionados con el nervio trigémino y una reducción significativa en la frecuencia e intensidad del dolor en el territorio del nervio glosofaríngeo. Dos años después de la cirugía, continúa con un tratamiento farmacológico en disminución y mantiene un control satisfactorio del dolor, con episodios muy esporádicos y tolerables en la zona glosofaríngea, especialmente al tragar.\n\nEste caso ilustra la importancia de identificar la compresión vascular en neuralgias craneales refractarias y la eficacia de la descompresión microvascular como tratamiento para mejorar la calidad de vida en pacientes con neuralgia del trigémino y del glosofaríngeo.",
+        "score": {
+          "ROUGE-L-Sum": 0.2815057283142389,
+          "BERTScore_F": 0.8028742074966431
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.5421899679054409
+        }
+      }
+    }
+  },
+  {
+    "id": 5,
+    "gold_summary": "Se trata de un hombre joven, bisexual, en profilaxis antirretroviral de pre-exposición al HIV, cuya forma de presentación fue faringitis exudativa sin otra etiología documentada y adenopatías que evolucionaron a la necrosis, presencia de lesiones asincrónicas características en cara, cuello, abdomen, extremidades y genitales. El diagnóstico fue por detección de ADN viral por reacción en cadena de la polimerasa en lesiones de piel, exudado de fauces y semen. El compromiso faríngeo con presencia de exudado luego del descarte de otras infecciones, podría ser una rareza para la forma epidémica de la enfermedad. El hallazgo del virus en semen ya reportado en otras publicaciones no es suficiente aún para confirmar la vía sexual como forma de trasmisión.",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Un hombre joven se enfermó con dolor de garganta y bultos en el cuello. También tuvo manchitas en la cara, cuello, barriga, brazos y partes íntimas. Los doctores encontraron un virus en su piel, en la garganta y en otra parte del cuerpo. Este virus es raro y puede causar estas manchas y dolor. Los doctores no están seguros si el virus se pasa por el contacto en el cuerpo. El hombre mejoró con ayuda de los doctores.",
+        "score": {
+          "ROUGE-L-Sum": 0.1792452830188679,
+          "BERTScore_F": 0.7223184704780579
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.4507818767484629
+        }
+      },
+      "B2": {
+        "text": "**Caso de un Hombre Joven con Viruela Símica**\n\nEste informe habla de un hombre de 36 años que es bisexual y estaba tomando medicamentos para prevenir el VIH antes de enfermarse. Él empezó con dolor de garganta, fiebre y dolor en el cuello. Además, tenía ganglios inflamados y dolorosos en el cuello. También aparecieron pequeñas lesiones en la cara, el pene y el escroto, que son áreas del cuerpo donde se pueden ver bultos o manchas.\n\nPara saber qué tenía, los médicos hicieron varios estudios. Tomaron muestras de las lesiones en la piel y las analizaron con una prueba llamada PCR, que busca el ADN del virus. Encontraron que tenía el virus de la viruela símica, una enfermedad causada por un virus parecido a la viruela común, pero menos grave. También encontraron el virus en la garganta y en el semen del paciente.\n\nDurante su enfermedad, el hombre desarrolló más lesiones en diferentes partes del cuerpo, como los glúteos, la zona alrededor del ano, el cuello y las manos. Además, tuvo un aumento en algunas enzimas del hígado, lo que indica que el virus afectó un poco este órgano. En el cuello, los ganglios inflamados mostraron signos de daño, pero no fue necesario hacer cirugía.\n\nAunque el virus se encontró en el semen, todavía no está claro si la viruela símica se transmite por contacto sexual. El dolor y la inflamación en la garganta con pus (exudado) que tuvo este paciente no es común en los casos que se han visto en la epidemia actual, por lo que es un detalle importante para los médicos.\n\nDespués de recibir tratamiento, el paciente mejoró y pudo salir del hospital. Este caso ayuda a entender mejor cómo puede presentarse la viruela símica y qué síntomas buscar para hacer un diagnóstico correcto.",
+        "score": {
+          "ROUGE-L-Sum": 0.18340611353711792,
+          "BERTScore_F": 0.7574628591537476
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.4704344863454327
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe presenta el caso de un hombre de 36 años, bisexual, que utiliza profilaxis antirretroviral de pre-exposición (PrEP) para prevenir la infección por VIH. Sin antecedentes de viajes recientes, asistió a un evento donde tuvo contacto con parejas sexuales ocasionales de identidad y antecedentes desconocidos. Diez días después comenzó con fiebre, dolor de garganta (odinofagia) y dolor en el cuello, síntomas que persistieron a pesar de tratamiento antibiótico inicial, lo que motivó su hospitalización.\n\n**Hallazgos Clave**  \nAl ingreso, el paciente mostró inflamación y exudado en la garganta, ganglios linfáticos cervicales inflamados y dolorosos en ambos lados, además de lesiones cutáneas características: pápulas umbilicadas (con un centro hundido) en el escroto y pene, y pústulas en la cara con cinco días de evolución. Se realizaron estudios de imagen, incluyendo tomografía computarizada (TC) de cuello con contraste, que descartó abscesos, y ecografía abdominal que evidenció un leve aumento del tamaño del hígado y bazo (hepatoesplenomegalia). Se inició tratamiento empírico con antibióticos ceftriaxona y azitromicina.\n\nSe tomaron muestras para cultivos, serologías y escarificación (raspado) de lesiones cutáneas, las cuales fueron enviadas a un laboratorio de referencia para realizar una prueba de reacción en cadena de la polimerasa (PCR) específica para Orthopoxvirus, confirmando la presencia de ADN viral de viruela símica (monkeypox). La secuenciación genética mostró alta similitud con cepas del clado de África Occidental, que es menos virulento que otros clados. Se descartaron otras posibles infecciones que podrían explicar los síntomas.\n\nDurante la evolución clínica, aparecieron nuevas lesiones en diferentes partes del cuerpo (glúteos, región perianal, ingle derecha, abdomen, frente, cuello, mano derecha y dorso del pie), sumando un total de aproximadamente 25 lesiones. Además, desarrolló una úlcera en la lengua. En análisis de laboratorio se detectó un aumento moderado de las enzimas hepáticas (transaminasas), sin otros hallazgos relevantes. Debido a la persistencia del dolor cervical, se realizó una nueva TC a los 14 días que mostró ganglios linfáticos agrandados con áreas centrales de necrosis (muerte del tejido), pero sin necesidad de intervención quirúrgica.\n\nAl día 17, se confirmó la presencia del virus mediante PCR en muestras de exudado faríngeo y semen. Dos días después, el paciente fue dado de alta con una mejoría clínica notable.\n\n**Interpretación Clínica**  \nEste caso destaca una presentación atípica de viruela símica en un adulto joven que utiliza profilaxis antirretroviral para VIH. La enfermedad se manifestó inicialmente como una faringitis exudativa (inflamación de la garganta con pus), acompañada de adenopatías cervicales que evolucionaron a necrosis, un cuadro poco común en la epidemia actual. Las lesiones cutáneas asincrónicas (que aparecen en diferentes momentos) en múltiples regiones del cuerpo son características de esta infección.\n\nLa confirmación diagnóstica se realizó mediante detección del ADN viral en las lesiones de piel, así como en muestras de exudado faríngeo y semen. Aunque la presencia del virus en el semen ha sido reportada en otros estudios, todavía no es suficiente para afirmar que la transmisión sexual sea la vía principal de contagio.\n\n**Próximos Pasos**  \nEl seguimiento clínico debe incluir la vigilancia de la evolución de las lesiones y la resolución de la inflamación ganglionar. Es importante continuar investigando las vías de transmisión del virus para mejorar las estrategias de prevención, especialmente en poblaciones con riesgo elevado. Además, este caso resalta la necesidad de considerar la viruela símica en el diagnóstico diferencial de faringitis exudativa persistente en contextos epidemiológicos compatibles.",
+        "score": {
+          "ROUGE-L-Sum": 0.21243523316062177,
+          "BERTScore_F": 0.7776002287864685
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.4950177309735451
+        }
+      }
+    }
+  },
+  {
+    "id": 6,
+    "gold_summary": "A continuación, se presenta el caso de un paciente sexo masculino de 23 años con diagnóstico de cardiomiopatía hipertrófica variante medio apical, en quien se documenta variante de la filamina C, ante la inadecuada respuesta y persistencia de sintomatología frente al manejo médico, se realizó el procedimiento de miectomía con abordaje transapical, con posterior mejoría de sintomatología clínica y obstrucción al tracto de salida.",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Un joven de 23 años tenía un problema en su corazón. Su corazón era más grueso en una parte. Esto le hacía sentir mal y cansado.\n\nLos doctores le hicieron una operación para quitar un poco de ese corazón grueso. Después de la operación, se sintió mejor y su corazón pudo trabajar mejor.",
+        "score": {
+          "ROUGE-L-Sum": 0.22857142857142856,
+          "BERTScore_F": 0.7332866191864014
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.48092902387891495
+        }
+      },
+      "B2": {
+        "text": "**Caso de un joven con problema en el corazón**\n\nEste es el caso de un joven de 23 años que tiene una enfermedad llamada cardiomiopatía hipertrófica. Esto significa que una parte de su corazón, especialmente en la zona media y hacia el ápice (la punta), está más gruesa de lo normal. Esta enfermedad puede dificultar que la sangre salga bien del corazón.\n\n**Qué encontraron en sus genes**\n\nAl hacerle un estudio genético, descubrieron que tiene un cambio en un gen llamado filamina C. Este cambio puede causar problemas en el corazón y es una forma hereditaria de la enfermedad.\n\n**Tratamiento y resultados**\n\nEl joven no mejoraba con los medicamentos que le daban, así que los doctores decidieron hacer una cirugía llamada miectomía. En esta operación, quitaron parte del músculo grueso del corazón para que la sangre pueda salir mejor. La cirugía se hizo por la punta del corazón (abordaje transapical).\n\nDespués de la operación, el paciente mejoró mucho. Su corazón ya no tenía tanta obstrucción y sus síntomas disminuyeron. Actualmente, está en buen estado y sigue un tratamiento con medicamentos para cuidar su corazón.",
+        "score": {
+          "ROUGE-L-Sum": 0.2261484098939929,
+          "BERTScore_F": 0.7411545515060425
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.4836514807000177
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe trata de un paciente masculino de 23 años, originario de Itagüí, Colombia, con antecedentes familiares relevantes de muerte súbita en su abuelo a los 50 años, sin otras enfermedades familiares o personales significativas. Desde la infancia, el paciente presentaba episodios repetidos de síncope (pérdida temporal del conocimiento) atribuibles a una disfunción del nodo sinusal (una alteración en el sistema eléctrico del corazón), por lo que se le implantó un marcapasos. Durante años, su condición se mantuvo estable hasta que en 2012, en Guayaquil, Ecuador, presentó una infección relacionada con el marcapasos que requirió la extracción del generador y el implante de uno nuevo en el lado opuesto, sin complicaciones posteriores ni nuevos episodios de síncope durante una década.\n\nSeis meses antes del ingreso actual, el paciente comenzó a mostrar un deterioro en su capacidad funcional (clasificación NYHA III, que indica limitación marcada en la actividad física), aunque sin otros síntomas adicionales. Se suspendió el tratamiento con betabloqueadores debido a mala tolerancia. En el examen físico se detectó un soplo cardíaco leve, sin signos de insuficiencia cardíaca. Los análisis de laboratorio fueron normales. El marcapasos mostró agotamiento de la batería, y el ecocardiograma reveló una hipertrofia severa y concéntrica del septum interventricular (pared que separa las cámaras del corazón), con un grosor de 26 mm y un gradiente de presión muy alto (117 mmHg) dentro del ventrículo, además de un movimiento anormal del velo mitral que causaba una regurgitación leve (retorno de sangre hacia la aurícula).\n\n**Hallazgos Clave**  \n- Hipertrofia severa del septum interventricular medio ventricular con obstrucción significativa al flujo sanguíneo dentro del ventrículo izquierdo.  \n- Movimiento sistólico anterior del velo mitral (SAM), que contribuye a la obstrucción y regurgitación mitral leve.  \n- Antecedentes familiares de muerte súbita y un riesgo calculado de muerte súbita del 16,8%, lo que indica un riesgo elevado.  \n- Imposibilidad de realizar resonancia magnética cardíaca debido a la incompatibilidad con el marcapasos y la presencia de electrodos abandonados.  \n- Confirmación genética de una variante probablemente patogénica en el gen FLNC (filamina C), asociada a miocardiopatía hipertrófica familiar tipo 26, que se hereda de forma autosómica dominante.\n\n**Interpretación Clínica**  \nEl paciente presenta una forma de miocardiopatía hipertrófica con predominio medio apical, caracterizada por un engrosamiento anormal del músculo cardíaco que obstruye el flujo de salida del ventrículo izquierdo y genera síntomas significativos. La variante genética encontrada en filamina C explica la naturaleza hereditaria y progresiva de su enfermedad. La persistencia de síntomas y la obstrucción significativa a pesar del tratamiento médico justificaron la realización de una miectomía medio ventricular (cirugía para remover parte del músculo engrosado), realizada mediante un abordaje transapical (a través del ápex del corazón). La cirugía fue exitosa, con reducción del gradiente de presión y desaparición del movimiento anormal del velo mitral.\n\nPosteriormente, el paciente presentó episodios de taquicardia ventricular (arritmias peligrosas) que requirieron la implantación de un cardiodesfibrilador implantable (CDI) compatible con resonancia magnética, para prevenir muerte súbita. Tras el implante, no se registraron nuevos episodios arrítmicos y el paciente evolucionó favorablemente.\n\n**Próximos Pasos**  \nActualmente, el paciente se encuentra en clase funcional I (sin limitaciones en la actividad física), sin arritmias detectadas en monitoreo continuo, y en tratamiento con bisoprolol (un betabloqueador) a dosis de 5 mg. Se ha iniciado un estudio genético ampliado en familiares directos para identificar portadores de la variante genética, aunque el acceso limitado a servicios de salud ha dificultado la realización completa de este estudio. El seguimiento continuo y la evaluación genética son fundamentales para el manejo integral del paciente y su familia, con el fin de prevenir complicaciones graves como la muerte súbita.",
+        "score": {
+          "ROUGE-L-Sum": 0.13811420982735723,
+          "BERTScore_F": 0.7460815906524658
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.4420979002399115
+        }
+      }
+    }
+  },
+  {
+    "id": 7,
+    "gold_summary": "Presentamos el caso de un HSH con infección por VIH, que consultó por un cuadro de uretritis y sifilis primaria, en el cual se aisló N. meningitidis en una muestra anorectal. Fue tratado en forma empírica con ceftriaxona y azitromicina, realizándose un cultivo de control post-tratamiento que fue negativo.",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Un hombre con VIH tenía una herida y dolor al orinar. Los doctores encontraron una bacteria en su cuerpo. Le dieron medicinas para curarlo. Después, la bacteria ya no estaba. Él mejoró mucho.",
+        "score": {
+          "ROUGE-L-Sum": 0.13636363636363635,
+          "BERTScore_F": 0.7228449583053589
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.4296042973344976
+        }
+      },
+      "B2": {
+        "text": "Caso de un hombre de 32 años con VIH que tuvo una infección en la uretra y una úlcera en el pene. Los médicos encontraron que tenía sífilis primaria, que es una infección de transmisión sexual. Además, en una muestra tomada del ano, detectaron una bacteria llamada Neisseria meningitidis, que normalmente no causa infecciones en esa zona. \n\nEl paciente recibió tratamiento con antibióticos llamados ceftriaxona y azitromicina para combatir las infecciones. Después del tratamiento, se hicieron pruebas de control y no encontraron más bacterias en las muestras tomadas de la uretra, la garganta y el ano. El paciente mejoró bien y la lesión en el pene y la inflamación en la ingle desaparecieron en dos semanas. \n\nEste caso muestra la importancia de revisar diferentes áreas del cuerpo en personas con conductas sexuales de riesgo y de usar tratamientos adecuados para varias posibles infecciones.",
+        "score": {
+          "ROUGE-L-Sum": 0.18181818181818182,
+          "BERTScore_F": 0.7584642767906189
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.4701412293044004
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe trata de un hombre de 32 años que vive con infección por VIH controlada mediante tratamiento antirretroviral, con carga viral indetectable y un recuento adecuado de células CD4. Además, tiene antecedentes de consumo de tabaco y drogas recreativas. Consultó en una unidad de salud sexual debido a una secreción mucosa por la uretra y una úlcera dolorosa en el pene, acompañadas de inflamación en los ganglios linfáticos inguinales del lado izquierdo. No presentaba fiebre ni otros síntomas sistémicos. En la entrevista, refirió múltiples parejas sexuales masculinas en el último año, con prácticas sexuales orales y anales, y uso irregular de preservativos. Cuatro semanas antes, tuvo una relación sexual sin protección con una persona conocida a través de una aplicación móvil.\n\n**Hallazgos Clave**  \nSe sospechó inicialmente una sífilis primaria y una uretritis de origen incierto. Se tomaron muestras de sangre y secreción uretral para análisis microbiológicos, así como un hisopado anorrectal debido al alto riesgo sexual. El diagnóstico serológico confirmó sífilis, con pruebas VDRL y MHA-TP positivas. Los cultivos de secreción uretral fueron negativos para bacterias comunes causantes de uretritis. Sin embargo, en la muestra anorrectal se identificó la presencia de Neisseria meningitidis (una bacteria que normalmente habita en la garganta y que en este caso se encontró en el recto), confirmada mediante espectrometría de masas MALDI-TOF MS.  \n\n**Interpretación Clínica**  \nEl paciente fue tratado empíricamente con penicilina benzatina para la sífilis, además de una dosis única de ceftriaxona y azitromicina para cubrir posibles infecciones bacterianas de transmisión sexual. La detección de N. meningitidis en la muestra anorrectal es relevante, ya que esta bacteria no es un patógeno típico en uretritis, pero puede colonizar el tracto genital o anal, especialmente en personas con conductas sexuales de riesgo. El tratamiento fue efectivo, ya que a las dos semanas el paciente mostró resolución de la secreción uretral, cicatrización de la úlcera y desaparición de la inflamación ganglionar. Los cultivos posteriores fueron negativos, confirmando la erradicación de las infecciones.  \n\n**Próximos Pasos**  \nSe realizó el estudio y tratamiento del contacto sexual reciente para prevenir la transmisión y reinfección, aunque este contacto no presentó síntomas ni cultivos positivos. Este caso subraya la importancia de considerar agentes menos comunes como N. meningitidis en infecciones del tracto genital y anorrectal en personas con alto riesgo sexual, y la necesidad de un abordaje diagnóstico y terapéutico integral en estos pacientes.",
+        "score": {
+          "ROUGE-L-Sum": 0.1212121212121212,
+          "BERTScore_F": 0.7347267270088196
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.4279694241104704
+        }
+      }
+    }
+  },
+  {
+    "id": 8,
+    "gold_summary": "Paciente: Hombre, 63 años\n\nDiagnóstico final: Edema pulmonar cardiovenoso hipertensivo\n\nSíntomas: falta de aire\n\nMedicación: —\n\nProcedimiento clínico: —\n\nEspecialidad: Medicina general e interna\n\nUn hombre hispano de 63 años con antecedentes de hipertensión, enfermedad de las arterias coronarias, insuficiencia cardiaca con una fracción de eyección reducida del 35 %, enfermedad renal crónica (ERC) y diabetes mellitus, se presentó como una emergencia con disnea aguda y grave. El paciente fue tratado inicialmente con 100 % de oxígeno suplementario y nitroglicerina intravenosa (IV) en dosis altas (30 mcg/min), que se ajustó cada 3 minutos, aumentando en 15 mcg/min hasta que se alcanzó una dosis de 120 mcg/min. Después de 18 minutos de terapia agresiva, la condición del paciente mejoró y ya no necesitaba ventilación mecánica.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Había un hombre de 63 años que se sentía muy mal. Le costaba mucho respirar y estaba muy cansado. Tenía problemas en el corazón y en los riñones desde hace tiempo.\n\nCuando llegó al hospital, le dieron aire con una máscara para ayudarlo a respirar mejor. También le pusieron un medicamento por la vena para que su corazón y su cuerpo se sintieran mejor.\n\nDespués de un rato, el hombre empezó a respirar mejor y se sintió más tranquilo. Los doctores cuidaron mucho de él y lo ayudaron a mejorar.",
+        "score": {
+          "ROUGE-L-Sum": 0.2175732217573222,
+          "BERTScore_F": 0.7199494242668152
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.4687613230120687
+        }
+      },
+      "B2": {
+        "text": "**Caso de un Hombre de 63 Años con Problemas del Corazón y Dificultad para Respirar**\n\n**Lo que Pasó:**  \nUn hombre de 63 años, que hablaba español y tenía varias enfermedades como presión alta (hipertensión), diabetes, problemas en las arterias del corazón y una enfermedad llamada insuficiencia cardíaca (que significa que su corazón no bombeaba bien la sangre), llegó al hospital muy enfermo. De repente, empezó a tener mucha dificultad para respirar, su corazón latía rápido y sudaba mucho. Antes de esto, estaba bien y podía hacer sus actividades normales.\n\n**Lo que Encontraron:**  \nAl examinarlo, su presión arterial estaba muy alta y tenía signos claros de que su corazón estaba trabajando mal. También tenía líquido en los pulmones, lo que se llama edema pulmonar, y eso dificultaba que el oxígeno llegara a su cuerpo. Las pruebas mostraron que su corazón estaba agrandado y que había problemas en la circulación de la sangre en sus pulmones.\n\n**Qué Hicieron para Ayudarlo:**  \nLe dieron oxígeno puro para que pudiera respirar mejor y empezaron a darle un medicamento llamado nitroglicerina por vía intravenosa (directamente en la vena). La nitroglicerina ayuda a bajar la presión arterial y a que el corazón trabaje menos. Comenzaron con una dosis baja y la aumentaron poco a poco cada pocos minutos. Después de 18 minutos, el paciente mejoró mucho: su presión bajó, su corazón latía más despacio y pudo respirar sin tanta dificultad. Ya no necesitó una máquina para ayudarlo a respirar.\n\n**Después del Tratamiento:**  \nLuego le dieron otros medicamentos para el corazón y para eliminar el exceso de líquido. El paciente se quedó en el hospital dos días y después pudo irse a casa. Continuó con controles médicos semanales y no volvió a tener problemas graves en los siguientes dos meses.\n\n**Resumen:**  \nEste caso muestra cómo un hombre con varias enfermedades del corazón y otros problemas puede sufrir una emergencia grave llamada edema pulmonar, que es cuando se acumula líquido en los pulmones por problemas del corazón. Con un tratamiento rápido y adecuado, que incluye oxígeno y medicamentos para bajar la presión y ayudar al corazón, el paciente pudo recuperarse sin complicaciones mayores.",
+        "score": {
+          "ROUGE-L-Sum": 0.22592592592592592,
+          "BERTScore_F": 0.7657008171081543
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.4958133715170401
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nUn hombre hispanoparlante de 63 años con antecedentes médicos complejos, incluyendo hipertensión arterial de larga evolución, diabetes mellitus, enfermedad coronaria con colocación previa de stent, insuficiencia cardíaca crónica con función del corazón reducida (fracción de eyección del 35 %) y enfermedad renal crónica en estadio avanzado, acudió al hospital en estado de emergencia debido a un inicio súbito de dificultad respiratoria severa, palpitaciones y sudoración intensa. Hasta poco antes de su ingreso, el paciente se encontraba en su estado habitual de salud y realizaba actividades cotidianas de forma independiente.\n\n**Hallazgos Clave**  \nAl examen físico, el paciente presentaba signos evidentes de insuficiencia cardíaca descompensada: presión arterial muy elevada (205/110 mmHg), frecuencia cardíaca rápida (118 latidos por minuto), dificultad respiratoria grave con saturación de oxígeno baja (82 % en aire ambiente), distensión venosa yugular marcada, crepitaciones pulmonares bilaterales, y un galope cardíaco junto con un soplo sistólico. La radiografía de tórax mostró cardiomegalia (aumento del tamaño del corazón), signos de congestión pulmonar y edema intersticial, confirmando la sospecha clínica de edema pulmonar cardiogénico hipertensivo. El electrocardiograma evidenció taquicardia sinusal, hipertrofia ventricular izquierda y cambios isquémicos.\n\nLos análisis de laboratorio posteriores revelaron un péptido natriurético cerebral (BNP) muy elevado (3,452 pg/ml), indicador de insuficiencia cardíaca descompensada, y una troponina normal, descartando daño cardíaco agudo. Se descartaron otras causas de dificultad respiratoria aguda, como embolia pulmonar e infecciones pulmonares, mediante pruebas específicas y criterios clínicos.\n\n**Interpretación Clínica**  \nEl cuadro clínico y los estudios complementarios fueron consistentes con un episodio agudo de edema pulmonar cardiogénico hipertensivo, una condición en la que la presión arterial muy alta y la insuficiencia cardíaca provocan acumulación rápida de líquido en los pulmones, dificultando la respiración. La rápida identificación y tratamiento de esta emergencia fueron cruciales para evitar complicaciones mayores.\n\n**Tratamiento y Evolución**  \nEl manejo inicial incluyó la administración de oxígeno al 100 % mediante máscara no reanimadora y la colocación del paciente en posición sentada para facilitar la respiración. Se inició tratamiento intravenoso con nitroglicerina, un vasodilatador que reduce la presión arterial y la carga sobre el corazón, comenzando con una dosis de 30 microgramos por minuto y aumentando progresivamente hasta 120 microgramos por minuto en 18 minutos. Esta terapia permitió una reducción significativa de la presión arterial y de la frecuencia cardíaca, con una mejora clínica rápida: el paciente pudo respirar sin dificultad y comunicarse con normalidad, y su saturación de oxígeno superó el 97 % con oxígeno suplementario.\n\nPosteriormente, se administraron enalapril (un inhibidor de la enzima convertidora de angiotensina) y furosemida (un diurético) por vía intravenosa para continuar el control de la presión arterial y eliminar el exceso de líquido. La nitroglicerina se fue disminuyendo hasta suspenderla, y se inició tratamiento oral con isosorbida dinitrato para mantener la vasodilatación.\n\nEl paciente fue hospitalizado en la unidad de medicina interna, donde se ajustó su tratamiento con medicamentos para insuficiencia cardíaca, incluyendo furosemida, carvedilol (un betabloqueador), sacubitril/valsartán (un inhibidor de la neprilisina combinado con un bloqueador del receptor de angiotensina), espironolactona (un antagonista de la aldosterona) e isosorbida mononitrato. Tras 48 horas de hospitalización, se dio de alta en condiciones estables y con seguimiento cardiológico programado.\n\n**Próximos Pasos y Seguimiento**  \nDurante al menos 60 días posteriores al alta, el paciente no requirió nuevas hospitalizaciones ni visitas a urgencias, lo que indica una adecuada respuesta al tratamiento y control de su enfermedad cardíaca. El seguimiento semanal con su cardiólogo permitió optimizar la terapia médica para prevenir futuras descompensaciones.\n\n---\n\nEste caso ilustra la importancia de un diagnóstico rápido y un manejo agresivo en pacientes con edema pulmonar cardiogénico hipertensivo, especialmente en aquellos con múltiples comorbilidades cardiovasculares y renales, para mejorar la supervivencia y la calidad de vida.",
+        "score": {
+          "ROUGE-L-Sum": 0.1870503597122302,
+          "BERTScore_F": 0.7904630899429321
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.48875672482758115
+        }
+      }
+    }
+  },
+  {
+    "id": 9,
+    "gold_summary": "Un niño de 12 años con una masa conjuntival pedunculada carnosa fue llevado al Centro Médico de la Universidad de Jimma con un historial de un mes de sensación de cuerpo extraño. Al paciente se le diagnosticó un papiloma pedunculado de células escamosas y se le realizó una biopsia excisional de la lesión. Se encontró que la masa era una lesión polipoide hiperplásica con numerosos quistes globulares dentro de la submucosa conjuntival, rodeados por un infiltrado inflamatorio pesado de linfocitos, células plasmáticas y neutrófilos, así como grandes esporas de paredes gruesas con numerosas endosporas en secciones microscópicas. Se diagnosticó histopatológicamente rinosporidiosis conjuntival.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Un niño tenía una bolita en el ojo que le molestaba. Los doctores le quitaron la bolita para verla mejor. \n\nAl mirar la bolita con un microscopio, vieron que tenía muchas cositas pequeñas dentro. Estas cositas eran como unas semillas que no son buenas. \n\nLos doctores dijeron que el niño tenía una infección en el ojo llamada rinosporidiosis. Después de quitar la bolita, el niño estuvo bien y no volvió a tener problema.",
+        "score": {
+          "ROUGE-L-Sum": 0.18181818181818182,
+          "BERTScore_F": 0.7142685055732727
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.4480433436957273
+        }
+      },
+      "B2": {
+        "text": "**Lo que pasó con el niño**  \nUn niño de 12 años tenía una sensación rara en el ojo y una masa blanda y rosada que crecía en la parte interna del párpado derecho. No había sufrido golpes ni tenía problemas similares en el otro ojo. Cuando lo revisaron, su vista estaba normal, pero encontraron esta masa que parecía un papiloma, que es un tipo de bulto benigno hecho de células de la piel.\n\n**Qué hicieron los médicos**  \nLe quitaron la masa para analizarla mejor. Esto se llama biopsia, que es cuando se saca un pedacito de tejido para estudiar qué es exactamente. En el laboratorio, vieron que la masa tenía muchas células inflamatorias, que son células que el cuerpo usa para defenderse cuando hay una infección o irritación. También encontraron estructuras llamadas esporangios, que son como pequeñas bolsas con esporas dentro. Las esporas son formas de reproducción de ciertos microorganismos.\n\n**Qué significa el diagnóstico**  \nEl análisis mostró que el niño tenía rinosporidiosis conjuntival, que es una infección causada por un microorganismo que forma esas esporas. Esta infección afecta la conjuntiva, que es la membrana que cubre el ojo y el interior del párpado. Después de quitar la masa, el niño no tuvo problemas ni volvió a tener la infección en el ojo ni en otras partes del cuerpo durante al menos siete meses.\n\n**En resumen**  \nEl niño tenía una infección poco común en el ojo que causó una masa. Gracias a la biopsia, los médicos pudieron identificar la infección y tratarla con cirugía, evitando que regresara.",
+        "score": {
+          "ROUGE-L-Sum": 0.18581907090464547,
+          "BERTScore_F": 0.76585853099823
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.4758388009514377
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nUn niño de 12 años acudió al hospital tras presentar durante un mes una sensación persistente de cuerpo extraño en el ojo derecho, acompañada de una masa carnosa y pedunculada (con un tallo que la une a la superficie) en la conjuntiva palpebral (la membrana que recubre el párpado). No había antecedentes de trauma ni lesiones similares en el otro ojo. La agudeza visual del niño era normal. Inicialmente, se sospechó que la lesión correspondía a un papiloma de células escamosas pedunculado, por lo que se decidió realizar una biopsia excisional para su análisis.\n\n**Hallazgos Clave**  \nEl tejido extraído, de aproximadamente 1,5 x 1 cm, fue examinado bajo el microscopio. Se observó una lesión polipoide hiperplásica (un crecimiento en forma de pólipo con aumento en el número de células) que contenía múltiples quistes globulares en la submucosa conjuntival (la capa debajo de la superficie de la conjuntiva). Además, había una intensa infiltración inflamatoria compuesta por linfocitos, células plasmáticas y neutrófilos, que son tipos de células del sistema inmunitario. De manera destacada, se identificaron grandes esporangios (estructuras que contienen esporas) con paredes gruesas, dentro de los cuales se encontraban numerosas endosporas (esporas internas). Algunas de estas esporas se liberaban tras la ruptura de los esporangios maduros.\n\n**Interpretación Clínica**  \nEl examen histopatológico confirmó que la masa no era un papiloma, sino que correspondía a una infección por rinosporidiosis conjuntival, una enfermedad causada por el microorganismo Rhinosporidium seeberi que afecta principalmente las mucosas y puede formar masas polipoides. Esta infección es poco común y se caracteriza por la presencia de esporangios con endosporas en el tejido afectado.\n\n**Próximos Pasos y Seguimiento**  \nTras la escisión quirúrgica completa de la lesión, el paciente fue monitoreado durante al menos siete meses, sin presentar recurrencia de la lesión ni signos de infección en el ojo ni en otras partes del cuerpo. Este seguimiento indica un buen pronóstico tras el tratamiento quirúrgico. Se recomienda continuar con controles periódicos para detectar cualquier posible reaparición.",
+        "score": {
+          "ROUGE-L-Sum": 0.2669404517453799,
+          "BERTScore_F": 0.8293812274932861
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.548160839619333
+        }
+      }
+    }
+  },
+  {
+    "id": 10,
+    "gold_summary": "Presentamos el caso clínico de un varón adolescente de 15 años sin antecedentes quirúrgicos previos, con clínica de dolor abdominal y vómitos, en el que la tomografía computarizada sugería un cuadro de obstrucción intestinal a causa de hernia interna a nivel del hiato de Winslow. Precisó de intervención quirúrgica mediante laparoscopia exploradora, reconvertida por mala visualización a laparotomía media supraumbilical, para reducción del asa de íleon herniada. Esta presentaba buen aspecto y no fue necesaria la resección intestinal. No se realizó ninguna técnica preventiva para disminuir el riesgo de recidiva. Postoperatoriamente, el paciente presentó una colección pélvica manejada de manera conservadora con antibióticos. Actualmente se encuentra en seguimiento en consultas externas de cirugía pediátrica.",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Un niño de 15 años tenía dolor en la barriga y vomitaba. Los doctores vieron que su intestino estaba tapado por un lugar raro. Hicieron una operación para ayudarlo. Sacaron el intestino que estaba atrapado y estaba bien. No cortaron nada. Después, el niño tuvo un poco de líquido en la barriga, pero con medicinas mejoró. Ahora está bien y los doctores lo revisan para que siga sano.",
+        "score": {
+          "ROUGE-L-Sum": 0.1523809523809524,
+          "BERTScore_F": 0.72305828332901
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.4377196178549812
+        }
+      },
+      "B2": {
+        "text": "**Caso Clínico de un Adolescente con Dolor Abdominal y Vómitos**\n\nUn chico de 15 años, sin problemas médicos anteriores, llegó al hospital con dolor en la parte superior del abdomen y vómitos que duraban cuatro días. Al principio, pensaron que tenía gastroenteritis, una infección del estómago, pero como no mejoraba, le hicieron más pruebas.\n\n**Lo que Encontraron**\n\nUna radiografía y una tomografía computarizada (una imagen detallada del cuerpo) mostraron que tenía una obstrucción en el intestino delgado. Esto ocurrió porque una parte del intestino se había metido por un espacio llamado hiato de Winslow, causando una hernia interna. Una hernia interna es cuando un órgano se mueve a un lugar donde no debería estar dentro del cuerpo.\n\n**Qué Hicieron**\n\nEl equipo médico decidió operar para arreglar la obstrucción. Comenzaron con una cirugía por laparoscopia, que es una operación con pequeñas incisiones y una cámara, pero tuvieron que cambiar a una cirugía abierta para ver mejor. Encontraron el intestino atrapado, pero estaba sano, así que no fue necesario cortar ninguna parte. No hicieron ninguna técnica para evitar que la hernia volviera a aparecer porque el espacio por donde se metió el intestino tenía un tamaño normal.\n\n**Después de la Cirugía**\n\nDespués de la operación, el chico tuvo un problema llamado íleo paralítico, que significa que el intestino tardó en empezar a funcionar normalmente. También desarrolló una acumulación de líquido en la pelvis, llamada colección pélvica, que trataron con antibióticos sin necesidad de otra cirugía. Finalmente, el paciente mejoró y fue dado de alta después de diez días.\n\n**Situación Actual**\n\nAhora, el adolescente sigue en control con el equipo de cirugía pediátrica para asegurarse de que se recupere bien y no tenga problemas futuros.",
+        "score": {
+          "ROUGE-L-Sum": 0.2782608695652174,
+          "BERTScore_F": 0.7795069217681885
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.5288838956667029
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe describe el caso de un adolescente de 15 años, sin antecedentes médicos ni quirúrgicos previos, que presentó durante cuatro días dolor abdominal en la parte superior del abdomen (epigastrio) acompañado de vómitos biliosos (con contenido similar a bilis), sin fiebre. Inicialmente fue tratado como una gastroenteritis, pero al no mejorar y mantener los síntomas, acudió nuevamente a urgencias.\n\n**Hallazgos Clave**  \nEn la evaluación física, el paciente estaba en buen estado general, afebril, con signos leves de deshidratación y abdomen distendido, pero sin signos de inflamación grave (peritonismo). Los ruidos intestinales estaban disminuidos. Los análisis de sangre no mostraron alteraciones significativas. Una radiografía abdominal sugirió la presencia de una obstrucción intestinal. Posteriormente, una tomografía computarizada (TC) reveló ascitis (líquido en la cavidad abdominal) y dilatación importante de las asas del intestino delgado, con una posible herniación interna a través del hiato de Winslow, un orificio natural en la cavidad abdominal.\n\n**Interpretación Clínica**  \nEl diagnóstico fue una hernia interna del intestino delgado a través del hiato de Winslow, una causa poco frecuente de obstrucción intestinal. Debido a la gravedad y persistencia de los síntomas, se decidió realizar una cirugía urgente. Inicialmente se intentó una laparoscopia exploradora (cirugía mínimamente invasiva), pero la visualización limitada y la distensión intestinal dificultaron la intervención, por lo que se convirtió a una laparotomía (cirugía abierta) supraumbilical media. Durante la cirugía se identificó un asa de íleon (parte final del intestino delgado) herniada a través del hiato de Winslow, con signos de congestión por la presión del hiato, pero sin daño irreversible, por lo que no fue necesaria la resección intestinal. El asa herniada fue reducida (devuelta a su posición normal). El hiato de Winslow tenía un tamaño normal, por lo que no se realizó ninguna maniobra para prevenir la recurrencia de la hernia.\n\nEn el postoperatorio, el paciente presentó un íleo paralítico (falta temporal de movimiento intestinal), que mejoró progresivamente, permitiendo retirar la sonda nasogástrica a los cinco días y comenzar la alimentación oral con buena tolerancia. Además, desarrolló una colección pélvica (acumulación localizada de líquido o pus) que se trató con antibióticos de forma conservadora, sin necesidad de intervención quirúrgica adicional. El paciente evolucionó favorablemente y fue dado de alta al décimo día después de la cirugía, manteniendo un buen estado general y sin fiebre.\n\n**Próximos Pasos**  \nActualmente, el paciente se encuentra en seguimiento ambulatorio en consultas de cirugía pediátrica para monitorizar su recuperación y detectar posibles complicaciones o recurrencias. Se mantiene estable y con tránsito intestinal conservado.",
+        "score": {
+          "ROUGE-L-Sum": 0.2745098039215686,
+          "BERTScore_F": 0.8097641468048096
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.542136975363189
+        }
+      }
+    }
+  },
+  {
+    "id": 11,
+    "gold_summary": "Un niño de 16 meses de edad con cardiomiopatía restrictiva que fue incluido en una lista para un trasplante cardiaco. A los 20 meses de edad, requirió un implante de un dispositivo de asistencia biventricular externo (Berlin Heart) y tuvo un accidente cerebrovascular en el hemisferio izquierdo a los 23 meses. Se utilizó un enfoque intraarterial y produjo buenos resultados clínicos. Un mes después, se realizó con éxito un trasplante cardiaco.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Había un niño que tenía un problema en su corazón. Tenía que esperar para recibir un corazón nuevo. Le pusieron una máquina para ayudar a su corazón a latir. Un día, su cerebro se enfermó un poco. Los doctores usaron una medicina especial para ayudar a su cerebro. Después, el niño recibió un corazón nuevo y se puso mejor.",
+        "score": {
+          "ROUGE-L-Sum": 0.2054794520547945,
+          "BERTScore_F": 0.7069401741027832
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.45620981307878883
+        }
+      },
+      "B2": {
+        "text": "**Lo que pasó con el niño**\n\nUn niño de 16 meses tenía un problema en el corazón llamado cardiomiopatía restrictiva, que hace que el corazón no funcione bien. Por eso, lo pusieron en una lista para recibir un trasplante de corazón. A los 20 meses, le pusieron un dispositivo especial llamado Berlin Heart, que ayuda al corazón a bombear sangre mientras espera el trasplante.\n\n**El problema del accidente cerebrovascular**\n\nCuando tenía 23 meses, el niño sufrió un accidente cerebrovascular, que es cuando una parte del cerebro no recibe suficiente sangre y se daña. En su caso, el problema ocurrió en el lado izquierdo del cerebro. Debido a que ya estaba tomando medicamentos para evitar coágulos, no se pudo usar un tratamiento común para este tipo de accidente.\n\n**El tratamiento que recibieron**\n\nLos médicos usaron una técnica llamada trombectomía intraarterial. Esto significa que, con anestesia, introdujeron un pequeño tubo por una arteria en la pierna para llegar hasta el cerebro y quitar el coágulo que bloqueaba la arteria. Lograron abrir la arteria en una sola vez y restaurar el flujo de sangre.\n\n**Qué pasó después**\n\nUn mes después del accidente, el niño recibió el trasplante de corazón que necesitaba. Como consecuencia del accidente cerebrovascular, quedó con un poco de rigidez en el brazo derecho, pero en general tuvo buenos resultados y pudo continuar con su tratamiento.\n\n**Por qué es importante este caso**\n\nEste caso muestra que, incluso en niños muy pequeños con problemas graves del corazón, es posible usar técnicas avanzadas para tratar accidentes cerebrovasculares y mejorar su salud antes de un trasplante.",
+        "score": {
+          "ROUGE-L-Sum": 0.2369146005509642,
+          "BERTScore_F": 0.7508296966552734
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.4938721486031188
+        }
+      },
+      "B3": {
+        "text": "**Contexto:**  \nSe presenta el caso de un niño de 23 meses con antecedentes complejos, incluyendo encefalopatía isquémica hipóxica al nacer con desarrollo psicomotor normal, y una cardiomiopatía restrictiva diagnosticada en la infancia. Debido a la gravedad de su insuficiencia cardíaca, fue incluido en un programa de trasplante cardiaco a los 16 meses. Posteriormente, a los 20 meses, se le implantó un dispositivo de asistencia ventricular biventricular externo (Berlin Heart) para apoyar la función cardíaca mientras esperaba el trasplante. Para prevenir la formación de coágulos, recibió tratamiento combinado con anticoagulantes y antiplaquetarios.\n\n**Hallazgos Clave:**  \nA los 23 meses, el niño presentó síntomas neurológicos agudos, incluyendo desconexión y hemiparesia (debilidad) en el lado derecho del cuerpo. Una tomografía computarizada reveló una obstrucción en la arteria cerebral media izquierda, responsable del suministro sanguíneo a una parte importante del cerebro, junto con un infarto crónico en el hemisferio derecho. Debido a que el tratamiento trombolítico intravenoso (que disuelve coágulos) estaba contraindicado por su régimen anticoagulante, se optó por una trombectomía mecánica intraarterial, un procedimiento endovascular que consiste en extraer el coágulo directamente desde la arteria afectada.\n\nDurante la intervención, realizada bajo anestesia general, se accedió a la arteria femoral derecha para introducir un catéter que permitió llegar hasta la arteria cerebral afectada. Se utilizó un dispositivo llamado stentriever para recuperar el flujo sanguíneo en una sola maniobra. Aunque se detectó una disección (una lesión en la pared arterial causada por el procedimiento), esta no tuvo consecuencias clínicas importantes debido a la circulación colateral cerebral. El procedimiento fue exitoso y permitió la recuperación del flujo en la arteria ocluida.\n\n**Interpretación Clínica:**  \nEste caso destaca la viabilidad y eficacia de la trombectomía mecánica en pacientes pediátricos con ictus isquémico, incluso en niños muy pequeños y con condiciones cardíacas complejas que contraindican el tratamiento trombolítico convencional. La intervención permitió minimizar el daño cerebral y preservar la función neurológica, limitando la secuela a una espasticidad en el brazo derecho.\n\n**Próximos Pasos:**  \nUn mes después de la recuperación del accidente cerebrovascular, el niño fue sometido con éxito a un trasplante de corazón, mejorando su pronóstico a largo plazo. El seguimiento neurológico y cardiológico continúa siendo fundamental para monitorizar la evolución y manejar posibles complicaciones futuras. Este caso aporta evidencia sobre el manejo multidisciplinario y personalizado en pacientes pediátricos con enfermedades cardíacas graves y complicaciones neurológicas.",
+        "score": {
+          "ROUGE-L-Sum": 0.1576923076923077,
+          "BERTScore_F": 0.7706815600395203
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.464186933865914
+        }
+      }
+    }
+  },
+  {
+    "id": 12,
+    "gold_summary": "Aquí se informa sobre el caso de una joven granjera de la zona rural de Etiopía que fue internada en un hospital local tras perder el conocimiento y presentar exceso de secreciones orales 2 horas después de haber ingerido, de manera suicida, un agente tóxico desconocido. Originalmente, se la trató por intoxicación con organofosforados y luego se la trasladó al Hospital Saint Peter's en Addis Abeba para recibir atención médica más intensiva. Allí, se confirmó la ingesta de 2,4-D y se le brindó atención médica de apoyo, ventilación mecánica y diuresis alcalina forzada. A pesar de estas intervenciones, falleció varios días después.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Una joven tomó un veneno para hacerse daño. Se puso muy mal y perdió el conocimiento. La llevaron al hospital para ayudarla. \n\nLos doctores le dieron medicinas y la cuidaron mucho. Pero su cuerpo no pudo mejorar. Después de unos días, ella murió. \n\nLos doctores hicieron todo lo que pudieron para ayudarla.",
+        "score": {
+          "ROUGE-L-Sum": 0.18497109826589597,
+          "BERTScore_F": 0.7440687417984009
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.4645199200321484
+        }
+      },
+      "B2": {
+        "text": "Caso de Intoxicación Grave en una Joven\n\nUna mujer de 23 años de una zona rural de Etiopía tomó un veneno llamado 2,4-D con la intención de suicidarse. Dos horas después, perdió el conocimiento y tenía mucha saliva. Al principio, pensaron que había tomado otro tipo de veneno y la trataron en un hospital pequeño. Luego, la llevaron a un hospital más grande llamado Saint Peter para recibir mejor atención.\n\nLo que Encontraron en el Hospital\n\nCuando llegó, la paciente estaba inconsciente y tenía signos de daño en sus nervios y músculos. Los exámenes de sangre y orina mostraron que sus riñones no funcionaban bien y que había daño muscular grave, causado por el veneno. Los médicos intentaron ayudarla con tratamientos para limpiar el veneno y proteger sus órganos, incluyendo ponerle un tubo para ayudarla a respirar.\n\nQué Pasó Después\n\nA pesar de los esfuerzos médicos, la paciente empeoró. Su presión sanguínea bajó mucho y los médicos tuvieron que usar medicamentos para mantenerla estable. Finalmente, después de tres días en cuidados intensivos, falleció debido a un fallo en su circulación sanguínea.\n\nImportancia del Caso\n\nEste caso muestra lo peligroso que puede ser el veneno 2,4-D y cómo puede afectar seriamente el cuerpo, especialmente los riñones y los músculos. También destaca la importancia de un diagnóstico correcto y tratamiento rápido en casos de intoxicación para intentar salvar vidas.",
+        "score": {
+          "ROUGE-L-Sum": 0.2506527415143603,
+          "BERTScore_F": 0.7890900373458862
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.5198713894301232
+        }
+      },
+      "B3": {
+        "text": "**Contexto**\n\nSe presenta el caso de una mujer joven de 23 años, proveniente de una zona rural de Etiopía, que ingresó al hospital tras perder el conocimiento y mostrar un exceso de secreciones orales aproximadamente dos horas después de ingerir intencionalmente una sustancia tóxica. Inicialmente fue atendida en un hospital local donde se sospechó intoxicación por organofosforados (un tipo común de pesticida) y recibió tratamiento con atropina y cimetidina durante tres días. Posteriormente, fue trasladada al Hospital Saint Peter en Addis Abeba para recibir cuidados más especializados.\n\n**Hallazgos Clave**\n\nEn el hospital de referencia se confirmó que la sustancia ingerida era 2,4-D, un herbicida tóxico. Al ingreso, la paciente estaba inconsciente con un nivel de conciencia muy bajo (Glasgow Coma Scale de 6/15), presentaba pupilas dilatadas pero reactivas, hipertonicidad (aumento anormal del tono muscular) y reflejos exagerados en las extremidades inferiores, así como un reflejo plantar anormal (reflejo de Babinski positivo). Sus signos vitales mostraban taquicardia (frecuencia cardíaca rápida), presión arterial y saturación de oxígeno dentro de rangos aceptables. Los análisis iniciales de sangre, función renal y hepática, así como glucosa, fueron normales. Sin embargo, no se pudieron medir niveles específicos de la toxina ni gases en sangre debido a limitaciones del hospital.\n\nDurante su estancia en la unidad de cuidados intensivos (UCI), la paciente fue intubada para proteger sus vías respiratorias y se inició diuresis alcalina forzada, una técnica para ayudar a eliminar la toxina a través de la orina. A pesar de esto, desarrolló insuficiencia renal aguda, evidenciada por un aumento significativo de creatinina y nitrógeno ureico en sangre, así como presencia de hemoglobina y glóbulos rojos en la orina. Además, presentó rabdomiólisis (descomposición del tejido muscular) inducida por la toxina, confirmada por niveles elevados de creatina fosfocinasa, una enzima muscular. Posteriormente, la paciente sufrió hipotensión (presión arterial baja) que requirió el uso de medicamentos vasopresores para mantener la presión arterial. Estudios de ecocardiografía y ecografía abdominal no mostraron alteraciones significativas.\n\n**Interpretación Clínica**\n\nLa intoxicación por 2,4-D es poco común pero grave, y puede causar daño multisistémico, incluyendo alteraciones neurológicas, musculares y renales. En este caso, la rápida progresión hacia insuficiencia renal y colapso circulatorio refleja la alta toxicidad de esta sustancia y la dificultad para manejar sus complicaciones, incluso con tratamiento intensivo y medidas de soporte avanzadas.\n\n**Próximos Pasos**\n\nEste caso subraya la importancia de un diagnóstico preciso y rápido en intoxicaciones, especialmente en regiones con recursos limitados. La disponibilidad de pruebas específicas para identificar toxinas y la implementación temprana de tratamientos dirigidos podrían mejorar el pronóstico. Además, es fundamental fortalecer la atención en salud mental y los servicios de prevención del suicidio para evitar intentos con sustancias altamente tóxicas.",
+        "score": {
+          "ROUGE-L-Sum": 0.20745542949756884,
+          "BERTScore_F": 0.8112509250640869
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.5093531772808279
+        }
+      }
+    }
+  },
+  {
+    "id": 13,
+    "gold_summary": "Una mujer negra de 35 años se presentó con falta de aire en reposo, ortopnea, disnea paroxística nocturna, dolor torácico, tos productiva teñida de sangre y fiebre durante 2 semanas. También tenía hinchazón progresiva del cuerpo, fatigabilidad fácil, pérdida de apetito y dolor abdominal durante la misma semana. La imagen corporal reveló grandes derrames pleurales y pericárdicos, lesiones hepáticas metastásicas y defectos de llenado segmentarios y subsegmentarios vasculares pulmonares bilaterales. La citología de los fluidos pericardio y pleural sugieren derrame maligno. Las lesiones hepáticas y la biopsia con aguja indicaron adenocarcinoma de origen desconocido, y el nivel de antígeno carcinoembriónico también aumentó significativamente.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Había una mujer que se sentía muy cansada y con dificultad para respirar. Su cuerpo se hinchó mucho y tenía dolor en el pecho. Los doctores vieron que tenía líquido en el pecho y alrededor del corazón. También encontraron que tenía un problema en el hígado y en los pulmones. El líquido que sacaron mostró que tenía células que no son buenas. Los doctores dijeron que tenía un tipo de cáncer que empezó en un lugar que no pudieron encontrar.",
+        "score": {
+          "ROUGE-L-Sum": 0.1308411214953271,
+          "BERTScore_F": 0.7150653600692749
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.422953240782301
+        }
+      },
+      "B2": {
+        "text": "**Lo que le Pasó a la Paciente**\n\nUna mujer de 35 años llegó al hospital porque tenía mucha dificultad para respirar, incluso cuando estaba en reposo. También tenía dolor en el pecho, tos con sangre, fiebre y una hinchazón que comenzó en sus piernas y se extendió por todo el cuerpo. Además, se sentía muy cansada, había perdido el apetito y tenía dolor en la parte superior del abdomen.\n\n**Lo que Encontraron en los Exámenes**\n\nLas imágenes médicas mostraron que tenía acumulación de líquido en los pulmones (llamado derrame pleural) y alrededor del corazón (derrame pericárdico). También encontraron lesiones en el hígado que parecían ser metástasis, es decir, que el cáncer se había extendido allí. En los vasos sanguíneos de sus pulmones había bloqueos que indicaban embolias pulmonares, que son coágulos que dificultan la circulación.\n\nAl analizar el líquido que rodeaba el corazón y los pulmones, los médicos encontraron células anormales que indicaban que el líquido estaba causado por un cáncer (derrame maligno). La biopsia del hígado confirmó que tenía un tipo de cáncer llamado adenocarcinoma, pero no pudieron encontrar dónde comenzó el cáncer originalmente.\n\nAdemás, un examen de sangre mostró que tenía un nivel muy alto de una sustancia llamada antígeno carcinoembrionario, que suele aumentar cuando hay ciertos tipos de cáncer.\n\n**Qué Significa Todo Esto**\n\nLa paciente tenía un cáncer avanzado que se había extendido a varias partes del cuerpo, incluyendo los pulmones, el corazón y el hígado. Esto causó problemas graves como dificultad para respirar, acumulación de líquidos y coágulos en la sangre. Aunque recibieron tratamiento para aliviar sus síntomas y para el cáncer, la enfermedad estaba muy avanzada y el origen del tumor principal no se pudo identificar.",
+        "score": {
+          "ROUGE-L-Sum": 0.2163355408388521,
+          "BERTScore_F": 0.7756541967391968
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.49599486878902443
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nUna mujer etíope de 35 años acudió al hospital presentando dificultad grave para respirar en reposo, dificultad para respirar al estar acostada (ortopnea), episodios repentinos de dificultad respiratoria nocturna (disnea paroxística nocturna), dolor en el pecho, tos con expectoración de sangre y vómitos de contenido alimenticio durante dos semanas. Además, manifestó una hinchazón progresiva que comenzó en las piernas y se extendió a todo el cuerpo, cansancio fácil, pérdida de apetito, fiebre alta intermitente y ardor en la parte superior del abdomen. También había experimentado pérdida de peso y fatiga durante los dos meses previos. No tenía antecedentes médicos relevantes ni factores de riesgo conocidos.\n\n**Hallazgos Clave**  \nEl examen físico y las pruebas de imagen revelaron derrames significativos de líquido tanto en la cavidad pleural (alrededor de los pulmones) como en el pericardio (la membrana que rodea el corazón). La tomografía computarizada mostró lesiones en el hígado compatibles con metástasis (diseminación del cáncer) y defectos en la circulación sanguínea pulmonar que indicaban embolias pulmonares bilaterales. El análisis del líquido extraído del pericardio y la pleura mostró células malignas, lo que sugiere que el líquido se debía a un derrame maligno. La biopsia hepática confirmó la presencia de un adenocarcinoma (un tipo de cáncer que se origina en células glandulares) de origen primario desconocido. Además, el nivel en sangre del antígeno carcinoembrionario (CEA), un marcador tumoral, estaba muy elevado, apoyando la presencia de un cáncer avanzado.\n\n**Interpretación Clínica**  \nLa paciente fue diagnosticada con insuficiencia cardíaca causada por un derrame pericárdico masivo de origen maligno, secundario a un adenocarcinoma diseminado que afectaba múltiples órganos, incluyendo pulmón, pleura, pericardio y tracto gastrointestinal. También se identificaron complicaciones como trombosis venosa profunda en el brazo izquierdo y embolia pulmonar, probablemente relacionadas con la enfermedad tumoral avanzada. Se detectó además una neumonía multifocal superpuesta y anemia leve asociada a enfermedad crónica.\n\n**Próximos Pasos y Tratamiento**  \nLa paciente recibió tratamiento urgente para aliviar el derrame pericárdico mediante pericardiocentesis y ventana pericárdica, así como drenaje del líquido pleural. Se inició tratamiento anticoagulante para la trombosis y embolia pulmonar, y antibióticos para la neumonía. Posteriormente, se administró quimioterapia con carboplatino y paclitaxel dirigida al cáncer de origen desconocido. A pesar de la mejoría inicial y el alta hospitalaria, la paciente falleció cuatro meses después debido a la progresión de la enfermedad.\n\nEste caso ilustra la complejidad del diagnóstico y manejo de un cáncer avanzado con origen primario desconocido, que se manifestó inicialmente con síntomas respiratorios y signos de insuficiencia cardíaca por derrame pericárdico maligno.",
+        "score": {
+          "ROUGE-L-Sum": 0.22445561139028475,
+          "BERTScore_F": 0.820339560508728
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.5223975859495064
+        }
+      }
+    }
+  },
+  {
+    "id": 14,
+    "gold_summary": "Adolescente de 17 años con enfermedad de Graves con manifestaciones clínicas descontroladas, la cual no respondió a tratamiento médico y se programó para tiroidectomia radical. Se obtuvieron 35 puntos en la Escala de Burch y Wartofsky. Se manejó con anestesia general y fueron disminuyendo los estímulos para control de vía aérea y regional a fin de disminuir los estímulos quirúrgicos. Se usaron medicamentos adyuvantes como sulfato de magnesio para la estabilidad transoperatoria.",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Una niña de 17 años tenía un problema en su cuello llamado enfermedad de Graves. Su cuerpo estaba muy acelerado y no mejoró con medicinas. Por eso, los doctores decidieron hacerle una operación para quitarle una parte del cuello. Durante la operación, los doctores usaron medicinas para que ella no sintiera dolor y para que su cuerpo estuviera tranquilo. También cuidaron mucho su respiración para que todo saliera bien.",
+        "score": {
+          "ROUGE-L-Sum": 0.1794871794871795,
+          "BERTScore_F": 0.7178597450256348
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.44867346225640714
+        }
+      },
+      "B2": {
+        "text": "**Caso de una Adolescente con Enfermedad de Graves**\n\nUna joven de 17 años tenía una enfermedad llamada Graves, que afecta la tiroides, una glándula en el cuello que controla muchas funciones del cuerpo. Su enfermedad estaba muy activa y no mejoró con los medicamentos que le dieron.\n\n**Lo que Pasó Antes de la Cirugía**\n\nLa paciente tenía síntomas como pérdida de peso, ansiedad, latidos rápidos del corazón y un aumento visible en el tamaño de su cuello debido al crecimiento de la tiroides. Los médicos usaron una escala llamada Burch y Wartofsky para medir qué tan grave estaba su condición, y obtuvo 35 puntos, lo que indica un problema serio.\n\n**Cómo Se Realizó la Cirugía**\n\nPara operarla, le pusieron anestesia general, que es un medicamento que la hizo dormir y no sentir dolor durante la cirugía. Los médicos cuidaron mucho la forma de manejar su respiración y usaron técnicas para reducir las molestias causadas por la operación. Además, le dieron medicamentos especiales, como sulfato de magnesio, para mantener su cuerpo estable mientras duraba la cirugía.\n\n**Por Qué Es Importante**\n\nEste caso muestra cómo se trata una enfermedad de Graves muy avanzada cuando los medicamentos no funcionan. La cirugía y el cuidado durante la operación son muy importantes para que la paciente esté segura y se recupere bien.",
+        "score": {
+          "ROUGE-L-Sum": 0.2367601246105919,
+          "BERTScore_F": 0.7390968203544617
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.4879284724825268
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe trata de una paciente femenina de 17 años diagnosticada con enfermedad de Graves, una condición autoinmune que provoca un aumento en la actividad de la glándula tiroides (hipertiroidismo) y crecimiento difuso del tiroides (bocio). Desde hace seis meses, presentó síntomas progresivos como pérdida de peso, ansiedad, fiebre leve, palpitaciones, dolor abdominal y diarrea. Posteriormente, desarrolló un aumento visible en la parte frontal del cuello y taquicardia (frecuencia cardíaca acelerada). El tratamiento inicial con tiamazol (un medicamento antitiroideo) fue suspendido debido a una complicación grave llamada agranulocitosis (disminución severa de glóbulos blancos). Se intentaron otros tratamientos sin éxito, por lo que se decidió administrar yodo radioactivo (I-131) para reducir la función tiroidea.\n\n**Hallazgos Clave**  \nEn la evaluación física, la paciente mostraba signos de hipertiroidismo activo: frecuencia cardíaca elevada (105 latidos por minuto), temperatura corporal ligeramente elevada (37.4 ºC), temblor fino, sudoración excesiva en las palmas y aumento de la sensibilidad al calor. Se observó un bocio grande (aproximadamente 7.5 x 7 x 10 cm) sin signos de dificultad respiratoria, aunque no se pudo evaluar completamente la movilidad de la tráquea debido al tamaño del tiroides. La escala de Burch y Wartofsky, que evalúa el riesgo de una crisis tiroidea grave llamada tormenta tiroidea, arrojó un puntaje de 40, indicando alta probabilidad de esta complicación.\n\nDurante la cirugía programada para extirpar la glándula tiroides (tiroidectomía radical), se utilizó anestesia general con técnicas avanzadas para asegurar la vía aérea, incluyendo videolaringoscopía, y ventilación mecánica controlada. Se aplicó un bloqueo nervioso cervical superficial guiado por ultrasonido para reducir el dolor y la respuesta al estímulo quirúrgico. Además, se emplearon varios medicamentos adyuvantes, como sulfato de magnesio, para mantener la estabilidad cardiovascular y mejorar el control del dolor durante la operación. La paciente se mantuvo estable durante todo el procedimiento, que duró aproximadamente 3 horas y 35 minutos.\n\n**Interpretación Clínica**  \nLa paciente presentaba un cuadro de enfermedad de Graves descontrolada, con signos y síntomas que indicaban un alto riesgo de tormenta tiroidea, una emergencia médica que puede ser potencialmente mortal. La falta de respuesta a tratamientos convencionales y la contraindicación del tiamazol por agranulocitosis hicieron necesaria la intervención quirúrgica. El manejo anestésico fue cuidadosamente planificado para minimizar los riesgos asociados a la hiperactividad tiroidea y al tamaño del bocio, utilizando técnicas que redujeron la estimulación del sistema nervioso y mantuvieron la estabilidad hemodinámica.\n\n**Próximos Pasos**  \nDespués de la cirugía, la paciente presentó analgesia efectiva durante 12 horas y requirió un solo rescate analgésico. Se observó disfonía (alteración de la voz) persistente, probablemente relacionada con la manipulación quirúrgica de los nervios laríngeos, pero sin dolor al tragar. Será importante realizar un seguimiento para evaluar la función vocal y ajustar el tratamiento hormonal tiroideo según sea necesario para evitar complicaciones a largo plazo. Además, se debe monitorizar la recuperación general y prevenir posibles efectos secundarios derivados de la cirugía y la enfermedad de base.",
+        "score": {
+          "ROUGE-L-Sum": 0.17124394184168015,
+          "BERTScore_F": 0.7332991361618042
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.45227153900174216
+        }
+      }
+    }
+  },
+  {
+    "id": 15,
+    "gold_summary": "Una mujer de 30 años presentó disminución de la micción durante 2 días después de una cesárea. La ecografía mostró una hidronefrosis izquierda grave y un fluido abdominal libre moderado. Una ureteroscopia reveló una oclusión total del uréter izquierdo y, posteriormente, se realizó una ureteroneocistostomía. Dos días después, la paciente presentó complicaciones con distensión abdominal que requirieron una nueva exploración. La exploración reveló lesiones en el colon (recto-sigmoide), peritonitis, endometritis y alteración de la anastomosis ureteral. Se realizó una colostomía, reparación de lesiones en el colon, histerectomía y derivación ureterocutánea. La estancia hospitalaria de la paciente fue complicada, con retracción estomal que requirió revisión quirúrgica y dehiscencia de la herida, que se trató de forma conservadora. Después de 6 meses, se cerró la colostomía y se anastomosó el uréter mediante el procedimiento de colgajo de Boari.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Una mujer tuvo un bebé con una operación. Después, le dolía y no podía hacer pipí bien. Los doctores vieron que un tubito que lleva la pipí estaba tapado. Hicieron una operación para arreglarlo.\n\nDespués, la mujer se sintió peor y su pancita se hizo grande. Los doctores encontraron que tenía heridas en su pancita y en otros lugares. Hicieron más operaciones para ayudarla y poner todo bien.\n\nLa mujer estuvo en el hospital mucho tiempo. Poco a poco, se fue mejorando. Después de seis meses, los doctores cerraron una abertura que le habían hecho y arreglaron el tubito de la pipí otra vez. Ahora está bien y sin dolor.",
+        "score": {
+          "ROUGE-L-Sum": 0.19014084507042256,
+          "BERTScore_F": 0.7307069897651672
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.46042391741779487
+        }
+      },
+      "B2": {
+        "text": "**Lo que pasó con la paciente**  \nUna mujer de 30 años tuvo problemas para orinar durante dos días después de una cesárea, que es una operación para sacar al bebé. Al hacerle una ecografía, los médicos vieron que tenía una hinchazón grave en el riñón izquierdo llamada hidronefrosis, causada por la acumulación de orina, y también encontraron líquido libre en su abdomen. Luego, con un examen llamado ureteroscopia, descubrieron que el tubo que lleva la orina desde el riñón a la vejiga (el uréter izquierdo) estaba completamente bloqueado.\n\n**Tratamiento inicial**  \nPara arreglar este problema, los médicos hicieron una cirugía llamada ureteroneocistostomía, que consiste en conectar el uréter a la vejiga de nuevo para que la orina pueda salir. Sin embargo, dos días después, la paciente tuvo dolor y su abdomen se hinchó más, lo que indicaba que algo no estaba bien.\n\n**Complicaciones y nuevas cirugías**  \nAl revisarla otra vez, encontraron que tenía una infección grave en el abdomen (peritonitis), una herida en el colon (parte del intestino) y una inflamación en el útero (endometritis). También la conexión del uréter que habían hecho estaba dañada. Por eso, los médicos tuvieron que hacer varias cirugías: quitaron el útero (histerectomía), repararon el colon y crearon una abertura en la piel para que la orina y las heces pudieran salir por separado (derivación ureterocutánea y colostomía).\n\n**Recuperación y seguimiento**  \nLa recuperación fue difícil porque la paciente tuvo problemas con las heridas y la abertura del colon se contrajo, lo que necesitó otra cirugía. También tuvo infecciones que se trataron con antibióticos y cuidados especiales. Después de seis meses, los médicos cerraron la abertura del colon y volvieron a conectar el uréter usando una técnica llamada colgajo de Boari, que usa parte de la vejiga para reparar el uréter.\n\n**Resultado final**  \nTras esta última cirugía, la paciente se recuperó bien. Los controles con ecografías y otros estudios mostraron que su vejiga y riñones funcionaban normalmente. Durante dos años de seguimiento, no tuvo problemas ni síntomas molestos.",
+        "score": {
+          "ROUGE-L-Sum": 0.2956204379562044,
+          "BERTScore_F": 0.7798705101013184
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.5377454740287614
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nUna mujer de 30 años, embarazada por tercera vez, fue sometida a una cesárea de emergencia debido a complicaciones durante el trabajo de parto, incluyendo sangrado prolongado y sufrimiento fetal. Tras la cesárea, presentó disminución en la cantidad de orina, dolor en el costado izquierdo y fiebre. Durante la cirugía se detectaron adherencias severas en el útero y lesiones compatibles con endometriosis, además de una pérdida significativa de sangre. La paciente no había recibido atención prenatal y no presentaba antecedentes médicos relevantes.\n\n**Hallazgos Clave**  \n- Exámenes iniciales mostraron leucocitosis con predominio neutrofílico (indicativo de infección), anemia moderada y deterioro de la función renal (elevación de creatinina).  \n- La ecografía evidenció una hidronefrosis grave (dilatación del riñón por obstrucción) en el lado izquierdo y presencia de líquido libre en la cavidad abdominal, que resultó ser orina al analizarse.  \n- La ureteroscopia urgente identificó una obstrucción completa del uréter izquierdo.  \n- Se realizó una cirugía para extirpar el segmento dañado del uréter y se reconstruyó la conexión entre el uréter y la vejiga (ureteroneocistostomía), con colocación de un stent para mantener el flujo urinario.\n\n**Interpretación Clínica**  \nPocos días después de la cirugía, la paciente desarrolló distensión abdominal progresiva, dolor y ausencia de expulsión de gases, signos sugestivos de complicaciones intraabdominales. Estudios por imagen mostraron aire y líquido libre en el abdomen, lo que indicaba una posible perforación intestinal. La laparotomía exploratoria confirmó perforación en el colon rectosigmoide, peritonitis (inflamación del revestimiento abdominal), infección del útero (endometritis) y problemas en la reparación del uréter. Debido a la complejidad y gravedad del cuadro, se realizaron múltiples intervenciones: histerectomía para controlar la infección uterina, derivación urinaria mediante ureterostomía para proteger el tracto urinario, y reparación del colon con creación de colostomía para desviar las heces.\n\nDurante la hospitalización, la paciente presentó complicaciones adicionales como retracción de la colostomía con infección y dehiscencia (apertura) de la herida abdominal, que requirieron revisiones quirúrgicas y tratamiento con antibióticos y cuidados locales. La recuperación fue gradual, y la paciente fue dada de alta en condiciones estables tras un mes de hospitalización.\n\n**Próximos Pasos y Seguimiento**  \nSeis meses después, se realizó el cierre de la colostomía y la reconstrucción definitiva del uréter mediante el procedimiento de colgajo de Boari, que utiliza un segmento de la vejiga para reemplazar la parte dañada del uréter. La recuperación postoperatoria fue satisfactoria, con estudios de imagen que mostraron una vejiga y tracto urinario superiores normales, y ureteroscopias que confirmaron un calibre adecuado del uréter. Durante dos años de seguimiento, la paciente no presentó síntomas urinarios ni gastrointestinales, evidenciando una recuperación completa y funcional.\n\n---\n\nEste caso ilustra la complejidad y gravedad de las complicaciones postoperatorias tras una cesárea en un contexto de falta de atención prenatal y lesiones previas, así como la importancia de un manejo multidisciplinario para resolver complicaciones urológicas, ginecológicas y gastrointestinales simultáneas.",
+        "score": {
+          "ROUGE-L-Sum": 0.2570621468926554,
+          "BERTScore_F": 0.8134866952896118
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.5352744210911335
+        }
+      }
+    }
+  },
+  {
+    "id": 16,
+    "gold_summary": "Mujer de 43 años que ingresó a un servicio de urgencias con datos de obstrucción intestinal. Se realizó tomografía simple de abdomen donde se identificó dilatación del colon e imagen que semejaba un grano de café invertido. Se hizo laparotomía exploradora y se identificó vólvulo cecal del tipo báscula, sin compromiso vascular. Se realizó desvolvulación, descompresión a través de apendicectomía, y cecopexia. Posterior a evento quirúrgico, la paciente se recuperó sin incidentes y fue dada de alta con controles adecuados por consulta externa.",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Una señora tenía dolor en su barriga y no podía ir al baño bien. Los doctores le hicieron una foto especial para ver su barriga. Vieron que un pedazo de su barriga estaba doblado y tapado. La señora tuvo una operación para arreglar ese problema. Los doctores quitaron la parte que estaba doblada y la dejaron bien. Después de la operación, la señora se sintió mejor y pudo ir al baño normalmente. Ahora está bien y los doctores la revisan para cuidar que siga sana.",
+        "score": {
+          "ROUGE-L-Sum": 0.1368421052631579,
+          "BERTScore_F": 0.694343626499176
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.41559286588116695
+        }
+      },
+      "B2": {
+        "text": "**Lo que pasó con la paciente**\n\nUna mujer de 43 años llegó al hospital porque tenía dolor en el abdomen, vómitos y problemas para evacuar. Los médicos hicieron estudios y vieron que una parte del intestino grueso, llamada colon, estaba muy inflamada y bloqueada. En la tomografía, que es una imagen especial del cuerpo, notaron una forma que parecía un \"grano de café\" invertido, lo que les hizo sospechar que había un problema llamado vólvulo, que es cuando el intestino se gira y se tapa.\n\n**Lo que hicieron los médicos**\n\nDecidieron hacer una cirugía urgente para ver qué pasaba. Durante la operación, encontraron que una parte del intestino llamada ciego estaba doblada y no estaba bien sujeta en su lugar. Esto causaba que el intestino se girara (vólvulo), pero sin dañar el flujo de sangre. Para arreglarlo, quitaron una banda de tejido que estaba causando el problema, hicieron una apendicectomía (que es sacar el apéndice) para descomprimir el intestino, y fijaron el ciego a la pared del abdomen para que no se moviera otra vez.\n\n**Qué pasó después**\n\nDespués de la cirugía, la paciente mejoró mucho. Empezó a evacuar normalmente y no tuvo más síntomas. Fue dada de alta y siguió controles médicos para asegurarse de que todo estuviera bien.",
+        "score": {
+          "ROUGE-L-Sum": 0.24539877300613497,
+          "BERTScore_F": 0.7365373969078064
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.4909680849569707
+        }
+      },
+      "B3": {
+        "text": "**Contexto:**  \nUna mujer de 43 años con antecedentes de hipertensión arterial, dos cesáreas previas y oclusión tubaria bilateral, ingresó al hospital presentando dolor abdominal intenso de tipo cólico en la parte baja del abdomen (hipogastrio), que se irradiaba hacia el lado izquierdo, acompañado de náuseas, vómitos y cambios en sus evacuaciones intestinales, incluyendo inicialmente heces semilíquidas y luego ausencia de evacuaciones y gases. En la exploración física, se detectó distensión abdominal y dolor localizado, especialmente en el lado izquierdo, con presencia de sonidos intestinales reducidos o ausentes en esa zona, pero sin signos de irritación peritoneal (inflamación de la membrana que recubre los órganos abdominales). Los análisis de sangre mostraron un aumento moderado de glóbulos blancos y proteína C reactiva, indicadores de inflamación o infección. La radiografía y la tomografía computarizada del abdomen revelaron una dilatación significativa del colon izquierdo y una imagen característica en forma de “grano de café”, que sugiere torsión intestinal.\n\n**Hallazgos Clave:**  \nAnte la sospecha de una obstrucción intestinal grave, posiblemente causada por torsión del colon (vólvulo de sigmoides) o adherencias (bandas de tejido cicatricial que pueden causar obstrucción), se decidió realizar una cirugía de emergencia (laparotomía). Durante la operación, se encontró que el ciego (la primera parte del colon) estaba anormalmente desplazado y flexionado hacia adelante y hacia la izquierda, sin estar fijado a la pared abdominal como es habitual. Esta torsión fue causada por una banda de adherencia sobre el colon ascendente. No se observaron signos de daño grave como falta de riego sanguíneo (isquemia), muerte del tejido (necrosis) o perforación. Se liberó la adherencia que causaba la torsión, se descomprimió el ciego mediante la extracción del apéndice (apendicectomía) y se fijó el ciego a la pared abdominal (cecopexia) para evitar futuras torsiones.\n\n**Interpretación Clínica:**  \nEl diagnóstico final fue un vólvulo cecal del tipo “báscula”, una torsión del ciego que puede provocar obstrucción intestinal pero que en este caso no comprometió la circulación sanguínea ni causó daño irreversible. La intervención quirúrgica oportuna permitió resolver la obstrucción, evitar complicaciones mayores y preservar la integridad del colon.\n\n**Próximos Pasos:**  \nTras la cirugía, la paciente mostró una recuperación favorable, con retorno normal de las evacuaciones intestinales y ausencia de síntomas. Fue dada de alta y se mantuvo en seguimiento ambulatorio con controles periódicos en consulta externa de cirugía, donde continuó asintomática y sin complicaciones. Este caso resalta la importancia del diagnóstico temprano y tratamiento quirúrgico adecuado en pacientes con obstrucción intestinal por vólvulo cecal.",
+        "score": {
+          "ROUGE-L-Sum": 0.1663716814159292,
+          "BERTScore_F": 0.7638235688209534
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.46509762511844127
+        }
+      }
+    }
+  },
+  {
+    "id": 17,
+    "gold_summary": "Paciente de 10 años que se presenta con síndrome nefrótico y bocio. Se pesquisa antecedente de tiroiditis autoinmu ne e hipotiroidismo no tratado. Se inicia terapia corticoidal y hormonal de sustitución (levotiroxina), logrando buena respuesta clínica y de laboratorio.",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Niña de 10 años con hinchazón en el cuerpo y cuello grande. Tenía un problema en la tiroides que no se había tratado. Le dieron medicinas para ayudar su cuerpo y se puso mejor.",
+        "score": {
+          "ROUGE-L-Sum": 0.24096385542168672,
+          "BERTScore_F": 0.7427579164505005
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.4918608859360936
+        }
+      },
+      "B2": {
+        "text": "**Lo que le Pasó a la Paciente**  \nUna niña de 10 años llegó al hospital con hinchazón en los ojos y las piernas, además de orina con espuma. Ella tenía un bocio, que es cuando la glándula tiroides en el cuello está agrandada. También se sabía que tenía tiroiditis autoinmune, una enfermedad donde el cuerpo ataca su propia tiroides, y no estaba tomando ningún medicamento para eso.\n\n**Qué Encontraron en los Exámenes**  \nLos análisis de orina mostraron mucha proteína, lo que indica que los riñones no estaban funcionando bien. Esto se llama síndrome nefrótico, una condición que causa que el cuerpo pierda proteínas importantes. Además, sus niveles de algunas hormonas de la tiroides estaban bajos y tenía anticuerpos que confirmaban la tiroiditis. La ecografía del cuello mostró inflamación en la tiroides, pero sin tumores.\n\n**Cómo la Trataron y Qué Pasó Después**  \nLe dieron un medicamento llamado prednisona, que es un corticoide para reducir la inflamación, y levotiroxina, que es una hormona para ayudar a su tiroides a funcionar mejor. Con este tratamiento, la hinchazón bajó y los análisis mejoraron rápidamente. Después de un año, la niña estaba bien, sin síntomas y con su tiroides controlada gracias a la medicación. No tuvo problemas nuevos en los riñones.",
+        "score": {
+          "ROUGE-L-Sum": 0.1408450704225352,
+          "BERTScore_F": 0.7025238275527954
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.42168444898766533
+        }
+      },
+      "B3": {
+        "text": "**Contexto:**  \nSe trata de una niña de 10 años con diagnóstico previo de bocio (aumento visible de la glándula tiroides) y tiroiditis autoinmune (una inflamación de la tiroides causada por el propio sistema inmunológico), sin tratamiento para su hipotiroidismo (función tiroidea disminuida) al momento de su ingreso hospitalario. Consultó por síntomas relacionados con síndrome nefrótico, que incluyen orina espumosa, edema (hinchazón) en párpados y extremidades, disminución de la cantidad de orina, dolor abdominal, vómitos y fiebre.\n\n**Hallazgos Clave:**  \n- En la evaluación inicial, se observó edema palpebral bilateral y en las piernas, así como un bocio evidente pero sin nódulos dolorosos. Además, presentó un soplo cardíaco leve.  \n- La presión arterial estaba en el límite superior normal para su edad.  \n- Los análisis de orina mostraron una proteinuria significativa (pérdida elevada de proteínas en la orina), sin signos de infección.  \n- En sangre, se detectó hipoalbuminemia (niveles bajos de albúmina, una proteína importante), hipercolesterolemia y niveles normales de creatinina, indicando función renal preservada.  \n- Los estudios inmunológicos confirmaron la presencia de anticuerpos antitiroideos elevados, compatibles con tiroiditis autoinmune, y niveles normales de otros marcadores inflamatorios y autoinmunes.  \n- La ecografía tiroidea mostró un tamaño normal de la glándula pero con aumento difuso de la vascularización, típico de tiroiditis.  \n- No se encontraron otras enfermedades autoinmunes o infecciones asociadas.\n\n**Interpretación Clínica:**  \nLa paciente presentó un síndrome nefrótico (una enfermedad renal caracterizada por pérdida excesiva de proteínas en la orina y edema) asociado a una tiroiditis autoinmune con hipotiroidismo no tratado. La coexistencia de estas dos condiciones autoinmunes sugiere un trastorno inmunológico subyacente que afecta tanto la tiroides como el riñón.\n\n**Próximos Pasos y Tratamiento:**  \nSe inició tratamiento con prednisona (un corticosteroide) para controlar el síndrome nefrótico, logrando una rápida mejoría clínica y normalización de la proteinuria en pocos días. Paralelamente, se comenzó terapia de reemplazo hormonal con levotiroxina para corregir el hipotiroidismo. La paciente fue dada de alta en buenas condiciones y, tras un seguimiento de 12 meses, se mantuvo asintomática, con función tiroidea controlada y sin recaídas del síndrome nefrótico.\n\nEste caso destaca la importancia de identificar y tratar de manera integral las enfermedades autoinmunes coexistentes para lograr una recuperación óptima y prevenir complicaciones a largo plazo.",
+        "score": {
+          "ROUGE-L-Sum": 0.12636165577342048,
+          "BERTScore_F": 0.7238638401031494
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.42511274793828496
+        }
+      }
+    }
+  },
+  {
+    "id": 18,
+    "gold_summary": "Mujer de 58 años sana que consultó por un trastorno de la marcha con caídas. La exploración neurológica mostró una apariencia facial característica (mirada fija, ojos muy abiertos, ceño fruncido y expresión fija hemifacial inferior), e hipocinesia-rigidez simétrica de predominio axial (postura retrocólica del tronco y el cuello). La exploración de la marcha reveló un trastorno de la marcha del nivel superior, caracterizado por una significativa vacilación inicial, que precisaba ayuda de objetos/personas cercanos. Al iniciar la marcha, los pasos mejoraban relativamente, pero reaparecía una deambulación inefectiva al girar. Presentaba zancadas cortas, congelación, base amplia de sustentación, desequilibrio, movimiento lento de las piernas, arrastre de los pies, y pérdida de la cadencia normal del tronco y las extremidades. Los reflejos posturales estaban alterados. La resonancia magnética cerebral desveló atrofia mesencefálica, dilatación de acueducto de Silvio y III ventrículo, atrofia frontal bilateral y el signo típico del colibrí. Finalmente, la paciente fue diagnosticada de una PSP probable.",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Había una señora que tenía problemas para caminar. Sus ojos se veían muy abiertos y su cara parecía quieta. Caminaba con pasos cortos y a veces se paraba sin poder seguir. Le costaba mucho girar y mantener el equilibrio. Su cuerpo estaba un poco rígido y lento. En el doctor, vieron que su cerebro estaba un poco cambiado. Por eso, dijeron que tenía una enfermedad que hace difícil caminar y moverse bien.",
+        "score": {
+          "ROUGE-L-Sum": 0.10810810810810811,
+          "BERTScore_F": 0.7260571718215942
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.4170826399648512
+        }
+      },
+      "B2": {
+        "text": "**Lo que Encontraron en la Paciente**\n\nUna mujer de 58 años, que antes estaba sana, empezó a tener problemas para caminar y se caía con frecuencia. Al examinarla, los médicos notaron que su cara tenía una expresión especial: sus ojos estaban muy abiertos y fijos, tenía el ceño fruncido y la parte baja de su cara parecía inmóvil. También tenía rigidez y movimientos lentos en el tronco y el cuello, con una postura inclinada hacia atrás.\n\nCuando caminaba, al principio dudaba mucho y necesitaba ayuda para no caerse. Después de unos pasos, mejoraba un poco, pero al girar volvía a tener problemas para caminar bien. Sus pasos eran cortos, a veces se quedaba paralizada (congelación), mantenía los pies separados para no perder el equilibrio, y arrastraba los pies. Además, sus movimientos eran lentos y perdía la forma normal de mover el cuerpo y las piernas. Los reflejos que ayudan a mantener el equilibrio también estaban afectados.\n\n**Lo que Vieron en el Cerebro**\n\nUna resonancia magnética, que es una imagen detallada del cerebro, mostró que algunas partes importantes estaban más pequeñas de lo normal. En especial, el mesencéfalo (una parte del cerebro que controla movimientos), el acueducto de Silvio y el tercer ventrículo (espacios llenos de líquido en el cerebro) estaban dilatados o agrandados. También había pérdida de tejido en los lóbulos frontales, que son áreas importantes para pensar y controlar movimientos. Además, apareció un signo especial llamado \"signo del colibrí\", que ayuda a los médicos a identificar esta enfermedad.\n\n**Qué Significa Todo Esto**\n\nCon estos síntomas y los resultados del examen, los médicos concluyeron que la paciente probablemente tiene una enfermedad llamada parálisis supranuclear progresiva (PSP). Esta enfermedad afecta el control de los movimientos, el equilibrio y la expresión facial, y suele empeorar con el tiempo. Aunque no tiene algunos síntomas típicos como problemas graves en la vejiga o cambios fuertes en la personalidad, sí muestra apatía, que es una falta de interés o motivación. Este diagnóstico ayudará a los médicos a planear el mejor cuidado para ella.",
+        "score": {
+          "ROUGE-L-Sum": 0.22898032200357782,
+          "BERTScore_F": 0.802615761756897
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.5157980418802374
+        }
+      },
+      "B3": {
+        "text": "**Contexto**\n\nUna mujer de 58 años, previamente sana, acudió a consulta debido a problemas para caminar acompañados de caídas frecuentes. La evaluación neurológica detallada reveló signos característicos en su rostro y movimientos, así como alteraciones específicas en su forma de caminar y en estudios de imagen cerebral.\n\n**Hallazgos Clave**\n\n- **Apariencia facial característica:** La paciente mostraba una mirada fija con los ojos muy abiertos, fruncimiento de la frente que generaba una expresión de ceño fruncido (conocido como signo del procerus) y una expresión fija en la parte inferior de la cara.\n\n- **Alteraciones motoras:** Presentaba hipocinesia (movimientos lentos) y rigidez simétrica, principalmente en la zona axial, es decir, en el tronco y cuello, con una postura inclinada hacia atrás (retrocolis).\n\n- **Trastorno de la marcha:** La forma de caminar mostraba un patrón típico de afectación del nivel superior del sistema nervioso. Inicialmente, la paciente vacilaba notablemente y necesitaba apoyo de objetos o personas para comenzar a caminar. Al avanzar, sus pasos mejoraban algo, pero al intentar girar reaparecía una marcha ineficaz. Además, caminaba con pasos cortos, episodios de congelación (parálisis temporal de la marcha), base amplia para mantener el equilibrio, desequilibrio general, movimientos lentos de las piernas, arrastre de los pies y pérdida de la fluidez normal del tronco y extremidades. Los reflejos posturales, que ayudan a mantener la estabilidad, estaban alterados.\n\n- **Movimientos oculares:** Se observaron alteraciones en los movimientos sacádicos (movimientos rápidos del ojo para cambiar la mirada), especialmente en la dirección vertical, con una oftalmoplejía supranuclear, que implica dificultad para mover los ojos hacia arriba o abajo debido a un problema en el cerebro.\n\n- **Ausencia de otros signos frontales:** No se detectaron rigidez paratónica (una rigidez muscular variable), reflejos de prensión (agarre involuntario), incontinencia urinaria ni déficits cognitivos frontales típicos (como problemas en la planificación, cambios de personalidad o impulsividad), salvo un estado de apatía progresiva.\n\n- **Imágenes cerebrales:** La resonancia magnética mostró atrofia (pérdida de volumen) del mesencéfalo (una parte del tronco cerebral), dilatación del acueducto de Silvio y del tercer ventrículo (estructuras por donde circula el líquido cefalorraquídeo), atrofia bilateral de los lóbulos frontales y la presencia de signos característicos conocidos como el “signo del colibrí” y la “gloria de la mañana”, que son patrones específicos de daño cerebral en esta enfermedad.\n\n**Interpretación Clínica**\n\nEl conjunto de síntomas, signos neurológicos y hallazgos en la resonancia magnética son compatibles con un diagnóstico probable de parálisis supranuclear progresiva (PSP), una enfermedad neurodegenerativa que afecta principalmente el control del movimiento, el equilibrio y los movimientos oculares, con daño en áreas profundas del cerebro.\n\n**Próximos Pasos**\n\nEl diagnóstico de PSP implica un seguimiento neurológico continuo para manejar los síntomas, prevenir caídas y mejorar la calidad de vida. Aunque actualmente no existe una cura, el tratamiento puede incluir terapias físicas, medicamentos para controlar la rigidez y la lentitud de movimientos, y apoyo multidisciplinario para abordar las dificultades motoras y cognitivas que puedan surgir.",
+        "score": {
+          "ROUGE-L-Sum": 0.3048951048951049,
+          "BERTScore_F": 0.8349832892417908
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5699391970684479
+        }
+      }
+    }
+  },
+  {
+    "id": 19,
+    "gold_summary": "Paciente: Mujer, 36 años\n\nDiagnóstico final: Shock cardiogénico • miocarditis\n\nSíntomas: Fiebre\n\nMedicación: —\n\nProcedimiento clínico: soporte circulatorio mecánico\n\nEspecialidad: Cirugía\n\n\nInforme del caso:\n\nReportamos el caso de una mujer de 36 años que desarrolló fiebre y shock cardiogénico 3 días después de una picadura de abeja. La angiografía cardíaca mostró arterias coronarias permeables y una función ventricular izquierda gravemente comprometida. Su hemodinámica permaneció inestable bajo una dosis alta de agentes inotrópicos y apoyo con un balón intraaórtico. El paro cardíaco intrahospitalario ocurrió 4 horas después del ingreso y recibió reanimación cardiopulmonar extracorpórea. Su oxigenación de membrana extracorpórea venosa periférica (VA ECMO) se cambió a dispositivos de asistencia ventricular bilateral (VAD) debido a una insuficiencia cardíaca derecha progresiva. El resultado de la biopsia endomiocárdica fue compatible con el cuadro de miocarditis por hipersensibilidad. Su corazón entró en paro persistente bajo apoyo circulatorio mecánico. Se sometió a un trasplante de corazón el día 49 del ingreso y permaneció clínicamente estable 6 meses después del alta.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Una mujer de 36 años fue picada por una abeja. Tres días después, tuvo fiebre y su corazón se puso muy débil. Los doctores le ayudaron con máquinas para que su corazón pudiera latir. Su corazón no mejoró y se detuvo. Entonces, le pusieron un corazón nuevo. Después de eso, ella estuvo bien y fuerte.",
+        "score": {
+          "ROUGE-L-Sum": 0.19157088122605362,
+          "BERTScore_F": 0.7264825701713562
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.4590267256987049
+        }
+      },
+      "B2": {
+        "text": "Caso de una mujer de 36 años con problemas graves en el corazón tras una picadura de abeja\n\nLo que pasó:  \nUna mujer sana de 36 años fue picada por un insecto parecido a una abeja. Tres días después, empezó a tener fiebre y problemas serios en el corazón, llamados shock cardiogénico, que significa que el corazón no podía bombear suficiente sangre. Cuando la revisaron, sus arterias del corazón estaban normales, pero el ventrículo izquierdo (una parte importante del corazón) no funcionaba bien.\n\nQué hicieron los médicos:  \nIntentaron ayudarla con medicamentos para mejorar la fuerza del corazón y usaron un balón intraaórtico, que es un dispositivo que ayuda a que el corazón trabaje mejor. Sin embargo, su estado empeoró y sufrió un paro cardíaco, que es cuando el corazón deja de latir. La reanimaron usando una máquina especial que hace el trabajo del corazón y los pulmones (oxigenación por membrana extracorpórea o ECMO). Más tarde, cambiaron esta máquina por dispositivos que ayudan a ambos lados del corazón (asistencia ventricular bilateral), porque la parte derecha del corazón también empezó a fallar.\n\nQué encontraron:  \nTomaron una pequeña muestra del músculo del corazón (biopsia endomiocárdica) y vieron que tenía inflamación causada por una reacción alérgica, llamada miocarditis por hipersensibilidad. Esto significa que el corazón estaba dañado por la respuesta del cuerpo a la picadura.\n\nQué pasó después:  \nEl corazón dejó de funcionar completamente a pesar de las máquinas que lo ayudaban. Por eso, le hicieron un trasplante de corazón el día 49 después de entrar al hospital. Se recuperó bien y estuvo estable durante al menos seis meses después de salir del hospital.\n\nEn resumen:  \nUna picadura de abeja causó una inflamación grave en el corazón de esta mujer, que llevó a una falla cardíaca muy seria. Gracias a tratamientos avanzados y un trasplante de corazón, pudo recuperarse. Este caso muestra lo importante que es tratar rápido y con cuidado las reacciones alérgicas que afectan al corazón.",
+        "score": {
+          "ROUGE-L-Sum": 0.32867132867132864,
+          "BERTScore_F": 0.8210815787315369
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5748764537014328
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe presenta el caso de una mujer de 36 años, previamente sana, que desarrolló un cuadro grave de insuficiencia cardíaca tras una picadura de abeja. Inicialmente, la paciente presentó hinchazón y enrojecimiento en la mano derecha, seguidos de fiebre en menos de 6 horas. A pesar del tratamiento inicial con esteroides y antibióticos, evolucionó con fiebre intermitente, taquicardia, hipotensión y alteraciones electrocardiográficas que indicaban compromiso cardíaco.\n\n**Hallazgos Clave**  \nAl ingreso, la paciente mostró signos de shock cardiogénico (presión arterial baja y ritmo cardíaco acelerado con fibrilación auricular), elevación significativa de marcadores cardíacos (troponina I y CK-MB), y una función ventricular izquierda gravemente reducida (fracción de eyección del 30,6%) sin evidencia de enfermedad coronaria obstructiva en el cateterismo. La ecocardiografía reveló además la presencia de trombos dentro del corazón. A pesar del soporte con balón intraaórtico y medicamentos para mejorar la función cardíaca, la paciente sufrió un paro cardíaco intrahospitalario que requirió reanimación cardiopulmonar asistida con soporte mecánico extracorpóreo (PCPS).\n\nDurante su evolución, la función cardíaca se deterioró progresivamente, afectando ambos ventrículos, y se desarrolló falla multiorgánica que requirió hemodiálisis y soporte ventilatorio avanzado. La biopsia endomiocárdica evidenció inflamación significativa con predominio de linfocitos y algunos eosinófilos, compatible con miocarditis por hipersensibilidad (una inflamación del músculo cardíaco probablemente desencadenada por una reacción alérgica o inmunológica). La paciente presentó complicaciones graves como hemorragias, infecciones y problemas en la cicatrización, que fueron manejados con intervenciones quirúrgicas y tratamientos antibióticos.\n\n**Interpretación Clínica**  \nEl cuadro clínico y los estudios realizados indican que la paciente desarrolló una miocarditis severa secundaria a una reacción de hipersensibilidad tras la picadura de abeja, que llevó a un shock cardiogénico refractario y paro cardíaco. La ausencia de enfermedad coronaria y la inflamación observada en la biopsia apoyan este diagnóstico. El soporte mecánico avanzado, incluyendo dispositivos de asistencia ventricular bilateral y oxigenación por membrana extracorpórea, fue fundamental para mantener la circulación y oxigenación mientras se evaluaba la posibilidad de trasplante cardíaco.\n\n**Próximos Pasos y Evolución**  \nDada la persistencia del fallo cardíaco y la ausencia de recuperación, la paciente fue registrada como candidata para trasplante de corazón y recibió el trasplante ortotópico en el día 49 de hospitalización. Posteriormente, se mantuvo bajo soporte postoperatorio con ECMO y fue monitoreada para detectar rechazo cardíaco, sin evidencia de este. A pesar de episodios de shock séptico y la necesidad de cirugía abdominal, la paciente logró estabilizarse, fue extubada y dada de alta al día 101. En el seguimiento a tres meses, se mantuvo clínicamente estable.\n\n**Resumen Final**  \nEste caso ilustra una forma grave y poco común de miocarditis por hipersensibilidad desencadenada por una picadura de abeja, que evolucionó rápidamente hacia un shock cardiogénico y paro cardíaco. El manejo multidisciplinario con soporte circulatorio mecánico avanzado y trasplante cardíaco fue esencial para la supervivencia y recuperación de la paciente.",
+        "score": {
+          "ROUGE-L-Sum": 0.2860998650472335,
+          "BERTScore_F": 0.8170465230941772
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5515731940707054
+        }
+      }
+    }
+  },
+  {
+    "id": 20,
+    "gold_summary": "Preocupaciones de los pacientes:\nUn hombre de 24 años fue admitido en nuestro departamento de medicina interna debido a disnea, ascitis e hinchazón de las piernas. El análisis de gases en sangre arterial reveló una hipoxemia grave con alcalosis respiratoria y metabólica. La radiografía de tórax mostró una congestión hilar.\n\nDiagnósticos:\nInsuficiencia cardíaca aguda descompensada recurrente con fracción de eyección reducida a pesar de la terapia médica óptima en la cardiomiopatía relacionada con el síndrome de Marfan.\n\nIntervenciones y resultados:\nSe agregó sacubitril/valsartan a la terapia médica óptima después de la estabilización hemodinámica, lo que permitió una mejora clínica, de laboratorio y ecocardiográfica progresiva. El paciente mantuvo una supervivencia libre de insuficiencia cardiaca y una buena calidad de vida hasta el seguimiento de 9 meses.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Un hombre joven estaba muy cansado y con las piernas hinchadas. Tenía problemas para respirar y mucho líquido en su barriga. Los doctores hicieron pruebas y vieron que su corazón no estaba funcionando bien.\n\nÉl tiene una enfermedad que hace que su corazón sea débil. Los doctores le dieron medicinas para ayudarlo. Luego, le dieron una medicina nueva llamada sacubitril/valsartan.\n\nDespués de tomar la medicina nueva, el hombre se sintió mejor. Su corazón empezó a trabajar mejor y pudo vivir sin problemas por mucho tiempo. Los doctores están contentos porque está más sano y feliz.",
+        "score": {
+          "ROUGE-L-Sum": 0.2151394422310757,
+          "BERTScore_F": 0.7512653470039368
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.48320239461750625
+        }
+      },
+      "B2": {
+        "text": "**Lo que le Pasó al Paciente**  \nUn joven de 24 años con síndrome de Marfan, una enfermedad que afecta el corazón y los vasos sanguíneos, fue llevado al hospital porque tenía dificultad para respirar, líquido en el abdomen (ascitis) y piernas hinchadas. Al hacerle un análisis de sangre, encontraron que tenía poco oxígeno en la sangre y un desequilibrio en los ácidos y bases de su cuerpo. La radiografía de su pecho mostró que sus pulmones estaban congestionados.\n\n**Qué Diagnosticaron**  \nEl paciente tenía insuficiencia cardíaca aguda descompensada, lo que significa que su corazón no podía bombear sangre correctamente y esto empeoraba de forma repetida. Además, su corazón tenía una fracción de eyección reducida, que es una medida de qué tan bien el corazón bombea la sangre. Esto ocurrió a pesar de que ya estaba recibiendo el mejor tratamiento médico disponible para su condición relacionada con el síndrome de Marfan.\n\n**Cómo lo Trataron y Qué Resultó**  \nDespués de estabilizar su estado, los médicos añadieron un medicamento llamado sacubitril/valsartán a su tratamiento. Este medicamento ayuda al corazón a funcionar mejor. Gracias a esto, el paciente mejoró poco a poco en su salud general, en los resultados de sus análisis de sangre y en los exámenes del corazón por ecocardiograma. Durante los siguientes nueve meses, el joven no tuvo nuevos episodios graves de insuficiencia cardíaca y pudo mantener una buena calidad de vida.",
+        "score": {
+          "ROUGE-L-Sum": 0.3902439024390244,
+          "BERTScore_F": 0.8059954643249512
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5981196833819877
+        }
+      },
+      "B3": {
+        "text": "**Contexto:**  \nUn hombre joven de 24 años con diagnóstico previo de síndrome de Marfan (una enfermedad genética que afecta el tejido conectivo y puede causar problemas cardiovasculares graves) fue ingresado en el hospital debido a dificultad para respirar, acumulación de líquido en el abdomen (ascitis) y edema en las piernas. Este paciente presentaba antecedentes complejos, incluyendo múltiples cirugías aórticas y valvulares, episodios repetidos de insuficiencia cardíaca aguda con función del corazón gravemente reducida, así como complicaciones neurológicas y respiratorias.\n\n**Hallazgos Clave:**  \nAl ingreso, el análisis de gases en sangre mostró una hipoxemia severa (bajo nivel de oxígeno en la sangre) acompañada de alcalosis respiratoria y metabólica, lo que indica un desequilibrio en el pH sanguíneo debido a problemas respiratorios y metabólicos. La radiografía de tórax reveló congestión en la zona hilar (área central del pulmón), cardiomegalia (aumento del tamaño del corazón) y consolidación pulmonar, además de una acumulación de líquido infectado en el mediastino (espacio entre los pulmones). El ecocardiograma evidenció una fracción de eyección ventricular izquierda (FEVI) reducida al 30%, presencia de prótesis valvulares mecánicas con fugas y regurgitación valvular, reflejando un deterioro significativo de la función cardíaca a pesar del tratamiento previo.\n\n**Interpretación Clínica:**  \nEl paciente sufría de insuficiencia cardíaca aguda descompensada recurrente con fracción de eyección reducida, a pesar de recibir la mejor terapia médica disponible hasta ese momento. Esta condición estaba relacionada con la miocardiopatía (enfermedad del músculo cardíaco) secundaria al síndrome de Marfan, que había provocado daños estructurales severos en el corazón y los vasos sanguíneos. La infección mediastínica y las complicaciones pulmonares añadían un riesgo significativo para su pronóstico.\n\n**Intervenciones y Resultados:**  \nTras estabilizar su condición hemodinámica, se incorporó a su tratamiento sacubitril/valsartán, un medicamento que combina un inhibidor de la neprilisina y un antagonista del receptor de angiotensina, conocido por mejorar la función cardíaca en insuficiencia cardíaca con fracción de eyección reducida. La introducción de este fármaco, junto con la terapia médica óptima previa (incluyendo diuréticos, betabloqueantes, inhibidores de la enzima convertidora de angiotensina, espironolactona y digoxina), permitió una mejora progresiva en sus síntomas clínicos, parámetros de laboratorio (disminución de marcadores como NT-proBNP, que indican estrés cardíaco) y en los estudios ecocardiográficos (aumento de la fracción de eyección y mejoría en las dimensiones y masa ventricular). Durante un seguimiento de nueve meses, el paciente no presentó nuevos episodios de insuficiencia cardíaca aguda y experimentó una mejora significativa en su calidad de vida.\n\n**Próximos Pasos:**  \nDado el éxito observado con sacubitril/valsartán en este caso, se sugiere considerar este tratamiento como una opción terapéutica en pacientes jóvenes con miocardiopatía asociada al síndrome de Marfan y fracción de eyección reducida, aunque se requiere más investigación para establecer pautas específicas de dosificación y manejo en esta población particular. Además, es fundamental continuar con un seguimiento estrecho para monitorear la función cardíaca, controlar las complicaciones infecciosas y ajustar la terapia según la evolución clínica.",
+        "score": {
+          "ROUGE-L-Sum": 0.3006896551724138,
+          "BERTScore_F": 0.8089167475700378
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5548032013712259
+        }
+      }
+    }
+  },
+  {
+    "id": 21,
+    "gold_summary": "Masculino de 41 años de edad que sufre fractura subtrocantérica derecha producto de un accidente de tránsito que requirió manejo de osteosíntesis. Con posterior ruptura del clavo cefalomedular en su tercio proximal, no unión de la fractura e infecciones en sitio de la fractura. Fue tratado con múltiples lavados quirúrgicos, antibioticoterapia y un procedimiento ortopédico y quirúrgico poco convencional como el uso de una placa de soporte condíleo de fémur distal y un injerto óseo endomedular con un segmento de 10 cm de peroné no vascularizado. Paciente con evolución satisfactoria y favorable.",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Un hombre se lastimó mucho la pierna en un accidente. Su hueso del muslo se rompió y tuvo que ir al doctor para arreglarlo. El doctor puso un palo especial para que el hueso se pegara. \n\nPero el palo se rompió y el hueso no sanaba bien. También tuvo una infección que le dolía mucho. Los doctores limpiaron muchas veces la herida y le dieron medicinas para la infección. \n\nDespués, hicieron una operación especial para poner un hueso nuevo y un soporte para ayudar a que su pierna sanara. Ahora, el hombre está mejor y su pierna está sanando bien.",
+        "score": {
+          "ROUGE-L-Sum": 0.14285714285714282,
+          "BERTScore_F": 0.7008233666419983
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.42184025474957054
+        }
+      },
+      "B2": {
+        "text": "**Lo que le pasó al paciente:**  \nUn hombre de 41 años tuvo un accidente de tránsito que le causó una fractura en la parte superior del fémur derecho, llamada fractura subtrocantérica. Para arreglarla, los doctores usaron un clavo especial dentro del hueso (osteosíntesis).  \n\n**Problemas que surgieron:**  \nCon el tiempo, el clavo se rompió y la fractura no sanó bien, lo que se llama \"no unión\". Además, la zona se infectó con bacterias, lo que complicó la recuperación.  \n\n**Tratamientos realizados:**  \nEl paciente necesitó varias cirugías para limpiar la infección y quitar el material roto. También recibió antibióticos fuertes para combatir las bacterias. Para ayudar a que el hueso sanara, los médicos usaron un método especial que incluyó colocar una placa metálica para sostener el hueso y un injerto óseo. Este injerto fue un pedazo de hueso tomado de su propia pierna (del peroné) que se colocó dentro del hueso fracturado para ayudar a que creciera y se uniera.  \n\n**Resultado final:**  \nDespués de todo este tratamiento, el paciente mejoró mucho. La herida sanó bien, la infección desapareció y la fractura se unió correctamente. Ahora puede usar su pierna sin dolor y con buena función.",
+        "score": {
+          "ROUGE-L-Sum": 0.2229299363057325,
+          "BERTScore_F": 0.7524992823600769
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.48771460933290467
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe trata de un hombre de 41 años que sufrió un accidente de tránsito en 2016, el cual le provocó múltiples lesiones, entre ellas fracturas en ambas piernas: una fractura subtrocantérica (zona proximal del fémur) en la cadera derecha y fracturas en los platillos tibiales izquierdos. Inicialmente, se le realizó una cirugía para estabilizar la fractura de cadera mediante un clavo cefalomedular largo, y posteriormente se corrigió la fractura de la tibia. Durante los primeros años, el paciente tuvo episodios esporádicos de dolor en la cadera derecha, pero sin limitación importante en sus actividades diarias.\n\n**Hallazgos Clave**  \nEn 2020, el dolor en la cadera derecha empeoró y se acompañó de dificultad para mover la pierna. Las radiografías mostraron que el clavo utilizado para fijar la fractura se había roto en su parte proximal y que la fractura no había sanado correctamente (no unión). Se intentó retirar el material de osteosíntesis en otro centro sin éxito, por lo que fue referido a un hospital especializado. Allí se realizó la extracción del material, limpieza quirúrgica de la zona afectada y se identificó una infección causada por la bacteria Klebsiella pneumoniae, que fue tratada con antibióticos intravenosos.  \n\nA pesar del tratamiento, la infección reapareció en marzo de 2020, detectándose otra bacteria llamada Enterobacter, lo que requirió múltiples cirugías adicionales para limpiar y desbridar (eliminar tejido infectado) la zona afectada, junto con un tratamiento combinado de antibióticos. Debido a la persistencia de la infección, en mayo se retiró nuevamente el material de fijación y se colocó un clavo recubierto con cemento impregnado con antibióticos para controlar la infección localmente.  \n\nFinalmente, se realizó una cirugía más compleja que incluyó la resección de los bordes de la fractura hasta llegar a hueso sano, la colocación de un injerto óseo endomedular (un segmento de 10 cm de hueso peroné tomado del mismo paciente, sin conexión vascular directa), y la fijación definitiva con una placa metálica especial para soportar la zona distal del fémur. Se utilizó además un sistema de vacío para favorecer la cicatrización de la herida.  \n\n**Interpretación Clínica**  \nEste caso representa una fractura compleja con complicaciones importantes como la no unión ósea y la infección crónica, que dificultaron la consolidación normal del hueso. La ruptura del clavo de fijación y la persistencia de bacterias resistentes requirieron un manejo multidisciplinario que combinó cirugía ortopédica avanzada, técnicas de control de infecciones y uso de injertos óseos autólogos (del propio paciente). El uso de un injerto no vascularizado de peroné y una placa de soporte condíleo fue una estrategia poco convencional pero necesaria para lograr la estabilidad y promover la curación ósea.  \n\n**Próximos Pasos**  \nTras la última cirugía y el tratamiento antibiótico, el paciente mostró una evolución favorable con cicatrización completa de la herida, remisión de la infección y evidencia radiológica de consolidación de la fractura. Actualmente se encuentra asintomático y conserva la función de la extremidad afectada. Se recomienda continuar con seguimiento clínico y radiológico para asegurar la estabilidad a largo plazo y prevenir posibles recaídas infecciosas o problemas mecánicos.",
+        "score": {
+          "ROUGE-L-Sum": 0.1961367013372957,
+          "BERTScore_F": 0.7600909471511841
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.47811382424423987
+        }
+      }
+    }
+  },
+  {
+    "id": 22,
+    "gold_summary": "Una adolescente de 17 años se presentó con su madre en nuestra clínica con un historial de dos meses de dolor en el pecho izquierdo y un historial de una semana de dolor en la parte media de la espalda. Diagnosticamos el síndrome de la columna vertebral basado en los hallazgos radiográficos del pecho y la columna vertebral y los síntomas de dolor en el pecho, palpitaciones y disnea. Tranquilizamos a la paciente de que la enfermedad era benigna y le aconsejamos que iniciara y continuara con la terapia quiropráctica. Todos los síntomas, incluido el dolor de espalda, desaparecieron en tres semanas.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Había una niña de 17 años que tenía dolor en el pecho y en la espalda. Ella fue al doctor para que la ayudara. El doctor miró sus huesos con una foto especial. El doctor dijo que sus huesos estaban un poco rectos y eso le dolía. Le dijo que no era algo peligroso. Le dio un tratamiento para ayudar a que su espalda se sintiera mejor. Después de unas semanas, la niña ya no tenía dolor. Ahora está bien y feliz.",
+        "score": {
+          "ROUGE-L-Sum": 0.2412060301507538,
+          "BERTScore_F": 0.7427793145179749
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.49199267233436433
+        }
+      },
+      "B2": {
+        "text": "**Lo que le pasaba a la paciente**  \nUna chica de 17 años llegó a la clínica porque tenía dolor en el lado izquierdo del pecho durante dos meses y dolor en la parte media de la espalda desde hacía una semana. Además, sentía palpitaciones (cuando el corazón late rápido o irregular) y dificultad para respirar algunas veces.\n\n**Qué encontraron los médicos**  \nDespués de hacerle varios estudios, como radiografías del pecho y la columna, vieron que su columna torácica (la parte media de la espalda) estaba más recta de lo normal. Esto se llama \"síndrome de la espalda recta\". No encontraron problemas en el corazón ni en los pulmones que explicaran el dolor y los otros síntomas.\n\n**Qué hicieron y qué pasó después**  \nLos médicos le dijeron que esta condición no era peligrosa. Le recomendaron hacer terapia quiropráctica, que es un tratamiento donde un especialista ayuda a mejorar la postura y la movilidad de la columna. Después de seguir este tratamiento, todos sus síntomas, incluyendo el dolor y las palpitaciones, desaparecieron en tres semanas.\n\n**Qué significa esto**  \nEl síndrome de la espalda recta puede causar dolor en el pecho y la espalda, pero no es una enfermedad grave. Con el tratamiento adecuado, como la terapia quiropráctica, los síntomas pueden mejorar y desaparecer. Es importante consultar al médico para recibir el diagnóstico correcto y el tratamiento adecuado.",
+        "score": {
+          "ROUGE-L-Sum": 0.3157894736842105,
+          "BERTScore_F": 0.8005552887916565
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5581723812379336
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nUna joven de 17 años acudió a nuestra clínica acompañada por su madre, presentando un cuadro de dos meses con dolor en el lado izquierdo del pecho y una semana con dolor en la parte media de la espalda, específicamente a nivel de la séptima vértebra torácica (T7). Además, experimentaba episodios de palpitaciones (sensación de latidos cardíacos acelerados o irregulares) y dificultad para respirar (disnea) varias veces por semana. Estos síntomas comenzaron a mejorar una semana antes de la consulta, aunque persistía un dolor sordo e intermitente en la zona afectada, que podía durar horas y ocurría tanto en reposo como durante la actividad física.\n\n**Hallazgos Clave**  \nEl examen físico no mostró signos de enfermedad cardíaca ni pulmonar: la presión arterial y el pulso estaban dentro de rangos normales, no se detectaron ruidos anormales en el corazón ni en los pulmones, y no había sensibilidad en músculos o huesos que sugiriera inflamación o lesión. Los estudios electrocardiográficos y de laboratorio, incluyendo pruebas de función tiroidea, fueron normales. Las radiografías del tórax revelaron una alteración en la curvatura normal de la columna torácica superior, conocida como pérdida de la cifosis (curvatura hacia adelante), y se descartaron fracturas o neumotórax (colapso pulmonar).\n\nCon base en estos hallazgos y los criterios diagnósticos establecidos en la literatura médica, se identificó un síndrome conocido como “síndrome de la espalda recta” o “síndrome de la columna vertebral rectificada”, que se caracteriza por la pérdida de la curvatura normal de la columna torácica y puede asociarse a dolor torácico y dorsal.\n\n**Interpretación Clínica**  \nEl síndrome de la espalda recta es una condición benigna, es decir, que no pone en riesgo la vida ni causa daño grave a largo plazo. En este caso, se relacionó con los síntomas de dolor en el pecho y la espalda, así como con las palpitaciones y la disnea, que probablemente estaban vinculados a la alteración postural y mecánica de la columna vertebral.\n\n**Próximos Pasos y Evolución**  \nSe recomendó iniciar y mantener un tratamiento quiropráctico, que consiste en técnicas manuales para mejorar la movilidad y la postura de la columna, con el objetivo de restaurar la curvatura torácica normal. Durante el seguimiento ambulatorio, los síntomas fueron mejorando progresivamente hasta desaparecer completamente en tres semanas. Una ecocardiografía (ultrasonido del corazón) realizada un mes después mostró una regurgitación mitral trivial (un leve retorno de sangre en una válvula cardíaca) sin prolapso (sin desplazamiento anormal), lo cual no requería tratamiento. La paciente fue tranquilizada sobre la naturaleza benigna de su condición y se le aconsejó continuar con la terapia quiropráctica. No presentó recaídas ni necesidad de atención médica adicional en el año siguiente.\n\n**Resumen Final**  \nUna adolescente con dolor torácico y dorsal, acompañado de palpitaciones y dificultad para respirar, fue diagnosticada con síndrome de la espalda recta tras estudios clínicos y radiográficos. Con tratamiento quiropráctico y seguimiento, sus síntomas desaparecieron completamente en pocas semanas, confirmando que se trataba de una condición benigna y manejable.",
+        "score": {
+          "ROUGE-L-Sum": 0.2261904761904762,
+          "BERTScore_F": 0.7868227958679199
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.5065066360291981
+        }
+      }
+    }
+  },
+  {
+    "id": 23,
+    "gold_summary": "Una mujer de 59 años con urolitiasis bilateral recurrente, insuficiencia cardiaca derecha, diabetes tipo 2 mal controlada y enfermedad renal crónica se presentó con dolor en el flanco derecho, fiebre y fatiga. Previamente se le había colocado un stent doble J derecho, pero se perdió su seguimiento. Una tomografía computarizada reveló una hidronefrosis, un stent calcificado y una piedra pélvica de 22 mm, lo que llevó a la realización de una nefrostomía percutánea. La paciente desarrolló un accidente cerebrovascular embólico tres días después y posteriormente presentó hematuria, hipotensión y anemia significativa. La angiografía por TC confirmó una FAV con sangrado activo, que se trató con éxito con embolización.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Una señora tenía dolor y fiebre. Tenía piedras en sus dos riñones. También tenía problemas con su corazón y azúcar alta. Le pusieron un tubito en el riñón, pero no fue al doctor para revisarlo. \n\nEl doctor vio que su riñón estaba muy hinchado y había una piedra grande. Le pusieron un tubito para sacar el líquido. \n\nDespués, la señora tuvo un problema en su cabeza y se cayó. Luego, empezó a tener sangre en la orina y se puso muy débil. \n\nLos doctores encontraron que estaba sangrando dentro del riñón. Hicieron un tratamiento para parar la sangre y la ayudaron mucho.",
+        "score": {
+          "ROUGE-L-Sum": 0.20833333333333331,
+          "BERTScore_F": 0.7287852168083191
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.4685592750708262
+        }
+      },
+      "B2": {
+        "text": "**Lo que le pasó a la paciente**  \nUna mujer de 59 años tenía piedras en ambos riñones que volvían a aparecer, además de problemas graves del corazón, diabetes mal controlada y enfermedad en los riñones. Ella sentía dolor en el lado derecho de su cuerpo, tenía fiebre y estaba cansada. Un año antes, le habían puesto un tubo llamado stent doble J en el riñón derecho para ayudar a que la orina pasara, pero no fue revisado después.  \n\n**Lo que encontraron en sus estudios**  \nUna tomografía (una especie de radiografía especial) mostró que su riñón derecho estaba inflamado por la acumulación de orina (hidronefrosis), que el stent estaba cubierto de calcio y que tenía una piedra grande en la pelvis del riñón. Por esto, le hicieron una nefrostomía, que es un procedimiento para drenar la orina directamente del riñón usando un tubo.  \n\n**Problemas que surgieron después**  \nTres días después, la mujer tuvo una convulsión y se descubrió que había sufrido un accidente cerebrovascular, que es cuando falta sangre en una parte del cerebro. Le dieron medicamentos para evitar más problemas en el cerebro.  \n\nLuego, presentó sangrado en la orina, presión baja y anemia (menos glóbulos rojos), lo que indicaba que estaba perdiendo mucha sangre. Un estudio con contraste mostró que tenía una fístula arteriovenosa (FAV), que es una conexión anormal entre una arteria y una vena en el riñón, causando sangrado.  \n\n**Cómo la trataron**  \nPara detener el sangrado, hicieron una embolización, que consiste en bloquear la fístula usando pequeños dispositivos llamados microespirales. Esto funcionó bien y la paciente se estabilizó.  \n\n**Seguimiento y tratamiento final**  \nDespués, continuaron con un tratamiento para eliminar el stent calcificado y las piedras en dos etapas, usando láser y endoscopios (instrumentos para ver y tratar dentro del cuerpo). Sin embargo, la salud de la paciente empeoró debido a sus otras enfermedades, lo que complicó completar el tratamiento.  \n\n**Qué significa todo esto**  \nEste caso muestra que cuando un stent se deja mucho tiempo sin control, puede causar problemas graves como infecciones, sangrados y daño renal. También destaca la importancia de un seguimiento médico cuidadoso para evitar complicaciones serias.",
+        "score": {
+          "ROUGE-L-Sum": 0.23300970873786406,
+          "BERTScore_F": 0.788503110408783
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.5107564095733235
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nUna mujer de 59 años con antecedentes complejos, incluyendo cálculos renales recurrentes en ambos riñones (urolitiasis bilateral), insuficiencia cardíaca del lado derecho, diabetes tipo 2 mal controlada y enfermedad renal crónica, acudió al hospital por dolor intenso en el costado derecho, fiebre y cansancio. Un año antes, se le había colocado un stent doble J (un tubo delgado que ayuda a drenar la orina desde el riñón hacia la vejiga) en el riñón derecho debido a una piedra renal, pero no se realizó un seguimiento adecuado de este dispositivo.\n\n**Hallazgos Clave**  \nAl realizar una tomografía computarizada (una exploración detallada con rayos X), se detectó que el riñón derecho presentaba hidronefrosis (acumulación de orina debido a una obstrucción), un stent doble J calcificado (con depósitos de calcio que dificultan su función) y una piedra renal grande de aproximadamente 35 × 28 mm. El riñón izquierdo también mostraba signos de daño, con una piedra más pequeña y reducción de tamaño. Debido a la obstrucción severa y el riesgo de infección, se realizó una nefrostomía percutánea bilateral urgente, que consiste en colocar tubos para drenar la orina directamente desde los riñones hacia el exterior, lo que mejoró significativamente su estado y normalizó los marcadores de inflamación y función renal.\n\nSin embargo, tres días después, la paciente sufrió una convulsión generalizada y dificultad para hablar. Un escáner cerebral mostró lesiones isquémicas (áreas con falta de riego sanguíneo) en diferentes partes del cerebro, confirmando un accidente cerebrovascular embólico (causado por un coágulo que bloqueó una arteria cerebral). Se inició tratamiento anticoagulante para prevenir nuevos eventos.\n\nPosteriormente, la paciente desarrolló signos de hemorragia activa: palidez, taquicardia, presión arterial baja y sangre visible en la orina. La hemoglobina, que mide la cantidad de glóbulos rojos, cayó drásticamente, indicando una pérdida significativa de sangre. Una tomografía con contraste evidenció una colección de sangre en el riñón con extravasación de contraste, señal clara de sangrado activo, y coágulos en la pelvis renal y vejiga. Se diagnosticó una fístula arteriovenosa (FAV), una conexión anormal entre una arteria y una vena en el riñón, probablemente causada por la nefrostomía y agravada por la anticoagulación.\n\n**Interpretación Clínica**  \nLa fístula arteriovenosa renal es una complicación rara pero grave que puede provocar hemorragias importantes. En este caso, la combinación de la lesión vascular por la nefrostomía y el tratamiento anticoagulante para el accidente cerebrovascular aumentó el riesgo de sangrado. La angiografía selectiva (una técnica que visualiza los vasos sanguíneos) confirmó la presencia de la FAV y un pequeño pseudoaneurisma (una dilatación anormal de la arteria).\n\n**Próximos Pasos y Tratamiento**  \nSe realizó una embolización superselectiva, un procedimiento mínimamente invasivo en el que se introdujeron microespirales y partículas especiales para bloquear la fístula y detener el sangrado. El procedimiento fue exitoso, restaurando la integridad vascular y estabilizando a la paciente. Posteriormente, se reintrodujo cuidadosamente la anticoagulación para tratar el accidente cerebrovascular, equilibrando el riesgo de hemorragia.\n\nEl manejo definitivo incluyó un enfoque multidisciplinario para tratar las piedras y el stent calcificado. En una primera etapa, se realizó una litotripsia endoscópica con láser para fragmentar el stent incrustado y se colocó un segundo stent para facilitar el drenaje, retirando la nefrostomía. Se planificó una segunda etapa para fragmentar la piedra pélvica y extraer completamente el stent calcificado, pero la salud general de la paciente, afectada por sus múltiples enfermedades crónicas y el accidente cerebrovascular, retrasó este procedimiento.\n\n**Resumen Final**  \nEsta paciente presentó una compleja combinación de problemas renales y vasculares, incluyendo obstrucción urinaria grave, infección, accidente cerebrovascular y una complicación hemorrágica por fístula arteriovenosa renal. El manejo requirió intervenciones urgentes y coordinadas para controlar la infección, detener el sangrado y tratar las piedras y el stent calcificado, destacando la importancia del seguimiento adecuado en pacientes con dispositivos urológicos y múltiples comorbilidades.",
+        "score": {
+          "ROUGE-L-Sum": 0.19471153846153846,
+          "BERTScore_F": 0.8157340884208679
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.5052228134412032
+        }
+      }
+    }
+  },
+  {
+    "id": 24,
+    "gold_summary": "Un hombre de 52 años fue derivado a nuestra institución para la evaluación de una taquicardia ventricular de inicio súbito. Su historia clínica incluía una reconstrucción del tracto de salida del ventrículo derecho a los 5 años de edad. La auscultación reveló un murmullo diastólico regurgitante agudo, un primer sonido cardiaco (S1) ampliamente dividido y un segundo sonido cardiaco (S2) único, lo que indicaba un ventrículo derecho severamente dilatado debido a una regurgitación pulmonar (RP) grave y la presencia de una válvula pulmonar no funcional. Además, el tercer sonido cardiaco (S3) y el cuarto sonido cardiaco (S4) del lado derecho estaban presentes, lo que era coherente con una presión de llenado del ventrículo derecho elevada y la presencia de un ventrículo derecho no conforme. Finalmente, el mencionado «quinteto de sonidos cardiacos» se confirmó mediante una evaluación multimodal como insuficiencia cardiaca del lado derecho con un ventrículo derecho concomitantemente severamente dilatado debido a la regresión completa de la válvula pulmonar y la consiguiente RP libre.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Un hombre tenía problemas con su corazón. Su corazón latía muy rápido y se cansaba mucho. Cuando el doctor escuchó su corazón, oyó sonidos raros. Estos sonidos decían que una parte del corazón estaba muy grande y no funcionaba bien. La válvula del corazón que ayuda a la sangre a salir no estaba trabajando. Esto hizo que el corazón se llenara mucho y se hiciera más grande. Los doctores usaron muchas pruebas para entenderlo mejor. Al final, vieron que el corazón tenía problemas para trabajar bien porque la válvula estaba rota.",
+        "score": {
+          "ROUGE-L-Sum": 0.1917808219178082,
+          "BERTScore_F": 0.7312657833099365
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.46152330261387237
+        }
+      },
+      "B2": {
+        "text": "**Lo que le pasó al paciente**  \nUn hombre de 52 años llegó al hospital porque tenía palpitaciones rápidas y se sentía muy cansado. Cuando era niño, a los 5 años, había tenido una operación en el corazón para corregir un problema llamado Tetralogía de Fallot, que afecta cómo la sangre sale del corazón. En esa operación, le reconstruyeron una parte del ventrículo derecho, que es una de las cámaras del corazón que envía sangre a los pulmones.\n\n**Lo que encontraron al examinarlo**  \nAl escuchar su corazón con un estetoscopio, los médicos notaron varios sonidos anormales. Había un murmullo que indicaba que la sangre estaba regresando por la válvula pulmonar, que no funcionaba bien. Además, escucharon sonidos llamados S1 y S2 que estaban cambiados, y también sonidos llamados S3 y S4 en el lado derecho del corazón. Estos sonidos indican que el ventrículo derecho estaba muy agrandado y tenía problemas para llenarse y bombear la sangre correctamente.\n\n**Qué significa todo esto**  \nEstos signos juntos, que los médicos llamaron el «quinteto de sonidos cardiacos», mostraron que el paciente tenía insuficiencia cardíaca en el lado derecho del corazón. Esto pasó porque la válvula pulmonar que le habían reconstruido cuando era niño ya no funcionaba y la sangre regresaba libremente hacia el ventrículo derecho, causando que este se agrandara mucho y trabajara mal.\n\n**Qué hicieron después**  \nPara confirmar todo, usaron varios estudios, como ecocardiogramas y resonancias magnéticas, que mostraron claramente el daño en la válvula y el agrandamiento del ventrículo derecho. Finalmente, el paciente recibió un reemplazo de la válvula pulmonar, y después de la operación, los sonidos anormales del corazón desaparecieron, lo que indica que su corazón mejoró.",
+        "score": {
+          "ROUGE-L-Sum": 0.27722772277227725,
+          "BERTScore_F": 0.794082760810852
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.5356552417915647
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nUn hombre de 52 años, con antecedentes de cirugía cardíaca infantil para corregir la tetralogía de Fallot (una malformación congénita del corazón), fue ingresado tras presentar palpitaciones repentinas y fatiga. En su niñez, se le realizó una reconstrucción del tracto de salida del ventrículo derecho y cierre de un defecto septal ventricular, pero no tuvo seguimiento médico posterior. En el hospital, se detectó una taquicardia ventricular (ritmo cardíaco acelerado originado en el ventrículo) que se corrigió mediante cardioversión eléctrica.\n\n**Hallazgos Clave**  \nAl examen físico, se identificaron varios sonidos cardíacos anormales: un murmullo diastólico regurgitante agudo (sonido producido por el flujo anormal de sangre hacia atrás durante la diástole), un primer sonido cardíaco (S1) ampliamente dividido, un segundo sonido cardíaco (S2) único, y la presencia de un tercer (S3) y cuarto sonido cardíaco (S4) en el lado derecho del corazón. Estos hallazgos indicaban un ventrículo derecho severamente dilatado y con función alterada.  \n\nLas pruebas complementarias confirmaron estos hallazgos:  \n- El electrocardiograma mostró bloqueo completo del haz de rama derecha y un complejo QRS prolongado, reflejando alteraciones en la conducción eléctrica ventricular.  \n- La radiografía de tórax evidenció cardiomegalia (aumento del tamaño del corazón) y dilatación de las arterias pulmonares.  \n- La ecocardiografía y la resonancia magnética cardíaca demostraron una regresión completa de la válvula pulmonar (una estructura que normalmente evita el reflujo de sangre hacia el ventrículo derecho), lo que causaba una regurgitación pulmonar libre y una dilatación importante del ventrículo derecho con disminución de su capacidad de bombeo (fracción de eyección del 36%).  \n- La evaluación hemodinámica mediante cateterismo cardíaco mostró presiones elevadas en la aurícula derecha y ventrículo derecho, con formas de onda características que correspondían a los sonidos cardíacos S3 y S4 detectados en la auscultación.\n\n**Interpretación Clínica**  \nEl conjunto de sonidos cardíacos anormales —denominado aquí como el «quinteto de sonidos cardíacos»— reflejaba una insuficiencia cardíaca derecha grave causada por la dilatación y disfunción del ventrículo derecho, secundaria a la ausencia funcional de la válvula pulmonar y la regurgitación pulmonar libre resultante. La presencia simultánea de estos cinco sonidos (murmullo diastólico regurgitante, S1 ampliamente dividido, S2 único, S3 y S4 derechos) fue confirmada mediante una evaluación clínica, hemodinámica y anatómica exhaustiva.\n\n**Próximos Pasos y Resultado**  \nEl paciente fue sometido a un reemplazo de la válvula pulmonar, procedimiento que restauró la función valvular y eliminó la regurgitación pulmonar. Posteriormente, el «quinteto de sonidos cardíacos» desapareció por completo, indicando una mejora significativa en la función y la dinámica del ventrículo derecho.\n\n---\n\nEste caso ilustra cómo una alteración valvular congénita corregida en la infancia puede evolucionar décadas después hacia una insuficiencia cardíaca derecha severa, y cómo la evaluación detallada de los sonidos cardíacos, junto con estudios de imagen y hemodinámicos, es fundamental para un diagnóstico preciso y un tratamiento efectivo.",
+        "score": {
+          "ROUGE-L-Sum": 0.31190150478796175,
+          "BERTScore_F": 0.8310191631317139
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5714603339598379
+        }
+      }
+    }
+  },
+  {
+    "id": 25,
+    "gold_summary": "Un hombre de 62 años con antecedentes de insuficiencia cardiaca inducida por cardiomiopatía no isquémica, post-puente de asistencia ventricular izquierda y trasplante cardiaco ortotópico, presentó distensión abdominal, dolor y leucocitosis seis días después del trasplante. La TAC de abdomen y pelvis reveló bucles intestinales dilatados, niveles de aire-líquido y un punto de transición en el intestino delgado proximal. Se diagnosticó al paciente una obstrucción intestinal y se le realizó una laparotomía exploratoria. Se encontró que tenía un conducto de LVAD intraabdominal retenido que estrangulaba un bucle de intestino delgado en el cuadrante superior izquierdo. Se retiró el conducto y se liberó la sección de intestino con el retorno de la perfusión.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Un hombre de 62 años se sentía mal en su barriga después de una operación en su corazón. Su barriga estaba hinchada y le dolía. Los doctores le hicieron una foto especial para ver dentro de su barriga. Vieron que su intestino estaba muy grande y apretado en un lugar. Los doctores hicieron una operación para mirar dentro. Encontraron un tubito que estaba apretando su intestino. Quitaron el tubito y el intestino volvió a estar bien. Ahora el hombre puede sentirse mejor.",
+        "score": {
+          "ROUGE-L-Sum": 0.2222222222222222,
+          "BERTScore_F": 0.7284793853759766
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.4753508037990994
+        }
+      },
+      "B2": {
+        "text": "**Lo que pasó con el paciente**  \nUn hombre de 62 años, que tenía problemas graves del corazón y había recibido un trasplante de corazón, comenzó a tener dolor y hinchazón en el abdomen seis días después de la operación. También tenía más glóbulos blancos en la sangre, lo que puede indicar infección o inflamación.\n\n**Qué encontraron los médicos**  \nLe hicieron una tomografía, que es un tipo de radiografía especial, y vieron que partes de su intestino estaban muy hinchadas y había señales de que algo bloqueaba el paso en el intestino delgado, que es la parte del intestino donde se absorben los nutrientes.\n\n**Qué hicieron para ayudarlo**  \nLos médicos lo operaron para ver qué causaba la obstrucción. Durante la cirugía, descubrieron que un tubo que se usaba para ayudar a su corazón (llamado LVAD) se había movido dentro del abdomen y estaba apretando un pedazo del intestino, bloqueando el paso.\n\n**Resultado de la cirugía**  \nQuitaron ese tubo que estaba causando el problema y liberaron el intestino. Después de unos minutos, el intestino volvió a funcionar bien y no había daño grave. Finalmente, cerraron la herida y el paciente pudo continuar con su recuperación.\n\n**Por qué es importante**  \nEste caso muestra que los dispositivos para ayudar al corazón pueden, en raras ocasiones, causar problemas en otras partes del cuerpo, como el intestino. Por eso, los médicos deben estar atentos a síntomas como dolor abdominal después de cirugías complejas.",
+        "score": {
+          "ROUGE-L-Sum": 0.24561403508771928,
+          "BERTScore_F": 0.746917724609375
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.49626587984854714
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nUn hombre de 62 años con antecedentes de insuficiencia cardíaca causada por una enfermedad del músculo cardíaco no relacionada con problemas de circulación (cardiomiopatía no isquémica), que había sido tratado previamente con un dispositivo de asistencia ventricular izquierdo (LVAD, un aparato que ayuda al corazón a bombear sangre), recibió un trasplante de corazón ortotópico (reemplazo del corazón en su posición normal). Durante su recuperación en la unidad de cuidados intensivos, seis días después de la cirugía, presentó un aumento progresivo de la distensión abdominal (hinchazón), dolor abdominal y un aumento en el número de glóbulos blancos (leucocitosis), indicativo de inflamación o infección.\n\n**Hallazgos Clave**  \nUna tomografía computarizada (TAC) del abdomen y la pelvis mostró múltiples segmentos del intestino delgado dilatados con niveles de aire y líquido, además de un punto de transición en el intestino delgado proximal en el cuadrante superior izquierdo del abdomen. Estos hallazgos sugirieron la presencia de una obstrucción intestinal. Dado que el paciente no tenía antecedentes de cirugías abdominales previas, lo que reduce la probabilidad de adherencias (bandas de tejido cicatricial que pueden causar obstrucción), se decidió realizar una laparotomía exploratoria (cirugía para abrir el abdomen y examinar los órganos).\n\nDurante la cirugía, se observó que el intestino estaba dilatado pero sin signos de daño irreversible (isquemia). Se identificó que una porción del intestino delgado estaba adherida a la pared abdominal anterior. Al investigar más a fondo, se descubrió que una línea motriz del LVAD, que había migrado y estaba dentro de la cavidad abdominal, estaba causando una estrangulación (compresión que impide el flujo sanguíneo) de un segmento del intestino delgado en el cuadrante superior izquierdo. Esta línea motriz fue liberada y retirada, y el segmento intestinal afectado recuperó su circulación sanguínea tras unos minutos.\n\nSe inspeccionó todo el intestino delgado desde el ligamento de Treitz (punto donde el duodeno se une al yeyuno) hasta el intestino ciego, encontrándose dilatado pero sin daño significativo. Se reparó una pequeña lesión en la capa externa del intestino (desgarro seroso) en el sitio donde estaba adherido a la línea motriz. Finalmente, el intestino fue reposicionado en la cavidad abdominal y se cerró la incisión quirúrgica.\n\n**Interpretación Clínica**  \nEste caso ilustra una complicación poco común pero grave en pacientes con dispositivos de asistencia ventricular izquierda: la migración intraabdominal de una línea motriz que puede causar obstrucción intestinal por estrangulación. La presentación clínica con distensión abdominal, dolor y leucocitosis, junto con los hallazgos radiológicos, orientaron hacia una obstrucción intestinal que requirió intervención quirúrgica urgente para evitar daño intestinal irreversible.\n\n**Próximos Pasos**  \nSe recomienda un seguimiento cuidadoso para detectar posibles complicaciones posteriores, como infecciones o recurrencia de obstrucción. Además, es importante evaluar la correcta colocación y manejo de los dispositivos de asistencia ventricular para prevenir migraciones similares. Este caso destaca la necesidad de un abordaje multidisciplinario en pacientes complejos post-trasplante cardíaco con dispositivos implantados.",
+        "score": {
+          "ROUGE-L-Sum": 0.27259259259259255,
+          "BERTScore_F": 0.8248342275619507
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5487134100772716
+        }
+      }
+    }
+  },
+  {
+    "id": 26,
+    "gold_summary": "Reportamos un caso único de un niño de 13 años que presentó una masa palpable agrandada en la región inguinal izquierda sin ningún síntoma constitucional. La extirpación quirúrgica de esta masa fue esencial para descartar causas preocupantes. El examen patológico reveló cambios proliferativos consistentes con el tipo de célula plasmática de la enfermedad de Castleman, que es una de las formas más raras de la enfermedad en niños. Hasta donde sabemos, este caso es el primer caso reportado de enfermedad de Castleman unicéntrica (UCD) en el área inguinal. Durante un período de seguimiento de 12 meses, no se reportaron agrandamientos adicionales de los ganglios linfáticos u otros síntomas.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Había un niño de 13 años con una bolita en la ingle. La bolita no le dolía ni le hacía sentir mal. Los doctores sacaron la bolita con una operación para ver qué era. \n\nDespués, miraron la bolita con un microscopio y vieron que era una cosa rara que a veces pasa en niños. Es muy poco común. \n\nEl niño estuvo bien y no tuvo más bolitas ni se enfermó en un año. Los doctores lo cuidaron mucho y él está contento.",
+        "score": {
+          "ROUGE-L-Sum": 0.24770642201834864,
+          "BERTScore_F": 0.7268944978713989
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.4873004599448738
+        }
+      },
+      "B2": {
+        "text": "Caso de un niño con una masa en la ingle\n\nUn niño de 13 años notó una masa o bulto en la parte izquierda de su ingle (la zona donde la pierna se une al cuerpo). No tenía otros síntomas como fiebre o pérdida de peso. Para entender qué era esa masa, los médicos decidieron quitarla con cirugía.\n\nQué encontraron en la biopsia\n\nDespués de la cirugía, examinaron la masa bajo el microscopio. Vieron que había un crecimiento anormal de ciertas células llamadas células plasmáticas, que forman parte del sistema inmunológico. Este hallazgo mostró que el niño tenía una enfermedad llamada enfermedad de Castleman, que es muy rara en niños y afecta los ganglios linfáticos.\n\nImportancia del caso y seguimiento\n\nEste es el primer caso conocido de esta enfermedad en un ganglio linfático de la ingle en un niño. Después de la cirugía, el niño recibió un medicamento llamado prednisolona para ayudar a controlar la enfermedad. Durante un año, los médicos lo revisaron regularmente con exámenes físicos y pruebas de imagen para asegurarse de que no aparecieran nuevos ganglios agrandados ni otros problemas. El niño se mantuvo sin síntomas y sin nuevos bultos durante todo ese tiempo.\n\nEn resumen, este caso muestra la importancia de investigar y tratar las masas en los ganglios linfáticos para encontrar enfermedades raras y cuidar bien la salud.",
+        "score": {
+          "ROUGE-L-Sum": 0.2698412698412698,
+          "BERTScore_F": 0.8054195642471313
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.5376304170442006
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nPresentamos el caso de un niño de 13 años que acudió al hospital debido a la presencia de una masa palpable en la región inguinal izquierda, sin presentar síntomas generales como fiebre, pérdida de peso o fatiga. Su historial médico previo incluía una cirugía en la columna vertebral tras un accidente, que le ocasionó parálisis y pérdida de sensibilidad en las piernas, lo que llevó a complicaciones como úlceras por presión en el pie izquierdo. No se identificaron otros signos clínicos relevantes ni indicios de infecciones o enfermedades sistémicas.\n\n**Hallazgos Clave**  \nLos análisis de laboratorio mostraron una velocidad de sedimentación globular (VSG) elevada, un marcador de inflamación, mientras que otros parámetros sanguíneos y pruebas de función orgánica se mantuvieron dentro de rangos normales. La tomografía computarizada (TAC) evidenció ganglios linfáticos aumentados de tamaño debajo del ligamento inguinal, siendo el mayor de aproximadamente 3,5 x 2,4 cm, sin afectación de otros órganos o ganglios. Para descartar enfermedades graves como linfoma o leucemia, se decidió realizar una cirugía para extirpar los ganglios afectados y analizarlos bajo el microscopio.\n\nEl examen histopatológico (microscópico) de los ganglios mostró una proliferación aumentada de células plasmáticas (un tipo de célula del sistema inmunitario) y células llamadas histiocitos, junto con un aumento en la formación de vasos sanguíneos, características compatibles con la forma de células plasmáticas de la enfermedad de Castleman. Esta enfermedad es una condición poco común que causa crecimiento anormal de ganglios linfáticos y puede presentarse en una única área (unicéntrica) o en múltiples regiones del cuerpo.\n\n**Interpretación Clínica**  \nEste caso representa una presentación rara de la enfermedad de Castleman unicéntrica en la región inguinal, un sitio poco frecuente para esta patología, especialmente en niños. La ausencia de síntomas sistémicos y la localización única de los ganglios afectados apoyan el diagnóstico de esta forma localizada de la enfermedad. La extirpación quirúrgica completa fue fundamental tanto para confirmar el diagnóstico como para tratar la condición.\n\n**Próximos Pasos y Seguimiento**  \nTras la cirugía, el paciente recibió tratamiento con prednisolona oral (un corticosteroide) y fue dado de alta después de 14 días sin complicaciones. Se estableció un seguimiento riguroso que incluyó evaluaciones clínicas, análisis de laboratorio y tomografías computarizadas cada tres meses para detectar cualquier recurrencia o aparición de nuevos ganglios agrandados. Durante un año de seguimiento, el paciente no presentó nuevos síntomas ni evidencia de enfermedad activa, lo que indica un buen pronóstico tras el tratamiento quirúrgico.\n\nEn resumen, este caso destaca la importancia de considerar la enfermedad de Castleman en el diagnóstico diferencial de masas ganglionares inguinales en niños, y demuestra que la resección quirúrgica puede ser curativa en la forma unicéntrica de esta enfermedad.",
+        "score": {
+          "ROUGE-L-Sum": 0.20625,
+          "BERTScore_F": 0.7986257672309875
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.5024378836154938
+        }
+      }
+    }
+  },
+  {
+    "id": 27,
+    "gold_summary": "Presentamos el caso de un hombre asiático de 55 años que había tenido un caso conocido de miocardiopatía dilatada durante 6 meses, que se presentó con las principales quejas de falta de aire al hacer ejercicio y disminución de la producción de orina. En el examen físico general, se observaron características que sugerían una ICC. El signo de Chvostek y Trousseau fue positivo. El paciente tenía antecedentes de cirugía de cataratas en ambos ojos 15 años atrás. Otras investigaciones revelaron una hipocalcemia. La ecografía mostró una grave hipocinesia global del ventrículo izquierdo con una fracción de eyección del ventrículo izquierdo del 15%. Esta ICC fue refractaria al tratamiento convencional, aunque, con la suplementación de calcio, el paciente mejoró sintomáticamente. En el seguimiento después de 3 meses, se observó una mejora en los parámetros ecocardiográficos con una fracción de eyección que mejoró al 25%.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Había un hombre que se sentía muy cansado y le costaba respirar cuando caminaba. También hacía menos pipí. El doctor vio que su corazón estaba muy débil. El hombre tenía señales en sus manos que mostraban que le faltaba calcio. Le dieron calcio para ayudarlo. Después de un tiempo, el corazón del hombre se puso un poco mejor y él se sintió mejor también.",
+        "score": {
+          "ROUGE-L-Sum": 0.1646090534979424,
+          "BERTScore_F": 0.7259277701377869
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.44526841181786464
+        }
+      },
+      "B2": {
+        "text": "**Caso de un Hombre con Problemas del Corazón y Bajos Niveles de Calcio**\n\nUn hombre de 55 años, que ya tenía un diagnóstico de miocardiopatía dilatada (una enfermedad del corazón donde el músculo del ventrículo izquierdo se debilita y agranda), llegó al hospital porque tenía dificultad para respirar al hacer ejercicio y producía menos orina de lo normal.\n\n**Lo que Encontraron en el Examen**\n\nAl revisarlo, los médicos notaron signos de insuficiencia cardíaca congestiva (cuando el corazón no bombea bien y se acumula líquido). También detectaron dos signos especiales llamados Chvostek y Trousseau, que indican que el cuerpo tiene poco calcio en la sangre. Además, el paciente había tenido cirugía de cataratas en ambos ojos hace 15 años.\n\n**Resultados de las Pruebas**\n\nLas pruebas mostraron que tenía hipocalcemia, es decir, niveles bajos de calcio en la sangre. El ultrasonido del corazón (ecocardiografía) reveló que su ventrículo izquierdo estaba muy debilitado, con una fracción de eyección del 15%, lo que significa que el corazón bombeaba muy poco sangre.\n\n**Tratamiento y Mejoría**\n\nEl paciente no mejoró con el tratamiento habitual para la insuficiencia cardíaca. Sin embargo, cuando le dieron calcio por vía intravenosa, su condición mejoró notablemente. Después de tres meses, su corazón funcionaba mejor, con una fracción de eyección aumentada al 25%.\n\n**Qué Significa Esto**\n\nEste caso muestra que la falta de calcio en la sangre, causada por un problema llamado hipoparatiroidismo (cuando una glándula llamada paratiroides no produce suficiente hormona para controlar el calcio), puede empeorar la función del corazón. Al corregir el calcio, se puede mejorar la salud del corazón en pacientes con miocardiopatía dilatada.",
+        "score": {
+          "ROUGE-L-Sum": 0.3847780126849895,
+          "BERTScore_F": 0.8075551390647888
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5961665758748892
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe presenta el caso de un hombre asiático de 55 años con diagnóstico previo de miocardiopatía dilatada (una enfermedad del músculo cardíaco que provoca su debilitamiento y agrandamiento) durante los últimos 6 meses. El paciente acudió al hospital debido a dificultad para respirar al realizar ejercicio (disnea) y una reducción en la cantidad de orina durante los últimos dos días. Su dificultad respiratoria había empeorado progresivamente, llegando a un grado severo según la clasificación de la Asociación del Corazón de Nueva York (NYHA). Además, presentaba hinchazón en ambas piernas y tos con expectoración espumosa, síntomas compatibles con insuficiencia cardíaca congestiva (ICC).\n\n**Hallazgos Clave**  \nEn el examen físico, el paciente mostraba signos típicos de insuficiencia cardíaca, como edema en las extremidades inferiores y aumento de la presión venosa yugular. Además, durante la toma de la presión arterial, se evidenciaron espasmos musculares en la muñeca, lo que llevó a descubrir signos positivos de Chvostek y Trousseau, indicativos de hipocalcemia (niveles bajos de calcio en sangre). El paciente también tenía antecedentes de cirugía de cataratas bilateral realizada 15 años antes.\n\nLos análisis de laboratorio confirmaron hipocalcemia severa junto con niveles elevados de fosfato y una hormona paratiroidea (PTH) muy baja, lo que sugiere hipoparatiroidismo (una condición en la que las glándulas paratiroides no producen suficiente hormona para regular el calcio). La ecocardiografía mostró un ventrículo izquierdo dilatado con una fracción de eyección muy baja (15%), reflejando una función cardíaca gravemente comprometida. Otras pruebas descartaron enfermedad coronaria y evidenciaron calcificaciones cerebrales simétricas.\n\n**Interpretación Clínica**  \nEl cuadro clínico y los resultados sugieren que la insuficiencia cardíaca del paciente no solo se debía a la miocardiopatía dilatada conocida, sino que estaba agravada por una cardiomiopatía secundaria a hipocalcemia causada por hipoparatiroidismo. La hipocalcemia puede afectar la contracción del músculo cardíaco, empeorando la función ventricular. Esto explica la falta de respuesta a los tratamientos convencionales para insuficiencia cardíaca.\n\n**Tratamiento y Evolución**  \nSe inició tratamiento estándar para insuficiencia cardíaca, incluyendo dobutamina y diuréticos, sin mejoría significativa. Al identificar la hipocalcemia e hipoparatiroidismo, se administró gluconato de calcio por vía intravenosa, seguido de calcio oral y calcitriol (una forma activa de vitamina D) para corregir el déficit de calcio. Tras esta intervención, el paciente mostró una mejoría clínica notable. También se trató la anemia megaloblástica con vitamina B12.\n\nEn el seguimiento a los tres meses, el paciente presentó mejoría en los niveles de calcio y en la función cardíaca, con una fracción de eyección que aumentó al 25%, lo que indica una recuperación parcial de la capacidad de bombeo del corazón. Sin embargo, el paciente rechazó realizar una biopsia endomiocárdica que podría haber ayudado a confirmar el diagnóstico definitivo.\n\n**Próximos Pasos**  \nSe recomienda continuar con el tratamiento de calcio y calcitriol para mantener niveles adecuados de calcio en sangre y prevenir complicaciones. Además, es fundamental el seguimiento cardiológico para monitorizar la función ventricular y ajustar la terapia para la insuficiencia cardíaca. La educación del paciente sobre la importancia de la adherencia al tratamiento es clave para evitar recaídas. En caso de que el paciente acepte, una biopsia cardíaca podría aportar información adicional para el manejo a largo plazo.",
+        "score": {
+          "ROUGE-L-Sum": 0.23605706874189367,
+          "BERTScore_F": 0.7951358556747437
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.5155964622083187
+        }
+      }
+    }
+  },
+  {
+    "id": 28,
+    "gold_summary": "A continuación, se describe un caso inusual de una paciente con HD de 54 años de edad que presentó HPE pocos días después de una colonoscopia. La causa de la HPE fue la ruptura de un quiste de DRCA. Consideramos que la colonoscopia fue un factor desencadenante y planteamos hipótesis sobre su etiopatogenia. La paciente se sometió a una nefrectomía izquierda exitosa.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Una señora de 54 años tenía un problema en sus riñones. Ella se hacía un tratamiento para limpiar su sangre. Unos días después de un examen en su barriga, empezó a sentir mucho dolor en un lado. Un quiste en su riñón se rompió y eso le dolió mucho. Los doctores le hicieron una operación para quitar ese riñón. Ahora ella está mejor y sigue con su tratamiento para limpiar su sangre.",
+        "score": {
+          "ROUGE-L-Sum": 0.2,
+          "BERTScore_F": 0.7318460941314697
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.46592304706573484
+        }
+      },
+      "B2": {
+        "text": "**Caso de una mujer con sangrado en el riñón después de una colonoscopia**\n\nUna mujer de 54 años que estaba en hemodiálisis, un tratamiento para personas con problemas graves en los riñones, tuvo un problema raro. Pocos días después de hacerse una colonoscopia (un examen para revisar el colon), comenzó a sentir un dolor fuerte en la parte baja de la espalda, del lado izquierdo, junto con náuseas y vómitos.\n\nLos médicos descubrieron que tenía un sangrado grande alrededor de su riñón izquierdo. Este sangrado ocurrió porque se rompió un quiste, que es una bolsa llena de líquido que se forma en el riñón. La ruptura del quiste causó un hematoma, que es una acumulación de sangre fuera de los vasos sanguíneos.\n\nCreen que la colonoscopia pudo haber sido la causa que desencadenó este problema, aunque no es común que esto pase. Para tratar la situación, los médicos le hicieron una cirugía para quitarle el riñón izquierdo, llamada nefrectomía. La operación fue exitosa y la paciente se recuperó bien, sin más sangrados.\n\nEste caso es importante porque muestra una complicación poco común después de una colonoscopia en una persona con enfermedad renal avanzada y hemodiálisis. Los médicos aprendieron que hay que estar atentos a síntomas como dolor intenso y sangrado después de estos procedimientos en pacientes con problemas renales.",
+        "score": {
+          "ROUGE-L-Sum": 0.22641509433962262,
+          "BERTScore_F": 0.7833319306373596
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.5048735124884911
+        }
+      },
+      "B3": {
+        "text": "**Contexto:**  \nSe presenta el caso poco común de una mujer de 54 años que se encuentra en hemodiálisis (HD) debido a una enfermedad renal crónica avanzada llamada glomeruloesclerosis segmentaria focal. Esta paciente desarrolló un hematoma perirrenal espontáneo (HPE), que es una acumulación de sangre alrededor del riñón, pocos días después de haberse sometido a una colonoscopia, un procedimiento para examinar el colon.\n\n**Hallazgos Clave:**  \nEl hematoma perirrenal se originó por la ruptura de un quiste renal asociado a una enfermedad renal crónica avanzada (DRCA). La tomografía computarizada mostró un gran hematoma intraparenquimatoso (dentro del tejido renal) y perirrenal (alrededor del riñón) en el riñón izquierdo, con signos de sangrado activo y compresión del sistema urinario. La paciente presentó dolor lumbar intenso, anemia progresiva y requerimientos de transfusión sanguínea. Durante la intervención quirúrgica, se confirmó que el parénquima renal estaba casi completamente reemplazado por el hematoma. Además, se identificó una pequeña lesión benigna llamada adenoma papilar.\n\n**Interpretación Clínica:**  \nSe considera que la colonoscopia, realizada días antes, pudo haber sido un factor desencadenante que contribuyó a la ruptura del quiste renal y la formación del hematoma. Aunque la relación causal no es completamente clara, la manipulación abdominal y los cambios en la presión intraabdominal durante la colonoscopia podrían haber favorecido este evento hemorrágico en un riñón ya debilitado por la enfermedad crónica y la presencia de quistes. La situación requirió una nefrectomía radical (extirpación completa del riñón afectado) para controlar el sangrado y evitar complicaciones mayores.\n\n**Próximos Pasos y Seguimiento:**  \nTras la cirugía, la paciente continuó con su tratamiento de hemodiálisis sin complicaciones adicionales y se mantuvo estable, sin signos de sangrado recurrente. Este caso resalta la importancia de considerar posibles complicaciones renales en pacientes con enfermedad renal crónica avanzada que se someten a procedimientos invasivos, y la necesidad de un manejo multidisciplinario para asegurar una recuperación adecuada.",
+        "score": {
+          "ROUGE-L-Sum": 0.19230769230769232,
+          "BERTScore_F": 0.748791515827179
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.4705496040674356
+        }
+      }
+    }
+  },
+  {
+    "id": 29,
+    "gold_summary": "El caso 2 fue el de una mujer de 30 años con antecedentes de dos meses de dolor progresivo y disminución de la visión en el ojo derecho. Se le diagnosticó uveítis anterior hipertensiva tras una paracentesis diagnóstica de la cámara anterior. A pesar de la terapia exitosa para la uveítis anterior, su presión intraocular se mantuvo elevada y requirió un procedimiento de filtración de glaucoma. Se recolectó una muestra de fluido ocular en el momento de la cirugía para el análisis de perfiles de citoquinas/quimioquinas, y se detectaron niveles de 7 citoquinas/quimioquinas, entre ellas, IL-6, IL-8, IL-18, MIP-1B, IP-10, MCP-1 e IL-1RA, siendo IL-1RA la citoquina más abundante.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Había una mujer que tenía dolor y no veía bien con un ojo. Los doctores encontraron que su ojo estaba inflamado y tenía mucha presión. Ella necesitó una operación para ayudar a que la presión bajara. Durante la operación, los doctores tomaron un poquito de líquido del ojo para ver qué había dentro. Encontraron unas cosas llamadas citoquinas, que son como mensajeros que dicen al cuerpo qué hacer. Una de estas citoquinas estaba más que las otras. Esto ayuda a los doctores a entender mejor qué pasa en el ojo.",
+        "score": {
+          "ROUGE-L-Sum": 0.16379310344827586,
+          "BERTScore_F": 0.7242751121520996
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.4440341078001877
+        }
+      },
+      "B2": {
+        "text": "**Caso de una Mujer con Problemas en el Ojo Derecho**\n\nUna mujer de 30 años tuvo dolor y pérdida de visión en su ojo derecho durante dos meses. Los médicos le diagnosticaron una inflamación llamada uveítis anterior hipertensiva, que significa que había inflamación en la parte frontal del ojo y la presión dentro del ojo estaba alta. Para confirmar esto, tomaron una pequeña muestra del líquido dentro del ojo, llamado fluido ocular.\n\nAunque recibió tratamiento para la inflamación, la presión en su ojo siguió siendo alta. Por eso, necesitó una cirugía llamada filtración de glaucoma, que ayuda a bajar la presión del ojo para evitar daños.\n\nDurante la cirugía, los médicos tomaron otra muestra del fluido ocular para estudiar unas sustancias llamadas citoquinas y quimioquinas. Estas sustancias son como señales que usan las células para comunicarse y controlar la inflamación. Encontraron siete de estas sustancias, entre ellas IL-6, IL-8, IL-18, MIP-1B, IP-10, MCP-1 y IL-1RA. La más abundante fue IL-1RA, que ayuda a reducir la inflamación en el cuerpo.\n\nEste análisis ayuda a entender mejor qué está pasando en el ojo durante la enfermedad y podría ayudar a mejorar los tratamientos en el futuro.",
+        "score": {
+          "ROUGE-L-Sum": 0.37883008356545955,
+          "BERTScore_F": 0.8024716377258301
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5906508606456449
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe evaluó a una mujer de 30 años que presentaba un cuadro de dos meses con dolor progresivo y disminución de la visión en su ojo derecho. Dos semanas antes del inicio de estos síntomas oculares, había comenzado a reducir la dosis de prednisona, un corticosteroide que utilizaba para tratar síntomas inflamatorios sistémicos relacionados con artritis inflamatoria y posibles enfermedades intestinales inflamatorias. Además, había experimentado una pérdida de peso significativa antes de la consulta.\n\n**Hallazgos Clave**  \nEn el examen ocular inicial, la agudeza visual era de 20/40 en el ojo derecho y 20/20 en el izquierdo. Se observaron pupilas anormalmente dilatadas y sin respuesta en el ojo derecho, con una presión intraocular (PIO) muy elevada de 65 mmHg (normalmente debe estar entre 10 y 21 mmHg), mientras que el ojo izquierdo estaba dentro de los parámetros normales. El examen con lámpara de hendidura reveló signos de inflamación en la parte frontal del ojo derecho, incluyendo células inflamatorias en la cámara anterior y depósitos granulomatosos pigmentados en la córnea. También se detectó atrofia del iris y otras alteraciones estructurales. La gonioscopia, que examina el ángulo donde drena el humor acuoso, mostró células pigmentadas inflamatorias. El fondo de ojo estaba normal en ambos ojos.\n\nUna prueba diagnóstica mediante paracentesis (extracción de fluido del ojo) confirmó la presencia de ADN del virus varicela-zóster (VVZ), responsable de la culebrilla, y los análisis serológicos indicaron anticuerpos contra este virus, confirmando la infección ocular. Se diagnosticó uveítis anterior hipertensiva asociada a VVZ, una inflamación del segmento anterior del ojo que causa aumento de la presión ocular. El tratamiento incluyó medicamentos para reducir la presión intraocular (acetazolamida, timolol, dorzolamida, brimonidina), un antiviral oral (valaciclovir) y corticosteroides tópicos (prednisolona).\n\nPosteriormente, la paciente sufrió un accidente cerebrovascular atribuido a una vasculopatía (enfermedad de los vasos sanguíneos) del sistema nervioso central relacionada con el VVZ, lo que requirió hospitalización. Durante su recuperación, los síntomas oculares mejoraron, pero dos meses después presentó un nuevo empeoramiento con aumento del dolor, disminución de la visión a 20/100 y presión intraocular elevada (39 mmHg). Se intensificó el tratamiento antiinflamatorio con difluprednato, pero la respuesta fue mínima, por lo que se realizó una cirugía de filtración para controlar la presión ocular, colocando una derivación de Ahmed.\n\n**Análisis de Citoquinas y Quimioquinas**  \nDurante la cirugía, se obtuvo una muestra del humor acuoso (fluido dentro del ojo) para analizar el perfil de citoquinas y quimioquinas, que son proteínas que regulan la inflamación y la respuesta inmune. Se evaluaron 22 de estas moléculas mediante una técnica avanzada llamada inmunoensayo de perlas múltiplex. Se detectaron niveles significativos de siete citoquinas/quimioquinas: interleucina-6 (IL-6), interleucina-8 (IL-8), interleucina-18 (IL-18), proteína quimioatrayente de macrófagos 1 beta (MIP-1b), proteína inducible por interferón gamma 10 (IP-10), proteína quimioatrayente de monocitos 1 (MCP-1) y antagonista del receptor de interleucina 1 (IL-1RA).\n\nDe estas, la IL-1RA fue la más abundante, con una concentración alrededor de 1000 pg/mL. Esta molécula actúa como un regulador que bloquea la acción de la interleucina 1, una citoquina proinflamatoria, y su presencia elevada sugiere un intento del organismo por controlar la inflamación ocular. IP-10 y MCP-1 fueron las segundas más abundantes, con niveles entre 150 y 200 pg/mL, y están involucradas en la atracción de células inmunitarias al sitio inflamado. Las otras citoquinas, incluyendo IL-6 e IL-8, estuvieron presentes en concentraciones más bajas (<10 pg/mL).\n\n**Interpretación Clínica**  \nEste caso ilustra una uveítis anterior hipertensiva causada por infección activa por VVZ, que además se complicó con un accidente cerebrovascular relacionado con la misma infección viral. La persistencia de la presión intraocular elevada a pesar del tratamiento médico requirió intervención quirúrgica. El análisis detallado del perfil inflamatorio en el humor acuoso reveló una respuesta inmunitaria compleja, con predominio de moléculas reguladoras como IL-1RA, lo que podría reflejar mecanismos de control de la inflamación en el ojo afectados por el virus.\n\n**Próximos Pasos**  \nEl manejo de esta paciente requiere un seguimiento estrecho para controlar la inflamación ocular y la presión intraocular, prevenir daños permanentes en la visión y vigilar posibles complicaciones neurológicas asociadas al VVZ. El análisis de citoquinas puede ofrecer información valiosa para ajustar terapias inmunomoduladoras y antivirales en casos similares.",
+        "score": {
+          "ROUGE-L-Sum": 0.21864951768488747,
+          "BERTScore_F": 0.7534587979316711
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.4860541578082793
+        }
+      }
+    }
+  },
+  {
+    "id": 30,
+    "gold_summary": "Presentamos un caso de NCS diagnosticado y tratado en base a los hallazgos del examen físico. La ecografía fetal mostró distensión de la vejiga, hidroceles bilaterales, dilatación de la uretra y ascitis abdominal que preocupaban por la obstrucción del tracto urinario inferior y posible ruptura de la vejiga. Una hora después del nacimiento, el examen de la extremidad superior izquierda del lactante no mostró movimiento espontáneo, la mano y el antebrazo parecían oscuros y la mano tenía una gran ampolla con descamación. No se detectó pulso distal a la fosa antecubital mediante ecografía Doppler. Se diagnosticó al lactante con NCS y se le practicó una fasciotomía urgente. La apariencia clínica y la perfusión de la extremidad superior izquierda mejoraron gradualmente. A los cuatro meses de edad, las heridas se habían curado y el paciente tenía un rango de movimiento pasivo completo de la extremidad superior izquierda. La recuperación del movimiento activo está en curso.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Un bebé nació y tenía problemas en su brazo izquierdo. El brazo estaba muy oscuro y no se movía solo. Tenía una burbuja grande en la mano. Los doctores no sentían el pulso en el brazo. Ellos hicieron una operación para ayudar al brazo. Poco a poco, el brazo se puso mejor. A los cuatro meses, las heridas estaban sanas. El bebé puede mover el brazo con ayuda. Los doctores siguen cuidando para que mejore más.",
+        "score": {
+          "ROUGE-L-Sum": 0.15810276679841898,
+          "BERTScore_F": 0.7469421625137329
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.45252246465607593
+        }
+      },
+      "B2": {
+        "text": "**Lo que Encontraron al Nacer**  \nUn bebé nació con problemas en su brazo izquierdo. Su mano y antebrazo estaban oscuros y tenían una ampolla grande con piel que se estaba cayendo. Además, no movía esa parte del cuerpo y los médicos no pudieron sentir el pulso en la muñeca usando un examen especial llamado ecografía Doppler, que sirve para ver el flujo de sangre.\n\n**Qué Significa el Diagnóstico**  \nLos doctores dijeron que el bebé tenía un problema llamado Síndrome de Compartment Neonatal (NCS). Esto ocurre cuando hay mucha presión dentro de los músculos, lo que puede dañar la sangre y los nervios. En este caso, probablemente fue causado por la presión dentro del útero antes de nacer.\n\n**Cómo lo Trataron**  \nPara ayudar, los médicos hicieron una cirugía llamada fasciotomía. Esta operación abre la piel y los músculos para bajar la presión y salvar el brazo. La cirugía se hizo unas seis horas después del nacimiento.\n\n**Resultados y Seguimiento**  \nDespués de la operación, el brazo del bebé mejoró poco a poco. A los tres días, el color y la circulación de la sangre en el brazo y la mano eran normales. Las heridas sanaron bien y, a los cuatro meses, el bebé podía mover pasivamente (con ayuda) su muñeca y dedos. Aunque todavía tiene poco movimiento activo (por sí mismo), especialmente en algunos dedos, puede mover el hombro y el codo. El bebé seguirá recibiendo terapia para mejorar su movimiento y evitar que las cicatrices causen problemas. Los médicos continuarán observando su recuperación con cuidado.",
+        "score": {
+          "ROUGE-L-Sum": 0.24945295404814002,
+          "BERTScore_F": 0.7831487059593201
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.5163008300037301
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe presenta el caso de un recién nacido prematuro (35 semanas y 3 días de gestación) que pesó 2021 gramos al nacer. La madre tenía antecedentes relevantes, incluyendo rasgo de células falciformes, edad avanzada y obesidad. Durante el embarazo se detectó oligohidramnios (disminución del líquido amniótico) y signos ecográficos preocupantes como distensión de la vejiga, hidroceles bilaterales (acumulación de líquido en las bolsas testiculares), dilatación de la uretra y ascitis abdominal, lo que sugería una posible obstrucción del tracto urinario inferior y ruptura de la vejiga. Debido a la disminución del movimiento fetal y un perfil biofísico bajo, se realizó una cesárea programada.\n\n**Hallazgos Clave**  \nAl nacer, el bebé presentó dificultad respiratoria y signos evidentes de compromiso en la extremidad superior izquierda: la mano y el antebrazo estaban oscuros (cianóticos), con una gran ampolla y descamación en el dorso de la mano, además de ausencia de movimiento espontáneo y falta de respuesta a estímulos. La ecografía Doppler mostró flujo arterial hasta la fosa antecubital, pero no se detectaron pulsos en las arterias radiales o cubitales, lo que indicaba compromiso circulatorio distal. Estos hallazgos fueron compatibles con un síndrome de compresión neuromuscular (NCS), probablemente causado por la presión ejercida sobre la extremidad dentro del útero debido al oligohidramnios.\n\n**Interpretación Clínica**  \nEl diagnóstico de NCS se basó en la combinación de los hallazgos físicos y ecográficos, que indicaban una isquemia (falta de flujo sanguíneo adecuado) en la extremidad superior izquierda. Para evitar daños permanentes, se decidió realizar una fasciotomía descompresiva urgente (una cirugía que libera la presión dentro de los compartimentos musculares del antebrazo y la mano, incluyendo el túnel carpiano) aproximadamente seis horas después del nacimiento. Esta intervención permitió restaurar la circulación y prevenir la necrosis (muerte del tejido).\n\n**Próximos Pasos y Evolución**  \nTras la cirugía, la apariencia y la perfusión de la extremidad mejoraron progresivamente. A los tres días de vida, el antebrazo y la mano mostraban una coloración normal y señales Doppler positivas en toda la extremidad, desde la arteria braquial hasta los dedos. Las heridas de la fasciotomía se dejaron curar de forma natural y se protegieron con una férula personalizada para mantener la muñeca y los dedos en posición adecuada. No se presentaron infecciones ni signos de isquemia persistente. A las seis semanas, las heridas estaban completamente cicatrizadas.\n\nEn la consulta de seguimiento a los cuatro meses, el bebé tenía un rango completo de movimiento pasivo en la muñeca y los dedos, aunque el movimiento activo era limitado, con ligera flexión y extensión en algunos dedos y buen movimiento activo en el hombro y codo. Se continúa con terapia ocupacional, uso de férulas y masaje de cicatrices para prevenir contracturas (rigidez anormal) y mejorar la función. Un equipo multidisciplinario sigue monitorizando su recuperación para optimizar los resultados funcionales a largo plazo.",
+        "score": {
+          "ROUGE-L-Sum": 0.2840746054519369,
+          "BERTScore_F": 0.8343223929405212
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5591984991962291
+        }
+      }
+    }
+  },
+  {
+    "id": 31,
+    "gold_summary": "Una mujer de 38 años se presentó con distensión abdominal progresiva. Las imágenes revelaron un quiste retroperitoneal gigante. Debido a los recursos limitados, se realizó una laparotomía abierta y se extirpó completamente un quiste de 33 cm que contenía 8 l de líquido transparente. La histopatología confirmó un quiste retroperitoneal idiopático gigante.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Una mujer tenía una barriga muy grande y le dolía un poco. Los doctores vieron que había una bolsa grande llena de líquido dentro de su barriga. La doctora hizo una operación para sacar la bolsa. La bolsa era muy grande y tenía mucho líquido adentro. Después de la operación, la mujer se sintió mejor y no volvió a tener la bolsa.",
+        "score": {
+          "ROUGE-L-Sum": 0.21374045801526714,
+          "BERTScore_F": 0.6941605806350708
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.45395051932516894
+        }
+      },
+      "B2": {
+        "text": "**Lo que le pasó a la paciente**  \nUna mujer de 38 años notó que su abdomen (la parte del cuerpo donde están el estómago y otros órganos) se hinchaba poco a poco durante cinco meses. También sentía un dolor leve y se llenaba rápido al comer. Al examinarla, los médicos encontraron una gran masa dentro de su abdomen, pero no tenía fiebre ni otros síntomas graves.\n\n**Qué encontraron los médicos**  \nLas pruebas de imagen, como la tomografía computarizada (una especie de radiografía avanzada), mostraron un quiste muy grande en la zona llamada retroperitoneo, que está detrás de los órganos principales del abdomen. Un quiste es una bolsa llena de líquido. Este quiste medía más de 30 centímetros y contenía alrededor de 8 litros de líquido. Debido a su tamaño, estaba presionando otros órganos importantes.\n\n**Cómo la trataron**  \nLos médicos decidieron hacer una cirugía abierta para quitar el quiste. Durante la operación, hicieron una incisión en el abdomen y sacaron el quiste, aspirando el líquido que tenía dentro. Luego, enviaron muestras del quiste para analizarlas y asegurarse de que no fuera canceroso.\n\n**Qué significan los resultados**  \nEl análisis mostró que el quiste no tenía células cancerosas y que estaba formado por tejido normal con algunas células inflamatorias. No encontraron una causa clara para el quiste, por lo que lo llamaron \"idiopático\", que significa que no se sabe exactamente por qué apareció.\n\n**Después de la cirugía**  \nLa paciente se recuperó bien y fue dada de alta una semana después. En los controles a los 6 y 12 meses no hubo problemas ni volvió a aparecer el quiste. Esto indica que la cirugía fue exitosa y que la paciente está en buen estado.",
+        "score": {
+          "ROUGE-L-Sum": 0.15957446808510636,
+          "BERTScore_F": 0.7165195345878601
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.4380470013364832
+        }
+      },
+      "B3": {
+        "text": "**Contexto:**  \nUna mujer de 38 años acudió al hospital debido a una hinchazón abdominal que había ido aumentando progresivamente durante cinco meses. Además, presentaba dolor abdominal leve y sensación de llenura rápida al comer. No tenía otros síntomas generales como pérdida de peso, problemas digestivos, fatiga o fiebre. En la exploración física, se observó una gran distensión del abdomen con una masa palpable que ocupaba gran parte de la cavidad abdominal, sin dolor ni signos de inflamación. También se detectó una leve palidez y un tinte amarillento en la parte blanca de los ojos (ictericia).\n\n**Hallazgos Clave:**  \nLos análisis de sangre mostraron anemia leve, bilirrubina elevada (lo que explica la ictericia), pero funciones hepáticas y renales normales. La ecografía y la tomografía computarizada (TC) con contraste revelaron un enorme quiste con paredes delgadas ubicado en la región retroperitoneal (la zona detrás del abdomen), que medía aproximadamente 33 cm en su mayor dimensión y contenía alrededor de 8 litros de líquido. Este quiste desplazaba órganos cercanos como el riñón derecho, el hígado, la vesícula biliar, el páncreas y los intestinos, pero no parecía originarse en ninguno de ellos.\n\n**Interpretación Clínica:**  \nDado el tamaño considerable del quiste y su efecto compresivo sobre órganos abdominales importantes, se decidió realizar una cirugía abierta (laparotomía) para extirparlo completamente. Durante la operación, se aspiraron 8 litros de líquido marrón del quiste y se removió la masa sin complicaciones. El análisis microscópico del tejido del quiste mostró que estaba formado por tejido suprarrenal (glándulas que se encuentran encima de los riñones) sin signos de células anormales o malignas, aunque había inflamación leve. La superficie interna del quiste no presentaba un revestimiento celular definido. Estos hallazgos sugieren que se trataba de un quiste retroperitoneal gigante idiopático, es decir, de origen desconocido y sin causa aparente.\n\n**Próximos Pasos:**  \nLa paciente tuvo una recuperación sin complicaciones y fue dada de alta siete días después de la cirugía. En los controles realizados a los 6 y 12 meses posteriores, no se detectó recurrencia del quiste ni problemas relacionados. Se recomienda continuar con seguimiento clínico periódico para asegurar que no aparezcan nuevas complicaciones o recidivas.",
+        "score": {
+          "ROUGE-L-Sum": 0.16344086021505375,
+          "BERTScore_F": 0.7469733953475952
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.4552071277813245
+        }
+      }
+    }
+  },
+  {
+    "id": 32,
+    "gold_summary": "Un hombre de 71 años con enfermedad de Chagas y angina estable en esfuerzo mínimo se sometió a una angiografía por tomografía computarizada y cineangiografía que reveló una enfermedad multivascular muy calcificada que afectaba a la arteria descendente anterior izquierda (LM). Debido al grado de calcificación, se decidió realizar una rotablation. La primera etapa de la intervención coronaria percutánea (ICP) con rotablation se realizó en la arteria descendente anterior izquierda (LM), la arteria descendente anterior izquierda y la segunda rama diagonal sin complicaciones. Casi 30 días después, volvió para una ICP de la arteria coronaria derecha (RCA). La estrategia propuesta fue la aterectomía rotativa en la arteria descendente anterior posterior (PDA) y la arteria posterolateral derecha (RPLA) con una fresa de 1,5 mm, seguida por la implantación de dos stents liberadores de fármacos (DES). A través del acceso a la arteria femoral derecha, la lesión de la RPLA se extirpó con éxito. Como no había signos de disección y se mantuvo el flujo TIMI 3, se reposicionó el RotaWire de 0,009″ para cruzar la lesión de la PDA y se realizó la extirpación de la lesión. Después de dos intentos, logramos cruzar la lesión con la fresa de 1,5 mm, sin embargo, se produjo el atrapamiento de la misma. El sistema se retiró hasta que el catéter guía penetró profundamente en la RCA, y se hicieron intentos para liberar el Rotablator moviéndolo hacia adelante y hacia atrás, pero la fresa ni siquiera giró. La arteria femoral contralateral se perforó y se insertó un catéter guía 6F JR, con el fin de mover un alambre guía y un pequeño globo de angioplastia tangencialmente a la fresa, pero sin éxito. Finalmente, avanzamos el alambre guía utilizando la técnica de «nudillo», aprovechando la torsión de la porción distal del alambre guía PT2, realizando una disección subintimal y reentrada, y pudimos cruzar fácilmente el globo, inflarlo y liberar la fresa atrapada. A través del sistema 6F, se implantaron dos DES programados y uno de rescate con éxito en la PDA, RPLA y RCA, obteniendo un flujo TIMI 3 final sin complicaciones.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Había un señor de 71 años con problemas en su corazón. Su corazón tenía partes muy duras y tapadas. Los doctores usaron una máquina especial para ver su corazón. \n\nPrimero, limpiaron unas partes del corazón con una herramienta que gira rápido. Esto ayudó a que la sangre pudiera pasar mejor. Después de un mes, volvieron a limpiar otras partes del corazón. \n\nEn una parte, la herramienta se quedó atrapada. Los doctores usaron un truco con un hilo para ayudar a que la herramienta se moviera otra vez. Al final, pusieron unos tubos pequeñitos para que la sangre siga fluyendo bien. \n\nEl señor quedó bien y sin problemas después de la ayuda.",
+        "score": {
+          "ROUGE-L-Sum": 0.14396887159533076,
+          "BERTScore_F": 0.7392184138298035
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.4415936427125671
+        }
+      },
+      "B2": {
+        "text": "**Lo que le pasó al paciente:**  \nUn hombre de 71 años con una enfermedad llamada Chagas y problemas en el corazón tuvo dolor en el pecho al hacer poco esfuerzo. Los médicos le hicieron estudios que mostraron que varias arterias del corazón estaban muy dañadas y tenían muchas calcificaciones, que son depósitos duros que bloquean el paso de la sangre.\n\n**Qué hicieron los médicos:**  \nPara ayudarlo, los doctores usaron una técnica llamada intervención coronaria percutánea (ICP). Esta técnica consiste en abrir las arterias del corazón usando pequeños tubos llamados stents, que ayudan a mantenerlas abiertas. Debido a que las arterias estaban muy duras por la calcificación, usaron una herramienta especial llamada rotablación. Esta herramienta tiene una pequeña fresa que gira rápido para eliminar la parte dura y permitir que el stent se coloque mejor.\n\n**Cómo fue el tratamiento:**  \nPrimero, trataron las arterias principales del lado izquierdo del corazón sin problemas. Después de casi un mes, regresó para tratar las arterias del lado derecho. Durante este segundo procedimiento, usaron la fresa para limpiar las arterias bloqueadas y pusieron stents para mantenerlas abiertas. Sin embargo, la fresa se quedó atrapada en una de las arterias, lo que complicó el procedimiento.\n\n**Cómo resolvieron el problema:**  \nPara liberar la fresa atrapada, los médicos usaron una técnica especial con un alambre guía que creó un nuevo camino dentro de la pared de la arteria para pasar un globo y liberar la fresa. Luego, colocaron los stents necesarios y lograron que la sangre fluyera bien por las arterias sin complicaciones.\n\n**Qué significa esto:**  \nEste caso muestra cómo los médicos pueden tratar arterias muy dañadas y duras usando herramientas avanzadas. Aunque hubo una complicación, pudieron solucionarla con éxito. El paciente salió en buen estado y con su corazón funcionando normalmente.",
+        "score": {
+          "ROUGE-L-Sum": 0.250351617440225,
+          "BERTScore_F": 0.792331337928772
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.5213414776844985
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nUn hombre de 71 años con antecedentes de enfermedad de Chagas y diabetes presentó una pérdida de peso significativa y un diagnóstico de megaesófago con obstrucción en el cardias. Durante la evaluación prequirúrgica, manifestó dolor torácico con mínimo esfuerzo. Estudios previos mostraron una enfermedad coronaria multivascular severamente calcificada, especialmente en la arteria coronaria izquierda. Se decidió realizar una intervención coronaria percutánea (ICP) debido al alto riesgo quirúrgico y la complejidad de las lesiones.\n\n**Hallazgos Clave**  \nLa angiografía coronaria reveló múltiples lesiones calcificadas: una estenosis del 90% en la arteria descendente anterior izquierda (LAD), lesiones severas en ramas diagonales, y oclusión de la arteria circunfleja izquierda (LCx) con circulación colateral. La arteria coronaria derecha (RCA) también presentaba lesiones significativas y calcificación. La función ventricular izquierda se mantenía conservada.\n\n**Intervención y Procedimientos**  \nSe planificó la ICP en dos etapas debido a la extensión y severidad de las lesiones. La primera intervención, realizada el 19 de febrero de 2016, incluyó la rotablation (una técnica que utiliza una fresa rotatoria para eliminar la calcificación) en la arteria descendente anterior, seguida de la implantación de stents liberadores de fármacos (DES) en la arteria descendente derecha y la circunfleja, logrando un flujo sanguíneo óptimo sin complicaciones.\n\nCasi un mes después, el 22 de marzo de 2016, se realizó la segunda ICP en las ramas de la arteria coronaria derecha (PDA y RPLA) también con rotablation y colocación de DES. Durante este procedimiento, se produjo una disección severa en la arteria coronaria derecha, causada por la manipulación del catéter, que fue rápidamente corregida con la implantación de un stent adicional. Se presentó un incidente de atrapamiento de la fresa rotatoria dentro de la arteria, que fue resuelto mediante una técnica avanzada que permitió liberar el dispositivo sin daños adicionales.\n\n**Interpretación Clínica**  \nEste caso ilustra la complejidad del manejo de enfermedad coronaria multivascular severamente calcificada en un paciente con comorbilidades importantes y alto riesgo quirúrgico. La utilización de rotablation permitió tratar las lesiones calcificadas que dificultan la expansión de los stents, mejorando el flujo sanguíneo coronario. La estrategia en dos tiempos y la cuidadosa planificación fueron fundamentales para minimizar riesgos y lograr un resultado exitoso.\n\n**Próximos Pasos**  \nEl paciente fue dado de alta en buenas condiciones tras una estancia corta en cuidados intensivos, con función ventricular preservada y sin complicaciones clínicas significativas. Se recomienda seguimiento cardiológico estrecho, control de factores de riesgo cardiovascular y terapia antiplaquetaria dual para prevenir eventos trombóticos. La arteria circunfleja, ocluida pero con circulación colateral, no fue intervenida debido a la dificultad técnica y el riesgo asociado.",
+        "score": {
+          "ROUGE-L-Sum": 0.29398148148148145,
+          "BERTScore_F": 0.8369128704071045
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.565447175944293
+        }
+      }
+    }
+  },
+  {
+    "id": 33,
+    "gold_summary": "Se diagnosticó a una mujer de 29 años con dolor intermitente en el flanco derecho y ardor urinario un quiste hidatídico (HC) de categoría 4 de Bosniak, tras dar positivo en anticuerpos de equinococo. Las imágenes confirmaron el diagnóstico, lo que derivó en un tratamiento de tres meses con albendazol, seguido de una nefrectomía derecha y una resección hepática parcial. El análisis histopatológico confirmó un HC y una pielonefritis crónica. La paciente se recuperó sin incidentes y volvió a sus actividades normales.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Una mujer tenía dolor en un lado de su cuerpo y ardor al hacer pipí. Los doctores encontraron un quiste grande en su riñón. Le dieron medicina por tres meses para ayudarla. Luego, le hicieron una operación para quitar el riñón y un poco del hígado. Después, ella se sintió bien y pudo hacer sus cosas normales otra vez.",
+        "score": {
+          "ROUGE-L-Sum": 0.2531645569620253,
+          "BERTScore_F": 0.7661888599395752
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5096767084508003
+        }
+      },
+      "B2": {
+        "text": "**Lo que Encontraron**  \nUna mujer de 29 años tenía dolor en el lado derecho de su espalda y a veces sentía ardor al orinar. Los médicos hicieron pruebas y encontraron que tenía anticuerpos contra un parásito llamado equinococo, que puede causar quistes en órganos. Las imágenes del riñón mostraron un quiste grande y complicado, clasificado como categoría 4 de Bosniak, lo que significa que podría ser peligroso.\n\n**Qué Hicieron**  \nPara tratarla, primero le dieron un medicamento llamado albendazol durante tres meses. Este medicamento ayuda a matar el parásito. Después, le hicieron una cirugía para quitar el riñón derecho y parte del hígado, porque el quiste estaba pegado a esos órganos.\n\n**Qué Significa el Diagnóstico**  \nAl analizar el quiste, confirmaron que era un quiste hidatídico, que es una bolsa llena de líquido causada por el parásito. También encontraron inflamación crónica en el riñón, llamada pielonefritis.  \n\n**Recuperación**  \nDespués de la operación, la paciente se recuperó bien, sin problemas. Su orina y signos vitales estaban normales. Pudo volver a sus actividades normales sin complicaciones.  \n\nEste caso muestra cómo una infección por parásitos puede afectar órganos importantes y cómo se puede tratar con medicamentos y cirugía.",
+        "score": {
+          "ROUGE-L-Sum": 0.27848101265822783,
+          "BERTScore_F": 0.7783060669898987
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.5283935398240632
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nUna mujer de 29 años consultó por dolor intermitente en el flanco derecho y episodios ocasionales de ardor al orinar, sin presencia de sangre en la orina. No presentaba síntomas sistémicos como tos, fatiga o pérdida de peso, y su estado general era estable. Destacaba una exposición frecuente a ovejas, factor de riesgo para infecciones parasitarias. Los análisis de laboratorio fueron normales, pero la prueba serológica detectó anticuerpos contra equinococos, un parásito causante de quistes hidatídicos.\n\n**Hallazgos Clave**  \nEl ultrasonido abdominal reveló una lesión quística grande en el riñón derecho, con paredes gruesas y sin flujo sanguíneo significativo. La tomografía computarizada con contraste mostró una masa quística con tabiques internos y una pared engrosada que se realzaba con el contraste, clasificada como categoría 4 en la escala de Bosniak, lo que indica una alta probabilidad de lesión compleja y potencialmente maligna o infecciosa. Además, la lesión involucraba el sistema colector renal y estaba en contacto con el hígado. La radiografía de tórax no mostró quistes pulmonares, descartando afectación pulmonar.\n\n**Interpretación Clínica**  \nEl diagnóstico presuntivo fue un quiste hidatídico renal (HC), una infección parasitaria causada por el equinococo, con posible extensión hepática. El tratamiento inicial consistió en albendazol, un medicamento antiparasitario, administrado durante tres meses para reducir la carga parasitaria y minimizar riesgos quirúrgicos. Posteriormente, se realizó una cirugía abierta mediante una incisión subcostal derecha (incisión de Kocher), que incluyó la extracción completa del riñón derecho (nefrectomía) y una resección parcial del hígado debido a adherencias entre ambos órganos. El estudio histopatológico confirmó la presencia del quiste hidatídico y evidenció pielonefritis crónica, una inflamación prolongada del tejido renal.\n\n**Próximos Pasos y Evolución**  \nTras la cirugía, la paciente mostró una recuperación favorable, con parámetros vitales estables y función urinaria adecuada. El catéter urinario se retiró a las 24 horas, y el drenaje renal se retiró en los días siguientes sin complicaciones. Finalmente, la paciente pudo retomar sus actividades habituales sin presentar efectos adversos ni recurrencias. Este caso destaca la importancia de considerar infecciones parasitarias en pacientes con lesiones quísticas renales, especialmente en contextos de exposición a animales de riesgo.",
+        "score": {
+          "ROUGE-L-Sum": 0.25101214574898784,
+          "BERTScore_F": 0.7808781266212463
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.5159451361851171
+        }
+      }
+    }
+  },
+  {
+    "id": 34,
+    "gold_summary": "Presentamos a una paciente de 46 años que fue admitida en nuestro hospital debido a opresión torácica y falta de aire que duró más de un mes. La ecocardiografía reveló un diámetro del ventrículo izquierdo (anteroposterior) de 54 mm, el electrocardiograma mostró bradicardia sinusal y duración del QRS de 90 ms. La paciente no experimentó opresión torácica o falta de aire, y hubo una marcada mejora en la tolerancia al ejercicio y calidad de vida después de la implantación de la modulación de la contractilidad cardiaca.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Una señora tenía dolor en el pecho y le costaba respirar mucho tiempo. Los doctores miraron su corazón con máquinas. Después de un tratamiento especial, ella se sintió mucho mejor. Ya no tenía dolor ni dificultad para respirar. Ahora puede jugar y caminar sin problema.",
+        "score": {
+          "ROUGE-L-Sum": 0.13333333333333333,
+          "BERTScore_F": 0.7106133699417114
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.42197335163752236
+        }
+      },
+      "B2": {
+        "text": "**Caso de una Paciente con Problemas del Corazón**\n\nUna mujer de 46 años llegó al hospital porque sentía opresión en el pecho y le costaba respirar desde hacía más de un mes. Para entender qué le pasaba, los médicos le hicieron varios estudios.\n\n**Lo que Encontraron**\n\nUn examen llamado ecocardiografía mostró que una parte de su corazón, llamada ventrículo izquierdo, estaba un poco agrandada (medía 54 mm). Otro examen, el electrocardiograma, mostró que su corazón latía más lento de lo normal (bradicardia sinusal) y que la señal eléctrica que controla el latido tenía una duración normal (QRS de 90 ms).\n\n**Qué Hicieron y Qué Pasó Después**\n\nPara ayudarla, los médicos le implantaron un dispositivo llamado modulador de la contractilidad cardiaca (CCM). Este aparato envía pequeñas señales eléctricas al corazón para mejorar su fuerza al latir. Después de la implantación, la paciente ya no tuvo opresión en el pecho ni dificultad para respirar. Además, pudo hacer ejercicio con más facilidad y su calidad de vida mejoró mucho.\n\nEn resumen, el tratamiento con CCM ayudó a mejorar la función de su corazón y su bienestar general.",
+        "score": {
+          "ROUGE-L-Sum": 0.33650793650793653,
+          "BERTScore_F": 0.795749306678772
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5661286215933543
+        }
+      },
+      "B3": {
+        "text": "**Contexto**\n\nUna mujer de 46 años fue hospitalizada por presentar opresión en el pecho y dificultad para respirar que persistían desde hacía más de un mes. Su historial incluía una cirugía parcial de tiroides y no tenía antecedentes de tabaquismo ni consumo de alcohol. A pesar de recibir tratamiento médico estándar para insuficiencia cardiaca, sus síntomas y función cardíaca no mejoraron adecuadamente. Los exámenes iniciales mostraron una fracción de eyección del ventrículo izquierdo (LVEF) muy reducida (28%), indicativa de una función cardíaca comprometida, y un electrocardiograma (ECG) con bradicardia sinusal y un complejo QRS estrecho (90 ms).\n\n**Hallazgos Clave**\n\n- Ecocardiografía: El ventrículo izquierdo tenía un diámetro anteroposterior de 54 mm, con una fracción de eyección del 28%, confirmando una cardiomiopatía dilatada con función cardíaca severamente reducida.\n- ECG: Bradicardia sinusal (ritmo cardíaco lento pero regular) y duración del QRS de 90 ms, lo que indica que la conducción eléctrica del corazón estaba relativamente normal.\n- Laboratorio: Elevación significativa del NT-proBNP (6245 pg/mL), marcador que refleja estrés y daño cardíaco.\n- Sintomatología: Opresión en el pecho y dificultad para realizar actividades físicas leves, clasificada como insuficiencia cardíaca clase III según la New York Heart Association (NYHA).\n\n**Interpretación Clínica**\n\nLa paciente presentaba insuficiencia cardíaca con función ventricular izquierda gravemente disminuida, a pesar del tratamiento médico óptimo. La cardiomiopatía dilatada y los síntomas persistentes indicaban la necesidad de una intervención adicional. Se decidió implantar un dispositivo de modulación de la contractilidad cardíaca (CCM), que es un tipo de terapia eléctrica que mejora la fuerza de contracción del corazón sin alterar el ritmo cardíaco normal.\n\nEl procedimiento de implantación fue similar al de un marcapasos tradicional, con cables colocados en el tabique del ventrículo derecho y un generador de impulsos programado para optimizar la función cardíaca. La implantación fue exitosa, sin complicaciones inmediatas.\n\n**Próximos Pasos y Resultados**\n\nTras la implantación del dispositivo CCM, la paciente fue monitoreada mediante ecocardiografía, análisis sanguíneos, pruebas de caminata y cuestionarios de calidad de vida. A los tres meses, se observó una mejora significativa en la función diastólica del ventrículo izquierdo, reducción de la presión de llenado ventricular y una disminución en los síntomas clínicos.\n\nLa paciente dejó de experimentar opresión en el pecho y dificultad para respirar, mostró una notable mejoría en la capacidad para realizar ejercicio y reportó una mejor calidad de vida. Estos resultados sugieren que la terapia con CCM puede ser una opción efectiva para pacientes con insuficiencia cardíaca avanzada que no responden adecuadamente al tratamiento médico convencional.",
+        "score": {
+          "ROUGE-L-Sum": 0.21694915254237288,
+          "BERTScore_F": 0.7655888199806213
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.4912689862614971
+        }
+      }
+    }
+  },
+  {
+    "id": 35,
+    "gold_summary": "Paciente de sexo femenino, de 61 años, que había estado en remisión de psoriasis durante 20 años. Sufrió una recaída de psoriasis en forma de placa pocos días después de comenzar el tratamiento con L-metilfolato a una dosis diaria de 15 mg.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Una señora de 61 años tuvo la piel con manchas hace mucho tiempo. Ella no tuvo esas manchas por 20 años. Pero cuando empezó a tomar una medicina nueva, las manchas volvieron rápido. Luego, dejó de tomar esa medicina y las manchas se fueron.",
+        "score": {
+          "ROUGE-L-Sum": 0.20408163265306126,
+          "BERTScore_F": 0.7053477168083191
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.45471467473069016
+        }
+      },
+      "B2": {
+        "text": "**Lo que pasó con la paciente**  \nUna mujer de 61 años había tenido psoriasis, que es una enfermedad de la piel que causa manchas rojas y escamosas. Sin embargo, no había tenido problemas con la psoriasis durante 20 años.  \n\n**Qué tratamiento recibió y qué pasó después**  \nElla empezó a tomar un medicamento llamado L-metilfolato, que es una forma de vitamina B9 que ayuda en el tratamiento de la depresión. Tomaba 15 mg al día. Pero pocos días después de comenzar este medicamento, la psoriasis volvió a aparecer en su piel.  \n\n**Qué hicieron los médicos**  \nAl ver que la psoriasis regresó, el doctor decidió quitarle el L-metilfolato. Cuatro días después de dejar el medicamento, las manchas en la piel comenzaron a mejorar y desaparecieron completamente en unas semanas.  \n\n**Qué significa esto**  \nEste caso muestra que, en esta paciente, el L-metilfolato pudo haber causado que la psoriasis regresara después de muchos años sin síntomas. Por eso, es importante que los médicos revisen bien los tratamientos y los posibles efectos en cada persona.",
+        "score": {
+          "ROUGE-L-Sum": 0.2510460251046025,
+          "BERTScore_F": 0.7537298798561096
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.5023879524803561
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe trata de una mujer de 61 años con antecedentes de psoriasis y depresión desde los 20 años. Durante dos décadas, desde los 41 años, no presentó brotes de psoriasis. Su tratamiento psiquiátrico actual incluía venlafaxina, lamotrigina y quetiapina, con buena respuesta y sin efectos adversos importantes. En 2019, se identificó que tenía una mutación genética heterozigótica en el gen MTHFR (C677T), lo que llevó a prescribirle L-metilfolato, un suplemento que puede ayudar en ciertos trastornos depresivos.\n\n**Hallazgos Clave**  \nPocos días después de iniciar el L-metilfolato a una dosis diaria de 15 mg, la paciente presentó una recaída de psoriasis en forma de placas, una manifestación cutánea que no había experimentado en 20 años. Al suspender el L-metilfolato, las lesiones comenzaron a mejorar en cuatro días y desaparecieron completamente en unas semanas. No se registraron nuevos brotes hasta casi un año después.\n\n**Interpretación Clínica**  \nEl caso sugiere una posible relación entre la administración de L-metilfolato y la reactivación de la psoriasis en esta paciente. Aunque el L-metilfolato es utilizado para mejorar la depresión, en este caso pudo haber desencadenado una respuesta inflamatoria cutánea, posiblemente relacionada con su predisposición genética y su historial de psoriasis. Este hallazgo es relevante para considerar el impacto de tratamientos coadyuvantes en enfermedades autoinmunes o inflamatorias crónicas.\n\n**Próximos Pasos**  \nSe recomienda un seguimiento cuidadoso en pacientes con antecedentes de psoriasis cuando se prescriben suplementos como el L-metilfolato. Además, es importante evaluar alternativas terapéuticas para la depresión que no exacerben enfermedades cutáneas. La comunicación estrecha entre dermatólogos y psiquiatras es fundamental para manejar casos similares y evitar recaídas.",
+        "score": {
+          "ROUGE-L-Sum": 0.15126050420168066,
+          "BERTScore_F": 0.7660607099533081
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.4586606070774944
+        }
+      }
+    }
+  },
+  {
+    "id": 36,
+    "gold_summary": "Este informe de caso se refiere a un paciente de 61 años con destrucción rápida de ambas articulaciones de la cadera debido a una artritis séptica que se trató con éxito con una implantación por etapas de prótesis de cadera recubiertas con plata con un recubrimiento ultrafino multicapa de plata. En un seguimiento de tres años, no hubo signos de infección, se observó un buen estado de todos los componentes protésicos y el resultado funcional fue excelente.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Había un señor con mucho dolor en sus dos caderas. Sus caderas se dañaron rápido por una infección. Los doctores le pusieron unas piezas nuevas en sus caderas. Estas piezas tenían una capa especial de plata para ayudar. Después de tres años, el señor está bien y sin dolor. Sus caderas funcionan muy bien y no hay infección.",
+        "score": {
+          "ROUGE-L-Sum": 0.22077922077922077,
+          "BERTScore_F": 0.7562254071235657
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.4885023139513932
+        }
+      },
+      "B2": {
+        "text": "**Lo que pasó con el paciente:**  \nUn hombre de 61 años tenía un problema grave en ambas caderas. Tenía una infección llamada artritis séptica, que hizo que sus articulaciones se dañaran muy rápido. Esta infección causó mucho dolor y dificultad para moverse.\n\n**Cómo lo trataron:**  \nPrimero, le quitaron las partes dañadas de las caderas y limpiaron bien las áreas infectadas. Luego, le pusieron unos espaciadores especiales con antibióticos para controlar la infección. Después de varias semanas y tratamientos con antibióticos fuertes, la infección mejoró.\n\nMás tarde, le pusieron prótesis nuevas en ambas caderas. Estas prótesis tenían un recubrimiento muy delgado de plata. La plata ayuda a evitar que las bacterias vuelvan a causar infección. Las cirugías se hicieron con técnicas que dañan poco los tejidos, para que la recuperación fuera mejor.\n\n**Qué pasó después:**  \nTres años después de las cirugías, el paciente estaba muy bien. No había señales de que la infección regresara. Las prótesis estaban firmes y funcionando bien. El paciente podía caminar normalmente y no sentía dolor ni rigidez en las caderas.\n\n**Por qué es importante:**  \nEste caso muestra que usar prótesis con un recubrimiento especial de plata puede ayudar a tratar infecciones graves en las articulaciones y mejorar la recuperación. Además, el seguimiento a largo plazo confirmó que el tratamiento fue exitoso y seguro.",
+        "score": {
+          "ROUGE-L-Sum": 0.2588235294117647,
+          "BERTScore_F": 0.7587051391601562
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.5087643342859605
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe trató a un paciente de 61 años con antecedentes de artritis reumatoide, que recibía tratamiento con esteroides, y que presentaba osteoartritis en ambas caderas junto con dolor en la ingle. Después de una inyección de ácido hialurónico en ambas articulaciones, el paciente desarrolló fiebre, deterioro general y un dolor intenso y progresivo en las caderas. Las radiografías mostraron una rápida destrucción ósea en ambas articulaciones, y la aspiración reveló pus, confirmando una infección grave llamada artritis séptica bilateral.\n\n**Hallazgos Clave**  \nSe realizó la extracción quirúrgica de las cabezas femorales (la parte superior del hueso del muslo que forma la articulación de la cadera) y se limpiaron las articulaciones, implantando espaciadores temporales cargados con antibióticos para controlar la infección. Inicialmente se administraron antibióticos de amplio espectro, pero al identificar la bacteria Escherichia coli, el tratamiento se ajustó a un antibiótico específico (meropenem). Debido a la persistencia del drenaje, se llevaron a cabo dos cirugías adicionales para cambiar los espaciadores antibióticos.\n\nTras controlar la infección, se realizaron reemplazos definitivos de ambas caderas mediante prótesis recubiertas con un revestimiento ultrafino multicapa de plata. Este recubrimiento libera iones de plata, conocidos por sus propiedades antimicrobianas, con el objetivo de prevenir nuevas infecciones. La cirugía se realizó mediante un abordaje mínimamente invasivo para reducir el daño a los tejidos.\n\nEl lado derecho se operó primero, con una prótesis sin cemento y recubierta de plata en las superficies clave. La cadera izquierda se intervino semanas después, utilizando una jaula de refuerzo también recubierta de plata para reparar un defecto óseo importante, junto con una copa de polietileno cementada y un vástago femoral sin cemento igualmente recubierto. El paciente recibió un tratamiento antibiótico prolongado (hasta 18 semanas) para asegurar la erradicación completa de la infección.\n\n**Interpretación Clínica**  \nEl uso de prótesis recubiertas con plata en este caso permitió un control efectivo de la infección y una recuperación funcional excelente. Las heridas cicatrizaron sin complicaciones, y el paciente pudo caminar sin muletas en pocas semanas. Tres años después de la cirugía, no se observaron signos de infección recurrente ni efectos secundarios relacionados con la plata, como la argiria (una pigmentación anormal de la piel). Las radiografías mostraron que las prótesis estaban bien integradas y estables, y la función de las caderas era casi normal, con muy poco dolor y rigidez.\n\n**Próximos Pasos**  \nEl seguimiento clínico y radiológico continuado es fundamental para detectar cualquier posible complicación a largo plazo. En este caso, el éxito del tratamiento sugiere que las prótesis con recubrimiento de plata pueden ser una opción valiosa para pacientes con infecciones severas en las articulaciones, especialmente cuando se requiere una reconstrucción compleja. Además, el abordaje mínimamente invasivo contribuyó a una recuperación más rápida y con menos cicatrices visibles.\n\nEn resumen, este caso demuestra que un tratamiento escalonado que combina cirugía, antibióticos específicos y prótesis con recubrimiento antimicrobiano puede lograr resultados excelentes en infecciones articulares graves, mejorando la calidad de vida del paciente a largo plazo.",
+        "score": {
+          "ROUGE-L-Sum": 0.15987460815047022,
+          "BERTScore_F": 0.7889248132705688
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.47439971071051956
+        }
+      }
+    }
+  },
+  {
+    "id": 37,
+    "gold_summary": "Una niña africana de raza negra bantú de 1 día de vida fue admitida en la unidad neonatal debido a múltiples anomalías congénitas. La madre no buscó atención médica hasta el inicio del tercer trimestre, cuando tuvo un desprendimiento de placenta. La madre nunca recibió suplementos de ácido fólico prenatal. La niña tenía microcefalia, orejas bajas, paladar hendido derecho y labio, micrognatia, contractura y extremidades más cortas. Una radiografía esquelética mostró hipoplasia femoral. Presentamos este caso poco habitual y destacamos los retos en el diagnóstico y el tratamiento.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Una bebé nació con problemas en su cuerpo. Su mamá no fue al doctor mucho cuando estaba embarazada. La bebé tenía la cabeza pequeña y orejas bajitas. También tenía un huequito en la boca y su labio estaba partido. Sus brazos y piernas eran más cortos y un hueso de la pierna estaba pequeño. Los doctores cuidaron mucho a la bebé, pero fue difícil ayudarla.",
+        "score": {
+          "ROUGE-L-Sum": 0.1839080459770115,
+          "BERTScore_F": 0.7343820929527283
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.4591450694648699
+        }
+      },
+      "B2": {
+        "text": "**Lo que pasó con la bebé**  \nUna niña africana nació prematura, con solo 32 semanas de gestación y pesando 1000 gramos. Fue llevada a una unidad especial para bebés recién nacidos porque tenía varios problemas desde el nacimiento. Su mamá no recibió atención médica durante la mayor parte del embarazo y no tomó ácido fólico, una vitamina importante para evitar defectos al nacer. Además, la mamá tuvo un problema llamado desprendimiento de placenta, que puede afectar al bebé.\n\n**Lo que encontraron en la bebé**  \nLa niña tenía la cabeza más pequeña de lo normal (microcefalia), orejas bajas, un paladar y labio hendidos (como un corte en el labio y el techo de la boca), mandíbula pequeña (micrognatia), y sus brazos y piernas eran más cortos y rígidos. Las radiografías mostraron que sus huesos de las piernas, especialmente los fémures, estaban subdesarrollados o faltaban partes. También tenía dificultad para respirar leve y un pequeño problema en el corazón.\n\n**Qué significa el diagnóstico**  \nLos médicos diagnosticaron a la bebé con un síndrome llamado femoro-facial. Esto significa que tiene problemas en los huesos de las piernas (fémur) y en la cara. Este síndrome es raro y puede parecerse a otro llamado síndrome de regresión caudal, pero en ese último no hay problemas en la cara, lo que ayuda a diferenciarlos. Además, algunas de sus características podrían estar relacionadas con problemas durante el embarazo, como la falta de control de azúcar en la mamá, aunque en este caso no se encontró diabetes.\n\n**Cómo trataron a la bebé y qué pasó después**  \nLa bebé recibió ayuda para respirar y antibióticos para prevenir infecciones. También la atendieron varios especialistas para planear cirugías y terapias que la ayudaran a mejorar su movilidad y corregir el paladar hendido. Sin embargo, a pesar de los cuidados, la bebé falleció a los 30 días de vida debido a una infección grave.\n\n**Resumen final**  \nEste caso muestra lo difícil que es diagnosticar y tratar a bebés con problemas congénitos raros, especialmente cuando la atención prenatal no es adecuada. Es importante que las mamás reciban cuidado médico temprano y tomen vitaminas como el ácido fólico para prevenir algunos defectos al nacer.",
+        "score": {
+          "ROUGE-L-Sum": 0.20392156862745095,
+          "BERTScore_F": 0.771990954875946
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.4879562617516985
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe presentó el caso de una recién nacida africana de raza negra, con un peso bajo al nacer (1000 gramos) y prematura (32 semanas de gestación), que fue ingresada en la unidad de cuidados intensivos neonatales debido a múltiples anomalías congénitas y dificultad respiratoria moderada. La madre, de 32 años, no recibió atención prenatal adecuada hasta el tercer trimestre, cuando sufrió un desprendimiento de placenta, y no tomó suplementos de ácido fólico durante el embarazo. El embarazo se caracterizó por oligohidramnios severo (disminución del líquido amniótico).\n\n**Hallazgos Clave**  \nAl momento del ingreso, la bebé estaba alerta pero presentaba signos leves de síndrome de dificultad respiratoria. Se observaron varias malformaciones físicas: microcefalia (cabeza pequeña), occipucio prominente (parte posterior de la cabeza sobresaliente), orejas bajas, paladar hendido y labio leporino en el lado derecho, micrognatia (mandíbula pequeña), contracturas en ambos codos y extremidades inferiores más cortas.  \n\nLas radiografías mostraron aplanamiento de las costillas, ausencia completa del fémur derecho (aplasia) y desarrollo insuficiente del fémur izquierdo (hipoplasia). Los análisis de laboratorio básicos fueron normales, la ecografía cerebral no mostró alteraciones, pero el ecocardiograma detectó un pequeño conducto arterioso permeable (una conexión anormal entre dos vasos sanguíneos del corazón).\n\n**Interpretación Clínica**  \nEl conjunto de características clínicas llevó al diagnóstico de síndrome femoro-facial, una condición poco común que se caracteriza por anomalías en los huesos del muslo (fémur) y rasgos faciales inusuales. Este diagnóstico se diferencia del síndrome de regresión caudal, que también afecta la parte inferior del cuerpo pero no presenta malformaciones faciales. Además, se consideraron otras causas posibles del labio leporino, como el síndrome de banda amniótica, pero la combinación de hallazgos apuntó al síndrome femoro-facial.  \n\nEs importante destacar que, aunque la hiperglucemia materna mal controlada (niveles altos de azúcar en sangre durante el embarazo) puede causar ambas condiciones, en este caso la madre no tenía diabetes diagnosticada.\n\n**Tratamiento y Manejo**  \nLa bebé recibió soporte respiratorio y tratamiento antibiótico preventivo. Se contó con la participación de un equipo multidisciplinario que incluyó cirujano ortopédico, otorrinolaringólogo y fisioterapeuta. Se planificó la reparación quirúrgica del paladar hendido a los seis meses de edad y la rehabilitación funcional antes de que la niña comenzara a caminar. Sin embargo, la cirugía para alargar las extremidades no está disponible en el centro donde fue atendida.\n\n**Resultado y Seguimiento**  \nLamentablemente, la paciente falleció a la edad de un mes debido a complicaciones derivadas de una sepsis neonatal grave (infección generalizada en el recién nacido) de inicio tardío, lo que refleja la gravedad y complejidad del cuadro clínico.\n\n---\n\nEste caso resalta los desafíos en el diagnóstico y manejo de anomalías congénitas complejas en un contexto con recursos limitados, así como la importancia de la atención prenatal temprana y adecuada para prevenir y detectar estas condiciones.",
+        "score": {
+          "ROUGE-L-Sum": 0.21760000000000002,
+          "BERTScore_F": 0.815362274646759
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.5164811373233795
+        }
+      }
+    }
+  },
+  {
+    "id": 38,
+    "gold_summary": "Paciente masculino de 18 años con diagnóstico desde la infancia de NF-1 que presenta múltiples nodulos ovalados en cara, zona occipital y muñeca, máculas rojo-azuladas en dorso y placa rosada atrófica en muslo. El estudio ecográfico de los nódulos fue compatible con neurofibromas y el estudio histopatológico de las lesiones de dorso y muslo compatibles con neurofibromas cutáneos.",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Un niño que ahora tiene 18 años tiene una enfermedad llamada NF-1 desde que era muy pequeño. En su piel hay bolitas redondas en la cara, la cabeza y la muñeca. También tiene manchas rojas y azules en la espalda. En el muslo tiene una mancha rosada y suave. Los doctores hicieron pruebas y vieron que esas bolitas y manchas son parte de su enfermedad. Todo está bien cuidado y los doctores lo están ayudando.",
+        "score": {
+          "ROUGE-L-Sum": 0.2368421052631579,
+          "BERTScore_F": 0.7114367485046387
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.4741394268838983
+        }
+      },
+      "B2": {
+        "text": "**Lo que encontraron en el paciente**  \nUn joven de 18 años, que desde pequeño tiene una enfermedad llamada Neurofibromatosis tipo 1 (NF-1), presentó varios bultos pequeños y redondeados en la cara, la parte de atrás de la cabeza (zona occipital) y la muñeca. También tenía manchas de color rojo-azulado en la espalda y una zona rosada y delgada en el muslo izquierdo.\n\n**Qué significan los estudios realizados**  \nSe usó una ecografía, que es una prueba con ondas sonoras para ver el interior de los bultos, y mostró que esos nódulos eran neurofibromas. Los neurofibromas son tumores benignos, es decir, no cancerosos, que crecen en los nervios. Además, se tomó una biopsia, que consiste en sacar un pequeño pedazo de piel para examinarlo bajo el microscopio. Esta prueba confirmó que las manchas en la espalda y la placa en el muslo también eran neurofibromas en la piel.\n\n**Importancia del diagnóstico**  \nEstos hallazgos ayudan a entender mejor cómo afecta la NF-1 a este paciente, mostrando que tiene diferentes tipos de neurofibromas en varias partes del cuerpo. Esto es importante para su seguimiento médico y para decidir el mejor tratamiento si fuera necesario.",
+        "score": {
+          "ROUGE-L-Sum": 0.2661870503597122,
+          "BERTScore_F": 0.7513245344161987
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.5087557923879554
+        }
+      },
+      "B3": {
+        "text": "**Contexto**\n\nSe trata de un joven de 18 años con diagnóstico clínico confirmado desde la infancia de Neurofibromatosis tipo 1 (NF1), una enfermedad genética que afecta el desarrollo de tejidos nerviosos y cutáneos. Su historia médica incluye retrasos en el desarrollo psicomotor y del lenguaje durante la infancia, así como un diagnóstico de Trastorno por Déficit de Atención e Hiperactividad en la adolescencia. Presenta además características típicas de NF1, como múltiples manchas café con leche en la piel, nódulos oculares llamados nódulos de Lisch, y una macrocefalia (cabeza de tamaño mayor al promedio).\n\n**Hallazgos Clínicos y Diagnósticos**\n\nA los 18 años, el paciente consultó por la aparición de una nueva mancha en el muslo izquierdo que llevaba un año, además de varios nódulos en la muñeca derecha, la zona supraciliar derecha (por encima de la ceja) y el cuero cabelludo, todos asintomáticos. En el examen físico se observaron:\n\n- Múltiples manchas café con leche distribuidas por todo el cuerpo.\n- Nódulos subcutáneos ovalados, bien delimitados y móviles, de aproximadamente 0,5 cm en la zona supraciliar derecha, occipital y muñeca derecha.\n- Una placa rosada de 25 mm en el muslo izquierdo, con pérdida de anexos cutáneos (como folículos pilosos) y consistencia blanda.\n- Múltiples máculas rojo-azuladas pequeñas, algunas ligeramente deprimidas, en la zona lumbar y pectoral.\n\nSe realizaron estudios complementarios:\n\n- Ecografía de los nódulos supraciliares y occipitales, que mostró características compatibles con neurofibromas nodulares subcutáneos (tumores benignos derivados de las células nerviosas).\n- Biopsias de las máculas rojo-azuladas del pecho y de la placa del muslo, cuyos resultados confirmaron la presencia de neurofibromas cutáneos.\n\n**Interpretación Clínica**\n\nEl diagnóstico se basó en la clasificación clínica propuesta por García-Martínez y colaboradores, identificando tres tipos de manifestaciones cutáneas en este paciente:\n\n1. Neurofibromas superficiales subcutáneos nodulares en la zona supraciliar derecha, occipital y muñeca derecha.\n2. Neurofibroma superficial cutáneo con aspecto pseudoatrófico (que simula una pérdida de tejido) en el muslo izquierdo.\n3. Neurofibromas superficiales cutáneos de color rojo-azulado en la zona lumbar y pectoral.\n\nEstos hallazgos son consistentes con la variedad de lesiones cutáneas que pueden presentarse en pacientes con NF1, reflejando la heterogeneidad clínica de la enfermedad.\n\n**Próximos Pasos**\n\nEl paciente debe continuar con seguimiento multidisciplinario, incluyendo dermatología, neurología y oftalmología, para monitorear la evolución de las lesiones cutáneas y detectar posibles complicaciones neurológicas o malignización de los neurofibromas. Además, es importante mantener el control de su desarrollo cognitivo y conductual, así como realizar evaluaciones periódicas mediante imágenes para descartar nuevas alteraciones. La educación y el apoyo psicosocial también son fundamentales para mejorar su calidad de vida.",
+        "score": {
+          "ROUGE-L-Sum": 0.1757469244288225,
+          "BERTScore_F": 0.7511939406394958
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.4634704325341592
+        }
+      }
+    }
+  },
+  {
+    "id": 39,
+    "gold_summary": "Preocupaciones de los pacientes:\nUn hombre de 38 años, previamente sano, fue admitido en nuestro hospital con una queja de disnea. Tenía un historial de haber sido golpeado en el pecho por un tornillo de alta velocidad mientras trabajaba en una fábrica 3 meses antes de ser admitido en el hospital.\n\nDiagnóstico:\nLuego de realizarse una angiografía coronaria y una ecocardiografía, finalmente se le diagnosticó un infarto de miocardio.\n\nIntervenciones:\nRecibió medicamentos optimizados, entre ellos, diuréticos, bloqueadores beta y estimulantes cardíacos.\n\nResultados:\nAl cabo de cuatro años de seguimiento, se le diagnosticó al paciente una insuficiencia cardíaca crónica con una fracción de eyección reducida.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Un hombre se lastimó el pecho con un tornillo grande. Tres meses después, le costaba mucho respirar. Los doctores le hicieron pruebas y vieron que su corazón estaba dañado. Le dieron medicinas para ayudar a su corazón a trabajar mejor. Cuatro años después, su corazón seguía un poco débil, pero los doctores siguen cuidándolo.",
+        "score": {
+          "ROUGE-L-Sum": 0.17679558011049726,
+          "BERTScore_F": 0.7433128952980042
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.4600542377042507
+        }
+      },
+      "B2": {
+        "text": "**Lo que le pasó al paciente**  \nUn hombre de 38 años, que estaba sano antes, sufrió un fuerte golpe en el pecho cuando un tornillo de alta velocidad lo alcanzó mientras trabajaba. Tres meses después, empezó a sentir dificultad para respirar y dolor en el pecho, por lo que fue llevado al hospital.\n\n**Qué encontraron los médicos**  \nDespués de hacerle varios exámenes, como una ecografía del corazón y una angiografía (que es una prueba para ver las arterias del corazón), descubrieron que había tenido un infarto de miocardio. Esto significa que una parte de su corazón no recibió suficiente sangre y se dañó.\n\n**Cómo lo trataron**  \nEl paciente recibió varios medicamentos para ayudar a su corazón a funcionar mejor. Entre ellos estaban diuréticos (que ayudan a eliminar el exceso de líquido), bloqueadores beta (que reducen la carga del corazón) y estimulantes cardíacos (que mejoran la fuerza del latido).\n\n**Qué pasó después**  \nDurante los siguientes cuatro años, los médicos lo siguieron controlando. Descubrieron que desarrolló insuficiencia cardíaca crónica, que es cuando el corazón no puede bombear sangre tan bien como antes. Esto se confirmó porque su fracción de eyección, que mide qué tan bien el corazón bombea, estaba baja.\n\nEn resumen, un golpe fuerte en el pecho causó daño en el corazón que llevó a un infarto y, con el tiempo, a problemas para que el corazón funcione correctamente. El paciente recibió tratamiento para mejorar su condición y sigue siendo monitoreado por los médicos.",
+        "score": {
+          "ROUGE-L-Sum": 0.3682864450127878,
+          "BERTScore_F": 0.8044003844261169
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5863434147194524
+        }
+      },
+      "B3": {
+        "text": "**Contexto:**  \nUn hombre de 38 años, previamente sano y sin factores de riesgo conocidos para enfermedad coronaria, sufrió un traumatismo torácico grave al ser impactado en el pecho por un tornillo de alta velocidad mientras trabajaba en una fábrica. Tras perder el conocimiento brevemente, fue atendido inicialmente en un hospital local donde se identificaron fracturas en el esternón y costillas, además de derrame pleural bilateral. Fue tratado con drenaje torácico y dado de alta sin realizar estudios cardíacos. Sin embargo, tres meses después, presentó síntomas persistentes como dolor y opresión en el pecho, dificultad para respirar al realizar esfuerzos y disnea nocturna, lo que motivó su ingreso en un hospital especializado para una evaluación más profunda.\n\n**Hallazgos Clave:**  \n- El examen físico reveló signos compatibles con derrame pleural residual en el pulmón derecho, pero sin alteraciones cardíacas evidentes a la auscultación.  \n- El electrocardiograma mostró alteraciones sugestivas de un infarto de miocardio antiguo en la región anterior del corazón, incluyendo inversión de ondas T y bloqueo de rama izquierda anterior.  \n- Los niveles de troponina (marcador de daño cardíaco agudo) fueron negativos, pero el NT-proBNP (marcador de insuficiencia cardíaca) estaba elevado, indicando estrés cardíaco.  \n- La ecocardiografía evidenció una función ventricular izquierda reducida (fracción de eyección del 32%), con adelgazamiento y disminución del movimiento en la pared anterior del ventrículo izquierdo y el tabique interventricular.  \n- La angiografía coronaria mostró una estenosis (estrechamiento) significativa del 70% en la arteria coronaria descendente anterior (LAD), confirmando la presencia de una lesión coronaria importante.  \n- No se encontraron signos de aterosclerosis en otras arterias principales, lo que sugiere que el infarto fue consecuencia directa del traumatismo torácico y no de enfermedad arterial previa.\n\n**Interpretación Clínica:**  \nEl paciente desarrolló un infarto de miocardio antiguo como complicación tardía del traumatismo torácico contundente. La lesión en la arteria coronaria descendente anterior, probablemente causada por el impacto, condujo a daño en el músculo cardíaco y a una reducción significativa de la función del ventrículo izquierdo. A pesar de la gravedad inicial, el paciente se mantuvo hemodinámicamente estable y respondió favorablemente a la terapia médica. Sin embargo, con el tiempo evolucionó hacia una insuficiencia cardíaca crónica con función ventricular reducida, condición que requiere manejo continuo y seguimiento.\n\n**Próximos Pasos y Manejo:**  \n- Se inició tratamiento médico optimizado que incluyó diuréticos para controlar la retención de líquidos, bloqueadores beta para reducir la carga cardíaca y mejorar la función, estatinas para protección vascular y estimulantes cardíacos.  \n- Posteriormente, el paciente se sometió a una intervención coronaria percutánea (ICP) para mejorar el flujo sanguíneo en la arteria afectada.  \n- Durante el seguimiento a largo plazo, se observó una mejoría parcial en la función cardíaca, aunque persistió una insuficiencia cardíaca leve a moderada.  \n- Se enfatizó la importancia de la adherencia estricta a la medicación para prevenir la progresión de la insuficiencia cardíaca y mejorar la calidad de vida.  \n- En controles posteriores, se mantuvo la función cardíaca reducida y síntomas leves de disnea tras esfuerzos, requiriendo ajuste y continuidad en el tratamiento farmacológico.\n\n**Resumen Final:**  \nEste caso ilustra cómo un traumatismo torácico severo puede ocasionar una lesión coronaria significativa que conduce a un infarto de miocardio y, eventualmente, a insuficiencia cardíaca crónica. La evaluación cuidadosa, el diagnóstico oportuno mediante imágenes cardíacas y la terapia médica adecuada son fundamentales para mejorar el pronóstico en estos pacientes. Además, la adherencia al tratamiento y el seguimiento a largo plazo son esenciales para controlar los síntomas y evitar complicaciones mayores.",
+        "score": {
+          "ROUGE-L-Sum": 0.2080624187256177,
+          "BERTScore_F": 0.7931231260299683
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.500592772377793
+        }
+      }
+    }
+  },
+  {
+    "id": 40,
+    "gold_summary": "Reportamos el caso de una neonata Han china de 0 días de vida que presentó trombocitopenia grave y hemorragia intracraneal, y que finalmente falleció por fallo multiorgánico e intracraneal el tercer día después del nacimiento. La secuenciación genética identificó una variante de cambio de marco heterocigótica, c.157_158del, dentro del gen MECOM. Esta variante condujo a una sustitución del 53.º aminoácido de metionina a glicina, terminando en el 54.º aminoácido. Una revisión exhaustiva de la literatura indicó que las mutaciones del gen MECOM incluían mutaciones sin sentido (68.3%), deleción (8.5%), sitio de empalme (8.5%), cambio de marco (7.3%) y sin sentido (7.3%). Las pacientes con mutaciones sin sentido frecuentemente presentaban sinostosis radiocubital, mientras que el fallo de la médula ósea se asociaba más comúnmente con los otros cuatro tipos de mutaciones.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Una bebé nació muy pequeñita y se puso muy enferma. Tenía problemas para que su sangre funcionara bien y sangraba en la cabeza. Los doctores buscaron en sus genes y encontraron un cambio que no estaba bien. Ese cambio hizo que su cuerpo no pudiera hacer una parte importante para estar sano. Por eso, la bebé se enfermó mucho y no pudo mejorar.",
+        "score": {
+          "ROUGE-L-Sum": 0.09174311926605505,
+          "BERTScore_F": 0.7084172964096069
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.400080207837831
+        }
+      },
+      "B2": {
+        "text": "**Caso de una recién nacida con un problema genético grave**\n\nPresentamos el caso de una bebé recién nacida de origen Han en China, que tenía un conteo muy bajo de plaquetas en la sangre, llamado trombocitopenia grave. Esto causó que tuviera sangrados dentro de su cabeza (hemorragia intracraneal). Lamentablemente, falleció al tercer día de vida debido a que varios órganos dejaron de funcionar correctamente.\n\n**Qué encontraron en sus genes**\n\nLos médicos analizaron el ADN de la bebé y encontraron un cambio en un gen llamado MECOM. Este cambio es una mutación que afecta cómo se produce una proteína importante. En concreto, la mutación cambió el aminoácido número 53 de metionina a glicina y provocó que la proteína se terminara de fabricar muy rápido, antes de tiempo. Esto afecta la función normal de la proteína.\n\n**Importancia de esta mutación**\n\nAl revisar otros casos en la literatura científica, se sabe que el gen MECOM puede tener diferentes tipos de mutaciones. La mayoría son mutaciones que detienen la producción normal de la proteína (llamadas mutaciones sin sentido), pero también hay otros tipos como deleciones o cambios en el marco de lectura del gen. Cada tipo de mutación puede causar distintos problemas. Por ejemplo, las mutaciones sin sentido suelen relacionarse con un problema en los huesos del brazo (sinostosis radiocubital), mientras que otras mutaciones, como la que tuvo esta bebé, están más asociadas con fallos en la médula ósea, que es donde se producen las células de la sangre.\n\n**Qué significa este caso**\n\nEste caso muestra cómo una mutación nueva en el gen MECOM puede causar una enfermedad muy grave desde el nacimiento. Entender estas mutaciones ayuda a los médicos a diagnosticar y estudiar mejor estas condiciones raras, aunque en este caso no fue posible salvar a la bebé.",
+        "score": {
+          "ROUGE-L-Sum": 0.27615062761506276,
+          "BERTScore_F": 0.8153815865516663
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5457661070833645
+        }
+      },
+      "B3": {
+        "text": "**Contexto del Caso**  \nSe trató de una recién nacida de origen Han, nacida a las 36 semanas de gestación mediante cesárea de urgencia debido a sufrimiento fetal. Al nacer, presentó signos graves como palidez, sangrado en mucosas, equimosis (moretones) dispersos y dificultad respiratoria que requirió ventilación mecánica. Los análisis iniciales mostraron anemia severa, trombocitopenia (bajo recuento de plaquetas) y leucopenia (bajo recuento de glóbulos blancos). Durante su ingreso en la unidad de cuidados intensivos neonatales, se diagnosticó coagulación intravascular diseminada (una alteración grave de la coagulación sanguínea) y hemorragias múltiples, incluyendo una hemorragia intracraneal masiva. A pesar de tratamientos intensivos, la paciente falleció al tercer día de vida por falla multiorgánica y hemorragia cerebral.\n\n**Hallazgos Genéticos**  \nSe realizó un estudio genético mediante secuenciación Sanger para identificar la causa subyacente de su enfermedad. Se detectó una mutación nueva y heterocigótica (presente en una sola copia del gen) en el gen MECOM, específicamente una deleción de dos nucleótidos (c.157_158del) que provocó un cambio en el marco de lectura del gen (mutación de cambio de marco). Esta alteración causó que el aminoácido número 53, metionina, fuera sustituido por glicina, seguida de una terminación prematura en la síntesis proteica, lo que probablemente afecta gravemente la función de la proteína MECOM. Esta mutación no se encontró en los padres ni en el hermano mayor, indicando que fue una mutación de novo (nueva en la paciente). Además, el residuo afectado está altamente conservado en mamíferos, lo que sugiere su importancia funcional.\n\n**Interpretación Clínica y Revisión Bibliográfica**  \nEl gen MECOM está implicado en la regulación del desarrollo de la médula ósea y la formación de células sanguíneas. Mutaciones en este gen se han asociado con síndromes que incluyen fallo medular y anomalías óseas. Una revisión exhaustiva de la literatura mostró que las mutaciones en MECOM pueden ser de varios tipos: mutaciones sin sentido (que generan una proteína truncada), deleciones, alteraciones en sitios de empalme (que afectan el procesamiento del ARN), cambios de marco y otras mutaciones sin sentido. Se observó que las mutaciones sin sentido se relacionan frecuentemente con sinostosis radiocubital (fusión anormal de huesos del antebrazo), mientras que el fallo de la médula ósea es más común en los otros tipos de mutaciones, incluyendo la de cambio de marco que presentó esta paciente.\n\n**Conclusiones y Relevancia**  \nEste caso ilustra la gravedad clínica que puede tener una mutación de novo en el gen MECOM, manifestada por una trombocitopenia severa, hemorragias masivas y fallo multiorgánico en un recién nacido. La identificación precisa de la mutación permitió confirmar el diagnóstico genético y ampliar el conocimiento sobre la diversidad de mutaciones en MECOM y sus manifestaciones clínicas. Este hallazgo es importante para el diagnóstico prenatal y el asesoramiento genético en familias con antecedentes similares.",
+        "score": {
+          "ROUGE-L-Sum": 0.2563338301043219,
+          "BERTScore_F": 0.8046420812606812
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.5304879556825015
+        }
+      }
+    }
+  },
+  {
+    "id": 41,
+    "gold_summary": "Esta señora de 74 años padecía tendinopatía insercional de Aquiles. Después del tratamiento con una inyección local de cortisona, sufrió una rotura total del tendón de Aquiles insercional. Esta rotura se trató de forma conservadora y, después del tratamiento, el tendón de Aquiles volvió a romperse en la zona de inserción. La rotura se trató entonces con reinserción en la zona de inserción calcánea. Al poco tiempo del postoperatorio, la paciente sufrió una infección de herida quirúrgica profunda y sepsis. Debido al pobre efecto del tratamiento con antibióticos y a la destrucción total del tendón, se extirpó todo el tendón de Aquiles. Después de la extirpación, se inmovilizó en un yeso, seguido de movilización y aumento gradual de la carga. En un seguimiento de un año, la paciente caminaba sin cojera, podía levantar el talón hasta la mitad mientras estaba de pie sobre una pierna, había un tendón de Aquiles palpable y el escaneado por ultrasonido mostró una estructura muy similar a un tendón de Aquiles tendinopático y ligeramente engrosado. Había una regeneración evidente de todo el tendón de Aquiles y la función del tendón era sorprendentemente buena.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Había una señora de 74 años con un problema en el hueso del talón y el hueso del muslo. Se lastimó el hueso del muslo cerca del talón después de una inyección. Primero, usó una bota especial para sanar. Pero se volvió a lastimar el mismo hueso. Entonces, los doctores hicieron una operación para arreglarlo. Después, tuvo una infección que no se quitaba con medicina. Por eso, los doctores tuvieron que quitar todo el hueso del muslo que estaba lastimado. Luego, la señora usó un yeso para que su pie sanara. Poco a poco, pudo mover el pie y caminar sin dolor. Un año después, su hueso del muslo estaba casi como nuevo y ella podía caminar bien y levantar el talón.",
+        "score": {
+          "ROUGE-L-Sum": 0.2116991643454039,
+          "BERTScore_F": 0.7721360325813293
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.49191759846336663
+        }
+      },
+      "B2": {
+        "text": "**Lo que le Pasó a la Paciente**  \nUna mujer de 74 años tenía un problema llamado tendinopatía insercional de Aquiles. Esto significa que el tendón de Aquiles, que conecta el músculo de la pantorrilla con el hueso del talón, estaba dañado cerca de donde se une al hueso. Para tratarlo, le pusieron una inyección de cortisona, que es un medicamento para reducir la inflamación. Sin embargo, después de esto, el tendón se rompió completamente en esa zona.\n\n**Tratamientos y Complicaciones**  \nPrimero intentaron curar la rotura sin cirugía, usando una bota especial para inmovilizar el pie. Pero luego, el tendón se rompió otra vez. Esta vez, hicieron una operación para volver a unir el tendón al hueso usando anclajes, que son pequeños dispositivos para sujetar el tendón. Poco después de la cirugía, la paciente tuvo una infección grave en la herida que no mejoró con antibióticos y causó sepsis, una infección que afecta todo el cuerpo.\n\n**Cirugía y Recuperación**  \nDurante otra operación para tratar la infección, los médicos vieron que el tendón estaba muy dañado y tuvieron que quitarlo completamente, dejando una gran herida. La piel se cerró sobre esa zona y la paciente usó un yeso para inmovilizar el pie durante varias semanas. También recibió antibióticos para curar la infección. Luego, poco a poco, empezó a mover el pie y a cargar peso al caminar, pero evitando estirar demasiado el tendón.\n\n**Resultados Después de un Año**  \nUn año después, la paciente podía caminar sin cojear y levantar el talón mientras estaba de pie sobre una pierna, lo que muestra que el tendón funcionaba bien. Un examen con ultrasonido, que es una imagen que muestra los tejidos, mostró que el tendón de Aquiles había crecido de nuevo y parecía casi normal, aunque un poco engrosado y con signos de daño leve. Esto indica que el tendón se regeneró sorprendentemente bien y que la función del pie mejoró mucho, a pesar de que el tendón original fue removido.",
+        "score": {
+          "ROUGE-L-Sum": 0.3394957983193278,
+          "BERTScore_F": 0.8189494013786316
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5792225998489797
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nLa paciente es una mujer de 74 años, físicamente activa, que desarrolló una tendinopatía insercional del tendón de Aquiles (una lesión en la zona donde el tendón se une al hueso del talón). Tras recibir una inyección local de cortisona para tratar esta lesión, sufrió una rotura completa del tendón en la zona de inserción. Inicialmente, esta rotura se manejó con tratamiento conservador, pero posteriormente el tendón volvió a romperse en el mismo lugar. Esta segunda rotura se trató mediante cirugía para reinsertar el tendón en el hueso del talón.\n\n**Hallazgos Clave**  \nPoco después de la cirugía, la paciente desarrolló una infección profunda en la herida quirúrgica que evolucionó a sepsis (una infección grave que afecta a todo el organismo). Debido a que los antibióticos no controlaron la infección y el tendón estaba gravemente dañado, fue necesario extirpar completamente el tendón de Aquiles distal (aproximadamente 7 cm). Tras la extirpación, la herida se cerró y la paciente fue inmovilizada con yesos durante varios meses, con un protocolo gradual para permitir la recuperación y evitar movimientos que pudieran dañar la zona.\n\n**Interpretación Clínica**  \nA pesar de la pérdida total del tendón de Aquiles, la paciente mostró una recuperación funcional sorprendentemente buena. Un año después, caminaba sin cojera, podía levantar el talón mientras se apoyaba sobre una pierna y se palpaba un tendón en la zona afectada. El ultrasonido reveló que el tendón había regenerado una estructura similar a un tendón de Aquiles, aunque con signos leves de tendinopatía (engrosamiento y alteraciones en la textura). Esto indica que, incluso tras la extirpación completa del tendón, el organismo fue capaz de formar un nuevo tejido tendinoso funcional.\n\n**Próximos Pasos**  \nSe ofreció a la paciente la opción de una reconstrucción quirúrgica con un injerto de otro tendón (flexor hallucis longus) para mejorar aún más la función, pero ella decidió esperar debido a la buena recuperación que presentaba. Se recomienda continuar con seguimiento clínico y funcional para monitorizar la evolución, especialmente considerando que la regeneración espontánea del tendón de Aquiles es poco común y puede ofrecer información valiosa para futuros tratamientos.",
+        "score": {
+          "ROUGE-L-Sum": 0.3783783783783783,
+          "BERTScore_F": 0.8590501546859741
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.6187142665321762
+        }
+      }
+    }
+  },
+  {
+    "id": 42,
+    "gold_summary": "Describimos el caso de una mujer de 47 años con antecedentes de dolor en el cuello izquierdo y en el oído, acompañado por una masa en el cuello que había ido aumentando gradualmente durante 2,5 años. Después de las evaluaciones iniciales y de múltiples diagnósticos diferenciales, la angiografía por TC reveló una masa ovalada de 30 × 50 mm en la bifurcación carotídea izquierda, lo que confirmó un CCT tipo II de Shamblin. Las evaluaciones preoperatorias demostraron CHB congénita en el electrocardiograma y la ecocardiografía. La paciente se sometió a una resección completa del tumor con todas las precauciones necesarias, incluida la colocación temporal de un marcapasos y un cuidadoso seguimiento.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Había una señora con dolor en su cuello y oído. Tenía una bolita en el cuello que creció poco a poco. Los doctores hicieron muchas pruebas y vieron la bolita en su cuello con una máquina especial. La bolita estaba cerca de unos tubos importantes del cuello. \n\nAntes de la operación, los doctores revisaron su corazón y vieron que tenía un problema que nació con ella. Para la operación, usaron un aparato para ayudar a su corazón a latir bien. Los doctores sacaron la bolita con mucho cuidado. Después, la señora se sintió mejor y no le dolió más.",
+        "score": {
+          "ROUGE-L-Sum": 0.23529411764705882,
+          "BERTScore_F": 0.7503740191459656
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.4928340683965122
+        }
+      },
+      "B2": {
+        "text": "**Lo que le pasó a la paciente**  \nUna mujer de 47 años tenía dolor en el lado izquierdo del cuello y en el oído izquierdo. También notó una bolita (masa) en el cuello que fue creciendo poco a poco durante más de dos años. Al principio, pensaron que tenía una infección en el oído, pero el dolor no mejoró con el tratamiento.\n\n**Lo que encontraron los médicos**  \nDespués de hacer varios estudios, usaron una tomografía computarizada (una especie de radiografía especial) para ver mejor el cuello. Descubrieron una masa ovalada de 3 por 5 centímetros en un lugar donde una arteria importante del cuello se divide. Esto confirmó que tenía un tumor llamado paraganglioma carotídeo, que es un tumor raro que crece cerca de las arterias del cuello.\n\nAdemás, al revisar su corazón, encontraron que tenía un bloqueo cardíaco congénito, que significa que su corazón late más lento de lo normal desde que nació. Por eso, antes de la cirugía, hicieron varios exámenes para asegurarse de que su corazón estaba estable.\n\n**Cómo la operaron y qué cuidados tuvieron**  \nPara quitar el tumor, los médicos planearon la cirugía con mucho cuidado. Le pusieron un marcapasos temporal, que es un dispositivo que ayuda a controlar el ritmo del corazón durante la operación. También usaron anestesia especial para que no tuviera problemas con la presión o el ritmo cardíaco.\n\nDurante la cirugía, hicieron una incisión en el cuello para llegar al tumor. Usaron pinzas para controlar el sangrado y monitorearon los nervios importantes para evitar dañarlos. El tumor fue separado cuidadosamente de las arterias y nervios cercanos. La operación duró poco más de dos horas y no hubo complicaciones graves.\n\n**Después de la cirugía y resultados**  \nLa paciente estuvo en cuidados intensivos un día para vigilar su estado. El marcapasos temporal se retiró al día siguiente porque su corazón mantenía un ritmo estable. Fue dada de alta tres días después, sin dolor ni problemas.\n\nEn los controles posteriores, los médicos vieron que el tumor no había vuelto a aparecer y que su corazón seguía funcionando bien. Además, el análisis mostró que la función de un nervio llamado nervio vago mejoró después de quitar el tumor, lo que ayudó a que su sistema nervioso autónomo trabajara mejor. La paciente también dijo que el dolor en el cuello y oído desapareció completamente.\n\n**Qué significa este caso**  \nEste caso muestra la importancia de hacer un diagnóstico correcto cuando hay dolor persistente y masas en el cuello. También destaca cómo los médicos deben planear cuidadosamente la cirugía en pacientes con problemas cardíacos para evitar riesgos. La operación fue exitosa y mejoró la calidad de vida de la paciente.",
+        "score": {
+          "ROUGE-L-Sum": 0.21202531645569622,
+          "BERTScore_F": 0.7772389054298401
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.49463211094276816
+        }
+      },
+      "B3": {
+        "text": "**Contexto del Caso**  \nSe presenta el caso de una mujer de 47 años que experimentaba dolor en el lado izquierdo del cuello y en el oído izquierdo, acompañado por la presencia de una masa en el mismo lado del cuello. Esta masa había sido detectada aproximadamente 30 meses antes y había ido aumentando de tamaño de forma progresiva. Inicialmente, el dolor se atribuyó a una infección del oído medio (otitis media), pero ante la persistencia de los síntomas, se realizaron estudios de imagen que identificaron una masa en la bifurcación de la arteria carótida izquierda.\n\n**Hallazgos Clave**  \nLa angiografía por tomografía computarizada (TC) mostró una masa ovalada de 30 × 50 mm ubicada en la bifurcación carotídea izquierda, característica de un tumor del cuerpo carotídeo (TCC) clasificado como tipo II según Shamblin, lo que indica un compromiso parcial de las arterias carótidas. Además, las evaluaciones cardiovasculares preoperatorias confirmaron que la paciente tenía un bloqueo auriculoventricular completo congénito (CHB), detectado mediante electrocardiograma (ECG) y corroborado por ecocardiografía, que mostró función ventricular normal sin anomalías estructurales.\n\n**Interpretación Clínica y Manejo**  \nDado el diagnóstico de TCC y la condición cardíaca de la paciente, se diseñó un plan quirúrgico y anestésico cuidadoso para minimizar riesgos. Se colocó un marcapasos temporal externo para mantener un ritmo cardíaco estable durante la cirugía y se monitorizó de forma continua la presión arterial y otros parámetros vitales. La cirugía se realizó mediante un abordaje abierto, con una incisión paralela al músculo esternocleidomastoideo para exponer la bifurcación carotídea y permitir la disección cuidadosa del tumor, preservando nervios importantes como el vago e hipogloso mediante neuromonitorización intraoperatoria.\n\nDurante la intervención, se aplicaron pinzas vasculares para controlar el flujo sanguíneo y evitar hemorragias, y se mantuvo una comunicación estrecha entre los equipos quirúrgico y anestésico para manejar cualquier cambio hemodinámico. La cirugía se completó exitosamente en poco más de dos horas, con sangrado mínimo y sin complicaciones inmediatas.\n\n**Próximos Pasos y Resultados a Largo Plazo**  \nDespués de la operación, la paciente fue vigilada en la unidad de cuidados intensivos y luego trasladada a planta general. El marcapasos temporal se retiró al día siguiente, ya que el ritmo cardíaco se mantuvo estable. La paciente fue dada de alta en buenas condiciones al tercer día postoperatorio, sin dolor ni otros síntomas. El examen histopatológico confirmó el diagnóstico de tumor del cuerpo carotídeo.\n\nEn el seguimiento a corto y largo plazo, que incluyó evaluaciones clínicas, electrocardiogramas y ecocardiografías, se observó que la función cardíaca permaneció estable y que el bloqueo cardíaco congénito no empeoró. Además, un análisis de la variabilidad de la frecuencia cardíaca mostró una mejora significativa en la actividad parasimpática después de la cirugía, lo que sugiere que la extirpación del tumor alivió la compresión del nervio vago y restauró la función autónoma normal. Los estudios de imagen realizados a los 6 meses y un año no evidenciaron recurrencia tumoral ni complicaciones vasculares. La paciente reportó la desaparición completa del dolor en cuello y oído, sin reaparición de síntomas durante el seguimiento.\n\nEn resumen, este caso ilustra la importancia de un diagnóstico preciso y un manejo multidisciplinario cuidadoso en pacientes con tumores carotídeos y condiciones cardíacas preexistentes, logrando una resección segura y resultados clínicos favorables a largo plazo.",
+        "score": {
+          "ROUGE-L-Sum": 0.2323097463284379,
+          "BERTScore_F": 0.8265654444694519
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.5294375953989449
+        }
+      }
+    }
+  },
+  {
+    "id": 43,
+    "gold_summary": "Reportamos el caso de una mujer de 19 años que presentó feocromocitoma sin experimentar una crisis, a pesar de tener una masa suprarrenal significativa y someterse a un tratamiento glucocorticoide de alta dosis. Las pruebas genéticas revelaron una mutación de sentido erróneo heterocigótica en el gen RET (c.1900T > C: p. Cys634Arg), asociada con MEN2A. La evaluación endocrina adicional identificó un nódulo tiroideo con niveles de calcitonina levemente elevados, pero niveles normales de electrolitos y hormona paratiroidea. Durante un seguimiento postoperatorio de 15 meses, la paciente exhibió hipercalcitonemia persistente leve con tamaño de nódulo tiroideo estable, mientras que la PTH y los niveles de calcio sérico mostraron un aumento progresivo. Se realizó una gammagrafía paratiroidea adicional utilizando 99mTc-MIBI, que arrojó un resultado negativo para el adenoma paratiroideo.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Había una chica de 19 años que tenía un bulto en una parte de su cuerpo llamada glándula suprarrenal. Este bulto no le causó un problema muy grande de repente. Los doctores le hicieron un examen especial y encontraron un cambio en sus genes. Este cambio puede causar problemas en algunas partes del cuerpo que hacen hormonas.\n\nTambién encontraron un pequeño bulto en su cuello, en una parte llamada tiroides. Ella tenía un poco más de una sustancia llamada calcitonina, pero otras cosas en su cuerpo estaban normales. Después de que le sacaron el bulto del cuerpo, los doctores la cuidaron por mucho tiempo. Vieron que la calcitonina seguía un poco alta y que otras cosas en su sangre subían poco a poco. Hicieron otro examen para buscar otro bulto, pero no encontraron nada malo. Los doctores siguen cuidándola para que esté bien.",
+        "score": {
+          "ROUGE-L-Sum": 0.17006802721088435,
+          "BERTScore_F": 0.7504714131355286
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.46026972017320644
+        }
+      },
+      "B2": {
+        "text": "**Caso de una joven con tumor suprarrenal y mutación genética**\n\nUna mujer de 19 años llegó al hospital con dolor de cabeza, náuseas, vómitos y fiebre. Tenía la presión arterial muy alta y signos de inflamación en su cuerpo. Los médicos encontraron una masa (un bulto) en su glándula suprarrenal izquierda, que está encima del riñón y produce hormonas importantes. Esta masa causaba que su cuerpo liberara muchas sustancias llamadas catecolaminas, que pueden subir mucho la presión arterial.\n\nSe hizo un análisis genético y descubrieron que tenía un cambio en un gen llamado RET. Este cambio puede causar un síndrome llamado MEN2A, que hace que se formen tumores en varias glándulas del cuerpo. Por eso, también revisaron su tiroides y encontraron un pequeño nódulo (una bolita) con niveles un poco altos de calcitonina, una hormona relacionada con la tiroides.\n\nDespués de tratarla con medicamentos para controlar su presión y frecuencia cardíaca, la paciente se sometió a una cirugía para quitar la masa suprarrenal. El examen del tumor confirmó que era un feocromocitoma, un tipo de tumor que produce muchas hormonas. Tras la operación, la paciente mejoró y no tuvo más síntomas.\n\nDurante los siguientes 15 meses, los médicos siguieron revisando su tiroides y sus niveles de calcio en sangre. Aunque el nódulo en la tiroides no creció, los niveles de calcitonina y calcio en sangre aumentaron un poco, lo que puede indicar cambios en las glándulas paratiroides, que ayudan a controlar el calcio en el cuerpo. Sin embargo, una prueba especial llamada gammagrafía no mostró tumores en esas glándulas.\n\n**¿Qué significa esto?**\n\nEste caso muestra cómo un tumor en la glándula suprarrenal puede causar problemas graves, pero también cómo una mutación genética puede afectar varias glándulas del cuerpo. Es importante hacer un seguimiento cuidadoso para detectar y tratar cualquier cambio en otras glándulas, como la tiroides o las paratiroides, que pueden estar relacionadas con esta mutación.",
+        "score": {
+          "ROUGE-L-Sum": 0.19758064516129034,
+          "BERTScore_F": 0.7905486822128296
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.49406466368706
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nPresentamos el caso de una mujer joven de 19 años que acudió al hospital con síntomas de cefalea, náuseas, vómitos y fiebre, acompañados de hipertensión severa y taquicardia. Durante la evaluación, se detectó incidentalmente una masa en la glándula suprarrenal izquierda. Los análisis de sangre y orina mostraron niveles muy elevados de catecolaminas (sustancias químicas producidas por la médula suprarrenal), lo que sugirió la presencia de un feocromocitoma, un tumor poco común que produce estas hormonas y puede causar hipertensión y otros síntomas.\n\n**Hallazgos Clave**  \n- La paciente tenía una masa suprarrenal de aproximadamente 4 cm detectada por tomografía computarizada.  \n- Los niveles plasmáticos y urinarios de catecolaminas y sus metabolitos estaban marcadamente elevados, confirmando la sospecha de feocromocitoma.  \n- Se identificó una mutación genética heterocigótica en el gen RET (c.1900T > C: p. Cys634Arg), conocida por estar asociada con el síndrome de neoplasia endocrina múltiple tipo 2A (MEN2A), una condición que predispone a tumores endocrinos múltiples.  \n- La evaluación adicional mostró un pequeño nódulo en la glándula tiroides con leves elevaciones en los niveles de calcitonina, una hormona que puede indicar la presencia de carcinoma medular de tiroides, común en MEN2A.  \n- Durante el seguimiento postoperatorio de 15 meses, la paciente mantuvo niveles ligeramente elevados de calcitonina y un nódulo tiroideo estable, pero los niveles de hormona paratiroidea (PTH) y calcio en sangre aumentaron progresivamente.  \n- Una gammagrafía paratiroidea con 99mTc-MIBI no mostró evidencia de adenoma paratiroideo (tumor benigno de la glándula paratiroides).\n\n**Interpretación Clínica**  \nEste caso destaca la presentación atípica de un feocromocitoma sin crisis hipertensiva grave, a pesar de la masa suprarrenal significativa y el uso de glucocorticoides de alta dosis, que normalmente podrían desencadenar una crisis. La mutación en el gen RET confirma la asociación con MEN2A, un síndrome que requiere vigilancia cuidadosa por el riesgo de tumores endocrinos múltiples, incluyendo carcinoma medular de tiroides y alteraciones paratiroideas. La persistencia de hipercalcitoninemia y el aumento progresivo de PTH y calcio sugieren la necesidad de un seguimiento continuo para detectar posibles complicaciones o desarrollo de hiperparatiroidismo.\n\n**Próximos Pasos**  \n- Continuar con el seguimiento endocrinológico regular para monitorizar el nódulo tiroideo y los niveles hormonales, especialmente calcitonina, PTH y calcio sérico.  \n- Realizar evaluaciones periódicas para detectar signos tempranos de carcinoma medular de tiroides o hiperparatiroidismo.  \n- Considerar intervenciones quirúrgicas o terapéuticas adicionales si se evidencian cambios significativos en el nódulo tiroideo o en la función paratiroidea.  \n- Mantener un control estricto de la presión arterial y la función cardiaca, dado el antecedente de feocromocitoma y miocarditis.  \n- Brindar asesoramiento genético y seguimiento familiar, dado el componente hereditario asociado a la mutación RET y el antecedente de muerte súbita en el padre.\n\nEste caso subraya la importancia de una evaluación multidisciplinaria y un seguimiento prolongado en pacientes jóvenes con feocromocitoma y mutaciones genéticas relacionadas con síndromes endocrinos múltiples.",
+        "score": {
+          "ROUGE-L-Sum": 0.293939393939394,
+          "BERTScore_F": 0.8221704959869385
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5580549449631662
+        }
+      }
+    }
+  },
+  {
+    "id": 44,
+    "gold_summary": "Presentamos el caso de una refugiada de 39 años, no diabética y no hipertensa, que inicialmente presentó insuficiencia cardiaca debido a anemia, por lo que recibió transfusiones de sangre. Más adelante, al ingresar, desarrolló convulsiones múltiples focales bilaterales, irritabilidad severa, afasia y hemiplejía derecha, lo que motivó su ingreso a la UCI. Un examen y un historial médico repetidos revelaron una mancha de vino de Oporto ocular izquierda leve que inicialmente pasó desapercibida y un historial remoto de convulsiones no provocadas 20 años atrás. Las imágenes revelaron calcificaciones parietales y confirmaron el diagnóstico de SWS. Por lo tanto, se adoptó un enfoque multidisciplinario para comprender plenamente el diagnóstico de la paciente y determinar una estrategia de tratamiento, que incluyó consultas con los departamentos de neurología, oftalmología, otorrinolaringología y fisioterapia. Se logró un control exitoso de las convulsiones mediante la administración de fenitoína IV durante 3 días y el aumento gradual de la carbamazepina oral a 1 g diario a través de una sonda nasogástrica. Lamentablemente, debido a la falta de personal o recursos, no se pudieron realizar otras evaluaciones importantes para pacientes con SWS, como evaluaciones avanzadas de neuroimagen, psiquiátricas, de cirugía plástica y neurocirugía, así como revisiones dentales.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Había una señora que estaba muy cansada y con el cuerpo hinchado. Ella tenía una manchita roja en la cara desde que nació. También tuvo muchos ataques donde se movía sin querer. Los doctores vieron que tenía un problema en el cerebro y en la cara. Le dieron medicinas para que los ataques pararan. Muchos doctores la ayudaron para que se sintiera mejor. A veces, no pudieron hacer todas las pruebas porque faltaban cosas en el hospital. Pero todos cuidaron mucho de ella para que estuviera tranquila.",
+        "score": {
+          "ROUGE-L-Sum": 0.11428571428571428,
+          "BERTScore_F": 0.7266535758972168
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.42046964509146556
+        }
+      },
+      "B2": {
+        "text": "**Caso de una mujer con Síndrome de Sturge-Weber (SWS)**\n\nPresentamos la historia de una mujer de 39 años que llegó al hospital con problemas de salud graves. Al principio, tenía insuficiencia cardíaca causada por anemia, que es cuando hay pocas células rojas en la sangre. Por eso, le dieron transfusiones de sangre para mejorar su condición.\n\nDespués, comenzó a tener varias convulsiones, que son movimientos involuntarios del cuerpo causados por actividad anormal en el cerebro. También mostró irritabilidad, dificultad para hablar (afasia) y debilidad en el lado derecho del cuerpo (hemiplejía). Debido a esto, fue ingresada en la unidad de cuidados intensivos (UCI) para recibir atención especial.\n\nAl revisar su historia médica y hacer un examen más detallado, los médicos notaron una mancha roja en el ojo izquierdo llamada mancha de vino de Oporto. Esta mancha estaba presente desde su nacimiento, pero no se había detectado antes. Además, la paciente había tenido convulsiones hace 20 años, aunque no se había tratado formalmente.\n\nUna tomografía computarizada (una imagen del cerebro) mostró calcificaciones en una parte del cerebro llamada área parietal. Estos hallazgos ayudaron a confirmar que la paciente tenía Síndrome de Sturge-Weber (SWS), una enfermedad rara que afecta la piel, el cerebro y a veces los ojos.\n\nPara tratarla, un equipo de diferentes especialistas trabajó junto: neurólogos (que cuidan del cerebro), oftalmólogos (que cuidan los ojos), otorrinolaringólogos (que cuidan oídos y garganta) y fisioterapeutas (que ayudan con la movilidad). Las convulsiones se controlaron con medicamentos llamados fenitoína y carbamazepina, administrados por vía intravenosa y a través de un tubo en la nariz.\n\nSin embargo, debido a la falta de personal y recursos en el hospital, no se pudieron hacer otros estudios importantes para pacientes con SWS, como imágenes más detalladas del cerebro, evaluaciones psicológicas, consultas para cirugía plástica o neurocirugía, ni revisiones dentales.\n\nEste caso muestra la importancia de un diagnóstico cuidadoso y un tratamiento multidisciplinario para manejar enfermedades complejas como el Síndrome de Sturge-Weber.",
+        "score": {
+          "ROUGE-L-Sum": 0.3247863247863248,
+          "BERTScore_F": 0.8080716729164124
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5664289988513685
+        }
+      },
+      "B3": {
+        "text": "**Contexto del Caso**  \nSe trata de una mujer refugiada de 39 años, embarazada, sin antecedentes de diabetes o hipertensión, que acudió al hospital con síntomas iniciales de insuficiencia cardíaca secundaria a anemia severa. Inicialmente recibió transfusiones sanguíneas para tratar esta condición. Sin embargo, durante su hospitalización, desarrolló múltiples convulsiones focales que se extendieron a ambos hemisferios cerebrales, acompañadas de irritabilidad intensa, dificultad para hablar (afasia) y parálisis parcial en el lado derecho del cuerpo (hemiplejía). Estos signos neurológicos graves motivaron su ingreso a la unidad de cuidados intensivos (UCI).\n\n**Hallazgos Clave**  \nUna revisión detallada de su historia clínica, junto con un examen físico repetido, reveló la presencia de una mancha de vino de Oporto (una lesión vascular congénita de color rojo púrpura) en la región ocular izquierda, que inicialmente no se había detectado. Además, se confirmó un antecedente remoto de convulsiones no provocadas ocurridas hace aproximadamente 20 años, que no había sido reportado inicialmente. La tomografía computarizada del cerebro mostró calcificaciones en la región parietal izquierda, hallazgo característico que, junto con la mancha cutánea y el cuadro clínico, permitió establecer el diagnóstico de síndrome de Sturge-Weber (SWS), una enfermedad neurocutánea rara que afecta vasos sanguíneos del cerebro y la piel.\n\n**Interpretación Clínica**  \nEl síndrome de Sturge-Weber se caracteriza por la presencia de malformaciones vasculares en la piel y el cerebro, que pueden provocar convulsiones, déficits neurológicos y problemas oftalmológicos. En este caso, la combinación de convulsiones recurrentes, hemiplejía, afasia y la mancha facial típica apoyaron el diagnóstico. La anemia y la insuficiencia cardíaca iniciales complicaron el cuadro clínico, pero el manejo neurológico fue prioritario tras la aparición de las convulsiones y el deterioro neurológico.\n\n**Estrategia de Tratamiento y Manejo Multidisciplinario**  \nSe implementó un enfoque integral que involucró a varios especialistas: neurología para el control de las convulsiones, oftalmología para evaluar posibles complicaciones oculares como el glaucoma (aunque la paciente estaba muy irritable y dificultó el examen), otorrinolaringología y fisioterapia para abordar las secuelas neurológicas. El control de las convulsiones se logró con éxito mediante la administración intravenosa de fenitoína durante tres días, seguida de un aumento progresivo de la dosis de carbamazepina oral hasta 1000 mg diarios, administrada a través de una sonda nasogástrica debido al estado de coma profundo de la paciente.\n\n**Limitaciones y Próximos Pasos**  \nDebido a limitaciones en recursos humanos y técnicos en el hospital, no fue posible realizar evaluaciones adicionales importantes para pacientes con SWS, como estudios avanzados de neuroimagen, evaluaciones psiquiátricas, consultas de cirugía plástica y neurocirugía, ni revisiones dentales, que suelen ser necesarias para un manejo completo de esta enfermedad. Se recomienda continuar con un seguimiento multidisciplinario para optimizar el tratamiento y mejorar la calidad de vida de la paciente.",
+        "score": {
+          "ROUGE-L-Sum": 0.3551912568306011,
+          "BERTScore_F": 0.8162996172904968
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5857454370605489
+        }
+      }
+    }
+  },
+  {
+    "id": 45,
+    "gold_summary": "Una paciente de 69 años de edad se presentó en la clínica quejándose de una pérdida progresiva de la visión. La evaluación oftálmica fue notable para una mejor agudeza visual corregida de contar los dedos a 5' en el ojo derecho y 3' en el ojo izquierdo. Las imágenes revelaron una atrofia profunda y extensa de la mácula central, una hiperplasia del pigmento epitelial y otras áreas de atrofia multifocal en el ojo derecho. Además, las imágenes de autofluorescencia del fondo de la mácula mostraron una hipoautofluorescencia central con expansión bilateral a la periferia en ambos ojos. Un electrorretinograma de campo completo mostró una respuesta normal de los bastones, con una respuesta disminuida de los conos, bilateralmente. Las pruebas genéticas fueron positivas para una mutación inotrópica homocigótica en el gen ABCA4 de la variante c.5714+5G>A.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Una señora de 69 años veía cada vez menos con sus ojos. El doctor le hizo muchas pruebas para mirar sus ojos. Vio que la parte del ojo que ayuda a ver bien estaba muy dañada. También encontró que algunas partes del ojo no funcionaban bien. El doctor hizo un examen especial y vio que unas células del ojo estaban normales y otras no. Luego, hicieron un examen de su sangre y encontraron un cambio en un gen que puede causar problemas en la vista.",
+        "score": {
+          "ROUGE-L-Sum": 0.1707317073170732,
+          "BERTScore_F": 0.732230007648468
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.4514808574827706
+        }
+      },
+      "B2": {
+        "text": "**Lo que le pasaba a la paciente**  \nUna mujer de 69 años empezó a perder la vista poco a poco. Cuando la examinaron, pudo ver solo lo suficiente para contar los dedos a una distancia muy corta: 5 pies en un ojo y 3 pies en el otro. Esto muestra que su visión estaba bastante afectada.\n\n**Qué encontraron en sus ojos**  \nAl mirar dentro de sus ojos con imágenes especiales, los médicos vieron que la parte central de la retina llamada mácula estaba muy dañada. Había zonas donde las células que ayudan a la vista estaban muertas o muy débiles. También notaron un aumento anormal de unas células llamadas pigmento epitelial. Las imágenes que muestran la luz que emite la retina (autofluorescencia) indicaron que la parte central de la mácula tenía menos luz de lo normal, lo que significa daño, y este daño se extendía hacia los lados en ambos ojos.\n\n**Cómo funcionaban sus células de la vista**  \nSe hizo un examen llamado electrorretinograma, que mide la actividad eléctrica de las células de la retina. Los resultados mostraron que las células llamadas bastones, que ayudan a ver en la oscuridad, funcionaban bien. Pero las células llamadas conos, que permiten ver colores y detalles, estaban debilitadas en ambos ojos.\n\n**Qué encontraron en sus genes**  \nAl analizar su ADN, descubrieron que tenía una mutación específica en un gen llamado ABCA4. Este gen es importante para la salud de la retina. La mutación encontrada puede causar problemas en la función de las células de la retina y explicar la pérdida de visión de la paciente.\n\n**En resumen**  \nLa paciente tiene una enfermedad llamada STGD1, que afecta la mácula y causa pérdida progresiva de la visión. Los exámenes clínicos y genéticos ayudaron a confirmar este diagnóstico.",
+        "score": {
+          "ROUGE-L-Sum": 0.2721649484536083,
+          "BERTScore_F": 0.7790645956993103
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.5256147720764592
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nUna mujer de 69 años acudió a consulta debido a una pérdida progresiva de la visión que había experimentado durante años. Su historia médica incluía un diagnóstico previo de retinitis pigmentosa desde hacía 27 años, antecedentes familiares de consanguinidad (sus padres eran primos hermanos), así como hiperlipidemia e hipotiroidismo. Además, había fumado durante 15 años.\n\n**Hallazgos Clave**  \nLa evaluación oftalmológica reveló una agudeza visual corregida muy reducida, con la paciente capaz solo de contar los dedos a 5 pies (aproximadamente 1.5 metros) con el ojo derecho y a 3 pies (menos de un metro) con el ojo izquierdo. La refracción mostró leves defectos de visión en ambos ojos. El examen del fondo de ojo evidenció una atrofia profunda y extensa de la mácula central (la zona responsable de la visión detallada), acompañada de hiperplasia (aumento) del pigmento epitelial y múltiples áreas de atrofia en el ojo derecho, mientras que el ojo izquierdo presentaba también atrofia macular. Las imágenes de autofluorescencia del fondo del ojo mostraron una zona central con baja autofluorescencia (hipoautofluorescencia), que se extendía desde el centro hacia la periferia en ambos ojos.\n\nLa tomografía de coherencia óptica (OCT), que permite visualizar las capas de la retina, indicó un grosor macular disminuido en ambos ojos, sin presencia de edema, quistes o líquido subretinal. Las pruebas de campo visual mostraron una pérdida significativa de sensibilidad en ambos ojos. El electrorretinograma (ERG), que mide la función de las células fotorreceptoras de la retina, evidenció una respuesta normal de los bastones (células responsables de la visión en condiciones de poca luz) pero una respuesta disminuida de los conos (células responsables de la visión en condiciones de luz y la percepción del color), de forma bilateral.\n\n**Interpretación Clínica**  \nCon base en estos hallazgos clínicos y funcionales, se estableció un diagnóstico de enfermedad de Stargardt tipo 1 (STGD1), una forma hereditaria de degeneración macular juvenil que afecta la visión central. El análisis genético confirmó la presencia de una mutación patogénica homocigótica (es decir, la misma alteración en ambas copias del gen) en el gen ABCA4, específicamente la variante intrónica c.5714+5G>A, conocida por estar asociada con esta enfermedad. Además, se identificaron seis variantes genéticas adicionales de significado incierto en otros genes relacionados con enfermedades retinianas, aunque su relevancia clínica no pudo ser determinada en este caso.\n\n**Próximos Pasos**  \nEl diagnóstico genético y clínico permite orientar el manejo y seguimiento de la paciente, que debe incluir controles oftalmológicos periódicos para evaluar la progresión de la enfermedad y la función visual. Aunque actualmente no existe una cura definitiva para la enfermedad de Stargardt, se pueden considerar opciones de apoyo visual y asesoramiento genético para la paciente y su familia. Asimismo, la identificación de la mutación específica puede facilitar la inclusión en estudios clínicos o terapias emergentes dirigidas a esta patología genética.",
+        "score": {
+          "ROUGE-L-Sum": 0.3299565846599132,
+          "BERTScore_F": 0.8312302231788635
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5805934039193883
+        }
+      }
+    }
+  },
+  {
+    "id": 46,
+    "gold_summary": "Describimos el caso de un niño de 19 meses que llegó a la sala de urgencias por un traumatismo en la cabeza. La evaluación clínica, sin embargo, reveló una dificultad respiratoria grave inexplicable que requería intubación traqueal. Después de nuestra evaluación, planteamos la hipótesis de que la dificultad respiratoria grave determinó un estado alterado de conciencia con el consiguiente traumatismo en la cabeza. Los hallazgos radiológicos levantaron la sospecha de aspiración de cuerpo extraño por la presencia de una atelectasia de todo el pulmón izquierdo. La tomografía computarizada mostró una interrupción abrupta del bronquio principal a 12 mm del casco. La siguiente broncoscopia identificó una amígdala de 2 cm.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Un niño pequeño se cayó y se lastimó la cabeza. Pero lo más importante es que no podía respirar bien. Los doctores pusieron un tubo para ayudarlo a respirar. Vieron que un huesito en su pulmón estaba tapado. Buscaron y sacaron una almendra que estaba en su pulmón. Después, el niño mejoró y pudo respirar bien otra vez.",
+        "score": {
+          "ROUGE-L-Sum": 0.15789473684210525,
+          "BERTScore_F": 0.7293487191200256
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.4436217279810655
+        }
+      },
+      "B2": {
+        "text": "Caso de un niño con dificultad para respirar y caída en la cabeza\n\nUn niño de 19 meses llegó a urgencias después de caerse de la trona donde comía. Aunque parecía estar bien al principio, tenía problemas para respirar y vomitó varias veces. Su ritmo de respiración y corazón estaba muy rápido, y el nivel de oxígeno en su sangre era muy bajo. Al examinarlo, notaron que tenía dificultad para respirar y menos sonidos en el pulmón izquierdo.\n\nLo que encontraron\n\nUsaron una máquina para ayudarlo a respirar, pero el nivel de oxígeno seguía bajando. Una ecografía del pulmón mostró que una parte del pulmón estaba sólida, lo que no es normal. Luego, una tomografía (una imagen detallada del pecho) mostró que el pulmón izquierdo estaba colapsado y que el tubo principal que lleva aire a ese pulmón estaba bloqueado.\n\nQué significaba esto\n\nPensaron que algo estaba bloqueando la vía aérea, posiblemente un objeto que el niño había inhalado sin querer. La madre recordó que el niño había tenido una tos fuerte días antes. Al hacer una broncoscopia, que es cuando se usa un tubo con cámara para mirar dentro de los pulmones, encontraron y sacaron una almendra de 2 cm que estaba bloqueando el bronquio izquierdo.\n\nRecuperación\n\nEl niño nunca había comido almendras antes y la había tragado por accidente. Después de quitar la almendra, mejoró rápidamente. Lo mantuvieron en observación y finalmente se recuperó completamente de sus problemas para respirar.",
+        "score": {
+          "ROUGE-L-Sum": 0.26237623762376233,
+          "BERTScore_F": 0.7713563442230225
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.5168662909233924
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe presenta el caso de un niño de 19 meses que fue llevado a urgencias tras una caída desde la trona mientras comía. Inicialmente, se pensó que el motivo principal era el traumatismo craneal provocado por la caída. Sin embargo, durante la evaluación clínica se detectó una dificultad respiratoria grave que no podía explicarse únicamente por el golpe.\n\n**Hallazgos Clave**  \nEl niño mostraba signos de insuficiencia respiratoria severa, con frecuencia respiratoria y cardíaca elevadas, saturación de oxígeno muy baja (menos del 80%) y dificultad para respirar evidenciada por retracciones subcostales y disminución de los sonidos respiratorios en la base del pulmón izquierdo. La saturación de oxígeno empeoraba incluso con ventilación asistida. La ecografía pulmonar reveló ausencia de las líneas A típicas y consolidación pulmonar, indicando que el tejido pulmonar estaba sólido en lugar de aireado. La tomografía computarizada (TC) de tórax mostró una atelectasia completa (colapso) del pulmón izquierdo y una interrupción abrupta del bronquio principal izquierdo a 12 mm de la bifurcación bronquial.\n\n**Interpretación Clínica**  \nEstos hallazgos sugirieron que la dificultad respiratoria grave fue la causa principal del estado alterado de conciencia y, por ende, del traumatismo craneal secundario a la caída. La interrupción del bronquio principal y la atelectasia indicaron la presencia de un cuerpo extraño que obstruía la vía aérea. La madre confirmó que el niño había tenido un episodio previo de tos intensa, lo que apoyó la sospecha de aspiración de un objeto. La broncoscopia rígida permitió identificar y extraer una almendra de 2 cm alojada en el bronquio izquierdo principal, que el niño había ingerido accidentalmente, siendo su primera exposición a frutos secos.\n\n**Próximos Pasos y Evolución**  \nTras la extracción del cuerpo extraño, el niño mostró una mejoría clínica progresiva. Se retiró la intubación después de 24 horas y fue trasladado de la unidad de cuidados intensivos a la sala de pediatría general, donde continuó su recuperación hasta la normalización completa de la función respiratoria. Este caso resalta la importancia de considerar la aspiración de cuerpos extraños en niños pequeños con dificultad respiratoria grave y síntomas atípicos, incluso cuando se presenta un traumatismo asociado.",
+        "score": {
+          "ROUGE-L-Sum": 0.2771535580524344,
+          "BERTScore_F": 0.8154815435409546
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5463175507966945
+        }
+      }
+    }
+  },
+  {
+    "id": 47,
+    "gold_summary": "Presentamos el caso de una mujer nulípara de 35 años de edad del norte de Tanzania con un historial de infertilidad de 10 años. Al presentarse, la paciente informó de un historial de tres años de dolor cíclico asociado a una masa umbilical. Una resonancia magnética abdominal reveló una masa mal definida que se intensificaba y medía 3 × 4 × 6 cm, localizada a lo largo de la pared abdominal anterior derecha. La masa estaba conectada a un tracto sinusal que se extendía hacia la región suprapúbica, pero no mostraba comunicación con la cavidad peritoneal, lo que sugería endometriosis. Además, las lesiones anexiales bilaterales demostraron señales hiperintensas con áreas hipointensas focales y restricciones variables, consistentes con endometriomas ováricos bilaterales. La paciente se sometió a la extirpación de la masa umbilical y el examen histopatológico confirmó el diagnóstico de endometriosis umbilical primaria. A pesar de su condición estable después del tratamiento, no concibió durante el año siguiente.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Había una mujer que tenía dolor en su pancita cerca del ombligo. El dolor venía y se iba, y a veces el ombligo sangraba. Los doctores vieron que tenía un bultito en el ombligo. Le sacaron el bultito con una operación. Cuando miraron el bultito, encontraron que era un problema llamado endometriosis. Ella se sintió mejor después de la operación. Pero todavía no pudo tener un bebé.",
+        "score": {
+          "ROUGE-L-Sum": 0.15139442231075698,
+          "BERTScore_F": 0.7357838153839111
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.44358911884733404
+        }
+      },
+      "B2": {
+        "text": "**Caso de una mujer con dolor y un bulto en el ombligo**\n\nUna mujer de 35 años, que nunca ha tenido hijos y ha tenido problemas para quedar embarazada durante 10 años, acudió al médico porque tenía dolor en el ombligo desde hace tres años. Este dolor aparecía de forma cíclica, es decir, se repetía cada mes, y estaba relacionado con un bulto en esa zona.\n\n**Lo que encontraron en las pruebas**\n\nSe le hizo una resonancia magnética, que es un tipo de imagen que muestra el interior del cuerpo. Esta prueba mostró una masa o bulto de 3 × 4 × 6 centímetros en la pared del abdomen, cerca del ombligo. La masa estaba conectada a un pequeño canal que llegaba hacia la parte baja del abdomen, pero no estaba unida a la cavidad donde están los órganos internos. Esto hizo pensar que podría tratarse de endometriosis, que es cuando un tejido parecido al que recubre el interior del útero crece en otros lugares del cuerpo.\n\nAdemás, se encontraron lesiones en ambos ovarios que también parecían ser endometriomas, que son quistes causados por la endometriosis en los ovarios.\n\n**Qué hicieron y qué pasó después**\n\nLa mujer se sometió a una cirugía para quitar el bulto del ombligo. El tejido extraído se analizó bajo el microscopio y confirmó que era endometriosis en el ombligo, algo poco común. Después de la operación, la paciente se recuperó bien y comenzó un tratamiento con medicamentos para controlar la endometriosis.\n\nDurante los siguientes ocho meses, no tuvo nuevos síntomas ni signos de que la enfermedad regresara. Sin embargo, aunque su salud mejoró, no logró quedar embarazada en el año siguiente.\n\nEste caso muestra cómo la endometriosis puede afectar diferentes partes del cuerpo y la importancia de un diagnóstico y tratamiento adecuados para mejorar la calidad de vida y la fertilidad.",
+        "score": {
+          "ROUGE-L-Sum": 0.308300395256917,
+          "BERTScore_F": 0.7901511788368225
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5492257870468698
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe presenta el caso de una mujer de 35 años, sin hijos y con un historial de infertilidad de una década, que acudió a consulta por un dolor cíclico y persistente en el ombligo durante tres años. Este dolor se asociaba a la presencia de un nódulo umbilical que sangraba coincidiendo con su menstruación. Además, refería síntomas ginecológicos como dolor menstrual intenso (dismenorrea), sangrado menstrual abundante (menorragia) y dolor durante las relaciones sexuales (dispareunia). La paciente había utilizado un dispositivo intrauterino (DIU) de cobre desde hacía tres años y recientemente había iniciado tratamiento hormonal combinado para aliviar el dolor.\n\n**Hallazgos Clave**  \nEl examen físico reveló una masa firme, hiperpigmentada, inmóvil y no dolorosa en el ombligo, sin conexión palpable con estructuras internas. La resonancia magnética mostró una masa mal definida de 3 × 4 × 6 cm en la pared abdominal anterior derecha, conectada a un tracto sinusal que se extendía hacia la región suprapúbica, pero sin comunicación con la cavidad peritoneal, lo que orientó hacia un diagnóstico de endometriosis umbilical primaria. Además, se identificaron lesiones en ambos ovarios con características compatibles con endometriomas (quistes ováricos formados por tejido endometrial), confirmando la afectación bilateral.\n\n**Interpretación Clínica**  \nEl diagnóstico diferencial incluyó diversas condiciones como hernia umbilical, granuloma, cicatriz queloide, tumores malignos y anomalías congénitas, pero la combinación de síntomas, hallazgos de imagen y la confirmación histopatológica establecieron la endometriosis umbilical primaria. La biopsia del nódulo extirpado mostró tejido endometrial (glándulas y estroma) dentro de la dermis, confirmando la presencia de endometriosis fuera del útero. Este tipo de endometriosis es poco frecuente y puede causar dolor cíclico y sangrado en la piel del ombligo.\n\n**Próximos Pasos y Seguimiento**  \nTras la cirugía, la paciente tuvo una recuperación sin complicaciones y fue dada de alta al segundo día postoperatorio. Se le indicó tratamiento hormonal con dienogest y anticonceptivos orales combinados para controlar la endometriosis y reducir el riesgo de recurrencia. Se le brindó asesoramiento sobre su fertilidad futura, incluyendo la posibilidad de recurrir a técnicas de reproducción asistida como la fertilización in vitro (FIV). Durante un seguimiento clínico de ocho meses no se observaron signos de recurrencia local, aunque la paciente no logró concebir en el año posterior al tratamiento.\n\nEste caso destaca la importancia de considerar la endometriosis umbilical en mujeres con dolor cíclico y nódulos en el ombligo, especialmente en el contexto de infertilidad, y subraya la necesidad de un manejo multidisciplinario para optimizar el control de los síntomas y la fertilidad.",
+        "score": {
+          "ROUGE-L-Sum": 0.330188679245283,
+          "BERTScore_F": 0.8472927808761597
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5887407300607214
+        }
+      }
+    }
+  },
+  {
+    "id": 48,
+    "gold_summary": "Presentamos a un neonato de 15 minutos de vida, hijo de una madre para-cuatro que no recordaba su LNMP pero que afirmaba estar amenorreica desde hacía nueve meses. El modo de parto fue por cesárea para extraer al neonato vivo, que pesaba 2,01 kg y tenía puntuaciones APGAR de 5 y 6 en el primer y quinto minutos, respectivamente. El neonato no lloró y fue reanimado durante cinco minutos. Después se lo trasladó a la unidad de cuidados intensivos neonatales para continuar con el tratamiento y las investigaciones. Sus signos vitales eran: pulso de 160 latidos por minuto, frecuencia respiratoria de 70 respiraciones por minuto, temperatura de 33,4 grados centígrados y saturación de oxígeno del 60%. La fontanela anterior del neonato medía 2 cm por 2 cm y tenía micrognatia y cuello corto. En el sistema respiratorio había retracciones intercostales y subcostales, respiración trabajosa y gruñidos. En el sistema musculoesquelético había acortamiento bilateral de la extremidad superior, la pierna derecha tenía una posición y estructura normales, la pierna izquierda giraba hacia adentro (se doblaba hacia la parte media) en la articulación de la rodilla y el pie tenía una estructura normal.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Un bebé nació hace muy poquito tiempo. Su mamá tuvo que ir al hospital para que lo sacaran con una operación especial. El bebé pesaba poquito y no pudo llorar al nacer. Los doctores lo ayudaron a respirar y lo llevaron a un lugar para cuidarlo mucho.\n\nEl bebé respiraba rápido y su corazón latía rápido también. Tenía frío y le faltaba un poco de aire. Su cabeza tenía una parte blanda y su cuello era cortito. Sus brazos eran más cortos de lo normal. Una pierna estaba normal, pero la otra estaba doblada hacia adentro. Sus pies estaban bien. Los doctores lo cuidaron mucho para que se sintiera mejor.",
+        "score": {
+          "ROUGE-L-Sum": 0.18072289156626506,
+          "BERTScore_F": 0.7612423896789551
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.4709826406226101
+        }
+      },
+      "B2": {
+        "text": "**Lo que pasó con el bebé al nacer**  \nUn bebé nació por cesárea después de que su mamá tuvo problemas en el embarazo. El bebé pesó 2,01 kg y sus primeras pruebas para saber cómo estaba (llamadas puntuaciones Apgar) fueron 5 y 6, lo que indica que necesitó ayuda para respirar. De hecho, el bebé no lloró al nacer y tuvo que ser reanimado durante cinco minutos para ayudarlo a respirar mejor.\n\n**Estado del bebé en la unidad de cuidados intensivos**  \nDespués de nacer, el bebé fue llevado a una unidad especial para recién nacidos que necesitan cuidados extra. Allí, los médicos notaron que su corazón latía rápido (160 latidos por minuto) y respiraba muy rápido (70 respiraciones por minuto). Además, tenía la temperatura baja (33,4 grados Celsius) y poca cantidad de oxígeno en la sangre (60%). La parte blanda en la cabeza del bebé (llamada fontanela anterior) medía 2 cm por 2 cm. También tenía micrognatia, que significa que la mandíbula era más pequeña de lo normal, y un cuello corto.\n\n**Problemas en la respiración y los huesos**  \nEl bebé tenía dificultad para respirar, con movimientos fuertes entre las costillas y sonidos de gruñidos al respirar. En cuanto a sus brazos, ambos eran más cortos de lo normal. La pierna derecha estaba normal, pero la pierna izquierda estaba doblada hacia adentro en la rodilla, aunque el pie tenía una forma normal.\n\n**Qué significa todo esto**  \nEstos signos muestran que el bebé tenía problemas para respirar y algunas malformaciones en sus extremidades. Estas condiciones pueden ser causadas por complicaciones durante el embarazo o problemas en el desarrollo del bebé. Los médicos le dieron oxígeno y otros tratamientos para ayudarlo, pero lamentablemente el bebé murió después de tres días en el hospital.",
+        "score": {
+          "ROUGE-L-Sum": 0.3707865168539326,
+          "BERTScore_F": 0.8246096968650818
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5976981068595072
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe presentó un recién nacido de apenas 15 minutos de vida, hijo de una mujer con antecedentes obstétricos de cuatro partos previos (para-cuatro). La madre no recordaba la fecha de su última menstruación, pero aseguró haber estado sin menstruar durante nueve meses, lo que indicaba un embarazo avanzado. Durante el embarazo, la madre recibió atención prenatal limitada y no se realizó una ecografía temprana. Al momento del ingreso hospitalario, la madre presentaba hemorragia vaginal prolongada, diagnóstico de desprendimiento prematuro de placenta, oligohidramnios severo (disminución del líquido amniótico) y presentación fetal de nalgas.\n\n**Hallazgos Clave del Neonato**  \nEl bebé nació mediante cesárea de urgencia con un peso de 2,01 kg y puntuaciones de Apgar de 5 y 6 al primer y quinto minuto, respectivamente, lo que indica una adaptación inicial comprometida. No lloró al nacer y requirió reanimación durante cinco minutos. Fue trasladado a la unidad de cuidados intensivos neonatales debido a dificultad respiratoria grave, con signos vitales alterados: frecuencia cardíaca elevada (160 latidos por minuto), respiración rápida (70 respiraciones por minuto), temperatura corporal baja (33,4 °C) y saturación de oxígeno muy baja (60%).\n\nEn el examen físico, se observaron características faciales anómalas como micrognatia (mandíbula inferior pequeña) y cuello corto. En el sistema respiratorio, el neonato presentaba retracciones intercostales y subcostales (movimientos visibles de los músculos entre las costillas y debajo de ellas al respirar), respiración dificultosa y sonidos respiratorios anormales (gruñidos). En el sistema musculoesquelético, había un acortamiento marcado de ambas extremidades superiores (brazo y antebrazo), mientras que la pierna derecha tenía una estructura y posición normales. La pierna izquierda estaba girada hacia adentro en la articulación de la rodilla (flexión mediolateral), aunque el pie mantenía una estructura normal.\n\nLos estudios complementarios revelaron una elevación significativa de los glóbulos blancos (30,000), indicando posible infección, con una proteína C reactiva positiva (marcador de inflamación), anemia moderada (hemoglobina de 8 g/dL) y plaquetas dentro de rango normal. La radiografía confirmó el acortamiento extremo de las extremidades superiores y la rotación interna de la pierna izquierda. La ecocardiografía fue normal, descartando malformaciones cardíacas.\n\n**Interpretación Clínica**  \nEl diagnóstico principal incluyó un neonato prematuro tardío (34 semanas de gestación), con bajo peso al nacer pero adecuado para su edad gestacional, que presentaba focomelia (una malformación congénita caracterizada por extremidades muy cortas o ausentes), asfixia perinatal (falta de oxígeno al nacer) y sepsis neonatal temprana (infección grave en los primeros días de vida). Estas condiciones explican la dificultad respiratoria, el compromiso hemodinámico y las anomalías físicas observadas.\n\n**Próximos Pasos y Evolución**  \nEl manejo incluyó soporte respiratorio con oxígeno, administración de líquidos por vía intravenosa y tratamiento antibiótico para la infección. A pesar de estas intervenciones, el neonato falleció a los tres días de hospitalización debido a la gravedad de sus condiciones clínicas y malformaciones congénitas asociadas. Este caso resalta la importancia de un control prenatal adecuado, diagnóstico temprano y manejo multidisciplinario para mejorar el pronóstico en embarazos complicados y neonatos con malformaciones severas.",
+        "score": {
+          "ROUGE-L-Sum": 0.38193548387096776,
+          "BERTScore_F": 0.8194915652275085
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.6007135245492381
+        }
+      }
+    }
+  },
+  {
+    "id": 49,
+    "gold_summary": "Oaciente de 61 años tratada con gemcitabina (11.744 mg/m² acumulados) por enfermedad metastásica, en un hospital general de cuarto nivel, privado, no oncológico, donde venía siendo manejada de forma ambulatoria. Presentó necrosis distal del segundo dedo de la mano derecha, por lo que se suspendió el tratamiento y se requirió amputación de este dedo. Se realizó una búsqueda en Embase, Medline y Lilacs. Se buscaron estudios de reporte y series de casos sobre necrosis distal inducida por gemcitabina. Se extrajeron datos de dosis, diagnóstico y tratamiento.",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Una señora de 61 años estaba muy enferma y recibió medicina para el cáncer. Esta medicina le hizo daño en un dedo de su mano derecha. El dedo se puso muy mal y tuvieron que cortarlo para que no le doliera más. Los doctores buscaron información para entender mejor este problema y cómo ayudar.",
+        "score": {
+          "ROUGE-L-Sum": 0.2051282051282051,
+          "BERTScore_F": 0.7432465553283691
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.4741873802282871
+        }
+      },
+      "B2": {
+        "text": "**Caso de una Mujer con Cáncer y Problemas en las Manos**\n\nUna mujer de 61 años estaba recibiendo un medicamento llamado gemcitabina para tratar su cáncer que se había extendido. Este medicamento se usó en un hospital privado que atiende casos complejos. Después de recibir una dosis acumulada bastante alta (11.744 mg/m²), comenzó a tener problemas graves en su mano derecha. El segundo dedo se puso negro y murió (necrosis), lo que hizo necesario suspender el medicamento y amputar ese dedo.\n\n**Búsqueda de Información sobre el Problema**\n\nLos médicos buscaron en varias bases de datos científicas (Embase, Medline y Lilacs) para encontrar otros casos similares donde la gemcitabina causara necrosis en los dedos. Revisaron estudios y reportes para entender mejor las dosis usadas, cómo se diagnosticó el problema y qué tratamientos se aplicaron.\n\n**Qué Significa Esto**\n\nEste caso muestra que, aunque la gemcitabina es útil para tratar ciertos tipos de cáncer, puede causar efectos secundarios graves en las manos, como la muerte de tejido en los dedos. Por eso, los médicos deben vigilar muy bien a los pacientes que reciben este medicamento para detectar cualquier señal temprana de daño y actuar rápido para evitar complicaciones mayores.",
+        "score": {
+          "ROUGE-L-Sum": 0.23376623376623376,
+          "BERTScore_F": 0.7950013279914856
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.5143837808788597
+        }
+      },
+      "B3": {
+        "text": "Resumen detallado para público no médico universitario\n\nContexto  \nSe trata de una mujer de 61 años con un historial complejo de cáncer de cuello uterino (carcinoma escamocelular), inicialmente diagnosticado en 2019 y tratado con cirugía, quimioterapia y radioterapia, logrando respuestas completas. Sin embargo, presentó varias recaídas localizadas y regionales entre 2021 y 2023, que requirieron diferentes líneas de tratamiento con quimioterapia y terapia inmunológica. En 2023, ante la progresión tumoral, se inició gemcitabina como segunda línea de tratamiento para la enfermedad recurrente.\n\nHallazgos clave  \nDurante el tratamiento con gemcitabina, acumuló una dosis total de 11.744 mg/m², pero desarrolló síntomas de isquemia digital, es decir, falta de flujo sanguíneo en los dedos de las manos, que se manifestó con dolor intenso, coloración azulada y necrosis (muerte del tejido) en el segundo dedo de la mano derecha. Esto llevó a la suspensión inmediata del medicamento y a la amputación quirúrgica de dicho dedo, confirmándose la necrosis mediante análisis histopatológico (examen microscópico del tejido).\n\nSe descartaron otras causas comunes de daño vascular o inflamación de los vasos sanguíneos (vasculitis) mediante pruebas serológicas y de autoinmunidad, todas negativas. Tampoco se encontraron problemas cardíacos que pudieran explicar la formación de coágulos o embolias. El equipo médico inició tratamiento con anticoagulantes, antiinflamatorios, vasodilatadores y medicamentos para mejorar la circulación, logrando cierta mejoría en los dedos restantes.\n\nInterpretación clínica  \nEl análisis de causalidad mediante la escala de Naranjo, una herramienta que ayuda a determinar si un medicamento es responsable de un efecto adverso, indicó que la gemcitabina fue probablemente la causa de la necrosis digital. Este efecto adverso es poco frecuente pero grave, y se relaciona con daño vascular inducido por el fármaco.\n\nPróximos pasos y evolución  \nPosteriormente, la paciente presentó complicaciones adicionales, incluyendo un sangrado vaginal masivo que requirió embolización (procedimiento para detener el sangrado) y un deterioro neurológico sin causa clara en estudios de imagen. Su estado general empeoró significativamente, con pérdida total de autonomía y un pronóstico de vida inferior a tres semanas. En consenso con la familia, se decidió suspender estudios invasivos y se implementó un manejo paliativo integral para mejorar su calidad de vida en el tiempo restante. Finalmente, la paciente falleció tras el alta hospitalaria.\n\nResumen de la revisión bibliográfica  \nSe realizó una búsqueda en bases de datos médicas (Embase, Medline y Lilacs) para identificar reportes y series de casos sobre necrosis distal inducida por gemcitabina, recopilando información sobre dosis, diagnóstico y manejo de esta complicación, con el fin de contextualizar y comparar el caso presentado.\n\nEste caso resalta la importancia de la vigilancia estrecha de efectos adversos vasculares graves en pacientes tratados con gemcitabina, especialmente en contextos de enfermedad avanzada y tratamientos prolongados.",
+        "score": {
+          "ROUGE-L-Sum": 0.21052631578947367,
+          "BERTScore_F": 0.7810689806938171
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.4957976482416454
+        }
+      }
+    }
+  },
+  {
+    "id": 50,
+    "gold_summary": "Mujer de 55 años con antecedente de AR que ingresó a un servicio de medicina interna por sangrado de tubo digestivo; presentó datos clínicos de trombosis venosa profunda en miembro pélvico izquierdo y síndrome consuntivo en estudio. Durante su abordaje se identificó con infartos esplénicos y hepáticos, así como múltiples conglomerados ganglionares, por lo que se practicó biopsia de ganglio axilar que reportó proliferación neoplásica de células linfoides y aspirado de médula ósea con presencia de infiltración linfoplasmocitaria, con lo que se determinó diagnóstico de linfoma no Hodgkin estadio IV. La paciente fue enviada a un hospital de tercer nivel para inicio de tratamiento.",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Había una señora que se sentía muy cansada y tenía dolor en una pierna. También tenía sangre en su pancita. Los doctores le hicieron muchas pruebas. Encontraron que tenía unos bultitos en su cuerpo que no estaban bien. Le hicieron una prueba en un lugar con bultitos y otra en su hueso. Vieron que tenía un tipo de enfermedad llamada linfoma. La señora fue a un hospital especial para que la cuiden y le den medicina para mejorar.",
+        "score": {
+          "ROUGE-L-Sum": 0.17647058823529413,
+          "BERTScore_F": 0.718192458152771
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.4473315231940326
+        }
+      },
+      "B2": {
+        "text": "**Lo que le pasó a la paciente**  \nUna mujer de 53 años, que tenía artritis reumatoide (una enfermedad que afecta las articulaciones), llegó al hospital porque estaba sangrando por el tubo digestivo (el camino que va desde la boca hasta el estómago y los intestinos). Además, tenía dolor y hinchazón en la pierna izquierda, y estaba muy cansada y pálida. También había perdido mucho peso sin querer.\n\n**Lo que encontraron en los exámenes**  \nLos médicos descubrieron que tenía una trombosis venosa profunda, que es un coágulo de sangre en una vena grande de la pierna. También encontraron daños en el bazo y el hígado, llamados infartos, que son áreas donde no llegó suficiente sangre. Al hacer una tomografía (una imagen especial del cuerpo), vieron que sus ganglios linfáticos (pequeñas glándulas que ayudan a combatir infecciones) estaban muy grandes y agrupados en varias partes del cuerpo.\n\nPara entender mejor qué pasaba, le hicieron una biopsia, que es cuando se toma un pequeño pedazo de tejido para analizarlo. La biopsia del ganglio linfático mostró que había un crecimiento anormal de células llamadas linfocitos, que son parte del sistema inmunológico. También examinaron su médula ósea (donde se producen las células de la sangre) y encontraron células anormales que indicaban que el problema estaba afectando varias partes del cuerpo.\n\n**Qué significa el diagnóstico**  \nCon toda esta información, los médicos diagnosticaron un linfoma no Hodgkin en estadio IV. El linfoma no Hodgkin es un tipo de cáncer que afecta a los linfocitos. El estadio IV significa que el cáncer está avanzado y se ha extendido a varias áreas del cuerpo.\n\n**Próximos pasos**  \nLa paciente fue enviada a un hospital especializado para hacer más estudios y comenzar un tratamiento con quimioterapia, que es un tipo de medicina para combatir el cáncer.",
+        "score": {
+          "ROUGE-L-Sum": 0.23162583518930957,
+          "BERTScore_F": 0.7549259066581726
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.4932758709237411
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe trata de una mujer de 53 años con diagnóstico previo de artritis reumatoide (AR) desde hace 15 años, en tratamiento con metotrexato. Ocho meses antes de su ingreso al hospital, comenzó a presentar síntomas progresivos como fatiga intensa (astenia), debilidad generalizada (adinamia), palidez en la piel, fiebre nocturna no cuantificada y una pérdida de peso no intencionada de aproximadamente 15 kg en seis meses. Tres meses después, desarrolló dificultad para respirar al realizar esfuerzos moderados. Cinco días antes de su ingreso, su condición empeoró con sangrado digestivo alto, manifestado por evacuaciones negras abundantes (melena) y vómitos con sangre (hematemesis), sin causa aparente. Además, presentó aumento de volumen, dolor, enrojecimiento y limitación de movimiento en la pierna izquierda, signos compatibles con trombosis venosa profunda (coágulo en una vena profunda).\n\n**Hallazgos Clave**  \nDurante la hospitalización, se confirmó anemia severa que requirió transfusión de glóbulos rojos. Un ultrasonido Doppler de la pierna izquierda confirmó la presencia de trombosis venosa profunda. El ultrasonido abdominal mostró infartos (áreas de tejido muerto por falta de riego sanguíneo) en el bazo y el hígado, junto con cambios hepáticos crónicos probablemente relacionados con el uso de metotrexato. La endoscopía digestiva evidenció varices pequeñas sin sangrado activo. La tomografía computarizada (TAC) de tórax y abdomen reveló agrandamiento del hígado y bazo (hepatoesplenomegalia) y múltiples conglomerados de ganglios linfáticos en axilas, mediastino y alrededor de la aorta, lo que sugirió una posible infiltración tumoral.  \n\nLa biopsia de un ganglio axilar derecho mostró proliferación anormal de células linfoides (células del sistema inmunitario). El aspirado de médula ósea evidenció infiltración por células plasmáticas anormales y células reticulares, confirmando la afectación linfoplasmocitaria. Estos hallazgos permitieron establecer el diagnóstico de linfoma no Hodgkin (LNH) en estadio IV, que indica una enfermedad avanzada con compromiso de múltiples órganos y tejidos.\n\n**Interpretación Clínica**  \nEl cuadro clínico y los estudios realizados indican que la paciente presenta un linfoma no Hodgkin difuso de células B, un tipo de cáncer que afecta a las células del sistema inmunitario. La enfermedad se encuentra en una etapa avanzada y ha provocado complicaciones como trombosis venosa profunda, infartos en órganos abdominales y sangrado digestivo. La asociación con su antecedente de artritis reumatoide y el tratamiento con metotrexato puede haber influido en la evolución y presentación clínica.\n\n**Próximos Pasos**  \nLa paciente fue referida a un hospital de tercer nivel para realizar estudios adicionales de inmunohistoquímica (técnicas que permiten caracterizar con precisión el tipo de células tumorales), completar la estadificación de la enfermedad y comenzar el tratamiento específico con quimioterapia. El manejo multidisciplinario es fundamental para optimizar el pronóstico y controlar tanto la enfermedad linfoproliferativa como las complicaciones asociadas.",
+        "score": {
+          "ROUGE-L-Sum": 0.19999999999999998,
+          "BERTScore_F": 0.7720091342926025
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.48600456714630125
+        }
+      }
+    }
+  },
+  {
+    "id": 51,
+    "gold_summary": "Paciente: Hombre, 56 años\n\nDiagnóstico final: Insuficiencia cardíaca derecha por embolia pulmonar\n\nSíntomas: síncope\n\nMedicación: —\n\nProcedimiento clínico: —\n\nEspecialidad: Cardiología\n\nSe trata de un informe de caso en el que se utilizó sildenafil como agente de rescate para lograr una mejora en el tamaño y la función del ventrículo derecho en un caso de inicio agudo de embolia pulmonar masiva con insuficiencia aguda del ventrículo derecho en el escenario en el que la terapia trombolítica sistémica estaba contraindicada.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Un hombre de 56 años se sintió muy cansado y se desmayó. Tenía problemas para respirar. Esto pasó porque tenía unos tapones en sus pulmones. Estos tapones hicieron que su corazón derecho se pusiera muy cansado. Los doctores no le pudieron dar una medicina fuerte para quitar los tapones porque él había tenido una operación hace poco. Entonces, le dieron otra medicina llamada sildenafil. Esta medicina ayudó a que su corazón mejorara y se hiciera más fuerte. Después de un tiempo, el hombre se sintió mejor y su corazón trabajó mejor. Los doctores cuidaron mucho de él y le explicaron todo a él y a su familia.",
+        "score": {
+          "ROUGE-L-Sum": 0.1826923076923077,
+          "BERTScore_F": 0.7196587920188904
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.45117554985559905
+        }
+      },
+      "B2": {
+        "text": "**Lo que le pasó al paciente**  \nUn hombre de 56 años tuvo problemas para respirar de repente y se desmayó mientras caminaba en su casa. Cinco días antes, había tenido una cirugía para tratar un cáncer de próstata. Después de la cirugía, parecía estar bien, pero luego presentó estos síntomas.\n\n**Qué encontraron los médicos**  \nEn el hospital, su presión arterial estaba baja y su corazón latía muy rápido. Tenía hinchazón en una pierna, lo que puede indicar un coágulo de sangre. Un examen especial llamado tomografía mostró que tenía coágulos grandes en las arterias de los pulmones, lo que se llama embolia pulmonar. Estos coágulos estaban afectando el lado derecho del corazón, que se encargaba de enviar sangre a los pulmones. También confirmaron que había un coágulo en la pierna.\n\n**Cómo lo trataron**  \nNo pudieron hacer una cirugía para quitar los coágulos porque la cirugía reciente del paciente era un riesgo. En lugar de eso, le dieron un medicamento llamado heparina para evitar que se formen más coágulos. Además, usaron óxido nítrico inhalado y un medicamento llamado sildenafil, que ayuda a relajar los vasos sanguíneos y mejora la función del corazón derecho.\n\n**Qué pasó después**  \nDespués de un día, el paciente estaba más estable. Dos días después, los exámenes mostraron que el corazón derecho había mejorado en tamaño y función. La presión en el corazón derecho bajó y su capacidad para bombear sangre mejoró. Los médicos recomendaron que siguiera tomando sildenafil y medicamentos para evitar coágulos durante un mes después de salir del hospital.\n\n**Por qué es importante este caso**  \nEste caso muestra que el sildenafil puede ayudar a mejorar la función del corazón derecho en personas con embolia pulmonar grave cuando no se puede usar la cirugía o medicamentos para disolver coágulos. Es una opción útil para tratar problemas del corazón causados por coágulos en los pulmones.",
+        "score": {
+          "ROUGE-L-Sum": 0.19607843137254902,
+          "BERTScore_F": 0.7343297600746155
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.46520409572358223
+        }
+      },
+      "B3": {
+        "text": "**Contexto**\n\nUn hombre de 56 años fue atendido en urgencias tras presentar una dificultad respiratoria súbita y un episodio de desmayo mientras caminaba en su casa. Cinco días antes, había sido sometido a una prostatectomía laparoscópica asistida por robot para tratar un cáncer de próstata, y su recuperación inicial había sido sin complicaciones. Al llegar al hospital, mostraba signos de inestabilidad hemodinámica, con presión arterial baja y frecuencia cardíaca elevada. Además, se detectó hinchazón en su pierna izquierda.\n\n**Hallazgos Clave**\n\n- El electrocardiograma mostró taquicardia sinusal sin alteraciones isquémicas.\n- La troponina, un marcador de daño cardíaco, estaba ligeramente elevada.\n- La tomografía computarizada del tórax reveló una embolia pulmonar bilateral extensa, es decir, coágulos grandes en ambas arterias pulmonares principales, causando insuficiencia aguda del ventrículo derecho (la cámara del corazón que bombea sangre hacia los pulmones).\n- Un estudio de ultrasonido vascular confirmó la presencia de un coágulo en la vena profunda de la pierna izquierda (trombosis venosa profunda).\n- El ecocardiograma evidenció que el ventrículo izquierdo funcionaba normalmente, pero el ventrículo derecho estaba dilatado y con función reducida, con signos de presión elevada en esta cavidad.\n\n**Interpretación Clínica**\n\nEl paciente presentaba insuficiencia cardíaca derecha aguda secundaria a una embolia pulmonar masiva. Debido a que la mayoría de los coágulos estaban en áreas distales y que la cirugía reciente representaba una contraindicación para tratamientos trombolíticos (medicamentos que disuelven coágulos), no se consideró adecuada la extracción quirúrgica ni la trombólisis sistémica.\n\nEn este contexto, se inició tratamiento con heparina para anticoagulación, óxido nítrico inhalado para mejorar la oxigenación y sildenafil oral (un inhibidor de la fosfodiesterasa tipo 5, que actúa como vasodilatador pulmonar) para reducir la presión en el ventrículo derecho y mejorar su función.\n\n**Evolución y Próximos Pasos**\n\nAl día siguiente, el paciente mostró estabilidad hemodinámica y mejoría en la función del ventrículo derecho, confirmada mediante ecocardiografía realizada 48 horas después del ingreso. La presión en el ventrículo derecho disminuyó significativamente y la capacidad de contracción mejoró.\n\nSe recomendó continuar con sildenafil durante un mes tras el alta hospitalaria, junto con anticoagulación oral, y realizar seguimiento ambulatorio para monitorear su recuperación. El paciente y su familia fueron informados detalladamente y dieron su consentimiento para el plan terapéutico.\n\n**Resumen**\n\nEste caso ilustra el uso exitoso de sildenafil como tratamiento complementario para mejorar la función del ventrículo derecho en un paciente con embolia pulmonar masiva y disfunción ventricular derecha aguda, en un escenario donde la trombólisis estaba contraindicada debido a una cirugía reciente. El manejo combinado permitió la estabilización clínica y la recuperación funcional sin necesidad de intervenciones quirúrgicas o trombolíticas.",
+        "score": {
+          "ROUGE-L-Sum": 0.21694915254237288,
+          "BERTScore_F": 0.7611064314842224
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.48902779201329766
+        }
+      }
+    }
+  },
+  {
+    "id": 52,
+    "gold_summary": "Presentamos el caso de un hombre de 78 años con una exacerbación de la insuficiencia cardiaca mientras viajaba a gran altitud. Se detectó un aumento de sus presiones arteriales pulmonares (PA) mediante su dispositivo CardioMEMS implantado. La comprensión del cambio esperado en los registros de presión de la PA ayudó a identificar una verdadera exacerbación de la insuficiencia cardiaca en nuestro paciente. Esto llevó a un cambio rápido en la terapia médica, que en última instancia evitó la hospitalización.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Había un hombre de 78 años que tenía problemas en su corazón. Él usaba un aparato especial para medir la presión en su corazón. Cuando viajó a un lugar muy alto, su corazón trabajó más fuerte y se sintió mal. El aparato mostró que su corazón estaba con mucha presión. Los doctores cambiaron sus medicinas rápido. Así, él no tuvo que ir al hospital y se mejoró.",
+        "score": {
+          "ROUGE-L-Sum": 0.20606060606060608,
+          "BERTScore_F": 0.7288413643836975
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.4674509852221518
+        }
+      },
+      "B2": {
+        "text": "**Lo que pasó con el paciente**  \nUn hombre de 78 años tenía problemas graves del corazón llamados insuficiencia cardiaca, que significa que su corazón no bombeaba la sangre tan bien como debería. Para ayudar a controlar su enfermedad, le pusieron un dispositivo llamado CardioMEMS, que mide la presión en una arteria del pulmón. Esto ayuda a los doctores a saber cómo está funcionando su corazón sin que él tenga que ir al hospital.\n\n**Qué sucedió durante su viaje**  \nEl paciente viajó a una ciudad alta llamada Denver, que está a mucha altura sobre el nivel del mar. Allí, las mediciones del CardioMEMS mostraron que la presión en su arteria pulmonar subió mucho. Esto fue un problema porque también empezó a sentir más dificultad para respirar y sus piernas se hincharon. Estas señales indicaron que su insuficiencia cardiaca empeoró.\n\n**Cómo ayudaron los doctores**  \nAunque no fue al hospital, el paciente llamó a su cardiólogo, quien le cambió el tratamiento aumentando la cantidad de un medicamento llamado diurético, que ayuda a eliminar el exceso de líquido del cuerpo. Gracias a este cambio rápido, sus síntomas mejoraron y evitó tener que ser hospitalizado.\n\n**Qué aprendimos de este caso**  \nEste caso muestra que el dispositivo CardioMEMS es muy útil para detectar cambios importantes en la presión del corazón, especialmente cuando una persona viaja a lugares con altitudes altas. Saber cómo cambian las presiones en estas situaciones ayuda a los médicos a actuar rápido y evitar complicaciones graves.",
+        "score": {
+          "ROUGE-L-Sum": 0.21468926553672316,
+          "BERTScore_F": 0.7605196237564087
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.48760444464656594
+        }
+      },
+      "B3": {
+        "text": "**Contexto**\n\nSe describe el caso de un hombre de 78 años con antecedentes de fibrilación auricular crónica, cardiopatía hipertensiva y miocardiopatía no isquémica, que presentaba insuficiencia cardiaca crónica en estadio C (según el Colegio Americano de Cardiología) con síntomas moderados a severos (clase III de la Asociación del Corazón de Nueva York). A pesar del tratamiento ambulatorio, experimentó un aumento significativo de peso y empeoramiento de la falta de aire, lo que llevó a una hospitalización y al implante de un dispositivo CardioMEMS para monitoreo invasivo de las presiones en la arteria pulmonar.\n\n**Hallazgos Clave**\n\nTras la implantación del CardioMEMS, el paciente mostró presiones pulmonares estables durante cuatro semanas en su entorno habitual en Michigan (a una altitud de 837 pies). Sin embargo, durante un viaje de cuatro días a Denver, Colorado (a 5280 pies de altitud), se registró un aumento marcado y sostenido de las presiones sistólica, media y diastólica en la arteria pulmonar. Paralelamente, el paciente experimentó un empeoramiento de sus síntomas de insuficiencia cardiaca, como aumento de la falta de aire y edema (hinchazón) en las extremidades inferiores.\n\n**Interpretación Clínica**\n\nEl aumento de las presiones pulmonares detectado por el CardioMEMS durante la estancia en altitud elevada reflejó una verdadera exacerbación de la insuficiencia cardiaca, más allá del efecto esperado por el cambio de altitud. Este monitoreo permitió diferenciar entre las variaciones fisiológicas normales y un deterioro clínico significativo. La rápida comunicación con el equipo médico facilitó la intensificación del tratamiento, incluyendo el aumento de la dosis de diuréticos y oxígeno suplementario, lo que mejoró los síntomas y evitó la necesidad de hospitalización.\n\n**Próximos Pasos**\n\nEl paciente continuó con un seguimiento estrecho mediante el dispositivo CardioMEMS tras su regreso a Michigan, donde las presiones pulmonares se normalizaron rápidamente. Se mantuvo con tratamiento diurético de mantenimiento y control diario de las presiones arteriales pulmonares para prevenir futuras descompensaciones. Este caso resalta la utilidad del monitoreo hemodinámico invasivo en pacientes con insuficiencia cardiaca, especialmente en situaciones que pueden alterar la fisiología cardiovascular, como los viajes a gran altitud.",
+        "score": {
+          "ROUGE-L-Sum": 0.2203023758099352,
+          "BERTScore_F": 0.7969661951065063
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.5086342854582208
+        }
+      }
+    }
+  },
+  {
+    "id": 53,
+    "gold_summary": "Preocupaciones del paciente: Un hombre de 55 años con un historial de 80 años fumando presenta al hospital con un historial de 3 semanas de fiebres, tos productiva, disnea y sibilancias. No tenía comorbilidades significativas.\n\nDiagnóstico: Extensas investigaciones radiológicas revelaron una gran masa en el hilum derecho que comprimía el bronquio inferior derecho con depósitos suprarrenales metastásicos. Las investigaciones bioquímicas confirmaron el síndrome de secreción inadecuada de la hormona antidiurética, y la histología identificó un CPCP.\n\nIntervenciones: A pesar de iniciar una quimioterapia combinada con carboplatino y etopósido, el paciente desarrolló parálisis motora progresiva y pérdida sensorial en el transcurso de 4 días, lo que derivó en un diagnóstico de polineuropatía motora y sensorial aguda paraneoplásica.\n\nResultados: Su estado empeoró rápidamente y falleció 14 días después de la aparición de los síntomas debido a una insuficiencia respiratoria, lo que pone de relieve la agresividad de los síndromes paraneoplásicos.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Había un hombre que estaba muy enfermo. Tenía tos, fiebre y le costaba respirar. \n\nLos doctores encontraron un bulto grande en su pulmón. También tenía un problema en otras partes de su cuerpo. \n\nLe dieron medicinas para el cáncer, pero empezó a perder fuerza en sus piernas y brazos. No podía sentir bien ni moverlos. \n\nMuy rápido, se puso muy mal y no pudo respirar bien. Después de unos días, se fue al cielo. \n\nLos doctores dijeron que su enfermedad fue muy fuerte y difícil de curar.",
+        "score": {
+          "ROUGE-L-Sum": 0.2344322344322344,
+          "BERTScore_F": 0.7291522026062012
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.4817922185192178
+        }
+      },
+      "B2": {
+        "text": "**Lo que le pasó al paciente**  \nUn hombre de 55 años que había fumado mucho durante muchos años llegó al hospital con fiebre, tos con flema, dificultad para respirar y silbidos al respirar. Estos síntomas habían durado tres semanas. Antes de esto, estaba sano y no tenía otras enfermedades importantes.\n\n**Qué encontraron los médicos**  \nLas pruebas de imagen mostraron una masa grande en una parte del pulmón derecho que estaba bloqueando una vía respiratoria importante. También encontraron que el cáncer se había extendido a las glándulas suprarrenales, que están encima de los riñones. Un análisis de sangre mostró que tenía un problema llamado síndrome de secreción inadecuada de hormona antidiurética, que afecta el equilibrio de líquidos en el cuerpo. Al analizar una muestra del tumor, confirmaron que tenía un tipo de cáncer de pulmón llamado cáncer de pulmón de células pequeñas (CPCP).\n\n**Tratamiento y complicaciones**  \nEl paciente comenzó a recibir quimioterapia con dos medicamentos, carboplatino y etopósido, que son comunes para tratar este tipo de cáncer. Sin embargo, en pocos días, empezó a perder fuerza en las piernas y luego en los brazos, además de perder sensibilidad. Los médicos diagnosticaron una polineuropatía motora y sensorial aguda paraneoplásica, que es una enfermedad nerviosa grave relacionada con el cáncer, donde los nervios dejan de funcionar correctamente.\n\n**Qué pasó al final**  \nA pesar de que el tratamiento contra el cáncer estaba funcionando y el tumor había disminuido de tamaño, la enfermedad nerviosa empeoró rápidamente. El paciente tuvo problemas para respirar y falleció dos semanas después de que aparecieron los síntomas nerviosos. Este caso muestra lo agresivos y difíciles de tratar que pueden ser los síndromes paraneoplásicos, que son enfermedades causadas por la reacción del cuerpo al cáncer.",
+        "score": {
+          "ROUGE-L-Sum": 0.4150197628458498,
+          "BERTScore_F": 0.8047367930412292
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.6098782779435395
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nUn hombre de 55 años, con un historial muy extenso de tabaquismo (equivalente a 80 paquetes-año) y sin enfermedades previas relevantes, acudió al hospital tras presentar durante tres semanas fiebre persistente, tos con expectoración, dificultad para respirar y sibilancias. Inicialmente fue tratado con antibióticos y corticoides, pero sus síntomas empeoraron, lo que motivó su ingreso hospitalario.\n\n**Hallazgos Clave**  \nLas pruebas radiológicas, incluyendo radiografía y tomografía computarizada (TC) de tórax, revelaron una masa grande en la región del hilio derecho del pulmón, que comprimía el bronquio inferior derecho, además de metástasis en las glándulas suprarrenales. Los análisis de sangre mostraron un síndrome de secreción inadecuada de hormona antidiurética (SIADH), que explica un nivel muy bajo de sodio en sangre. La biopsia pulmonar confirmó el diagnóstico de cáncer de pulmón de células pequeñas (CPCP), un tipo agresivo de tumor pulmonar.\n\n**Interpretación Clínica**  \nA pesar de iniciar un tratamiento estándar con quimioterapia combinada de carboplatino y etopósido, el paciente desarrolló rápidamente una polineuropatía aguda, es decir, un daño progresivo en múltiples nervios que afectó tanto la función motora (movimiento) como sensorial (sensaciones). En pocos días, presentó debilidad grave en las extremidades inferiores que progresó a parálisis completa de brazos y piernas, acompañada de pérdida sensorial. Las pruebas de imágenes cerebrales y de la médula espinal no mostraron metástasis ni compresión nerviosa, y los análisis de líquido cefalorraquídeo descartaron infección o infiltración tumoral directa. Los estudios electrofisiológicos indicaron una combinación de daño axonal (afectación de las fibras nerviosas) y desmielinizante (pérdida de la cubierta protectora de los nervios), un patrón atípico para síndromes paraneoplásicos clásicos, que suelen afectar principalmente la sensibilidad.\n\nSe inició tratamiento inmunomodulador con dexametasona (un corticoide) e inmunoglobulina intravenosa, pero no se observó mejoría neurológica. La rápida progresión de la debilidad llevó a insuficiencia respiratoria, requiriendo soporte ventilatorio.\n\n**Próximos Pasos y Resultado Final**  \nTras una cuidadosa discusión multidisciplinaria y con el paciente plenamente informado, se decidió no continuar con soporte ventilatorio invasivo debido a la baja probabilidad de recuperación neurológica y la mala calidad de vida esperada. El paciente falleció tres semanas después del inicio de los síntomas neurológicos.\n\nEste caso ilustra la agresividad y complejidad de los síndromes paraneoplásicos asociados al cáncer de pulmón de células pequeñas, donde la respuesta favorable al tratamiento oncológico puede contrastar con un deterioro neurológico rápido e irreversible. Además, resalta la importancia de abordar las decisiones éticas y de calidad de vida en el manejo de estas complicaciones graves.",
+        "score": {
+          "ROUGE-L-Sum": 0.3677811550151976,
+          "BERTScore_F": 0.8232091069221497
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5954951309686736
+        }
+      }
+    }
+  },
+  {
+    "id": 54,
+    "gold_summary": "Se describió el caso de un paciente de 66 años con disfagia por atragantamiento con sólidos y reflujo nasal de alimentos desde hacía un año. La videoendoscopia de la deglución mostró una protuberancia en la pared posterior de la faringe y, al ofrecer alimentos sólidos, una restricción de la retroflexión de la epiglotis, reflujo nasal de alimentos y una gran cantidad de residuos de alimentos sobre la lesión. La tomografía computarizada de la columna cervical identificó la presencia de osteofitos cervicales anteriores entre las vértebras C3 y C6, el más grande con una longitud anteroposterior de 12 milímetros, que estrechaba la columna aérea a nivel de la orofaringe e hipofaringe. El paciente fue tratado adecuadamente con fonoterapia para la deglución.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Un señor de 66 años tenía problemas para tragar comida dura. A veces, la comida se le iba por la nariz. Los doctores vieron que tenía un bulto en la garganta. También había huesos grandes que apretaban su garganta. Para ayudarlo, le enseñaron ejercicios para tragar mejor. Ahora puede comer sin problemas y está bien cuidado.",
+        "score": {
+          "ROUGE-L-Sum": 0.16161616161616163,
+          "BERTScore_F": 0.6953634023666382
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.4284897819913999
+        }
+      },
+      "B2": {
+        "text": "**Lo que Encontraron**\n\nUn hombre de 66 años tenía problemas para tragar alimentos sólidos y notaba que la comida a veces regresaba por la nariz desde hacía un año. Al hacerle un examen llamado videoendoscopia de la deglución, que consiste en usar una cámara pequeña para ver cómo traga, se vio una protuberancia (una especie de bulto) en la parte de atrás de su garganta. Cuando comía alimentos sólidos, su epiglotis (una parte que ayuda a que la comida no vaya a los pulmones) no se movía bien, y parte de la comida subía hacia la nariz, quedando residuos sobre el bulto.\n\n**Qué Significa**\n\nPara entender mejor la causa, le hicieron una tomografía computarizada, que es un tipo de radiografía especial que muestra imágenes detalladas de los huesos y tejidos. En esta imagen, encontraron que tenía unos crecimientos óseos llamados osteofitos en su columna cervical (el cuello), entre las vértebras C3 y C6. El más grande medía 12 milímetros y estaba presionando la vía aérea en la garganta, dificultando el paso normal de la comida.\n\n**Cómo lo Trataron**\n\nEl paciente recibió terapia para mejorar la forma en que traga, llamada fonoterapia. Esta terapia incluyó ejercicios para la lengua y cambios en la postura al comer, como inclinar la cabeza hacia adelante para facilitar el paso de la comida. También modificaron su dieta para evitar alimentos muy duros o secos. Gracias a este tratamiento, pudo mejorar su capacidad para tragar sin necesidad de cirugía y sigue siendo controlado regularmente para asegurarse de que no tenga problemas nuevos.",
+        "score": {
+          "ROUGE-L-Sum": 0.30622009569377984,
+          "BERTScore_F": 0.7903397083282471
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5482799020110134
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe presentó el caso de un hombre de 66 años que acudió a consulta por dificultad para tragar alimentos sólidos, acompañada de sensación de atragantamiento y reflujo nasal de alimentos, síntomas que persistían desde hacía un año. Entre sus antecedentes médicos destacaba un accidente automovilístico ocurrido 13 años antes y diabetes.  \n\n**Hallazgos Clave**  \nMediante una videoendoscopia de la deglución, se identificó una protuberancia en la pared posterior de la hipofaringe (parte baja de la garganta), con acumulación de saliva sobre esta lesión. Al ofrecer alimentos sólidos, se observó que la epiglotis (estructura que ayuda a proteger las vías respiratorias durante la deglución) tenía dificultad para doblarse hacia atrás, además de reflujo nasal de alimentos y una gran cantidad de restos alimentarios acumulados por encima de la protuberancia.  \n\nUna tomografía computarizada (TC) de la columna cervical reveló la presencia de osteofitos (crecimientos óseos anormales) en la parte anterior de las vértebras cervicales C3 a C6, siendo el más grande de 12 milímetros. Estos osteofitos comprimían la vía aérea en la región de la orofaringe e hipofaringe, lo que explicaba la dificultad para tragar.  \n\n**Interpretación Clínica**  \nEl diagnóstico principal fue disfagia mecánica causada por osteofitos cervicales que estrechaban la vía aérea y alteraban el mecanismo normal de la deglución. Se descartaron otras posibles causas de disfagia.  \n\n**Tratamiento y Seguimiento**  \nEl paciente recibió terapia de deglución personalizada, que incluyó:  \n- Modificación de la dieta para evitar alimentos sólidos y secos, facilitando la ingesta.  \n- Maniobras posturales durante la deglución, especialmente la flexión de la cabeza hacia adelante (chin tuck), que mejora el paso del alimento y reduce el reflujo nasal.  \n- Ejercicios de fortalecimiento de la lengua para superar la obstrucción mecánica y facilitar la expulsión del alimento.  \n\nAdemás, se prescribió omeprazol para tratar el reflujo faringolaríngeo (reflujo de ácido hacia la garganta). El paciente mostró una respuesta favorable tras seis sesiones de terapia y se mantuvo bajo seguimiento regular durante dos años, con controles trimestrales en el primer año y semestrales posteriormente.  \n\nSe evaluó la posibilidad de tratamiento quirúrgico para eliminar los osteofitos, pero se decidió continuar con un manejo conservador debido a la buena compensación clínica. Se recomendó continuar con ejercicios en casa y mantener evaluaciones periódicas al menos una vez al año, para detectar a tiempo cualquier deterioro en la función de la deglución asociado al envejecimiento o a nuevos factores.  \n\n**Conclusión**  \nEste caso ilustra cómo los osteofitos cervicales pueden causar disfagia mecánica significativa, y cómo un tratamiento integral basado en terapia de deglución y modificaciones dietéticas puede lograr una adecuada compensación funcional, evitando la necesidad de cirugía y mejorando la calidad de vida del paciente.",
+        "score": {
+          "ROUGE-L-Sum": 0.3454833597464342,
+          "BERTScore_F": 0.8382336497306824
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5918585047385583
+        }
+      }
+    }
+  },
+  {
+    "id": 55,
+    "gold_summary": "Una paciente de 18 años de edad se presentó en nuestra clínica con múltiples bultos palpables en sus senos bilateralmente. En el examen físico, la paciente también tenía múltiples lesiones pigmentadas lentigosas en su cara, cuerpo y esclerótica, nevos azules en su tronco y extremidades superiores y un rostro redondo con forma de luna. El diagnóstico del síndrome de Carney se decidió mediante imágenes, biopsias y análisis genético. La paciente se sometió a una mastectomía bilateral como plan de tratamiento profiláctico con colocación de expansores de tejidos.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Una niña de 18 años tenía muchos bultos en sus pechos. También tenía manchas de colores en su cara y cuerpo. Los doctores hicieron pruebas y encontraron una enfermedad llamada síndrome de Carney. Para ayudarla, le quitaron los pechos y pusieron cosas suaves para que su cuerpo se vea bien.",
+        "score": {
+          "ROUGE-L-Sum": 0.2893081761006289,
+          "BERTScore_F": 0.7721976637840271
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.530752919942328
+        }
+      },
+      "B2": {
+        "text": "**Lo que Encontraron en la Paciente**  \nUna joven de 18 años llegó a la clínica porque tenía varios bultos en ambos senos. Al examinarla, también notaron manchas oscuras en su piel y ojos, así como lunares azules en su cuerpo. Su cara tenía una forma redonda, parecida a una luna llena. Estas señales indicaron que podría tener algo llamado síndrome de Carney, que es una enfermedad rara que causa tumores benignos (no cancerosos) en diferentes partes del cuerpo.\n\n**Cómo Confirmaron el Diagnóstico**  \nPara estar seguros, los médicos hicieron varias pruebas. Usaron imágenes especiales como ultrasonidos y resonancias magnéticas para ver los bultos en sus senos. Además, tomaron pequeñas muestras de esos bultos (biopsias) para analizarlas bajo el microscopio. También hicieron un examen genético y encontraron un cambio en un gen llamado PRHAR1A, que está relacionado con este síndrome.\n\n**Qué Tratamiento Eligieron**  \nDespués de discutir varias opciones, decidieron hacer una mastectomía bilateral. Esto significa que le quitaron ambos senos para evitar problemas futuros, ya que los bultos seguían creciendo y causaban dolor. Para ayudar a que la piel se mantuviera y poder reconstruir después, colocaron unos dispositivos llamados expansores de tejidos, que poco a poco estiran la piel. Más tarde, estos expansores se reemplazaron por implantes de silicona para que la paciente tuviera una apariencia natural.\n\n**Importancia del Caso**  \nEste caso muestra cómo es importante combinar diferentes pruebas para diagnosticar enfermedades raras como el síndrome de Carney. También destaca que, a veces, el tratamiento puede ser difícil y requiere decisiones importantes para mejorar la calidad de vida del paciente.",
+        "score": {
+          "ROUGE-L-Sum": 0.21134020618556698,
+          "BERTScore_F": 0.7698163986206055
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.4905783024030862
+        }
+      },
+      "B3": {
+        "text": "**Contexto**\n\nUna joven caucásica de 18 años acudió a la clínica debido a la presencia de múltiples bultos palpables en ambos senos. Durante el examen físico, se observaron varias lesiones pigmentadas llamadas lentigos (manchas oscuras) en la cara, el cuerpo y la esclerótica (parte blanca del ojo), además de nevos azules (manchas pigmentadas) en el tronco y extremidades superiores, y una característica forma redonda de su rostro, conocida como cara en forma de luna.\n\n**Hallazgos Clave**\n\n- Estudios por ultrasonido y resonancia magnética revelaron múltiples nódulos compactos en ambos senos, identificados como fibroadenomas mixoides, siendo el más grande de 7,8 cm en el seno izquierdo.\n- Se realizaron biopsias por escisión de algunos nódulos, confirmando el diagnóstico de fibroadenomas mixtos.\n- Se detectó una anomalía en el mediastino anterior (área entre los pulmones), consistente con un timo prominente, y ganglios linfáticos axilares e internos aumentados de tamaño.\n- Los análisis hormonales no mostraron alteraciones significativas.\n- Un estudio genético identificó una mutación en el gen PRKAR1A, asociada con el síndrome de Carney, una enfermedad rara que se caracteriza por la presencia de tumores benignos en diferentes órganos y lesiones pigmentadas en la piel.\n\n**Interpretación Clínica**\n\nEl conjunto de hallazgos clínicos, imagenológicos, histopatológicos y genéticos permitió establecer el diagnóstico del síndrome de Carney. Este síndrome explica la presencia simultánea de múltiples fibroadenomas mamarios, lesiones pigmentadas cutáneas y otras anomalías observadas en la paciente.\n\n**Próximos Pasos y Tratamiento**\n\nDado que las cirugías previas para extirpar los fibroadenomas grandes solo proporcionaron alivio temporal y afectaban negativamente la calidad de vida de la paciente, se consideraron opciones de tratamiento más definitivas. Tras una evaluación psicológica y médica exhaustiva, se decidió realizar una mastectomía bilateral (extirpación completa de ambos senos) con conservación de la piel, seguida de la colocación subcutánea de expansores de tejidos para permitir la reconstrucción mamaria gradual.\n\nEl cuidado postoperatorio incluyó el uso de un sujetador médico y visitas regulares para el llenado progresivo de los expansores. Un año después, se reemplazaron estos expansores por implantes permanentes de silicona colocados debajo del músculo, con un manejo mínimo de la herida y seguimiento ambulatorio.\n\nEste enfoque permitió controlar los síntomas, mejorar la calidad de vida de la paciente y manejar de manera efectiva las manifestaciones mamarias del síndrome de Carney.",
+        "score": {
+          "ROUGE-L-Sum": 0.2943396226415095,
+          "BERTScore_F": 0.7879701256752014
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.5411548741583554
+        }
+      }
+    }
+  },
+  {
+    "id": 56,
+    "gold_summary": "Se presenta el caso de una paciente adolescente femenino que, tras tratamiento conservador con férula de una fractura fisaria Peterson tipo I en radio, sufre a las seis semanas déficit agudo de extensión del pulgar, diagnosticada mediante examen clínico radiológico de rotura espontánea del extensor pollicis longus. Es tratada por medio de transferencia del extensor propio del índice (EPI) con resultados satisfactorios y recuperación de su actividad habitual al mes postoperatorio.",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Una niña de 13 años se cayó y se lastimó la muñeca. Le pusieron una tablita para que su hueso sanara. \n\nDespués de quitarle la tablita, su dedo pulgar no podía moverse bien. Los doctores vieron que un hilo que mueve el dedo se había roto. \n\nElla tuvo una operación para arreglar ese hilo con otro hilo de su mano. \n\nDespués de un mes, su dedo volvió a moverse bien y pudo hacer todo como antes.",
+        "score": {
+          "ROUGE-L-Sum": 0.12345679012345678,
+          "BERTScore_F": 0.7038714289665222
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.4136641095449895
+        }
+      },
+      "B2": {
+        "text": "Caso de una adolescente de 13 años con fractura en la muñeca que fue tratada con una férula. Seis semanas después, comenzó a tener dificultad para estirar el pulgar de la mano izquierda. Los médicos descubrieron que uno de los tendones que mueve el pulgar, llamado extensor largo del pulgar, se había roto sin que ella hiciera un esfuerzo fuerte. Para arreglarlo, realizaron una cirugía donde usaron otro tendón del dedo índice para reemplazar el que estaba roto. Después de la operación y un periodo de inmovilización, la paciente recuperó completamente el movimiento del pulgar y pudo volver a sus actividades normales en un mes.",
+        "score": {
+          "ROUGE-L-Sum": 0.2061855670103093,
+          "BERTScore_F": 0.7668335437774658
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.48650955539388757
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe trata de una adolescente de 13 años, sin antecedentes médicos relevantes, que sufrió una caída mientras patinaba, ocasionándole dolor e incapacidad para mover la muñeca izquierda. Fue diagnosticada con una fractura en la parte distal del radio (hueso del antebrazo), específicamente una lesión fisaria clasificada como Peterson tipo I, y se le inmovilizó la muñeca con una férula durante cuatro semanas.\n\n**Hallazgos Clave**  \nDos semanas después de retirar la férula, la paciente volvió a urgencias tras sentir un crujido en la muñeca sin haber realizado un esfuerzo adicional. Presentaba incapacidad para extender (levantar) el primer dedo de la mano izquierda, hinchazón local y asimetría visible en comparación con la mano contraria. La exploración clínica mostró un déficit en la extensión activa del dedo y un signo llamado tenodesis patológico, que indica alteración en la función tendinosa. La resonancia magnética confirmó la ruptura del tendón extensor largo del pulgar (EPL), que es el tendón responsable de estirar el pulgar.\n\n**Interpretación Clínica**  \nLa ruptura espontánea del tendón extensor largo del pulgar es una complicación poco frecuente pero grave que puede ocurrir después de fracturas en la muñeca, incluso cuando el tratamiento inicial es conservador. Debido a la pérdida de función del EPL, se decidió realizar una cirugía para restaurar la movilidad del pulgar. El procedimiento consistió en transferir el tendón extensor propio del índice (EPI), que normalmente mueve el dedo índice, para sustituir la función del tendón lesionado del pulgar. La sutura se realizó mediante una técnica llamada Pulvertaft, que asegura una unión firme entre los tendones.\n\n**Próximos Pasos y Resultados**  \nTras la cirugía, la muñeca se inmovilizó durante cuatro semanas para favorecer la cicatrización. Posteriormente, se permitió la movilidad y la paciente mostró una recuperación completa de la extensión del pulgar sin dolor ni limitaciones funcionales. En los controles realizados a las 6, 12 semanas y al año, no se observaron complicaciones, y la paciente recuperó completamente su actividad habitual, con una puntuación de 0 en la escala PRWE, que indica ausencia de dolor y discapacidad en la muñeca.\n\nEn resumen, este caso ilustra cómo una complicación inesperada tras una fractura en la muñeca puede ser tratada con éxito mediante una transferencia tendinosa, logrando una recuperación funcional completa en una paciente adolescente.",
+        "score": {
+          "ROUGE-L-Sum": 0.18253968253968256,
+          "BERTScore_F": 0.7451465725898743
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.4638431275647784
+        }
+      }
+    }
+  },
+  {
+    "id": 57,
+    "gold_summary": "Un hombre de 73 años con enfermedad de Castleman, tratado con TCZ, se sometió a un reemplazo de la válvula aórtica por medio de esternotomía mediana para la regurgitación de la válvula aórtica con falta de aire al hacer ejercicio. Se implementaron medidas integrales para prevenir la infección del sitio quirúrgico junto con un examen minucioso durante el período perioperatorio. Tocilizumab se interrumpió 26 días antes de la cirugía y se reanudó 30 días después de la cirugía, durante los cuales los niveles de IL-6 en plasma disminuyeron. No hubo evidencia de infección o exacerbación de la enfermedad de Castleman. Los niveles del factor de crecimiento endotelial vascular aumentaron antes de un aumento en los niveles de proteína C reactiva después del alta hospitalaria y antes de la reanudación de TCZ.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Un hombre de 73 años estaba enfermo y tenía problemas en su corazón. Tenía dificultad para respirar cuando caminaba. Los doctores le hicieron una operación para cambiar una parte del corazón llamada válvula.\n\nAntes de la operación, dejaron de darle un medicamento llamado TCZ para que no tuviera problemas. También cuidaron mucho que no se le hiciera una infección en la herida.\n\nDespués de la operación, el hombre se fue mejorando. No tuvo infecciones ni se puso más enfermo. Cuando estuvo listo, le dieron otra vez el medicamento para ayudarlo.\n\nLos doctores vieron que su cuerpo estaba mejor y que el medicamento funcionaba bien. El hombre pudo salir del hospital sin problemas.",
+        "score": {
+          "ROUGE-L-Sum": 0.19494584837545126,
+          "BERTScore_F": 0.7461668252944946
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.47055633683497294
+        }
+      },
+      "B2": {
+        "text": "**Lo que le pasaba al paciente:**  \nUn hombre de 73 años tenía una enfermedad llamada enfermedad de Castleman, que afecta a los ganglios linfáticos y causa inflamación. También tenía un problema en el corazón llamado regurgitación de la válvula aórtica, que significa que la válvula no cerraba bien y eso le causaba dificultad para respirar al hacer ejercicio.\n\n**Qué tratamiento recibió:**  \nPara mejorar su corazón, los médicos le hicieron una cirugía para reemplazar la válvula aórtica. Antes de la operación, el paciente recibía un medicamento llamado tocilizumab (TCZ), que ayuda a controlar la inflamación en la enfermedad de Castleman. Este medicamento se detuvo 26 días antes de la cirugía para evitar problemas durante la operación y se volvió a empezar 30 días después, cuando ya estaba seguro.\n\n**Cómo cuidaron al paciente durante la cirugía:**  \nLos médicos tomaron muchas precauciones para evitar infecciones en la herida de la cirugía. Revisaron si tenía bacterias en la nariz, limpiaron bien la piel antes de operar, usaron antibióticos preventivos y controlaron su azúcar en sangre. Además, usaron una técnica especial llamada terapia de presión negativa en la herida para ayudar a que sanara sin infecciones.\n\n**Qué pasó después de la cirugía:**  \nEl paciente no tuvo infecciones ni empeoramiento de su enfermedad durante el tiempo que estuvo sin tomar el medicamento. Los niveles en sangre de una proteína llamada IL-6, que está relacionada con la inflamación, bajaron después de la cirugía y subieron nuevamente cuando volvió a tomar el medicamento. También observaron cambios en otras proteínas relacionadas con la inflamación, pero el paciente se recuperó bien y pudo salir del hospital sin problemas.\n\n**En resumen:**  \nEste caso muestra que es posible hacer una cirugía importante en un paciente con enfermedad de Castleman que usa tocilizumab, siempre que se tomen medidas cuidadosas para prevenir infecciones y se controle bien el tratamiento antes y después de la operación.",
+        "score": {
+          "ROUGE-L-Sum": 0.26666666666666666,
+          "BERTScore_F": 0.7905909419059753
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.528628804286321
+        }
+      },
+      "B3": {
+        "text": "**Contexto:**  \nUn hombre de 73 años con diagnóstico de enfermedad de Castleman idiopática multicéntrica (iMCD), un trastorno inflamatorio caracterizado por crecimiento anormal de ganglios linfáticos y producción elevada de interleucina-6 (IL-6), fue tratado con tocilizumab (TCZ), un medicamento que bloquea la acción de esta proteína inflamatoria. Además, presentaba regurgitación valvular aórtica (fuga en la válvula del corazón que permite el retorno de sangre), que causaba dificultad progresiva para respirar durante el esfuerzo, y se decidió realizar un reemplazo quirúrgico de la válvula aórtica (SAVR) mediante una incisión en el esternón (esternotomía media).\n\n**Hallazgos Clave y Manejo Perioperatorio:**  \nAntes de la cirugía, el paciente recibió cuidados especializados para minimizar el riesgo de infecciones en el sitio quirúrgico, incluyendo la detección y manejo de bacterias en la nariz, preparación cuidadosa de la piel, uso profiláctico de antibióticos y control estricto del azúcar en sangre. El tratamiento con tocilizumab se suspendió 26 días antes de la operación para reducir posibles complicaciones inmunológicas, mientras que la administración de esteroides continuó para controlar la inflamación. La cirugía se realizó con éxito bajo circulación extracorpórea (máquina que mantiene la circulación y oxigenación de la sangre durante la operación), requiriendo transfusiones de sangre, y el paciente fue extubado al día siguiente sin complicaciones inmediatas.\n\nDurante el postoperatorio, no se observaron signos de infección en la herida quirúrgica, y se utilizó terapia de presión negativa (una técnica para favorecer la cicatrización y prevenir infecciones) hasta el día 13 después de la cirugía. El paciente fue dado de alta el día 17 sin evidencia de infección ni recurrencia de los síntomas de la enfermedad de Castleman, como erupciones cutáneas o aumento de ganglios linfáticos.\n\n**Interpretación Clínica:**  \nLos niveles de IL-6 en plasma aumentaron temporalmente en los primeros días tras la cirugía, lo cual es esperado debido a la respuesta inflamatoria postoperatoria, pero luego disminuyeron progresivamente hasta el día 24. Posteriormente, al reanudarse el tratamiento con tocilizumab el día 30, los niveles de IL-6 volvieron a aumentar, reflejando la acción del medicamento. La proteína C reactiva (PCR), un marcador de inflamación, mostró un leve aumento sin evidencia de infección, y se observó un incremento previo en el factor de crecimiento endotelial vascular, una proteína relacionada con la reparación y formación de vasos sanguíneos, lo que podría indicar procesos de recuperación tisular.\n\nLa función renal mostró un aumento temporal en los niveles de creatinina después de la cirugía, pero volvió a los valores previos al alta, indicando una recuperación adecuada de la función renal.\n\n**Próximos Pasos y Conclusiones:**  \nEl manejo cuidadoso del tratamiento inmunosupresor y las medidas preventivas implementadas permitieron realizar con éxito el reemplazo valvular en un paciente con enfermedad de Castleman sin complicaciones infecciosas ni exacerbación de la enfermedad. La reanudación del tocilizumab se realizó de forma segura tras confirmar la ausencia de infección. Este caso resalta la importancia de una planificación multidisciplinaria y un seguimiento riguroso en pacientes con enfermedades inflamatorias complejas sometidos a cirugía mayor.",
+        "score": {
+          "ROUGE-L-Sum": 0.25449515905947445,
+          "BERTScore_F": 0.8027184009552002
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.5286067800073373
+        }
+      }
+    }
+  },
+  {
+    "id": 58,
+    "gold_summary": "Se presenta el caso de un infante con enfermedad granulomatosa crónica y aspergilosis invasiva. Se trata de un lactante de sexo masculino de cuatro meses de edad, de madre hipotiroidea y con quien convive en la celda de la cárcel. El infante presentó tumores en la región axilar izquierda y la radiografía de tórax sugirió fracturas costales; fue hospitalizado ante la sospecha de maltrato infantil. En la tomografía de tórax se observó un absceso axilar, osteólisis de costillas, neumonía y nódulos pulmonares; el paciente recibió antibióticos de amplio espectro y fue dado de alta. A los ocho meses, reingresó por fiebre y extensión del absceso purulento hacia la región escapular izquierda; en la tomografía se observaron imágenes de empeoramiento de la condición. Se aisló Aspergillus fumigatus de la secreción del absceso y se diagnosticó aspergilosis invasiva; se inició tratamiento con voriconazol por 28 días. Mediante la prueba de dihidrorrodamina, se diagnosticó enfermedad granulomatosa crónica causada por la variante patógena c.80_83del/Y del gen CYBB, portada por la madre (c.80_83del/WT). A los 12 meses, el paciente reingresó nuevamente por aspergilosis invasiva, resistente al tratamiento, con desenlace fatal.",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Había un bebé que estaba muy enfermo. Tenía un bulto doloroso en su brazo y problemas para respirar. Los doctores lo cuidaron mucho y le dieron medicinas para que mejorara.\n\nDespués, el bebé se volvió a enfermar. Tenía fiebre y otro bulto que dolía mucho. Los doctores encontraron un hongo que le hacía daño. Le dieron medicinas especiales para el hongo.\n\nLos doctores hicieron pruebas y vieron que el bebé tenía un problema en su cuerpo que no lo dejaba pelear bien contra las enfermedades. Su mamá también tenía ese problema, pero no estaba enferma.\n\nEl bebé estuvo en el hospital muchas veces. Aunque los doctores hicieron todo lo posible, el bebé se puso muy mal y no pudo mejorar. Los doctores y su familia lo cuidaron con mucho amor.",
+        "score": {
+          "ROUGE-L-Sum": 0.12535612535612536,
+          "BERTScore_F": 0.7042726874351501
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.41481440639563777
+        }
+      },
+      "B2": {
+        "text": "**Caso de un Bebé con Problemas en el Sistema Inmunológico y una Infección Grave**\n\nEste es el caso de un bebé de cuatro meses que vivía con su madre en una cárcel. Su madre tenía problemas de tiroides y durante el embarazo tomó medicamentos. El bebé nació con buen peso y tamaño, pero luego presentó un bulto doloroso en la axila izquierda. Al hacerle una radiografía, los médicos vieron posibles fracturas en sus costillas, por lo que pensaron que podría estar sufriendo maltrato. Fue hospitalizado para recibir atención.\n\nEn estudios más detallados, encontraron un absceso (una acumulación de pus) en la axila, daño en varias costillas, neumonía y nódulos en los pulmones. El bebé recibió antibióticos fuertes y fue dado de alta después de mejorar un poco.\n\nA los ocho meses, volvió al hospital con fiebre y un absceso que se extendió hacia la parte superior de la espalda. Nuevas imágenes mostraron que la infección había empeorado. En el pus del absceso encontraron un hongo llamado Aspergillus fumigatus, que puede causar infecciones graves, especialmente en personas con defensas bajas. Por eso, le dieron un medicamento antifúngico llamado voriconazol.\n\nLos médicos sospecharon que el bebé tenía un problema en su sistema inmunológico, que es el que nos protege de las infecciones. Hicieron una prueba llamada dihidrorrodamina, que mostró que sus células defensivas no podían producir sustancias necesarias para combatir gérmenes. Esto confirmó que tenía una enfermedad llamada enfermedad granulomatosa crónica, que afecta la capacidad del cuerpo para luchar contra ciertas infecciones. Esta enfermedad fue causada por un cambio en un gen llamado CYBB, que heredó de su madre.\n\nA pesar del tratamiento, a los 12 meses el bebé volvió a enfermar gravemente por la misma infección de Aspergillus. La infección no respondió bien a los medicamentos y, lamentablemente, el bebé falleció debido a una falla de varios órganos.\n\n**Qué Significa Este Caso**\n\nEste caso muestra cómo un problema genético en el sistema inmunológico puede hacer que un bebé sea muy vulnerable a infecciones graves, como las causadas por hongos. También resalta la importancia de diagnosticar estas enfermedades temprano para intentar proteger a los pacientes con tratamientos adecuados.",
+        "score": {
+          "ROUGE-L-Sum": 0.27574750830564787,
+          "BERTScore_F": 0.799397885799408
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.5375726970525279
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe describe el caso de un lactante varón de cuatro meses originario del centro de México, cuya madre presentaba hipotiroidismo y con quien vivía en condiciones precarias dentro de una cárcel. El bebé nació con peso y talla adecuados, pero a los cuatro meses desarrolló un tumor doloroso en la axila izquierda. Ante la sospecha inicial de maltrato infantil, debido a fracturas costales observadas en radiografías, fue hospitalizado para evaluación y tratamiento.\n\n**Hallazgos Clave**  \nDurante la hospitalización inicial, las imágenes de tomografía mostraron un absceso en la axila izquierda, lesiones destructivas en varias costillas (osteólisis), neumonía en el lóbulo superior del pulmón izquierdo y nódulos pulmonares bilaterales, además de ganglios linfáticos aumentados de tamaño. El análisis de sangre reveló anemia, elevación de leucocitos y marcadores inflamatorios, indicativos de infección activa. A pesar de recibir antibióticos de amplio espectro, el paciente presentó recurrencia de la infección a los ocho meses, manifestada por fiebre y un absceso supurante que se extendió hacia la región escapular izquierda. Nuevas imágenes mostraron empeoramiento con consolidación pulmonar, bronquiectasias (dilatación anormal de las vías respiratorias), lesiones óseas adicionales y formación de fístulas. En el cultivo de la secreción del absceso se aisló Aspergillus fumigatus, un hongo que causa infecciones invasivas en personas con alteraciones inmunológicas.\n\n**Interpretación Clínica**  \nLa recurrencia y gravedad de las infecciones, junto con la presencia de infecciones fúngicas invasivas, sugirieron un defecto en la inmunidad innata. La prueba funcional de dihidrorrodamina, que evalúa la capacidad de los neutrófilos (un tipo de glóbulo blanco) para producir especies reactivas de oxígeno necesarias para eliminar microorganismos, fue negativa. Además, no se detectó la proteína gp91^phox en neutrófilos, confirmando el diagnóstico de enfermedad granulomatosa crónica ligada al cromosoma X, una condición genética que afecta la capacidad del sistema inmunitario para combatir ciertas infecciones. La secuenciación genética identificó una mutación patógena específica (c.80_83del/Y) en el gen CYBB, responsable de esta enfermedad, y se confirmó que la madre era portadora de esta variante.\n\n**Próximos Pasos y Evolución**  \nTras el diagnóstico, el paciente recibió tratamiento antifúngico con voriconazol y profilaxis antibiótica y antifúngica para prevenir nuevas infecciones. Sin embargo, a la edad de un año, volvió a ingresar al hospital con neumonía multifocal grave causada nuevamente por Aspergillus fumigatus, que requirió soporte respiratorio avanzado. A pesar del tratamiento, el paciente desarrolló falla orgánica múltiple y falleció un mes después.\n\n**Resumen Final**  \nEste caso ilustra la presentación clínica y evolución de un lactante con enfermedad granulomatosa crónica ligada al cromosoma X, caracterizada por infecciones recurrentes graves, incluyendo aspergilosis invasiva. La identificación temprana de esta enfermedad genética es crucial para el manejo adecuado y la prevención de complicaciones fatales, aunque en este caso la gravedad y recurrencia de las infecciones condujeron a un desenlace fatal.",
+        "score": {
+          "ROUGE-L-Sum": 0.3233695652173913,
+          "BERTScore_F": 0.8289984464645386
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.576184005840965
+        }
+      }
+    }
+  },
+  {
+    "id": 59,
+    "gold_summary": "Presentamos el caso de un varón de 66 años de edad oriundo de la ciudad Juan Bautista Alberdi de la provincia de Buenos Aires con antecedentes de hipertensión arterial y trastorno obsesivo compulsivo. Consultó por fiebre súbita de cuatro días de evolución, con desarrollo de encefalopatía durante su internación. La punción lumbar mostró un líquido cefalorraquídeo cristalino, aunque inflamatorio de predominio mononuclear. La RMN de encéfalo informó hiperintensidad en secuencias FLAIR y T2 en el dorso del tronco encefálico. Ingresó a terapia intensiva por deterioro neurológico y acidosis respiratoria grave, requiriendo asistencia ventilatoria mecánica. Luego de 10 días presentó mejoría neurológica, sin déficit motor pero con hipoventilación alveolar que dificultaron el destete del respirador.",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Un hombre de 66 años se puso muy enfermo. Tenía fiebre y estaba confundido. Los doctores le hicieron una prueba con líquido de su espalda. El líquido estaba un poco inflamado. Le hicieron fotos especiales a su cabeza y vieron partes que estaban diferentes. El hombre tuvo que ir a un lugar especial del hospital para que lo cuidaran mucho. No podía respirar bien solo y necesitó una máquina para ayudarlo a respirar. Después de 10 días, empezó a mejorar y podía moverse bien. Pero todavía le costaba respirar sin la máquina. Los doctores lo están cuidando para que se ponga mejor.",
+        "score": {
+          "ROUGE-L-Sum": 0.1935483870967742,
+          "BERTScore_F": 0.7192491292953491
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.4563987581960617
+        }
+      },
+      "B2": {
+        "text": "**Caso de un Hombre con Fiebre y Problemas Cerebrales**\n\nUn hombre de 66 años, que vivía en Juan Bautista Alberdi, Buenos Aires, tenía antecedentes de presión alta y un trastorno llamado obsesivo compulsivo. Él llegó al hospital porque tenía fiebre alta durante cuatro días. Al principio, estaba consciente y sin problemas en sus movimientos o sensibilidad.\n\n**Lo que Encontraron**\n\nDespués de un día, empezó a confundirse y a estar somnoliento. Le hicieron una punción lumbar, que es cuando se extrae un poco de líquido del cerebro para analizarlo. Este líquido estaba claro pero mostraba signos de inflamación, especialmente con células llamadas mononucleares, que son parte del sistema inmunológico. Una resonancia magnética (una imagen del cerebro) mostró zonas inflamadas en una parte del cerebro llamada tronco encefálico.\n\n**Qué Pasó Después**\n\nSu estado empeoró y tuvo problemas para respirar bien, por lo que fue llevado a la unidad de cuidados intensivos. Allí, necesitó un respirador para ayudarle a respirar porque su cuerpo no eliminaba bien el dióxido de carbono, lo que causaba un problema llamado acidosis respiratoria. Después de 10 días, mejoró en cuanto a la conciencia y no tenía problemas para mover sus brazos y piernas, pero seguía teniendo dificultades para respirar por sí solo, lo que complicó que pudiera dejar el respirador.\n\n**Resumen**\n\nEste caso muestra cómo una infección o inflamación en el cerebro puede causar fiebre, confusión y problemas graves para respirar. Aunque el paciente mejoró su estado mental y motor, la función respiratoria tardó más en recuperarse.",
+        "score": {
+          "ROUGE-L-Sum": 0.30656934306569344,
+          "BERTScore_F": 0.7814697623252869
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5440195526954902
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe trata de un hombre de 66 años con antecedentes de hipertensión arterial y trastorno obsesivo compulsivo, que residía en Juan Bautista Alberdi, provincia de Buenos Aires. Fue hospitalizado tras presentar fiebre alta (39ºC) durante cuatro días sin otros síntomas iniciales. En el ingreso, estaba consciente y sin signos neurológicos focales, pero a las 24 horas desarrolló episodios alternantes de desorientación y somnolencia, junto con temblor en las extremidades.\n\n**Hallazgos Clave**  \n- La punción lumbar reveló un líquido cefalorraquídeo (LCR) claro pero con signos de inflamación, mostrando un aumento de leucocitos con predominio mixto (mononucleares y polimorfonucleares), proteínas elevadas y glucosa normal.  \n- Los cultivos de sangre y orina fueron negativos, así como las pruebas PCR para virus herpes simple y encefalopatía equina del oeste en LCR. Sin embargo, la detección de anticuerpos IgM específicos para encefalopatía equina del este (EEO) fue positiva tanto en suero como en LCR, confirmando la infección viral.  \n- La resonancia magnética (RMN) cerebral mostró áreas de mayor intensidad en secuencias FLAIR y T2 localizadas en la región dorsal del tronco encefálico (incluyendo protuberancia, bulbo y mesencéfalo), ambos pedúnculos cerebrales y ganglios basales, con afectación bilateral y predominio en el ganglio basal derecho. También se observaron múltiples lesiones en la sustancia blanca de ambos hemisferios cerebrales.  \n- El paciente presentó deterioro neurológico progresivo con disminución del nivel de conciencia (escala de Glasgow reducida a 8/15), requiriendo ingreso a unidad de terapia intensiva (UTI), intubación y ventilación mecánica debido a insuficiencia respiratoria con acidosis respiratoria grave (pH 7.11, pCO2 136 mmHg).  \n- Posteriormente, mostró mejoría neurológica parcial, con apertura ocular y respuesta a órdenes simples, sin déficit motor significativo, pero persistió con hipoventilación alveolar (disminución de la capacidad para ventilar adecuadamente los pulmones), lo que dificultó el destete de la ventilación mecánica y motivó la realización de traqueostomía.  \n- La RMN de control evidenció reducción de las lesiones inflamatorias previamente observadas.\n\n**Interpretación Clínica**  \nEl cuadro clínico y los estudios complementarios son compatibles con una encefalitis viral causada por el virus de la encefalopatía equina del este, una infección poco frecuente en humanos pero con potencial severo. La inflamación del tronco encefálico y ganglios basales explica el deterioro neurológico y la afectación respiratoria, dado que estas áreas controlan funciones vitales como la respiración. La hipoventilación persistente refleja compromiso del centro respiratorio, dificultando la recuperación completa y la independencia ventilatoria.\n\n**Próximos Pasos**  \nEl manejo continuó con soporte ventilatorio adaptado a la capacidad respiratoria del paciente, monitorización neurológica estrecha y seguimiento por imágenes para evaluar la evolución de las lesiones cerebrales. Se recomienda rehabilitación neurológica y respiratoria para mejorar la función muscular y ventilatoria. Además, es fundamental mantener vigilancia para posibles complicaciones infecciosas o neurológicas asociadas. El pronóstico dependerá de la recuperación neurológica y la capacidad para mantener una ventilación adecuada sin soporte mecánico.",
+        "score": {
+          "ROUGE-L-Sum": 0.2560240963855422,
+          "BERTScore_F": 0.8133718967437744
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.5346979965646583
+        }
+      }
+    }
+  },
+  {
+    "id": 60,
+    "gold_summary": "Presentamos el caso de una mujer de 27 años que consultó por sangrado vaginal y en quien se evidenció en la colposcopia, una lesión polipoide blanquecina que se exteriorizaba a través del orificio cervical externo. El estudio histológico reveló sectores celulares alternados por áreas laxas, mixoides, junto a glándulas ístmico-endometriales típicas. La proliferación fusocelular atípica, se disponía en nidos, constituidos por células de amplio citoplasma eosinófilo con estriaciones citoplasmáticas transversales y núcleos excéntricos con cromatina homogénea. Se exhibían áreas de células densamente condensadas inmediatas y próximas al revestimiento epitelial intacto, pero separadas de él, por una fina capa de estroma laxo (capa cambial). El perfil de inmunomarcación resultó positivo para desmina, actina músculo específico y miogenina, y negativo para actina músculo liso. Se realizó diagnóstico de rabdomiosarcoma embrionario botroide de cuerpo uterino.",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Una mujer joven tenía sangrado y una bolita en su cuerpo. Los doctores miraron la bolita con cuidado. Vieron que estaba hecha de muchas células diferentes. Estas células eran especiales y venían de un músculo. Los doctores dijeron que la bolita era un tipo de enfermedad que necesita tratamiento. Ellos cuidarán mucho a la mujer para ayudarla a estar mejor.",
+        "score": {
+          "ROUGE-L-Sum": 0.15315315315315314,
+          "BERTScore_F": 0.7209252715110779
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.4370392123321155
+        }
+      },
+      "B2": {
+        "text": "Caso de una mujer joven con sangrado vaginal\n\nUna mujer de 27 años fue al médico porque tenía sangrado vaginal. Al examinarla con un colposcopio (un instrumento que permite ver el cuello del útero), encontraron una lesión con forma de pólipo que salía por el orificio del cuello uterino. Esta lesión era de color blanquecino y tenía una superficie irregular.\n\nLo que encontraron en el laboratorio\n\nSe tomó una muestra de la lesión para analizarla bajo el microscopio. Los científicos vieron diferentes tipos de células: algunas estaban agrupadas en nidos y tenían un citoplasma (la parte de la célula fuera del núcleo) amplio y con un color rosado. Estas células también mostraban unas líneas transversales llamadas estriaciones, que indican que son células musculares especiales. Cerca de la superficie de la lesión, había una capa delgada de células muy densas, separadas del revestimiento normal por una capa de tejido blando llamada estroma laxo. Esta capa se llama “capa cambial” y es característica de ciertos tumores.\n\nCómo confirmaron el diagnóstico\n\nPara saber qué tipo de tumor era, usaron pruebas especiales que detectan proteínas en las células. Encontraron que las células tenían proteínas llamadas desmina, actina músculo específico y miogenina, que están presentes en músculos estriados (los músculos que usamos para movernos). No encontraron actina de músculo liso, que es otro tipo de músculo. Con esta información y la apariencia de las células, diagnosticaron un rabdomiosarcoma embrionario botrioide. Este es un tipo raro de tumor canceroso que se origina en células musculares jóvenes y se presenta en el cuerpo uterino.\n\nEn resumen, esta paciente tenía un tumor maligno muscular en el cuello del útero que se identificó gracias a la combinación de estudios visuales, microscópicos y de proteínas. El diagnóstico permitió iniciar un tratamiento adecuado para su condición.",
+        "score": {
+          "ROUGE-L-Sum": 0.28169014084507044,
+          "BERTScore_F": 0.8144324421882629
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5480612915166667
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe presenta el caso de una mujer joven de 27 años, sin antecedentes médicos relevantes, que consultó debido a sangrado vaginal. Durante la colposcopia (un examen visual del cuello uterino), se identificó una lesión con forma de pólipo blanquecino que sobresalía a través del orificio cervical externo (la abertura del cuello uterino hacia la vagina). Inicialmente, se sospechó un mioma nascens (un tipo de tumor benigno), pero la biopsia reveló un diagnóstico diferente.\n\n**Hallazgos Clave**  \nEl análisis microscópico del tejido mostró una combinación de áreas celulares densas y otras más laxas con características mixoides (tejido con apariencia gelatinosa), junto con glándulas típicas del istmo y endometrio (zonas del cuello y cuerpo uterino). La proliferación celular predominante estaba formada por células fusiformes (alargadas) atípicas organizadas en grupos o nidos. Estas células tenían un citoplasma amplio y rosado (eosinófilo), con estriaciones transversales visibles en el citoplasma, y núcleos excéntricos con cromatina homogénea, aunque algunos mostraban variabilidad en forma y tamaño (pleomorfismo).  \n\nAdemás, se observaron áreas específicas de células muy condensadas justo debajo del revestimiento epitelial intacto, separadas de este por una delgada capa de tejido conectivo laxo, conocida como “capa cambial”. Esta característica es importante para clasificar el tumor.  \n\nLas pruebas inmunohistoquímicas, que detectan proteínas específicas en las células, mostraron positividad para desmina, actina músculo específico y miogenina, marcadores que indican la presencia de células musculares estriadas (músculo esquelético). Por otro lado, la actina de músculo liso fue negativa, lo que ayudó a descartar otros tipos de tumores musculares.\n\n**Interpretación Clínica**  \nCon base en las características morfológicas y los resultados inmunohistoquímicos, se estableció el diagnóstico de rabdomiosarcoma embrionario botrioide, un tipo raro y agresivo de tumor maligno que se origina en células musculares estriadas y que en este caso afectaba el cuello uterino. La presencia de la capa cambial y la agrupación de rabdomioblastos (células tumorales características) fueron fundamentales para identificar esta variante específica.\n\n**Próximos Pasos**  \nTras el diagnóstico, la paciente recibió tratamiento con quimioterapia para reducir el tamaño del tumor. Posteriormente, se realizó una cirugía de histerectomía total con anexos (extirpación del útero, trompas y ovarios) para eliminar completamente la lesión. El seguimiento y manejo continuarán en función de la respuesta al tratamiento y la evolución clínica.  \n\nEste caso resalta la importancia de una evaluación cuidadosa y multidisciplinaria para diagnosticar correctamente tumores poco comunes que pueden presentarse con síntomas comunes como el sangrado vaginal.",
+        "score": {
+          "ROUGE-L-Sum": 0.3333333333333333,
+          "BERTScore_F": 0.8415259718894958
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5874296526114146
+        }
+      }
+    }
+  },
+  {
+    "id": 61,
+    "gold_summary": "Un hombre de 52 años con insuficiencia renal en fase terminal que requería hemodiálisis se sometió a una ecocardiografía anual de seguimiento para detectar una disfunción valvular aórtica. La ecocardiografía reveló una masa circular bien definida de 22 × 17 mm en el anillo de la valva mitral posterior que no se había detectado 2 años antes. En función de las características de la imagen, se sospechó que la masa era un CCMA. Se había agrandado rápidamente y suponía un riesgo potencial de embolia; por lo tanto, se extirpó al mismo tiempo que la sustitución de la válvula aórtica. Aunque se sospechó un CCMA en función de los hallazgos intraoperativos, el diagnóstico histopatológico fue un CAT. Tras el análisis histológico de la muestra de miocardio del ventrículo izquierdo y la válvula aórtica extirpada, se observó una infiltración de células inflamatorias crónicas; por lo tanto, se diagnosticó una cardiomiopatía inflamatoria crónica.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Había un hombre que tenía problemas en sus riñones. Tenía un huesito en su corazón que creció mucho y podía hacerle daño. Los doctores vieron el huesito con una máquina especial. Decidieron quitarlo para que el hombre estuviera mejor. También le pusieron una nueva parte en su corazón para que funcione bien. Cuando miraron el huesito con un microscopio, vieron que había muchas células que estaban peleando dentro. Eso les dijo que su corazón estaba un poco enfermo por dentro. Ahora el hombre está más seguro y los doctores lo cuidan mucho.",
+        "score": {
+          "ROUGE-L-Sum": 0.1543859649122807,
+          "BERTScore_F": 0.716454029083252
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.43541999699776635
+        }
+      },
+      "B2": {
+        "text": "**Lo que pasó con el paciente**  \nUn hombre de 52 años tenía problemas graves en sus riñones y necesitaba hemodiálisis, que es un tratamiento para limpiar la sangre cuando los riñones no funcionan bien. Cada año, le hacían una ecocardiografía, que es un examen con ultrasonido para ver cómo está funcionando su corazón y sus válvulas.\n\n**Lo que encontraron en el corazón**  \nEn el último examen, vieron una masa redonda de 22 × 17 mm en una parte del corazón llamada anillo mitral posterior. Esta masa no estaba ahí dos años antes. Por las imágenes, pensaron que podía ser una calcificación caseosa del anillo mitral (CCMA), que es una acumulación dura y blanda de calcio en esa zona. La masa había crecido rápido y podía causar problemas si pedazos se soltaban y viajaban por la sangre (embolias).\n\n**Qué hicieron los médicos**  \nDecidieron quitar la masa y al mismo tiempo reemplazar la válvula aórtica, que también estaba dañada. Durante la cirugía, vieron que la masa tenía un aspecto cremoso, lo que apoyaba la idea de que era una CCMA.\n\n**Lo que mostraron los análisis después de la cirugía**  \nCuando examinaron la masa bajo el microscopio, encontraron que no era solo calcio, sino también muchas células inflamatorias, lo que indicaba una inflamación crónica en el corazón. Además, analizaron muestras del músculo del corazón y de la válvula aórtica y vieron signos similares de inflamación. Por eso, diagnosticaron al paciente con una cardiomiopatía inflamatoria crónica, que es una enfermedad donde el músculo del corazón está inflamado por mucho tiempo.\n\n**Estado después de la cirugía**  \nSeis meses después, el corazón no mostró que la masa hubiera vuelto, y la válvula nueva funcionaba bien. Sin embargo, la función del ventrículo izquierdo, que es la parte del corazón que bombea la sangre, no mejoró mucho.\n\n**Resumen final**  \nEste caso muestra cómo una masa en el corazón que parecía ser una calcificación pudo ser en realidad una inflamación crónica del músculo cardíaco. La cirugía ayudó a prevenir posibles problemas graves, pero la función del corazón seguía afectada.",
+        "score": {
+          "ROUGE-L-Sum": 0.2910958904109589,
+          "BERTScore_F": 0.7796725034713745
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.5353841969411667
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nUn hombre de 53 años con insuficiencia renal terminal en hemodiálisis, causada por nefropatía diabética o nefroesclerosis, fue seguido durante 10 años en un servicio de nefrología. Presentaba estenosis valvular aórtica progresiva y regurgitación moderada, con función ventricular izquierda inicialmente normal. En controles ecocardiográficos anuales se detectó la aparición y rápido crecimiento de una masa en el anillo mitral posterior, que generó preocupación por riesgo de embolia.\n\n**Hallazgos Clave**  \nLa ecocardiografía mostró una masa redonda, bien delimitada, de 22 × 17 mm en el anillo mitral posterior, con características ecogénicas sugestivas de calcificación. La función del ventrículo izquierdo se deterioró progresivamente en dos años, con disminución de la fracción de eyección del 64 % al 42 %. La tomografía computarizada y la resonancia magnética descartaron tumores comunes como mixomas o fibroelastomas papilares, y no hubo evidencia de infección ni endocarditis. Por el contexto clínico y las imágenes, se sospechó una calcificación caseosa del anillo mitral (CCMA), una forma rara de calcificación valvular.\n\nDado el rápido crecimiento de la masa y el riesgo de embolia, se decidió extirparla quirúrgicamente junto con el reemplazo de la válvula aórtica. Durante la cirugía, se observó una masa con contenido cremoso típica de CCMA. Sin embargo, el análisis histopatológico reveló que la masa correspondía a un tumor calcificado atípico (CAT), caracterizado por calcificaciones nodulares y una infiltración inflamatoria crónica con células como neutrófilos, linfocitos, macrófagos y células plasmáticas. Además, la biopsia del músculo cardíaco del ventrículo izquierdo y la válvula aórtica resecada mostraron infiltración similar, lo que llevó al diagnóstico de una cardiomiopatía inflamatoria crónica (CICM). No se pudo determinar la causa exacta de esta inflamación.\n\n**Interpretación Clínica**  \nEste caso ilustra la complejidad diagnóstica de masas en el anillo mitral en pacientes con insuficiencia renal terminal y hemodiálisis, donde la calcificación caseosa puede simular tumores o lesiones inflamatorias. La progresión rápida y el riesgo embolígeno justificaron la cirugía. El diagnóstico definitivo mediante histología fue fundamental para identificar una cardiomiopatía inflamatoria crónica asociada, que podría explicar la disfunción ventricular progresiva observada.\n\n**Próximos Pasos**  \nSe realizó un seguimiento ecocardiográfico a los 6 meses postoperatorios que mostró ausencia de recurrencia de la masa, función normal de la válvula aórtica protésica y estabilidad de la regurgitación mitral, aunque sin mejoría en la función ventricular izquierda (fracción de eyección 41 %). El paciente recibió tratamiento anticoagulante y manejo para fibrilación auricular paroxística. Se recomienda continuar el seguimiento cardiológico para monitorizar la función ventricular y detectar posibles complicaciones asociadas a la cardiomiopatía inflamatoria crónica.",
+        "score": {
+          "ROUGE-L-Sum": 0.2916053019145803,
+          "BERTScore_F": 0.8212445974349976
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.556424949674789
+        }
+      }
+    }
+  },
+  {
+    "id": 62,
+    "gold_summary": "Se comunica el caso de un paciente masculino de 28 años, que acude a consulta de dermatología con cuadro de 48 horas de evolución de dos placas eritematosas con ampollas centrales más ulceración superficial localizadas en cara flexora de brazo y antebrazo derecho, acompañadas de una sensación de ardor y prurito en el lugar de las lesiones, sin síntomas acompañantes. Como antecedente refiere que se encontraba de vacaciones en la región costera de Ecuador al momento de aparecer las lesiones. Se realizó una biopsia incisional y por las características clínicas y el antecedente de viaje a una región tropical se diagnosticó como dermatitis por Paederus y se indicó tratamiento con antihistamínicos, esteroides tópicos y compresas frías. Después de 8 días de tratamiento, las lesiones remitieron dejando una hiperpigmentación postinflamatoria.",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Un hombre se lastimó la piel en su brazo. Tenía dos manchas rojas con ampollas y le picaban y quemaban. Esto pasó después de estar de vacaciones en un lugar con mucho calor y bichos. El doctor vio su piel y dijo que era una irritación por un bicho llamado Paederus. Le dieron medicinas para calmar la picazón y poner frío en su brazo. Después de unos días, la piel mejoró, pero quedó un poco de color diferente donde estaban las manchas.",
+        "score": {
+          "ROUGE-L-Sum": 0.21940928270042193,
+          "BERTScore_F": 0.7402103543281555
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.4798098185142887
+        }
+      },
+      "B2": {
+        "text": "Caso de un joven de 28 años con lesiones en la piel\n\nUn hombre de 28 años fue al dermatólogo porque tenía dos manchas rojas en el brazo y antebrazo derecho. Estas manchas tenían ampollas (pequeñas burbujas llenas de líquido) en el centro y una pequeña herida superficial. Además, sentía ardor y picazón en esas áreas. No tenía otros síntomas ni había tomado medicamentos por su cuenta.\n\nLo que encontraron y cómo lo trataron\n\nEl paciente contó que estaba de vacaciones en la costa de Ecuador cuando aparecieron las lesiones. Para entender mejor qué pasaba, los médicos tomaron una biopsia, que es cuando se extrae un pequeño pedazo de piel para examinarlo bajo el microscopio. En el análisis, vieron cambios en las capas de la piel y células inflamatorias, lo que ayudó a confirmar que tenía dermatitis por Paederus. Esta dermatitis es una irritación causada por un insecto llamado Paederus, común en zonas tropicales.\n\nEl tratamiento incluyó medicamentos para reducir la picazón (antihistamínicos), cremas con esteroides para bajar la inflamación, y compresas frías para aliviar el ardor. Después de ocho días, las lesiones mejoraron, pero quedaron manchas oscuras en la piel, llamadas hiperpigmentación postinflamatoria, que suelen desaparecer con el tiempo.",
+        "score": {
+          "ROUGE-L-Sum": 0.31830238726790455,
+          "BERTScore_F": 0.8232541680335999
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5707782776507522
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe presenta el caso de un hombre de 28 años, sin antecedentes médicos relevantes, que consultó en dermatología debido a la aparición de lesiones cutáneas durante las últimas 48 horas. Estas lesiones consistían en dos placas rojas (eritematosas) con ampollas en el centro y una ulceración superficial, localizadas en la parte interna del brazo y antebrazo derecho, equidistantes del pliegue del codo. El paciente describió sensación de ardor y picazón en las zonas afectadas, sin presentar otros síntomas generales ni haber tomado medicamentos por su cuenta. Como antecedente importante, refirió que se encontraba de vacaciones en una zona costera tropical de Ecuador cuando aparecieron las lesiones.\n\n**Hallazgos Clave**  \nSe realizó una biopsia incisional de la piel afectada, cuyo análisis microscópico mostró:  \n- Engrosamiento de la epidermis (acantosis)  \n- Presencia de células muertas con núcleo (paraqueratosis)  \n- Acumulación de líquido entre las células epidérmicas (espongiosis)  \n- Infiltración de neutrófilos (un tipo de glóbulo blanco) en la capa más superficial de la piel (estrato córneo)  \n- Presencia de un infiltrado inflamatorio linfocitario alrededor de los vasos sanguíneos en las capas superficiales, medias y profundas de la dermis (la capa intermedia de la piel).\n\n**Interpretación Clínica**  \nLa combinación de las características clínicas, el antecedente de exposición en una región tropical y los hallazgos histológicos permitió establecer el diagnóstico de dermatitis por Paederus. Esta condición es una inflamación cutánea causada por el contacto con un insecto del género Paederus, que libera una toxina irritante al ser aplastado sobre la piel.\n\n**Próximos Pasos y Tratamiento**  \nEl tratamiento indicado incluyó antihistamínicos para aliviar la picazón, esteroides tópicos para reducir la inflamación y la aplicación de compresas frías para calmar la zona afectada. Tras ocho días de tratamiento, las lesiones desaparecieron, aunque dejaron una hiperpigmentación postinflamatoria, es decir, una mancha oscura residual en la piel debido a la inflamación previa.\n\nEste caso resalta la importancia de considerar la dermatitis por Paederus en pacientes con lesiones cutáneas agudas tras viajes a regiones tropicales, y la efectividad del tratamiento tópico combinado para su resolución.",
+        "score": {
+          "ROUGE-L-Sum": 0.39697542533081287,
+          "BERTScore_F": 0.8174276947975159
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.6072015600641644
+        }
+      }
+    }
+  },
+  {
+    "id": 63,
+    "gold_summary": "Un hombre de 35 años de edad sufrió múltiples lesiones tras un accidente de tráfico y fue trasladado a nuestro hospital en estado de shock. La tomografía computarizada reveló una fractura de TAI de grado IV que se extendía hasta la cavidad torácica y una fractura pélvica. Poco tiempo después de realizar un relleno pélvico preperitoneal y una embolización arterial transcatéter para la fractura pélvica, se realizó un TEVAR en el quirófano híbrido sin trasladar al paciente. El paciente fue trasladado a un hospital de rehabilitación el día 41 después de la operación.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Un hombre se lastimó mucho en un accidente. Su pierna estaba muy dañada y tenía huesos rotos en el cuerpo. Los doctores le hicieron muchas cosas para ayudarlo a estar mejor. Usaron una máquina para ver dentro de su cuerpo y encontraron problemas grandes. Luego, le pusieron un tubo especial para arreglar su corazón y sus huesos. El hombre se quedó en el hospital mucho tiempo. Después, fue a otro lugar para aprender a caminar y estar fuerte otra vez.",
+        "score": {
+          "ROUGE-L-Sum": 0.19387755102040816,
+          "BERTScore_F": 0.7327959537506104
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.46333675238550925
+        }
+      },
+      "B2": {
+        "text": "**Lo que pasó con el paciente**  \nUn hombre de 35 años tuvo un accidente de tráfico grave y llegó al hospital en estado muy delicado. Tenía varias heridas, incluyendo una fractura en la pelvis y una lesión grave en la arteria principal del pecho llamada aorta. Esta lesión se llama fractura de TAI de grado IV y puede ser muy peligrosa porque afecta el flujo de sangre al cuerpo.\n\n**Tratamientos que recibió**  \nPrimero, los médicos hicieron un procedimiento llamado relleno pélvico preperitoneal, que ayuda a controlar el sangrado en la pelvis. También realizaron una embolización arterial transcatéter, que es cuando se bloquea una arteria para detener una hemorragia. Después, sin mover al paciente a otro lugar, hicieron una cirugía llamada TEVAR en un quirófano especial que combina imagen y cirugía. En esta operación, colocaron un tubo especial llamado injerto de stent dentro de la arteria dañada para repararla y permitir que la sangre fluya bien.\n\n**Qué pasó después**  \nGracias a estos tratamientos, el paciente se estabilizó y pudo continuar su recuperación. Después de 41 días, fue enviado a un hospital de rehabilitación para seguir mejorando su salud.",
+        "score": {
+          "ROUGE-L-Sum": 0.36363636363636365,
+          "BERTScore_F": 0.8127251267433167
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5881807451898402
+        }
+      },
+      "B3": {
+        "text": "**Contexto:**  \nUn hombre de 35 años sufrió un grave accidente de tráfico que le provocó múltiples lesiones, incluyendo una fractura grave en la arteria aorta torácica (TAI, por sus siglas en inglés) y fracturas óseas en la pelvis y el fémur derecho. Fue trasladado a un hospital equipado con un quirófano híbrido, donde recibió atención de emergencia.\n\n**Hallazgos Clave:**  \nA su llegada, el paciente presentaba signos de shock, con presión arterial muy baja y frecuencia cardíaca elevada. La tomografía computarizada (TAC) mostró un hemotórax (acumulación de sangre en el tórax), ensanchamiento del mediastino (zona central del tórax que contiene el corazón y grandes vasos), una fractura pélvica y una lesión de grado IV en la arteria aorta torácica que se extendía hacia la cavidad torácica izquierda. Además, la pierna derecha estaba acortada y girada, indicando fractura del fémur.\n\n**Interpretación Clínica:**  \nDebido a la gravedad y la inestabilidad hemodinámica del paciente, se realizaron procedimientos de emergencia para controlar el sangrado y estabilizarlo, incluyendo intubación, relleno pélvico preperitoneal (una técnica para controlar hemorragias pélvicas) y transfusión masiva. Posteriormente, se realizó una embolización arterial transcatéter (TAE) para controlar el sangrado de la fractura pélvica y se fijó externamente la fractura del fémur. Finalmente, sin necesidad de trasladar al paciente, se llevó a cabo una reparación endovascular de la aorta torácica (TEVAR) en el quirófano híbrido, utilizando un injerto de stent que se colocó desde justo después de la arteria carótida común izquierda hasta la octava vértebra torácica. Para asegurar un flujo sanguíneo adecuado, se decidió sacrificar la arteria subclavia izquierda, ya que la circulación cerebral estaba garantizada por la arteria vertebral izquierda. Durante la cirugía se administró heparina para prevenir coágulos.\n\n**Próximos Pasos y Resultado:**  \nEl paciente evolucionó favorablemente sin signos de isquemia (falta de riego sanguíneo) tras la intervención. Fue dado de alta al hospital de rehabilitación 41 días después de la cirugía, donde continuó su recuperación.",
+        "score": {
+          "ROUGE-L-Sum": 0.3146997929606626,
+          "BERTScore_F": 0.8125516772270203
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5636257350938414
+        }
+      }
+    }
+  },
+  {
+    "id": 64,
+    "gold_summary": "Se reporta el caso de un hombre de 31 años que presenta este síndrome luego de la aplicación de penicilina benzatínica intramuscular. La biopsia apoyó el diagnóstico. Recibió tratamiento con enoxaparina y cilostazol con posterior mejoría.",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Un hombre se puso una medicina en el glúteo. Después, le dolió mucho y le salió una mancha en la piel. El doctor vio que la piel estaba lastimada por la medicina. Le dieron medicinas para ayudar y se fue mejorando poco a poco. Ahora está mejor y la piel está sanando.",
+        "score": {
+          "ROUGE-L-Sum": 0.14583333333333334,
+          "BERTScore_F": 0.6992650032043457
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.42254916826883954
+        }
+      },
+      "B2": {
+        "text": "Caso de Síndrome de Nicolau tras Inyección de Penicilina\n\nUn hombre de 31 años recibió una inyección de penicilina para tratar una posible infección por sífilis, debido a que su pareja tenía esta enfermedad. Poco después, comenzó a sentir dolor en la nalga derecha que se extendía hasta el pie. Además, apareció una lesión en la piel cerca del lugar de la inyección, con forma de anillo y bordes irregulares, y otras heridas en el escroto y la planta del pie.\n\nPara entender qué pasaba, los médicos hicieron una ecografía que mostró inflamación en los músculos y tejidos cerca de la lesión. También se hicieron análisis de sangre que indicaron inflamación y daño muscular. Se descartaron otras infecciones como VIH y hepatitis.\n\nSe tomó una biopsia, que es cuando se extrae un pequeño pedazo de piel para examinarlo. Esta mostró que la piel estaba dañada por falta de sangre, pero sin inflamación de los vasos sanguíneos. Todo esto confirmó que el paciente tenía el síndrome de Nicolau, una reacción rara que puede ocurrir después de una inyección y que causa daño en la piel y músculos por bloqueo de vasos sanguíneos.\n\nEl tratamiento incluyó medicamentos para evitar coágulos (enoxaparina) y para mejorar la circulación (cilostazol), además de analgésicos para el dolor. Con este cuidado, el paciente mejoró, sus análisis de sangre volvieron casi a la normalidad y las lesiones en la piel sanaron, quedando solo algunas cicatrices leves.\n\nEste caso muestra la importancia de reconocer el síndrome de Nicolau para tratarlo rápido y evitar daños mayores.",
+        "score": {
+          "ROUGE-L-Sum": 0.14159292035398233,
+          "BERTScore_F": 0.6841760277748108
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.41288447406439654
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe trata de un hombre de 31 años con antecedentes de consumo de alcohol, tabaco y cocaína inhalada, además de haber tenido tuberculosis pulmonar tratada, y cirugías previas de nefrectomía izquierda y esplenectomía tras un trauma. Consultó en urgencias debido a un cuadro que comenzó una semana antes, inmediatamente después de recibir una inyección intramuscular de penicilina benzatínica, administrada por contacto sexual con una pareja diagnosticada con sífilis.\n\n**Hallazgos Clínicos y Diagnósticos**  \nEl paciente presentó dolor intenso en la región glútea derecha que se irradiaba hacia el pie, acompañado de una erupción cutánea purpúrica (manchas violáceas) en el sitio de la inyección. Esta lesión tenía forma de placa anular (con un borde en forma de anillo irregular) de aproximadamente 15 centímetros, con piel sana en el centro. Además, tenía una pequeña úlcera (escara) en el escroto y una lesión extensa en la planta del pie derecho con aspecto livedoide (patrón vascular irregular), que se extendía desde el talón hasta la punta de los dedos.\n\nLa ecografía del glúteo mostró alteraciones en el músculo mayor, con pérdida de su estructura normal, aumento de grosor y edema (hinchazón por acumulación de líquido) tanto en el músculo como en el tejido subcutáneo (debajo de la piel). Se observó edema también en la región plantar del pie y en el escroto.\n\nLos análisis de sangre revelaron leucocitosis (aumento de glóbulos blancos) y elevación de proteína C reactiva, indicadores de inflamación aguda. Además, hubo un aumento significativo de enzimas hepáticas (transaminasas) y de marcadores musculares como la creatina quinasa y la lactato deshidrogenasa, lo que sugiere daño muscular.\n\nLas pruebas serológicas para sífilis, VIH, hepatitis B y C fueron negativas.\n\nLa biopsia de piel del glúteo evidenció necrosis (muerte celular) epidérmica y afectación del epitelio folicular, con formación de ampollas debido a la reparación de la piel, pero sin signos de vasculitis (inflamación de vasos sanguíneos) ni trombosis (coágulos), lo que apoyó el diagnóstico de síndrome de Nicolau o embolia cutis medicamentosa en fase aguda. Este síndrome es una reacción adversa poco frecuente que ocurre tras la inyección intramuscular de ciertos medicamentos, causando daño vascular y necrosis en la piel y tejidos subyacentes.\n\n**Interpretación Clínica**  \nEl cuadro clínico, la historia temporal relacionada con la inyección de penicilina y los hallazgos histológicos confirmaron el diagnóstico de síndrome de Nicolau. Este diagnóstico explicó el dolor intenso, las lesiones cutáneas y el compromiso muscular observado.\n\n**Tratamiento y Evolución**  \nSe inició tratamiento con anticoagulación mediante enoxaparina (un anticoagulante) y cilostazol (un medicamento que mejora la circulación sanguínea), además de analgésicos para controlar el dolor. Durante la hospitalización, el paciente mostró una franca mejoría, con descenso progresivo de las enzimas hepáticas y musculares a valores cercanos a la normalidad.\n\nNo se realizaron estudios inmunológicos adicionales, dado que el diagnóstico clínico y patológico fue suficiente para explicar el cuadro.\n\nAl alta, el paciente continuó con cilostazol y analgésicos, y en el control ambulatorio a los tres meses presentó mejoría significativa del dolor y de las lesiones cutáneas. Quedaron secuelas en forma de cicatrices con alteraciones en la pigmentación y descamación fina en el glúteo derecho, así como cicatrices similares y mínimas lesiones livedoides en la planta del pie derecho.\n\n**Próximos Pasos**  \nSe recomienda seguimiento clínico para evaluar la evolución de las cicatrices y el manejo del dolor residual, así como evitar futuras inyecciones intramusculares en la zona afectada para prevenir recurrencias. Además, es importante la educación al paciente sobre los riesgos asociados a la administración de medicamentos por vía intramuscular y la vigilancia temprana de síntomas similares.",
+        "score": {
+          "ROUGE-L-Sum": 0.08207934336525308,
+          "BERTScore_F": 0.7026351094245911
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.3923572263949221
+        }
+      }
+    }
+  },
+  {
+    "id": 65,
+    "gold_summary": "Un bebé de cuatro días de edad, a término, varón, nacido por parto vaginal sin complicaciones, con un curso de enfermería significativo para la falta de audición, se presentó en un departamento de emergencias (DE) con dificultad respiratoria y estridor en aumento. Fue trasladado a una unidad de cuidados intensivos neonatales (UCIN) de nivel III para una evaluación posterior y se le practicó una intubación debido a la hipercarbia progresiva. La laringoscopia reveló una parálisis unilateral de las cuerdas vocales (PCV) del lado izquierdo. Se le sometió a una evaluación posterior que incluyó un cerebro, cuello y tórax normales en una resonancia magnética. Se consultó a genética por la preocupación de los rasgos dismórficos en el examen físico. Después de las pruebas del panel de genes, la PCV se atribuyó a la asociación conocida con el síndrome CHARGE. Se observó un edema de las vías respiratorias en la laringoscopia que impidió la extubación hasta los dos meses de edad. Se identificaron otras características del síndrome CHARGE, incluidos los colobomas, el glaucoma, la pérdida auditiva neurosensorial y las anomalías genitales. Se le dio de alta con aire ambiente y después de la colocación de un tubo de gastrostomía con seguimiento de otorrinolaringología.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Un bebé de cuatro días tenía problemas para respirar y hacer ruido al respirar. Lo llevaron al hospital para que lo cuidaran mucho. Los doctores vieron que una cuerda en su garganta no se movía bien. Hicieron pruebas y encontraron que tenía un problema llamado síndrome CHARGE. Este problema puede hacer que los ojos, los oídos y otras partes del cuerpo no estén como deben. El bebé estuvo en el hospital hasta que pudo respirar mejor. Luego, le pusieron un tubito para ayudarlo a comer. Ahora, los doctores lo cuidan para que siga mejorando.",
+        "score": {
+          "ROUGE-L-Sum": 0.17575757575757572,
+          "BERTScore_F": 0.7463215589523315
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.46103956735495366
+        }
+      },
+      "B2": {
+        "text": "**Lo que pasó con el bebé**  \nUn bebé de cuatro días, que nació sin problemas y a término, llegó al hospital porque tenía dificultad para respirar y un sonido extraño al inhalar llamado estridor. En el hospital, los médicos notaron que su respiración empeoraba y que tenía una cuerda vocal izquierda que no se movía, lo que se llama parálisis unilateral de las cuerdas vocales. Esto dificultaba que respirara bien.\n\n**Qué hicieron los médicos**  \nEl bebé fue llevado a una unidad especial para recién nacidos y le pusieron un tubo para ayudarlo a respirar mejor. Le hicieron varios estudios, incluyendo una resonancia magnética, que mostró que su cerebro, cuello y tórax estaban normales. También notaron que tenía algunas características físicas diferentes, como orejas bajas y ojos pequeños, por lo que pidieron ayuda a especialistas en genética.\n\n**El diagnóstico y su significado**  \nDespués de hacer pruebas genéticas, descubrieron que el bebé tenía una condición llamada síndrome CHARGE. Este síndrome puede causar problemas en varias partes del cuerpo, como los ojos (colobomas y glaucoma), pérdida de audición y problemas en los genitales. La parálisis de la cuerda vocal izquierda estaba relacionada con este síndrome.\n\n**El tratamiento y el seguimiento**  \nEl bebé tuvo inflamación en las vías respiratorias, lo que dificultó quitarle el tubo para respirar hasta que tenía dos meses. También le pusieron un tubo especial para alimentarse directamente al estómago (tubo de gastrostomía) a los tres meses. Finalmente, fue dado de alta para seguir en casa, pero continúa con controles médicos para vigilar su respiración y otros problemas relacionados con el síndrome CHARGE.",
+        "score": {
+          "ROUGE-L-Sum": 0.30131826741996237,
+          "BERTScore_F": 0.8120449185371399
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5566815929785511
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nUn recién nacido varón a término, sin complicaciones durante el parto, fue llevado al servicio de urgencias a los cuatro días de vida debido a un empeoramiento de la dificultad para respirar y la presencia de estridor (un sonido respiratorio agudo causado por la obstrucción de las vías aéreas). Estos síntomas se agravaban con la alimentación y al estar acostado boca arriba. En el examen inicial, se detectó también una deformidad torácica llamada pectus excavatum. La dificultad respiratoria mejoraba al colocarlo boca abajo o de lado.  \n\n**Hallazgos Clave**  \n- La evaluación inicial mostró acidosis respiratoria, lo que indica una acumulación de dióxido de carbono en la sangre por dificultad para respirar adecuadamente.  \n- Se inició soporte respiratorio con cánula nasal de alto flujo y posteriormente con presión positiva continua en la vía aérea (CPAP).  \n- La laringoscopia flexible (una exploración visual de la laringe) reveló parálisis unilateral de la cuerda vocal izquierda y edema (hinchazón) en varias estructuras de las vías respiratorias superiores.  \n- Se identificaron rasgos físicos sutiles que sugerían una posible condición genética, incluyendo orejas de implantación baja, mandíbula pequeña (retromicrognatia), ojos pequeños (microftalmia) y deformidades en los dedos de los pies.  \n- La resonancia magnética del cerebro, cuello y tórax fue normal, descartando lesiones estructurales en los nervios laríngeos recurrentes, que controlan las cuerdas vocales.  \n- El análisis genético confirmó la presencia de una mutación patogénica en el gen CHD7, diagnóstico que confirma el síndrome CHARGE, una enfermedad genética que afecta múltiples órganos y sistemas.  \n\n**Interpretación Clínica**  \nLa parálisis de la cuerda vocal izquierda se atribuyó a la asociación conocida con el síndrome CHARGE, que también explicó otros hallazgos clínicos como colobomas bilaterales (defectos en el ojo), glaucoma, pérdida auditiva neurosensorial y anomalías genitales. El edema persistente en las vías respiratorias superiores dificultó la extubación (retirar el tubo de respiración) hasta los dos meses de edad, requiriendo múltiples tratamientos con corticosteroides y antibióticos tópicos aplicados directamente sobre las cuerdas vocales. Posteriormente, se observó una nueva parálisis de la cuerda vocal derecha, cuya causa no está clara, aunque ambas cuerdas vocales mostraron mejoría progresiva.  \n\n**Próximos Pasos y Seguimiento**  \nEl paciente fue dado de alta respirando aire ambiente a los cuatro meses de edad, tras la colocación de un tubo de gastrostomía para alimentación directa al estómago, debido a las dificultades para alimentarse por vía oral. Continúa bajo seguimiento estrecho con otorrinolaringología para monitorizar la función de las cuerdas vocales y el estado de las vías respiratorias. Este caso resalta la importancia de una evaluación multidisciplinaria en recién nacidos con síntomas respiratorios y rasgos dismórficos, para identificar condiciones genéticas complejas como el síndrome CHARGE y manejar sus múltiples complicaciones.",
+        "score": {
+          "ROUGE-L-Sum": 0.3058186738836265,
+          "BERTScore_F": 0.8212672472000122
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5635429605418194
+        }
+      }
+    }
+  },
+  {
+    "id": 66,
+    "gold_summary": "Describimos aquí el caso de una paciente de 17 años con diagnóstico de neumocitoma esclerosante con presentación infrecuente.",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Una niña de 17 años tenía un bulto en su pulmón. Los doctores lo sacaron con una operación para que ella esté mejor. El bulto no era peligroso.",
+        "score": {
+          "ROUGE-L-Sum": 0.25925925925925924,
+          "BERTScore_F": 0.7484920620918274
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5038756606755433
+        }
+      },
+      "B2": {
+        "text": "Caso de una joven con un tumor pulmonar poco común\n\nUna chica de 17 años de Tucumán fue al médico porque tenía síntomas en las vías respiratorias y tos con un poco de sangre. Se le hizo una tomografía, que es una imagen especial del pecho, y mostraba una bolita redonda en el pulmón derecho. Esta bolita tenía paredes lisas y un borde un poco borroso. Para entender mejor, le hicieron una resonancia magnética, que confirmó que la imagen parecía un líquido dentro de esa bolita.\n\nComo la lesión estaba en una zona difícil, los médicos decidieron sacar la parte superior del pulmón derecho usando una cirugía asistida por video, que es menos invasiva. Durante la operación, no pudieron saber exactamente qué era la lesión, así que también quitaron algunos ganglios cercanos para analizarlos.\n\nDespués de estudiar el tejido con un microscopio, los especialistas confirmaron que se trataba de un neumocitoma esclerosante. Este es un tipo raro de tumor en el pulmón que generalmente no es canceroso. Para asegurarse, usaron pruebas especiales que detectan ciertas proteínas en las células, y estas pruebas dieron resultados positivos para marcadores típicos de este tumor.\n\nEn resumen, este caso muestra cómo se identificó y trató un tumor pulmonar poco común en una paciente joven, usando diferentes estudios de imagen y cirugía para llegar a un diagnóstico claro.",
+        "score": {
+          "ROUGE-L-Sum": 0.11678832116788321,
+          "BERTScore_F": 0.6545872688293457
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.38568779499861444
+        }
+      },
+      "B3": {
+        "text": "**Contexto:**  \nSe presenta el caso de una joven de 17 años originaria de Tucumán que consultó por síntomas respiratorios superiores acompañados de hemoptisis leve (expectoración con sangre). Los estudios iniciales incluyeron una tomografía computarizada (TC) de tórax que reveló una lesión redondeada de aproximadamente 2.5 cm en el lóbulo superior derecho del pulmón, con bordes regulares y un halo periférico de vidrio esmerilado, sin captación de contraste. Posteriormente, una resonancia magnética (RMN) confirmó la presencia de esta lesión con características líquidas.\n\n**Hallazgos Clave:**  \nDebido a la ubicación central de la lesión, se decidió realizar una lobectomía superior derecha mediante cirugía videoasistida. Durante la operación, el estudio anatomopatológico preliminar no permitió un diagnóstico definitivo, por lo que se amplió la cirugía para incluir un vaciamiento ganglionar mediastínico (extirpación de ganglios linfáticos en el mediastino). El examen histológico final identificó la lesión como un neumocitoma esclerosante, un tumor pulmonar poco frecuente, de tamaño aproximado de 2 x 1.7 cm. Los marcadores inmunohistoquímicos fueron positivos para TTF1, CK, CK7 y napsina, proteínas que ayudan a confirmar el origen pulmonar y la naturaleza del tumor.\n\n**Interpretación Clínica:**  \nEl neumocitoma esclerosante es una neoplasia pulmonar rara que suele presentarse en adultos jóvenes y tiene un comportamiento generalmente benigno o de bajo grado maligno. En este caso, la presentación con hemoptisis y la localización central del tumor hicieron necesaria una intervención quirúrgica completa para su diagnóstico y tratamiento. La confirmación mediante inmunomarcadores es fundamental para diferenciarlo de otras lesiones pulmonares.\n\n**Próximos Pasos:**  \nSe recomienda un seguimiento clínico y radiológico periódico para vigilar la posible recurrencia o complicaciones postoperatorias. La cirugía completa y el vaciamiento ganglionar mediastínico realizados constituyen un manejo adecuado para este tipo de tumor, aunque su pronóstico suele ser favorable. En caso de aparición de nuevos síntomas o hallazgos, se deberá reevaluar para descartar progresión o complicaciones.",
+        "score": {
+          "ROUGE-L-Sum": 0.08488063660477453,
+          "BERTScore_F": 0.6761677265167236
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.3805241815607491
+        }
+      }
+    }
+  },
+  {
+    "id": 67,
+    "gold_summary": "Preocupaciones de la paciente: Una mujer de 28 años de edad vino a nuestro hospital para recibir tratamiento debido al descubrimiento de una masa pélvica 10 meses antes. Después de la admisión, la paciente se sometió a tratamiento quirúrgico y fue dada de alta en 1 semana. Recibió tratamiento médico durante 3 años después del alta. Después de la retirada de la medicación, la paciente quedó embarazada y dio a luz a un niño sin recurrencia durante el seguimiento.\n\nDiagnósticos: Los diagnósticos iniciales al ingreso fueron «¿masa pelviana inflamatoria?» y «¿endometriosis?». Después de 10 meses, la paciente volvió a ser internada en el hospital debido a un aumento gradual de la masa, y se le diagnosticó endometriosis.\n\nIntervenciones: El paciente fue tratado con terapia antiinfecciosa de rehidratación por primera vez, y el paciente fue tratado quirúrgicamente por segunda vez, seguido de agonista de la hormona liberadora de gonadotropina (GnRH-α) y tratamiento con dienogest (DNG) después de la cirugía.\n\nResultados: Después de 6 ciclos de tratamiento con GnRH-α y 3 años de tratamiento con DNG, un hijo nació con éxito tras la interrupción de la medicación y, hasta ahora, no se han producido reacciones adversas ni recurrencias durante el período de seguimiento.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Había una mujer que tenía un bulto en su barriga por mucho tiempo. Los doctores la ayudaron con una operación y medicina para que se sintiera mejor. \n\nDespués de tomar la medicina por mucho tiempo, la mujer pudo tener un bebé sano. Ella y su bebé están bien y felices.",
+        "score": {
+          "ROUGE-L-Sum": 0.15053763440860216,
+          "BERTScore_F": 0.7145168781280518
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.43252725626832694
+        }
+      },
+      "B2": {
+        "text": "**Lo que le pasó a la paciente:**  \nUna mujer de 28 años tenía una masa, que es una especie de bulto, en la parte baja de su abdomen desde hacía 10 meses. Fue al hospital para tratarse. Al principio, pensaron que podía ser una inflamación o una enfermedad llamada endometriosis, que ocurre cuando un tejido parecido al que está dentro del útero crece fuera de él y causa dolor o problemas.\n\n**Qué hicieron los médicos:**  \nPrimero, le dieron un tratamiento para la inflamación y la hidratación. Pero como la masa creció, la operaron para quitarla y examinarla mejor. Después de la cirugía, le dieron medicamentos especiales que ayudan a controlar la endometriosis. Estos medicamentos incluyen un tipo que afecta las hormonas del cuerpo (llamado agonista de GnRH) y otro llamado dienogest, que tomaba por varios años.\n\n**Qué pasó después:**  \nTras el tratamiento y la cirugía, la paciente pudo quedar embarazada de forma natural. Tuvo un bebé sano y no volvió a tener problemas ni síntomas de la enfermedad durante el tiempo que la siguieron en el hospital.\n\n**En resumen:**  \nEsta paciente con endometriosis y una masa pélvica recibió cirugía y tratamiento hormonal. Gracias a esto, pudo tener un embarazo normal y no tuvo complicaciones después del tratamiento.",
+        "score": {
+          "ROUGE-L-Sum": 0.38839285714285715,
+          "BERTScore_F": 0.8199443221092224
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.6041685896260398
+        }
+      },
+      "B3": {
+        "text": "Resumen detallado para público general universitario\n\n**Contexto y motivo de consulta**  \nUna mujer asiática de 28 años acudió al hospital tras haber detectado una masa en la pelvis que persistía desde hacía 10 meses. Antes de esto, su menstruación era regular, con un volumen moderado y dolor menstrual (dismenorrea). No presentaba antecedentes de embarazos exitosos, pero sí un aborto espontáneo. Durante el examen físico, se encontró que la parte posterior del útero estaba agrandada (aproximadamente 8 cm) y con poca movilidad, aunque sin otras anomalías evidentes. La paciente no había experimentado dolor abdominal significativo durante esos meses previos.\n\n**Hallazgos diagnósticos iniciales**  \nLa ecografía reveló una masa heterogénea de unos 4 cm en la parte superior derecha del útero y un pequeño nódulo en el epiplón mayor (una capa de tejido graso en el abdomen) de 2 cm. Además, el análisis sanguíneo mostró un nivel elevado de CA125 (416 mU/mL), una proteína que puede aumentar en enfermedades inflamatorias o tumorales del área pélvica. Se sospechó inicialmente que la masa correspondía a endometriosis (una condición en la que tejido similar al endometrio crece fuera del útero) o a una masa inflamatoria pélvica.\n\n**Evolución y revaluación**  \nTras un tratamiento inicial con líquidos y antibióticos, la paciente mejoró y fue dada de alta. Los niveles de CA125 disminuyeron progresivamente hasta normalizarse en 6 semanas. Sin embargo, la masa pélvica continuó creciendo, alcanzando dimensiones de aproximadamente 8 cm, con características ecográficas que sugerían posible malignidad, lo que llevó a recomendar cirugía.\n\n**Intervenciones quirúrgicas y hallazgos intraoperatorios**  \nEl 14 de noviembre de 2018, la paciente fue sometida a una cirugía abdominal para liberar adherencias (tejido cicatricial que une órganos) en la pelvis e intestinos, así como para extirpar tejido afectado en el epiplón, ovarios, peritoneo (membrana que recubre la cavidad abdominal) y el útero. Durante la operación se drenaron 600 ml de líquido abdominal con sangre (ascitis hemorrágica). Se observaron lesiones características de endometriosis, incluyendo depósitos marrones en múltiples superficies abdominales y uterinas, y una masa blanda en el epiplón que parecía tejido necrótico. No fue posible eliminar todas las lesiones, por lo que algunas áreas se trataron con electrocoagulación para reducir su actividad.\n\n**Resultados del análisis patológico**  \nEl examen microscópico confirmó la presencia de endometriosis en el tejido adiposo del epiplón, con inflamación crónica y cambios en el tejido uterino compatibles con adenomiosis (una forma de endometriosis dentro del músculo uterino). No se detectaron células tumorales malignas en el líquido ascítico. También se observaron fibrosis (formación de tejido cicatricial) y proliferación de fibroblastos (células que forman tejido conectivo).\n\n**Tratamiento posterior y seguimiento**  \nDespués de la cirugía, la paciente recibió terapia hormonal con un agonista de la hormona liberadora de gonadotropina (GnRH-α), específicamente leuprorelina, administrada mensualmente durante 6 meses para suprimir la actividad ovárica y reducir la endometriosis. Posteriormente, continuó con dienogest (un progestágeno oral) durante 3 años para mantener el control de la enfermedad. Tras suspender la medicación durante 3 meses, la paciente logró concebir de forma natural.\n\n**Resultados obstétricos y estado actual**  \nLa paciente tuvo un embarazo normal y dio a luz por vía vaginal a término (39 semanas y 3 días) a un bebé sano de 3300 gramos. Durante el seguimiento posterior, no se observaron recurrencias de la endometriosis ni efectos adversos relacionados con el tratamiento o el embarazo.\n\n---\n\n**Interpretación clínica**  \nEste caso ilustra la complejidad del diagnóstico y manejo de la endometriosis con masas pélvicas grandes y elevación del marcador CA125, que puede simular malignidad. La combinación de cirugía para el control de lesiones extensas y terapia hormonal prolongada fue efectiva para controlar la enfermedad y preservar la fertilidad, permitiendo un embarazo exitoso sin complicaciones.\n\n**Próximos pasos y recomendaciones**  \nEl seguimiento clínico continuo es fundamental para detectar posibles recurrencias. La terapia hormonal prolongada puede ser necesaria para mantener la remisión. Además, este caso destaca la importancia de un enfoque multidisciplinario para el manejo de endometriosis avanzada, especialmente en mujeres jóvenes que desean conservar la fertilidad.",
+        "score": {
+          "ROUGE-L-Sum": 0.2976066597294485,
+          "BERTScore_F": 0.7883642315864563
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.5429854456579524
+        }
+      }
+    }
+  },
+  {
+    "id": 68,
+    "gold_summary": "Paciente de 76 años con una enfermedad pulmonar intersticial difusa preexistente, que experimentó un ictus masivo debido a un neumomediastino espontáneo. Su presentación incluyó confusión, convulsiones y debilidad motora. Las pruebas de imagen revelaron burbujas de aire en los surcos cerebrales y áreas hipodensas en el cerebelo y parietooccipitales. Además, se observó neumotórax y aire en el mediastino superior en las radiografías de tórax y la tomografía torácica. A pesar de las medidas terapéuticas como el oxígeno hiperbárico, la paciente lamentablemente falleció debido al fallo multiorgánico.",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Había una señora de 76 años que estaba muy enferma y se sentía muy cansada. Ella tenía problemas en sus pulmones desde antes. Un día, su cerebro se enfermó mucho porque había aire donde no debía estar. Esto hizo que ella se confundiera y se sintiera muy débil. Los doctores vieron en sus fotos que había aire en su cabeza y en su pecho. Aunque trataron de ayudarla mucho, ella se puso muy mal y no pudo mejorar. Los doctores estaban tristes porque ella se fue al cielo.",
+        "score": {
+          "ROUGE-L-Sum": 0.17171717171717174,
+          "BERTScore_F": 0.7144455313682556
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.44308135154271366
+        }
+      },
+      "B2": {
+        "text": "Paciente de 76 años con una enfermedad pulmonar que afecta sus pulmones, llamada enfermedad pulmonar intersticial difusa. Ella llegó al hospital con confusión, somnolencia y debilidad en sus brazos y piernas. Los médicos hicieron una tomografía cerebral, que es una imagen detallada del cerebro, y encontraron burbujas de aire dentro de su cerebro y áreas dañadas en partes del cerebelo y otras zonas del cerebro. También hicieron radiografías y una tomografía del pecho, donde vieron que tenía un neumotórax, que es aire fuera del pulmón, y aire en una zona llamada mediastino, que está en el centro del pecho. Estos problemas causaron que el aire entrara en el cerebro, lo que provocó un tipo de accidente cerebrovascular llamado embolismo gaseoso. Aunque la paciente recibió tratamiento, incluyendo oxígeno especial para eliminar el aire, su estado empeoró y falleció por el fallo de varios órganos.",
+        "score": {
+          "ROUGE-L-Sum": 0.2901960784313726,
+          "BERTScore_F": 0.8061822652816772
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5481891718565249
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe presenta el caso de una mujer de 76 años con antecedentes de enfermedad pulmonar intersticial difusa, dislipemia e hipertensión arterial, que fue ingresada en urgencias debido a un estado de conciencia disminuido y tendencia al sueño. En la exploración física, la paciente estaba en estupor, sin respuesta a estímulos, con debilidad en las cuatro extremidades y desviación de la mirada hacia la derecha, sin fiebre y con signos leves de deshidratación.\n\n**Hallazgos Clave**  \nLa evaluación neurológica llevó a la realización urgente de una tomografía computarizada (TC) cerebral, que mostró múltiples burbujas de aire localizadas en los surcos cerebrales, el cuerpo calloso y ambos tálamos, además de áreas con menor densidad en la corteza y la sustancia subcortical del cerebelo izquierdo y regiones parietooccipitales bilaterales. Estas imágenes son compatibles con un daño cerebral por isquemia (falta de flujo sanguíneo) secundaria a embolismo gaseoso (bloqueo causado por burbujas de aire).  \n\nDado el antecedente pulmonar, se realizaron radiografías y una TC de tórax que evidenciaron un neumotórax apical izquierdo (colapso parcial del pulmón en la parte superior) y presencia de aire fuera de lugar en el mediastino superior (neumomediastino), lo que sugiere que el aire escapó desde el pulmón hacia estructuras cercanas.\n\n**Interpretación Clínica**  \nLa paciente sufrió un ictus masivo debido a la entrada de aire en la circulación cerebral, probablemente originado por el neumotórax y el neumomediastino espontáneos relacionados con su enfermedad pulmonar intersticial. Esta situación es grave porque las burbujas de aire pueden bloquear vasos sanguíneos y causar daño cerebral extenso. A pesar de la atención especializada y las medidas terapéuticas, incluyendo el soporte en la Unidad de Ictus, la evolución fue desfavorable.\n\n**Próximos Pasos y Resultado**  \nLa paciente falleció al segundo día de ingreso debido a un fallo multiorgánico, que es la incapacidad progresiva de varios órganos vitales. Este caso resalta la importancia de reconocer rápidamente el embolismo gaseoso cerebral como una complicación potencialmente mortal en pacientes con enfermedades pulmonares crónicas y neumotórax espontáneo.",
+        "score": {
+          "ROUGE-L-Sum": 0.23504273504273507,
+          "BERTScore_F": 0.7911680340766907
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.5131053845597129
+        }
+      }
+    }
+  },
+  {
+    "id": 69,
+    "gold_summary": "Un paciente de 24 años de edad, de etnia persa, se presentó con una queja principal de halitosis tras recuperarse de la enfermedad por coronavirus 2019 en el consultorio de su dentista general. Los exámenes intraorales y extraorales no revelaron ningún problema específico. En la sesión de seguimiento tras el tratamiento periodontal de fase I, la sensibilidad de los dientes al estímulo frío era evidente, y las radiografías revelaron una gran lesión intraósea lítica en la mandíbula. Una biopsia incisional reveló células de Langerhans y una reacción positiva a Langerina y al grupo de diferenciación 1a, por lo que se le diagnosticó histiocitosis de células de Langerhans. Después de realizar una tomografía por emisión de positrones con fluoro-2-desoxiglucosa y una tomografía computarizada, una resonancia magnética y una tomografía computarizada de haz cónico, debido a la implicación generalizada de la enfermedad, el paciente fue derivado a un oncólogo. En última instancia, se descubrió que los problemas de salud infantil del paciente, incluidos los problemas endocrinos, probablemente fueron causados por una histiocitosis de células de Langerhans no diagnosticada. El oncólogo eligió un régimen de denosumab, vinblastina, etopósido, 6-mercaptopurina, metotrexato y pegfilgrastim. El seguimiento no fue posible ya que el paciente falleció tras un accidente.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Había un hombre joven que tenía mal olor en la boca. Esto pasó después de que se enfermó con un virus. El dentista vio que algunos dientes le dolían con el frío. También encontró un hueco grande en el hueso de su mandíbula.\n\nEl doctor tomó un pedacito de ese hueso para mirar con un microscopio. Vieron unas células especiales llamadas células de Langerhans. Esto dijo que tenía una enfermedad llamada histiocitosis de células de Langerhans.\n\nEl hombre fue a ver a otro doctor que sabe de enfermedades graves. Le hicieron muchas pruebas para ver dónde estaba la enfermedad. Los doctores dijeron que la enfermedad estaba en muchas partes de su cuerpo.\n\nEl doctor le dio medicinas fuertes para ayudarlo. Pero el hombre tuvo un accidente y no pudo seguir con el tratamiento. Los doctores estaban muy tristes por eso.",
+        "score": {
+          "ROUGE-L-Sum": 0.2227979274611399,
+          "BERTScore_F": 0.7735073566436768
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.49815264205240833
+        }
+      },
+      "B2": {
+        "text": "**Lo que le pasó al paciente**  \nUn joven de 24 años, después de recuperarse de un caso leve de COVID-19, fue al dentista porque tenía mal olor en la boca. Al principio, no se encontraron problemas visibles en su boca ni en su cara. Sin embargo, después de un tratamiento para limpiar sus dientes, empezó a sentir sensibilidad al frío en algunos dientes. Las radiografías mostraron una lesión grande en el hueso de la mandíbula.\n\n**Qué encontraron los médicos**  \nPara entender mejor la lesión, los médicos tomaron una biopsia, que es cuando se extrae un pequeño pedazo de tejido para examinarlo bajo el microscopio. En esta muestra, vieron células especiales llamadas células de Langerhans. Estas células reaccionaron a ciertas pruebas que confirmaron que el paciente tenía una enfermedad llamada histiocitosis de células de Langerhans (LCH). Esta enfermedad puede afectar varios órganos y huesos.\n\n**Estudios adicionales y diagnóstico**  \nEl paciente se sometió a varios estudios, como tomografías y resonancias magnéticas, que mostraron que la enfermedad estaba en varias partes de su cuerpo, incluyendo huesos de la cabeza y las piernas, y también afectaba algunas áreas del cerebro. Además, descubrieron que algunos problemas de salud que tuvo cuando era niño, como problemas hormonales y frecuentes infecciones de oído, probablemente estaban relacionados con esta enfermedad que no se había detectado antes.\n\n**Tratamiento y resultado**  \nDebido a que la enfermedad estaba extendida, el paciente fue enviado a un especialista en cáncer para recibir quimioterapia, que es un tratamiento con medicamentos para combatir células enfermas. El médico eligió un plan con varios medicamentos para tratar la enfermedad. Lamentablemente, no se pudo hacer un seguimiento del tratamiento porque el paciente falleció debido a un accidente.  \n\nEste caso muestra la importancia de investigar a fondo cuando aparecen problemas inusuales en la boca, ya que pueden ser señales de enfermedades más serias en el cuerpo.",
+        "score": {
+          "ROUGE-L-Sum": 0.3181818181818182,
+          "BERTScore_F": 0.8166985511779785
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5674401846798983
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nUn hombre persa de 24 años acudió a su dentista quejándose de mal olor en la boca (halitosis) poco después de recuperarse de una infección leve por COVID-19. Inicialmente, no se encontraron problemas visibles en su boca ni en el examen externo. Sin embargo, tras un tratamiento periodontal inicial, el paciente comenzó a experimentar sensibilidad dental al frío, lo que llevó a la realización de radiografías que mostraron una lesión ósea anormal en la mandíbula.\n\n**Hallazgos Clave**  \nUna biopsia de la lesión reveló la presencia de células de Langerhans, un tipo específico de células inmunitarias, confirmada mediante pruebas inmunohistoquímicas positivas para marcadores como Langerina (CD-207) y CD1a. Estos hallazgos permitieron diagnosticar una enfermedad llamada histiocitosis de células de Langerhans (LCH), que es una condición poco común caracterizada por la proliferación anormal de estas células. Estudios de imagen adicionales, incluyendo tomografía computarizada de haz cónico (TCFC), tomografía por emisión de positrones con fluor-2-desoxiglucosa (FDG PET/CT) y resonancia magnética cerebral, revelaron que la enfermedad afectaba múltiples áreas óseas, incluyendo varias regiones del cráneo y huesos largos, así como inflamación en estructuras cercanas al oído y la hipófisis (glándula cerebral que regula varias funciones endocrinas).\n\n**Interpretación Clínica**  \nEl diagnóstico de LCH explicó no solo la lesión mandibular sino también varios problemas de salud que el paciente había tenido desde la infancia, como episodios recurrentes de otitis (infección del oído), alteraciones endocrinas relacionadas con un síndrome de silla turca vacía (una anomalía en la glándula hipófisis), y otros síntomas sistémicos. La enfermedad mostró un compromiso multifocal, lo que significa que afectaba varias áreas del cuerpo, complicando su pronóstico. Además, se detectó una mutación en el oncogen BRAF, un factor genético que puede influir en el comportamiento de la enfermedad y en las opciones de tratamiento.\n\n**Próximos Pasos y Tratamiento**  \nDebido a la extensión y gravedad de la enfermedad, el paciente fue remitido al departamento de oncología para recibir quimioterapia sistémica. El régimen elegido incluyó varios medicamentos: denosumab (que ayuda a inhibir la destrucción ósea), vinblastina, etopósido, 6-mercaptopurina, metotrexato y pegfilgrastim (que estimula la producción de células sanguíneas). Lamentablemente, no fue posible realizar un seguimiento del tratamiento porque el paciente falleció posteriormente a causa de un accidente.\n\n**Resumen Final**  \nEste caso ilustra cómo una enfermedad poco común como la histiocitosis de células de Langerhans puede manifestarse inicialmente con síntomas aparentemente leves, como mal aliento y sensibilidad dental, y estar relacionada con problemas médicos complejos desde la infancia. La detección temprana y el diagnóstico preciso mediante biopsia y estudios de imagen son fundamentales para orientar un tratamiento adecuado, aunque el pronóstico puede ser reservado cuando la enfermedad afecta múltiples órganos.",
+        "score": {
+          "ROUGE-L-Sum": 0.3203230148048452,
+          "BERTScore_F": 0.8333604335784912
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5768417241916682
+        }
+      }
+    }
+  },
+  {
+    "id": 70,
+    "gold_summary": "Una mujer de 66 años que en la década de 1980 había recibido varios tratamientos de rayos gamma en el cuero cabelludo desarrolló múltiples carcinomas basocelulares en la zona. Se le habían realizado más de 30 cirugías de escisión, incluida la cirugía de Mohs, en el pasado, con muchas complicaciones locales, pero, no obstante, los cánceres recurrentes. Los tratamientos con HIFU aplicados a ocho carcinomas basocelulares y dos lesiones precancerosas dieron como resultado una limpieza completa en el control a los 12 meses, pero una recurrencia después de 15 meses.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Había una señora de 66 años con problemas en su cabeza. Hace mucho tiempo, le dieron unos rayos para ayudar su piel que le picaba. Pero después, le salieron muchos bultitos malos en la cabeza.\n\nElla tuvo muchas operaciones para quitar esos bultitos. A veces, le dolía mucho y los bultitos volvían a salir. Luego, los doctores usaron un tratamiento especial con un aparato que usa calor para quitar los bultitos.\n\nDespués de un año, casi todos los bultitos se fueron. Pero después de un poco más de un año, uno volvió a salir. Los doctores la cuidaron y trataron otra vez. Ella está siendo cuidada con mucho cariño.",
+        "score": {
+          "ROUGE-L-Sum": 0.19819819819819817,
+          "BERTScore_F": 0.744246244430542
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.4712222213143701
+        }
+      },
+      "B2": {
+        "text": "**Caso de una mujer con cáncer en el cuero cabelludo**\n\nUna mujer de 66 años recibió hace muchos años, en la década de 1980, un tratamiento con rayos especiales en su cuero cabelludo para aliviar una enfermedad llamada psoriasis, que causa picor y enrojecimiento. Después de ese tratamiento, su piel se volvió sensible y se dañó con el tiempo.\n\nAproximadamente 35 años después, empezaron a aparecer en su cuero cabelludo varios tumores llamados carcinomas basocelulares (que son un tipo de cáncer de piel) y lesiones que podrían volverse cancerosas. Para tratar estos tumores, le hicieron más de 30 cirugías, incluyendo una técnica especial llamada cirugía de Mohs, que busca eliminar el cáncer sin dañar mucho la piel sana. Sin embargo, los tumores seguían apareciendo y la piel estaba muy dañada y sensible.\n\n**Nuevo tratamiento con ultrasonido de alta intensidad (HIFU)**\n\nEn 2022, los médicos decidieron probar un nuevo tratamiento llamado HIFU, que usa ondas de ultrasonido para destruir los tumores sin necesidad de cirugía. Antes de aplicar el tratamiento, marcaron las lesiones y usaron anestesia local para evitar el dolor.\n\nDurante 15 meses, trataron con HIFU diez lesiones: ocho eran carcinomas basocelulares y dos eran lesiones precancerosas. Siete de los ocho tumores desaparecieron completamente después de un año. Solo uno volvió a aparecer después de 15 meses, y fue tratado nuevamente con HIFU. Las lesiones precancerosas también sanaron sin problemas.\n\n**Qué significa esto**\n\nEste caso muestra que el tratamiento con HIFU puede ser una opción efectiva para eliminar ciertos cánceres de piel y lesiones precancerosas en pacientes con piel sensible y dañada, evitando cirugías complicadas. Aunque algunos tumores pueden volver, el HIFU ofrece una alternativa menos invasiva y con buena tolerancia para controlar estos problemas.",
+        "score": {
+          "ROUGE-L-Sum": 0.2857142857142857,
+          "BERTScore_F": 0.7967180609703064
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.541216173342296
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe trata de una mujer de 66 años que, durante la década de 1980, recibió múltiples tratamientos con rayos grenz (una forma de radiación de baja energía) en el cuero cabelludo para aliviar la psoriasis, una enfermedad inflamatoria de la piel. Estos tratamientos, junto con otros medicamentos tópicos, lograron cierto alivio, pero con el tiempo provocaron adelgazamiento del cabello, sensibilidad dolorosa y cicatrización en la piel del cuero cabelludo. Aproximadamente 35 años después de finalizar la radioterapia, la paciente desarrolló numerosos carcinomas basocelulares (un tipo común de cáncer de piel) y queratosis actínicas (lesiones precancerosas) en la misma zona.\n\n**Hallazgos Clave**  \nEntre 2020 y 2022, la paciente fue sometida a múltiples tratamientos convencionales, incluyendo más de 30 cirugías para extirpar los carcinomas basocelulares, algunas de ellas mediante cirugía de Mohs, una técnica especializada para eliminar tumores de piel con precisión. También recibió crioterapia para las lesiones precancerosas. Sin embargo, los tumores continuaron apareciendo, y la sensibilidad y daño en el cuero cabelludo dificultaban la aplicación de otros tratamientos tópicos o fotodinámicos.\n\nEn septiembre de 2022, se detectaron nuevos carcinomas basocelulares confirmados mediante biopsia. Para evaluar la extensión y profundidad de las lesiones, se utilizó un ultrasonido especializado que mostró tumores de entre 0,5 y 1,3 mm de grosor. La paciente aceptó someterse a un tratamiento con ultrasonido focalizado de alta intensidad (HIFU, por sus siglas en inglés), una técnica que utiliza ondas de ultrasonido para destruir tejido tumoral sin cirugía.\n\nAntes del tratamiento, se aplicó anestesia local para minimizar el dolor, y las lesiones fueron cuidadosamente marcadas y mapeadas para su seguimiento. El HIFU se administró con parámetros específicos (dosis de 150 ms y energía de 0.9 julios por dosis), aplicando entre 20 y 200 dosis según el tamaño de cada lesión.\n\n**Interpretación Clínica**  \nDurante los 15 meses posteriores al tratamiento inicial con HIFU, se trataron un total de 10 lesiones (8 carcinomas basocelulares y 2 queratosis actínicas) que, según los protocolos habituales, habrían requerido biopsia y cirugía. Todas las lesiones sanaron espontáneamente en pocos días sin complicaciones ni necesidad de tratamientos adicionales.\n\nEn el seguimiento a 12 meses, se observó una eliminación completa de 7 de las 8 lesiones de carcinoma basocelular y de ambas lesiones precancerosas. Solo una lesión pequeña de carcinoma basocelular recidivó después de 15 meses y fue nuevamente tratada con HIFU con éxito.\n\n**Próximos Pasos**  \nEl uso de HIFU en esta paciente representa una alternativa prometedora para el manejo de carcinomas basocelulares recurrentes en un cuero cabelludo dañado y sensible, donde las opciones quirúrgicas y tópicas son limitadas o generan complicaciones. Se recomienda continuar con controles periódicos cada 3 a 6 meses para detectar nuevas lesiones o recurrencias y evaluar la tolerancia a largo plazo del tratamiento. Además, la experiencia obtenida sugiere que el HIFU podría ser una modalidad terapéutica eficaz y menos invasiva para casos similares en el futuro.",
+        "score": {
+          "ROUGE-L-Sum": 0.20537124802527648,
+          "BERTScore_F": 0.795607328414917
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.5004892882200968
+        }
+      }
+    }
+  },
+  {
+    "id": 71,
+    "gold_summary": "Se sometió a un trasplante de corazón ortotópico a un niño de 12 años con insuficiencia cardiaca en fase terminal debido a una miocardiopatía restrictiva. La disfunción primaria del injerto precisó oxigenación con membrana extracorpórea venosa arterial. La función cardiaca se normalizó, pero el bloqueo auriculoventricular completo persistió después de 3 semanas. Se realizó un marcapaso bicameral con marcapaso transvenoso del ventrículo izquierdo a través del seno coronario. Tras 5 años de seguimiento, el paciente se encuentra estable con el mismo sistema de marcapaso y con la función ventricular preservada.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Un niño de 12 años recibió un nuevo corazón porque su corazón estaba muy enfermo. Al principio, su nuevo corazón tuvo problemas y necesitó ayuda para funcionar. Después de un tiempo, el corazón empezó a trabajar bien. Pero el niño tenía un problema con el ritmo del corazón. Por eso, los doctores le pusieron un pequeño aparato llamado marcapasos para ayudar a que su corazón latiera bien. Cinco años después, el niño está bien y su corazón funciona muy bien con el marcapasos.",
+        "score": {
+          "ROUGE-L-Sum": 0.22660098522167488,
+          "BERTScore_F": 0.7465301156044006
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.48656555041303773
+        }
+      },
+      "B2": {
+        "text": "**Trasplante de Corazón y Uso de Marcapasos en una Niña de 12 Años**\n\nUna niña de 12 años con un problema grave en el corazón llamado miocardiopatía restrictiva, que causa que el corazón no funcione bien, recibió un trasplante de corazón. Durante la operación, el nuevo corazón tuvo dificultades para funcionar correctamente, por lo que los médicos usaron una máquina especial llamada oxigenación por membrana extracorpórea. Esta máquina ayuda a oxigenar la sangre cuando el corazón está débil.\n\nDespués de cuatro días, el corazón trasplantado comenzó a funcionar bien. Sin embargo, la niña tuvo un problema llamado bloqueo auriculoventricular completo, que significa que las señales eléctricas entre las partes superiores e inferiores del corazón no se transmitían bien. Este problema duró más de tres semanas.\n\nPara ayudar a su corazón a latir de manera sincronizada y evitar daños, los médicos le implantaron un marcapasos especial. Un marcapasos es un dispositivo que envía señales eléctricas para controlar el ritmo del corazón. En este caso, colocaron un marcapasos que estimula ambos ventrículos del corazón (las partes inferiores) usando cables que pasan por las venas hasta llegar al corazón.\n\nEl procedimiento se hizo con anestesia local y sedación suave, y los cables se colocaron cuidadosamente en las venas del corazón. El marcapasos se programó para adaptarse a las necesidades del corazón de la niña. Después de la operación, los exámenes mostraron que el corazón latía de forma sincronizada y sin problemas.\n\nCinco años después, la niña está estable, con buena función del corazón y sigue usando el mismo marcapasos sin complicaciones. Esto muestra que el tratamiento fue exitoso para mejorar su calidad de vida.",
+        "score": {
+          "ROUGE-L-Sum": 0.23474178403755866,
+          "BERTScore_F": 0.7946245074272156
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.5146831457323872
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nUna niña de 12 años con insuficiencia cardíaca avanzada causada por una miocardiopatía restrictiva (una enfermedad que limita la capacidad del corazón para llenarse de sangre) fue sometida a un trasplante cardíaco ortotópico, que consiste en reemplazar el corazón enfermo por uno sano en la misma posición anatómica. Durante la cirugía, presentó una disfunción grave del nuevo corazón (injerto), lo que requirió soporte temporal con oxigenación por membrana extracorpórea venosa arterial (una técnica que ayuda a oxigenar la sangre y mantener la circulación mientras el corazón se recupera).\n\n**Hallazgos Clave**  \n- La función cardíaca del injerto se recuperó completamente en 4 días.  \n- Posteriormente, la paciente desarrolló un bloqueo auriculoventricular completo (una interrupción total en la transmisión eléctrica entre las aurículas y los ventrículos del corazón) que persistió por más de tres semanas.  \n- Para evitar problemas relacionados con la descoordinación del ventrículo izquierdo y el daño potencial al ventrículo derecho por las biopsias repetidas que se realizan para vigilar el rechazo del trasplante, se decidió implantar un marcapasos biventricular transvenoso. Este dispositivo estimula eléctricamente ambos ventrículos para mantener un ritmo cardíaco sincronizado.  \n- El electrodo del ventrículo izquierdo se colocó a través de la vena coronaria (una vena del corazón) usando un catéter guiado, mientras que otro electrodo se implantó en la aurícula derecha.  \n- Ambos electrodos se conectaron a un marcapasos adaptable a la frecuencia, ubicado en una bolsa muscular debajo de la clavícula izquierda.  \n- Las mediciones eléctricas del marcapasos mostraron parámetros estables y adecuados para un funcionamiento óptimo.  \n- El electrocardiograma posterior mostró una morfología compatible con bloqueo de rama derecha, pero la ecocardiografía confirmó que no existían desincronías en la contracción de las cámaras cardíacas.\n\n**Interpretación Clínica**  \nEl uso de un marcapasos biventricular con estimulación del ventrículo izquierdo a través del seno coronario resultó ser una estrategia efectiva para manejar el bloqueo auriculoventricular prolongado en esta paciente trasplantada. Este enfoque permitió mantener la sincronía en la contracción del corazón, evitando complicaciones que podrían afectar la función ventricular. La estabilidad de los parámetros eléctricos y la ausencia de disincronías evidenciadas por ecocardiografía respaldan la eficacia del tratamiento.\n\n**Próximos Pasos y Seguimiento**  \nA cinco años del implante del marcapasos, la paciente se mantiene en clase funcional I (sin limitaciones para realizar actividades físicas normales), con función ventricular preservada y sin necesidad de cambios en el sistema de estimulación. Esto indica un pronóstico favorable y una buena calidad de vida a largo plazo. Se recomienda continuar con el seguimiento cardiológico regular para monitorear la función del marcapasos y del injerto cardíaco, así como para detectar cualquier posible complicación futura.",
+        "score": {
+          "ROUGE-L-Sum": 0.22553897180762852,
+          "BERTScore_F": 0.8178963661193848
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.5217176689635067
+        }
+      }
+    }
+  },
+  {
+    "id": 72,
+    "gold_summary": "Presentamos un caso de nudos ileocecales en una paciente posparto con distensión abdominal, vómitos y ausencia de heces y flatos. La radiografía abdominal simple reveló bucles intestinales dilatados con múltiples niveles de aire y fluidos. Se realizó una laparotomía exploratoria con hallazgo intraoperatorio de nudos ileocecales con intestino viable, ciego móvil y colon ascendente y punta gangrenosa del apéndice. Deshicimos el nudo y realizamos una apendectomía. Debido a la inestabilidad intraoperatoria de los signos vitales de la paciente, se aplazó la hemicolectomía derecha y se fijaron el ciego y el colon ascendente a la pared abdominal posterolateral derecha.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Había una niña que acababa de tener un bebé. Su barriga estaba muy grande y le dolía mucho. No podía hacer popó ni tirar gases y vomitaba mucho.\n\nLos doctores le hicieron una radiografía y vieron que sus intestinos estaban muy hinchados. La niña fue al hospital y los doctores la operaron para ver qué pasaba.\n\nDentro, encontraron que sus intestinos estaban enredados como un nudo. También vieron que una parte pequeña llamada apéndice estaba dañada. Los doctores deshicieron el nudo y quitaron el apéndice malo.\n\nComo la niña estaba muy débil, los doctores hicieron algo para que sus intestinos no se movieran mucho y la cuidaron mucho después.",
+        "score": {
+          "ROUGE-L-Sum": 0.23478260869565215,
+          "BERTScore_F": 0.7265211939811707
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.4806519013384114
+        }
+      },
+      "B2": {
+        "text": "**Lo que le pasó a la paciente:**  \nUna joven de 20 años, que acababa de tener un bebé por cesárea, llegó al hospital con el abdomen muy hinchado, dolor y vómitos. Además, no podía expulsar gases ni hacer sus necesidades. Estos síntomas indicaban que algo estaba bloqueando su intestino.\n\n**Lo que encontraron en las pruebas:**  \nLa radiografía mostró que partes del intestino estaban muy dilatadas y había niveles de aire y líquido, lo que sugiere una obstrucción. Por eso, los médicos decidieron hacer una cirugía para ver qué estaba pasando.\n\n**Lo que vieron durante la operación:**  \nDescubrieron que una parte del intestino delgado (íleon) estaba enredada alrededor del ciego y el colon ascendente, formando un nudo llamado \"nudo ileocecal\". El intestino estaba en buen estado, pero la punta del apéndice estaba dañada (gangrenosa). Los médicos deshicieron el nudo y quitaron el apéndice enfermo (apendectomía).\n\n**Cómo continuó el tratamiento:**  \nLa paciente tuvo problemas con su presión arterial durante la cirugía, por lo que no pudieron hacer una cirugía más grande (hemicolectomía derecha) en ese momento. En cambio, fijaron el ciego y el colon a la pared abdominal para evitar que se movieran y causaran más problemas.\n\n**Qué significa esto:**  \nEl nudo ileocecal es una causa rara de bloqueo intestinal que puede ser grave. En este caso, la cirugía ayudó a liberar el intestino y a quitar la parte dañada. Sin embargo, la paciente tuvo complicaciones después, lo que muestra que este tipo de problemas necesita atención rápida y cuidadosa.",
+        "score": {
+          "ROUGE-L-Sum": 0.2649350649350649,
+          "BERTScore_F": 0.7657347321510315
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.5153348985430481
+        }
+      },
+      "B3": {
+        "text": "**Contexto:**  \nSe trató de una mujer joven de 20 años que, tras un parto por cesárea debido a problemas con el ritmo cardíaco fetal, comenzó a presentar una distensión abdominal progresiva acompañada de calambres, vómitos frecuentes y la incapacidad para expulsar gases y heces. No tenía antecedentes de cirugías abdominales ni enfermedades crónicas. Su estado general era grave, con signos de dolor abdominal intenso, presión arterial baja y taquicardia (latidos rápidos del corazón). Las pruebas iniciales mostraron una disminución en el número de glóbulos blancos y plaquetas, además de una radiografía abdominal que evidenció dilatación de los intestinos y acumulación de líquido en la cavidad abdominal.\n\n**Hallazgos Clave:**  \nDurante la cirugía exploratoria, se encontró que una parte del intestino delgado (íleon distal) estaba enredada alrededor del ciego y el colon ascendente, formando un nudo intestinal (nudo ileocecal). Aunque el intestino estaba viable (sin daño irreversible), la punta del apéndice estaba gangrenosa (tejido muerto por falta de circulación). Se observó también una gran cantidad de líquido seroso en la cavidad abdominal. La paciente presentó inestabilidad hemodinámica (presión arterial muy baja) durante la operación, lo que complicó el manejo quirúrgico.\n\n**Interpretación Clínica:**  \nEl nudo ileocecal es una causa rara pero grave de obstrucción intestinal que puede provocar compromiso vascular y gangrena si no se trata oportunamente. En este caso, la viabilidad del intestino permitió deshacer el nudo y realizar la extirpación del apéndice afectado (apendicectomía). Debido a la inestabilidad de la paciente, se decidió posponer la resección mayor (hemicolectomía derecha) y en su lugar se fijaron el ciego y el colon ascendente para evitar una nueva torsión.\n\n**Próximos Pasos y Evolución:**  \nA pesar de las intervenciones quirúrgicas y el soporte con líquidos y medicamentos para estabilizar la presión arterial, la paciente desarrolló una infección grave denominada gangrena de Fournier, que afectó la región genital y suprapúbica. Se requirió un desbridamiento quirúrgico radical y tratamiento antibiótico intensivo. Sin embargo, la paciente evolucionó hacia un shock séptico refractario (una infección generalizada que no responde al tratamiento) y finalmente falleció debido a un fallo multiorgánico en el segundo día postoperatorio.\n\nEste caso resalta la complejidad y gravedad de las complicaciones abdominales posparto, la importancia del diagnóstico temprano y la dificultad de manejo en pacientes con inestabilidad hemodinámica y recursos limitados.",
+        "score": {
+          "ROUGE-L-Sum": 0.2271880819366853,
+          "BERTScore_F": 0.771922767162323
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.49955542454950413
+        }
+      }
+    }
+  },
+  {
+    "id": 73,
+    "gold_summary": "Aquí, reportamos un caso de insuficiencia cardiaca debido al síndrome de Carney que resultó en mixoma cardiaco combinado con cardiomiopatía dilatada. Un hombre de 35 años de edad fue admitido en el hospital hace tres años debido a opresión torácica repentina y falta de aire. La ecocardiografía indicó mixoma, y una combinación de cribado genético y examen físico confirmó el síndrome de Carney con mixoma cardiaco. Después del tratamiento sintomático, fue dado de alta. Las intervenciones quirúrgicas no fueron consideradas en ese momento. Sin embargo, la opresión torácica y los síntomas de falta de aire del paciente empeoraron, y volvió al hospital. Se confirmó una función cardiaca de grado IV de la New York Heart Association, y la ecocardiografía indicó la presencia de cardiomiopatía dilatada acompañada de mixoma cardiaco. En última instancia, la insuficiencia cardiaca del paciente fue tratada con éxito con un trasplante cardiaco.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Había un hombre que se sentía muy cansado y le dolía el pecho. Tenía un bulto en su corazón que no era bueno. Los doctores le hicieron pruebas y encontraron que tenía una enfermedad llamada síndrome de Carney. Al principio, le dieron medicinas para sentirse mejor y se fue a su casa. Pero después, se sintió peor y volvió al hospital. Su corazón estaba muy débil y tenía el bulto grande. Los doctores le dieron un corazón nuevo con una operación. Ahora, el hombre está mejor y puede vivir feliz.",
+        "score": {
+          "ROUGE-L-Sum": 0.17843866171003717,
+          "BERTScore_F": 0.7281399965286255
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.45328932911933134
+        }
+      },
+      "B2": {
+        "text": "**Lo que le pasó al paciente**\n\nUn hombre de 35 años tuvo problemas en el corazón que le causaban dolor en el pecho y dificultad para respirar. Al principio, los médicos encontraron una masa en su corazón llamada mixoma, que es un tipo de tumor benigno, y también detectaron que tenía el síndrome de Carney, una enfermedad rara que puede causar tumores y otros problemas en el cuerpo. En ese momento, solo le dieron medicamentos para aliviar los síntomas y no le hicieron cirugía.\n\n**Cómo empeoró su condición**\n\nCon el tiempo, sus síntomas se hicieron más graves. Volvió al hospital porque le costaba mucho respirar y su corazón estaba muy débil. Los médicos descubrieron que tenía cardiomiopatía dilatada, que significa que su corazón estaba agrandado y no podía bombear la sangre bien. Además, el mixoma seguía presente en su corazón.\n\n**Qué hicieron los médicos**\n\nDebido a que su corazón estaba muy dañado y tenía insuficiencia cardíaca avanzada, los médicos decidieron hacerle un trasplante de corazón. Esto significa que le pusieron un corazón nuevo de un donante para reemplazar el suyo enfermo.\n\n**Cómo fue la cirugía y la recuperación**\n\nLa operación fue complicada, pero exitosa. Los médicos quitaron el corazón enfermo y el tumor, y pusieron el corazón nuevo. Después de la cirugía, el paciente recibió medicamentos para evitar que su cuerpo rechazara el nuevo corazón y para prevenir infecciones. Poco a poco, su corazón comenzó a funcionar bien y sus síntomas mejoraron mucho.\n\n**Qué significa este caso**\n\nEste caso muestra cómo el síndrome de Carney puede causar problemas graves en el corazón, como tumores y debilidad del músculo cardíaco. También enseña que, cuando el corazón está muy dañado, un trasplante puede ser la mejor opción para salvar la vida del paciente.",
+        "score": {
+          "ROUGE-L-Sum": 0.23529411764705882,
+          "BERTScore_F": 0.7736754417419434
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.5044847796945011
+        }
+      },
+      "B3": {
+        "text": "**Contexto**\n\nPresentamos el caso de un hombre de 38 años diagnosticado con el síndrome de Carney (CNC), una enfermedad genética rara caracterizada por tumores cardíacos benignos llamados mixomas, pigmentación cutánea y otras anomalías. Este paciente inicialmente se presentó hace tres años con síntomas de opresión en el pecho y dificultad para respirar, y fue diagnosticado con un mixoma en el corazón izquierdo mediante ecocardiografía. Además, el examen físico reveló manchas pigmentadas en las orejas, y estudios de imagen detectaron múltiples lesiones hepáticas y quistes renales. Las pruebas genéticas confirmaron mutaciones en los genes TTN y PRKAR1A, asociadas con CNC y cardiomiopatía dilatada (una enfermedad que afecta la capacidad del corazón para bombear sangre). En ese momento, recibió tratamiento para aliviar los síntomas y fue dado de alta, rechazando la cirugía.\n\n**Evolución y Hallazgos Clínicos**\n\nEn septiembre de 2023, el paciente regresó con empeoramiento de la opresión torácica y dificultad respiratoria, incluyendo intolerancia a la posición acostada. El examen físico evidenció signos de insuficiencia cardíaca avanzada, como distensión de la vena yugular, ritmo cardíaco irregular (fibrilación auricular), murmullo en la válvula mitral y estertores pulmonares. También se observaron un hígado aumentado de tamaño y edema en las piernas. La ecocardiografía mostró un corazón globalmente agrandado, dilatación de grandes vasos, regurgitación mitral moderada y una masa irregular de 54 × 43 mm en la aurícula izquierda, compatible con mixoma. La función del ventrículo izquierdo estaba gravemente reducida, con una fracción de eyección del 23,1 % (normalmente >55 %). La electrocardiografía confirmó fibrilación auricular y alteraciones en las derivaciones precordiales. El diagnóstico final incluyó cardiomiopatía dilatada (DCM) y síndrome de Carney con mixoma cardíaco, en contexto de insuficiencia cardíaca terminal.\n\n**Procedimiento Quirúrgico**\n\nDada la gravedad de la insuficiencia cardíaca y la presencia del mixoma, se decidió realizar un trasplante de corazón. Durante la cirugía, se realizó una esternotomía media para acceder al corazón agrandado y debilitado. Se extirparon las aurículas y ventrículos enfermos junto con la masa tumoral, y se implantó el corazón donante mediante suturas meticulosas para conectar las estructuras vasculares y auriculares. El corazón trasplantado recuperó el ritmo sinusal espontáneamente y sin complicaciones hemorrágicas. El examen histopatológico confirmó la presencia de mixoma y cardiomiopatía dilatada en el tejido removido.\n\n**Manejo Postoperatorio y Resultados**\n\nEn el postoperatorio inmediato, el paciente mostró una producción urinaria adecuada y niveles elevados pero decrecientes de marcadores cardíacos (troponina T y NT-proBNP), indicadores de daño y estrés cardíaco. La ecocardiografía evidenció una función ventricular normalizada con fracción de eyección del 65 % y estructura valvular sin anomalías. Se instauró un régimen inmunosupresor con metilprednisolona, prednisona, micofenolato de mofetilo y tacrolimus para prevenir el rechazo del trasplante, junto con tratamiento antibiótico y antifúngico para evitar infecciones. La recuperación fue favorable, con normalización progresiva de los parámetros clínicos y de laboratorio. En el seguimiento a largo plazo, el paciente mantuvo un buen estado general sin signos de rechazo ni complicaciones, y fue dado de alta con un pronóstico positivo.\n\n**Interpretación Clínica**\n\nEste caso ilustra la complejidad del síndrome de Carney cuando se asocia con mixoma cardíaco y cardiomiopatía dilatada, condiciones que pueden conducir a insuficiencia cardíaca grave. La identificación temprana mediante ecocardiografía, examen físico detallado y pruebas genéticas es fundamental para el diagnóstico. Aunque inicialmente se manejó de forma conservadora, el deterioro progresivo de la función cardíaca requirió un trasplante de corazón, que resultó ser una opción terapéutica eficaz para tratar simultáneamente la insuficiencia cardíaca terminal y la masa tumoral. La cirugía y el manejo postoperatorio cuidadoso permitieron una recuperación exitosa y mejoraron significativamente la calidad de vida del paciente.\n\n**Próximos Pasos**\n\nSe recomienda continuar con controles regulares para monitorear la función cardíaca y detectar posibles signos de rechazo o recurrencia de la enfermedad. Además, el seguimiento genético y clínico es importante para evaluar otras manifestaciones del síndrome de Carney y prevenir complicaciones asociadas. La educación del paciente sobre la adherencia al tratamiento inmunosupresor y la vigilancia de síntomas es esencial para mantener un resultado favorable a largo plazo.",
+        "score": {
+          "ROUGE-L-Sum": 0.19658119658119655,
+          "BERTScore_F": 0.8091896772384644
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.5028854369098305
+        }
+      }
+    }
+  },
+  {
+    "id": 74,
+    "gold_summary": "Un paciente caucásico de 52 años de edad con hipertensión pulmonar (HP) confirmada por ecocardiografía fue admitido en el departamento de cardiología debido a disnea de esfuerzo y signos de insuficiencia ventricular derecha. La exploración rutinaria para detectar causas de HP secundaria fue negativa. El cateterismo cardiaco derecho (CCR) confirmó una HP arterial de alto grado [presión arterial pulmonar media (PAPm); 50,6 mmHg, presión de enclavamiento pulmonar (PWP); 11,3 mmHg, resistencia vascular pulmonar (PVR); 11,9 unidades de Wood (UW)] irreversible en la prueba con óxido nítrico inhalado. La saturación de oxígeno (SaO2) de las muestras de sangre obtenidas durante el primer CCR osciló entre 69,3 y 73,2%. Se diagnosticó hipertensión arterial pulmonar idiopática. Se inició el tratamiento con iloprost inhalado y sildenafil.\n\nEl control RHC, realizado 5 meses después, mostró valores de mPAP (59,7 mmHg) y PVR (13,4 WU) más altos en comparación con la medición inicial. El SaO2 de sangre obtenida durante el RHC de la arteria del lóbulo superior del pulmón derecho fue elevado y ascendió al 89,7 %.\n\nLuego se realizó una arteriografía pulmonar. Se encontró falta de contraste en la arteria del lóbulo superior derecho con evidencia de flujo sanguíneo retrógrado visible como contraste negativo en la arteria pulmonar derecha. Después, una arteriografía de la arteria subclavia derecha detectó una enorme malformación vascular que se comunicaba con la arteria del lóbulo superior derecho. Después, un angiograma por tomografía computarizada (angio-CT) reveló adicionalmente el agrandamiento de las arterias bronquiales que se originaban en las fístulas hacia la arteria pulmonar del lóbulo superior derecho.\n\nA pesar del tratamiento farmacológico intensivo, que incluyó la terapia de la hipertensión pulmonar y la embolización percutánea de las fístulas, el estado del paciente siguió deteriorándose. Falleció tres meses después de la embolización debido a una insuficiencia cardiaca grave complicada por neumonía.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Había un hombre de 52 años que tenía problemas para respirar. Su corazón y pulmones no funcionaban bien. Los doctores hicieron muchas pruebas para entender qué pasaba.\n\nEncontraron que la presión en sus pulmones era muy alta. Le dieron medicinas para ayudar, pero no mejoró mucho.\n\nLuego vieron que tenía unos tubos raros en sus pulmones que no estaban bien. Intentaron taparlos para ayudar, pero el hombre se puso más enfermo.\n\nAl final, el hombre murió porque su corazón se cansó mucho y tuvo una infección en los pulmones. Los doctores hicieron todo lo que pudieron para ayudarlo.",
+        "score": {
+          "ROUGE-L-Sum": 0.13656387665198236,
+          "BERTScore_F": 0.7129381895065308
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.42475103307925655
+        }
+      },
+      "B2": {
+        "text": "**Caso de un Paciente con Hipertensión Pulmonar y Problemas en las Arterias del Pulmón**\n\nUn hombre de 52 años tenía dificultad para respirar y problemas en el lado derecho de su corazón. Los médicos confirmaron que tenía hipertensión pulmonar, que es cuando la presión en las arterias de los pulmones está muy alta. Para entender mejor su enfermedad, le hicieron un examen llamado cateterismo cardiaco derecho, que mide la presión y el flujo de sangre en el corazón y los pulmones. Los resultados mostraron que su hipertensión pulmonar era grave y no mejoraba con el tratamiento con óxido nítrico inhalado. Además, la cantidad de oxígeno en su sangre estaba baja, entre 69% y 73%.\n\nLos médicos pensaron que tenía hipertensión arterial pulmonar idiopática, que significa que la causa es desconocida. Por eso, comenzaron un tratamiento con dos medicamentos: iloprost inhalado y sildenafil, que ayudan a bajar la presión en las arterias pulmonares.\n\nCinco meses después, hicieron otro cateterismo y encontraron que la presión en sus pulmones había aumentado aún más, y la resistencia al flujo sanguíneo también era mayor. Sin embargo, la cantidad de oxígeno en la sangre de una parte específica del pulmón derecho había subido a casi 90%, lo que era extraño.\n\nPara investigar esto, realizaron una arteriografía, que es una prueba que usa un contraste para ver las arterias con rayos X. Descubrieron que la arteria del lóbulo superior del pulmón derecho no se llenaba bien con el contraste y que la sangre estaba fluyendo en dirección contraria en esa arteria. Luego, hicieron otra arteriografía en la arteria subclavia derecha (una arteria cerca del hombro) y encontraron una gran malformación, que es una conexión anormal entre vasos sanguíneos, que se comunicaba con la arteria del pulmón derecho.\n\nTambién un estudio por tomografía computarizada mostró que las arterias bronquiales, que normalmente llevan sangre a los pulmones, estaban agrandadas y formaban fístulas. Las fístulas son conexiones anormales entre arterias que pueden causar problemas en el flujo sanguíneo.\n\nAunque el paciente recibió tratamiento médico y se intentó cerrar estas fístulas mediante un procedimiento llamado embolización (que bloquea estas conexiones anormales), su salud empeoró. Tres meses después de este procedimiento, falleció debido a insuficiencia cardiaca grave, que fue complicada por una infección pulmonar llamada neumonía.\n\n**Qué Significa Este Caso**\n\nEste caso muestra que en algunos pacientes con hipertensión pulmonar grave, pueden existir conexiones anormales entre arterias que afectan el flujo de sangre y el oxígeno en los pulmones. Aunque se usen medicamentos y procedimientos para tratar estas malformaciones, la enfermedad puede avanzar y causar complicaciones serias. Por eso, es importante hacer estudios detallados para entender todas las causas y buscar el mejor tratamiento posible.",
+        "score": {
+          "ROUGE-L-Sum": 0.4360189573459715,
+          "BERTScore_F": 0.8125137686729431
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.6242663630094574
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe trata de un hombre caucásico de 52 años con hipertensión pulmonar (HP) grave, inicialmente diagnosticada mediante ecocardiografía, que presentaba dificultad para respirar al esfuerzo y signos de insuficiencia del ventrículo derecho del corazón. A lo largo de su evolución, se descartaron causas secundarias comunes de hipertensión pulmonar mediante estudios exhaustivos, incluyendo pruebas de imagen y análisis de laboratorio.\n\n**Hallazgos Clave**  \nEl cateterismo cardiaco derecho (CCR), una prueba invasiva que mide directamente las presiones y flujos en el corazón y pulmones, confirmó una hipertensión arterial pulmonar severa e irreversible, con una presión arterial pulmonar media elevada (50,6 mmHg), presión de enclavamiento pulmonar normal (11,3 mmHg) y resistencia vascular pulmonar alta (11,9 unidades de Wood). La saturación de oxígeno en la sangre obtenida durante este procedimiento fue moderadamente reducida (entre 69,3% y 73,2%), lo que indicaba un intercambio de oxígeno comprometido.\n\nCinco meses después, un nuevo cateterismo mostró un empeoramiento de las presiones pulmonares (presión media de 59,7 mmHg) y de la resistencia vascular (13,4 unidades de Wood). Sin embargo, la saturación de oxígeno en la arteria del lóbulo superior derecho del pulmón aumentó notablemente hasta 89,7%, lo que sugería la presencia de un flujo anormal de sangre.\n\nUna angiografía pulmonar (estudio de imagen con contraste para visualizar las arterias pulmonares) reveló ausencia de contraste en la arteria del lóbulo superior derecho y flujo sanguíneo retrógrado (en sentido contrario al habitual) en la arteria pulmonar derecha. Posteriormente, una arteriografía de la arteria subclavia derecha identificó una gran malformación vascular que conectaba esta arteria con la arteria del lóbulo superior derecho del pulmón. Un estudio adicional con angiografía por tomografía computarizada (angio-TC) mostró además un aumento del tamaño de las arterias bronquiales que formaban fístulas (conexiones anormales) hacia la arteria pulmonar del mismo lóbulo.\n\n**Interpretación Clínica**  \nEl diagnóstico final fue hipertensión arterial pulmonar idiopática (sin causa identificable) complicada por la presencia de fístulas arterio-arteriales entre las arterias sistémicas (subclavia y bronquiales) y las arterias pulmonares del lóbulo superior derecho. Estas conexiones anómalas alteraban el flujo sanguíneo normal, contribuyendo al empeoramiento de la insuficiencia cardiaca derecha y a la hipoxemia (bajo nivel de oxígeno en sangre).\n\nA pesar del tratamiento médico intensivo con vasodilatadores pulmonares (iloprost inhalado y sildenafil oral) y de la embolización percutánea (procedimiento para cerrar las fístulas mediante la introducción de materiales que bloquean el flujo anormal), la condición del paciente continuó deteriorándose.\n\n**Próximos Pasos y Resultado**  \nEl paciente falleció tres meses después de la embolización debido a insuficiencia cardiaca grave, agravada por una neumonía. Este caso resalta la complejidad y gravedad de la hipertensión pulmonar idiopática cuando se asocia a malformaciones vasculares, y la dificultad para controlar la progresión a pesar de las terapias disponibles.",
+        "score": {
+          "ROUGE-L-Sum": 0.5473441108545035,
+          "BERTScore_F": 0.8484379053115845
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.697891008083044
+        }
+      }
+    }
+  },
+  {
+    "id": 75,
+    "gold_summary": "Paciente 73 años, dependiente, polimedicada y pluripatológica contacta telefónicamente con la farmacia comunitaria para solicitar información sobre un tratamiento de nueva prescripción para una infección de orina y un déficit de vitamina D. La dispensación de la medicación a su cuidadora deriva en mayores dudas a la paciente, por lo que se le ofrece el servicio de revisión del uso del medicamento (RUM). Durante la prestación del servicio se detectan varias incidencias en su tratamiento, por lo que se decide realizar un informe de derivación al médico de atención primaria para una revisión completa del tratamiento y poder así derivar a la paciente al servicio de Sistema Personalizado de Dosificación (SPD) con el fin de garantizar la seguridad farmacoterapéutica de la paciente y mejorar su adherencia al tratamiento.",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Una señora de 73 años se siente confundida con sus medicinas nuevas. Ella no puede salir de casa y su cuidadora siempre le ayuda con sus pastillas. La señora llamó a la farmacia para preguntar. \n\nLa farmacia revisó todas sus medicinas y vio que había problemas. Algunas pastillas estaban mal guardadas y había medicinas repetidas. \n\nPor eso, la farmacia habló con su doctor para ayudarla mejor. El doctor cambió algunas medicinas y pidió que la señora tenga un organizador especial para sus pastillas. Así, será más fácil y seguro tomar sus medicinas.",
+        "score": {
+          "ROUGE-L-Sum": 0.19591836734693877,
+          "BERTScore_F": 0.721239447593689
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.4585789074703139
+        }
+      },
+      "B2": {
+        "text": "**Información sobre la Paciente y su Situación**\n\nUna mujer de 73 años, que depende totalmente de otras personas para su cuidado y toma muchos medicamentos por varias enfermedades, llamó a la farmacia para preguntar sobre un nuevo tratamiento. Este tratamiento era para una infección de orina y para un problema de falta de vitamina D, que le habían diagnosticado en un hospital.\n\n**Problemas Detectados con la Medicación**\n\nAunque su cuidadora recogió los medicamentos, la paciente se confundió porque ya tomaba otras pastillas para la vitamina D y no entendía bien los cambios. Además, su cuidadora habitual ya no podía ayudarla, lo que complicaba más la situación. Por eso, la farmacia le ofreció un servicio llamado Revisión del Uso del Medicamento (RUM). Este servicio ayuda a revisar si la paciente entiende bien sus medicinas y si las está tomando correctamente.\n\nAl revisar los medicamentos, encontraron varios problemas: había medicinas vencidas, instrucciones equivocadas, pastillas partidas que no debían estar así y varios envases del mismo medicamento. Como la paciente no podía manejar bien su tratamiento y estaba sin su cuidadora, se decidió que necesitaba un Sistema Personalizado de Dosificación (SPD). Este sistema organiza las medicinas en pastilleros para que sea más fácil y seguro tomarlas.\n\n**Acciones y Cambios Realizados**\n\nSe preparó un informe para el médico de atención primaria explicando la situación y recomendando la revisión completa del tratamiento. El médico hizo algunos cambios importantes, como:\n\n- Cambiar la vitamina D para evitar tomar dos tipos diferentes al mismo tiempo.\n\n- Ajustar la dosis de un analgésico llamado tramadol.\n\n- Cambiar el tipo de pañales para facilitar su uso debido a la dependencia de la paciente.\n\n- Mantener el tratamiento para la enfermedad pulmonar, pero con supervisión diaria para asegurar que la paciente use bien el inhalador.\n\n**Conclusión**\n\nGracias a la revisión y coordinación entre la farmacia y el médico, se mejoró la seguridad y el manejo del tratamiento de la paciente. Además, se implementó un sistema que facilitará que tome sus medicamentos correctamente, lo cual es muy importante para su salud y bienestar.",
+        "score": {
+          "ROUGE-L-Sum": 0.3229571984435798,
+          "BERTScore_F": 0.8109643459320068
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5669607721877933
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe trata de una paciente de 73 años con múltiples enfermedades crónicas, incluyendo enfermedad pulmonar obstructiva crónica (EPOC), hipertensión arterial, trastorno bipolar, ansiedad, depresión, hipotiroidismo y artritis reumatoide. Es totalmente dependiente para sus actividades diarias y no sale de casa; su cuidadora habitual se encargaba de gestionar y recoger su medicación. Recientemente, tras una analítica en urgencias, se le diagnosticó una infección de orina y un déficit de vitamina D, para los cuales se le prescribió un nuevo tratamiento.\n\n**Hallazgos Clave**  \nLa paciente contactó con la farmacia comunitaria para aclarar dudas sobre la nueva medicación, ya que existía confusión debido a la coexistencia de tratamientos previos para el déficit de vitamina D y la reciente prescripción. Además, la cuidadora habitual informó que ya no podría continuar asistiendo a la paciente, lo que generó preocupación sobre la correcta administración de los medicamentos. Se ofreció entonces el servicio de Revisión del Uso del Medicamento (RUM) para evaluar el conocimiento de la paciente y su cuidadora sobre las patologías y tratamientos, y para identificar posibles errores en la gestión farmacológica.\n\nDurante la revisión, se detectaron múltiples problemas: medicamentos caducados, instrucciones incorrectas, comprimidos partidos indebidamente y acumulación de envases duplicados. También se identificaron errores potenciales en la prescripción, como duplicidad en el tratamiento para la vitamina D y una pauta inadecuada para tramadol. Además, se observaron dificultades en el manejo del inhalador para la EPOC y problemas relacionados con la elección del absorbente para la incontinencia urinaria, que complicaban la correcta atención de la paciente.\n\n**Interpretación Clínica**  \nDada la complejidad del caso, la dependencia de la paciente y la ausencia de su cuidadora habitual, se consideró necesario derivar a la paciente al servicio de Sistema Personalizado de Dosificación (SPD), que facilita la organización y administración segura de la medicación. Se elaboró un informe detallado para el médico de Atención Primaria, incluyendo recomendaciones específicas para ajustar el tratamiento, como la sustitución del calcifediol por colecalciferol para el déficit de vitamina D, la modificación de la pauta de tramadol y el cambio del tipo de absorbente para mejorar la comodidad y manejo.\n\nEn cuanto al tratamiento para la EPOC, el médico decidió mantener la medicación actual pero reforzar la supervisión diaria por parte de la cuidadora para asegurar la correcta utilización del inhalador.\n\n**Próximos Pasos**  \nEl médico de Atención Primaria recibió el informe y coordinó con la farmacia comunitaria la implementación del Sistema Personalizado de Dosificación. Este enfoque busca mejorar la seguridad en la administración de los medicamentos, evitar errores y aumentar la adherencia al tratamiento, aspectos fundamentales para el bienestar y la calidad de vida de la paciente. Además, se estableció un seguimiento estrecho para supervisar la evolución clínica y la correcta gestión terapéutica en el contexto de la nueva situación de dependencia y ausencia de la cuidadora habitual.",
+        "score": {
+          "ROUGE-L-Sum": 0.26307922272047835,
+          "BERTScore_F": 0.8119956254959106
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.5375374241081945
+        }
+      }
+    }
+  },
+  {
+    "id": 76,
+    "gold_summary": "A continuación, describimos un caso de cetoacidosis en una mujer japonesa de 83 años sin diabetes a la que se le administraron inhibidores de SGLT2 para la insuficiencia cardiaca (fracción de eyección: aproximadamente 30 %). Dos semanas antes de su ingreso, había sufrido una fractura vertebral y una fractura de costilla debido a una caída, a la que siguió una anorexia, pero continuó tomando inhibidores de SGLT2. En el momento del ingreso, los resultados de los análisis de sangre revelaron un nivel de glucosa en sangre de 124 mg/dL, un nivel de hemoglobina A1C del 5,9 %, un pH de 7,329, una concentración de HCO₃⁻ de 14,3 mmol/L y una concentración de β-hidroxibutirato de 5150 μmol/L, lo que condujo a un diagnóstico de cetoacidosis euglucémica. El nivel de péptido C de la paciente coincidía con los niveles de glucosa en sangre en el momento del ingreso, lo que indicaba que tenía una secreción de insulina adecuada. La paciente fue tratada únicamente con administración de glucosa sin insulina y fue dada de alta tras la interrupción del inhibidor de SGLT2.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Había una señora de 83 años que no tenía diabetes. Ella tenía un problema en el corazón. Tomaba una medicina para ayudar su corazón. \n\nUn día, se cayó y se lastimó mucho. Le dolían los huesos y no quería comer. Pero siguió tomando su medicina. \n\nCuando llegó al hospital, los doctores le hicieron pruebas. Vieron que su sangre estaba un poco rara, pero no tenía mucha azúcar. \n\nElla tenía un problema llamado cetoacidosis, que pasa cuando el cuerpo usa mucha energía y se cansa. Los doctores le dieron agua con azúcar para ayudarla. No le dieron insulina porque su cuerpo todavía hacía insulina sola. \n\nDespués de un tiempo, ella se sintió mejor y pudo irse a su casa. Ya no tomó esa medicina para el corazón.",
+        "score": {
+          "ROUGE-L-Sum": 0.16231884057971016,
+          "BERTScore_F": 0.7344109416007996
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.44836489109025485
+        }
+      },
+      "B2": {
+        "text": "Caso de una mujer mayor con problemas del corazón y un medicamento especial\n\nUna mujer japonesa de 83 años tenía insuficiencia cardíaca, que significa que su corazón no bombeaba sangre tan bien como debería. Para ayudarla, le dieron un medicamento llamado inhibidor de SGLT2, que normalmente se usa para la diabetes, pero ella no tenía diabetes. Este medicamento ayuda al corazón, pero puede causar un problema llamado cetoacidosis, que es cuando el cuerpo produce sustancias ácidas llamadas cetonas.\n\nLo que pasó antes de ir al hospital\n\nDos semanas antes de entrar al hospital, la mujer se cayó y se fracturó una vértebra y una costilla. Por el dolor, dejó de comer bien y se debilitó mucho. A pesar de esto, siguió tomando el medicamento inhibidor de SGLT2.\n\nLo que encontraron en el hospital\n\nCuando llegó al hospital, sus análisis de sangre mostraron que tenía niveles normales de azúcar en la sangre (124 mg/dL), pero su cuerpo estaba en cetoacidosis, porque el pH de su sangre estaba bajo (7.3), el bicarbonato (HCO3–) estaba bajo (14 mmol/L) y tenía muchas cetonas (β-hidroxibutirato alto). Esto significa que su cuerpo estaba produciendo ácidos, aunque el azúcar en sangre no estaba alto, por eso se llama cetoacidosis euglucémica. Además, su cuerpo todavía producía insulina, la hormona que controla el azúcar en sangre, lo que se confirmó con un análisis llamado péptido C.\n\nCómo la trataron y qué pasó después\n\nLos médicos dejaron de darle el medicamento inhibidor de SGLT2 y no le pusieron insulina porque su cuerpo seguía produciéndola. En cambio, le dieron líquidos con glucosa (azúcar) para ayudar a su cuerpo a recuperarse. Poco a poco, sus análisis mejoraron y las cetonas desaparecieron. Cuando pudo volver a comer bien, dejaron de darle glucosa por vía intravenosa. Aunque su azúcar en sangre se mantuvo normal, todavía eliminaba glucosa por la orina durante varios días después de dejar el medicamento. Después de rehabilitación para recuperarse de las fracturas y el cansancio, pudo caminar sola y fue dada de alta del hospital. No volvieron a darle el medicamento inhibidor de SGLT2.\n\nResumen\n\nEste caso muestra que los inhibidores de SGLT2 pueden causar cetoacidosis en personas sin diabetes, especialmente si están débiles o comen poco. Es importante vigilar a los pacientes que usan este medicamento y suspenderlo si aparecen síntomas como náuseas, vómitos o debilidad.",
+        "score": {
+          "ROUGE-L-Sum": 0.3011093502377179,
+          "BERTScore_F": 0.8151559233665466
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5581326368021322
+        }
+      },
+      "B3": {
+        "text": "**Contexto:**  \nSe presenta el caso de una mujer japonesa de 83 años con insuficiencia cardíaca crónica, caracterizada por una fracción de eyección del 30 %, que recibió tratamiento con inhibidores del cotransportador sodio-glucosa tipo 2 (SGLT2), medicamentos usados para mejorar la función cardíaca y controlar la glucosa en sangre. La paciente no tenía diagnóstico previo de diabetes, con una hemoglobina A1c del 5.9 % antes de iniciar el tratamiento. Aproximadamente dos semanas antes de su ingreso hospitalario, sufrió fracturas vertebrales y de costillas tras una caída, lo que le provocó dolor intenso, dificultad para caminar y una marcada disminución en su ingesta alimentaria, aunque continuó tomando dapagliflozina, un inhibidor de SGLT2.\n\n**Hallazgos Clave:**  \nAl ingresar al hospital, la paciente estaba consciente y estable en signos vitales, pero los análisis de sangre mostraron:  \n- Glucosa en sangre de 124 mg/dL (dentro del rango normal).  \n- pH sanguíneo de 7.3, indicando acidosis (un aumento en la acidez de la sangre).  \n- Bicarbonato (HCO₃⁻) de 14 mmol/L, bajo, lo que confirma acidosis metabólica.  \n- Brecha aniónica elevada (20 mEq/L), que sugiere la presencia de ácidos en la sangre.  \n- Elevada concentración de β-hidroxibutirato (5150 μmol/L), una cetona que indica cetosis.  \nEstos resultados permitieron diagnosticar una cetoacidosis euglucémica, una condición en la que hay acumulación de ácidos cetónicos en sangre sin hiperglucemia significativa. Además, el nivel de péptido C, un marcador de producción de insulina, era adecuado, lo que indicaba que la paciente seguía produciendo insulina de forma suficiente.\n\n**Interpretación Clínica:**  \nLa cetoacidosis euglucémica en esta paciente fue probablemente inducida por el uso de inhibidores de SGLT2 en el contexto de una ingesta alimentaria muy reducida y estrés físico debido a las fracturas. Estos medicamentos pueden aumentar la producción de cuerpos cetónicos al promover la eliminación de glucosa por la orina y reducir la insulina circulante, favoreciendo la cetosis incluso cuando los niveles de glucosa en sangre no están elevados. La secreción adecuada de insulina descartó la necesidad de administrar insulina exógena.\n\n**Próximos Pasos y Evolución:**  \nSe suspendió el tratamiento con inhibidores de SGLT2 y se inició terapia con infusión intravenosa de glucosa y líquidos para corregir la acidosis y mantener la ingesta energética, sin administrar insulina. La paciente mostró mejoría rápida en los parámetros ácido-base al día siguiente y la cetosis desapareció en cuatro días. La infusión de glucosa se ajustó según su capacidad para alimentarse y se suspendió una vez que pudo consumir comidas completas. Durante ocho días posteriores a la suspensión del medicamento, la paciente continuó excretando glucosa en la orina, un efecto residual conocido de la dapagliflozina. Tras rehabilitación para recuperar la movilidad afectada por las fracturas y el desuso, la paciente fue dada de alta en buen estado y sin reiniciar los inhibidores de SGLT2.\n\n---\n\nEste caso ilustra la importancia de reconocer la cetoacidosis euglucémica como una complicación potencial de los inhibidores de SGLT2, especialmente en pacientes sin diabetes que presentan factores de riesgo como ingesta insuficiente y estrés físico. La intervención temprana con suspensión del medicamento y soporte nutricional adecuado puede conducir a una recuperación favorable sin necesidad de insulina.",
+        "score": {
+          "ROUGE-L-Sum": 0.32727272727272727,
+          "BERTScore_F": 0.8510010242462158
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5891368757594715
+        }
+      }
+    }
+  },
+  {
+    "id": 77,
+    "gold_summary": "Informamos sobre un neonato al que se le diagnosticó ACC de grupo G-V asociado con fetus papyraceus de un embarazo gemelar di-coriónico y di-amniótico. Nacida de una madre asiática de 28 años, esta niña presentaba lesiones extensas, cicatrizadas, similares a las cicatrices en sus flancos y muslos superiores. Estas lesiones eran consistentes con la distribución en forma de «H» comúnmente descrita en ACC ligada a fetus papyraceus. A pesar de las manifestaciones dermatológicas significativas, la niña no mostró otras anormalidades externas o implicación sistémica, y las evaluaciones exhaustivas, incluidos los ultrasonidos y el microarray cromosómico, fueron normales.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Una bebé nació con marcas en la piel que parecían cicatrices. Estas marcas estaban en sus lados y muslos. La mamá tuvo dos bebés, pero uno no creció bien en la barriga. \n\nLa bebé con las marcas está sana y fuerte. Los doctores revisaron su cuerpo y todo está bien. No tiene otras partes malas en su cuerpo. \n\nLas marcas en su piel se hicieron mientras estaba en la barriga. Los doctores solo le pusieron crema para cuidar su piel. La bebé está bien y seguirá creciendo feliz.",
+        "score": {
+          "ROUGE-L-Sum": 0.15841584158415842,
+          "BERTScore_F": 0.731499969959259
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.44495790577170874
+        }
+      },
+      "B2": {
+        "text": "**Caso de una recién nacida con lesiones en la piel**\n\nLes presentamos el caso de una bebé que nació con unas marcas especiales en la piel, llamadas aplasia cutis congénita (ACC) grupo V. Estas marcas aparecieron porque tuvo un gemelo que no sobrevivió durante el embarazo, lo que se conoce como fetus papyraceus (un gemelo aplastado y no viable).\n\n**Lo que encontraron en la bebé**\n\nLa niña, nacida de una madre asiática de 28 años, tenía lesiones en la piel que parecían cicatrices en forma de “H” en sus costados y muslos superiores. Estas marcas son típicas en casos de ACC cuando hay un fetus papyraceus. A pesar de estas lesiones, la bebé estaba saludable en general. No tenía otros problemas visibles ni síntomas en su cuerpo. Las pruebas médicas, como ecografías del cerebro, corazón y abdomen, y un análisis genético llamado microarreglo cromosómico, mostraron resultados normales.\n\n**Qué significa este diagnóstico**\n\nLa ACC grupo V es una condición rara que afecta la piel y está relacionada con la pérdida de un gemelo durante el embarazo. Aunque las marcas en la piel pueden ser grandes, no siempre causan otros problemas de salud. En este caso, la bebé solo necesitó cuidados para mantener la piel hidratada y fue seguida por especialistas en dermatología y cirugía plástica para asegurar una buena recuperación.\n\nEn resumen, esta niña nació con lesiones en la piel causadas por la pérdida de su gemelo, pero su salud general es buena y no presenta otras complicaciones.",
+        "score": {
+          "ROUGE-L-Sum": 0.28124999999999994,
+          "BERTScore_F": 0.7858619689941406
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.5335559844970703
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe presenta el caso de una recién nacida diagnosticada con aplasia cutis congénita (ACC) del grupo V, una condición caracterizada por la ausencia localizada de piel, en asociación con fetus papyraceus (un gemelo fetal muerto y comprimido) en un embarazo gemelar bicorial y biamniótico. La bebé nació de una madre asiática de 28 años, producto de un embarazo espontáneo gemelar, en el que uno de los fetos no sobrevivió desde etapas tempranas.\n\n**Hallazgos Clave**  \nAl momento del nacimiento, la niña mostró lesiones cutáneas extensas, con un patrón simétrico en forma de «H» en ambos flancos y muslos superiores, que se asemejaban a cicatrices. Estas lesiones son típicas de la ACC grupo V cuando se asocia con fetus papyraceus. A pesar de la apariencia notable de la piel, la bebé no presentó otras anomalías externas ni signos de afectación en órganos o sistemas. Los exámenes clínicos y de laboratorio, incluyendo ecografías cerebrales, abdominales y cardíacas, así como pruebas para infecciones congénitas (TORCH) y análisis cromosómicos mediante microarreglo, no mostraron alteraciones.\n\n**Interpretación Clínica**  \nLa distribución y características de las lesiones cutáneas, junto con la historia del embarazo gemelar con un gemelo no viable, apoyan el diagnóstico de aplasia cutis congénita grupo V. Esta forma de ACC se relaciona con la presencia de fetus papyraceus y suele manifestarse con lesiones simétricas en la piel, pero sin compromiso sistémico. La ausencia de otras anomalías y la normalidad de las pruebas complementarias indican un pronóstico favorable.\n\n**Próximos Pasos**  \nEl tratamiento consistió en cuidados locales con emolientes para favorecer la hidratación y cicatrización de la piel. La bebé fue dada de alta tras 48 horas de observación y se programaron controles en dermatología pediátrica y cirugía plástica para seguimiento y manejo de las lesiones cutáneas. A las dos semanas, no se observaron cambios ni aparición de nuevos síntomas, confirmando la estabilidad clínica del caso.",
+        "score": {
+          "ROUGE-L-Sum": 0.2618025751072961,
+          "BERTScore_F": 0.8199762105941772
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.5408893928507367
+        }
+      }
+    }
+  },
+  {
+    "id": 78,
+    "gold_summary": "Preocupaciones del paciente: Presentamos el caso de un hombre de 44 años con fuga anastomótica tardía después del cierre de la ileostomía, causada por la compresión de un hematoma intraabdominal que se curó rápidamente después de la dilatación fluoroscópica con globo del área de la estenosis intestinal.\n\nDiagnósticos: Se produjo sangrado postoperatorio y shock hemorrágico el día 1 postoperatorio tras el cierre de la ileostomía. Los signos vitales se estabilizaron tras la transfusión de sangre, y se realizó con éxito un drenaje guiado por tomografía computarizada para reducir el volumen del hematoma. Sin embargo, el hematoma residual comprimió el íleon en el lado anal de la anastomosis, lo que provocó una fuga anastomótica tardía.\n\nIntervenciones/resultados: Se realizó con éxito la dilatación con balón fluoroscópico del área estenótica a través del drenaje y la fuga anastomótica se curó rápidamente.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Había un hombre que se lastimó su tripita después de una operación. Tenía un bulto con sangre que apretaba su intestino y eso hizo que se hiciera un agujero pequeño. \n\nLos doctores le pusieron una bolsita con aire para hacer más grande el lugar apretado. Así, el agujero se cerró y el hombre empezó a sentirse mejor. \n\nDespués, pudo comer y hacer popó sin problema. Los doctores cuidaron mucho de él y se fue a su casa feliz.",
+        "score": {
+          "ROUGE-L-Sum": 0.24096385542168672,
+          "BERTScore_F": 0.7178401947021484
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.4794020250619176
+        }
+      },
+      "B2": {
+        "text": "Caso del paciente  \nUn hombre de 44 años tuvo una complicación después de una cirugía para cerrar una ileostomía, que es una abertura temporal en el abdomen para sacar los desechos del intestino. Esta complicación se llamó fuga anastomótica tardía, que significa que la unión hecha entre partes del intestino empezó a tener una filtración de líquidos.\n\nQué pasó después de la cirugía  \nAl día siguiente de cerrar la ileostomía, el paciente sufrió una hemorragia interna que causó un shock, una condición grave donde la presión de la sangre baja mucho. Los médicos le transfundieron sangre y drenaron un hematoma, que es una acumulación de sangre fuera de los vasos sanguíneos dentro del abdomen. Aunque esto ayudó, quedó un hematoma pequeño que presionaba una parte del intestino llamada íleon, causando que la unión intestinal se filtrara.\n\nTratamiento y resultados  \nPara solucionar la fuga, los médicos usaron una técnica llamada dilatación con balón fluoroscópico. Esto consiste en insertar un pequeño globo dentro del área estrecha del intestino y luego inflarlo para abrir el paso. Esta intervención se hizo a través del drenaje ya colocado y ayudó a aliviar la presión causada por el hematoma. Después del tratamiento, la fuga se cerró rápidamente, el drenaje disminuyó y el paciente pudo volver a comer y tener movimientos intestinales normales. Fue dado de alta sin más problemas y no ha tenido recurrencias.",
+        "score": {
+          "ROUGE-L-Sum": 0.39906103286384975,
+          "BERTScore_F": 0.8010533452033997
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.6000571890336247
+        }
+      },
+      "B3": {
+        "text": "**Contexto del Caso**  \nSe presenta el caso de un hombre de 44 años que inicialmente fue hospitalizado por síntomas de neumaturia (presencia de aire en la orina) y episodios repetidos de cistitis (infección de la vejiga). Tenía antecedentes de hipotiroidismo. Estudios de imagen y endoscopía revelaron una fístula (una conexión anormal) entre el colon sigmoide y la vejiga, acompañada de múltiples divertículos (pequeñas bolsas) en el colon. Debido a la inflamación severa y adherencias entre intestino y vejiga, se realizó una cirugía laparoscópica compleja que incluyó la resección del colon afectado, cierre de la fístula vesical, resección parcial del intestino delgado y creación temporal de una ileostomía (una abertura en el abdomen para desviar las heces).\n\n**Hallazgos y Complicaciones Postoperatorias**  \nAl día siguiente del cierre de la ileostomía, el paciente presentó un shock hemorrágico debido a una hemorragia interna, evidenciada por una caída significativa de hemoglobina y acumulación de líquido denso en la cavidad abdominal detectada por tomografía computarizada (TC). Se estabilizó con transfusiones y drenaje guiado por TC de un hematoma (acumulación de sangre) intraabdominal. A pesar de la hemostasia, persistió una inflamación intensa y distensión abdominal. Posteriormente, el drenaje mostró presencia de jugo intestinal, lo que indicó una fuga en la anastomosis (la unión quirúrgica entre segmentos intestinales) en el sitio del cierre de la ileostomía. Esta fuga anastomótica tardía se atribuyó a la compresión del íleon (parte final del intestino delgado) por un hematoma residual que causaba estenosis (estrechamiento) en esa zona.\n\n**Intervención Terapéutica**  \nDado el alto riesgo de una nueva cirugía debido a las adherencias y complicaciones previas, se optó por un tratamiento menos invasivo. Se realizó una dilatación con balón guiada por fluoroscopía (una técnica de imagen en tiempo real) a través del drenaje existente para ampliar el área estenótica del íleon comprimido. Este procedimiento consistió en introducir un catéter y un globo inflable en el sitio estrechado y expandirlo cuidadosamente para aliviar la compresión.\n\n**Resultados y Seguimiento**  \nTras la dilatación con balón, la cantidad de drenaje intestinal disminuyó notablemente y el paciente recuperó la función intestinal normal, con evacuaciones por vía natural. Una semana después, la fuga anastomótica se resolvió completamente, permitiendo la retirada progresiva del drenaje. El paciente mantuvo una buena ingesta oral y movimientos intestinales regulares, y fue dado de alta 45 días después de la cirugía inicial. Hasta la fecha, no se ha reportado recurrencia de la estenosis ni de la fuga anastomótica.\n\n---\n\nEste caso ilustra cómo una complicación grave tras cirugía intestinal, como una fuga anastomótica causada por compresión de un hematoma residual, puede ser tratada eficazmente mediante una dilatación endovascular guiada por imágenes, evitando una cirugía adicional de alto riesgo.",
+        "score": {
+          "ROUGE-L-Sum": 0.3228699551569507,
+          "BERTScore_F": 0.8026958703994751
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5627829127782129
+        }
+      }
+    }
+  },
+  {
+    "id": 79,
+    "gold_summary": "Se realizó un levantamiento de seno maxilar sin injerto óseo en una paciente de sexo femenino de 23 años que requería la colocación de un implante dental en la zona edéntula de la pieza 16. La evaluación clínica y tomográfica permitieron planificar y realizar la elevación de seno maxilar mediante el abordaje transcrestal y sin la necesidad de injerto óseo. El reborde residual de 6 mm permitió la colocación de un implante dental simultáneo. Luego de 6 meses de seguimiento tomográfico, antes de la carga protésica, se consiguió una altura ósea vertical de 8,83 mm, lo que dio como resultado una ganancia ósea vertical de 2,83 mm. Adicionalmente, se observa una adecuada integración del implante dental sin complicaciones posoperatorias.",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Una joven de 23 años necesitaba un diente nuevo. El doctor hizo un pequeño espacio en su hueso cerca de la nariz. No usó nada más para llenar ese espacio. Puso un tornillo especial para el diente. Después de un tiempo, el hueso creció un poquito más. El diente nuevo quedó bien y sin problemas. Todo está sanando muy bien.",
+        "score": {
+          "ROUGE-L-Sum": 0.14070351758793972,
+          "BERTScore_F": 0.6906163096427917
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.41565991361536575
+        }
+      },
+      "B2": {
+        "text": "**Lo que hicieron y encontraron**\n\nUna joven de 23 años necesitaba un implante dental porque le faltaba un molar superior derecho. Los doctores revisaron su boca y tomaron imágenes para medir el hueso donde se colocaría el implante. Vieron que había 6 mm de hueso en esa zona, lo que era suficiente para poner un implante, pero necesitaban levantar un poco el seno maxilar. El seno maxilar es un espacio lleno de aire dentro del hueso de la cara, cerca de los dientes superiores. Para hacer espacio para el implante, realizaron una cirugía llamada elevación de seno maxilar usando un método que no requiere poner hueso nuevo (injerto).\n\n**Cómo fue la cirugía**\n\nDurante la operación, anestesiaron la zona para que no sintiera dolor. Hicieron una pequeña incisión y usaron herramientas especiales para levantar el suelo del seno maxilar unos 2 mm. Luego colocaron un implante dental de 8 mm de largo en el hueso existente. Después, cerraron la herida con puntos y le dieron medicamentos para evitar infecciones y controlar el dolor. También le indicaron cuidados para que la zona sanara bien.\n\n**Qué pasó después**\n\nA los 7 días, la herida estaba sanando bien y retiraron los puntos. Después de 6 meses, las imágenes mostraron que el hueso había crecido 2,83 mm más en altura, alcanzando un total de 8,83 mm. Esto significa que el implante estaba bien integrado y estable, sin problemas después de la cirugía.\n\n**Por qué es importante**\n\nEste caso muestra que es posible levantar el seno maxilar y colocar un implante al mismo tiempo sin usar hueso extra. Esto puede hacer que el tratamiento sea más rápido y menos complicado para pacientes que necesitan implantes en esa zona.",
+        "score": {
+          "ROUGE-L-Sum": 0.19909502262443438,
+          "BERTScore_F": 0.7628958225250244
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.4809954225747294
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nUna mujer de 23 años, sin antecedentes médicos relevantes (clasificación ASA I), acudió a un centro de salud para la colocación de un implante dental en el espacio dejado por la extracción previa de su primer molar superior derecho (pieza 1.6). La paciente había perdido este diente debido a una fractura y se le realizó una exodoncia atraumática. Durante la evaluación clínica se observó la ausencia del diente, un tipo de encía delgada y una reducción en la altura del reborde óseo (zona del hueso donde se apoya el diente), clasificada como Seibert tipo II. Las imágenes tomográficas mostraron que el reborde óseo residual tenía una altura de 6 mm desde el piso del seno maxilar, con un ancho adecuado para la colocación del implante, y se identificó un seno maxilar de forma ovoide.\n\n**Hallazgos Clave y Procedimiento Realizado**  \nSe planificó una elevación del seno maxilar mediante un abordaje transcrestal (acceso a través de la cresta ósea donde se colocará el implante) sin necesidad de utilizar injerto óseo. Durante la cirugía, se realizó anestesia local, incisiones precisas para levantar un colgajo de encía, y se preparó el sitio para el implante con fresas de diferentes diámetros, respetando una distancia segura de 1 mm al piso del seno maxilar. Se elevó la membrana del seno maxilar 2 mm con un osteótomo (instrumento para levantar el seno), permitiendo colocar un implante dental de 4,8 mm de diámetro por 8 mm de longitud. La inserción se realizó con un torque adecuado (20 N), y se cerró la zona con suturas. Se indicó un tratamiento antibiótico, antiinflamatorio, antihistamínico y enjuagues con clorhexidina, además de recomendaciones estrictas para evitar complicaciones, como reposo absoluto y evitar esfuerzos que puedan afectar la zona quirúrgica.\n\n**Interpretación Clínica**  \nEl procedimiento permitió aumentar la altura ósea vertical disponible para el implante sin necesidad de injerto óseo, aprovechando el reborde óseo residual de 6 mm para colocar el implante simultáneamente con la elevación del seno maxilar. El seguimiento tomográfico realizado a los 7 días mostró una elevación de la membrana del seno de aproximadamente 2,83 mm, y controles posteriores a los 35 y 56 días confirmaron una adecuada cicatrización de los tejidos blandos sin complicaciones. Se logró una ganancia ósea vertical total de 2,83 mm, alcanzando una altura ósea de 8,83 mm antes de la colocación de la prótesis dental.\n\n**Próximos Pasos**  \nCon la adecuada integración del implante y la ganancia ósea confirmada, el siguiente paso será la carga protésica, es decir, la colocación de la corona o diente artificial sobre el implante para restaurar la función masticatoria y estética. Se continuará con controles periódicos para asegurar la estabilidad del implante y la salud de los tejidos circundantes.",
+        "score": {
+          "ROUGE-L-Sum": 0.2563291139240506,
+          "BERTScore_F": 0.8103326559066772
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.533330884915364
+        }
+      }
+    }
+  },
+  {
+    "id": 80,
+    "gold_summary": "Describimos el caso de una mujer de 42 años con antecedentes de aumento de senos bilateral con fines cosméticos 21 años antes, que desarrolló seroma recurrente del lado izquierdo. Buscó ayuda de su primer cirujano, quien realizó 2 procedimientos de intercambio de implantes mamarios, colocando dispositivos texturados y, finalmente, una extracción bilateral de implantes mamarios en el transcurso de dos décadas. La paciente no recibió capsulectomías en los intercambios de implantes anteriores y recibió una muestra de la cápsula anterior en el último procedimiento, donde se diagnosticó BIA-ALCL en el lado izquierdo. Fue derivada a un centro de cáncer terciario donde el examen preoperatorio confirmó la presencia de enfermedad residual local. Después de la gestión del equipo multidisciplinario, se sometió a una revisión de capsulectomía en bloque del lado izquierdo sin necesidad de tratamientos adicionales. El curso postoperatorio fue sin incidentes y sin signos de recurrencias locales a los 18 meses de seguimiento.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Había una mujer que se puso pechos nuevos hace mucho tiempo. Con el tiempo, su pecho izquierdo se llenó de líquido muchas veces. Fue al doctor varias veces y le cambiaron los pechos dos veces. Al final, le quitaron los pechos nuevos. \n\nEl doctor vio que había unas células raras en el pecho izquierdo. La llevaron a un hospital especial para ayudarla. Allí le hicieron una operación para sacar todo lo raro. \n\nDespués de la operación, la mujer estuvo bien. Los doctores la revisaron muchas veces y no encontraron nada malo. Ahora está sana y sigue yendo al doctor para cuidarse.",
+        "score": {
+          "ROUGE-L-Sum": 0.1897810218978102,
+          "BERTScore_F": 0.7329142689704895
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.46134764543414986
+        }
+      },
+      "B2": {
+        "text": "**Caso de una mujer con problemas en sus implantes mamarios**\n\nUna mujer de 42 años se hizo un aumento de senos cuando tenía 21 años. Con el tiempo, comenzó a tener un problema llamado seroma, que es cuando se acumula líquido alrededor del implante. Esto pasó especialmente en su seno izquierdo y volvió varias veces.\n\n**Tratamientos previos y diagnóstico**\n\nLa mujer visitó a su cirujano varias veces y se le cambiaron los implantes dos veces. En la última cirugía, le quitaron ambos implantes, pero no retiraron toda la cápsula, que es el tejido que se forma alrededor del implante. Al analizar una muestra de esta cápsula, los médicos encontraron células anormales que indicaban una enfermedad llamada linfoma anaplásico de células grandes asociado a implantes mamarios (BIA-ALCL). Este es un tipo raro de cáncer que puede aparecer en personas con implantes mamarios.\n\n**Atención en un centro especializado**\n\nDespués de este diagnóstico, la paciente fue enviada a un hospital especializado en cáncer. Allí, un equipo de diferentes especialistas revisó su caso y confirmó que todavía había enfermedad en la cápsula del seno izquierdo. La paciente se sometió a una cirugía para quitar toda la cápsula afectada y el líquido acumulado, sin necesidad de tratamientos como quimioterapia o radioterapia.\n\n**Resultado y seguimiento**\n\nLa operación fue exitosa y no hubo complicaciones. Durante 18 meses después de la cirugía, la mujer fue revisada varias veces y no se detectó que el cáncer regresara. Actualmente, sigue en control médico para asegurarse de que se mantenga sana.\n\nEn resumen, este caso muestra la importancia de detectar y tratar a tiempo un tipo raro de cáncer que puede aparecer en personas con implantes mamarios, y cómo un equipo médico especializado puede ayudar a manejarlo con éxito.",
+        "score": {
+          "ROUGE-L-Sum": 0.2716049382716049,
+          "BERTScore_F": 0.7972925305366516
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.5344487344041282
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nPresentamos el caso de una mujer de 42 años que, tras haberse sometido a un aumento bilateral de senos con implantes mamarios hace 21 años, desarrolló un seroma (acumulación anormal de líquido) recurrente en el seno izquierdo. A lo largo de dos décadas, la paciente consultó repetidamente a su cirujano original, quien realizó dos procedimientos para reemplazar los implantes, utilizando dispositivos texturados (implantes con superficie rugosa), y finalmente llevó a cabo una extracción bilateral de los implantes. Durante estos procedimientos previos, no se realizaron capsulectomías completas (extirpación total de la cápsula fibrosa que se forma alrededor del implante). En el último procedimiento, se tomó una muestra de la cápsula del lado izquierdo que reveló la presencia de un linfoma anaplásico de células grandes asociado a implantes mamarios (BIA-ALCL, por sus siglas en inglés), un tipo raro de cáncer que afecta el tejido alrededor del implante.\n\n**Hallazgos Clave**  \nAl ser remitida a un centro terciario especializado en cáncer, se confirmó mediante estudios preoperatorios que la enfermedad persistía localmente en el seno izquierdo. El equipo multidisciplinario, compuesto por cirujanos plásticos, hematopatólogos, hematólogos, oncólogos, radiólogos y radioterapeutas, evaluó cuidadosamente el caso. Se realizó una capsulectomía en bloque (extirpación completa de la cápsula y el tejido circundante) en el lado afectado, sin encontrar necesidad de tratamientos adicionales como quimioterapia o radioterapia. El examen histopatológico mostró infiltración tumoral limitada a la cápsula periprostética, con márgenes quirúrgicos libres de enfermedad y sin afectación ganglionar.\n\n**Interpretación Clínica**  \nEste caso ilustra la importancia de la vigilancia y el diagnóstico temprano del BIA-ALCL, especialmente en pacientes con implantes texturados que presentan seromas persistentes o recurrentes. La ausencia de capsulectomías completas en procedimientos previos pudo haber contribuido a la persistencia de la enfermedad. La intervención quirúrgica radical, sin necesidad de tratamientos complementarios, fue suficiente para controlar la enfermedad en estadio temprano (IC según la clasificación MD Anderson-TNM).\n\n**Próximos Pasos**  \nLa paciente ha seguido un riguroso protocolo de seguimiento con estudios de imagen, incluyendo tomografías por emisión de positrones (PET/CT) a los 6, 12 y 18 meses postcirugía, sin evidencia de recurrencia local ni a distancia. Continúa bajo vigilancia médica estrecha para detectar cualquier signo de reaparición del linfoma, manteniendo hasta la fecha una supervivencia libre de enfermedad más allá de 18 meses. Este caso subraya la eficacia del manejo multidisciplinario y la cirugía completa en el tratamiento del BIA-ALCL en estadios iniciales.",
+        "score": {
+          "ROUGE-L-Sum": 0.30065359477124187,
+          "BERTScore_F": 0.8288935422897339
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5647735685304879
+        }
+      }
+    }
+  },
+  {
+    "id": 81,
+    "gold_summary": "Se trata de un paciente de 50 años que se presentó con una queja de dolor e hinchazón de la lengua de tres días de duración. Asociado a esto, tenía dolor al tragar, dificultad para abrir la boca, falta de aire y babeo. Asimismo, tenía fiebre alta y un tipo de dolor de cabeza global. En el examen físico, había una hinchazón significativa de la lengua en el área anterolateral izquierda, fluctuante a la palpación, y tenía un borde eritematoso. Después de que se tomó el consentimiento informado, el paciente fue trasladado al quirófano con el diagnóstico de absceso de la lengua. Posteriormente, se hizo una incisión y drenaje bajo anestesia general, y se drenaron unos 30 ml de pus espeso. El bolsillo se lavó con solución salina normal y peróxido de hidrógeno al 2%. El paciente fue trasladado a la sala de cirugía con signos vitales estables y había estado tomando antibióticos. Fue dado de alta después de dos días de estancia en el hospital.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Un hombre tenía la lengua muy hinchada y le dolía mucho. También le costaba abrir la boca y respirar bien. Tenía fiebre y dolor de cabeza. Los doctores vieron que su lengua estaba muy inflamada y con una bolita de pus. Lo llevaron al hospital para limpiar la lengua y sacar el pus. Le dieron medicinas para que no se enfermara más. Después de dos días, se sintió mejor y pudo ir a su casa.",
+        "score": {
+          "ROUGE-L-Sum": 0.22878228782287818,
+          "BERTScore_F": 0.779066801071167
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5039245444470226
+        }
+      },
+      "B2": {
+        "text": "**Lo que le Pasó al Paciente**  \nUn hombre de 50 años llegó al hospital porque tenía dolor e hinchazón en la lengua desde hacía tres días. También le dolía al tragar, le costaba abrir la boca, tenía dificultad para respirar y babeaba mucho. Además, tenía fiebre alta y un dolor de cabeza que sentía en toda la cabeza.\n\n**Lo que Encontraron en el Examen**  \nCuando lo examinaron, vieron que la parte izquierda de su lengua estaba muy hinchada y blanda al tocarla. La piel alrededor estaba roja. También tenía muchos dientes con caries, que son daños en los dientes causados por bacterias.\n\n**Qué Hicieron para Ayudarlo**  \nLos médicos decidieron que tenía un absceso en la lengua. Un absceso es una acumulación de pus, que es un líquido lleno de bacterias y células muertas, causado por una infección. Para tratarlo, lo llevaron al quirófano y, bajo anestesia general (cuando el paciente está dormido y no siente dolor), hicieron una pequeña abertura para sacar el pus, aproximadamente 30 mililitros. Luego limpiaron la zona con agua salada y peróxido de hidrógeno, que ayuda a eliminar las bacterias.\n\n**Recuperación y Tratamiento**  \nDespués de la operación, el paciente recibió antibióticos por vía intravenosa para combatir la infección. Su estado mejoró y, tras dos días en el hospital, pudo irse a su casa con medicamentos para seguir tomando y asegurar que la infección desapareciera completamente.",
+        "score": {
+          "ROUGE-L-Sum": 0.36888888888888893,
+          "BERTScore_F": 0.8243212699890137
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5966050794389512
+        }
+      },
+      "B3": {
+        "text": "**Contexto**\n\nUn hombre de 50 años acudió al hospital debido a dolor e inflamación en la lengua que había persistido durante tres días. Además, presentaba dificultad para tragar, problemas para abrir la boca, sensación de falta de aire y babeo excesivo. También tenía fiebre alta y un dolor de cabeza generalizado. No reportaba antecedentes recientes de traumatismos en la boca, procedimientos dentales, tabaquismo ni enfermedades crónicas como diabetes o hipertensión. Sin embargo, había experimentado dolor dental agudo en los seis meses previos y tenía hábitos de masticar khat desde la niñez, junto con una higiene oral deficiente.\n\n**Hallazgos Clave**\n\nDurante el examen físico, el paciente se mostró visiblemente enfermo. Sus signos vitales indicaron fiebre (39 °C), pulso acelerado (120 latidos por minuto), presión arterial normal (115/70 mmHg), frecuencia respiratoria de 20 respiraciones por minuto y saturación de oxígeno ligeramente disminuida (92%). En la exploración de cabeza y cuello, se observó una inflamación notable en la parte anterolateral izquierda de la lengua, que al tacto era fluctuante (lo que sugiere acumulación de líquido) y presentaba un borde enrojecido (eritematoso). Además, se detectaron múltiples caries en los dientes superiores e inferiores.\n\n**Interpretación Clínica**\n\nEl cuadro clínico y los hallazgos físicos fueron compatibles con un absceso lingual, que es una acumulación de pus en la lengua debido a una infección. Esta condición puede ser grave porque la inflamación y el pus pueden dificultar la respiración y la deglución, como ocurrió en este paciente.\n\n**Próximos Pasos y Tratamiento**\n\nCon el consentimiento informado del paciente, se decidió realizar una intervención quirúrgica para drenar el absceso. Bajo anestesia general, se hizo una incisión en la lengua y se extrajeron aproximadamente 30 mililitros de pus espeso. La cavidad se limpió cuidadosamente con solución salina y peróxido de hidrógeno al 2% para eliminar restos de infección. Posteriormente, el paciente recibió tratamiento antibiótico intravenoso con ceftriaxona y metronidazol durante dos días. Su estado se mantuvo estable y, tras mejorar, fue dado de alta con indicaciones para continuar con antibióticos orales (Augmentin) durante cinco días más.\n\nEste manejo oportuno permitió controlar la infección y evitar complicaciones mayores, destacando la importancia de un diagnóstico rápido y un tratamiento adecuado en casos de abscesos en la lengua.",
+        "score": {
+          "ROUGE-L-Sum": 0.3537190082644628,
+          "BERTScore_F": 0.8128181099891663
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5832685591268145
+        }
+      }
+    }
+  },
+  {
+    "id": 82,
+    "gold_summary": "Presentamos un caso de origen latinoamericano que inicialmente se manifestó con síntomas sistémicos de más de 6 años de evolución, con posteriores alteraciones cognitivas. Después presentó alteraciones de la marcha y síntomas motores sugestivos de parkinsonismo con datos atípicos y datos de enfermedad de motoneurona. Se hicieron estudios de extensión que confirmaron hallazgos compatibles con afectación en motoneurona superior e inferior. Observamos mutación en gen POLG, relacionada con síndrome de depleción mitocondrial.",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Un señor empezó a sentirse mal hace mucho tiempo. Primero, tenía problemas para oler, escuchar y dormir. Luego, se le olvidaban cosas y le costaba hacer tareas fáciles.\n\nDespués, le costaba caminar y se caía mucho. También tenía los músculos débiles y se movía lento. Los doctores hicieron pruebas y vieron que sus nervios y músculos no funcionaban bien.\n\nEncontraron un cambio en un gen que puede causar problemas en el cuerpo. Los doctores le explicaron todo con calma. Ahora, lo cuidan para que esté lo más cómodo posible.",
+        "score": {
+          "ROUGE-L-Sum": 0.13903743315508021,
+          "BERTScore_F": 0.7028262615203857
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.420931847337733
+        }
+      },
+      "B2": {
+        "text": "**Lo que pasó con el paciente:**  \nUn hombre latinoamericano de 73 años tuvo síntomas durante más de seis años. Primero, presentó problemas en su cuerpo como dificultad para oler, escuchar y dormir. Luego, comenzó a tener problemas con la memoria y a olvidar cosas de su vida diaria. Más adelante, tuvo problemas para caminar y debilidad en sus músculos, lo que afectó sus movimientos y le causó caídas frecuentes.\n\n**Qué encontraron los médicos:**  \nAl hacerle pruebas, vieron que tenía signos de parkinsonismo, que es un conjunto de síntomas parecidos a los del Parkinson, pero con algunas diferencias. También encontraron que sus nervios y músculos estaban dañados, mostrando que tenía problemas en las motoneuronas. Las motoneuronas son células nerviosas que controlan los músculos, y en su caso, tanto las motoneuronas superiores como las inferiores estaban afectadas.\n\n**Resultados genéticos importantes:**  \nSe le hizo un examen genético y encontraron una mutación en un gen llamado POLG. Este gen está relacionado con un problema llamado síndrome de depleción mitocondrial, que afecta la energía que producen las células. Esta mutación puede causar enfermedades que afectan los músculos y el sistema nervioso.\n\n**Qué significa todo esto:**  \nEl caso es complejo porque el paciente tiene síntomas que involucran tanto problemas de memoria como de movimiento y debilidad muscular. La combinación de parkinsonismo atípico y enfermedad de motoneurona, junto con la mutación genética, ayuda a entender mejor su enfermedad y a buscar tratamientos adecuados.",
+        "score": {
+          "ROUGE-L-Sum": 0.2735042735042735,
+          "BERTScore_F": 0.7455653548240662
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.5095348141641698
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe trata de un hombre latinoamericano de 73 años con antecedentes familiares de enfermedades neurodegenerativas, incluyendo Alzheimer, esclerosis lateral amiotrófica (ELA) y Parkinson. Su cuadro clínico comenzó en 2016 con síntomas no específicos como disminución del olfato (hiposmia), pérdida auditiva leve (hipoacusia), estreñimiento e insomnio. En 2020, aparecieron problemas de memoria, dificultades en actividades cotidianas y debilidad muscular progresiva, especialmente en manos. En 2021, desarrolló alteraciones de la marcha con caídas frecuentes, rigidez y lentitud de movimientos, además de signos neurológicos que sugerían afectación tanto de la motoneurona superior como inferior.\n\n**Hallazgos Clave**  \n- Evaluación cognitiva mostró deterioro en funciones ejecutivas, memoria y habilidades visuoespaciales.  \n- Examen neurológico reveló rigidez, bradicinesia (lentitud de movimientos), reflejos anormales, fasciculaciones musculares (contracciones involuntarias) y alteraciones en la marcha con congelamiento.  \n- Estudios electromiográficos (EMG) y de velocidad de conducción nerviosa confirmaron daño en las motoneuronas superiores e inferiores, compatible con enfermedad de motoneurona.  \n- La resonancia magnética cerebral no mostró hallazgos específicos que expliquen el cuadro.  \n- Un panel genético amplio fue negativo para mutaciones comunes en enfermedades neurodegenerativas, pero identificó una variante patogénica en el gen POLG, asociado a síndromes de depleción mitocondrial, que afectan la función celular energética.  \n- En etapas avanzadas, el paciente presentó afasia (pérdida del lenguaje), disfagia (dificultad para tragar) y dependencia para movilizarse, requiriendo gastrostomía para alimentación.\n\n**Interpretación Clínica**  \nEste caso ilustra una enfermedad neurodegenerativa compleja con síntomas iniciales sistémicos y progresión hacia un síndrome mixto que combina características de parkinsonismo atípico y enfermedad de motoneurona. La presencia de la mutación en POLG sugiere un trastorno mitocondrial subyacente que podría estar contribuyendo a la degeneración neuronal. La afectación simultánea de motoneuronas superiores e inferiores y la falta de respuesta a levodopa apoyan un diagnóstico fuera del parkinsonismo típico. La evolución rápida hacia discapacidad severa y alteraciones del lenguaje y la deglución reflejan la gravedad del proceso.\n\n**Próximos Pasos**  \n- Continuar con manejo multidisciplinario que incluya neurología, rehabilitación, nutrición y apoyo psicológico.  \n- Monitorizar complicaciones respiratorias y nutricionales, dado el compromiso neuromuscular avanzado.  \n- Realizar asesoramiento genético familiar para evaluar riesgos y orientar a los parientes.  \n- Considerar terapias sintomáticas y soporte paliativo conforme avance la enfermedad, dado que no existen tratamientos curativos para esta condición.  \n\nEste caso destaca la importancia de una evaluación integral en pacientes con síntomas neurológicos progresivos y la utilidad de estudios genéticos para identificar causas poco frecuentes que pueden influir en el pronóstico y manejo.",
+        "score": {
+          "ROUGE-L-Sum": 0.2230483271375465,
+          "BERTScore_F": 0.7837454080581665
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.5033968675978565
+        }
+      }
+    }
+  },
+  {
+    "id": 83,
+    "gold_summary": "Una mujer de 33 años de edad, con antecedentes de fiebre y disnea de unos pocos días de evolución, fue hospitalizada con un síndrome lupoide, con hemocultivos positivos para Haemophilus spp. El ecocardiograma reveló una masa gigante que involucraba ambas valvas mitrales, con una severa regurgitación mitral que requería un reemplazo valvular mitral biológico. La microscopía reveló un mixoma infectado y la paciente fue dada de alta asintomática tras finalizar la terapia con antibióticos. Ella tuvo un buen seguimiento.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Había una mujer que se sentía muy mal. Tenía fiebre y le costaba mucho respirar. \n\nLos doctores la llevaron al hospital. Le encontraron una bolita grande en el corazón. Esa bolita hacía que su corazón no funcionara bien. \n\nLos doctores le pusieron una nueva parte en el corazón para ayudarla. También le dieron medicinas para que se mejorara. \n\nDespués de un tiempo, ella se sintió bien y pudo irse a su casa. Los doctores la cuidaron mucho y ella estuvo sana.",
+        "score": {
+          "ROUGE-L-Sum": 0.16759776536312848,
+          "BERTScore_F": 0.7100065350532532
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.4388021502081908
+        }
+      },
+      "B2": {
+        "text": "**Lo que le pasó a la paciente**  \nUna mujer de 33 años comenzó con dificultad para respirar, fiebre alta y otros síntomas graves. Fue hospitalizada porque tenía una infección en la sangre causada por una bacteria llamada Haemophilus. Además, su corazón tenía un problema: una masa grande creció en la válvula mitral, que es una parte importante para que la sangre fluya bien en el corazón.\n\n**Qué encontraron los médicos**  \nUn examen llamado ecocardiograma mostró que esta masa afectaba ambas partes de la válvula mitral y causaba que la sangre regresara hacia el corazón, lo que se llama regurgitación mitral grave. Por eso, fue necesario reemplazar esa válvula por una nueva hecha de material biológico. Cuando analizaron la masa con un microscopio, descubrieron que era un mixoma infectado, que es un tumor benigno pero que en este caso tenía infección.\n\n**Cómo terminó el caso**  \nDespués de la cirugía y de recibir antibióticos durante varias semanas, la paciente mejoró mucho y pudo salir del hospital sin síntomas. En el seguimiento durante un año, no hubo problemas ni regreso del tumor. Este caso es muy raro y muestra la importancia de un diagnóstico rápido y un tratamiento adecuado para este tipo de infecciones en el corazón.",
+        "score": {
+          "ROUGE-L-Sum": 0.2445141065830721,
+          "BERTScore_F": 0.7772552967071533
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.5108847016451127
+        }
+      },
+      "B3": {
+        "text": "**Contexto**\n\nUna mujer de 33 años, previamente sana, comenzó a experimentar dificultad para respirar progresiva, fiebre alta, sudores nocturnos y pérdida de peso durante un mes. Fue ingresada en un hospital con insuficiencia respiratoria aguda, shock séptico, sangrado pulmonar (hemoptisis), ictericia (coloración amarillenta de piel y mucosas) y petequias (pequeñas manchas rojas) en las piernas. Presentaba además un soplo cardíaco en la válvula mitral, leucocitosis (aumento de glóbulos blancos), plaquetopenia (disminución de plaquetas), disfunción hepática y renal, y alteraciones en pruebas inmunológicas.\n\n**Hallazgos Clave**\n\n- Se descartaron infecciones virales comunes en la región (fiebre amarilla, dengue, chikungunya, VIH, hepatitis).\n- Hemocultivos confirmaron infección por Haemophilus spp., un tipo de bacteria del grupo HACEK, conocida por afectar las válvulas cardíacas.\n- Ecocardiograma mostró una masa grande y irregular que afectaba ambas valvas de la válvula mitral, causando una regurgitación grave (flujo sanguíneo anormal hacia atrás) debido a daño estructural.\n- Resonancia magnética detectó pequeños abscesos en el bazo y un aneurisma micótico (una dilatación arterial causada por infección) en una arteria cerebral, tratado con embolización (bloqueo del vaso).\n- La paciente fue sometida a reemplazo exitoso de la válvula mitral por una prótesis biológica tras resección completa del tumor.\n- El examen patológico confirmó que la masa era un mixoma valvular mitral infectado, un tumor cardíaco benigno pero con infección bacteriana.\n- Se observó además regurgitación aórtica moderada por lesión en la estructura entre la válvula mitral y la aórtica, manejada sin cirugía.\n- Recibió tratamiento antibiótico con ceftriaxona y gentamicina durante 28 días.\n\n**Interpretación Clínica**\n\nEste caso representa una forma rara y grave de mixoma valvular mitral infectado, que es poco frecuente en la literatura médica y con alto riesgo de complicaciones embólicas (formación de coágulos que pueden viajar a otros órganos). La infección por Haemophilus spp. del grupo HACEK es especialmente relevante por su asociación con endocarditis (infección de las válvulas cardíacas). La presentación clínica puede ser similar a la de tumores no infectados, pero el riesgo de complicaciones es mayor.\n\nEl manejo combinado de cirugía para remover el tumor y reemplazar la válvula dañada, junto con terapia antibiótica prolongada, permitió una recuperación exitosa. La paciente mostró buena evolución clínica y no presentó recurrencia ni complicaciones significativas durante un seguimiento de un año.\n\n**Próximos Pasos**\n\n- Continuar con controles cardiológicos periódicos para monitorear la función valvular y detectar posibles complicaciones tardías.\n- Mantener vigilancia clínica para signos de infección o embolias.\n- Considerar la importancia de un diagnóstico precoz en casos similares para reducir la mortalidad y mejorar los resultados quirúrgicos.\n- Difundir el conocimiento sobre esta entidad rara para facilitar su reconocimiento y tratamiento oportuno en la práctica clínica.",
+        "score": {
+          "ROUGE-L-Sum": 0.17171717171717174,
+          "BERTScore_F": 0.7700591087341309
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.4708881402256513
+        }
+      }
+    }
+  },
+  {
+    "id": 84,
+    "gold_summary": "Describimos el caso confirmado de botulismo alimentario en una paciente atendida en nuestro hospital en septiembre de 2020. La instauración en pocos días de una afectación bilateral de pares craneales, incluyendo disfagia, disnea y disartria, junto con midriasis y tetraparesia graves, precedida de diarrea, constituyó la presentación clínica en el primer caso; mientras que en su familiar cursó con síntomas inespecíficos y transitorios. Constatamos disautonomía consistente en hipotensión arterial. Teniendo en cuenta la situación pandémica en aquel momento, se descartó repetidamente la infección por SARS-CoV-2 antes de plantear alternativas diagnósticas. La neurotoxina B de C. botulinum fue detectada en las heces de la paciente, confirmando el diagnóstico de botulismo, que relacionamos con la ingesta de una conserva casera de alubias. Se completó el diagnóstico diferencial del cuadro descartando otras posibles etiologías.",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Una señora se enfermó después de comer unas alubias hechas en casa. Ella se puso muy débil y le costaba hablar, tragar y respirar. También tenía los ojos muy abiertos y los músculos muy flojos. Los doctores buscaron otras enfermedades, pero no encontró ninguna. Por eso, supieron que tenía una enfermedad llamada botulismo. Ella recibió ayuda en el hospital y poco a poco se fue mejorando hasta poder caminar con ayuda.",
+        "score": {
+          "ROUGE-L-Sum": 0.12334801762114538,
+          "BERTScore_F": 0.7431336045265198
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.43324081107383255
+        }
+      },
+      "B2": {
+        "text": "**Lo que pasó con la paciente**  \nUna mujer de 71 años llegó al hospital con debilidad que empeoraba rápidamente. Antes, había tenido diarrea leve y dolor de barriga. Luego, empezó a tener problemas para respirar, tragar y hablar. En el examen, los médicos vieron que tenía caída de los párpados, parálisis en la cara, pupilas que no reaccionaban a la luz, debilidad en brazos y piernas, y dificultad para mover los ojos. A pesar de estos síntomas, estaba consciente y sus reflejos y sensibilidad estaban normales.\n\n**Qué descubrieron los médicos**  \nBuscaron si tenía COVID-19, pero las pruebas fueron negativas varias veces. También hicieron otros estudios que no mostraron problemas en el pecho ni en el corazón. Detectaron que tenía presión baja en la sangre y falta de oxígeno en la sangre. Finalmente, encontraron una toxina llamada neurotoxina B producida por una bacteria llamada Clostridium botulinum en sus heces. Esta bacteria puede causar botulismo, una enfermedad grave que afecta los nervios y los músculos. Creen que la paciente se enfermó por comer una conserva casera de alubias contaminada.\n\n**Qué significa este diagnóstico**  \nEl botulismo es una enfermedad rara pero peligrosa que puede causar debilidad muscular grave y problemas para respirar. En este caso, la enfermedad afectó varios nervios importantes y causó síntomas como dificultad para tragar y hablar. Los médicos descartaron otras causas posibles antes de confirmar el botulismo. Gracias al tratamiento y cuidados, la paciente mejoró poco a poco y se recuperó completamente en unas semanas.\n\n**Resumen final**  \nEste caso muestra cómo el botulismo puede aparecer después de comer alimentos contaminados y causar síntomas graves. Es importante diagnosticarlo rápido para dar el tratamiento adecuado y evitar complicaciones. También se destacó que, durante la pandemia, fue necesario descartar COVID-19 antes de llegar a este diagnóstico.",
+        "score": {
+          "ROUGE-L-Sum": 0.21656050955414013,
+          "BERTScore_F": 0.7670260071754456
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.4917932583647928
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe presenta el caso de una mujer de 71 años que ingresó en el Hospital de Mataró (Barcelona) en septiembre de 2020 con debilidad progresiva y síntomas neurológicos graves. Inicialmente, había experimentado diarrea leve y dolor abdominal, seguidos de dificultad para respirar (disnea), dificultad para tragar (disfagia), y alteraciones en el habla (disartria). La evolución clínica incluyó afectación bilateral de varios nervios craneales y debilidad en las cuatro extremidades.\n\n**Hallazgos Clave**  \nLa paciente mostró signos característicos de afectación neurológica severa: caída de los párpados (ptosis) en ambos ojos, parálisis facial bilateral, pupilas dilatadas que no respondían a la luz ni a la acomodación (midriasis arreactiva), y parálisis de los movimientos oculares en varias direcciones (oftalmoparesia). Además, presentaba debilidad moderada en brazos y piernas (tetraparesia), voz ronca (disfonía) y dificultad grave para tragar. A pesar de estos síntomas, estaba consciente y mantenía un lenguaje coherente, con reflejos y sensibilidad normales. La prueba del hielo, que consiste en aplicar frío sobre los párpados para evaluar la mejora temporal de la ptosis, fue positiva, lo que orientó hacia un trastorno neuromuscular.\n\nSe descartó repetidamente la infección por SARS-CoV-2 mediante pruebas PCR, dada la pandemia vigente en ese momento. Otros estudios complementarios, como radiografía de tórax, análisis de sangre y electrocardiograma, no mostraron alteraciones relevantes. La gasometría arterial reveló hipoxemia moderada, indicando un nivel bajo de oxígeno en sangre.\n\n**Interpretación Clínica**  \nEl cuadro clínico y la evolución sugirieron un botulismo alimentario, una enfermedad causada por la neurotoxina producida por la bacteria *Clostridium botulinum*, que afecta la función nerviosa y muscular. La confirmación diagnóstica se obtuvo al detectar la neurotoxina tipo B en las heces de la paciente. Se estableció que la fuente probable de la intoxicación fue la ingesta de una conserva casera de alubias. Además, la paciente presentó disautonomía, manifestada por hipotensión arterial, que requirió manejo con fluidos intravenosos.\n\nSe realizó un diagnóstico diferencial exhaustivo para descartar otras causas neurológicas que pudieran explicar los síntomas, asegurando así la precisión del diagnóstico.\n\n**Próximos Pasos y Evolución**  \nLa paciente recibió tratamiento de soporte, incluyendo oxígeno, nutrición por sonda nasogástrica y cuidados para prevenir complicaciones. Su condición se estabilizó en los primeros días y comenzó a mejorar lentamente a partir del octavo día, tolerando progresivamente la alimentación adaptada a su disfagia. Posteriormente, inició rehabilitación física, con buena respuesta, y fue trasladada a un centro especializado para continuar su recuperación. Seis semanas después, en la consulta de seguimiento neurológico, la paciente había recuperado completamente su función neuromuscular y capacidad para caminar con ayuda.\n\nEste caso destaca la importancia de considerar el botulismo alimentario en pacientes con debilidad neuromuscular progresiva y afectación de nervios craneales, especialmente cuando se descartan infecciones virales prevalentes como el SARS-CoV-2. Además, resalta la necesidad de un diagnóstico rápido y un manejo multidisciplinario para lograr una recuperación completa.",
+        "score": {
+          "ROUGE-L-Sum": 0.25183016105417283,
+          "BERTScore_F": 0.7996926307678223
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.5257613959109976
+        }
+      }
+    }
+  },
+  {
+    "id": 85,
+    "gold_summary": "Un hombre de 52 años se quejó de pérdida de visión en el ojo derecho (OD) dos días después de un IVI anti-VEGF sin complicaciones para el tratamiento de la neovascularización coroidea secundaria a estrías angioides. Su historial médico incluía PE, miopía patológica y una vitrectomía pars plana (PPV) previa debido a un desprendimiento de retina. La agudeza visual mejor corregida (BCVA) en el OD disminuyó de 6/12 a 6/18 después del IVI. La presión intraocular (IOP) era de 3 mmHg y se observaron pliegues corio-retinianos en el polo posterior. Se prescribió dexametasona tópica y atropina, y se observó una recuperación completa después de tres días. Cuatro meses después, el paciente desarrolló un nuevo episodio de pérdida de visión después de otro IVI. Su BCVA era contar los dedos, la IOP era de 2 mmHg, y se observaron pliegues corio-retinianos más evidentes. Esta vez, una herida escleral abierta en el sitio de inyección era evidente y fue necesaria una sutura escleral. Una vez más, el paciente se recuperó bien.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Un hombre tuvo problemas para ver con su ojo derecho. Esto pasó después de que le pusieron una medicina en el ojo. Su ojo estaba un poco débil y la presión dentro del ojo era baja. El doctor le dio unas gotas para ayudar. Después de tres días, su vista mejoró.\n\nCuatro meses después, le pusieron otra vez la medicina. Otra vez, su vista se puso muy mala. Esta vez, el ojo tenía una pequeña herida. El doctor la cerró con puntitos. Después, el hombre volvió a ver mejor.",
+        "score": {
+          "ROUGE-L-Sum": 0.2356902356902357,
+          "BERTScore_F": 0.7715692520141602
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5036297438521979
+        }
+      },
+      "B2": {
+        "text": "### Lo que le pasó al paciente\n\nUn hombre de 52 años perdió visión en su ojo derecho dos días después de recibir una inyección en la vena para tratar un problema en la parte trasera del ojo llamado neovascularización coroidea, que es cuando crecen vasos sanguíneos anormales. Él tenía antecedentes de miopía fuerte, una cirugía previa en el ojo por desprendimiento de retina y otros problemas oculares.\n\n### Qué encontraron los doctores\n\nDespués de la inyección, su visión empeoró y la presión dentro del ojo bajó mucho, a solo 3 mmHg (lo normal es más alta). Al examinar el ojo, vieron pliegues en la capa del ojo llamada coroides y retina, que son señales de que el ojo estaba muy débil por la baja presión. Le dieron medicamentos en gotas para ayudar a que el ojo se recuperara, y en tres días su visión y presión volvieron a la normalidad.\n\n### Qué pasó después\n\nCuatro meses más tarde, el hombre recibió otra inyección similar y volvió a perder visión al día siguiente. Esta vez, la presión en el ojo bajó aún más, y los pliegues en la retina eran más visibles. Además, los doctores encontraron una herida abierta en la pared del ojo donde pusieron la inyección. Para arreglarla, tuvieron que coser esa herida. Después del tratamiento, el paciente mejoró y recuperó buena visión y presión normal en el ojo.\n\n### Qué significa esto\n\nEste caso muestra que, aunque las inyecciones en el ojo suelen ser seguras, pueden causar problemas como baja presión ocular y daño temporal en la retina. Es importante revisar bien el ojo después de cada inyección para detectar heridas o complicaciones y tratarlas rápido para evitar pérdida permanente de visión.",
+        "score": {
+          "ROUGE-L-Sum": 0.29118773946360155,
+          "BERTScore_F": 0.8094509243965149
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5503193319300582
+        }
+      },
+      "B3": {
+        "text": "**Contexto:**  \nUn hombre de 52 años con antecedentes de preeclampsia (PE), miopía alta y una cirugía previa llamada vitrectomía pars plana (PPV) en su ojo derecho debido a un desprendimiento de retina, recibía tratamiento mensual con inyecciones intravenosas (IVI) de ranibizumab, un medicamento anti-VEGF (factor de crecimiento endotelial vascular), para tratar una neovascularización coroidea secundaria a estrías angioides (formación anormal de vasos sanguíneos en la capa vascular del ojo).\n\n**Hallazgos Clave:**  \nDos días después de una inyección intravenosa que inicialmente parecía no presentar complicaciones, el paciente notó una disminución de la agudeza visual en su ojo derecho. La agudeza visual mejor corregida (BCVA) bajó de 6/12 a 6/18, y la presión intraocular (IOP) estaba muy baja, en 3 mmHg (el rango normal es aproximadamente 10-21 mmHg). El examen con lámpara de hendidura no mostró alteraciones en la parte frontal del ojo, pero el examen del fondo de ojo y las imágenes por tomografía de coherencia óptica (OCT) revelaron pliegues en las capas coroideas y retinianas en la parte posterior del ojo. Estos hallazgos, junto con la baja presión intraocular, llevaron al diagnóstico de hipotensión maculopatía, una condición en la que la baja presión dentro del ojo causa cambios estructurales que afectan la visión.\n\nSe inició tratamiento con dexametasona tópica (un corticosteroide para reducir la inflamación) y atropina (un medicamento que ayuda a relajar el cuerpo ciliar, facilitando la producción de humor acuoso y aumentando la presión intraocular). En tres días, la presión intraocular volvió a la normalidad y la visión mejoró, con desaparición de los pliegues corio-retinianos.\n\nCuatro meses después, tras una nueva inyección intravenosa anti-VEGF aplicada en la zona inferolateral del ojo, el paciente presentó nuevamente una disminución significativa de la visión al día siguiente, con una BCVA reducida a “contar los dedos” (una medida de visión muy pobre) y una presión intraocular aún más baja, de 2 mmHg. Esta vez, los pliegues corio-retinianos eran más evidentes. El examen con lámpara de hendidura detectó una herida abierta en la esclerótica (la capa externa blanca del ojo) en el sitio de la inyección, lo que indicaba una filtración o fuga de líquido ocular. Esta herida fue reparada mediante sutura con un hilo muy fino (monofilamento 10-0). Se repitió el tratamiento con dexametasona tópica y atropina, y el paciente se recuperó satisfactoriamente, alcanzando una BCVA de 6/12 y una presión intraocular de 12 mmHg.\n\n**Interpretación Clínica:**  \nEste caso muestra que, aunque las inyecciones intravenosas de anti-VEGF son generalmente seguras, pueden presentarse complicaciones poco comunes como la hipotensión maculopatía causada por una baja presión intraocular. La presencia de pliegues corio-retinianos y la disminución de la visión son signos importantes que deben alertar al médico. Además, la aparición de una herida escleral abierta en el sitio de la inyección puede causar una fuga de líquido y empeorar la hipotensión ocular, requiriendo reparación quirúrgica.\n\n**Próximos Pasos:**  \nEs fundamental monitorizar cuidadosamente la presión intraocular y la integridad de la esclera después de las inyecciones anti-VEGF, especialmente en pacientes con antecedentes de cirugía ocular previa o miopía alta, que pueden tener mayor riesgo de complicaciones. El tratamiento temprano con corticosteroides tópicos y atropina puede ayudar a restaurar la presión intraocular y la función visual. En casos de filtración escleral, la reparación quirúrgica es necesaria para evitar daños permanentes. Además, se recomienda evaluar la técnica de inyección para minimizar el riesgo de heridas escleral abiertas en futuras aplicaciones.",
+        "score": {
+          "ROUGE-L-Sum": 0.2746478873239437,
+          "BERTScore_F": 0.8299232721328735
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5522855797284086
+        }
+      }
+    }
+  },
+  {
+    "id": 86,
+    "gold_summary": "Una mujer de 82 años con antecedentes de hipertensión arterial e hipotiroidismo acudió al servicio de urgencias por dolor abdominal, diarrea, confusión y deterioro de su estado general de varios días de evolución. A su admisión, la paciente se encontraba febril y la analítica mostró una elevación de la proteína C reactiva sin leucocitosis (8.9 × 10^9/L). En ese contexto se realizó exudado nasofaríngeo para SARS-CoV-2 que fue negativo. Con estos resultados, la sospecha inicial era la de un cuadro infeccioso de origen digestivo. La muestra de orina era maloliente con presencia de leucocitos y nitritos enviándose a cultivo microbiológico. Se inició tratamiento antibiótico empírico con una cefalosporina de tercera generación ante la sospecha de une posible infección urinaria. Se decidió la realización de una tomografía tóraco-abdomino-pélvica con el objetivo de evaluar la presencia de otros focos infecciosos en una paciente de edad avanzada. Este estudio mostró una cistitis enfisematosa, una enfermedad poco frecuente en una paciente sin ninguno de los factores de riesgo clásicos para esta entidad. Los cultivos de orina y sangre fueron positivos para Escherichia coli sensible al antibiótico empírico por lo que se continuó para completar 7 días de tratamiento. La evolución clínica fue favorable.",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Una señora de 82 años se sentía muy mal. Tenía dolor en la barriga y estaba confundida. \n\nLos doctores le hicieron pruebas y vieron que tenía una infección en la orina. Le dieron medicina para ayudarla. \n\nTambién hicieron una foto especial de su cuerpo. Vieron que su vejiga estaba un poco dañada por la infección. \n\nLa medicina funcionó y la señora mejoró mucho. Después de una semana, pudo irse a su casa feliz.",
+        "score": {
+          "ROUGE-L-Sum": 0.19047619047619047,
+          "BERTScore_F": 0.7307484745979309
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.4606123325370607
+        }
+      },
+      "B2": {
+        "text": "**Lo que Encontraron**  \nUna mujer de 82 años llegó al hospital porque tenía dolor en el abdomen, diarrea, estaba confundida y se sentía muy mal desde hacía varios días. Tenía fiebre y algunos análisis de sangre mostraron que tenía inflamación, pero no un aumento en los glóbulos blancos, que son células que ayudan a combatir infecciones. También le hicieron una prueba para detectar COVID-19, que salió negativa.\n\n**Qué Significa la Orina y el Tratamiento**  \nLa orina de la paciente olía mal y tenía señales de infección, como leucocitos (células blancas) y nitritos. Por eso, enviaron una muestra para ver qué bacteria causaba la infección. Mientras esperaban, comenzaron a darle un antibiótico llamado ceftriaxona, que es fuerte y puede combatir muchas bacterias.\n\n**Descubrimiento Importante con la Tomografía**  \nPara asegurarse de que no hubiera una infección más grave en el cuerpo, le hicieron una tomografía, que es una imagen especial del cuerpo. Esta prueba mostró que tenía una cistitis enfisematosa, que es una infección rara en la vejiga donde se forman burbujas de gas en la pared de este órgano. Esto es inusual porque la paciente no tenía los factores de riesgo típicos para esta enfermedad.\n\n**Resultados del Cultivo y Evolución**  \nLos cultivos de la orina y la sangre mostraron que la bacteria causante era Escherichia coli, que respondía bien al antibiótico que ya le estaban dando. Por eso, continuaron con el tratamiento durante 7 días. La paciente mejoró mucho y pudo salir del hospital.  \n\nEn resumen, esta mujer tuvo una infección urinaria grave y poco común que se detectó a tiempo y se trató con éxito gracias a los exámenes y al antibiótico adecuado.",
+        "score": {
+          "ROUGE-L-Sum": 0.2888888888888889,
+          "BERTScore_F": 0.8012082576751709
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5450485732820299
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nUna mujer de 82 años con antecedentes médicos de hipertensión arterial e hipotiroidismo acudió al servicio de urgencias debido a varios días de dolor abdominal, diarrea, confusión y un deterioro general de su estado de salud. Al examen físico, presentaba fiebre y signos de deshidratación, con un abdomen doloroso a la palpación pero sin signos de irritación peritoneal.  \n\n**Hallazgos Clave**  \nLos análisis de sangre revelaron una elevación significativa de la proteína C reactiva (un marcador de inflamación) sin aumento en el número de glóbulos blancos (leucocitosis), lo que sugiere una respuesta inflamatoria sin infección bacteriana evidente en sangre. La prueba para detectar infección por SARS-CoV-2 fue negativa. La orina presentaba mal olor, nitritos positivos y presencia de leucocitos y glóbulos rojos, indicativos de infección urinaria.  \n\nSe inició tratamiento antibiótico empírico con ceftriaxona, una cefalosporina de tercera generación, ante la sospecha de infección urinaria. Para descartar la existencia de infecciones profundas o complicaciones, se realizó una tomografía computarizada (TC) del tórax, abdomen y pelvis. Este estudio identificó una neumatosis vesical parietal, es decir, presencia de gas en la pared de la vejiga, compatible con cistitis enfisematosa, una infección urinaria grave y poco frecuente caracterizada por la acumulación de gas en la vejiga.  \n\nLos cultivos microbiológicos confirmaron la presencia de Escherichia coli, una bacteria comúnmente responsable de infecciones urinarias, tanto en la orina como en la sangre, y que resultó sensible al antibiótico administrado.  \n\n**Interpretación Clínica**  \nLa cistitis enfisematosa es una infección poco común que suele presentarse en pacientes con factores de riesgo como diabetes o inmunosupresión, pero en este caso la paciente no presentaba estos antecedentes clásicos, lo que hace el diagnóstico más inusual. La detección temprana mediante imagen y el inicio rápido de tratamiento antibiótico adecuado fueron fundamentales para la evolución favorable del cuadro.  \n\n**Próximos Pasos**  \nLa paciente fue ingresada en el servicio de medicina interna para continuar el tratamiento antibiótico durante siete días. Durante su hospitalización, mostró mejoría clínica y analítica, lo que permitió su alta hospitalaria sin complicaciones. Se recomienda seguimiento médico para controlar posibles recurrencias o complicaciones y mantener el control de sus condiciones crónicas.",
+        "score": {
+          "ROUGE-L-Sum": 0.40442338072669826,
+          "BERTScore_F": 0.8511063456535339
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.627764863190116
+        }
+      }
+    }
+  },
+  {
+    "id": 87,
+    "gold_summary": "Recién nacido de sexo masculino, nacido a término, derivado por vómitos, evacuaciones escasas y distensión abdominal. A los 8 días de vida y tras excluir diversas causas de distensión abdominal se sometió a laparotomía exploradora, identificando una hernia transmesentérica y dos sitios de atresia intestinal. Se realizó resección del segmento atrésico y anastomosis primaria, con buena evolución.",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Un bebé nació sin problemas. Tenía dolor en la barriga y no podía hacer popó bien. Los doctores buscaron qué pasaba y lo operaron. Encontraron dos partes del intestino que estaban tapadas. Quitaron las partes malas y unieron el intestino bueno. El bebé mejoró mucho después de la operación.",
+        "score": {
+          "ROUGE-L-Sum": 0.1487603305785124,
+          "BERTScore_F": 0.7114591598510742
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.4301097452147933
+        }
+      },
+      "B2": {
+        "text": "**Lo que pasó con el bebé:**  \nUn bebé varón nació a término y, durante su primera semana de vida, tuvo problemas como vómitos, pocas evacuaciones y el abdomen hinchado. Estos síntomas indicaban que algo no estaba funcionando bien en su intestino.\n\n**Qué encontraron los médicos:**  \nDespués de hacer varios estudios para entender la causa de la hinchazón abdominal, los doctores decidieron hacer una cirugía llamada laparotomía exploradora. En esta operación, descubrieron que el bebé tenía una hernia transmesentérica, que es cuando una parte del intestino queda atrapada en un defecto del tejido que lo sostiene. Además, encontraron dos lugares donde el intestino estaba bloqueado, lo que se llama atresia intestinal.\n\n**Qué hicieron para ayudar:**  \nLos médicos quitaron la parte del intestino que estaba bloqueada (resección del segmento atrésico) y unieron las partes sanas del intestino (anastomosis primaria) para que el alimento pudiera pasar normalmente.\n\n**Cómo le fue al bebé:**  \nDespués de la cirugía, el bebé mejoró bien, comenzó a alimentarse por vía oral y pudo irse a casa sin complicaciones. Un año después, sigue sano, come bien y tiene evacuaciones normales.",
+        "score": {
+          "ROUGE-L-Sum": 0.2878228782287823,
+          "BERTScore_F": 0.7293546795845032
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.5085887789066428
+        }
+      },
+      "B3": {
+        "text": "Resumen detallado para público general universitario\n\n**Contexto:**  \nSe trata de un recién nacido varón, nacido a término (38 semanas de gestación) mediante un parto normal sin complicaciones, con un peso al nacer de 2.678 gramos. No contó con controles prenatales durante el embarazo. En las primeras horas de vida presentó dificultad para alimentarse debido a una succión débil y vómitos con contenido biliar (color verde), lo que motivó su ingreso a la unidad de cuidados intensivos neonatales. Las primeras radiografías abdominales mostraron una imagen sugestiva de obstrucción intestinal, pero con presencia de gas en intestino distal. A los pocos días presentó distensión abdominal y vómitos persistentes, lo que llevó a sospechar una enterocolitis necrotizante (una inflamación grave del intestino en recién nacidos), por lo que se inició tratamiento con ayuno, nutrición intravenosa y antibióticos.\n\n**Hallazgos clave:**  \nA pesar del tratamiento, los síntomas no mejoraron, por lo que fue trasladado a un centro especializado. Allí se realizaron estudios radiológicos que evidenciaron un colon muy pequeño (microcolon) y ausencia de progresión del tránsito intestinal, lo que sugirió la presencia de una atresia intestinal (una obstrucción causada por la ausencia o cierre de una parte del intestino). Durante la cirugía exploratoria se encontró una hernia interna a través de un defecto en el mesenterio (tejido que sostiene los intestinos) con atrapamiento de un segmento del intestino delgado (asa yeyunal), además de dos áreas de atresia en el intestino delgado (tipo IV, que implica múltiples segmentos afectados). Se observó un segmento intermedio con meconio (primera materia fecal) y cambios de coloración, pero sin perforación. La relación entre el diámetro del intestino proximal y distal era de 3 a 1, indicando una diferencia significativa en tamaño.\n\n**Interpretación clínica:**  \nSe realizó la resección del segmento intestinal afectado y una anastomosis término-oblicua yeyunoileal (unión quirúrgica entre dos partes del intestino delgado), asegurando la permeabilidad del intestino distal. El análisis histopatológico confirmó la atresia múltiple con inflamación crónica leve del intestino. El paciente mostró una evolución favorable tras la cirugía, iniciando alimentación oral progresivamente desde el quinto día postoperatorio y retirando la nutrición parenteral al octavo día. Presentó deposiciones normales y fue dado de alta a los 20 días de vida sin complicaciones.\n\n**Próximos pasos y seguimiento:**  \nA los doce meses de edad, el niño continúa asintomático, con un adecuado aumento de peso y tolerancia normal a la alimentación complementaria, manteniendo deposiciones diarias de características normales. Este caso resalta la importancia de un diagnóstico oportuno y tratamiento quirúrgico adecuado en atresias intestinales múltiples para lograr una recuperación exitosa en recién nacidos.",
+        "score": {
+          "ROUGE-L-Sum": 0.1335740072202166,
+          "BERTScore_F": 0.7327772974967957
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.43317565235850614
+        }
+      }
+    }
+  },
+  {
+    "id": 88,
+    "gold_summary": "Se remitió a un hombre de 86 años para la implantación de una válvula aórtica transfemoral. La ecocardiografía transtorácica reveló una estenosis grave (gradiente medio: 58 mmHg, área de la válvula aórtica: 0,4 cm2), y después de una discusión multidisciplinaria, se consideró que el riesgo de la cirugía era demasiado alto (Euroscore logístico: 51%), y se propuso al paciente para la implantación de una válvula aórtica transfemoral (TAVI). Al llegar al quirófano, se observó que el paciente, completamente consciente, tenía respiración de Cheyne-Stokes (CSB), que persistió después de la administración de oxígeno al 40%. El procedimiento TAVI fue exitoso, y el patrón CSB se interrumpió en 8 s.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Había un señor de 86 años que tenía un problema en su corazón. Su corazón tenía una puerta muy pequeña y difícil para que la sangre pasara.\n\nLos doctores dijeron que una operación grande era muy peligrosa para él. Entonces, decidieron ponerle una válvula nueva con un tubo pequeño por la pierna.\n\nCuando llegó al lugar para la operación, el señor respiraba de una forma rara que subía y bajaba. Le dieron aire para ayudar, pero seguía igual.\n\nLa operación salió muy bien. Después, su forma de respirar rara se detuvo rápido. El señor se sintió mejor y todo salió bien.",
+        "score": {
+          "ROUGE-L-Sum": 0.2766798418972332,
+          "BERTScore_F": 0.734175443649292
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5054276427732626
+        }
+      },
+      "B2": {
+        "text": "**Lo que le pasaba al paciente:**  \nUn hombre de 86 años tenía un problema grave en su corazón llamado estenosis aórtica, que significa que la válvula que controla el flujo de sangre desde el corazón hacia el cuerpo estaba muy estrecha. Esto hacía que su corazón trabajara mucho más duro para bombear la sangre. Los médicos usaron una ecografía especial para ver que la válvula estaba muy dañada y que el área por donde pasa la sangre era muy pequeña.\n\n**Por qué eligieron un tratamiento especial:**  \nDebido a que el paciente era mayor y tenía otros problemas de salud, los médicos pensaron que una cirugía tradicional para cambiar la válvula era demasiado riesgosa. En lugar de eso, decidieron hacer un procedimiento menos invasivo llamado TAVI, que consiste en implantar una nueva válvula a través de una arteria en la pierna, sin abrir el pecho.\n\n**Lo que ocurrió durante el procedimiento:**  \nCuando el paciente llegó al quirófano, estaba despierto y mostraba un tipo de respiración llamada Cheyne-Stokes. Esta respiración es irregular y se caracteriza por períodos en los que la persona respira muy rápido y otros en los que casi no respira. Aunque le dieron oxígeno, esta respiración continuó. Durante el procedimiento para poner la nueva válvula, todo salió bien y, justo después, la respiración irregular desapareció en pocos segundos.\n\n**Qué significa esto:**  \nEl éxito del procedimiento no solo mejoró la función de la válvula del corazón, sino que también ayudó a normalizar la respiración del paciente. Esto muestra que tratar la estenosis aórtica puede mejorar otros problemas relacionados con el corazón y la forma en que el cuerpo respira.",
+        "score": {
+          "ROUGE-L-Sum": 0.25512528473804097,
+          "BERTScore_F": 0.7622049450874329
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.5086651149127369
+        }
+      },
+      "B3": {
+        "text": "**Contexto**\n\nUn hombre de 86 años con antecedentes importantes, incluyendo tabaquismo intenso en el pasado, fibrilación auricular paroxística tratada con anticoagulación y marcapasos por bradicardia, fue diagnosticado con estenosis aórtica severa calcificada. Presentaba síntomas de insuficiencia cardíaca, como disnea y edemas, además de deterioro significativo de la función ventricular izquierda (fracción de eyección del 27-29%) y hipertensión pulmonar. Debido a su alto riesgo quirúrgico (Euroscore logístico del 51%), se decidió realizar un reemplazo valvular aórtico mediante un procedimiento menos invasivo conocido como implantación de válvula aórtica transfemoral (TAVI).\n\n**Hallazgos Clave**\n\n- La ecocardiografía mostró una estenosis aórtica severa con un área valvular muy reducida (0,4-0,5 cm²) y un gradiente medio elevado (55-58 mmHg), junto con disfunción ventricular izquierda y dilatación de las aurículas.\n- El paciente presentaba un patrón respiratorio anormal llamado respiración de Cheyne-Stokes (CSB), caracterizado por ciclos periódicos de respiración rápida seguidos de pausas (apneas), que persistió incluso tras la administración de oxígeno al 40%.\n- Durante el procedimiento TAVI, que se realizó bajo sedación consciente, se monitorizaron cuidadosamente la función cardíaca, la saturación de oxígeno y la respiración.\n- El procedimiento incluyó la valvuloplastia con balón y la implantación de una válvula protésica de 26 mm, con inducción temporal de ritmo cardíaco rápido para facilitar la expansión valvular.\n- El paciente mantuvo la respiración espontánea durante todo el procedimiento, sin despertar ni presentar complicaciones respiratorias.\n- Tras la implantación, se observó una interrupción inmediata del patrón de respiración de Cheyne-Stokes, con estabilización de la presión arterial y mejora hemodinámica.\n- La función valvular mejoró notablemente, con aumento del área valvular a 1,6 cm² y reducción del gradiente a 15 mmHg. La presión pulmonar también disminuyó progresivamente en el seguimiento.\n\n**Interpretación Clínica**\n\nEste caso ilustra la complejidad del manejo de un paciente anciano con estenosis aórtica severa y disfunción ventricular avanzada, en quien la cirugía convencional representaba un riesgo muy alto. La elección del TAVI permitió una intervención efectiva y menos invasiva. La presencia de respiración de Cheyne-Stokes, un patrón respiratorio asociado a insuficiencia cardíaca avanzada y alteraciones en el control respiratorio, fue un hallazgo relevante que se resolvió tras la mejora hemodinámica conseguida con la corrección valvular. Esto sugiere que la disfunción cardíaca contribuye directamente a la aparición de este patrón respiratorio anormal.\n\n**Próximos Pasos**\n\n- Continuar con el seguimiento clínico y ecocardiográfico para evaluar la función valvular y ventricular a largo plazo.\n- Monitorizar la presión arterial pulmonar y la función respiratoria, dado que la mejoría observada puede influir favorablemente en la calidad de vida y pronóstico.\n- Mantener el control de factores de riesgo cardiovascular y la anticoagulación adecuada, considerando la historia de fibrilación auricular y la implantación del marcapasos.\n- Evaluar y manejar cualquier síntoma residual o complicación relacionada con la insuficiencia cardíaca o el patrón respiratorio, aunque la desaparición de la respiración de Cheyne-Stokes tras el procedimiento es un signo alentador.\n\nEn resumen, la implantación de la válvula aórtica transfemoral en este paciente de alto riesgo fue exitosa y produjo una mejora significativa tanto en la función cardíaca como en la estabilidad respiratoria, evidenciando la importancia de un enfoque multidisciplinario y personalizado en casos complejos.",
+        "score": {
+          "ROUGE-L-Sum": 0.22192513368983957,
+          "BERTScore_F": 0.8174276947975159
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.5196764142436777
+        }
+      }
+    }
+  },
+  {
+    "id": 89,
+    "gold_summary": "Una mujer blanca norteafricana de 62 años de edad, diagnosticada con la enfermedad de Von Hippel-Lindau en 2021, presentó múltiples manifestaciones, entre ellas, un tumor del hueso petroso izquierdo, feocromocitoma izquierdo, carcinoma de células renales izquierdo, riñón derecho con múltiples quistes y masas pancreáticas. Se sometió a varios tratamientos, entre ellos, radioterapia, adrenalectomía, nefrectomía y duodenopancreatectomía cefálica. Los exámenes de ultrasonografía y resonancia magnética revelaron una masa quística sólida en la región anexial izquierda. La laparoscopia identificó tumores quísticos en la mesosalpinx derecha e izquierda. Después de una histerectomía con anexectomía bilateral, el examen histológico reveló cistadenomas papilares de células claras bilaterales de la mesosalpinx y el ligamento ancho, compatibles con la enfermedad de Von Hippel-Lindau.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Había una señora que tenía una enfermedad llamada Von Hippel-Lindau. Esta enfermedad le hizo tener bultos en partes de su cuerpo. Los doctores le hicieron varias operaciones para quitar esos bultos. \n\nUn día, los doctores encontraron otro bulto cerca de su barriga. Le hicieron una cirugía para quitarlo. Cuando miraron el bulto con el microscopio, vieron que era un tipo de bulto que pasa con su enfermedad. \n\nDespués de la operación, la señora se sintió bien y los doctores la cuidaron mucho para que siga sana.",
+        "score": {
+          "ROUGE-L-Sum": 0.2127659574468085,
+          "BERTScore_F": 0.7245652079582214
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.46866558270251496
+        }
+      },
+      "B2": {
+        "text": "**Lo que le Pasó a la Paciente**  \nUna mujer de 62 años fue diagnosticada con la enfermedad de Von Hippel-Lindau, que es una condición genética que causa tumores en diferentes partes del cuerpo. Ella tuvo varios tumores en lugares como el hueso cerca del oído, las glándulas suprarrenales, los riñones y el páncreas. Para tratar estos tumores, se sometió a diferentes cirugías y radioterapia.\n\n**Descubrimiento de una Nueva Masa**  \nDurante un control médico, los doctores encontraron una masa sólida y con líquido (quística) en la zona de los órganos reproductores femeninos, específicamente cerca del ovario izquierdo. Usaron ultrasonido y resonancia magnética para verla mejor.\n\n**Cirugía y Resultados**  \nLos médicos hicieron una cirugía para quitar la masa y también extirparon el útero y ambos anexos (que incluyen las trompas de Falopio y los ovarios). Al analizar el tejido, encontraron que la masa era un tipo de tumor llamado cistadenoma papilar de células claras. Este tumor es raro y está relacionado con la enfermedad de Von Hippel-Lindau.\n\n**Qué Significa Esto**  \nEstos tumores no eran cancerosos, pero están asociados con la enfermedad genética que tiene la paciente. Después de la cirugía, la mujer se recuperó bien y no tuvo problemas durante los dos años siguientes, aunque tuvo que regresar para tratar un tumor cerebral que volvió a aparecer.\n\nEn resumen, esta paciente con una enfermedad genética complicada tuvo varios tumores en diferentes órganos. Gracias a los controles y cirugías, los médicos pudieron identificar y tratar un tumor nuevo en su sistema reproductor, ayudándola a mantenerse estable por un tiempo.",
+        "score": {
+          "ROUGE-L-Sum": 0.3004694835680751,
+          "BERTScore_F": 0.7873086333274841
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5438890584477796
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nUna mujer tunecina de 62 años fue diagnosticada en 2021 con la enfermedad de Von Hippel-Lindau, un trastorno genético que predispone al desarrollo de múltiples tumores en diferentes órganos. A lo largo de su evolución clínica, presentó diversas manifestaciones relacionadas con esta enfermedad, incluyendo tumores en el hueso petroso (una parte del cráneo cerca del oído), glándula suprarrenal, riñón y páncreas. Su tratamiento incluyó radioterapia y varias cirugías importantes para extirpar estos tumores.\n\n**Hallazgos Clave**  \nDurante el seguimiento posoperatorio, se detectó de forma incidental mediante tomografía computarizada una masa sólida y quística de 4 cm en la región anexial izquierda (área ovárica y estructuras cercanas). Esta masa fue confirmada por ultrasonido transvaginal y resonancia magnética, clasificándose como de alta sospecha de malignidad según el sistema O-RADS. Sin embargo, la paciente no presentaba síntomas ginecológicos ni signos físicos evidentes de masa pélvica.\n\nSe decidió realizar una cirugía mediante laparotomía para evaluar y tratar la masa. Durante la intervención, se encontró una masa quística sólida bien delimitada en el anexo izquierdo, sin evidencia de diseminación tumoral en la cavidad abdominal. Se realizó la extirpación del anexo izquierdo y, debido a la edad posmenopáusica de la paciente y la sospecha de enfermedad bilateral, también se llevó a cabo la anexectomía derecha y la histerectomía total.\n\nEl análisis histológico posterior mostró la presencia de cistadenomas papilares de células claras en ambas trompas de Falopio y en el ligamento ancho (estructuras que sostienen el útero y las trompas), con tamaños de 4 cm en el lado izquierdo y 0,5 cm en el derecho. Estos tumores, caracterizados por papilas densamente agrupadas cubiertas por una capa única de células epiteliales, son una manifestación típica de la enfermedad de Von Hippel-Lindau.\n\n**Interpretación Clínica**  \nLos cistadenomas papilares de células claras bilaterales en las trompas de Falopio y el ligamento ancho representan una manifestación poco común pero reconocida de la enfermedad de Von Hippel-Lindau. La ausencia de síntomas ginecológicos y la detección incidental subrayan la importancia de un seguimiento cuidadoso en pacientes con esta enfermedad multisistémica. La cirugía fue necesaria para confirmar el diagnóstico y prevenir posibles complicaciones asociadas a estas masas.\n\n**Próximos Pasos**  \nEl postoperatorio inmediato fue favorable y, durante un seguimiento de dos años con controles ecográficos pélvicos regulares, no se observaron recurrencias ni nuevas lesiones en la región pélvica. No obstante, la paciente fue recientemente readmitida en neurocirugía debido a la recurrencia de un tumor cerebral, lo que refleja la naturaleza crónica y multisistémica de la enfermedad de Von Hippel-Lindau. Se recomienda continuar con un seguimiento multidisciplinario riguroso para manejar las diferentes manifestaciones de esta condición.",
+        "score": {
+          "ROUGE-L-Sum": 0.23197492163009406,
+          "BERTScore_F": 0.7889845967292786
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.5104797591796864
+        }
+      }
+    }
+  },
+  {
+    "id": 90,
+    "gold_summary": "Presentamos un informe de caso de una primera mutación descrita de un feto masculino diagnosticado prenatalmente con síndrome de Milroy a través de amniocentesis. El feto tenía edema bilateral de miembros inferiores, y las pruebas genéticas confirmaron el diagnóstico de síndrome de Milroy. La paciente fue monitoreada de cerca durante todo el embarazo, y después del parto, el lactante fue tratado con terapias apropiadas, incluyendo prendas de compresión y drenaje linfático manual. Los padres recibieron asesoramiento y apoyo apropiados.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Un bebé niño tenía sus piernas un poco hinchadas cuando estaba en la barriga de su mamá. Los doctores hicieron pruebas para entender por qué. Descubrieron que el bebé tenía una condición llamada síndrome de Milroy. La mamá fue cuidada con mucho cariño durante todo el embarazo. Cuando el bebé nació, los doctores le ayudaron para que sus piernas estuvieran mejor. Los papás también recibieron ayuda para cuidar bien al bebé. Todo está hecho para que el bebé crezca fuerte y feliz.",
+        "score": {
+          "ROUGE-L-Sum": 0.22346368715083798,
+          "BERTScore_F": 0.7278441786766052
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.4756539329137216
+        }
+      },
+      "B2": {
+        "text": "**Lo que Encontraron**\n\nEn este caso, una mujer embarazada fue examinada con ultrasonido y se descubrió que su bebé tenía hinchazón (edema) en ambas piernas antes de nacer. Para entender mejor qué pasaba, los médicos hicieron una amniocentesis, que es cuando se toma un poco del líquido que rodea al bebé para estudiar sus genes. Encontraron una mutación, que es un cambio en un gen llamado FLT4, que causa una enfermedad llamada síndrome de Milroy. Esta enfermedad hace que el sistema que ayuda a drenar el líquido del cuerpo no funcione bien, causando hinchazón.\n\n**Qué Significa**\n\nEl diagnóstico se confirmó antes del nacimiento, lo que permitió a los médicos seguir de cerca el embarazo y prepararse para cuidar al bebé después del parto. El bebé nació con hinchazón en las piernas, pero recibió tratamientos especiales, como usar prendas que aprietan suavemente y masajes para ayudar a mover el líquido acumulado. Además, los padres recibieron información y apoyo para entender la enfermedad y cómo cuidar a su hijo.\n\nEste caso muestra la importancia de las pruebas genéticas y el seguimiento durante el embarazo para detectar y manejar enfermedades raras como el síndrome de Milroy.",
+        "score": {
+          "ROUGE-L-Sum": 0.2733333333333334,
+          "BERTScore_F": 0.7524345517158508
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.5128839425245921
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nEste informe describe el caso de una mujer embarazada de 31 años cuyo feto masculino fue diagnosticado antes del nacimiento con síndrome de Milroy, una forma hereditaria de linfedema (acumulación anormal de líquido linfático que causa hinchazón). La paciente no presentaba antecedentes familiares relevantes ni factores de riesgo conocidos, y las pruebas iniciales durante el embarazo no mostraron anomalías.\n\n**Hallazgos Clave**  \nDurante la ecografía morfológica realizada en la semana 20 de gestación, se detectó un edema significativo en ambas extremidades inferiores del feto, aunque el líquido amniótico estaba dentro de los parámetros normales. Un seguimiento a las 23 semanas confirmó la persistencia de este edema subcutáneo. Ante estos hallazgos, se realizó una amniocentesis para obtener líquido amniótico y realizar estudios genéticos detallados.  \n\nEl análisis cromosómico mostró un cariotipo normal (46, XY), y se descartó el síndrome de Noonan mediante pruebas moleculares. Sin embargo, la secuenciación genética identificó una mutación patogénica inédita en el gen FLT4 (c.3116C>A p. (Ala1039Asp)), responsable del desarrollo del sistema linfático. Esta mutación confirmó el diagnóstico prenatal de linfedema hereditario tipo 1A, conocido como enfermedad de Milroy. Además, el análisis de sangre materno reveló que la madre también portaba esta mutación, lo que permitió realizar un asesoramiento genético adecuado a la familia.\n\nEl parto se llevó a cabo mediante cesárea a las 38 semanas y 6 días, naciendo un niño con buen peso y condición general (puntuación de Apgar 9/10). Tras el nacimiento, se observó edema en las extremidades inferiores, consistente con el diagnóstico prenatal. Los estudios histopatológicos de la placenta y membranas no mostraron infecciones ni otras patologías.\n\n**Interpretación Clínica**  \nEl síndrome de Milroy es una enfermedad genética que afecta el desarrollo y funcionamiento del sistema linfático, provocando linfedema desde etapas tempranas de la vida. La detección prenatal mediante ecografía y pruebas genéticas permite un diagnóstico temprano, lo que facilita la planificación del manejo clínico y el apoyo familiar. La identificación de una mutación previamente no descrita en el gen FLT4 amplía el conocimiento sobre la variabilidad genética de esta enfermedad.\n\n**Próximos Pasos**  \nDespués del nacimiento, el lactante recibió tratamiento especializado para el linfedema, que incluyó el uso de prendas de compresión y drenaje linfático manual, con el objetivo de controlar la hinchazón y mejorar la calidad de vida. La familia recibió asesoramiento genético para comprender el origen hereditario de la enfermedad, las implicaciones para futuros embarazos y las opciones disponibles. El seguimiento clínico continuo es esencial para monitorizar la evolución del linfedema y adaptar el tratamiento según sea necesario.",
+        "score": {
+          "ROUGE-L-Sum": 0.17132867132867133,
+          "BERTScore_F": 0.7638388872146606
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.467583779271666
+        }
+      }
+    }
+  },
+  {
+    "id": 91,
+    "gold_summary": "Un hombre de 50 años se presentó con dolor abdominal agudo, anemia y signos de inestabilidad hemodinámica. Las imágenes de diagnóstico, incluida la CTA, revelaron un aneurisma de la arteria gastroduodenal grande y trombosado con evidencia de ruptura. El paciente se sometió a exploración y reparación quirúrgica abierta para abordar tanto el aneurisma como la perforación duodenal. La recuperación del paciente fue satisfactoria y fue dado de alta en condiciones estables.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Un hombre tenía mucho dolor en su barriga. Estaba muy cansado y débil. Los doctores vieron que tenía un bulto grande en una de sus venas. Ese bulto estaba lastimado y había sangre. Los doctores hicieron una operación para arreglar el bulto y la herida. Después, el hombre se sintió mejor y pudo ir a su casa.",
+        "score": {
+          "ROUGE-L-Sum": 0.19580419580419578,
+          "BERTScore_F": 0.704924464225769
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.45036433001498244
+        }
+      },
+      "B2": {
+        "text": "### Lo que le pasó al paciente\n\nUn hombre de 50 años llegó al hospital con un dolor fuerte en el abdomen que había durado una semana. También estaba muy cansado y tenía anemia, que es cuando la sangre no tiene suficientes glóbulos rojos para llevar oxígeno al cuerpo. Su presión arterial estaba baja y su pulso rápido, lo que indicaba que su cuerpo estaba débil.\n\n### Lo que encontraron los médicos\n\nLos médicos hicieron varias pruebas, incluyendo imágenes especiales llamadas tomografía computarizada (CTA). Estas mostraron que tenía un aneurisma grande en una arteria llamada gastroduodenal. Un aneurisma es una zona donde la pared de un vaso sanguíneo está débil y se hincha, como un globo. Además, había coágulos de sangre dentro del aneurisma y parecía que se había roto, lo que es muy peligroso.\n\n### Qué hicieron los médicos\n\nPara salvarlo, los médicos hicieron una cirugía abierta. Abrieron el abdomen para encontrar y reparar el aneurisma. También encontraron una pequeña herida (perforación) en el duodeno, que es la primera parte del intestino delgado, y la repararon. Durante la cirugía, limpiaron la sangre acumulada y cerraron cuidadosamente las heridas.\n\n### Cómo fue la recuperación\n\nDespués de la operación, el paciente estuvo en cuidados intensivos para que lo vigilaran bien. Su recuperación fue buena, sin problemas importantes. Diez días después, pudo salir del hospital en buen estado y continuó con controles médicos para asegurarse de que siguiera mejorando.",
+        "score": {
+          "ROUGE-L-Sum": 0.20630372492836677,
+          "BERTScore_F": 0.7320066690444946
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.4691551969864307
+        }
+      },
+      "B3": {
+        "text": "**Contexto:**  \nUn hombre de 50 años con antecedentes de diabetes e hipertensión, que no seguía un tratamiento constante, acudió al hospital tras una semana de dolor abdominal intenso en la parte superior del abdomen, que se irradiaba hacia la espalda. Además, presentaba distensión abdominal, náuseas, vómitos, fatiga y antecedentes recientes de sangrado digestivo (melena). Dos días antes había recibido una transfusión de sangre debido a anemia.\n\n**Hallazgos Clave:**  \nEn la evaluación inicial, el paciente estaba consciente pero pálido, con presión arterial baja (90/60 mmHg) y pulso acelerado (120 latidos/minuto), signos que indicaban inestabilidad hemodinámica. El examen físico mostró distensión abdominal y sensibilidad leve en la zona del dolor. Los análisis de sangre revelaron anemia severa (hemoglobina de 6 g/dL), aumento de glóbulos blancos (16,000), y otros parámetros dentro de límites aceptables. Las imágenes diagnósticas, incluyendo una tomografía computarizada con angiografía (CTA), identificaron un hematoma grande en la región abdominal paraumbilical y un aneurisma (una dilatación anormal de un vaso sanguíneo) de la arteria gastroduodenal, con signos de trombosis (coágulos) y posible ruptura. También se observó una hernia diafragmática con desplazamiento de órganos abdominales hacia el tórax y acumulación de líquido en la cavidad abdominal.\n\n**Interpretación Clínica:**  \nEl diagnóstico principal fue un aneurisma gigante y trombosado de la arteria gastroduodenal con ruptura, que causaba hemorragia interna y perforación en la primera parte del duodeno (segmento inicial del intestino delgado). Esta situación representaba una emergencia quirúrgica debido al riesgo de sangrado masivo y complicaciones graves.\n\n**Próximos Pasos y Tratamiento:**  \nEl paciente fue estabilizado con líquidos intravenosos y transfusiones sanguíneas antes de ser llevado a cirugía de urgencia. Durante la operación, se evacuaron aproximadamente dos litros de sangre acumulada, se identificó y reparó el aneurisma mediante suturas, y se cerró la perforación duodenal en dos capas. Se colocó un drenaje abdominal para controlar posibles fugas y se monitorizó estrechamente en la unidad de cuidados intensivos. La recuperación fue favorable, sin complicaciones postoperatorias, y el paciente fue dado de alta diez días después en condiciones estables, con seguimiento ambulatorio programado.\n\nEn resumen, este caso ilustra la importancia de un diagnóstico rápido y un manejo quirúrgico oportuno en pacientes con aneurisma roto de la arteria gastroduodenal, una condición rara pero potencialmente mortal.",
+        "score": {
+          "ROUGE-L-Sum": 0.20675944333996027,
+          "BERTScore_F": 0.7629655003547668
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.48486247184736353
+        }
+      }
+    }
+  },
+  {
+    "id": 92,
+    "gold_summary": "Una mujer de 60 años con antecedentes de estenosis congénita de la válvula pulmonar desarrolló insuficiencia cardíaca derecha, cirrosis hepática y enfermedad renal en fase terminal que requería terapia de reemplazo renal. La cirrosis hepática se complicó con hipertensión portal, lo que provocó hemorragias gastrointestinales intratables a pesar del tratamiento óptimo con betabloqueantes y la ligadura endoscópica de la banda. Debido al temor de que empeorara la insuficiencia cardíaca derecha, inicialmente se rechazó la colocación de una derivación intrahepática transyugular (TIPS). Sin embargo, como los problemas de hemorragia intratables persistieron y causaron grandes necesidades de transfusión, la TIPS se realizó finalmente como un procedimiento de rescate. Aunque la TIPS redujo con éxito el gradiente de presión venosa hepática de 16 mmHg a 4 mmHg, la presión portal se mantuvo alta a 14 mmHg debido a la persistencia de la insuficiencia cardíaca derecha con presión venosa central elevada. La encefalopatía hepática se desarrolló poco después de la colocación de la TIPS y culminó en una falla multiorgánica después de otro episodio de hemorragia gastrointestinal. En este punto, la familia del paciente decidió retirar la atención y el paciente falleció posteriormente.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Había una señora de 60 años que tenía problemas en el corazón y en el hígado. Su hígado estaba muy enfermo y le dolía mucho la barriga. También tenía problemas para que la sangre no sangrara mucho por dentro.\n\nLos doctores intentaron ayudarla con medicinas y tratamientos, pero la sangre seguía saliendo. Entonces, hicieron una operación para ayudar a que la sangre pasara mejor por el hígado.\n\nDespués de la operación, la señora se sintió peor y tuvo más problemas en su cuerpo. Al final, su familia decidió que ya no la trataran más y la señora se fue al cielo.",
+        "score": {
+          "ROUGE-L-Sum": 0.20298507462686569,
+          "BERTScore_F": 0.7324523329734802
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.46771870380017294
+        }
+      },
+      "B2": {
+        "text": "**Historia Clínica y Problemas Principales**  \nUna mujer de 60 años tenía varios problemas de salud desde joven, incluyendo una enfermedad del corazón llamada estenosis congénita de la válvula pulmonar. Con el tiempo, desarrolló insuficiencia cardíaca derecha, que significa que el lado derecho de su corazón no funcionaba bien. También tenía cirrosis hepática, una enfermedad del hígado que causa daño y cicatrices, y enfermedad renal en etapa terminal, por lo que necesitaba diálisis para limpiar su sangre.\n\n**Complicaciones y Tratamientos**  \nLa cirrosis causó hipertensión portal, que es una presión alta en las venas del hígado. Esto provocó sangrados graves en su estómago y esófago que no se podían controlar fácilmente. A pesar de usar medicamentos llamados betabloqueantes, que ayudan a bajar la presión, y hacer tratamientos endoscópicos para detener el sangrado, las hemorragias continuaron. Por miedo a que un procedimiento llamado TIPS (una derivación que ayuda a bajar la presión en el hígado) empeorara su insuficiencia cardíaca, inicialmente no se realizó.\n\n**Procedimiento TIPS y Resultados**  \nFinalmente, debido a que las hemorragias seguían siendo muy graves y necesitaba muchas transfusiones de sangre, se decidió hacer el TIPS como último recurso. Este procedimiento logró bajar la presión en las venas del hígado de 16 a 4 mmHg, lo que es una mejora importante. Sin embargo, la presión en la vena principal del hígado siguió siendo alta porque su corazón derecho seguía funcionando mal.\n\n**Complicaciones Finales y Desenlace**  \nDespués del TIPS, la paciente desarrolló encefalopatía hepática, que es un problema en el cerebro causado por la acumulación de toxinas cuando el hígado no funciona bien. También tuvo otro sangrado en el estómago y su estado general empeoró, con fallas en varios órganos. Finalmente, la familia decidió suspender el tratamiento y la paciente falleció 43 días después del procedimiento.\n\n**Qué Significa Este Caso**  \nEste caso muestra lo difícil que es tratar a pacientes con problemas graves en el corazón, hígado y riñones al mismo tiempo. Aunque el TIPS puede ayudar a bajar la presión en el hígado y controlar el sangrado, no siempre es suficiente si el corazón no puede manejar los cambios. Además, el procedimiento puede causar complicaciones como la encefalopatía hepática. Por eso, cada caso necesita un cuidado muy cuidadoso y personalizado.",
+        "score": {
+          "ROUGE-L-Sum": 0.30141287284144425,
+          "BERTScore_F": 0.8180091977119446
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5597110352766944
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe presenta el caso de una mujer de 60 años con un complejo historial médico que incluye una estenosis congénita de la válvula pulmonar diagnosticada en la infancia, seguida de múltiples complicaciones cardíacas como fibrilación auricular, insuficiencia cardíaca derecha y regurgitación valvular severa. Estas condiciones condujeron a una congestión venosa sistémica persistente, que a su vez provocó cirrosis hepática y enfermedad renal en etapa terminal, requiriendo hemodiálisis. Además, la paciente sufrió hemorragias gastrointestinales graves y recurrentes, difíciles de controlar, que demandaron numerosas transfusiones sanguíneas.\n\n**Hallazgos Clave**  \n- La cirrosis hepática se acompañó de hipertensión portal, evidenciada por un gradiente de presión venosa hepática elevado (16 mmHg).  \n- A pesar del tratamiento con betabloqueantes (propranolol) y procedimientos endoscópicos para controlar las hemorragias gástricas, estas continuaron siendo incontrolables.  \n- Inicialmente, se evitó la colocación de una derivación portosistémica intrahepática transyugular (TIPS) debido al riesgo de empeoramiento de la insuficiencia cardíaca derecha.  \n- Finalmente, se realizó el procedimiento TIPS como medida de rescate, logrando reducir el gradiente de presión venosa hepática a 4 mmHg; sin embargo, la presión portal permaneció elevada (14 mmHg) debido a la presión venosa central alta secundaria a la insuficiencia cardíaca derecha persistente.  \n- Posterior a la colocación del TIPS, la paciente desarrolló encefalopatía hepática (una alteración cerebral causada por la acumulación de toxinas debido a la insuficiencia hepática), con niveles elevados de amoníaco en sangre y síntomas neurológicos.  \n- Se presentó un nuevo episodio de sangrado gástrico, con evidencia endoscópica de úlcera antral y cambios isquémicos en la mucosa gástrica.  \n- La función hepática no mostró deterioro significativo en los análisis de laboratorio tras el TIPS, y la ecocardiografía reveló que la función cardíaca derecha permaneció comprometida.  \n- Finalmente, la paciente desarrolló una falla multiorgánica acompañada de infección pulmonar, lo que llevó a la decisión familiar de retirar el soporte terapéutico.\n\n**Interpretación Clínica**  \nEste caso ilustra la compleja interacción entre la insuficiencia cardíaca derecha crónica y sus consecuencias sistémicas, incluyendo la hipertensión portal secundaria y la cirrosis hepática. La hipertensión portal generó hemorragias gastrointestinales difíciles de controlar, que agravaron el estado general de la paciente. La colocación del TIPS, aunque efectiva para reducir el gradiente hepático, no logró normalizar la presión portal debido a la persistente congestión venosa por insuficiencia cardíaca. Además, el procedimiento desencadenó encefalopatía hepática, complicación frecuente en estos casos, y no previno nuevos episodios hemorrágicos. La evolución desfavorable culminó en falla multiorgánica y muerte.\n\n**Próximos Pasos y Reflexiones**  \nEste caso subraya la dificultad de manejar la hipertensión portal y sus complicaciones en pacientes con insuficiencia cardíaca derecha avanzada. La decisión de realizar un TIPS debe sopesar cuidadosamente los riesgos de empeoramiento cardíaco y encefalopatía hepática. En situaciones similares, se requiere un enfoque multidisciplinario que incluya cardiología, hepatología y nefrología para optimizar el tratamiento y considerar alternativas terapéuticas. Además, es fundamental el diálogo con la familia para establecer objetivos realistas y respetar las decisiones sobre el cuidado al final de la vida.",
+        "score": {
+          "ROUGE-L-Sum": 0.3490445859872612,
+          "BERTScore_F": 0.8575050234794617
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.6032748047333614
+        }
+      }
+    }
+  },
+  {
+    "id": 93,
+    "gold_summary": "Reportamos el caso de una mujer de 62 años de edad con antecedentes de hipertensión arterial mal controlada que presentó pérdida visual bilateral súbita y cefalea durante 5 días. Negó antecedentes de traumatismo craneal. En el examen, sus agudezas visuales eran de no percepción de luz (NLP) con pupilas fijas en ambos ojos. La motilidad ocular de ambos ojos era limitada en todas las direcciones. Era difícil abrir ambos párpados. El examen del segmento anterior reveló quemosis bilateral y vasos del sacacorchos episclerales. La presión intraocular era de 45 y 48 mmHg en los ojos derecho e izquierdo, respectivamente. La gonioscopia reveló sangre en el canal de Schlemm en el ángulo nasal del ojo derecho. El examen del fondo de ojo mostró venas retinianas ligeramente dilatadas y tortuosas con discos ópticos de apariencia normal en ambos ojos. Las relaciones entre la copa y el disco eran de 0,3 bilateralmente. Otros exámenes neurológicos no presentaron anormalidades. La resonancia magnética demostró dilatación de las venas oftálmicas superiores bilaterales (SOV) y congestión orbital y periorbital bilateral marcada. Sin embargo, no hubo compresión o estiramiento de los nervios ópticos bilaterales. Se reveló una restricción de la difusión en la difusión ponderada por la difusión, con la correspondiente reducción del coeficiente de difusión aparente, en todo el segmento orbital bilateral de los nervios ópticos, consistente con PION bilateral. La angiografía por resonancia magnética reveló arterialización de los senos cavernosos bilaterales y las SOV. La angiografía cerebral confirmó el diagnóstico de CCF bilaterales de drenaje anterior. El tratamiento con embolización de bobina transvenosa fue exitoso. Tres meses después de la embolización, el examen oftálmico demostró una mejora progresiva de los signos oftálmicos antes mencionados; sin embargo, sus agudezas visuales permanecieron como NLP en ambos ojos.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Una señora mayor se enfermó y no pudo ver con sus ojos. Tenía dolor en la cabeza. Sus ojos estaban muy cansados y no se movían bien. Abrir los ojos era difícil. Los ojos estaban hinchados y con vasos raros. Tenía mucha presión dentro de los ojos. Los doctores hicieron fotos especiales de su cabeza y ojos. Vieron que las venas de sus ojos estaban muy grandes y llenas de sangre. También vieron que los nervios de sus ojos estaban dañados. Encontraron un problema con las venas que llevaba sangre en su cabeza. Los doctores hicieron una operación para arreglar las venas. Después de la operación, sus ojos se veían mejor, pero ella no pudo recuperar la vista. Los doctores la cuidaron mucho y trataron de ayudarla.",
+        "score": {
+          "ROUGE-L-Sum": 0.1735357917570499,
+          "BERTScore_F": 0.7590242624282837
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.4662800270926668
+        }
+      },
+      "B2": {
+        "text": "**Caso de una Mujer con Pérdida Súbita de la Vista**\n\nUna mujer de 62 años, que tenía presión arterial alta sin control, comenzó a perder la vista en ambos ojos de forma repentina y también tenía dolor de cabeza durante cinco días. No había sufrido golpes en la cabeza antes.\n\n**Lo que Encontraron en el Examen**\n\nCuando la revisaron, no podía ver nada con ninguno de sus ojos y sus pupilas no reaccionaban a la luz. Además, no podía mover bien los ojos y le costaba abrir los párpados. En sus ojos había hinchazón y vasos sanguíneos con forma torcida. La presión dentro de sus ojos estaba muy alta, mucho más de lo normal. También encontraron sangre en un canal especial dentro del ojo derecho. Al mirar el fondo del ojo, las venas estaban un poco dilatadas, pero el nervio óptico parecía normal. Otros exámenes del cerebro y nervios no mostraron problemas.\n\n**Lo que Mostraron las Imágenes Médicas**\n\nUna resonancia magnética (una imagen del cerebro y ojos) mostró que las venas grandes que drenan la sangre de los ojos estaban muy dilatadas y había mucha congestión alrededor de los ojos. No había daño visible en los nervios ópticos, pero una prueba especial mostró que esos nervios tenían daño por falta de oxígeno, llamado neuropatía óptica isquémica posterior (PION), en ambos ojos. Otra imagen mostró que unas venas en el cerebro estaban recibiendo sangre de arterias, lo que no es normal.\n\n**Diagnóstico y Tratamiento**\n\nCon una angiografía cerebral (un estudio para ver los vasos sanguíneos), confirmaron que tenía fístulas carotídeo-cavernosas durales bilaterales. Esto significa que había conexiones anormales entre arterias y venas en una parte del cerebro llamada seno cavernoso, lo que causaba que la sangre fluyera mal y afectara los ojos. Para tratarlo, hicieron una embolización con bobinas, que es un procedimiento para cerrar esas conexiones anormales.\n\n**Resultado Después del Tratamiento**\n\nTres meses después, los signos de hinchazón y congestión en los ojos mejoraron, pero la mujer no recuperó la visión y seguía sin poder percibir luz en ambos ojos. Esto indica que el daño en los nervios ópticos fue muy grave y no se pudo revertir.",
+        "score": {
+          "ROUGE-L-Sum": 0.26373626373626374,
+          "BERTScore_F": 0.8085418939590454
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.5361390788476545
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe presentó el caso de una mujer tailandesa de 62 años con antecedentes de hipertensión arterial mal controlada, quien experimentó una pérdida súbita de la visión en ambos ojos acompañada de cefalea durante cinco días. No reportó antecedentes de traumatismo craneal ni otros síntomas neurológicos adicionales.\n\n**Hallazgos Clave**  \nEn la evaluación oftalmológica inicial, la paciente tenía una agudeza visual de no percepción de luz (NLP) en ambos ojos, con pupilas fijas y motilidad ocular limitada en todas las direcciones. La apertura de ambos párpados fue dificultosa. El examen del segmento anterior mostró quemosis (hinchazón de la conjuntiva) bilateral y vasos episclerales con aspecto de “sacacorchos”, indicativos de congestión vascular. La presión intraocular estaba elevada, con valores de 45 mmHg en el ojo derecho y 48 mmHg en el izquierdo. La gonioscopia (evaluación del ángulo de drenaje ocular) reveló presencia de sangre en el canal de Schlemm del ojo derecho, lo que sugiere hemorragia en el sistema de drenaje ocular. El fondo de ojo mostró venas retinianas levemente dilatadas y tortuosas, pero los discos ópticos tenían una apariencia normal, con una relación copa-disco de 0.3 en ambos ojos, lo que indica ausencia de daño glaucomatoso avanzado. Otros exámenes neurológicos no mostraron alteraciones.\n\nLa resonancia magnética (MRI) con contraste evidenció dilatación de las venas oftálmicas superiores (SOV) en ambos ojos, junto con congestión marcada en las regiones orbital y periorbital. No se observaron signos de compresión o estiramiento de los nervios ópticos. Sin embargo, la resonancia ponderada en difusión (DWI) mostró restricción en la difusión con reducción del coeficiente de difusión aparente (ADC) en el segmento orbital bilateral de los nervios ópticos, hallazgo compatible con neuropatía isquémica óptica posterior (PION) bilateral, una lesión causada por falta de flujo sanguíneo en los nervios ópticos. La angiografía por resonancia magnética (MRA) reveló arterialización (flujo arterial anormal) de los senos cavernosos y las venas oftálmicas superiores bilaterales.\n\nLa angiografía cerebral confirmó la presencia de fístulas carotídeo-cavernosas (CCF) durales bilaterales con drenaje anterior. Estas fístulas eran alimentadas por ramas durales de la arteria carótida interna (ICA) y externa (ECA) en ambos lados, y contribuían al flujo arterial anómalo en las venas oftálmicas superiores, incluyendo comunicación entre ambos senos cavernosos. No se detectó reflujo venoso cortical, lo que indica que no había afectación directa de la circulación cerebral superficial.\n\n**Interpretación Clínica**  \nLa paciente presentó una forma rara y grave de fístulas carotídeo-cavernosas durales bilaterales que causaron congestión venosa orbital severa, elevación de la presión intraocular y daño isquémico bilateral en los nervios ópticos, manifestado como neuropatía isquémica óptica posterior. Esta condición explicó la pérdida visual súbita e irreversible, a pesar de la ausencia de compresión directa de los nervios ópticos.\n\n**Próximos Pasos y Evolución**  \nSe realizó una embolización transvenosa mediante colocación de bobinas para ocluir las fístulas en ambos senos cavernosos, logrando el cierre completo de las comunicaciones anómalas según la angiografía postprocedimiento. Tres meses después, la congestión y los signos oftálmicos mejoraron progresivamente, incluyendo la reducción del edema y la congestión vascular; sin embargo, la agudeza visual permaneció sin recuperación, con no percepción de luz en ambos ojos, reflejando daño irreversible en los nervios ópticos.\n\nEste caso destaca la importancia de un diagnóstico temprano y tratamiento oportuno en fístulas carotídeo-cavernosas para prevenir complicaciones graves como la pérdida visual irreversible por neuropatía isquémica óptica.",
+        "score": {
+          "ROUGE-L-Sum": 0.45388601036269427,
+          "BERTScore_F": 0.8707153797149658
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.66230069503883
+        }
+      }
+    }
+  },
+  {
+    "id": 94,
+    "gold_summary": "Describimos el caso de un niño de 15 años con pérdida auditiva total bilateral postlingual tras la administración de medicamentos ototóxicos durante su estancia en la unidad de cuidados intensivos pediátricos. El paciente recibió el implante de corazón artificial total SynCardia (50 ml; SynCardia Systems, Inc., Tucson, AZ, EE. UU.) para la insuficiencia cardiaca biventricular en fase terminal como puente para el trasplante cardiaco. Durante su estancia en la lista de espera de trasplantes cardiacos urgentes, se sometió a una implantación coclear satisfactoria tras optimizar el estado de coagulación y hemostasis y una preparación anestésica adecuada.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Un niño de 15 años tuvo problemas para oír después de tomar medicinas en el hospital. Su corazón estaba muy enfermo y le pusieron un corazón artificial para ayudarlo. Mientras esperaba un nuevo corazón, le pusieron un aparato especial en el oído para que pudiera oír mejor. Los doctores cuidaron mucho que todo saliera bien en la operación. Ahora puede oír mejor y está más feliz.",
+        "score": {
+          "ROUGE-L-Sum": 0.2162162162162162,
+          "BERTScore_F": 0.7314521074295044
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.4738341618228603
+        }
+      },
+      "B2": {
+        "text": "**Caso de un Adolescente con Problemas del Corazón y Pérdida de Audición**\n\nUn joven de 15 años tenía un problema grave en su corazón llamado insuficiencia cardiaca biventricular, que significa que ambos lados de su corazón no funcionaban bien. Para ayudarlo mientras esperaba un trasplante de corazón, le pusieron un corazón artificial llamado SynCardia. \n\nDurante su tratamiento en cuidados intensivos, recibió un medicamento llamado amikacina, que puede dañar el oído y causar pérdida de audición. Después de un tiempo, el paciente empezó a perder la audición en ambos oídos. Los médicos hicieron varios exámenes y confirmaron que tenía una pérdida auditiva profunda en los dos oídos, aunque sus oídos y nervios estaban físicamente normales.\n\nPara mejorar su audición y ayudarlo a comunicarse mejor, el equipo médico decidió ponerle un implante coclear en el oído derecho. Un implante coclear es un dispositivo que ayuda a las personas con pérdida auditiva severa a escuchar sonidos. Antes de la cirugía, ajustaron cuidadosamente sus medicamentos para evitar problemas con la coagulación de la sangre, ya que él tomaba medicinas para el corazón que afectan esto.\n\nLa operación para colocar el implante coclear fue exitosa y sin complicaciones. Después de la cirugía, el paciente mejoró su capacidad para oír y entender el habla, lo que es muy importante para su calidad de vida y para prepararse para el futuro trasplante de corazón.\n\nEn resumen, este caso muestra cómo un adolescente con un corazón artificial y pérdida auditiva causada por medicamentos pudo recibir un implante coclear con buenos resultados, gracias al trabajo de un equipo médico especializado y una cuidadosa preparación.",
+        "score": {
+          "ROUGE-L-Sum": 0.2524271844660194,
+          "BERTScore_F": 0.7746181488037109
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.5135226666348651
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nPresentamos el caso de un adolescente de 15 años con insuficiencia cardiaca biventricular avanzada, que requirió el implante de un corazón artificial total SynCardia como medida temporal mientras esperaba un trasplante de corazón. Durante su hospitalización en cuidados intensivos, recibió amikacina, un antibiótico conocido por su potencial daño al oído (ototoxicidad). Posteriormente, desarrolló una pérdida auditiva profunda bilateral, detectada aproximadamente 131 días después de la implantación del corazón artificial.\n\n**Hallazgos Clave**  \n- El paciente no tenía antecedentes previos de pérdida auditiva ni factores familiares que sugirieran sordera.  \n- Las pruebas audiológicas confirmaron una pérdida auditiva profunda en ambos oídos, mientras que los estudios de imagen mostraron estructuras normales del oído interno y nervios cocleares intactos.  \n- La evaluación multidisciplinaria concluyó que un implante coclear era la mejor opción para mejorar su audición y facilitar su adaptación cognitiva y funcional en el contexto del trasplante cardíaco.  \n- La cirugía de implante coclear se realizó con éxito, tras una cuidadosa preparación para manejar los riesgos relacionados con la anticoagulación y la función del corazón artificial.  \n- No hubo complicaciones perioperatorias significativas, y la activación del implante coclear mostró una mejora progresiva en la audición y la percepción del habla en los meses siguientes.\n\n**Interpretación Clínica**  \nEste caso ilustra cómo la ototoxicidad inducida por medicamentos puede causar una pérdida auditiva severa en pacientes críticos, incluso en adolescentes sin antecedentes previos. La coordinación entre múltiples especialidades fue fundamental para manejar los riesgos asociados a la anticoagulación y la anestesia en un paciente con un dispositivo cardíaco artificial, permitiendo una intervención auditiva efectiva que mejoró significativamente su calidad de vida y capacidad de comunicación.\n\n**Próximos Pasos**  \nSe recomienda continuar con el seguimiento audiológico y rehabilitación auditiva para maximizar los beneficios del implante coclear. Además, se debe mantener una vigilancia estrecha de la función cardíaca y del estado anticoagulante, especialmente en el contexto del trasplante cardíaco futuro. Este caso destaca la importancia de la detección temprana y el manejo multidisciplinario de las complicaciones auditivas en pacientes con enfermedades cardíacas complejas.",
+        "score": {
+          "ROUGE-L-Sum": 0.19262295081967215,
+          "BERTScore_F": 0.7912415266036987
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.49193223871168545
+        }
+      }
+    }
+  },
+  {
+    "id": 95,
+    "gold_summary": "Este informe de caso describe a un hombre de 25 años que desarrolló una RM grave y lesión renal aguda (LRA) después de la administración intramuscular (IM) de heroína como usuario por primera vez. El uso de la heroína IM puede inducir niveles más altos de CPK debido a la toxicidad directa de los miocitos y el trauma mecánico. Los músculos glúteos altamente vascularizados con fibras tipo 1 en el sitio de la inyección probablemente exacerbaron la gravedad. Los factores adicionales incluyeron una menor densidad mitocondrial en los hombres y la exposición al alcohol. A pesar de la reanimación agresiva con líquidos, se requirió la terapia de reemplazo renal (RRT) y el paciente respondió bien a la hemodiálisis.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Un hombre joven se lastimó el músculo de su nalga. Esto pasó porque se puso una medicina mala llamada heroína en esa parte. Su cuerpo se enfermó mucho y sus riñones también se lastimaron. \n\nLos doctores le dieron muchos líquidos para ayudarlo. Pero su riñón no mejoró solo. Entonces, usaron una máquina especial para limpiar su sangre. Después, el hombre empezó a sentirse mejor.",
+        "score": {
+          "ROUGE-L-Sum": 0.16585365853658537,
+          "BERTScore_F": 0.7319269776344299
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.44889031808550767
+        }
+      },
+      "B2": {
+        "text": "**Lo que pasó con el paciente**  \nUn hombre de 25 años usó heroína por primera vez y se la inyectó en el músculo de la nalga derecha. Después de eso, empezó a sentirse muy mal, con dolor, vómitos y agresividad. Cuando llegó al hospital, no encontraron heridas, pero sus síntomas empeoraron al día siguiente.\n\n**Qué encontraron los médicos**  \nLos análisis de sangre mostraron que tenía niveles muy altos de una enzima llamada CPK, que indica daño en los músculos. También tenía problemas en los riñones, con niveles altos de creatinina y urea, que son sustancias que el riñón normalmente limpia. La orina estaba de color rojo-marrón, pero sin sangre visible, lo que es un signo de daño muscular y renal. La tomografía mostró inflamación en el músculo de la nalga donde se inyectó la droga.\n\n**Qué significa todo esto**  \nEl hombre sufrió una condición llamada rabdomiólisis, que es cuando los músculos se dañan mucho y liberan sustancias que pueden dañar los riñones. Esto ocurrió por la inyección directa de heroína en el músculo, que causó daño tanto por la droga como por el trauma de la aguja. Además, factores como el alcohol y diferencias en el cuerpo de los hombres pueden haber empeorado la situación.\n\n**Cómo lo trataron**  \nLe dieron líquidos por vía intravenosa para ayudar a limpiar sus riñones, pero esto no fue suficiente. Por eso, tuvo que recibir un tratamiento especial llamado hemodiálisis, que es una máquina que hace el trabajo de los riñones cuando están muy dañados. Después de varios días, su función renal mejoró y pudo dejar el tratamiento.\n\n**Conclusión**  \nEste caso muestra que inyectarse heroína en el músculo puede causar un daño muscular grave y problemas serios en los riñones, incluso en personas que la usan por primera vez. Es importante buscar ayuda médica rápido si alguien presenta síntomas después de usar drogas de esta forma.",
+        "score": {
+          "ROUGE-L-Sum": 0.25250501002004005,
+          "BERTScore_F": 0.7714748382568359
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.511989924138438
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nEste caso clínico presenta a un hombre de 25 años que sufrió una lesión muscular grave conocida como rabdomiólisis (RM) y una lesión renal aguda (LRA) tras administrarse heroína por primera vez mediante una inyección intramuscular (IM) en la región glútea derecha. La rabdomiólisis es una condición en la que el daño muscular libera sustancias tóxicas en la sangre, lo que puede afectar negativamente a los riñones.\n\n**Hallazgos Clave**  \nEl paciente fue encontrado después de una noche de consumo de sustancias, con síntomas de vómitos, agresividad y dolor intenso en la zona glútea derecha. Inicialmente, no se detectaron lesiones traumáticas, pero al empeorar sus síntomas, se realizaron análisis que mostraron niveles extremadamente elevados de creatina fosfoquinasa (CPK) sérica (42,527 IU/l), un marcador que indica daño muscular severo. Además, presentó alteraciones en la función renal, evidenciadas por un aumento significativo de creatinina y urea en sangre, así como cambios en el análisis de orina, que mostraba orina de color rojo-marrón sin glóbulos rojos, proteinuria (presencia de proteínas) y glucosuria (presencia de glucosa), signos compatibles con daño renal. La toxicología confirmó una concentración elevada de heroína en sangre, y el paciente finalmente admitió haberse inyectado heroína en el glúteo la noche previa.\n\nUna tomografía computarizada reveló inflamación y edema (hinchazón) muscular en la región glútea derecha, confirmando la miositis (inflamación muscular) localizada.\n\n**Interpretación Clínica**  \nLa administración intramuscular de heroína puede causar daño muscular directo debido a la toxicidad de la droga sobre las células musculares (miocitos) y al trauma mecánico producido por la inyección. La región glútea, por su alta vascularización y predominancia de fibras musculares tipo 1 (que tienen características metabólicas específicas), probablemente contribuyó a la gravedad del daño. Además, factores como una menor densidad mitocondrial en hombres (las mitocondrias son las \"centrales energéticas\" de las células) y la exposición al alcohol podrían haber exacerbado la lesión muscular y renal.\n\nA pesar de iniciar un tratamiento convencional con líquidos intravenosos para intentar revertir la lesión renal, el daño progresó, requiriendo la implementación de terapia de reemplazo renal mediante hemodiálisis. Tras este tratamiento, la función renal del paciente mejoró, permitiendo su alta hospitalaria después de nueve días.\n\n**Próximos Pasos**  \nEl seguimiento posterior del paciente fue limitado debido a su falta de asistencia a controles médicos, lo que dificulta evaluar su recuperación a largo plazo y la prevención de complicaciones futuras. Este caso resalta la importancia de la detección temprana y el manejo adecuado de la rabdomiólisis inducida por drogas, así como la necesidad de apoyo y seguimiento continuo en pacientes con consumo de sustancias para evitar daños graves y mejorar los resultados clínicos.",
+        "score": {
+          "ROUGE-L-Sum": 0.28482972136222906,
+          "BERTScore_F": 0.7831206321716309
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.53397517676693
+        }
+      }
+    }
+  },
+  {
+    "id": 96,
+    "gold_summary": "Una mujer de 63 años de edad acudió a la sala de urgencias con un historial de fiebre aguda, postración y disnea. Se le diagnosticó un caso grave de COVID-19 y síndrome de dificultad respiratoria aguda. A pesar de recibir atención médica intensiva, cumplía con los requisitos para someterse a una oxigenación por membrana extracorpórea. El día 34, luego de siete días de haber suspendido la sedación y de que su cuadro neurológico hubiera evolucionado de manera positiva, presentó una crisis tónico-clónica generalizada limitada, que no guardaba relación con un desequilibrio hidroelectrolítico o metabólico, lo que hizo necesario realizar una investigación diagnóstica. Los estudios de imágenes cerebrales revelaron un síndrome de encefalopatía posterior reversible.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Una señora muy enferma tenía fiebre y le costaba respirar. Tenía un virus que le hizo mucho daño en los pulmones. Los doctores le pusieron una máquina para ayudarla a respirar mejor.\n\nDespués de muchos días, la señora empezó a mejorar. Pero un día tuvo un problema en su cabeza que la asustó. Los doctores hicieron unas fotos especiales de su cerebro. Vieron que su cerebro estaba un poco dañado, pero podía mejorar.\n\nLa señora se puso mejor y los doctores la cuidaron mucho para que se sintiera bien otra vez.",
+        "score": {
+          "ROUGE-L-Sum": 0.19087136929460582,
+          "BERTScore_F": 0.741770327091217
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.4663208481929114
+        }
+      },
+      "B2": {
+        "text": "**Lo que le pasó a la paciente**  \nUna mujer de 63 años llegó al hospital con fiebre alta, mucho cansancio y dificultad para respirar. Los médicos descubrieron que tenía COVID-19 muy grave y un problema llamado síndrome de dificultad respiratoria aguda, que afecta los pulmones y dificulta la respiración. Aunque recibió cuidados intensivos, su condición empeoró y necesitó un tratamiento especial llamado oxigenación por membrana extracorpórea (VV-ECMO). Este tratamiento ayuda a oxigenar la sangre cuando los pulmones no funcionan bien.\n\n**Qué pasó después**  \nDespués de 34 días en el hospital y tras dejar la sedación (medicamentos para dormirla) durante una semana, la paciente tuvo una crisis convulsiva, que es un movimiento fuerte y descontrolado del cuerpo. Esta crisis no se debió a problemas con líquidos o sustancias en su cuerpo, por lo que los médicos hicieron más estudios para entender la causa.\n\n**Lo que mostraron los estudios**  \nLas imágenes del cerebro mostraron un problema llamado síndrome de encefalopatía posterior reversible. Esto significa que algunas partes del cerebro estaban inflamadas o dañadas temporalmente, pero que esta condición puede mejorar con tratamiento. Gracias a la atención médica y la rehabilitación, la paciente casi recuperó completamente sus funciones cerebrales y fue dada de alta después de 44 días en el hospital.",
+        "score": {
+          "ROUGE-L-Sum": 0.28418230563002683,
+          "BERTScore_F": 0.784900426864624
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.5345413662473254
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nUna mujer de 63 años con antecedentes de obesidad e hipertensión presentó un cuadro de siete días con fiebre, tos seca, pérdida del olfato (hiposmia) y dolores musculares. Al ingresar al hospital, mostró signos de insuficiencia respiratoria leve y fue diagnosticada con COVID-19 mediante una prueba PCR. Su condición respiratoria empeoró rápidamente, desarrollando un síndrome de dificultad respiratoria aguda (SDRA) que requirió intubación y ventilación mecánica. Debido a la gravedad del compromiso pulmonar, fue sometida a oxigenación por membrana extracorpórea venovenosa (VV-ECMO), un soporte avanzado para mantener la oxigenación cuando los pulmones no funcionan adecuadamente.\n\n**Hallazgos Clave**  \nTras 34 días de hospitalización y después de haber suspendido la sedación durante una semana con mejoría neurológica, la paciente sufrió una crisis epiléptica generalizada limitada. Esta convulsión no se relacionó con alteraciones metabólicas o desequilibrios hidroelectrolíticos, por lo que se inició una investigación neurológica. La resonancia magnética cerebral mostró un patrón característico de síndrome de encefalopatía posterior reversible (SEPR), que se manifiesta por áreas de inflamación y edema en la sustancia blanca del cerebro, especialmente en regiones occipitales y parietales, sin daño permanente. Además, se detectaron microhemorragias puntiformes en la sustancia blanca, pero el líquido cefalorraquídeo no mostró infección ni inflamación activa.\n\n**Interpretación Clínica**  \nEl SEPR es una condición neurológica que puede presentarse en pacientes críticos y se caracteriza por síntomas como convulsiones, alteraciones visuales y cefalea, acompañados de cambios reversibles en el cerebro. En este caso, la aparición del SEPR después de una infección grave por COVID-19 y soporte con VV-ECMO sugiere una relación con la inflamación sistémica y posibles alteraciones vasculares inducidas por el virus o el tratamiento intensivo. La ausencia de infección directa del virus en el sistema nervioso central y la normalidad del líquido cefalorraquídeo apoyan esta hipótesis.\n\n**Próximos Pasos y Evolución**  \nLa paciente recibió tratamiento adecuado para la crisis epiléptica y cuidados de soporte neurológico. A pesar de la miopatía asociada a la enfermedad crítica, logró una recuperación casi completa de sus funciones neurológicas. Fue dada de alta tras 44 días de hospitalización y remitida a un centro de rehabilitación, donde continuó mejorando hasta recuperar prácticamente su estado mental previo al ingreso.\n\nEste caso resalta la importancia de la vigilancia neurológica en pacientes con COVID-19 grave, especialmente aquellos sometidos a terapias avanzadas como la VV-ECMO, para detectar y tratar complicaciones como el síndrome de encefalopatía posterior reversible.",
+        "score": {
+          "ROUGE-L-Sum": 0.25496688741721857,
+          "BERTScore_F": 0.8144162893295288
+        },
+        "quality": {
+          "category": "good",
+          "is_good": true,
+          "combined_score": 0.5346915883733737
+        }
+      }
+    }
+  },
+  {
+    "id": 97,
+    "gold_summary": "mujer de 65 años con el antecedente de ser portadora de infección por virus de inmunodeficiencia humana (VIH), que presentó un carcinoma verrugoso asociado a una úlcera de Marjolin secundaria a herpes zóster e infección de tejidos blandos en pierna derecha, con un periodo de latencia de 10 años desde el proceso infeccioso inicial hasta la confirmación histopatológica.",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Una señora de 65 años tuvo una herida en su pierna. La herida empezó hace mucho tiempo por una infección. La herida no sanó bien y cambió. Los doctores vieron que la herida tenía una enfermedad que puede crecer. Ella recibe ayuda para mejorar.",
+        "score": {
+          "ROUGE-L-Sum": 0.1592920353982301,
+          "BERTScore_F": 0.7290577292442322
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.44417488232123115
+        }
+      },
+      "B2": {
+        "text": "### Lo que pasó con la paciente\n\nUna mujer de 65 años, que vive en la Ciudad de México y tiene VIH controlado desde hace varios años, desarrolló un problema en la piel de su pierna derecha. Hace 10 años, tuvo una infección llamada herpes zóster, que afectó esa zona. Después, sufrió una infección en los tejidos blandos (la parte blanda bajo la piel), llamada celulitis. Esto causó una herida o úlcera que no sanaba bien.\n\n### Lo que encontraron\n\nA pesar de varios tratamientos, incluyendo cirugías para poner injertos de piel, la úlcera siguió abierta y le causaba dolor. Cuando la revisaron, vieron una lesión con una herida de 1.5 cm en el muslo derecho. Tomaron una biopsia, que es cuando se extrae un pequeño pedazo de piel para examinarlo bajo el microscopio. El examen mostró que la úlcera tenía un tipo de cáncer llamado carcinoma verrugoso, que es un tumor que crece lentamente y parece una verruga.\n\n### Qué significa\n\nEsta úlcera se llama úlcera de Marjolin, que es una herida crónica que puede convertirse en cáncer después de muchos años. En este caso, la úlcera apareció después de la infección por herpes zóster y la celulitis, y tardó 10 años en transformarse en cáncer. Debido a esto, la paciente fue enviada a un hospital especializado para recibir tratamiento con radioterapia, que usa rayos para destruir las células cancerosas.\n\nEn resumen, una infección antigua en la pierna causó una herida que no sanó y, con el tiempo, se convirtió en un tipo de cáncer en la piel. Por eso es importante cuidar bien las heridas que no se curan y revisarlas con el médico.",
+        "score": {
+          "ROUGE-L-Sum": 0.19726027397260273,
+          "BERTScore_F": 0.7400614023208618
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.46866083814673226
+        }
+      },
+      "B3": {
+        "text": "Contexto  \nSe trata de una mujer de 65 años con diagnóstico de infección por VIH desde hace 20 años, con carga viral indetectable y buen conteo de células CD4, además de otras condiciones crónicas como hipotiroidismo, cardiopatía isquémica, osteoporosis y dislipidemia, todas bajo control médico. Hace 10 años, tras un episodio de herpes zóster en la pierna derecha que se complicó con una infección de tejidos blandos (celulitis), desarrolló una úlcera en esa zona. A pesar de múltiples intervenciones quirúrgicas con injertos cutáneos y seguimiento especializado, la úlcera persistió y causó dolor local.\n\nHallazgos Clave  \nDurante la evaluación clínica, se observó una lesión en la cara lateral del muslo derecho consistente en una neoformación aplanada con una úlcera de 1.5 cm de diámetro, bordes elevados, piel circundante oscura y engrosada, y una cicatriz atrófica. La biopsia de piel reveló la presencia de un carcinoma verrugoso, que es un tipo de cáncer de piel de crecimiento lento y aspecto verrugoso (similar a una verruga). Este hallazgo confirmó que la úlcera crónica correspondía a una úlcera de Marjolin, que es una lesión maligna que puede desarrollarse en cicatrices o heridas crónicas.\n\nInterpretación Clínica  \nLa paciente presentó un carcinoma verrugoso asociado a una úlcera de Marjolin que se originó como secuela de una infección previa por herpes zóster y celulitis en la pierna derecha. El periodo de latencia entre el evento infeccioso inicial y la aparición del cáncer fue de aproximadamente 10 años. Esta condición es poco frecuente pero importante, ya que las úlceras crónicas pueden transformarse en lesiones malignas, especialmente en pacientes con factores de riesgo como el VIH.\n\nPróximos Pasos  \nLa paciente fue referida al hospital de oncología para recibir tratamiento con radioterapia, que es una modalidad adecuada para este tipo de carcinoma. Se requiere un seguimiento estrecho para evaluar la respuesta al tratamiento y prevenir complicaciones adicionales. Además, es fundamental mantener un control riguroso de sus condiciones crónicas y del estado inmunológico para optimizar su recuperación.",
+        "score": {
+          "ROUGE-L-Sum": 0.22119815668202766,
+          "BERTScore_F": 0.7808136343955994
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.5010058955388135
+        }
+      }
+    }
+  },
+  {
+    "id": 98,
+    "gold_summary": "Una mujer de 90 años de edad, proveniente de una zona rural, presentó una hinchazón de crecimiento lento en el muslo posteromedial durante tres años. No tenía antecedentes de traumatismos ni síntomas sistémicos. El examen clínico reveló una masa firme y no dolorosa. Las imágenes sugieren una lesión quística, y la serología confirmó la infección por Echinococcus. Se realizó la extirpación quirúrgica, y la histopatología confirmó un quiste hidatídico. La paciente recibió un tratamiento posoperatorio de albendazol durante seis semanas. Su recuperación fue sin incidentes, sin recurrencia en el seguimiento.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Había una abuela de 90 años con una bola en su muslo. La bola creció muy despacito por tres años. No le dolía ni tenía fiebre. El doctor vio que la bola era dura y no hacía daño. Hicieron unas fotos especiales y encontraron que había un bichito dentro. El doctor sacó la bola con una operación. Luego, la abuela tomó medicina para quitar el bichito. Ella se puso bien y no volvió a salir la bola.",
+        "score": {
+          "ROUGE-L-Sum": 0.2694300518134715,
+          "BERTScore_F": 0.715766191482544
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.49259812164800776
+        }
+      },
+      "B2": {
+        "text": "**Lo que Encontraron**  \nUna mujer de 90 años que vivía en una zona rural notó una hinchazón en la parte trasera y media de su muslo izquierdo, justo encima de la rodilla. Esta hinchazón creció lentamente durante tres años. No tenía dolor ni otros síntomas como fiebre o enrojecimiento. Al examinarla, los médicos encontraron una masa firme y que no dolía al tocarla.\n\n**Qué Significan las Pruebas**  \nLas imágenes por ecografía y resonancia mostraron que la hinchazón era un quiste grande, que es una bolsa llena de líquido. Además, la prueba de sangre confirmó que estaba infectada por un parásito llamado Echinococcus, que puede causar un quiste hidatídico. Este tipo de quiste se forma cuando el parásito crea una bolsa en el cuerpo.\n\n**El Tratamiento y Resultado**  \nLos médicos operaron para quitar el quiste completo, con mucho cuidado para no romperlo y evitar que el parásito se esparciera. Después de la cirugía, la muestra del quiste fue analizada y confirmó el diagnóstico. La paciente tomó un medicamento llamado albendazol durante seis semanas para eliminar cualquier parásito restante. Su recuperación fue buena y no tuvo problemas ni volvió a aparecer la hinchazón en las revisiones posteriores.\n\nEn resumen, esta mujer tuvo un quiste causado por un parásito, que fue tratado con cirugía y medicina, y se recuperó sin complicaciones.",
+        "score": {
+          "ROUGE-L-Sum": 0.34659090909090906,
+          "BERTScore_F": 0.7862579226493835
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5664244158701464
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nUna mujer de 90 años, originaria de una zona rural y con antecedentes de hepatitis C y tabaquismo prolongado, consultó por una hinchazón en la parte posterior y medial del muslo izquierdo, justo por encima de la rodilla. Esta masa había aparecido hace tres años y había ido aumentando de tamaño de forma gradual. La paciente no presentaba dolor, fiebre, picazón ni otros síntomas asociados, y no refería antecedentes de traumatismos recientes. Además, tenía historial de contacto con animales debido a su entorno rural.\n\n**Hallazgos Clave**  \nEn el examen físico, se detectó una masa esférica, firme, fija y no dolorosa, de aproximadamente 14 × 10 cm, con bordes bien definidos y piel sobre la lesión que se podía pellizcar, mostrando venas prominentes pero sin aumento de temperatura local. La ecografía reveló una lesión quística grande con múltiples quistes pequeños en su interior, originada en la articulación de la rodilla y extendiéndose hacia la mitad del muslo, sin vascularización interna. La resonancia magnética confirmó estas características, mostrando además extensión intramuscular e intermuscular en músculos específicos del muslo. Estos hallazgos fueron altamente sugestivos de un quiste hidatídico (una infección parasitaria causada por el Echinococcus). La confirmación diagnóstica se realizó mediante una prueba serológica de hemaglutinación para Echinococcus. Estudios adicionales, como radiografía de tórax y ecografía abdominal, no mostraron afectación en otros órganos.\n\n**Interpretación Clínica**  \nEl diagnóstico de quiste hidatídico en el muslo, aunque poco común, fue confirmado mediante imágenes, pruebas serológicas y análisis histopatológico. La lesión representaba una masa quística con múltiples compartimentos, infiltrando tejidos musculares pero sin comunicación con la articulación de la rodilla. La histología mostró una pared quística con infiltración inflamatoria y material característico del parásito, confirmando la naturaleza hidatídica de la lesión.\n\n**Próximos Pasos y Tratamiento**  \nSe planificó y llevó a cabo la extirpación quirúrgica completa del quiste mediante una incisión en forma de S, con una disección cuidadosa para evitar la ruptura y contaminación del área. El sitio quirúrgico fue irrigado con solución salina para minimizar riesgos de diseminación. El postoperatorio transcurrió sin complicaciones, y la paciente recibió tratamiento antiparasitario con albendazol durante seis semanas para asegurar la erradicación del parásito. Se realizaron controles periódicos a las 1, 3, 6, 9 y 12 semanas posteriores a la cirugía, durante los cuales no se evidenció recurrencia ni complicaciones.\n\nEn resumen, este caso ilustra la importancia de considerar infecciones parasitarias como causa de masas quísticas en pacientes de zonas rurales, y demuestra que un abordaje quirúrgico cuidadoso combinado con terapia antiparasitaria puede conducir a una recuperación exitosa sin recurrencia.",
+        "score": {
+          "ROUGE-L-Sum": 0.24543946932006636,
+          "BERTScore_F": 0.7895590662956238
+        },
+        "quality": {
+          "category": "good",
+          "is_good": false,
+          "combined_score": 0.517499267807845
+        }
+      }
+    }
+  },
+  {
+    "id": 99,
+    "gold_summary": "En este informe de caso, presentamos a una mujer soltera de 21 años con un fuerte historial familiar de neoplasia endocrina. Fue derivada a nuestro hospital para quimioterapia debido a un diagnóstico de feocromocitoma maligno, que había hecho metástasis en la vejiga urinaria, los huesos y los pulmones. Además, desarrolló anemia hemolítica microangiopática como un síndrome paraneoplásico.\n",
+    "synthetic_summary": {
+      "B1": {
+        "text": "Esta es la historia de una joven de 21 años. Ella tiene un tipo de enfermedad que hace que su cuerpo tenga bultos malos. Estos bultos están en partes como la vejiga, los huesos y los pulmones. También, su sangre estaba muy débil y no estaba bien. Los doctores le dieron medicinas para ayudarla a mejorar. Ahora, ella está más fuerte y se siente mejor.",
+        "score": {
+          "ROUGE-L-Sum": 0.2647058823529411,
+          "BERTScore_F": 0.7404709458351135
+        },
+        "quality": {
+          "category": "best",
+          "is_good": true,
+          "combined_score": 0.5025884140940273
+        }
+      },
+      "B2": {
+        "text": "### Caso de una joven con cáncer y anemia especial\n\nPresentamos la historia de una mujer de 21 años que tiene un tipo de tumor llamado feocromocitoma maligno. Este tumor se originó en sus glándulas suprarrenales y se ha extendido a otros órganos, como la vejiga, los huesos y los pulmones. Además, su familia tiene antecedentes de tumores similares, lo que indica que puede haber una causa genética.\n\n### Qué le pasó a la paciente\n\nLa paciente también desarrolló un problema en la sangre llamado anemia hemolítica microangiopática. Esto significa que sus glóbulos rojos se destruyen más rápido de lo normal debido a pequeños daños en los vasos sanguíneos. Esta anemia está relacionada con su cáncer y se llama síndrome paraneoplásico, porque ocurre como una consecuencia del tumor, aunque no sea directamente causado por él.\n\n### Tratamiento y evolución\n\nElla recibió quimioterapia adaptada para evitar empeorar la anemia. Después de varios ciclos, su sangre mejoró y ya no tenía signos de anemia ni problemas en las células sanguíneas. Esto muestra que el tratamiento ayudó tanto al cáncer como a la anemia causada por él.\n\nEn resumen, este caso muestra cómo un cáncer puede afectar otras partes del cuerpo, como la sangre, y cómo un tratamiento adecuado puede mejorar la salud general de la paciente.",
+        "score": {
+          "ROUGE-L-Sum": 0.25742574257425743,
+          "BERTScore_F": 0.7475435733795166
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.502484657976887
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe trata de una mujer joven de 21 años con antecedentes familiares significativos de tumores endocrinos malignos, en particular feocromocitomas (tumores que producen hormonas y se originan en las glándulas suprarrenales o tejidos relacionados). La paciente fue ingresada en el hospital debido a un feocromocitoma metastásico, es decir, un tumor maligno que se ha extendido a otros órganos, incluyendo la vejiga, los huesos y los pulmones. Además, presentaba hipertensión arterial difícil de controlar y síntomas relacionados con su enfermedad avanzada.\n\n**Hallazgos Clave**  \nDurante su hospitalización, se detectó que la paciente tenía anemia severa causada por un proceso llamado anemia hemolítica microangiopática (MAHA). Esta condición implica la destrucción acelerada de glóbulos rojos debido a daños en los pequeños vasos sanguíneos, y en este caso se relaciona directamente con su cáncer avanzado, constituyendo un síndrome paraneoplásico (un efecto indirecto del tumor sobre el organismo). Los análisis de sangre mostraron anemia significativa, signos de destrucción de glóbulos rojos (como aumento de reticulocitos y bilirrubina indirecta), y alteraciones en el frotis sanguíneo que confirmaron la presencia de células fragmentadas características de MAHA.\n\n**Interpretación Clínica**  \nLa anemia hemolítica microangiopática en esta paciente se considera una complicación secundaria al feocromocitoma metastásico, reflejando la gravedad y la actividad del tumor. El tratamiento con quimioterapia adaptada (excluyendo ciertos fármacos que podrían empeorar la anemia) logró controlar tanto la anemia como la progresión del cáncer, evidenciado por la normalización de los parámetros sanguíneos y la desaparición de las células anormales en el frotis. Esto confirma la relación directa entre la actividad tumoral y la anemia hemolítica.\n\n**Próximos Pasos**  \nLa paciente fue dada de alta con un régimen farmacológico para manejar sus síntomas y prevenir complicaciones, incluyendo corticosteroides, medicamentos para controlar la presión arterial, antieméticos y suplementos. En el seguimiento posterior, mostró una mejoría clínica significativa, con parámetros sanguíneos dentro de rangos normales y un estado general activo y estable. Continuará bajo vigilancia estrecha para monitorear la evolución de su enfermedad y ajustar el tratamiento según sea necesario.",
+        "score": {
+          "ROUGE-L-Sum": 0.18666666666666665,
+          "BERTScore_F": 0.7351530194282532
+        },
+        "quality": {
+          "category": "worst",
+          "is_good": false,
+          "combined_score": 0.4609098430474599
+        }
+      }
+    }
+  }
+]
\ No newline at end of file
diff --git a/generating_data/score/es_synthetic_fh.json b/generating_data/score/es_synthetic_fh.json
new file mode 100644
index 0000000000000000000000000000000000000000..71eb707e603d4e88f763f2cc6fd8cec7b0561883
--- /dev/null
+++ b/generating_data/score/es_synthetic_fh.json
@@ -0,0 +1,1802 @@
+[
+    {
+        "article": "Información para el paciente\nUn hombre de 27 años y fumador estuvo involucrado en un accidente de tráfico; se cayó de su motocicleta sin casco. El hombre llevó la motocicleta al hospital e informó de un dolor de cabeza y heridas hemorrágicas en la frente.\n\nEl paciente no tiene antecedentes patológicos y trabaja en una zona rural.\n\nHallazgos clínicos\nTras su ingreso en urgencias, perdió el conocimiento y sufrió dos convulsiones. En la exploración física, la escala de coma de Glasgow fue de 6/15 (no abrió los ojos, se retiró al sentir dolor, no respondió verbalmente) con midriasis bilateral, dificultad hemodinámica y buena saturación. Se identificó una lesión craneal penetrante con una profusa hemorragia intracraneal.\n\nLínea de tiempo\nTras caerse de la motocicleta, el paciente volvió a montarse en ella e inmediatamente fue al hospital, quejándose de dolores de cabeza y de una herida en la frente por la que sangraba. Recibió tratamiento de urgencia para estabilizar sus funciones respiratorias y hemodinámicas. Ese mismo día, fue trasladado inconsciente a un centro mejor equipado, donde se le realizó un TAC y se sometió a una operación quirúrgica con éxito.\n\nEvaluación diagnóstica\nSu nivel de hemoglobina era de 6 g/dL y su grupo sanguíneo era O positivo. El hospital no tenía ni una unidad de cuidados intensivos ni un escáner. El único diagnóstico sugerido fue el de traumatismo agudo en la cabeza, complicado por hemorragia intracraneal que provocó shock y convulsiones. El pronóstico vital, basado en la presentación clínica, era malo.\n\nIntervención terapéutica\nUna intervención inicial consiste en un relleno intracraneal a través de la fractura craneal, seguido de un vendaje cefálico que ayuda a detener el sangrado. El tratamiento involucró la estabilización de la columna cervical, intubación orotraqueal con oxígeno a 6 L por minuto y la inserción de un catéter Foley. Se usaron dos puertos venosos periféricos para administrar NaCl 0.9 % 1000 CC, Geloplasma* 500 CC, Manitol 20 % 250 CC; Phenobarbital inj 40 mg/2 ml: 100 mg, luego Thiopental 250 mg: bolo de 100 mg × 2 debido a otras convulsiones; Amoxicillin + Clavulanic Acid injection 2 g; Gentamycin 160 mg intramuscularmente. Se realizó un suero antitetánico de 1500 IU y una transfusión de 450 CC de sangre.\n\nEl paciente fue trasladado inconsciente a un equipo en un hospital de primera categoría, sin intubación y en un estado hemodinámico estable.\n\nEl primer día después de la transferencia, el paciente evolucionó bien; estaba consciente y podía caminar, sin problemas neurológicos, hemodinámicos o respiratorios. La tomografía computarizada reveló un edema bifrontal agudo, una contusión hemorrágica del parénquima predominantemente en el lado derecho, una capa de hematoma subdural agudo (3 mm) en la región fronto-parieto-temporo-occipital izquierda, una hernia subfalcular izquierda de 5 mm, una compresión discreta del ventrículo lateral derecho, una hemorragia subaracnoidea superior bifrontal aguda, una fractura frontal deprimida con rotura osteomeníngea y una fractura de la tercera vértebra cervical con compresión de la médula espinal. El paciente se sometió a una operación exitosa en el hospital de primera categoría.\n\nSeguimiento y resultados\nEl período postoperatorio estuvo marcado por convulsiones, para las cuales se le administró anticonvulsivos al paciente, con un buen resultado.\n",
+        "gold_summary": "Un hombre de 27 años, fumador sin antecedentes patológicos, estuvo involucrado en un accidente de tráfico, al caerse de una motocicleta sin casco. En el ingreso al hospital de nuestro distrito rural, la escala de coma de Glasgow durante el examen físico fue de 6/15 con midriasis bilateral, distrés hemodinámico y buena saturación. Se identificó una lesión penetrante en la cabeza con profusa hemorragia intracraneal. Se usó el relleno intracraneal conocido en la neurocirugía de control de daños para taponar la hemorragia intracraneal grave y que es una maniobra neuroquirúrgica que salva vidas. El paciente fue trasladado inconsciente a un hospital de primera categoría, libre de intubación y en un estado hemodinámico estable. El período postoperatorio estuvo marcado por convulsiones, por lo que el paciente fue puesto en anticonvulsivos con un buen resultado.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un hombre de 27 años se cayó de su motocicleta sin casco. Se golpeó muy fuerte la cabeza y sangraba por la frente. Al llegar al hospital quedó muy dormido y tuvo dos convulsiones (ataques o “fits”). Tenía la sangre muy baja y estaba en peligro.\n\nEn el hospital pequeño no había todo lo que necesita la gente con heridas así. Los médicos taparon la herida dentro del cráneo para detener la sangre. Le pusieron líquidos, medicinas, y le dieron sangre. Luego lo llevaron a un hospital grande para más ayuda.\n\nEn el hospital grande le hicieron una prueba especial (una tomografía) y vieron golpes y hinchazón en el cerebro, una fractura en la frente y otra en el cuello. Le operaron con éxito. Después de la operación todavía tuvo convulsiones, pero le dieron medicinas para controlarlas. Al final mejoró: recuperó la conciencia y pudo caminar. Los médicos dicen que su resultado fue bueno.",
+                "fh_score": 78.65
+            },
+            "B2": {
+                "text": "Resumen (nivel B2, lenguaje claro y comprensible)\n\nUn hombre de 27 años que fuma sufrió una caída de una motocicleta sin llevar casco. Al llegar al hospital de su zona rural estaba en mal estado: la escala de coma de Glasgow era 6/15 (esto indica que estaba muy inconsciente), tenía las pupilas dilatadas en ambos ojos (un signo de lesión cerebral grave), y presentaba inestabilidad hemodinámica (problemas para mantener la presión y el flujo de sangre). Se detectó una lesión penetrante en la cabeza con hemorragia dentro del cráneo.\n\nEn ese hospital se realizó una maniobra de emergencia llamada relleno intracraneal o “taponamiento” para controlar la hemorragia; es una técnica de neurocirugía de control de daños que puede salvar la vida al detener sangrados cerebrales masivos. Posteriormente el paciente fue llevado, aún inconsciente, a un centro de mayor complejidad para cirugía. Llegó sin intubación y en un estado hemodinámico estable.\n\nDespués de la operación tuvo episodios de convulsiones, que se trataron con medicamentos anticonvulsivos, y la evolución fue buena. Este caso muestra cómo una intervención rápida para controlar la hemorragia puede ser determinante y subraya la importancia de medidas preventivas como el uso del casco al conducir una motocicleta.",
+                "fh_score": 49.34
+            },
+            "B3": {
+                "text": "Resumen (nivel lector universitario)\n\nPaciente\n- Hombre de 27 años, fumador, sin antecedentes médicos conocidos. Sufrió una caída de motocicleta sin casco.\n\nPresentación inicial (hallazgos anormales y normales)\n- Al ingreso en el hospital rural: pérdida de conciencia y dos convulsiones. Glasgow Coma Scale 6/15 (no abre ojos, retirada a dolor, sin respuesta verbal) — esto indica un daño cerebral grave.  \n- Midriasis bilateral (dilatación de pupilas) y distrés hemodinámico (inestabilidad de la presión/ritmo circulatorio) — signos de lesión neurológica y estado crítico.  \n- Buena saturación de oxígeno (hallazgo relativamente normal), pero hemoglobina muy baja: 6 g/dL (anemia grave).  \n- Se constató una lesión craneal penetrante con hemorragia intracraneal profusa.\n\nActuación inicial en el centro rural\n- Medidas de soporte: inmovilización cervical, intubación orotraqueal y oxígeno, acceso venoso y reposición de líquidos, administración de manitol (para disminuir presión intracraneal), anticonvulsivantes (fenobarbital, thiopental), antibióticos, suero antitetánico y transfusión sanguínea parcial.  \n- Se practicó un taponamiento (relleno) a través de la fractura craneal para controlar la hemorragia — una maniobra de control de daños neuroquirúrgico destinada a detener sangrado masivo cuando no hay recursos avanzados.  \n- El hospital rural no disponía de TAC ni de unidad de cuidados intensivos, por lo que el paciente fue trasladado a un centro de mayor complejidad estando inconsciente pero hemodinámicamente estable tras la estabilización inicial.\n\nEvaluación en el hospital de referencia y hallazgos por TAC (anormales relevantes)\n- Edema bifrontal agudo y contusión hemorrágica del parénquima, predominante en el lado derecho.  \n- Hematoma subdural agudo (capa de 3 mm) en la región fronto-parieto-temporo-occipital izquierda.  \n- Hernia subfalcular izquierda de 5 mm (desplazamiento del tejido cerebral hacia la línea media), con compresión moderada del ventrículo lateral derecho — ambos son signos de aumento de la presión intracraneal y riesgo de lesión cerebral adicional.  \n- Hemorragia subaracnoidea bifrontal superior.  \n- Fractura frontal deprimida con ruptura osteomeníngea (fractura que comunica el cráneo con las meninges), lo que aumenta el riesgo de infección y fuga de líquido cefalorraquídeo.  \n- Fractura de la tercera vértebra cervical (C3) con compresión de la médula espinal — lesión adicional que requiere manejo espinal especializado.\n\nTratamiento definitivo y evolución\n- El paciente fue intervenido quirúrgicamente con éxito en el hospital de referencia.  \n- En el postoperatorio presentó convulsiones recurrentes, que fueron tratadas con anticonvulsivantes. Bajo ese tratamiento tuvo buena evolución clínica: al primer día tras la transferencia se informó que estaba consciente y caminando, sin déficit neurológico, hemodinámico o respiratorio evidente.\n\nImplicaciones y pasos a seguir recomendados\n- El cuadro inicial era de muy mal pronóstico, pero la intervención de control de daño y la cirugía definitiva permitieron una recuperación inicial favorable.  \n- Seguimiento necesario: continuidad de la terapia anticonvulsivante y vigilancia neurológica para detectar convulsiones tardías o déficits cognitivos/neurológicos; control de la fractura craneal abierta por riesgo de infección y posible reparación adicional si hay fuga de líquido cefalorraquídeo; evaluación y manejo específico de la fractura cervical y de la médula (riesgo de lesión medular tardía, rehabilitación y posible cirugía vertebral según evaluación neuroquirúrgica/ortopédica); control imagenológico de evolución (TAC o RMN) y rehabilitación física/neurológica según necesidades.  \n- También es importante continuar la vigilancia hematológica (recuperación de la anemia) y la prevención de complicaciones infecciosas.\n\nComentario empático\n- Se trata de un adulto joven sin enfermedades previas que sufrió lesiones cerebrales y medulares graves. Recibió intervenciones de emergencia que resultaron en una recuperación inicial notable, pero requiere seguimiento especializado y rehabilitación para maximizar la recuperación y reducir riesgos futuros.",
+                "fh_score": 30.44
+            }
+        }
+    },
+    {
+        "article": "La paciente era una madre de 54 años que provenía de una zona rural y que llegó al Hospital Especializado de Compresión de Nekemte con la queja de una masa en su vagina de 3 años de duración. Hace tres años, encontró una protuberancia de masa a través de su vagina, que gradualmente creció en tamaño con el tiempo. Había tenido dos bebés, el último hace 12 años. Ambos partos fueron en casa, ya que el centro de salud está demasiado lejos de su área de residencia, y fue asistida por una comadrona tradicional. Ella afirmó que todo había sido sin problemas. Inicialmente, hace tres años, hubo sangrado y una descarga ofensiva de la masa, pero eso se detuvo en el último año. Desarrolló laceraciones en la masa hace seis meses. Por esta razón, se divorció y se aisló de toda la vida social durante este largo período de tiempo. Ahora, su hermana mayor y otro familiar la trajeron al hospital específicamente por la laceración de la masa. No tenía ninguna otra enfermedad médica crónica conocida.\n\nHallazgo pertinente del PE\nSigno vital: PA = 100/60 mm hg, FC = 84 lpm, FR = 20 lpm, T° = 36.5°C, peso = 47 kg.\n\nGUS: hay una masa rosada en la vagina que se encuentra a unos 7 cm del anillo del himen.\n\nEl fondo uterino es la parte principal de la masa.\n\nHabía una laceración longitudinal de unos 5 cm en el lado derecho de la masa.\n\nNo hubo sangrado ni secreción de la masa ni del área de la laceración.\n\nLaboratorio\nCBC: hemoglobina = 12 g/dl, PLT = 285 mil, neutrófilos = 74%.\n\nAnálisis de orina: resultado normal.\n\nGrupo sanguíneo = A, RH = positivo.\n\nPrueba de VIH = negativa.\n\nHBSAg = negativo.\n\nEcografía: vejiga parcialmente llena visible en el abdomen, útero no visible en el abdomen. Por lo demás, no se observaron otros hallazgos pertinentes.\n\nRadiografía de tórax: radiografía de tórax normal.\n\nPor este motivo, se le diagnosticó una inversión uterina crónica. Se tomaron imágenes preoperatorias y postoperatorias, el fondo uterino era el punto principal de la masa que sobresalía completamente a través de la vagina y había una laceración crónica desarrollada en la superficie endometrial. Después de la operación, se observó un canal vaginal normal. Después de revisar las opciones de tratamiento con ella y su familia, se programó una cirugía y se realizó una histerectomía abdominal al día siguiente. Era una cirugía abdominal y era fácil introducir el útero en el abdomen. Como el tejido era redundante y distorsionado, es difícil identificar la referencia anatómica y los puntos de referencia quirúrgicos. Debido a esto, la cirugía fue difícil y hubo una lesión ureteral derecha transaccional intraoperatoria y se realizó una anastomosis de extremo a extremo. Se dio de alta el décimo día de la operación y se encontró que estaba mejorando. Se le dio una cita de seguimiento dos semanas después y cuando se evaluó se encontró que estaba bien.\n",
+        "gold_summary": "Una mujer de 54 años de edad acudió a nuestro hospital con la queja de una masa indolora en su vagina de 3 años de duración. Hace tres años, encontró una protuberancia de masa a través de su vagina, que gradualmente creció en tamaño con el tiempo. En el examen físico, el fondo uterino fue el punto principal de la masa y sobresalía 7 cm por debajo del anillo del himen. Como resultado, se le diagnosticó inversión uterina crónica y se le sometió a una histerectomía abdominal. Fue dada de alta en casa mejorada. Presentamos este caso debido a un factor no identificado que provocó la inversión uterina, la presentación tardía de la enfermedad y la dificultad en el tratamiento quirúrgico.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Esta es la historia de una mamá de 54 años que vivía en el campo. Hace tres años notó una bolita que salía por su vagina. La bolita fue creciendo poco a poco. Al final, era la parte superior del útero (el lugar donde crecen los bebés) que se había dado vuelta y salido por la vagina. Esto se llama inversión uterina.\n\nTenía una grieta en esa zona desde hace meses. Vivía lejos del hospital y no pidió ayuda antes. Su hermana la llevó cuando la herida empeoró.\n\nLos médicos la revisaron y le hicieron estudios. Todo lo demás estaba bien. Le explicaron las opciones y la operaron al día siguiente. Le quitaron el útero con una cirugía por el abdomen. La operación fue difícil porque los órganos estaban muy cambiados. Durante la cirugía, se cortó sin querer un tubito que lleva la orina del riñón a la vejiga (eso se llama uréter). Los cirujanos lo arreglaron uniendo los dos extremos.\n\nElla mejoró después de la operación. Salió del hospital diez días después y en la cita de control estaba bien. Los médicos compartieron el caso porque la causa de que el útero se volteara no quedó clara y porque la operación fue complicada.",
+                "fh_score": 82.34
+            },
+            "B2": {
+                "text": "Resumen comprensible (nivel secundaria)\n\nUna mujer de 54 años que vive en una zona rural llegó al hospital porque tenía desde hacía 3 años una masa que le salía por la vagina. Al principio la masa sangraba y tenía mal olor, pero eso paró hace aproximadamente un año. Hace seis meses se le abrió una herida (laceración) en la masa, lo que la aisló socialmente y la llevó incluso a un divorcio. No tenía otras enfermedades crónicas conocidas.\n\nEn la exploración, la parte superior del útero (llamada fondo uterino) era la parte principal de la masa y sobresalía por la vagina unos 7 cm más allá del anillo del himen. Esto llevó al diagnóstico de inversión uterina crónica. La inversión uterina ocurre cuando el útero se voltea hacia dentro y puede salir por la vagina; es algo raro en mujeres no embarazadas y suele requerir tratamiento quirúrgico si es crónica.\n\nSe hicieron pruebas: hemoglobina y otros análisis fueron normales, la ecografía no mostró el útero en el abdomen (porque estaba fuera) y las pruebas de VIH y hepatitis B fueron negativas. Tras hablar con la paciente y su familia, se realizó una histerectomía abdominal (operación para quitar el útero). Durante la cirugía fue difícil reconocer las estructuras porque los tejidos estaban muy deformados; esto causó una lesión accidental en el uréter derecho (el conducto que lleva la orina del riñón a la vejiga), que se reparó con una sutura de extremo a extremo.\n\nLa paciente mejoró después de la operación, estuvo ingresada diez días y en la consulta de control dos semanas después estaba bien. Este caso llama la atención por la causa no identificada de la inversión, la presentación tardía (probablemente influida por el acceso limitado a servicios de salud) y las dificultades técnicas durante la cirugía.",
+                "fh_score": 57.08
+            },
+            "B3": {
+                "text": "Presentación clínica\nUna mujer de 54 años, procedente de zona rural, consultó por una masa vaginal que había notado desde hacía 3 años y que fue creciendo gradualmente. Inicialmente la masa produjo sangrado y secreción fétida (que cesaron en el último año); hace seis meses se desarrolló una laceración sobre la masa. Por esta condición la paciente sufrió aislamiento social y divorcio y acudió al hospital acompañada por familiares. No refería otras enfermedades crónicas conocidas.\n\nExamen físico y pruebas\n- Signos vitales estables (PA 100/60 mmHg, FC 84 lpm, FR 20, T 36.5 °C). Peso 47 kg.  \n- Inspección genital: masa rosada que protruye por la vagina y cuyo punto principal es el fondo uterino, ubicado 7 cm por debajo del anillo himenal. Se observó una laceración longitudinal de unos 5 cm en el lado derecho de la masa sin sangrado activo ni secreción en el momento del examen.  \n- Analítica: hemoglobina 12 g/dl, plaquetas 285.000/µl, neutrófilos 74%. Orina normal. Serologías: VIH negativo, HBsAg negativo. Grupo sanguíneo A Rh+.  \n- Imagen: ecografía abdominal no visualizó el útero en su localización habitual; radiografía de tórax normal.\n\nDiagnóstico y tratamiento\nCon estos hallazgos se diagnosticó inversión uterina crónica: el útero estaba volteado de manera que su fondo sobresalía a través de la vagina. Tras discutir opciones, se realizó una histerectomía abdominal programada al día siguiente. Durante la cirugía el útero pudo reintegrarse al abdomen, pero el tejido estaba muy redundante y distorsionado, lo que dificultó identificar referencias anatómicas. Esto provocó una lesión transaccional del uréter derecho, que se reparó mediante anastomosis término-terminal intraoperatoria. La paciente evolucionó bien, fue dada de alta al décimo día y en la cita de control a las dos semanas se encontró sin problemas aparentes.\n\nInterpretación y consideraciones\n- Hallazgos normales: signos vitales y pruebas básicas (hemograma, orina, radiografía de tórax) sin alteraciones importantes; ausencia de infección por VIH o hepatitis B.  \n- Hallazgos anormales: inversión uterina crónica con protrusión del fondo uterino y laceración endometrial crónica; distorsión anatómica que complicó la cirugía y conllevó lesión ureteral iatrogénica tratada en el mismo acto.  \n- Etiología: la causa precisa de la inversión no pudo establecerse. La inversión uterina crónica suele relacionarse con eventos obstétricos (p. ej., manipulación uterina) pero en este caso la paciente no informó de un episodio agudo claro en el puerperio —su último parto fue hace 12 años, en casa— lo que sugiere un caso de presentación tardía o una causa no identificada.  \n- Impacto psicosocial: la larga evolución, la secreción y la laceración contribuyeron al estigma social y aislamiento de la paciente, subrayando barreras de acceso a la atención en áreas rurales.\n\nRecomendaciones y seguimiento\n- Seguimiento urológico para vigilar la viabilidad y el drenaje del uréter derecho (evaluación clínica, creatinina renal y, si procede, imagen como urografía por TC o ecografía renal).  \n- Control ginecológico de la herida y recuperación posoperatoria.  \n- Apoyo psicosocial y, si procede, orientación para acceso a servicios de salud reproductiva y atención primaria para prevenir demoras en futuros problemas.  \n- Documentación y discusión multidisciplinaria de casos similares pueden ayudar a identificar factores de riesgo y mejorar la atención en áreas con acceso limitado.\n\nResumen breve\nMujer de 54 años con inversión uterina crónica que protruyó por la vagina durante 3 años, tratada mediante histerectomía abdominal. La cirugía fue compleja por la alteración anatómica y se asoció a lesión ureteral reparada intraoperatoriamente. La paciente mejoró y presentó buena evolución en controles. El caso destaca la presentación tardía, la dificultad quirúrgica y las consecuencias psicosociales en un entorno rural con acceso limitado a atención obstétrica.",
+                "fh_score": 49.19
+            }
+        }
+    },
+    {
+        "article": "Varón de 20 años, HIV negativo, con TB pulmonar y tratamiento irregular en 2020-2021. Se internó por síndrome de impregnación bacilar, dolor e impotencia funcional del hombro derecho. Presentaba mal estado general, adelgazado, hipotrofia muscular grave, lesiones tumorales frías fluctuantes fistulizadas en dorso, calota craneana y tórax anterior con secreción caseosa, sin presentar déficits motores ni sensitivos. El examen molecular rápido (GeneXpert Mtb/Rif) de secreción del tórax fue positivo para Mycobacterium tuberculosis, sensible a rifampicina (el antibiograma fenotípico mostró una cepa pansensible). La TC demostró consolidaciones pulmonares y árbol en brote, junto con el compromiso óseo de columna cervical, dorsal y lumbar con imágenes líticas y colecciones pre y paraespinales. En la RMN se observaron imágenes infiltrativas desde C4 a C6; D4 a D6, D9 a D12; fractura patológica de D6 y D10 e infiltración en L1, L2 y L3. Inició tratamiento anti-TB con esquema estándar de primera línea (isoniacida, rifampicina, pirazinamida, etambutol). Dada la extensa destrucción y el peligro de cuadriplejía/paraplejía por el compromiso cervical y/o dorsal, se indicó posición decúbito dorsal permanente, collar de Filadelfia, asistencia kinésica y conducta neuroquirúrgica en forma programada en los niveles cervicales, D6 y D10. Previo a la cirugía programada presentó un cuadro agudo de paraplejía con nivel sensitivo D8, con compromiso vesical. Se interpretó como nivel de compresión aguda en D6. Se indicó neurocirugía de urgencia con descompresión medular vía posterior con laminectomía dorsal 6 y parcialmente D5 y 7 y evacuación de una colección epidural. Fue recuperando la función motora y sensitiva en forma progresiva. Posteriormente se realizó la cirugía programada cervical vía anterior con corporectomía de C4, C5, C6 y C7 más artrodesis de C3 a D1 con reemplazo de cuerpo vertebral más injerto autólogo, placa y tornillos. En la TC de control se evidenció luxación posterior de D6 con compresión del canal espinal y deterioro neurológico por compresión medular. Se reconsideró la táctica quirúrgica debido a la inestabilidad mecánica y neurológica. Se realizó descompresión y alineación del nivel luxado con artrodesis posterior de los tres niveles espinales no adyacentes, cervical, dorsal 6 y dorsal 10 en un solo tiempo quirúrgico. Se fijó desde  C3 hasta D12 con tornillos poliaxiales y barra de transición cervicodorsal. En cada tiempo quirúrgico se evidenció evacuación espontánea de material caseoso, BAAR positivo, y se realizaron lavados profusos.  Presentó mejoría clínica, bacteriológica y resolución de las lesiones pulmonares. Recuperó movilidad con rehabilitación kinésica sumada al tratamiento específico (3 meses de primera fase e indicación de continuación con isoniacida y rifampicina hasta completar los 12 meses). Egresó caminando por sus propios medios, luego de una prolongada internación de 5 meses.",
+        "gold_summary": "Se presenta el caso de un varón de 20 años con espondilitis tuberculosa multinivel no contigua (cervical, dorsal 6, dorsal 10 y lumbar). Se trata de un paciente HIV negativo con tuberculosis diseminada con grave compromiso de su estado general y múltiples localizaciones de la enfermedad. Algunas tenían fistulas que secretaban caseum. El paciente presentó paraplejía aguda que requirió, teniendo en cuenta el nivel sensitivo a nivel dorsal 6, una primera cirugía urgente de descompresión por vía posterior. Luego se efectuó la cirugía programada. En primera instancia, la región cervical por vía anterior, con corporectomía, colocación de reemplazo de cuerpo vertebral más injerto autólogo y placa con tornillos. Posteriormente se evidenció luxación del nivel dorsal 6 hacia atrás comprimiendo la médula espinal y, dada la inestabilidad mecánica, se indicó un tercer tiempo quirúrgico por vía posterior que comprendió reducción, descompresión y fijación, resolviendo los tres niveles por vía posterior con barras y tornillos. El tratamiento quirúrgico, médico y kinésico de esta forma poco frecuente del mal de Pott fue exitoso, con recuperación de su estabilidad mecánica y progresiva recuperación de su estado neurológico.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un joven de 20 años tuvo tuberculosis que se extendió a los pulmones y a varios huesos de la columna. Tenía heridas que supuraban material blando y estaba muy delgado y débil. \n\nEmpezó tratamiento contra la tuberculosis con antibióticos especiales. Pero un día perdió fuerza en las piernas y no podía controlar la vejiga. Los médicos vieron que la médula espinal estaba siendo aplastada en la parte media de la espalda. Hicieron una cirugía urgente por detrás para quitar la presión y drenar una colección de material infectado. Después de esa operación fue mejorando poco a poco.\n\nLuego le hicieron una cirugía programada en el cuello por delante. Le quitaron partes de varias vértebras enfermas y las reemplazaron, con injerto y una placa para dejar el cuello firme. Más tarde se comprobó que una vértebra de la espalda se había movido hacia atrás y volvía a apretar la médula. Por eso hicieron otra operación desde atrás para alinear, descomprimir y fijar la columna con tornillos y barras, abarcando los niveles afectados.\n\nEn las operaciones encontraron material típico de la tuberculosis y lo lavaron bien. Con los medicamentos antituberculosos (incluyendo isoniacida y rifampicina) y la rehabilitación con fisioterapia, el joven mejoró mucho. Sus pulmones también sanaron. Continuó el tratamiento hasta completar 12 meses. Tras cinco meses de hospital, salió caminando por sus propios medios.",
+                "fh_score": 64.01
+            },
+            "B2": {
+                "text": "This is the case of a 20-year-old man with widespread tuberculosis (TB) that affected his lungs and many parts of his spine. He was HIV-negative and had a history of not finishing TB treatment. He was very weak and thin, and had several soft swellings on his back, skull, and chest that leaked a thick, cheese-like fluid (this is dead tissue caused by TB).\n\nTests on the chest fluid confirmed Mycobacterium tuberculosis that was sensitive to usual drugs. Scans showed lung damage and multiple areas of bone destruction in the cervical (neck), dorsal (upper and mid-back), and lumbar (lower back) spine. MRI also found broken vertebrae and collections of infected material pressing near the spinal cord.\n\nDoctors began standard first-line TB medicine (isoniazid, rifampicin, pyrazinamide, ethambutol). Because the spine was badly damaged and there was a real risk of losing movement (paralysis), they planned spinal surgery and kept him in a stable position with a neck collar while preparing.\n\nBefore the planned surgery, he suddenly developed paraplegia (loss of leg movement) and a sensory level at the mid-back, with bladder problems. This was judged to be sudden spinal cord compression at the sixth dorsal vertebra (D6). He had emergency posterior surgery to relieve the pressure (laminectomy, which means removing part of the back of the vertebra) and the surgeons drained an epidural collection of infected material. He recovered some movement and feeling after that operation.\n\nLater, the team performed the planned neck surgery from the front: they removed damaged vertebral bodies in the neck (corporectomy of C4–C7), replaced them, and fused the spine from C3 to D1 using the patient’s bone graft and metal hardware. In a follow-up scan, D6 had shifted backwards and was again pressing on the spinal cord, causing new neurologic problems. Because the spine was mechanically unstable, surgeons performed another operation from the back to realign, decompress, and stabilize the damaged levels. In total, they fixed the spine from C3 down to D12 with rods and screws in a combined approach.\n\nThroughout the surgeries, the teams found and washed out caseous (cheesy) TB material; samples were positive for TB bacteria. With combined medical therapy, repeated surgical drainage and stabilization, and intensive physical rehabilitation, the patient improved. His lung infections healed, bacteria tests became negative, and he regained the ability to walk. He continued TB medication to complete a year of treatment and was discharged walking after a five-month hospital stay.\n\nThis case shows a severe, multi-level form of spinal TB (Pott disease) that required urgent and staged surgical care together with long-term antibiotics and rehab. The combined approach led to recovery of spinal stability and gradual neurological improvement.",
+                "fh_score": 80.38
+            },
+            "B3": {
+                "text": "Resumen clínico breve (empatía y contexto)\n- Paciente: varón de 20 años, VIH negativo, con antecedente de tratamiento antituberculoso irregular en 2020–2021.\n- Presentación: deterioro general marcado, pérdida de peso y atrofia muscular; lesiones frias fistulizadas en dorso, calota y tórax con secreción caseosa. Inicialmente sin déficit neurológico motor o sensitivo, pero con dolor e impotencia funcional del hombro derecho.\n\nHallazgos diagnósticos principales\n- Microbiología: GeneXpert positivo para Mycobacterium tuberculosis sensible a rifampicina; cultivos/antibiograma fenotípico: cepa pansensible.\n- Imágenes torácicas: consolidaciones y patrón árbol en brote (típico de TB pulmonar).\n- Columna: lesiones líticas y colecciones pre/paraespinales en niveles cervical, dorsal y lumbar. RMN con infiltración en C4–C6; D4–D6; D9–D12; fracturas patológicas en D6 y D10; compromiso de L1–L3.\n- Diagnóstico anatómico: espondilitis tuberculosa multisegmentaria no contigua (mal de Pott), con abscesos epidurales que amenazaban la médula.\n\nTratamiento realizado (médico, quirúrgico y rehabilitador)\n- Tratamiento antituberculoso inicial estándar de primera línea (isoniacida, rifampicina, pirazinamida, etambutol); esquema prolongado hasta 12 meses (fase intensiva 3 meses, continuación con isoniacida + rifampicina).\n- Manejo preventivo inicial: posición supina, collar cervical de Filadelfia y kinesiterapia, plan quirúrgico programado por compromiso multisegmentario.\n- Evento agudo: antes de la cirugía programada el paciente desarrolló paraplejía aguda con nivel sensitivo en D8 y trastorno vesical → interpretado como compresión aguda en D6.\n  - Urgencia: descompresión posterior con laminectomía (D6 ± D5–D7) y evacuación de colección epidural → recuperación progresiva sensitivo-motora.\n- Cirugías programadas posteriores:\n  1) Vía anterior cervical: corporectomías cervicales (C4–C7), reemplazo de cuerpos vertebrales con injerto autólogo, artrodesis C3–D1 y fijación anterior (placa y tornillos).\n  2) Tras observar luxación posterior en D6 con nueva compresión y inestabilidad, se realizó en un solo tiempo posterior: reducción/descompresión y artrodesis posterior que incluyó fijación desde C3 hasta D12 con tornillos poliaxiales y barra de transición cervicodorsal; se abordaron los tres niveles comprometidos (cervical, D6 y D10). En todas las cirugías se evacuó material caseoso y se comprobó BAAR positivo.\n- Rehabilitación kinésica intensiva complementaria.\n\nEvolución y resultado\n- Mejoría clínica y microbiológica: resolución de lesiones pulmonares y negativización progresiva.\n- Recuperación neurológica: recuperación de la función motora y sensitiva de forma progresiva; al alta el paciente caminaba por sus propios medios.\n- Hospitalización prolongada: 5 meses; seguimiento con continuidad del tratamiento antituberculoso hasta completar 12 meses.\n\nImplicaciones clínicas y lecciones principales\n- Este caso ilustra una forma poco frecuente y grave de TB ósea: espondilitis tuberculosa multisegmentaria no contigua con abscesos epidurales y riesgo real de lesión medular irreversible.\n- Mensajes relevantes:\n  - Ante déficit neurológico agudo por compresión medular por TB, la descompresión urgente puede permitir recuperación neurológica.\n  - Las lesiones tuberculosas vertebrales pueden requerir una combinación de abordajes (anterior para reconstrucción vertebral y posterior para estabilización) y fijación extensa cuando hay inestabilidad mecánica.\n  - El tratamiento antibiótico prolongado y la rehabilitación son esenciales para la resolución infectológica y funcional.\n  - La adherencia al tratamiento antituberculoso y el seguimiento son claves para prevenir diseminación y complicaciones graves.\n\nComentario final (empatía)\nEl caso muestra que, aun frente a una TB diseminada y compromiso medular serio, la combinación de tratamiento antituberculoso apropiado, intervenciones quirúrgicas oportunas y rehabilitación puede conducir a una recuperación funcional significativa.",
+                "fh_score": 24.78
+            }
+        }
+    },
+    {
+        "article": "Un hombre japonés de 23 años fue admitido en nuestro hospital debido al empeoramiento de la disnea de esfuerzo. Había mostrado dificultad para correr a los dos años y se le diagnosticó EDMD con una mutación genética de LMNA (Lamin A/C) en el exón 1 de leucina 102 a prolina. De acuerdo con las manifestaciones típicas de EDMD, sus codos, rodillas y tendones de Aquiles se habían contraído a los cinco años, y sus músculos cervicales posteriores se habían vuelto rígidos; sin embargo, continuó con su vida diaria habitual, aunque con una leve restricción de ejercicio. Su padre también había sido diagnosticado con EDMD y murió repentinamente a los 40 años.\n\nCuando el paciente tenía 19 años, fue admitido en un hospital por primera vez debido a una insuficiencia cardiaca congestiva. Los signos de insuficiencia de la RV, tales como edema de las piernas y congestión hepática, fueron prominentes, como lo indica el alto nivel de bilirrubina en sangre (2,5 mg/dL). La ecocardiografía mostró que la excursión sistólica del plano anular tricúspide (TAPSE) era de 5,7 mm, la velocidad de la RV de 5,1 cm/s y el cambio del área fraccional de la RV (RVFAC) del 19 %, lo que indica una marcada disfunción de la RV. Se introdujeron diuréticos de alta dosis además de carvedilol (10 mg/día) y enalapril (2,5 mg/día). A pesar de esos medicamentos, fue readmitido debido al empeoramiento de la insuficiencia de la RV.\n\nA los 22 años, se le implantó un desfibrilador cardioversor implantable (ICD) debido a su taquicardia ventricular no sostenida (VT) y a la historia familiar de muerte súbita cardiaca. En este momento, el cateterismo cardiaco derecho (RHC) mostró una presión de la cuña de la arteria pulmonar (PAWP) de 22 mmHg, presión auricular derecha (RAP) de 17 mmHg, e índice de trabajo de accidente cerebrovascular ventricular derecho (RVSWI) de 6.47, lo que sugiere una disfunción severa sostenida del RV. Como tal, el fallo del RV probablemente fue la principal condición patológica a lo largo de su curso clínico.\n\nTenía insuficiencia cardiaca sintomática con la clasificación III de la New York Heart Association con dosis máximas de medicación guiada por directrices, y su electrocardiograma mostraba un ritmo sinusal regular y bloqueo de rama izquierda con ancho QRS (150 ms). Su fracción de eyección del ventrículo izquierdo (LVEF) era ≤35 % en la ecocardiografía. Por lo tanto, se consideró que estaba indicado para CRT y se le actualizó a ICD a los 23 años.\n\nAl ingreso, su presión arterial era de 106/65 mmHg y su frecuencia cardíaca de 60 latidos/min con un ritmo regular. El examen físico reveló un tercer sonido cardíaco y un soplo pan sistólico (Levine II/VI) en la región apical. Los sonidos respiratorios eran claros, mientras que una vena yugular distendida y un edema de miembros inferiores eran evidentes. La radiografía de tórax indicó un aumento de la relación cardiotorácica (59%) sin congestión pulmonar.\n\nEl electrocardiograma mostró un ritmo biventricular debido a la TRC. La ecocardiografía reveló una ligera dilatación en ambos ventrículos (diámetro final diastólico del LV: 54 mm, diámetro del RV: 50 mm) con una reducción de la LVEF (30%). La función del RV también se redujo, como lo indican una reducción de la RVFAC (11%) y un bajo TAPSE (8 mm). Ambos ventrículos agrandados causaron una pérdida de sujeción y coaptación de las valvas que resultó en una regurgitación mitral moderada y una regurgitación tricuspídea severa. La vena cava inferior se dilató a 23 mm con una reducción de la fluctuación respiratoria.\n\nEn los hallazgos histológicos de los músculos cervicales posteriores realizados más tarde en la autopsia, se observó un aumento en la variación del tamaño de la fibra muscular con una infiltración moderada de tejido conectivo, lo que fue compatible con la EDMD. Los análisis de sangre revelaron péptido natriurético cerebral (BNP) 196.1 pg/mL, bilirrubina total 1.4 mg/dL, aspartato aminotransferasa (AST) 39 U/L, alanina aminotransferasa (ALT) 43 U/L, y gamma glutamil transpeptidasa (gamma-GTP) 451 U/L, lo que sugirió una disfunción hepática. Aunque las arterias coronarias estaban intactas en la angiografía, una biopsia endocárdica del VD reveló una hipertrofia cardiaca con un aumento de la magnitud del núcleo y el miocardio.\n\nLa microscopía electrónica demostró hallazgos típicos de la EDMD: un número reducido de miofibrillas, necrosis y la formación de pseudo- o verdaderas inclusiones. Dado que se descartaron otras cardiomiopatías secundarias mediante estos hallazgos clínicos e histológicos, diagnosticamos una cardiomiopatía relacionada con la EDMD.\n\n\nEl curso clínico del paciente. El cateterismo cardiaco derecho (RHC) en el día 11 mostró disfunción y congestión severa del LV/RV, y se iniciaron algunos inótropos. Aunque la hemodinámica del paciente mejoró, su función renal empeoró progresivamente en el día 38. Preocupados por el empeoramiento de su función renal debido a la disminución de la presión arterial, se iniciaron la dopamina y el soporte mecánico (IABP y CRRT), y la función renal y la hemodinámica del paciente mejoraron. Sin embargo, desarrolló insuficiencia hepática aguda junto con insuficiencia severa del RV indicada por los datos del RHC en el día 68. Aunque se introdujo ECMO veno-atrial en el día 71, la disfunción hepática y la DIC causaron diátesis hemorrágica sistémica, y el paciente falleció por fallo multiorgánico en el día 100. CRRT: terapia de reemplazo renal continua, DIC: coagulación intravascular diseminada, ECMO: oxigenación por membrana extracorpórea, IABP: bombeo de globo intraaórtico, LV: ventrículo izquierdo, RV: ventrículo derecho\n\nEl RHC en el día 11 mostró que el índice cardiaco (IC) era de 2,0 L/min/m2 (método de Fick), y la PAP era de 15 mmHg, lo que indicaba un subgrupo IV de Forrester. La presión arterial pulmonar (PAP) era de 29/12 (18) mmHg, y la RAP era de 15 mmHg. El RVSWI, uno de los parámetros hemodinámicos para la función del RV, se calculó con la siguiente fórmula: RVSWI (g·m/m2/latido)=[presión arterial pulmonar media (mPAP)-presión atrial derecha media (mRAP)]×índice de volumen de latido (SVI)×0.0136. Su RVSWI era de 1.36 g·m/m2/latido, lo que indicaba una disfunción severa del RV. Para compensar el síndrome de baja producción del paciente y la congestión, comenzamos una infusión continua de dobutamina (3.0 μg/kg/min) y añadimos milrinona (0.125 μg/kg/min) en el día 16.\n\n\nEn el día 32, los datos de RHC mejoraron, con un aumento del IC (2,48 L/min/m2), una reducción de la PAWP (13 mmHg) y un aumento de la RVSWI (2,8 g·m/m2/latido). Sin embargo, en el día 38, la función renal del paciente empeoró progresivamente, posiblemente debido a una presión venosa central alta (CVP) e hipotensión, ya que la presión arterial había sido de alrededor de 70/40 mmHg varios días antes del empeoramiento de la función renal. Para aumentar su presión arterial, se inició una infusión continua de dopamina (2,0 μg/kg/min); se redujo la milrinona y se interrumpieron el enalapril y la eplerenona. Además, se necesitaron temporalmente el bombeo de globo intraaórtico (IABP) y la terapia de reemplazo renal continuo (CRRT). A medida que la hemodinámica del paciente mejoró en respuesta al aumento de la saturación de oxígeno venoso mixto (SvO2, 70-80%) y el IC (3,0-3,5 L/min/m2), se retiraron el IABP y la CRRT en el día 45.\n\nSin embargo, el día 68, el IC volvió a disminuir a 1,25 l/min/m2 y la congestión pulmonar y la retención de fluidos del paciente se deterioraron; la PAWP era tan alta como la RAP, a 22 mmHg. Además, los niveles de bilirrubina en suero y las transaminasas hepáticas del paciente aumentaron drásticamente, lo que sugiere el desarrollo de insuficiencia hepática. El día 71, se inició la ECMO VA a través de una vena femoral a la arteria subclavia, pero debido a la diátesis hemorrágica sistémica acompañada por la coagulación intravascular diseminada (CID), el paciente falleció de insuficiencia multiorgánica el día 100.\n\nUna autopsia realizada con el consentimiento informado de la familia del paciente reveló un agrandamiento eferente en ambos ventrículos con un espesor de pared delgado. El examen histopatológico reveló que la hipertrofia miocárdica leve a moderada y la fibrosis severa eran evidentes en el RV y el LV. El peso del hígado aumentó significativamente a 2298 g, y se detectaron congestión hepática macroscópica y colestasis. En las imágenes microscópicas, el área de la vena porta apenas cambió, y se observó atrofia o pérdida de hepatocitos alrededor de las venas centrales, lo que indica un «hígado de shock». En los pulmones, se observó una hemorragia alveolar extensa, y se observó una colección de macrófagos que habían ingerido hemosiderina, lo que refleja una diátesis hemorrágica sistémica.\n\nMH - Adulto\nMH - Insuficiencia cardiaca/*etiología/fisiopatología/terapia\nMH - Humanos\nMH - Lamin tipo A/genética\nMH - Hombre\nMH - Distrofia muscular, Emery-Dreifuss/*complicaciones/diagnóstico/genética/terapia\nMH - Mutación\n",
+        "gold_summary": "Un hombre de 23 años tenía debilidad muscular progresiva y distrofia muscular de Emery-Dreifuss (EDMD) debido a una mutación de LMNA (lamina A/C). Insuficiencia cardiaca congestiva diagnosticada a los 19 años de edad. El tratamiento farmacológico máximo/resincronización cardiaca no logró mejorar la función cardiaca. Por lo tanto, fue hospitalizado debido a insuficiencia cardiaca. A pesar de la oxigenación por membrana extracorpórea, desarrolló una disfunción cardiaca derecha grave y falleció (fallo multiorgánico).\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había un joven japonés de 23 años con una enfermedad heredada llamada distrofia muscular de Emery-Dreifuss. Esta enfermedad hace que los músculos y también el corazón se debiliten. Desde niño tuvo problemas para moverse y con el tiempo su corazón empezó a fallar.\n\nA los 19 años su corazón ya no bombeaba bien, sobre todo el lado derecho. Le dieron medicinas y le pusieron un aparato que protege el corazón y otro que ayuda a que los dos lados latan al mismo tiempo. Aun así su estado empeoró y lo ingresaron al hospital.\n\nLos médicos usaron muchos tratamientos fuertes. Le dieron medicinas que ayudan al corazón, una máquina para apoyar la circulación, una máquina para limpiar la sangre cuando los riñones fallan y otra para ayudar a los pulmones y al corazón. Al principio mejoró, pero después su hígado y otros órganos sufrieron mucho.\n\nLamentablemente, después de varios días con cuidados intensivos presentó sangrados y una falla de varios órganos, y falleció. La autopsia mostró que los dos ventrículos del corazón estaban agrandados y con mucho daño, y que el hígado y los pulmones también estaban muy dañados por la mala circulación. Su caso muestra cómo esta forma de distrofia muscular puede afectar gravemente al corazón y a todo el cuerpo.",
+                "fh_score": 67.97
+            },
+            "B2": {
+                "text": "Here is a clear, compassionate summary of the case:\n\nA 23-year-old Japanese man had Emery–Dreifuss muscular dystrophy (EDMD). EDMD is a genetic disease that weakens muscles and causes stiff joints. His condition came from a change (mutation) in the LMNA gene, which makes a protein important for cell structure. He had muscle problems and joint contractures from early childhood, and his father—who also had EDMD—died suddenly at 40.\n\nAt 19 he developed congestive heart failure. This means his heart could not pump blood well, and fluid built up in his body. Tests showed the right side of his heart (the right ventricle, RV) was especially weak. He needed strong medicines for heart failure, but his condition later got worse again. At 22 he received an implantable cardioverter-defibrillator (ICD) because of dangerous heart rhythms and family history of sudden death. At 23, because his left heart pumping (left ventricular ejection fraction) was low and he had severe symptoms, his device was upgraded to cardiac resynchronization therapy (CRT) to try to help both sides of the heart work together.\n\nDuring the hospital stay his blood pressures and heart pressures showed severe right and left heart failure. Doctors tried many treatments: inotropic medicines (drugs that help the heart pump), dopamine and dobutamine, milrinone, a balloon pump placed in the aorta (IABP) to support circulation, continuous dialysis (CRRT) when his kidneys failed, and finally veno-arterial extracorporeal membrane oxygenation (VA-ECMO), which is an external machine that supports heart and lung function. At times his condition improved, but he later developed worsening kidney failure, then severe liver failure and a disorder of blood clotting (disseminated intravascular coagulation, DIC) that caused bleeding throughout the body.\n\nDespite all treatments, he died on day 100 of multiorgan failure. An autopsy showed both heart ventricles were enlarged with thin walls and had severe scarring (fibrosis). The liver was very congested and showed changes called “shock liver” from poor blood flow. The lungs had bleeding and signs of widespread bleeding problems.\n\nDoctors concluded his heart disease was a cardiomyopathy caused by EDMD (linked to the LMNA mutation). This report shows how a genetic muscle disease can especially damage the heart and, despite many advanced treatments, can lead to fatal heart and organ failure. My condolences to his family—this was a serious, progressive illness that proved hard to control.",
+                "fh_score": 83.92
+            },
+            "B3": {
+                "text": "Resumen clínico (lectores universitarios)\n\nPaciente: hombre japonés, 23 años. Historia familiar relevante: padre con diagnóstico de distrofia muscular de Emery–Dreifuss (EDMD) que falleció súbitamente a los 40 años. Genética: mutación heterocigota en LMNA (lamina A/C), cambio L102P (leucina 102 → prolina, exón 1).\n\nAntecedentes musculares y diagnóstico\n- Desde la infancia presentó debilidad muscular progresiva y contracturas típicas de EDMD (codos, rodillas, tendones de Aquiles; rigidez cervical), diagnóstico confirmado por hallazgos histológicos musculares (variación del tamaño de fibras y fibrosis) en la autopsia.\n- La mutación en LMNA explica la combinación de miopatía, afectación del sistema de conducción y cardiomiopatía.\n\nCurso cardíaco y hallazgos iniciales\n- A los 19 años ingresó por insuficiencia cardiaca congestiva con signos predominantes de insuficiencia del ventrículo derecho (RV): edema, congestión hepática y bilirrubina elevada (2,5 mg/dL).\n- Ecocardiografía inicial: marcada disfunción del RV (TAPSE 5,7 mm; velocidad tisular RV 5,1 cm/s; RVFAC 19%).\n- Se inició tratamiento médico (diuréticos, carvedilol, enalapril) pero con episodios recurrentes de descompensación.\n\nArritmias y dispositivos\n- A los 22 años recibió un desfibrilador cardioversor implantable (ICD) por taquicardia ventricular no sostenida y antecedentes familiares de muerte súbita.\n- Debido a insuficiencia cardiaca sintomática (NYHA III), LVEF ≤35% y bloqueo de rama izquierda con QRS ancho (150 ms), se actualizó a resincronizador (CRT‑D) a los 23 años.\n\nIngreso y evaluación hemodinámica reciente\n- Al ingreso presentaba hipotensión relativa (106/65 mmHg), ritmo biventricular por CRT, hepatomegalia congestiva, vena yugular distendida y edema. Radiografía: cardiomegalia (ITC 59%) sin edema pulmonar marcado.\n- Ecocardiograma: dilatación leve de ambos ventrículos, LVEF ≈30%, RV muy deteriorado (RVFAC 11%, TAPSE 8 mm), insuficiencia tricuspídea severa secundaria a dilatación.\n- Laboratorio: BNP elevado (196 pg/mL), enzimas hepáticas y gamma‑GTP marcadamente elevadas (gamma‑GTP 451 U/L), signos de disfunción hepática.\n- Angiografía coronaria normal; biopsia endomiocárdica del RV mostró hipertrofia miocárdica, necrosis y en la microscopía electrónica hallazgos característicos de EDMD (pérdida de miofibrillas e inclusiones).\n\nEvolución hospitalaria y terapias avanzadas\n- RHC (día 11): bajo índice cardíaco (IC 2,0 L/min/m2 por Fick), RAP y PAWP elevadas; RVSWI muy reducido (1,36 g·m/m2/latido), consistente con insuficiencia grave del RV. Se inició dobutamina y luego milrinona.\n- Respuesta transitoria: mejoría hemodinámica (IC 2,48 L/min/m2, RVSWI 2,8 g·m/m2/día 32). Posteriormente empeoramiento renal (probablemente por hipotensión sostenida y alta presión venosa central) → dopamina, suspensión de inhibidores del SRA, IABP e inicio de terapia de reemplazo renal continua (CRRT). Estas medidas mejoraron la hemodinámica y se retiraron IABP/CRRT.\n- Recaída y órgano terminal: en día 68 nuevo descenso del IC (1,25 L/min/m2), agravamiento de congestión y colestasis/hepatopatía aguda. Se instauró ECMO veno‑arterial (día 71), pero el paciente desarrolló coagulación intravascular diseminada (CID) con diátesis hemorrágica y falleció por fallo multiorgánico en el día 100.\n\nHallazgos post‑mortem\n- Corazón: dilatación biventricular con paredes adelgazadas; histología con fibrosis severa y moderada hipertrofia en ambos ventrículos.\n- Hígado: peso aumentado (2298 g), congestión macroscópica, colestasis y atrofia centrolobulillar de hepatocitos compatible con “hígado de shock” por congestión/hipoperfusión.\n- Pulmones: hemorragia alveolar extensa y macrófagos con hemosiderina (reflejan diátesis hemorrágica).\n- Musculatura cervical: cambios compatibles con EDMD.\n\nInterpretación y lecciones clínicas (implicaciones)\n- En esta persona la cardiomiopatía relacionada con LMNA/EDMD se presentó con afectación dominante del ventrículo derecho y evolución fulminante pese a terapia médica óptima y resincronización. Las mutaciones en LMNA predisponen a arritmias malignas y a una cardiomiopatía progresiva que puede no responder a terapias convencionales.\n- Puntos clínicos relevantes para casos similares: vigilancia temprana y seriada de la función del RV (ecocardiografía y, si procede, RHC), consideración precoz de derivación a trasplante o asistencia ventricular cuando existe disfunción biventricular progresiva y falla orgánica recurrente, y cribado genético/familiar y asesoramiento genético por el riesgo hereditario.\n- El caso también subraya las limitaciones de las terapias de soporte (inótropos, IABP, ECMO) cuando la miocardiopatía está avanzada y la fibrosis es extensa, y los riesgos de complicaciones como CID y fallo multiorgánico.\n\nComentario humano y empatía\nEste caso ejemplifica la carga grave y rápida que puede comportar la cardiomiopatía por LMNA en pacientes jóvenes con EDMD. A pesar de intervenciones agresivas y tecnología avanzada, la enfermedad puede progresar a insuficiencia orgánica irreversible. El manejo óptimo incluye vigilancia cardiaca estrecha, planificación anticipada de terapias avanzadas y apoyo a la familia con información y asesoramiento genético.",
+                "fh_score": 38.18
+            }
+        }
+    },
+    {
+        "article": "Mujer de 65 años sin antecedentes patológicos destacables que en 2004 inició paroxismos lancinantes en los territorios V2 y V3 derechos, con desencadenantes clásicos, por lo que se le diagnosticó una neuralgia del trigémino derecho. En las resonancias magnéticas cerebrales hasta 2021 no se habían realizado las secuencias que permiten identificar si hay un cruce neurovascular. Desde el inicio, el control del dolor con carboxamidas fue difícil. En 2021 presentó exacerbación de los paroxismos previos que aparecieron en V1. La neuralgia se volvió refractaria, sin respuesta a las carboxamidas y la lamotrigina, y muy escasa al clonacepam, por lo que requirió perfusiones de fenitoína y/o lidocaína en las exacerbaciones graves. Simultáneamente inició paroxismos lancinantes en la parte posterior de la lengua y la pared lateral derecha de la orofaringe, que se exacerbaron con la deglución y que aumentaron progresivamente en intensidad y frecuencia. Se orientó como el inicio de una neuralgia del nervio glosofaríngeo derecho. Se repitió la resonancia magnética cerebral con secuencia CISS (del inglés, constructive interference in steady state), que mostró un contacto arterial significativo entre la arteria cerebelosa superior derecha y el origen del V par craneal derecho, y de la arteria cerebelosa anteroinferior con el origen de los pares craneales bajos derechos. Ante un caso de neuralgia del nervio trigémino y neuralgia del nervio glosofaríngeo clásicas, concomitantes y refractarias, se planteó una doble descompresión microvascular en un tiempo como mejor opción terapéutica.\n\nEn marzo de 2021 se realizó una craniectomía retrosigmoidea derecha con exposición de la cisterna perimesencefálica y las cisternas basales. Se procedió a la liberación del V par craneal, y se apreció un íntimo contacto con la arteria cerebelosa superior en su parte sensitiva y adelgazamiento en la zona de entrada de la raíz nerviosa. Se procedió a la colocación de teflón entre la arteria cerebelosa superior y el V par craneal en todo su trayecto. Posteriormente, se exploró la cisterna basal y se apreció loop vascular de la arteria cerebelosa anteroinferior en íntimo contacto con el IX par craneal, donde se colocó teflón y sellante dural encima. El postoperatorio cursó sin incidencias, con resolución completa de la neuralgia del nervio trigémino y reducción >50% de la intensidad de los paroxismos en el territorio glosofaríngeo. A los dos años continúa sin paroxismos trigeminales y presenta <1 paroxismo/mes de intensidad tolerable en el territorio glosofaríngeo desencadenado con la deglución. El tratamiento farmacológico continúa en pauta descendente sin que ello haya supuesto la reaparición de los paroxismos.",
+        "gold_summary": "Mujer de 65 años con NT derecho (inicialmente en V2-V3) desde 2004 con control regular con carboxamidas. Diecisiete años después empeoraron los paroxismos en V2-V3, aparecieron también en V1 y en el territorio del nervio glosofaríngeo derecho (oído derecho y fosa amigdalar al hablar y deglutir). La resonancia magnética cerebral mostró contacto arterial significativo entre arteria cerebelosa superior (ACS) con origen del V par craneal derecho y de la arteria cerebelosa antero-inferior (AICA) con el origen de pares craneales bajos derechos. Se realizó DMV de ambos pares craneales en un mismo tiempo quirúrgico mediante craniectomía retrosigmoidea, y se procedió a la liberación del V par craneal, en contacto íntimo con la ACS, y del IX par craneal en contacto con la AICA derecha, para lo que se puso teflón entre ellas. La paciente tuvo una resolución inmediata de los paroxismos trigeminales y una mejoría considerable en intensidad y frecuencia de los glosofaríngeos. A los 2 años de la intervención continúa la desescalada de tratamiento neuromodulador con buena respuesta.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Esta es la historia de una mujer de 65 años que tuvo dolores muy fuertes y repentinos en la cara desde 2004. Esos dolores se llaman neuralgia del trigémino. Al principio los medicamentos ayudaban, pero con los años los dolores empeoraron. En 2021 empezó también a tener pinchazos muy fuertes en la parte de atrás de la lengua y la garganta al tragar. Los medicamentos ya no bastaban.\n\nLos médicos hicieron una resonancia especial y vieron que dos arterias tocaban los nervios que causaban el dolor. Esto puede provocar esos pinchazos. Decidieron hacer una operación pequeña en la parte de atrás de la cabeza. Durante la cirugía separaron las arterias de los nervios y pusieron una pequeña almohadilla de material (teflón) para que no se volvieran a rozar.\n\nDespués de la operación se fue el dolor de la cara por completo. Los pinchazos en la lengua y la garganta bajaron mucho (más del 50%). Dos años después sigue sin dolor en la cara y casi no tiene ataques en la garganta (menos de uno al mes y tolerable). Los médicos han bajado poco a poco los medicamentos y ella está bien.",
+                "fh_score": 78.76
+            },
+            "B2": {
+                "text": "Resumen comprensible (nivel B2)\n\nUna mujer de 65 años empezó en 2004 con episodios de dolor punzante, breves y muy intensos en la cara, localizados en las zonas V2 y V3 del nervio trigémino derecho (V2 = zona media de la cara, V3 = mandíbula). Al principio los analgésicos habituales (como la carbamazepina) funcionaban con dificultad. En 2021 el dolor empeoró: los episodios aparecieron también en V1 (zona superior de la cara) y comenzaron además dolores parecidos en la parte posterior de la lengua y la pared lateral derecha de la garganta al tragar, compatibles con neuralgia del nervio glosofaríngeo. Los medicamentos dejaron de controlar bien los ataques; en crisis graves requirió perfusiones de fenitoína o lidocaína.\n\nSe repitió una resonancia magnética con una secuencia especial (CISS) que permitió ver contactos importantes entre vasos sanguíneos y nervios: la arteria cerebelosa superior tocaba el origen del nervio trigémino derecho, y la arteria cerebelosa antero-inferior estaba en íntimo contacto con los nervios craneales bajos (incluido el glosofaríngeo) del lado derecho. Este tipo de contacto vascular puede causar los dolores paroxísticos.\n\nComo los dos tipos de neuralgia eran clásicos, simultáneos y resistentes a fármacos, se decidió realizar una descompresión microvascular (cirugía para separar el vaso del nervio). En marzo de 2021 se hizo una craniectomía retrosigmoidea derecha (acceso por detrás del oído). Durante la operación se colocaron pequeñas almohadillas de teflón entre la arteria y cada nervio para evitar el roce directo.\n\nEl postoperatorio fue bueno. El dolor trigeminal desapareció por completo y el dolor glosofaríngeo mejoró más del 50% en intensidad y frecuencia. A los dos años la paciente sigue sin ataques trigeminales y tiene menos de uno por mes de dolor en la garganta, de intensidad tolerable y desencadenado al tragar. Los medicamentos se están reduciendo progresivamente sin que los dolores reaparezcan.\n\nComentario final: La descompresión microvascular puede ser una opción eficaz cuando la neuralgia facial o glosofaríngea está causada por el roce de una arteria sobre el nervio y no responde a medicación. El seguimiento clínico y la disminución controlada de fármacos son pasos habituales tras una buena respuesta quirúrgica.",
+                "fh_score": 49.53
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel universitario, lectura B3)\n\nPresentación\n- Paciente: mujer de 65 años, sin antecedentes relevantes.\n- Historia: desde 2004 presentó neuralgia del trigémino derecho con paroxismos lancinantes en los territorios V2 y V3, con desencadenantes típicos (p. ej., tacto, masticación). El dolor fue difícil de controlar con carboxamidas (p. ej., carbamazepina).\n- En 2021 hubo empeoramiento: los paroxismos se extendieron a V1 y aparecieron además episodios dolorosos en la parte posterior de la lengua y la pared lateral derecha de la orofaringe, provocados y agravados por la deglución. Estos hallazgos orientaron a neuralgia glosofaríngea derecha concomitante.\n\nInvestigaciones\n- Resonancias magnéticas previas no incluían secuencias de alta resolución para ver un contacto neurovascular.\n- Se repitió la RM con secuencia CISS (secuencia de alta resolución que muestra bien vasos y raíces nerviosas). Encontró:\n  - Compresión significativa del nervio trigémino derecho por la arteria cerebelosa superior (ACS) en su zona sensitiva, con adelgazamiento de la raíz.\n  - Un asa de la arteria cerebelosa anteroinferior (AICA) en íntimo contacto con las raíces de los pares craneales bajos derechos (incluido el IX).\n\nTratamiento quirúrgico\n- En marzo de 2021 se realizó una descompresión microvascular (DMV) por vía retrosigmoidea derecha en un solo tiempo para ambos nervios.\n- Hallazgos operatorios: contacto íntimo y daño por compresión del V por la ACS; asa de AICA en contacto con el IX.\n- Procedimiento: se colocó material de teflón entre cada arteria y la raíz nerviosa afectada (con sellante dural sobre la colocación en la zona del IX).\n\nEvolución y resultado\n- Postoperatorio sin complicaciones inmediatas.\n- Resultado precoz: resolución completa de los paroxismos trigeminales y reducción >50% de la intensidad de los episodios glosofaríngeos.\n- A los 2 años: ausencia de paroxismos trigeminales; menos de 1 paroxismo glosofaríngeo por mes, de intensidad tolerable y desencadenado por la deglución. El tratamiento farmacológico se ha ido reduciendo (desescalada) sin recrudecimiento de los síntomas.\n\nInterpretación y consideraciones\n- El caso ilustra una neuralgia trigeminal y una neuralgia glosofaríngea clásicas causadas por conflicto neurovascular (arterias en contacto directo con la raíz nerviosa). Estas condiciones pueden volverse refractarias a medicación y requerir intervención quirúrgica.\n- La descompresión microvascular, que separa el vaso de la raíz nerviosa y coloca un acolchado (teflón), es una opción terapéutica eficaz en casos refractarios y en este caso logró un control clínico sostenido a 2 años.\n- Seguimiento recomendável: control neurológico y neuroquirúrgico para monitorizar recurrencias, manejo gradual de fármacos y vigilancia de posibles complicaciones tardías aunque la paciente no las presentó hasta el momento informado.",
+                "fh_score": 46.8
+            }
+        }
+    },
+    {
+        "article": "Hombre de 36 años, bisexual, en profilaxis antirretroviral de pre-exposición al HIV, sin antecedentes de viaje, que refirió haber asistido a un evento donde tuvo contactos con parejas ocasionales cuya identidad y antecedentes se desconocen. Diez días después comenzó con fiebre, odinofagia y dolor cervical por lo que consultó en varias oportunidades, hasta que a los siete días del inicio de los síntomas se internó por persistencia de los mismos a pesar del tratamiento antibiótico indicado. Al ingreso presentó exudado faríngeo, adenopatías cervicales bilaterales dolorosas y pápulas umbilicadas en escroto y pene y pústulas en cara de cinco días de evolución. Se realizó tomografía computarizada de cuello con contraste endovenoso que descartó colección, ecografía abdominal con leve hepatoesplenomegalia, e inició tratamiento empírico con ceftriaxona y azitromicina. Se tomaron muestras para cultivo, para serologías, y escarificación de dos lesiones de la cara que se enviaron al Laboratorio Nacional de Referencia, INEI-ANLIS Dr. Carlos G. Malbrán, para PCR de punto final para Orthopoxvirus, con resultado DETECTABLE, confirmando así el diagnóstico de viruela símica. La secuenciación arrojó un alto porcentaje de homología con secuencias del clado de África Occidental (MPV-ARG003-2022, Genbank_ID ON800897). Otros diagnósticos diferenciales fueron descartados. El paciente evolucionó con aparición de una úlcera en lengua y nuevas lesiones asincrónicas en glúteos, región perianal, inguinal derecha, umbilical, frontal, cuello, mano derecha y dorso de pie en un total de no más de 25. En el laboratorio se constató un aumento de transaminasas en 2.2 veces el valor normal, sin otros datos significativos.  Por persistencia del dolor cervical se solicitó nueva tomografía computarizada a los 14 días del inicio de los síntomas que evidenció adenomegalias con centro hipodenso de aspecto necrótico, que no requirieron drenaje quirúrgico. Al día 17 se realizó PCR en muestras de exudado de fauces y semen las que también resultaron positivas para virus de viruela símica. Se externó con franca mejoría clínica dos días después. El paciente dio su consentimiento informado escrito para la publicación de este informe de caso y las imágenes que lo acompañan.",
+        "gold_summary": "Se trata de un hombre joven, bisexual, en profilaxis antirretroviral de pre-exposición al HIV, cuya forma de presentación fue faringitis exudativa sin otra etiología documentada y adenopatías que evolucionaron a la necrosis, presencia de lesiones asincrónicas características en cara, cuello, abdomen, extremidades y genitales. El diagnóstico fue por detección de ADN viral por reacción en cadena de la polimerasa en lesiones de piel, exudado de fauces y semen. El compromiso faríngeo con presencia de exudado luego del descarte de otras infecciones, podría ser una rareza para la forma epidémica de la enfermedad. El hallazgo del virus en semen ya reportado en otras publicaciones no es suficiente aún para confirmar la vía sexual como forma de trasmisión.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "This is a simple story about a man of 36 years. He takes medicine to help prevent HIV. He went to an event and had contact with people he did not know. Ten days later he had fever, sore throat, and neck pain.\n\nWhen he went to the hospital, doctors found white stuff in his throat, painful swollen neck glands, and small bumps and pus spots on his face and private parts. Scans showed no pus collection, but his liver and spleen were a little big. Blood tests showed his liver enzymes were a bit high.\n\nDoctors tested skin sores and other samples. A lab test found monkeypox virus. The virus’s genetic code matched the West African type. The virus was also found in a throat sample and in semen. Finding the virus in semen does not prove that sex is how it spreads.\n\nHe developed new skin sores in several places, and one sore on his tongue. Some neck glands looked damaged on a later scan, but they did not need surgery. He got better with time and went home two days after the last test. Other possible illnesses were ruled out.",
+                "fh_score": 109.11
+            },
+            "B2": {
+                "text": "Resumen claro y amable:\n\nUn hombre de 36 años que usa profilaxis previa al VIH (PrEP) asistió a un evento donde tuvo contacto con parejas ocasionales. Diez días después empezó con fiebre, dolor de garganta y dolor en el cuello. Siete días tras el inicio de los síntomas fue internado porque no mejoraba con antibióticos.\n\nAl ingreso tenía pus en la garganta (exudado), ganglios dolorosos en ambos lados del cuello y lesiones en piel: pequeñas pápulas con hoyuelo en escroto y pene, y pústulas en la cara. Se hicieron estudios por imágenes: una tomografía de cuello descartó una colección purulenta y una ecografía abdominal mostró el hígado y bazo algo aumentados. Empezó tratamiento antibiótico mientras se recogían muestras para pruebas.\n\nEl laboratorio nacional detectó ADN de Orthopoxvirus por PCR en dos lesiones de la cara, confirmando infección por viruela símica (mpox). La secuenciación del virus mostró gran semejanza con el clado (variante) de África Occidental. Otros diagnósticos posibles fueron descartados. Durante la evolución apareció una úlcera en la lengua y nuevas lesiones en glúteos, región perianal, ingle, ombligo, frente, cuello, mano y pie, hasta unas 25 en total. Un análisis de sangre mostró aumento moderado de las enzimas hepáticas.\n\nA los 14 días una nueva tomografía mostró ganglios con zonas de aspecto necrosado (áreas donde el tejido estaba dañado), pero no fue necesario realizar cirugía. El día 17 se encontró PCR positiva para el virus en exudado de garganta y en semen. Dos días después el paciente fue dado de alta por clara mejoría. El hallazgo del virus en semen se ha visto en otros estudios, pero por ahora no basta para probar que la transmisión sea sexual. La presentación con pus en la garganta, tras descartar otras infecciones, puede ser menos común en los brotes actuales.",
+                "fh_score": 65.89
+            },
+            "B3": {
+                "text": "Resumen clínico breve\nUn hombre de 36 años, bisexual y en profilaxis preexposición para VIH (PrEP), asistió a un evento con contactos sexuales ocasionales. Diez días después desarrolló fiebre, odinofagia (dolor al tragar) y dolor cervical. Siete días tras el inicio de los síntomas fue internado por persistencia pese a tratamiento antibiótico.\n\nHallazgos clave al ingreso\n- Exudado faríngeo y adenopatías cervicales bilaterales dolorosas.  \n- Lesiones cutáneas: pápulas umbilicadas en escroto y pene; pústulas en la cara (5 días de evolución).  \n- Tomografía de cuello inicial: sin colección. Ecografía abdominal: leve hepatoesplenomegalia.  \n- Laboratorio: aumento moderado de transaminasas (≈2,2× el valor normal); resto sin hallazgos significativos.\n\nDiagnóstico microbiológico y genético\n- PCR final para Orthopoxvirus en lesiones cutáneas: detectable → diagnóstico confirmado de viruela símica (monkeypox).  \n- Secuenciación: alta homología con el clado de África Occidental (MPV-ARG003-2022, Genbank ID ON800897).  \n- PCR posterior positiva también en exudado de fauces y en semen.\n\nEvolución clínica\n- Aparecieron nuevas lesiones asincrónicas (máx. 25 en total) en lengua (úlcera), glúteos, región perianal, inguinal, abdomen, cara, cuello y extremidades.  \n- A los 14 días, nueva TC mostró adenomegalias con centros hipodensos de aspecto necrótico; no requirieron drenaje quirúrgico.  \n- Mejoría clínica progresiva; egresó dos días después de la PCR positiva en orina y semen. El paciente prestó consentimiento para la publicación del caso.\n\nInterpretación y consideraciones prácticas\n- Presentación atípica: la afectación faríngea con exudado como manifestación predominante, después de descartar otras infecciones, es poco frecuente en la forma epidémica descrita de viruela símica y debe alertar al clínico.  \n- Detección viral en semen confirma presencia de ARN/ADN viral en ese fluido, pero no prueba por sí sola la vía sexual de transmisión; otros estudios epidemiológicos y virológicos son necesarios para documentarla.  \n- La evolución fue moderada y no requirió intervenciones invasivas ni terapia antiviral específica en este caso; hubo un aumento leve-moderado de transaminasas que conviene monitorizar.  \n- Implicaciones de salud pública: identificar y notificar contactos sexuales, ofrecer pruebas a parejas potencialmente expuestas y aconsejar medidas de aislamiento y prácticas sexuales seguras hasta resolución de lesiones son pasos razonables en la gestión de casos confirmados.\n\nRecomendaciones para manejo y seguimiento (generales)\n- Confirmar diagnóstico por PCR en lesiones cutáneas; considerar muestreo adicional (fauces, semen) según contexto clínico.  \n- Vigilar signos de complicación (infección secundaria, compromiso mucoso extenso, linfadenopatía necrotizante, alteración hepática).  \n- Control de laboratorio seriado (función hepática) y seguimiento clínico hasta cicatrización completa de las lesiones.  \n- Notificar a salud pública y realizar rastreo de contactos sexuales; ofrecer consejería sobre reducción de riesgo y pruebas para ITS/VIH según corresponda.\n\nTono final\nEl caso ilustra una forma de presentación algo atípica de viruela símica —predominio de faringitis exudativa y adenopatías que evolucionaron a necrosis— y subraya la importancia de considerar este diagnóstico ante la combinación de síntomas sistémicos, adenopatías y lesiones genitales o cutáneas; asimismo muestra que la detección del virus en semen, aunque relevante, no aclara por sí sola las rutas de transmisión.",
+                "fh_score": 38.59
+            }
+        }
+    },
+    {
+        "article": "Paciente de sexo masculino de 23 años, natural de Itagüí - Colombia, antecedente familiar de muerte súbita de etiología no clara en abuelo a los 50 años, sin otros antecedentes familiares o personales de importancia. Venía en seguimiento externo por episodios sincopales a repetición con diagnóstico desde la infancia de disfunción del nodo sinusal sintomática por lo que se le implantó un marcapaso.\n\nDurante controles posteriores no hay reporte de deterioro de clase funcional hasta el año 2012 en Guayaquil-Ecuador. Durante su hospitalización se realiza el cambio de generador; en el primer mes postoperatorio presenta como complicación temprana una infección de bolsillo de marcapaso por lo que requirió el explante de la unidad generadora con posterior abandono de electrodo ventricular previamente implantado. Se realiza un nuevo implante de marcapaso en el lado contralateral sin complicaciones ni registro de nuevos eventos sincopales en los siguientes 10 años de seguimiento.\n\nSeis meses antes del ingreso presentaba deterioro de clase funcional NYHA III, sin otros síntomas y sin reportes de evaluaciones por servicio de electrofisiología desde el último implante de generador de marcapaso en 2012. Durante controles ambulatorios se reportó la suspensión del tratamiento con beta bloqueador debido a la pobre tolerancia.\n\nAl examen físico se encontró soplo sistólico en foco aórtico II/VI sin irradiación, no presentó signos de congestión central o periférica. Dentro de los laboratorios no se evidenció alteración en función renal, electrolítica ni del perfil hematológico. Se programó el marcapaso con evidencia de agotamiento de la batería de generador. Se realizó un ecocardiograma transtorácico donde se encontró hipertrofia concéntrica severa del septum interventricular a nivel medio ventricular, de 26 mm con gradiente intracavitario pico de 117 mmHg y movimiento sistólico anterior del velo mitral (SAM) el cual generaba una regurgitación mitral leve.\n\nFue evaluado por Heart Team, debido al score de riesgo de muerte súbita (16,8%) además de tener antecedentes familiares de muerte súbita considerando EUROSCORE II 0,67%; en cuanto a los electrodos abandonados previamente y la contraindicación de realización de resonancia magnética cardiaca, dado a la incompatibilidad del marcapaso, se realiza un estudio tomográfico y se consideró la realización de miectomía por sintomatología y variante documentada.\n\nFue programado para realización de miectomía medio ventricular por abordaje transapical con retiro de electrodos; se realizó la ventriculotomía izquierda en el ápex, con posterior resección del septum desde el parte medio ventricular hasta la base, con posterior retiro de electrodos adheridos a velo septal tricúspideo. No hubo complicaciones intraoperatorias y posteriormente se presentó disminución del gradiente intracavitario sin presencia del fenómeno SAM. Durante su estancia en Unidad de Cuidados Intensivos el paciente cursó con dos episodios documentados de taquicardia ventricular con inestabilidad hemodinámica por lo cual se le colocó un cardiodesfibrilador implantable (CDI) compatible con resonancia magnética (MRI) ST Jude sin presentar nuevos episodios de TV. El paciente cursó sin nuevas intercurrencias y se iniciaron los estudios ambulatorios de estudio genético debido a sus antecedente familiares.\n\nEl paciente presentó una evolución posoperatoria favorable luego del implante de CDI. En los estudios genéticos se encontró una variante, probablemente patogénica, en heterocigosis del FLNC, c 4636G>A consistente con miocardiopatía familiar hipertrófica tipo 26 autosómica dominante.\n\nActualmente, el paciente se encuentra en clase funcional I, sin arritmias evidenciadas en la telemetría y en tratamiento regular con Bisoprolol 5 mg. Se inició ampliación de estudio genético a familiares directos, sin embargo, debido al difícil acceso a servicios de salud su ejecución fue limitada.",
+        "gold_summary": "A continuación, se presenta el caso de un paciente sexo masculino de 23 años con diagnóstico de cardiomiopatía hipertrófica variante medio apical, en quien se documenta variante de la filamina C, ante la inadecuada respuesta y persistencia de sintomatología frente al manejo médico, se realizó el procedimiento de miectomía con abordaje transapical, con posterior mejoría de sintomatología clínica y obstrucción al tracto de salida.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Este es un resumen sencillo y amable del caso.\n\nUn joven de 23 años tenía desde niño desmayos porque su corazón a veces no marcaba bien el ritmo. Le pusieron un marcapasos, que es una pequeña máquina que ayuda al corazón a latir. Más tarde tuvo una infección en el lugar del marcapasos y le cambiaron el aparato y los cables.\n\nA los 23 años empezó a cansarse mucho al hacer cosas normales. Un ecocardiograma (una ecografía del corazón) mostró que el músculo del corazón, sobre todo en el tabique entre las dos cámaras, estaba muy grueso. Ese músculo grueso hacía que la sangre se encontrara con una “pared” dentro del corazón. También una parte de la válvula se movía de forma incorrecta y dejaba pasar un poco de sangre. Todo esto podía explicar por qué se cansaba y tenía riesgo de problemas con el ritmo del corazón.\n\nLos médicos decidieron hacer una operación llamada miectomía. En esa operación quitaron una parte del músculo muy grueso para dejar más espacio para la sangre. También retiraron unos cables viejos que estaban pegados. La operación salió bien. Después de la cirugía el flujo de sangre mejoró y la válvula dejó de moverse mal.\n\nEn cuidados intensivos tuvo dos episodios de latidos peligrosos llamados taquicardia ventricular. Para cuidarlo mejor le pusieron un desfibrilador implantable (un aparato que puede dar una descarga si el corazón tiene un latido muy peligroso). Luego no presentó más episodios.\n\nLos estudios genéticos mostraron un cambio en un gen llamado FLNC. Ese cambio puede causar una forma de “miocardiopatía hipertrófica”, que significa que el músculo del corazón tiende a volverse más grueso. Esta enfermedad puede pasar de padres a hijos. Por eso empezaron a ofrecer pruebas a la familia, aunque fue difícil que todos pudieran hacerse los estudios.\n\nHoy el paciente está bien. Se cansa menos y está en buena clase funcional. Toma un medicamento para el corazón (bisoprolol). Los médicos siguen revisándolo y buscan ayudar a su familia con las pruebas genéticas.\n\nSi tienes preguntas sobre alguna palabra, puedo explicarla con más calma.",
+                "fh_score": 71.22
+            },
+            "B2": {
+                "text": "Resumen (nivel B2, lenguaje claro y cuidado)\n\nSe presenta el caso de un hombre de 23 años con antecedentes de desmayos desde la infancia por un problema del nodo sinusal (el marcapasos natural del corazón), por lo que tenía un marcapasos. Tenía además antecedente familiar de muerte súbita en un abuelo. Tras un recambio de generador en 2012 sufrió infección del bolsillo del marcapasos, se retiró el generador y se dejó un electrodo ventricular abandonado; se colocó después un nuevo marcapasos en el otro lado y estuvo sin eventos durante 10 años.\n\nSeis meses antes del ingreso empeoró su capacidad para hacer actividad física (clase funcional NYHA III). Un ecocardiograma mostró hipertrofia severa del tabique entre los ventrículos (26 mm) con una obstrucción dentro de la cavidad del ventrículo izquierdo que producía un gradiente elevado (117 mmHg). Además había movimiento sistólico anterior (SAM) de la válvula mitral, que favoreció una insuficiencia mitral leve. El marcapasos y los electrodos abandonados impedían hacer una resonancia magnética, por lo que se solicitó una tomografía.\n\nEl equipo médico decidió una miectomía medio-ventricular por vía transapical (cirugía para resecar el músculo hipertrofiado desde el ápex —la punta— del corazón) y retirar los electrodos adheridos. La cirugía transcurrió sin complicaciones y redujo la obstrucción; el fenómeno SAM desapareció. En el posoperatorio presentó dos episodios de taquicardia ventricular con inestabilidad (arritmias peligrosas), por lo que se le implantó un desfibrilador automático implantable (CDI) compatible con resonancia magnética. Tras el implante no tuvo nuevas arritmias.\n\nEl estudio genético mostró una variante probablemente patogénica en el gen FLNC (miocardiopatía hipertrófica tipo 26, herencia autosómica dominante). Se inició el rastreo genético en familiares, aunque el acceso a pruebas fue limitado. Actualmente el paciente está en clase funcional I (sintomático mínimo o ninguno), toma bisoprolol 5 mg y no se han registrado arritmias en la monitorización.\n\nComentarios finales sencillos\n- La cirugía (miectomía) fue necesaria porque el músculo del corazón estaba obstruyendo el flujo y los síntomas empeoraban pese al tratamiento médico.  \n- La variante genética encontrada puede explicar la enfermedad y hace importante ofrecer pruebas a familiares directos.  \n- El desfibrilador se colocó como prevención ante el riesgo de arritmias graves y muerte súbita.  \n\nSi tienes dudas sobre algún término médico, puedo explicarlo con más detalle.",
+                "fh_score": 47.04
+            },
+            "B3": {
+                "text": "Resumen clínico\n\nPaciente masculino de 23 años, con antecedente de síncopes desde la infancia que motivaron el implante de un marcapasos por disfunción del nodo sinusal. Historia importante: cambio de generador en 2012 complicado por infección de bolsillo que obligó a explante del generador y abandono del electrodo ventricular; luego se implantó un nuevo marcapasos en el lado contralateral y estuvo estable 10 años. Antecedente familiar relevante: abuelo con muerte súbita a los 50 años.\n\nPresentación y hallazgos principales\n- Seis meses antes del ingreso el paciente empeoró su clase funcional a NYHA III (disnea con actividad cotidiana). Se había suspendido un betabloqueador por mala tolerancia.  \n- En el examen físico solo se objetivó un soplo sistólico aórtico II/VI; sin signos de congestión.  \n- Ecocardiograma transtorácico: hipertrofia septal concéntrica severa (septum 26 mm), gradiente intraventricular pico 117 mmHg (obstrucción importante del tracto de salida del ventrículo izquierdo) y presencia de movimiento sistólico anterior (SAM) de la valva mitral, con regurgitación mitral leve.  \n- El marcapasos mostraba agotamiento de batería; además, los electrodos abandonados y la incompatibilidad con resonancia magnética llevaron a realizar un estudio tomográfico para evaluar la anatomía.  \n- Score de riesgo de muerte súbita calculado en 16,8% (riesgo aumentado); EUROSCORE II 0,67% (bajo riesgo quirúrgico).\n\nDecisión terapéutica y procedimiento\n- Tras evaluación por Heart Team y dada la sintomatología refractaria y la obstrucción documentada, se decidió realizar una miectomía medio-ventricular por abordaje transapical y retirar los electrodos abandonados.  \n- Durante la cirugía se hizo ventriculotomía apical izquierda, resección del septum desde la zona media hasta la base y extracción de electrodos adheridos. No hubo complicaciones intraoperatorias y el SAM desapareció con disminución del gradiente intraventricular.\n\nEventos posoperatorios y manejo adicional\n- En UCI presentó dos episodios de taquicardia ventricular con inestabilidad hemodinámica; por esto se implantó un cardiodesfibrilador implantable (CDI) compatible con resonancia magnética (marca St. Jude). Tras el implante no se registraron nuevas taquiarritmias.  \n- Evolución posterior favorable: paciente en clase funcional I, sin arritmias en telemetría y en tratamiento con bisoprolol 5 mg.\n\nHallazgo genético y recomendaciones\n- El estudio genético detectó una variante probablemente patogénica heterocigota en FLNC (c.4636G>A), consistente con miocardiopatía hipertrófica familiar tipo 26 de herencia autosómica dominante.  \n- Implicaciones: la variante en FLNC explica la cardiomiopatía y aumenta el riesgo arrítmico; se recomienda estudio genético y seguimiento cardiológico en familiares de primer grado (cribado y consejería genética). En este caso, la extensión del estudio familiar fue limitada por dificultades de acceso a servicios de salud.\n\nInterpretación y pasos siguientes\n- Diagnóstico final: miocardiopatía hipertrófica con obstrucción septal medio-ventricular, complicación arrítmica posoperatoria que requirió CDI, y variante probablemente patogénica en FLNC.  \n- El procedimiento quirúrgico resolvió la obstrucción y mejoró la capacidad funcional; el CDI fue necesario por episodios de taquicardia ventricular.  \n- Recomendaciones clínicas: seguimiento cardiológico periódico (función ventricular, síntomas, registro de arritmias por el CDI), optimización del tratamiento farmacológico según tolerancia, y realización de estudio genético y evaluación cardiológica a familiares directos para detección precoz y manejo preventivo.\n\nComentario empático\nEl paciente tuvo una mejora clínica clara tras la cirugía y el control de arritmias, pero el hallazgo genético tiene implicaciones familiares importantes. Se sugiere apoyo para facilitar el acceso al cribado y a la consejería genética de sus familiares cercanos, dado el potencial riesgo hereditario.",
+                "fh_score": 33.89
+            }
+        }
+    },
+    {
+        "article": "Varón de 32 años, con antecedentes de infección por VIH en terapia anti-retroviral (carga viral indetectable y recuento de CD4 de 454 céls/mm3) y consumo de tabaco y drogas (marihuana, éxtasis y ketamina). Consultó en nuestra unidad de salud sexual por una historia de dos semanas de secreción uretral de aspecto mucoso con escaso ardor local, asociado a una úlcera eritematosa indurada en el surco balanoprepucial de 1,5 cm de diámetro, dolorosa y exudativa. Al examen físico presentaba una adenopatía inguinal izquierda de 2 cm, sensible a palpación, blanda, no adherida a planos profundos ni asociada a signos inflamatorios cutáneos. No presentaba fiebre ni otros síntomas asociados. En la anamnesis dirigida, refirió 20 parejas sexuales hombres en el último año, con relaciones sexuales orales y anales insertivas y receptivas, con uso ocasional de preservativo. No tenía antecedente de viajes fuera de Chile. Cuatro semanas antes del inicio de los síntomas, había tenido un contacto sexual de riesgo sin preservativo con una pareja contactada mediante una aplicación de telefonía móvil. Con el diagnóstico presuntivo de una sífilis primaria y uretritis en estudio, se tomaron muestras de sangre y secreción uretral para estudio microbiológico. Por la conducta sexual de alto riesgo, se tomó también un hisopado anorrectal para tinción de Gram y cultivo. De acuerdo con la norma vigente en Chile, se administraron tres dosis de 2,4 millones de UI de penicilina benzatina intramuscular separadas por una semana, además de 250 mg de ceftriaxona intramuscular y 1 g de azitromicina oral, ambas por una vez. El estudio de laboratorio confirmó el diagnóstico de sífilis, con un VDRL (Venereal disease research laboratory) reactivo con dilución de 1:2 y MHA-TP (Microhemagglutination assay for antibody to Treponema pallidum) reactivo. La tinción de Gram y los cultivos de secreción uretral (agar sangre y Thayer Martin) fueron negativos. La muestra anorrectal mostró escasos diplococos gramnegativos en la tinción de Gram, con desarrollo abundante de N. meningitidis y microbiota comensal en el cultivo corriente. La identificación bacteriana se realizó a través de espectrometría de masas MALDI-TOF MS. El paciente evolucionó favorablemente, sin secreción uretral y con regresión de la lesión ulcerada genital y la adenopatía inguinal a las dos semanas de seguimiento. Las tinciones de Gram y los cultivos de control de secreción uretral, faríngea y anorrectal resultaron negativos. Se citó al contacto sexual reciente para estudio y tratamiento. Sin embargo, éste se encontraba asintomático y los cultivos faríngeo, anorrectal y uretral realizados fueron negativos.",
+        "gold_summary": "Presentamos el caso de un HSH con infección por VIH, que consultó por un cuadro de uretritis y sifilis primaria, en el cual se aisló N. meningitidis en una muestra anorectal. Fue tratado en forma empírica con ceftriaxona y azitromicina, realizándose un cultivo de control post-tratamiento que fue negativo.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un hombre de 32 años con VIH controlado vino al consultorio porque tenía una secreción en la uretra y una llaga dolorosa en el glande. También tenía un ganglio inflamado en la ingle. Había tenido muchas parejas y un encuentro sin preservativo unas semanas antes.\n\nLos médicos pensaron que podía ser sífilis, que es una infección que causa llagas. Le hicieron análisis de sangre y muestras de la secreción y del recto. Los exámenes confirmaron sífilis. En la muestra del recto encontraron otra bacteria llamada Neisseria meningitidis, que normalmente vive en la garganta pero a veces aparece en otras partes del cuerpo.\n\nRecibió antibióticos por inyección y una pastilla. En dos semanas la secreción desapareció, la llaga y el ganglio mejoraron, y los controles dieron negativo. También llamaron a la pareja reciente para que le hicieran pruebas y tratamiento; esa persona estaba sin síntomas y los cultivos salieron negativos.",
+                "fh_score": 66.0
+            },
+            "B2": {
+                "text": "Resumen claro y directo:\n\nUn hombre de 32 años con VIH controlado (carga viral indetectable y recuento de defensas razonable) consultó por dos semanas de secreción uretral y una úlcera dolorosa en el pene. En los exámenes se confirmó sífilis (pruebas VDRL y MHA-TP positivas). Además, en un cultivo de la muestra anorrectal se aisló Neisseria meningitidis, una bacteria que normalmente vive en la garganta pero que a veces puede aparecer en la zona genital o anal y causar infección.\n\nPor el cuadro y el riesgo sexual se le dio tratamiento empírico con antibióticos (ceftriaxona y azitromicina) y, según la norma local para sífilis, recibió tres dosis semanales de penicilina benzatina. A las dos semanas mejoró clínicamente: la secreción desapareció y la úlcera y la adenopatía (ganglio inflamado) disminuyeron. Los cultivos de control (uretral, faríngeo y anorrectal) fueron negativos después del tratamiento. El contacto sexual reciente fue citado para estudio y tratamiento; estaba sin síntomas y sus cultivos resultaron negativos.",
+                "fh_score": 49.96
+            },
+            "B3": {
+                "text": "Resumen clínico\n\nContexto y presentación\nUn hombre de 32 años, con infección por VIH en tratamiento antirretroviral (carga viral indetectable, recuento de CD4 454 céls/mm3) y consumo de tabaco y drogas recreativas, consultó por dos semanas de secreción uretral mucosa con leve ardor y una úlcera eritematosa, indurada y dolorosa de 1,5 cm en el surco balanoprepucial. Además presentó una adenopatía inguinal izquierda sensible de 2 cm. No había fiebre ni otros síntomas sistémicos. En la anamnesis refirió múltiples parejas sexuales masculinas y prácticas de riesgo con uso ocasional de preservativo; cuatro semanas antes había tenido un contacto sexual sin protección por una aplicación móvil.\n\nInvestigaciones y diagnóstico\nSe investigaron causas de uretritis y lesiones genitales. Se tomaron muestras de sangre, secreción uretral y un hisopado anorrectal. Los serológicos confirmaron sífilis (VDRL reactivo 1:2 y MHA-TP reactivo). La tinción de Gram y los cultivos de la secreción uretral resultaron negativos. En la muestra anorrectal se observaron escasos diplococos gramnegativos en la tinción, y el cultivo mostró crecimiento abundante de Neisseria meningitidis junto con flora comensal; la identificación se realizó mediante espectrometría de masas (MALDI-TOF MS).\n\nTratamiento inicial\nSiguiendo la normativa local, se administraron: tres dosis semanales de penicilina benzatina 2,4 millones UI intramuscular (tratamiento para sífilis) y, de forma empírica por uretritis/posible gonorrea, una dosis única de ceftriaxona 250 mg IM y una dosis única de azitromicina 1 g VO.\n\nEvolución y control\nA las dos semanas el paciente mostró resolución de la secreción uretral y regresión de la úlcera y la adenopatía. Los controles microbiológicos (tinciones y cultivos de secreción uretral, faríngea y anorrectal) fueron negativos tras el tratamiento. El contacto sexual reciente fue citado, estaba asintomático y sus cultivos faríngeo, anorrectal y uretral resultaron negativos.\n\nImplicaciones y observaciones\n- Encontrar N. meningitidis en un hisopado anorrectal es notable: aunque esta especie es clásica como agente de meningitis/sepsis, puede colonizar o infectar mucosas urogenitales y anorectales y en la práctica puede confundirse con Neisseria gonorrhoeae.  \n- En este caso el aislamiento en anorrectal podría representar colonización o infección local; no hubo evidencia de infección invasiva.  \n- El tratamiento empírico con ceftriaxona (utilizado para sospecha de gonorrea) es activo frente a muchas cepas de N. meningitidis, y el paciente respondió clínicamente.  \n- Es importante identificar la especie mediante métodos como MALDI-TOF y, cuando sea posible, realizar pruebas de susceptibilidad para orientar terapias y vigilancia epidemiológica.\n\nRecomendaciones prácticas (derivadas del caso)\n- Considerar N. meningitidis en el diagnóstico diferencial de infecciones anorrectales/urogenitales en hombres que tienen sexo con hombres (HSH) u otras poblaciones con prácticas de riesgo.  \n- Notificar y estudiar contactos sexuales según protocolos locales.  \n- Seguimiento serológico de sífilis y control clínico si persisten síntomas.  \n\nEl caso ilustra la utilidad de la identificación bacteriana precisa y la importancia del abordaje integral (tratamiento empírico, confirmación diagnóstica y estudio de contactos) en infecciones de transmisión sexual en redes de alto riesgo.",
+                "fh_score": 41.47
+            }
+        }
+    },
+    {
+        "article": "Un paciente hispanoparlante de 63 años de edad se presentó en el hospital como una emergencia con inicio repentino de dificultad respiratoria severa, palpitaciones y sudoración profusa. Estaba en su estado habitual de salud y podía deambular con actividades independientes de la vida diaria hasta 30 minutos antes de su llegada a la sala de urgencias. Tenía un historial de 20 años de hipertensión, un historial de 15 años de diabetes mellitus, enfermedad de la arteria coronaria que requería la inserción de un stent de la arteria coronaria cinco años antes, un historial de diez años de insuficiencia cardiaca de la clase II de la New York Heart Association (NYHA) con una fracción de eyección reducida (EF) del 35 %, enfermedad renal crónica (CKD) en estadio 3B. Al ingresar en el hospital, sus medicamentos incluían carvedilol (25 mg dos veces al día), lisinopril (20 mg diario), espironolactona (25 mg diario), furosemida (20 mg diario), insulina glargina (20 unidades al acostarse), inyección de insulina lispro (7 unidades tres veces al día), atorvastatina (40 mg diario), y aspirina (81 mg diario), sin alergias a medicamentos conocidas.\n\nAl examen, su presión arterial era de 205/110 mmHg, su frecuencia respiratoria de 29 respiraciones/min, su frecuencia cardíaca de 118 latidos/min, la oximetría de pulso era de 82% (en aire ambiente) y su temperatura de 36.2°C. Su peso era de 72 kg y su estatura de 68 pulgadas, lo que resultó en un índice de masa corporal (IMC) de 24.13 kg/m2. Al examen físico, el paciente estaba en grave dificultad respiratoria, sudaba y no podía hablar con claridad. Su presión venosa yugular era elevada, como se muestra por la distensión de la vena yugular (3+). Al auscultar el tórax, se observaron crepitaciones bilaterales en todos los campos pulmonares. La auscultación cardíaca fue notable por un galope con una frecuencia regular y un murmullo sistólico 3/6 que se oía en la línea medioclavicular izquierda, al nivel del quinto espacio intercostal. El punto de impulso cardíaco máximo se desplazó hacia la izquierda (en la línea medioaxilar anterior) y no se observó distensión abdominal ni ascitis, con edema de los miembros inferiores (1+) hasta el nivel de la mitad de la pantorrilla.\n\nEl paciente fue trasladado a la zona de reanimación cardiopulmonar (RCP), donde se midieron los gases sanguíneos en el aire y se solicitaron pruebas de laboratorio. El paciente fue tratado con oxígeno al 100% utilizando una máscara no reanadora y se le colocó en posición de 90°, lo que produjo una mejora en la oximetría de pulso, que aumentó hasta el 90%. Un electrocardiograma (ECG) mostró taquicardia sinusal, depresión del ST del conductor lateral (de 1 mV), desviación del eje izquierdo e hipertrofia del ventrículo izquierdo. Se obtuvo una radiografía de tórax portátil que fue notable por una silueta cardiaca agrandada, señal de asta de ciervo de desviación venosa pulmonar del lóbulo superior (cefalización), y líneas B de Kerley, que indican edema intersticial.\n\nAunque se solicitaron pruebas de laboratorio, debido a que el paciente estaba gravemente enfermo y no se podía demorar el tratamiento, se inició un tratamiento inicial basado en los hallazgos clínicos, el historial clínico, el ECG, los gases arteriales en sangre y los hallazgos de rayos X. En vista de los hallazgos de las investigaciones iniciales y la ausencia de fiebre, se descartó la neumonía y se realizó un diagnóstico de edema pulmonar cardiogénico hipertensivo. Se inició un tratamiento intravenoso (IV) con nitroglicerina, comenzando a 30 mcg/min y aumentando en 15 mcg/min cada 3 minutos, con oximetría de pulso continua y monitoreo de los signos vitales cada 3 minutos. Después de 18 minutos, se tituló la nitroglicerina hasta 120 mcg/min y su presión arterial disminuyó a 148/82 mmHg, su presión arterial sistólica se redujo en un 29%, su presión arterial diastólica se redujo en un 25%, y su frecuencia cardíaca disminuyó a 87 latidos por minuto. Se hizo una rápida mejora clínica y el paciente pudo comunicarse con oraciones completas y pudo respirar sin el uso de músculos accesorios. La oximetría de pulso mostró una saturación de oxígeno >97%, y la suplementación de oxígeno continuó con el uso de una cánula nasal a 3 L/min y la medición de la oximetría de pulso del paciente fue >96%.\n\nDespués de 25 minutos, el paciente fue tratado con enalapril (2,5 mg IV) combinado con furosemida (20 mg IV). La nitroglicerina se redujo a una tasa de 10 mcg/min cada 5 minutos hasta que se interrumpió, seguido de una dosis oral de isosorbida dinitrato (30 mg). Después de la estabilización clínica completa, los resultados de los laboratorios mostraron un recuento de glóbulos blancos (WBC) de 11,43 × 109/uL, hemoglobina de 10,9 g/dl, hematocrito de 31,8%, plaquetas de 74 × 109/L, sodio de 144 mmol/L, potasio de 3,9 mmol/L, cloruro de 107 mmol/L, dióxido de carbono (CO2) de 25 mmol/L, nitrógeno ureico en sangre (BUN) de 27 mg/dL, creatinina de 1,4 mg/dL, péptido natriurético cerebral (BNP) de 3,452 pg/ml, y troponina I <0,05 ng/ml. Las mediciones de gases en sangre en aire incluyeron pH de 7,381, pCO2 de 44,8 mmHg, pO2 de 57 mmHg, HCO3 de 25,8 mmol/L, y saturación de oxígeno de 84%.\n\nSe evaluó al paciente para detectar la presencia de una posible embolia pulmonar (EP) subyacente, utilizando los criterios de estratificación de riesgo de EP de Wells, y se lo estratificó como de bajo riesgo, con una evaluación posterior con un nivel de dímero D de 340 ng/ml, que se interpretó como negativo. La evaluación para detectar hipertiroidismo mostró un valor normal de la medición ultrasensible del ensayo de la hormona estimulante de la tiroides en plasma (usTSH) de 2,56 μU/mL y tiroxina libre (T4) de 6,87 μU/mL.\n\nEl paciente fue admitido en la sala de hospital de medicina interna con un diagnóstico de edema pulmonar cardiogénico hipertensivo y fue dado de alta 48 horas después. Al momento del alta hospitalaria, su medicación incluía furosemida (40 mg diarios), carvedilol (12.5 mg dos veces al día), sacubitril/valsartan (24 mg/26 mg dos veces al día), espironolactona (25 mg diarios) e isosorbida mononitrato (60 mg diarios). El paciente fue sometido a seguimiento semanal por su cardiólogo, quien optimizó la terapia medicinal. No se registraron visitas a urgencias ni hospitalizaciones, al menos durante los siguientes 60 días.\n\nMH - Insuficiencia cardiaca/*complicaciones\nMH - Humanos\nMH - Hipertensión/*complicaciones\nMH - Infusiones, intravenosas\nMH - Hombre\nMH - Edad Media\nMH - Nitroglicerina/*administración y dosificación\nMH - Edema pulmonar/*terapia farmacológica/etiología\nMH - Insuficiencia respiratoria/*terapia farmacológica/etiología\nMH - Agentes vasodilatadores/*administración y dosificación\n",
+        "gold_summary": "Paciente: Hombre, 63 años\n\nDiagnóstico final: Edema pulmonar cardiovenoso hipertensivo\n\nSíntomas: falta de aire\n\nMedicación: —\n\nProcedimiento clínico: —\n\nEspecialidad: Medicina general e interna\n\nUn hombre hispano de 63 años con antecedentes de hipertensión, enfermedad de las arterias coronarias, insuficiencia cardiaca con una fracción de eyección reducida del 35 %, enfermedad renal crónica (ERC) y diabetes mellitus, se presentó como una emergencia con disnea aguda y grave. El paciente fue tratado inicialmente con 100 % de oxígeno suplementario y nitroglicerina intravenosa (IV) en dosis altas (30 mcg/min), que se ajustó cada 3 minutos, aumentando en 15 mcg/min hasta que se alcanzó una dosis de 120 mcg/min. Después de 18 minutos de terapia agresiva, la condición del paciente mejoró y ya no necesitaba ventilación mecánica.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un hombre hispano de 63 años, con presión alta, diabetes, problemas del corazón y del riñón, llegó al hospital porque de pronto no podía respirar bien. Tenía mucha sudoración y palpitaciones. \n\nEn la sala su tensión arterial estaba muy alta y su oxígeno en la sangre estaba bajo. Al escucharlo, los médicos oyeron líquido en sus pulmones y signos de que el corazón no estaba trabajando bien. Esto se llama edema pulmonar cardiogénico: es cuando el corazón no bombea bien y se acumula líquido en los pulmones.\n\nLe dieron oxígeno y un medicamento por la vena llamado nitroglicerina. Ese medicamento ayuda a relajar las venas y bajar la presión. En unos 18 minutos empezó a sentirse mucho mejor. Pudo hablar y respirar con menos esfuerzo. Después recibió otros medicamentos y fue cuidado en el hospital.\n\nLas pruebas mostraron que el corazón estaba muy cargado, pero no había un ataque al corazón. Fue dado de alta a las 48 horas con medicinas nuevas y seguimiento con su cardiólogo. No volvió a urgencias en los siguientes 60 días. \n\nFue una situación grave y asustadora, pero recibió tratamiento rápido y mejoró.",
+                "fh_score": 72.19
+            },
+            "B2": {
+                "text": "Resumen comprensible y amable\n\nPaciente: hombre de 63 años.\n\nQué pasó: Llegó al servicio de urgencias con una falta de aire muy fuerte, palpitaciones y sudoración. Hasta media hora antes estaba bien y podía caminar solo.\n\nAntecedentes importantes: tenía hipertensión (20 años), diabetes (15 años), enfermedad coronaria con un stent (hace 5 años), insuficiencia cardiaca crónica con función reducida del corazón (fracción de eyección 35 %) y enfermedad renal crónica (estadio 3B).\n\nQué encontraron al llegar:\n- Presión arterial muy alta (205/110 mmHg), respiración rápida y saturación de oxígeno baja (82 % en aire).\n- Venas del cuello hinchadas, crepitaciones en ambos pulmones (ruidos que sugieren líquido) y un sonido extra en el corazón (galope). También tenía un soplo y algo de hinchazón en las piernas.\n- Radiografía de tórax: corazón agrandado y signos de acumulación de líquido en los pulmones.\n- ECG: ritmo sinusal rápido y señales de sobrecarga del ventrículo izquierdo.\n- Análisis: péptido natriurético (BNP) muy alto (3,452 pg/ml), lo que indica estrés o fallo del corazón; troponina baja (sin evidencia de infarto); plaquetas bajas (74 × 10^9/L) y anemia leve. Gasometría arterial mostró bajo oxígeno en sangre al aire ambiente.\n\nDiagnóstico: edema pulmonar cardiogénico hipertensivo (es decir, líquido en los pulmones provocado por que el corazón no estaba manejando bien la presión alta).\n\nTratamiento inicial y evolución:\n- Se le dio oxígeno al 100 % y se colocó erguido; luego se administró nitroglicerina por vía intravenosa (un medicamento que dilata los vasos y reduce la carga del corazón). La dosis se aumentó rápidamente hasta 120 mcg/min.\n- En 18 minutos mejoró mucho: bajó la presión arterial, la frecuencia cardíaca y su respiración; pudo hablar en oraciones y la saturación subió por encima del 97 %. Luego se mantuvo con cánula nasal a 3 L/min.\n- Después se le dio enalapril IV y furosemida IV (diurético para eliminar líquido). La nitroglicerina se fue retirando y se inició medicación oral para mantener el control.\n\nResultados y seguimiento:\n- Fue ingresado en medicina interna y dado de alta a las 48 horas con tratamiento oral actualizado: diurético (furosemida), betabloqueante (carvedilol, dosis reducida), sacubitril/valsartán (medicamento para la insuficiencia cardiaca), espironolactona e isosorbida mononitrato.\n- Se programaron controles semanales con su cardiólogo y no tuvo nuevas visitas a urgencias ni reingresos durante, al menos, los siguientes 60 días.\n\nComentario en palabras sencillas: El paciente tuvo una emergencia por acumulación de líquido en los pulmones causada por presión arterial muy alta y un corazón que ya estaba debilitado. Con oxígeno y medicamentos que bajaron la presión y ayudaron al corazón y a eliminar líquido, mejoró rápido y pudo volver a casa bajo control médico. Algunas pruebas mostraron otros datos (por ejemplo, plaquetas bajas y anemia leve) que requerirán seguimiento con su equipo de salud.",
+                "fh_score": 54.0
+            },
+            "B3": {
+                "text": "Summary — Hypertensive cardiogenic pulmonary edema in a 63-year-old man\n\nBrief clinical picture\n- A 63-year-old Hispanic man with long-standing hypertension (20 years), type 2 diabetes, coronary artery disease with prior stent, chronic heart failure (NYHA class II, LVEF ≈35%), and chronic kidney disease (stage 3B) presented suddenly with severe shortness of breath, palpitations and heavy sweating. He had been independent and ambulatory until about 30 minutes before arrival.\n\nImportant abnormal findings on arrival\n- Vital signs: blood pressure 205/110 mmHg (severely elevated), heart rate 118/min (tachycardia), respiratory rate 29/min, O2 saturation 82% on room air.\n- Exam: marked respiratory distress, jugular venous distension (JVD 3+), bilateral crackles throughout the lungs, an S3 gallop and a 3/6 systolic murmur, displaced point of maximal impulse, mild bilateral leg edema.\n- Chest x-ray: enlarged cardiac silhouette, cephalization of pulmonary vessels and Kerley B lines — consistent with pulmonary interstitial edema.\n- ECG: sinus tachycardia, left axis deviation, left ventricular hypertrophy, and lateral ST depression.\n- Arterial blood gas (on room air): pO2 57 mmHg, O2 saturation 84% (hypoxemia).\n- Blood tests after initial stabilization: BNP 3,452 pg/mL (markedly elevated → supports acute cardiac failure), troponin I <0.05 ng/mL (no biochemical evidence of acute myocardial infarction), creatinine 1.4 mg/dL (mildly elevated for CKD), mild anemia (Hb 10.9 g/dL) and thrombocytopenia (platelets 74 × 10^9/L) — both notable and require follow-up. WBC slightly elevated (11.4 × 10^9/L). D-dimer 340 ng/mL (not suggestive of pulmonary embolism in this low-risk patient). Thyroid tests normal.\n\nWorking diagnosis\n- Hypertensive cardiogenic (cardiogenic) pulmonary edema — acute heart-failure exacerbation driven by very high blood pressure, with resultant pulmonary congestion and hypoxemia. Infection and pulmonary embolism were considered unlikely based on clinical course, absence of fever, and negative testing.\n\nTreatment and response\n- Immediate care: high-flow oxygen (initially 100% by non-rebreather), upright positioning, and rapid medical therapy targeted at lowering afterload and relieving pulmonary congestion.\n- Nitroglycerin IV was started at 30 mcg/min and titrated every 3 minutes by 15 mcg/min to 120 mcg/min. Within 18 minutes the patient’s blood pressure fell to 148/82 mmHg, heart rate slowed to 87/min, breathing and mental status improved rapidly, and oxygen saturation rose to >97% on supplemental oxygen. Aggressive IV nitrates likely reduced preload/afterload and avoided need for mechanical ventilation.\n- Additional therapy included IV enalapril 2.5 mg and IV furosemide 20 mg to promote diuresis. Nitroglycerin was tapered and transitioned to oral nitrates (isosorbide dinitrate then long-acting isosorbide mononitrate).\n- No evidence of acute myocardial infarction; treatment focused on decongestion and blood-pressure control.\n\nHospital course and disposition\n- Admitted to internal medicine, clinically stabilized within 48 hours and discharged home.\n- Discharge medications included: furosemide 40 mg daily, carvedilol 12.5 mg twice daily, sacubitril/valsartan 24/26 mg twice daily (ARNI added/optimized), spironolactone 25 mg daily, and isosorbide mononitrate 60 mg daily.\n- Outpatient cardiology follow-up was arranged weekly for medication optimization. No emergency visits or readmissions were reported during at least the subsequent 60 days.\n\nKey points, implications and recommended follow-up\n- This was an acute, severe hypertensive cardiogenic pulmonary edema responding rapidly to high-dose IV nitrates plus diuretic and afterload reduction — demonstrating that early vasodilator therapy can reverse life‑threatening pulmonary congestion and avoid intubation when used carefully.\n- Important supportive findings that helped exclude other causes: very high BNP (supports heart-failure cause), negative troponin (argues against large acute MI), low Wells score and negative D-dimer (makes pulmonary embolism unlikely), and no fever or focal consolidation on imaging (less likely pneumonia).\n- Issues requiring ongoing attention: his chronic kidney disease (monitor renal function, BUN/creatinine, and electrolytes with diuretics and RAAS/ARNI therapy); new or unexplained thrombocytopenia and mild anemia (needs hematology review and repeat testing to identify cause); blood-pressure control and optimization of heart‑failure medications; careful outpatient monitoring for hypotension, renal effects, and potassium abnormalities after starting sacubitril/valsartan and spironolactone.\n- Follow-up with cardiology and primary care, with repeat labs and clinical checks in the near term, is appropriate to ensure safe medication titration and to investigate low platelets and anemia.\n\nIf you would like, I can produce a brief patient-facing version (simpler language) for explanation to the patient or a checklist for the outpatient follow-up plan.",
+                "fh_score": 64.3
+            }
+        }
+    },
+    {
+        "article": "Historial clínico\nUn niño de 12 años se presentó en nuestro hospital con un mes de historia de sensación de cuerpo extraño y una masa conjuntival pedunculada carnosa que creció con el tiempo. No había historia de trauma o lesiones similares en el otro lado del cuerpo. Se descubrió una masa pedunculada carnosa rosácea de 15 mm de la conjuntiva palpebral derecha durante un examen oftalmológico. La agudeza visual estaba dentro de los límites normales. Se diagnosticó al niño como papiloma de células escamosas pedunculadas y se le realizó una biopsia excisional de la lesión.\n\nHallazgos macroscópicos y microscópicos\nRecibimos un fragmento de tejido blanco grisáceo, pequeño, firme, ovoide, fijado en formalina, de 1,5 x 1 cm, para su análisis patológico. En las secciones microscópicas se encontró una lesión poliopóidea hiperplásica con múltiples quistes globulares en la submucosa conjuntival, junto con una importante infiltración inflamatoria constituida por linfocitos, células plasmáticas y neutrófilos, así como enormes esporangios de paredes gruesas con numerosas endosporas. Las endosporas se liberaron después de que algunos de los esporangios maduros se rompieran. La rinosporidiosis conjuntival se diagnosticó histopatológicamente. No hubo recurrencia ni signo de rinosporidiosis en el ojo ni en ninguna otra área del cuerpo en el último examen del paciente, que fue 7 meses después de la escisión quirúrgica.\n",
+        "gold_summary": "Un niño de 12 años con una masa conjuntival pedunculada carnosa fue llevado al Centro Médico de la Universidad de Jimma con un historial de un mes de sensación de cuerpo extraño. Al paciente se le diagnosticó un papiloma pedunculado de células escamosas y se le realizó una biopsia excisional de la lesión. Se encontró que la masa era una lesión polipoide hiperplásica con numerosos quistes globulares dentro de la submucosa conjuntival, rodeados por un infiltrado inflamatorio pesado de linfocitos, células plasmáticas y neutrófilos, así como grandes esporas de paredes gruesas con numerosas endosporas en secciones microscópicas. Se diagnosticó histopatológicamente rinosporidiosis conjuntival.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un niño de 12 años tenía desde hace un mes una bolita carnosa dentro del párpado derecho. Decía que sentía algo en el ojo, pero su vista estaba bien. Los médicos quitaron la bolita y la miraron con un microscopio. Vieron muchas bolsitas grandes llenas de pequeñas esporas y mucho material de defensa del cuerpo alrededor. Esto se llama rinosporidiosis, una infección rara que hace crecer bultos en la conjuntiva del ojo. Después de la operación el niño se recuperó. Siete meses más tarde no había vuelto a aparecer y no había señales de la infección en otras partes.",
+                "fh_score": 75.44
+            },
+            "B2": {
+                "text": "A 12-year-old boy had one month of feeling something in his right eye and a slowly growing, fleshy bump on the inner surface of his eyelid. His sight was normal. Doctors first thought it was a benign papilloma (a wart-like growth) and removed the lump by excisional biopsy.\n\nUnder the microscope, the tissue showed a polyp-like overgrowth with many round, cyst-like spaces under the surface, and a heavy inflammatory reaction (lots of immune cells). Pathologists also saw large, thick-walled sacs filled with many smaller spores; some sacs had burst and released those spores. These changes are typical of conjunctival rinosporidiosis — an infection that causes polyp-like growths on mucous membranes and is diagnosed by finding these distinctive spore-filled sacs.\n\nThe lesion had been completely removed, and at a follow-up exam 7 months later there was no sign of the infection coming back. Surgical removal is the usual step, and continued follow-up is recommended because these growths can sometimes recur.",
+                "fh_score": 84.35
+            },
+            "B3": {
+                "text": "Resumen clínico y hallazgos principales\n\n- Paciente: niño de 12 años con un mes de sensación de cuerpo extraño en el ojo derecho y una masa conjuntival pedunculada, carnosa, rosácea de 15 mm. La agudeza visual era normal.\n- Manejo inicial: la lesión se interpretó clínicamente como un papiloma escamoso pedunculado y se realizó biopsia excisional.\n\nHallazgos macroscópicos y microscópicos\n\n- Macroscópico: fragmento de tejido fijo, blanco‑grisáceo, firme, ovoide, de 1,5 × 1 cm.\n- Microscópico: lesión polipoidea hiperplásica de la conjuntiva con múltiples quistes globulares en la submucosa y un infiltrado inflamatorio intenso (linfocitos, células plasmáticas y neutrófilos). Se observaron grandes esporangios de pared gruesa conteniendo numerosas endosporas; algunos esporangios maduros se habían roto liberando endosporas.\n- Diagnóstico histopatológico: rinosporidiosis conjuntival.\n\nEvolución y consideraciones clínicas\n\n- El paciente no presentó recurrencia ni signos de rinosporidiosis en el ojo ni en otras localizaciones a los 7 meses tras la escisión.\n- La rinosporidiosis es una infección granulomatosa crónica que suele identificarse por la presencia característica de esporangios y endosporas en el tejido; el tratamiento habitual es la escisión quirúrgica completa, y existe riesgo de recurrencia si la extirpación es incompleta.\n- Recomendaciones prácticas (habituales en este contexto): vigilancia clínica periódica de la misma zona y evaluación de otras mucosas (por ejemplo cavidad nasal) para buscar lesiones adicionales; aconsejar medidas para reducir la exposición a posibles fuentes de contagio según la epidemiología local.  \n\nSi desea, puedo redactar una versión breve para familiares o añadir sugerencias específicas de seguimiento y prevención adaptadas al entorno del paciente.",
+                "fh_score": 32.11
+            }
+        }
+    },
+    {
+        "article": "Presentamos el caso clínico de un varón de quince años, sin antecedentes médicos ni intervenciones previas, que acude al servicio de urgencias de pediatría con clínica de vómitos y dolor abdominal epigástrico de cuatro días de evolución, manteniéndose afebril durante la evolución del cuadro.\n\nInicialmente fue manejado como gastroenteritis, pero ante la ausencia de mejoría, con persistencia del dolor abdominal de tipo cólico a nivel epigástrico y de los vómitos de aspecto bilioso, acude a urgencias para nueva valoración.\n\nA la exploración física el paciente presentaba aceptable estado general, se encontraba afebril, con signos leves de deshidratación. El abdomen se encontraba distendido, sin datos de peritonismo y con ruidos hidroaéreos disminuidos. La analítica no presentaba hallazgos significativos, realizándose una radiografía de abdomen con hallazgos sugestivos de obstrucción intestinal.\n\nDada la evolución se decide realizar una tomografía computarizada urgente, en la que se observó presencia de ascitis e importante dilatación de asas de intestino delgado, sugiriendo la interposición de un asa de intestino delgado en el inicio de la transcavidad de los epiplones, con cambio de calibre a nivel del hiato de Winslow.\n\nSe realizó intervención quirúrgica urgente, realizando inicialmente una laparoscopia exploradora. Se observaban asas de intestino delgado dilatadas, e íleon terminal, ciego y colon ascendente de calibre normal pero localizados en hipocondrio derecho, con el ciego muy móvil y sin presentar adherencias al espacio parietocólico derecho. Siguiendo proximalmente el íleon terminal, se observaron asas de intestino delgado de distinto calibre desde la profundidad de la teórica localización del hiato de Winslow. Se consiguió traccionar de ciego e íleon terminal hasta desplazarlos a fosa iliaca derecha, pero sin llegar a identificar correctamente el punto de cambio de calibre, ya que la interposición del borde inferior del hígado y la distensión de asas de intestino delgado dificultaban la técnica. Se intentó mejorar la visualización mediante punción percutánea de un asa dilatada para vaciar el gas, sin mejoría. Para asegurar la resolución del cuadro obstructivo se decidió realizar una laparotomía media supraumbilical. Al acceder a cavidad se evidenciaba el cambio de calibre en íleon, a unos 40 centímetros de la válvula ileocecal, con signos compatibles con herniación de un tramo de unos cinco centímetros de íleon a través de hiato de Winslow. En ambos extremos del asa herniada observamos la impronta congestiva del hiato sobre el asa (Fig. 3). Se identificó el hiato de Winslow, de calibre normal, por lo que no se realizó ninguna técnica preventiva para disminuir el riesgo de recidiva.\n\nDurante los primeros días del postoperatorio el paciente presentó un íleo paralítico, pudiendo retirar la sonda nasogástrica a los cinco días de la cirugía e iniciando tolerancia oral con buena respuesta. Simultáneamente desarrolló una colección pélvica que se manejó de forma conservadora con antibióticos, con buena evolución. Finalmente, el paciente fue dado de alta a los diez días de la intervención, con tránsito conservado, manteniéndose afebril y con buen estado general.\n\nActualmente el paciente está en seguimiento en consultas externas de cirugía pediátrica.",
+        "gold_summary": "Presentamos el caso clínico de un varón adolescente de 15 años sin antecedentes quirúrgicos previos, con clínica de dolor abdominal y vómitos, en el que la tomografía computarizada sugería un cuadro de obstrucción intestinal a causa de hernia interna a nivel del hiato de Winslow. Precisó de intervención quirúrgica mediante laparoscopia exploradora, reconvertida por mala visualización a laparotomía media supraumbilical, para reducción del asa de íleon herniada. Esta presentaba buen aspecto y no fue necesaria la resección intestinal. No se realizó ninguna técnica preventiva para disminuir el riesgo de recidiva. Postoperatoriamente, el paciente presentó una colección pélvica manejada de manera conservadora con antibióticos. Actualmente se encuentra en seguimiento en consultas externas de cirugía pediátrica.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Este es el caso de un chico de 15 años que empezó con dolor de barriga y vómitos. Al principio pensaron que era una infección del estómago, pero no mejoró. Una tomografía (una imagen del interior del cuerpo) mostró que parte del intestino estaba atascado porque se metió por un pequeño agujero dentro del abdomen cerca del hígado.  \n\nLos médicos operaron para mirar dentro con una cámara y luego abrieron un poco más para poder sacar el trozo de intestino. El intestino estaba sano y no hubo que quitar ninguna parte. No se hizo ninguna técnica extra para evitar que vuelva a ocurrir.  \n\nDespués de la operación tuvo el intestino un poco lento y también una pequeña bolsa de líquido en la pelvis. Le quitaron la sonda del estómago a los cinco días y trataron la bolsa con antibióticos. Salió del hospital a los diez días, sin fiebre y en buen estado. Ahora sigue en controles con los médicos para ver cómo va.",
+                "fh_score": 75.0
+            },
+            "B2": {
+                "text": "Resumen claro y comprensible:\n\nUn chico de 15 años, sin cirugías previas, acudió por varios días de vómitos y dolor en la parte alta del abdomen. Al principio se pensó que tenía una gastroenteritis, pero como no mejoró y los vómitos eran biliosos (con contenido del intestino), le hicieron pruebas de imagen. La tomografía mostró líquido en la barriga y asas delgadas del intestino muy dilatadas, lo que sugería una obstrucción por una hernia interna a través del hiato de Winslow (una abertura dentro del abdomen donde, raramente, puede quedar atrapada una porción del intestino).\n\nEl equipo realizó primero una laparoscopia (cirugía con pequeñas incisiones y cámara), pero por mala visualización la convirtieron en una laparotomía media (incisión abdominal mayor). Encontraron un tramo de íleon (la parte final del intestino delgado) de unos 5 cm atrapado en el hiato; lo redujeron (lo sacaron) y el intestino estaba viable, por lo que no fue necesario cortar ninguna porción. No se practicó ninguna maniobra adicional para intentar evitar que la hernia vuelva a ocurrir.\n\nEn los días posteriores presentó un íleo paralítico (cuando el intestino se mueve muy poco de forma temporal) y desarrolló una colección en la pelvis que se trató con antibióticos y observación. Se le retiró la sonda nasogástrica al quinto día, empezó a tolerar alimentos y fue dado de alta al décimo día con buena evolución. Actualmente sigue en revisión en consultas de cirugía pediátrica.",
+                "fh_score": 53.14
+            },
+            "B3": {
+                "text": "Presentación clínica\nUn varón de 15 años sin antecedentes médicos ni cirugías previas acudió por 4 días de vómitos y dolor abdominal epigástrico. Inicialmente fue tratado como gastroenteritis, pero los síntomas persistieron y el vómito se volvió bilioso. A la exploración estaba afebril, con leve deshidratación, abdomen distendido, ruidos hidroaéreos disminuidos y sin signos de peritonismo.\n\nHallazgos diagnósticos\n- Analítica: sin hallazgos relevantes.  \n- Radiografía abdominal: imágenes sugestivas de obstrucción intestinal.  \n- Tomografía computarizada urgente: ascitis, marcada dilatación de asas de intestino delgado y un cambio de calibre a nivel del hiato (foramen) de Winslow, hallazgos compatibles con una herniación interna de asa ileal hacia la cavidad del epiplón menor.\n\nProcedimiento quirúrgico y hallazgos intraoperatorios\nSe realizó laparoscopia exploradora que mostró asas delgado dilatadas y ciego/íleon terminal móviles, localizados en hipocondrio derecho. La visualización quedó limitada por el borde hepático y la distensión intestinal; se intentó descomprimir una asa por punción sin éxito visual. Se convirtió a laparotomía media supraumbilical. Al abrir la cavidad se identificó un cambio de calibre en el íleon a unos 40 cm de la válvula ileocecal: un segmento de aproximadamente 5 cm de íleon había herniado a través del hiato de Winslow. Se observaron impresiones congestivas en los extremos del asa herniada. El foramen de Winslow tenía calibre normal. El asa reducida tenía buena viabilidad, por lo que no fue necesaria resección intestinal. No se realizó maniobra preventiva adicional para reducir el riesgo de recurrencia dado el aspecto y el calibre normal del hiato.\n\nEvolución postoperatoria\nEl postoperatorio inmediato cursó con íleo paralítico; la sonda nasogástrica se retiró al quinto día y se inició tolerancia oral progresiva con buena respuesta. Además desarrolló una colección pélvica que se manejó de forma conservadora con antibióticos, con buena evolución clínica. Fue dado de alta al décimo día tras mantener tránsito intestinal y buen estado general. Actualmente está en seguimiento en consultas externas de cirugía pediátrica.\n\nImplicaciones y recomendaciones\n- Diagnóstico: hernia interna a través del foramen de Winslow provocando obstrucción intestinal; es una causa poco frecuente de obstrucción en pacientes sin cirugía previa.  \n- Manejo realizado: reducción quirúrgica por laparotomía tras intento laparoscópico; no hubo necrosis intestinal ni resección.  \n- Seguimiento: vigilancia clínica en consultas de cirugía para detectar signos de recurrencia (dolor abdominal agudo, vómitos biliosos, distensión) o complicaciones infecciosas residuales. Si reaparecen síntomas, estaría indicado estudio por imagen y valoración quirúrgica precoz.  \n- Riesgo de recidiva: no se practicó cierre ni fijación específica del hiato en esta intervención porque el foramen tenía aspecto normal; el equipo mantiene seguimiento por si fuera necesario intervenir en el futuro.\n\nResumen empático\nSe trata de un adolescente previamente sano con una hernia interna poco habitual por el foramen de Winslow que provocó obstrucción intestinal. Gracias al diagnóstico por TC y la intervención oportuna se redujo el asa intestinal sin necesidad de resección, y el paciente evolucionó favorablemente tras un inicio postoperatorio complicado pero controlado. Continúa en seguimiento para asegurar recuperación completa y detectar cualquier signo de recurrencia.",
+                "fh_score": 41.18
+            }
+        }
+    },
+    {
+        "article": "Un niño de 23 meses de edad con encefalopatía isquémica hipóxica al nacer, con buen potencial motor cerebral y desarrollo psicomotor normal. Tenía antecedentes personales de miocardiopatía restrictiva y fue incluido en un programa de trasplante cardiaco cuando tenía 16 meses de edad. También fue necesario implantarle un dispositivo de asistencia biventricular Berlin Heart externo. Para evitar eventos embólicos, se le administró un tratamiento antiplaquetario doble y anticoagulante. Cuando tenía 23 meses de edad, presentó desconexión y hemiparesia derecha. Una tomografía computarizada (TC) mostró una arteria cerebral media (ACM) izquierda hiperdensa, así como un infarto parietotemporal derecho crónico. Su análisis de sangre mostró: glóbulos rojos 4.16 × 106 µ/L; hemoglobina 11.4 g/gL; tiempo de tromboplastina parcial activada (TTPA) 93 segundos y relación internacional normalizada (INR) 1.08.\n\nEl tratamiento trombolítico intravenoso estaba contraindicado debido al doble tratamiento antiplaquetario y anticoagulante a la dosis completa con heparina, por lo que se realizó una trombectomía intraarterial. Aunque el paciente tenía 23 meses de edad, se encontraba en el tercer percentil de la curva de peso (10 kg). Bajo anestesia general, se perforó la arteria femoral derecha y se colocó una funda 4F de 11 cm de largo (Cordis, Irlanda). Se usó un catéter vertebral Radiofocus 4F (Glidecath de Terumo, Bélgica) para confirmar la oclusión del segmento M1 de la MCA izquierda. La arteria se recanalizó mediante trombectomía mecánica con un stentriever utilizando el catéter vertebral 4F como tutor, colocándolo en el segmento petroso de la arteria carótida. Se usó un dispositivo Trevo XP Pro Vue de 3 mm x 20 mm (Stryker, Países Bajos), con un microcatéter Rapid Transit recto (Codman Neurovascular, Reino Unido), abriendo la arteria en una sola pasada. Se retiró todo el sistema (catéter tutor, microcatéter y stentriever) simultáneamente. En la prueba de control, se detectó una disección iatrogénica de la arteria carótida interna izquierda, que no tuvo importancia clínica, ya que el hemisferio izquierdo se irrigaba a través de la arteria comunicante anterior.\n\nUn mes después, se realizó con éxito el trasplante de corazón. La única secuela neurológica a largo plazo que surgió como resultado del accidente cerebrovascular fue la espasticidad del miembro superior derecho.\n\nMH - Cardiomiopatía, Dilatada/complicaciones/cirugía\nMH - Cardiomiopatía, restrictiva/complicaciones/cirugía\nMH - Angiografía cerebral\nMH - Procedimientos/métodos endovasculares\nMH - Mujer\nMH - Estudios de seguimiento\nMH - Insuficiencia cardiaca/*complicaciones/tratamiento\nMH - Trasplante de corazón\nMH - *Dispositivos de asistencia cardíaca\nMH - Humanos\nMH - Infantil\nMH - Hombre\nMH - Arteria cerebral media/imágenes diagnósticas\nMH - Estudios Retrospectivos\nMH - Ictus/complicaciones/diagnóstico por imágenes/cirugía\nMH - Resultado del tratamiento\n",
+        "gold_summary": "Un niño de 16 meses de edad con cardiomiopatía restrictiva que fue incluido en una lista para un trasplante cardiaco. A los 20 meses de edad, requirió un implante de un dispositivo de asistencia biventricular externo (Berlin Heart) y tuvo un accidente cerebrovascular en el hemisferio izquierdo a los 23 meses. Se utilizó un enfoque intraarterial y produjo buenos resultados clínicos. Un mes después, se realizó con éxito un trasplante cardiaco.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Este es el resumen de la historia de un niño pequeño contado con palabras sencillas.\n\n- Cuando nació tuvo un problema en el cerebro por falta de oxígeno, pero creció con un desarrollo normal y movía bien su cuerpo.\n- Tenía una enfermedad del corazón llamada cardiomiopatía. A los 16 meses lo pusieron en la lista para un trasplante de corazón.\n- Más tarde le pusieron una máquina externa (Berlin Heart) para ayudar a su corazón a bombear. Por eso tomaba medicinas para hacer la sangre menos pegajosa.\n- A los 23 meses tuvo un accidente cerebrovascular (un coágulo que tapó una arteria del lado izquierdo del cerebro). Esto hizo que su brazo y pierna derechos quedaran débiles.\n- Los médicos no pudieron darle la medicina que disuelve coágulos porque ya estaba con medicinas que adelgazan la sangre. En vez de eso, hicieron una operación por dentro de los vasos.\n- Introdujeron un catéter por la pierna, llegaron hasta la arteria del cerebro y usaron un pequeño aparato para sacar el coágulo. Lo lograron en una sola vez.\n- Durante el procedimiento apareció una pequeña rotura en una arteria del cuello. No fue grave porque otra arteria seguía dando sangre al cerebro.\n- Un mes después le hicieron el trasplante de corazón con éxito. La única secuela que le quedó fue rigidez (espasticidad) en el brazo derecho.\n- En general, los doctores pudieron arreglar el problema de la arteria y después recibió el nuevo corazón. Esto ayudó mucho a su salud.",
+                "fh_score": 71.64
+            },
+            "B2": {
+                "text": "Resumen comprensible para lectores jóvenes (11–17 años):\n\nUn niño de 23 meses que había sufrido una lesión cerebral por falta de oxígeno al nacer (pero que se había desarrollado bien en cuanto al movimiento y al desarrollo general) tenía una cardiomiopatía restrictiva —una enfermedad del corazón que dificulta que el ventrículo se llene bien— y fue incluido en la lista para un trasplante de corazón cuando tenía 16 meses. Más adelante necesitó un dispositivo de asistencia cardiaca externo (llamado Berlin Heart) para ayudar al corazón a bombear.\n\nPara evitar coágulos, recibía dos medicamentos antiplaquetarios y también anticoagulación completa con heparina. A los 23 meses presentó una pérdida súbita de conciencia y debilidad marcada en el lado derecho del cuerpo. Una tomografía mostró lo que parecía ser un coágulo en la arteria cerebral media izquierda (la arteria que lleva sangre a gran parte del lado izquierdo del cerebro). Debido a los medicamentos que estaba tomando, no se pudo dar el tratamiento trombolítico por vía intravenosa (el fármaco que disuelve coágulos). Por eso los médicos realizaron una trombectomía mecánica intraarterial: introdujeron catéteres por la arteria femoral, llegaron hasta la arteria bloqueada y retiraron el coágulo con un dispositivo especial llamado stent retriever. Abrieron la arteria en una sola pasada.\n\nDurante el procedimiento se produjo una pequeña disección iatrogénica (un desgarro en la pared de la arteria causado por el procedimiento), pero no causó problemas porque la parte izquierda del cerebro seguía recibiendo sangre por otra vía (la arteria comunicante anterior). Un mes después el niño pudo recibir con éxito el trasplante de corazón. La única secuela neurológica duradera fue espasticidad (rigidez y tensión) en el brazo derecho.\n\nQué significa esto de forma sencilla:\n- Cuando hay un coágulo grande en una arteria cerebral, a veces no puede usarse el tratamiento que disuelve coágulos si el paciente ya toma anticoagulantes; entonces los médicos pueden quitar el coágulo usando instrumentos que llegan por dentro de las arterias.\n- Aunque el procedimiento tuvo una pequeña complicación en la arteria, la circulación alternativa protegió el cerebro.\n- El niño se recuperó lo suficiente para recibir el trasplante, pero quedó con algo de rigidez en el brazo derecho.",
+                "fh_score": 47.65
+            },
+            "B3": {
+                "text": "Resumen\n\nUn niño de 23 meses con antecedentes de encefalopatía hipóxico-isquémica neonatal (con desarrollo psicomotor y función motora cerebral considerados buenos) y cardiomiopatía restrictiva fue incluido en lista para trasplante cardiaco en la infancia y recibió un dispositivo de asistencia biventricular externo (Berlin Heart). Pesaba 10 kg, en el tercer percentil para su edad.\n\nPresentación y hallazgos\n- A los 23 meses tuvo una desconexión neurológica y hemiparesia derecha.  \n- La TC craneal mostró una arteria cerebral media (ACM) izquierda hiperdensa compatible con oclusión aguda; además existía un infarto crónico en el hemisferio derecho (parietotemporal).  \n- Analíticas: hematíes 4.16 × 10^6/µL, hemoglobina 11.4 g/dL; tiempo de tromboplastina parcial activada (TTPA) prolongado a 93 s (por anticoagulación con heparina) e INR 1.08.  \n\nDecisiones terapéuticas\n- La terapia trombolítica intravenosa se consideró contraindicada por estar en tratamiento antiplaquetario doble y anticoagulación a dosis completa.  \n- Se optó por una trombectomía mecánica endovascular, procedimiento dirigido a retirar el trombo y restaurar el flujo arterial.\n\nProcedimiento\n- Bajo anestesia general, se accedió por arteria femoral derecha con una vaina 4F y se navegó hasta la carótida para confirmar oclusión del segmento M1 de la ACM izquierda.  \n- Se realizó trombectomía con un stent-retriever (Trevo XP ProVue 3 × 20 mm) colocado mediante microcatéter; la arteria se recanalizó en una sola pasada.  \n- Tras la retirada simultánea del sistema, se identificó una disección iatrogénica de la arteria carótida interna izquierda, pero ésta no produjo déficit clínico porque el hemisferio izquierdo seguía recibiendo irrigación por la arteria comunicante anterior.\n\nEvolución y resultados\n- La recanalización fue exitosa y permitió la resolución del evento isquémico agudo.  \n- Un mes después se realizó con éxito el trasplante cardiaco.  \n- A largo plazo la única secuela neurológica señalada fue espasticidad del miembro superior derecho.\n\nImplicaciones y consideraciones\n- Este caso muestra que la trombectomía mecánica puede ser factible y eficaz en lactantes pequeños con ictus isquémico agudo, incluso cuando la trombólisis sistémica está contraindicada por anticoagulación/antiplaquetarios.  \n- Riesgos específicos incluyen lesión o disección vascular iatrogénica; por eso estos procedimientos requieren equipos y experiencia en neurointervencionismo pediátrico y acceso vascular adaptado al tamaño del niño.  \n- El seguimiento debe incluir rehabilitación neurológica dirigida a la espasticidad (fisioterapia, terapias del tono, y si procede, intervención rehabilitadora adicional) y vigilancia neurovascular y neurofuncional tras el trasplante.\n\nEste informe es esperanzador respecto a la posibilidad de tratar ictus isquémicos en niños muy pequeños con técnicas endovasculares cuando la trombólisis no es una opción, pero subraya la necesidad de centros especializados y un seguimiento rehabilitador estrecho.",
+                "fh_score": 34.88
+            }
+        }
+    },
+    {
+        "article": "Una mujer de 23 años de edad se presentó al departamento de urgencias con pérdida de conciencia y exceso de secreciones orales 2 horas después de la ingestión de un veneno no especificado. No tenía movimientos corporales anormales, fiebre, diarrea, vómitos o sudoración. Inicialmente la habían llevado a un hospital primario cercano, donde fue tratada por posible intoxicación por OP con atropina y cimetidina durante 3 días, antes de ser trasladada al hospital Saint Peter. Después de un interrogatorio exhaustivo, se descubrió que la paciente había consumido unos 30 ml de 2,4-D en un intento de suicidio, precipitado por problemas financieros. No tenía antecedentes conocidos de enfermedad psiquiátrica, intentos de suicidio, episodios depresivos o abuso de sustancias. No se observaron trastornos cardíacos, renales o metabólicos previos.\n\nAl llegar al departamento de urgencias, la paciente estaba inconsciente. Sus constantes vitales eran PR 110/min, BP 120/70 mmHg, RR 21/min, y SPO2 96% en aire ambiente. Los resultados del examen físico fueron notables: un GCS de 6 sobre 15, pupilas dilatadas y reactivas, extremidades inferiores hipertónicas e hiperreflexivas, y reflejo plantar ascendente. Tras la investigación inicial, el recuento completo de células sanguíneas, la prueba de la función renal, la prueba de la función hepática, y la glucosa en sangre aleatoria fueron normales. Su electrocardiograma mostró taquicardia sinusal, mientras que la radiografía de tórax no fue notable. El análisis de gases en sangre arterial y el nivel sérico de la toxina no pudieron determinarse, ya que ninguno de los medios de prueba estaba disponible en el hospital.\n\nLa paciente fue trasladada a la unidad de cuidados intensivos (UCI), se le introdujo una sonda para proteger las vías respiratorias y se le inició inmediatamente una diuresis alcalina forzada. Su evolución en la UCI fue notable por el desarrollo de una insuficiencia renal (creatinina 3,1 ml/dL [intervalo de referencia 0,5-1,2 mg/dL], BUN 133 mg/dL [intervalo de referencia 16,6-48,5 mg/dL], análisis de orina 3+ hemoglobina y muchos glóbulos rojos), debido a una rabdomiolisis inducida por toxinas (nivel de creatina fosfocinasa de 1330 µg/L). Posteriormente, la paciente se volvió hipotensa y se le inició un tratamiento con vasopresores. La ecocardiografía y la ecografía abdominal no fueron significativas. A pesar de estos esfuerzos, falleció por colapso circulatorio el tercer día de estancia en la UCI.\n",
+        "gold_summary": "Aquí se informa sobre el caso de una joven granjera de la zona rural de Etiopía que fue internada en un hospital local tras perder el conocimiento y presentar exceso de secreciones orales 2 horas después de haber ingerido, de manera suicida, un agente tóxico desconocido. Originalmente, se la trató por intoxicación con organofosforados y luego se la trasladó al Hospital Saint Peter's en Addis Abeba para recibir atención médica más intensiva. Allí, se confirmó la ingesta de 2,4-D y se le brindó atención médica de apoyo, ventilación mecánica y diuresis alcalina forzada. A pesar de estas intervenciones, falleció varios días después.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una mujer de 23 años tomó 30 ml de 2,4-D, un veneno que se usa contra las malas hierbas. Lo hizo porque tenía problemas de dinero. Dos horas después la encontraron inconsciente y con mucha saliva. La llevaron a un hospital pequeño. Allí pensaron que era otro veneno y le dieron medicinas. Luego la trasladaron a un hospital más grande.\n\nAl llegar estaba muy dormida y no respondía. Al principio sus análisis de sangre y la radiografía no mostraron problemas grandes. En la unidad de cuidados intensivos le pusieron una sonda para proteger su respiración y le dieron líquidos y medicinas para ayudar a sacar el veneno por la orina.\n\nPero su situación empeoró. Los músculos se dañaron, y eso lesionó sus riñones. Empezó a orinar sangre y sus riñones dejaron de funcionar bien. También bajó demasiado su presión y tuvo que recibir medicinas para subirla. A pesar de los tratamientos, falleció al tercer día por un fallo circulatorio.\n\nEs una historia triste. Los médicos hicieron lo posible, pero algunos venenos son muy peligrosos y difíciles de tratar.",
+                "fh_score": 76.03
+            },
+            "B2": {
+                "text": "Resumen clínico (nivel B2, lectura para adolescentes)\n\nUna mujer de 23 años intentó suicidarse bebiendo cerca de 30 ml de 2,4-D, un herbicida (un producto para matar malezas). Dos horas después fue llevada al servicio de urgencias porque había perdido el conocimiento y tenía mucha saliva en la boca. Al principio la trataron en un hospital cercano pensando que se había intoxicado con organofosforados (otro tipo de veneno) y le dieron atropina y cimetidina durante 3 días antes de transferirla a un hospital más grande.\n\nAl llegar al Hospital Saint Peter:\n- Estaba inconsciente con una puntuación de 6/15 en la escala de Glasgow (una forma de medir el nivel de conciencia).\n- Tenía pupilas dilatadas pero que respondían a la luz, y las piernas estaban rígidas y con reflejos exagerados; el reflejo plantar estaba anormal (signo de daño en la vía nerviosa).\n- Ritmo cardiaco rápido (taquicardia) y otras pruebas iniciales (sangre, hígado, glucosa) salieron normales.\n- No se pudo medir el gas en sangre ni el nivel de la toxina porque el hospital no tenía esas pruebas.\n\nQué se hizo y cómo evolucionó:\n- Fue llevada a cuidados intensivos, se le puso un tubo para proteger la vía aérea y se inició diuresis alcalina forzada (una medida para intentar eliminar el veneno por la orina).\n- Desarrolló rabdomiólisis: las células musculares se dañaron y liberaron sustancias al torrente sanguíneo (el valor de creatina quinasa estaba alto), lo que dañó los riñones.\n- Apareció insuficiencia renal: la creatinina y el nitrógeno ureico en sangre (BUN), que muestran función renal, se elevaron mucho; en la orina se veía hemoglobina y muchos glóbulos rojos.\n- Se volvió hipotensa (presión arterial baja) y necesitaron medicación para subir la presión (vasopresores).\n- Ecocardiograma y ecografía abdominal no mostraron hallazgos importantes.\n- A pesar de las medidas de apoyo, falleció por colapso circulatorio al tercer día en la UCI.\n\nComentario y lecciones importantes (explicado con calma):\n- El 2,4-D es un herbicida que no tiene un antídoto específico; el tratamiento es sobre todo de soporte: proteger la respiración, controlar la presión, eliminar la toxina si es posible y cuidar los riñones.\n- En este caso hubo limitaciones en las pruebas disponibles (no se pudo medir la sustancia ni el gasometría), lo que complica el manejo.\n- La rabdomiólisis y la insuficiencia renal fueron complicaciones graves que contribuyeron al empeoramiento.\n- En intoxicaciones graves como esta, además de la atención intensiva, a veces se considera diálisis para ayudar a eliminar la toxina y apoyar los riñones.\n\nEs una situación triste: una joven sin antecedentes psiquiátricos que tomó esta decisión por problemas económicos. Casos así recuerdan la importancia de tener acceso rápido a pruebas y tratamientos específicos, así como apoyo emocional y social para prevenir intentos de suicidio.",
+                "fh_score": 52.45
+            },
+            "B3": {
+                "text": "Resumen clínico (paciente: mujer, 23 años)\n\nBreve introducción\n- Se presenta el caso de una mujer joven que intentó suicidarse ingiriendo aproximadamente 30 ml de 2,4-diclorofenoxiacético (2,4‑D), un herbicida. Fue llevada al servicio de urgencias 2 horas después de la ingestión y, tras tratamiento inicial en un hospital local por sospecha de intoxicación por organofosforados, fue trasladada a un centro terciario para manejo intensivo.\n\nAntecedentes y motivo de la ingesta\n- Intento de suicidio motivado por problemas financieros.\n- Sin antecedentes documentados de enfermedad psiquiátrica, consumo de tóxicos, intentos previos ni enfermedad cardíaca, renal o metabólica conocida.\n\nHallazgos al ingreso\n- Estado neurológico: conciencia gravemente alterada (GCS 6/15), pupilas dilatadas pero reactivas, hipertonicidad e hiperreflexia en miembros inferiores con signo de extensión plantar (anormal).\n- Signos vitales: frecuencia cardiaca 110/min, presión arterial 120/70 mmHg, frecuencia respiratoria 21/min, saturación de O2 96% en aire ambiente.\n- Pruebas iniciales normales: hemograma, pruebas hepáticas, pruebas renales y glucemia al ingreso fueron normales. ECG: taquicardia sinusal. Radiografía de tórax sin hallazgos.\n- No fue posible medir gases arteriales ni niveles séricos del tóxico por falta de disponibilidad.\n\nTratamiento inicial y medidas en UCI\n- Protección de vía aérea con tubo endotraqueal.\n- Diuresis alcalina forzada como medida para aumentar eliminación renal del tóxico.\n- Antes del traslado, recibió atropina y cimetidina en el hospital local por sospecha de organofosforados.\n\nEvolución y complicaciones\n- Desarrollo de rabdomiólisis: creatina fosfocinasa elevada (1.330 µg/L).\n- Insuficiencia renal aguda: creatinina 3,1 mg/dL (valor referencia 0,5–1,2), BUN 133 mg/dL (ref. 16,6–48,5). Análisis de orina: 3+ hemoglobina y numerosos glóbulos rojos.\n- Posteriormente se volvió hipotensa y requirió vasopresores.\n- Ecocardiograma y ecografía abdominal sin hallazgos relevantes.\n- Falleció por colapso circulatorio al tercer día en la UCI.\n\nInterpretación y puntos clave\n- 2,4‑D puede causar afectación neurológica severa, daño muscular (rabdomiólisis), fallo renal y alteraciones hemodinámicas; en este caso la progresión fue rápida y fatal a pesar de medidas de soporte intensivo.\n- La ausencia de pruebas toxicológicas y de gasometría limitó la monitorización específica del envenenamiento.\n- El diagnóstico inicial por error como intoxicación por organofosforados motivó tratamiento empírico (atropina), lo que ilustra cómo la identificación temprana del agente es importante para orientar intervenciones específicas.\n\nLecciones prácticas y siguientes pasos razonables (generales)\n- En intoxicaciones por herbicidas como 2,4‑D, la atención es mayoritariamente de soporte: estabilizar vía aérea, circulación y función renal; medidas de descontaminación precoz cuando procede; y considerar diálisis o soporte renal de reemplazo si hay insuficiencia renal grave o acumulación del tóxico.\n- Contar con pruebas analíticas (niveles séricos del tóxico, gasometría) facilita el manejo y el pronóstico.\n- Es clave la evaluación y el soporte psiquiátrico tras intentos de suicidio para prevención secundaria.\n\nComentario final\nEste caso ilustra la gravedad potencial de la ingestión de 2,4‑D y los límites que imponen la presentación tardía o el diagnóstico incierto y la falta de recursos diagnósticos. Lamento la trágica evolución de la paciente; el reporte subraya la necesidad de recursos de toxicología, acceso a terapias de reemplazo renal y servicios de salud mental en entornos con exposiciones a pesticidas.",
+                "fh_score": 43.7
+            }
+        }
+    },
+    {
+        "article": "Una paciente etíope de 35 años de edad se presentó en el departamento de urgencias del Colegio Médico del Hospital Yekatitit 12 con síntomas de falta de aire en reposo, ortopnea, disnea paroxística nocturna significativa, dolor torácico, tos productiva teñida de sangre y vómitos de materia ingerida (2-3 episodios por día) durante 2 semanas. Presentaba una hinchazón progresiva del cuerpo que comenzó en las extremidades inferiores y luego afectó a todo el cuerpo, fatigabilidad fácil, pérdida de apetito, fiebre intermitente de alto grado y sensación de ardor epigástrico durante la misma semana y con la misma duración. La paciente también experimentó una pérdida de peso y fatiga no especificadas durante los últimos 2 meses. Por lo demás, no tenía comorbilidades conocidas, ni comportamientos de riesgo, como fumar o beber alcohol, medicamentos o antecedentes familiares de neoplasia. Estaba casada, tenía cuatro hijos y no tenía antecedentes obstétricos negativos. Su ocupación era la agricultura y había vivido en una zona rural. Nunca había sido admitida por una queja similar.\n\nLa escala de coma de Glasgow (GCS) de la paciente fue de 15 sobre 15, y no había anormalidades de memoria, potencia o tono. La paciente estaba en grave dificultad respiratoria con saturación de oxígeno del 70% con aire atmosférico, frecuencia respiratoria de 30-35 latidos/minuto, y frecuencia del pulso de 120 por minuto. Tenía registros de fiebre de alto grado hasta el nivel de 39.5 0C y puede mantener su presión arterial. El examen de mama con ultrasonido y mamografía fue supuestamente normal. No se detectó linfadenopatía en áreas accesibles.\n\nEl examen del tórax reveló signos de derrame pleural que también se observaron en las imágenes y se analizaron. Una tomografía computarizada (TC) del tórax con contraste mostró derrame pericárdico y neumonía multifocal. La angiografía por TC mostró un defecto de llenado arterial pulmonar segmentario del lóbulo inferior en ambos lados, lo que sugiere embolia pulmonar y derrame pleural en ambos lados. Los frotis citológicos se informaron con láminas de células mesoteliales, neutrófilos y grupos dispersos de células grandes atípicas con nucleolos prominentes que sugieren derrame maligno. El análisis del líquido pleural mostró un líquido con predominio linfocítico con glucosa normal (82 mg/dl), proteínas (2,2 g/dl) y lactato deshidrogenasa (LDH) de 592 mg/dl.\n\nLa presión venosa yugular aumentó con los sonidos cardiacos apagados. La ecocardiografía mostró derrame pericárdico masivo con características de taponamiento cardiaco, fracción de eyección preservada (65%), y excursión sistólica del plano anular tricuspídeo (TAPSE) mayor a 18 mm. Un electrocardiograma (ECG) reveló solo taquicardia sinusal y desviación del eje. Se realizó una pericardiocentesis inmediata, se extrajo un drenaje de aproximadamente 250 ml de fluido hemorrágico y se aseguró la ventana pericárdica. La repetida ecocardiografía reveló una reducción del tamaño. El informe de citología del fluido pericárdico mostró numerosos linfocitos junto con células malignas atípicas que tenían prominentes nucleolos, lo que sugería un derrame maligno.\n\nEn el examen abdominal, mostró signos positivos de acumulación de fluidos sin órgano hinchable. La tomografía computarizada abdominal y pélvica mostró un aumento en el tamaño del hígado con múltiples lesiones hepáticas hipointensas que sugerían metástasis. Los órganos pélvicos, incluidos los ovarios y el útero, no presentaron lesiones identificadas. Se realizó una biopsia con aguja de la lesión hepática y los resultados revelaron un adenocarcinoma secundario.\n\nSe realizó un diagnóstico de insuficiencia cardíaca causada por una efusión pericárdica masiva maligna secundaria a un adenocarcinoma diseminado y un carcinoma de origen primario desconocido que afectaba al pulmón, la pleura, el pericardio y el tracto gastrointestinal. Se le diagnosticó a la paciente una trombosis venosa profunda extensa en la extremidad superior izquierda, una embolia pulmonar bilateral y segmentaria, posiblemente debido a la CUP diseminada. Los hallazgos también mostraron una neumonía multifocal superpuesta y una anemia leve de enfermedad crónica.\n\nEl recuento sanguíneo completo inicial reveló leucocitosis con un recuento de glóbulos blancos de 24 × 103 por ml, neutrófilos predominantes (91%), recuento de glóbulos rojos de 3.7 × 106 por µl, anemia normocítica leve (hemoglobina (Hgb) 11.2 mg/dl), volumen corpuscular medio (MCV) de 81.2 fl, y trombocitopenia severa (66 × 103/µl). Después del tratamiento antibiótico para neumonía, el recuento sanguíneo completo volvió a la normalidad (excepto para Hgb). Con niveles normales de bilirrubina, la aspartato aminotransferasa (AST) aumentó más de siete veces (263 U/L), mientras que la alanina transaminasa (ALT) aumentó más de nueve veces (332 U/L). Los electrolitos séricos (excepto para Na + con hiponatremia leve, 129 mEq/L) y las pruebas de función renal fueron normales. La albúmina era baja (2.12 g/dl). Los niveles de lactato deshidrogenasa (LDH) aumentaron casi dos veces desde el inicio (592 U/L). Los virus del virus de inmunodeficiencia humana, hepatitis B y hepatitis C no fueron reactivos. La sangre y el cultivo del líquido pleural no tuvieron crecimiento. Un antígeno carcinoembrionario (CEA) aumentó más de 400 veces (1000 µg/L) del inicio.\n\nLa paciente fue admitida en la sala general. Se realizó una ventana pericárdica y una inserción de un tubo torácico derecho con un cirujano cardiotorácico junto con un cardiólogo (ver la cantidad de aspirado antes). Se realizó una aspiración pleural terapéutica intermitente para el derrame pleural maligno. Una vez que la dosis de carga (60 mg) de frusemida produjo suficiente producción de orina, esta dosis se mantuvo tres veces (TID) al día. Esto se redujo y se dio de alta a la paciente con una dosis oral de 20 mg dos veces al día (BID). Se inició una dosis estándar de enoxaparina para el tromboembolismo pulmonar y la trombosis venosa profunda aguda extensa en la extremidad superior izquierda. Se administró enoxaparina por vía subcutánea 40 mg BID durante la hospitalización, que se cambió a 5 mg de warfarina oral diaria durante el alta debido a problemas financieros. La neumonía multifocal se trató con ceftazidima (1 g intravenoso TID) y vancomicina (1 g intravenoso BID) según el protocolo de tratamiento estándar nacional. El dolor se controló con un potente medicamento contra el dolor (morfina 5 mg intravenosa TID) y se redujo y suspendió. También estaba en la profilaxis de la úlcera. La paciente fue dada de alta de la sala médica con una mejora significativa después de 14 días de hospitalización y fue asignada a la unidad de oncología del hospital. Por lo tanto, para el cáncer de origen primario desconocido, se le dio un ciclo de quimioterapia (carboplatino/paclitaxel). Se perdió el seguimiento debido a problemas financieros, y la paciente murió en su casa cuatro meses después del alta.\n\nMH - Humanos\nMH - Mujer\nMH - *Insuficiencia cardiaca/etiología\nMH - Adulto\nMH - *Neoplasias, complicaciones/primaria desconocida",
+        "gold_summary": "Una mujer negra de 35 años se presentó con falta de aire en reposo, ortopnea, disnea paroxística nocturna, dolor torácico, tos productiva teñida de sangre y fiebre durante 2 semanas. También tenía hinchazón progresiva del cuerpo, fatigabilidad fácil, pérdida de apetito y dolor abdominal durante la misma semana. La imagen corporal reveló grandes derrames pleurales y pericárdicos, lesiones hepáticas metastásicas y defectos de llenado segmentarios y subsegmentarios vasculares pulmonares bilaterales. La citología de los fluidos pericardio y pleural sugieren derrame maligno. Las lesiones hepáticas y la biopsia con aguja indicaron adenocarcinoma de origen desconocido, y el nivel de antígeno carcinoembriónico también aumentó significativamente.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una mujer de 35 años fue al hospital porque le costaba mucho respirar. Tenía dolor en el pecho, tos con algo de sangre, fiebre, hinchazón por todo el cuerpo, y se sentía muy cansada y había bajado de peso.\n\nLos médicos encontraron mucho líquido alrededor de sus pulmones y alrededor del corazón. El líquido alrededor del corazón estaba apretando el corazón y por eso le costaba respirar. Le sacaron ese líquido y ella mejoró. Al mirar ese líquido, vieron células de cáncer.\n\nLas pruebas y una biopsia (un pequeño pedazo de tejido tomado con una aguja) mostraron que el cáncer había llegado al hígado y a las membranas del pecho y del corazón. No pudieron encontrar con seguridad de dónde empezó el cáncer. También tuvo coágulos de sangre en una vena del brazo y en los pulmones.\n\nLa trataron en el hospital. Le hicieron una pequeña operación para drenar el líquido del corazón y le pusieron un tubo en el pecho para sacar el líquido de los pulmones. Le dieron antibióticos para la infección, medicinas para bajar la hinchazón, calmantes y medicinas para los coágulos. Le dieron una sesión de quimioterapia (medicinas fuertes para tratar el cáncer).\n\nDespués de 14 días en el hospital, ella estaba mejor y salió a su casa. No pudo seguir el tratamiento por problemas de dinero. Cuatro meses después murió en su casa. Fue un caso triste de cáncer que ya se había extendido y que fue difícil de curar.",
+                "fh_score": 76.55
+            },
+            "B2": {
+                "text": "Summary (upper-intermediate / suitable for ages 14–17)\n\nA 35-year-old Ethiopian woman went to the emergency room with two weeks of worsening breathlessness (even at rest), trouble breathing when lying flat (orthopnea), sudden night-time breathlessness, chest pain, coughing up blood-stained mucus, vomiting, fever, and swelling that began in her legs and spread through her body. She had also lost weight and felt tired for about two months.\n\nImportant findings and tests\n- She was very sick on arrival: low oxygen (about 70%), fast breathing and heart rate, and high fever.\n- Chest scans showed large amounts of fluid around both lungs (pleural effusion) and around the heart (pericardial effusion). There was also pneumonia in several places and small blood clots in lung arteries (pulmonary emboli).\n- The heart ultrasound showed a large pericardial effusion causing cardiac tamponade. Cardiac tamponade means the fluid was pressing on the heart and stopping it from working normally.\n- Doctors drained blood-stained fluid from around the heart (about 250 ml) with a needle (pericardiocentesis) and made a surgical opening (pericardial window) so fluid could drain more easily.\n- Cell studies (cytology) of the fluid around the heart and lungs showed cancer cells, which suggested the effusions were caused by cancer.\n- An abdominal CT scan showed an enlarged liver with many lesions. A needle biopsy of a liver lesion showed metastatic adenocarcinoma — a common type of cancer that started somewhere else and spread to the liver.\n- Blood tests showed high white blood cells (infection/inflammation), low platelets at first (which later improved), low blood protein (albumin), very high liver enzymes, and a very high carcinoembryonic antigen (CEA), a marker often raised in some cancers.\n\nDiagnosis and other problems\n- The team diagnosed heart failure caused by a large malignant pericardial effusion, due to widely spread adenocarcinoma of unknown primary origin (called cancer of unknown primary, CUP). The cancer involved the lungs, pleura (lining of the lungs), pericardium (lining of the heart), and likely the digestive tract.\n- She also had a large blood clot in a vein of her left arm (deep vein thrombosis), pulmonary emboli (clots in the lungs), and multifocal pneumonia.\n\nTreatment and outcome\n- Emergency drainage of the heart and chest was done, repeated draining of the pleural fluid was performed, and a chest tube was placed.\n- She received diuretics (to remove extra fluid), antibiotics for pneumonia, strong pain relief, and blood thinners for the clots (started with enoxaparin, later changed to warfarin for cost reasons).\n- After 14 days in hospital she improved and was sent to the oncology unit. She began chemotherapy (carboplatin and paclitaxel) aimed at the cancer of unknown primary.\n- Due to financial difficulties she stopped follow-up care and died at home four months after leaving the hospital.\n\nWhat this means (in simple terms)\n- The patient had an aggressive cancer that spread to several places in her body and caused dangerous fluid build-up around her heart and lungs. Drainage and medical treatments helped in hospital, but the cancer was advanced and the exact original site could not be found. Financial and access problems affected ongoing care, and she died a few months later.\n\nThis case shows how cancer can present first with life-threatening fluid around the heart and lungs, and how serious complications (like clots and liver spread) make treatment harder. The medical team acted quickly to relieve the pressure on her heart and to treat infections and clots, but the advanced stage of disease made the outlook poor.",
+                "fh_score": 82.7
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel lector universitario)\n\nPresentación y síntoma principal\n- Mujer etíope de 35 años acudió por reciente insuficiencia respiratoria: disnea en reposo, ortopnea y disnea paroxística nocturna durante 2 semanas, acompañadas de dolor torácico, tos productiva con sangre, vómitos alimentarios, fiebre intermitente y edema progresivo generalizado. Además refirió pérdida de peso y fatigabilidad durante 2 meses.\n\nHallazgos iniciales y examen físico\n- Estado neurológico intacto (GCS 15), sin déficit motor o de memoria. Estaba taquipneica (FR 30–35/min), taquicárdica (pulso 120/min) y con saturación de oxígeno del 70% en aire ambiente. Tenía fiebre hasta 39.5 °C pero tensión arterial mantenida.\n- No se palparon adenopatías accesibles; examen mamario (ecografía y mamografía) informados como normales.\n\nImágenes y procedimientos urgentes\n- TC torácica con contraste: derrame pericárdico masivo, neumonía multifocal y derrames pleurales bilaterales. Angio-TC mostró defectos de llenado segmentarios bilaterales en arterias pulmonares, compatibles con embolia pulmonar.\n- Ecocardiograma: derrame pericárdico masivo con signos de taponamiento cardiaco; fracción de eyección conservada (~65%).\n- Se practicó pericardiocentesis urgente y se creó una ventana pericárdica; se extrajeron ≈250 ml de líquido hemorrágico, con reducción del derrame en la ecografía posterior. Se colocó drenaje torácico derecho y se realizaron aspiraciones pleurales terapéuticas.\n\nLaboratorio y citología\n- Sangre: leucocitosis marcada (24 × 10^3/µL) con neutrofilia (91%), anemia leve normocítica (Hb 11.2 g/dL), trombocitopenia severa inicial (66 × 10^3/µL) que luego mejoró tras tratamiento.\n- Bioquímica: elevación notable de transaminasas (AST 263 U/L, ALT 332 U/L), LDH aumentada (~592 U/L), albúmina baja (2.12 g/dL) e hiponatremia leve (Na+ 129 mEq/L). Pruebas virales (VIH, hepatitis B y C) negativas. Hemocultivos y cultivo de líquido pleural negativos.\n- Marcador tumoral: antígeno carcinoembrionario (CEA) muy elevado (>1000 µg/L).\n- Citología de líquido pleural y pericárdico: presencia de células malignas atípicas con nucleolos prominentes; líquido pleural linfocítico con glucosa normal, proteína aumentada y LDH elevada — compatibles con derrame maligno.\n\nHallazgos abdominales y diagnóstico histológico\n- TAC abdominopélvico: hepatomegalia con múltiples lesiones hipointensas en hígado sugestivas de metástasis; ovarios y útero sin lesiones identificadas.\n- Biopsia hepática por aguja: adenocarcinoma metastásico.\n- Se diagnosticó cáncer de origen primario desconocido (CUP) con afectación pleuro-pericárdica, pulmonar y hepática.\n\nComplicaciones adicionales\n- Trombosis venosa profunda extensa en miembro superior izquierdo y embolia pulmonar bilateral segmentaria, atribuibles al estado pro-trombótico paraneoplásico.\n- Neumonía multifocal superpuesta y anemia de enfermedad crónica.\n\nTratamiento y evolución\n- Manejo agudo: pericardiocentesis y ventana pericárdica, drenaje pleural derecho, diuréticos (furosemida) para congestión, anticoagulación con enoxaparina (cambiada a warfarina al alta por limitaciones económicas), y antibióticos (ceftazidima + vancomicina) para la neumonía. Analgesia y profilaxis de úlcera también.\n- Oncología: un ciclo de quimioterapia con carboplatino/paclitaxel para cáncer de origen desconocido.\n- Alta tras 14 días con mejoría clínica, pero la paciente perdió seguimiento por dificultades económicas y falleció en su domicilio cuatro meses después.\n\nInterpretación y implicaciones\n- El cuadro es compatible con un adenocarcinoma metastásico avanzado que se presentó inicialmente por complicaciones cardiopulmonares (derrame pericárdico maligno con taponamiento y derrames pleurales), además de tromboembolismo venoso masivo. La elevación muy marcada del CEA y la citología positiva apoyan origen adenocarcinomatoso, pero no se identificó de forma concluyente el tumor primario.\n- El pronóstico en este contexto era reservado/malo: derrame pericárdico maligno con taponamiento y enfermedad metastásica múltiple suelen asociarse a supervivencia limitada, a pesar del control sintomático y la quimioterapia paliativa.\n\nPasos diagnósticos y terapéuticos razonables (general)\n- En casos similares valorar tinción inmunohistoquímica de la biopsia hepática e investigación molecular para intentar identificar el tumor primario y detectar alteraciones tratables (cuando los recursos lo permitan).\n- PET-CT y estudios dirigidos según el panel inmunohistoquímico pueden ayudar a localizar el primario.\n- Enfoque multidisciplinario (oncología, cardiología, cuidados paliativos) para control sintomático, tratamiento antitromboembólico y planificación oncológica según estado funcional y objetivos de la paciente.\n\nComentario final (tono empático)\n- Esta paciente joven presentó una forma agresiva y avanzada de cáncer con complicaciones potencialmente mortales (taponamiento cardíaco, embolia pulmonar y metástasis hepáticas). A pesar de intervenciones urgentes y tratamiento paliativo, la enfermedad era sistémica y el desenlace fue fatal pocos meses después del alta. La atención integrada y el acceso a estudios diagnósticos y terapias más amplios pueden, en otros casos, ayudar a orientar tratamientos más específicos, aunque el pronóstico sigue siendo a menudo reservado en CUP con derrames malignos extensos.",
+                "fh_score": 28.8
+            }
+        }
+    },
+    {
+        "article": "Paciente del sexo femenino de 17 años con diagnóstico de enfermedad de Graves con bocio difuso, la cual negó otros antecedentes de importancia.\n\nSu cuadro comenzó seis meses antes con pérdida de peso progresiva, episodios de ansiedad y agitación, temperaturas de 37.4 a 37.9 ºC, palpitaciones, dolor abdominal y diarrea intermitente. A los dos meses se agregó como síntoma el crecimiento de la cara anterior del cuello; al tercer mes presentó taquicardia de hasta 130 latidos por minuto. Al ser valorada por Endocrinología se le administró tiamazol de 15 mg cada 8 horas, el cual fue suspendido por cuadro de agranulocitosis. Por lo tanto, se le comenzó a administrar lugol y propanol de 20 mg cada 8 horas, sin respuesta adecuada. Por ende, se decidió aplicar una dosis terapéutica de yodo 131 (I-131) 10 mcU.\n\n\nExploración física\nA la exploración física, la paciente presentó como signos basales una presión arterial no invasiva (PANI) 137/75 mmHg, frecuencia cardiaca (FC) 105 lpm, frecuencia respiratoria (FR) 16 rpm, SpO2 95%, temperatura 37.4ºC. La paciente ingresó deambulando, con agitación leve, con actitud cooperadora; estaba hidratada y sin datos clínicos de vía aérea difícil, pero no se valoró movilidad de tráquea por crecimiento tiroideo de aproximadamente 7.5 x 7 x 10 cm). La superficie del cuello era regular y su movilidad tenía una adecuada extensión. A la auscultación cardiopulmonar no hubo ruidos agregados y la paciente tenía ruidos cardiacos aumentados en frecuencia; asimismo, abdomen blando, depresible, no doloroso, con peristalsis presente. Extremidades integras, sensibilidad con aumento de la percepción del calor, hiperhidrosis palmar, fuerza 5/5, y temblor fino.\n\nSe empleó la escala de Burch y Wartofsky y se obtuvieron 40 puntos con elevada probabilidad de tormenta tiroidea, por lo cual se decidió manejo con anestesia multimodal.\n\nEn la monitorización tipo 2 la paciente presentó signos vitales iniciales PANI 137/75 mmHg, frecuencia cardiaca 96 latidos por minuto, frecuencia respiratoria 16 respiraciones por minuto, 95% Spo2, monitoreo invasivo de tensión arterial.\n\nPor inducción endovenosa se le administraron a la paciente 2 mg de midazolam; 150 mcg de fentanilo; 5 mg de cisatracurio y 50 mg de propofol.\n\nEl abordaje de la vía aérea se hizo con videolaringoscopía Glide Scope con hoja hiperangular 3 sin complicaciones. La ventilación mecánica invasiva modo volumen presentó flujos bajos FIO2 (40%).\n\nSe llevó a cabo bloqueo cervical superficial bilateral ecoguiado con 4 mL de ropivacaina al 0.2% en cada lado (16 mg en total).\n\nPara el mantenimiento se empleó sevoflorano CAM 0.8, infusión de dexmedetomedina 0.7 a 0.4 mcg/kg/hora, infusión de lidocaína 25 mcg/kg/hora, concentración plasmática de fentanilo 0.001 mcg/mL.\n\nEn cuanto a los adyuvantes se empleó paracetamol 750 mg + parecoxib 40 mg + ketorolaco intravenoso 30 + sulfato de magnesio 1250 g en infusión para una hora. El balance de líquidos fue negativo. El tiempo anestésico fue de 215 minutos. En el transoperatorio, la paciente estuvo hemodinámicamente estable, con presión arterial media de 67 a 75 mmHg, que se considera adecuada para la perfusión de órganos.\n\nEn el postoperatorio la paciente presentó analgesia durante 12 horas. Rescate con 1 g de metamizol por razón necesaria, utilizando un solo rescate. Disfonía postoperatoria persistente, sin presencia de odinofagia.",
+        "gold_summary": "Adolescente de 17 años con enfermedad de Graves con manifestaciones clínicas descontroladas, la cual no respondió a tratamiento médico y se programó para tiroidectomia radical. Se obtuvieron 35 puntos en la Escala de Burch y Wartofsky. Se manejó con anestesia general y fueron disminuyendo los estímulos para control de vía aérea y regional a fin de disminuir los estímulos quirúrgicos. Se usaron medicamentos adyuvantes como sulfato de magnesio para la estabilidad transoperatoria.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Esta es la historia de una chica de 17 años con una enfermedad llamada Graves. En Graves la tiroides, que está en el cuello, trabaja demasiado y hace que el cuerpo se acelere. Ella perdió peso, se sentía muy nerviosa y agitada, tenía el pulso rápido, sudaba y su cuello se hizo grande porque la tiroides creció.\n\nLe dieron un medicamento para bajar la tiroides, pero tuvo un problema serio en la sangre y el médico tuvo que dejar de dárselo. Probaron otros tratamientos que no funcionaron bien. Por eso decidieron quitar la tiroides con una operación.\n\nAntes de la operación, los médicos vieron que tenía alto riesgo de una complicación llamada “tormenta tiroidea”, que es cuando el cuerpo se altera mucho por la tiroides. Por eso prepararon todo con mucho cuidado.\n\nDurante la operación:\n- Le pusieron anestesia para que durmiera y no sintiera dolor.\n- Le cuidaron la respiración con una cámara especial para ver la garganta.\n- Pusieron medicinas que ayudan a mantener el corazón y la presión estables.\n- También usaron una inyección cerca del cuello para reducir el dolor.\n- La operación duró más de tres horas y la paciente estuvo estable todo el tiempo.\n\nDespués de la operación:\n- Estuvo sin dolor por 12 horas. Solo necesitó una medicina extra para el dolor una vez.\n- Quedó con la voz ronca por un tiempo, pero no tenía dolor al tragar.\n\nEn resumen: la chica tenía la tiroides muy activa y la medicina le causó un problema. Por eso le quitaron la tiroides con una operación. Los médicos la cuidaron muy bien antes, durante y después de la cirugía.",
+                "fh_score": 75.43
+            },
+            "B2": {
+                "text": "Here is a clear, caring summary written for a teenage reader:\n\n- Patient: 17-year-old girl with Graves disease. Graves disease is an autoimmune condition that makes the thyroid gland overactive and often causes the gland to grow (a goiter).\n\n- Symptoms before surgery: Over six months she lost weight, felt anxious and agitated, had mild fevers (about 37.4–37.9 °C), fast heartbeats (up to 130 beats/min), belly pain and intermittent diarrhea, and noticed a growing lump at the front of her neck. On exam she had a fast heartbeat, sweating, a fine tremor, and an enlarged thyroid about 7.5 × 7 × 10 cm.\n\n- Treatments tried: She was given thiamazole (a medicine that lowers thyroid hormone) but developed agranulocytosis, a serious drop in white blood cells, so that drug had to be stopped. She then received iodine and propranolol (a medicine to slow the heart), but her condition did not improve enough. A dose of radioactive iodine (I-131) was given, and because medical treatment was not controlling the disease, surgery to remove the thyroid (thyroidectomy) was planned.\n\n- Risk before surgery: Doctors used the Burch and Wartofsky score, a checklist that estimates the chance of a dangerous complication called “thyroid storm” (a sudden, severe increase in thyroid effects). Her score was 40, which means a high risk. Because of this, the anesthesia team prepared extra measures to keep her safe.\n\n- Anesthesia and pain control: She received general anesthesia using a combination of medicines to sedate her, control pain, and relax her muscles. Her airway was managed successfully with a video laryngoscope (a device that helps place the breathing tube) without problems. The team also performed a guided bilateral superficial cervical block (a local anesthetic injected around the neck) to reduce surgical pain and stress. Other medicines given during surgery helped keep her blood pressure and heart rate stable and decreased pain after surgery.\n\n- How she did during surgery: The operation and anesthesia lasted about 215 minutes (just over 3.5 hours). She remained hemodynamically stable (blood pressure and circulation were adequate), with a mean arterial pressure of about 67–75 mmHg, which is acceptable for organ blood flow. Fluid balance was slightly negative. There were no breathing or heart complications recorded during the operation.\n\n- After surgery: She had good pain relief for about 12 hours and needed only one extra dose of pain medicine (1 g metamizole). She had persistent hoarseness (voice change) after the operation but did not have painful swallowing. No other major problems were reported.\n\nTakeaway: This teenager had a severe, hard-to-control form of hyperthyroidism. Because medicines either caused a bad side effect or did not work well, surgery was chosen. The anesthesia team used several drug strategies and a local neck block to keep her safe and comfortable. She recovered from surgery without major complications, although she had lasting hoarseness that will need follow-up.",
+                "fh_score": 84.76
+            },
+            "B3": {
+                "text": "Resumen clínico\n\nPaciente femenina de 17 años con enfermedad de Graves y bocio difuso que consultó por seis meses de síntomas progresivos: pérdida de peso, episodios de ansiedad y agitación, febrícula (37.4–37.9 ºC), palpitaciones, dolor abdominal y diarrea intermitente. A los 2–3 meses apareció aumento del tamaño del cuello y taquicardia hasta 130 lpm. El tratamiento antitiroideo con tiamazol se suspendió por agranulocitosis (una reacción grave que disminuye los glóbulos blancos); los bloqueantes adrenérgicos y lugol no fueron suficientes, por lo que se administró yodo-131 y se programó tiroidectomía radical.\n\nHallazgos relevantes antes y durante la cirugía\n- Signos vitales preoperatorios: PA 137/75 mmHg, FC 105 lpm, T 37.4 ºC, SpO2 95%.  \n- Examen físico: paciente levemente agitada, hidratada, sin signos de dificultad respiratoria evidente; bocio grande (aprox. 7.5 x 7 x 10 cm). No se valoró movilidad traqueal debido al volumen tiroideo. Presentaba intolerancia al calor, hiperhidrosis palmar y temblor fino.  \n- Escala de Burch y Wartofsky: 40 puntos, valor que indica alta probabilidad de tormenta tiroidea — por ello se planificó manejo anestésico multimodal para minimizar riesgo hemodinámico-perioperatorio.  \n- Monitorización: invasiva para tensión arterial. Inducción con midazolam, fentanilo, propofol y cisatracurio; intubación con videolaringoscopio GlideScope sin complicaciones. Ventilación mecánica con FiO2 40%.  \n- Bloqueo cervical superficial bilateral bajo ecografía con ropivacaína 0,2% (4 mL por lado; 16 mg total).  \n- Mantenimiento anestésico: sevoflurano, infusión de dexmedetomidina (0.7→0.4 mcg/kg/h), lidocaína IV (25 mcg/kg/h) y fentanilo (concentración plasmática reportada).  \n- Adyuvantes analgésicos y estabilizadores: paracetamol 750 mg, parecoxib 40 mg, ketorolaco 30 mg IV y sulfato de magnesio (el informe menciona \"1250 g\", lo más probable es que sea 1250 mg = 1,25 g; parece un error tipográfico). Balance hídrico intraoperatorio fue negativo; tiempo anestésico 215 minutos.  \n- Transoperatoriamente la paciente permaneció hemodinámicamente estable; presión arterial media entre 67–75 mmHg (adecuada para perfusión).  \n\nEvolución postoperatoria\n- Analgesia efectiva por 12 horas; requirió un rescate único con 1 g de metamizol.  \n- Presentó disfonía persistente en el postoperatorio sin odinofagia (sin dolor al tragar). No se reportó tormenta tiroidea ni complicaciones hemodinámicas mayores.\n\nInterpretación y posibles pasos siguientes (implicaciones)\n- El manejo anestésico multimodal y la intubación guiada facilitaron una cirugía segura en una paciente con tirotoxicosis severa y riesgo elevado de tormenta tiroidea.  \n- La disfonía postoperatoria puede reflejar irritación o lesión temporal del nervio laríngeo recurrente o edema de cuerdas vocales; se recomienda evaluación otorrinolaringológica con laringoscopia y seguimiento vocal.  \n- Tras tiroidectomía es importante monitorizar calcio sérico (por riesgo de hipocalcemia por afectación de paratiroides), signos de hipotiroidismo y ajustar terapia de reemplazo hormonal tiroidea cuando proceda.  \n- Dado el antecedente de agranulocitosis por tiamazol, debe evitarse reexposición a ese fármaco y documentarse la alergia/efecto adverso en la historia clínica.\n\nComentario final\nLa intervención se desarrolló sin eventos hemodinámicos mayores y con control del dolor postoperatorio; sin embargo la paciente precisa seguimiento para la disfonía y vigilancia de complicaciones propias de la tiroidectomía (calcemia, función tiroidea y evaluación de nervio laríngeo). Si desea, puedo formular un plan de seguimiento detallado o una explicación más amplia sobre los riesgos habituales después de una tiroidectomía.",
+                "fh_score": 42.9
+            }
+        }
+    },
+    {
+        "article": "Una mujer de 30 años de edad, embarazada de 3, para 3, se presentó con disminución de la micción, dolor en el flanco izquierdo y fiebre durante 2 días después de una cesárea de emergencia por primera vez, indicada debido a la angustia materna y fetal secundaria al trabajo de parto prolongado y sangrado vaginal prolongado en el hospital Al-Thora, Ibb, Yemen. A pesar de los esfuerzos de reanimación, su recién nacido falleció después de 45 minutos. Durante la cesárea, se identificaron severas adherencias uterinas (ya que había lesiones de endometriosis y adherencias entre la pared posterior del útero y el colon sigmoide), y una pérdida de sangre estimada de 1500 cc, según el informe del ginecólogo. La paciente no recibió atención prenatal durante su embarazo. No es fumadora y negó condiciones médicas crónicas, abuso de drogas, intoxicación accidental o antecedentes quirúrgicos previos.\n\nEn el examen físico, el paciente se veía pálido, enfermo y febril durante la evaluación inicial, con una temperatura oral de 38 °C, pulso de 80 latidos por minuto y presión arterial de 95/70 mm Hg. El abdomen del paciente estaba levemente distendido, con sensibilidad moderada, principalmente en el cuadrante inferior izquierdo.\n\nLos datos de laboratorio fueron los siguientes: el recuento de glóbulos blancos (WBC) fue de 15,3 × 103/mL, con 90% de neutrófilos polimórficos (leucocitosis con predominio neutrofílico), la hemoglobina fue de 7,5 g/dL, el recuento de plaquetas fue de 200 × 103/µL, el nitrógeno ureico en sangre (BUN) fue de 23 mg/dl y la creatinina fue de 3,8 mg/dl. Otros análisis de sangre, como los de la función hepática y los de coagulación, estuvieron dentro de los rangos normales. La ecografía (US) mostró una hidronefrosis izquierda grave y un fluido libre moderado en la cavidad abdominal. Se realizó la aspiración de la punción abdominal y la creatinina en el punto fue de 52 mg/dL, lo que indica que el fluido era orina.\n\nLa paciente fue resucitada con glóbulos rojos concentrados y una amplia cobertura antibiótica. Después de esto, se le realizó una ureteroscopia urgente que mostró una oclusión total del uréter izquierdo. Se tomó la decisión de realizar una exploración quirúrgica, dada la inestabilidad hemodinámica, la falta de equipos de nefrostomía percutánea y la evidencia de contaminación intraabdominal. Durante la operación, se encontró fluido libre moderado en la cavidad abdominal. El uréter izquierdo fue aplastado y ligado con una sutura Vicryl (5 agujas) a unos 5 cm de su parte distal. Después de evacuar el fluido, se extirpó el segmento lesionado del uréter y se realizó una ureteroneocistostomía de forma refluyente tras distender la vejiga con solución salina a través del catéter. Además, diseccionamos el uréter, con cuidado, de los tejidos circundantes en dirección cefálica, espatulamos el extremo distal del uréter e insertamos un stent doble. Se implantó el uréter en la cúpula posterior de la vejiga urinaria con anastomosis sin tensión y se suturó con Vicryl 4-0 a través del uréter de espesor completo, luego la capa mucosa de la vejiga y la capa detrusora. Se insertó un drenaje Jackson-Pratt (JP) cerca de la anastomosis y se cerró la pared abdominal tras evaluar el contenido intraperitoneal.\n\n\nSeguimiento y resultado\nSe iniciaron líquidos transparentes el segundo día postoperatorio. La paciente tenía distensión abdominal leve, dolor y náuseas. El tercer día postoperatorio, tenía una distensión abdominal creciente y dejó de expulsar flatos. La ecografía abdominal mostró una gran cantidad de acumulación en la cavidad peritoneal. Los datos de laboratorio de sangre mostraron una leucocitosis (WBC de 22 × 103/mL con un cambio a la izquierda).\n\nUna tomografía computarizada (TC) del abdomen y la pelvis con contraste reveló una cantidad significativa de aire libre y líquido en todo el abdomen y la pelvis adyacente a la pared abdominal anterior. También se observaron múltiples localizaciones de gas libre en el mesenterio, con realce de contraste de múltiples bucles intestinales pequeños, sin evidencia de extravasación de contraste. Los hallazgos sugirieron una víscera perforada. Después de consultar al equipo de cirugía general, la paciente fue llevada inmediatamente al quirófano para una laparotomía exploratoria, que reveló una pequeña perforación en la parte rectosigmoidea con algo de derrame, peritonitis con edema del asa intestinal y alteración de la anastomosis ureteral. La complejidad de este caso nos obligó a realizar intervenciones en varias etapas de manera multidisciplinaria. En primer lugar, el ginecólogo realizó una histerectomía debido a endometritis (confirmada histopatológicamente), supuración severa y alteración de la sutura del útero. En segundo lugar, un urólogo realizó una derivación ureterocutánea del uréter izquierdo y se creó una urostomía en el lado izquierdo. Por último, el cirujano general realizó el procedimiento de colostomía después de reparar la lesión del colon y se creó una colostomía en el lado izquierdo. En el quinto día postoperatorio, se produjo retracción de la colostomía con infección de la herida y se observó comunicación entre la colostomía y la urostomía. Se decidió realizar una reexploración para reubicar la colostomía sigmoidea y se realizó una colostomía transversal derecha. Una semana después de la operación, la paciente experimentó una infección superficial de la pared abdominal complicada con dehiscencia de la herida e hipoalbuminemia (albúmina: 2 g/dL) que requirió tratamiento con varios desbridamientos, irrigación de la herida, antibióticos y terapia de apoyo. Los antibióticos recomendados fueron linezolid (600 mg IV cada 12 horas durante 7 días), luego cambiaron a ceftriaxona (1 g IV cada 12 horas durante 5 días) más metronidazol (500 mg IV cada 12 horas durante 5 días) y cambiaron a ciprofloxacina oral (500 mg cada 12 horas por vía oral durante 7 días). Gradualmente, reanudó su dieta normal y fue dada de alta 30 días después en condiciones estables. Requería atención domiciliaria para ayudarla con la colostomía, la ureterostomía y la deambulación.\n\nSeis meses después, se cerró la colostomía y se anastomosó el uréter mediante el procedimiento de colgajo de vejiga tabular de Boari (la vejiga se abrió en su superficie anterior y se volteó un colgajo de vejiga de espesor completo caudalmente y se tabularizó para anastomosis al segmento ureteral proximal después de la inserción de la endoprótesis doble J). Después de una recuperación postoperatoria sin incidentes, se dio de alta a la paciente el séptimo día postoperatorio. El seguimiento de un mes mediante ecografía y cistouretrografía miccional mostró un aspecto normal de la vejiga con capacidad vesical adecuada y un sistema del tracto urinario superior normal. Tres meses después, la ureteroscopia retrógrada mostró un calibre adecuado del uréter. Se hizo un seguimiento regular de la paciente con ecografía durante 3 meses durante un año. La paciente no tuvo síntomas irritativos o gastrointestinales en los 2 años de seguimiento.\n",
+        "gold_summary": "Una mujer de 30 años presentó disminución de la micción durante 2 días después de una cesárea. La ecografía mostró una hidronefrosis izquierda grave y un fluido abdominal libre moderado. Una ureteroscopia reveló una oclusión total del uréter izquierdo y, posteriormente, se realizó una ureteroneocistostomía. Dos días después, la paciente presentó complicaciones con distensión abdominal que requirieron una nueva exploración. La exploración reveló lesiones en el colon (recto-sigmoide), peritonitis, endometritis y alteración de la anastomosis ureteral. Se realizó una colostomía, reparación de lesiones en el colon, histerectomía y derivación ureterocutánea. La estancia hospitalaria de la paciente fue complicada, con retracción estomal que requirió revisión quirúrgica y dehiscencia de la herida, que se trató de forma conservadora. Después de 6 meses, se cerró la colostomía y se anastomosó el uréter mediante el procedimiento de colgajo de Boari.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había una mujer de 30 años que tuvo una cesárea de emergencia. Después de la operación, habló que orinaba menos, tenía dolor en el lado izquierdo y fiebre. \n\nLos médicos vieron que el riñón izquierdo estaba muy hinchado porque el conducto que lleva la orina (el uréter) estaba totalmente tapado. También había líquido en la barriga que resultó ser orina. Hicieron una operación para quitar la parte dañada del uréter y unirlo al lugar correcto en la vejiga. Pusieron un pequeño tubo dentro para que la orina pasara bien.\n\nUnos días después, la mujer tuvo mucho dolor y la barriga se puso peor. Un examen mostró que había una perforación, es decir, un orificio en el intestino (parte rectosigmoidea) y una infección dentro de la barriga llamada peritonitis. También había infección en el útero y el arreglo del uréter se había estropeado. \n\nPor la gravedad del problema, varios médicos trabajaron juntos. Hicieron:\n- una histerectomía (quitaron el útero) por infección,\n- una colostomía (hicieron que las heces salieran a una bolsa en la piel) tras reparar el intestino,\n- y una derivación del uréter a la piel (para que la orina saliera a una bolsa).\n\nTuvo más problemas: la colostomía se retrajo y la herida se infectó. Recibió más operaciones, limpieza de la herida y antibióticos. Poco a poco mejoró y salió del hospital a los 30 días. Necesitó ayuda en casa para cuidar las bolsas y caminar.\n\nSeis meses después le cerraron la colostomía y reconstruyeron el uréter usando un colgajo de la vejiga (llamado procedimiento de Boari). Le pusieron un stent temporal y la operación fue bien. En los controles posteriores, la vejiga y los riñones estaban normales. Tras un año y más, la mujer no tenía problemas y estaba bien.  \n\nAunque fue una situación muy difícil, al final recibió varias operaciones y cuidados, y se recuperó.",
+                "fh_score": 69.27
+            },
+            "B2": {
+                "text": "Summary (readability: upper-intermediate, for ages 11–17)\n\nA 30-year-old woman who had no prenatal care had an emergency cesarean section after a long labor and heavy bleeding. Sadly, her baby died shortly after birth. During the cesarean the surgeons found severe scar tissue in the pelvis (from endometriosis) and she lost a large amount of blood.\n\nTwo days after surgery she had very little urine, left-side belly pain, fever, and felt unwell. Blood tests showed infection (high white blood cells), severe anemia (low hemoglobin), and kidney injury (high creatinine). An ultrasound showed a very swollen left kidney (hydronephrosis — this means urine was backing up into the kidney) and fluid in the belly. The fluid was tested and found to be urine, meaning the urinary tract had been damaged and urine was leaking into the abdomen.\n\nShe received blood transfusions and antibiotics. An urgent scope of the ureter (the tube that carries urine from the kidney to the bladder) showed the left ureter was completely blocked. Because she was unstable and a tube from the kidney to the skin (nephrostomy) was not available, the team opened her belly. They removed the injured segment of the left ureter and reconnected the ureter to the bladder (ureteroneocystostomy) and put in a stent to keep it open. A drain was left near the repair.\n\nA few days later her belly became much more swollen, she stopped passing gas, and her white blood cell count rose. A CT scan showed free air and fluid in the abdomen, suggesting a hole in the bowel. Emergency surgery found a small perforation in the rectosigmoid (part of the colon), peritonitis (infection and inflammation of the abdominal cavity), an infected uterus, and a problem with the ureter repair.\n\nBecause of these problems, several teams operated together. The gynecologist removed the uterus (hysterectomy) because of severe infection. The urologist created a left ureterostomy (bringing the ureter to the skin to drain urine into a bag). The general surgeon repaired the colon and made a left colostomy (bringing part of the colon to the skin to divert stool). The patient then had more problems: the colostomy retracted and became infected, and there was communication between the colostomy and the urostomy. The team re-explored and moved the colostomy to the right side. She also developed a wound infection and the surgical wound partly opened; low blood protein (hypoalbuminemia) made healing harder. She was treated with antibiotics, repeated wound cleaning, and supportive care.\n\nAfter a difficult hospital stay of 30 days she was discharged in stable condition with help at home to manage the colostomy and urostomy. Six months later the surgeons closed the colostomy and repaired the ureter using a Boari flap (a piece of bladder tissue is reshaped and used to bridge the gap to the ureter) with a new stent. Her recovery after that operation was smooth. Follow-up tests over the next months showed normal bladder capacity and normal upper urinary tract, and ureteroscopy showed the ureter was wide enough. At two years after these events she had no urinary or bowel symptoms.\n\nOverall outcome: despite a very serious and complex course with multiple operations and complications, the patient recovered well, had her stomas closed, and had normal urinary and bowel function on follow-up. The case shows how pelvic scarring, heavy bleeding, and surgery can lead to accidental injury of the urinary tract and bowel, and how staged, team-based surgery and close follow-up can restore function.",
+                "fh_score": 84.08
+            },
+            "B3": {
+                "text": "Resumen clínico — caso de lesión ureteral compleja tras cesárea\n\nPresentación y contexto\n- Paciente: mujer de 30 años, embarazada de término, sin controles prenatales, sometida a cesárea de urgencia por trabajo de parto prolongado y sangrado vaginal. Durante la cesárea hubo pérdidas sanguíneas importantes (≈1.500 ml) y se describieron adherencias severas por endometriosis. El recién nacido falleció; la paciente presentó 2 días después disminución de la micción, dolor en flanco izquierdo y fiebre.\n\nHallazgos iniciales (anormales)\n- Signos vitales: febril (38 °C), algo hipotensa (PA 95/70 mm Hg).\n- Laboratorio: leucocitosis (WBC 15,3 ×10^3/µL, 90% neutrófilos), anemia grave (Hb 7,5 g/dL), elevación de creatinina sérica (3,8 mg/dL) y BUN 23 mg/dL — compatible con daño renal agudo y sepsis/hipoperfusión.\n- Ecografía: hidronefrosis izquierda severa y líquido libre abdominal moderado.\n- Análisis del líquido abdominal: creatinina 52 mg/dL (muy superior a la sérica) — esto confirma que el fluido era orina (urinoma) por lesión ureteral.\n- Ureteroscopia urgente: oclusión total del uréter izquierdo.\n\nIntervenciones iniciales\n- Reanimación con glóbulos rojos concentrados y antibióticos de amplio espectro.\n- Dadas la inestabilidad hemodinámica, la falta de acceso a nefrostomía percutánea y la contaminación abdominal, se optó por laparotomía urgente. Se encontró el uréter izquierdo aplastado y ligado a 5 cm de su porción distal. Se reseca el segmento lesionado y se realizó ureteroneocistostomía refluyente con colocación de stent doble J y drenaje JP.\n\nEvolución y complicaciones posteriores\n- A los 3 días: distensión abdominal progresiva, ileo (sin expulsión de flatos), incremento de leucocitos (WBC 22 ×10^3/µL).\n- TC abdominal: abundante líquido y aire libre en peritoneo, con gas en mesenterio y realce de asas intestinales — sugerente de perforación visceral.\n- Laparotomía exploratoria: perforación en rectosigma, peritonitis, edema intestinal y compromiso de la anastomosis ureteral.\n- Manejo multidisciplinario en varias etapas:\n  1. Histerectomía por endometritis y sutura uterina deteriorada (confirmada histopatológicamente).\n  2. Derivación ureterocutánea del uréter izquierdo (urostomía) por fallo de la anastomosis ureteral.\n  3. Reparación de la lesión colónica y colostomía izquierda.\n- Complicaciones posoperatorias: retracción de la colostomía con infección de herida y comunicación entre colostomía y urostomía; se reexploró y se reubicó la colostomía a transversal derecha. Posteriormente presentó infección superficial de la pared abdominal con dehiscencia y hipoalbuminemia (albúmina 2 g/dL), tratadas con desbridamientos, irrigación, antibióticos y soporte nutricional.\n\nAlta y reconstrucciones diferidas\n- La paciente fue dada de alta estable 30 días después, con cuidados en domicilio para colostomía y ureterostomía.\n- A los 6 meses se cerró la colostomía y se reconstruyó el uréter mediante colgajo de Boari (flap vesical tabularizado) con colocación de doble J. Recuperación postoperatoria sin incidentes; dada de alta al 7.º día.\n- Controles por imagen (ecografía, cistouretrografía miccional) a 1 mes mostraron vejiga con capacidad adecuada y tracto urinario superior normal. Ureteroscopia a los 3 meses mostró calibre ureteral adecuado. Seguimiento clínico/por ecografía hasta 1 año y evaluación clínica a 2 años sin síntomas urinarios o gastrointestinales.\n\nImplicaciones y puntos clave\n- Este caso ejemplifica una lesión ureteral iatrogénica grave tras cesárea complicada por adherencias y sangrado, que fue inicialmente reconocida por oliguria, dolor en flanco e hidronefrosis y confirmada por análisis de líquido abdominal (elevada creatinina).\n- La ausencia de recursos (no disponibilidad de nefrostomía percutánea) y la inestabilidad hemodinámica condicionaron la necesidad de terapia quirúrgica inmediata.\n- La anastomosis ureteral primaria fracasó en el contexto de contaminación abdominal y sepsis, obligando a derivaciones temporales (urostomía y colostomía) y posterior reconstrucción diferida (Boari flap), que dio buen resultado a largo plazo.\n- Complicaciones serias incluyeron peritonitis por perforación colo-rectal, infección de herida, dehiscencia y hipoalbuminemia; todas requirieron manejo multidisciplinario intensivo.\n\nConsejos prácticos (para pacientes y cuidadores)\n- La recuperación fue prolongada y requirió cuidados especializados de estomas y rehabilitación; la planificación precoz de apoyo nutricional y cuidado de la herida es importante en casos similares.\n- Cuando hay disminución de la orina, dolor lumbar y fiebre después de cirugía pélvica, es crítico investigar lesión ureteral o urinoma cuanto antes para reducir riesgo de sepsis y daño renal definitivo.\n\nTono final\n- La paciente tuvo un curso muy complejo y doloroso, pero gracias a intervenciones secuenciales y manejo multidisciplinario se logró restaurar la anatomía y la función urinaria y digestiva con buena recuperación a largo plazo.",
+                "fh_score": 38.93
+            }
+        }
+    },
+    {
+        "article": "Mujer de 43 años, con antecedente de hipertensión arterial con tratamiento con losartán, dos cesáreas y oclusión tubaria bilateral. Ingresó a nuestro hospital y refirió dolor de 24 horas de evolución, tipo cólico en hipogastrio e irradiación a fosa iliaca izquierda, además de náusea y vómito en dos ocasiones. Se agregaron evacuaciones semilíquidas en forma inicial y posteriormente cese en las evacuaciones y en la canalización de gases. A la exploración física, la paciente presentó dolor en el abdomen, así como distensión, especialmente hacia el flanco izquierdo. En el mesogastrio y el flanco izquierdo hubo la presencia de timpanismo. La peristalsis estaba presente, mínima, abolida en flanco izquierdo y mesogastrio. La irritación peritoneal estuvo ausente. Se colocó sonda nasogástrica, con gasto mínimo gástrico y sin mejoría en la sintomatología. Los estudios de laboratorio demostraron: 9700 leucocitos con un 87% de neutrófilos, creatinina de 0.7 mg/dL, urea de 22 mg/dL y proteína C reactiva de 5.0 mg/L. En la radiografía simple de abdomen presentó dilatación importante del lado izquierdo del colon, con niveles hidroaéreos. La tomografía muestra la dilatación del colon del lado izquierdo, con imagen que simula grano de café en el corte coronal.\n\nAnte estos hallazgos clínicos y de imagen, se decidió hacer laparotomía de urgencia ante la sospecha de la presencia de vólvulo de sigmoides o de síndrome adherencial complicado. Durante la cirugía se evidenció un ciego flexionado hacia adelante y a la izquierda, carente de fijación retroperitoneal. El punto de flexión fue producido por una banda de adherencia colocada sobre el colon ascendente. Se realizó liberación de la adherencia y se corroboró continuidad adecuada hacia el colon distal. No se evidenció la presencia de isquemia, necrosis o perforación del ciego. Se realizó apendicectomía con descompresión del ciego a través de base apendicular y posteriormente ligadura de esta. Se llevó a cabo cecopexia hacia pared de fosa iliaca derecha. Después de la cirugía, hubo mejoría clínica de la paciente, que tuvo evacuaciones presentes normales. La paciente siguió controles correctos en consulta externa de cirugía y se mantuvo asintomática.",
+        "gold_summary": "Mujer de 43 años que ingresó a un servicio de urgencias con datos de obstrucción intestinal. Se realizó tomografía simple de abdomen donde se identificó dilatación del colon e imagen que semejaba un grano de café invertido. Se hizo laparotomía exploradora y se identificó vólvulo cecal del tipo báscula, sin compromiso vascular. Se realizó desvolvulación, descompresión a través de apendicectomía, y cecopexia. Posterior a evento quirúrgico, la paciente se recuperó sin incidentes y fue dada de alta con controles adecuados por consulta externa.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una mujer de 43 años llegó al hospital con dolor de barriga, náuseas, vómitos y que no podía hacer caca ni sacar gases. Las radiografías y la tomografía mostraron que una parte del intestino grueso estaba muy hinchada y parecía torcida.  \n\nEn la operación se encontró que el ciego (el inicio del intestino grueso, que normalmente está en la parte derecha) se había doblado y girado hacia la izquierda por una banda de tejido que lo tenía pegado. Esa torsión se llama vólvulo y puede tapar el paso dentro del intestino. Por suerte, el intestino no estaba dañado ni muerto.  \n\nLos médicos quitaron la banda que pegaba el intestino, sacaron el apéndice para poder desinflar el ciego y fijaron el ciego a la pared para que no volviera a moverse. Después de la cirugía la mujer mejoró, empezó a evacuar normalmente y se fue a casa con controles. Está bien y no ha vuelto a tener problemas.",
+                "fh_score": 71.79
+            },
+            "B2": {
+                "text": "Mujer de 43 años que llegó al hospital con dolor abdominal, náuseas y vómitos, y luego dejó de tener deposiciones y expulsión de gases, signos que sugerían una obstrucción intestinal. La radiografía y la tomografía mostraron una gran dilatación del colon izquierdo y una imagen en \"grano de café\" que sugiere un intestino girado o comprimido. Ante la falta de mejoría con medidas iniciales se decidió operar de urgencia.\n\nEn la cirugía se encontró el ciego (la primera parte del colon, donde se une el intestino delgado) plegado hacia adelante y hacia la izquierda porque una banda de adherencia lo doblaba. Esto se describió como un vólvulo cecal del tipo “báscula” (el ciego se volcó o se giró sobre sí mismo). No había evidencia de falta de riego sanguíneo (isquemia), necrosis ni perforación. Los cirujanos liberaron la adherencia, descomprimieron el ciego quitando el apéndice (apendicectomía para vaciar el intestino por su base) y fijaron el ciego a la pared abdominal (cecopexia) para evitar que volviera a girarse.\n\nLa paciente mejoró después de la operación: recuperó las deposiciones normales y, en controles posteriores, permaneció sin síntomas. En resumen, se trató un vólvulo cecal sin daño tisular mediante desvolvulación, descompresión y fijación, con buena recuperación.",
+                "fh_score": 53.49
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel universitario)\n\nPaciente: mujer de 43 años con hipertensión arterial tratada con losartán; antecedentes quirúrgicos: dos cesáreas y oclusión tubaria bilateral.\n\nPresentación y examen:\n- Cuadro de 24 horas de evolución con dolor cólico en hipogastrio que irradiaba a la fosa ilíaca izquierda, náuseas, dos vómitos y cambio en las deposiciones: al inicio heces semilíquidas y luego detención de las evacuaciones y de la eliminación de gases (íleo obstructivo).\n- Exploración: distensión abdominal predominante en hemiabdomen izquierdo, timpanismo en mesogastrio y flanco izquierdo, peristalsis presente pero muy disminuida (prácticamente abolida en mesogastrio y flanco izquierdo). No hubo signos de irritación peritoneal.\n- Sonda nasogástrica con escaso drenaje y sin mejoría sintomática.\n\nPruebas complementarias:\n- Laboratorio: leucocitos 9 700/µL con 87% neutrófilos (predominio neutrofílico), creatinina y urea normales, PCR 5,0 mg/L (ligera elevación de marcador inflamatorio).\n- Radiografía de abdomen: importante dilatación del colon izquierdo con niveles hidroaéreos.\n- Tomografía abdominal: dilatación colónica izquierda con imagen en \"grano de café\" en cortes coronales, sugestiva de volvulus (torsión intestinal).\n\nDiagnóstico presuntivo y conducta:\n- Se planteó vólvulo de sigma versus obstrucción por adherencias complicada; por la gravedad del cuadro se realizó laparotomía exploradora urgente.\n\nHallazgos intraoperatorios y tratamiento:\n- Se identificó un vólvulo cecal del tipo báscula: el ciego estaba plegado hacia adelante y hacia la izquierda y carecía de su fijación retroperitoneal habitual.\n- El punto de flexión fue producido por una banda de adherencia sobre el colon ascendente. No había isquemia, necrosis ni perforación del ciego.\n- Se liberó la adherencia, se confirmó la continuidad intestinal distal y se procedió a desvolvulación. Para descompresión del ciego se realizó apendicectomía con descompresión por la base apendicular y posterior ligadura. Finalmente se realizó cecopexia (fijación del ciego a la pared abdominal en fosa iliaca derecha) para reducir el riesgo de recurrencia.\n\nEvolución y pronóstico:\n- La paciente mejoró clínicamente tras la cirugía; recuperó deposiciones normales y fue seguida en consulta externa de cirugía sin síntomas residuales.\n- Al no existir compromiso vascular del ciego no fue necesaria la resección intestinal, lo que favorece un pronóstico bueno a corto y medio plazo.\n\nImplicaciones y consideraciones:\n- El vólvulo cecal puede simular otros cuadros obstructivos; la imagen en \"grano de café\" en TC y la presentación clínica orientan al diagnóstico, pero la confirmación y el manejo definitivo pueden requerir cirugía urgente.\n- En ausencia de isquemia, las maniobras conservadoras de desvolvulación, descompresión y fijación (cecopexia) son adecuadas; cuando existe necrosis o perforación está indicada la resección.\n- Seguimiento ambulatorio y vigilancia ante signos de obstrucción recurrente o complicaciones posoperatorias son necesarios. Se puede considerar medidas para reducir formación de nuevas adherencias según la práctica quirúrgica.",
+                "fh_score": 37.92
+            }
+        }
+    },
+    {
+        "article": "Paciente de sexo femenino de 10 años, sin historia familiar de enfermedad tiroidea, portadora de bocio diagnosticado a los 9 años (ecografía tiroidea con sig nos compatibles de tiroiditis crónica) con presencia de anticuerpos antitiroideos positivos. Sin tratamiento al momento del ingreso hospitalario. Consultó por orina de aspecto espumoso de 5 días de evolución, asociado a dolor abdominal, vómitos profusos y diarrea. Evo lucionó con edema palpebral y de extremidades, disminución de la diuresis, decaimiento y fiebre de 38° C el día previo a su ingreso. Al momento de su eva luación en el servicio de urgencia destacó una pacien te con edema palpebral bilateral y pretibial, con bocio evidente (indoloro y sin nódulos palpables) y presen cia de soplo sistólico eyectivo en foco pulmonar IV/VI sin irradiación. Resto del examen sin alteraciones de significancia. Presión arterial 120/78 mmHg (percentil 95), temperatura 38,1°C, peso: 33.9 Kg, talla: 131,5 cm (p7), IMC 19,8 (p83).\n\nDentro de sus exámenes de admisión destacaron examen de orina completa con proteinuria +++, sin bacterias, sin nitritos, leucocitos 7 cel/uL (VN: 0-10 cel/uL), eritrocitos 4 cel/uL (VN: 0-15 cel/uL), índice proteinuria/creatininuria (IPC) 2 mg/mg, proteínas totales de 3.8 g/dL, hipoalbuminemia de 2,1 g/dL, hipercolesterolemia de 416 mg/dL, hipertrigliceridemia de 127 mg/dL y creatinina plasmática de 0,46 mg/dL (aclaramiento de creatinina calculado por fórmula de Schwartz: 125 ml/min/1,73 m2). Gases venosos, elec trolitos plasmáticos y hemograma dentro de rangos normales. En cuanto al estudio inmunológico destacó: inmunoglobulina A 181 mg/dL (VN 45-236), inmunoglobulina M 131 mg/dL (VN 52-242), inmunoglobulina G 208 (VN 608-1572) mg/dL, C3 125 mg/dL (VN 80-150), C4 37,3 mg/dL (VN 12-36). Ecografía renal normal. Se ingresó a la paciente con diagnóstico de SN y tiroiditis autoinmune.\n\nEn el contexto de SN se inició tratamiento con prednisona (60 mg/m2/día), con buena respuesta, logrando fundir edema y disminuir progresivamente la proteinuria hasta alcanzar rangos normales previo al egreso (IPC de egreso: 0.09, a los 6 días).\n\nDel punto de vista de función tiroidea su estudio mostró hormona tiroestimulante (TSH) 4,4 UI/ml (VN: 0,67-4,16 UI/ml), tiroxina (T4) libre 0,80 ng/ dL (VN: 0,86-1,4 ng/dL), anticuerpos antiperoxidasa (Anti Tpo) 120 U/ml (VN: 0-60 U/ml), anticuerpos antitiroglobulina (Anti-Tg) 82 U/ml (VN: 0-60 U/ ml), por lo que se inició terapia de sustitución con levotiroxina (25 mcg/día). La ecografía tiroidea descri bió tiroides de tamaño normal con leve aumento de vascularización difusa al Doppler, sin lesiones focales sólidas ni quísticas, siendo estos hallazgos sugerentes de tiroiditis. Resto del estudio (PCR para SARS CoV-2, anticuerpos anti citoplasma de neutrófilos, anticuer pos anti nucleares, anticuerpos anti DNA, anticuerpos anti estreptolisina O, anticuerpos anticardiolipinas, anticuerpos anti mieloperoxidasa y anticuerpos anti proteinasa 3) resultó negativo.\n\nA los 6 días de ingresada la paciente se encontraba en buenas condiciones, siendo dada de alta con prednisona (60 mg al día) y levotiroxina (25 ucg al día). En el seguimiento a los 12 meses la paciente se encontraba asintomática, con su patología tiroidea bajo control (TSH 1,11 UI/ml) con tratamiento de sustitución. No ha presentado recaídas del SN (examen de orina sin proteinuria y creatinina 0,44 mg/dL).",
+        "gold_summary": "Paciente de 10 años que se presenta con síndrome nefrótico y bocio. Se pesquisa antecedente de tiroiditis autoinmu ne e hipotiroidismo no tratado. Se inicia terapia corticoidal y hormonal de sustitución (levotiroxina), logrando buena respuesta clínica y de laboratorio.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había una niña de 10 años que tenía un bulto en el cuello porque su tiroides (la glándula del cuello) no trabajaba bien por una enfermedad del sistema que cuida al cuerpo. Un día llegó al hospital porque su orina estaba espumosa, tenía dolor de panza, vómitos, diarrea y después le salieron hinchazón en los párpados y las piernas. Los médicos encontraron que sus riñones perdían mucha proteína en la orina. Esa pérdida hizo que tuviera poco proteína en la sangre y mucho colesterol. \n\nLa niña recibió dos medicinas: una pastilla que baja la inflamación (prednisona) para cuidar los riñones, y otra que reemplaza la hormona de la tiroides (levotiroxina). Con las medicinas la hinchazón bajó y la orina dejó de tener tanta proteína en pocos días. Fue dada de alta y, al año, estaba muy bien: la tiroides funcionaba con la pastilla y los riñones no habían vuelto a fallar. Los médicos vieron que todo estaba bajo control y ella no tuvo recaídas.",
+                "fh_score": 70.69
+            },
+            "B2": {
+                "text": "Resumen claro y amable:\n\nSe trata de una niña de 10 años que llegó al hospital con orina espumosa, dolor abdominal, vómitos, diarrea y aparición de hinchazón en párpados y piernas. Tenía desde los 9 años un bocio (aumento de la glándula tiroides) diagnosticado como tiroiditis autoinmune —es decir, el propio sistema inmunitario ataca la tiroides— pero no estaba recibiendo tratamiento.\n\nDiagnósticos principales\n- Síndrome nefrótico: esto es un cuadro en el que los riñones pierden mucha proteína en la orina, lo que produce hinchazón, baja proteína en la sangre y niveles altos de colesterol. En esta paciente se confirmó por proteinuria alta (índice proteinuria/creatinina 2 mg/mg), albúmina baja (2,1 g/dL) y colesterol elevado (416 mg/dL). La función renal (creatinina) estaba normal y la ecografía renal no mostró alteraciones.\n- Tiroiditis autoinmune con hipotiroidismo leve: tenía anticuerpos tiroideos positivos y pruebas que mostraron TSH algo alta y T4 libre algo baja, por lo que se consideró necesario iniciar tratamiento.\n\nTratamiento y evolución\n- Para el síndrome nefrótico se le dio prednisona (un corticoide) a dosis alta. Respondió muy bien: la hinchazón cedió y la proteinuria mejoró hasta valores normales en seis días.\n- Para la tiroiditis se inició levotiroxina (hormona tiroidea) en dosis de 25 µg/día. La ecografía tiroidea apoyó el diagnóstico de tiroiditis.\n- Otros estudios de autoinmunidad fueron negativos.\n\nAlta y seguimiento\n- Fue dada de alta a los 6 días tomando prednisona y levotiroxina. A los 12 meses estaba asintomática, la función tiroidea controlada con el tratamiento (TSH 1,11 UI/ml) y sin recaídas del síndrome nefrótico (orina sin proteinuria).\n\nComentario final (calmado y práctico)\nLa niña tuvo dos problemas relacionados con el sistema inmune: uno que afectó la tiroides y otro que afectó los riñones. Ambos se trataron con medicamentos apropiados y la respuesta fue buena. Es importante el seguimiento médico para ajustar la hormona tiroidea y vigilar que el síndrome nefrótico no reaparezca.",
+                "fh_score": 54.84
+            },
+            "B3": {
+                "text": "Resumen clínico (empatético y claro)\n\nPaciente: niña de 10 años con antecedente de bocio e investigación previa compatible con tiroiditis crónica autoinmune (anticuerpos antitiroideos positivos), sin tratamiento hormonal al ingreso.\n\nPresentación y evolución inicial\n- Síntomas de 5 días: orina espumosa, dolor abdominal, vómitos profusos y diarrea. Posteriormente desarrolló edema palpebral y de extremidades, menor diuresis, decaimiento y fiebre (≈38 °C).\n- En el examen: edema palpebral bilateral y pretibial, bocio visible (indoloro, sin nódulos) y soplo sistólico eyectivo grado IV/VI en foco pulmonar. Presión arterial 120/78 mmHg (alrededor del percentil 95 para su edad), temperatura 38,1 °C, IMC en percentil 83.\n\nHallazgos de laboratorio y estudio imagenológico\n- Orina: proteinuria marcada (+++); cociente proteína/creatinina (IPC) en orina 2 mg/mg (rango nefrótico).\n- Sangre: proteínas totales 3,8 g/dL, albúmina 2,1 g/dL (hipoalbuminemia), colesterol total 416 mg/dL (hipercolesterolemia), triglicéridos 127 mg/dL; creatinina 0,46 mg/dL (aclaramiento según Schwartz ≈125 ml/min/1,73 m2).\n- Inmunología: IgG baja (208 mg/dL; rango referido 608–1572), IgA e IgM en rangos normales; C3 y C4 sin alteraciones clínicamente relevantes. La disminución de IgG es coherente con pérdidas urinarias en síndrome nefrótico.\n- Tiroides: TSH 4,4 UI/ml (ligeramente elevada), T4 libre 0,80 ng/dL (límite bajo), anti-TPO 120 U/ml y anti-Tg 82 U/ml (ambos positivos). Ecografía tiroidea: tamaño normal con aumento difuso de la vascularización (compatible con tiroiditis).\n- Ecografía renal normal. Estudios serológicos/autoinmunes adicionales (ANA, ANCA, anti‑DNA, PCR SARS‑CoV‑2, etc.) negativos.\n\nDiagnóstico\n- Síndrome nefrótico (probablemente de tipo minimal change o similar por rápida respuesta a corticoides), asociado a tiroiditis autoinmune con disfunción tiroidea leve/incipiente (hipotiroidismo subclínico/levemente franco).\n\nTratamiento y evolución\n- Se inició prednisona 60 mg/m2/día. Respuesta rápida y completa: desaparición del edema y normalización progresiva de la proteinuria; IPC al alta 0,09 (normal) a los 6 días.\n- Se inició levotiroxina 25 µg/día por alteración de la función tiroidea y anticuerpos positivos.\n- Alta hospitalaria al día 6 con prednisona y levotiroxina.\n- Seguimiento a 12 meses: asintomática, función tiroidea controlada con TSH 1,11 UI/ml en terapia de reemplazo; sin recaídas de síndrome nefrótico (orina sin proteinuria) y creatinina estable.\n\nImplicaciones y recomendaciones prácticas\n- El cuadro ilustra la coexistencia de enfermedad renal con pérdida proteica y una tiroiditis autoinmune que requiere tratamiento de reemplazo. En el síndrome nefrótico es habitual la pérdida urinaria de proteínas plasmáticas (albúmina, inmunoglobulinas, proteínas transportadoras) que puede agravar o revelar trastornos tiroideos y aumentar el riesgo de infecciones.\n- Buen pronóstico inmediato por la respuesta completa a esteroides; es necesario seguimiento continuado para:\n  - Vigilar recaídas del síndrome nefrótico y adaptación de la terapia esteroidea si aparecen recaídas o efectos adversos.\n  - Controlar función tiroidea y ajustar levotiroxina según crecimiento y cambios puberales.\n  - Monitorizar parámetros cardiovasculares y lípidos (dada la hiperlipidemia), estado vacunal y riesgo trombótico asociado con síndrome nefrótico.\n- En conjunto, la niña evolucionó favorablemente y permanece estable a 12 meses, pero requiere seguimiento pediátrico/nefrológico y endocrinológico periódicos.\n\nSi desea, puedo redactar una versión más breve para familiares o una hoja de seguimiento con los controles y signos de alarma que deben observar.",
+                "fh_score": 43.46
+            }
+        }
+    },
+    {
+        "article": "La exploración neurológica exhaustiva puso de manifiesto una apariencia facial característica: mirada fija con los ojos muy abiertos, fruncimiento de la frente con una expresión de ceño fruncido (signo del procerus) y expresión fija de la parte inferior de la cara. La paciente presentaba hipocinesia-rigidez simétrica de predominio axial con postura retrocólica del tronco y el cuello. El examen de la deambulación reveló un patrón de la marcha del nivel superior caracterizado por una llamativa vacilación inicial que requería ayuda de objetos/personas cercanas. Una vez que comenzaba a caminar, los pasos mejoraban relativamente, pero volvía a aparecer una marcha inefectiva cuando intentaba girar. Exhibía zancadas cortas, congelación, base amplia de sustentación, desequilibrio, movimiento lento de los miembros inferiores, arrastre de los pies y pérdida de la fluidez normal del tronco y las extremidades. Los reflejos posturales estaban alterados. Asimismo, existía una dificultad grave para la bipedestación tras la sedestación y dificultad para darse la vuelta en la cama. Sin embargo, los signos frontales, como la rigidez paratónica, los reflejos de prensión, la incontinencia urinaria y las características de los déficits cognitivos frontales (por ejemplo, cambios disejecutivos y de personalidad e impulsividad) estaban ausentes, excepto por un estado apático progresivo. Los movimientos oculares sacádicos verticales estaban alterados, con amplitudes relativamente normales y movimientos sacádicos horizontales. Se evidenciaron sacadas de onda cuadrada y una oftalmoplejía supranuclear. La resonancia magnética del cerebro reveló atrofia del mesencéfalo, dilatación del acueducto de Silvio y del III ventrículo y atrofia de los lóbulos frontales, y los signos típicos del colibrí y de la gloria de la mañana. Finalmente, la paciente fue diagnosticada de una PSP probable.",
+        "gold_summary": "Mujer de 58 años sana que consultó por un trastorno de la marcha con caídas. La exploración neurológica mostró una apariencia facial característica (mirada fija, ojos muy abiertos, ceño fruncido y expresión fija hemifacial inferior), e hipocinesia-rigidez simétrica de predominio axial (postura retrocólica del tronco y el cuello). La exploración de la marcha reveló un trastorno de la marcha del nivel superior, caracterizado por una significativa vacilación inicial, que precisaba ayuda de objetos/personas cercanos. Al iniciar la marcha, los pasos mejoraban relativamente, pero reaparecía una deambulación inefectiva al girar. Presentaba zancadas cortas, congelación, base amplia de sustentación, desequilibrio, movimiento lento de las piernas, arrastre de los pies, y pérdida de la cadencia normal del tronco y las extremidades. Los reflejos posturales estaban alterados. La resonancia magnética cerebral desveló atrofia mesencefálica, dilatación de acueducto de Silvio y III ventrículo, atrofia frontal bilateral y el signo típico del colibrí. Finalmente, la paciente fue diagnosticada de una PSP probable.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una mujer de 58 años fue a la consulta porque tenía problemas para caminar y se caía.  \nSu cara parecía rígida: miraba fijamente, tenía los ojos muy abiertos y el ceño fruncido.  \nEl cuerpo y el cuello estaban tiesos y se movía muy despacio.  \nAl empezar a andar, dudaba mucho y necesitaba apoyarse en cosas o en otras personas.  \nCuando ya llevaba unos pasos, caminaba un poco mejor, pero al girar volvía a fallar.  \nSus pasos eran cortos, a veces se quedaba “pegada” (congelación), arrastraba los pies y perdía el equilibrio.  \nLe costaba ponerse de pie después de estar sentada y también girarse en la cama.  \nLos movimientos de los ojos hacia arriba y abajo estaban alterados.  \nLa resonancia mostró que algunas partes del cerebro estaban más pequeñas y que unos espacios con líquido estaban más grandes.  \nLos médicos vieron cambios en la imagen que son típicos de una enfermedad llamada PSP.  \nPSP es una enfermedad que afecta el movimiento, el equilibrio y la mirada.  \nPor todo esto, la diagnosis final fue de PSP probable. Esto puede ser duro, y la persona necesita apoyo y cuidados.",
+                "fh_score": 74.18
+            },
+            "B2": {
+                "text": "Here is a clear summary written for readers at an upper-intermediate (B2) level:\n\nA 58-year-old woman went to the doctor because she had trouble walking and had fallen. On exam she had a striking facial look: a fixed stare, very wide-open eyes, a deeply furrowed brow (called the procerus sign), and a lower face that looked less expressive. She moved more slowly and was stiff, especially in the trunk and neck, which were bent slightly backward.\n\nHer walking showed a typical “higher-level” gait problem: she hesitated a lot before starting to walk and often needed to hold on to things or people to begin. Once she started, her steps improved a bit, but she had trouble when turning and her walking became ineffective again. Other features were short steps, episodes of “freezing” where she could not start stepping, a wide stance for balance, unsteadiness, slow leg movements, dragging of the feet, and loss of normal smooth movement of the trunk and limbs. Her automatic balance reactions (postural reflexes) were reduced, and she had trouble standing up from a sitting position and turning over in bed.\n\nEye movement testing showed problems with vertical saccades (quick up-and-down eye movements) and signs of supranuclear ophthalmoplegia — an eye movement disorder caused by brain control problems rather than muscle weakness. Small involuntary eye movements called square-wave jerks were also seen. Brain MRI showed shrinkage (atrophy) in the midbrain and frontal lobes, enlargement of fluid-filled spaces including the aqueduct of Sylvius and the third ventricle, and imaging patterns often called the “hummingbird” and “morning glory” signs, which are typical in this condition.\n\nPutting these findings together, the doctors diagnosed probable progressive supranuclear palsy (PSP). PSP is a neurodegenerative disease that mainly affects balance, walking, posture, and eye movements. The MRI and the clinical signs supported this diagnosis.",
+                "fh_score": 78.58
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel universitario, lectura B3)\n\nPaciente: mujer de 58 años que consultó por alteración de la marcha con caídas.\n\nHallazgos principales\n- Apariencia facial característica: mirada fija con ojos muy abiertos, ceño fruncido (signo del procerus) y expresión fija en la parte inferior de la cara — un patrón distintivo en ciertas enfermedades neurodegenerativas.\n- Trastorno motor axial simétrico: hipocinesia (movimiento reducido) y rigidez predominantemente en el tronco y el cuello, con postura retrocólica (el tronco y la cabeza inclinados hacia atrás).\n- Trastorno de la marcha de “nivel superior”: inicio vacilante que requiere apoyo, mejoría relativa al comenzar a andar pero marcada dificultad al girar; pasos cortos, episodios de congelación, base de sustentación amplia, arrastre de los pies, lentitud de las piernas y pérdida de la cadencia normal. Los reflejos posturales estaban alterados; también había dificultad importante para ponerse de pie desde la sedestación y para darse la vuelta en la cama.\n- Función frontal: no se documentaron los signos frontales típicos (rigidez paratónica, reflejos de prensión, incontinencia urinaria ni déficits cognitivos frontales claros como desinhibición o impulsividad). Sí existía un cuadro de apatía progresiva.\n- Oculomotricidad: alteración de las sacadas verticales con presencia de sacadas “onda cuadrada” y oftalmoplejía supranuclear (limitación de los movimientos oculares por un defecto supranuclear), mientras que las sacadas horizontales eran relativamente preservadas.\n- Imagen por resonancia magnética (RM): atrofia del mesencéfalo (signo del “colibrí” o “hummingbird”), dilatación del acueducto de Silvio y del tercer ventrículo y atrofia frontal bilateral (también descrito como el signo de la “gloria de la mañana”).\n\nImpresión diagnóstica\n- Diagnóstico final: probable PSP (parálisis supranuclear progresiva), una enfermedad neurodegenerativa que típicamente produce problemas de equilibrio y marcha, alteraciones de la mirada supranuclear (especialmente vertical) y cambios en el comportamiento o la motivación.\n\nImplicaciones y pasos siguientes sugeridos\n- Pronóstico: progresiva a lo largo de varios años, con aumento del riesgo de caídas y limitación funcional; la progresión y el tiempo varían entre pacientes.\n- Manejo inmediato y a medio plazo: evaluación por un equipo de trastornos del movimiento (neurólogo especialista), fisioterapia enfocada en equilibrio y estrategias para disminuir caídas, terapia ocupacional para adaptar actividades y el hogar, evaluación de la deglución y terapia del habla según necesidad, y apoyo psicológico/social para paciente y cuidadores.\n- Tratamiento farmacológico: no existe cura; algunos fármacos (p. ej., prueba con levodopa) pueden probarse pero la respuesta suele ser limitada. El tratamiento es mayormente sintomático y de soporte.\n- Seguimiento: controles periódicos para monitorizar progresión, ajustar medidas de seguridad y planificar cuidados a largo plazo; considerar derivación a servicios de cuidados paliativos cuando los síntomas sean avanzados.\n\nComentario empático\nEsta situación suele ser difícil para la paciente y su familia. Es importante ofrecer información clara, apoyo multidisciplinario y medidas concretas para reducir el riesgo de caídas y mantener la autonomía el mayor tiempo posible.",
+                "fh_score": 34.62
+            }
+        }
+    },
+    {
+        "article": "Una mujer de 36 años, previamente sana, fue picada una vez por un insecto Hymenoptera desconocido, lo que le provocó hinchazón y eritema en la parte dorsal de la mano derecha. La fiebre punzante apareció en un plazo de 6 horas, a pesar de que el sitio de la picadura se volvió irreconocible gradualmente. Acudió a una clínica local donde le recetaron esteroides orales (prednisolona 20 mg/día) y antibióticos. Tres días después, acudió a nuestro departamento de urgencias por una fiebre intermitente. Presentaba una temperatura elevada (38,9°C), taquicardia e hipotensión (presión arterial 80/52 mmHg) en el momento de la clasificación. La electrocardiografía mostró fibrilación auricular con una frecuencia ventricular rápida de alrededor de 130 latidos por minuto y elevación difusa del ST. La radiografía de tórax mostró una relación cardiotorácica normal sin signos de infiltración o congestión. El hemograma no mostró eosinofilia, leucocitosis, leucopenia o desviación a la izquierda. La isoenzima MB de creatina cinasa (CK-MB) y la troponina cardíaca I se elevaron a 96,0 ng/mL y 8,0 ng/mL, respectivamente. La proteína C reactiva fue de 10,5 mg/L y la procalcitonina fue de 0,32 ng/mL. El NT-proBNP fue de 20 700 pg/mL. La ecocardiografía mostró una hipocinesia global del ventrículo izquierdo con una fracción de eyección del 30,6% y sin derrame pericárdico. El cateterismo cardíaco emergente no reveló lesiones de las arterias coronarias o vasospasmo. Se insertó un globo intraaórtico durante el procedimiento para el shock cardiogénico. La hipotensión progresó acompañada de taquicardia ventricular y fibrilación ventricular, y luego se produjo un paro cardíaco intrahospitalario. La reanimación cardiopulmonar manual no tuvo éxito durante 25 minutos y se usó el soporte cardiopulmonar percutáneo (PCPS, CAPIOX® Centrifugal Pump Controller SP-200, Terumo). La circulación espontánea se estableció 25 minutos después con una recuperación total de la conciencia.\n\nLa prueba rápida de antígeno de influenza (Directigen EZ Flu A+B; BD, Franklin Lakes, NJ, EE. UU.), los cultivos de esputo, los cultivos de sangre y los exámenes serológicos para los virus respiratorios recolectados al ingreso fueron negativos. En el día 2 del ingreso, los niveles séricos de CK-MB y troponina I alcanzaron un máximo de >303 ng/ml y >81 ng/ml, respectivamente. La ecocardiografía de seguimiento 24 horas después del inicio del PCPS mostró deterioro de la función ventricular izquierda, cierre persistente de las válvulas aórticas y trombos intracardiacos en la aurícula izquierda y el ventrículo izquierdo, aproximadamente 24 horas después del inicio del soporte mecánico. En el día 3, el shock progresó con falla multiorgánica. Se aplicó hemodiálisis venovenosa continua debido a la acidosis metabólica y oliguria. En el día 4, la función ventricular derecha también se deterioró gravemente y la actividad eléctrica del corazón desapareció gradualmente. El PCPS se cambió a soportes mecánicos bi-ventriculares a través de canalizaciones hacia la aurícula derecha, el tronco pulmonar, el ápex del ventrículo izquierdo y la aorta ascendente. Ambos sistemas se establecieron utilizando bombas de sangre centrífugas MEDTRONIC Affinity CP. Debido a la hemorragia pulmonar con consolidación bilateral severa de los pulmones, se usó un oxigenador de membrana para lograr una oxigenación adecuada. El flujo sanguíneo se estableció a 3.5 L/minuto, lo que podría mantener la presión arterial media en torno a 65 mmHg. Se realizó una biopsia endomiocárdica del ventrículo izquierdo y la patología reveló una inflamación significativa compuesta principalmente por linfocitos y algunos eosinófilos. El daño miocárdico con necrosis estuvo presente, pero no extenso. En términos de ajustes de ventilador, la presión de conducción y la presión de meseta se establecieron en torno a 15 y 30 cmH2O respectivamente para la protección pulmonar. Se usó la fibra broncoscopia repetidamente para eliminar los coágulos de sangre que obstruían las vías respiratorias principales. En el día 13 del ingreso, la actividad eléctrica del corazón del paciente permaneció ausente y ambas bombas de sangre se cambiaron a los sistemas de asistencia ventricular Levitronix Centri-Mag (Levitronix LLC, Waltham, MA, EE. UU.) para un mejor soporte. El paciente fue trasladado a un centro de trasplantes y se registró como candidato para un trasplante de corazón. En el día 14 se insertó otra cánula en la vena femoral común izquierda para aumentar el flujo de entrada del VAD derecho. Desde el día 14 hasta el día 48, el paciente sufrió episodios de sangrado masivo del mediastino y la vagina, infección de la herida esternal con formación de abscesos, infecciones por úlceras de presión y progresiva hiperbilirrubinemia. Su condición se estabilizó después de desbridamiento, hemostasia quirúrgica y uso de antibióticos fuertes. Se sometió a 5 cursos de intercambio de plasma terapéutico para evitar el rechazo mediado por anticuerpos y recibió un trasplante de corazón ortotópico el día 49. El estudio patológico del corazón del paciente mostró pancarditis de ambos ventrículos y ninguna alteración específica de las 3 arterias coronarias. La ECMO de VA se mantuvo hasta el día 58 para el apoyo postoperatorio del fallo cardiaco. La biopsia endomiocárdica repetida después del trasplante no mostró evidencia de rechazo celular o humoral. La paciente experimentó episodios de shock séptico bajo inmunosupresión y se sometió a una laparoscopia exploratoria y apendicectomía el día 93. La extubación se realizó el día 96 y se dio de alta el día 101. La paciente permaneció clínicamente estable en el seguimiento de 3 meses.\n\nMH - Adulto\nMH - Animales\nMH - Abejas\nMH - Picaduras y mordeduras/*complicaciones\nMH - Oxigenación por membrana extracorpórea\nMH - Mujer\nMH - Paro cardiaco/*etiología/tratamiento\nMH - Insuficiencia cardiaca/*etiología/terapia\nMH - *Trasplante de corazón\nMH - Dispositivos de asistencia cardiaca\nMH - Humanos\nMH - Hipersensibilidad/*diagnóstico\nMH - Miocarditis/*diagnóstico\nMH - Shock, Cardiogénico/*etiología/terapia\n",
+        "gold_summary": "Paciente: Mujer, 36 años\n\nDiagnóstico final: Shock cardiogénico • miocarditis\n\nSíntomas: Fiebre\n\nMedicación: —\n\nProcedimiento clínico: soporte circulatorio mecánico\n\nEspecialidad: Cirugía\n\n\nInforme del caso:\n\nReportamos el caso de una mujer de 36 años que desarrolló fiebre y shock cardiogénico 3 días después de una picadura de abeja. La angiografía cardíaca mostró arterias coronarias permeables y una función ventricular izquierda gravemente comprometida. Su hemodinámica permaneció inestable bajo una dosis alta de agentes inotrópicos y apoyo con un balón intraaórtico. El paro cardíaco intrahospitalario ocurrió 4 horas después del ingreso y recibió reanimación cardiopulmonar extracorpórea. Su oxigenación de membrana extracorpórea venosa periférica (VA ECMO) se cambió a dispositivos de asistencia ventricular bilateral (VAD) debido a una insuficiencia cardíaca derecha progresiva. El resultado de la biopsia endomiocárdica fue compatible con el cuadro de miocarditis por hipersensibilidad. Su corazón entró en paro persistente bajo apoyo circulatorio mecánico. Se sometió a un trasplante de corazón el día 49 del ingreso y permaneció clínicamente estable 6 meses después del alta.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había una mujer de 36 años que fue picada por un insecto en la mano. La picadura se hinchó y poco después ella tuvo fiebre. Tres días más tarde fue al hospital porque estuvo muy enferma. Tenía el pulso muy rápido y la presión baja. Su corazón no podía bombear bien la sangre. Los médicos vieron que las arterias del corazón estaban normales, pero el músculo del corazón estaba inflamado. Esto se llama miocarditis. Es como si algunas células del cuerpo hubieran atacado al corazón.\n\nLa mujer sufrió un paro cardíaco dentro del hospital. Recibió muchos cuidados y se usó una máquina que bombea y oxigena la sangre por fuera del cuerpo. También le pusieron otros dispositivos para ayudar los dos lados del corazón. Durante su enfermedad tuvo sangrados, infecciones y problemas con los riñones. Los médicos llegaron a la conclusión de que su corazón no iba a mejorar. Por eso, después de muchos días le hicieron un trasplante de corazón nuevo.\n\nDespués de la operación, la mujer fue cuidada mucho tiempo. Mejoró poco a poco. Salió del hospital y estuvo estable meses después. Los médicos creen que la inflamación del corazón pudo estar relacionada con la reacción a la picadura. Aunque fue un caso muy grave, recibió tratamiento y finalmente pudo recuperarse.",
+                "fh_score": 77.66
+            },
+            "B2": {
+                "text": "Resumen (nivel B2, para lectores de 11–17 años)\n\nQué pasó\n- Una mujer de 36 años recibió la picadura de un insecto del grupo Hymenoptera (por ejemplo, una abeja). En las horas siguientes tuvo hinchazón y enrojecimiento en la mano y empezó a tener fiebre.\n- Tres días después acudió al hospital con fiebre, pulso muy rápido y presión arterial baja. En el electrocardiograma tenía una arritmia (fibrilación auricular) y cambios que sugerían daño al corazón.\n- Las pruebas de sangre mostraron elevación marcada de las enzimas cardíacas (troponina y CK‑MB), que indican lesión del músculo del corazón. La ecocardiografía mostró que el ventrículo izquierdo funcionaba muy mal (fracción de eyección baja).\n\nDiagnóstico probable\n- Los médicos concluyeron que tenía miocarditis, es decir, inflamación del músculo cardíaco. En este caso parecía ser miocarditis por hipersensibilidad: una reacción del sistema inmune (posible reacción alérgica) que daña el corazón después de la picadura.\n\nQué tratamientos recibió\n- Le hicieron un cateterismo para ver las arterias coronarias; estaban abiertas, por lo que no había ataque al corazón por obstrucción.\n- Empezó con soporte farmacológico y un balón intraaórtico, pero su situación empeoró: sufrió arritmias graves y paro cardíaco dentro del hospital.\n- La reanimación manual no fue suficiente, por lo que se conectó a soporte cardiopulmonar percutáneo (ECMO/PCPS), una máquina que hace temporalmente el trabajo del corazón y los pulmones.\n- Su corazón empeoró y desarrolló trombos dentro de las cámaras y fallo de ambos ventrículos, por lo que el equipo cambió a dispositivos de asistencia ventricular (VAD) para mantener la circulación.\n- A lo largo de su ingreso tuvo complicaciones (sangrados graves, infecciones, fallo renal que necesitó diálisis). Se le practicaron biopsias del corazón que mostraron inflamación con linfocitos y algunos eosinófilos, compatible con miocarditis por hipersensibilidad.\n- Fue incluida en lista para trasplante y recibió un trasplante de corazón el día 49. Tras el trasplante no mostró rechazo en las biopsias posteriores.\n\nEvolución y resultado\n- Tras el trasplante y cuidados intensivos prolongados (incluyendo soporte ECMO temporal), la paciente mejoró. Tuvo episodios de infección que requirieron cirugía, pero fue extubada el día 96 y dada de alta el día 101.\n- En el seguimiento a 3 meses estaba clínicamente estable.\n\nMensaje clave (explicado con calma)\n- La picadura de un insecto rara vez puede desencadenar una reacción inmunológica grave que dañe el corazón (miocarditis).  \n- La miocarditis puede provocar fallo cardíaco y paro, y a veces necesita soporte mecánico largo y hasta un trasplante de corazón.  \n- Gracias a la atención intensiva y al trasplante, esta paciente sobrevivió y mejoró con el tiempo.\n\nSi tienes preguntas sobre alguno de los términos (miocarditis, ECMO, VAD), puedo explicarlos con más detalle.",
+                "fh_score": 55.94
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel universitario, lenguaje no especializado)\n\nCaso y presentación\n- Paciente: mujer de 36 años, previamente sana.\n- Antecedente inmediato: picadura única por un insecto del orden Hymenoptera (probablemente abeja) con eritema y edema local.\n- Curso temprano: en las siguientes 6 horas desarrolló fiebre; 3 días después consultó por fiebre intermitente y signos de insuficiencia hemodinámica.\n\nHallazgos iniciales y pruebas\n- Signos vitales al ingreso: fiebre 38,9 °C, taquicardia, hipotensión (PA 80/52 mmHg).\n- ECG: fibrilación auricular con respuesta ventricular rápida (~130 lpm) y elevación difusa del segmento ST.\n- Radiografía de tórax: sin congestión ni infiltrados al ingreso.\n- Marcadores cardíacos: CK‑MB y troponina I marcadamente elevados (CK‑MB 96 ng/mL al ingreso, pico >303 ng/mL; troponina I 8,0 ng/mL al ingreso, pico >81 ng/mL). NT‑proBNP 20.700 pg/mL.\n- Hemograma: sin eosinofilia ni leucocitosis significativa.\n- Microbiología: pruebas iniciales (antígeno de influenza, cultivos de sangre y esputo, serologías respiratorias) negativas.\n- Ecocardiograma: hipocinesia global del ventrículo izquierdo, fracción de eyección ≈30,6%, sin derrame pericárdico.\n- Angiografía coronaria emergente: arterias coronarias sin lesiones ni vasoespasmo (descarta infarto coronario como causa primaria).\n\nEvolución clínica y tratamientos empleados\n- Shock cardiogénico progresivo a pesar de inotrópicos y balón intraaórtico; evolución a paro cardíaco intrahospitalario con taquicardia ventricular/fibrilación ventricular.\n- Reanimación: reanimación avanzada sin retorno inmediato; se inició soporte cardiopulmonar percutáneo (PCPS/VA‑ECMO) y se obtuvo retorno de la circulación tras ~25 minutos.\n- Complicaciones tempranas: empeoramiento de la función ventricular izquierda, aparición de trombos intracardiacos (aurícula y ventrículo izquierdo) 24 horas tras iniciar soporte mecánico.\n- Progresión a insuficiencia multiorgánica: oliguria y acidosis que requirieron hemodiálisis venovenosa continua.\n- Deterioro de la función ventricular derecha → cambio de soporte a dispositivos de asistencia ventricular biventricular (VADs) y uso de oxigenador de membrana para soporte respiratorio por hemorragia pulmonar y consolidación bilateral.\n- Manejo quirúrgico y procedimientos adicionales: extracción repetida de coágulos por broncoscopia, desbridamiento y control quirúrgico de sangrados, intercambio plasmático terapéutico (5 sesiones) para reducir riesgo de rechazo inmunológico cuando se planificó trasplante.\n- A lo largo del ingreso presentó episodios de sangrados masivos (mediastino, vagina), infección de herida esternal con absceso, úlceras por presión e hiperbilirrubinemia; recibió antibioticoterapia dirigida y cuidados quirúrgicos.\n\nPatología y diagnóstico etiológico\n- Biopsia endomiocárdica del ventrículo izquierdo: inflamación significativa formada principalmente por linfocitos con presencia de algunos eosinófilos; daño miocárdico con necrosis focal (no extensa).\n- Estudio patológico del corazón explantado tras trasplante: pancarditis de ambos ventrículos; coronarias sin lesiones.\n- Interpretación final: miocarditis de tipo hipersensibilidad (probable relación temporal con la picadura de insecto), que provocó fallo cardiaco fulminante y shock cardiogénico refractario.\n\nResultado y seguimiento\n- Debido a paro cardíaco persistente y fallo biventricular refractario, se realizó trasplante cardíaco ortotópico el día 49 de ingreso.\n- Soporte mecánico posoperatorio (ECMO venoarterial) mantenido hasta el día 58.\n- Biopsias endomiocárdicas posteriores al trasplante: sin evidencia de rechazo celular o humoral.\n- Complicaciones tardías: episodios sépticos bajo inmunosupresión; laparoscopia exploratoria y apendicectomía en día 93.\n- Alta hospitalaria en día 101; paciente clínicamente estable en el control a 3 meses.\n\nImplicaciones clínicas y lecciones\n- Una reacción sistémica a una picadura de insecto puede, en casos raros, desencadenar una miocarditis por hipersensibilidad que progresa rápidamente a fracaso cardiaco fulminante.\n- En pacientes con insuficiencia cardíaca aguda y marcadores de daño miocárdico elevados pero coronarias normales, la miocarditis debe sospecharse; la biopsia endomiocárdica puede aportar diagnóstico histológico.\n- La ausencia de eosinofilia periférica no excluye la miocarditis por hipersensibilidad (en este caso hubo pocos eosinófilos en la biopsia).\n- El manejo puede requerir escalada a soporte circulatorio mecánico avanzado (ECMO, VAD biventricular) y, cuando la recuperación miocárdica es imposible, trasplante cardíaco.\n- Este caso subraya la rapidez con la que puede evolucionar la enfermedad y la necesidad de un abordaje multidisciplinario (cardiología, cirugía cardiaca, cuidados intensivos, infectología, cirugía).\n\nTono final\nEste caso describe una complicación rara pero grave tras una picadura de insecto que llevó a miocarditis fulminante y a la necesidad de soporte mecánico prolongado y trasplante. La paciente sobrevivió y estaba estable a los 3 meses, lo que ilustra tanto la gravedad potencial de la miocarditis por hipersensibilidad como la eficacia del tratamiento intensivo y del trasplante en centros especializados.",
+                "fh_score": 29.08
+            }
+        }
+    },
+    {
+        "article": "Un hombre de 24 años con complicaciones cardiovasculares relacionadas con MFS fue admitido en nuestro departamento de medicina interna debido a 3 episodios consecutivos de insuficiencia cardiaca aguda descompensada con fracción de eyección reducida (ADHFrEF) de 2014 a 2017. Su historia médica restante incluye hipertensión arterial, dislipidemia, hipertiroidismo, shock anafiláctico debido a flecainida y hábito tabágico previo.\n\nEl diagnóstico de MFS se realizó en 2010, cuando se llevó a cabo la sustitución de la aorta ascendente y la válvula aórtica con prótesis mecánica debido a una disección aórtica aguda tipo A en presencia de antecedentes familiares (madre, padre y 3 hijos con MFS). Durante el período intraoperatorio, se produjo un síndrome coronario agudo inferior y se trató con cirugía de injerto de derivación de la arteria coronaria.\n\nEn mayo de 2014, se realizó la implantación de una prótesis mecánica de aorta descendente y arco aórtico debido a un aneurisma disecante crónico. El hematoma peri-aórtico y la isquemia medular complicaron la cirugía y causaron paraplejia de las extremidades inferiores, dolor y hipoestesia térmica, e incontinencia rectal. Después de 2 meses, durante su primera admisión por ADHFrEF, las pruebas de laboratorio fueron notables para N-terminal pro-BNP (NT-proBNP) de 12,000 pg/mL y el ecocardiograma transtorácico mostró una función de la prótesis normal, dilatación de todas las cámaras cardiacas (principalmente las izquierdas) con insuficiencia mitral y tricuspídea moderada, hipertrofia ventricular izquierda, acinesia de la pared inferior, discinesia septal e hipocinesia de las paredes restantes con reducción severa de la fracción de eyección ventricular izquierda (LVEF) −20%. Se le trató con diuréticos intravenosos y desfibrilador cardiaco interno (St. Jude Ellipse DR, modo DDD) sin terapia de resincronización cardiaca (criterios de electrocardiograma no cumplidos) y se le dio de alta con la máxima terapia médica (furosemida, carvedilol, ramipril, espironolactona, digoxina y amlodipina).\n\nEn agosto de 2017, se produjo un nuevo episodio de ADHFrEF. Los valores de laboratorio de admisión notables incluían NT-proBNP de 2719 pg/mL y midregional-proadrenomedullin (MR-proADM) de 1.61 nmol/L, mientras que el ecocardiograma transtorácico y transesofágico mostró un LVEF de 35%, función de prótesis normal, severa regurgitación tricuspídea, y ruptura de la valva anterior de la chorda tendineae con severa regurgitación mitral. Los pacientes fueron tratados con diuréticos intravenosos y digoxina y dados de alta con una terapia médica óptima (furosemida, carvedilol, ramipril, espironolactona, digoxina, y amlodipina).\n\nPor último, volvió a ser admitido en nuestro departamento de medicina interna en noviembre de 2017 debido a un tercer episodio de ADHFrEF y una acumulación de líquido mediastinal infectado secundaria a una corrección quirúrgica de insuficiencia valvular severa un mes antes con implantación de prótesis mecánica mitral (31 mm ST Jude) y anuloplastia tricúspide De Vega.\n\nEl examen físico reveló una presión arterial de 120/80 mm Hg, pulso de 82 bpm, frecuencia respiratoria de 26 apm, saturación de O2 de 87% en aire ambiente con posición ortopneica obligatoria, y un habitus marfanoide (peso de 147 kg, altura de 2.2 m). La evaluación cardiopulmonar reveló un segundo sonido cardíaco metálico, percusión opaca con reducción del frémito vocal táctil y crepitaciones en la base de los pulmones, disminución amplia de los sonidos respiratorios vesiculares, presencia de ascitis abundante e hinchazón de las piernas.\n\nLos valores de laboratorio notables incluyeron NT-proBNP de 10,132 pg/mL y MR-proADM de 2,36 nmoL/mL.\n\nEl análisis de gases arteriales reveló una hipoxemia grave con alcalosis respiratoria y metabólica (pH 7,56, pO2 46 mm Hg, pCO2 24,8 mm Hg, HCO3− 21,9 mm mol/L, gradiente alveolar-arterial 31 mm Hg). Aunque el electrocardiograma resaltó fibrilación auricular con frecuencia ventricular de 80 bpm, hipertrofia ventricular izquierda e isquemia subepicárdica infralateral, el ecocardiograma transtorácico mostró las mismas características que el anterior, excepto por una FEVI de 30 %, presencia de prótesis mecánicas mitrales con fuga paravalvular y gradiente medio de 9 mm Hg, e insuficiencia tricuspídea leve.\n\n\nEn la radiografía de tórax y en la tomografía computarizada de alta resolución se observa una congestión hilar con cardiomegalia, consolidación pulmonar en el lóbulo superior derecho y acumulación de líquido mediastínico infectado.\n\nEl paciente fue tratado con 250 mg de furosemida intravenosa por día, 100 mg de canrenona por día, 4,5 g de piperacilina/tazobactam cada 6 horas y 12 mg/kg de teicoplanina por día, y luego 12 mg/kg por día. El día 9, una vez alcanzada la estabilización hemodinámica, se agregó una dosis intermedia de sacubitril/valsartan de 49/51 mg por día a 3,125 mg de carvedilol por día, 100 mg de espironolactona por día, 250 mg de furosemida por día y 0,25 mg de digoxina por día.\n\nEn el seguimiento de 1 mes, sacubitril/valsartan se aumentó a 97/103 mg b.i.d. para la buena condición clínica del paciente, lo que permitió una reducción persistente y progresiva de los parámetros clínicos, de laboratorio (reducción de NT-proBNP e incremento de MR-proADM), de los parámetros ecocardiográficos (aumento del EFV final del ventrículo izquierdo (42 % vs 30 %), del diámetro final del ventrículo izquierdo, del diámetro diastólico final del ventrículo izquierdo, de la masa del ventrículo izquierdo y del índice de masa del ventrículo izquierdo) y una mejora de la calidad de vida sin nuevos episodios de ADHFrEF hasta el seguimiento de 9 meses (Fig. (Fig.1B1B y D; Tabla 1).1). Debido a la falta de un régimen de dosificación específico para sacubitril/valsartan en la miocardiopatía relacionada con la EM, utilizamos el esquema terapéutico recomendado.\n\nMH - Aminobutiratos/uso terapéutico\nMH - Antagonistas de los receptores de la angiotensina/*uso terapéutico\nMH - Compuestos de bifenilo\nMH - Combinaciones de fármacos\nMH - Insuficiencia cardiaca/*terapia farmacológica/*etiología\nMH - Humanos\nMH - Hombre\nMH - Síndrome de Marfan/*complicaciones\nMH - Tetrazoles/uso terapéutico\nMH - Resultado del tratamiento\nMH - Valsartán\nMH - Adultos jóvenes\n",
+        "gold_summary": "Preocupaciones de los pacientes:\nUn hombre de 24 años fue admitido en nuestro departamento de medicina interna debido a disnea, ascitis e hinchazón de las piernas. El análisis de gases en sangre arterial reveló una hipoxemia grave con alcalosis respiratoria y metabólica. La radiografía de tórax mostró una congestión hilar.\n\nDiagnósticos:\nInsuficiencia cardíaca aguda descompensada recurrente con fracción de eyección reducida a pesar de la terapia médica óptima en la cardiomiopatía relacionada con el síndrome de Marfan.\n\nIntervenciones y resultados:\nSe agregó sacubitril/valsartan a la terapia médica óptima después de la estabilización hemodinámica, lo que permitió una mejora clínica, de laboratorio y ecocardiográfica progresiva. El paciente mantuvo una supervivencia libre de insuficiencia cardiaca y una buena calidad de vida hasta el seguimiento de 9 meses.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había un hombre joven de 24 años con síndrome de Marfan. Esto es una condición que puede hacer que las paredes de los vasos y las válvulas del corazón sean débiles. Él ya había tenido varias operaciones en el corazón y en la aorta. Después de una operación quedó sin poder mover bien las piernas y con menos sensibilidad en ellas.\n\nDurante varios años tuvo episodios en los que su corazón fallaba y no bombeaba suficiente sangre. Esto le causaba falta de aire, líquido en el abdomen y en los pulmones, y mucho hinchazón en las piernas. También tenía infección en líquido cerca del corazón y necesitó antibióticos.\n\nLos médicos le dieron muchos medicamentos para el corazón y lo estabilizaron. Cuando estuvo más estable, le añadieron un medicamento nuevo llamado sacubitril/valsartan. Con ese cambio, su respiración mejoró. El líquido en el cuerpo bajó. Las pruebas y el ecocardiograma mostraron que su corazón empezó a bombear mejor. No tuvo nuevos ataques de falla del corazón durante por lo menos nueve meses y su calidad de vida mejoró.\n\nEn resumen: era un joven con muchas operaciones y problemas cardíacos. Tras estabilizarlo, los médicos usaron un medicamento nuevo que ayudó a que se sintiera mejor y que su corazón trabajara con más fuerza.",
+                "fh_score": 71.92
+            },
+            "B2": {
+                "text": "Resumen para lectores jóvenes (nivel secundaria — B2)\n\nEste informe cuenta la historia de un hombre de 24 años con síndrome de Marfan, una enfermedad genética que afecta el tejido conectivo y suele dañar la aorta y las válvulas del corazón. Desde 2010 ha tenido varias cirugías mayores en el corazón y la aorta, y complicaciones importantes: en una operación sufrió un infarto y requirió un bypass coronario; en otra intervención de la aorta descendente quedó con paraplejia (pérdida de movimiento de las piernas), dolor y problemas de sensibilidad e incontinencia.\n\nProblema principal\nEntre 2014 y 2017 el paciente presentó tres episodios de insuficiencia cardíaca aguda descompensada con fracción de eyección reducida. La fracción de eyección (FE) es una medida de la capacidad del corazón para bombear sangre; valores bajos (por ejemplo 20–35 %) indican fallo importante del bombeo. En sus ingresos se detectaron también niveles muy altos de NT‑proBNP, un análisis de sangre que sube cuando el corazón está estresado.\n\nQué le pasó en la última hospitalización (noviembre de 2017)\n- Allí tenía dificultad para respirar, ascitis (líquido en el abdomen) e hinchazón de piernas. Su saturación de oxígeno era baja.\n- Tenía prótesis mecánicas en válvulas cardíacas y fugas alrededor de una prótesis (fuga paravalvular).\n- Además se encontró una acumulación de líquido mediastínico infectado (líquido infectado en el área entre los pulmones), que se trató con antibióticos fuertes.\n- Tras estabilizarlo con diuréticos y tratamiento para la infección, se añadió sacubitril/valsartán —un fármaco combinado recomendado para ciertos tipos de insuficiencia cardíaca— a la terapia ya óptima que estaba recibiendo (betabloqueante, espironolactona, diuréticos, digoxina, entre otros).\n\nResultados tras la nueva medicación\n- En el seguimiento a 1 mes y hasta 9 meses, el paciente mejoró de forma sostenida: mejor estado clínico, menos signos en sangre de fallo cardíaco (NT‑proBNP disminuyó) y mejorías en el ecocardiograma.\n- La fracción de eyección del ventrículo izquierdo aumentó de alrededor del 30 % a 42 %, lo que significa que el corazón bombeaba mejor.\n- No tuvo nuevos episodios de insuficiencia cardíaca aguda hasta el control a 9 meses y su calidad de vida mejoró.\n\nImportancia y enseñanza\nEste caso muestra a una persona joven con síndrome de Marfan y cardiomiopatía severa que, a pesar de muchas cirugías y complicaciones, tuvo mejoría clínica y ecocardiográfica tras añadir sacubitril/valsartán a la terapia médica óptima. En pacientes con enfermedades complejas como ésta, los cambios en el tratamiento pueden traducirse en mejor función cardíaca y menos hospitalizaciones, aunque se necesita vigilancia continua y adaptación del tratamiento individualmente.",
+                "fh_score": 43.41
+            },
+            "B3": {
+                "text": "Paciente\nUn hombre de 24 años con síndrome de Marfan (antecedente familiar claro) que ha sufrido varias cirugías aórticas y valvulares y complicaciones graves (incluida paraplejia tras cirugía de aorta en 2014) ingresó por disnea intensa, ortopnea, ascitis y edemas de piernas. Tenía saturación de O2 en aire ambiente del 87% y signos clínicos de congestión pulmonar y sobrecarga sistémica.\n\nAntecedentes relevantes\n- Diagnóstico de síndrome de Marfan en 2010; cirugía de sustitución de aorta ascendente y válvula aórtica por disección tipo A, con injerto coronario tras infarto intraoperatorio.  \n- En 2014 reemplazo de aorta descendente y arco aórtico por aneurisma disecante; complicaciones: hematoma peri-aórtico, isquemia medular y paraplejia.  \n- Implante previo de desfibrilador (St. Jude Ellipse DR); múltiples episodios previos de insuficiencia cardiaca aguda descompensada con fracción de eyección reducida (HFrEF).  \n- Un mes antes del ingreso más reciente se había colocado una prótesis mecánica mitral (31 mm) y se realizó anuloplastia tricuspídea De Vega; luego presentó colección mediastínica infectada.\n\nHallazgos clínicos y pruebas\n- Gasometría: hipoxemia grave (pO2 46 mm Hg) con alcalosis respiratoria y metabólica (pH 7,56).  \n- ECG: fibrilación auricular con respuesta ventricular lenta (~80 lpm), hipertrofia ventricular izquierda e isquemia subepicárdica infralateral.  \n- Ecocardiograma: fracción de eyección del ventrículo izquierdo (LVEF) reducida (30% en el ingreso más reciente), prótesis valvulares presentes con fuga paravalvular mitral y gradiente medio 9 mm Hg; regurgitación tricuspídea variable en los episodios previos.  \n- Marcadores: NT‑proBNP marcadamente elevado en episodios (12,000 pg/mL en 2014; 2,719 pg/mL en agosto de 2017; 10,132 pg/mL en noviembre de 2017), MR‑proADM también elevado (1.61 nmol/L en agosto 2017, 2.36 nmol/L en noviembre 2017).  \n- Imagen torácica: cardiomegalia, congestión hilar y consolidación pulmonar; colección mediastínica infectada confirmada por TC.\n\nTratamiento durante esta hospitalización\n- Manejo inicial: diuréticos intravenosos intensivos (furosemida 250 mg/día), antagonistas mineralocorticoides (canrenona/espironolactona), control de ritmo/anticongestión y antibióticos para mediastinitis (piperacilina/tazobactam y teicoplanina).  \n- Tras estabilización hemodinámica (día 9) se añadió sacubitril/valsartán (inhibidor de neprilisina + valsartán) 49/51 mg/día junto con la terapia médica óptima ya en curso (carvedilol, espironolactona, digoxina, diuréticos).  \n- A 1 mes se incrementó sacubitril/valsartán a 97/103 mg dos veces al día siguiendo el esquema recomendado para insuficiencia cardiaca con fracción reducida.\n\nEvolución y resultados\n- Clínicamente mejoró de forma sostenida: reducción de disnea y congestión, mejor tolerancia funcional y mejor calidad de vida.  \n- Biológicamente disminuyó el NT‑proBNP (marcador de tensión cardiaca). MR‑proADM aumentó (el significado pronóstico de este cambio en este contexto no está del todo aclarado).  \n- Ecocardiograma de control mostró aumento de LVEF de ~30% a 42% y cambios favorables en parámetros del ventrículo izquierdo.  \n- A los 9 meses de seguimiento no presentó nuevos episodios de insuficiencia cardiaca aguda descompensada.\n\nInterpretación y recomendaciones\n- En este paciente joven con cardiomiopatía asociada a síndrome de Marfan y HFrEF recurrente, la adición de sacubitril/valsartán a la terapia médica óptima se asoció a mejoría clínica, descenso de NT‑proBNP y recuperación parcial de la función ventricular izquierda.  \n- Limitaciones importantes: se trata de un único caso observacional; no puede establecerse causalidad ni generalizarse la eficacia o seguridad del tratamiento para todos los pacientes con Marfan. Además, no existe un régimen de dosificación específico para la miocardiopatía relacionada con Marfan, por lo que se siguió el esquema estándar para HFrEF.  \n- Pasos siguientes razonables para pacientes similares: seguimiento estrecho (función renal, potasio, tensión arterial), monitorizar prótesis valvulares y complicaciones infecciosas, considerar indicaciones para terapia de resincronización o intervenciones sobre fugas paravalvulares si persisten, y evaluar la acumulación de evidencia mediante series de casos o estudios controlados.\n\nComentario final (tono empático)\nEste caso sugiere que, en circunstancias seleccionadas y con monitorización cuidadosa, un inhibidor de neprilisina/ARA II (sacubitril/valsartán) puede ayudar a recuperar función ventricular y mejorar síntomas en HFrEF asociada a Marfan. Es alentador para el paciente y su equipo tratar de alcanzar estabilidad y calidad de vida, pero se necesitan más datos sistemáticos para confirmar este enfoque en poblaciones similares.",
+                "fh_score": 36.98
+            }
+        }
+    },
+    {
+        "article": "Paciente masculino de 41 años de edad quien ingresó en 2016 al servicio de urgencia con politraumatismo producto de accidente de tránsito; con trauma en miembros inferioA B res, en los rayos X se observa fractura de platillos tibiales izquierdos y fractura subtrocanteriana derecha, trauma toracoabdominal y trauma craneoencefálico leve.\nSe le practica osteosíntesis de fémur con clavo cefalomedular largo a foco cerrado corrigiendo la fractura subtrocanteriana y se le aplica tutor externo transarticular de rodilla como medida de control de daño local provisional; 15 días después se realiza osteosíntesis definitiva de su fractura de platillos tibiales. Evolución adecuada y satisfactoria de platillos tibiales.\nEntre 2016 y 2019 tuvo episodios esporádicos de dolor en cadera derecha que cedían fácilmente al manejo con antiinflamatorios y analgésicos sin limitar las actividades de la vida diaria y en la toma de rayos X se observaba fatiga de los bloqueos distales con dudas de la consolidación de la fractura.\nEn 2020 se incrementa el dolor en la cadera que no cede con el tratamiento médico y se acompaña de limitación funcional. En los rayos X de control se evidencia ruptura del clavo cefalomedular en su tercio proximal y no unión de la fractura subtrocantérica.\nEn Febrero de 2020 intento fallido de extracción de material de osteosíntesis (extrainstitucional), por lo que es remitido a nuestra institución. Se lleva a cirugía el 8 de Febrero, se realiza retiro de material de osteosíntesis, curetaje y toma de cultivo de foco de no unión. Cultivo positivo para Klebsiella pneumoniae recibiendo tratamiento con meropenem intravenoso por 10 días. Posteriormente se le realizó un lavado quirúrgico con drenaje de hematoma para el 20 de Febrero realizar nueva osteosíntesis con clavo cefalomedular + injerto óseo autólogo (tomado de ambas crestas iliacas) en foco de no unión.\nReactivación de la infección en Marzo de 2020, requiriendo nuevamente cirugía para lavados y desbridamiento quirúrgicos seriados (#5). Se aísla nueva bacteria Enterobacter que es manejada con vancomicina y meropenem. A f inales de Abril completa tratamiento médico y se le da salida en condiciones estables.\nEn Mayo de 2020 por persistencia de la infección se retira el material de osteosíntesis, se deja un clavo TENS endomedular recubierto de cemento con antibióticos (gentamicina).\nA finales de Mayo después de dos lavados quirúrgicos se retiró el clavo TENS, resección de bordes de fractura (hasta hueso sano) injerto óseo endomedular con un segmento de 10 cm de peroné no vascularizado (autólogo) y fijación de la fractura con una placa de soporte condíleo de fémur distal; colocación de sistema VAC y cierre definitivo de la herida en un segundo tiempo el 28 de Mayo de 2020. El paciente evolucionó adecuadamente, la herida quirúrgica cicatrizó por completo hasta el día de hoy con infección en remisión y evidencia radiológica de consolidación de la fractura, además paciente asintomático con función preservada de la extremidad.",
+        "gold_summary": "Masculino de 41 años de edad que sufre fractura subtrocantérica derecha producto de un accidente de tránsito que requirió manejo de osteosíntesis. Con posterior ruptura del clavo cefalomedular en su tercio proximal, no unión de la fractura e infecciones en sitio de la fractura. Fue tratado con múltiples lavados quirúrgicos, antibioticoterapia y un procedimiento ortopédico y quirúrgico poco convencional como el uso de una placa de soporte condíleo de fémur distal y un injerto óseo endomedular con un segmento de 10 cm de peroné no vascularizado. Paciente con evolución satisfactoria y favorable.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un hombre de 41 años se rompió el hueso del muslo derecho en un accidente de coche en 2016. Le pusieron un clavo dentro del hueso para sujetar la fractura. También le hicieron otras operaciones en la rodilla y la tibia.\n\nEn los años siguientes tuvo dolor a veces. En 2020 el clavo se rompió y el hueso no había sanado. Le operaron para quitar el material y tomaron muestras. Salieron bacterias (gérmenes) en los análisis. Recibió antibióticos fuertes por vía intravenosa.\n\nSe le hicieron varios lavados y limpiezas quirúrgicas porque la infección volvió. Le pusieron y quitaron distintos dispositivos con antibióticos. Finalmente le quitaron el material roto y pusieron un injerto de hueso: un trozo de 10 cm del peroné del propio paciente, metido dentro del hueso para ayudar a que sane. También le pusieron una placa metálica grande para dar soporte. Usaron un sistema de vacío (VAC) para ayudar a cerrar la herida.\n\nEl proceso fue largo y requirió varias cirugías y medicinas. Al final la infección desapareció. La herida cicatrizó bien. Las radiografías muestran que el hueso consolidó. El paciente está sin dolor y puede usar la pierna. Esto fue un buen resultado después de un tratamiento difícil.",
+                "fh_score": 76.35
+            },
+            "B2": {
+                "text": "Resumen (nivel B2, claro y empático)\n\nHombre de 41 años que en 2016 sufrió un accidente de tráfico con varias fracturas, entre ellas una fractura subtrocantérea del fémur derecho (justo debajo del trocánter, una parte de la cadera). Inicialmente se le colocó un clavo cefalomedular largo (un clavo metálico dentro del hueso para sujetar la fractura) y otros dispositivos para controlar el daño.\n\nEntre 2016 y 2019 tuvo dolor intermitente en la cadera; en 2020 el dolor aumentó y la fractura no había consolidado (no unión = el hueso no había cicatrizado). Además, el clavo se rompió en su tercio proximal. Tras un intento fallido de extracción del material, fue operado en febrero de 2020: se retiró el material, se limpió la zona afectada (curetaje) y se tomaron cultivos, que dieron positivo para Klebsiella pneumoniae. Recibió antibióticos intravenosos (meropenem) y se le colocó de nuevo un clavo junto con injerto óseo autólogo (hueso propio de las crestas ilíacas).\n\nEn marzo la infección reapareció; requirió varios lavados y desbridamientos (cirugías para limpiar tejido infectado) y se aisló una nueva bacteria, Enterobacter, tratada con vancomicina y meropenem. A pesar del tratamiento, la infección persistió y en mayo se retiró el material de osteosíntesis y se dejó temporalmente un clavo TENS recubierto con cemento que contiene antibiótico (esto ayuda a dar estabilidad y liberar antibiótico localmente).\n\nA finales de mayo se decidió un tratamiento reconstructivo: retirada del clavo TENS, resección de los bordes de la fractura hasta hueso sano, colocación de un injerto endomedular con un segmento de 10 cm del peroné del propio paciente (injerto no vascularizado = hueso sin reconexión directa de vasos sanguíneos) y fijación con una placa de soporte condílea en el fémur distal. Se utilizó también sistema VAC (terapia de presión negativa para ayudar a que la herida sane) y el cierre definitivo se hizo en un segundo tiempo. \n\nEvolución final: la herida cicatrizó completamente, la infección quedó en remisión y las imágenes radiológicas mostraron consolidación de la fractura. El paciente está asintomático y mantiene función en la extremidad. Este caso muestra el uso combinado de limpiezas repetidas, antibióticos y técnicas reconstructivas poco convencionales para controlar infección y lograr la curación ósea.",
+                "fh_score": 45.51
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel universitario)\n\n- Presentación inicial\n  - Hombre de 41 años con politraumatismo por accidente de tránsito en 2016. Entre sus lesiones destacaron una fractura subtrocantérica derecha (por debajo del trocánter femoral), fractura de platillos tibiales izquierdos y fractura subtrocantérica derecha; además trauma toracoabdominal y craneoencefálico leve.\n  - Tratamiento agudo: osteosíntesis del fémur con clavo cefalomedular largo (clavo intramedular que estabiliza el cuello y la diáfisis femoral) y tutor externo transarticular de rodilla; 15 días después se fijaron los platillos tibiales. Evolución inicial satisfactoria de la tibia.\n\n- Curso clínico y complicaciones\n  - Entre 2016 y 2019 tuvo dolor intermitente en cadera derecha controlable con AINEs. Radiografías mostraban fatiga de los bloqueos distales del clavo y duda de consolidación.\n  - En 2020 empeoró el dolor y la función; radiografías mostraron ruptura del clavo cefalomedular en su tercio proximal y ausencia de unión de la fractura (no unión).\n\n- Manejo en 2020\n  - Febrero 2020: intento fallido extradicional de extracción del material; fue remitido y el 8 de febrero se retiró el material, se realizó curetaje y se tomó cultivo del foco de no unión. Cultivo positivo para Klebsiella pneumoniae → tratamiento con meropenem IV 10 días.\n  - Segunda cirugía: lavado y drenaje de hematoma; el 20 de febrero se realizó nueva osteosíntesis con clavo cefalomedular y injerto óseo autólogo tomado de ambas crestas ilíacas.\n  - Marzo 2020: reactivación de infección, necesitó múltiples lavados y desbridamientos seriados (cinco procedimientos). Se aisló Enterobacter; se trató con vancomicina y meropenem. Alta clínica estable a finales de abril.\n  - Mayo 2020: por persistencia de infección se retiró el material; se colocó temporalmente un clavo TENS endomedular recubierto con cemento impregnado de gentamicina (técnica para administrar antibiótico local).\n  - Finales de mayo 2020: tras dos lavados adicionales se retiró el clavo TENS, se resecaron los bordes de fractura hasta hueso sano, se colocó un injerto óseo endomedular con un segmento autólogo de peroné no vascularizado de 10 cm (injerto interpuesto dentro del canal medular) y se fijó la fractura con una placa soporte condílea de fémur distal. Se usó sistema VAC (vacío) y cierre definitivo el 28 de mayo.\n\n- Hallazgos y desenlace\n  - Tras estos procedimientos el paciente evolucionó favorablemente: la herida cicatrizó completamente, la infección está en remisión, hay evidencia radiológica de consolidación ósea y el paciente está asintomático con función preservada de la extremidad.\n\n- Interpretación y consideraciones\n  - Problema principal: no unión de fractura subtrocantérica complicada por infección posoperatoria y fractura/ruptura del implante, lo que requirió manejo secuencial: control de infección (desbridamiento, antibióticos sistémicos y locales), retirada y sustitución de material, y reconstrucción ósea con injerto autólogo.\n  - Técnicas destacadas: uso temporal de clavo con cemento antibiótico para control local de infección, injerto endomedular con peroné no vascularizado y fijación con placa de soporte inusual para esta localización — todas medidas de salvamento que evitaron resultados más adversos como la pérdida funcional o amputación.\n\n- Recomendaciones posteriores (seguimiento)\n  - Continuar seguimiento clínico y radiológico para detectar recidiva de infección o fallo de consolidación.\n  - Monitorizar marcadores inflamatorios/infecciosos si hay signos sugestivos.\n  - Programa de rehabilitación para potenciar la recuperación funcional y control del dolor.\n  - Considerar control ortopédico periódico y evaluación por rehabilitación y, si procede, por infectología para manejo a largo plazo.\n\nLa evolución final fue satisfactoria: infección en remisión, consolidación radiológica y función de la extremidad preservada. Si desea, puedo preparar una versión más breve o una explicación de cualquiera de los procedimientos y términos usados.",
+                "fh_score": 37.18
+            }
+        }
+    },
+    {
+        "article": "Una adolescente de 17 años se presentó en nuestra clínica con una historia de dos meses de dolor torácico en el lado izquierdo y una historia de una semana de dolor en la espalda en el nivel de T7. El dolor torácico se acompañaba de palpitaciones y disnea que ocurrían de tres a cuatro días por semana. Una semana antes de la primera visita, las palpitaciones y la disnea se hicieron menos frecuentes, y desarrolló un dolor sordo diario intermitente en el lado izquierdo del pecho y la parte media de la espalda sin radiación, en la mayoría de los casos. El dolor ocurría tanto con el ejercicio como en reposo, y duraba horas, sin factores agravantes o atenuantes. Informó una intensidad del dolor de 2 a 6 en una escala de 10 puntos. La intensidad cambiaba durante un ataque, y el promedio era 4. Estaba sana por lo demás. No había limitación en la vida diaria. Visitó a un médico local un mes antes de visitar nuestra clínica. Los resultados de los exámenes electrocardiográficos y de laboratorio de Holter fueron normales. Su historial médico incluía migraña durante tres años. Sus medicamentos regulares eran lomerizina, loxoprofen y naratriptan para la prevención y el tratamiento agudo de la migraña. Su migraña estaba bien controlada, y rara vez experimentaba ataques. Negó trauma o cirugías previas. Negó síntomas sospechosos o antecedentes familiares de afecciones autoinmunes o inflamatorias.\n\nSu presión arterial era de 107/60 mmHg y su pulso de 62 latidos/min. Medía 162 cm de altura y pesaba 43 kg, con un índice de masa corporal de 16,4 kg/m2. No se escuchaba ningún murmullo ni arritmia en su examen cardiovascular. Los pulmones estaban limpios a la auscultación bilateral. La palpación del tórax provocó un dolor local no reproducible en las articulaciones inferiores esterno-costales; la maniobra de tracción del brazo horizontal y la maniobra del gallo cantando no provocaron dolor. No había sensibilidad en los músculos y huesos de la parte superior del cuerpo.\n\nLos hallazgos electrocardiográficos y de laboratorio, incluida la función tiroidea, fueron normales. El examen radiográfico torácico y torácico mostró el enderezamiento de la columna torácica superior y una pérdida de la curvatura cifótica normal. Las radiografías de las costillas inferiores no revelaron fractura ni neumotórax. Sospechamos un síndrome de la espalda recta, de acuerdo con los dos criterios diagnósticos diferentes propuestos por Davies et al. y DeLeon et al. La distancia entre la mitad del borde anterior de T8 y una línea vertical que conecta T4 a T12 fue de 0.91 cm. El diámetro anteroposterior fue de 74.0 cm, y el diámetro transversal fue de 243.2 cm. Le aconsejamos que comenzara y continuara la terapia quiropráctica para aumentar la cifosis torácica. Procedimos con una espera vigilante durante un mes en atención ambulatoria.\n\nDespués de esta primera visita, el dolor de pecho y de espalda se alivió gradualmente. Las palpitaciones y la disnea apenas se produjeron. Todos los síntomas desaparecieron en tres semanas. En la visita de seguimiento de un mes, se realizó una ecocardiografía, que reveló una regurgitación mitral trivial sin prolapso. Confirmamos el diagnóstico de síndrome de espalda recta. Reaseguramos a la paciente de que la enfermedad es benigna y le aconsejamos que continuara con la terapia quiropráctica. No ha tenido recaída de síntomas graves ni necesidad de visitar el hospital. Nunca volvió a visitar nuestra clínica en el año siguiente.\n",
+        "gold_summary": "Una adolescente de 17 años se presentó con su madre en nuestra clínica con un historial de dos meses de dolor en el pecho izquierdo y un historial de una semana de dolor en la parte media de la espalda. Diagnosticamos el síndrome de la columna vertebral basado en los hallazgos radiográficos del pecho y la columna vertebral y los síntomas de dolor en el pecho, palpitaciones y disnea. Tranquilizamos a la paciente de que la enfermedad era benigna y le aconsejamos que iniciara y continuara con la terapia quiropráctica. Todos los síntomas, incluido el dolor de espalda, desaparecieron en tres semanas.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una chica de 17 años vino con su mamá porque tenía dolor en el lado izquierdo del pecho desde hace dos meses y dolor en la mitad de la espalda desde hace una semana. También sentía a veces que el corazón le latía fuerte y que le faltaba el aire. Las pruebas del corazón y la sangre salieron normales. Las radiografías mostraron que la parte de la columna en el pecho estaba demasiado recta. Los médicos dijeron que tenía “síndrome de la espalda recta”, que puede causar esos dolores y molestias pero no es grave. Le recomendaron terapia quiropráctica y vigilancia. En tres semanas todos los síntomas desaparecieron. Los médicos la tranquilizaron y no volvió a tener problemas en el año siguiente.",
+                "fh_score": 76.2
+            },
+            "B2": {
+                "text": "A 17-year-old girl came to the clinic with two months of left-sided chest pain and one week of dull mid‑back pain. She also had episodes of palpitations (feelings of a fast or strong heartbeat) and shortness of breath, but heart rhythm tests and blood work were normal. Chest and spine X‑rays showed a loss of the normal upper‑back curve, a finding consistent with straight‑back syndrome — a harmless condition in which the upper spine is unusually straight and can sometimes cause chest symptoms. The team advised chiropractic therapy to help restore the thoracic curve and watched her as an outpatient. Her chest and back pain and the palpitations improved and then completely went away within three weeks. A follow‑up heart ultrasound (echocardiogram) showed only a very small leak in the mitral valve (trivial mitral regurgitation) without valve prolapse, which is not expected to cause problems. She was reassured that the condition is benign, advised to continue therapy, and had no serious recurrence during the next year.",
+                "fh_score": 87.64
+            },
+            "B3": {
+                "text": "Presentación\nUna adolescente de 17 años acudió con dolor en el lado izquierdo del pecho durante dos meses y dolor intermitente en la parte media de la espalda (nivel T7) desde hace una semana. Inicialmente también presentaba palpitaciones y disnea tres o cuatro días por semana; con el tiempo estas molestias respiratorias disminuyeron y quedó un dolor sordo diario en el pecho y la espalda (intensidad media 4/10). No refería traumatismo ni antecedentes familiares relevantes; tenía una historia de migraña controlada con medicación.\n\nExploración y pruebas\n- Signos vitales dentro de límites normales (PA 107/60 mmHg, pulso 62/min); índice de masa corporal 16,4 kg/m2.\n- Examen cardiopulmonar sin soplos ni ruidos patológicos; palpación torácica provocó dolor local no reproducible en articulaciones esternocostales inferiores.\n- ECG, monitor Holter y análisis de laboratorio, incluida la función tiroidea, normales.\n- Radiografías de tórax/columna mostraron rectificación de la columna torácica superior y pérdida de la curvatura cifótica normal; radiografías de costillas sin fractura ni neumotórax.\n- Ecocardiograma realizado en el seguimiento mostró una regurgitación mitral trivial sin prolapso.\n\nDiagnóstico\nCon base en los hallazgos clínicos y radiográficos se diagnosticó síndrome de la espalda recta (straight back syndrome): una disminución de la curvatura cifótica torácica que puede asociarse a síntomas torácicos y palpitaciones pero suele ser benigno.\n\nTratamiento y evolución\nSe recomendó iniciar y continuar terapia quiropráctica dirigida a restaurar la cifosis torácica y se realizó vigilancia ambulatoria. Los síntomas (dolor torácico, dolor dorsal, palpitaciones y disnea) mejoraron gradualmente y desaparecieron en tres semanas. A un año no hubo recaídas que requirieran atención hospitalaria.\n\nImplicaciones y recomendaciones\n- El cuadro fue benigno y respondió a manejo conservador; la ecocardiografía descartó una afección estructural cardiaca significativa.\n- Recomendaciones prácticas: continuar la terapia postural/quiropraxia y vigilancia; solicitar nueva evaluación (incluida ecocardiografía) si reaparecen palpitaciones intensas, disnea persistente, síncope o dolor torácico severo.\n- Aunque infrecuente, cuando los síntomas torácicos y palpitaciones aparecen en pacientes jóvenes, conviene correlacionar examen clínico, ECG y radiografías para diferenciar causas musculoesqueléticas/estructurales benignas de enfermedades cardiacas.",
+                "fh_score": 32.3
+            }
+        }
+    },
+    {
+        "article": "Una mujer de 59 años con urolitiasis bilateral recurrente se presentó con dolor en el flanco derecho, fiebre y fatiga. Se le había colocado un stent doble J derecho un año antes para una piedra pélvica sintomática, pero no se le dio seguimiento. Tenía insuficiencia cardíaca derecha, diabetes tipo 2 mal controlada y enfermedad renal crónica (nadir de creatinina: 18 mg/L).\nEstable clínicamente, tenía una escala de coma de Glasgow de 14/15 (respuesta verbal ligeramente alterada), fiebre (38,3 °C), sensibilidad en el flanco derecho y una producción de orina de 800 cc en 24 horas.\nLos resultados de laboratorio revelaron una lesión renal aguda, con un nivel de creatinina sérica de 107 mg/L (normal: 6-12 mg/L) y urea sanguínea de 3 g/L (normal: 0.15-0.45 g/L). Los marcadores inflamatorios estaban elevados, con un nivel de proteína C reactiva de 300 mg/L (normal: <5 mg/L) y un recuento de glóbulos blancos de 17,000/mm3 (normal: 4000-10,000/mm3). Además, el paciente exhibió anemia normocítica (hemoglobina: 7.6 g/dL; normal: 12-16 g/dL) e hipercalemia leve (potasio sérico: 5.4 mEq/L; normal: 3.5-5.1 mEq/L). El análisis de orina y el cultivo de orina fueron negativos para infección bacteriana.\nUna tomografía computarizada abdominal y pélvica sin contraste reveló una hidronefrosis del lado derecho, un stent de doble J calcificado en espiral en ambos extremos y una piedra en la pelvis derecha de 35 × 28 mm (588 UH). El riñón izquierdo está reducido en tamaño, con hidronefrosis y una piedra en la pelvis de 12 × 7 mm (531 UH).\n\nDebido a la obstructiva severa de la pielonefritis, en particular causada por la endoprótesis incrustada, se realizó una nefrostomía percutánea bilateral urgente, lo que produjo una importante mejora clínica y normalización de los marcadores inflamatorios y la función renal.\nTres días después, la paciente experimentó una convulsión generalizada asociada con disartria. Una tomografía computarizada urgente del cerebro mostró lesiones isquémicas en los lóbulos occipitales izquierdo y frontal derecho, lo que indicaba un accidente cerebrovascular embólico. Se le inició un tratamiento con enoxaparina (0,4 cc diarios) y Kardegic (160 mg diarios) para la prevención de accidentes cerebrovasculares.\nA pesar de la mejora neurológica, cuatro días después, la paciente desarrolló palidez mucocutánea progresiva, taquicardia (110 latidos por minuto), hipotensión (80/50 mmHg) y hematuria macroscópica por el catéter urinario. Los niveles de hemoglobina descendieron de 7,5 g/dL a 4,4 g/dL, lo que levantó sospechas de hemorragia activa. Se administró fluidoterapia, vasopresores intravenosos y transfusiones de sangre, estabilizando su estado para una exploración de angiografía por TAC con contraste.\nLa tomografía computarizada reveló una colección polar media heterogénea de 17 mm de espesor con extravasación de contraste en las fases arterial y portal, lo que indica una hemorragia activa de las arterias del polo superior y medio. También había coágulos intraluminales en la pelvis renal y la vejiga. Se hizo un diagnóstico de fístula arteriovenosa postnefrostomía, exacerbada por la terapia anticoagulante para el accidente cerebrovascular.\nSe realizó una arteriografía renal urgente a través del acceso a la arteria femoral derecha, utilizando un catéter de diagnóstico de calibre 5. La angiografía selectiva reveló una FAV en el polo inferior del riñón con drenaje venoso temprano hacia la vena cava inferior, junto con un pequeño pseudoaneurisma. La embolización superselectiva con microespirales de 3 mm y 5 mm logró ocluir con éxito la fístula, y se usaron partículas de Gelfoam para evitar el sangrado retrógrado. Una inyección final de contraste confirmó la oclusión completa de la fístula, restaurando la integridad arterial y deteniendo la hemorragia.\n\nDespués de la embolización, se vigiló de cerca al paciente en la UCI. La hemodinámica se mantuvo estable y se tomó la decisión colegiada de reintroducir la anticoagulación con monitorización del INR para controlar el accidente cerebrovascular isquémico mientras se equilibraba el riesgo de hemorragia. La hematuria se resolvió, la función renal se normalizó y la nefrostomía siguió siendo funcional.\nSe adoptó un enfoque multidisciplinario para el tratamiento definitivo. La primera etapa involucró la litotripsia endoscópica con láser del bucle inferior calcificado del stent de JJ, la inserción de un segundo stent de JJ en paralelo con el incrustado y la extracción de la nefrostomía, que se completó con éxito. La segunda etapa, programada seis semanas después, incluyó una ureteroscopia derecha flexible para liberar el bucle superior del stent de JJ calcificado, la fragmentación de la piedra pélvica derecha mediante litotripsia con láser y la extracción completa del stent incrustado. Lamentablemente, la salud del paciente se deterioró debido a múltiples factores, entre ellos, insuficiencia cardíaca, diabetes mal controlada, enfermedad renal crónica y un accidente cerebrovascular previo, lo que demoró la finalización de la segunda etapa del tratamiento planificado.\n",
+        "gold_summary": "Una mujer de 59 años con urolitiasis bilateral recurrente, insuficiencia cardiaca derecha, diabetes tipo 2 mal controlada y enfermedad renal crónica se presentó con dolor en el flanco derecho, fiebre y fatiga. Previamente se le había colocado un stent doble J derecho, pero se perdió su seguimiento. Una tomografía computarizada reveló una hidronefrosis, un stent calcificado y una piedra pélvica de 22 mm, lo que llevó a la realización de una nefrostomía percutánea. La paciente desarrolló un accidente cerebrovascular embólico tres días después y posteriormente presentó hematuria, hipotensión y anemia significativa. La angiografía por TC confirmó una FAV con sangrado activo, que se trató con éxito con embolización.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una mujer de 59 años con problemas de salud y piedras en los riñones vino al hospital con dolor en el costado, fiebre y cansancio. Tenía un pequeño tubo llamado stent en el riñón que se le había puesto antes, pero nadie lo revisó después. Las pruebas y una tomografía mostraron que el stent estaba lleno de calcio y que había piedras grandes que bloqueaban el paso de la orina. Esto hacía que el riñón se hinchara y se infectara.\n\nLos médicos pusieron tubos desde la piel hasta los riñones (nefrostomías) para drenar la orina. Esto ayudó y la infección mejoró. Tres días después, la mujer tuvo una convulsión y luego un pequeño derrame cerebral por un coágulo. Le dieron medicinas para evitar más coágulos.\n\nMás tarde empezó a sangrar mucho por la orina, se puso muy pálida y su presión bajó. Las pruebas mostraron que había una conexión anormal entre una arteria y una vena en el riñón (llamada fístula arteriovenosa), que probablemente apareció después de poner los tubos y se empeoró por las medicinas para el coágulo. Los médicos hicieron una angiografía (una prueba que mira las arterias) y cerraron la conexión con pequeños espirales y material que hace tapón. Esto paró el sangrado.\n\nDespués del procedimiento ella estuvo en la UCI y se recuperó: la sangre en la orina desapareció y la función del riñón volvió a la normalidad. Los médicos planearon dos pasos para quitar el stent calcificado y romper las piedras con láser. La primera parte se hizo con éxito. La segunda parte se programó más tarde, pero se demoró porque la mujer tenía otros problemas de salud (corazón, diabetes y riñones) que la hicieron más frágil.",
+                "fh_score": 73.12
+            },
+            "B2": {
+                "text": "A 59-year-old woman with a history of repeated kidney stones, right-sided heart failure, poorly controlled type 2 diabetes, and chronic kidney disease came to the hospital with right-side flank pain, fever, and tiredness. A CT scan showed a large stone in the right kidney (about 35 × 28 mm), swelling of the right kidney from blocked urine flow (hydronephrosis), and a calcified “double‑J” ureteral stent on the right that had been left in place a year earlier. Because she had signs of an infected, obstructed kidney, doctors put in urgent percutaneous nephrostomies (tubes through the skin into each kidney to drain urine). Her infection and kidney tests improved after drainage.\n\nThree days later she had a generalized seizure and imaging showed embolic strokes (small clots in the brain). She was started on blood thinners for stroke prevention. A few days after that she developed heavy visible blood in the urine, fast heartbeat, low blood pressure, and a sharp drop in hemoglobin, indicating major bleeding. CT angiography found active bleeding from an arteriovenous fistula (an abnormal connection between an artery and a vein) in the kidney, likely created by the nephrostomy and made worse by anticoagulation.\n\nInterventional radiology performed a superselective renal angiography and treated the bleeding with coil embolization and Gelfoam particles to block the abnormal vessel. The procedure stopped the hemorrhage, the visible blood in the urine resolved, and kidney function returned to normal. Anticoagulation was restarted carefully with close monitoring because of her stroke.\n\nA multidisciplinary plan was made to remove the heavily calcified stent and treat the kidney stones in two stages using endoscopic laser procedures. The first stage (breaking the lower stent loop, adding a parallel stent, and removing the nephrostomy) was done successfully. The second stage (freeing the upper loop, fragmenting the pelvic stone, and removing the remaining stent) was planned for six weeks later but was delayed because her overall health—heart failure, poorly controlled diabetes, chronic kidney disease, and the recent stroke—worsened. The bleeding complication was managed successfully, but her complex medical problems made completing definitive treatment more difficult.",
+                "fh_score": 73.06
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel universitario, lectura cuidada y empática)\n\nPaciente: mujer de 59 años con antecedentes importantes: urolitiasis bilateral recurrente, insuficiencia cardíaca derecha, diabetes tipo 2 mal controlada y enfermedad renal crónica.\n\nPresentación y hallazgos iniciales\n- Síntomas: dolor en flanco derecho, fiebre y fatiga. Tenía un stent ureteral doble J derecho colocado un año antes y sin seguimiento; el stent estaba muy calcificado.\n- Pruebas: TAC abdominopélvico mostró hidronefrosis derecha, stent doble J con incrustación en ambos extremos y una litiasis pélvica derecha grande (aprox. 35 × 28 mm). El riñón izquierdo estaba atrófico con hidronefrosis y otra piedra menor.\n- Laboratorio: marcadores inflamatorios marcadamente elevados (p. ej., PCR muy alta) y leucocitosis, lesión renal aguda con elevación de creatinina y urea, anemia normocítica y ligera hipercaliemia. El urocultivo fue negativo.\n\nPrimer manejo y respuesta\n- Por la obstrucción severa y la sospecha de pielonefritis obstructiva causada por el stent incrustado se colocaron nefrostomías percutáneas bilaterales de urgencia. Tras esto hubo mejoría clínica importante y normalización de inflamación y función renal.\n\nComplicaciones posteriores\n- A los tres días tuvo un accidente cerebrovascular isquémico embólico (lesiones en lóbulos occipital y frontal). Se inició anticoagulación (enoxaparina) y antiagregación (ácido acetilsalicílico) para prevención secundaria.\n- Cuatro días después desarrolló hematuria macroscópica, hipotensión, taquicardia y una caída rápida de la hemoglobina (de ~7,5 a 4,4 g/dL), compatible con hemorragia activa. Se estabilizó con líquidos, vasopresores y transfusiones.\n- La angio-TAC mostró extravasación de contraste desde ramas renales (hemorragia activa) y coágulos intraluminales. Se diagnosticó una fístula arteriovenosa (FAV) post-nefrostomía, posiblemente favorecida por la anticoagulación.\n\nTratamiento definitivo de la hemorragia\n- Se realizó arteriografía selectiva y embolización superselectiva (microespirales + Gelfoam). La oclusión de la fístula y del pseudoaneurisma fue exitosa y detuvo la hemorragia. Tras la embolización la hemodinámica y la hematuria se resolvieron; la nefrostomía siguió funcionando y la función renal se normalizó.\n\nPlan urológico y evolución\n- Se decidió un enfoque multidisciplinario en dos etapas: 1) litotripsia endoscópica y corte/fragmentación del asa inferior calcificada del stent, colocación de un segundo stent paralelo y retirada de la nefrostomía; 2) seis semanas después, ureteroscopia flexible para liberar y extraer el asa superior calcificada y fragmentar la litiasis pélvica derecha. La primera etapa se completó con éxito; la segunda se retrasó y no se realizó por deterioro clínico global relacionado con sus comorbilidades (insuficiencia cardíaca, diabetes mal controlada, enfermedad renal crónica y el ACV).\n\nPuntos clave e implicaciones\n- El stent ureteral retenido y muy incrustado produjo obstrucción e infección que requirieron drenaje urgente. La falta de seguimiento de los stents puede causar complicaciones graves.\n- La nefrostomía percutánea salvó la función renal y la vida al aliviar la obstrucción, pero la punción renal puede producir complicaciones vasculares raras como fístulas arteriovenosas; estas pueden sangrar de forma masiva, especialmente si el paciente recibe anticoagulación.\n- La embolización arterial selectiva es una opción eficaz y preservadora de órgano para controlar hemorragias renales por FAV/pseudoaneurisma.\n- El manejo en estos casos exige coordinación estrecha entre urólogos, radiólogos intervencionistas, intensivistas y neurológos, y un delicado balance entre prevenir eventos embólicos (requiriendo anticoagulación) y minimizar riesgo de sangrado.\n\nEmpatía y pronóstico\nEste caso ilustra la complejidad de manejar pacientes con múltiples enfermedades crónicas y procedimientos urológicos retenidos. Aunque las intervenciones endovasculares y endourológicas fueron exitosas para las complicaciones inmediatas, las comorbilidades y el ACV complicaron la recuperación y retrasaron el tratamiento definitivo. La prevención (seguimiento y extracción programada de stents) y la vigilancia estrecha tras procedimientos invasivos son medidas esenciales para evitar desenlaces similares.",
+                "fh_score": 32.92
+            }
+        }
+    },
+    {
+        "article": "Un hombre de 52 años fue admitido en un hospital debido a palpitaciones repentinas y fatiga general. La electrocardiografía reveló taquicardia ventricular con una frecuencia cardíaca de 180 lpm. Su ritmo cardíaco volvió a un ritmo sinusal después de una cardioversión inmediata y luego fue derivado a nuestra institución para una investigación adicional. Su historial médico pasado incluía reconstrucción del tracto de salida del ventrículo derecho utilizando un injerto homólogo y cierre de un defecto septal ventricular para TOF, que se realizó 47 años antes. Sin embargo, se perdió su seguimiento posterior. Tras ser derivado a nuestra institución, su presión arterial era de 116/70 mmHg, frecuencia cardíaca de 80 lpm, y saturación de oxígeno del 99% (con aire ambiente). Al inspeccionar la pulsación de la vena yugular, se observaron claramente una onda prominente y un descenso profundo, que eran consistentes con el aumento de la presión de llenado del ventrículo derecho y la compensación del aumento de la contracción de la RA. Cabe destacar que la auscultación reveló un murmullo diastólico regurgitante agudo en el tercer espacio intercostal izquierdo, un primer sonido cardíaco ampliamente dividido (S1) y un segundo sonido cardíaco (S2), lo que indicaba un ventrículo derecho severamente dilatado debido a la liberación de PR libre y la presencia de una válvula pulmonar no funcional. Además, se auscultó un tercer sonido cardíaco (S3) en el cuarto borde paraesternal, que era consistente con un S3 derecho. El electrocardiograma reveló bloqueo completo del haz de rama derecha, con una duración de QRS de 200 lpm. La radiografía de tórax mostró cardiomegalia con dilatación de las arterias pulmonares bilaterales. La ecocardiografía transtorácica reveló una regresión completa de la válvula pulmonar, que resultó en PR libre y una dilatación prominente del ventrículo derecho. La evaluación volumétrica del ventrículo derecho se realizó utilizando una resonancia magnética cardíaca, que reveló un volumen final diastólico del ventrículo derecho de 428 ml (índice de volumen final diastólico del ventrículo derecho de 240 ml/m2), una fracción de eyección del ventrículo derecho del 36% y una fracción de eyección de PR del 74%. Además, la tomografía computarizada multidetector mostró claramente una regresión completa de la válvula pulmonar del injerto homólogo.\n\nEl paciente se sometió a un examen con catéter para investigar más a fondo su estado hemodinámico. Su forma de onda de presión RA fue particularmente notable, ya que consistía en una onda a prominente y un descenso y, que coincidían con el cuarto sonido cardiaco (S4) y S3 en un fonocardiograma, respectivamente. Además, se reveló que la presión arterial pulmonar final diastólica y la presión final diastólica del VD eran casi idénticas debido al PR libre. Por lo tanto, la evaluación clínica del «quinteto de sonidos cardiacos», que incluye un murmullo diastólico regurgitante agudo, un S1 ampliamente dividido, un S2 único y la presencia de un S3 y un S4 derechos, se confirmó mediante una evaluación hemodinámica y anatómica multimodal como insuficiencia cardiaca derecha grave concomitante con un VD significativamente dilatado debido a la regresión completa de la válvula pulmonar y el PR libre resultante.\n\nDespués del reemplazo de la válvula pulmonar, el «quinteto de sonidos del corazón» se resolvió por completo.\n\nMH - Insuficiencia cardiaca/*etiología\nMH - Murmullos cardiacos/*diagnóstico\nMH - *Sonidos del corazón\nMH - Humanos\nMH - Hombre\nMH - Edad Media\nMH - Insuficiencia de la válvula pulmonar/*complicaciones/diagnóstico\nMH - Taquicardia, ventricular/etiología\nMH - Tetralogía de Fallot/*cirugía\nMH - Disfunción ventricular, derecha/etiología\n",
+        "gold_summary": "Un hombre de 52 años fue derivado a nuestra institución para la evaluación de una taquicardia ventricular de inicio súbito. Su historia clínica incluía una reconstrucción del tracto de salida del ventrículo derecho a los 5 años de edad. La auscultación reveló un murmullo diastólico regurgitante agudo, un primer sonido cardiaco (S1) ampliamente dividido y un segundo sonido cardiaco (S2) único, lo que indicaba un ventrículo derecho severamente dilatado debido a una regurgitación pulmonar (RP) grave y la presencia de una válvula pulmonar no funcional. Además, el tercer sonido cardiaco (S3) y el cuarto sonido cardiaco (S4) del lado derecho estaban presentes, lo que era coherente con una presión de llenado del ventrículo derecho elevada y la presencia de un ventrículo derecho no conforme. Finalmente, el mencionado «quinteto de sonidos cardiacos» se confirmó mediante una evaluación multimodal como insuficiencia cardiaca del lado derecho con un ventrículo derecho concomitantemente severamente dilatado debido a la regresión completa de la válvula pulmonar y la consiguiente RP libre.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había un hombre de 52 años que llegó al hospital porque su corazón empezó a latir muy, muy rápido y se sentía muy cansado. Los médicos lo trataron para que el latido volviera a la normalidad. \n\nCuando le escucharon el pecho, oyeron ruidos raros. Esos ruidos decían que la válvula que va del corazón a los pulmones no funcionaba. Esa válvula estaba rota y dejaba que la sangre volviera hacia atrás. Por eso, la parte derecha del corazón (la que manda sangre a los pulmones) estaba muy grande y cansada.\n\nLos médicos hicieron ecografías, una tomografía y una resonancia. También pasaron un tubito fino para medir las presiones dentro del corazón. Todo mostró lo mismo: la válvula estaba fallando por completo y el lado derecho del corazón trabajaba mal.\n\nLe cambiaron la válvula por una nueva. Después de la operación, los ruidos raros desaparecieron. En resumen: su corazón tuvo un problema grande por una válvula rota. Los médicos lo arreglaron con una operación y eso solucionó los sonidos y la falla del corazón.",
+                "fh_score": 73.61
+            },
+            "B2": {
+                "text": "Here is a clear, patient summary you can understand at a high-school level.\n\nWhat happened\n- A 52-year-old man went to the hospital because he suddenly felt very fast heartbeats (ventricular tachycardia) and was tired. Doctors restored his normal heart rhythm with an emergency shock (cardioversion).\n- As a child he had surgery for tetralogy of Fallot (a congenital heart defect). That surgery included rebuilding the outlet of the right ventricle and placing a homograft (a donated valve). He did not have follow-up care after that.\n\nKey findings and what they mean\n- Physical exam found a loud blowing sound during the heart’s filling phase (a diastolic regurgitant murmur). This comes from blood leaking backward through the pulmonary valve into the right ventricle. This leak is called pulmonary regurgitation (PR).\n- Additional heart sounds were unusual: a widely split first heart sound (S1), a single second heart sound (S2), and two extra low-pitched sounds on the right side called S3 and S4. These signs together (the authors call them a “quintet” of heart sounds) point to a severely dilated, poorly working right ventricle with high filling pressure.\n- Imaging tests confirmed the problem:\n  - Chest X-ray showed an enlarged heart and big pulmonary arteries.\n  - Echocardiography and CT showed the homograft pulmonary valve had completely failed (no working leaflets), causing free pulmonary regurgitation.\n  - Cardiac MRI measured a very large right ventricle: end-diastolic volume 428 ml (indexed 240 ml/m2) — much larger than normal — and right ventricular ejection fraction 36% (reduced pump function). The regurgitation fraction was 74% (meaning most blood was leaking back).\n- A catheter study (direct pressure measurements from inside the heart) supported these findings. Pressures in the pulmonary artery and right ventricle were almost the same at end-diastole because blood flowed freely backward through the failed valve. The wave patterns in the right atrium matched the S4 and S3 sounds heard with the stethoscope.\n\nDiagnosis and outcome\n- The team diagnosed severe right-sided heart failure caused by complete degeneration of the pulmonary homograft and massive pulmonary regurgitation. This also likely contributed to the episode of ventricular tachycardia.\n- The patient had the failed pulmonary valve replaced. After surgery, the unusual “quintet” of heart sounds disappeared, showing the valve replacement fixed the abnormal blood flow and reduced the load on the right ventricle.\n\nTakeaway (in simple terms)\n- A valve placed in childhood can wear out decades later and cause the right side of the heart to become very large and weak if not checked.\n- Symptoms can include fast, dangerous heart rhythms and tiredness. Careful physical exam, imaging, and pressure measurements can show the problem.\n- Replacing the failed valve can stop the backward leak and improve the heart’s function and sounds. Regular long-term follow-up after congenital heart surgery is important to catch valve failure early.",
+                "fh_score": 85.75
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel universitario)\n\nUn hombre de 52 años ingresó tras un episodio de taquicardia ventricular súbita (180 lpm) que requirió cardioversión eléctrica. Tenía antecedentes de reparación de la tetralogía de Fallot a los 5 años (reconstrucción del tracto de salida del ventrículo derecho con un injerto homólogo y cierre de un defecto septal ventricular) y había perdido el seguimiento desde entonces.\n\nHallazgos clínicos y pruebas\n- Signos vitales al ingreso: PA 116/70 mmHg, FC 80 lpm, SaO2 99% en aire ambiente.\n- Inspección: pulso yugular con una onda prominente y un descenso profundo, compatibles con aumento de la presión de llenado del ventrículo derecho (VD) y mayor contracción auricular derecha.\n- Auscultación: \"quinteto\" de hallazgos anormales — un soplo diastólico regurgitante agudo (compatible con insuficiencia pulmonar libre), primer ruido cardíaco (S1) ampliamente dividido, segundo ruido (S2) único (ausencia de componente pulmonar), y ruidos del lado derecho S3 y S4. Estos signos apuntaban a un VD severamente dilatado y a insuficiencia cardíaca derecha.\n- ECG: bloqueo completo de rama derecha con QRS muy ancho (200 ms).\n- Radiografía de tórax: cardiomegalia y dilatación de las arterias pulmonares.\n- Ecocardiografía transtorácica y TC multicorte: regresión completa/degeneración de la válvula pulmonar del injerto homólogo y regurgitación pulmonar (RP) libre, con dilatación prominente del VD.\n- Resonancia cardíaca (evaluación volumétrica): volumen telesistólico/diastólico derecho muy aumentado — volumen telediastólico del VD 428 ml (índice 240 ml/m2), fracción de eyección del VD 36%; fracción regurgitante pulmonar 74% (indicativa de RP severa).\n- Cateterismo derecho: la onda auricular derecha mostró a una prominente y un descenso pronunciado que se correlacionaron con S4 y S3 en el fonocardiograma; la presión diastólica final pulmonar y la presión diastólica final del VD fueron casi iguales, hallazgo esperado en RP libre.\n\nInterpretación y significado\n- La regresión/degeneración completa de la válvula pulmonar del injerto causó regurgitación pulmonar libre, lo que produjo sobrecarga de volumen crónica del VD. Esto llevó a dilatación ventricular derecha marcada, disfunción sistólica (RVEF reducida) y elevación de las presiones de llenado derechas.\n- La dilatación y la alteración de la geometría ventricular, junto con la conducción alterada (QRS ancho), explican la presentación con arritmia ventricular y aumentan el riesgo de eventos arrítmicos.\n- El conjunto característico de cinco hallazgos auscultatorios (soplo diastólico regurgitante agudo, S1 ampliamente dividido, S2 único, S3 y S4 derechos) fue confirmado por estudios hemodinámicos e imagenológicos como manifestación clínica de insuficiencia cardíaca derecha por RP severa.\n\nTratamiento y evolución\n- Se realizó reemplazo de la válvula pulmonar. Tras la cirugía, los cinco hallazgos auscultatorios desaparecieron por completo, lo que refleja la corrección inmediata de la regurgitación y la mejora hemodinámica.\n\nImplicaciones prácticas\n- Los pacientes reparados de tetralogía de Fallot necesitan seguimiento cardiológico de por vida; la degeneración tardía de válvulas biológicas o injertos puede causar RP progresiva, dilatación del VD y arritmias potencialmente graves.\n- La evaluación periódica con ecocardiografía y, cuando sea necesario, resonancia cardíaca permite detectar indicación de reemplazo valvular pulmonar antes de un deterioro irreversible del VD.\n- En pacientes con RP severa y VD dilatado o síntomas/taquiarritmias, el reemplazo valvular pulmonar puede normalizar la hemodinámica y reducir los síntomas y riesgos arrítmicos.\n\nComentario empático\nEste caso ilustra la importancia del seguimiento a largo plazo después de la reparación de cardiopatías congénitas. El diagnóstico y tratamiento oportunos permitieron revertir hallazgos clínicos claros y mejorar la situación hemodinámica del paciente.",
+                "fh_score": 36.36
+            }
+        }
+    },
+    {
+        "article": "Un hombre de 62 años con antecedentes médicos de cardiopatía no isquémica que derivó en insuficiencia cardíaca, en estado postoperatorio de un dispositivo de asistencia ventricular izquierdo, se sometió a un trasplante cardíaco ortotópico. Mientras se recuperaba en la UCI quirúrgica, desarrolló un empeoramiento de la distensión abdominal, sensibilidad y leucocitosis, lo que motivó la evaluación por el equipo de cirugía general 6 días después del trasplante. El paciente no había evacuado ni expulsado gases desde su cirugía y no había respondido a los enemas administrados ni a la metoclopramida oral por un presunto íleo posoperatorio. Se realizó una tomografía computarizada del abdomen y la pelvis, que reveló múltiples bucles intestinales dilatados con niveles de aire-líquido y un punto de transición en el intestino delgado proximal en el cuadrante superior izquierdo, lo que generó preocupación por una obstrucción. En función de estos hallazgos y del hecho de que el paciente no había sido sometido a cirugías abdominales previas, lo que hacía que la obstrucción intestinal fuera secundaria a las adherencias, se llevó al paciente al quirófano para una laparotomía exploratoria. En el quirófano, se encontró que el intestino estaba dilatado de forma difusa sin ninguna área de isquemia aparente. Se encontró que una porción del intestino delgado estaba adherida a la pared abdominal anterior en el cuadrante superior izquierdo. Tras una exploración adicional, se encontró que una línea motriz de LVAD retenida estaba tunelizada en la cavidad peritoneal, estrangulando un bucle de intestino delgado en el cuadrante superior izquierdo. La línea motriz se liberó de la pared abdominal y se retiró, y se liberó el bucle de intestino afectado. Se encontró que era viable después de unos minutos de reperfusión. Se examinó el intestino delgado en su totalidad, desde el ligamento de Trietz distalmente hasta el intestino ciego, y se encontró que estaba dilatado pero en general era normal. Se reparó una pequeña área de desgarro seroso en el punto de adhesión a la línea motriz, principalmente. Se devolvió el intestino a la cavidad abdominal y se cerró la fascia y la piel con suturas corrientes y grapas cutáneas.\n\nMH - *Eliminación de dispositivo\nMH - Migración de cuerpos extraños/*complicaciones\nMH - Insuficiencia cardiaca/*terapia\nMH - *Trasplante de corazón\nMH - Dispositivos de asistencia cardíaca/*efectos adversos\nMH - Humanos\nMH - Obstrucción intestinal/diagnóstico por imágenes/*etiología\nMH - Laparotomía\nMH - Hombre\nMH - Edad Media\nMH - Tomografía computarizada por rayos X\nMH - Estados Unidos\n",
+        "gold_summary": "Un hombre de 62 años con antecedentes de insuficiencia cardiaca inducida por cardiomiopatía no isquémica, post-puente de asistencia ventricular izquierda y trasplante cardiaco ortotópico, presentó distensión abdominal, dolor y leucocitosis seis días después del trasplante. La TAC de abdomen y pelvis reveló bucles intestinales dilatados, niveles de aire-líquido y un punto de transición en el intestino delgado proximal. Se diagnosticó al paciente una obstrucción intestinal y se le realizó una laparotomía exploratoria. Se encontró que tenía un conducto de LVAD intraabdominal retenido que estrangulaba un bucle de intestino delgado en el cuadrante superior izquierdo. Se retiró el conducto y se liberó la sección de intestino con el retorno de la perfusión.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un hombre de 62 años tuvo un trasplante de corazón. Antes, llevaba un aparato de asistencia que tenía un cable que salía del cuerpo. Seis días después de la operación, su barriga se hinchó, le dolía y no podía hacer caca ni expulsar gases. Los médicos vieron en una tomografía que su intestino estaba bloqueado.\n\nAbrieron la barriga para mirar. Encontraron que el cable del aparato había quedado dentro y rodeaba un tramo del intestino. El cable estaba apretando el intestino. Los cirujanos quitaron el cable y soltaron el intestino. Después de unos minutos la sangre volvió a correr y el intestino estaba bien. Repararon una pequeña rotura en la superficie y cerraron la herida.\n\nLos médicos resolvieron el problema y el intestino quedó sano. Esto muestra que a veces partes de aparatos antiguos pueden causar problemas, pero los médicos pueden encontrarlos y corregirlos.",
+                "fh_score": 70.85
+            },
+            "B2": {
+                "text": "Here is a clear summary in plain language:\n\nA 62-year-old man who had severe heart failure and previously used a left ventricular assist device (LVAD) received a new heart (orthotopic heart transplant). Six days after the transplant he developed increasing belly swelling, pain, and a high white blood cell count. He had not passed stool or gas since the surgery and did not improve with enemas or medicines for a suspected postoperative ileus (an ileus is when the intestines are slow or stopped but not blocked).\n\nA CT scan of the belly showed many dilated small-bowel loops, air–fluid levels, and a clear “transition point” in the upper left side of the small intestine — findings that suggested a mechanical bowel obstruction. Because he had not had previous abdominal surgery (making adhesions less likely), the team took him to the operating room for an exploratory laparotomy (surgically opening the abdomen to look inside).\n\nDuring surgery the small intestine was very dilated. The surgeons found that a portion of small bowel was stuck to the front abdominal wall. Further inspection revealed that the retained LVAD driveline (the cable that connects the LVAD pump to outside power) had been tunneled into the abdominal cavity and was strangling a loop of small intestine. The driveline was freed from the wall and removed, and the trapped bowel loop was released. After a few minutes of restoring blood flow (reperfusion), the affected bowel looked viable (alive and likely to recover). The surgeons checked the rest of the small intestine from the ligament of Treitz down to the cecum; it was dilated but otherwise normal. A small tear in the bowel’s outer layer where it had adhered to the driveline was repaired. The abdomen was closed.\n\nIn short: a retained LVAD driveline caused a strangulating small-bowel obstruction after heart transplant. The driveline was removed and the bowel was saved. The patient would be monitored afterward for return of bowel function, signs of infection, and healing.",
+                "fh_score": 83.81
+            },
+            "B3": {
+                "text": "Resumen (nivel universitario)\n\nUn hombre de 62 años, con insuficiencia cardiaca por miocardiopatía no isquémica que había recibido previamente un dispositivo de asistencia ventricular izquierdo (LVAD) y posteriormente un trasplante cardíaco ortotópico, desarrolló seis días después del trasplante distensión abdominal progresiva, dolor y leucocitosis. No había evacuado ni expulsado gases desde la cirugía y no respondió a medidas conservadoras (enemas y metoclopramida), por lo que se solicitó una tomografía abdominal.\n\nLa TC mostró múltiples asas intestinales dilatadas con niveles hidroaéreos y un punto de transición en el intestino delgado proximal, hallazgos compatibles con una obstrucción del intestino delgado. Dado que el paciente no tenía cirugías abdominales previas que explicaran adherencias, se decidió una laparotomía exploratoria.\n\nEn quirófano se observó dilatación intestinal generalizada pero sin zonas necróticas. El hallazgo clave fue que una línea motriz (driveline) del LVAD, retenida y tunelizada hacia la cavidad peritoneal, estaba estrangulando un asa de intestino delgado en el cuadrante superior izquierdo. El equipo liberó y retiró la línea motriz de la pared abdominal y desestranguló el asa intestinal; tras unos minutos de reperfusión la víscera quedó viable, por lo que no fue necesaria resección. Se reparó una pequeña rotura serosa en el punto de adherencia y se cerró la pared abdominal.\n\nImplicaciones y recomendaciones prácticas\n- Este caso ilustra que cuerpos extraños o componentes retenidos de dispositivos cardíacos (como la línea motriz de un LVAD) pueden migrar y producir una obstrucción mecánica por estrangulación, incluso en pacientes sin cirugías abdominales previas.  \n- La ausencia de isquemia intestinal y la recuperación tras la liberación son resultados favorables; sin embargo, la situación exigió intervención quirúrgica urgente para evitar necrosis intestinal.  \n- Es importante la revisión y eliminación completa de componentes extracorpóreos al retirar o explantar dispositivos, y mantener alta sospecha clínica de obstrucción mecánica cuando un paciente con dispositivo implantado presenta distensión y ausencia de tránsito intestinal.  \n- El seguimiento debe incluir vigilancia de la función intestinal, signos de infección o complicaciones de la herida y control cardíaco postrasplante.  \n\nSe reporta un desenlace inmediato favorable tras la intervención, con preservación del intestino afectado.",
+                "fh_score": 32.64
+            }
+        }
+    },
+    {
+        "article": "Un paciente de 13 años de edad, del sexo masculino, fue admitido en el Hospital de Niños de Damasco tras notar una masa palpable agrandada en la región inguinal izquierda. Su historial médico no fue notable, excepto por una intervención quirúrgica en su columna vertebral 6 años atrás, debido a un accidente, que resultó en la pérdida de la función motora y la sensación en ambas extremidades inferiores.\n\nDebido al largo período que había pasado en la cama, el paciente desarrolló úlceras de decúbito en su pie izquierdo. El único hallazgo en el examen clínico fue una masa en el área inguinal izquierda, que era móvil en las estructuras profundas y también lo era la piel que la cubría. La masa no era sensible a la palpación y no se observaron signos de inflamación local.\n\nLos exámenes de laboratorio revelaron una ESR elevada (119 mm/h en la primera hora). Se solicitaron otros exámenes básicos de laboratorio, que incluían (recuento sanguíneo completo, pruebas de función hepática, electrolitos, urea, creatinina y LDH) y estaban dentro de los rangos normales para la edad. La realización de estos exámenes fue esencial para descartar enfermedades sistémicas. Dada la ausencia de hallazgos físicos indicativos de trastornos sistémicos o inmunodeficiencias, se consideró innecesario realizar exámenes adicionales como los de VIH o antiglobulina directa.\n\nLa tomografía computarizada del abdomen, el tórax y la pelvis mostró ganglios linfáticos agrandados por debajo del ligamento inguinal, el más grande de aproximadamente 3,5 por 2,4 cm. Otros órganos y ganglios estaban dentro de los límites normales.\n\nTodas las investigaciones mencionadas fueron esenciales para descartar otros diagnósticos de alto riesgo, como linfoma y leucemia. Sin embargo, no fueron suficientes para llegar al diagnóstico definitivo, por lo que se tomó la decisión de realizar una resección quirúrgica de los ganglios.\n\nPara confirmar los diagnósticos y descartar otras posibles diferencias que pudieran presentarse con ganglios linfáticos agrandados, se realizó la extirpación quirúrgica de todos estos ganglios agrandados bajo anestesia general y se enviaron biopsias para su estudio microscópico.\n\nLa biopsia mostró una arquitectura ganglionar hiperplásica con proliferación de histiocitos y células plasmáticas con proliferación vascular, lo que es compatible con el subtipo de enfermedad de Castleman de células plasmáticas.\n\nEl paciente fue dado de alta del hospital después de 14 días, tras comprobar que no había ganglios linfáticos agrandados. La única recomendación fue prednisolona oral. El paciente se sometió a un seguimiento mediante TAC de cuerpo entero cada tres meses. Durante cada visita al hospital, se realizó un examen clínico exhaustivo y pruebas de laboratorio (por ejemplo, análisis de sangre completo, VSG, proteína C reactiva, pruebas de función hepática, pruebas de función renal), además del TAC. Después de un período de seguimiento de 12 meses, el paciente no informó de nuevos síntomas o ganglios linfáticos agrandados. Además, no se observaron anomalías durante el examen clínico o en las pruebas de laboratorio.\n",
+        "gold_summary": "Reportamos un caso único de un niño de 13 años que presentó una masa palpable agrandada en la región inguinal izquierda sin ningún síntoma constitucional. La extirpación quirúrgica de esta masa fue esencial para descartar causas preocupantes. El examen patológico reveló cambios proliferativos consistentes con el tipo de célula plasmática de la enfermedad de Castleman, que es una de las formas más raras de la enfermedad en niños. Hasta donde sabemos, este caso es el primer caso reportado de enfermedad de Castleman unicéntrica (UCD) en el área inguinal. Durante un período de seguimiento de 12 meses, no se reportaron agrandamientos adicionales de los ganglios linfáticos u otros síntomas.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había un niño de 13 años que encontró un bulto en la ingle izquierda. El bulto no dolía. El niño había pasado mucho tiempo en cama antes y tenía una úlcera en el pie, pero por lo demás estaba bien.\n\nLos médicos hicieron análisis de sangre. Una prueba mostró algo de inflamación. Otras pruebas estaban normales. También le hicieron una tomografía (una foto grande del cuerpo) y vieron ganglios linfáticos agrandados en la ingle. Los ganglios son pequeños “guardianes” que ayudan al cuerpo a luchar contra gérmenes.\n\nLos médicos sacaron los ganglios con cirugía para ver qué eran. Miraron el tejido con un microscopio. Dijeron que era enfermedad de Castleman, tipo de células plasmáticas. Esto es una enfermedad rara donde un ganglio crece más de lo normal, pero no es lo mismo que un cáncer. En este niño, solo un grupo de ganglios estaba afectado (esto se llama “unicéntrica”). Es muy raro en niños y puede ser el primer caso descrito en la ingle.\n\nEl niño salió del hospital a las dos semanas. Le dieron un medicamento para bajar la inflamación. Lo revisaron con pruebas y tomografías cada tres meses. Después de un año no tenía nuevos bultos ni otros problemas. Esto es una buena noticia.",
+                "fh_score": 81.9
+            },
+            "B2": {
+                "text": "Resumen para lectores jóvenes (nivel B2, 11–17 años)\n\nUn niño de 13 años acudió al hospital porque notó una masa en la ingle izquierda. El chico había perdido la movilidad y la sensibilidad en las piernas años antes tras un accidente y una operación de columna, por lo que pasó mucho tiempo en cama y tenía úlceras por presión en el pie. Aparte de eso, no tenía otros síntomas como fiebre, pérdida de peso ni cansancio extremo.\n\nQué encontraron los médicos\n- En la exploración física solo se vio una masa en la ingle: era móvil, no dolorosa y la piel sobre ella estaba normal.  \n- Un análisis de sangre mostró la velocidad de sedimentación globular (VSG) elevada, que indica inflamación, pero el resto de las pruebas básicas salió dentro de lo esperado.  \n- La tomografía (TAC) reveló ganglios linfáticos agrandados por debajo del ligamento inguinal; el mayor medía 3,5 × 2,4 cm. No había agrandamiento en otros órganos o ganglios.\n\nQué hicieron y por qué\n- Para descartar enfermedades graves como linfoma o leucemia y para saber exactamente qué era la masa, los médicos decidieron extirpar quirúrgicamente los ganglios agrandados y enviarlos a estudio microscópico (biopsia).  \n- La biopsia mostró un patrón llamado “subtipo de células plasmáticas” de la enfermedad de Castleman. La enfermedad de Castleman es un trastorno raro en el que los ganglios linfáticos se agrandan por cambios en las células del sistema inmune. Cuando afecta a un solo grupo de ganglios se llama “unicéntrica”.\n\nTratamiento y seguimiento\n- El paciente recibió prednisolona oral y quedó ingresado 14 días antes del alta.  \n- Se programaron controles completos cada tres meses que incluyeron TAC de cuerpo entero y análisis de sangre (para vigilar inflamación y función de órganos).  \n- Tras 12 meses de seguimiento no hubo nuevos ganglios aumentados, ni síntomas ni alteraciones en las pruebas.\n\nImportancia del caso\n- La resección quirúrgica fue clave tanto para lograr el diagnóstico como para excluir enfermedades más graves.  \n- Según los autores, este sería el primer caso descrito de enfermedad de Castleman unicéntrica en la región inguinal en un niño.\n\nSi tienes preguntas sobre esto: es normal sentir curiosidad o preocupación por enfermedades raras. Los médicos suelen usar imágenes y biopsias para saber exactamente qué ocurre y así ofrecer el mejor tratamiento.",
+                "fh_score": 60.67
+            },
+            "B3": {
+                "text": "Resumen clínico — enfermedad de Castleman unicéntrica (subtipo plasmocítico) en un niño de 13 años\n\nPresentación y antecedentes\n- Paciente: varón de 13 años, sin antecedentes médicos relevantes salvo una cirugía vertebral 6 años antes que lo dejó con pérdida de función motora y sensibilidad en ambas piernas. Por inmovilidad prolongada tenía úlceras por presión en el pie izquierdo.\n- Motivo de consulta: masa palpable en la región inguinal izquierda, indolora, móvil respecto a las estructuras profundas y a la piel, sin signos locales de inflamación ni síntomas generales (febrícula, pérdida de peso, sudoración nocturna).\n\nHallazgos iniciales\n- Laboratorio: velocidad de sedimentación globular (VSG/ESR) muy elevada (119 mm/h), lo que indica inflamación sistémica. Resto de pruebas básicas (hemograma, función hepática, electrolitos, urea, creatinina, LDH) dentro de rangos normales.\n- Imagen: tomografía computarizada (abdomen, tórax y pelvis) mostró ganglios linfáticos aumentados de volumen por debajo del ligamento inguinal; el mayor medía ≈ 3,5 × 2,4 cm. Otros órganos y ganglios normales.\n\nQué se hizo y por qué\n- Dada la preocupación por diagnósticos de alto riesgo (linfoma, leucemia) y la imposibilidad de diagnosticar con certeza solo con pruebas de imagen y laboratorio, se decidió la resección quirúrgica de los ganglios agrandados.\n- La cirugía tuvo finalidad diagnóstica y terapéutica: extirpación completa de las adenopatías con envío de biopsias para estudio histológico.\n\nDiagnóstico final (biopsia)\n- Anatomía patológica: arquitectura ganglionar hiperplásica con proliferación de histiocitos y abundantes células plasmáticas junto con proliferación vascular.\n- Interpretación: compatible con enfermedad de Castleman unicéntrica, subtipo plasmocítico. Breve nota explicativa: la enfermedad de Castleman es un trastorno linfoproliferativo poco frecuente; la forma unicéntrica afecta a un solo grupo ganglionar y suele curarse con la extirpación completa. El subtipo plasmocítico se caracteriza por abundantes células plasmáticas e inflamación.\n\nTratamiento, seguimiento y evolución\n- Alta hospitalaria: a los 14 días, sin adenopatías palpables. Se indicó prednisolona oral.\n- Vigilancia: tomografía corporal cada 3 meses y controles clínicos y analíticos regulares (hemograma, VSG, proteína C reactiva, función hepática y renal).\n- Resultado a 12 meses: asintomático, sin recurrencia de adenopatías ni alteraciones en el examen físico o en las pruebas de laboratorio.\n\nImplicaciones y puntos clave\n- La resección quirúrgica fue clave tanto para establecer el diagnóstico definitivo como para tratar la enfermedad; en la enfermedad de Castleman unicéntrica la extirpación completa suele ser curativa.\n- La VSG muy elevada señaló un proceso inflamatorio aunque el niño no mostró síntomas sistémicos.\n- Se descartaron causas graves como linfoma o leucemia mediante imagen y, finalmente, por la histología.\n- Según los autores, este es el primer caso reportado de enfermedad de Castleman unicéntrica localizada en la región inguinal en un niño, lo que subraya su rareza.\n- Recomendación razonable: continuar seguimiento periódico para detectar recurrencia o aparición de enfermedad multicéntrica, aunque el pronóstico tras resección completa es generalmente bueno.\n\nEmpatía\n- El diagnóstico fue infrecuente pero tratable. El paciente respondió bien al tratamiento y permanece sin evidencia de enfermedad a los 12 meses. Es importante que las familias mantengan el seguimiento médico programado y consulten ante cualquier nuevo bulto, fiebre persistente o pérdida de peso.",
+                "fh_score": 40.03
+            }
+        }
+    },
+    {
+        "article": "Un hombre asiático de 55 años de edad, que había estado recibiendo tratamiento irregularmente (el paciente no cumplía con el tratamiento) para DCMP durante los últimos 6 meses, acudió con quejas de disnea al hacer ejercicio durante 1 semana y disminución de la producción de orina durante 2 días. El paciente aparentemente estaba bien hace 1 semana cuando empezó a desarrollar disnea, inicio insidioso, gradualmente progresiva, inicialmente de grado II de la New York Heart Association (NYHA) pero progresó a grado IV de la NYHA asociada con pesadez en el pecho. La historia de ortopnea y disnea nocturna paroxística estuvo presente. Esto estuvo asociado con tos con una cantidad moderada de expectoración espumosa, no purulenta. El paciente también se quejó de hinchazón de las extremidades inferiores bilaterales. No hubo historia de hinchazón periorbital, orina espumosa o hematuria. No hubo historia de palpitación, síncope, dolor de pecho o hemoptisis. El paciente también dio una historia de una sensación de hormigueo en ambas manos y pies durante 1 mes.\n\nEl paciente había tenido un episodio similar 6 meses atrás, por el que fue hospitalizado y tratado de manera conservadora como un caso de DCMP. Se le había practicado una cirugía de cataratas en ambos ojos 15 años atrás.\n\nEn el examen físico general, el paciente estaba consciente y orientado en cuanto al tiempo, el lugar y la persona, y afebril con una presión arterial de 90/60 mmHg en el brazo derecho en posición supina y una frecuencia de pulso de 110/min, que era de bajo volumen y todos los pulsos periféricos eran palpables. Presentaba taquipnea con una frecuencia respiratoria de 28/min y palidez. Tenía un edema de pedal B/L, que era de tipo lento con presión venosa yugular elevada (JVP). No se observó ictericia, cianosis, clubbing ni linfadenopatía. Mientras se medía la presión arterial, el paciente empezó a tener espasmos en la muñeca, lo que nos dio una pista para examinar más a fondo y revelar un signo de Chvostek positivo. El signo de Trousseau también fue positivo a los 10 segundos.\n\nEl examen del sistema cardiovascular reveló un latido apical localizado en el sexto espacio intercostal izquierdo, a 1 cm fuera de la línea medioclavicular, de carácter hiperdinámico. Se escucharon S1 y S2 con normalidad en todas las áreas.\n\nEl examen del sistema respiratorio reveló una reducción de la entrada de aire en las bases pulmonares bilaterales con crepitación fina al final de la inspiración bilateral. El examen del sistema nervioso abdominal y central no reveló nada de interés.\n\n\nInvestigaciones\n\nEn el momento del ingreso, el ECG mostró bloqueo completo de rama izquierda (B-R) con un intervalo QT prolongado. La hemoglobina era de 58 g/l (133-162) con un cuadro dimórfico. El volumen corpuscular medio era de 110 fL (80,0-100,0 fL), la hemoglobina corpuscular media era de 34 pg/mL (27,0-32,0 pg/mL), la concentración media de hemoglobina corpuscular era de 36,2 g/dL (32,0-35,0 g/dL). Otros análisis revelaron niveles séricos de vitamina B12 de 135 pg/mL (211-911 pg/mL). El nivel sérico de ácido fólico era de 5,40 ng/mL (>5,38 ng/mL). El nitrógeno ureico en sangre era de 53 mg/dL (10-50) con creatinina de 0,8 mg/dL (0,7-1,3). Los resultados de las pruebas de función hepática (LFT) estaban dentro de los límites normales. El perfil de calcio mostró 4,3 mg/dL de S.calcium (8,5-10,5), fosfato 7,1 mg/dL (2,5-4,5), 3,06 g/dL de S.albumin (3,5-5,5). En vista de la hipocalcemia e hiperfosfatemia, se realizó un estudio del nivel de hormona paratiroidea intacta, que resultó ser <0,23 ng/mL (14-72). El S.magnesium era de 2,0 mg/dL (1,7-2,2). El análisis de gases en sangre arterial (ABG) fue sugestivo de una acidosis metabólica leve. El perfil tiroideo y los niveles de IgAtTG estaban dentro de los límites normales. Los niveles de ferritina y ceruloplasmina séricos estaban dentro de los límites normales. El ultrasonido abdominal y torácico mostró derrame pleural bilateral en posición supina. La vena cava inferior (IVC) y las venas hepáticas eran prominentes. El reposo dentro de los límites normales. La radiografía de tórax mostró un aplanamiento de los ángulos costofrénicos bilaterales que sugería derrame pleural bilateral. La ecocardiografía reveló un ventrículo izquierdo dilatado (LV) con una fracción de eyección del ventrículo izquierdo del 15 %, que sugería DCMP con disfunción severa del LV. Se realizó un arteriograma coronario basal que fue normal. La TC sin contraste de la cabeza mostró calcificación simétrica bilateral (B/L) en el hemisferio cerebeloso B/L, ganglios basales B/L y calcificación cortical/subcortical en la región B/L fronto-parieto-occipital. El reposo dentro de los límites normales.\n\n\nTratamiento\n\nPara el CHF, se inició al paciente con dobutamina intravenosa a una dosis de 6 µg/kg y furosemida intravenosa 20 mg BD para la descongestión. Sin embargo, el paciente no mostró una mejora significativa con el tratamiento anterior. En vista de la hipocalcemia con hiperfosfatemia y bajos niveles de hormona paratiroidea, se consideró un diagnóstico de cardiomiopatía hipocalcemica con hipoparatiroidismo y se inició al paciente con inyección de gluconato de calcio 1 g (90 mg de calcio elemental) administrado por vía intravenosa seguido de infusión de gluconato de calcio en 500 ml de dextrosa al 5% a una velocidad de 37,5 mg/hora de calcio elemental. El paciente mostró una mejora significativa después de iniciar el gluconato de calcio. El paciente fue dado de alta en condiciones estables con comprimidos de calcio por vía oral 3 g/día junto con calcitriol 0,5 µg/día. También se inició con benzotiazida con triamtereno (25/50 mg) OD, ramipril 5 mg una vez al día y carvedilol 3,125 mg dos veces al día. Para la anemia megaloblástica, se administraron inyecciones de cianocobalamina según el protocolo.\n\n\nResultado y seguimiento\n\nAl cabo de tres meses, el paciente había mejorado notablemente.\n\nLas investigaciones mostraron S.calcium 7.7, S.phosphate 6.0 y albúmina 3.6. La hemoglobina fue de 10.1 g/dL. El eco mostró una mejora en la función del LV con una fracción de eyección del 25%. Se planificó una biopsia endomiocardial, pero el paciente se negó, por lo que no pudo realizarse.\n\nMH - Gluconato de calcio/administración y dosificación/uso terapéutico\nMH - Cardiomiopatía, Dilatada/*complicaciones/diagnóstico\nMH - Ecocardiografía/métodos\nMH - Insuficiencia cardiaca/terapia farmacológica/*etiología/fisiopatología\nMH - Humanos\nMH - Hipocalcemia/*complicaciones/diagnóstico/terapia farmacológica/fisiopatología\nMH - Hipoparatiroidismo/*complicaciones/terapia farmacológica\nMH - Hombre\nMH - Edad Media\nMH - Volumen de carrera\nMH - Resultado del tratamiento\nMH - Disfunción ventricular izquierda/diagnóstico por imágenes\n",
+        "gold_summary": "Presentamos el caso de un hombre asiático de 55 años que había tenido un caso conocido de miocardiopatía dilatada durante 6 meses, que se presentó con las principales quejas de falta de aire al hacer ejercicio y disminución de la producción de orina. En el examen físico general, se observaron características que sugerían una ICC. El signo de Chvostek y Trousseau fue positivo. El paciente tenía antecedentes de cirugía de cataratas en ambos ojos 15 años atrás. Otras investigaciones revelaron una hipocalcemia. La ecografía mostró una grave hipocinesia global del ventrículo izquierdo con una fracción de eyección del ventrículo izquierdo del 15%. Esta ICC fue refractaria al tratamiento convencional, aunque, con la suplementación de calcio, el paciente mejoró sintomáticamente. En el seguimiento después de 3 meses, se observó una mejora en los parámetros ecocardiográficos con una fracción de eyección que mejoró al 25%.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un hombre de 55 años llegó al hospital porque le costaba respirar al hacer esfuerzo y había reducido la cantidad de orina. También tenía hinchazón en las piernas y tos con algo de esputo espumoso.\n\nLos médicos vieron que su corazón estaba muy débil. Esto se llama miocardiopatía dilatada. Su corazón estaba agrandado y no bombeaba bien. También tenía signos de falta de calcio en la sangre. Por ejemplo, se le contrajo la mano cuando le pusieron la presión y tuvo pequeños espasmos en la cara. Los exámenes mostraron calcio muy bajo y una hormona llamada paratiroidea muy baja. Tenía además anemia por falta de vitamina B12.\n\nLos médicos le dieron calcio por la vena y medicinas para el corazón. También le dieron vitamina B12. Después de empezar el calcio por vía intravenosa, mejoró rápido. Tres meses después estaba mucho mejor. Su sangre y sus niveles de calcio habían mejorado. La ecografía del corazón mostró que ahora bombeaba mejor (mejoró de 15% a 25% de fracción de eyección).\n\nEn resumen: su corazón estaba débil por falta de calcio causada por un problema en las glándulas paratiroides. Al darle calcio y otros tratamientos, el paciente mejoró y se sentía mucho mejor después de tres meses.",
+                "fh_score": 76.66
+            },
+            "B2": {
+                "text": "Here is a clear, caring summary of the case:\n\nA 55-year-old man with a known weak, enlarged heart (dilated cardiomyopathy — a condition where the heart cannot pump well) came to the hospital with worsening shortness of breath, trouble breathing when lying down, swollen legs, and reduced urine output. On exam he had signs of heart failure and low blood pressure. He also had two physical signs (Chvostek and Trousseau) that suggest very low blood calcium.\n\nImportant test results:\n- Very low blood calcium (4.3 mg/dL; normal is about 8.5–10.5), high blood phosphate, and a very low parathyroid hormone (PTH) level — this points to hypoparathyroidism (the parathyroid glands are not making enough hormone, which causes low calcium).\n- Severe anemia and low vitamin B12.\n- ECG showed changes (left bundle branch block and a prolonged QT interval) that can happen with low calcium.\n- Echocardiogram showed a very weak left ventricle with ejection fraction (EF) 15% (normal EF is ~55–70%).\n- Brain CT showed symmetric calcium deposits in several brain areas, which can occur with long-standing low calcium.\n\nCourse and treatment:\nStandard heart-failure medicines and a drip to support the heart did not help much at first. When doctors started intravenous calcium (calcium gluconate) because of the low calcium and low PTH, the patient improved noticeably. He was sent home on oral calcium, active vitamin D (calcitriol), heart-failure medicines, and vitamin B12 injections. A heart biopsy was offered later but the patient declined.\n\nOutcome:\nAfter three months the patient was doing much better. His calcium had risen, hemoglobin improved, and heart function showed partial recovery (EF rose to 25%). The findings suggest his severe heart weakness was at least partly caused by very low calcium from hypoparathyroidism, and correcting the calcium helped the heart.\n\nWhat this means and possible next steps:\n- Low blood calcium can cause serious heart problems; treating the calcium deficiency can improve heart function.\n- Ongoing follow-up is needed to keep calcium and phosphate balanced, to monitor heart function, and to continue treating anemia and vitamin B12 deficiency.\n- If uncertainty about the heart’s cause remains, a biopsy can be considered, but it requires patient consent.",
+                "fh_score": 90.92
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel universitario — lectura avanzada)\n\nPresentación y contexto\n- Hombre asiático de 55 años con miocardiopatía dilatada (DCMP) conocida durante 6 meses y tratamiento irregular.\n- Ingresó por empeoramiento rápido de la insuficiencia cardíaca: disnea progresiva (de NYHA II a IV en una semana), ortopnea, disnea paroxística nocturna, tos con esputo espumoso y disminución del volumen urinario durante 2 días. También refería parestesias en manos y pies durante el último mes.\n- Antecedente relevante: cirugía de cataratas bilateral hace 15 años. Hospitalizado previamente por DCMP hace 6 meses.\n\nExploración física y hallazgos relevantes\n- Signos de insuficiencia cardiacas: taquipnea (FR 28/min), taquicardia (FC 110/min), hipotensión (PA 90/60 mmHg), ingurgitación yugular, edema periférico bilateral y crepitantes finos basales pulmonares.\n- Signos neuromusculares positivos para hipocalcemia: Chvostek y Trousseau positivos.\n- Latido apical desplazado (indicador de corazón dilatado).\n- ECG: bloqueo completo de rama izquierda y QT prolongado.\n- Radiografía/ultrasonido: derrame pleural bilateral.\n\nPruebas de laboratorio e imagen\n- Anemia severa: hemoglobina 58 g/L (5.8 g/dL) con cuadro dimórfico y macrocitosis (VCM 110 fL). Niveles bajos de vitamina B12 (135 pg/mL) — compatible con anemia megaloblástica.\n- Función renal y hepática: creatinina normal (0,8 mg/dL), BUN algo elevado (53 mg/dL), LFT dentro de límites normales.\n- Alteraciones electrolíticas críticas:\n  - Calcio sérico total muy bajo: 4.3 mg/dL (normal 8.5–10.5).\n  - Fósforo elevado: 7.1 mg/dL (normal 2.5–4.5).\n  - Albúmina baja: 3.06 g/dL.\n  - Hormona paratiroidea intacta (PTH) suprimida: <0.23 ng/mL (normal 14–72) — indica hipoparatiroidismo.\n  - Magnesio normal.\n- Ecocardiograma: ventrículo izquierdo dilatado con fracción de eyección (FE) del 15% — disfunción ventricular izquierda severa.\n- Coronariografía: arterias coronarias normales (descarta isquemia coronaria como causa principal).\n- TAC craneal: calcificaciones bilaterales en ganglios basales, cerebelo y córtico-subcortical fronto-parieto-occipital — hallazgo compatible con hipoparatiroidismo crónico.\n\nDiagnóstico clínico\n- Insuficiencia cardíaca por miocardiopatía dilatada agravada por hipocalcemia severa: cardiomiopatía hipocalcémica secundaria a hipoparatiroidismo.\n- Anemia megaloblástica por déficit de vitamina B12.\n\nTratamiento y evolución\n- Terapia inicial para insuficiencia cardíaca (dobutamina IV y furosemida) proporcionó respuesta clínica insuficiente.\n- Tras identificar hipocalcemia con PTH baja, se inició reposición con gluconato de calcio IV (bolo 1 g seguido de infusión continua) y posteriormente suplemento oral de calcio (3 g/día) y calcitriol (0,5 µg/día).\n- También recibió tratamiento para la anemia con inyecciones de cianocobalamina.\n- Se añadieron terapia establecida para insuficiencia cardíaca (ramipril, carvedilol, tiazídico combinado con triamtereno).\n- Respuesta: mejoría clínica rápida tras la corrección de calcio; a los 3 meses, calcio sérico 7.7 mg/dL, fósforo 6.0 mg/dL, Hb 10.1 g/dL y FE del VI aumentó a 25% (mejoría parcial). Se planeó biopsia endomiocárdica, pero el paciente la rechazó.\n\nInterpretación e implicaciones\n- La hipocalcemia grave por hipoparatiroidismo fue el factor reversible que agravó la función ventricular en este paciente. La normalidad arterial coronaria y la mejoría de la FE tras corregir el calcio apoyan la relación causal (cardiomiopatía hipocalcémica).\n- Las calcificaciones intracraneales y la presencia de signos clínicos de hipocalcemia (Chvostek/Trousseau) sugieren un hipoparatiroidismo de larga evolución.\n- La anemia megaloblástica coexistente probablemente contribuyó a la fatiga y la anemia severa al ingreso; mejoró con suplementación de vitamina B12.\n\nRecomendaciones y próximos pasos clínicos (prácticos)\n- Continuar substitución oral de calcio y calcitriol, con controles periódicos de calcio total y calcio corregido por albúmina, fósforo, magnesio y función renal.\n- Vigilar signos de exceso de tratamiento (hipercalcemia, hiperparatiroidismo secundario renal, riesgo de nefrolitiasis) y realizar control de calcio urinario si procede.\n- Investigar la causa subyacente del hipoparatiroidismo (quirúrgica, autoinmune, genética, etc.) y considerar pruebas específicas según la sospecha clínica.\n- Seguimiento cardiológico con ecocardiogramas seriados para valorar recuperación ventricular y ajuste de terapia para insuficiencia cardíaca.\n- Adherencia al tratamiento y educación del paciente sobre síntomas de hipocalcemia/hipercalcemia.\n- Evaluación continua y suplementación para la anemia por déficit de B12 si persiste.\n\nComentario final (tono humano)\nEste caso ilustra que causas metabólicas tratables, como la hipocalcemia por hipoparatiroidismo, pueden precipitar o agravar una miocardiopatía grave. La identificación y corrección de la alteración electrolítica permitió una mejoría clínica y parcial recuperación de la función cardíaca. Es importante el seguimiento estrecho y la investigación de la causa del hipoparatiroidismo para evitar recurrencias y complicaciones a largo plazo.",
+                "fh_score": 42.53
+            }
+        }
+    },
+    {
+        "article": "Una mujer de 54 años de edad, libanesa, en hemodiálisis (HD) de mantenimiento tres veces por semana para glomeruloesclerosis segmentaria focal (GSF) fue admitida en el departamento de urgencias, luego de haber sido sometida a su HD programada la noche anterior, debido al inicio repentino de un dolor lumbar agudo en el lado izquierdo, náuseas y vómitos. El dolor había comenzado repentinamente cerca de 12 horas antes de su presentación y se agravó rápidamente. En una nota al margen, un hiperparatiroidismo secundario grave con calcificación cutánea vascular fue tratado con cinacalcet durante 3 años sin respuesta, lo que demandó una paratiroidectomía (hiperplasia de cuatro glándulas) 8 meses antes de su presentación actual. Cinco días antes de su presentación, fue admitida en el hospital debido a anemia grave y rectorragia. Su evaluación por ultrasonido renal mostró riñones bilaterales pequeños con parénquima delgado que contenía quistes de hasta 3 cm y calcificaciones vasculares sin hidronefrosis. Cuatro días antes de su presentación, la colonoscopia a través del íleo terminal reveló un pólipo de 7 mm en el colon descendente izquierdo, que fue removido por mucosectomía. La microscopía volvió como adenoma tubular sésil con displasia de bajo grado. La paciente negó fiebre o antecedentes de trauma. No hubo antecedentes previos de uso de antiplaquetarios. En la emergencia, su presión arterial y pulso fueron de 112/65 mmHg y 96 bpm, su temperatura fue de 36.8°C y presentaba abdomen levemente distendido, con dolor importante en el ángulo costovertebral izquierdo. Los hallazgos de laboratorio mostraron hemoglobina de 9.0 g/dL mientras que el hematocrito fue de 29.7%, recuento total de leucocitos 12.2 × 1000/microlitro, creatinina de 6.06 mg/dL, y nivel de proteína C reactiva de 6 mg/L. Además, el TP fue de 83% y el INR fue de 1.13. En el día de la presentación (es decir, 4 días después de la colonoscopia), se realizó una tomografía computarizada (TC) multifásica del tórax, abdomen y pelvis con y sin contraste intravenoso. El examen reveló un gran quiste y enormes hematomas intraparenquimatosos perirrenales izquierdos con una colección subcapsular de hasta 1,8 cm de espesor con colección hemática en todo el compartimiento renal que alcanzaba un diámetro de más de 9 × 4 cm, hidronefrosis izquierda y edema alrededor de la grasa en todo el flanco y calcificaciones en el hilo. Para la descompresión del sistema pélvico renal y drenaje, optamos por tratarla con inserción retrógrada de doble stent ureteral a la izquierda, que identificó un coágulo en la parte media del uréter izquierdo. Se realizaron cultivo de orina y citología y los resultados fueron negativos. Una simple radiografía del abdomen mostró el doble J en su lugar. La paciente permaneció hemodinámicamente estable, pero presentó una nueva caída en la hemoglobina (6.1 g/dL) la misma noche, lo que exigió una transfusión de una unidad de concentrado de eritrocitos leucodepleados para estabilización. Se tomó la decisión de explorar quirúrgicamente con diagnóstico presuntivo de hematoma perirrenal izquierdo subagudo y para excluir una malignidad subyacente. Se sometió a una sesión de HD sin heparina. En el tercer día, se sometió a una nefrectomía radical abierta a la izquierda con conservación de la glándula suprarrenal. Recibió 2 unidades más de concentrado de eritrocitos leucodepleados durante la intervención. El parénquima renal fue casi totalmente reemplazado por un hematoma que medía 9 × 9 × 7 cm y se extendía hasta la grasa perirrenal. Una pequeña masa papilar fue enviada por separado para análisis. La evaluación histopatológica detallada reveló un parénquima renal con lesiones de nefritis crónica mutilada por grandes áreas hemorrágicas que se extendían hasta la grasa perirrenal. Además, había una proliferación neoplásica de 2 mm, con arquitectura papilar cubierta por pequeñas células cúbicas atípicas y macrófagos espumosos en el eje, compatibles con adenoma papilar. Al día siguiente de la operación, la paciente fue sometida a HD y recibió un paquete de eritrocitos leucodepleados. El período postoperatorio fue sin intercorrerencias. El nivel de hemoglobina se mantuvo alrededor de 10 g/dL. La paciente se recuperó sin signos o síntomas de sangrado. La paciente permanece bien y asintomática y actualmente se encuentra en HD de mantenimiento regular.\n",
+        "gold_summary": "A continuación, se describe un caso inusual de una paciente con HD de 54 años de edad que presentó HPE pocos días después de una colonoscopia. La causa de la HPE fue la ruptura de un quiste de DRCA. Consideramos que la colonoscopia fue un factor desencadenante y planteamos hipótesis sobre su etiopatogenia. La paciente se sometió a una nefrectomía izquierda exitosa.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Esta es la historia en palabras sencillas.\n\nUna mujer de 54 años hacía diálisis tres veces por semana. La diálisis es cuando una máquina limpia su sangre porque sus riñones no trabajan bien.\n\nCuatro días después de hacerse una colonoscopia (un examen del intestino), comenzó a sentir un dolor fuerte en el costado izquierdo. También tenía náuseas y vómitos. Fue al hospital.\n\nLas pruebas por imágenes mostraron que tenía un gran coágulo de sangre alrededor del riñón izquierdo. Esto ocurrió porque se rompió un quiste (una bolsita con líquido) en ese riñón. Los médicos piensan que la colonoscopia pudo haber sido la causa que lo desencadenó.\n\nPrimero le pusieron un tubo para ayudar a drenar la orina y un coágulo dentro del uréter. Pero como el riñón estaba muy dañado y lleno de sangre, la tuvieron que sacar en una operación (nefrectomía), es decir, remover el riñón izquierdo. Durante la cirugía recibió transfusiones de sangre.\n\nEl estudio del riñón mostró que había mucho daño por sangrado. También encontraron una pequeña masa que resultó ser un adenoma papilar, que es un tumor pequeño y benigno (no canceroso).\n\nDespués de la operación, la mujer se recuperó bien. No volvió a sangrar y su hemoglobina se mantuvo estable. Sigue en diálisis regular. Los médicos la vigilan y está bien ahora.",
+                "fh_score": 74.82
+            },
+            "B2": {
+                "text": "Here is a clear, patient-friendly summary of the case.\n\nA 54-year-old woman on long-term hemodialysis (dialysis is a machine treatment that filters the blood when the kidneys do not work) came to the emergency room with sudden, severe pain in her left side, nausea, and vomiting. This happened four days after she had a colonoscopy in which a small polyp was removed.\n\nKey findings and what the doctors did\n- A CT scan showed a large bleed around and inside her left kidney (a perirenal and intraparenchymal hematoma). There was also fluid collecting under the kidney capsule and swelling of the kidney collecting system (hydronephrosis).\n- The team placed a ureteral stent (a small tube that helps urine drain from the kidney to the bladder) and found a blood clot in the ureter. She received blood transfusions because her hemoglobin dropped dangerously low.\n- Because the kidney was mostly replaced by the blood collection and the cause needed to be clarified, the doctors performed a left radical nephrectomy (surgical removal of the left kidney). The adrenal gland was left in place.\n\nWhat the tests showed\n- Pathology (microscope examination) found that the kidney had chronic damage from long-term kidney disease and large hemorrhagic (bleeding) areas that extended into the fat around the kidney.\n- A tiny 2 mm papillary adenoma (a small benign tumor) was also found, but no cancer was identified.\n- The bleeding was caused by rupture of a cyst related to acquired cystic kidney disease (this is common in people on long-term dialysis and means small cysts form in the kidneys).\n\nOutcome and possible cause\n- After surgery she recovered without complications, received further dialysis and blood transfusion as needed, and remained stable with no more signs of bleeding.\n- The team thinks the recent colonoscopy may have triggered the cyst rupture and bleeding, although the exact reason is uncertain.\n\nIn simple terms: a woman on long-term dialysis developed a sudden, serious kidney bleed a few days after a colonoscopy. Treatment included a drain tube, blood transfusions, and removal of the damaged kidney. She recovered well, and the bleeding was linked to a ruptured dialysis-related kidney cyst.",
+                "fh_score": 84.41
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel universitario — lectura avanzada)\n\nPresentación y antecedentes\n- Paciente: mujer libanesa de 54 años en hemodiálisis crónica (3 veces/semana) por esclerosis focal y segmentaria.\n- Antecedentes relevantes: enfermedad renal crónica con riñones pequeños y quistes (en ecografía), múltiples calcificaciones vasculares; hiperparatiroidismo secundario tratado finalmente con paratiroidectomía 8 meses antes. No tomaba antiplaquetarios.\n- Procedimientos recientes: 5 días antes tuvo anemia y rectorragia; 4 días antes se le realizó colonoscopia con polipectomía (pólipo de 7 mm, adenoma tubular sésil con displasia de bajo grado).\n\nCuadro actual y hallazgos iniciales\n- Motivo de ingreso: dolor lumbar izquierdo agudo, náuseas y vómitos con inicio súbito ~12 horas antes de la consulta.\n- Signos vitales: hemodinámica relativamente estable; dolor a la palpación en ángulo costovertebral izquierdo.\n- Laboratorio: anemia (Hb 9 g/dL al ingreso), leucocitosis leve, creatinina elevada (6.06 mg/dL — esperado en paciente en HD), inflamación leve (PCR 6 mg/L), coagulación dentro de límites aceptables (INR 1.13).\n- Imagen: TC multifásica mostró hematoma intrarrenal e importante colección hemática perirrenal izquierda (subcapsular y que ocupaba el compartimento renal, hasta >9 × 4 cm), quiste renal grande, hidronefrosis izquierda y edema de la grasa perirrenal.\n\nManejo inicial\n- Se realizó colocación retrógrada de stent ureteral doble-J izquierdo para descomprimir el sistema pielocalicial; se observó un coágulo en el uréter medio.\n- Cultivo urinario y citología: negativos.\n- A pesar de estabilidad hemodinámica inicial, la paciente presentó caída de hemoglobina a 6.1 g/dL la misma noche, que requirió transfusión de glóbulos rojos leucodepletados.\n\nDecisión terapéutica y hallazgos quirúrgicos\n- Dado el hematoma perirrenal subagudo de gran tamaño y la necesidad de excluir una lesión maligna subyacente, se optó por cirugía exploratoria.\n- Tercero día: nefrectomía radical izquierda abierta (suprarrenal preservada). Durante la intervención se transfundieron 2 unidades adicionales.\n- Hallazgo operatorio: el parénquima renal casi totalmente reemplazado por un hematoma de 9 × 9 × 7 cm que se extendía a la grasa perirrenal; se remitió además una pequeña masa papilar para estudio.\n\nAnatomía patológica y diagnóstico final\n- Macroscópicamente y microscópicamente: riñón con cambios crónicos (nefritis crónica) y áreas extensas de hemorragia que invadían la grasa perirrenal.\n- pequeña lesión neoplásica (2 mm) con arquitectura papilar y células cúbicas atípicas, compatible con adenoma papilar (lesión benigna).\n- Conclusión clínica: hematoma perirrenal izquierdo secundario a ruptura de un quiste asociado a enfermedad renal quística adquirida (DRCA/ACKD) en un paciente en hemodiálisis.\n\nEvolución y desenlace\n- Postoperatorio sin complicaciones significativas; pacientes continuó en HD (sin heparina previa a la cirugía) y recibió transfusiones según necesidad.\n- Hemoglobina estabilizada alrededor de 10 g/dL; sin signos de sangrado recurrente.\n- Actualmente asintomática y en hemodiálisis de mantenimiento.\n\nInterpretación y puntos clave (implicaciones clínicas)\n- Complicación rara pero grave: la rotura espontánea de quistes renales en pacientes con enfermedad renal crónica en diálisis puede producir hematoma intrarrenal/perirrenal masivo que amenaza la estabilidad y puede requerir nefrectomía.\n- Factores predisponentes: enfermedad renal crónica avanzada con quistes (ACKD), alteraciones vasculares y procedimientos recientes (en este caso se plantea que la colonoscopia/polipectomía pudo ser un factor desencadenante, aunque la relación causal no puede probarse definitivamente).\n- Manejo recomendado en casos similares: evaluación rápida con TC, estabilización hemodinámica y transfusional, medidas de descompresión si procede (p. ej., stent ureteral) y, cuando existe hemorragia extensa o duda sobre malignidad, exploración quirúrgica/nephrectomía. La histología es esencial para descartar cáncer renal, que tiene mayor incidencia en ACKD.\n- Resultado favorable en este caso: resolución del sangrado, lesión papilar benigna en anatomía patológica y recuperación sin recurrencia de hemorragia.\n\nComentario empático\nLa paciente presentó un evento agudo grave que exigió intervenciones rápidas y finalmente una nefrectomía. Aunque la situación fue seria, la atención multidisciplinaria permitió controlar la hemorragia, confirmar el diagnóstico y lograr una buena recuperación. Este caso resalta la importancia de la vigilancia en pacientes en diálisis con quistes renales y la necesidad de considerar complicaciones hemorrágicas después de procedimientos endoscópicos, aun cuando la relación causal no esté confirmada.",
+                "fh_score": 33.73
+            }
+        }
+    },
+    {
+        "article": "Se evaluó a una mujer de 30 años de edad con antecedentes de dos meses de dolor progresivo y disminución de la visión OD. Dos semanas antes del desarrollo de los síntomas oculares, la paciente comenzó a disminuir la prednisona como tratamiento para sus síntomas inflamatorios sistémicos. Los antecedentes médicos incluyen artritis inflamatoria, síntomas gastrointestinales que sugieren enfermedad intestinal inflamatoria y pérdida de peso de 20 libras antes de la presentación. Los detalles completos del caso de la paciente se informaron previamente y se resumen aquí junto con análisis adicionales de quimiocina y citoquina de fluido ocular.13\n\nEn el examen, las BCVAs fueron 20/40 OD y 20/20 OS, y las pupilas fueron 9 mm y akinéticas OD y 5 mm con una rápida reactividad a la luz OS. Las presiones intraoculares fueron 65 mmHg OD y 21 mmHg OS. El examen con lámpara de hendidura mostró precipitados queráticos granulomatosos pigmentados (KP) dentro de la córnea inferior, 3+ células de la cámara anterior, atrofia difusa del iris con pigmento en las zónulas, y ectropion uvea OD, y OS fue normal. La gonioscopia mostró 3+ células pigmentadas dentro del ángulo inferior OD. El examen del fondo fue normal en ambos ojos. Una paracentesis anterior diagnóstica fue positiva para ADN de VZV mediante pruebas de PCR, y las pruebas serológicas fueron positivas para anticuerpos IgG de VZV. Posteriormente, se le diagnosticó uveítis anterior hipertensiva asociada a VZV, lo que provocó el inicio de acetazolamida oral y timolol oftálmico, dorzolamida, y brimonidina para la hipertensión ocular, así como valaciclovir 1 g TID y acetato de prednisolona 1% cada 2 horas. El curso de la enfermedad de la paciente y otros detalles de su tratamiento se describieron previamente.13\n\nLa paciente fue diagnosticada con un accidente cerebrovascular (ACV), que se cree que se debe a una vasculopatía del SNC asociada al VVZ, y fue hospitalizada durante 2 semanas, durante las cuales sus síntomas oculares mejoraron gradualmente. Sin embargo, dos meses después de su ACV, desarrolló un empeoramiento del dolor y la visión en el ojo derecho, y su BCVA disminuyó a 20/100 con una PIO elevada de 39 mmHg OD. El examen reveló una inyección ciliar 1+ y 3+ células de la cámara anterior, y se cambió de prednisolona a difluprednato con una mejora mínima. Posteriormente, se sometió a un procedimiento de filtración de glaucoma con una derivación de Ahmed debido a su PIO elevada persistente a pesar de la máxima tolerancia de la terapia ocular hipertensiva. Se obtuvo una muestra de humor acuoso del ojo derecho durante la cirugía de filtración para un análisis de perfil de quimiocina/citoquina. Se estimaron los niveles de 22 citoquinas y quimioquinas, incluidos IFN-Y, IL-10, IL-12p70, IL-17A, IL-1B, IL-2, IL-5, IL-6, IL-8, TNF-a, IL-18, IL-1RA, IL-1a, IL-1a, IP-10, MCP-1, MIP-1a, MIP-1B, SDF-1a, IL-21, IL-22, IL-23 e IL-27, utilizando la técnica de inmunoensayo de perlas múltiplex. Se detectaron niveles de concentración de 7 citoquinas/quimioquinas, incluidos IL-6, IL-8, IL-18, MIP-1b, IP-10, MCP-1, e IL-1RA. La IL-1RA fue la citoquina más abundante (1000 pg/mL), mientras que IP-10 y MCP-1 fueron las segundas citoquinas más abundantes (150–200 pg/mL). Se detectaron niveles de 10–20 pg/mL de IL-18 y MCP-1b, pero a niveles mínimos en esta muestra de AqH. Se detectaron niveles de IL-6 e IL-8, pero se encontró que eran las citoquinas menos abundantes, cada una con niveles de <10 pg/mL.\n\n",
+        "gold_summary": "El caso 2 fue el de una mujer de 30 años con antecedentes de dos meses de dolor progresivo y disminución de la visión en el ojo derecho. Se le diagnosticó uveítis anterior hipertensiva tras una paracentesis diagnóstica de la cámara anterior. A pesar de la terapia exitosa para la uveítis anterior, su presión intraocular se mantuvo elevada y requirió un procedimiento de filtración de glaucoma. Se recolectó una muestra de fluido ocular en el momento de la cirugía para el análisis de perfiles de citoquinas/quimioquinas, y se detectaron niveles de 7 citoquinas/quimioquinas, entre ellas, IL-6, IL-8, IL-18, MIP-1B, IP-10, MCP-1 e IL-1RA, siendo IL-1RA la citoquina más abundante.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "This is a simple and kind summary of the case.\n\nA 30-year-old woman had two months of pain and worse sight in her right eye. She also had body inflammation and had been lowering her steroid medicine. Doctors found her right eye was very inflamed and the eye pressure was very high. A special test found varicella zoster virus (the chickenpox/shingles virus) in the front part of her eye. This caused “anterior hypertensive uveitis,” which means the front of the eye was inflamed and the eye pressure went up.\n\nShe was given medicine for the virus, eye drops, and steroid drops. Later she had a stroke that doctors thought was linked to the same virus. Her eye got a little better, but the eye pressure stayed high. Because the pressure would not fall with medicines, she had glaucoma surgery (an Ahmed valve) to help drain fluid and lower the pressure.\n\nDuring the surgery, doctors took a tiny sample of eye fluid to study inflammation signals called cytokines and chemokines. They tested for 22 different signals and found 7 of them. The most common signal was IL-1RA (about 1000 units). Two others (IP-10 and MCP-1) were next highest (about 150–200). Several others were present at low amounts.\n\nWhat this means: the virus caused inflammation in the eye and high pressure. The surgery was needed because medicines could not control the pressure. The fluid test helped doctors see which inflammation signals were active in her eye.",
+                "fh_score": 98.19
+            },
+            "B2": {
+                "text": "Here is a clear summary of the case in plain, caring language.\n\nA 30-year-old woman had two months of increasing pain and worsening vision in her right eye. She also had a history of inflammatory arthritis, gut symptoms that suggested inflammatory bowel disease, and recent weight loss. Two weeks before her eye problems began she had reduced the dose of prednisone, a steroid she had been taking for inflammation.\n\nOn exam her right vision was worse than the left and her right pupil was large and not reacting to light. The pressure inside her right eye was very high (65 mmHg; normal is under about 21 mmHg). The front part of the eye showed signs of inflammation: pigmented deposits on the cornea, many inflammatory cells in the front chamber, and damage to the iris. A small sample of fluid from the front of the eye (an anterior chamber paracentesis) tested positive by PCR for varicella zoster virus (VZV), the virus that causes chickenpox and shingles. This led to a diagnosis of VZV-associated hypertensive anterior uveitis. (“Uveitis” means inflammation inside the eye; “hypertensive” here means it caused high eye pressure.)\n\nShe was treated with antiviral medication (valacyclovir), topical and oral medicines to lower eye pressure, and steroid eye drops to reduce inflammation. While hospitalized later with a stroke believed to be caused by VZV affecting blood vessels in the brain, her eye symptoms improved. But two months after the stroke she had a flare: increased pain, worse vision in the right eye (20/100), and a high pressure of 39 mmHg despite strong medical therapy. Steroid drops were switched with little benefit, so she underwent glaucoma filtration surgery with an Ahmed drainage valve to control the pressure.\n\nAt the time of surgery a sample of the eye fluid was tested for immune signaling proteins called cytokines and chemokines. These small proteins help the immune system communicate during inflammation. Of 22 tested, seven were detected: IL-6, IL-8, IL-18, MIP-1β, IP-10, MCP-1, and IL-1RA. The most abundant was IL-1RA (about 1,000 pg/mL), a natural blocker that can reduce inflammation. IP-10 and MCP-1 were present at moderate levels (around 150–200 pg/mL). IL-18 and MIP-1β were low (about 10–20 pg/mL), and IL-6 and IL-8 were very low (<10 pg/mL).\n\nIn short: this patient had VZV-related inflammation inside the eye that led to very high eye pressure and eventually required surgical drainage. Testing of her eye fluid showed a mix of immune signals, with IL-1RA notably high, which may reflect the eye’s attempt to limit inflammation. Continued antiviral treatment and pressure control were key parts of her care.",
+                "fh_score": 86.75
+            },
+            "B3": {
+                "text": "Resumen (nivel B3)\n\nPresentación y antecedentes\n- Mujer de 30 años con dos meses de dolor progresivo y pérdida de visión en el ojo derecho (OD). Dos semanas antes de los síntomas oculares había reducido la prednisona que tomaba por cuadros inflamatorios sistémicos (artritis, síntomas gastrointestinales y pérdida de peso).\n- Importante antecedente: evolución posterior complicada por un accidente cerebrovascular (ACV), atribuido a vasculopatía del sistema nervioso central asociada a varicela zóster (VVZ).\n\nHallazgos clínicos clave\n- Agudeza visual mejor corregida: 20/40 OD (ojo afectado) y 20/20 OS (ojo izquierdo).\n- Pupila derecha dilatada (9 mm) y acinética; pupil izquierda con reacción rápida.\n- Presiones intraoculares: 65 mmHg OD (muy alta; normal ≈ 10–21 mmHg) y 21 mmHg OS.\n- Examen con lámpara de hendidura en OD: precipitados queráticos granulomatosos pigmentados, 3+ células en cámara anterior (inflamación activa), atrofia difusa del iris con pigmento en zónulas y ectropion uvea. Gonioscopia: células pigmentadas en el ángulo. Fondo de ojo normal en ambos.\n- Prueba diagnóstica en humor acuoso positiva por PCR para ADN de VVZ; serología positiva para IgG de VVZ.\n\nDiagnóstico y tratamiento\n- Diagnóstico: uveítis anterior hipertensiva secundaria a infección por VVZ, con hipertonía ocular persistente a pesar de terapia médica máxima.\n- Tratamiento inicial: antivírico oral (valaciclovir 1 g tres veces al día), corticoides tópicos (acetato de prednisolona 1% cada 2 horas, luego cambio a difluprednato), y múltiples fármacos para reducir la presión intraocular (acetazolamida oral; timolol, dorzolamida y brimonidina tópicas).\n- Debido a la presión intraocular refractaria (persistió elevada tras tratamiento), se realizó cirugía filtrante con implante de válvula de Ahmed. Durante la cirugía se obtuvo humor acuoso para análisis de citoquinas/quimioquinas.\n\nAnálisis de citoquinas/quimioquinas en humor acuoso\n- Se midieron 22 mediadores; se detectaron 7: IL-1RA, IP-10 (CXCL10), MCP-1 (CCL2), IL-18, MIP-1β, IL-6 e IL-8.\n- Concentraciones observadas (aprox.):\n  - IL-1RA: la más alta, ~1000 pg/mL.\n  - IP-10 y MCP-1: segundas más abundantes, ~150–200 pg/mL.\n  - IL-18 y MIP-1β: ~10–20 pg/mL (niveles bajos).\n  - IL-6 e IL-8: <10 pg/mL (las menos abundantes en esta muestra).\n- Interpretación preliminar: el alto nivel de IL-1RA (antagonista de la señalización proinflamatoria de IL-1) sugiere una fuerte respuesta antiinflamatoria compensatoria en el ojo. IP-10 y MCP-1 son quimioquinas relacionadas con reclutamiento de linfocitos T y monocitos, consistentes con una respuesta inmune dirigida frente a infección viral. Niveles bajos de IL-6/IL-8 son llamativos y pueden reflejar la fase de la enfermedad, efecto del tratamiento o particularidades de la respuesta inmune local en VVZ.\n\nImplicaciones y pasos a seguir\n- Clínicamente, la paciente necesitó cirugía por glaucoma secundario a uveítis por VVZ; el ACV atribuido a vasculopatía por VVZ subraya la naturaleza sistémica y potencialmente grave de la infección.\n- El perfil de citoquinas aporta información sobre la inflamación intraocular: la elevada IL-1RA podría indicar control parcial de la inflamación, mientras que IP-10 y MCP-1 respaldan la participación de respuestas celulares frente al virus.\n- Recomendaciones prácticas: seguimiento estrecho de la presión intraocular y de la función visual, mantenimiento/ajuste del tratamiento antiviral según evolución, control neurológico por riesgo de recurrencia de vasculopatía por VVZ, y considerar investigación adicional (serie de pacientes) para correlacionar perfiles de citoquinas con pronóstico y respuesta terapéutica.\n\nComentario empático\n- Este caso muestra cómo una infección por VVZ ocular puede provocar inflamación intensa, glaucoma secundario y complicaciones sistémicas graves. Es comprensible que la situación haya sido angustiante; el manejo incluyó terapia antiviral, antiinflamatoria y cirugía para proteger la visión, y los hallazgos de laboratorio ayudan a entender la respuesta inmunitaria local.",
+                "fh_score": 48.31
+            }
+        }
+    },
+    {
+        "article": "Un varón negro de 2021 g de peso nació a las 35 semanas y tres días de edad gestacional estimada por repetición de cesárea debido a la preocupación por la disminución del movimiento fetal en el contexto de una puntuación de perfil biofísico baja (basada en el tono muscular, la frecuencia cardíaca, el movimiento, la respiración y el volumen de líquido amniótico). La historia materna fue notable por el rasgo de células falciformes, la edad materna avanzada y la obesidad. La historia del embarazo fue notable por oligohidramnios observados por ultrasonografía a las 31 semanas. La ecografía fetal también mostró distensión de la vejiga, hidroceles bilaterales, dilatación de la uretra y ascitis abdominal preocupantes por la obstrucción del tracto urinario inferior y la posible ruptura de la vejiga. La ruptura de membranas ocurrió al momento del parto.\n\nAl nacer, el bebé experimentó dificultad respiratoria y fue tratado con ventilación con presión positiva, oxígeno suplementario e intubación. Las puntuaciones de Apgar fueron de dos y siete a un minuto y cinco minutos de vida, respectivamente. El examen mostró hematomas sustanciales y oscurecimiento de la extremidad superior izquierda. El bebé fue trasladado a la unidad de cuidados intensivos neonatales para el tratamiento de la dificultad respiratoria y sospecha de obstrucción del tracto urinario inferior. En la evaluación realizada dentro de la hora posterior al nacimiento por especialistas en ortopedia y cirugía plástica, el tercio distal del antebrazo y la mano estaban cianóticos, y una gran ampolla y área circundante de descamación eran evidentes en el dorso de la mano. No se observó movimiento espontáneo de la extremidad superior izquierda, y no se provocó la retirada o respuesta a los estímulos. La ecografía Doppler mostró flujo arterial al nivel de la fosa antecubital, pero no se detectaron pulsos radiales o cubitales. Los hallazgos del examen físico fueron consistentes con NCS, probablemente debido a la compresión de la pared uterina debido a oligohidramnios durante el embarazo.\n\nDespués de aproximadamente 5 horas de exámenes en serie, así como una amplia discusión con los equipos de ortopedia, cirugía plástica, neonatología y anestesia pediátrica, así como con los padres del bebé, se tomó la decisión de realizar una fasciotomía descompresiva del antebrazo, la mano y el túnel carpiano para permitir el rescate de la extremidad. La fasciotomía se realizó aproximadamente 6 horas después del nacimiento. El bebé fue monitoreado de cerca durante los siguientes días. La apariencia de la extremidad superior izquierda mejoró gradualmente. Al tercer día de vida, el antebrazo y la mano habían mejorado notablemente en color y parecían bien vascularizados. Las señales Doppler estaban presentes en todo momento, desde la arteria braquial hasta cada dedo. Se permitió que las heridas de la fasciotomía se curaran por intención secundaria, y se aplicó una férula personalizada con la muñeca en posición neutra y los dedos extendidos. No hubo signos de infección o isquemia en curso. Las heridas se curaron bien a las seis semanas de edad. En la visita de seguimiento a los cuatro meses de edad, las heridas se curaron por completo. El paciente tenía un rango de movimiento pasivo completo de la muñeca y los dedos. Se observó que tenía una ligera flexión y extensión del dedo anular y meñique, pero por lo demás, un movimiento activo mínimo de la muñeca o la mano en este momento. Tenía un movimiento activo del hombro y el codo. El paciente continuará recibiendo terapia ocupacional, así como férulas y masaje de cicatrices para prevenir/minimizar las contracturas. Los equipos multidisciplinarios continuarán siguiendo su progreso y recuperación de cerca.\n",
+        "gold_summary": "Presentamos un caso de NCS diagnosticado y tratado en base a los hallazgos del examen físico. La ecografía fetal mostró distensión de la vejiga, hidroceles bilaterales, dilatación de la uretra y ascitis abdominal que preocupaban por la obstrucción del tracto urinario inferior y posible ruptura de la vejiga. Una hora después del nacimiento, el examen de la extremidad superior izquierda del lactante no mostró movimiento espontáneo, la mano y el antebrazo parecían oscuros y la mano tenía una gran ampolla con descamación. No se detectó pulso distal a la fosa antecubital mediante ecografía Doppler. Se diagnosticó al lactante con NCS y se le practicó una fasciotomía urgente. La apariencia clínica y la perfusión de la extremidad superior izquierda mejoraron gradualmente. A los cuatro meses de edad, las heridas se habían curado y el paciente tenía un rango de movimiento pasivo completo de la extremidad superior izquierda. La recuperación del movimiento activo está en curso.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un bebé nació un poco antes de tiempo. Antes de nacer, las ecografías mostraron poco líquido alrededor del bebé y problemas en su barriga. Los médicos pensaron que eso pudo haber apretado al bebé dentro de la mamá.\n\nAl nacer, la mano y el antebrazo izquierdos del bebé estaban muy oscuros. No se movían. Los médicos creyeron que había mucha presión dentro del brazo. Esto puede dañar músculos y nervios. A eso se le llama síndrome compartimental neonatal. Para salvar el brazo, le hicieron una operación urgente llamada fasciotomía. En esa operación se cortan unas capas muy apretadas para que la sangre pueda volver a pasar.\n\nDespués de la operación, el brazo mejoró poco a poco. En los primeros días el color y la circulación mejoraron. Las heridas sanaron bien en unas semanas. A los cuatro meses, las cicatrices estaban cerradas y el brazo podía moverse pasivamente (otra persona podía moverlo) completamente. El bebé ya movía un poco algunos dedos, pero todavía tenía poco movimiento por sí mismo en la mano y la muñeca. \n\nLos médicos y terapeutas seguirán cuidando al bebé. Hará terapia de manos y usará férulas para ayudar su recuperación. Los doctores esperan que siga mejorando con tiempo y tratamiento.",
+                "fh_score": 72.68
+            },
+            "B2": {
+                "text": "Presentamos el caso de un recién nacido que desarrolló un problema serio en el brazo izquierdo debido a presión prolongada dentro del útero. La madre tenía un embarazo con pocas semanas de gestación restantes y se había observado oligohidramnios (poco líquido amniótico). En una ecografía prenatal se vio la vejiga muy distendida, hidroceles en ambos lados (acumulación de líquido en el escroto), dilatación de la uretra y ascitis (líquido en el abdomen), hallazgos que hacían sospechar una obstrucción del aparato urinario fetal y posible ruptura de la vejiga. Por disminución del movimiento fetal y una prueba llamada perfil biofísico baja, se decidió realizar una cesárea.\n\nAl nacer, el bebé necesitó ayuda para respirar y mostró un brazo izquierdo muy pálido/azulado, sin movimiento espontáneo, con una ampolla grande en la mano. Un examen con Doppler (una ecografía que mide el flujo sanguíneo) mostró flujo en la parte superior del brazo pero no en las arterias del antebrazo y la mano. Los especialistas concluyeron que el bebé tenía un síndrome compartimental neonatal (NCS). Esto significa que la presión dentro del antebrazo era tan alta que comprimía los vasos sanguíneos y los nervios, poniendo en riesgo la viabilidad de la extremidad.\n\nPara salvar el brazo se realizó una fasciotomía de emergencia unas seis horas después del nacimiento. La fasciotomía es una operación en la que se abre la fascia (la cubierta de los músculos) para aliviar la presión y restablecer la circulación. Tras la cirugía la apariencia y la perfusión (flujo sanguíneo) del brazo mejoraron de forma gradual; los registros por Doppler mostraron flujo hasta los dedos. Las heridas se dejaron curar poco a poco (por segunda intención) y se colocó una férula para mantener la mano en buena posición.\n\nA las seis semanas las heridas estaban bien curadas y, a los cuatro meses, la piel estaba completamente cicatrizada. El bebé tenía movilidad pasiva completa de la muñeca y los dedos (puede moverse con ayuda), y movimiento activo en el hombro y el codo. Por ahora muestra poco movimiento activo de la muñeca y la mano, salvo una ligera función de dos dedos; esto puede mejorar con el tiempo. El plan es continuar con terapia ocupacional, usar férulas y masajes en la cicatriz para prevenir contracturas, y que el equipo multidisciplinario siga de cerca su recuperación.\n\nEste caso muestra la importancia de reconocer y tratar rápidamente el síndrome compartimental en recién nacidos: una intervención temprana puede ayudar a salvar la extremidad y mejorar el resultado funcional.",
+                "fh_score": 55.19
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel lector universitario)\n\nAntecedentes y presentación\n- Recién nacido masculino, 35+3 semanas, peso 2 021 g. Cesárea repetida por disminución del movimiento fetal y perfil biofísico bajo.\n- Embarazo complicado por oligohidramnios (ecografía a 31 semanas) y hallazgos fetales sugestivos de obstrucción del tracto urinario inferior (vejiga distendida, hidrocéles bilaterales, dilatación de la uretra y ascitis), con posible ruptura vesical.\n- Madre con rasgo falciforme, edad materna avanzada y obesidad.\n\nEvento al nacimiento\n- Dificultad respiratoria al nacer: precisó ventilación a presión positiva, oxígeno e intubación. Apgar 2 y 7 al minuto y a los cinco minutos.\n- Desde la primera hora de vida, la extremidad superior izquierda era cianótica en su tercio distal; existía una gran ampolla dorsal con descamación, sin movimiento espontáneo ni respuesta a estímulos. No se palparon pulsos radiales ni cubitales; Doppler mostró flujo arterial a nivel de la fosa antecubital pero ausencia de señales distales.\n- Diagnóstico clínico: síndrome compartimental neonatal (NCS), probablemente secundario a compresión intrauterina asociada a oligohidramnios.\n\nTratamiento\n- Tras evaluación multidisciplinaria (ortopedia, cirugía plástica, neonatología, anestesia) y discusión con la familia, se realizó fasciotomía descompresiva del antebrazo, mano y túnel carpiano aproximadamente 6 horas tras el nacimiento para intentar salvar la extremidad.\n- Las heridas se dejaron cerrar por intención secundaria y se colocó una férula personalizada con muñeca neutra y dedos extendidos.\n\nEvolución y resultados\n- Mejoría progresiva de la perfusión y del color de la extremidad en los días siguientes. En todo momento hubo señales Doppler desde la arteria braquial hasta cada dedo.\n- No hubo signos de infección ni isquemia continuada. Cicatrización buena a las 6 semanas.\n- A los 4 meses: heridas completamente cerradas; rango de movimiento pasivo completo en muñeca y dedos. Movilidad activa limitada en mano y muñeca (leve flexo-extensión del anular y meñique), con movimiento activo preservado en hombro y codo.\n\nPlan y consideraciones\n- Continuará terapia ocupacional, uso de férulas y masaje de cicatrices para reducir el riesgo de contracturas y favorecer la recuperación funcional.\n- Seguimiento multidisciplinario continuo para monitorizar la recuperación motora a largo plazo.\n- Nota clave: el NCS neonatal es una emergencia; el reconocimiento temprano y la fasciotomía descompresiva pueden restaurar la perfusión y salvar tejido, pero la recuperación motora puede ser parcial y requiere rehabilitación prolongada.",
+                "fh_score": 39.21
+            }
+        }
+    },
+    {
+        "article": "Una mujer de 38 años de edad fue admitida en la sala de cirugía en noviembre de 2022 con la principal queja de una hinchazón abdominal progresiva que se asoció con un dolor abdominal leve y una saciedad precoz durante cinco meses. No tenía síntomas sistémicos como pérdida de peso, estreñimiento, diarrea, deseo de alimentos salados, fatigabilidad fácil o dolor de cabeza.\nEn el examen, parecía estar bien alimentada, pero presentaba una gran distensión abdominal, un leve palidez, afebril y con un tinte de ictericia en la esclerótica.\nLa palpación abdominal reveló una gran masa intraabdominal, no dolorosa, que ocupaba todo el abdomen inferior y se extendía hacia el superior, sin signos de irritación peritoneal u organomegalia.\nLos análisis de sangre mostraron un recuento de glóbulos blancos (5,7 × 109/l), hemoglobina (9,8 g/dl), bilirrubina (103 mg/dl) con recuentos normales de plaquetas (393 × 109/l). Las enzimas hepáticas, AST (24,0 U/l), ALT (21,0 U/l), albúmina 42,7 g/l. Creatinina sérica (53 μmol/l) y ESR (80 mm/h). Todos los demás análisis de sangre fueron normales. Una ecografía abdominal reveló un complejo quiste abdominal, ambos riñones eran de tamaño normal y con una ecografía normal, el hígado parecía normal. La TC abdominal y pélvica de contraste, vistas axiales y coronales, demostraron un gran quiste suprarrenal de paredes delgadas (flechas azules) que medía aproximadamente 23,5 cm (AP) x 20,3 cm (T) x 32,2 cm (CC) con un volumen de 8 l. El gran quiste desplaza el riñón derecho (flechas rojas) inferomedial a través de la línea media y ejerce presión sobre el hígado, la vesícula biliar, el páncreas y los intestinos delgados. Se extiende hasta la fosa ilíaca derecha. Como había un tinte de esclerosis ictérica, pero la masa era separada del hígado, el páncreas, los conductos biliares y el riñón derecho. Dado el tamaño del quiste y sus efectos compresivos, se planificó una intervención quirúrgica. Se eligió un enfoque quirúrgico abierto.\n\nSe le practicó una laparotomía al paciente. Se le hizo una incisión abdominal en la línea media, bajo anestesia general, y tras abrir las capas de la pared abdominal, se identificó un enorme quiste retroperitoneal que ocupaba toda la cavidad abdominal.\n\nSe abrió el quiste para acceder al fluido que se aspiraba, como se demostró en la cistectomía que se realizó con éxito. Se aspiraron unos 8 l de fluido de color marrón de la masa. Se enviaron muestras de la pared quística y del fluido para su análisis histológico.\n\nLa paciente se recuperó sin incidentes y fue dada de alta el día 7 después de la operación. El seguimiento a los 6 y 12 meses no mostró recurrencia ni complicaciones. El examen citológico de la muestra informó la presencia de material amorfo, no hubo evidencia de malignidad. Los resultados histológicos indicaron que la pared quística contenía tejido suprarrenal sin atipia, había infiltración de la pared quística por células inflamatorias mononucleares. La superficie interna de la pared no estaba revestida por células específicas reconocibles. En cuanto a los hallazgos clínicos intraoperativos, donde el origen del quiste era incierto, los hallazgos fueron más sugerentes de un quiste gigante idiopático retroperitoneal.\n\n",
+        "gold_summary": "Una mujer de 38 años se presentó con distensión abdominal progresiva. Las imágenes revelaron un quiste retroperitoneal gigante. Debido a los recursos limitados, se realizó una laparotomía abierta y se extirpó completamente un quiste de 33 cm que contenía 8 l de líquido transparente. La histopatología confirmó un quiste retroperitoneal idiopático gigante.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una mujer de 38 años vino al hospital porque su barriga había crecido mucho y se sentía llena. Los médicos hicieron pruebas y encontraron un quiste grande. Un quiste es una bolsita llena de líquido. Este quiste estaba detrás de los órganos de la barriga y empujaba todo a su alrededor.\n\nLos médicos abrieron la barriga con una operación y sacaron el quiste. Del quiste salieron unos 8 litros de líquido. Mandaron partes del quiste y el líquido al laboratorio. Allí no vieron cáncer. El tejido parecía venir de una glándula cerca del riñón y había un poco de inflamación.\n\nLa mujer se recuperó bien. Salió del hospital al séptimo día. A los 6 y 12 meses no había vuelto a aparecer el quiste. Esto fue una buena noticia.",
+                "fh_score": 82.3
+            },
+            "B2": {
+                "text": "Resumen (nivel B2)\n\nUna mujer de 38 años consultó por una hinchazón abdominal progresiva durante cinco meses, con dolor leve y sensación de llenura temprana. En la exploración se observó gran distensión abdominal, ligera palidez y tinción amarilla de las escleróticas (ictericia). Los análisis mostraron una anemia leve y una velocidad de sedimentación elevada; las pruebas de función hepática estaban dentro de límites normales.\n\nLa ecografía y la tomografía computarizada revelaron un quiste grande en el espacio retroperitoneal (zona detrás de los órganos abdominales) que medía alrededor de 23–33 cm y contenía unos 8 litros de líquido, desplazando riñón, hígado y otros órganos. Por el tamaño y el efecto compresivo se decidió una cirugía abierta (laparotomía), se drenó y retiró el quiste por completo; se extrajeron aproximadamente 8 litros de líquido marrón y se enviaron muestras para análisis.\n\nLa paciente tuvo una recuperación sin complicaciones y recibió el alta al séptimo día; a los controles a los 6 y 12 meses no hubo recidiva. Los estudios de la pared quística mostraron tejido suprarrenal sin signos de malignidad y células inflamatorias; la citología del líquido no detectó tumor. En conjunto, los hallazgos fueron compatibles con un quiste retroperitoneal gigante idiopático (es decir, de causa desconocida).",
+                "fh_score": 44.6
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel universitario, lectura B3)\n\nPresentación\n- Paciente: mujer de 38 años.\n- Síntomas: distensión abdominal progresiva durante 5 meses, dolor abdominal leve y saciedad precoz. No refirió pérdida de peso ni otros síntomas sistémicos significativos.\n- Examen: gran distensión abdominal con una masa intraabdominal no dolorosa que ocupaba gran parte del abdomen; ligera palidez y tinción ictérica de la esclerótica. No hubo signos de irritación peritoneal.\n\nInvestigaciones\n- Analíticas: leucocitos dentro de rango, anemia moderada (Hb 9,8 g/dl), elevación marcada de bilirrubina (correlando con la ictericia) y velocidad de sedimentación elevada (ESR 80 mm/h). Función hepática (AST/ALT) y albúmina normales; creatinina normal.\n- Imagen: ecografía detectó un quiste abdominal complejo. La tomografía contrastada mostró un quiste retroperitoneal de pared delgada, muy grande (aprox. 23,5 × 20,3 × 32,2 cm; volumen estimado ≈ 8 L) que desplazaba el riñón derecho y comprimía hígado, vesícula, páncreas e intestino delgado. El quiste estaba separado de órganos sólidos y conductos biliares.\n\nTratamiento\n- Se realizó laparotomía media abierta (decisión influida por recursos limitados) y resección del quiste.\n- Durante la cirugía se aspiraron ≈ 8 L de líquido marrón desde el quiste y se completó la cistectomía.\n\nHallazgos anatomopatológicos\n- Citología del líquido: material amorfo, sin evidencia de malignidad.\n- Anatomía patológica de la pared quística: presencia de tejido suprarrenal sin atipia y infiltrado inflamatorio mononuclear; la superficie interna no mostró un revestimiento celular específico reconocible.\n- Dado que el origen exacto no pudo confirmarse intraoperatoriamente, los hallazgos se interpretaron como un quiste retroperitoneal gigante idiopático, con elementos sugestivos de origen suprarrenal pero sin signos de malignidad.\n\nEvolución y pronóstico\n- Recuperación postoperatoria sin complicaciones; alta al día 7.\n- Seguimiento a 6 y 12 meses sin recurrencia ni problemas detectados.\n- Prognosis favorable: resección completa y ausencia de malignidad sugieren bajo riesgo de recidiva, aunque se recomienda vigilancia clínica/imaginológica periódica.\n\nInterpretación y pasos a considerar\n- Este caso es un ejemplo de un quiste retroperitoneal gigante que, por su tamaño, produjo síntomas por efecto compresivo aunque sin evidencia de invasión maligna.\n- Hallazgos clave a vigilar: recuperación de la anemia, normalización de la bilirrubina y control imagenológico para descartar recurrencia.\n- En general, el tratamiento definitivo de quistes retroperitoneales sintomáticos es quirúrgico; la histología confirma la naturaleza benigna en este caso, por lo que no se precisó tratamiento oncológico adicional.\n\nNota empática: la paciente recibió atención quirúrgica oportuna y evolucionó bien; el pronóstico a medio plazo es bueno, pero las revisiones periódicas son razonables para asegurar que no haya recurrencia.",
+                "fh_score": 36.8
+            }
+        }
+    },
+    {
+        "article": "Un hombre de 71 años con diabetes y enfermedad de Chagas había perdido recientemente mucho peso (60 kg). La investigación clínica dio lugar a un diagnóstico de megaesófago asociado a una obstrucción significativa a nivel del cardias. Se realizó una dilatación esofágica con balón, recuperando con éxito el tránsito digestivo. Mientras tanto, durante la evaluación del riesgo quirúrgico, el paciente también presentó dolor torácico con el mínimo esfuerzo. La angiografía por tomografía computarizada coronaria realizada tres años antes mostró una enfermedad multivascular muy calcificada que afectaba a la arteria coronaria izquierda; en ese momento no se había realizado ninguna otra investigación. Esta vez, se lo derivó a nosotros para un cateterismo cardíaco.\nEl examen realizado el 16 de febrero de 2016 mostró: arteria coronaria derecha (RCA) con importante calcificación y una lesión del 50% en el tercio medio; arteria descendente posterior (PDA) y arteria posterolateral derecha (RPLA), con severa calcificación y lesiones del 80% y 70%, respectivamente; LM con 80% de lesiones calcificadas en el tercio distal; arteria descendente anterior izquierda (LAD) con significativa calcificación y 90% de lesión en el tercio medio; ramas diagonales (DG1 y DG2) con lesiones calcificadas del 70% y 80%, en el origen y en el tercio proximal, respectivamente; y arteria circunfleja izquierda (LCx) ocluida y calcificada, recibiendo colaterales grado II de múltiples orígenes. El volumen ventricular izquierdo y la contractilidad se conservaron.\n\nCon esta imagen angiográfica, una puntuación de riesgo de la Society of Thoracic Surgeons del 15,8 % para morbilidad o mortalidad, una puntuación EuroSCORE II del 4,67 %, y una debilidad significativa debido a una pérdida de peso importante y reciente, el equipo cardiaco decidió realizar una intervención coronaria percutánea (ICP) de la LM, LAD, DG1 y DG2 inicialmente y, en un segundo procedimiento después de 30 días, una ICP de las ramas de la RCA. En ambos procedimientos, también se indicó una RA debido a una calcificación significativa. No se abordaría la LCx, ya que angiográficamente el vaso no estaba tan gravemente afectado y también considerando la dificultad técnica de la recanalización, debido a la longitud del CTO y también a las paredes muy calcificadas (puntuación J-CTO 4). La LCx ya estaba recibiendo una circulación collateral de grado II.\nEl 19 de febrero de 2016, tras comenzar una terapia antiplaquetaria dual con aspirina y clopidogrel, el paciente se sometió a una angioplastia de la arteria descendente anterior, la arteria circunfleja y la arteria descendente derecha con una fresa de 1,5 mm, seguida de una predilatación con un balón de 3,0 mm x 20 mm a 14 atm y la implantación de stents liberadores de fármacos en la arteria descendente derecha y la arteria circunfleja, utilizando una técnica de mini-aplastamiento y un balón de contacto al final. Se realizó un balón de contacto en la bifurcación de la arteria descendente derecha/arteria circunfleja y, finalmente, se implantó el tercer stent liberador de fármacos desde el origen de la arteria descendente derecha para superponerse con el stent de la arteria descendente derecha. Se logró un éxito procedimental con un flujo TIMI de 3 y sin complicaciones clínicas o angiográficas.\nEl 22 de marzo de 2016, el paciente volvió para una PCI con un RotaWire PCI en el PDA y RPLA con una fresa de 1,5 mm, seguido por la implantación de dos DES de 2,75 mm x 20 mm y 2,75 mm x 16 mm a 12 atm en el PDA y RPLA, respectivamente, sin ninguna predilatación adicional. También observamos la presencia de una disección larga y severa en el tercio medio del RCA, sin duda causada por un manejo excesivo e intentos de remover la fresa, lo que causó una penetración profunda por el catéter guía 7F. Esta disección se corrigió rápidamente con la implantación de un tercer DES de 4,0 mm x 32 mm, y se obtuvo un flujo TIMI 3 final sin complicaciones clínicas o electrocardiográficas. Los dos sitios de punción femoral se ocluyeron con dispositivos AngioSeal 8F y 6F, respectivamente. El paciente permaneció en la unidad de cuidados intensivos durante 48 horas, la única anormalidad fue la elevación de CK-MB (el doble del valor de referencia). Fue dado de alta el día 3 en excelentes condiciones generales. El ecocardiograma de control mostró una contractilidad ventricular izquierda normal.\n",
+        "gold_summary": "Un hombre de 71 años con enfermedad de Chagas y angina estable en esfuerzo mínimo se sometió a una angiografía por tomografía computarizada y cineangiografía que reveló una enfermedad multivascular muy calcificada que afectaba a la arteria descendente anterior izquierda (LM). Debido al grado de calcificación, se decidió realizar una rotablation. La primera etapa de la intervención coronaria percutánea (ICP) con rotablation se realizó en la arteria descendente anterior izquierda (LM), la arteria descendente anterior izquierda y la segunda rama diagonal sin complicaciones. Casi 30 días después, volvió para una ICP de la arteria coronaria derecha (RCA). La estrategia propuesta fue la aterectomía rotativa en la arteria descendente anterior posterior (PDA) y la arteria posterolateral derecha (RPLA) con una fresa de 1,5 mm, seguida por la implantación de dos stents liberadores de fármacos (DES). A través del acceso a la arteria femoral derecha, la lesión de la RPLA se extirpó con éxito. Como no había signos de disección y se mantuvo el flujo TIMI 3, se reposicionó el RotaWire de 0,009″ para cruzar la lesión de la PDA y se realizó la extirpación de la lesión. Después de dos intentos, logramos cruzar la lesión con la fresa de 1,5 mm, sin embargo, se produjo el atrapamiento de la misma. El sistema se retiró hasta que el catéter guía penetró profundamente en la RCA, y se hicieron intentos para liberar el Rotablator moviéndolo hacia adelante y hacia atrás, pero la fresa ni siquiera giró. La arteria femoral contralateral se perforó y se insertó un catéter guía 6F JR, con el fin de mover un alambre guía y un pequeño globo de angioplastia tangencialmente a la fresa, pero sin éxito. Finalmente, avanzamos el alambre guía utilizando la técnica de «nudillo», aprovechando la torsión de la porción distal del alambre guía PT2, realizando una disección subintimal y reentrada, y pudimos cruzar fácilmente el globo, inflarlo y liberar la fresa atrapada. A través del sistema 6F, se implantaron dos DES programados y uno de rescate con éxito en la PDA, RPLA y RCA, obteniendo un flujo TIMI 3 final sin complicaciones.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un hombre de 71 años con enfermedad de Chagas y mucho adelgazamiento tenía dolor en el pecho con poco esfuerzo. Las pruebas mostraron que varias arterias del corazón estaban muy duras y estrechas por la calcificación. Los médicos decidieron abrirlas en dos veces usando una técnica especial.\n\nPrimero, le hicieron una angioplastia con rotablación. Rotablación es usar una pequeña fresa que quita el calcio de las arterias. Después pusieron stents, que son tubitos pequeños que mantienen la arteria abierta. Esta primera intervención salió bien. La sangre fluía bien y no hubo problemas.\n\nUnas cuatro semanas después volvieron a tratar otras arterias del lado derecho del corazón. En esa segunda intervención también usaron la fresa y pusieron más stents. Durante el procedimiento se formó una rasgadura en la arteria por el manejo de los instrumentos. Los médicos la arreglaron rápido poniendo un stent más grande. Al final la circulación quedó buena.\n\nEl paciente estuvo 48 horas en cuidados intensivos. Solo subió un poco una prueba de sangre del corazón. Fue dado de alta al tercer día en buen estado. El ecocardiograma mostró que su corazón latía y se movía normalmente.",
+                "fh_score": 73.6
+            },
+            "B2": {
+                "text": "Resumen claro y comprensible:\n\nUn hombre de 71 años con enfermedad de Chagas y pérdida de peso importante tuvo dolor en el pecho al mínimo esfuerzo. Un estudio de imagen y una arteriografía mostraron enfermedad coronaria muy calcificada en múltiples vasos (arterias que llevan sangre al corazón). Su función del ventrículo izquierdo (la principal cámara del corazón) estaba conservada, pero el riesgo de cirugía abierta era alto, así que el equipo decidió tratar las lesiones con intervenciones coronarias percutáneas (ICP) en dos etapas usando además rotablación (una técnica que usa una pequeña fresa giratoria para “lijar” la calcificación dentro de la arteria) y luego colocando stents liberadores de fármaco (pequeños tubos metálicos recubiertos que mantienen la arteria abierta y liberan medicamento para reducir la reestenosis).\n\nPrimera sesión (19 de febrero de 2016)\n- Se inició terapia antiplaquetaria dual (aspirina y clopidogrel) y se realizó rotablación con fresa de 1,5 mm y angioplastia con balón.  \n- Se implantaron varios stents liberadores de fármaco en las arterias tratadas usando técnicas especiales para bifurcaciones.  \n- El procedimiento fue exitoso con flujo sanguíneo final normal (TIMI 3) y sin complicaciones clínicas.\n\nSegunda sesión (22 de marzo de 2016)\n- Se usó de nuevo rotablación en la arteria descendente posterior (PDA) y la arteria posterolateral derecha (RPLA) y se colocaron dos stents DES en esas ramas.  \n- Durante el procedimiento apareció una disección larga y severa (una rotura o desgarro en la capa interna de la arteria), probablemente por manipulación excesiva al intentar retirar la fresa.  \n- La disección se trató rápidamente con la colocación de un stent de rescate más grande (4,0 mm x 32 mm), con buen resultado y flujo TIMI 3 final.\n\nCuidados posteriores y resultado\n- Los accesos femorales se cerraron con dispositivos hemostáticos. El paciente estuvo 48 horas en la unidad de cuidados intensivos; la única anomalía fue un aumento moderado de una enzima cardíaca (CK‑MB).  \n- Fue dado de alta al tercer día en buen estado general. El ecocardiograma de control mostró función ventricular izquierda normal.\n\nInterpretación y próxima etapa\n- En un corazón con mucha calcificación, la rotablación seguida de stent es una estrategia usada para facilitar la apertura de las arterias.  \n- Aunque hubo una complicación (disección), se manejó con éxito en la misma intervención. El resultado inmediato fue bueno, con recuperación rápida y función cardíaca preservada.  \n- El equipo decidió no intentar recanalizar una arteria circunfleja muy calcificada y crónicamente ocluida porque ya recibía circulación colateral y la intervención habría sido técnicamente muy difícil.\n\nEn resumen: el paciente de 71 años con enfermedad coronaria severa y muy calcificada fue tratado en dos procedimientos mediante rotablación y colocación de stents. A pesar de una complicación tratada con éxito, terminó con buen flujo coronario y fue dado de alta con función cardíaca normal.",
+                "fh_score": 47.73
+            },
+            "B3": {
+                "text": "Resumen (nivel universitario, lectura clara y empática)\n\nPaciente y contexto\n- Hombre de 71 años con diabetes y enfermedad de Chagas. Había sufrido una pérdida de peso importante y reciente (60 kg) y recibió tratamiento por megaesófago antes de la evaluación cardiológica.\n- Consultó por dolor torácico al mínimo esfuerzo. Tres años antes ya tenía una tomografía coronaria que mostraba enfermedad coronaria calcificada multivaso.\n\nHallazgos principales\n- Coronariografía (16 feb 2016): enfermedad coronaria multivaso muy calcificada:\n  - LM: lesión calcificada del 80% en tercio distal.\n  - LAD: lesión del 90% en tercio medio; DG1 y DG2 con lesiones calcificadas del 70–80%.\n  - RCA: lesión del 50% en tercio medio; PDA 80% y RPLA 70% (ambas muy calcificadas).\n  - LCx: ocluida y muy calcificada, con circulación colateral grado II desde otras arterias.\n- Función ventricular: volumen y contractilidad del ventrículo izquierdo conservados (es decir, función global preservada).\n\nRazonamiento terapéutico\n- El paciente tenía alto riesgo quirúrgico (STS 15,8% para morbimortalidad) y cierta fragilidad por la pérdida de peso; por ello el equipo eligió una estrategia percutánea y escalonada en dos tiempos, en lugar de cirugía cardíaca.\n- Debido a la calcificación severa, las intervenciones incluyeron aterectomía rotatoria (rotablación) antes de implantar stents liberadores de fármaco (DES).\n- No se intentó recanalizar la LCx porque era una oclusión crónica larga y muy calcificada (J‑CTO 4) y ya recibía colaterales; esto aumentaría notablemente la complejidad y el riesgo.\n\nProcedimientos y resultado\n1) Primera sesión (19 feb 2016)\n   - Se inició doble antiagregación (aspirina + clopidogrel).\n   - Rotablación con fresa 1,5 mm y predilatación con balón (3,0 × 20 mm a 14 atm).\n   - Implante de DES en arterias afectadas (incluida técnica de mini‑crush en bifurcación y balón de contacto final).\n   - Resultado: flujo TIMI 3, sin complicaciones clínicas ni angiográficas inmediatas.\n\n2) Segunda sesión (22 mar 2016)\n   - Rotablación en PDA y RPLA con fresa 1,5 mm; se implantaron dos DES (2,75 × 20 mm y 2,75 × 16 mm) sin predilatación adicional.\n   - Durante el procedimiento apareció una disección larga y severa en el tercio medio de la RCA, atribuida a manipulación excesiva y a la penetración profunda del catéter guía.\n   - La disección se trató rápidamente con un tercer DES (4,0 × 32 mm).\n   - Resultado final: flujo TIMI 3, sin complicaciones clínicas ni cambios electrocardiográficos relevantes.\n\nEvolución hospitalaria y controles\n- Hemostasia de los accesos femorales con AngioSeal (8F y 6F).\n- Permaneció 48 horas en UCI; la única alteración fue elevación moderada de CK‑MB (≈2 veces el valor de referencia).\n- Ecocardiograma de control mostró contractilidad ventricular izquierda normal.\n- Alta al tercer día en muy buenas condiciones generales.\n\nImplicaciones y pasos siguientes (interpretación)\n- Lo positivo: revascularización percutánea multivaso con rotablación fue técnicamente exitosa y dejó flujo coronario normal (TIMI 3) conservando la función ventricular; el paciente salió en buen estado.\n- Riesgos y elementos a vigilar: la calcificación extensa y la oclusión crónica de la LCx dejan una parte de la enfermedad sin tratamiento directo; la disección de la RCA durante la intervención muestra la complejidad y el riesgo procedimental en arterias muy calcificadas. La elevación de CK‑MB indica lesión miocárdica procedimental leve a moderada.\n- Seguimiento razonable: continuar doble antiagregación según indicación cardiológica, control clínico y electrocardiográfico, vigilancia de marcadores cardíacos si reaparecen síntomas, ecocardiograma de control y rehabilitación cardiaca. Si reaparecen síntomas anginosos o hay isquemia recurrente, valorar estrategias adicionales (reintervención percutánea en otros segmentos o reconsiderar cirugía en un equipo multidisciplinario, aunque el riesgo quirúrgico sigue siendo alto).\n\nComentario final (empatía)\nEste fue un caso complejo por la edad, la comorbilidad y la calcificación difusa de las arterias. El equipo adaptó la estrategia al riesgo del paciente y logró una revascularización percutánea eficaz con buena recuperación inicial; sin embargo, precisa seguimiento estrecho y manejo multidisciplinario.",
+                "fh_score": 46.61
+            }
+        }
+    },
+    {
+        "article": "Una paciente de 29 años se presentó al departamento de urología con dolor intermittent en el flanco derecho durante un año y sensación de ardor urinaria ocasional sin hematuria; su estado general era estable. La paciente no mostró signos de tos, fatiga, pérdida de peso, no había tenido cirugías previas, pero había estado expuesta frecuentemente a ovejas. A pesar de los exámenes de laboratorio normales, el examen de anticuerpos de equinococos arrojó un resultado positivo. El ultrasonido abdominal posterior reveló una lesión quística grande en el riñón derecho, que medía aproximadamente 63 mm con paredes gruesas y sin flujo de doppler significativo. La tomografía computarizada con contraste, tanto en vista transversal como coronal, reveló una masa quística con septos en el lado lateral del riñón derecho, que presentaba una pared gruesa y regular que se intensificaba con el contraste. Esta lesión se clasificó como categoría 4 de Bosniak, con imágenes de tomografía computarizada en vista coronal que mostraban la participación del sistema colector y el contacto con el hígado. Se sospechó de HC en base a las evaluaciones clínicas y radiológicas. Los hallazgos de la radiografía de tórax no fueron significativos, sin evidencia de quistes pulmonares. Después de un régimen de tres meses de albendazol 400 mg administrado dos veces al día, la paciente se sometió a una intervención quirúrgica. Se realizó un procedimiento abierto a través de una incisión subcostal derecha de Kocher, lo que resultó en una nefrectomía derecha y una resección hepática parcial debido a las adherencias. El espécimen, que pesaba 372 g y medía 13 × 8 × 6 cm, mostró un gran quiste blanco con paredes delgadas que contenían una membrana desprendida, que afectaba los cálices renales y la pelvis. El diagnóstico final fue HC del riñón acompañado de pielonefritis crónica. Los exámenes de laboratorio posteriores al procedimiento mostraron resultados normales, con una producción urinaria estable y signos vitales. El catéter urinario se retiró después de 24 horas debido a una producción urinaria adecuada (2 L). El drenaje renal se retiró después de 3 días, con volúmenes de drenaje de 200 ml, 100 ml y ninguno en días consecutivos. La paciente volvió a sus actividades normales sin complicaciones.\n",
+        "gold_summary": "Se diagnosticó a una mujer de 29 años con dolor intermitente en el flanco derecho y ardor urinario un quiste hidatídico (HC) de categoría 4 de Bosniak, tras dar positivo en anticuerpos de equinococo. Las imágenes confirmaron el diagnóstico, lo que derivó en un tratamiento de tres meses con albendazol, seguido de una nefrectomía derecha y una resección hepática parcial. El análisis histopatológico confirmó un HC y una pielonefritis crónica. La paciente se recuperó sin incidentes y volvió a sus actividades normales.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había una mujer de 29 años que tuvo dolor en el costado derecho y a veces ardor al orinar durante un año. Vivía cerca de ovejas. Esto es importante porque un parásito que vive en ovejas puede causar un quiste en los órganos.\n\nLas pruebas de sangre mostraron que su cuerpo había visto ese parásito. Las ecografías y la tomografía mostraron un quiste grande en el riñón derecho. Los médicos dijeron que era “Bosniak 4”, que quiere decir que el quiste parecía serio y necesitaba tratamiento.\n\nLa mujer tomó un medicamento llamado albendazol durante tres meses. Este medicamento ayuda a matar al parásito. Luego tuvo una operación. Le quitaron todo el riñón derecho y también sacaron una parte pequeña del hígado porque el quiste estaba pegado allí.\n\nEl examen del quiste confirmó que era un quiste hidatídico (un saco con una membrana causado por el parásito) y además había una infección crónica del riñón llamada pielonefritis. Después de la operación estuvo bien. No tuvo problemas, le quitaron los tubos y volvió a sus actividades normales.",
+                "fh_score": 68.99
+            },
+            "B2": {
+                "text": "Here is a clear, caring summary written for a high-school reader:\n\nA 29-year-old woman had on-and-off pain in her right side for about a year and sometimes felt a burning when she urinated. She had often been around sheep, which is important because certain parasites carried by sheep can infect people. Blood tests were otherwise normal, but a test for antibodies against the Echinococcus parasite (which causes hydatid disease) was positive.\n\nAn ultrasound and a contrast CT scan showed a large cystic mass (about 6.3 cm) in the right kidney with thick walls and internal divisions. Radiologists labeled it Bosniak category 4 — this means the cyst looked complex and suspicious on imaging, so surgery was recommended. No abnormal cysts were seen in the lungs.\n\nThe medical team gave the patient albendazole (an anti-parasite medicine) for three months before surgery. She then had an open operation through a right-sided Kocher incision. Because the kidney cyst was stuck to the nearby liver, the surgeons removed the whole right kidney (right nephrectomy) and part of the liver. The removed tissue contained a large white cyst with a detached inner membrane — a typical finding for a hydatid cyst.\n\nLab examination of the removed tissue confirmed a hydatid cyst (caused by Echinococcus) and chronic pyelonephritis (long-standing kidney inflammation/infection). After surgery her lab tests and urine output were good, tubes and drains were removed over the next few days, and she recovered without complications. She returned to normal activities.\n\nKey points to remember:\n- A hydatid cyst is a parasitic cyst that can form after contact with animals like sheep.  \n- Imaging sometimes makes these cysts look like dangerous kidney tumors, so surgery is often needed to be sure and to treat the problem.  \n- Pretreatment with albendazole helps reduce the risk of spreading the parasite during surgery.  \n\nIf you have questions about any term or step in the treatment, I can explain it in more detail.",
+                "fh_score": 85.08
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel universitario — lectura B3)\n\nPresentación\n- Mujer de 29 años con un año de dolor intermitente en el flanco derecho y episodios ocasionales de ardor al orinar. No presentó fiebre, tos, fatiga ni pérdida de peso, y no tenía antecedentes quirúrgicos relevantes.\n- Antecedente epidemiológico: exposición frecuente a ovejas, factor de riesgo para enfermedad por Echinococcus (hidatidosis).\n\nExploraciones y hallazgos\n- Laboratorio: resultados generales normales; no hubo hematuria.\n- Serología: anticuerpos contra Echinococcus positivos, lo que sugiere infección hidatídica.\n- Ecografía abdominal: lesión quística derecha grande (~63 mm) con paredes gruesas y sin flujo Doppler significativo.\n- Tomografía computarizada con contraste: quiste renal complejo con tabiques y pared gruesa que realzaba con contraste; se clasificó como Bosniak 4 (categoría que habitualmente sugiere una lesión quística con alto riesgo de malignidad). La imagen mostró además contacto con el hígado y compromiso del sistema colector renal.\n- Radiografía de tórax: sin signos de quistes pulmonares.\n\nImpresión diagnóstica antes de la cirugía\n- Sospecha de quiste hidatídico renal (HC) sobre la base de la serología, la imagen y los antecedentes; la lesión simulaba una lesión quística compleja (Bosniak 4), lo que motivó manejo quirúrgico por riesgo de enfermedad grave o malignidad.\n\nTratamiento\n- Terapia antiparasitaria preoperatoria: albendazol 400 mg, dos veces al día durante 3 meses.\n- Intervención quirúrgica abierta por incisión subcostal derecha (Kocher): se realizó nefrectomía derecha y resección hepática parcial debido a adherencias entre el quiste y el hígado.\n\nHallazgos anatomopatológicos y diagnóstico definitivo\n- Especimen: 372 g, 13 × 8 × 6 cm; gran quiste blanco con membrana desprendida, que afectaba cálices y pelvis renales.\n- Diagnóstico final: quiste hidatídico renal (HC) asociado a pielonefritis crónica (inflamación/infección crónica del parénquima renal).\n\nEvolución y alta\n- Postoperatorio sin complicaciones: parámetros hemodinámicos y laboratorios dentro de la normalidad, adecuada producción de orina (alrededor de 2 L) — catéter retirado a las 24 h; drenaje renal retirado a los 3 días.\n- La paciente se recuperó y retomó sus actividades habituales.\n\nComentarios e implicaciones\n- La hidatidosis renal es rara y puede imitar radiológicamente lesiones quísticas complejas (Bosniak 4), que suelen hacer pensar en cáncer renal; por ello la combinación de antecedentes epidemiológicos y serología fue clave para orientar el diagnóstico.\n- El tratamiento combinó terapia antiparasitaria preoperatoria y resección quirúrgica extensa, lo cual es apropiado para reducir riesgo de diseminación y tratar la lesión que comprometía la función renal.\n- Recomendaciones prácticas (no detalladas en el informe, pero usualmente indicadas): seguimiento clínico y por imagen para vigilar recidiva, control de la función hepática y renal, y considerar controles serológicos periódicos según protocolo local.\n\nEmpatía\n- La paciente recibió tratamiento dirigido y se recuperó sin complicaciones; el manejo multidisciplinario (urología, cirugía y tratamiento antiparasitario) contribuyó a este buen resultado.",
+                "fh_score": 33.29
+            }
+        }
+    },
+    {
+        "article": "Una paciente de 46 años de edad fue admitida en nuestro hospital debido a opresión en el pecho y falta de aire que había durado más de un mes. Su historial médico incluía una tiroidectomía parcial, y no tenía antecedentes de tabaquismo o consumo de alcohol. Fue tratada con medicamentos regulares (comprimidos de liberación prolongada de succinato de metoprolol, comprimidos de sacubitril valsartán sodio, espironolactona, comprimidos de dapagliflozina) para la IC, pero la respuesta fue pobre. Durante el examen físico, la paciente estaba consciente y bien orientada. Su frecuencia cardíaca era de 68 latidos por minuto, la presión arterial era de 150/98 mm Hg, la frecuencia respiratoria era de 20 latidos por minuto. No había signos de sangrado o ictericia en la piel o membranas mucosas, y no se observó distensión de la vena yugular. La glándula tiroides no estaba agrandada. Los sonidos respiratorios eran gruesos en ambos pulmones, con roncus húmedos presentes en las bases pulmonares. La frecuencia cardíaca era de 68 lpm con un ritmo regular. El abdomen era suave, sin sensibilidad o sensibilidad de rebote, y el hígado y el bazo no eran palpables por debajo de la caja torácica. El signo de reflujo hepatoyugular fue negativo, pero había edema en ambas extremidades inferiores.\n\nLa paciente fue hospitalizada y se le realizaron los exámenes pertinentes. Los análisis bioquímicos mostraron una hormona estimulante de la tiroides (TSH) de 7,190 uIU/mL, triglicéridos de 0,81 mmol/L, colesterol de lipoproteínas de baja densidad (LDL-C) de 2,61 mmol/L, lipoproteína (a) de suero de 435 mg/L y NT-proBNP de 6245 pg/mL. Un examen de electrocardiograma (ECG) mostró bradicardia sinusal, anomalías de la onda T-U y duración del QRS de 90 ms. Un examen ecocardiográfico transtorácico posterior reveló un diámetro de la aurícula izquierda (LA) (anteroposterior) de 41 mm, un diámetro del ventrículo izquierdo (LVD) (anteroposterior) de 54 mm, un espesor del tabique interventricular en diástole (IVSD) de 9 mm, un espesor de la pared posterior del ventrículo izquierdo en la fase final de la diástole (LVPWd) de 9 mm, una fracción de eyección del ventrículo izquierdo (LVEF) del 28% (M-mode), una fracción de acortamiento (FS) del 13% y una presión de la arteria pulmonar de 29 mm Hg. No se observaron lesiones coronarias significativas en la angiografía coronaria computarizada (CCA). Se diagnosticó a la paciente con cardiomiopatía dilatada, insuficiencia cardiaca de clase III con LVEF reducida según la New York Heart Association (NYHA). En combinación con los parámetros, se puede observar que los volúmenes de la aurícula izquierda y el ventrículo izquierdo se reducen gradualmente, lo que indica que la función diastólica del ventrículo izquierdo está mejorando. El tratamiento con CCM revierte la remodelación miocárdica. Además, E/e′ refleja la presión de llenado ventricular izquierdo. El valor normal debe ser inferior a 8. Se puede observar que en este caso, E/e′ vuelve al valor normal tres meses después de la implantación de CCM. Estos dos puntos reflejan el papel de CCM en la mejora de la función diastólica miocárdica en el tratamiento de la insuficiencia cardiaca. En resumen, la paciente tenía las siguientes características: (1) LVEF mejoró pero se mantuvo tan bajo como el 30% después de la terapia óptima para la insuficiencia cardiaca; (2) opresión en el pecho y malestar con ligera actividad, grado de función cardiaca III; (3) ECG muestra QRS estrecho. Teniendo en cuenta el resultado positivo de la prueba preoperatoria de levosimendan, después de una discusión general y una comunicación completa con el paciente y su familia, se decidió realizar el tratamiento con CCM.\n\nEl procedimiento de implantación del CCM fue similar al de la implantación de un marcapasos tradicional. El paciente se colocó en posición supina, se desinfectó con una toalla y se perforó la vena subclavia izquierda dos veces bajo anestesia local, y se hizo la bolsa capsular después de insertar el alambre guía. Bajo la guía del alambre guía, se introdujeron dos vainas de desprendimiento, y se introdujeron dos cables de estimulación ventricular (Medtronic 3830-69) a través de la vaina, y se ajustó la posición de los cables a la superficie del tabique ventricular derecho con una distancia de 3 cm. Durante la operación, se probó el electrodo de campo cercano (RV), que mostró un umbral de estimulación de 0,5 V, una amplitud de la onda R detectada mayor de 10 mV, y una impedancia del cable de 1080 Ω; el electrodo de campo lejano (LS) mostró un umbral de estimulación de 0,5 V, una amplitud de la onda R detectada mayor de 15 mV, y una impedancia del cable de 900 Ω. Estas mediciones cumplieron los criterios para una implantación exitosa del electrodo. Ambos cables se anclaron de forma segura en el tabique ventricular derecho. Después de asegurarse de que no había estimulación diafragmática palpable con un pulso de estimulación de 10 V y una anchura de pulso de 0,4 ms, se conectaron los cables al generador de impulsos Optimizer Smart. Posteriormente, se ajustaron los impulsos de salida y se programaron y optimizaron los parámetros.\n\nLa monitorización del ECG postoperatorio inmediato indicó un suministro normal de impulsos CCM (Figura 1C). Observamos la respuesta de los pacientes al CCM al adherirnos a un protocolo de seguimiento estandarizado. Utilizando una amplia variedad de herramientas de evaluación, que incluían ultrasonografía Doppler cardiaca a color, análisis de sangre NT-ProBNP, pruebas de caminata de seis minutos (6MW) y el Cuestionario de Minnesota para Vivir con Insuficiencia Cardiaca (MLHFQ), evaluamos sistemáticamente el estado clínico de los pacientes. El paciente no experimentó opresión en el pecho ni falta de aire, y hubo una marcada mejora en la tolerancia al ejercicio y la calidad de vida.\n",
+        "gold_summary": "Presentamos a una paciente de 46 años que fue admitida en nuestro hospital debido a opresión torácica y falta de aire que duró más de un mes. La ecocardiografía reveló un diámetro del ventrículo izquierdo (anteroposterior) de 54 mm, el electrocardiograma mostró bradicardia sinusal y duración del QRS de 90 ms. La paciente no experimentó opresión torácica o falta de aire, y hubo una marcada mejora en la tolerancia al ejercicio y calidad de vida después de la implantación de la modulación de la contractilidad cardiaca.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Esta es la historia de una mujer de 46 años que se sentía con el pecho apretado y le faltaba el aire por más de un mes. Los médicos vieron que su corazón estaba débil y no bombeaba bien. En una ecografía su corazón tenía una fracción de eyección baja (esto quiere decir que no soltaba suficiente sangre cada latido). No tenía vasos del corazón tapados.\n\nLe pusieron un aparato llamado CCM. Este aparato se pone como un marcapasos. Envía pequeñas señales al músculo del corazón para ayudarle a contraerse mejor. La operación fue bien y las pruebas durante la cirugía salieron normales.\n\nTras poner el aparato, la mujer empezó a sentirse mucho mejor. Ya no tenía la opresión en el pecho y podía hacer más ejercicio sin cansarse tanto. Las ecografías y otras pruebas mostraron que la función del corazón fue mejorando con el tiempo. En resumen: recibió un tratamiento con un dispositivo que ayudó a su corazón y mejoró su vida.",
+                "fh_score": 76.67
+            },
+            "B2": {
+                "text": "Resumen para lectores de nivel B2 (adolescentes):\n\nUna mujer de 46 años ingresó por más de un mes con sensación de opresión en el pecho y falta de aire. Tenía antecedente de tiroidectomía parcial y estaba recibiendo tratamiento médico estándar para insuficiencia cardiaca, pero no mejoró lo suficiente. Las pruebas mostraron: una fracción de eyección del ventrículo izquierdo (LVEF) muy baja (28%), marcadores de insuficiencia cardiaca elevados (NT‑proBNP 6245 pg/mL) y un electrocardiograma con bradicardia sinusal y un QRS estrecho (90 ms). La angiografía coronaria no mostró obstrucciones importantes, por lo que se diagnosticó miocardiopatía dilatada con insuficiencia cardiaca clase III (NYHA).\n\nTras una prueba positiva con levosimendan (un fármaco que ayuda a predecir la respuesta a terapias eléctricas), se decidió implantar un dispositivo de modulación de la contractilidad cardiaca (CCM). El implante es similar al de un marcapasos: se colocaron dos electrodos en el tabique del ventrículo derecho y se conectaron a un generador. Las mediciones durante la cirugía fueron adecuadas y no hubo estimulación del diafragma.\n\nEn el seguimiento, con ecocardiografías, análisis de sangre, la prueba de caminata de seis minutos y cuestionarios de calidad de vida, la paciente mostró mejoría clara: desapareció la opresión torácica y la disnea, mejoró la tolerancia al ejercicio y su calidad de vida. Además, indicadores ecocardiográficos de función diastólica (como E/e′) volvieron a valores normales a los tres meses, y los volúmenes del corazón disminuyeron, lo que sugiere una reversión favorable del remodelado cardiaco tras la terapia CCM. En conjunto, el tratamiento fue seguro y produjo una mejora clínica importante en esta paciente con insuficiencia cardiaca avanzada.",
+                "fh_score": 44.06
+            },
+            "B3": {
+                "text": "Resumen clínico conciso y comprensible\n\nCaso\n- Mujer de 46 años ingresada por opresión torácica y disnea persistentes >1 mes. Antecedente de tiroidectomía parcial; no fumadora ni consumidora de alcohol. Recibía tratamiento farmacológico óptimo para insuficiencia cardiaca (metoprolol de liberación prolongada, sacubitril/valsartán, espironolactona, dapagliflozina) pero con mala respuesta sintomática.\n\nExploración y pruebas iniciales (hallazgos relevantes)\n- Signos vitales: FC 68 lpm (normal), TA 150/98 mm Hg (elevada), FR 20 rpm (límite alto).\n- Examen: crepitantes y roncus húmedos en bases pulmonares; edema en ambas piernas; sin distensión yugular ni hepatomegalia.\n- Analítica: TSH 7,19 μIU/mL (elevada → sugiere hipotiroidismo subyacente), NT‑proBNP 6.245 pg/mL (muy elevado, indica fallo cardiaco), lipoproteína (a) 435 mg/L (elevada, factor de riesgo).\n- ECG: bradicardia sinusal, alteraciones de onda T‑U, QRS estrecho (90 ms).\n- Ecocardiograma: aurícula izquierda 41 mm, ventrículo izquierdo diástole 54 mm, fracción de eyección (LVEF) 28% (disfunción sistólica importante), acortamiento (FS) 13%, presión arterial pulmonar 29 mm Hg.\n- Angio‑TC coronaria: sin lesiones coronarias significativas.\n\nDiagnóstico\n- Miocardiopatía dilatada con insuficiencia cardiaca sistólica (HFrEF), clase funcional NYHA III (síntomas con actividad ligera).\n\nRazonamiento para la intervención\n- Persistencia de LVEF reducida (~30%) y síntomas limitantes a pesar de terapia médica óptima.\n- QRS estrecho contraindica o reduce la probabilidad de respuesta a resincronización (CRT).\n- Prueba preoperatoria con levosimendan fue positiva, lo que apoyó la probabilidad de respuesta a terapia eléctrica dirigida a mejorar la contractilidad.\n\nIntervención: implantación de modulación de la contractilidad cardiaca (CCM)\n- Procedimiento similar al de un marcapasos: vías de abordaje por vena subclavia izquierda, colocación de dos electrodos (Medtronic 3830‑69) fijados en el tabique ventricular derecho con 3 cm de separación, y conexión al generador Optimizer Smart.\n- Parámetros intraoperatorios: umbrales de estimulación bajos (0,5 V), buena detección de ondas R (>10–15 mV) e impedancias dentro de rango; ausencia de estimulación diafragmática con estimulación hasta 10 V.\n- Implantación técnica satisfactoria y entrega correcta de impulsos CCM en el ECG postoperatorio.\n\nEvolución y seguimiento\n- Evaluaciones seriadas incluyeron ecocardiografía Doppler, NT‑proBNP, prueba de caminata de 6 minutos y cuestionario MLHFQ.\n- A los 3 meses: reducción progresiva de volúmenes auricular y ventricular izquierdos y normalización del cociente E/e′ (marcador de presión de llenado diastólico), lo que indica mejora de la función diastólica; desaparición de opresión torácica y disnea; aumento de la tolerancia al ejercicio y mejora clara en calidad de vida.\n- No se describieron complicaciones agudas relacionadas con el implante.\n\nImplicaciones y próximos pasos recomendados\n- La CCM puede ser una opción útil en pacientes con HFrEF sintomática, LVEF moderadamente baja y QRS estrecho que no responden a terapia médica y no son candidatos claros para CRT.\n- Seguimiento a largo plazo: monitorizar función clínica, pruebas serológicas (NT‑proBNP), ecocardiografía y control del dispositivo (umbrales, detección, ausencia de estimulación diafragmática).\n- Tratar condiciones asociadas que pueden influir en el pronóstico: ajustar manejo tiroideo (TSH elevada), control de factores de riesgo lipídico (LDL y lipoproteína (a) elevada) y optimización farmacológica según guías.\n- Comunicación continua con la paciente sobre expectativas, señalización de síntomas de alarma y adherencia al seguimiento.\n\nConclusión\nEn esta paciente con miocardiopatía dilatada y LVEF severamente reducida, la implantación de CCM fue técnicamente exitosa y se asoció a mejoría objetiva de la función cardiaca (sistólica y diastólica) y a alivio sintomático significativo. Esto sugiere que la CCM puede revertir parcialmente la remodelación miocárdica y mejorar la calidad de vida en pacientes seleccionados con insuficiencia cardiaca refractaria a tratamiento médico.",
+                "fh_score": 37.73
+            }
+        }
+    },
+    {
+        "article": "Paciente de sexo femenino, 61 años, caucásica, casada, dos hijos, informó empeoramiento de los síntomas de la psoriasis tras el inicio de L-metilfolato 15 mg al día para tratamiento coadyuvante de la depresión. Informó depresión y psoriasis desde los 20 años. Desde los 41 años, la paciente no había tenido recidivas de las lesiones psoriáticas.\n\nPor su historial de depresiones, se le indicó carbonato de litio, pero no lo tomó debido a la psoriasis. En 2000, su cuadro depresivo mejoró con venlafaxina 225 mg al día. En 2016, debido a las oscilaciones de humor, se le agregó lamotrigina 100 mg al día y, para mejorar el sueño, se le sumó quetiapina 50 mg al día.\n\nEstas fueron las dosis actuales, con una mejora en la depresión, la calidad de vida y sin efectos adversos significativos.\n\nEn enero de 2019, se detectó polimorfismo en el gen MTHFR, con una mutación heterozigótica en C677T, y se le recetó a la paciente 15 mg diarios de L-metilfolato. Antes de que finalizara la primera semana de uso de L-metilfolato, aparecieron lesiones psoriáticas que no se habían manifestado en 20 años. Se informó lo ocurrido al psiquiatra, quien retiró la medicación y, 4 días después, las lesiones psoriáticas comenzaron a remitir, desapareciendo por completo al cabo de unas semanas. La paciente no volvió a registrar manifestaciones hasta principios de 2020.\n",
+        "gold_summary": "Paciente de sexo femenino, de 61 años, que había estado en remisión de psoriasis durante 20 años. Sufrió una recaída de psoriasis en forma de placa pocos días después de comenzar el tratamiento con L-metilfolato a una dosis diaria de 15 mg.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una mujer de 61 años tenía psoriasis y depresión desde joven. Durante 20 años no tuvo brotes de psoriasis. Tomaba medicinas para la depresión que le iban bien.\n\nLe hicieron una prueba y vieron un cambio en un gen llamado MTHFR. Eso puede cambiar cómo el cuerpo usa una vitamina llamada folato. Por eso le recetaron L‑metilfolato, que es una forma de esa vitamina, 15 mg al día.\n\nA los pocos días de tomarlo le volvieron las placas de psoriasis. Se lo contó al médico y dejaron de darle L‑metilfolato. Cuatro días después las manchas empezaron a mejorar y, en unas semanas, desaparecieron. No volvió a tener brotes hasta principios de 2020.\n\nParece que, en este caso, el L‑metilfolato pudo haber causado la recaída de la psoriasis.",
+                "fh_score": 80.32
+            },
+            "B2": {
+                "text": "Resumen breve y claro:\n\nUna mujer de 61 años, con antecedentes de depresión desde los 20 años y psoriasis (una enfermedad de la piel que causa placas rojas y escamosas), estuvo 20 años sin brotes de psoriasis. En enero de 2019, se le encontró una variante del gen MTHFR (que puede cambiar cómo el cuerpo usa el folato, una vitamina) y le recetaron L‑metilfolato 15 mg al día. L‑metilfolato es la forma activa del folato y a veces se añade para ayudar con la depresión.\n\nA menos de una semana de comenzar L‑metilfolato aparecieron de nuevo las lesiones de psoriasis. Su psiquiatra suspendió el medicamento y, cuatro días después, las lesiones empezaron a mejorar y desaparecieron por completo en pocas semanas. Antes de esto, su tratamiento con venlafaxina, lamotrigina y quetiapina estaba controlando bien la depresión sin efectos adversos importantes.\n\nEsto sugiere que el inicio de L‑metilfolato se asoció en el tiempo con la recaída de psoriasis, ya que las lesiones remitieron al retirar el fármaco. Un paso razonable en casos así es detener el medicamento sospechoso y vigilar la respuesta; también puede considerarse consultar con un dermatólogo y discutir alternativas para el tratamiento de la depresión.",
+                "fh_score": 55.84
+            },
+            "B3": {
+                "text": "Resumen clínico\n\nPaciente mujer de 61 años, con antecedentes de psoriasis desde los 20 años y en remisión completa durante aproximadamente 20 años (desde los 41). También presenta episodio(s) depresivo(s) crónico(s) controlados con medicación psiquiátrica estable: venlafaxina 225 mg/día, lamotrigina 100 mg/día y quetiapina 50 mg/día. Por motivos de tratamiento adyuvante de la depresión y tras detectarse un polimorfismo heterocigoto C677T en el gen MTHFR, se le prescribió L‑metilfolato 15 mg/día.\n\nDescripción del evento adverso\n- Normal previo: psoriasis en remisión durante 20 años; estado depresivo relativamente estable con la medicación actual y sin efectos adversos importantes.\n- Evento anómalo: a los pocos días (antes de finalizar la primera semana) de iniciar L‑metilfolato 15 mg/día, la paciente desarrolló lesiones psoriáticas en placa, reaparición que no había ocurrido en dos décadas.\n- Curso tras suspensión: el psiquiatra retiró L‑metilfolato; cuatro días después las lesiones comenzaron a remitir y desaparecieron por completo en unas semanas. La paciente no volvió a presentar manifestaciones cutáneas hasta principios de 2020.\n\nInterpretación y significado clínico\n- La temporalidad (inicio de la psoriasis pocos días después de comenzar L‑metilfolato) y la resolución tras la suspensión (dechallenge positivo) sugieren una relación probable entre L‑metilfolato 15 mg/día y la recaída psoriásica en esta paciente.\n- No se identificaron otros cambios en medicación o factores obvios que expliquen la reactivación, y las terapias psiquiátricas previas se toleraban bien.\n- Aunque no se puede probar causalidad definitiva con un solo caso, el patrón temporal hace razonable considerar el L‑metilfolato como el desencadenante más probable.\n\nRecomendaciones prácticas\n- Para pacientes con historia de psoriasis, especialmente de larga evolución, considerar con cautela el uso de altas dosis de L‑metilfolato y discutir el balance riesgo/beneficio.\n- Si se decide iniciar L‑metilfolato, recomendar seguimiento dermatológico estrecho y vigilancia temprana de cualquier signo cutáneo.\n- Ante reaparición de lesiones, suspender el fármaco y coordinar con dermatología y psiquiatría para alternativas antidepresivas seguras.\n- Notificar el evento adverso a los registros farmacovigilantes para mejorar la información sobre seguridad.\n\nComentario final\nEste caso subraya la importancia de revisar antecedentes dermatológicos antes de introducir suplementos o fármacos nuevos. La paciente tuvo resolución completa tras retirar L‑metilfolato, lo que permitió controlar la recaída; seguir un plan conjunto entre psiquiatría y dermatología ayudará a mantener tanto la salud mental como la cutánea de forma segura.",
+                "fh_score": 40.11
+            }
+        }
+    },
+    {
+        "article": "Se diagnosticó osteoartritis bilateral de las articulaciones de la cadera en un paciente de 61 años de edad con tratamiento con esteroides para la artritis reumatoide y dolencias en la ingle bilateral. [9] Recibió una inyección intraarticular bilateral de ácido hialurónico y se presentó doce semanas después en nuestro departamento de urgencias con fiebre, un estado general reducido y un dolor cada vez más incapacitante. Las radiografías de la pelvis mostraron una destrucción progresiva y rápida de ambas articulaciones de la cadera con una osteólisis extensa, subluxación concomitante y un defecto óseo acetabular del lado izquierdo. La aspiración de la articulación mostró pus en ambas articulaciones de la cadera y se hizo el diagnóstico de artritis séptica bilateral progresiva rápida. Se realizó una resección bilateral de ambas cabezas femorales con desbridamiento de la articulación de la cadera y la implantación de espaciadores de PMMA cargados con antibióticos a través de un enfoque anterolateral mínimamente invasivo.\n\nSe inició un tratamiento antibiótico sistémico empírico con vancomicina y ampicilina por vía intravenosa. Se detectó E. coli en muestras de tejido de ambas articulaciones de la cadera y se adaptó el tratamiento antibiótico sistémico a meropenem por vía intravenosa. Se realizaron dos procedimientos quirúrgicos de seguimiento con intercambio de los espaciadores de PMMA cargados con antibiótico para controlar la infección debido al drenaje persistente.\n\nDoce semanas después de la resección de la cabeza femoral y el control exitoso de la infección, el paciente recibió una artroplastia total de cadera con el uso adicional de un revestimiento multicapa de plata (HyProtect®, Bio-Gate, Nürnberg, Alemania). Este revestimiento consiste en una capa de siloxano ultrafina directamente sobre la superficie del implante (10 a 30 nm), de la que se liberan iones de plata.\n\n12 semanas después de la resección de la cabeza femoral, se realizó una artroplastia total de cadera en el lado derecho con una copa estándar sin cemento (Allofit®, ZimmerBiomet, Varsovia, EE. UU.) y un vástago femoral sin cemento (Avenir®, ZimmerBiomet, Varsovia, EE. UU.) a través del enfoque anterolateral mínimamente invasivo previamente utilizado con este revestimiento multicapa de plata ultrafino. Tanto la superficie posterior de la copa como todo el eje femoral se revistieron con plata.\n\nLa cadera izquierda se trató 18 semanas después de la resección de la cabeza femoral con una jaula de refuerzo recubierta de plata (Burch-Schneider®, ZimmerBiomet, Varsovia, EE. UU.) para un defecto acetabular tipo IIB de Paprosky y una copa de polietileno cementada (Durasul®, ZimmerBiomet, Varsovia, EE. UU.). El vástago femoral sin cemento (Avenir®, ZimmerBiomet, Varsovia, EE. UU.) también se recubrió de plata en toda su parte intramedular. Esta intervención también se realizó mediante el enfoque anterolateral mínimamente invasivo utilizado previamente. El paciente se sometió a una terapia antibiótica sistémica durante un período de tratamiento total de 18 semanas después de la implantación del lado derecho. Se aplicó ertapenem 1 g por vía intravenosa durante este período de tiempo una vez al día, después de la descarga en un entorno ambulatorio. Esto permitió una cobertura antibiótica del lado derecho de 18 semanas y del lado izquierdo de 12 semanas de tratamiento antibiótico.\n\nSe recomendó el uso parcial de peso con 20 kg en el lado operado y el uso de muletas durante 6 semanas después de las intervenciones.\n\nLas heridas de ambos lados se curaron sin incidentes. El paciente fue visto regularmente para un seguimiento clínico y radiológico. Se logró el apoyo total del peso sin el uso de muletas 7 semanas después de la operación en ambos lados. No hubo signos de PIJ y no fue necesaria una cirugía de revisión adicional.\n\nEn un seguimiento final tres años después de la implantación de las prótesis recubiertas de plata, la paciente mostró un aspecto normal de la piel con mínimas cicatrices después de enfoques antero-laterales mínimamente invasivos en ambos lados sin signos de argiria. Hubo un excelente resultado funcional de ambas caderas con marcha normal y una puntuación WOMAC de 6 en ambos lados (dolor: 0, rigidez: 0, función física: 6). El recuento de leucocitos en sangre fue de 7,29/nl (referencia: 4,23-9,1) y el nivel de proteína C reactiva (PCR) fue de 12,4 mg/l (referencia: <5 mg/l). El nivel ligeramente elevado de PCR es atribuible a la artritis reumatoide subyacente de la paciente. Las radiografías revelaron componentes protésicos de cadera bien integrados y no sueltos en ambos lados tres años después de la implantación con una articulación correcta.\n",
+        "gold_summary": "Este informe de caso se refiere a un paciente de 61 años con destrucción rápida de ambas articulaciones de la cadera debido a una artritis séptica que se trató con éxito con una implantación por etapas de prótesis de cadera recubiertas con plata con un recubrimiento ultrafino multicapa de plata. En un seguimiento de tres años, no hubo signos de infección, se observó un buen estado de todos los componentes protésicos y el resultado funcional fue excelente.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un paciente de 61 años tuvo una infección grave en las dos caderas. Antes tenía artritis y tomaba medicinas con esteroides. Después de una inyección en las caderas, se puso muy enfermo. Tenía fiebre y mucho dolor. Las radiografías mostraron que las caderas se estaban destruyendo. Al sacar líquido de las caderas, los médicos encontraron pus. Esto quería decir que había una infección con gusanos (gérmenes).\n\nPrimero le quitaron las partes dañadas del hueso y limpiaron las caderas. Pusieron piezas temporales con antibiótico para combatir los gérmenes. Le dieron antibióticos por la vena. Más tarde, cuando la infección estuvo controlada, le pusieron reemplazos de cadera permanentes. Las piezas nuevas tenían un recubrimiento muy fino con plata. La plata ayuda a impedir que vuelvan las infecciones.\n\nEl paciente usó muletas y caminó con cuidado al principio. Las heridas sanaron bien. Tres años después estaba muy bien. Caminaba normalmente y no tenía señales de infección. La piel se veía normal y las prótesis estaban firmes. Los análisis de sangre estaban casi normales; una prueba pequeña estaba un poco alta porque todavía tenía artritis. En resumen: los médicos controlaron la infección y las nuevas caderas funcionaron muy bien.",
+                "fh_score": 71.97
+            },
+            "B2": {
+                "text": "Resumen comprensible (nivel B2)\n\nUn hombre de 61 años con artritis reumatoide y que estaba tomando esteroides desarrolló dolor en ambas ingles y tenía artrosis de cadera. Recibió inyecciones en las articulaciones y, 12 semanas después, llegó a urgencias con fiebre, empeoramiento general y dolor muy intenso. Las radiografías mostraron una destrucción rápida de las dos caderas y la extracción de líquido articular mostró pus; se diagnosticó artritis séptica, es decir, infección grave dentro de ambas articulaciones.\n\nPara controlar la infección se retiraron las cabezas femorales (parte superior del hueso del muslo) y se limpiaron las articulaciones. Se colocaron espaciadores de PMMA (una especie de cemento que libera antibiótico localmente) y se inició tratamiento antibiótico por vía intravenosa. Las muestras de tejido crecieron E. coli, por lo que los antibióticos se adaptaron a ese germen. Debido a drenaje persistente, se cambiaron los espaciadores en dos ocasiones antes de considerar la reconstrucción definitiva.\n\nCuando la infección estuvo controlada, se realizó la artroplastia total de cadera en dos tiempos: primero el lado derecho y después el izquierdo. Las prótesis y algunos refuerzos usados en la cirugía recibieron un recubrimiento multicapa muy fino de plata, que libera iones de plata y ayuda a reducir el riesgo de que las bacterias vuelvan a crecer. Además, el paciente recibió antibióticos intravenosos durante varias semanas tras las cirugías y caminó con apoyo parcial durante las primeras semanas.\n\nLas heridas cicatrizaron bien y, a las siete semanas, pudo apoyar todo el peso sin muletas. Tres años después las caderas funcionaban muy bien (puntuación WOMAC de 6 en cada lado), no hubo signos de nueva infección ni problemas por la plata en la piel, los implantes estaban bien fijados en las radiografías y las pruebas de sangre fueron razonables (la PCR algo elevada se atribuyó a su artritis reumatoide). En resumen, el tratamiento por etapas con espaciadores antibióticos, antibióticos intravenosos prolongados y prótesis recubiertas de plata logró controlar la infección y obtuvo un buen resultado funcional a tres años.",
+                "fh_score": 50.94
+            },
+            "B3": {
+                "text": "Summary (readability band B3)\n\nPatient and presentation\n- A 61-year-old patient with rheumatoid arthritis on long-term steroids developed bilateral groin pain and was treated with intra‑articular hyaluronic acid injections. Twelve weeks later they presented with fever, worsening general condition and progressive, severe hip pain.\n- Imaging showed rapid, destructive changes in both hip joints with extensive bone loss and subluxation. Joint aspiration yielded pus from both hips, and the diagnosis was rapidly progressive bilateral septic arthritis.\n\nTreatment course\n- Initial surgery: both femoral heads were resected, the hips were extensively debrided, and antibiotic‑loaded polymethylmethacrylate (PMMA) spacers were placed via a minimally invasive anterolateral approach.\n- Empiric intravenous antibiotics (vancomycin + ampicillin) were started. Cultures from joint tissue grew Escherichia coli, so systemic therapy was changed to meropenem. Because drainage persisted, two additional operations were done to exchange the antibiotic spacers.\n- After infection control, staged total hip arthroplasties were performed: the right hip 12 weeks after resection and the left hip 18 weeks after resection. Both procedures used implants with a multilayer ultrathin silver coating (a siloxane layer that releases silver ions). The left side required a silver‑coated reinforcement cage for a Paprosky type IIB acetabular defect and a cemented polyethylene cup.\n- Systemic intravenous ertapenem 1 g daily was continued as outpatient therapy for a total of 18 weeks after the right‑side implantation (resulting in 18 weeks of antibiotic coverage for the right hip and 12 weeks for the left).\n\nRecovery and follow‑up\n- The surgical wounds healed without complication. The patient progressed to full weight bearing without crutches by seven weeks after each operation.\n- At three years after implantation there were no clinical or radiographic signs of recurrent periprosthetic joint infection. The hips showed well‑integrated, stable prosthetic components.\n- Function was excellent: normal gait and a WOMAC score of 6 on each side (pain 0, stiffness 0, physical function 6). There were no signs of argyria (skin discoloration from silver).\n- Laboratory tests at three years: normal white blood cell count (7.29/nl) and a mildly elevated C‑reactive protein (CRP 12.4 mg/L), attributed to the patient’s underlying rheumatoid arthritis rather than implant infection.\n\nInterpretation and implications\n- This case demonstrates successful management of bilateral, rapidly destructive septic arthritis in an immunosuppressed patient using a staged approach: aggressive debridement with antibiotic spacers, culture‑directed prolonged IV antibiotics, and delayed total hip arthroplasty using implants with an ultrathin silver coating.\n- The silver coating was well tolerated in this patient (no argyria) and infection did not recur over three years, suggesting that silver‑coated implants can be a useful adjunct in high‑risk or previously infected reconstructions. However, this is a single case—broader studies are needed to define safety, long‑term outcomes and comparative effectiveness.\n- Practical points for similar cases: obtain culture guidance, use staged exchange with antibiotic spacers when infection is active, provide prolonged culture‑directed antibiotics, monitor clinical, radiographic and laboratory markers for recurrence, and counsel patients about the risks and uncertain long‑term benefits of silver‑coated implants.",
+                "fh_score": 65.8
+            }
+        }
+    },
+    {
+        "article": "Una niña africana de raza negra, con 1000 g de peso, nacida a las 32 semanas de gestación, de madre viva, fue derivada a nuestra unidad de cuidados intensivos neonatales debido a múltiples anomalías congénitas y dificultad respiratoria moderada. La madre tiene 32 años y está en un matrimonio no consanguíneo. La madre no buscó atención médica hasta el inicio del tercer trimestre de embarazo, debido a un desprendimiento de placenta. El primer ultrasonido prenatal reveló oligohidramnios severos. No era diabética (la glucosa en sangre aleatoria fue de 5.1 mmol/L) y no recibió suplementos de ácido fólico durante el embarazo.\n\nAl ingreso, la bebé estaba alerta con características leves del síndrome de dificultad respiratoria. Presentaba múltiples rasgos dismórficos, entre ellos, microcefalia (circunferencia de la cabeza < 10%), occipucio prominente, orejas bajas, paladar hendido y labio derecho, micrognatia, contractura bilateral de los codos e inferiores más cortos.\n\n\nEl peso al nacer fue de 1000 g, la longitud del bebé fue de 40 cm y la circunferencia occipitofrontal fue de 30 cm.\n\nInvestigaciones\nLa radiografía esquelética mostró aplanamiento de las costillas, aplasia del fémur derecho e hipoplasia del fémur izquierdo. Los análisis de laboratorio incluyeron: hemograma completo, proteína C reactiva, creatinina, urea en sangre y electrolitos, todos dentro de los valores normales. La ecografía craneal fue normal, pero la ecocardiografía reveló un pequeño conducto arterioso permeable.\n\nDiagnóstico diferencial\nLa paciente presentaba aplasia femoral bilateral y facies inusuales. Estas características clínicas llevaron al diagnóstico de síndrome femoro-facial.\n\nLa similitud en la etiopatogénesis hace que el síndrome de regresión caudal sea el diagnóstico diferencial común. Ambos pueden ser causados por una hiperglucemia materna mal controlada. Sin embargo, los defectos faciales están ausentes en el síndrome de regresión caudal, la característica diagnóstica clave.\n\nLa hipoplasia femoral focal proximal y las anomalías craneofaciales suelen estar ausentes.\n\nEntre las condiciones que pueden provocar el labio leporino se incluye el síndrome de banda amniótica grave.\n\nTratamiento\nEl bebé recibió asistencia respiratoria y antibióticos empíricos. Participaron un cirujano ortopédico, un otorrinolaringólogo y un fisioterapeuta. Está previsto reparar quirúrgicamente el paladar hendido a los 6 meses de edad. La rehabilitación funcional está prevista antes de que el paciente comience a deambular. La cirugía de alargamiento de extremidades no se realiza actualmente en nuestro entorno.\n\nResultado y seguimiento\nEl paciente falleció a la edad de un mes por complicaciones de una sepsis neonatal grave de inicio tardío.\n",
+        "gold_summary": "Una niña africana de raza negra bantú de 1 día de vida fue admitida en la unidad neonatal debido a múltiples anomalías congénitas. La madre no buscó atención médica hasta el inicio del tercer trimestre, cuando tuvo un desprendimiento de placenta. La madre nunca recibió suplementos de ácido fólico prenatal. La niña tenía microcefalia, orejas bajas, paladar hendido derecho y labio, micrognatia, contractura y extremidades más cortas. Una radiografía esquelética mostró hipoplasia femoral. Presentamos este caso poco habitual y destacamos los retos en el diagnóstico y el tratamiento.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Esta es la historia de una bebé muy pequeña. Nació antes de tiempo, a las 32 semanas. Pesó 1 kilo. La mamá tiene 32 años y no tuvo controles con el médico hasta muy tarde en el embarazo. No tomó ácido fólico. Durante el embarazo hubo poco líquido alrededor del bebé.\n\nAl nacer, la niña estaba despierta pero respiraba con dificultad leve. Tenía la cabeza más pequeña de lo esperado. Tenía orejas bajas, un labio y paladar partidos en el lado derecho (esto se llama paladar hendido), y la mandíbula pequeña. También tenía los codos apretados y las piernas más cortas.\n\nLas radiografías mostraron que faltaba el hueso del muslo derecho y que el muslo izquierdo estaba pequeño. El ultrasonido de la cabeza fue normal, y algunas pruebas de sangre también estuvieron dentro de lo esperado. El corazón tenía un pequeño orificio llamado ductus arterioso persistente.\n\nLos médicos pensaron que tenía un problema llamado síndrome femoro-facial. Trataron a la bebé con ayuda para respirar y con antibióticos. También la vieron un cirujano de huesos, un especialista de oídos y garganta, y un fisioterapeuta. Planeaban arreglar el paladar cuando tuviera 6 meses y hacer terapia para ayudarla a caminar.\n\nCon mucho dolor, la bebé murió a la edad de un mes por una infección grave en la sangre. Es una historia triste. Los médicos aprendieron sobre un caso poco común y los desafíos para cuidar a bebés con muchos problemas al nacer.",
+                "fh_score": 73.26
+            },
+            "B2": {
+                "text": "Resumen claro y amable\n\nPresentación\nUna recién nacida africana de 32 semanas (muy prematura) y 1 000 g fue ingresada en la unidad neonatal por varias malformaciones congénitas y dificultad respiratoria leve. La madre tenía 32 años, no recibió control prenatal hasta el tercer trimestre porque presentó un desprendimiento de la placenta, y no tomó suplementos de ácido fólico durante el embarazo. El primer ultrasonido mostró oligohidramnios severo (poco líquido alrededor del feto).\n\nHallazgos en la bebé\n- Cabeza pequeña (microcefalia: circunferencia por debajo del rango esperado).\n- Occipucio prominente (parte posterior de la cabeza más sobresaliente).\n- Orejas bajas.\n- Labio y paladar hendidos en el lado derecho (hendidura en el labio y en el techo de la boca).\n- Micrognatia (mandíbula pequeña).\n- Contracciones en ambas articulaciones de los codos y extremidades inferiores más cortas de lo habitual.\n- Radiografía ósea: ausencia del fémur derecho y fémur izquierdo más pequeño (aplasia e hipoplasia femoral).\n- Ecocardiograma: pequeño conducto arterioso permeable (PDA), que es un vaso que normalmente se cierra después del nacimiento.\n- Ecografía cerebral y pruebas de sangre básicas dentro de la normalidad al ingreso.\n\nDiagnóstico y consideraciones\nLos médicos consideraron el síndrome femoro-facial, que combina problemas en los huesos del muslo con rasgos faciales anormales. Como diagnóstico alternativo se evaluó el síndrome de regresión caudal (otro trastorno relacionado con la formación de la parte baja del cuerpo), pero este último generalmente no tiene defectos faciales, lo que apoyó el diagnóstico de femoro-facial en este caso. Algunas condiciones como bandas amnióticas pueden causar labio leporino, por lo que también se tuvieron en cuenta otras causas. Aunque algunos síndromes se han asociado con diabetes materna mal controlada, en este caso la madre no era diabética según la glucosa registrada.\n\nTratamiento y seguimiento\nLa bebé recibió soporte respiratorio y antibióticos empíricos. Fueron consultados ortopedia, otorrinolaringología y fisioterapia. Se planificó reparar el paladar hendido a los 6 meses y comenzar rehabilitación antes de que la niña empezara a caminar. Algunas operaciones complejas, como alargamiento de las extremidades, no estaban disponibles en el centro.\n\nResultado\nLa bebé falleció a la edad de un mes por una sepsis neonatal severa de inicio tardío (infección generalizada grave adquirida después del período inmediato del nacimiento).\n\nComentario final (empatía y contexto)\nEste caso muestra un cuadro poco frecuente y los retos que existen para diagnosticar y tratar malformaciones complejas en recién nacidos, especialmente cuando el control prenatal es tardío y hay limitaciones de recursos. Es una situación triste; las decisiones médicas intentaron ofrecer apoyo y planificar intervenciones futuras, pero la infección grave complicó el curso.",
+                "fh_score": 47.09
+            },
+            "B3": {
+                "text": "Case summary\nA preterm Black African female infant (32 weeks’ gestation, birth weight 1,000 g, length 40 cm, head circumference 30 cm) was referred to the neonatal intensive care unit on day 1 of life for multiple congenital anomalies and moderate respiratory distress. The mother (32 years) had no consanguinity with the father, sought prenatal care late (first seen in the third trimester after placental abruption), had severe oligohydramnios on ultrasound, did not take prenatal folic acid, and was not known to be diabetic (random maternal glucose 5.1 mmol/L).\n\nAbnormal findings (clinical and imaging)\n- Craniofacial and head: microcephaly (head circumference <10th centile), prominent occiput, low-set ears, right-sided cleft lip and cleft palate, and micrognathia (small lower jaw).  \n- Limbs and musculoskeletal: bilateral elbow contractures and markedly shortened lower limbs. Skeletal X-ray showed right femoral aplasia (absence) and left femoral hypoplasia, with flattened ribs.  \n- Cardiac: small patent ductus arteriosus on echocardiography.  \n- Respiratory: mild features of neonatal respiratory distress syndrome requiring respiratory support.\n\nNormal or unremarkable findings\n- Basic laboratory tests, including complete blood count, C-reactive protein, renal function (creatinine, urea) and electrolytes, were within reference ranges at admission.  \n- Cranial ultrasound was normal.\n\nWorking diagnosis and differential\n- The clinical picture (proximal femoral deficiency with characteristic facial anomalies) led to a diagnosis of femoral-facial syndrome.  \n- Caudal regression syndrome is an important differential because both disorders can be associated with maternal hyperglycemia; however, caudal regression typically lacks the facial anomalies seen here.  \n- Severe amniotic band syndrome can cause cleft lip/palate and other limb defects and was considered as another differential.\n\nManagement and course\n- Initial care included respiratory support and empirical antibiotics. Multidisciplinary involvement included orthopedics, otolaryngology, and physiotherapy.  \n- Planned interventions included surgical repair of the cleft palate at about 6 months of age and pre-ambulation functional rehabilitation. Limb-lengthening or advanced orthopedic reconstruction was not available in the treating center.  \n- The infant developed late-onset neonatal sepsis and died at one month of age.\n\nImplications and recommendations\n- This is a rare and severe presentation of femoral-facial syndrome, highlighting diagnostic challenges and limited therapeutic options in a resource-constrained setting.  \n- Important preventive and investigational points for future pregnancies: timely prenatal care, folic acid supplementation, and screening for maternal diabetes (since maternal hyperglycemia can be associated with similar anomalies).  \n- Families should be offered multidisciplinary counseling (genetic counseling when available, discussion of recurrence risk, and psychosocial support).  \n- Where possible, referral to specialized centers for orthopedic planning and advanced neonatal surgical care can improve access to reconstructive options and long-term rehabilitation.\n\nTone and context\n- The case illustrates both the medical complexity of congenital limb–facial syndromes and the vulnerability of neonates to infectious complications. The outcome was tragic; compassionate follow-up and support for the family are important components of care.",
+                "fh_score": 56.54
+            }
+        }
+    },
+    {
+        "article": "Paciente de sexo masculino de 18 años, con diag nóstico clínico de Neurofibromatosis tipo 1 desde el primer año de vida. Entre sus antecedentes destaca que tiene educación completa, sus padres no son consan guíneos, y no tiene antecedentes familiares de manchas café con leche. Desde el punto de vista neurológico desarrolló durante la infancia retraso del desarrollo psicomotor fino y grueso, trastorno del lenguaje de predominio expresivo, con alteración fonológica y semántica del lenguaje, por lo que fue manejado con fonoaudiología en Escuela de Lenguaje, además de ki- nesioterapia y terapia ocupacional durante la infancia. Durante la adolescencia se le diagnosticó Trastorno por Déficit Atencional e Hiperactividad, que fue manejado con metilfenidato, manteniendo regular rendimiento escolar. Tuvo desarrollo puberal normal. Oftalmológi camente presentó nódulos de Lisch desde los 4 años de edad, euriblefaron y astigmatismo. Se mantuvo en control anual en Oftalmología y Neuropediatría. Su última Resonancia Magnética de cerebro fue realiza da 6 meses previo a la consulta en Dermatología, sin hallazgos patológicos y en la Resonancia Magnética de columna se evidenció discopatía L5-S1 y realce perifacetario en T11-T12 y T12-L1. A los 16 años se reali zó estudio genético que demostró deleción de exones 5-47 del gen NF1.\n\nA los 18 años consultó en servicio de Dermatología del Centro de Referencia en Salud Peñalolén Cordille ra Oriente por aparición de nueva mancha en muslo izquierdo de 1 año evolución, asintomática. Además, refirió aparición de nódulos en muñeca derecha, su praciliar derecho y cuero cabelludo, de unos meses de evolución, asintomáticos.\n\nAl examen físico destacaba presión arterial normal, macrocefalia (CC: 60 cm) y múltiples manchas café con leche generalizadas, efélides en axilas, y en zona supraciliar derecha, occipital y muñeca derecha nódulos subcutáneos ovalados de 0,5 cm, bien delimitados, móviles. En muslo izquierdo lateral pre sentaba placa de 25 mm algo rosada, con pérdida de anexos, y de consistencia blanda. Por último, en zona lumbar y pectoral, múltiples máculas rojo- azuladas pequeñas, de menos de 5 mm cada una, algu nas levemente deprimidas.\n\nSe realizó biopsia cutánea de máculas azuladas en pecho y de placa muslo, resultando ambas compatibles con NF. Se realizó una ecografía de nódulos supraciliar y occipital que resultó compatible con NF nodular subcutáneo.\n\nUsando la clasificación clínica de García-Martínez et al.1 se diagnosticó al paciente con NF superficial sub cutáneo nodular en zona supraciliar derecha, occipital y muñeca derecha, NF superficial cutáneo pseudoatró fico en muslo izquierdo lateral y NF superficial cutáneo rojo azulado en zona lumbar y pectoral.",
+        "gold_summary": "Paciente masculino de 18 años con diagnóstico desde la infancia de NF-1 que presenta múltiples nodulos ovalados en cara, zona occipital y muñeca, máculas rojo-azuladas en dorso y placa rosada atrófica en muslo. El estudio ecográfico de los nódulos fue compatible con neurofibromas y el estudio histopatológico de las lesiones de dorso y muslo compatibles con neurofibromas cutáneos.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Resumen simple y amable:\n\nEste joven tiene 18 años y desde bebé sabe que tiene neurofibromatosis tipo 1. Esa enfermedad causa manchas en la piel y a veces bultos pequeños.\n\nCuando era niño recibió terapia del habla, fisioterapia y apoyo escolar. También le diagnosticaron TDAH y tomó medicina para eso. Tiene nódulos en los ojos llamados nódulos de Lisch y la cabeza un poco más grande de lo habitual.\n\nA los 17–18 años le salieron nuevas lesiones en la piel. Apareció una mancha rosada en el muslo que mide unos 2,5 cm. También notó bultitos pequeños y móviles en la frente, la nuca y la muñeca derecha. Además había pequeñas manchas rojo-azuladas en la espalda y el pecho. Los bultos no le dolían.\n\nHicieron estudios: la ecografía de los nódulos y las biopsias de la mancha del muslo y de las manchas del pecho mostraron que son neurofibromas. La resonancia del cerebro fue normal. La resonancia de la columna mostró cambios en un disco y en unas articulaciones. Un estudio genético confirmó un cambio en el gen NF1, que explica la enfermedad.\n\nEn resumen: tiene múltiples neurofibromas en la piel y algunas manchas. Los exámenes confirmaron que las nuevas lesiones son parte de su neurofibromatosis.",
+                "fh_score": 76.75
+            },
+            "B2": {
+                "text": "Resumen comprensible (nivel secundaria — B2)\n\nEste informe describe a un joven de 18 años con diagnóstico de neurofibromatosis tipo 1 (NF1) desde el primer año de vida. NF1 es una condición genética que causa manchas en la piel y tumores benignos que nacen de los nervios (estos tumores se llaman neurofibromas).\n\nAntecedentes importantes\n- Tuvo retrasos en el desarrollo motor y en el lenguaje en la infancia; recibió terapia del lenguaje, fisioterapia y terapia ocupacional.  \n- Durante la adolescencia fue diagnosticado con TDAH y recibió metilfenidato.  \n- Tuvo pubertad normal.  \n- Desde los 4 años tenía nódulos en el iris del ojo llamados nódulos de Lisch (manchitas en el ojo que suelen aparecer en NF1), además de astigmatismo y una diferencia en el párpado (euriblefaron).  \n- Estudio genético a los 16 años mostró una eliminación grande en el gen NF1 (deleción de exones 5-47), lo que confirma la causa genética de su NF1.  \n- La resonancia del cerebro hecha 6 meses antes fue normal; la de columna mostró algo de desgaste de disco en L5-S1.\n\nQué consultó ahora\n- Nueva mancha en el muslo izquierdo que apareció hace 1 año (no duele ni molesta).  \n- Nódulos pequeños en la frente (sobre la ceja derecha), en la nuca (occipucio) y en la muñeca derecha que salieron hace meses, también sin dolor.  \n- Varias manchas rojo-azuladas pequeñas en la espalda y el pecho.\n\nHallazgos al examen y estudios\n- Múltiples manchas “café con leche” y efélides (pecas) en las axilas. Cabeza mayor de lo habitual (microcefalia no, sino macrocefalia: circunferencia 60 cm).  \n- Nódulos subcutáneos ovalados, móviles, de ~0,5 cm en frente, nuca y muñeca.  \n- Placa en muslo izquierdo de 25 mm, algo rosada, con pérdida de pelo local y consistencia blanda.  \n- Pequeñas máculas rojo-azuladas (<5 mm) en zona lumbar y pectoral, algunas ligeramente hundidas.  \n- Ecografía de los nódulos y biopsias de la zona del pecho y del muslo: todos los hallazgos fueron compatibles con neurofibromas (tumores benignos asociados a NF1).\n\nDiagnóstico final (clasificación clínica)\n- Neurofibromas subcutáneos nodulares: frente (supraciliar derecha), occipucio y muñeca derecha.  \n- Neurofibroma cutáneo pseudoatrófico: placa rosada en muslo izquierdo.  \n- Neurofibromas cutáneos rojo-azulados: zonas lumbar y pectoral.\n\nQué significa y siguientes pasos\n- Las lesiones encontradas son compatibes con los tipos comunes de neurofibromas en NF1 y actualmente son asintomáticas.  \n- Es importante mantener seguimiento médico regular (dermatología, neurología y oftalmología).  \n- Se vigilarán cambios en tamaño, dolor, sangrado o pérdida de función; si alguno aparece, se puede considerar extirpar el tumor o hacer estudios adicionales para descartar complicaciones.  \n- Dado que la prueba genética mostró una deleción grande en NF1, también puede ser recomendable asesoría genética para la familia.\n\nSi tienes preguntas sobre qué observar en casa o sobre opciones de tratamiento, los médicos del equipo pueden explicar los riesgos, beneficios y pasos siguientes de forma clara y paciente.",
+                "fh_score": 56.43
+            },
+            "B3": {
+                "text": "Resumen clínico breve (nivel universitario)\n\nAntecedentes relevantes\n- Paciente masculino de 18 años, con diagnóstico clínico de neurofibromatosis tipo 1 (NF1) desde el primer año de vida. El estudio genético a los 16 años mostró una deleción de los exones 5–47 del gen NF1, confirmando la enfermedad a nivel molecular.\n- Desarrollo neurológico: retraso psicomotor fino y grueso en la infancia, trastorno del lenguaje (predominio expresivo) tratado con fonoaudiología, kinesioterapia y terapia ocupacional. Diagnosticado luego con trastorno por déficit de atención e hiperactividad (TDAH) tratado con metilfenidato.\n- Ojos: nódulos de Lisch (pequeñas lesiones en el iris) desde los 4 años. Pubertad y presión arterial normales.\n- Imágenes: resonancia magnética cerebral hecha 6 meses antes de la consulta sin hallazgos patológicos; resonancia de columna con discopatía L5–S1 y realce perifacetario en T11–T12 y T12–L1.\n\nPresentación actual\n- Consulta por aparición, durante el último año, de una nueva placa en el muslo izquierdo (asintomática) y, durante meses, de nódulos subcutáneos asintomáticos en la región supraciliar derecha, cuero cabelludo (occipital) y muñeca derecha.\n- Examen físico: macrocefalia (circunferencia craneal 60 cm), múltiples manchas café con leche y efélides axilares. Nódulos subcutáneos ovalados, bien delimitados y móviles (≈0,5 cm). Placa en muslo lateral izquierdo de 25 mm, de aspecto algo rosado, con pérdida de anexos (pelo) y consistencia blanda. Varias máculas rojo‑azuladas pequeñas (<5 mm) en región lumbar y pectoral, algunas levemente deprimidas.\n\nEstudios realizados y diagnóstico\n- Biopsias cutáneas de las máculas rojo‑azuladas del pecho y de la placa del muslo: resultados compatibles con neurofibromas cutáneos.\n- Ecografía de los nódulos supraciliar y occipital: compatible con neurofibromas subcutáneos nodulares.\n- Clasificación clínica (según García‑Martínez et al.): coexistencia de tres fenotipos cutáneos en este paciente — NF superficial subcutáneo nodular (supraciliar derecho, occipital, muñeca derecha), NF superficial cutáneo pseudoatrófico (muslo izquierdo lateral) y NF superficial cutáneo rojo‑azulado (zona lumbar y pectoral).\n\nQué es normal y qué es anómalo aquí\n- Coincide con NF1: macrocefalia, manchas café‑con‑leche, efélides axilares, nódulos (neurofibromas) y nódulos de Lisch son hallazgos típicos de NF1.\n- Anómalo o relevante para seguimiento: aparición de nuevas lesiones cutáneas y subcutáneas confirmadas como neurofibromas; la deleción amplia en NF1 (exones 5–47) puede asociarse con mayor carga de enfermedad en algunos casos, por lo que requiere vigilancia más estrecha.\n\nImplicaciones y recomendaciones prácticas\n- Seguimiento multidisciplinario continuo: control dermatológico, neurología/neuropediatría y oftalmología según protocolo de NF1. Dada la genética confirmada, ofrecer asesoría genética si considera tener descendencia.\n- Vigilancia activa de lesiones: indicar control y reevaluación si cualquier neurofibroma crece rápidamente, duele, causa déficit neurológico o cambia de aspecto (motivos para imagen adicional y posible derivación a cirugía). Biopsia o resección se justifica si hay duda diagnóstica o sintomas.\n- Imagen y clínica de columna: correlacionar con síntomas de dolor o signos neurológicos; la discopatía y el realce facetario pueden requerir manejo ortopédico/neuroquirúrgico si hay clínica.\n- Riesgos a explicar al paciente: aunque la mayoría de los neurofibromas son benignos, existe un riesgo (bajo) de transformación maligna en algunos casos (tumor maligno de la vaina nerviosa); por eso la observación periódica es importante.\n- Soporte psicosocial y educativo: dado el antecedente de dificultades del desarrollo y TDAH, mantener soporte rehabilitador y educativo según necesidad.\n\nComentario final (empático)\nUsted presenta las manifestaciones cutáneas y sistémicas esperables de NF1, confirmadas por estudios histológicos y por la deleción genética amplia. Lo más importante ahora es mantener controles periódicos con los especialistas, vigilar cambios en las lesiones cutáneas o síntomas nuevos, y recibir orientación genética si planea tener hijos. Si desea, puedo ayudar a redactar preguntas para llevar a la próxima consulta o a preparar una lista de señales de alarma que justifiquen consultar antes.",
+                "fh_score": 38.12
+            }
+        }
+    },
+    {
+        "article": "Un hombre de 38 años de edad fue ingresado en el hospital por traumatismo torácico contundente. El paciente estaba generalmente sano y no tenía factores de riesgo de enfermedad coronaria. Fue golpeado en el pecho por un tornillo de alta velocidad que tenía aproximadamente 6 cm de diámetro mientras trabajaba en una fábrica. Voló aproximadamente 4 metros de distancia debido a la fuerza y presión del tornillo de alta velocidad. Perdió el conocimiento de inmediato, pero recuperó la conciencia varios minutos después. Fue trasladado inmediatamente a la sala de urgencias de un hospital local. Su puntaje en la escala de coma de Glasgow fue de 15. Se quejó de dolor torácico intenso y persistente, opresión y disnea. La tomografía computarizada del tórax mostró derrame pleural bilateral y fracturas de esternón y costillas. Por lo tanto, se insertó un tubo torácico durante varios días. Luego, fue dado de alta sin someterse a un electrocardiograma (ECG) u otros exámenes cardiovasculares.\n\nTres meses después del alta hospitalaria, durante un chequeo de seguimiento de rutina, todavía había presencia de derrame pleural con síntomas acompañantes de opresión en el pecho, falta de aire después de la actividad física, e incluso disnea por la noche, lo que motivó su ingreso en nuestro hospital. Sus constantes vitales durante el ingreso fueron las siguientes: frecuencia cardíaca regular de 98 latidos/min, presión arterial de 110/70 mmHg, y frecuencia respiratoria de 20 respiraciones/min. El examen físico mostró una pulsación carotídea y yugular normal. El movimiento respiratorio torácico bilateral y la actividad fueron normales, la fibrilación del lenguaje táctil del pulmón derecho disminuyó, la percusión del pulmón derecho presentó un sonido sordo, y los sonidos respiratorios disminuyeron. No hubo roncus ni estertores evidentes durante la auscultación pulmonar. No hubo murmullos en la auscultación cardíaca. Los exámenes del abdomen y las extremidades revelaron hallazgos normales. El primer ECG mostró evaluación ST e inversión de la onda T en las derivaciones I, aVL y V2-V5 y en el bloqueo de rama anterior izquierdo. La prueba de troponina-I fue negativa, y el nivel de NT-proBNP fue de 706 pg/ml (rango normal: 0-104 pg/ml), lo que sugiere un infarto de miocardio anterior antiguo. La ecocardiografía transtorácica mostró una aurícula izquierda de 26,4 mm, un ventrículo izquierdo de 51,8 mm, y una fracción de eyección ventricular izquierda (EF) del 32% (modo M). La pared anterior del LV e interventricular septum mostraron adelgazamiento a 6,6 mm, con un eco de movimiento notablemente reducido.\n\nAl examinar las arterias carótidas, intracraneales y de las extremidades inferiores del paciente, no se encontraron placas ateroscleróticas evidentes. Todos los hallazgos apoyaron el diagnóstico de infarto de miocardio antiguo (OMI), en lugar de arteriosclerosis. Sin embargo, el paciente era hemodinámicamente estable. Después de someterse a una terapia diurética, se le administraron bloqueadores beta, estatinas y estimulantes cardíacos, lo que alivió su malestar. La angiografía por tomografía computarizada coronaria mostró una estenosis moderada en la arteria LAD proximal. Para confirmar la estenosis y examinar el estado de la íntima coronaria, se realizó CAG 3 meses después del traumatismo torácico, que mostró un estrechamiento aproximado del 70% del lumen en la LAD proximal y el segmento coronario tenía una lesión curva. La arteria circunfleja izquierda (LCX) y la arteria coronaria derecha (RCA) eran normales. Los resultados de CAG confirmaron el diagnóstico de OMI, pero debido a la carga de costos, el paciente rechazó el examen IVUS. El paciente se sometió a una terapia conservadora y fue dado de alta del hospital varios días después.\n\nUn mes después, el 9 de diciembre de 2014, volvió al hospital para someterse a una intervención coronaria percutánea (ICP). Después de someterse a una terapia con fármacos, sus condiciones habían mejorado ligeramente. El examen físico y el ECG revelaron resultados casi normales. La ecocardiografía transtorácica mostró una mejora en la función sistólica del LV y EF del 45%. Se sometió a otra CAG 4 meses después del traumatismo torácico, que mostró una ligera mejora de la estenosis. Había aproximadamente un 60% de estrechamiento del lumen. Se realizó un IVUS y reveló que la gravedad de la lesión era del 55.9%, y la placa de bajo eco apareció antes de la formación de trombos después de la rotura subintimal. Completamos el examen sin más intervención porque solo se encontró un 55.9% de estrechamiento del lumen y el paciente tenía una hemodinámica estable sin evidencia de isquemia miocárdica constante. Se le recetó al paciente la medicación óptima, y su incomodidad se alivió gradualmente. El 17 de julio de 2018, 4 años después del traumatismo, la evaluación de seguimiento reveló que el paciente todavía experimentaba dificultad para respirar después de trabajar, pero se alivió poco después de descansar. El examen físico mostró los siguientes resultados: presión arterial de 114/80 mmHg, frecuencia cardíaca de 66 latidos/min, ausencia de anomalías obvias en la auscultación pulmonar y cardíaca; y ausencia de edema obvio en ambas extremidades inferiores. El ECG de seguimiento reveló los siguientes hallazgos: rS en las derivaciones V2-V4, inversión de la onda T en las derivaciones I, AVL y V2-V5 y bloqueo de rama izquierda. La ecocardiografía transtorácica mostró agrandamiento del ventrículo izquierdo con una aurícula izquierda de 39 mm, un ventrículo izquierdo de 54.7 mm y una EF del LV del 41% (Simpson's). También se observó adelgazamiento de la pared anterior del LV y del tabique interventricular, con la parte más delgada de 4.7 mm; el movimiento casi había desaparecido y el eco se había mejorado. Sin embargo, las arterias carótidas, intracraneales y de las extremidades inferiores seguían siendo normales. Además, descubrimos que los medicamentos recetados para tratar la insuficiencia cardíaca no se tomaron religiosamente después del alta; por lo tanto, recetamos 23.75 mg de metoprolol, 2.5 mg de benazepril y 20 mg de espironolactona para tomar una vez al día, y coenzima para tomar cada 10 horas.\n\nMH - Adulto\nMH - Errores de diagnóstico\nMH - Insuficiencia cardiaca/etiología\nMH - Humanos\nMH - Hombre\nMH - Infarto de miocardio/complicaciones/*etiología\nMH - Lesiones torácicas/*complicaciones\nMH - Tiempo hasta el tratamiento\nMH - Heridas, no penetrantes/complicaciones\n",
+        "gold_summary": "Preocupaciones de los pacientes:\nUn hombre de 38 años, previamente sano, fue admitido en nuestro hospital con una queja de disnea. Tenía un historial de haber sido golpeado en el pecho por un tornillo de alta velocidad mientras trabajaba en una fábrica 3 meses antes de ser admitido en el hospital.\n\nDiagnóstico:\nLuego de realizarse una angiografía coronaria y una ecocardiografía, finalmente se le diagnosticó un infarto de miocardio.\n\nIntervenciones:\nRecibió medicamentos optimizados, entre ellos, diuréticos, bloqueadores beta y estimulantes cardíacos.\n\nResultados:\nAl cabo de cuatro años de seguimiento, se le diagnosticó al paciente una insuficiencia cardíaca crónica con una fracción de eyección reducida.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un hombre de 38 años se golpeó muy fuerte el pecho con un tornillo mientras trabajaba. Perdió el conocimiento por un rato y tuvo mucho dolor en el pecho. Primero lo atendieron en el hospital, pero no le hicieron pruebas del corazón.\n\nTres meses después todavía tenía falta de aire. Los médicos le hicieron imágenes especiales del corazón. Descubrieron que había tenido un ataque al corazón cuando se lastimó el pecho. Eso dañó una parte del corazón y lo dejó más débil.\n\nLe dieron medicinas para ayudar al corazón y para quitarle líquido del cuerpo. Mejoró un poco, pero el corazón no volvió a ser del todo fuerte. Cuatro años después seguía con el corazón débil y tenía lo que llaman insuficiencia cardíaca crónica. También se notó que no siempre tomaba sus medicinas como debía, por eso los doctores le recetaron nuevos medicamentos y le pidieron que los tome todos los días.",
+                "fh_score": 77.09
+            },
+            "B2": {
+                "text": "Patient story (in simple terms)\nA previously healthy 38-year-old man was hit hard in the chest by a large, high-speed screw while working in a factory. He lost consciousness briefly and had broken ribs and a broken breastbone. He was treated for chest injuries and a fluid build-up around the lungs, then sent home. No heart tests were done at that first discharge.\n\nWhat happened next\nThree months later he still had chest tightness and shortness of breath. Tests at our hospital showed changes on his ECG (a heart tracing) and a high NT-proBNP blood level (a marker that can mean the heart is strained). An ultrasound of the heart (echocardiogram) showed the front wall of his left heart was thin and not moving well, and his left ventricular ejection fraction (EF) — the percent of blood the heart pumps out each beat — was low (about 32%). These findings meant he had an old heart attack (myocardial infarction), most likely caused by the blunt chest trauma rather than usual artery disease, because scans did not show plaque elsewhere.\n\nFurther checks and treatment\nCoronary imaging (angiography and later CT angiography) showed the left anterior descending (LAD) artery had a significant narrowing. At first he considered a stent procedure (percutaneous coronary intervention), but he was treated with medicines (diuretics, beta blocker, statin and other heart drugs). Later, intravascular ultrasound (IVUS) measured the narrowing at about 56%, which is moderate; because he was stable and not having ongoing chest pain or clear signs of ongoing ischemia (lack of blood flow), no stent was placed. He was sent home on optimal medical therapy.\n\nOutcome and follow-up\nOver four years he continued to have some breathlessness with activity. His heart size was slightly larger and EF stayed reduced (about 41%), so he developed chronic heart failure with reduced ejection fraction — a long-term effect of the earlier heart attack. It was also noted he had not always taken his heart medicines as prescribed, so doctors restarted guideline medications (a beta blocker, an ACE inhibitor, and spironolactone).\n\nWhat this means and next steps\nBlunt chest trauma can sometimes injure a coronary artery and cause a heart attack. Important steps are close follow-up, taking prescribed medicines, lifestyle changes, and regular cardiology checks (including repeat imaging or stress tests if symptoms change). Staying on medications and keeping appointments can help protect heart function and reduce symptoms.",
+                "fh_score": 85.93
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel universitario, lectura B3)\n\nPresentación y antecedente inmediato\n- Hombre de 38 años, previamente sano, recibió un fuerte golpe en el pecho por un tornillo de alta velocidad durante el trabajo; perdió la conciencia brevemente. \n- En el hospital inicial se identificaron derrame pleural bilateral y fracturas de esternón y costillas; se colocó tubo torácico. Fue dado de alta sin electrocardiograma (ECG) ni evaluación coronaria.\n\nSíntomas y hallazgos al ingreso a los 3 meses\n- Motivo de ingreso: disnea de esfuerzo persistente, opresión torácica y derrame pleural residual.\n- Signos vitales relativamente estables (FC ≈ 98 lpm, PA 110/70 mmHg).\n- ECG: alteraciones de la repolarización (inversión de onda T en I, aVL y V2–V5) y bloqueo de rama izquierda anterior — cambios sugestivos de lesión miocárdica previa.\n- Troponina I negativa (no lesión aguda evidente en ese momento); NT‑proBNP elevado (706 pg/ml; normal 0–104) — compatible con estrés ventricular/insuficiencia cardiaca.\n- Ecocardiograma transtorácico: ventrículo izquierdo dilatado, fracción de eyección (FE) reducida (32% por modo M) y adelgazamiento / movilidad severamente reducida de la pared anterior y del septo interventricular — hallazgos consistentes con infarto de miocardio antiguo (OMI).\n\nEvaluación coronaria y etiología\n- Arterias carotídeas, intracraneales y de extremidades sin placas ateroscleróticas significativas, lo que sugiere que la causa no fue una aterosclerosis difusa.\n- Tomografía coronaria y posteriormente angiografía coronaria (CAG) mostraron estenosis en la arteria descendente anterior (LAD) proximal: ~70% en la primera CAG realizada 3 meses tras el trauma. LCX y RCA normales.\n- IVUS (realizado más tarde) mostró que la lesión tenía un 55.9% de estrechamiento y una placa hipoecoica antes de formación trombótica por ruptura subintimal. Esto sugiere lesión intimal/traumática de la LAD seguida de trombosis y embolización que causó el infarto, en lugar de enfermedad aterosclerótica crónica.\n\nTratamiento y evolución\n- Inicialmente manejo médico conservador: diuréticos, betabloqueantes, estatinas y fármacos inotrópicos según necesidad; luego terapia óptima para insuficiencia cardíaca.\n- No se realizó intervención revascularizadora inmediata por falta de evidencia de isquemia persistente y por el grado moderado de estenosis en IVUS; además, el paciente rechazó IVUS en una ocasión por motivos económicos.\n- Tras terapia médica la función mejoró parcialmente (FE hasta 45% un mes después; luego estabilizada alrededor de 41% a los 4 años), pero persistió disnea de esfuerzo leve-moderada.\n- A los 4 años se constató insuficiencia cardíaca crónica con FE reducida, ventrículo izquierdo dilatado y zonas akiné­ticas/adelgazadas en pared anterior; se documentó además incumplimiento terapéutico intermitente.\n\nInterpretación clínica y lecciones\n- Probable lesión coronaria traumática (LAD) secundaria a trauma torácico cerrado que llevó a ruptura intimal, trombosis y un infarto de miocardio que no fue detectado ni tratado en el momento agudo.\n- Hallazgos normales en otras arterias y la historia clínica del trauma apoyan la etiología traumática más que la aterosclerótica.\n- El retraso en la sospecha/diagnóstico coronario tras traumatismo torácico tuvo como consecuencia daño miocárdico irreversible y evolución a insuficiencia cardíaca crónica con FE reducida.\n\nImplicaciones y recomendaciones prácticas\n- Tras traumatismo torácico de alta energía, es importante realizar evaluación cardíaca precoz: ECG seriados, troponinas y ecocardiograma según la clínica. Si hay sospecha de lesión coronaria, considerar angiografía y/o imagen intracoronaria (IVUS/OCT) para guiar la revascularización.\n- En pacientes con disfunción ventricular tras posible infarto, instaurar y garantizar adherencia a terapia cardioprotectora y para insuficiencia cardíaca (betabloqueantes, IEC/ARA-II, antagonistas de aldosterona, estatinas cuando indicada).\n- Seguimiento prolongado: monitorizar función ventricular, síntomas, adherencia a tratamiento y considerar revascularización si hay isquemia documentada o progresión de la lesión; valorar terapia dispositivo si persiste FE ≤35% pese a terapia óptima.\n- Educar al paciente sobre la importancia de la adherencia farmacológica y seguimiento cardiológico para mejorar pronóstico.\n\nTono final\nEste caso subraya la posibilidad, aunque poco frecuente, de lesión coronaria por traumatismo cerrado del tórax y la importancia de una evaluación cardiológica temprana. Con una detección y manejo oportunos se puede reducir el riesgo de daño miocárdico irreversible y de progresión a insuficiencia cardíaca crónica. Se recomienda atención continuada y cumplimiento estricto de la terapia guiada por las guías.",
+                "fh_score": 35.09
+            }
+        }
+    },
+    {
+        "article": "La paciente era una recién nacida de 0 días de edad, de etnia Han, que nació a las 36 semanas de gestación de una mujer embarazada de 3, para 2, con un peso de 2650 g. Se le practicó una cesárea de urgencia debido a la angustia fetal, con puntuaciones de Apgar de 6 a 1 min y 5 min. Su grupo sanguíneo era O y RhD positivo. Al nacer, presentaba palidez, equimosis dispersas en múltiples áreas del cuerpo, sangrado de las mucosas e insuficiencia respiratoria, con un leve flujo de sangre hemorrágica también observado en los sitios de punción venosa. El análisis de gases en sangre de la arteria umbilical mostró un hematocrito de 0.08 y una hemoglobina de 23 g/L. La paciente requirió intubación endotraqueal y ventilación mecánica. Después de la transfusión de una suspensión de glóbulos rojos, los recuentos sanguíneos iniciales revelaron una trombocitopenia severa (recuento de plaquetas de 12 × 109/L), anemia (hemoglobina de 46 g/L) y leucopenia (recuento de leucocitos de 1.11 × 109/L).\n\nLa paciente fue ingresada en la unidad de cuidados intensivos neonatales a las 3 horas de vida para recibir tratamiento adicional. Durante la hospitalización, se le diagnosticó coagulación intravascular diseminada (CID), con tiempo de tromboplastina parcial activada (TTPA) de 73,10 segundos, tiempo de protrombina (TP) de 25,4 segundos, fibrinógeno (FIB) de 1,01 g/L, razón internacional normalizada (INR) de 2,26 y dímero D > 20 mg/L. Se le administró ventilación mecánica, corrección de la acidosis y transfusión de plasma fresco congelado. A pesar de múltiples transfusiones de glóbulos rojos y plaquetas, los niveles de hemoglobina y plaquetas permanecieron por debajo de lo normal (hemoglobina 106 g/L y plaquetas 11 × 109/L el día 3). También recibió tratamiento antiinfeccioso, cardiotónico, vasopresor y otro tratamiento sintomático. Un frotis periférico mostró áreas de tinción pálida agrandadas de glóbulos rojos, con una proporción de reticulocitos del 1,5% y un resultado negativo en la prueba directa de Coombs. No se realizó aspiración de médula ósea debido a su grave estado. No hubo evidencia clínica o de laboratorio de sepsis neonatal, y las pruebas para toxoplasma, rubéola, citomegalovirus y virus del herpes simple (TORCH); virus de hepatitis; y Treponema pallidum fueron negativas. El examen físico de admisión reveló un estado mental deficiente, disminución del tono muscular en las extremidades y reflejo pupilar lento a la luz. Todos los demás hallazgos fueron normales. El ultrasonido craneal y electroencefalograma de cabecera revelaron hemorragia intracraneal grave y bajo voltaje, respectivamente. Los hallazgos del ecocardiograma sugirieron un conducto arterioso patente, foramen oval permeable e hipertensión pulmonar. El ultrasonido abdominal indicó hemorragia gastrointestinal. A pesar de todos los esfuerzos, la paciente falleció el tercer día de vida debido a falla multiorgánica y hemorragia intracraneal masiva (la información detallada se puede encontrar en el Informe Suplementario).\n\nLos padres de la paciente no eran consanguíneos y ambos tenían talasemia. La madre, que compartía el mismo tipo de sangre que la paciente, tuvo una anemia leve durante el embarazo (nivel de hemoglobina de 97 g/L) y un historial de aborto inducido. Los exámenes prenatales no mostraron anomalías, ni tampoco hidrops fetal, y no recibió ninguna medicación durante el embarazo que pudiera provocar una enfermedad hemorrágica de inicio temprano en el recién nacido. La paciente también tenía un hermano de 1 año que gozaba de buena salud. Su abuelo tenía un historial de anemia leve (detalles desconocidos).\n\nSe obtuvo el consentimiento informado de los padres del paciente y se realizó un secuenciamiento de Sanger para descubrir la causa de la enfermedad. Se detectó una nueva mutación de MECOM de desplazamiento de marco heterocigótica [NM_001105078: c.157_158del (p.Met53Glyfs*2)] en el probando. Esta variante cambió el aminoácido 53 de metionina (codón ATG) a glicina (codón GGT), seguido de una terminación temprana. La mutación no se encontró en los padres o en el hermano mayor. La variante se clasificó como patogénica según las directrices del Colegio Americano de Genética Médica (ACMG) [14]. El algoritmo “AutoPVS1” brindó un fuerte apoyo para la interpretación de PVS1 de p.Met53Glyfs*2, lo que indica patogenicidad. La variante no se ha informado previamente en la Base de Datos de Mutación Genética Humana (HGMD) o en Clinvar. El análisis de conservación mostró que el residuo Met53 está altamente conservado en todas las especies de mamíferos (incluidos humanos, ratones, ratas, chimpancés y bovinos) utilizando Clustal Omega. Se generaron modelos de estructura de proteínas tridimensionales de las proteínas MECOM de tipo salvaje y mutantes utilizando SWISS-MODEL, lo que indica que la mutación de desplazamiento de marco causó una terminación temprana de la síntesis de aminoácidos, alterando significativamente la estructura de la proteína.\n",
+        "gold_summary": "Reportamos el caso de una neonata Han china de 0 días de vida que presentó trombocitopenia grave y hemorragia intracraneal, y que finalmente falleció por fallo multiorgánico e intracraneal el tercer día después del nacimiento. La secuenciación genética identificó una variante de cambio de marco heterocigótica, c.157_158del, dentro del gen MECOM. Esta variante condujo a una sustitución del 53.º aminoácido de metionina a glicina, terminando en el 54.º aminoácido. Una revisión exhaustiva de la literatura indicó que las mutaciones del gen MECOM incluían mutaciones sin sentido (68.3%), deleción (8.5%), sitio de empalme (8.5%), cambio de marco (7.3%) y sin sentido (7.3%). Las pacientes con mutaciones sin sentido frecuentemente presentaban sinostosis radiocubital, mientras que el fallo de la médula ósea se asociaba más comúnmente con los otros cuatro tipos de mutaciones.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Esta es la historia de una bebé que nació muy débil a las pocas semanas de embarazo.  \nAl nacer estaba muy pálida, tenía moretones por todo el cuerpo y sangraba. También tenía problemas para respirar y necesitó ayuda con un tubo y una máquina para respirar.\n\nLos médicos encontraron que tenía muy pocas plaquetas. Las plaquetas son pequeñas partes de la sangre que ayudan a detener el sangrado. También tenía pocos glóbulos rojos, que llevan el oxígeno por el cuerpo. A pesar de recibir transfusiones y medicinas, la bebé sufrió una hemorragia grande en el cerebro y fallaron varios órganos. Murió al tercer día de vida. Esto fue muy triste para la familia y para el equipo médico.\n\nBuscaron la causa y no encontraron infección. Hicieron un estudio del ADN y hallaron un cambio nuevo en un gen llamado MECOM. Un gen es como una instrucción que le dice al cuerpo cómo funcionar. Ese cambio hizo que las instrucciones no funcionaran bien. Por eso su cuerpo no pudo producir bien las células de la sangre y no pudo parar las hemorragias.  \nEl cambio no estaba en la mamá, el papá ni en su hermano, así que apareció por primera vez en ella.\n\nLos médicos creen que este tipo de cambios en el gen MECOM puede causar problemas graves en la médula ósea y en la sangre. Lamentamos mucho la pérdida de la bebé.",
+                "fh_score": 81.62
+            },
+            "B2": {
+                "text": "Summary (clear, age 11–17 level)\n\nThis report describes a newborn baby girl of Han Chinese background who was born at 36 weeks by emergency cesarean because of fetal distress. Soon after birth she looked very pale, had bruises and bleeding from her mouth and from IV sites, and had trouble breathing. Blood tests showed very low red blood cells, very low white blood cells, and a critically low number of platelets (platelets are the blood cells that help stop bleeding). scans showed a large bleed inside her brain. Despite breathing support, many blood transfusions, and other intensive care treatments, she died on the third day of life from multiple organ failure and massive brain bleeding.\n\nDoctors tested for infections and other common causes of newborn bleeding; these were negative. Her lab tests also showed disseminated intravascular coagulation (DIC) — a serious condition where the clotting system becomes overactive and then fails, causing both dangerous clots and severe bleeding. An ultrasound of her belly showed bleeding in the gut, and an ultrasound of the heart showed small birth-related openings and high pressure in the lung blood vessels.\n\nGenetic testing (Sanger sequencing) found a new, harmful change in one copy of the gene called MECOM. This change is a small deletion (called c.157_158del) that shifts the gene’s “reading frame” so the protein is cut off very early (written p.Met53Glyfs*2). Because the change causes early termination of the protein, it is predicted to stop the protein from working properly. The same mutation was not found in either parent or her older brother, so it likely happened for the first time in this baby (a de novo mutation). Computer analyses showed the affected part of the protein is conserved in mammals and that the mutation severely alters the protein’s 3D structure. Using standard clinical guidelines, the change was classified as pathogenic (disease-causing).\n\nPutting this case in context, other reports of MECOM mutations show several types of changes: most are nonsense mutations (which also make a short, nonworking protein), and others include deletions, splice-site changes, frameshifts, and missense changes (which swap one amino acid for another). People with nonsense mutations often have bone and limb findings such as radioulnar synostosis (fusion of forearm bones), while bone marrow failure and very low blood counts are more commonly seen with the other mutation types.\n\nWhy this matters (kind note)\nThis baby’s illness was caused by a new harmful change in MECOM that led to rapid bone marrow failure and life‑threatening bleeding. Reporting new mutations helps doctors recognize similar cases sooner, offer genetic counseling to families, and improve understanding of how MECOM variants lead to disease. I’m sorry for this tragic outcome; the information may help prevent or better treat future cases.",
+                "fh_score": 82.32
+            },
+            "B3": {
+                "text": "Summary\n\nThis report describes a full-term–near (36 weeks) Han Chinese neonate who presented at birth with severe bleeding and bone‑marrow failure and died on day 3 of life from multiorgan failure and massive intracranial hemorrhage. The case was caused by a de novo, heterozygous frameshift mutation in the MECOM gene (c.157_158del; p.Met53Glyfs*2), classified as pathogenic.\n\nClinical course and key findings\n- Delivery and immediate condition: emergency cesarean for fetal distress; Apgar scores 6 and 5. The newborn was pale with widespread bruising, mucosal bleeding, respiratory failure, and active bleeding from venipuncture sites.  \n- Hematology at birth and early life: umbilical arterial gas analysis showed extremely low hematocrit and hemoglobin; after transfusion the neonate had severe thrombocytopenia (platelets 12 × 10^9/L), marked anemia (hemoglobin 46 g/L), and leukopenia (WBC 1.11 × 10^9/L). Reticulocyte proportion 1.5%; direct Coombs test negative.  \n- Coagulopathy and organ involvement: diagnosed with disseminated intravascular coagulation (prolonged PT/TTPA, low fibrinogen, D‑dimer >20 mg/L). Cranial ultrasound and EEG showed major intracranial hemorrhage and low-voltage activity. Echocardiography revealed patent ductus arteriosus, patent foramen ovale, and pulmonary hypertension. Abdominal ultrasound suggested gastrointestinal bleeding. The patient required intubation, mechanical ventilation, blood product support (RBCs, plasma, platelets), antibiotics, inotropes and vasopressors, and correction of acidosis. Bone marrow aspiration was not performed because the infant was clinically unstable. Despite aggressive support, the infant died on day 3.\n\nInvestigations for cause\n- Infectious and metabolic workup was negative: cultures/markers for neonatal sepsis, TORCH infections, hepatitis viruses and syphilis were negative.  \n- Family history: parents nonconsanguineous; both reported to have thalassemia (mother had mild antenatal anemia). An older sibling is well. The MECOM variant was not detected in either parent or the sibling, indicating a de novo mutation.\n\nGenetic result and interpretation\n- A novel heterozygous frameshift deletion in MECOM (c.157_158del, p.Met53Glyfs*2) was identified by Sanger sequencing. The change introduces a premature stop codon soon after residue 53. The altered residue (Met53) is highly conserved across mammals. In silico structural modeling predicted major disruption of the MECOM protein. The variant was classified pathogenic under ACMG criteria with strong PVS1 support and is not reported in public mutation databases.\n\nClinical implications and recommended next steps\n- MECOM encodes transcriptional regulators (including EVI1) required for normal hematopoiesis. Pathogenic MECOM variants are a recognized cause of congenital bone‑marrow failure syndromes, often presenting as severe thrombocytopenia and risk of life‑threatening bleeding in the neonatal period. Some variant types are also associated with skeletal anomalies (for example, radioulnar synostosis) though findings are variable.  \n- For the family: this appears to be a de novo event, so recurrence risk for future pregnancies is low but not zero (gonadal mosaicism is possible). Genetic counseling is indicated. Options to discuss include targeted prenatal testing or preimplantation testing in future pregnancies.  \n- For clinicians: in suspected neonatal bone‑marrow failure, early genetic testing can clarify diagnosis and guide planning (for example, timing of hematopoietic stem cell transplant for survivors). When infants survive initial instability, hematology referral and consideration of definitive therapy (HSCT) may be necessary. Reporting novel pathogenic variants to databases and considering autopsy or postmortem genetic/hematopathology when feasible can improve knowledge for future cases.\n\nThe case underscores how a de novo MECOM loss‑of‑function variant can produce catastrophic neonatal marrow failure and bleeding despite intensive supportive care. Condolences to the family for this tragic outcome.",
+                "fh_score": 63.46
+            }
+        }
+    },
+    {
+        "article": "La paciente es una mujer de 74 años de edad, físicamente activa, que practica senderismo y equitación. Un mes después del tratamiento con inyección de cortisona de la tendinopatía insercional de Aquiles, sufrió una rotura total del tendón de Aquiles insercional al intentar dar un paso mientras montaba en bicicleta. Esta rotura se trató de forma conservadora con una bota de Walker durante 8 semanas. Después, mientras montaba a caballo, un intento de dar un paso provocó una nueva rotura total del tendón de Aquiles en la inserción. La rotura se trató quirúrgicamente con reinserción del tendón de Aquiles en el calcáneo, utilizando anclajes de sutura. Esto fue seguido por inmovilización en un yeso. Después de la operación, la paciente sufrió una infección profunda que no respondía a los antibióticos, signos de sepsis, y se indicó exploración quirúrgica. Durante la cirugía, se encontró que todo el tendón de Aquiles estaba gravemente afectado por la infección, más o menos destruido, y hubo que retirar el tendón de Aquiles distal de 7 cm (todo el tendón libre de Aquiles). Esto dejó una gran herida sin tejido tendinoso, y la piel se suturó sobre la herida. Después de este procedimiento, la inmovilización y el tratamiento con antibióticos de cloxacilina curaron la infección y la herida se curó adecuadamente. El pie se inmovilizó en un yeso durante las primeras 10 semanas, desde la máxima flexión plantar inicialmente, y luego la flexión plantar disminuyó gradualmente hasta alcanzar la posición neutra. Esto fue seguido por inmovilización en un yeso dorsal, evitando la extensión del tendón de Aquiles en flexión plantar, durante otros 3 meses. Se le dijo que aumentara gradualmente la carga al caminar, pero que evitara la extensión durante un total de 6 meses. Después de 6 meses se le ofreció reconstrucción quirúrgica con un injerto de flexor hallucis longus, pero como entonces tenía una función satisfactoria, decidió esperar y ver. Su función mejoró gradualmente, y un año después de la operación, cuando buscó ayuda por el dolor en el otro tendón de Aquiles, se notó la buena función en el lado operado. La exploración por ultrasonido mostró sorprendentemente un tendón que se parecía mucho a un tendón de Aquiles ligeramente tendinopático.\n",
+        "gold_summary": "Esta señora de 74 años padecía tendinopatía insercional de Aquiles. Después del tratamiento con una inyección local de cortisona, sufrió una rotura total del tendón de Aquiles insercional. Esta rotura se trató de forma conservadora y, después del tratamiento, el tendón de Aquiles volvió a romperse en la zona de inserción. La rotura se trató entonces con reinserción en la zona de inserción calcánea. Al poco tiempo del postoperatorio, la paciente sufrió una infección de herida quirúrgica profunda y sepsis. Debido al pobre efecto del tratamiento con antibióticos y a la destrucción total del tendón, se extirpó todo el tendón de Aquiles. Después de la extirpación, se inmovilizó en un yeso, seguido de movilización y aumento gradual de la carga. En un seguimiento de un año, la paciente caminaba sin cojera, podía levantar el talón hasta la mitad mientras estaba de pie sobre una pierna, había un tendón de Aquiles palpable y el escaneado por ultrasonido mostró una estructura muy similar a un tendón de Aquiles tendinopático y ligeramente engrosado. Había una regeneración evidente de todo el tendón de Aquiles y la función del tendón era sorprendentemente buena.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había una señora de 74 años que hacía ejercicio y montaba a caballo. Tenía dolor en el lugar donde el tendón de Aquiles se une al talón. El tendón de Aquiles es una cuerda fuerte detrás del tobillo que ayuda a caminar y saltar.\n\nLe pusieron una inyección para el dolor. Un mes después, al dar un paso en la bicicleta, el tendón se rompió por completo. La trataron con una bota especial durante ocho semanas. Más tarde, al montar a caballo, el tendón volvió a romperse en el mismo sitio. Entonces le hicieron una operación para volver a fijar el tendón al hueso del talón.\n\nDespués de la operación, la herida se infectó. La infección fue grave y no mejoró con antibióticos. Los médicos tuvieron que quitar todo el tendón de Aquiles que estaba dañado. Cerraron la piel sobre la herida y siguieron con antibióticos y yesos hasta que la infección sanó.\n\nLa pierna estuvo inmovilizada muchos meses. Poco a poco la mujer empezó a apoyar el pie y caminar de nuevo. Le ofrecieron otra operación para reconstruir el tendón, pero ella tenía suficiente función y decidió esperar.\n\nUn año después caminaba sin cojear. Podía subir el talón a la mitad estando en una pierna. La ecografía (una imagen con sonido) mostró algo que se parecía mucho a un tendón, aunque algo engrosado. Fue sorprendente ver que se formó tejido parecido al tendón y que la función del pie era buena después de tanto problema.",
+                "fh_score": 78.76
+            },
+            "B2": {
+                "text": "Resumen comprensible (nivel B2, pensado para lectores de 11–17 años)\n\nUna mujer activa de 74 años, que practica senderismo y monta a caballo, tenía una tendinopatía insercional del tendón de Aquiles (es decir, dolor y daño en la parte donde el tendón se une al hueso del talón). Recibió una inyección local de cortisona (un antiinflamatorio) y, un mes después, sufrió una rotura completa del tendón de Aquiles en la inserción al intentar dar un paso. Esa primera rotura se trató de forma conservadora con una bota de apoyo durante 8 semanas. Más tarde, al montar a caballo, volvió a romperse el tendón en la misma zona. Entonces se operó para reinsertar el tendón en el hueso del talón usando anclajes de sutura.\n\nPoco después de la operación apareció una infección profunda de la herida y signos de sepsis (una infección grave que afecta a todo el cuerpo). Como los antibióticos no controlaron bien la infección, fue necesaria una nueva cirugía. En esa intervención se halló que casi todo el tendón había quedado destruido por la infección, por lo que se retiró por completo el segmento distal libre del tendón (unos 7 cm). La herida se cerró y, con antibióticos (cloxacilina) y reposo en yeso, la infección sanó.\n\nEl pie se inmovilizó durante muchos meses para proteger la zona: primero 10 semanas en una posición con el pie apuntando hacia abajo (flexión plantar), y después se fue llevando poco a poco a posición neutra; más tarde se usó un yeso que impedía estirar el tendón otros 3 meses. En total se le indicó evitar la extensión del tendón durante 6 meses y aumentar la carga al caminar de forma gradual. A los 6 meses le ofrecieron reconstruir el tendón con un injerto del músculo flexor largo del dedo gordo del pie (es una operación que usa otro tendón para reemplazar el que falta), pero como su función ya era aceptable, ella prefirió esperar.\n\nA los 12 meses del último tratamiento estaba caminando sin cojear, podía levantarse sobre una pierna y elevar el talón hasta la mitad, y se notaba un tendón al palpar. La ecografía mostró una estructura sorprendentemente parecida a un tendón de Aquiles algo tendinopático y engrosado, lo que indica que hubo una regeneración importante del tendón y que su función final fue mejor de lo esperado.\n\nComentario final suave: aunque la paciente pasó por complicaciones serias (roturas repetidas e infección que obligó a retirar el tendón), con cirugía, antibióticos y una reeducación lenta, consiguió recuperar una función sorprendentemente buena. Se le ofreció una reconstrucción adicional, pero decidió esperar porque su capacidad para caminar y ponerse de puntillas era satisfactoria.",
+                "fh_score": 56.43
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel lector universitario)\n\nPaciente: mujer de 74 años, físicamente activa (senderismo y equitación).\n\nAntecedente inicial\n- Tenía tendinopatía insercional del tendón de Aquiles (dolor y degeneración en la zona donde el tendón se une al hueso del talón).\n- Recibió una inyección local de cortisona para esa tendinopatía.\n\nEpisodios posteriores y tratamientos\n1. Primer evento (1 mes después de la inyección): rotura total del tendón de Aquiles en la inserción al intentar dar un paso. Tratamiento inicial conservador: bota tipo “walker” durante 8 semanas.\n2. Recaída: meses después, al montar a caballo, volvió a romperse el tendón en la misma zona. Se realizó una reinserción quirúrgica en el calcáneo con anclajes de sutura.\n3. Complicación postoperatoria grave: desarrolló infección profunda de la herida y signos de sepsis que no respondieron bien a antibióticos. En la exploración quirúrgica se observó que el tendón estaba gravemente destruido; se retiró la porción distal afectada (unos 7 cm, es decir, la totalidad del “tendón libre” distal).\n4. Manejo de la infección y rehabilitación inicial: cierre de la piel sobre la herida, tratamiento con cloxacilina y prolongada inmovilización en yeso: primero en máxima flexión plantar y progresivamente hacia neutro durante ~10 semanas, seguido de un yeso dorsal que evitaba la extensión durante alrededor de 3 meses más. Se indicó aumento gradual de carga al caminar y evitar la extensión forzada del tobillo durante unos 6 meses en total.\n5. Oferta de reconstrucción: a los 6 meses se ofreció reconstrucción mediante trasferencia de tendón flexor hallucis longus (FHL), pero la paciente tenía función satisfactoria y prefirió esperar.\n\nEvolución y hallazgos al año\n- A 1 año, la paciente caminaba sin cojear y podía levantar el talón hasta la mitad en apoyo monopodal (prueba funcional útil para valorar la fuerza del tríceps sural).\n- A la palpación había una estructura en la región posterior del tobillo que se asemejaba a un tendón.\n- Ecografía: mostró una estructura muy parecida a un tendón de Aquiles con cambios compatibles con tendinopatía leve y engrosamiento.\n- Conclusión clínica: hubo regeneración o reemplazo por tejido que aporta función tendinosa suficiente; la recuperación funcional fue sorprendentemente buena pese a la extirpación completa del tendón libre distal.\n\nPuntos importantes y consideraciones\n- Riesgos asociados: la inyección local de cortisona en tendones insercionales puede debilitar tejido y aumentar el riesgo de rotura; la cirugía de reinserción tiene riesgo de infección profunda, la cual puede requerir desbridamiento extenso e incluso pérdida del tendón.\n- Recuperación sin reconstrucción: en este caso, a pesar de la extirpación del tendón, la paciente obtuvo una recuperación funcional satisfactoria sin injerto reconstructivo; esto sugiere que, en algunos pacientes, la cicatrización y remodelado pueden restaurar función suficiente.\n- Seguimiento y opciones futuras: si apareciese debilidad funcional persistente o dolor incapacitante, la reconstrucción con transferencia tendinosa (por ejemplo FHL) sigue siendo una opción razonable. La rehabilitación progresiva y ejercicios de fortalecimiento son claves para optimizar la función.\n- Prevención y alerta temprana: ante signos de infección postoperatoria (fiebre, enrojecimiento intenso, dolor creciente, secreción) se debe actuar rápido: cultivo, antibióticos dirigidos y, si es necesario, limpieza quirúrgica.\n\nTono y mensaje final\nEsta paciente vivió complicaciones graves (roturas recurrentes e infección con pérdida del tendón), pero con manejo quirúrgico/agresivo de la infección, inmovilización adecuada y rehabilitación coherente consiguió una recuperación funcional notable a un año. El caso recuerda la necesidad de evaluar riesgos y beneficios de inyecciones de cortisona en tendones, la vigilancia estrecha tras cirugía y la posibilidad de resultados funcionales aceptables incluso después de pérdidas anatómicas importantes.",
+                "fh_score": 44.82
+            }
+        }
+    },
+    {
+        "article": "Una mujer de 47 años con antecedentes de CHB congénita se presentó con quejas de dolor en el cuello del lado izquierdo y dolor en el oído izquierdo. Aproximadamente 30 meses antes de la presentación, la paciente había notado una pequeña masa en el lado izquierdo de su cuello, que había aumentado gradualmente de tamaño. El dolor se localizó inicialmente en la región del cuello, pero se intensificó con el tiempo y se extendió al área del oído izquierdo.\nInicialmente, debido al dolor en el oído izquierdo, el paciente consultó a varios otorrinolaringólogos y fue tratado por un diagnóstico preliminar de otitis media. Sin embargo, a pesar de los tratamientos, el dolor persistió. Finalmente, un otorrinolaringólogo derivó al paciente para una ecografía, que reveló una masa en el lado izquierdo del cuello, lo que llevó a una derivación quirúrgica. Después de las evaluaciones iniciales, se solicitó una angiografía por TC, que reveló una masa de forma ovalada que medía 30 por 50 mm en la bifurcación de la arteria carótida izquierda, lo que sugiere un CBT tipo II de Shamblin.\n\nEvaluaciones cardiovasculares preoperatorias\nDada la historia del paciente de CHB congénita, se realizó una evaluación cardiovascular preoperatoria exhaustiva. Esto incluyó un electrocardiograma (ECG) de 12 derivaciones, que confirmó la presencia de CHB con un ritmo de escape ventricular estable. Se realizó una ecocardiografía transtorácica para evaluar la estructura y función cardiaca, revelando una función sistólica ventricular normal sin evidencia de anormalidades estructurales. Además, se obtuvo una consulta de cardiología para evaluar la aptitud del paciente para la cirugía y optimizar el manejo perioperatorio.\n\nConsideraciones anestésicas\nDebido a la CHB congénita del paciente y al potencial de inestabilidad hemodinámica durante la cirugía, se formuló un plan anestésico detallado. El paciente fue clasificado como estado físico III de la Sociedad Estadounidense de Anestesiología (ASA). Preoperativamente, se le colocó un marcapasos externo temporal para garantizar un control adecuado de la frecuencia cardíaca y se le insertó un catéter arterial para el monitoreo continuo de la presión arterial. La inducción de la anestesia se realizó utilizando una combinación de etomidato (0,3 mg/kg) y fentanilo (2 μg/kg) para minimizar las fluctuaciones hemodinámicas. El mantenimiento se logró con sevoflurano (1-2 %) y rocuronio (0,6 mg/kg) para la relajación muscular. Los parámetros hemodinámicos, incluida la frecuencia cardíaca, la presión arterial y la saturación de oxígeno, se controlaron de forma continua. Además, se le colocó un catéter venoso central para monitorear la presión venosa central y administrar medicamentos vasoactivos si fuera necesario. El equipo de anestesia mantuvo una comunicación estrecha con el equipo quirúrgico para abordar de forma inmediata cualquier cambio hemodinámico intraoperatorio.\n\nEnfoque quirúrgico\nEl paciente fue sometido a cirugía el 19 de mayo de 2024, después de la localización precisa de la TCC mediante angiografía por TC. El enfoque quirúrgico se eligió en base a la clasificación de Shamblin tipo II, que indica un encasamiento parcial de las arterias carótidas. Dada la proximidad del tumor a estructuras neurovasculares críticas, incluidos los nervios vago e hipogloso, se consideró que el enfoque quirúrgico abierto era el más apropiado para garantizar una resección completa y minimizar las complicaciones.\nTras la inducción de la anestesia general, se colocó al paciente en posición supina con el cuello extendido y rotado hacia la derecha. Se realizó una incisión oblicua paralela al músculo esternocleidomastoideo izquierdo, que se extendía desde la apófisis mastoidea hasta la escotadura esternal. Tras la incisión de la piel y la disección del platisma, se expuso con cuidado la vaina carotídea. Se identificaron la arteria carótida común y su bifurcación en las arterias carótidas internas y externas. Se observó el tumor, de 30 × 50 mm, en la bifurcación carotídea y se diseccionó con cuidado de los tejidos circundantes.\n\nManobras y precauciones específicas\n1.\nSe aplicaron pinzas vasculares temporales en las arterias carótidas internas y externas para controlar el flujo sanguíneo durante la disección del tumor. Esto minimizó el sangrado y proporcionó un campo quirúrgico despejado.\n2.\nSe utilizó neuromonitorización intraoperativa para evaluar la integridad de los nervios vago e hipogloso. La retroalimentación continua garantizó que las estructuras neurales se preservaran durante la disección.\n3.\nEl tumor se separó cuidadosamente de las arterias carótidas y las estructuras neurales circundantes, mediante una combinación de disección aguda y roma. Se logró la hemostasis mediante cauterización bipolar y pinzas quirúrgicas para minimizar el sangrado.\n4.\nEl marcapasos externo se monitoreó activamente durante todo el procedimiento para garantizar un ritmo cardíaco estable. El equipo de anestesia estaba preparado para administrar atropina o epinefrina si se producía una bradicardia o hipotensión significativas.\n2.5. Manejo postoperatorio\nTras asegurarse de que no había hemorragia activa y restablecer el flujo sanguíneo, se devolvieron los tejidos a su posición original y se cerró la herida en múltiples capas. Se aplicó un vendaje apropiado. La cirugía se completó sin complicaciones y con un sangrado mínimo en 2 h y 10 min. El paciente fue trasladado a la UCI vascular para una estrecha monitorización.\nDespués de la operación, se controló al paciente en la UCI durante 24 horas y, más tarde, se le trasladó a la planta general tras mejorar su estado clínico. El marcapasos externo se retiró el día 1 después de la operación, ya que el paciente mantenía un ritmo de escape ventricular estable. El paciente fue dado de alta en buenas condiciones generales el día 3 después de la operación, sin quejas específicas.\n2.6. Seguimiento y resultados a largo plazo\nEl examen histopatológico confirmó el diagnóstico definitivo de TCC en la paciente. Se realizaron evaluaciones de seguimiento a las 2 semanas, 1 mes, 6 meses y 1 año posteriores a la cirugía para evaluar los resultados quirúrgicos y cardíacos. En cada visita, la paciente se sometió a un ECG de 12 derivaciones para monitorear el CHB congénito, que permaneció sin cambios durante todo el período de seguimiento. Se repitió la ecocardiografía transtorácica a los 6 meses y un año, sin deterioro de la función cardíaca y con una función sistólica ventricular estable.\n\nPara evaluar el impacto de la extirpación del tumor en la función cardiaca, se realizó un análisis de la variabilidad de la frecuencia cardiaca (VFC) antes de la operación y a los 6 meses después de la misma. El análisis de la VFC antes de la operación demostró una reducción de la actividad parasimpática, probablemente debido a la compresión del nervio vago por el tumor. El análisis de la VFC después de la operación mostró una mejora significativa del tono parasimpático, lo que sugiere que la extirpación del tumor alivió la compresión del nervio vago y restauró la función autónoma normal.\nAsimismo, el paciente manifestó que el dolor en el cuello y en el oído había desaparecido por completo después de la cirugía, sin que se produjera una reaparición de los síntomas durante el período de seguimiento. Se realizaron estudios de imagen, que incluyeron ultrasonido Doppler y angiografía por TAC, a los 6 meses y al año, que no mostraron evidencia de reaparición del tumor o complicaciones vasculares.\n",
+        "gold_summary": "Describimos el caso de una mujer de 47 años con antecedentes de dolor en el cuello izquierdo y en el oído, acompañado por una masa en el cuello que había ido aumentando gradualmente durante 2,5 años. Después de las evaluaciones iniciales y de múltiples diagnósticos diferenciales, la angiografía por TC reveló una masa ovalada de 30 × 50 mm en la bifurcación carotídea izquierda, lo que confirmó un CCT tipo II de Shamblin. Las evaluaciones preoperatorias demostraron CHB congénita en el electrocardiograma y la ecocardiografía. La paciente se sometió a una resección completa del tumor con todas las precauciones necesarias, incluida la colocación temporal de un marcapasos y un cuidadoso seguimiento.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había una mujer de 47 años que tenía una bola en el lado izquierdo del cuello. La bola creció poco a poco por unos 2 años y medio. También le dolía el cuello y el oído izquierdo. Al principio pensaron que era una infección del oído, pero los tratamientos no ayudaron.\n\nUnos médicos le hicieron una ecografía y una angiografía por TAC. Vieron una masa de 3 x 5 cm en la división de la arteria del cuello. Los médicos dijeron que era un tumor llamado cuerpo carotídeo (un tipo de tumor cerca de la arteria). Estaba muy cerca de nervios y vasos importantes.\n\nAntes de la operación, revisaron su corazón. Ella tenía un bloqueo cardíaco desde que nació. Esto significa que el corazón late con un ritmo diferente, pero su función estaba bien. Los cardiólogos ayudaron a preparar todo para la cirugía.\n\nPara la operación, los médicos pusieron un marcapasos temporal por fuera para cuidar el latido del corazón. Durante la cirugía cuidaron mucho las arterias y los nervios. Usaron monitoreo para ver los nervios en tiempo real. Quitaron el tumor con cuidado. La operación duró unas 2 horas y 10 minutos y hubo poco sangrado.\n\nDespués de la operación, la mujer estuvo en la unidad de cuidados intensivos 24 horas. El marcapasos temporal se retiró al día siguiente porque su ritmo era estable. Ella salió del hospital al tercer día en buen estado.\n\nEl estudio del tumor confirmó el diagnóstico. En las visitas de control a las 2 semanas, 1 mes, 6 meses y 1 año, estaba bien. El dolor del cuello y del oído desapareció. El bloqueo del corazón no empeoró y la función del corazón se mantuvo normal. Pruebas mostraron que un nervio que estaba comprimido por el tumor mejoró después de quitarlo. No hubo señal de que el tumor volviera.",
+                "fh_score": 80.78
+            },
+            "B2": {
+                "text": "Resumen comprensible y atento\n\nPresentamos el caso de una mujer de 47 años que notó una pequeña masa en el lado izquierdo del cuello que creció durante unos 30 meses y acabó causando dolor en el cuello y en el oído izquierdo. Al principio fue tratada como una otitis (infección del oído), pero el dolor no cedió. Una ecografía y luego una angiografía por TC mostraron una masa ovalada de 30 × 50 mm en la bifurcación de la arteria carótida izquierda. Esto fue diagnosticado como un tumor del cuerpo carotídeo (también llamado paraganglioma o CBT) tipo II de Shamblin, lo que significa que el tumor rodeaba parcialmente las arterias carótidas.\n\nAntecedentes cardíacos y preparaciones\nLa paciente tenía un bloqueo cardíaco completo congénito (CHB). Esto es un problema del ritmo del corazón en el que las señales eléctricas entre las partes superiores e inferiores del corazón no pasan con normalidad; la paciente tenía un “ritmo de escape” ventricular estable que mantenía el latido, pero requería precaución. Antes de la operación se hicieron un ECG y una ecocardiografía: la función de bombeo del corazón era normal. Un equipo de cardiología revisó al caso para asegurar que la paciente era apta para la cirugía y para planear cuidados especiales.\n\nCuidados durante la anestesia y la cirugía\nPor seguridad se colocó un marcapasos externo temporal y un catéter arterial para monitorizar la presión arterial constantemente. La anestesia fue cuidadosamente elegida para evitar cambios bruscos en la presión o la frecuencia cardíaca; también se colocó un catéter venoso central por si era necesario dar medicación para el corazón. Se mantuvo comunicación estrecha entre anestesiólogos y cirujanos durante todo el procedimiento.\n\nLa cirugía se realizó por vía abierta (incisión en el lado izquierdo del cuello) debido a la cercanía del tumor a vasos y nervios importantes. Se usaron pinzas vasculares temporales para controlar el sangrado y monitorización neurológica intraoperatoria para proteger nervios importantes como el vago (que ayuda a controlar funciones como la frecuencia cardíaca) y el hipogloso (que mueve la lengua). La operación duró 2 horas y 10 minutos, con sangrado mínimo, y se completó sin complicaciones.\n\nRecuperación y controles\nLa paciente pasó 24 horas en la UCI vascular y luego fue a planta. El marcapasos externo se retiró al día 1 porque el ritmo de escape ventricular siguió siendo estable. Fue dada de alta al tercer día en buen estado y sin dolor en cuello ni oído. El examen de laboratorio confirmó que la masa era un tumor del cuerpo carotídeo.\n\nA largo plazo se hicieron seguimientos a las 2 semanas, 1 mes, 6 meses y 1 año. El bloqueo cardíaco congénito no empeoró y la función del corazón se mantuvo estable en ecocardiografías repetidas. Además, antes de la operación el análisis de la variabilidad de la frecuencia cardíaca (una forma de medir el balance del sistema nervioso que controla el corazón) mostró menos actividad del sistema parasimpático, probablemente porque el tumor comprimía el nervio vago. Se observó una mejora en esa medida a los 6 meses tras la extirpación, lo que sugiere que quitar el tumor alivió la compresión nerviosa. Las imágenes de control (Doppler y angiografía por TC) a los 6 meses y 1 año no mostraron recurrencia del tumor ni problemas vasculares.\n\nConclusión práctica\nEste caso muestra que, incluso con un bloqueo cardíaco congénito, una planificación cuidadosa (marcapasos temporal, monitorización intensiva y comunicación entre equipos) permite realizar con seguridad la resección de un tumor carotídeo. La paciente se recuperó bien, el dolor desapareció y las pruebas mostraron mejora en la función nerviosa relacionada con el corazón y ausencia de recurrencia tumoral en el primer año.",
+                "fh_score": 53.95
+            },
+            "B3": {
+                "text": "Resumen clínico (lenguaje dirigido a lector universitario)\n\nPresentación y diagnóstico\n- Paciente: mujer de 47 años con bloqueo auriculoventricular completo (CHB) congénito.\n- Síntomas: masa progresiva en el lado izquierdo del cuello por ~30 meses, dolor cervical izquierdo y otalgia (dolor de oído) que no respondieron a tratamientos para otitis media.\n- Estudios de imagen: angiografía por tomografía computarizada (angio‑TAC) mostró una masa ovalada de 30 × 50 mm en la bifurcación de la arteria carótida izquierda, compatible con tumor del cuerpo carotídeo (TCC, paraganglioma) Shamblin tipo II (encasamiento parcial de las carótidas).\n\nEvaluación preoperatoria y consideraciones cardíacas\n- ECG de 12 derivaciones confirmó CHB con ritmo de escape ventricular estable (hallazgo anormal, pero hemodinámicamente tolerado).\n- Ecocardiograma transtorácico: función sistólica ventricular normal (hallazgo normal).\n- Consulta cardiológica para valorar aptitud para cirugía y planificar manejo perioperatorio.\n\nPlan anestésico y medidas de seguridad\n- Clasificada ASA III por su cardiopatía.\n- Se colocó un marcapasos externo temporal y un catéter arterial para monitorización continua; además se insertó catéter venoso central.\n- Inducción con etomidato y fentanilo para minimizar cambios hemodinámicos; mantenimiento con sevoflurano y rocuronio.\n- Monitorización continua de ritmo, presión arterial y saturación; preparación para tratamiento rápido de bradicardia o hipotensión.\n\nCirugía y técnicas intraoperatorias\n- Fecha: 19 de mayo de 2024. Enfoque abierto por la localización y relación del tumor con estructuras neurovasculares (vago e hipogloso).\n- Incisión paralela al esternocleidomastoideo izquierdo; exposición de la bifurcación carotídea y disección cuidadosa del tumor.\n- Medidas específicas: clampaje temporal de arterias carótidas interna y externa para controlar flujo, neuromonitorización intraoperatoria de nervios craneales, disección combinada (aguda y roma), hemostasia con cauterio bipolar.\n- El marcapasos externo se monitorizó activamente durante todo el procedimiento.\n- Duración: 2 h 10 min; sangrado mínimo; resección completa sin complicaciones inmediatas.\n\nEvolución postoperatoria y seguimiento\n- Postoperatorio inmediato: vigilancia en UCI vascular 24 h; marcapasos externo retirado al día 1 porque persistía ritmo de escape ventricular estable.\n- Alta hospitalaria al día 3 en buenas condiciones y sin síntomas.\n- Anatomía patológica confirmó TCC.\n- Seguimiento a 2 semanas, 1 mes, 6 meses y 1 año: ECG mostró CHB sin cambios (estable); ecocardiogramas a 6 meses y 1 año sin deterioro de función ventricular.\n- Estudios de imagen (Doppler y angio‑TAC) a 6 meses y 1 año sin recidiva tumoral ni complicaciones vasculares.\n- Análisis de variabilidad de la frecuencia cardíaca: antes de la cirugía hubo disminución del tono parasimpático (probablemente por compresión del nervio vago por el tumor); a los 6 meses se observó mejoría significativa, lo que sugiere alivio de la compresión vagal tras la resección.\n- Síntomas (dolor cervical y otalgia) desaparecieron y no recurrieron durante el seguimiento.\n\nImplicaciones y puntos clave\n- El caso muestra que un TCC carotídeo mayor, parcialmente encasante (Shamblin II), puede producir síntomas vagales y afectar la regulación autonómica; su resección puede restaurar función parasimpática.\n- En pacientes con CHB congénito, la planificación perioperatoria cuidadosa (marcapasos temporal, monitorización invasiva, equipo coordinado) permitió una cirugía segura sin necesidad inmediata de marcapasos definitivo, dado el ritmo de escape estable.\n- Riesgos potenciales de este tipo de cirugía incluyen lesión de nervios craneales, sangrado, isquemia cerebral o necesidad de reconstrucción vascular; ninguno de estos ocurrió en este caso.\n- Recomendaciones prácticas: continuar con vigilancia cardiológica (evaluar necesidad de marcapasos permanente si el ritmo se vuelve inestable o aparecen síntomas) y con imágenes periódicas para detectar recidiva del paraganglioma.",
+                "fh_score": 33.07
+            }
+        }
+    },
+    {
+        "article": "Una mujer de 19 años de edad acudió al servicio de urgencias de nuestro hospital con una queja principal de dos días de historia de cefalea, acompañada de náuseas recurrentes, vómitos y fiebre de un día. En el ingreso, su examen físico reveló una fiebre alta de 39.1°C, presión arterial elevada de 189/120 mmHg y una frecuencia cardíaca de 148 latidos por minuto. Los resultados de laboratorio indicaron un recuento de glóbulos blancos elevado de 14.77×10^9/L y un recuento de neutrófilos de 13.55×10^9/L, lo que sugiere una posible infección o respuesta inflamatoria. Se administró un tratamiento empírico inicial con antibióticos debido a la sospecha de infección, pero sus síntomas persistieron. Dados sus signos vitales anormales, marcadores inflamatorios elevados y falta de mejora de los síntomas, la paciente fue admitida para una evaluación diagnóstica adicional y transferida a la unidad de cuidados intensivos para una estrecha monitorización. Un año antes, la paciente había presentado síntomas similares y se le diagnosticó miocarditis en un hospital local en base a los hallazgos clínicos en ese momento. Durante esa hospitalización, también se le diagnosticó hipertensión y se le prescribieron medicamentos antihipertensivos. Sin embargo, después del alta, la paciente no se adhirió al tratamiento antihipertensivo prescrito y no controló regularmente su presión arterial. Además, es notable que su padre tenía antecedentes de muerte súbita inexplicable.\n\nPara investigar la etiología subyacente de los síntomas del paciente, se realizó una tomografía computarizada (TC) de tórax. De forma incidental, esta exploración reveló una masa suprarrenal izquierda con densidad de tejido blando, que medía 43 mm × 36 mm. No se observaron hallazgos patológicos en las exploraciones de TC de cabeza y tórax. El electrocardiograma demostró taquicardia sinusal con un intervalo PR acortado y ondas P altas y puntiagudas en las derivaciones II, III y aVF. La ecocardiografía transtorácica no reveló ninguna anomalía significativa.\n\nEn el segundo día de ingreso, el paciente mostró niveles crecientes de péptido natriurético cerebral (BNP) y troponina I (TnI). El cardiólogo diagnosticó provisionalmente al paciente con miocarditis de etiología incierta, basándose en la presentación clínica, los biomarcadores cardiacos elevados (BNP y TnI) y los hallazgos del electrocardiograma de apoyo. Se inició el tratamiento con metilprednisolona (0,25 g diarios) para abordar la posible inflamación miocárdica debida a la sospecha de miocarditis. Se administraron furosemida (20 mg cada 12 horas) y espironolactona (20 mg cada 12 horas) como diuréticos para controlar la retención de líquidos y reducir la carga de trabajo cardiaco. Se prescribió perindopril amlodipina (10 mg: 5 mg diarios) como inhibidor de la enzima convertidora de la angiotensina y bloqueador del canal del calcio para controlar la presión arterial y reducir la poscarga. Se usó tartrato de metoprolol (25 mg cada 12 horas) para controlar la frecuencia cardiaca y disminuir la demanda de oxígeno miocárdico, mientras que se administró esmolol (0,2 g/hora por infusión intravenosa), un bloqueador beta de acción corta, para controlar la frecuencia cardiaca aguda adicional debido a la taquicardia sinusal. Debido a la preocupación por una posible infección, se agregó moxifloxacina como terapia antibiótica empírica.\n\nDada la presentación del paciente con una masa suprarrenal e hipertensión, el endocrinólogo recomendó una evaluación de la relación aldosterona/renina, cortisol plasmático, catecolaminas plasmáticas y catecolaminas urinarias de 24 horas, junto con sus metabolitos. En posición supina, los niveles de catecolaminas plasmáticas y urinarias estaban marcadamente elevados (Tabla 1), incluyendo dopamina plasmática a 524,5 pmol/L, norepinefrina a 83975 pmol/L y epinefrina a 10579,3 pmol/L. Además, los niveles urinarios de 24 horas mostraron adrenalina libre a 4368,89 nmol/24 horas, norepinefrina libre superior a 12697,60 nmol/24 horas, normetaneprina a 8312 nmol/24 horas, metaneprinas a 4078 nmol/24 horas y ácido vanilmandélico a 58,1 mg/24 horas. Estos hallazgos apoyaron un diagnóstico clínico de feocromocitoma. En el quinto día posterior al ingreso, se interrumpió la terapia glucocorticoide y se sustituyó perindopril amlodipina con terazosin para un control más dirigido de la presión arterial.\n\nUna tomografía computarizada abdominal mejorada confirmó una masa suprarrenal izquierda, muy sugestiva de feocromocitoma. Además, después de obtener el consentimiento informado, se realizó una secuenciación del exoma completo, que reveló una mutación sin sentido heterocigótica, c.1900T > C: p. Cys634Arg, en el gen RET, que conduce a una sustitución de cisteína por arginina en el codón 634. Esta mutación levantó sospechas de un síndrome de neoplasia endocrina múltiple, lo que impulsó una evaluación adicional de las glándulas tiroides y paratiroides. La ecografía Doppler en color de la tiroides identificó una masa hipoecoica que medía 6 mm × 4 mm en el lóbulo tiroideo izquierdo, y se observó una leve elevación en los niveles de calcitonina. No se detectaron anormalidades significativas adicionales.\n\nA medida que la condición del paciente mejoró gradualmente, los niveles de cortisol en plasma y ACTH volvieron a la normalidad. El paciente fue dado de alta con una prescripción de tartrato de metoprolol (100 mg cada 12 horas) e hidrocloruro de ivabradina (5 mg cada 12 horas) para el tratamiento en el hogar. Tres meses después, después de lograr un estado clínico estable, el paciente se sometió a una resección del tumor suprarrenal izquierdo, que medía 50 mm × 40 mm × 30 mm. El análisis inmunohistoquímico confirmó una tinción positiva para Vim, CD56, Syn, CgA y NSE, con S-100 positivo en las células de Sertoli, mientras que CKpan, CD10, MART-1/Melan-A y Melan-A fueron negativos. El índice Ki67 fue del 1 %, lo que llevó a un diagnóstico definitivo de feocromocitoma suprarrenal. El paciente fue dado de alta sin más medicamentos y desde entonces se le ha dado seguimiento regular postoperatorio sin recurrencia de síntomas. Durante un seguimiento postoperatorio de 15 meses, el paciente exhibió hipercalcinotemia persistente leve con un tamaño de nódulo tiroideo estable, mientras que los niveles de PTH y calcio en suero mostraron un aumento progresivo (Tabla 2). Se realizó una gammagrafía paratiroidea adicional utilizando 99mTc-MIBI, y la conclusión fue un resultado negativo para el adenoma paratiroideo.\n",
+        "gold_summary": "Reportamos el caso de una mujer de 19 años que presentó feocromocitoma sin experimentar una crisis, a pesar de tener una masa suprarrenal significativa y someterse a un tratamiento glucocorticoide de alta dosis. Las pruebas genéticas revelaron una mutación de sentido erróneo heterocigótica en el gen RET (c.1900T > C: p. Cys634Arg), asociada con MEN2A. La evaluación endocrina adicional identificó un nódulo tiroideo con niveles de calcitonina levemente elevados, pero niveles normales de electrolitos y hormona paratiroidea. Durante un seguimiento postoperatorio de 15 meses, la paciente exhibió hipercalcitonemia persistente leve con tamaño de nódulo tiroideo estable, mientras que la PTH y los niveles de calcio sérico mostraron un aumento progresivo. Se realizó una gammagrafía paratiroidea adicional utilizando 99mTc-MIBI, que arrojó un resultado negativo para el adenoma paratiroideo.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Esta es la historia de una joven de 19 años. Ella vino al hospital con dolor de cabeza, náuseas, vómitos y fiebre. Tenía la presión muy alta y el corazón latía muy rápido. Al principio pensaron que tenía infección y le dieron antibióticos, pero no mejoró.\n\nUna tomografía mostró por casualidad un bulto en una glándula encima del riñón. Esa glándula se llama suprarrenal. Esos bultos a veces hacen muchas “hormonas del estrés”. Las pruebas de sangre y orina mostraron que tenía muchísima de esas hormonas. Por eso los médicos dijeron que el bulto era muy probablemente un feocromocitoma. Un feocromocitoma es un tumor que hace hormonas que suben la presión y aceleran el corazón.\n\nTambién le hicieron pruebas del corazón. Unos análisis del músculo del corazón estaban un poco altos, y por eso la cuidaron en intensivo y le dieron medicinas para bajar la presión y el ritmo del corazón. Una ecografía del corazón salió normal, lo cual fue una buena noticia.\n\nSe hizo un examen genético. Encontraron un cambio en el gen RET que puede pasar en familias. Ese cambio está ligado a un síndrome llamado MEN2A. MEN2A hace que a veces aparezcan tumores en la tiroides, las glándulas paratiroides y las suprarrenales. Por eso buscaron en la tiroides y hallaron un pequeño nódulo y un leve aumento de una sustancia llamada calcitonina.\n\nTres meses después, cuando estuvo mejor, le sacaron el tumor de la suprarrenal con cirugía. La biopsia confirmó que era un feocromocitoma. Después de la operación se fue recuperando bien y no tuvo más síntomas por ahora.\n\nEn el seguimiento de más de un año, la calcitonina siguió algo alta y los niveles de PTH y calcio subieron un poco. Hicieron una prueba para buscar un problema en las paratiroides y no encontraron un tumor allí. Los médicos siguen controlándola porque el cambio genético puede afectar otras glándulas con el tiempo.\n\nEn resumen:\n- Tenía un tumor en la suprarrenal que producía muchas hormonas del estrés (feocromocitoma).\n- Le quitaron el tumor y mejoró.\n- Tiene una mutación genética que necesita controles médicos continuos.\n- Los médicos la siguen de cerca para vigilar la tiroides y las paratiroides.",
+                "fh_score": 72.09
+            },
+            "B2": {
+                "text": "Resumen comprensible y amable:\n\nUna mujer de 19 años llegó al hospital con dolor de cabeza, náuseas, vómitos y fiebre. En la exploración tenía presión arterial muy alta y latidos rápidos del corazón. Una tomografía detectó, de forma accidental, una masa en la glándula suprarrenal izquierda (las glándulas suprarrenales están encima de los riñones y pueden producir hormonas). Las pruebas de sangre y orina mostraron niveles muy altos de catecolaminas, que son hormonas como la adrenalina y la noradrenalina. Estos resultados apoyaron el diagnóstico de feocromocitoma, un tumor de la glándula suprarrenal que produce esas hormonas y puede causar presión alta y palpitaciones.\n\nAdemás, se hizo una prueba genética y se encontró una mutación en el gen RET (c.1900T>C, p.Cys634Arg). Esta mutación está asociada con un síndrome hereditario llamado MEN2A (neoplasia endocrina múltiple tipo 2A). En MEN2A suelen aparecer tres problemas: feocromocitoma, cáncer medular de tiroides y enfermedades de las glándulas paratiroides. Por ello, los médicos estudiaron también la tiroides y las paratiroides: encontraron un pequeño nódulo tiroideo y una leve elevación de calcitonina (una hormona producida por la tiroides que puede subir si hay enfermedad tiroidea), pero no hallaron un adenoma claro de la paratiroides en la gammagrafía (una prueba que busca tumores paratiroideos).\n\nAntes de la cirugía, la paciente recibió medicamentos para controlar la presión y la frecuencia cardíaca y también un tratamiento breve con glucocorticoides. A pesar del tamaño del tumor y de ese tratamiento, no sufrió una crisis por la liberación masiva de hormonas (lo que a veces ocurre con los feocromocitomas). Tras estabilizarse, se realizó la extirpación del tumor suprarrenal. El examen del tejido confirmó que se trataba de un feocromocitoma benigno.\n\nEn el control a 15 meses después de la operación, la paciente seguía sin recurrencia del tumor suprarrenal. Tenía una calcitonina ligeramente alta y un nódulo tiroideo estable; además, los niveles de hormona paratiroidea (PTH) y calcio en sangre fueron aumentando con el tiempo, aunque la gammagrafía no mostró un adenoma paratiroideo claro. Estos hallazgos sugieren la necesidad de seguimiento continuo para vigilar la tiroides y las paratiroides, porque la mutación RET aumenta el riesgo de problemas en esas glándulas.\n\nQué significa esto para la paciente:\n- El diagnóstico de feocromocitoma fue tratado con éxito mediante cirugía.\n- La mutación genética encontrada implica que necesita seguimiento endocrinológico a largo plazo (control de tiroides y paratiroides) y consejo genético; familiares pueden necesitar hacerse pruebas.\n- Los médicos continuarán monitorizando calcitonina, calcio y PTH, y harán más estudios si los resultados cambian.\n\nSi tienes preguntas sobre alguno de los términos o sobre lo que sigue para esta paciente, te lo explico con gusto.",
+                "fh_score": 51.19
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel de lectura universitario)\n\nPaciente y presentación inicial\n- Mujer de 19 años que acudió por 2 días de cefalea, náuseas, vómitos y un día de fiebre. Al ingreso presentaba hipertensión severa (189/120 mmHg), taquicardia (148 lpm) y fiebre (39.1 °C). Tenía leucocitosis (WBC 14.77×10^9/L), lo que orientó inicialmente a posible infección.\n- Ante la persistencia de la taquicardia y el aumento de biomarcadores cardíacos (BNP y troponina I), el equipo consideró miocarditis y se inició tratamiento con glucocorticoides, diuréticos, bloqueadores beta y fármacos para la presión arterial.\n\nHallazgos relevantes y diagnóstico de feocromocitoma\n- Una tomografía toraco-abdominal realizada para investigar la causa mostró de forma incidental una masa suprarrenal izquierda de ≈43 × 36 mm. Estudios bioquímicos en decúbito supino revelaron elevaciones marcadas de catecolaminas plasmáticas y en orina de 24 h (adrenalina, noradrenalina, metanefrinas, ácido vanilmandélico), compatibles con feocromocitoma —un tumor de la médula suprarrenal que secreta catecolaminas.\n- Tras la confirmación bioquímica, se cambió la estrategia antihipertensiva a bloqueo alfa (terazosina) antes de la cirugía, y se suspendieron los glucocorticoides.\n\nTratamiento y anatomía patológica\n- Tres meses después de estabilizarse, la paciente se sometió a adrenalectomía izquierda. La pieza medía 50 × 40 × 30 mm; la inmunohistoquímica fue compatible con feocromocitoma (marcadores neuroendocrinos positivos) y el índice Ki-67 fue bajo (1 %). Tras la cirugía no requirió medicación antihipertensiva y no hubo recurrencia clínica en el seguimiento inicial.\n\nHallazgo genético y evaluación endocrina asociada\n- La secuenciación del exoma mostró una mutación heterocigota de sentido erróneo en el gen RET (c.1900T>C; p.Cys634Arg). Esta variante está asociada con el síndrome de neoplasia endocrina múltiple tipo 2A (MEN2A), cuyo espectro incluye feocromocitoma, carcinoma medular de tiroides (MTC) y hiperparatiroidismo primario.\n- La ecografía tiroidea mostró un nódulo hipoecoico pequeño (6 × 4 mm) y la calcitonina sérica estaba ligeramente elevada, hallazgos que plantean la posibilidad de enfermedad tiroidea medular incipiente.\n- Durante 15 meses de seguimiento postoperatorio persistió una leve hipercalcitoninemia y, de forma preocupante, hubo un aumento progresivo de PTH y calcio séricos, lo que sugiere desarrollo de hiperparatiroidismo primario. Una gammagrafía paratiroidea con 99mTc‑MIBI fue negativa para adenoma localizado, lo que no descarta hiperplasia o adenomas pequeños.\n\nInterpretación y implicaciones clínicas\n- El cuadro inicial que parecía miocarditis probablemente incluyó contribuciones de catecolaminas (cardiomiopatía por exceso de catecolaminas), dado el feocromocitoma subyacente. Los esteroides pueden precipitar crisis adrenérgicas en pacientes con feocromocitoma, pero en este caso la paciente no desarrolló una crisis aguda a pesar de dosis altas.\n- La mutación RET p.Cys634Arg es de alto riesgo para MTC y se asocia con aparición temprana y mayor agresividad. Por ello, la combinación de feocromocitoma + mutación RET obliga a vigilancia y manejo proactivo de la tiroides y las paratiroides.\n\nRecomendaciones prácticas y seguimiento sugerido\n- Consulta genética y asesoramiento familiar: ofrecer prueba genética a familiares de primer grado (por la mutación RET) y consejo reproductivo.\n- Vigilancia tiroidea: monitoreo estrecho de calcitonina y CEA, ecografías tiroideas periódicas; en mutaciones de alto riesgo como Cys634 suele considerarse tiroidectomía profiláctica temprana o evaluar su necesidad según tendencias de calcitonina y hallazgos ecográficos, en discusión con endocrinología y cirugía.\n- Evaluación de paratiroides: seguimiento de calcio y PTH; si la hipercalcemia y/o síntomas progresan, valorar imagenología adicional (p. ej., sustracción selectiva o PET/CT con trazadores específicos) y discusión quirúrgica, ya que el MIBI negativo no excluye enfermedad paratiroidea.\n- Seguimiento por endocrinología de por vida: controles periódicos para detectar recurrencia de feocromocitoma, progresión de MTC o aparición de hiperparatiroidismo, y ajuste de intervenciones según evolución.\n- Evaluación cardiológica continua hasta normalización completa de función y biomarcadores.\n\nTono y pronóstico\n- La paciente respondió bien al tratamiento del feocromocitoma y la cirugía fue curativa para el tumor suprarrenal. Sin embargo, la mutación RET implica riesgo real de enfermedad tiroidea y paratiroidea futura; con vigilancia apropiada y manejo temprano (incluyendo opciones quirúrgicas cuando esté indicado), el pronóstico puede ser favorable. Es importante el seguimiento estrecho y la implicación familiar en el rastreo genético y clínico.\n\nSi desea, puedo preparar un resumen para familiares que explique qué es MEN2A, qué pruebas deben hacerse a los parientes, y qué señales clínicas deben vigilarse.",
+                "fh_score": 37.1
+            }
+        }
+    },
+    {
+        "article": "Una refugiada etíope embarazada de 39 años (Gravida 3 Para 2+0) fue derivada a nuestro departamento de urgencias de medicina interna en el Hospital Universitario de Gadarif, Gadarif State, Sudán, con hinchazón generalizada progresiva, falta de aire y fatiga durante 6 semanas y una revisión sistémica sin importancia. La paciente fue admitida en el sitio de admisión de casos críticos y su historia, tomada con la ayuda de un intérprete de idiomas más tarde en la admisión, reveló un episodio remoto inicialmente no revelado de tres convulsiones tónico-clónicas generalizadas no provocadas hace 21 años que se trataron tradicionalmente. Sin embargo, no había antecedentes de traumatismo craneal o antecedentes familiares de convulsiones. El examen general de la paciente reveló un PWS del lado izquierdo que involucraba la división oftálmica del nervio trigémino. Sin embargo, este hallazgo se perdió inicialmente en la inspección pero luego fue confirmado por el cónyuge de la paciente para estar presente desde el nacimiento. La paciente también estaba muy pálida y tenía derrames pleurales bilaterales, hepatomegalia blanda e hinchazón bilateral de las extremidades inferiores.\n\nLas investigaciones iniciales revelaron un nivel de hemoglobina de 8,84 g/dl. Por lo tanto, se diagnosticó insuficiencia cardíaca debido a anemia y se trató a la paciente en consecuencia. Sin embargo, ocho días después de su ingreso, la paciente había desarrollado aproximadamente seis episodios de convulsiones tónico-clónicas focales a bilaterales que respondieron bien a la fenitoína, pero que dejaron a la paciente en un estado comatoso profundo con un GCS de tres. Fue posteriormente admitida en la unidad de cuidados intensivos (UCI) y se le insertó un tubo nasogástrico para ayudarla con su nutrición y administración de fármacos. Además, para evitar más convulsiones, se le inició un tratamiento con comprimidos de carbamazepina de 200 mg administrados a través del tubo nasogástrico.\n\nSe retrasó una tomografía computarizada (TC) sin contraste del cerebro para el día posterior a la estabilización, ya que solo había una máquina de tomografía computarizada en el estado de Gadarif y funcionaba de forma intermitente debido a la falta de un número suficiente de técnicos radiólogos. La tomografía computarizada reveló calcificaciones corticales en la parte posterior del área parietal izquierda, lo que planteó el diagnóstico diferencial de SWS. En consecuencia, se realizó un examen físico de repetición, que mostró la presencia de una lesión plana de color rojo púrpura en la frente y el ojo. Al interrogar al cónyuge, se confirmó la presencia de esta lesión y que no había cambiado desde el nacimiento, lo que nos ayudó a descartar el diagnóstico de una mancha salmón, ya que esta lesión no se desvaneció, por lo que se diagnosticó como PWS. Además, no tenía características de megalencefalia, síndrome de malformación capilar que por lo general incluye un gran tamaño de la cabeza o del cerebro, problemas en las articulaciones y malformaciones capilares en la piel. Tampoco tenía hipertrofia de extremidades, anomalías del drenaje linfático o excrecencias óseas o de tejidos blandos que sugieran el síndrome de Klippel-Trenaunay-Weber. Por lo tanto, en función de los hallazgos de la tomografía computarizada y la presentación típica, llegamos a la conclusión del diagnóstico de SWS.\n\nDos días después de ingresar en la UCI, la paciente experimentó un cambio fluctuante en su estado de conciencia y una nueva aparición de hemiparesia contralateral (contralateral al SPW), así como afasia y labilidad emocional. Desafortunadamente, cuatro días después de ingresar en la UCI, la paciente empezó a experimentar sangrado vaginal; por ello, se consultó al departamento de obstetricia y ginecología y se descubrió que la paciente tenía un embarazo no viable (28 semanas + 1 día) y se realizó una inducción sin incidentes. Durante el mismo período, la paciente se volvió combativa y poco cooperativa, lo que llevó a que se la inmovilizara físicamente. Tres días después, la paciente desarrolló nuevos ataques focales bilaterales que comenzaron como episodios mioclónicos faciales y, tras consultar con el departamento de neurología, se aumentó la dosis de carbamazepina de la paciente a 1000 mg diarios, lo que ayudó a prevenir la recurrencia de los ataques. Cabe mencionar que, en su segundo trimestre y antes de recibir el resultado de la tomografía computarizada, se exploró un diagnóstico de eclampsia, pero sus constantes lecturas de presión arterial con una presión sistólica superior a la normal de 139 la mayoría de los días y una presión diastólica con un máximo de 97 mmHg y un rango bajo de proteinuria, así como la ausencia de características sistémicas como deterioro renal o hepático, excluyeron este diagnóstico. Después de alcanzar el diagnóstico de SW, se puso en juego un enfoque multidisciplinario; por ello, se realizó una consulta oftalmológica para descartar glaucoma. Sin embargo, la paciente estaba muy irritable y era difícil realizar un examen de fondo de ojo. Además, la paciente fue trasladada a la sala de medicina interna tras la estabilización.\n",
+        "gold_summary": "Presentamos el caso de una refugiada de 39 años, no diabética y no hipertensa, que inicialmente presentó insuficiencia cardiaca debido a anemia, por lo que recibió transfusiones de sangre. Más adelante, al ingresar, desarrolló convulsiones múltiples focales bilaterales, irritabilidad severa, afasia y hemiplejía derecha, lo que motivó su ingreso a la UCI. Un examen y un historial médico repetidos revelaron una mancha de vino de Oporto ocular izquierda leve que inicialmente pasó desapercibida y un historial remoto de convulsiones no provocadas 20 años atrás. Las imágenes revelaron calcificaciones parietales y confirmaron el diagnóstico de SWS. Por lo tanto, se adoptó un enfoque multidisciplinario para comprender plenamente el diagnóstico de la paciente y determinar una estrategia de tratamiento, que incluyó consultas con los departamentos de neurología, oftalmología, otorrinolaringología y fisioterapia. Se logró un control exitoso de las convulsiones mediante la administración de fenitoína IV durante 3 días y el aumento gradual de la carbamazepina oral a 1 g diario a través de una sonda nasogástrica. Lamentablemente, debido a la falta de personal o recursos, no se pudieron realizar otras evaluaciones importantes para pacientes con SWS, como evaluaciones avanzadas de neuroimagen, psiquiátricas, de cirugía plástica y neurocirugía, así como revisiones dentales.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Esta es la historia de una mujer de 39 años que había huido de su país. Llegó al hospital porque estaba muy cansada y tenía hinchazón. Tenía anemia, que hizo que su corazón trabajara mal. Le dieron sangre para ayudarla.\n\nAl poco tiempo empezó a tener ataques: convulsiones son movimientos fuertes y pérdida de lo que hace la persona. Fue llevada a la unidad de cuidados intensivos (una sala para pacientes muy enfermos). Los médicos encontraron que tenía desde niña una mancha roja en la frente y el ojo izquierdo. También dijo que tuvo convulsiones hace muchos años.\n\nUna exploración del cerebro mostró pequeñas zonas duras llamadas calcificaciones. Juntos, la mancha en la cara y las cosas del cerebro hicieron que los médicos pensaran en el síndrome de Sturge‑Weber. Este síndrome es algo con lo que se nace. Puede causar convulsiones y problemas con el lado del cuerpo opuesto a la mancha.\n\nLos médicos usaron medicinas para parar las convulsiones. Primero le dieron fenitoína en la vena. Luego le subieron la dosis de carbamazepina hasta 1.000 mg al día por una sonda en la nariz. Con eso las convulsiones se controlaron. También la vieron especialistas de neurología, oftalmología, otorrinolaringología y fisioterapia para ayudarla.\n\nLa paciente estaba embarazada, pero desgraciadamente el embarazo no siguió adelante y se hizo la inducción. Por falta de personal y recursos, no pudieron hacer algunas pruebas y tratamientos más complejos que a veces se hacen para este síndrome.\n\nEn resumen: la mujer tenía anemia y convulsiones. Los médicos diagnosticaron síndrome de Sturge‑Weber por la mancha y las pruebas. Controlaron las convulsiones con medicinas y la atendió un equipo de especialistas, aunque faltaron recursos para más estudios.",
+                "fh_score": 69.84
+            },
+            "B2": {
+                "text": "Resumen comprensible y amable:\n\nPresentamos el caso de una mujer refugiada de 39 años que llegó al hospital embarazada y con síntomas de fatiga, dificultad para respirar e hinchazón generalizada. Al principio se pensó que tenía insuficiencia cardíaca por anemia severa y recibió tratamiento con transfusiones. Más tarde, durante la hospitalización, sufrió varias crisis convulsivas (ataques cerebrales que causan movimientos incontrolados y pérdida de conciencia) y quedó en coma breve con un GCS muy bajo (GCS 3 indica nivel de conciencia muy reducido).\n\nAl investigar más a fondo se descubrió una mancha rojiza plana en la frente y el ojo izquierdo presente desde el nacimiento, llamada mancha en “vino de Oporto” (port-wine stain). Una tomografía computarizada (TC) mostró calcificaciones en la parte parietal del cerebro. Estos hallazgos, junto con la historia de convulsiones antiguas, llevaron al diagnóstico de síndrome de Sturge–Weber (SWS). SWS es una condición congénita (desde el nacimiento) que afecta los vasos sanguíneos de la piel, el cerebro y a veces el ojo; puede causar manchas en la piel, convulsiones y aumentar el riesgo de problemas oculares como el glaucoma (aumento de la presión en el ojo).\n\nDurante la estancia la paciente desarrolló debilidad en la mitad del cuerpo opuesta a la mancha (hemiparesia), dificultades para hablar (afasia) y cambios emocionales. El embarazo resultó no viable a las 28 semanas y se indujo el parto. Para controlar las convulsiones se administró fenitoína por vía intravenosa y después se aumentó la carbamazepina oral hasta 1 g al día a través de una sonda nasogástrica; con esto las convulsiones quedaron mejor controladas. Se hicieron consultas con neurología y oftalmología, y se empleó un enfoque multidisciplinario que también incluyó fisioterapia.\n\nDebido a limitaciones de recursos y personal, no se pudieron realizar otras pruebas importantes para SWS (como estudios de neuroimagen más avanzados, valoración psiquiátrica, cirugía plástica o estudios dentales). En estos casos, los próximos pasos recomendables suelen incluir seguimiento neurológico y oftalmológico regular (para vigilar glaucoma), rehabilitación para la debilidad, ajustes de medicación anticonvulsiva y, cuando sea posible, estudios adicionales de imagen y consultas con cirugía o psiquiatría para planificar cuidados a largo plazo.\n\nSentimos la difícil situación de la paciente; el equipo logró estabilizar y controlar sus convulsiones, pero destacó la necesidad de más recursos para completar una evaluación y seguimiento completos del síndrome de Sturge–Weber.",
+                "fh_score": 42.92
+            },
+            "B3": {
+                "text": "Summary — Sturge‑Weber syndrome (SWS) diagnosed in a pregnant refugee with new seizures\n\nPatient and presentation\n- A 39‑year‑old Ethiopian refugee (gravida 3, para 2) presented with 6 weeks of progressive generalized swelling, shortness of breath and fatigue. She was markedly pale (hemoglobin 8.8 g/dL) and had bilateral pleural effusions and soft hepatomegaly. These findings led initially to a working diagnosis of heart failure secondary to severe anemia and she received supportive care and blood transfusion.\n- Her history—obtained later with an interpreter—included three unprovoked generalized tonic‑clonic seizures about 20–21 years earlier (treated outside conventional medicine), a detail not disclosed at first.\n\nCritical deterioration and neurological findings\n- On hospital day 8 she developed multiple focal‑onset seizures that generalized. Seizures responded to IV phenytoin but she became deeply comatose (GCS 3) and required ICU care with nasogastric feeding and anticonvulsant therapy.\n- Repeated examination revealed a left‑sided port‑wine stain (PWS) in the territory of the ophthalmic branch of the trigeminal nerve; the lesion had been present since birth and had been missed on initial inspection.\n- Non‑contrast CT brain (delayed because of intermittent CT availability) showed cortical calcifications in the left parietal region, consistent with leptomeningeal vascular malformation.\n- Over the ICU stay she developed fluctuating consciousness, new right‑sided hemiparesis, aphasia and emotional lability — all signs of focal brain dysfunction contralateral to the facial PWS.\n\nDiagnosis and management\n- The combination of a congenital facial port‑wine stain in the V1 (ophthalmic) distribution, remote seizure history, recent focal seizures with neurologic deficits, and ipsilateral cortical calcifications led to a clinical diagnosis of Sturge‑Weber syndrome (SWS).\n- Seizures were treated acutely with IV phenytoin and later with enteral carbamazepine via the nasogastric tube, gradually increased to 1,000 mg/day, which helped control recurrent attacks.\n- An ophthalmology consult was arranged to evaluate for glaucoma (a known risk in SWS), but a complete eye exam was limited by the patient’s agitation.\n- Obstetric evaluation: at 28 weeks + 1 day she developed vaginal bleeding and the fetus was judged nonviable; induction was performed without incident. Eclampsia was considered earlier but deemed unlikely because blood pressures were only mildly elevated at times, proteinuria was low and there were no renal or hepatic dysfunction signs.\n\nImportant exclusions and resource limits\n- The team excluded other syndromes that can produce vascular skin lesions and limb or brain overgrowth (for example, Klippel‑Trenaunay‑Weber and megalencephaly‑capillary malformation) based on the absence of limb hypertrophy, lymphatic abnormalities or large head size.\n- Advanced investigations and specialist input (MRI with contrast, detailed neuroimaging, formal EEG, psychiatric assessment, plastic surgery, neurosurgery and dental review) were not available or were limited by staffing and resources.\n\nWhat this implies and suggested next steps\n- SWS is a congenital neurocutaneous disorder caused by leptomeningeal and facial vascular malformations; main concerns are refractory seizures, stroke‑like neurological deficits, and glaucoma. Early and ongoing multidisciplinary care improves outcomes.\n- In this patient, priorities going forward (as resources permit) would include:\n  - Complete neuroimaging (MRI with contrast) and EEG to better define the extent of leptomeningeal disease and seizure focus.\n  - Full ophthalmologic assessment including intraocular pressure and optic nerve evaluation to detect glaucoma.\n  - Neurology follow‑up to optimize antiseizure therapy and consider surgical options if seizures remain medically refractory.\n  - Rehabilitation (physiotherapy, speech therapy) for hemiparesis and aphasia.\n  - Psychosocial support and counseling, including reproductive counseling and coordination of care given refugee status and limited local resources.\n- If advanced care is not locally available, referral pathways to centers with pediatric/adult neurovascular and neurosurgical expertise should be sought.\n\nTone and context\n- The case highlights diagnostic delay because the facial PWS and remote seizure history were initially missed, and illustrates how limited imaging access and staffing can restrict comprehensive care. The clinical team used a pragmatic multidisciplinary approach to control seizures and stabilize the patient despite resource constraints.\n\nIf you would like, I can produce a one‑page clinical snapshot for clinicians (timeline, key investigations, medications and recommended referrals) or a patient‑facing explanation of SWS and its implications.",
+                "fh_score": 55.75
+            }
+        }
+    },
+    {
+        "article": "Una paciente de 69 años se quejaba de una pérdida progresiva de la visión. Sus padres eran primos hermanos. Le habían diagnosticado retinitis pigmentosa 27 años antes. La paciente había fumado durante 15 años. Tenía antecedentes de hiperlipidemia e hipotiroidismo.\n\nTras una evaluación oftalmológica completa, se determinó que el paciente tenía una agudeza visual corregida (AVC) de contar los dedos a 5’ y 3’ en los ojos derecho e izquierdo, respectivamente. La retinoscopia mostró una refracción de –1.00 + 0.50×70 y –2.00 + 1.00×5 en los ojos derecho e izquierdo, respectivamente. El paciente tenía discos ópticos pálidos con una atrofia profunda extensa de la mácula central, hiperplasia del pigmento epitelial y otras áreas de atrofia multifocal en el ojo derecho. Además, el paciente tenía atrofia macular en el ojo izquierdo. En la imagen de autofluorescencia del fondo del ojo (FAF) del paciente, había evidencia de una hipoautofluorescencia central de la mácula, con una extensión centrífuga difusa desde su centro hasta su periferia.\n\nLa tomografía de coherencia óptica macular (OCT) determinó que el espesor macular promedio era de 191 µM y 193 µM en los ojos derecho e izquierdo, respectivamente. El volumen macular era de 6.9 mm3 y 7.0 mm3 en los ojos derecho e izquierdo, respectivamente. No se encontró edema macular, quistes o fluido subretinal en ninguno de los ojos.\n\nUna prueba de campo visual reveló que el paciente tenía desviaciones medias de –23.75 dB y –24.56 dB en los ojos derecho e izquierdo, respectivamente. Las desviaciones estándar de patrón fueron de +3.69 dB y +4.69 dB en los ojos derecho e izquierdo, respectivamente. Los resultados de un electrorretinograma de campo completo (ERG) mostraron una respuesta normal de bastones y una respuesta de conos disminuida, bilateralmente. Por estas razones, se realizó un diagnóstico clínico de enfermedad STGD1.\n\nSe encontró una variante patogénica homocigótica intrónica c.5714+5G>A del gen ABCA4 tras el análisis de secuenciación y eliminación/duplicación utilizando secuenciación de próxima generación (Invitae Corporation, San Francisco, California). Tenía seis variantes adicionales de significación incierta (VUS) en los genes CACNA1F, EYS, KCNV2, KLHL7, MKKS y USH2A.\n",
+        "gold_summary": "Una paciente de 69 años de edad se presentó en la clínica quejándose de una pérdida progresiva de la visión. La evaluación oftálmica fue notable para una mejor agudeza visual corregida de contar los dedos a 5' en el ojo derecho y 3' en el ojo izquierdo. Las imágenes revelaron una atrofia profunda y extensa de la mácula central, una hiperplasia del pigmento epitelial y otras áreas de atrofia multifocal en el ojo derecho. Además, las imágenes de autofluorescencia del fondo de la mácula mostraron una hipoautofluorescencia central con expansión bilateral a la periferia en ambos ojos. Un electrorretinograma de campo completo mostró una respuesta normal de los bastones, con una respuesta disminuida de los conos, bilateralmente. Las pruebas genéticas fueron positivas para una mutación inotrópica homocigótica en el gen ABCA4 de la variante c.5714+5G>A.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una mujer de 69 años tenía pérdida de la vista que empeoraba con el tiempo. Esto la hacía ver solo grandes cosas: podía contar dedos a poca distancia. Los médicos miraron sus ojos con muchas pruebas. Vieron que la parte central de la retina (la mácula), que nos ayuda a ver caras y detalles, estaba muy dañada en los dos ojos. No había hinchazón ni líquido en la mácula, lo cual es algo bueno.\n\nUna prueba llamada ERG mostró que las células que nos ayudan a ver con poca luz (bastones) funcionaban bien. Pero las células que nos ayudan a ver colores y detalles (conos) estaban dañadas. Por eso tiene problemas para ver con claridad y para distinguir detalles.\n\nLos médicos dijeron que tiene enfermedad de Stargardt (STGD1). Esta es una enfermedad heredada que afecta la visión central. La prueba genética encontró un cambio en el gen ABCA4 que explica su enfermedad. Los padres de la paciente eran primos, y eso puede aumentar la probabilidad de tener el mismo cambio en ambos genes. También se hallaron otras pequeñas variantes en varios genes, pero su importancia no está clara.",
+                "fh_score": 79.75
+            },
+            "B2": {
+                "text": "Resumen claro y amable:\n\nUna mujer de 69 años acudió por una pérdida progresiva de visión. Tenía antecedentes familiares cercanos (sus padres eran primos) y otros problemas de salud como hiperlipidemia e hipotiroidismo. En la exploración oftalmológica su agudeza visual corregida era muy reducida: podía contar dedos a 5 pies en el ojo derecho y a 3 pies en el izquierdo. Las imágenes de la retina mostraron una atrofia profunda de la mácula, que es la zona central de la retina responsable de la visión fina y de los detalles, y cambios en el epitelio pigmentario (capa que apoya a las células de la retina). La autofluorescencia del fondo de ojo mostró una área oscura (hipoautofluorescencia) en la mácula que se extendía hacia la periferia, lo que indica daño y pérdida de tejido macular.\n\nEl electrorretinograma (ERG), una prueba que mide la respuesta eléctrica de la retina, encontró respuestas normales de los bastones (células que ayudan a ver en la oscuridad) y respuestas disminuidas de los conos (células que permiten ver los colores y los detalles), lo que explica la pérdida de visión central.\n\nEl estudio genético encontró que la paciente es homocigótica para una variante patogénica (dañina) en el gen ABCA4 (c.5714+5G>A). \"Homocigótica\" significa que la misma variante proviene de ambos progenitores, lo que aumenta la probabilidad de enfermedad hereditaria. Esta mutación se asoció con un diagnóstico clínico de enfermedad STGD1 (Stargardt), una forma hereditaria de degeneración macular juvenil-adulta que causa pérdida de la visión central. También se hallaron seis variantes adicionales de significado incierto en otros genes; estas requieren más estudio para saber si tienen importancia.\n\nQué puede seguirse haciendo (pasos razonables):\n- Derivación a consejo genético para explicar el resultado, sus implicaciones familiares y la posibilidad de hacer pruebas a familiares.\n- Soporte de baja visión (ayudas ópticas y rehabilitación) para mejorar la independencia en las actividades diarias.\n- Seguimiento oftalmológico regular para vigilar la progresión.\n- Considerar evaluación para ensayos clínicos o terapias en investigación si procede.\n\nSi necesita, puedo ayudar a redactar preguntas para el equipo médico o explicar con más detalle qué significan las pruebas.",
+                "fh_score": 49.59
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel universitario)\n\nPresentación y antecedentes\n- Mujer de 69 años con pérdida progresiva de la visión. Sus padres eran primos hermanos (consanguinidad).\n- Historia previa de retinitis pigmentosa diagnosticada hace 27 años. Fumó durante 15 años. Antecedentes médicos: hiperlipidemia e hipotiroidismo.\n\nHallazgos oftalmológicos clave\n- Agudeza visual corregida: contar los dedos a 5 pies (ojo derecho) y a 3 pies (ojo izquierdo) — pérdida visual central marcada.\n- Exploración del segmento posterior: discos ópticos pálidos; atrofia macular central profunda y extensa con hiperplasia del epitelio pigmentario y áreas de atrofia multifocal especialmente en el ojo derecho; atrofia macular también en el izquierdo.\n- Autofluorescencia del fondo (FAF): hipoautofluorescencia central de la mácula con extensión centrifuga difusa hacia la periferia — hallazgo anormal compatible con pérdida del epitelio pigmentario y de los fotorreceptores en la región macular.\n- Tomografía de coherencia óptica (OCT) macular: espesor macular promedio ~191–193 µm y volúmenes 6.9–7.0 mm3; no se observaron edema macular, quistes ni líquido subretinal (esto indica ausencia de edema o exudación activa).\n- Campo visual: desviaciones medias severas (−23.75 dB y −24.56 dB), compatible con importante pérdida del campo funcional.\n- Electrorretinograma (ERG) global: respuesta de bastones (visión escotópica) normal; respuesta de conos (visión fotópica/central y color) disminuida bilateralmente — patrón típico de afectación predominantemente de conos.\n\nDiagnóstico clínico y genético\n- Diagnóstico clínico final: enfermedad STGD1 (Stargardt tipo 1), enfermedad hereditaria de la mácula que provoca atrofia macular y pérdida de visión central.\n- Genética: se identificó una variante homocigótica intrónica c.5714+5G>A en el gen ABCA4, reportada como patogénica. Además se hallaron seis variantes de significado incierto (VUS) en CACNA1F, EYS, KCNV2, KLHL7, MKKS y USH2A.\n- Interpretación genética: la variante homocigótica en ABCA4 confirma que la enfermedad es causada por mutaciones en ABCA4 (forma autosómica recesiva), y la consanguinidad parental aumenta la probabilidad de homocigosidad. Las VUS requieren más estudio para determinar si contribuyen a la enfermedad.\n\nImplicaciones clínicas y pasos recomendados\n- Pronóstico: enfermedad progresiva con deterioro persistente de la visión central; la preservación de la función de bastones sugiere que la visión periférica y la adaptación a la oscuridad pueden conservarse más tiempo, pero la visión central y la agudeza seguirán comprometiéndose.\n- Manejo inmediato razonable: derivación a servicios de baja visión (rehabilitación visual, ayudas ópticas), protección solar y fotoprotección, control de factores modificables (p. ej., cesación del tabaquismo si procede).\n- Seguimiento y estudios adicionales: consulta de genética clínica para asesoramiento familiar y oferta de prueba genética a parientes (pruebas de portador/cascade testing); considerar confirmación funcional o segregación familiar para las VUS. Evaluación periódica oftalmológica para detectar complicaciones (p. ej. neovascularización coroidea) y para seguimiento de la progresión.\n- Investigación y ensayos: información sobre ensayos clínicos en enfermedades ABCA4/STGD1 y registro en bases de pacientes podría ofrecer acceso a terapias experimentales en el futuro.\n\nComentario final (tono empático)\nLos hallazgos estructurales (atrofia macular extensa y cambios en FAF) junto con la pérdida selectiva de la función de conos y la variante patogénica homocigota en ABCA4 respaldan fuertemente el diagnóstico de Stargardt (STGD1). Entiendo que esta es una noticia difícil; el paso siguiente más útil es coordinar atención multidisciplinaria (oftalmología, genética, baja visión) para optimizar la calidad de vida y explorar opciones de apoyo y, cuando proceda, participación en investigación.",
+                "fh_score": 41.57
+            }
+        }
+    },
+    {
+        "article": "Un niño de 19 meses de edad fue admitido en el departamento de urgencias porque se cayó de la trona en la que comía. Esta caída ocurrió en un aparente bienestar, sin la presencia de signos o síntomas anticipados. Primero, se cayó sobre su glúteo y luego se golpeó la cabeza (occipucio) contra el suelo. Vomitó (tres episodios) y estaba muy irritable. Su frecuencia respiratoria y cardíaca eran >60 respiraciones y >150 latidos por minuto, mientras que la saturación de oxígeno era <80%. Tras el examen físico, el niño estaba hidratado y consciente, pero irritable. Más importante aún, observamos retracciones subcostal y, al auscultar, disminución de los sonidos respiratorios en la parte basal izquierda del tórax. El paciente fue ventilado con un balón de AMBU conectado a una fuente de oxígeno y monitorizado con un oxímetro de pulso. A pesar de nuestra intervención, la saturación de oxígeno cayó por debajo del 70% y cuanto más ventilábamos, más caía la saturación. La ecografía pulmonar mostró la ausencia de las típicas líneas A y la consolidación del pulmón, que se visualizó directamente como un parénquima sólido. Sobre la base del mal estado clínico, el paciente se sometió a intubación orotraqueal con un tubo endotraqueal con manguito. Después de que el bebé se estabilizó, se sometió a una tomografía computarizada (TC) de tórax que mostró una atelectasia completa del pulmón izquierdo con una interrupción del bronquio izquierdo principal a 12 cm de la bifurcación bronquial. Se sospechó un FBA ya que la madre también declaró que el bebé en los días anteriores había tenido un ataque de tos intenso y desapareció en 24 h sin ningún tratamiento. Por lo tanto, se realizó una broncoscopia rígida y se encontró y se eliminó rápidamente una almendra de 2 cm de diámetro en el bronquio izquierdo principal.\n\nEl paciente nunca había consumido antes almendras u otros frutos secos y, en esta ocasión, ingirió la almendra por accidente.\n\nEl bebé mostró una mejora clínica progresiva y, después de 24 horas, se le retiró la sonda y se le dio de alta de la unidad de cuidados intensivos para ser ingresado en la sala de pediatría general durante unos días, con una recuperación gradual y total de la función respiratoria.\n",
+        "gold_summary": "Describimos el caso de un niño de 19 meses que llegó a la sala de urgencias por un traumatismo en la cabeza. La evaluación clínica, sin embargo, reveló una dificultad respiratoria grave inexplicable que requería intubación traqueal. Después de nuestra evaluación, planteamos la hipótesis de que la dificultad respiratoria grave determinó un estado alterado de conciencia con el consiguiente traumatismo en la cabeza. Los hallazgos radiológicos levantaron la sospecha de aspiración de cuerpo extraño por la presencia de una atelectasia de todo el pulmón izquierdo. La tomografía computarizada mostró una interrupción abrupta del bronquio principal a 12 mm del casco. La siguiente broncoscopia identificó una amígdala de 2 cm.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un niño de 19 meses se cayó de la trona y se golpeó la cabeza. Vomitó varias veces y estaba muy irritable. También tenía mucha dificultad para respirar y el nivel de oxígeno en su sangre estaba muy bajo.\n\nLos médicos escucharon menos aire en el lado izquierdo del pecho. Le pusieron una máscara y luego un tubo para ayudarle a respirar. Una tomografía mostró que todo el pulmón izquierdo estaba colapsado. Esto pasó porque algo tapaba el bronquio principal izquierdo, que es el conducto por donde entra el aire al pulmón.\n\nLa madre contó que el niño había tenido una tos fuerte unos días antes. Por eso los médicos pensaron que podía haber inhalado algo sin querer. Hicieron una broncoscopia, que es meter una pequeña cámara por la garganta para ver los pulmones. Encontraron y sacaron una almendra de 2 cm que estaba atascada.\n\nEl niño mejoró poco a poco. Al día siguiente le quitaron el tubo y, después de unos días en el hospital, se recuperó totalmente. No había comido almendras antes; se la tragó por accidente.",
+                "fh_score": 76.82
+            },
+            "B2": {
+                "text": "Resumen para alumnos (nivel B2, edad 11–17)\n\nUn niño de 19 meses llegó a urgencias tras caerse de la trona y golpearse la cabeza. Aunque parecía consciente, tenía problemas para respirar: respiraba muy rápido (>60 respiraciones/min), su corazón latía muy deprisa (>150 lpm) y su saturación de oxígeno estaba muy baja (<80% y luego <70%), incluso cuando se le ventilaba con una bolsa de oxígeno. En la exploración se vieron retracciones debajo de las costillas (señal de dificultad para respirar) y menos sonidos respiratorios en la parte baja del pulmón izquierdo.\n\nSe le puso un tubo en la tráquea para ayudarle a respirar (intubación). Una ecografía y después una tomografía del tórax mostraron que todo el pulmón izquierdo estaba colapsado (atelectasia: cuando una parte del pulmón deja de llenarse de aire) y que el conducto principal del pulmón (bronquio izquierdo) estaba bloqueado poco después de la bifurcación de las vías aéreas, a aproximadamente 1 cm. La familia recordó que el niño había tenido un episodio intenso de tos días antes que se resolvió solo, lo que hizo sospechar que había aspirado (tragado) algo.\n\nSe realizó una broncoscopia rígida (una exploración con un tubo rígido por la vía aérea) y se extrajo inmediatamente una almendra de unos 2 cm atrapada en el bronquio izquierdo. El niño no había comido almendras antes; la ingesta fue accidental. Tras la retirada del cuerpo extraño mejoró rápidamente: se le retiró el tubo tras 24 horas y fue trasladado de la UCI a planta, recuperando por completo la función respiratoria.\n\nMensaje final: la inhalación de alimentos o objetos pequeños puede causar bloqueo grave de una vía aérea. Si un niño tiene dificultad respiratoria, tos intensa o colapso de un pulmón en las pruebas, los médicos pueden necesitar imágenes y una broncoscopia para encontrar y quitar el cuerpo extraño.",
+                "fh_score": 55.3
+            },
+            "B3": {
+                "text": "Presentación clínica\nUn niño de 19 meses fue traído a urgencias tras caerse de la trona y golpearse la nuca. En el examen inicial estaba hidratado y consciente pero muy irritable. Tenía signos vitales anormales: taquipnea (>60 respiraciones/min), taquicardia (>150 lpm) y saturación de oxígeno marcadamente baja (<80%, llegando por debajo del 70% a pesar de ventilación con bolsa y oxígeno). Además presentaba retracciones subcostales y disminución de los ruidos respiratorios en la base del hemitórax izquierdo.\n\nHallazgos de imagen y procedimientos\n- Ecografía pulmonar: ausencia de las líneas A normales y presencia de consolidación en el pulmón izquierdo, visualizada como parénquima sólido.  \n- Debido al deterioro respiratorio se realizó intubación orotraqueal.  \n- Tomografía torácica: atelectasia completa del pulmón izquierdo y un corte abrupto del bronquio principal izquierdo situado a 12 mm (≈1,2 cm) desde la carina, lo que sugiere obstrucción bronquial.  \n- Ante la sospecha de aspiración de cuerpo extraño (la madre refirió un episodio reciente de tos intensa que cedió espontáneamente), se realizó broncoscopia rígida: se extrajo una almendra de 2 cm alojada en el bronquio principal izquierdo.\n\nDiagnóstico e interpretación\nEl cuadro corresponde a una obstrucción bronquial por cuerpo extraño (almendra) que provocó atelectasia total del pulmón izquierdo y una insuficiencia respiratoria grave. Es plausible que el episodio respiratorio agudo (hipoxia/alteración del nivel de conciencia) precediera y causara la caída y el traumatismo craneal, más que al revés.\n\nTratamiento y evolución\nLa extracción endoscópica del objeto fue curativa. El niño mejoró progresivamente, fue extubado a las 24 horas, trasladado a planta y tuvo recuperación completa de la función respiratoria en los días siguientes.\n\nImplicaciones y recomendaciones\n- En niños pequeños con insuficiencia respiratoria aguda, hipoxemia inexplicable o atelectasia unilateral, debe considerarse de inmediato la posibilidad de aspiración de cuerpo extraño.  \n- La tomografía y la ecografía pueden orientar, pero la broncoscopia rígida es diagnóstica y terapéutica.  \n- Prevención: los frutos secos enteros representan un riesgo alto de aspiración en menores de 3–4 años; es importante evitar darles nueces o almendras enteras y vigilar la alimentación.\n\nNota final (tono humano)\nEl caso subraya cuán rápido y grave puede ser la aspiración de un cuerpo extraño en lactantes y la importancia de una respuesta urgente. Afortunadamente, en este caso la extracción fue efectiva y el niño se recuperó completamente.",
+                "fh_score": 44.17
+            }
+        }
+    },
+    {
+        "article": "Una mujer nulípara de 35 años con antecedentes de infertilidad se presentó en la consulta externa. Informó de un antecedente de tres años de dolor sordo cíclico en el ombligo. El dolor se asoció a un nódulo umbilical que sangraba durante la menstruación. Cabe destacar que el dolor empeoraba durante la menstruación y se aliviaba con analgésicos. La paciente también informó de dismenorrea, menorragia y dispareunia. La paciente se había insertado un DIU de cobre 3 años antes y había estado usando Zinnia P (levonorgestrel y etinilestradiol) durante los últimos 3-4 meses para intentar aliviar el dolor. Su historial ginecológico previo no fue notable y tenía un ciclo menstrual regular. No había antecedentes médicos, quirúrgicos o sociales de importancia.\nAl examinarla, sus constantes vitales eran estables. Se observó una hinchazón hiperpigmentada (3 × 2 cm) en el ombligo al examinar el abdomen. La hinchazón era firme, inmóvil, no dolorosa, no reductible y no estaba ligada a estructuras subyacentes. Una resonancia magnética abdominal reveló una masa de mejora mal definida que medía 3 × 4 × 6 cm ubicada a lo largo de la pared abdominal anterior derecha y estaba conectada a un tracto sinusal que se extendía hacia la región suprapúbica, pero no se comunicaba con la cavidad peritoneal, hallazgos que sugieren endometriosis. El diagnóstico diferencial fue amplio, incluida una hernia umbilical, granuloma, cicatriz queloide, neoplasias malignas nodulares y anomalías embriológicas. Además, se observaron lesiones anexiales bilaterales, eran hiperintensas con áreas hipointensas focales y restricciones variables, la lesión del lado derecho medía 1,6 × 1,7 cm y la lesión del lado izquierdo medía 2,0 × 0,8 cm, hallazgos consistentes con endometriosis ovárica bilateral.\n\nSe programó al paciente para la extirpación quirúrgica del nódulo umbilical. La muestra se envió para un examen histopatológico. Los resultados revelaron una epidermis normal con glándulas endometriales dispersas y estroma dentro de la dermis. La fotomicroscopía resaltó la presencia de estroma endometrial y tejido graso subcutáneo. Esta morfología es consistente con la endometriosis. La recuperación postoperatoria de la paciente fue sin incidentes, y se la consideró apta para el alta el día 2 postoperatorio. Recibió asesoramiento sobre su fertilidad futura y la posibilidad de FIV, riesgo de recurrencia y se programó una visita de seguimiento en dos semanas. Se le inició con Dienogest, Visanne y un anticonceptivo oral combinado para el tratamiento de la endometriosis. Se la ha monitoreado clínicamente cada cuatro semanas, y no se han observado síntomas o signos de recurrencia local durante el período de seguimiento de 8 meses. Cabe destacar que, a pesar de que su condición permaneció estable después del tratamiento, no concibió en el transcurso del año siguiente.\n",
+        "gold_summary": "Presentamos el caso de una mujer nulípara de 35 años de edad del norte de Tanzania con un historial de infertilidad de 10 años. Al presentarse, la paciente informó de un historial de tres años de dolor cíclico asociado a una masa umbilical. Una resonancia magnética abdominal reveló una masa mal definida que se intensificaba y medía 3 × 4 × 6 cm, localizada a lo largo de la pared abdominal anterior derecha. La masa estaba conectada a un tracto sinusal que se extendía hacia la región suprapúbica, pero no mostraba comunicación con la cavidad peritoneal, lo que sugería endometriosis. Además, las lesiones anexiales bilaterales demostraron señales hiperintensas con áreas hipointensas focales y restricciones variables, consistentes con endometriomas ováricos bilaterales. La paciente se sometió a la extirpación de la masa umbilical y el examen histopatológico confirmó el diagnóstico de endometriosis umbilical primaria. A pesar de su condición estable después del tratamiento, no concibió durante el año siguiente.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "A 35-year-old woman who had not had children came to the clinic. She had three years of dull pain at her belly button. The pain got worse and the small lump at the belly button bled when she had her period. She also had painful and heavy periods.\n\nAn MRI scan showed a lump at the belly button and spots on both ovaries. Doctors thought this was endometriosis. Endometriosis is when tissue like the inside of the womb grows where it should not. This can make pain and bleeding.\n\nThe doctors removed the belly-button lump with a small operation. The lab looked at the removed tissue and found womb-like tissue in the skin. That confirmed endometriosis. The woman healed well and went home two days after surgery.\n\nShe was given hormone medicines to help keep the endometriosis quiet. She had check-ups every month. There was no sign that the lump came back for eight months. Even so, she did not become pregnant during the next year. Doctors talked with her about her future fertility and possible help such as IVF.",
+                "fh_score": 109.15
+            },
+            "B2": {
+                "text": "Summary (clear, age-appropriate)\n\nA 35-year-old woman who had never given birth and had been unable to get pregnant for many years came to clinic because she had three years of a dull, monthly pain at her belly button. The spot at her belly button sometimes formed a small lump that bled during her periods. She also had painful periods, heavy bleeding, and pain during sex.\n\nExams and scans\n- On physical exam the doctors saw a firm, darkened lump at the belly button.\n- An MRI scan showed a larger mass in the front abdominal wall connected by a small tract toward the lower belly. The scan did not show the mass opening into the main belly cavity. The MRI also showed small cyst-like lesions on both ovaries. These findings suggested endometriosis. \n- Endometriosis means tissue similar to the lining of the uterus grows outside the uterus. This can cause pain, bleeding, and sometimes ovarian cysts (called endometriomas).\n\nTreatment and outcome\n- The doctors surgically removed the belly-button lump. Looking at the removed tissue under a microscope (histopathology) showed endometrial glands and stroma in the skin — confirming primary umbilical endometriosis, a rare form of the condition.\n- She recovered well and left the hospital two days after surgery. She was given hormonal medicines (including dienogest and a combined birth-control pill) to help control endometriosis and was advised about future fertility options such as in vitro fertilization (IVF) and the chance the disease could come back.\n- During follow-up over eight months there were no signs that the belly-button problem had returned. However, she did not become pregnant in the year after treatment.\n\nThis case shows how endometriosis can sometimes appear in unusual places, such as the belly button, and how doctors use scans, surgery, and tissue tests to find and treat it.",
+                "fh_score": 88.73
+            },
+            "B3": {
+                "text": "Presentación breve\nUna mujer nulípara de 35 años con antecedentes de infertilidad consultó por un nódulo umbilical doloroso de aparición cíclica. El dolor era sordo, empeoraba durante la menstruación y el nódulo llegaba a sangrar en esos episodios. También refería dismenorrea (dolor menstrual intenso), menorragia (sangrado abundante) y dispareunia (dolor con las relaciones sexuales).\n\nHallazgos clínicos y de imagen\n- Exploración: lesión umbilical hiperpigmentada, firme, inmóvil, de unos 3 × 2 cm; no reducible y sin clara conexión con estructuras profundas a la palpación.\n- Resonancia magnética abdominal: masa mal definida de 3 × 4 × 6 cm en la pared abdominal anterior derecha, conectada por un tracto sinusal hacia la región suprapúbica pero sin comunicación con la cavidad peritoneal — hallazgos compatibles con endometriosis cutánea. Además, lesiones anexiales bilaterales con características (hiperintensas/hipo-intensas) compatibles con endometriomas ováricos (derecha 1,6 × 1,7 cm; izquierda 2,0 × 0,8 cm).\n\nDiagnóstico diferencial considerado\nhernia umbilical, granuloma, queloide, nódulos malignos o malformaciones congénitas. La combinación de clínica cíclica y hallazgos por imagen orientó hacia endometriosis umbilical (endometriosis primaria de la pared) asociada a enfermedad ovárica.\n\nTratamiento y confirmación diagnóstica\nSe realizó exéresis quirúrgica del nódulo umbilical. El examen histopatológico mostró epidermis normal con glándulas endometriales y estroma en la dermis y tejido graso subcutáneo, confirmando endometriosis umbilical primaria.\n\nEvolución y manejo posterior\n- Recuperación postoperatoria sin incidencias; alta al segundo día.\n- Inicio de tratamiento médico con dienogest (Visanne) y anticonceptivo oral combinado.\n- Consejería sobre fertilidad futura, posibilidad de FIV y riesgo de recurrencia; seguimiento clínico cada 4 semanas.\n- Durante 8 meses de seguimiento no hubo signos clínicos de recurrencia local. A pesar del tratamiento, la paciente no logró concebir en el año siguiente.\n\nImplicaciones y recomendaciones prácticas\n- La endometriosis umbilical primaria es poco frecuente pero debe sospecharse ante un nódulo umbilical con dolor y sangrado cíclico.  \n- La presencia simultánea de endometriomas ováricos sugiere enfermedad pélvica relacionada, lo que puede contribuir a la infertilidad.  \n- El manejo eficaz suele combinar cirugía (exéresis completa) y terapia hormonal para reducir síntomas y riesgo de recurrencia.  \n- Para pacientes que desean embarazo, es razonable la derivación a reproducción asistida (incluida la valoración para FIV) y la coordinación entre ginecología quirúrgica y reproducción asistida.  \n- Mantener seguimiento clínico e imagenológico si aparecen síntomas nuevos, por el riesgo —aunque bajo— de recurrencia o complicaciones.\n\nSi desea, puedo preparar un resumen más breve para uso clínico, una lista de preguntas para la consulta de fertilidad, o una explicación más detallada sobre los tratamientos hormonales y sus efectos sobre la fertilidad.",
+                "fh_score": 34.53
+            }
+        }
+    },
+    {
+        "article": "Presentamos a un recién nacido de 15 minutos de edad, hijo de una madre para-cuatro que no recordaba su LNMP pero que afirmaba haber estado amenorreica durante los últimos nueve meses. Su madre había recibido atención prenatal en el centro de salud cercano dos veces y no había tenido incidentes. Sin embargo, no se le había realizado un ultrasonido obstétrico temprano. Por lo demás, no tiene antecedentes de enfermedades crónicas como diabetes mellitus e hipertensión. Durante su embarazo actual, no tuvo fiebre, dolor de cabeza o visión borrosa. Nunca había usado ninguna droga aparte de sulfato ferroso durante este embarazo. Sus hijos anteriores están todos sanos y vivos. A su llegada a nuestro hospital, tuvo una hemorragia vaginal de dos horas de duración. Posteriormente, fue admitida con un diagnóstico de embarazo de tercer trimestre más multigravida más hemorragia anteparto secundaria a desprendimiento de placenta más oligohidramnios severo más presentación de nalgas.\n\nEn el examen pélvico, tenía un sangrado vaginal activo. Se le realizó una ecografía obstétrica al llegar. En consecuencia, la edad gestacional era de 34 semanas, la placenta estaba en el fondo con un coágulo retroplacentario y el líquido amniótico había disminuido significativamente con un único bolsillo más profundo de 1,5 cm. El peso fetal estimado era de 2,4 kg y presentación de nalgas. Otras investigaciones de la madre son grupo sanguíneo AB+, VDRL=negativo, RBS=120 mg/dL, en CBC, glóbulos blancos=9000, hemoglobina=11 gm/dL, plaqueta=180,000 y neutrófilo=60%.\n\nTras obtener el consentimiento informado por escrito, se realizó una cesárea de urgencia por las indicaciones ya mencionadas para extraer un neonato vivo de 2,01 kg de peso con puntuaciones de 5 y 6 en las pruebas de Apgar en el primer y el quinto minuto, respectivamente.\n\nEl neonato no lloró y fue reanimado durante cinco minutos. Luego fue trasladado a la unidad de cuidados intensivos neonatales para recibir atención e investigaciones adicionales. Al llegar, el neonato estaba en dificultad respiratoria. Sus signos vitales eran de 160 latidos por minuto, 70 respiraciones por minuto, temperatura de 33,4 grados centígrados y saturación de oxígeno del 60%. La fontanela anterior del neonato medía 2 cm por 2 cm y tenía micrognatia y cuello corto. En el sistema respiratorio, había retracciones intercostales y subcostales, respiración trabajosa y gruñidos. En el examen precordial, se escucharon bien los sonidos s1 y s2, no había murmullo ni ritmo de galope. En el sistema musculoesquelético, había acortamiento bilateral de las extremidades superiores, la extremidad inferior derecha estaba normal en posición y estructura, la pierna izquierda giraba hacia adentro (flexión mediolateral) en la articulación de la rodilla y la estructura del pie era normal. En el examen neurológico, estaba letárgico, el tono era normotónico en la extremidad inferior derecha y el reflejo de Moro era difícil de evaluar. La investigación de laboratorio mostró grupo sanguíneo = A+, CRP = reactivo, WBC = 30,000, neutrófilos = 54%, linfocitos = 21.1%, HGB = 8 gm/dL y plaquetas = 150,000. Se realizó una radiografía que mostró un acortamiento extremo de las extremidades superiores. La extremidad inferior izquierda estaba internamente girada. La ecocardiografía fue normal. Con una evaluación de prematuro tardío (34-36 semanas por puntaje de Ballard) más bajo peso al nacer más apropiado para la edad gestacional más focomelia más asfixia perinatal más sepsis neonatal temprana, se manejó con apoyo de oxígeno, fluido de mantenimiento e antibióticos intravenosos. El neonato murió después de tres días de hospitalización.\n",
+        "gold_summary": "Presentamos a un neonato de 15 minutos de vida, hijo de una madre para-cuatro que no recordaba su LNMP pero que afirmaba estar amenorreica desde hacía nueve meses. El modo de parto fue por cesárea para extraer al neonato vivo, que pesaba 2,01 kg y tenía puntuaciones APGAR de 5 y 6 en el primer y quinto minutos, respectivamente. El neonato no lloró y fue reanimado durante cinco minutos. Después se lo trasladó a la unidad de cuidados intensivos neonatales para continuar con el tratamiento y las investigaciones. Sus signos vitales eran: pulso de 160 latidos por minuto, frecuencia respiratoria de 70 respiraciones por minuto, temperatura de 33,4 grados centígrados y saturación de oxígeno del 60%. La fontanela anterior del neonato medía 2 cm por 2 cm y tenía micrognatia y cuello corto. En el sistema respiratorio había retracciones intercostales y subcostales, respiración trabajosa y gruñidos. En el sistema musculoesquelético había acortamiento bilateral de la extremidad superior, la pierna derecha tenía una posición y estructura normales, la pierna izquierda giraba hacia adentro (se doblaba hacia la parte media) en la articulación de la rodilla y el pie tenía una estructura normal.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Resumen sencillo y amable:\n\nUna madre llegó al hospital con sangrado antes del parto. Le hicieron una cesárea de urgencia porque la placenta se había separado y el bebé estaba en presentación de nalgas. La madre había tenido poco control prenatal y no se hizo una ecografía temprana.\n\nNació un bebé que pesó 2,01 kg. Al nacer tuvo puntuaciones de Apgar 5 y 6, no lloró y tuvo que ser reanimado por cinco minutos. Lo llevaron a la unidad de cuidados intensivos neonatales.\n\nEl bebé tenía dificultad para respirar. Tenía la piel fría y la temperatura era baja (33,4 °C). Su oxígeno en la sangre era muy bajo (60%). Tenía la frente blanda (fontanela 2 x 2 cm), la mandíbula pequeña (micrognatia) y el cuello corto. Se le veía respirar con esfuerzo y hacía gruñidos.\n\nEn el cuerpo se encontró que los brazos estaban muy cortos en ambos lados (esto se llama focomelia). La pierna izquierda estaba girada hacia adentro. La ecografía del corazón fue normal. Los análisis de sangre mostraron signos de infección y anemia.\n\nEl equipo le dio oxígeno, líquidos y antibióticos por vena. A pesar de los cuidados, el bebé falleció después de tres días en el hospital. Es una noticia triste, y los médicos actuaron rápido para intentar ayudar.",
+                "fh_score": 78.56
+            },
+            "B2": {
+                "text": "This report describes a baby born by emergency cesarean section after the mother had heavy vaginal bleeding caused by a placental abruption (the placenta partly detaching from the uterus). The mother had limited prenatal checks and an ultrasound at arrival showed the pregnancy was about 34 weeks, the baby was in breech position, and the amniotic fluid was very low (oligohydramnios).\n\nThe baby was alive at birth but weak, weighing 2.01 kg, and had low Apgar scores (5 at 1 minute, 6 at 5 minutes), which are quick tests of a newborn’s health. The infant did not cry at first and needed five minutes of resuscitation. In the neonatal intensive care unit the baby had serious breathing problems: fast breathing, chest retractions, grunting, low oxygen saturation (60%), and a low body temperature (33.4 °C). These signs show respiratory distress and possible birth-related oxygen shortage (perinatal asphyxia).\n\nOn exam and X-ray the baby had very short upper arms (phocomelia, a condition where parts of the limbs are missing or very shortened), a small lower jaw (micrognathia), and a short neck. One lower leg was turned inward at the knee. Heart ultrasound was normal. Blood tests suggested infection (high white blood cell count and positive CRP) and anemia (hemoglobin 8 g/dL).\n\nDoctors treated the newborn with oxygen, fluids, and intravenous antibiotics for suspected early neonatal sepsis (a bloodstream infection). Despite care, the baby died after three days in hospital.\n\nWhen infants have severe limb differences and early problems like these, doctors often consider further investigations such as genetic testing and specialist counseling for the family, along with explaining the causes, likely outcomes, and options for future pregnancies. The tone of this case is one of serious illness and sadness; families in similar situations are usually offered support, clear information, and follow-up care.",
+                "fh_score": 83.69
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel universitario, tono empático)\n\nPresentación y antecedentes maternos\n- Madre multípara (para 4) con dos controles prenatales en centro de salud; no se hizo ecografía temprana. No refiere enfermedades crónicas ni uso de fármacos teratógenos declarados (solo sulfato ferroso). Reportó amenorrea de nueve meses.\n- Acudió por hemorragia vaginal de 2 horas; fue diagnosticada de probable desprendimiento de placenta con oligohidramnios severo y presentación de nalgas. Ecografía al ingreso: edad gestacional estimada 34 semanas, placenta fundal con colección retroplacentaria, bolsillo amniótico más profundo 1,5 cm, peso fetal estimado 2,4 kg.\n\nParto y reanimación\n- Se realizó cesárea de urgencia por las indicaciones maternas/fetales. Se extrajo un neonato vivo que pesó 2,01 kg (APGAR 5 al 1’ y 6 al 5’). No lloró al nacer y precisó reanimación por 5 minutos antes de traslado a UCI neonatal.\n\nExamen inicial del neonato y hallazgos relevantes\n- Signos vitales al ingreso: FC 160/min, FR 70/min, temperatura 33,4 °C (hipotermia), SaO2 60% (hipoxia).\n- Estado general: dificultad respiratoria con retracciones inter- y subcostales y gruñidos; letárgico.\n- Cabeza/cara/cuello: fontanela anterior 2 × 2 cm, micrognatia (mandíbula pequeña) y cuello corto.\n- Sistema cardiovascular: sonidos normales sin soplos.\n- Sistema musculoesquelético: acortamiento bilateral marcado de ambas extremidades superiores (focomelia en radiografía). Extremidad inferior derecha con aspecto normal; extremidad inferior izquierda con rotación interna en la rodilla, pie con estructura normal.\n- Neurológico: tono conservado en la extremidad inferior derecha; reflejo de Moro difícil de evaluar.\n- Laboratorio: grupo sanguíneo A+; CRP reactiva; leucocitos 30 000/µL, neutrófilos 54%, linfocitos 21.1%; hemoglobina 8 g/dL; plaquetas 150 000/µL.\n- Ecocardiograma normal. Radiografía confirmó acortamiento extremo de los miembros superiores.\n\nDiagnóstico y manejo inicial\n- Diagnósticos planteados: recién nacido prematuro tardío (≈34 semanas), bajo peso al nacer (2,01 kg), apropiado para la edad gestacional según evaluación, focomelia bilateral de miembros superiores, asfixia perinatal, y sospecha de sepsis neonatal temprana (CRP alta, leucocitosis).\n- Tratamiento: soporte con oxígeno, control térmico, líquidos de mantenimiento y antibióticos intravenosos empíricos.\n- Evolución: fallecimiento tras 3 días de hospitalización.\n\nInterpretación y consideraciones importantes\n- Los hallazgos estructurales (focomelia bilateral de miembros superiores y malposición de la pierna izquierda) indican una malformación congénita significativa. Las causas posibles incluyen alteraciones en el desarrollo embrionario por factores genéticos, alteraciones vasculares durante la organogénesis o exposición a teratógenos (p. ej., fármacos como talidomida), aunque la madre negó uso de fármacos distintos al hierro. No se puede concluir la causa sin estudios adicionales.\n- La combinación de desprendimiento placentario, oligohidramnios, parto pretérmino y las anomalías respiratorias y térmicas contribuía a la asfixia perinatal y al riesgo de sepsis. La anemia (Hb 8 g/dL) y la hipoxia/hipotermia empeoran el pronóstico neonatal.\n- La discordancia entre el peso fetal estimado por ecografía (2,4 kg) y el peso real (2,01 kg) sugiere estimación prenatal imprecisa o pérdida de peso por las condiciones perinatales.\n\nRecomendaciones y pasos siguientes sugeridos (para la familia y el equipo clínico)\n- Considerar estudio postmortem (autopsia) y examen patológico de la placenta para investigar desprendimiento, infecciones o causas vasculares.\n- Estudios genéticos y/o consulta con genética clínica para evaluar etiologías hereditarias o síndromes asociados a focomelia.\n- Revisión detallada de la historia de exposición materna a medicamentos, sustancias o infecciones durante el embarazo.\n- Cultivos y PCR para agentes infecciosos (si no se hicieron) y revisión de resultados microbiológicos para confirmar o descartar sepsis neonatal.\n- Apoyo psicosocial y consejería para la familia sobre hallazgos, pruebas adicionales y planificación de embarazos futuros.\n\nLamento profundamente la pérdida de este recién nacido. Si la familia o el equipo clínico lo desean, los pasos descritos pueden ayudar a aclarar la causa y orientar el manejo en futuros embarazos; el apoyo emocional y la comunicación clara son fundamentales en este proceso.",
+                "fh_score": 42.51
+            }
+        }
+    },
+    {
+        "article": "Mujer de 61 años con antecedente de carcinoma escamocelular de cuello uterino estadio FIGO IIB, diagnosticado en febrero de 2019, tratada en un hospital privado de cuarto nivel de atención, donde se ofrece cuidado ambulatorio y hospitalario para pacientes con condiciones complejas oncológicas y no oncológicas. Al momento del diagnóstico se realizó histerectomía radical con linfadenectomía pélvica, que descartó compromiso nodal. El tratamiento complementario de primera línea incluyó seis ciclos de quimioterapia con cisplatino, y braquiterapia y radioterapia, alcanzando una respuesta tumoral completa. En 2021, tras detectarse una recaída aislada en la región ilíaca, mediante tomografía, se administró cisplatino y 30 sesiones de radioterapia, logrando una nueva respuesta completa. En septiembre de 2022, una tomografía reveló otra recaída con compromiso del parametrio izquierdo, el uréter y la cadena ilíaca ipsilateral, por lo que se decidió primera línea para enfermedad recurrente con carboplatino, paclitaxel y pembrolizumab. Durante este régimen, la paciente presentó hipersensibilidad al platino en el quinto ciclo, gestionada con un protocolo de desensibilización, continuando con el pembrolizumab. En septiembre de 2023, ante la progresión en imágenes de una masa retroperitoneal única, debido a la falta de respuesta óptima, se inició gemcitabina, según guías de manejo, segunda línea de enfermedad recurrente, recibiendo una dosis acumulada de 8.544 mg/m2 hasta enero de 2024. Sin embargo, desarrolló síntomas de isquemia digital en manos, por lo que el tratamiento fue suspendido tras la segunda dosis del tercer ciclo, acumulando 11.744 mg/m2 de gemcitabina.\n\nEn febrero de 2024, la paciente ingresó al servicio de urgencias del mismo hospital donde era valorada de forma ambulatoria, remitida por oncología debido a progresión de los síntomas en sus extremidades. La paciente refería dolor lancinante y coloración azulada en dedos de manos; al examen físico se evidencia necrosis en el segundo dedo de la mano derecha, coloración ocre y fenómeno de Raynaud en los dedos de la mano izquierda. Las extremidades inferiores mostraban edema grado II en el miembro inferior izquierdo y pulsos presentes. Los estudios para autoinmunidad y vasculitis resultaron negativos, incluyendo anticuerpos anticitoplasma de neutrófilos (ANCAS), anticuerpos antinucleares (ANAS), anticuerpos antidesoxirribonucleicos (anti-DNA), cardiolipinas, prueba confirmatoria de anticoagulante lúpico, perfil de anticuerpos contra antígenos nucleares extraíbles (ENAS), anticuerpos contra proteinasa 3, anticuerpos antimieloperoxidasa y anticuerpos dirigidos contra la ADN topoisomerasa I (antiSCL). Además, el factor reumatoide y los niveles de complemento 3 (C3) y complemento 4 (C4) también fueron normales. Prueba serológica para sífilis (VDRL - Venereal Disease Research Laboratory) negativa, ecocardiograma transtorácico sin hallazgos de un foco cardioembólico.\n\nSe inició anticoagulación con heparina de bajo peso molecular, junto con ácido acetilsalicílico, estatina y un calcioantagonista. El equipo de cirugía de mano realizó amputación del segundo dedo de la mano derecha, confirmando necrosis por licuefacción en el estudio histopatológico.\n\nDurante el posoperatorio se agregó sildenafil al tratamiento, logrando una mejoría progresiva en los signos de isquemia de los dedos restantes. Durante la hospitalización, la paciente presenta complicación por sangrado vaginal masivo, requiriendo embolización de arterias uterinas.\n\nEl servicio de reumatología aplicó la escala de causalidad de Naranjo para determinar el papel de la gemcitabina en la vasculitis, con un puntaje de 8, lo que indicó que el medicamento probablemente provocó la necrosis.\n\nPosteriormente, a los 20 días de ingreso a hospitalización desarrolló deterioro neurológico, sin hallazgos significativos en la tomografía de cráneo. Evaluada por cuidados paliativos, su estado funcional se clasificó con un Barthel de 0/30, ECOG de 4 y Karnofsky de 10 %, con pronóstico de vida inferior a tres semanas según el Índice Pronóstico de Paciente (PPI: + 6 puntos). En consenso con la familia, se suspendieron estudios adicionales y se implementó un manejo paliativo integral. La paciente falleció tras el alta hospitalaria.",
+        "gold_summary": "Oaciente de 61 años tratada con gemcitabina (11.744 mg/m² acumulados) por enfermedad metastásica, en un hospital general de cuarto nivel, privado, no oncológico, donde venía siendo manejada de forma ambulatoria. Presentó necrosis distal del segundo dedo de la mano derecha, por lo que se suspendió el tratamiento y se requirió amputación de este dedo. Se realizó una búsqueda en Embase, Medline y Lilacs. Se buscaron estudios de reporte y series de casos sobre necrosis distal inducida por gemcitabina. Se extrajeron datos de dosis, diagnóstico y tratamiento.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había una mujer de 61 años que había tenido cáncer en la parte baja del vientre. Los médicos le dieron muchos tratamientos con medicina fuerte (quimioterapia). Cuando volvió a empeorar, le dieron un medicamento llamado gemcitabina.\n\nDespués de varias dosis, empezó a tener mucho dolor y sus dedos de las manos se pusieron de color azul y después algunas partes se murieron (necrosis). Los médicos hicieron muchas pruebas para ver si otra enfermedad estaba causando eso. Esas pruebas salieron normales. También revisaron el corazón y no encontraron que hubiera coágulos saliendo del corazón.\n\nLos médicos pensaron, usando una lista de comprobación, que probablemente la gemcitabina causó el problema. Dejaron de dar ese medicamento. Tuvieron que quitar el segundo dedo de la mano derecha porque esa parte estaba muerta. Le dieron otras medicinas y, con eso, los otros dedos mejoraron un poco.\n\nMientras estuvo en el hospital sufrió un sangrado fuerte en la zona del vientre y los médicos tuvieron que hacer un procedimiento para parar la sangre. Más tarde empezó a empeorar mucho de salud en general. La familia y el equipo médico acordaron darle cuidados de confort para que no sufriera más. Poco después de salir del hospital, la mujer falleció.\n\nLo importante: los médicos creen que un medicamento pudo haber causado que un dedo se dañara. Buscaron otras causas y no las encontraron. Los cuidaron y, al final, decidieron darle alivio y acompañamiento.",
+                "fh_score": 69.44
+            },
+            "B2": {
+                "text": "Here is a clear, gentle summary of the case written for a teenage reader.\n\nSummary:\n- A 61-year-old woman had a type of cervical cancer (squamous cell carcinoma) first treated successfully with surgery, chemotherapy, and radiotherapy. After two separate recurrences over several years, she received different chemotherapy drugs.\n- In September 2023 her cancer progressed and doctors started gemcitabine, a chemotherapy drug. By January 2024 she had received a total dose of 11,744 mg/m² of gemcitabine when she developed problems in her hands.\n- She came to the hospital with severe, stabbing pain and blue coloring of her fingers. On exam, the right index finger (second finger) was dead tissue (necrosis), and the left hand showed a Raynaud-like pattern (fingers turning pale or blue when stressed). Her lower legs had some swelling but blood pulses were present.\n- Doctors checked for other causes that can block blood flow or cause inflammation of vessels (vasculitis). Tests for autoimmune diseases and infections (for example, ANCA, ANA, anti-DNA, antiphospholipid tests, complements C3/C4, and syphilis test) were all negative. A heart ultrasound showed no blood-clot source from the heart.\n- Because of the worsening ischemia (lack of blood flow), the medical team stopped gemcitabine. They started blood thinners (low-molecular-weight heparin), aspirin, a cholesterol-lowering drug (statin), and a calcium-channel blocker to try to open blood vessels. The damaged right index finger was surgically removed; the tissue exam confirmed liquefactive necrosis (tissue breakdown due to lack of blood).\n- After surgery doctors added sildenafil (a drug that can help improve blood flow) and the remaining fingers gradually improved. During the hospital stay she also had heavy vaginal bleeding that required embolization (a procedure to block the bleeding uterine artery).\n- Rheumatology used the Naranjo scale (a standard checklist) to see whether gemcitabine likely caused the blood-vessel damage. The score was 8, which means it was a probable cause.\n- About 20 days after admission she developed sudden neurological decline. Brain CT did not show a clear cause. Her overall condition became very poor: she could not perform daily activities and scores used to measure function and prognosis indicated a very limited life expectancy (under three weeks). After discussion with her family, further invasive testing was stopped and palliative (comfort-focused) care was started. The patient died after discharge.\n\nWhat this means (in simple terms):\n- Gemcitabine is a chemotherapy drug that can, rarely, cause severe problems with blood flow to the fingers and toes, leading to pain, color change, and sometimes tissue death. In this case the pattern, the timing after gemcitabine, and the negative tests for other causes made the drug the most likely reason.\n- When such signs appear, doctors usually stop the suspected drug, use medicines to improve blood flow and prevent clots, and may need surgery for dead tissue. If a patient’s overall health worsens, the focus may shift to comfort care in discussion with the family.\n\nThis case shows how rare but serious side effects of chemotherapy can develop, and how teams work together to diagnose, treat, and support the patient and family.",
+                "fh_score": 82.11
+            },
+            "B3": {
+                "text": "Resumen clínico (lectores universitarios)\n\nAntecedentes y tratamiento oncológico\n- Mujer de 61 años con carcinoma epidermoide de cuello uterino estadio FIGO IIB diagnosticado en 2019. Fue sometida a histerectomía radical y linfadenectomía pélvica (sin afectación nodal) y recibió quimioterapia con cisplatino, braquiterapia y radioterapia, con respuesta completa.\n- En 2021 presentó recurrencia ilíaca tratada con cisplatino y radioterapia (respuesta completa). En 2022 hubo nueva recaída con compromiso del parametrio izquierdo, uréter y cadena ilíaca ipsilateral; se inició carboplatino + paclitaxel + pembrolizumab. Se documentó hipersensibilidad al platino en el 5.º ciclo, manejada con desensibilización.\n- Por progresión en 2023 se inició gemcitabina como segunda línea. La paciente recibió una dosis acumulada total de 11.744 mg/m² antes de suspender el fármaco por aparición de síntomas isquémicos en las manos.\n\nPresentación y hallazgos\n- En febrero de 2024 consultó por dolor intenso y acrocianosis en los dedos. Al examen: necrosis del segundo dedo de la mano derecha, coloración ocre y fenómeno de Raynaud en la mano izquierda; miembros inferiores con edema grado II y pulsos presentes.\n- Se descartaron causas autoinmunes y vasculitis: pruebas negativas (ANCA, ANA, anti‑DNA, ENA, anticardiolipinas, anticoagulante lúpico, anti‑PR3, anti‑MPO, anti‑Scl‑70), factor reumatoide y C3/C4 normales. Serología para sífilis negativa. Ecocardiograma transtorácico sin foco cardioembólico.\n\nManejo realizado\n- Suspensión de gemcitabina. Inicio de anticoagulación con heparina de bajo peso molecular, ácido acetilsalicílico, estatina y un calcioantagonista (vasodilatador).\n- Amputación del segundo dedo derecho por necrosis; anatomía patológica compatible con necrosis por licuefacción.\n- Posteriormente se añadió sildenafil (vasodilatador), con mejoría progresiva de la isquemia en los dedos restantes.\n- Complicación durante la hospitalización: hemorragia vaginal masiva que requirió embolización de las arterias uterinas.\n\nCausalidad y evolución\n- El equipo de reumatología aplicó la escala de Naranjo (herramienta para estimar probabilidad de reacción adversa a un fármaco); el puntaje fue 8, lo que sugiere que gemcitabina fue una causa probable de la vasculopatía/digital necrosis.\n- A los 20 días de hospitalización la paciente presentó deterioro neurológico sin hallazgos significativos en la tomografía cerebral. Su estado funcional empeoró (Barthel 0/30, ECOG 4, Karnofsky 10 %) y el índice pronóstico (PPI) indicó expectativa de vida inferior a tres semanas.\n- En consenso con la familia se limitaron estudios y se inició manejo paliativo integral. La paciente falleció tras el egreso.\n\nInterpretación y consideraciones\n- Se trata de un cuadro de isquemia digital grave y necrosis distal aparecido durante tratamiento con gemcitabina, tras excluir causas autoinmunes y cardioembólicas. Aunque raro, la gemcitabina se ha asociado con vasculopatías y fenómenos tromboembólicos que pueden ocasionar isquemia tisular.\n- Implicaciones prácticas: ante signos tempranos de isquemia digital en pacientes que reciben gemcitabina, debe considerarse la suspensión inmediata del fármaco, evaluación exhaustiva para excluir otras causas (trombosis, embolia, vasculitis), tratamiento médico con anticoagulación y vasodilatadores, y cirugía cuando exista necrosis establecida. La notificación del evento adverso y la evaluación de causalidad son recomendables.\n- En pacientes con enfermedad avanzada y deterioro funcional marcado, la atención paliativa temprana y la toma de decisiones compartida con la familia son fundamentales.\n\nEmpatía\n- Este caso ilustra una complicación grave y devastadora en el contexto de cáncer avanzado. La toma rápida de decisiones terapéuticas y el apoyo paliativo fueron elementos clave en el manejo hacia el final de la vida.",
+                "fh_score": 38.21
+            }
+        }
+    },
+    {
+        "article": "Mujer de 53 años, con antecedente de AR de 15 años de diagnóstico en tratamiento con metotrexato, resto de antecedentes sin datos de importancia, la cual presentó cuadro clínico 8 meses antes (de acudir a nuestro servicio) con astenia y adinamia de forma progresiva, palidez de tegumentos, alzas térmicas no cuantificadas de predominio nocturno, pérdida de peso no intencionada de 15 kg en 6 meses aproximadamente, sin valoración ni seguimiento médico, a lo que se agregó 3 meses después disnea de grandes a medianos esfuerzos, y cuya sintomatología se agudizó 5 días antes (de acudir a nuestro servicio), aunada a sangrado de tubo digestivo alto (STDA), caracterizado por evacuaciones melénicas abundantes, 3 evacuaciones en 24 horas, hematemesis en 2 ocasiones, escasas, sin causa aparente. La paciente negó consumo de analgésicos no esteroideos (AINE) y tuvo aumento de volumen en la pierna izquierda, la cual le dolía y tenía la presencia de edema y eritema, con limitación a la movilidad, motivo por el cual acudió a (nuestro) Servicio de Urgencias.\n\nDurante su hospitalización con anemia severa sin repercusión hemodinámica, se transfundieron 3 concentrados eritrocitarios sin complicaciones aparentes. Después de su estabilización, se inició abordaje diagnóstico para síndrome consuntivo. Por el cuadro clínico de miembro inferior izquierdo se hizo US Doppler que evidenció trombosis venosa profunda. Se realizó ultrasonido de abdomen por probable hepatopatía por metotrexato, el cual reportó infartos esplénicos y hepáticos, así como presencia de cambios crónicos hepáticos. Se llevó a cabo endoscopía con evidencia de varices pequeñas, sin sangrado activo. Debido a la sospecha de neoplasia por los antecedentes y el cuadro clínico de la paciente, se llevó a cabo tomografía axial simple y contrastada de tórax y abdomen y se encontró hepatoesplenomegalia y múltiples conglomerados ganglionares axilares, mediastinales y paraaórticos que sugerían actividad infiltrativa. Esto se valoró por el Servicio de Cirugía General para la realización de biopsia de ganglio axilar derecho, donde se reportó proliferación neoplásica de células linfoides. Posteriormente se valoró por el Servicio de Hematología de la unidad, se solicitaron estudios de laboratorio (cuadro I) y se realizó aspirado de médula ósea en el que se evidenciaron células plasmáticas displásicas y células reticulares, por lo cual se concluyó que había la presencia de infiltración linfoplasmocitaria. Con los antecedentes, el cuadro clínico y los estudios complementarios se diagnosticó LNH estadio IV y la paciente fue enviada a hospital de tercer nivel para realización de inmunohistoquímica, estadificación e inicio de tratamiento. En tercer nivel se identificó linfoma difuso de células B con inmunofenotipo B CD20 con sobrecrecimiento de células dendríticas, y la paciente fue valorada para inicio de tratamiento con quimioterapia.",
+        "gold_summary": "Mujer de 55 años con antecedente de AR que ingresó a un servicio de medicina interna por sangrado de tubo digestivo; presentó datos clínicos de trombosis venosa profunda en miembro pélvico izquierdo y síndrome consuntivo en estudio. Durante su abordaje se identificó con infartos esplénicos y hepáticos, así como múltiples conglomerados ganglionares, por lo que se practicó biopsia de ganglio axilar que reportó proliferación neoplásica de células linfoides y aspirado de médula ósea con presencia de infiltración linfoplasmocitaria, con lo que se determinó diagnóstico de linfoma no Hodgkin estadio IV. La paciente fue enviada a un hospital de tercer nivel para inicio de tratamiento.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una mujer de 53 años llegó al hospital porque estaba muy cansada, había bajado mucho de peso y tenía fiebre por las noches. También tenía sangre en las heces y vomitó sangre. Su pierna izquierda se hinchó y le dolía. \n\nEn el hospital le pusieron sangre porque estaba muy baja de sangre. Hicieron muchas pruebas. En la pierna encontraron un coágulo en una vena. En el abdomen vieron zonas del bazo y del hígado que dejaron de recibir sangre. También encontraron muchos ganglios inflamados en el cuerpo. \n\nSacaron una muestra de un ganglio y del hueso para mirar las células. Vieron que unas células del sistema inmune estaban creciendo sin control. Por eso diagnosticaron linfoma no Hodgkin en estadio IV. Esto es un tipo de cáncer que afecta ganglios y médula. \n\nLa enviaron a un hospital más grande para hacer más estudios y empezar tratamiento con quimioterapia. Los médicos la estaban cuidando y le darán el tratamiento que necesita.",
+                "fh_score": 79.78
+            },
+            "B2": {
+                "text": "Resumen claro y amable:\n\nUna mujer de 53 años con artritis reumatoide tratada con metotrexato llegó al hospital por cansancio progresivo, pérdida de peso fuerte (unos 15 kg en 6 meses), palidez, fiebre nocturna y dificultad para respirar. Cinco días antes de la consulta presentó además sangrado digestivo alto: heces negras por sangre (melena) y dos episodios de vómito con sangre (hematemesis). También tenía hinchazón, dolor y enrojecimiento en la pierna izquierda, que limitaban su movimiento.\n\nEn el hospital presentaba anemia severa y recibió tres transfusiones de sangre. Un ecodoppler de la pierna mostró una trombosis venosa profunda (un coágulo en una vena profunda). Un ecografía abdominal encontró infartos en el bazo y el hígado y cambios hepáticos crónicos. La endoscopia mostró varices pequeñas sin sangrado activo. La tomografía (TAC) mostró aumento de tamaño del hígado y del bazo (hepatosplenomegalia) y muchos ganglios agrandados en axilas, mediastino y alrededor de la aorta, lo que sugirió una enfermedad infiltrativa (posible tumor).\n\nSe tomó una biopsia de un ganglio axilar y un aspirado de médula ósea (muestras para mirar las células al microscopio). Estos estudios mostraron proliferación de células linfoides e infiltración linfoplasmocitaria, por lo que se diagnosticó un linfoma no Hodgkin en estadio IV (un tipo de cáncer de los linfocitos que ya afecta varios órganos). La paciente fue enviada a un hospital de tercer nivel para confirmar el diagnóstico con inmunohistoquímica; allí identificaron un linfoma difuso de células B positivo para CD20 y se planificó el inicio de quimioterapia.\n\nQué significa esto y próximos pasos: la paciente tiene un cáncer del sistema inmunitario que requiere tratamiento especializado (quimioterapia). Ya se completaron estudios diagnósticos y fue derivada para recibir tratamiento y seguimiento en un centro con experiencia.",
+                "fh_score": 48.46
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel universitario)\n\nPaciente: mujer de 53 años con artritis reumatoide de 15 años en tratamiento con metotrexato.\n\nPresentación y evolución\n- Hace 8 meses inició astenia progresiva, pérdida de fuerza, palidez, febrículas nocturnas y pérdida de peso no intencional de ~15 kg. No recibió seguimiento médico inicial.\n- A los 3 meses apareció disnea a esfuerzos moderados.\n- Cinco días antes del ingreso presentó sangrado digestivo alto: evacuaciones melénicas abundantes (3 en 24 h) y dos episodios de hematemesis leves. Negó consumo de AINE.\n- También refirió aumento de volumen, dolor, eritema y edema en la pierna izquierda con limitación funcional.\n\nHallazgos durante la hospitalización\n- Anemia severa que requirió transfusión de 3 concentrados eritrocitarios sin complicaciones hemodinámicas aparentes.\n- Doppler venoso de miembro inferior izquierdo: trombosis venosa profunda (complicación trombótica confirmada).\n- Endoscopia digestiva alta: varices pequeñas sin sangrado activo en el momento del estudio.\n- Ecografía abdominal (realizada por sospecha de hepatopatía relacionada con metotrexato): infartos esplénicos y hepáticos y signos de cambios hepáticos crónicos.\n- Tomografía (tórax y abdomen, con contraste): hepatoesplenomegalia y múltiples conglomerados ganglionares axilares, mediastinales y paraaórticos, sugestivos de proceso infiltrativo/linfoproliferativo.\n- Biopsia de ganglio axilar derecho: proliferación neoplásica de células linfoides.\n- Aspirado de médula ósea: presencia de células plasmáticas displásicas y células reticulares; se documentó infiltración linfoplasmocitaria.\n\nDiagnóstico y manejo inicial\n- Con los antecedentes, la clínica y los estudios anatomopatológicos se diagnosticó linfoma no Hodgkin (LNH) en estadio IV.\n- Fue remitida a un hospital de tercer nivel para completar inmunohistoquímica, estadificación definitiva e inicio de tratamiento. En el centro de referencia se identificó linfoma difuso de células B CD20+, con sobrecrecimiento de células dendríticas, y se valoró el inicio de quimioterapia.\n\nImplicaciones clínicas y consideraciones importantes\n- El cuadro combina complicaciones graves: sangrado digestivo, anemia significativa, trombosis venosa profunda e infartos esplénicos/hepáticos, todas ellas asociadas al proceso neoplásico sistémico y que requieren manejo multidisciplinario.\n- Necesidades inmediatas y siguientes pasos esperables: confirmación inmunohistoquímica y estadificación completa (para planificar quimioterapia), discusión del riesgo/beneficio de anticoagulación por la trombosis frente al reciente sangrado digestivo, soporte transfusional y manejo de complicaciones infecciosas y hepáticas, y valoración por hematología/oncología para iniciar esquema específico dirigido a LNH difuso de células B (CD20+).\n- La historia de tratamiento con metotrexato es relevante porque la inmunosupresión crónica puede aumentar el riesgo de linfomas, pero la relación causal debe evaluarse en el contexto clínico y patológico.\n\nResumen empático\nSe trata de una mujer con pérdida progresiva de salud y complicaciones serias atribuibles a un linfoma sistémico avanzado. Fue correctamente evaluada y derivada para confirmación diagnóstica y tratamiento oncohematológico especializado. El enfoque inmediato combina control de complicaciones (anemia, sangrado, trombosis) y el inicio temprano de quimioterapia apropiada según la subclasificación del linfoma.",
+                "fh_score": 24.53
+            }
+        }
+    },
+    {
+        "article": "Un hombre de 56 años se presentó en el departamento de urgencias de nuestro hospital debido a una falta de aire repentina y un episodio de síncope mientras caminaba dentro de su casa. Se sometió a una prostatectomía laparoscópica asistida por robot para el carcinoma de próstata, 5 días antes de su presentación en el departamento de urgencias. Su curso postoperatorio en el hospital fue sin incidentes. En el departamento de urgencias, su presión arterial era de 94/54 mmHg, frecuencia cardiaca de 121 latidos por minuto, frecuencia respiratoria de 20 respiraciones por minuto, no tenía fiebre y su saturación de oxígeno era de 92% con 6 L por minuto de oxígeno a través de una cánula nasal. El examen cardiaco reveló S1S2, regular, taquicardia, sin murmullos/galopes/ruidos respiratorios. El examen respiratorio reveló ruidos respiratorios vesiculares normales bilaterales. Se observó que tenía edema de extremidad inferior izquierdo asimétrico. El electrocardiograma (ECG) reveló taquicardia sinusal, sin cambios en la onda ST-T. La troponina estaba levemente elevada a 0.120 ng/mL (rango de referencia: 0 a 0.020). La angiografía por tomografía computarizada (CTA) del tórax mostró embolia pulmonar bilateral extensa, con una gran carga de coágulos en ambas arterias pulmonares principales, evidencia de insuficiencia ventricular derecha aguda. El examen dúplex venoso mostró trombosis venosa profunda izquierda aguda. El ecocardiograma mostró fracción de eyección ventricular izquierda normal del 60% al 65%, movimiento septal anormal y aplanamiento del tabique interventricular, presión sistólica ventricular derecha de 49.7 mmHg, ventrículo derecho moderadamente dilatado, función ventricular derecha disminuida, excursión sistólica tricuspídea de 12.1 mm (normal 15 a 20 mm). Como la mayoría de la carga de coágulos era distal, no se consideró susceptible de extracción quirúrgica, ya que la cirugía reciente era una contraindicación importante para la trombólisis. El paciente comenzó con un goteo de heparina e inhaló óxido nítrico a 20 ppm junto con 40 mg de sildenafil oral cada 8 horas. Al día siguiente, el paciente estaba hemodinámicamente estable y su óxido nítrico inhalado se redujo. Repetir el ecocardiograma 48 horas desde la presentación inicial mostró un tamaño y función del ventrículo derecho mejorados. Su presión sistólica ventricular derecha disminuyó a 22.4 mmHg y su excursión sistólica tricuspídea mejoró a 17.8 mm. Recomendamos que continuara con sildenafil durante el mes siguiente después del alta junto con anticoagulación oral con un plan de seguimiento como paciente ambulatorio. El paciente dio su consentimiento por escrito para el tratamiento durante su hospitalización. El paciente y sus familiares estaban bien informados sobre el plan de atención completo y estuvieron de acuerdo con el plan de atención.\n\nMH - Insuficiencia cardiaca/*terapia farmacológica/etiología\nMH - Humanos\nMH - Hombre\nMH - Edad Media\nMH - Inhibidores de la fosfodiesterasa 5/*uso terapéutico\nMH - Embolismo pulmonar/*complicaciones\nMH - Agentes vasodilatadores/*uso terapéutico\nMH - Disfunción ventricular, derecha/terapia/etiología\n",
+        "gold_summary": "Paciente: Hombre, 56 años\n\nDiagnóstico final: Insuficiencia cardíaca derecha por embolia pulmonar\n\nSíntomas: síncope\n\nMedicación: —\n\nProcedimiento clínico: —\n\nEspecialidad: Cardiología\n\nSe trata de un informe de caso en el que se utilizó sildenafil como agente de rescate para lograr una mejora en el tamaño y la función del ventrículo derecho en un caso de inicio agudo de embolia pulmonar masiva con insuficiencia aguda del ventrículo derecho en el escenario en el que la terapia trombolítica sistémica estaba contraindicada.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Resumen sencillo\n\nUn hombre de 56 años tuvo una emergencia. Cinco días antes, se había operado de la próstata. Mientras caminaba en su casa, de repente no podía respirar bien y se desmayó.\n\nQué tenía:\n- Tenía una trombosis en la pierna izquierda (un coágulo de sangre).\n- Ese coágulo viajó a sus pulmones. Esto se llama embolia pulmonar. Los médicos encontraron muchos coágulos en ambos pulmones.\n- La parte derecha del corazón estaba muy estresada y un poco agrandada por los coágulos. La parte izquierda del corazón estaba normal.\n\nQué le hicieron los médicos:\n- No le pudieron dar el remedio fuerte para disolver coágulos porque acababa de operarse. Eso sería peligroso.\n- Le pusieron un medicamento que evita que la sangre forme más coágulos (heparina).\n- También le dieron óxido nítrico para respirar y un medicamento por boca llamado sildenafil. Estos ayudan a abrir los vasos en los pulmones y a que el corazón derecho trabaje mejor.\n\nQué pasó después:\n- Al día siguiente estaba más estable.\n- Dos días después el corazón derecho estaba más pequeño y funcionaba mejor.\n- Lo dieron de alta con pastillas para seguir abriendo los vasos y con anticoagulantes (medicina para que no se formen más coágulos). Debía volver a control con los médicos.\n\nMensaje amable:\nLos médicos cuidaron al paciente con cuidado porque no podían usar el tratamiento habitual por su cirugía reciente. Con otros medicamentos, él mejoró y pudo volver a casa.",
+                "fh_score": 72.12
+            },
+            "B2": {
+                "text": "Resumen para lectores jóvenes (nivel B2)\n\nUn hombre de 56 años llegó a urgencias 5 días después de una operación de próstata por haber sentido una falta de aire repentina y desmayarse mientras caminaba. Tenía la presión baja y el pulso alto. Además se notó que su pierna izquierda estaba más hinchada que la derecha.\n\nQué encontraron los médicos\n- Una tomografía del tórax mostró grandes coágulos en ambas arterias pulmonares: esto se llama embolia pulmonar. Significa que fragmentos de coágulos (normalmente venas de las piernas) viajaron hasta los pulmones y bloquearon el flujo de sangre.\n- Un estudio de las venas de la pierna encontró una trombosis venosa profunda (coágulo) en la pierna izquierda.\n- El ecocardiograma (una ecografía del corazón) mostró que el ventrículo izquierdo funcionaba bien, pero el ventrículo derecho estaba agrandado y no trabajaba bien. Esto indica insuficiencia o “agotamiento” del ventrículo derecho por la carga que pusieron los coágulos en los pulmones.\n  - Medidas importantes: presión sistólica del ventrículo derecho elevada (49.7 mmHg) y una medida de movimiento del ventrículo derecho baja (TAPSE 12.1 mm; lo normal es 15–20 mm).\n\nPor qué no se usó trombólisis (disolver coágulos)\n- Aunque en algunos casos graves se usan medicamentos para disolver los coágulos o se sacan quirúrgicamente, el paciente había tenido una cirugía reciente. Eso aumentaba mucho el riesgo de sangrado, por lo que esos tratamientos no eran seguros.\n\nTratamiento que recibió\n- Anticoagulación con heparina (para evitar que se formen más coágulos).\n- Óxido nítrico inhalado (un vasodilatador que ayuda a bajar la presión en las arterias pulmonares y alivia al ventrículo derecho).\n- Sildenafil oral (un medicamento que también dilata los vasos sanguíneos pulmonares) 40 mg cada 8 horas como terapia de rescate.\n\nEvolución y alta\n- Al día siguiente el paciente estaba más estable y se redujo el óxido nítrico inhalado.\n- A las 48 horas, el ecocardiograma mostró mejoría del tamaño y la función del ventrículo derecho: la presión descendió a 22.4 mmHg y el TAPSE mejoró a 17.8 mm.\n- Se le dio el alta con anticoagulante oral y se recomendó continuar sildenafil durante un mes, con seguimiento ambulatorio.\n\nConclusión simple y amable\nEste caso muestra que, cuando no se pueden usar tratamientos que disuelven coágulos por riesgo de sangrado después de una cirugía, combinar anticoagulación con medidas que bajan la presión en las arterias pulmonares (óxido nítrico y sildenafil) puede ayudar al ventrículo derecho a recuperarse. El equipo explicó todo al paciente y su familia y obtuvo su consentimiento para el tratamiento.",
+                "fh_score": 59.33
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel universitario, tono empático)\n\nPaciente\n- Hombre de 56 años, cinco días después de prostatectomía laparoscópica asistida por robot por cáncer de próstata.\n\nPresentación\n- Llegó a urgencias con disnea súbita y un episodio de síncope mientras caminaba en su casa.\n- Signos iniciales: PA 94/54 mmHg, FC 121 lpm, FR 20 rpm, SatO2 92% con 6 L/min por cánula nasal.\n\nHallazgos relevantes\n- Exploración: taquicardia sin otros ruidos cardíacos anormales; ruidos respiratorios vesiculares bilaterales conservados; edema asimétrico en la pierna izquierda.\n- ECG: taquicardia sinusal sin cambios isquémicos.\n- Troponina: levemente elevada (0,120 ng/mL; referencia 0–0,020).\n- Angio-TC torácica: embolia pulmonar bilateral extensa con gran carga de trombos en ambas arterias pulmonares principales y signos de insuficiencia ventricular derecha aguda.\n- Eco-Doppler venoso: trombosis venosa profunda (Trombosis venosa profunda) aguda en miembro inferior izquierdo.\n- Ecocardiograma: \n  - Fracción de eyección del ventrículo izquierdo normal (60–65%).\n  - Aplanamiento del septo interventricular y movimiento septal anormal (señales de sobrecarga derecha).\n  - Ventrículo derecho moderadamente dilatado y función reducida.\n  - Presión sistólica ventricular derecha estimada 49.7 mmHg (elevada).\n  - TAPSE (excursión sistólica tricuspídea) 12.1 mm (normal 15–20 mm) — indicador de función sistólica del ventrículo derecho disminuida.\n\nDiagnóstico\n- Insuficiencia ventricular derecha aguda secundaria a embolia pulmonar masiva, con TEP secundario a TEP venosa profunda postoperatoria.\n\nRazonamiento terapéutico y tratamiento aplicado\n- El paciente no fue candidato a trombólisis sistémica por la cirugía reciente (riesgo alto de sangrado) y la mayoría de los trombos eran demasiado distales para extracción quirúrgica.\n- Se inició:\n  - Heparina intravenosa (anticoagulación).\n  - Óxido nítrico inhalado (20 ppm) como vasodilatador pulmonar selectivo.\n  - Sildenafil oral 40 mg cada 8 horas (inhibidor de la fosfodiesterasa tipo 5, usado aquí como vasodilatador pulmonar de rescate) — uso fuera de ficha técnica en este contexto, empleado para reducir la poscarga del ventrículo derecho.\n- Consentimiento informado obtenido.\n\nEvolución y resultado\n- A las 24 horas el paciente estaba hemodinámicamente estable y se redujo la dosis de óxido nítrico inhalado.\n- A las 48 horas, ecocardiograma mostró mejoría significativa del ventrículo derecho: presión sistólica derecha disminuyó a 22.4 mmHg y TAPSE mejoró a 17.8 mm.\n- Alta hospitalaria con plan de continuar sildenafil durante un mes y anticoagulación oral indefinida según seguimiento ambulatorio.\n\nImplicaciones prácticas y consideraciones\n- Este caso ilustra el uso de vasodilatadores pulmonares (sildenafil e óxido nítrico inhalado) como medida de rescate en insuficiencia ventricular derecha aguda por embolia pulmonar cuando la trombólisis está contraindicada.\n- Mecanismo: la vasodilatación pulmonar reduce la resistencia vascular pulmonar y la poscarga del ventrículo derecho, permitiendo recuperación funcional.\n- Limitaciones: evidencia basada en un caso clínico; no prueba causal definitiva. El uso de sildenafil en este contexto es off-label y requiere monitorización estrecha por riesgo de hipotensión y contraindicaciones (por ejemplo, nitratos sistémicos).\n- Seguimiento recomendado: control clínico y ecocardiográfico, manejo continuo de anticoagulación y vigilancia de efectos adversos.\n\nComentario final (empático)\nEl equipo tratante adoptó una estrategia terapéutica prudente y multidisciplinaria frente a una situación de alto riesgo (TEP masivo con contraindicación para trombólisis). El paciente respondió bien al tratamiento combinado, con recuperación rápida de la función del ventrículo derecho. Casos como este subrayan la necesidad de más estudios para definir el papel de fármacos vasodilatadores sistémicos u inhalados como terapia puente o de rescate en pacientes con embolia pulmonar y falla ventricular derecha cuando las opciones estándar están limitadas.",
+                "fh_score": 37.27
+            }
+        }
+    },
+    {
+        "article": "Presentamos el caso de un hombre de 78 años con antecedentes conocidos de fibrilación auricular crónica, cardiopatía hipertensiva y miocardiopatía no isquémica. Tenía una reducción global de la fracción de eyección del ventrículo izquierdo del 40-45 %, y su ecocardiograma no mostraba anomalías significativas. El paciente había sido seguido en la clínica de cardiología ambulatoria, donde fue tratado por insuficiencia cardiaca crónica en estadio C del Colegio Americano de Cardiología (ACC) con síntomas de clase III de la Asociación del Corazón de Nueva York (NYHA). A pesar de varios cambios en sus diuréticos e intentos de controlar su estado de líquidos, ganó 40 libras de peso en un período de 3 meses, con un aumento significativo de la falta de aire. A medida que su descompensación de la insuficiencia cardiaca progresó, fue hospitalizado durante 8 días y tratado con furosemida intravenosa (IV). Debido a su clasificación de la NYHA y su ingreso al hospital por exacerbación de la insuficiencia cardiaca, se indicó y se realizó un monitoreo hemodinámico invasivo con implantación de CardioMEMS. La implantación de su CardioMEMS se realizó en Grand Blanc, Michigan, a una altitud de 837 pies con una presión atmosférica de 731.2 el 9 de abril de 2019. Las mediciones hemodinámicas iniciales del cateterismo cardiaco mostraron una presión sistólica PA de 45 mmHg, presión diastólica PA de 16 mmHg y una presión PA media de 30 mmHg. La presión auricular derecha fue de 21 mmHg, presión ventricular derecha de 44/17 mmHg y la presión media de la cuña pulmonar fue de 24 mmHg. El procedimiento se completó sin complicaciones y el paciente fue dado de alta el mismo día.\n\nTras la implantación de CardioMEMS, el paciente permaneció estable durante 4 semanas sin empeoramiento de los síntomas de insuficiencia cardiaca. Cumplió con las lecturas diarias de CardioMEMS con una PA media que osciló entre 27 y 31 mmHg, y una presión diastólica de PA de 17 a 21 mmHg. Estos hallazgos hemodinámicos globales fueron estables en comparación con los del momento de la implantación.\n\nEl paciente viajó a Denver, Colorado, durante cuatro días a una altitud de 5280 pies con una presión atmosférica de 596.8 atm el 5 de mayo de 2019. Las grabaciones del primer día de su visita mostraron un aumento de la presión sistólica de 44 mmHg a 73 mmHg, un aumento de la presión media de 30 mmHg a 53 mmHg y un aumento de la presión diastólica de 20 mmHg a 40 mmHg. Al mismo tiempo, notó un aumento significativo de la falta de aire y la hinchazón de las extremidades inferiores. No buscó atención médica, sino que se contactó con su cardiólogo primario en Michigan. Su oxígeno nasal de referencia se incrementó de 1 litro a 2 litros y su dosis de furosemida se duplicó de 40 mg diarios a dos veces al día. Afortunadamente, este tratamiento mejoró los síntomas del paciente y evitó la admisión hospitalaria. Debido a que se evitó la admisión hospitalaria, no se dispuso de valores de laboratorio, imágenes de diagnóstico y signos vitales clínicos.\n\nDurante su estancia hospitalaria de 4 días, sus presiones invasivas se mantuvieron altas, pero disminuyeron lentamente y se estabilizaron con una PA sistólica de 72 mmHg, una PA media de 49 mmHg y una PA diastólica de 35 mmHg el día previo a su regreso a Michigan. El quinto día, volvió a Michigan y sus mediciones de presión invasiva se normalizaron rápidamente, con una presión PA media de 29 mmHg y una presión PA diastólica de 20 mmHg. Ha seguido estando bien mientras estuvo en Michigan con diuréticos de mantenimiento continuos y un control diario de las presiones PA con su dispositivo CardioMEMS.\n\nMH - Envejecido\nMH - *Altitud\nMH - Monitoreo de presión arterial, ambulatorio\nMH - *Insuficiencia cardiaca/diagnóstico/etiología\nMH - Hospitalización\nMH - Humanos\nMH - Hombre\nMH - Arteria Pulmonar\n",
+        "gold_summary": "Presentamos el caso de un hombre de 78 años con una exacerbación de la insuficiencia cardiaca mientras viajaba a gran altitud. Se detectó un aumento de sus presiones arteriales pulmonares (PA) mediante su dispositivo CardioMEMS implantado. La comprensión del cambio esperado en los registros de presión de la PA ayudó a identificar una verdadera exacerbación de la insuficiencia cardiaca en nuestro paciente. Esto llevó a un cambio rápido en la terapia médica, que en última instancia evitó la hospitalización.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Este cuento habla de un hombre de 78 años con problemas del corazón. Le pusieron un pequeño sensor dentro de una arteria del pulmón. El sensor mide la presión y ayuda a los médicos a ver cómo está su corazón.\n\nDurante un mes estuvo estable. Luego viajó a Denver, que está muy alto sobre el nivel del mar. Allí el sensor mostró que la presión en sus pulmones subió mucho. Él tuvo más falta de aire y las piernas se le hincharon.\n\nNo fue al hospital. Llamó a su médico. Le subieron el oxígeno y le dieron más pastillas para sacar el líquido del cuerpo. Con eso mejoró y no tuvo que quedarse en el hospital. Cuando volvió a su ciudad, la presión volvió a la normalidad.\n\nEl sensor ayudó a encontrar el problema rápido. Gracias a eso cambiaron su tratamiento a tiempo y él se recuperó sin entrar al hospital.",
+                "fh_score": 90.54
+            },
+            "B2": {
+                "text": "Resumen para lectores jóvenes (nivel secundaria)\n\nPresentamos el caso de un hombre de 78 años con insuficiencia cardiaca crónica que llevaba implantado un pequeño sensor llamado CardioMEMS. CardioMEMS se coloca en la arteria pulmonar (el vaso que lleva la sangre del corazón a los pulmones) y mide la presión allí cada día. Los médicos usan esas cifras para ver si el corazón está trabajando bien o si hay acumulación de líquido en el cuerpo.\n\nAntes del viaje, sus lecturas eran estables: la presión media en la arteria pulmonar estaba alrededor de 27–31 mmHg. Viajó a Denver (5.280 pies de altitud) y, durante los primeros días, el sensor mostró un aumento grande de las presiones (por ejemplo, la presión media subió de 30 a 53 mmHg). Al mismo tiempo, el paciente tuvo más dificultad para respirar y notó hinchazón en las piernas. La elevación de la presión pulmonar puede deberse al cambio de altitud, pero también puede señalar que la insuficiencia cardiaca empeora.\n\nEl paciente llamó a su cardiólogo. Le aumentaron el oxígeno y duplicaron la dosis de furosemida (un diurético que ayuda a eliminar el exceso de líquido). Con ese tratamiento, sus síntomas mejoraron y se evitó la hospitalización. Mientras estuvo en Denver las presiones fueron bajando lentamente; al volver a la altitud baja, las lecturas del CardioMEMS volvieron rápidamente a valores cercanos a los iniciales.\n\nQué podemos aprender de este caso\n- El monitoreo remoto con CardioMEMS permitió detectar rápido un aumento importante de la presión pulmonar y relacionarlo con síntomas reales.\n- El viaje a gran altitud puede aumentar las presiones pulmonares, pero ante síntomas (más falta de aire y edema) es importante tratar como una descompensación de insuficiencia cardiaca.\n- La comunicación rápida con el equipo médico y ajustes de tratamiento (más oxígeno y diuréticos) pueden evitar la hospitalización.\n- Seguir con controles y diuréticos de mantenimiento fue clave para mantener al paciente estable después del regreso.\n\nEste caso muestra cómo la vigilancia continua y respuestas médicas rápidas ayudan a cuidar a personas con insuficiencia cardiaca, especialmente cuando viajan a lugares de mucha altitud.",
+                "fh_score": 58.31
+            },
+            "B3": {
+                "text": "Presentamos el caso de un hombre de 78 años con fibrilación auricular crónica, cardiopatía hipertensiva y miocardiopatía no isquémica, seguido por insuficiencia cardíaca crónica estadio C (NYHA clase III). Su fracción de eyección del ventrículo izquierdo era de 40–45 % y el ecocardiograma no mostraba hallazgos significativos. Debido a una descompensación con ganancia de peso y empeoramiento de la disnea después de intentos de manejo ambulatorio, se implantó un sensor CardioMEMS para monitorización invasiva ambulatoria de la presión arterial pulmonar (PA) el 9 de abril de 2019 en Grand Blanc, Michigan (altitud 837 pies).\n\nHallazgos hemodinámicos y evolución\n- Mediciones iniciales en el cateterismo: PA sistólica 45 mmHg, PA diastólica 16 mmHg, PA media 30 mmHg; presión auricular derecha 21 mmHg; presión de cuña 24 mmHg. El procedimiento fue sin complicaciones.\n- En las 4 semanas posteriores a la implantación, las lecturas diarias del CardioMEMS se mantuvieron estables (PA media 27–31 mmHg; PA diastólica 17–21 mmHg) y el paciente se encontró clínicamente estable.\n- El 5 de mayo de 2019 el paciente viajó a Denver (altitud 5.280 pies). Ese mismo día el CardioMEMS mostró un aumento marcado de las presiones: PA sistólica de 44→73 mmHg, PA media de 30→53 mmHg, PA diastólica de 20→40 mmHg. Coincidiendo con estos cambios, el paciente presentó incremento significativo de disnea e edema en miembros inferiores.\n- No requirió ingreso: el cardiólogo aumentó el oxígeno domiciliario de 1 L a 2 L y duplicó la furosemida oral (de 40 mg una vez diaria a 40 mg dos veces al día). Los síntomas mejoraron y el paciente evitó hospitalización.\n- Durante su estancia en Denver las presiones se mantuvieron elevadas pero fueron descendiendo lentamente (el día antes del regreso PA sistólica ≈72 mmHg, PA media 49 mmHg, PA diastólica 35 mmHg). Tras volver a Michigan las lecturas se normalizaron rápidamente (PA media 29 mmHg, PA diastólica 20 mmHg) y el paciente permaneció estable con tratamiento de mantenimiento.\n\nInterpretación y puntos clave\n- Lo anormal: aumentos agudos y marcados en las presiones arteriales pulmonares durante la estancia en altitud elevada, acompañados de empeoramiento sintomático (disnea y edema), indicaron una verdadera descompensación hemodinámica.\n- Probable mecanismo: la hipoxia asociada con la altitud alta produce vasoconstricción pulmonar, lo que eleva las resistencias y las presiones en la circulación pulmonar; en un paciente con insuficiencia cardíaca esto puede precipitar o agravar la congestión.\n- Papel del CardioMEMS: la monitorización invasiva ambulatoria permitió detección inmediata del cambio hemodinámico mientras el paciente estaba fuera de su centro habitual, lo que facilitó ajustes médicos remotos rápidos y evitó la hospitalización.\n\nImplicaciones clínicas y recomendaciones prácticas\n- Para pacientes con insuficiencia cardíaca y dispositivos de monitorización hemodinámica: considerar el efecto de la altitud en las lecturas del dispositivo y en la clínica del paciente; interpretar cambios absolutos en contexto (síntomas, uso de oxígeno, altitud).\n- Antes de viajar a altitudes altas, aconsejar evaluación y planificación: posible ajuste profiláctico de diuréticos, disponer de oxígeno suplementario si está indicado, y acordar un plan de contacto y manejo remoto con el equipo de cardiología.\n- El monitoreo remoto invasivo puede mejorar la seguridad de pacientes con insuficiencia cardíaca al permitir intervenciones tempranas y reducir admissions, pero se necesitan datos adicionales para guiar protocolos específicos sobre viajes a altitud.\n\nConclusión\nEn este caso, el aumento de las presiones pulmonares detectado por CardioMEMS durante un viaje a gran altitud se correlacionó con empeoramiento clínico; la intervención médica precoz y ambulatoria (más oxígeno y mayor diurético) estabilizó al paciente y evitó la hospitalización. Este caso ilustra la importancia de reconocer cómo factores ambientales como la altitud pueden afectar las mediciones hemodinámicas y el curso de la insuficiencia cardíaca.",
+                "fh_score": 40.77
+            }
+        }
+    },
+    {
+        "article": "Un hombre de 55 años, previamente sano, fue derivado al servicio de urgencias por su médico de cabecera, quejándose de una fiebre de 3 semanas de evolución, tos productiva, disnea y sibilancias. Tenía un historial de 80 paquetes-año de consumo de tabaco y un historial familiar positivo de cáncer de pulmón. Había sido tratado por su médico de cabecera con un ciclo de amoxicilina oral y prednisona oral, pero sus síntomas empeoraron. Cuando llegó al servicio de urgencias, su recuento de glóbulos blancos era de 16,4 × 109/L (rango normal: 4,0-10,0 × 109/L), el recuento de neutrófilos de 13,8 × 109/L (rango normal: 2,0-7,0 × 109/L), la proteína C reactiva era de 118 mg/L (normal: 0-5 mg/L) y el sodio sérico era de 112 mmol/L (rango normal: 136-145 mmol/L). Otros marcadores bioquímicos estaban dentro de los límites normales. Una radiografía de tórax mostró consolidación del lóbulo medio e inferior derecho con derrame pleural moderado asociado. Fue admitido y tratado como neumonía adquirida en la comunidad y el estudio confirmó el diagnóstico de SIADH.\n\nEl paciente empeoró a pesar de la administración intravenosa de piperacilina-tazobactam y de claritromicina oral, con empeoramiento de la consolidación en la repetición de la radiografía de tórax. El paciente fue trasladado a la unidad de cuidados intensivos y, posteriormente, se le realizó una intubación y ventilación. Una tomografía computarizada (TC) de su tórax reveló una masa hilar derecha con afectación mediastinal y adenopatía hilar derecha con consolidación de espacio aéreo extenso superpuesta. Una biopsia realizada durante la broncoscopia reveló células pequeñas, histológicamente monótonas, con núcleos ovoides oscuros. No se observaron nucleolos, y varias figuras mitóticas estaban presentes. Las células tienen un citoplasma estrecho y mal definido. La inmunohistoquímica realizada en las células tumorales mostró negatividad a CD45, AE1/AE3, positividad a TTF1. También se observaron sinapsina mínima focal y positividad a cromogranina A. Este perfil inmunohistoquímico fue consistente con un diagnóstico de cáncer de pulmón de células pequeñas.\n\nLa estadificación completa, que consistió en una tomografía computarizada del cerebro y tórax-abdomen-pelvis, confirmó una enfermedad en estadio extenso con metástasis suprarrenales. El estado funcional ECOG de la paciente era deficiente debido a una combinación de SCLC y dificultad respiratoria que requería ventilación artificial. Como las tasas de respuesta con quimioterapia en SCLC son generalmente altas, se inició un tratamiento quimioterápico doble en forma de carboplatino y etopósido mientras la paciente estaba intubada en la UCI.\n\nEl paciente respondió bien al tratamiento y fue extubado y trasladado a la sala de ventilación no invasiva. Una nueva tomografía computarizada de tórax después de 1 ciclo mostró una buena respuesta parcial al tratamiento.\n\nEn el día 3 del ciclo 2 de quimioterapia, la paciente desarrolló dolor en la parte inferior de la espalda y debilidad bilateral en las extremidades inferiores. El examen identificó paresia motora bilateral en las extremidades inferiores (grado 3 del Consejo de Investigación Médica [MRC]) y paresia sensorial. El examen sensorial reveló ausencia de tacto ligero, pinchazo, coordinación y propiocepción en las extremidades inferiores. El día 3 de etopósido se retrasó como resultado de los nuevos hallazgos neurológicos.\n\nSe realizaron un TAC cerebral, resonancia magnética (RM) cerebral y resonancia magnética (RM) de la columna para investigar los nuevos hallazgos neurológicos. Todos los resultados radiológicos fueron normales, sin evidencia de metástasis intracerebrales, accidente cerebrovascular, mielitis o enfermedad leptomeníngea. Además, no hubo evidencia radiográfica obvia de compresión de la médula espinal, ya sea por compresión extrínseca por depósito metastásico óseo o depósitos intramedulares o leptomeníngeos.\n\nDos días después, un examen neurológico de seguimiento reveló tetraplejía, MRC grado 0 en las extremidades superiores e inferiores. Todos los reflejos tendinosos profundos estaban ausentes. Los músculos de la cabeza y el cuello, la cognición y el habla no se vieron afectados, y el examen de los nervios craneales fue normal.\n\nLos análisis de sangre de rutina, incluida la proteína C reactiva y la velocidad de sedimentación de eritrocitos, fueron normales. Los análisis de sangre específicos, incluidos los de vitamina B12 en suero, folato, serología del VIH, serología de la enfermedad de Lyme, serología del virus de Epstein-Barr, serología de Brucella, anticuerpos tiroideos, pruebas de función tiroidea, ANCA, ENA, ANA y electroforesis de proteínas séricas, fueron negativos o normales. Se enviaron anticuerpos para las pruebas de sangre Hu, Ri y Yo, y todos fueron negativos. En este momento, se sospechó un diagnóstico de polineuropatía simétrica ascendente aguda motora y sensorial y se realizó una punción lumbar. Los resultados del líquido cefalorraquídeo (LCR) revelaron una proteína total elevada de 3.32 g/L (normal 0.15–0.45), y otros parámetros fueron normales, con una repetición 3 días después que mostró resultados similares. La citología del LCR fue negativa para la malignidad y el cultivo del LCR también fue negativo.\n\nLa electromiografía fue consistente con una polineuropatía difusa predominantemente motora; los potenciales sensoriales se conservaron, pero fueron de pequeña amplitud. Las conducciones motoras mostraron características axonales/desmielinizantes mixtas, que no eran típicas del síndrome de Guillain-Barré.\n\nSe realizaron estudios de electromiografía y conducción nerviosa para investigar la polineuropatía motora y sensorial aguda del paciente. Los estudios de conducción nerviosa revelaron lo siguiente:\n\n•Nervios motores:\n◦Las amplitudes del potencial de acción muscular compuesto (CMAP) se redujeron notablemente en los nervios tibial y cubital de forma bilateral (tibial: 1,2 mV; normal > 4 mV; cubital: 0,8 mV; normal > 3 mV).\n◦Las velocidades de conducción motora (MCV) se desaceleraron en los nervios tibial y cubital (tibial: 30 m/s; normal > 40 m/s; cubital: 34 m/s; normal > 50 m/s), lo que es coherente con la desmielinización.\n◦Las latencias motoras distales se prolongaron, con un patrón mixto axonal y desmielinizante.\n•Nervios sensoriales:\n◦Las amplitudes del potencial de acción nerviosa sensorial (SNAP) se conservaron, pero fueron de poca amplitud en los nervios surales y medianos (sural: 4 μV; normal > 10 μV; mediano: 6 μV; normal > 15 μV).\n◦Las velocidades de conducción sensorial (VCS) se encontraban dentro de los límites normales.\nLos hallazgos electrofisiológicos revelaron una polineuropatía predominantemente motora con características axonales y desmielinizantes mixtas, atípicas para los síndromes paraneoplásicos clásicos, que generalmente son predominantemente sensoriales y se caracterizan por la ausencia de SNAP.\n\nMientras tanto, mientras estas investigaciones estaban en curso, se inició al paciente con dexametasona intravenosa y 0.4 g/kg/día de inmunoglobulina intravenosa sin ninguna mejora sintomática.\n\n3. Resultados y seguimiento\nA pesar de una importante respuesta oncológica inicial a la quimioterapia, el estado neurológico del paciente se deterioró rápidamente. Después de 1 ciclo de carboplatino y etopósido, las imágenes confirmaron una respuesta parcial con una reducción en el tamaño del tumor. Sin embargo, el inicio de una polineuropatía motora y sensorial grave y ascendente condujo a un compromiso respiratorio. Esta disociación entre las respuestas oncológicas y neurológicas destaca la naturaleza agresiva y refractaria del SNP, incluso cuando el tratamiento del cáncer es efectivo. Aunque la dexametasona intravenosa y la inmunoglobulina intravenosa se administraron rápidamente, no lograron mejorar los resultados neurológicos.\n\nSe llevaron a cabo largas y repetidas discusiones multidisciplinares con el paciente y su familia sobre la admisión en la unidad de cuidados intensivos para recibir apoyo ventilatorio. El paciente estaba bien informado y consciente de que era poco probable que sus síntomas neurológicos fueran reversibles y, por lo tanto, optó por el mejor tratamiento de apoyo. El paciente falleció 3 semanas después de los síntomas iniciales. La decisión del paciente de rechazar el apoyo ventilatorio invasivo en favor de los cuidados paliativos pone de relieve las consideraciones éticas que rodean la calidad de vida en los síndromes paraneoplásicos de progresión rápida.\n",
+        "gold_summary": "Preocupaciones del paciente: Un hombre de 55 años con un historial de 80 años fumando presenta al hospital con un historial de 3 semanas de fiebres, tos productiva, disnea y sibilancias. No tenía comorbilidades significativas.\n\nDiagnóstico: Extensas investigaciones radiológicas revelaron una gran masa en el hilum derecho que comprimía el bronquio inferior derecho con depósitos suprarrenales metastásicos. Las investigaciones bioquímicas confirmaron el síndrome de secreción inadecuada de la hormona antidiurética, y la histología identificó un CPCP.\n\nIntervenciones: A pesar de iniciar una quimioterapia combinada con carboplatino y etopósido, el paciente desarrolló parálisis motora progresiva y pérdida sensorial en el transcurso de 4 días, lo que derivó en un diagnóstico de polineuropatía motora y sensorial aguda paraneoplásica.\n\nResultados: Su estado empeoró rápidamente y falleció 14 días después de la aparición de los síntomas debido a una insuficiencia respiratoria, lo que pone de relieve la agresividad de los síndromes paraneoplásicos.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había un hombre de 55 años que fumaba mucho. Durante tres semanas tuvo fiebre, tos y le faltaba el aire. Su doctor le dio antibióticos y pastillas, pero no mejoró.\n\nEn el hospital le hicieron una radiografía y un escáner. Tenía una masa grande en el pulmón derecho y la enfermedad ya había llegado a las glándulas suprarrenales. Un trocito de la masa (biopsia) mostró que era cáncer de pulmón de células pequeñas. También tenía la sangre con muy poco sodio, un problema llamado SIADH.\n\nEmpezó quimioterapia mientras estaba en la unidad de cuidados intensivos. El tumor se hizo más pequeño con el primer ciclo de tratamiento. Pero después, en el segundo ciclo, empezó a perder fuerza en las piernas. En pocos días quedó paralizado en brazos y piernas. También perdió la sensibilidad de abajo hacia arriba.\n\nHicieron muchas pruebas. Las imágenes del cerebro y de la médula fueron normales. El líquido que rodea el cerebro y la médula tenía mucha proteína, pero no había células de cáncer. Los estudios de los nervios mostraron daño serio. Los médicos pensaron que su propio cuerpo estaba atacando los nervios por culpa del cáncer; esto se llama síndrome paraneoplásico, y a veces pasa con este tipo de cáncer.\n\nLe dieron medicinas para el sistema inmune, pero no mejoró. La respiración empeoró. El paciente habló con su familia y decidió no recibir más respiración artificial. Recibió cuidados para estar cómodo y murió unas tres semanas después de que empezaron los problemas de los nervios.\n\nEste caso muestra que, aunque el cáncer pudiera responder al tratamiento, a veces las enfermedades que el cáncer provoca en los nervios pueden avanzar muy rápido y ser fatales. Los médicos y la familia tomaron las decisiones cuidando lo que él quería.",
+                "fh_score": 75.33
+            },
+            "B2": {
+                "text": "Summary (for older children / teens)\n\nWhat happened\n- A 55-year-old man who had smoked heavily came to hospital after 3 weeks of fever, a cough that made mucus, shortness of breath and wheeze. Initial antibiotics and steroids did not help.\n- Tests showed infection-like blood changes, very low blood sodium (112 mmol/L) caused by SIADH — a condition where the body makes too much antidiuretic hormone and keeps extra water — and a chest X-ray with a blockage and fluid in the right lung.\n- A CT scan and a biopsy showed small cell lung cancer (a fast-growing type of lung cancer) that had already spread to the adrenal glands. He became very breathless and needed ventilator support in the intensive care unit.\n\nTreatment and tumour response\n- Because small cell lung cancer often responds to chemotherapy, doctors started carboplatin and etoposide while he remained in hospital on a ventilator.\n- The cancer did shrink with treatment and he was able to come off the ventilator to less invasive breathing support.\n\nNew and serious neurological problems\n- During the second cycle of chemotherapy, he developed sudden lower back pain and weakness in both legs. Over two days the weakness spread to all four limbs and he lost reflexes, though his thinking and cranial nerves (face and head muscles) stayed normal.\n- Brain and spine scans were normal — there was no stroke, no tumour pressing on the spinal cord, and no obvious spread into the brain or spinal fluid on imaging.\n- A lumbar puncture (spinal tap) showed very high protein in the cerebrospinal fluid, but no cancer cells or infection.\n- Nerve tests (EMG and nerve conduction studies) showed a widespread nerve problem that mainly affected motor nerves and had both axonal (nerve-fibre) and demyelinating (insulation) features. Sensory nerve signals were reduced but not completely absent. This pattern was not typical for the usual paraneoplastic nerve syndromes, which are often mainly sensory.\n- Blood tests for common paraneoplastic antibodies (Hu, Ri, Yo) and many other causes were negative.\n\nResponse to immune treatment and outcome\n- Doctors gave high-dose steroids (dexamethasone) and intravenous immunoglobulin (IVIG), treatments used for immune-related nerve damage, but he did not improve.\n- The neurologic condition led to breathing failure despite the cancer responding to chemotherapy. After long discussions with his family, he chose comfort-focused care rather than further invasive ventilator support. He died three weeks after his first symptoms.\n\nWhat this shows\n- This case shows a rare, very fast, and severe paraneoplastic peripheral neuropathy — a nerve disease caused by the body’s reaction to a cancer — that can progress quickly and not get better with usual immune treatments.\n- It also highlights a difficult situation where the cancer itself responds to treatment, but the immune-related neurological damage continues to get worse, which can lead to serious disability and life-threatening breathing failure.\n- Decisions about aggressive life support are personal and were made here after careful discussion with the patient and family.",
+                "fh_score": 78.74
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel lector universitario)\n\nPresentación\n- Hombre de 55 años, fumador importante (80 paquetes-año), sin comorbilidades previas conocidas.\n- Síntomas iniciales: fiebre durante 3 semanas, tos productiva, disnea y sibilancias. Tratado en atención primaria con amoxicilina y prednisona sin mejora.\n\nHallazgos clave y diagnóstico oncológico\n- Analíticas anormales al ingreso: leucocitosis (16,4 × 10^9/L), neutrofilia (13,8 × 10^9/L), proteína C reactiva elevada (118 mg/L) e hiponatremia marcada (Na 112 mmol/L) consistente con SIADH (síndrome de secreción inadecuada de hormona antidiurética).\n- Radiografía/TC torácica: consolidación extensa en lóbulo medio e inferior derecho, derrame pleural moderado y masa hiliar derecha con afectación mediastinal y adenopatía.\n- Biopsia broncoscópica: tumor de células pequeñas de pulmón (small‑cell lung cancer, SCLC) — inmunohistoquímica: TTF1 positiva, CD45 y AE1/AE3 negativas; sinapsina focal mínima y cromogranina A positiva.\n- Estadificación: enfermedad en estadio extenso con metástasis suprarrenales.\n- Situación funcional comprometida por insuficiencia respiratoria que precisó ventilación mecánica.\n\nTratamiento inicial y respuesta tumoral\n- Se inició quimioterapia combinada (carboplatino + etopósido) incluso mientras el paciente estaba intubado, dado que SCLC suele responder a quimioterapia.\n- Buena respuesta oncológica inicial: reducción tumoral documentada tras 1 ciclo y posibilitó extubación.\n\nDesarrollo neurológico agudo\n- Durante el ciclo 2 (día 3) apareció dolor lumbar y debilidad bilateral de las piernas, progresando en 48–72 horas a tetraplejía completa con arreflexia generalizada; función bulbar, nervios craneales y cognición preservadas.\n- Estudios por imagen (TC cerebral, RNM cerebral y de columna) normales: sin metástasis intracraneal, compresión medular, mielitis ni enfermedad leptomeníngea evidente.\n- Punción lumbar: proteína total muy elevada (3,32 g/L) con recuento celular normal — hallazgo de “disociación albúmino-citológica”.\n- Citología y cultivos de LCR negativos para malignidad o infección.\n- Serologías y panel extendido (incluyendo anticuerpos paraneoplásicos Hu, Ri, Yo) negativos; otras causas metabólicas/infecciosas/autoinmunes descartadas por pruebas de rutina.\n- Electrofisiología (EMG/velocidades de conducción): polineuropatía difusa predominantemente motora con rasgos mixtos axonal y desmielinizante; potenciales sensoriales conservados pero de baja amplitud. Estos hallazgos no eran típicos de los síndromes paraneoplásicos clásicos (que suelen ser predominantemente sensoriales con ausencia de SNAP).\n- Diagnóstico clínico: polineuropatía motora y sensorial aguda de probable origen paraneoplásico, atípica en su patrón electrofisiológico y de evolución muy rápida.\n\nTratamiento neurológico y resultado\n- Se administraron dexametasona IV e inmunoglobulina IV (0,4 g/kg/día) sin mejoría neurológica.\n- El cuadro progresó rápidamente hasta provocar insuficiencia respiratoria por debilidad respiratoria. Tras discusión multidisciplinaria y conversación informada con el paciente y su familia, el paciente optó por cuidados de soporte y no reintubación invasiva.\n- Falleció tres semanas después del inicio de los síntomas neurológicos.\n\nInterpretación e implicaciones\n- Este caso muestra una disociación clínica importante: tumor pulmonar de células pequeñas con buena respuesta inicial a quimioterapia, pero aparición de una polineuropatía paraneoplásica motora-sensorial fulminante que no respondió a inmunoterapia aguda y condujo al fallecimiento.\n- Hallazgos que apoyan origen paraneoplásico: inicio subagudo en contexto de cáncer de pulmón de células pequeñas, LCR con proteinorraquia aislada y exclusión de otras causas (infección, metástasis, compresión medular). Sin embargo, la ausencia de anticuerpos paraneoplásicos conocidos y el patrón electrofisiológico mixto hacen el caso atípico.\n- Pronóstico: las neuropatías paraneoplásicas pueden ser rápidamente debilitantes y, en algunos subtipos, refractarias al tratamiento inmunomodulador; cuando afectan la musculatura respiratoria, el pronóstico es pobre.\n\nRecomendaciones generales para casos similares\n- Evaluación precoz y urgente ante signos de debilidad progresiva en pacientes oncológicos: neuroimagen, LCR, estudio electrofisiológico y pruebas serológicas paraneoplásicas.\n- Tratamiento temprano con inmunoterapia (IVIG, plasmaféresis, esteroides) suele intentarse, aunque la respuesta es variable; la identificación temprana no garantiza recuperación.\n- Discutir de forma proactiva las metas de tratamiento y preferencias del paciente (incluido soporte ventilatorio) dada la posibilidad de deterioro rápido.\n- Considerar manejo multidisciplinario (oncología, neurología, cuidados intensivos, cuidados paliativos) desde fases tempranas.\n\nComentario final (tono humano)\nLamento el desenlace de este caso. A pesar de un tratamiento oncológico eficaz sobre la lesión primaria, la aparición de una neuropatía paraneoplásica fulminante mostró cómo las complicaciones neurológicas pueden ser devastadoras y poco previsibles. En situaciones así, las conversaciones honestas sobre pronóstico y las decisiones compartidas con el paciente y la familia son fundamentales.",
+                "fh_score": 24.43
+            }
+        }
+    },
+    {
+        "article": "El paciente presentado firmó el Consentimiento Informado y se cumplieron los demás principios éticos, respetando la Resolución 466/12 del Consejo Nacional de Ética en Investigación. Este informe de caso fue aprobado por el Comité de Ética en Investigación de la Universidad Federal de São Paulo (UNIFESP), bajo el dictamen número 4.455.365.\n\nEl paciente, de 66 años de edad y sexo masculino, acudió a una consulta de otorrinolaringología por presentar disfagia tipo atragantamiento con sólidos y reflujo nasal de alimentos desde hacía un año. Había sufrido un accidente automovilístico 13 años atrás y era diabético. Se le realizó una videoendoscopia de la deglución (VED), en la que se observó, en la evaluación estructural, una protuberancia de la pared posterior de la hipofaringe con residuo salival sobre la lesión. En la evaluación funcional, tras la ingesta de alimentos sólidos, se observó una restricción de la retroflexión de la epiglotis, una limitación de la elevación de la laringe y un reflujo nasal de alimentos, con gran cantidad de residuo alimentario por encima de la lesión, en la pared posterior de la faringe. En la prueba de maniobras posturales, empeoró la disfagia al extender el cuello y mejoró la eliminación al flexionar la cabeza. Se le realizó una tomografía computarizada (TC) de la columna cervical, solicitada para evaluar la naturaleza de la lesión, que mostró la presencia de osteofitos cervicales anteriores entre las vértebras C3 y C6, el mayor de 12 milímetros (mm) de longitud, que estrechaba la columna aérea al nivel de la orofaringe e hipofaringe. Se descartaron otras causas de disfagia y se trató al paciente con terapia de deglución y omeprazol, dirigido al reflujo faringolaríngeo. Se realizaron 6 sesiones de terapia de deglución individualizada, con el objetivo de compensar el mecanismo de deglución ante un obstáculo mecánico en la región faríngea. Los principales aspectos trabajados fueron: modificación de la textura de la dieta, evitando alimentos sólidos y secos; maniobras posturales de deglución, probadas durante la VED, especialmente el chin tuck (“cabeza hacia abajo” o “flexión de la cabeza”), que aumenta el espacio de la válvula (“abre la válvula”) y mejora la presión de transferencia faríngea del alimento; y ejercicios de fortalecimiento de la lengua, para superar la barrera mecánica de la orofaringe durante la expulsión del alimento. Se recomendó, si fuera necesario, alternar la ingesta de alimentos sólidos con líquidos, ante la percepción de alimentos estancados en la faringe. Se le indicó que repitiera los ejercicios de lengua en el hogar, 2 a 3 veces al día. Después de las sesiones iniciales, el paciente presentó una respuesta satisfactoria, y se lo controló trimestralmente durante el primer año y semestralmente a partir del segundo año. Se lo derivó para una evaluación ortopédica para analizar la viabilidad quirúrgica, y se optó por un tratamiento conservador debido a la buena compensación con medidas clínicas. Sigue en seguimiento ambulatorio desde hace 2 años, y mantiene una deglución eficiente, sin incidencia de complicaciones relacionadas con la disfagia. Se optó por mantener reevaluaciones periódicas, al menos una vez al año, para detectar precozmente un posible nuevo desequilibrio de la homeostasis de la deglución relacionado con el deterioro gradual de las funciones en el contexto de la presbifagia o el surgimiento de un nuevo factor agresor.\n",
+        "gold_summary": "Se describió el caso de un paciente de 66 años con disfagia por atragantamiento con sólidos y reflujo nasal de alimentos desde hacía un año. La videoendoscopia de la deglución mostró una protuberancia en la pared posterior de la faringe y, al ofrecer alimentos sólidos, una restricción de la retroflexión de la epiglotis, reflujo nasal de alimentos y una gran cantidad de residuos de alimentos sobre la lesión. La tomografía computarizada de la columna cervical identificó la presencia de osteofitos cervicales anteriores entre las vértebras C3 y C6, el más grande con una longitud anteroposterior de 12 milímetros, que estrechaba la columna aérea a nivel de la orofaringe e hipofaringe. El paciente fue tratado adecuadamente con fonoterapia para la deglución.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había un hombre de 66 años que tenía dificultad para tragar alimentos sólidos y a veces la comida subía por la nariz desde hacía un año. Le hicieron una cámara para ver la garganta cuando tragaba. Vieron un bulto en la parte de atrás de la garganta. También notaron que una pequeña “tapa” que cierra la entrada de la tráquea (epiglotis) no se movía bien y que había mucha comida parada encima del bulto. Cuando estiraba el cuello, le iba peor; cuando bajaba la cabeza (chin tuck), mejoraba.\n\nLuego le hicieron una tomografía del cuello. Encontraron unos “bultos de hueso” en las vértebras del cuello (osteofitos) entre C3 y C6. Uno era bastante grande (unos 1,2 cm) y estrechaba el paso del aire y de la comida en la parte de atrás de la garganta.\n\nLos médicos descartaron otras causas. No operaron. Le dieron terapia para aprender a tragar mejor y medicina para el reflujo. En las sesiones le enseñaron a comer alimentos más blandos, a usar la postura de “cabeza hacia abajo” y a hacer ejercicios con la lengua. También tenía ejercicios para hacer en casa.\n\nDespués de seis sesiones mejoró mucho. Sigue con controles médicos desde hace dos años y puede tragar bien. Los médicos pidieron que siga con revisiones al menos una vez al año para revisar que todo siga bien.",
+                "fh_score": 78.63
+            },
+            "B2": {
+                "text": "Resumen comprensible (nivel B2, lectura para jóvenes)\n\nEste caso describe a un hombre de 66 años que llevaba un año teniendo problemas para tragar alimentos sólidos y a veces le regresaban alimentos por la nariz. El paciente dio su consentimiento y el informe contó con aprobación ética.\n\nQué encontraron los doctores\n- En la evaluación con endoscopia de la deglución (una cámara pequeña para ver la garganta) vieron una protuberancia en la parte posterior de la faringe y restos de saliva y comida encima de esa zona.\n- Al darle alimentos sólidos, la epiglotis (una tapa de cartílago que protege la vía aérea cuando tragamos) no se doblaba bien hacia atrás, la laringe no subía lo suficiente y parte de la comida subía hacia la nariz. Todo esto hacía que se acumulara mucha comida sobre la protuberancia.\n- En la tomografía de la columna cervical encontraron osteofitos anteriores entre las vértebras C3 y C6. Los osteofitos son pequeñas crestas o \"protuberancias\" de hueso (a veces llamadas bone spurs). El mayor medía 12 mm y estrechaba el espacio por donde pasa el alimento en la parte alta de la garganta.\n\nTratamiento y resultado\n- Los médicos descartaron otras causas de la dificultad para tragar y trataron al paciente con terapia de la deglución (ejercicios y maniobras prácticas) y omeprazol para controlar el reflujo hacia la garganta.\n- Hicieron 6 sesiones individuales de terapia: cambiaron la textura de la dieta (evitando alimentos sólidos y secos), enseñaron maniobras posturales que probó en la endoscopia (especialmente el \"chin tuck\" o flexionar la cabeza hacia adelante, que ayuda a empujar la comida y a proteger la vía aérea) y ejercicios para fortalecer la lengua.\n- Le recomendaron alternar sólidos con líquidos si sentía que la comida se atascaba, y repetir los ejercicios en casa 2–3 veces al día.\n\nSeguimiento\n- El paciente respondió bien al tratamiento. Se le revisó cada tres meses el primer año y cada seis meses después. Fue valorado por ortopedia para estudiar cirugía, pero se decidió manejarlo de forma conservadora porque la terapia daba buenos resultados.\n- Lleva 2 años en seguimiento ambulatorio con una deglución eficiente y sin complicaciones. Mantendrán controles periódicos, al menos una vez al año, para detectar cambios tempranos relacionados con el envejecimiento de la deglución (presbifagia) o nuevos problemas.\n\nEn resumen: la dificultad para tragar se debió a protuberancias óseas en la columna cervical que estrechaban la parte alta de la garganta. Con terapia de deglución dirigida y medidas para el reflujo, el paciente mejoró y se optó por evitar la cirugía mientras siga estable.",
+                "fh_score": 55.11
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel universitario)\n\nContexto y aspectos éticos\n- Se presentó un paciente varón de 66 años con consentimiento informado; el caso contó con aprobación del comité de ética de la UNIFESP.  \n\nPresentación clínica\n- Síntomas: disfagia del tipo “atragantamiento” con alimentos sólidos y reflujo nasal de alimentos de aproximadamente 1 año de evolución.  \n- Antecedentes relevantes: accidente de tráfico hace 13 años y diabetes mellitus.\n\nExploraciones y hallazgos (normales vs anormales)\n- Videoendoscopia de la deglución (VED): hallazgo estructural anormal — protuberancia en la pared posterior de la hipofaringe con residuo salival sobre ella. Evaluación funcional anormal al ofrecer sólidos: restricción de la retroflexión de la epiglotis (la epiglotis no se pliega con normalidad para proteger la vía aérea), limitación de la elevación laríngea, reflujo nasal de alimento y gran cantidad de residuo por encima de la lesión.  \n- Maniobras posturales: la extensión de cuello empeoró la disfagia; la flexión del cuello (chin tuck) mejoró la eliminación del alimento.  \n- Tomografía computarizada cervical: hallazgo anatómico anormal — osteofitos anteriores (excrecencias óseas) entre C3 y C6, el mayor de 12 mm, que estrechaban el paso aéreo a nivel de orofaringe e hipofaringe.  \n- Se descartaron otras causas de disfagia en el estudio.\n\nDiagnóstico funcional y etiológico\n- Disfagia mecánica secundaria a osteofitos cervicales anteriores que generan una barrera en la región faríngea, con compromiso protector de la vía aérea (epiglotis y elevación laríngea) y reflujo faringolaríngeo concurrente.\n\nTratamiento aplicado\n- Manejo conservador elegido por buena respuesta clínica:\n  - Terapia fonoaudiológica de deglución: 6 sesiones individualizadas centradas en:\n    - Modificación de la textura dietética (evitar sólidos secos; alternativas liquidar/mezclar según percepción de estancamiento).\n    - Maniobras posturales validadas por VED, sobre todo el chin tuck, que reduce el espacio afectado y mejora la transferencia faríngea.\n    - Ejercicios de fortalecimiento lingual para ayudar a vencer la barrera mecánica durante la propulsión del bolo.\n    - Repetición domiciliaria de ejercicios 2–3 veces/día y recomendaciones para alternar sólidos con líquidos si hay sensación de retención.\n  - Omeprazol para control del reflujo faringolaríngeo.\n  - Derivación a ortopedia para valorar viabilidad quirúrgica (se consideró, pero se optó por conducta conservadora).\n\nEvolución y seguimiento\n- Respuesta clínica satisfactoria tras las sesiones iniciales.  \n- Seguimiento ambulatorio: controles trimestrales el primer año y semestrales desde el segundo año; al cabo de 2 años mantiene deglución eficiente sin complicaciones relacionadas con la disfagia.  \n- Plan: reevaluaciones periódicas, al menos anuales, para detectar precozmente empeoramiento (por ejemplo por presbifagia —cambios por envejecimiento— o aparición de nuevos factores).\n\nImplicaciones clínicas y recomendaciones prácticas\n- Los osteofitos cervicales pueden producir una obstrucción mecánica de la faringe y aumentar el riesgo de aspiración y residuos alimentarios; en casos graves existe la opción quirúrgica (osteofitectomía anterior), pero la terapia rehabilitadora y las modificaciones dietéticas pueden ser eficaces cuando el paciente compensa bien.  \n- Señales de alarma que justificarían revaluación urgente: pérdida de peso, infecciones respiratorias recurrentes (neumonía por aspiración), empeoramiento marcado de la disfagia o incapacidad para hidratarse/alimentarse.  \n- Mantener las medidas aprendidas (ejercicios y posturas) y controles periódicos para preservar la seguridad alimentaria y la calidad de vida.\n\nComentario empático\n- El manejo multidisciplinario y la adherencia a la terapia permitieron al paciente recuperar una deglución funcional sin cirugía. Es razonable y prudente mantener vigilancia periódica para detectar cambios precoces y adaptar el tratamiento si la situación evoluciona.",
+                "fh_score": 30.41
+            }
+        }
+    },
+    {
+        "article": "Una paciente caucásica de 18 años de edad se presentó en nuestra clínica con quejas de múltiples bultos palpables en sus senos bilateralmente. En el examen físico, la paciente tenía múltiples lesiones pigmentadas lentigosas en su cara, cuerpo y esclerótica bilateralmente, nevos azules en su tronco y extremidades superiores y una cara redonda con forma de luna.\n\nTras la evaluación ultrasonográfica, se encontraron múltiples nódulos compactos (fibroadenomas) en ambos senos, siendo el más grande en el cuadrante superior externo del seno izquierdo, con un diámetro de 7,8 cm.\n\nEn 2018, se le había practicado una tiroidectomía total con el diagnóstico de adenoma folicular y la extirpación de un nódulo grande del seno izquierdo, debido a su gran tamaño y al dolor que causaba, con un informe de histopatología que sugería un fibroadenoma con estroma mixóide.\n\nSe realizó una biopsia por escisión de dos nódulos de la mama derecha con diagnóstico de fibroadenoma mixto, lo que respaldó nuestro diagnóstico de complejo de Carney.\n\nEn la resonancia magnética se encontraron múltiples fibroadenomas compactos en ambos senos, con alta intensidad de señal en las imágenes T2 y T2/FS, con tabiques internos sin restricción de difusión, compatibles con múltiples fibroadenomas mixoides.\n\nAdemás, había un par de ganglios linfáticos axilares y prominentes ganglios linfáticos mamarios internos bilaterales.\n\nAdemás, se observó una anomalía en la densidad de los tejidos blandos en el mediastino anterior, que medía 11 mm de espesor máximo, lo que sugería un timo prominente.\n\nTodos los hallazgos anteriores sugerían la posibilidad de un complejo de Carney. Se realizó una evaluación adicional en el laboratorio. Los análisis hormonales no mostraron anomalías en los niveles de testosterona, prolactina, PTH y DHEA-S.\n\nLuego se realizó un análisis genético que arrojó como resultado la mutación del gen PRHAR1A, heterocigótico para una variante sin sentido de significancia incierta en el exón 3 de este gen. Esta mutación nunca se había informado en la base de datos gnomAD.\n\nSe realizaron pruebas genéticas a los padres y se determinó que solo el padre era portador de la misma mutación genética.\n\nSe discutieron con la paciente varios planes de tratamiento conservadores, pero ninguno demostró proporcionar una solución/tratamiento definitivo. En el pasado se realizó la extirpación de los lóbulos grandes con alivio temporal de los síntomas de dolor de la paciente y las cirugías recurrentes estaban afectando su calidad de vida. La paciente también tuvo varias sesiones con la psicóloga de nuestra clínica y fue evaluada a fondo antes de decidir la solución final de una mastectomía bilateral.\n\nLa paciente se sometió a una mastectomía bilateral con conservación de la piel y colocación subcutánea de expansores de tejidos (suave, Motiva Flora®). La histopatología informó múltiples fibroadenomas mixóides en ambos senos, compatibles con el síndrome de Carney, con interrupción de la arquitectura normal del parénquima mamario. Las figuras muestran el fibroadenoma de forma macroscópica e histológica.\n\nEl cuidado de la herida fue mínimo, se le recomendó a la paciente usar un sujetador médico y visitas regulares a la clínica ambulatoria para seguimiento y rellenado adicional de los expansores de tejidos a intervalos regulares hasta que se alcanzó el tamaño deseado. Paciente antes y después de la mastectomía. Después de un año se realizó una segunda cirugía y los expansores se reemplazaron con implantes de silicona permanentes (suaves, Motiva Ergonomic®) submusculares, con los mismos requisitos mínimos de cuidado de la herida y colocación del sujetador.\n",
+        "gold_summary": "Una paciente de 18 años de edad se presentó en nuestra clínica con múltiples bultos palpables en sus senos bilateralmente. En el examen físico, la paciente también tenía múltiples lesiones pigmentadas lentigosas en su cara, cuerpo y esclerótica, nevos azules en su tronco y extremidades superiores y un rostro redondo con forma de luna. El diagnóstico del síndrome de Carney se decidió mediante imágenes, biopsias y análisis genético. La paciente se sometió a una mastectomía bilateral como plan de tratamiento profiláctico con colocación de expansores de tejidos.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había una paciente de 18 años que notó muchos bultos en los dos pechos. También tenía manchas oscuras en la piel, lunares azules y una cara redonda.  \n\nLos doctores hicieron exámenes y biopsias. Descubrieron que los bultos eran fibroadenomas. Eso quiere decir que eran bolitas no cancerosas, pero grandes y que le dolían.  \n\nLe hicieron pruebas de sangre y las hormonas salieron normales. También hicieron un estudio del ADN y encontraron un cambio en un gen que puede causar este conjunto de problemas. El padre tenía el mismo cambio.  \n\nLa joven ya había tenido otras cirugías que ayudaban solo por un tiempo. Ella se sentía cansada de las operaciones repetidas y habló con psicólogos. Al final decidió quitarse los pechos para evitar más problemas.  \n\nLe hicieron una mastectomía en los dos pechos y pusieron unas bolsitas temporales llamadas expansores. Después, un año más tarde, cambiaron las bolsitas por implantes de silicona. La herida sanó bien y la paciente siguió controles médicos.  \n\nEsta operación era para mejorar su salud y su vida diaria. Los doctores la acompañaron con cuidado y apoyo durante todo el proceso.",
+                "fh_score": 74.13
+            },
+            "B2": {
+                "text": "An 18-year-old woman came to the clinic because she felt many lumps in both breasts. On exam she also had many small dark spots on her skin and eyes (lentigines), blue‑colored moles (blue nevi), and a round, “moon‑shaped” face. She had previously had her thyroid removed in 2018 for a benign tumor.\n\nImaging with ultrasound and MRI showed many compact breast tumors called fibroadenomas (benign lumps made of gland and fibrous tissue). The largest lump was 7.8 cm in the upper outer part of the left breast. Some nearby lymph nodes looked larger than usual and there was a slightly prominent thymus (a small gland in the chest). Biopsies of breast nodules confirmed mixed (myxoid) fibroadenomas — “myxoid” means the tissue has a soft, jelly‑like stroma.\n\nThese findings suggested Carney complex, a rare genetic condition that can cause skin spots, benign tumors, and endocrine problems. Blood hormone tests were normal. Genetic testing found a previously unreported change (a heterozygous nonsense variant of uncertain significance) in the PRHAR1A gene; the same change was also found in her father. This supports an inherited cause, so family genetic counseling was offered.\n\nBecause repeated lump removals had only given temporary relief and were affecting her quality of life, after psychological support she chose a preventive surgery: bilateral mastectomy with skin preservation and temporary tissue expanders placed under the skin. Pathology of the removed breasts confirmed multiple myxoid fibroadenomas that had disrupted the normal breast tissue, which fits with Carney complex. One year later the expanders were replaced with permanent silicone implants under the muscle. Wound healing was uncomplicated and she continues outpatient follow‑up and implant care.\n\nThis approach aimed to stop the cycle of repeated surgeries, reduce pain and distress, and improve her quality of life. Genetic counseling and follow‑up for other possible features of Carney complex remain important for her and her family.",
+                "fh_score": 84.21
+            },
+            "B3": {
+                "text": "Presentación y contexto\nUna mujer caucásica de 18 años acudió por múltiples nódulos palpables en ambos senos. En el examen físico también se observaron múltiples lentigos pigmentados en cara, cuerpo y esclerótica, nevos azules en tronco y extremidades superiores y una facies redondeada tipo “luna”. En 2018 había recibido tiroidectomía total por un adenoma folicular y, en el pasado, se extirpó un gran nódulo mamario izquierdo por dolor.\n\nHallazgos clínicos, de imagen y anatomía patológica\n- Imágenes (ecografía y resonancia): múltiples nódulos compactos en ambos senos compatibles con fibroadenomas mixoides; el mayor medía 7,8 cm en el cuadrante superior externo izquierdo. En RM los nódulos eran hiperintensos en T2/T2-FS, con tabiques internos y sin restricción en difusión. Se informaron además ganglios axilares e internos mamarios prominentes y una densidad de tejidos blandos de 11 mm en mediastino anterior sugestiva de timo prominente.\n- Biopsias y pieza quirúrgica: resecciones previas y biopsia por escisión de nódulos confirmaron fibroadenomas mixtos/mixoides. La histología definitiva tras la segunda intervención mostró múltiples fibroadenomas mixoides y alteración de la arquitectura normal del parénquima mamario.\n- Laboratorio endocrino: niveles normales de testosterona, prolactina, PTH y DHEA‑S.\n- Genética: se identificó una variante heterocigota sin sentido de significado incierto en el exón 3 del gen reportado en el artículo como PRHAR1A (probablemente correspondiente al gen PRKAR1A, conocido por asociarse al complejo de Carney). La variante no estaba en la base de datos gnomAD. El mismo cambio genético fue hallado en el padre de la paciente.\n\nDiagnóstico y decisión terapéutica\n- Conjuntamente, los hallazgos clínicos, radiológicos, histológicos y la variante genética apoyaron el diagnóstico de complejo de Carney (síndrome que asocia lentigos, tumores mamarios mixoides/fibroadenomas, neoplasias y alteraciones endocrinas).\n- Se discutieron opciones conservadoras, pero las resecciones repetidas daban solo alivio temporal y afectaban la calidad de vida. Tras valoración psicológica y consenso informado, la paciente optó por una mastectomía bilateral profiláctica con conservación de piel.\n\nTratamiento y evolución\n- Primera intervención: mastectomía bilateral skin‑sparing y colocación subcutánea de expansores de tejidos (Motiva Flora®). Cuidados posoperatorios mínimos, uso de sujetador médico y controles para relleno progresivo de expansores.\n- Segunda intervención (un año después): sustitución de expansores por implantes de silicona submusculares permanentes (Motiva Ergonomic®). La anatomía patológica confirmó la presencia de múltiples fibroadenomas mixoides bilaterales.\n\nImplicaciones y recomendaciones razonables\n- El hallazgo genético (variante sin sentido heterocigota no reportada previamente) y la identificación de la misma variante en el padre sugieren una forma familiar del complejo de Carney, aunque la variante fue catalogada como de significado incierto; se requieren más datos para clasificarla definitivamente.\n- Dado el diagnóstico de complejo de Carney, se recomiendan seguimientos dirigidos a detectar otras manifestaciones del síndrome: cribado cardiológico (ecocardiograma para excluir mixomas cardiacos), vigilancia endocrina periódica (tiroides, glándulas suprarrenales, etc.), examen dermatológico y controles ginecológicos según indicación. También se aconseja asesoramiento genético para la paciente y la familia.\n- Los ganglios mamarios y axilares descritos eran prominentes en imagen pero no se informó malignidad; la ausencia de restricción en difusión en la RM favorece benignidad, aunque el seguimiento es pertinente.\n\nTono y conclusión\nLa paciente recibió un tratamiento definitivo que alivió el problema recurrente y la carga sintomática de lesiones mamarias extensas. Dado el carácter genético y sistémico del complejo de Carney, el pronóstico dependerá del control y la detección precoz de otras posibles lesiones asociadas; el seguimiento multidisciplinario y el consejo genético son pasos clave. Lamento la carga emocional y física que esta enfermedad ha supuesto para la paciente y destaco la importancia del apoyo psicológico y de un plan de vigilancia a largo plazo.",
+                "fh_score": 34.86
+            }
+        }
+    },
+    {
+        "article": "Una adolescente femenino de 13 años sin antecedentes médico-quirúrgicos de interés acude a Urgencias por dolor e impotencia funcional en muñeca izquierda tras caída mientras patinaba. Diagnosticada de lesión en torus metafisaria con extensión fisaria de radio distal clasificada como lesión Peterson tipo I, es inmovilizada durante cuatro semanas con férula antebraquiopalmar. Dos semanas después de la retirada de la férula, acude nuevamente a Urgencias al sentir un crujido en la muñeca, sin sobreesfuerzo asociado e impotencia para movilizar el primer dedo de la mano izquierda. Clínicamente presenta déficit de extensión activa interfalángica, efecto tenodesis patológico, edema local y asimetría macroscópica a la comparación con la extremidad contralateral. Se estudia con resonancia magnética nuclear (RMN), identificando imagen de solución de continuidad del EPL. Con la paciente bajo anestesia general, se procede al tratamiento quirúrgico mediante transferencia tendinosa del extensor propio del índice (EPI) al remanente distal del EPL con sutura tipo Pulvertaft de monofilamento no absorbible. En el postoperatorio se inmovilizó la extremidad las cuatro primeras semanas.\n\nTras cuatro semanas, se autorizó movilidad evidenciando recuperación de extensión del primer dedo de la mano izquierda y cicatrices discretamente hipertróficas, sin dolor. El seguimiento a la sexta, duodécima semana y al año no reporta complicaciones, con una restitución completa de la función y una puntuación de 0 en la escala PRWE (Patient Rated Wrist Evaluation).",
+        "gold_summary": "Se presenta el caso de una paciente adolescente femenino que, tras tratamiento conservador con férula de una fractura fisaria Peterson tipo I en radio, sufre a las seis semanas déficit agudo de extensión del pulgar, diagnosticada mediante examen clínico radiológico de rotura espontánea del extensor pollicis longus. Es tratada por medio de transferencia del extensor propio del índice (EPI) con resultados satisfactorios y recuperación de su actividad habitual al mes postoperatorio.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una niña de 13 años se cayó mientras patinaba y se lastimó la muñeca. Los médicos le pusieron una férula y la inmovilizaron por cuatro semanas porque se había hecho una pequeña fractura en el hueso cerca de la muñeca.  \n\nDos semanas después de quitar la férula, notó un crujido en la muñeca y no pudo mover el pulgar. Al hacer pruebas y una imagen por resonancia, vieron que se había roto un tendón que sirve para levantar el pulgar.  \n\nLe hicieron una operación. Los cirujanos usaron un tendón del dedo índice para reemplazar el tendón roto del pulgar. El brazo quedó quieto otra vez durante cuatro semanas para sanar.  \n\nA las cuatro semanas después de la cirugía, pudo mover el pulgar otra vez y no tenía dolor. Quedó con una pequeña cicatriz. En los controles a las 6 y 12 semanas y al año, no hubo problemas y recuperó totalmente la función de la mano.",
+                "fh_score": 78.62
+            },
+            "B2": {
+                "text": "Resumen\n\nUna adolescente de 13 años se presentó tras una caída mientras patinaba con una fractura en la parte distal del radio (clasificada como lesión de torus con extensión a la fisis, Peterson tipo I). Se trató de forma conservadora con una férula antebraquiopalmar durante cuatro semanas. Dos semanas después de retirar la férula (seis semanas tras la caída) notó un “crujido” en la muñeca y perdió la capacidad para extender el pulgar: el examen mostró imposibilidad de extender la articulación interfalángica del pulgar, edema local y asimetría con la mano sana. La resonancia magnética confirmó la rotura del tendón extensor largo del pulgar (EPL).\n\nCon la paciente bajo anestesia general se realizó una transferencia tendinosa, utilizando el extensor propio del índice (EPI) para reemplazar la función del EPL, suturando los tendones con la técnica de Pulvertaft (una forma firme de unir tendones). La muñeca se inmovilizó cuatro semanas después de la cirugía. A las cuatro semanas la paciente había recuperado la extensión del pulgar, con cicatrices levemente sobreelevadas y sin dolor. En los controles a las 6 y 12 semanas y al año no hubo complicaciones y la función se restauró por completo; la paciente obtuvo 0 puntos en la escala PRWE (una puntuación de 0 indica ausencia de dolor y limitación funcional). En resumen, una rotura espontánea del EPL tras una fractura distal del radio fue resuelta con éxito mediante transferencia tendinosa, permitiendo la recuperación completa de la actividad habitual.",
+                "fh_score": 50.98
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel B3)\n\nPresentación\n- Paciente: adolescente femenina de 13 años, sin antecedentes relevantes.\n- Evento inicial: caída mientras patinaba → dolor e incapacidad funcional de la muñeca izquierda.\n- Diagnóstico inicial: lesión en torus metafisaria con extensión fisaria del radio distal (Peterson tipo I).\n- Tratamiento inicial: inmovilización con férula antebraquiopalmar durante 4 semanas.\n\nEvolución y hallazgos anormales\n- Dos semanas tras retirar la férula (6 semanas desde la fractura) la paciente siente un crujido en la muñeca y presenta incapacidad para extender el pulgar izquierdo.\n- Examen clínico: déficit de extensión interfalángica del pulgar, efecto tenodesis patológico (movimientos pasivos que no se traducen en extensión activa), edema local y asimetría evidente respecto al lado sano.\n- Imagen: resonancia magnética (RMN) mostró solución de continuidad (rotura) del extensor pollicis longus (EPL), el tendón encargado de la extensión del pulgar.\n\nTratamiento realizado\n- Bajo anestesia general se efectuó transferencia tendinosa: se tomó el extensor propio del índice (EPI) y se suturó al remanente distal del EPL mediante técnica de Pulvertaft con monofilamento no absorbible.\n- Postoperatorio: inmovilización de la extremidad durante las primeras 4 semanas.\n\nResultados y seguimiento\n- A las 4 semanas postoperatorias se permitió movilización: recuperación de la extensión del pulgar y cicatrices ligeramente hipertróficas, sin dolor.\n- Controles a 6 y 12 semanas y a 1 año: sin complicaciones, restitución completa de la función, puntuación 0 en la escala PRWE (Patient Rated Wrist Evaluation), es decir, ausencia de limitación percibida por la paciente.\n\nInterpretación y puntos clave\n- La ruptura espontánea del EPL es una complicación conocida tras fracturas distales de radio, incluso cuando la fractura es leve o tratada de forma conservadora. Mecanismos posibles: daño directo, pinzamiento sobre callo óseo o alteración del aporte vascular al tendón.\n- La transferencia del EPI es una solución quirúrgica bien establecida y eficaz: restituye la extensión del pulgar con mínima pérdida funcional del índice.\n- En pacientes con fractura distal de radio que desarrollan pérdida aguda de extensión del pulgar debe sospecharse lesión de EPL; la RMN o la ecografía ayudan a confirmar la rotura y guiar el tratamiento.\n- El pronóstico tras una transferencia tendinosa orientada y una rehabilitación adecuada suele ser excelente, como se observó en este caso.\n\nRecomendaciones prácticas\n- Vigilar la función tendinosa del pulgar tras fracturas distales de radio y valorar imágenes si aparece déficit funcional.\n- Derivar a cirugía de mano/rehabilitación temprana cuando se confirma rotura tendinosa.\n- Informar al paciente y a la familia sobre la alta probabilidad de recuperación funcional tras transferencia tendinosa y sobre el posible cambio mínimo en la función del índice.",
+                "fh_score": 41.72
+            }
+        }
+    },
+    {
+        "article": "Se remitió a un hombre de 73 años para una SAVR para tratar la regurgitación valvular aórtica sintomática (AR). Dos años antes, había presentado múltiples lesiones exantématicas. Una biopsia de piel reveló infiltración de células plasmáticas, lo que motivó la derivación a un hematólogo. La tomografía computarizada reveló linfadenopatía sistémica y hepatoesplenomegalia. Una biopsia renal realizada por disfunción renal confirmó la amiloidosis AA; una biopsia de ganglios linfáticos mostró plasmocitosis interfolicular y un centro germinal hiperplásico, consistente con el subtipo plasmático de iMCD, apoyado por niveles elevados de IL-6 en plasma. Se administró al paciente TCZ intravenoso (640 mg cada 2 semanas), junto con prednisolona (10 mg diarios). La erupción cutánea y la linfadenopatía se resolvieron. La ecocardiografía reveló AR puro moderado y agrandamiento ventricular izquierdo. Dado que el paciente experimentó gradualmente disnea de esfuerzo con agrandamiento ventricular izquierdo progresivo, se consideró necesaria la SAVR.\n\nDebido al sangrado por hemorroides y a la hepatosplenomegalia, se consultó a un hepatólogo; se diagnosticó cirrosis hepática de Child-Pugh grado A y varices esofágicas. Se realizó una conferencia preoperatoria del equipo, en la que participaron un intensivista y un farmacéutico, en la que se revisaron los mecanismos de acción de TCZ, las posibles complicaciones y el tratamiento perioperatorio. La cirugía se realizó 26 días después de la última dosis de TCZ. Durante el período perioperatorio, se suspendió el tratamiento con TCZ, mientras que se continuó con los esteroides por vía oral o intravenosa. Las medidas preventivas para las infecciones del sitio quirúrgico (SSI) incluyeron la detección de portadores nasales de Staphylococcus aureus resistentes a la meticilina, la preparación antiséptica de la piel, la terapia antibiótica profiláctica y el control de la hiperglucemia. El cultivo nasal fue positivo para Staphylococcus coagulasa negativo. Se realizó el reemplazo de la válvula aórtica quirúrgica a través de una esternotomía media bajo circulación extracorpórea, con 65 minutos de tiempo de isquemia cardiaca y 128 minutos de tiempo de circulación extracorpórea. Se requirieron transfusiones de sangre, incluidos glóbulos rojos, plasma y plaquetas; el paciente fue extubado al día siguiente. Los hallazgos patológicos revelaron un espesamiento fibroso focal sin depósitos amiloides.\n\nLa herida quirúrgica no mostró signos de infección en el día 2 postoperatorio; se inició la terapia de presión negativa en la herida (NPWT) en la herida quirúrgica cerrada para evitar SSI. La terapia de presión negativa en la herida se interrumpió en el día 13 postoperatorio, sin aparente SSI. El paciente fue dado de alta en el día 17 postoperatorio sin ningún signo de infección.\n\nAunque los niveles de IL-6 aumentaron temporalmente los días 1 y 2 después de la operación, disminuyeron progresivamente hasta el día 24 después de la operación, y luego volvieron a aumentar al reanudarse el tratamiento con TCZ. Los niveles de proteína C reactiva (PCR) estaban ligeramente elevados, alcanzando un máximo de 0,56 mg/dL el día 2 después de la operación. Para el día 24 después de la operación, la PCR había aumentado a 1,06 mg/dL sin infección. Antes del aumento de la PCR, los niveles del factor de crecimiento endotelial vascular aumentaron el día 13 después de la operación.\n\nEl paciente no experimentó recurrencia de erupción cutánea o linfadenopatía durante el período perioperatorio. Los niveles de creatinina postoperatorios aumentaron temporalmente, pero volvieron a los niveles preoperatorios el día 24. Se reanudó el tratamiento con tocilizumab el día 30 postoperatorio tras confirmar la ausencia de infección, incluida la IFI.\n",
+        "gold_summary": "Un hombre de 73 años con enfermedad de Castleman, tratado con TCZ, se sometió a un reemplazo de la válvula aórtica por medio de esternotomía mediana para la regurgitación de la válvula aórtica con falta de aire al hacer ejercicio. Se implementaron medidas integrales para prevenir la infección del sitio quirúrgico junto con un examen minucioso durante el período perioperatorio. Tocilizumab se interrumpió 26 días antes de la cirugía y se reanudó 30 días después de la cirugía, durante los cuales los niveles de IL-6 en plasma disminuyeron. No hubo evidencia de infección o exacerbación de la enfermedad de Castleman. Los niveles del factor de crecimiento endotelial vascular aumentaron antes de un aumento en los niveles de proteína C reactiva después del alta hospitalaria y antes de la reanudación de TCZ.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Resumen sencillo:\n\nUn hombre de 73 años tenía una enfermedad llamada Castleman. Esa enfermedad le hacía hinchar los ganglios y tener sarpullido, pero mejoró con una medicina llamada tocilizumab (TCZ).\n\nTenía problemas en una válvula del corazón. Esto le daba falta de aire al caminar. Los médicos le hicieron una operación para cambiar la válvula por una nueva.\n\nAntes de la operación, dejaron de darle TCZ unas cuatro semanas. Hicieron muchas cosas para evitar infecciones. Revisaron si tenía gérmenes en la nariz, limpiaron bien la piel, dieron antibiótico para prevenir infecciones y cuidaron su azúcar en la sangre.\n\nLa operación salió bien. No hubo infección en la herida. El hombre salió del hospital 17 días después de la operación.\n\nReanudaron la medicina TCZ cerca de 4 semanas después de la operación, cuando comprobaron que no había infección. Las pruebas de sangre mostraron que una sustancia llamada IL-6 bajó mientras la medicina estuvo parada y volvió a subir cuando la medicina se reanudó. Otra prueba (PCR) subió un poco más tarde, pero no hubo infección ni empeoramiento de la enfermedad.\n\nEn pocas palabras: la operación fue necesaria y se hizo con cuidado para evitar infecciones. El paciente se recuperó bien y volvió a su tratamiento sin que su enfermedad empeorara.",
+                "fh_score": 69.17
+            },
+            "B2": {
+                "text": "Resumen sencillo y claro\n\nUn hombre de 73 años con enfermedad de Castleman multicéntrica (una enfermedad en la que el sistema inmunitario está alterado) y amiloidosis AA (acumulación anormal de proteína en órganos) necesitó un reemplazo de la válvula aórtica porque tenía regurgitación aórtica (la válvula no cerraba bien) y dificultad para respirar al hacer ejercicio.\n\nTratamiento previo y preparación para la cirugía\n- Recibía tocilizumab (TCZ), un medicamento que bloquea la proteína inflamatoria IL‑6, y prednisolona (un esteroide).\n- Tenía también hepatomegalia y cirrosis hepática leve (Child‑Pugh A) y várices esofágicas, por lo que un equipo médico evaluó cuidadosamente los riesgos.\n- El equipo decidió suspender TCZ 26 días antes de la operación; los esteroides se mantuvieron. La cirugía se hizo por esternotomía media con circulación extracorpórea (máquina corazón‑pulmón).\n\nMedidas para evitar infección y cuidados quirúrgicos\n- Se tomaron varias precauciones para prevenir infecciones de la herida: búsqueda de portadores nasales de bacterias, antisepsia de la piel, antibiótico profiláctico y control de la glucosa.\n- Tras la operación, se usó terapia de presión negativa sobre la herida (un vendaje con succión que ayuda a prevenir infección). Esta terapia se interrumpió el día 13 sin problemas y el paciente salió del hospital al día 17 sin signos de infección.\n\nEvolución de pruebas y medicamentos después de la operación\n- Tras la cirugía, los niveles de IL‑6 subieron de forma temporal en los primeros días y luego bajaron hasta el día 24; aumentaron otra vez cuando se reanudó TCZ.\n- La proteína C reactiva (PCR), un marcador de inflamación, se elevó levemente (máximo 0,56 mg/dL el día 2) y luego a 1,06 mg/dL el día 24, también sin evidencia de infección.\n- El factor de crecimiento endotelial vascular (VEGF) subió antes del segundo aumento de la PCR.\n- La función renal mostró un aumento temporal de creatinina que regresó a los valores previos al día 24.\n- No reaparecieron la erupción cutánea ni la linfadenopatía relacionadas con la enfermedad de Castleman.\n- TCZ se reanudó el día 30 tras comprobar que no había infección, incluida infección fúngica invasiva.\n\nResultados y conclusión\n- La operación fue técnicamente exitosa; la biopsia de la válvula mostró fibrosis localizada pero sin depósitos de amiloide.\n- Con las medidas tomadas, no hubo infección de la herida ni empeoramiento de la enfermedad de Castleman durante el periodo perioperatorio.\n- En resumen: la suspensión planificada de TCZ antes de la cirugía, la vigilancia estrecha y las medidas preventivas permitieron realizar el reemplazo valvular con buena recuperación y reanudar el tratamiento inmunológico de forma segura.",
+                "fh_score": 50.93
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel lector universitario)\n\nPresentación y antecedentes\n- Paciente: hombre de 73 años con enfermedad de Castleman multicéntrica idiopática (subtipo plasmocítico) confirmada por biopsia de ganglio y niveles elevados de IL‑6, y amiloidosis AA secundaria (biopsia renal). Tenía antecedentes de erupciones cutáneas y hepatoesplenomegalia.\n- Tratamiento crónico previo a la cirugía: tocilizumab intravenoso (640 mg cada 2 semanas) más prednisolona 10 mg/día. La terapia con tocilizumab controló la erupción y la linfadenopatía.\n- Motivo de la cirugía: insuficiencia aórtica (regurgitación aórtica pura moderada) con dilatación ventricular izquierda y progresiva disnea de esfuerzo → decisión de realizar reemplazo quirúrgico de válvula aórtica (SAVR).\n\nEvaluación preoperatoria y riesgos\n- Hallazgos relevantes: sangrado por hemorroides, hepatólogo diagnosticó cirrosis hepática Child‑Pugh A y varices esofágicas.\n- Gestión del riesgo inmunosupresor: discusión multidisciplinaria (incluyendo intensivista y farmacéutico) sobre los efectos de tocilizumab y estrategias perioperatorias.\n- Plan: suspender tocilizumab antes de la cirugía (última dosis 26 días antes) y mantener esteroides; aplicar medidas intensivas para prevenir infección del sitio quirúrgico (screening nasal para Staphylococcus aureus resistente, antisepsia cutánea, antibiótico profiláctico, control de glucemia). Cultivo nasal positivo para estafilococos coagulasa‑negativos.\n\nCurso quirúrgico y postoperatorio\n- Procedimiento: reemplazo valvular aórtico por esternotomía media bajo circulación extracorpórea (tiempo de isquemia 65 min; circulación 128 min). Requirió transfusiones y fue extubado al día siguiente.\n- Anatomía patológica de la válvula: engrosamiento fibroso focal sin depósitos amiloides.\n- Herida y complicaciones infecciosas: sin signos clínicos de infección; se empleó terapia de presión negativa en herida cerrada (NPWT) desde el día 2 al 13 postoperatorio; alta hospitalaria en el día 17 sin infección aparente.\n- Función renal: creatinina aumentó transitoriamente pero volvió al nivel preoperatorio al día 24.\n\nBiomarcadores y reanudación de tocilizumab\n- IL‑6: aumento transitorio en los días 1–2 posoperatorios, luego disminución progresiva hasta el día 24; aumentó de nuevo tras la reintroducción de tocilizumab.\n- PCR (proteína C reactiva): ligera elevación máxima 0,56 mg/dL el día 2; subió a 1,06 mg/dL al día 24 sin evidencia de infección.\n- VEGF: aumento detectado el día 13, precediendo el incremento de la PCR.\n- Reinicio de tocilizumab: se reanudó el día 30 postoperatorio tras confirmar ausencia de infección, incluida la infección fúngica invasora (IFI).\n- Clínica de Castleman: sin recurrencia de erupción ni linfadenopatía durante el período perioperatorio.\n\nInterpretación y puntos prácticos\n- Resultado: SAVR exitoso sin infección del sitio quirúrgico ni reactivación clínica de la enfermedad de Castleman, gracias a una planificación perioperatoria cuidadosa.\n- Implicaciones:\n  - Suspender tocilizumab varias semanas antes de cirugía y reanudarlo después de confirmar ausencia de infección fue una estrategia segura en este caso, pero debe individualizarse según el riesgo infeccioso y la gravedad de la enfermedad subyacente.\n  - Monitorizar biomarcadores (IL‑6, PCR, VEGF) puede ayudar a distinguir respuestas inflamatorias posoperatorias esperadas de infecciones o actividad de la enfermedad; sin embargo, los inmunomoduladores cambian la interpretación de estos marcadores.\n  - Medidas preventivas (screening nasal, antisepsia, profilaxis antibiótica, control glucémico) y el uso de NPWT en herida cerrada pueden contribuir a reducir el riesgo de SSI en pacientes inmunocomprometidos.\n  - La decisión sobre timing de suspensión/rehabilitación de agentes biológicos requiere un enfoque multidisciplinario, especialmente cuando hay comorbilidades como cirrosis.\n\nComentario empático\nEste caso muestra que, con evaluación y coordinación cuidadosas, es posible realizar cirugías mayores en pacientes con enfermedades inflamatorias tratadas con biológicos sin provocar infección ni reactivación clínica. Las decisiones sobre manejo perioperatorio de inmunosupresión deben discutirse de forma individualizada y con seguimiento estrecho.",
+                "fh_score": 30.71
+            }
+        }
+    },
+    {
+        "article": "Se trata de un paciente de sexo masculino de cuatro meses de edad, originario del centro de México y con dos hermanos hombres sanos. Durante el primer trimestre de gestación, su madre hipotiroidea consumió drogas. No obstante, el infante nació con peso y talla adecuados, fue alimentado con leche materna y recibió la vacuna del bacilo de Calmette-Guérin (BCG), sin desarrollo de cicatriz. La madre del paciente era prisionera en una cárcel y, junto con el bebé, compartían una celda insalubre con dos personas más.A los cuatro meses, el paciente fue valorado médicamente por un tumor doloroso en la región axilar izquierda. En la radiografía de tórax se observaron imágenes sugestivas de fracturas costales; se sospechó de maltrato infantil por parte de la madre, y el infante fue hospitalizado en un hospital pediátrico. Se determinó el peso (4.190 g) y la talla (58 cm) –por debajo del percentil tres–, saturación de oxígeno del 70 %, fiebre, tos, aumento de volumen en la región axilar izquierda, además de dolor, rubor y calor. En el cuadro hemático se encontró: hemoglobina de 8,8 g/dl (11,0 - 12,6), 29,3 × 109 leucocitos/L (6,0 - 17,5), 18,4 × 109 neutrófilos/L (1,0 - 8,5), 7,0 × 109 linfocitos/L (4,0 - 13,5), 3,5 × 109 monocitos/L, 459 × 109 plaquetas/L (150 - 350) y proteína C reactiva igual a 16 mg/L (< 3,0). En la primera tomografía toracoabdominal se observaron imágenes de un absceso en la región axilar izquierda, lesiones líticas en las costillas 3 a 6, neumonía apical izquierda, nódulos pulmonares en ambos pulmones y ganglios linfáticos cervicales y mediastinales incrementados de tamaño. En la biopsia del absceso axilar izquierdo se reportó miositis y paniculitis supurativa. Solo se hizo cultivo para bacterias del líquido broncoalveolar, el cual fue negativo, y la PCR para el complejo Mycobacterium tuberculosis fue negativa. Después de 41 días de hospitalización y de haber recibido dos esquemas de antimicrobianos –ceftriaxona-clindamicina y cefepima-vancomicina–, el paciente fue dado de alta.\n\nDos meses después, a los ocho meses de edad, reingresó al hospital por fiebre, irritabilidad y un absceso supurante en la escápula izquierda. En el cuadro hemático se encontró: hemoglobina de 10,8 g/dl (10,5 - 12), 21,2 × 109 leucocitos/L (6 - 17), 12,2 × 109 neutrófilos/L (1,5 - 8,5), 7,5 × 109 linfocitos/L (4 - 10,5), 1,2 × 109 monocitos/L (600), y 583 × 109 plaquetas/L (150 - 350); la prueba para la detección sérica de HIV fue negativa. En la tomografía de tórax se observó una consolidación apical izquierda, bronquiectasias, lesiones líticas en las costillas 2 a 7 y en las vértebras dorsales 2 a 7, además de una colección de líquido multiloculado; en el ultrasonido se encontró una fístula asociada con el absceso escapular. El paciente recibió piperacilina-tazobactam, que se sustituyó después por voriconazol al detectarse Aspergillus fumigatus en el cultivo de la muestra de secreción del absceso. Dada la recurrencia y la gravedad de la infección, se sospechó un error innato de la inmunidad. La prueba de dihidrorrodamina resultó sin producción de especies reactivas de oxígeno y la expresión de gp91phox en los neutrófilos fue nula, estableciéndose así el diagnóstico de enfermedad granulomatosa crónica ligada al cromosoma X. La variante patógena detectada por la secuenciación de nueva generación fue c.80_83del/Y (p.Val27Glyfs*33) en CYBB. La madre resultó portadora de la variante (c.80_83del/WT). No fue posible estudiar genéticamente a sus dos hermanos mayores, de sexo masculino, y aparentemente sanos. El paciente fue dado de alta después de 65 días de hospitalización y tratamiento con voriconazol por 28 días. Se inició profilaxis antibiótica diaria con trimetoprim-sulfametoxazol y profilaxis antifúngica con fluconazol dos veces a la semana. Dos meses después, al año de edad, el infante reingresó debido a una neumonía multifocal, por la cual requirió asistencia respiratoria mecánica. Se detectó el antígeno galactomanano en el suero y A. fumigatusen el cultivo del líquido del lavado broncoalveolar, por lo que se inició nuevamente tratamiento con voriconazol. El paciente sufrió una falla orgánica múltiple y falleció un mes después de su ingreso.\n",
+        "gold_summary": "Se presenta el caso de un infante con enfermedad granulomatosa crónica y aspergilosis invasiva. Se trata de un lactante de sexo masculino de cuatro meses de edad, de madre hipotiroidea y con quien convive en la celda de la cárcel. El infante presentó tumores en la región axilar izquierda y la radiografía de tórax sugirió fracturas costales; fue hospitalizado ante la sospecha de maltrato infantil. En la tomografía de tórax se observó un absceso axilar, osteólisis de costillas, neumonía y nódulos pulmonares; el paciente recibió antibióticos de amplio espectro y fue dado de alta. A los ocho meses, reingresó por fiebre y extensión del absceso purulento hacia la región escapular izquierda; en la tomografía se observaron imágenes de empeoramiento de la condición. Se aisló Aspergillus fumigatus de la secreción del absceso y se diagnosticó aspergilosis invasiva; se inició tratamiento con voriconazol por 28 días. Mediante la prueba de dihidrorrodamina, se diagnosticó enfermedad granulomatosa crónica causada por la variante patógena c.80_83del/Y del gen CYBB, portada por la madre (c.80_83del/WT). A los 12 meses, el paciente reingresó nuevamente por aspergilosis invasiva, resistente al tratamiento, con desenlace fatal.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Este es el cuento triste de un bebé que nació con un problema en sus defensas.\n\nEl niño era un bebé varón. Vivía con su mamá en una celda sucia. Cuando tenía cuatro meses, apareció un bulto doloroso en la axila. También le dolía el pecho y tenía fiebre. Los médicos pensaron al principio que podía haber sido maltrato porque se vieron lesiones en las costillas. Lo ingresaron al hospital y le dieron antibióticos.\n\nEl bebé mejoró un poco y salió del hospital. Pero a los ocho meses volvió con fiebre y un absceso que supuraba cerca del omóplato. En el cultivo del pus crecieron hongos llamados Aspergillus. Le dieron un medicamento para los hongos, pero la infección seguía preocupando a los médicos.\n\nLos especialistas pensaron que el niño no podía luchar bien contra gérmenes y le hicieron pruebas. Descubrieron que sus glóbulos blancos no funcionaban para matar microbios. Esto se llama enfermedad granulomatosa crónica (CGD). Es un problema en un gen llamado CYBB. La mamá era portadora de ese cambio en el gen. Por eso el bebé nació con este problema.\n\nLe dieron medicinas para prevenir infecciones y para el hongo. Aun así, al año volvió muy enfermo con neumonía por el mismo hongo. Necesitó respirador y, a pesar del tratamiento, su cuerpo dejó de trabajar y murió un mes después.\n\nEs una historia triste. El bebé sufrió por muchas infecciones porque su sistema de defensa no funcionaba. Los médicos encontraron la causa y cuidaron de él, pero no fue suficiente.",
+                "fh_score": 79.95
+            },
+            "B2": {
+                "text": "This is the story of a baby boy who became very sick from a rare immune problem and a serious fungal infection.\n\nBackground and first illness\n- The child was born apparently healthy and lived with his mother, who had thyroid disease, in a poor and crowded jail cell. At 4 months old he developed a painful swollen lump under his left armpit. A chest X‑ray also suggested broken ribs, so doctors first worried about possible child abuse and admitted him to hospital.\n- At admission he was very small for his age, had low oxygen levels, fever, cough, and a painful, red axillary (armpit) abscess. Blood tests showed anemia and signs of infection. A CT scan found an abscess under the arm, areas where the ribs had been destroyed, pneumonia in the top of the left lung, small lung nodules, and enlarged lymph nodes. A biopsy of the abscess showed inflammation and pus. Tests for common bacteria and for tuberculosis were negative.\n- He received broad‑spectrum antibiotics in hospital and was sent home after about six weeks.\n\nSecond illness, diagnosis, and treatment\n- At 8 months he returned with fever, irritability, and a new draining abscess near his left shoulder blade. Imaging showed worse lung disease (including bronchiectasis, which means damaged airways), more bone destruction of ribs and spinal vertebrae, and collections of infected fluid with a fistula (an abnormal draining tract).\n- A fungus called Aspergillus fumigatus grew from the abscess. Treatment was changed to the antifungal drug voriconazole. Because the infections kept coming back and were unusual for an infant, doctors tested his immune system.\n- A dihydrorhodamine (DHR) test showed his white blood cells could not produce reactive oxygen species—chemicals immune cells normally use to kill certain germs. A further test showed no gp91phox protein. Genetic testing found a damaging change (called c.80_83del in the CYBB gene) that explains the condition: X‑linked chronic granulomatous disease (CGD). In CGD, some immune cells cannot destroy certain bacteria and fungi, so people get repeated, severe infections. The mother was found to be a carrier of the same gene change.\n\nFinal course and outcome\n- He received antifungal therapy and daily antibiotic prevention (trimethoprim‑sulfamethoxazole) plus twice‑weekly fluconazole to try to prevent new infections. Despite this, at about 12 months he was readmitted with widespread pneumonia, needed a breathing machine, and tests again found Aspergillus in his lungs. He developed multiple organ failure and died about one month later.\n\nWhat this means (calmly)\n- This case shows how CGD, an inherited immune defect that mainly affects boys when it is X‑linked, can lead to life‑threatening infections with organisms like Aspergillus. Early diagnosis of primary immunodeficiency can allow targeted care (antifungal and antibiotic treatment, infection prevention, and sometimes bone marrow transplant) that might improve outcomes. The medical team also had to consider and rule out other problems, such as child abuse, because of the unusual bone findings. The situation was made harder by the child’s difficult living conditions and the delayed recognition of the underlying immune disorder.",
+                "fh_score": 82.57
+            },
+            "B3": {
+                "text": "Resumen clínico empatético y orientado a no especialistas (nivel lector universitario)\n\nPaciente y contexto\n- Lactante masculino, originario del centro de México. Madre con hipotiroidismo, privada de libertad; vivían en una celda con condiciones insalubres. Nacimiento con peso y talla adecuados; lactancia materna y vacuna BCG aplicada sin formación de cicatriz.\n- Dos hermanos varones aparentemente sanos, no fue posible estudiarles genéticamente.\n\nCurso clínico y hallazgos principales\n1) Primer ingreso (4 meses)\n- Motivo: tumor doloroso en la axila izquierda. Radiografía de tórax sugirió fracturas costales, por lo que se consideró inicialmente maltrato infantil.\n- Signos anormales: saturación de oxígeno 70% (muy baja), fiebre, crecimiento por debajo del percentil 3, dolor e inflamación axilar.\n- Laboratorio: anemia (Hb 8,8 g/dl), leucocitosis marcada (29,3 ×10^9/L) con neutrofilia, PCR elevada (16 mg/L) y trombocitosis.\n- Imágenes: tomografía mostró absceso axilar izquierdo, lesiones líticas en costillas (3–6), neumonía apical izquierda, nódulos pulmonares bilaterales y adenopatías cervicales y mediastinales.\n- Biopsia del absceso: miositis y paniculitis supurativa. Cultivo de LBA y PCR para Mycobacterium tuberculosis negativos.\n- Tratamiento: antibióticos de amplio espectro (esquemas secuenciales). Alta tras 41 días.\n\n2) Segundo ingreso (8 meses)\n- Motivo: fiebre y absceso supurante en región escapular izquierda que formó fístula.\n- Hallazgos: nuevas lesiones líticas en costillas y vértebras (D2–D7), bronquiectasias, colección multiloculada en tórax.\n- Microbiología: Aspergillus fumigatus aislado del secreción del absceso. Se cambió a voriconazol.\n- Dada la recurrencia y gravedad, se sospechó inmunodeficiencia.\n\nDiagnóstico de enfermedad granulomatosa crónica (EGC)\n- Prueba de dihidrorrodamina (DHR): ausencia de producción de especies reactivas de oxígeno en neutrófilos.\n- Flujo: ausencia de expresión de gp91phox.\n- Genética: secuenciación identificó una variante patógena en el gen CYBB: c.80_83del (p.Val27Glyfs*33), consistente con EGC ligada al cromosoma X. La madre resultó portadora de la misma variante.\n- Explicación breve: la EGC es un defecto hereditario del complejo NADPH oxidasa de los fagocitos; impide la producción de especies reactivas necesarias para matar ciertos bacterias y hongos, por lo que hay infecciones recurrentes, especialmente por organismos como Aspergillus.\n\nTratamiento, profilaxis y desenlace\n- Tras el segundo ingreso se administró voriconazol (28 días) y se instauró profilaxis diaria con trimetoprim‑sulfametoxazol y antifúngico profiláctico (fluconazol dos veces por semana).\n- A los 12 meses presentó neumonía multifocal por A. fumigatus (galactomanano sérico positivo), requirió ventilación mecánica, evolucionó a falla multiorgánica y falleció un mes después.\n\nImplicaciones clínicas y lecciones\n- Signos que deben alertar sobre una inmunodeficiencia primaria en lactantes: infecciones graves o recurrentes por hongos u otros patógenos inusuales, abscesos recurrentes, osteólisis/osteomielitis y mala respuesta a tratamientos convencionales.\n- La DHR es una prueba diagnóstica rápida y sensible para EGC; la confirmación genética permite identificar portadores y ofrecer consejo genético.\n- Manejo recomendado en EGC: profilaxis antibiótica/antifúngica, tratamiento agresivo de infecciones invasivas, evaluación para trasplante de progenitores hematopoyéticos (terapia potencialmente curativa) y seguimiento familiar. En este caso, el diagnóstico llegó después de infecciones ya avanzadas y aunque se iniciaron medidas profilácticas, no fue suficiente para evitar el desenlace fatal.\n- Es importante evaluar y ofrecer estudio genético a hermanos varones y apoyo social/psicosocial dada la situación familiar y el riesgo para otros varones portadores.\n\nComentario final (empático)\nEste caso ilustra cómo una enfermedad genética del sistema inmune (EGC ligada al X) puede manifestarse precozmente con infecciones fúngicas y lesiones óseas graves. El diagnóstico temprano y la coordinación entre microbiología, inmunología, genética y cuidado social son claves para ofrecer intervenciones que puedan cambiar el pronóstico. Lamento el desenlace desfavorable para el lactante y subrayo la importancia del estudio y consejo genético para la familia.",
+                "fh_score": 38.39
+            }
+        }
+    },
+    {
+        "article": "Se trata de un hombre de 66 años de edad que vive en la ciudad de Juan Bautista Alberdi de la provincia de Buenos Aires, con antecedentes de hipertensión arterial y trastorno obsesivo compulsivo. Su medicación habitual incluía amlodipina, quetiapina, venlafaxina y ácido valproico. Consultó por presentar fiebre de 39ºC de cuatro días de evolución sin síntomas asociados y se internó para estudio en sala general. Al examen de ingreso se constató un paciente lúcido, sin foco motor, sin trastorno sensitivo ni rigidez de nuca (escala de coma de Glasgow (GCS) 15/15). El resto del examen físico y el laboratorio general no presentaron particularidades. Los cultivos de sangre y orina resultaron negativos, y la tomografía computarizada de encéfalo, tórax, abdomen y pelvis no mostró afecciones. A las 24 horas agregó episodios de desorientación témporo-espacial que alternaban con otros de somnolencia (GCS 13/15). Al examen físico se constató temblor grueso distal en los cuatro miembros. El examen del LCR informó: líquido incoloro, límpido, y aspecto post centrifugado también límpido. Recuento de leucocitos 310/mm3 (mononucleares 54%, polimorfonucleares 46%), hematíes < de 1000/mm3, proteínas 0.76 g/l, glucosa 54 mg/dl (glucemia 120 mg/dl), y ácido láctico 21 mg/dl. Se inició tratamiento empírico con aciclovir 10 mg/kg endovenoso cada 8 horas. Se solicitaron en LCR: PCR para virus de herpes simple (VHS) y para virus de encefalopatía equina del oeste (VEEO) que resultaron no reactivas. Sin embargo, la IgM (ELISA) para EEO resultó positiva en suero y en LCR a los diez días. La RMN de encéfalo evidenció aumento en la intensidad en secuencias FLAIR y T2 a nivel de la región dorsal del tronco encefálico (tanto protuberancial, como también bulbar y mesencefálico), ambos pedúnculos cerebrales y ganglios de la base, con afectación bilateral y ligero predominio ganglio basal derecho. También se observaron múltiples imágenes focales hiperintensas en la sustancia blanca de ambos hemisferios cerebrales. El paciente evolucionó con deterioro del sensorio (GCS 8/15), sin protección de la vía aérea, por lo que ingresó a UTI. Requirió intubación y ventilación mecánica, con utilización de sedación y analgesia. Al ingreso a UTI presentaba: estado ácido-base (EAB) arterial: pH 7.11, pCO2 136 mmHg, pO2 75 mmHg, bicarbonato 43 mEq/l, exceso de base 11 mEq/l, saturación 88% (Con FIO2 21%), ácido láctico 11.5 mg/dl. Se inició la ventilación mecánica con un volumen minuto respiratorio (VMR) de 9.8 litros (volumen tidal 490 ml que corresponde a 6 ml/kg de peso teórico, frecuencia respiratoria 20 por minuto, presión positiva al final de espiración (PEEP) 5 cmH2 O, fracción inspirada de oxígeno 30%) se extrajo sangre para EAB arterial: pH 7.40, pCO2 41 mmHg, pO2 65 mmHg, bicarbonato 28 mEq/l, exceso de base 0 mEq/l, saturación 93%, PAFI 216. Evolucionó sin fiebre, estable hemodinámicamente, con adecuada oxigenación y ritmo diurético. Al suspender sedantes presentó GCS de 3 puntos sobre 10 (correspondiente con evaluación ocular 1 y motor 2 puntos), con rigidez generalizada y reflejos osteotendinosos adecuados, con movimientos rítmicos linguales y peribucales. El electroencefalograma de 12 canales no evidenció descargas patológicas. Al décimo día de inicio de los síntomas presentó apertura ocular y menor rigidez, pero no toleraba la modalidad respiratoria espontánea por hipoventilación e hipercapnia que lo llevaron a hipoxemia transitoria. En el EAB arterial presentó: pH 7.31, pCO2 70 mmHg, pO2 76 mmHg, bicarbonato 35 mEq/l, exceso de base 8 mEq/l bajo asistencia ventilatoria en modalidad espontánea de presión soporte de 5 cmH2 O, frecuencia respiratoria 6 por minuto, PEEP 5 cmH2 O y volumen tidal entre 120-150 ml. Los siguientes días el paciente se conectó, respondiendo órdenes simples y complejas, y movilizó simétricamente los miembros con cierta debilidad. Por intolerancia a las pruebas ventilatorias espontáneas fue traqueostomizado. En la evaluación funcional respiratoria presentaba presión inspiratoria máxima menor a -40 cm de H2 O, presión espiratoria máxima mayor a 80 cm de H2 O, pero continuaba con hipercapnia en la prueba ventilatoria espontánea, por lo que requirió soporte ventilatorio con modalidad controlada. Se realizó ecocardiograma transtorácico que informó cavidades derechas normales, sin signos de hipertensión pulmonar. En la nueva RMN de encéfalo se evidenció disminución de las áreas hiperintensas en secuencias FLAIR y T2 visibles previamente.\n\nEl enfermo evolucionó con requerimiento de menor soporte ventilatorio en forma progresiva al momento del desarrollo de este informe.",
+        "gold_summary": "Presentamos el caso de un varón de 66 años de edad oriundo de la ciudad Juan Bautista Alberdi de la provincia de Buenos Aires con antecedentes de hipertensión arterial y trastorno obsesivo compulsivo. Consultó por fiebre súbita de cuatro días de evolución, con desarrollo de encefalopatía durante su internación. La punción lumbar mostró un líquido cefalorraquídeo cristalino, aunque inflamatorio de predominio mononuclear. La RMN de encéfalo informó hiperintensidad en secuencias FLAIR y T2 en el dorso del tronco encefálico. Ingresó a terapia intensiva por deterioro neurológico y acidosis respiratoria grave, requiriendo asistencia ventilatoria mecánica. Luego de 10 días presentó mejoría neurológica, sin déficit motor pero con hipoventilación alveolar que dificultaron el destete del respirador.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un hombre de 66 años llegó al hospital con fiebre. Tenía presión alta y un problema de ansiedad. Al principio estaba despierto y sin signos de infección en el cuerpo.  \n\nAl día siguiente empezó a estar confundido y muy somnoliento. Le hicieron una punción lumbar (sacaron líquido de la espalda) y ese líquido mostró signos de infección. Le hicieron una resonancia del cerebro (una prueba por imágenes) y vieron cambios en el tronco del cerebro y otras áreas. Los médicos pensaron que tenía una infección viral del cerebro llamada encefalitis. Pruebas en sangre y en el líquido de la espalda mostraron anticuerpos que apoyaron la idea de una infección por el virus de la encefalitis equina del este.  \n\nEl paciente empeoró y perdió parte de su capacidad para respirar solo. Lo conectaron a un respirador en la unidad de cuidados intensivos. Con el tiempo mejoró en la parte del cerebro: abrió los ojos y respondía. Pero seguía respirando de forma lenta y no podía dejar el respirador, por lo que le hicieron una pequeña apertura en la garganta (traqueostomía) para ayudarle a respirar mejor.  \n\nLa segunda resonancia mostró que las áreas dañadas empezaban a mejorar. Al momento del informe, necesitaba menos ayuda del respirador y su estado general estaba mejorando. Aunque había mejoría, seguía con debilidad y problemas para respirar por su cuenta. Los médicos continuaban cuidándolo y dándole apoyo.",
+                "fh_score": 68.0
+            },
+            "B2": {
+                "text": "Resumen amable y claro:\n\nUn hombre de 66 años, con hipertensión y trastorno obsesivo-compulsivo, consultó por fiebre de cuatro días y fue hospitalizado. Al principio estaba lúcido, pero al día siguiente comenzó con desorientación y somnolencia, además de temblor en las manos y pies.\n\nSe le practicó una punción lumbar (extracción de líquido que rodea el cerebro y la médula, llamado líquido cefalorraquídeo o LCR). El LCR estaba claro pero mostraba signos de inflamación (aumento de glóbulos blancos y proteínas), lo que sugiere infección o inflamación en el sistema nervioso. Se inició tratamiento empírico con aciclovir (un antiviral usado para sospecha de infección por herpes) mientras se hacían pruebas. La PCR para virus herpes y otro virus equino fue negativa, pero a los diez días la prueba de anticuerpos IgM fue positiva tanto en sangre como en LCR, lo que indica una infección reciente por un virus equino (virus de encefalitis equina del oeste).\n\nLa resonancia magnética (RMN) del cerebro mostró zonas anormales en la parte posterior del tronco encefálico (incluyendo puente, bulbo y mesencéfalo), en los pedúnculos cerebrales y en los ganglios basales, además de algunas lesiones en la sustancia blanca de ambos hemisferios. Estas imágenes son compatibles con inflamación del cerebro por virus.\n\nPor empeoramiento neurológico (bajó el nivel de conciencia) y una respiración muy insuficiente con retención de dióxido de carbono (hipercapnia), fue trasladado a la unidad de cuidados intensivos y conectado a ventilación mecánica (respirador). Tras estabilizar los gases sanguíneos y suspender sedación, estuvo con reflejos y movimientos anormales, y el electroencefalograma no mostró crisis epilépticas. Diez días después empezó a mejorar neurocognitivamente (respondía órdenes y movía los brazos y piernas), pero no podía respirar bien por sí mismo: respiraba muy despacio y con volúmenes pequeños, lo que causaba alta CO2 y episodios de baja oxigenación. Por eso se le practicó traqueostomía (una abertura en la garganta para ayudar la ventilación) y siguió recibiendo apoyo ventilatorio.\n\nUna resonancia de control mostró reducción de las zonas anormales, y al momento del informe requería cada vez menos asistencia del respirador, aunque aún no estaba totalmente independiente para respirar solo.\n\nQué significa y posibles pasos siguientes:\n- El cuadro es compatible con una encefalitis viral (inflamación del cerebro) por un virus de encefalitis equina occidental, confirmada por anticuerpos IgM.  \n- El tratamiento principal fue de soporte en UCI (respirador, control de gases, cuidado neurológico); no existe un tratamiento específico para algunos de estos virus, por eso el manejo es de apoyo.  \n- Los próximos pasos suelen incluir rehabilitación respiratoria y neurológica, seguimiento con nuevas imágenes y control clínico para ver la recuperación funcional y respiratoria.\n\nEs comprensible que este proceso sea angustiante; la evolución mostrada aquí es alentadora porque hubo mejoría neurológica y disminución de las lesiones en la RMN, aunque aún requiere cuidado para lograr el alta completa.",
+                "fh_score": 43.76
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel universitario — lectura avanzada, tono empático)\n\nPresentación\n- Paciente: varón de 66 años, antecedentes de hipertensión arterial y trastorno obsesivo‑compulsivo; toma amlodipina, quetiapina, venlafaxina y ácido valproico.\n- Motivo de consulta: fiebre de 39 °C durante 4 días, sin focalidad infecciosa aparente al ingreso.\n- Inicialmente lúcido (GCS 15/15), sin rigidez de nuca ni déficit neurológico focal. Estudios iniciales (cultivos de sangre y orina, tomografías de cráneo, tórax, abdomen y pelvis) sin hallazgos.\n\nHallazgos clínicos y de laboratorio relevantes\n- A las 24 horas desarrolló desorientación témporo‑espacial y somnolencia intermitente, con temblor grueso distal en las cuatro extremidades.\n- Punción lumbar: LCR claro pero inflamatorio — pleocitosis 310 leucocitos/mm3 (predominio mononuclear 54%), proteínas elevadas (0.76 g/L), glucosa 54 mg/dL (glicemia concomitante 120 mg/dL), hematíes <1000/mm3. Estos valores indican inflamación meníngea/encefálica.\n- PCR en LCR para virus herpes simple y para virus equino (pruebas realizadas inicialmente) negativas.\n- Serología (ELISA IgM) para encefalitis equina oriental (EEO) positiva en suero y en LCR a los 10 días, lo que apoya infección aguda por este arbovirus (presencia de IgM en LCR sugiere producción intratecal).\n- EEG de 12 canales sin descargas epileptiformes, a pesar de movimientos periorales rítmicos y rigidez generalizada.\n\nImagenología\n- RMN cerebral: hiperintensidades en FLAIR y T2 en el dorso del tronco encefálico (protuberancia, bulbo y mesencéfalo), ambos pedúnculos cerebrales y núcleos de la base (predominio relativo en el ganglio basal derecho), además de múltiples focos en la sustancia blanca de ambos hemisferios. Estos hallazgos son compatibles con encefalitis que afecta preferentemente tronco cerebral y ganglios basales.\n- RMN de control mostró reducción de las áreas hiperintensas, coincidiendo con mejoría radiológica.\n\nEvolución clínica y manejo\n- Deterioro neurológico progresivo hasta GCS 8/15; ingreso a unidad de terapia intensiva e intubación por pérdida de protección de vía aérea.\n- Presentó acidosis respiratoria grave por hipoventilación (pCO2 muy elevado) y requirió ventilación mecánica; después de ventilación controlada los gases arteriales se normalizaron.\n- Tras suspensión de sedación, persistió un bajo nivel de conciencia (GCS reducido) con rigidez y movimientos orofaciales; no hubo evidencia electroencefalográfica de estatus epiléptico.\n- A los 10 días mejoría neurológica: apertura ocular y disminución de rigidez; sin embargo, hipoventilación alveolar (central) persistente que dificultó el destete ventilatorio. Se realizó traqueostomía por intolerancia a las pruebas de ventilación espontánea.\n- Ecocardiograma transtorácico sin alteraciones significativas.\n- En el momento del informe, el paciente requería progresivamente menos soporte ventilatorio.\n\nInterpretación y puntos clave\n- Diagnóstico probable: encefalitis por virus de la encefalitis equina oriental (EEO/“Eastern equine encephalitis”), confirmado por IgM positiva en suero y LCR. La PCR puede ser negativa por baja carga viral o ventana temporal de muestreo; la serología IgM en LCR respalda infección activa del SNC.\n- La localización predominantemente en el dorso del tronco encefálico explica la insuficiencia ventilatoria central (afección de centros respiratorios bulboprotuberanciales) y la necesidad de ventilación prolongada.\n- La ausencia de foco infeccioso sistémico y la imagen típica en RMN, junto con la pleocitosis del LCR, son concordantes con encefalitis viral.\n- Tratamiento específico para EEO es de soporte; a su ingreso se inició aciclovir empírico hasta descartar herpesvirus, pero no existe terapia antiviral eficaz específica para EEO establecida en práctica clínica.\n\nImplicaciones y recomendaciones prácticas\n- Pronóstico: la encefalitis por EEO puede tener evolución grave y mortalidad elevada; sin embargo, algunos pacientes muestran recuperación parcial o gradual, como en este caso donde hubo mejoría neurológica pero persistió hipoventilación. El pronóstico funcional dependerá de la extensión del daño encefálico y de complicaciones respiratorias y neurológicas residuales.\n- Seguimiento: ventilatorio prolongado y rehabilitación neurológica motora y respiratoria; control seriado por neuroimagen y evaluación neurofisiológica si cambian los movimientos anormales; vigilancia de complicaciones nosocomiales en UTI.\n- Consideraciones epidemiológicas: notificar a salud pública y evaluar riesgo de transmisión vectorial en la región, ya que EEO es un arbovirus transmitido por mosquitos.\n\nTono final\nEste caso ilustra una forma severa de encefalitis viral con compromiso troncoencefálico y falla ventilatoria central, confirmada por serología en LCR. El cuidado ha sido predominantemente de soporte intensivo y manejo de complicaciones; la mejora clínica y la disminución de las lesiones en la RMN son alentadoras, aunque la capacidad respiratoria central comprometida requerirá tiempo y rehabilitación especializada. Si desea, puedo preparar una versión más técnica orientada a médicos o una guía de seguimiento y rehabilitación para el equipo tratante.",
+                "fh_score": 33.7
+            }
+        }
+    },
+    {
+        "article": "Mujer de 27 años de edad oriunda del interior de la Provincia de Buenos Aires sin antecedentes personales o familiares de relevancia, consultó por sangrado vaginal. El estudio colposcópico evidenció formación polipoide que protruía por el orificio cervical externo (OCE). Se arribó clínicamente al diagnóstico de mioma nascens y se tomó una muestra de biopsia para su evaluación. Ante el diagnóstico patológico de sarcoma, se instauró quimioterapia, con el fin de reducir la masa lesional. Una vez lograda la reducción del tamaño, se decidió derivarla a nuestra institución para realizar tratamiento quirúrgico. Se recibió una pieza de histerectomía total con anexos, f ijada en formol al 10%. Cuerpo de 5 × 5 × 3.2 cm, cuello de 3.5 × 3 × 2 cm, ambas trompas de 4.5 × 0.7 cm y ovarios de 4 × 2.5 × 2.5 cm. A la apertura de la pieza, se observó a nivel de la unión cérvico-ístmica una formación polipoide pediculada de 8.5 cm de diámetro, que emergía hacia el canal endocervical y se exteriorizaba por el OCE. La superficie externa era parda, lobulada, con sectores rojizos. Al corte, se observaba blanquecina, blanda, con sectores de aspecto gelatinoso y formaciones quísticas de hasta 0,6 cm de dimensión máxima. Luego del procesamiento de rutina, se efectuaron secciones histológicas y se colorearon con hematoxilina-eosina (H-E), las cuales evidenciaron sectores celulares alternados por áreas laxas, mixoides junto a glándulas ístmico-endometriales típicas. La proliferación, predominantemente fusocelular atípica se disponía en nidos, constituidos por células de amplio citoplasma eosinófilo y núcleos excéntricos con cromatina homogénea, algunos pleomórficos. Se apreciaron estriaciones citoplasmáticas transversales en dichas células. El estroma era ampliamente mixoide y ricamente vascularizado. Se destacaban focalmente áreas celulares densamente condensadas inmediatas y próximas al revestimiento epitelial intacto, pero separadas de él, por una fina capa de estroma laxo. Esto se conoce como cambium layer o capa cambial. Se realizaron técnicas de inmunohistoquímica para desmina, actina músculo específico (AME) y miogenina (MYF4), las cuales resultaron positivas, mientras que la actina músculo liso fue negativa. Esta inmunomarcación permitió comprobar la estirpe muscular estriada y en última instancia arribar al diagnóstico, junto al cuadro morfológico, de RMS embrionario. Asimismo, la presencia de rabdomioblastos agrupados constituyendo la capa cambial a nivel subepitelial resultó fundamental y necesario para tipificar al RMS embrionario como botrioide, independientemente de la presentación macroscópica en forma de racimos polipoides.",
+        "gold_summary": "Presentamos el caso de una mujer de 27 años que consultó por sangrado vaginal y en quien se evidenció en la colposcopia, una lesión polipoide blanquecina que se exteriorizaba a través del orificio cervical externo. El estudio histológico reveló sectores celulares alternados por áreas laxas, mixoides, junto a glándulas ístmico-endometriales típicas. La proliferación fusocelular atípica, se disponía en nidos, constituidos por células de amplio citoplasma eosinófilo con estriaciones citoplasmáticas transversales y núcleos excéntricos con cromatina homogénea. Se exhibían áreas de células densamente condensadas inmediatas y próximas al revestimiento epitelial intacto, pero separadas de él, por una fina capa de estroma laxo (capa cambial). El perfil de inmunomarcación resultó positivo para desmina, actina músculo específico y miogenina, y negativo para actina músculo liso. Se realizó diagnóstico de rabdomiosarcoma embrionario botroide de cuerpo uterino.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una mujer de 27 años fue a la consulta porque tenía sangrado por la vagina.  \nLos médicos miraron el cuello del útero y vieron una especie de bulto que salía por el orificio del cuello.  \nTomaron un pedacito del bulto (biopsia) para verlo en el microscopio.  \nEn el laboratorio encontraron que el bulto era un cáncer raro que nace de células del músculo. Ese cáncer se llama rabdomiosarcoma.  \nAntes de operar, le dieron quimioterapia para hacerlo más pequeño. Luego le quitaron el útero con sus anexos.  \nAl abrir la pieza y al mirarla con el microscopio, vieron un tumor polipoide grande con zonas gelatinosas y quistes pequeños.  \nTambién encontraron una capa muy delgada de muchas células del tumor justo debajo de la capa interna: eso se llama “capa cambial” y ayuda a identificar un tipo especial del tumor.  \nHicieron pruebas con colorantes especiales que detectan proteínas de músculo y esas pruebas salieron positivas.  \nCon todo eso, los médicos dieron el diagnóstico de rabdomiosarcoma embrionario tipo botrioide. “Botrioide” significa que el tumor tiene aspecto parecido a racimos o a uvas.  \nLos médicos actuaron con pruebas y tratamientos para manejar este problema de manera cuidadosa.",
+                "fh_score": 65.79
+            },
+            "B2": {
+                "text": "A 27-year-old woman from the Buenos Aires province went to the doctor for vaginal bleeding. On exam, a polyp-like mass was seen coming through the cervical opening. At first it was thought to be a type of fibroid, but a biopsy showed a sarcoma (a cancer of soft-tissue cells). She received chemotherapy to shrink the tumor and was then referred for surgery.\n\nThe removed uterus showed a pedunculated (on a stalk) polypoid mass about 8.5 cm wide at the cervico-isthmic area that projected through the cervical opening. On cut section the lesion was soft, partly gelatinous, and had small cystic spaces.\n\nUnder the microscope, the tumor had areas of loose, myxoid (mucus-like) stroma mixed with denser cellular nests. Tumor cells were spindle-shaped to rounded, had abundant pink (eosinophilic) cytoplasm and eccentric nuclei, and some showed transverse striations—features suggesting muscle-type cells. Right beneath the intact surface epithelium there was a dense layer of tumor cells separated from the epithelium by a thin loose stroma; this dense zone is called a cambium layer and is characteristic of the botryoid form of certain tumors.\n\nSpecial stains (immunohistochemistry) were positive for desmin, muscle-specific actin, and myogenin, and negative for smooth muscle actin. These results point to a skeletal muscle cell origin rather than smooth muscle, supporting the diagnosis.\n\nPutting the microscopic appearance and the immunostains together, the final diagnosis was embryonal rhabdomyosarcoma, botryoid type, of the uterine cervix. Rhabdomyosarcoma is a cancer that shows skeletal muscle features; the botryoid type often forms grape-like polypoid masses and is identified by the cambium layer. The patient was treated with chemotherapy followed by total hysterectomy (removal of the uterus and nearby reproductive structures). Ongoing cancer follow-up and care by a specialist team are needed to monitor recovery and any further treatment.",
+                "fh_score": 78.8
+            },
+            "B3": {
+                "text": "Resumen clínico y patológico\n\nPresentamos el caso de una mujer de 27 años sin antecedentes relevantes que consultó por sangrado vaginal. En la colposcopia se mostró una formación polipoide que protruyó por el orificio cervical externo y fue inicialmente interpretada como un mioma nascens; se tomó biopsia y, ante el resultado de sarcoma, se indicó quimioterapia neoadyuvante para reducir la masa antes del tratamiento definitivo. Tras disminución del tumor, se practicó histerectomía total con anexos.\n\nHallazgos macroscópicos: pieza con tumor polipoide pediculado de 8,5 cm en la unión cérvico-ístmica, de superficie parda y lobulada; en el corte, tejido blanquecino con áreas blandas, gelatinosas y quistes de hasta 0,6 cm.\n\nHallazgos histológicos e inmunohistoquímicos: el tumor mostró zonas celulares alternando con estroma laxo y mixoide, y glándulas ístmico-endometriales adyacentes. La proliferación fusocelular atípica se organizó en nidos con células de citoplasma eosinófilo, núcleos excéntricos y estriaciones citoplasmáticas transversales (rhabdomioblastos). Se observó una capa cambial —una banda subepitelial de células densamente condensadas—, característica del tipo botrioide. La inmunohistoquímica fue positiva para desmina, actina músculo-específica y miogenina, y negativa para actina de músculo liso, confirmando diferenciación hacia músculo estriado. En conjunto, estos hallazgos permiten el diagnóstico de rabdomiosarcoma embrionario, variante botrioide, del cuerpo uterino.\n\nImplicaciones y recomendaciones: el rabdomiosarcoma uterino es raro en adultas; la variante botrioide tiene rasgos morfológicos característicos pero requiere manejo oncológico multidisciplinario. Dado que la paciente recibió histerectomía, existe pérdida de fertilidad; se recomienda seguimiento oncológico estrecho (estadificación por imagen si no realizada, valoración en oncología médica y radioterápica según protocolos locales, vigilancia por recidiva). El pronóstico y el tratamiento adyuvante dependen del estadío, la resección completa y la respuesta a quimioterapia, por lo que es importante coordinar un plan terapéutico individualizado.",
+                "fh_score": 24.24
+            }
+        }
+    },
+    {
+        "article": "Un hombre de 53 años de edad, que inició diálisis por disfunción renal en etapa terminal debido a nefropatía diabética o nefroesclerosis en nuestro departamento de nefrología 10 años antes, se sometió a una ecocardiografía de seguimiento anual para estenosis valvular aórtica progresiva (AVS) y regurgitación moderada con fracción de eyección ventricular izquierda (LVEF) normal. Un año antes, se observaron calcificaciones que sugerían MAC en el anillo mitral posterior, que no se habían visto dos años antes. En el último seguimiento, la ecocardiografía reveló una masa redonda de superficie lisa de 22 × 17 mm con alta ecogenicidad en el área circundante y un brillo interno ligeramente disminuido en el anillo mitral posterior del lado auricular izquierdo. El paciente no tenía síntomas significativos ni hallazgos físicos, excepto un soplo sistólico.\n\nLa ecocardiografía también reveló una VS moderada con un flujo de pico valvular transaórtico de 3,76 m/s y una regurgitación valvular aórtica moderada. Se observó una regurgitación mitral leve pero no estenosis. El patrón de velocidad de flujo de entrada del VI mostró un patrón pseudo-normal con un agrandamiento de la aurícula izquierda de 47 mm de diámetro. La ecocardiografía en serie durante dos años reveló un agrandamiento del VI y una disminución de la FEVI. El diámetro final diastólico/final sistólico del VI y la FEVI fueron de 50/33 mm y 64 %, respectivamente, hace dos años; 57/41 mm y 52 % hace un año; y 59/47 mm y 42 % en el último seguimiento.\n\nTeniendo en cuenta el estado de la hemodiálisis, predijimos la progresión a una AVS casi severa, con empeoramiento de la disfunción sistólica del LV, que se convertiría en una indicación para el reemplazo de la válvula aórtica (AVR) en un futuro cercano.\n\nLa tomografía computarizada (TC) reveló una masa de alta densidad sin realce de contraste. La resonancia magnética (MRI) mostró una masa bien definida de alta intensidad en el centro, con un borde hipointenso en la imagen T1 y una señal desprovista en T2. Se excluyeron los neoplasmas, incluidos los mixomas y los fibroelastomas papilares, en función de sus características de imagen. Los hallazgos de laboratorio no indicaron infección, y no se sospechó de vegetación con endocarditis infecciosa. Teniendo en cuenta la disfunción renal en etapa terminal en la hemodiálisis y los hallazgos de imagen, se sospechó CCMA. El rápido agrandamiento de la masa generó preocupación sobre una potencial embolia. En consecuencia, la masa se resecó con AVR.\n\nLa incisión del atrio izquierdo reveló una masa por debajo del endocardio auricular en el anillo de la válvula mitral (P1-2); se observaron sustancias cremosas en la incisión de la masa, lo que sugiere CCMA. Después de la extirpación y desbridamiento del tejido, el sitio de la incisión se suturó con prolina. Se realizó el reemplazo de la válvula aórtica utilizando una válvula SJM de 21 mm. La retirada del bypass cardiopulmonar fue relativamente suave. Al momento del alta, se prescribió warfarina y aspirina, junto con bisoprolol para la fibrilación auricular paroxística después de la cirugía.\n\nNo se observaron eventos embólicos antes o después de la cirugía.\n\nEl examen histopatológico reveló calcificaciones granulares y nodulares dispersas, que consistían principalmente en infiltración de células inflamatorias y proliferación vascular de neutrófilos, linfocitos, células espumosas, macrófagos tisulares y células plasmáticas, con osificación parcial compatible con CICM. La biopsia miocárdica LV para descartar cardiomiopatía secundaria y la válvula aórtica resecada mostraron células inflamatorias similares a las observadas en CICM. Por lo tanto, se diagnosticó CICM en base a la disminución del movimiento de la pared y la fibrosis miocárdica, con infiltración de células inflamatorias > 14 mm2, células T CD3 positivas > 7/mm2 y negatividad de tenascina C (4C8).7 Sin embargo, no se pudo determinar la causa de CICM.\n\nLa ecocardiografía 6 meses después de la resección no mostró recurrencia del tumor (ver material complementario en línea), ni progresión de la regurgitación mitral, función normal de la válvula aórtica protésica y ninguna mejora de la FEVI (41 %)\n\n",
+        "gold_summary": "Un hombre de 52 años con insuficiencia renal en fase terminal que requería hemodiálisis se sometió a una ecocardiografía anual de seguimiento para detectar una disfunción valvular aórtica. La ecocardiografía reveló una masa circular bien definida de 22 × 17 mm en el anillo de la valva mitral posterior que no se había detectado 2 años antes. En función de las características de la imagen, se sospechó que la masa era un CCMA. Se había agrandado rápidamente y suponía un riesgo potencial de embolia; por lo tanto, se extirpó al mismo tiempo que la sustitución de la válvula aórtica. Aunque se sospechó un CCMA en función de los hallazgos intraoperativos, el diagnóstico histopatológico fue un CAT. Tras el análisis histológico de la muestra de miocardio del ventrículo izquierdo y la válvula aórtica extirpada, se observó una infiltración de células inflamatorias crónicas; por lo tanto, se diagnosticó una cardiomiopatía inflamatoria crónica.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había un hombre de 53 años que necesitaba hemodiálisis. Eso quiere decir que una máquina limpiaba su sangre porque sus riñones estaban muy enfermos. Los médicos le hacían una ecografía del corazón cada año para ver sus válvulas.\n\nUn año vieron un bulto nuevo cerca de una válvula del corazón. El bulto medía como 2 cm. El hombre no tenía dolor, sólo un sonido extraño cuando el corazón latía. Las pruebas con tomografía y resonancia mostraron que el bulto tenía calcio y no parecía un tumor ni una infección. Los médicos temieron que el bulto pudiera soltar algo y viajar por la sangre. Por eso lo quitaron con cirugía. También cambiaron la válvula aórtica por una nueva.\n\nDentro del bulto hallaron una sustancia cremosa y calcio. El examen con el microscopio mostró muchas células de inflamación. Los médicos dijeron que tenía una inflamación crónica del corazón. No hubo señales de que algo se hubiera desprendido antes o después de la operación. Tras la operación, el hombre recibió medicinas para el ritmo del corazón y para evitar coágulos.\n\nSeis meses después, la ecografía mostró que el bulto no volvió. La válvula nueva funcionaba bien. Pero la fuerza del corazón no había mejorado mucho. Los médicos siguen cuidándolo y dándole medicinas.",
+                "fh_score": 75.33
+            },
+            "B2": {
+                "text": "Here is a clear, kind summary written for a secondary-school reader:\n\nA 53-year-old man who has been on hemodialysis for kidney failure had routine heart scans because of worsening aortic valve disease. Over two years his left heart pumping function (called left ventricular ejection fraction, or LVEF) fell from 64% to about 42%. In the most recent scan doctors found a new, round 22 × 17 mm mass on the back part of the ring of the mitral valve. The patient had no new symptoms besides a heart murmur.\n\nImaging tests (CT and MRI) suggested the mass might be “caseous calcification of the mitral annulus” (CCMA). CCMA is a rare, non-cancerous lump where calcium and other material build up in the valve ring. Because the mass had grown quickly and might break off and cause an embolus (a dangerous blockage), the team removed it during surgery and also replaced the aortic valve at the same time.\n\nUnder the microscope the removed mass looked like a calcified amorphous tumor (CAT) — another non-cancerous, calcium-containing mass — and showed many inflammatory cells. Samples from the left heart muscle and the removed aortic valve also had similar chronic inflammation. Based on these findings, doctors diagnosed chronic inflammatory cardiomyopathy (a long-lasting inflammation of the heart muscle) as the reason for the reduced heart function. The exact cause of that inflammation was not found.\n\nThe patient recovered from surgery without any embolic events. He went home on blood thinners (warfarin and aspirin) and a beta-blocker for occasional atrial fibrillation. Six months later there was no sign the mass had come back, the artificial aortic valve worked well, and mitral valve leakage had not worsened — but the heart’s pumping function had not improved.\n\nTakeaway: The team treated a new, quickly growing calcified mass in the mitral valve ring with surgery because of embolic risk. Pathology showed a non-cancerous calcified tumor and chronic inflammation of the heart muscle, which likely explains the falling heart function. Continued follow-up and medical care are needed to monitor heart function and look for causes of the inflammation.",
+                "fh_score": 85.94
+            },
+            "B3": {
+                "text": "Summary\n\nBackground and context\n- A 53-year-old man on chronic hemodialysis for end‑stage renal disease (ESRD) — started 10 years earlier for diabetic nephropathy or nephroesclerosis — was followed with annual echocardiography for progressive aortic valve disease (aortic stenosis and moderate regurgitation).\n\nKey findings (what was normal and what was abnormal)\n- Symptoms and exam: the patient had no new symptoms and only a systolic murmur on exam.\n- Echocardiography (latest): a new, smooth, round mass 22 × 17 mm located at the posterior mitral annulus on the left‑atrial side; the mass was highly echogenic with slightly reduced internal brightness. Other findings: moderate aortic stenosis (peak transaortic velocity 3.76 m/s), moderate aortic regurgitation, mild mitral regurgitation without stenosis, a pseudonormal LV inflow pattern, and left atrial enlargement (47 mm).\n- Serial LV measurements (progressive worsening over 2 years): \n  - 2 years ago: LV end‑diastolic/systolic diameters 50/33 mm, LVEF 64%\n  - 1 year ago: 57/41 mm, LVEF 52%\n  - Latest: 59/47 mm, LVEF 42% (clear progressive LV dilation and falling ejection fraction).\n- CT: high‑density (calcified) mass without contrast enhancement.\n- Cardiac MRI: well‑defined central high signal with a hypointense rim on T1 and signal void on T2 — Imaging features argued against cardiac tumors (myxoma, papillary fibroelastoma) and against infective vegetation. Laboratory testing did not indicate infection.\n\nWorking diagnosis before surgery\n- Because the mass appeared calcified, grew rapidly, and the patient has ESRD (a risk factor for mitral annular calcification), the team suspected caseous calcification of the mitral annulus (CCMA). Rapid enlargement raised concern for embolic risk and, together with predicted near‑severe aortic stenosis and worsening LV dysfunction, led to a decision for surgery.\n\nTreatment and surgical findings\n- The patient underwent resection of the mitral‑annulus mass at the time of aortic valve replacement (AVR) with a mechanical 21 mm SJM valve.\n- Intraoperative appearance: mass beneath the left atrial endocardium at the posterior mitral annulus (P1–2) contained a creamy substance — an appearance suggestive of CCMA.\n- Postoperative course: uneventful weaning from bypass. Discharged on warfarin and aspirin (for the mechanical valve) and bisoprolol for new paroxysmal atrial fibrillation. No clinical embolic events occurred before or after surgery.\n\nPathology and final diagnosis\n- Histopathology of the resected specimen showed dispersed granular and nodular calcifications with abundant inflammatory cell infiltrates (neutrophils, lymphocytes, foam cells, tissue macrophages, plasma cells), vascular proliferation and partial ossification.\n- Similar inflammatory findings were present in the left ventricular biopsy and in the excised aortic valve tissue.\n- Based on wall‑motion abnormalities, myocardial fibrosis and quantitative inflammatory cell criteria (inflammatory cell infiltration and CD3+ T‑cell density above diagnostic thresholds), the final diagnosis was chronic inflammatory cardiomyopathy (CICM). The exact cause of the inflammatory cardiomyopathy remained unknown.\n\nOutcomes and follow‑up\n- Six months after surgery: echocardiography showed no recurrence of the mitral annulus mass, no progression of mitral regurgitation, normal prosthetic aortic valve function, but persistent LV systolic dysfunction (LVEF ~41%) with no improvement in ejection fraction.\n\nImplications and reasonable next steps\n- What this means: the mass was initially suspected to be a benign caseous calcification of the mitral annulus based on imaging and intraoperative appearance, but histology demonstrated a chronic inflammatory process involving both the annulus and myocardium. The patient also has progressive LV systolic dysfunction consistent with inflammatory cardiomyopathy.\n- Clinical implications: persistent LV dysfunction despite removal of the mass suggests that myocardial inflammation and fibrosis are established and are the likely drivers of heart failure risk. ESRD patients are prone to annular calcification and complex valve pathology; the presence of inflammatory cardiomyopathy complicates prognosis.\n- Reasonable next steps in care (individualized by the treating team):\n  - Ongoing surveillance of LV function and valve prosthesis by echocardiography.\n  - Guideline‑directed heart failure management as appropriate (medications, rate/rhythm control for atrial fibrillation).\n  - Further evaluation to seek an underlying cause of the inflammatory cardiomyopathy if clinically indicated (infectious, autoimmune, metabolic, or drug‑related causes), and consideration of specialty input (cardiology with heart failure and possibly myocarditis/inflammatory cardiomyopathy expertise).\n  - Long‑term monitoring for embolic events and prosthetic valve management (anticoagulation).\n\nEmpathy note\n- The team acted preemptively because of the mass’s rapid growth and the patient’s declining cardiac function, aiming to reduce embolic risk and address worsening aortic valve disease. Although surgery removed the mass and replaced the aortic valve successfully, the persistent LV dysfunction highlights the need for careful long‑term cardiology follow‑up and targeted management of the underlying inflammatory cardiomyopathy.",
+                "fh_score": 59.15
+            }
+        }
+    },
+    {
+        "article": "Paciente masculino de 28 años, sin antecedentes de importancia, acude a consulta de dermatología con un cuadro cutáneo de 48 horas de evolución caracterizado por dos placas eritematosas con ampollas centrales más ulceración superficial localizadas en cara flexora de brazo y antebrazo derecho equidistantes del pliegue del codo, acompañadas de una sensación de ardor y prurito en el lugar de las lesiones. No presentó síntomas sistémicos ni se automedicó. Como antecedente refiere que se encontraba de vacaciones en la región costera de Ecuador al momento de aparecer las lesiones. Se realizó una biopsia incisional que reportó epidermis con acantosis, paraqueratosis y espongiosis, neutrófilos en estrato córneo e infiltrado linfocitario perivascular en dermis superficial, media y profunda. Por las características clínicas, el antecedente de viaje a una región tropical y los hallazgos histológicos se diagnosticó como dermatitis por Paederus. Se indicó tratamiento con antihistamínicos, esteroides tópicos y compresas frías. Después de 8 días de tratamiento, las lesiones remitieron dejando una hiperpigmentación postinflamatoria.",
+        "gold_summary": "Se comunica el caso de un paciente masculino de 28 años, que acude a consulta de dermatología con cuadro de 48 horas de evolución de dos placas eritematosas con ampollas centrales más ulceración superficial localizadas en cara flexora de brazo y antebrazo derecho, acompañadas de una sensación de ardor y prurito en el lugar de las lesiones, sin síntomas acompañantes. Como antecedente refiere que se encontraba de vacaciones en la región costera de Ecuador al momento de aparecer las lesiones. Se realizó una biopsia incisional y por las características clínicas y el antecedente de viaje a una región tropical se diagnosticó como dermatitis por Paederus y se indicó tratamiento con antihistamínicos, esteroides tópicos y compresas frías. Después de 8 días de tratamiento, las lesiones remitieron dejando una hiperpigmentación postinflamatoria.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un hombre de 28 años fue al doctor por dos manchas rojas en el brazo y el antebrazo derecho. Tenían ampollas en el centro y un poco de herida. Le dolía y le picaba. No tuvo fiebre ni otros problemas. Él había estado de vacaciones en la costa de Ecuador cuando aparecieron las lesiones.\n\nLos médicos hicieron una pequeña prueba en la piel que mostró inflamación. Juntando eso con su viaje, dijeron que era dermatitis por Paederus. Esto ocurre cuando un insecto pequeño (un escarabajo llamado Paederus) toca la piel y deja una sustancia que la irrita.\n\nLe dieron antihistamínicos para la picazón, cremas con esteroide para bajar la inflamación y compresas frías. Después de 8 días las heridas mejoraron, pero quedó una mancha más oscura en la piel donde estuvieron las lesiones.",
+                "fh_score": 75.53
+            },
+            "B2": {
+                "text": "A 28-year-old man went to a skin doctor after 48 hours of two red patches on the inner (flexor) side of his right upper arm and forearm. Each patch had a central blister and a shallow ulcer, and he felt burning and itching where the lesions were. He had no other symptoms and had not treated the spots himself; he said the lesions began while he was on vacation in coastal Ecuador. A skin biopsy showed changes that mean inflammation of the outer skin layers and a band of immune cells around blood vessels in the deeper skin. Based on the look of the lesions, the biopsy, and the travel to a tropical area, doctors diagnosed Paederus dermatitis — a skin reaction that can happen after contact with a small beetle that releases a toxin. He was treated with antihistamines (to reduce itching), topical steroids (to lower inflammation), and cold compresses. After eight days the lesions improved, leaving a darker area of skin called postinflammatory hyperpigmentation.",
+                "fh_score": 88.01
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel universitario, tono empático)\n\nPresentación y síntomas:\nUn hombre de 28 años, sin antecedentes relevantes, consultó por lesiones cutáneas de 48 horas de evolución: dos placas eritematosas con ampollas centrales y ulceración superficial en la cara flexora del brazo y antebrazo derechos, equidistantes del pliegue del codo. Las lesiones producían ardor y prurito local; no hubo síntomas sistémicos ni automedicación. Como antecedente relevante, el paciente estaba de vacaciones en la zona costera de Ecuador cuando aparecieron las lesiones.\n\nHallazgos histológicos:\nSe realizó una biopsia incisional. El informe describió: engrosamiento epidérmico (acantosis), retención de núcleos en la capa córnea (parakeratosis), edema intercelular epidérmico (espongiosis), presencia de neutrófilos en el estrato córneo y un infiltrado linfocitario perivascular que afectaba dermis superficial, media y profunda. Estos cambios son compatibles con una reacción inflamatoria aguda de la piel.\n\nDiagnóstico y explicación breve:\nPor la apariencia clínica, el antecedente de exposición en una región tropical y los hallazgos histológicos, se diagnosticó dermatitis por Paederus. Esta es una dermatitis irritativa causada por la liberación del tóxico pederina cuando se aplasta un escarabajo del género Paederus; típicamente provoca placas eritematosas, ampollas o lesiones lineales en áreas expuestas.\n\nTratamiento y evolución:\nSe indicó manejo conservador: antihistamínicos para el prurito, esteroides tópicos y compresas frías. Tras 8 días de tratamiento las lesiones remitieron, dejando hiperpigmentación postinflamatoria en la zona.\n\nImplicaciones y recomendaciones prácticas:\n- Prognóstico: buena respuesta al tratamiento en este caso; la hiperpigmentación postinflamatoria puede tardar semanas o meses en atenuarse.  \n- Seguimiento: acudir si las lesiones se extienden, aparecen signos de infección (dolor creciente, supuración, fiebre) o si la pigmentación persiste y causa preocupación estética.  \n- Prevención: evitar aplastar escarabajos Paederus en la piel (si contacta con uno, lavar con agua y jabón y no frotar), usar mosquiteros y minimizar la luz nocturna directa que atrae a estos insectos en regiones endémicas.  \n- Tratamientos adicionales: para hiperpigmentación persistente pueden considerarse medidas dermatológicas (fotoprotección, cremas despigmentantes, procedimientos) tras valoración por dermatólogo.\n\nSi desea, puedo redactar una versión aún más breve para registro clínico o preparar materiales para el paciente con recomendaciones de cuidado de la piel y prevención.",
+                "fh_score": 30.76
+            }
+        }
+    },
+    {
+        "article": "Un hombre de 35 años de edad, herido en un accidente de tráfico, fue trasladado a nuestro hospital, que está equipado con un ER híbrido. Había sufrido una lesión potencialmente mortal, con su pierna derecha acortada y girada. Los signos vitales del paciente a su llegada fueron los siguientes: frecuencia respiratoria de 24 respiraciones/min, saturación de oxígeno del 99 % con 12 L de administración de oxígeno, frecuencia cardiaca de 143 latidos/min, presión arterial de 80/40 mmHg, y puntuación de Glasgow Coma Scale de E4V4M6. Intentamos realizar un TAC y resucitar al paciente. El TAC reveló un hemotórax izquierdo, ensanchamiento del mediastino, y fractura pélvica. Como la presión arterial del paciente cayó rápidamente antes del TAC, se administraron procedimientos de salvamento, como intubación de emergencia, preperitoneal pelvic packing, y transfusión masiva, con un cuidadoso control de la presión arterial en el ER híbrido. Después de la estabilización de los signos vitales con estos procedimientos, el TAC con contraste reveló una fractura de BTAI de grado IV que se extendía hacia la cavidad torácica izquierda. La embolización arterial transcatéter (TAE) para la fractura pélvica y la fijación esquelética externa de la fractura del fémur derecho se realizaron primero, ya que el radiólogo y el cirujano cardiovascular, que realizan TEVAR en nuestro centro médico, no estaban disponibles en ese momento. Posteriormente, se realizó TEVAR utilizando un injerto de stent (GORE C-TAG 26 × 150 mm; WL Gore & Associates, Flagstaff, Arizona, EE. UU.) en el ER híbrido sin transferir al paciente. Se desplegó un injerto de stent justo distal de la arteria carótida común izquierda (zona II) y el extremo distal del injerto de stent se posicionó en el nivel de Th 8. Decidimos sacrificar LSCA ya que el flujo sanguíneo de la arteria vertebral izquierda fue suficiente según lo evaluado por angiografía. El paciente no tuvo síntomas que sugirieran isquemia después de TEVER. Durante la cirugía, se administraron 50 unidades/kg (3000 unidades) de heparina. El paciente fue trasladado a un hospital de rehabilitación el día 41 postoperatorio.\n",
+        "gold_summary": "Un hombre de 35 años de edad sufrió múltiples lesiones tras un accidente de tráfico y fue trasladado a nuestro hospital en estado de shock. La tomografía computarizada reveló una fractura de TAI de grado IV que se extendía hasta la cavidad torácica y una fractura pélvica. Poco tiempo después de realizar un relleno pélvico preperitoneal y una embolización arterial transcatéter para la fractura pélvica, se realizó un TEVAR en el quirófano híbrido sin trasladar al paciente. El paciente fue trasladado a un hospital de rehabilitación el día 41 después de la operación.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un hombre de 35 años tuvo un choque de coche y llegó muy herido. Tenía el muslo derecho roto y el cuerpo herido por dentro. Los médicos vieron que tenía sangre en el pecho y una grave rotura en una arteria del tórax. También tenía una fractura en la pelvis.\n\nPrimero los doctores lo ayudaron a respirar con un tubo y le dieron mucha sangre. Pusieron compresas dentro de la pelvis para detener la hemorragia. Luego cerraron los vasos de la pelvis con un catéter para parar el sangrado y pusieron una fijación externa en la pierna rota.\n\nDespués, sin moverlo del cuarto de urgencias, los médicos arreglaron la arteria rota en el pecho colocando un injerto por dentro de la arteria. Para eso usaron un “tubo” especial que evita que la arteria siga perdiendo sangre. Tuvieron que cerrar una rama pequeña de la arteria, pero otra arteria daba suficiente sangre, y el paciente no tuvo problemas por eso. También le dieron un medicamento para evitar coágulos durante la cirugía.\n\nEl hombre se recuperó y, 41 días después, lo enviaron a un hospital de rehabilitación para seguir mejorando.",
+                "fh_score": 74.05
+            },
+            "B2": {
+                "text": "Un hombre de 35 años llegó al hospital después de un accidente de tráfico con la pierna derecha visiblemente dañada y signos de shock (pulso rápido y presión arterial muy baja). En la tomografía se vio sangre en el pecho (hemotórax izquierdo), ensanchamiento del mediastino (un hallazgo que puede indicar lesión de un gran vaso) y una fractura pélvica. Como su presión arterial bajó rápido, el equipo realizó maniobras de emergencia en la sala híbrida (una sala con imagen y recursos quirúrgicos): intubación para ayudar a respirar, colocaron compresas en la pelvis para detener el sangrado y le dieron una transfusión masiva.\n\nTras estabilizarlo, la tomografía con contraste mostró una lesión grave en la aorta torácica (fractura de aorta por traumatismo, grado IV). Primero controlaron el sangrado de la pelvis con embolización (bloqueo de vasos desde un catéter) y fijaron la fractura del fémur. Luego realizaron una reparación endovascular de la aorta (TEVAR): colocaron un injerto o “stent” dentro de la aorta en la misma sala híbrida sin mover al paciente. Para asegurar el flujo cerebral, decidieron cerrar la arteria subclavia izquierda porque la arteria vertebral izquierda suministraba suficiente sangre; el paciente no presentó síntomas de falta de riego después del procedimiento. Durante la operación se usó heparina para evitar coágulos.\n\nEl paciente evolucionó bien y fue trasladado a un hospital de rehabilitación 41 días después de la cirugía.",
+                "fh_score": 51.98
+            },
+            "B3": {
+                "text": "Resumen clínico (lectores con formación universitaria)\n\nPresentación\n- Hombre de 35 años, víctima de accidente de tráfico, ingresó en estado de choque con la pierna derecha acortada y girada. A su llegada presentaba taquicardia (FC 143/min), hipotensión (PA 80/40 mmHg), frecuencia respiratoria 24/min y puntuación de Glasgow 14 (E4V4M6). Recibía 12 L de oxígeno con saturación del 99 %.\n\nHallazgos radiológicos y lesiones principales (anormales)\n- Tomografía computarizada (TAC) mostró hemotórax izquierdo, ensanchamiento del mediastino y fractura pélvica.\n- TAC con contraste posterior evidenció una lesión aórtica por traumatismo torácico (BTAI) grado IV que se extendía hacia la cavidad torácica izquierda — lesión potencialmente letal.\n\nIntervenciones realizadas\n- Manejo inicial de emergencia en el servicio de urgencias híbrido: intubación, preperitoneal pelvic packing (para controlar sangrado pélvico) y transfusión masiva, logrando estabilizar hemodinámicamente al paciente.\n- Procedimientos por prioridad: embolización arterial transcatéter (TAE) para la fractura pélvica y fijación externa de la fractura femoral derecha (realizados primero porque el equipo de TEVAR no estaba disponible inmediatamente).\n- Una vez disponible el equipo, se realizó TEVAR (colocación endovascular de stent endoluminal) en el quirófano/ER híbrido sin traslado del paciente. Se usó un graft GORE C-TAG 26 × 150 mm, implantado desde justo distal a la arteria carótida común izquierda (zona II) hasta aproximadamente T8.\n- Se decidió cubrir (sacrificar) la arteria subclavia izquierda (LSCA) porque la angiografía mostró flujo vertebral izquierdo suficiente. Durante el procedimiento se administraron 50 U/kg de heparina (3.000 U).\n\nResultados y evolución\n- No aparecieron síntomas sugestivos de isquemia vertebrobasilar o de miembro superior tras la cobertura de la LSCA.\n- El paciente fue trasladado a un centro de rehabilitación al día 41 posoperatorio.\n\nComentarios e implicaciones\n- El manejo escalonado —control urgente del sangrado pélvico y estabilización hemodinámica, seguido de reparación endovascular de la lesión aórtica— fue decisivo para la supervivencia.\n- La cobertura de la subclavia izquierda es una decisión frecuente cuando es necesario para lograr un sellado aórtico; requiere evaluar el flujo vertebral y vigilancia posterior por riesgo teórico de isquemia cerebral posterior, del brazo o de la médula espinal. En este caso no hubo signos clínicos de complicaciones inmediatas.\n- El uso del ER híbrido permitió realizar intervenciones simultáneas y evitar traslados riesgosos en un paciente inestable.\n\nSi desea, puedo añadir una breve explicación sobre qué implican las clasificaciones de lesiones aórticas (grado IV) o sobre los riesgos a medio-largo plazo tras TEVAR.",
+                "fh_score": 42.84
+            }
+        }
+    },
+    {
+        "article": "Hombre de 31 años con antecedentes de consumo de alcohol, tabaco, cocaína inhalada, tuberculosis pulmonar tratada, nefrectomía izquierda y esplenectomía post-traumática. Consultó al servicio de urgencias por cuadro de una semana de evolución que inició inmediatamente posterior a la aplicación intramuscular de penicilina por contacto sexual con pareja con sífilis, caracterizado por dolor en región glútea derecha que irradiaba hasta pie, con posterior aparición de dermatosis purpúrica relacionada con sitio de inyección, siendo una lesión tipo placa configurada en forma anular, con bordes irregulares y distribución racemosa que medía 15 centímetros (cm), con piel sana en su interior. También presentaba una pequeña escara escrotal y una extensa lesión plantar derecha de aspecto livedoide desde la zona talar hasta la punta de los dedos que no respetaba margen estricto. Se realizó ecografía del glúteo mayor, que mostró pérdida del patrón fibrilar heterogéneo, aumento del espesor del mismo a nivel de su tercio medio de aspecto edematoso, además de edema del tejido celular subcutáneo (TCS); en región plantar homolateral y en escroto edema de TCS. En el laboratorio presentó leucocitosis de 13.7 × 109/L, proteína C reactiva de 3.2 mg/dL (normal hasta 0.5 mg/dL), que se interpretaron como reactantes de fase aguda, también aumento de transaminasas con aspartato aminotransferasa de 175 UI/L (normal hasta 32), alanino aminotransferasa de 245 UI/L (normal hasta 33), creatina kinasa con un valor de 2741 UI/L (normal hasta 170) y lactato deshidrogenasa de 2499 UI/L (normal hasta 250) representando compromiso muscular. Se realizaron serologías completas para sífilis, con venereal disease research laboratory (VDRL y anticuerpos treponémicos), virus de la inmunodeficiencia humana (HIV) hepatitis B, hepatitis C, con resultados negativos. La cronología, las manifestaciones clínicas y la posterior biopsia, respaldaron el diagnóstico de síndrome de Nicolau, para lo cual se inició anticoagulación con enoxaparina 1 mg/ kg c/12 hs vía subcutánea, cilostazol 100 mg cada 12 horas y tramadol, por 10 días. Se realizó biopsia de piel de glúteo que evidenció necrosis epidérmica y extensión a epitelio folicular, con formación de ampolla secundaria a reepitelización, sin vasculitis ni trombosis vascular, vinculable a embolia cutis medicamentosa en fase aguda, hubo franca mejoría con descenso de valores de transaminasas, con aspartato aminotransferasa de 39 UI/L, alanino aminotransferasa de 77 UI/L y creatin kinasa de 167 UI/L.  No se solicitó perfil inmunológico, basados en que nuestro diagnóstico presuntivo inicial no justificaba la búsqueda de otras etiologías. Se otorgó alta con cilostazol y analgésicos, control ambulatorio a los 3 meses con mejoría del dolor y de las lesiones, quedando en glúteo derecho cicatriz discrómica con presencia de descamación fina y en pie derecho cicatriz discrómica con zonas de descamación gruesas en región de apoyo tarso metatarsiano asociado a mínimas lesiones livedoides en planta del mismo pie.",
+        "gold_summary": "Se reporta el caso de un hombre de 31 años que presenta este síndrome luego de la aplicación de penicilina benzatínica intramuscular. La biopsia apoyó el diagnóstico. Recibió tratamiento con enoxaparina y cilostazol con posterior mejoría.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un hombre de 31 años recibió una inyección de penicilina en la nalga. Poco después tuvo mucho dolor en esa zona y apareció una mancha grande y morada en la piel. También tuvo una pequeña llaga en el escroto y una lesión en la planta del pie.\n\nLas pruebas de sangre mostraron inflamación y que algunos músculos y el hígado estaban dañados. Las pruebas para sífilis y otros virus fueron negativas. Los médicos pensaron que tenía síndrome de Nicolau. Esto es una reacción rara después de una inyección que puede dañar la piel y el músculo.\n\nLe hicieron una biopsia (tomaron un pedacito de piel) que mostró daño en la piel y apoyó el diagnóstico. Lo trataron con medicamentos para mejorar la circulación y evitar coágulos (enoxaparina), con otro que ayuda la sangre a fluir mejor (cilostazol) y con analgésicos para el dolor. Con el tratamiento mejoró mucho. Las pruebas de sangre volvieron casi a la normalidad.\n\nAl salir del hospital quedó con pequeñas cicatrices y algo de piel seca en la nalga y en la planta del pie, y tenía menos dolor. Fue un caso raro, pero con tratamiento el hombre se recuperó. Si alguien siente mucho dolor o ve una lesión después de una inyección, debe avisar al médico.",
+                "fh_score": 76.87
+            },
+            "B2": {
+                "text": "Here is a clear, reader-friendly summary of the case:\n\nA 31-year-old man developed a painful skin and muscle problem after receiving an intramuscular injection of benzathine penicillin. He had pain in his right buttock that spread down to his foot. At the injection site a large purplish, ring-shaped plaque formed (15 cm across), with healthy-looking skin in the middle. He also had a small scab on the scrotum and a wide, net-like discolored area on the sole of the right foot.\n\nTests and imaging\n- Ultrasound of the buttock showed swelling and loss of the normal muscle pattern, and swelling under the skin. Swelling was also seen in the sole and scrotum.\n- Blood tests showed signs of inflammation and marked muscle injury: white blood cell count slightly high, CRP (an inflammation marker) elevated, and very high muscle enzymes (creatine kinase and LDH). Liver enzymes were also raised but later improved.\n- Tests for syphilis, HIV, hepatitis B and C were negative.\n\nDiagnosis and what it means\n- Based on the timing, how the symptoms developed, and a skin biopsy, doctors diagnosed Nicolau syndrome (also called medicamentous cutaneous embolism). This is a rare reaction after an injection that can cause blockage of small blood vessels and local tissue damage, leading to severe pain, skin necrosis (dead skin), and swelling.\n\nTreatment and outcome\n- He was treated with a blood thinner (enoxaparin), cilostazol (a medicine that can improve blood flow), and pain control (tramadol) for 10 days. The skin biopsy showed dead skin cells and damage around hair follicles, but no clear blood-vessel inflammation or clot in the sampled tissue, which fit the diagnosis.\n- His pain and lab tests improved: muscle and liver enzymes fell toward normal. He was discharged with cilostazol and pain medicines.\n- At 3-month follow-up he was much better. The main lasting effects were discolored scars at the right buttock and foot, with some flaky skin and small remaining mottled areas on the sole.\n\nNotes for readers\n- Nicolau syndrome is uncommon but can happen after injections. Early recognition and treatment can limit damage. If someone has severe pain, changing color, or skin breakdown after an injection, they should seek medical care right away.",
+                "fh_score": 89.48
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel universitario)\n\nPresentación\n- Hombre de 31 años con antecedentes de consumo de alcohol, tabaco y cocaína inhalada, tuberculosis pulmonar tratada, nefrectomía izquierda y esplenectomía por trauma.\n- Una semana después de recibir una inyección intramuscular de penicilina benzatínica (administrada por exposición sexual a una pareja con sífilis), desarrolló dolor intenso en glúteo derecho irradiado al pie y, posteriormente, lesiones cutáneas purpúricas en el sitio de inyección.\n\nHallazgos clínicos y complementarios\n- Lesión principal: placa anular de 15 cm en glúteo derecho, bordes irregulares y aspecto racemoso, con piel sana en el centro.\n- Otras lesiones: pequeña escara escrotal y extensa lesión livedoide en la planta del pie derecho que abarcaba desde la región talar hasta las puntas de los dedos.\n- Ecografía: pérdida del patrón fibrilar y engrosamiento edematoso del glúteo mayor en su tercio medio; edema del tejido celular subcutáneo en zona plantar y escrotal.\n- Laboratorio: leucocitosis (13.7 × 10^9/L) y proteína C reactiva elevada (3.2 mg/dL) —indicadores de reacción inflamatoria—; marcadores de daño muscular marcadamente altos: AST 175 UI/L, ALT 245 UI/L, CK 2741 UI/L, LDH 2499 UI/L.\n- Serologías para sífilis (VDRL y pruebas treponémicas), VIH, hepatitis B y C: todas negativas.\n\nDiagnóstico\n- La combinación de inicio inmediato tras la inyección, la apariencia cutánea y la biopsia condujeron al diagnóstico de síndrome de Nicolau (también llamado embolia cutis medicamentosa).  \n- Biopsia cutánea: necrosis epidérmica que llega hasta epitelio folicular y formación de ampolla secundaria a reepitelización; no se observó vasculitis ni trombosis vascular, hallazgo compatible con fase aguda de embolia cutis medicamentosa.\n\nTratamiento y evolución\n- Tratamiento instaurado: anticoagulación con enoxaparina subcutánea (1 mg/kg cada 12 h), cilostazol 100 mg cada 12 h y analgesia (tramadol) durante 10 días.\n- Respuesta: mejoría clínica y marcadores bioquímicos (AST 39 UI/L, ALT 77 UI/L, CK 167 UI/L), alta hospitalaria con cilostazol y analgésicos.\n- Seguimiento a 3 meses: disminución del dolor y de las lesiones; secuelas residuales: cicatriz discrómica y descamación fina en glúteo derecho; en planta del pie derecho cicatriz discrómica con descamación gruesa en zona de apoyo tarsometatarsiana y pequeñas áreas livedoides.\n\nPuntos clave e implicaciones\n- El síndrome de Nicolau es una complicación rara pero grave de inyecciones intramusculares que provoca isquemia y necrosis en el tejido local; el diagnóstico se basa en la historia temporal, el examen y la biopsia.\n- En este caso hubo afectación muscular y elevación enzimática importante, lo que sugiere compromiso más allá de la piel; la respuesta favorable a anticoagulación y vasodilatación (cilostazol) es consistente con un proceso isquémico/embólico reversible en su fase aguda.\n- Las serologías negativas indican que la penicilina se administró por exposición, no por confirmación serológica de sífilis.\n- No se completó un perfil inmunológico porque el equipo consideró que la presentación clínica y la biopsia justificaban el diagnóstico sin buscar otras etiologías.\n\nRecomendaciones prácticas (consideraciones para el seguimiento)\n- Continuar vigilancia clínica de las secuelas cutáneas y dolor; cuidado local de la piel para evitar infección.  \n- Valoración por dermatología y, si la cicatriz es funcional o estéticamente problemática, considerar evaluación por cirugía plástica.  \n- Si aparecieran signos de infección o empeoramiento, reconsulta urgente.  \n- En futuros procedimientos intramusculares, notificar a los profesionales de salud sobre este antecedente para evitar riesgo de recurrencia.\n\nEste resumen respeta la evolución y decisiones del equipo tratante y subraya que el paciente mejoró con tratamiento conservador, quedando secuelas cutáneas residuales que requieren manejo y seguimiento.",
+                "fh_score": 38.96
+            }
+        }
+    },
+    {
+        "article": "Un varón de cuatro días de edad, nacido a las 39 semanas y 4 días de gestación, acude a un servicio de urgencias con un empeoramiento de la dificultad respiratoria y el estridor, que se ve agravado por la alimentación y la posición supina.\n\nNació de una madre de 31 años con serología significativa para una prueba de Coomb positiva indirecta, con un parto vaginal sin complicaciones y puntuaciones de APGAR de ocho y nueve en el primer y quinto minuto, respectivamente. Su peso al nacer fue de 3050 g. La ecografía fetal mostró preocupación por un foco intracardíaco, con un embarazo sin complicaciones. El curso de enfermería fue significativo solo por una prueba de audición bilateral fallida y un ecocardiograma normal. El bebé fue dado de alta en el día dos de vida. Se observó que tenía congestión nasal en el momento de la descarga. Se instruyó a la familia para que le aspirara la nariz y usara gotas salinas según fuera necesario.\n\nEn el día cuatro de vida, la madre del lactante notó estridor asociado con dificultad para alimentarse y el pediatra lo derivó al servicio de urgencias. El examen en el servicio de urgencias es significativo para el estridor inspiratorio agudo con tirones traqueales y retracciones subcostal. Además, se observa que tiene pectus excavatum. El estridor y el aumento del trabajo respiratorio mejoran con la posición prona o lateral. La evaluación de laboratorio es significativa para la acidosis respiratoria en el gas sanguíneo venoso [pH 7.18 y CO2 73 mmHg (9,732 Pa)] y el análisis de orina que revela bacterias moderadas y 11-20 glóbulos blancos sin la presencia de nitrito urinario o esterasa leucocitaria. Un recuento sanguíneo completo es tranquilizador. Se le coloca una cánula nasal de alto flujo y se inicia con ampicilina y gentamicina después de obtener cultivos de sangre.\n\nSe le aumentó la presión positiva continua en la vía aérea (CPAP) y se lo trasladó a una unidad de cuidados intensivos neonatales de nivel III para continuar con el tratamiento y la evaluación de otorrinolaringología. Se le introdujo un tubo nasogástrico por las dos fosas nasales sin dificultad. La laringoscopia flexible mostró una cuerda vocal izquierda inmóvil y cavidades nasales estrechas con edema de los cornetes nasales, aritenoides bilaterales y cuerdas vocales. La broncoscopia no reveló ninguna otra anormalidad. El examen físico posterior se caracterizó por rasgos dismórficos sutiles, que incluían orejas de implantación baja, retromicrognatia, microftalmia y clinodactilia de los dedos de los pies. Se interrumpió el tratamiento antibiótico empírico tras un examen infeccioso tranquilizador. Se consultó a un equipo multidisciplinario.\n\nEl paciente finalmente requirió intubación a las dos semanas de vida debido al empeoramiento del fallo respiratorio. Se administraron ciprofloxacina nasal y dexametasona para el edema de las vías respiratorias superiores. Una resonancia magnética del cerebro, cuello y tórax mostró un curso normal de los nervios laríngeos recurrentes. La evaluación genética incluyó un análisis de microarreglo cromosómico normal (CMA). La prueba adicional del panel genético fue positiva para la variante patogénica en el gen CHD7, consistente con el síndrome CHARGE. En este caso, el VFP se atribuyó a la asociación conocida con el síndrome CHARGE. La evaluación continua reveló otras características consistentes con el síndrome CHARGE, incluidos colobomas bilaterales, glaucoma, pérdida auditiva confirmada y anomalías genitales.\n\nLa repetición de la broncoscopia en el día 42 de vida demostró una mejora en el edema laríngeo general, pero continuó con un edema leve de las cuerdas vocales bilaterales. El paciente fue extubado después de la broncoscopia en el marco de un edema de las vías respiratorias mejorado. Sin embargo, fue re-intubado el día 46 de vida debido al empeoramiento de la insuficiencia respiratoria. La repetición de la laringoscopia ese día mostró un edema continuado. En este momento, el paciente ya había recibido múltiples ciclos cortos de Dexamethasone en un intento de disminuir el edema de las vías respiratorias. Debido a la necesidad de re-intubación, fue tratado con Tobramycin tópico y Dexamethasone aplicado directamente a las cuerdas vocales mediante laringoscopia directa durante cinco días. Después de este tratamiento, fue extubado con éxito a los dos meses de edad y se le colocó un tubo de gastrostomía a los tres meses.\n\nEn el momento de la colocación del tubo de gastrotomía, se le realizó una broncoscopia y una microlaringoscopia adicionales que demostraron que la cuerda vocal izquierda afectada originalmente era totalmente móvil, pero que mostraba una nueva inmovilidad de la cuerda derecha; la etiología de esto no está clara. Ambas cuerdas vocales seguían estando ligeramente edematosas, pero habían mejorado mucho desde la evaluación anterior. El paciente fue dado de alta en aire ambiente a los cuatro meses de edad y continúa siendo seguido de cerca por el otorrinolaringólogo. En la laringoscopia ambulatoria de repetición a los cuatro meses de edad, ambas cuerdas aparecían móviles con un edema de las vías respiratorias continuado.\n\n",
+        "gold_summary": "Un bebé de cuatro días de edad, a término, varón, nacido por parto vaginal sin complicaciones, con un curso de enfermería significativo para la falta de audición, se presentó en un departamento de emergencias (DE) con dificultad respiratoria y estridor en aumento. Fue trasladado a una unidad de cuidados intensivos neonatales (UCIN) de nivel III para una evaluación posterior y se le practicó una intubación debido a la hipercarbia progresiva. La laringoscopia reveló una parálisis unilateral de las cuerdas vocales (PCV) del lado izquierdo. Se le sometió a una evaluación posterior que incluyó un cerebro, cuello y tórax normales en una resonancia magnética. Se consultó a genética por la preocupación de los rasgos dismórficos en el examen físico. Después de las pruebas del panel de genes, la PCV se atribuyó a la asociación conocida con el síndrome CHARGE. Se observó un edema de las vías respiratorias en la laringoscopia que impidió la extubación hasta los dos meses de edad. Se identificaron otras características del síndrome CHARGE, incluidos los colobomas, el glaucoma, la pérdida auditiva neurosensorial y las anomalías genitales. Se le dio de alta con aire ambiente y después de la colocación de un tubo de gastrostomía con seguimiento de otorrinolaringología.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Este es un resumen sencillo y amable del caso.\n\nUn bebé de cuatro días tenía mucha dificultad para respirar. Hacía un sonido fuerte al respirar (estridor). Comía mal y estaba peor cuando lo acostaban boca arriba. Nació a término y al principio parecía bien. En el hospital le hicieron pruebas y vieron que tenía mucho CO2 en la sangre, lo que significa que no respiraba bien.\n\nLos médicos usaron una máquina para ayudarle a respirar. Miraron dentro de su garganta con una cámara y vieron que una cuerda vocal (una de las dos pequeñas “telitas” que ayudan a hablar y a respirar) no se movía y que había hinchazón en la garganta. Le pusieron antibióticos al principio, pero luego los dejaron cuando las pruebas no mostraron infección.\n\nA las dos semanas el bebé empeoró y le pusieron un tubo para ayudarle a respirar mejor (intubación). Le hicieron una resonancia y los nervios grandes estaban normales, lo cual fue una buena noticia. También hicieron pruebas genéticas y encontraron un cambio en un gen llamado CHD7. Ese cambio explica que el bebé tiene el síndrome CHARGE. Ese síndrome puede causar problemas en los ojos, la audición, la garganta y otras partes del cuerpo. En este bebé también encontraron problemas en los ojos, pérdida de audición y algunas diferencias en los genitales.\n\nLa hinchazón en la garganta hizo difícil quitar el tubo por varias semanas. Usaron medicinas y trataron la garganta directamente con medicamentos. A los dos meses pudieron quitar el tubo y a los tres meses le pusieron un tubito para darle comida directo al estómago porque comer seguía siendo difícil. Al principio solo la cuerda vocal izquierda estaba paralizada, luego mejoró, y por un tiempo la cuerda derecha también dejó de moverse; los médicos no saben por qué pasó eso. Al final, a los cuatro meses, las dos cuerdas vocales ya se movían y el bebé pudo irse a casa respirando aire normal. Sigue con control del otorrinolaringólogo (especialista de garganta y oídos).\n\nEn palabras simples: el bebé tuvo problemas de respiración por la hinchazón y por una cuerda vocal que no se movía. Los médicos le ayudaron a respirar, lo cuidaron con medicinas y pruebas, y encontraron que tenía el síndrome CHARGE. Poco a poco mejoró y pudo volver a casa.",
+                "fh_score": 72.69
+            },
+            "B2": {
+                "text": "Summary (B2 level)\n\nA baby boy, born at full term and healthy at birth, came to the emergency room at four days old because he had loud noisy breathing (called stridor) and trouble feeding. The noisy breathing was worse when he lay on his back and during feeding, and got better when he was placed on his side or stomach.\n\nOn arrival he had signs of poor breathing and a blood test showed respiratory acidosis (high carbon dioxide in the blood), so he was given support with high-flow oxygen and later CPAP (a breathing machine that helps keep the airway open). Ear–nose–throat doctors (ENT) looked inside his throat with a flexible scope and found that his left vocal cord was not moving (vocal fold paralysis). When a vocal cord does not move it can make breathing and swallowing hard. His nasal passages were also narrow and swollen. Other small physical differences were found, for example low-set ears, small jaw, small eyes, and toe differences.\n\nBecause of worsening breathing, he needed a breathing tube (intubation) at two weeks of age. An MRI of the brain, neck and chest was normal for the nerves that go to the larynx. Genetic tests first showed a normal chromosome microarray, but a later gene panel found a disease-causing change in the CHD7 gene, which confirmed CHARGE syndrome. CHARGE is a genetic condition that can cause eye problems (colobomas), hearing loss, heart and genital differences, and facial and airway anomalies. In this baby the diagnosis explained the vocal cord paralysis and other features (colobomas, glaucoma, confirmed hearing loss, and genital differences).\n\nHe had repeated scopes and treatment for airway swelling, including steroid medicine and topical antibiotic applied to the vocal cords. Over time the swelling got much better. The left cord, which had been immobile, later moved again, and at times both cords were moving on follow-up exams. He was successfully taken off the breathing tube at about two months. Because he had ongoing feeding problems, a feeding tube into the stomach (gastrostomy) was placed at three months. He was discharged home breathing room air at four months and continues close follow-up with ENT and genetics.\n\nWhat this means and next steps\n- Vocal cord paralysis in newborns can cause serious breathing and feeding problems. In this case it was part of CHARGE syndrome.  \n- Children with CHARGE need multiple specialists: ENT, genetics, eye and hearing doctors, and feeding teams.  \n- The baby received breathing support, medicines to reduce airway swelling, and a feeding tube until he could feed safely. Ongoing follow-up will monitor breathing, voice, hearing, vision and development, and help plan future care.  \n\nThis was a stressful and complex condition for the family, but the team managed the airway and feeding needs while identifying the underlying genetic cause so the baby can get the right long-term care.",
+                "fh_score": 89.66
+            },
+            "B3": {
+                "text": "Resumen clínico (lectores universitarios)\n\nPresentación y curso inicial\nUn recién nacido varón a término (39+4 semanas), con parto eutócico y pruebas de Apgar normales, fue dado de alta al día 2 pero reingresó a los 4 días por estridor inspiratorio y dificultad para alimentarse, empeoradas en decúbito supino y al alimentarse. En urgencias presentaba tiraje y signos de insuficiencia respiratoria; la gasometría mostró acidosis respiratoria (pH 7,18; pCO2 73 mmHg). Se inició soporte respiratorio (cánula nasal de alto flujo y luego CPAP), se obtuvieron cultivos y se administraron antibióticos empíricos que se suspendieron tras descartar infección significativa.\n\nHallazgos otorrinolaringológicos y anatómicos\nLa laringoscopia flexible mostró parálisis de la cuerda vocal izquierda (parálisis vocal unilateral) junto con edema laríngeo y estrechez nasal por edema de los cornetes. La broncoscopia no mostró otras anormalidades. Estudios por imagen (RM de cerebro, cuello y tórax) no identificaron anomalía en el trayecto de los nervios laríngeos recurrentes. El examen físico también reveló rasgos dismórficos sutiles: orejas de implantación baja, retromicrognatia, microftalmia y clinodactilia podal.\n\nEvolución y manejo\nA las dos semanas el paciente precisó intubación por empeoramiento respiratorio. Se administraron corticoides sistémicos y tratamientos tópicos (antibiótico nasal y posteriormente aplicación directa de dexametasona y tobramicina sobre las cuerdas vocales) para reducir el edema laríngeo. Tras varios intentos de extubación exitosos y reintubaciones, finalmente fue extubado de forma sostenida alrededor de los 2 meses. Se colocó una sonda de gastrostomía a los 3 meses por seguridad alimentaria. Repetidas laringoscopias mostraron mejoría progresiva del edema; la movilidad de las cuerdas vocales cambió en el tiempo (recuperación de la izquierda y, de forma transitoria, inmovilidad derecha), y a los 4 meses ambas cuerdas eran móviles con edema residual. El alta se produjo en aire ambiente con seguimiento otorrinolaringológico ambulatorio.\n\nDiagnóstico etiológico y hallazgos asociados\nEl cariotipo microarray fue normal, pero un panel genético identificó una variante patogénica en el gen CHD7, diagnóstico compatible con síndrome CHARGE. Tras esto se detectaron otras manifestaciones típicas del síndrome: colobomas bilaterales, glaucoma, hipoacusia confirmada y anomalías genitales. La parálisis vocal en este caso se interpretó como parte de las manifestaciones del síndrome CHARGE más que como lesión quirúrgica o nerviosa focal identificable por imagen.\n\nImplicaciones y seguimiento\n- Las parálisis de cuerdas vocales en recién nacidos pueden provocar compromiso respiratorio y dificultades de alimentación; requieren manejo multidisciplinario urgente (neonatología, otorrinolaringología, genética, audiología, oftalmología y, según el caso, cirugía pediátrica/urología).  \n- El diagnóstico de CHARGE implica vigilancia y tratamiento multisistémico a largo plazo: corrección/rehabilitación visual y auditiva, control del crecimiento y desarrollo, manejo de anomalías genitales y nutricionales, y planificación de soporte respiratorio o intervenciones laríngeas si la obstrucción persiste.  \n- El pronóstico laríngeo es variable; en este caso hubo recuperación funcional con tratamiento conservador y procedimientos endoscópicos locales, pero algunos pacientes precisan traqueostomía o intervenciones quirúrgicas si la obstrucción o la aspiración alimentaria son persistentes.\n\nComentario final (empático)\nEste caso ilustra cómo una presentación respiratoria neonatal aparentemente aislada puede ser la primera señal de un síndrome genético multisistémico. La coordinación rápida entre equipos y el diagnóstico genético permitieron orientar el seguimiento y las intervenciones necesarias para proteger la vía aérea, la nutrición y el desarrollo del niño.",
+                "fh_score": 26.04
+            }
+        }
+    },
+    {
+        "article": "Mujer de 17 años oriunda de Tucumán, acudió a la consulta por cuadro de vías aéreas superiores y hemoptisis leve. La tomografía computarizada de tórax informó, en lóbulo superior derecho, una imagen redondeada de paredes regulares y lisas de 25x24x24 mm, rodeado de un tenue halo periférico en vidrio esmerilado. No se observaba realce ante la administración de contraste endovenoso. Se sugirió un posible quiste broncogénico, por lo que se realizó una RMN de tórax que informó imagen redondeada de paredes regulares y lisas que alcanzó un diámetro anteroposterior de 25 x 24 x 24.5 mm con intensidad de señal líquida. Debido a la localización central de la lesión, se realizó una lobectomía superior derecha videoasistida. Dado que el estudio anatomopatológico intraoperatorio fue indeterminado, se complementó la resección pulmonar con un vaciamiento ganglionar mediastínico. La anatomía patológica definitiva informó neumocitoma esclerosante de 2 x 1.7 cm. La inmunomarcación fue positiva para TTF1, CK, CK7 y napsina.",
+        "gold_summary": "Describimos aquí el caso de una paciente de 17 años con diagnóstico de neumocitoma esclerosante con presentación infrecuente.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Resumen sencillo y amable:\n\n- Una joven de 17 años vino al médico porque tenía mocos y tos. También sacó un poco de sangre al toser.  \n- Le hicieron una tomografía y una resonancia. Vieron una bolita redonda de unos 2.5 cm en la parte superior del pulmón derecho.  \n- Al principio pensaron que podía ser un quiste. Como la bolita estaba en una zona difícil, los médicos quitaron la parte superior del pulmón derecho usando una cirugía con cámara (una operación menos grande que la abierta).  \n- Durante la operación, la prueba rápida no dio un resultado claro. Por eso, además quitaron algunos ganglios cercanos para estudiar mejor.  \n- El examen final del tejido dijo que la bolita era un neumocitoma esclerosante. Es un tipo de tumor del pulmón que se encontró en esta paciente.  \n- Hicieron pruebas especiales en el tumor que dieron positivo para varias proteínas (TTF1, CK, CK7 y napsina). Esas pruebas ayudaron a confirmar el diagnóstico.  \n\nEste caso muestra a una persona joven con un tumor poco común en el pulmón. La cirugía permitió quitar la lesión y obtener el diagnóstico.",
+                "fh_score": 73.87
+            },
+            "B2": {
+                "text": "A 17-year-old woman from Tucumán went to the doctor because of upper respiratory symptoms and a small amount of coughing up blood. A chest CT scan found a round, smooth-walled lesion about 2.5 cm wide in the right upper lung lobe, with a faint “ground-glass” halo around it. The lesion did not take up contrast, so doctors first thought it might be a bronchogenic cyst (a fluid-filled birth-related lung cyst). An MRI showed the mass had a fluid-like signal and the same size.\n\nBecause the lesion was centrally located in the lung, surgeons removed the right upper lobe using a minimally invasive video-assisted technique (VATS lobectomy). The quick exam of tissue taken during surgery (frozen section) could not give a clear diagnosis, so the team also removed nearby mediastinal lymph nodes to check for spread. The final pathology report identified the tumor as a sclerosing pneumocytoma (also called pneumocitoma esclerosante) measuring about 2 x 1.7 cm. This is a rare lung tumor that is usually benign; special lab stains (TTF‑1, cytokeratins CK and CK7, and napsin) were positive and supported a lung origin.\n\nThis case is unusual because sclerosing pneumocytoma typically appears in older adults, not teenagers. The standard treatment is surgical removal, which was done here. After a complete resection with negative lymph nodes, the usual next steps are routine follow-up visits and imaging to watch for any recurrence. Overall prognosis is generally good after full removal.",
+                "fh_score": 87.35
+            },
+            "B3": {
+                "text": "Presentamos el caso de una mujer de 17 años que consultó por síntomas de vías respiratorias superiores y hemoptisis leve. La tomografía computada de tórax mostró en el lóbulo superior derecho una lesión redondeada, de paredes lisas, de aproximadamente 25 x 24 x 24 mm, con un tenue halo periférico en vidrio esmerilado; no hubo realce tras contraste intravenoso. Una resonancia confirmó una lesión bien delimitada con señal compatible con contenido líquido. Inicialmente se planteó como posible quiste broncogénico, pero por la localización central de la lesión se decidió realizar una lobectomía superior derecha asistida por video (VATS).\n\nDurante la cirugía, el estudio anatomopatológico intraoperatorio (congelación) no fue concluyente, por lo que se completó la resección con vaciamiento ganglionar mediastínico. El examen histopatológico definitivo identificó un neumocitoma esclerosante de 2 x 1,7 cm. La inmunohistoquímica fue positiva para TTF‑1, CK, CK7 y napsina A, un perfil que apoya el origen pneumocítico de la lesión.\n\nComentarios clínicos y manejo: el neumocitoma esclerosante es un tumor pulmonar poco frecuente que suele aparecer en mujeres jóvenes y suele comportarse de forma benigna; sin embargo, puede simular quistes o neoplasias malignas en estudios por imagen. La resección quirúrgica completa suele ser curativa y, cuando el diagnóstico no es claro en el intraoperatorio, puede justificarse ampliar el acto quirúrgico (por ejemplo, con vaciamiento ganglionar) para asegurar un tratamiento definitivo. El pronóstico después de resección completa es generalmente excelente, aunque se recomienda seguimiento clínico e imágenes periódicas para vigilar recidiva o complicaciones.",
+                "fh_score": 36.87
+            }
+        }
+    },
+    {
+        "article": "Una mujer asiática de 28 años fue admitida en el hospital para el tratamiento de «una masa pélvica durante 10 meses» el 11 de noviembre de 2018. La paciente solía tener menstruación regular, volumen menstrual moderado, dismenorrea y un G1P0L0A1. Examen ginecológico: la parte posterior del útero tenía aproximadamente 8 cm de diámetro con poca actividad y sensibilidad, pero no se observaron otras anomalías. La paciente no tenía una causa obvia de dolor abdominal durante los primeros 10 meses previos al ingreso. El examen de ultrasonido reveló una masa heterogénea en la parte superior derecha del útero con un diámetro de aproximadamente 4 cm, un nódulo del epiplón mayor con un diámetro de aproximadamente 2 cm y un nivel de CA125 sérico de 416 mU/mL. Se diagnosticó como «endometriosis, masas pélvicas inflamatorias». Se administró una terapia de rehidratación antiinfecciosa y se dio de alta a la paciente con alivio del dolor. Dos semanas después del alta, el nivel de CA125 sérico de la paciente disminuyó a 106 mU/mL y volvió a la normalidad después de 6 semanas. Sin embargo, la masa pélvica aumentó gradualmente. El reexamen de la ecografía pélvica realizada mostró una masa ecoica mixta de 7.7 cm x 7.4 cm x 8.2 cm en el lado derecho del útero con un límite claro, eco puntiforme fino en el quiste y derrame abdominal y pélvico. La ecografía de contraste mostró que la pared del quiste de la masa pélvica estaba significativamente mejorada, se sospechaba malignidad y se recomendó un tratamiento quirúrgico. El 14 de noviembre de 2018, la paciente se sometió a liberación de adherencias pélvicas e intestinales transabdominales, omento, ovarios bilaterales, peritoneo multipunto y múltiples adenomiosis y histerectomía. Durante la operación, se aspiraron aproximadamente 600 ml de ascitis hemorrágica. Tras la exploración, se observó una masa de color rojo grisáceo con un diámetro de aproximadamente 8 cm en la superficie del epiplón mayor, que era suave y se asemejaba a carne podrida. Se encontraron depósitos de celulosa marrón difusos en la superficie del útero, ovarios bilaterales, pared abdominal, tracto intestinal, surco lateral del recto y pared anterior del recto. Las lesiones no se eliminaron por completo y algunas áreas se electrocoagularon. El examen patológico de la muestra resecada mostró endometriosis del tejido retiniano con vasodilatación, ampollas, infiltración linfocítica difusa y focal, folículos ováricos císticos bilaterales, fibrosis peritoneal dentro de la necrosis del tejido adiposo, proliferación de fibroblastos, aumento de la infiltración de células espumosas y adenomiosis uterina. La patología de ascitis mostró muchos glóbulos rojos, un pequeño número de linfocitos y neutrófilos y ninguna célula tumoral. Después de la operación, la paciente se recuperó sin problemas y se trató con agonista de la hormona liberadora de gonadotropina (GnRH-α). Se inició leuprorelina una vez al mes durante 6 meses, seguido de dienogest oral (DNG) durante 3 años, después de lo cual se interrumpió la medicación durante 3 meses. La paciente concibió de forma natural y tuvo un embarazo normal. Se dio a luz a un bebé de 3300 g por vía vaginal a las 39 semanas + 3 días de gestación. Tanto la madre como el bebé estaban sanos, sin recurrencia ni reacciones adversas durante el seguimiento.\n\nMH - Humanos\nMH - Mujer\nMH - *Endometriosis/complicaciones/terapia\nMH - Adulto",
+        "gold_summary": "Preocupaciones de la paciente: Una mujer de 28 años de edad vino a nuestro hospital para recibir tratamiento debido al descubrimiento de una masa pélvica 10 meses antes. Después de la admisión, la paciente se sometió a tratamiento quirúrgico y fue dada de alta en 1 semana. Recibió tratamiento médico durante 3 años después del alta. Después de la retirada de la medicación, la paciente quedó embarazada y dio a luz a un niño sin recurrencia durante el seguimiento.\n\nDiagnósticos: Los diagnósticos iniciales al ingreso fueron «¿masa pelviana inflamatoria?» y «¿endometriosis?». Después de 10 meses, la paciente volvió a ser internada en el hospital debido a un aumento gradual de la masa, y se le diagnosticó endometriosis.\n\nIntervenciones: El paciente fue tratado con terapia antiinfecciosa de rehidratación por primera vez, y el paciente fue tratado quirúrgicamente por segunda vez, seguido de agonista de la hormona liberadora de gonadotropina (GnRH-α) y tratamiento con dienogest (DNG) después de la cirugía.\n\nResultados: Después de 6 ciclos de tratamiento con GnRH-α y 3 años de tratamiento con DNG, un hijo nació con éxito tras la interrupción de la medicación y, hasta ahora, no se han producido reacciones adversas ni recurrencias durante el período de seguimiento.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una mujer de 28 años tuvo una bolita y dolor en la tripa durante 10 meses. Los médicos vieron en una ecografía una masa cerca del útero. También midieron una prueba en la sangre que estaba alta al principio, pero volvió a la normalidad después.\n\nLos médicos pensaron que era endometriosis. Eso quiere decir que un tejido que normalmente está dentro del útero estaba creciendo en otros sitios del cuerpo. A veces esto causa bultos, dolor y líquido en la barriga.\n\nLa mujer tuvo una operación. Se sacó líquido de la barriga y se quitó la masa que encontraron. Los exámenes del tejido demostraron que no había cáncer. Confirmaron que era endometriosis.\n\nDespués de la operación recibió medicinas para controlar la endometriosis: inyecciones una vez al mes durante 6 meses y luego una pastilla por 3 años. Tres meses después de dejar las medicinas, quedó embarazada de forma natural. Tuvo un parto normal a las 39 semanas. El bebé pesó 3300 g. Madre y bebé están sanos. No ha vuelto la enfermedad durante el seguimiento.",
+                "fh_score": 76.03
+            },
+            "B2": {
+                "text": "Resumen claro y amable\n\nQué sentía la paciente:\n- Una mujer de 28 años acudió al hospital porque le habían encontrado una masa en la pelvis hacía 10 meses. Tenía regla regular, dolor menstrual (dismenorrea) y no había una causa clara para su dolor abdominal al principio.\n\nQué encontraron los médicos:\n- Ecografía inicial: una masa heterogénea cerca del útero (unos 4 cm) y un pequeño nódulo en el epiplón (2 cm).\n- Análisis de sangre: CA125 elevado (416 mU/mL). CA125 es una sustancia que puede aumentar en enfermedades como la endometriosis o en algunos cánceres, pero no es una prueba definitiva.\n- Tras un primer tratamiento para aliviar el dolor e infección, el CA125 bajó y se normalizó en unas semanas. Sin embargo, la masa siguió creciendo hasta medir alrededor de 8 cm, y hubo líquido en el abdomen (ascitis).\n\nDecisión y operación:\n- Debido al crecimiento de la masa y a que la imagen sugería posible malignidad, se realizó una cirugía el 14 de noviembre de 2018.\n- En la operación se encontraron aproximadamente 600 ml de líquido con sangre en el abdomen y una masa en el epiplón (tejido graso del abdomen). Había además muchas pequeñas lesiones oscuras (depósitos de «celulosa» típicos de endometriosis) en la superficie del útero, ovarios, peritoneo y partes del intestino.\n- No se pudieron quitar todas las lesiones; algunas se trataron con electrocoagulación (quemado controlado para destruir tejido).\n\nResultados de la biopsia:\n- El examen de los tejidos confirmó endometriosis en el epiplón y cambios relacionados (fibrosis, necrosis grasa, células inflamatorias). También se observó adenomiosis (cuando tejido parecido al que recubre el útero crece dentro del músculo uterino).\n- El líquido del abdomen no mostró células tumorales, lo que ayuda a descartar cáncer.\n\nTratamiento después de la operación:\n- Buena recuperación postoperatoria.\n- Tratamiento hormonal: 6 inyecciones mensuales de un agonista de la hormona liberadora de gonadotropina (GnRH-α, leuprorelina) y luego dienogest por vía oral durante 3 años. Estas medicaciones reducen la actividad de la endometriosis y el dolor.\n\nEvolución y resultado final:\n- Tras suspender la medicación durante 3 meses, la paciente quedó embarazada de manera natural.\n- Tuvo un embarazo normal y dio a luz por vía vaginal a término a un bebé sano de 3300 g.\n- En el seguimiento no hubo recurrencia de la enfermedad ni efectos adversos reportados.\n\nMensaje final (con calma):\n- Este caso muestra que la endometriosis puede producir masas grandes y líquido en el abdomen, pero con cirugía adecuada, confirmación por biopsia y tratamiento hormonal prolongado, una mujer joven pudo recuperarse y lograr un embarazo sano. Si te interesa saber más sobre qué es la endometriosis o cómo afectan estos tratamientos a la fertilidad, puedo explicarlo de forma sencilla.",
+                "fh_score": 55.49
+            },
+            "B3": {
+                "text": "Summary (college-level, empathetic tone)\n\nPresentation and background\n- A 28‑year‑old Asian woman presented with a pelvic mass that had been present for about 10 months. She reported regular menstrual cycles with moderate flow and painful periods (dysmenorrhea). There was no clear trigger for abdominal pain during the initial 10 months.\n\nKey findings (abnormal vs normal)\n- Abnormal:\n  - Pelvic mass on ultrasound that grew from about 4 cm to roughly 8 cm over time.\n  - An omental nodule (~2–8 cm) and approximately 600 mL of hemorrhagic ascites (blood‑tinged fluid in the abdomen) found at surgery.\n  - Serum CA125 was markedly elevated to 416 U/mL on admission, fell to 106 U/mL two weeks later and normalized by six weeks.\n  - Contrast ultrasound suggested cyst wall enhancement and raised concern for possible malignancy.\n- Normal/benign findings:\n  - Cytology of the ascitic fluid showed many red blood cells and only small numbers of inflammatory cells; no malignant cells were found.\n\nInterventions\n- Initial conservative treatment included rehydration and anti‑infective therapy, which relieved pain and reduced CA125 levels.\n- Because the pelvic mass enlarged and imaging raised concern, she underwent abdominal surgery for release of pelvic and intestinal adhesions, removal or treatment of omental and peritoneal lesions, and coagulation of residual implants. (The operative report described multiple brown “powder‑burn” implants typical of endometriosis.)\n- Post‑operative medical therapy to suppress endometriosis was given: monthly GnRH‑agonist (leuprorelin) for 6 months, followed by oral dienogest for 3 years.\n\nPathology\n- Surgical specimens showed extensive endometriosis involving the omentum and peritoneum, with vascular dilation, inflammatory cell infiltrates, peritoneal fibrosis and foamy cell changes; the uterus showed adenomyosis (endometrial tissue within the uterine muscle). No cancer cells were identified in the ascitic fluid.\n\nOutcome\n- Recovery from surgery was uncomplicated.\n- After finishing hormonal treatment and a 3‑month medication break, the patient conceived naturally and had an uneventful full‑term vaginal delivery (3,300 g infant) at 39+3 weeks.\n- During follow‑up there was no reported recurrence of disease or treatment‑related adverse effects.\n\nClinical points and implications\n- Endometriosis can mimic ovarian or peritoneal malignancy on imaging and can produce very high CA125 and hemorrhagic ascites; these findings are not specific for cancer and require tissue diagnosis when imaging is suspicious.\n- The case illustrates effective combined management: surgical removal or ablation of disease burden followed by prolonged hormonal suppression to reduce recurrence risk and preserve fertility.\n- For patients with similar findings, recommended next steps typically include regular follow‑up (clinical exam and symptom assessment, targeted imaging as needed), fertility counselling if pregnancy is desired, and discussion of long‑term medical options to manage recurrence and symptoms.\n\nIf you would like, I can summarize the pathology in simpler terms, outline the typical side effects and monitoring needs for leuprorelin and dienogest, or suggest key questions to discuss with a treating gynecologist.",
+                "fh_score": 65.24
+            }
+        }
+    },
+    {
+        "article": "Presentamos una paciente de 76 años de edad, que es traída al servicio de urgencias por bajo nivel de conciencia con tendencia al sueño.\n\nComo antecedentes médicos de interés destaca una enfermedad pulmonar intersticial difusa, dislipemia e hipertensión arterial.\n\nA la exploración física el paciente se encuentra estuporosa, arreactiva, con atonía de las 4 extremidades y desviación conjugada de la mirada hacia la derecha, sin fiebre y con una leve sequedad en piel y mucosas. La analítica sanguínea no muestra alteraciones significativas.\n\nEl paciente es valorado por el servicio de neurología que considera la realización de una TC cerebral urgente ante la sospecha de patología intracraneal de evolución aguda. Las pruebas de imagen ponen de manifiesto la presencia de numerosas burbujas aéreas que se disponen en los surcos cerebrales, cuerpo calloso y ambos tálamos así como áreas hipodensas cortico-subcorticales de distribución parcheada en hemisferio cerebeloso izquierdo y parietooccipitales bilaterales, todo ello compatible con isquemia cerebral subaguda secundaria a embolismo gaseoso.\n\nAnte los antecedentes personales de enfermedad pulmonar intersticial difusa se decide también realizar una placa de tórax en proyección anteroposterior y una TC torácica que objetivan un neumotórax apical izquierdo y aire ectópico en mediastino superior.\n\nSe decide el ingreso en la Unidad de Ictus del centro para control estrecho de constantes, sin embargo, la paciente presenta una evolución tórpida con el fallecimiento el segundo día de ingreso debido a fracaso multiorgánico.",
+        "gold_summary": "Paciente de 76 años con una enfermedad pulmonar intersticial difusa preexistente, que experimentó un ictus masivo debido a un neumomediastino espontáneo. Su presentación incluyó confusión, convulsiones y debilidad motora. Las pruebas de imagen revelaron burbujas de aire en los surcos cerebrales y áreas hipodensas en el cerebelo y parietooccipitales. Además, se observó neumotórax y aire en el mediastino superior en las radiografías de tórax y la tomografía torácica. A pesar de las medidas terapéuticas como el oxígeno hiperbárico, la paciente lamentablemente falleció debido al fallo multiorgánico.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Esta historia trata de una mujer de 76 años que llegó al hospital porque estaba muy dormida y no respondía bien.\n\nElla ya tenía una enfermedad en los pulmones, además de colesterol alto y tensión alta. En la consulta estaba muy atontada, con los brazos y piernas muy flojos y la mirada fija hacia la derecha. Los análisis de sangre salieron normales.\n\nLas pruebas de imagen de la cabeza mostraron muchas burbujas de aire dentro del cerebro y zonas donde el cerebro no recibía bien la sangre. Los médicos dijeron que esto era un ictus provocado por burbujas de aire que viajaron por la sangre y taparon vasos del cerebro.\n\nComo ella tenía enfermedad pulmonar, hicieron placas y una tomografía del tórax. Vieron aire fuera del pulmón izquierdo (neumotórax) y aire en el espacio del medio del pecho (neumomediastino). Es probable que ese aire escapado de los pulmones haya entrado en la sangre y causado el problema en el cerebro.\n\nLa ingresaron en la unidad de ictus para vigilarla muy de cerca. Aun así, la paciente empeoró y falleció al segundo día por un fallo de varios órganos. Fue un caso grave y muy triste.",
+                "fh_score": 74.88
+            },
+            "B2": {
+                "text": "Resumen claro y cordial:\n\nUna mujer de 76 años con enfermedad pulmonar intersticial (una afección crónica del pulmón que daña el tejido y dificulta la respiración) fue traída a urgencias porque estaba muy somnolienta y con nivel de conciencia bajo. En la exploración estaba en estupor, no respondía bien, tenía flacidez en los cuatro miembros y la mirada desviada hacia la derecha. La analítica de sangre no mostró alteraciones relevantes.\n\nLa tomografía craneal urgente mostró muchas burbujas de aire dentro del cerebro (embolia gaseosa) y áreas oscuras en el cerebelo y en zonas parietooccipitales, hallazgos compatibles con lesiones por falta de riego sanguíneo (isquemia) debidas a esos émbolos de aire. Dado su antecedente pulmonar, se hicieron también radiografía y tomografía de tórax, que revelaron un neumotórax apical izquierdo (colapso parcial del pulmón por aire en el espacio pleural) y aire en el mediastino superior (neumomediastino).\n\nLa paciente ingresó en la Unidad de Ictus para vigilancia estrecha, pero su estado empeoró y falleció al segundo día por fallo multiorgánico. En casos como este, los médicos suelen investigar las causas del aire en el tórax y valorar medidas urgentes para intentar limitar el daño cerebral, aunque en este informe no se detallan otras intervenciones concretas. Lamento la triste evolución de la paciente.",
+                "fh_score": 49.49
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel universitario)\n\nCaso: mujer de 76 años con enfermedad pulmonar intersticial difusa, dislipemia e hipertensión arterial, que ingresó por disminución del nivel de conciencia y somnolencia progresiva.\n\nExploración y pruebas:\n- Examen: estupor, no reactiva, hipotono en las cuatro extremidades y desviación conjugada de la mirada hacia la derecha; sin fiebre; leve sequedad de piel y mucosas.\n- Analítica sanguínea: sin alteraciones significativas.\n- TAC cerebral urgente: numerosas burbujas de aire en los surcos corticales, cuerpo calloso y ambos tálamos, y áreas hipodensas parcheadas cortico-subcorticales en el hemisferio cerebeloso izquierdo y en regiones parietooccipitales bilaterales. Estos hallazgos son compatibles con isquemia cerebral subaguda secundaria a embolismo gaseoso (embolismo por aire).\n- Radiografía y TAC torácica: neumotórax apical izquierdo y aire ectópico en el mediastino superior (neumomediastino).\n\nInterpretación y relación causal:\n- El cuadro se interpretó como un ictus masivo por embolismo aéreo cerebral, probablemente secundario a ruptura alveolar relacionada con la enfermedad pulmonar intersticial, que provocó neumotórax y aire en el mediastino y facilitó el paso de burbujas de aire a la circulación cerebral.\n- Mecanismo plausible: aire que atraviesa el circuito pulmonar (por rotura alveolar, fistulización o por un shunt derecho-izquierdo) alcanza la circulación arterial y ocluye vasos cerebrales, produciendo isquemia.\n\nEvolución y resultado:\n- Ingreso en la Unidad de Ictus para monitorización intensiva. Evolución tórpida; fallecimiento al segundo día por fracaso multiorgánico.\n\nImplicaciones clínicas y lecciones:\n- En pacientes con enfermedad pulmonar crónica, la aparición súbita de déficit neurológico o alteración del nivel de conciencia debe hacer sospechar embolismo gaseoso si hay antecedentes de neumotórax o neumomediastino.\n- El diagnóstico precoz mediante TAC y la identificación del origen torácico son cruciales. Las medidas que se consideran en estos casos incluyen oxigenoterapia de alto flujo, tratamiento del neumotórax/neumomediastino y, cuando está indicado y disponible, oxigenoterapia hiperbárica; sin embargo, el pronóstico depende del volumen de aire y de la extensión del daño cerebral.\n- Este caso ilustra la gravedad potencial del neumomediastino/neumotórax espontáneo en pacientes con enfermedad pulmonar intersticial y la necesidad de alta sospecha clínica.\n\nLamento la pérdida de la paciente; el caso subraya la rapidez con la que puede progresar un embolismo aéreo cerebral y la dificultad de tratamiento cuando el compromiso es extenso.",
+                "fh_score": 31.56
+            }
+        }
+    },
+    {
+        "article": "Un hombre de 24 años de edad, de etnia persa, presentó una queja principal de mal olor bucal después de un período de recuperación de la enfermedad leve por coronavirus 2019 (COVID-19), que quería resolver lo antes posible. Su dentista notó pérdida ósea y sangrado al explorar el área interproximal de los dientes número 18 y 19 clínicamente. Se realizó un escalamiento y un aplanamiento radicular, y se ordenaron radiografías periapicales y panorámicas para la evaluación del paciente. Sin embargo, el paciente se negó a tomar radiografías. La halitosis del paciente disminuyó después de 1 semana de tratamiento. Después de 2 meses, el paciente volvió a su dentista con la queja principal de sensibilidad al frío en sus incisivos mandibulares. El dentista realizó una prueba de vitalidad, y los dientes eran vitales excepto los números 23 y 24. El dentista tomó una radiografía periapical, y una lesión radiolucente en la mandíbula anterior era evidente.\n\nEn la radiografía panorámica, se evidenció una lesión radiolúcida lítica grande y bien definida con bordes festoneados que se extendían desde el diente número 31 en el lado derecho hasta el ramus ascendente izquierdo. Un estudio posterior de tomografía computarizada de haz cónico (TCFC) reveló una lesión lítica multilocular grande, con un margen relativamente distinto, que causó adelgazamiento y perforación de los cortexes bucales y linguales y signos de festoneado.\n\nTras el examen, se remitió al paciente a un cirujano oral y maxilofacial. En la entrevista médica, el paciente explicó su prolapso de la válvula mitral; antecedentes de episodios recurrentes de otitis desde el primer año de vida; antecedentes de septicemia de origen desconocido cuando tenía un año de edad, tras episodios de diarrea y vómitos; antecedentes de uso de broncodilatadores para la alergia estacional; antecedentes de uso de levotiroxina, cabergolina, acetato de desmopresina (DDAVP) en spray y gel de testosterona durante 4 años tras el diagnóstico de síndrome de silla turca vacía, tras poliúria y polidipsia; y, por último, antecedentes de infección reciente por COVID-19 (3 meses antes). Su historia familiar reveló tiroiditis de Hashimoto en su familia materna; su abuelo, su madre y sus tres tías padecían este tipo de hipotiroidismo. El historial quirúrgico previo del paciente incluía una reparación de una hernia inguinal 10 años antes sin complicaciones. Además, el paciente era obeso, con un índice de masa corporal (IMC) de 34,5.\n\nEn el examen clínico, los hallazgos extraorales e intraorales no fueron relevantes. Los exámenes de laboratorio, incluido el recuento sanguíneo completo (CBC), fueron normales, excepto por un aumento en la velocidad de sedimentación globular (ESR) y los niveles de proteína C reactiva (CRP). Se realizó una biopsia incisional en la mandíbula anterior y la muestra se envió al departamento de patología oral y maxilofacial de la Universidad de Ciencias Médicas Shahid Beheshti. Las secciones mostraron una infiltración difusa de grandes células de tinción pálida, como los histiocitos, con eosinófilos dentados y numerosos en el fondo fibroso. Un examen de inmunohistoquímica (IHC) reveló un positivo disperso para el grupo de diferenciación 1a (CD-1a) (+ +), un positivo fuerte para Langerin (CD-207) (+ + +), y más del 50% positivo para S-100.\n\nDe acuerdo con los datos clínicos, radiológicos e histopatológicos, se llegó al diagnóstico de LCH. Los diagnósticos diferenciales fueron osteomielitis, granuloma eosinófilo y metástasis ósea. Sin embargo, debido a las pruebas de laboratorio, los datos radiológicos y el historial clínico, se confirmó el diagnóstico de LCH. Por lo tanto, para un examen más a fondo, el paciente fue derivado al departamento de medicina nuclear para una tomografía por emisión de positrones con fluor-2-desoxiglucosa y una tomografía computarizada (FDG PET/CT), que reveló lesiones líticas hipermetabólicas en la mandíbula, el parietal derecho, el frontal izquierdo y el esfenoidal izquierdo, y opacidad hipermetabólica en el seno etmoidal izquierdo. Además, se observó una actividad metabólica aumentada en la región sellar, hidrocefalia comunicante y amígdalas palatinas hipermetabólicas prominentes. Además, se evidenció una actividad metabólica heterogénea aumentada en las tibias y fémures bilaterales.\n\nUna resonancia magnética del cerebro reveló una notable ampliación de la intensidad del material del líquido cefalorraquídeo (LCR) que contiene la silla turca. La adenohipófisis apareció como una capa delgada en la base de la silla turca agrandada, y se observaron cambios homogéneos e inflamatorios en las células aéreas mastoideas izquierdas. Se observó la extensión de la inflamación hacia el oído medio izquierdo (es de destacar que el paciente había sufrido de otitis durante muchos años). De acuerdo con la implicación multifocal de la enfermedad y su pronóstico cuestionable, el paciente fue derivado al departamento de oncología para quimioterapia sistémica. Pruebas posteriores revelaron mutaciones en el oncogen BRAF y no se detectaron mutaciones en KRAS y NRAS. El oncólogo eligió un régimen de denosumab, vinblastina, etopósido, 6-mercaptopurina, metotrexato y pegfilgrastim; sin embargo, el seguimiento no fue posible ya que el paciente falleció tras un accidente.\n",
+        "gold_summary": "Un paciente de 24 años de edad, de etnia persa, se presentó con una queja principal de halitosis tras recuperarse de la enfermedad por coronavirus 2019 en el consultorio de su dentista general. Los exámenes intraorales y extraorales no revelaron ningún problema específico. En la sesión de seguimiento tras el tratamiento periodontal de fase I, la sensibilidad de los dientes al estímulo frío era evidente, y las radiografías revelaron una gran lesión intraósea lítica en la mandíbula. Una biopsia incisional reveló células de Langerhans y una reacción positiva a Langerina y al grupo de diferenciación 1a, por lo que se le diagnosticó histiocitosis de células de Langerhans. Después de realizar una tomografía por emisión de positrones con fluoro-2-desoxiglucosa y una tomografía computarizada, una resonancia magnética y una tomografía computarizada de haz cónico, debido a la implicación generalizada de la enfermedad, el paciente fue derivado a un oncólogo. En última instancia, se descubrió que los problemas de salud infantil del paciente, incluidos los problemas endocrinos, probablemente fueron causados por una histiocitosis de células de Langerhans no diagnosticada. El oncólogo eligió un régimen de denosumab, vinblastina, etopósido, 6-mercaptopurina, metotrexato y pegfilgrastim. El seguimiento no fue posible ya que el paciente falleció tras un accidente.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un hombre de 24 años fue al dentista porque tenía mal olor en la boca después de recuperarse del COVID-19. El dentista vio pérdida de hueso cerca de unos dientes y, después, el paciente tuvo dolor con el frío. Las radiografías mostraron una gran zona dañada en la mandíbula.\n\nLos médicos tomaron una pequeña muestra del hueso (biopsia). Al mirar esa muestra al microscopio, encontraron un tipo especial de células. Con eso dieron el diagnóstico de histiocitosis de células de Langerhans (LCH). LCH es una enfermedad rara en la que ciertas células del cuerpo crecen de más y pueden hacer daño en los huesos y en otros órganos.\n\nHicieron más pruebas de imagen y vieron que la enfermedad estaba en varias partes del cuerpo: huesos de la cara y del cráneo, senos nasales, piernas y la zona de la hipófisis en el cerebro. Los médicos pensaron que los problemas de salud que el paciente tuvo cuando era niño (como problemas hormonales y muchas otitis) probablemente fueron por esta misma enfermedad sin ser diagnosticada.\n\nDebido a que la enfermedad afectaba muchas zonas, lo derivaron a oncología para tratamiento con medicamentos fuertes. Sin embargo, el seguimiento no fue posible porque el paciente murió en un accidente.",
+                "fh_score": 70.76
+            },
+            "B2": {
+                "text": "Resumen comprensible (nivel B2)\n\nUn hombre persa de 24 años acudió al dentista porque tenía mal aliento (halitosis) poco después de recuperarse de una infección leve por COVID-19. Al explorar la zona entre dos muelas, el dentista notó pérdida de hueso y sangrado. Se hizo un tratamiento periodontal básico (raspado y alisado radicular) y el mal aliento mejoró. El paciente rehusó radiografías en esa primera visita.\n\nDos meses después regresó por sensibilidad al frío en los incisivos inferiores. Entonces se le practicaron radiografías y se vio una gran lesión en la mandíbula. Una tomografía computarizada con haz cónico (un tipo de imagen 3D, parecida a un TAC) mostró una lesión con varias “cavidades” que estaba haciendo el hueso más delgado y hasta lo perforaba. Se tomó una biopsia (pequeña muestra de tejido) de la lesión.\n\nEl examen microscópico y las pruebas de inmunohistoquímica mostraron células de Langerhans (un tipo de célula del sistema inmune) positivas para marcadores como CD1a y Langerina. Esos hallazgos llevaron al diagnóstico de histiocitosis de células de Langerhans (LCH), una enfermedad rara en la que este tipo de células se acumulan y dañan hueso u otros tejidos.\n\nAntes y después del diagnóstico se recogió más información clínica: tenía antecedentes desde la infancia de otitis (infecciones de oído) y una septicemia de niño; le habían diagnosticado “silla turca vacía” (una forma en la que la glándula pituitaria queda muy aplanada, lo que puede afectar hormonas) y recibía varios tratamientos hormonales. Era obeso (IMC 34,5) y tenía antecedes familiares de tiroiditis de Hashimoto. En análisis sanguíneos, los marcadores de inflamación (velocidad de sedimentación y proteína C reactiva) estaban elevados.\n\nPara buscar más lesiones, se hizo una FDG PET/CT (una exploración que detecta zonas metabólicamente activas). Esta prueba mostró lesiones líticas activas en la mandíbula y en varios huesos del cráneo, además de cambios en el seno etmoidal y actividad aumentada en fémures y tibias. Una resonancia magnética del cráneo confirmó cambios en la silla turca y signos de inflamación en las celdillas mastoideas izquierdas, lo que concuerda con sus episodios crónicos de otitis.\n\nDado que la enfermedad afectaba varias áreas (enfermedad multifocal) y tenía un pronóstico incierto, fue derivado a oncología para tratamiento sistémico. Se detectó una mutación en el gen BRAF, y el equipo decidió un régimen que incluía denosumab (que actúa en el hueso) y varios fármacos de quimioterapia (vinblastina, etopósido, 6‑mercaptopurina, metotrexato) junto con pegfilgrastim (para proteger las células blancas). No se llegó a documentar el seguimiento del tratamiento porque el paciente falleció en un accidente.\n\nPuntos clave y explicación breve de términos\n- Histiocitosis de células de Langerhans (LCH): enfermedad rara donde células del sistema inmune llamadas células de Langerhans se acumulan y dañan hueso u otros órganos.  \n- Biopsia e inmunohistoquímica: la biopsia permite ver las células al microscopio; las pruebas de inmunohistoquímica usan marcadores (CD1a, Langerina, S‑100) para confirmar el tipo celular.  \n- FDG PET/CT: imagen que muestra áreas con actividad metabólica alta, útil para detectar lesiones en todo el cuerpo.  \n- Silla turca vacía: la glándula pituitaria aparece muy aplanada en su cavidad; puede explicar problemas hormonales.\n\nEste caso muestra cómo un problema dental puede ser la primera señal de una enfermedad más amplia. El diagnóstico requirió imágenes, biopsia y estudios adicionales, y el tratamiento planificado fue sistémico por la afectación multifocal.",
+                "fh_score": 50.5
+            },
+            "B3": {
+                "text": "Summary\n\nA 24-year-old Persian man first saw his dentist because of new bad breath (halitosis) shortly after recovering from a mild COVID-19 infection. Initial oral and extraoral exams were essentially normal, and his halitosis improved after routine periodontal treatment. Two months later he developed cold sensitivity in his lower front teeth. Dental vitality testing and imaging then revealed a large, destructive bone lesion in the lower jaw.\n\nKey findings\n- Clinical: initially unremarkable oral exam; later cold sensitivity of mandibular incisors.  \n- Imaging: periapical and panoramic radiographs showed a large, well-defined multilocular radiolucent lesion of the mandible with scalloped borders; cone-beam CT confirmed a multilocular lytic mass causing cortical thinning and perforation.  \n- Laboratory: routine blood count normal; inflammatory markers elevated (ESR and CRP).  \n- Pathology: incisional biopsy showed sheets of pale histiocyte-like cells with numerous eosinophils. Immunohistochemistry was strongly positive for Langerin (CD207), positive for CD1a, and >50% positive for S-100—findings diagnostic of Langerhans cell histiocytosis (LCH).  \n- Staging: FDG PET/CT showed additional hypermetabolic lytic lesions in skull bones (right parietal, left frontal, left sphenoid), hypermetabolic opacity in the left ethmoid sinus, increased activity in the sellar region, and increased uptake in both tibias and femurs. Brain MRI showed an enlarged, CSF-filled (empty) sella turcica with a thin anterior pituitary and inflammatory changes in the left mastoid and middle ear.\n\nRelevant medical history\n- Longstanding issues that likely relate to LCH involvement of the pituitary/central nervous system: empty-sella syndrome, years of polyuria/polydipsia requiring desmopressin (DDAVP), and four years of hormone replacement (levothyroxine and testosterone).  \n- Recurrent childhood otitis media and an episode of infantile sepsis.  \n- Mitral valve prolapse and obesity (BMI 34.5).  \n- Family history of Hashimoto thyroiditis.  \n- Recent COVID-19 infection three months before presentation.\n\nDiagnosis and management\n- A final diagnosis of multifocal Langerhans cell histiocytosis was made based on clinical, radiologic, and histopathologic evidence. Differential diagnoses such as osteomyelitis and metastatic disease were considered but excluded by the combined findings.  \n- Molecular testing identified a BRAF oncogene mutation (KRAS and NRAS were negative). BRAF status can influence therapy choices because targeted BRAF inhibitors may be effective in some patients.  \n- Because disease involved multiple bones and the central skull base/pituitary region, the patient was referred for systemic therapy. The oncology team planned a multiagent treatment regimen (denosumab, vinblastine, etoposide, 6‑mercaptopurine, methotrexate, and pegfilgrastim). No clinical follow-up of treatment response was possible because the patient later died in an unrelated accident.\n\nInterpretation and implications\n- This case illustrates LCH presenting first to dental care with a jaw lesion discovered after a trivial symptom (halitosis) and a normal initial exam.  \n- The patient’s prior endocrine problems (empty sella, diabetes insipidus treated with DDAVP, long‑term hormone replacement) and chronic otitis are most consistent with longstanding, previously unrecognized LCH involving the pituitary and temporal bones. Such involvement can cause permanent endocrine dysfunction and often signifies more extensive disease.  \n- Elevated inflammatory markers and multifocal PET/CT uptake confirm systemic activity and justify systemic therapy rather than local treatment alone. BRAF mutation offers a potential option for targeted therapy in appropriate cases.\n\nEmpathetic note\nThis was a complex and progressive illness that affected multiple systems and ultimately required coordinated care across dentistry, oral surgery, radiology, pathology, endocrinology, and oncology. The report underscores the importance of careful investigation of unusual oral findings, thorough systemic staging of LCH, and early multidisciplinary management when pituitary or multifocal bone involvement is suspected.",
+                "fh_score": 59.63
+            }
+        }
+    },
+    {
+        "article": "La paciente es una mujer de 66 años de edad que goza de buena salud. A mediados de la década de 1980, recibió varias sesiones de tratamiento con rayos grenz en el cuero cabelludo para aliviar el picor asociado con la psoriasis del cuero cabelludo. Con un tratamiento regular de aproximadamente una sesión al mes durante un período de 5 años, que se complementó de vez en cuando con alquitrán de hulla, ácido salicílico y prednisona, logró cierto alivio de su enfermedad. Con el tiempo, su cabello se adelgazó; la piel en toda el área del cuero cabelludo se volvió sensible al dolor y se produjo cicatrización. Los tratamientos con rayos grenz se habían administrado en una clínica privada; no se disponía de detalles del tratamiento, como la dosis única y acumulada. No había sufrido radiodermitis.\n\nEn un período muy breve en 2020, unos 35 años después de que cesara el tratamiento de radiación, aparecieron numerosos BCC y queratosis actínicas premalignas (AK) en su cuero cabelludo. Se inició un régimen de tratamiento de extirpación quirúrgica de BCC verificado por histología preoperatoria y crioterapia de AK por evaluación del médico. La terapia fotodinámica o los tratamientos tópicos no eran aplicables debido a la sensibilidad al dolor y las secuelas de la cirugía. De 2020 a 2022, recibió varios tratamientos de criocirugía y curetaje y un total de 13 extirpaciones quirúrgicas de BCC por cirugía de Mohs. Se estima que su número total de extirpaciones a lo largo del tiempo es de unos 30. Los BCC recalcitrantes y de novo en el cuero cabelludo cada vez más dañado, obviamente, son un desafío eterno; por lo tanto, los cirujanos plásticos y los dermatólogos buscaban otra modalidad de tratamiento con un mejor índice terapéutico.\n\nEn septiembre de 2022, aparecieron nuevos CCB confirmados histológicamente en el cuero cabelludo. La exploración por ultrasonido (DermaScan C, Cortex Technology ApS, Aalborg, Dinamarca) mostró tumores ecolucidos de 0,5-1,3 mm de espesor en ambos sitios analizados histológicamente, así como en algunas lesiones adicionales que pudieron identificarse en base al examen clínico y dermatoscópico. La paciente, tras ser informada, dio su consentimiento por escrito para el tratamiento con HIFU, con o sin biopsia de pretratamiento de las lesiones sospechosas.\n\nSe delinearon las lesiones elegibles para el tratamiento con un rotulador impermeable, incluyendo un margen perilesional de 2 mm. Se mapeó cada lesión seleccionada en una lámina transparente para ayudar a determinar la ubicación precisa en el seguimiento. Se usó el ultrasonido de 20 MHz para confirmar la profundidad de las lesiones identificadas al inicio y en las visitas de seguimiento posteriores. Debido al estado del cuero cabelludo conocido por ser sensible al dolor, se administró anestesia local (lidocaína 25 mg/ml + adrenalina 5 mg/ml, Amgros I/S, Copenhagen, Dinamarca) a todas las lesiones 10-15 minutos antes del tratamiento.\n\nLas lesiones fueron tratadas con HIFU utilizando la sonda de 1.3 mm; ajustes de 150 ms/dosis y energía acústica de 0.9 J/dosis. Se aplicaron 20-200 dosis a las lesiones, dependiendo de la extensión de la lesión. Las lesiones tratadas se curaron de forma espontánea sin complicaciones o necesidad de tratamiento especial. Se programaron visitas de seguimiento cada 3-6 meses para controlar la tasa de curación/recaída, tolerancia local y lesiones nuevas no identificadas anteriormente.\n\nDurante los 15 meses posteriores a la limpieza inicial con HIFU, se trataron con HIFU un total de 10 lesiones que, de acuerdo con las rutinas, hubieran requerido una biopsia seguida de una cirugía de escisión, en sesiones de unos 30 minutos. Las lesiones se curaron en unos pocos días sin complicaciones ni necesidad de intervención. Se observó una limpieza total en 7 de 8 lesiones de BCC tratadas y en ambas lesiones de AK. La única lesión recurrente de BCC de pequeño tamaño se observó después de 15 meses entre las primeras seis lesiones tratadas; la lesión se volvió a tratar con HIFU. Ejemplos de lesiones curadas 15 meses después del tratamiento con HIFU; el tumor con recurrencia.\n",
+        "gold_summary": "Una mujer de 66 años que en la década de 1980 había recibido varios tratamientos de rayos gamma en el cuero cabelludo desarrolló múltiples carcinomas basocelulares en la zona. Se le habían realizado más de 30 cirugías de escisión, incluida la cirugía de Mohs, en el pasado, con muchas complicaciones locales, pero, no obstante, los cánceres recurrentes. Los tratamientos con HIFU aplicados a ocho carcinomas basocelulares y dos lesiones precancerosas dieron como resultado una limpieza completa en el control a los 12 meses, pero una recurrencia después de 15 meses.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Esta es la historia de una mujer de 66 años. Cuando era más joven recibió radiación en el cuero cabelludo para tratar la psoriasis. Con el tiempo eso dejó la piel más fina, con cicatrices y dolor. Muchas décadas después le salieron muchas lesiones en la piel del cuero cabelludo. Algunas eran cáncer de piel llamado carcinoma basocelular (BCC). Otras eran manchas que a veces pueden volverse cáncer, llamadas queratosis actínicas (AK).\n\nLa paciente tuvo muchas cirugías antes (más de 30), incluidas varias con una técnica especial llamada Mohs. Aun así, los problemas seguían apareciendo. En 2022 los médicos probaron otro método llamado HIFU. HIFU usa ultrasonido para calentar y destruir la lesión sin cortar la piel. Buscaron las lesiones con una ecografía y pusieron anestesia local para que no doliera.\n\nTrataron 10 lesiones con HIFU (8 BCC y 2 AK). Las sesiones duraban alrededor de 30 minutos. Las heridas se curaron en pocos días y no hubo problemas importantes. Después de revisar a la paciente hasta 15 meses, encontraron que 7 de los 8 BCC y las 2 AK habían desaparecido. Una lesión pequeña volvió a aparecer a los 15 meses y la trataron otra vez con HIFU.\n\nEn resumen: muchos problemas de piel parecían estar relacionados con la radiación antigua. El HIFU ayudó a curar la mayoría de las lesiones en este caso. El tratamiento fue rápido y bien tolerado. Una lesión volvió a aparecer y se volvió a tratar.",
+                "fh_score": 77.23
+            },
+            "B2": {
+                "text": "Here is a clear, student-level summary of the case report:\n\nA 66-year-old woman who had repeated low-dose X-ray treatment to her scalp in the 1980s developed many skin problems decades later. The earlier radiation, given for scalp psoriasis, left her scalp thin, sensitive, and scarred. About 35 years after those treatments, multiple basal cell carcinomas (BCCs — a common type of skin cancer) and actinic keratoses (AKs — rough, sun-related patches that can become cancerous) appeared on her scalp. Over the years she had about 30 surgical removals, including Mohs surgery, but new and recurring tumors kept appearing.\n\nIn 2022 doctors tried a different approach: high-intensity focused ultrasound (HIFU). HIFU uses tightly focused sound waves to heat and destroy small tumors without cutting the skin. Before treatment, doctors used a 20 MHz ultrasound to measure how deep each lesion was (they were 0.5–1.3 mm thick) and marked the spots. Because her scalp was sensitive, each area was numbed with local anesthetic. The HIFU settings used a small 1.3 mm probe, short pulses (150 ms) and a set energy for each pulse; each lesion received between about 20 and 200 pulses depending on size.\n\nOver 15 months of follow-up, ten lesions that otherwise would have needed biopsy and surgery were treated with HIFU in short (≈30-minute) sessions. The treated spots healed in a few days without complications or extra care. Of eight BCCs treated, seven showed complete clearance at follow-up. Both AKs also cleared. One small BCC recurred after 15 months and was treated again with HIFU.\n\nWhat this means: In this single case, HIFU was well tolerated and cleared most small, thin BCCs and AKs on a previously damaged scalp. The results are promising, but this is a small series with limited follow-up. Longer monitoring and more patients are needed to know how well HIFU compares to standard treatments and how often recurrences happen. For this patient, ongoing check-ups and the option to re-treat with HIFU were used to manage new or returning lesions.",
+                "fh_score": 93.1
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel universitario, lectura B3)\n\nPaciente y antecedentes\n- Mujer de 66 años, por lo demás en buena salud.\n- En la década de 1980 recibió sesiones repetidas de radioterapia superficial (rayos grenz) en el cuero cabelludo durante unos 5 años (aprox. una sesión/mes), además de tratamientos tópicos ocasionales (alquitrán de hulla, ácido salicílico) y corticoide sistémico (prednisona). No hay datos sobre dosis acumulada y no refirió radiodermitis aguda.\n- A largo plazo desarrolló adelgazamiento del cabello, piel del cuero cabelludo dolorosa y cicatrizada.\n\nProblema actual\n- Unos 35 años después de la radioterapia (alrededor de 2020) apareció un brote de múltiples carcinomas basocelulares (BCC) y queratosis actínicas (AK, lesiones precancerosas) en el cuero cabelludo.\n- Entre 2020 y 2022 recibió múltiples tratamientos quirúrgicos (incluidas 13 resecciones por cirugía de Mohs) y criocirugía; se estiman unas 30 extirpaciones a lo largo del tiempo, con recidivas y aparición de lesiones nuevas.\n\nNueva estrategia terapéutica: HIFU\n- En septiembre de 2022 se documentaron nuevos BCC confirmados por biopsia. La ecografía cutánea (20 MHz) mostró tumores con espesor entre 0,5 y 1,3 mm.\n- La paciente consintió tratamiento con HIFU (ultrasonido focalizado de alta intensidad), seleccionándose y mapeando las lesiones con un margen perilesional de 2 mm.\n- Por sensibilidad dolorosa del cuero cabelludo se administró anestesia local (lidocaína con adrenalina) antes del procedimiento.\n- Parámetros de HIFU: sonda 1,3 mm, 150 ms por disparo, 0,9 J por disparo; se aplicaron entre 20 y 200 disparos según el tamaño de la lesión. Cada sesión duró aproximadamente 30 minutos.\n\nResultados\n- Durante 15 meses de seguimiento se trataron con HIFU 10 lesiones que, según la práctica habitual, habrían precisado biopsia y escisión.\n- Las zonas tratadas cicatrizaron espontáneamente en pocos días sin complicaciones locales ni necesidad de cuidados especiales.\n- Resultado clínico: limpieza total observada en 7 de 8 BCC tratados y en las 2 AK tratadas. Una lesión BCC pequeña recidivó a los 15 meses entre las primeras seis tratadas y fue nuevamente tratada con HIFU.\n- Controles programados cada 3–6 meses con ecografía para vigilar curación, recidiva y aparición de nuevas lesiones.\n\nInterpretación y consideraciones prácticas\n- HIFU se mostró como una opción local no quirúrgica, bien tolerada y rápida, capaz de conseguir resolución clínica en la mayoría de las lesiones pequeñas (espesor ≤1,3 mm) en este caso particular de cuero cabelludo previamente irradiado y doloroso.\n- Ventajas observadas: tratamiento ambulatorio corto, curación rápida, mínima morbilidad y posibilidad de repetir el tratamiento en caso de recidiva.\n- Limitaciones importantes: serie de un solo paciente, número pequeño de lesiones tratadas, seguimiento limitado (15 meses) y ausencia de datos completos sobre la radiación previa (dosis acumulada). La confirmación histológica de curación a largo plazo no consta en todos los casos.\n\nRecomendaciones y próximos pasos\n- Mantener vigilancia dermatológica estrecha con examen clínico y ecografía; biopsiar cualquier lesión sospechosa o recurrente.\n- Considerar HIFU como alternativa en pacientes con múltiples lesiones superficiales pequeñas o en cueros cabelludos con secuelas de radiación donde la cirugía es difícil o dolorosa.\n- Se necesitan series más amplias y con seguimiento prolongado para evaluar la eficacia real, la seguridad a largo plazo y comparar HIFU con terapias estándar (cirugía, tratamientos tópicos, fotodinámica).\n\nNota empática\n- El manejo de múltiples BCC en un cuero cabelludo previamente irradiado es complejo y puede ser emocionalmente agotador para la paciente. Las opciones que minimizan las intervenciones quirúrgicas y el dolor, como HIFU en este caso, pueden mejorar la calidad de vida, pero requieren seguimiento atento y comunicación clara entre paciente y equipo médico.",
+                "fh_score": 44.76
+            }
+        }
+    },
+    {
+        "article": "Se realizó un trasplante cardíaco ortotópico a una niña de 12 años con insuficiencia cardíaca en fase terminal debido a una miocardiopatía restrictiva. Durante la operación, se presentó una disfunción primaria grave del injerto, que requirió el uso de oxigenación por membrana extracorpórea venosa arterial. La función cardíaca se recuperó completamente después de 4 días, y su período postoperatorio se complicó por una insuficiencia renal aguda transitoria y un bloqueo auriculoventricular completo que duró >3 semanas después de la operación. Para evitar la disincronía del ventrículo izquierdo y el posible daño de la derivación del ventrículo derecho debido a las biopsias endomiocárdicas de vigilancia de rechazo múltiple, se indicó un marcapasos biventricular transvenoso que utiliza un marcapasos del ventrículo izquierdo aislado a través de la vena coronaria.\n\nBajo anestesia local y sedación suave, se cortó la vena cefálica izquierda y se introdujo un catéter guía en la vena subclavia y se colocó en el seno coronario inicialmente para realizar un venograma cardiaco. Se implantó un electrodo de estimulación endocárdica de elución de esteroides unipolar con mecanismo de fijación activa (Attain StarFix® 4195, Medtronic, Minneapolis, MN) en la rama de la vena interventricular anterior. Las medidas en el momento del implante fueron las siguientes: umbral 2 V a 0,4 ms, onda R 6 mV e impedancia 300 Ω a 4,8 mA. Se implantó un segundo electrodo de estimulación endocárdica de elución de esteroides bipolar con fijación activa (2088T®, St. Jude Medical, Minneapolis, MN) en la aurícula derecha.\n\nAmbos cables se aseguraron y se conectaron a un marcapasos adaptable a la frecuencia (Accent DR®, St. Jude Medical, Minneapolis, MN) que se colocó en una bolsa muscular infraclavicular izquierda y se programó a VDD. Las mediciones de los cables electrofisiológicos fueron estables después del implante: umbral ventricular 1.5 V a 0.7 ms, onda R 4.5 mV, onda P 4.3 mV (bipolar), impedancia ventricular 260 Ω y vida útil estimada de la batería de 5 años.\n\nEl electrocardiograma posterior al implante mostró complejos de morfología de bloqueo de rama derecha, y la evaluación ecocardiográfica mostró ausencia de disincronías auriculoventriculares, interventriculares e intraventriculares. En el seguimiento a 5 años, el paciente permaneció en Clase Funcional I con el mismo sistema de estimulación y conservó la función ventricular.\n\nMH - Bloqueo auriculoventricular/etiología/*terapia\nMH - Niño\nMH - Sinus coronario\nMH - Mujer\nMH - Insuficiencia cardiaca/cirugía\nMH - Trasplante de corazón/*efectos adversos\nMH - Ventrículos del corazón\nMH - Humanos\nMH - *Marcapasos, artificial\nMH - Disfunción/complicaciones/tratamiento del injerto primario\n",
+        "gold_summary": "Se sometió a un trasplante de corazón ortotópico a un niño de 12 años con insuficiencia cardiaca en fase terminal debido a una miocardiopatía restrictiva. La disfunción primaria del injerto precisó oxigenación con membrana extracorpórea venosa arterial. La función cardiaca se normalizó, pero el bloqueo auriculoventricular completo persistió después de 3 semanas. Se realizó un marcapaso bicameral con marcapaso transvenoso del ventrículo izquierdo a través del seno coronario. Tras 5 años de seguimiento, el paciente se encuentra estable con el mismo sistema de marcapaso y con la función ventricular preservada.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una niña de 12 años recibió un trasplante de corazón porque su propio corazón estaba muy enfermo.  \nDurante la operación, el corazón nuevo no funcionó bien al principio. Los médicos usaron una máquina que ayuda al corazón y a los pulmones (ECMO) durante cuatro días. Después de eso, el corazón se recuperó por completo.  \n\nLa niña tuvo dos problemas después: el riñón dejó de funcionar bien por un tiempo y las señales eléctricas del corazón no pasaban normalmente (esto se llama bloqueo auriculoventricular). Ese bloqueo duró más de tres semanas.  \n\nPara ayudar, los médicos le pusieron un marcapasos. Un marcapasos es un aparato con cables que envía pequeñas señales para que el corazón lata al ritmo correcto. Uno de los cables fue colocado en una vena del lado izquierdo del corazón para que los dos lados del corazón latan juntos y no se dañara el lado derecho con muchas pruebas. El procedimiento se hizo con anestesia local y sedación suave.  \n\nDespués de poner el marcapasos, las ecografías mostraron que el corazón latía de forma sincronizada y funcionaba bien. Cinco años después, la niña está bien, hace sus actividades y el marcapasos sigue funcionando correctamente.",
+                "fh_score": 68.49
+            },
+            "B2": {
+                "text": "Resumen claro y amable:\n\nUna niña de 12 años con insuficiencia cardíaca terminal por una miocardiopatía restrictiva (el corazón está muy rígido y no se llena bien) recibió un trasplante de corazón. Tras la operación el nuevo corazón tuvo una insuficiencia primaria grave y fue necesario conectarla a circulación extracorpórea (ECMO veno‑arterial), un soporte que sustituye temporalmente la función del corazón y los pulmones. La función cardíaca se recuperó completamente en 4 días.\n\nEn el postoperatorio tuvo una insuficiencia renal aguda transitoria y desarrolló un bloqueo auriculoventricular completo (el impulso eléctrico entre las aurículas y los ventrículos no pasaba) que persistió más de 3 semanas. Para tratar ese bloqueo y, al mismo tiempo, evitar que el ventrículo izquierdo se desincronizara —y también para proteger el ventrículo derecho de posibles daños por las biopsias que se hacen para vigilar el rechazo— se decidió implantar un marcapasos transvenoso especial que estimula el ventrículo izquierdo a través de la vena coronaria.\n\nEl procedimiento se realizó con sedación leve y anestesia local. Por la vena cefálica/subclavia se accedió al seno coronario y se colocó un cable activo de fijación para el ventrículo izquierdo en una rama de la vena interventricular anterior. Se colocó otro cable en la aurícula derecha. Ambos cables se conectaron a un marcapasos colocado en una bolsa muscular bajo la clavícula izquierda y se programó para asegurar una buena coordinación entre las cámaras del corazón.\n\nLas pruebas inmediatas mostraron parámetros eléctricos estables y, en la ecocardiografía, no había desincronía entre las cámaras del corazón. En el electrocardiograma apareció una morfología de bloqueo de rama derecha, lo cual es un hallazgo esperado después de este tipo de implantación. A los 5 años de seguimiento, la niña estaba estable en Clase Funcional I (sin limitación de la actividad), mantenía el mismo sistema de estimulación y tenía función ventricular preservada.\n\nComentario breve y humano: aunque tuvo complicaciones serias al principio, el equipo usó soportes temporales y un marcapasos diseñado para proteger la función del nuevo corazón. El resultado a medio plazo fue muy bueno, y la paciente siguió con buena calidad de vida.",
+                "fh_score": 46.74
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel universitario, lectura B3)\n\nUna niña de 12 años con miocardiopatía restrictiva en insuficiencia cardiaca terminal recibió un trasplante cardiaco ortotópico. Durante la cirugía presentó una disfunción primaria grave del injerto que exigió soporte con oxigenación por membrana extracorpórea veno‑arterial (VA‑ECMO). La función cardíaca se recuperó completamente en 4 días. En el posoperatorio inmediato hubo además una insuficiencia renal aguda transitoria. No obstante, persistió un bloqueo auriculoventricular completo durante más de 3 semanas.\n\nPor dos motivos se evitó implantar un cable ventricular derecho: (1) prevenir la disincronía del ventrículo izquierdo que puede derivarse del marcapaseo ventricular derecho exclusivo, y (2) reducir el riesgo de daño del electrodo derecho por las repetidas biopsias endomiocárdicas necesarias para el control del rechazo en trasplante. Se decidió, por tanto, un sistema transvenoso que estimulase el ventrículo izquierdo a través de la vena coronaria, combinado con estimulación auricular.\n\nProcedimiento y hallazgos técnicos\n- Bajo anestesia local y sedación ligera se abordó la vena cefálica izquierda y, tras cateterizar la subclavia y localizar el seno coronario con venograma, se implantó:\n  - Un electrodo unipolar de fijación activa y liberación de esteroides (Attain StarFix® 4195, Medtronic) en una rama de la vena interventricular anterior (vía coronaria) para estimular el ventrículo izquierdo. Parámetros iniciales: umbral 2 V a 0,4 ms; onda R 6 mV; impedancia 300 Ω.\n  - Un electrodo bipolar de fijación activa y liberación de esteroides (2088T®, St. Jude) en la aurícula derecha.\n- Ambos cables se aseguraron y se conectaron a un generador bicameral con adaptación de frecuencia (Accent DR®, St. Jude), ubicado en bolsa muscular infraclavicular izquierda y programado en modo VDD (sensado auricular con estimulación ventricular).\n- Mediciones posoperatorias: umbral ventricular 1,5 V a 0,7 ms; onda R 4,5 mV; onda P (bipolar) 4,3 mV; impedancia ventricular 260 Ω; autonomía estimada de la batería ≈ 5 años.\n\nEvolución y control\n- El electrocardiograma posimplante mostró complejos con morfología de bloqueo de rama derecha (compatible con estimulación ventricular izquierda).\n- Ecocardiografía: no se evidenciaron disincronías auriculoventriculares, interventriculares ni intraventriculares.\n- Seguimiento a 5 años: la paciente permaneció en clase funcional I (sin limitación clínica), conservó la función ventricular y seguía con el mismo sistema de estimulación.\n\nInterpretación y consideraciones\n- Este caso muestra que, en un niño trasplantado con bloqueo auriculoventricular persistente y necesidad de biopsias frecuentes, la estimulación ventricular izquierda transvenosa (a través del seno coronario) puede ser una alternativa eficaz para evitar disincronía y el riesgo de lesión del electrodo derecho.\n- Factores a considerar al valorar esta estrategia: anatomía coronaria favorable para colocación del cable, estabilidad del electrodo coronario, posibles complicaciones (p. ej., estimulación faríngea/frenica, desplazamiento del cable, problemas de umbral a largo plazo) y la vida útil del generador.\n- En este caso concreto, la solución fue bien tolerada y estable a mediano-largo plazo, con recuperación funcional y sin evidencia de disincronía.\n\nEmpatía y conclusión\nLa paciente superó una complicación grave del trasplante y, tras recibir un sistema de marcapaseo diseñado para minimizar riesgos en el contexto del trasplante, logró una recuperación funcional completa y estable a 5 años. Este enfoque aporta una opción valiosa cuando el riesgo de daño del electrodo derecho por biopsias o la posibilidad de disincronía ventricular hacen preferible estimular el ventrículo izquierdo por vía coronaria.",
+                "fh_score": 38.55
+            }
+        }
+    },
+    {
+        "article": "Una paciente de 20 años de edad se presentó con distensión abdominal progresiva asociada con calambres abdominales, incapacidad para expulsar flatos y heces, así como vómitos frecuentes de materia ingerida y biliar de un día de duración. El día anterior, dio a luz por cesárea por una indicación de bradicardia fetal severa. También tenía preeclampsia sin signos de gravedad y desnutrición de inicio en la edad adulta con un índice de masa corporal (IMC) de 16,5 kg/M2. No tenía antecedentes de cirugía abdominal previa. Negó cualquier queja similar en el pasado o antecedentes de cambio de hábitos intestinales o estreñimiento con paso de heces sanguinolentas. No tenía ninguna enfermedad médica crónica conocida.\n\nEn el examen físico, la paciente se veía enferma y con dolor. Su presión arterial era de 90/70 mmHg, su pulso oscilaba entre 116 y 120 latidos por minuto, y su frecuencia respiratoria era de 22 a 24 respiraciones por minuto. No se registró fiebre. Su abdomen estaba muy distendido y simétrico, con visibles movimientos intestinales peristálticos. Había una difusa sensibilidad directa en todo su abdomen, más en el cuadrante inferior derecho. Había un signo positivo de acumulación de fluido intraperitoneal con opacidad cambiante. Había una herida quirúrgica suprapúbica bien aproximada con un vendaje limpio. El examen rectal digital no mostró nada destacable. Tenía una herida superficial lineal de 3 cm de largo, orientada verticalmente, en su labio mayor izquierdo, que el equipo de obstetricia pensó inicialmente que era una quemadura de yodo en la piel.\n\nSe le introdujo un catéter y se le resucitó con dos bolsas de solución salina normal y produjo 200 ml de orina en una hora. Se le introdujo una sonda nasogástrica (NGT) pero no hubo una salida significativa. Se le realizó un hemograma completo y una radiografía abdominal simple. Su recuento de glóbulos blancos era de 1780 células/µl con predominio de neutrófilos del 88 %, hemoglobina de 12,7 mg/dl y un recuento de plaquetas de 78 x 103/ µl. Su prueba de función renal era normal y sus enzimas hepáticas estaban ligeramente elevadas por encima del rango normal pero no fue significativo. Su radiografía abdominal simple muestra múltiples niveles de aire-líquido ubicados centralmente con un bucle intestinal grande dilatado ubicado periféricamente y blanqueamiento del espacio pélvico que indica una acumulación de líquido. No se solicitó una tomografía computarizada abdominal (CT) porque trabajamos en un entorno con recursos limitados y para pacientes con obstrucción intestinal, solicitamos una tomografía computarizada cuando existe la posibilidad de un diagnóstico alternativo o cuando se sospecha una obstrucción tumoral.\n\nTras obtener el consentimiento informado por escrito, se exploró a la paciente bajo anestesia general con un diagnóstico de abdomen agudo secundario a obstrucción intestinal mixta secundaria a vólvulo del intestino delgado. El hallazgo intraoperatorio fue un íleon distal que rodeaba el ciego y el colon ascendente proximal, ambos móviles y no adheridos a la pared abdominal posterolateral derecha. Tanto el íleon como el ciego, así como el colon ascendente, eran viables. La punta del apéndice estaba enredada con el nudo ileal y estaba gangrenoso. El intestino delgado proximal y el intestino grueso distal estaban muy distendidos, pero en su ubicación normal. Había unos cuatro litros de líquido intraperitoneal seroso.\n\nDurante la operación, la paciente se mantuvo hipotensa (80/50 mmHg) desde que se le indujo la anestesia y se le administró un vasopresor. Debido a la inestabilidad de la paciente y a la viabilidad de los intestinos afectados por el nudo, se procedió a una hemicolectomía derecha. Se realizó una descompresión proximal y distal de los intestinos delgado y grueso distendidos, respectivamente. Se fijó el ciego y el colon ascendente a la pared abdominal posterolateral derecha con suturas seromusculares interrumpidas con hilo no absorbible (Silk 2-0).\n\nDespués del procedimiento, se le retiró la intubación y se le dio alimentación por vía oral (NPO) durante 24 horas y se le administró un fluido de mantenimiento con reposición de la pérdida. A pesar de la reanimación con fluidos y el apoyo con vasopresores, ella se encontraba persistentemente hipotensa, por lo que se le administró un tratamiento antibiótico doble con ceftriaxona 1 g, IV, BID y metronidazol 500 mg, IV, TID, en vista de un posible shock séptico de origen genitourinario. Su estado empeoró gradualmente y, tras una nueva evaluación el primer día postoperatorio, la herida superficial en su vulva se había extendido hacia la zona suprapúbica con signos clínicos de gangrena de Fournier. Por ello, revisamos su tratamiento antibiótico a meropenem 1 g, IV, BID, vancomicina 1 g, IV, BID y metronidazol 500 mg, IV, TID. Después de obtener el consentimiento informado por escrito, se la volvió a llevar al quirófano para un desbridamiento radical de la gangrena de Fournier y, posteriormente, se la trasladó a la unidad de cuidados intensivos quirúrgicos (ICU) intubada debido a un shock séptico persistente y un retraso en la recuperación de la anestesia. Lamentablemente, falleció con fallo multiorgánico debido a un shock séptico refractario en su segundo día postoperatorio, después de la exploración inicial.\n",
+        "gold_summary": "Presentamos un caso de nudos ileocecales en una paciente posparto con distensión abdominal, vómitos y ausencia de heces y flatos. La radiografía abdominal simple reveló bucles intestinales dilatados con múltiples niveles de aire y fluidos. Se realizó una laparotomía exploratoria con hallazgo intraoperatorio de nudos ileocecales con intestino viable, ciego móvil y colon ascendente y punta gangrenosa del apéndice. Deshicimos el nudo y realizamos una apendectomía. Debido a la inestabilidad intraoperatoria de los signos vitales de la paciente, se aplazó la hemicolectomía derecha y se fijaron el ciego y el colon ascendente a la pared abdominal posterolateral derecha.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Este es el caso de una mujer joven que acababa de tener un bebé. Tenía la barriga muy hinchada, vomitaba y no podía expulsar gases ni hacer caca.  \nLa radiografía mostró muchos huecos con aire y líquido en los intestinos. Eso dejó claro que algo bloqueaba el paso en su tripa.  \n\nEn la operación encontraron un nudo entre el intestino delgado y la parte de inicio del intestino grueso (el ciego). El nudo se llama \"nudo ileocecal\". La parte del intestino que estaba en el nudo estaba viva, pero la punta del apéndice estaba dañada.  \nLos cirujanos deshicieron el nudo y sacaron el apéndice enfermo. Como la paciente estaba muy inestable, no pudieron quitar una parte grande del colon. En vez de eso, fijaron el ciego y el colon a la pared para que no se movieran.  \n\nEs un problema raro y serio. Los médicos actuaron rápido para salvar el intestino y cuidar a la paciente.",
+                "fh_score": 77.43
+            },
+            "B2": {
+                "text": "Presentamos el caso de una paciente posparto que acudió con distensión abdominal, vómitos y ausencia de expulsión de gases y heces. La radiografía abdominal mostró asas intestinales muy dilatadas con varios niveles de aire y líquido, hallazgos compatibles con una obstrucción intestinal. Al abrir el abdomen (laparotomía exploradora) se encontró un nudo entre el íleon (la parte final del intestino delgado) y la región ileocecal; el intestino afectado estaba todavía viable (es decir, con buena circulación), el ciego y el colon ascendente eran móviles, y la punta del apéndice estaba gangrenosa (tejido muerto). Se deshizo el nudo y se realizó una apendicectomía (extirpación del apéndice). Dado que la paciente presentó inestabilidad de las constantes vitales durante la operación, se decidió posponer una hemicolectomía derecha (extirpar la porción derecha del colon) y, en su lugar, fijar el ciego y el colon ascendente a la pared abdominal para prevenir nueva torsión.",
+                "fh_score": 40.34
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel lector universitario)\n\nPresentación y antecedentes\n- Mujer de 20 años, un día después de una cesárea por bradicardia fetal severa. Antecedentes relevantes: preeclampsia (sin signos de gravedad) y desnutrición crónica reciente (IMC 16,5 kg/m2). Sin cirugías abdominales previas.\n- Síntomas al ingreso: distensión abdominal progresiva, calambres, ausencia de flatos y deposiciones (obstipación), vómitos alimentarios y biliosos de 1 día de evolución.\n\nExamen físico y pruebas iniciales\n- Signos vitales anormales: hipotensión (90/70 mmHg), taquicardia (116–120 lpm), taquipnea (22–24 rpm), afebril.\n- Abdomen: muy distendido, movimientos peristálticos visibles, sensibilidad generalizada con mayor dolor en cuadrante inferior derecho; signo de onda de líquido positivo (sugiere líquido intraperitoneal).\n- Hallazgo cutáneo inicial: lesión lineal superficial de 3 cm en labio mayor izquierdo, interpretada en primera instancia como quemadura de yodo.\n- Laboratorio: leucopenia marcada (GB 1.780/µl) con predominio de neutrófilos (88%), hemoglobina 12,7 g/dl, trombocitopenia (plaquetas 78 x10^3/µl). Función renal normal; enzimas hepáticas ligeramente elevadas.\n- Radiografía abdominal simple: múltiples niveles hidroaéreos centrales y asas dilatadas; borramiento del espacio pélvico compatible con líquido libre/colección. No se realizó TC por limitaciones de recursos.\n\nDiagnóstico preoperatorio\n- Abdomen agudo por sospecha de obstrucción intestinal por vólvulo del intestino delgado (obstrucción alta).\n\nHallazgos y conducta intraoperatoria\n- Exploración con anestesia general: nudo ileocecal (íleon distal enroscado alrededor del ciego y colon ascendente proximal). El íleon, el ciego y el colon ascendente eran móviles y, en apariencia, viables. La punta del apéndice estaba enredada en el nudo y presentaba gangrena local. Existían ≈4 litros de líquido seroso intraperitoneal.\n- Durante la cirugía la paciente se volvió hemodinámicamente inestable (PA 80/50 mmHg) y requirió vasopresores. Según el informe, se procedió a una hemicolectomía derecha, descompresión proximal y distal de los tramos intestinales dilatados, y fijación (cecopexia) del ciego y colon ascendente a la pared abdominal posterolateral.  \n\nEvolución postoperatoria y desenlace\n- Inicialmente fue extubada y mantenida NPO; recibió reposición hídrica y soporte vasopresor. Persistió hipotensa a pesar de líquidos y vasopresores.\n- Se inició terapia antibiótica empírica (ceftriaxona + metronidazol) por sospecha de shock séptico de posible origen genitourinario.\n- En el primer día posoperatorio la lesión vulvar se extendió hacia la región suprapúbica con signos clínicos compatibles con gangrena de Fournier (necrosis de tejidos blandos del periné). Antibióticos escalados a meropenem + vancomicina + metronidazol.\n- Se realizó desbridamiento radical de la zona afectada y la paciente fue trasladada a UCI quirúrgica intubada por shock séptico persistente y retraso en la recuperación anestésica.\n- Falleció en el segundo día posoperatorio por shock séptico refractario y fallo multiorgánico.\n\nInterpretación y puntos clave\n- Diagnóstico anatómico: nudo ileocecal (ileocecal knot) que produjo obstrucción intestinal aguda; apéndice con gangrena focal por enredo. El nudo puede causar compromiso vascular rápido y requiere manejo quirúrgico urgente.\n- Complicaciones críticas en este caso: inestabilidad hemodinámica intraoperatoria, insuficiencia de respuesta a resucitación, y evolución hacia gangrena de Fournier con sepsis rápida y refractaria.\n- Factores que probablemente contribuyeron al desenlace adverso: estado posparto inmediato, desnutrición, citopenias (leucopenia y trombocitopenia), posible foco infeccioso perineal precoz y limitaciones en recursos diagnósticos (no TC). La leucopenia con neutrofilia relativa y la trombocitopenia sugieren un estado sistémico grave que pudo empeorar la capacidad de respuesta a la infección.\n- Enseñanzas prácticas: el nudo ileocecal es una causa rara pero potencialmente letal de obstrucción intestinal; requiere diagnóstico y tratamiento quirúrgicos rápidos. Una lesión perineal aparentemente menor en un contexto posoperatorio o posparto debe vigilarse estrechamente porque puede progresar a infección necrotizante (Fournier) con rapidez. En entornos con recursos limitados, la vigilancia clínica y la intervención temprana son decisivas, pero aun así existe alto riesgo de mortalidad cuando concurren factores de riesgo sistémicos.\n\nEmpatía final\nEste caso ilustra cómo una complicación intestinal aguda combinada con una infección necrotizante del periné y un estado sistémico comprometido pueden evolucionar rápidamente a sepsis refractaria, pese a intervención quirúrgica activa. Es una pérdida trágica de una paciente joven; reconozco el impacto emocional y clínico que este desenlace tiene para la familia y el equipo tratante.",
+                "fh_score": 34.48
+            }
+        }
+    },
+    {
+        "article": "Un hombre de 38 años se presentó en el hospital con opresión en el pecho y falta de aire. Tres años antes, había experimentado síntomas similares después de la actividad y recibió tratamiento en nuestro hospital. La ecocardiografía ambulatoria indicó una masa de eco del corazón izquierdo que sugería un mixoma, lo que llevó a su ingreso para una evaluación adicional. El examen físico reveló pigmentación de las orejas del paciente caracterizada por múltiples puntos pequeños de color café y negro. La tomografía computarizada abdominal (TC) mostró múltiples hígados y pequeños quistes en el riñón izquierdo. Las pruebas genéticas identificaron mutaciones en los genes TTN y PRKAR1A. El diagnóstico de CNC se confirmó mediante examen clínico, imágenes y pruebas genéticas. Después del tratamiento sintomático, la condición del paciente mejoró; sin embargo, rechazó la intervención quirúrgica. El 20 de septiembre de 2023, el paciente se presentó en nuestro hospital con opresión en el pecho y falta de aire exacerbadas. Informó dificultad para permanecer acostado boca arriba y necesidad de sentarse erguido para respirar. El examen físico reveló distensión de la vena yugular, desplazamiento hacia la izquierda y hacia abajo del límite del corazón, ritmo cardíaco irregular en la auscultación y un murmullo de la válvula mitral de intensidad 2/6-3/6 en el cuarto espacio intercostal a lo largo del margen izquierdo del esternón. Se escucharon estertores húmedos en ambos campos pulmonares medio e inferior. La palpación reveló un hígado firme que se extendía tres dedos por debajo del proceso xifoides y dos dedos por debajo de la caja torácica, junto con un edema de pitting leve en ambas extremidades inferiores. Las imágenes ecocardiográficas indicaron un agrandamiento global del corazón, dilatación del seno aórtico y arteria pulmonar, regurgitación mitral pequeña a moderada y una masa ecógena irregular que medía 54 mm × 43 mm en la cámara izquierda unida al tabique auricular. La fracción de eyección del ventrículo izquierdo (FEVI) fue del 23,1 %, con acortamiento fraccional (FS) del 10,9 %. La electrocardiografía demostró fibrilación auricular (frecuencia ventricular promedio, 150 latidos/min) y ondas Q anormales en las derivaciones V1-V3. Basándose en la historia del paciente, el diagnóstico incluyó DCM y CNC con mixoma cardíaco. Dada la presencia de insuficiencia cardíaca en etapa terminal y mixoma cardíaco concurrente, el paciente fue hospitalizado y se consideró el trasplante de corazón como una opción terapéutica viable para abordar ambas afecciones simultáneamente. Un corazón de donante adecuado estuvo disponible para su trasplante inmediato el 1 de octubre de 2024.\n\n\nProcedimiento quirúrgico\n\nLa piel y los tejidos subcutáneos se incisionaron cuidadosamente capa por capa a través de una esternotomía media. El esternón se abrió longitudinalmente y se controló el sangrado mediante electrocoagulación y cera ósea. La exploración extracardíaca reveló un agrandamiento global del corazón, más prominente en el ventrículo izquierdo. El corazón mostró una disminución de la fuerza contráctil. La aorta y la arteria pulmonar principal (AP) se diseccionaron desde la región supravalvular. Algunos tejidos se conservaron para suturarlos posteriormente, mientras que la mayor parte de la aurícula derecha enferma, la aurícula izquierda (AL), el ventrículo derecho y el ventrículo izquierdo se extirparon. La resección reveló una masa mucoide de color blanco grisáceo. Los tejidos de la aurícula izquierda del donante y del receptor se suturaron utilizando hilos Prolene 3/0 dobles continuos. La anastomosis se inspeccionó meticulosamente varias veces y no se observó sangrado significativo. De forma similar, la anastomosis término-terminal de la aorta ascendente del donante y la arteria pulmonar del receptor se realizó utilizando suturas Prolene 5/0 continuas, y una inspección cuidadosa no reveló sangrado.\n\nAdemás, la LA del donante y la PA del receptor se cerraron de forma segura utilizando suturas Prolene 5/0 dobles y continuas. Los tejidos de la vena cava inferior tanto del donante como del receptor se suturaron de forma similar con suturas Prolene 5/0, y se realizaron varias inspecciones para confirmar que no había presencia de sangrado significativo. El lado izquierdo del corazón se desinfló y, a medida que comenzó el recalentamiento, se restableció la oxigenación, se soltó la aorta ascendente y el corazón volvió espontáneamente al ritmo sinusal. Se aplicó sutura continua con Prolene 5/0 tanto a la vena cava superior del donante como del receptor y se inspeccionó de forma diligente para garantizar la ausencia de sangrado significativo. Después de la interrupción exitosa de la circulación asistida, se descanuló la cavidad venosa. Se recogieron muestras de tejido del corazón izquierdo y de la materia gris del paciente para un examen histopatológico, y se confirmó el diagnóstico de DCM y mixoma cardiaco.\n\n\nManejo postoperatorio\n\nEl primer día después del trasplante de corazón, el paciente produjo 1200 ml de orina. Los exámenes de laboratorio revelaron un nivel de troponina T hipersensible de 796.70 ng/L y un nivel de NT-proBNP de 10798 pg/ml. El recuento completo de sangre mostró un recuento de glóbulos blancos de 17.15 × 109/L, sin anomalías significativas en otros resultados de exámenes. El ecocardiógrafo mostró un EFV del 65 %, FS del 35 %, un espesor de la pared ventricular normal y ecogenicidad, y no se observaron anomalías discernibles en la morfología y estructura de la válvula. Después del trasplante de corazón, se administró una terapia hormonal intravenosa de succinato sódico de metilprednisolona (0.25 g) para mejorar la inmunidad, y se proporcionó un tratamiento intravenoso antiinfeccioso con cefoperazona y sulbactam sódico (2 g). El paciente recibió una solución nutriente y tiopronina en el primer día después de la cirugía. En el día tres postoperatorio, se reemplazó el succinato sódico de metilprednisolona con acetato de prednisona oral (25 mg). Se administraron cápsulas de micofenolato de mofetilo (0.5 g) por vía oral para minimizar el rechazo del corazón, y se administró acetato de carpofénico intravenoso (50 mg) para prevenir infecciones fúngicas. La producción de orina del paciente fue de 2000 ml, con niveles de troponina T hipersensible de 390 ng/L, niveles de NT-proBNP de 7877 pg/ml, y un recuento de leucocitos de 12.15 × 109/L. En el día siete postoperatorio, se introdujeron cápsulas de tacrolimus a una dosis oral de (1 mg) para minimizar el rechazo del paciente al corazón del donante, con un cuidadoso monitoreo de las concentraciones sanguíneas. Subsiguientemente, la dosis oral de acetato de prednisona se redujo gradualmente a (10 mg) mientras se ajustaba la concentración sanguínea de tacrolimus a 10.90 ng/L. La recuperación del paciente mejoró. El 20 de octubre de 2023, la ecocardiografía de seguimiento (Fig. 6) no mostró anomalías, con niveles de troponina T de 85 ng/L, NT-proBNP de 210 pg/ml, y todos los demás resultados de exámenes dentro de los rangos normales. El paciente exhibió una excelente recuperación postoperatoria y fue dado de alta. Las visitas regulares de seguimiento a nuestro departamento después del alta mostraron que el paciente permanece en buen estado.\n\nMH - Humanos\nMH - *Cardiomiopatía, Dilatada/cirugía/etiología/diagnóstico/diagnóstico por imágenes\nMH - Hombre\nMH - *Complejo de Carney/genética/diagnóstico/cirugía/complicaciones\nMH - Adulto\nMH - *Trasplante de corazón\nMH - *Mixoma/complicaciones/cirugía/diagnóstico por imágenes/diagnóstico/genética\nMH - *Insuficiencia cardiaca/etiología/diagnóstico/cirugía\nMH - *Neoplasias cardiacas/cirugía/complicaciones/diagnóstico por imágenes/diagnóstico/genética\nMH - Resultado del tratamiento\nMH - Subunidad/genética de la proteína quinasa Rlalpha dependiente de AMP cíclico\n",
+        "gold_summary": "Aquí, reportamos un caso de insuficiencia cardiaca debido al síndrome de Carney que resultó en mixoma cardiaco combinado con cardiomiopatía dilatada. Un hombre de 35 años de edad fue admitido en el hospital hace tres años debido a opresión torácica repentina y falta de aire. La ecocardiografía indicó mixoma, y una combinación de cribado genético y examen físico confirmó el síndrome de Carney con mixoma cardiaco. Después del tratamiento sintomático, fue dado de alta. Las intervenciones quirúrgicas no fueron consideradas en ese momento. Sin embargo, la opresión torácica y los síntomas de falta de aire del paciente empeoraron, y volvió al hospital. Se confirmó una función cardiaca de grado IV de la New York Heart Association, y la ecocardiografía indicó la presencia de cardiomiopatía dilatada acompañada de mixoma cardiaco. En última instancia, la insuficiencia cardiaca del paciente fue tratada con éxito con un trasplante cardiaco.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Este es el cuento de un hombre que tuvo problemas con su corazón. Tenía 38 años y se sentía con opresión en el pecho y le costaba respirar. Hace tres años ya había tenido síntomas parecidos. Los médicos vieron en una ecografía que tenía una masa dentro del corazón. Esa masa se llama mixoma, que es un tumor que crece en el corazón.\n\nTambién tenía pequeñas manchas oscuras en las orejas y quistes en el hígado y en un riñón. Las pruebas de genética mostraron cambios en dos genes. Todo eso ayudó a los médicos a decir que tenía el síndrome de Carney. El síndrome de Carney es una condición que puede causar manchas en la piel y tumores como el mixoma.\n\nCon el tiempo, su corazón se hizo muy grande y se volvió muy débil. Esto se llama cardiomiopatía dilatada. Sus síntomas empeoraron mucho hasta que ya no podía acostarse boca arriba sin sentirse mal. Los médicos pensaron que la mejor opción era darle un corazón nuevo.\n\nEl 1 de octubre de 2024 recibió un trasplante de corazón. La operación fue compleja, pero salió bien. Después de la cirugía, su nuevo corazón funcionó correctamente. Recibió medicinas para evitar infecciones y para que su cuerpo no rechazara el nuevo corazón. Con el tiempo, sus pruebas volvieron a la normalidad y se recuperó muy bien.\n\nHoy está en buen estado y sigue con controles médicos regulares. Los médicos lo vigilan para asegurarse de que siga mejorando.",
+                "fh_score": 80.71
+            },
+            "B2": {
+                "text": "Resumen comprensible (nivel B2, para lectores de 11–17 años)\n\nUn hombre de 38 años llegó al hospital porque sentía opresión en el pecho y le costaba respirar. Tres años antes había presentado síntomas parecidos y, tras pruebas, se detectó en su corazón una masa que parecía un mixoma, un tumor benigno que puede crecer dentro de las cavidades del corazón y causar problemas.\n\nAl explorarlo, los médicos vieron que tenía manchas oscuras en las orejas y que en una tomografía abdominal había pequeños quistes en el hígado y el riñón. Las pruebas genéticas encontraron cambios en dos genes: PRKAR1A, que se asocia con el síndrome de Carney (una enfermedad hereditaria que puede causar tumores y pigmentación de la piel), y TTN, que puede relacionarse con debilidad del músculo cardíaco. Con estos datos —los hallazgos físicos, las imágenes y los genes— se confirmó el diagnóstico de síndrome de Carney con mixoma cardíaco y además cardiomiopatía dilatada (DCM), que significa que el corazón estaba agrandado y no latía con suficiente fuerza.\n\nCon el paso del tiempo, los síntomas empeoraron: el paciente ya no podía estar tumbado boca arriba porque le costaba respirar y tenía signos de insuficiencia cardíaca grave, como hinchazón en las piernas y acumulación de líquido en los pulmones. Las pruebas mostraron una fracción de eyección del ventrículo izquierdo muy baja (23 %) —esto indica que el corazón bombeaba poco— y fibrilación auricular (un ritmo cardíaco irregular). Dado que tenía insuficiencia cardíaca en fase terminal y un mixoma, los médicos consideraron el trasplante de corazón la mejor opción para tratar las dos condiciones a la vez.\n\nUn corazón de donante adecuado estuvo disponible y se realizó el trasplante. En la operación, se retiró el corazón enfermo y se implantó el corazón del donante. Los cirujanos revisaron cuidadosamente las uniones entre vasos y cavidades para evitar sangrado. Se tomaron muestras del tejido retirado y el examen posterior confirmó la cardiomiopatía dilatada y el mixoma.\n\nDespués de la cirugía, el paciente recibió cuidados intensivos: medicamentos para prevenir el rechazo del nuevo corazón (inmunosupresores como prednisona, micofenolato y tacrolimus), antibióticos y fármacos para evitar infecciones fúngicas. En los primeros días había marcadores cardíacos y algunas cifras inflamatorias elevadas, lo cual es esperado tras una cirugía mayor, pero con el tratamiento esos valores bajaron. La ecocardiografía mostró que el nuevo corazón funcionaba bien (fracción de eyección alrededor del 65 %) y no había problemas visibles con las válvulas o la estructura. El paciente se recuperó bien, fue dado de alta y, en los controles posteriores, permaneció en buen estado.\n\nQué significa esto y próximos pasos: el trasplante resolvió tanto la falla del músculo cardíaco como el problema del mixoma. El paciente necesitará controles médicos regulares y tratamiento con medicamentos inmunosupresores de por vida para prevenir el rechazo del órgano. También será importante el seguimiento por genética y para detectar posibles otros problemas relacionados con el síndrome de Carney.\n\nEste caso muestra cómo una enfermedad genética poco frecuente puede afectar al corazón y cómo, en casos graves, el trasplante puede ser una solución que salva la vida. El equipo médico actuó con cuidado durante la cirugía y en el manejo posterior, y el paciente tuvo una buena recuperación.",
+                "fh_score": 50.29
+            },
+            "B3": {
+                "text": "Resumen clínico comprensible y empático\n\nPaciente y presentación\n- Hombre de 38 años con episodios recurrentes de opresión torácica y disnea. Tres años antes ya había presentado síntomas similares; en ese momento una ecocardiografía ambulatoria detectó una masa en el corazón izquierdo compatible con mixoma.\n- La exploración reveló pigmentación cutánea en las orejas (múltiples máculas café/negro). La tomografía abdominal mostró alteraciones hepáticas y pequeños quistes renales. El estudio genético identificó mutaciones en PRKAR1A y TTN.\n- Con esos hallazgos —masa cardiaca, pigmentación cutánea y mutación en PRKAR1A— se confirmó el diagnóstico de complejo de Carney (CNC). La mutación en TTN apoyó la presencia de una miocardiopatía dilatada (DCM).\n\nCómo progresó la enfermedad\n- Tras tratamiento sintomático inicial el paciente mejoró pero rechazó cirugía en ese momento. Más tarde volvió con empeoramiento marcado: ortopnea (incapacidad para permanecer acostado por dificultad respiratoria), ingurgitación yugular, soplo mitral, estertores pulmonares, hepatomegalia y edema periférico.\n- Ecocardiograma: corazón globalmente dilatado, dilatación de seno aórtico y arteria pulmonar, regurgitación mitral leve-moderada y una masa ecogénica de 54 × 43 mm en la aurícula izquierda adherida al septo interauricular. Función sistólica muy reducida: fracción de eyección del ventrículo izquierdo (FEVI) 23,1% (normal ≈55–70%).\n- ECG: fibrilación auricular con respuesta ventricular rápida (≈150 lpm) y ondas Q patológicas en V1–V3.\n- Diagnóstico final antes de cirugía: miocardiopatía dilatada terminal con mixoma cardíaco en el contexto de complejo de Carney.\n\nDecisión terapéutica y cirugía\n- Debido a insuficiencia cardíaca en estadio terminal y a la masa intracardíaca, se consideró el trasplante cardíaco como la opción que podía resolver simultáneamente ambos problemas. Se obtuvo un corazón donante y se realizó trasplante por esternotomía media con técnica bicava/anastomosis habituales.\n- Durante la intervención se extirpó el corazón enfermo; la pieza mostró mixoma mucoide grisáceo. La anatomía y las anastomosis fueron verificadas varias veces sin sangrado significativo.\n- El examen histopatológico confirmó la miocardiopatía dilatada y el mixoma.\n\nEvolución postoperatoria\n- En las primeras 48–72 horas hubo elevación esperable de marcadores (troponina T y NT-proBNP) y leucocitosis, pero buena diuresis. La ecocardiografía temprana mostró FEVI normalizada (≈65%) y grosor de pared ventricular normal, sin alteraciones valvulares.\n- Esquema de inmunosupresión e profilaxis: metilprednisolona intravenosa inicialmente, transición a prednisona oral, micofenolato de mofetilo y, desde el día 7, tacrolimus con control de niveles sanguíneos. Antibióticos y antifúngicos de profilaxis también administrados.\n- Progresivamente los marcadores cardiacos y los síntomas mejoraron; en el control el corazón funcionaba bien, los valores de troponina y NT-proBNP descendieron y el paciente fue dado de alta en buen estado. Seguimientos ambulatorios posteriores mostraron recuperación sostenida.\n\nSignificado clínico y recomendaciones\n- Qué significa el diagnóstico: el complejo de Carney es un síndrome genético (frecuentemente por mutaciones en PRKAR1A) que predispone a mixomas cardíacos, pigmentación cutánea y tumores endocrinos u otras neoplasias. La mutación en TTN está asociada a miocardiopatía dilatada familiar. Ambos hallazgos explican la combinación de tumor cardíaco y fallo ventricular en este paciente.\n- Por qué se eligió el trasplante: el paciente tenía insuficiencia cardíaca avanzada con función ventricular gravemente reducida; el trasplante resolvió la falla mecánica y eliminó la masa tumoral intracardíaca.\n- Qué sigue para el paciente: vigilancia y manejo a largo plazo incluyen\n  - Terapia inmunosupresora de por vida con monitorización de niveles (p. ej., tacrolimus), y vigilancia estrecha para rechazo, infecciones y efectos adversos.\n  - Controles cardiológicos periódicos (ecocardiogramas, marcadores).\n  - Seguimiento por genética y cribado familiar: las mutaciones identificadas justifican consejo genético y estudio de familiares de primer grado.\n  - Vigilancia para otras manifestaciones del CNC (evaluación endocrinológica y cribado para nuevos tumores).\n  - Atención a la adherencia a la medicación y campañas de prevención (vacunación, profilaxis según indicación).\n\nComentario empático final\nEste caso muestra cómo una enfermedad genética poco frecuente puede combinar un tumor cardiaco benigno pero potencialmente peligroso (mixoma) con una miocardiopatía que progresa a insuficiencia terminal. El trasplante permitió recuperar función cardíaca y síntomas, pero impone una nueva etapa de cuidados crónicos y seguimiento multidisciplinario. El equipo clínico y el paciente han logrado una recuperación favorable hasta la última visita de control.",
+                "fh_score": 35.69
+            }
+        }
+    },
+    {
+        "article": "Un paciente de 52 años de edad con un diagnóstico inicial de arteria pulmonar fue admitido en el departamento de cardiología para una evaluación médica y una decisión sobre el tratamiento posterior. El paciente tenía un historial de neumotórax espontáneo del lado derecho, tratado con toracocentesis y drenaje por vacío 35 años antes. El paciente sentía una disnea creciente al hacer ejercicio. También se quejaba de signos de insuficiencia ventricular derecha y cianosis. Cuatro años antes, el paciente fue hospitalizado tres veces por fibrilación auricular paroxística que se convirtió en ritmo sinusal por cardioversión eléctrica, además de que el examen electrocardiográfico era normal.\n\nEn ese mismo año, la angiografía coronaria indicó arterias coronarias normales. La ecocardiografía reveló una hipertensión pulmonar leve con una presión sistólica calculada en el ventrículo derecho de 36 mmHg sin dilatación de ese ventrículo.\n\nEn los años siguientes, se observó insuficiencia cardiaca progresiva con aumento de la presión arterial pulmonar en la ecocardiografía. Se realizó angio-CT en dos ocasiones y se excluyó la hipertensión pulmonar tromboembólica crónica en cada ocasión. La tomografía computarizada de alta resolución excluyó la patología pulmonar intersticial. La espirometría fue normal. La detección de enfermedades autoinmunes y la infección por VIH fue negativa.\n\n\nLínea de tiempo: historia, curso de la enfermedad, diagnóstico y tratamiento\n\n1976  neumotórax derecho\n2007 Hospitalizado tres veces por fibrilación auricular e insuficiencia cardiaca. Se le realizaron ecocardiografías, cardioversiones y coronografías. En cada ocasión, fue dado de alta de los servicios con diagnósticos de fibrilación auricular, insuficiencia cardiaca e insuficiencia cardiaca de clase II de la NYHA.\n2010-2011: Aumento de la falta de aire y síntomas de insuficiencia cardiaca. El paciente fue hospitalizado tres veces. Se detectaron características indirectas de hipertensión pulmonar en ecocardiografía. Se realizó tres veces un examen de tórax por TAC; se excluyó la embolia pulmonar o la hipertensión arterial pulmonar tromboembólica crónica (2 x angio-TAC) o la fibrosis pulmonar (tomografía computarizada de alta resolución).\nSe estableció el diagnóstico de hipertensión pulmonar, clase III de la OMS.\nDEC-2011 Admisión a la clínica de cardiología – ecocardiografía (TTE, TEE), prueba de caminata de 6 minutos, NT-proBNP, cateterización cardiaca derecha, prueba de vasoreactividad pulmonar.\nSe estableció el diagnóstico de hipertensión pulmonar arterial irreversible.\nSe ha iniciado el tratamiento con iloprost y sildenafil\nEn enero de 2012, visita de control: mejora en la clase de la OMS, disminución de la concentración de NT-proBNP e incremento de la distancia en la prueba de 6 minutos.\nMAY-2012. Control RHC. La SaO2 de las muestras de sangre obtenidas durante el RHC de la arteria del lóbulo superior del pulmón derecho fue del 87 %.\nEl diagnóstico angiográfico de las arterias pulmonares reveló fístulas de HAP entre las arterias subclavianas y el lóbulo superior del pulmón derecho.\nJUN 2012  angiografía por TC de las arterias sistémicas reveló la presencia adicional de fístulas arteriales bronquiales en el lóbulo superior de las arterias del pulmón derecho\nIII-2013 Embolización de fístulas\nVI-2013. Muerte como resultado del empeoramiento de la insuficiencia cardiaca, combinado con neumonía.\n\n\n\nEn el ingreso a nuestra clínica, la clase funcional del paciente fue evaluada como OMS III. En el examen físico, el segundo sonido cardiaco (S2) fue acentuado con S2 dividido ensanchado. Además, la auscultación cardiaca indicó un murmullo holosistólico de regurgitación tricuspídea. La auscultación del tórax no mostró un murmullo vascular. La cianosis periférica y central fue marcada. Se examinaron la hepatomegalia, el edema periférico y las venas varicosas bilateralmente.\n\nLa SaO2 obtenida por el método de oximetría de pulso se redujo al 88 %. La electrocardiografía reveló fibrilación auricular, desviación del eje derecho y onda T negativa en las derivaciones precordiales v1-v3. Las pruebas adicionales fueron las siguientes: concentración de NT-proBNP - 3383 pg/ml, distancia de la prueba de caminata de seis minutos - 373 m con 7/10 puntos en la escala de disnea de Borg.\n\nLa ecocardiografía mostró características de hipertensión pulmonar grave: agrandamiento del ventrículo derecho a 44 mm (cuatro cámaras), con función deprimida del TAPSE del ventrículo derecho de 9 mm, agrandamiento del área de la aurícula derecha a 40 cm2, regurgitación tricuspídea grave (++++), aumento del PSVR calculado a 112 mmHg, acortamiento del tiempo de aceleración de la arteria pulmonar a 60 ms y derrame pericárdico leve. No hubo defecto en el tabique interventricular. La ecocardiografía transesofágica tampoco mostró un defecto en el tabique auricular, lo que se confirmó más tarde con angio-TAC.\n\n\nLa SaO2 de la sangre obtenida de la arteria radial se redujo al 87,8%. Se realizó un cateterismo cardiaco derecho. La SaO2 de las muestras de sangre obtenidas durante el RHC de la vena cava superior, la vena cava inferior, la aurícula derecha, el tronco pulmonar, la arteria del lóbulo medio del pulmón derecho y la arteria pulmonar izquierda ascendieron respectivamente a: 64,8%; 77,4%; 73,2%; 70,2%; 69,3%; 71,2% y no indicaron la presencia de un shunt de izquierda a derecha.\n\nLas mediciones hemodinámicas mostraron una hipertensión pulmonar precapilar grave, irreversible en las pruebas de vasoreactividad con óxido nítrico inhalado (80 ppm) y una combinación de sildenafil oral (50 mg) y óxido nítrico inhalado (80 ppm).\n\nEn base a todos los datos clínicos y los resultados de la RHC, se estableció un diagnóstico de hipertensión pulmonar idiopática irreversible.\n\nSe inició el tratamiento con iloprost inhalado (Ventavis) 6 × 5 µg y sildenafil (Revatio) por vía oral 3 × 20 mg. Además, se administraron digoxina (0,1 mg diarios), warfarina (INR rango: 2-3), furosemida (40 mg por vía oral diarios) y espironolactona (100 mg diarios).\n\nUn mes después se realizó un seguimiento no invasivo. El paciente manifestó una mejoría en la capacidad física, clase II según la OMS, concentración de NT-proBNP: 1014 pg/ml. Distancia en la prueba de caminata de seis minutos: 471 m.\n\nCinco meses después se realizó una evaluación invasiva. La RHC mostró valores de PAP más elevados que en las mediciones iniciales [75,4/51,8 (59,7) mm Hg] y PVR (13,4 WU) (Tabla 22 – control RHC).\n\nLa saturación de oxígeno de las muestras de sangre obtenidas durante la RHC de la arteria lobular superior del pulmón derecho fue elevada y ascendió al 89.7%.\n\nEn la angiografía pulmonar se detectó la reducción del trazo vascular periférico típico de la hipertensión arterial pulmonar y la falta de contraste de la arteria del lóbulo superior derecho. Además, se encontró evidencia de flujo sanguíneo retrógrado visible como un contraste negativo en la arteria pulmonar derecha. Después, se realizó una arteriografía de la arteria subclavia derecha y se detectó una enorme malformación vascular que se comunicaba con la arteria del lóbulo superior derecho.\n\nLa angio-TC de las arterias sistémicas confirmó la presencia de las fístulas previamente descritas y reveló la presencia adicional de fístulas de la arteria bronquial en el lóbulo superior de las arterias del pulmón derecho.\n\nSe realizó embolización selectiva de las fístulas (mezcla al 50% de Lipiodol y pegamento monomérico de n-butil-2-cianoacrilato). La embolización no produjo ningún cambio clínico en el estado del paciente.\n\nMH - Fístula arterio-arterial/*complicaciones\nMH - *Cateterización cardiaca\nMH - Angiografía por tomografía computarizada\nMH - Hipertensión pulmonar primaria familiar/*diagnóstico/terapia farmacológica\nMH - Resultado fatal\nMH - Insuficiencia cardiaca/fisiopatología\nMH - Humanos",
+        "gold_summary": "Un paciente caucásico de 52 años de edad con hipertensión pulmonar (HP) confirmada por ecocardiografía fue admitido en el departamento de cardiología debido a disnea de esfuerzo y signos de insuficiencia ventricular derecha. La exploración rutinaria para detectar causas de HP secundaria fue negativa. El cateterismo cardiaco derecho (CCR) confirmó una HP arterial de alto grado [presión arterial pulmonar media (PAPm); 50,6 mmHg, presión de enclavamiento pulmonar (PWP); 11,3 mmHg, resistencia vascular pulmonar (PVR); 11,9 unidades de Wood (UW)] irreversible en la prueba con óxido nítrico inhalado. La saturación de oxígeno (SaO2) de las muestras de sangre obtenidas durante el primer CCR osciló entre 69,3 y 73,2%. Se diagnosticó hipertensión arterial pulmonar idiopática. Se inició el tratamiento con iloprost inhalado y sildenafil.\n\nEl control RHC, realizado 5 meses después, mostró valores de mPAP (59,7 mmHg) y PVR (13,4 WU) más altos en comparación con la medición inicial. El SaO2 de sangre obtenida durante el RHC de la arteria del lóbulo superior del pulmón derecho fue elevado y ascendió al 89,7 %.\n\nLuego se realizó una arteriografía pulmonar. Se encontró falta de contraste en la arteria del lóbulo superior derecho con evidencia de flujo sanguíneo retrógrado visible como contraste negativo en la arteria pulmonar derecha. Después, una arteriografía de la arteria subclavia derecha detectó una enorme malformación vascular que se comunicaba con la arteria del lóbulo superior derecho. Después, un angiograma por tomografía computarizada (angio-CT) reveló adicionalmente el agrandamiento de las arterias bronquiales que se originaban en las fístulas hacia la arteria pulmonar del lóbulo superior derecho.\n\nA pesar del tratamiento farmacológico intensivo, que incluyó la terapia de la hipertensión pulmonar y la embolización percutánea de las fístulas, el estado del paciente siguió deteriorándose. Falleció tres meses después de la embolización debido a una insuficiencia cardiaca grave complicada por neumonía.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Este es el cuento de un hombre de 52 años que tuvo mucha dificultad para respirar y problemas en el lado derecho del corazón.\n\nQué le pasaba\n- Tenía cada vez más falta de aire cuando caminaba o hacía esfuerzos.  \n- Su piel se veía un poco azulada por falta de oxígeno.  \n- El lado derecho del corazón estaba cansado y tenía líquido en el cuerpo (hinchazón).\n\nQué hicieron los médicos\n- Le hicieron muchas pruebas para buscar una causa. No encontraron trombos en los pulmones ni otras enfermedades del pulmón.  \n- Mediante una prueba especial con un catéter en el corazón comprobaron que la presión en las arterias del pulmón era muy alta. Eso se llama hipertensión pulmonar. Es como si las tuberías del pulmón tuvieran mucha presión y el corazón tuviera que esforzarse mucho.  \n- Los médicos pensaron que era una forma sin causa clara (hipertensión arterial pulmonar idiopática). Le dieron medicinas para bajar la presión en los pulmones y ayudar al corazón. Al principio se sintió mejor.\n\nQué encontraron después\n- Más tarde, vieron que la sangre en una parte del pulmón derecho tenía más oxígeno de lo esperado.  \n- Nuevas pruebas de imagen mostraron vasos sanguíneos anormales que conectaban arterias grandes del cuerpo con una arteria del pulmón derecho. Esas conexiones se llaman fístulas. Por allí pasaba sangre de forma equivocada.  \n- Intentaron cerrar esas fístulas con un procedimiento llamado embolización. Esto consiste en introducir material para taponar los vasos anormales.\n\nQué pasó al final\n- Aunque intentaron tratarlo con medicinas y con la embolización, su estado empeoró.  \n- Murió tres meses después por fallo del corazón y una infección en los pulmones.\n\nMensaje final (con cariño)\n- Los médicos hicieron muchas pruebas y trataron de ayudarlo.  \n- A veces, las enfermedades del corazón y de los pulmones son difíciles de curar.  \n- Es triste que este paciente no mejorara, pero su historia ayuda a los médicos a entender mejor estas situaciones para ayudar a otros en el futuro.",
+                "fh_score": 69.5
+            },
+            "B2": {
+                "text": "Here is a clear, gentle summary of the case:\n\nA 52-year-old man developed gradually worsening shortness of breath and signs of right‑sided heart failure. He had a past right lung collapse (pneumothorax) decades earlier and episodes of irregular heartbeat (atrial fibrillation). Over several years doctors ruled out common causes of lung blood‑vessel disease: repeated CT scans excluded chronic blood clots in the lungs and high‑resolution CT showed no lung scarring. Blood tests for autoimmune disease and HIV were negative, and basic lung function tests were normal.\n\nTests and key findings\n- Echocardiograms showed severe pulmonary hypertension (high pressure in the lung arteries) with a large, poorly working right ventricle and severe leakage of the tricuspid valve. He was cyanotic (bluish skin) and had low oxygen levels by pulse oximetry (~88%).\n- Right heart catheterization (RHC), a test that directly measures pressures inside the heart and lung arteries, confirmed very high pulmonary artery pressure and very high vascular resistance. These findings were not improved by inhaled nitric oxide, so the hypertension was judged irreversible.\n  - Initial RHC: mean pulmonary artery pressure about 50.6 mmHg (normal is much lower) and pulmonary vascular resistance 11.9 Wood units (very high).\n  - Five months later: pressures and resistance were even higher (mean pressure ~59.7 mmHg, resistance 13.4 WU).\n- Oxygen measurements from blood samples taken in the heart and lungs were generally low (around 69–73%), but an unusually high oxygen level (about 89.7%) was found in the artery that supplies the right upper lung. A high oxygen level in a pulmonary artery is abnormal and suggested that oxygenated blood from the body’s arteries was entering the pulmonary circulation.\n- Detailed angiography (imaging of blood vessels) showed large abnormal connections (fistulas) between systemic arteries (including the right subclavian artery and enlarged bronchial arteries) and the right upper-lobe pulmonary artery. These are direct vascular shunts that let oxygen-rich blood from the body’s arteries flow into the lung arteries.\n\nDiagnosis and treatment\n- The working diagnosis was idiopathic pulmonary arterial hypertension that had become irreversible. In addition, large systemic-to-pulmonary arterial fistulas were found in the right upper lung.\n- He was started on targeted pulmonary hypertension medications (inhaled iloprost and oral sildenafil) plus standard heart‑failure medicines (digoxin, diuretics, anticoagulation).\n- He initially felt better: after one month his walking distance and heart‑failure blood marker (NT‑proBNP) improved.\n- After the worsening seen on repeat RHC, the fistulas were treated by selective embolization (a minimally invasive procedure that blocks abnormal vessels using glue-like material). The embolization itself did not improve his symptoms.\n\nOutcome\n- Despite medical therapy and embolization, his heart failure progressed. He died three months after the embolization from worsening heart failure complicated by pneumonia.\n\nSimple explanations of a few terms\n- Pulmonary hypertension: high blood pressure inside the arteries that carry blood through the lungs; this makes the right side of the heart work harder and can lead to heart failure.\n- Right heart catheterization (RHC): a test where thin tubes measure pressures and oxygen levels inside the heart and lung arteries; it gives exact information about how severe the problem is.\n- Fistula: an abnormal connection between two blood vessels; here, arteries that normally belong to the systemic circulation were directly connected to lung arteries.\n- Embolization: a procedure to block an abnormal blood vessel to stop unwanted blood flow.\n\nOverall message\nThis was a complex case of severe pulmonary arterial hypertension that was made worse by hidden abnormal blood vessel connections in the right upper lung. Even with advanced medications and a targeted procedure to block the abnormal vessels, the disease progressed and the patient died. The case highlights how rare vascular abnormalities can complicate pulmonary hypertension and how difficult some forms of this disease are to treat. My condolences to the patient’s family — this was a serious, heartbreaking illness.",
+                "fh_score": 75.98
+            },
+            "B3": {
+                "text": "Resumen clínico breve y comprensible\n\nPaciente varón caucásico de 52 años con disnea progresiva al esfuerzo, cianosis y signos de insuficiencia ventricular derecha. Antecedentes relevantes: neumotórax espontáneo derecho hace 35 años y episodios previos de fibrilación auricular que precisaron cardioversión.\n\nPresentación y hallazgos iniciales\n- Clase funcional OMS III a la admisión; SaO2 por pulsioximetría ≈ 88 % (hipoxemia).\n- Exploración: acentuación del segundo ruido cardiaco, soplo holosistólico por insuficiencia tricuspídea severa, hepatomegalia y edemas periféricos.\n- Ecocardiografía: hipertensión pulmonar grave con ventrículo derecho dilatado (44 mm), función sistólica derecha deprimida (TAPSE 9 mm), aurícula derecha aumentada (40 cm2), insuficiencia tricuspídea cuantiosa y PAsistólica estimada elevada (PSVR ≈ 112 mmHg). Pequeño derrame pericárdico.\n- Analítica: NT‑proBNP elevado 3.383 pg/ml (marcador de sobrecarga cardiaca). Prueba de caminata de 6 minutos: 373 m.\n\nInvestigaciones diagnósticas\n- Estudios para causas secundarias de hipertensión pulmonar (embolia crónica, enfermedad pulmonar intersticial, autoinmunidad, VIH) fueron negativos.\n- Cateterismo cardiaco derecho (RHC) inicial confirmó hipertensión pulmonar precapilar severa: presión arterial pulmonar media (mPAP) ≈ 50,6 mmHg, presión de enclavamiento pulmonar 11,3 mmHg, resistencia vascular pulmonar (PVR) ≈ 11,9 Wood units. Prueba de vasorreactividad negativa → lesión vascular irreversible.\n- Saturaciones durante el primer RHC no mostraron shunt izquierda‑derecha.\n- Tras tratamiento médico hubo mejoría clínica y biomarcadores a 1 mes (NT‑proBNP descendió a 1.014 pg/ml; 6MWD aumentó a 471 m).\n- A los 5 meses, RHC de control mostró empeoramiento hemodinámico (mPAP ≈ 59,7 mmHg, PVR 13,4 WU). Llama la atención una saturación anormalmente alta (≈ 89,7 %) en la arteria lobar superior derecha.\n- Arteriografía y angio‑TAC sistémica demostraron fístulas arteriales sistémico → pulmonar: una gran malformación entre la arteria subclavia derecha y la arteria del lóbulo superior derecho, además de fístulas de arterias bronquiales hacia la misma arteria pulmonar.\n\nDiagnóstico y tratamiento\n- Diagnóstico final: hipertensión arterial pulmonar de alto grado inicialmente catalogada como idiopática/irrevocable, sobreañadida a una malformación arteriovenosa/arterio‑arterial sistémico → pulmonar en el lóbulo superior derecho.\n- Terapia médica para hipertensión pulmonar iniciada: iloprost inhalado (6 × 5 µg) y sildenafil oral (3 × 20 mg); además digoxina, anticoagulación con warfarina, furosemida y espironolactona.\n- Se realizó embolización selectiva de las fístulas con mezcla 50 % Lipiodol y adhesivo (n‑butil‑2‑cianoacrilato). La embolización no produjo mejoría clínica evidente.\n\nEvolución y desenlace\n- Pese al tratamiento médico y a la embolización, el paciente continuó deteriorándose y falleció tres meses después de la embolización por insuficiencia cardiaca descompensada complicada con neumonía.\n\nInterpretación y puntos clave para clínicos y pacientes\n- El paciente presentó hipertensión pulmonar precapilar severa e irreversible con repercusión derecha importante. Aunque inicialmente se clasificó como idiopática, las imágenes y la elevada saturación localizada en la arteria lobar superior derecha revelaron fístulas sistémico → pulmonar que pueden haber contribuido o agravado la hipertensión y la sobrecarga derecha.\n- Las fístulas arteriales sistémico → pulmonar (incluidas malformaciones de arteria bronquial o conexión desde la subclavia) pueden introducir flujo arterial sistémico en la circulación pulmonar, alterar las saturaciones y aumentar la carga hemodinámica. Su detección requiere alto índice de sospecha y estudios angiográficos dirigidos.\n- La prueba de vasorreactividad negativa y las cifras de PVR altas indicaron daño vascular establecido, lo que limita la reversibilidad con vasodilatadores. La embolización puede ser una opción, pero no siempre revierte la insuficiencia cardiaca si la hipertensión y la remodelación vascular están avanzadas.\n- En pacientes con hipertensión pulmonar severa y hallazgos discordantes de saturación o ausencia de contraste en un segmento pulmonar, es razonable investigar fístulas arteriales sistémicas mediante angio‑TAC/arteriografía sistémica lo antes posible, porque su cierre precoz podría modificar el curso en algunos casos.\n\nEmpatía\nEste caso ilustra la complejidad de la hipertensión pulmonar avanzada y cómo una malformación vascular poco frecuente puede complicar el diagnóstico y el tratamiento. A pesar de los esfuerzos terapéuticos, la enfermedad puede progresar rápidamente; el enfoque multidisciplinario precoz y la exploración angiográfica dirigida son importantes cuando aparece evidencia clínica o radiológica sugestiva de comunicaciones vasculares anómalas.",
+                "fh_score": 31.98
+            }
+        }
+    },
+    {
+        "article": "Paciente de 73 años, diagnosticada de enfermedad pulmonar obstructiva crónica (EPOC), hipertensión arterial (HTA), trastorno bipolar, ansiedad, depresión, hipotiroidismo y artritis reumatoide, condiciones para las cuales tiene prescrito el tratamiento reflejado en el Anexo I.\n\nRealiza una llamada telefónica a la farmacia comunitaria para solicitar información sobre una nueva medicación prescrita para el tratamiento de una infección de orina y un déficit de vitamina D, diagnosticados tras la realización de una analítica completa en el servicio de urgencias de un hospital privado.\n\nLa paciente es totalmente dependiente y no sale de casa, siendo su cuidadora la persona que siempre va a retirar su medicación y elabora los pastilleros semanales.\n\nLos fármacos prescritos para el tratamiento de la infección de orina fueron cefuroxima 250 mg (1 comprimido cada 12 horas durante 5 días) y butilescopolamina 10 mg (1 comprimido en la mañana si presentaba molestias).\n\nPara el déficit de vitamina D se le prescribió colecalciferol 50.000 U.I. (1 cápsula una vez al mes durante dos meses) y colecalciferol 25.000 UI (1 cápsula una vez al mes tras finalizar el envase de 50.000 U.I.).\n\nESTUDIO Y EVALUACIÓN\nSe lleva a cabo el servicio de dispensación (SD) sin incidencias, siguiendo la metodología expuesta en la Guía práctica para los Servicios Profesionales Farmacéuticos Asistenciales en la Farmacia Comunitaria. Posteriormente, la paciente contacta con la farmacia comunitaria, preocupada porque la nueva medicación le ha generado confusión, ya que ella tomaba unas cápsulas naranjas para su déficit de vitamina D prescritas por su médico de Atención Primaria hace unos meses y en la parte del informe de urgencias en la que figura el tratamiento venía reflejado una medicación nueva para ese mismo problema de salud. Además, coincidió con que su cuidadora habitual ya no podrá trabajar más con ella y no la podrá ayudar con su medicación. Por ello, se le propone a la paciente el servicio de Revisión del Uso del Medicamento (RUM) con el objetivo de evaluar el grado de conocimiento que tienen la paciente con respecto a sus patologías y su tratamiento, a la par que poder resolver posibles errores en la administración de los distintos fármacos que forman parte del mismo. Se le explica en qué consiste todo el procedimiento y decide aceptar.\n\nTras esto, se procedió a citar a la cuidadora en la farmacia con la tarjeta sanitaria de la paciente, su bolsa de medicación para hacer una revisión exhaustiva de su botiquín y el último informe de urgencias con el objetivo de recopilar toda la información necesaria para realizar el servicio asistencial vía telefónica. Durante la llamada con la paciente, se procede a cumplimentar el formulario RUM, el cual se volcó posteriormente en la plataforma SEFAC e_XPERT ®. Además, para poder evaluar correctamente todo el tratamiento farmacológico, se emplearon herramientas como el CIMA (donde se consultaron las fichas técnicas de los medicamentos) y el BotPlus (donde se consultaron las posibles interacciones farmacológicas).\n\nINTERVENCIÓN\nTras la primera toma de contacto a través de la entrevista telefónica y hacer revisión del botiquín, se pudo detectar que la paciente y su cuidadora no estaban haciendo una gestión apropiada de la medicación. Tras la revisión de su botiquín, se hallaron envases caducados y con anotaciones erróneas sobre su uso, blísteres con comprimidos partidos que no deberían de estarlo y acúmulo de varios envases de un mismo fármaco. Al tratarse de una paciente dependiente, polimedicada y con problemas para gestionar correctamente su tratamiento antes y durante la ausencia de su cuidadora habitual se decidió con el fin de garantizar la seguridad farmacoterapéutica y mejorar la adherencia al tratamiento derivar al servicio de sistema personalizado de dosificación (SPD). A través de la plataforma de SEFAC e_XPERT ® se procedió a redactar un informe de derivación a su médico de Atención Primaria (MAP) del Sistema Nacional de Salud (SNS) (ver Anexo II), donde se detallaba la inclusión de la paciente en el servicio de Revisión del Uso de la Medicación y su posterior derivación al servicio de SPD. Además, quedaron recogidas las siguientes propuestas de intervención:\n\nRevisión de la pauta posológica de tramadol 50 mg de liberación retardada por la existencia de un posible error en la prescripción.\n\nRevisión del tratamiento prescrito para el déficit de vitamina D por la existencia de una duplicidad terapéutica.\n\nCambio del absorbente de incontinencia de tipo pants a elástico alegando la situación de dependencia de la paciente y las dificultades para realizar una correcta colocación por parte de la cuidadora al pasar encamada la mayor parte del tiempo. Se aportaron los Códigos Nacionales (CN) correspondientes.\n\nRevisión del tratamiento para la EPOC por dificultades de empleo del inhalador y falta de adherencia terapéutica.\n\nRESULTADOS\nDurante la cita médica, la médico de atención primaria recibe el informe de derivación entregado a la cuidadora donde, además, se solicita contacto con la farmacia comunitaria para poder iniciar de forma correcta el servicio de SPD. Tras hablar con ella vía telefónica, se realizaron los siguientes cambios en su tratamiento:\n\nDéficit de vitamina D: anulación de calcifediol y sustitución por colecalciferol prescrito en el Servicio de Urgencias.\n\nArtritis reumatoide: modificación de pauta de tramadol de liberación prolongada a 1-0-1 y empleo de paracetamol 1000 mg 1-1-1 si precisa.\n\nIncontinencia urinaria: sustitución de absorbente tipo pants por elástico.\n\nEPOC: no se realizó un cambio de tratamiento. La médico de atención primaria consideró oportuno llevar a cabo una supervisión diaria por parte de la cuidadora en cada una de las tomas del inhalador.",
+        "gold_summary": "Paciente 73 años, dependiente, polimedicada y pluripatológica contacta telefónicamente con la farmacia comunitaria para solicitar información sobre un tratamiento de nueva prescripción para una infección de orina y un déficit de vitamina D. La dispensación de la medicación a su cuidadora deriva en mayores dudas a la paciente, por lo que se le ofrece el servicio de revisión del uso del medicamento (RUM). Durante la prestación del servicio se detectan varias incidencias en su tratamiento, por lo que se decide realizar un informe de derivación al médico de atención primaria para una revisión completa del tratamiento y poder así derivar a la paciente al servicio de Sistema Personalizado de Dosificación (SPD) con el fin de garantizar la seguridad farmacoterapéutica de la paciente y mejorar su adherencia al tratamiento.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "La señora tiene 73 años y muchas enfermedades. No puede salir de casa. Su cuidadora siempre le daba las medicinas, pero ahora ya no podrá ayudarla.\n\nFue al servicio de urgencias por una infección de orina y le dijeron que tiene falta de vitamina D (una vitamina que ayuda a los huesos). Le dieron medicinas nuevas. La paciente y su cuidadora se confundieron con las pastillas.\n\nLa farmacia ofreció revisar todas sus medicinas. Encontraron problemas: algunos envases estaban caducados, había notas equivocadas, pastillas partidas y medicinas repetidas. La paciente toma muchos medicamentos y tiene dificultad para organizarlos sola.\n\nLa farmacia habló con la doctora de su centro de salud y pidió cambiar y coordinar tratamientos. Hicieron estos cambios:\n- Quitaron una de las medicinas de vitamina D y dejaron la que le dio urgencias.\n- Cambiaron la forma de tomar el medicamento para el dolor.\n- Pusieron paracetamol (si necesita) para dolor leve.\n- Cambiaron el tipo de protector para la incontinencia por otro más fácil de poner.\n- Para el inhalador del pulmón, la doctora pidió que la cuidadora supervise cada toma.\n\nTambién la enviaron al servicio de Sistema Personalizado de Dosificación (SPD). En ese servicio la farmacia prepara las pastillas en pastilleros por días y tomas. Así es más fácil y seguro tomar las medicinas correctas.\n\nTodo esto se hizo para que la señora tome sus medicinas bien y no haya errores. La doctora y la farmacia hablaron para ayudarla.",
+                "fh_score": 67.16
+            },
+            "B2": {
+                "text": "Resumen claro y amable\n\nUna mujer de 73 años, con varias enfermedades crónicas (como EPOC —problemas para respirar—, hipertensión, artritis reumatoide y otras) vive completamente dependiente y recibe ayuda de una cuidadora para sus medicinas. Tras una analítica en urgencias le recetaron tratamiento para una infección de orina (cefuroxima y un antiespasmódico) y suplementos de vitamina D (colecalciferol). La paciente se puso confusa porque ya tomaba otras cápsulas para la vitamina D y su cuidadora habitual dejó de poder ayudarla.\n\nQué hizo la farmacia\n- La farmacia ofreció un servicio llamado Revisión del Uso del Medicamento (RUM): es una entrevista y revisión para ver si la persona entiende sus medicinas y si hay problemas que puedan causar errores.\n- La cuidadora llevó la bolsa con todos los envases y la tarjeta sanitaria; la farmacia revisó los medicamentos y habló con la paciente por teléfono.\n- Encontraron varios problemas: envases caducados, instrucciones equivocadas, pastillas partido que no deberían partirse y duplicidad de medicamentos (más de un envase para la misma cosa).\n\nProblemas detectados y propuestas\n- Duplicidad en el tratamiento de la vitamina D (dos medicamentos para lo mismo).\n- Posible error o necesidad de revisar la dosis de tramadol (analgésico para el dolor).\n- Dificultad para poner los absorbentes de incontinencia tipo “pants” debido a que la paciente está encamada; propusieron cambiar a absorbentes elásticos más fáciles de poner.\n- Problemas con el uso del inhalador para la EPOC y falta de supervisión para garantizar que lo use correctamente.\n\nAcciones con el médico y resultados\n- La farmacia envió un informe al médico de Atención Primaria y propuso incluir a la paciente en un servicio llamado Sistema Personalizado de Dosificación (SPD). SPD significa que los medicamentos se organizan en pastilleros por día y hora para evitar errores y mejorar el cumplimiento.\n- El médico aceptó las recomendaciones: anuló un medicamento duplicado para la vitamina D y dejó el colecalciferol recetado en urgencias; cambió la pauta del tramadol (ahora 1-0-1, es decir una dosis por la mañana y otra por la noche) y recomendó paracetamol si hace falta; sustituyó los absorbentes por otros elásticos; y decidió no cambiar la medicación de la EPOC pero pidió que la cuidadora supervise cada uso del inhalador.\n\nPor qué es importante\nEstas acciones ayudan a reducir la confusión, evitar errores en la medicación y mejorar la seguridad de la paciente. El SPD y la supervisión diaria del inhalador buscan que la mujer reciba las medicinas correctas en el momento correcto, lo que es especialmente importante cuando depende de otros para su cuidado.",
+                "fh_score": 44.14
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel universitario, lectura B3)\n\nPaciente: mujer de 73 años, totalmente dependiente, polimedicada y con múltiples patologías crónicas: EPOC, hipertensión, trastorno bipolar, ansiedad, depresión, hipotiroidismo y artritis reumatoide. Vive en casa y su cuidadora habitual gestionaba la medicación; la cuidadora ha comunicado que dejará de prestar cuidados, lo que aumenta el riesgo sobre el manejo de fármacos.\n\nMotivo de contacto: la paciente llamó a la farmacia preocupada por confusión tras una receta nueva emitida en urgencias para una infección urinaria y un déficit de vitamina D. Ella recordaba cápsulas naranjas previas para vitamina D prescritas por su médico de Atención Primaria, y el informe de urgencias parecía duplicar ese tratamiento. Aceptó una Revisión del Uso del Medicamento (RUM).\n\nQué hizo la farmacia\n- Servicio de dispensación realizado sin incidencias iniciales.  \n- Se ofreció y realizó una RUM: entrevista telefónica con la paciente, revisión del botiquín (con la cuidadora en farmacia) y consulta de bases de datos (CIMA, BotPlus) para fichas técnicas e interacciones.  \n- Se detectaron problemas de gestión de la medicación: envases caducados, anotaciones erróneas, comprimidos partidos que no deberían partirse y duplicidad/acumulación de envases de un mismo fármaco.\n\nProblemas clínicos detectados (anormales)\n- Duplicidad en el tratamiento para déficit de vitamina D (medicación previa de Atención Primaria y nueva prescripción de urgencias). Esto incrementa riesgo teórico de sobredosificación y efectos adversos (p. ej., hipercalcemia).  \n- Posible error en la pauta de tramadol de liberación prolongada (riesgo de dosis inadecuada, efectos adversos y posibles interacciones con los psicofármacos de la paciente).  \n- Dificultades prácticas para el manejo del absorbente tipo pants por dependencia de la paciente (problemas en colocación y confort).  \n- Problemas de manejo y adherencia del tratamiento inhalatorio para EPOC por dificultades con el inhalador.\n\nIntervenciones realizadas\n- Elaboración y envío de un informe de derivación al médico de Atención Primaria solicitando revisión y propuesta de inclusión en el Servicio Personalizado de Dosificación (SPD; blísteres preparados por dosis).  \n- Propuestas concretas a AP: revisar tramadol, corregir duplicidad de vitamina D, cambiar tipo de absorbente y revisar EPOC/inhalador.  \n- Plan de derivación al SPD para mejorar seguridad y adherencia dada la dependencia y polimedicación.\n\nResultados tras contacto con el médico de Atención Primaria\n- Vitamina D: anulación de calcifediol y sustitución por colecalciferol recetado en urgencias (eliminó la duplicidad).  \n- Artritis y dolor: modificación de tramadol de liberación prolongada a pauta 1-0-1 (mañana-noche) y recomendación de paracetamol 1 g hasta tres veces al día si precisa.  \n- Incontinencia: cambio de absorbente tipo pants por absorbente elástico (más fácil de colocar en paciente dependiente).  \n- EPOC: no se cambió la medicación, pero se estableció que la cuidadora supervise diariamente la administración del inhalador para mejorar adherencia y técnica.  \n- Se acordó iniciar el proceso para el SPD contactando farmacia y AP.\n\nImplicaciones y siguientes pasos recomendados\n- Inicio del SPD para centralizar y simplificar tomas: expectable mejora de seguridad (evitar dosis erróneas, duplicidades) y adherencia.  \n- Monitorizar los niveles clínicos y efectos adversos: vigilar síntomas de hipercalcemia tras ajuste de vitamina D (aunque la duplicidad fue corregida), evaluar eficacia y tolerancia del nuevo esquema de tramadol/paracetamol, y controlar efectos sobre el ánimo dado el historial psiquiátrico.  \n- Formación y coordinación: instruir a la nueva cuidadora (o redes de apoyo) sobre el SPD, supervisión del inhalador y señales de alarma (sueño excesivo, confusión, signos de hipercalcemia, empeoramiento respiratorio).  \n- Seguimiento farmacéutico periódico (RUM o consulta en farmacia) para revisar adherencia, interacciones y necesidad de ajustes.\n\nMensaje final (empatía)\nLa intervención farmacéutica detectó problemas prácticos y clínicos que aumentaban el riesgo para esta paciente dependiente. Las correcciones acordadas con el médico (eliminación de duplicidad de vitamina D, ajuste del analgesia, cambio de absorbente y supervisión del inhalador) y la derivación al SPD son medidas concretas que reducen riesgos y facilitan la gestión diaria. Es importante mantener seguimiento cercano mientras se incorpora a un nuevo cuidador y se inicia el SPD.",
+                "fh_score": 39.66
+            }
+        }
+    },
+    {
+        "article": "Nuestra paciente era una mujer japonesa de 83 años con insuficiencia cardiaca crónica (fracción de eyección: aproximadamente 30 %) que inició un tratamiento con empagliflozina 10 mg diarios unos 8 meses antes de su ingreso. Nunca se le había diagnosticado diabetes mellitus (HbA1c 5.9 % antes de iniciar el tratamiento con empagliflozina). Unos 6 meses antes de su ingreso, su tratamiento se cambió a dapagliflozina 5 mg. Sus diuréticos y otros medicamentos cardiacos no se ajustaron durante ese tiempo. Dos semanas antes de su ingreso, tropezó y cayó, sufriendo fracturas vertebrales y de costillas. La paciente se debilitó significativamente por el dolor de las fracturas, lo que le causó dificultad para caminar y anorexia. Solo podía comer el 50-70 % de su ingesta dietética habitual. Esto empeoró en la semana siguiente, cuando también desarrolló náuseas y vómitos y redujo aún más su ingesta de alimentos a solo el 10-20 % de la cantidad habitual. Durante este período, continuó tomando dapagliflozina. Fue ingresada en el hospital.\nAl ingreso, la paciente estaba consciente con una temperatura corporal de 37.4°C, presión arterial de 124/68 mmHg, frecuencia cardiaca de 91 bpm y saturación de oxígeno de 98% en aire ambiente. Los análisis de sangre revelaron un nivel de glucosa en sangre de 124 mg/dL, pH de 7.3, concentración de HCO3– de 14 mmol/L, exceso de base de -10 mEq/L, brecha aniónica de 20 mEq/L y concentración de b-hidroxibutirato de 5150 umol/L (Tabla 1). Estos hallazgos fueron consistentes con el diagnóstico de cetoacidosis normoglucémica. La paciente no tenía antecedentes de consumo de alcohol, tabaquismo o uso de drogas.\nSe descartaron otras causas de acidosis con alto déficit aniónico. Su nivel de péptido C era coherente con los niveles de glucosa en sangre en el ingreso, lo que indicaba que tenía una secreción de insulina adecuada; por lo tanto, no se inició la administración de insulina. Se interrumpió el uso de inhibidores de SGLT2 y la paciente se trató inicialmente con solución salina isotónica y una infusión de mantenimiento de aproximadamente 170 g de glucosa diarios.\nA pesar de no haber iniciado la insulina, su pH (7.418), concentración de HCO3– (20.7 mmol/L) y brecha aniónica (13.3 mEq/L) mejoraron al día siguiente de su ingreso. Se inició la dieta Carb 60, pero se continuaron las infusiones intravenosas de glucosa porque la ingesta de alimentos de la paciente era escasa. La cantidad de infusión de glucosa administrada se ajustó según su ingesta de alimentos. En el cuarto día de hospitalización, las cetonas urinarias desaparecieron.\nLa infusión de glucosa se interrumpió el día 12 de la hospitalización, una vez que el paciente pudo comer comidas completas. Aunque el nivel de glucosa en sangre del paciente estaba dentro del rango normal, la excreción de glucosa en la orina fue de 3+ (>500 mg/dL) durante 8 días después de la última dosis de dapagliflozina.\nAl ingreso, la paciente no podía caminar debido al dolor de la fractura, la fatiga general y el síndrome de desuso, pero después de la rehabilitación pudo hacerlo de forma independiente. Fue dada de alta el día 19 de hospitalización, tras someterse a rehabilitación.\nLos inhibidores de SGLT2 no se reiniciaron.\n\nMH - Humanos\nMH - Mujer\nMH - *Insuficiencia cardiaca/inducida químicamente\nMH - *Inhibidores del transportador de glucosa y sodio 2/efectos adversos\nMH - Edad 80 años y más\nMH - Cetosis/químicamente inducida\nMH - glucósidos/efectos adversos\nMH - Cetoacidosis diabética/inducida químicamente\n",
+        "gold_summary": "A continuación, describimos un caso de cetoacidosis en una mujer japonesa de 83 años sin diabetes a la que se le administraron inhibidores de SGLT2 para la insuficiencia cardiaca (fracción de eyección: aproximadamente 30 %). Dos semanas antes de su ingreso, había sufrido una fractura vertebral y una fractura de costilla debido a una caída, a la que siguió una anorexia, pero continuó tomando inhibidores de SGLT2. En el momento del ingreso, los resultados de los análisis de sangre revelaron un nivel de glucosa en sangre de 124 mg/dL, un nivel de hemoglobina A1C del 5,9 %, un pH de 7,329, una concentración de HCO₃⁻ de 14,3 mmol/L y una concentración de β-hidroxibutirato de 5150 μmol/L, lo que condujo a un diagnóstico de cetoacidosis euglucémica. El nivel de péptido C de la paciente coincidía con los niveles de glucosa en sangre en el momento del ingreso, lo que indicaba que tenía una secreción de insulina adecuada. La paciente fue tratada únicamente con administración de glucosa sin insulina y fue dada de alta tras la interrupción del inhibidor de SGLT2.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Esta es la historia de una mujer japonesa de 83 años. Tenía enfermedad del corazón y tomaba un medicamento llamado inhibidor de SGLT2. Este medicamento ayuda al corazón y hace que el riñón saque azúcar en la orina. Ella no tenía diabetes (su HbA1c fue 5,9 % antes de empezar el medicamento).\n\nHace poco se cayó y se rompió una vértebra y algunas costillas. El dolor le quitó las ganas de comer. Cada vez comía menos. Igual siguió tomando el medicamento.\n\nCuando llegó al hospital estaba consciente pero débil. Su azúcar en sangre estaba casi normal (124 mg/dL). Aun así, su sangre estaba demasiado ácida porque su cuerpo había hecho muchas cetonas. Las cetonas son unas sustancias que el cuerpo usa cuando no recibe comida suficiente. Esto se llama cetoacidosis, y en su caso la azúcar estaba casi normal, por eso se llama “cetoacidosis con azúcar normal”.\n\nLos médicos pararon el medicamento SGLT2. No le pusieron insulina porque su cuerpo todavía fabricaba algo de insulina. Le dieron líquidos y azúcar por vía intravenosa para que su cuerpo dejara de hacer cetonas. Al día siguiente su sangre empezó a mejorar. Después de algunos días las cetonas desaparecieron. Aunque su azúcar en sangre estaba normal, su orina siguió mostrando azúcar durante varios días.\n\nHizo rehabilitación para poder caminar otra vez. Mejoró y salió del hospital el día 19. No le volvieron a dar el medicamento SGLT2.",
+                "fh_score": 73.39
+            },
+            "B2": {
+                "text": "Resumen sencillo y amable\n\nPresentamos el caso de una mujer japonesa de 83 años con insuficiencia cardiaca que recibía un medicamento llamado inhibidor de SGLT2 (se cambió de empagliflozina a dapagliflozina). Estos fármacos se usan para el corazón y también en la diabetes, pero esta paciente no tenía diabetes (su HbA1c antes del tratamiento era 5,9 %, un valor normal).\n\nDos semanas antes de ir al hospital, se cayó y se fracturó la columna y varias costillas. El dolor la dejó muy débil y comió mucho menos de lo habitual; luego empezó con náuseas y vómitos y llegó a comer solo el 10–20 % de lo normal. Durante ese tiempo siguió tomando dapagliflozina.\n\nAl ingresar, tenía la glucosa en sangre casi normal (124 mg/dL) pero presentaba acidosis metabólica (pH bajo y bicarbonato bajo) y niveles muy altos de una cetona llamada β-hidroxibutirato (5150 µmol/L). Esto llevó al diagnóstico de cetoacidosis euglucémica: es cetoacidosis (acumulación de ácidos llamados cetonas) que ocurre con glucosa en sangre normal o solo ligeramente elevada. El péptido C, una medida que refleja si el cuerpo produce insulina, estaba acorde con su glucosa, lo que sugiere que no tenía falta importante de insulina.\n\nTratamiento y evolución\n- Se suspendió el inhibidor de SGLT2.  \n- No se administró insulina porque la secreción de insulina no parecía insuficiente.  \n- Se le dio suero y una infusión de glucosa para corregir el problema y prevenir más formación de cetonas mientras no comía bien.  \n- Los cuerpos cetónicos en orina desaparecieron al cuarto día.  \n- La infusión de glucosa se retiró al día 12, cuando la paciente volvió a comer normalmente.  \n- Aunque su glucosa en sangre fue normal, la orina mostró glucosa alta durante 8 días después de la última dosis de dapagliflozina (esto puede pasar porque el fármaco actúa varios días).  \n- Tras rehabilitación por las fracturas y la debilidad, pudo caminar y fue dada de alta el día 19. El medicamento SGLT2 no se reanudó.\n\nMensaje importante (explicado con calma)\nLos inhibidores de SGLT2 pueden, en casos raros, provocar cetoacidosis incluso en personas sin diabetes, sobre todo si están enfermas, comen muy poco o tienen estrés físico (como fracturas). Si alguien que toma estos fármacos deja de comer, tiene vómitos o está muy debilitado, es importante que los profesionales de la salud consideren suspender el medicamento y tratar con líquidos y glucosa.",
+                "fh_score": 59.51
+            },
+            "B3": {
+                "text": "Resumen del caso\nUna mujer japonesa de 83 años con insuficiencia cardiaca (fracción de eyección ~30 %) que no tenía diabetes diagnosticada (HbA1c 5,9 %) estaba recibiendo inhibidores de SGLT2 para su insuficiencia cardiaca: empagliflozina 10 mg durante unos 8 meses y, desde 6 meses antes del ingreso, dapagliflozina 5 mg. Dos semanas antes de la hospitalización sufrió una caída con fracturas vertebrales y costales; el dolor y las náuseas la dejaron con apetito muy reducido (10–70 % de lo habitual) durante días, pero continuó tomando dapagliflozina. Fue ingresada por debilidad progresiva.\n\nHallazgos principales (normales vs anormales)\n- Signos vitales: estables en admisión (temperatura 37.4 °C, PA 124/68 mmHg, FC 91 lpm, Sat O2 98 %).  \n- Glucemia: 124 mg/dL (normal).  \n- Metabólicos: pH 7,30 (acidemia), HCO3– 14 mmol/L (bajo), exceso de base –10 mEq/L, brecha aniónica 20 mEq/L (elevada).  \n- Cetosis: β-hidroxibutirato 5.150 μmol/L (marcadamente elevado) → diagnóstico de cetoacidosis normoglucémica (euglucémica).  \n- Péptido C: coherente con la glucemia de ingreso, indicando secreción de insulina endógena adecuada.  \n- Historia: sin consumo de alcohol ni drogas; se descartaron otras causas de acidosis aniónica elevada.\n\nTratamiento y evolución\n- Se interrumpió el inhibidor de SGLT2.  \n- Recibió solución salina isotónica y una perfusión de glucosa de mantenimiento (≈170 g/día), ajustada según la ingesta oral. No se administró insulina debido a la evidencia de secreción de insulina adecuada.  \n- Mejoría rápida: al día siguiente pH 7,418, HCO3– 20,7 mmol/L, brecha aniónica 13,3 mEq/L.  \n- Dieta Carb 60 iniciada; las perfusiones de glucosa continuaron hasta que pudo alimentarse por completo. Las cetonas urinarias desaparecieron en el día 4.  \n- La glucosuria persistió (3+ en tira >500 mg/dL) durante 8 días después de la última dosis de dapagliflozina.  \n- Rehabilitación mejoró la movilidad; alta al día 19. No se reiniciaron los inhibidores de SGLT2.\n\nImplicaciones clínicas y recomendaciones prácticas\n- Los inhibidores de SGLT2 pueden provocar cetoacidosis euglucémica incluso en pacientes sin diabetes, sobre todo en situaciones de ingesta reducida, estrés agudo, enfermedad o tras un traumatismo.  \n- Signos de alerta: náuseas/vómitos, anorexia, fatiga y dolor con cetonas elevadas aunque la glucosa esté normal o ligeramente elevada.  \n- Manejo apropiado incluye suspender el SGLT2, corregir la volemia, aportar glucosa (para frenar la cetogénesis) y monitorizar cetonas, electrólitos y equilibrio ácido-base. La insulina puede no ser necesaria si hay secreción endógena suficiente, pero la decisión debe basarse en la evaluación clínica y de laboratorio.  \n- La glucosuria puede persistir días después de suspender el fármaco, por lo que no excluirá la responsabilidad del SGLT2.  \n- Prevención: evitar o suspender inhibidores de SGLT2 durante periodos de ayuno, enfermedad aguda, cirugía o trauma; educar al paciente y cuidadores sobre señales de alarma y cuándo buscar atención.\n\nTono y resultado\nLa paciente respondió bien al tratamiento conservador (fluido y glucosa), recuperó la capacidad de caminar con rehabilitación y fue dada de alta sin reiniciar los inhibidores de SGLT2. Este caso subraya la necesidad de precaución al usar SGLT2 en personas mayores o en quienes pueden presentar pérdida de ingesta o estrés fisiológico.",
+                "fh_score": 52.89
+            }
+        }
+    },
+    {
+        "article": "Una recién nacida fue evaluada en la sala de neonatos poco tiempo después del parto debido a la presencia de extensas lesiones similares a cicatrices en sus flancos y muslos superiores. La bebé, nacida de una madre asiática de 28 años a las 39 semanas de gestación, formaba parte de un embarazo gemelar espontáneo. Su madre, que ya había tenido cinco hijos, había tenido un aborto espontáneo en el primer trimestre durante su segundo embarazo.\n\nLos padres eran primos hermanos y no habían tenido problemas de salud en sus tres hijos vivos. La ecografía a las 13 semanas confirmó un embarazo bicorial y diacítico y la ausencia de actividad cardíaca en uno de los gemelos. Las ecografías posteriores mostraron un feto que se desarrollaba con normalidad junto a un gemelo no viable.\n\nDurante el embarazo, la madre no informó sobre el uso de medicamentos o síntomas como fiebre y erupción cutánea. Dio negativo para estreptococo del grupo B y fue admitida en el departamento de urgencias obstétricas con dolores de parto. La niña fue entregada por vía vaginal, pesando 2,83 kg, y fue vigorosa al nacer. A la placenta se le unió un remanente fetal no viable comprimido que medía 6 × 2 cm. La placenta pesaba 460 g y parecía normal al examen.\n\nLa niña presentaba lesiones cutáneas extensas e irregulares, que se caracterizaban por un aspecto estrellado en ambos flancos, que se extendían lateralmente sobre la zona glútea y el muslo superior. Las lesiones eran simétricas en ambos flancos. No obstante, las lesiones en los muslos eran notablemente más leves en el lado izquierdo. Sus constantes vitales eran estables y no presentaba otras anomalías externas. El examen clínico de sus sistemas respiratorio, cardiovascular, gastrointestinal y neurológico reveló resultados normales, y no se observaron otras anomalías cutáneas, incluida la ausencia de lesiones ampollosas.\n\nDada la naturaleza simétrica de las anomalías cutáneas y el contexto de embarazo de mellizos con FP, se realizó un diagnóstico de aplasia cutis congénita grupo V. Los exámenes de laboratorio, que incluían hemograma completo, electrolitos y pruebas de función renal e hepática, arrojaron resultados normales. Los exámenes de detección de toxoplasmosis, rubéola, citomegalovirus, herpes simple y VIH (TORCH) arrojaron resultados negativos. La ecografía del cerebro, abdomen y corazón no reveló anomalías.\n\nDado que las lesiones se curaron en el útero, solo se prescribieron emolientes locales. Después de 48 horas de observación, el bebé fue dado de alta en su casa, con derivaciones a clínicas de dermatología pediátrica y cirugía plástica. En el seguimiento de 2 semanas, no se observaron cambios en las lesiones de la piel ni nuevos síntomas. Su análisis de microarreglo cromosómico fue reportado como normal.\n",
+        "gold_summary": "Informamos sobre un neonato al que se le diagnosticó ACC de grupo G-V asociado con fetus papyraceus de un embarazo gemelar di-coriónico y di-amniótico. Nacida de una madre asiática de 28 años, esta niña presentaba lesiones extensas, cicatrizadas, similares a las cicatrices en sus flancos y muslos superiores. Estas lesiones eran consistentes con la distribución en forma de «H» comúnmente descrita en ACC ligada a fetus papyraceus. A pesar de las manifestaciones dermatológicas significativas, la niña no mostró otras anormalidades externas o implicación sistémica, y las evaluaciones exhaustivas, incluidos los ultrasonidos y el microarray cromosómico, fueron normales.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "A baby girl was born with wide, scar-like marks on both sides of her tummy and top of her legs. The marks looked like an H shape. She was strong when she was born and had no other problems.\n\nBefore she was born, she was one of two twins. The other twin had died early in the pregnancy and was very small and pressed against the placenta. This can sometimes cause the kind of skin marks the baby had.\n\nDoctors checked the baby carefully. Blood tests, scans of her brain, belly, and heart, and a chromosome test all came back normal. The doctors said the marks were a type of birth skin problem called aplasia cutis congenita group V (this means skin was missing or scarred in places because of the twin situation). The baby only needed soft skin cream. She went home after two days and stayed well on follow-up.",
+                "fh_score": 112.26
+            },
+            "B2": {
+                "text": "Resumen (nivel B2, para lectores jóvenes)\n\nUn recién nacido fue diagnosticado con aplasia cutis congénita (ACC) grupo V, una condición en la que faltan partes de la piel desde el nacimiento. En este caso, las lesiones eran simétricas y extensas en los flancos y la parte superior de los muslos, formando una distribución en “H” que a menudo se ve cuando hay un fetus papyraceus: un gemelo que murió antes del nacimiento y quedó aplastado y reducido dentro del útero.\n\nLa niña nació a término, pesó 2,83 kg y estaba vigorosa. No había otras anomalías externas ni problemas en los sistemas respiratorio, cardíaco, digestivo o neurológico. Pruebas de laboratorio básicas, ecografías del cerebro, abdomen y corazón, análisis para infecciones comunes en embarazos (TORCH) y un estudio genético por microarreglo resultaron normales. Los médicos consideraron que las lesiones ya se habían curado parcialmente en el útero, por lo que solo se prescribieron emolientes (cremas hidratantes) y seguimiento por dermatología pediátrica y cirugía plástica.\n\nTras 48 horas de observación la bebé fue dada de alta; a las dos semanas no hubo cambios ni nuevos síntomas. En conjunto, a pesar de las marcas en la piel, la bebé estaba bien y no hubo afectación sistémica evidente.",
+                "fh_score": 55.54
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel B3, lectura universitaria)\n\nPresentamos el caso de una recién nacida de 39 semanas, producto de un embarazo gemelar bicorial y biamniótico, en el que uno de los gemelos había fallecido en el primer trimestre y quedó como un remanente fetal comprimido (fetus papyraceus) adherido a la placenta. La madre, de 28 años, no refirió antecedentes infecciosos ni uso de fármacos relevantes durante la gestación; los padres son primos hermanos.\n\nHallazgos principales (anormales)\n- La niña mostró, al nacer, extensas lesiones cutáneas simétricas en ambos flancos y en la región glútea y muslos superiores. Las lesiones tenían aspecto cicatricial y seguían la distribución en “H” típica de la aplasia cutis congénita (ACC) grupo V, una forma de pérdida localizada de piel asociada a la presencia de un fetus papyraceus. Las lesiones en el muslo izquierdo eran algo menos marcadas.\n\nHallazgos normales (sin implicación sistémica)\n- La paciente estaba vigorosa al nacer, con constantes estables y sin otras anomalías externas. Exámenes dirigidos —hemograma, electrolitos, función renal y hepática— fueron normales. Pruebas infecciosas TORCH y VIH fueron negativas. Ecografías cerebrales, abdominales y cardiacas no mostraron alteraciones. El microarreglo cromosómico fue normal.\n\nInterpretación y manejo\n- El cuadro es coherente con ACC grupo V secundaria a fetus papyraceus: se interpreta como una lesión localizada por un evento intrauterino (probablemente alteración vascular relacionada con la muerte del gemelo) más que por una causa genética o infección sistémica. Dado que no hubo compromiso sistemático, el manejo inicial fue conservador: cuidados locales con emolientes. La paciente fue dada de alta tras 48 horas y derivada a dermatología pediátrica y cirugía plástica.\n\nPronóstico y pasos a seguir\n- El pronóstico funcional inmediato es bueno porque no hay afectación interna ni signos de infección. Sin embargo, las cicatrices pueden persistir y, según la evolución estética o funcional, podría considerarse tratamiento reconstructivo en el futuro. Se recomienda seguimiento por dermatología y cirugía plástica para vigilancia del área afectada, control del crecimiento y desarrollo, y para planificar intervenciones si son necesarias.",
+                "fh_score": 45.81
+            }
+        }
+    },
+    {
+        "article": "Información para el paciente\nUn hombre de 44 años de edad fue ingresado en nuestro hospital con quejas principales de neumaturia y cistitis repetida. El paciente también tenía antecedentes de hipotiroidismo.\n\nLa tomografía computarizada con contraste mejorado reveló múltiples divertículos del colon sigmoide, y el límite entre el divertículo y la vejiga no estaba claro. La endoscopia gastrointestinal inferior reveló una fístula en el colon rectosigmoide aproximadamente a 15 cm del borde anal. La cistoscopia reveló una fístula en la pared posterior izquierda de la vejiga. Se diagnosticó una fístula vesicovaginal y se planificó una cirugía laparoscópica. Los hallazgos intraoperatorios revelaron una inflamación severa alrededor de la fístula vesicovaginal, y también se habían formado adhesiones severas entre el íleon y la vejiga. El íleon y la vejiga eran difíciles de exfoliar debido a las adhesiones severas. Por lo tanto, decidimos realizar una resección intestinal combinada. El colon rectosigmoide, incluida la fístula, se movilizó y se resecó. La fístula vesical se seccionó y se cerró con una sutura de púas sin nudos (V-LocTM 180, Covidien, Mansfield). La anastomosis sigmoide-rectal se reconstruyó utilizando la técnica de doble grapado. La resección parcial del íleon se reconstruyó con una anastomosis funcional de extremo a extremo (FEEA). Además de la presencia de una anastomosis de 2 sitios, había una inflamación severa en el área circundante, y considerando el riesgo de fuga anastomótica, se creó una ileostomía de derivación 30 cm proximal a la anastomosis ileo-ileal.\n\nLos procedimientos quirúrgicos incluyeron resección anterior alta laparoscópica, resección parcial del intestino delgado, cistectomía parcial y derivación en forma de asa. La operación duró 236 minutos y la pérdida de sangre fue de 50 ml. El curso postoperatorio fue sin incidentes y el cierre de la ileostomía se planificó 1 mes después de la cirugía inicial. Con ayuda laparoscópica, se eliminaron las adherencias entre el omento y la pared abdominal alrededor del estoma. Se realizó una movilización completa alrededor del estoma y el intestino se sacó hacia afuera. El íleon se reconstruyó utilizando FEEA. El procedimiento quirúrgico implicó el cierre de la ileostomía asistida por laparoscopia. La operación duró 100 minutos y la pérdida de sangre fue de 30 ml.\n\nHallazgos clínicos\nAl día siguiente de la cirugía, se produjo un shock sintomático debido a la presión arterial baja (<80 mm Hg) y la taquicardia. Los análisis de sangre mostraron que la hemoglobina disminuyó de 15.3 antes de la cirugía a 8.6 g/dL después de la cirugía.\n\nEvaluación diagnóstica\nLa tomografía computarizada abdominal (TC) reveló una gran cantidad de fluido de alta densidad en la cavidad abdominal. El diagnóstico fue sangrado posoperatorio y shock hemorrágico. Se insertó un catéter venoso central y se administraron 8 unidades de glóbulos rojos y 8 unidades de plasma fresco congelado para estabilizar los signos vitales. Los signos vitales se estabilizaron y no se observó progresión de la anemia después de eso. Aunque se logró la hemostasia, la distensión abdominal severa y los altos niveles de respuesta inflamatoria (proteína C reactiva [CRP] a 42.9 mg/dL y recuento de glóbulos blancos [WBC] de 18,500/uL) persistieron 7 días después de la cirugía.\n\nLa TC con contraste reveló que el hematoma intraabdominal se localizaba en el abdomen inferior izquierdo y derecho, y se consideró posible el drenaje percutáneo. En el día 8 posoperatorio, se insertaron tubos de drenaje de 18 Fr en el abdomen inferior izquierdo y derecho a través de una punción guiada por TC, y se drenó una gran cantidad de sangre antigua. Después del drenaje, la reacción inflamatoria y la distensión abdominal causadas por la infección del hematoma residual mejoraron (CRP a 1,9 mg/dL y WBC de 5000/μL). No se observó progresión de la anemia. En el día 14 posoperatorio, el drenaje en el abdomen inferior derecho cambió de sangre antigua a jugo intestinal. Una angiografía de drenaje reveló fuga anastomótica tardía en el sitio de cierre de la ileostomía. No hubo signos de peritonitis con buen drenaje, pero el drenaje fue de aproximadamente 100 a 200 ml, y el flato del drenaje continuó. No se observó disminución del drenaje durante los siguientes 14 días.\n\nIntervención terapéutica\nAunque se consideró la posibilidad de una nueva operación, se esperaban adhesiones intraabdominales severas debido a la historia de cirugías anteriores, sangrado postoperatorio y fuga anastomótica. Por lo tanto, se consideró que la nueva operación era un procedimiento de alto riesgo. La tomografía computarizada con contraste mostró que un hematoma organizado permanecía en el mesenterio del intestino delgado y el íleon en el lado distal de 10 cm de la anastomosis estaba comprimido cerca del hematoma restante. Teniendo en cuenta la estenosis del íleon en el lado anal de la anastomosis debido a un hematoma residual como la causa de fuga anastomótica, se intentó la dilatación radioscópica del área de estenosis a través del drenaje en el día 24 postoperatorio. Se colocó un introductor de funda Cordis BRITE TIP® (8 Fr × 23 cm) en la fístula donde ocurrió la fuga anastomótica después del drenaje angiográfico. Se usó un hilo radioscópico GT (0.016 pulgadas, 180 cm, 90°) (Terumo, Tokio, Japón) y un microcatéter Renegade HI-FLO (135 × 20 cm) (Boston Scientific, Tokio, Japón) para alcanzar el íleon terminal. Usando el catéter Selecon MP II (6 Fr, 80 cm, φ20 mm) (Terumo), se identificó el área de estenosis en el íleon debido a la compresión del hematoma donde el globo no podía pasar.\n\nSe realizó dilatación con globo fluoroscópica en la estenosis del íleo utilizando un globo guiado por alambre CRE PRO GI (180 cm, 15-18 mm) (Boston Scientific), inflado a 16,5 mm de diámetro a 4,5 atm durante 3 minutos.\n\nSeguimiento y resultados\nDesde el día posterior a la dilatación con globo, la cantidad de drenaje disminuyó notablemente, y se observaron flatos y defecaciones desde el ano. Una semana después de la dilatación con globo, el drenaje fue casi nulo, y se determinó que la fuga anastomótica se había resuelto. El drenaje se eliminó gradualmente. La ingesta oral fue buena, y tuvo movimientos intestinales regulares. Fue dado de alta el día 45 posterior a la operación. Desde entonces, no se ha informado de ninguna recurrencia de la estenosis o fuga anastomótica.\n",
+        "gold_summary": "Preocupaciones del paciente: Presentamos el caso de un hombre de 44 años con fuga anastomótica tardía después del cierre de la ileostomía, causada por la compresión de un hematoma intraabdominal que se curó rápidamente después de la dilatación fluoroscópica con globo del área de la estenosis intestinal.\n\nDiagnósticos: Se produjo sangrado postoperatorio y shock hemorrágico el día 1 postoperatorio tras el cierre de la ileostomía. Los signos vitales se estabilizaron tras la transfusión de sangre, y se realizó con éxito un drenaje guiado por tomografía computarizada para reducir el volumen del hematoma. Sin embargo, el hematoma residual comprimió el íleon en el lado anal de la anastomosis, lo que provocó una fuga anastomótica tardía.\n\nIntervenciones/resultados: Se realizó con éxito la dilatación con balón fluoroscópico del área estenótica a través del drenaje y la fuga anastomótica se curó rápidamente.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había un hombre de 44 años que tuvo una operación para reparar el intestino. Después, le cerraron una ileostomía. La ileostomía es una salida en la barriga para que las heces salgan a una bolsa mientras el intestino se cura.\n\nAl día siguiente tuvo un sangrado fuerte dentro de la barriga. Los médicos le dieron sangre y le pusieron tubos para sacar la sangre acumulada. Ese líquido pegado (hematoma) quedó en un sitio cerca del intestino y apretó una parte del intestino. Esto hizo que la unión del intestino (donde se habían cosido dos trozos) se abriera y saliera líquido por el tubo de drenaje. Eso se llama fuga.\n\nHacer otra operación era muy peligroso porque había mucha cicatriz y riesgo de sangrar otra vez. Entonces los médicos usaron rayos X para ver y pasaron un pequeño globo por el tubo. Inflaron el globo en la parte apretada para abrirla. Después de eso, el drenaje bajó mucho. El hombre pudo expulsar gases y hacer caca por el ano. La fuga se cerró y fue dado de alta al día 45 después de la operación. No ha vuelto a tener ese problema.",
+                "fh_score": 79.19
+            },
+            "B2": {
+                "text": "Here is a clear, kind summary of the case:\n\nWhat happened first\n- A 44-year-old man went to the hospital because he had air in his urine (neumaturia) and repeated bladder infections. Scans showed many diverticula (small pouches) in the sigmoid colon and a fistula (an abnormal connection) between his colon and bladder.  \n- He had laparoscopic surgery to remove the diseased part of the colon, repair the bladder, remove a small part of the small intestine (ileum) that was stuck to the bladder, and make a temporary ileostomy. An ileostomy is a short-term opening of the small intestine to the skin so waste can leave the body while the inside heals.\n\nWhat happened after closing the ileostomy\n- One month later the ileostomy was closed (the two ends of intestine were reconnected). The next day he went into hemorrhagic shock — his blood pressure fell and his hemoglobin dropped a lot because of bleeding inside the belly. He received blood and plasma and his vital signs stabilized.\n- Scans showed a large blood collection (hematoma) inside the abdomen. On day 8 after the closure, doctors drained much of this old blood through tubes placed with CT imaging. This improved his inflammation and belly swelling.\n\nThe late leak and why it happened\n- On day 14 the right-side drain began to show intestinal juice instead of blood. Imaging showed a late anastomotic leak where the bowel had been reconnected. The leak was caused because a remaining, organized hematoma was pressing on the ileum below the anastomosis and creating a narrowing (stenosis). This pressure caused the join to fail and leak.\n- Because the patient already had difficult surgeries, bleeding, and likely severe scar tissue (adhesions), another open operation would be high risk.\n\nHow the team fixed it without major surgery\n- On day 24, the team used the already placed drain route to reach the narrowed part of the ileum under X-ray guidance (fluoroscopy). They passed wires and tiny catheters to the narrowed area and inflated a balloon inside the ileum to stretch the narrowed segment. This is called balloon (or dilatation) treatment.\n- The balloon was inflated to widen the area that the hematoma had compressed.\n\nResult and follow-up\n- The day after balloon dilatation the amount of drainage fell a lot, and the patient had gas and bowel movements again. One week later the drain output was nearly zero and the leak was judged to be healed. The drains were removed gradually.\n- He ate well, had normal bowel movements, and was discharged on postoperative day 45. There was no return of the narrowing or leak during follow-up.\n\nWhy this matters\n- This case shows that a late leak after ileostomy closure can be caused by an internal blood clot pressing on the bowel. In a patient for whom another major operation is risky, a minimally invasive approach — draining the hematoma and dilating the narrowed bowel with a balloon under X-ray — can treat the problem and avoid reoperation.",
+                "fh_score": 86.13
+            },
+            "B3": {
+                "text": "Resumen clínico (edad 44)\n\nMotivo de consulta\nUn hombre de 44 años fue ingresado inicialmente por neumaturia y cistitis recurrente; se diagnosticó una fístula colo-vesical y se realizó cirugía laparoscópica mayor (resección sigmoide-rectal, resección parcial de íleon, cierre de fístula vesical y creación de ileostomía de derivación).\n\nCurso inmediato y complicaciones\n- Tras el cierre de la ileostomía, al día siguiente presentó shock hemorrágico: presión arterial <80 mmHg, taquicardia y caída de hemoglobina de 15.3 a 8.6 g/dL.  \n- Se diagnosticó sangrado posoperatorio y se logró hemostasia; el paciente recibió 8 unidades de glóbulos rojos y 8 unidades de plasma fresco congelado para estabilizarlo.  \n- Persistió distensión abdominal e inflamación intensa (CRP 42.9 mg/dL, WBC 18.500/µL). La TAC mostró hematoma intraabdominal en ambos cuadrantes inferiores.\n\nIntervenciones no quirúrgicas tempranas\n- Día 8: drenajes percutáneos guiados por TAC colocados en ambos cuadrantes inferiores; drenaron abundante sangre antigua y mejoraron la inflamación (CRP 1.9 mg/dL, WBC 5.000/µL).  \n- Día 14: el drenaje derecho cambió a contenido intestinal; la angiografía de drenaje confirmó una fuga anastomótica tardía en el sitio de cierre de la ileostomía. El drenaje continuó (≈100–200 ml/día) durante 2 semanas sin signos de peritonitis.\n\nCausa de la fuga y razonamiento terapéutico\n- La TAC mostró un hematoma organizado en el mesenterio que comprimía el íleon en el lado distal (10 cm desde la anastomosis). Se interpretó que esa compresión provocó estenosis intestinal distal, aumento de presión y finalmente fuga anastomótica.  \n- Debido a múltiples cirugías previas, sangrado y riesgo elevado por adherencias extensas, una reoperación se consideró de alto riesgo. Se optó por una estrategia mínimamente invasiva: dilatación con balón por vía radiológica a través del tracto de drenaje.\n\nProcedimiento de dilatación (día 24 posoperatorio)\n- Se accedió a la fístula a través del drenaje; se avanzaron hilo guía y microcatéter hasta el íleon terminal y se localizó la estenosis.  \n- Se realizó dilatación fluoroscópica con balón (diámetro inflado 16.5 mm, 4.5 atm, 3 minutos).\n\nResultados y seguimiento\n- A partir del día siguiente a la dilatación disminuyó marcadamente el volumen de drenaje; se observaron expulsión de flatos y heces por vía natural.  \n- Una semana después, el drenaje fue casi nulo y se consideró resuelta la fuga anastomótica; los tubos se retiraron progresivamente.  \n- El paciente toleró la vía oral, recuperó tránsito intestinal normal y fue dado de alta al día 45 posoperatorio. No se ha registrado recidiva de estenosis ni de la fuga hasta el último seguimiento.\n\nLecciones y recomendaciones prácticas\n- Una fuga anastomótica tardía puede deberse no solo a fallo técnico, sino a estenosis distal por compresión (p. ej., hematoma organizado).  \n- En pacientes con alto riesgo de reintervención, la dilatación endovascular/fluoroscópica de una estenosis compresiva puede ser una alternativa eficaz y menos invasiva para permitir el drenaje y la cicatrización de la anastomosis.  \n- Seguimiento clínico e imagenológico estrecho es necesario tras la resolución; si la estenosis o la fuga persisten, puede precisarse intervención quirúrgica. También conviene monitorizar nutrición, infección y función intestinal.\n\nComentario empático\nEl equipo tratante evitó una reoperación de alto riesgo y consiguió la resolución mediante técnicas percutáneas y endovasculares. Este enfoque permitió al paciente recuperarse sin nueva cirugía mayor; sin embargo, requiere vigilancia continua para detectar recurrencias y asegurar una recuperación completa.",
+                "fh_score": 51.66
+            }
+        }
+    },
+    {
+        "article": "Paciente femenino de 23 años, ASA I, acude al Centro de Salud de la Universidad Peruana de Ciencias Aplicadas (CUS-UPC) para colocarle un implante en la zona edéntula de la pieza 1.6. Durante la evaluación, la paciente refiere que hace unos meses se le fracturó la primera molar superior derecha y, como consecuencia, le realizaron la exodoncia atraumática de dicha pieza dentaria.\n\nTras la inspección clínica, se observó la ausencia de la pieza dentaria 1.6, fenotipo gingival delgado y disminución en altura de reborde edéntulo Seibert tipo II 13. Tomográficamente, se registraron medidas de la altura del reborde óseo residual en relación con el piso del seno maxilar (6 mm) y el ancho de la cresta ósea a nivel cervical (11,20 mm), medio (11,80 mm) y apical (12,40 mm), con lo que se identifica la presencia de un seno maxilar ovoide, según Nie et al. Se realizó la planificación quirúrgica para la realización de una elevación del seno maxilar con abordaje transcrestal y la colocación de un implante dental de 4,8 x 8 mm.\n\nSe inició el procedimiento quirúrgico, que consistió en lo siguiente:\n\n• Asepsia y antisepsia\n\n• Técnica anestesia infiltrativa por vestibular y palatino de la zona edéntula 1.6 utilizando 2 cartuchos de lidocaína al 2% con epinefrina 1:80.000.\n\n• Incisión supracrestal en la zona edéntula 1.6 e incisiones sulculares en mesial de la pieza dentaria 1.7 y en distal de la pieza dentaria 1.5.\n\n• Decolado del colgajo a espesor parcial y, luego, se procedió a probar la guía quirúrgica para realizar la secuencia de fresado hasta una longitud de 6 mm, dejando 1 mm de distancia al piso del seno maxilar, el cual fue comprobado con los calibradores de profundidad, según el diámetro de la fresa que se utilizó durante la osteotomía. La secuencia de fresado se realizó hasta la fresa 3,5 mm de diámetro y luego se procedió a realizar el levantamiento de 2 mm del seno maxilar con la técnica de abordaje transcrestal mediante el uso de un osteótomo, hasta llegar a una longitud de 8 mm.\n\n• Colocación del implante φ 4,8 x 8 mm (Bone Level tapered, Straumann®) y tornillo de cierre, ambos con un torque de inserción de 20 N.\n\n• Sutura con puntos interrumpidos con ácido poliglicólico 5/0 y lavado de la zona quirúrgica con suero fisiológico al 0,09%.\n\n• Radiografía posquirúrgica del implante en zona edéntula 1.6.\n\n• Indicación de tomar amoxicilina de 500 mg + ácido clavulánico 125 mg cada 8 horas durante 7 días, ketorolaco de 10 mg cada 8 horas por 3 días, cetirizina de 10 mg cada 24 horas por 3 días y clorhexidina al 0,12%, 2 veces al día, por 10 días. Entre las indicaciones posquirúrgicas se le indicó a la paciente reposo absoluto, sin esfuerzo físico, dieta blanda, no sonarse la nariz, no succionar líquidos por dos semanas, no sumergir la cabeza en agua, tampoco estornudar o toser con la boca abierta, mantener la cabeza elevada y aplicarse compresas de hielo durante las primeras 4 horas.\n\nSe realizó un control posquirúrgico a los 7 días, el cual evidenció tejidos blandos en proceso de cicatrización, por lo que se procedió al retiro de puntos y lavado con suero fisiológico al 0,9%, y se realizó una tomografía de control que evidenció la elevación de seno maxilar, con 2,83 mm aproximadamente. Asimismo, se realizaron controles posquirúrgicos a los 35 y 56 días, en los cueles se hallaron tejidos blandos en completo proceso de cicatrización.",
+        "gold_summary": "Se realizó un levantamiento de seno maxilar sin injerto óseo en una paciente de sexo femenino de 23 años que requería la colocación de un implante dental en la zona edéntula de la pieza 16. La evaluación clínica y tomográfica permitieron planificar y realizar la elevación de seno maxilar mediante el abordaje transcrestal y sin la necesidad de injerto óseo. El reborde residual de 6 mm permitió la colocación de un implante dental simultáneo. Luego de 6 meses de seguimiento tomográfico, antes de la carga protésica, se consiguió una altura ósea vertical de 8,83 mm, lo que dio como resultado una ganancia ósea vertical de 2,83 mm. Adicionalmente, se observa una adecuada integración del implante dental sin complicaciones posoperatorias.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había una joven de 23 años que necesitaba poner un implante en el lugar donde le habían sacado un molar arriba a la derecha. Debajo de ese diente hay un espacio con aire llamado seno. Para poner el implante había que levantar un poco el suelo de ese espacio.  \n\nLos doctores vieron en la radiografía que quedaba 6 mm de hueso. Eso era suficiente para hacer la operación sin añadir hueso extra. Durante la cirugía limpiaron y adormecieron la zona. Con cuidado levantaron 2 mm del piso del seno por la misma abertura donde iba el implante. Pusieron un implante pequeño (4,8 x 8 mm) y cerraron la encía con puntos. Le dieron medicinas y le explicaron cómo cuidarse en casa.  \n\nA los 7 días la herida estaba sanando y quitaron los puntos. En controles posteriores la encía siguió cicatrizando bien. A los 6 meses, la radiografía mostró que había crecido casi 3 mm de hueso más, quedando cerca de 9 mm. El implante estaba integrado y no hubo problemas.  \n\nTodo salió bien y la paciente se recuperó sin complicaciones.",
+                "fh_score": 78.29
+            },
+            "B2": {
+                "text": "Resumen (nivel B2, lenguaje claro y amable)\n\nUna mujer de 23 años acudió para colocar un implante dental en el lugar donde faltaba la muela superior derecha (pieza 1.6), después de una extracción previa. La evaluación clínica y una tomografía mostraron que había 6 mm de hueso vertical entre la cresta alveolar y el suelo del seno maxilar (una cavidad aérea situada sobre las muelas), y un ancho de cresta suficiente (unos 11–12 mm). Por estas medidas se planificó un levantamiento de seno maxilar por vía transcrestal (es decir, accediendo desde la propia cresta donde va el implante) y la colocación simultánea de un implante de 4,8 x 8 mm, sin usar injerto óseo.\n\nDurante la cirugía se usó anestesia local y se talló un colgajo parcial. Se fresó hasta 6 mm de profundidad (dejando 1 mm del suelo del seno), y con un osteótomo se elevó el piso del seno alrededor de 2 mm para alcanzar la longitud necesaria. Se colocó el implante con un par de inserción de 20 N·cm y se suturó la zona. Se indicaron antibióticos, analgésicos, enjuague con clorhexidina y medidas postoperatorias cuidadosas (reposo, dieta blanda, evitar sonarse la nariz o succionar, mantener la cabeza elevada, hielo las primeras horas) para proteger la elevación del seno.\n\nEn el control a los 7 días la herida evolucionaba bien; la tomografía mostró una elevación del seno de aproximadamente 2,83 mm. En controles posteriores (35 y 56 días) la cicatrización fue completa. Tras seguimiento tomográfico antes de la carga protésica se reportó una altura ósea vertical final de 8,83 mm, lo que supone una ganancia ósea de 2,83 mm. No se registraron complicaciones y el implante mostró buena integración.\n\nComentario final (claro y tranquilizador): en este caso, debido a la altura residual de hueso, fue posible levantar el seno y colocar el implante al mismo tiempo sin usar injerto. La ganancia ósea y la buena cicatrización indican un resultado exitoso y sin problemas inmediatos.",
+                "fh_score": 61.14
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel universitario)\n\nPaciente y motivo\n- Mujer de 23 años, ASA I, que acudió para la colocación de un implante en el espacio edéntulo del primer molar superior derecho (pieza 1.6). Refería exodoncia atraumática previa de esa pieza tras una fractura.\n\nHallazgos iniciales\n- Examen clínico: ausencia de la pieza 1.6, fenotipo gingival delgado y reducción del reborde edéntulo tipo Seibert II (pérdida moderada de altura).\n- Tomografía (CBCT): altura ósea residual de 6 mm desde la cresta hasta el piso del seno maxilar; anchos crestal de 11,20 mm (cervical), 11,80 mm (medio) y 12,40 mm (apical). Se describió un seno maxilar de morfología ovoide (criterios de Nie et al.).\n\nPlan y técnica quirúrgica\n- Se planificó una elevación de seno maxilar por abordaje transcrestal sin injerto óseo y la colocación inmediata de un implante.\n- Procedimiento relevante:\n  - Anestesia infiltrativa vestibular y palatina con lidocaína 2% + epinefrina.\n  - Incisión supracrestal y despegamiento de espesor parcial.\n  - Fresado guiado hasta 6 mm (1 mm por debajo del piso sin perforar), luego osteotomía con osteótomo para elevar 2 mm el piso del seno y alcanzar una profundidad total de 8 mm.\n  - Colocación de implante Bone Level tapered Straumann de 4,8 x 8 mm y tornillo de cierre con torque de inserción registrado de 20 N.\n  - Sutura con puntos interrumpidos (ácido poliglicólico 5/0) y lavado con suero fisiológico.\n\nTratamiento posoperatorio y cuidados\n- Medicación: amoxicilina/ácido clavulánico 500/125 mg cada 8 h por 7 días; ketorolaco 10 mg cada 8 h por 3 días; cetirizina 10 mg cada 24 h por 3 días; enjuagues con clorhexidina 0,12% dos veces al día por 10 días.\n- Indicaciones: reposo, dieta blanda, evitar sonarse la nariz, succión, inmersión en agua, estornudar o toser con la boca cerrada, mantener la cabeza elevada y aplicar frío local las primeras 4 horas.\n\nEvolución y resultados\n- Control a los 7 días: buena cicatrización de tejidos blandos; retirada de puntos. CBCT de control mostró una elevación del seno de aproximadamente 2,83 mm respecto al piso previo.\n- Controles a los 35 y 56 días: tejidos blandos en completo proceso de cicatrización.\n- Antes de la carga protésica, a los 6 meses de seguimiento tomográfico, se constató una altura ósea vertical total de ~8,83 mm (ganancia vertical ≈ 2,83 mm) y buena integración del implante sin complicaciones clínicas registradas.\n\nInterpretación e implicaciones\n- Con una altura residual de 6 mm, la técnica transcrestal sin relleno fue suficiente para elevar el piso sin injerto y colocar el implante simultáneamente, logrando una ganancia ósea vertical cercana a 3 mm y estabilidad sin evidencia de complicaciones en el seguimiento reportado.\n- Esta estrategia puede ser una alternativa menos invasiva cuando la altura residual permite soporte primario del implante; reduce el uso de biomateriales y la morbilidad asociada a procedimientos más extensos.\n\nRecomendaciones y consideraciones\n- Seguimiento prolongado (radiográfico y clínico) hasta la carga definitiva y más allá para confirmar estabilidad a largo plazo del hueso y del implante.\n- Vigilar signos de complicación: dolor persistente, aumento de inflamación, secreción purulenta, o síntomas de sinusitis que podrían indicar perforación de la membrana, infección o fracaso de la osteointegración.\n- Antes de la rehabilitación protésica final, confirmar por CBCT y pruebas clínicas la integración y la calidad ósea obtenida.\n\nComentario final (tono empático)\nEl procedimiento fue exitoso en esta paciente joven, con buena cicatrización y aumento óseo suficiente para la rehabilitación protésica planificada. Es importante mantener controles periódicos y seguir las recomendaciones para minimizar riesgos y asegurar un resultado funcional y estable a largo plazo.",
+                "fh_score": 50.89
+            }
+        }
+    },
+    {
+        "article": "Una paciente de 42 años de edad fue remitida a nuestro centro terciario de cáncer con antecedentes de seroma recurrente del seno izquierdo. La paciente se había sometido a una extracción bilateral de implantes mamarios con una capsulotomía parcial 11 meses antes de su primera visita a nuestro centro. La paciente no presentaba ninguna comorbilidad notable y tenía antecedentes de aumento bilateral de senos con implantes mamarios en el plano submuscular en 2003, a la edad de 21 años. No se pudo localizar ninguna información sobre el tipo de implantes que había recibido originalmente. La paciente volvió a consultar al mismo cirujano en 2008, quejándose de seroma bilateral, para someterse a un primer reemplazo bilateral de implantes mamarios con implantes mamarios anatómicos texturados de 425 cc (Sebbin LSA TF 425). En 2013, se sometió a un segundo procedimiento de reemplazo de implantes para aumentar el tamaño con implantes mamarios de 480 cc del mismo fabricante (Sebbin LSA TF 480). En 2017, la paciente volvió para una revisión en la que se quejaba de dolor y aumento del volumen del seno bilateralmente. En ese momento, se le realizó una exploración por ultrasonido que identificó efusiones periprostéticas bilaterales sin linfadenopatía o masas palpables en las regiones mamarias. Las efusiones se drenaron sin análisis, pero reaparecieron a lo largo de los años, cuando la paciente buscó ayuda del mismo cirujano y se sometió a un tercer procedimiento de revisión en 2022, con un reemplazo bilateral de implantes mamarios y una toma de muestras de la cápsula anterior. El cirujano envió dos especímenes desde el lado derecho (9 x 1 cm y 3 x 3 cm) y uno desde el lado izquierdo (2 x 1 cm). El informe histopatológico del espécimen encontró «material proteico amorfo celular acellular» en el lado derecho y «tejido fibroso escleroso con inflamación de linfocitos-monocitos, que requiere correlación con la presentación clínica» en el lado izquierdo. A pesar de la extracción, el seroma reapareció en el lado izquierdo, y se envió para pruebas citopatológicas que identificaron «una población de células pleomórficas atípicas irregulares con contornos irregulares que sugieren un proceso linfoproliferativo con CD30+ elementos» para los que se recomendaron pruebas diagnósticas adicionales. Por esta razón, la paciente buscó tratamiento en nuestra institución, donde el caso fue gestionado por un equipo multidisciplinario (MDT) que incluía a un cirujano plástico, un hematopatólogo, un hematólogo, un oncólogo, un radioterapeuta, un oncólogo quirúrgico y un radiólogo de mama. El espécimen histopatológico original de la toma de la cápsula se revisó por un hematopatólogo de nuestro centro de referencia, que identificó células CD30+ grandes y escasas atípicas con contornos irregulares que se consideraron compatibles con el diagnóstico de BIA-ALCL. Las células presentaron el siguiente fenotipo: CD30+, CD3-, CD7-, CD5-, CD4-, CD8-, Granzima B+/-, TIA1-, ALK1-, PAX5-, CD79a-, CD68-, CD15-/+. La paciente recibió una exploración por ultrasonido con aspiración por aguja fina y citopatología de la efusión recurrente que confirmó un proceso CD30+ linfoproliferativo atípico con captación de 18F-FDG (fluorodeoxiglucosa) (SUV máx. 1,8). No se pudieron localizar otras áreas de captación en todos los demás segmentos corporales explorados. La paciente también recibió una exploración por resonancia magnética de ambos senos con medio de contraste para completar la estadificación preoperativa, confirmando el seroma del lado izquierdo. Los portaobjetos del espécimen de la cirugía anterior se revisaron por el hematopatólogo que consideró los hallazgos suficientes para identificar BIA-ALCL con infiltración temprana de la cápsula periprostética (pT2 según el sistema de estadificación MD Anderson-TNM). Tres semanas después de la visita inicial, la paciente se sometió a cirugía radical con capsulotomía en bloque que contenía solo 150 cc de efusión serosa sin implante. El contenido líquido se envió para cultivo y citopatología, mientras que el espécimen sólido se envió para examen histopatológico. Además, la paciente se sometió a biopsia de ganglio linfático centinela de 2 ganglios axilares identificados preoperativamente a través de linfografía segmentaria. Los ganglios linfáticos presentaron una linfadenopatía silicona-asociada reactiva crónica sin signos de linfadenopatía metastásica. El informe histopatológico de la cápsula reveló agregados celulares infiltrantes en la cápsula periprostética, pero márgenes de resección claros y sin signos de infiltración más allá de la cápsula. Como tal, la paciente recibió un estadio IC (pT3pN0M0). El curso postoperatorio fue sin incidentes, y no se consideraron necesarios más tratamientos adyuvantes por el MDT. La paciente continuó su estricto protocolo de seguimiento, con PET/CT de 6, 12 y 18 meses posteriores a la cirugía que no mostró signos de recurrencia de enfermedad local o distante. Como está, la paciente continúa sus visitas de seguimiento y exploraciones, con supervivencia libre de enfermedad más allá de 18 meses.\n",
+        "gold_summary": "Describimos el caso de una mujer de 42 años con antecedentes de aumento de senos bilateral con fines cosméticos 21 años antes, que desarrolló seroma recurrente del lado izquierdo. Buscó ayuda de su primer cirujano, quien realizó 2 procedimientos de intercambio de implantes mamarios, colocando dispositivos texturados y, finalmente, una extracción bilateral de implantes mamarios en el transcurso de dos décadas. La paciente no recibió capsulectomías en los intercambios de implantes anteriores y recibió una muestra de la cápsula anterior en el último procedimiento, donde se diagnosticó BIA-ALCL en el lado izquierdo. Fue derivada a un centro de cáncer terciario donde el examen preoperatorio confirmó la presencia de enfermedad residual local. Después de la gestión del equipo multidisciplinario, se sometió a una revisión de capsulectomía en bloque del lado izquierdo sin necesidad de tratamientos adicionales. El curso postoperatorio fue sin incidentes y sin signos de recurrencias locales a los 18 meses de seguimiento.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Esta es la historia de una mujer de 42 años que se había puesto implantes de seno cuando era joven. Con los años tuvo varias cirugías y a veces se le formó líquido alrededor del implante en el seno izquierdo. Ese líquido volvió muchas veces.\n\nCuando le quitaron los implantes y mandaron a mirar el tejido, los médicos encontraron un tipo raro de cáncer llamado BIA-ALCL. Eso es un cáncer de las células del sistema que a veces aparece cerca de implantes de seno. Los médicos la mandaron a un centro especializado para estudiar mejor el caso.\n\nAllí le hicieron más pruebas y vieron que el cáncer estaba solo en la cápsula (el tejido cicatricial) alrededor del seno izquierdo. Le hicieron una cirugía para quitar toda la cápsula y el líquido de una sola vez. También revisaron los ganglios (pequeñas bolitas que revisan si el cáncer se ha movido) y no encontraron cáncer en ellos. Los márgenes de la cirugía quedaron limpios, es decir, quitó todo lo que hacía falta.\n\nDespués de la operación no necesitó más tratamientos. Los controles con imágenes a los 6, 12 y 18 meses no mostraron enfermedad. La paciente sigue controlándose y, hasta ahora, está libre de cáncer más de 18 meses después.",
+                "fh_score": 76.18
+            },
+            "B2": {
+                "text": "Resumen claro y amable:\n\nUna mujer de 42 años que había recibido implantes mamarios por estética desde los 21 años desarrolló repetidos acúmulos de líquido (seromas) en el seno izquierdo. Un seroma es una acumulación de líquido que puede formarse alrededor de un implante. A lo largo de casi dos décadas la paciente tuvo varios recambios de implantes y en 2022 se le retiraron los implantes y se tomaron muestras de la cápsula (la bolsa de tejido fibroso que el cuerpo forma alrededor del implante).\n\nTras la extracción, el seroma volvió a aparecer en el lado izquierdo. El examen del líquido y de la cápsula encontró células anormales que daban positivo para una proteína llamada CD30. Eso hizo sospechar un tipo raro de linfoma asociado a implantes mamarios, llamado BIA‑ALCL (un linfoma no Hodgkin que puede aparecer en el líquido o la cápsula alrededor de implantes). El caso fue enviado a un equipo especializado (cirujanos, hematólogos, patólogos, radiólogos y oncólogos) para decidir el mejor tratamiento.\n\nLas pruebas por imagen (ecografía, PET/CT y resonancia magnética) mostraron enfermedad localizada en el seno izquierdo sin signos de extensión a otras partes del cuerpo. Los patólogos revisaron las muestras y vieron células CD30+ compatibles con BIA‑ALCL con infiltración temprana de la cápsula.\n\nTres semanas después de la evaluación, la paciente se sometió a una cirugía para retirar en bloque la cápsula afectada y el líquido acumulado (capsulectomía en bloque). También se hicieron biopsias de los ganglios linfáticos sentinel para comprobar si el cáncer se había diseminado. Los ganglios mostraron cambios reactivos por la silicona, pero no había metástasis. La pieza quirúrgica tenía márgenes limpios y no se encontró enfermedad fuera de la cápsula.\n\nEl diagnóstico final fue BIA‑ALCL en estadio local (estadio IC, pT3 pN0 M0), y el equipo decidió que no eran necesarias más terapias (quimioterapia o radioterapia). La recuperación fue buena y las revisiones con PET/CT a los 6, 12 y 18 meses no mostraron recurrencia. Al momento del informe la paciente seguía libre de enfermedad más allá de 18 meses.\n\nComentario y pasos a seguir: BIA‑ALCL es raro y a menudo se identifica por seromas tardíos alrededor de implantes. El manejo ideal cuando la enfermedad está limitada a la cápsula suele ser cirugía completa para retirar la cápsula y el implante, seguida de controles periódicos por imagen. En este caso la respuesta fue buena y el seguimiento hasta ahora es favorable.",
+                "fh_score": 59.72
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel lector universitario)\n\nPresentación y antecedentes\n- Mujer de 42 años con antecedente de aumento mamario en 2003 y múltiples revisiones/reemplazos de implantes durante las dos décadas siguientes. En 2008 y 2013 se usaron implantes anatómicos texturados (Sebbin LSA TF 425 y 480). No se dispone de datos del implante original de 2003.\n- Desde 2017 presentó efusiones (seromas) periprotésicos recurrentes del lado izquierdo que se drenaron en varias ocasiones. En 2022 se realizó un tercer procedimiento de revisión; 11 meses antes de la derivación al centro terciario se hicieron extracción bilateral de implantes con capsulotomía parcial.\n- Tras la extracción persistió el seroma izquierdo, y la citología detectó una población atípica CD30+ que orientó a un proceso linfoproliferativo.\n\nEvaluaciones diagnósticas\n- Revisión por un equipo multidisciplinario en el centro oncológico; examen histopatológico y revisión por hematopatólogo identificaron células grandes CD30+ y ALK-, hallazgo compatible con BIA‑ALCL (linfoma anaplásico de células grandes asociado a implante mamario).\n- Inmunofenotipo relevante: CD30+, ALK1–, negativos para marcadores B (PAX5, CD79a) y en su mayoría para marcadores T habituales (CD3, CD4, CD5, CD7, CD8); granzima B variable.\n- Ecografía con punción aspirativa del derrame confirmó proceso linfoproliferativo CD30+. PET/CT mostró captación de FDG limitada al foco mamario izquierdo (SUV máx 1,8) sin otras lesiones a distancia. RM con contraste confirmó el seroma izquierdo.\n- Biopsia de ganglios centinela axilares (2 ganglios) mostró linfadenopatía reactiva crónica asociada a silicona, sin compromiso metastásico.\n\nTratamiento y estadificación\n- Se realizó capsulotomía en bloque lateral izquierdo (extirpación completa de la cápsula periprotésica con el contenido seroso —150 cc—). El examen histológico mostró agregados celulares infiltrantes en la cápsula, márgenes quirúrgicos libres y ausencia de extensión más allá de la cápsula.\n- Estadio postoperatorio informado: IC (pT3 pN0 M0) según el sistema MD Anderson–TNM. El equipo multidisciplinario consideró que, dada la resección completa y la ausencia de afectación ganglionar o a distancia, no se requerían tratamientos adyuvantes (quimioterapia o radioterapia).\n\nEvolución y seguimiento\n- Recuperación postoperatoria sin complicaciones.\n- Vigilancia con PET/CT a los 6, 12 y 18 meses: sin evidencia de recidiva local ni enfermedad a distancia.\n- Actualmente la paciente permanece en seguimiento activo, con supervivencia libre de enfermedad >18 meses.\n\nInterpretación y puntos prácticos\n- BIA‑ALCL es un linfoma raro asociado con implantes mamarios, con mayor relación reportada en implantes texturados; se caracteriza por células CD30+ y generalmente ALK–.\n- En este caso, la enfermedad estuvo confinada a la cápsula periprotésica y fue tratada con resección en bloque completa, lo que se asocia con buen pronóstico cuando la resección es completa y no hay afectación ganglionar o sistémica.\n- Importa la vigilancia continua: seguimiento clínico e imagenológico para detectar recurrencia precoz. El manejo se beneficia de un enfoque multidisciplinario que incluye cirugía, hematopatología e imagen.\n\nNota empática\n- La paciente atravesó múltiples revisiones y procedimientos antes del diagnóstico definitivo. El resultado temprano y localizado, la intervención quirúrgica completa y el seguimiento riguroso han permitido hasta ahora una evolución favorable.",
+                "fh_score": 41.33
+            }
+        }
+    },
+    {
+        "article": "Se trata de un paciente de 50 años que se presentó con una queja de dolor e hinchazón de la lengua de tres días de duración. Asociado a esto, tenía dolor al tragar, dificultad para abrir la boca, falta de aire y babeo. Asimismo, tenía fiebre alta y un tipo de dolor de cabeza global. Por lo demás, no tenía traumatismo en la lengua, ni procedimientos dentales u orales recientes, ni antecedentes de tabaquismo ni de enfermedad médica crónica como diabetes mellitus, enfermedad cardiaca e hipertensión. Históricamente, había tenido un dolor dental agudo en los últimos seis meses antes de su queja actual. Había masticado khat desde su niñez y tenía una mala higiene oral.\n\nEn el examen físico, se veía muy enfermo y sus signos vitales eran: presión arterial 115 por 70 mmHg, pulso 120 latidos por minuto, frecuencia respiratoria 20, temperatura 39 grados centígrados y saturación de oxígeno 92% de oxígeno. En el examen HEENT, había una hinchazón significativa de la lengua en el área anterolateral izquierdo, fluctuante a la palpación, y tenía un borde eritematoso. Hay múltiples caries en las áreas maxilares y mandibulares. No hubo hallazgos pertinentes en los sistemas restantes.\n\nTras obtener el consentimiento informado, el paciente fue trasladado al quirófano con el diagnóstico de absceso lingual. Posteriormente, se realizó la incisión y el drenaje bajo anestesia general, y se drenaron unos 30 ml de pus espeso. La bolsa se lavó con solución salina normal y peróxido de hidrógeno al 2 %. El paciente fue trasladado a la sala de cirugía con signos vitales estables y había tomado ceftriaxona 1 g por vía intravenosa dos veces al día y metronidazol 500 mg por vía intravenosa tres veces al día durante dos días. Fue dado de alta después de dos días de estancia en el hospital con mejoría y Augmentin 625 mg por vía oral tres veces al día durante cinco días.\n",
+        "gold_summary": "Se trata de un paciente de 50 años que se presentó con una queja de dolor e hinchazón de la lengua de tres días de duración. Asociado a esto, tenía dolor al tragar, dificultad para abrir la boca, falta de aire y babeo. Asimismo, tenía fiebre alta y un tipo de dolor de cabeza global. En el examen físico, había una hinchazón significativa de la lengua en el área anterolateral izquierda, fluctuante a la palpación, y tenía un borde eritematoso. Después de que se tomó el consentimiento informado, el paciente fue trasladado al quirófano con el diagnóstico de absceso de la lengua. Posteriormente, se hizo una incisión y drenaje bajo anestesia general, y se drenaron unos 30 ml de pus espeso. El bolsillo se lavó con solución salina normal y peróxido de hidrógeno al 2%. El paciente fue trasladado a la sala de cirugía con signos vitales estables y había estado tomando antibióticos. Fue dado de alta después de dos días de estancia en el hospital.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un hombre de 50 años llegó al hospital porque tenía la lengua hinchada y dolorida desde hacía tres días. Le dolía al tragar. Tenía dificultad para abrir la boca, le salía saliva y le costaba un poco respirar. También tenía fiebre y dolor de cabeza.\n\nEn la boca se vio una hinchazón grande en la parte izquierda de la lengua. Esa zona estaba blanda y al tocarla parecía haber líquido dentro. Los médicos dijeron que era un absceso de la lengua. Un absceso es una bolsa con pus, que es líquido amarillo que se forma cuando hay infección.\n\nCon el permiso del paciente, lo llevaron al quirófano. Lo pusieron a dormir para la operación. Le hicieron un pequeño corte y sacaron unos 30 ml de pus espeso. Limpiaron la herida con agua salada y peróxido de hidrógeno al 2 %. Después lo cuidaron con antibióticos por vía intravenosa en el hospital.\n\nEl hombre mejoró y, tras dos días, lo dejaron ir a su casa con más antibiótico para tomar por cinco días. Está bien decir que recibió tratamiento y mejoró.",
+                "fh_score": 82.71
+            },
+            "B2": {
+                "text": "Resumen sencillo y claro:\n\nUn hombre de 50 años llegó al hospital porque desde hacía tres días tenía dolor e hinchazón en la lengua. También le dolía al tragar, tenía dificultad para abrir la boca, le salía saliva sin control (babeo), se quedaba sin aliento y tenía fiebre alta y dolor de cabeza general. No había sufrido un golpe en la lengua ni se había hecho tratamientos dentales recientes. No tenía enfermedades crónicas conocidas como diabetes o problemas del corazón, ni fumaba. Sí había tenido un dolor dental agudo en los últimos seis meses, masticaba khat y tenía mala higiene bucal.\n\nAl examinarlo se veía muy enfermo. Sus signos vitales fueron: presión 115/70 mmHg, pulso rápido 120 latidos por minuto, respiración 20 por minuto, temperatura 39 °C y saturación de oxígeno 92%. En la boca se observó una hinchazón importante en el lado izquierdo y hacia la parte frontal de la lengua; esa zona se sentía blanda y llena de líquido al tocarla (fluctuación) y tenía el borde enrojecido. Además había muchas caries en los dientes superiores e inferiores.\n\nEl diagnóstico fue absceso de la lengua. Un absceso es una acumulación de pus causada por una infección. Bajo anestesia general se hizo una incisión para abrir y drenar el absceso; salieron unos 30 ml de pus espeso. La cavidad se limpió con suero salino y peróxido de hidrógeno al 2%. Después del procedimiento el paciente quedó estable y recibió antibióticos por vía intravenosa (ceftriaxona y metronidazol) durante dos días.\n\nFue dado de alta tras dos días en el hospital porque mejoró. Al salir recibió antibiótico oral (Augmentin 625 mg, tres veces al día por cinco días).\n\nQué significa y próximos pasos prácticos:\n- El problema principal era una infección localizada que necesitó drenaje y antibióticos, lo que suele resolver la infección.  \n- Es importante seguir la receta y volver si empeora la hinchazón, aparece dificultad para respirar más grave, fiebre alta persistente o dolor que no cede.  \n- También se recomienda atención dental y mejorar la higiene bucal para evitar que caries o infecciones dentales vuelvan a provocar problemas.",
+                "fh_score": 65.96
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel B3)\n\n- Presentación: Hombre de 50 años con 3 días de dolor e hinchazón de la lengua, asociados a odinofagia (dolor al tragar), dificultad para abrir la boca (trismo), disnea leve y babeo. También tuvo fiebre alta y cefalea difusa.\n\n- Antecedentes relevantes: No refirió traumatismo lingual ni procedimientos dentales u orales recientes, ni enfermedades crónicas conocidas (por ejemplo diabetes, cardiopatía o hipertensión). Historia de dolor dental agudo en los últimos seis meses, masticación crónica de khat y mala higiene bucal, lo que sugiere una probable fuente odontogénica de la infección.\n\n- Exploración: Paciente en estado general comprometido. Signos vitales anormales: taquicardia (FC 120/min), fiebre (39 °C) y saturación de oxígeno algo reducida (92%); tensión arterial y frecuencia respiratoria dentro de límites aceptables. En HEENT hallazgo clave: masa fluctuante y eritematosa en la región anterolateral izquierda de la lengua (absceso lingual). Múltiples caries dentales en maxilar y mandíbula. No se reportaron otros hallazgos sistémicos importantes.\n\n- Diagnóstico y manejo inmediato: Diagnóstico de absceso lingual. Tras consentimiento informado, se realizó drenaje quirúrgico bajo anestesia general; se evacuaron aproximadamente 30 ml de pus espeso y el bolsillo se irrigó con solución salina y peróxido de hidrógeno al 2%. Se inició antibioterapia empírica intravenosa: ceftriaxona 1 g cada 12 horas y metronidazol 500 mg cada 8 horas durante 2 días.\n\n- Evolución y alta: Mejoró tras el drenaje y la terapia intravenosa; fue trasladado a sala quirúrgica en situación estable y dado de alta tras 48 horas con tratamiento oral (amoxicilina/ácido clavulánico 625 mg cada 8 horas por 5 días).\n\n- Interpretación y puntos a considerar: El absceso lingual es una infección rara pero potencialmente grave por riesgo de compromiso de la vía aérea y extensión a espacios profundos del cuello. En este caso, la presencia de múltiples caries y antecedente de dolor dental hacen probable un origen odontogénico. La saturación de 92% y la taquicardia justificaron manejo urgente y vigilancia del estado respiratorio. No se mencionó cultivo del pus ni pruebas metabólicas (p. ej., glucemia) en el informe; obtener cultivo y evaluar factores de riesgo inmunológicos puede ser útil en casos similares para orientar el tratamiento antimicrobiano y prevenir recurrencias.\n\n- Recomendaciones sugeridas tras el alta: seguimiento dental para tratar la fuente (caries), mejora de higiene oral, consejo para suspender masticación de khat y control ambulatorio para confirmar resolución completa y vigilar signos de recurrencia o extensión (fiebre persistente, empeoramiento de la respiración, dolor cervical). Si aparecieran nuevos síntomas, reconsulta urgente por riesgo de complicaciones.",
+                "fh_score": 46.88
+            }
+        }
+    },
+    {
+        "article": "Hombre de 73 años de edad de origen latinoamericano, con antecedente de madre con diagnóstico de demencia tipo Alzheimer con panel genético negativo; hermano con diagnóstico de ELA; hermana con diagnóstico de enfermedad de Parkinson. La sintomatología progresiva comenzó desde el año 2016 y se caracterizó por síntomas progresivos de hiposmia, hipoacusia, estreñimiento e insomnio, los cuales ameritaron valoración por otorrinolaringología y audiología, sin conclusión diagnóstica. En el año 2020 los familiares notaron que el paciente presentaba problemas en la memoria episódica, olvidos de objetos de la vida cotidiana, problemas de ganancias en su negocio (de comercio). Estos síntomas fueron progresivos hasta que el paciente empezó a tener limitación en las tareas diarias, como al manejar y al cambiar las velocidades, además de al salir de su casa. A finales de ese año el paciente comenzó a presentar debilidad muscular distal, manifestada al abrir botellas, cepillarse los dientes, lo cual progresó de forma insidiosa, no fluctuante, sin predominio de horario.\n\nEn enero de 2021 el paciente comenzó con alteraciones de la marcha, las cuales condicionaron caídas frecuentes hasta más de 6 veces a la semana, esto debido a inestabilidad postural. El paciente acudió a valoración en mayo. Se le hizo test de MoCA de 16 puntos con alteraciones en la fluidez del lenguaje y repetición de oraciones; en la abstracción, recuerdo diferido y problemas visuoespaciales y disejecutivos. El test de Luria dio positivo. El paciente presentó facie hipomímica, emitió con hipofonía, entrecortado y lento, y presentó reflejo nauseoso disminuido, rigidez generalizada de predominio izquierdo, hipotrofia generalizada, bradicinesia de predominio izquierdo, fuerza 4/5 generalizada, reflejos de estiramientos musculares 3/4, reflejos abdominocutáneos abolidos, signos de Hoffmann y Trömner presentes de forma bilateral, respuesta plantar extensora bilateral, fasciculaciones en extremidades inferiores evocadas al tacto, marcha con pasos cortos, congelamiento de la marcha al giro, pull test positivo (inestabilidad postural). Se manejó con levodopa carbidopa a una dosis gradual. Al seguimiento a los 3 meses el paciente había presentado nula mejoría en cuanto a los síntomas parkinsónicos, aumento de la debilidad muscular y persistieron los datos de motoneurona inferior y superior. Con estos hallazgos se realizó resonancia magnética (RM) del encéfalo. La velocidad de neuroconducción (VCN) presentó neuropatía axonal motora de miembros torácicos en relación con atrofia y neuroconducción sensitiva sin alteraciones. La electromiografía (EMG) presentó datos de denervación activa (aumento de actividad insercional, potenciales de fibrilación, fasciculación) y reinervación crónica (potenciales de acción de la unidad motora polifásicos, y bajo reclutamiento a la contracción máxima) en los 5 segmentos corporales, lo cual es compatible con enfermedad de motoneurona.\n\n\nLa EMG mostró un aumento de actividad insercional en músculos deltoides, bíceps, tríceps, extensor digital común bilateral y músculos linguales de forma bilateral. Se observaron abundantes potenciales de fibrilación y predominó la fasciculación en los músculos de los miembros torácicos. Durante la contracción, se observó una activación del potencial de acción de la unidad motora (PAUM) de forma polifásica y de gran amplitud. Y a máxima contracción se observó una disminución del reclutamiento en la mayoría de los músculos evaluados.\n\nEl paciente perdió seguimiento un año. Al vover a valoración se encontraba con postración en cama, afásico, aumento de los datos de parkinsonismo y síndrome de motoneurona. Se decidió realizar panel genético que resultó negativo para C9ORF72, así como para 143 genes más involucrados en enfermedades neuromusculares y neurodegenerativas, incluidos los genes VCP, MAT3, asociados a ELA, NOTCH3, asociado a demencia frontotemporal, sin alteraciones. Se reportó resultado de variante patogénica para el gen POLG: C.2209G>C, p.(Gly737Arg), relacionado con síndrome de depleción mitocondrial autosómico dominante y recesivo. Se realizó sesión de asesoramiento genético y el paciente fue informado. En mayo de 2022, el paciente presentaba disfagia y acudió en silla de ruedas, por lo que fue enviado a que se le practicara una gastrostomía.",
+        "gold_summary": "Presentamos un caso de origen latinoamericano que inicialmente se manifestó con síntomas sistémicos de más de 6 años de evolución, con posteriores alteraciones cognitivas. Después presentó alteraciones de la marcha y síntomas motores sugestivos de parkinsonismo con datos atípicos y datos de enfermedad de motoneurona. Se hicieron estudios de extensión que confirmaron hallazgos compatibles con afectación en motoneurona superior e inferior. Observamos mutación en gen POLG, relacionada con síndrome de depleción mitocondrial.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Este es el cuento de un hombre de 73 años. Al principio, hace varios años, empezó a perder el olfato y algo de oído. También tenía estreñimiento y no podía dormir bien. Con el tiempo tuvo problemas para recordar cosas y eso le afectó su trabajo y la vida diaria.\n\nLuego le costó abrir frascos y cepillarse los dientes. Empezó a caerse muchas veces cuando caminaba. Los médicos le hicieron pruebas. Una prueba de la memoria y el pensamiento salió baja. Las pruebas que miran los nervios y los músculos mostraron que muchas células que mandan órdenes a los músculos estaban dañadas. Eso explica la debilidad y los temblores que tuvo.\n\nLe probaron un medicamento para el Parkinson, pero no mejoró. También le hicieron un examen de los genes. En muchos genes no encontraron cambios. Sí hallaron un cambio en un gen llamado POLG. Ese gen ayuda a las \"baterías\" de las células (mitocondrias). Cuando ese gen cambia, las células pueden quedarse sin energía y eso causa problemas.\n\nCon el tiempo se puso peor. Quedó en cama, perdió el habla y tuvo dificultad para tragar. Los médicos le pusieron una sonda para poder darle comida directamente al estómago.\n\nEn resumen: tenía problemas de memoria y de movimiento. Tenía señales de dos cosas: un tipo de problema parecido al Parkinson y también daño en las células que mueven los músculos. Los médicos encontraron un cambio en el gen POLG que puede explicar por qué las células no tenían energía. Fue una enfermedad difícil y fue empeorando con el tiempo.",
+                "fh_score": 80.98
+            },
+            "B2": {
+                "text": "Resumen comprensible y amable:\n\nPresentamos el caso de un hombre latinoamericano de 73 años cuya enfermedad comenzó de forma lenta desde 2016. Al principio tuvo pérdida del olfato (hiposmia), disminución de la audición, estreñimiento e insomnio. En 2020 la familia notó problemas de memoria para eventos recientes y olvidos que afectaron su trabajo. Más adelante empezó a presentar debilidad en manos y brazos, que fue empeorando sin aparecer y desaparecer.\n\nEn enero de 2021 tuvo dificultades para caminar y caídas frecuentes por inestabilidad. En la valoración neurológica obtuvo 16/30 en la prueba MoCA, con problemas en el lenguaje, memoria diferida, funciones visuoespaciales y planificación. El examen mostró rasgos de parkinsonismo (cara con poca expresión, voz baja y lenta, rigidez y lentitud de movimientos), junto con signos de afectación de la motoneurona superior e inferior: reflejos anormales, respuesta plantar extensora, fasciculaciones (contracciones musculares visibles) y debilidad. Al darle levodopa-carbidopa no mejoró el parkinsonismo.\n\nSe hicieron estudios eléctricos: la velocidad de conducción nerviosa mostró daño axonal motor en los brazos y la electromiografía (EMG) mostró signos de denervación activa (fibrilaciones y fasciculaciones) y cambios de reinervación crónica en varios segmentos del cuerpo. Estos hallazgos son compatibles con enfermedad de la motoneurona (un grupo de enfermedades que incluye a la ELA). Posteriormente el paciente empeoró: quedó en cama, con dificultad para hablar (afasia) y problemas para tragar, lo que requirió la colocación de una gastrostomía (tubo para alimentar directamente al estómago).\n\nSe realizó un estudio genético extenso. No se encontraron alteraciones en genes habitualmente asociados a ELA u otras demencias (por ejemplo C9ORF72, VCP, NOTCH3). Sí se identificó una variante patogénica en el gen POLG (c.2209G>C, p.Gly737Arg). Mutaciones en POLG se asocian con síndromes de depleción mitocondrial, que afectan la función de las mitocondrias (las “plantas de energía” de las células) y pueden provocar síntomas neurológicos. El equipo ofreció asesoría genética al paciente y la familia.\n\nQué significa todo esto, en términos sencillos:\n- El cuadro clínico combina signos de parkinsonismo que no respondieron a levodopa y criterios eléctricos que indican daño tanto de la motoneurona superior como inferior.\n- La variante en POLG podría estar relacionada con el problema, pero su papel exacto debe interpretarse junto con la clínica y otros estudios por especialistas en genética y neurología.\n- El manejo ya incluyó terapia sintomática y soporte nutricional; los siguientes pasos suelen ser seguimiento neurológico, apoyo multidisciplinario (rehabilitación, nutrición, cuidados respiratorios si hace falta) y valoración genética familiar si procede.\n\nLamento la situación difícil del paciente y su familia; este caso ilustra cómo enfermedades neurológicas complejas pueden superponerse y por qué se necesitan estudios clínicos, eléctricos e genéticos para entenderlas mejor.",
+                "fh_score": 45.17
+            },
+            "B3": {
+                "text": "Presentamos el caso de un hombre latinoamericano de 73 años con un cuadro progresivo multisistémico que comenzó en 2016 y que, a lo largo de varios años, combinó síntomas motores, cognitivos y autonómicos.\n\nCronología y síntomas principales\n- 2016 en adelante: síntomas prodrómicos no específicos pero relevantes — hiposmia (pérdida del olfato), hipoacusia, estreñimiento e insomnio. Fueron evaluados por otorrinolaringología y audiología sin diagnóstico concluyente.  \n- 2020: inicio de deterioro cognitivo episódico (olvidos de objetos, problemas en la gestión de su negocio) que progresó hasta afectar las actividades diarias (conducción, salir de casa).  \n- Finales 2020: debilidad distal insidiosa (dificultad para abrir botellas, cepillarse los dientes).  \n- Enero 2021: alteración de la marcha con inestabilidad postural y caídas frecuentes (>6/semana).  \n- Mayo 2021: valoración neurológica con MoCA 16/30 (déficits en fluidez verbal, repetición, abstracción, memoria retrasada, visoespacial y funciones ejecutivas). Signos clínicos notables: facie hipomímica, hipofonía, rigidez generalizada (predominio izquierdo), bradicinesia (predominio izquierdo), hipotrofia muscular, reflejos profundos aumentados, abolición de reflejos abdominales cutáneos, signos de neurona motora superior (Hoffmann, Trömner, respuesta plantar extensora bilateral), fasciculaciones en miembros inferiores, marcha con pasos cortos y congelamiento al girar, test de pull positivo. Se inició levodopa-carbidopa sin mejoría.  \n- Empeoramiento electromiográfico y neurofisiológico compatible con enfermedad de motoneurona (ver abajo).  \n- Pérdida de seguimiento durante un año; al retorno estaba postrado, afásico y con agravamiento del parkinsonismo y del síndrome de motoneurona. En mayo 2022 presentaba disfagia y necesitó gastrostomía.\n\nEstudios complementarios relevantes\n- Velocidad de conducción nerviosa: neuropatía axonal motora en miembros superiores (asociada a atrofia); conducción sensitiva normal.  \n- Electromiografía (EMG): actividad de denervación activa (aumento de la actividad insercional, fibrilaciones, fasciculaciones) y signos de reinervación crónica (potenciales de unidad motora polifásicos y bajo reclutamiento) en los cinco segmentos estudiados — hallazgos compatibles con afectación de motoneurona superior e inferior (fenotipo similar a esclerosis lateral amiotrófica / enfermedad motoneurona). Se observó afectación de músculos deltoides, bíceps, tríceps, extensores digitales y lengua.  \n- Resonancia magnética cerebral: mencionada, sin detalles en el informe resumido.  \n- Panel genético amplio (144 genes) y prueba para expansión C9ORF72: negativos para genes clásicos de ELA (incluidos VCP, MATR3) y para NOTCH3.  \n- Se identificó una variante patogénica en POLG: c.2209G>C, p.(Gly737Arg), asociada a síndromes por depleción mitocondrial (herencia autosómica dominante y recesiva). Se brindó asesoramiento genético.\n\nInterpretación y consideraciones\n- El paciente presentó una combinación atípica de parkinsonismo (con pobre respuesta a levodopa), deterioro cognitivo y signos claros de enfermedad de motoneurona. Este patrón sugiere traslapo clínico entre trastornos extrapiramidales y enfermedades de la motoneurona; no se identificó la causa genética clásica de ELA/FTD (C9ORF72 negativo).  \n- La presencia de una variante patogénica en POLG introduce una posible explicación alternativa: las mutaciones en POLG producen alteraciones del ADN mitocondrial y pueden dar síndromes neuromusculares y neurodegenerativos variados (neuropatía, ataxia, parkinsonismo, miopatía, epilepsia, depleción de ADN mitocondrial). No obstante, la relación causal entre la variante POLG encontrada y el cuadro clínico concreto requiere evaluación adicional (correlación fenotípica, estudios funcionales, análisis de linaje familiar y pruebas complementarias de mitocondria).  \n- Dada la rápida progresión hasta la dependencia funcional (afasia, postración, disfagia), el pronóstico fue grave y exigió intervención de soporte nutricional (gastrostomía).\n\nRecomendaciones y pasos siguientes plausibles (según práctica clínica)\n- Confirmación y caracterización de la afectación mitocondrial: determinación de lactato en sangre/CSF, estudio de ADN mitocondrial (carga heteroplásmica), conteo de copias de mtDNA y, si procede, biopsia muscular con estudios bioquímicos mitocondriales.  \n- Revisión y seguimiento genético familiar: ofrecer prueba dirigida a parientes para la variante POLG y asesoramiento genético, dado el hallazgo patogénico y las implicaciones familiares.  \n- Manejo multidisciplinario: cuidados paliativos/rehabilitación, nutrición (gastrostomía ya realizada), fisioterapia, terapia del lenguaje, manejo de complicaciones respiratorias y control sintomático del parkinsonismo y de la rigidez.  \n- Considerar derivación a centros especializados en enfermedades mitocondriales y en enfermedades de motoneurona para discusión de diagnóstico y posibilidades de investigación/ensayos clínicos.\n\nConclusión\nEste paciente mayor presentó un cuadro progresivo complejo que asoció síntomas prodrómicos (olfato, audición, función autonómica), deterioro cognitivo y un síndrome mixto de parkinsonismo y enfermedad de motoneurona. Los estudios neurofisiológicos confirmaron compromiso de motoneurona superior e inferior. El hallazgo de una variante patogénica en POLG abre la posibilidad de un trastorno mitocondrial como explicación o contribución genética al fenotipo, aunque la relación causal no está totalmente establecida sin estudios funcionales y correlación familiar. El caso subraya la importancia de una evaluación genética amplia y de un manejo multidisciplinario en cuadros neurodegenerativos atípicos.",
+                "fh_score": 23.93
+            }
+        }
+    },
+    {
+        "article": "Mujer de 33 años, previamente sana, presentó disnea progresiva, fiebre alta, sudores nocturnos y pérdida de peso en diciembre de 2017. Después de un mes de evolución, fue ingresada en un hospital general con insuficiencia respiratoria aguda y shock séptico con infiltrados alveolares difusos, ictericia, hemoptisis y petequias en las extremidades inferiores. Fue intubada y necesitó soporte hemodinámico. Se detectó un soplo sistólico mitral a la ausculta del precordio. Había leucocitosis acentuada con desviación a la izquierda, plaquetopenia, disfunción hepática y renal asociada a proteinuria subnefrótica y consumo de complemento. El resultado de los anticuerpos antinucleares fue de 1/80, a pesar de los niveles normales de anti-DNA de doble cadena, anti-SM y anti-PR3. Después de la administración de ceftriaxona, mejoró clínicamente. Fiebre amarilla, dengue, chikungunya, leptospirosis, VIH y hepatitis virales fueron descartados. Las hemoculturas fueron positivas para Haemophilus spp. en las seis muestras recolectadas. El ecocardiograma transtorácico (ETT) demostró una masa ecogénica amorfa con superficie irregular y algunos elementos móviles que envolvían ambos folletos de la válvula mitral, midiendo 20x17 mm en el folleto anterior y 19 mm en su mayor diámetro en los folletos posteriores, resultando en regurgitación grave por flail mitral y perforación. La resonancia magnética mostró pequeños abscesos esplénicos, tratados de manera conservadora. Un aneurisma micótico no complicado de la arteria cerebral media izquierda fue tratado por embolización percutánea. Treinta días después de la hospitalización, se sometió a un reemplazo de la válvula mitral con éxito por una prótesis valvular biológica de tamaño 29 mm y después de una extensa resección del tumor. Se evidenció regurgitación aórtica moderada debido a lesión de la fibrosa intervalvar mitroaórtica y retracción de la cúspide no coronaria, tratada de manera conservadora. El examen patológico confirmó la presencia de un mixoma valvular mitral infectado. La paciente completó 28 días de ceftriaxona y gentamicina, recibiendo el alta hospitalaria asintomática. En el seguimiento de un año, no hubo evidencia de recurrencia y se constató solamente regurgitación aórtica leve. Los mixomas infectados presentan mayor riesgo de eventos embólicos, aunque las manifestaciones clínicas son indistinguibles de tumores no infectados.2 El presente caso parece ser el sexto de mixoma valvular mitral infectado relatado en la literatura, llenando criterios definitivos para el diagnóstico, y el tercero causado por un microorganismo del grupo HACEK.3 - 8 De los 64 mixomas valvulares mitrales publicados de 2006 a 2012, los síntomas eran cardiovasculares en 36,7%; 9,5 a 21,6% de los mixomas de la válvula mitral fueron sometidos al cambio de válvula y el tiempo del diagnóstico hasta la cirugía varió de algunas horas a 42 días.2 , 9 La mortalidad operatoria y general fue relatada como siendo, respectivamente, 2,6 a 3% y 5,1 a 21%.2 , 10 En la presente serie, la mayoría de los pacientes presentó insuficiencia cardiaca sintomática, fueron sometidos al cambio de válvula mitral y todos presentaron buenos resultados en el seguimiento.\n",
+        "gold_summary": "Una mujer de 33 años de edad, con antecedentes de fiebre y disnea de unos pocos días de evolución, fue hospitalizada con un síndrome lupoide, con hemocultivos positivos para Haemophilus spp. El ecocardiograma reveló una masa gigante que involucraba ambas valvas mitrales, con una severa regurgitación mitral que requería un reemplazo valvular mitral biológico. La microscopía reveló un mixoma infectado y la paciente fue dada de alta asintomática tras finalizar la terapia con antibióticos. Ella tuvo un buen seguimiento.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había una mujer de 33 años que se sentía muy enferma. Tenía fiebre, dificultad para respirar y perdía peso. Llegó al hospital con una infección grave y tuvo que usar una máquina para ayudarla a respirar.\n\nLos médicos encontraron gérmenes en su sangre. También vieron en el corazón una masa grande en la válvula mitral. La válvula es como una puerta que ayuda a la sangre a ir en la dirección correcta. La masa estaba dañando la puerta y la sangre no circulaba bien.\n\nElla recibió antibióticos fuertes y los médicos trataron otros problemas, como un pequeño absceso en el bazo y un aneurisma en una arteria del cerebro (eso es una bolita en una arteria que puede ser peligrosa; la arreglaron con un procedimiento sin abrir la cabeza). Un mes después le cambiaron la válvula mitral por una nueva de material biológico y quitaron la masa.\n\nEl examen del tejido mostró que la masa era un mixoma infectado. Después de 28 días de antibióticos, la mujer salió del hospital sin síntomas. Un año después estaba bien y no había vuelto a aparecer la masa. Los médicos dicen que estos mixomas infectados son raros, pero pueden ser graves. Gracias al tratamiento a tiempo, ella se recuperó.",
+                "fh_score": 74.74
+            },
+            "B2": {
+                "text": "Resumen comprensible y amable:\n\nUna mujer sana de 33 años comenzó con fiebre, pérdida de peso y dificultad para respirar. Al mes empeoró y fue hospitalizada con insuficiencia respiratoria y shock séptico; además presentó tos con sangre, ictericia (piel y ojos amarillos) y pequeñas manchas en las piernas llamadas petequias. Los análisis mostraron infección y afectación del hígado y los riñones, y los hemocultivos crecieron Haemophilus spp., una bacteria que puede infectar el corazón.\n\nUna ecocardiografía mostró una masa grande y irregular en la válvula mitral (la válvula entre dos cámaras del corazón) que dañaba ambos velos y producía una regurgitación grave: la sangre volvía en lugar de seguir su camino normal. Se detectaron también pequeños abscesos en el bazo y un aneurisma micótico (una dilatación de una arteria causada por la infección) en una arteria cerebral, que se trató con embolización.\n\nTras estabilizarla con antibióticos (ceftriaxona y gentamicina) y tratar las complicaciones, a los 30 días se le sustituyó la válvula mitral por una prótesis biológica y se resecaron los tejidos infectados. El examen microscópico confirmó que la masa era un mixoma (un tumor benigno del corazón) que estaba infectado. Completó 28 días de antibióticos, recibió el alta sin síntomas y, al año, no había recurrencia; solo quedó una insuficiencia aórtica leve.\n\nComentario final: los mixomas infectados son raros y tienen mayor riesgo de que fragmentos viajen por la sangre y provoquen embolias, pero sus síntomas suelen ser parecidos a los de los mixomas no infectados. En este caso el tratamiento combinado (antibióticos y cirugía) fue exitoso.",
+                "fh_score": 51.29
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel universitario)\n\nCaso: mujer de 33 años previamente sana que consultó por disnea progresiva, fiebre alta, sudores nocturnos y pérdida de peso. Tras aproximadamente un mes empeoró hasta ingreso por insuficiencia respiratoria aguda y shock séptico, con infiltrados alveolares difusos, ictericia, hemoptisis y petequias en las piernas. Requirió intubación y soporte hemodinámico.\n\nHallazgos importantes\n- Signos y laboratorio: soplo sistólico mitral al examen; leucocitosis con desviación a la izquierda, trombocitopenia, disfunción hepática y renal, proteinuria subnefrótica y consumo de complemento. Anticuerpos antinucleares 1/80, demás autoanticuerpos relevantes negativos.\n- Microbiología: hemocultivos positivos en las seis muestras para Haemophilus spp. (miembro del grupo HACEK).\n- Ecocardiografía transtorácica: masa ecogénica, irregular y parcialmente móvil que involucraba ambas valvas mitrales (aprox. 20×17 mm), con flail y perforación de la válvula causando regurgitación mitral grave.\n- Complicaciones y procedimientos: pequeños abscesos esplénicos (tratados de forma conservadora) y un aneurisma micótico de la arteria cerebral media izquierda tratado por embolización percutánea.\n- Tratamiento y evolución: recibió ceftriaxona (y gentamicina), mejoró clínicamente; a los 30 días se realizó resección extensa y reemplazo de la válvula mitral por una prótesis biológica de 29 mm. Se observó regurgitación aórtica moderada por lesión de la zona intervalvar mitroaórtica, manejada conservadoramente.\n- Anatomía patológica: confirmación de mixoma (tumor cardiacógeno) de la válvula mitral infectado.\n- Alta y seguimiento: completó 28 días de antibioterapia, egresó asintomática; a 1 año no hubo recidiva del mixoma y quedó con regurgitación aórtica leve.\n\nInterpretación y puntos clave\n- Se trató de un mixoma valvular mitral infectado por Haemophilus spp., un cuadro raro (pocos casos descritos) que combina infección sistémica grave y afectación valvular tumoral. Aunque clínicamente los mixomas infectados pueden parecerse a los no infectados, la infección aumenta el riesgo de embolias y complicaciones sépticas.\n- El diagnóstico combinó hallazgos clínicos, hemocultivos positivos, imágenes (ecocardiograma) y confirmación histológica —cumpliendo criterios definitivos.\n- Manejo efectivo incluyó antibioterapia dirigida, tratamiento de complicaciones embólicas/aneurismas y tratamiento quirúrgico (resección y reemplazo valvular) cuando fue necesario.\n\nImplicaciones prácticas y recomendaciones razonables\n- Los mixomas valvulares infectados requieren un enfoque multidisciplinario: cardiología, cirugía cardíaca, infectología y neurología/intervencionismo si hay aneurismas o embolias cerebrales.\n- Tras el alta, el seguimiento debe centrarse en: controles seriados por ecocardiografía para vigilar la prótesis y la regurgitación aórtica, vigilancia neurológica por el antecedente de aneurisma micótico, y control clínico/infectológico para detectar recurrencia o complicaciones tardías.\n- En infecciones por HACEK, ceftriaxona es tratamiento apropiado; la duración y combinación con aminoglucósidos varía según la situación clínica, el tipo de intervención y la respuesta.\n\nPronóstico\n- En este caso la paciente evolucionó favorablemente: recuperación clínica, resección del tumor infectado, y ausencia de recidiva a 1 año, aunque persiste regurgitación aórtica leve que requiere seguimiento.\n\nComentario final (empatía)\nEste fue un cuadro grave y poco frecuente cuyo manejo coordinado —antibiótico adecuado, tratamiento de complicaciones y cirugía valvular— permitió una recuperación completa y sin recidiva a un año. Para la paciente, el seguimiento cardiológico y neurológico continuo será importante para vigilar la función valvular y prevenir complicaciones futuras.",
+                "fh_score": 26.77
+            }
+        }
+    },
+    {
+        "article": "Mujer de 71 años, que fue atendida en urgencias del Hospital de Mataró (Barcelona, España) el 9 de septiembre de 2020 con debilidad progresiva, por lo que se decidió su ingreso en neurología. Como antecedentes patológicos destacaban hipertensión arterial, temblor esencial, artrosis y trastorno de ansiedad leve, en tratamiento con gabapentina, sertralina y tramadol. La paciente había consultado a su médico de cabecera el 1 de septiembre de 2020 por dolor abdominal, junto con diarrea leve que duró 24 horas. Al día siguiente comenzó a sentirse débil y, a lo largo de los días siguientes, apareció disnea y disfagia, por lo que se sospechó laringitis y se le recetó prednisona. El 8 de septiembre de 2020 fue visitada nuevamente por su médico de cabecera por empeoramiento global de la debilidad; presentaba, además, disartria, disfagia y ptosis bilateral, por lo que fue derivada a urgencias del hospital.\n\nA su llegada no presentaba fiebre, la presión arterial y la frecuencia cardíaca eran normales, y la exploración física era normal, a excepción de taquipnea moderada. El examen neurológico mostró ptosis palpebral bilateral, parálisis facial bilateral, midriasis bilateral arreactiva a la luz y a la acomodación, oftalmoparesia bilateral tanto para la suprainfraversión como para la mirada horizontal bilateral, tetraparesia moderada en las extremidades (3/5), y disfonía y disfagia graves. Ella estaba consciente y el contenido del lenguaje era normal, al igual que los reflejos miotáticos, la sensibilidad y la coordinación. Las maniobras de fatigabilidad no fueron concluyentes y se realizó la prueba del hielo, que resultó positiva, mejorando –transitoriamente– la ptosis.\n\nLa reacción en cadena de la polimerasa (PCR) para el SARS-CoV-2 fue repetidamente negativa (en su ambulatorio y en el hospital). La gasometría arterial mostró hipoxemia: 75, con SO2 al 95%, y el resto de las exploraciones realizadas en urgencias resultaron normales (radiografía de tórax, análisis de sangre de rutina, electrocardiograma).\n\nSe inició tratamiento de soporte con oxígeno, sueroterapia, nutrición por sonda nasogástrica y medidas encaminadas a la prevención de complicaciones. El cuadro se estabilizó el tercer día del ingreso en planta, sin requerir soporte ventilatorio avanzado, y comenzó una mejoría lenta a partir del octavo día, iniciando tolerancia a la dieta adaptada de disfagia. Durante la primera semana presentaba hipotensión arterial, que fue corrigiéndose con la sueroterapia. A partir de la segunda semana, pudo iniciar rehabilitación física, con buena evolución, por lo que fue trasladada a un centro específico de rehabilitación al 19.º día, y entonces fue capaz de deambular con ayuda bilateral. En la visita de control en consultas externas de neurología seis semanas después, la paciente estaba completamente recuperada.",
+        "gold_summary": "Describimos el caso confirmado de botulismo alimentario en una paciente atendida en nuestro hospital en septiembre de 2020. La instauración en pocos días de una afectación bilateral de pares craneales, incluyendo disfagia, disnea y disartria, junto con midriasis y tetraparesia graves, precedida de diarrea, constituyó la presentación clínica en el primer caso; mientras que en su familiar cursó con síntomas inespecíficos y transitorios. Constatamos disautonomía consistente en hipotensión arterial. Teniendo en cuenta la situación pandémica en aquel momento, se descartó repetidamente la infección por SARS-CoV-2 antes de plantear alternativas diagnósticas. La neurotoxina B de C. botulinum fue detectada en las heces de la paciente, confirmando el diagnóstico de botulismo, que relacionamos con la ingesta de una conserva casera de alubias. Se completó el diagnóstico diferencial del cuadro descartando otras posibles etiologías.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Esta es la historia de una mujer de 71 años que se puso muy débil después de tener diarrea. Al principio tenía dolor de barriga y un día de diarrea. Luego empezó a sentirse débil, con dificultad para respirar, tragar y hablar. La vieron en urgencias y la ingresaron en neurología.\n\nEn el hospital tenía los párpados caídos en los dos ojos, la cara muy floja, las pupilas grandes que no cambiaban con la luz, y los ojos casi no se movían. También tenía debilidad en los cuatro brazos y piernas y mucha dificultad para tragar y hablar. Estaba despierta y pensaba con normalidad. Le hicieron una prueba con hielo y los párpados mejoraron un rato.\n\nLe hicieron pruebas para COVID y salieron negativas. Tenía el oxígeno un poco bajo, pero la radiografía de tórax y las analíticas salieron bien. Empezaron cuidados con oxígeno, sueros y nutrición por sonda para que no se atragantara. No necesitó respirador.\n\nAl tercer día se estabilizó. Empezó a mejorar despacio desde el octavo día. Tuvo bajadas de tensión que mejoraron con sueros. En la segunda semana pudo empezar rehabilitación. El día 19 la llevaron a un centro de rehabilitación y pudo andar con ayuda. Se recuperó por completo a las seis semanas.\n\nLos médicos encontraron la toxina B de Clostridium botulinum en sus heces. Esto confirmó que tuvo botulismo alimentario. Creen que fue por comer una conserva casera de alubias. Un familiar tuvo síntomas leves y breves. Los médicos descartaron otras causas antes de dar el diagnóstico.\n\nResumen claro: fue un botulismo por comida. La paciente recibió cuidados y rehabilitación. Al final se recuperó totalmente.",
+                "fh_score": 75.99
+            },
+            "B2": {
+                "text": "Resumen para alumnos de secundaria (lectura clara y amable)\n\nEste informe cuenta el caso de una mujer de 71 años que en septiembre de 2020 desarrolló debilidad y problemas para mover los ojos y la cara, así como dificultad para hablar, tragar y respirar. Antes de estos síntomas tuvo un episodio breve de diarrea. Al llegar al hospital se descartó repetidamente que tuviera COVID-19 (las PCR fueron negativas).\n\nLos médicos observaron que tenía afectación de varios nervios craneales (es decir, los nervios que controlan los ojos, la cara, la deglución y la voz), pupilas dilatadas que no reaccionaban a la luz, debilidad en los cuatro miembros y baja presión arterial. Estos signos sugirieron botulismo alimentario: una intoxicación causada por una toxina producida por la bacteria Clostridium botulinum que puede provocar parálisis y afectar funciones automáticas del cuerpo (como la presión arterial).\n\nEl diagnóstico se confirmó al encontrar la neurotoxina B de C. botulinum en las heces de la paciente. Se relacionó el caso con la ingesta de una conserva casera de judías (alubias). Otra persona de su familia sólo tuvo síntomas leves y pasajeros.\n\nEl tratamiento fue principalmente de apoyo: oxígeno, líquidos por vía venosa, alimentación por sonda mientras no podía tragar y medidas para prevenir complicaciones. No necesitó ventilación invasiva. Empezó rehabilitación física en la segunda semana, mejoró poco a poco y fue trasladada a un centro de rehabilitación. Se recuperó completamente en unas seis semanas. Los médicos también descartaron otras causas posibles antes de llegar a este diagnóstico.",
+                "fh_score": 57.08
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel lector universitario)\n\nPresentación y antecedente inmediato\n- Paciente mujer de 71 años, con hipertensión, temblor esencial, artrosis y ansiedad, en tratamiento con gabapentina, sertralina y tramadol.\n- El 1 de septiembre de 2020 consultó por dolor abdominal y diarrea leve de 24 horas. Desde el día siguiente empezó con debilidad progresiva; en los días posteriores apareció disnea y disfagia. Inicialmente se sospechó laringitis y se le pautó prednisona. El 8 de septiembre presentó empeoramiento: disartria, disfagia y ptosis bilateral, por lo que fue derivada al hospital; ingresó el 9 de septiembre.\n\nExploración y hallazgos clave\n- Signos vitales: sin fiebre; presión arterial y frecuencia cardiaca dentro de límites normales al ingreso; respiración algo acelerada. Gasometría arterial con leve hipoxemia (PaO2 ≈ 75 mmHg; saturación ≈ 95%).\n- Estado neurológico: consciente, lenguaje con contenido normal; reflejos tendinosos, sensibilidad y coordinación preservados.\n- Defectos motores y neurológicos importantes y bilaterales: ptosis palpebral, parálisis facial, midriasis bilateral no reactiva a la luz ni a la acomodación, oftalmoparesia (movimientos oculares limitados vertical y horizontalmente), tetraparesia moderada (fuerza 3/5) y disfonía y disfagia graves.\n- Prueba del hielo positiva (mejora transitoria de la ptosis), maniobras de fatigabilidad no concluyentes.\n- Pruebas de imagen y analítica de rutina sin alteraciones significativas; PCR para SARS‑CoV‑2 repetidamente negativa.\n\nEvolución clínica y tratamiento\n- Se instauró tratamiento de soporte: oxígeno, fluidoterapia, nutrición por sonda nasogástrica y medidas para prevenir complicaciones.\n- No requirió ventilación mecánica avanzada. Presentó hipotensión durante la primera semana, que se corrigió con fluidos.\n- Estabilización al tercer día; mejoría lenta desde el día 8 con progresiva tolerancia oral. Inició rehabilitación en la segunda semana; fue transferida a un centro de rehabilitación el día 19 y pudo deambular con ayuda bilateral.\n- En la consulta de neurología a las seis semanas la paciente estaba completamente recuperada.\n\nDiagnóstico y etiología\n- Se confirmó botulismo alimentario: se detectó neurotoxina tipo B de Clostridium botulinum en las heces de la paciente. La intoxicación se relacionó con la ingestión de una conserva casera de alubias.\n- Se documentó además disautonomía (hipotensión). Un familiar presentó síntomas leves y transitorios.\n- Se completó el diagnóstico diferencial y se descartaron otras etiologías relevantes, incluidas repetidas pruebas de COVID‑19 en el contexto pandémico.\n\nBreve explicación del mecanismo (para comprensión)\n- El botulismo alimentario es causado por una toxina que bloquea la liberación de acetilcolina en la unión neuromuscular y en sinapsis autonómicas, provocando una parálisis motora descendente y posible afectación autonómica. Suele comenzar con síntomas cráneo‑bulbares (ptosis, diplopía, disfagia, disartria) y puede progresar a debilidad generalizada y riesgo respiratorio.\n\nImplicaciones prácticas\n- Ante un cuadro agudo de pares craneales bilaterales con debilidad y antecedentes de ingestión de conservas caseras, debe considerarse botulismo y recogerse muestras de heces y alimentos para análisis. El manejo inmediato es sobre todo soporte respiratorio y nutricional, monitorización estrecha y rehabilitación; la identificación del alimento implicado es clave para medidas de salud pública.\n- La recuperación completa es posible pero puede requerir semanas de soporte y rehabilitación, como ilustra este caso.\n\nComentario final\nEste caso muestra una presentación clásica de botulismo alimentario con recuperación completa tras manejo de soporte y rehabilitación. La evaluación incluyó descartar infecciones prevalentes en la época (SARS‑CoV‑2) antes de confirmar la etiología por toxina B de C. botulinum.",
+                "fh_score": 37.99
+            }
+        }
+    },
+    {
+        "article": "Un hombre de 52 años presentó pérdida de agudeza visual en su ojo derecho (OD) dos días después de una inyección intravenosa no complicada de ranibizumab con una aguja de 30 G. Su historial médico incluía PE, miopía alta y vitrectomía pars plana en el OD debido a desprendimiento de retina. Recibía tratamiento mensual con ranibizumab debido a neovascularización coroidea secundaria a estrías angioides, con 78 inyecciones previas en el OD. En el momento de la presentación, su BCVA era de 6/18 y la presión intraocular (IOP) era de 3 mmHg. El examen con lámpara de hendidura del segmento anterior no mostró nada de particular. El examen de fondo de ojo y los escaneos OCT revelaron pliegues corio-retinianos posteriores. En conjunto, la baja presión intraocular y los hallazgos del fondo de ojo llevaron al diagnóstico de hipotensión maculopatía. Se prescribió dexametasona tópica y atropina para mejorar la función del cuerpo ciliar. La IOP se normalizó en tres días con recuperación de la agudeza visual y resolución de los pliegues corio-retinianos. Cuatro meses después, se realizó una nueva inyección intravenosa anti-VEGF en el cuadrante inferolateral y el paciente informó disminución de la agudeza visual en el día siguiente a la inyección. La BCVA era contar los dedos y la IOP era de 2 mmHg. Los pliegues corio-retinianos en el polo posterior estaban presentes, incluso más prominentemente esta vez. El examen con lámpara de hendidura reveló una herida abierta en la esclerótica en el sitio de la inyección. La herida se suturó con monofilamento 10-0 y se prescribió dexametasona tópica y atropina. El paciente se recuperó bien y presentó una BCVA de 6/12 y una IOP de 12 mmHg.\n",
+        "gold_summary": "Un hombre de 52 años se quejó de pérdida de visión en el ojo derecho (OD) dos días después de un IVI anti-VEGF sin complicaciones para el tratamiento de la neovascularización coroidea secundaria a estrías angioides. Su historial médico incluía PE, miopía patológica y una vitrectomía pars plana (PPV) previa debido a un desprendimiento de retina. La agudeza visual mejor corregida (BCVA) en el OD disminuyó de 6/12 a 6/18 después del IVI. La presión intraocular (IOP) era de 3 mmHg y se observaron pliegues corio-retinianos en el polo posterior. Se prescribió dexametasona tópica y atropina, y se observó una recuperación completa después de tres días. Cuatro meses después, el paciente desarrolló un nuevo episodio de pérdida de visión después de otro IVI. Su BCVA era contar los dedos, la IOP era de 2 mmHg, y se observaron pliegues corio-retinianos más evidentes. Esta vez, una herida escleral abierta en el sitio de inyección era evidente y fue necesaria una sutura escleral. Una vez más, el paciente se recuperó bien.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un hombre de 52 años perdió visión en su ojo derecho dos días después de que le pusieran una inyección dentro del ojo para tratar vasos anormales. Él ya había tenido antes una operación en ese ojo y usa estas inyecciones desde hace tiempo.\n\nDespués de la primera inyección, el ojo tenía muy baja presión. Esto hizo que la parte de atrás del ojo tuviera pliegues y que viera menos. Los médicos le dieron gotas para ayudar al ojo a curarse y a subir la presión. Tres días después, la presión volvió a la normalidad y su vista mejoró.\n\nCuatro meses después, volvió a tener pérdida de visión después de otra inyección. Esta vez la presión era aún más baja. Al mirar con lupa encontraron una pequeña herida en la pared blanca del ojo donde se había puesto la inyección. Los médicos cerraron la herida con una puntada y le dieron las mismas gotas. El ojo sanó y su vista volvió a mejorar.\n\nEn resumen: las inyecciones dentro del ojo causaron que la presión bajara y que la visión empeorara. Con tratamiento rápido, primero con gotas y luego con una puntada cuando hubo una fuga, el ojo se recuperó bien.",
+                "fh_score": 81.05
+            },
+            "B2": {
+                "text": "This report describes a 52-year-old man who had two episodes of sudden vision loss in his right eye shortly after routine intravitreal injections (IVIs) of an anti-VEGF drug (ranibizumab). Anti-VEGF injections are medicines placed inside the eye to stop abnormal new blood vessels; he was receiving these monthly for choroidal neovascularization (abnormal blood vessel growth under the retina) caused by angioid streaks. His eye history included high myopia (strong nearsightedness) and a past pars plana vitrectomy (surgery that removed the eye’s inner gel) for a retinal detachment. He had already had many injections in that eye.\n\nFirst episode\n- Two days after an injection, his corrected vision fell from 6/12 to 6/18 and his intraocular pressure (IOP) was very low (3 mmHg). Low IOP is called hypotony.\n- The front of the eye looked normal, but retinal imaging showed chorioretinal folds (wrinkles in the layers at the back of the eye).\n- These findings led to the diagnosis of hypotony maculopathy — vision problems caused by very low eye pressure that distort the central retina.\n- He was treated with topical dexamethasone (a steroid) and atropine (a medicine that relaxes the eye’s focusing muscle). His pressure and vision returned to normal within three days and the retinal folds resolved.\n\nSecond episode (four months later)\n- After another injection, he had rapid vision loss the next day (vision reduced to counting fingers) and a very low IOP (2 mmHg). The retinal folds were more obvious.\n- This time the exam found an open wound in the sclera (the white wall of the eye) at the injection site. A leaking wound can cause hypotony.\n- The wound was closed with a very fine suture and he received the same topical treatments. He recovered well, with vision improving to 6/12 and IOP rising to 12 mmHg.\n\nKey points and lessons\n- Repeated injections, prior vitrectomy, and high myopia can raise the risk that an injection site might leak and cause hypotony.\n- Hypotony maculopathy can often be treated successfully by sealing a leak (if present) and using medicines to reduce inflammation and help the eye’s ciliary body restore normal pressure.\n- Prompt examination and treatment after sudden vision change following an injection are important and can lead to full recovery, as happened in this case.\n\nIf you or someone notices sudden vision loss after an eye injection, they should seek urgent eye care so the cause can be checked and treated quickly.",
+                "fh_score": 83.53
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel universitario)\n\nUn hombre de 52 años sufrió pérdida aguda de visión en su ojo derecho (OD) dos días después de una inyección intravítrea (IVI) de ranibizumab con aguja 30 G, administrada como parte de un tratamiento mensual por neovascularización coroidea secundaria a estrías angioides (había recibido 78 inyecciones previas en ese ojo). Sus antecedentes incluían miopía alta y una vitrectomía pars plana previa por desprendimiento de retina.\n\nPrimer episodio\n- Presentación: agudeza visual mejor corregida (BCVA) bajó a 6/18; presión intraocular (PIO) muy baja, 3 mmHg.  \n- Examen: segmento anterior sin hallazgos relevantes; fondo de ojo y OCT mostraron pliegues corio-retinianos en el polo posterior.  \n- Interpretación: conjunto de hipotensión ocular con maculopatía (hipotonía macular) secundaria a fuga/defecto de la pared ocular tras la IVI.  \n- Tratamiento y evolución: terapia tópica con dexametasona y atropina para mejorar la función del cuerpo ciliar y controlar la inflamación. La PIO se normalizó en tres días, con resolución de los pliegues y recuperación de la agudeza visual.\n\nSegundo episodio (4 meses después)\n- Tras una nueva IVI en el cuadrante inferolateral, el paciente refirió disminución de visión al día siguiente. BCVA fue contar dedos, PIO 2 mmHg. Los pliegues corio-retinianos eran ahora más prominentes.  \n- Examen con lámpara de hendidura mostró una herida escleral abierta en el sitio de la inyección.  \n- Manejo: sutura escleral con monofilamento 10-0 y nuevamente dexametasona tópica y atropina. Resultado favorable: recuperación a BCVA 6/12 e IOP 12 mmHg.\n\nComentarios y enseñanzas clave (implicaciones)\n- La hipotensión ocular tras IVI puede presentarse con visión reducida y pliegues corio-retinianos en el polo posterior; la PIO baja es un dato crítico para el diagnóstico.  \n- En ojos vitrectomizados y/o miopes altos existe mayor riesgo de fuga por el sitio de inyección y de hipotensión prolongada.  \n- El manejo inicial puede ser conservador (ciclopléjicos y antiinflamatorios tópicos) si la fuga es mínima y la PIO se recupera; cuando hay una herida escleral franca o fuga persistente, es necesaria reparación quirúrgica (sutura).  \n- Vigilancia estrecha tras IVI —evaluación de la PIO y del sitio de inyección— permite detectar y tratar la hipotensión antes de que cause daño macular permanente.\n\nEmpático cierre\nEl paciente evolucionó bien tras ambos episodios gracias a la detección rápida y al tratamiento apropiado. Para pacientes con características de alto riesgo (vitrectomía previa, miopía patológica) es razonable una vigilancia más cuidadosa tras las IVI y discutir con el equipo las medidas preventivas y las alternativas terapéuticas.",
+                "fh_score": 50.1
+            }
+        }
+    },
+    {
+        "article": "Una mujer de 82 años acudió al servicio de urgencias por dolor abdominal, diarrea, confusión y deterioro de su estado general de varios días de evolución. Entre sus antecedentes médicos destacaban hipertensión arterial tratada e hipotiroidismo en tratamiento sustitutivo. No se recogieron antecedentes quirúrgicos ni hábitos tóxicos de interés. A la exploración física, la frecuencia cardíaca era de 84 lpm, tensión arterial de 105/82 mmHg, temperatura de 38 °C y saturación de oxígeno de 95% en aire ambiente. Las mucosas estaban secas y el abdomen era difusamente doloroso a la palpación sin masas palpables ni reacción peritoneal. La analítica realizada mostró una hemoglobina de 13.1 g/dL, proteína C reactiva a 122.9 mg/L sin leucocitosis (8.9 × 10^9/L), hiponatremia (130 mmol/L), hipopotasemia (2.9 mmol/L), pruebas de función renal, hepáticas, lipasa y enzimas cardiacas normales. El frotis para SARSCoV-2 fue negativo. La orina era maloliente con presencia de nitritos positivos, hematíes (+++) y leucocitos (+) por lo que se envió la muestra para cultivo microbiológico. Ante estos hallazgos se inició antibioticoterapia probabilista con ceftriaxona ante la sospecha de una posible infección urinaria y se decidió realizar una tomografía tóraco-abdomino-pélvica para descartar la presencia de un foco infeccioso profundo. Este examen reveló la presencia de signos de broncopatía crónica y una neumatosis vesical parietal a nivel abdominal compatible con una cistitis enfisematosa. El cultivo de orina reveló la presencia de Escherichia coli (> 100 000 UFC/m) sensible a la antibioticoterapia prescrita empíricamente y los hemocultivos fueron positivos al mismo germen. Se decidió el ingreso de la paciente en servicio de medicina interna y se continuó el tratamiento antibiótico durante 7 días con una evolución favorable desde el punto de vista clínico y analítico, permitiendo el alta hospitalaria.",
+        "gold_summary": "Una mujer de 82 años con antecedentes de hipertensión arterial e hipotiroidismo acudió al servicio de urgencias por dolor abdominal, diarrea, confusión y deterioro de su estado general de varios días de evolución. A su admisión, la paciente se encontraba febril y la analítica mostró una elevación de la proteína C reactiva sin leucocitosis (8.9 × 10^9/L). En ese contexto se realizó exudado nasofaríngeo para SARS-CoV-2 que fue negativo. Con estos resultados, la sospecha inicial era la de un cuadro infeccioso de origen digestivo. La muestra de orina era maloliente con presencia de leucocitos y nitritos enviándose a cultivo microbiológico. Se inició tratamiento antibiótico empírico con una cefalosporina de tercera generación ante la sospecha de une posible infección urinaria. Se decidió la realización de una tomografía tóraco-abdomino-pélvica con el objetivo de evaluar la presencia de otros focos infecciosos en una paciente de edad avanzada. Este estudio mostró una cistitis enfisematosa, una enfermedad poco frecuente en una paciente sin ninguno de los factores de riesgo clásicos para esta entidad. Los cultivos de orina y sangre fueron positivos para Escherichia coli sensible al antibiótico empírico por lo que se continuó para completar 7 días de tratamiento. La evolución clínica fue favorable.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una mujer de 82 años fue al hospital porque tenía dolor de barriga, diarrea y estaba confundida. Llevaba varios días encontrándose mal y tenía un poco de fiebre.\n\nLa orina olía mal y las pruebas mostraron signos de infección. Los médicos empezaron un antibiótico mientras esperaban los resultados. Hicieron una radiografía especial (tomografía) y vieron gas en la pared de la vejiga. Eso se llama cistitis enfisematosa. Es una infección rara en la vejiga que puede formar gas.\n\nLas muestras de orina y de sangre mostraron que la bacteria Escherichia coli causaba la infección. Esa bacteria respondió bien al antibiótico que le dieron. La mujer estuvo ingresada y recibió antibióticos durante 7 días. Mejoró con el tratamiento y pudo volver a casa.",
+                "fh_score": 71.1
+            },
+            "B2": {
+                "text": "Una mujer de 82 años con hipertensión e hipotiroidismo llegó a urgencias tras varios días con dolor abdominal, diarrea, confusión y empeoramiento general. Tenía fiebre (38 °C), mucosas secas y dolor abdominal difuso a la palpación.\n\nEn los análisis destacó una proteína C reactiva elevada (marcador de inflamación), sin aumento del recuento de glóbulos blancos, además de sodio y potasio bajos. La orina olía mal y en el examen se detectaron nitritos y leucocitos, hallazgos que suelen indicar infección urinaria; por eso se envió la orina a cultivo y se empezó tratamiento antibiótico empírico con ceftriaxona.\n\nSe realizó una tomografía toraco-abdominopélvica para buscar focos de infección más profundos. El estudio mostró neumatosis de la pared vesical, es decir, gas en la pared de la vejiga, hallazgo compatible con cistitis enfisematosa. La cistitis enfisematosa es una infección de la vejiga que produce gas en la pared y suele ser más frecuente en pacientes con factores de riesgo (por ejemplo, diabetes), aunque en esta paciente no había esos factores clásicos.\n\nLos cultivos confirmaron Escherichia coli en orina (>100 000 UFC/mL) y en sangre, sensible al antibiótico iniciado. La presencia de E. coli en sangre indica que la infección llegó a la circulación (bacteriemia), por lo que la paciente fue ingresada y continuó con antibiótico durante 7 días.\n\nLa evolución fue favorable desde el punto de vista clínico y analítico, y la paciente pudo recibir el alta. En resumen: infección urinaria complicada por cistitis enfisematosa y bacteriemia por E. coli, tratada con antibiótico adecuado con buena respuesta.",
+                "fh_score": 55.97
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel lector universitario)\n\nPresentación\n- Mujer de 82 años que consultó por varios días de dolor abdominal, diarrea, confusión y deterioro del estado general.\n- Antecedentes: hipertensión arterial e hipotiroidismo en tratamiento. No se refirieron antecedentes quirúrgicos ni hábitos tóxicos relevantes.\n\nExploración y pruebas iniciales\n- Signos vitales: taquicardia moderada (84 lpm), tensión arterial 105/82 mmHg, febrícula (38 °C) y saturación de O2 95% en aire ambiente. Mucosas secas; abdomen doloroso de manera difusa sin defensa ni signos de peritonismo.\n- Analítica: hemoglobina 13.1 g/dL; proteína C reactiva elevada (122.9 mg/L); recuento de leucocitos dentro de rango (8.9 × 10^9/L). Alteraciones electrolíticas: hiponatremia leve (Na 130 mmol/L) e hipopotasemia (K 2.9 mmol/L). Función renal, hepática, lipasa y enzimas cardiacas normales.\n- Frotis nasofaríngeo para SARS‑CoV‑2: negativo.\n- Orina maloliente con nitritos positivos, hematíes y leucocitos; se envió cultivo urinario.\n\nHallazgos de imagen y microbiología\n- Tomografía tóraco-abdomino-pélvica: signos de broncopatía crónica y neumatosis parietal vesical compatible con cistitis enfisematosa (presencia de gas en la pared de la vejiga).\n- Cultivos: urocultivo con Escherichia coli (>100 000 UFC/mL) sensible a la ceftriaxona; hemocultivos también positivos para el mismo germen (bacteriemia por E. coli).\n\nDiagnóstico y manejo\n- Diagnóstico principal: cistitis enfisematosa complicada por bacteriemia por Escherichia coli.\n- Tratamiento: antibioterapia empírica inicial con ceftriaxona (cefalosporina de tercera generación), que resultó adecuada según la sensibilidad; antibioticoterapia mantenida durante 7 días.\n- Evolución: respuesta clínica y analítica favorable, con alta hospitalaria.\n\nPuntos clave e implicaciones\n- La cistitis enfisematosa es una infección del tracto urinario poco frecuente, caracterizada por formación de gas en la pared vesical. Suele asociarse a factores de riesgo como diabetes mellitus o inmunosupresión; en este caso no se describieron esos factores clásicos.\n- La presencia de bacteriemia (hemocultivos positivos) indica infección sistémica y justifica la hospitalización y tratamiento intravenoso hasta control clínico.\n- Hallazgos relevantes que requirieron seguimiento: hipopotasemia significativa (K 2.9 mmol/L) e hiponatremia leve, que deben corregirse y monitorizarse; y la necesidad de vigilar la resolución de la infección y posibles complicaciones.\n- Consideraciones prácticas tras el alta: control clínico y analítico para confirmar resolución, valorar investigación de factores predisponentes (por ejemplo, despistaje de diabetes si no se ha realizado) y medidas para prevenir recurrencias del tracto urinario.\n\nComentario final (tono empático)\nLa paciente anciana presentó una forma rara pero tratable de infección urinaria complicada, con detección rápida del germen y respuesta favorable al tratamiento antibiótico. Es comprensible la preocupación ante una infecció n sistémica en edad avanzada; el manejo oportuno y el seguimiento han permitido una evolución positiva.",
+                "fh_score": 39.49
+            }
+        }
+    },
+    {
+        "article": "Varón nacido a las 38 semanas de gestación y sin controles obstétricos prenatales, producto de un parto eutócico sin complicaciones con un peso de 2.678 g y Apgar 7 y 8 al minuto y a los cinco minutos de vida, respectivamente; derivado por sospecha de enterocolitis necrotizante a los siete días de vida. Al nacimiento, en su hospital de origen, se descartaron malformaciones congénitas externas y se colocó una sonda orogástrica para verificar la permeabilidad esofágica, obteniendo 200 mL de líquido amniótico. Posteriormente inició alimentación vía oral pero debido a succión débil y vómitos biliosos fue ingresado en la unidad de cuidados intensivos neonatales. A las 4 horas de vida se realizó radiografía abdominal observando una imagen de doble burbuja atípica, por lo cual realizaron un control radiológico 48 horas después identificando gas intestinal aparentemente distal, y presentó meconiorrexis a las 50 horas de vida. Dos días después reinició la alimentación oral, tras lo cual presentó nuevamente vómitos de aspecto biliar y distensión abdominal que mejoró con el ayuno y sonda orogástrica; por lo cual se sospechó enterocolitis necrotizante indicándose dieta absoluta, nutrición parenteral total y antibioterapia con ampicilina y amikacina. A los siete días de vida y debido a la persistencia de los síntomas pese al tratamiento instaurado, fue derivado a nuestro centro. A su llegada presentaba distensión abdominal, sin ruidos intestinales ni signos de irritación peritoneal, por lo que se realizó tránsito intestinal sin progresión distal y colon por enema con hallazgo de microcolon, todo ello sugestivo de atresia intestinal yeyunoileal. Tras la realización de los estudios de imagen y con la sospecha de atresia intestinal se realizó una laparotomía exploradora mediante abordaje supraumbilical transverso, observando adherencias hepatoileales, una hernia interna a través de un defecto mesentérico con incarceración de un asa yeyunal y atresia yeyunoileal tipo IV. Se identificaron dos sitios de atresia a 56 cm del ángulo de Treitz y a 36 cm de la válvula ileocecal, con un segmento interatrésico de 10 cm con meconio intraluminal y cambios de coloración con aspecto violáceo pero sin perforación; la diferencia de diámetros intestinales proximal a distal tenía una relación 3:1. Se decidió disecar el mesenterio y resecar el asa ciega (10 cm) para realizar una anastomosis término-oblicua yeyunoileal, corroborando la permeabilidad distal con sonda intraluminal y administración de solución fisiológica hasta que presentó evacuación rectal. El reporte de histopatología confirmó una atresia yeyunoileal tipo IV con enteritis crónica leve. El paciente evolucionó favorablemente y al 5º día postoperatorio inició alimentación oral con adecuada tolerancia progresiva y descenso paulatino de la nutrición parenteral total con retirada al 8º día postoperatorio. Al 6° día de la intervención presentó deposiciones espontáneas y a los 20 días de vida fue dado de alta sin complicaciones. Doce meses después el paciente continúa asintomático con adecuada ganancia ponderal y tolerancia a la alimentación complementaria con deposiciones diarias de características normales.",
+        "gold_summary": "Recién nacido de sexo masculino, nacido a término, derivado por vómitos, evacuaciones escasas y distensión abdominal. A los 8 días de vida y tras excluir diversas causas de distensión abdominal se sometió a laparotomía exploradora, identificando una hernia transmesentérica y dos sitios de atresia intestinal. Se realizó resección del segmento atrésico y anastomosis primaria, con buena evolución.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un bebé varón nació a término. Tenía vómitos, pocas deposiciones y la barriga hinchada. A los 8 días no mejoró y lo llevaron a cirugía. Al abrir la barriga, los médicos encontraron una hernia en el mesenterio (un hueco que dejó pasar parte del intestino) y dos zonas del intestino que estaban cerradas, es decir, bloqueadas (atresias). Quitaron la parte dañada y unieron los extremos del intestino para que volviera a funcionar. El bebé se recuperó bien. Empezó a comer poco a poco y salió del hospital sin problemas. A los 12 meses seguía sano, comiendo bien y subiendo de peso.",
+                "fh_score": 77.53
+            },
+            "B2": {
+                "text": "Resumen para lectores jóvenes (nivel B2)\n\nUn recién nacido varón, nacido a término (38 semanas) y sin controles prenatales, presentó desde los primeros días vómitos con bilis, distensión abdominal y poca cantidad de deposiciones. Inicialmente se sospechó una enterocolitis necrotizante (una infección/inflamación grave del intestino en recién nacidos) y se trató con ayuno, nutrición por vena y antibióticos, pero los síntomas persistieron. Las radiografías y un enema mostraron un colon muy pequeño (microcolon) y ausencia de paso de contraste hacia el intestino distal, lo que hizo sospechar una atresia intestinal (cuando una parte del intestino está ausente o cerrada).\n\nSe realizó una cirugía exploradora en la que encontraron una hernia interna a través del mesenterio (un defecto en el tejido que sostiene el intestino) que tenía un asa intestinal atrapada, y además hallaron atresias múltiples del intestino delgado (atresia yeyunoileal tipo IV). Se resecaron los segmentos no funcionales y se unieron los extremos sanos del intestino (anastomosis). El informe de biopsia confirmó la atresia múltiple y cambios leves de inflamación.\n\nLa recuperación fue buena: empezó a tomar por boca al quinto día después de la operación, la nutrición por vía venosa se retiró al octavo día, tuvo deposiciones normales y fue dado de alta a los 20 días de vida. A los 12 meses seguía sin síntomas, con buen aumento de peso y alimentación normal.",
+                "fh_score": 47.67
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel B3)\n\nPaciente: recién nacido varón, nacido a término (38 semanas) sin controles prenatales, parto eutócico, peso 2.678 g, Apgar 7/8. Al nacimiento no se observaron malformaciones externas; se colocó sonda orogástrica para comprobar permeabilidad esofágica y se aspiraron 200 mL de líquido amniótico.\n\nPresentación y evolución inicial: en las primeras horas de vida presentó succión débil y vómitos biliosos, por lo que fue ingresado en la unidad neonatal. La radiografía abdominal inicial mostró una imagen de “doble burbuja” atípica; 48 h después apareció gas intestinal distal y hubo eliminación de meconio a las ~50 h de vida. Tras reiniciar alimentación reaparecieron vómitos biliosos y distensión abdominal que cedieron con ayuno y sonda orogástrica. Por sospecha de enterocolitis necrotizante se instituyeron dieta absoluta, nutrición parenteral total (NPT) y antibióticos (ampicilina + amikacina). Al persistir los síntomas fue transferido a otro centro al día 7 de vida.\n\nHallazgos al ingreso y estudios: a su llegada había distensión abdominal, ausencia de ruidos intestinales y sin signos de peritonitis. El tránsito intestinal no mostró progresión distal y el enema opaco evidenció microcolon. Estos hallazgos son sugestivos de obstrucción intestinal alta (p. ej. atresia yeyunoileal): el microcolon indica un colon poco utilizado por una obstrucción proximal.\n\nIntervención quirúrgica y hallazgos intraoperatorios: se realizó laparotomía exploradora por abordaje supraumbilical transverso. Se encontraron adherencias hepatoileales, una hernia interna por defecto mesentérico con encarcelamiento de un asa yeyunal y atresia yeyunoileal tipo IV (atresias múltiples). Se identificaron dos atresias: una a 56 cm del ángulo de Treitz y otra a 36 cm de la válvula ileocecal, con un segmento interatrésico de 10 cm lleno de meconio y con coloración violácea, pero sin perforación. La relación de calibre proximal:distal era aproximadamente 3:1. Se resecaron 10 cm del asa ciega y se realizó una anastomosis término-oblicua yeyunoileal; se comprobó la permeabilidad distal mediante sonda y lavado salino hasta evacuación rectal. La histopatología confirmó atresia yeyunoileal tipo IV con enteritis crónica leve.\n\nCurso postoperatorio y seguimiento: evolución favorable. Inició alimentación oral al 5º día postoperatorio con buena tolerancia; la NPT se retiró al 8º día. Tuvo deposiciones espontáneas al 6º día postoperatorio y fue dado de alta a los 20 días de vida sin complicaciones. A los 12 meses permanece asintomático, con ganancia ponderal adecuada y tolerancia a alimentación complementaria; deposiciones diarias normales.\n\nInterpretación y puntos clave (implicaciones):\n- Diagnóstico final: atresia yeyunoileal múltiple (tipo IV) asociada a hernia transmesentérica con encarcelamiento de asa intestinal. Las atresias intestinales en neonatos suelen relacionarse con eventos isquémicos intraútero o perinatales que interrumpen la vascularización; la hernia transmesentérica pudo contribuir al compromiso vascular/ischemia y a la aparición de atresias.\n- Diagnóstico diferencial inicial incluyó enterocolitis necrotizante; la falta de respuesta al manejo médico y las imágenes (microcolon, ausencia de progresión distal) orientaron hacia obstrucción congénita que requiere corrección quirúrgica.\n- Buen pronóstico en este caso: preservación suficiente de longitud intestinal para evitar síndrome de intestino corto, anastomosis primaria satisfactoria y recuperación sin secuelas en el primer año. Sin embargo, los pacientes con atresias múltiples requieren seguimiento para vigilar complicaciones tardías (estenosis anastomótica, problemas de motilidad, retraso de crecimiento), por lo que el control pediátrico y nutricional es importante.\n\nComentario empático: el bebé recibió diagnóstico y tratamiento quirúrgico oportuno y ha mostrado una recuperación excelente. Es comprensible la preocupación de la familia frente a vómitos biliosos y la necesidad de cirugía en los primeros días de vida; el seguimiento continuo ha confirmado una evolución favorable.",
+                "fh_score": 38.7
+            }
+        }
+    },
+    {
+        "article": "Se remitió a un hombre de 86 años para que se le implantara una válvula aórtica transfemoral.\n\nLa historia significativa incluyó el hecho de fumar 40 cajetillas al año (hasta fines de la década de 1980) y la fibrilación auricular paroxística que requería anticoagulación con Coumadin desde 1999, seguida poco después por la implantación de un marcapasos ventricular debido a bradicardia. Fue admitido por síncope en mayo de 2011 y se le diagnosticó una estenosis aórtica calcificada severa. Era eupneico y no mostraba signos de insuficiencia cardiaca o retención de líquidos. La ecocardiografía transtorácica reveló una estenosis aórtica severa (gradiente medio: 58 mmHg, área de la válvula aórtica: 0,4 cm2) con hipertrofia ventricular izquierda, fracción de eyección ventricular izquierda deteriorada (29%), acinesia inferior apical y obstrucción septal subvalvular (septum: 18 mm) con dilatación biauricular e hipertensión pulmonar con dilatación de la vena cava.\n\nLa angiografía coronaria mostró una estenosis del 75% de la arteria descendente anterior izquierda. El examen de eco-Doppler encontró vasos normales en el cuello. Se agregó aspirina 80 mg diariamente a su tratamiento; el paciente fue programado para un reemplazo de la válvula aórtica, pero no llegó hasta agosto, cuando fue readmitido en urgencias por disnea aguda y confusión. Había ganado 6 kg de peso, con edemas en las piernas y signos clínicos de derrame pleural. En ese momento, su SpO2 era del 92% y la proteína B-natriurética estaba elevada a 2336 pg·mL−1 (normal < 100 pg·mL−1).\n\nTras la terapia diurética y la eliminación de 850 ml de derrame pleural, se realizó una valvuloplastia de balón percutáneo aórtico de emergencia (Cristal Balloon, 23 mm) e inmediatamente después se le implantó un stent de metal desnudo (Biotronik-Pro-Kinetic 2.74 × 10.0) en la arteria descendente anterior izquierda. El gradiente medio transvalvular disminuyó de 59 a 38 mmHg. Se observaron algunas torsades de pointe el día 6 después de la intervención, que desaparecieron cuando la frecuencia más baja del marcapasos se aceleró a 80 latidos/min. Su estado mejoró drásticamente y se le dio el alta con furosemida, aldactazina y clopidogrel. Tras una revisión cuidadosa del expediente del paciente por parte del equipo cardiaco, se consideró que el riesgo de una cirugía valvular era demasiado alto (Euroscore logístico: 51%), y se propuso al paciente un implante de válvula aórtica transfemoral.\n\nLas notas de las enfermeras mencionan la hiperventilación nocturna y las crisis de ansiedad. El paciente era semiautónomo y vivía con su hija.\n\nLa implantación de la válvula aórtica transfemoral se programó para octubre de 2011. En el ingreso, 2 días antes del procedimiento, el paciente se describió como «ansioso e hiperventilante»; su peso era de 67 kg para una altura de 168 cm; el volumen espiratorio forzado en 1 s (FEV1) era de 1,1 L (50% del valor previsto) y la capacidad vital forzada de 1,7 L (55%); la presión arterial sistémica era de 120/60 mmHg; la concentración de hemoglobina era de 167 g·L−1; la creatinina era de 12,7 g·L−1; la tasa de filtración glomerular se calculó en 54 ml·min−1·m−2; el potasio era de 3,7 mEq·L−1; el sodio era de 141 mEq·L−1; el bicarbonato era de 22 mEq·L−1; y la proteína B natriurética era de 2.073 pg·mL−1. La ecografía describió un área de superficie de la válvula aórtica de 0,5 cm2 con un gradiente aórtico medio de 55 mmHg y acinesia inferoapical en el ventrículo izquierdo. La fracción de eyección se midió en 27% por el método Simpson biplano con regurgitación mitral moderada con dilatación biauricular y se estimó la presión pulmonar sistólica en >69 mmHg. La radiografía de tórax no mostró derrame pleural significativo. El paciente era totalmente dependiente del marcapasos.\n\nDos horas antes de la intervención, el paciente recibió 1 g de acetaminofeno por vía oral. Al llegar al quirófano, el paciente, plenamente consciente, presentaba respiración de Cheyne-Stokes periódica; cada ciclo duraba unos 85 s, con apneas de entre 15 y 20 s y grandes oscilaciones de la SpO2 entre el 88 % y el 99 %. Se le colocó dos catéteres intravenosos periféricos y uno arterial. El trazado arterial también mostraba oscilaciones de 85 s y una presión sistólica de 130 a 150 mmHg. Se le aplicó una máscara facial de oxígeno al 40 % con ventilación no invasiva; la SpO2 alcanzó un rango más estable (92 %-99 %). Diez minutos después, los análisis de gases en sangre mostraron un pH de 7,39, Pao2 de 108 mmHg, Paco2 de 40 mmHg, SaO2 del 97 %, y oscilaciones de lactato de 1,2 mEq·L−1. Se instaló una línea de muestreo capnógrafo dentro de la máscara facial para monitorizar la frecuencia respiratoria (Carescape Monitor B650, GE Healthcare, Helsinki, Finlandia). La monitorización también incluía un ECG de 12 derivaciones, oximetría de pulso, y oximetría cerebral regional (rSO2) mediante espectroscopia infrarroja cercana en el frente (INVOS, Somanetics). La capnografía reveló que las oscilaciones de la presión arterial eran sincrónicas con el ritmo de la respiración y que la presión disminuía durante los períodos apneicos e hipopneicos y aumentaba durante la hiperventilación; la rSO2 seguía el mismo patrón, a pesar de que la SpO2 del dedo permanecía a un nivel constante de 99 %. Se inició una infusión de propofol a una concentración objetivo de 0,2 µg·mL−1; se administraron 2,5 µg de sufentanilo antes de que los operadores infiltraran cada ingle con 200 mg de mepivacaína; el paciente se quedó dormido pero se mantuvo despierto al menor contacto con su cara o cuando su nombre se susurraba al oído; se administraron otros 2,5 µg de sufentanilo antes de la dilatación femoral de la arteria, un procedimiento requerido antes del reemplazo de la válvula. Los ciclos de ventilación se desaceleraron a un máximo de 120 s con 24 s de apneas centrales. Cuando la angiografía y los catéteres operativos estaban en su lugar en la aorta ascendente y se introdujo un marcapasos temporal en el ventrículo derecho, se indujo un ritmo rápido de 200 latidos/min para permitir una nueva dilatación de la válvula calcificada. Este procedimiento duró <25 s, durante el cual el paciente permaneció consciente y continuó respirando de la forma habitual, el ritmo se indujo justo después del final de un período apneico. Se preparó una válvula de 26 mm (SAPIEN, Edwards Lifesciences) y se introdujo en el orificio aórtico. Se dio una señal a los operadores una vez que la respiración se reanudó al final de un período apneico; se inició un ritmo ventricular rápido que llevó a la asistolia a una presión arterial media de 45 mmHg, y la válvula se expandió con balón y la angiografía confirmó la ausencia de fuga paravalvular. El balón se desinfló justo antes de que se detuviera el ritmo rápido, y el corazón volvió a latir a 80 latidos/min bajo la estimulación del marcapasos implantado. La secuencia completa se filmó; duró 31 s, durante los cuales el paciente siguió respirando regularmente (8 veces durante la detención circulatoria, es decir, una tasa de 16 veces por minuto) y no se despertó. Las expulsiones de sangre se reanudaron inmediatamente después de la deflación del balón, con una presión sistólica de 80 mmHg. Después de unas respiraciones profundas, la respiración se hizo regular; no se produjeron nuevos períodos apneicos ni oscilaciones de la presión arterial o rSO2. La hipertensión sistémica se desarrolló rápidamente, culminando después de 1 min a 190 mmHg y se controló con 40 mg de urapidil intravenoso durante los siguientes 15 min. La ecografía transtorácica midió el área valvular a 1,6 cm2 y el gradiente transvalvular máximo a 15 mmHg. La estimación de la presión arterial pulmonar mediante ecografía transtorácica mostró un gradiente sistólico de la presión ventricular derecha-aurícula derecha de 69 mmHg 1 día antes del procedimiento y 45 mmHg 2 días después. Un mes después, era de 28 mmHg. La evolución posterior no tuvo incidentes, y el paciente fue dado de alta 72 h después sin haber vuelto a la respiración periódica.\n\nMH - Edad 80 años y más\nMH - Cirugía de la válvula aórtica\nMH - *Estenosis/cirugía de la válvula aórtica\nMH - *Respiración de Cheyne-Stokes\nMH - Ecocardiografía\nMH - *Insuficiencia cardiaca\nMH - *Implantación de prótesis valvulares cardíacas\nMH - Hemodinámica\nMH - Humanos\nMH - Hombre\nMH - Resultado del tratamiento\n",
+        "gold_summary": "Se remitió a un hombre de 86 años para la implantación de una válvula aórtica transfemoral. La ecocardiografía transtorácica reveló una estenosis grave (gradiente medio: 58 mmHg, área de la válvula aórtica: 0,4 cm2), y después de una discusión multidisciplinaria, se consideró que el riesgo de la cirugía era demasiado alto (Euroscore logístico: 51%), y se propuso al paciente para la implantación de una válvula aórtica transfemoral (TAVI). Al llegar al quirófano, se observó que el paciente, completamente consciente, tenía respiración de Cheyne-Stokes (CSB), que persistió después de la administración de oxígeno al 40%. El procedimiento TAVI fue exitoso, y el patrón CSB se interrumpió en 8 s.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un hombre de 86 años tenía la válvula del corazón muy estrecha. Los médicos dijeron que una operación grande era demasiado peligrosa. En lugar de eso, le pusieron una válvula nueva usando un tubo por la pierna.  \n\nAntes de la operación y durante el procedimiento notaron que respiraba de forma muy irregular. A esto se le llama respiración de Cheyne‑Stokes. Significa que a veces respiraba muy rápido y otras veces dejaba de respirar por un rato. Le dieron oxígeno y cuidado para mantenerlo tranquilo. \n\nPara colocar la nueva válvula, los médicos pararon el latido del corazón por un momento de forma controlada. El corazón volvió a latir bien y la válvula quedó en su sitio. Después del procedimiento, su respiración volvió a ser normal y no volvió a tener los episodios raros. Se recuperó bien y salió del hospital a los pocos días.",
+                "fh_score": 74.32
+            },
+            "B2": {
+                "text": "Here is a clear, caring summary of the case written for readers aged about 11–17:\n\nAn 86-year-old man with severe heart disease was treated with a less-invasive aortic valve replacement called TAVI (transfemoral transcatheter aortic valve implantation). He had very tight narrowing of his aortic valve (the valve that blood leaves the heart through), with the valve opening area only about 0.4–0.5 cm² (normal is much larger). He also had a weak left heart pump (ejection fraction about 27–29%), high pressure in his lungs, and a serious blockage (75%) in one of the heart arteries. Because he was frail and had a very high risk for open-heart surgery, doctors chose TAVI instead.\n\nBefore the procedure, the medical team noticed the patient was breathing in a Cheyne–Stokes pattern. Cheyne–Stokes breathing is a type of “periodic” breathing seen in people with advanced heart failure: it causes cycles of faster, deeper breaths followed by short pauses (central apneas). This can make the oxygen level and blood pressure swing up and down and is a sign of unstable heart and breathing control.\n\nDuring TAVI the team used light sedation and gave oxygen. To place and expand the new valve they briefly switched the heart into a very fast paced rhythm for about 25–31 seconds so the valve could be positioned safely. Even during that brief period of almost stopped circulation, the patient continued to breathe fairly regularly and did not suffer a bad event. After the valve was deployed, blood flow and valve measurements improved (valve area increased to about 1.6 cm² and pressure gradients dropped). The Cheyne–Stokes breathing pattern stopped soon after the procedure and did not come back. The patient’s lung blood pressure also fell over the next days and weeks. He recovered without further problems and was discharged three days later.\n\nWhy this matters: The patient had severe valve disease and heart failure, and Cheyne–Stokes breathing showed his circulation and breathing control were unstable. The team successfully used a less-invasive valve procedure, which quickly improved blood flow and stopped the dangerous breathing pattern. The outcome was good.",
+                "fh_score": 90.48
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel universitario)\n\nPresentación y contexto\n- Paciente: hombre de 86 años con estenosis aórtica calcificada grave, fibrilación auricular anticoagulada, marcapasos ventricular por bradicardia y fracción de eyección baja (FEVI ≈ 27–29%). Tenía además estenosis coronaria significativa en la arteria descendente anterior.\n- Antecedentes inmediatos: ingreso previo por insuficiencia cardiaca aguda que requirió diuréticos, evacuación de derrame pleural, valvuloplastia con balón de urgencia y colocación de un stent en la arteria descendente anterior. La cirugía abierta valvular fue considerada de muy alto riesgo (Euroscore logístico 51%), por lo que se planificó un implante transcatéter de válvula aórtica transfemoral (TAVI).\n\nHallazgos preoperatorios relevantes\n- Ecocardiograma: estenosis aórtica severa (área valvular 0,4–0,5 cm2; gradiente medio 55–59 mmHg), FEVI 27–29%, acinesia inferoapical, regurgitación mitral moderada, dilatación auricular y presión pulmonar elevada.\n- Función respiratoria moderadamente reducida (FEV1 ≈ 50% previsto).\n- Durante la evaluación preoperatoria y en quirófano el paciente presentó respiración de Cheyne‑Stokes (respiración periódica con ciclos de hiperventilación seguidos de apneas centrales). Los ciclos duraban ~85 s, con apneas centrales de 15–24 s y oscilaciones marcadas en la presión arterial y en la saturación cerebral regional (rSO2), aunque la SpO2 periférica permanecía alta. La respiración periódica persistió a pesar de oxígeno al 40%.\n\nProcedimiento y monitorización\n- Anestesia y sedación: sedación ligera con propofol a baja concentración y dosis pequeñas de opioide; analgesia local para acceso femoral. Monitorización exhaustiva incluyó ECG de 12 derivaciones, oximetría periférica, oximetría cerebral por infrarrojo cercano (rSO2), capnografía perimascara y línea arterial.\n- Durante la implantación de la prótesis (válvula SAPIEN 26 mm), se indujo ritmo de marcapasos ventricular rápido (≈200 latidos/min) para inmovilizar el corazón y permitir la expansión valvular. Esta maniobra provocó una parada circulatoria breve y una presión arterial media muy baja durante la inflación del balón.\n- Duración total de la secuencia de parada y expansión: 31 s. El paciente permaneció espontáneamente respirando (8 inspiraciones en esos 31 s), no se despertó ni requirió ventilación asistida durante el episodio.\n\nEvolución inmediata y resultados\n- La válvula se implantó con éxito y sin fuga paravalvular significativa. El área valvular mejoró a 1,6 cm2 y el gradiente máximo transvalvular descendió (ej. gradiente máximo 15 mmHg postoperatorio).\n- Tras el procedimiento hubo recuperación inmediata del latido con presión sistólica inicial baja (≈80 mmHg), seguida de hipertensión transitoria controlada con urapidil. La presión pulmonar estimada disminuyó rápidamente en los días siguientes (ej.: estimación ecocardiográfica de la presión sistólica pulmonar: 69 mmHg preop, 45 mmHg 2 días después, 28 mmHg a 1 mes).\n- Importante: el patrón de respiración de Cheyne‑Stokes desapareció tras la corrección de la estenosis aórtica y no reapareció durante la hospitalización; el paciente fue dado de alta 72 h después sin recurrencia.\n\nInterpretación y puntos clave\n- Cheyne‑Stokes (respiración periódica con apneas centrales) se asocia en pacientes con insuficiencia cardiaca y baja fracción de eyección. En este caso era clínicamente evidente y producía fluctuaciones hemodinámicas y de perfusión cerebral que se correlacionaban con la ventilación.\n- La corrección de la obstrucción aórtica mediante TAVI mejoró rápidamente la hemodinámica (mayor gasto cardiaco, reducción de presiones pulmonares) y se asoció a la desaparición del patrón respiratorio anómalo. Esto sugiere que la insuficiencia cardiaca avanzada y la inestabilidad hemodinámica eran mecanismos importantes de la respiración de Cheyne‑Stokes en este paciente.\n- La maniobra de estimulación ventricular rápida (breve parada circulatoria) durante la implantación no llevó a despertar ni a paro respiratorio significativo, probablemente porque el paciente tuvo respiración espontánea mantenida y se monitorizó estrechamente (capnografía, rSO2). La supervisión neurológica y hemodinámica fue clave para la seguridad del procedimiento.\n\nImplicaciones clínicas y recomendaciones\n- En pacientes con estenosis aórtica severa e insuficiencia cardiaca, la TAVI puede corregir no solo la válvula sino también reducir la apnea central relacionada con la insuficiencia cardiaca.\n- Para enfermos con respiración periódica es esencial monitorizar no solo la SpO2 periférica sino también la capnografía y la oxigenación cerebral (rSO2), ya que la saturación periférica puede permanecer normal mientras la perfusión cerebral y la presión arterial oscilan.\n- Vigilancia postoperatoria: control hemodinámico, ajuste de la terapia antiarrítmica y del marcapasos según necesidad, y seguimiento ecocardiográfico y de la presión pulmonar. Si las alteraciones respiratorias persistieran, considerar evaluación por sueño y tratamiento específico.\n\nTono final\nEl caso muestra que, con adecuada selección y monitorización, el TAVI puede realizarse de forma segura en un paciente anciano con respiración de Cheyne‑Stokes y disfunción ventricular severa, y que la corrección valvular puede resolver la apnea central secundaria a la insuficiencia cardiaca. Se requirió una estrecha vigilancia multidisciplinaria y medios de monitorización avanzados para garantizar un resultado favorable.",
+                "fh_score": 34.88
+            }
+        }
+    },
+    {
+        "article": "Una mujer árabe tunecina de 62 años, diagnosticada con la enfermedad de Von Hippel-Lindau en 2021, presentó varias manifestaciones relacionadas con la enfermedad. Tenía antecedentes de múltiples cirugías, principalmente por tumores renales, suprarrenales y pancreáticos, con hallazgos incidentales de masas ováricas.\n\nLa paciente no presentaba síntomas desde el punto de vista ginecológico, pero se quejaba principalmente de dolores de cabeza antes de someterse a una cirugía cerebral. No tenía antecedentes familiares o psicosociales significativos.\n\nSu historial quirúrgico incluye\n2021: Un tumor no operable (6 cm) del saco endolinfático del hueso petroso izquierdo, tratado con radioterapia.\n\n2021: Adrenalectomía izquierda por un feocromocitoma de 6 cm. El examen patológico reveló un feocromocitoma.\n\n2021: Nefrectomía izquierda por un tumor renal izquierdo roto. La microscopía mostró un carcinoma renal multifocal de células claras de grado nuclear 2.\n\n2022: Duodenopancreatectomía cefálica por una masa en el páncreas. El examen histológico confirmó tres cistadenomas serosos y dos tumores neuroendocrinos bien diferenciados.\n\nEn enero de 2021, durante la vigilancia posoperatoria con una tomografía computarizada (TC) abdominal-pélvica, se descubrió incidentalmente una masa anexial izquierda sólida de 4 cm, lo que levantó sospechas de malignidad. La masa se confirmó mediante ultrasonido transvaginal e IRM pélvica, clasificada como Sistema de Reporte y Datos Ováricos-Anexiales (O-RADS) 5 (alta sospecha de malignidad).\n\nExamen ginecológico e historial quirúrgico\nExamen físico: No se detectó masa abdominal-pélvica.\n\nExamen con espéculo: cuello uterino sano.\n\nSe observaron cicatrices quirúrgicas de una nefrectomía izquierda y una duodenopancreatectomía cefálica anteriores.\n\nUna reunión multidisciplinaria del personal concluyó que era necesaria la cirugía. Se realizó una laparotomía a través de una incisión en la línea media por debajo del ombligo, que reveló una masa quística sólida bien definida en el anexo izquierdo. No había ascitis ni signos de carcinomatosis peritoneal, y el anexo derecho parecía normal, sin signos macroscópicos de malignidad observados intraoperatoriamente, incluida la ausencia de vegetaciones exocísticas.\n\nSe realizó una citología junto con una anexectomía izquierda y la muestra se envió para un examen de sección congelada. Los resultados no fueron concluyentes, lo que planteó la posibilidad de tumores de margen o específicos del síndrome de Von Hippel-Lindau. Teniendo en cuenta el estado posmenopáusico de la paciente, se realizó una anexectomía derecha y una histerectomía total.\n\nEl examen histológico posterior reveló cistadenomas papilares de células claras bilaterales de las trompas de Falopio y el ligamento ancho, característicos de la enfermedad de Von Hippel-Lindau (0,5 cm en el lado derecho y 4 cm en el lado izquierdo). Los tumores consistían en papilas densamente compactadas con núcleos fibrosos, cubiertos por un epitelio monocapa.\n\nEl período postoperatorio inmediato transcurrió sin incidentes y, en el seguimiento de 1 mes, no se detectaron anomalías. Desde entonces, se ha hecho un seguimiento al paciente cada 4 meses con ecografías pélvicas normales. Durante estos 2 años de seguimiento, no han surgido complicaciones, pero el paciente fue readmitido recientemente en el departamento de neurocirugía por la recurrencia de un tumor cerebral.\n",
+        "gold_summary": "Una mujer blanca norteafricana de 62 años de edad, diagnosticada con la enfermedad de Von Hippel-Lindau en 2021, presentó múltiples manifestaciones, entre ellas, un tumor del hueso petroso izquierdo, feocromocitoma izquierdo, carcinoma de células renales izquierdo, riñón derecho con múltiples quistes y masas pancreáticas. Se sometió a varios tratamientos, entre ellos, radioterapia, adrenalectomía, nefrectomía y duodenopancreatectomía cefálica. Los exámenes de ultrasonografía y resonancia magnética revelaron una masa quística sólida en la región anexial izquierda. La laparoscopia identificó tumores quísticos en la mesosalpinx derecha e izquierda. Después de una histerectomía con anexectomía bilateral, el examen histológico reveló cistadenomas papilares de células claras bilaterales de la mesosalpinx y el ligamento ancho, compatibles con la enfermedad de Von Hippel-Lindau.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Here is a short, easy-to-understand summary:\n\nA 62-year-old woman from Tunisia has a condition called Von Hippel-Lindau (VHL). VHL is a problem some people are born with that can cause many different tumors in the body.\n\nSince 2021 she had several health problems and surgeries. Doctors treated tumors in her brain area, her left adrenal gland, her left kidney, and her pancreas. During a follow-up scan, they also found a new lump near her left ovary.\n\nShe did not have belly pain or other symptoms from this lump. Scans showed the lump might be cancer, so doctors did surgery. They removed her uterus and both adnexa (the left and right fallopian tube/ovary areas). In the operation they did not see signs that the cancer had spread.\n\nThe lab tests on the removed tissue showed small growths called clear cell papillary cystadenomas. These growths are known to happen with VHL. One was 4 cm on the left and a small one (0.5 cm) on the right.\n\nAfter the operation she recovered well. Follow-up checks every 4 months with pelvic ultrasound were normal for two years. Recently she went back to the hospital because a brain tumor came back and she is being treated by neurosurgery.\n\nOverall: the pelvic surgery worked and the pelvic scans stayed normal. But because VHL can cause tumors in many places, she needs ongoing care.",
+                "fh_score": 104.55
+            },
+            "B2": {
+                "text": "Resumen comprensible (nivel B2, dirigido a lectores de secundaria)\n\nUna mujer tunecina de 62 años fue diagnosticada en 2021 con la enfermedad de Von Hippel–Lindau (VHL). VHL es un trastorno genético que predispone a desarrollar varios tipos de tumores en diferentes órganos.\n\nAntes y desde el diagnóstico tuvo varios problemas relacionados con VHL:\n- Tumor del saco endolinfático en el hueso petroso izquierdo tratado con radioterapia.\n- Feocromocitoma (un tumor de la glándula suprarrenal) en el lado izquierdo, extirpado mediante cirugía.\n- Carcinoma renal de células claras multifocal en el riñón izquierdo, por el que se realizó una nefrectomía.\n- Masas en el páncreas que requirieron una duodenopancreatectomía; el tejido mostró cistadenomas serosos y dos tumores neuroendocrinos bien diferenciados.\n\nEn enero de 2021, durante un control con tomografía abdominal-pélvica se encontró por casualidad una masa sólida y quística de 4 cm en el anexo izquierdo (zona de ovario/trompa). Las ecografías y una resonancia la clasificaron como O-RADS 5, que indica alta sospecha de malignidad en la imagen.\n\nLa paciente no tenía síntomas ginecológicos ni masa palpable en la exploración. Se decidió operar y, durante una laparotomía, se vio una masa quística sólida bien definida en el anexo izquierdo. No había líquido de ascitis ni signos abiertos de cáncer en la cavidad abdominal; el anexo derecho parecía normal a simple vista.\n\nSe tomó una muestra para citología y se realizó una sección congelada durante la operación, pero los resultados fueron inconclusos. Dado que la paciente era posmenopáusica y para evitar dejar tejido enfermo, se completó la cirugía con anexectomía derecha (retirada de ambos anexos) y una histerectomía total.\n\nEl examen definitivo del tejido mostró cistadenomas papilares de células claras en ambas trompas de Falopio y en el ligamento ancho (mesosalpinx): lesiones benignas pero típicas de la enfermedad de Von Hippel–Lindau (0,5 cm a la derecha y 4 cm a la izquierda). Estas formaciones estaban hechas de papilas compactas cubiertas por una sola capa de células.\n\nLa recuperación inmediata fue buena. Al mes no se encontraron anomalías, y durante dos años se hizo seguimiento con ecografías pélvicas cada cuatro meses que permanecieron normales. No hubo complicaciones relacionadas con la cirugía pélvica. Recientemente la paciente volvió a ingresar en neurocirugía por la recurrencia de un tumor cerebral, lo que sugiere que seguirá recibiendo tratamiento y controles específicos para ese problema.\n\nComentario final: en personas con VHL es común encontrar tumores en distintas partes del cuerpo. Aunque las imágenes podían parecer sospechosas de cáncer, en este caso las lesiones pélvicas resultaron ser cistadenomas asociados al síndrome. El manejo incluyó cirugía para quitar las lesiones y control estrecho con imágenes; la paciente se mantiene en seguimiento por sus otras afecciones relacionadas con VHL.",
+                "fh_score": 51.18
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel universitario)\n\nPaciente: mujer tunecina árabe de 62 años, diagnosticada con la enfermedad de Von Hippel–Lindau (VHL) en 2021.\n\nAntecedentes relevantes\n- Enfermedad de VHL con múltiples manifestaciones tratadas previamente:\n  - Tumor del saco endolinfático del hueso petroso izquierdo (6 cm), no resecable → radioterapia.\n  - Feocromocitoma izquierdo (glándula suprarrenal) → adrenalectomía; confirmación patológica.\n  - Carcinoma renal de células claras multifocal del riñón izquierdo → nefrectomía izquierda.\n  - Masa pancreática → duodenopancreatectomía cefálica; hallazgos: cistadenomas serosos y dos tumores neuroendocrinos bien diferenciados.\n- Sin síntomas ginecológicos reportados y sin antecedentes familiares o psicosociales relevantes.\n\nHallazgo actual que motivó intervención\n- En una tomografía abdominal-pélvica de control (enero 2021) se detectó una masa anexial izquierda sólida de 4 cm, confirmada por ecografía transvaginal y resonancia magnética pélvica. Clasificada como O-RADS 5, lo que indica alta sospecha de malignidad.\n- Examen físico y ginecológico: sin masa palpable ni anormalidades del cuello uterino.\n\nIntervención quirúrgica y hallazgos intraoperatorios\n- Se realizó laparotomía por línea media infraumbilical. Se encontró una masa quístico-sólida bien delimitada en el anexo izquierdo; no había ascitis ni signos macroscópicos de carcinomatosis peritoneal. El anexo derecho parecía macroscópicamente normal.\n- Se tomaron citología y se practicó anexectomía izquierda con envío a sección congelada; el resultado intraoperatorio fue no concluyente.\n- Dado que la paciente estaba posmenopáusica y ante la incertidumbre diagnóstica, se completó histerectomía total con anexectomía derecha.\n\nResultado histológico definitivo\n- Lesiones bilaterales localizadas en la mesosalpinx y ligamento ancho (no en el ovario): papilares cistadenomas de células claras, compatibles con la VHL.\n  - Tamaños: 4 cm en el anexo izquierdo y 0,5 cm en el derecho.\n  - Morfología: papilas densamente compactadas con núcleos en el eje fibroso, revestidas por epitelio monocapa.\n- Estas lesiones tienen un patrón característico descrito en pacientes con VHL.\n\nEvolución y seguimiento\n- Período postoperatorio inmediato sin complicaciones.\n- Control al mes sin anomalías.\n- Seguimiento con ecografías pélvicas cada 4 meses durante 2 años, todas normales.\n- Reciente reingreso en neurocirugía por recurrencia de un tumor cerebral (relacionado con la VHL).\n\nInterpretación y consideraciones\n- Normal vs anormal: el examen ginecológico fue normal, pero la imagen detectó una masa anexial que resultó ser un tumor asociado a VHL. No hubo evidencia macroscópica de diseminación peritoneal ni signos de malignidad intraoperatorios; la histología describió lesiones benignas típicas de VHL.\n- Implicaciones: las cistadenomas papilares de células claras en la mesosalpinx son lesiones asociadas a VHL y, en este contexto, su hallazgo es coherente con la naturaleza multiorgánica de la enfermedad. La decisión de extirpar ambos anexos y el útero fue razonable dada la edad posmenopáusica y la inconclusión de la biopsia intraoperatoria.\n- Próximos pasos prudentes: continuar vigilancia multidisciplinaria para VHL (incluyendo control neurológico por la recurrencia cerebral, imágenes periódicas renales, suprarrenales y pancreáticas, y vigilancia por si aparecen nuevas lesiones), además de manejo específico del tumor cerebral recurrente por neurocirugía.\n\nComentario final (empatía)\nLa paciente ha recibido un manejo integral frente a una enfermedad sistémica compleja. El hallazgo pélvico se resolvió con tratamiento quirúrgico y la evolución inmediata fue favorable; sin embargo, la naturaleza heterogénea y recidivante de la VHL exige seguimiento estrecho y coordinación entre especialidades.",
+                "fh_score": 32.6
+            }
+        }
+    },
+    {
+        "article": "Una mujer embarazada de 31 años que había sido sometida a una cesárea fue derivada a la unidad de ultrasonido de nuestro departamento para un examen de ultrasonido morfológico de segundo trimestre. La paciente no tenía antecedentes familiares destacables y no había tomado medicamentos ni había estado expuesta a teratógenos durante el primer trimestre del embarazo. Los exámenes serológicos para diversas enfermedades infecciosas fueron negativos y un examen de ultrasonido previo a las 14 semanas fue normal. El triple examen para anomalías fetales también fue negativo a las 16 semanas.\n\nDurante la ecografía de la semana 20, se observó un feto masculino con una edad sonográfica compuesta de 20 semanas y 2 días que presentaba un edema significativo de las extremidades inferiores y líquido amniótico normal. Se recomendó un examen de seguimiento en 2 semanas, junto con pruebas de TORCH y pruebas de Coombs indirectas.\n\nSin embargo, se observó nuevamente edema subcutáneo en ambas extremidades inferiores durante la ecografía morfológica de la semana 23, lo que sugiere un posible diagnóstico de EM. Debido al linfedema persistente en las extremidades inferiores, se realizó una amniocentesis.\n\nLos exámenes posteriores revelaron que el cariotipo masculino era normal (46, XY), y el análisis molecular para el síndrome de Noonan fue negativo. Se realizó la secuenciación de nucleótidos del líquido amniótico con la secuenciación Illumina de 150 bases. Se aplicó el sistema de bioinformática (North-Oehler Aligarh, GATX) mientras se verificaba adicionalmente la existencia de deleciones/duplicaciones/CNV (Copy Number Variations) en el gen FLT4. El análisis identificó una mutación c.3116C>A p. (Ala1039Asp), que es una variante patogénica no conocida en el gen FLT4, lo que confirma el diagnóstico de linfedema hereditario tipo 1A – enfermedad de Milroy. El análisis de sangre materno confirmó la mutación materna y se realizó el asesoramiento genético.\n\nLa cesárea se realizó a las 38 semanas y 6 días de gestación y nació un neonato de sexo masculino que pesaba 3850 g y medía 46 cm con una puntuación de Apgar de 9/10. Después del parto se reconoció un edema en la extremidad inferior. El examen histopatológico de la placenta, el cordón umbilical y el saco amniótico no mostró signos de corioamnionitis u otra patología.\n",
+        "gold_summary": "Presentamos un informe de caso de una primera mutación descrita de un feto masculino diagnosticado prenatalmente con síndrome de Milroy a través de amniocentesis. El feto tenía edema bilateral de miembros inferiores, y las pruebas genéticas confirmaron el diagnóstico de síndrome de Milroy. La paciente fue monitoreada de cerca durante todo el embarazo, y después del parto, el lactante fue tratado con terapias apropiadas, incluyendo prendas de compresión y drenaje linfático manual. Los padres recibieron asesoramiento y apoyo apropiados.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una mujer embarazada de 31 años tuvo controles normales al principio del embarazo. A las 20 semanas, el bebé en su vientre mostró hinchazón en las piernas. Esto se llama linfedema. Los médicos volvieron a ver la hinchazón a las 23 semanas y pidieron una prueba del líquido que rodea al bebé (amniocentesis).  \n\nLas pruebas de los genes mostraron un cambio en un gen llamado FLT4. Ese cambio confirma un tipo de linfedema que se llama enfermedad de Milroy. La misma cambio se vio también en la sangre de la mamá, por eso se dijo que la condición es heredada. Los padres tuvieron explicación y apoyo con información genética.  \n\nEl bebé nació por cesárea a las 38 semanas y pesó 3850 g. Nació sano en general (puntuación de Apgar 9/10), pero tenía hinchazón en una pierna, como se esperaba. La placenta y los tejidos alrededor del bebé estaban normales.  \n\nDespués del nacimiento, al bebé le dieron cuidados para ayudar a bajar la hinchazón. Le pusieron prendas de compresión y le hicieron drenaje linfático manual, que son tratamientos para que el líquido salga y las piernas se sientan mejor. Los padres siguen recibiendo apoyo y consejos para cuidar al bebé.",
+                "fh_score": 77.97
+            },
+            "B2": {
+                "text": "This report describes a pregnant 31-year-old woman whose baby was found to have swelling in both lower legs on routine ultrasound in the second trimester. Because the swelling (called lymphedema — extra fluid that builds up when the body’s lymph vessels do not drain well) persisted, doctors performed an amniocentesis (a test that takes a small sample of the fluid around the baby to check the baby’s genes).\n\nStandard chromosome testing (karyotype) and tests for Noonan syndrome were normal, but detailed gene sequencing found a new harmful change in the FLT4 gene. Changes in FLT4 are known to cause Milroy disease, a hereditary form of lymphedema (type 1A). Blood testing showed the mother carried the same mutation, so the condition was inherited. The family received genetic counseling and support.\n\nThe baby was delivered by cesarean at 38 weeks and 6 days, weighing 3850 g, with good Apgar scores (9 and 10). The newborn had the same leg swelling at birth; the placenta and umbilical cord appeared normal. After birth the infant was treated with helpful measures such as compression garments and manual lymphatic drainage to reduce swelling. Early diagnosis allowed the team to plan appropriate care and provide the parents with information and support.",
+                "fh_score": 86.02
+            },
+            "B3": {
+                "text": "Resumen (nivel B3)\n\nPresentación y antecedentes\n- Mujer de 31 años con cesárea previa, embarazo controlado sin exposición a teratógenos ni historias familiares relevantes.\n- Serologías maternas y cribado bioquímico (triple test a las 16 semanas) fueron normales; ecografía previa a las 14 semanas sin hallazgos.\n\nHallazgos prenatales y pruebas realizadas\n- A las 20 semanas se detectó edema significativo en las extremidades inferiores del feto masculino (edad gestacional ecográfica 20+2), con líquido amniótico normal. Se programó control.\n- A las 23 semanas el edema subcutáneo en ambas piernas persistió, lo que orientó a linfedema fetal. Debido a la persistencia del linfedema se practicó amniocentesis.\n- Cariotipo fetal normal (46,XY). Test molecular para síndrome de Noonan negativo.\n- Secuenciación del ADN del líquido amniótico (Illumina, lectura de 150 pb) e inspección de variaciones en número de copias en el gen FLT4 revelaron la variante c.3116C>A p.(Ala1039Asp) en FLT4, no previamente descrita y considerada patogénica. Diagnóstico: linfedema hereditario tipo 1A (enfermedad de Milroy).\n- Análisis genético materno confirmó que la madre portaba la misma mutación; se dio asesoramiento genético.\n\nNacimiento y evolución postnatal\n- Cesárea a las 38+6 semanas; recién nacido masculino de 3.850 g, 46 cm, Apgar 9/10.\n- Al nacimiento se observó edema en las extremidades inferiores, concordante con la sospecha prenatal.\n- Anatomía patológica de placenta, cordón y saco amniótico sin signos de infección o patología (no corioamnionitis).\n\nImplicaciones clínicas y manejo\n- La enfermedad de Milroy es un linfedema hereditario por alteración del desarrollo de los vasos linfáticos (mutaciones en FLT4/VEGFR3). Se manifiesta por edema crónico de las extremidades, que puede detectarse prenatalmente cuando es evidente en ecografía.\n- No hay cura definitiva; el tratamiento es de soporte y sintomático: cuidados de la piel, prendas de compresión, drenaje linfático manual y seguimiento con especialistas en linfedema y genética. En el caso descrito, el lactante recibió terapias conservadoras adecuadas.\n- La confirmación de la misma mutación en la madre indica herencia autosómica dominante y permite estimar riesgo de recurrencia en futuros embarazos y la posibilidad de evaluar a otros familiares.\n- El diagnóstico prenatal mediante ecografía seguido de estudio genético permitió planificación perinatal, consejo genético y preparación para el manejo neonatal.\n\nComentario final (tono empático)\nEste caso ilustra cómo un edema fetal persistente en ecografía puede conducir a un diagnóstico genético temprano de linfedema hereditario (Milroy). La identificación de una mutación patogénica, incluida su confirmación en la madre, permitió ofrecer a la familia información concreta, apoyo y opciones de manejo desde la etapa prenatal. Aunque el linfedema será probablemente una condición crónica, el control especializado y las medidas conservadoras pueden mejorar la calidad de vida del niño.",
+                "fh_score": 46.31
+            }
+        }
+    },
+    {
+        "article": "Un paciente de 50 años con antecedentes médicos conocidos de diabetes mellitus (DM) e hipertensión (HTN), que se manejaba de manera irregular, se presentó en nuestro hospital en la ciudad de Sana’a, Yemen, el 25 de mayo de 2022, a las 5:30 p. m. El paciente fue derivado a otro hospital y manifestó un dolor abdominal agudo que había durado una semana antes del ingreso. El dolor se localizaba en la región epigástrica, de inicio repentino, empeoramiento progresivo y radiación hacia la espalda. Además, el paciente experimentó distensión abdominal generalizada, náuseas, vómitos y fatiga significativa. También se informó un historial de melena y vómitos relacionados con los alimentos durante el mes pasado. Dos días antes del ingreso, el paciente había recibido una transfusión de sangre de 2 unidades. No había antecedentes de cirugías previas ni antecedentes familiares de neoplasias.\n\nAl examinar al paciente, se constató que estaba consciente y alerta, pero que presentaba un aspecto pálido. La presión arterial era de 90/60 mmHg y el pulso de 120 latidos por minuto. Se observó distensión abdominal generalizada, particularmente prominente en la región supraumbilical con desplazamiento hacia abajo del ombligo. Se constató una leve sensibilidad en la zona epigástrica, junto con sonidos intestinales positivos, el examen rectal digital reveló un tono normal del esfínter anal y no se detectó ninguna masa palpable.\n\nLos exámenes hematológicos y bioquímicos revelaron anemia microcítica hipocrómica con un nivel de hemoglobina de 6 g/dL (rango normal: 12-15.5 g/dL), un recuento de glóbulos blancos de 16,000 (rango normal: 4-10,000), y un recuento de plaquetas de 303. El nivel de nitrógeno ureico en sangre fue de 7 mg/dL (rango normal: 10-20 mg/dL), la creatinina fue de 0.49 mg/dL (rango normal: 0.7-1.5% / dL), el índice internacional normalizado fue de 1.34 (rango normal: 0.62-1.3), el tiempo de protrombina (PT) fue de 16.9, el tiempo de tromboplastina parcial (PTT) fue de 30, el calcio fue de 8.0 mg/dL (rango normal: 8.5-10.1 mg / dL) y el ácido láctico fue de 1.9 mmol/L (rango normal: 0.5-2.2% / L). Los niveles de enzimas hepáticas y amilasa estuvieron dentro de los límites normales.\n\nSe realizaron estudios de diagnóstico por imágenes, que incluyeron una radiografía de tórax y una ecografía abdominal. La radiografía de tórax no reveló aire subdiafragmático, pero se observó una elevación en el diafragma izquierdo. La ecografía abdominal demostró la presencia de una acumulación de líquido intraabdominal. Posteriormente, se realizó una angiografía por TC abdominal, que reveló un hematoma de aproximadamente 14,3 × 8,8 cm en la región paraumbilical. En el interior del hematoma, se identificó un aneurisma arterial de 3,4 × 2,2 cm conectado a la arteria gastroduodenal, acompañado de cambios edematosos circundantes. Estos hallazgos sugieren la presencia de un aneurisma trombosado grande en la arteria gastroduodenal. Además, se observó la evisceración del diafragma izquierdo, que contiene el bazo y parte del estómago, junto con una acumulación de líquido intraperitoneal leve a moderada. No se detectó evidencia de un aneurisma aórtico.\n\nPara estabilizar al paciente, se inició la reanimación con 1000 ml de lactato de Ringer y se transfundieron tres unidades de sangre fresca. Se obtuvo el consentimiento informado para la intervención de alto riesgo y el paciente fue llevado inmediatamente al quirófano. Bajo anestesia general, en posición supina y con estricta adhesión a las técnicas asépticas, se realizó una incisión de laparotomía en la línea media. Cuando se abrió el peritoneo, se evacuó aproximadamente 2000 ml de sangre, revelando una masa pulsátil ocluida en el duodeno. Se logró una exposición adecuada utilizando un retractor auto-reforzado. La flexión del hígado y el colon transverso se movilizaron inferiormente desde la cabeza del páncreas y se eliminó la sangre coagulada del intestino delgado. Se realizó una disección meticulosa sobre el gran aneurisma ocluido pulsátil en la arteria gastroduodenal abriendo el ligamento gastrohepático. La movilización del píloro y el duodeno lejos de la cabeza del páncreas expuso una fístula que conectaba el duodeno y el aneurisma, sin contenido digestivo. Después de la heparinización, se realizó un pinzamiento proximal y distal de la arteria gastroduodenal. Posteriormente, se abrió el pseudoaneurisma y se evacuó una cantidad significativa de trombo. Se realizó una aneurismorrafía utilizando suturas de prolina 7.0. La perforación en la primera parte del duodeno se reparó en dos capas y se insertó una sonda nasogástrica más allá de la perforación. Se logró una irrigación exhaustiva con solución salina normal y una hemostasia meticulosa. Se colocó un drenaje abdominal y se cerró la incisión abdominal en capas. El paciente fue trasladado a la unidad de cuidados intensivos (UCI) para una estrecha monitorización y observación.\n\nDurante el período postoperatorio, el drenaje abdominal recolectó aproximadamente 100 ml de fluido seroso, que se eliminó el tercer día después de la operación. La recuperación de la paciente progresó sin complicaciones. Diez días después de la cirugía, la paciente fue dada de alta en condiciones favorables. Se programaron citas de seguimiento en el departamento ambulatorio y se mantuvo una comunicación regular por teléfono, con la condición de la paciente reportada como satisfactoria.\n",
+        "gold_summary": "Un hombre de 50 años se presentó con dolor abdominal agudo, anemia y signos de inestabilidad hemodinámica. Las imágenes de diagnóstico, incluida la CTA, revelaron un aneurisma de la arteria gastroduodenal grande y trombosado con evidencia de ruptura. El paciente se sometió a exploración y reparación quirúrgica abierta para abordar tanto el aneurisma como la perforación duodenal. La recuperación del paciente fue satisfactoria y fue dado de alta en condiciones estables.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un señor de 50 años llegó al hospital porque tenía muchísimos dolores en la panza que se iban hacia la espalda. También estaba muy cansado, vomitaba y había perdido sangre en las heces. Tenía la presión baja y estaba pálido.\n\nLos médicos hicieron estudios y vieron una gran bolita en una arteria cerca del estómago. Esa bolita era como un globo en la pared de la arteria y tenía dentro coágulos (sangre pegada). Esa bolita se había roto y había hecho un hoyo en la primera parte del intestino (duodeno). Por eso había mucha sangre dentro de la panza.\n\nLo llevaron de urgencia al quirófano. Abrieron el abdomen, sacaron mucha sangre y arreglaron la arteria y el hoyo del intestino. Le pusieron sangre para ayudarlo y lo cuidaron en la unidad de cuidados intensivos.\n\nSe recuperó bien después de la operación. Diez días más tarde pudo irse a su casa y volvió a sus citas de control. Los médicos dijeron que su estado era estable y que mejoraba.",
+                "fh_score": 77.23
+            },
+            "B2": {
+                "text": "Here is a clear, kind summary of the case:\n\nA 50-year-old man with diabetes and high blood pressure came to the hospital with one week of sudden, severe upper-abdominal pain that spread to his back. He also had belly swelling, nausea, vomiting, tiredness, and black stools (melena), and he was already very anemic from bleeding. On arrival he looked pale, his blood pressure was low and his heart rate fast, and blood tests showed a very low hemoglobin (6 g/dL) and a raised white blood cell count.\n\nImaging with a CT angiogram showed a large blood collection (hematoma) near the belly and a 3.4 × 2.2 cm aneurysm of the gastroduodenal artery. An aneurysm is a ballooning or bulge in an artery. This aneurysm was partly filled with clot (thrombosed) and had likely ruptured, causing internal bleeding. The scan also showed that part of the spleen and stomach had moved upward through the left side of the diaphragm (a type of herniation) and there was a moderate amount of fluid inside the abdomen.\n\nBecause of ongoing bleeding and the patient’s unstable condition, the team gave fluids and several units of blood and took him immediately to emergency surgery. During an open operation (a midline laparotomy), the surgeons removed about 2 liters of blood from the abdomen and found a pulsating mass connected to the duodenum (first part of the small intestine). They discovered a fistula — an abnormal hole or connection — between the aneurysm and the duodenum. After temporarily controlling the artery, they opened the aneurysm, removed the clot, repaired the artery, and stitched the hole in the duodenum in two layers. They placed a drain and a nasogastric tube (a tube through the nose into the stomach) and moved him to the intensive care unit for close monitoring.\n\nThe patient recovered well after surgery. The abdominal drain produced a small amount of clear fluid and was removed on day 3. He had no major complications and was discharged in good condition on day 10, with outpatient follow-up arranged.\n\nIn short: the patient had a ruptured, partly clot-filled aneurysm of the gastroduodenal artery that caused major internal bleeding. Emergency open surgery successfully controlled the bleeding, repaired the artery and the duodenal injury, and the patient recovered.",
+                "fh_score": 86.49
+            },
+            "B3": {
+                "text": "Resumen clínico\n\nUn hombre de 50 años con diabetes e hipertensión mal controladas llegó al hospital con una semana de dolor epigástrico intenso y de inicio súbito que irradiaba a la espalda, distensión abdominal, náuseas, vómitos y fatiga. También refería melena (heces oscuras por sangrado) y había recibido transfusión sanguínea días antes. Al ingreso estaba pálido, hipotenso (90/60 mmHg) y taquicárdico (120 lpm), lo que indica inestabilidad hemodinámica.\n\nHallazgos clave (anormales)\n- Hemoglobina muy baja: 6 g/dL (anemia microcítica hipocrómica severa).\n- Leucocitosis: 16.000 /µL (inflamación o reacción al sangrado).\n- Radiografía: elevación del hemidiafragma izquierdo, sin aire libre subdiafragmático.\n- Ecografía: líquido intraabdominal (anfiperitoneo).\n- Angio-TC abdominal: hematoma paraumbilical grande (14,3 × 8,8 cm) y un aneurisma de la arteria gastroduodenal de 3,4 × 2,2 cm, parcialmente trombosado, con signos de ruptura hacia el peritoneo. Se observó además herniación del bazo y parte del estómago a través del hemidiafragma izquierdo.\n\nDiagnóstico y manejo\n- Diagnóstico principal: aneurisma roto (pseudoaneurisma) de la arteria gastroduodenal con hemoperitoneo y fístula hacia el duodeno.\n- Manejo inmediato: reanimación con líquidos y transfusión de sangre; consentimiento y traslado urgente a quirófano.\n- Procedimiento quirúrgico: laparotomía media con evacuación de ~2000 mL de sangre; identificación de un aneurisma ocluido en relación con el duodeno y una fístula duodenal. Tras heparinización, se pinzó la arteria gastroduodenal proximal y distal, se abrió el pseudoaneurisma y se evacuó trombo; se reparó el saco aneurismático (aneurismorrafia) y se suturó la perforación duodenal en dos capas; se colocó sonda nasogástrica y drenaje abdominal.\n\nEvolución y pronóstico\n- Postoperatorio sin complicaciones significativas: drenaje seroso retirado al tercer día; alta al décimo día en condiciones estables.\n- Se programaron controles ambulatorios y seguimiento telefónico, con reporte de buena recuperación.\n\nImplicaciones y recomendaciones prácticas\n- Este caso muestra una causa rara pero potencialmente mortal de dolor abdominal agudo: ruptura de un aneurisma visceral (arteria gastroduodenal), que requiere diagnóstico rápido y control quirúrgico u endovascular inmediato.\n- Pasos razonables a seguir tras el alta: control estricto de los factores de riesgo cardiovascular (mejorar control de diabetes e hipertensión), corrección y seguimiento de la anemia, y vigilancia por imagen (según indicación del equipo tratante) para asegurar que no haya recurrencia o nuevos aneurismas.  \n- La coordinación con cirugía vascular/gastroenterología en consultas de seguimiento es recomendable.\n\nEstoy disponible si desea una versión más breve, una lista de términos explicados con más detalle, o recomendaciones específicas para el control de factores de riesgo.",
+                "fh_score": 38.84
+            }
+        }
+    },
+    {
+        "article": "Una mujer de 60 años fue admitida en el departamento de nefrología con dolor epigástrico, hematemesis y edema en la pierna. La presión arterial era de 90/50 mmHg, dentro del rango normal para esta paciente.\nLos resultados de laboratorio fueron notables para las enzimas hepáticas alteradas con un patrón colestático: los niveles de alanina amino transferasa (ALT) y aspartato amino transferasa (AST) fueron ligeramente elevados a 28 U/L y 61 U/L, respectivamente, mientras que los niveles de fosfatasa alcalina (388 U/L) y gamma glutamiltransferasa (291 U/L) fueron muy elevados. Los niveles de albúmina en suero fueron de 24 g/L y el índice internacional normalizado fue normal a 1.02.\nOtros resultados de laboratorio, incluidos la bilirrubina total (0,32 mg/dL), la bilirrubina directa (0,26 mg/dL), el recuento total de plaquetas (176 000 plaquetas por microlitro) y el recuento de glóbulos blancos (8400 células por microlitro), se encontraban dentro de los valores normales.\nEl paciente tenía un extenso historial de enfermedades cardiacas y renales. A los 11 años, se le diagnosticó estenosis congénita de la válvula pulmonar, por lo que se le practicó una valvulotomía. Más adelante, desarrolló fibrilación auricular y aleteo auricular, que no toleró bien y para los que se intentó, sin éxito, la ablación del aleteo. Como el paciente seguía teniendo síntomas, se le practicó una ablación del nódulo auriculoventricular con colocación de un marcapasos.\nSe inició anticoagulación oral con fenprocoumon debido a una puntuación CHA2DS2-Vasc de 3 (mujer, insuficiencia cardiaca y enfermedad vascular periférica). A la edad de 55 años, se desarrolló una insuficiencia cardiaca derecha manifiesta y la paciente continuó luchando con ascitis y edemas periféricos que requerían múltiples ingresos hospitalarios. Además, también desarrolló un problema de efusiones pleurales transudativas recurrentes de etiología poco clara.\nLa ecocardiografía en ese momento mostró una severa regurgitación pulmonar y tricuspídea con un ventrículo derecho moderadamente dilatado y una aurícula derecha. El ventrículo izquierdo estaba ligeramente dilatado con una regurgitación mitral moderada. El cateterismo cardiaco derecho demostró presiones arteriales pulmonares de 74/30 mmHg con una presión venosa central de 28 mmHg. Se colocó un homotransplante pulmonar cuando el paciente tenía 57 años y se realizó una anuloplastia tricuspídea concomitante. A pesar de una presión venosa central más baja de 13 mmHg, el paciente seguía siendo readmitido varias veces por signos y síntomas de insuficiencia cardiaca derecha. La congestión venosa sistémica persistente finalmente dio lugar a una enfermedad renal en fase terminal para la que se inició una terapia de reemplazo renal a través de hemodiálisis intermitente. El caso se complicó por hemorragias gastrointestinales graves recurrentes, que requerían transfusiones de sangre frecuentes con hasta 60 unidades de glóbulos rojos por año. A pesar de esto, en combinación con la sustitución intravenosa de hierro, los niveles de hemoglobina variaron entre 5.3-8.8 g/dL. Debido a estos problemas de sangrado intratables, la anticoagulación oral con fenprocoumon se detuvo a la edad de 59 años.\nUna gastroscopia mostró una gastropatía erosiva con una mucosa difusa congestiva y friable. Como prevención de primera línea de las hemorragias gástricas recurrentes en el marco de la cirrosis, se inició el propranolol a una dosis de 5 mg por vía oral dos veces al día (el paciente no toleró una dosificación superior debido a la presión arterial baja). Además, se realizó una coagulación endoscópica de un angioma fúndico y un recorte de una lesión de Dieulafoy.\nSe creía que estas lesiones eran causadas por una gastropatía hipertensiva. Sin embargo, las hemorragias intractables persistieron.\nEl gradiente de presión venosa hepática se midió a 16 mmHg (27 mmHg-11 mmHg). Aunque hubo cierta reticencia debido al temor de empeorar la insuficiencia cardiaca derecha, se tomó la decisión de crear un TIPS. El procedimiento fue sin incidentes. Después de la colocación del TIPS, el gradiente de presión venosa hepática disminuyó a 4 mmHg (14 mmHg-10 mmHg). Por lo tanto, aunque el TIPS redujo considerablemente el gradiente venoso hepático, la presión portal se mantuvo alta debido a la elevada presión venosa central.\nDespués de la colocación del TIPS, el paciente desarrolló signos de encefalopatía hepática y se midieron niveles de amoniaco de 77 umol/L. Se inició el tratamiento con lactulosa oral y enemas, con poca mejora. En ese momento, se produjo otro episodio de sangrado gástrico.\nLa ecografía abdominal mostró buena permeabilidad del TIPS con flujo Doppler normal. Se detectó sangrado gástrico de una úlcera antral con endoscopia, a pesar de que la hiperemia gástrica disminuyó visualmente en comparación con la situación antes del TIPS. Se realizó una biopsia que mostró una mucosa foveolar edematosa, lo que sugiere isquemia de la mucosa. El sangrado fue demasiado difuso para una ligadura endoscópica adicional. No se encontró empeoramiento de la función hepática en los resultados de laboratorio, con el índice internacional normalizado 1.01 en este momento. La ecocardiografía no mostró cambios significativos en comparación con la situación antes de la colocación del TIPS. El ventrículo derecho permaneció moderadamente dilatado con una función longitudinal deficiente y una regurgitación tricuspídea severa persistente. Sin embargo, el estado general del paciente se deterioró y se desarrolló fiebre con consolidaciones pulmonares bilaterales.\nSe produjo una falla multiorgánica y, en ese momento, la familia del paciente decidió retirar el tratamiento. El paciente falleció finalmente 43 días después del procedimiento TIPS.\n\nMH - Resultado fatal\nMH - Mujer\nMH - Insuficiencia cardiaca/*complicaciones/fisiopatología\nMH - Encefalopatía hepática/etiología\nMH - Humanos\nMH - Hipertensión, Portal/etiología/fisiopatología/*cirugía\nMH - Cirrosis hepática/*complicaciones\nMH - Edad Media\nMH - Presión del portal\nMH - *Derivación portosistémica, intrahepática transyugular\nMH - Fracaso del tratamiento\n",
+        "gold_summary": "Una mujer de 60 años con antecedentes de estenosis congénita de la válvula pulmonar desarrolló insuficiencia cardíaca derecha, cirrosis hepática y enfermedad renal en fase terminal que requería terapia de reemplazo renal. La cirrosis hepática se complicó con hipertensión portal, lo que provocó hemorragias gastrointestinales intratables a pesar del tratamiento óptimo con betabloqueantes y la ligadura endoscópica de la banda. Debido al temor de que empeorara la insuficiencia cardíaca derecha, inicialmente se rechazó la colocación de una derivación intrahepática transyugular (TIPS). Sin embargo, como los problemas de hemorragia intratables persistieron y causaron grandes necesidades de transfusión, la TIPS se realizó finalmente como un procedimiento de rescate. Aunque la TIPS redujo con éxito el gradiente de presión venosa hepática de 16 mmHg a 4 mmHg, la presión portal se mantuvo alta a 14 mmHg debido a la persistencia de la insuficiencia cardíaca derecha con presión venosa central elevada. La encefalopatía hepática se desarrolló poco después de la colocación de la TIPS y culminó en una falla multiorgánica después de otro episodio de hemorragia gastrointestinal. En este punto, la familia del paciente decidió retirar la atención y el paciente falleció posteriormente.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Esta es la historia de una mujer de 60 años con muchos problemas de salud. Desde niña tuvo un problema de la válvula del corazón. Con los años su corazón derecho dejó de funcionar bien. Por eso tuvo líquido en el vientre y en las piernas. También tuvo daño en el hígado (llamado cirrosis) y los riñones dejaron de funcionar, por lo que necesitaba diálisis.\n\nTenía hemorragias del estómago que no podían detenerse. Recibió muchas transfusiones de sangre. Los médicos probaron medicinas y tratamientos por endoscopia, pero las hemorragias siguieron.\n\nComo último intento, le hicieron un TIPS. Eso es poner un pequeño tubo dentro del hígado para bajar la presión en las venas del hígado. El tubo bajó la presión dentro del hígado, pero la presión en todo su cuerpo seguía alta porque su corazón derecho seguía muy enfermo.\n\nDespués del TIPS empezó a confundirse por problemas del hígado (encefalopatía hepática). Siguió sangrando y su salud empeoró. Tuvo fiebre y problemas en los pulmones y varios órganos empezaron a fallar. La familia decidió dejar de tratarla y ella murió 43 días después del procedimiento.\n\nEs una historia triste. Los médicos intentaron muchos tratamientos, pero no pudieron salvarla.",
+                "fh_score": 73.8
+            },
+            "B2": {
+                "text": "Summary (clear, kind, upper‑intermediate level)\n\nA 60‑year‑old woman with a long history of heart problems (including a narrow pulmonary valve from birth and later severe right‑sided heart failure) developed liver disease (cirrhosis) and kidney failure that needed dialysis. Because of the liver damage she had portal hypertension — high blood pressure in the veins that go into the liver — which caused repeated, hard‑to‑stop stomach and gut bleeding. Despite medicines to lower portal pressure (a beta‑blocker) and endoscopic treatments (procedures inside the stomach), the bleeding continued and she needed many blood transfusions.\n\nDoctors were worried that creating a TIPS (a transjugular intrahepatic portosystemic shunt — a small tube placed through the liver to lower portal pressure) might make her right heart failure worse. But because the bleeding was life‑threatening, they performed TIPS as a last‑rescue option. The procedure worked to lower the measured pressure difference in the liver (from 16 mmHg to 4 mmHg), but the overall portal pressure stayed high because her central venous pressure (the pressure returned to the heart) remained elevated from the bad right heart function.\n\nAfter TIPS she developed hepatic encephalopathy — a brain problem caused by the liver not removing toxins (her blood ammonia was high) — and had another major stomach bleed. Imaging showed the TIPS was open and working. A stomach biopsy suggested that the stomach lining had areas of poor blood supply (ischemia). Her heart scans did not show big new changes, but she got worse overall, developed fever and lung problems, and then multiorgan failure.\n\nGiven the poor outlook, the family chose to stop life‑support treatments, and she died 43 days after the TIPS procedure.\n\nKey points and explanations\n- Portal hypertension: high pressure in the liver’s blood vessels that can cause dangerous bleeding from the stomach or esophagus.  \n- TIPS: a tube placed inside the liver to lower that pressure; it can stop bleeding but may cause or worsen brain symptoms (encephalopathy) and can increase the load on a weak heart.  \n- In this case, TIPS lowered liver pressure measures but could not fix high portal pressure because the patient’s failing right heart kept central venous pressure high.  \n- Outcome: despite treatment, complications (encephalopathy, recurrent bleeding, infection, organ failure) led to death.\n\nThis case shows how complex decisions can be when severe liver disease and severe heart disease exist together: treatments that help one problem can make the other worse. The medical team tried several options, but the combined illnesses led to a poor outcome. My condolences to the patient’s family.",
+                "fh_score": 77.63
+            },
+            "B3": {
+                "text": "Resumen clínico (lectores universitarios)\n\nPaciente: mujer de 60 años con historia larga de cardiopatía congénita (estenosis pulmonar), arritmias (fibrilación y aleteo auricular tratadas con ablación del nódulo y marcapasos), insuficiencia cardíaca derecha progresiva y enfermedad renal crónica que evolucionó a insuficiencia renal terminal en hemodiálisis.\n\nProblema principal: cirrosis hepática por congestión venosa crónica (congestive hepatopathy) con hipertensión portal y hemorragias gastrointestinales recurrentes e intratables que requirieron transfusiones masivas.\n\nHallazgos relevantes\n- Laboratorio hepático: patrón colestático (ALP 388 U/L y GGT 291 U/L muy elevadas); ALT y AST solo ligeramente aumentadas. Albúmina baja (24 g/L). Bilirrubinas totales y directas, recuentos de plaquetas y leucocitos e INR estaban dentro de límites normales o apenas alterados, lo que sugiere función sintética hepática relativamente conservada a pesar de la congestión.\n- Hemodinámica: gradiente de presión venosa hepática (HVPG) de 16 mmHg antes del procedimiento; presión venosa central (PVC) crónicamente elevada por insuficiencia cardíaca derecha.\n- Clínica endoscópica: gastropatía congestiva difusa, lesión tipo Dieulafoy y úlceras antrales isquémicas; los sangrados fueron difusos y difíciles de controlar endoscópicamente.\n- Intervenciones previas: beta‑bloqueo (propranolol a baja dosis por hipotensión), múltiples tratamientos endoscópicos; anticoagulación oral suspendida por sangrados masivos.\n\nDecisión terapéutica y evolución\n- Se decidió implantar una derivación portosistémica intrahepática transyugular (TIPS) como última opción para reducir el riesgo hemorrágico. Riesgo teórico de empeoramiento de la insuficiencia cardíaca derecha motivó inicialmente reticencia.\n- Resultado hemodinámico: el TIPS redujo el HVPG de 16 a 4 mmHg, pero la presión portal absoluta se mantuvo elevada (≈14 mmHg) debido a la PVC alta persistente por la insuficiencia cardíaca derecha. Es decir, el gradiente hepático mejoró, pero la presión portal no se normalizó por el fallo cardíaco coexistente.\n- Complicaciones post‑procedimiento: el paciente desarrolló encefalopatía hepática (amonio 77 μmol/L) con respuesta clínica limitada a lactulosa y enemas. Persistió sangrado gástrico por úlceras antrales con cambios mucosos de tipo isquémico. Posteriormente se añadieron fiebre y consolidaciones pulmonares, progresión a fallo multiorgánico y, tras decisión familiar de retirar el soporte, falleció 43 días después del TIPS.\n\nInterpretación y lecciones clínicas\n- Este caso ilustra una forma de cirrosis secundaria a congestión venosa por insuficiencia cardíaca derecha, en la que la hipertensión portal tiene un componente prehepático/poshepático por PVC elevada. En tales pacientes, un TIPS puede reducir el gradiente portal pero no normalizar la presión portal si la presión venosa central sigue alta.\n- El TIPS conlleva riesgo de encefalopatía hepática y puede ofrecer beneficio limitado cuando la causa principal de la hipertensión portal es la insuficiencia cardíaca. Por ello, la selección de candidatos debe ser muy cuidadosa y multidisciplinaria (hepatología, cardiología y radiología intervencionista).\n- En pacientes similares, las alternativas o medidas complementarias a valorar incluyen optimización del estado cardíaco antes del TIPS, tratamiento dirigido de focos hemorrágicos localizados cuando sea posible, y planificación anticipada sobre riesgos de encefalopatía y manejo de infecciones nosocomiales.\n\nCierre\nSe trata de un caso complejo en el que la coexistencia de insuficiencia cardíaca derecha avanzada, hipertensión portal y sangrado digestivo masivo limitó las opciones terapéuticas y contribuyó a un desenlace fatal. La situación subraya la necesidad de evaluación individualizada y coordinación estrecha entre especialidades frente a decisiones invasivas como el TIPS. Mi más sentido pésame por el resultado adverso.",
+                "fh_score": 30.03
+            }
+        }
+    },
+    {
+        "article": "Una mujer tailandesa de 62 años presentó pérdida visual bilateral súbita y cefalea durante 5 días. Negó antecedentes de traumatismo craneal. Su historia clínica era significativa por presentar hipertensión mal controlada.\n\nLos signos vitales fueron normales, excepto por la presión arterial de 200/105 mmHg. La agudeza visual fue de no percepción de luz (NLP) con pupilas fijas en ambos ojos. La motilidad ocular de ambos ojos fue limitada en todas las direcciones. Ambas párpados fueron difíciles de abrir. Las medidas del exoftalmómetro de Hertel fueron de 16 mm en el ojo derecho y 14 mm en el ojo izquierdo. Había quemosis significativa y vasos de sacacorchos episclerales en ambos ojos. Ambas córneas mostraron un edema estromal leve y difuso sin infiltración. Las cámaras anteriores fueron profundas y tranquilas en ambos ojos. Las presiones intraoculares fueron de 45 mmHg y 48 mmHg en los ojos derecho e izquierdo, respectivamente. La gonioscopia reveló sangre en el canal de Schlemm en el ángulo nasal del ojo derecho. El examen del fondo de ojo mostró venas de la retina ligeramente dilatadas y tortuosas con discos ópticos de apariencia normal en ambos ojos. La relación taza-disco fue de 0.3 bilateralmente. La tomografía de coherencia óptica demostró un espesor normal de la mácula en cada ojo. No hubo ruido audible. Otros exámenes neurológicos fueron normales.\n\nLa resonancia magnética (MRI) con gadolinio del cerebro y las órbitas demostró la dilatación de las venas oftálmicas superiores bilaterales (SOVs) y un grado marcado de congestión orbital y periorbital bilateralmente. Sin embargo, no se observó ni compresión ni estiramiento de los nervios ópticos bilaterales. Es interesante destacar que la restricción de la difusión, con la correspondiente reducción del coeficiente de difusión aparente (ADC), en todo el segmento orbital de los nervios ópticos bilateralmente se reveló en la resonancia magnética ponderada en difusión (DWI). Esto es consistente con el PION bilateral. La angiografía por resonancia magnética (MRA) del cerebro y las órbitas reveló arterialización de los senos cavernosos bilaterales y de las SOVs.\n\nLa angiografía cerebral confirmó el diagnóstico de CCF durales bilaterales de drenaje anterior. La CCF dural derecha se alimentaba de las ramas durales de la ICA (tronco meningo-hipofisario derecho). La CCF dural izquierda se alimentaba de las ramas durales de la ECA (arteria meningo-hipofisaria izquierda y la arteria izquierda del foramen redondo y las ramas durales de la ICA (tronco meningo-hipofisario izquierdo). Cada lado de la CCF dural contribuía con flujo sanguíneo arterial a los SOV bilaterales (SOV contralateral a través de la comunicación inter-cavernosa). No se observó reflujo venoso cortical del flujo sanguíneo arterial. Basándose en estos hallazgos, se realizó una embolización transvenosa de la bobina. Los senos cavernosos bilaterales se embolizaron utilizando bobinas para ocluir los vasos de alimentación de las ramas durales de la ICA y la ECA. La angiografía cerebral inmediata posterior a la embolización mostró el cierre completo de las fístulas.\n\nTres meses después de la embolización, el examen oftálmico demostró una mejora progresiva de los signos oftálmicos antes mencionados; no obstante, la agudeza visual del paciente se mantuvo en NLP en ambos ojos.\n",
+        "gold_summary": "Reportamos el caso de una mujer de 62 años de edad con antecedentes de hipertensión arterial mal controlada que presentó pérdida visual bilateral súbita y cefalea durante 5 días. Negó antecedentes de traumatismo craneal. En el examen, sus agudezas visuales eran de no percepción de luz (NLP) con pupilas fijas en ambos ojos. La motilidad ocular de ambos ojos era limitada en todas las direcciones. Era difícil abrir ambos párpados. El examen del segmento anterior reveló quemosis bilateral y vasos del sacacorchos episclerales. La presión intraocular era de 45 y 48 mmHg en los ojos derecho e izquierdo, respectivamente. La gonioscopia reveló sangre en el canal de Schlemm en el ángulo nasal del ojo derecho. El examen del fondo de ojo mostró venas retinianas ligeramente dilatadas y tortuosas con discos ópticos de apariencia normal en ambos ojos. Las relaciones entre la copa y el disco eran de 0,3 bilateralmente. Otros exámenes neurológicos no presentaron anormalidades. La resonancia magnética demostró dilatación de las venas oftálmicas superiores bilaterales (SOV) y congestión orbital y periorbital bilateral marcada. Sin embargo, no hubo compresión o estiramiento de los nervios ópticos bilaterales. Se reveló una restricción de la difusión en la difusión ponderada por la difusión, con la correspondiente reducción del coeficiente de difusión aparente, en todo el segmento orbital bilateral de los nervios ópticos, consistente con PION bilateral. La angiografía por resonancia magnética reveló arterialización de los senos cavernosos bilaterales y las SOV. La angiografía cerebral confirmó el diagnóstico de CCF bilaterales de drenaje anterior. El tratamiento con embolización de bobina transvenosa fue exitoso. Tres meses después de la embolización, el examen oftálmico demostró una mejora progresiva de los signos oftálmicos antes mencionados; sin embargo, sus agudezas visuales permanecieron como NLP en ambos ojos.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había una mujer de 62 años que tenía la presión arterial alta y mal controlada. Un día empezó con dolor de cabeza y, en cinco días, dejó de ver con los dos ojos. No tuvo golpe en la cabeza.\n\nCuando la vieron en el hospital no veía nada en ninguno de los dos ojos. Sus pupilas no reaccionaban y los ojos casi no se podían mover. Tenía los párpados hinchados y costaba abrirlos. Los ojos estaban enrojecidos y con venas muy marcadas. La presión dentro de los ojos estaba muy alta. En uno de los ojos se encontró sangre en un canal del ángulo del ojo.\n\nLas partes que se miran dentro del ojo, como el disco del nervio óptico y la mácula, parecían normales en las pruebas. Pero en la resonancia magnética se vieron venas muy agrandadas detrás de los ojos y mucho hinchazón alrededor. También se vio que las señales del nervio que lleva la vista estaban dañadas por falta de riego. Esto significa que el nervio quedó herido por no recibir suficiente sangre. Los médicos llamaron a eso PION, que es un daño del nervio óptico por falta de sangre.\n\nLa causa fue una conexión anormal entre arterias y venas cerca de los ojos, llamada fístula carotídeo-cavernosa. Esa conexión hacía que llegara demasiada sangre a las venas de los ojos. Los médicos confirmaron esto con una angiografía, que es una prueba que mira los vasos.\n\nPara arreglarlo, los médicos metieron pequeñas bobinas por dentro de las venas para cerrar esas conexiones malas. Inmediatamente después, las pruebas mostraron que las fístulas se habían cerrado.\n\nTres meses después, la hinchazón y el enrojecimiento de los ojos mejoraron. Pero, aunque los ojos se veían mejor, la mujer no recuperó la visión y seguía sin poder ver nada con ninguno de los dos ojos.\n\nEn resumen: una fístula cerca del ojo causó hinchazón y daño al nervio de la vista. Los médicos la cerraron con un tratamiento que funcionó para parar el flujo malo, pero el daño al nervio ya era muy grande y la persona no recuperó la vista.",
+                "fh_score": 80.58
+            },
+            "B2": {
+                "text": "Resumen corto y claro (nivel B2, para lectores de secundaria)\n\nUna mujer tailandesa de 62 años con hipertensión arterial mal controlada acudió por una pérdida súbita de visión en ambos ojos y cefalea durante 5 días. No había sufrido traumatismo. En la consulta tenía presión arterial alta (200/105 mmHg). Su visión era “no percepción de luz” (NLP) en los dos ojos, es decir, no podía ver nada ni siquiera luz. Las pupilas estaban fijas, los movimientos oculares muy limitados y le costaba abrir los párpados.\n\nEn el examen de los ojos se vieron signos de congestión venosa: quemosis (hinchazón de la conjuntiva), vasos en “sacacorchos” (muy tortuosos) y leve edema de la córnea. La presión dentro de los ojos era muy alta (45 y 48 mmHg; valores normales están por debajo de 21 mmHg). Al mirar dentro del ojo, los vasos de la retina estaban algo dilatados y tortuosos, pero los discos ópticos parecían normales. Una tomografía (OCT) mostró máculas de grosor normal.\n\nLa resonancia magnética con contraste mostró venas oftálmicas superiores muy dilatadas y congestión marcada alrededor de las órbitas (la zona del ojo). En la resonancia de difusión se vio que toda la parte orbital de los nervios ópticos tenía “restricción de difusión” con reducción del ADC; esto indica lesión por falta de riego y es compatible con una neuropatía óptica isquémica posterior (PION). La angiografía por RM mostró “arterialización” de los senos cavernosos y de las venas oftálmicas, lo que sugería un flujo arterial anormal hacia las venas.\n\nLa angiografía cerebral confirmó la causa: fístulas carótido-cavernosas durales bilaterales (CCF) con drenaje hacia adelante. Una fístula carótido-cavernosa es una conexión anormal entre arterias y el seno cavernoso (una vena grande en la base del cráneo); eso pone mucha presión en las venas del ojo y produce los signos que se vieron. Cada fístula recibía sangre de ramas arteriales diferentes y ambas aportaban flujo a las venas oftálmicas. No había reflujo hacia las venas corticales del cerebro.\n\nSe trató realizando una embolización transvenosa con bobinas: mediante catéteres se colocaron bobinas dentro de los senos cavernosos para cerrar las fístulas. La angiografía inmediatamente después mostró cierre completo de las comunicaciones anormales. Tres meses tras el procedimiento, muchos signos en los ojos (hinchazón, congestión) habían mejorado, pero la visión no se recuperó y seguía siendo NLP en ambos ojos.\n\nComentarios prácticos y tono cuidadoso\n- El daño observado en la resonancia (PION) explica por qué la visión no volvió: hubo falta de riego y lesión del segmento orbital de los nervios ópticos, y ese daño suele ser irreversible.  \n- El tratamiento endovascular cerró la fístula y mejoró la congestión ocular, lo que fue positivo para la salud ocular general y para evitar más daño.  \n- En casos similares es importante controlar factores de riesgo (como la hipertensión) y buscar atención urgente ante cambios visuales repentinos. También puede necesitarse apoyo de rehabilitación visual si la pérdida es permanente.\n\nEste resumen describe los hallazgos y el tratamiento del caso de forma sencilla y respetuosa. Si quieres, puedo explicar con dibujos o comparar las estructuras implicadas para entender mejor cómo una fístula afecta al ojo.",
+                "fh_score": 59.25
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel universitario, sensible y claro)\n\nPresentación y antecedentes\n- Paciente: mujer tailandesa de 62 años con hipertensión mal controlada.\n- Síntomas: pérdida visual súbita en ambos ojos y cefalea durante 5 días. Niega traumatismo craneal.\n- Signos vitales relevantes: presión arterial 200/105 mmHg.\n\nExploración oftalmológica (hallazgos anormales principales)\n- Agudeza visual: no percepción de luz (NLP) en ambos ojos — pérdida visual completa.\n- Pupilas fijas y motilidad ocular limitada en todas las direcciones; apertura palpebral dificultosa.\n- Quemosis (hinchazón de la conjuntiva) bilateral y vasos episclerales en “sacacorchos” (tortuosos).\n- Exoftalometría (Hertel): 16 mm OD, 14 mm OI (ligera protrusión derecha).\n- Presiones intraoculares muy elevadas: 45 mmHg (OD) y 48 mmHg (OI) — (normal ≈ 10–21 mmHg).\n- Gonioscopia: sangre en el canal de Schlemm en el ángulo nasal derecho (signo de hipertensión venosa ocular).\n- Fondo de ojo: venas retinianas levemente dilatadas/tortuosas; discos ópticos con aspecto normal (copa/disco 0,3 bilaterales).\n- Otros exámenes neurológicos normales.\n\nImágenes e interpretación (cómo se llegó al diagnóstico)\n- Resonancia magnética (RM) orbitarias con gadolinio: dilatación de las venas oftálmicas superiores bilaterales (SOV) y congestión orbital/periorbital marcada. No hubo compresión ni estiramiento visible de los nervios ópticos.\n- RM ponderada en difusión (DWI) con descenso del coeficiente de difusión aparente (ADC) en todo el segmento orbital de ambos nervios ópticos → compatible con neuropatía óptica isquémica posterior bilateral (PION), es decir, lesión por falta de riego en la porción posterior del nervio óptico.\n- Angio-RM: “arterialización” de los senos cavernosos bilaterales y de las SOVs (indica paso anormal de sangre arterial a las venas).\n- Angiografía cerebral: confirmó fístulas carotídeo-cavernosas (CCF) durales bilaterales con drenaje anterior. Las fístulas estaban alimentadas por ramas durales de la arteria carótida interna (ICA) y de la arteria carótida externa (ECA); había comunicación inter-cavernosa que permitía arterializar ambas SOVs. No se observó reflujo venoso cortical (lo que reduce, pero no elimina, otros riesgos neurológicos).\n\nDiagnóstico final\n- CCF durales bilaterales con drenaje anterior que causaron congestión venosa orbital intensa y elevación marcada de la presión intraocular, y PION bilateral que explica la ceguera aguda.\n\nTratamiento y evolución\n- Se realizó embolización transvenosa con bobinas de los senos cavernosos bilaterales para ocluir las ramas durales suministradoras (ICA y ECA). La angiografía inmediatamente posterior mostró cierre completo de las fístulas.\n- A los 3 meses: mejora progresiva de los signos externos oculares (quemosis, congestión, vascularización episcleral), pero la agudeza visual permaneció NLP en ambos ojos. Esto sugiere que la lesión isquémica del nervio óptico fue irreversible a pesar del cierre exitoso de las fístulas.\n\nImplicaciones clínicas y recomendaciones (qué significa y qué seguir)\n- Etiología y riesgo: las CCF durales pueden aparecer sin traumatismo y en pacientes con factores vasculares (como hipertensión). El drenaje venoso anómalo eleva la presión venosa orbital, aumentando la presión intraocular y el riesgo de isquemia del nervio óptico.\n- Importancia del diagnóstico precoz: cuanto antes se trate la fístula, mayor la probabilidad de prevenir daño isquémico irreversible. Sin embargo, si ya hay PION establecida, la recuperación visual puede no ser posible.\n- Seguimiento y manejo: control estricto de la presión arterial, control de la presión intraocular y vigilancia de complicaciones oculares y neurológicas. Evaluación para rehabilitación visual y apoyo psicosocial dada la ceguera bilateral persistente.\n- Consejos al equipo tratante: documentar función residual, ofrecer baja visión/rehabilitación, controlar factores de riesgo cardiovascular y planear seguimiento a largo plazo de la anatomía vascular mediante imágenes si hubiera síntomas nuevos.\n\nComentario empático final\nEste caso muestra cómo una fístula carotídeo-cavernosa dural puede producir una congestión orbital severa y daño isquémico del nervio óptico a pesar de un tratamiento endovascular exitoso. Lamentablemente, la lesión establecida en los nervios ópticos llevó a una ceguera permanente; sin embargo, el cierre de la fístula redujo la congestión y evitará probablemente nuevas complicaciones. Es importante ofrecer a la paciente apoyo multidisciplinario (cardiovascular, oftalmológico y de rehabilitación visual) y manejo riguroso de la hipertensión para prevenir futuras crisis.",
+                "fh_score": 41.13
+            }
+        }
+    },
+    {
+        "article": "Un paciente de 15 años de edad (altura = 161 cm; peso = 66 kg; superficie corporal = 1,70; grupo sanguíneo = B positivo) con cardiomiopatía dilatada fue derivado a la Universidad de Ankara con pérdida de conciencia y shock cardiogénico en julio de 2016. El apoyo de oxigenación de membrana extracorpórea venosa arterial se realizó aproximadamente 1 semana después. Su fracción de eyección ventricular izquierda fue del 22%. Ocho días después, el paciente recibió un implante de corazón artificial total SynCardia (50 ml; SynCardia Systems, Inc., Tucson, AZ, EE. UU.). En el día 131 postoperatorio después de la cirugía TAH, el paciente se quejó de pérdida de audición bilateral y fue derivado al departamento de oído, nariz y garganta.\n\nLos antecedentes médicos previos no revelaron evidencia de pérdida auditiva, antecedentes familiares de sordera o cualquier anomalía adicional en su niñez. Sus registros médicos no revelaron evidencia de meningitis. Sin embargo, había recibido amikacina (15 mg/kg), un antibiótico ototóxico, contra patógenos gramnegativos importantes durante su estancia en la unidad de cuidados intensivos. El paciente fue incluido en la lista de espera de trasplantes de corazón de alta urgencia y era móvil en el Freedom Driver portátil (SynCardia).\n\nEl examen otoscópico del paciente fue normal. La audiometría de tonos puros y la respuesta auditiva del tronco encefálico revelaron una pérdida auditiva profunda bilateral. La timpanometría mostró timpanogramas normales de tipo A bilaterales. Tanto la tomografía computarizada como la resonancia magnética confirmaron la morfología normal del laberinto y nervios cocleares intactos.\n\nFue examinado por un equipo multidisciplinario (cirugía cardiovascular, cuidados intensivos pediátricos, cardiología pediátrica, psiquiatría de consulta y enlace, fisioterapia y rehabilitación, enfermedades infecciosas y microbiología clínica, anestesiología, audiología y otorrinolaringología) para realizar un implante coclear. Después de analizar las posibles opciones con el paciente y sus padres, se decidió que se beneficiaría de un implante coclear debido a la pérdida auditiva y la reducción de la función cognitiva y la adaptación necesaria para el trasplante de corazón. Después de analizar su caso con el equipo multidisciplinario, se decidió un implante coclear del lado derecho (Nucleus CI24RE con Contour Advance Electrode; Cochlear, Macquarie University, Australia).\n\nEl paciente tomaba warfarina (10 mg/día), que se interrumpió tres días antes de la cirugía, y se inició la heparinización (dosis de carga de 50 U/kg y dosis de mantenimiento de 20 U/kg/h) cuando el tiempo de protrombina (cociente internacional normalizado [INR]) era inferior a 1,5. Dos horas antes de la cirugía, se interrumpió la heparinización. En el quirófano, se disponía de un dispositivo de reserva para un posible fallo del dispositivo TAH. El equipo de anestesia y el perfusionista controlaron de cerca los resultados del flujo para el TAH. El flujo sanguíneo no pulsátil afecta de forma negativa al control de los signos vitales, y la presión arterial no invasiva no fue suficiente en nuestro paciente. Bajo anestesia local, se realizó un cateterismo radial arterial invasivo. Además, se dejó la vena yugular interna izquierda en su lugar, lo que permitió el control de la presión venosa central y su uso como reemplazo de fluidos de gran volumen cuando fue necesario. Después de iniciar el control, se administraron con precaución 2 mg/kg de propofol, 1 mg/kg de bromuro de rocuronio y 1 µg/kg de fentanilo, y se intubió al paciente por vía oral. Se utilizó sevoflurano con una concentración alveolar mínima de 1 a 1,5 en oxígeno al 40 % para el mantenimiento. El óxido nítrico inhalado también estaba listo para usarse en caso de una posible crisis hipertensiva pulmonar.\n\nEl día 250 después del implante TAH, se realizó la cirugía de implante coclear con abordaje de ventana redonda sin complicaciones perioperatorias; el paciente tuvo una pérdida de sangre mínima (solo 50 ml). La duración de la operación fue de 120 minutos. El paciente fue extubado en el quirófano sin problemas circulatorios y respiratorios. La heparinización se inició a la hora 6 posoperatoria. Comenzamos con la warfarina el día 1 posoperatorio, y la heparinización se detuvo después de alcanzar un INR de 2.0. No se observaron complicaciones (infecciones, hematoma) en el seguimiento posoperatorio.\n\nEl implante coclear se activó en la semana 4 después de la operación. El equipo de audiología lo revisó 4 y 8 semanas después; mostró una mejora continua en su audición, con impedancias normales. Sus resultados de percepción del habla mejoraron significativamente 3 meses después del implante coclear.\n\nMH - Adolescente\nMH - Niño\nMH - *Implantación coclear\nMH - *Insuficiencia cardiaca/diagnóstico/etiología/cirugía\nMH - *Efectos adversos del trasplante de corazón\nMH - *Corazón, Artificial\nMH - Humanos\nMH - Hombre\nMH - Resultado del tratamiento\n",
+        "gold_summary": "Describimos el caso de un niño de 15 años con pérdida auditiva total bilateral postlingual tras la administración de medicamentos ototóxicos durante su estancia en la unidad de cuidados intensivos pediátricos. El paciente recibió el implante de corazón artificial total SynCardia (50 ml; SynCardia Systems, Inc., Tucson, AZ, EE. UU.) para la insuficiencia cardiaca biventricular en fase terminal como puente para el trasplante cardiaco. Durante su estancia en la lista de espera de trasplantes cardiacos urgentes, se sometió a una implantación coclear satisfactoria tras optimizar el estado de coagulación y hemostasis y una preparación anestésica adecuada.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un chico de 15 años tenía el corazón muy débil. Le pusieron un corazón artificial para ayudarle mientras esperaba un trasplante. Después de estar en la unidad de cuidados intensivos, dejó de oír en los dos oídos. Los médicos creyeron que fue por un antibiótico que puede dañar el oído.\n\nLas pruebas mostraron que la parte del oído y el nervio estaban bien, pero él tenía pérdida de audición profunda en los dos oídos. Un equipo de muchos médicos decidió ponerle un implante coclear en el oído derecho. Un implante coclear es un pequeño aparato que se coloca en la cabeza para devolver la sensación de sonido.\n\nAntes de la operación, los doctores cambiaron sus medicinas para la sangre con mucho cuidado. La cirugía fue corta y sin problemas. No hubo sangrado ni infección. El implante se activó cuatro semanas después. Con el tiempo, empezó a oír mejor y sus pruebas de habla mejoraron mucho a los tres meses.\n\nLos médicos cuidaron bien todos los pasos. El tratamiento ayudó al joven a recuperar parte de su audición y a prepararse mejor para su trasplante de corazón.",
+                "fh_score": 79.1
+            },
+            "B2": {
+                "text": "Summary:\n\nA 15-year-old boy with severe dilated cardiomyopathy was treated at a university center after losing consciousness and going into cardiogenic shock. He received extracorporeal membrane oxygenation (ECMO) for a week and, because his heart function was very poor (left ventricular ejection fraction 22%), he had a total artificial heart (TAH, a mechanical heart device) implanted eight days later as a bridge to transplant. About four months after the TAH surgery, he noticed sudden, severe hearing loss in both ears.\n\nTests showed profound bilateral sensorineural hearing loss (damage to the inner ear or hearing nerve), while ear anatomy and the cochlear nerves looked normal on CT and MRI. During his intensive care stay he had been given amikacin, an antibiotic that can be ototoxic (it can damage hearing), and this was the likely cause. A multidisciplinary team agreed that a cochlear implant (an electronic device that bypasses the damaged inner ear and stimulates the hearing nerve) would help him—both for communication and to support his care while waiting for a heart transplant. They chose a right-sided implant (Nucleus CI24RE with Contour Advance electrode).\n\nBecause he was taking warfarin (a blood thinner) for the TAH, the team carefully managed his anticoagulation: warfarin was stopped three days before surgery and he was switched to heparin (short-acting anticoagulant), which was paused two hours before the operation. The team used invasive blood-pressure and central venous monitoring during anesthesia to keep the TAH functioning safely. The cochlear implant surgery (round-window approach) was done about 250 days after the TAH implant without complications, with very little blood loss. He was extubated in the operating room and anticoagulation was restarted after surgery; warfarin was resumed on day 1 post-op and heparin stopped once the target INR was reached.\n\nThe implant was activated four weeks later. Follow-up audiology at 4 and 8 weeks showed improving hearing and normal device function, and his speech perception had improved significantly by three months. There were no infections, hematomas, or other complications. Overall, the case shows that, with careful planning and multidisciplinary care, a cochlear implant can be safely and successfully performed in a patient supported by a total artificial heart.",
+                "fh_score": 72.74
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel universitario, lectura clara y empática)\n\nCaso\n- Paciente varón de 15 años con miocardiopatía dilatada e insuficiencia cardíaca biventricular terminal que requirió soporte con oxigenación por membrana extracorpórea y, después, implante de corazón artificial total (TAH SynCardia 50 ml) como puente al trasplante. La fracción de eyección del ventrículo izquierdo era del 22%.\n\nPresentación otológica\n- A los 131 días tras el implante del TAH el paciente refería pérdida auditiva bilateral. No había antecedentes previos de hipoacusia, meningitis ni sordera familiar. Durante su ingreso en la UCI se administró amikacina, un antibiótico con riesgo ototóxico.\n\nHallazgos objetivo\n- Examen otoscópico: normal.\n- Audiometría tonal y potenciales evocados auditivos del tronco cerebral (ABR): pérdida auditiva profunda bilateral (sensorioneural).\n- Timpanometría: curvas tipo A bilaterales (órganos medioauriculares normales).\n- TAC y resonancia magnética: morfología normal del laberinto y nervios cocleares intactos (anatomía favorable para implante coclear).\n- Conclusión clínica: pérdida auditiva postlingual profunda, muy probablemente asociada a ototoxicidad por aminoglucósido (amikacina).\n\nDecisión terapéutica\n- Un equipo multidisciplinario (cardiología, cirugía cardiovascular, cuidados intensivos pediátricos, anestesiología, infectología, ORL/audiología, rehabilitación, psiquiatría, perfusionista) evaluó riesgos y beneficios. Se optó por implante coclear unilateral derecho (Nucleus CI24RE con electrodo Contour Advance) para recuperar audición, mejorar función cognitiva y facilitar la adaptación al eventual trasplante cardíaco.\n\nManejo perioperatorio y anestésico (aspectos clave)\n- Anticoagulación: warfarina (10 mg/día) suspendida 3 días antes; puente con heparina (carga 50 U/kg, mantenimiento 20 U/kg/h) hasta INR < 1,5; heparina detenida 2 h antes de la cirugía; reiniciada 6 h posoperatorias y warfarina reintroducida el día 1 posoperatorio; heparina suspendida al alcanzar INR 2,0.\n- Monitoreo: presión arterial invasiva radial debido a flujo no pulsátil del TAH (la presión no invasiva fue insuficiente); control de presión venosa central mediante catéter yugular existente; perfusionista y equipo de anestesia supervisando flujo y dispositivo TAH; dispositivo de reserva disponible.\n- Anestesia: inducción y mantenimiento con dosis ajustadas de propofol, rocuronio, fentanilo y sevoflurano; óxido nítrico inhalado disponible para crisis hipertensiva pulmonar.\n- Procedimiento: implante por abordaje de ventana redonda sin complicaciones perioperatorias; tiempo quirúrgico 120 minutos; pérdida sanguínea mínima (50 ml). Extubado en quirófano sin problemas respiratorios o circulatorios.\n\nEvolución y resultados\n- Sin complicaciones posoperatorias (sin infección ni hematoma).\n- Activación del implante: semana 4 tras la cirugía.\n- Seguimiento audiológico a las semanas 4 y 8: impedancias normales y mejora progresiva de la audición.\n- Evaluación a los 3 meses: mejora marcada en percepción del habla.\n\nImplicaciones y enseñanzas clave\n- Es factible y seguro realizar implante coclear en pacientes con soporte circulatorio complejo (TAH) si se planifica y coordina cuidadosamente la anticoagulación, el control hemodinámico y el manejo anestésico.\n- La preservación de la anatomía coclear y de la vía auditiva en las pruebas de imagen favoreció el éxito del implante.\n- En pacientes que han recibido aminoglucósidos, debe sospecharse ototoxicidad si aparece disminución auditiva; la intervención temprana con implante coclear puede restaurar comunicación verbal y apoyar la rehabilitación global y la elegibilidad para trasplante.\n- Próximos pasos: rehabilitación audiológica continuada, seguimiento del TAH y del estado para trasplante cardiaco, y vigilancia de la anticoagulación.\n\nTono y enfoque\n- El tratamiento se diseñó teniendo en cuenta la seguridad del dispositivo cardíaco, la prevención de sangrado y trombosis, y el bienestar funcional y cognitivo del adolescente. El resultado funcional inicial fue favorable y supuso una mejora significativa en su comunicación y calidad de vida.",
+                "fh_score": 29.35
+            }
+        }
+    },
+    {
+        "article": "Se encontró a un hombre de 25 años de edad recostado por familiares después de una noche de fiesta, con vómitos, agresión y dolor localizado en la región glútea e inferior derecha. La evaluación inicial en el departamento de urgencias no reveló lesiones traumáticas; sin embargo, el empeoramiento de los síntomas llevó a una nueva evaluación al día siguiente. Los resultados de laboratorio revelaron un recuento sanguíneo completo sin alteraciones, niveles elevados de CPK sérica (42 527 IU/l), creatinina sérica (735 µmol/l), urea (44,3 mmol/l) y potasio (5,7 mmol/l). El análisis de orina reveló orina de color rojo-marrón sin glóbulos rojos, proteinuria (+1), glucosuria (+1) y WBC (9-10/hpf). Estos resultados confirmaron la RM y la IRA. La toxicología estableció la administración de 1796 µg/l de heroína (> 5 veces el nivel basal) sin detección de ninguna otra sustancia. Aunque inicialmente negó haber tomado medicamentos, después del análisis toxicológico, el paciente admitió que había administrado heroína una vez por vía intramuscular en la región glútea derecha la noche del incidente.\n\nUna tomografía computarizada demostró edema muscular glúteo y miositis localizada en la región glútea derecha. Al comenzar el tratamiento convencional con resucitación de fluidos intravenosos (IV), el tratamiento de la IRA fracasó, lo que hizo necesario el TRR con hemodiálisis debido a la progresión de la azotemia con un aumento de la creatinina sérica a 1052 µmol/l. La función renal mejoró tras el cese del TRR con una duración total de la estancia (LOS) de 9 días. El seguimiento posterior del paciente fue incompleto debido a la falta de asistencia.\n",
+        "gold_summary": "Este informe de caso describe a un hombre de 25 años que desarrolló una RM grave y lesión renal aguda (LRA) después de la administración intramuscular (IM) de heroína como usuario por primera vez. El uso de la heroína IM puede inducir niveles más altos de CPK debido a la toxicidad directa de los miocitos y el trauma mecánico. Los músculos glúteos altamente vascularizados con fibras tipo 1 en el sitio de la inyección probablemente exacerbaron la gravedad. Los factores adicionales incluyeron una menor densidad mitocondrial en los hombres y la exposición al alcohol. A pesar de la reanimación agresiva con líquidos, se requirió la terapia de reemplazo renal (RRT) y el paciente respondió bien a la hemodiálisis.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Este cuento habla de un hombre de 25 años que se puso muy enfermo después de una noche de fiesta. Él recibió una sola inyección de heroína en el glúteo (la nalga). Al día siguiente tenía vómitos y mucho dolor en esa nalga.\n\nLa inyección dañó los músculos. Cuando los músculos se rompen, meten cosas en la sangre que pueden dañar los riñones. Sus análisis mostraron que tenía daño fuerte en los músculos y que los riñones no funcionaban bien. Los médicos le dieron líquidos por vena, pero sus riñones siguieron empeorando. Por eso necesitó hemodiálisis. La hemodiálisis es una máquina que limpia la sangre cuando los riñones no pueden hacerlo.\n\nDespués de la hemodiálisis y el tratamiento, sus riñones mejoraron. Estuvo en el hospital 9 días y salió después. No se sabe bien cómo siguió porque no volvió a las citas. Esto nos recuerda que inyectar drogas puede causar daño grave y que beber alcohol puede empeorar las cosas.",
+                "fh_score": 81.41
+            },
+            "B2": {
+                "text": "Resumen del caso (nivel escolar, B2)\n\nUn hombre de 25 años fue encontrado por su familia después de una noche de fiesta con vómitos, comportamiento agresivo y dolor en la nalga derecha. Al principio no se vieron heridas graves, pero al empeorar los síntomas volvió al hospital al día siguiente.\n\nQué se encontró\n- Tenía una prueba sanguínea con CPK muy alta (42 527 IU/L). La CPK es una enzima que sube cuando el músculo se destruye; niveles tan altos indican rabdomiólisis, es decir, daño muscular importante.  \n- La creatinina y la urea (marcadores de función renal) estaban muy elevadas: la creatinina llegó a 735 µmol/L y luego subió a 1052 µmol/L. Esto mostró una lesión renal aguda (insuficiencia renal súbita).  \n- La orina era de color rojo-marrón pero sin glóbulos rojos, lo que sugiere que la orina contenía productos del músculo dañado (mioglobina).  \n- La toxina detectada fue heroína en una concentración muy alta; el paciente finalmente admitió que había inyectado heroína por vía intramuscular en la nalga derecha esa noche (era su primer uso así).\n\nImágenes y tratamiento\n- Una tomografía mostró inflamación y edema del músculo glúteo derecho (miositis localizada).  \n- Comenzaron líquidos por vía intravenosa para intentar proteger los riñones, pero la función renal siguió empeorando. Por ello fue necesario aplicar terapia de reemplazo renal (hemodiálisis). Tras ese tratamiento la función renal mejoró y el paciente estuvo 9 días en el hospital. El seguimiento posterior no fue completo porque el paciente dejó de acudir a control.\n\nPor qué pudo pasar esto\n- La inyección intramuscular de heroína puede dañar el músculo de dos maneras: por la propia toxicidad de la sustancia sobre las células musculares y por el trauma mecánico de la aguja y del volumen inyectado.  \n- Los músculos glúteos, por su estructura y vascularización, pudieron favorecer una lesión más intensa en ese sitio.  \n- También se mencionan factores que pueden aumentar el riesgo, como el consumo de alcohol y diferencias biológicas entre hombres y mujeres.\n\nQué significa esto y qué sigue\n- La rabdomiólisis grave puede provocar fallo renal si los productos del músculo dañado llegan al riñón. El tratamiento urgente incluye líquidos y, si no es suficiente, diálisis para reemplazar la función renal temporalmente.  \n- Es importante el seguimiento médico para comprobar la recuperación completa del riñón y recibir apoyo para problemas relacionados con el consumo de drogas.\n\nTono final\nSucedió un daño muscular serio tras una inyección de heroína que terminó afectando los riñones. El tratamiento médico fue efectivo para recuperar la función renal en el hospital, pero el control ambulatorio fue incompleto. Si alguien tiene una situación parecida, debe buscar atención médica urgente y ayuda para el consumo de sustancias.",
+                "fh_score": 58.34
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel lector universitario)\n\nPresentación y hallazgos principales\n- Hombre de 25 años fue encontrado somnoliento después de una noche de fiesta con vómitos, comportamiento agresivo y dolor localizado en la región glútea derecha.\n- La primera evaluación en urgencias no mostró signos de traumatismo externo. Al día siguiente empeoró y se repitió la valoración.\n- Hemograma dentro de límites normales; hallazgos anormales clave: CPK sérica muy elevada (42 527 IU/L), creatinina 735 µmol/L, urea 44,3 mmol/L y potasio 5,7 mmol/L.\n- Orina de color rojo‑marrón sin glóbulos rojos visibles, con proteinuria y glucosuria leves y leucocitos 9–10/campo: esto sugiere mioglobinuria (presencia de mioglobina en orina) secundaria a destrucción muscular, no sangrado urinario.\n- Tomografía mostró edema y miositis en el músculo glúteo derecho.\n\nDiagnóstico y causa probable\n- Se diagnosticó rabdomiólisis (destrucción aguda de músculo esquelético) con lesión renal aguda (LRA) secundaria.\n- La toxicología detectó una concentración elevada de heroína (1 796 µg/L) y el paciente, tras inicialmente negarlo, admitió haberse inyectado heroína intramuscularmente en la región glútea la noche previa. Fue su primer uso por esa vía.\n- La combinación de toxicidad directa sobre los miocitos, trauma mecánico por la inyección y factores locales (glúteo con gran vascularización y cierta composición de fibras musculares) probablemente aumentó la destrucción muscular. Otros factores contribuyentes mencionados fueron sexo masculino y consumo de alcohol.\n\nTratamiento y evolución\n- Se inició reanimación con líquidos IV (tratamiento estándar inicial para rabdomiólisis) pero la función renal no mejoró: la creatinina progresó hasta 1 052 µmol/L.\n- Fue necesario realizar terapia de reemplazo renal (TRR) mediante hemodiálisis. Tras el tratamiento renal la función renal mejoró.\n- Estancia hospitalaria total: 9 días. El seguimiento posterior fue incompleto por falta de asistencia.\n\nImplicaciones clínicas y recomendaciones prácticas\n- La inyección intramuscular de heroína puede provocar rabdomiólisis grave y LRA incluso en usuarios primerizos; por tanto, es importante sospecharlo si hay dolor local intenso, orina oscura y síntomas sistémicos tras consumo o inyección.\n- Signos de alarma que requieren valoración urgente: CPK muy elevada, hiperkalemia, oliguria/anuria, elevación rápida de creatinina o alteraciones ácido‑base.\n- Primeros pasos: hidratación IV agresiva, monitorización estrecha de electrolitos (especialmente potasio), diuresis y función renal; consultar precozmente a nefrología para valorar TRR si la clínica o los valores no responden.\n- También es importante abordar el consumo de sustancias: asesoramiento, programas de reducción de daños y seguimiento para evitar recurrencias y complicaciones a largo plazo.\n\nTono y contexto\n- El caso subraya que una conducta de consumo puntual puede tener consecuencias médicas graves y potencialmente reversibles con tratamiento oportuno. La atención médica temprana y el seguimiento son claves.",
+                "fh_score": 43.89
+            }
+        }
+    },
+    {
+        "article": "Una mujer de 63 años con antecedentes de obesidad e hipertensión arterial acudió a la sala de urgencias de un hospital de nivel secundario con un historial de siete días de fiebre, tos seca, hiposmia y mialgia. Al momento del ingreso, se encontraba alerta, con una frecuencia respiratoria de 22 ciclos por minuto, pulso de 90 latidos por minuto y saturación de oxígeno de 90 %. Los análisis de laboratorio revelaron linfopenia (1,55 x 109) y niveles elevados de proteína C reactiva (10,62 mg/dL). Se realizó una prueba de reacción en cadena de la polimerasa para COVID-19 a partir de un hisopado nasofaríngeo y de la garganta, que resultó positivo para el coronavirus del síndrome respiratorio agudo severo 2 (SARS-CoV-2).\n\nLa situación evolucionó rápidamente con fiebre, postración y empeoramiento de la disnea. La gasometría arterial reveló una insuficiencia respiratoria grave, mientras que la radiografía de tórax evidenció infiltrados pulmonares bilaterales. La paciente fue intubada y sometida a ventilación mecánica, pero su condición respiratoria continuó deteriorándose, a pesar de los mejores cuidados críticos, incluyendo ventilación en posición prona y bloqueo neuromuscular. Su examen de tomografía computarizada del tórax, tras la intubación, reveló extensas opacificaciones multifocales bilaterales en vidrio molido, sin signos de embolia pulmonar. Los ajustes iniciales del ventilador fueron: ventilación controlada por volumen con volumen corriente de 360 ml (6 ml/kg de peso corporal ideal), frecuencia respiratoria de 14 respiraciones por minuto, presión espiratoria positiva final (PEEP) de 14 cmH2O y complacencia estática de 44 cmH2O.\n\nEn el segundo día de internación, la gasometría arterial mostró pH de 7,34, presión parcial de dióxido de carbono (PaCO2) de 53 mmHg, presión parcial de oxígeno (PaO2) de 102 mmHg y bicarbonato (HCO3) de 29,7 mmol/L, con una proporción presión parcial de oxígeno/fracción inspirada de oxígeno (PaO2/FiO2) de 98. Ella cumplía los criterios para indicación de VV-ECMO y fue transferida a la unidad de terapia intensiva (UTI), que disponía de un programa establecido para VV-ECMO. El procedimiento fue realizado con seguridad, no habiendo ocurrido complicaciones. El análisis de la gasometría arterial 3 horas después del inicio de la VV-ECMO mostró pH de 7,386, PaCO2 de 43 mmHg, PaO2 de 94,3 mmHg y HCO3 de 25,4 mmol/L, sin cualquier variación abruta de la PaCO2. Tuvieron inicio la nutrición y la rehabilitación precoces tras la introducción de la VV-ECMO. En el 14º día de internación, la paciente desarrolló neumonía asociada al ventilador causada por Pseudomonas aeruginosa, siendo sometida a 7 días de antibioticoterapia con ceftazidima y vancomicina, con respuesta favorable. En el 20º día de internación, su radiografía del tórax y la complacencia mejoraron, y la paciente fue retirada de la VV-ECMO con éxito tras 455 horas de soporte, siendo traqueostomizada 7 días después. La paciente mantuvo buena función renal durante toda la internación.\n\nEn el día 34 de internación, luego de 7 días de destete de la sedación, con evolución positiva de su cuadro neurológico, ocurrió una crisis epiléptica generalizada limitada, que llevó a la investigación diagnóstica.\n\nInvestigación\nLos análisis de sangre de laboratorio revelaron una disminución de los niveles de proteína C reactiva (6,11 mg/dL), procalcitonina (0,07 ng/mL), fibrinógeno (307 ng/mL) y ferritina (2802 ng/mL), pero un aumento en los niveles de dímero D (18021 ng/mL) e interleucina 6 (10,4 pg/mL) en el día anterior al inicio de los síntomas. No se asoció ninguno de los fármacos administrados a la paciente con el SEPR, es decir, fármacos inmunosupresores, inmunomoduladores y quimioterápicos.\n\nSe realizó una resonancia magnética (RM) del cerebro y las imágenes de recuperación de inversión atenuada por fluidos (FLAIR) demostraron una hiperintensidad simétrica y confluente que afectaba a la sustancia blanca justa y subcortical, principalmente en las regiones occipital y parietal, pero también en la región frontal, temporal y cerebelosa izquierda. Los núcleos grises profundos se conservaron y no había presencia de ninguna área con restricción del contraste. Las imágenes ponderadas por susceptibilidad mostraron múltiples microhemorragias puntiformes que afectaban a la sustancia blanca superficial y profunda, pero que no afectaban al área con hiperintensidad en FLAIR. Las microhemorragias puntiformes involucraban predominantemente a la sustancia blanca justacortical y al cuerpo calloso (especialmente el codo y el esplenio). Además, había tres hemorragias subagudas de menos de 1 cm en las cápsulas externas, con hiperintensidad en T1.\n\nLa muestra de líquido cefalorraquídeo dio negativo para SARS-CoV-2 y los niveles de proteínas (31 mg/dL), glucosa (74 mg/dL) y lactato (1,89 mmol/L) se encontraban dentro de los parámetros normales.\n\nDesvelado\nLa paciente logró una recuperación casi total de los déficits neurológicos, a pesar de la miopatía de la enfermedad crítica, y fue dada de alta después de 44 días en el hospital. Se la derivó a un hospital secundario para su rehabilitación y prácticamente recuperó su estado mental previo.\n",
+        "gold_summary": "Una mujer de 63 años de edad acudió a la sala de urgencias con un historial de fiebre aguda, postración y disnea. Se le diagnosticó un caso grave de COVID-19 y síndrome de dificultad respiratoria aguda. A pesar de recibir atención médica intensiva, cumplía con los requisitos para someterse a una oxigenación por membrana extracorpórea. El día 34, luego de siete días de haber suspendido la sedación y de que su cuadro neurológico hubiera evolucionado de manera positiva, presentó una crisis tónico-clónica generalizada limitada, que no guardaba relación con un desequilibrio hidroelectrolítico o metabólico, lo que hizo necesario realizar una investigación diagnóstica. Los estudios de imágenes cerebrales revelaron un síndrome de encefalopatía posterior reversible.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "A 63-year-old woman got very sick with COVID-19. She had fever, cough, and trouble breathing. Doctors put a breathing tube in and used a special machine called ECMO. ECMO helps give oxygen to the blood when the lungs cannot.\n\nAfter many days, she woke and seemed to get better. Then she had a seizure, which is when the brain makes sudden, uncontrolled movements. Doctors did brain scans. The scans showed a problem called posterior reversible encephalopathy syndrome, or PRES. PRES means some parts of the brain get swollen and can cause seizures. The scans also showed a few very small bleeds, but the spinal fluid test did not show infection.\n\nThe doctors treated her and gave time to recover. She got better almost all the way and left the hospital after 44 days. She went to rehab and nearly returned to how she was before. This was a serious illness, but she improved a lot.",
+                "fh_score": 106.85
+            },
+            "B2": {
+                "text": "A 63-year-old woman with obesity and high blood pressure went to the emergency room after seven days of fever, dry cough, loss of smell, muscle pain and shortness of breath. Tests showed low lymphocytes (a type of white blood cell) and a high C‑reactive protein (CRP, a blood marker of inflammation). A PCR test was positive for SARS‑CoV‑2, the virus that causes COVID‑19.\n\nHer breathing got much worse and she developed severe lung failure (acute respiratory distress syndrome, or ARDS). She was put on a breathing tube (intubation) and a ventilator, but still did not get enough oxygen. On the second day her oxygenation was very poor (PaO2/FiO2 ratio 98), so she was started on venovenous extracorporeal membrane oxygenation (VV‑ECMO). ECMO is a machine that takes blood out of the body, adds oxygen and removes carbon dioxide, and then returns the blood — it is used when the lungs cannot work well enough by themselves. ECMO was started safely and she spent about 455 hours (almost 19 days) on it. During her ICU stay she also had early nutrition and physical rehabilitation. She developed a ventilator‑associated pneumonia due to Pseudomonas bacteria on day 14 and was treated with antibiotics and improved. Her kidneys worked well the whole time. She was taken off ECMO on day 20 and later had a tracheostomy (a small opening in the neck to help breathing) as part of recovery.\n\nOn day 34, after seven days without sedative drugs and after showing overall neurological improvement, she had a single generalized tonic‑clonic seizure (a convulsion affecting the whole body). Doctors checked blood tests, spinal fluid and did brain imaging to find the cause. Blood tests the day before showed that some inflammation markers had gone down (CRP, procalcitonin, fibrinogen, ferritin) but D‑dimer (a marker linked to blood clotting) and interleukin‑6 (IL‑6, an inflammatory molecule) were high. No medicines she had received were known to cause the brain syndrome identified.\n\nBrain MRI scans showed a pattern typical of posterior reversible encephalopathy syndrome (PRES). PRES is a condition where parts of the brain become swollen and can cause headaches, confusion, visual changes or seizures; it is often linked to severe illness, blood pressure problems, inflammation, or certain drugs. The MRI (FLAIR images) found symmetrical areas of swelling in the white matter, especially in the back of the brain (occipital and parietal lobes) and also in other regions. Another MRI sequence showed many tiny microbleeds (small spots of bleeding) in the white matter and in the corpus callosum. Spinal fluid tests were normal and did not show the virus.\n\nShe received supportive care, and her neurological state improved almost completely despite weakness from prolonged critical illness. She left the hospital on day 44 and was sent for rehabilitation; her mental status returned nearly to how it had been before illness.\n\nWhat this means and possible next steps\n- PRES is often reversible when the underlying problem is treated. In this case, diagnosis was made by MRI and by ruling out other causes.\n- Typical care includes controlling blood pressure if needed, treating infections or inflammation, preventing and treating seizures, and close monitoring with follow‑up imaging and rehabilitation.\n- The patient’s good recovery is encouraging and shows that even severe COVID‑19 cases with serious brain findings can improve with timely, supportive ICU care.\n\nIf you have questions about any term or part of the case, I can explain it more simply.",
+                "fh_score": 83.27
+            },
+            "B3": {
+                "text": "Resumen breve y empático\nUna mujer de 63 años con obesidad e hipertensión desarrolló COVID-19 grave con síndrome de distrés respiratorio agudo (SDRA). Requirió ventilación mecánica y soporte con oxigenación por membrana extracorpórea venovenosa (VV-ECMO). Tras una recuperación respiratoria progresiva y retirada de la sedación, presentó una crisis convulsiva generalizada; las imágenes cerebrales y las pruebas complementarias apoyaron el diagnóstico de encefalopatía posterior reversible (PRES). La paciente evolucionó favorablemente, recuperó casi por completo sus funciones neurológicas y fue dada de alta para rehabilitación.\n\nDatos clínicos y evolución\n- Presentación inicial: fiebre, tos seca, pérdida del olfato, mialgias y disnea tras 7 días de síntomas; saturación de oxígeno 90 % al ingreso. Laboratorio con linfopenia y proteína C reactiva elevada. PCR nasofaríngea positiva para SARS‑CoV‑2.  \n- Deterioro respiratorio progresivo con insuficiencia respiratoria y radiografía con infiltrados bilaterales → intubación y ventilación mecánica. A pesar de maniobras (prono, bloqueo neuromuscular) la oxigenación fue insuficiente (PaO2/FiO2 ≈ 98), por lo que se indicó VV‑ECMO.  \n- Soporte con VV‑ECMO realizado sin complicaciones; 455 horas de soporte (≈19 días). Durante la internación presentó neumonía asociada a ventilador por Pseudomonas aeruginosa tratada con ceftazidima y vancomicina con buena respuesta. Función renal conservada. Traqueostomía realizada 7 días después de retirar ECMO.  \n- Día 34 de internación, y 7 días después del destete de sedación, tuvo una crisis tónico‑clónica generalizada limitada, lo que motivó estudios neurológicos.\n\nInvestigaciones neurológicas y hallazgos\n- Resonancia magnética cerebral (FLAIR): hiperintensidad simétrica y confluente predominantemente en la sustancia blanca justa y subcortical de regiones occipitales y parietales, con afectación también en frontal, temporal y cerebelo izquierdo. Estos hallazgos son típicos de edema vasogénico en PRES.  \n- Secuencia de susceptibilidad: múltiples microhemorragias puntiformes en sustancia blanca superficial y profunda, afectando especialmente la sustancia blanca justacortical y el cuerpo calloso; además, tres hemorragias subagudas <1 cm en cápsulas externas (T1 hiperintenso).  \n- Líquido cefalorraquídeo: parámetros normales (proteínas, glucosa, lactato) y PCR para SARS‑CoV‑2 negativa.  \n- Laboratorio en el día previo a la crisis: descenso de PCR, procalcitonina, fibrinógeno y ferritina respecto a fases previas; aumento marcado de dímero D (18 021 ng/mL) e interleucina‑6 (10,4 pg/mL). No se habían administrado fármacos inmunosupresores, inmunomoduladores ni quimioterápicos asociados a PRES.\n\nInterpretación diagnóstica\n- Diagnóstico principal: PRES (síndrome de encefalopatía posterior reversible) manifestado por convulsión y por patrón típico de edema vasogénico en regiones posteriores en la RM.  \n- Hallazgos atípicos pero relevantes: microhemorragias y pequeñas hemorragias subagudas, que pueden acompañar a PRES en contextos de disfunción endotelial o coagulopatía.  \n- Factores de riesgo plausibles en este caso: COVID‑19 grave con respuesta inflamatoria y alteración de la coagulación, necesidad de VV‑ECMO y estancia prolongada en UCI. No se identificó causa medicamentosa directa.\n\nTratamiento y resultado\n- Manejo dirigido a soportar la función vital y controlar la convulsión; cuidados neuroprotectores y rehabilitación precoz.  \n- La paciente sufrió miopatía secundaria a enfermedad crítica pero alcanzó una recuperación neurológica casi completa. Fue dada de alta tras 44 días de hospitalización y remitida para rehabilitación, recuperando prácticamente su estado mental previo.\n\nImplicaciones y recomendaciones prácticas\n- En pacientes con COVID‑19 grave y estancia prolongada en UCI, nuevas manifestaciones neurológicas (especialmente convulsiones, alteración del estado mental o déficits visuales) deben investigarse con imagen cerebral (RM) y estudios básicos (laboratorio, LCR) para descartar PRES u otras complicaciones.  \n- PRES puede ser reversible si se identifica y trata a tiempo; sin embargo, puede coexistir con hemorragias microvascularizadas y coagulopatía, por lo que es importante monitorizar parámetros inflamatorios y de coagulación.  \n- La detección precoz y la rehabilitación son claves para una buena recuperación funcional.\n\nMensaje final empático\nEsta paciente afrontó una enfermedad muy grave y complicaciones importantes, pero gracias a una atención intensiva multidisciplinaria y evaluación neurológica oportuna logró recuperar su función neurológica en gran medida. La historia subraya la importancia de vigilar complicaciones neurológicas en COVID‑19 severo y de un abordaje integral que incluya imagen, control de la inflamación y rehabilitación.",
+                "fh_score": 33.0
+            }
+        }
+    },
+    {
+        "article": "Mujer de 65 años, originaria y residente de la Ciudad de México, con antecedente de infección por VIH de 20 años de diagnóstico con carga viral indetectable desde 2020 y con cuenta de CD4 de 1220 células por mililitro en febrero de 2022, hipotiroidismo de 29 años, cardiopatía isquémica de 9 años de diagnóstico, osteoporosis y dislipidemia, en tratamiento y bajo control médico.\n\nSu dermatosis problema se inició 10 años atrás, después de un cuadro de herpes zóster localizado en la extremidad inferior derecha y se complicó con una infección de tejidos blandos, referida como celulitis. Como secuela de este evento la paciente desarrolló úlcera, la cual ameritó corrección del defecto con 4 injertos cutáneos en diferentes tiempos quirúrgicos por cirugía plástica, con acompañamiento por parte de la clínica de heridas. Durante el seguimiento y a pesar de las medidas tomadas, no logró resolución completa y persistió con una úlcera asociada a dolor local, motivo de su envío a nuestro servicio.\n\nA la exploración física presentaba una dermatosis localizada en la extremidad inferior derecha, en la cara lateral del muslo, caracterizada por una neoformación aplanada sobre la que se asentaba una úlcera de 1.5 cm de diámetro, con fondo limpio, con costra sero-amarillenta, bordes sobreelevados, piel perilesional hiperpigmentada y queratósica, una cicatriz atrófica e hiperpigmentada. Se inició abordaje de la dermatosis mediante biopsia de piel, con reporte histopatológico de carcinoma verrugoso, por lo que se concluyó como úlcera de Marjolin asociada a carcinoma verrugoso en paciente portadora de VIH. Se canalizó al hospital de oncología para manejo con radioterapia.",
+        "gold_summary": "mujer de 65 años con el antecedente de ser portadora de infección por virus de inmunodeficiencia humana (VIH), que presentó un carcinoma verrugoso asociado a una úlcera de Marjolin secundaria a herpes zóster e infección de tejidos blandos en pierna derecha, con un periodo de latencia de 10 años desde el proceso infeccioso inicial hasta la confirmación histopatológica.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Resumen simple y amable:\n\nUna mujer de 65 años de la Ciudad de México tenía varias enfermedades, entre ellas VIH que estaba bien controlado. Hace 10 años tuvo culebrilla (herpes zóster) en la pierna derecha y la zona se infectó. Quedó una llaga que no sanó. Le pusieron cuatro injertos de piel, pero la herida siguió dando problemas y le dolía.\n\nAl revisarla encontraron una lesión en el muslo derecho con una úlcera pequeña. Hicieron una biopsia (toman un pedacito para mirar al microscopio). El resultado mostró que la llaga se había convertido en un tipo de tumor llamado carcinoma verrugoso. Cuando una llaga vieja se transforma en cáncer se llama úlcera de Marjolin. \n\nLa paciente fue enviada al hospital de oncología para recibir radioterapia, que son rayos que ayudan a tratar el cáncer. Es una situación seria, pero ya la están atendiendo por especialistas.",
+                "fh_score": 70.39
+            },
+            "B2": {
+                "text": "Summary\n\nA 65-year-old woman from Mexico City, who has lived with HIV for 20 years and has been well controlled (undetectable viral load since 2020, CD4 count 1220 in 2022), developed a chronic skin problem on her right thigh. Ten years ago she had a shingles infection (herpes zoster) on the same leg that became complicated by a soft tissue infection (cellulitis). After that episode she developed a long‑standing ulcer (a nonhealing sore) that required four skin grafts and ongoing wound care, but the ulcer did not heal and caused local pain.\n\nOn exam doctors found a flattened new growth on the outside of her right thigh with a 1.5 cm ulcer in the center, raised edges, a clean base with a yellowish crust, and darkened, thickened skin around the sore. A skin biopsy (a small sample of tissue) showed verrucous carcinoma. This led to the diagnosis of a Marjolin ulcer — that is, a cancer that developed in a chronic wound or scar — associated with verrucous carcinoma (a slow‑growing, wart‑like form of squamous cell skin cancer).\n\nBecause the lesion is cancerous, the patient was referred to an oncology hospital for treatment with radiotherapy (radiation treatment). The key points are the long 10‑year delay between the original infection and the cancer, and that chronic, nonhealing ulcers can sometimes turn into cancer, so they need careful follow‑up and prompt treatment.",
+                "fh_score": 83.23
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel universitario)\n\nPaciente: mujer de 65 años de la Ciudad de México.\n\nAntecedentes relevantes:\n- Infección por VIH desde hace 20 años; carga viral indetectable desde 2020 y recuento de CD4 de 1,220 células/mm3 (febrero 2022), es decir, control virológico y buena inmunidad en registros recientes.\n- Hipotiroidismo (29 años), cardiopatía isquémica (9 años), osteoporosis y dislipidemia, todas en tratamiento y control médico.\n\nHistoria de la lesión:\n- Hace 10 años sufrió herpes zóster localizado en la pierna derecha, complicándose con infección de partes blandas (celulitis).\n- Como secuela desarrolló una úlcera crónica en la cara lateral del muslo derecho que requirió cuatro injertos cutáneos en diferentes tiempos y seguimiento en clínica de heridas.\n- A pesar de los tratamientos la úlcera persistió y generó dolor local, por lo que fue remitida al servicio especializado.\n\nExploración física:\n- Neoformación aplanada en la cara lateral del muslo derecho sobre la que se asienta una úlcera de 1,5 cm de diámetro.\n- Fondo limpio con costra sero‑amarillenta, bordes sobreelevados, piel perilesional hiperpigmentada y queratósica, y cicatriz atrófica hiperpigmentada.\n\nDiagnóstico:\n- Biopsia cutánea con reporte histopatológico de carcinoma verrugoso.\n- Conclusión clínica: úlcera de Marjolin (malignización de una lesión crónica) asociada a carcinoma verrugoso en paciente portadora de VIH.\n\nInterpretación e implicaciones:\n- Una úlcera de Marjolin es la transformación maligna de una lesión crónica o cicatriz y suele aparecer tras procesos inflamatorios o traumáticos; la latencia de 10 años en este caso es compatible con ese patrón.\n- El carcinoma verrugoso es una variante bien diferenciada del carcinoma epidermoide (escamoso): tiende a crecer localmente y rara vez hace metástasis, pero puede ser destructivo en la zona afectada.\n- Aunque la paciente tiene VIH, sus registros recientes muestran buen control inmunológico, lo que es favorable para el manejo y pronóstico; no obstante, la historia de infección crónica fue el factor más relevante en la génesis de la lesión.\n\nPlan y siguientes pasos recomendados:\n- La paciente fue canalizada al hospital de oncología para manejo con radioterapia.\n- Es aconsejable un abordaje multidisciplinario: discusión en comité tumoral con cirugía oncológica y plastica, oncología radioterápica, medicina interna/infectología y clínica de heridas.\n- Considerar evaluación imagenológica local y ganglionar (ecografía o TC/RM) para determinar extensión y descartar compromiso profundo o adenopatías.\n- El tratamiento de elección para úlceras de Marjolin suele ser la escisión amplia con márgenes claros; la radioterapia puede usarse en determinados contextos, pero la decisión debe individualizarse según extensión, localización y comorbilidades.\n- Mantener control del dolor, cuidado local de la herida y seguimiento estrecho por riesgo de recurrencia.\n\nTono y perspectiva:\n- Se trata de una transformación maligna seria pero con opciones terapéuticas. El control virológico y el estado general de la paciente son datos favorables; una evaluación multidisciplinaria facilitará definir el mejor tratamiento y el seguimiento adecuado.",
+                "fh_score": 38.85
+            }
+        }
+    },
+    {
+        "article": "Una mujer de 90 años con hepatitis C y un historial de tabaquismo de 60 años proveniente de una zona rural presentó una hinchazón en la cara posteromedial del muslo izquierdo justo por encima de la rodilla. La hinchazón se notó por primera vez hace 3 años y aumentó gradualmente de tamaño durante este período. Ella sintió un leve malestar, pero niega cualquier síntoma asociado de dolor, picazón, secreción, fiebre o inmovilidad articular. Como provenía de una zona rural, también tenía un historial de exposición a animales.\nEn el examen físico, la hinchazón tenía una forma esférica de 14 × 10, era firme, fija y no sensible, con márgenes bien definidos en el aspecto posteromedial del muslo izquierdo, justo por encima de la rodilla. La piel que la recubría era pellizcable y mostraba venas prominentes, y la temperatura era comparable a la de la piel circundante.\nLa ecografía reveló una lesión quística grande con varios quistes pequeños en su interior, que medían 13,2 × 11 × 13,6 cm y un volumen de 1046 ml. Se originaba en la articulación de la rodilla izquierda y se extendía hasta la mitad del muslo. La ecografía Doppler en color no mostró vascularización en su interior. Se realizó una resonancia magnética que mostró una lesión quística grande (21 × 9,9 × 8,1 cm) con múltiples lesiones pequeñas dispersas, con extensión intramuscular e intermuscular que afectaban al aductor largo y al gracilis de manera medial y al bíceps femoral de manera posterior. Todas estas características eran indicativas de un quiste hidatídico. El diagnóstico se confirmó mediante una prueba de hemaglutinación para Echinococcus. La radiografía de tórax y la ecografía abdominal fueron normales.\nSe planificó la escisión quirúrgica de la tumefacción quística y se realizó una incisión en forma de S en la piel, seguida de una disección cuidadosa a través del tejido subcutáneo para acceder al quiste. La lesión estaba bien definida dentro de los planos intermuscular e intramuscular. Se realizó una disección meticulosa para aislar y extraer el quiste intacto, asegurando que no se derramara su contenido. Para minimizar el riesgo de contaminación, se irrigó a fondo el sitio quirúrgico con solución salina normal después de la escisión.\nLos hallazgos intraoperatorios revelaron una gran hinchazón quística intermuscular de 22 × 14 cm, que involucraba los compartimentos posterior y medial del muslo izquierdo. El quiste demostró extensión intramuscular hacia el aductor largo y el gracilis medialmente y hacia el bíceps femoral posteriormente, extendiéndose hasta la fosa poplítea. Cabe destacar que no había comunicación entre el quiste y la articulación de la rodilla. Una biopsia enviada al laboratorio confirmó aún más el diagnóstico. El examen histopatológico de la muestra extirpada reveló una pared quística fibrocondrogénica revestida por epitelio atenuado con infiltración inflamatoria. La presencia de material queratinoso focal caracterizó aún más la lesión. Estos hallazgos, junto con las características macroscópicas, favorecieron el diagnóstico de un quiste hidatídico. El curso postoperatorio fue sin complicaciones y el paciente fue dado de alta con una terapia antihelmíntica durante seis semanas. Se programaron visitas de seguimiento a la semana, tres semanas, seis semanas, nueve semanas y doce semanas. Durante estas visitas, el paciente no mostró signos de recurrencia o complicaciones.\n",
+        "gold_summary": "Una mujer de 90 años de edad, proveniente de una zona rural, presentó una hinchazón de crecimiento lento en el muslo posteromedial durante tres años. No tenía antecedentes de traumatismos ni síntomas sistémicos. El examen clínico reveló una masa firme y no dolorosa. Las imágenes sugieren una lesión quística, y la serología confirmó la infección por Echinococcus. Se realizó la extirpación quirúrgica, y la histopatología confirmó un quiste hidatídico. La paciente recibió un tratamiento posoperatorio de albendazol durante seis semanas. Su recuperación fue sin incidentes, sin recurrencia en el seguimiento.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una mujer de 90 años que vive en el campo tuvo una hinchazón en la parte de atrás y adentro del muslo izquierdo. La hinchazón creció despacio durante tres años. No le dolía y no tenía fiebre ni otros problemas. Las imágenes mostraron que era un gran saco lleno de líquido que venía de la rodilla y se metía entre los músculos. Un análisis de sangre dijo que había un parásito llamado Echinococcus. Los médicos quitaron el quiste con una operación y lo sacaron entero para que no se rompiera. El examen del tejido en el laboratorio confirmó que era un quiste hidatídico (un saco causado por ese parásito). Después de la operación, la paciente tomó un medicamento contra los parásitos durante seis semanas. Se recuperó bien y las revisiones no mostraron que el quiste volviera.",
+                "fh_score": 73.63
+            },
+            "B2": {
+                "text": "Resumen claro y amable:\n\nUna mujer de 90 años que vivía en zona rural notó durante tres años una hinchazón que fue creciendo lentamente en la parte trasera y medial del muslo izquierdo, justo por encima de la rodilla. Tenía un leve malestar pero sin dolor fuerte, fiebre, secreción ni problemas para mover la articulación. Por su historia, también había tenido contacto con animales, un dato importante en este caso.\n\nLas pruebas por imagen (ecografía y resonancia magnética) mostraron una gran lesión llena de líquido con muchas “pequeñas bolsas” dentro, que ocupaba espacio entre y dentro de varios músculos del muslo. Los resultados sugerían un quiste hidatídico, que es una bolsa formada por un parásito llamado Echinococcus (un tipo de gusano que puede contagiarse por animales). Un análisis de sangre específico (prueba de hemaglutinación) confirmó la infección. Radiografías del tórax y ecografía abdominal fueron normales, lo que indica que no había quistes visibles en pulmón o hígado.\n\nSe decidió operar y extraer la lesión. Los cirujanos hicieron una incisión, separaron cuidadosamente los planos musculares y sacaron el quiste entero sin romperlo (esto es importante para evitar que el parásito se disemine). Luego limpiaron la zona y enviaron tejido al laboratorio. El examen del tejido confirmó el diagnóstico de quiste hidatídico. La recuperación después de la cirugía fue buena; la paciente recibió albendazol (un medicamento antiparasitario) durante seis semanas y tuvo controles regulares en las semanas siguientes sin señales de recurrencia ni complicaciones.\n\nEn resumen: se trató de un quiste hidatídico grande en el muslo de una paciente mayor, confirmado por pruebas y tratado con cirugía cuidadosa y medicación antiparasitaria, con buena evolución.",
+                "fh_score": 51.38
+            },
+            "B3": {
+                "text": "Resumen clínico (nivel de lectura universitario)\n\nUna mujer de 90 años, procedente de zona rural con exposición a animales y antecedentes de hepatitis C y tabaquismo prolongado, consultó por una masa de crecimiento lento en la cara posteromedial del muslo izquierdo, detectada desde hace 3 años. La lesión era una tumoración esférica, firme, fija y no dolorosa, con piel intacta y venas superficiales prominentes.\n\nLa ecografía y la resonancia magnética mostraron una lesión predominantemente quística grande con múltiples “quistes hijos”, situada en planos intramuscular e intermuscular (afectando aductor largo, gracilis y bíceps femoral) y extendiéndose hasta la fosa poplítea; el Doppler no mostró vascularización. La serología por hemaglutinación fue positiva para Echinococcus, y las pruebas de extensión (radiografía de tórax y ecografía abdominal) no identificaron enfermedad en pulmón o hígado. Estos hallazgos apoyaron el diagnóstico de quiste hidatídico (hidatidosis) localizado en el muslo, una presentación poco frecuente.\n\nSe realizó resección quirúrgica cuidadosa mediante incisión en S y disección para extraer el quiste intacto —medida clave para evitar derrames que aumenten el riesgo de diseminación o reacción anafiláctica—; el espécimen medía alrededor de 22 × 14 cm y no tenía comunicación con la articulación de la rodilla. La histopatología confirmó pared quística con epitelio atenuado, infiltrado inflamatorio y material queratinoso, consistente con quiste hidatídico. El posoperatorio transcurrió sin complicaciones; recibió albendazol (terapia antihelmíntica) seis semanas y controles periódicos a 1, 3, 6, 9 y 12 semanas sin evidencia de recurrencia.\n\nImplicaciones y recomendaciones: la hidatidosis muscular es rara pero debe considerarse frente a masas quísticas en pacientes con exposición animal. El manejo combina cirugía (evitando abrir el quiste) y tratamiento farmacológico para reducir riesgo de recurrencia; se recomienda seguimiento a más largo plazo y evaluación serológica/imaginológica si aparecen nuevos síntomas.",
+                "fh_score": 26.22
+            }
+        }
+    },
+    {
+        "article": "Una paciente de 21 años de edad, soltera, con antecedentes de hipertensión y feocromocitoma metastásico, se presentó en nuestro hospital. Su cáncer se ha metastatizado en la vejiga, los huesos y los pulmones. También tiene un fuerte historial familiar de neoplasias, en particular de feocromocitoma. La paciente fue admitida debido a la hipertensión no controlada y los síntomas crónicos relacionados con su enfermedad.\n\nEn el ingreso (09/06/2024), la paciente era normotensa (PA: 104/66 mmHg), su frecuencia cardiaca era de aproximadamente 90 latidos por minuto, afebril a 36.9°C, y tenía una saturación de oxígeno de 99% en aire ambiente. El examen físico indicó un estado de desempeño del Grupo Cooperativo de Oncología del Este (ECOG) de 2, palidez consistente con anemia crónica, latido cardiaco regular sin murmullos o sonidos adicionales. El examen abdominal no fue notable, y no se observó edema o equimosis en las extremidades inferiores.\n\nLa paciente tiene antecedentes de hipertensión y paraganglioma, su medicación incluye (Doxazosin 2 mg, Labetalol 100 mg, Oxibutinina 5 mg, Aceite de parafina, Nifedipina 30 mg). Su historial quirúrgico incluye una adrenalectomía derecha a los diez años, y ha recibido varios tratamientos, incluidos análogos de somatostatina y radioterapia paliativa. El historial familiar revela una mutación familiar de la subunidad B de la deshidrogenasa del succinato (mutación SDBH) con un importante historial de tumores malignos endocrinos, incluidos feocromocitomas en su padre y hermana y cáncer de páncreas en su abuela.\n\nLas investigaciones de laboratorio, incluido el recuento sanguíneo completo, revelaron anemia significativa, con un nivel de hemoglobina de 7.5 g/dl. Había evidencia de hemólisis, como lo indican el alto recuento de reticulocitos, la bilirrubina indirecta y la lactato deshidrogenasa. La haptoglobina era baja. Los resultados de laboratorio se muestran en. El perfil de coagulación excluyó la coagulación intravascular diseminada (DIC), que muestra (PT: 15.6, PTT: 23.3, fibrinógeno: 489, dímero D: 0.63). La prueba de Coombs directa para excluir la anemia hemolítica autoinmune fue negativa. Los frotis de sangre periférica mostraron la presencia de esquistocitos, equinocitos y algunas células en forma de lágrima, además de trombocitopenia, todo lo cual apuntaba a la anemia hemolítica microangiopática (MAHA). Dado el contexto del cáncer metastásico, el paciente fue diagnosticado con anemia hemolítica microangiopática paraneoplásica en marzo/2024.\n\nEl paciente fue programado para el protocolo CVD (ciclofosfamida, vincristina y doxorrubicina), pero sin ciclofosfamida debido al efecto inductor de anemia de los agentes alquilantes. El paciente recibió un total de 5 ciclos. Como indicador de respuesta clínica, el paciente ya no experimentó anemia o trombocitopenia. Un nuevo frotis de sangre periférica reveló células normales, lo que sugiere una respuesta clínica al MAHA que coincide con la mejora de la neoplasia subyacente. Esto se alinea con la definición de MAHA como un síndrome paraneoplásico.\n\nLos medicamentos que se le suministran al paciente al momento del alta son: comprimidos de dexametasona de 2 mg, 4 mg por vía oral (PO) una vez al día (OD) durante 3 días, comprimidos de ondansetrón de 8 mg por vía oral (PO) una vez al día (OD) durante 3 días, comprimidos de metoclopramida de 10 mg por vía oral (PO) tres veces al día durante 3 días, calcio de 600 mg con vitamina D por vía oral (PO) una vez al día (OD) durante 1 día, comprimidos de labetalol de 100 mg por vía oral (PO) dos veces al día durante 1 día, comprimidos de doxazocina de 2 mg por vía oral (PO) dos veces al día durante 1 día, comprimidos de citalopram de 20 mg por vía oral (PO) durante 1 día, comprimidos de omeprazol de 20 mg, 40 mg por vía oral (PO) durante 1 día, comprimidos de paracetamol de 500 mg, 1000 mg por vía oral (PO) dos veces al día durante 1 día, cápsulas de aprepitant de 125 mg/80 mg, 1 cápsula por vía oral (PO) dos veces al día durante 3 días (con prescripción médica).\n\nEl paciente fue objeto de seguimiento el 01/07/2024, y su aspecto clínico era bueno y activo. El paciente se sometió a exámenes de laboratorio que incluían un recuento sanguíneo completo (WBC 6.59 10e3/ul, RBC 4.47 × 10^6/ul, HGB 13.2 g/dl, 40.0%, MCV 89.4 fL, PLT 41.5 10e3/ul), nitrógeno ureico en sangre 33.8 mg/dl, creatina cinasa-MB 36.1 u/l, creatinina sérica 0.97 mg/dl, cloruro 101.5 mmol/l, potasio 4.52 mmol/l, sodio 135 mmol/l.\n",
+        "gold_summary": "En este informe de caso, presentamos a una mujer soltera de 21 años con un fuerte historial familiar de neoplasia endocrina. Fue derivada a nuestro hospital para quimioterapia debido a un diagnóstico de feocromocitoma maligno, que había hecho metástasis en la vejiga urinaria, los huesos y los pulmones. Además, desarrolló anemia hemolítica microangiopática como un síndrome paraneoplásico.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Esta es la historia de una mujer de 21 años con un tumor llamado feocromocitoma. El tumor se había extendido a la vejiga, los huesos y los pulmones. Muchas personas en su familia también han tenido tumores parecidos.\n\nEl tumor le causó una anemia especial. Esto quiere decir que sus glóbulos rojos se rompían dentro de vasos muy pequeños. Por eso estaba muy cansada y su sangre estaba baja. Los médicos hicieron pruebas y vieron que las células se rompían, pero que no era por una enfermedad del sistema que ataca la sangre.\n\nLe dieron quimioterapia para tratar el cáncer. Después de cinco ciclos de tratamiento, su sangre mejoró. Ya no tenía la anemia y el examen de sangre se veía mejor. Al salir del hospital le dieron medicinas para ayudar con los efectos del tratamiento. En el control posterior se veía activa y con la hemoglobina en un nivel normal.\n\nLos médicos piensan que la anemia fue causada por el cáncer. Al mejorar el cáncer, también mejoró la anemia. Esto es algo que puede pasar cuando un tumor causa problemas en otras partes del cuerpo.",
+                "fh_score": 81.93
+            },
+            "B2": {
+                "text": "Summary (B2 level, for readers aged ~11–17)\n\nThis report describes a 21-year-old woman with a rare and serious cancer called pheochromocytoma that had spread (metastasized) to her bladder, bones, and lungs. Pheochromocytoma is a tumor that starts in hormone-making cells of the adrenal glands. She also has a strong family history of similar tumors and a known inherited change (SDHB mutation) that raises the risk of these cancers.\n\nWhat happened\n- She was admitted because her cancer was causing ongoing problems and high blood pressure in the past. At admission her vital signs were stable.\n- Blood tests showed a severe drop in red blood cells (hemoglobin 7.5 g/dl) and signs that red blood cells were being destroyed inside small blood vessels. This condition is called microangiopathic hemolytic anemia (MAHA). MAHA is a type of anemia where red cells are broken into pieces as they pass through damaged tiny blood vessels. The blood smear (a slide of blood looked at under a microscope) showed broken red cells (schistocytes) and other abnormal cells. Tests ruled out autoimmune causes and widespread blood clotting (DIC).\n- Because her MAHA appeared together with advanced cancer, doctors diagnosed it as a paraneoplastic syndrome — a problem caused by the cancer but happening away from the tumor itself.\n\nTreatment and response\n- She was treated with a chemotherapy plan called CVD (vincristine and doxorubicin were used; cyclophosphamide was left out because it can worsen anemia). She received five cycles.\n- After treatment her anemia and the appearance of broken red cells improved, which suggests the MAHA got better as the cancer came under control.\n- On follow-up about a month later her hemoglobin was back to normal (13.2 g/dl). However, her platelet count was still low (41.5 × 10^3/µl), so some blood abnormalities persisted and need continued monitoring.\n\nOther notes\n- Discharge medicines included short courses of steroids and anti-nausea drugs, and her usual blood-pressure medicines.\n- The case shows how a cancer can cause serious blood problems (like MAHA) and that treating the underlying tumor can improve those problems. It also highlights the role of family genetics (SDHB mutation) in this patient’s illness.\n\nWhat comes next (typical steps)\n- Continued cancer treatment and close follow-up with blood tests to watch red cells and platelets.\n- Supportive care as needed (for example, blood transfusions if blood counts fall again).\n- Genetic counseling and family screening may be important because of the inherited SDHB change.\n\nThis summary aims to explain the case simply and calmly. If you have questions about any terms or want the information in Spanish, I can help with that.",
+                "fh_score": 88.84
+            },
+            "B3": {
+                "text": "Summary (college-level, empathetic)\n\nPatient and background\n- A 21‑year‑old woman with metastatic pheochromocytoma (spread to bladder, bones and lungs). She has a strong family history of endocrine cancers and a known familial SDHB mutation (pheochromocytomas in father and sister; pancreatic cancer in grandmother). She previously had a right adrenalectomy (age 10) and received somatostatin analogues and palliative radiotherapy.\n\nPresentation and examination\n- Admitted for uncontrolled hypertension and cancer‑related symptoms but on admission she was hemodynamically stable: blood pressure 104/66 mmHg, heart rate ~90/min, afebrile, oxygen saturation 99% on room air. Performance status was ECOG 2. Physical exam showed pallor consistent with chronic anemia; abdomen and lower limbs were unremarkable.\n\nKey laboratory and diagnostic findings\n- Severe anemia at presentation: hemoglobin 7.5 g/dL.\n- Evidence of hemolysis: high reticulocyte count, elevated indirect bilirubin and LDH, and low haptoglobin.\n- Peripheral blood smear: schistocytes (fragmented red cells), echinocytes, some teardrop cells, and thrombocytopenia — findings consistent with microangiopathic hemolytic anemia (MAHA).\n- Direct Coombs (direct antiglobulin) test was negative, arguing against autoimmune hemolysis.\n- Coagulation tests argued against disseminated intravascular coagulation (DIC) (PT 15.6 s, PTT 23.3 s, fibrinogen 489 mg/dL, D‑dimer 0.63).\n- Clinical impression: MAHA as a paraneoplastic syndrome related to her metastatic pheochromocytoma (diagnosed March 2024).\n\nTreatment course and response\n- She was treated with a modified CVD chemotherapy protocol (vincristine and doxorubicin were given; cyclophosphamide was omitted because of its anemia‑inducing effects). She completed five cycles.\n- Clinical response: the team reported resolution of anemia and normalization of the peripheral smear, which supports the interpretation that the MAHA was paraneoplastic and improved as the cancer was treated.\n\nFollow‑up (01/07/2024)\n- Clinically she appeared well and active.\n- Labs at follow‑up showed hemoglobin 13.2 g/dL and otherwise acceptable renal and electrolyte values. The platelet count was reported as 41.5 × 10^3/µL (marked thrombocytopenia), which contrasts with the statement that thrombocytopenia had resolved; this discrepancy warrants attention and close monitoring.\n\nMedications at discharge (summary)\n- Short steroid and antiemetic courses (dexamethasone, ondansetron, metoclopramide, aprepitant), ongoing blood‑pressure management (doxazosin, labetalol), supportive agents (calcium with vitamin D, paracetamol, omeprazole), and an SSRI (citalopram). (Exact dosages were used in the chart.)\n\nInterpretation and implications\n- MAHA in this case appears to be a paraneoplastic phenomenon linked to metastatic pheochromocytoma. Improvement of the hemolysis and anemia after systemic chemotherapy supports that the hematologic syndrome was driven by the cancer.\n- Persistent or recurrent thrombocytopenia at follow‑up (if confirmed) is concerning and should be investigated; causes could include ongoing marrow suppression, immune mechanisms, consumptive processes, or disease progression.\n- Management priorities going forward: continued oncologic treatment and surveillance of the cancer; regular CBC and hemolysis markers (LDH, bilirubin, haptoglobin, reticulocyte count); blood‑pressure control and symptomatic/supportive care; hematology input if the platelet count remains low or if hemolysis recurs; and genetic counseling/testing given the SDHB mutation and strong family history.\n\nEmpathetic note\n- This is a young patient facing advanced cancer and a serious paraneoplastic complication. The improvement in hemoglobin after cancer‑directed therapy is encouraging. Close multidisciplinary follow‑up (oncology, hematology, genetics, and supportive care) and clear communication with the patient and family about goals of care and next steps will be important.",
+                "fh_score": 60.97
+            }
+        }
+    }
+]
\ No newline at end of file
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@@ -0,0 +1,1802 @@
+[
+    {
+        "article": "Información para el paciente\nUn hombre de 27 años y fumador estuvo involucrado en un accidente de tráfico; se cayó de su motocicleta sin casco. El hombre llevó la motocicleta al hospital e informó de un dolor de cabeza y heridas hemorrágicas en la frente.\n\nEl paciente no tiene antecedentes patológicos y trabaja en una zona rural.\n\nHallazgos clínicos\nTras su ingreso en urgencias, perdió el conocimiento y sufrió dos convulsiones. En la exploración física, la escala de coma de Glasgow fue de 6/15 (no abrió los ojos, se retiró al sentir dolor, no respondió verbalmente) con midriasis bilateral, dificultad hemodinámica y buena saturación. Se identificó una lesión craneal penetrante con una profusa hemorragia intracraneal.\n\nLínea de tiempo\nTras caerse de la motocicleta, el paciente volvió a montarse en ella e inmediatamente fue al hospital, quejándose de dolores de cabeza y de una herida en la frente por la que sangraba. Recibió tratamiento de urgencia para estabilizar sus funciones respiratorias y hemodinámicas. Ese mismo día, fue trasladado inconsciente a un centro mejor equipado, donde se le realizó un TAC y se sometió a una operación quirúrgica con éxito.\n\nEvaluación diagnóstica\nSu nivel de hemoglobina era de 6 g/dL y su grupo sanguíneo era O positivo. El hospital no tenía ni una unidad de cuidados intensivos ni un escáner. El único diagnóstico sugerido fue el de traumatismo agudo en la cabeza, complicado por hemorragia intracraneal que provocó shock y convulsiones. El pronóstico vital, basado en la presentación clínica, era malo.\n\nIntervención terapéutica\nUna intervención inicial consiste en un relleno intracraneal a través de la fractura craneal, seguido de un vendaje cefálico que ayuda a detener el sangrado. El tratamiento involucró la estabilización de la columna cervical, intubación orotraqueal con oxígeno a 6 L por minuto y la inserción de un catéter Foley. Se usaron dos puertos venosos periféricos para administrar NaCl 0.9 % 1000 CC, Geloplasma* 500 CC, Manitol 20 % 250 CC; Phenobarbital inj 40 mg/2 ml: 100 mg, luego Thiopental 250 mg: bolo de 100 mg × 2 debido a otras convulsiones; Amoxicillin + Clavulanic Acid injection 2 g; Gentamycin 160 mg intramuscularmente. Se realizó un suero antitetánico de 1500 IU y una transfusión de 450 CC de sangre.\n\nEl paciente fue trasladado inconsciente a un equipo en un hospital de primera categoría, sin intubación y en un estado hemodinámico estable.\n\nEl primer día después de la transferencia, el paciente evolucionó bien; estaba consciente y podía caminar, sin problemas neurológicos, hemodinámicos o respiratorios. La tomografía computarizada reveló un edema bifrontal agudo, una contusión hemorrágica del parénquima predominantemente en el lado derecho, una capa de hematoma subdural agudo (3 mm) en la región fronto-parieto-temporo-occipital izquierda, una hernia subfalcular izquierda de 5 mm, una compresión discreta del ventrículo lateral derecho, una hemorragia subaracnoidea superior bifrontal aguda, una fractura frontal deprimida con rotura osteomeníngea y una fractura de la tercera vértebra cervical con compresión de la médula espinal. El paciente se sometió a una operación exitosa en el hospital de primera categoría.\n\nSeguimiento y resultados\nEl período postoperatorio estuvo marcado por convulsiones, para las cuales se le administró anticonvulsivos al paciente, con un buen resultado.\n",
+        "gold_summary": "Un hombre de 27 años, fumador sin antecedentes patológicos, estuvo involucrado en un accidente de tráfico, al caerse de una motocicleta sin casco. En el ingreso al hospital de nuestro distrito rural, la escala de coma de Glasgow durante el examen físico fue de 6/15 con midriasis bilateral, distrés hemodinámico y buena saturación. Se identificó una lesión penetrante en la cabeza con profusa hemorragia intracraneal. Se usó el relleno intracraneal conocido en la neurocirugía de control de daños para taponar la hemorragia intracraneal grave y que es una maniobra neuroquirúrgica que salva vidas. El paciente fue trasladado inconsciente a un hospital de primera categoría, libre de intubación y en un estado hemodinámico estable. El período postoperatorio estuvo marcado por convulsiones, por lo que el paciente fue puesto en anticonvulsivos con un buen resultado.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un hombre se cayó de su moto y se lastimó la cabeza. No llevaba casco y se hizo una herida que sangraba mucho. Cuando llegó al hospital, estaba muy dormido y no podía hablar ni abrir los ojos. \n\nLos doctores pusieron algo para parar la sangre dentro de su cabeza. Luego lo llevaron a otro hospital donde lo cuidaron mejor. Después de la operación, tuvo algunos temblores, pero le dieron medicina y se mejoró.",
+                "fh_score": 80.75
+            },
+            "B2": {
+                "text": "**Lo que pasó con el paciente**  \nUn hombre de 27 años que fuma tuvo un accidente al caerse de su motocicleta sin usar casco. Cuando llegó al hospital en una zona rural, estaba muy grave. No respondía bien, tenía las pupilas dilatadas en ambos ojos y sangraba mucho dentro de su cabeza por una herida penetrante.\n\n**Qué hicieron los médicos**  \nPara detener la hemorragia dentro de su cráneo, los médicos usaron una técnica llamada relleno intracraneal. Esto significa que colocaron un material especial para tapar la herida y controlar el sangrado, lo cual es una cirugía que puede salvar vidas en casos graves. Luego, lo trasladaron a un hospital mejor equipado, donde estaba inconsciente pero estable en cuanto a su circulación y respiración.\n\n**Qué pasó después de la operación**  \nDespués de la cirugía, el paciente tuvo convulsiones, que son movimientos involuntarios causados por problemas en el cerebro. Por eso, le dieron medicamentos llamados anticonvulsivos para controlar estas convulsiones. Gracias a este tratamiento, el paciente mejoró y tuvo una buena recuperación.",
+                "fh_score": 60.16
+            },
+            "B3": {
+                "text": "Resumen detallado para público general universitario\n\nContexto  \nUn hombre de 27 años, fumador y sin antecedentes médicos previos, sufrió un accidente de tráfico al caerse de una motocicleta sin usar casco. Tras la caída, presentó dolor de cabeza y una herida sangrante en la frente, por lo que acudió al hospital local en una zona rural.\n\nHallazgos clínicos y evaluación inicial  \nAl llegar al hospital, el paciente perdió el conocimiento y tuvo dos convulsiones. La evaluación neurológica mostró una escala de coma de Glasgow de 6 sobre 15, lo que indica un estado de coma profundo (no abría los ojos, respondía solo con movimientos para evitar el dolor y no hablaba). Además, presentaba midriasis bilateral (dilatación anormal de ambas pupilas), dificultad para mantener la presión arterial (distrés hemodinámico) y buena saturación de oxígeno. Se detectó una lesión penetrante en el cráneo con una hemorragia intracraneal abundante, lo que significa que la sangre estaba acumulándose dentro del cerebro debido a la lesión.\n\nIntervención inicial y traslado  \nEn el hospital rural, donde no había unidad de cuidados intensivos ni tomografía computarizada (TAC), se aplicó un tratamiento de emergencia para controlar el sangrado intracraneal mediante una técnica quirúrgica llamada relleno intracraneal, que consiste en taponar la fractura del cráneo para detener la hemorragia y estabilizar al paciente. Además, se estabilizó la columna cervical, se realizó intubación orotraqueal para asegurar la respiración, se administraron líquidos intravenosos, medicamentos anticonvulsivos para controlar las convulsiones, antibióticos para prevenir infecciones y una transfusión sanguínea debido a la anemia severa (hemoglobina de 6 g/dL). Posteriormente, el paciente fue trasladado inconsciente pero hemodinámicamente estable a un hospital de mayor nivel con mejores recursos.\n\nDiagnóstico y tratamiento avanzado  \nEn el hospital de referencia, se realizó una tomografía computarizada que reveló múltiples lesiones cerebrales graves: edema cerebral (hinchazón del cerebro) en ambas áreas frontales, contusión hemorrágica (moretón con sangrado) en el tejido cerebral del lado derecho, un hematoma subdural agudo (acumulación de sangre entre el cerebro y la membrana que lo cubre) en el lado izquierdo, una hernia subfalcular (desplazamiento del cerebro hacia un lado), compresión ventricular leve, hemorragia subaracnoidea (sangrado en el espacio que rodea el cerebro), fractura deprimida del hueso frontal con ruptura de las membranas que cubren el cerebro, y fractura de la tercera vértebra cervical con compresión de la médula espinal. El paciente fue sometido a una cirugía exitosa para tratar estas lesiones.\n\nEvolución y seguimiento  \nDurante el postoperatorio, el paciente presentó convulsiones que fueron controladas con medicamentos anticonvulsivos, logrando una buena respuesta clínica. Al día siguiente de la cirugía, el paciente estaba consciente, podía caminar y no mostraba problemas neurológicos, respiratorios ni circulatorios.\n\nInterpretación clínica  \nEste caso ilustra la gravedad de los traumatismos craneoencefálicos penetrantes y la importancia de una intervención rápida y adecuada, incluso en entornos con recursos limitados. La técnica de relleno intracraneal utilizada inicialmente fue fundamental para controlar la hemorragia y estabilizar al paciente antes del traslado. La atención especializada posterior y el manejo multidisciplinario permitieron una recuperación favorable a pesar de las múltiples lesiones cerebrales y de la médula espinal.\n\nPróximos pasos  \nSe recomienda continuar con el seguimiento neurológico y rehabilitación para evaluar y tratar posibles secuelas a largo plazo, así como mantener el control de las convulsiones con medicación adecuada. Además, es fundamental promover el uso de casco y medidas de seguridad vial para prevenir este tipo de accidentes.",
+                "fh_score": 30.06
+            }
+        }
+    },
+    {
+        "article": "La paciente era una madre de 54 años que provenía de una zona rural y que llegó al Hospital Especializado de Compresión de Nekemte con la queja de una masa en su vagina de 3 años de duración. Hace tres años, encontró una protuberancia de masa a través de su vagina, que gradualmente creció en tamaño con el tiempo. Había tenido dos bebés, el último hace 12 años. Ambos partos fueron en casa, ya que el centro de salud está demasiado lejos de su área de residencia, y fue asistida por una comadrona tradicional. Ella afirmó que todo había sido sin problemas. Inicialmente, hace tres años, hubo sangrado y una descarga ofensiva de la masa, pero eso se detuvo en el último año. Desarrolló laceraciones en la masa hace seis meses. Por esta razón, se divorció y se aisló de toda la vida social durante este largo período de tiempo. Ahora, su hermana mayor y otro familiar la trajeron al hospital específicamente por la laceración de la masa. No tenía ninguna otra enfermedad médica crónica conocida.\n\nHallazgo pertinente del PE\nSigno vital: PA = 100/60 mm hg, FC = 84 lpm, FR = 20 lpm, T° = 36.5°C, peso = 47 kg.\n\nGUS: hay una masa rosada en la vagina que se encuentra a unos 7 cm del anillo del himen.\n\nEl fondo uterino es la parte principal de la masa.\n\nHabía una laceración longitudinal de unos 5 cm en el lado derecho de la masa.\n\nNo hubo sangrado ni secreción de la masa ni del área de la laceración.\n\nLaboratorio\nCBC: hemoglobina = 12 g/dl, PLT = 285 mil, neutrófilos = 74%.\n\nAnálisis de orina: resultado normal.\n\nGrupo sanguíneo = A, RH = positivo.\n\nPrueba de VIH = negativa.\n\nHBSAg = negativo.\n\nEcografía: vejiga parcialmente llena visible en el abdomen, útero no visible en el abdomen. Por lo demás, no se observaron otros hallazgos pertinentes.\n\nRadiografía de tórax: radiografía de tórax normal.\n\nPor este motivo, se le diagnosticó una inversión uterina crónica. Se tomaron imágenes preoperatorias y postoperatorias, el fondo uterino era el punto principal de la masa que sobresalía completamente a través de la vagina y había una laceración crónica desarrollada en la superficie endometrial. Después de la operación, se observó un canal vaginal normal. Después de revisar las opciones de tratamiento con ella y su familia, se programó una cirugía y se realizó una histerectomía abdominal al día siguiente. Era una cirugía abdominal y era fácil introducir el útero en el abdomen. Como el tejido era redundante y distorsionado, es difícil identificar la referencia anatómica y los puntos de referencia quirúrgicos. Debido a esto, la cirugía fue difícil y hubo una lesión ureteral derecha transaccional intraoperatoria y se realizó una anastomosis de extremo a extremo. Se dio de alta el décimo día de la operación y se encontró que estaba mejorando. Se le dio una cita de seguimiento dos semanas después y cuando se evaluó se encontró que estaba bien.\n",
+        "gold_summary": "Una mujer de 54 años de edad acudió a nuestro hospital con la queja de una masa indolora en su vagina de 3 años de duración. Hace tres años, encontró una protuberancia de masa a través de su vagina, que gradualmente creció en tamaño con el tiempo. En el examen físico, el fondo uterino fue el punto principal de la masa y sobresalía 7 cm por debajo del anillo del himen. Como resultado, se le diagnosticó inversión uterina crónica y se le sometió a una histerectomía abdominal. Fue dada de alta en casa mejorada. Presentamos este caso debido a un factor no identificado que provocó la inversión uterina, la presentación tardía de la enfermedad y la dificultad en el tratamiento quirúrgico.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había una señora que tenía una bolita en su cuerpo. Esa bolita estaba en un lugar muy especial dentro de ella. La bolita creció poco a poco durante mucho tiempo. Los doctores vieron que esa bolita era parte de un órgano que estaba fuera de su lugar. Ella tuvo que ir al hospital para que los doctores la ayudaran con una operación. Después de la operación, la señora se sintió mejor y pudo ir a su casa. Los doctores contaron esta historia para que otros puedan aprender.",
+                "fh_score": 80.37
+            },
+            "B2": {
+                "text": "**Lo que le Pasó a la Paciente**  \nUna mujer de 54 años notó hace tres años una masa o bulto que salía de su vagina. Esta masa fue creciendo poco a poco y no le causaba dolor. Al principio, tuvo sangrado y mal olor, pero eso paró hace un año. También se lastimó la masa hace seis meses, lo que la hizo sentirse mal y alejarse de su familia y amigos.\n\n**Qué Encontraron los Médicos**  \nCuando la examinaron, vieron que la masa era parte del útero que había salido hacia afuera por la vagina. Esto se llama inversión uterina crónica, que es cuando el útero se da vuelta y sale fuera del cuerpo. Había una herida larga en la masa, pero no estaba sangrando en ese momento. Los exámenes de sangre y orina estaban normales, y no tenía infecciones como VIH o hepatitis.\n\n**Cómo la Ayudaron**  \nLos médicos decidieron hacer una cirugía para quitar el útero, llamada histerectomía abdominal. La operación fue complicada porque el tejido estaba muy cambiado y era difícil saber dónde estaban las partes normales. Durante la cirugía, se lastimó un conducto que lleva la orina desde el riñón a la vejiga, pero lo repararon en el mismo momento. Después de la operación, la paciente mejoró y pudo volver a casa. En el control dos semanas después, estaba bien y sin problemas.\n\n**Por Qué es Importante Este Caso**  \nEste caso es especial porque la inversión uterina es rara y no se sabe exactamente qué la causó en esta mujer. Además, ella llegó al hospital muy tarde, cuando la situación ya era difícil de tratar. La cirugía fue complicada, pero al final tuvo un buen resultado. Esto muestra la importancia de buscar ayuda médica a tiempo cuando se tiene una masa o bulto en el cuerpo.",
+                "fh_score": 72.79
+            },
+            "B3": {
+                "text": "Resumen para Público General Educado\n\nContexto  \nUna mujer de 54 años, originaria de una zona rural, acudió al hospital tras presentar durante tres años una masa que sobresalía por su vagina. Esta masa fue creciendo lentamente y, en sus primeros años, estuvo acompañada de sangrado y secreción con mal olor, aunque estos síntomas desaparecieron en el último año. La paciente había tenido dos partos en casa, asistida por una comadrona tradicional, sin complicaciones aparentes. Debido a la masa y a una herida (laceración) que apareció en ella hace seis meses, la paciente sufrió aislamiento social y divorcio. Finalmente, fue llevada al hospital por familiares para recibir atención médica.\n\nHallazgos Clínicos  \nAl examen físico, se encontró una masa de color rosado ubicada aproximadamente a 7 centímetros del borde del himen (la membrana que rodea la entrada de la vagina). La parte principal de esta masa correspondía al fondo uterino, que es la parte superior del útero. En la masa había una herida longitudinal de unos 5 centímetros, pero no se observó sangrado ni secreción en ese momento. Los signos vitales de la paciente estaban dentro de rangos normales y los análisis de sangre y orina no mostraron alteraciones significativas. La ecografía abdominal no logró visualizar el útero en su posición habitual, lo que apoyó el diagnóstico.\n\nDiagnóstico e Interpretación Clínica  \nSe diagnosticó a la paciente con inversión uterina crónica, una condición poco común en la que el útero se voltea hacia adentro y puede protruir a través de la vagina. En este caso, la inversión era completa y prolongada, lo que causó la formación de la masa visible y la laceración en su superficie. La causa exacta que originó esta inversión uterina no pudo ser identificada, lo que hace este caso especialmente relevante.\n\nTratamiento y Evolución  \nDespués de discutir las opciones con la paciente y su familia, se decidió realizar una histerectomía abdominal, que consiste en la extirpación quirúrgica del útero a través del abdomen. Durante la cirugía, se encontró que el tejido estaba muy distorsionado y redundante, lo que dificultó la identificación de las estructuras anatómicas normales. Esto llevó a una complicación quirúrgica: una lesión en el uréter derecho (el conducto que conecta el riñón con la vejiga), que fue reparada mediante una anastomosis (unión quirúrgica) de extremo a extremo. La paciente fue dada de alta diez días después de la operación, con mejoría clínica, y en el control posterior mostró una recuperación satisfactoria, con un canal vaginal normal.\n\nImportancia del Caso  \nEste caso destaca la presentación tardía y poco común de una inversión uterina crónica en una mujer rural, así como las dificultades quirúrgicas asociadas a esta condición. La ausencia de atención médica temprana y la falta de acceso a centros de salud contribuyeron a la evolución prolongada y compleja del caso. La experiencia subraya la necesidad de mejorar el acceso a servicios médicos y la educación sanitaria en áreas rurales para prevenir complicaciones graves.",
+                "fh_score": 49.21
+            }
+        }
+    },
+    {
+        "article": "Varón de 20 años, HIV negativo, con TB pulmonar y tratamiento irregular en 2020-2021. Se internó por síndrome de impregnación bacilar, dolor e impotencia funcional del hombro derecho. Presentaba mal estado general, adelgazado, hipotrofia muscular grave, lesiones tumorales frías fluctuantes fistulizadas en dorso, calota craneana y tórax anterior con secreción caseosa, sin presentar déficits motores ni sensitivos. El examen molecular rápido (GeneXpert Mtb/Rif) de secreción del tórax fue positivo para Mycobacterium tuberculosis, sensible a rifampicina (el antibiograma fenotípico mostró una cepa pansensible). La TC demostró consolidaciones pulmonares y árbol en brote, junto con el compromiso óseo de columna cervical, dorsal y lumbar con imágenes líticas y colecciones pre y paraespinales. En la RMN se observaron imágenes infiltrativas desde C4 a C6; D4 a D6, D9 a D12; fractura patológica de D6 y D10 e infiltración en L1, L2 y L3. Inició tratamiento anti-TB con esquema estándar de primera línea (isoniacida, rifampicina, pirazinamida, etambutol). Dada la extensa destrucción y el peligro de cuadriplejía/paraplejía por el compromiso cervical y/o dorsal, se indicó posición decúbito dorsal permanente, collar de Filadelfia, asistencia kinésica y conducta neuroquirúrgica en forma programada en los niveles cervicales, D6 y D10. Previo a la cirugía programada presentó un cuadro agudo de paraplejía con nivel sensitivo D8, con compromiso vesical. Se interpretó como nivel de compresión aguda en D6. Se indicó neurocirugía de urgencia con descompresión medular vía posterior con laminectomía dorsal 6 y parcialmente D5 y 7 y evacuación de una colección epidural. Fue recuperando la función motora y sensitiva en forma progresiva. Posteriormente se realizó la cirugía programada cervical vía anterior con corporectomía de C4, C5, C6 y C7 más artrodesis de C3 a D1 con reemplazo de cuerpo vertebral más injerto autólogo, placa y tornillos. En la TC de control se evidenció luxación posterior de D6 con compresión del canal espinal y deterioro neurológico por compresión medular. Se reconsideró la táctica quirúrgica debido a la inestabilidad mecánica y neurológica. Se realizó descompresión y alineación del nivel luxado con artrodesis posterior de los tres niveles espinales no adyacentes, cervical, dorsal 6 y dorsal 10 en un solo tiempo quirúrgico. Se fijó desde  C3 hasta D12 con tornillos poliaxiales y barra de transición cervicodorsal. En cada tiempo quirúrgico se evidenció evacuación espontánea de material caseoso, BAAR positivo, y se realizaron lavados profusos.  Presentó mejoría clínica, bacteriológica y resolución de las lesiones pulmonares. Recuperó movilidad con rehabilitación kinésica sumada al tratamiento específico (3 meses de primera fase e indicación de continuación con isoniacida y rifampicina hasta completar los 12 meses). Egresó caminando por sus propios medios, luego de una prolongada internación de 5 meses.",
+        "gold_summary": "Se presenta el caso de un varón de 20 años con espondilitis tuberculosa multinivel no contigua (cervical, dorsal 6, dorsal 10 y lumbar). Se trata de un paciente HIV negativo con tuberculosis diseminada con grave compromiso de su estado general y múltiples localizaciones de la enfermedad. Algunas tenían fistulas que secretaban caseum. El paciente presentó paraplejía aguda que requirió, teniendo en cuenta el nivel sensitivo a nivel dorsal 6, una primera cirugía urgente de descompresión por vía posterior. Luego se efectuó la cirugía programada. En primera instancia, la región cervical por vía anterior, con corporectomía, colocación de reemplazo de cuerpo vertebral más injerto autólogo y placa con tornillos. Posteriormente se evidenció luxación del nivel dorsal 6 hacia atrás comprimiendo la médula espinal y, dada la inestabilidad mecánica, se indicó un tercer tiempo quirúrgico por vía posterior que comprendió reducción, descompresión y fijación, resolviendo los tres niveles por vía posterior con barras y tornillos. El tratamiento quirúrgico, médico y kinésico de esta forma poco frecuente del mal de Pott fue exitoso, con recuperación de su estabilidad mecánica y progresiva recuperación de su estado neurológico.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había un joven de 20 años muy enfermo con un hueso del cuello y la espalda roto por una infección. Esta infección era muy fuerte y estaba en muchos lugares de su cuerpo. A veces, de sus heridas salía una cosa blanda y fea. \n\nUn día, el joven no pudo mover sus piernas. Los doctores hicieron una operación rápida para ayudar a su espalda y que pudiera sentir y mover mejor. Después, le hicieron otra operación para arreglar los huesos del cuello con partes nuevas y tornillos. \n\nLuego, vieron que un hueso de su espalda estaba fuera de lugar y apretaba la parte que mueve y siente el cuerpo. Entonces, hicieron otra operación para poner todo en su lugar con barras y tornillos. \n\nCon medicinas, ejercicios y las operaciones, el joven mejoró mucho. Ahora puede caminar y está más fuerte. Los doctores están contentos porque él está mejor.",
+                "fh_score": 80.01
+            },
+            "B2": {
+                "text": "**Caso de Tuberculosis en la Columna Vertebral**\n\nEste es el caso de un joven de 20 años que tenía tuberculosis, una infección causada por una bacteria llamada Mycobacterium tuberculosis. Aunque no tenía VIH, la infección estaba muy extendida y afectaba varias partes de su columna vertebral: el cuello (cervical), la parte media de la espalda (dorsal) y la zona baja (lumbar). Algunas áreas tenían heridas abiertas que soltaban una sustancia llamada caseum, que es un material parecido a queso que se forma por la infección.\n\n**Problemas y Tratamiento Inicial**\n\nEl paciente sufrió una pérdida súbita de movimiento y sensibilidad en las piernas, llamada paraplejía, debido a que la médula espinal estaba comprimida en la zona dorsal 6 (parte media de la espalda). Por eso, tuvo que someterse a una cirugía urgente para aliviar la presión en la médula, llamada descompresión, realizada por la parte trasera de la columna.\n\nDespués, se hizo una cirugía programada en el cuello, por la parte delantera, donde se removieron varios cuerpos vertebrales dañados (corporectomía). Para reemplazarlos, se usaron injertos, que son partes de hueso tomadas del propio paciente, junto con placas y tornillos para estabilizar la columna.\n\n**Complicación y Cirugía Final**\n\nMás adelante, se descubrió que una vértebra en la zona dorsal 6 se había desplazado hacia atrás, presionando otra vez la médula espinal y causando inestabilidad en la columna. Por esta razón, se realizó una tercera cirugía por la parte trasera para corregir el desplazamiento, aliviar la presión y fijar la columna con barras y tornillos desde el cuello hasta la parte media de la espalda.\n\n**Resultado**\n\nCon el tratamiento combinado de medicamentos para la tuberculosis, cirugías y rehabilitación física, el paciente mejoró mucho. Recuperó la estabilidad de su columna y la función de sus piernas, pudiendo caminar por sí mismo después de una larga hospitalización de cinco meses. Este caso muestra cómo, aunque la tuberculosis en la columna puede ser grave y complicada, un tratamiento adecuado puede llevar a una buena recuperación.",
+                "fh_score": 49.76
+            },
+            "B3": {
+                "text": "**Contexto**  \nSe describe el caso de un joven de 20 años, sin infección por VIH, que presentó tuberculosis pulmonar y ósea diseminada, con afectación de múltiples niveles de la columna vertebral (cervical, dorsal y lumbar) en forma no contigua. El paciente tenía un estado general muy deteriorado, con pérdida de peso, atrofia muscular severa y lesiones tumorales en la piel que secretaban material caseoso (una sustancia similar a queso, típica de la tuberculosis). Estas lesiones estaban fistulizadas, es decir, comunicadas con el exterior, en regiones como el dorso, el cráneo y el tórax anterior.\n\n**Hallazgos Clave**  \n- Confirmación microbiológica de Mycobacterium tuberculosis sensible a rifampicina y otros antibióticos habituales.  \n- Imágenes de tomografía computarizada y resonancia magnética que mostraron consolidaciones pulmonares, lesiones óseas líticas (áreas de destrucción ósea) en varios niveles vertebrales y colecciones (acumulaciones de líquido o pus) pre y paraespinales.  \n- Fracturas patológicas en las vértebras dorsales D6 y D10, con infiltración tumoral desde C4 a C6, D4 a D6, D9 a D12 y L1 a L3.  \n- Episodio agudo de paraplejía (pérdida de movimiento y sensibilidad en las piernas) con nivel sensitivo en D8 y compromiso vesical, atribuible a compresión medular aguda en D6.\n\n**Interpretación Clínica**  \nEl paciente presentó una forma grave y poco común de tuberculosis ósea conocida como mal de Pott, con afectación de múltiples niveles vertebrales no contiguos. La destrucción ósea extensa y la presencia de colecciones pusieron en riesgo la integridad neurológica, con riesgo de parálisis permanente. La paraplejía aguda requirió una intervención quirúrgica urgente para descomprimir la médula espinal mediante laminectomía (extirpación de parte de la vértebra) y evacuación de la colección epidural. Posteriormente, se realizó una cirugía programada en la región cervical por vía anterior, que incluyó la extracción de varios cuerpos vertebrales afectados (corporectomía), reconstrucción con injerto óseo autólogo y fijación con placa y tornillos. Sin embargo, se detectó una luxación posterior en D6 que comprimía nuevamente la médula, causando inestabilidad mecánica y deterioro neurológico. Esto motivó una tercera cirugía por vía posterior para reducir la luxación, descomprimir la médula y fijar los niveles cervical y dorsales afectados con tornillos y barras, estabilizando la columna desde C3 hasta D12.\n\n**Próximos Pasos y Evolución**  \nEl tratamiento combinado, que incluyó terapia antituberculosa estándar de primera línea durante al menos 12 meses, intervenciones quirúrgicas escalonadas y rehabilitación kinésica intensiva, permitió la recuperación progresiva de la función motora y sensitiva del paciente. Además, se logró la resolución de las lesiones pulmonares y la estabilidad mecánica de la columna vertebral. Tras una prolongada hospitalización de cinco meses, el paciente egresó caminando por sus propios medios, evidenciando una evolución favorable en un caso complejo y de alta gravedad.",
+                "fh_score": 35.9
+            }
+        }
+    },
+    {
+        "article": "Un hombre japonés de 23 años fue admitido en nuestro hospital debido al empeoramiento de la disnea de esfuerzo. Había mostrado dificultad para correr a los dos años y se le diagnosticó EDMD con una mutación genética de LMNA (Lamin A/C) en el exón 1 de leucina 102 a prolina. De acuerdo con las manifestaciones típicas de EDMD, sus codos, rodillas y tendones de Aquiles se habían contraído a los cinco años, y sus músculos cervicales posteriores se habían vuelto rígidos; sin embargo, continuó con su vida diaria habitual, aunque con una leve restricción de ejercicio. Su padre también había sido diagnosticado con EDMD y murió repentinamente a los 40 años.\n\nCuando el paciente tenía 19 años, fue admitido en un hospital por primera vez debido a una insuficiencia cardiaca congestiva. Los signos de insuficiencia de la RV, tales como edema de las piernas y congestión hepática, fueron prominentes, como lo indica el alto nivel de bilirrubina en sangre (2,5 mg/dL). La ecocardiografía mostró que la excursión sistólica del plano anular tricúspide (TAPSE) era de 5,7 mm, la velocidad de la RV de 5,1 cm/s y el cambio del área fraccional de la RV (RVFAC) del 19 %, lo que indica una marcada disfunción de la RV. Se introdujeron diuréticos de alta dosis además de carvedilol (10 mg/día) y enalapril (2,5 mg/día). A pesar de esos medicamentos, fue readmitido debido al empeoramiento de la insuficiencia de la RV.\n\nA los 22 años, se le implantó un desfibrilador cardioversor implantable (ICD) debido a su taquicardia ventricular no sostenida (VT) y a la historia familiar de muerte súbita cardiaca. En este momento, el cateterismo cardiaco derecho (RHC) mostró una presión de la cuña de la arteria pulmonar (PAWP) de 22 mmHg, presión auricular derecha (RAP) de 17 mmHg, e índice de trabajo de accidente cerebrovascular ventricular derecho (RVSWI) de 6.47, lo que sugiere una disfunción severa sostenida del RV. Como tal, el fallo del RV probablemente fue la principal condición patológica a lo largo de su curso clínico.\n\nTenía insuficiencia cardiaca sintomática con la clasificación III de la New York Heart Association con dosis máximas de medicación guiada por directrices, y su electrocardiograma mostraba un ritmo sinusal regular y bloqueo de rama izquierda con ancho QRS (150 ms). Su fracción de eyección del ventrículo izquierdo (LVEF) era ≤35 % en la ecocardiografía. Por lo tanto, se consideró que estaba indicado para CRT y se le actualizó a ICD a los 23 años.\n\nAl ingreso, su presión arterial era de 106/65 mmHg y su frecuencia cardíaca de 60 latidos/min con un ritmo regular. El examen físico reveló un tercer sonido cardíaco y un soplo pan sistólico (Levine II/VI) en la región apical. Los sonidos respiratorios eran claros, mientras que una vena yugular distendida y un edema de miembros inferiores eran evidentes. La radiografía de tórax indicó un aumento de la relación cardiotorácica (59%) sin congestión pulmonar.\n\nEl electrocardiograma mostró un ritmo biventricular debido a la TRC. La ecocardiografía reveló una ligera dilatación en ambos ventrículos (diámetro final diastólico del LV: 54 mm, diámetro del RV: 50 mm) con una reducción de la LVEF (30%). La función del RV también se redujo, como lo indican una reducción de la RVFAC (11%) y un bajo TAPSE (8 mm). Ambos ventrículos agrandados causaron una pérdida de sujeción y coaptación de las valvas que resultó en una regurgitación mitral moderada y una regurgitación tricuspídea severa. La vena cava inferior se dilató a 23 mm con una reducción de la fluctuación respiratoria.\n\nEn los hallazgos histológicos de los músculos cervicales posteriores realizados más tarde en la autopsia, se observó un aumento en la variación del tamaño de la fibra muscular con una infiltración moderada de tejido conectivo, lo que fue compatible con la EDMD. Los análisis de sangre revelaron péptido natriurético cerebral (BNP) 196.1 pg/mL, bilirrubina total 1.4 mg/dL, aspartato aminotransferasa (AST) 39 U/L, alanina aminotransferasa (ALT) 43 U/L, y gamma glutamil transpeptidasa (gamma-GTP) 451 U/L, lo que sugirió una disfunción hepática. Aunque las arterias coronarias estaban intactas en la angiografía, una biopsia endocárdica del VD reveló una hipertrofia cardiaca con un aumento de la magnitud del núcleo y el miocardio.\n\nLa microscopía electrónica demostró hallazgos típicos de la EDMD: un número reducido de miofibrillas, necrosis y la formación de pseudo- o verdaderas inclusiones. Dado que se descartaron otras cardiomiopatías secundarias mediante estos hallazgos clínicos e histológicos, diagnosticamos una cardiomiopatía relacionada con la EDMD.\n\n\nEl curso clínico del paciente. El cateterismo cardiaco derecho (RHC) en el día 11 mostró disfunción y congestión severa del LV/RV, y se iniciaron algunos inótropos. Aunque la hemodinámica del paciente mejoró, su función renal empeoró progresivamente en el día 38. Preocupados por el empeoramiento de su función renal debido a la disminución de la presión arterial, se iniciaron la dopamina y el soporte mecánico (IABP y CRRT), y la función renal y la hemodinámica del paciente mejoraron. Sin embargo, desarrolló insuficiencia hepática aguda junto con insuficiencia severa del RV indicada por los datos del RHC en el día 68. Aunque se introdujo ECMO veno-atrial en el día 71, la disfunción hepática y la DIC causaron diátesis hemorrágica sistémica, y el paciente falleció por fallo multiorgánico en el día 100. CRRT: terapia de reemplazo renal continua, DIC: coagulación intravascular diseminada, ECMO: oxigenación por membrana extracorpórea, IABP: bombeo de globo intraaórtico, LV: ventrículo izquierdo, RV: ventrículo derecho\n\nEl RHC en el día 11 mostró que el índice cardiaco (IC) era de 2,0 L/min/m2 (método de Fick), y la PAP era de 15 mmHg, lo que indicaba un subgrupo IV de Forrester. La presión arterial pulmonar (PAP) era de 29/12 (18) mmHg, y la RAP era de 15 mmHg. El RVSWI, uno de los parámetros hemodinámicos para la función del RV, se calculó con la siguiente fórmula: RVSWI (g·m/m2/latido)=[presión arterial pulmonar media (mPAP)-presión atrial derecha media (mRAP)]×índice de volumen de latido (SVI)×0.0136. Su RVSWI era de 1.36 g·m/m2/latido, lo que indicaba una disfunción severa del RV. Para compensar el síndrome de baja producción del paciente y la congestión, comenzamos una infusión continua de dobutamina (3.0 μg/kg/min) y añadimos milrinona (0.125 μg/kg/min) en el día 16.\n\n\nEn el día 32, los datos de RHC mejoraron, con un aumento del IC (2,48 L/min/m2), una reducción de la PAWP (13 mmHg) y un aumento de la RVSWI (2,8 g·m/m2/latido). Sin embargo, en el día 38, la función renal del paciente empeoró progresivamente, posiblemente debido a una presión venosa central alta (CVP) e hipotensión, ya que la presión arterial había sido de alrededor de 70/40 mmHg varios días antes del empeoramiento de la función renal. Para aumentar su presión arterial, se inició una infusión continua de dopamina (2,0 μg/kg/min); se redujo la milrinona y se interrumpieron el enalapril y la eplerenona. Además, se necesitaron temporalmente el bombeo de globo intraaórtico (IABP) y la terapia de reemplazo renal continuo (CRRT). A medida que la hemodinámica del paciente mejoró en respuesta al aumento de la saturación de oxígeno venoso mixto (SvO2, 70-80%) y el IC (3,0-3,5 L/min/m2), se retiraron el IABP y la CRRT en el día 45.\n\nSin embargo, el día 68, el IC volvió a disminuir a 1,25 l/min/m2 y la congestión pulmonar y la retención de fluidos del paciente se deterioraron; la PAWP era tan alta como la RAP, a 22 mmHg. Además, los niveles de bilirrubina en suero y las transaminasas hepáticas del paciente aumentaron drásticamente, lo que sugiere el desarrollo de insuficiencia hepática. El día 71, se inició la ECMO VA a través de una vena femoral a la arteria subclavia, pero debido a la diátesis hemorrágica sistémica acompañada por la coagulación intravascular diseminada (CID), el paciente falleció de insuficiencia multiorgánica el día 100.\n\nUna autopsia realizada con el consentimiento informado de la familia del paciente reveló un agrandamiento eferente en ambos ventrículos con un espesor de pared delgado. El examen histopatológico reveló que la hipertrofia miocárdica leve a moderada y la fibrosis severa eran evidentes en el RV y el LV. El peso del hígado aumentó significativamente a 2298 g, y se detectaron congestión hepática macroscópica y colestasis. En las imágenes microscópicas, el área de la vena porta apenas cambió, y se observó atrofia o pérdida de hepatocitos alrededor de las venas centrales, lo que indica un «hígado de shock». En los pulmones, se observó una hemorragia alveolar extensa, y se observó una colección de macrófagos que habían ingerido hemosiderina, lo que refleja una diátesis hemorrágica sistémica.\n\nMH - Adulto\nMH - Insuficiencia cardiaca/*etiología/fisiopatología/terapia\nMH - Humanos\nMH - Lamin tipo A/genética\nMH - Hombre\nMH - Distrofia muscular, Emery-Dreifuss/*complicaciones/diagnóstico/genética/terapia\nMH - Mutación\n",
+        "gold_summary": "Un hombre de 23 años tenía debilidad muscular progresiva y distrofia muscular de Emery-Dreifuss (EDMD) debido a una mutación de LMNA (lamina A/C). Insuficiencia cardiaca congestiva diagnosticada a los 19 años de edad. El tratamiento farmacológico máximo/resincronización cardiaca no logró mejorar la función cardiaca. Por lo tanto, fue hospitalizado debido a insuficiencia cardiaca. A pesar de la oxigenación por membrana extracorpórea, desarrolló una disfunción cardiaca derecha grave y falleció (fallo multiorgánico).\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había un hombre joven con músculos muy débiles. Tenía una enfermedad que hace que los músculos se pongan muy rígidos y duros. Su corazón también se puso muy cansado y no podía trabajar bien. Los doctores le dieron medicinas y una máquina para ayudar su corazón. Pero su corazón se puso peor y se enfermó mucho. Al final, su cuerpo no pudo seguir y él murió.",
+                "fh_score": 86.53
+            },
+            "B2": {
+                "text": "**Lo que le pasaba al paciente:**  \nUn joven japonés de 23 años tenía una enfermedad llamada distrofia muscular de Emery-Dreifuss (EDMD). Esta enfermedad afecta los músculos y está causada por un cambio en un gen llamado LMNA, que produce una proteína importante para las células. Desde pequeño, él tenía problemas para moverse bien y sus músculos se ponían rígidos. A los 19 años, comenzó a tener problemas graves en su corazón, especialmente en la parte derecha, lo que causaba insuficiencia cardiaca, es decir, que el corazón no podía bombear sangre correctamente.\n\n**Tratamientos y evolución:**  \nEl paciente recibió varios medicamentos para mejorar su corazón y un dispositivo llamado desfibrilador para prevenir ritmos cardiacos peligrosos. Más tarde, le pusieron un tratamiento llamado terapia de resincronización cardiaca, que ayuda a que las partes del corazón trabajen juntas mejor. Sin embargo, ninguno de estos tratamientos logró mejorar suficientemente la función de su corazón.\n\n**Lo que ocurrió en el hospital:**  \nFue ingresado en el hospital por empeoramiento de su insuficiencia cardiaca. Los médicos usaron máquinas especiales para ayudar a su corazón y a sus órganos, como la oxigenación por membrana extracorpórea (ECMO), que es un sistema que ayuda a oxigenar la sangre cuando el corazón y los pulmones no funcionan bien. A pesar de estos esfuerzos, su corazón derecho siguió fallando gravemente, lo que provocó que otros órganos también dejaran de funcionar, y lamentablemente falleció.\n\n**Qué significa este caso:**  \nEste caso muestra cómo la distrofia muscular de Emery-Dreifuss puede afectar no solo los músculos, sino también el corazón, causando insuficiencia cardiaca severa que es difícil de tratar. La mutación genética en LMNA juega un papel importante en esta enfermedad. Aunque existen tratamientos avanzados, en algunos casos la enfermedad puede progresar y causar complicaciones graves que llevan a la muerte.",
+                "fh_score": 52.87
+            },
+            "B3": {
+                "text": "**Contexto**  \nSe presenta el caso de un hombre japonés de 23 años con distrofia muscular de Emery-Dreifuss (EDMD), una enfermedad genética causada por una mutación en el gen LMNA que codifica la proteína lamina A/C. Esta mutación específica (leucina 102 a prolina en el exón 1) provocó debilidad muscular progresiva desde la infancia, contracturas articulares y rigidez muscular, manifestaciones típicas de esta enfermedad. Además, existía un antecedente familiar importante, ya que su padre también padeció EDMD y falleció súbitamente a los 40 años.\n\n**Hallazgos Clave**  \nA los 19 años, el paciente desarrolló insuficiencia cardíaca congestiva, principalmente por disfunción severa del ventrículo derecho (RV), evidenciada por síntomas como edema en las piernas y congestión hepática, así como por estudios ecocardiográficos y cateterismo cardíaco que mostraron una función ventricular deteriorada. A pesar de recibir tratamiento farmacológico intensivo con diuréticos, betabloqueantes y inhibidores de la enzima convertidora de angiotensina, la función cardíaca no mejoró. A los 22 años se le implantó un desfibrilador cardioversor implantable (ICD) debido a episodios de taquicardia ventricular y riesgo de muerte súbita.\n\nCuando la insuficiencia cardíaca progresó a una etapa avanzada (clasificación funcional III de la New York Heart Association), se le realizó una terapia de resincronización cardíaca (CRT) para mejorar la función del corazón. Sin embargo, al ingreso hospitalario a los 23 años, persistían signos de insuficiencia cardíaca derecha grave, con dilatación de ambos ventrículos, reducción significativa de la fracción de eyección del ventrículo izquierdo (LVEF 30%) y disfunción severa del ventrículo derecho, acompañada de insuficiencia valvular mitral y tricuspídea.\n\nDurante su hospitalización, el paciente presentó empeoramiento progresivo de la función renal y hepática, complicaciones que reflejaban la insuficiencia multiorgánica secundaria a la falla cardíaca avanzada. Se implementaron tratamientos de soporte hemodinámico, incluyendo infusiones de medicamentos inotrópicos, bombeo de globo intraaórtico (IABP), terapia de reemplazo renal continua (CRRT) y finalmente oxigenación por membrana extracorpórea (ECMO) veno-arterial. A pesar de estas intervenciones, desarrolló coagulación intravascular diseminada (CID) y una diátesis hemorrágica sistémica, que culminaron en su fallecimiento por fallo multiorgánico al día 100 de hospitalización.\n\n**Interpretación Clínica**  \nEste caso ilustra la evolución grave y progresiva de la insuficiencia cardíaca en un paciente con EDMD causada por una mutación en LMNA, destacando la predominancia de la disfunción del ventrículo derecho como factor principal en su deterioro clínico. La resistencia a los tratamientos convencionales y avanzados, como la terapia farmacológica máxima, resincronización cardíaca y soporte mecánico, refleja la complejidad y severidad de la cardiomiopatía asociada a esta enfermedad genética. Los hallazgos histopatológicos post mortem confirmaron la presencia de hipertrofia miocárdica, fibrosis severa en ambos ventrículos y daño hepático compatible con congestión crónica y “hígado de shock”.\n\n**Próximos Pasos y Consideraciones**  \nEste caso subraya la necesidad de un diagnóstico temprano y un seguimiento riguroso en pacientes con EDMD, especialmente aquellos con mutaciones en LMNA, dado el alto riesgo de insuficiencia cardíaca progresiva y muerte súbita. La identificación de disfunción ventricular derecha precoz podría orientar intervenciones más agresivas o la consideración temprana de trasplante cardíaco. Además, se requiere investigación continua para desarrollar terapias específicas que puedan modificar el curso de la cardiomiopatía en EDMD y mejorar la supervivencia y calidad de vida de estos pacientes.",
+                "fh_score": 26.08
+            }
+        }
+    },
+    {
+        "article": "Mujer de 65 años sin antecedentes patológicos destacables que en 2004 inició paroxismos lancinantes en los territorios V2 y V3 derechos, con desencadenantes clásicos, por lo que se le diagnosticó una neuralgia del trigémino derecho. En las resonancias magnéticas cerebrales hasta 2021 no se habían realizado las secuencias que permiten identificar si hay un cruce neurovascular. Desde el inicio, el control del dolor con carboxamidas fue difícil. En 2021 presentó exacerbación de los paroxismos previos que aparecieron en V1. La neuralgia se volvió refractaria, sin respuesta a las carboxamidas y la lamotrigina, y muy escasa al clonacepam, por lo que requirió perfusiones de fenitoína y/o lidocaína en las exacerbaciones graves. Simultáneamente inició paroxismos lancinantes en la parte posterior de la lengua y la pared lateral derecha de la orofaringe, que se exacerbaron con la deglución y que aumentaron progresivamente en intensidad y frecuencia. Se orientó como el inicio de una neuralgia del nervio glosofaríngeo derecho. Se repitió la resonancia magnética cerebral con secuencia CISS (del inglés, constructive interference in steady state), que mostró un contacto arterial significativo entre la arteria cerebelosa superior derecha y el origen del V par craneal derecho, y de la arteria cerebelosa anteroinferior con el origen de los pares craneales bajos derechos. Ante un caso de neuralgia del nervio trigémino y neuralgia del nervio glosofaríngeo clásicas, concomitantes y refractarias, se planteó una doble descompresión microvascular en un tiempo como mejor opción terapéutica.\n\nEn marzo de 2021 se realizó una craniectomía retrosigmoidea derecha con exposición de la cisterna perimesencefálica y las cisternas basales. Se procedió a la liberación del V par craneal, y se apreció un íntimo contacto con la arteria cerebelosa superior en su parte sensitiva y adelgazamiento en la zona de entrada de la raíz nerviosa. Se procedió a la colocación de teflón entre la arteria cerebelosa superior y el V par craneal en todo su trayecto. Posteriormente, se exploró la cisterna basal y se apreció loop vascular de la arteria cerebelosa anteroinferior en íntimo contacto con el IX par craneal, donde se colocó teflón y sellante dural encima. El postoperatorio cursó sin incidencias, con resolución completa de la neuralgia del nervio trigémino y reducción >50% de la intensidad de los paroxismos en el territorio glosofaríngeo. A los dos años continúa sin paroxismos trigeminales y presenta <1 paroxismo/mes de intensidad tolerable en el territorio glosofaríngeo desencadenado con la deglución. El tratamiento farmacológico continúa en pauta descendente sin que ello haya supuesto la reaparición de los paroxismos.",
+        "gold_summary": "Mujer de 65 años con NT derecho (inicialmente en V2-V3) desde 2004 con control regular con carboxamidas. Diecisiete años después empeoraron los paroxismos en V2-V3, aparecieron también en V1 y en el territorio del nervio glosofaríngeo derecho (oído derecho y fosa amigdalar al hablar y deglutir). La resonancia magnética cerebral mostró contacto arterial significativo entre arteria cerebelosa superior (ACS) con origen del V par craneal derecho y de la arteria cerebelosa antero-inferior (AICA) con el origen de pares craneales bajos derechos. Se realizó DMV de ambos pares craneales en un mismo tiempo quirúrgico mediante craniectomía retrosigmoidea, y se procedió a la liberación del V par craneal, en contacto íntimo con la ACS, y del IX par craneal en contacto con la AICA derecha, para lo que se puso teflón entre ellas. La paciente tuvo una resolución inmediata de los paroxismos trigeminales y una mejoría considerable en intensidad y frecuencia de los glosofaríngeos. A los 2 años de la intervención continúa la desescalada de tratamiento neuromodulador con buena respuesta.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había una señora de 65 años que tenía dolor fuerte en la cara desde hace mucho tiempo. El dolor estaba en un lado de su cara y a veces se hacía más fuerte. También empezó a dolerle la garganta y el oído cuando comía o hablaba.\n\nLos doctores le hicieron una foto especial de su cabeza. Vieron que unas partes de su cuerpo, que son como tubitos, estaban tocando nervios que causaban el dolor.\n\nEntonces, los doctores hicieron una operación para poner un pedacito suave entre los tubitos y los nervios. Esto ayudó mucho a que el dolor se fuera.\n\nDespués de la operación, la señora se sintió mucho mejor. El dolor casi no volvió y pudo tomar menos medicina. Está feliz y tranquila.",
+                "fh_score": 82.9
+            },
+            "B2": {
+                "text": "**Lo que le Pasó a la Paciente**  \nUna mujer de 65 años tuvo un dolor muy fuerte y repentino en la cara desde 2004. Este dolor afectaba principalmente dos zonas de su cara, llamadas V2 y V3, que son partes del nervio trigémino, un nervio que ayuda a sentir la cara. A pesar de tomar medicamentos llamados carboxamidas para controlar el dolor, este empeoró después de muchos años. Además, el dolor apareció en otra zona llamada V1 y también en el área de la garganta y oído derecho, que están conectados con otro nervio llamado glosofaríngeo.\n\n**Lo que Encontraron en las Pruebas**  \nSe le hizo una resonancia magnética especial que mostró que dos arterias (vasos sanguíneos) estaban presionando los nervios afectados. Una arteria llamada cerebelosa superior estaba tocando el nervio trigémino, y otra llamada cerebelosa antero-inferior estaba en contacto con el nervio glosofaríngeo. Esta presión puede causar los dolores intensos que ella sentía.\n\n**Qué Hicieron para Ayudarla**  \nLos médicos realizaron una cirugía llamada descompresión microvascular. En esta operación, hicieron una pequeña apertura en el cráneo para llegar a los nervios y separar las arterias que los estaban presionando. Para evitar que las arterias volvieran a tocar los nervios, colocaron un material llamado teflón entre ellos.\n\n**Resultados Después de la Cirugía**  \nDespués de la operación, el dolor en la cara (del nervio trigémino) desapareció completamente. El dolor en la garganta y oído (del nervio glosofaríngeo) mejoró mucho, con menos intensidad y frecuencia. Dos años después, la paciente sigue mejor, con muy pocos episodios de dolor que puede controlar fácilmente y ha podido reducir los medicamentos que tomaba.\n\n**En Resumen**  \nEsta paciente tenía dolores fuertes causados por arterias que presionaban nervios en su cabeza. La cirugía para separar esas arterias de los nervios fue exitosa y mejoró mucho su calidad de vida.",
+                "fh_score": 58.8
+            },
+            "B3": {
+                "text": "**Contexto**  \nSe trata de una mujer de 65 años que desde 2004 presentaba episodios de dolor intenso y punzante en las ramas V2 y V3 del nervio trigémino derecho (que corresponden a zonas de la cara como el maxilar y la mandíbula). Estos episodios, conocidos como neuralgia del trigémino, inicialmente se controlaban con medicamentos llamados carboxamidas. Sin embargo, diecisiete años después, el dolor empeoró, extendiéndose también a la rama V1 (zona de la frente) y aparecieron nuevos episodios dolorosos en el territorio del nervio glosofaríngeo derecho, afectando áreas como el oído y la parte lateral de la garganta, especialmente al hablar y tragar.\n\n**Hallazgos Clave**  \nUna resonancia magnética cerebral con una técnica especial (secuencia CISS) reveló que dos arterias cerebrales —la arteria cerebelosa superior (ACS) y la arteria cerebelosa anteroinferior (AICA)— estaban en contacto directo y presionando los orígenes de los nervios afectados: la ACS sobre el nervio trigémino derecho y la AICA sobre los nervios craneales inferiores, incluido el nervio glosofaríngeo derecho.\n\n**Interpretación Clínica**  \nEsta compresión vascular es una causa conocida de neuralgias craneales, ya que la presión constante puede irritar los nervios y provocar los episodios de dolor intenso. En este caso, la paciente presentaba neuralgia del trigémino y neuralgia del glosofaríngeo simultáneamente, ambas resistentes al tratamiento farmacológico habitual.\n\n**Próximos Pasos y Tratamiento**  \nSe decidió realizar una cirugía llamada descompresión microvascular (DMV) en un solo procedimiento, mediante una craniectomía retrosigmoidea (una apertura quirúrgica en la parte posterior del cráneo). Durante la intervención, se liberaron ambos nervios de la presión arterial colocando pequeñas almohadillas de teflón entre las arterias y los nervios para evitar el contacto directo.  \n\n**Resultados y Seguimiento**  \nLa paciente experimentó una resolución inmediata de los episodios dolorosos relacionados con el nervio trigémino y una reducción significativa en la frecuencia e intensidad del dolor en el territorio del nervio glosofaríngeo. Dos años después de la cirugía, continúa con un tratamiento farmacológico en disminución y mantiene un control satisfactorio del dolor, con episodios muy esporádicos y tolerables en la zona glosofaríngea, especialmente al tragar.\n\nEste caso ilustra la importancia de identificar la compresión vascular en neuralgias craneales refractarias y la eficacia de la descompresión microvascular como tratamiento para mejorar la calidad de vida en pacientes con neuralgia del trigémino y del glosofaríngeo.",
+                "fh_score": 29.7
+            }
+        }
+    },
+    {
+        "article": "Hombre de 36 años, bisexual, en profilaxis antirretroviral de pre-exposición al HIV, sin antecedentes de viaje, que refirió haber asistido a un evento donde tuvo contactos con parejas ocasionales cuya identidad y antecedentes se desconocen. Diez días después comenzó con fiebre, odinofagia y dolor cervical por lo que consultó en varias oportunidades, hasta que a los siete días del inicio de los síntomas se internó por persistencia de los mismos a pesar del tratamiento antibiótico indicado. Al ingreso presentó exudado faríngeo, adenopatías cervicales bilaterales dolorosas y pápulas umbilicadas en escroto y pene y pústulas en cara de cinco días de evolución. Se realizó tomografía computarizada de cuello con contraste endovenoso que descartó colección, ecografía abdominal con leve hepatoesplenomegalia, e inició tratamiento empírico con ceftriaxona y azitromicina. Se tomaron muestras para cultivo, para serologías, y escarificación de dos lesiones de la cara que se enviaron al Laboratorio Nacional de Referencia, INEI-ANLIS Dr. Carlos G. Malbrán, para PCR de punto final para Orthopoxvirus, con resultado DETECTABLE, confirmando así el diagnóstico de viruela símica. La secuenciación arrojó un alto porcentaje de homología con secuencias del clado de África Occidental (MPV-ARG003-2022, Genbank_ID ON800897). Otros diagnósticos diferenciales fueron descartados. El paciente evolucionó con aparición de una úlcera en lengua y nuevas lesiones asincrónicas en glúteos, región perianal, inguinal derecha, umbilical, frontal, cuello, mano derecha y dorso de pie en un total de no más de 25. En el laboratorio se constató un aumento de transaminasas en 2.2 veces el valor normal, sin otros datos significativos.  Por persistencia del dolor cervical se solicitó nueva tomografía computarizada a los 14 días del inicio de los síntomas que evidenció adenomegalias con centro hipodenso de aspecto necrótico, que no requirieron drenaje quirúrgico. Al día 17 se realizó PCR en muestras de exudado de fauces y semen las que también resultaron positivas para virus de viruela símica. Se externó con franca mejoría clínica dos días después. El paciente dio su consentimiento informado escrito para la publicación de este informe de caso y las imágenes que lo acompañan.",
+        "gold_summary": "Se trata de un hombre joven, bisexual, en profilaxis antirretroviral de pre-exposición al HIV, cuya forma de presentación fue faringitis exudativa sin otra etiología documentada y adenopatías que evolucionaron a la necrosis, presencia de lesiones asincrónicas características en cara, cuello, abdomen, extremidades y genitales. El diagnóstico fue por detección de ADN viral por reacción en cadena de la polimerasa en lesiones de piel, exudado de fauces y semen. El compromiso faríngeo con presencia de exudado luego del descarte de otras infecciones, podría ser una rareza para la forma epidémica de la enfermedad. El hallazgo del virus en semen ya reportado en otras publicaciones no es suficiente aún para confirmar la vía sexual como forma de trasmisión.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un hombre joven se enfermó con dolor de garganta y bultos en el cuello. También tuvo manchitas en la cara, cuello, barriga, brazos y partes íntimas. Los doctores encontraron un virus en su piel, en la garganta y en otra parte del cuerpo. Este virus es raro y puede causar estas manchas y dolor. Los doctores no están seguros si el virus se pasa por el contacto en el cuerpo. El hombre mejoró con ayuda de los doctores.",
+                "fh_score": 89.73
+            },
+            "B2": {
+                "text": "**Caso de un Hombre Joven con Viruela Símica**\n\nEste informe habla de un hombre de 36 años que es bisexual y estaba tomando medicamentos para prevenir el VIH antes de enfermarse. Él empezó con dolor de garganta, fiebre y dolor en el cuello. Además, tenía ganglios inflamados y dolorosos en el cuello. También aparecieron pequeñas lesiones en la cara, el pene y el escroto, que son áreas del cuerpo donde se pueden ver bultos o manchas.\n\nPara saber qué tenía, los médicos hicieron varios estudios. Tomaron muestras de las lesiones en la piel y las analizaron con una prueba llamada PCR, que busca el ADN del virus. Encontraron que tenía el virus de la viruela símica, una enfermedad causada por un virus parecido a la viruela común, pero menos grave. También encontraron el virus en la garganta y en el semen del paciente.\n\nDurante su enfermedad, el hombre desarrolló más lesiones en diferentes partes del cuerpo, como los glúteos, la zona alrededor del ano, el cuello y las manos. Además, tuvo un aumento en algunas enzimas del hígado, lo que indica que el virus afectó un poco este órgano. En el cuello, los ganglios inflamados mostraron signos de daño, pero no fue necesario hacer cirugía.\n\nAunque el virus se encontró en el semen, todavía no está claro si la viruela símica se transmite por contacto sexual. El dolor y la inflamación en la garganta con pus (exudado) que tuvo este paciente no es común en los casos que se han visto en la epidemia actual, por lo que es un detalle importante para los médicos.\n\nDespués de recibir tratamiento, el paciente mejoró y pudo salir del hospital. Este caso ayuda a entender mejor cómo puede presentarse la viruela símica y qué síntomas buscar para hacer un diagnóstico correcto.",
+                "fh_score": 71.21
+            },
+            "B3": {
+                "text": "**Contexto**  \nSe presenta el caso de un hombre de 36 años, bisexual, que utiliza profilaxis antirretroviral de pre-exposición (PrEP) para prevenir la infección por VIH. Sin antecedentes de viajes recientes, asistió a un evento donde tuvo contacto con parejas sexuales ocasionales de identidad y antecedentes desconocidos. Diez días después comenzó con fiebre, dolor de garganta (odinofagia) y dolor en el cuello, síntomas que persistieron a pesar de tratamiento antibiótico inicial, lo que motivó su hospitalización.\n\n**Hallazgos Clave**  \nAl ingreso, el paciente mostró inflamación y exudado en la garganta, ganglios linfáticos cervicales inflamados y dolorosos en ambos lados, además de lesiones cutáneas características: pápulas umbilicadas (con un centro hundido) en el escroto y pene, y pústulas en la cara con cinco días de evolución. Se realizaron estudios de imagen, incluyendo tomografía computarizada (TC) de cuello con contraste, que descartó abscesos, y ecografía abdominal que evidenció un leve aumento del tamaño del hígado y bazo (hepatoesplenomegalia). Se inició tratamiento empírico con antibióticos ceftriaxona y azitromicina.\n\nSe tomaron muestras para cultivos, serologías y escarificación (raspado) de lesiones cutáneas, las cuales fueron enviadas a un laboratorio de referencia para realizar una prueba de reacción en cadena de la polimerasa (PCR) específica para Orthopoxvirus, confirmando la presencia de ADN viral de viruela símica (monkeypox). La secuenciación genética mostró alta similitud con cepas del clado de África Occidental, que es menos virulento que otros clados. Se descartaron otras posibles infecciones que podrían explicar los síntomas.\n\nDurante la evolución clínica, aparecieron nuevas lesiones en diferentes partes del cuerpo (glúteos, región perianal, ingle derecha, abdomen, frente, cuello, mano derecha y dorso del pie), sumando un total de aproximadamente 25 lesiones. Además, desarrolló una úlcera en la lengua. En análisis de laboratorio se detectó un aumento moderado de las enzimas hepáticas (transaminasas), sin otros hallazgos relevantes. Debido a la persistencia del dolor cervical, se realizó una nueva TC a los 14 días que mostró ganglios linfáticos agrandados con áreas centrales de necrosis (muerte del tejido), pero sin necesidad de intervención quirúrgica.\n\nAl día 17, se confirmó la presencia del virus mediante PCR en muestras de exudado faríngeo y semen. Dos días después, el paciente fue dado de alta con una mejoría clínica notable.\n\n**Interpretación Clínica**  \nEste caso destaca una presentación atípica de viruela símica en un adulto joven que utiliza profilaxis antirretroviral para VIH. La enfermedad se manifestó inicialmente como una faringitis exudativa (inflamación de la garganta con pus), acompañada de adenopatías cervicales que evolucionaron a necrosis, un cuadro poco común en la epidemia actual. Las lesiones cutáneas asincrónicas (que aparecen en diferentes momentos) en múltiples regiones del cuerpo son características de esta infección.\n\nLa confirmación diagnóstica se realizó mediante detección del ADN viral en las lesiones de piel, así como en muestras de exudado faríngeo y semen. Aunque la presencia del virus en el semen ha sido reportada en otros estudios, todavía no es suficiente para afirmar que la transmisión sexual sea la vía principal de contagio.\n\n**Próximos Pasos**  \nEl seguimiento clínico debe incluir la vigilancia de la evolución de las lesiones y la resolución de la inflamación ganglionar. Es importante continuar investigando las vías de transmisión del virus para mejorar las estrategias de prevención, especialmente en poblaciones con riesgo elevado. Además, este caso resalta la necesidad de considerar la viruela símica en el diagnóstico diferencial de faringitis exudativa persistente en contextos epidemiológicos compatibles.",
+                "fh_score": 42.32
+            }
+        }
+    },
+    {
+        "article": "Paciente de sexo masculino de 23 años, natural de Itagüí - Colombia, antecedente familiar de muerte súbita de etiología no clara en abuelo a los 50 años, sin otros antecedentes familiares o personales de importancia. Venía en seguimiento externo por episodios sincopales a repetición con diagnóstico desde la infancia de disfunción del nodo sinusal sintomática por lo que se le implantó un marcapaso.\n\nDurante controles posteriores no hay reporte de deterioro de clase funcional hasta el año 2012 en Guayaquil-Ecuador. Durante su hospitalización se realiza el cambio de generador; en el primer mes postoperatorio presenta como complicación temprana una infección de bolsillo de marcapaso por lo que requirió el explante de la unidad generadora con posterior abandono de electrodo ventricular previamente implantado. Se realiza un nuevo implante de marcapaso en el lado contralateral sin complicaciones ni registro de nuevos eventos sincopales en los siguientes 10 años de seguimiento.\n\nSeis meses antes del ingreso presentaba deterioro de clase funcional NYHA III, sin otros síntomas y sin reportes de evaluaciones por servicio de electrofisiología desde el último implante de generador de marcapaso en 2012. Durante controles ambulatorios se reportó la suspensión del tratamiento con beta bloqueador debido a la pobre tolerancia.\n\nAl examen físico se encontró soplo sistólico en foco aórtico II/VI sin irradiación, no presentó signos de congestión central o periférica. Dentro de los laboratorios no se evidenció alteración en función renal, electrolítica ni del perfil hematológico. Se programó el marcapaso con evidencia de agotamiento de la batería de generador. Se realizó un ecocardiograma transtorácico donde se encontró hipertrofia concéntrica severa del septum interventricular a nivel medio ventricular, de 26 mm con gradiente intracavitario pico de 117 mmHg y movimiento sistólico anterior del velo mitral (SAM) el cual generaba una regurgitación mitral leve.\n\nFue evaluado por Heart Team, debido al score de riesgo de muerte súbita (16,8%) además de tener antecedentes familiares de muerte súbita considerando EUROSCORE II 0,67%; en cuanto a los electrodos abandonados previamente y la contraindicación de realización de resonancia magnética cardiaca, dado a la incompatibilidad del marcapaso, se realiza un estudio tomográfico y se consideró la realización de miectomía por sintomatología y variante documentada.\n\nFue programado para realización de miectomía medio ventricular por abordaje transapical con retiro de electrodos; se realizó la ventriculotomía izquierda en el ápex, con posterior resección del septum desde el parte medio ventricular hasta la base, con posterior retiro de electrodos adheridos a velo septal tricúspideo. No hubo complicaciones intraoperatorias y posteriormente se presentó disminución del gradiente intracavitario sin presencia del fenómeno SAM. Durante su estancia en Unidad de Cuidados Intensivos el paciente cursó con dos episodios documentados de taquicardia ventricular con inestabilidad hemodinámica por lo cual se le colocó un cardiodesfibrilador implantable (CDI) compatible con resonancia magnética (MRI) ST Jude sin presentar nuevos episodios de TV. El paciente cursó sin nuevas intercurrencias y se iniciaron los estudios ambulatorios de estudio genético debido a sus antecedente familiares.\n\nEl paciente presentó una evolución posoperatoria favorable luego del implante de CDI. En los estudios genéticos se encontró una variante, probablemente patogénica, en heterocigosis del FLNC, c 4636G>A consistente con miocardiopatía familiar hipertrófica tipo 26 autosómica dominante.\n\nActualmente, el paciente se encuentra en clase funcional I, sin arritmias evidenciadas en la telemetría y en tratamiento regular con Bisoprolol 5 mg. Se inició ampliación de estudio genético a familiares directos, sin embargo, debido al difícil acceso a servicios de salud su ejecución fue limitada.",
+        "gold_summary": "A continuación, se presenta el caso de un paciente sexo masculino de 23 años con diagnóstico de cardiomiopatía hipertrófica variante medio apical, en quien se documenta variante de la filamina C, ante la inadecuada respuesta y persistencia de sintomatología frente al manejo médico, se realizó el procedimiento de miectomía con abordaje transapical, con posterior mejoría de sintomatología clínica y obstrucción al tracto de salida.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un joven de 23 años tenía un problema en su corazón. Su corazón era más grueso en una parte. Esto le hacía sentir mal y cansado.\n\nLos doctores le hicieron una operación para quitar un poco de ese corazón grueso. Después de la operación, se sintió mejor y su corazón pudo trabajar mejor.",
+                "fh_score": 85.08
+            },
+            "B2": {
+                "text": "**Caso de un joven con problema en el corazón**\n\nEste es el caso de un joven de 23 años que tiene una enfermedad llamada cardiomiopatía hipertrófica. Esto significa que una parte de su corazón, especialmente en la zona media y hacia el ápice (la punta), está más gruesa de lo normal. Esta enfermedad puede dificultar que la sangre salga bien del corazón.\n\n**Qué encontraron en sus genes**\n\nAl hacerle un estudio genético, descubrieron que tiene un cambio en un gen llamado filamina C. Este cambio puede causar problemas en el corazón y es una forma hereditaria de la enfermedad.\n\n**Tratamiento y resultados**\n\nEl joven no mejoraba con los medicamentos que le daban, así que los doctores decidieron hacer una cirugía llamada miectomía. En esta operación, quitaron parte del músculo grueso del corazón para que la sangre pueda salir mejor. La cirugía se hizo por la punta del corazón (abordaje transapical).\n\nDespués de la operación, el paciente mejoró mucho. Su corazón ya no tenía tanta obstrucción y sus síntomas disminuyeron. Actualmente, está en buen estado y sigue un tratamiento con medicamentos para cuidar su corazón.",
+                "fh_score": 66.84
+            },
+            "B3": {
+                "text": "**Contexto**  \nSe trata de un paciente masculino de 23 años, originario de Itagüí, Colombia, con antecedentes familiares relevantes de muerte súbita en su abuelo a los 50 años, sin otras enfermedades familiares o personales significativas. Desde la infancia, el paciente presentaba episodios repetidos de síncope (pérdida temporal del conocimiento) atribuibles a una disfunción del nodo sinusal (una alteración en el sistema eléctrico del corazón), por lo que se le implantó un marcapasos. Durante años, su condición se mantuvo estable hasta que en 2012, en Guayaquil, Ecuador, presentó una infección relacionada con el marcapasos que requirió la extracción del generador y el implante de uno nuevo en el lado opuesto, sin complicaciones posteriores ni nuevos episodios de síncope durante una década.\n\nSeis meses antes del ingreso actual, el paciente comenzó a mostrar un deterioro en su capacidad funcional (clasificación NYHA III, que indica limitación marcada en la actividad física), aunque sin otros síntomas adicionales. Se suspendió el tratamiento con betabloqueadores debido a mala tolerancia. En el examen físico se detectó un soplo cardíaco leve, sin signos de insuficiencia cardíaca. Los análisis de laboratorio fueron normales. El marcapasos mostró agotamiento de la batería, y el ecocardiograma reveló una hipertrofia severa y concéntrica del septum interventricular (pared que separa las cámaras del corazón), con un grosor de 26 mm y un gradiente de presión muy alto (117 mmHg) dentro del ventrículo, además de un movimiento anormal del velo mitral que causaba una regurgitación leve (retorno de sangre hacia la aurícula).\n\n**Hallazgos Clave**  \n- Hipertrofia severa del septum interventricular medio ventricular con obstrucción significativa al flujo sanguíneo dentro del ventrículo izquierdo.  \n- Movimiento sistólico anterior del velo mitral (SAM), que contribuye a la obstrucción y regurgitación mitral leve.  \n- Antecedentes familiares de muerte súbita y un riesgo calculado de muerte súbita del 16,8%, lo que indica un riesgo elevado.  \n- Imposibilidad de realizar resonancia magnética cardíaca debido a la incompatibilidad con el marcapasos y la presencia de electrodos abandonados.  \n- Confirmación genética de una variante probablemente patogénica en el gen FLNC (filamina C), asociada a miocardiopatía hipertrófica familiar tipo 26, que se hereda de forma autosómica dominante.\n\n**Interpretación Clínica**  \nEl paciente presenta una forma de miocardiopatía hipertrófica con predominio medio apical, caracterizada por un engrosamiento anormal del músculo cardíaco que obstruye el flujo de salida del ventrículo izquierdo y genera síntomas significativos. La variante genética encontrada en filamina C explica la naturaleza hereditaria y progresiva de su enfermedad. La persistencia de síntomas y la obstrucción significativa a pesar del tratamiento médico justificaron la realización de una miectomía medio ventricular (cirugía para remover parte del músculo engrosado), realizada mediante un abordaje transapical (a través del ápex del corazón). La cirugía fue exitosa, con reducción del gradiente de presión y desaparición del movimiento anormal del velo mitral.\n\nPosteriormente, el paciente presentó episodios de taquicardia ventricular (arritmias peligrosas) que requirieron la implantación de un cardiodesfibrilador implantable (CDI) compatible con resonancia magnética, para prevenir muerte súbita. Tras el implante, no se registraron nuevos episodios arrítmicos y el paciente evolucionó favorablemente.\n\n**Próximos Pasos**  \nActualmente, el paciente se encuentra en clase funcional I (sin limitaciones en la actividad física), sin arritmias detectadas en monitoreo continuo, y en tratamiento con bisoprolol (un betabloqueador) a dosis de 5 mg. Se ha iniciado un estudio genético ampliado en familiares directos para identificar portadores de la variante genética, aunque el acceso limitado a servicios de salud ha dificultado la realización completa de este estudio. El seguimiento continuo y la evaluación genética son fundamentales para el manejo integral del paciente y su familia, con el fin de prevenir complicaciones graves como la muerte súbita.",
+                "fh_score": 34.75
+            }
+        }
+    },
+    {
+        "article": "Varón de 32 años, con antecedentes de infección por VIH en terapia anti-retroviral (carga viral indetectable y recuento de CD4 de 454 céls/mm3) y consumo de tabaco y drogas (marihuana, éxtasis y ketamina). Consultó en nuestra unidad de salud sexual por una historia de dos semanas de secreción uretral de aspecto mucoso con escaso ardor local, asociado a una úlcera eritematosa indurada en el surco balanoprepucial de 1,5 cm de diámetro, dolorosa y exudativa. Al examen físico presentaba una adenopatía inguinal izquierda de 2 cm, sensible a palpación, blanda, no adherida a planos profundos ni asociada a signos inflamatorios cutáneos. No presentaba fiebre ni otros síntomas asociados. En la anamnesis dirigida, refirió 20 parejas sexuales hombres en el último año, con relaciones sexuales orales y anales insertivas y receptivas, con uso ocasional de preservativo. No tenía antecedente de viajes fuera de Chile. Cuatro semanas antes del inicio de los síntomas, había tenido un contacto sexual de riesgo sin preservativo con una pareja contactada mediante una aplicación de telefonía móvil. Con el diagnóstico presuntivo de una sífilis primaria y uretritis en estudio, se tomaron muestras de sangre y secreción uretral para estudio microbiológico. Por la conducta sexual de alto riesgo, se tomó también un hisopado anorrectal para tinción de Gram y cultivo. De acuerdo con la norma vigente en Chile, se administraron tres dosis de 2,4 millones de UI de penicilina benzatina intramuscular separadas por una semana, además de 250 mg de ceftriaxona intramuscular y 1 g de azitromicina oral, ambas por una vez. El estudio de laboratorio confirmó el diagnóstico de sífilis, con un VDRL (Venereal disease research laboratory) reactivo con dilución de 1:2 y MHA-TP (Microhemagglutination assay for antibody to Treponema pallidum) reactivo. La tinción de Gram y los cultivos de secreción uretral (agar sangre y Thayer Martin) fueron negativos. La muestra anorrectal mostró escasos diplococos gramnegativos en la tinción de Gram, con desarrollo abundante de N. meningitidis y microbiota comensal en el cultivo corriente. La identificación bacteriana se realizó a través de espectrometría de masas MALDI-TOF MS. El paciente evolucionó favorablemente, sin secreción uretral y con regresión de la lesión ulcerada genital y la adenopatía inguinal a las dos semanas de seguimiento. Las tinciones de Gram y los cultivos de control de secreción uretral, faríngea y anorrectal resultaron negativos. Se citó al contacto sexual reciente para estudio y tratamiento. Sin embargo, éste se encontraba asintomático y los cultivos faríngeo, anorrectal y uretral realizados fueron negativos.",
+        "gold_summary": "Presentamos el caso de un HSH con infección por VIH, que consultó por un cuadro de uretritis y sifilis primaria, en el cual se aisló N. meningitidis en una muestra anorectal. Fue tratado en forma empírica con ceftriaxona y azitromicina, realizándose un cultivo de control post-tratamiento que fue negativo.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un hombre con VIH tenía una herida y dolor al orinar. Los doctores encontraron una bacteria en su cuerpo. Le dieron medicinas para curarlo. Después, la bacteria ya no estaba. Él mejoró mucho.",
+                "fh_score": 81.93
+            },
+            "B2": {
+                "text": "Caso de un hombre de 32 años con VIH que tuvo una infección en la uretra y una úlcera en el pene. Los médicos encontraron que tenía sífilis primaria, que es una infección de transmisión sexual. Además, en una muestra tomada del ano, detectaron una bacteria llamada Neisseria meningitidis, que normalmente no causa infecciones en esa zona. \n\nEl paciente recibió tratamiento con antibióticos llamados ceftriaxona y azitromicina para combatir las infecciones. Después del tratamiento, se hicieron pruebas de control y no encontraron más bacterias en las muestras tomadas de la uretra, la garganta y el ano. El paciente mejoró bien y la lesión en el pene y la inflamación en la ingle desaparecieron en dos semanas. \n\nEste caso muestra la importancia de revisar diferentes áreas del cuerpo en personas con conductas sexuales de riesgo y de usar tratamientos adecuados para varias posibles infecciones.",
+                "fh_score": 59.71
+            },
+            "B3": {
+                "text": "**Contexto**  \nSe trata de un hombre de 32 años que vive con infección por VIH controlada mediante tratamiento antirretroviral, con carga viral indetectable y un recuento adecuado de células CD4. Además, tiene antecedentes de consumo de tabaco y drogas recreativas. Consultó en una unidad de salud sexual debido a una secreción mucosa por la uretra y una úlcera dolorosa en el pene, acompañadas de inflamación en los ganglios linfáticos inguinales del lado izquierdo. No presentaba fiebre ni otros síntomas sistémicos. En la entrevista, refirió múltiples parejas sexuales masculinas en el último año, con prácticas sexuales orales y anales, y uso irregular de preservativos. Cuatro semanas antes, tuvo una relación sexual sin protección con una persona conocida a través de una aplicación móvil.\n\n**Hallazgos Clave**  \nSe sospechó inicialmente una sífilis primaria y una uretritis de origen incierto. Se tomaron muestras de sangre y secreción uretral para análisis microbiológicos, así como un hisopado anorrectal debido al alto riesgo sexual. El diagnóstico serológico confirmó sífilis, con pruebas VDRL y MHA-TP positivas. Los cultivos de secreción uretral fueron negativos para bacterias comunes causantes de uretritis. Sin embargo, en la muestra anorrectal se identificó la presencia de Neisseria meningitidis (una bacteria que normalmente habita en la garganta y que en este caso se encontró en el recto), confirmada mediante espectrometría de masas MALDI-TOF MS.  \n\n**Interpretación Clínica**  \nEl paciente fue tratado empíricamente con penicilina benzatina para la sífilis, además de una dosis única de ceftriaxona y azitromicina para cubrir posibles infecciones bacterianas de transmisión sexual. La detección de N. meningitidis en la muestra anorrectal es relevante, ya que esta bacteria no es un patógeno típico en uretritis, pero puede colonizar el tracto genital o anal, especialmente en personas con conductas sexuales de riesgo. El tratamiento fue efectivo, ya que a las dos semanas el paciente mostró resolución de la secreción uretral, cicatrización de la úlcera y desaparición de la inflamación ganglionar. Los cultivos posteriores fueron negativos, confirmando la erradicación de las infecciones.  \n\n**Próximos Pasos**  \nSe realizó el estudio y tratamiento del contacto sexual reciente para prevenir la transmisión y reinfección, aunque este contacto no presentó síntomas ni cultivos positivos. Este caso subraya la importancia de considerar agentes menos comunes como N. meningitidis en infecciones del tracto genital y anorrectal en personas con alto riesgo sexual, y la necesidad de un abordaje diagnóstico y terapéutico integral en estos pacientes.",
+                "fh_score": 46.35
+            }
+        }
+    },
+    {
+        "article": "Un paciente hispanoparlante de 63 años de edad se presentó en el hospital como una emergencia con inicio repentino de dificultad respiratoria severa, palpitaciones y sudoración profusa. Estaba en su estado habitual de salud y podía deambular con actividades independientes de la vida diaria hasta 30 minutos antes de su llegada a la sala de urgencias. Tenía un historial de 20 años de hipertensión, un historial de 15 años de diabetes mellitus, enfermedad de la arteria coronaria que requería la inserción de un stent de la arteria coronaria cinco años antes, un historial de diez años de insuficiencia cardiaca de la clase II de la New York Heart Association (NYHA) con una fracción de eyección reducida (EF) del 35 %, enfermedad renal crónica (CKD) en estadio 3B. Al ingresar en el hospital, sus medicamentos incluían carvedilol (25 mg dos veces al día), lisinopril (20 mg diario), espironolactona (25 mg diario), furosemida (20 mg diario), insulina glargina (20 unidades al acostarse), inyección de insulina lispro (7 unidades tres veces al día), atorvastatina (40 mg diario), y aspirina (81 mg diario), sin alergias a medicamentos conocidas.\n\nAl examen, su presión arterial era de 205/110 mmHg, su frecuencia respiratoria de 29 respiraciones/min, su frecuencia cardíaca de 118 latidos/min, la oximetría de pulso era de 82% (en aire ambiente) y su temperatura de 36.2°C. Su peso era de 72 kg y su estatura de 68 pulgadas, lo que resultó en un índice de masa corporal (IMC) de 24.13 kg/m2. Al examen físico, el paciente estaba en grave dificultad respiratoria, sudaba y no podía hablar con claridad. Su presión venosa yugular era elevada, como se muestra por la distensión de la vena yugular (3+). Al auscultar el tórax, se observaron crepitaciones bilaterales en todos los campos pulmonares. La auscultación cardíaca fue notable por un galope con una frecuencia regular y un murmullo sistólico 3/6 que se oía en la línea medioclavicular izquierda, al nivel del quinto espacio intercostal. El punto de impulso cardíaco máximo se desplazó hacia la izquierda (en la línea medioaxilar anterior) y no se observó distensión abdominal ni ascitis, con edema de los miembros inferiores (1+) hasta el nivel de la mitad de la pantorrilla.\n\nEl paciente fue trasladado a la zona de reanimación cardiopulmonar (RCP), donde se midieron los gases sanguíneos en el aire y se solicitaron pruebas de laboratorio. El paciente fue tratado con oxígeno al 100% utilizando una máscara no reanadora y se le colocó en posición de 90°, lo que produjo una mejora en la oximetría de pulso, que aumentó hasta el 90%. Un electrocardiograma (ECG) mostró taquicardia sinusal, depresión del ST del conductor lateral (de 1 mV), desviación del eje izquierdo e hipertrofia del ventrículo izquierdo. Se obtuvo una radiografía de tórax portátil que fue notable por una silueta cardiaca agrandada, señal de asta de ciervo de desviación venosa pulmonar del lóbulo superior (cefalización), y líneas B de Kerley, que indican edema intersticial.\n\nAunque se solicitaron pruebas de laboratorio, debido a que el paciente estaba gravemente enfermo y no se podía demorar el tratamiento, se inició un tratamiento inicial basado en los hallazgos clínicos, el historial clínico, el ECG, los gases arteriales en sangre y los hallazgos de rayos X. En vista de los hallazgos de las investigaciones iniciales y la ausencia de fiebre, se descartó la neumonía y se realizó un diagnóstico de edema pulmonar cardiogénico hipertensivo. Se inició un tratamiento intravenoso (IV) con nitroglicerina, comenzando a 30 mcg/min y aumentando en 15 mcg/min cada 3 minutos, con oximetría de pulso continua y monitoreo de los signos vitales cada 3 minutos. Después de 18 minutos, se tituló la nitroglicerina hasta 120 mcg/min y su presión arterial disminuyó a 148/82 mmHg, su presión arterial sistólica se redujo en un 29%, su presión arterial diastólica se redujo en un 25%, y su frecuencia cardíaca disminuyó a 87 latidos por minuto. Se hizo una rápida mejora clínica y el paciente pudo comunicarse con oraciones completas y pudo respirar sin el uso de músculos accesorios. La oximetría de pulso mostró una saturación de oxígeno >97%, y la suplementación de oxígeno continuó con el uso de una cánula nasal a 3 L/min y la medición de la oximetría de pulso del paciente fue >96%.\n\nDespués de 25 minutos, el paciente fue tratado con enalapril (2,5 mg IV) combinado con furosemida (20 mg IV). La nitroglicerina se redujo a una tasa de 10 mcg/min cada 5 minutos hasta que se interrumpió, seguido de una dosis oral de isosorbida dinitrato (30 mg). Después de la estabilización clínica completa, los resultados de los laboratorios mostraron un recuento de glóbulos blancos (WBC) de 11,43 × 109/uL, hemoglobina de 10,9 g/dl, hematocrito de 31,8%, plaquetas de 74 × 109/L, sodio de 144 mmol/L, potasio de 3,9 mmol/L, cloruro de 107 mmol/L, dióxido de carbono (CO2) de 25 mmol/L, nitrógeno ureico en sangre (BUN) de 27 mg/dL, creatinina de 1,4 mg/dL, péptido natriurético cerebral (BNP) de 3,452 pg/ml, y troponina I <0,05 ng/ml. Las mediciones de gases en sangre en aire incluyeron pH de 7,381, pCO2 de 44,8 mmHg, pO2 de 57 mmHg, HCO3 de 25,8 mmol/L, y saturación de oxígeno de 84%.\n\nSe evaluó al paciente para detectar la presencia de una posible embolia pulmonar (EP) subyacente, utilizando los criterios de estratificación de riesgo de EP de Wells, y se lo estratificó como de bajo riesgo, con una evaluación posterior con un nivel de dímero D de 340 ng/ml, que se interpretó como negativo. La evaluación para detectar hipertiroidismo mostró un valor normal de la medición ultrasensible del ensayo de la hormona estimulante de la tiroides en plasma (usTSH) de 2,56 μU/mL y tiroxina libre (T4) de 6,87 μU/mL.\n\nEl paciente fue admitido en la sala de hospital de medicina interna con un diagnóstico de edema pulmonar cardiogénico hipertensivo y fue dado de alta 48 horas después. Al momento del alta hospitalaria, su medicación incluía furosemida (40 mg diarios), carvedilol (12.5 mg dos veces al día), sacubitril/valsartan (24 mg/26 mg dos veces al día), espironolactona (25 mg diarios) e isosorbida mononitrato (60 mg diarios). El paciente fue sometido a seguimiento semanal por su cardiólogo, quien optimizó la terapia medicinal. No se registraron visitas a urgencias ni hospitalizaciones, al menos durante los siguientes 60 días.\n\nMH - Insuficiencia cardiaca/*complicaciones\nMH - Humanos\nMH - Hipertensión/*complicaciones\nMH - Infusiones, intravenosas\nMH - Hombre\nMH - Edad Media\nMH - Nitroglicerina/*administración y dosificación\nMH - Edema pulmonar/*terapia farmacológica/etiología\nMH - Insuficiencia respiratoria/*terapia farmacológica/etiología\nMH - Agentes vasodilatadores/*administración y dosificación\n",
+        "gold_summary": "Paciente: Hombre, 63 años\n\nDiagnóstico final: Edema pulmonar cardiovenoso hipertensivo\n\nSíntomas: falta de aire\n\nMedicación: —\n\nProcedimiento clínico: —\n\nEspecialidad: Medicina general e interna\n\nUn hombre hispano de 63 años con antecedentes de hipertensión, enfermedad de las arterias coronarias, insuficiencia cardiaca con una fracción de eyección reducida del 35 %, enfermedad renal crónica (ERC) y diabetes mellitus, se presentó como una emergencia con disnea aguda y grave. El paciente fue tratado inicialmente con 100 % de oxígeno suplementario y nitroglicerina intravenosa (IV) en dosis altas (30 mcg/min), que se ajustó cada 3 minutos, aumentando en 15 mcg/min hasta que se alcanzó una dosis de 120 mcg/min. Después de 18 minutos de terapia agresiva, la condición del paciente mejoró y ya no necesitaba ventilación mecánica.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había un hombre de 63 años que se sentía muy mal. Le costaba mucho respirar y estaba muy cansado. Tenía problemas en el corazón y en los riñones desde hace tiempo.\n\nCuando llegó al hospital, le dieron aire con una máscara para ayudarlo a respirar mejor. También le pusieron un medicamento por la vena para que su corazón y su cuerpo se sintieran mejor.\n\nDespués de un rato, el hombre empezó a respirar mejor y se sintió más tranquilo. Los doctores cuidaron mucho de él y lo ayudaron a mejorar.",
+                "fh_score": 83.73
+            },
+            "B2": {
+                "text": "**Caso de un Hombre de 63 Años con Problemas del Corazón y Dificultad para Respirar**\n\n**Lo que Pasó:**  \nUn hombre de 63 años, que hablaba español y tenía varias enfermedades como presión alta (hipertensión), diabetes, problemas en las arterias del corazón y una enfermedad llamada insuficiencia cardíaca (que significa que su corazón no bombeaba bien la sangre), llegó al hospital muy enfermo. De repente, empezó a tener mucha dificultad para respirar, su corazón latía rápido y sudaba mucho. Antes de esto, estaba bien y podía hacer sus actividades normales.\n\n**Lo que Encontraron:**  \nAl examinarlo, su presión arterial estaba muy alta y tenía signos claros de que su corazón estaba trabajando mal. También tenía líquido en los pulmones, lo que se llama edema pulmonar, y eso dificultaba que el oxígeno llegara a su cuerpo. Las pruebas mostraron que su corazón estaba agrandado y que había problemas en la circulación de la sangre en sus pulmones.\n\n**Qué Hicieron para Ayudarlo:**  \nLe dieron oxígeno puro para que pudiera respirar mejor y empezaron a darle un medicamento llamado nitroglicerina por vía intravenosa (directamente en la vena). La nitroglicerina ayuda a bajar la presión arterial y a que el corazón trabaje menos. Comenzaron con una dosis baja y la aumentaron poco a poco cada pocos minutos. Después de 18 minutos, el paciente mejoró mucho: su presión bajó, su corazón latía más despacio y pudo respirar sin tanta dificultad. Ya no necesitó una máquina para ayudarlo a respirar.\n\n**Después del Tratamiento:**  \nLuego le dieron otros medicamentos para el corazón y para eliminar el exceso de líquido. El paciente se quedó en el hospital dos días y después pudo irse a casa. Continuó con controles médicos semanales y no volvió a tener problemas graves en los siguientes dos meses.\n\n**Resumen:**  \nEste caso muestra cómo un hombre con varias enfermedades del corazón y otros problemas puede sufrir una emergencia grave llamada edema pulmonar, que es cuando se acumula líquido en los pulmones por problemas del corazón. Con un tratamiento rápido y adecuado, que incluye oxígeno y medicamentos para bajar la presión y ayudar al corazón, el paciente pudo recuperarse sin complicaciones mayores.",
+                "fh_score": 57.49
+            },
+            "B3": {
+                "text": "**Contexto**  \nUn hombre hispanoparlante de 63 años con antecedentes médicos complejos, incluyendo hipertensión arterial de larga evolución, diabetes mellitus, enfermedad coronaria con colocación previa de stent, insuficiencia cardíaca crónica con función del corazón reducida (fracción de eyección del 35 %) y enfermedad renal crónica en estadio avanzado, acudió al hospital en estado de emergencia debido a un inicio súbito de dificultad respiratoria severa, palpitaciones y sudoración intensa. Hasta poco antes de su ingreso, el paciente se encontraba en su estado habitual de salud y realizaba actividades cotidianas de forma independiente.\n\n**Hallazgos Clave**  \nAl examen físico, el paciente presentaba signos evidentes de insuficiencia cardíaca descompensada: presión arterial muy elevada (205/110 mmHg), frecuencia cardíaca rápida (118 latidos por minuto), dificultad respiratoria grave con saturación de oxígeno baja (82 % en aire ambiente), distensión venosa yugular marcada, crepitaciones pulmonares bilaterales, y un galope cardíaco junto con un soplo sistólico. La radiografía de tórax mostró cardiomegalia (aumento del tamaño del corazón), signos de congestión pulmonar y edema intersticial, confirmando la sospecha clínica de edema pulmonar cardiogénico hipertensivo. El electrocardiograma evidenció taquicardia sinusal, hipertrofia ventricular izquierda y cambios isquémicos.\n\nLos análisis de laboratorio posteriores revelaron un péptido natriurético cerebral (BNP) muy elevado (3,452 pg/ml), indicador de insuficiencia cardíaca descompensada, y una troponina normal, descartando daño cardíaco agudo. Se descartaron otras causas de dificultad respiratoria aguda, como embolia pulmonar e infecciones pulmonares, mediante pruebas específicas y criterios clínicos.\n\n**Interpretación Clínica**  \nEl cuadro clínico y los estudios complementarios fueron consistentes con un episodio agudo de edema pulmonar cardiogénico hipertensivo, una condición en la que la presión arterial muy alta y la insuficiencia cardíaca provocan acumulación rápida de líquido en los pulmones, dificultando la respiración. La rápida identificación y tratamiento de esta emergencia fueron cruciales para evitar complicaciones mayores.\n\n**Tratamiento y Evolución**  \nEl manejo inicial incluyó la administración de oxígeno al 100 % mediante máscara no reanimadora y la colocación del paciente en posición sentada para facilitar la respiración. Se inició tratamiento intravenoso con nitroglicerina, un vasodilatador que reduce la presión arterial y la carga sobre el corazón, comenzando con una dosis de 30 microgramos por minuto y aumentando progresivamente hasta 120 microgramos por minuto en 18 minutos. Esta terapia permitió una reducción significativa de la presión arterial y de la frecuencia cardíaca, con una mejora clínica rápida: el paciente pudo respirar sin dificultad y comunicarse con normalidad, y su saturación de oxígeno superó el 97 % con oxígeno suplementario.\n\nPosteriormente, se administraron enalapril (un inhibidor de la enzima convertidora de angiotensina) y furosemida (un diurético) por vía intravenosa para continuar el control de la presión arterial y eliminar el exceso de líquido. La nitroglicerina se fue disminuyendo hasta suspenderla, y se inició tratamiento oral con isosorbida dinitrato para mantener la vasodilatación.\n\nEl paciente fue hospitalizado en la unidad de medicina interna, donde se ajustó su tratamiento con medicamentos para insuficiencia cardíaca, incluyendo furosemida, carvedilol (un betabloqueador), sacubitril/valsartán (un inhibidor de la neprilisina combinado con un bloqueador del receptor de angiotensina), espironolactona (un antagonista de la aldosterona) e isosorbida mononitrato. Tras 48 horas de hospitalización, se dio de alta en condiciones estables y con seguimiento cardiológico programado.\n\n**Próximos Pasos y Seguimiento**  \nDurante al menos 60 días posteriores al alta, el paciente no requirió nuevas hospitalizaciones ni visitas a urgencias, lo que indica una adecuada respuesta al tratamiento y control de su enfermedad cardíaca. El seguimiento semanal con su cardiólogo permitió optimizar la terapia médica para prevenir futuras descompensaciones.\n\n---\n\nEste caso ilustra la importancia de un diagnóstico rápido y un manejo agresivo en pacientes con edema pulmonar cardiogénico hipertensivo, especialmente en aquellos con múltiples comorbilidades cardiovasculares y renales, para mejorar la supervivencia y la calidad de vida.",
+                "fh_score": 20.06
+            }
+        }
+    },
+    {
+        "article": "Historial clínico\nUn niño de 12 años se presentó en nuestro hospital con un mes de historia de sensación de cuerpo extraño y una masa conjuntival pedunculada carnosa que creció con el tiempo. No había historia de trauma o lesiones similares en el otro lado del cuerpo. Se descubrió una masa pedunculada carnosa rosácea de 15 mm de la conjuntiva palpebral derecha durante un examen oftalmológico. La agudeza visual estaba dentro de los límites normales. Se diagnosticó al niño como papiloma de células escamosas pedunculadas y se le realizó una biopsia excisional de la lesión.\n\nHallazgos macroscópicos y microscópicos\nRecibimos un fragmento de tejido blanco grisáceo, pequeño, firme, ovoide, fijado en formalina, de 1,5 x 1 cm, para su análisis patológico. En las secciones microscópicas se encontró una lesión poliopóidea hiperplásica con múltiples quistes globulares en la submucosa conjuntival, junto con una importante infiltración inflamatoria constituida por linfocitos, células plasmáticas y neutrófilos, así como enormes esporangios de paredes gruesas con numerosas endosporas. Las endosporas se liberaron después de que algunos de los esporangios maduros se rompieran. La rinosporidiosis conjuntival se diagnosticó histopatológicamente. No hubo recurrencia ni signo de rinosporidiosis en el ojo ni en ninguna otra área del cuerpo en el último examen del paciente, que fue 7 meses después de la escisión quirúrgica.\n",
+        "gold_summary": "Un niño de 12 años con una masa conjuntival pedunculada carnosa fue llevado al Centro Médico de la Universidad de Jimma con un historial de un mes de sensación de cuerpo extraño. Al paciente se le diagnosticó un papiloma pedunculado de células escamosas y se le realizó una biopsia excisional de la lesión. Se encontró que la masa era una lesión polipoide hiperplásica con numerosos quistes globulares dentro de la submucosa conjuntival, rodeados por un infiltrado inflamatorio pesado de linfocitos, células plasmáticas y neutrófilos, así como grandes esporas de paredes gruesas con numerosas endosporas en secciones microscópicas. Se diagnosticó histopatológicamente rinosporidiosis conjuntival.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un niño tenía una bolita en el ojo que le molestaba. Los doctores le quitaron la bolita para verla mejor. \n\nAl mirar la bolita con un microscopio, vieron que tenía muchas cositas pequeñas dentro. Estas cositas eran como unas semillas que no son buenas. \n\nLos doctores dijeron que el niño tenía una infección en el ojo llamada rinosporidiosis. Después de quitar la bolita, el niño estuvo bien y no volvió a tener problema.",
+                "fh_score": 77.72
+            },
+            "B2": {
+                "text": "**Lo que pasó con el niño**  \nUn niño de 12 años tenía una sensación rara en el ojo y una masa blanda y rosada que crecía en la parte interna del párpado derecho. No había sufrido golpes ni tenía problemas similares en el otro ojo. Cuando lo revisaron, su vista estaba normal, pero encontraron esta masa que parecía un papiloma, que es un tipo de bulto benigno hecho de células de la piel.\n\n**Qué hicieron los médicos**  \nLe quitaron la masa para analizarla mejor. Esto se llama biopsia, que es cuando se saca un pedacito de tejido para estudiar qué es exactamente. En el laboratorio, vieron que la masa tenía muchas células inflamatorias, que son células que el cuerpo usa para defenderse cuando hay una infección o irritación. También encontraron estructuras llamadas esporangios, que son como pequeñas bolsas con esporas dentro. Las esporas son formas de reproducción de ciertos microorganismos.\n\n**Qué significa el diagnóstico**  \nEl análisis mostró que el niño tenía rinosporidiosis conjuntival, que es una infección causada por un microorganismo que forma esas esporas. Esta infección afecta la conjuntiva, que es la membrana que cubre el ojo y el interior del párpado. Después de quitar la masa, el niño no tuvo problemas ni volvió a tener la infección en el ojo ni en otras partes del cuerpo durante al menos siete meses.\n\n**En resumen**  \nEl niño tenía una infección poco común en el ojo que causó una masa. Gracias a la biopsia, los médicos pudieron identificar la infección y tratarla con cirugía, evitando que regresara.",
+                "fh_score": 67.22
+            },
+            "B3": {
+                "text": "**Contexto**  \nUn niño de 12 años acudió al hospital tras presentar durante un mes una sensación persistente de cuerpo extraño en el ojo derecho, acompañada de una masa carnosa y pedunculada (con un tallo que la une a la superficie) en la conjuntiva palpebral (la membrana que recubre el párpado). No había antecedentes de trauma ni lesiones similares en el otro ojo. La agudeza visual del niño era normal. Inicialmente, se sospechó que la lesión correspondía a un papiloma de células escamosas pedunculado, por lo que se decidió realizar una biopsia excisional para su análisis.\n\n**Hallazgos Clave**  \nEl tejido extraído, de aproximadamente 1,5 x 1 cm, fue examinado bajo el microscopio. Se observó una lesión polipoide hiperplásica (un crecimiento en forma de pólipo con aumento en el número de células) que contenía múltiples quistes globulares en la submucosa conjuntival (la capa debajo de la superficie de la conjuntiva). Además, había una intensa infiltración inflamatoria compuesta por linfocitos, células plasmáticas y neutrófilos, que son tipos de células del sistema inmunitario. De manera destacada, se identificaron grandes esporangios (estructuras que contienen esporas) con paredes gruesas, dentro de los cuales se encontraban numerosas endosporas (esporas internas). Algunas de estas esporas se liberaban tras la ruptura de los esporangios maduros.\n\n**Interpretación Clínica**  \nEl examen histopatológico confirmó que la masa no era un papiloma, sino que correspondía a una infección por rinosporidiosis conjuntival, una enfermedad causada por el microorganismo Rhinosporidium seeberi que afecta principalmente las mucosas y puede formar masas polipoides. Esta infección es poco común y se caracteriza por la presencia de esporangios con endosporas en el tejido afectado.\n\n**Próximos Pasos y Seguimiento**  \nTras la escisión quirúrgica completa de la lesión, el paciente fue monitoreado durante al menos siete meses, sin presentar recurrencia de la lesión ni signos de infección en el ojo ni en otras partes del cuerpo. Este seguimiento indica un buen pronóstico tras el tratamiento quirúrgico. Se recomienda continuar con controles periódicos para detectar cualquier posible reaparición.",
+                "fh_score": 45.4
+            }
+        }
+    },
+    {
+        "article": "Presentamos el caso clínico de un varón de quince años, sin antecedentes médicos ni intervenciones previas, que acude al servicio de urgencias de pediatría con clínica de vómitos y dolor abdominal epigástrico de cuatro días de evolución, manteniéndose afebril durante la evolución del cuadro.\n\nInicialmente fue manejado como gastroenteritis, pero ante la ausencia de mejoría, con persistencia del dolor abdominal de tipo cólico a nivel epigástrico y de los vómitos de aspecto bilioso, acude a urgencias para nueva valoración.\n\nA la exploración física el paciente presentaba aceptable estado general, se encontraba afebril, con signos leves de deshidratación. El abdomen se encontraba distendido, sin datos de peritonismo y con ruidos hidroaéreos disminuidos. La analítica no presentaba hallazgos significativos, realizándose una radiografía de abdomen con hallazgos sugestivos de obstrucción intestinal.\n\nDada la evolución se decide realizar una tomografía computarizada urgente, en la que se observó presencia de ascitis e importante dilatación de asas de intestino delgado, sugiriendo la interposición de un asa de intestino delgado en el inicio de la transcavidad de los epiplones, con cambio de calibre a nivel del hiato de Winslow.\n\nSe realizó intervención quirúrgica urgente, realizando inicialmente una laparoscopia exploradora. Se observaban asas de intestino delgado dilatadas, e íleon terminal, ciego y colon ascendente de calibre normal pero localizados en hipocondrio derecho, con el ciego muy móvil y sin presentar adherencias al espacio parietocólico derecho. Siguiendo proximalmente el íleon terminal, se observaron asas de intestino delgado de distinto calibre desde la profundidad de la teórica localización del hiato de Winslow. Se consiguió traccionar de ciego e íleon terminal hasta desplazarlos a fosa iliaca derecha, pero sin llegar a identificar correctamente el punto de cambio de calibre, ya que la interposición del borde inferior del hígado y la distensión de asas de intestino delgado dificultaban la técnica. Se intentó mejorar la visualización mediante punción percutánea de un asa dilatada para vaciar el gas, sin mejoría. Para asegurar la resolución del cuadro obstructivo se decidió realizar una laparotomía media supraumbilical. Al acceder a cavidad se evidenciaba el cambio de calibre en íleon, a unos 40 centímetros de la válvula ileocecal, con signos compatibles con herniación de un tramo de unos cinco centímetros de íleon a través de hiato de Winslow. En ambos extremos del asa herniada observamos la impronta congestiva del hiato sobre el asa (Fig. 3). Se identificó el hiato de Winslow, de calibre normal, por lo que no se realizó ninguna técnica preventiva para disminuir el riesgo de recidiva.\n\nDurante los primeros días del postoperatorio el paciente presentó un íleo paralítico, pudiendo retirar la sonda nasogástrica a los cinco días de la cirugía e iniciando tolerancia oral con buena respuesta. Simultáneamente desarrolló una colección pélvica que se manejó de forma conservadora con antibióticos, con buena evolución. Finalmente, el paciente fue dado de alta a los diez días de la intervención, con tránsito conservado, manteniéndose afebril y con buen estado general.\n\nActualmente el paciente está en seguimiento en consultas externas de cirugía pediátrica.",
+        "gold_summary": "Presentamos el caso clínico de un varón adolescente de 15 años sin antecedentes quirúrgicos previos, con clínica de dolor abdominal y vómitos, en el que la tomografía computarizada sugería un cuadro de obstrucción intestinal a causa de hernia interna a nivel del hiato de Winslow. Precisó de intervención quirúrgica mediante laparoscopia exploradora, reconvertida por mala visualización a laparotomía media supraumbilical, para reducción del asa de íleon herniada. Esta presentaba buen aspecto y no fue necesaria la resección intestinal. No se realizó ninguna técnica preventiva para disminuir el riesgo de recidiva. Postoperatoriamente, el paciente presentó una colección pélvica manejada de manera conservadora con antibióticos. Actualmente se encuentra en seguimiento en consultas externas de cirugía pediátrica.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un niño de 15 años tenía dolor en la barriga y vomitaba. Los doctores vieron que su intestino estaba tapado por un lugar raro. Hicieron una operación para ayudarlo. Sacaron el intestino que estaba atrapado y estaba bien. No cortaron nada. Después, el niño tuvo un poco de líquido en la barriga, pero con medicinas mejoró. Ahora está bien y los doctores lo revisan para que siga sano.",
+                "fh_score": 75.17
+            },
+            "B2": {
+                "text": "**Caso Clínico de un Adolescente con Dolor Abdominal y Vómitos**\n\nUn chico de 15 años, sin problemas médicos anteriores, llegó al hospital con dolor en la parte superior del abdomen y vómitos que duraban cuatro días. Al principio, pensaron que tenía gastroenteritis, una infección del estómago, pero como no mejoraba, le hicieron más pruebas.\n\n**Lo que Encontraron**\n\nUna radiografía y una tomografía computarizada (una imagen detallada del cuerpo) mostraron que tenía una obstrucción en el intestino delgado. Esto ocurrió porque una parte del intestino se había metido por un espacio llamado hiato de Winslow, causando una hernia interna. Una hernia interna es cuando un órgano se mueve a un lugar donde no debería estar dentro del cuerpo.\n\n**Qué Hicieron**\n\nEl equipo médico decidió operar para arreglar la obstrucción. Comenzaron con una cirugía por laparoscopia, que es una operación con pequeñas incisiones y una cámara, pero tuvieron que cambiar a una cirugía abierta para ver mejor. Encontraron el intestino atrapado, pero estaba sano, así que no fue necesario cortar ninguna parte. No hicieron ninguna técnica para evitar que la hernia volviera a aparecer porque el espacio por donde se metió el intestino tenía un tamaño normal.\n\n**Después de la Cirugía**\n\nDespués de la operación, el chico tuvo un problema llamado íleo paralítico, que significa que el intestino tardó en empezar a funcionar normalmente. También desarrolló una acumulación de líquido en la pelvis, llamada colección pélvica, que trataron con antibióticos sin necesidad de otra cirugía. Finalmente, el paciente mejoró y fue dado de alta después de diez días.\n\n**Situación Actual**\n\nAhora, el adolescente sigue en control con el equipo de cirugía pediátrica para asegurarse de que se recupere bien y no tenga problemas futuros.",
+                "fh_score": 54.29
+            },
+            "B3": {
+                "text": "**Contexto**  \nSe describe el caso de un adolescente de 15 años, sin antecedentes médicos ni quirúrgicos previos, que presentó durante cuatro días dolor abdominal en la parte superior del abdomen (epigastrio) acompañado de vómitos biliosos (con contenido similar a bilis), sin fiebre. Inicialmente fue tratado como una gastroenteritis, pero al no mejorar y mantener los síntomas, acudió nuevamente a urgencias.\n\n**Hallazgos Clave**  \nEn la evaluación física, el paciente estaba en buen estado general, afebril, con signos leves de deshidratación y abdomen distendido, pero sin signos de inflamación grave (peritonismo). Los ruidos intestinales estaban disminuidos. Los análisis de sangre no mostraron alteraciones significativas. Una radiografía abdominal sugirió la presencia de una obstrucción intestinal. Posteriormente, una tomografía computarizada (TC) reveló ascitis (líquido en la cavidad abdominal) y dilatación importante de las asas del intestino delgado, con una posible herniación interna a través del hiato de Winslow, un orificio natural en la cavidad abdominal.\n\n**Interpretación Clínica**  \nEl diagnóstico fue una hernia interna del intestino delgado a través del hiato de Winslow, una causa poco frecuente de obstrucción intestinal. Debido a la gravedad y persistencia de los síntomas, se decidió realizar una cirugía urgente. Inicialmente se intentó una laparoscopia exploradora (cirugía mínimamente invasiva), pero la visualización limitada y la distensión intestinal dificultaron la intervención, por lo que se convirtió a una laparotomía (cirugía abierta) supraumbilical media. Durante la cirugía se identificó un asa de íleon (parte final del intestino delgado) herniada a través del hiato de Winslow, con signos de congestión por la presión del hiato, pero sin daño irreversible, por lo que no fue necesaria la resección intestinal. El asa herniada fue reducida (devuelta a su posición normal). El hiato de Winslow tenía un tamaño normal, por lo que no se realizó ninguna maniobra para prevenir la recurrencia de la hernia.\n\nEn el postoperatorio, el paciente presentó un íleo paralítico (falta temporal de movimiento intestinal), que mejoró progresivamente, permitiendo retirar la sonda nasogástrica a los cinco días y comenzar la alimentación oral con buena tolerancia. Además, desarrolló una colección pélvica (acumulación localizada de líquido o pus) que se trató con antibióticos de forma conservadora, sin necesidad de intervención quirúrgica adicional. El paciente evolucionó favorablemente y fue dado de alta al décimo día después de la cirugía, manteniendo un buen estado general y sin fiebre.\n\n**Próximos Pasos**  \nActualmente, el paciente se encuentra en seguimiento ambulatorio en consultas de cirugía pediátrica para monitorizar su recuperación y detectar posibles complicaciones o recurrencias. Se mantiene estable y con tránsito intestinal conservado.",
+                "fh_score": 40.63
+            }
+        }
+    },
+    {
+        "article": "Un niño de 23 meses de edad con encefalopatía isquémica hipóxica al nacer, con buen potencial motor cerebral y desarrollo psicomotor normal. Tenía antecedentes personales de miocardiopatía restrictiva y fue incluido en un programa de trasplante cardiaco cuando tenía 16 meses de edad. También fue necesario implantarle un dispositivo de asistencia biventricular Berlin Heart externo. Para evitar eventos embólicos, se le administró un tratamiento antiplaquetario doble y anticoagulante. Cuando tenía 23 meses de edad, presentó desconexión y hemiparesia derecha. Una tomografía computarizada (TC) mostró una arteria cerebral media (ACM) izquierda hiperdensa, así como un infarto parietotemporal derecho crónico. Su análisis de sangre mostró: glóbulos rojos 4.16 × 106 µ/L; hemoglobina 11.4 g/gL; tiempo de tromboplastina parcial activada (TTPA) 93 segundos y relación internacional normalizada (INR) 1.08.\n\nEl tratamiento trombolítico intravenoso estaba contraindicado debido al doble tratamiento antiplaquetario y anticoagulante a la dosis completa con heparina, por lo que se realizó una trombectomía intraarterial. Aunque el paciente tenía 23 meses de edad, se encontraba en el tercer percentil de la curva de peso (10 kg). Bajo anestesia general, se perforó la arteria femoral derecha y se colocó una funda 4F de 11 cm de largo (Cordis, Irlanda). Se usó un catéter vertebral Radiofocus 4F (Glidecath de Terumo, Bélgica) para confirmar la oclusión del segmento M1 de la MCA izquierda. La arteria se recanalizó mediante trombectomía mecánica con un stentriever utilizando el catéter vertebral 4F como tutor, colocándolo en el segmento petroso de la arteria carótida. Se usó un dispositivo Trevo XP Pro Vue de 3 mm x 20 mm (Stryker, Países Bajos), con un microcatéter Rapid Transit recto (Codman Neurovascular, Reino Unido), abriendo la arteria en una sola pasada. Se retiró todo el sistema (catéter tutor, microcatéter y stentriever) simultáneamente. En la prueba de control, se detectó una disección iatrogénica de la arteria carótida interna izquierda, que no tuvo importancia clínica, ya que el hemisferio izquierdo se irrigaba a través de la arteria comunicante anterior.\n\nUn mes después, se realizó con éxito el trasplante de corazón. La única secuela neurológica a largo plazo que surgió como resultado del accidente cerebrovascular fue la espasticidad del miembro superior derecho.\n\nMH - Cardiomiopatía, Dilatada/complicaciones/cirugía\nMH - Cardiomiopatía, restrictiva/complicaciones/cirugía\nMH - Angiografía cerebral\nMH - Procedimientos/métodos endovasculares\nMH - Mujer\nMH - Estudios de seguimiento\nMH - Insuficiencia cardiaca/*complicaciones/tratamiento\nMH - Trasplante de corazón\nMH - *Dispositivos de asistencia cardíaca\nMH - Humanos\nMH - Infantil\nMH - Hombre\nMH - Arteria cerebral media/imágenes diagnósticas\nMH - Estudios Retrospectivos\nMH - Ictus/complicaciones/diagnóstico por imágenes/cirugía\nMH - Resultado del tratamiento\n",
+        "gold_summary": "Un niño de 16 meses de edad con cardiomiopatía restrictiva que fue incluido en una lista para un trasplante cardiaco. A los 20 meses de edad, requirió un implante de un dispositivo de asistencia biventricular externo (Berlin Heart) y tuvo un accidente cerebrovascular en el hemisferio izquierdo a los 23 meses. Se utilizó un enfoque intraarterial y produjo buenos resultados clínicos. Un mes después, se realizó con éxito un trasplante cardiaco.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había un niño que tenía un problema en su corazón. Tenía que esperar para recibir un corazón nuevo. Le pusieron una máquina para ayudar a su corazón a latir. Un día, su cerebro se enfermó un poco. Los doctores usaron una medicina especial para ayudar a su cerebro. Después, el niño recibió un corazón nuevo y se puso mejor.",
+                "fh_score": 79.86
+            },
+            "B2": {
+                "text": "**Lo que pasó con el niño**\n\nUn niño de 16 meses tenía un problema en el corazón llamado cardiomiopatía restrictiva, que hace que el corazón no funcione bien. Por eso, lo pusieron en una lista para recibir un trasplante de corazón. A los 20 meses, le pusieron un dispositivo especial llamado Berlin Heart, que ayuda al corazón a bombear sangre mientras espera el trasplante.\n\n**El problema del accidente cerebrovascular**\n\nCuando tenía 23 meses, el niño sufrió un accidente cerebrovascular, que es cuando una parte del cerebro no recibe suficiente sangre y se daña. En su caso, el problema ocurrió en el lado izquierdo del cerebro. Debido a que ya estaba tomando medicamentos para evitar coágulos, no se pudo usar un tratamiento común para este tipo de accidente.\n\n**El tratamiento que recibieron**\n\nLos médicos usaron una técnica llamada trombectomía intraarterial. Esto significa que, con anestesia, introdujeron un pequeño tubo por una arteria en la pierna para llegar hasta el cerebro y quitar el coágulo que bloqueaba la arteria. Lograron abrir la arteria en una sola vez y restaurar el flujo de sangre.\n\n**Qué pasó después**\n\nUn mes después del accidente, el niño recibió el trasplante de corazón que necesitaba. Como consecuencia del accidente cerebrovascular, quedó con un poco de rigidez en el brazo derecho, pero en general tuvo buenos resultados y pudo continuar con su tratamiento.\n\n**Por qué es importante este caso**\n\nEste caso muestra que, incluso en niños muy pequeños con problemas graves del corazón, es posible usar técnicas avanzadas para tratar accidentes cerebrovasculares y mejorar su salud antes de un trasplante.",
+                "fh_score": 59.3
+            },
+            "B3": {
+                "text": "**Contexto:**  \nSe presenta el caso de un niño de 23 meses con antecedentes complejos, incluyendo encefalopatía isquémica hipóxica al nacer con desarrollo psicomotor normal, y una cardiomiopatía restrictiva diagnosticada en la infancia. Debido a la gravedad de su insuficiencia cardíaca, fue incluido en un programa de trasplante cardiaco a los 16 meses. Posteriormente, a los 20 meses, se le implantó un dispositivo de asistencia ventricular biventricular externo (Berlin Heart) para apoyar la función cardíaca mientras esperaba el trasplante. Para prevenir la formación de coágulos, recibió tratamiento combinado con anticoagulantes y antiplaquetarios.\n\n**Hallazgos Clave:**  \nA los 23 meses, el niño presentó síntomas neurológicos agudos, incluyendo desconexión y hemiparesia (debilidad) en el lado derecho del cuerpo. Una tomografía computarizada reveló una obstrucción en la arteria cerebral media izquierda, responsable del suministro sanguíneo a una parte importante del cerebro, junto con un infarto crónico en el hemisferio derecho. Debido a que el tratamiento trombolítico intravenoso (que disuelve coágulos) estaba contraindicado por su régimen anticoagulante, se optó por una trombectomía mecánica intraarterial, un procedimiento endovascular que consiste en extraer el coágulo directamente desde la arteria afectada.\n\nDurante la intervención, realizada bajo anestesia general, se accedió a la arteria femoral derecha para introducir un catéter que permitió llegar hasta la arteria cerebral afectada. Se utilizó un dispositivo llamado stentriever para recuperar el flujo sanguíneo en una sola maniobra. Aunque se detectó una disección (una lesión en la pared arterial causada por el procedimiento), esta no tuvo consecuencias clínicas importantes debido a la circulación colateral cerebral. El procedimiento fue exitoso y permitió la recuperación del flujo en la arteria ocluida.\n\n**Interpretación Clínica:**  \nEste caso destaca la viabilidad y eficacia de la trombectomía mecánica en pacientes pediátricos con ictus isquémico, incluso en niños muy pequeños y con condiciones cardíacas complejas que contraindican el tratamiento trombolítico convencional. La intervención permitió minimizar el daño cerebral y preservar la función neurológica, limitando la secuela a una espasticidad en el brazo derecho.\n\n**Próximos Pasos:**  \nUn mes después de la recuperación del accidente cerebrovascular, el niño fue sometido con éxito a un trasplante de corazón, mejorando su pronóstico a largo plazo. El seguimiento neurológico y cardiológico continúa siendo fundamental para monitorizar la evolución y manejar posibles complicaciones futuras. Este caso aporta evidencia sobre el manejo multidisciplinario y personalizado en pacientes pediátricos con enfermedades cardíacas graves y complicaciones neurológicas.",
+                "fh_score": 31.46
+            }
+        }
+    },
+    {
+        "article": "Una mujer de 23 años de edad se presentó al departamento de urgencias con pérdida de conciencia y exceso de secreciones orales 2 horas después de la ingestión de un veneno no especificado. No tenía movimientos corporales anormales, fiebre, diarrea, vómitos o sudoración. Inicialmente la habían llevado a un hospital primario cercano, donde fue tratada por posible intoxicación por OP con atropina y cimetidina durante 3 días, antes de ser trasladada al hospital Saint Peter. Después de un interrogatorio exhaustivo, se descubrió que la paciente había consumido unos 30 ml de 2,4-D en un intento de suicidio, precipitado por problemas financieros. No tenía antecedentes conocidos de enfermedad psiquiátrica, intentos de suicidio, episodios depresivos o abuso de sustancias. No se observaron trastornos cardíacos, renales o metabólicos previos.\n\nAl llegar al departamento de urgencias, la paciente estaba inconsciente. Sus constantes vitales eran PR 110/min, BP 120/70 mmHg, RR 21/min, y SPO2 96% en aire ambiente. Los resultados del examen físico fueron notables: un GCS de 6 sobre 15, pupilas dilatadas y reactivas, extremidades inferiores hipertónicas e hiperreflexivas, y reflejo plantar ascendente. Tras la investigación inicial, el recuento completo de células sanguíneas, la prueba de la función renal, la prueba de la función hepática, y la glucosa en sangre aleatoria fueron normales. Su electrocardiograma mostró taquicardia sinusal, mientras que la radiografía de tórax no fue notable. El análisis de gases en sangre arterial y el nivel sérico de la toxina no pudieron determinarse, ya que ninguno de los medios de prueba estaba disponible en el hospital.\n\nLa paciente fue trasladada a la unidad de cuidados intensivos (UCI), se le introdujo una sonda para proteger las vías respiratorias y se le inició inmediatamente una diuresis alcalina forzada. Su evolución en la UCI fue notable por el desarrollo de una insuficiencia renal (creatinina 3,1 ml/dL [intervalo de referencia 0,5-1,2 mg/dL], BUN 133 mg/dL [intervalo de referencia 16,6-48,5 mg/dL], análisis de orina 3+ hemoglobina y muchos glóbulos rojos), debido a una rabdomiolisis inducida por toxinas (nivel de creatina fosfocinasa de 1330 µg/L). Posteriormente, la paciente se volvió hipotensa y se le inició un tratamiento con vasopresores. La ecocardiografía y la ecografía abdominal no fueron significativas. A pesar de estos esfuerzos, falleció por colapso circulatorio el tercer día de estancia en la UCI.\n",
+        "gold_summary": "Aquí se informa sobre el caso de una joven granjera de la zona rural de Etiopía que fue internada en un hospital local tras perder el conocimiento y presentar exceso de secreciones orales 2 horas después de haber ingerido, de manera suicida, un agente tóxico desconocido. Originalmente, se la trató por intoxicación con organofosforados y luego se la trasladó al Hospital Saint Peter's en Addis Abeba para recibir atención médica más intensiva. Allí, se confirmó la ingesta de 2,4-D y se le brindó atención médica de apoyo, ventilación mecánica y diuresis alcalina forzada. A pesar de estas intervenciones, falleció varios días después.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una joven tomó un veneno para hacerse daño. Se puso muy mal y perdió el conocimiento. La llevaron al hospital para ayudarla. \n\nLos doctores le dieron medicinas y la cuidaron mucho. Pero su cuerpo no pudo mejorar. Después de unos días, ella murió. \n\nLos doctores hicieron todo lo que pudieron para ayudarla.",
+                "fh_score": 79.26
+            },
+            "B2": {
+                "text": "Caso de Intoxicación Grave en una Joven\n\nUna mujer de 23 años de una zona rural de Etiopía tomó un veneno llamado 2,4-D con la intención de suicidarse. Dos horas después, perdió el conocimiento y tenía mucha saliva. Al principio, pensaron que había tomado otro tipo de veneno y la trataron en un hospital pequeño. Luego, la llevaron a un hospital más grande llamado Saint Peter para recibir mejor atención.\n\nLo que Encontraron en el Hospital\n\nCuando llegó, la paciente estaba inconsciente y tenía signos de daño en sus nervios y músculos. Los exámenes de sangre y orina mostraron que sus riñones no funcionaban bien y que había daño muscular grave, causado por el veneno. Los médicos intentaron ayudarla con tratamientos para limpiar el veneno y proteger sus órganos, incluyendo ponerle un tubo para ayudarla a respirar.\n\nQué Pasó Después\n\nA pesar de los esfuerzos médicos, la paciente empeoró. Su presión sanguínea bajó mucho y los médicos tuvieron que usar medicamentos para mantenerla estable. Finalmente, después de tres días en cuidados intensivos, falleció debido a un fallo en su circulación sanguínea.\n\nImportancia del Caso\n\nEste caso muestra lo peligroso que puede ser el veneno 2,4-D y cómo puede afectar seriamente el cuerpo, especialmente los riñones y los músculos. También destaca la importancia de un diagnóstico correcto y tratamiento rápido en casos de intoxicación para intentar salvar vidas.",
+                "fh_score": 63.05
+            },
+            "B3": {
+                "text": "**Contexto**\n\nSe presenta el caso de una mujer joven de 23 años, proveniente de una zona rural de Etiopía, que ingresó al hospital tras perder el conocimiento y mostrar un exceso de secreciones orales aproximadamente dos horas después de ingerir intencionalmente una sustancia tóxica. Inicialmente fue atendida en un hospital local donde se sospechó intoxicación por organofosforados (un tipo común de pesticida) y recibió tratamiento con atropina y cimetidina durante tres días. Posteriormente, fue trasladada al Hospital Saint Peter en Addis Abeba para recibir cuidados más especializados.\n\n**Hallazgos Clave**\n\nEn el hospital de referencia se confirmó que la sustancia ingerida era 2,4-D, un herbicida tóxico. Al ingreso, la paciente estaba inconsciente con un nivel de conciencia muy bajo (Glasgow Coma Scale de 6/15), presentaba pupilas dilatadas pero reactivas, hipertonicidad (aumento anormal del tono muscular) y reflejos exagerados en las extremidades inferiores, así como un reflejo plantar anormal (reflejo de Babinski positivo). Sus signos vitales mostraban taquicardia (frecuencia cardíaca rápida), presión arterial y saturación de oxígeno dentro de rangos aceptables. Los análisis iniciales de sangre, función renal y hepática, así como glucosa, fueron normales. Sin embargo, no se pudieron medir niveles específicos de la toxina ni gases en sangre debido a limitaciones del hospital.\n\nDurante su estancia en la unidad de cuidados intensivos (UCI), la paciente fue intubada para proteger sus vías respiratorias y se inició diuresis alcalina forzada, una técnica para ayudar a eliminar la toxina a través de la orina. A pesar de esto, desarrolló insuficiencia renal aguda, evidenciada por un aumento significativo de creatinina y nitrógeno ureico en sangre, así como presencia de hemoglobina y glóbulos rojos en la orina. Además, presentó rabdomiólisis (descomposición del tejido muscular) inducida por la toxina, confirmada por niveles elevados de creatina fosfocinasa, una enzima muscular. Posteriormente, la paciente sufrió hipotensión (presión arterial baja) que requirió el uso de medicamentos vasopresores para mantener la presión arterial. Estudios de ecocardiografía y ecografía abdominal no mostraron alteraciones significativas.\n\n**Interpretación Clínica**\n\nLa intoxicación por 2,4-D es poco común pero grave, y puede causar daño multisistémico, incluyendo alteraciones neurológicas, musculares y renales. En este caso, la rápida progresión hacia insuficiencia renal y colapso circulatorio refleja la alta toxicidad de esta sustancia y la dificultad para manejar sus complicaciones, incluso con tratamiento intensivo y medidas de soporte avanzadas.\n\n**Próximos Pasos**\n\nEste caso subraya la importancia de un diagnóstico preciso y rápido en intoxicaciones, especialmente en regiones con recursos limitados. La disponibilidad de pruebas específicas para identificar toxinas y la implementación temprana de tratamientos dirigidos podrían mejorar el pronóstico. Además, es fundamental fortalecer la atención en salud mental y los servicios de prevención del suicidio para evitar intentos con sustancias altamente tóxicas.",
+                "fh_score": 34.27
+            }
+        }
+    },
+    {
+        "article": "Una paciente etíope de 35 años de edad se presentó en el departamento de urgencias del Colegio Médico del Hospital Yekatitit 12 con síntomas de falta de aire en reposo, ortopnea, disnea paroxística nocturna significativa, dolor torácico, tos productiva teñida de sangre y vómitos de materia ingerida (2-3 episodios por día) durante 2 semanas. Presentaba una hinchazón progresiva del cuerpo que comenzó en las extremidades inferiores y luego afectó a todo el cuerpo, fatigabilidad fácil, pérdida de apetito, fiebre intermitente de alto grado y sensación de ardor epigástrico durante la misma semana y con la misma duración. La paciente también experimentó una pérdida de peso y fatiga no especificadas durante los últimos 2 meses. Por lo demás, no tenía comorbilidades conocidas, ni comportamientos de riesgo, como fumar o beber alcohol, medicamentos o antecedentes familiares de neoplasia. Estaba casada, tenía cuatro hijos y no tenía antecedentes obstétricos negativos. Su ocupación era la agricultura y había vivido en una zona rural. Nunca había sido admitida por una queja similar.\n\nLa escala de coma de Glasgow (GCS) de la paciente fue de 15 sobre 15, y no había anormalidades de memoria, potencia o tono. La paciente estaba en grave dificultad respiratoria con saturación de oxígeno del 70% con aire atmosférico, frecuencia respiratoria de 30-35 latidos/minuto, y frecuencia del pulso de 120 por minuto. Tenía registros de fiebre de alto grado hasta el nivel de 39.5 0C y puede mantener su presión arterial. El examen de mama con ultrasonido y mamografía fue supuestamente normal. No se detectó linfadenopatía en áreas accesibles.\n\nEl examen del tórax reveló signos de derrame pleural que también se observaron en las imágenes y se analizaron. Una tomografía computarizada (TC) del tórax con contraste mostró derrame pericárdico y neumonía multifocal. La angiografía por TC mostró un defecto de llenado arterial pulmonar segmentario del lóbulo inferior en ambos lados, lo que sugiere embolia pulmonar y derrame pleural en ambos lados. Los frotis citológicos se informaron con láminas de células mesoteliales, neutrófilos y grupos dispersos de células grandes atípicas con nucleolos prominentes que sugieren derrame maligno. El análisis del líquido pleural mostró un líquido con predominio linfocítico con glucosa normal (82 mg/dl), proteínas (2,2 g/dl) y lactato deshidrogenasa (LDH) de 592 mg/dl.\n\nLa presión venosa yugular aumentó con los sonidos cardiacos apagados. La ecocardiografía mostró derrame pericárdico masivo con características de taponamiento cardiaco, fracción de eyección preservada (65%), y excursión sistólica del plano anular tricuspídeo (TAPSE) mayor a 18 mm. Un electrocardiograma (ECG) reveló solo taquicardia sinusal y desviación del eje. Se realizó una pericardiocentesis inmediata, se extrajo un drenaje de aproximadamente 250 ml de fluido hemorrágico y se aseguró la ventana pericárdica. La repetida ecocardiografía reveló una reducción del tamaño. El informe de citología del fluido pericárdico mostró numerosos linfocitos junto con células malignas atípicas que tenían prominentes nucleolos, lo que sugería un derrame maligno.\n\nEn el examen abdominal, mostró signos positivos de acumulación de fluidos sin órgano hinchable. La tomografía computarizada abdominal y pélvica mostró un aumento en el tamaño del hígado con múltiples lesiones hepáticas hipointensas que sugerían metástasis. Los órganos pélvicos, incluidos los ovarios y el útero, no presentaron lesiones identificadas. Se realizó una biopsia con aguja de la lesión hepática y los resultados revelaron un adenocarcinoma secundario.\n\nSe realizó un diagnóstico de insuficiencia cardíaca causada por una efusión pericárdica masiva maligna secundaria a un adenocarcinoma diseminado y un carcinoma de origen primario desconocido que afectaba al pulmón, la pleura, el pericardio y el tracto gastrointestinal. Se le diagnosticó a la paciente una trombosis venosa profunda extensa en la extremidad superior izquierda, una embolia pulmonar bilateral y segmentaria, posiblemente debido a la CUP diseminada. Los hallazgos también mostraron una neumonía multifocal superpuesta y una anemia leve de enfermedad crónica.\n\nEl recuento sanguíneo completo inicial reveló leucocitosis con un recuento de glóbulos blancos de 24 × 103 por ml, neutrófilos predominantes (91%), recuento de glóbulos rojos de 3.7 × 106 por µl, anemia normocítica leve (hemoglobina (Hgb) 11.2 mg/dl), volumen corpuscular medio (MCV) de 81.2 fl, y trombocitopenia severa (66 × 103/µl). Después del tratamiento antibiótico para neumonía, el recuento sanguíneo completo volvió a la normalidad (excepto para Hgb). Con niveles normales de bilirrubina, la aspartato aminotransferasa (AST) aumentó más de siete veces (263 U/L), mientras que la alanina transaminasa (ALT) aumentó más de nueve veces (332 U/L). Los electrolitos séricos (excepto para Na + con hiponatremia leve, 129 mEq/L) y las pruebas de función renal fueron normales. La albúmina era baja (2.12 g/dl). Los niveles de lactato deshidrogenasa (LDH) aumentaron casi dos veces desde el inicio (592 U/L). Los virus del virus de inmunodeficiencia humana, hepatitis B y hepatitis C no fueron reactivos. La sangre y el cultivo del líquido pleural no tuvieron crecimiento. Un antígeno carcinoembrionario (CEA) aumentó más de 400 veces (1000 µg/L) del inicio.\n\nLa paciente fue admitida en la sala general. Se realizó una ventana pericárdica y una inserción de un tubo torácico derecho con un cirujano cardiotorácico junto con un cardiólogo (ver la cantidad de aspirado antes). Se realizó una aspiración pleural terapéutica intermitente para el derrame pleural maligno. Una vez que la dosis de carga (60 mg) de frusemida produjo suficiente producción de orina, esta dosis se mantuvo tres veces (TID) al día. Esto se redujo y se dio de alta a la paciente con una dosis oral de 20 mg dos veces al día (BID). Se inició una dosis estándar de enoxaparina para el tromboembolismo pulmonar y la trombosis venosa profunda aguda extensa en la extremidad superior izquierda. Se administró enoxaparina por vía subcutánea 40 mg BID durante la hospitalización, que se cambió a 5 mg de warfarina oral diaria durante el alta debido a problemas financieros. La neumonía multifocal se trató con ceftazidima (1 g intravenoso TID) y vancomicina (1 g intravenoso BID) según el protocolo de tratamiento estándar nacional. El dolor se controló con un potente medicamento contra el dolor (morfina 5 mg intravenosa TID) y se redujo y suspendió. También estaba en la profilaxis de la úlcera. La paciente fue dada de alta de la sala médica con una mejora significativa después de 14 días de hospitalización y fue asignada a la unidad de oncología del hospital. Por lo tanto, para el cáncer de origen primario desconocido, se le dio un ciclo de quimioterapia (carboplatino/paclitaxel). Se perdió el seguimiento debido a problemas financieros, y la paciente murió en su casa cuatro meses después del alta.\n\nMH - Humanos\nMH - Mujer\nMH - *Insuficiencia cardiaca/etiología\nMH - Adulto\nMH - *Neoplasias, complicaciones/primaria desconocida",
+        "gold_summary": "Una mujer negra de 35 años se presentó con falta de aire en reposo, ortopnea, disnea paroxística nocturna, dolor torácico, tos productiva teñida de sangre y fiebre durante 2 semanas. También tenía hinchazón progresiva del cuerpo, fatigabilidad fácil, pérdida de apetito y dolor abdominal durante la misma semana. La imagen corporal reveló grandes derrames pleurales y pericárdicos, lesiones hepáticas metastásicas y defectos de llenado segmentarios y subsegmentarios vasculares pulmonares bilaterales. La citología de los fluidos pericardio y pleural sugieren derrame maligno. Las lesiones hepáticas y la biopsia con aguja indicaron adenocarcinoma de origen desconocido, y el nivel de antígeno carcinoembriónico también aumentó significativamente.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había una mujer que se sentía muy cansada y con dificultad para respirar. Su cuerpo se hinchó mucho y tenía dolor en el pecho. Los doctores vieron que tenía líquido en el pecho y alrededor del corazón. También encontraron que tenía un problema en el hígado y en los pulmones. El líquido que sacaron mostró que tenía células que no son buenas. Los doctores dijeron que tenía un tipo de cáncer que empezó en un lugar que no pudieron encontrar.",
+                "fh_score": 85.24
+            },
+            "B2": {
+                "text": "**Lo que le Pasó a la Paciente**\n\nUna mujer de 35 años llegó al hospital porque tenía mucha dificultad para respirar, incluso cuando estaba en reposo. También tenía dolor en el pecho, tos con sangre, fiebre y una hinchazón que comenzó en sus piernas y se extendió por todo el cuerpo. Además, se sentía muy cansada, había perdido el apetito y tenía dolor en la parte superior del abdomen.\n\n**Lo que Encontraron en los Exámenes**\n\nLas imágenes médicas mostraron que tenía acumulación de líquido en los pulmones (llamado derrame pleural) y alrededor del corazón (derrame pericárdico). También encontraron lesiones en el hígado que parecían ser metástasis, es decir, que el cáncer se había extendido allí. En los vasos sanguíneos de sus pulmones había bloqueos que indicaban embolias pulmonares, que son coágulos que dificultan la circulación.\n\nAl analizar el líquido que rodeaba el corazón y los pulmones, los médicos encontraron células anormales que indicaban que el líquido estaba causado por un cáncer (derrame maligno). La biopsia del hígado confirmó que tenía un tipo de cáncer llamado adenocarcinoma, pero no pudieron encontrar dónde comenzó el cáncer originalmente.\n\nAdemás, un examen de sangre mostró que tenía un nivel muy alto de una sustancia llamada antígeno carcinoembrionario, que suele aumentar cuando hay ciertos tipos de cáncer.\n\n**Qué Significa Todo Esto**\n\nLa paciente tenía un cáncer avanzado que se había extendido a varias partes del cuerpo, incluyendo los pulmones, el corazón y el hígado. Esto causó problemas graves como dificultad para respirar, acumulación de líquidos y coágulos en la sangre. Aunque recibieron tratamiento para aliviar sus síntomas y para el cáncer, la enfermedad estaba muy avanzada y el origen del tumor principal no se pudo identificar.",
+                "fh_score": 55.7
+            },
+            "B3": {
+                "text": "**Contexto**  \nUna mujer etíope de 35 años acudió al hospital presentando dificultad grave para respirar en reposo, dificultad para respirar al estar acostada (ortopnea), episodios repentinos de dificultad respiratoria nocturna (disnea paroxística nocturna), dolor en el pecho, tos con expectoración de sangre y vómitos de contenido alimenticio durante dos semanas. Además, manifestó una hinchazón progresiva que comenzó en las piernas y se extendió a todo el cuerpo, cansancio fácil, pérdida de apetito, fiebre alta intermitente y ardor en la parte superior del abdomen. También había experimentado pérdida de peso y fatiga durante los dos meses previos. No tenía antecedentes médicos relevantes ni factores de riesgo conocidos.\n\n**Hallazgos Clave**  \nEl examen físico y las pruebas de imagen revelaron derrames significativos de líquido tanto en la cavidad pleural (alrededor de los pulmones) como en el pericardio (la membrana que rodea el corazón). La tomografía computarizada mostró lesiones en el hígado compatibles con metástasis (diseminación del cáncer) y defectos en la circulación sanguínea pulmonar que indicaban embolias pulmonares bilaterales. El análisis del líquido extraído del pericardio y la pleura mostró células malignas, lo que sugiere que el líquido se debía a un derrame maligno. La biopsia hepática confirmó la presencia de un adenocarcinoma (un tipo de cáncer que se origina en células glandulares) de origen primario desconocido. Además, el nivel en sangre del antígeno carcinoembrionario (CEA), un marcador tumoral, estaba muy elevado, apoyando la presencia de un cáncer avanzado.\n\n**Interpretación Clínica**  \nLa paciente fue diagnosticada con insuficiencia cardíaca causada por un derrame pericárdico masivo de origen maligno, secundario a un adenocarcinoma diseminado que afectaba múltiples órganos, incluyendo pulmón, pleura, pericardio y tracto gastrointestinal. También se identificaron complicaciones como trombosis venosa profunda en el brazo izquierdo y embolia pulmonar, probablemente relacionadas con la enfermedad tumoral avanzada. Se detectó además una neumonía multifocal superpuesta y anemia leve asociada a enfermedad crónica.\n\n**Próximos Pasos y Tratamiento**  \nLa paciente recibió tratamiento urgente para aliviar el derrame pericárdico mediante pericardiocentesis y ventana pericárdica, así como drenaje del líquido pleural. Se inició tratamiento anticoagulante para la trombosis y embolia pulmonar, y antibióticos para la neumonía. Posteriormente, se administró quimioterapia con carboplatino y paclitaxel dirigida al cáncer de origen desconocido. A pesar de la mejoría inicial y el alta hospitalaria, la paciente falleció cuatro meses después debido a la progresión de la enfermedad.\n\nEste caso ilustra la complejidad del diagnóstico y manejo de un cáncer avanzado con origen primario desconocido, que se manifestó inicialmente con síntomas respiratorios y signos de insuficiencia cardíaca por derrame pericárdico maligno.",
+                "fh_score": 32.31
+            }
+        }
+    },
+    {
+        "article": "Paciente del sexo femenino de 17 años con diagnóstico de enfermedad de Graves con bocio difuso, la cual negó otros antecedentes de importancia.\n\nSu cuadro comenzó seis meses antes con pérdida de peso progresiva, episodios de ansiedad y agitación, temperaturas de 37.4 a 37.9 ºC, palpitaciones, dolor abdominal y diarrea intermitente. A los dos meses se agregó como síntoma el crecimiento de la cara anterior del cuello; al tercer mes presentó taquicardia de hasta 130 latidos por minuto. Al ser valorada por Endocrinología se le administró tiamazol de 15 mg cada 8 horas, el cual fue suspendido por cuadro de agranulocitosis. Por lo tanto, se le comenzó a administrar lugol y propanol de 20 mg cada 8 horas, sin respuesta adecuada. Por ende, se decidió aplicar una dosis terapéutica de yodo 131 (I-131) 10 mcU.\n\n\nExploración física\nA la exploración física, la paciente presentó como signos basales una presión arterial no invasiva (PANI) 137/75 mmHg, frecuencia cardiaca (FC) 105 lpm, frecuencia respiratoria (FR) 16 rpm, SpO2 95%, temperatura 37.4ºC. La paciente ingresó deambulando, con agitación leve, con actitud cooperadora; estaba hidratada y sin datos clínicos de vía aérea difícil, pero no se valoró movilidad de tráquea por crecimiento tiroideo de aproximadamente 7.5 x 7 x 10 cm). La superficie del cuello era regular y su movilidad tenía una adecuada extensión. A la auscultación cardiopulmonar no hubo ruidos agregados y la paciente tenía ruidos cardiacos aumentados en frecuencia; asimismo, abdomen blando, depresible, no doloroso, con peristalsis presente. Extremidades integras, sensibilidad con aumento de la percepción del calor, hiperhidrosis palmar, fuerza 5/5, y temblor fino.\n\nSe empleó la escala de Burch y Wartofsky y se obtuvieron 40 puntos con elevada probabilidad de tormenta tiroidea, por lo cual se decidió manejo con anestesia multimodal.\n\nEn la monitorización tipo 2 la paciente presentó signos vitales iniciales PANI 137/75 mmHg, frecuencia cardiaca 96 latidos por minuto, frecuencia respiratoria 16 respiraciones por minuto, 95% Spo2, monitoreo invasivo de tensión arterial.\n\nPor inducción endovenosa se le administraron a la paciente 2 mg de midazolam; 150 mcg de fentanilo; 5 mg de cisatracurio y 50 mg de propofol.\n\nEl abordaje de la vía aérea se hizo con videolaringoscopía Glide Scope con hoja hiperangular 3 sin complicaciones. La ventilación mecánica invasiva modo volumen presentó flujos bajos FIO2 (40%).\n\nSe llevó a cabo bloqueo cervical superficial bilateral ecoguiado con 4 mL de ropivacaina al 0.2% en cada lado (16 mg en total).\n\nPara el mantenimiento se empleó sevoflorano CAM 0.8, infusión de dexmedetomedina 0.7 a 0.4 mcg/kg/hora, infusión de lidocaína 25 mcg/kg/hora, concentración plasmática de fentanilo 0.001 mcg/mL.\n\nEn cuanto a los adyuvantes se empleó paracetamol 750 mg + parecoxib 40 mg + ketorolaco intravenoso 30 + sulfato de magnesio 1250 g en infusión para una hora. El balance de líquidos fue negativo. El tiempo anestésico fue de 215 minutos. En el transoperatorio, la paciente estuvo hemodinámicamente estable, con presión arterial media de 67 a 75 mmHg, que se considera adecuada para la perfusión de órganos.\n\nEn el postoperatorio la paciente presentó analgesia durante 12 horas. Rescate con 1 g de metamizol por razón necesaria, utilizando un solo rescate. Disfonía postoperatoria persistente, sin presencia de odinofagia.",
+        "gold_summary": "Adolescente de 17 años con enfermedad de Graves con manifestaciones clínicas descontroladas, la cual no respondió a tratamiento médico y se programó para tiroidectomia radical. Se obtuvieron 35 puntos en la Escala de Burch y Wartofsky. Se manejó con anestesia general y fueron disminuyendo los estímulos para control de vía aérea y regional a fin de disminuir los estímulos quirúrgicos. Se usaron medicamentos adyuvantes como sulfato de magnesio para la estabilidad transoperatoria.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una niña de 17 años tenía un problema en su cuello llamado enfermedad de Graves. Su cuerpo estaba muy acelerado y no mejoró con medicinas. Por eso, los doctores decidieron hacerle una operación para quitarle una parte del cuello. Durante la operación, los doctores usaron medicinas para que ella no sintiera dolor y para que su cuerpo estuviera tranquilo. También cuidaron mucho su respiración para que todo saliera bien.",
+                "fh_score": 64.94
+            },
+            "B2": {
+                "text": "**Caso de una Adolescente con Enfermedad de Graves**\n\nUna joven de 17 años tenía una enfermedad llamada Graves, que afecta la tiroides, una glándula en el cuello que controla muchas funciones del cuerpo. Su enfermedad estaba muy activa y no mejoró con los medicamentos que le dieron.\n\n**Lo que Pasó Antes de la Cirugía**\n\nLa paciente tenía síntomas como pérdida de peso, ansiedad, latidos rápidos del corazón y un aumento visible en el tamaño de su cuello debido al crecimiento de la tiroides. Los médicos usaron una escala llamada Burch y Wartofsky para medir qué tan grave estaba su condición, y obtuvo 35 puntos, lo que indica un problema serio.\n\n**Cómo Se Realizó la Cirugía**\n\nPara operarla, le pusieron anestesia general, que es un medicamento que la hizo dormir y no sentir dolor durante la cirugía. Los médicos cuidaron mucho la forma de manejar su respiración y usaron técnicas para reducir las molestias causadas por la operación. Además, le dieron medicamentos especiales, como sulfato de magnesio, para mantener su cuerpo estable mientras duraba la cirugía.\n\n**Por Qué Es Importante**\n\nEste caso muestra cómo se trata una enfermedad de Graves muy avanzada cuando los medicamentos no funcionan. La cirugía y el cuidado durante la operación son muy importantes para que la paciente esté segura y se recupere bien.",
+                "fh_score": 58.1
+            },
+            "B3": {
+                "text": "**Contexto**  \nSe trata de una paciente femenina de 17 años diagnosticada con enfermedad de Graves, una condición autoinmune que provoca un aumento en la actividad de la glándula tiroides (hipertiroidismo) y crecimiento difuso del tiroides (bocio). Desde hace seis meses, presentó síntomas progresivos como pérdida de peso, ansiedad, fiebre leve, palpitaciones, dolor abdominal y diarrea. Posteriormente, desarrolló un aumento visible en la parte frontal del cuello y taquicardia (frecuencia cardíaca acelerada). El tratamiento inicial con tiamazol (un medicamento antitiroideo) fue suspendido debido a una complicación grave llamada agranulocitosis (disminución severa de glóbulos blancos). Se intentaron otros tratamientos sin éxito, por lo que se decidió administrar yodo radioactivo (I-131) para reducir la función tiroidea.\n\n**Hallazgos Clave**  \nEn la evaluación física, la paciente mostraba signos de hipertiroidismo activo: frecuencia cardíaca elevada (105 latidos por minuto), temperatura corporal ligeramente elevada (37.4 ºC), temblor fino, sudoración excesiva en las palmas y aumento de la sensibilidad al calor. Se observó un bocio grande (aproximadamente 7.5 x 7 x 10 cm) sin signos de dificultad respiratoria, aunque no se pudo evaluar completamente la movilidad de la tráquea debido al tamaño del tiroides. La escala de Burch y Wartofsky, que evalúa el riesgo de una crisis tiroidea grave llamada tormenta tiroidea, arrojó un puntaje de 40, indicando alta probabilidad de esta complicación.\n\nDurante la cirugía programada para extirpar la glándula tiroides (tiroidectomía radical), se utilizó anestesia general con técnicas avanzadas para asegurar la vía aérea, incluyendo videolaringoscopía, y ventilación mecánica controlada. Se aplicó un bloqueo nervioso cervical superficial guiado por ultrasonido para reducir el dolor y la respuesta al estímulo quirúrgico. Además, se emplearon varios medicamentos adyuvantes, como sulfato de magnesio, para mantener la estabilidad cardiovascular y mejorar el control del dolor durante la operación. La paciente se mantuvo estable durante todo el procedimiento, que duró aproximadamente 3 horas y 35 minutos.\n\n**Interpretación Clínica**  \nLa paciente presentaba un cuadro de enfermedad de Graves descontrolada, con signos y síntomas que indicaban un alto riesgo de tormenta tiroidea, una emergencia médica que puede ser potencialmente mortal. La falta de respuesta a tratamientos convencionales y la contraindicación del tiamazol por agranulocitosis hicieron necesaria la intervención quirúrgica. El manejo anestésico fue cuidadosamente planificado para minimizar los riesgos asociados a la hiperactividad tiroidea y al tamaño del bocio, utilizando técnicas que redujeron la estimulación del sistema nervioso y mantuvieron la estabilidad hemodinámica.\n\n**Próximos Pasos**  \nDespués de la cirugía, la paciente presentó analgesia efectiva durante 12 horas y requirió un solo rescate analgésico. Se observó disfonía (alteración de la voz) persistente, probablemente relacionada con la manipulación quirúrgica de los nervios laríngeos, pero sin dolor al tragar. Será importante realizar un seguimiento para evaluar la función vocal y ajustar el tratamiento hormonal tiroideo según sea necesario para evitar complicaciones a largo plazo. Además, se debe monitorizar la recuperación general y prevenir posibles efectos secundarios derivados de la cirugía y la enfermedad de base.",
+                "fh_score": 36.04
+            }
+        }
+    },
+    {
+        "article": "Una mujer de 30 años de edad, embarazada de 3, para 3, se presentó con disminución de la micción, dolor en el flanco izquierdo y fiebre durante 2 días después de una cesárea de emergencia por primera vez, indicada debido a la angustia materna y fetal secundaria al trabajo de parto prolongado y sangrado vaginal prolongado en el hospital Al-Thora, Ibb, Yemen. A pesar de los esfuerzos de reanimación, su recién nacido falleció después de 45 minutos. Durante la cesárea, se identificaron severas adherencias uterinas (ya que había lesiones de endometriosis y adherencias entre la pared posterior del útero y el colon sigmoide), y una pérdida de sangre estimada de 1500 cc, según el informe del ginecólogo. La paciente no recibió atención prenatal durante su embarazo. No es fumadora y negó condiciones médicas crónicas, abuso de drogas, intoxicación accidental o antecedentes quirúrgicos previos.\n\nEn el examen físico, el paciente se veía pálido, enfermo y febril durante la evaluación inicial, con una temperatura oral de 38 °C, pulso de 80 latidos por minuto y presión arterial de 95/70 mm Hg. El abdomen del paciente estaba levemente distendido, con sensibilidad moderada, principalmente en el cuadrante inferior izquierdo.\n\nLos datos de laboratorio fueron los siguientes: el recuento de glóbulos blancos (WBC) fue de 15,3 × 103/mL, con 90% de neutrófilos polimórficos (leucocitosis con predominio neutrofílico), la hemoglobina fue de 7,5 g/dL, el recuento de plaquetas fue de 200 × 103/µL, el nitrógeno ureico en sangre (BUN) fue de 23 mg/dl y la creatinina fue de 3,8 mg/dl. Otros análisis de sangre, como los de la función hepática y los de coagulación, estuvieron dentro de los rangos normales. La ecografía (US) mostró una hidronefrosis izquierda grave y un fluido libre moderado en la cavidad abdominal. Se realizó la aspiración de la punción abdominal y la creatinina en el punto fue de 52 mg/dL, lo que indica que el fluido era orina.\n\nLa paciente fue resucitada con glóbulos rojos concentrados y una amplia cobertura antibiótica. Después de esto, se le realizó una ureteroscopia urgente que mostró una oclusión total del uréter izquierdo. Se tomó la decisión de realizar una exploración quirúrgica, dada la inestabilidad hemodinámica, la falta de equipos de nefrostomía percutánea y la evidencia de contaminación intraabdominal. Durante la operación, se encontró fluido libre moderado en la cavidad abdominal. El uréter izquierdo fue aplastado y ligado con una sutura Vicryl (5 agujas) a unos 5 cm de su parte distal. Después de evacuar el fluido, se extirpó el segmento lesionado del uréter y se realizó una ureteroneocistostomía de forma refluyente tras distender la vejiga con solución salina a través del catéter. Además, diseccionamos el uréter, con cuidado, de los tejidos circundantes en dirección cefálica, espatulamos el extremo distal del uréter e insertamos un stent doble. Se implantó el uréter en la cúpula posterior de la vejiga urinaria con anastomosis sin tensión y se suturó con Vicryl 4-0 a través del uréter de espesor completo, luego la capa mucosa de la vejiga y la capa detrusora. Se insertó un drenaje Jackson-Pratt (JP) cerca de la anastomosis y se cerró la pared abdominal tras evaluar el contenido intraperitoneal.\n\n\nSeguimiento y resultado\nSe iniciaron líquidos transparentes el segundo día postoperatorio. La paciente tenía distensión abdominal leve, dolor y náuseas. El tercer día postoperatorio, tenía una distensión abdominal creciente y dejó de expulsar flatos. La ecografía abdominal mostró una gran cantidad de acumulación en la cavidad peritoneal. Los datos de laboratorio de sangre mostraron una leucocitosis (WBC de 22 × 103/mL con un cambio a la izquierda).\n\nUna tomografía computarizada (TC) del abdomen y la pelvis con contraste reveló una cantidad significativa de aire libre y líquido en todo el abdomen y la pelvis adyacente a la pared abdominal anterior. También se observaron múltiples localizaciones de gas libre en el mesenterio, con realce de contraste de múltiples bucles intestinales pequeños, sin evidencia de extravasación de contraste. Los hallazgos sugirieron una víscera perforada. Después de consultar al equipo de cirugía general, la paciente fue llevada inmediatamente al quirófano para una laparotomía exploratoria, que reveló una pequeña perforación en la parte rectosigmoidea con algo de derrame, peritonitis con edema del asa intestinal y alteración de la anastomosis ureteral. La complejidad de este caso nos obligó a realizar intervenciones en varias etapas de manera multidisciplinaria. En primer lugar, el ginecólogo realizó una histerectomía debido a endometritis (confirmada histopatológicamente), supuración severa y alteración de la sutura del útero. En segundo lugar, un urólogo realizó una derivación ureterocutánea del uréter izquierdo y se creó una urostomía en el lado izquierdo. Por último, el cirujano general realizó el procedimiento de colostomía después de reparar la lesión del colon y se creó una colostomía en el lado izquierdo. En el quinto día postoperatorio, se produjo retracción de la colostomía con infección de la herida y se observó comunicación entre la colostomía y la urostomía. Se decidió realizar una reexploración para reubicar la colostomía sigmoidea y se realizó una colostomía transversal derecha. Una semana después de la operación, la paciente experimentó una infección superficial de la pared abdominal complicada con dehiscencia de la herida e hipoalbuminemia (albúmina: 2 g/dL) que requirió tratamiento con varios desbridamientos, irrigación de la herida, antibióticos y terapia de apoyo. Los antibióticos recomendados fueron linezolid (600 mg IV cada 12 horas durante 7 días), luego cambiaron a ceftriaxona (1 g IV cada 12 horas durante 5 días) más metronidazol (500 mg IV cada 12 horas durante 5 días) y cambiaron a ciprofloxacina oral (500 mg cada 12 horas por vía oral durante 7 días). Gradualmente, reanudó su dieta normal y fue dada de alta 30 días después en condiciones estables. Requería atención domiciliaria para ayudarla con la colostomía, la ureterostomía y la deambulación.\n\nSeis meses después, se cerró la colostomía y se anastomosó el uréter mediante el procedimiento de colgajo de vejiga tabular de Boari (la vejiga se abrió en su superficie anterior y se volteó un colgajo de vejiga de espesor completo caudalmente y se tabularizó para anastomosis al segmento ureteral proximal después de la inserción de la endoprótesis doble J). Después de una recuperación postoperatoria sin incidentes, se dio de alta a la paciente el séptimo día postoperatorio. El seguimiento de un mes mediante ecografía y cistouretrografía miccional mostró un aspecto normal de la vejiga con capacidad vesical adecuada y un sistema del tracto urinario superior normal. Tres meses después, la ureteroscopia retrógrada mostró un calibre adecuado del uréter. Se hizo un seguimiento regular de la paciente con ecografía durante 3 meses durante un año. La paciente no tuvo síntomas irritativos o gastrointestinales en los 2 años de seguimiento.\n",
+        "gold_summary": "Una mujer de 30 años presentó disminución de la micción durante 2 días después de una cesárea. La ecografía mostró una hidronefrosis izquierda grave y un fluido abdominal libre moderado. Una ureteroscopia reveló una oclusión total del uréter izquierdo y, posteriormente, se realizó una ureteroneocistostomía. Dos días después, la paciente presentó complicaciones con distensión abdominal que requirieron una nueva exploración. La exploración reveló lesiones en el colon (recto-sigmoide), peritonitis, endometritis y alteración de la anastomosis ureteral. Se realizó una colostomía, reparación de lesiones en el colon, histerectomía y derivación ureterocutánea. La estancia hospitalaria de la paciente fue complicada, con retracción estomal que requirió revisión quirúrgica y dehiscencia de la herida, que se trató de forma conservadora. Después de 6 meses, se cerró la colostomía y se anastomosó el uréter mediante el procedimiento de colgajo de Boari.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una mujer tuvo un bebé con una operación. Después, le dolía y no podía hacer pipí bien. Los doctores vieron que un tubito que lleva la pipí estaba tapado. Hicieron una operación para arreglarlo.\n\nDespués, la mujer se sintió peor y su pancita se hizo grande. Los doctores encontraron que tenía heridas en su pancita y en otros lugares. Hicieron más operaciones para ayudarla y poner todo bien.\n\nLa mujer estuvo en el hospital mucho tiempo. Poco a poco, se fue mejorando. Después de seis meses, los doctores cerraron una abertura que le habían hecho y arreglaron el tubito de la pipí otra vez. Ahora está bien y sin dolor.",
+                "fh_score": 81.55
+            },
+            "B2": {
+                "text": "**Lo que pasó con la paciente**  \nUna mujer de 30 años tuvo problemas para orinar durante dos días después de una cesárea, que es una operación para sacar al bebé. Al hacerle una ecografía, los médicos vieron que tenía una hinchazón grave en el riñón izquierdo llamada hidronefrosis, causada por la acumulación de orina, y también encontraron líquido libre en su abdomen. Luego, con un examen llamado ureteroscopia, descubrieron que el tubo que lleva la orina desde el riñón a la vejiga (el uréter izquierdo) estaba completamente bloqueado.\n\n**Tratamiento inicial**  \nPara arreglar este problema, los médicos hicieron una cirugía llamada ureteroneocistostomía, que consiste en conectar el uréter a la vejiga de nuevo para que la orina pueda salir. Sin embargo, dos días después, la paciente tuvo dolor y su abdomen se hinchó más, lo que indicaba que algo no estaba bien.\n\n**Complicaciones y nuevas cirugías**  \nAl revisarla otra vez, encontraron que tenía una infección grave en el abdomen (peritonitis), una herida en el colon (parte del intestino) y una inflamación en el útero (endometritis). También la conexión del uréter que habían hecho estaba dañada. Por eso, los médicos tuvieron que hacer varias cirugías: quitaron el útero (histerectomía), repararon el colon y crearon una abertura en la piel para que la orina y las heces pudieran salir por separado (derivación ureterocutánea y colostomía).\n\n**Recuperación y seguimiento**  \nLa recuperación fue difícil porque la paciente tuvo problemas con las heridas y la abertura del colon se contrajo, lo que necesitó otra cirugía. También tuvo infecciones que se trataron con antibióticos y cuidados especiales. Después de seis meses, los médicos cerraron la abertura del colon y volvieron a conectar el uréter usando una técnica llamada colgajo de Boari, que usa parte de la vejiga para reparar el uréter.\n\n**Resultado final**  \nTras esta última cirugía, la paciente se recuperó bien. Los controles con ecografías y otros estudios mostraron que su vejiga y riñones funcionaban normalmente. Durante dos años de seguimiento, no tuvo problemas ni síntomas molestos.",
+                "fh_score": 52.21
+            },
+            "B3": {
+                "text": "**Contexto**  \nUna mujer de 30 años, embarazada por tercera vez, fue sometida a una cesárea de emergencia debido a complicaciones durante el trabajo de parto, incluyendo sangrado prolongado y sufrimiento fetal. Tras la cesárea, presentó disminución en la cantidad de orina, dolor en el costado izquierdo y fiebre. Durante la cirugía se detectaron adherencias severas en el útero y lesiones compatibles con endometriosis, además de una pérdida significativa de sangre. La paciente no había recibido atención prenatal y no presentaba antecedentes médicos relevantes.\n\n**Hallazgos Clave**  \n- Exámenes iniciales mostraron leucocitosis con predominio neutrofílico (indicativo de infección), anemia moderada y deterioro de la función renal (elevación de creatinina).  \n- La ecografía evidenció una hidronefrosis grave (dilatación del riñón por obstrucción) en el lado izquierdo y presencia de líquido libre en la cavidad abdominal, que resultó ser orina al analizarse.  \n- La ureteroscopia urgente identificó una obstrucción completa del uréter izquierdo.  \n- Se realizó una cirugía para extirpar el segmento dañado del uréter y se reconstruyó la conexión entre el uréter y la vejiga (ureteroneocistostomía), con colocación de un stent para mantener el flujo urinario.\n\n**Interpretación Clínica**  \nPocos días después de la cirugía, la paciente desarrolló distensión abdominal progresiva, dolor y ausencia de expulsión de gases, signos sugestivos de complicaciones intraabdominales. Estudios por imagen mostraron aire y líquido libre en el abdomen, lo que indicaba una posible perforación intestinal. La laparotomía exploratoria confirmó perforación en el colon rectosigmoide, peritonitis (inflamación del revestimiento abdominal), infección del útero (endometritis) y problemas en la reparación del uréter. Debido a la complejidad y gravedad del cuadro, se realizaron múltiples intervenciones: histerectomía para controlar la infección uterina, derivación urinaria mediante ureterostomía para proteger el tracto urinario, y reparación del colon con creación de colostomía para desviar las heces.\n\nDurante la hospitalización, la paciente presentó complicaciones adicionales como retracción de la colostomía con infección y dehiscencia (apertura) de la herida abdominal, que requirieron revisiones quirúrgicas y tratamiento con antibióticos y cuidados locales. La recuperación fue gradual, y la paciente fue dada de alta en condiciones estables tras un mes de hospitalización.\n\n**Próximos Pasos y Seguimiento**  \nSeis meses después, se realizó el cierre de la colostomía y la reconstrucción definitiva del uréter mediante el procedimiento de colgajo de Boari, que utiliza un segmento de la vejiga para reemplazar la parte dañada del uréter. La recuperación postoperatoria fue satisfactoria, con estudios de imagen que mostraron una vejiga y tracto urinario superiores normales, y ureteroscopias que confirmaron un calibre adecuado del uréter. Durante dos años de seguimiento, la paciente no presentó síntomas urinarios ni gastrointestinales, evidenciando una recuperación completa y funcional.\n\n---\n\nEste caso ilustra la complejidad y gravedad de las complicaciones postoperatorias tras una cesárea en un contexto de falta de atención prenatal y lesiones previas, así como la importancia de un manejo multidisciplinario para resolver complicaciones urológicas, ginecológicas y gastrointestinales simultáneas.",
+                "fh_score": 29.8
+            }
+        }
+    },
+    {
+        "article": "Mujer de 43 años, con antecedente de hipertensión arterial con tratamiento con losartán, dos cesáreas y oclusión tubaria bilateral. Ingresó a nuestro hospital y refirió dolor de 24 horas de evolución, tipo cólico en hipogastrio e irradiación a fosa iliaca izquierda, además de náusea y vómito en dos ocasiones. Se agregaron evacuaciones semilíquidas en forma inicial y posteriormente cese en las evacuaciones y en la canalización de gases. A la exploración física, la paciente presentó dolor en el abdomen, así como distensión, especialmente hacia el flanco izquierdo. En el mesogastrio y el flanco izquierdo hubo la presencia de timpanismo. La peristalsis estaba presente, mínima, abolida en flanco izquierdo y mesogastrio. La irritación peritoneal estuvo ausente. Se colocó sonda nasogástrica, con gasto mínimo gástrico y sin mejoría en la sintomatología. Los estudios de laboratorio demostraron: 9700 leucocitos con un 87% de neutrófilos, creatinina de 0.7 mg/dL, urea de 22 mg/dL y proteína C reactiva de 5.0 mg/L. En la radiografía simple de abdomen presentó dilatación importante del lado izquierdo del colon, con niveles hidroaéreos. La tomografía muestra la dilatación del colon del lado izquierdo, con imagen que simula grano de café en el corte coronal.\n\nAnte estos hallazgos clínicos y de imagen, se decidió hacer laparotomía de urgencia ante la sospecha de la presencia de vólvulo de sigmoides o de síndrome adherencial complicado. Durante la cirugía se evidenció un ciego flexionado hacia adelante y a la izquierda, carente de fijación retroperitoneal. El punto de flexión fue producido por una banda de adherencia colocada sobre el colon ascendente. Se realizó liberación de la adherencia y se corroboró continuidad adecuada hacia el colon distal. No se evidenció la presencia de isquemia, necrosis o perforación del ciego. Se realizó apendicectomía con descompresión del ciego a través de base apendicular y posteriormente ligadura de esta. Se llevó a cabo cecopexia hacia pared de fosa iliaca derecha. Después de la cirugía, hubo mejoría clínica de la paciente, que tuvo evacuaciones presentes normales. La paciente siguió controles correctos en consulta externa de cirugía y se mantuvo asintomática.",
+        "gold_summary": "Mujer de 43 años que ingresó a un servicio de urgencias con datos de obstrucción intestinal. Se realizó tomografía simple de abdomen donde se identificó dilatación del colon e imagen que semejaba un grano de café invertido. Se hizo laparotomía exploradora y se identificó vólvulo cecal del tipo báscula, sin compromiso vascular. Se realizó desvolvulación, descompresión a través de apendicectomía, y cecopexia. Posterior a evento quirúrgico, la paciente se recuperó sin incidentes y fue dada de alta con controles adecuados por consulta externa.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una señora tenía dolor en su barriga y no podía ir al baño bien. Los doctores le hicieron una foto especial para ver su barriga. Vieron que un pedazo de su barriga estaba doblado y tapado. La señora tuvo una operación para arreglar ese problema. Los doctores quitaron la parte que estaba doblada y la dejaron bien. Después de la operación, la señora se sintió mejor y pudo ir al baño normalmente. Ahora está bien y los doctores la revisan para cuidar que siga sana.",
+                "fh_score": 78.69
+            },
+            "B2": {
+                "text": "**Lo que pasó con la paciente**\n\nUna mujer de 43 años llegó al hospital porque tenía dolor en el abdomen, vómitos y problemas para evacuar. Los médicos hicieron estudios y vieron que una parte del intestino grueso, llamada colon, estaba muy inflamada y bloqueada. En la tomografía, que es una imagen especial del cuerpo, notaron una forma que parecía un \"grano de café\" invertido, lo que les hizo sospechar que había un problema llamado vólvulo, que es cuando el intestino se gira y se tapa.\n\n**Lo que hicieron los médicos**\n\nDecidieron hacer una cirugía urgente para ver qué pasaba. Durante la operación, encontraron que una parte del intestino llamada ciego estaba doblada y no estaba bien sujeta en su lugar. Esto causaba que el intestino se girara (vólvulo), pero sin dañar el flujo de sangre. Para arreglarlo, quitaron una banda de tejido que estaba causando el problema, hicieron una apendicectomía (que es sacar el apéndice) para descomprimir el intestino, y fijaron el ciego a la pared del abdomen para que no se moviera otra vez.\n\n**Qué pasó después**\n\nDespués de la cirugía, la paciente mejoró mucho. Empezó a evacuar normalmente y no tuvo más síntomas. Fue dada de alta y siguió controles médicos para asegurarse de que todo estuviera bien.",
+                "fh_score": 63.71
+            },
+            "B3": {
+                "text": "**Contexto:**  \nUna mujer de 43 años con antecedentes de hipertensión arterial, dos cesáreas previas y oclusión tubaria bilateral, ingresó al hospital presentando dolor abdominal intenso de tipo cólico en la parte baja del abdomen (hipogastrio), que se irradiaba hacia el lado izquierdo, acompañado de náuseas, vómitos y cambios en sus evacuaciones intestinales, incluyendo inicialmente heces semilíquidas y luego ausencia de evacuaciones y gases. En la exploración física, se detectó distensión abdominal y dolor localizado, especialmente en el lado izquierdo, con presencia de sonidos intestinales reducidos o ausentes en esa zona, pero sin signos de irritación peritoneal (inflamación de la membrana que recubre los órganos abdominales). Los análisis de sangre mostraron un aumento moderado de glóbulos blancos y proteína C reactiva, indicadores de inflamación o infección. La radiografía y la tomografía computarizada del abdomen revelaron una dilatación significativa del colon izquierdo y una imagen característica en forma de “grano de café”, que sugiere torsión intestinal.\n\n**Hallazgos Clave:**  \nAnte la sospecha de una obstrucción intestinal grave, posiblemente causada por torsión del colon (vólvulo de sigmoides) o adherencias (bandas de tejido cicatricial que pueden causar obstrucción), se decidió realizar una cirugía de emergencia (laparotomía). Durante la operación, se encontró que el ciego (la primera parte del colon) estaba anormalmente desplazado y flexionado hacia adelante y hacia la izquierda, sin estar fijado a la pared abdominal como es habitual. Esta torsión fue causada por una banda de adherencia sobre el colon ascendente. No se observaron signos de daño grave como falta de riego sanguíneo (isquemia), muerte del tejido (necrosis) o perforación. Se liberó la adherencia que causaba la torsión, se descomprimió el ciego mediante la extracción del apéndice (apendicectomía) y se fijó el ciego a la pared abdominal (cecopexia) para evitar futuras torsiones.\n\n**Interpretación Clínica:**  \nEl diagnóstico final fue un vólvulo cecal del tipo “báscula”, una torsión del ciego que puede provocar obstrucción intestinal pero que en este caso no comprometió la circulación sanguínea ni causó daño irreversible. La intervención quirúrgica oportuna permitió resolver la obstrucción, evitar complicaciones mayores y preservar la integridad del colon.\n\n**Próximos Pasos:**  \nTras la cirugía, la paciente mostró una recuperación favorable, con retorno normal de las evacuaciones intestinales y ausencia de síntomas. Fue dada de alta y se mantuvo en seguimiento ambulatorio con controles periódicos en consulta externa de cirugía, donde continuó asintomática y sin complicaciones. Este caso resalta la importancia del diagnóstico temprano y tratamiento quirúrgico adecuado en pacientes con obstrucción intestinal por vólvulo cecal.",
+                "fh_score": 34.78
+            }
+        }
+    },
+    {
+        "article": "Paciente de sexo femenino de 10 años, sin historia familiar de enfermedad tiroidea, portadora de bocio diagnosticado a los 9 años (ecografía tiroidea con sig nos compatibles de tiroiditis crónica) con presencia de anticuerpos antitiroideos positivos. Sin tratamiento al momento del ingreso hospitalario. Consultó por orina de aspecto espumoso de 5 días de evolución, asociado a dolor abdominal, vómitos profusos y diarrea. Evo lucionó con edema palpebral y de extremidades, disminución de la diuresis, decaimiento y fiebre de 38° C el día previo a su ingreso. Al momento de su eva luación en el servicio de urgencia destacó una pacien te con edema palpebral bilateral y pretibial, con bocio evidente (indoloro y sin nódulos palpables) y presen cia de soplo sistólico eyectivo en foco pulmonar IV/VI sin irradiación. Resto del examen sin alteraciones de significancia. Presión arterial 120/78 mmHg (percentil 95), temperatura 38,1°C, peso: 33.9 Kg, talla: 131,5 cm (p7), IMC 19,8 (p83).\n\nDentro de sus exámenes de admisión destacaron examen de orina completa con proteinuria +++, sin bacterias, sin nitritos, leucocitos 7 cel/uL (VN: 0-10 cel/uL), eritrocitos 4 cel/uL (VN: 0-15 cel/uL), índice proteinuria/creatininuria (IPC) 2 mg/mg, proteínas totales de 3.8 g/dL, hipoalbuminemia de 2,1 g/dL, hipercolesterolemia de 416 mg/dL, hipertrigliceridemia de 127 mg/dL y creatinina plasmática de 0,46 mg/dL (aclaramiento de creatinina calculado por fórmula de Schwartz: 125 ml/min/1,73 m2). Gases venosos, elec trolitos plasmáticos y hemograma dentro de rangos normales. En cuanto al estudio inmunológico destacó: inmunoglobulina A 181 mg/dL (VN 45-236), inmunoglobulina M 131 mg/dL (VN 52-242), inmunoglobulina G 208 (VN 608-1572) mg/dL, C3 125 mg/dL (VN 80-150), C4 37,3 mg/dL (VN 12-36). Ecografía renal normal. Se ingresó a la paciente con diagnóstico de SN y tiroiditis autoinmune.\n\nEn el contexto de SN se inició tratamiento con prednisona (60 mg/m2/día), con buena respuesta, logrando fundir edema y disminuir progresivamente la proteinuria hasta alcanzar rangos normales previo al egreso (IPC de egreso: 0.09, a los 6 días).\n\nDel punto de vista de función tiroidea su estudio mostró hormona tiroestimulante (TSH) 4,4 UI/ml (VN: 0,67-4,16 UI/ml), tiroxina (T4) libre 0,80 ng/ dL (VN: 0,86-1,4 ng/dL), anticuerpos antiperoxidasa (Anti Tpo) 120 U/ml (VN: 0-60 U/ml), anticuerpos antitiroglobulina (Anti-Tg) 82 U/ml (VN: 0-60 U/ ml), por lo que se inició terapia de sustitución con levotiroxina (25 mcg/día). La ecografía tiroidea descri bió tiroides de tamaño normal con leve aumento de vascularización difusa al Doppler, sin lesiones focales sólidas ni quísticas, siendo estos hallazgos sugerentes de tiroiditis. Resto del estudio (PCR para SARS CoV-2, anticuerpos anti citoplasma de neutrófilos, anticuer pos anti nucleares, anticuerpos anti DNA, anticuerpos anti estreptolisina O, anticuerpos anticardiolipinas, anticuerpos anti mieloperoxidasa y anticuerpos anti proteinasa 3) resultó negativo.\n\nA los 6 días de ingresada la paciente se encontraba en buenas condiciones, siendo dada de alta con prednisona (60 mg al día) y levotiroxina (25 ucg al día). En el seguimiento a los 12 meses la paciente se encontraba asintomática, con su patología tiroidea bajo control (TSH 1,11 UI/ml) con tratamiento de sustitución. No ha presentado recaídas del SN (examen de orina sin proteinuria y creatinina 0,44 mg/dL).",
+        "gold_summary": "Paciente de 10 años que se presenta con síndrome nefrótico y bocio. Se pesquisa antecedente de tiroiditis autoinmu ne e hipotiroidismo no tratado. Se inicia terapia corticoidal y hormonal de sustitución (levotiroxina), logrando buena respuesta clínica y de laboratorio.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Niña de 10 años con hinchazón en el cuerpo y cuello grande. Tenía un problema en la tiroides que no se había tratado. Le dieron medicinas para ayudar su cuerpo y se puso mejor.",
+                "fh_score": 91.16
+            },
+            "B2": {
+                "text": "**Lo que le Pasó a la Paciente**  \nUna niña de 10 años llegó al hospital con hinchazón en los ojos y las piernas, además de orina con espuma. Ella tenía un bocio, que es cuando la glándula tiroides en el cuello está agrandada. También se sabía que tenía tiroiditis autoinmune, una enfermedad donde el cuerpo ataca su propia tiroides, y no estaba tomando ningún medicamento para eso.\n\n**Qué Encontraron en los Exámenes**  \nLos análisis de orina mostraron mucha proteína, lo que indica que los riñones no estaban funcionando bien. Esto se llama síndrome nefrótico, una condición que causa que el cuerpo pierda proteínas importantes. Además, sus niveles de algunas hormonas de la tiroides estaban bajos y tenía anticuerpos que confirmaban la tiroiditis. La ecografía del cuello mostró inflamación en la tiroides, pero sin tumores.\n\n**Cómo la Trataron y Qué Pasó Después**  \nLe dieron un medicamento llamado prednisona, que es un corticoide para reducir la inflamación, y levotiroxina, que es una hormona para ayudar a su tiroides a funcionar mejor. Con este tratamiento, la hinchazón bajó y los análisis mejoraron rápidamente. Después de un año, la niña estaba bien, sin síntomas y con su tiroides controlada gracias a la medicación. No tuvo problemas nuevos en los riñones.",
+                "fh_score": 63.37
+            },
+            "B3": {
+                "text": "**Contexto:**  \nSe trata de una niña de 10 años con diagnóstico previo de bocio (aumento visible de la glándula tiroides) y tiroiditis autoinmune (una inflamación de la tiroides causada por el propio sistema inmunológico), sin tratamiento para su hipotiroidismo (función tiroidea disminuida) al momento de su ingreso hospitalario. Consultó por síntomas relacionados con síndrome nefrótico, que incluyen orina espumosa, edema (hinchazón) en párpados y extremidades, disminución de la cantidad de orina, dolor abdominal, vómitos y fiebre.\n\n**Hallazgos Clave:**  \n- En la evaluación inicial, se observó edema palpebral bilateral y en las piernas, así como un bocio evidente pero sin nódulos dolorosos. Además, presentó un soplo cardíaco leve.  \n- La presión arterial estaba en el límite superior normal para su edad.  \n- Los análisis de orina mostraron una proteinuria significativa (pérdida elevada de proteínas en la orina), sin signos de infección.  \n- En sangre, se detectó hipoalbuminemia (niveles bajos de albúmina, una proteína importante), hipercolesterolemia y niveles normales de creatinina, indicando función renal preservada.  \n- Los estudios inmunológicos confirmaron la presencia de anticuerpos antitiroideos elevados, compatibles con tiroiditis autoinmune, y niveles normales de otros marcadores inflamatorios y autoinmunes.  \n- La ecografía tiroidea mostró un tamaño normal de la glándula pero con aumento difuso de la vascularización, típico de tiroiditis.  \n- No se encontraron otras enfermedades autoinmunes o infecciones asociadas.\n\n**Interpretación Clínica:**  \nLa paciente presentó un síndrome nefrótico (una enfermedad renal caracterizada por pérdida excesiva de proteínas en la orina y edema) asociado a una tiroiditis autoinmune con hipotiroidismo no tratado. La coexistencia de estas dos condiciones autoinmunes sugiere un trastorno inmunológico subyacente que afecta tanto la tiroides como el riñón.\n\n**Próximos Pasos y Tratamiento:**  \nSe inició tratamiento con prednisona (un corticosteroide) para controlar el síndrome nefrótico, logrando una rápida mejoría clínica y normalización de la proteinuria en pocos días. Paralelamente, se comenzó terapia de reemplazo hormonal con levotiroxina para corregir el hipotiroidismo. La paciente fue dada de alta en buenas condiciones y, tras un seguimiento de 12 meses, se mantuvo asintomática, con función tiroidea controlada y sin recaídas del síndrome nefrótico.\n\nEste caso destaca la importancia de identificar y tratar de manera integral las enfermedades autoinmunes coexistentes para lograr una recuperación óptima y prevenir complicaciones a largo plazo.",
+                "fh_score": 33.22
+            }
+        }
+    },
+    {
+        "article": "La exploración neurológica exhaustiva puso de manifiesto una apariencia facial característica: mirada fija con los ojos muy abiertos, fruncimiento de la frente con una expresión de ceño fruncido (signo del procerus) y expresión fija de la parte inferior de la cara. La paciente presentaba hipocinesia-rigidez simétrica de predominio axial con postura retrocólica del tronco y el cuello. El examen de la deambulación reveló un patrón de la marcha del nivel superior caracterizado por una llamativa vacilación inicial que requería ayuda de objetos/personas cercanas. Una vez que comenzaba a caminar, los pasos mejoraban relativamente, pero volvía a aparecer una marcha inefectiva cuando intentaba girar. Exhibía zancadas cortas, congelación, base amplia de sustentación, desequilibrio, movimiento lento de los miembros inferiores, arrastre de los pies y pérdida de la fluidez normal del tronco y las extremidades. Los reflejos posturales estaban alterados. Asimismo, existía una dificultad grave para la bipedestación tras la sedestación y dificultad para darse la vuelta en la cama. Sin embargo, los signos frontales, como la rigidez paratónica, los reflejos de prensión, la incontinencia urinaria y las características de los déficits cognitivos frontales (por ejemplo, cambios disejecutivos y de personalidad e impulsividad) estaban ausentes, excepto por un estado apático progresivo. Los movimientos oculares sacádicos verticales estaban alterados, con amplitudes relativamente normales y movimientos sacádicos horizontales. Se evidenciaron sacadas de onda cuadrada y una oftalmoplejía supranuclear. La resonancia magnética del cerebro reveló atrofia del mesencéfalo, dilatación del acueducto de Silvio y del III ventrículo y atrofia de los lóbulos frontales, y los signos típicos del colibrí y de la gloria de la mañana. Finalmente, la paciente fue diagnosticada de una PSP probable.",
+        "gold_summary": "Mujer de 58 años sana que consultó por un trastorno de la marcha con caídas. La exploración neurológica mostró una apariencia facial característica (mirada fija, ojos muy abiertos, ceño fruncido y expresión fija hemifacial inferior), e hipocinesia-rigidez simétrica de predominio axial (postura retrocólica del tronco y el cuello). La exploración de la marcha reveló un trastorno de la marcha del nivel superior, caracterizado por una significativa vacilación inicial, que precisaba ayuda de objetos/personas cercanos. Al iniciar la marcha, los pasos mejoraban relativamente, pero reaparecía una deambulación inefectiva al girar. Presentaba zancadas cortas, congelación, base amplia de sustentación, desequilibrio, movimiento lento de las piernas, arrastre de los pies, y pérdida de la cadencia normal del tronco y las extremidades. Los reflejos posturales estaban alterados. La resonancia magnética cerebral desveló atrofia mesencefálica, dilatación de acueducto de Silvio y III ventrículo, atrofia frontal bilateral y el signo típico del colibrí. Finalmente, la paciente fue diagnosticada de una PSP probable.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había una señora que tenía problemas para caminar. Sus ojos se veían muy abiertos y su cara parecía quieta. Caminaba con pasos cortos y a veces se paraba sin poder seguir. Le costaba mucho girar y mantener el equilibrio. Su cuerpo estaba un poco rígido y lento. En el doctor, vieron que su cerebro estaba un poco cambiado. Por eso, dijeron que tenía una enfermedad que hace difícil caminar y moverse bien.",
+                "fh_score": 80.52
+            },
+            "B2": {
+                "text": "**Lo que Encontraron en la Paciente**\n\nUna mujer de 58 años, que antes estaba sana, empezó a tener problemas para caminar y se caía con frecuencia. Al examinarla, los médicos notaron que su cara tenía una expresión especial: sus ojos estaban muy abiertos y fijos, tenía el ceño fruncido y la parte baja de su cara parecía inmóvil. También tenía rigidez y movimientos lentos en el tronco y el cuello, con una postura inclinada hacia atrás.\n\nCuando caminaba, al principio dudaba mucho y necesitaba ayuda para no caerse. Después de unos pasos, mejoraba un poco, pero al girar volvía a tener problemas para caminar bien. Sus pasos eran cortos, a veces se quedaba paralizada (congelación), mantenía los pies separados para no perder el equilibrio, y arrastraba los pies. Además, sus movimientos eran lentos y perdía la forma normal de mover el cuerpo y las piernas. Los reflejos que ayudan a mantener el equilibrio también estaban afectados.\n\n**Lo que Vieron en el Cerebro**\n\nUna resonancia magnética, que es una imagen detallada del cerebro, mostró que algunas partes importantes estaban más pequeñas de lo normal. En especial, el mesencéfalo (una parte del cerebro que controla movimientos), el acueducto de Silvio y el tercer ventrículo (espacios llenos de líquido en el cerebro) estaban dilatados o agrandados. También había pérdida de tejido en los lóbulos frontales, que son áreas importantes para pensar y controlar movimientos. Además, apareció un signo especial llamado \"signo del colibrí\", que ayuda a los médicos a identificar esta enfermedad.\n\n**Qué Significa Todo Esto**\n\nCon estos síntomas y los resultados del examen, los médicos concluyeron que la paciente probablemente tiene una enfermedad llamada parálisis supranuclear progresiva (PSP). Esta enfermedad afecta el control de los movimientos, el equilibrio y la expresión facial, y suele empeorar con el tiempo. Aunque no tiene algunos síntomas típicos como problemas graves en la vejiga o cambios fuertes en la personalidad, sí muestra apatía, que es una falta de interés o motivación. Este diagnóstico ayudará a los médicos a planear el mejor cuidado para ella.",
+                "fh_score": 58.19
+            },
+            "B3": {
+                "text": "**Contexto**\n\nUna mujer de 58 años, previamente sana, acudió a consulta debido a problemas para caminar acompañados de caídas frecuentes. La evaluación neurológica detallada reveló signos característicos en su rostro y movimientos, así como alteraciones específicas en su forma de caminar y en estudios de imagen cerebral.\n\n**Hallazgos Clave**\n\n- **Apariencia facial característica:** La paciente mostraba una mirada fija con los ojos muy abiertos, fruncimiento de la frente que generaba una expresión de ceño fruncido (conocido como signo del procerus) y una expresión fija en la parte inferior de la cara.\n\n- **Alteraciones motoras:** Presentaba hipocinesia (movimientos lentos) y rigidez simétrica, principalmente en la zona axial, es decir, en el tronco y cuello, con una postura inclinada hacia atrás (retrocolis).\n\n- **Trastorno de la marcha:** La forma de caminar mostraba un patrón típico de afectación del nivel superior del sistema nervioso. Inicialmente, la paciente vacilaba notablemente y necesitaba apoyo de objetos o personas para comenzar a caminar. Al avanzar, sus pasos mejoraban algo, pero al intentar girar reaparecía una marcha ineficaz. Además, caminaba con pasos cortos, episodios de congelación (parálisis temporal de la marcha), base amplia para mantener el equilibrio, desequilibrio general, movimientos lentos de las piernas, arrastre de los pies y pérdida de la fluidez normal del tronco y extremidades. Los reflejos posturales, que ayudan a mantener la estabilidad, estaban alterados.\n\n- **Movimientos oculares:** Se observaron alteraciones en los movimientos sacádicos (movimientos rápidos del ojo para cambiar la mirada), especialmente en la dirección vertical, con una oftalmoplejía supranuclear, que implica dificultad para mover los ojos hacia arriba o abajo debido a un problema en el cerebro.\n\n- **Ausencia de otros signos frontales:** No se detectaron rigidez paratónica (una rigidez muscular variable), reflejos de prensión (agarre involuntario), incontinencia urinaria ni déficits cognitivos frontales típicos (como problemas en la planificación, cambios de personalidad o impulsividad), salvo un estado de apatía progresiva.\n\n- **Imágenes cerebrales:** La resonancia magnética mostró atrofia (pérdida de volumen) del mesencéfalo (una parte del tronco cerebral), dilatación del acueducto de Silvio y del tercer ventrículo (estructuras por donde circula el líquido cefalorraquídeo), atrofia bilateral de los lóbulos frontales y la presencia de signos característicos conocidos como el “signo del colibrí” y la “gloria de la mañana”, que son patrones específicos de daño cerebral en esta enfermedad.\n\n**Interpretación Clínica**\n\nEl conjunto de síntomas, signos neurológicos y hallazgos en la resonancia magnética son compatibles con un diagnóstico probable de parálisis supranuclear progresiva (PSP), una enfermedad neurodegenerativa que afecta principalmente el control del movimiento, el equilibrio y los movimientos oculares, con daño en áreas profundas del cerebro.\n\n**Próximos Pasos**\n\nEl diagnóstico de PSP implica un seguimiento neurológico continuo para manejar los síntomas, prevenir caídas y mejorar la calidad de vida. Aunque actualmente no existe una cura, el tratamiento puede incluir terapias físicas, medicamentos para controlar la rigidez y la lentitud de movimientos, y apoyo multidisciplinario para abordar las dificultades motoras y cognitivas que puedan surgir.",
+                "fh_score": 28.73
+            }
+        }
+    },
+    {
+        "article": "Una mujer de 36 años, previamente sana, fue picada una vez por un insecto Hymenoptera desconocido, lo que le provocó hinchazón y eritema en la parte dorsal de la mano derecha. La fiebre punzante apareció en un plazo de 6 horas, a pesar de que el sitio de la picadura se volvió irreconocible gradualmente. Acudió a una clínica local donde le recetaron esteroides orales (prednisolona 20 mg/día) y antibióticos. Tres días después, acudió a nuestro departamento de urgencias por una fiebre intermitente. Presentaba una temperatura elevada (38,9°C), taquicardia e hipotensión (presión arterial 80/52 mmHg) en el momento de la clasificación. La electrocardiografía mostró fibrilación auricular con una frecuencia ventricular rápida de alrededor de 130 latidos por minuto y elevación difusa del ST. La radiografía de tórax mostró una relación cardiotorácica normal sin signos de infiltración o congestión. El hemograma no mostró eosinofilia, leucocitosis, leucopenia o desviación a la izquierda. La isoenzima MB de creatina cinasa (CK-MB) y la troponina cardíaca I se elevaron a 96,0 ng/mL y 8,0 ng/mL, respectivamente. La proteína C reactiva fue de 10,5 mg/L y la procalcitonina fue de 0,32 ng/mL. El NT-proBNP fue de 20 700 pg/mL. La ecocardiografía mostró una hipocinesia global del ventrículo izquierdo con una fracción de eyección del 30,6% y sin derrame pericárdico. El cateterismo cardíaco emergente no reveló lesiones de las arterias coronarias o vasospasmo. Se insertó un globo intraaórtico durante el procedimiento para el shock cardiogénico. La hipotensión progresó acompañada de taquicardia ventricular y fibrilación ventricular, y luego se produjo un paro cardíaco intrahospitalario. La reanimación cardiopulmonar manual no tuvo éxito durante 25 minutos y se usó el soporte cardiopulmonar percutáneo (PCPS, CAPIOX® Centrifugal Pump Controller SP-200, Terumo). La circulación espontánea se estableció 25 minutos después con una recuperación total de la conciencia.\n\nLa prueba rápida de antígeno de influenza (Directigen EZ Flu A+B; BD, Franklin Lakes, NJ, EE. UU.), los cultivos de esputo, los cultivos de sangre y los exámenes serológicos para los virus respiratorios recolectados al ingreso fueron negativos. En el día 2 del ingreso, los niveles séricos de CK-MB y troponina I alcanzaron un máximo de >303 ng/ml y >81 ng/ml, respectivamente. La ecocardiografía de seguimiento 24 horas después del inicio del PCPS mostró deterioro de la función ventricular izquierda, cierre persistente de las válvulas aórticas y trombos intracardiacos en la aurícula izquierda y el ventrículo izquierdo, aproximadamente 24 horas después del inicio del soporte mecánico. En el día 3, el shock progresó con falla multiorgánica. Se aplicó hemodiálisis venovenosa continua debido a la acidosis metabólica y oliguria. En el día 4, la función ventricular derecha también se deterioró gravemente y la actividad eléctrica del corazón desapareció gradualmente. El PCPS se cambió a soportes mecánicos bi-ventriculares a través de canalizaciones hacia la aurícula derecha, el tronco pulmonar, el ápex del ventrículo izquierdo y la aorta ascendente. Ambos sistemas se establecieron utilizando bombas de sangre centrífugas MEDTRONIC Affinity CP. Debido a la hemorragia pulmonar con consolidación bilateral severa de los pulmones, se usó un oxigenador de membrana para lograr una oxigenación adecuada. El flujo sanguíneo se estableció a 3.5 L/minuto, lo que podría mantener la presión arterial media en torno a 65 mmHg. Se realizó una biopsia endomiocárdica del ventrículo izquierdo y la patología reveló una inflamación significativa compuesta principalmente por linfocitos y algunos eosinófilos. El daño miocárdico con necrosis estuvo presente, pero no extenso. En términos de ajustes de ventilador, la presión de conducción y la presión de meseta se establecieron en torno a 15 y 30 cmH2O respectivamente para la protección pulmonar. Se usó la fibra broncoscopia repetidamente para eliminar los coágulos de sangre que obstruían las vías respiratorias principales. En el día 13 del ingreso, la actividad eléctrica del corazón del paciente permaneció ausente y ambas bombas de sangre se cambiaron a los sistemas de asistencia ventricular Levitronix Centri-Mag (Levitronix LLC, Waltham, MA, EE. UU.) para un mejor soporte. El paciente fue trasladado a un centro de trasplantes y se registró como candidato para un trasplante de corazón. En el día 14 se insertó otra cánula en la vena femoral común izquierda para aumentar el flujo de entrada del VAD derecho. Desde el día 14 hasta el día 48, el paciente sufrió episodios de sangrado masivo del mediastino y la vagina, infección de la herida esternal con formación de abscesos, infecciones por úlceras de presión y progresiva hiperbilirrubinemia. Su condición se estabilizó después de desbridamiento, hemostasia quirúrgica y uso de antibióticos fuertes. Se sometió a 5 cursos de intercambio de plasma terapéutico para evitar el rechazo mediado por anticuerpos y recibió un trasplante de corazón ortotópico el día 49. El estudio patológico del corazón del paciente mostró pancarditis de ambos ventrículos y ninguna alteración específica de las 3 arterias coronarias. La ECMO de VA se mantuvo hasta el día 58 para el apoyo postoperatorio del fallo cardiaco. La biopsia endomiocárdica repetida después del trasplante no mostró evidencia de rechazo celular o humoral. La paciente experimentó episodios de shock séptico bajo inmunosupresión y se sometió a una laparoscopia exploratoria y apendicectomía el día 93. La extubación se realizó el día 96 y se dio de alta el día 101. La paciente permaneció clínicamente estable en el seguimiento de 3 meses.\n\nMH - Adulto\nMH - Animales\nMH - Abejas\nMH - Picaduras y mordeduras/*complicaciones\nMH - Oxigenación por membrana extracorpórea\nMH - Mujer\nMH - Paro cardiaco/*etiología/tratamiento\nMH - Insuficiencia cardiaca/*etiología/terapia\nMH - *Trasplante de corazón\nMH - Dispositivos de asistencia cardiaca\nMH - Humanos\nMH - Hipersensibilidad/*diagnóstico\nMH - Miocarditis/*diagnóstico\nMH - Shock, Cardiogénico/*etiología/terapia\n",
+        "gold_summary": "Paciente: Mujer, 36 años\n\nDiagnóstico final: Shock cardiogénico • miocarditis\n\nSíntomas: Fiebre\n\nMedicación: —\n\nProcedimiento clínico: soporte circulatorio mecánico\n\nEspecialidad: Cirugía\n\n\nInforme del caso:\n\nReportamos el caso de una mujer de 36 años que desarrolló fiebre y shock cardiogénico 3 días después de una picadura de abeja. La angiografía cardíaca mostró arterias coronarias permeables y una función ventricular izquierda gravemente comprometida. Su hemodinámica permaneció inestable bajo una dosis alta de agentes inotrópicos y apoyo con un balón intraaórtico. El paro cardíaco intrahospitalario ocurrió 4 horas después del ingreso y recibió reanimación cardiopulmonar extracorpórea. Su oxigenación de membrana extracorpórea venosa periférica (VA ECMO) se cambió a dispositivos de asistencia ventricular bilateral (VAD) debido a una insuficiencia cardíaca derecha progresiva. El resultado de la biopsia endomiocárdica fue compatible con el cuadro de miocarditis por hipersensibilidad. Su corazón entró en paro persistente bajo apoyo circulatorio mecánico. Se sometió a un trasplante de corazón el día 49 del ingreso y permaneció clínicamente estable 6 meses después del alta.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una mujer de 36 años fue picada por una abeja. Tres días después, tuvo fiebre y su corazón se puso muy débil. Los doctores le ayudaron con máquinas para que su corazón pudiera latir. Su corazón no mejoró y se detuvo. Entonces, le pusieron un corazón nuevo. Después de eso, ella estuvo bien y fuerte.",
+                "fh_score": 86.22
+            },
+            "B2": {
+                "text": "Caso de una mujer de 36 años con problemas graves en el corazón tras una picadura de abeja\n\nLo que pasó:  \nUna mujer sana de 36 años fue picada por un insecto parecido a una abeja. Tres días después, empezó a tener fiebre y problemas serios en el corazón, llamados shock cardiogénico, que significa que el corazón no podía bombear suficiente sangre. Cuando la revisaron, sus arterias del corazón estaban normales, pero el ventrículo izquierdo (una parte importante del corazón) no funcionaba bien.\n\nQué hicieron los médicos:  \nIntentaron ayudarla con medicamentos para mejorar la fuerza del corazón y usaron un balón intraaórtico, que es un dispositivo que ayuda a que el corazón trabaje mejor. Sin embargo, su estado empeoró y sufrió un paro cardíaco, que es cuando el corazón deja de latir. La reanimaron usando una máquina especial que hace el trabajo del corazón y los pulmones (oxigenación por membrana extracorpórea o ECMO). Más tarde, cambiaron esta máquina por dispositivos que ayudan a ambos lados del corazón (asistencia ventricular bilateral), porque la parte derecha del corazón también empezó a fallar.\n\nQué encontraron:  \nTomaron una pequeña muestra del músculo del corazón (biopsia endomiocárdica) y vieron que tenía inflamación causada por una reacción alérgica, llamada miocarditis por hipersensibilidad. Esto significa que el corazón estaba dañado por la respuesta del cuerpo a la picadura.\n\nQué pasó después:  \nEl corazón dejó de funcionar completamente a pesar de las máquinas que lo ayudaban. Por eso, le hicieron un trasplante de corazón el día 49 después de entrar al hospital. Se recuperó bien y estuvo estable durante al menos seis meses después de salir del hospital.\n\nEn resumen:  \nUna picadura de abeja causó una inflamación grave en el corazón de esta mujer, que llevó a una falla cardíaca muy seria. Gracias a tratamientos avanzados y un trasplante de corazón, pudo recuperarse. Este caso muestra lo importante que es tratar rápido y con cuidado las reacciones alérgicas que afectan al corazón.",
+                "fh_score": 57.96
+            },
+            "B3": {
+                "text": "**Contexto**  \nSe presenta el caso de una mujer de 36 años, previamente sana, que desarrolló un cuadro grave de insuficiencia cardíaca tras una picadura de abeja. Inicialmente, la paciente presentó hinchazón y enrojecimiento en la mano derecha, seguidos de fiebre en menos de 6 horas. A pesar del tratamiento inicial con esteroides y antibióticos, evolucionó con fiebre intermitente, taquicardia, hipotensión y alteraciones electrocardiográficas que indicaban compromiso cardíaco.\n\n**Hallazgos Clave**  \nAl ingreso, la paciente mostró signos de shock cardiogénico (presión arterial baja y ritmo cardíaco acelerado con fibrilación auricular), elevación significativa de marcadores cardíacos (troponina I y CK-MB), y una función ventricular izquierda gravemente reducida (fracción de eyección del 30,6%) sin evidencia de enfermedad coronaria obstructiva en el cateterismo. La ecocardiografía reveló además la presencia de trombos dentro del corazón. A pesar del soporte con balón intraaórtico y medicamentos para mejorar la función cardíaca, la paciente sufrió un paro cardíaco intrahospitalario que requirió reanimación cardiopulmonar asistida con soporte mecánico extracorpóreo (PCPS).\n\nDurante su evolución, la función cardíaca se deterioró progresivamente, afectando ambos ventrículos, y se desarrolló falla multiorgánica que requirió hemodiálisis y soporte ventilatorio avanzado. La biopsia endomiocárdica evidenció inflamación significativa con predominio de linfocitos y algunos eosinófilos, compatible con miocarditis por hipersensibilidad (una inflamación del músculo cardíaco probablemente desencadenada por una reacción alérgica o inmunológica). La paciente presentó complicaciones graves como hemorragias, infecciones y problemas en la cicatrización, que fueron manejados con intervenciones quirúrgicas y tratamientos antibióticos.\n\n**Interpretación Clínica**  \nEl cuadro clínico y los estudios realizados indican que la paciente desarrolló una miocarditis severa secundaria a una reacción de hipersensibilidad tras la picadura de abeja, que llevó a un shock cardiogénico refractario y paro cardíaco. La ausencia de enfermedad coronaria y la inflamación observada en la biopsia apoyan este diagnóstico. El soporte mecánico avanzado, incluyendo dispositivos de asistencia ventricular bilateral y oxigenación por membrana extracorpórea, fue fundamental para mantener la circulación y oxigenación mientras se evaluaba la posibilidad de trasplante cardíaco.\n\n**Próximos Pasos y Evolución**  \nDada la persistencia del fallo cardíaco y la ausencia de recuperación, la paciente fue registrada como candidata para trasplante de corazón y recibió el trasplante ortotópico en el día 49 de hospitalización. Posteriormente, se mantuvo bajo soporte postoperatorio con ECMO y fue monitoreada para detectar rechazo cardíaco, sin evidencia de este. A pesar de episodios de shock séptico y la necesidad de cirugía abdominal, la paciente logró estabilizarse, fue extubada y dada de alta al día 101. En el seguimiento a tres meses, se mantuvo clínicamente estable.\n\n**Resumen Final**  \nEste caso ilustra una forma grave y poco común de miocarditis por hipersensibilidad desencadenada por una picadura de abeja, que evolucionó rápidamente hacia un shock cardiogénico y paro cardíaco. El manejo multidisciplinario con soporte circulatorio mecánico avanzado y trasplante cardíaco fue esencial para la supervivencia y recuperación de la paciente.",
+                "fh_score": 26.44
+            }
+        }
+    },
+    {
+        "article": "Un hombre de 24 años con complicaciones cardiovasculares relacionadas con MFS fue admitido en nuestro departamento de medicina interna debido a 3 episodios consecutivos de insuficiencia cardiaca aguda descompensada con fracción de eyección reducida (ADHFrEF) de 2014 a 2017. Su historia médica restante incluye hipertensión arterial, dislipidemia, hipertiroidismo, shock anafiláctico debido a flecainida y hábito tabágico previo.\n\nEl diagnóstico de MFS se realizó en 2010, cuando se llevó a cabo la sustitución de la aorta ascendente y la válvula aórtica con prótesis mecánica debido a una disección aórtica aguda tipo A en presencia de antecedentes familiares (madre, padre y 3 hijos con MFS). Durante el período intraoperatorio, se produjo un síndrome coronario agudo inferior y se trató con cirugía de injerto de derivación de la arteria coronaria.\n\nEn mayo de 2014, se realizó la implantación de una prótesis mecánica de aorta descendente y arco aórtico debido a un aneurisma disecante crónico. El hematoma peri-aórtico y la isquemia medular complicaron la cirugía y causaron paraplejia de las extremidades inferiores, dolor y hipoestesia térmica, e incontinencia rectal. Después de 2 meses, durante su primera admisión por ADHFrEF, las pruebas de laboratorio fueron notables para N-terminal pro-BNP (NT-proBNP) de 12,000 pg/mL y el ecocardiograma transtorácico mostró una función de la prótesis normal, dilatación de todas las cámaras cardiacas (principalmente las izquierdas) con insuficiencia mitral y tricuspídea moderada, hipertrofia ventricular izquierda, acinesia de la pared inferior, discinesia septal e hipocinesia de las paredes restantes con reducción severa de la fracción de eyección ventricular izquierda (LVEF) −20%. Se le trató con diuréticos intravenosos y desfibrilador cardiaco interno (St. Jude Ellipse DR, modo DDD) sin terapia de resincronización cardiaca (criterios de electrocardiograma no cumplidos) y se le dio de alta con la máxima terapia médica (furosemida, carvedilol, ramipril, espironolactona, digoxina y amlodipina).\n\nEn agosto de 2017, se produjo un nuevo episodio de ADHFrEF. Los valores de laboratorio de admisión notables incluían NT-proBNP de 2719 pg/mL y midregional-proadrenomedullin (MR-proADM) de 1.61 nmol/L, mientras que el ecocardiograma transtorácico y transesofágico mostró un LVEF de 35%, función de prótesis normal, severa regurgitación tricuspídea, y ruptura de la valva anterior de la chorda tendineae con severa regurgitación mitral. Los pacientes fueron tratados con diuréticos intravenosos y digoxina y dados de alta con una terapia médica óptima (furosemida, carvedilol, ramipril, espironolactona, digoxina, y amlodipina).\n\nPor último, volvió a ser admitido en nuestro departamento de medicina interna en noviembre de 2017 debido a un tercer episodio de ADHFrEF y una acumulación de líquido mediastinal infectado secundaria a una corrección quirúrgica de insuficiencia valvular severa un mes antes con implantación de prótesis mecánica mitral (31 mm ST Jude) y anuloplastia tricúspide De Vega.\n\nEl examen físico reveló una presión arterial de 120/80 mm Hg, pulso de 82 bpm, frecuencia respiratoria de 26 apm, saturación de O2 de 87% en aire ambiente con posición ortopneica obligatoria, y un habitus marfanoide (peso de 147 kg, altura de 2.2 m). La evaluación cardiopulmonar reveló un segundo sonido cardíaco metálico, percusión opaca con reducción del frémito vocal táctil y crepitaciones en la base de los pulmones, disminución amplia de los sonidos respiratorios vesiculares, presencia de ascitis abundante e hinchazón de las piernas.\n\nLos valores de laboratorio notables incluyeron NT-proBNP de 10,132 pg/mL y MR-proADM de 2,36 nmoL/mL.\n\nEl análisis de gases arteriales reveló una hipoxemia grave con alcalosis respiratoria y metabólica (pH 7,56, pO2 46 mm Hg, pCO2 24,8 mm Hg, HCO3− 21,9 mm mol/L, gradiente alveolar-arterial 31 mm Hg). Aunque el electrocardiograma resaltó fibrilación auricular con frecuencia ventricular de 80 bpm, hipertrofia ventricular izquierda e isquemia subepicárdica infralateral, el ecocardiograma transtorácico mostró las mismas características que el anterior, excepto por una FEVI de 30 %, presencia de prótesis mecánicas mitrales con fuga paravalvular y gradiente medio de 9 mm Hg, e insuficiencia tricuspídea leve.\n\n\nEn la radiografía de tórax y en la tomografía computarizada de alta resolución se observa una congestión hilar con cardiomegalia, consolidación pulmonar en el lóbulo superior derecho y acumulación de líquido mediastínico infectado.\n\nEl paciente fue tratado con 250 mg de furosemida intravenosa por día, 100 mg de canrenona por día, 4,5 g de piperacilina/tazobactam cada 6 horas y 12 mg/kg de teicoplanina por día, y luego 12 mg/kg por día. El día 9, una vez alcanzada la estabilización hemodinámica, se agregó una dosis intermedia de sacubitril/valsartan de 49/51 mg por día a 3,125 mg de carvedilol por día, 100 mg de espironolactona por día, 250 mg de furosemida por día y 0,25 mg de digoxina por día.\n\nEn el seguimiento de 1 mes, sacubitril/valsartan se aumentó a 97/103 mg b.i.d. para la buena condición clínica del paciente, lo que permitió una reducción persistente y progresiva de los parámetros clínicos, de laboratorio (reducción de NT-proBNP e incremento de MR-proADM), de los parámetros ecocardiográficos (aumento del EFV final del ventrículo izquierdo (42 % vs 30 %), del diámetro final del ventrículo izquierdo, del diámetro diastólico final del ventrículo izquierdo, de la masa del ventrículo izquierdo y del índice de masa del ventrículo izquierdo) y una mejora de la calidad de vida sin nuevos episodios de ADHFrEF hasta el seguimiento de 9 meses (Fig. (Fig.1B1B y D; Tabla 1).1). Debido a la falta de un régimen de dosificación específico para sacubitril/valsartan en la miocardiopatía relacionada con la EM, utilizamos el esquema terapéutico recomendado.\n\nMH - Aminobutiratos/uso terapéutico\nMH - Antagonistas de los receptores de la angiotensina/*uso terapéutico\nMH - Compuestos de bifenilo\nMH - Combinaciones de fármacos\nMH - Insuficiencia cardiaca/*terapia farmacológica/*etiología\nMH - Humanos\nMH - Hombre\nMH - Síndrome de Marfan/*complicaciones\nMH - Tetrazoles/uso terapéutico\nMH - Resultado del tratamiento\nMH - Valsartán\nMH - Adultos jóvenes\n",
+        "gold_summary": "Preocupaciones de los pacientes:\nUn hombre de 24 años fue admitido en nuestro departamento de medicina interna debido a disnea, ascitis e hinchazón de las piernas. El análisis de gases en sangre arterial reveló una hipoxemia grave con alcalosis respiratoria y metabólica. La radiografía de tórax mostró una congestión hilar.\n\nDiagnósticos:\nInsuficiencia cardíaca aguda descompensada recurrente con fracción de eyección reducida a pesar de la terapia médica óptima en la cardiomiopatía relacionada con el síndrome de Marfan.\n\nIntervenciones y resultados:\nSe agregó sacubitril/valsartan a la terapia médica óptima después de la estabilización hemodinámica, lo que permitió una mejora clínica, de laboratorio y ecocardiográfica progresiva. El paciente mantuvo una supervivencia libre de insuficiencia cardiaca y una buena calidad de vida hasta el seguimiento de 9 meses.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un hombre joven estaba muy cansado y con las piernas hinchadas. Tenía problemas para respirar y mucho líquido en su barriga. Los doctores hicieron pruebas y vieron que su corazón no estaba funcionando bien.\n\nÉl tiene una enfermedad que hace que su corazón sea débil. Los doctores le dieron medicinas para ayudarlo. Luego, le dieron una medicina nueva llamada sacubitril/valsartan.\n\nDespués de tomar la medicina nueva, el hombre se sintió mejor. Su corazón empezó a trabajar mejor y pudo vivir sin problemas por mucho tiempo. Los doctores están contentos porque está más sano y feliz.",
+                "fh_score": 75.34
+            },
+            "B2": {
+                "text": "**Lo que le Pasó al Paciente**  \nUn joven de 24 años con síndrome de Marfan, una enfermedad que afecta el corazón y los vasos sanguíneos, fue llevado al hospital porque tenía dificultad para respirar, líquido en el abdomen (ascitis) y piernas hinchadas. Al hacerle un análisis de sangre, encontraron que tenía poco oxígeno en la sangre y un desequilibrio en los ácidos y bases de su cuerpo. La radiografía de su pecho mostró que sus pulmones estaban congestionados.\n\n**Qué Diagnosticaron**  \nEl paciente tenía insuficiencia cardíaca aguda descompensada, lo que significa que su corazón no podía bombear sangre correctamente y esto empeoraba de forma repetida. Además, su corazón tenía una fracción de eyección reducida, que es una medida de qué tan bien el corazón bombea la sangre. Esto ocurrió a pesar de que ya estaba recibiendo el mejor tratamiento médico disponible para su condición relacionada con el síndrome de Marfan.\n\n**Cómo lo Trataron y Qué Resultó**  \nDespués de estabilizar su estado, los médicos añadieron un medicamento llamado sacubitril/valsartán a su tratamiento. Este medicamento ayuda al corazón a funcionar mejor. Gracias a esto, el paciente mejoró poco a poco en su salud general, en los resultados de sus análisis de sangre y en los exámenes del corazón por ecocardiograma. Durante los siguientes nueve meses, el joven no tuvo nuevos episodios graves de insuficiencia cardíaca y pudo mantener una buena calidad de vida.",
+                "fh_score": 55.75
+            },
+            "B3": {
+                "text": "**Contexto:**  \nUn hombre joven de 24 años con diagnóstico previo de síndrome de Marfan (una enfermedad genética que afecta el tejido conectivo y puede causar problemas cardiovasculares graves) fue ingresado en el hospital debido a dificultad para respirar, acumulación de líquido en el abdomen (ascitis) y edema en las piernas. Este paciente presentaba antecedentes complejos, incluyendo múltiples cirugías aórticas y valvulares, episodios repetidos de insuficiencia cardíaca aguda con función del corazón gravemente reducida, así como complicaciones neurológicas y respiratorias.\n\n**Hallazgos Clave:**  \nAl ingreso, el análisis de gases en sangre mostró una hipoxemia severa (bajo nivel de oxígeno en la sangre) acompañada de alcalosis respiratoria y metabólica, lo que indica un desequilibrio en el pH sanguíneo debido a problemas respiratorios y metabólicos. La radiografía de tórax reveló congestión en la zona hilar (área central del pulmón), cardiomegalia (aumento del tamaño del corazón) y consolidación pulmonar, además de una acumulación de líquido infectado en el mediastino (espacio entre los pulmones). El ecocardiograma evidenció una fracción de eyección ventricular izquierda (FEVI) reducida al 30%, presencia de prótesis valvulares mecánicas con fugas y regurgitación valvular, reflejando un deterioro significativo de la función cardíaca a pesar del tratamiento previo.\n\n**Interpretación Clínica:**  \nEl paciente sufría de insuficiencia cardíaca aguda descompensada recurrente con fracción de eyección reducida, a pesar de recibir la mejor terapia médica disponible hasta ese momento. Esta condición estaba relacionada con la miocardiopatía (enfermedad del músculo cardíaco) secundaria al síndrome de Marfan, que había provocado daños estructurales severos en el corazón y los vasos sanguíneos. La infección mediastínica y las complicaciones pulmonares añadían un riesgo significativo para su pronóstico.\n\n**Intervenciones y Resultados:**  \nTras estabilizar su condición hemodinámica, se incorporó a su tratamiento sacubitril/valsartán, un medicamento que combina un inhibidor de la neprilisina y un antagonista del receptor de angiotensina, conocido por mejorar la función cardíaca en insuficiencia cardíaca con fracción de eyección reducida. La introducción de este fármaco, junto con la terapia médica óptima previa (incluyendo diuréticos, betabloqueantes, inhibidores de la enzima convertidora de angiotensina, espironolactona y digoxina), permitió una mejora progresiva en sus síntomas clínicos, parámetros de laboratorio (disminución de marcadores como NT-proBNP, que indican estrés cardíaco) y en los estudios ecocardiográficos (aumento de la fracción de eyección y mejoría en las dimensiones y masa ventricular). Durante un seguimiento de nueve meses, el paciente no presentó nuevos episodios de insuficiencia cardíaca aguda y experimentó una mejora significativa en su calidad de vida.\n\n**Próximos Pasos:**  \nDado el éxito observado con sacubitril/valsartán en este caso, se sugiere considerar este tratamiento como una opción terapéutica en pacientes jóvenes con miocardiopatía asociada al síndrome de Marfan y fracción de eyección reducida, aunque se requiere más investigación para establecer pautas específicas de dosificación y manejo en esta población particular. Además, es fundamental continuar con un seguimiento estrecho para monitorear la función cardíaca, controlar las complicaciones infecciosas y ajustar la terapia según la evolución clínica.",
+                "fh_score": 18.19
+            }
+        }
+    },
+    {
+        "article": "Paciente masculino de 41 años de edad quien ingresó en 2016 al servicio de urgencia con politraumatismo producto de accidente de tránsito; con trauma en miembros inferioA B res, en los rayos X se observa fractura de platillos tibiales izquierdos y fractura subtrocanteriana derecha, trauma toracoabdominal y trauma craneoencefálico leve.\nSe le practica osteosíntesis de fémur con clavo cefalomedular largo a foco cerrado corrigiendo la fractura subtrocanteriana y se le aplica tutor externo transarticular de rodilla como medida de control de daño local provisional; 15 días después se realiza osteosíntesis definitiva de su fractura de platillos tibiales. Evolución adecuada y satisfactoria de platillos tibiales.\nEntre 2016 y 2019 tuvo episodios esporádicos de dolor en cadera derecha que cedían fácilmente al manejo con antiinflamatorios y analgésicos sin limitar las actividades de la vida diaria y en la toma de rayos X se observaba fatiga de los bloqueos distales con dudas de la consolidación de la fractura.\nEn 2020 se incrementa el dolor en la cadera que no cede con el tratamiento médico y se acompaña de limitación funcional. En los rayos X de control se evidencia ruptura del clavo cefalomedular en su tercio proximal y no unión de la fractura subtrocantérica.\nEn Febrero de 2020 intento fallido de extracción de material de osteosíntesis (extrainstitucional), por lo que es remitido a nuestra institución. Se lleva a cirugía el 8 de Febrero, se realiza retiro de material de osteosíntesis, curetaje y toma de cultivo de foco de no unión. Cultivo positivo para Klebsiella pneumoniae recibiendo tratamiento con meropenem intravenoso por 10 días. Posteriormente se le realizó un lavado quirúrgico con drenaje de hematoma para el 20 de Febrero realizar nueva osteosíntesis con clavo cefalomedular + injerto óseo autólogo (tomado de ambas crestas iliacas) en foco de no unión.\nReactivación de la infección en Marzo de 2020, requiriendo nuevamente cirugía para lavados y desbridamiento quirúrgicos seriados (#5). Se aísla nueva bacteria Enterobacter que es manejada con vancomicina y meropenem. A f inales de Abril completa tratamiento médico y se le da salida en condiciones estables.\nEn Mayo de 2020 por persistencia de la infección se retira el material de osteosíntesis, se deja un clavo TENS endomedular recubierto de cemento con antibióticos (gentamicina).\nA finales de Mayo después de dos lavados quirúrgicos se retiró el clavo TENS, resección de bordes de fractura (hasta hueso sano) injerto óseo endomedular con un segmento de 10 cm de peroné no vascularizado (autólogo) y fijación de la fractura con una placa de soporte condíleo de fémur distal; colocación de sistema VAC y cierre definitivo de la herida en un segundo tiempo el 28 de Mayo de 2020. El paciente evolucionó adecuadamente, la herida quirúrgica cicatrizó por completo hasta el día de hoy con infección en remisión y evidencia radiológica de consolidación de la fractura, además paciente asintomático con función preservada de la extremidad.",
+        "gold_summary": "Masculino de 41 años de edad que sufre fractura subtrocantérica derecha producto de un accidente de tránsito que requirió manejo de osteosíntesis. Con posterior ruptura del clavo cefalomedular en su tercio proximal, no unión de la fractura e infecciones en sitio de la fractura. Fue tratado con múltiples lavados quirúrgicos, antibioticoterapia y un procedimiento ortopédico y quirúrgico poco convencional como el uso de una placa de soporte condíleo de fémur distal y un injerto óseo endomedular con un segmento de 10 cm de peroné no vascularizado. Paciente con evolución satisfactoria y favorable.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un hombre se lastimó mucho la pierna en un accidente. Su hueso del muslo se rompió y tuvo que ir al doctor para arreglarlo. El doctor puso un palo especial para que el hueso se pegara. \n\nPero el palo se rompió y el hueso no sanaba bien. También tuvo una infección que le dolía mucho. Los doctores limpiaron muchas veces la herida y le dieron medicinas para la infección. \n\nDespués, hicieron una operación especial para poner un hueso nuevo y un soporte para ayudar a que su pierna sanara. Ahora, el hombre está mejor y su pierna está sanando bien.",
+                "fh_score": 83.69
+            },
+            "B2": {
+                "text": "**Lo que le pasó al paciente:**  \nUn hombre de 41 años tuvo un accidente de tránsito que le causó una fractura en la parte superior del fémur derecho, llamada fractura subtrocantérica. Para arreglarla, los doctores usaron un clavo especial dentro del hueso (osteosíntesis).  \n\n**Problemas que surgieron:**  \nCon el tiempo, el clavo se rompió y la fractura no sanó bien, lo que se llama \"no unión\". Además, la zona se infectó con bacterias, lo que complicó la recuperación.  \n\n**Tratamientos realizados:**  \nEl paciente necesitó varias cirugías para limpiar la infección y quitar el material roto. También recibió antibióticos fuertes para combatir las bacterias. Para ayudar a que el hueso sanara, los médicos usaron un método especial que incluyó colocar una placa metálica para sostener el hueso y un injerto óseo. Este injerto fue un pedazo de hueso tomado de su propia pierna (del peroné) que se colocó dentro del hueso fracturado para ayudar a que creciera y se uniera.  \n\n**Resultado final:**  \nDespués de todo este tratamiento, el paciente mejoró mucho. La herida sanó bien, la infección desapareció y la fractura se unió correctamente. Ahora puede usar su pierna sin dolor y con buena función.",
+                "fh_score": 65.91
+            },
+            "B3": {
+                "text": "**Contexto**  \nSe trata de un hombre de 41 años que sufrió un accidente de tránsito en 2016, el cual le provocó múltiples lesiones, entre ellas fracturas en ambas piernas: una fractura subtrocantérica (zona proximal del fémur) en la cadera derecha y fracturas en los platillos tibiales izquierdos. Inicialmente, se le realizó una cirugía para estabilizar la fractura de cadera mediante un clavo cefalomedular largo, y posteriormente se corrigió la fractura de la tibia. Durante los primeros años, el paciente tuvo episodios esporádicos de dolor en la cadera derecha, pero sin limitación importante en sus actividades diarias.\n\n**Hallazgos Clave**  \nEn 2020, el dolor en la cadera derecha empeoró y se acompañó de dificultad para mover la pierna. Las radiografías mostraron que el clavo utilizado para fijar la fractura se había roto en su parte proximal y que la fractura no había sanado correctamente (no unión). Se intentó retirar el material de osteosíntesis en otro centro sin éxito, por lo que fue referido a un hospital especializado. Allí se realizó la extracción del material, limpieza quirúrgica de la zona afectada y se identificó una infección causada por la bacteria Klebsiella pneumoniae, que fue tratada con antibióticos intravenosos.  \n\nA pesar del tratamiento, la infección reapareció en marzo de 2020, detectándose otra bacteria llamada Enterobacter, lo que requirió múltiples cirugías adicionales para limpiar y desbridar (eliminar tejido infectado) la zona afectada, junto con un tratamiento combinado de antibióticos. Debido a la persistencia de la infección, en mayo se retiró nuevamente el material de fijación y se colocó un clavo recubierto con cemento impregnado con antibióticos para controlar la infección localmente.  \n\nFinalmente, se realizó una cirugía más compleja que incluyó la resección de los bordes de la fractura hasta llegar a hueso sano, la colocación de un injerto óseo endomedular (un segmento de 10 cm de hueso peroné tomado del mismo paciente, sin conexión vascular directa), y la fijación definitiva con una placa metálica especial para soportar la zona distal del fémur. Se utilizó además un sistema de vacío para favorecer la cicatrización de la herida.  \n\n**Interpretación Clínica**  \nEste caso representa una fractura compleja con complicaciones importantes como la no unión ósea y la infección crónica, que dificultaron la consolidación normal del hueso. La ruptura del clavo de fijación y la persistencia de bacterias resistentes requirieron un manejo multidisciplinario que combinó cirugía ortopédica avanzada, técnicas de control de infecciones y uso de injertos óseos autólogos (del propio paciente). El uso de un injerto no vascularizado de peroné y una placa de soporte condíleo fue una estrategia poco convencional pero necesaria para lograr la estabilidad y promover la curación ósea.  \n\n**Próximos Pasos**  \nTras la última cirugía y el tratamiento antibiótico, el paciente mostró una evolución favorable con cicatrización completa de la herida, remisión de la infección y evidencia radiológica de consolidación de la fractura. Actualmente se encuentra asintomático y conserva la función de la extremidad afectada. Se recomienda continuar con seguimiento clínico y radiológico para asegurar la estabilidad a largo plazo y prevenir posibles recaídas infecciosas o problemas mecánicos.",
+                "fh_score": 39.36
+            }
+        }
+    },
+    {
+        "article": "Una adolescente de 17 años se presentó en nuestra clínica con una historia de dos meses de dolor torácico en el lado izquierdo y una historia de una semana de dolor en la espalda en el nivel de T7. El dolor torácico se acompañaba de palpitaciones y disnea que ocurrían de tres a cuatro días por semana. Una semana antes de la primera visita, las palpitaciones y la disnea se hicieron menos frecuentes, y desarrolló un dolor sordo diario intermitente en el lado izquierdo del pecho y la parte media de la espalda sin radiación, en la mayoría de los casos. El dolor ocurría tanto con el ejercicio como en reposo, y duraba horas, sin factores agravantes o atenuantes. Informó una intensidad del dolor de 2 a 6 en una escala de 10 puntos. La intensidad cambiaba durante un ataque, y el promedio era 4. Estaba sana por lo demás. No había limitación en la vida diaria. Visitó a un médico local un mes antes de visitar nuestra clínica. Los resultados de los exámenes electrocardiográficos y de laboratorio de Holter fueron normales. Su historial médico incluía migraña durante tres años. Sus medicamentos regulares eran lomerizina, loxoprofen y naratriptan para la prevención y el tratamiento agudo de la migraña. Su migraña estaba bien controlada, y rara vez experimentaba ataques. Negó trauma o cirugías previas. Negó síntomas sospechosos o antecedentes familiares de afecciones autoinmunes o inflamatorias.\n\nSu presión arterial era de 107/60 mmHg y su pulso de 62 latidos/min. Medía 162 cm de altura y pesaba 43 kg, con un índice de masa corporal de 16,4 kg/m2. No se escuchaba ningún murmullo ni arritmia en su examen cardiovascular. Los pulmones estaban limpios a la auscultación bilateral. La palpación del tórax provocó un dolor local no reproducible en las articulaciones inferiores esterno-costales; la maniobra de tracción del brazo horizontal y la maniobra del gallo cantando no provocaron dolor. No había sensibilidad en los músculos y huesos de la parte superior del cuerpo.\n\nLos hallazgos electrocardiográficos y de laboratorio, incluida la función tiroidea, fueron normales. El examen radiográfico torácico y torácico mostró el enderezamiento de la columna torácica superior y una pérdida de la curvatura cifótica normal. Las radiografías de las costillas inferiores no revelaron fractura ni neumotórax. Sospechamos un síndrome de la espalda recta, de acuerdo con los dos criterios diagnósticos diferentes propuestos por Davies et al. y DeLeon et al. La distancia entre la mitad del borde anterior de T8 y una línea vertical que conecta T4 a T12 fue de 0.91 cm. El diámetro anteroposterior fue de 74.0 cm, y el diámetro transversal fue de 243.2 cm. Le aconsejamos que comenzara y continuara la terapia quiropráctica para aumentar la cifosis torácica. Procedimos con una espera vigilante durante un mes en atención ambulatoria.\n\nDespués de esta primera visita, el dolor de pecho y de espalda se alivió gradualmente. Las palpitaciones y la disnea apenas se produjeron. Todos los síntomas desaparecieron en tres semanas. En la visita de seguimiento de un mes, se realizó una ecocardiografía, que reveló una regurgitación mitral trivial sin prolapso. Confirmamos el diagnóstico de síndrome de espalda recta. Reaseguramos a la paciente de que la enfermedad es benigna y le aconsejamos que continuara con la terapia quiropráctica. No ha tenido recaída de síntomas graves ni necesidad de visitar el hospital. Nunca volvió a visitar nuestra clínica en el año siguiente.\n",
+        "gold_summary": "Una adolescente de 17 años se presentó con su madre en nuestra clínica con un historial de dos meses de dolor en el pecho izquierdo y un historial de una semana de dolor en la parte media de la espalda. Diagnosticamos el síndrome de la columna vertebral basado en los hallazgos radiográficos del pecho y la columna vertebral y los síntomas de dolor en el pecho, palpitaciones y disnea. Tranquilizamos a la paciente de que la enfermedad era benigna y le aconsejamos que iniciara y continuara con la terapia quiropráctica. Todos los síntomas, incluido el dolor de espalda, desaparecieron en tres semanas.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había una niña de 17 años que tenía dolor en el pecho y en la espalda. Ella fue al doctor para que la ayudara. El doctor miró sus huesos con una foto especial. El doctor dijo que sus huesos estaban un poco rectos y eso le dolía. Le dijo que no era algo peligroso. Le dio un tratamiento para ayudar a que su espalda se sintiera mejor. Después de unas semanas, la niña ya no tenía dolor. Ahora está bien y feliz.",
+                "fh_score": 93.21
+            },
+            "B2": {
+                "text": "**Lo que le pasaba a la paciente**  \nUna chica de 17 años llegó a la clínica porque tenía dolor en el lado izquierdo del pecho durante dos meses y dolor en la parte media de la espalda desde hacía una semana. Además, sentía palpitaciones (cuando el corazón late rápido o irregular) y dificultad para respirar algunas veces.\n\n**Qué encontraron los médicos**  \nDespués de hacerle varios estudios, como radiografías del pecho y la columna, vieron que su columna torácica (la parte media de la espalda) estaba más recta de lo normal. Esto se llama \"síndrome de la espalda recta\". No encontraron problemas en el corazón ni en los pulmones que explicaran el dolor y los otros síntomas.\n\n**Qué hicieron y qué pasó después**  \nLos médicos le dijeron que esta condición no era peligrosa. Le recomendaron hacer terapia quiropráctica, que es un tratamiento donde un especialista ayuda a mejorar la postura y la movilidad de la columna. Después de seguir este tratamiento, todos sus síntomas, incluyendo el dolor y las palpitaciones, desaparecieron en tres semanas.\n\n**Qué significa esto**  \nEl síndrome de la espalda recta puede causar dolor en el pecho y la espalda, pero no es una enfermedad grave. Con el tratamiento adecuado, como la terapia quiropráctica, los síntomas pueden mejorar y desaparecer. Es importante consultar al médico para recibir el diagnóstico correcto y el tratamiento adecuado.",
+                "fh_score": 61.18
+            },
+            "B3": {
+                "text": "**Contexto**  \nUna joven de 17 años acudió a nuestra clínica acompañada por su madre, presentando un cuadro de dos meses con dolor en el lado izquierdo del pecho y una semana con dolor en la parte media de la espalda, específicamente a nivel de la séptima vértebra torácica (T7). Además, experimentaba episodios de palpitaciones (sensación de latidos cardíacos acelerados o irregulares) y dificultad para respirar (disnea) varias veces por semana. Estos síntomas comenzaron a mejorar una semana antes de la consulta, aunque persistía un dolor sordo e intermitente en la zona afectada, que podía durar horas y ocurría tanto en reposo como durante la actividad física.\n\n**Hallazgos Clave**  \nEl examen físico no mostró signos de enfermedad cardíaca ni pulmonar: la presión arterial y el pulso estaban dentro de rangos normales, no se detectaron ruidos anormales en el corazón ni en los pulmones, y no había sensibilidad en músculos o huesos que sugiriera inflamación o lesión. Los estudios electrocardiográficos y de laboratorio, incluyendo pruebas de función tiroidea, fueron normales. Las radiografías del tórax revelaron una alteración en la curvatura normal de la columna torácica superior, conocida como pérdida de la cifosis (curvatura hacia adelante), y se descartaron fracturas o neumotórax (colapso pulmonar).\n\nCon base en estos hallazgos y los criterios diagnósticos establecidos en la literatura médica, se identificó un síndrome conocido como “síndrome de la espalda recta” o “síndrome de la columna vertebral rectificada”, que se caracteriza por la pérdida de la curvatura normal de la columna torácica y puede asociarse a dolor torácico y dorsal.\n\n**Interpretación Clínica**  \nEl síndrome de la espalda recta es una condición benigna, es decir, que no pone en riesgo la vida ni causa daño grave a largo plazo. En este caso, se relacionó con los síntomas de dolor en el pecho y la espalda, así como con las palpitaciones y la disnea, que probablemente estaban vinculados a la alteración postural y mecánica de la columna vertebral.\n\n**Próximos Pasos y Evolución**  \nSe recomendó iniciar y mantener un tratamiento quiropráctico, que consiste en técnicas manuales para mejorar la movilidad y la postura de la columna, con el objetivo de restaurar la curvatura torácica normal. Durante el seguimiento ambulatorio, los síntomas fueron mejorando progresivamente hasta desaparecer completamente en tres semanas. Una ecocardiografía (ultrasonido del corazón) realizada un mes después mostró una regurgitación mitral trivial (un leve retorno de sangre en una válvula cardíaca) sin prolapso (sin desplazamiento anormal), lo cual no requería tratamiento. La paciente fue tranquilizada sobre la naturaleza benigna de su condición y se le aconsejó continuar con la terapia quiropráctica. No presentó recaídas ni necesidad de atención médica adicional en el año siguiente.\n\n**Resumen Final**  \nUna adolescente con dolor torácico y dorsal, acompañado de palpitaciones y dificultad para respirar, fue diagnosticada con síndrome de la espalda recta tras estudios clínicos y radiográficos. Con tratamiento quiropráctico y seguimiento, sus síntomas desaparecieron completamente en pocas semanas, confirmando que se trataba de una condición benigna y manejable.",
+                "fh_score": 37.87
+            }
+        }
+    },
+    {
+        "article": "Una mujer de 59 años con urolitiasis bilateral recurrente se presentó con dolor en el flanco derecho, fiebre y fatiga. Se le había colocado un stent doble J derecho un año antes para una piedra pélvica sintomática, pero no se le dio seguimiento. Tenía insuficiencia cardíaca derecha, diabetes tipo 2 mal controlada y enfermedad renal crónica (nadir de creatinina: 18 mg/L).\nEstable clínicamente, tenía una escala de coma de Glasgow de 14/15 (respuesta verbal ligeramente alterada), fiebre (38,3 °C), sensibilidad en el flanco derecho y una producción de orina de 800 cc en 24 horas.\nLos resultados de laboratorio revelaron una lesión renal aguda, con un nivel de creatinina sérica de 107 mg/L (normal: 6-12 mg/L) y urea sanguínea de 3 g/L (normal: 0.15-0.45 g/L). Los marcadores inflamatorios estaban elevados, con un nivel de proteína C reactiva de 300 mg/L (normal: <5 mg/L) y un recuento de glóbulos blancos de 17,000/mm3 (normal: 4000-10,000/mm3). Además, el paciente exhibió anemia normocítica (hemoglobina: 7.6 g/dL; normal: 12-16 g/dL) e hipercalemia leve (potasio sérico: 5.4 mEq/L; normal: 3.5-5.1 mEq/L). El análisis de orina y el cultivo de orina fueron negativos para infección bacteriana.\nUna tomografía computarizada abdominal y pélvica sin contraste reveló una hidronefrosis del lado derecho, un stent de doble J calcificado en espiral en ambos extremos y una piedra en la pelvis derecha de 35 × 28 mm (588 UH). El riñón izquierdo está reducido en tamaño, con hidronefrosis y una piedra en la pelvis de 12 × 7 mm (531 UH).\n\nDebido a la obstructiva severa de la pielonefritis, en particular causada por la endoprótesis incrustada, se realizó una nefrostomía percutánea bilateral urgente, lo que produjo una importante mejora clínica y normalización de los marcadores inflamatorios y la función renal.\nTres días después, la paciente experimentó una convulsión generalizada asociada con disartria. Una tomografía computarizada urgente del cerebro mostró lesiones isquémicas en los lóbulos occipitales izquierdo y frontal derecho, lo que indicaba un accidente cerebrovascular embólico. Se le inició un tratamiento con enoxaparina (0,4 cc diarios) y Kardegic (160 mg diarios) para la prevención de accidentes cerebrovasculares.\nA pesar de la mejora neurológica, cuatro días después, la paciente desarrolló palidez mucocutánea progresiva, taquicardia (110 latidos por minuto), hipotensión (80/50 mmHg) y hematuria macroscópica por el catéter urinario. Los niveles de hemoglobina descendieron de 7,5 g/dL a 4,4 g/dL, lo que levantó sospechas de hemorragia activa. Se administró fluidoterapia, vasopresores intravenosos y transfusiones de sangre, estabilizando su estado para una exploración de angiografía por TAC con contraste.\nLa tomografía computarizada reveló una colección polar media heterogénea de 17 mm de espesor con extravasación de contraste en las fases arterial y portal, lo que indica una hemorragia activa de las arterias del polo superior y medio. También había coágulos intraluminales en la pelvis renal y la vejiga. Se hizo un diagnóstico de fístula arteriovenosa postnefrostomía, exacerbada por la terapia anticoagulante para el accidente cerebrovascular.\nSe realizó una arteriografía renal urgente a través del acceso a la arteria femoral derecha, utilizando un catéter de diagnóstico de calibre 5. La angiografía selectiva reveló una FAV en el polo inferior del riñón con drenaje venoso temprano hacia la vena cava inferior, junto con un pequeño pseudoaneurisma. La embolización superselectiva con microespirales de 3 mm y 5 mm logró ocluir con éxito la fístula, y se usaron partículas de Gelfoam para evitar el sangrado retrógrado. Una inyección final de contraste confirmó la oclusión completa de la fístula, restaurando la integridad arterial y deteniendo la hemorragia.\n\nDespués de la embolización, se vigiló de cerca al paciente en la UCI. La hemodinámica se mantuvo estable y se tomó la decisión colegiada de reintroducir la anticoagulación con monitorización del INR para controlar el accidente cerebrovascular isquémico mientras se equilibraba el riesgo de hemorragia. La hematuria se resolvió, la función renal se normalizó y la nefrostomía siguió siendo funcional.\nSe adoptó un enfoque multidisciplinario para el tratamiento definitivo. La primera etapa involucró la litotripsia endoscópica con láser del bucle inferior calcificado del stent de JJ, la inserción de un segundo stent de JJ en paralelo con el incrustado y la extracción de la nefrostomía, que se completó con éxito. La segunda etapa, programada seis semanas después, incluyó una ureteroscopia derecha flexible para liberar el bucle superior del stent de JJ calcificado, la fragmentación de la piedra pélvica derecha mediante litotripsia con láser y la extracción completa del stent incrustado. Lamentablemente, la salud del paciente se deterioró debido a múltiples factores, entre ellos, insuficiencia cardíaca, diabetes mal controlada, enfermedad renal crónica y un accidente cerebrovascular previo, lo que demoró la finalización de la segunda etapa del tratamiento planificado.\n",
+        "gold_summary": "Una mujer de 59 años con urolitiasis bilateral recurrente, insuficiencia cardiaca derecha, diabetes tipo 2 mal controlada y enfermedad renal crónica se presentó con dolor en el flanco derecho, fiebre y fatiga. Previamente se le había colocado un stent doble J derecho, pero se perdió su seguimiento. Una tomografía computarizada reveló una hidronefrosis, un stent calcificado y una piedra pélvica de 22 mm, lo que llevó a la realización de una nefrostomía percutánea. La paciente desarrolló un accidente cerebrovascular embólico tres días después y posteriormente presentó hematuria, hipotensión y anemia significativa. La angiografía por TC confirmó una FAV con sangrado activo, que se trató con éxito con embolización.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una señora tenía dolor y fiebre. Tenía piedras en sus dos riñones. También tenía problemas con su corazón y azúcar alta. Le pusieron un tubito en el riñón, pero no fue al doctor para revisarlo. \n\nEl doctor vio que su riñón estaba muy hinchado y había una piedra grande. Le pusieron un tubito para sacar el líquido. \n\nDespués, la señora tuvo un problema en su cabeza y se cayó. Luego, empezó a tener sangre en la orina y se puso muy débil. \n\nLos doctores encontraron que estaba sangrando dentro del riñón. Hicieron un tratamiento para parar la sangre y la ayudaron mucho.",
+                "fh_score": 84.08
+            },
+            "B2": {
+                "text": "**Lo que le pasó a la paciente**  \nUna mujer de 59 años tenía piedras en ambos riñones que volvían a aparecer, además de problemas graves del corazón, diabetes mal controlada y enfermedad en los riñones. Ella sentía dolor en el lado derecho de su cuerpo, tenía fiebre y estaba cansada. Un año antes, le habían puesto un tubo llamado stent doble J en el riñón derecho para ayudar a que la orina pasara, pero no fue revisado después.  \n\n**Lo que encontraron en sus estudios**  \nUna tomografía (una especie de radiografía especial) mostró que su riñón derecho estaba inflamado por la acumulación de orina (hidronefrosis), que el stent estaba cubierto de calcio y que tenía una piedra grande en la pelvis del riñón. Por esto, le hicieron una nefrostomía, que es un procedimiento para drenar la orina directamente del riñón usando un tubo.  \n\n**Problemas que surgieron después**  \nTres días después, la mujer tuvo una convulsión y se descubrió que había sufrido un accidente cerebrovascular, que es cuando falta sangre en una parte del cerebro. Le dieron medicamentos para evitar más problemas en el cerebro.  \n\nLuego, presentó sangrado en la orina, presión baja y anemia (menos glóbulos rojos), lo que indicaba que estaba perdiendo mucha sangre. Un estudio con contraste mostró que tenía una fístula arteriovenosa (FAV), que es una conexión anormal entre una arteria y una vena en el riñón, causando sangrado.  \n\n**Cómo la trataron**  \nPara detener el sangrado, hicieron una embolización, que consiste en bloquear la fístula usando pequeños dispositivos llamados microespirales. Esto funcionó bien y la paciente se estabilizó.  \n\n**Seguimiento y tratamiento final**  \nDespués, continuaron con un tratamiento para eliminar el stent calcificado y las piedras en dos etapas, usando láser y endoscopios (instrumentos para ver y tratar dentro del cuerpo). Sin embargo, la salud de la paciente empeoró debido a sus otras enfermedades, lo que complicó completar el tratamiento.  \n\n**Qué significa todo esto**  \nEste caso muestra que cuando un stent se deja mucho tiempo sin control, puede causar problemas graves como infecciones, sangrados y daño renal. También destaca la importancia de un seguimiento médico cuidadoso para evitar complicaciones serias.",
+                "fh_score": 57.16
+            },
+            "B3": {
+                "text": "**Contexto**  \nUna mujer de 59 años con antecedentes complejos, incluyendo cálculos renales recurrentes en ambos riñones (urolitiasis bilateral), insuficiencia cardíaca del lado derecho, diabetes tipo 2 mal controlada y enfermedad renal crónica, acudió al hospital por dolor intenso en el costado derecho, fiebre y cansancio. Un año antes, se le había colocado un stent doble J (un tubo delgado que ayuda a drenar la orina desde el riñón hacia la vejiga) en el riñón derecho debido a una piedra renal, pero no se realizó un seguimiento adecuado de este dispositivo.\n\n**Hallazgos Clave**  \nAl realizar una tomografía computarizada (una exploración detallada con rayos X), se detectó que el riñón derecho presentaba hidronefrosis (acumulación de orina debido a una obstrucción), un stent doble J calcificado (con depósitos de calcio que dificultan su función) y una piedra renal grande de aproximadamente 35 × 28 mm. El riñón izquierdo también mostraba signos de daño, con una piedra más pequeña y reducción de tamaño. Debido a la obstrucción severa y el riesgo de infección, se realizó una nefrostomía percutánea bilateral urgente, que consiste en colocar tubos para drenar la orina directamente desde los riñones hacia el exterior, lo que mejoró significativamente su estado y normalizó los marcadores de inflamación y función renal.\n\nSin embargo, tres días después, la paciente sufrió una convulsión generalizada y dificultad para hablar. Un escáner cerebral mostró lesiones isquémicas (áreas con falta de riego sanguíneo) en diferentes partes del cerebro, confirmando un accidente cerebrovascular embólico (causado por un coágulo que bloqueó una arteria cerebral). Se inició tratamiento anticoagulante para prevenir nuevos eventos.\n\nPosteriormente, la paciente desarrolló signos de hemorragia activa: palidez, taquicardia, presión arterial baja y sangre visible en la orina. La hemoglobina, que mide la cantidad de glóbulos rojos, cayó drásticamente, indicando una pérdida significativa de sangre. Una tomografía con contraste evidenció una colección de sangre en el riñón con extravasación de contraste, señal clara de sangrado activo, y coágulos en la pelvis renal y vejiga. Se diagnosticó una fístula arteriovenosa (FAV), una conexión anormal entre una arteria y una vena en el riñón, probablemente causada por la nefrostomía y agravada por la anticoagulación.\n\n**Interpretación Clínica**  \nLa fístula arteriovenosa renal es una complicación rara pero grave que puede provocar hemorragias importantes. En este caso, la combinación de la lesión vascular por la nefrostomía y el tratamiento anticoagulante para el accidente cerebrovascular aumentó el riesgo de sangrado. La angiografía selectiva (una técnica que visualiza los vasos sanguíneos) confirmó la presencia de la FAV y un pequeño pseudoaneurisma (una dilatación anormal de la arteria).\n\n**Próximos Pasos y Tratamiento**  \nSe realizó una embolización superselectiva, un procedimiento mínimamente invasivo en el que se introdujeron microespirales y partículas especiales para bloquear la fístula y detener el sangrado. El procedimiento fue exitoso, restaurando la integridad vascular y estabilizando a la paciente. Posteriormente, se reintrodujo cuidadosamente la anticoagulación para tratar el accidente cerebrovascular, equilibrando el riesgo de hemorragia.\n\nEl manejo definitivo incluyó un enfoque multidisciplinario para tratar las piedras y el stent calcificado. En una primera etapa, se realizó una litotripsia endoscópica con láser para fragmentar el stent incrustado y se colocó un segundo stent para facilitar el drenaje, retirando la nefrostomía. Se planificó una segunda etapa para fragmentar la piedra pélvica y extraer completamente el stent calcificado, pero la salud general de la paciente, afectada por sus múltiples enfermedades crónicas y el accidente cerebrovascular, retrasó este procedimiento.\n\n**Resumen Final**  \nEsta paciente presentó una compleja combinación de problemas renales y vasculares, incluyendo obstrucción urinaria grave, infección, accidente cerebrovascular y una complicación hemorrágica por fístula arteriovenosa renal. El manejo requirió intervenciones urgentes y coordinadas para controlar la infección, detener el sangrado y tratar las piedras y el stent calcificado, destacando la importancia del seguimiento adecuado en pacientes con dispositivos urológicos y múltiples comorbilidades.",
+                "fh_score": 32.92
+            }
+        }
+    },
+    {
+        "article": "Un hombre de 52 años fue admitido en un hospital debido a palpitaciones repentinas y fatiga general. La electrocardiografía reveló taquicardia ventricular con una frecuencia cardíaca de 180 lpm. Su ritmo cardíaco volvió a un ritmo sinusal después de una cardioversión inmediata y luego fue derivado a nuestra institución para una investigación adicional. Su historial médico pasado incluía reconstrucción del tracto de salida del ventrículo derecho utilizando un injerto homólogo y cierre de un defecto septal ventricular para TOF, que se realizó 47 años antes. Sin embargo, se perdió su seguimiento posterior. Tras ser derivado a nuestra institución, su presión arterial era de 116/70 mmHg, frecuencia cardíaca de 80 lpm, y saturación de oxígeno del 99% (con aire ambiente). Al inspeccionar la pulsación de la vena yugular, se observaron claramente una onda prominente y un descenso profundo, que eran consistentes con el aumento de la presión de llenado del ventrículo derecho y la compensación del aumento de la contracción de la RA. Cabe destacar que la auscultación reveló un murmullo diastólico regurgitante agudo en el tercer espacio intercostal izquierdo, un primer sonido cardíaco ampliamente dividido (S1) y un segundo sonido cardíaco (S2), lo que indicaba un ventrículo derecho severamente dilatado debido a la liberación de PR libre y la presencia de una válvula pulmonar no funcional. Además, se auscultó un tercer sonido cardíaco (S3) en el cuarto borde paraesternal, que era consistente con un S3 derecho. El electrocardiograma reveló bloqueo completo del haz de rama derecha, con una duración de QRS de 200 lpm. La radiografía de tórax mostró cardiomegalia con dilatación de las arterias pulmonares bilaterales. La ecocardiografía transtorácica reveló una regresión completa de la válvula pulmonar, que resultó en PR libre y una dilatación prominente del ventrículo derecho. La evaluación volumétrica del ventrículo derecho se realizó utilizando una resonancia magnética cardíaca, que reveló un volumen final diastólico del ventrículo derecho de 428 ml (índice de volumen final diastólico del ventrículo derecho de 240 ml/m2), una fracción de eyección del ventrículo derecho del 36% y una fracción de eyección de PR del 74%. Además, la tomografía computarizada multidetector mostró claramente una regresión completa de la válvula pulmonar del injerto homólogo.\n\nEl paciente se sometió a un examen con catéter para investigar más a fondo su estado hemodinámico. Su forma de onda de presión RA fue particularmente notable, ya que consistía en una onda a prominente y un descenso y, que coincidían con el cuarto sonido cardiaco (S4) y S3 en un fonocardiograma, respectivamente. Además, se reveló que la presión arterial pulmonar final diastólica y la presión final diastólica del VD eran casi idénticas debido al PR libre. Por lo tanto, la evaluación clínica del «quinteto de sonidos cardiacos», que incluye un murmullo diastólico regurgitante agudo, un S1 ampliamente dividido, un S2 único y la presencia de un S3 y un S4 derechos, se confirmó mediante una evaluación hemodinámica y anatómica multimodal como insuficiencia cardiaca derecha grave concomitante con un VD significativamente dilatado debido a la regresión completa de la válvula pulmonar y el PR libre resultante.\n\nDespués del reemplazo de la válvula pulmonar, el «quinteto de sonidos del corazón» se resolvió por completo.\n\nMH - Insuficiencia cardiaca/*etiología\nMH - Murmullos cardiacos/*diagnóstico\nMH - *Sonidos del corazón\nMH - Humanos\nMH - Hombre\nMH - Edad Media\nMH - Insuficiencia de la válvula pulmonar/*complicaciones/diagnóstico\nMH - Taquicardia, ventricular/etiología\nMH - Tetralogía de Fallot/*cirugía\nMH - Disfunción ventricular, derecha/etiología\n",
+        "gold_summary": "Un hombre de 52 años fue derivado a nuestra institución para la evaluación de una taquicardia ventricular de inicio súbito. Su historia clínica incluía una reconstrucción del tracto de salida del ventrículo derecho a los 5 años de edad. La auscultación reveló un murmullo diastólico regurgitante agudo, un primer sonido cardiaco (S1) ampliamente dividido y un segundo sonido cardiaco (S2) único, lo que indicaba un ventrículo derecho severamente dilatado debido a una regurgitación pulmonar (RP) grave y la presencia de una válvula pulmonar no funcional. Además, el tercer sonido cardiaco (S3) y el cuarto sonido cardiaco (S4) del lado derecho estaban presentes, lo que era coherente con una presión de llenado del ventrículo derecho elevada y la presencia de un ventrículo derecho no conforme. Finalmente, el mencionado «quinteto de sonidos cardiacos» se confirmó mediante una evaluación multimodal como insuficiencia cardiaca del lado derecho con un ventrículo derecho concomitantemente severamente dilatado debido a la regresión completa de la válvula pulmonar y la consiguiente RP libre.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un hombre tenía problemas con su corazón. Su corazón latía muy rápido y se cansaba mucho. Cuando el doctor escuchó su corazón, oyó sonidos raros. Estos sonidos decían que una parte del corazón estaba muy grande y no funcionaba bien. La válvula del corazón que ayuda a la sangre a salir no estaba trabajando. Esto hizo que el corazón se llenara mucho y se hiciera más grande. Los doctores usaron muchas pruebas para entenderlo mejor. Al final, vieron que el corazón tenía problemas para trabajar bien porque la válvula estaba rota.",
+                "fh_score": 77.22
+            },
+            "B2": {
+                "text": "**Lo que le pasó al paciente**  \nUn hombre de 52 años llegó al hospital porque tenía palpitaciones rápidas y se sentía muy cansado. Cuando era niño, a los 5 años, había tenido una operación en el corazón para corregir un problema llamado Tetralogía de Fallot, que afecta cómo la sangre sale del corazón. En esa operación, le reconstruyeron una parte del ventrículo derecho, que es una de las cámaras del corazón que envía sangre a los pulmones.\n\n**Lo que encontraron al examinarlo**  \nAl escuchar su corazón con un estetoscopio, los médicos notaron varios sonidos anormales. Había un murmullo que indicaba que la sangre estaba regresando por la válvula pulmonar, que no funcionaba bien. Además, escucharon sonidos llamados S1 y S2 que estaban cambiados, y también sonidos llamados S3 y S4 en el lado derecho del corazón. Estos sonidos indican que el ventrículo derecho estaba muy agrandado y tenía problemas para llenarse y bombear la sangre correctamente.\n\n**Qué significa todo esto**  \nEstos signos juntos, que los médicos llamaron el «quinteto de sonidos cardiacos», mostraron que el paciente tenía insuficiencia cardíaca en el lado derecho del corazón. Esto pasó porque la válvula pulmonar que le habían reconstruido cuando era niño ya no funcionaba y la sangre regresaba libremente hacia el ventrículo derecho, causando que este se agrandara mucho y trabajara mal.\n\n**Qué hicieron después**  \nPara confirmar todo, usaron varios estudios, como ecocardiogramas y resonancias magnéticas, que mostraron claramente el daño en la válvula y el agrandamiento del ventrículo derecho. Finalmente, el paciente recibió un reemplazo de la válvula pulmonar, y después de la operación, los sonidos anormales del corazón desaparecieron, lo que indica que su corazón mejoró.",
+                "fh_score": 51.96
+            },
+            "B3": {
+                "text": "**Contexto**  \nUn hombre de 52 años, con antecedentes de cirugía cardíaca infantil para corregir la tetralogía de Fallot (una malformación congénita del corazón), fue ingresado tras presentar palpitaciones repentinas y fatiga. En su niñez, se le realizó una reconstrucción del tracto de salida del ventrículo derecho y cierre de un defecto septal ventricular, pero no tuvo seguimiento médico posterior. En el hospital, se detectó una taquicardia ventricular (ritmo cardíaco acelerado originado en el ventrículo) que se corrigió mediante cardioversión eléctrica.\n\n**Hallazgos Clave**  \nAl examen físico, se identificaron varios sonidos cardíacos anormales: un murmullo diastólico regurgitante agudo (sonido producido por el flujo anormal de sangre hacia atrás durante la diástole), un primer sonido cardíaco (S1) ampliamente dividido, un segundo sonido cardíaco (S2) único, y la presencia de un tercer (S3) y cuarto sonido cardíaco (S4) en el lado derecho del corazón. Estos hallazgos indicaban un ventrículo derecho severamente dilatado y con función alterada.  \n\nLas pruebas complementarias confirmaron estos hallazgos:  \n- El electrocardiograma mostró bloqueo completo del haz de rama derecha y un complejo QRS prolongado, reflejando alteraciones en la conducción eléctrica ventricular.  \n- La radiografía de tórax evidenció cardiomegalia (aumento del tamaño del corazón) y dilatación de las arterias pulmonares.  \n- La ecocardiografía y la resonancia magnética cardíaca demostraron una regresión completa de la válvula pulmonar (una estructura que normalmente evita el reflujo de sangre hacia el ventrículo derecho), lo que causaba una regurgitación pulmonar libre y una dilatación importante del ventrículo derecho con disminución de su capacidad de bombeo (fracción de eyección del 36%).  \n- La evaluación hemodinámica mediante cateterismo cardíaco mostró presiones elevadas en la aurícula derecha y ventrículo derecho, con formas de onda características que correspondían a los sonidos cardíacos S3 y S4 detectados en la auscultación.\n\n**Interpretación Clínica**  \nEl conjunto de sonidos cardíacos anormales —denominado aquí como el «quinteto de sonidos cardíacos»— reflejaba una insuficiencia cardíaca derecha grave causada por la dilatación y disfunción del ventrículo derecho, secundaria a la ausencia funcional de la válvula pulmonar y la regurgitación pulmonar libre resultante. La presencia simultánea de estos cinco sonidos (murmullo diastólico regurgitante, S1 ampliamente dividido, S2 único, S3 y S4 derechos) fue confirmada mediante una evaluación clínica, hemodinámica y anatómica exhaustiva.\n\n**Próximos Pasos y Resultado**  \nEl paciente fue sometido a un reemplazo de la válvula pulmonar, procedimiento que restauró la función valvular y eliminó la regurgitación pulmonar. Posteriormente, el «quinteto de sonidos cardíacos» desapareció por completo, indicando una mejora significativa en la función y la dinámica del ventrículo derecho.\n\n---\n\nEste caso ilustra cómo una alteración valvular congénita corregida en la infancia puede evolucionar décadas después hacia una insuficiencia cardíaca derecha severa, y cómo la evaluación detallada de los sonidos cardíacos, junto con estudios de imagen y hemodinámicos, es fundamental para un diagnóstico preciso y un tratamiento efectivo.",
+                "fh_score": 24.67
+            }
+        }
+    },
+    {
+        "article": "Un hombre de 62 años con antecedentes médicos de cardiopatía no isquémica que derivó en insuficiencia cardíaca, en estado postoperatorio de un dispositivo de asistencia ventricular izquierdo, se sometió a un trasplante cardíaco ortotópico. Mientras se recuperaba en la UCI quirúrgica, desarrolló un empeoramiento de la distensión abdominal, sensibilidad y leucocitosis, lo que motivó la evaluación por el equipo de cirugía general 6 días después del trasplante. El paciente no había evacuado ni expulsado gases desde su cirugía y no había respondido a los enemas administrados ni a la metoclopramida oral por un presunto íleo posoperatorio. Se realizó una tomografía computarizada del abdomen y la pelvis, que reveló múltiples bucles intestinales dilatados con niveles de aire-líquido y un punto de transición en el intestino delgado proximal en el cuadrante superior izquierdo, lo que generó preocupación por una obstrucción. En función de estos hallazgos y del hecho de que el paciente no había sido sometido a cirugías abdominales previas, lo que hacía que la obstrucción intestinal fuera secundaria a las adherencias, se llevó al paciente al quirófano para una laparotomía exploratoria. En el quirófano, se encontró que el intestino estaba dilatado de forma difusa sin ninguna área de isquemia aparente. Se encontró que una porción del intestino delgado estaba adherida a la pared abdominal anterior en el cuadrante superior izquierdo. Tras una exploración adicional, se encontró que una línea motriz de LVAD retenida estaba tunelizada en la cavidad peritoneal, estrangulando un bucle de intestino delgado en el cuadrante superior izquierdo. La línea motriz se liberó de la pared abdominal y se retiró, y se liberó el bucle de intestino afectado. Se encontró que era viable después de unos minutos de reperfusión. Se examinó el intestino delgado en su totalidad, desde el ligamento de Trietz distalmente hasta el intestino ciego, y se encontró que estaba dilatado pero en general era normal. Se reparó una pequeña área de desgarro seroso en el punto de adhesión a la línea motriz, principalmente. Se devolvió el intestino a la cavidad abdominal y se cerró la fascia y la piel con suturas corrientes y grapas cutáneas.\n\nMH - *Eliminación de dispositivo\nMH - Migración de cuerpos extraños/*complicaciones\nMH - Insuficiencia cardiaca/*terapia\nMH - *Trasplante de corazón\nMH - Dispositivos de asistencia cardíaca/*efectos adversos\nMH - Humanos\nMH - Obstrucción intestinal/diagnóstico por imágenes/*etiología\nMH - Laparotomía\nMH - Hombre\nMH - Edad Media\nMH - Tomografía computarizada por rayos X\nMH - Estados Unidos\n",
+        "gold_summary": "Un hombre de 62 años con antecedentes de insuficiencia cardiaca inducida por cardiomiopatía no isquémica, post-puente de asistencia ventricular izquierda y trasplante cardiaco ortotópico, presentó distensión abdominal, dolor y leucocitosis seis días después del trasplante. La TAC de abdomen y pelvis reveló bucles intestinales dilatados, niveles de aire-líquido y un punto de transición en el intestino delgado proximal. Se diagnosticó al paciente una obstrucción intestinal y se le realizó una laparotomía exploratoria. Se encontró que tenía un conducto de LVAD intraabdominal retenido que estrangulaba un bucle de intestino delgado en el cuadrante superior izquierdo. Se retiró el conducto y se liberó la sección de intestino con el retorno de la perfusión.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un hombre de 62 años se sentía mal en su barriga después de una operación en su corazón. Su barriga estaba hinchada y le dolía. Los doctores le hicieron una foto especial para ver dentro de su barriga. Vieron que su intestino estaba muy grande y apretado en un lugar. Los doctores hicieron una operación para mirar dentro. Encontraron un tubito que estaba apretando su intestino. Quitaron el tubito y el intestino volvió a estar bien. Ahora el hombre puede sentirse mejor.",
+                "fh_score": 76.39
+            },
+            "B2": {
+                "text": "**Lo que pasó con el paciente**  \nUn hombre de 62 años, que tenía problemas graves del corazón y había recibido un trasplante de corazón, comenzó a tener dolor y hinchazón en el abdomen seis días después de la operación. También tenía más glóbulos blancos en la sangre, lo que puede indicar infección o inflamación.\n\n**Qué encontraron los médicos**  \nLe hicieron una tomografía, que es un tipo de radiografía especial, y vieron que partes de su intestino estaban muy hinchadas y había señales de que algo bloqueaba el paso en el intestino delgado, que es la parte del intestino donde se absorben los nutrientes.\n\n**Qué hicieron para ayudarlo**  \nLos médicos lo operaron para ver qué causaba la obstrucción. Durante la cirugía, descubrieron que un tubo que se usaba para ayudar a su corazón (llamado LVAD) se había movido dentro del abdomen y estaba apretando un pedazo del intestino, bloqueando el paso.\n\n**Resultado de la cirugía**  \nQuitaron ese tubo que estaba causando el problema y liberaron el intestino. Después de unos minutos, el intestino volvió a funcionar bien y no había daño grave. Finalmente, cerraron la herida y el paciente pudo continuar con su recuperación.\n\n**Por qué es importante**  \nEste caso muestra que los dispositivos para ayudar al corazón pueden, en raras ocasiones, causar problemas en otras partes del cuerpo, como el intestino. Por eso, los médicos deben estar atentos a síntomas como dolor abdominal después de cirugías complejas.",
+                "fh_score": 61.15
+            },
+            "B3": {
+                "text": "**Contexto**  \nUn hombre de 62 años con antecedentes de insuficiencia cardíaca causada por una enfermedad del músculo cardíaco no relacionada con problemas de circulación (cardiomiopatía no isquémica), que había sido tratado previamente con un dispositivo de asistencia ventricular izquierdo (LVAD, un aparato que ayuda al corazón a bombear sangre), recibió un trasplante de corazón ortotópico (reemplazo del corazón en su posición normal). Durante su recuperación en la unidad de cuidados intensivos, seis días después de la cirugía, presentó un aumento progresivo de la distensión abdominal (hinchazón), dolor abdominal y un aumento en el número de glóbulos blancos (leucocitosis), indicativo de inflamación o infección.\n\n**Hallazgos Clave**  \nUna tomografía computarizada (TAC) del abdomen y la pelvis mostró múltiples segmentos del intestino delgado dilatados con niveles de aire y líquido, además de un punto de transición en el intestino delgado proximal en el cuadrante superior izquierdo del abdomen. Estos hallazgos sugirieron la presencia de una obstrucción intestinal. Dado que el paciente no tenía antecedentes de cirugías abdominales previas, lo que reduce la probabilidad de adherencias (bandas de tejido cicatricial que pueden causar obstrucción), se decidió realizar una laparotomía exploratoria (cirugía para abrir el abdomen y examinar los órganos).\n\nDurante la cirugía, se observó que el intestino estaba dilatado pero sin signos de daño irreversible (isquemia). Se identificó que una porción del intestino delgado estaba adherida a la pared abdominal anterior. Al investigar más a fondo, se descubrió que una línea motriz del LVAD, que había migrado y estaba dentro de la cavidad abdominal, estaba causando una estrangulación (compresión que impide el flujo sanguíneo) de un segmento del intestino delgado en el cuadrante superior izquierdo. Esta línea motriz fue liberada y retirada, y el segmento intestinal afectado recuperó su circulación sanguínea tras unos minutos.\n\nSe inspeccionó todo el intestino delgado desde el ligamento de Treitz (punto donde el duodeno se une al yeyuno) hasta el intestino ciego, encontrándose dilatado pero sin daño significativo. Se reparó una pequeña lesión en la capa externa del intestino (desgarro seroso) en el sitio donde estaba adherido a la línea motriz. Finalmente, el intestino fue reposicionado en la cavidad abdominal y se cerró la incisión quirúrgica.\n\n**Interpretación Clínica**  \nEste caso ilustra una complicación poco común pero grave en pacientes con dispositivos de asistencia ventricular izquierda: la migración intraabdominal de una línea motriz que puede causar obstrucción intestinal por estrangulación. La presentación clínica con distensión abdominal, dolor y leucocitosis, junto con los hallazgos radiológicos, orientaron hacia una obstrucción intestinal que requirió intervención quirúrgica urgente para evitar daño intestinal irreversible.\n\n**Próximos Pasos**  \nSe recomienda un seguimiento cuidadoso para detectar posibles complicaciones posteriores, como infecciones o recurrencia de obstrucción. Además, es importante evaluar la correcta colocación y manejo de los dispositivos de asistencia ventricular para prevenir migraciones similares. Este caso destaca la necesidad de un abordaje multidisciplinario en pacientes complejos post-trasplante cardíaco con dispositivos implantados.",
+                "fh_score": 33.08
+            }
+        }
+    },
+    {
+        "article": "Un paciente de 13 años de edad, del sexo masculino, fue admitido en el Hospital de Niños de Damasco tras notar una masa palpable agrandada en la región inguinal izquierda. Su historial médico no fue notable, excepto por una intervención quirúrgica en su columna vertebral 6 años atrás, debido a un accidente, que resultó en la pérdida de la función motora y la sensación en ambas extremidades inferiores.\n\nDebido al largo período que había pasado en la cama, el paciente desarrolló úlceras de decúbito en su pie izquierdo. El único hallazgo en el examen clínico fue una masa en el área inguinal izquierda, que era móvil en las estructuras profundas y también lo era la piel que la cubría. La masa no era sensible a la palpación y no se observaron signos de inflamación local.\n\nLos exámenes de laboratorio revelaron una ESR elevada (119 mm/h en la primera hora). Se solicitaron otros exámenes básicos de laboratorio, que incluían (recuento sanguíneo completo, pruebas de función hepática, electrolitos, urea, creatinina y LDH) y estaban dentro de los rangos normales para la edad. La realización de estos exámenes fue esencial para descartar enfermedades sistémicas. Dada la ausencia de hallazgos físicos indicativos de trastornos sistémicos o inmunodeficiencias, se consideró innecesario realizar exámenes adicionales como los de VIH o antiglobulina directa.\n\nLa tomografía computarizada del abdomen, el tórax y la pelvis mostró ganglios linfáticos agrandados por debajo del ligamento inguinal, el más grande de aproximadamente 3,5 por 2,4 cm. Otros órganos y ganglios estaban dentro de los límites normales.\n\nTodas las investigaciones mencionadas fueron esenciales para descartar otros diagnósticos de alto riesgo, como linfoma y leucemia. Sin embargo, no fueron suficientes para llegar al diagnóstico definitivo, por lo que se tomó la decisión de realizar una resección quirúrgica de los ganglios.\n\nPara confirmar los diagnósticos y descartar otras posibles diferencias que pudieran presentarse con ganglios linfáticos agrandados, se realizó la extirpación quirúrgica de todos estos ganglios agrandados bajo anestesia general y se enviaron biopsias para su estudio microscópico.\n\nLa biopsia mostró una arquitectura ganglionar hiperplásica con proliferación de histiocitos y células plasmáticas con proliferación vascular, lo que es compatible con el subtipo de enfermedad de Castleman de células plasmáticas.\n\nEl paciente fue dado de alta del hospital después de 14 días, tras comprobar que no había ganglios linfáticos agrandados. La única recomendación fue prednisolona oral. El paciente se sometió a un seguimiento mediante TAC de cuerpo entero cada tres meses. Durante cada visita al hospital, se realizó un examen clínico exhaustivo y pruebas de laboratorio (por ejemplo, análisis de sangre completo, VSG, proteína C reactiva, pruebas de función hepática, pruebas de función renal), además del TAC. Después de un período de seguimiento de 12 meses, el paciente no informó de nuevos síntomas o ganglios linfáticos agrandados. Además, no se observaron anomalías durante el examen clínico o en las pruebas de laboratorio.\n",
+        "gold_summary": "Reportamos un caso único de un niño de 13 años que presentó una masa palpable agrandada en la región inguinal izquierda sin ningún síntoma constitucional. La extirpación quirúrgica de esta masa fue esencial para descartar causas preocupantes. El examen patológico reveló cambios proliferativos consistentes con el tipo de célula plasmática de la enfermedad de Castleman, que es una de las formas más raras de la enfermedad en niños. Hasta donde sabemos, este caso es el primer caso reportado de enfermedad de Castleman unicéntrica (UCD) en el área inguinal. Durante un período de seguimiento de 12 meses, no se reportaron agrandamientos adicionales de los ganglios linfáticos u otros síntomas.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había un niño de 13 años con una bolita en la ingle. La bolita no le dolía ni le hacía sentir mal. Los doctores sacaron la bolita con una operación para ver qué era. \n\nDespués, miraron la bolita con un microscopio y vieron que era una cosa rara que a veces pasa en niños. Es muy poco común. \n\nEl niño estuvo bien y no tuvo más bolitas ni se enfermó en un año. Los doctores lo cuidaron mucho y él está contento.",
+                "fh_score": 91.72
+            },
+            "B2": {
+                "text": "Caso de un niño con una masa en la ingle\n\nUn niño de 13 años notó una masa o bulto en la parte izquierda de su ingle (la zona donde la pierna se une al cuerpo). No tenía otros síntomas como fiebre o pérdida de peso. Para entender qué era esa masa, los médicos decidieron quitarla con cirugía.\n\nQué encontraron en la biopsia\n\nDespués de la cirugía, examinaron la masa bajo el microscopio. Vieron que había un crecimiento anormal de ciertas células llamadas células plasmáticas, que forman parte del sistema inmunológico. Este hallazgo mostró que el niño tenía una enfermedad llamada enfermedad de Castleman, que es muy rara en niños y afecta los ganglios linfáticos.\n\nImportancia del caso y seguimiento\n\nEste es el primer caso conocido de esta enfermedad en un ganglio linfático de la ingle en un niño. Después de la cirugía, el niño recibió un medicamento llamado prednisolona para ayudar a controlar la enfermedad. Durante un año, los médicos lo revisaron regularmente con exámenes físicos y pruebas de imagen para asegurarse de que no aparecieran nuevos ganglios agrandados ni otros problemas. El niño se mantuvo sin síntomas y sin nuevos bultos durante todo ese tiempo.\n\nEn resumen, este caso muestra la importancia de investigar y tratar las masas en los ganglios linfáticos para encontrar enfermedades raras y cuidar bien la salud.",
+                "fh_score": 63.2
+            },
+            "B3": {
+                "text": "**Contexto**  \nPresentamos el caso de un niño de 13 años que acudió al hospital debido a la presencia de una masa palpable en la región inguinal izquierda, sin presentar síntomas generales como fiebre, pérdida de peso o fatiga. Su historial médico previo incluía una cirugía en la columna vertebral tras un accidente, que le ocasionó parálisis y pérdida de sensibilidad en las piernas, lo que llevó a complicaciones como úlceras por presión en el pie izquierdo. No se identificaron otros signos clínicos relevantes ni indicios de infecciones o enfermedades sistémicas.\n\n**Hallazgos Clave**  \nLos análisis de laboratorio mostraron una velocidad de sedimentación globular (VSG) elevada, un marcador de inflamación, mientras que otros parámetros sanguíneos y pruebas de función orgánica se mantuvieron dentro de rangos normales. La tomografía computarizada (TAC) evidenció ganglios linfáticos aumentados de tamaño debajo del ligamento inguinal, siendo el mayor de aproximadamente 3,5 x 2,4 cm, sin afectación de otros órganos o ganglios. Para descartar enfermedades graves como linfoma o leucemia, se decidió realizar una cirugía para extirpar los ganglios afectados y analizarlos bajo el microscopio.\n\nEl examen histopatológico (microscópico) de los ganglios mostró una proliferación aumentada de células plasmáticas (un tipo de célula del sistema inmunitario) y células llamadas histiocitos, junto con un aumento en la formación de vasos sanguíneos, características compatibles con la forma de células plasmáticas de la enfermedad de Castleman. Esta enfermedad es una condición poco común que causa crecimiento anormal de ganglios linfáticos y puede presentarse en una única área (unicéntrica) o en múltiples regiones del cuerpo.\n\n**Interpretación Clínica**  \nEste caso representa una presentación rara de la enfermedad de Castleman unicéntrica en la región inguinal, un sitio poco frecuente para esta patología, especialmente en niños. La ausencia de síntomas sistémicos y la localización única de los ganglios afectados apoyan el diagnóstico de esta forma localizada de la enfermedad. La extirpación quirúrgica completa fue fundamental tanto para confirmar el diagnóstico como para tratar la condición.\n\n**Próximos Pasos y Seguimiento**  \nTras la cirugía, el paciente recibió tratamiento con prednisolona oral (un corticosteroide) y fue dado de alta después de 14 días sin complicaciones. Se estableció un seguimiento riguroso que incluyó evaluaciones clínicas, análisis de laboratorio y tomografías computarizadas cada tres meses para detectar cualquier recurrencia o aparición de nuevos ganglios agrandados. Durante un año de seguimiento, el paciente no presentó nuevos síntomas ni evidencia de enfermedad activa, lo que indica un buen pronóstico tras el tratamiento quirúrgico.\n\nEn resumen, este caso destaca la importancia de considerar la enfermedad de Castleman en el diagnóstico diferencial de masas ganglionares inguinales en niños, y demuestra que la resección quirúrgica puede ser curativa en la forma unicéntrica de esta enfermedad.",
+                "fh_score": 36.01
+            }
+        }
+    },
+    {
+        "article": "Un hombre asiático de 55 años de edad, que había estado recibiendo tratamiento irregularmente (el paciente no cumplía con el tratamiento) para DCMP durante los últimos 6 meses, acudió con quejas de disnea al hacer ejercicio durante 1 semana y disminución de la producción de orina durante 2 días. El paciente aparentemente estaba bien hace 1 semana cuando empezó a desarrollar disnea, inicio insidioso, gradualmente progresiva, inicialmente de grado II de la New York Heart Association (NYHA) pero progresó a grado IV de la NYHA asociada con pesadez en el pecho. La historia de ortopnea y disnea nocturna paroxística estuvo presente. Esto estuvo asociado con tos con una cantidad moderada de expectoración espumosa, no purulenta. El paciente también se quejó de hinchazón de las extremidades inferiores bilaterales. No hubo historia de hinchazón periorbital, orina espumosa o hematuria. No hubo historia de palpitación, síncope, dolor de pecho o hemoptisis. El paciente también dio una historia de una sensación de hormigueo en ambas manos y pies durante 1 mes.\n\nEl paciente había tenido un episodio similar 6 meses atrás, por el que fue hospitalizado y tratado de manera conservadora como un caso de DCMP. Se le había practicado una cirugía de cataratas en ambos ojos 15 años atrás.\n\nEn el examen físico general, el paciente estaba consciente y orientado en cuanto al tiempo, el lugar y la persona, y afebril con una presión arterial de 90/60 mmHg en el brazo derecho en posición supina y una frecuencia de pulso de 110/min, que era de bajo volumen y todos los pulsos periféricos eran palpables. Presentaba taquipnea con una frecuencia respiratoria de 28/min y palidez. Tenía un edema de pedal B/L, que era de tipo lento con presión venosa yugular elevada (JVP). No se observó ictericia, cianosis, clubbing ni linfadenopatía. Mientras se medía la presión arterial, el paciente empezó a tener espasmos en la muñeca, lo que nos dio una pista para examinar más a fondo y revelar un signo de Chvostek positivo. El signo de Trousseau también fue positivo a los 10 segundos.\n\nEl examen del sistema cardiovascular reveló un latido apical localizado en el sexto espacio intercostal izquierdo, a 1 cm fuera de la línea medioclavicular, de carácter hiperdinámico. Se escucharon S1 y S2 con normalidad en todas las áreas.\n\nEl examen del sistema respiratorio reveló una reducción de la entrada de aire en las bases pulmonares bilaterales con crepitación fina al final de la inspiración bilateral. El examen del sistema nervioso abdominal y central no reveló nada de interés.\n\n\nInvestigaciones\n\nEn el momento del ingreso, el ECG mostró bloqueo completo de rama izquierda (B-R) con un intervalo QT prolongado. La hemoglobina era de 58 g/l (133-162) con un cuadro dimórfico. El volumen corpuscular medio era de 110 fL (80,0-100,0 fL), la hemoglobina corpuscular media era de 34 pg/mL (27,0-32,0 pg/mL), la concentración media de hemoglobina corpuscular era de 36,2 g/dL (32,0-35,0 g/dL). Otros análisis revelaron niveles séricos de vitamina B12 de 135 pg/mL (211-911 pg/mL). El nivel sérico de ácido fólico era de 5,40 ng/mL (>5,38 ng/mL). El nitrógeno ureico en sangre era de 53 mg/dL (10-50) con creatinina de 0,8 mg/dL (0,7-1,3). Los resultados de las pruebas de función hepática (LFT) estaban dentro de los límites normales. El perfil de calcio mostró 4,3 mg/dL de S.calcium (8,5-10,5), fosfato 7,1 mg/dL (2,5-4,5), 3,06 g/dL de S.albumin (3,5-5,5). En vista de la hipocalcemia e hiperfosfatemia, se realizó un estudio del nivel de hormona paratiroidea intacta, que resultó ser <0,23 ng/mL (14-72). El S.magnesium era de 2,0 mg/dL (1,7-2,2). El análisis de gases en sangre arterial (ABG) fue sugestivo de una acidosis metabólica leve. El perfil tiroideo y los niveles de IgAtTG estaban dentro de los límites normales. Los niveles de ferritina y ceruloplasmina séricos estaban dentro de los límites normales. El ultrasonido abdominal y torácico mostró derrame pleural bilateral en posición supina. La vena cava inferior (IVC) y las venas hepáticas eran prominentes. El reposo dentro de los límites normales. La radiografía de tórax mostró un aplanamiento de los ángulos costofrénicos bilaterales que sugería derrame pleural bilateral. La ecocardiografía reveló un ventrículo izquierdo dilatado (LV) con una fracción de eyección del ventrículo izquierdo del 15 %, que sugería DCMP con disfunción severa del LV. Se realizó un arteriograma coronario basal que fue normal. La TC sin contraste de la cabeza mostró calcificación simétrica bilateral (B/L) en el hemisferio cerebeloso B/L, ganglios basales B/L y calcificación cortical/subcortical en la región B/L fronto-parieto-occipital. El reposo dentro de los límites normales.\n\n\nTratamiento\n\nPara el CHF, se inició al paciente con dobutamina intravenosa a una dosis de 6 µg/kg y furosemida intravenosa 20 mg BD para la descongestión. Sin embargo, el paciente no mostró una mejora significativa con el tratamiento anterior. En vista de la hipocalcemia con hiperfosfatemia y bajos niveles de hormona paratiroidea, se consideró un diagnóstico de cardiomiopatía hipocalcemica con hipoparatiroidismo y se inició al paciente con inyección de gluconato de calcio 1 g (90 mg de calcio elemental) administrado por vía intravenosa seguido de infusión de gluconato de calcio en 500 ml de dextrosa al 5% a una velocidad de 37,5 mg/hora de calcio elemental. El paciente mostró una mejora significativa después de iniciar el gluconato de calcio. El paciente fue dado de alta en condiciones estables con comprimidos de calcio por vía oral 3 g/día junto con calcitriol 0,5 µg/día. También se inició con benzotiazida con triamtereno (25/50 mg) OD, ramipril 5 mg una vez al día y carvedilol 3,125 mg dos veces al día. Para la anemia megaloblástica, se administraron inyecciones de cianocobalamina según el protocolo.\n\n\nResultado y seguimiento\n\nAl cabo de tres meses, el paciente había mejorado notablemente.\n\nLas investigaciones mostraron S.calcium 7.7, S.phosphate 6.0 y albúmina 3.6. La hemoglobina fue de 10.1 g/dL. El eco mostró una mejora en la función del LV con una fracción de eyección del 25%. Se planificó una biopsia endomiocardial, pero el paciente se negó, por lo que no pudo realizarse.\n\nMH - Gluconato de calcio/administración y dosificación/uso terapéutico\nMH - Cardiomiopatía, Dilatada/*complicaciones/diagnóstico\nMH - Ecocardiografía/métodos\nMH - Insuficiencia cardiaca/terapia farmacológica/*etiología/fisiopatología\nMH - Humanos\nMH - Hipocalcemia/*complicaciones/diagnóstico/terapia farmacológica/fisiopatología\nMH - Hipoparatiroidismo/*complicaciones/terapia farmacológica\nMH - Hombre\nMH - Edad Media\nMH - Volumen de carrera\nMH - Resultado del tratamiento\nMH - Disfunción ventricular izquierda/diagnóstico por imágenes\n",
+        "gold_summary": "Presentamos el caso de un hombre asiático de 55 años que había tenido un caso conocido de miocardiopatía dilatada durante 6 meses, que se presentó con las principales quejas de falta de aire al hacer ejercicio y disminución de la producción de orina. En el examen físico general, se observaron características que sugerían una ICC. El signo de Chvostek y Trousseau fue positivo. El paciente tenía antecedentes de cirugía de cataratas en ambos ojos 15 años atrás. Otras investigaciones revelaron una hipocalcemia. La ecografía mostró una grave hipocinesia global del ventrículo izquierdo con una fracción de eyección del ventrículo izquierdo del 15%. Esta ICC fue refractaria al tratamiento convencional, aunque, con la suplementación de calcio, el paciente mejoró sintomáticamente. En el seguimiento después de 3 meses, se observó una mejora en los parámetros ecocardiográficos con una fracción de eyección que mejoró al 25%.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había un hombre que se sentía muy cansado y le costaba respirar cuando caminaba. También hacía menos pipí. El doctor vio que su corazón estaba muy débil. El hombre tenía señales en sus manos que mostraban que le faltaba calcio. Le dieron calcio para ayudarlo. Después de un tiempo, el corazón del hombre se puso un poco mejor y él se sintió mejor también.",
+                "fh_score": 89.09
+            },
+            "B2": {
+                "text": "**Caso de un Hombre con Problemas del Corazón y Bajos Niveles de Calcio**\n\nUn hombre de 55 años, que ya tenía un diagnóstico de miocardiopatía dilatada (una enfermedad del corazón donde el músculo del ventrículo izquierdo se debilita y agranda), llegó al hospital porque tenía dificultad para respirar al hacer ejercicio y producía menos orina de lo normal.\n\n**Lo que Encontraron en el Examen**\n\nAl revisarlo, los médicos notaron signos de insuficiencia cardíaca congestiva (cuando el corazón no bombea bien y se acumula líquido). También detectaron dos signos especiales llamados Chvostek y Trousseau, que indican que el cuerpo tiene poco calcio en la sangre. Además, el paciente había tenido cirugía de cataratas en ambos ojos hace 15 años.\n\n**Resultados de las Pruebas**\n\nLas pruebas mostraron que tenía hipocalcemia, es decir, niveles bajos de calcio en la sangre. El ultrasonido del corazón (ecocardiografía) reveló que su ventrículo izquierdo estaba muy debilitado, con una fracción de eyección del 15%, lo que significa que el corazón bombeaba muy poco sangre.\n\n**Tratamiento y Mejoría**\n\nEl paciente no mejoró con el tratamiento habitual para la insuficiencia cardíaca. Sin embargo, cuando le dieron calcio por vía intravenosa, su condición mejoró notablemente. Después de tres meses, su corazón funcionaba mejor, con una fracción de eyección aumentada al 25%.\n\n**Qué Significa Esto**\n\nEste caso muestra que la falta de calcio en la sangre, causada por un problema llamado hipoparatiroidismo (cuando una glándula llamada paratiroides no produce suficiente hormona para controlar el calcio), puede empeorar la función del corazón. Al corregir el calcio, se puede mejorar la salud del corazón en pacientes con miocardiopatía dilatada.",
+                "fh_score": 53.38
+            },
+            "B3": {
+                "text": "**Contexto**  \nSe presenta el caso de un hombre asiático de 55 años con diagnóstico previo de miocardiopatía dilatada (una enfermedad del músculo cardíaco que provoca su debilitamiento y agrandamiento) durante los últimos 6 meses. El paciente acudió al hospital debido a dificultad para respirar al realizar ejercicio (disnea) y una reducción en la cantidad de orina durante los últimos dos días. Su dificultad respiratoria había empeorado progresivamente, llegando a un grado severo según la clasificación de la Asociación del Corazón de Nueva York (NYHA). Además, presentaba hinchazón en ambas piernas y tos con expectoración espumosa, síntomas compatibles con insuficiencia cardíaca congestiva (ICC).\n\n**Hallazgos Clave**  \nEn el examen físico, el paciente mostraba signos típicos de insuficiencia cardíaca, como edema en las extremidades inferiores y aumento de la presión venosa yugular. Además, durante la toma de la presión arterial, se evidenciaron espasmos musculares en la muñeca, lo que llevó a descubrir signos positivos de Chvostek y Trousseau, indicativos de hipocalcemia (niveles bajos de calcio en sangre). El paciente también tenía antecedentes de cirugía de cataratas bilateral realizada 15 años antes.\n\nLos análisis de laboratorio confirmaron hipocalcemia severa junto con niveles elevados de fosfato y una hormona paratiroidea (PTH) muy baja, lo que sugiere hipoparatiroidismo (una condición en la que las glándulas paratiroides no producen suficiente hormona para regular el calcio). La ecocardiografía mostró un ventrículo izquierdo dilatado con una fracción de eyección muy baja (15%), reflejando una función cardíaca gravemente comprometida. Otras pruebas descartaron enfermedad coronaria y evidenciaron calcificaciones cerebrales simétricas.\n\n**Interpretación Clínica**  \nEl cuadro clínico y los resultados sugieren que la insuficiencia cardíaca del paciente no solo se debía a la miocardiopatía dilatada conocida, sino que estaba agravada por una cardiomiopatía secundaria a hipocalcemia causada por hipoparatiroidismo. La hipocalcemia puede afectar la contracción del músculo cardíaco, empeorando la función ventricular. Esto explica la falta de respuesta a los tratamientos convencionales para insuficiencia cardíaca.\n\n**Tratamiento y Evolución**  \nSe inició tratamiento estándar para insuficiencia cardíaca, incluyendo dobutamina y diuréticos, sin mejoría significativa. Al identificar la hipocalcemia e hipoparatiroidismo, se administró gluconato de calcio por vía intravenosa, seguido de calcio oral y calcitriol (una forma activa de vitamina D) para corregir el déficit de calcio. Tras esta intervención, el paciente mostró una mejoría clínica notable. También se trató la anemia megaloblástica con vitamina B12.\n\nEn el seguimiento a los tres meses, el paciente presentó mejoría en los niveles de calcio y en la función cardíaca, con una fracción de eyección que aumentó al 25%, lo que indica una recuperación parcial de la capacidad de bombeo del corazón. Sin embargo, el paciente rechazó realizar una biopsia endomiocárdica que podría haber ayudado a confirmar el diagnóstico definitivo.\n\n**Próximos Pasos**  \nSe recomienda continuar con el tratamiento de calcio y calcitriol para mantener niveles adecuados de calcio en sangre y prevenir complicaciones. Además, es fundamental el seguimiento cardiológico para monitorizar la función ventricular y ajustar la terapia para la insuficiencia cardíaca. La educación del paciente sobre la importancia de la adherencia al tratamiento es clave para evitar recaídas. En caso de que el paciente acepte, una biopsia cardíaca podría aportar información adicional para el manejo a largo plazo.",
+                "fh_score": 38.74
+            }
+        }
+    },
+    {
+        "article": "Una mujer de 54 años de edad, libanesa, en hemodiálisis (HD) de mantenimiento tres veces por semana para glomeruloesclerosis segmentaria focal (GSF) fue admitida en el departamento de urgencias, luego de haber sido sometida a su HD programada la noche anterior, debido al inicio repentino de un dolor lumbar agudo en el lado izquierdo, náuseas y vómitos. El dolor había comenzado repentinamente cerca de 12 horas antes de su presentación y se agravó rápidamente. En una nota al margen, un hiperparatiroidismo secundario grave con calcificación cutánea vascular fue tratado con cinacalcet durante 3 años sin respuesta, lo que demandó una paratiroidectomía (hiperplasia de cuatro glándulas) 8 meses antes de su presentación actual. Cinco días antes de su presentación, fue admitida en el hospital debido a anemia grave y rectorragia. Su evaluación por ultrasonido renal mostró riñones bilaterales pequeños con parénquima delgado que contenía quistes de hasta 3 cm y calcificaciones vasculares sin hidronefrosis. Cuatro días antes de su presentación, la colonoscopia a través del íleo terminal reveló un pólipo de 7 mm en el colon descendente izquierdo, que fue removido por mucosectomía. La microscopía volvió como adenoma tubular sésil con displasia de bajo grado. La paciente negó fiebre o antecedentes de trauma. No hubo antecedentes previos de uso de antiplaquetarios. En la emergencia, su presión arterial y pulso fueron de 112/65 mmHg y 96 bpm, su temperatura fue de 36.8°C y presentaba abdomen levemente distendido, con dolor importante en el ángulo costovertebral izquierdo. Los hallazgos de laboratorio mostraron hemoglobina de 9.0 g/dL mientras que el hematocrito fue de 29.7%, recuento total de leucocitos 12.2 × 1000/microlitro, creatinina de 6.06 mg/dL, y nivel de proteína C reactiva de 6 mg/L. Además, el TP fue de 83% y el INR fue de 1.13. En el día de la presentación (es decir, 4 días después de la colonoscopia), se realizó una tomografía computarizada (TC) multifásica del tórax, abdomen y pelvis con y sin contraste intravenoso. El examen reveló un gran quiste y enormes hematomas intraparenquimatosos perirrenales izquierdos con una colección subcapsular de hasta 1,8 cm de espesor con colección hemática en todo el compartimiento renal que alcanzaba un diámetro de más de 9 × 4 cm, hidronefrosis izquierda y edema alrededor de la grasa en todo el flanco y calcificaciones en el hilo. Para la descompresión del sistema pélvico renal y drenaje, optamos por tratarla con inserción retrógrada de doble stent ureteral a la izquierda, que identificó un coágulo en la parte media del uréter izquierdo. Se realizaron cultivo de orina y citología y los resultados fueron negativos. Una simple radiografía del abdomen mostró el doble J en su lugar. La paciente permaneció hemodinámicamente estable, pero presentó una nueva caída en la hemoglobina (6.1 g/dL) la misma noche, lo que exigió una transfusión de una unidad de concentrado de eritrocitos leucodepleados para estabilización. Se tomó la decisión de explorar quirúrgicamente con diagnóstico presuntivo de hematoma perirrenal izquierdo subagudo y para excluir una malignidad subyacente. Se sometió a una sesión de HD sin heparina. En el tercer día, se sometió a una nefrectomía radical abierta a la izquierda con conservación de la glándula suprarrenal. Recibió 2 unidades más de concentrado de eritrocitos leucodepleados durante la intervención. El parénquima renal fue casi totalmente reemplazado por un hematoma que medía 9 × 9 × 7 cm y se extendía hasta la grasa perirrenal. Una pequeña masa papilar fue enviada por separado para análisis. La evaluación histopatológica detallada reveló un parénquima renal con lesiones de nefritis crónica mutilada por grandes áreas hemorrágicas que se extendían hasta la grasa perirrenal. Además, había una proliferación neoplásica de 2 mm, con arquitectura papilar cubierta por pequeñas células cúbicas atípicas y macrófagos espumosos en el eje, compatibles con adenoma papilar. Al día siguiente de la operación, la paciente fue sometida a HD y recibió un paquete de eritrocitos leucodepleados. El período postoperatorio fue sin intercorrerencias. El nivel de hemoglobina se mantuvo alrededor de 10 g/dL. La paciente se recuperó sin signos o síntomas de sangrado. La paciente permanece bien y asintomática y actualmente se encuentra en HD de mantenimiento regular.\n",
+        "gold_summary": "A continuación, se describe un caso inusual de una paciente con HD de 54 años de edad que presentó HPE pocos días después de una colonoscopia. La causa de la HPE fue la ruptura de un quiste de DRCA. Consideramos que la colonoscopia fue un factor desencadenante y planteamos hipótesis sobre su etiopatogenia. La paciente se sometió a una nefrectomía izquierda exitosa.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una señora de 54 años tenía un problema en sus riñones. Ella se hacía un tratamiento para limpiar su sangre. Unos días después de un examen en su barriga, empezó a sentir mucho dolor en un lado. Un quiste en su riñón se rompió y eso le dolió mucho. Los doctores le hicieron una operación para quitar ese riñón. Ahora ella está mejor y sigue con su tratamiento para limpiar su sangre.",
+                "fh_score": 85.43
+            },
+            "B2": {
+                "text": "**Caso de una mujer con sangrado en el riñón después de una colonoscopia**\n\nUna mujer de 54 años que estaba en hemodiálisis, un tratamiento para personas con problemas graves en los riñones, tuvo un problema raro. Pocos días después de hacerse una colonoscopia (un examen para revisar el colon), comenzó a sentir un dolor fuerte en la parte baja de la espalda, del lado izquierdo, junto con náuseas y vómitos.\n\nLos médicos descubrieron que tenía un sangrado grande alrededor de su riñón izquierdo. Este sangrado ocurrió porque se rompió un quiste, que es una bolsa llena de líquido que se forma en el riñón. La ruptura del quiste causó un hematoma, que es una acumulación de sangre fuera de los vasos sanguíneos.\n\nCreen que la colonoscopia pudo haber sido la causa que desencadenó este problema, aunque no es común que esto pase. Para tratar la situación, los médicos le hicieron una cirugía para quitarle el riñón izquierdo, llamada nefrectomía. La operación fue exitosa y la paciente se recuperó bien, sin más sangrados.\n\nEste caso es importante porque muestra una complicación poco común después de una colonoscopia en una persona con enfermedad renal avanzada y hemodiálisis. Los médicos aprendieron que hay que estar atentos a síntomas como dolor intenso y sangrado después de estos procedimientos en pacientes con problemas renales.",
+                "fh_score": 61.76
+            },
+            "B3": {
+                "text": "**Contexto:**  \nSe presenta el caso poco común de una mujer de 54 años que se encuentra en hemodiálisis (HD) debido a una enfermedad renal crónica avanzada llamada glomeruloesclerosis segmentaria focal. Esta paciente desarrolló un hematoma perirrenal espontáneo (HPE), que es una acumulación de sangre alrededor del riñón, pocos días después de haberse sometido a una colonoscopia, un procedimiento para examinar el colon.\n\n**Hallazgos Clave:**  \nEl hematoma perirrenal se originó por la ruptura de un quiste renal asociado a una enfermedad renal crónica avanzada (DRCA). La tomografía computarizada mostró un gran hematoma intraparenquimatoso (dentro del tejido renal) y perirrenal (alrededor del riñón) en el riñón izquierdo, con signos de sangrado activo y compresión del sistema urinario. La paciente presentó dolor lumbar intenso, anemia progresiva y requerimientos de transfusión sanguínea. Durante la intervención quirúrgica, se confirmó que el parénquima renal estaba casi completamente reemplazado por el hematoma. Además, se identificó una pequeña lesión benigna llamada adenoma papilar.\n\n**Interpretación Clínica:**  \nSe considera que la colonoscopia, realizada días antes, pudo haber sido un factor desencadenante que contribuyó a la ruptura del quiste renal y la formación del hematoma. Aunque la relación causal no es completamente clara, la manipulación abdominal y los cambios en la presión intraabdominal durante la colonoscopia podrían haber favorecido este evento hemorrágico en un riñón ya debilitado por la enfermedad crónica y la presencia de quistes. La situación requirió una nefrectomía radical (extirpación completa del riñón afectado) para controlar el sangrado y evitar complicaciones mayores.\n\n**Próximos Pasos y Seguimiento:**  \nTras la cirugía, la paciente continuó con su tratamiento de hemodiálisis sin complicaciones adicionales y se mantuvo estable, sin signos de sangrado recurrente. Este caso resalta la importancia de considerar posibles complicaciones renales en pacientes con enfermedad renal crónica avanzada que se someten a procedimientos invasivos, y la necesidad de un manejo multidisciplinario para asegurar una recuperación adecuada.",
+                "fh_score": 32.79
+            }
+        }
+    },
+    {
+        "article": "Se evaluó a una mujer de 30 años de edad con antecedentes de dos meses de dolor progresivo y disminución de la visión OD. Dos semanas antes del desarrollo de los síntomas oculares, la paciente comenzó a disminuir la prednisona como tratamiento para sus síntomas inflamatorios sistémicos. Los antecedentes médicos incluyen artritis inflamatoria, síntomas gastrointestinales que sugieren enfermedad intestinal inflamatoria y pérdida de peso de 20 libras antes de la presentación. Los detalles completos del caso de la paciente se informaron previamente y se resumen aquí junto con análisis adicionales de quimiocina y citoquina de fluido ocular.13\n\nEn el examen, las BCVAs fueron 20/40 OD y 20/20 OS, y las pupilas fueron 9 mm y akinéticas OD y 5 mm con una rápida reactividad a la luz OS. Las presiones intraoculares fueron 65 mmHg OD y 21 mmHg OS. El examen con lámpara de hendidura mostró precipitados queráticos granulomatosos pigmentados (KP) dentro de la córnea inferior, 3+ células de la cámara anterior, atrofia difusa del iris con pigmento en las zónulas, y ectropion uvea OD, y OS fue normal. La gonioscopia mostró 3+ células pigmentadas dentro del ángulo inferior OD. El examen del fondo fue normal en ambos ojos. Una paracentesis anterior diagnóstica fue positiva para ADN de VZV mediante pruebas de PCR, y las pruebas serológicas fueron positivas para anticuerpos IgG de VZV. Posteriormente, se le diagnosticó uveítis anterior hipertensiva asociada a VZV, lo que provocó el inicio de acetazolamida oral y timolol oftálmico, dorzolamida, y brimonidina para la hipertensión ocular, así como valaciclovir 1 g TID y acetato de prednisolona 1% cada 2 horas. El curso de la enfermedad de la paciente y otros detalles de su tratamiento se describieron previamente.13\n\nLa paciente fue diagnosticada con un accidente cerebrovascular (ACV), que se cree que se debe a una vasculopatía del SNC asociada al VVZ, y fue hospitalizada durante 2 semanas, durante las cuales sus síntomas oculares mejoraron gradualmente. Sin embargo, dos meses después de su ACV, desarrolló un empeoramiento del dolor y la visión en el ojo derecho, y su BCVA disminuyó a 20/100 con una PIO elevada de 39 mmHg OD. El examen reveló una inyección ciliar 1+ y 3+ células de la cámara anterior, y se cambió de prednisolona a difluprednato con una mejora mínima. Posteriormente, se sometió a un procedimiento de filtración de glaucoma con una derivación de Ahmed debido a su PIO elevada persistente a pesar de la máxima tolerancia de la terapia ocular hipertensiva. Se obtuvo una muestra de humor acuoso del ojo derecho durante la cirugía de filtración para un análisis de perfil de quimiocina/citoquina. Se estimaron los niveles de 22 citoquinas y quimioquinas, incluidos IFN-Y, IL-10, IL-12p70, IL-17A, IL-1B, IL-2, IL-5, IL-6, IL-8, TNF-a, IL-18, IL-1RA, IL-1a, IL-1a, IP-10, MCP-1, MIP-1a, MIP-1B, SDF-1a, IL-21, IL-22, IL-23 e IL-27, utilizando la técnica de inmunoensayo de perlas múltiplex. Se detectaron niveles de concentración de 7 citoquinas/quimioquinas, incluidos IL-6, IL-8, IL-18, MIP-1b, IP-10, MCP-1, e IL-1RA. La IL-1RA fue la citoquina más abundante (1000 pg/mL), mientras que IP-10 y MCP-1 fueron las segundas citoquinas más abundantes (150–200 pg/mL). Se detectaron niveles de 10–20 pg/mL de IL-18 y MCP-1b, pero a niveles mínimos en esta muestra de AqH. Se detectaron niveles de IL-6 e IL-8, pero se encontró que eran las citoquinas menos abundantes, cada una con niveles de <10 pg/mL.\n\n",
+        "gold_summary": "El caso 2 fue el de una mujer de 30 años con antecedentes de dos meses de dolor progresivo y disminución de la visión en el ojo derecho. Se le diagnosticó uveítis anterior hipertensiva tras una paracentesis diagnóstica de la cámara anterior. A pesar de la terapia exitosa para la uveítis anterior, su presión intraocular se mantuvo elevada y requirió un procedimiento de filtración de glaucoma. Se recolectó una muestra de fluido ocular en el momento de la cirugía para el análisis de perfiles de citoquinas/quimioquinas, y se detectaron niveles de 7 citoquinas/quimioquinas, entre ellas, IL-6, IL-8, IL-18, MIP-1B, IP-10, MCP-1 e IL-1RA, siendo IL-1RA la citoquina más abundante.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había una mujer que tenía dolor y no veía bien con un ojo. Los doctores encontraron que su ojo estaba inflamado y tenía mucha presión. Ella necesitó una operación para ayudar a que la presión bajara. Durante la operación, los doctores tomaron un poquito de líquido del ojo para ver qué había dentro. Encontraron unas cosas llamadas citoquinas, que son como mensajeros que dicen al cuerpo qué hacer. Una de estas citoquinas estaba más que las otras. Esto ayuda a los doctores a entender mejor qué pasa en el ojo.",
+                "fh_score": 76.39
+            },
+            "B2": {
+                "text": "**Caso de una Mujer con Problemas en el Ojo Derecho**\n\nUna mujer de 30 años tuvo dolor y pérdida de visión en su ojo derecho durante dos meses. Los médicos le diagnosticaron una inflamación llamada uveítis anterior hipertensiva, que significa que había inflamación en la parte frontal del ojo y la presión dentro del ojo estaba alta. Para confirmar esto, tomaron una pequeña muestra del líquido dentro del ojo, llamado fluido ocular.\n\nAunque recibió tratamiento para la inflamación, la presión en su ojo siguió siendo alta. Por eso, necesitó una cirugía llamada filtración de glaucoma, que ayuda a bajar la presión del ojo para evitar daños.\n\nDurante la cirugía, los médicos tomaron otra muestra del fluido ocular para estudiar unas sustancias llamadas citoquinas y quimioquinas. Estas sustancias son como señales que usan las células para comunicarse y controlar la inflamación. Encontraron siete de estas sustancias, entre ellas IL-6, IL-8, IL-18, MIP-1B, IP-10, MCP-1 y IL-1RA. La más abundante fue IL-1RA, que ayuda a reducir la inflamación en el cuerpo.\n\nEste análisis ayuda a entender mejor qué está pasando en el ojo durante la enfermedad y podría ayudar a mejorar los tratamientos en el futuro.",
+                "fh_score": 64.45
+            },
+            "B3": {
+                "text": "**Contexto**  \nSe evaluó a una mujer de 30 años que presentaba un cuadro de dos meses con dolor progresivo y disminución de la visión en su ojo derecho. Dos semanas antes del inicio de estos síntomas oculares, había comenzado a reducir la dosis de prednisona, un corticosteroide que utilizaba para tratar síntomas inflamatorios sistémicos relacionados con artritis inflamatoria y posibles enfermedades intestinales inflamatorias. Además, había experimentado una pérdida de peso significativa antes de la consulta.\n\n**Hallazgos Clave**  \nEn el examen ocular inicial, la agudeza visual era de 20/40 en el ojo derecho y 20/20 en el izquierdo. Se observaron pupilas anormalmente dilatadas y sin respuesta en el ojo derecho, con una presión intraocular (PIO) muy elevada de 65 mmHg (normalmente debe estar entre 10 y 21 mmHg), mientras que el ojo izquierdo estaba dentro de los parámetros normales. El examen con lámpara de hendidura reveló signos de inflamación en la parte frontal del ojo derecho, incluyendo células inflamatorias en la cámara anterior y depósitos granulomatosos pigmentados en la córnea. También se detectó atrofia del iris y otras alteraciones estructurales. La gonioscopia, que examina el ángulo donde drena el humor acuoso, mostró células pigmentadas inflamatorias. El fondo de ojo estaba normal en ambos ojos.\n\nUna prueba diagnóstica mediante paracentesis (extracción de fluido del ojo) confirmó la presencia de ADN del virus varicela-zóster (VVZ), responsable de la culebrilla, y los análisis serológicos indicaron anticuerpos contra este virus, confirmando la infección ocular. Se diagnosticó uveítis anterior hipertensiva asociada a VVZ, una inflamación del segmento anterior del ojo que causa aumento de la presión ocular. El tratamiento incluyó medicamentos para reducir la presión intraocular (acetazolamida, timolol, dorzolamida, brimonidina), un antiviral oral (valaciclovir) y corticosteroides tópicos (prednisolona).\n\nPosteriormente, la paciente sufrió un accidente cerebrovascular atribuido a una vasculopatía (enfermedad de los vasos sanguíneos) del sistema nervioso central relacionada con el VVZ, lo que requirió hospitalización. Durante su recuperación, los síntomas oculares mejoraron, pero dos meses después presentó un nuevo empeoramiento con aumento del dolor, disminución de la visión a 20/100 y presión intraocular elevada (39 mmHg). Se intensificó el tratamiento antiinflamatorio con difluprednato, pero la respuesta fue mínima, por lo que se realizó una cirugía de filtración para controlar la presión ocular, colocando una derivación de Ahmed.\n\n**Análisis de Citoquinas y Quimioquinas**  \nDurante la cirugía, se obtuvo una muestra del humor acuoso (fluido dentro del ojo) para analizar el perfil de citoquinas y quimioquinas, que son proteínas que regulan la inflamación y la respuesta inmune. Se evaluaron 22 de estas moléculas mediante una técnica avanzada llamada inmunoensayo de perlas múltiplex. Se detectaron niveles significativos de siete citoquinas/quimioquinas: interleucina-6 (IL-6), interleucina-8 (IL-8), interleucina-18 (IL-18), proteína quimioatrayente de macrófagos 1 beta (MIP-1b), proteína inducible por interferón gamma 10 (IP-10), proteína quimioatrayente de monocitos 1 (MCP-1) y antagonista del receptor de interleucina 1 (IL-1RA).\n\nDe estas, la IL-1RA fue la más abundante, con una concentración alrededor de 1000 pg/mL. Esta molécula actúa como un regulador que bloquea la acción de la interleucina 1, una citoquina proinflamatoria, y su presencia elevada sugiere un intento del organismo por controlar la inflamación ocular. IP-10 y MCP-1 fueron las segundas más abundantes, con niveles entre 150 y 200 pg/mL, y están involucradas en la atracción de células inmunitarias al sitio inflamado. Las otras citoquinas, incluyendo IL-6 e IL-8, estuvieron presentes en concentraciones más bajas (<10 pg/mL).\n\n**Interpretación Clínica**  \nEste caso ilustra una uveítis anterior hipertensiva causada por infección activa por VVZ, que además se complicó con un accidente cerebrovascular relacionado con la misma infección viral. La persistencia de la presión intraocular elevada a pesar del tratamiento médico requirió intervención quirúrgica. El análisis detallado del perfil inflamatorio en el humor acuoso reveló una respuesta inmunitaria compleja, con predominio de moléculas reguladoras como IL-1RA, lo que podría reflejar mecanismos de control de la inflamación en el ojo afectados por el virus.\n\n**Próximos Pasos**  \nEl manejo de esta paciente requiere un seguimiento estrecho para controlar la inflamación ocular y la presión intraocular, prevenir daños permanentes en la visión y vigilar posibles complicaciones neurológicas asociadas al VVZ. El análisis de citoquinas puede ofrecer información valiosa para ajustar terapias inmunomoduladoras y antivirales en casos similares.",
+                "fh_score": 39.8
+            }
+        }
+    },
+    {
+        "article": "Un varón negro de 2021 g de peso nació a las 35 semanas y tres días de edad gestacional estimada por repetición de cesárea debido a la preocupación por la disminución del movimiento fetal en el contexto de una puntuación de perfil biofísico baja (basada en el tono muscular, la frecuencia cardíaca, el movimiento, la respiración y el volumen de líquido amniótico). La historia materna fue notable por el rasgo de células falciformes, la edad materna avanzada y la obesidad. La historia del embarazo fue notable por oligohidramnios observados por ultrasonografía a las 31 semanas. La ecografía fetal también mostró distensión de la vejiga, hidroceles bilaterales, dilatación de la uretra y ascitis abdominal preocupantes por la obstrucción del tracto urinario inferior y la posible ruptura de la vejiga. La ruptura de membranas ocurrió al momento del parto.\n\nAl nacer, el bebé experimentó dificultad respiratoria y fue tratado con ventilación con presión positiva, oxígeno suplementario e intubación. Las puntuaciones de Apgar fueron de dos y siete a un minuto y cinco minutos de vida, respectivamente. El examen mostró hematomas sustanciales y oscurecimiento de la extremidad superior izquierda. El bebé fue trasladado a la unidad de cuidados intensivos neonatales para el tratamiento de la dificultad respiratoria y sospecha de obstrucción del tracto urinario inferior. En la evaluación realizada dentro de la hora posterior al nacimiento por especialistas en ortopedia y cirugía plástica, el tercio distal del antebrazo y la mano estaban cianóticos, y una gran ampolla y área circundante de descamación eran evidentes en el dorso de la mano. No se observó movimiento espontáneo de la extremidad superior izquierda, y no se provocó la retirada o respuesta a los estímulos. La ecografía Doppler mostró flujo arterial al nivel de la fosa antecubital, pero no se detectaron pulsos radiales o cubitales. Los hallazgos del examen físico fueron consistentes con NCS, probablemente debido a la compresión de la pared uterina debido a oligohidramnios durante el embarazo.\n\nDespués de aproximadamente 5 horas de exámenes en serie, así como una amplia discusión con los equipos de ortopedia, cirugía plástica, neonatología y anestesia pediátrica, así como con los padres del bebé, se tomó la decisión de realizar una fasciotomía descompresiva del antebrazo, la mano y el túnel carpiano para permitir el rescate de la extremidad. La fasciotomía se realizó aproximadamente 6 horas después del nacimiento. El bebé fue monitoreado de cerca durante los siguientes días. La apariencia de la extremidad superior izquierda mejoró gradualmente. Al tercer día de vida, el antebrazo y la mano habían mejorado notablemente en color y parecían bien vascularizados. Las señales Doppler estaban presentes en todo momento, desde la arteria braquial hasta cada dedo. Se permitió que las heridas de la fasciotomía se curaran por intención secundaria, y se aplicó una férula personalizada con la muñeca en posición neutra y los dedos extendidos. No hubo signos de infección o isquemia en curso. Las heridas se curaron bien a las seis semanas de edad. En la visita de seguimiento a los cuatro meses de edad, las heridas se curaron por completo. El paciente tenía un rango de movimiento pasivo completo de la muñeca y los dedos. Se observó que tenía una ligera flexión y extensión del dedo anular y meñique, pero por lo demás, un movimiento activo mínimo de la muñeca o la mano en este momento. Tenía un movimiento activo del hombro y el codo. El paciente continuará recibiendo terapia ocupacional, así como férulas y masaje de cicatrices para prevenir/minimizar las contracturas. Los equipos multidisciplinarios continuarán siguiendo su progreso y recuperación de cerca.\n",
+        "gold_summary": "Presentamos un caso de NCS diagnosticado y tratado en base a los hallazgos del examen físico. La ecografía fetal mostró distensión de la vejiga, hidroceles bilaterales, dilatación de la uretra y ascitis abdominal que preocupaban por la obstrucción del tracto urinario inferior y posible ruptura de la vejiga. Una hora después del nacimiento, el examen de la extremidad superior izquierda del lactante no mostró movimiento espontáneo, la mano y el antebrazo parecían oscuros y la mano tenía una gran ampolla con descamación. No se detectó pulso distal a la fosa antecubital mediante ecografía Doppler. Se diagnosticó al lactante con NCS y se le practicó una fasciotomía urgente. La apariencia clínica y la perfusión de la extremidad superior izquierda mejoraron gradualmente. A los cuatro meses de edad, las heridas se habían curado y el paciente tenía un rango de movimiento pasivo completo de la extremidad superior izquierda. La recuperación del movimiento activo está en curso.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un bebé nació y tenía problemas en su brazo izquierdo. El brazo estaba muy oscuro y no se movía solo. Tenía una burbuja grande en la mano. Los doctores no sentían el pulso en el brazo. Ellos hicieron una operación para ayudar al brazo. Poco a poco, el brazo se puso mejor. A los cuatro meses, las heridas estaban sanas. El bebé puede mover el brazo con ayuda. Los doctores siguen cuidando para que mejore más.",
+                "fh_score": 88.49
+            },
+            "B2": {
+                "text": "**Lo que Encontraron al Nacer**  \nUn bebé nació con problemas en su brazo izquierdo. Su mano y antebrazo estaban oscuros y tenían una ampolla grande con piel que se estaba cayendo. Además, no movía esa parte del cuerpo y los médicos no pudieron sentir el pulso en la muñeca usando un examen especial llamado ecografía Doppler, que sirve para ver el flujo de sangre.\n\n**Qué Significa el Diagnóstico**  \nLos doctores dijeron que el bebé tenía un problema llamado Síndrome de Compartment Neonatal (NCS). Esto ocurre cuando hay mucha presión dentro de los músculos, lo que puede dañar la sangre y los nervios. En este caso, probablemente fue causado por la presión dentro del útero antes de nacer.\n\n**Cómo lo Trataron**  \nPara ayudar, los médicos hicieron una cirugía llamada fasciotomía. Esta operación abre la piel y los músculos para bajar la presión y salvar el brazo. La cirugía se hizo unas seis horas después del nacimiento.\n\n**Resultados y Seguimiento**  \nDespués de la operación, el brazo del bebé mejoró poco a poco. A los tres días, el color y la circulación de la sangre en el brazo y la mano eran normales. Las heridas sanaron bien y, a los cuatro meses, el bebé podía mover pasivamente (con ayuda) su muñeca y dedos. Aunque todavía tiene poco movimiento activo (por sí mismo), especialmente en algunos dedos, puede mover el hombro y el codo. El bebé seguirá recibiendo terapia para mejorar su movimiento y evitar que las cicatrices causen problemas. Los médicos continuarán observando su recuperación con cuidado.",
+                "fh_score": 70.99
+            },
+            "B3": {
+                "text": "**Contexto**  \nSe presenta el caso de un recién nacido prematuro (35 semanas y 3 días de gestación) que pesó 2021 gramos al nacer. La madre tenía antecedentes relevantes, incluyendo rasgo de células falciformes, edad avanzada y obesidad. Durante el embarazo se detectó oligohidramnios (disminución del líquido amniótico) y signos ecográficos preocupantes como distensión de la vejiga, hidroceles bilaterales (acumulación de líquido en las bolsas testiculares), dilatación de la uretra y ascitis abdominal, lo que sugería una posible obstrucción del tracto urinario inferior y ruptura de la vejiga. Debido a la disminución del movimiento fetal y un perfil biofísico bajo, se realizó una cesárea programada.\n\n**Hallazgos Clave**  \nAl nacer, el bebé presentó dificultad respiratoria y signos evidentes de compromiso en la extremidad superior izquierda: la mano y el antebrazo estaban oscuros (cianóticos), con una gran ampolla y descamación en el dorso de la mano, además de ausencia de movimiento espontáneo y falta de respuesta a estímulos. La ecografía Doppler mostró flujo arterial hasta la fosa antecubital, pero no se detectaron pulsos en las arterias radiales o cubitales, lo que indicaba compromiso circulatorio distal. Estos hallazgos fueron compatibles con un síndrome de compresión neuromuscular (NCS), probablemente causado por la presión ejercida sobre la extremidad dentro del útero debido al oligohidramnios.\n\n**Interpretación Clínica**  \nEl diagnóstico de NCS se basó en la combinación de los hallazgos físicos y ecográficos, que indicaban una isquemia (falta de flujo sanguíneo adecuado) en la extremidad superior izquierda. Para evitar daños permanentes, se decidió realizar una fasciotomía descompresiva urgente (una cirugía que libera la presión dentro de los compartimentos musculares del antebrazo y la mano, incluyendo el túnel carpiano) aproximadamente seis horas después del nacimiento. Esta intervención permitió restaurar la circulación y prevenir la necrosis (muerte del tejido).\n\n**Próximos Pasos y Evolución**  \nTras la cirugía, la apariencia y la perfusión de la extremidad mejoraron progresivamente. A los tres días de vida, el antebrazo y la mano mostraban una coloración normal y señales Doppler positivas en toda la extremidad, desde la arteria braquial hasta los dedos. Las heridas de la fasciotomía se dejaron curar de forma natural y se protegieron con una férula personalizada para mantener la muñeca y los dedos en posición adecuada. No se presentaron infecciones ni signos de isquemia persistente. A las seis semanas, las heridas estaban completamente cicatrizadas.\n\nEn la consulta de seguimiento a los cuatro meses, el bebé tenía un rango completo de movimiento pasivo en la muñeca y los dedos, aunque el movimiento activo era limitado, con ligera flexión y extensión en algunos dedos y buen movimiento activo en el hombro y codo. Se continúa con terapia ocupacional, uso de férulas y masaje de cicatrices para prevenir contracturas (rigidez anormal) y mejorar la función. Un equipo multidisciplinario sigue monitorizando su recuperación para optimizar los resultados funcionales a largo plazo.",
+                "fh_score": 41.52
+            }
+        }
+    },
+    {
+        "article": "Una mujer de 38 años de edad fue admitida en la sala de cirugía en noviembre de 2022 con la principal queja de una hinchazón abdominal progresiva que se asoció con un dolor abdominal leve y una saciedad precoz durante cinco meses. No tenía síntomas sistémicos como pérdida de peso, estreñimiento, diarrea, deseo de alimentos salados, fatigabilidad fácil o dolor de cabeza.\nEn el examen, parecía estar bien alimentada, pero presentaba una gran distensión abdominal, un leve palidez, afebril y con un tinte de ictericia en la esclerótica.\nLa palpación abdominal reveló una gran masa intraabdominal, no dolorosa, que ocupaba todo el abdomen inferior y se extendía hacia el superior, sin signos de irritación peritoneal u organomegalia.\nLos análisis de sangre mostraron un recuento de glóbulos blancos (5,7 × 109/l), hemoglobina (9,8 g/dl), bilirrubina (103 mg/dl) con recuentos normales de plaquetas (393 × 109/l). Las enzimas hepáticas, AST (24,0 U/l), ALT (21,0 U/l), albúmina 42,7 g/l. Creatinina sérica (53 μmol/l) y ESR (80 mm/h). Todos los demás análisis de sangre fueron normales. Una ecografía abdominal reveló un complejo quiste abdominal, ambos riñones eran de tamaño normal y con una ecografía normal, el hígado parecía normal. La TC abdominal y pélvica de contraste, vistas axiales y coronales, demostraron un gran quiste suprarrenal de paredes delgadas (flechas azules) que medía aproximadamente 23,5 cm (AP) x 20,3 cm (T) x 32,2 cm (CC) con un volumen de 8 l. El gran quiste desplaza el riñón derecho (flechas rojas) inferomedial a través de la línea media y ejerce presión sobre el hígado, la vesícula biliar, el páncreas y los intestinos delgados. Se extiende hasta la fosa ilíaca derecha. Como había un tinte de esclerosis ictérica, pero la masa era separada del hígado, el páncreas, los conductos biliares y el riñón derecho. Dado el tamaño del quiste y sus efectos compresivos, se planificó una intervención quirúrgica. Se eligió un enfoque quirúrgico abierto.\n\nSe le practicó una laparotomía al paciente. Se le hizo una incisión abdominal en la línea media, bajo anestesia general, y tras abrir las capas de la pared abdominal, se identificó un enorme quiste retroperitoneal que ocupaba toda la cavidad abdominal.\n\nSe abrió el quiste para acceder al fluido que se aspiraba, como se demostró en la cistectomía que se realizó con éxito. Se aspiraron unos 8 l de fluido de color marrón de la masa. Se enviaron muestras de la pared quística y del fluido para su análisis histológico.\n\nLa paciente se recuperó sin incidentes y fue dada de alta el día 7 después de la operación. El seguimiento a los 6 y 12 meses no mostró recurrencia ni complicaciones. El examen citológico de la muestra informó la presencia de material amorfo, no hubo evidencia de malignidad. Los resultados histológicos indicaron que la pared quística contenía tejido suprarrenal sin atipia, había infiltración de la pared quística por células inflamatorias mononucleares. La superficie interna de la pared no estaba revestida por células específicas reconocibles. En cuanto a los hallazgos clínicos intraoperativos, donde el origen del quiste era incierto, los hallazgos fueron más sugerentes de un quiste gigante idiopático retroperitoneal.\n\n",
+        "gold_summary": "Una mujer de 38 años se presentó con distensión abdominal progresiva. Las imágenes revelaron un quiste retroperitoneal gigante. Debido a los recursos limitados, se realizó una laparotomía abierta y se extirpó completamente un quiste de 33 cm que contenía 8 l de líquido transparente. La histopatología confirmó un quiste retroperitoneal idiopático gigante.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una mujer tenía una barriga muy grande y le dolía un poco. Los doctores vieron que había una bolsa grande llena de líquido dentro de su barriga. La doctora hizo una operación para sacar la bolsa. La bolsa era muy grande y tenía mucho líquido adentro. Después de la operación, la mujer se sintió mejor y no volvió a tener la bolsa.",
+                "fh_score": 84.84
+            },
+            "B2": {
+                "text": "**Lo que le pasó a la paciente**  \nUna mujer de 38 años notó que su abdomen (la parte del cuerpo donde están el estómago y otros órganos) se hinchaba poco a poco durante cinco meses. También sentía un dolor leve y se llenaba rápido al comer. Al examinarla, los médicos encontraron una gran masa dentro de su abdomen, pero no tenía fiebre ni otros síntomas graves.\n\n**Qué encontraron los médicos**  \nLas pruebas de imagen, como la tomografía computarizada (una especie de radiografía avanzada), mostraron un quiste muy grande en la zona llamada retroperitoneo, que está detrás de los órganos principales del abdomen. Un quiste es una bolsa llena de líquido. Este quiste medía más de 30 centímetros y contenía alrededor de 8 litros de líquido. Debido a su tamaño, estaba presionando otros órganos importantes.\n\n**Cómo la trataron**  \nLos médicos decidieron hacer una cirugía abierta para quitar el quiste. Durante la operación, hicieron una incisión en el abdomen y sacaron el quiste, aspirando el líquido que tenía dentro. Luego, enviaron muestras del quiste para analizarlas y asegurarse de que no fuera canceroso.\n\n**Qué significan los resultados**  \nEl análisis mostró que el quiste no tenía células cancerosas y que estaba formado por tejido normal con algunas células inflamatorias. No encontraron una causa clara para el quiste, por lo que lo llamaron \"idiopático\", que significa que no se sabe exactamente por qué apareció.\n\n**Después de la cirugía**  \nLa paciente se recuperó bien y fue dada de alta una semana después. En los controles a los 6 y 12 meses no hubo problemas ni volvió a aparecer el quiste. Esto indica que la cirugía fue exitosa y que la paciente está en buen estado.",
+                "fh_score": 65.44
+            },
+            "B3": {
+                "text": "**Contexto:**  \nUna mujer de 38 años acudió al hospital debido a una hinchazón abdominal que había ido aumentando progresivamente durante cinco meses. Además, presentaba dolor abdominal leve y sensación de llenura rápida al comer. No tenía otros síntomas generales como pérdida de peso, problemas digestivos, fatiga o fiebre. En la exploración física, se observó una gran distensión del abdomen con una masa palpable que ocupaba gran parte de la cavidad abdominal, sin dolor ni signos de inflamación. También se detectó una leve palidez y un tinte amarillento en la parte blanca de los ojos (ictericia).\n\n**Hallazgos Clave:**  \nLos análisis de sangre mostraron anemia leve, bilirrubina elevada (lo que explica la ictericia), pero funciones hepáticas y renales normales. La ecografía y la tomografía computarizada (TC) con contraste revelaron un enorme quiste con paredes delgadas ubicado en la región retroperitoneal (la zona detrás del abdomen), que medía aproximadamente 33 cm en su mayor dimensión y contenía alrededor de 8 litros de líquido. Este quiste desplazaba órganos cercanos como el riñón derecho, el hígado, la vesícula biliar, el páncreas y los intestinos, pero no parecía originarse en ninguno de ellos.\n\n**Interpretación Clínica:**  \nDado el tamaño considerable del quiste y su efecto compresivo sobre órganos abdominales importantes, se decidió realizar una cirugía abierta (laparotomía) para extirparlo completamente. Durante la operación, se aspiraron 8 litros de líquido marrón del quiste y se removió la masa sin complicaciones. El análisis microscópico del tejido del quiste mostró que estaba formado por tejido suprarrenal (glándulas que se encuentran encima de los riñones) sin signos de células anormales o malignas, aunque había inflamación leve. La superficie interna del quiste no presentaba un revestimiento celular definido. Estos hallazgos sugieren que se trataba de un quiste retroperitoneal gigante idiopático, es decir, de origen desconocido y sin causa aparente.\n\n**Próximos Pasos:**  \nLa paciente tuvo una recuperación sin complicaciones y fue dada de alta siete días después de la cirugía. En los controles realizados a los 6 y 12 meses posteriores, no se detectó recurrencia del quiste ni problemas relacionados. Se recomienda continuar con seguimiento clínico periódico para asegurar que no aparezcan nuevas complicaciones o recidivas.",
+                "fh_score": 45.13
+            }
+        }
+    },
+    {
+        "article": "Un hombre de 71 años con diabetes y enfermedad de Chagas había perdido recientemente mucho peso (60 kg). La investigación clínica dio lugar a un diagnóstico de megaesófago asociado a una obstrucción significativa a nivel del cardias. Se realizó una dilatación esofágica con balón, recuperando con éxito el tránsito digestivo. Mientras tanto, durante la evaluación del riesgo quirúrgico, el paciente también presentó dolor torácico con el mínimo esfuerzo. La angiografía por tomografía computarizada coronaria realizada tres años antes mostró una enfermedad multivascular muy calcificada que afectaba a la arteria coronaria izquierda; en ese momento no se había realizado ninguna otra investigación. Esta vez, se lo derivó a nosotros para un cateterismo cardíaco.\nEl examen realizado el 16 de febrero de 2016 mostró: arteria coronaria derecha (RCA) con importante calcificación y una lesión del 50% en el tercio medio; arteria descendente posterior (PDA) y arteria posterolateral derecha (RPLA), con severa calcificación y lesiones del 80% y 70%, respectivamente; LM con 80% de lesiones calcificadas en el tercio distal; arteria descendente anterior izquierda (LAD) con significativa calcificación y 90% de lesión en el tercio medio; ramas diagonales (DG1 y DG2) con lesiones calcificadas del 70% y 80%, en el origen y en el tercio proximal, respectivamente; y arteria circunfleja izquierda (LCx) ocluida y calcificada, recibiendo colaterales grado II de múltiples orígenes. El volumen ventricular izquierdo y la contractilidad se conservaron.\n\nCon esta imagen angiográfica, una puntuación de riesgo de la Society of Thoracic Surgeons del 15,8 % para morbilidad o mortalidad, una puntuación EuroSCORE II del 4,67 %, y una debilidad significativa debido a una pérdida de peso importante y reciente, el equipo cardiaco decidió realizar una intervención coronaria percutánea (ICP) de la LM, LAD, DG1 y DG2 inicialmente y, en un segundo procedimiento después de 30 días, una ICP de las ramas de la RCA. En ambos procedimientos, también se indicó una RA debido a una calcificación significativa. No se abordaría la LCx, ya que angiográficamente el vaso no estaba tan gravemente afectado y también considerando la dificultad técnica de la recanalización, debido a la longitud del CTO y también a las paredes muy calcificadas (puntuación J-CTO 4). La LCx ya estaba recibiendo una circulación collateral de grado II.\nEl 19 de febrero de 2016, tras comenzar una terapia antiplaquetaria dual con aspirina y clopidogrel, el paciente se sometió a una angioplastia de la arteria descendente anterior, la arteria circunfleja y la arteria descendente derecha con una fresa de 1,5 mm, seguida de una predilatación con un balón de 3,0 mm x 20 mm a 14 atm y la implantación de stents liberadores de fármacos en la arteria descendente derecha y la arteria circunfleja, utilizando una técnica de mini-aplastamiento y un balón de contacto al final. Se realizó un balón de contacto en la bifurcación de la arteria descendente derecha/arteria circunfleja y, finalmente, se implantó el tercer stent liberador de fármacos desde el origen de la arteria descendente derecha para superponerse con el stent de la arteria descendente derecha. Se logró un éxito procedimental con un flujo TIMI de 3 y sin complicaciones clínicas o angiográficas.\nEl 22 de marzo de 2016, el paciente volvió para una PCI con un RotaWire PCI en el PDA y RPLA con una fresa de 1,5 mm, seguido por la implantación de dos DES de 2,75 mm x 20 mm y 2,75 mm x 16 mm a 12 atm en el PDA y RPLA, respectivamente, sin ninguna predilatación adicional. También observamos la presencia de una disección larga y severa en el tercio medio del RCA, sin duda causada por un manejo excesivo e intentos de remover la fresa, lo que causó una penetración profunda por el catéter guía 7F. Esta disección se corrigió rápidamente con la implantación de un tercer DES de 4,0 mm x 32 mm, y se obtuvo un flujo TIMI 3 final sin complicaciones clínicas o electrocardiográficas. Los dos sitios de punción femoral se ocluyeron con dispositivos AngioSeal 8F y 6F, respectivamente. El paciente permaneció en la unidad de cuidados intensivos durante 48 horas, la única anormalidad fue la elevación de CK-MB (el doble del valor de referencia). Fue dado de alta el día 3 en excelentes condiciones generales. El ecocardiograma de control mostró una contractilidad ventricular izquierda normal.\n",
+        "gold_summary": "Un hombre de 71 años con enfermedad de Chagas y angina estable en esfuerzo mínimo se sometió a una angiografía por tomografía computarizada y cineangiografía que reveló una enfermedad multivascular muy calcificada que afectaba a la arteria descendente anterior izquierda (LM). Debido al grado de calcificación, se decidió realizar una rotablation. La primera etapa de la intervención coronaria percutánea (ICP) con rotablation se realizó en la arteria descendente anterior izquierda (LM), la arteria descendente anterior izquierda y la segunda rama diagonal sin complicaciones. Casi 30 días después, volvió para una ICP de la arteria coronaria derecha (RCA). La estrategia propuesta fue la aterectomía rotativa en la arteria descendente anterior posterior (PDA) y la arteria posterolateral derecha (RPLA) con una fresa de 1,5 mm, seguida por la implantación de dos stents liberadores de fármacos (DES). A través del acceso a la arteria femoral derecha, la lesión de la RPLA se extirpó con éxito. Como no había signos de disección y se mantuvo el flujo TIMI 3, se reposicionó el RotaWire de 0,009″ para cruzar la lesión de la PDA y se realizó la extirpación de la lesión. Después de dos intentos, logramos cruzar la lesión con la fresa de 1,5 mm, sin embargo, se produjo el atrapamiento de la misma. El sistema se retiró hasta que el catéter guía penetró profundamente en la RCA, y se hicieron intentos para liberar el Rotablator moviéndolo hacia adelante y hacia atrás, pero la fresa ni siquiera giró. La arteria femoral contralateral se perforó y se insertó un catéter guía 6F JR, con el fin de mover un alambre guía y un pequeño globo de angioplastia tangencialmente a la fresa, pero sin éxito. Finalmente, avanzamos el alambre guía utilizando la técnica de «nudillo», aprovechando la torsión de la porción distal del alambre guía PT2, realizando una disección subintimal y reentrada, y pudimos cruzar fácilmente el globo, inflarlo y liberar la fresa atrapada. A través del sistema 6F, se implantaron dos DES programados y uno de rescate con éxito en la PDA, RPLA y RCA, obteniendo un flujo TIMI 3 final sin complicaciones.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había un señor de 71 años con problemas en su corazón. Su corazón tenía partes muy duras y tapadas. Los doctores usaron una máquina especial para ver su corazón. \n\nPrimero, limpiaron unas partes del corazón con una herramienta que gira rápido. Esto ayudó a que la sangre pudiera pasar mejor. Después de un mes, volvieron a limpiar otras partes del corazón. \n\nEn una parte, la herramienta se quedó atrapada. Los doctores usaron un truco con un hilo para ayudar a que la herramienta se moviera otra vez. Al final, pusieron unos tubos pequeñitos para que la sangre siga fluyendo bien. \n\nEl señor quedó bien y sin problemas después de la ayuda.",
+                "fh_score": 80.92
+            },
+            "B2": {
+                "text": "**Lo que le pasó al paciente:**  \nUn hombre de 71 años con una enfermedad llamada Chagas y problemas en el corazón tuvo dolor en el pecho al hacer poco esfuerzo. Los médicos le hicieron estudios que mostraron que varias arterias del corazón estaban muy dañadas y tenían muchas calcificaciones, que son depósitos duros que bloquean el paso de la sangre.\n\n**Qué hicieron los médicos:**  \nPara ayudarlo, los doctores usaron una técnica llamada intervención coronaria percutánea (ICP). Esta técnica consiste en abrir las arterias del corazón usando pequeños tubos llamados stents, que ayudan a mantenerlas abiertas. Debido a que las arterias estaban muy duras por la calcificación, usaron una herramienta especial llamada rotablación. Esta herramienta tiene una pequeña fresa que gira rápido para eliminar la parte dura y permitir que el stent se coloque mejor.\n\n**Cómo fue el tratamiento:**  \nPrimero, trataron las arterias principales del lado izquierdo del corazón sin problemas. Después de casi un mes, regresó para tratar las arterias del lado derecho. Durante este segundo procedimiento, usaron la fresa para limpiar las arterias bloqueadas y pusieron stents para mantenerlas abiertas. Sin embargo, la fresa se quedó atrapada en una de las arterias, lo que complicó el procedimiento.\n\n**Cómo resolvieron el problema:**  \nPara liberar la fresa atrapada, los médicos usaron una técnica especial con un alambre guía que creó un nuevo camino dentro de la pared de la arteria para pasar un globo y liberar la fresa. Luego, colocaron los stents necesarios y lograron que la sangre fluyera bien por las arterias sin complicaciones.\n\n**Qué significa esto:**  \nEste caso muestra cómo los médicos pueden tratar arterias muy dañadas y duras usando herramientas avanzadas. Aunque hubo una complicación, pudieron solucionarla con éxito. El paciente salió en buen estado y con su corazón funcionando normalmente.",
+                "fh_score": 59.13
+            },
+            "B3": {
+                "text": "**Contexto**  \nUn hombre de 71 años con antecedentes de enfermedad de Chagas y diabetes presentó una pérdida de peso significativa y un diagnóstico de megaesófago con obstrucción en el cardias. Durante la evaluación prequirúrgica, manifestó dolor torácico con mínimo esfuerzo. Estudios previos mostraron una enfermedad coronaria multivascular severamente calcificada, especialmente en la arteria coronaria izquierda. Se decidió realizar una intervención coronaria percutánea (ICP) debido al alto riesgo quirúrgico y la complejidad de las lesiones.\n\n**Hallazgos Clave**  \nLa angiografía coronaria reveló múltiples lesiones calcificadas: una estenosis del 90% en la arteria descendente anterior izquierda (LAD), lesiones severas en ramas diagonales, y oclusión de la arteria circunfleja izquierda (LCx) con circulación colateral. La arteria coronaria derecha (RCA) también presentaba lesiones significativas y calcificación. La función ventricular izquierda se mantenía conservada.\n\n**Intervención y Procedimientos**  \nSe planificó la ICP en dos etapas debido a la extensión y severidad de las lesiones. La primera intervención, realizada el 19 de febrero de 2016, incluyó la rotablation (una técnica que utiliza una fresa rotatoria para eliminar la calcificación) en la arteria descendente anterior, seguida de la implantación de stents liberadores de fármacos (DES) en la arteria descendente derecha y la circunfleja, logrando un flujo sanguíneo óptimo sin complicaciones.\n\nCasi un mes después, el 22 de marzo de 2016, se realizó la segunda ICP en las ramas de la arteria coronaria derecha (PDA y RPLA) también con rotablation y colocación de DES. Durante este procedimiento, se produjo una disección severa en la arteria coronaria derecha, causada por la manipulación del catéter, que fue rápidamente corregida con la implantación de un stent adicional. Se presentó un incidente de atrapamiento de la fresa rotatoria dentro de la arteria, que fue resuelto mediante una técnica avanzada que permitió liberar el dispositivo sin daños adicionales.\n\n**Interpretación Clínica**  \nEste caso ilustra la complejidad del manejo de enfermedad coronaria multivascular severamente calcificada en un paciente con comorbilidades importantes y alto riesgo quirúrgico. La utilización de rotablation permitió tratar las lesiones calcificadas que dificultan la expansión de los stents, mejorando el flujo sanguíneo coronario. La estrategia en dos tiempos y la cuidadosa planificación fueron fundamentales para minimizar riesgos y lograr un resultado exitoso.\n\n**Próximos Pasos**  \nEl paciente fue dado de alta en buenas condiciones tras una estancia corta en cuidados intensivos, con función ventricular preservada y sin complicaciones clínicas significativas. Se recomienda seguimiento cardiológico estrecho, control de factores de riesgo cardiovascular y terapia antiplaquetaria dual para prevenir eventos trombóticos. La arteria circunfleja, ocluida pero con circulación colateral, no fue intervenida debido a la dificultad técnica y el riesgo asociado.",
+                "fh_score": 36.63
+            }
+        }
+    },
+    {
+        "article": "Una paciente de 29 años se presentó al departamento de urología con dolor intermittent en el flanco derecho durante un año y sensación de ardor urinaria ocasional sin hematuria; su estado general era estable. La paciente no mostró signos de tos, fatiga, pérdida de peso, no había tenido cirugías previas, pero había estado expuesta frecuentemente a ovejas. A pesar de los exámenes de laboratorio normales, el examen de anticuerpos de equinococos arrojó un resultado positivo. El ultrasonido abdominal posterior reveló una lesión quística grande en el riñón derecho, que medía aproximadamente 63 mm con paredes gruesas y sin flujo de doppler significativo. La tomografía computarizada con contraste, tanto en vista transversal como coronal, reveló una masa quística con septos en el lado lateral del riñón derecho, que presentaba una pared gruesa y regular que se intensificaba con el contraste. Esta lesión se clasificó como categoría 4 de Bosniak, con imágenes de tomografía computarizada en vista coronal que mostraban la participación del sistema colector y el contacto con el hígado. Se sospechó de HC en base a las evaluaciones clínicas y radiológicas. Los hallazgos de la radiografía de tórax no fueron significativos, sin evidencia de quistes pulmonares. Después de un régimen de tres meses de albendazol 400 mg administrado dos veces al día, la paciente se sometió a una intervención quirúrgica. Se realizó un procedimiento abierto a través de una incisión subcostal derecha de Kocher, lo que resultó en una nefrectomía derecha y una resección hepática parcial debido a las adherencias. El espécimen, que pesaba 372 g y medía 13 × 8 × 6 cm, mostró un gran quiste blanco con paredes delgadas que contenían una membrana desprendida, que afectaba los cálices renales y la pelvis. El diagnóstico final fue HC del riñón acompañado de pielonefritis crónica. Los exámenes de laboratorio posteriores al procedimiento mostraron resultados normales, con una producción urinaria estable y signos vitales. El catéter urinario se retiró después de 24 horas debido a una producción urinaria adecuada (2 L). El drenaje renal se retiró después de 3 días, con volúmenes de drenaje de 200 ml, 100 ml y ninguno en días consecutivos. La paciente volvió a sus actividades normales sin complicaciones.\n",
+        "gold_summary": "Se diagnosticó a una mujer de 29 años con dolor intermitente en el flanco derecho y ardor urinario un quiste hidatídico (HC) de categoría 4 de Bosniak, tras dar positivo en anticuerpos de equinococo. Las imágenes confirmaron el diagnóstico, lo que derivó en un tratamiento de tres meses con albendazol, seguido de una nefrectomía derecha y una resección hepática parcial. El análisis histopatológico confirmó un HC y una pielonefritis crónica. La paciente se recuperó sin incidentes y volvió a sus actividades normales.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una mujer tenía dolor en un lado de su cuerpo y ardor al hacer pipí. Los doctores encontraron un quiste grande en su riñón. Le dieron medicina por tres meses para ayudarla. Luego, le hicieron una operación para quitar el riñón y un poco del hígado. Después, ella se sintió bien y pudo hacer sus cosas normales otra vez.",
+                "fh_score": 85.99
+            },
+            "B2": {
+                "text": "**Lo que Encontraron**  \nUna mujer de 29 años tenía dolor en el lado derecho de su espalda y a veces sentía ardor al orinar. Los médicos hicieron pruebas y encontraron que tenía anticuerpos contra un parásito llamado equinococo, que puede causar quistes en órganos. Las imágenes del riñón mostraron un quiste grande y complicado, clasificado como categoría 4 de Bosniak, lo que significa que podría ser peligroso.\n\n**Qué Hicieron**  \nPara tratarla, primero le dieron un medicamento llamado albendazol durante tres meses. Este medicamento ayuda a matar el parásito. Después, le hicieron una cirugía para quitar el riñón derecho y parte del hígado, porque el quiste estaba pegado a esos órganos.\n\n**Qué Significa el Diagnóstico**  \nAl analizar el quiste, confirmaron que era un quiste hidatídico, que es una bolsa llena de líquido causada por el parásito. También encontraron inflamación crónica en el riñón, llamada pielonefritis.  \n\n**Recuperación**  \nDespués de la operación, la paciente se recuperó bien, sin problemas. Su orina y signos vitales estaban normales. Pudo volver a sus actividades normales sin complicaciones.  \n\nEste caso muestra cómo una infección por parásitos puede afectar órganos importantes y cómo se puede tratar con medicamentos y cirugía.",
+                "fh_score": 57.4
+            },
+            "B3": {
+                "text": "**Contexto**  \nUna mujer de 29 años consultó por dolor intermitente en el flanco derecho y episodios ocasionales de ardor al orinar, sin presencia de sangre en la orina. No presentaba síntomas sistémicos como tos, fatiga o pérdida de peso, y su estado general era estable. Destacaba una exposición frecuente a ovejas, factor de riesgo para infecciones parasitarias. Los análisis de laboratorio fueron normales, pero la prueba serológica detectó anticuerpos contra equinococos, un parásito causante de quistes hidatídicos.\n\n**Hallazgos Clave**  \nEl ultrasonido abdominal reveló una lesión quística grande en el riñón derecho, con paredes gruesas y sin flujo sanguíneo significativo. La tomografía computarizada con contraste mostró una masa quística con tabiques internos y una pared engrosada que se realzaba con el contraste, clasificada como categoría 4 en la escala de Bosniak, lo que indica una alta probabilidad de lesión compleja y potencialmente maligna o infecciosa. Además, la lesión involucraba el sistema colector renal y estaba en contacto con el hígado. La radiografía de tórax no mostró quistes pulmonares, descartando afectación pulmonar.\n\n**Interpretación Clínica**  \nEl diagnóstico presuntivo fue un quiste hidatídico renal (HC), una infección parasitaria causada por el equinococo, con posible extensión hepática. El tratamiento inicial consistió en albendazol, un medicamento antiparasitario, administrado durante tres meses para reducir la carga parasitaria y minimizar riesgos quirúrgicos. Posteriormente, se realizó una cirugía abierta mediante una incisión subcostal derecha (incisión de Kocher), que incluyó la extracción completa del riñón derecho (nefrectomía) y una resección parcial del hígado debido a adherencias entre ambos órganos. El estudio histopatológico confirmó la presencia del quiste hidatídico y evidenció pielonefritis crónica, una inflamación prolongada del tejido renal.\n\n**Próximos Pasos y Evolución**  \nTras la cirugía, la paciente mostró una recuperación favorable, con parámetros vitales estables y función urinaria adecuada. El catéter urinario se retiró a las 24 horas, y el drenaje renal se retiró en los días siguientes sin complicaciones. Finalmente, la paciente pudo retomar sus actividades habituales sin presentar efectos adversos ni recurrencias. Este caso destaca la importancia de considerar infecciones parasitarias en pacientes con lesiones quísticas renales, especialmente en contextos de exposición a animales de riesgo.",
+                "fh_score": 36.21
+            }
+        }
+    },
+    {
+        "article": "Una paciente de 46 años de edad fue admitida en nuestro hospital debido a opresión en el pecho y falta de aire que había durado más de un mes. Su historial médico incluía una tiroidectomía parcial, y no tenía antecedentes de tabaquismo o consumo de alcohol. Fue tratada con medicamentos regulares (comprimidos de liberación prolongada de succinato de metoprolol, comprimidos de sacubitril valsartán sodio, espironolactona, comprimidos de dapagliflozina) para la IC, pero la respuesta fue pobre. Durante el examen físico, la paciente estaba consciente y bien orientada. Su frecuencia cardíaca era de 68 latidos por minuto, la presión arterial era de 150/98 mm Hg, la frecuencia respiratoria era de 20 latidos por minuto. No había signos de sangrado o ictericia en la piel o membranas mucosas, y no se observó distensión de la vena yugular. La glándula tiroides no estaba agrandada. Los sonidos respiratorios eran gruesos en ambos pulmones, con roncus húmedos presentes en las bases pulmonares. La frecuencia cardíaca era de 68 lpm con un ritmo regular. El abdomen era suave, sin sensibilidad o sensibilidad de rebote, y el hígado y el bazo no eran palpables por debajo de la caja torácica. El signo de reflujo hepatoyugular fue negativo, pero había edema en ambas extremidades inferiores.\n\nLa paciente fue hospitalizada y se le realizaron los exámenes pertinentes. Los análisis bioquímicos mostraron una hormona estimulante de la tiroides (TSH) de 7,190 uIU/mL, triglicéridos de 0,81 mmol/L, colesterol de lipoproteínas de baja densidad (LDL-C) de 2,61 mmol/L, lipoproteína (a) de suero de 435 mg/L y NT-proBNP de 6245 pg/mL. Un examen de electrocardiograma (ECG) mostró bradicardia sinusal, anomalías de la onda T-U y duración del QRS de 90 ms. Un examen ecocardiográfico transtorácico posterior reveló un diámetro de la aurícula izquierda (LA) (anteroposterior) de 41 mm, un diámetro del ventrículo izquierdo (LVD) (anteroposterior) de 54 mm, un espesor del tabique interventricular en diástole (IVSD) de 9 mm, un espesor de la pared posterior del ventrículo izquierdo en la fase final de la diástole (LVPWd) de 9 mm, una fracción de eyección del ventrículo izquierdo (LVEF) del 28% (M-mode), una fracción de acortamiento (FS) del 13% y una presión de la arteria pulmonar de 29 mm Hg. No se observaron lesiones coronarias significativas en la angiografía coronaria computarizada (CCA). Se diagnosticó a la paciente con cardiomiopatía dilatada, insuficiencia cardiaca de clase III con LVEF reducida según la New York Heart Association (NYHA). En combinación con los parámetros, se puede observar que los volúmenes de la aurícula izquierda y el ventrículo izquierdo se reducen gradualmente, lo que indica que la función diastólica del ventrículo izquierdo está mejorando. El tratamiento con CCM revierte la remodelación miocárdica. Además, E/e′ refleja la presión de llenado ventricular izquierdo. El valor normal debe ser inferior a 8. Se puede observar que en este caso, E/e′ vuelve al valor normal tres meses después de la implantación de CCM. Estos dos puntos reflejan el papel de CCM en la mejora de la función diastólica miocárdica en el tratamiento de la insuficiencia cardiaca. En resumen, la paciente tenía las siguientes características: (1) LVEF mejoró pero se mantuvo tan bajo como el 30% después de la terapia óptima para la insuficiencia cardiaca; (2) opresión en el pecho y malestar con ligera actividad, grado de función cardiaca III; (3) ECG muestra QRS estrecho. Teniendo en cuenta el resultado positivo de la prueba preoperatoria de levosimendan, después de una discusión general y una comunicación completa con el paciente y su familia, se decidió realizar el tratamiento con CCM.\n\nEl procedimiento de implantación del CCM fue similar al de la implantación de un marcapasos tradicional. El paciente se colocó en posición supina, se desinfectó con una toalla y se perforó la vena subclavia izquierda dos veces bajo anestesia local, y se hizo la bolsa capsular después de insertar el alambre guía. Bajo la guía del alambre guía, se introdujeron dos vainas de desprendimiento, y se introdujeron dos cables de estimulación ventricular (Medtronic 3830-69) a través de la vaina, y se ajustó la posición de los cables a la superficie del tabique ventricular derecho con una distancia de 3 cm. Durante la operación, se probó el electrodo de campo cercano (RV), que mostró un umbral de estimulación de 0,5 V, una amplitud de la onda R detectada mayor de 10 mV, y una impedancia del cable de 1080 Ω; el electrodo de campo lejano (LS) mostró un umbral de estimulación de 0,5 V, una amplitud de la onda R detectada mayor de 15 mV, y una impedancia del cable de 900 Ω. Estas mediciones cumplieron los criterios para una implantación exitosa del electrodo. Ambos cables se anclaron de forma segura en el tabique ventricular derecho. Después de asegurarse de que no había estimulación diafragmática palpable con un pulso de estimulación de 10 V y una anchura de pulso de 0,4 ms, se conectaron los cables al generador de impulsos Optimizer Smart. Posteriormente, se ajustaron los impulsos de salida y se programaron y optimizaron los parámetros.\n\nLa monitorización del ECG postoperatorio inmediato indicó un suministro normal de impulsos CCM (Figura 1C). Observamos la respuesta de los pacientes al CCM al adherirnos a un protocolo de seguimiento estandarizado. Utilizando una amplia variedad de herramientas de evaluación, que incluían ultrasonografía Doppler cardiaca a color, análisis de sangre NT-ProBNP, pruebas de caminata de seis minutos (6MW) y el Cuestionario de Minnesota para Vivir con Insuficiencia Cardiaca (MLHFQ), evaluamos sistemáticamente el estado clínico de los pacientes. El paciente no experimentó opresión en el pecho ni falta de aire, y hubo una marcada mejora en la tolerancia al ejercicio y la calidad de vida.\n",
+        "gold_summary": "Presentamos a una paciente de 46 años que fue admitida en nuestro hospital debido a opresión torácica y falta de aire que duró más de un mes. La ecocardiografía reveló un diámetro del ventrículo izquierdo (anteroposterior) de 54 mm, el electrocardiograma mostró bradicardia sinusal y duración del QRS de 90 ms. La paciente no experimentó opresión torácica o falta de aire, y hubo una marcada mejora en la tolerancia al ejercicio y calidad de vida después de la implantación de la modulación de la contractilidad cardiaca.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una señora tenía dolor en el pecho y le costaba respirar mucho tiempo. Los doctores miraron su corazón con máquinas. Después de un tratamiento especial, ella se sintió mucho mejor. Ya no tenía dolor ni dificultad para respirar. Ahora puede jugar y caminar sin problema.",
+                "fh_score": 76.33
+            },
+            "B2": {
+                "text": "**Caso de una Paciente con Problemas del Corazón**\n\nUna mujer de 46 años llegó al hospital porque sentía opresión en el pecho y le costaba respirar desde hacía más de un mes. Para entender qué le pasaba, los médicos le hicieron varios estudios.\n\n**Lo que Encontraron**\n\nUn examen llamado ecocardiografía mostró que una parte de su corazón, llamada ventrículo izquierdo, estaba un poco agrandada (medía 54 mm). Otro examen, el electrocardiograma, mostró que su corazón latía más lento de lo normal (bradicardia sinusal) y que la señal eléctrica que controla el latido tenía una duración normal (QRS de 90 ms).\n\n**Qué Hicieron y Qué Pasó Después**\n\nPara ayudarla, los médicos le implantaron un dispositivo llamado modulador de la contractilidad cardiaca (CCM). Este aparato envía pequeñas señales eléctricas al corazón para mejorar su fuerza al latir. Después de la implantación, la paciente ya no tuvo opresión en el pecho ni dificultad para respirar. Además, pudo hacer ejercicio con más facilidad y su calidad de vida mejoró mucho.\n\nEn resumen, el tratamiento con CCM ayudó a mejorar la función de su corazón y su bienestar general.",
+                "fh_score": 62.07
+            },
+            "B3": {
+                "text": "**Contexto**\n\nUna mujer de 46 años fue hospitalizada por presentar opresión en el pecho y dificultad para respirar que persistían desde hacía más de un mes. Su historial incluía una cirugía parcial de tiroides y no tenía antecedentes de tabaquismo ni consumo de alcohol. A pesar de recibir tratamiento médico estándar para insuficiencia cardiaca, sus síntomas y función cardíaca no mejoraron adecuadamente. Los exámenes iniciales mostraron una fracción de eyección del ventrículo izquierdo (LVEF) muy reducida (28%), indicativa de una función cardíaca comprometida, y un electrocardiograma (ECG) con bradicardia sinusal y un complejo QRS estrecho (90 ms).\n\n**Hallazgos Clave**\n\n- Ecocardiografía: El ventrículo izquierdo tenía un diámetro anteroposterior de 54 mm, con una fracción de eyección del 28%, confirmando una cardiomiopatía dilatada con función cardíaca severamente reducida.\n- ECG: Bradicardia sinusal (ritmo cardíaco lento pero regular) y duración del QRS de 90 ms, lo que indica que la conducción eléctrica del corazón estaba relativamente normal.\n- Laboratorio: Elevación significativa del NT-proBNP (6245 pg/mL), marcador que refleja estrés y daño cardíaco.\n- Sintomatología: Opresión en el pecho y dificultad para realizar actividades físicas leves, clasificada como insuficiencia cardíaca clase III según la New York Heart Association (NYHA).\n\n**Interpretación Clínica**\n\nLa paciente presentaba insuficiencia cardíaca con función ventricular izquierda gravemente disminuida, a pesar del tratamiento médico óptimo. La cardiomiopatía dilatada y los síntomas persistentes indicaban la necesidad de una intervención adicional. Se decidió implantar un dispositivo de modulación de la contractilidad cardíaca (CCM), que es un tipo de terapia eléctrica que mejora la fuerza de contracción del corazón sin alterar el ritmo cardíaco normal.\n\nEl procedimiento de implantación fue similar al de un marcapasos tradicional, con cables colocados en el tabique del ventrículo derecho y un generador de impulsos programado para optimizar la función cardíaca. La implantación fue exitosa, sin complicaciones inmediatas.\n\n**Próximos Pasos y Resultados**\n\nTras la implantación del dispositivo CCM, la paciente fue monitoreada mediante ecocardiografía, análisis sanguíneos, pruebas de caminata y cuestionarios de calidad de vida. A los tres meses, se observó una mejora significativa en la función diastólica del ventrículo izquierdo, reducción de la presión de llenado ventricular y una disminución en los síntomas clínicos.\n\nLa paciente dejó de experimentar opresión en el pecho y dificultad para respirar, mostró una notable mejoría en la capacidad para realizar ejercicio y reportó una mejor calidad de vida. Estos resultados sugieren que la terapia con CCM puede ser una opción efectiva para pacientes con insuficiencia cardíaca avanzada que no responden adecuadamente al tratamiento médico convencional.",
+                "fh_score": 39.84
+            }
+        }
+    },
+    {
+        "article": "Paciente de sexo femenino, 61 años, caucásica, casada, dos hijos, informó empeoramiento de los síntomas de la psoriasis tras el inicio de L-metilfolato 15 mg al día para tratamiento coadyuvante de la depresión. Informó depresión y psoriasis desde los 20 años. Desde los 41 años, la paciente no había tenido recidivas de las lesiones psoriáticas.\n\nPor su historial de depresiones, se le indicó carbonato de litio, pero no lo tomó debido a la psoriasis. En 2000, su cuadro depresivo mejoró con venlafaxina 225 mg al día. En 2016, debido a las oscilaciones de humor, se le agregó lamotrigina 100 mg al día y, para mejorar el sueño, se le sumó quetiapina 50 mg al día.\n\nEstas fueron las dosis actuales, con una mejora en la depresión, la calidad de vida y sin efectos adversos significativos.\n\nEn enero de 2019, se detectó polimorfismo en el gen MTHFR, con una mutación heterozigótica en C677T, y se le recetó a la paciente 15 mg diarios de L-metilfolato. Antes de que finalizara la primera semana de uso de L-metilfolato, aparecieron lesiones psoriáticas que no se habían manifestado en 20 años. Se informó lo ocurrido al psiquiatra, quien retiró la medicación y, 4 días después, las lesiones psoriáticas comenzaron a remitir, desapareciendo por completo al cabo de unas semanas. La paciente no volvió a registrar manifestaciones hasta principios de 2020.\n",
+        "gold_summary": "Paciente de sexo femenino, de 61 años, que había estado en remisión de psoriasis durante 20 años. Sufrió una recaída de psoriasis en forma de placa pocos días después de comenzar el tratamiento con L-metilfolato a una dosis diaria de 15 mg.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una señora de 61 años tuvo la piel con manchas hace mucho tiempo. Ella no tuvo esas manchas por 20 años. Pero cuando empezó a tomar una medicina nueva, las manchas volvieron rápido. Luego, dejó de tomar esa medicina y las manchas se fueron.",
+                "fh_score": 83.8
+            },
+            "B2": {
+                "text": "**Lo que pasó con la paciente**  \nUna mujer de 61 años había tenido psoriasis, que es una enfermedad de la piel que causa manchas rojas y escamosas. Sin embargo, no había tenido problemas con la psoriasis durante 20 años.  \n\n**Qué tratamiento recibió y qué pasó después**  \nElla empezó a tomar un medicamento llamado L-metilfolato, que es una forma de vitamina B9 que ayuda en el tratamiento de la depresión. Tomaba 15 mg al día. Pero pocos días después de comenzar este medicamento, la psoriasis volvió a aparecer en su piel.  \n\n**Qué hicieron los médicos**  \nAl ver que la psoriasis regresó, el doctor decidió quitarle el L-metilfolato. Cuatro días después de dejar el medicamento, las manchas en la piel comenzaron a mejorar y desaparecieron completamente en unas semanas.  \n\n**Qué significa esto**  \nEste caso muestra que, en esta paciente, el L-metilfolato pudo haber causado que la psoriasis regresara después de muchos años sin síntomas. Por eso, es importante que los médicos revisen bien los tratamientos y los posibles efectos en cada persona.",
+                "fh_score": 67.58
+            },
+            "B3": {
+                "text": "**Contexto**  \nSe trata de una mujer de 61 años con antecedentes de psoriasis y depresión desde los 20 años. Durante dos décadas, desde los 41 años, no presentó brotes de psoriasis. Su tratamiento psiquiátrico actual incluía venlafaxina, lamotrigina y quetiapina, con buena respuesta y sin efectos adversos importantes. En 2019, se identificó que tenía una mutación genética heterozigótica en el gen MTHFR (C677T), lo que llevó a prescribirle L-metilfolato, un suplemento que puede ayudar en ciertos trastornos depresivos.\n\n**Hallazgos Clave**  \nPocos días después de iniciar el L-metilfolato a una dosis diaria de 15 mg, la paciente presentó una recaída de psoriasis en forma de placas, una manifestación cutánea que no había experimentado en 20 años. Al suspender el L-metilfolato, las lesiones comenzaron a mejorar en cuatro días y desaparecieron completamente en unas semanas. No se registraron nuevos brotes hasta casi un año después.\n\n**Interpretación Clínica**  \nEl caso sugiere una posible relación entre la administración de L-metilfolato y la reactivación de la psoriasis en esta paciente. Aunque el L-metilfolato es utilizado para mejorar la depresión, en este caso pudo haber desencadenado una respuesta inflamatoria cutánea, posiblemente relacionada con su predisposición genética y su historial de psoriasis. Este hallazgo es relevante para considerar el impacto de tratamientos coadyuvantes en enfermedades autoinmunes o inflamatorias crónicas.\n\n**Próximos Pasos**  \nSe recomienda un seguimiento cuidadoso en pacientes con antecedentes de psoriasis cuando se prescriben suplementos como el L-metilfolato. Además, es importante evaluar alternativas terapéuticas para la depresión que no exacerben enfermedades cutáneas. La comunicación estrecha entre dermatólogos y psiquiatras es fundamental para manejar casos similares y evitar recaídas.",
+                "fh_score": 44.1
+            }
+        }
+    },
+    {
+        "article": "Se diagnosticó osteoartritis bilateral de las articulaciones de la cadera en un paciente de 61 años de edad con tratamiento con esteroides para la artritis reumatoide y dolencias en la ingle bilateral. [9] Recibió una inyección intraarticular bilateral de ácido hialurónico y se presentó doce semanas después en nuestro departamento de urgencias con fiebre, un estado general reducido y un dolor cada vez más incapacitante. Las radiografías de la pelvis mostraron una destrucción progresiva y rápida de ambas articulaciones de la cadera con una osteólisis extensa, subluxación concomitante y un defecto óseo acetabular del lado izquierdo. La aspiración de la articulación mostró pus en ambas articulaciones de la cadera y se hizo el diagnóstico de artritis séptica bilateral progresiva rápida. Se realizó una resección bilateral de ambas cabezas femorales con desbridamiento de la articulación de la cadera y la implantación de espaciadores de PMMA cargados con antibióticos a través de un enfoque anterolateral mínimamente invasivo.\n\nSe inició un tratamiento antibiótico sistémico empírico con vancomicina y ampicilina por vía intravenosa. Se detectó E. coli en muestras de tejido de ambas articulaciones de la cadera y se adaptó el tratamiento antibiótico sistémico a meropenem por vía intravenosa. Se realizaron dos procedimientos quirúrgicos de seguimiento con intercambio de los espaciadores de PMMA cargados con antibiótico para controlar la infección debido al drenaje persistente.\n\nDoce semanas después de la resección de la cabeza femoral y el control exitoso de la infección, el paciente recibió una artroplastia total de cadera con el uso adicional de un revestimiento multicapa de plata (HyProtect®, Bio-Gate, Nürnberg, Alemania). Este revestimiento consiste en una capa de siloxano ultrafina directamente sobre la superficie del implante (10 a 30 nm), de la que se liberan iones de plata.\n\n12 semanas después de la resección de la cabeza femoral, se realizó una artroplastia total de cadera en el lado derecho con una copa estándar sin cemento (Allofit®, ZimmerBiomet, Varsovia, EE. UU.) y un vástago femoral sin cemento (Avenir®, ZimmerBiomet, Varsovia, EE. UU.) a través del enfoque anterolateral mínimamente invasivo previamente utilizado con este revestimiento multicapa de plata ultrafino. Tanto la superficie posterior de la copa como todo el eje femoral se revistieron con plata.\n\nLa cadera izquierda se trató 18 semanas después de la resección de la cabeza femoral con una jaula de refuerzo recubierta de plata (Burch-Schneider®, ZimmerBiomet, Varsovia, EE. UU.) para un defecto acetabular tipo IIB de Paprosky y una copa de polietileno cementada (Durasul®, ZimmerBiomet, Varsovia, EE. UU.). El vástago femoral sin cemento (Avenir®, ZimmerBiomet, Varsovia, EE. UU.) también se recubrió de plata en toda su parte intramedular. Esta intervención también se realizó mediante el enfoque anterolateral mínimamente invasivo utilizado previamente. El paciente se sometió a una terapia antibiótica sistémica durante un período de tratamiento total de 18 semanas después de la implantación del lado derecho. Se aplicó ertapenem 1 g por vía intravenosa durante este período de tiempo una vez al día, después de la descarga en un entorno ambulatorio. Esto permitió una cobertura antibiótica del lado derecho de 18 semanas y del lado izquierdo de 12 semanas de tratamiento antibiótico.\n\nSe recomendó el uso parcial de peso con 20 kg en el lado operado y el uso de muletas durante 6 semanas después de las intervenciones.\n\nLas heridas de ambos lados se curaron sin incidentes. El paciente fue visto regularmente para un seguimiento clínico y radiológico. Se logró el apoyo total del peso sin el uso de muletas 7 semanas después de la operación en ambos lados. No hubo signos de PIJ y no fue necesaria una cirugía de revisión adicional.\n\nEn un seguimiento final tres años después de la implantación de las prótesis recubiertas de plata, la paciente mostró un aspecto normal de la piel con mínimas cicatrices después de enfoques antero-laterales mínimamente invasivos en ambos lados sin signos de argiria. Hubo un excelente resultado funcional de ambas caderas con marcha normal y una puntuación WOMAC de 6 en ambos lados (dolor: 0, rigidez: 0, función física: 6). El recuento de leucocitos en sangre fue de 7,29/nl (referencia: 4,23-9,1) y el nivel de proteína C reactiva (PCR) fue de 12,4 mg/l (referencia: <5 mg/l). El nivel ligeramente elevado de PCR es atribuible a la artritis reumatoide subyacente de la paciente. Las radiografías revelaron componentes protésicos de cadera bien integrados y no sueltos en ambos lados tres años después de la implantación con una articulación correcta.\n",
+        "gold_summary": "Este informe de caso se refiere a un paciente de 61 años con destrucción rápida de ambas articulaciones de la cadera debido a una artritis séptica que se trató con éxito con una implantación por etapas de prótesis de cadera recubiertas con plata con un recubrimiento ultrafino multicapa de plata. En un seguimiento de tres años, no hubo signos de infección, se observó un buen estado de todos los componentes protésicos y el resultado funcional fue excelente.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había un señor con mucho dolor en sus dos caderas. Sus caderas se dañaron rápido por una infección. Los doctores le pusieron unas piezas nuevas en sus caderas. Estas piezas tenían una capa especial de plata para ayudar. Después de tres años, el señor está bien y sin dolor. Sus caderas funcionan muy bien y no hay infección.",
+                "fh_score": 89.39
+            },
+            "B2": {
+                "text": "**Lo que pasó con el paciente:**  \nUn hombre de 61 años tenía un problema grave en ambas caderas. Tenía una infección llamada artritis séptica, que hizo que sus articulaciones se dañaran muy rápido. Esta infección causó mucho dolor y dificultad para moverse.\n\n**Cómo lo trataron:**  \nPrimero, le quitaron las partes dañadas de las caderas y limpiaron bien las áreas infectadas. Luego, le pusieron unos espaciadores especiales con antibióticos para controlar la infección. Después de varias semanas y tratamientos con antibióticos fuertes, la infección mejoró.\n\nMás tarde, le pusieron prótesis nuevas en ambas caderas. Estas prótesis tenían un recubrimiento muy delgado de plata. La plata ayuda a evitar que las bacterias vuelvan a causar infección. Las cirugías se hicieron con técnicas que dañan poco los tejidos, para que la recuperación fuera mejor.\n\n**Qué pasó después:**  \nTres años después de las cirugías, el paciente estaba muy bien. No había señales de que la infección regresara. Las prótesis estaban firmes y funcionando bien. El paciente podía caminar normalmente y no sentía dolor ni rigidez en las caderas.\n\n**Por qué es importante:**  \nEste caso muestra que usar prótesis con un recubrimiento especial de plata puede ayudar a tratar infecciones graves en las articulaciones y mejorar la recuperación. Además, el seguimiento a largo plazo confirmó que el tratamiento fue exitoso y seguro.",
+                "fh_score": 67.2
+            },
+            "B3": {
+                "text": "**Contexto**  \nSe trató a un paciente de 61 años con antecedentes de artritis reumatoide, que recibía tratamiento con esteroides, y que presentaba osteoartritis en ambas caderas junto con dolor en la ingle. Después de una inyección de ácido hialurónico en ambas articulaciones, el paciente desarrolló fiebre, deterioro general y un dolor intenso y progresivo en las caderas. Las radiografías mostraron una rápida destrucción ósea en ambas articulaciones, y la aspiración reveló pus, confirmando una infección grave llamada artritis séptica bilateral.\n\n**Hallazgos Clave**  \nSe realizó la extracción quirúrgica de las cabezas femorales (la parte superior del hueso del muslo que forma la articulación de la cadera) y se limpiaron las articulaciones, implantando espaciadores temporales cargados con antibióticos para controlar la infección. Inicialmente se administraron antibióticos de amplio espectro, pero al identificar la bacteria Escherichia coli, el tratamiento se ajustó a un antibiótico específico (meropenem). Debido a la persistencia del drenaje, se llevaron a cabo dos cirugías adicionales para cambiar los espaciadores antibióticos.\n\nTras controlar la infección, se realizaron reemplazos definitivos de ambas caderas mediante prótesis recubiertas con un revestimiento ultrafino multicapa de plata. Este recubrimiento libera iones de plata, conocidos por sus propiedades antimicrobianas, con el objetivo de prevenir nuevas infecciones. La cirugía se realizó mediante un abordaje mínimamente invasivo para reducir el daño a los tejidos.\n\nEl lado derecho se operó primero, con una prótesis sin cemento y recubierta de plata en las superficies clave. La cadera izquierda se intervino semanas después, utilizando una jaula de refuerzo también recubierta de plata para reparar un defecto óseo importante, junto con una copa de polietileno cementada y un vástago femoral sin cemento igualmente recubierto. El paciente recibió un tratamiento antibiótico prolongado (hasta 18 semanas) para asegurar la erradicación completa de la infección.\n\n**Interpretación Clínica**  \nEl uso de prótesis recubiertas con plata en este caso permitió un control efectivo de la infección y una recuperación funcional excelente. Las heridas cicatrizaron sin complicaciones, y el paciente pudo caminar sin muletas en pocas semanas. Tres años después de la cirugía, no se observaron signos de infección recurrente ni efectos secundarios relacionados con la plata, como la argiria (una pigmentación anormal de la piel). Las radiografías mostraron que las prótesis estaban bien integradas y estables, y la función de las caderas era casi normal, con muy poco dolor y rigidez.\n\n**Próximos Pasos**  \nEl seguimiento clínico y radiológico continuado es fundamental para detectar cualquier posible complicación a largo plazo. En este caso, el éxito del tratamiento sugiere que las prótesis con recubrimiento de plata pueden ser una opción valiosa para pacientes con infecciones severas en las articulaciones, especialmente cuando se requiere una reconstrucción compleja. Además, el abordaje mínimamente invasivo contribuyó a una recuperación más rápida y con menos cicatrices visibles.\n\nEn resumen, este caso demuestra que un tratamiento escalonado que combina cirugía, antibióticos específicos y prótesis con recubrimiento antimicrobiano puede lograr resultados excelentes en infecciones articulares graves, mejorando la calidad de vida del paciente a largo plazo.",
+                "fh_score": 36.87
+            }
+        }
+    },
+    {
+        "article": "Una niña africana de raza negra, con 1000 g de peso, nacida a las 32 semanas de gestación, de madre viva, fue derivada a nuestra unidad de cuidados intensivos neonatales debido a múltiples anomalías congénitas y dificultad respiratoria moderada. La madre tiene 32 años y está en un matrimonio no consanguíneo. La madre no buscó atención médica hasta el inicio del tercer trimestre de embarazo, debido a un desprendimiento de placenta. El primer ultrasonido prenatal reveló oligohidramnios severos. No era diabética (la glucosa en sangre aleatoria fue de 5.1 mmol/L) y no recibió suplementos de ácido fólico durante el embarazo.\n\nAl ingreso, la bebé estaba alerta con características leves del síndrome de dificultad respiratoria. Presentaba múltiples rasgos dismórficos, entre ellos, microcefalia (circunferencia de la cabeza < 10%), occipucio prominente, orejas bajas, paladar hendido y labio derecho, micrognatia, contractura bilateral de los codos e inferiores más cortos.\n\n\nEl peso al nacer fue de 1000 g, la longitud del bebé fue de 40 cm y la circunferencia occipitofrontal fue de 30 cm.\n\nInvestigaciones\nLa radiografía esquelética mostró aplanamiento de las costillas, aplasia del fémur derecho e hipoplasia del fémur izquierdo. Los análisis de laboratorio incluyeron: hemograma completo, proteína C reactiva, creatinina, urea en sangre y electrolitos, todos dentro de los valores normales. La ecografía craneal fue normal, pero la ecocardiografía reveló un pequeño conducto arterioso permeable.\n\nDiagnóstico diferencial\nLa paciente presentaba aplasia femoral bilateral y facies inusuales. Estas características clínicas llevaron al diagnóstico de síndrome femoro-facial.\n\nLa similitud en la etiopatogénesis hace que el síndrome de regresión caudal sea el diagnóstico diferencial común. Ambos pueden ser causados por una hiperglucemia materna mal controlada. Sin embargo, los defectos faciales están ausentes en el síndrome de regresión caudal, la característica diagnóstica clave.\n\nLa hipoplasia femoral focal proximal y las anomalías craneofaciales suelen estar ausentes.\n\nEntre las condiciones que pueden provocar el labio leporino se incluye el síndrome de banda amniótica grave.\n\nTratamiento\nEl bebé recibió asistencia respiratoria y antibióticos empíricos. Participaron un cirujano ortopédico, un otorrinolaringólogo y un fisioterapeuta. Está previsto reparar quirúrgicamente el paladar hendido a los 6 meses de edad. La rehabilitación funcional está prevista antes de que el paciente comience a deambular. La cirugía de alargamiento de extremidades no se realiza actualmente en nuestro entorno.\n\nResultado y seguimiento\nEl paciente falleció a la edad de un mes por complicaciones de una sepsis neonatal grave de inicio tardío.\n",
+        "gold_summary": "Una niña africana de raza negra bantú de 1 día de vida fue admitida en la unidad neonatal debido a múltiples anomalías congénitas. La madre no buscó atención médica hasta el inicio del tercer trimestre, cuando tuvo un desprendimiento de placenta. La madre nunca recibió suplementos de ácido fólico prenatal. La niña tenía microcefalia, orejas bajas, paladar hendido derecho y labio, micrognatia, contractura y extremidades más cortas. Una radiografía esquelética mostró hipoplasia femoral. Presentamos este caso poco habitual y destacamos los retos en el diagnóstico y el tratamiento.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una bebé nació con problemas en su cuerpo. Su mamá no fue al doctor mucho cuando estaba embarazada. La bebé tenía la cabeza pequeña y orejas bajitas. También tenía un huequito en la boca y su labio estaba partido. Sus brazos y piernas eran más cortos y un hueso de la pierna estaba pequeño. Los doctores cuidaron mucho a la bebé, pero fue difícil ayudarla.",
+                "fh_score": 82.25
+            },
+            "B2": {
+                "text": "**Lo que pasó con la bebé**  \nUna niña africana nació prematura, con solo 32 semanas de gestación y pesando 1000 gramos. Fue llevada a una unidad especial para bebés recién nacidos porque tenía varios problemas desde el nacimiento. Su mamá no recibió atención médica durante la mayor parte del embarazo y no tomó ácido fólico, una vitamina importante para evitar defectos al nacer. Además, la mamá tuvo un problema llamado desprendimiento de placenta, que puede afectar al bebé.\n\n**Lo que encontraron en la bebé**  \nLa niña tenía la cabeza más pequeña de lo normal (microcefalia), orejas bajas, un paladar y labio hendidos (como un corte en el labio y el techo de la boca), mandíbula pequeña (micrognatia), y sus brazos y piernas eran más cortos y rígidos. Las radiografías mostraron que sus huesos de las piernas, especialmente los fémures, estaban subdesarrollados o faltaban partes. También tenía dificultad para respirar leve y un pequeño problema en el corazón.\n\n**Qué significa el diagnóstico**  \nLos médicos diagnosticaron a la bebé con un síndrome llamado femoro-facial. Esto significa que tiene problemas en los huesos de las piernas (fémur) y en la cara. Este síndrome es raro y puede parecerse a otro llamado síndrome de regresión caudal, pero en ese último no hay problemas en la cara, lo que ayuda a diferenciarlos. Además, algunas de sus características podrían estar relacionadas con problemas durante el embarazo, como la falta de control de azúcar en la mamá, aunque en este caso no se encontró diabetes.\n\n**Cómo trataron a la bebé y qué pasó después**  \nLa bebé recibió ayuda para respirar y antibióticos para prevenir infecciones. También la atendieron varios especialistas para planear cirugías y terapias que la ayudaran a mejorar su movilidad y corregir el paladar hendido. Sin embargo, a pesar de los cuidados, la bebé falleció a los 30 días de vida debido a una infección grave.\n\n**Resumen final**  \nEste caso muestra lo difícil que es diagnosticar y tratar a bebés con problemas congénitos raros, especialmente cuando la atención prenatal no es adecuada. Es importante que las mamás reciban cuidado médico temprano y tomen vitaminas como el ácido fólico para prevenir algunos defectos al nacer.",
+                "fh_score": 58.39
+            },
+            "B3": {
+                "text": "**Contexto**  \nSe presentó el caso de una recién nacida africana de raza negra, con un peso bajo al nacer (1000 gramos) y prematura (32 semanas de gestación), que fue ingresada en la unidad de cuidados intensivos neonatales debido a múltiples anomalías congénitas y dificultad respiratoria moderada. La madre, de 32 años, no recibió atención prenatal adecuada hasta el tercer trimestre, cuando sufrió un desprendimiento de placenta, y no tomó suplementos de ácido fólico durante el embarazo. El embarazo se caracterizó por oligohidramnios severo (disminución del líquido amniótico).\n\n**Hallazgos Clave**  \nAl momento del ingreso, la bebé estaba alerta pero presentaba signos leves de síndrome de dificultad respiratoria. Se observaron varias malformaciones físicas: microcefalia (cabeza pequeña), occipucio prominente (parte posterior de la cabeza sobresaliente), orejas bajas, paladar hendido y labio leporino en el lado derecho, micrognatia (mandíbula pequeña), contracturas en ambos codos y extremidades inferiores más cortas.  \n\nLas radiografías mostraron aplanamiento de las costillas, ausencia completa del fémur derecho (aplasia) y desarrollo insuficiente del fémur izquierdo (hipoplasia). Los análisis de laboratorio básicos fueron normales, la ecografía cerebral no mostró alteraciones, pero el ecocardiograma detectó un pequeño conducto arterioso permeable (una conexión anormal entre dos vasos sanguíneos del corazón).\n\n**Interpretación Clínica**  \nEl conjunto de características clínicas llevó al diagnóstico de síndrome femoro-facial, una condición poco común que se caracteriza por anomalías en los huesos del muslo (fémur) y rasgos faciales inusuales. Este diagnóstico se diferencia del síndrome de regresión caudal, que también afecta la parte inferior del cuerpo pero no presenta malformaciones faciales. Además, se consideraron otras causas posibles del labio leporino, como el síndrome de banda amniótica, pero la combinación de hallazgos apuntó al síndrome femoro-facial.  \n\nEs importante destacar que, aunque la hiperglucemia materna mal controlada (niveles altos de azúcar en sangre durante el embarazo) puede causar ambas condiciones, en este caso la madre no tenía diabetes diagnosticada.\n\n**Tratamiento y Manejo**  \nLa bebé recibió soporte respiratorio y tratamiento antibiótico preventivo. Se contó con la participación de un equipo multidisciplinario que incluyó cirujano ortopédico, otorrinolaringólogo y fisioterapeuta. Se planificó la reparación quirúrgica del paladar hendido a los seis meses de edad y la rehabilitación funcional antes de que la niña comenzara a caminar. Sin embargo, la cirugía para alargar las extremidades no está disponible en el centro donde fue atendida.\n\n**Resultado y Seguimiento**  \nLamentablemente, la paciente falleció a la edad de un mes debido a complicaciones derivadas de una sepsis neonatal grave (infección generalizada en el recién nacido) de inicio tardío, lo que refleja la gravedad y complejidad del cuadro clínico.\n\n---\n\nEste caso resalta los desafíos en el diagnóstico y manejo de anomalías congénitas complejas en un contexto con recursos limitados, así como la importancia de la atención prenatal temprana y adecuada para prevenir y detectar estas condiciones.",
+                "fh_score": 33.69
+            }
+        }
+    },
+    {
+        "article": "Paciente de sexo masculino de 18 años, con diag nóstico clínico de Neurofibromatosis tipo 1 desde el primer año de vida. Entre sus antecedentes destaca que tiene educación completa, sus padres no son consan guíneos, y no tiene antecedentes familiares de manchas café con leche. Desde el punto de vista neurológico desarrolló durante la infancia retraso del desarrollo psicomotor fino y grueso, trastorno del lenguaje de predominio expresivo, con alteración fonológica y semántica del lenguaje, por lo que fue manejado con fonoaudiología en Escuela de Lenguaje, además de ki- nesioterapia y terapia ocupacional durante la infancia. Durante la adolescencia se le diagnosticó Trastorno por Déficit Atencional e Hiperactividad, que fue manejado con metilfenidato, manteniendo regular rendimiento escolar. Tuvo desarrollo puberal normal. Oftalmológi camente presentó nódulos de Lisch desde los 4 años de edad, euriblefaron y astigmatismo. Se mantuvo en control anual en Oftalmología y Neuropediatría. Su última Resonancia Magnética de cerebro fue realiza da 6 meses previo a la consulta en Dermatología, sin hallazgos patológicos y en la Resonancia Magnética de columna se evidenció discopatía L5-S1 y realce perifacetario en T11-T12 y T12-L1. A los 16 años se reali zó estudio genético que demostró deleción de exones 5-47 del gen NF1.\n\nA los 18 años consultó en servicio de Dermatología del Centro de Referencia en Salud Peñalolén Cordille ra Oriente por aparición de nueva mancha en muslo izquierdo de 1 año evolución, asintomática. Además, refirió aparición de nódulos en muñeca derecha, su praciliar derecho y cuero cabelludo, de unos meses de evolución, asintomáticos.\n\nAl examen físico destacaba presión arterial normal, macrocefalia (CC: 60 cm) y múltiples manchas café con leche generalizadas, efélides en axilas, y en zona supraciliar derecha, occipital y muñeca derecha nódulos subcutáneos ovalados de 0,5 cm, bien delimitados, móviles. En muslo izquierdo lateral pre sentaba placa de 25 mm algo rosada, con pérdida de anexos, y de consistencia blanda. Por último, en zona lumbar y pectoral, múltiples máculas rojo- azuladas pequeñas, de menos de 5 mm cada una, algu nas levemente deprimidas.\n\nSe realizó biopsia cutánea de máculas azuladas en pecho y de placa muslo, resultando ambas compatibles con NF. Se realizó una ecografía de nódulos supraciliar y occipital que resultó compatible con NF nodular subcutáneo.\n\nUsando la clasificación clínica de García-Martínez et al.1 se diagnosticó al paciente con NF superficial sub cutáneo nodular en zona supraciliar derecha, occipital y muñeca derecha, NF superficial cutáneo pseudoatró fico en muslo izquierdo lateral y NF superficial cutáneo rojo azulado en zona lumbar y pectoral.",
+        "gold_summary": "Paciente masculino de 18 años con diagnóstico desde la infancia de NF-1 que presenta múltiples nodulos ovalados en cara, zona occipital y muñeca, máculas rojo-azuladas en dorso y placa rosada atrófica en muslo. El estudio ecográfico de los nódulos fue compatible con neurofibromas y el estudio histopatológico de las lesiones de dorso y muslo compatibles con neurofibromas cutáneos.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un niño que ahora tiene 18 años tiene una enfermedad llamada NF-1 desde que era muy pequeño. En su piel hay bolitas redondas en la cara, la cabeza y la muñeca. También tiene manchas rojas y azules en la espalda. En el muslo tiene una mancha rosada y suave. Los doctores hicieron pruebas y vieron que esas bolitas y manchas son parte de su enfermedad. Todo está bien cuidado y los doctores lo están ayudando.",
+                "fh_score": 83.39
+            },
+            "B2": {
+                "text": "**Lo que encontraron en el paciente**  \nUn joven de 18 años, que desde pequeño tiene una enfermedad llamada Neurofibromatosis tipo 1 (NF-1), presentó varios bultos pequeños y redondeados en la cara, la parte de atrás de la cabeza (zona occipital) y la muñeca. También tenía manchas de color rojo-azulado en la espalda y una zona rosada y delgada en el muslo izquierdo.\n\n**Qué significan los estudios realizados**  \nSe usó una ecografía, que es una prueba con ondas sonoras para ver el interior de los bultos, y mostró que esos nódulos eran neurofibromas. Los neurofibromas son tumores benignos, es decir, no cancerosos, que crecen en los nervios. Además, se tomó una biopsia, que consiste en sacar un pequeño pedazo de piel para examinarlo bajo el microscopio. Esta prueba confirmó que las manchas en la espalda y la placa en el muslo también eran neurofibromas en la piel.\n\n**Importancia del diagnóstico**  \nEstos hallazgos ayudan a entender mejor cómo afecta la NF-1 a este paciente, mostrando que tiene diferentes tipos de neurofibromas en varias partes del cuerpo. Esto es importante para su seguimiento médico y para decidir el mejor tratamiento si fuera necesario.",
+                "fh_score": 60.37
+            },
+            "B3": {
+                "text": "**Contexto**\n\nSe trata de un joven de 18 años con diagnóstico clínico confirmado desde la infancia de Neurofibromatosis tipo 1 (NF1), una enfermedad genética que afecta el desarrollo de tejidos nerviosos y cutáneos. Su historia médica incluye retrasos en el desarrollo psicomotor y del lenguaje durante la infancia, así como un diagnóstico de Trastorno por Déficit de Atención e Hiperactividad en la adolescencia. Presenta además características típicas de NF1, como múltiples manchas café con leche en la piel, nódulos oculares llamados nódulos de Lisch, y una macrocefalia (cabeza de tamaño mayor al promedio).\n\n**Hallazgos Clínicos y Diagnósticos**\n\nA los 18 años, el paciente consultó por la aparición de una nueva mancha en el muslo izquierdo que llevaba un año, además de varios nódulos en la muñeca derecha, la zona supraciliar derecha (por encima de la ceja) y el cuero cabelludo, todos asintomáticos. En el examen físico se observaron:\n\n- Múltiples manchas café con leche distribuidas por todo el cuerpo.\n- Nódulos subcutáneos ovalados, bien delimitados y móviles, de aproximadamente 0,5 cm en la zona supraciliar derecha, occipital y muñeca derecha.\n- Una placa rosada de 25 mm en el muslo izquierdo, con pérdida de anexos cutáneos (como folículos pilosos) y consistencia blanda.\n- Múltiples máculas rojo-azuladas pequeñas, algunas ligeramente deprimidas, en la zona lumbar y pectoral.\n\nSe realizaron estudios complementarios:\n\n- Ecografía de los nódulos supraciliares y occipitales, que mostró características compatibles con neurofibromas nodulares subcutáneos (tumores benignos derivados de las células nerviosas).\n- Biopsias de las máculas rojo-azuladas del pecho y de la placa del muslo, cuyos resultados confirmaron la presencia de neurofibromas cutáneos.\n\n**Interpretación Clínica**\n\nEl diagnóstico se basó en la clasificación clínica propuesta por García-Martínez y colaboradores, identificando tres tipos de manifestaciones cutáneas en este paciente:\n\n1. Neurofibromas superficiales subcutáneos nodulares en la zona supraciliar derecha, occipital y muñeca derecha.\n2. Neurofibroma superficial cutáneo con aspecto pseudoatrófico (que simula una pérdida de tejido) en el muslo izquierdo.\n3. Neurofibromas superficiales cutáneos de color rojo-azulado en la zona lumbar y pectoral.\n\nEstos hallazgos son consistentes con la variedad de lesiones cutáneas que pueden presentarse en pacientes con NF1, reflejando la heterogeneidad clínica de la enfermedad.\n\n**Próximos Pasos**\n\nEl paciente debe continuar con seguimiento multidisciplinario, incluyendo dermatología, neurología y oftalmología, para monitorear la evolución de las lesiones cutáneas y detectar posibles complicaciones neurológicas o malignización de los neurofibromas. Además, es importante mantener el control de su desarrollo cognitivo y conductual, así como realizar evaluaciones periódicas mediante imágenes para descartar nuevas alteraciones. La educación y el apoyo psicosocial también son fundamentales para mejorar su calidad de vida.",
+                "fh_score": 39.34
+            }
+        }
+    },
+    {
+        "article": "Un hombre de 38 años de edad fue ingresado en el hospital por traumatismo torácico contundente. El paciente estaba generalmente sano y no tenía factores de riesgo de enfermedad coronaria. Fue golpeado en el pecho por un tornillo de alta velocidad que tenía aproximadamente 6 cm de diámetro mientras trabajaba en una fábrica. Voló aproximadamente 4 metros de distancia debido a la fuerza y presión del tornillo de alta velocidad. Perdió el conocimiento de inmediato, pero recuperó la conciencia varios minutos después. Fue trasladado inmediatamente a la sala de urgencias de un hospital local. Su puntaje en la escala de coma de Glasgow fue de 15. Se quejó de dolor torácico intenso y persistente, opresión y disnea. La tomografía computarizada del tórax mostró derrame pleural bilateral y fracturas de esternón y costillas. Por lo tanto, se insertó un tubo torácico durante varios días. Luego, fue dado de alta sin someterse a un electrocardiograma (ECG) u otros exámenes cardiovasculares.\n\nTres meses después del alta hospitalaria, durante un chequeo de seguimiento de rutina, todavía había presencia de derrame pleural con síntomas acompañantes de opresión en el pecho, falta de aire después de la actividad física, e incluso disnea por la noche, lo que motivó su ingreso en nuestro hospital. Sus constantes vitales durante el ingreso fueron las siguientes: frecuencia cardíaca regular de 98 latidos/min, presión arterial de 110/70 mmHg, y frecuencia respiratoria de 20 respiraciones/min. El examen físico mostró una pulsación carotídea y yugular normal. El movimiento respiratorio torácico bilateral y la actividad fueron normales, la fibrilación del lenguaje táctil del pulmón derecho disminuyó, la percusión del pulmón derecho presentó un sonido sordo, y los sonidos respiratorios disminuyeron. No hubo roncus ni estertores evidentes durante la auscultación pulmonar. No hubo murmullos en la auscultación cardíaca. Los exámenes del abdomen y las extremidades revelaron hallazgos normales. El primer ECG mostró evaluación ST e inversión de la onda T en las derivaciones I, aVL y V2-V5 y en el bloqueo de rama anterior izquierdo. La prueba de troponina-I fue negativa, y el nivel de NT-proBNP fue de 706 pg/ml (rango normal: 0-104 pg/ml), lo que sugiere un infarto de miocardio anterior antiguo. La ecocardiografía transtorácica mostró una aurícula izquierda de 26,4 mm, un ventrículo izquierdo de 51,8 mm, y una fracción de eyección ventricular izquierda (EF) del 32% (modo M). La pared anterior del LV e interventricular septum mostraron adelgazamiento a 6,6 mm, con un eco de movimiento notablemente reducido.\n\nAl examinar las arterias carótidas, intracraneales y de las extremidades inferiores del paciente, no se encontraron placas ateroscleróticas evidentes. Todos los hallazgos apoyaron el diagnóstico de infarto de miocardio antiguo (OMI), en lugar de arteriosclerosis. Sin embargo, el paciente era hemodinámicamente estable. Después de someterse a una terapia diurética, se le administraron bloqueadores beta, estatinas y estimulantes cardíacos, lo que alivió su malestar. La angiografía por tomografía computarizada coronaria mostró una estenosis moderada en la arteria LAD proximal. Para confirmar la estenosis y examinar el estado de la íntima coronaria, se realizó CAG 3 meses después del traumatismo torácico, que mostró un estrechamiento aproximado del 70% del lumen en la LAD proximal y el segmento coronario tenía una lesión curva. La arteria circunfleja izquierda (LCX) y la arteria coronaria derecha (RCA) eran normales. Los resultados de CAG confirmaron el diagnóstico de OMI, pero debido a la carga de costos, el paciente rechazó el examen IVUS. El paciente se sometió a una terapia conservadora y fue dado de alta del hospital varios días después.\n\nUn mes después, el 9 de diciembre de 2014, volvió al hospital para someterse a una intervención coronaria percutánea (ICP). Después de someterse a una terapia con fármacos, sus condiciones habían mejorado ligeramente. El examen físico y el ECG revelaron resultados casi normales. La ecocardiografía transtorácica mostró una mejora en la función sistólica del LV y EF del 45%. Se sometió a otra CAG 4 meses después del traumatismo torácico, que mostró una ligera mejora de la estenosis. Había aproximadamente un 60% de estrechamiento del lumen. Se realizó un IVUS y reveló que la gravedad de la lesión era del 55.9%, y la placa de bajo eco apareció antes de la formación de trombos después de la rotura subintimal. Completamos el examen sin más intervención porque solo se encontró un 55.9% de estrechamiento del lumen y el paciente tenía una hemodinámica estable sin evidencia de isquemia miocárdica constante. Se le recetó al paciente la medicación óptima, y su incomodidad se alivió gradualmente. El 17 de julio de 2018, 4 años después del traumatismo, la evaluación de seguimiento reveló que el paciente todavía experimentaba dificultad para respirar después de trabajar, pero se alivió poco después de descansar. El examen físico mostró los siguientes resultados: presión arterial de 114/80 mmHg, frecuencia cardíaca de 66 latidos/min, ausencia de anomalías obvias en la auscultación pulmonar y cardíaca; y ausencia de edema obvio en ambas extremidades inferiores. El ECG de seguimiento reveló los siguientes hallazgos: rS en las derivaciones V2-V4, inversión de la onda T en las derivaciones I, AVL y V2-V5 y bloqueo de rama izquierda. La ecocardiografía transtorácica mostró agrandamiento del ventrículo izquierdo con una aurícula izquierda de 39 mm, un ventrículo izquierdo de 54.7 mm y una EF del LV del 41% (Simpson's). También se observó adelgazamiento de la pared anterior del LV y del tabique interventricular, con la parte más delgada de 4.7 mm; el movimiento casi había desaparecido y el eco se había mejorado. Sin embargo, las arterias carótidas, intracraneales y de las extremidades inferiores seguían siendo normales. Además, descubrimos que los medicamentos recetados para tratar la insuficiencia cardíaca no se tomaron religiosamente después del alta; por lo tanto, recetamos 23.75 mg de metoprolol, 2.5 mg de benazepril y 20 mg de espironolactona para tomar una vez al día, y coenzima para tomar cada 10 horas.\n\nMH - Adulto\nMH - Errores de diagnóstico\nMH - Insuficiencia cardiaca/etiología\nMH - Humanos\nMH - Hombre\nMH - Infarto de miocardio/complicaciones/*etiología\nMH - Lesiones torácicas/*complicaciones\nMH - Tiempo hasta el tratamiento\nMH - Heridas, no penetrantes/complicaciones\n",
+        "gold_summary": "Preocupaciones de los pacientes:\nUn hombre de 38 años, previamente sano, fue admitido en nuestro hospital con una queja de disnea. Tenía un historial de haber sido golpeado en el pecho por un tornillo de alta velocidad mientras trabajaba en una fábrica 3 meses antes de ser admitido en el hospital.\n\nDiagnóstico:\nLuego de realizarse una angiografía coronaria y una ecocardiografía, finalmente se le diagnosticó un infarto de miocardio.\n\nIntervenciones:\nRecibió medicamentos optimizados, entre ellos, diuréticos, bloqueadores beta y estimulantes cardíacos.\n\nResultados:\nAl cabo de cuatro años de seguimiento, se le diagnosticó al paciente una insuficiencia cardíaca crónica con una fracción de eyección reducida.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un hombre se lastimó el pecho con un tornillo grande. Tres meses después, le costaba mucho respirar. Los doctores le hicieron pruebas y vieron que su corazón estaba dañado. Le dieron medicinas para ayudar a su corazón a trabajar mejor. Cuatro años después, su corazón seguía un poco débil, pero los doctores siguen cuidándolo.",
+                "fh_score": 76.94
+            },
+            "B2": {
+                "text": "**Lo que le pasó al paciente**  \nUn hombre de 38 años, que estaba sano antes, sufrió un fuerte golpe en el pecho cuando un tornillo de alta velocidad lo alcanzó mientras trabajaba. Tres meses después, empezó a sentir dificultad para respirar y dolor en el pecho, por lo que fue llevado al hospital.\n\n**Qué encontraron los médicos**  \nDespués de hacerle varios exámenes, como una ecografía del corazón y una angiografía (que es una prueba para ver las arterias del corazón), descubrieron que había tenido un infarto de miocardio. Esto significa que una parte de su corazón no recibió suficiente sangre y se dañó.\n\n**Cómo lo trataron**  \nEl paciente recibió varios medicamentos para ayudar a su corazón a funcionar mejor. Entre ellos estaban diuréticos (que ayudan a eliminar el exceso de líquido), bloqueadores beta (que reducen la carga del corazón) y estimulantes cardíacos (que mejoran la fuerza del latido).\n\n**Qué pasó después**  \nDurante los siguientes cuatro años, los médicos lo siguieron controlando. Descubrieron que desarrolló insuficiencia cardíaca crónica, que es cuando el corazón no puede bombear sangre tan bien como antes. Esto se confirmó porque su fracción de eyección, que mide qué tan bien el corazón bombea, estaba baja.\n\nEn resumen, un golpe fuerte en el pecho causó daño en el corazón que llevó a un infarto y, con el tiempo, a problemas para que el corazón funcione correctamente. El paciente recibió tratamiento para mejorar su condición y sigue siendo monitoreado por los médicos.",
+                "fh_score": 62.83
+            },
+            "B3": {
+                "text": "**Contexto:**  \nUn hombre de 38 años, previamente sano y sin factores de riesgo conocidos para enfermedad coronaria, sufrió un traumatismo torácico grave al ser impactado en el pecho por un tornillo de alta velocidad mientras trabajaba en una fábrica. Tras perder el conocimiento brevemente, fue atendido inicialmente en un hospital local donde se identificaron fracturas en el esternón y costillas, además de derrame pleural bilateral. Fue tratado con drenaje torácico y dado de alta sin realizar estudios cardíacos. Sin embargo, tres meses después, presentó síntomas persistentes como dolor y opresión en el pecho, dificultad para respirar al realizar esfuerzos y disnea nocturna, lo que motivó su ingreso en un hospital especializado para una evaluación más profunda.\n\n**Hallazgos Clave:**  \n- El examen físico reveló signos compatibles con derrame pleural residual en el pulmón derecho, pero sin alteraciones cardíacas evidentes a la auscultación.  \n- El electrocardiograma mostró alteraciones sugestivas de un infarto de miocardio antiguo en la región anterior del corazón, incluyendo inversión de ondas T y bloqueo de rama izquierda anterior.  \n- Los niveles de troponina (marcador de daño cardíaco agudo) fueron negativos, pero el NT-proBNP (marcador de insuficiencia cardíaca) estaba elevado, indicando estrés cardíaco.  \n- La ecocardiografía evidenció una función ventricular izquierda reducida (fracción de eyección del 32%), con adelgazamiento y disminución del movimiento en la pared anterior del ventrículo izquierdo y el tabique interventricular.  \n- La angiografía coronaria mostró una estenosis (estrechamiento) significativa del 70% en la arteria coronaria descendente anterior (LAD), confirmando la presencia de una lesión coronaria importante.  \n- No se encontraron signos de aterosclerosis en otras arterias principales, lo que sugiere que el infarto fue consecuencia directa del traumatismo torácico y no de enfermedad arterial previa.\n\n**Interpretación Clínica:**  \nEl paciente desarrolló un infarto de miocardio antiguo como complicación tardía del traumatismo torácico contundente. La lesión en la arteria coronaria descendente anterior, probablemente causada por el impacto, condujo a daño en el músculo cardíaco y a una reducción significativa de la función del ventrículo izquierdo. A pesar de la gravedad inicial, el paciente se mantuvo hemodinámicamente estable y respondió favorablemente a la terapia médica. Sin embargo, con el tiempo evolucionó hacia una insuficiencia cardíaca crónica con función ventricular reducida, condición que requiere manejo continuo y seguimiento.\n\n**Próximos Pasos y Manejo:**  \n- Se inició tratamiento médico optimizado que incluyó diuréticos para controlar la retención de líquidos, bloqueadores beta para reducir la carga cardíaca y mejorar la función, estatinas para protección vascular y estimulantes cardíacos.  \n- Posteriormente, el paciente se sometió a una intervención coronaria percutánea (ICP) para mejorar el flujo sanguíneo en la arteria afectada.  \n- Durante el seguimiento a largo plazo, se observó una mejoría parcial en la función cardíaca, aunque persistió una insuficiencia cardíaca leve a moderada.  \n- Se enfatizó la importancia de la adherencia estricta a la medicación para prevenir la progresión de la insuficiencia cardíaca y mejorar la calidad de vida.  \n- En controles posteriores, se mantuvo la función cardíaca reducida y síntomas leves de disnea tras esfuerzos, requiriendo ajuste y continuidad en el tratamiento farmacológico.\n\n**Resumen Final:**  \nEste caso ilustra cómo un traumatismo torácico severo puede ocasionar una lesión coronaria significativa que conduce a un infarto de miocardio y, eventualmente, a insuficiencia cardíaca crónica. La evaluación cuidadosa, el diagnóstico oportuno mediante imágenes cardíacas y la terapia médica adecuada son fundamentales para mejorar el pronóstico en estos pacientes. Además, la adherencia al tratamiento y el seguimiento a largo plazo son esenciales para controlar los síntomas y evitar complicaciones mayores.",
+                "fh_score": 34.73
+            }
+        }
+    },
+    {
+        "article": "La paciente era una recién nacida de 0 días de edad, de etnia Han, que nació a las 36 semanas de gestación de una mujer embarazada de 3, para 2, con un peso de 2650 g. Se le practicó una cesárea de urgencia debido a la angustia fetal, con puntuaciones de Apgar de 6 a 1 min y 5 min. Su grupo sanguíneo era O y RhD positivo. Al nacer, presentaba palidez, equimosis dispersas en múltiples áreas del cuerpo, sangrado de las mucosas e insuficiencia respiratoria, con un leve flujo de sangre hemorrágica también observado en los sitios de punción venosa. El análisis de gases en sangre de la arteria umbilical mostró un hematocrito de 0.08 y una hemoglobina de 23 g/L. La paciente requirió intubación endotraqueal y ventilación mecánica. Después de la transfusión de una suspensión de glóbulos rojos, los recuentos sanguíneos iniciales revelaron una trombocitopenia severa (recuento de plaquetas de 12 × 109/L), anemia (hemoglobina de 46 g/L) y leucopenia (recuento de leucocitos de 1.11 × 109/L).\n\nLa paciente fue ingresada en la unidad de cuidados intensivos neonatales a las 3 horas de vida para recibir tratamiento adicional. Durante la hospitalización, se le diagnosticó coagulación intravascular diseminada (CID), con tiempo de tromboplastina parcial activada (TTPA) de 73,10 segundos, tiempo de protrombina (TP) de 25,4 segundos, fibrinógeno (FIB) de 1,01 g/L, razón internacional normalizada (INR) de 2,26 y dímero D > 20 mg/L. Se le administró ventilación mecánica, corrección de la acidosis y transfusión de plasma fresco congelado. A pesar de múltiples transfusiones de glóbulos rojos y plaquetas, los niveles de hemoglobina y plaquetas permanecieron por debajo de lo normal (hemoglobina 106 g/L y plaquetas 11 × 109/L el día 3). También recibió tratamiento antiinfeccioso, cardiotónico, vasopresor y otro tratamiento sintomático. Un frotis periférico mostró áreas de tinción pálida agrandadas de glóbulos rojos, con una proporción de reticulocitos del 1,5% y un resultado negativo en la prueba directa de Coombs. No se realizó aspiración de médula ósea debido a su grave estado. No hubo evidencia clínica o de laboratorio de sepsis neonatal, y las pruebas para toxoplasma, rubéola, citomegalovirus y virus del herpes simple (TORCH); virus de hepatitis; y Treponema pallidum fueron negativas. El examen físico de admisión reveló un estado mental deficiente, disminución del tono muscular en las extremidades y reflejo pupilar lento a la luz. Todos los demás hallazgos fueron normales. El ultrasonido craneal y electroencefalograma de cabecera revelaron hemorragia intracraneal grave y bajo voltaje, respectivamente. Los hallazgos del ecocardiograma sugirieron un conducto arterioso patente, foramen oval permeable e hipertensión pulmonar. El ultrasonido abdominal indicó hemorragia gastrointestinal. A pesar de todos los esfuerzos, la paciente falleció el tercer día de vida debido a falla multiorgánica y hemorragia intracraneal masiva (la información detallada se puede encontrar en el Informe Suplementario).\n\nLos padres de la paciente no eran consanguíneos y ambos tenían talasemia. La madre, que compartía el mismo tipo de sangre que la paciente, tuvo una anemia leve durante el embarazo (nivel de hemoglobina de 97 g/L) y un historial de aborto inducido. Los exámenes prenatales no mostraron anomalías, ni tampoco hidrops fetal, y no recibió ninguna medicación durante el embarazo que pudiera provocar una enfermedad hemorrágica de inicio temprano en el recién nacido. La paciente también tenía un hermano de 1 año que gozaba de buena salud. Su abuelo tenía un historial de anemia leve (detalles desconocidos).\n\nSe obtuvo el consentimiento informado de los padres del paciente y se realizó un secuenciamiento de Sanger para descubrir la causa de la enfermedad. Se detectó una nueva mutación de MECOM de desplazamiento de marco heterocigótica [NM_001105078: c.157_158del (p.Met53Glyfs*2)] en el probando. Esta variante cambió el aminoácido 53 de metionina (codón ATG) a glicina (codón GGT), seguido de una terminación temprana. La mutación no se encontró en los padres o en el hermano mayor. La variante se clasificó como patogénica según las directrices del Colegio Americano de Genética Médica (ACMG) [14]. El algoritmo “AutoPVS1” brindó un fuerte apoyo para la interpretación de PVS1 de p.Met53Glyfs*2, lo que indica patogenicidad. La variante no se ha informado previamente en la Base de Datos de Mutación Genética Humana (HGMD) o en Clinvar. El análisis de conservación mostró que el residuo Met53 está altamente conservado en todas las especies de mamíferos (incluidos humanos, ratones, ratas, chimpancés y bovinos) utilizando Clustal Omega. Se generaron modelos de estructura de proteínas tridimensionales de las proteínas MECOM de tipo salvaje y mutantes utilizando SWISS-MODEL, lo que indica que la mutación de desplazamiento de marco causó una terminación temprana de la síntesis de aminoácidos, alterando significativamente la estructura de la proteína.\n",
+        "gold_summary": "Reportamos el caso de una neonata Han china de 0 días de vida que presentó trombocitopenia grave y hemorragia intracraneal, y que finalmente falleció por fallo multiorgánico e intracraneal el tercer día después del nacimiento. La secuenciación genética identificó una variante de cambio de marco heterocigótica, c.157_158del, dentro del gen MECOM. Esta variante condujo a una sustitución del 53.º aminoácido de metionina a glicina, terminando en el 54.º aminoácido. Una revisión exhaustiva de la literatura indicó que las mutaciones del gen MECOM incluían mutaciones sin sentido (68.3%), deleción (8.5%), sitio de empalme (8.5%), cambio de marco (7.3%) y sin sentido (7.3%). Las pacientes con mutaciones sin sentido frecuentemente presentaban sinostosis radiocubital, mientras que el fallo de la médula ósea se asociaba más comúnmente con los otros cuatro tipos de mutaciones.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una bebé nació muy pequeñita y se puso muy enferma. Tenía problemas para que su sangre funcionara bien y sangraba en la cabeza. Los doctores buscaron en sus genes y encontraron un cambio que no estaba bien. Ese cambio hizo que su cuerpo no pudiera hacer una parte importante para estar sano. Por eso, la bebé se enfermó mucho y no pudo mejorar.",
+                "fh_score": 81.61
+            },
+            "B2": {
+                "text": "**Caso de una recién nacida con un problema genético grave**\n\nPresentamos el caso de una bebé recién nacida de origen Han en China, que tenía un conteo muy bajo de plaquetas en la sangre, llamado trombocitopenia grave. Esto causó que tuviera sangrados dentro de su cabeza (hemorragia intracraneal). Lamentablemente, falleció al tercer día de vida debido a que varios órganos dejaron de funcionar correctamente.\n\n**Qué encontraron en sus genes**\n\nLos médicos analizaron el ADN de la bebé y encontraron un cambio en un gen llamado MECOM. Este cambio es una mutación que afecta cómo se produce una proteína importante. En concreto, la mutación cambió el aminoácido número 53 de metionina a glicina y provocó que la proteína se terminara de fabricar muy rápido, antes de tiempo. Esto afecta la función normal de la proteína.\n\n**Importancia de esta mutación**\n\nAl revisar otros casos en la literatura científica, se sabe que el gen MECOM puede tener diferentes tipos de mutaciones. La mayoría son mutaciones que detienen la producción normal de la proteína (llamadas mutaciones sin sentido), pero también hay otros tipos como deleciones o cambios en el marco de lectura del gen. Cada tipo de mutación puede causar distintos problemas. Por ejemplo, las mutaciones sin sentido suelen relacionarse con un problema en los huesos del brazo (sinostosis radiocubital), mientras que otras mutaciones, como la que tuvo esta bebé, están más asociadas con fallos en la médula ósea, que es donde se producen las células de la sangre.\n\n**Qué significa este caso**\n\nEste caso muestra cómo una mutación nueva en el gen MECOM puede causar una enfermedad muy grave desde el nacimiento. Entender estas mutaciones ayuda a los médicos a diagnosticar y estudiar mejor estas condiciones raras, aunque en este caso no fue posible salvar a la bebé.",
+                "fh_score": 60.24
+            },
+            "B3": {
+                "text": "**Contexto del Caso**  \nSe trató de una recién nacida de origen Han, nacida a las 36 semanas de gestación mediante cesárea de urgencia debido a sufrimiento fetal. Al nacer, presentó signos graves como palidez, sangrado en mucosas, equimosis (moretones) dispersos y dificultad respiratoria que requirió ventilación mecánica. Los análisis iniciales mostraron anemia severa, trombocitopenia (bajo recuento de plaquetas) y leucopenia (bajo recuento de glóbulos blancos). Durante su ingreso en la unidad de cuidados intensivos neonatales, se diagnosticó coagulación intravascular diseminada (una alteración grave de la coagulación sanguínea) y hemorragias múltiples, incluyendo una hemorragia intracraneal masiva. A pesar de tratamientos intensivos, la paciente falleció al tercer día de vida por falla multiorgánica y hemorragia cerebral.\n\n**Hallazgos Genéticos**  \nSe realizó un estudio genético mediante secuenciación Sanger para identificar la causa subyacente de su enfermedad. Se detectó una mutación nueva y heterocigótica (presente en una sola copia del gen) en el gen MECOM, específicamente una deleción de dos nucleótidos (c.157_158del) que provocó un cambio en el marco de lectura del gen (mutación de cambio de marco). Esta alteración causó que el aminoácido número 53, metionina, fuera sustituido por glicina, seguida de una terminación prematura en la síntesis proteica, lo que probablemente afecta gravemente la función de la proteína MECOM. Esta mutación no se encontró en los padres ni en el hermano mayor, indicando que fue una mutación de novo (nueva en la paciente). Además, el residuo afectado está altamente conservado en mamíferos, lo que sugiere su importancia funcional.\n\n**Interpretación Clínica y Revisión Bibliográfica**  \nEl gen MECOM está implicado en la regulación del desarrollo de la médula ósea y la formación de células sanguíneas. Mutaciones en este gen se han asociado con síndromes que incluyen fallo medular y anomalías óseas. Una revisión exhaustiva de la literatura mostró que las mutaciones en MECOM pueden ser de varios tipos: mutaciones sin sentido (que generan una proteína truncada), deleciones, alteraciones en sitios de empalme (que afectan el procesamiento del ARN), cambios de marco y otras mutaciones sin sentido. Se observó que las mutaciones sin sentido se relacionan frecuentemente con sinostosis radiocubital (fusión anormal de huesos del antebrazo), mientras que el fallo de la médula ósea es más común en los otros tipos de mutaciones, incluyendo la de cambio de marco que presentó esta paciente.\n\n**Conclusiones y Relevancia**  \nEste caso ilustra la gravedad clínica que puede tener una mutación de novo en el gen MECOM, manifestada por una trombocitopenia severa, hemorragias masivas y fallo multiorgánico en un recién nacido. La identificación precisa de la mutación permitió confirmar el diagnóstico genético y ampliar el conocimiento sobre la diversidad de mutaciones en MECOM y sus manifestaciones clínicas. Este hallazgo es importante para el diagnóstico prenatal y el asesoramiento genético en familias con antecedentes similares.",
+                "fh_score": 42.2
+            }
+        }
+    },
+    {
+        "article": "La paciente es una mujer de 74 años de edad, físicamente activa, que practica senderismo y equitación. Un mes después del tratamiento con inyección de cortisona de la tendinopatía insercional de Aquiles, sufrió una rotura total del tendón de Aquiles insercional al intentar dar un paso mientras montaba en bicicleta. Esta rotura se trató de forma conservadora con una bota de Walker durante 8 semanas. Después, mientras montaba a caballo, un intento de dar un paso provocó una nueva rotura total del tendón de Aquiles en la inserción. La rotura se trató quirúrgicamente con reinserción del tendón de Aquiles en el calcáneo, utilizando anclajes de sutura. Esto fue seguido por inmovilización en un yeso. Después de la operación, la paciente sufrió una infección profunda que no respondía a los antibióticos, signos de sepsis, y se indicó exploración quirúrgica. Durante la cirugía, se encontró que todo el tendón de Aquiles estaba gravemente afectado por la infección, más o menos destruido, y hubo que retirar el tendón de Aquiles distal de 7 cm (todo el tendón libre de Aquiles). Esto dejó una gran herida sin tejido tendinoso, y la piel se suturó sobre la herida. Después de este procedimiento, la inmovilización y el tratamiento con antibióticos de cloxacilina curaron la infección y la herida se curó adecuadamente. El pie se inmovilizó en un yeso durante las primeras 10 semanas, desde la máxima flexión plantar inicialmente, y luego la flexión plantar disminuyó gradualmente hasta alcanzar la posición neutra. Esto fue seguido por inmovilización en un yeso dorsal, evitando la extensión del tendón de Aquiles en flexión plantar, durante otros 3 meses. Se le dijo que aumentara gradualmente la carga al caminar, pero que evitara la extensión durante un total de 6 meses. Después de 6 meses se le ofreció reconstrucción quirúrgica con un injerto de flexor hallucis longus, pero como entonces tenía una función satisfactoria, decidió esperar y ver. Su función mejoró gradualmente, y un año después de la operación, cuando buscó ayuda por el dolor en el otro tendón de Aquiles, se notó la buena función en el lado operado. La exploración por ultrasonido mostró sorprendentemente un tendón que se parecía mucho a un tendón de Aquiles ligeramente tendinopático.\n",
+        "gold_summary": "Esta señora de 74 años padecía tendinopatía insercional de Aquiles. Después del tratamiento con una inyección local de cortisona, sufrió una rotura total del tendón de Aquiles insercional. Esta rotura se trató de forma conservadora y, después del tratamiento, el tendón de Aquiles volvió a romperse en la zona de inserción. La rotura se trató entonces con reinserción en la zona de inserción calcánea. Al poco tiempo del postoperatorio, la paciente sufrió una infección de herida quirúrgica profunda y sepsis. Debido al pobre efecto del tratamiento con antibióticos y a la destrucción total del tendón, se extirpó todo el tendón de Aquiles. Después de la extirpación, se inmovilizó en un yeso, seguido de movilización y aumento gradual de la carga. En un seguimiento de un año, la paciente caminaba sin cojera, podía levantar el talón hasta la mitad mientras estaba de pie sobre una pierna, había un tendón de Aquiles palpable y el escaneado por ultrasonido mostró una estructura muy similar a un tendón de Aquiles tendinopático y ligeramente engrosado. Había una regeneración evidente de todo el tendón de Aquiles y la función del tendón era sorprendentemente buena.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había una señora de 74 años con un problema en el hueso del talón y el hueso del muslo. Se lastimó el hueso del muslo cerca del talón después de una inyección. Primero, usó una bota especial para sanar. Pero se volvió a lastimar el mismo hueso. Entonces, los doctores hicieron una operación para arreglarlo. Después, tuvo una infección que no se quitaba con medicina. Por eso, los doctores tuvieron que quitar todo el hueso del muslo que estaba lastimado. Luego, la señora usó un yeso para que su pie sanara. Poco a poco, pudo mover el pie y caminar sin dolor. Un año después, su hueso del muslo estaba casi como nuevo y ella podía caminar bien y levantar el talón.",
+                "fh_score": 82.76
+            },
+            "B2": {
+                "text": "**Lo que le Pasó a la Paciente**  \nUna mujer de 74 años tenía un problema llamado tendinopatía insercional de Aquiles. Esto significa que el tendón de Aquiles, que conecta el músculo de la pantorrilla con el hueso del talón, estaba dañado cerca de donde se une al hueso. Para tratarlo, le pusieron una inyección de cortisona, que es un medicamento para reducir la inflamación. Sin embargo, después de esto, el tendón se rompió completamente en esa zona.\n\n**Tratamientos y Complicaciones**  \nPrimero intentaron curar la rotura sin cirugía, usando una bota especial para inmovilizar el pie. Pero luego, el tendón se rompió otra vez. Esta vez, hicieron una operación para volver a unir el tendón al hueso usando anclajes, que son pequeños dispositivos para sujetar el tendón. Poco después de la cirugía, la paciente tuvo una infección grave en la herida que no mejoró con antibióticos y causó sepsis, una infección que afecta todo el cuerpo.\n\n**Cirugía y Recuperación**  \nDurante otra operación para tratar la infección, los médicos vieron que el tendón estaba muy dañado y tuvieron que quitarlo completamente, dejando una gran herida. La piel se cerró sobre esa zona y la paciente usó un yeso para inmovilizar el pie durante varias semanas. También recibió antibióticos para curar la infección. Luego, poco a poco, empezó a mover el pie y a cargar peso al caminar, pero evitando estirar demasiado el tendón.\n\n**Resultados Después de un Año**  \nUn año después, la paciente podía caminar sin cojear y levantar el talón mientras estaba de pie sobre una pierna, lo que muestra que el tendón funcionaba bien. Un examen con ultrasonido, que es una imagen que muestra los tejidos, mostró que el tendón de Aquiles había crecido de nuevo y parecía casi normal, aunque un poco engrosado y con signos de daño leve. Esto indica que el tendón se regeneró sorprendentemente bien y que la función del pie mejoró mucho, a pesar de que el tendón original fue removido.",
+                "fh_score": 63.38
+            },
+            "B3": {
+                "text": "**Contexto**  \nLa paciente es una mujer de 74 años, físicamente activa, que desarrolló una tendinopatía insercional del tendón de Aquiles (una lesión en la zona donde el tendón se une al hueso del talón). Tras recibir una inyección local de cortisona para tratar esta lesión, sufrió una rotura completa del tendón en la zona de inserción. Inicialmente, esta rotura se manejó con tratamiento conservador, pero posteriormente el tendón volvió a romperse en el mismo lugar. Esta segunda rotura se trató mediante cirugía para reinsertar el tendón en el hueso del talón.\n\n**Hallazgos Clave**  \nPoco después de la cirugía, la paciente desarrolló una infección profunda en la herida quirúrgica que evolucionó a sepsis (una infección grave que afecta a todo el organismo). Debido a que los antibióticos no controlaron la infección y el tendón estaba gravemente dañado, fue necesario extirpar completamente el tendón de Aquiles distal (aproximadamente 7 cm). Tras la extirpación, la herida se cerró y la paciente fue inmovilizada con yesos durante varios meses, con un protocolo gradual para permitir la recuperación y evitar movimientos que pudieran dañar la zona.\n\n**Interpretación Clínica**  \nA pesar de la pérdida total del tendón de Aquiles, la paciente mostró una recuperación funcional sorprendentemente buena. Un año después, caminaba sin cojera, podía levantar el talón mientras se apoyaba sobre una pierna y se palpaba un tendón en la zona afectada. El ultrasonido reveló que el tendón había regenerado una estructura similar a un tendón de Aquiles, aunque con signos leves de tendinopatía (engrosamiento y alteraciones en la textura). Esto indica que, incluso tras la extirpación completa del tendón, el organismo fue capaz de formar un nuevo tejido tendinoso funcional.\n\n**Próximos Pasos**  \nSe ofreció a la paciente la opción de una reconstrucción quirúrgica con un injerto de otro tendón (flexor hallucis longus) para mejorar aún más la función, pero ella decidió esperar debido a la buena recuperación que presentaba. Se recomienda continuar con seguimiento clínico y funcional para monitorizar la evolución, especialmente considerando que la regeneración espontánea del tendón de Aquiles es poco común y puede ofrecer información valiosa para futuros tratamientos.",
+                "fh_score": 45.95
+            }
+        }
+    },
+    {
+        "article": "Una mujer de 47 años con antecedentes de CHB congénita se presentó con quejas de dolor en el cuello del lado izquierdo y dolor en el oído izquierdo. Aproximadamente 30 meses antes de la presentación, la paciente había notado una pequeña masa en el lado izquierdo de su cuello, que había aumentado gradualmente de tamaño. El dolor se localizó inicialmente en la región del cuello, pero se intensificó con el tiempo y se extendió al área del oído izquierdo.\nInicialmente, debido al dolor en el oído izquierdo, el paciente consultó a varios otorrinolaringólogos y fue tratado por un diagnóstico preliminar de otitis media. Sin embargo, a pesar de los tratamientos, el dolor persistió. Finalmente, un otorrinolaringólogo derivó al paciente para una ecografía, que reveló una masa en el lado izquierdo del cuello, lo que llevó a una derivación quirúrgica. Después de las evaluaciones iniciales, se solicitó una angiografía por TC, que reveló una masa de forma ovalada que medía 30 por 50 mm en la bifurcación de la arteria carótida izquierda, lo que sugiere un CBT tipo II de Shamblin.\n\nEvaluaciones cardiovasculares preoperatorias\nDada la historia del paciente de CHB congénita, se realizó una evaluación cardiovascular preoperatoria exhaustiva. Esto incluyó un electrocardiograma (ECG) de 12 derivaciones, que confirmó la presencia de CHB con un ritmo de escape ventricular estable. Se realizó una ecocardiografía transtorácica para evaluar la estructura y función cardiaca, revelando una función sistólica ventricular normal sin evidencia de anormalidades estructurales. Además, se obtuvo una consulta de cardiología para evaluar la aptitud del paciente para la cirugía y optimizar el manejo perioperatorio.\n\nConsideraciones anestésicas\nDebido a la CHB congénita del paciente y al potencial de inestabilidad hemodinámica durante la cirugía, se formuló un plan anestésico detallado. El paciente fue clasificado como estado físico III de la Sociedad Estadounidense de Anestesiología (ASA). Preoperativamente, se le colocó un marcapasos externo temporal para garantizar un control adecuado de la frecuencia cardíaca y se le insertó un catéter arterial para el monitoreo continuo de la presión arterial. La inducción de la anestesia se realizó utilizando una combinación de etomidato (0,3 mg/kg) y fentanilo (2 μg/kg) para minimizar las fluctuaciones hemodinámicas. El mantenimiento se logró con sevoflurano (1-2 %) y rocuronio (0,6 mg/kg) para la relajación muscular. Los parámetros hemodinámicos, incluida la frecuencia cardíaca, la presión arterial y la saturación de oxígeno, se controlaron de forma continua. Además, se le colocó un catéter venoso central para monitorear la presión venosa central y administrar medicamentos vasoactivos si fuera necesario. El equipo de anestesia mantuvo una comunicación estrecha con el equipo quirúrgico para abordar de forma inmediata cualquier cambio hemodinámico intraoperatorio.\n\nEnfoque quirúrgico\nEl paciente fue sometido a cirugía el 19 de mayo de 2024, después de la localización precisa de la TCC mediante angiografía por TC. El enfoque quirúrgico se eligió en base a la clasificación de Shamblin tipo II, que indica un encasamiento parcial de las arterias carótidas. Dada la proximidad del tumor a estructuras neurovasculares críticas, incluidos los nervios vago e hipogloso, se consideró que el enfoque quirúrgico abierto era el más apropiado para garantizar una resección completa y minimizar las complicaciones.\nTras la inducción de la anestesia general, se colocó al paciente en posición supina con el cuello extendido y rotado hacia la derecha. Se realizó una incisión oblicua paralela al músculo esternocleidomastoideo izquierdo, que se extendía desde la apófisis mastoidea hasta la escotadura esternal. Tras la incisión de la piel y la disección del platisma, se expuso con cuidado la vaina carotídea. Se identificaron la arteria carótida común y su bifurcación en las arterias carótidas internas y externas. Se observó el tumor, de 30 × 50 mm, en la bifurcación carotídea y se diseccionó con cuidado de los tejidos circundantes.\n\nManobras y precauciones específicas\n1.\nSe aplicaron pinzas vasculares temporales en las arterias carótidas internas y externas para controlar el flujo sanguíneo durante la disección del tumor. Esto minimizó el sangrado y proporcionó un campo quirúrgico despejado.\n2.\nSe utilizó neuromonitorización intraoperativa para evaluar la integridad de los nervios vago e hipogloso. La retroalimentación continua garantizó que las estructuras neurales se preservaran durante la disección.\n3.\nEl tumor se separó cuidadosamente de las arterias carótidas y las estructuras neurales circundantes, mediante una combinación de disección aguda y roma. Se logró la hemostasis mediante cauterización bipolar y pinzas quirúrgicas para minimizar el sangrado.\n4.\nEl marcapasos externo se monitoreó activamente durante todo el procedimiento para garantizar un ritmo cardíaco estable. El equipo de anestesia estaba preparado para administrar atropina o epinefrina si se producía una bradicardia o hipotensión significativas.\n2.5. Manejo postoperatorio\nTras asegurarse de que no había hemorragia activa y restablecer el flujo sanguíneo, se devolvieron los tejidos a su posición original y se cerró la herida en múltiples capas. Se aplicó un vendaje apropiado. La cirugía se completó sin complicaciones y con un sangrado mínimo en 2 h y 10 min. El paciente fue trasladado a la UCI vascular para una estrecha monitorización.\nDespués de la operación, se controló al paciente en la UCI durante 24 horas y, más tarde, se le trasladó a la planta general tras mejorar su estado clínico. El marcapasos externo se retiró el día 1 después de la operación, ya que el paciente mantenía un ritmo de escape ventricular estable. El paciente fue dado de alta en buenas condiciones generales el día 3 después de la operación, sin quejas específicas.\n2.6. Seguimiento y resultados a largo plazo\nEl examen histopatológico confirmó el diagnóstico definitivo de TCC en la paciente. Se realizaron evaluaciones de seguimiento a las 2 semanas, 1 mes, 6 meses y 1 año posteriores a la cirugía para evaluar los resultados quirúrgicos y cardíacos. En cada visita, la paciente se sometió a un ECG de 12 derivaciones para monitorear el CHB congénito, que permaneció sin cambios durante todo el período de seguimiento. Se repitió la ecocardiografía transtorácica a los 6 meses y un año, sin deterioro de la función cardíaca y con una función sistólica ventricular estable.\n\nPara evaluar el impacto de la extirpación del tumor en la función cardiaca, se realizó un análisis de la variabilidad de la frecuencia cardiaca (VFC) antes de la operación y a los 6 meses después de la misma. El análisis de la VFC antes de la operación demostró una reducción de la actividad parasimpática, probablemente debido a la compresión del nervio vago por el tumor. El análisis de la VFC después de la operación mostró una mejora significativa del tono parasimpático, lo que sugiere que la extirpación del tumor alivió la compresión del nervio vago y restauró la función autónoma normal.\nAsimismo, el paciente manifestó que el dolor en el cuello y en el oído había desaparecido por completo después de la cirugía, sin que se produjera una reaparición de los síntomas durante el período de seguimiento. Se realizaron estudios de imagen, que incluyeron ultrasonido Doppler y angiografía por TAC, a los 6 meses y al año, que no mostraron evidencia de reaparición del tumor o complicaciones vasculares.\n",
+        "gold_summary": "Describimos el caso de una mujer de 47 años con antecedentes de dolor en el cuello izquierdo y en el oído, acompañado por una masa en el cuello que había ido aumentando gradualmente durante 2,5 años. Después de las evaluaciones iniciales y de múltiples diagnósticos diferenciales, la angiografía por TC reveló una masa ovalada de 30 × 50 mm en la bifurcación carotídea izquierda, lo que confirmó un CCT tipo II de Shamblin. Las evaluaciones preoperatorias demostraron CHB congénita en el electrocardiograma y la ecocardiografía. La paciente se sometió a una resección completa del tumor con todas las precauciones necesarias, incluida la colocación temporal de un marcapasos y un cuidadoso seguimiento.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había una señora con dolor en su cuello y oído. Tenía una bolita en el cuello que creció poco a poco. Los doctores hicieron muchas pruebas y vieron la bolita en su cuello con una máquina especial. La bolita estaba cerca de unos tubos importantes del cuello. \n\nAntes de la operación, los doctores revisaron su corazón y vieron que tenía un problema que nació con ella. Para la operación, usaron un aparato para ayudar a su corazón a latir bien. Los doctores sacaron la bolita con mucho cuidado. Después, la señora se sintió mejor y no le dolió más.",
+                "fh_score": 80.88
+            },
+            "B2": {
+                "text": "**Lo que le pasó a la paciente**  \nUna mujer de 47 años tenía dolor en el lado izquierdo del cuello y en el oído izquierdo. También notó una bolita (masa) en el cuello que fue creciendo poco a poco durante más de dos años. Al principio, pensaron que tenía una infección en el oído, pero el dolor no mejoró con el tratamiento.\n\n**Lo que encontraron los médicos**  \nDespués de hacer varios estudios, usaron una tomografía computarizada (una especie de radiografía especial) para ver mejor el cuello. Descubrieron una masa ovalada de 3 por 5 centímetros en un lugar donde una arteria importante del cuello se divide. Esto confirmó que tenía un tumor llamado paraganglioma carotídeo, que es un tumor raro que crece cerca de las arterias del cuello.\n\nAdemás, al revisar su corazón, encontraron que tenía un bloqueo cardíaco congénito, que significa que su corazón late más lento de lo normal desde que nació. Por eso, antes de la cirugía, hicieron varios exámenes para asegurarse de que su corazón estaba estable.\n\n**Cómo la operaron y qué cuidados tuvieron**  \nPara quitar el tumor, los médicos planearon la cirugía con mucho cuidado. Le pusieron un marcapasos temporal, que es un dispositivo que ayuda a controlar el ritmo del corazón durante la operación. También usaron anestesia especial para que no tuviera problemas con la presión o el ritmo cardíaco.\n\nDurante la cirugía, hicieron una incisión en el cuello para llegar al tumor. Usaron pinzas para controlar el sangrado y monitorearon los nervios importantes para evitar dañarlos. El tumor fue separado cuidadosamente de las arterias y nervios cercanos. La operación duró poco más de dos horas y no hubo complicaciones graves.\n\n**Después de la cirugía y resultados**  \nLa paciente estuvo en cuidados intensivos un día para vigilar su estado. El marcapasos temporal se retiró al día siguiente porque su corazón mantenía un ritmo estable. Fue dada de alta tres días después, sin dolor ni problemas.\n\nEn los controles posteriores, los médicos vieron que el tumor no había vuelto a aparecer y que su corazón seguía funcionando bien. Además, el análisis mostró que la función de un nervio llamado nervio vago mejoró después de quitar el tumor, lo que ayudó a que su sistema nervioso autónomo trabajara mejor. La paciente también dijo que el dolor en el cuello y oído desapareció completamente.\n\n**Qué significa este caso**  \nEste caso muestra la importancia de hacer un diagnóstico correcto cuando hay dolor persistente y masas en el cuello. También destaca cómo los médicos deben planear cuidadosamente la cirugía en pacientes con problemas cardíacos para evitar riesgos. La operación fue exitosa y mejoró la calidad de vida de la paciente.",
+                "fh_score": 65.92
+            },
+            "B3": {
+                "text": "**Contexto del Caso**  \nSe presenta el caso de una mujer de 47 años que experimentaba dolor en el lado izquierdo del cuello y en el oído izquierdo, acompañado por la presencia de una masa en el mismo lado del cuello. Esta masa había sido detectada aproximadamente 30 meses antes y había ido aumentando de tamaño de forma progresiva. Inicialmente, el dolor se atribuyó a una infección del oído medio (otitis media), pero ante la persistencia de los síntomas, se realizaron estudios de imagen que identificaron una masa en la bifurcación de la arteria carótida izquierda.\n\n**Hallazgos Clave**  \nLa angiografía por tomografía computarizada (TC) mostró una masa ovalada de 30 × 50 mm ubicada en la bifurcación carotídea izquierda, característica de un tumor del cuerpo carotídeo (TCC) clasificado como tipo II según Shamblin, lo que indica un compromiso parcial de las arterias carótidas. Además, las evaluaciones cardiovasculares preoperatorias confirmaron que la paciente tenía un bloqueo auriculoventricular completo congénito (CHB), detectado mediante electrocardiograma (ECG) y corroborado por ecocardiografía, que mostró función ventricular normal sin anomalías estructurales.\n\n**Interpretación Clínica y Manejo**  \nDado el diagnóstico de TCC y la condición cardíaca de la paciente, se diseñó un plan quirúrgico y anestésico cuidadoso para minimizar riesgos. Se colocó un marcapasos temporal externo para mantener un ritmo cardíaco estable durante la cirugía y se monitorizó de forma continua la presión arterial y otros parámetros vitales. La cirugía se realizó mediante un abordaje abierto, con una incisión paralela al músculo esternocleidomastoideo para exponer la bifurcación carotídea y permitir la disección cuidadosa del tumor, preservando nervios importantes como el vago e hipogloso mediante neuromonitorización intraoperatoria.\n\nDurante la intervención, se aplicaron pinzas vasculares para controlar el flujo sanguíneo y evitar hemorragias, y se mantuvo una comunicación estrecha entre los equipos quirúrgico y anestésico para manejar cualquier cambio hemodinámico. La cirugía se completó exitosamente en poco más de dos horas, con sangrado mínimo y sin complicaciones inmediatas.\n\n**Próximos Pasos y Resultados a Largo Plazo**  \nDespués de la operación, la paciente fue vigilada en la unidad de cuidados intensivos y luego trasladada a planta general. El marcapasos temporal se retiró al día siguiente, ya que el ritmo cardíaco se mantuvo estable. La paciente fue dada de alta en buenas condiciones al tercer día postoperatorio, sin dolor ni otros síntomas. El examen histopatológico confirmó el diagnóstico de tumor del cuerpo carotídeo.\n\nEn el seguimiento a corto y largo plazo, que incluyó evaluaciones clínicas, electrocardiogramas y ecocardiografías, se observó que la función cardíaca permaneció estable y que el bloqueo cardíaco congénito no empeoró. Además, un análisis de la variabilidad de la frecuencia cardíaca mostró una mejora significativa en la actividad parasimpática después de la cirugía, lo que sugiere que la extirpación del tumor alivió la compresión del nervio vago y restauró la función autónoma normal. Los estudios de imagen realizados a los 6 meses y un año no evidenciaron recurrencia tumoral ni complicaciones vasculares. La paciente reportó la desaparición completa del dolor en cuello y oído, sin reaparición de síntomas durante el seguimiento.\n\nEn resumen, este caso ilustra la importancia de un diagnóstico preciso y un manejo multidisciplinario cuidadoso en pacientes con tumores carotídeos y condiciones cardíacas preexistentes, logrando una resección segura y resultados clínicos favorables a largo plazo.",
+                "fh_score": 36.14
+            }
+        }
+    },
+    {
+        "article": "Una mujer de 19 años de edad acudió al servicio de urgencias de nuestro hospital con una queja principal de dos días de historia de cefalea, acompañada de náuseas recurrentes, vómitos y fiebre de un día. En el ingreso, su examen físico reveló una fiebre alta de 39.1°C, presión arterial elevada de 189/120 mmHg y una frecuencia cardíaca de 148 latidos por minuto. Los resultados de laboratorio indicaron un recuento de glóbulos blancos elevado de 14.77×10^9/L y un recuento de neutrófilos de 13.55×10^9/L, lo que sugiere una posible infección o respuesta inflamatoria. Se administró un tratamiento empírico inicial con antibióticos debido a la sospecha de infección, pero sus síntomas persistieron. Dados sus signos vitales anormales, marcadores inflamatorios elevados y falta de mejora de los síntomas, la paciente fue admitida para una evaluación diagnóstica adicional y transferida a la unidad de cuidados intensivos para una estrecha monitorización. Un año antes, la paciente había presentado síntomas similares y se le diagnosticó miocarditis en un hospital local en base a los hallazgos clínicos en ese momento. Durante esa hospitalización, también se le diagnosticó hipertensión y se le prescribieron medicamentos antihipertensivos. Sin embargo, después del alta, la paciente no se adhirió al tratamiento antihipertensivo prescrito y no controló regularmente su presión arterial. Además, es notable que su padre tenía antecedentes de muerte súbita inexplicable.\n\nPara investigar la etiología subyacente de los síntomas del paciente, se realizó una tomografía computarizada (TC) de tórax. De forma incidental, esta exploración reveló una masa suprarrenal izquierda con densidad de tejido blando, que medía 43 mm × 36 mm. No se observaron hallazgos patológicos en las exploraciones de TC de cabeza y tórax. El electrocardiograma demostró taquicardia sinusal con un intervalo PR acortado y ondas P altas y puntiagudas en las derivaciones II, III y aVF. La ecocardiografía transtorácica no reveló ninguna anomalía significativa.\n\nEn el segundo día de ingreso, el paciente mostró niveles crecientes de péptido natriurético cerebral (BNP) y troponina I (TnI). El cardiólogo diagnosticó provisionalmente al paciente con miocarditis de etiología incierta, basándose en la presentación clínica, los biomarcadores cardiacos elevados (BNP y TnI) y los hallazgos del electrocardiograma de apoyo. Se inició el tratamiento con metilprednisolona (0,25 g diarios) para abordar la posible inflamación miocárdica debida a la sospecha de miocarditis. Se administraron furosemida (20 mg cada 12 horas) y espironolactona (20 mg cada 12 horas) como diuréticos para controlar la retención de líquidos y reducir la carga de trabajo cardiaco. Se prescribió perindopril amlodipina (10 mg: 5 mg diarios) como inhibidor de la enzima convertidora de la angiotensina y bloqueador del canal del calcio para controlar la presión arterial y reducir la poscarga. Se usó tartrato de metoprolol (25 mg cada 12 horas) para controlar la frecuencia cardiaca y disminuir la demanda de oxígeno miocárdico, mientras que se administró esmolol (0,2 g/hora por infusión intravenosa), un bloqueador beta de acción corta, para controlar la frecuencia cardiaca aguda adicional debido a la taquicardia sinusal. Debido a la preocupación por una posible infección, se agregó moxifloxacina como terapia antibiótica empírica.\n\nDada la presentación del paciente con una masa suprarrenal e hipertensión, el endocrinólogo recomendó una evaluación de la relación aldosterona/renina, cortisol plasmático, catecolaminas plasmáticas y catecolaminas urinarias de 24 horas, junto con sus metabolitos. En posición supina, los niveles de catecolaminas plasmáticas y urinarias estaban marcadamente elevados (Tabla 1), incluyendo dopamina plasmática a 524,5 pmol/L, norepinefrina a 83975 pmol/L y epinefrina a 10579,3 pmol/L. Además, los niveles urinarios de 24 horas mostraron adrenalina libre a 4368,89 nmol/24 horas, norepinefrina libre superior a 12697,60 nmol/24 horas, normetaneprina a 8312 nmol/24 horas, metaneprinas a 4078 nmol/24 horas y ácido vanilmandélico a 58,1 mg/24 horas. Estos hallazgos apoyaron un diagnóstico clínico de feocromocitoma. En el quinto día posterior al ingreso, se interrumpió la terapia glucocorticoide y se sustituyó perindopril amlodipina con terazosin para un control más dirigido de la presión arterial.\n\nUna tomografía computarizada abdominal mejorada confirmó una masa suprarrenal izquierda, muy sugestiva de feocromocitoma. Además, después de obtener el consentimiento informado, se realizó una secuenciación del exoma completo, que reveló una mutación sin sentido heterocigótica, c.1900T > C: p. Cys634Arg, en el gen RET, que conduce a una sustitución de cisteína por arginina en el codón 634. Esta mutación levantó sospechas de un síndrome de neoplasia endocrina múltiple, lo que impulsó una evaluación adicional de las glándulas tiroides y paratiroides. La ecografía Doppler en color de la tiroides identificó una masa hipoecoica que medía 6 mm × 4 mm en el lóbulo tiroideo izquierdo, y se observó una leve elevación en los niveles de calcitonina. No se detectaron anormalidades significativas adicionales.\n\nA medida que la condición del paciente mejoró gradualmente, los niveles de cortisol en plasma y ACTH volvieron a la normalidad. El paciente fue dado de alta con una prescripción de tartrato de metoprolol (100 mg cada 12 horas) e hidrocloruro de ivabradina (5 mg cada 12 horas) para el tratamiento en el hogar. Tres meses después, después de lograr un estado clínico estable, el paciente se sometió a una resección del tumor suprarrenal izquierdo, que medía 50 mm × 40 mm × 30 mm. El análisis inmunohistoquímico confirmó una tinción positiva para Vim, CD56, Syn, CgA y NSE, con S-100 positivo en las células de Sertoli, mientras que CKpan, CD10, MART-1/Melan-A y Melan-A fueron negativos. El índice Ki67 fue del 1 %, lo que llevó a un diagnóstico definitivo de feocromocitoma suprarrenal. El paciente fue dado de alta sin más medicamentos y desde entonces se le ha dado seguimiento regular postoperatorio sin recurrencia de síntomas. Durante un seguimiento postoperatorio de 15 meses, el paciente exhibió hipercalcinotemia persistente leve con un tamaño de nódulo tiroideo estable, mientras que los niveles de PTH y calcio en suero mostraron un aumento progresivo (Tabla 2). Se realizó una gammagrafía paratiroidea adicional utilizando 99mTc-MIBI, y la conclusión fue un resultado negativo para el adenoma paratiroideo.\n",
+        "gold_summary": "Reportamos el caso de una mujer de 19 años que presentó feocromocitoma sin experimentar una crisis, a pesar de tener una masa suprarrenal significativa y someterse a un tratamiento glucocorticoide de alta dosis. Las pruebas genéticas revelaron una mutación de sentido erróneo heterocigótica en el gen RET (c.1900T > C: p. Cys634Arg), asociada con MEN2A. La evaluación endocrina adicional identificó un nódulo tiroideo con niveles de calcitonina levemente elevados, pero niveles normales de electrolitos y hormona paratiroidea. Durante un seguimiento postoperatorio de 15 meses, la paciente exhibió hipercalcitonemia persistente leve con tamaño de nódulo tiroideo estable, mientras que la PTH y los niveles de calcio sérico mostraron un aumento progresivo. Se realizó una gammagrafía paratiroidea adicional utilizando 99mTc-MIBI, que arrojó un resultado negativo para el adenoma paratiroideo.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había una chica de 19 años que tenía un bulto en una parte de su cuerpo llamada glándula suprarrenal. Este bulto no le causó un problema muy grande de repente. Los doctores le hicieron un examen especial y encontraron un cambio en sus genes. Este cambio puede causar problemas en algunas partes del cuerpo que hacen hormonas.\n\nTambién encontraron un pequeño bulto en su cuello, en una parte llamada tiroides. Ella tenía un poco más de una sustancia llamada calcitonina, pero otras cosas en su cuerpo estaban normales. Después de que le sacaron el bulto del cuerpo, los doctores la cuidaron por mucho tiempo. Vieron que la calcitonina seguía un poco alta y que otras cosas en su sangre subían poco a poco. Hicieron otro examen para buscar otro bulto, pero no encontraron nada malo. Los doctores siguen cuidándola para que esté bien.",
+                "fh_score": 76.87
+            },
+            "B2": {
+                "text": "**Caso de una joven con tumor suprarrenal y mutación genética**\n\nUna mujer de 19 años llegó al hospital con dolor de cabeza, náuseas, vómitos y fiebre. Tenía la presión arterial muy alta y signos de inflamación en su cuerpo. Los médicos encontraron una masa (un bulto) en su glándula suprarrenal izquierda, que está encima del riñón y produce hormonas importantes. Esta masa causaba que su cuerpo liberara muchas sustancias llamadas catecolaminas, que pueden subir mucho la presión arterial.\n\nSe hizo un análisis genético y descubrieron que tenía un cambio en un gen llamado RET. Este cambio puede causar un síndrome llamado MEN2A, que hace que se formen tumores en varias glándulas del cuerpo. Por eso, también revisaron su tiroides y encontraron un pequeño nódulo (una bolita) con niveles un poco altos de calcitonina, una hormona relacionada con la tiroides.\n\nDespués de tratarla con medicamentos para controlar su presión y frecuencia cardíaca, la paciente se sometió a una cirugía para quitar la masa suprarrenal. El examen del tumor confirmó que era un feocromocitoma, un tipo de tumor que produce muchas hormonas. Tras la operación, la paciente mejoró y no tuvo más síntomas.\n\nDurante los siguientes 15 meses, los médicos siguieron revisando su tiroides y sus niveles de calcio en sangre. Aunque el nódulo en la tiroides no creció, los niveles de calcitonina y calcio en sangre aumentaron un poco, lo que puede indicar cambios en las glándulas paratiroides, que ayudan a controlar el calcio en el cuerpo. Sin embargo, una prueba especial llamada gammagrafía no mostró tumores en esas glándulas.\n\n**¿Qué significa esto?**\n\nEste caso muestra cómo un tumor en la glándula suprarrenal puede causar problemas graves, pero también cómo una mutación genética puede afectar varias glándulas del cuerpo. Es importante hacer un seguimiento cuidadoso para detectar y tratar cualquier cambio en otras glándulas, como la tiroides o las paratiroides, que pueden estar relacionadas con esta mutación.",
+                "fh_score": 61.19
+            },
+            "B3": {
+                "text": "**Contexto**  \nPresentamos el caso de una mujer joven de 19 años que acudió al hospital con síntomas de cefalea, náuseas, vómitos y fiebre, acompañados de hipertensión severa y taquicardia. Durante la evaluación, se detectó incidentalmente una masa en la glándula suprarrenal izquierda. Los análisis de sangre y orina mostraron niveles muy elevados de catecolaminas (sustancias químicas producidas por la médula suprarrenal), lo que sugirió la presencia de un feocromocitoma, un tumor poco común que produce estas hormonas y puede causar hipertensión y otros síntomas.\n\n**Hallazgos Clave**  \n- La paciente tenía una masa suprarrenal de aproximadamente 4 cm detectada por tomografía computarizada.  \n- Los niveles plasmáticos y urinarios de catecolaminas y sus metabolitos estaban marcadamente elevados, confirmando la sospecha de feocromocitoma.  \n- Se identificó una mutación genética heterocigótica en el gen RET (c.1900T > C: p. Cys634Arg), conocida por estar asociada con el síndrome de neoplasia endocrina múltiple tipo 2A (MEN2A), una condición que predispone a tumores endocrinos múltiples.  \n- La evaluación adicional mostró un pequeño nódulo en la glándula tiroides con leves elevaciones en los niveles de calcitonina, una hormona que puede indicar la presencia de carcinoma medular de tiroides, común en MEN2A.  \n- Durante el seguimiento postoperatorio de 15 meses, la paciente mantuvo niveles ligeramente elevados de calcitonina y un nódulo tiroideo estable, pero los niveles de hormona paratiroidea (PTH) y calcio en sangre aumentaron progresivamente.  \n- Una gammagrafía paratiroidea con 99mTc-MIBI no mostró evidencia de adenoma paratiroideo (tumor benigno de la glándula paratiroides).\n\n**Interpretación Clínica**  \nEste caso destaca la presentación atípica de un feocromocitoma sin crisis hipertensiva grave, a pesar de la masa suprarrenal significativa y el uso de glucocorticoides de alta dosis, que normalmente podrían desencadenar una crisis. La mutación en el gen RET confirma la asociación con MEN2A, un síndrome que requiere vigilancia cuidadosa por el riesgo de tumores endocrinos múltiples, incluyendo carcinoma medular de tiroides y alteraciones paratiroideas. La persistencia de hipercalcitoninemia y el aumento progresivo de PTH y calcio sugieren la necesidad de un seguimiento continuo para detectar posibles complicaciones o desarrollo de hiperparatiroidismo.\n\n**Próximos Pasos**  \n- Continuar con el seguimiento endocrinológico regular para monitorizar el nódulo tiroideo y los niveles hormonales, especialmente calcitonina, PTH y calcio sérico.  \n- Realizar evaluaciones periódicas para detectar signos tempranos de carcinoma medular de tiroides o hiperparatiroidismo.  \n- Considerar intervenciones quirúrgicas o terapéuticas adicionales si se evidencian cambios significativos en el nódulo tiroideo o en la función paratiroidea.  \n- Mantener un control estricto de la presión arterial y la función cardiaca, dado el antecedente de feocromocitoma y miocarditis.  \n- Brindar asesoramiento genético y seguimiento familiar, dado el componente hereditario asociado a la mutación RET y el antecedente de muerte súbita en el padre.\n\nEste caso subraya la importancia de una evaluación multidisciplinaria y un seguimiento prolongado en pacientes jóvenes con feocromocitoma y mutaciones genéticas relacionadas con síndromes endocrinos múltiples.",
+                "fh_score": 31.7
+            }
+        }
+    },
+    {
+        "article": "Una refugiada etíope embarazada de 39 años (Gravida 3 Para 2+0) fue derivada a nuestro departamento de urgencias de medicina interna en el Hospital Universitario de Gadarif, Gadarif State, Sudán, con hinchazón generalizada progresiva, falta de aire y fatiga durante 6 semanas y una revisión sistémica sin importancia. La paciente fue admitida en el sitio de admisión de casos críticos y su historia, tomada con la ayuda de un intérprete de idiomas más tarde en la admisión, reveló un episodio remoto inicialmente no revelado de tres convulsiones tónico-clónicas generalizadas no provocadas hace 21 años que se trataron tradicionalmente. Sin embargo, no había antecedentes de traumatismo craneal o antecedentes familiares de convulsiones. El examen general de la paciente reveló un PWS del lado izquierdo que involucraba la división oftálmica del nervio trigémino. Sin embargo, este hallazgo se perdió inicialmente en la inspección pero luego fue confirmado por el cónyuge de la paciente para estar presente desde el nacimiento. La paciente también estaba muy pálida y tenía derrames pleurales bilaterales, hepatomegalia blanda e hinchazón bilateral de las extremidades inferiores.\n\nLas investigaciones iniciales revelaron un nivel de hemoglobina de 8,84 g/dl. Por lo tanto, se diagnosticó insuficiencia cardíaca debido a anemia y se trató a la paciente en consecuencia. Sin embargo, ocho días después de su ingreso, la paciente había desarrollado aproximadamente seis episodios de convulsiones tónico-clónicas focales a bilaterales que respondieron bien a la fenitoína, pero que dejaron a la paciente en un estado comatoso profundo con un GCS de tres. Fue posteriormente admitida en la unidad de cuidados intensivos (UCI) y se le insertó un tubo nasogástrico para ayudarla con su nutrición y administración de fármacos. Además, para evitar más convulsiones, se le inició un tratamiento con comprimidos de carbamazepina de 200 mg administrados a través del tubo nasogástrico.\n\nSe retrasó una tomografía computarizada (TC) sin contraste del cerebro para el día posterior a la estabilización, ya que solo había una máquina de tomografía computarizada en el estado de Gadarif y funcionaba de forma intermitente debido a la falta de un número suficiente de técnicos radiólogos. La tomografía computarizada reveló calcificaciones corticales en la parte posterior del área parietal izquierda, lo que planteó el diagnóstico diferencial de SWS. En consecuencia, se realizó un examen físico de repetición, que mostró la presencia de una lesión plana de color rojo púrpura en la frente y el ojo. Al interrogar al cónyuge, se confirmó la presencia de esta lesión y que no había cambiado desde el nacimiento, lo que nos ayudó a descartar el diagnóstico de una mancha salmón, ya que esta lesión no se desvaneció, por lo que se diagnosticó como PWS. Además, no tenía características de megalencefalia, síndrome de malformación capilar que por lo general incluye un gran tamaño de la cabeza o del cerebro, problemas en las articulaciones y malformaciones capilares en la piel. Tampoco tenía hipertrofia de extremidades, anomalías del drenaje linfático o excrecencias óseas o de tejidos blandos que sugieran el síndrome de Klippel-Trenaunay-Weber. Por lo tanto, en función de los hallazgos de la tomografía computarizada y la presentación típica, llegamos a la conclusión del diagnóstico de SWS.\n\nDos días después de ingresar en la UCI, la paciente experimentó un cambio fluctuante en su estado de conciencia y una nueva aparición de hemiparesia contralateral (contralateral al SPW), así como afasia y labilidad emocional. Desafortunadamente, cuatro días después de ingresar en la UCI, la paciente empezó a experimentar sangrado vaginal; por ello, se consultó al departamento de obstetricia y ginecología y se descubrió que la paciente tenía un embarazo no viable (28 semanas + 1 día) y se realizó una inducción sin incidentes. Durante el mismo período, la paciente se volvió combativa y poco cooperativa, lo que llevó a que se la inmovilizara físicamente. Tres días después, la paciente desarrolló nuevos ataques focales bilaterales que comenzaron como episodios mioclónicos faciales y, tras consultar con el departamento de neurología, se aumentó la dosis de carbamazepina de la paciente a 1000 mg diarios, lo que ayudó a prevenir la recurrencia de los ataques. Cabe mencionar que, en su segundo trimestre y antes de recibir el resultado de la tomografía computarizada, se exploró un diagnóstico de eclampsia, pero sus constantes lecturas de presión arterial con una presión sistólica superior a la normal de 139 la mayoría de los días y una presión diastólica con un máximo de 97 mmHg y un rango bajo de proteinuria, así como la ausencia de características sistémicas como deterioro renal o hepático, excluyeron este diagnóstico. Después de alcanzar el diagnóstico de SW, se puso en juego un enfoque multidisciplinario; por ello, se realizó una consulta oftalmológica para descartar glaucoma. Sin embargo, la paciente estaba muy irritable y era difícil realizar un examen de fondo de ojo. Además, la paciente fue trasladada a la sala de medicina interna tras la estabilización.\n",
+        "gold_summary": "Presentamos el caso de una refugiada de 39 años, no diabética y no hipertensa, que inicialmente presentó insuficiencia cardiaca debido a anemia, por lo que recibió transfusiones de sangre. Más adelante, al ingresar, desarrolló convulsiones múltiples focales bilaterales, irritabilidad severa, afasia y hemiplejía derecha, lo que motivó su ingreso a la UCI. Un examen y un historial médico repetidos revelaron una mancha de vino de Oporto ocular izquierda leve que inicialmente pasó desapercibida y un historial remoto de convulsiones no provocadas 20 años atrás. Las imágenes revelaron calcificaciones parietales y confirmaron el diagnóstico de SWS. Por lo tanto, se adoptó un enfoque multidisciplinario para comprender plenamente el diagnóstico de la paciente y determinar una estrategia de tratamiento, que incluyó consultas con los departamentos de neurología, oftalmología, otorrinolaringología y fisioterapia. Se logró un control exitoso de las convulsiones mediante la administración de fenitoína IV durante 3 días y el aumento gradual de la carbamazepina oral a 1 g diario a través de una sonda nasogástrica. Lamentablemente, debido a la falta de personal o recursos, no se pudieron realizar otras evaluaciones importantes para pacientes con SWS, como evaluaciones avanzadas de neuroimagen, psiquiátricas, de cirugía plástica y neurocirugía, así como revisiones dentales.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había una señora que estaba muy cansada y con el cuerpo hinchado. Ella tenía una manchita roja en la cara desde que nació. También tuvo muchos ataques donde se movía sin querer. Los doctores vieron que tenía un problema en el cerebro y en la cara. Le dieron medicinas para que los ataques pararan. Muchos doctores la ayudaron para que se sintiera mejor. A veces, no pudieron hacer todas las pruebas porque faltaban cosas en el hospital. Pero todos cuidaron mucho de ella para que estuviera tranquila.",
+                "fh_score": 80.58
+            },
+            "B2": {
+                "text": "**Caso de una mujer con Síndrome de Sturge-Weber (SWS)**\n\nPresentamos la historia de una mujer de 39 años que llegó al hospital con problemas de salud graves. Al principio, tenía insuficiencia cardíaca causada por anemia, que es cuando hay pocas células rojas en la sangre. Por eso, le dieron transfusiones de sangre para mejorar su condición.\n\nDespués, comenzó a tener varias convulsiones, que son movimientos involuntarios del cuerpo causados por actividad anormal en el cerebro. También mostró irritabilidad, dificultad para hablar (afasia) y debilidad en el lado derecho del cuerpo (hemiplejía). Debido a esto, fue ingresada en la unidad de cuidados intensivos (UCI) para recibir atención especial.\n\nAl revisar su historia médica y hacer un examen más detallado, los médicos notaron una mancha roja en el ojo izquierdo llamada mancha de vino de Oporto. Esta mancha estaba presente desde su nacimiento, pero no se había detectado antes. Además, la paciente había tenido convulsiones hace 20 años, aunque no se había tratado formalmente.\n\nUna tomografía computarizada (una imagen del cerebro) mostró calcificaciones en una parte del cerebro llamada área parietal. Estos hallazgos ayudaron a confirmar que la paciente tenía Síndrome de Sturge-Weber (SWS), una enfermedad rara que afecta la piel, el cerebro y a veces los ojos.\n\nPara tratarla, un equipo de diferentes especialistas trabajó junto: neurólogos (que cuidan del cerebro), oftalmólogos (que cuidan los ojos), otorrinolaringólogos (que cuidan oídos y garganta) y fisioterapeutas (que ayudan con la movilidad). Las convulsiones se controlaron con medicamentos llamados fenitoína y carbamazepina, administrados por vía intravenosa y a través de un tubo en la nariz.\n\nSin embargo, debido a la falta de personal y recursos en el hospital, no se pudieron hacer otros estudios importantes para pacientes con SWS, como imágenes más detalladas del cerebro, evaluaciones psicológicas, consultas para cirugía plástica o neurocirugía, ni revisiones dentales.\n\nEste caso muestra la importancia de un diagnóstico cuidadoso y un tratamiento multidisciplinario para manejar enfermedades complejas como el Síndrome de Sturge-Weber.",
+                "fh_score": 49.19
+            },
+            "B3": {
+                "text": "**Contexto del Caso**  \nSe trata de una mujer refugiada de 39 años, embarazada, sin antecedentes de diabetes o hipertensión, que acudió al hospital con síntomas iniciales de insuficiencia cardíaca secundaria a anemia severa. Inicialmente recibió transfusiones sanguíneas para tratar esta condición. Sin embargo, durante su hospitalización, desarrolló múltiples convulsiones focales que se extendieron a ambos hemisferios cerebrales, acompañadas de irritabilidad intensa, dificultad para hablar (afasia) y parálisis parcial en el lado derecho del cuerpo (hemiplejía). Estos signos neurológicos graves motivaron su ingreso a la unidad de cuidados intensivos (UCI).\n\n**Hallazgos Clave**  \nUna revisión detallada de su historia clínica, junto con un examen físico repetido, reveló la presencia de una mancha de vino de Oporto (una lesión vascular congénita de color rojo púrpura) en la región ocular izquierda, que inicialmente no se había detectado. Además, se confirmó un antecedente remoto de convulsiones no provocadas ocurridas hace aproximadamente 20 años, que no había sido reportado inicialmente. La tomografía computarizada del cerebro mostró calcificaciones en la región parietal izquierda, hallazgo característico que, junto con la mancha cutánea y el cuadro clínico, permitió establecer el diagnóstico de síndrome de Sturge-Weber (SWS), una enfermedad neurocutánea rara que afecta vasos sanguíneos del cerebro y la piel.\n\n**Interpretación Clínica**  \nEl síndrome de Sturge-Weber se caracteriza por la presencia de malformaciones vasculares en la piel y el cerebro, que pueden provocar convulsiones, déficits neurológicos y problemas oftalmológicos. En este caso, la combinación de convulsiones recurrentes, hemiplejía, afasia y la mancha facial típica apoyaron el diagnóstico. La anemia y la insuficiencia cardíaca iniciales complicaron el cuadro clínico, pero el manejo neurológico fue prioritario tras la aparición de las convulsiones y el deterioro neurológico.\n\n**Estrategia de Tratamiento y Manejo Multidisciplinario**  \nSe implementó un enfoque integral que involucró a varios especialistas: neurología para el control de las convulsiones, oftalmología para evaluar posibles complicaciones oculares como el glaucoma (aunque la paciente estaba muy irritable y dificultó el examen), otorrinolaringología y fisioterapia para abordar las secuelas neurológicas. El control de las convulsiones se logró con éxito mediante la administración intravenosa de fenitoína durante tres días, seguida de un aumento progresivo de la dosis de carbamazepina oral hasta 1000 mg diarios, administrada a través de una sonda nasogástrica debido al estado de coma profundo de la paciente.\n\n**Limitaciones y Próximos Pasos**  \nDebido a limitaciones en recursos humanos y técnicos en el hospital, no fue posible realizar evaluaciones adicionales importantes para pacientes con SWS, como estudios avanzados de neuroimagen, evaluaciones psiquiátricas, consultas de cirugía plástica y neurocirugía, ni revisiones dentales, que suelen ser necesarias para un manejo completo de esta enfermedad. Se recomienda continuar con un seguimiento multidisciplinario para optimizar el tratamiento y mejorar la calidad de vida de la paciente.",
+                "fh_score": 25.67
+            }
+        }
+    },
+    {
+        "article": "Una paciente de 69 años se quejaba de una pérdida progresiva de la visión. Sus padres eran primos hermanos. Le habían diagnosticado retinitis pigmentosa 27 años antes. La paciente había fumado durante 15 años. Tenía antecedentes de hiperlipidemia e hipotiroidismo.\n\nTras una evaluación oftalmológica completa, se determinó que el paciente tenía una agudeza visual corregida (AVC) de contar los dedos a 5’ y 3’ en los ojos derecho e izquierdo, respectivamente. La retinoscopia mostró una refracción de –1.00 + 0.50×70 y –2.00 + 1.00×5 en los ojos derecho e izquierdo, respectivamente. El paciente tenía discos ópticos pálidos con una atrofia profunda extensa de la mácula central, hiperplasia del pigmento epitelial y otras áreas de atrofia multifocal en el ojo derecho. Además, el paciente tenía atrofia macular en el ojo izquierdo. En la imagen de autofluorescencia del fondo del ojo (FAF) del paciente, había evidencia de una hipoautofluorescencia central de la mácula, con una extensión centrífuga difusa desde su centro hasta su periferia.\n\nLa tomografía de coherencia óptica macular (OCT) determinó que el espesor macular promedio era de 191 µM y 193 µM en los ojos derecho e izquierdo, respectivamente. El volumen macular era de 6.9 mm3 y 7.0 mm3 en los ojos derecho e izquierdo, respectivamente. No se encontró edema macular, quistes o fluido subretinal en ninguno de los ojos.\n\nUna prueba de campo visual reveló que el paciente tenía desviaciones medias de –23.75 dB y –24.56 dB en los ojos derecho e izquierdo, respectivamente. Las desviaciones estándar de patrón fueron de +3.69 dB y +4.69 dB en los ojos derecho e izquierdo, respectivamente. Los resultados de un electrorretinograma de campo completo (ERG) mostraron una respuesta normal de bastones y una respuesta de conos disminuida, bilateralmente. Por estas razones, se realizó un diagnóstico clínico de enfermedad STGD1.\n\nSe encontró una variante patogénica homocigótica intrónica c.5714+5G>A del gen ABCA4 tras el análisis de secuenciación y eliminación/duplicación utilizando secuenciación de próxima generación (Invitae Corporation, San Francisco, California). Tenía seis variantes adicionales de significación incierta (VUS) en los genes CACNA1F, EYS, KCNV2, KLHL7, MKKS y USH2A.\n",
+        "gold_summary": "Una paciente de 69 años de edad se presentó en la clínica quejándose de una pérdida progresiva de la visión. La evaluación oftálmica fue notable para una mejor agudeza visual corregida de contar los dedos a 5' en el ojo derecho y 3' en el ojo izquierdo. Las imágenes revelaron una atrofia profunda y extensa de la mácula central, una hiperplasia del pigmento epitelial y otras áreas de atrofia multifocal en el ojo derecho. Además, las imágenes de autofluorescencia del fondo de la mácula mostraron una hipoautofluorescencia central con expansión bilateral a la periferia en ambos ojos. Un electrorretinograma de campo completo mostró una respuesta normal de los bastones, con una respuesta disminuida de los conos, bilateralmente. Las pruebas genéticas fueron positivas para una mutación inotrópica homocigótica en el gen ABCA4 de la variante c.5714+5G>A.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una señora de 69 años veía cada vez menos con sus ojos. El doctor le hizo muchas pruebas para mirar sus ojos. Vio que la parte del ojo que ayuda a ver bien estaba muy dañada. También encontró que algunas partes del ojo no funcionaban bien. El doctor hizo un examen especial y vio que unas células del ojo estaban normales y otras no. Luego, hicieron un examen de su sangre y encontraron un cambio en un gen que puede causar problemas en la vista.",
+                "fh_score": 88.63
+            },
+            "B2": {
+                "text": "**Lo que le pasaba a la paciente**  \nUna mujer de 69 años empezó a perder la vista poco a poco. Cuando la examinaron, pudo ver solo lo suficiente para contar los dedos a una distancia muy corta: 5 pies en un ojo y 3 pies en el otro. Esto muestra que su visión estaba bastante afectada.\n\n**Qué encontraron en sus ojos**  \nAl mirar dentro de sus ojos con imágenes especiales, los médicos vieron que la parte central de la retina llamada mácula estaba muy dañada. Había zonas donde las células que ayudan a la vista estaban muertas o muy débiles. También notaron un aumento anormal de unas células llamadas pigmento epitelial. Las imágenes que muestran la luz que emite la retina (autofluorescencia) indicaron que la parte central de la mácula tenía menos luz de lo normal, lo que significa daño, y este daño se extendía hacia los lados en ambos ojos.\n\n**Cómo funcionaban sus células de la vista**  \nSe hizo un examen llamado electrorretinograma, que mide la actividad eléctrica de las células de la retina. Los resultados mostraron que las células llamadas bastones, que ayudan a ver en la oscuridad, funcionaban bien. Pero las células llamadas conos, que permiten ver colores y detalles, estaban debilitadas en ambos ojos.\n\n**Qué encontraron en sus genes**  \nAl analizar su ADN, descubrieron que tenía una mutación específica en un gen llamado ABCA4. Este gen es importante para la salud de la retina. La mutación encontrada puede causar problemas en la función de las células de la retina y explicar la pérdida de visión de la paciente.\n\n**En resumen**  \nLa paciente tiene una enfermedad llamada STGD1, que afecta la mácula y causa pérdida progresiva de la visión. Los exámenes clínicos y genéticos ayudaron a confirmar este diagnóstico.",
+                "fh_score": 66.78
+            },
+            "B3": {
+                "text": "**Contexto**  \nUna mujer de 69 años acudió a consulta debido a una pérdida progresiva de la visión que había experimentado durante años. Su historia médica incluía un diagnóstico previo de retinitis pigmentosa desde hacía 27 años, antecedentes familiares de consanguinidad (sus padres eran primos hermanos), así como hiperlipidemia e hipotiroidismo. Además, había fumado durante 15 años.\n\n**Hallazgos Clave**  \nLa evaluación oftalmológica reveló una agudeza visual corregida muy reducida, con la paciente capaz solo de contar los dedos a 5 pies (aproximadamente 1.5 metros) con el ojo derecho y a 3 pies (menos de un metro) con el ojo izquierdo. La refracción mostró leves defectos de visión en ambos ojos. El examen del fondo de ojo evidenció una atrofia profunda y extensa de la mácula central (la zona responsable de la visión detallada), acompañada de hiperplasia (aumento) del pigmento epitelial y múltiples áreas de atrofia en el ojo derecho, mientras que el ojo izquierdo presentaba también atrofia macular. Las imágenes de autofluorescencia del fondo del ojo mostraron una zona central con baja autofluorescencia (hipoautofluorescencia), que se extendía desde el centro hacia la periferia en ambos ojos.\n\nLa tomografía de coherencia óptica (OCT), que permite visualizar las capas de la retina, indicó un grosor macular disminuido en ambos ojos, sin presencia de edema, quistes o líquido subretinal. Las pruebas de campo visual mostraron una pérdida significativa de sensibilidad en ambos ojos. El electrorretinograma (ERG), que mide la función de las células fotorreceptoras de la retina, evidenció una respuesta normal de los bastones (células responsables de la visión en condiciones de poca luz) pero una respuesta disminuida de los conos (células responsables de la visión en condiciones de luz y la percepción del color), de forma bilateral.\n\n**Interpretación Clínica**  \nCon base en estos hallazgos clínicos y funcionales, se estableció un diagnóstico de enfermedad de Stargardt tipo 1 (STGD1), una forma hereditaria de degeneración macular juvenil que afecta la visión central. El análisis genético confirmó la presencia de una mutación patogénica homocigótica (es decir, la misma alteración en ambas copias del gen) en el gen ABCA4, específicamente la variante intrónica c.5714+5G>A, conocida por estar asociada con esta enfermedad. Además, se identificaron seis variantes genéticas adicionales de significado incierto en otros genes relacionados con enfermedades retinianas, aunque su relevancia clínica no pudo ser determinada en este caso.\n\n**Próximos Pasos**  \nEl diagnóstico genético y clínico permite orientar el manejo y seguimiento de la paciente, que debe incluir controles oftalmológicos periódicos para evaluar la progresión de la enfermedad y la función visual. Aunque actualmente no existe una cura definitiva para la enfermedad de Stargardt, se pueden considerar opciones de apoyo visual y asesoramiento genético para la paciente y su familia. Asimismo, la identificación de la mutación específica puede facilitar la inclusión en estudios clínicos o terapias emergentes dirigidas a esta patología genética.",
+                "fh_score": 41.84
+            }
+        }
+    },
+    {
+        "article": "Un niño de 19 meses de edad fue admitido en el departamento de urgencias porque se cayó de la trona en la que comía. Esta caída ocurrió en un aparente bienestar, sin la presencia de signos o síntomas anticipados. Primero, se cayó sobre su glúteo y luego se golpeó la cabeza (occipucio) contra el suelo. Vomitó (tres episodios) y estaba muy irritable. Su frecuencia respiratoria y cardíaca eran >60 respiraciones y >150 latidos por minuto, mientras que la saturación de oxígeno era <80%. Tras el examen físico, el niño estaba hidratado y consciente, pero irritable. Más importante aún, observamos retracciones subcostal y, al auscultar, disminución de los sonidos respiratorios en la parte basal izquierda del tórax. El paciente fue ventilado con un balón de AMBU conectado a una fuente de oxígeno y monitorizado con un oxímetro de pulso. A pesar de nuestra intervención, la saturación de oxígeno cayó por debajo del 70% y cuanto más ventilábamos, más caía la saturación. La ecografía pulmonar mostró la ausencia de las típicas líneas A y la consolidación del pulmón, que se visualizó directamente como un parénquima sólido. Sobre la base del mal estado clínico, el paciente se sometió a intubación orotraqueal con un tubo endotraqueal con manguito. Después de que el bebé se estabilizó, se sometió a una tomografía computarizada (TC) de tórax que mostró una atelectasia completa del pulmón izquierdo con una interrupción del bronquio izquierdo principal a 12 cm de la bifurcación bronquial. Se sospechó un FBA ya que la madre también declaró que el bebé en los días anteriores había tenido un ataque de tos intenso y desapareció en 24 h sin ningún tratamiento. Por lo tanto, se realizó una broncoscopia rígida y se encontró y se eliminó rápidamente una almendra de 2 cm de diámetro en el bronquio izquierdo principal.\n\nEl paciente nunca había consumido antes almendras u otros frutos secos y, en esta ocasión, ingirió la almendra por accidente.\n\nEl bebé mostró una mejora clínica progresiva y, después de 24 horas, se le retiró la sonda y se le dio de alta de la unidad de cuidados intensivos para ser ingresado en la sala de pediatría general durante unos días, con una recuperación gradual y total de la función respiratoria.\n",
+        "gold_summary": "Describimos el caso de un niño de 19 meses que llegó a la sala de urgencias por un traumatismo en la cabeza. La evaluación clínica, sin embargo, reveló una dificultad respiratoria grave inexplicable que requería intubación traqueal. Después de nuestra evaluación, planteamos la hipótesis de que la dificultad respiratoria grave determinó un estado alterado de conciencia con el consiguiente traumatismo en la cabeza. Los hallazgos radiológicos levantaron la sospecha de aspiración de cuerpo extraño por la presencia de una atelectasia de todo el pulmón izquierdo. La tomografía computarizada mostró una interrupción abrupta del bronquio principal a 12 mm del casco. La siguiente broncoscopia identificó una amígdala de 2 cm.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un niño pequeño se cayó y se lastimó la cabeza. Pero lo más importante es que no podía respirar bien. Los doctores pusieron un tubo para ayudarlo a respirar. Vieron que un huesito en su pulmón estaba tapado. Buscaron y sacaron una almendra que estaba en su pulmón. Después, el niño mejoró y pudo respirar bien otra vez.",
+                "fh_score": 83.19
+            },
+            "B2": {
+                "text": "Caso de un niño con dificultad para respirar y caída en la cabeza\n\nUn niño de 19 meses llegó a urgencias después de caerse de la trona donde comía. Aunque parecía estar bien al principio, tenía problemas para respirar y vomitó varias veces. Su ritmo de respiración y corazón estaba muy rápido, y el nivel de oxígeno en su sangre era muy bajo. Al examinarlo, notaron que tenía dificultad para respirar y menos sonidos en el pulmón izquierdo.\n\nLo que encontraron\n\nUsaron una máquina para ayudarlo a respirar, pero el nivel de oxígeno seguía bajando. Una ecografía del pulmón mostró que una parte del pulmón estaba sólida, lo que no es normal. Luego, una tomografía (una imagen detallada del pecho) mostró que el pulmón izquierdo estaba colapsado y que el tubo principal que lleva aire a ese pulmón estaba bloqueado.\n\nQué significaba esto\n\nPensaron que algo estaba bloqueando la vía aérea, posiblemente un objeto que el niño había inhalado sin querer. La madre recordó que el niño había tenido una tos fuerte días antes. Al hacer una broncoscopia, que es cuando se usa un tubo con cámara para mirar dentro de los pulmones, encontraron y sacaron una almendra de 2 cm que estaba bloqueando el bronquio izquierdo.\n\nRecuperación\n\nEl niño nunca había comido almendras antes y la había tragado por accidente. Después de quitar la almendra, mejoró rápidamente. Lo mantuvieron en observación y finalmente se recuperó completamente de sus problemas para respirar.",
+                "fh_score": 64.63
+            },
+            "B3": {
+                "text": "**Contexto**  \nSe presenta el caso de un niño de 19 meses que fue llevado a urgencias tras una caída desde la trona mientras comía. Inicialmente, se pensó que el motivo principal era el traumatismo craneal provocado por la caída. Sin embargo, durante la evaluación clínica se detectó una dificultad respiratoria grave que no podía explicarse únicamente por el golpe.\n\n**Hallazgos Clave**  \nEl niño mostraba signos de insuficiencia respiratoria severa, con frecuencia respiratoria y cardíaca elevadas, saturación de oxígeno muy baja (menos del 80%) y dificultad para respirar evidenciada por retracciones subcostales y disminución de los sonidos respiratorios en la base del pulmón izquierdo. La saturación de oxígeno empeoraba incluso con ventilación asistida. La ecografía pulmonar reveló ausencia de las líneas A típicas y consolidación pulmonar, indicando que el tejido pulmonar estaba sólido en lugar de aireado. La tomografía computarizada (TC) de tórax mostró una atelectasia completa (colapso) del pulmón izquierdo y una interrupción abrupta del bronquio principal izquierdo a 12 mm de la bifurcación bronquial.\n\n**Interpretación Clínica**  \nEstos hallazgos sugirieron que la dificultad respiratoria grave fue la causa principal del estado alterado de conciencia y, por ende, del traumatismo craneal secundario a la caída. La interrupción del bronquio principal y la atelectasia indicaron la presencia de un cuerpo extraño que obstruía la vía aérea. La madre confirmó que el niño había tenido un episodio previo de tos intensa, lo que apoyó la sospecha de aspiración de un objeto. La broncoscopia rígida permitió identificar y extraer una almendra de 2 cm alojada en el bronquio izquierdo principal, que el niño había ingerido accidentalmente, siendo su primera exposición a frutos secos.\n\n**Próximos Pasos y Evolución**  \nTras la extracción del cuerpo extraño, el niño mostró una mejoría clínica progresiva. Se retiró la intubación después de 24 horas y fue trasladado de la unidad de cuidados intensivos a la sala de pediatría general, donde continuó su recuperación hasta la normalización completa de la función respiratoria. Este caso resalta la importancia de considerar la aspiración de cuerpos extraños en niños pequeños con dificultad respiratoria grave y síntomas atípicos, incluso cuando se presenta un traumatismo asociado.",
+                "fh_score": 45.57
+            }
+        }
+    },
+    {
+        "article": "Una mujer nulípara de 35 años con antecedentes de infertilidad se presentó en la consulta externa. Informó de un antecedente de tres años de dolor sordo cíclico en el ombligo. El dolor se asoció a un nódulo umbilical que sangraba durante la menstruación. Cabe destacar que el dolor empeoraba durante la menstruación y se aliviaba con analgésicos. La paciente también informó de dismenorrea, menorragia y dispareunia. La paciente se había insertado un DIU de cobre 3 años antes y había estado usando Zinnia P (levonorgestrel y etinilestradiol) durante los últimos 3-4 meses para intentar aliviar el dolor. Su historial ginecológico previo no fue notable y tenía un ciclo menstrual regular. No había antecedentes médicos, quirúrgicos o sociales de importancia.\nAl examinarla, sus constantes vitales eran estables. Se observó una hinchazón hiperpigmentada (3 × 2 cm) en el ombligo al examinar el abdomen. La hinchazón era firme, inmóvil, no dolorosa, no reductible y no estaba ligada a estructuras subyacentes. Una resonancia magnética abdominal reveló una masa de mejora mal definida que medía 3 × 4 × 6 cm ubicada a lo largo de la pared abdominal anterior derecha y estaba conectada a un tracto sinusal que se extendía hacia la región suprapúbica, pero no se comunicaba con la cavidad peritoneal, hallazgos que sugieren endometriosis. El diagnóstico diferencial fue amplio, incluida una hernia umbilical, granuloma, cicatriz queloide, neoplasias malignas nodulares y anomalías embriológicas. Además, se observaron lesiones anexiales bilaterales, eran hiperintensas con áreas hipointensas focales y restricciones variables, la lesión del lado derecho medía 1,6 × 1,7 cm y la lesión del lado izquierdo medía 2,0 × 0,8 cm, hallazgos consistentes con endometriosis ovárica bilateral.\n\nSe programó al paciente para la extirpación quirúrgica del nódulo umbilical. La muestra se envió para un examen histopatológico. Los resultados revelaron una epidermis normal con glándulas endometriales dispersas y estroma dentro de la dermis. La fotomicroscopía resaltó la presencia de estroma endometrial y tejido graso subcutáneo. Esta morfología es consistente con la endometriosis. La recuperación postoperatoria de la paciente fue sin incidentes, y se la consideró apta para el alta el día 2 postoperatorio. Recibió asesoramiento sobre su fertilidad futura y la posibilidad de FIV, riesgo de recurrencia y se programó una visita de seguimiento en dos semanas. Se le inició con Dienogest, Visanne y un anticonceptivo oral combinado para el tratamiento de la endometriosis. Se la ha monitoreado clínicamente cada cuatro semanas, y no se han observado síntomas o signos de recurrencia local durante el período de seguimiento de 8 meses. Cabe destacar que, a pesar de que su condición permaneció estable después del tratamiento, no concibió en el transcurso del año siguiente.\n",
+        "gold_summary": "Presentamos el caso de una mujer nulípara de 35 años de edad del norte de Tanzania con un historial de infertilidad de 10 años. Al presentarse, la paciente informó de un historial de tres años de dolor cíclico asociado a una masa umbilical. Una resonancia magnética abdominal reveló una masa mal definida que se intensificaba y medía 3 × 4 × 6 cm, localizada a lo largo de la pared abdominal anterior derecha. La masa estaba conectada a un tracto sinusal que se extendía hacia la región suprapúbica, pero no mostraba comunicación con la cavidad peritoneal, lo que sugería endometriosis. Además, las lesiones anexiales bilaterales demostraron señales hiperintensas con áreas hipointensas focales y restricciones variables, consistentes con endometriomas ováricos bilaterales. La paciente se sometió a la extirpación de la masa umbilical y el examen histopatológico confirmó el diagnóstico de endometriosis umbilical primaria. A pesar de su condición estable después del tratamiento, no concibió durante el año siguiente.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había una mujer que tenía dolor en su pancita cerca del ombligo. El dolor venía y se iba, y a veces el ombligo sangraba. Los doctores vieron que tenía un bultito en el ombligo. Le sacaron el bultito con una operación. Cuando miraron el bultito, encontraron que era un problema llamado endometriosis. Ella se sintió mejor después de la operación. Pero todavía no pudo tener un bebé.",
+                "fh_score": 79.76
+            },
+            "B2": {
+                "text": "**Caso de una mujer con dolor y un bulto en el ombligo**\n\nUna mujer de 35 años, que nunca ha tenido hijos y ha tenido problemas para quedar embarazada durante 10 años, acudió al médico porque tenía dolor en el ombligo desde hace tres años. Este dolor aparecía de forma cíclica, es decir, se repetía cada mes, y estaba relacionado con un bulto en esa zona.\n\n**Lo que encontraron en las pruebas**\n\nSe le hizo una resonancia magnética, que es un tipo de imagen que muestra el interior del cuerpo. Esta prueba mostró una masa o bulto de 3 × 4 × 6 centímetros en la pared del abdomen, cerca del ombligo. La masa estaba conectada a un pequeño canal que llegaba hacia la parte baja del abdomen, pero no estaba unida a la cavidad donde están los órganos internos. Esto hizo pensar que podría tratarse de endometriosis, que es cuando un tejido parecido al que recubre el interior del útero crece en otros lugares del cuerpo.\n\nAdemás, se encontraron lesiones en ambos ovarios que también parecían ser endometriomas, que son quistes causados por la endometriosis en los ovarios.\n\n**Qué hicieron y qué pasó después**\n\nLa mujer se sometió a una cirugía para quitar el bulto del ombligo. El tejido extraído se analizó bajo el microscopio y confirmó que era endometriosis en el ombligo, algo poco común. Después de la operación, la paciente se recuperó bien y comenzó un tratamiento con medicamentos para controlar la endometriosis.\n\nDurante los siguientes ocho meses, no tuvo nuevos síntomas ni signos de que la enfermedad regresara. Sin embargo, aunque su salud mejoró, no logró quedar embarazada en el año siguiente.\n\nEste caso muestra cómo la endometriosis puede afectar diferentes partes del cuerpo y la importancia de un diagnóstico y tratamiento adecuados para mejorar la calidad de vida y la fertilidad.",
+                "fh_score": 62.2
+            },
+            "B3": {
+                "text": "**Contexto**  \nSe presenta el caso de una mujer de 35 años, sin hijos y con un historial de infertilidad de una década, que acudió a consulta por un dolor cíclico y persistente en el ombligo durante tres años. Este dolor se asociaba a la presencia de un nódulo umbilical que sangraba coincidiendo con su menstruación. Además, refería síntomas ginecológicos como dolor menstrual intenso (dismenorrea), sangrado menstrual abundante (menorragia) y dolor durante las relaciones sexuales (dispareunia). La paciente había utilizado un dispositivo intrauterino (DIU) de cobre desde hacía tres años y recientemente había iniciado tratamiento hormonal combinado para aliviar el dolor.\n\n**Hallazgos Clave**  \nEl examen físico reveló una masa firme, hiperpigmentada, inmóvil y no dolorosa en el ombligo, sin conexión palpable con estructuras internas. La resonancia magnética mostró una masa mal definida de 3 × 4 × 6 cm en la pared abdominal anterior derecha, conectada a un tracto sinusal que se extendía hacia la región suprapúbica, pero sin comunicación con la cavidad peritoneal, lo que orientó hacia un diagnóstico de endometriosis umbilical primaria. Además, se identificaron lesiones en ambos ovarios con características compatibles con endometriomas (quistes ováricos formados por tejido endometrial), confirmando la afectación bilateral.\n\n**Interpretación Clínica**  \nEl diagnóstico diferencial incluyó diversas condiciones como hernia umbilical, granuloma, cicatriz queloide, tumores malignos y anomalías congénitas, pero la combinación de síntomas, hallazgos de imagen y la confirmación histopatológica establecieron la endometriosis umbilical primaria. La biopsia del nódulo extirpado mostró tejido endometrial (glándulas y estroma) dentro de la dermis, confirmando la presencia de endometriosis fuera del útero. Este tipo de endometriosis es poco frecuente y puede causar dolor cíclico y sangrado en la piel del ombligo.\n\n**Próximos Pasos y Seguimiento**  \nTras la cirugía, la paciente tuvo una recuperación sin complicaciones y fue dada de alta al segundo día postoperatorio. Se le indicó tratamiento hormonal con dienogest y anticonceptivos orales combinados para controlar la endometriosis y reducir el riesgo de recurrencia. Se le brindó asesoramiento sobre su fertilidad futura, incluyendo la posibilidad de recurrir a técnicas de reproducción asistida como la fertilización in vitro (FIV). Durante un seguimiento clínico de ocho meses no se observaron signos de recurrencia local, aunque la paciente no logró concebir en el año posterior al tratamiento.\n\nEste caso destaca la importancia de considerar la endometriosis umbilical en mujeres con dolor cíclico y nódulos en el ombligo, especialmente en el contexto de infertilidad, y subraya la necesidad de un manejo multidisciplinario para optimizar el control de los síntomas y la fertilidad.",
+                "fh_score": 35.26
+            }
+        }
+    },
+    {
+        "article": "Presentamos a un recién nacido de 15 minutos de edad, hijo de una madre para-cuatro que no recordaba su LNMP pero que afirmaba haber estado amenorreica durante los últimos nueve meses. Su madre había recibido atención prenatal en el centro de salud cercano dos veces y no había tenido incidentes. Sin embargo, no se le había realizado un ultrasonido obstétrico temprano. Por lo demás, no tiene antecedentes de enfermedades crónicas como diabetes mellitus e hipertensión. Durante su embarazo actual, no tuvo fiebre, dolor de cabeza o visión borrosa. Nunca había usado ninguna droga aparte de sulfato ferroso durante este embarazo. Sus hijos anteriores están todos sanos y vivos. A su llegada a nuestro hospital, tuvo una hemorragia vaginal de dos horas de duración. Posteriormente, fue admitida con un diagnóstico de embarazo de tercer trimestre más multigravida más hemorragia anteparto secundaria a desprendimiento de placenta más oligohidramnios severo más presentación de nalgas.\n\nEn el examen pélvico, tenía un sangrado vaginal activo. Se le realizó una ecografía obstétrica al llegar. En consecuencia, la edad gestacional era de 34 semanas, la placenta estaba en el fondo con un coágulo retroplacentario y el líquido amniótico había disminuido significativamente con un único bolsillo más profundo de 1,5 cm. El peso fetal estimado era de 2,4 kg y presentación de nalgas. Otras investigaciones de la madre son grupo sanguíneo AB+, VDRL=negativo, RBS=120 mg/dL, en CBC, glóbulos blancos=9000, hemoglobina=11 gm/dL, plaqueta=180,000 y neutrófilo=60%.\n\nTras obtener el consentimiento informado por escrito, se realizó una cesárea de urgencia por las indicaciones ya mencionadas para extraer un neonato vivo de 2,01 kg de peso con puntuaciones de 5 y 6 en las pruebas de Apgar en el primer y el quinto minuto, respectivamente.\n\nEl neonato no lloró y fue reanimado durante cinco minutos. Luego fue trasladado a la unidad de cuidados intensivos neonatales para recibir atención e investigaciones adicionales. Al llegar, el neonato estaba en dificultad respiratoria. Sus signos vitales eran de 160 latidos por minuto, 70 respiraciones por minuto, temperatura de 33,4 grados centígrados y saturación de oxígeno del 60%. La fontanela anterior del neonato medía 2 cm por 2 cm y tenía micrognatia y cuello corto. En el sistema respiratorio, había retracciones intercostales y subcostales, respiración trabajosa y gruñidos. En el examen precordial, se escucharon bien los sonidos s1 y s2, no había murmullo ni ritmo de galope. En el sistema musculoesquelético, había acortamiento bilateral de las extremidades superiores, la extremidad inferior derecha estaba normal en posición y estructura, la pierna izquierda giraba hacia adentro (flexión mediolateral) en la articulación de la rodilla y la estructura del pie era normal. En el examen neurológico, estaba letárgico, el tono era normotónico en la extremidad inferior derecha y el reflejo de Moro era difícil de evaluar. La investigación de laboratorio mostró grupo sanguíneo = A+, CRP = reactivo, WBC = 30,000, neutrófilos = 54%, linfocitos = 21.1%, HGB = 8 gm/dL y plaquetas = 150,000. Se realizó una radiografía que mostró un acortamiento extremo de las extremidades superiores. La extremidad inferior izquierda estaba internamente girada. La ecocardiografía fue normal. Con una evaluación de prematuro tardío (34-36 semanas por puntaje de Ballard) más bajo peso al nacer más apropiado para la edad gestacional más focomelia más asfixia perinatal más sepsis neonatal temprana, se manejó con apoyo de oxígeno, fluido de mantenimiento e antibióticos intravenosos. El neonato murió después de tres días de hospitalización.\n",
+        "gold_summary": "Presentamos a un neonato de 15 minutos de vida, hijo de una madre para-cuatro que no recordaba su LNMP pero que afirmaba estar amenorreica desde hacía nueve meses. El modo de parto fue por cesárea para extraer al neonato vivo, que pesaba 2,01 kg y tenía puntuaciones APGAR de 5 y 6 en el primer y quinto minutos, respectivamente. El neonato no lloró y fue reanimado durante cinco minutos. Después se lo trasladó a la unidad de cuidados intensivos neonatales para continuar con el tratamiento y las investigaciones. Sus signos vitales eran: pulso de 160 latidos por minuto, frecuencia respiratoria de 70 respiraciones por minuto, temperatura de 33,4 grados centígrados y saturación de oxígeno del 60%. La fontanela anterior del neonato medía 2 cm por 2 cm y tenía micrognatia y cuello corto. En el sistema respiratorio había retracciones intercostales y subcostales, respiración trabajosa y gruñidos. En el sistema musculoesquelético había acortamiento bilateral de la extremidad superior, la pierna derecha tenía una posición y estructura normales, la pierna izquierda giraba hacia adentro (se doblaba hacia la parte media) en la articulación de la rodilla y el pie tenía una estructura normal.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un bebé nació hace muy poquito tiempo. Su mamá tuvo que ir al hospital para que lo sacaran con una operación especial. El bebé pesaba poquito y no pudo llorar al nacer. Los doctores lo ayudaron a respirar y lo llevaron a un lugar para cuidarlo mucho.\n\nEl bebé respiraba rápido y su corazón latía rápido también. Tenía frío y le faltaba un poco de aire. Su cabeza tenía una parte blanda y su cuello era cortito. Sus brazos eran más cortos de lo normal. Una pierna estaba normal, pero la otra estaba doblada hacia adentro. Sus pies estaban bien. Los doctores lo cuidaron mucho para que se sintiera mejor.",
+                "fh_score": 83.73
+            },
+            "B2": {
+                "text": "**Lo que pasó con el bebé al nacer**  \nUn bebé nació por cesárea después de que su mamá tuvo problemas en el embarazo. El bebé pesó 2,01 kg y sus primeras pruebas para saber cómo estaba (llamadas puntuaciones Apgar) fueron 5 y 6, lo que indica que necesitó ayuda para respirar. De hecho, el bebé no lloró al nacer y tuvo que ser reanimado durante cinco minutos para ayudarlo a respirar mejor.\n\n**Estado del bebé en la unidad de cuidados intensivos**  \nDespués de nacer, el bebé fue llevado a una unidad especial para recién nacidos que necesitan cuidados extra. Allí, los médicos notaron que su corazón latía rápido (160 latidos por minuto) y respiraba muy rápido (70 respiraciones por minuto). Además, tenía la temperatura baja (33,4 grados Celsius) y poca cantidad de oxígeno en la sangre (60%). La parte blanda en la cabeza del bebé (llamada fontanela anterior) medía 2 cm por 2 cm. También tenía micrognatia, que significa que la mandíbula era más pequeña de lo normal, y un cuello corto.\n\n**Problemas en la respiración y los huesos**  \nEl bebé tenía dificultad para respirar, con movimientos fuertes entre las costillas y sonidos de gruñidos al respirar. En cuanto a sus brazos, ambos eran más cortos de lo normal. La pierna derecha estaba normal, pero la pierna izquierda estaba doblada hacia adentro en la rodilla, aunque el pie tenía una forma normal.\n\n**Qué significa todo esto**  \nEstos signos muestran que el bebé tenía problemas para respirar y algunas malformaciones en sus extremidades. Estas condiciones pueden ser causadas por complicaciones durante el embarazo o problemas en el desarrollo del bebé. Los médicos le dieron oxígeno y otros tratamientos para ayudarlo, pero lamentablemente el bebé murió después de tres días en el hospital.",
+                "fh_score": 65.49
+            },
+            "B3": {
+                "text": "**Contexto**  \nSe presentó un recién nacido de apenas 15 minutos de vida, hijo de una mujer con antecedentes obstétricos de cuatro partos previos (para-cuatro). La madre no recordaba la fecha de su última menstruación, pero aseguró haber estado sin menstruar durante nueve meses, lo que indicaba un embarazo avanzado. Durante el embarazo, la madre recibió atención prenatal limitada y no se realizó una ecografía temprana. Al momento del ingreso hospitalario, la madre presentaba hemorragia vaginal prolongada, diagnóstico de desprendimiento prematuro de placenta, oligohidramnios severo (disminución del líquido amniótico) y presentación fetal de nalgas.\n\n**Hallazgos Clave del Neonato**  \nEl bebé nació mediante cesárea de urgencia con un peso de 2,01 kg y puntuaciones de Apgar de 5 y 6 al primer y quinto minuto, respectivamente, lo que indica una adaptación inicial comprometida. No lloró al nacer y requirió reanimación durante cinco minutos. Fue trasladado a la unidad de cuidados intensivos neonatales debido a dificultad respiratoria grave, con signos vitales alterados: frecuencia cardíaca elevada (160 latidos por minuto), respiración rápida (70 respiraciones por minuto), temperatura corporal baja (33,4 °C) y saturación de oxígeno muy baja (60%).\n\nEn el examen físico, se observaron características faciales anómalas como micrognatia (mandíbula inferior pequeña) y cuello corto. En el sistema respiratorio, el neonato presentaba retracciones intercostales y subcostales (movimientos visibles de los músculos entre las costillas y debajo de ellas al respirar), respiración dificultosa y sonidos respiratorios anormales (gruñidos). En el sistema musculoesquelético, había un acortamiento marcado de ambas extremidades superiores (brazo y antebrazo), mientras que la pierna derecha tenía una estructura y posición normales. La pierna izquierda estaba girada hacia adentro en la articulación de la rodilla (flexión mediolateral), aunque el pie mantenía una estructura normal.\n\nLos estudios complementarios revelaron una elevación significativa de los glóbulos blancos (30,000), indicando posible infección, con una proteína C reactiva positiva (marcador de inflamación), anemia moderada (hemoglobina de 8 g/dL) y plaquetas dentro de rango normal. La radiografía confirmó el acortamiento extremo de las extremidades superiores y la rotación interna de la pierna izquierda. La ecocardiografía fue normal, descartando malformaciones cardíacas.\n\n**Interpretación Clínica**  \nEl diagnóstico principal incluyó un neonato prematuro tardío (34 semanas de gestación), con bajo peso al nacer pero adecuado para su edad gestacional, que presentaba focomelia (una malformación congénita caracterizada por extremidades muy cortas o ausentes), asfixia perinatal (falta de oxígeno al nacer) y sepsis neonatal temprana (infección grave en los primeros días de vida). Estas condiciones explican la dificultad respiratoria, el compromiso hemodinámico y las anomalías físicas observadas.\n\n**Próximos Pasos y Evolución**  \nEl manejo incluyó soporte respiratorio con oxígeno, administración de líquidos por vía intravenosa y tratamiento antibiótico para la infección. A pesar de estas intervenciones, el neonato falleció a los tres días de hospitalización debido a la gravedad de sus condiciones clínicas y malformaciones congénitas asociadas. Este caso resalta la importancia de un control prenatal adecuado, diagnóstico temprano y manejo multidisciplinario para mejorar el pronóstico en embarazos complicados y neonatos con malformaciones severas.",
+                "fh_score": 32.26
+            }
+        }
+    },
+    {
+        "article": "Mujer de 61 años con antecedente de carcinoma escamocelular de cuello uterino estadio FIGO IIB, diagnosticado en febrero de 2019, tratada en un hospital privado de cuarto nivel de atención, donde se ofrece cuidado ambulatorio y hospitalario para pacientes con condiciones complejas oncológicas y no oncológicas. Al momento del diagnóstico se realizó histerectomía radical con linfadenectomía pélvica, que descartó compromiso nodal. El tratamiento complementario de primera línea incluyó seis ciclos de quimioterapia con cisplatino, y braquiterapia y radioterapia, alcanzando una respuesta tumoral completa. En 2021, tras detectarse una recaída aislada en la región ilíaca, mediante tomografía, se administró cisplatino y 30 sesiones de radioterapia, logrando una nueva respuesta completa. En septiembre de 2022, una tomografía reveló otra recaída con compromiso del parametrio izquierdo, el uréter y la cadena ilíaca ipsilateral, por lo que se decidió primera línea para enfermedad recurrente con carboplatino, paclitaxel y pembrolizumab. Durante este régimen, la paciente presentó hipersensibilidad al platino en el quinto ciclo, gestionada con un protocolo de desensibilización, continuando con el pembrolizumab. En septiembre de 2023, ante la progresión en imágenes de una masa retroperitoneal única, debido a la falta de respuesta óptima, se inició gemcitabina, según guías de manejo, segunda línea de enfermedad recurrente, recibiendo una dosis acumulada de 8.544 mg/m2 hasta enero de 2024. Sin embargo, desarrolló síntomas de isquemia digital en manos, por lo que el tratamiento fue suspendido tras la segunda dosis del tercer ciclo, acumulando 11.744 mg/m2 de gemcitabina.\n\nEn febrero de 2024, la paciente ingresó al servicio de urgencias del mismo hospital donde era valorada de forma ambulatoria, remitida por oncología debido a progresión de los síntomas en sus extremidades. La paciente refería dolor lancinante y coloración azulada en dedos de manos; al examen físico se evidencia necrosis en el segundo dedo de la mano derecha, coloración ocre y fenómeno de Raynaud en los dedos de la mano izquierda. Las extremidades inferiores mostraban edema grado II en el miembro inferior izquierdo y pulsos presentes. Los estudios para autoinmunidad y vasculitis resultaron negativos, incluyendo anticuerpos anticitoplasma de neutrófilos (ANCAS), anticuerpos antinucleares (ANAS), anticuerpos antidesoxirribonucleicos (anti-DNA), cardiolipinas, prueba confirmatoria de anticoagulante lúpico, perfil de anticuerpos contra antígenos nucleares extraíbles (ENAS), anticuerpos contra proteinasa 3, anticuerpos antimieloperoxidasa y anticuerpos dirigidos contra la ADN topoisomerasa I (antiSCL). Además, el factor reumatoide y los niveles de complemento 3 (C3) y complemento 4 (C4) también fueron normales. Prueba serológica para sífilis (VDRL - Venereal Disease Research Laboratory) negativa, ecocardiograma transtorácico sin hallazgos de un foco cardioembólico.\n\nSe inició anticoagulación con heparina de bajo peso molecular, junto con ácido acetilsalicílico, estatina y un calcioantagonista. El equipo de cirugía de mano realizó amputación del segundo dedo de la mano derecha, confirmando necrosis por licuefacción en el estudio histopatológico.\n\nDurante el posoperatorio se agregó sildenafil al tratamiento, logrando una mejoría progresiva en los signos de isquemia de los dedos restantes. Durante la hospitalización, la paciente presenta complicación por sangrado vaginal masivo, requiriendo embolización de arterias uterinas.\n\nEl servicio de reumatología aplicó la escala de causalidad de Naranjo para determinar el papel de la gemcitabina en la vasculitis, con un puntaje de 8, lo que indicó que el medicamento probablemente provocó la necrosis.\n\nPosteriormente, a los 20 días de ingreso a hospitalización desarrolló deterioro neurológico, sin hallazgos significativos en la tomografía de cráneo. Evaluada por cuidados paliativos, su estado funcional se clasificó con un Barthel de 0/30, ECOG de 4 y Karnofsky de 10 %, con pronóstico de vida inferior a tres semanas según el Índice Pronóstico de Paciente (PPI: + 6 puntos). En consenso con la familia, se suspendieron estudios adicionales y se implementó un manejo paliativo integral. La paciente falleció tras el alta hospitalaria.",
+        "gold_summary": "Oaciente de 61 años tratada con gemcitabina (11.744 mg/m² acumulados) por enfermedad metastásica, en un hospital general de cuarto nivel, privado, no oncológico, donde venía siendo manejada de forma ambulatoria. Presentó necrosis distal del segundo dedo de la mano derecha, por lo que se suspendió el tratamiento y se requirió amputación de este dedo. Se realizó una búsqueda en Embase, Medline y Lilacs. Se buscaron estudios de reporte y series de casos sobre necrosis distal inducida por gemcitabina. Se extrajeron datos de dosis, diagnóstico y tratamiento.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una señora de 61 años estaba muy enferma y recibió medicina para el cáncer. Esta medicina le hizo daño en un dedo de su mano derecha. El dedo se puso muy mal y tuvieron que cortarlo para que no le doliera más. Los doctores buscaron información para entender mejor este problema y cómo ayudar.",
+                "fh_score": 76.4
+            },
+            "B2": {
+                "text": "**Caso de una Mujer con Cáncer y Problemas en las Manos**\n\nUna mujer de 61 años estaba recibiendo un medicamento llamado gemcitabina para tratar su cáncer que se había extendido. Este medicamento se usó en un hospital privado que atiende casos complejos. Después de recibir una dosis acumulada bastante alta (11.744 mg/m²), comenzó a tener problemas graves en su mano derecha. El segundo dedo se puso negro y murió (necrosis), lo que hizo necesario suspender el medicamento y amputar ese dedo.\n\n**Búsqueda de Información sobre el Problema**\n\nLos médicos buscaron en varias bases de datos científicas (Embase, Medline y Lilacs) para encontrar otros casos similares donde la gemcitabina causara necrosis en los dedos. Revisaron estudios y reportes para entender mejor las dosis usadas, cómo se diagnosticó el problema y qué tratamientos se aplicaron.\n\n**Qué Significa Esto**\n\nEste caso muestra que, aunque la gemcitabina es útil para tratar ciertos tipos de cáncer, puede causar efectos secundarios graves en las manos, como la muerte de tejido en los dedos. Por eso, los médicos deben vigilar muy bien a los pacientes que reciben este medicamento para detectar cualquier señal temprana de daño y actuar rápido para evitar complicaciones mayores.",
+                "fh_score": 56.52
+            },
+            "B3": {
+                "text": "Resumen detallado para público no médico universitario\n\nContexto  \nSe trata de una mujer de 61 años con un historial complejo de cáncer de cuello uterino (carcinoma escamocelular), inicialmente diagnosticado en 2019 y tratado con cirugía, quimioterapia y radioterapia, logrando respuestas completas. Sin embargo, presentó varias recaídas localizadas y regionales entre 2021 y 2023, que requirieron diferentes líneas de tratamiento con quimioterapia y terapia inmunológica. En 2023, ante la progresión tumoral, se inició gemcitabina como segunda línea de tratamiento para la enfermedad recurrente.\n\nHallazgos clave  \nDurante el tratamiento con gemcitabina, acumuló una dosis total de 11.744 mg/m², pero desarrolló síntomas de isquemia digital, es decir, falta de flujo sanguíneo en los dedos de las manos, que se manifestó con dolor intenso, coloración azulada y necrosis (muerte del tejido) en el segundo dedo de la mano derecha. Esto llevó a la suspensión inmediata del medicamento y a la amputación quirúrgica de dicho dedo, confirmándose la necrosis mediante análisis histopatológico (examen microscópico del tejido).\n\nSe descartaron otras causas comunes de daño vascular o inflamación de los vasos sanguíneos (vasculitis) mediante pruebas serológicas y de autoinmunidad, todas negativas. Tampoco se encontraron problemas cardíacos que pudieran explicar la formación de coágulos o embolias. El equipo médico inició tratamiento con anticoagulantes, antiinflamatorios, vasodilatadores y medicamentos para mejorar la circulación, logrando cierta mejoría en los dedos restantes.\n\nInterpretación clínica  \nEl análisis de causalidad mediante la escala de Naranjo, una herramienta que ayuda a determinar si un medicamento es responsable de un efecto adverso, indicó que la gemcitabina fue probablemente la causa de la necrosis digital. Este efecto adverso es poco frecuente pero grave, y se relaciona con daño vascular inducido por el fármaco.\n\nPróximos pasos y evolución  \nPosteriormente, la paciente presentó complicaciones adicionales, incluyendo un sangrado vaginal masivo que requirió embolización (procedimiento para detener el sangrado) y un deterioro neurológico sin causa clara en estudios de imagen. Su estado general empeoró significativamente, con pérdida total de autonomía y un pronóstico de vida inferior a tres semanas. En consenso con la familia, se decidió suspender estudios invasivos y se implementó un manejo paliativo integral para mejorar su calidad de vida en el tiempo restante. Finalmente, la paciente falleció tras el alta hospitalaria.\n\nResumen de la revisión bibliográfica  \nSe realizó una búsqueda en bases de datos médicas (Embase, Medline y Lilacs) para identificar reportes y series de casos sobre necrosis distal inducida por gemcitabina, recopilando información sobre dosis, diagnóstico y manejo de esta complicación, con el fin de contextualizar y comparar el caso presentado.\n\nEste caso resalta la importancia de la vigilancia estrecha de efectos adversos vasculares graves en pacientes tratados con gemcitabina, especialmente en contextos de enfermedad avanzada y tratamientos prolongados.",
+                "fh_score": 33.44
+            }
+        }
+    },
+    {
+        "article": "Mujer de 53 años, con antecedente de AR de 15 años de diagnóstico en tratamiento con metotrexato, resto de antecedentes sin datos de importancia, la cual presentó cuadro clínico 8 meses antes (de acudir a nuestro servicio) con astenia y adinamia de forma progresiva, palidez de tegumentos, alzas térmicas no cuantificadas de predominio nocturno, pérdida de peso no intencionada de 15 kg en 6 meses aproximadamente, sin valoración ni seguimiento médico, a lo que se agregó 3 meses después disnea de grandes a medianos esfuerzos, y cuya sintomatología se agudizó 5 días antes (de acudir a nuestro servicio), aunada a sangrado de tubo digestivo alto (STDA), caracterizado por evacuaciones melénicas abundantes, 3 evacuaciones en 24 horas, hematemesis en 2 ocasiones, escasas, sin causa aparente. La paciente negó consumo de analgésicos no esteroideos (AINE) y tuvo aumento de volumen en la pierna izquierda, la cual le dolía y tenía la presencia de edema y eritema, con limitación a la movilidad, motivo por el cual acudió a (nuestro) Servicio de Urgencias.\n\nDurante su hospitalización con anemia severa sin repercusión hemodinámica, se transfundieron 3 concentrados eritrocitarios sin complicaciones aparentes. Después de su estabilización, se inició abordaje diagnóstico para síndrome consuntivo. Por el cuadro clínico de miembro inferior izquierdo se hizo US Doppler que evidenció trombosis venosa profunda. Se realizó ultrasonido de abdomen por probable hepatopatía por metotrexato, el cual reportó infartos esplénicos y hepáticos, así como presencia de cambios crónicos hepáticos. Se llevó a cabo endoscopía con evidencia de varices pequeñas, sin sangrado activo. Debido a la sospecha de neoplasia por los antecedentes y el cuadro clínico de la paciente, se llevó a cabo tomografía axial simple y contrastada de tórax y abdomen y se encontró hepatoesplenomegalia y múltiples conglomerados ganglionares axilares, mediastinales y paraaórticos que sugerían actividad infiltrativa. Esto se valoró por el Servicio de Cirugía General para la realización de biopsia de ganglio axilar derecho, donde se reportó proliferación neoplásica de células linfoides. Posteriormente se valoró por el Servicio de Hematología de la unidad, se solicitaron estudios de laboratorio (cuadro I) y se realizó aspirado de médula ósea en el que se evidenciaron células plasmáticas displásicas y células reticulares, por lo cual se concluyó que había la presencia de infiltración linfoplasmocitaria. Con los antecedentes, el cuadro clínico y los estudios complementarios se diagnosticó LNH estadio IV y la paciente fue enviada a hospital de tercer nivel para realización de inmunohistoquímica, estadificación e inicio de tratamiento. En tercer nivel se identificó linfoma difuso de células B con inmunofenotipo B CD20 con sobrecrecimiento de células dendríticas, y la paciente fue valorada para inicio de tratamiento con quimioterapia.",
+        "gold_summary": "Mujer de 55 años con antecedente de AR que ingresó a un servicio de medicina interna por sangrado de tubo digestivo; presentó datos clínicos de trombosis venosa profunda en miembro pélvico izquierdo y síndrome consuntivo en estudio. Durante su abordaje se identificó con infartos esplénicos y hepáticos, así como múltiples conglomerados ganglionares, por lo que se practicó biopsia de ganglio axilar que reportó proliferación neoplásica de células linfoides y aspirado de médula ósea con presencia de infiltración linfoplasmocitaria, con lo que se determinó diagnóstico de linfoma no Hodgkin estadio IV. La paciente fue enviada a un hospital de tercer nivel para inicio de tratamiento.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había una señora que se sentía muy cansada y tenía dolor en una pierna. También tenía sangre en su pancita. Los doctores le hicieron muchas pruebas. Encontraron que tenía unos bultitos en su cuerpo que no estaban bien. Le hicieron una prueba en un lugar con bultitos y otra en su hueso. Vieron que tenía un tipo de enfermedad llamada linfoma. La señora fue a un hospital especial para que la cuiden y le den medicina para mejorar.",
+                "fh_score": 85.47
+            },
+            "B2": {
+                "text": "**Lo que le pasó a la paciente**  \nUna mujer de 53 años, que tenía artritis reumatoide (una enfermedad que afecta las articulaciones), llegó al hospital porque estaba sangrando por el tubo digestivo (el camino que va desde la boca hasta el estómago y los intestinos). Además, tenía dolor y hinchazón en la pierna izquierda, y estaba muy cansada y pálida. También había perdido mucho peso sin querer.\n\n**Lo que encontraron en los exámenes**  \nLos médicos descubrieron que tenía una trombosis venosa profunda, que es un coágulo de sangre en una vena grande de la pierna. También encontraron daños en el bazo y el hígado, llamados infartos, que son áreas donde no llegó suficiente sangre. Al hacer una tomografía (una imagen especial del cuerpo), vieron que sus ganglios linfáticos (pequeñas glándulas que ayudan a combatir infecciones) estaban muy grandes y agrupados en varias partes del cuerpo.\n\nPara entender mejor qué pasaba, le hicieron una biopsia, que es cuando se toma un pequeño pedazo de tejido para analizarlo. La biopsia del ganglio linfático mostró que había un crecimiento anormal de células llamadas linfocitos, que son parte del sistema inmunológico. También examinaron su médula ósea (donde se producen las células de la sangre) y encontraron células anormales que indicaban que el problema estaba afectando varias partes del cuerpo.\n\n**Qué significa el diagnóstico**  \nCon toda esta información, los médicos diagnosticaron un linfoma no Hodgkin en estadio IV. El linfoma no Hodgkin es un tipo de cáncer que afecta a los linfocitos. El estadio IV significa que el cáncer está avanzado y se ha extendido a varias áreas del cuerpo.\n\n**Próximos pasos**  \nLa paciente fue enviada a un hospital especializado para hacer más estudios y comenzar un tratamiento con quimioterapia, que es un tipo de medicina para combatir el cáncer.",
+                "fh_score": 59.22
+            },
+            "B3": {
+                "text": "**Contexto**  \nSe trata de una mujer de 53 años con diagnóstico previo de artritis reumatoide (AR) desde hace 15 años, en tratamiento con metotrexato. Ocho meses antes de su ingreso al hospital, comenzó a presentar síntomas progresivos como fatiga intensa (astenia), debilidad generalizada (adinamia), palidez en la piel, fiebre nocturna no cuantificada y una pérdida de peso no intencionada de aproximadamente 15 kg en seis meses. Tres meses después, desarrolló dificultad para respirar al realizar esfuerzos moderados. Cinco días antes de su ingreso, su condición empeoró con sangrado digestivo alto, manifestado por evacuaciones negras abundantes (melena) y vómitos con sangre (hematemesis), sin causa aparente. Además, presentó aumento de volumen, dolor, enrojecimiento y limitación de movimiento en la pierna izquierda, signos compatibles con trombosis venosa profunda (coágulo en una vena profunda).\n\n**Hallazgos Clave**  \nDurante la hospitalización, se confirmó anemia severa que requirió transfusión de glóbulos rojos. Un ultrasonido Doppler de la pierna izquierda confirmó la presencia de trombosis venosa profunda. El ultrasonido abdominal mostró infartos (áreas de tejido muerto por falta de riego sanguíneo) en el bazo y el hígado, junto con cambios hepáticos crónicos probablemente relacionados con el uso de metotrexato. La endoscopía digestiva evidenció varices pequeñas sin sangrado activo. La tomografía computarizada (TAC) de tórax y abdomen reveló agrandamiento del hígado y bazo (hepatoesplenomegalia) y múltiples conglomerados de ganglios linfáticos en axilas, mediastino y alrededor de la aorta, lo que sugirió una posible infiltración tumoral.  \n\nLa biopsia de un ganglio axilar derecho mostró proliferación anormal de células linfoides (células del sistema inmunitario). El aspirado de médula ósea evidenció infiltración por células plasmáticas anormales y células reticulares, confirmando la afectación linfoplasmocitaria. Estos hallazgos permitieron establecer el diagnóstico de linfoma no Hodgkin (LNH) en estadio IV, que indica una enfermedad avanzada con compromiso de múltiples órganos y tejidos.\n\n**Interpretación Clínica**  \nEl cuadro clínico y los estudios realizados indican que la paciente presenta un linfoma no Hodgkin difuso de células B, un tipo de cáncer que afecta a las células del sistema inmunitario. La enfermedad se encuentra en una etapa avanzada y ha provocado complicaciones como trombosis venosa profunda, infartos en órganos abdominales y sangrado digestivo. La asociación con su antecedente de artritis reumatoide y el tratamiento con metotrexato puede haber influido en la evolución y presentación clínica.\n\n**Próximos Pasos**  \nLa paciente fue referida a un hospital de tercer nivel para realizar estudios adicionales de inmunohistoquímica (técnicas que permiten caracterizar con precisión el tipo de células tumorales), completar la estadificación de la enfermedad y comenzar el tratamiento específico con quimioterapia. El manejo multidisciplinario es fundamental para optimizar el pronóstico y controlar tanto la enfermedad linfoproliferativa como las complicaciones asociadas.",
+                "fh_score": 33.38
+            }
+        }
+    },
+    {
+        "article": "Un hombre de 56 años se presentó en el departamento de urgencias de nuestro hospital debido a una falta de aire repentina y un episodio de síncope mientras caminaba dentro de su casa. Se sometió a una prostatectomía laparoscópica asistida por robot para el carcinoma de próstata, 5 días antes de su presentación en el departamento de urgencias. Su curso postoperatorio en el hospital fue sin incidentes. En el departamento de urgencias, su presión arterial era de 94/54 mmHg, frecuencia cardiaca de 121 latidos por minuto, frecuencia respiratoria de 20 respiraciones por minuto, no tenía fiebre y su saturación de oxígeno era de 92% con 6 L por minuto de oxígeno a través de una cánula nasal. El examen cardiaco reveló S1S2, regular, taquicardia, sin murmullos/galopes/ruidos respiratorios. El examen respiratorio reveló ruidos respiratorios vesiculares normales bilaterales. Se observó que tenía edema de extremidad inferior izquierdo asimétrico. El electrocardiograma (ECG) reveló taquicardia sinusal, sin cambios en la onda ST-T. La troponina estaba levemente elevada a 0.120 ng/mL (rango de referencia: 0 a 0.020). La angiografía por tomografía computarizada (CTA) del tórax mostró embolia pulmonar bilateral extensa, con una gran carga de coágulos en ambas arterias pulmonares principales, evidencia de insuficiencia ventricular derecha aguda. El examen dúplex venoso mostró trombosis venosa profunda izquierda aguda. El ecocardiograma mostró fracción de eyección ventricular izquierda normal del 60% al 65%, movimiento septal anormal y aplanamiento del tabique interventricular, presión sistólica ventricular derecha de 49.7 mmHg, ventrículo derecho moderadamente dilatado, función ventricular derecha disminuida, excursión sistólica tricuspídea de 12.1 mm (normal 15 a 20 mm). Como la mayoría de la carga de coágulos era distal, no se consideró susceptible de extracción quirúrgica, ya que la cirugía reciente era una contraindicación importante para la trombólisis. El paciente comenzó con un goteo de heparina e inhaló óxido nítrico a 20 ppm junto con 40 mg de sildenafil oral cada 8 horas. Al día siguiente, el paciente estaba hemodinámicamente estable y su óxido nítrico inhalado se redujo. Repetir el ecocardiograma 48 horas desde la presentación inicial mostró un tamaño y función del ventrículo derecho mejorados. Su presión sistólica ventricular derecha disminuyó a 22.4 mmHg y su excursión sistólica tricuspídea mejoró a 17.8 mm. Recomendamos que continuara con sildenafil durante el mes siguiente después del alta junto con anticoagulación oral con un plan de seguimiento como paciente ambulatorio. El paciente dio su consentimiento por escrito para el tratamiento durante su hospitalización. El paciente y sus familiares estaban bien informados sobre el plan de atención completo y estuvieron de acuerdo con el plan de atención.\n\nMH - Insuficiencia cardiaca/*terapia farmacológica/etiología\nMH - Humanos\nMH - Hombre\nMH - Edad Media\nMH - Inhibidores de la fosfodiesterasa 5/*uso terapéutico\nMH - Embolismo pulmonar/*complicaciones\nMH - Agentes vasodilatadores/*uso terapéutico\nMH - Disfunción ventricular, derecha/terapia/etiología\n",
+        "gold_summary": "Paciente: Hombre, 56 años\n\nDiagnóstico final: Insuficiencia cardíaca derecha por embolia pulmonar\n\nSíntomas: síncope\n\nMedicación: —\n\nProcedimiento clínico: —\n\nEspecialidad: Cardiología\n\nSe trata de un informe de caso en el que se utilizó sildenafil como agente de rescate para lograr una mejora en el tamaño y la función del ventrículo derecho en un caso de inicio agudo de embolia pulmonar masiva con insuficiencia aguda del ventrículo derecho en el escenario en el que la terapia trombolítica sistémica estaba contraindicada.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un hombre de 56 años se sintió muy cansado y se desmayó. Tenía problemas para respirar. Esto pasó porque tenía unos tapones en sus pulmones. Estos tapones hicieron que su corazón derecho se pusiera muy cansado. Los doctores no le pudieron dar una medicina fuerte para quitar los tapones porque él había tenido una operación hace poco. Entonces, le dieron otra medicina llamada sildenafil. Esta medicina ayudó a que su corazón mejorara y se hiciera más fuerte. Después de un tiempo, el hombre se sintió mejor y su corazón trabajó mejor. Los doctores cuidaron mucho de él y le explicaron todo a él y a su familia.",
+                "fh_score": 75.83
+            },
+            "B2": {
+                "text": "**Lo que le pasó al paciente**  \nUn hombre de 56 años tuvo problemas para respirar de repente y se desmayó mientras caminaba en su casa. Cinco días antes, había tenido una cirugía para tratar un cáncer de próstata. Después de la cirugía, parecía estar bien, pero luego presentó estos síntomas.\n\n**Qué encontraron los médicos**  \nEn el hospital, su presión arterial estaba baja y su corazón latía muy rápido. Tenía hinchazón en una pierna, lo que puede indicar un coágulo de sangre. Un examen especial llamado tomografía mostró que tenía coágulos grandes en las arterias de los pulmones, lo que se llama embolia pulmonar. Estos coágulos estaban afectando el lado derecho del corazón, que se encargaba de enviar sangre a los pulmones. También confirmaron que había un coágulo en la pierna.\n\n**Cómo lo trataron**  \nNo pudieron hacer una cirugía para quitar los coágulos porque la cirugía reciente del paciente era un riesgo. En lugar de eso, le dieron un medicamento llamado heparina para evitar que se formen más coágulos. Además, usaron óxido nítrico inhalado y un medicamento llamado sildenafil, que ayuda a relajar los vasos sanguíneos y mejora la función del corazón derecho.\n\n**Qué pasó después**  \nDespués de un día, el paciente estaba más estable. Dos días después, los exámenes mostraron que el corazón derecho había mejorado en tamaño y función. La presión en el corazón derecho bajó y su capacidad para bombear sangre mejoró. Los médicos recomendaron que siguiera tomando sildenafil y medicamentos para evitar coágulos durante un mes después de salir del hospital.\n\n**Por qué es importante este caso**  \nEste caso muestra que el sildenafil puede ayudar a mejorar la función del corazón derecho en personas con embolia pulmonar grave cuando no se puede usar la cirugía o medicamentos para disolver coágulos. Es una opción útil para tratar problemas del corazón causados por coágulos en los pulmones.",
+                "fh_score": 65.05
+            },
+            "B3": {
+                "text": "**Contexto**\n\nUn hombre de 56 años fue atendido en urgencias tras presentar una dificultad respiratoria súbita y un episodio de desmayo mientras caminaba en su casa. Cinco días antes, había sido sometido a una prostatectomía laparoscópica asistida por robot para tratar un cáncer de próstata, y su recuperación inicial había sido sin complicaciones. Al llegar al hospital, mostraba signos de inestabilidad hemodinámica, con presión arterial baja y frecuencia cardíaca elevada. Además, se detectó hinchazón en su pierna izquierda.\n\n**Hallazgos Clave**\n\n- El electrocardiograma mostró taquicardia sinusal sin alteraciones isquémicas.\n- La troponina, un marcador de daño cardíaco, estaba ligeramente elevada.\n- La tomografía computarizada del tórax reveló una embolia pulmonar bilateral extensa, es decir, coágulos grandes en ambas arterias pulmonares principales, causando insuficiencia aguda del ventrículo derecho (la cámara del corazón que bombea sangre hacia los pulmones).\n- Un estudio de ultrasonido vascular confirmó la presencia de un coágulo en la vena profunda de la pierna izquierda (trombosis venosa profunda).\n- El ecocardiograma evidenció que el ventrículo izquierdo funcionaba normalmente, pero el ventrículo derecho estaba dilatado y con función reducida, con signos de presión elevada en esta cavidad.\n\n**Interpretación Clínica**\n\nEl paciente presentaba insuficiencia cardíaca derecha aguda secundaria a una embolia pulmonar masiva. Debido a que la mayoría de los coágulos estaban en áreas distales y que la cirugía reciente representaba una contraindicación para tratamientos trombolíticos (medicamentos que disuelven coágulos), no se consideró adecuada la extracción quirúrgica ni la trombólisis sistémica.\n\nEn este contexto, se inició tratamiento con heparina para anticoagulación, óxido nítrico inhalado para mejorar la oxigenación y sildenafil oral (un inhibidor de la fosfodiesterasa tipo 5, que actúa como vasodilatador pulmonar) para reducir la presión en el ventrículo derecho y mejorar su función.\n\n**Evolución y Próximos Pasos**\n\nAl día siguiente, el paciente mostró estabilidad hemodinámica y mejoría en la función del ventrículo derecho, confirmada mediante ecocardiografía realizada 48 horas después del ingreso. La presión en el ventrículo derecho disminuyó significativamente y la capacidad de contracción mejoró.\n\nSe recomendó continuar con sildenafil durante un mes tras el alta hospitalaria, junto con anticoagulación oral, y realizar seguimiento ambulatorio para monitorear su recuperación. El paciente y su familia fueron informados detalladamente y dieron su consentimiento para el plan terapéutico.\n\n**Resumen**\n\nEste caso ilustra el uso exitoso de sildenafil como tratamiento complementario para mejorar la función del ventrículo derecho en un paciente con embolia pulmonar masiva y disfunción ventricular derecha aguda, en un escenario donde la trombólisis estaba contraindicada debido a una cirugía reciente. El manejo combinado permitió la estabilización clínica y la recuperación funcional sin necesidad de intervenciones quirúrgicas o trombolíticas.",
+                "fh_score": 30.71
+            }
+        }
+    },
+    {
+        "article": "Presentamos el caso de un hombre de 78 años con antecedentes conocidos de fibrilación auricular crónica, cardiopatía hipertensiva y miocardiopatía no isquémica. Tenía una reducción global de la fracción de eyección del ventrículo izquierdo del 40-45 %, y su ecocardiograma no mostraba anomalías significativas. El paciente había sido seguido en la clínica de cardiología ambulatoria, donde fue tratado por insuficiencia cardiaca crónica en estadio C del Colegio Americano de Cardiología (ACC) con síntomas de clase III de la Asociación del Corazón de Nueva York (NYHA). A pesar de varios cambios en sus diuréticos e intentos de controlar su estado de líquidos, ganó 40 libras de peso en un período de 3 meses, con un aumento significativo de la falta de aire. A medida que su descompensación de la insuficiencia cardiaca progresó, fue hospitalizado durante 8 días y tratado con furosemida intravenosa (IV). Debido a su clasificación de la NYHA y su ingreso al hospital por exacerbación de la insuficiencia cardiaca, se indicó y se realizó un monitoreo hemodinámico invasivo con implantación de CardioMEMS. La implantación de su CardioMEMS se realizó en Grand Blanc, Michigan, a una altitud de 837 pies con una presión atmosférica de 731.2 el 9 de abril de 2019. Las mediciones hemodinámicas iniciales del cateterismo cardiaco mostraron una presión sistólica PA de 45 mmHg, presión diastólica PA de 16 mmHg y una presión PA media de 30 mmHg. La presión auricular derecha fue de 21 mmHg, presión ventricular derecha de 44/17 mmHg y la presión media de la cuña pulmonar fue de 24 mmHg. El procedimiento se completó sin complicaciones y el paciente fue dado de alta el mismo día.\n\nTras la implantación de CardioMEMS, el paciente permaneció estable durante 4 semanas sin empeoramiento de los síntomas de insuficiencia cardiaca. Cumplió con las lecturas diarias de CardioMEMS con una PA media que osciló entre 27 y 31 mmHg, y una presión diastólica de PA de 17 a 21 mmHg. Estos hallazgos hemodinámicos globales fueron estables en comparación con los del momento de la implantación.\n\nEl paciente viajó a Denver, Colorado, durante cuatro días a una altitud de 5280 pies con una presión atmosférica de 596.8 atm el 5 de mayo de 2019. Las grabaciones del primer día de su visita mostraron un aumento de la presión sistólica de 44 mmHg a 73 mmHg, un aumento de la presión media de 30 mmHg a 53 mmHg y un aumento de la presión diastólica de 20 mmHg a 40 mmHg. Al mismo tiempo, notó un aumento significativo de la falta de aire y la hinchazón de las extremidades inferiores. No buscó atención médica, sino que se contactó con su cardiólogo primario en Michigan. Su oxígeno nasal de referencia se incrementó de 1 litro a 2 litros y su dosis de furosemida se duplicó de 40 mg diarios a dos veces al día. Afortunadamente, este tratamiento mejoró los síntomas del paciente y evitó la admisión hospitalaria. Debido a que se evitó la admisión hospitalaria, no se dispuso de valores de laboratorio, imágenes de diagnóstico y signos vitales clínicos.\n\nDurante su estancia hospitalaria de 4 días, sus presiones invasivas se mantuvieron altas, pero disminuyeron lentamente y se estabilizaron con una PA sistólica de 72 mmHg, una PA media de 49 mmHg y una PA diastólica de 35 mmHg el día previo a su regreso a Michigan. El quinto día, volvió a Michigan y sus mediciones de presión invasiva se normalizaron rápidamente, con una presión PA media de 29 mmHg y una presión PA diastólica de 20 mmHg. Ha seguido estando bien mientras estuvo en Michigan con diuréticos de mantenimiento continuos y un control diario de las presiones PA con su dispositivo CardioMEMS.\n\nMH - Envejecido\nMH - *Altitud\nMH - Monitoreo de presión arterial, ambulatorio\nMH - *Insuficiencia cardiaca/diagnóstico/etiología\nMH - Hospitalización\nMH - Humanos\nMH - Hombre\nMH - Arteria Pulmonar\n",
+        "gold_summary": "Presentamos el caso de un hombre de 78 años con una exacerbación de la insuficiencia cardiaca mientras viajaba a gran altitud. Se detectó un aumento de sus presiones arteriales pulmonares (PA) mediante su dispositivo CardioMEMS implantado. La comprensión del cambio esperado en los registros de presión de la PA ayudó a identificar una verdadera exacerbación de la insuficiencia cardiaca en nuestro paciente. Esto llevó a un cambio rápido en la terapia médica, que en última instancia evitó la hospitalización.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había un hombre de 78 años que tenía problemas en su corazón. Él usaba un aparato especial para medir la presión en su corazón. Cuando viajó a un lugar muy alto, su corazón trabajó más fuerte y se sintió mal. El aparato mostró que su corazón estaba con mucha presión. Los doctores cambiaron sus medicinas rápido. Así, él no tuvo que ir al hospital y se mejoró.",
+                "fh_score": 86.2
+            },
+            "B2": {
+                "text": "**Lo que pasó con el paciente**  \nUn hombre de 78 años tenía problemas graves del corazón llamados insuficiencia cardiaca, que significa que su corazón no bombeaba la sangre tan bien como debería. Para ayudar a controlar su enfermedad, le pusieron un dispositivo llamado CardioMEMS, que mide la presión en una arteria del pulmón. Esto ayuda a los doctores a saber cómo está funcionando su corazón sin que él tenga que ir al hospital.\n\n**Qué sucedió durante su viaje**  \nEl paciente viajó a una ciudad alta llamada Denver, que está a mucha altura sobre el nivel del mar. Allí, las mediciones del CardioMEMS mostraron que la presión en su arteria pulmonar subió mucho. Esto fue un problema porque también empezó a sentir más dificultad para respirar y sus piernas se hincharon. Estas señales indicaron que su insuficiencia cardiaca empeoró.\n\n**Cómo ayudaron los doctores**  \nAunque no fue al hospital, el paciente llamó a su cardiólogo, quien le cambió el tratamiento aumentando la cantidad de un medicamento llamado diurético, que ayuda a eliminar el exceso de líquido del cuerpo. Gracias a este cambio rápido, sus síntomas mejoraron y evitó tener que ser hospitalizado.\n\n**Qué aprendimos de este caso**  \nEste caso muestra que el dispositivo CardioMEMS es muy útil para detectar cambios importantes en la presión del corazón, especialmente cuando una persona viaja a lugares con altitudes altas. Saber cómo cambian las presiones en estas situaciones ayuda a los médicos a actuar rápido y evitar complicaciones graves.",
+                "fh_score": 60.11
+            },
+            "B3": {
+                "text": "**Contexto**\n\nSe describe el caso de un hombre de 78 años con antecedentes de fibrilación auricular crónica, cardiopatía hipertensiva y miocardiopatía no isquémica, que presentaba insuficiencia cardiaca crónica en estadio C (según el Colegio Americano de Cardiología) con síntomas moderados a severos (clase III de la Asociación del Corazón de Nueva York). A pesar del tratamiento ambulatorio, experimentó un aumento significativo de peso y empeoramiento de la falta de aire, lo que llevó a una hospitalización y al implante de un dispositivo CardioMEMS para monitoreo invasivo de las presiones en la arteria pulmonar.\n\n**Hallazgos Clave**\n\nTras la implantación del CardioMEMS, el paciente mostró presiones pulmonares estables durante cuatro semanas en su entorno habitual en Michigan (a una altitud de 837 pies). Sin embargo, durante un viaje de cuatro días a Denver, Colorado (a 5280 pies de altitud), se registró un aumento marcado y sostenido de las presiones sistólica, media y diastólica en la arteria pulmonar. Paralelamente, el paciente experimentó un empeoramiento de sus síntomas de insuficiencia cardiaca, como aumento de la falta de aire y edema (hinchazón) en las extremidades inferiores.\n\n**Interpretación Clínica**\n\nEl aumento de las presiones pulmonares detectado por el CardioMEMS durante la estancia en altitud elevada reflejó una verdadera exacerbación de la insuficiencia cardiaca, más allá del efecto esperado por el cambio de altitud. Este monitoreo permitió diferenciar entre las variaciones fisiológicas normales y un deterioro clínico significativo. La rápida comunicación con el equipo médico facilitó la intensificación del tratamiento, incluyendo el aumento de la dosis de diuréticos y oxígeno suplementario, lo que mejoró los síntomas y evitó la necesidad de hospitalización.\n\n**Próximos Pasos**\n\nEl paciente continuó con un seguimiento estrecho mediante el dispositivo CardioMEMS tras su regreso a Michigan, donde las presiones pulmonares se normalizaron rápidamente. Se mantuvo con tratamiento diurético de mantenimiento y control diario de las presiones arteriales pulmonares para prevenir futuras descompensaciones. Este caso resalta la utilidad del monitoreo hemodinámico invasivo en pacientes con insuficiencia cardiaca, especialmente en situaciones que pueden alterar la fisiología cardiovascular, como los viajes a gran altitud.",
+                "fh_score": 30.65
+            }
+        }
+    },
+    {
+        "article": "Un hombre de 55 años, previamente sano, fue derivado al servicio de urgencias por su médico de cabecera, quejándose de una fiebre de 3 semanas de evolución, tos productiva, disnea y sibilancias. Tenía un historial de 80 paquetes-año de consumo de tabaco y un historial familiar positivo de cáncer de pulmón. Había sido tratado por su médico de cabecera con un ciclo de amoxicilina oral y prednisona oral, pero sus síntomas empeoraron. Cuando llegó al servicio de urgencias, su recuento de glóbulos blancos era de 16,4 × 109/L (rango normal: 4,0-10,0 × 109/L), el recuento de neutrófilos de 13,8 × 109/L (rango normal: 2,0-7,0 × 109/L), la proteína C reactiva era de 118 mg/L (normal: 0-5 mg/L) y el sodio sérico era de 112 mmol/L (rango normal: 136-145 mmol/L). Otros marcadores bioquímicos estaban dentro de los límites normales. Una radiografía de tórax mostró consolidación del lóbulo medio e inferior derecho con derrame pleural moderado asociado. Fue admitido y tratado como neumonía adquirida en la comunidad y el estudio confirmó el diagnóstico de SIADH.\n\nEl paciente empeoró a pesar de la administración intravenosa de piperacilina-tazobactam y de claritromicina oral, con empeoramiento de la consolidación en la repetición de la radiografía de tórax. El paciente fue trasladado a la unidad de cuidados intensivos y, posteriormente, se le realizó una intubación y ventilación. Una tomografía computarizada (TC) de su tórax reveló una masa hilar derecha con afectación mediastinal y adenopatía hilar derecha con consolidación de espacio aéreo extenso superpuesta. Una biopsia realizada durante la broncoscopia reveló células pequeñas, histológicamente monótonas, con núcleos ovoides oscuros. No se observaron nucleolos, y varias figuras mitóticas estaban presentes. Las células tienen un citoplasma estrecho y mal definido. La inmunohistoquímica realizada en las células tumorales mostró negatividad a CD45, AE1/AE3, positividad a TTF1. También se observaron sinapsina mínima focal y positividad a cromogranina A. Este perfil inmunohistoquímico fue consistente con un diagnóstico de cáncer de pulmón de células pequeñas.\n\nLa estadificación completa, que consistió en una tomografía computarizada del cerebro y tórax-abdomen-pelvis, confirmó una enfermedad en estadio extenso con metástasis suprarrenales. El estado funcional ECOG de la paciente era deficiente debido a una combinación de SCLC y dificultad respiratoria que requería ventilación artificial. Como las tasas de respuesta con quimioterapia en SCLC son generalmente altas, se inició un tratamiento quimioterápico doble en forma de carboplatino y etopósido mientras la paciente estaba intubada en la UCI.\n\nEl paciente respondió bien al tratamiento y fue extubado y trasladado a la sala de ventilación no invasiva. Una nueva tomografía computarizada de tórax después de 1 ciclo mostró una buena respuesta parcial al tratamiento.\n\nEn el día 3 del ciclo 2 de quimioterapia, la paciente desarrolló dolor en la parte inferior de la espalda y debilidad bilateral en las extremidades inferiores. El examen identificó paresia motora bilateral en las extremidades inferiores (grado 3 del Consejo de Investigación Médica [MRC]) y paresia sensorial. El examen sensorial reveló ausencia de tacto ligero, pinchazo, coordinación y propiocepción en las extremidades inferiores. El día 3 de etopósido se retrasó como resultado de los nuevos hallazgos neurológicos.\n\nSe realizaron un TAC cerebral, resonancia magnética (RM) cerebral y resonancia magnética (RM) de la columna para investigar los nuevos hallazgos neurológicos. Todos los resultados radiológicos fueron normales, sin evidencia de metástasis intracerebrales, accidente cerebrovascular, mielitis o enfermedad leptomeníngea. Además, no hubo evidencia radiográfica obvia de compresión de la médula espinal, ya sea por compresión extrínseca por depósito metastásico óseo o depósitos intramedulares o leptomeníngeos.\n\nDos días después, un examen neurológico de seguimiento reveló tetraplejía, MRC grado 0 en las extremidades superiores e inferiores. Todos los reflejos tendinosos profundos estaban ausentes. Los músculos de la cabeza y el cuello, la cognición y el habla no se vieron afectados, y el examen de los nervios craneales fue normal.\n\nLos análisis de sangre de rutina, incluida la proteína C reactiva y la velocidad de sedimentación de eritrocitos, fueron normales. Los análisis de sangre específicos, incluidos los de vitamina B12 en suero, folato, serología del VIH, serología de la enfermedad de Lyme, serología del virus de Epstein-Barr, serología de Brucella, anticuerpos tiroideos, pruebas de función tiroidea, ANCA, ENA, ANA y electroforesis de proteínas séricas, fueron negativos o normales. Se enviaron anticuerpos para las pruebas de sangre Hu, Ri y Yo, y todos fueron negativos. En este momento, se sospechó un diagnóstico de polineuropatía simétrica ascendente aguda motora y sensorial y se realizó una punción lumbar. Los resultados del líquido cefalorraquídeo (LCR) revelaron una proteína total elevada de 3.32 g/L (normal 0.15–0.45), y otros parámetros fueron normales, con una repetición 3 días después que mostró resultados similares. La citología del LCR fue negativa para la malignidad y el cultivo del LCR también fue negativo.\n\nLa electromiografía fue consistente con una polineuropatía difusa predominantemente motora; los potenciales sensoriales se conservaron, pero fueron de pequeña amplitud. Las conducciones motoras mostraron características axonales/desmielinizantes mixtas, que no eran típicas del síndrome de Guillain-Barré.\n\nSe realizaron estudios de electromiografía y conducción nerviosa para investigar la polineuropatía motora y sensorial aguda del paciente. Los estudios de conducción nerviosa revelaron lo siguiente:\n\n•Nervios motores:\n◦Las amplitudes del potencial de acción muscular compuesto (CMAP) se redujeron notablemente en los nervios tibial y cubital de forma bilateral (tibial: 1,2 mV; normal > 4 mV; cubital: 0,8 mV; normal > 3 mV).\n◦Las velocidades de conducción motora (MCV) se desaceleraron en los nervios tibial y cubital (tibial: 30 m/s; normal > 40 m/s; cubital: 34 m/s; normal > 50 m/s), lo que es coherente con la desmielinización.\n◦Las latencias motoras distales se prolongaron, con un patrón mixto axonal y desmielinizante.\n•Nervios sensoriales:\n◦Las amplitudes del potencial de acción nerviosa sensorial (SNAP) se conservaron, pero fueron de poca amplitud en los nervios surales y medianos (sural: 4 μV; normal > 10 μV; mediano: 6 μV; normal > 15 μV).\n◦Las velocidades de conducción sensorial (VCS) se encontraban dentro de los límites normales.\nLos hallazgos electrofisiológicos revelaron una polineuropatía predominantemente motora con características axonales y desmielinizantes mixtas, atípicas para los síndromes paraneoplásicos clásicos, que generalmente son predominantemente sensoriales y se caracterizan por la ausencia de SNAP.\n\nMientras tanto, mientras estas investigaciones estaban en curso, se inició al paciente con dexametasona intravenosa y 0.4 g/kg/día de inmunoglobulina intravenosa sin ninguna mejora sintomática.\n\n3. Resultados y seguimiento\nA pesar de una importante respuesta oncológica inicial a la quimioterapia, el estado neurológico del paciente se deterioró rápidamente. Después de 1 ciclo de carboplatino y etopósido, las imágenes confirmaron una respuesta parcial con una reducción en el tamaño del tumor. Sin embargo, el inicio de una polineuropatía motora y sensorial grave y ascendente condujo a un compromiso respiratorio. Esta disociación entre las respuestas oncológicas y neurológicas destaca la naturaleza agresiva y refractaria del SNP, incluso cuando el tratamiento del cáncer es efectivo. Aunque la dexametasona intravenosa y la inmunoglobulina intravenosa se administraron rápidamente, no lograron mejorar los resultados neurológicos.\n\nSe llevaron a cabo largas y repetidas discusiones multidisciplinares con el paciente y su familia sobre la admisión en la unidad de cuidados intensivos para recibir apoyo ventilatorio. El paciente estaba bien informado y consciente de que era poco probable que sus síntomas neurológicos fueran reversibles y, por lo tanto, optó por el mejor tratamiento de apoyo. El paciente falleció 3 semanas después de los síntomas iniciales. La decisión del paciente de rechazar el apoyo ventilatorio invasivo en favor de los cuidados paliativos pone de relieve las consideraciones éticas que rodean la calidad de vida en los síndromes paraneoplásicos de progresión rápida.\n",
+        "gold_summary": "Preocupaciones del paciente: Un hombre de 55 años con un historial de 80 años fumando presenta al hospital con un historial de 3 semanas de fiebres, tos productiva, disnea y sibilancias. No tenía comorbilidades significativas.\n\nDiagnóstico: Extensas investigaciones radiológicas revelaron una gran masa en el hilum derecho que comprimía el bronquio inferior derecho con depósitos suprarrenales metastásicos. Las investigaciones bioquímicas confirmaron el síndrome de secreción inadecuada de la hormona antidiurética, y la histología identificó un CPCP.\n\nIntervenciones: A pesar de iniciar una quimioterapia combinada con carboplatino y etopósido, el paciente desarrolló parálisis motora progresiva y pérdida sensorial en el transcurso de 4 días, lo que derivó en un diagnóstico de polineuropatía motora y sensorial aguda paraneoplásica.\n\nResultados: Su estado empeoró rápidamente y falleció 14 días después de la aparición de los síntomas debido a una insuficiencia respiratoria, lo que pone de relieve la agresividad de los síndromes paraneoplásicos.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había un hombre que estaba muy enfermo. Tenía tos, fiebre y le costaba respirar. \n\nLos doctores encontraron un bulto grande en su pulmón. También tenía un problema en otras partes de su cuerpo. \n\nLe dieron medicinas para el cáncer, pero empezó a perder fuerza en sus piernas y brazos. No podía sentir bien ni moverlos. \n\nMuy rápido, se puso muy mal y no pudo respirar bien. Después de unos días, se fue al cielo. \n\nLos doctores dijeron que su enfermedad fue muy fuerte y difícil de curar.",
+                "fh_score": 92.84
+            },
+            "B2": {
+                "text": "**Lo que le pasó al paciente**  \nUn hombre de 55 años que había fumado mucho durante muchos años llegó al hospital con fiebre, tos con flema, dificultad para respirar y silbidos al respirar. Estos síntomas habían durado tres semanas. Antes de esto, estaba sano y no tenía otras enfermedades importantes.\n\n**Qué encontraron los médicos**  \nLas pruebas de imagen mostraron una masa grande en una parte del pulmón derecho que estaba bloqueando una vía respiratoria importante. También encontraron que el cáncer se había extendido a las glándulas suprarrenales, que están encima de los riñones. Un análisis de sangre mostró que tenía un problema llamado síndrome de secreción inadecuada de hormona antidiurética, que afecta el equilibrio de líquidos en el cuerpo. Al analizar una muestra del tumor, confirmaron que tenía un tipo de cáncer de pulmón llamado cáncer de pulmón de células pequeñas (CPCP).\n\n**Tratamiento y complicaciones**  \nEl paciente comenzó a recibir quimioterapia con dos medicamentos, carboplatino y etopósido, que son comunes para tratar este tipo de cáncer. Sin embargo, en pocos días, empezó a perder fuerza en las piernas y luego en los brazos, además de perder sensibilidad. Los médicos diagnosticaron una polineuropatía motora y sensorial aguda paraneoplásica, que es una enfermedad nerviosa grave relacionada con el cáncer, donde los nervios dejan de funcionar correctamente.\n\n**Qué pasó al final**  \nA pesar de que el tratamiento contra el cáncer estaba funcionando y el tumor había disminuido de tamaño, la enfermedad nerviosa empeoró rápidamente. El paciente tuvo problemas para respirar y falleció dos semanas después de que aparecieron los síntomas nerviosos. Este caso muestra lo agresivos y difíciles de tratar que pueden ser los síndromes paraneoplásicos, que son enfermedades causadas por la reacción del cuerpo al cáncer.",
+                "fh_score": 54.84
+            },
+            "B3": {
+                "text": "**Contexto**  \nUn hombre de 55 años, con un historial muy extenso de tabaquismo (equivalente a 80 paquetes-año) y sin enfermedades previas relevantes, acudió al hospital tras presentar durante tres semanas fiebre persistente, tos con expectoración, dificultad para respirar y sibilancias. Inicialmente fue tratado con antibióticos y corticoides, pero sus síntomas empeoraron, lo que motivó su ingreso hospitalario.\n\n**Hallazgos Clave**  \nLas pruebas radiológicas, incluyendo radiografía y tomografía computarizada (TC) de tórax, revelaron una masa grande en la región del hilio derecho del pulmón, que comprimía el bronquio inferior derecho, además de metástasis en las glándulas suprarrenales. Los análisis de sangre mostraron un síndrome de secreción inadecuada de hormona antidiurética (SIADH), que explica un nivel muy bajo de sodio en sangre. La biopsia pulmonar confirmó el diagnóstico de cáncer de pulmón de células pequeñas (CPCP), un tipo agresivo de tumor pulmonar.\n\n**Interpretación Clínica**  \nA pesar de iniciar un tratamiento estándar con quimioterapia combinada de carboplatino y etopósido, el paciente desarrolló rápidamente una polineuropatía aguda, es decir, un daño progresivo en múltiples nervios que afectó tanto la función motora (movimiento) como sensorial (sensaciones). En pocos días, presentó debilidad grave en las extremidades inferiores que progresó a parálisis completa de brazos y piernas, acompañada de pérdida sensorial. Las pruebas de imágenes cerebrales y de la médula espinal no mostraron metástasis ni compresión nerviosa, y los análisis de líquido cefalorraquídeo descartaron infección o infiltración tumoral directa. Los estudios electrofisiológicos indicaron una combinación de daño axonal (afectación de las fibras nerviosas) y desmielinizante (pérdida de la cubierta protectora de los nervios), un patrón atípico para síndromes paraneoplásicos clásicos, que suelen afectar principalmente la sensibilidad.\n\nSe inició tratamiento inmunomodulador con dexametasona (un corticoide) e inmunoglobulina intravenosa, pero no se observó mejoría neurológica. La rápida progresión de la debilidad llevó a insuficiencia respiratoria, requiriendo soporte ventilatorio.\n\n**Próximos Pasos y Resultado Final**  \nTras una cuidadosa discusión multidisciplinaria y con el paciente plenamente informado, se decidió no continuar con soporte ventilatorio invasivo debido a la baja probabilidad de recuperación neurológica y la mala calidad de vida esperada. El paciente falleció tres semanas después del inicio de los síntomas neurológicos.\n\nEste caso ilustra la agresividad y complejidad de los síndromes paraneoplásicos asociados al cáncer de pulmón de células pequeñas, donde la respuesta favorable al tratamiento oncológico puede contrastar con un deterioro neurológico rápido e irreversible. Además, resalta la importancia de abordar las decisiones éticas y de calidad de vida en el manejo de estas complicaciones graves.",
+                "fh_score": 29.68
+            }
+        }
+    },
+    {
+        "article": "El paciente presentado firmó el Consentimiento Informado y se cumplieron los demás principios éticos, respetando la Resolución 466/12 del Consejo Nacional de Ética en Investigación. Este informe de caso fue aprobado por el Comité de Ética en Investigación de la Universidad Federal de São Paulo (UNIFESP), bajo el dictamen número 4.455.365.\n\nEl paciente, de 66 años de edad y sexo masculino, acudió a una consulta de otorrinolaringología por presentar disfagia tipo atragantamiento con sólidos y reflujo nasal de alimentos desde hacía un año. Había sufrido un accidente automovilístico 13 años atrás y era diabético. Se le realizó una videoendoscopia de la deglución (VED), en la que se observó, en la evaluación estructural, una protuberancia de la pared posterior de la hipofaringe con residuo salival sobre la lesión. En la evaluación funcional, tras la ingesta de alimentos sólidos, se observó una restricción de la retroflexión de la epiglotis, una limitación de la elevación de la laringe y un reflujo nasal de alimentos, con gran cantidad de residuo alimentario por encima de la lesión, en la pared posterior de la faringe. En la prueba de maniobras posturales, empeoró la disfagia al extender el cuello y mejoró la eliminación al flexionar la cabeza. Se le realizó una tomografía computarizada (TC) de la columna cervical, solicitada para evaluar la naturaleza de la lesión, que mostró la presencia de osteofitos cervicales anteriores entre las vértebras C3 y C6, el mayor de 12 milímetros (mm) de longitud, que estrechaba la columna aérea al nivel de la orofaringe e hipofaringe. Se descartaron otras causas de disfagia y se trató al paciente con terapia de deglución y omeprazol, dirigido al reflujo faringolaríngeo. Se realizaron 6 sesiones de terapia de deglución individualizada, con el objetivo de compensar el mecanismo de deglución ante un obstáculo mecánico en la región faríngea. Los principales aspectos trabajados fueron: modificación de la textura de la dieta, evitando alimentos sólidos y secos; maniobras posturales de deglución, probadas durante la VED, especialmente el chin tuck (“cabeza hacia abajo” o “flexión de la cabeza”), que aumenta el espacio de la válvula (“abre la válvula”) y mejora la presión de transferencia faríngea del alimento; y ejercicios de fortalecimiento de la lengua, para superar la barrera mecánica de la orofaringe durante la expulsión del alimento. Se recomendó, si fuera necesario, alternar la ingesta de alimentos sólidos con líquidos, ante la percepción de alimentos estancados en la faringe. Se le indicó que repitiera los ejercicios de lengua en el hogar, 2 a 3 veces al día. Después de las sesiones iniciales, el paciente presentó una respuesta satisfactoria, y se lo controló trimestralmente durante el primer año y semestralmente a partir del segundo año. Se lo derivó para una evaluación ortopédica para analizar la viabilidad quirúrgica, y se optó por un tratamiento conservador debido a la buena compensación con medidas clínicas. Sigue en seguimiento ambulatorio desde hace 2 años, y mantiene una deglución eficiente, sin incidencia de complicaciones relacionadas con la disfagia. Se optó por mantener reevaluaciones periódicas, al menos una vez al año, para detectar precozmente un posible nuevo desequilibrio de la homeostasis de la deglución relacionado con el deterioro gradual de las funciones en el contexto de la presbifagia o el surgimiento de un nuevo factor agresor.\n",
+        "gold_summary": "Se describió el caso de un paciente de 66 años con disfagia por atragantamiento con sólidos y reflujo nasal de alimentos desde hacía un año. La videoendoscopia de la deglución mostró una protuberancia en la pared posterior de la faringe y, al ofrecer alimentos sólidos, una restricción de la retroflexión de la epiglotis, reflujo nasal de alimentos y una gran cantidad de residuos de alimentos sobre la lesión. La tomografía computarizada de la columna cervical identificó la presencia de osteofitos cervicales anteriores entre las vértebras C3 y C6, el más grande con una longitud anteroposterior de 12 milímetros, que estrechaba la columna aérea a nivel de la orofaringe e hipofaringe. El paciente fue tratado adecuadamente con fonoterapia para la deglución.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un señor de 66 años tenía problemas para tragar comida dura. A veces, la comida se le iba por la nariz. Los doctores vieron que tenía un bulto en la garganta. También había huesos grandes que apretaban su garganta. Para ayudarlo, le enseñaron ejercicios para tragar mejor. Ahora puede comer sin problemas y está bien cuidado.",
+                "fh_score": 80.53
+            },
+            "B2": {
+                "text": "**Lo que Encontraron**\n\nUn hombre de 66 años tenía problemas para tragar alimentos sólidos y notaba que la comida a veces regresaba por la nariz desde hacía un año. Al hacerle un examen llamado videoendoscopia de la deglución, que consiste en usar una cámara pequeña para ver cómo traga, se vio una protuberancia (una especie de bulto) en la parte de atrás de su garganta. Cuando comía alimentos sólidos, su epiglotis (una parte que ayuda a que la comida no vaya a los pulmones) no se movía bien, y parte de la comida subía hacia la nariz, quedando residuos sobre el bulto.\n\n**Qué Significa**\n\nPara entender mejor la causa, le hicieron una tomografía computarizada, que es un tipo de radiografía especial que muestra imágenes detalladas de los huesos y tejidos. En esta imagen, encontraron que tenía unos crecimientos óseos llamados osteofitos en su columna cervical (el cuello), entre las vértebras C3 y C6. El más grande medía 12 milímetros y estaba presionando la vía aérea en la garganta, dificultando el paso normal de la comida.\n\n**Cómo lo Trataron**\n\nEl paciente recibió terapia para mejorar la forma en que traga, llamada fonoterapia. Esta terapia incluyó ejercicios para la lengua y cambios en la postura al comer, como inclinar la cabeza hacia adelante para facilitar el paso de la comida. También modificaron su dieta para evitar alimentos muy duros o secos. Gracias a este tratamiento, pudo mejorar su capacidad para tragar sin necesidad de cirugía y sigue siendo controlado regularmente para asegurarse de que no tenga problemas nuevos.",
+                "fh_score": 56.04
+            },
+            "B3": {
+                "text": "**Contexto**  \nSe presentó el caso de un hombre de 66 años que acudió a consulta por dificultad para tragar alimentos sólidos, acompañada de sensación de atragantamiento y reflujo nasal de alimentos, síntomas que persistían desde hacía un año. Entre sus antecedentes médicos destacaba un accidente automovilístico ocurrido 13 años antes y diabetes.  \n\n**Hallazgos Clave**  \nMediante una videoendoscopia de la deglución, se identificó una protuberancia en la pared posterior de la hipofaringe (parte baja de la garganta), con acumulación de saliva sobre esta lesión. Al ofrecer alimentos sólidos, se observó que la epiglotis (estructura que ayuda a proteger las vías respiratorias durante la deglución) tenía dificultad para doblarse hacia atrás, además de reflujo nasal de alimentos y una gran cantidad de restos alimentarios acumulados por encima de la protuberancia.  \n\nUna tomografía computarizada (TC) de la columna cervical reveló la presencia de osteofitos (crecimientos óseos anormales) en la parte anterior de las vértebras cervicales C3 a C6, siendo el más grande de 12 milímetros. Estos osteofitos comprimían la vía aérea en la región de la orofaringe e hipofaringe, lo que explicaba la dificultad para tragar.  \n\n**Interpretación Clínica**  \nEl diagnóstico principal fue disfagia mecánica causada por osteofitos cervicales que estrechaban la vía aérea y alteraban el mecanismo normal de la deglución. Se descartaron otras posibles causas de disfagia.  \n\n**Tratamiento y Seguimiento**  \nEl paciente recibió terapia de deglución personalizada, que incluyó:  \n- Modificación de la dieta para evitar alimentos sólidos y secos, facilitando la ingesta.  \n- Maniobras posturales durante la deglución, especialmente la flexión de la cabeza hacia adelante (chin tuck), que mejora el paso del alimento y reduce el reflujo nasal.  \n- Ejercicios de fortalecimiento de la lengua para superar la obstrucción mecánica y facilitar la expulsión del alimento.  \n\nAdemás, se prescribió omeprazol para tratar el reflujo faringolaríngeo (reflujo de ácido hacia la garganta). El paciente mostró una respuesta favorable tras seis sesiones de terapia y se mantuvo bajo seguimiento regular durante dos años, con controles trimestrales en el primer año y semestrales posteriormente.  \n\nSe evaluó la posibilidad de tratamiento quirúrgico para eliminar los osteofitos, pero se decidió continuar con un manejo conservador debido a la buena compensación clínica. Se recomendó continuar con ejercicios en casa y mantener evaluaciones periódicas al menos una vez al año, para detectar a tiempo cualquier deterioro en la función de la deglución asociado al envejecimiento o a nuevos factores.  \n\n**Conclusión**  \nEste caso ilustra cómo los osteofitos cervicales pueden causar disfagia mecánica significativa, y cómo un tratamiento integral basado en terapia de deglución y modificaciones dietéticas puede lograr una adecuada compensación funcional, evitando la necesidad de cirugía y mejorando la calidad de vida del paciente.",
+                "fh_score": 37.05
+            }
+        }
+    },
+    {
+        "article": "Una paciente caucásica de 18 años de edad se presentó en nuestra clínica con quejas de múltiples bultos palpables en sus senos bilateralmente. En el examen físico, la paciente tenía múltiples lesiones pigmentadas lentigosas en su cara, cuerpo y esclerótica bilateralmente, nevos azules en su tronco y extremidades superiores y una cara redonda con forma de luna.\n\nTras la evaluación ultrasonográfica, se encontraron múltiples nódulos compactos (fibroadenomas) en ambos senos, siendo el más grande en el cuadrante superior externo del seno izquierdo, con un diámetro de 7,8 cm.\n\nEn 2018, se le había practicado una tiroidectomía total con el diagnóstico de adenoma folicular y la extirpación de un nódulo grande del seno izquierdo, debido a su gran tamaño y al dolor que causaba, con un informe de histopatología que sugería un fibroadenoma con estroma mixóide.\n\nSe realizó una biopsia por escisión de dos nódulos de la mama derecha con diagnóstico de fibroadenoma mixto, lo que respaldó nuestro diagnóstico de complejo de Carney.\n\nEn la resonancia magnética se encontraron múltiples fibroadenomas compactos en ambos senos, con alta intensidad de señal en las imágenes T2 y T2/FS, con tabiques internos sin restricción de difusión, compatibles con múltiples fibroadenomas mixoides.\n\nAdemás, había un par de ganglios linfáticos axilares y prominentes ganglios linfáticos mamarios internos bilaterales.\n\nAdemás, se observó una anomalía en la densidad de los tejidos blandos en el mediastino anterior, que medía 11 mm de espesor máximo, lo que sugería un timo prominente.\n\nTodos los hallazgos anteriores sugerían la posibilidad de un complejo de Carney. Se realizó una evaluación adicional en el laboratorio. Los análisis hormonales no mostraron anomalías en los niveles de testosterona, prolactina, PTH y DHEA-S.\n\nLuego se realizó un análisis genético que arrojó como resultado la mutación del gen PRHAR1A, heterocigótico para una variante sin sentido de significancia incierta en el exón 3 de este gen. Esta mutación nunca se había informado en la base de datos gnomAD.\n\nSe realizaron pruebas genéticas a los padres y se determinó que solo el padre era portador de la misma mutación genética.\n\nSe discutieron con la paciente varios planes de tratamiento conservadores, pero ninguno demostró proporcionar una solución/tratamiento definitivo. En el pasado se realizó la extirpación de los lóbulos grandes con alivio temporal de los síntomas de dolor de la paciente y las cirugías recurrentes estaban afectando su calidad de vida. La paciente también tuvo varias sesiones con la psicóloga de nuestra clínica y fue evaluada a fondo antes de decidir la solución final de una mastectomía bilateral.\n\nLa paciente se sometió a una mastectomía bilateral con conservación de la piel y colocación subcutánea de expansores de tejidos (suave, Motiva Flora®). La histopatología informó múltiples fibroadenomas mixóides en ambos senos, compatibles con el síndrome de Carney, con interrupción de la arquitectura normal del parénquima mamario. Las figuras muestran el fibroadenoma de forma macroscópica e histológica.\n\nEl cuidado de la herida fue mínimo, se le recomendó a la paciente usar un sujetador médico y visitas regulares a la clínica ambulatoria para seguimiento y rellenado adicional de los expansores de tejidos a intervalos regulares hasta que se alcanzó el tamaño deseado. Paciente antes y después de la mastectomía. Después de un año se realizó una segunda cirugía y los expansores se reemplazaron con implantes de silicona permanentes (suaves, Motiva Ergonomic®) submusculares, con los mismos requisitos mínimos de cuidado de la herida y colocación del sujetador.\n",
+        "gold_summary": "Una paciente de 18 años de edad se presentó en nuestra clínica con múltiples bultos palpables en sus senos bilateralmente. En el examen físico, la paciente también tenía múltiples lesiones pigmentadas lentigosas en su cara, cuerpo y esclerótica, nevos azules en su tronco y extremidades superiores y un rostro redondo con forma de luna. El diagnóstico del síndrome de Carney se decidió mediante imágenes, biopsias y análisis genético. La paciente se sometió a una mastectomía bilateral como plan de tratamiento profiláctico con colocación de expansores de tejidos.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una niña de 18 años tenía muchos bultos en sus pechos. También tenía manchas de colores en su cara y cuerpo. Los doctores hicieron pruebas y encontraron una enfermedad llamada síndrome de Carney. Para ayudarla, le quitaron los pechos y pusieron cosas suaves para que su cuerpo se vea bien.",
+                "fh_score": 81.29
+            },
+            "B2": {
+                "text": "**Lo que Encontraron en la Paciente**  \nUna joven de 18 años llegó a la clínica porque tenía varios bultos en ambos senos. Al examinarla, también notaron manchas oscuras en su piel y ojos, así como lunares azules en su cuerpo. Su cara tenía una forma redonda, parecida a una luna llena. Estas señales indicaron que podría tener algo llamado síndrome de Carney, que es una enfermedad rara que causa tumores benignos (no cancerosos) en diferentes partes del cuerpo.\n\n**Cómo Confirmaron el Diagnóstico**  \nPara estar seguros, los médicos hicieron varias pruebas. Usaron imágenes especiales como ultrasonidos y resonancias magnéticas para ver los bultos en sus senos. Además, tomaron pequeñas muestras de esos bultos (biopsias) para analizarlas bajo el microscopio. También hicieron un examen genético y encontraron un cambio en un gen llamado PRHAR1A, que está relacionado con este síndrome.\n\n**Qué Tratamiento Eligieron**  \nDespués de discutir varias opciones, decidieron hacer una mastectomía bilateral. Esto significa que le quitaron ambos senos para evitar problemas futuros, ya que los bultos seguían creciendo y causaban dolor. Para ayudar a que la piel se mantuviera y poder reconstruir después, colocaron unos dispositivos llamados expansores de tejidos, que poco a poco estiran la piel. Más tarde, estos expansores se reemplazaron por implantes de silicona para que la paciente tuviera una apariencia natural.\n\n**Importancia del Caso**  \nEste caso muestra cómo es importante combinar diferentes pruebas para diagnosticar enfermedades raras como el síndrome de Carney. También destaca que, a veces, el tratamiento puede ser difícil y requiere decisiones importantes para mejorar la calidad de vida del paciente.",
+                "fh_score": 55.02
+            },
+            "B3": {
+                "text": "**Contexto**\n\nUna joven caucásica de 18 años acudió a la clínica debido a la presencia de múltiples bultos palpables en ambos senos. Durante el examen físico, se observaron varias lesiones pigmentadas llamadas lentigos (manchas oscuras) en la cara, el cuerpo y la esclerótica (parte blanca del ojo), además de nevos azules (manchas pigmentadas) en el tronco y extremidades superiores, y una característica forma redonda de su rostro, conocida como cara en forma de luna.\n\n**Hallazgos Clave**\n\n- Estudios por ultrasonido y resonancia magnética revelaron múltiples nódulos compactos en ambos senos, identificados como fibroadenomas mixoides, siendo el más grande de 7,8 cm en el seno izquierdo.\n- Se realizaron biopsias por escisión de algunos nódulos, confirmando el diagnóstico de fibroadenomas mixtos.\n- Se detectó una anomalía en el mediastino anterior (área entre los pulmones), consistente con un timo prominente, y ganglios linfáticos axilares e internos aumentados de tamaño.\n- Los análisis hormonales no mostraron alteraciones significativas.\n- Un estudio genético identificó una mutación en el gen PRKAR1A, asociada con el síndrome de Carney, una enfermedad rara que se caracteriza por la presencia de tumores benignos en diferentes órganos y lesiones pigmentadas en la piel.\n\n**Interpretación Clínica**\n\nEl conjunto de hallazgos clínicos, imagenológicos, histopatológicos y genéticos permitió establecer el diagnóstico del síndrome de Carney. Este síndrome explica la presencia simultánea de múltiples fibroadenomas mamarios, lesiones pigmentadas cutáneas y otras anomalías observadas en la paciente.\n\n**Próximos Pasos y Tratamiento**\n\nDado que las cirugías previas para extirpar los fibroadenomas grandes solo proporcionaron alivio temporal y afectaban negativamente la calidad de vida de la paciente, se consideraron opciones de tratamiento más definitivas. Tras una evaluación psicológica y médica exhaustiva, se decidió realizar una mastectomía bilateral (extirpación completa de ambos senos) con conservación de la piel, seguida de la colocación subcutánea de expansores de tejidos para permitir la reconstrucción mamaria gradual.\n\nEl cuidado postoperatorio incluyó el uso de un sujetador médico y visitas regulares para el llenado progresivo de los expansores. Un año después, se reemplazaron estos expansores por implantes permanentes de silicona colocados debajo del músculo, con un manejo mínimo de la herida y seguimiento ambulatorio.\n\nEste enfoque permitió controlar los síntomas, mejorar la calidad de vida de la paciente y manejar de manera efectiva las manifestaciones mamarias del síndrome de Carney.",
+                "fh_score": 34.57
+            }
+        }
+    },
+    {
+        "article": "Una adolescente femenino de 13 años sin antecedentes médico-quirúrgicos de interés acude a Urgencias por dolor e impotencia funcional en muñeca izquierda tras caída mientras patinaba. Diagnosticada de lesión en torus metafisaria con extensión fisaria de radio distal clasificada como lesión Peterson tipo I, es inmovilizada durante cuatro semanas con férula antebraquiopalmar. Dos semanas después de la retirada de la férula, acude nuevamente a Urgencias al sentir un crujido en la muñeca, sin sobreesfuerzo asociado e impotencia para movilizar el primer dedo de la mano izquierda. Clínicamente presenta déficit de extensión activa interfalángica, efecto tenodesis patológico, edema local y asimetría macroscópica a la comparación con la extremidad contralateral. Se estudia con resonancia magnética nuclear (RMN), identificando imagen de solución de continuidad del EPL. Con la paciente bajo anestesia general, se procede al tratamiento quirúrgico mediante transferencia tendinosa del extensor propio del índice (EPI) al remanente distal del EPL con sutura tipo Pulvertaft de monofilamento no absorbible. En el postoperatorio se inmovilizó la extremidad las cuatro primeras semanas.\n\nTras cuatro semanas, se autorizó movilidad evidenciando recuperación de extensión del primer dedo de la mano izquierda y cicatrices discretamente hipertróficas, sin dolor. El seguimiento a la sexta, duodécima semana y al año no reporta complicaciones, con una restitución completa de la función y una puntuación de 0 en la escala PRWE (Patient Rated Wrist Evaluation).",
+        "gold_summary": "Se presenta el caso de una paciente adolescente femenino que, tras tratamiento conservador con férula de una fractura fisaria Peterson tipo I en radio, sufre a las seis semanas déficit agudo de extensión del pulgar, diagnosticada mediante examen clínico radiológico de rotura espontánea del extensor pollicis longus. Es tratada por medio de transferencia del extensor propio del índice (EPI) con resultados satisfactorios y recuperación de su actividad habitual al mes postoperatorio.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una niña de 13 años se cayó y se lastimó la muñeca. Le pusieron una tablita para que su hueso sanara. \n\nDespués de quitarle la tablita, su dedo pulgar no podía moverse bien. Los doctores vieron que un hilo que mueve el dedo se había roto. \n\nElla tuvo una operación para arreglar ese hilo con otro hilo de su mano. \n\nDespués de un mes, su dedo volvió a moverse bien y pudo hacer todo como antes.",
+                "fh_score": 87.34
+            },
+            "B2": {
+                "text": "Caso de una adolescente de 13 años con fractura en la muñeca que fue tratada con una férula. Seis semanas después, comenzó a tener dificultad para estirar el pulgar de la mano izquierda. Los médicos descubrieron que uno de los tendones que mueve el pulgar, llamado extensor largo del pulgar, se había roto sin que ella hiciera un esfuerzo fuerte. Para arreglarlo, realizaron una cirugía donde usaron otro tendón del dedo índice para reemplazar el que estaba roto. Después de la operación y un periodo de inmovilización, la paciente recuperó completamente el movimiento del pulgar y pudo volver a sus actividades normales en un mes.",
+                "fh_score": 61.42
+            },
+            "B3": {
+                "text": "**Contexto**  \nSe trata de una adolescente de 13 años, sin antecedentes médicos relevantes, que sufrió una caída mientras patinaba, ocasionándole dolor e incapacidad para mover la muñeca izquierda. Fue diagnosticada con una fractura en la parte distal del radio (hueso del antebrazo), específicamente una lesión fisaria clasificada como Peterson tipo I, y se le inmovilizó la muñeca con una férula durante cuatro semanas.\n\n**Hallazgos Clave**  \nDos semanas después de retirar la férula, la paciente volvió a urgencias tras sentir un crujido en la muñeca sin haber realizado un esfuerzo adicional. Presentaba incapacidad para extender (levantar) el primer dedo de la mano izquierda, hinchazón local y asimetría visible en comparación con la mano contraria. La exploración clínica mostró un déficit en la extensión activa del dedo y un signo llamado tenodesis patológico, que indica alteración en la función tendinosa. La resonancia magnética confirmó la ruptura del tendón extensor largo del pulgar (EPL), que es el tendón responsable de estirar el pulgar.\n\n**Interpretación Clínica**  \nLa ruptura espontánea del tendón extensor largo del pulgar es una complicación poco frecuente pero grave que puede ocurrir después de fracturas en la muñeca, incluso cuando el tratamiento inicial es conservador. Debido a la pérdida de función del EPL, se decidió realizar una cirugía para restaurar la movilidad del pulgar. El procedimiento consistió en transferir el tendón extensor propio del índice (EPI), que normalmente mueve el dedo índice, para sustituir la función del tendón lesionado del pulgar. La sutura se realizó mediante una técnica llamada Pulvertaft, que asegura una unión firme entre los tendones.\n\n**Próximos Pasos y Resultados**  \nTras la cirugía, la muñeca se inmovilizó durante cuatro semanas para favorecer la cicatrización. Posteriormente, se permitió la movilidad y la paciente mostró una recuperación completa de la extensión del pulgar sin dolor ni limitaciones funcionales. En los controles realizados a las 6, 12 semanas y al año, no se observaron complicaciones, y la paciente recuperó completamente su actividad habitual, con una puntuación de 0 en la escala PRWE, que indica ausencia de dolor y discapacidad en la muñeca.\n\nEn resumen, este caso ilustra cómo una complicación inesperada tras una fractura en la muñeca puede ser tratada con éxito mediante una transferencia tendinosa, logrando una recuperación funcional completa en una paciente adolescente.",
+                "fh_score": 43.9
+            }
+        }
+    },
+    {
+        "article": "Se remitió a un hombre de 73 años para una SAVR para tratar la regurgitación valvular aórtica sintomática (AR). Dos años antes, había presentado múltiples lesiones exantématicas. Una biopsia de piel reveló infiltración de células plasmáticas, lo que motivó la derivación a un hematólogo. La tomografía computarizada reveló linfadenopatía sistémica y hepatoesplenomegalia. Una biopsia renal realizada por disfunción renal confirmó la amiloidosis AA; una biopsia de ganglios linfáticos mostró plasmocitosis interfolicular y un centro germinal hiperplásico, consistente con el subtipo plasmático de iMCD, apoyado por niveles elevados de IL-6 en plasma. Se administró al paciente TCZ intravenoso (640 mg cada 2 semanas), junto con prednisolona (10 mg diarios). La erupción cutánea y la linfadenopatía se resolvieron. La ecocardiografía reveló AR puro moderado y agrandamiento ventricular izquierdo. Dado que el paciente experimentó gradualmente disnea de esfuerzo con agrandamiento ventricular izquierdo progresivo, se consideró necesaria la SAVR.\n\nDebido al sangrado por hemorroides y a la hepatosplenomegalia, se consultó a un hepatólogo; se diagnosticó cirrosis hepática de Child-Pugh grado A y varices esofágicas. Se realizó una conferencia preoperatoria del equipo, en la que participaron un intensivista y un farmacéutico, en la que se revisaron los mecanismos de acción de TCZ, las posibles complicaciones y el tratamiento perioperatorio. La cirugía se realizó 26 días después de la última dosis de TCZ. Durante el período perioperatorio, se suspendió el tratamiento con TCZ, mientras que se continuó con los esteroides por vía oral o intravenosa. Las medidas preventivas para las infecciones del sitio quirúrgico (SSI) incluyeron la detección de portadores nasales de Staphylococcus aureus resistentes a la meticilina, la preparación antiséptica de la piel, la terapia antibiótica profiláctica y el control de la hiperglucemia. El cultivo nasal fue positivo para Staphylococcus coagulasa negativo. Se realizó el reemplazo de la válvula aórtica quirúrgica a través de una esternotomía media bajo circulación extracorpórea, con 65 minutos de tiempo de isquemia cardiaca y 128 minutos de tiempo de circulación extracorpórea. Se requirieron transfusiones de sangre, incluidos glóbulos rojos, plasma y plaquetas; el paciente fue extubado al día siguiente. Los hallazgos patológicos revelaron un espesamiento fibroso focal sin depósitos amiloides.\n\nLa herida quirúrgica no mostró signos de infección en el día 2 postoperatorio; se inició la terapia de presión negativa en la herida (NPWT) en la herida quirúrgica cerrada para evitar SSI. La terapia de presión negativa en la herida se interrumpió en el día 13 postoperatorio, sin aparente SSI. El paciente fue dado de alta en el día 17 postoperatorio sin ningún signo de infección.\n\nAunque los niveles de IL-6 aumentaron temporalmente los días 1 y 2 después de la operación, disminuyeron progresivamente hasta el día 24 después de la operación, y luego volvieron a aumentar al reanudarse el tratamiento con TCZ. Los niveles de proteína C reactiva (PCR) estaban ligeramente elevados, alcanzando un máximo de 0,56 mg/dL el día 2 después de la operación. Para el día 24 después de la operación, la PCR había aumentado a 1,06 mg/dL sin infección. Antes del aumento de la PCR, los niveles del factor de crecimiento endotelial vascular aumentaron el día 13 después de la operación.\n\nEl paciente no experimentó recurrencia de erupción cutánea o linfadenopatía durante el período perioperatorio. Los niveles de creatinina postoperatorios aumentaron temporalmente, pero volvieron a los niveles preoperatorios el día 24. Se reanudó el tratamiento con tocilizumab el día 30 postoperatorio tras confirmar la ausencia de infección, incluida la IFI.\n",
+        "gold_summary": "Un hombre de 73 años con enfermedad de Castleman, tratado con TCZ, se sometió a un reemplazo de la válvula aórtica por medio de esternotomía mediana para la regurgitación de la válvula aórtica con falta de aire al hacer ejercicio. Se implementaron medidas integrales para prevenir la infección del sitio quirúrgico junto con un examen minucioso durante el período perioperatorio. Tocilizumab se interrumpió 26 días antes de la cirugía y se reanudó 30 días después de la cirugía, durante los cuales los niveles de IL-6 en plasma disminuyeron. No hubo evidencia de infección o exacerbación de la enfermedad de Castleman. Los niveles del factor de crecimiento endotelial vascular aumentaron antes de un aumento en los niveles de proteína C reactiva después del alta hospitalaria y antes de la reanudación de TCZ.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un hombre de 73 años estaba enfermo y tenía problemas en su corazón. Tenía dificultad para respirar cuando caminaba. Los doctores le hicieron una operación para cambiar una parte del corazón llamada válvula.\n\nAntes de la operación, dejaron de darle un medicamento llamado TCZ para que no tuviera problemas. También cuidaron mucho que no se le hiciera una infección en la herida.\n\nDespués de la operación, el hombre se fue mejorando. No tuvo infecciones ni se puso más enfermo. Cuando estuvo listo, le dieron otra vez el medicamento para ayudarlo.\n\nLos doctores vieron que su cuerpo estaba mejor y que el medicamento funcionaba bien. El hombre pudo salir del hospital sin problemas.",
+                "fh_score": 71.67
+            },
+            "B2": {
+                "text": "**Lo que le pasaba al paciente:**  \nUn hombre de 73 años tenía una enfermedad llamada enfermedad de Castleman, que afecta a los ganglios linfáticos y causa inflamación. También tenía un problema en el corazón llamado regurgitación de la válvula aórtica, que significa que la válvula no cerraba bien y eso le causaba dificultad para respirar al hacer ejercicio.\n\n**Qué tratamiento recibió:**  \nPara mejorar su corazón, los médicos le hicieron una cirugía para reemplazar la válvula aórtica. Antes de la operación, el paciente recibía un medicamento llamado tocilizumab (TCZ), que ayuda a controlar la inflamación en la enfermedad de Castleman. Este medicamento se detuvo 26 días antes de la cirugía para evitar problemas durante la operación y se volvió a empezar 30 días después, cuando ya estaba seguro.\n\n**Cómo cuidaron al paciente durante la cirugía:**  \nLos médicos tomaron muchas precauciones para evitar infecciones en la herida de la cirugía. Revisaron si tenía bacterias en la nariz, limpiaron bien la piel antes de operar, usaron antibióticos preventivos y controlaron su azúcar en sangre. Además, usaron una técnica especial llamada terapia de presión negativa en la herida para ayudar a que sanara sin infecciones.\n\n**Qué pasó después de la cirugía:**  \nEl paciente no tuvo infecciones ni empeoramiento de su enfermedad durante el tiempo que estuvo sin tomar el medicamento. Los niveles en sangre de una proteína llamada IL-6, que está relacionada con la inflamación, bajaron después de la cirugía y subieron nuevamente cuando volvió a tomar el medicamento. También observaron cambios en otras proteínas relacionadas con la inflamación, pero el paciente se recuperó bien y pudo salir del hospital sin problemas.\n\n**En resumen:**  \nEste caso muestra que es posible hacer una cirugía importante en un paciente con enfermedad de Castleman que usa tocilizumab, siempre que se tomen medidas cuidadosas para prevenir infecciones y se controle bien el tratamiento antes y después de la operación.",
+                "fh_score": 50.32
+            },
+            "B3": {
+                "text": "**Contexto:**  \nUn hombre de 73 años con diagnóstico de enfermedad de Castleman idiopática multicéntrica (iMCD), un trastorno inflamatorio caracterizado por crecimiento anormal de ganglios linfáticos y producción elevada de interleucina-6 (IL-6), fue tratado con tocilizumab (TCZ), un medicamento que bloquea la acción de esta proteína inflamatoria. Además, presentaba regurgitación valvular aórtica (fuga en la válvula del corazón que permite el retorno de sangre), que causaba dificultad progresiva para respirar durante el esfuerzo, y se decidió realizar un reemplazo quirúrgico de la válvula aórtica (SAVR) mediante una incisión en el esternón (esternotomía media).\n\n**Hallazgos Clave y Manejo Perioperatorio:**  \nAntes de la cirugía, el paciente recibió cuidados especializados para minimizar el riesgo de infecciones en el sitio quirúrgico, incluyendo la detección y manejo de bacterias en la nariz, preparación cuidadosa de la piel, uso profiláctico de antibióticos y control estricto del azúcar en sangre. El tratamiento con tocilizumab se suspendió 26 días antes de la operación para reducir posibles complicaciones inmunológicas, mientras que la administración de esteroides continuó para controlar la inflamación. La cirugía se realizó con éxito bajo circulación extracorpórea (máquina que mantiene la circulación y oxigenación de la sangre durante la operación), requiriendo transfusiones de sangre, y el paciente fue extubado al día siguiente sin complicaciones inmediatas.\n\nDurante el postoperatorio, no se observaron signos de infección en la herida quirúrgica, y se utilizó terapia de presión negativa (una técnica para favorecer la cicatrización y prevenir infecciones) hasta el día 13 después de la cirugía. El paciente fue dado de alta el día 17 sin evidencia de infección ni recurrencia de los síntomas de la enfermedad de Castleman, como erupciones cutáneas o aumento de ganglios linfáticos.\n\n**Interpretación Clínica:**  \nLos niveles de IL-6 en plasma aumentaron temporalmente en los primeros días tras la cirugía, lo cual es esperado debido a la respuesta inflamatoria postoperatoria, pero luego disminuyeron progresivamente hasta el día 24. Posteriormente, al reanudarse el tratamiento con tocilizumab el día 30, los niveles de IL-6 volvieron a aumentar, reflejando la acción del medicamento. La proteína C reactiva (PCR), un marcador de inflamación, mostró un leve aumento sin evidencia de infección, y se observó un incremento previo en el factor de crecimiento endotelial vascular, una proteína relacionada con la reparación y formación de vasos sanguíneos, lo que podría indicar procesos de recuperación tisular.\n\nLa función renal mostró un aumento temporal en los niveles de creatinina después de la cirugía, pero volvió a los valores previos al alta, indicando una recuperación adecuada de la función renal.\n\n**Próximos Pasos y Conclusiones:**  \nEl manejo cuidadoso del tratamiento inmunosupresor y las medidas preventivas implementadas permitieron realizar con éxito el reemplazo valvular en un paciente con enfermedad de Castleman sin complicaciones infecciosas ni exacerbación de la enfermedad. La reanudación del tocilizumab se realizó de forma segura tras confirmar la ausencia de infección. Este caso resalta la importancia de una planificación multidisciplinaria y un seguimiento riguroso en pacientes con enfermedades inflamatorias complejas sometidos a cirugía mayor.",
+                "fh_score": 30.51
+            }
+        }
+    },
+    {
+        "article": "Se trata de un paciente de sexo masculino de cuatro meses de edad, originario del centro de México y con dos hermanos hombres sanos. Durante el primer trimestre de gestación, su madre hipotiroidea consumió drogas. No obstante, el infante nació con peso y talla adecuados, fue alimentado con leche materna y recibió la vacuna del bacilo de Calmette-Guérin (BCG), sin desarrollo de cicatriz. La madre del paciente era prisionera en una cárcel y, junto con el bebé, compartían una celda insalubre con dos personas más.A los cuatro meses, el paciente fue valorado médicamente por un tumor doloroso en la región axilar izquierda. En la radiografía de tórax se observaron imágenes sugestivas de fracturas costales; se sospechó de maltrato infantil por parte de la madre, y el infante fue hospitalizado en un hospital pediátrico. Se determinó el peso (4.190 g) y la talla (58 cm) –por debajo del percentil tres–, saturación de oxígeno del 70 %, fiebre, tos, aumento de volumen en la región axilar izquierda, además de dolor, rubor y calor. En el cuadro hemático se encontró: hemoglobina de 8,8 g/dl (11,0 - 12,6), 29,3 × 109 leucocitos/L (6,0 - 17,5), 18,4 × 109 neutrófilos/L (1,0 - 8,5), 7,0 × 109 linfocitos/L (4,0 - 13,5), 3,5 × 109 monocitos/L, 459 × 109 plaquetas/L (150 - 350) y proteína C reactiva igual a 16 mg/L (< 3,0). En la primera tomografía toracoabdominal se observaron imágenes de un absceso en la región axilar izquierda, lesiones líticas en las costillas 3 a 6, neumonía apical izquierda, nódulos pulmonares en ambos pulmones y ganglios linfáticos cervicales y mediastinales incrementados de tamaño. En la biopsia del absceso axilar izquierdo se reportó miositis y paniculitis supurativa. Solo se hizo cultivo para bacterias del líquido broncoalveolar, el cual fue negativo, y la PCR para el complejo Mycobacterium tuberculosis fue negativa. Después de 41 días de hospitalización y de haber recibido dos esquemas de antimicrobianos –ceftriaxona-clindamicina y cefepima-vancomicina–, el paciente fue dado de alta.\n\nDos meses después, a los ocho meses de edad, reingresó al hospital por fiebre, irritabilidad y un absceso supurante en la escápula izquierda. En el cuadro hemático se encontró: hemoglobina de 10,8 g/dl (10,5 - 12), 21,2 × 109 leucocitos/L (6 - 17), 12,2 × 109 neutrófilos/L (1,5 - 8,5), 7,5 × 109 linfocitos/L (4 - 10,5), 1,2 × 109 monocitos/L (600), y 583 × 109 plaquetas/L (150 - 350); la prueba para la detección sérica de HIV fue negativa. En la tomografía de tórax se observó una consolidación apical izquierda, bronquiectasias, lesiones líticas en las costillas 2 a 7 y en las vértebras dorsales 2 a 7, además de una colección de líquido multiloculado; en el ultrasonido se encontró una fístula asociada con el absceso escapular. El paciente recibió piperacilina-tazobactam, que se sustituyó después por voriconazol al detectarse Aspergillus fumigatus en el cultivo de la muestra de secreción del absceso. Dada la recurrencia y la gravedad de la infección, se sospechó un error innato de la inmunidad. La prueba de dihidrorrodamina resultó sin producción de especies reactivas de oxígeno y la expresión de gp91phox en los neutrófilos fue nula, estableciéndose así el diagnóstico de enfermedad granulomatosa crónica ligada al cromosoma X. La variante patógena detectada por la secuenciación de nueva generación fue c.80_83del/Y (p.Val27Glyfs*33) en CYBB. La madre resultó portadora de la variante (c.80_83del/WT). No fue posible estudiar genéticamente a sus dos hermanos mayores, de sexo masculino, y aparentemente sanos. El paciente fue dado de alta después de 65 días de hospitalización y tratamiento con voriconazol por 28 días. Se inició profilaxis antibiótica diaria con trimetoprim-sulfametoxazol y profilaxis antifúngica con fluconazol dos veces a la semana. Dos meses después, al año de edad, el infante reingresó debido a una neumonía multifocal, por la cual requirió asistencia respiratoria mecánica. Se detectó el antígeno galactomanano en el suero y A. fumigatusen el cultivo del líquido del lavado broncoalveolar, por lo que se inició nuevamente tratamiento con voriconazol. El paciente sufrió una falla orgánica múltiple y falleció un mes después de su ingreso.\n",
+        "gold_summary": "Se presenta el caso de un infante con enfermedad granulomatosa crónica y aspergilosis invasiva. Se trata de un lactante de sexo masculino de cuatro meses de edad, de madre hipotiroidea y con quien convive en la celda de la cárcel. El infante presentó tumores en la región axilar izquierda y la radiografía de tórax sugirió fracturas costales; fue hospitalizado ante la sospecha de maltrato infantil. En la tomografía de tórax se observó un absceso axilar, osteólisis de costillas, neumonía y nódulos pulmonares; el paciente recibió antibióticos de amplio espectro y fue dado de alta. A los ocho meses, reingresó por fiebre y extensión del absceso purulento hacia la región escapular izquierda; en la tomografía se observaron imágenes de empeoramiento de la condición. Se aisló Aspergillus fumigatus de la secreción del absceso y se diagnosticó aspergilosis invasiva; se inició tratamiento con voriconazol por 28 días. Mediante la prueba de dihidrorrodamina, se diagnosticó enfermedad granulomatosa crónica causada por la variante patógena c.80_83del/Y del gen CYBB, portada por la madre (c.80_83del/WT). A los 12 meses, el paciente reingresó nuevamente por aspergilosis invasiva, resistente al tratamiento, con desenlace fatal.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había un bebé que estaba muy enfermo. Tenía un bulto doloroso en su brazo y problemas para respirar. Los doctores lo cuidaron mucho y le dieron medicinas para que mejorara.\n\nDespués, el bebé se volvió a enfermar. Tenía fiebre y otro bulto que dolía mucho. Los doctores encontraron un hongo que le hacía daño. Le dieron medicinas especiales para el hongo.\n\nLos doctores hicieron pruebas y vieron que el bebé tenía un problema en su cuerpo que no lo dejaba pelear bien contra las enfermedades. Su mamá también tenía ese problema, pero no estaba enferma.\n\nEl bebé estuvo en el hospital muchas veces. Aunque los doctores hicieron todo lo posible, el bebé se puso muy mal y no pudo mejorar. Los doctores y su familia lo cuidaron con mucho amor.",
+                "fh_score": 82.25
+            },
+            "B2": {
+                "text": "**Caso de un Bebé con Problemas en el Sistema Inmunológico y una Infección Grave**\n\nEste es el caso de un bebé de cuatro meses que vivía con su madre en una cárcel. Su madre tenía problemas de tiroides y durante el embarazo tomó medicamentos. El bebé nació con buen peso y tamaño, pero luego presentó un bulto doloroso en la axila izquierda. Al hacerle una radiografía, los médicos vieron posibles fracturas en sus costillas, por lo que pensaron que podría estar sufriendo maltrato. Fue hospitalizado para recibir atención.\n\nEn estudios más detallados, encontraron un absceso (una acumulación de pus) en la axila, daño en varias costillas, neumonía y nódulos en los pulmones. El bebé recibió antibióticos fuertes y fue dado de alta después de mejorar un poco.\n\nA los ocho meses, volvió al hospital con fiebre y un absceso que se extendió hacia la parte superior de la espalda. Nuevas imágenes mostraron que la infección había empeorado. En el pus del absceso encontraron un hongo llamado Aspergillus fumigatus, que puede causar infecciones graves, especialmente en personas con defensas bajas. Por eso, le dieron un medicamento antifúngico llamado voriconazol.\n\nLos médicos sospecharon que el bebé tenía un problema en su sistema inmunológico, que es el que nos protege de las infecciones. Hicieron una prueba llamada dihidrorrodamina, que mostró que sus células defensivas no podían producir sustancias necesarias para combatir gérmenes. Esto confirmó que tenía una enfermedad llamada enfermedad granulomatosa crónica, que afecta la capacidad del cuerpo para luchar contra ciertas infecciones. Esta enfermedad fue causada por un cambio en un gen llamado CYBB, que heredó de su madre.\n\nA pesar del tratamiento, a los 12 meses el bebé volvió a enfermar gravemente por la misma infección de Aspergillus. La infección no respondió bien a los medicamentos y, lamentablemente, el bebé falleció debido a una falla de varios órganos.\n\n**Qué Significa Este Caso**\n\nEste caso muestra cómo un problema genético en el sistema inmunológico puede hacer que un bebé sea muy vulnerable a infecciones graves, como las causadas por hongos. También resalta la importancia de diagnosticar estas enfermedades temprano para intentar proteger a los pacientes con tratamientos adecuados.",
+                "fh_score": 59.3
+            },
+            "B3": {
+                "text": "**Contexto**  \nSe describe el caso de un lactante varón de cuatro meses originario del centro de México, cuya madre presentaba hipotiroidismo y con quien vivía en condiciones precarias dentro de una cárcel. El bebé nació con peso y talla adecuados, pero a los cuatro meses desarrolló un tumor doloroso en la axila izquierda. Ante la sospecha inicial de maltrato infantil, debido a fracturas costales observadas en radiografías, fue hospitalizado para evaluación y tratamiento.\n\n**Hallazgos Clave**  \nDurante la hospitalización inicial, las imágenes de tomografía mostraron un absceso en la axila izquierda, lesiones destructivas en varias costillas (osteólisis), neumonía en el lóbulo superior del pulmón izquierdo y nódulos pulmonares bilaterales, además de ganglios linfáticos aumentados de tamaño. El análisis de sangre reveló anemia, elevación de leucocitos y marcadores inflamatorios, indicativos de infección activa. A pesar de recibir antibióticos de amplio espectro, el paciente presentó recurrencia de la infección a los ocho meses, manifestada por fiebre y un absceso supurante que se extendió hacia la región escapular izquierda. Nuevas imágenes mostraron empeoramiento con consolidación pulmonar, bronquiectasias (dilatación anormal de las vías respiratorias), lesiones óseas adicionales y formación de fístulas. En el cultivo de la secreción del absceso se aisló Aspergillus fumigatus, un hongo que causa infecciones invasivas en personas con alteraciones inmunológicas.\n\n**Interpretación Clínica**  \nLa recurrencia y gravedad de las infecciones, junto con la presencia de infecciones fúngicas invasivas, sugirieron un defecto en la inmunidad innata. La prueba funcional de dihidrorrodamina, que evalúa la capacidad de los neutrófilos (un tipo de glóbulo blanco) para producir especies reactivas de oxígeno necesarias para eliminar microorganismos, fue negativa. Además, no se detectó la proteína gp91^phox en neutrófilos, confirmando el diagnóstico de enfermedad granulomatosa crónica ligada al cromosoma X, una condición genética que afecta la capacidad del sistema inmunitario para combatir ciertas infecciones. La secuenciación genética identificó una mutación patógena específica (c.80_83del/Y) en el gen CYBB, responsable de esta enfermedad, y se confirmó que la madre era portadora de esta variante.\n\n**Próximos Pasos y Evolución**  \nTras el diagnóstico, el paciente recibió tratamiento antifúngico con voriconazol y profilaxis antibiótica y antifúngica para prevenir nuevas infecciones. Sin embargo, a la edad de un año, volvió a ingresar al hospital con neumonía multifocal grave causada nuevamente por Aspergillus fumigatus, que requirió soporte respiratorio avanzado. A pesar del tratamiento, el paciente desarrolló falla orgánica múltiple y falleció un mes después.\n\n**Resumen Final**  \nEste caso ilustra la presentación clínica y evolución de un lactante con enfermedad granulomatosa crónica ligada al cromosoma X, caracterizada por infecciones recurrentes graves, incluyendo aspergilosis invasiva. La identificación temprana de esta enfermedad genética es crucial para el manejo adecuado y la prevención de complicaciones fatales, aunque en este caso la gravedad y recurrencia de las infecciones condujeron a un desenlace fatal.",
+                "fh_score": 33.5
+            }
+        }
+    },
+    {
+        "article": "Se trata de un hombre de 66 años de edad que vive en la ciudad de Juan Bautista Alberdi de la provincia de Buenos Aires, con antecedentes de hipertensión arterial y trastorno obsesivo compulsivo. Su medicación habitual incluía amlodipina, quetiapina, venlafaxina y ácido valproico. Consultó por presentar fiebre de 39ºC de cuatro días de evolución sin síntomas asociados y se internó para estudio en sala general. Al examen de ingreso se constató un paciente lúcido, sin foco motor, sin trastorno sensitivo ni rigidez de nuca (escala de coma de Glasgow (GCS) 15/15). El resto del examen físico y el laboratorio general no presentaron particularidades. Los cultivos de sangre y orina resultaron negativos, y la tomografía computarizada de encéfalo, tórax, abdomen y pelvis no mostró afecciones. A las 24 horas agregó episodios de desorientación témporo-espacial que alternaban con otros de somnolencia (GCS 13/15). Al examen físico se constató temblor grueso distal en los cuatro miembros. El examen del LCR informó: líquido incoloro, límpido, y aspecto post centrifugado también límpido. Recuento de leucocitos 310/mm3 (mononucleares 54%, polimorfonucleares 46%), hematíes < de 1000/mm3, proteínas 0.76 g/l, glucosa 54 mg/dl (glucemia 120 mg/dl), y ácido láctico 21 mg/dl. Se inició tratamiento empírico con aciclovir 10 mg/kg endovenoso cada 8 horas. Se solicitaron en LCR: PCR para virus de herpes simple (VHS) y para virus de encefalopatía equina del oeste (VEEO) que resultaron no reactivas. Sin embargo, la IgM (ELISA) para EEO resultó positiva en suero y en LCR a los diez días. La RMN de encéfalo evidenció aumento en la intensidad en secuencias FLAIR y T2 a nivel de la región dorsal del tronco encefálico (tanto protuberancial, como también bulbar y mesencefálico), ambos pedúnculos cerebrales y ganglios de la base, con afectación bilateral y ligero predominio ganglio basal derecho. También se observaron múltiples imágenes focales hiperintensas en la sustancia blanca de ambos hemisferios cerebrales. El paciente evolucionó con deterioro del sensorio (GCS 8/15), sin protección de la vía aérea, por lo que ingresó a UTI. Requirió intubación y ventilación mecánica, con utilización de sedación y analgesia. Al ingreso a UTI presentaba: estado ácido-base (EAB) arterial: pH 7.11, pCO2 136 mmHg, pO2 75 mmHg, bicarbonato 43 mEq/l, exceso de base 11 mEq/l, saturación 88% (Con FIO2 21%), ácido láctico 11.5 mg/dl. Se inició la ventilación mecánica con un volumen minuto respiratorio (VMR) de 9.8 litros (volumen tidal 490 ml que corresponde a 6 ml/kg de peso teórico, frecuencia respiratoria 20 por minuto, presión positiva al final de espiración (PEEP) 5 cmH2 O, fracción inspirada de oxígeno 30%) se extrajo sangre para EAB arterial: pH 7.40, pCO2 41 mmHg, pO2 65 mmHg, bicarbonato 28 mEq/l, exceso de base 0 mEq/l, saturación 93%, PAFI 216. Evolucionó sin fiebre, estable hemodinámicamente, con adecuada oxigenación y ritmo diurético. Al suspender sedantes presentó GCS de 3 puntos sobre 10 (correspondiente con evaluación ocular 1 y motor 2 puntos), con rigidez generalizada y reflejos osteotendinosos adecuados, con movimientos rítmicos linguales y peribucales. El electroencefalograma de 12 canales no evidenció descargas patológicas. Al décimo día de inicio de los síntomas presentó apertura ocular y menor rigidez, pero no toleraba la modalidad respiratoria espontánea por hipoventilación e hipercapnia que lo llevaron a hipoxemia transitoria. En el EAB arterial presentó: pH 7.31, pCO2 70 mmHg, pO2 76 mmHg, bicarbonato 35 mEq/l, exceso de base 8 mEq/l bajo asistencia ventilatoria en modalidad espontánea de presión soporte de 5 cmH2 O, frecuencia respiratoria 6 por minuto, PEEP 5 cmH2 O y volumen tidal entre 120-150 ml. Los siguientes días el paciente se conectó, respondiendo órdenes simples y complejas, y movilizó simétricamente los miembros con cierta debilidad. Por intolerancia a las pruebas ventilatorias espontáneas fue traqueostomizado. En la evaluación funcional respiratoria presentaba presión inspiratoria máxima menor a -40 cm de H2 O, presión espiratoria máxima mayor a 80 cm de H2 O, pero continuaba con hipercapnia en la prueba ventilatoria espontánea, por lo que requirió soporte ventilatorio con modalidad controlada. Se realizó ecocardiograma transtorácico que informó cavidades derechas normales, sin signos de hipertensión pulmonar. En la nueva RMN de encéfalo se evidenció disminución de las áreas hiperintensas en secuencias FLAIR y T2 visibles previamente.\n\nEl enfermo evolucionó con requerimiento de menor soporte ventilatorio en forma progresiva al momento del desarrollo de este informe.",
+        "gold_summary": "Presentamos el caso de un varón de 66 años de edad oriundo de la ciudad Juan Bautista Alberdi de la provincia de Buenos Aires con antecedentes de hipertensión arterial y trastorno obsesivo compulsivo. Consultó por fiebre súbita de cuatro días de evolución, con desarrollo de encefalopatía durante su internación. La punción lumbar mostró un líquido cefalorraquídeo cristalino, aunque inflamatorio de predominio mononuclear. La RMN de encéfalo informó hiperintensidad en secuencias FLAIR y T2 en el dorso del tronco encefálico. Ingresó a terapia intensiva por deterioro neurológico y acidosis respiratoria grave, requiriendo asistencia ventilatoria mecánica. Luego de 10 días presentó mejoría neurológica, sin déficit motor pero con hipoventilación alveolar que dificultaron el destete del respirador.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un hombre de 66 años se puso muy enfermo. Tenía fiebre y estaba confundido. Los doctores le hicieron una prueba con líquido de su espalda. El líquido estaba un poco inflamado. Le hicieron fotos especiales a su cabeza y vieron partes que estaban diferentes. El hombre tuvo que ir a un lugar especial del hospital para que lo cuidaran mucho. No podía respirar bien solo y necesitó una máquina para ayudarlo a respirar. Después de 10 días, empezó a mejorar y podía moverse bien. Pero todavía le costaba respirar sin la máquina. Los doctores lo están cuidando para que se ponga mejor.",
+                "fh_score": 79.38
+            },
+            "B2": {
+                "text": "**Caso de un Hombre con Fiebre y Problemas Cerebrales**\n\nUn hombre de 66 años, que vivía en Juan Bautista Alberdi, Buenos Aires, tenía antecedentes de presión alta y un trastorno llamado obsesivo compulsivo. Él llegó al hospital porque tenía fiebre alta durante cuatro días. Al principio, estaba consciente y sin problemas en sus movimientos o sensibilidad.\n\n**Lo que Encontraron**\n\nDespués de un día, empezó a confundirse y a estar somnoliento. Le hicieron una punción lumbar, que es cuando se extrae un poco de líquido del cerebro para analizarlo. Este líquido estaba claro pero mostraba signos de inflamación, especialmente con células llamadas mononucleares, que son parte del sistema inmunológico. Una resonancia magnética (una imagen del cerebro) mostró zonas inflamadas en una parte del cerebro llamada tronco encefálico.\n\n**Qué Pasó Después**\n\nSu estado empeoró y tuvo problemas para respirar bien, por lo que fue llevado a la unidad de cuidados intensivos. Allí, necesitó un respirador para ayudarle a respirar porque su cuerpo no eliminaba bien el dióxido de carbono, lo que causaba un problema llamado acidosis respiratoria. Después de 10 días, mejoró en cuanto a la conciencia y no tenía problemas para mover sus brazos y piernas, pero seguía teniendo dificultades para respirar por sí solo, lo que complicó que pudiera dejar el respirador.\n\n**Resumen**\n\nEste caso muestra cómo una infección o inflamación en el cerebro puede causar fiebre, confusión y problemas graves para respirar. Aunque el paciente mejoró su estado mental y motor, la función respiratoria tardó más en recuperarse.",
+                "fh_score": 57.24
+            },
+            "B3": {
+                "text": "**Contexto**  \nSe trata de un hombre de 66 años con antecedentes de hipertensión arterial y trastorno obsesivo compulsivo, que residía en Juan Bautista Alberdi, provincia de Buenos Aires. Fue hospitalizado tras presentar fiebre alta (39ºC) durante cuatro días sin otros síntomas iniciales. En el ingreso, estaba consciente y sin signos neurológicos focales, pero a las 24 horas desarrolló episodios alternantes de desorientación y somnolencia, junto con temblor en las extremidades.\n\n**Hallazgos Clave**  \n- La punción lumbar reveló un líquido cefalorraquídeo (LCR) claro pero con signos de inflamación, mostrando un aumento de leucocitos con predominio mixto (mononucleares y polimorfonucleares), proteínas elevadas y glucosa normal.  \n- Los cultivos de sangre y orina fueron negativos, así como las pruebas PCR para virus herpes simple y encefalopatía equina del oeste en LCR. Sin embargo, la detección de anticuerpos IgM específicos para encefalopatía equina del este (EEO) fue positiva tanto en suero como en LCR, confirmando la infección viral.  \n- La resonancia magnética (RMN) cerebral mostró áreas de mayor intensidad en secuencias FLAIR y T2 localizadas en la región dorsal del tronco encefálico (incluyendo protuberancia, bulbo y mesencéfalo), ambos pedúnculos cerebrales y ganglios basales, con afectación bilateral y predominio en el ganglio basal derecho. También se observaron múltiples lesiones en la sustancia blanca de ambos hemisferios cerebrales.  \n- El paciente presentó deterioro neurológico progresivo con disminución del nivel de conciencia (escala de Glasgow reducida a 8/15), requiriendo ingreso a unidad de terapia intensiva (UTI), intubación y ventilación mecánica debido a insuficiencia respiratoria con acidosis respiratoria grave (pH 7.11, pCO2 136 mmHg).  \n- Posteriormente, mostró mejoría neurológica parcial, con apertura ocular y respuesta a órdenes simples, sin déficit motor significativo, pero persistió con hipoventilación alveolar (disminución de la capacidad para ventilar adecuadamente los pulmones), lo que dificultó el destete de la ventilación mecánica y motivó la realización de traqueostomía.  \n- La RMN de control evidenció reducción de las lesiones inflamatorias previamente observadas.\n\n**Interpretación Clínica**  \nEl cuadro clínico y los estudios complementarios son compatibles con una encefalitis viral causada por el virus de la encefalopatía equina del este, una infección poco frecuente en humanos pero con potencial severo. La inflamación del tronco encefálico y ganglios basales explica el deterioro neurológico y la afectación respiratoria, dado que estas áreas controlan funciones vitales como la respiración. La hipoventilación persistente refleja compromiso del centro respiratorio, dificultando la recuperación completa y la independencia ventilatoria.\n\n**Próximos Pasos**  \nEl manejo continuó con soporte ventilatorio adaptado a la capacidad respiratoria del paciente, monitorización neurológica estrecha y seguimiento por imágenes para evaluar la evolución de las lesiones cerebrales. Se recomienda rehabilitación neurológica y respiratoria para mejorar la función muscular y ventilatoria. Además, es fundamental mantener vigilancia para posibles complicaciones infecciosas o neurológicas asociadas. El pronóstico dependerá de la recuperación neurológica y la capacidad para mantener una ventilación adecuada sin soporte mecánico.",
+                "fh_score": 32.04
+            }
+        }
+    },
+    {
+        "article": "Mujer de 27 años de edad oriunda del interior de la Provincia de Buenos Aires sin antecedentes personales o familiares de relevancia, consultó por sangrado vaginal. El estudio colposcópico evidenció formación polipoide que protruía por el orificio cervical externo (OCE). Se arribó clínicamente al diagnóstico de mioma nascens y se tomó una muestra de biopsia para su evaluación. Ante el diagnóstico patológico de sarcoma, se instauró quimioterapia, con el fin de reducir la masa lesional. Una vez lograda la reducción del tamaño, se decidió derivarla a nuestra institución para realizar tratamiento quirúrgico. Se recibió una pieza de histerectomía total con anexos, f ijada en formol al 10%. Cuerpo de 5 × 5 × 3.2 cm, cuello de 3.5 × 3 × 2 cm, ambas trompas de 4.5 × 0.7 cm y ovarios de 4 × 2.5 × 2.5 cm. A la apertura de la pieza, se observó a nivel de la unión cérvico-ístmica una formación polipoide pediculada de 8.5 cm de diámetro, que emergía hacia el canal endocervical y se exteriorizaba por el OCE. La superficie externa era parda, lobulada, con sectores rojizos. Al corte, se observaba blanquecina, blanda, con sectores de aspecto gelatinoso y formaciones quísticas de hasta 0,6 cm de dimensión máxima. Luego del procesamiento de rutina, se efectuaron secciones histológicas y se colorearon con hematoxilina-eosina (H-E), las cuales evidenciaron sectores celulares alternados por áreas laxas, mixoides junto a glándulas ístmico-endometriales típicas. La proliferación, predominantemente fusocelular atípica se disponía en nidos, constituidos por células de amplio citoplasma eosinófilo y núcleos excéntricos con cromatina homogénea, algunos pleomórficos. Se apreciaron estriaciones citoplasmáticas transversales en dichas células. El estroma era ampliamente mixoide y ricamente vascularizado. Se destacaban focalmente áreas celulares densamente condensadas inmediatas y próximas al revestimiento epitelial intacto, pero separadas de él, por una fina capa de estroma laxo. Esto se conoce como cambium layer o capa cambial. Se realizaron técnicas de inmunohistoquímica para desmina, actina músculo específico (AME) y miogenina (MYF4), las cuales resultaron positivas, mientras que la actina músculo liso fue negativa. Esta inmunomarcación permitió comprobar la estirpe muscular estriada y en última instancia arribar al diagnóstico, junto al cuadro morfológico, de RMS embrionario. Asimismo, la presencia de rabdomioblastos agrupados constituyendo la capa cambial a nivel subepitelial resultó fundamental y necesario para tipificar al RMS embrionario como botrioide, independientemente de la presentación macroscópica en forma de racimos polipoides.",
+        "gold_summary": "Presentamos el caso de una mujer de 27 años que consultó por sangrado vaginal y en quien se evidenció en la colposcopia, una lesión polipoide blanquecina que se exteriorizaba a través del orificio cervical externo. El estudio histológico reveló sectores celulares alternados por áreas laxas, mixoides, junto a glándulas ístmico-endometriales típicas. La proliferación fusocelular atípica, se disponía en nidos, constituidos por células de amplio citoplasma eosinófilo con estriaciones citoplasmáticas transversales y núcleos excéntricos con cromatina homogénea. Se exhibían áreas de células densamente condensadas inmediatas y próximas al revestimiento epitelial intacto, pero separadas de él, por una fina capa de estroma laxo (capa cambial). El perfil de inmunomarcación resultó positivo para desmina, actina músculo específico y miogenina, y negativo para actina músculo liso. Se realizó diagnóstico de rabdomiosarcoma embrionario botroide de cuerpo uterino.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una mujer joven tenía sangrado y una bolita en su cuerpo. Los doctores miraron la bolita con cuidado. Vieron que estaba hecha de muchas células diferentes. Estas células eran especiales y venían de un músculo. Los doctores dijeron que la bolita era un tipo de enfermedad que necesita tratamiento. Ellos cuidarán mucho a la mujer para ayudarla a estar mejor.",
+                "fh_score": 70.64
+            },
+            "B2": {
+                "text": "Caso de una mujer joven con sangrado vaginal\n\nUna mujer de 27 años fue al médico porque tenía sangrado vaginal. Al examinarla con un colposcopio (un instrumento que permite ver el cuello del útero), encontraron una lesión con forma de pólipo que salía por el orificio del cuello uterino. Esta lesión era de color blanquecino y tenía una superficie irregular.\n\nLo que encontraron en el laboratorio\n\nSe tomó una muestra de la lesión para analizarla bajo el microscopio. Los científicos vieron diferentes tipos de células: algunas estaban agrupadas en nidos y tenían un citoplasma (la parte de la célula fuera del núcleo) amplio y con un color rosado. Estas células también mostraban unas líneas transversales llamadas estriaciones, que indican que son células musculares especiales. Cerca de la superficie de la lesión, había una capa delgada de células muy densas, separadas del revestimiento normal por una capa de tejido blando llamada estroma laxo. Esta capa se llama “capa cambial” y es característica de ciertos tumores.\n\nCómo confirmaron el diagnóstico\n\nPara saber qué tipo de tumor era, usaron pruebas especiales que detectan proteínas en las células. Encontraron que las células tenían proteínas llamadas desmina, actina músculo específico y miogenina, que están presentes en músculos estriados (los músculos que usamos para movernos). No encontraron actina de músculo liso, que es otro tipo de músculo. Con esta información y la apariencia de las células, diagnosticaron un rabdomiosarcoma embrionario botrioide. Este es un tipo raro de tumor canceroso que se origina en células musculares jóvenes y se presenta en el cuerpo uterino.\n\nEn resumen, esta paciente tenía un tumor maligno muscular en el cuello del útero que se identificó gracias a la combinación de estudios visuales, microscópicos y de proteínas. El diagnóstico permitió iniciar un tratamiento adecuado para su condición.",
+                "fh_score": 54.98
+            },
+            "B3": {
+                "text": "**Contexto**  \nSe presenta el caso de una mujer joven de 27 años, sin antecedentes médicos relevantes, que consultó debido a sangrado vaginal. Durante la colposcopia (un examen visual del cuello uterino), se identificó una lesión con forma de pólipo blanquecino que sobresalía a través del orificio cervical externo (la abertura del cuello uterino hacia la vagina). Inicialmente, se sospechó un mioma nascens (un tipo de tumor benigno), pero la biopsia reveló un diagnóstico diferente.\n\n**Hallazgos Clave**  \nEl análisis microscópico del tejido mostró una combinación de áreas celulares densas y otras más laxas con características mixoides (tejido con apariencia gelatinosa), junto con glándulas típicas del istmo y endometrio (zonas del cuello y cuerpo uterino). La proliferación celular predominante estaba formada por células fusiformes (alargadas) atípicas organizadas en grupos o nidos. Estas células tenían un citoplasma amplio y rosado (eosinófilo), con estriaciones transversales visibles en el citoplasma, y núcleos excéntricos con cromatina homogénea, aunque algunos mostraban variabilidad en forma y tamaño (pleomorfismo).  \n\nAdemás, se observaron áreas específicas de células muy condensadas justo debajo del revestimiento epitelial intacto, separadas de este por una delgada capa de tejido conectivo laxo, conocida como “capa cambial”. Esta característica es importante para clasificar el tumor.  \n\nLas pruebas inmunohistoquímicas, que detectan proteínas específicas en las células, mostraron positividad para desmina, actina músculo específico y miogenina, marcadores que indican la presencia de células musculares estriadas (músculo esquelético). Por otro lado, la actina de músculo liso fue negativa, lo que ayudó a descartar otros tipos de tumores musculares.\n\n**Interpretación Clínica**  \nCon base en las características morfológicas y los resultados inmunohistoquímicos, se estableció el diagnóstico de rabdomiosarcoma embrionario botrioide, un tipo raro y agresivo de tumor maligno que se origina en células musculares estriadas y que en este caso afectaba el cuello uterino. La presencia de la capa cambial y la agrupación de rabdomioblastos (células tumorales características) fueron fundamentales para identificar esta variante específica.\n\n**Próximos Pasos**  \nTras el diagnóstico, la paciente recibió tratamiento con quimioterapia para reducir el tamaño del tumor. Posteriormente, se realizó una cirugía de histerectomía total con anexos (extirpación del útero, trompas y ovarios) para eliminar completamente la lesión. El seguimiento y manejo continuarán en función de la respuesta al tratamiento y la evolución clínica.  \n\nEste caso resalta la importancia de una evaluación cuidadosa y multidisciplinaria para diagnosticar correctamente tumores poco comunes que pueden presentarse con síntomas comunes como el sangrado vaginal.",
+                "fh_score": 30.81
+            }
+        }
+    },
+    {
+        "article": "Un hombre de 53 años de edad, que inició diálisis por disfunción renal en etapa terminal debido a nefropatía diabética o nefroesclerosis en nuestro departamento de nefrología 10 años antes, se sometió a una ecocardiografía de seguimiento anual para estenosis valvular aórtica progresiva (AVS) y regurgitación moderada con fracción de eyección ventricular izquierda (LVEF) normal. Un año antes, se observaron calcificaciones que sugerían MAC en el anillo mitral posterior, que no se habían visto dos años antes. En el último seguimiento, la ecocardiografía reveló una masa redonda de superficie lisa de 22 × 17 mm con alta ecogenicidad en el área circundante y un brillo interno ligeramente disminuido en el anillo mitral posterior del lado auricular izquierdo. El paciente no tenía síntomas significativos ni hallazgos físicos, excepto un soplo sistólico.\n\nLa ecocardiografía también reveló una VS moderada con un flujo de pico valvular transaórtico de 3,76 m/s y una regurgitación valvular aórtica moderada. Se observó una regurgitación mitral leve pero no estenosis. El patrón de velocidad de flujo de entrada del VI mostró un patrón pseudo-normal con un agrandamiento de la aurícula izquierda de 47 mm de diámetro. La ecocardiografía en serie durante dos años reveló un agrandamiento del VI y una disminución de la FEVI. El diámetro final diastólico/final sistólico del VI y la FEVI fueron de 50/33 mm y 64 %, respectivamente, hace dos años; 57/41 mm y 52 % hace un año; y 59/47 mm y 42 % en el último seguimiento.\n\nTeniendo en cuenta el estado de la hemodiálisis, predijimos la progresión a una AVS casi severa, con empeoramiento de la disfunción sistólica del LV, que se convertiría en una indicación para el reemplazo de la válvula aórtica (AVR) en un futuro cercano.\n\nLa tomografía computarizada (TC) reveló una masa de alta densidad sin realce de contraste. La resonancia magnética (MRI) mostró una masa bien definida de alta intensidad en el centro, con un borde hipointenso en la imagen T1 y una señal desprovista en T2. Se excluyeron los neoplasmas, incluidos los mixomas y los fibroelastomas papilares, en función de sus características de imagen. Los hallazgos de laboratorio no indicaron infección, y no se sospechó de vegetación con endocarditis infecciosa. Teniendo en cuenta la disfunción renal en etapa terminal en la hemodiálisis y los hallazgos de imagen, se sospechó CCMA. El rápido agrandamiento de la masa generó preocupación sobre una potencial embolia. En consecuencia, la masa se resecó con AVR.\n\nLa incisión del atrio izquierdo reveló una masa por debajo del endocardio auricular en el anillo de la válvula mitral (P1-2); se observaron sustancias cremosas en la incisión de la masa, lo que sugiere CCMA. Después de la extirpación y desbridamiento del tejido, el sitio de la incisión se suturó con prolina. Se realizó el reemplazo de la válvula aórtica utilizando una válvula SJM de 21 mm. La retirada del bypass cardiopulmonar fue relativamente suave. Al momento del alta, se prescribió warfarina y aspirina, junto con bisoprolol para la fibrilación auricular paroxística después de la cirugía.\n\nNo se observaron eventos embólicos antes o después de la cirugía.\n\nEl examen histopatológico reveló calcificaciones granulares y nodulares dispersas, que consistían principalmente en infiltración de células inflamatorias y proliferación vascular de neutrófilos, linfocitos, células espumosas, macrófagos tisulares y células plasmáticas, con osificación parcial compatible con CICM. La biopsia miocárdica LV para descartar cardiomiopatía secundaria y la válvula aórtica resecada mostraron células inflamatorias similares a las observadas en CICM. Por lo tanto, se diagnosticó CICM en base a la disminución del movimiento de la pared y la fibrosis miocárdica, con infiltración de células inflamatorias > 14 mm2, células T CD3 positivas > 7/mm2 y negatividad de tenascina C (4C8).7 Sin embargo, no se pudo determinar la causa de CICM.\n\nLa ecocardiografía 6 meses después de la resección no mostró recurrencia del tumor (ver material complementario en línea), ni progresión de la regurgitación mitral, función normal de la válvula aórtica protésica y ninguna mejora de la FEVI (41 %)\n\n",
+        "gold_summary": "Un hombre de 52 años con insuficiencia renal en fase terminal que requería hemodiálisis se sometió a una ecocardiografía anual de seguimiento para detectar una disfunción valvular aórtica. La ecocardiografía reveló una masa circular bien definida de 22 × 17 mm en el anillo de la valva mitral posterior que no se había detectado 2 años antes. En función de las características de la imagen, se sospechó que la masa era un CCMA. Se había agrandado rápidamente y suponía un riesgo potencial de embolia; por lo tanto, se extirpó al mismo tiempo que la sustitución de la válvula aórtica. Aunque se sospechó un CCMA en función de los hallazgos intraoperativos, el diagnóstico histopatológico fue un CAT. Tras el análisis histológico de la muestra de miocardio del ventrículo izquierdo y la válvula aórtica extirpada, se observó una infiltración de células inflamatorias crónicas; por lo tanto, se diagnosticó una cardiomiopatía inflamatoria crónica.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había un hombre que tenía problemas en sus riñones. Tenía un huesito en su corazón que creció mucho y podía hacerle daño. Los doctores vieron el huesito con una máquina especial. Decidieron quitarlo para que el hombre estuviera mejor. También le pusieron una nueva parte en su corazón para que funcione bien. Cuando miraron el huesito con un microscopio, vieron que había muchas células que estaban peleando dentro. Eso les dijo que su corazón estaba un poco enfermo por dentro. Ahora el hombre está más seguro y los doctores lo cuidan mucho.",
+                "fh_score": 77.72
+            },
+            "B2": {
+                "text": "**Lo que pasó con el paciente**  \nUn hombre de 52 años tenía problemas graves en sus riñones y necesitaba hemodiálisis, que es un tratamiento para limpiar la sangre cuando los riñones no funcionan bien. Cada año, le hacían una ecocardiografía, que es un examen con ultrasonido para ver cómo está funcionando su corazón y sus válvulas.\n\n**Lo que encontraron en el corazón**  \nEn el último examen, vieron una masa redonda de 22 × 17 mm en una parte del corazón llamada anillo mitral posterior. Esta masa no estaba ahí dos años antes. Por las imágenes, pensaron que podía ser una calcificación caseosa del anillo mitral (CCMA), que es una acumulación dura y blanda de calcio en esa zona. La masa había crecido rápido y podía causar problemas si pedazos se soltaban y viajaban por la sangre (embolias).\n\n**Qué hicieron los médicos**  \nDecidieron quitar la masa y al mismo tiempo reemplazar la válvula aórtica, que también estaba dañada. Durante la cirugía, vieron que la masa tenía un aspecto cremoso, lo que apoyaba la idea de que era una CCMA.\n\n**Lo que mostraron los análisis después de la cirugía**  \nCuando examinaron la masa bajo el microscopio, encontraron que no era solo calcio, sino también muchas células inflamatorias, lo que indicaba una inflamación crónica en el corazón. Además, analizaron muestras del músculo del corazón y de la válvula aórtica y vieron signos similares de inflamación. Por eso, diagnosticaron al paciente con una cardiomiopatía inflamatoria crónica, que es una enfermedad donde el músculo del corazón está inflamado por mucho tiempo.\n\n**Estado después de la cirugía**  \nSeis meses después, el corazón no mostró que la masa hubiera vuelto, y la válvula nueva funcionaba bien. Sin embargo, la función del ventrículo izquierdo, que es la parte del corazón que bombea la sangre, no mejoró mucho.\n\n**Resumen final**  \nEste caso muestra cómo una masa en el corazón que parecía ser una calcificación pudo ser en realidad una inflamación crónica del músculo cardíaco. La cirugía ayudó a prevenir posibles problemas graves, pero la función del corazón seguía afectada.",
+                "fh_score": 60.6
+            },
+            "B3": {
+                "text": "**Contexto**  \nUn hombre de 53 años con insuficiencia renal terminal en hemodiálisis, causada por nefropatía diabética o nefroesclerosis, fue seguido durante 10 años en un servicio de nefrología. Presentaba estenosis valvular aórtica progresiva y regurgitación moderada, con función ventricular izquierda inicialmente normal. En controles ecocardiográficos anuales se detectó la aparición y rápido crecimiento de una masa en el anillo mitral posterior, que generó preocupación por riesgo de embolia.\n\n**Hallazgos Clave**  \nLa ecocardiografía mostró una masa redonda, bien delimitada, de 22 × 17 mm en el anillo mitral posterior, con características ecogénicas sugestivas de calcificación. La función del ventrículo izquierdo se deterioró progresivamente en dos años, con disminución de la fracción de eyección del 64 % al 42 %. La tomografía computarizada y la resonancia magnética descartaron tumores comunes como mixomas o fibroelastomas papilares, y no hubo evidencia de infección ni endocarditis. Por el contexto clínico y las imágenes, se sospechó una calcificación caseosa del anillo mitral (CCMA), una forma rara de calcificación valvular.\n\nDado el rápido crecimiento de la masa y el riesgo de embolia, se decidió extirparla quirúrgicamente junto con el reemplazo de la válvula aórtica. Durante la cirugía, se observó una masa con contenido cremoso típica de CCMA. Sin embargo, el análisis histopatológico reveló que la masa correspondía a un tumor calcificado atípico (CAT), caracterizado por calcificaciones nodulares y una infiltración inflamatoria crónica con células como neutrófilos, linfocitos, macrófagos y células plasmáticas. Además, la biopsia del músculo cardíaco del ventrículo izquierdo y la válvula aórtica resecada mostraron infiltración similar, lo que llevó al diagnóstico de una cardiomiopatía inflamatoria crónica (CICM). No se pudo determinar la causa exacta de esta inflamación.\n\n**Interpretación Clínica**  \nEste caso ilustra la complejidad diagnóstica de masas en el anillo mitral en pacientes con insuficiencia renal terminal y hemodiálisis, donde la calcificación caseosa puede simular tumores o lesiones inflamatorias. La progresión rápida y el riesgo embolígeno justificaron la cirugía. El diagnóstico definitivo mediante histología fue fundamental para identificar una cardiomiopatía inflamatoria crónica asociada, que podría explicar la disfunción ventricular progresiva observada.\n\n**Próximos Pasos**  \nSe realizó un seguimiento ecocardiográfico a los 6 meses postoperatorios que mostró ausencia de recurrencia de la masa, función normal de la válvula aórtica protésica y estabilidad de la regurgitación mitral, aunque sin mejoría en la función ventricular izquierda (fracción de eyección 41 %). El paciente recibió tratamiento anticoagulante y manejo para fibrilación auricular paroxística. Se recomienda continuar el seguimiento cardiológico para monitorizar la función ventricular y detectar posibles complicaciones asociadas a la cardiomiopatía inflamatoria crónica.",
+                "fh_score": 31.7
+            }
+        }
+    },
+    {
+        "article": "Paciente masculino de 28 años, sin antecedentes de importancia, acude a consulta de dermatología con un cuadro cutáneo de 48 horas de evolución caracterizado por dos placas eritematosas con ampollas centrales más ulceración superficial localizadas en cara flexora de brazo y antebrazo derecho equidistantes del pliegue del codo, acompañadas de una sensación de ardor y prurito en el lugar de las lesiones. No presentó síntomas sistémicos ni se automedicó. Como antecedente refiere que se encontraba de vacaciones en la región costera de Ecuador al momento de aparecer las lesiones. Se realizó una biopsia incisional que reportó epidermis con acantosis, paraqueratosis y espongiosis, neutrófilos en estrato córneo e infiltrado linfocitario perivascular en dermis superficial, media y profunda. Por las características clínicas, el antecedente de viaje a una región tropical y los hallazgos histológicos se diagnosticó como dermatitis por Paederus. Se indicó tratamiento con antihistamínicos, esteroides tópicos y compresas frías. Después de 8 días de tratamiento, las lesiones remitieron dejando una hiperpigmentación postinflamatoria.",
+        "gold_summary": "Se comunica el caso de un paciente masculino de 28 años, que acude a consulta de dermatología con cuadro de 48 horas de evolución de dos placas eritematosas con ampollas centrales más ulceración superficial localizadas en cara flexora de brazo y antebrazo derecho, acompañadas de una sensación de ardor y prurito en el lugar de las lesiones, sin síntomas acompañantes. Como antecedente refiere que se encontraba de vacaciones en la región costera de Ecuador al momento de aparecer las lesiones. Se realizó una biopsia incisional y por las características clínicas y el antecedente de viaje a una región tropical se diagnosticó como dermatitis por Paederus y se indicó tratamiento con antihistamínicos, esteroides tópicos y compresas frías. Después de 8 días de tratamiento, las lesiones remitieron dejando una hiperpigmentación postinflamatoria.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un hombre se lastimó la piel en su brazo. Tenía dos manchas rojas con ampollas y le picaban y quemaban. Esto pasó después de estar de vacaciones en un lugar con mucho calor y bichos. El doctor vio su piel y dijo que era una irritación por un bicho llamado Paederus. Le dieron medicinas para calmar la picazón y poner frío en su brazo. Después de unos días, la piel mejoró, pero quedó un poco de color diferente donde estaban las manchas.",
+                "fh_score": 88.27
+            },
+            "B2": {
+                "text": "Caso de un joven de 28 años con lesiones en la piel\n\nUn hombre de 28 años fue al dermatólogo porque tenía dos manchas rojas en el brazo y antebrazo derecho. Estas manchas tenían ampollas (pequeñas burbujas llenas de líquido) en el centro y una pequeña herida superficial. Además, sentía ardor y picazón en esas áreas. No tenía otros síntomas ni había tomado medicamentos por su cuenta.\n\nLo que encontraron y cómo lo trataron\n\nEl paciente contó que estaba de vacaciones en la costa de Ecuador cuando aparecieron las lesiones. Para entender mejor qué pasaba, los médicos tomaron una biopsia, que es cuando se extrae un pequeño pedazo de piel para examinarlo bajo el microscopio. En el análisis, vieron cambios en las capas de la piel y células inflamatorias, lo que ayudó a confirmar que tenía dermatitis por Paederus. Esta dermatitis es una irritación causada por un insecto llamado Paederus, común en zonas tropicales.\n\nEl tratamiento incluyó medicamentos para reducir la picazón (antihistamínicos), cremas con esteroides para bajar la inflamación, y compresas frías para aliviar el ardor. Después de ocho días, las lesiones mejoraron, pero quedaron manchas oscuras en la piel, llamadas hiperpigmentación postinflamatoria, que suelen desaparecer con el tiempo.",
+                "fh_score": 59.84
+            },
+            "B3": {
+                "text": "**Contexto**  \nSe presenta el caso de un hombre de 28 años, sin antecedentes médicos relevantes, que consultó en dermatología debido a la aparición de lesiones cutáneas durante las últimas 48 horas. Estas lesiones consistían en dos placas rojas (eritematosas) con ampollas en el centro y una ulceración superficial, localizadas en la parte interna del brazo y antebrazo derecho, equidistantes del pliegue del codo. El paciente describió sensación de ardor y picazón en las zonas afectadas, sin presentar otros síntomas generales ni haber tomado medicamentos por su cuenta. Como antecedente importante, refirió que se encontraba de vacaciones en una zona costera tropical de Ecuador cuando aparecieron las lesiones.\n\n**Hallazgos Clave**  \nSe realizó una biopsia incisional de la piel afectada, cuyo análisis microscópico mostró:  \n- Engrosamiento de la epidermis (acantosis)  \n- Presencia de células muertas con núcleo (paraqueratosis)  \n- Acumulación de líquido entre las células epidérmicas (espongiosis)  \n- Infiltración de neutrófilos (un tipo de glóbulo blanco) en la capa más superficial de la piel (estrato córneo)  \n- Presencia de un infiltrado inflamatorio linfocitario alrededor de los vasos sanguíneos en las capas superficiales, medias y profundas de la dermis (la capa intermedia de la piel).\n\n**Interpretación Clínica**  \nLa combinación de las características clínicas, el antecedente de exposición en una región tropical y los hallazgos histológicos permitió establecer el diagnóstico de dermatitis por Paederus. Esta condición es una inflamación cutánea causada por el contacto con un insecto del género Paederus, que libera una toxina irritante al ser aplastado sobre la piel.\n\n**Próximos Pasos y Tratamiento**  \nEl tratamiento indicado incluyó antihistamínicos para aliviar la picazón, esteroides tópicos para reducir la inflamación y la aplicación de compresas frías para calmar la zona afectada. Tras ocho días de tratamiento, las lesiones desaparecieron, aunque dejaron una hiperpigmentación postinflamatoria, es decir, una mancha oscura residual en la piel debido a la inflamación previa.\n\nEste caso resalta la importancia de considerar la dermatitis por Paederus en pacientes con lesiones cutáneas agudas tras viajes a regiones tropicales, y la efectividad del tratamiento tópico combinado para su resolución.",
+                "fh_score": 31.14
+            }
+        }
+    },
+    {
+        "article": "Un hombre de 35 años de edad, herido en un accidente de tráfico, fue trasladado a nuestro hospital, que está equipado con un ER híbrido. Había sufrido una lesión potencialmente mortal, con su pierna derecha acortada y girada. Los signos vitales del paciente a su llegada fueron los siguientes: frecuencia respiratoria de 24 respiraciones/min, saturación de oxígeno del 99 % con 12 L de administración de oxígeno, frecuencia cardiaca de 143 latidos/min, presión arterial de 80/40 mmHg, y puntuación de Glasgow Coma Scale de E4V4M6. Intentamos realizar un TAC y resucitar al paciente. El TAC reveló un hemotórax izquierdo, ensanchamiento del mediastino, y fractura pélvica. Como la presión arterial del paciente cayó rápidamente antes del TAC, se administraron procedimientos de salvamento, como intubación de emergencia, preperitoneal pelvic packing, y transfusión masiva, con un cuidadoso control de la presión arterial en el ER híbrido. Después de la estabilización de los signos vitales con estos procedimientos, el TAC con contraste reveló una fractura de BTAI de grado IV que se extendía hacia la cavidad torácica izquierda. La embolización arterial transcatéter (TAE) para la fractura pélvica y la fijación esquelética externa de la fractura del fémur derecho se realizaron primero, ya que el radiólogo y el cirujano cardiovascular, que realizan TEVAR en nuestro centro médico, no estaban disponibles en ese momento. Posteriormente, se realizó TEVAR utilizando un injerto de stent (GORE C-TAG 26 × 150 mm; WL Gore & Associates, Flagstaff, Arizona, EE. UU.) en el ER híbrido sin transferir al paciente. Se desplegó un injerto de stent justo distal de la arteria carótida común izquierda (zona II) y el extremo distal del injerto de stent se posicionó en el nivel de Th 8. Decidimos sacrificar LSCA ya que el flujo sanguíneo de la arteria vertebral izquierda fue suficiente según lo evaluado por angiografía. El paciente no tuvo síntomas que sugirieran isquemia después de TEVER. Durante la cirugía, se administraron 50 unidades/kg (3000 unidades) de heparina. El paciente fue trasladado a un hospital de rehabilitación el día 41 postoperatorio.\n",
+        "gold_summary": "Un hombre de 35 años de edad sufrió múltiples lesiones tras un accidente de tráfico y fue trasladado a nuestro hospital en estado de shock. La tomografía computarizada reveló una fractura de TAI de grado IV que se extendía hasta la cavidad torácica y una fractura pélvica. Poco tiempo después de realizar un relleno pélvico preperitoneal y una embolización arterial transcatéter para la fractura pélvica, se realizó un TEVAR en el quirófano híbrido sin trasladar al paciente. El paciente fue trasladado a un hospital de rehabilitación el día 41 después de la operación.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un hombre se lastimó mucho en un accidente. Su pierna estaba muy dañada y tenía huesos rotos en el cuerpo. Los doctores le hicieron muchas cosas para ayudarlo a estar mejor. Usaron una máquina para ver dentro de su cuerpo y encontraron problemas grandes. Luego, le pusieron un tubo especial para arreglar su corazón y sus huesos. El hombre se quedó en el hospital mucho tiempo. Después, fue a otro lugar para aprender a caminar y estar fuerte otra vez.",
+                "fh_score": 81.93
+            },
+            "B2": {
+                "text": "**Lo que pasó con el paciente**  \nUn hombre de 35 años tuvo un accidente de tráfico grave y llegó al hospital en estado muy delicado. Tenía varias heridas, incluyendo una fractura en la pelvis y una lesión grave en la arteria principal del pecho llamada aorta. Esta lesión se llama fractura de TAI de grado IV y puede ser muy peligrosa porque afecta el flujo de sangre al cuerpo.\n\n**Tratamientos que recibió**  \nPrimero, los médicos hicieron un procedimiento llamado relleno pélvico preperitoneal, que ayuda a controlar el sangrado en la pelvis. También realizaron una embolización arterial transcatéter, que es cuando se bloquea una arteria para detener una hemorragia. Después, sin mover al paciente a otro lugar, hicieron una cirugía llamada TEVAR en un quirófano especial que combina imagen y cirugía. En esta operación, colocaron un tubo especial llamado injerto de stent dentro de la arteria dañada para repararla y permitir que la sangre fluya bien.\n\n**Qué pasó después**  \nGracias a estos tratamientos, el paciente se estabilizó y pudo continuar su recuperación. Después de 41 días, fue enviado a un hospital de rehabilitación para seguir mejorando su salud.",
+                "fh_score": 60.19
+            },
+            "B3": {
+                "text": "**Contexto:**  \nUn hombre de 35 años sufrió un grave accidente de tráfico que le provocó múltiples lesiones, incluyendo una fractura grave en la arteria aorta torácica (TAI, por sus siglas en inglés) y fracturas óseas en la pelvis y el fémur derecho. Fue trasladado a un hospital equipado con un quirófano híbrido, donde recibió atención de emergencia.\n\n**Hallazgos Clave:**  \nA su llegada, el paciente presentaba signos de shock, con presión arterial muy baja y frecuencia cardíaca elevada. La tomografía computarizada (TAC) mostró un hemotórax (acumulación de sangre en el tórax), ensanchamiento del mediastino (zona central del tórax que contiene el corazón y grandes vasos), una fractura pélvica y una lesión de grado IV en la arteria aorta torácica que se extendía hacia la cavidad torácica izquierda. Además, la pierna derecha estaba acortada y girada, indicando fractura del fémur.\n\n**Interpretación Clínica:**  \nDebido a la gravedad y la inestabilidad hemodinámica del paciente, se realizaron procedimientos de emergencia para controlar el sangrado y estabilizarlo, incluyendo intubación, relleno pélvico preperitoneal (una técnica para controlar hemorragias pélvicas) y transfusión masiva. Posteriormente, se realizó una embolización arterial transcatéter (TAE) para controlar el sangrado de la fractura pélvica y se fijó externamente la fractura del fémur. Finalmente, sin necesidad de trasladar al paciente, se llevó a cabo una reparación endovascular de la aorta torácica (TEVAR) en el quirófano híbrido, utilizando un injerto de stent que se colocó desde justo después de la arteria carótida común izquierda hasta la octava vértebra torácica. Para asegurar un flujo sanguíneo adecuado, se decidió sacrificar la arteria subclavia izquierda, ya que la circulación cerebral estaba garantizada por la arteria vertebral izquierda. Durante la cirugía se administró heparina para prevenir coágulos.\n\n**Próximos Pasos y Resultado:**  \nEl paciente evolucionó favorablemente sin signos de isquemia (falta de riego sanguíneo) tras la intervención. Fue dado de alta al hospital de rehabilitación 41 días después de la cirugía, donde continuó su recuperación.",
+                "fh_score": 40.45
+            }
+        }
+    },
+    {
+        "article": "Hombre de 31 años con antecedentes de consumo de alcohol, tabaco, cocaína inhalada, tuberculosis pulmonar tratada, nefrectomía izquierda y esplenectomía post-traumática. Consultó al servicio de urgencias por cuadro de una semana de evolución que inició inmediatamente posterior a la aplicación intramuscular de penicilina por contacto sexual con pareja con sífilis, caracterizado por dolor en región glútea derecha que irradiaba hasta pie, con posterior aparición de dermatosis purpúrica relacionada con sitio de inyección, siendo una lesión tipo placa configurada en forma anular, con bordes irregulares y distribución racemosa que medía 15 centímetros (cm), con piel sana en su interior. También presentaba una pequeña escara escrotal y una extensa lesión plantar derecha de aspecto livedoide desde la zona talar hasta la punta de los dedos que no respetaba margen estricto. Se realizó ecografía del glúteo mayor, que mostró pérdida del patrón fibrilar heterogéneo, aumento del espesor del mismo a nivel de su tercio medio de aspecto edematoso, además de edema del tejido celular subcutáneo (TCS); en región plantar homolateral y en escroto edema de TCS. En el laboratorio presentó leucocitosis de 13.7 × 109/L, proteína C reactiva de 3.2 mg/dL (normal hasta 0.5 mg/dL), que se interpretaron como reactantes de fase aguda, también aumento de transaminasas con aspartato aminotransferasa de 175 UI/L (normal hasta 32), alanino aminotransferasa de 245 UI/L (normal hasta 33), creatina kinasa con un valor de 2741 UI/L (normal hasta 170) y lactato deshidrogenasa de 2499 UI/L (normal hasta 250) representando compromiso muscular. Se realizaron serologías completas para sífilis, con venereal disease research laboratory (VDRL y anticuerpos treponémicos), virus de la inmunodeficiencia humana (HIV) hepatitis B, hepatitis C, con resultados negativos. La cronología, las manifestaciones clínicas y la posterior biopsia, respaldaron el diagnóstico de síndrome de Nicolau, para lo cual se inició anticoagulación con enoxaparina 1 mg/ kg c/12 hs vía subcutánea, cilostazol 100 mg cada 12 horas y tramadol, por 10 días. Se realizó biopsia de piel de glúteo que evidenció necrosis epidérmica y extensión a epitelio folicular, con formación de ampolla secundaria a reepitelización, sin vasculitis ni trombosis vascular, vinculable a embolia cutis medicamentosa en fase aguda, hubo franca mejoría con descenso de valores de transaminasas, con aspartato aminotransferasa de 39 UI/L, alanino aminotransferasa de 77 UI/L y creatin kinasa de 167 UI/L.  No se solicitó perfil inmunológico, basados en que nuestro diagnóstico presuntivo inicial no justificaba la búsqueda de otras etiologías. Se otorgó alta con cilostazol y analgésicos, control ambulatorio a los 3 meses con mejoría del dolor y de las lesiones, quedando en glúteo derecho cicatriz discrómica con presencia de descamación fina y en pie derecho cicatriz discrómica con zonas de descamación gruesas en región de apoyo tarso metatarsiano asociado a mínimas lesiones livedoides en planta del mismo pie.",
+        "gold_summary": "Se reporta el caso de un hombre de 31 años que presenta este síndrome luego de la aplicación de penicilina benzatínica intramuscular. La biopsia apoyó el diagnóstico. Recibió tratamiento con enoxaparina y cilostazol con posterior mejoría.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un hombre se puso una medicina en el glúteo. Después, le dolió mucho y le salió una mancha en la piel. El doctor vio que la piel estaba lastimada por la medicina. Le dieron medicinas para ayudar y se fue mejorando poco a poco. Ahora está mejor y la piel está sanando.",
+                "fh_score": 88.92
+            },
+            "B2": {
+                "text": "Caso de Síndrome de Nicolau tras Inyección de Penicilina\n\nUn hombre de 31 años recibió una inyección de penicilina para tratar una posible infección por sífilis, debido a que su pareja tenía esta enfermedad. Poco después, comenzó a sentir dolor en la nalga derecha que se extendía hasta el pie. Además, apareció una lesión en la piel cerca del lugar de la inyección, con forma de anillo y bordes irregulares, y otras heridas en el escroto y la planta del pie.\n\nPara entender qué pasaba, los médicos hicieron una ecografía que mostró inflamación en los músculos y tejidos cerca de la lesión. También se hicieron análisis de sangre que indicaron inflamación y daño muscular. Se descartaron otras infecciones como VIH y hepatitis.\n\nSe tomó una biopsia, que es cuando se extrae un pequeño pedazo de piel para examinarlo. Esta mostró que la piel estaba dañada por falta de sangre, pero sin inflamación de los vasos sanguíneos. Todo esto confirmó que el paciente tenía el síndrome de Nicolau, una reacción rara que puede ocurrir después de una inyección y que causa daño en la piel y músculos por bloqueo de vasos sanguíneos.\n\nEl tratamiento incluyó medicamentos para evitar coágulos (enoxaparina) y para mejorar la circulación (cilostazol), además de analgésicos para el dolor. Con este cuidado, el paciente mejoró, sus análisis de sangre volvieron casi a la normalidad y las lesiones en la piel sanaron, quedando solo algunas cicatrices leves.\n\nEste caso muestra la importancia de reconocer el síndrome de Nicolau para tratarlo rápido y evitar daños mayores.",
+                "fh_score": 60.86
+            },
+            "B3": {
+                "text": "**Contexto**  \nSe trata de un hombre de 31 años con antecedentes de consumo de alcohol, tabaco y cocaína inhalada, además de haber tenido tuberculosis pulmonar tratada, y cirugías previas de nefrectomía izquierda y esplenectomía tras un trauma. Consultó en urgencias debido a un cuadro que comenzó una semana antes, inmediatamente después de recibir una inyección intramuscular de penicilina benzatínica, administrada por contacto sexual con una pareja diagnosticada con sífilis.\n\n**Hallazgos Clínicos y Diagnósticos**  \nEl paciente presentó dolor intenso en la región glútea derecha que se irradiaba hacia el pie, acompañado de una erupción cutánea purpúrica (manchas violáceas) en el sitio de la inyección. Esta lesión tenía forma de placa anular (con un borde en forma de anillo irregular) de aproximadamente 15 centímetros, con piel sana en el centro. Además, tenía una pequeña úlcera (escara) en el escroto y una lesión extensa en la planta del pie derecho con aspecto livedoide (patrón vascular irregular), que se extendía desde el talón hasta la punta de los dedos.\n\nLa ecografía del glúteo mostró alteraciones en el músculo mayor, con pérdida de su estructura normal, aumento de grosor y edema (hinchazón por acumulación de líquido) tanto en el músculo como en el tejido subcutáneo (debajo de la piel). Se observó edema también en la región plantar del pie y en el escroto.\n\nLos análisis de sangre revelaron leucocitosis (aumento de glóbulos blancos) y elevación de proteína C reactiva, indicadores de inflamación aguda. Además, hubo un aumento significativo de enzimas hepáticas (transaminasas) y de marcadores musculares como la creatina quinasa y la lactato deshidrogenasa, lo que sugiere daño muscular.\n\nLas pruebas serológicas para sífilis, VIH, hepatitis B y C fueron negativas.\n\nLa biopsia de piel del glúteo evidenció necrosis (muerte celular) epidérmica y afectación del epitelio folicular, con formación de ampollas debido a la reparación de la piel, pero sin signos de vasculitis (inflamación de vasos sanguíneos) ni trombosis (coágulos), lo que apoyó el diagnóstico de síndrome de Nicolau o embolia cutis medicamentosa en fase aguda. Este síndrome es una reacción adversa poco frecuente que ocurre tras la inyección intramuscular de ciertos medicamentos, causando daño vascular y necrosis en la piel y tejidos subyacentes.\n\n**Interpretación Clínica**  \nEl cuadro clínico, la historia temporal relacionada con la inyección de penicilina y los hallazgos histológicos confirmaron el diagnóstico de síndrome de Nicolau. Este diagnóstico explicó el dolor intenso, las lesiones cutáneas y el compromiso muscular observado.\n\n**Tratamiento y Evolución**  \nSe inició tratamiento con anticoagulación mediante enoxaparina (un anticoagulante) y cilostazol (un medicamento que mejora la circulación sanguínea), además de analgésicos para controlar el dolor. Durante la hospitalización, el paciente mostró una franca mejoría, con descenso progresivo de las enzimas hepáticas y musculares a valores cercanos a la normalidad.\n\nNo se realizaron estudios inmunológicos adicionales, dado que el diagnóstico clínico y patológico fue suficiente para explicar el cuadro.\n\nAl alta, el paciente continuó con cilostazol y analgésicos, y en el control ambulatorio a los tres meses presentó mejoría significativa del dolor y de las lesiones cutáneas. Quedaron secuelas en forma de cicatrices con alteraciones en la pigmentación y descamación fina en el glúteo derecho, así como cicatrices similares y mínimas lesiones livedoides en la planta del pie derecho.\n\n**Próximos Pasos**  \nSe recomienda seguimiento clínico para evaluar la evolución de las cicatrices y el manejo del dolor residual, así como evitar futuras inyecciones intramusculares en la zona afectada para prevenir recurrencias. Además, es importante la educación al paciente sobre los riesgos asociados a la administración de medicamentos por vía intramuscular y la vigilancia temprana de síntomas similares.",
+                "fh_score": 38.91
+            }
+        }
+    },
+    {
+        "article": "Un varón de cuatro días de edad, nacido a las 39 semanas y 4 días de gestación, acude a un servicio de urgencias con un empeoramiento de la dificultad respiratoria y el estridor, que se ve agravado por la alimentación y la posición supina.\n\nNació de una madre de 31 años con serología significativa para una prueba de Coomb positiva indirecta, con un parto vaginal sin complicaciones y puntuaciones de APGAR de ocho y nueve en el primer y quinto minuto, respectivamente. Su peso al nacer fue de 3050 g. La ecografía fetal mostró preocupación por un foco intracardíaco, con un embarazo sin complicaciones. El curso de enfermería fue significativo solo por una prueba de audición bilateral fallida y un ecocardiograma normal. El bebé fue dado de alta en el día dos de vida. Se observó que tenía congestión nasal en el momento de la descarga. Se instruyó a la familia para que le aspirara la nariz y usara gotas salinas según fuera necesario.\n\nEn el día cuatro de vida, la madre del lactante notó estridor asociado con dificultad para alimentarse y el pediatra lo derivó al servicio de urgencias. El examen en el servicio de urgencias es significativo para el estridor inspiratorio agudo con tirones traqueales y retracciones subcostal. Además, se observa que tiene pectus excavatum. El estridor y el aumento del trabajo respiratorio mejoran con la posición prona o lateral. La evaluación de laboratorio es significativa para la acidosis respiratoria en el gas sanguíneo venoso [pH 7.18 y CO2 73 mmHg (9,732 Pa)] y el análisis de orina que revela bacterias moderadas y 11-20 glóbulos blancos sin la presencia de nitrito urinario o esterasa leucocitaria. Un recuento sanguíneo completo es tranquilizador. Se le coloca una cánula nasal de alto flujo y se inicia con ampicilina y gentamicina después de obtener cultivos de sangre.\n\nSe le aumentó la presión positiva continua en la vía aérea (CPAP) y se lo trasladó a una unidad de cuidados intensivos neonatales de nivel III para continuar con el tratamiento y la evaluación de otorrinolaringología. Se le introdujo un tubo nasogástrico por las dos fosas nasales sin dificultad. La laringoscopia flexible mostró una cuerda vocal izquierda inmóvil y cavidades nasales estrechas con edema de los cornetes nasales, aritenoides bilaterales y cuerdas vocales. La broncoscopia no reveló ninguna otra anormalidad. El examen físico posterior se caracterizó por rasgos dismórficos sutiles, que incluían orejas de implantación baja, retromicrognatia, microftalmia y clinodactilia de los dedos de los pies. Se interrumpió el tratamiento antibiótico empírico tras un examen infeccioso tranquilizador. Se consultó a un equipo multidisciplinario.\n\nEl paciente finalmente requirió intubación a las dos semanas de vida debido al empeoramiento del fallo respiratorio. Se administraron ciprofloxacina nasal y dexametasona para el edema de las vías respiratorias superiores. Una resonancia magnética del cerebro, cuello y tórax mostró un curso normal de los nervios laríngeos recurrentes. La evaluación genética incluyó un análisis de microarreglo cromosómico normal (CMA). La prueba adicional del panel genético fue positiva para la variante patogénica en el gen CHD7, consistente con el síndrome CHARGE. En este caso, el VFP se atribuyó a la asociación conocida con el síndrome CHARGE. La evaluación continua reveló otras características consistentes con el síndrome CHARGE, incluidos colobomas bilaterales, glaucoma, pérdida auditiva confirmada y anomalías genitales.\n\nLa repetición de la broncoscopia en el día 42 de vida demostró una mejora en el edema laríngeo general, pero continuó con un edema leve de las cuerdas vocales bilaterales. El paciente fue extubado después de la broncoscopia en el marco de un edema de las vías respiratorias mejorado. Sin embargo, fue re-intubado el día 46 de vida debido al empeoramiento de la insuficiencia respiratoria. La repetición de la laringoscopia ese día mostró un edema continuado. En este momento, el paciente ya había recibido múltiples ciclos cortos de Dexamethasone en un intento de disminuir el edema de las vías respiratorias. Debido a la necesidad de re-intubación, fue tratado con Tobramycin tópico y Dexamethasone aplicado directamente a las cuerdas vocales mediante laringoscopia directa durante cinco días. Después de este tratamiento, fue extubado con éxito a los dos meses de edad y se le colocó un tubo de gastrostomía a los tres meses.\n\nEn el momento de la colocación del tubo de gastrotomía, se le realizó una broncoscopia y una microlaringoscopia adicionales que demostraron que la cuerda vocal izquierda afectada originalmente era totalmente móvil, pero que mostraba una nueva inmovilidad de la cuerda derecha; la etiología de esto no está clara. Ambas cuerdas vocales seguían estando ligeramente edematosas, pero habían mejorado mucho desde la evaluación anterior. El paciente fue dado de alta en aire ambiente a los cuatro meses de edad y continúa siendo seguido de cerca por el otorrinolaringólogo. En la laringoscopia ambulatoria de repetición a los cuatro meses de edad, ambas cuerdas aparecían móviles con un edema de las vías respiratorias continuado.\n\n",
+        "gold_summary": "Un bebé de cuatro días de edad, a término, varón, nacido por parto vaginal sin complicaciones, con un curso de enfermería significativo para la falta de audición, se presentó en un departamento de emergencias (DE) con dificultad respiratoria y estridor en aumento. Fue trasladado a una unidad de cuidados intensivos neonatales (UCIN) de nivel III para una evaluación posterior y se le practicó una intubación debido a la hipercarbia progresiva. La laringoscopia reveló una parálisis unilateral de las cuerdas vocales (PCV) del lado izquierdo. Se le sometió a una evaluación posterior que incluyó un cerebro, cuello y tórax normales en una resonancia magnética. Se consultó a genética por la preocupación de los rasgos dismórficos en el examen físico. Después de las pruebas del panel de genes, la PCV se atribuyó a la asociación conocida con el síndrome CHARGE. Se observó un edema de las vías respiratorias en la laringoscopia que impidió la extubación hasta los dos meses de edad. Se identificaron otras características del síndrome CHARGE, incluidos los colobomas, el glaucoma, la pérdida auditiva neurosensorial y las anomalías genitales. Se le dio de alta con aire ambiente y después de la colocación de un tubo de gastrostomía con seguimiento de otorrinolaringología.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un bebé de cuatro días tenía problemas para respirar y hacer ruido al respirar. Lo llevaron al hospital para que lo cuidaran mucho. Los doctores vieron que una cuerda en su garganta no se movía bien. Hicieron pruebas y encontraron que tenía un problema llamado síndrome CHARGE. Este problema puede hacer que los ojos, los oídos y otras partes del cuerpo no estén como deben. El bebé estuvo en el hospital hasta que pudo respirar mejor. Luego, le pusieron un tubito para ayudarlo a comer. Ahora, los doctores lo cuidan para que siga mejorando.",
+                "fh_score": 80.6
+            },
+            "B2": {
+                "text": "**Lo que pasó con el bebé**  \nUn bebé de cuatro días, que nació sin problemas y a término, llegó al hospital porque tenía dificultad para respirar y un sonido extraño al inhalar llamado estridor. En el hospital, los médicos notaron que su respiración empeoraba y que tenía una cuerda vocal izquierda que no se movía, lo que se llama parálisis unilateral de las cuerdas vocales. Esto dificultaba que respirara bien.\n\n**Qué hicieron los médicos**  \nEl bebé fue llevado a una unidad especial para recién nacidos y le pusieron un tubo para ayudarlo a respirar mejor. Le hicieron varios estudios, incluyendo una resonancia magnética, que mostró que su cerebro, cuello y tórax estaban normales. También notaron que tenía algunas características físicas diferentes, como orejas bajas y ojos pequeños, por lo que pidieron ayuda a especialistas en genética.\n\n**El diagnóstico y su significado**  \nDespués de hacer pruebas genéticas, descubrieron que el bebé tenía una condición llamada síndrome CHARGE. Este síndrome puede causar problemas en varias partes del cuerpo, como los ojos (colobomas y glaucoma), pérdida de audición y problemas en los genitales. La parálisis de la cuerda vocal izquierda estaba relacionada con este síndrome.\n\n**El tratamiento y el seguimiento**  \nEl bebé tuvo inflamación en las vías respiratorias, lo que dificultó quitarle el tubo para respirar hasta que tenía dos meses. También le pusieron un tubo especial para alimentarse directamente al estómago (tubo de gastrostomía) a los tres meses. Finalmente, fue dado de alta para seguir en casa, pero continúa con controles médicos para vigilar su respiración y otros problemas relacionados con el síndrome CHARGE.",
+                "fh_score": 55.64
+            },
+            "B3": {
+                "text": "**Contexto**  \nUn recién nacido varón a término, sin complicaciones durante el parto, fue llevado al servicio de urgencias a los cuatro días de vida debido a un empeoramiento de la dificultad para respirar y la presencia de estridor (un sonido respiratorio agudo causado por la obstrucción de las vías aéreas). Estos síntomas se agravaban con la alimentación y al estar acostado boca arriba. En el examen inicial, se detectó también una deformidad torácica llamada pectus excavatum. La dificultad respiratoria mejoraba al colocarlo boca abajo o de lado.  \n\n**Hallazgos Clave**  \n- La evaluación inicial mostró acidosis respiratoria, lo que indica una acumulación de dióxido de carbono en la sangre por dificultad para respirar adecuadamente.  \n- Se inició soporte respiratorio con cánula nasal de alto flujo y posteriormente con presión positiva continua en la vía aérea (CPAP).  \n- La laringoscopia flexible (una exploración visual de la laringe) reveló parálisis unilateral de la cuerda vocal izquierda y edema (hinchazón) en varias estructuras de las vías respiratorias superiores.  \n- Se identificaron rasgos físicos sutiles que sugerían una posible condición genética, incluyendo orejas de implantación baja, mandíbula pequeña (retromicrognatia), ojos pequeños (microftalmia) y deformidades en los dedos de los pies.  \n- La resonancia magnética del cerebro, cuello y tórax fue normal, descartando lesiones estructurales en los nervios laríngeos recurrentes, que controlan las cuerdas vocales.  \n- El análisis genético confirmó la presencia de una mutación patogénica en el gen CHD7, diagnóstico que confirma el síndrome CHARGE, una enfermedad genética que afecta múltiples órganos y sistemas.  \n\n**Interpretación Clínica**  \nLa parálisis de la cuerda vocal izquierda se atribuyó a la asociación conocida con el síndrome CHARGE, que también explicó otros hallazgos clínicos como colobomas bilaterales (defectos en el ojo), glaucoma, pérdida auditiva neurosensorial y anomalías genitales. El edema persistente en las vías respiratorias superiores dificultó la extubación (retirar el tubo de respiración) hasta los dos meses de edad, requiriendo múltiples tratamientos con corticosteroides y antibióticos tópicos aplicados directamente sobre las cuerdas vocales. Posteriormente, se observó una nueva parálisis de la cuerda vocal derecha, cuya causa no está clara, aunque ambas cuerdas vocales mostraron mejoría progresiva.  \n\n**Próximos Pasos y Seguimiento**  \nEl paciente fue dado de alta respirando aire ambiente a los cuatro meses de edad, tras la colocación de un tubo de gastrostomía para alimentación directa al estómago, debido a las dificultades para alimentarse por vía oral. Continúa bajo seguimiento estrecho con otorrinolaringología para monitorizar la función de las cuerdas vocales y el estado de las vías respiratorias. Este caso resalta la importancia de una evaluación multidisciplinaria en recién nacidos con síntomas respiratorios y rasgos dismórficos, para identificar condiciones genéticas complejas como el síndrome CHARGE y manejar sus múltiples complicaciones.",
+                "fh_score": 34.42
+            }
+        }
+    },
+    {
+        "article": "Mujer de 17 años oriunda de Tucumán, acudió a la consulta por cuadro de vías aéreas superiores y hemoptisis leve. La tomografía computarizada de tórax informó, en lóbulo superior derecho, una imagen redondeada de paredes regulares y lisas de 25x24x24 mm, rodeado de un tenue halo periférico en vidrio esmerilado. No se observaba realce ante la administración de contraste endovenoso. Se sugirió un posible quiste broncogénico, por lo que se realizó una RMN de tórax que informó imagen redondeada de paredes regulares y lisas que alcanzó un diámetro anteroposterior de 25 x 24 x 24.5 mm con intensidad de señal líquida. Debido a la localización central de la lesión, se realizó una lobectomía superior derecha videoasistida. Dado que el estudio anatomopatológico intraoperatorio fue indeterminado, se complementó la resección pulmonar con un vaciamiento ganglionar mediastínico. La anatomía patológica definitiva informó neumocitoma esclerosante de 2 x 1.7 cm. La inmunomarcación fue positiva para TTF1, CK, CK7 y napsina.",
+        "gold_summary": "Describimos aquí el caso de una paciente de 17 años con diagnóstico de neumocitoma esclerosante con presentación infrecuente.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una niña de 17 años tenía un bulto en su pulmón. Los doctores lo sacaron con una operación para que ella esté mejor. El bulto no era peligroso.",
+                "fh_score": 88.03
+            },
+            "B2": {
+                "text": "Caso de una joven con un tumor pulmonar poco común\n\nUna chica de 17 años de Tucumán fue al médico porque tenía síntomas en las vías respiratorias y tos con un poco de sangre. Se le hizo una tomografía, que es una imagen especial del pecho, y mostraba una bolita redonda en el pulmón derecho. Esta bolita tenía paredes lisas y un borde un poco borroso. Para entender mejor, le hicieron una resonancia magnética, que confirmó que la imagen parecía un líquido dentro de esa bolita.\n\nComo la lesión estaba en una zona difícil, los médicos decidieron sacar la parte superior del pulmón derecho usando una cirugía asistida por video, que es menos invasiva. Durante la operación, no pudieron saber exactamente qué era la lesión, así que también quitaron algunos ganglios cercanos para analizarlos.\n\nDespués de estudiar el tejido con un microscopio, los especialistas confirmaron que se trataba de un neumocitoma esclerosante. Este es un tipo raro de tumor en el pulmón que generalmente no es canceroso. Para asegurarse, usaron pruebas especiales que detectan ciertas proteínas en las células, y estas pruebas dieron resultados positivos para marcadores típicos de este tumor.\n\nEn resumen, este caso muestra cómo se identificó y trató un tumor pulmonar poco común en una paciente joven, usando diferentes estudios de imagen y cirugía para llegar a un diagnóstico claro.",
+                "fh_score": 56.29
+            },
+            "B3": {
+                "text": "**Contexto:**  \nSe presenta el caso de una joven de 17 años originaria de Tucumán que consultó por síntomas respiratorios superiores acompañados de hemoptisis leve (expectoración con sangre). Los estudios iniciales incluyeron una tomografía computarizada (TC) de tórax que reveló una lesión redondeada de aproximadamente 2.5 cm en el lóbulo superior derecho del pulmón, con bordes regulares y un halo periférico de vidrio esmerilado, sin captación de contraste. Posteriormente, una resonancia magnética (RMN) confirmó la presencia de esta lesión con características líquidas.\n\n**Hallazgos Clave:**  \nDebido a la ubicación central de la lesión, se decidió realizar una lobectomía superior derecha mediante cirugía videoasistida. Durante la operación, el estudio anatomopatológico preliminar no permitió un diagnóstico definitivo, por lo que se amplió la cirugía para incluir un vaciamiento ganglionar mediastínico (extirpación de ganglios linfáticos en el mediastino). El examen histológico final identificó la lesión como un neumocitoma esclerosante, un tumor pulmonar poco frecuente, de tamaño aproximado de 2 x 1.7 cm. Los marcadores inmunohistoquímicos fueron positivos para TTF1, CK, CK7 y napsina, proteínas que ayudan a confirmar el origen pulmonar y la naturaleza del tumor.\n\n**Interpretación Clínica:**  \nEl neumocitoma esclerosante es una neoplasia pulmonar rara que suele presentarse en adultos jóvenes y tiene un comportamiento generalmente benigno o de bajo grado maligno. En este caso, la presentación con hemoptisis y la localización central del tumor hicieron necesaria una intervención quirúrgica completa para su diagnóstico y tratamiento. La confirmación mediante inmunomarcadores es fundamental para diferenciarlo de otras lesiones pulmonares.\n\n**Próximos Pasos:**  \nSe recomienda un seguimiento clínico y radiológico periódico para vigilar la posible recurrencia o complicaciones postoperatorias. La cirugía completa y el vaciamiento ganglionar mediastínico realizados constituyen un manejo adecuado para este tipo de tumor, aunque su pronóstico suele ser favorable. En caso de aparición de nuevos síntomas o hallazgos, se deberá reevaluar para descartar progresión o complicaciones.",
+                "fh_score": 35.61
+            }
+        }
+    },
+    {
+        "article": "Una mujer asiática de 28 años fue admitida en el hospital para el tratamiento de «una masa pélvica durante 10 meses» el 11 de noviembre de 2018. La paciente solía tener menstruación regular, volumen menstrual moderado, dismenorrea y un G1P0L0A1. Examen ginecológico: la parte posterior del útero tenía aproximadamente 8 cm de diámetro con poca actividad y sensibilidad, pero no se observaron otras anomalías. La paciente no tenía una causa obvia de dolor abdominal durante los primeros 10 meses previos al ingreso. El examen de ultrasonido reveló una masa heterogénea en la parte superior derecha del útero con un diámetro de aproximadamente 4 cm, un nódulo del epiplón mayor con un diámetro de aproximadamente 2 cm y un nivel de CA125 sérico de 416 mU/mL. Se diagnosticó como «endometriosis, masas pélvicas inflamatorias». Se administró una terapia de rehidratación antiinfecciosa y se dio de alta a la paciente con alivio del dolor. Dos semanas después del alta, el nivel de CA125 sérico de la paciente disminuyó a 106 mU/mL y volvió a la normalidad después de 6 semanas. Sin embargo, la masa pélvica aumentó gradualmente. El reexamen de la ecografía pélvica realizada mostró una masa ecoica mixta de 7.7 cm x 7.4 cm x 8.2 cm en el lado derecho del útero con un límite claro, eco puntiforme fino en el quiste y derrame abdominal y pélvico. La ecografía de contraste mostró que la pared del quiste de la masa pélvica estaba significativamente mejorada, se sospechaba malignidad y se recomendó un tratamiento quirúrgico. El 14 de noviembre de 2018, la paciente se sometió a liberación de adherencias pélvicas e intestinales transabdominales, omento, ovarios bilaterales, peritoneo multipunto y múltiples adenomiosis y histerectomía. Durante la operación, se aspiraron aproximadamente 600 ml de ascitis hemorrágica. Tras la exploración, se observó una masa de color rojo grisáceo con un diámetro de aproximadamente 8 cm en la superficie del epiplón mayor, que era suave y se asemejaba a carne podrida. Se encontraron depósitos de celulosa marrón difusos en la superficie del útero, ovarios bilaterales, pared abdominal, tracto intestinal, surco lateral del recto y pared anterior del recto. Las lesiones no se eliminaron por completo y algunas áreas se electrocoagularon. El examen patológico de la muestra resecada mostró endometriosis del tejido retiniano con vasodilatación, ampollas, infiltración linfocítica difusa y focal, folículos ováricos císticos bilaterales, fibrosis peritoneal dentro de la necrosis del tejido adiposo, proliferación de fibroblastos, aumento de la infiltración de células espumosas y adenomiosis uterina. La patología de ascitis mostró muchos glóbulos rojos, un pequeño número de linfocitos y neutrófilos y ninguna célula tumoral. Después de la operación, la paciente se recuperó sin problemas y se trató con agonista de la hormona liberadora de gonadotropina (GnRH-α). Se inició leuprorelina una vez al mes durante 6 meses, seguido de dienogest oral (DNG) durante 3 años, después de lo cual se interrumpió la medicación durante 3 meses. La paciente concibió de forma natural y tuvo un embarazo normal. Se dio a luz a un bebé de 3300 g por vía vaginal a las 39 semanas + 3 días de gestación. Tanto la madre como el bebé estaban sanos, sin recurrencia ni reacciones adversas durante el seguimiento.\n\nMH - Humanos\nMH - Mujer\nMH - *Endometriosis/complicaciones/terapia\nMH - Adulto",
+        "gold_summary": "Preocupaciones de la paciente: Una mujer de 28 años de edad vino a nuestro hospital para recibir tratamiento debido al descubrimiento de una masa pélvica 10 meses antes. Después de la admisión, la paciente se sometió a tratamiento quirúrgico y fue dada de alta en 1 semana. Recibió tratamiento médico durante 3 años después del alta. Después de la retirada de la medicación, la paciente quedó embarazada y dio a luz a un niño sin recurrencia durante el seguimiento.\n\nDiagnósticos: Los diagnósticos iniciales al ingreso fueron «¿masa pelviana inflamatoria?» y «¿endometriosis?». Después de 10 meses, la paciente volvió a ser internada en el hospital debido a un aumento gradual de la masa, y se le diagnosticó endometriosis.\n\nIntervenciones: El paciente fue tratado con terapia antiinfecciosa de rehidratación por primera vez, y el paciente fue tratado quirúrgicamente por segunda vez, seguido de agonista de la hormona liberadora de gonadotropina (GnRH-α) y tratamiento con dienogest (DNG) después de la cirugía.\n\nResultados: Después de 6 ciclos de tratamiento con GnRH-α y 3 años de tratamiento con DNG, un hijo nació con éxito tras la interrupción de la medicación y, hasta ahora, no se han producido reacciones adversas ni recurrencias durante el período de seguimiento.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había una mujer que tenía un bulto en su barriga por mucho tiempo. Los doctores la ayudaron con una operación y medicina para que se sintiera mejor. \n\nDespués de tomar la medicina por mucho tiempo, la mujer pudo tener un bebé sano. Ella y su bebé están bien y felices.",
+                "fh_score": 83.69
+            },
+            "B2": {
+                "text": "**Lo que le pasó a la paciente:**  \nUna mujer de 28 años tenía una masa, que es una especie de bulto, en la parte baja de su abdomen desde hacía 10 meses. Fue al hospital para tratarse. Al principio, pensaron que podía ser una inflamación o una enfermedad llamada endometriosis, que ocurre cuando un tejido parecido al que está dentro del útero crece fuera de él y causa dolor o problemas.\n\n**Qué hicieron los médicos:**  \nPrimero, le dieron un tratamiento para la inflamación y la hidratación. Pero como la masa creció, la operaron para quitarla y examinarla mejor. Después de la cirugía, le dieron medicamentos especiales que ayudan a controlar la endometriosis. Estos medicamentos incluyen un tipo que afecta las hormonas del cuerpo (llamado agonista de GnRH) y otro llamado dienogest, que tomaba por varios años.\n\n**Qué pasó después:**  \nTras el tratamiento y la cirugía, la paciente pudo quedar embarazada de forma natural. Tuvo un bebé sano y no volvió a tener problemas ni síntomas de la enfermedad durante el tiempo que la siguieron en el hospital.\n\n**En resumen:**  \nEsta paciente con endometriosis y una masa pélvica recibió cirugía y tratamiento hormonal. Gracias a esto, pudo tener un embarazo normal y no tuvo complicaciones después del tratamiento.",
+                "fh_score": 65.04
+            },
+            "B3": {
+                "text": "Resumen detallado para público general universitario\n\n**Contexto y motivo de consulta**  \nUna mujer asiática de 28 años acudió al hospital tras haber detectado una masa en la pelvis que persistía desde hacía 10 meses. Antes de esto, su menstruación era regular, con un volumen moderado y dolor menstrual (dismenorrea). No presentaba antecedentes de embarazos exitosos, pero sí un aborto espontáneo. Durante el examen físico, se encontró que la parte posterior del útero estaba agrandada (aproximadamente 8 cm) y con poca movilidad, aunque sin otras anomalías evidentes. La paciente no había experimentado dolor abdominal significativo durante esos meses previos.\n\n**Hallazgos diagnósticos iniciales**  \nLa ecografía reveló una masa heterogénea de unos 4 cm en la parte superior derecha del útero y un pequeño nódulo en el epiplón mayor (una capa de tejido graso en el abdomen) de 2 cm. Además, el análisis sanguíneo mostró un nivel elevado de CA125 (416 mU/mL), una proteína que puede aumentar en enfermedades inflamatorias o tumorales del área pélvica. Se sospechó inicialmente que la masa correspondía a endometriosis (una condición en la que tejido similar al endometrio crece fuera del útero) o a una masa inflamatoria pélvica.\n\n**Evolución y revaluación**  \nTras un tratamiento inicial con líquidos y antibióticos, la paciente mejoró y fue dada de alta. Los niveles de CA125 disminuyeron progresivamente hasta normalizarse en 6 semanas. Sin embargo, la masa pélvica continuó creciendo, alcanzando dimensiones de aproximadamente 8 cm, con características ecográficas que sugerían posible malignidad, lo que llevó a recomendar cirugía.\n\n**Intervenciones quirúrgicas y hallazgos intraoperatorios**  \nEl 14 de noviembre de 2018, la paciente fue sometida a una cirugía abdominal para liberar adherencias (tejido cicatricial que une órganos) en la pelvis e intestinos, así como para extirpar tejido afectado en el epiplón, ovarios, peritoneo (membrana que recubre la cavidad abdominal) y el útero. Durante la operación se drenaron 600 ml de líquido abdominal con sangre (ascitis hemorrágica). Se observaron lesiones características de endometriosis, incluyendo depósitos marrones en múltiples superficies abdominales y uterinas, y una masa blanda en el epiplón que parecía tejido necrótico. No fue posible eliminar todas las lesiones, por lo que algunas áreas se trataron con electrocoagulación para reducir su actividad.\n\n**Resultados del análisis patológico**  \nEl examen microscópico confirmó la presencia de endometriosis en el tejido adiposo del epiplón, con inflamación crónica y cambios en el tejido uterino compatibles con adenomiosis (una forma de endometriosis dentro del músculo uterino). No se detectaron células tumorales malignas en el líquido ascítico. También se observaron fibrosis (formación de tejido cicatricial) y proliferación de fibroblastos (células que forman tejido conectivo).\n\n**Tratamiento posterior y seguimiento**  \nDespués de la cirugía, la paciente recibió terapia hormonal con un agonista de la hormona liberadora de gonadotropina (GnRH-α), específicamente leuprorelina, administrada mensualmente durante 6 meses para suprimir la actividad ovárica y reducir la endometriosis. Posteriormente, continuó con dienogest (un progestágeno oral) durante 3 años para mantener el control de la enfermedad. Tras suspender la medicación durante 3 meses, la paciente logró concebir de forma natural.\n\n**Resultados obstétricos y estado actual**  \nLa paciente tuvo un embarazo normal y dio a luz por vía vaginal a término (39 semanas y 3 días) a un bebé sano de 3300 gramos. Durante el seguimiento posterior, no se observaron recurrencias de la endometriosis ni efectos adversos relacionados con el tratamiento o el embarazo.\n\n---\n\n**Interpretación clínica**  \nEste caso ilustra la complejidad del diagnóstico y manejo de la endometriosis con masas pélvicas grandes y elevación del marcador CA125, que puede simular malignidad. La combinación de cirugía para el control de lesiones extensas y terapia hormonal prolongada fue efectiva para controlar la enfermedad y preservar la fertilidad, permitiendo un embarazo exitoso sin complicaciones.\n\n**Próximos pasos y recomendaciones**  \nEl seguimiento clínico continuo es fundamental para detectar posibles recurrencias. La terapia hormonal prolongada puede ser necesaria para mantener la remisión. Además, este caso destaca la importancia de un enfoque multidisciplinario para el manejo de endometriosis avanzada, especialmente en mujeres jóvenes que desean conservar la fertilidad.",
+                "fh_score": 38.25
+            }
+        }
+    },
+    {
+        "article": "Presentamos una paciente de 76 años de edad, que es traída al servicio de urgencias por bajo nivel de conciencia con tendencia al sueño.\n\nComo antecedentes médicos de interés destaca una enfermedad pulmonar intersticial difusa, dislipemia e hipertensión arterial.\n\nA la exploración física el paciente se encuentra estuporosa, arreactiva, con atonía de las 4 extremidades y desviación conjugada de la mirada hacia la derecha, sin fiebre y con una leve sequedad en piel y mucosas. La analítica sanguínea no muestra alteraciones significativas.\n\nEl paciente es valorado por el servicio de neurología que considera la realización de una TC cerebral urgente ante la sospecha de patología intracraneal de evolución aguda. Las pruebas de imagen ponen de manifiesto la presencia de numerosas burbujas aéreas que se disponen en los surcos cerebrales, cuerpo calloso y ambos tálamos así como áreas hipodensas cortico-subcorticales de distribución parcheada en hemisferio cerebeloso izquierdo y parietooccipitales bilaterales, todo ello compatible con isquemia cerebral subaguda secundaria a embolismo gaseoso.\n\nAnte los antecedentes personales de enfermedad pulmonar intersticial difusa se decide también realizar una placa de tórax en proyección anteroposterior y una TC torácica que objetivan un neumotórax apical izquierdo y aire ectópico en mediastino superior.\n\nSe decide el ingreso en la Unidad de Ictus del centro para control estrecho de constantes, sin embargo, la paciente presenta una evolución tórpida con el fallecimiento el segundo día de ingreso debido a fracaso multiorgánico.",
+        "gold_summary": "Paciente de 76 años con una enfermedad pulmonar intersticial difusa preexistente, que experimentó un ictus masivo debido a un neumomediastino espontáneo. Su presentación incluyó confusión, convulsiones y debilidad motora. Las pruebas de imagen revelaron burbujas de aire en los surcos cerebrales y áreas hipodensas en el cerebelo y parietooccipitales. Además, se observó neumotórax y aire en el mediastino superior en las radiografías de tórax y la tomografía torácica. A pesar de las medidas terapéuticas como el oxígeno hiperbárico, la paciente lamentablemente falleció debido al fallo multiorgánico.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había una señora de 76 años que estaba muy enferma y se sentía muy cansada. Ella tenía problemas en sus pulmones desde antes. Un día, su cerebro se enfermó mucho porque había aire donde no debía estar. Esto hizo que ella se confundiera y se sintiera muy débil. Los doctores vieron en sus fotos que había aire en su cabeza y en su pecho. Aunque trataron de ayudarla mucho, ella se puso muy mal y no pudo mejorar. Los doctores estaban tristes porque ella se fue al cielo.",
+                "fh_score": 86.97
+            },
+            "B2": {
+                "text": "Paciente de 76 años con una enfermedad pulmonar que afecta sus pulmones, llamada enfermedad pulmonar intersticial difusa. Ella llegó al hospital con confusión, somnolencia y debilidad en sus brazos y piernas. Los médicos hicieron una tomografía cerebral, que es una imagen detallada del cerebro, y encontraron burbujas de aire dentro de su cerebro y áreas dañadas en partes del cerebelo y otras zonas del cerebro. También hicieron radiografías y una tomografía del pecho, donde vieron que tenía un neumotórax, que es aire fuera del pulmón, y aire en una zona llamada mediastino, que está en el centro del pecho. Estos problemas causaron que el aire entrara en el cerebro, lo que provocó un tipo de accidente cerebrovascular llamado embolismo gaseoso. Aunque la paciente recibió tratamiento, incluyendo oxígeno especial para eliminar el aire, su estado empeoró y falleció por el fallo de varios órganos.",
+                "fh_score": 52.46
+            },
+            "B3": {
+                "text": "**Contexto**  \nSe presenta el caso de una mujer de 76 años con antecedentes de enfermedad pulmonar intersticial difusa, dislipemia e hipertensión arterial, que fue ingresada en urgencias debido a un estado de conciencia disminuido y tendencia al sueño. En la exploración física, la paciente estaba en estupor, sin respuesta a estímulos, con debilidad en las cuatro extremidades y desviación de la mirada hacia la derecha, sin fiebre y con signos leves de deshidratación.\n\n**Hallazgos Clave**  \nLa evaluación neurológica llevó a la realización urgente de una tomografía computarizada (TC) cerebral, que mostró múltiples burbujas de aire localizadas en los surcos cerebrales, el cuerpo calloso y ambos tálamos, además de áreas con menor densidad en la corteza y la sustancia subcortical del cerebelo izquierdo y regiones parietooccipitales bilaterales. Estas imágenes son compatibles con un daño cerebral por isquemia (falta de flujo sanguíneo) secundaria a embolismo gaseoso (bloqueo causado por burbujas de aire).  \n\nDado el antecedente pulmonar, se realizaron radiografías y una TC de tórax que evidenciaron un neumotórax apical izquierdo (colapso parcial del pulmón en la parte superior) y presencia de aire fuera de lugar en el mediastino superior (neumomediastino), lo que sugiere que el aire escapó desde el pulmón hacia estructuras cercanas.\n\n**Interpretación Clínica**  \nLa paciente sufrió un ictus masivo debido a la entrada de aire en la circulación cerebral, probablemente originado por el neumotórax y el neumomediastino espontáneos relacionados con su enfermedad pulmonar intersticial. Esta situación es grave porque las burbujas de aire pueden bloquear vasos sanguíneos y causar daño cerebral extenso. A pesar de la atención especializada y las medidas terapéuticas, incluyendo el soporte en la Unidad de Ictus, la evolución fue desfavorable.\n\n**Próximos Pasos y Resultado**  \nLa paciente falleció al segundo día de ingreso debido a un fallo multiorgánico, que es la incapacidad progresiva de varios órganos vitales. Este caso resalta la importancia de reconocer rápidamente el embolismo gaseoso cerebral como una complicación potencialmente mortal en pacientes con enfermedades pulmonares crónicas y neumotórax espontáneo.",
+                "fh_score": 33.53
+            }
+        }
+    },
+    {
+        "article": "Un hombre de 24 años de edad, de etnia persa, presentó una queja principal de mal olor bucal después de un período de recuperación de la enfermedad leve por coronavirus 2019 (COVID-19), que quería resolver lo antes posible. Su dentista notó pérdida ósea y sangrado al explorar el área interproximal de los dientes número 18 y 19 clínicamente. Se realizó un escalamiento y un aplanamiento radicular, y se ordenaron radiografías periapicales y panorámicas para la evaluación del paciente. Sin embargo, el paciente se negó a tomar radiografías. La halitosis del paciente disminuyó después de 1 semana de tratamiento. Después de 2 meses, el paciente volvió a su dentista con la queja principal de sensibilidad al frío en sus incisivos mandibulares. El dentista realizó una prueba de vitalidad, y los dientes eran vitales excepto los números 23 y 24. El dentista tomó una radiografía periapical, y una lesión radiolucente en la mandíbula anterior era evidente.\n\nEn la radiografía panorámica, se evidenció una lesión radiolúcida lítica grande y bien definida con bordes festoneados que se extendían desde el diente número 31 en el lado derecho hasta el ramus ascendente izquierdo. Un estudio posterior de tomografía computarizada de haz cónico (TCFC) reveló una lesión lítica multilocular grande, con un margen relativamente distinto, que causó adelgazamiento y perforación de los cortexes bucales y linguales y signos de festoneado.\n\nTras el examen, se remitió al paciente a un cirujano oral y maxilofacial. En la entrevista médica, el paciente explicó su prolapso de la válvula mitral; antecedentes de episodios recurrentes de otitis desde el primer año de vida; antecedentes de septicemia de origen desconocido cuando tenía un año de edad, tras episodios de diarrea y vómitos; antecedentes de uso de broncodilatadores para la alergia estacional; antecedentes de uso de levotiroxina, cabergolina, acetato de desmopresina (DDAVP) en spray y gel de testosterona durante 4 años tras el diagnóstico de síndrome de silla turca vacía, tras poliúria y polidipsia; y, por último, antecedentes de infección reciente por COVID-19 (3 meses antes). Su historia familiar reveló tiroiditis de Hashimoto en su familia materna; su abuelo, su madre y sus tres tías padecían este tipo de hipotiroidismo. El historial quirúrgico previo del paciente incluía una reparación de una hernia inguinal 10 años antes sin complicaciones. Además, el paciente era obeso, con un índice de masa corporal (IMC) de 34,5.\n\nEn el examen clínico, los hallazgos extraorales e intraorales no fueron relevantes. Los exámenes de laboratorio, incluido el recuento sanguíneo completo (CBC), fueron normales, excepto por un aumento en la velocidad de sedimentación globular (ESR) y los niveles de proteína C reactiva (CRP). Se realizó una biopsia incisional en la mandíbula anterior y la muestra se envió al departamento de patología oral y maxilofacial de la Universidad de Ciencias Médicas Shahid Beheshti. Las secciones mostraron una infiltración difusa de grandes células de tinción pálida, como los histiocitos, con eosinófilos dentados y numerosos en el fondo fibroso. Un examen de inmunohistoquímica (IHC) reveló un positivo disperso para el grupo de diferenciación 1a (CD-1a) (+ +), un positivo fuerte para Langerin (CD-207) (+ + +), y más del 50% positivo para S-100.\n\nDe acuerdo con los datos clínicos, radiológicos e histopatológicos, se llegó al diagnóstico de LCH. Los diagnósticos diferenciales fueron osteomielitis, granuloma eosinófilo y metástasis ósea. Sin embargo, debido a las pruebas de laboratorio, los datos radiológicos y el historial clínico, se confirmó el diagnóstico de LCH. Por lo tanto, para un examen más a fondo, el paciente fue derivado al departamento de medicina nuclear para una tomografía por emisión de positrones con fluor-2-desoxiglucosa y una tomografía computarizada (FDG PET/CT), que reveló lesiones líticas hipermetabólicas en la mandíbula, el parietal derecho, el frontal izquierdo y el esfenoidal izquierdo, y opacidad hipermetabólica en el seno etmoidal izquierdo. Además, se observó una actividad metabólica aumentada en la región sellar, hidrocefalia comunicante y amígdalas palatinas hipermetabólicas prominentes. Además, se evidenció una actividad metabólica heterogénea aumentada en las tibias y fémures bilaterales.\n\nUna resonancia magnética del cerebro reveló una notable ampliación de la intensidad del material del líquido cefalorraquídeo (LCR) que contiene la silla turca. La adenohipófisis apareció como una capa delgada en la base de la silla turca agrandada, y se observaron cambios homogéneos e inflamatorios en las células aéreas mastoideas izquierdas. Se observó la extensión de la inflamación hacia el oído medio izquierdo (es de destacar que el paciente había sufrido de otitis durante muchos años). De acuerdo con la implicación multifocal de la enfermedad y su pronóstico cuestionable, el paciente fue derivado al departamento de oncología para quimioterapia sistémica. Pruebas posteriores revelaron mutaciones en el oncogen BRAF y no se detectaron mutaciones en KRAS y NRAS. El oncólogo eligió un régimen de denosumab, vinblastina, etopósido, 6-mercaptopurina, metotrexato y pegfilgrastim; sin embargo, el seguimiento no fue posible ya que el paciente falleció tras un accidente.\n",
+        "gold_summary": "Un paciente de 24 años de edad, de etnia persa, se presentó con una queja principal de halitosis tras recuperarse de la enfermedad por coronavirus 2019 en el consultorio de su dentista general. Los exámenes intraorales y extraorales no revelaron ningún problema específico. En la sesión de seguimiento tras el tratamiento periodontal de fase I, la sensibilidad de los dientes al estímulo frío era evidente, y las radiografías revelaron una gran lesión intraósea lítica en la mandíbula. Una biopsia incisional reveló células de Langerhans y una reacción positiva a Langerina y al grupo de diferenciación 1a, por lo que se le diagnosticó histiocitosis de células de Langerhans. Después de realizar una tomografía por emisión de positrones con fluoro-2-desoxiglucosa y una tomografía computarizada, una resonancia magnética y una tomografía computarizada de haz cónico, debido a la implicación generalizada de la enfermedad, el paciente fue derivado a un oncólogo. En última instancia, se descubrió que los problemas de salud infantil del paciente, incluidos los problemas endocrinos, probablemente fueron causados por una histiocitosis de células de Langerhans no diagnosticada. El oncólogo eligió un régimen de denosumab, vinblastina, etopósido, 6-mercaptopurina, metotrexato y pegfilgrastim. El seguimiento no fue posible ya que el paciente falleció tras un accidente.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había un hombre joven que tenía mal olor en la boca. Esto pasó después de que se enfermó con un virus. El dentista vio que algunos dientes le dolían con el frío. También encontró un hueco grande en el hueso de su mandíbula.\n\nEl doctor tomó un pedacito de ese hueso para mirar con un microscopio. Vieron unas células especiales llamadas células de Langerhans. Esto dijo que tenía una enfermedad llamada histiocitosis de células de Langerhans.\n\nEl hombre fue a ver a otro doctor que sabe de enfermedades graves. Le hicieron muchas pruebas para ver dónde estaba la enfermedad. Los doctores dijeron que la enfermedad estaba en muchas partes de su cuerpo.\n\nEl doctor le dio medicinas fuertes para ayudarlo. Pero el hombre tuvo un accidente y no pudo seguir con el tratamiento. Los doctores estaban muy tristes por eso.",
+                "fh_score": 81.43
+            },
+            "B2": {
+                "text": "**Lo que le pasó al paciente**  \nUn joven de 24 años, después de recuperarse de un caso leve de COVID-19, fue al dentista porque tenía mal olor en la boca. Al principio, no se encontraron problemas visibles en su boca ni en su cara. Sin embargo, después de un tratamiento para limpiar sus dientes, empezó a sentir sensibilidad al frío en algunos dientes. Las radiografías mostraron una lesión grande en el hueso de la mandíbula.\n\n**Qué encontraron los médicos**  \nPara entender mejor la lesión, los médicos tomaron una biopsia, que es cuando se extrae un pequeño pedazo de tejido para examinarlo bajo el microscopio. En esta muestra, vieron células especiales llamadas células de Langerhans. Estas células reaccionaron a ciertas pruebas que confirmaron que el paciente tenía una enfermedad llamada histiocitosis de células de Langerhans (LCH). Esta enfermedad puede afectar varios órganos y huesos.\n\n**Estudios adicionales y diagnóstico**  \nEl paciente se sometió a varios estudios, como tomografías y resonancias magnéticas, que mostraron que la enfermedad estaba en varias partes de su cuerpo, incluyendo huesos de la cabeza y las piernas, y también afectaba algunas áreas del cerebro. Además, descubrieron que algunos problemas de salud que tuvo cuando era niño, como problemas hormonales y frecuentes infecciones de oído, probablemente estaban relacionados con esta enfermedad que no se había detectado antes.\n\n**Tratamiento y resultado**  \nDebido a que la enfermedad estaba extendida, el paciente fue enviado a un especialista en cáncer para recibir quimioterapia, que es un tratamiento con medicamentos para combatir células enfermas. El médico eligió un plan con varios medicamentos para tratar la enfermedad. Lamentablemente, no se pudo hacer un seguimiento del tratamiento porque el paciente falleció debido a un accidente.  \n\nEste caso muestra la importancia de investigar a fondo cuando aparecen problemas inusuales en la boca, ya que pueden ser señales de enfermedades más serias en el cuerpo.",
+                "fh_score": 55.05
+            },
+            "B3": {
+                "text": "**Contexto**  \nUn hombre persa de 24 años acudió a su dentista quejándose de mal olor en la boca (halitosis) poco después de recuperarse de una infección leve por COVID-19. Inicialmente, no se encontraron problemas visibles en su boca ni en el examen externo. Sin embargo, tras un tratamiento periodontal inicial, el paciente comenzó a experimentar sensibilidad dental al frío, lo que llevó a la realización de radiografías que mostraron una lesión ósea anormal en la mandíbula.\n\n**Hallazgos Clave**  \nUna biopsia de la lesión reveló la presencia de células de Langerhans, un tipo específico de células inmunitarias, confirmada mediante pruebas inmunohistoquímicas positivas para marcadores como Langerina (CD-207) y CD1a. Estos hallazgos permitieron diagnosticar una enfermedad llamada histiocitosis de células de Langerhans (LCH), que es una condición poco común caracterizada por la proliferación anormal de estas células. Estudios de imagen adicionales, incluyendo tomografía computarizada de haz cónico (TCFC), tomografía por emisión de positrones con fluor-2-desoxiglucosa (FDG PET/CT) y resonancia magnética cerebral, revelaron que la enfermedad afectaba múltiples áreas óseas, incluyendo varias regiones del cráneo y huesos largos, así como inflamación en estructuras cercanas al oído y la hipófisis (glándula cerebral que regula varias funciones endocrinas).\n\n**Interpretación Clínica**  \nEl diagnóstico de LCH explicó no solo la lesión mandibular sino también varios problemas de salud que el paciente había tenido desde la infancia, como episodios recurrentes de otitis (infección del oído), alteraciones endocrinas relacionadas con un síndrome de silla turca vacía (una anomalía en la glándula hipófisis), y otros síntomas sistémicos. La enfermedad mostró un compromiso multifocal, lo que significa que afectaba varias áreas del cuerpo, complicando su pronóstico. Además, se detectó una mutación en el oncogen BRAF, un factor genético que puede influir en el comportamiento de la enfermedad y en las opciones de tratamiento.\n\n**Próximos Pasos y Tratamiento**  \nDebido a la extensión y gravedad de la enfermedad, el paciente fue remitido al departamento de oncología para recibir quimioterapia sistémica. El régimen elegido incluyó varios medicamentos: denosumab (que ayuda a inhibir la destrucción ósea), vinblastina, etopósido, 6-mercaptopurina, metotrexato y pegfilgrastim (que estimula la producción de células sanguíneas). Lamentablemente, no fue posible realizar un seguimiento del tratamiento porque el paciente falleció posteriormente a causa de un accidente.\n\n**Resumen Final**  \nEste caso ilustra cómo una enfermedad poco común como la histiocitosis de células de Langerhans puede manifestarse inicialmente con síntomas aparentemente leves, como mal aliento y sensibilidad dental, y estar relacionada con problemas médicos complejos desde la infancia. La detección temprana y el diagnóstico preciso mediante biopsia y estudios de imagen son fundamentales para orientar un tratamiento adecuado, aunque el pronóstico puede ser reservado cuando la enfermedad afecta múltiples órganos.",
+                "fh_score": 31.17
+            }
+        }
+    },
+    {
+        "article": "La paciente es una mujer de 66 años de edad que goza de buena salud. A mediados de la década de 1980, recibió varias sesiones de tratamiento con rayos grenz en el cuero cabelludo para aliviar el picor asociado con la psoriasis del cuero cabelludo. Con un tratamiento regular de aproximadamente una sesión al mes durante un período de 5 años, que se complementó de vez en cuando con alquitrán de hulla, ácido salicílico y prednisona, logró cierto alivio de su enfermedad. Con el tiempo, su cabello se adelgazó; la piel en toda el área del cuero cabelludo se volvió sensible al dolor y se produjo cicatrización. Los tratamientos con rayos grenz se habían administrado en una clínica privada; no se disponía de detalles del tratamiento, como la dosis única y acumulada. No había sufrido radiodermitis.\n\nEn un período muy breve en 2020, unos 35 años después de que cesara el tratamiento de radiación, aparecieron numerosos BCC y queratosis actínicas premalignas (AK) en su cuero cabelludo. Se inició un régimen de tratamiento de extirpación quirúrgica de BCC verificado por histología preoperatoria y crioterapia de AK por evaluación del médico. La terapia fotodinámica o los tratamientos tópicos no eran aplicables debido a la sensibilidad al dolor y las secuelas de la cirugía. De 2020 a 2022, recibió varios tratamientos de criocirugía y curetaje y un total de 13 extirpaciones quirúrgicas de BCC por cirugía de Mohs. Se estima que su número total de extirpaciones a lo largo del tiempo es de unos 30. Los BCC recalcitrantes y de novo en el cuero cabelludo cada vez más dañado, obviamente, son un desafío eterno; por lo tanto, los cirujanos plásticos y los dermatólogos buscaban otra modalidad de tratamiento con un mejor índice terapéutico.\n\nEn septiembre de 2022, aparecieron nuevos CCB confirmados histológicamente en el cuero cabelludo. La exploración por ultrasonido (DermaScan C, Cortex Technology ApS, Aalborg, Dinamarca) mostró tumores ecolucidos de 0,5-1,3 mm de espesor en ambos sitios analizados histológicamente, así como en algunas lesiones adicionales que pudieron identificarse en base al examen clínico y dermatoscópico. La paciente, tras ser informada, dio su consentimiento por escrito para el tratamiento con HIFU, con o sin biopsia de pretratamiento de las lesiones sospechosas.\n\nSe delinearon las lesiones elegibles para el tratamiento con un rotulador impermeable, incluyendo un margen perilesional de 2 mm. Se mapeó cada lesión seleccionada en una lámina transparente para ayudar a determinar la ubicación precisa en el seguimiento. Se usó el ultrasonido de 20 MHz para confirmar la profundidad de las lesiones identificadas al inicio y en las visitas de seguimiento posteriores. Debido al estado del cuero cabelludo conocido por ser sensible al dolor, se administró anestesia local (lidocaína 25 mg/ml + adrenalina 5 mg/ml, Amgros I/S, Copenhagen, Dinamarca) a todas las lesiones 10-15 minutos antes del tratamiento.\n\nLas lesiones fueron tratadas con HIFU utilizando la sonda de 1.3 mm; ajustes de 150 ms/dosis y energía acústica de 0.9 J/dosis. Se aplicaron 20-200 dosis a las lesiones, dependiendo de la extensión de la lesión. Las lesiones tratadas se curaron de forma espontánea sin complicaciones o necesidad de tratamiento especial. Se programaron visitas de seguimiento cada 3-6 meses para controlar la tasa de curación/recaída, tolerancia local y lesiones nuevas no identificadas anteriormente.\n\nDurante los 15 meses posteriores a la limpieza inicial con HIFU, se trataron con HIFU un total de 10 lesiones que, de acuerdo con las rutinas, hubieran requerido una biopsia seguida de una cirugía de escisión, en sesiones de unos 30 minutos. Las lesiones se curaron en unos pocos días sin complicaciones ni necesidad de intervención. Se observó una limpieza total en 7 de 8 lesiones de BCC tratadas y en ambas lesiones de AK. La única lesión recurrente de BCC de pequeño tamaño se observó después de 15 meses entre las primeras seis lesiones tratadas; la lesión se volvió a tratar con HIFU. Ejemplos de lesiones curadas 15 meses después del tratamiento con HIFU; el tumor con recurrencia.\n",
+        "gold_summary": "Una mujer de 66 años que en la década de 1980 había recibido varios tratamientos de rayos gamma en el cuero cabelludo desarrolló múltiples carcinomas basocelulares en la zona. Se le habían realizado más de 30 cirugías de escisión, incluida la cirugía de Mohs, en el pasado, con muchas complicaciones locales, pero, no obstante, los cánceres recurrentes. Los tratamientos con HIFU aplicados a ocho carcinomas basocelulares y dos lesiones precancerosas dieron como resultado una limpieza completa en el control a los 12 meses, pero una recurrencia después de 15 meses.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había una señora de 66 años con problemas en su cabeza. Hace mucho tiempo, le dieron unos rayos para ayudar su piel que le picaba. Pero después, le salieron muchos bultitos malos en la cabeza.\n\nElla tuvo muchas operaciones para quitar esos bultitos. A veces, le dolía mucho y los bultitos volvían a salir. Luego, los doctores usaron un tratamiento especial con un aparato que usa calor para quitar los bultitos.\n\nDespués de un año, casi todos los bultitos se fueron. Pero después de un poco más de un año, uno volvió a salir. Los doctores la cuidaron y trataron otra vez. Ella está siendo cuidada con mucho cariño.",
+                "fh_score": 82.33
+            },
+            "B2": {
+                "text": "**Caso de una mujer con cáncer en el cuero cabelludo**\n\nUna mujer de 66 años recibió hace muchos años, en la década de 1980, un tratamiento con rayos especiales en su cuero cabelludo para aliviar una enfermedad llamada psoriasis, que causa picor y enrojecimiento. Después de ese tratamiento, su piel se volvió sensible y se dañó con el tiempo.\n\nAproximadamente 35 años después, empezaron a aparecer en su cuero cabelludo varios tumores llamados carcinomas basocelulares (que son un tipo de cáncer de piel) y lesiones que podrían volverse cancerosas. Para tratar estos tumores, le hicieron más de 30 cirugías, incluyendo una técnica especial llamada cirugía de Mohs, que busca eliminar el cáncer sin dañar mucho la piel sana. Sin embargo, los tumores seguían apareciendo y la piel estaba muy dañada y sensible.\n\n**Nuevo tratamiento con ultrasonido de alta intensidad (HIFU)**\n\nEn 2022, los médicos decidieron probar un nuevo tratamiento llamado HIFU, que usa ondas de ultrasonido para destruir los tumores sin necesidad de cirugía. Antes de aplicar el tratamiento, marcaron las lesiones y usaron anestesia local para evitar el dolor.\n\nDurante 15 meses, trataron con HIFU diez lesiones: ocho eran carcinomas basocelulares y dos eran lesiones precancerosas. Siete de los ocho tumores desaparecieron completamente después de un año. Solo uno volvió a aparecer después de 15 meses, y fue tratado nuevamente con HIFU. Las lesiones precancerosas también sanaron sin problemas.\n\n**Qué significa esto**\n\nEste caso muestra que el tratamiento con HIFU puede ser una opción efectiva para eliminar ciertos cánceres de piel y lesiones precancerosas en pacientes con piel sensible y dañada, evitando cirugías complicadas. Aunque algunos tumores pueden volver, el HIFU ofrece una alternativa menos invasiva y con buena tolerancia para controlar estos problemas.",
+                "fh_score": 52.69
+            },
+            "B3": {
+                "text": "**Contexto**  \nSe trata de una mujer de 66 años que, durante la década de 1980, recibió múltiples tratamientos con rayos grenz (una forma de radiación de baja energía) en el cuero cabelludo para aliviar la psoriasis, una enfermedad inflamatoria de la piel. Estos tratamientos, junto con otros medicamentos tópicos, lograron cierto alivio, pero con el tiempo provocaron adelgazamiento del cabello, sensibilidad dolorosa y cicatrización en la piel del cuero cabelludo. Aproximadamente 35 años después de finalizar la radioterapia, la paciente desarrolló numerosos carcinomas basocelulares (un tipo común de cáncer de piel) y queratosis actínicas (lesiones precancerosas) en la misma zona.\n\n**Hallazgos Clave**  \nEntre 2020 y 2022, la paciente fue sometida a múltiples tratamientos convencionales, incluyendo más de 30 cirugías para extirpar los carcinomas basocelulares, algunas de ellas mediante cirugía de Mohs, una técnica especializada para eliminar tumores de piel con precisión. También recibió crioterapia para las lesiones precancerosas. Sin embargo, los tumores continuaron apareciendo, y la sensibilidad y daño en el cuero cabelludo dificultaban la aplicación de otros tratamientos tópicos o fotodinámicos.\n\nEn septiembre de 2022, se detectaron nuevos carcinomas basocelulares confirmados mediante biopsia. Para evaluar la extensión y profundidad de las lesiones, se utilizó un ultrasonido especializado que mostró tumores de entre 0,5 y 1,3 mm de grosor. La paciente aceptó someterse a un tratamiento con ultrasonido focalizado de alta intensidad (HIFU, por sus siglas en inglés), una técnica que utiliza ondas de ultrasonido para destruir tejido tumoral sin cirugía.\n\nAntes del tratamiento, se aplicó anestesia local para minimizar el dolor, y las lesiones fueron cuidadosamente marcadas y mapeadas para su seguimiento. El HIFU se administró con parámetros específicos (dosis de 150 ms y energía de 0.9 julios por dosis), aplicando entre 20 y 200 dosis según el tamaño de cada lesión.\n\n**Interpretación Clínica**  \nDurante los 15 meses posteriores al tratamiento inicial con HIFU, se trataron un total de 10 lesiones (8 carcinomas basocelulares y 2 queratosis actínicas) que, según los protocolos habituales, habrían requerido biopsia y cirugía. Todas las lesiones sanaron espontáneamente en pocos días sin complicaciones ni necesidad de tratamientos adicionales.\n\nEn el seguimiento a 12 meses, se observó una eliminación completa de 7 de las 8 lesiones de carcinoma basocelular y de ambas lesiones precancerosas. Solo una lesión pequeña de carcinoma basocelular recidivó después de 15 meses y fue nuevamente tratada con HIFU con éxito.\n\n**Próximos Pasos**  \nEl uso de HIFU en esta paciente representa una alternativa prometedora para el manejo de carcinomas basocelulares recurrentes en un cuero cabelludo dañado y sensible, donde las opciones quirúrgicas y tópicas son limitadas o generan complicaciones. Se recomienda continuar con controles periódicos cada 3 a 6 meses para detectar nuevas lesiones o recurrencias y evaluar la tolerancia a largo plazo del tratamiento. Además, la experiencia obtenida sugiere que el HIFU podría ser una modalidad terapéutica eficaz y menos invasiva para casos similares en el futuro.",
+                "fh_score": 40.58
+            }
+        }
+    },
+    {
+        "article": "Se realizó un trasplante cardíaco ortotópico a una niña de 12 años con insuficiencia cardíaca en fase terminal debido a una miocardiopatía restrictiva. Durante la operación, se presentó una disfunción primaria grave del injerto, que requirió el uso de oxigenación por membrana extracorpórea venosa arterial. La función cardíaca se recuperó completamente después de 4 días, y su período postoperatorio se complicó por una insuficiencia renal aguda transitoria y un bloqueo auriculoventricular completo que duró >3 semanas después de la operación. Para evitar la disincronía del ventrículo izquierdo y el posible daño de la derivación del ventrículo derecho debido a las biopsias endomiocárdicas de vigilancia de rechazo múltiple, se indicó un marcapasos biventricular transvenoso que utiliza un marcapasos del ventrículo izquierdo aislado a través de la vena coronaria.\n\nBajo anestesia local y sedación suave, se cortó la vena cefálica izquierda y se introdujo un catéter guía en la vena subclavia y se colocó en el seno coronario inicialmente para realizar un venograma cardiaco. Se implantó un electrodo de estimulación endocárdica de elución de esteroides unipolar con mecanismo de fijación activa (Attain StarFix® 4195, Medtronic, Minneapolis, MN) en la rama de la vena interventricular anterior. Las medidas en el momento del implante fueron las siguientes: umbral 2 V a 0,4 ms, onda R 6 mV e impedancia 300 Ω a 4,8 mA. Se implantó un segundo electrodo de estimulación endocárdica de elución de esteroides bipolar con fijación activa (2088T®, St. Jude Medical, Minneapolis, MN) en la aurícula derecha.\n\nAmbos cables se aseguraron y se conectaron a un marcapasos adaptable a la frecuencia (Accent DR®, St. Jude Medical, Minneapolis, MN) que se colocó en una bolsa muscular infraclavicular izquierda y se programó a VDD. Las mediciones de los cables electrofisiológicos fueron estables después del implante: umbral ventricular 1.5 V a 0.7 ms, onda R 4.5 mV, onda P 4.3 mV (bipolar), impedancia ventricular 260 Ω y vida útil estimada de la batería de 5 años.\n\nEl electrocardiograma posterior al implante mostró complejos de morfología de bloqueo de rama derecha, y la evaluación ecocardiográfica mostró ausencia de disincronías auriculoventriculares, interventriculares e intraventriculares. En el seguimiento a 5 años, el paciente permaneció en Clase Funcional I con el mismo sistema de estimulación y conservó la función ventricular.\n\nMH - Bloqueo auriculoventricular/etiología/*terapia\nMH - Niño\nMH - Sinus coronario\nMH - Mujer\nMH - Insuficiencia cardiaca/cirugía\nMH - Trasplante de corazón/*efectos adversos\nMH - Ventrículos del corazón\nMH - Humanos\nMH - *Marcapasos, artificial\nMH - Disfunción/complicaciones/tratamiento del injerto primario\n",
+        "gold_summary": "Se sometió a un trasplante de corazón ortotópico a un niño de 12 años con insuficiencia cardiaca en fase terminal debido a una miocardiopatía restrictiva. La disfunción primaria del injerto precisó oxigenación con membrana extracorpórea venosa arterial. La función cardiaca se normalizó, pero el bloqueo auriculoventricular completo persistió después de 3 semanas. Se realizó un marcapaso bicameral con marcapaso transvenoso del ventrículo izquierdo a través del seno coronario. Tras 5 años de seguimiento, el paciente se encuentra estable con el mismo sistema de marcapaso y con la función ventricular preservada.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un niño de 12 años recibió un nuevo corazón porque su corazón estaba muy enfermo. Al principio, su nuevo corazón tuvo problemas y necesitó ayuda para funcionar. Después de un tiempo, el corazón empezó a trabajar bien. Pero el niño tenía un problema con el ritmo del corazón. Por eso, los doctores le pusieron un pequeño aparato llamado marcapasos para ayudar a que su corazón latiera bien. Cinco años después, el niño está bien y su corazón funciona muy bien con el marcapasos.",
+                "fh_score": 74.9
+            },
+            "B2": {
+                "text": "**Trasplante de Corazón y Uso de Marcapasos en una Niña de 12 Años**\n\nUna niña de 12 años con un problema grave en el corazón llamado miocardiopatía restrictiva, que causa que el corazón no funcione bien, recibió un trasplante de corazón. Durante la operación, el nuevo corazón tuvo dificultades para funcionar correctamente, por lo que los médicos usaron una máquina especial llamada oxigenación por membrana extracorpórea. Esta máquina ayuda a oxigenar la sangre cuando el corazón está débil.\n\nDespués de cuatro días, el corazón trasplantado comenzó a funcionar bien. Sin embargo, la niña tuvo un problema llamado bloqueo auriculoventricular completo, que significa que las señales eléctricas entre las partes superiores e inferiores del corazón no se transmitían bien. Este problema duró más de tres semanas.\n\nPara ayudar a su corazón a latir de manera sincronizada y evitar daños, los médicos le implantaron un marcapasos especial. Un marcapasos es un dispositivo que envía señales eléctricas para controlar el ritmo del corazón. En este caso, colocaron un marcapasos que estimula ambos ventrículos del corazón (las partes inferiores) usando cables que pasan por las venas hasta llegar al corazón.\n\nEl procedimiento se hizo con anestesia local y sedación suave, y los cables se colocaron cuidadosamente en las venas del corazón. El marcapasos se programó para adaptarse a las necesidades del corazón de la niña. Después de la operación, los exámenes mostraron que el corazón latía de forma sincronizada y sin problemas.\n\nCinco años después, la niña está estable, con buena función del corazón y sigue usando el mismo marcapasos sin complicaciones. Esto muestra que el tratamiento fue exitoso para mejorar su calidad de vida.",
+                "fh_score": 56.69
+            },
+            "B3": {
+                "text": "**Contexto**  \nUna niña de 12 años con insuficiencia cardíaca avanzada causada por una miocardiopatía restrictiva (una enfermedad que limita la capacidad del corazón para llenarse de sangre) fue sometida a un trasplante cardíaco ortotópico, que consiste en reemplazar el corazón enfermo por uno sano en la misma posición anatómica. Durante la cirugía, presentó una disfunción grave del nuevo corazón (injerto), lo que requirió soporte temporal con oxigenación por membrana extracorpórea venosa arterial (una técnica que ayuda a oxigenar la sangre y mantener la circulación mientras el corazón se recupera).\n\n**Hallazgos Clave**  \n- La función cardíaca del injerto se recuperó completamente en 4 días.  \n- Posteriormente, la paciente desarrolló un bloqueo auriculoventricular completo (una interrupción total en la transmisión eléctrica entre las aurículas y los ventrículos del corazón) que persistió por más de tres semanas.  \n- Para evitar problemas relacionados con la descoordinación del ventrículo izquierdo y el daño potencial al ventrículo derecho por las biopsias repetidas que se realizan para vigilar el rechazo del trasplante, se decidió implantar un marcapasos biventricular transvenoso. Este dispositivo estimula eléctricamente ambos ventrículos para mantener un ritmo cardíaco sincronizado.  \n- El electrodo del ventrículo izquierdo se colocó a través de la vena coronaria (una vena del corazón) usando un catéter guiado, mientras que otro electrodo se implantó en la aurícula derecha.  \n- Ambos electrodos se conectaron a un marcapasos adaptable a la frecuencia, ubicado en una bolsa muscular debajo de la clavícula izquierda.  \n- Las mediciones eléctricas del marcapasos mostraron parámetros estables y adecuados para un funcionamiento óptimo.  \n- El electrocardiograma posterior mostró una morfología compatible con bloqueo de rama derecha, pero la ecocardiografía confirmó que no existían desincronías en la contracción de las cámaras cardíacas.\n\n**Interpretación Clínica**  \nEl uso de un marcapasos biventricular con estimulación del ventrículo izquierdo a través del seno coronario resultó ser una estrategia efectiva para manejar el bloqueo auriculoventricular prolongado en esta paciente trasplantada. Este enfoque permitió mantener la sincronía en la contracción del corazón, evitando complicaciones que podrían afectar la función ventricular. La estabilidad de los parámetros eléctricos y la ausencia de disincronías evidenciadas por ecocardiografía respaldan la eficacia del tratamiento.\n\n**Próximos Pasos y Seguimiento**  \nA cinco años del implante del marcapasos, la paciente se mantiene en clase funcional I (sin limitaciones para realizar actividades físicas normales), con función ventricular preservada y sin necesidad de cambios en el sistema de estimulación. Esto indica un pronóstico favorable y una buena calidad de vida a largo plazo. Se recomienda continuar con el seguimiento cardiológico regular para monitorear la función del marcapasos y del injerto cardíaco, así como para detectar cualquier posible complicación futura.",
+                "fh_score": 33.35
+            }
+        }
+    },
+    {
+        "article": "Una paciente de 20 años de edad se presentó con distensión abdominal progresiva asociada con calambres abdominales, incapacidad para expulsar flatos y heces, así como vómitos frecuentes de materia ingerida y biliar de un día de duración. El día anterior, dio a luz por cesárea por una indicación de bradicardia fetal severa. También tenía preeclampsia sin signos de gravedad y desnutrición de inicio en la edad adulta con un índice de masa corporal (IMC) de 16,5 kg/M2. No tenía antecedentes de cirugía abdominal previa. Negó cualquier queja similar en el pasado o antecedentes de cambio de hábitos intestinales o estreñimiento con paso de heces sanguinolentas. No tenía ninguna enfermedad médica crónica conocida.\n\nEn el examen físico, la paciente se veía enferma y con dolor. Su presión arterial era de 90/70 mmHg, su pulso oscilaba entre 116 y 120 latidos por minuto, y su frecuencia respiratoria era de 22 a 24 respiraciones por minuto. No se registró fiebre. Su abdomen estaba muy distendido y simétrico, con visibles movimientos intestinales peristálticos. Había una difusa sensibilidad directa en todo su abdomen, más en el cuadrante inferior derecho. Había un signo positivo de acumulación de fluido intraperitoneal con opacidad cambiante. Había una herida quirúrgica suprapúbica bien aproximada con un vendaje limpio. El examen rectal digital no mostró nada destacable. Tenía una herida superficial lineal de 3 cm de largo, orientada verticalmente, en su labio mayor izquierdo, que el equipo de obstetricia pensó inicialmente que era una quemadura de yodo en la piel.\n\nSe le introdujo un catéter y se le resucitó con dos bolsas de solución salina normal y produjo 200 ml de orina en una hora. Se le introdujo una sonda nasogástrica (NGT) pero no hubo una salida significativa. Se le realizó un hemograma completo y una radiografía abdominal simple. Su recuento de glóbulos blancos era de 1780 células/µl con predominio de neutrófilos del 88 %, hemoglobina de 12,7 mg/dl y un recuento de plaquetas de 78 x 103/ µl. Su prueba de función renal era normal y sus enzimas hepáticas estaban ligeramente elevadas por encima del rango normal pero no fue significativo. Su radiografía abdominal simple muestra múltiples niveles de aire-líquido ubicados centralmente con un bucle intestinal grande dilatado ubicado periféricamente y blanqueamiento del espacio pélvico que indica una acumulación de líquido. No se solicitó una tomografía computarizada abdominal (CT) porque trabajamos en un entorno con recursos limitados y para pacientes con obstrucción intestinal, solicitamos una tomografía computarizada cuando existe la posibilidad de un diagnóstico alternativo o cuando se sospecha una obstrucción tumoral.\n\nTras obtener el consentimiento informado por escrito, se exploró a la paciente bajo anestesia general con un diagnóstico de abdomen agudo secundario a obstrucción intestinal mixta secundaria a vólvulo del intestino delgado. El hallazgo intraoperatorio fue un íleon distal que rodeaba el ciego y el colon ascendente proximal, ambos móviles y no adheridos a la pared abdominal posterolateral derecha. Tanto el íleon como el ciego, así como el colon ascendente, eran viables. La punta del apéndice estaba enredada con el nudo ileal y estaba gangrenoso. El intestino delgado proximal y el intestino grueso distal estaban muy distendidos, pero en su ubicación normal. Había unos cuatro litros de líquido intraperitoneal seroso.\n\nDurante la operación, la paciente se mantuvo hipotensa (80/50 mmHg) desde que se le indujo la anestesia y se le administró un vasopresor. Debido a la inestabilidad de la paciente y a la viabilidad de los intestinos afectados por el nudo, se procedió a una hemicolectomía derecha. Se realizó una descompresión proximal y distal de los intestinos delgado y grueso distendidos, respectivamente. Se fijó el ciego y el colon ascendente a la pared abdominal posterolateral derecha con suturas seromusculares interrumpidas con hilo no absorbible (Silk 2-0).\n\nDespués del procedimiento, se le retiró la intubación y se le dio alimentación por vía oral (NPO) durante 24 horas y se le administró un fluido de mantenimiento con reposición de la pérdida. A pesar de la reanimación con fluidos y el apoyo con vasopresores, ella se encontraba persistentemente hipotensa, por lo que se le administró un tratamiento antibiótico doble con ceftriaxona 1 g, IV, BID y metronidazol 500 mg, IV, TID, en vista de un posible shock séptico de origen genitourinario. Su estado empeoró gradualmente y, tras una nueva evaluación el primer día postoperatorio, la herida superficial en su vulva se había extendido hacia la zona suprapúbica con signos clínicos de gangrena de Fournier. Por ello, revisamos su tratamiento antibiótico a meropenem 1 g, IV, BID, vancomicina 1 g, IV, BID y metronidazol 500 mg, IV, TID. Después de obtener el consentimiento informado por escrito, se la volvió a llevar al quirófano para un desbridamiento radical de la gangrena de Fournier y, posteriormente, se la trasladó a la unidad de cuidados intensivos quirúrgicos (ICU) intubada debido a un shock séptico persistente y un retraso en la recuperación de la anestesia. Lamentablemente, falleció con fallo multiorgánico debido a un shock séptico refractario en su segundo día postoperatorio, después de la exploración inicial.\n",
+        "gold_summary": "Presentamos un caso de nudos ileocecales en una paciente posparto con distensión abdominal, vómitos y ausencia de heces y flatos. La radiografía abdominal simple reveló bucles intestinales dilatados con múltiples niveles de aire y fluidos. Se realizó una laparotomía exploratoria con hallazgo intraoperatorio de nudos ileocecales con intestino viable, ciego móvil y colon ascendente y punta gangrenosa del apéndice. Deshicimos el nudo y realizamos una apendectomía. Debido a la inestabilidad intraoperatoria de los signos vitales de la paciente, se aplazó la hemicolectomía derecha y se fijaron el ciego y el colon ascendente a la pared abdominal posterolateral derecha.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había una niña que acababa de tener un bebé. Su barriga estaba muy grande y le dolía mucho. No podía hacer popó ni tirar gases y vomitaba mucho.\n\nLos doctores le hicieron una radiografía y vieron que sus intestinos estaban muy hinchados. La niña fue al hospital y los doctores la operaron para ver qué pasaba.\n\nDentro, encontraron que sus intestinos estaban enredados como un nudo. También vieron que una parte pequeña llamada apéndice estaba dañada. Los doctores deshicieron el nudo y quitaron el apéndice malo.\n\nComo la niña estaba muy débil, los doctores hicieron algo para que sus intestinos no se movieran mucho y la cuidaron mucho después.",
+                "fh_score": 72.28
+            },
+            "B2": {
+                "text": "**Lo que le pasó a la paciente:**  \nUna joven de 20 años, que acababa de tener un bebé por cesárea, llegó al hospital con el abdomen muy hinchado, dolor y vómitos. Además, no podía expulsar gases ni hacer sus necesidades. Estos síntomas indicaban que algo estaba bloqueando su intestino.\n\n**Lo que encontraron en las pruebas:**  \nLa radiografía mostró que partes del intestino estaban muy dilatadas y había niveles de aire y líquido, lo que sugiere una obstrucción. Por eso, los médicos decidieron hacer una cirugía para ver qué estaba pasando.\n\n**Lo que vieron durante la operación:**  \nDescubrieron que una parte del intestino delgado (íleon) estaba enredada alrededor del ciego y el colon ascendente, formando un nudo llamado \"nudo ileocecal\". El intestino estaba en buen estado, pero la punta del apéndice estaba dañada (gangrenosa). Los médicos deshicieron el nudo y quitaron el apéndice enfermo (apendectomía).\n\n**Cómo continuó el tratamiento:**  \nLa paciente tuvo problemas con su presión arterial durante la cirugía, por lo que no pudieron hacer una cirugía más grande (hemicolectomía derecha) en ese momento. En cambio, fijaron el ciego y el colon a la pared abdominal para evitar que se movieran y causaran más problemas.\n\n**Qué significa esto:**  \nEl nudo ileocecal es una causa rara de bloqueo intestinal que puede ser grave. En este caso, la cirugía ayudó a liberar el intestino y a quitar la parte dañada. Sin embargo, la paciente tuvo complicaciones después, lo que muestra que este tipo de problemas necesita atención rápida y cuidadosa.",
+                "fh_score": 60.61
+            },
+            "B3": {
+                "text": "**Contexto:**  \nSe trató de una mujer joven de 20 años que, tras un parto por cesárea debido a problemas con el ritmo cardíaco fetal, comenzó a presentar una distensión abdominal progresiva acompañada de calambres, vómitos frecuentes y la incapacidad para expulsar gases y heces. No tenía antecedentes de cirugías abdominales ni enfermedades crónicas. Su estado general era grave, con signos de dolor abdominal intenso, presión arterial baja y taquicardia (latidos rápidos del corazón). Las pruebas iniciales mostraron una disminución en el número de glóbulos blancos y plaquetas, además de una radiografía abdominal que evidenció dilatación de los intestinos y acumulación de líquido en la cavidad abdominal.\n\n**Hallazgos Clave:**  \nDurante la cirugía exploratoria, se encontró que una parte del intestino delgado (íleon distal) estaba enredada alrededor del ciego y el colon ascendente, formando un nudo intestinal (nudo ileocecal). Aunque el intestino estaba viable (sin daño irreversible), la punta del apéndice estaba gangrenosa (tejido muerto por falta de circulación). Se observó también una gran cantidad de líquido seroso en la cavidad abdominal. La paciente presentó inestabilidad hemodinámica (presión arterial muy baja) durante la operación, lo que complicó el manejo quirúrgico.\n\n**Interpretación Clínica:**  \nEl nudo ileocecal es una causa rara pero grave de obstrucción intestinal que puede provocar compromiso vascular y gangrena si no se trata oportunamente. En este caso, la viabilidad del intestino permitió deshacer el nudo y realizar la extirpación del apéndice afectado (apendicectomía). Debido a la inestabilidad de la paciente, se decidió posponer la resección mayor (hemicolectomía derecha) y en su lugar se fijaron el ciego y el colon ascendente para evitar una nueva torsión.\n\n**Próximos Pasos y Evolución:**  \nA pesar de las intervenciones quirúrgicas y el soporte con líquidos y medicamentos para estabilizar la presión arterial, la paciente desarrolló una infección grave denominada gangrena de Fournier, que afectó la región genital y suprapúbica. Se requirió un desbridamiento quirúrgico radical y tratamiento antibiótico intensivo. Sin embargo, la paciente evolucionó hacia un shock séptico refractario (una infección generalizada que no responde al tratamiento) y finalmente falleció debido a un fallo multiorgánico en el segundo día postoperatorio.\n\nEste caso resalta la complejidad y gravedad de las complicaciones abdominales posparto, la importancia del diagnóstico temprano y la dificultad de manejo en pacientes con inestabilidad hemodinámica y recursos limitados.",
+                "fh_score": 36.54
+            }
+        }
+    },
+    {
+        "article": "Un hombre de 38 años se presentó en el hospital con opresión en el pecho y falta de aire. Tres años antes, había experimentado síntomas similares después de la actividad y recibió tratamiento en nuestro hospital. La ecocardiografía ambulatoria indicó una masa de eco del corazón izquierdo que sugería un mixoma, lo que llevó a su ingreso para una evaluación adicional. El examen físico reveló pigmentación de las orejas del paciente caracterizada por múltiples puntos pequeños de color café y negro. La tomografía computarizada abdominal (TC) mostró múltiples hígados y pequeños quistes en el riñón izquierdo. Las pruebas genéticas identificaron mutaciones en los genes TTN y PRKAR1A. El diagnóstico de CNC se confirmó mediante examen clínico, imágenes y pruebas genéticas. Después del tratamiento sintomático, la condición del paciente mejoró; sin embargo, rechazó la intervención quirúrgica. El 20 de septiembre de 2023, el paciente se presentó en nuestro hospital con opresión en el pecho y falta de aire exacerbadas. Informó dificultad para permanecer acostado boca arriba y necesidad de sentarse erguido para respirar. El examen físico reveló distensión de la vena yugular, desplazamiento hacia la izquierda y hacia abajo del límite del corazón, ritmo cardíaco irregular en la auscultación y un murmullo de la válvula mitral de intensidad 2/6-3/6 en el cuarto espacio intercostal a lo largo del margen izquierdo del esternón. Se escucharon estertores húmedos en ambos campos pulmonares medio e inferior. La palpación reveló un hígado firme que se extendía tres dedos por debajo del proceso xifoides y dos dedos por debajo de la caja torácica, junto con un edema de pitting leve en ambas extremidades inferiores. Las imágenes ecocardiográficas indicaron un agrandamiento global del corazón, dilatación del seno aórtico y arteria pulmonar, regurgitación mitral pequeña a moderada y una masa ecógena irregular que medía 54 mm × 43 mm en la cámara izquierda unida al tabique auricular. La fracción de eyección del ventrículo izquierdo (FEVI) fue del 23,1 %, con acortamiento fraccional (FS) del 10,9 %. La electrocardiografía demostró fibrilación auricular (frecuencia ventricular promedio, 150 latidos/min) y ondas Q anormales en las derivaciones V1-V3. Basándose en la historia del paciente, el diagnóstico incluyó DCM y CNC con mixoma cardíaco. Dada la presencia de insuficiencia cardíaca en etapa terminal y mixoma cardíaco concurrente, el paciente fue hospitalizado y se consideró el trasplante de corazón como una opción terapéutica viable para abordar ambas afecciones simultáneamente. Un corazón de donante adecuado estuvo disponible para su trasplante inmediato el 1 de octubre de 2024.\n\n\nProcedimiento quirúrgico\n\nLa piel y los tejidos subcutáneos se incisionaron cuidadosamente capa por capa a través de una esternotomía media. El esternón se abrió longitudinalmente y se controló el sangrado mediante electrocoagulación y cera ósea. La exploración extracardíaca reveló un agrandamiento global del corazón, más prominente en el ventrículo izquierdo. El corazón mostró una disminución de la fuerza contráctil. La aorta y la arteria pulmonar principal (AP) se diseccionaron desde la región supravalvular. Algunos tejidos se conservaron para suturarlos posteriormente, mientras que la mayor parte de la aurícula derecha enferma, la aurícula izquierda (AL), el ventrículo derecho y el ventrículo izquierdo se extirparon. La resección reveló una masa mucoide de color blanco grisáceo. Los tejidos de la aurícula izquierda del donante y del receptor se suturaron utilizando hilos Prolene 3/0 dobles continuos. La anastomosis se inspeccionó meticulosamente varias veces y no se observó sangrado significativo. De forma similar, la anastomosis término-terminal de la aorta ascendente del donante y la arteria pulmonar del receptor se realizó utilizando suturas Prolene 5/0 continuas, y una inspección cuidadosa no reveló sangrado.\n\nAdemás, la LA del donante y la PA del receptor se cerraron de forma segura utilizando suturas Prolene 5/0 dobles y continuas. Los tejidos de la vena cava inferior tanto del donante como del receptor se suturaron de forma similar con suturas Prolene 5/0, y se realizaron varias inspecciones para confirmar que no había presencia de sangrado significativo. El lado izquierdo del corazón se desinfló y, a medida que comenzó el recalentamiento, se restableció la oxigenación, se soltó la aorta ascendente y el corazón volvió espontáneamente al ritmo sinusal. Se aplicó sutura continua con Prolene 5/0 tanto a la vena cava superior del donante como del receptor y se inspeccionó de forma diligente para garantizar la ausencia de sangrado significativo. Después de la interrupción exitosa de la circulación asistida, se descanuló la cavidad venosa. Se recogieron muestras de tejido del corazón izquierdo y de la materia gris del paciente para un examen histopatológico, y se confirmó el diagnóstico de DCM y mixoma cardiaco.\n\n\nManejo postoperatorio\n\nEl primer día después del trasplante de corazón, el paciente produjo 1200 ml de orina. Los exámenes de laboratorio revelaron un nivel de troponina T hipersensible de 796.70 ng/L y un nivel de NT-proBNP de 10798 pg/ml. El recuento completo de sangre mostró un recuento de glóbulos blancos de 17.15 × 109/L, sin anomalías significativas en otros resultados de exámenes. El ecocardiógrafo mostró un EFV del 65 %, FS del 35 %, un espesor de la pared ventricular normal y ecogenicidad, y no se observaron anomalías discernibles en la morfología y estructura de la válvula. Después del trasplante de corazón, se administró una terapia hormonal intravenosa de succinato sódico de metilprednisolona (0.25 g) para mejorar la inmunidad, y se proporcionó un tratamiento intravenoso antiinfeccioso con cefoperazona y sulbactam sódico (2 g). El paciente recibió una solución nutriente y tiopronina en el primer día después de la cirugía. En el día tres postoperatorio, se reemplazó el succinato sódico de metilprednisolona con acetato de prednisona oral (25 mg). Se administraron cápsulas de micofenolato de mofetilo (0.5 g) por vía oral para minimizar el rechazo del corazón, y se administró acetato de carpofénico intravenoso (50 mg) para prevenir infecciones fúngicas. La producción de orina del paciente fue de 2000 ml, con niveles de troponina T hipersensible de 390 ng/L, niveles de NT-proBNP de 7877 pg/ml, y un recuento de leucocitos de 12.15 × 109/L. En el día siete postoperatorio, se introdujeron cápsulas de tacrolimus a una dosis oral de (1 mg) para minimizar el rechazo del paciente al corazón del donante, con un cuidadoso monitoreo de las concentraciones sanguíneas. Subsiguientemente, la dosis oral de acetato de prednisona se redujo gradualmente a (10 mg) mientras se ajustaba la concentración sanguínea de tacrolimus a 10.90 ng/L. La recuperación del paciente mejoró. El 20 de octubre de 2023, la ecocardiografía de seguimiento (Fig. 6) no mostró anomalías, con niveles de troponina T de 85 ng/L, NT-proBNP de 210 pg/ml, y todos los demás resultados de exámenes dentro de los rangos normales. El paciente exhibió una excelente recuperación postoperatoria y fue dado de alta. Las visitas regulares de seguimiento a nuestro departamento después del alta mostraron que el paciente permanece en buen estado.\n\nMH - Humanos\nMH - *Cardiomiopatía, Dilatada/cirugía/etiología/diagnóstico/diagnóstico por imágenes\nMH - Hombre\nMH - *Complejo de Carney/genética/diagnóstico/cirugía/complicaciones\nMH - Adulto\nMH - *Trasplante de corazón\nMH - *Mixoma/complicaciones/cirugía/diagnóstico por imágenes/diagnóstico/genética\nMH - *Insuficiencia cardiaca/etiología/diagnóstico/cirugía\nMH - *Neoplasias cardiacas/cirugía/complicaciones/diagnóstico por imágenes/diagnóstico/genética\nMH - Resultado del tratamiento\nMH - Subunidad/genética de la proteína quinasa Rlalpha dependiente de AMP cíclico\n",
+        "gold_summary": "Aquí, reportamos un caso de insuficiencia cardiaca debido al síndrome de Carney que resultó en mixoma cardiaco combinado con cardiomiopatía dilatada. Un hombre de 35 años de edad fue admitido en el hospital hace tres años debido a opresión torácica repentina y falta de aire. La ecocardiografía indicó mixoma, y una combinación de cribado genético y examen físico confirmó el síndrome de Carney con mixoma cardiaco. Después del tratamiento sintomático, fue dado de alta. Las intervenciones quirúrgicas no fueron consideradas en ese momento. Sin embargo, la opresión torácica y los síntomas de falta de aire del paciente empeoraron, y volvió al hospital. Se confirmó una función cardiaca de grado IV de la New York Heart Association, y la ecocardiografía indicó la presencia de cardiomiopatía dilatada acompañada de mixoma cardiaco. En última instancia, la insuficiencia cardiaca del paciente fue tratada con éxito con un trasplante cardiaco.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había un hombre que se sentía muy cansado y le dolía el pecho. Tenía un bulto en su corazón que no era bueno. Los doctores le hicieron pruebas y encontraron que tenía una enfermedad llamada síndrome de Carney. Al principio, le dieron medicinas para sentirse mejor y se fue a su casa. Pero después, se sintió peor y volvió al hospital. Su corazón estaba muy débil y tenía el bulto grande. Los doctores le dieron un corazón nuevo con una operación. Ahora, el hombre está mejor y puede vivir feliz.",
+                "fh_score": 86.03
+            },
+            "B2": {
+                "text": "**Lo que le pasó al paciente**\n\nUn hombre de 35 años tuvo problemas en el corazón que le causaban dolor en el pecho y dificultad para respirar. Al principio, los médicos encontraron una masa en su corazón llamada mixoma, que es un tipo de tumor benigno, y también detectaron que tenía el síndrome de Carney, una enfermedad rara que puede causar tumores y otros problemas en el cuerpo. En ese momento, solo le dieron medicamentos para aliviar los síntomas y no le hicieron cirugía.\n\n**Cómo empeoró su condición**\n\nCon el tiempo, sus síntomas se hicieron más graves. Volvió al hospital porque le costaba mucho respirar y su corazón estaba muy débil. Los médicos descubrieron que tenía cardiomiopatía dilatada, que significa que su corazón estaba agrandado y no podía bombear la sangre bien. Además, el mixoma seguía presente en su corazón.\n\n**Qué hicieron los médicos**\n\nDebido a que su corazón estaba muy dañado y tenía insuficiencia cardíaca avanzada, los médicos decidieron hacerle un trasplante de corazón. Esto significa que le pusieron un corazón nuevo de un donante para reemplazar el suyo enfermo.\n\n**Cómo fue la cirugía y la recuperación**\n\nLa operación fue complicada, pero exitosa. Los médicos quitaron el corazón enfermo y el tumor, y pusieron el corazón nuevo. Después de la cirugía, el paciente recibió medicamentos para evitar que su cuerpo rechazara el nuevo corazón y para prevenir infecciones. Poco a poco, su corazón comenzó a funcionar bien y sus síntomas mejoraron mucho.\n\n**Qué significa este caso**\n\nEste caso muestra cómo el síndrome de Carney puede causar problemas graves en el corazón, como tumores y debilidad del músculo cardíaco. También enseña que, cuando el corazón está muy dañado, un trasplante puede ser la mejor opción para salvar la vida del paciente.",
+                "fh_score": 63.55
+            },
+            "B3": {
+                "text": "**Contexto**\n\nPresentamos el caso de un hombre de 38 años diagnosticado con el síndrome de Carney (CNC), una enfermedad genética rara caracterizada por tumores cardíacos benignos llamados mixomas, pigmentación cutánea y otras anomalías. Este paciente inicialmente se presentó hace tres años con síntomas de opresión en el pecho y dificultad para respirar, y fue diagnosticado con un mixoma en el corazón izquierdo mediante ecocardiografía. Además, el examen físico reveló manchas pigmentadas en las orejas, y estudios de imagen detectaron múltiples lesiones hepáticas y quistes renales. Las pruebas genéticas confirmaron mutaciones en los genes TTN y PRKAR1A, asociadas con CNC y cardiomiopatía dilatada (una enfermedad que afecta la capacidad del corazón para bombear sangre). En ese momento, recibió tratamiento para aliviar los síntomas y fue dado de alta, rechazando la cirugía.\n\n**Evolución y Hallazgos Clínicos**\n\nEn septiembre de 2023, el paciente regresó con empeoramiento de la opresión torácica y dificultad respiratoria, incluyendo intolerancia a la posición acostada. El examen físico evidenció signos de insuficiencia cardíaca avanzada, como distensión de la vena yugular, ritmo cardíaco irregular (fibrilación auricular), murmullo en la válvula mitral y estertores pulmonares. También se observaron un hígado aumentado de tamaño y edema en las piernas. La ecocardiografía mostró un corazón globalmente agrandado, dilatación de grandes vasos, regurgitación mitral moderada y una masa irregular de 54 × 43 mm en la aurícula izquierda, compatible con mixoma. La función del ventrículo izquierdo estaba gravemente reducida, con una fracción de eyección del 23,1 % (normalmente >55 %). La electrocardiografía confirmó fibrilación auricular y alteraciones en las derivaciones precordiales. El diagnóstico final incluyó cardiomiopatía dilatada (DCM) y síndrome de Carney con mixoma cardíaco, en contexto de insuficiencia cardíaca terminal.\n\n**Procedimiento Quirúrgico**\n\nDada la gravedad de la insuficiencia cardíaca y la presencia del mixoma, se decidió realizar un trasplante de corazón. Durante la cirugía, se realizó una esternotomía media para acceder al corazón agrandado y debilitado. Se extirparon las aurículas y ventrículos enfermos junto con la masa tumoral, y se implantó el corazón donante mediante suturas meticulosas para conectar las estructuras vasculares y auriculares. El corazón trasplantado recuperó el ritmo sinusal espontáneamente y sin complicaciones hemorrágicas. El examen histopatológico confirmó la presencia de mixoma y cardiomiopatía dilatada en el tejido removido.\n\n**Manejo Postoperatorio y Resultados**\n\nEn el postoperatorio inmediato, el paciente mostró una producción urinaria adecuada y niveles elevados pero decrecientes de marcadores cardíacos (troponina T y NT-proBNP), indicadores de daño y estrés cardíaco. La ecocardiografía evidenció una función ventricular normalizada con fracción de eyección del 65 % y estructura valvular sin anomalías. Se instauró un régimen inmunosupresor con metilprednisolona, prednisona, micofenolato de mofetilo y tacrolimus para prevenir el rechazo del trasplante, junto con tratamiento antibiótico y antifúngico para evitar infecciones. La recuperación fue favorable, con normalización progresiva de los parámetros clínicos y de laboratorio. En el seguimiento a largo plazo, el paciente mantuvo un buen estado general sin signos de rechazo ni complicaciones, y fue dado de alta con un pronóstico positivo.\n\n**Interpretación Clínica**\n\nEste caso ilustra la complejidad del síndrome de Carney cuando se asocia con mixoma cardíaco y cardiomiopatía dilatada, condiciones que pueden conducir a insuficiencia cardíaca grave. La identificación temprana mediante ecocardiografía, examen físico detallado y pruebas genéticas es fundamental para el diagnóstico. Aunque inicialmente se manejó de forma conservadora, el deterioro progresivo de la función cardíaca requirió un trasplante de corazón, que resultó ser una opción terapéutica eficaz para tratar simultáneamente la insuficiencia cardíaca terminal y la masa tumoral. La cirugía y el manejo postoperatorio cuidadoso permitieron una recuperación exitosa y mejoraron significativamente la calidad de vida del paciente.\n\n**Próximos Pasos**\n\nSe recomienda continuar con controles regulares para monitorear la función cardíaca y detectar posibles signos de rechazo o recurrencia de la enfermedad. Además, el seguimiento genético y clínico es importante para evaluar otras manifestaciones del síndrome de Carney y prevenir complicaciones asociadas. La educación del paciente sobre la adherencia al tratamiento inmunosupresor y la vigilancia de síntomas es esencial para mantener un resultado favorable a largo plazo.",
+                "fh_score": 33.06
+            }
+        }
+    },
+    {
+        "article": "Un paciente de 52 años de edad con un diagnóstico inicial de arteria pulmonar fue admitido en el departamento de cardiología para una evaluación médica y una decisión sobre el tratamiento posterior. El paciente tenía un historial de neumotórax espontáneo del lado derecho, tratado con toracocentesis y drenaje por vacío 35 años antes. El paciente sentía una disnea creciente al hacer ejercicio. También se quejaba de signos de insuficiencia ventricular derecha y cianosis. Cuatro años antes, el paciente fue hospitalizado tres veces por fibrilación auricular paroxística que se convirtió en ritmo sinusal por cardioversión eléctrica, además de que el examen electrocardiográfico era normal.\n\nEn ese mismo año, la angiografía coronaria indicó arterias coronarias normales. La ecocardiografía reveló una hipertensión pulmonar leve con una presión sistólica calculada en el ventrículo derecho de 36 mmHg sin dilatación de ese ventrículo.\n\nEn los años siguientes, se observó insuficiencia cardiaca progresiva con aumento de la presión arterial pulmonar en la ecocardiografía. Se realizó angio-CT en dos ocasiones y se excluyó la hipertensión pulmonar tromboembólica crónica en cada ocasión. La tomografía computarizada de alta resolución excluyó la patología pulmonar intersticial. La espirometría fue normal. La detección de enfermedades autoinmunes y la infección por VIH fue negativa.\n\n\nLínea de tiempo: historia, curso de la enfermedad, diagnóstico y tratamiento\n\n1976  neumotórax derecho\n2007 Hospitalizado tres veces por fibrilación auricular e insuficiencia cardiaca. Se le realizaron ecocardiografías, cardioversiones y coronografías. En cada ocasión, fue dado de alta de los servicios con diagnósticos de fibrilación auricular, insuficiencia cardiaca e insuficiencia cardiaca de clase II de la NYHA.\n2010-2011: Aumento de la falta de aire y síntomas de insuficiencia cardiaca. El paciente fue hospitalizado tres veces. Se detectaron características indirectas de hipertensión pulmonar en ecocardiografía. Se realizó tres veces un examen de tórax por TAC; se excluyó la embolia pulmonar o la hipertensión arterial pulmonar tromboembólica crónica (2 x angio-TAC) o la fibrosis pulmonar (tomografía computarizada de alta resolución).\nSe estableció el diagnóstico de hipertensión pulmonar, clase III de la OMS.\nDEC-2011 Admisión a la clínica de cardiología – ecocardiografía (TTE, TEE), prueba de caminata de 6 minutos, NT-proBNP, cateterización cardiaca derecha, prueba de vasoreactividad pulmonar.\nSe estableció el diagnóstico de hipertensión pulmonar arterial irreversible.\nSe ha iniciado el tratamiento con iloprost y sildenafil\nEn enero de 2012, visita de control: mejora en la clase de la OMS, disminución de la concentración de NT-proBNP e incremento de la distancia en la prueba de 6 minutos.\nMAY-2012. Control RHC. La SaO2 de las muestras de sangre obtenidas durante el RHC de la arteria del lóbulo superior del pulmón derecho fue del 87 %.\nEl diagnóstico angiográfico de las arterias pulmonares reveló fístulas de HAP entre las arterias subclavianas y el lóbulo superior del pulmón derecho.\nJUN 2012  angiografía por TC de las arterias sistémicas reveló la presencia adicional de fístulas arteriales bronquiales en el lóbulo superior de las arterias del pulmón derecho\nIII-2013 Embolización de fístulas\nVI-2013. Muerte como resultado del empeoramiento de la insuficiencia cardiaca, combinado con neumonía.\n\n\n\nEn el ingreso a nuestra clínica, la clase funcional del paciente fue evaluada como OMS III. En el examen físico, el segundo sonido cardiaco (S2) fue acentuado con S2 dividido ensanchado. Además, la auscultación cardiaca indicó un murmullo holosistólico de regurgitación tricuspídea. La auscultación del tórax no mostró un murmullo vascular. La cianosis periférica y central fue marcada. Se examinaron la hepatomegalia, el edema periférico y las venas varicosas bilateralmente.\n\nLa SaO2 obtenida por el método de oximetría de pulso se redujo al 88 %. La electrocardiografía reveló fibrilación auricular, desviación del eje derecho y onda T negativa en las derivaciones precordiales v1-v3. Las pruebas adicionales fueron las siguientes: concentración de NT-proBNP - 3383 pg/ml, distancia de la prueba de caminata de seis minutos - 373 m con 7/10 puntos en la escala de disnea de Borg.\n\nLa ecocardiografía mostró características de hipertensión pulmonar grave: agrandamiento del ventrículo derecho a 44 mm (cuatro cámaras), con función deprimida del TAPSE del ventrículo derecho de 9 mm, agrandamiento del área de la aurícula derecha a 40 cm2, regurgitación tricuspídea grave (++++), aumento del PSVR calculado a 112 mmHg, acortamiento del tiempo de aceleración de la arteria pulmonar a 60 ms y derrame pericárdico leve. No hubo defecto en el tabique interventricular. La ecocardiografía transesofágica tampoco mostró un defecto en el tabique auricular, lo que se confirmó más tarde con angio-TAC.\n\n\nLa SaO2 de la sangre obtenida de la arteria radial se redujo al 87,8%. Se realizó un cateterismo cardiaco derecho. La SaO2 de las muestras de sangre obtenidas durante el RHC de la vena cava superior, la vena cava inferior, la aurícula derecha, el tronco pulmonar, la arteria del lóbulo medio del pulmón derecho y la arteria pulmonar izquierda ascendieron respectivamente a: 64,8%; 77,4%; 73,2%; 70,2%; 69,3%; 71,2% y no indicaron la presencia de un shunt de izquierda a derecha.\n\nLas mediciones hemodinámicas mostraron una hipertensión pulmonar precapilar grave, irreversible en las pruebas de vasoreactividad con óxido nítrico inhalado (80 ppm) y una combinación de sildenafil oral (50 mg) y óxido nítrico inhalado (80 ppm).\n\nEn base a todos los datos clínicos y los resultados de la RHC, se estableció un diagnóstico de hipertensión pulmonar idiopática irreversible.\n\nSe inició el tratamiento con iloprost inhalado (Ventavis) 6 × 5 µg y sildenafil (Revatio) por vía oral 3 × 20 mg. Además, se administraron digoxina (0,1 mg diarios), warfarina (INR rango: 2-3), furosemida (40 mg por vía oral diarios) y espironolactona (100 mg diarios).\n\nUn mes después se realizó un seguimiento no invasivo. El paciente manifestó una mejoría en la capacidad física, clase II según la OMS, concentración de NT-proBNP: 1014 pg/ml. Distancia en la prueba de caminata de seis minutos: 471 m.\n\nCinco meses después se realizó una evaluación invasiva. La RHC mostró valores de PAP más elevados que en las mediciones iniciales [75,4/51,8 (59,7) mm Hg] y PVR (13,4 WU) (Tabla 22 – control RHC).\n\nLa saturación de oxígeno de las muestras de sangre obtenidas durante la RHC de la arteria lobular superior del pulmón derecho fue elevada y ascendió al 89.7%.\n\nEn la angiografía pulmonar se detectó la reducción del trazo vascular periférico típico de la hipertensión arterial pulmonar y la falta de contraste de la arteria del lóbulo superior derecho. Además, se encontró evidencia de flujo sanguíneo retrógrado visible como un contraste negativo en la arteria pulmonar derecha. Después, se realizó una arteriografía de la arteria subclavia derecha y se detectó una enorme malformación vascular que se comunicaba con la arteria del lóbulo superior derecho.\n\nLa angio-TC de las arterias sistémicas confirmó la presencia de las fístulas previamente descritas y reveló la presencia adicional de fístulas de la arteria bronquial en el lóbulo superior de las arterias del pulmón derecho.\n\nSe realizó embolización selectiva de las fístulas (mezcla al 50% de Lipiodol y pegamento monomérico de n-butil-2-cianoacrilato). La embolización no produjo ningún cambio clínico en el estado del paciente.\n\nMH - Fístula arterio-arterial/*complicaciones\nMH - *Cateterización cardiaca\nMH - Angiografía por tomografía computarizada\nMH - Hipertensión pulmonar primaria familiar/*diagnóstico/terapia farmacológica\nMH - Resultado fatal\nMH - Insuficiencia cardiaca/fisiopatología\nMH - Humanos",
+        "gold_summary": "Un paciente caucásico de 52 años de edad con hipertensión pulmonar (HP) confirmada por ecocardiografía fue admitido en el departamento de cardiología debido a disnea de esfuerzo y signos de insuficiencia ventricular derecha. La exploración rutinaria para detectar causas de HP secundaria fue negativa. El cateterismo cardiaco derecho (CCR) confirmó una HP arterial de alto grado [presión arterial pulmonar media (PAPm); 50,6 mmHg, presión de enclavamiento pulmonar (PWP); 11,3 mmHg, resistencia vascular pulmonar (PVR); 11,9 unidades de Wood (UW)] irreversible en la prueba con óxido nítrico inhalado. La saturación de oxígeno (SaO2) de las muestras de sangre obtenidas durante el primer CCR osciló entre 69,3 y 73,2%. Se diagnosticó hipertensión arterial pulmonar idiopática. Se inició el tratamiento con iloprost inhalado y sildenafil.\n\nEl control RHC, realizado 5 meses después, mostró valores de mPAP (59,7 mmHg) y PVR (13,4 WU) más altos en comparación con la medición inicial. El SaO2 de sangre obtenida durante el RHC de la arteria del lóbulo superior del pulmón derecho fue elevado y ascendió al 89,7 %.\n\nLuego se realizó una arteriografía pulmonar. Se encontró falta de contraste en la arteria del lóbulo superior derecho con evidencia de flujo sanguíneo retrógrado visible como contraste negativo en la arteria pulmonar derecha. Después, una arteriografía de la arteria subclavia derecha detectó una enorme malformación vascular que se comunicaba con la arteria del lóbulo superior derecho. Después, un angiograma por tomografía computarizada (angio-CT) reveló adicionalmente el agrandamiento de las arterias bronquiales que se originaban en las fístulas hacia la arteria pulmonar del lóbulo superior derecho.\n\nA pesar del tratamiento farmacológico intensivo, que incluyó la terapia de la hipertensión pulmonar y la embolización percutánea de las fístulas, el estado del paciente siguió deteriorándose. Falleció tres meses después de la embolización debido a una insuficiencia cardiaca grave complicada por neumonía.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había un hombre de 52 años que tenía problemas para respirar. Su corazón y pulmones no funcionaban bien. Los doctores hicieron muchas pruebas para entender qué pasaba.\n\nEncontraron que la presión en sus pulmones era muy alta. Le dieron medicinas para ayudar, pero no mejoró mucho.\n\nLuego vieron que tenía unos tubos raros en sus pulmones que no estaban bien. Intentaron taparlos para ayudar, pero el hombre se puso más enfermo.\n\nAl final, el hombre murió porque su corazón se cansó mucho y tuvo una infección en los pulmones. Los doctores hicieron todo lo que pudieron para ayudarlo.",
+                "fh_score": 78.18
+            },
+            "B2": {
+                "text": "**Caso de un Paciente con Hipertensión Pulmonar y Problemas en las Arterias del Pulmón**\n\nUn hombre de 52 años tenía dificultad para respirar y problemas en el lado derecho de su corazón. Los médicos confirmaron que tenía hipertensión pulmonar, que es cuando la presión en las arterias de los pulmones está muy alta. Para entender mejor su enfermedad, le hicieron un examen llamado cateterismo cardiaco derecho, que mide la presión y el flujo de sangre en el corazón y los pulmones. Los resultados mostraron que su hipertensión pulmonar era grave y no mejoraba con el tratamiento con óxido nítrico inhalado. Además, la cantidad de oxígeno en su sangre estaba baja, entre 69% y 73%.\n\nLos médicos pensaron que tenía hipertensión arterial pulmonar idiopática, que significa que la causa es desconocida. Por eso, comenzaron un tratamiento con dos medicamentos: iloprost inhalado y sildenafil, que ayudan a bajar la presión en las arterias pulmonares.\n\nCinco meses después, hicieron otro cateterismo y encontraron que la presión en sus pulmones había aumentado aún más, y la resistencia al flujo sanguíneo también era mayor. Sin embargo, la cantidad de oxígeno en la sangre de una parte específica del pulmón derecho había subido a casi 90%, lo que era extraño.\n\nPara investigar esto, realizaron una arteriografía, que es una prueba que usa un contraste para ver las arterias con rayos X. Descubrieron que la arteria del lóbulo superior del pulmón derecho no se llenaba bien con el contraste y que la sangre estaba fluyendo en dirección contraria en esa arteria. Luego, hicieron otra arteriografía en la arteria subclavia derecha (una arteria cerca del hombro) y encontraron una gran malformación, que es una conexión anormal entre vasos sanguíneos, que se comunicaba con la arteria del pulmón derecho.\n\nTambién un estudio por tomografía computarizada mostró que las arterias bronquiales, que normalmente llevan sangre a los pulmones, estaban agrandadas y formaban fístulas. Las fístulas son conexiones anormales entre arterias que pueden causar problemas en el flujo sanguíneo.\n\nAunque el paciente recibió tratamiento médico y se intentó cerrar estas fístulas mediante un procedimiento llamado embolización (que bloquea estas conexiones anormales), su salud empeoró. Tres meses después de este procedimiento, falleció debido a insuficiencia cardiaca grave, que fue complicada por una infección pulmonar llamada neumonía.\n\n**Qué Significa Este Caso**\n\nEste caso muestra que en algunos pacientes con hipertensión pulmonar grave, pueden existir conexiones anormales entre arterias que afectan el flujo de sangre y el oxígeno en los pulmones. Aunque se usen medicamentos y procedimientos para tratar estas malformaciones, la enfermedad puede avanzar y causar complicaciones serias. Por eso, es importante hacer estudios detallados para entender todas las causas y buscar el mejor tratamiento posible.",
+                "fh_score": 52.36
+            },
+            "B3": {
+                "text": "**Contexto**  \nSe trata de un hombre caucásico de 52 años con hipertensión pulmonar (HP) grave, inicialmente diagnosticada mediante ecocardiografía, que presentaba dificultad para respirar al esfuerzo y signos de insuficiencia del ventrículo derecho del corazón. A lo largo de su evolución, se descartaron causas secundarias comunes de hipertensión pulmonar mediante estudios exhaustivos, incluyendo pruebas de imagen y análisis de laboratorio.\n\n**Hallazgos Clave**  \nEl cateterismo cardiaco derecho (CCR), una prueba invasiva que mide directamente las presiones y flujos en el corazón y pulmones, confirmó una hipertensión arterial pulmonar severa e irreversible, con una presión arterial pulmonar media elevada (50,6 mmHg), presión de enclavamiento pulmonar normal (11,3 mmHg) y resistencia vascular pulmonar alta (11,9 unidades de Wood). La saturación de oxígeno en la sangre obtenida durante este procedimiento fue moderadamente reducida (entre 69,3% y 73,2%), lo que indicaba un intercambio de oxígeno comprometido.\n\nCinco meses después, un nuevo cateterismo mostró un empeoramiento de las presiones pulmonares (presión media de 59,7 mmHg) y de la resistencia vascular (13,4 unidades de Wood). Sin embargo, la saturación de oxígeno en la arteria del lóbulo superior derecho del pulmón aumentó notablemente hasta 89,7%, lo que sugería la presencia de un flujo anormal de sangre.\n\nUna angiografía pulmonar (estudio de imagen con contraste para visualizar las arterias pulmonares) reveló ausencia de contraste en la arteria del lóbulo superior derecho y flujo sanguíneo retrógrado (en sentido contrario al habitual) en la arteria pulmonar derecha. Posteriormente, una arteriografía de la arteria subclavia derecha identificó una gran malformación vascular que conectaba esta arteria con la arteria del lóbulo superior derecho del pulmón. Un estudio adicional con angiografía por tomografía computarizada (angio-TC) mostró además un aumento del tamaño de las arterias bronquiales que formaban fístulas (conexiones anormales) hacia la arteria pulmonar del mismo lóbulo.\n\n**Interpretación Clínica**  \nEl diagnóstico final fue hipertensión arterial pulmonar idiopática (sin causa identificable) complicada por la presencia de fístulas arterio-arteriales entre las arterias sistémicas (subclavia y bronquiales) y las arterias pulmonares del lóbulo superior derecho. Estas conexiones anómalas alteraban el flujo sanguíneo normal, contribuyendo al empeoramiento de la insuficiencia cardiaca derecha y a la hipoxemia (bajo nivel de oxígeno en sangre).\n\nA pesar del tratamiento médico intensivo con vasodilatadores pulmonares (iloprost inhalado y sildenafil oral) y de la embolización percutánea (procedimiento para cerrar las fístulas mediante la introducción de materiales que bloquean el flujo anormal), la condición del paciente continuó deteriorándose.\n\n**Próximos Pasos y Resultado**  \nEl paciente falleció tres meses después de la embolización debido a insuficiencia cardiaca grave, agravada por una neumonía. Este caso resalta la complejidad y gravedad de la hipertensión pulmonar idiopática cuando se asocia a malformaciones vasculares, y la dificultad para controlar la progresión a pesar de las terapias disponibles.",
+                "fh_score": 29.78
+            }
+        }
+    },
+    {
+        "article": "Paciente de 73 años, diagnosticada de enfermedad pulmonar obstructiva crónica (EPOC), hipertensión arterial (HTA), trastorno bipolar, ansiedad, depresión, hipotiroidismo y artritis reumatoide, condiciones para las cuales tiene prescrito el tratamiento reflejado en el Anexo I.\n\nRealiza una llamada telefónica a la farmacia comunitaria para solicitar información sobre una nueva medicación prescrita para el tratamiento de una infección de orina y un déficit de vitamina D, diagnosticados tras la realización de una analítica completa en el servicio de urgencias de un hospital privado.\n\nLa paciente es totalmente dependiente y no sale de casa, siendo su cuidadora la persona que siempre va a retirar su medicación y elabora los pastilleros semanales.\n\nLos fármacos prescritos para el tratamiento de la infección de orina fueron cefuroxima 250 mg (1 comprimido cada 12 horas durante 5 días) y butilescopolamina 10 mg (1 comprimido en la mañana si presentaba molestias).\n\nPara el déficit de vitamina D se le prescribió colecalciferol 50.000 U.I. (1 cápsula una vez al mes durante dos meses) y colecalciferol 25.000 UI (1 cápsula una vez al mes tras finalizar el envase de 50.000 U.I.).\n\nESTUDIO Y EVALUACIÓN\nSe lleva a cabo el servicio de dispensación (SD) sin incidencias, siguiendo la metodología expuesta en la Guía práctica para los Servicios Profesionales Farmacéuticos Asistenciales en la Farmacia Comunitaria. Posteriormente, la paciente contacta con la farmacia comunitaria, preocupada porque la nueva medicación le ha generado confusión, ya que ella tomaba unas cápsulas naranjas para su déficit de vitamina D prescritas por su médico de Atención Primaria hace unos meses y en la parte del informe de urgencias en la que figura el tratamiento venía reflejado una medicación nueva para ese mismo problema de salud. Además, coincidió con que su cuidadora habitual ya no podrá trabajar más con ella y no la podrá ayudar con su medicación. Por ello, se le propone a la paciente el servicio de Revisión del Uso del Medicamento (RUM) con el objetivo de evaluar el grado de conocimiento que tienen la paciente con respecto a sus patologías y su tratamiento, a la par que poder resolver posibles errores en la administración de los distintos fármacos que forman parte del mismo. Se le explica en qué consiste todo el procedimiento y decide aceptar.\n\nTras esto, se procedió a citar a la cuidadora en la farmacia con la tarjeta sanitaria de la paciente, su bolsa de medicación para hacer una revisión exhaustiva de su botiquín y el último informe de urgencias con el objetivo de recopilar toda la información necesaria para realizar el servicio asistencial vía telefónica. Durante la llamada con la paciente, se procede a cumplimentar el formulario RUM, el cual se volcó posteriormente en la plataforma SEFAC e_XPERT ®. Además, para poder evaluar correctamente todo el tratamiento farmacológico, se emplearon herramientas como el CIMA (donde se consultaron las fichas técnicas de los medicamentos) y el BotPlus (donde se consultaron las posibles interacciones farmacológicas).\n\nINTERVENCIÓN\nTras la primera toma de contacto a través de la entrevista telefónica y hacer revisión del botiquín, se pudo detectar que la paciente y su cuidadora no estaban haciendo una gestión apropiada de la medicación. Tras la revisión de su botiquín, se hallaron envases caducados y con anotaciones erróneas sobre su uso, blísteres con comprimidos partidos que no deberían de estarlo y acúmulo de varios envases de un mismo fármaco. Al tratarse de una paciente dependiente, polimedicada y con problemas para gestionar correctamente su tratamiento antes y durante la ausencia de su cuidadora habitual se decidió con el fin de garantizar la seguridad farmacoterapéutica y mejorar la adherencia al tratamiento derivar al servicio de sistema personalizado de dosificación (SPD). A través de la plataforma de SEFAC e_XPERT ® se procedió a redactar un informe de derivación a su médico de Atención Primaria (MAP) del Sistema Nacional de Salud (SNS) (ver Anexo II), donde se detallaba la inclusión de la paciente en el servicio de Revisión del Uso de la Medicación y su posterior derivación al servicio de SPD. Además, quedaron recogidas las siguientes propuestas de intervención:\n\nRevisión de la pauta posológica de tramadol 50 mg de liberación retardada por la existencia de un posible error en la prescripción.\n\nRevisión del tratamiento prescrito para el déficit de vitamina D por la existencia de una duplicidad terapéutica.\n\nCambio del absorbente de incontinencia de tipo pants a elástico alegando la situación de dependencia de la paciente y las dificultades para realizar una correcta colocación por parte de la cuidadora al pasar encamada la mayor parte del tiempo. Se aportaron los Códigos Nacionales (CN) correspondientes.\n\nRevisión del tratamiento para la EPOC por dificultades de empleo del inhalador y falta de adherencia terapéutica.\n\nRESULTADOS\nDurante la cita médica, la médico de atención primaria recibe el informe de derivación entregado a la cuidadora donde, además, se solicita contacto con la farmacia comunitaria para poder iniciar de forma correcta el servicio de SPD. Tras hablar con ella vía telefónica, se realizaron los siguientes cambios en su tratamiento:\n\nDéficit de vitamina D: anulación de calcifediol y sustitución por colecalciferol prescrito en el Servicio de Urgencias.\n\nArtritis reumatoide: modificación de pauta de tramadol de liberación prolongada a 1-0-1 y empleo de paracetamol 1000 mg 1-1-1 si precisa.\n\nIncontinencia urinaria: sustitución de absorbente tipo pants por elástico.\n\nEPOC: no se realizó un cambio de tratamiento. La médico de atención primaria consideró oportuno llevar a cabo una supervisión diaria por parte de la cuidadora en cada una de las tomas del inhalador.",
+        "gold_summary": "Paciente 73 años, dependiente, polimedicada y pluripatológica contacta telefónicamente con la farmacia comunitaria para solicitar información sobre un tratamiento de nueva prescripción para una infección de orina y un déficit de vitamina D. La dispensación de la medicación a su cuidadora deriva en mayores dudas a la paciente, por lo que se le ofrece el servicio de revisión del uso del medicamento (RUM). Durante la prestación del servicio se detectan varias incidencias en su tratamiento, por lo que se decide realizar un informe de derivación al médico de atención primaria para una revisión completa del tratamiento y poder así derivar a la paciente al servicio de Sistema Personalizado de Dosificación (SPD) con el fin de garantizar la seguridad farmacoterapéutica de la paciente y mejorar su adherencia al tratamiento.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una señora de 73 años se siente confundida con sus medicinas nuevas. Ella no puede salir de casa y su cuidadora siempre le ayuda con sus pastillas. La señora llamó a la farmacia para preguntar. \n\nLa farmacia revisó todas sus medicinas y vio que había problemas. Algunas pastillas estaban mal guardadas y había medicinas repetidas. \n\nPor eso, la farmacia habló con su doctor para ayudarla mejor. El doctor cambió algunas medicinas y pidió que la señora tenga un organizador especial para sus pastillas. Así, será más fácil y seguro tomar sus medicinas.",
+                "fh_score": 71.85
+            },
+            "B2": {
+                "text": "**Información sobre la Paciente y su Situación**\n\nUna mujer de 73 años, que depende totalmente de otras personas para su cuidado y toma muchos medicamentos por varias enfermedades, llamó a la farmacia para preguntar sobre un nuevo tratamiento. Este tratamiento era para una infección de orina y para un problema de falta de vitamina D, que le habían diagnosticado en un hospital.\n\n**Problemas Detectados con la Medicación**\n\nAunque su cuidadora recogió los medicamentos, la paciente se confundió porque ya tomaba otras pastillas para la vitamina D y no entendía bien los cambios. Además, su cuidadora habitual ya no podía ayudarla, lo que complicaba más la situación. Por eso, la farmacia le ofreció un servicio llamado Revisión del Uso del Medicamento (RUM). Este servicio ayuda a revisar si la paciente entiende bien sus medicinas y si las está tomando correctamente.\n\nAl revisar los medicamentos, encontraron varios problemas: había medicinas vencidas, instrucciones equivocadas, pastillas partidas que no debían estar así y varios envases del mismo medicamento. Como la paciente no podía manejar bien su tratamiento y estaba sin su cuidadora, se decidió que necesitaba un Sistema Personalizado de Dosificación (SPD). Este sistema organiza las medicinas en pastilleros para que sea más fácil y seguro tomarlas.\n\n**Acciones y Cambios Realizados**\n\nSe preparó un informe para el médico de atención primaria explicando la situación y recomendando la revisión completa del tratamiento. El médico hizo algunos cambios importantes, como:\n\n- Cambiar la vitamina D para evitar tomar dos tipos diferentes al mismo tiempo.\n\n- Ajustar la dosis de un analgésico llamado tramadol.\n\n- Cambiar el tipo de pañales para facilitar su uso debido a la dependencia de la paciente.\n\n- Mantener el tratamiento para la enfermedad pulmonar, pero con supervisión diaria para asegurar que la paciente use bien el inhalador.\n\n**Conclusión**\n\nGracias a la revisión y coordinación entre la farmacia y el médico, se mejoró la seguridad y el manejo del tratamiento de la paciente. Además, se implementó un sistema que facilitará que tome sus medicamentos correctamente, lo cual es muy importante para su salud y bienestar.",
+                "fh_score": 52.87
+            },
+            "B3": {
+                "text": "**Contexto**  \nSe trata de una paciente de 73 años con múltiples enfermedades crónicas, incluyendo enfermedad pulmonar obstructiva crónica (EPOC), hipertensión arterial, trastorno bipolar, ansiedad, depresión, hipotiroidismo y artritis reumatoide. Es totalmente dependiente para sus actividades diarias y no sale de casa; su cuidadora habitual se encargaba de gestionar y recoger su medicación. Recientemente, tras una analítica en urgencias, se le diagnosticó una infección de orina y un déficit de vitamina D, para los cuales se le prescribió un nuevo tratamiento.\n\n**Hallazgos Clave**  \nLa paciente contactó con la farmacia comunitaria para aclarar dudas sobre la nueva medicación, ya que existía confusión debido a la coexistencia de tratamientos previos para el déficit de vitamina D y la reciente prescripción. Además, la cuidadora habitual informó que ya no podría continuar asistiendo a la paciente, lo que generó preocupación sobre la correcta administración de los medicamentos. Se ofreció entonces el servicio de Revisión del Uso del Medicamento (RUM) para evaluar el conocimiento de la paciente y su cuidadora sobre las patologías y tratamientos, y para identificar posibles errores en la gestión farmacológica.\n\nDurante la revisión, se detectaron múltiples problemas: medicamentos caducados, instrucciones incorrectas, comprimidos partidos indebidamente y acumulación de envases duplicados. También se identificaron errores potenciales en la prescripción, como duplicidad en el tratamiento para la vitamina D y una pauta inadecuada para tramadol. Además, se observaron dificultades en el manejo del inhalador para la EPOC y problemas relacionados con la elección del absorbente para la incontinencia urinaria, que complicaban la correcta atención de la paciente.\n\n**Interpretación Clínica**  \nDada la complejidad del caso, la dependencia de la paciente y la ausencia de su cuidadora habitual, se consideró necesario derivar a la paciente al servicio de Sistema Personalizado de Dosificación (SPD), que facilita la organización y administración segura de la medicación. Se elaboró un informe detallado para el médico de Atención Primaria, incluyendo recomendaciones específicas para ajustar el tratamiento, como la sustitución del calcifediol por colecalciferol para el déficit de vitamina D, la modificación de la pauta de tramadol y el cambio del tipo de absorbente para mejorar la comodidad y manejo.\n\nEn cuanto al tratamiento para la EPOC, el médico decidió mantener la medicación actual pero reforzar la supervisión diaria por parte de la cuidadora para asegurar la correcta utilización del inhalador.\n\n**Próximos Pasos**  \nEl médico de Atención Primaria recibió el informe y coordinó con la farmacia comunitaria la implementación del Sistema Personalizado de Dosificación. Este enfoque busca mejorar la seguridad en la administración de los medicamentos, evitar errores y aumentar la adherencia al tratamiento, aspectos fundamentales para el bienestar y la calidad de vida de la paciente. Además, se estableció un seguimiento estrecho para supervisar la evolución clínica y la correcta gestión terapéutica en el contexto de la nueva situación de dependencia y ausencia de la cuidadora habitual.",
+                "fh_score": 31.22
+            }
+        }
+    },
+    {
+        "article": "Nuestra paciente era una mujer japonesa de 83 años con insuficiencia cardiaca crónica (fracción de eyección: aproximadamente 30 %) que inició un tratamiento con empagliflozina 10 mg diarios unos 8 meses antes de su ingreso. Nunca se le había diagnosticado diabetes mellitus (HbA1c 5.9 % antes de iniciar el tratamiento con empagliflozina). Unos 6 meses antes de su ingreso, su tratamiento se cambió a dapagliflozina 5 mg. Sus diuréticos y otros medicamentos cardiacos no se ajustaron durante ese tiempo. Dos semanas antes de su ingreso, tropezó y cayó, sufriendo fracturas vertebrales y de costillas. La paciente se debilitó significativamente por el dolor de las fracturas, lo que le causó dificultad para caminar y anorexia. Solo podía comer el 50-70 % de su ingesta dietética habitual. Esto empeoró en la semana siguiente, cuando también desarrolló náuseas y vómitos y redujo aún más su ingesta de alimentos a solo el 10-20 % de la cantidad habitual. Durante este período, continuó tomando dapagliflozina. Fue ingresada en el hospital.\nAl ingreso, la paciente estaba consciente con una temperatura corporal de 37.4°C, presión arterial de 124/68 mmHg, frecuencia cardiaca de 91 bpm y saturación de oxígeno de 98% en aire ambiente. Los análisis de sangre revelaron un nivel de glucosa en sangre de 124 mg/dL, pH de 7.3, concentración de HCO3– de 14 mmol/L, exceso de base de -10 mEq/L, brecha aniónica de 20 mEq/L y concentración de b-hidroxibutirato de 5150 umol/L (Tabla 1). Estos hallazgos fueron consistentes con el diagnóstico de cetoacidosis normoglucémica. La paciente no tenía antecedentes de consumo de alcohol, tabaquismo o uso de drogas.\nSe descartaron otras causas de acidosis con alto déficit aniónico. Su nivel de péptido C era coherente con los niveles de glucosa en sangre en el ingreso, lo que indicaba que tenía una secreción de insulina adecuada; por lo tanto, no se inició la administración de insulina. Se interrumpió el uso de inhibidores de SGLT2 y la paciente se trató inicialmente con solución salina isotónica y una infusión de mantenimiento de aproximadamente 170 g de glucosa diarios.\nA pesar de no haber iniciado la insulina, su pH (7.418), concentración de HCO3– (20.7 mmol/L) y brecha aniónica (13.3 mEq/L) mejoraron al día siguiente de su ingreso. Se inició la dieta Carb 60, pero se continuaron las infusiones intravenosas de glucosa porque la ingesta de alimentos de la paciente era escasa. La cantidad de infusión de glucosa administrada se ajustó según su ingesta de alimentos. En el cuarto día de hospitalización, las cetonas urinarias desaparecieron.\nLa infusión de glucosa se interrumpió el día 12 de la hospitalización, una vez que el paciente pudo comer comidas completas. Aunque el nivel de glucosa en sangre del paciente estaba dentro del rango normal, la excreción de glucosa en la orina fue de 3+ (>500 mg/dL) durante 8 días después de la última dosis de dapagliflozina.\nAl ingreso, la paciente no podía caminar debido al dolor de la fractura, la fatiga general y el síndrome de desuso, pero después de la rehabilitación pudo hacerlo de forma independiente. Fue dada de alta el día 19 de hospitalización, tras someterse a rehabilitación.\nLos inhibidores de SGLT2 no se reiniciaron.\n\nMH - Humanos\nMH - Mujer\nMH - *Insuficiencia cardiaca/inducida químicamente\nMH - *Inhibidores del transportador de glucosa y sodio 2/efectos adversos\nMH - Edad 80 años y más\nMH - Cetosis/químicamente inducida\nMH - glucósidos/efectos adversos\nMH - Cetoacidosis diabética/inducida químicamente\n",
+        "gold_summary": "A continuación, describimos un caso de cetoacidosis en una mujer japonesa de 83 años sin diabetes a la que se le administraron inhibidores de SGLT2 para la insuficiencia cardiaca (fracción de eyección: aproximadamente 30 %). Dos semanas antes de su ingreso, había sufrido una fractura vertebral y una fractura de costilla debido a una caída, a la que siguió una anorexia, pero continuó tomando inhibidores de SGLT2. En el momento del ingreso, los resultados de los análisis de sangre revelaron un nivel de glucosa en sangre de 124 mg/dL, un nivel de hemoglobina A1C del 5,9 %, un pH de 7,329, una concentración de HCO₃⁻ de 14,3 mmol/L y una concentración de β-hidroxibutirato de 5150 μmol/L, lo que condujo a un diagnóstico de cetoacidosis euglucémica. El nivel de péptido C de la paciente coincidía con los niveles de glucosa en sangre en el momento del ingreso, lo que indicaba que tenía una secreción de insulina adecuada. La paciente fue tratada únicamente con administración de glucosa sin insulina y fue dada de alta tras la interrupción del inhibidor de SGLT2.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había una señora de 83 años que no tenía diabetes. Ella tenía un problema en el corazón. Tomaba una medicina para ayudar su corazón. \n\nUn día, se cayó y se lastimó mucho. Le dolían los huesos y no quería comer. Pero siguió tomando su medicina. \n\nCuando llegó al hospital, los doctores le hicieron pruebas. Vieron que su sangre estaba un poco rara, pero no tenía mucha azúcar. \n\nElla tenía un problema llamado cetoacidosis, que pasa cuando el cuerpo usa mucha energía y se cansa. Los doctores le dieron agua con azúcar para ayudarla. No le dieron insulina porque su cuerpo todavía hacía insulina sola. \n\nDespués de un tiempo, ella se sintió mejor y pudo irse a su casa. Ya no tomó esa medicina para el corazón.",
+                "fh_score": 81.24
+            },
+            "B2": {
+                "text": "Caso de una mujer mayor con problemas del corazón y un medicamento especial\n\nUna mujer japonesa de 83 años tenía insuficiencia cardíaca, que significa que su corazón no bombeaba sangre tan bien como debería. Para ayudarla, le dieron un medicamento llamado inhibidor de SGLT2, que normalmente se usa para la diabetes, pero ella no tenía diabetes. Este medicamento ayuda al corazón, pero puede causar un problema llamado cetoacidosis, que es cuando el cuerpo produce sustancias ácidas llamadas cetonas.\n\nLo que pasó antes de ir al hospital\n\nDos semanas antes de entrar al hospital, la mujer se cayó y se fracturó una vértebra y una costilla. Por el dolor, dejó de comer bien y se debilitó mucho. A pesar de esto, siguió tomando el medicamento inhibidor de SGLT2.\n\nLo que encontraron en el hospital\n\nCuando llegó al hospital, sus análisis de sangre mostraron que tenía niveles normales de azúcar en la sangre (124 mg/dL), pero su cuerpo estaba en cetoacidosis, porque el pH de su sangre estaba bajo (7.3), el bicarbonato (HCO3–) estaba bajo (14 mmol/L) y tenía muchas cetonas (β-hidroxibutirato alto). Esto significa que su cuerpo estaba produciendo ácidos, aunque el azúcar en sangre no estaba alto, por eso se llama cetoacidosis euglucémica. Además, su cuerpo todavía producía insulina, la hormona que controla el azúcar en sangre, lo que se confirmó con un análisis llamado péptido C.\n\nCómo la trataron y qué pasó después\n\nLos médicos dejaron de darle el medicamento inhibidor de SGLT2 y no le pusieron insulina porque su cuerpo seguía produciéndola. En cambio, le dieron líquidos con glucosa (azúcar) para ayudar a su cuerpo a recuperarse. Poco a poco, sus análisis mejoraron y las cetonas desaparecieron. Cuando pudo volver a comer bien, dejaron de darle glucosa por vía intravenosa. Aunque su azúcar en sangre se mantuvo normal, todavía eliminaba glucosa por la orina durante varios días después de dejar el medicamento. Después de rehabilitación para recuperarse de las fracturas y el cansancio, pudo caminar sola y fue dada de alta del hospital. No volvieron a darle el medicamento inhibidor de SGLT2.\n\nResumen\n\nEste caso muestra que los inhibidores de SGLT2 pueden causar cetoacidosis en personas sin diabetes, especialmente si están débiles o comen poco. Es importante vigilar a los pacientes que usan este medicamento y suspenderlo si aparecen síntomas como náuseas, vómitos o debilidad.",
+                "fh_score": 59.56
+            },
+            "B3": {
+                "text": "**Contexto:**  \nSe presenta el caso de una mujer japonesa de 83 años con insuficiencia cardíaca crónica, caracterizada por una fracción de eyección del 30 %, que recibió tratamiento con inhibidores del cotransportador sodio-glucosa tipo 2 (SGLT2), medicamentos usados para mejorar la función cardíaca y controlar la glucosa en sangre. La paciente no tenía diagnóstico previo de diabetes, con una hemoglobina A1c del 5.9 % antes de iniciar el tratamiento. Aproximadamente dos semanas antes de su ingreso hospitalario, sufrió fracturas vertebrales y de costillas tras una caída, lo que le provocó dolor intenso, dificultad para caminar y una marcada disminución en su ingesta alimentaria, aunque continuó tomando dapagliflozina, un inhibidor de SGLT2.\n\n**Hallazgos Clave:**  \nAl ingresar al hospital, la paciente estaba consciente y estable en signos vitales, pero los análisis de sangre mostraron:  \n- Glucosa en sangre de 124 mg/dL (dentro del rango normal).  \n- pH sanguíneo de 7.3, indicando acidosis (un aumento en la acidez de la sangre).  \n- Bicarbonato (HCO₃⁻) de 14 mmol/L, bajo, lo que confirma acidosis metabólica.  \n- Brecha aniónica elevada (20 mEq/L), que sugiere la presencia de ácidos en la sangre.  \n- Elevada concentración de β-hidroxibutirato (5150 μmol/L), una cetona que indica cetosis.  \nEstos resultados permitieron diagnosticar una cetoacidosis euglucémica, una condición en la que hay acumulación de ácidos cetónicos en sangre sin hiperglucemia significativa. Además, el nivel de péptido C, un marcador de producción de insulina, era adecuado, lo que indicaba que la paciente seguía produciendo insulina de forma suficiente.\n\n**Interpretación Clínica:**  \nLa cetoacidosis euglucémica en esta paciente fue probablemente inducida por el uso de inhibidores de SGLT2 en el contexto de una ingesta alimentaria muy reducida y estrés físico debido a las fracturas. Estos medicamentos pueden aumentar la producción de cuerpos cetónicos al promover la eliminación de glucosa por la orina y reducir la insulina circulante, favoreciendo la cetosis incluso cuando los niveles de glucosa en sangre no están elevados. La secreción adecuada de insulina descartó la necesidad de administrar insulina exógena.\n\n**Próximos Pasos y Evolución:**  \nSe suspendió el tratamiento con inhibidores de SGLT2 y se inició terapia con infusión intravenosa de glucosa y líquidos para corregir la acidosis y mantener la ingesta energética, sin administrar insulina. La paciente mostró mejoría rápida en los parámetros ácido-base al día siguiente y la cetosis desapareció en cuatro días. La infusión de glucosa se ajustó según su capacidad para alimentarse y se suspendió una vez que pudo consumir comidas completas. Durante ocho días posteriores a la suspensión del medicamento, la paciente continuó excretando glucosa en la orina, un efecto residual conocido de la dapagliflozina. Tras rehabilitación para recuperar la movilidad afectada por las fracturas y el desuso, la paciente fue dada de alta en buen estado y sin reiniciar los inhibidores de SGLT2.\n\n---\n\nEste caso ilustra la importancia de reconocer la cetoacidosis euglucémica como una complicación potencial de los inhibidores de SGLT2, especialmente en pacientes sin diabetes que presentan factores de riesgo como ingesta insuficiente y estrés físico. La intervención temprana con suspensión del medicamento y soporte nutricional adecuado puede conducir a una recuperación favorable sin necesidad de insulina.",
+                "fh_score": 43.98
+            }
+        }
+    },
+    {
+        "article": "Una recién nacida fue evaluada en la sala de neonatos poco tiempo después del parto debido a la presencia de extensas lesiones similares a cicatrices en sus flancos y muslos superiores. La bebé, nacida de una madre asiática de 28 años a las 39 semanas de gestación, formaba parte de un embarazo gemelar espontáneo. Su madre, que ya había tenido cinco hijos, había tenido un aborto espontáneo en el primer trimestre durante su segundo embarazo.\n\nLos padres eran primos hermanos y no habían tenido problemas de salud en sus tres hijos vivos. La ecografía a las 13 semanas confirmó un embarazo bicorial y diacítico y la ausencia de actividad cardíaca en uno de los gemelos. Las ecografías posteriores mostraron un feto que se desarrollaba con normalidad junto a un gemelo no viable.\n\nDurante el embarazo, la madre no informó sobre el uso de medicamentos o síntomas como fiebre y erupción cutánea. Dio negativo para estreptococo del grupo B y fue admitida en el departamento de urgencias obstétricas con dolores de parto. La niña fue entregada por vía vaginal, pesando 2,83 kg, y fue vigorosa al nacer. A la placenta se le unió un remanente fetal no viable comprimido que medía 6 × 2 cm. La placenta pesaba 460 g y parecía normal al examen.\n\nLa niña presentaba lesiones cutáneas extensas e irregulares, que se caracterizaban por un aspecto estrellado en ambos flancos, que se extendían lateralmente sobre la zona glútea y el muslo superior. Las lesiones eran simétricas en ambos flancos. No obstante, las lesiones en los muslos eran notablemente más leves en el lado izquierdo. Sus constantes vitales eran estables y no presentaba otras anomalías externas. El examen clínico de sus sistemas respiratorio, cardiovascular, gastrointestinal y neurológico reveló resultados normales, y no se observaron otras anomalías cutáneas, incluida la ausencia de lesiones ampollosas.\n\nDada la naturaleza simétrica de las anomalías cutáneas y el contexto de embarazo de mellizos con FP, se realizó un diagnóstico de aplasia cutis congénita grupo V. Los exámenes de laboratorio, que incluían hemograma completo, electrolitos y pruebas de función renal e hepática, arrojaron resultados normales. Los exámenes de detección de toxoplasmosis, rubéola, citomegalovirus, herpes simple y VIH (TORCH) arrojaron resultados negativos. La ecografía del cerebro, abdomen y corazón no reveló anomalías.\n\nDado que las lesiones se curaron en el útero, solo se prescribieron emolientes locales. Después de 48 horas de observación, el bebé fue dado de alta en su casa, con derivaciones a clínicas de dermatología pediátrica y cirugía plástica. En el seguimiento de 2 semanas, no se observaron cambios en las lesiones de la piel ni nuevos síntomas. Su análisis de microarreglo cromosómico fue reportado como normal.\n",
+        "gold_summary": "Informamos sobre un neonato al que se le diagnosticó ACC de grupo G-V asociado con fetus papyraceus de un embarazo gemelar di-coriónico y di-amniótico. Nacida de una madre asiática de 28 años, esta niña presentaba lesiones extensas, cicatrizadas, similares a las cicatrices en sus flancos y muslos superiores. Estas lesiones eran consistentes con la distribución en forma de «H» comúnmente descrita en ACC ligada a fetus papyraceus. A pesar de las manifestaciones dermatológicas significativas, la niña no mostró otras anormalidades externas o implicación sistémica, y las evaluaciones exhaustivas, incluidos los ultrasonidos y el microarray cromosómico, fueron normales.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una bebé nació con marcas en la piel que parecían cicatrices. Estas marcas estaban en sus lados y muslos. La mamá tuvo dos bebés, pero uno no creció bien en la barriga. \n\nLa bebé con las marcas está sana y fuerte. Los doctores revisaron su cuerpo y todo está bien. No tiene otras partes malas en su cuerpo. \n\nLas marcas en su piel se hicieron mientras estaba en la barriga. Los doctores solo le pusieron crema para cuidar su piel. La bebé está bien y seguirá creciendo feliz.",
+                "fh_score": 93.23
+            },
+            "B2": {
+                "text": "**Caso de una recién nacida con lesiones en la piel**\n\nLes presentamos el caso de una bebé que nació con unas marcas especiales en la piel, llamadas aplasia cutis congénita (ACC) grupo V. Estas marcas aparecieron porque tuvo un gemelo que no sobrevivió durante el embarazo, lo que se conoce como fetus papyraceus (un gemelo aplastado y no viable).\n\n**Lo que encontraron en la bebé**\n\nLa niña, nacida de una madre asiática de 28 años, tenía lesiones en la piel que parecían cicatrices en forma de “H” en sus costados y muslos superiores. Estas marcas son típicas en casos de ACC cuando hay un fetus papyraceus. A pesar de estas lesiones, la bebé estaba saludable en general. No tenía otros problemas visibles ni síntomas en su cuerpo. Las pruebas médicas, como ecografías del cerebro, corazón y abdomen, y un análisis genético llamado microarreglo cromosómico, mostraron resultados normales.\n\n**Qué significa este diagnóstico**\n\nLa ACC grupo V es una condición rara que afecta la piel y está relacionada con la pérdida de un gemelo durante el embarazo. Aunque las marcas en la piel pueden ser grandes, no siempre causan otros problemas de salud. En este caso, la bebé solo necesitó cuidados para mantener la piel hidratada y fue seguida por especialistas en dermatología y cirugía plástica para asegurar una buena recuperación.\n\nEn resumen, esta niña nació con lesiones en la piel causadas por la pérdida de su gemelo, pero su salud general es buena y no presenta otras complicaciones.",
+                "fh_score": 62.48
+            },
+            "B3": {
+                "text": "**Contexto**  \nSe presenta el caso de una recién nacida diagnosticada con aplasia cutis congénita (ACC) del grupo V, una condición caracterizada por la ausencia localizada de piel, en asociación con fetus papyraceus (un gemelo fetal muerto y comprimido) en un embarazo gemelar bicorial y biamniótico. La bebé nació de una madre asiática de 28 años, producto de un embarazo espontáneo gemelar, en el que uno de los fetos no sobrevivió desde etapas tempranas.\n\n**Hallazgos Clave**  \nAl momento del nacimiento, la niña mostró lesiones cutáneas extensas, con un patrón simétrico en forma de «H» en ambos flancos y muslos superiores, que se asemejaban a cicatrices. Estas lesiones son típicas de la ACC grupo V cuando se asocia con fetus papyraceus. A pesar de la apariencia notable de la piel, la bebé no presentó otras anomalías externas ni signos de afectación en órganos o sistemas. Los exámenes clínicos y de laboratorio, incluyendo ecografías cerebrales, abdominales y cardíacas, así como pruebas para infecciones congénitas (TORCH) y análisis cromosómicos mediante microarreglo, no mostraron alteraciones.\n\n**Interpretación Clínica**  \nLa distribución y características de las lesiones cutáneas, junto con la historia del embarazo gemelar con un gemelo no viable, apoyan el diagnóstico de aplasia cutis congénita grupo V. Esta forma de ACC se relaciona con la presencia de fetus papyraceus y suele manifestarse con lesiones simétricas en la piel, pero sin compromiso sistémico. La ausencia de otras anomalías y la normalidad de las pruebas complementarias indican un pronóstico favorable.\n\n**Próximos Pasos**  \nEl tratamiento consistió en cuidados locales con emolientes para favorecer la hidratación y cicatrización de la piel. La bebé fue dada de alta tras 48 horas de observación y se programaron controles en dermatología pediátrica y cirugía plástica para seguimiento y manejo de las lesiones cutáneas. A las dos semanas, no se observaron cambios ni aparición de nuevos síntomas, confirmando la estabilidad clínica del caso.",
+                "fh_score": 47.37
+            }
+        }
+    },
+    {
+        "article": "Información para el paciente\nUn hombre de 44 años de edad fue ingresado en nuestro hospital con quejas principales de neumaturia y cistitis repetida. El paciente también tenía antecedentes de hipotiroidismo.\n\nLa tomografía computarizada con contraste mejorado reveló múltiples divertículos del colon sigmoide, y el límite entre el divertículo y la vejiga no estaba claro. La endoscopia gastrointestinal inferior reveló una fístula en el colon rectosigmoide aproximadamente a 15 cm del borde anal. La cistoscopia reveló una fístula en la pared posterior izquierda de la vejiga. Se diagnosticó una fístula vesicovaginal y se planificó una cirugía laparoscópica. Los hallazgos intraoperatorios revelaron una inflamación severa alrededor de la fístula vesicovaginal, y también se habían formado adhesiones severas entre el íleon y la vejiga. El íleon y la vejiga eran difíciles de exfoliar debido a las adhesiones severas. Por lo tanto, decidimos realizar una resección intestinal combinada. El colon rectosigmoide, incluida la fístula, se movilizó y se resecó. La fístula vesical se seccionó y se cerró con una sutura de púas sin nudos (V-LocTM 180, Covidien, Mansfield). La anastomosis sigmoide-rectal se reconstruyó utilizando la técnica de doble grapado. La resección parcial del íleon se reconstruyó con una anastomosis funcional de extremo a extremo (FEEA). Además de la presencia de una anastomosis de 2 sitios, había una inflamación severa en el área circundante, y considerando el riesgo de fuga anastomótica, se creó una ileostomía de derivación 30 cm proximal a la anastomosis ileo-ileal.\n\nLos procedimientos quirúrgicos incluyeron resección anterior alta laparoscópica, resección parcial del intestino delgado, cistectomía parcial y derivación en forma de asa. La operación duró 236 minutos y la pérdida de sangre fue de 50 ml. El curso postoperatorio fue sin incidentes y el cierre de la ileostomía se planificó 1 mes después de la cirugía inicial. Con ayuda laparoscópica, se eliminaron las adherencias entre el omento y la pared abdominal alrededor del estoma. Se realizó una movilización completa alrededor del estoma y el intestino se sacó hacia afuera. El íleon se reconstruyó utilizando FEEA. El procedimiento quirúrgico implicó el cierre de la ileostomía asistida por laparoscopia. La operación duró 100 minutos y la pérdida de sangre fue de 30 ml.\n\nHallazgos clínicos\nAl día siguiente de la cirugía, se produjo un shock sintomático debido a la presión arterial baja (<80 mm Hg) y la taquicardia. Los análisis de sangre mostraron que la hemoglobina disminuyó de 15.3 antes de la cirugía a 8.6 g/dL después de la cirugía.\n\nEvaluación diagnóstica\nLa tomografía computarizada abdominal (TC) reveló una gran cantidad de fluido de alta densidad en la cavidad abdominal. El diagnóstico fue sangrado posoperatorio y shock hemorrágico. Se insertó un catéter venoso central y se administraron 8 unidades de glóbulos rojos y 8 unidades de plasma fresco congelado para estabilizar los signos vitales. Los signos vitales se estabilizaron y no se observó progresión de la anemia después de eso. Aunque se logró la hemostasia, la distensión abdominal severa y los altos niveles de respuesta inflamatoria (proteína C reactiva [CRP] a 42.9 mg/dL y recuento de glóbulos blancos [WBC] de 18,500/uL) persistieron 7 días después de la cirugía.\n\nLa TC con contraste reveló que el hematoma intraabdominal se localizaba en el abdomen inferior izquierdo y derecho, y se consideró posible el drenaje percutáneo. En el día 8 posoperatorio, se insertaron tubos de drenaje de 18 Fr en el abdomen inferior izquierdo y derecho a través de una punción guiada por TC, y se drenó una gran cantidad de sangre antigua. Después del drenaje, la reacción inflamatoria y la distensión abdominal causadas por la infección del hematoma residual mejoraron (CRP a 1,9 mg/dL y WBC de 5000/μL). No se observó progresión de la anemia. En el día 14 posoperatorio, el drenaje en el abdomen inferior derecho cambió de sangre antigua a jugo intestinal. Una angiografía de drenaje reveló fuga anastomótica tardía en el sitio de cierre de la ileostomía. No hubo signos de peritonitis con buen drenaje, pero el drenaje fue de aproximadamente 100 a 200 ml, y el flato del drenaje continuó. No se observó disminución del drenaje durante los siguientes 14 días.\n\nIntervención terapéutica\nAunque se consideró la posibilidad de una nueva operación, se esperaban adhesiones intraabdominales severas debido a la historia de cirugías anteriores, sangrado postoperatorio y fuga anastomótica. Por lo tanto, se consideró que la nueva operación era un procedimiento de alto riesgo. La tomografía computarizada con contraste mostró que un hematoma organizado permanecía en el mesenterio del intestino delgado y el íleon en el lado distal de 10 cm de la anastomosis estaba comprimido cerca del hematoma restante. Teniendo en cuenta la estenosis del íleon en el lado anal de la anastomosis debido a un hematoma residual como la causa de fuga anastomótica, se intentó la dilatación radioscópica del área de estenosis a través del drenaje en el día 24 postoperatorio. Se colocó un introductor de funda Cordis BRITE TIP® (8 Fr × 23 cm) en la fístula donde ocurrió la fuga anastomótica después del drenaje angiográfico. Se usó un hilo radioscópico GT (0.016 pulgadas, 180 cm, 90°) (Terumo, Tokio, Japón) y un microcatéter Renegade HI-FLO (135 × 20 cm) (Boston Scientific, Tokio, Japón) para alcanzar el íleon terminal. Usando el catéter Selecon MP II (6 Fr, 80 cm, φ20 mm) (Terumo), se identificó el área de estenosis en el íleon debido a la compresión del hematoma donde el globo no podía pasar.\n\nSe realizó dilatación con globo fluoroscópica en la estenosis del íleo utilizando un globo guiado por alambre CRE PRO GI (180 cm, 15-18 mm) (Boston Scientific), inflado a 16,5 mm de diámetro a 4,5 atm durante 3 minutos.\n\nSeguimiento y resultados\nDesde el día posterior a la dilatación con globo, la cantidad de drenaje disminuyó notablemente, y se observaron flatos y defecaciones desde el ano. Una semana después de la dilatación con globo, el drenaje fue casi nulo, y se determinó que la fuga anastomótica se había resuelto. El drenaje se eliminó gradualmente. La ingesta oral fue buena, y tuvo movimientos intestinales regulares. Fue dado de alta el día 45 posterior a la operación. Desde entonces, no se ha informado de ninguna recurrencia de la estenosis o fuga anastomótica.\n",
+        "gold_summary": "Preocupaciones del paciente: Presentamos el caso de un hombre de 44 años con fuga anastomótica tardía después del cierre de la ileostomía, causada por la compresión de un hematoma intraabdominal que se curó rápidamente después de la dilatación fluoroscópica con globo del área de la estenosis intestinal.\n\nDiagnósticos: Se produjo sangrado postoperatorio y shock hemorrágico el día 1 postoperatorio tras el cierre de la ileostomía. Los signos vitales se estabilizaron tras la transfusión de sangre, y se realizó con éxito un drenaje guiado por tomografía computarizada para reducir el volumen del hematoma. Sin embargo, el hematoma residual comprimió el íleon en el lado anal de la anastomosis, lo que provocó una fuga anastomótica tardía.\n\nIntervenciones/resultados: Se realizó con éxito la dilatación con balón fluoroscópico del área estenótica a través del drenaje y la fuga anastomótica se curó rápidamente.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había un hombre que se lastimó su tripita después de una operación. Tenía un bulto con sangre que apretaba su intestino y eso hizo que se hiciera un agujero pequeño. \n\nLos doctores le pusieron una bolsita con aire para hacer más grande el lugar apretado. Así, el agujero se cerró y el hombre empezó a sentirse mejor. \n\nDespués, pudo comer y hacer popó sin problema. Los doctores cuidaron mucho de él y se fue a su casa feliz.",
+                "fh_score": 80.5
+            },
+            "B2": {
+                "text": "Caso del paciente  \nUn hombre de 44 años tuvo una complicación después de una cirugía para cerrar una ileostomía, que es una abertura temporal en el abdomen para sacar los desechos del intestino. Esta complicación se llamó fuga anastomótica tardía, que significa que la unión hecha entre partes del intestino empezó a tener una filtración de líquidos.\n\nQué pasó después de la cirugía  \nAl día siguiente de cerrar la ileostomía, el paciente sufrió una hemorragia interna que causó un shock, una condición grave donde la presión de la sangre baja mucho. Los médicos le transfundieron sangre y drenaron un hematoma, que es una acumulación de sangre fuera de los vasos sanguíneos dentro del abdomen. Aunque esto ayudó, quedó un hematoma pequeño que presionaba una parte del intestino llamada íleon, causando que la unión intestinal se filtrara.\n\nTratamiento y resultados  \nPara solucionar la fuga, los médicos usaron una técnica llamada dilatación con balón fluoroscópico. Esto consiste en insertar un pequeño globo dentro del área estrecha del intestino y luego inflarlo para abrir el paso. Esta intervención se hizo a través del drenaje ya colocado y ayudó a aliviar la presión causada por el hematoma. Después del tratamiento, la fuga se cerró rápidamente, el drenaje disminuyó y el paciente pudo volver a comer y tener movimientos intestinales normales. Fue dado de alta sin más problemas y no ha tenido recurrencias.",
+                "fh_score": 56.22
+            },
+            "B3": {
+                "text": "**Contexto del Caso**  \nSe presenta el caso de un hombre de 44 años que inicialmente fue hospitalizado por síntomas de neumaturia (presencia de aire en la orina) y episodios repetidos de cistitis (infección de la vejiga). Tenía antecedentes de hipotiroidismo. Estudios de imagen y endoscopía revelaron una fístula (una conexión anormal) entre el colon sigmoide y la vejiga, acompañada de múltiples divertículos (pequeñas bolsas) en el colon. Debido a la inflamación severa y adherencias entre intestino y vejiga, se realizó una cirugía laparoscópica compleja que incluyó la resección del colon afectado, cierre de la fístula vesical, resección parcial del intestino delgado y creación temporal de una ileostomía (una abertura en el abdomen para desviar las heces).\n\n**Hallazgos y Complicaciones Postoperatorias**  \nAl día siguiente del cierre de la ileostomía, el paciente presentó un shock hemorrágico debido a una hemorragia interna, evidenciada por una caída significativa de hemoglobina y acumulación de líquido denso en la cavidad abdominal detectada por tomografía computarizada (TC). Se estabilizó con transfusiones y drenaje guiado por TC de un hematoma (acumulación de sangre) intraabdominal. A pesar de la hemostasia, persistió una inflamación intensa y distensión abdominal. Posteriormente, el drenaje mostró presencia de jugo intestinal, lo que indicó una fuga en la anastomosis (la unión quirúrgica entre segmentos intestinales) en el sitio del cierre de la ileostomía. Esta fuga anastomótica tardía se atribuyó a la compresión del íleon (parte final del intestino delgado) por un hematoma residual que causaba estenosis (estrechamiento) en esa zona.\n\n**Intervención Terapéutica**  \nDado el alto riesgo de una nueva cirugía debido a las adherencias y complicaciones previas, se optó por un tratamiento menos invasivo. Se realizó una dilatación con balón guiada por fluoroscopía (una técnica de imagen en tiempo real) a través del drenaje existente para ampliar el área estenótica del íleon comprimido. Este procedimiento consistió en introducir un catéter y un globo inflable en el sitio estrechado y expandirlo cuidadosamente para aliviar la compresión.\n\n**Resultados y Seguimiento**  \nTras la dilatación con balón, la cantidad de drenaje intestinal disminuyó notablemente y el paciente recuperó la función intestinal normal, con evacuaciones por vía natural. Una semana después, la fuga anastomótica se resolvió completamente, permitiendo la retirada progresiva del drenaje. El paciente mantuvo una buena ingesta oral y movimientos intestinales regulares, y fue dado de alta 45 días después de la cirugía inicial. Hasta la fecha, no se ha reportado recurrencia de la estenosis ni de la fuga anastomótica.\n\n---\n\nEste caso ilustra cómo una complicación grave tras cirugía intestinal, como una fuga anastomótica causada por compresión de un hematoma residual, puede ser tratada eficazmente mediante una dilatación endovascular guiada por imágenes, evitando una cirugía adicional de alto riesgo.",
+                "fh_score": 37.66
+            }
+        }
+    },
+    {
+        "article": "Paciente femenino de 23 años, ASA I, acude al Centro de Salud de la Universidad Peruana de Ciencias Aplicadas (CUS-UPC) para colocarle un implante en la zona edéntula de la pieza 1.6. Durante la evaluación, la paciente refiere que hace unos meses se le fracturó la primera molar superior derecha y, como consecuencia, le realizaron la exodoncia atraumática de dicha pieza dentaria.\n\nTras la inspección clínica, se observó la ausencia de la pieza dentaria 1.6, fenotipo gingival delgado y disminución en altura de reborde edéntulo Seibert tipo II 13. Tomográficamente, se registraron medidas de la altura del reborde óseo residual en relación con el piso del seno maxilar (6 mm) y el ancho de la cresta ósea a nivel cervical (11,20 mm), medio (11,80 mm) y apical (12,40 mm), con lo que se identifica la presencia de un seno maxilar ovoide, según Nie et al. Se realizó la planificación quirúrgica para la realización de una elevación del seno maxilar con abordaje transcrestal y la colocación de un implante dental de 4,8 x 8 mm.\n\nSe inició el procedimiento quirúrgico, que consistió en lo siguiente:\n\n• Asepsia y antisepsia\n\n• Técnica anestesia infiltrativa por vestibular y palatino de la zona edéntula 1.6 utilizando 2 cartuchos de lidocaína al 2% con epinefrina 1:80.000.\n\n• Incisión supracrestal en la zona edéntula 1.6 e incisiones sulculares en mesial de la pieza dentaria 1.7 y en distal de la pieza dentaria 1.5.\n\n• Decolado del colgajo a espesor parcial y, luego, se procedió a probar la guía quirúrgica para realizar la secuencia de fresado hasta una longitud de 6 mm, dejando 1 mm de distancia al piso del seno maxilar, el cual fue comprobado con los calibradores de profundidad, según el diámetro de la fresa que se utilizó durante la osteotomía. La secuencia de fresado se realizó hasta la fresa 3,5 mm de diámetro y luego se procedió a realizar el levantamiento de 2 mm del seno maxilar con la técnica de abordaje transcrestal mediante el uso de un osteótomo, hasta llegar a una longitud de 8 mm.\n\n• Colocación del implante φ 4,8 x 8 mm (Bone Level tapered, Straumann®) y tornillo de cierre, ambos con un torque de inserción de 20 N.\n\n• Sutura con puntos interrumpidos con ácido poliglicólico 5/0 y lavado de la zona quirúrgica con suero fisiológico al 0,09%.\n\n• Radiografía posquirúrgica del implante en zona edéntula 1.6.\n\n• Indicación de tomar amoxicilina de 500 mg + ácido clavulánico 125 mg cada 8 horas durante 7 días, ketorolaco de 10 mg cada 8 horas por 3 días, cetirizina de 10 mg cada 24 horas por 3 días y clorhexidina al 0,12%, 2 veces al día, por 10 días. Entre las indicaciones posquirúrgicas se le indicó a la paciente reposo absoluto, sin esfuerzo físico, dieta blanda, no sonarse la nariz, no succionar líquidos por dos semanas, no sumergir la cabeza en agua, tampoco estornudar o toser con la boca abierta, mantener la cabeza elevada y aplicarse compresas de hielo durante las primeras 4 horas.\n\nSe realizó un control posquirúrgico a los 7 días, el cual evidenció tejidos blandos en proceso de cicatrización, por lo que se procedió al retiro de puntos y lavado con suero fisiológico al 0,9%, y se realizó una tomografía de control que evidenció la elevación de seno maxilar, con 2,83 mm aproximadamente. Asimismo, se realizaron controles posquirúrgicos a los 35 y 56 días, en los cueles se hallaron tejidos blandos en completo proceso de cicatrización.",
+        "gold_summary": "Se realizó un levantamiento de seno maxilar sin injerto óseo en una paciente de sexo femenino de 23 años que requería la colocación de un implante dental en la zona edéntula de la pieza 16. La evaluación clínica y tomográfica permitieron planificar y realizar la elevación de seno maxilar mediante el abordaje transcrestal y sin la necesidad de injerto óseo. El reborde residual de 6 mm permitió la colocación de un implante dental simultáneo. Luego de 6 meses de seguimiento tomográfico, antes de la carga protésica, se consiguió una altura ósea vertical de 8,83 mm, lo que dio como resultado una ganancia ósea vertical de 2,83 mm. Adicionalmente, se observa una adecuada integración del implante dental sin complicaciones posoperatorias.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una joven de 23 años necesitaba un diente nuevo. El doctor hizo un pequeño espacio en su hueso cerca de la nariz. No usó nada más para llenar ese espacio. Puso un tornillo especial para el diente. Después de un tiempo, el hueso creció un poquito más. El diente nuevo quedó bien y sin problemas. Todo está sanando muy bien.",
+                "fh_score": 91.1
+            },
+            "B2": {
+                "text": "**Lo que hicieron y encontraron**\n\nUna joven de 23 años necesitaba un implante dental porque le faltaba un molar superior derecho. Los doctores revisaron su boca y tomaron imágenes para medir el hueso donde se colocaría el implante. Vieron que había 6 mm de hueso en esa zona, lo que era suficiente para poner un implante, pero necesitaban levantar un poco el seno maxilar. El seno maxilar es un espacio lleno de aire dentro del hueso de la cara, cerca de los dientes superiores. Para hacer espacio para el implante, realizaron una cirugía llamada elevación de seno maxilar usando un método que no requiere poner hueso nuevo (injerto).\n\n**Cómo fue la cirugía**\n\nDurante la operación, anestesiaron la zona para que no sintiera dolor. Hicieron una pequeña incisión y usaron herramientas especiales para levantar el suelo del seno maxilar unos 2 mm. Luego colocaron un implante dental de 8 mm de largo en el hueso existente. Después, cerraron la herida con puntos y le dieron medicamentos para evitar infecciones y controlar el dolor. También le indicaron cuidados para que la zona sanara bien.\n\n**Qué pasó después**\n\nA los 7 días, la herida estaba sanando bien y retiraron los puntos. Después de 6 meses, las imágenes mostraron que el hueso había crecido 2,83 mm más en altura, alcanzando un total de 8,83 mm. Esto significa que el implante estaba bien integrado y estable, sin problemas después de la cirugía.\n\n**Por qué es importante**\n\nEste caso muestra que es posible levantar el seno maxilar y colocar un implante al mismo tiempo sin usar hueso extra. Esto puede hacer que el tratamiento sea más rápido y menos complicado para pacientes que necesitan implantes en esa zona.",
+                "fh_score": 66.89
+            },
+            "B3": {
+                "text": "**Contexto**  \nUna mujer de 23 años, sin antecedentes médicos relevantes (clasificación ASA I), acudió a un centro de salud para la colocación de un implante dental en el espacio dejado por la extracción previa de su primer molar superior derecho (pieza 1.6). La paciente había perdido este diente debido a una fractura y se le realizó una exodoncia atraumática. Durante la evaluación clínica se observó la ausencia del diente, un tipo de encía delgada y una reducción en la altura del reborde óseo (zona del hueso donde se apoya el diente), clasificada como Seibert tipo II. Las imágenes tomográficas mostraron que el reborde óseo residual tenía una altura de 6 mm desde el piso del seno maxilar, con un ancho adecuado para la colocación del implante, y se identificó un seno maxilar de forma ovoide.\n\n**Hallazgos Clave y Procedimiento Realizado**  \nSe planificó una elevación del seno maxilar mediante un abordaje transcrestal (acceso a través de la cresta ósea donde se colocará el implante) sin necesidad de utilizar injerto óseo. Durante la cirugía, se realizó anestesia local, incisiones precisas para levantar un colgajo de encía, y se preparó el sitio para el implante con fresas de diferentes diámetros, respetando una distancia segura de 1 mm al piso del seno maxilar. Se elevó la membrana del seno maxilar 2 mm con un osteótomo (instrumento para levantar el seno), permitiendo colocar un implante dental de 4,8 mm de diámetro por 8 mm de longitud. La inserción se realizó con un torque adecuado (20 N), y se cerró la zona con suturas. Se indicó un tratamiento antibiótico, antiinflamatorio, antihistamínico y enjuagues con clorhexidina, además de recomendaciones estrictas para evitar complicaciones, como reposo absoluto y evitar esfuerzos que puedan afectar la zona quirúrgica.\n\n**Interpretación Clínica**  \nEl procedimiento permitió aumentar la altura ósea vertical disponible para el implante sin necesidad de injerto óseo, aprovechando el reborde óseo residual de 6 mm para colocar el implante simultáneamente con la elevación del seno maxilar. El seguimiento tomográfico realizado a los 7 días mostró una elevación de la membrana del seno de aproximadamente 2,83 mm, y controles posteriores a los 35 y 56 días confirmaron una adecuada cicatrización de los tejidos blandos sin complicaciones. Se logró una ganancia ósea vertical total de 2,83 mm, alcanzando una altura ósea de 8,83 mm antes de la colocación de la prótesis dental.\n\n**Próximos Pasos**  \nCon la adecuada integración del implante y la ganancia ósea confirmada, el siguiente paso será la carga protésica, es decir, la colocación de la corona o diente artificial sobre el implante para restaurar la función masticatoria y estética. Se continuará con controles periódicos para asegurar la estabilidad del implante y la salud de los tejidos circundantes.",
+                "fh_score": 45.04
+            }
+        }
+    },
+    {
+        "article": "Una paciente de 42 años de edad fue remitida a nuestro centro terciario de cáncer con antecedentes de seroma recurrente del seno izquierdo. La paciente se había sometido a una extracción bilateral de implantes mamarios con una capsulotomía parcial 11 meses antes de su primera visita a nuestro centro. La paciente no presentaba ninguna comorbilidad notable y tenía antecedentes de aumento bilateral de senos con implantes mamarios en el plano submuscular en 2003, a la edad de 21 años. No se pudo localizar ninguna información sobre el tipo de implantes que había recibido originalmente. La paciente volvió a consultar al mismo cirujano en 2008, quejándose de seroma bilateral, para someterse a un primer reemplazo bilateral de implantes mamarios con implantes mamarios anatómicos texturados de 425 cc (Sebbin LSA TF 425). En 2013, se sometió a un segundo procedimiento de reemplazo de implantes para aumentar el tamaño con implantes mamarios de 480 cc del mismo fabricante (Sebbin LSA TF 480). En 2017, la paciente volvió para una revisión en la que se quejaba de dolor y aumento del volumen del seno bilateralmente. En ese momento, se le realizó una exploración por ultrasonido que identificó efusiones periprostéticas bilaterales sin linfadenopatía o masas palpables en las regiones mamarias. Las efusiones se drenaron sin análisis, pero reaparecieron a lo largo de los años, cuando la paciente buscó ayuda del mismo cirujano y se sometió a un tercer procedimiento de revisión en 2022, con un reemplazo bilateral de implantes mamarios y una toma de muestras de la cápsula anterior. El cirujano envió dos especímenes desde el lado derecho (9 x 1 cm y 3 x 3 cm) y uno desde el lado izquierdo (2 x 1 cm). El informe histopatológico del espécimen encontró «material proteico amorfo celular acellular» en el lado derecho y «tejido fibroso escleroso con inflamación de linfocitos-monocitos, que requiere correlación con la presentación clínica» en el lado izquierdo. A pesar de la extracción, el seroma reapareció en el lado izquierdo, y se envió para pruebas citopatológicas que identificaron «una población de células pleomórficas atípicas irregulares con contornos irregulares que sugieren un proceso linfoproliferativo con CD30+ elementos» para los que se recomendaron pruebas diagnósticas adicionales. Por esta razón, la paciente buscó tratamiento en nuestra institución, donde el caso fue gestionado por un equipo multidisciplinario (MDT) que incluía a un cirujano plástico, un hematopatólogo, un hematólogo, un oncólogo, un radioterapeuta, un oncólogo quirúrgico y un radiólogo de mama. El espécimen histopatológico original de la toma de la cápsula se revisó por un hematopatólogo de nuestro centro de referencia, que identificó células CD30+ grandes y escasas atípicas con contornos irregulares que se consideraron compatibles con el diagnóstico de BIA-ALCL. Las células presentaron el siguiente fenotipo: CD30+, CD3-, CD7-, CD5-, CD4-, CD8-, Granzima B+/-, TIA1-, ALK1-, PAX5-, CD79a-, CD68-, CD15-/+. La paciente recibió una exploración por ultrasonido con aspiración por aguja fina y citopatología de la efusión recurrente que confirmó un proceso CD30+ linfoproliferativo atípico con captación de 18F-FDG (fluorodeoxiglucosa) (SUV máx. 1,8). No se pudieron localizar otras áreas de captación en todos los demás segmentos corporales explorados. La paciente también recibió una exploración por resonancia magnética de ambos senos con medio de contraste para completar la estadificación preoperativa, confirmando el seroma del lado izquierdo. Los portaobjetos del espécimen de la cirugía anterior se revisaron por el hematopatólogo que consideró los hallazgos suficientes para identificar BIA-ALCL con infiltración temprana de la cápsula periprostética (pT2 según el sistema de estadificación MD Anderson-TNM). Tres semanas después de la visita inicial, la paciente se sometió a cirugía radical con capsulotomía en bloque que contenía solo 150 cc de efusión serosa sin implante. El contenido líquido se envió para cultivo y citopatología, mientras que el espécimen sólido se envió para examen histopatológico. Además, la paciente se sometió a biopsia de ganglio linfático centinela de 2 ganglios axilares identificados preoperativamente a través de linfografía segmentaria. Los ganglios linfáticos presentaron una linfadenopatía silicona-asociada reactiva crónica sin signos de linfadenopatía metastásica. El informe histopatológico de la cápsula reveló agregados celulares infiltrantes en la cápsula periprostética, pero márgenes de resección claros y sin signos de infiltración más allá de la cápsula. Como tal, la paciente recibió un estadio IC (pT3pN0M0). El curso postoperatorio fue sin incidentes, y no se consideraron necesarios más tratamientos adyuvantes por el MDT. La paciente continuó su estricto protocolo de seguimiento, con PET/CT de 6, 12 y 18 meses posteriores a la cirugía que no mostró signos de recurrencia de enfermedad local o distante. Como está, la paciente continúa sus visitas de seguimiento y exploraciones, con supervivencia libre de enfermedad más allá de 18 meses.\n",
+        "gold_summary": "Describimos el caso de una mujer de 42 años con antecedentes de aumento de senos bilateral con fines cosméticos 21 años antes, que desarrolló seroma recurrente del lado izquierdo. Buscó ayuda de su primer cirujano, quien realizó 2 procedimientos de intercambio de implantes mamarios, colocando dispositivos texturados y, finalmente, una extracción bilateral de implantes mamarios en el transcurso de dos décadas. La paciente no recibió capsulectomías en los intercambios de implantes anteriores y recibió una muestra de la cápsula anterior en el último procedimiento, donde se diagnosticó BIA-ALCL en el lado izquierdo. Fue derivada a un centro de cáncer terciario donde el examen preoperatorio confirmó la presencia de enfermedad residual local. Después de la gestión del equipo multidisciplinario, se sometió a una revisión de capsulectomía en bloque del lado izquierdo sin necesidad de tratamientos adicionales. El curso postoperatorio fue sin incidentes y sin signos de recurrencias locales a los 18 meses de seguimiento.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había una mujer que se puso pechos nuevos hace mucho tiempo. Con el tiempo, su pecho izquierdo se llenó de líquido muchas veces. Fue al doctor varias veces y le cambiaron los pechos dos veces. Al final, le quitaron los pechos nuevos. \n\nEl doctor vio que había unas células raras en el pecho izquierdo. La llevaron a un hospital especial para ayudarla. Allí le hicieron una operación para sacar todo lo raro. \n\nDespués de la operación, la mujer estuvo bien. Los doctores la revisaron muchas veces y no encontraron nada malo. Ahora está sana y sigue yendo al doctor para cuidarse.",
+                "fh_score": 83.67
+            },
+            "B2": {
+                "text": "**Caso de una mujer con problemas en sus implantes mamarios**\n\nUna mujer de 42 años se hizo un aumento de senos cuando tenía 21 años. Con el tiempo, comenzó a tener un problema llamado seroma, que es cuando se acumula líquido alrededor del implante. Esto pasó especialmente en su seno izquierdo y volvió varias veces.\n\n**Tratamientos previos y diagnóstico**\n\nLa mujer visitó a su cirujano varias veces y se le cambiaron los implantes dos veces. En la última cirugía, le quitaron ambos implantes, pero no retiraron toda la cápsula, que es el tejido que se forma alrededor del implante. Al analizar una muestra de esta cápsula, los médicos encontraron células anormales que indicaban una enfermedad llamada linfoma anaplásico de células grandes asociado a implantes mamarios (BIA-ALCL). Este es un tipo raro de cáncer que puede aparecer en personas con implantes mamarios.\n\n**Atención en un centro especializado**\n\nDespués de este diagnóstico, la paciente fue enviada a un hospital especializado en cáncer. Allí, un equipo de diferentes especialistas revisó su caso y confirmó que todavía había enfermedad en la cápsula del seno izquierdo. La paciente se sometió a una cirugía para quitar toda la cápsula afectada y el líquido acumulado, sin necesidad de tratamientos como quimioterapia o radioterapia.\n\n**Resultado y seguimiento**\n\nLa operación fue exitosa y no hubo complicaciones. Durante 18 meses después de la cirugía, la mujer fue revisada varias veces y no se detectó que el cáncer regresara. Actualmente, sigue en control médico para asegurarse de que se mantenga sana.\n\nEn resumen, este caso muestra la importancia de detectar y tratar a tiempo un tipo raro de cáncer que puede aparecer en personas con implantes mamarios, y cómo un equipo médico especializado puede ayudar a manejarlo con éxito.",
+                "fh_score": 56.65
+            },
+            "B3": {
+                "text": "**Contexto**  \nPresentamos el caso de una mujer de 42 años que, tras haberse sometido a un aumento bilateral de senos con implantes mamarios hace 21 años, desarrolló un seroma (acumulación anormal de líquido) recurrente en el seno izquierdo. A lo largo de dos décadas, la paciente consultó repetidamente a su cirujano original, quien realizó dos procedimientos para reemplazar los implantes, utilizando dispositivos texturados (implantes con superficie rugosa), y finalmente llevó a cabo una extracción bilateral de los implantes. Durante estos procedimientos previos, no se realizaron capsulectomías completas (extirpación total de la cápsula fibrosa que se forma alrededor del implante). En el último procedimiento, se tomó una muestra de la cápsula del lado izquierdo que reveló la presencia de un linfoma anaplásico de células grandes asociado a implantes mamarios (BIA-ALCL, por sus siglas en inglés), un tipo raro de cáncer que afecta el tejido alrededor del implante.\n\n**Hallazgos Clave**  \nAl ser remitida a un centro terciario especializado en cáncer, se confirmó mediante estudios preoperatorios que la enfermedad persistía localmente en el seno izquierdo. El equipo multidisciplinario, compuesto por cirujanos plásticos, hematopatólogos, hematólogos, oncólogos, radiólogos y radioterapeutas, evaluó cuidadosamente el caso. Se realizó una capsulectomía en bloque (extirpación completa de la cápsula y el tejido circundante) en el lado afectado, sin encontrar necesidad de tratamientos adicionales como quimioterapia o radioterapia. El examen histopatológico mostró infiltración tumoral limitada a la cápsula periprostética, con márgenes quirúrgicos libres de enfermedad y sin afectación ganglionar.\n\n**Interpretación Clínica**  \nEste caso ilustra la importancia de la vigilancia y el diagnóstico temprano del BIA-ALCL, especialmente en pacientes con implantes texturados que presentan seromas persistentes o recurrentes. La ausencia de capsulectomías completas en procedimientos previos pudo haber contribuido a la persistencia de la enfermedad. La intervención quirúrgica radical, sin necesidad de tratamientos complementarios, fue suficiente para controlar la enfermedad en estadio temprano (IC según la clasificación MD Anderson-TNM).\n\n**Próximos Pasos**  \nLa paciente ha seguido un riguroso protocolo de seguimiento con estudios de imagen, incluyendo tomografías por emisión de positrones (PET/CT) a los 6, 12 y 18 meses postcirugía, sin evidencia de recurrencia local ni a distancia. Continúa bajo vigilancia médica estrecha para detectar cualquier signo de reaparición del linfoma, manteniendo hasta la fecha una supervivencia libre de enfermedad más allá de 18 meses. Este caso subraya la eficacia del manejo multidisciplinario y la cirugía completa en el tratamiento del BIA-ALCL en estadios iniciales.",
+                "fh_score": 33.72
+            }
+        }
+    },
+    {
+        "article": "Se trata de un paciente de 50 años que se presentó con una queja de dolor e hinchazón de la lengua de tres días de duración. Asociado a esto, tenía dolor al tragar, dificultad para abrir la boca, falta de aire y babeo. Asimismo, tenía fiebre alta y un tipo de dolor de cabeza global. Por lo demás, no tenía traumatismo en la lengua, ni procedimientos dentales u orales recientes, ni antecedentes de tabaquismo ni de enfermedad médica crónica como diabetes mellitus, enfermedad cardiaca e hipertensión. Históricamente, había tenido un dolor dental agudo en los últimos seis meses antes de su queja actual. Había masticado khat desde su niñez y tenía una mala higiene oral.\n\nEn el examen físico, se veía muy enfermo y sus signos vitales eran: presión arterial 115 por 70 mmHg, pulso 120 latidos por minuto, frecuencia respiratoria 20, temperatura 39 grados centígrados y saturación de oxígeno 92% de oxígeno. En el examen HEENT, había una hinchazón significativa de la lengua en el área anterolateral izquierdo, fluctuante a la palpación, y tenía un borde eritematoso. Hay múltiples caries en las áreas maxilares y mandibulares. No hubo hallazgos pertinentes en los sistemas restantes.\n\nTras obtener el consentimiento informado, el paciente fue trasladado al quirófano con el diagnóstico de absceso lingual. Posteriormente, se realizó la incisión y el drenaje bajo anestesia general, y se drenaron unos 30 ml de pus espeso. La bolsa se lavó con solución salina normal y peróxido de hidrógeno al 2 %. El paciente fue trasladado a la sala de cirugía con signos vitales estables y había tomado ceftriaxona 1 g por vía intravenosa dos veces al día y metronidazol 500 mg por vía intravenosa tres veces al día durante dos días. Fue dado de alta después de dos días de estancia en el hospital con mejoría y Augmentin 625 mg por vía oral tres veces al día durante cinco días.\n",
+        "gold_summary": "Se trata de un paciente de 50 años que se presentó con una queja de dolor e hinchazón de la lengua de tres días de duración. Asociado a esto, tenía dolor al tragar, dificultad para abrir la boca, falta de aire y babeo. Asimismo, tenía fiebre alta y un tipo de dolor de cabeza global. En el examen físico, había una hinchazón significativa de la lengua en el área anterolateral izquierda, fluctuante a la palpación, y tenía un borde eritematoso. Después de que se tomó el consentimiento informado, el paciente fue trasladado al quirófano con el diagnóstico de absceso de la lengua. Posteriormente, se hizo una incisión y drenaje bajo anestesia general, y se drenaron unos 30 ml de pus espeso. El bolsillo se lavó con solución salina normal y peróxido de hidrógeno al 2%. El paciente fue trasladado a la sala de cirugía con signos vitales estables y había estado tomando antibióticos. Fue dado de alta después de dos días de estancia en el hospital.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un hombre tenía la lengua muy hinchada y le dolía mucho. También le costaba abrir la boca y respirar bien. Tenía fiebre y dolor de cabeza. Los doctores vieron que su lengua estaba muy inflamada y con una bolita de pus. Lo llevaron al hospital para limpiar la lengua y sacar el pus. Le dieron medicinas para que no se enfermara más. Después de dos días, se sintió mejor y pudo ir a su casa.",
+                "fh_score": 94.31
+            },
+            "B2": {
+                "text": "**Lo que le Pasó al Paciente**  \nUn hombre de 50 años llegó al hospital porque tenía dolor e hinchazón en la lengua desde hacía tres días. También le dolía al tragar, le costaba abrir la boca, tenía dificultad para respirar y babeaba mucho. Además, tenía fiebre alta y un dolor de cabeza que sentía en toda la cabeza.\n\n**Lo que Encontraron en el Examen**  \nCuando lo examinaron, vieron que la parte izquierda de su lengua estaba muy hinchada y blanda al tocarla. La piel alrededor estaba roja. También tenía muchos dientes con caries, que son daños en los dientes causados por bacterias.\n\n**Qué Hicieron para Ayudarlo**  \nLos médicos decidieron que tenía un absceso en la lengua. Un absceso es una acumulación de pus, que es un líquido lleno de bacterias y células muertas, causado por una infección. Para tratarlo, lo llevaron al quirófano y, bajo anestesia general (cuando el paciente está dormido y no siente dolor), hicieron una pequeña abertura para sacar el pus, aproximadamente 30 mililitros. Luego limpiaron la zona con agua salada y peróxido de hidrógeno, que ayuda a eliminar las bacterias.\n\n**Recuperación y Tratamiento**  \nDespués de la operación, el paciente recibió antibióticos por vía intravenosa para combatir la infección. Su estado mejoró y, tras dos días en el hospital, pudo irse a su casa con medicamentos para seguir tomando y asegurar que la infección desapareciera completamente.",
+                "fh_score": 64.75
+            },
+            "B3": {
+                "text": "**Contexto**\n\nUn hombre de 50 años acudió al hospital debido a dolor e inflamación en la lengua que había persistido durante tres días. Además, presentaba dificultad para tragar, problemas para abrir la boca, sensación de falta de aire y babeo excesivo. También tenía fiebre alta y un dolor de cabeza generalizado. No reportaba antecedentes recientes de traumatismos en la boca, procedimientos dentales, tabaquismo ni enfermedades crónicas como diabetes o hipertensión. Sin embargo, había experimentado dolor dental agudo en los seis meses previos y tenía hábitos de masticar khat desde la niñez, junto con una higiene oral deficiente.\n\n**Hallazgos Clave**\n\nDurante el examen físico, el paciente se mostró visiblemente enfermo. Sus signos vitales indicaron fiebre (39 °C), pulso acelerado (120 latidos por minuto), presión arterial normal (115/70 mmHg), frecuencia respiratoria de 20 respiraciones por minuto y saturación de oxígeno ligeramente disminuida (92%). En la exploración de cabeza y cuello, se observó una inflamación notable en la parte anterolateral izquierda de la lengua, que al tacto era fluctuante (lo que sugiere acumulación de líquido) y presentaba un borde enrojecido (eritematoso). Además, se detectaron múltiples caries en los dientes superiores e inferiores.\n\n**Interpretación Clínica**\n\nEl cuadro clínico y los hallazgos físicos fueron compatibles con un absceso lingual, que es una acumulación de pus en la lengua debido a una infección. Esta condición puede ser grave porque la inflamación y el pus pueden dificultar la respiración y la deglución, como ocurrió en este paciente.\n\n**Próximos Pasos y Tratamiento**\n\nCon el consentimiento informado del paciente, se decidió realizar una intervención quirúrgica para drenar el absceso. Bajo anestesia general, se hizo una incisión en la lengua y se extrajeron aproximadamente 30 mililitros de pus espeso. La cavidad se limpió cuidadosamente con solución salina y peróxido de hidrógeno al 2% para eliminar restos de infección. Posteriormente, el paciente recibió tratamiento antibiótico intravenoso con ceftriaxona y metronidazol durante dos días. Su estado se mantuvo estable y, tras mejorar, fue dado de alta con indicaciones para continuar con antibióticos orales (Augmentin) durante cinco días más.\n\nEste manejo oportuno permitió controlar la infección y evitar complicaciones mayores, destacando la importancia de un diagnóstico rápido y un tratamiento adecuado en casos de abscesos en la lengua.",
+                "fh_score": 46.68
+            }
+        }
+    },
+    {
+        "article": "Hombre de 73 años de edad de origen latinoamericano, con antecedente de madre con diagnóstico de demencia tipo Alzheimer con panel genético negativo; hermano con diagnóstico de ELA; hermana con diagnóstico de enfermedad de Parkinson. La sintomatología progresiva comenzó desde el año 2016 y se caracterizó por síntomas progresivos de hiposmia, hipoacusia, estreñimiento e insomnio, los cuales ameritaron valoración por otorrinolaringología y audiología, sin conclusión diagnóstica. En el año 2020 los familiares notaron que el paciente presentaba problemas en la memoria episódica, olvidos de objetos de la vida cotidiana, problemas de ganancias en su negocio (de comercio). Estos síntomas fueron progresivos hasta que el paciente empezó a tener limitación en las tareas diarias, como al manejar y al cambiar las velocidades, además de al salir de su casa. A finales de ese año el paciente comenzó a presentar debilidad muscular distal, manifestada al abrir botellas, cepillarse los dientes, lo cual progresó de forma insidiosa, no fluctuante, sin predominio de horario.\n\nEn enero de 2021 el paciente comenzó con alteraciones de la marcha, las cuales condicionaron caídas frecuentes hasta más de 6 veces a la semana, esto debido a inestabilidad postural. El paciente acudió a valoración en mayo. Se le hizo test de MoCA de 16 puntos con alteraciones en la fluidez del lenguaje y repetición de oraciones; en la abstracción, recuerdo diferido y problemas visuoespaciales y disejecutivos. El test de Luria dio positivo. El paciente presentó facie hipomímica, emitió con hipofonía, entrecortado y lento, y presentó reflejo nauseoso disminuido, rigidez generalizada de predominio izquierdo, hipotrofia generalizada, bradicinesia de predominio izquierdo, fuerza 4/5 generalizada, reflejos de estiramientos musculares 3/4, reflejos abdominocutáneos abolidos, signos de Hoffmann y Trömner presentes de forma bilateral, respuesta plantar extensora bilateral, fasciculaciones en extremidades inferiores evocadas al tacto, marcha con pasos cortos, congelamiento de la marcha al giro, pull test positivo (inestabilidad postural). Se manejó con levodopa carbidopa a una dosis gradual. Al seguimiento a los 3 meses el paciente había presentado nula mejoría en cuanto a los síntomas parkinsónicos, aumento de la debilidad muscular y persistieron los datos de motoneurona inferior y superior. Con estos hallazgos se realizó resonancia magnética (RM) del encéfalo. La velocidad de neuroconducción (VCN) presentó neuropatía axonal motora de miembros torácicos en relación con atrofia y neuroconducción sensitiva sin alteraciones. La electromiografía (EMG) presentó datos de denervación activa (aumento de actividad insercional, potenciales de fibrilación, fasciculación) y reinervación crónica (potenciales de acción de la unidad motora polifásicos, y bajo reclutamiento a la contracción máxima) en los 5 segmentos corporales, lo cual es compatible con enfermedad de motoneurona.\n\n\nLa EMG mostró un aumento de actividad insercional en músculos deltoides, bíceps, tríceps, extensor digital común bilateral y músculos linguales de forma bilateral. Se observaron abundantes potenciales de fibrilación y predominó la fasciculación en los músculos de los miembros torácicos. Durante la contracción, se observó una activación del potencial de acción de la unidad motora (PAUM) de forma polifásica y de gran amplitud. Y a máxima contracción se observó una disminución del reclutamiento en la mayoría de los músculos evaluados.\n\nEl paciente perdió seguimiento un año. Al vover a valoración se encontraba con postración en cama, afásico, aumento de los datos de parkinsonismo y síndrome de motoneurona. Se decidió realizar panel genético que resultó negativo para C9ORF72, así como para 143 genes más involucrados en enfermedades neuromusculares y neurodegenerativas, incluidos los genes VCP, MAT3, asociados a ELA, NOTCH3, asociado a demencia frontotemporal, sin alteraciones. Se reportó resultado de variante patogénica para el gen POLG: C.2209G>C, p.(Gly737Arg), relacionado con síndrome de depleción mitocondrial autosómico dominante y recesivo. Se realizó sesión de asesoramiento genético y el paciente fue informado. En mayo de 2022, el paciente presentaba disfagia y acudió en silla de ruedas, por lo que fue enviado a que se le practicara una gastrostomía.",
+        "gold_summary": "Presentamos un caso de origen latinoamericano que inicialmente se manifestó con síntomas sistémicos de más de 6 años de evolución, con posteriores alteraciones cognitivas. Después presentó alteraciones de la marcha y síntomas motores sugestivos de parkinsonismo con datos atípicos y datos de enfermedad de motoneurona. Se hicieron estudios de extensión que confirmaron hallazgos compatibles con afectación en motoneurona superior e inferior. Observamos mutación en gen POLG, relacionada con síndrome de depleción mitocondrial.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un señor empezó a sentirse mal hace mucho tiempo. Primero, tenía problemas para oler, escuchar y dormir. Luego, se le olvidaban cosas y le costaba hacer tareas fáciles.\n\nDespués, le costaba caminar y se caía mucho. También tenía los músculos débiles y se movía lento. Los doctores hicieron pruebas y vieron que sus nervios y músculos no funcionaban bien.\n\nEncontraron un cambio en un gen que puede causar problemas en el cuerpo. Los doctores le explicaron todo con calma. Ahora, lo cuidan para que esté lo más cómodo posible.",
+                "fh_score": 82.82
+            },
+            "B2": {
+                "text": "**Lo que pasó con el paciente:**  \nUn hombre latinoamericano de 73 años tuvo síntomas durante más de seis años. Primero, presentó problemas en su cuerpo como dificultad para oler, escuchar y dormir. Luego, comenzó a tener problemas con la memoria y a olvidar cosas de su vida diaria. Más adelante, tuvo problemas para caminar y debilidad en sus músculos, lo que afectó sus movimientos y le causó caídas frecuentes.\n\n**Qué encontraron los médicos:**  \nAl hacerle pruebas, vieron que tenía signos de parkinsonismo, que es un conjunto de síntomas parecidos a los del Parkinson, pero con algunas diferencias. También encontraron que sus nervios y músculos estaban dañados, mostrando que tenía problemas en las motoneuronas. Las motoneuronas son células nerviosas que controlan los músculos, y en su caso, tanto las motoneuronas superiores como las inferiores estaban afectadas.\n\n**Resultados genéticos importantes:**  \nSe le hizo un examen genético y encontraron una mutación en un gen llamado POLG. Este gen está relacionado con un problema llamado síndrome de depleción mitocondrial, que afecta la energía que producen las células. Esta mutación puede causar enfermedades que afectan los músculos y el sistema nervioso.\n\n**Qué significa todo esto:**  \nEl caso es complejo porque el paciente tiene síntomas que involucran tanto problemas de memoria como de movimiento y debilidad muscular. La combinación de parkinsonismo atípico y enfermedad de motoneurona, junto con la mutación genética, ayuda a entender mejor su enfermedad y a buscar tratamientos adecuados.",
+                "fh_score": 54.83
+            },
+            "B3": {
+                "text": "**Contexto**  \nSe trata de un hombre latinoamericano de 73 años con antecedentes familiares de enfermedades neurodegenerativas, incluyendo Alzheimer, esclerosis lateral amiotrófica (ELA) y Parkinson. Su cuadro clínico comenzó en 2016 con síntomas no específicos como disminución del olfato (hiposmia), pérdida auditiva leve (hipoacusia), estreñimiento e insomnio. En 2020, aparecieron problemas de memoria, dificultades en actividades cotidianas y debilidad muscular progresiva, especialmente en manos. En 2021, desarrolló alteraciones de la marcha con caídas frecuentes, rigidez y lentitud de movimientos, además de signos neurológicos que sugerían afectación tanto de la motoneurona superior como inferior.\n\n**Hallazgos Clave**  \n- Evaluación cognitiva mostró deterioro en funciones ejecutivas, memoria y habilidades visuoespaciales.  \n- Examen neurológico reveló rigidez, bradicinesia (lentitud de movimientos), reflejos anormales, fasciculaciones musculares (contracciones involuntarias) y alteraciones en la marcha con congelamiento.  \n- Estudios electromiográficos (EMG) y de velocidad de conducción nerviosa confirmaron daño en las motoneuronas superiores e inferiores, compatible con enfermedad de motoneurona.  \n- La resonancia magnética cerebral no mostró hallazgos específicos que expliquen el cuadro.  \n- Un panel genético amplio fue negativo para mutaciones comunes en enfermedades neurodegenerativas, pero identificó una variante patogénica en el gen POLG, asociado a síndromes de depleción mitocondrial, que afectan la función celular energética.  \n- En etapas avanzadas, el paciente presentó afasia (pérdida del lenguaje), disfagia (dificultad para tragar) y dependencia para movilizarse, requiriendo gastrostomía para alimentación.\n\n**Interpretación Clínica**  \nEste caso ilustra una enfermedad neurodegenerativa compleja con síntomas iniciales sistémicos y progresión hacia un síndrome mixto que combina características de parkinsonismo atípico y enfermedad de motoneurona. La presencia de la mutación en POLG sugiere un trastorno mitocondrial subyacente que podría estar contribuyendo a la degeneración neuronal. La afectación simultánea de motoneuronas superiores e inferiores y la falta de respuesta a levodopa apoyan un diagnóstico fuera del parkinsonismo típico. La evolución rápida hacia discapacidad severa y alteraciones del lenguaje y la deglución reflejan la gravedad del proceso.\n\n**Próximos Pasos**  \n- Continuar con manejo multidisciplinario que incluya neurología, rehabilitación, nutrición y apoyo psicológico.  \n- Monitorizar complicaciones respiratorias y nutricionales, dado el compromiso neuromuscular avanzado.  \n- Realizar asesoramiento genético familiar para evaluar riesgos y orientar a los parientes.  \n- Considerar terapias sintomáticas y soporte paliativo conforme avance la enfermedad, dado que no existen tratamientos curativos para esta condición.  \n\nEste caso destaca la importancia de una evaluación integral en pacientes con síntomas neurológicos progresivos y la utilidad de estudios genéticos para identificar causas poco frecuentes que pueden influir en el pronóstico y manejo.",
+                "fh_score": 20.86
+            }
+        }
+    },
+    {
+        "article": "Mujer de 33 años, previamente sana, presentó disnea progresiva, fiebre alta, sudores nocturnos y pérdida de peso en diciembre de 2017. Después de un mes de evolución, fue ingresada en un hospital general con insuficiencia respiratoria aguda y shock séptico con infiltrados alveolares difusos, ictericia, hemoptisis y petequias en las extremidades inferiores. Fue intubada y necesitó soporte hemodinámico. Se detectó un soplo sistólico mitral a la ausculta del precordio. Había leucocitosis acentuada con desviación a la izquierda, plaquetopenia, disfunción hepática y renal asociada a proteinuria subnefrótica y consumo de complemento. El resultado de los anticuerpos antinucleares fue de 1/80, a pesar de los niveles normales de anti-DNA de doble cadena, anti-SM y anti-PR3. Después de la administración de ceftriaxona, mejoró clínicamente. Fiebre amarilla, dengue, chikungunya, leptospirosis, VIH y hepatitis virales fueron descartados. Las hemoculturas fueron positivas para Haemophilus spp. en las seis muestras recolectadas. El ecocardiograma transtorácico (ETT) demostró una masa ecogénica amorfa con superficie irregular y algunos elementos móviles que envolvían ambos folletos de la válvula mitral, midiendo 20x17 mm en el folleto anterior y 19 mm en su mayor diámetro en los folletos posteriores, resultando en regurgitación grave por flail mitral y perforación. La resonancia magnética mostró pequeños abscesos esplénicos, tratados de manera conservadora. Un aneurisma micótico no complicado de la arteria cerebral media izquierda fue tratado por embolización percutánea. Treinta días después de la hospitalización, se sometió a un reemplazo de la válvula mitral con éxito por una prótesis valvular biológica de tamaño 29 mm y después de una extensa resección del tumor. Se evidenció regurgitación aórtica moderada debido a lesión de la fibrosa intervalvar mitroaórtica y retracción de la cúspide no coronaria, tratada de manera conservadora. El examen patológico confirmó la presencia de un mixoma valvular mitral infectado. La paciente completó 28 días de ceftriaxona y gentamicina, recibiendo el alta hospitalaria asintomática. En el seguimiento de un año, no hubo evidencia de recurrencia y se constató solamente regurgitación aórtica leve. Los mixomas infectados presentan mayor riesgo de eventos embólicos, aunque las manifestaciones clínicas son indistinguibles de tumores no infectados.2 El presente caso parece ser el sexto de mixoma valvular mitral infectado relatado en la literatura, llenando criterios definitivos para el diagnóstico, y el tercero causado por un microorganismo del grupo HACEK.3 - 8 De los 64 mixomas valvulares mitrales publicados de 2006 a 2012, los síntomas eran cardiovasculares en 36,7%; 9,5 a 21,6% de los mixomas de la válvula mitral fueron sometidos al cambio de válvula y el tiempo del diagnóstico hasta la cirugía varió de algunas horas a 42 días.2 , 9 La mortalidad operatoria y general fue relatada como siendo, respectivamente, 2,6 a 3% y 5,1 a 21%.2 , 10 En la presente serie, la mayoría de los pacientes presentó insuficiencia cardiaca sintomática, fueron sometidos al cambio de válvula mitral y todos presentaron buenos resultados en el seguimiento.\n",
+        "gold_summary": "Una mujer de 33 años de edad, con antecedentes de fiebre y disnea de unos pocos días de evolución, fue hospitalizada con un síndrome lupoide, con hemocultivos positivos para Haemophilus spp. El ecocardiograma reveló una masa gigante que involucraba ambas valvas mitrales, con una severa regurgitación mitral que requería un reemplazo valvular mitral biológico. La microscopía reveló un mixoma infectado y la paciente fue dada de alta asintomática tras finalizar la terapia con antibióticos. Ella tuvo un buen seguimiento.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había una mujer que se sentía muy mal. Tenía fiebre y le costaba mucho respirar. \n\nLos doctores la llevaron al hospital. Le encontraron una bolita grande en el corazón. Esa bolita hacía que su corazón no funcionara bien. \n\nLos doctores le pusieron una nueva parte en el corazón para ayudarla. También le dieron medicinas para que se mejorara. \n\nDespués de un tiempo, ella se sintió bien y pudo irse a su casa. Los doctores la cuidaron mucho y ella estuvo sana.",
+                "fh_score": 83.59
+            },
+            "B2": {
+                "text": "**Lo que le pasó a la paciente**  \nUna mujer de 33 años comenzó con dificultad para respirar, fiebre alta y otros síntomas graves. Fue hospitalizada porque tenía una infección en la sangre causada por una bacteria llamada Haemophilus. Además, su corazón tenía un problema: una masa grande creció en la válvula mitral, que es una parte importante para que la sangre fluya bien en el corazón.\n\n**Qué encontraron los médicos**  \nUn examen llamado ecocardiograma mostró que esta masa afectaba ambas partes de la válvula mitral y causaba que la sangre regresara hacia el corazón, lo que se llama regurgitación mitral grave. Por eso, fue necesario reemplazar esa válvula por una nueva hecha de material biológico. Cuando analizaron la masa con un microscopio, descubrieron que era un mixoma infectado, que es un tumor benigno pero que en este caso tenía infección.\n\n**Cómo terminó el caso**  \nDespués de la cirugía y de recibir antibióticos durante varias semanas, la paciente mejoró mucho y pudo salir del hospital sin síntomas. En el seguimiento durante un año, no hubo problemas ni regreso del tumor. Este caso es muy raro y muestra la importancia de un diagnóstico rápido y un tratamiento adecuado para este tipo de infecciones en el corazón.",
+                "fh_score": 59.9
+            },
+            "B3": {
+                "text": "**Contexto**\n\nUna mujer de 33 años, previamente sana, comenzó a experimentar dificultad para respirar progresiva, fiebre alta, sudores nocturnos y pérdida de peso durante un mes. Fue ingresada en un hospital con insuficiencia respiratoria aguda, shock séptico, sangrado pulmonar (hemoptisis), ictericia (coloración amarillenta de piel y mucosas) y petequias (pequeñas manchas rojas) en las piernas. Presentaba además un soplo cardíaco en la válvula mitral, leucocitosis (aumento de glóbulos blancos), plaquetopenia (disminución de plaquetas), disfunción hepática y renal, y alteraciones en pruebas inmunológicas.\n\n**Hallazgos Clave**\n\n- Se descartaron infecciones virales comunes en la región (fiebre amarilla, dengue, chikungunya, VIH, hepatitis).\n- Hemocultivos confirmaron infección por Haemophilus spp., un tipo de bacteria del grupo HACEK, conocida por afectar las válvulas cardíacas.\n- Ecocardiograma mostró una masa grande y irregular que afectaba ambas valvas de la válvula mitral, causando una regurgitación grave (flujo sanguíneo anormal hacia atrás) debido a daño estructural.\n- Resonancia magnética detectó pequeños abscesos en el bazo y un aneurisma micótico (una dilatación arterial causada por infección) en una arteria cerebral, tratado con embolización (bloqueo del vaso).\n- La paciente fue sometida a reemplazo exitoso de la válvula mitral por una prótesis biológica tras resección completa del tumor.\n- El examen patológico confirmó que la masa era un mixoma valvular mitral infectado, un tumor cardíaco benigno pero con infección bacteriana.\n- Se observó además regurgitación aórtica moderada por lesión en la estructura entre la válvula mitral y la aórtica, manejada sin cirugía.\n- Recibió tratamiento antibiótico con ceftriaxona y gentamicina durante 28 días.\n\n**Interpretación Clínica**\n\nEste caso representa una forma rara y grave de mixoma valvular mitral infectado, que es poco frecuente en la literatura médica y con alto riesgo de complicaciones embólicas (formación de coágulos que pueden viajar a otros órganos). La infección por Haemophilus spp. del grupo HACEK es especialmente relevante por su asociación con endocarditis (infección de las válvulas cardíacas). La presentación clínica puede ser similar a la de tumores no infectados, pero el riesgo de complicaciones es mayor.\n\nEl manejo combinado de cirugía para remover el tumor y reemplazar la válvula dañada, junto con terapia antibiótica prolongada, permitió una recuperación exitosa. La paciente mostró buena evolución clínica y no presentó recurrencia ni complicaciones significativas durante un seguimiento de un año.\n\n**Próximos Pasos**\n\n- Continuar con controles cardiológicos periódicos para monitorear la función valvular y detectar posibles complicaciones tardías.\n- Mantener vigilancia clínica para signos de infección o embolias.\n- Considerar la importancia de un diagnóstico precoz en casos similares para reducir la mortalidad y mejorar los resultados quirúrgicos.\n- Difundir el conocimiento sobre esta entidad rara para facilitar su reconocimiento y tratamiento oportuno en la práctica clínica.",
+                "fh_score": 40.24
+            }
+        }
+    },
+    {
+        "article": "Mujer de 71 años, que fue atendida en urgencias del Hospital de Mataró (Barcelona, España) el 9 de septiembre de 2020 con debilidad progresiva, por lo que se decidió su ingreso en neurología. Como antecedentes patológicos destacaban hipertensión arterial, temblor esencial, artrosis y trastorno de ansiedad leve, en tratamiento con gabapentina, sertralina y tramadol. La paciente había consultado a su médico de cabecera el 1 de septiembre de 2020 por dolor abdominal, junto con diarrea leve que duró 24 horas. Al día siguiente comenzó a sentirse débil y, a lo largo de los días siguientes, apareció disnea y disfagia, por lo que se sospechó laringitis y se le recetó prednisona. El 8 de septiembre de 2020 fue visitada nuevamente por su médico de cabecera por empeoramiento global de la debilidad; presentaba, además, disartria, disfagia y ptosis bilateral, por lo que fue derivada a urgencias del hospital.\n\nA su llegada no presentaba fiebre, la presión arterial y la frecuencia cardíaca eran normales, y la exploración física era normal, a excepción de taquipnea moderada. El examen neurológico mostró ptosis palpebral bilateral, parálisis facial bilateral, midriasis bilateral arreactiva a la luz y a la acomodación, oftalmoparesia bilateral tanto para la suprainfraversión como para la mirada horizontal bilateral, tetraparesia moderada en las extremidades (3/5), y disfonía y disfagia graves. Ella estaba consciente y el contenido del lenguaje era normal, al igual que los reflejos miotáticos, la sensibilidad y la coordinación. Las maniobras de fatigabilidad no fueron concluyentes y se realizó la prueba del hielo, que resultó positiva, mejorando –transitoriamente– la ptosis.\n\nLa reacción en cadena de la polimerasa (PCR) para el SARS-CoV-2 fue repetidamente negativa (en su ambulatorio y en el hospital). La gasometría arterial mostró hipoxemia: 75, con SO2 al 95%, y el resto de las exploraciones realizadas en urgencias resultaron normales (radiografía de tórax, análisis de sangre de rutina, electrocardiograma).\n\nSe inició tratamiento de soporte con oxígeno, sueroterapia, nutrición por sonda nasogástrica y medidas encaminadas a la prevención de complicaciones. El cuadro se estabilizó el tercer día del ingreso en planta, sin requerir soporte ventilatorio avanzado, y comenzó una mejoría lenta a partir del octavo día, iniciando tolerancia a la dieta adaptada de disfagia. Durante la primera semana presentaba hipotensión arterial, que fue corrigiéndose con la sueroterapia. A partir de la segunda semana, pudo iniciar rehabilitación física, con buena evolución, por lo que fue trasladada a un centro específico de rehabilitación al 19.º día, y entonces fue capaz de deambular con ayuda bilateral. En la visita de control en consultas externas de neurología seis semanas después, la paciente estaba completamente recuperada.",
+        "gold_summary": "Describimos el caso confirmado de botulismo alimentario en una paciente atendida en nuestro hospital en septiembre de 2020. La instauración en pocos días de una afectación bilateral de pares craneales, incluyendo disfagia, disnea y disartria, junto con midriasis y tetraparesia graves, precedida de diarrea, constituyó la presentación clínica en el primer caso; mientras que en su familiar cursó con síntomas inespecíficos y transitorios. Constatamos disautonomía consistente en hipotensión arterial. Teniendo en cuenta la situación pandémica en aquel momento, se descartó repetidamente la infección por SARS-CoV-2 antes de plantear alternativas diagnósticas. La neurotoxina B de C. botulinum fue detectada en las heces de la paciente, confirmando el diagnóstico de botulismo, que relacionamos con la ingesta de una conserva casera de alubias. Se completó el diagnóstico diferencial del cuadro descartando otras posibles etiologías.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una señora se enfermó después de comer unas alubias hechas en casa. Ella se puso muy débil y le costaba hablar, tragar y respirar. También tenía los ojos muy abiertos y los músculos muy flojos. Los doctores buscaron otras enfermedades, pero no encontró ninguna. Por eso, supieron que tenía una enfermedad llamada botulismo. Ella recibió ayuda en el hospital y poco a poco se fue mejorando hasta poder caminar con ayuda.",
+                "fh_score": 72.23
+            },
+            "B2": {
+                "text": "**Lo que pasó con la paciente**  \nUna mujer de 71 años llegó al hospital con debilidad que empeoraba rápidamente. Antes, había tenido diarrea leve y dolor de barriga. Luego, empezó a tener problemas para respirar, tragar y hablar. En el examen, los médicos vieron que tenía caída de los párpados, parálisis en la cara, pupilas que no reaccionaban a la luz, debilidad en brazos y piernas, y dificultad para mover los ojos. A pesar de estos síntomas, estaba consciente y sus reflejos y sensibilidad estaban normales.\n\n**Qué descubrieron los médicos**  \nBuscaron si tenía COVID-19, pero las pruebas fueron negativas varias veces. También hicieron otros estudios que no mostraron problemas en el pecho ni en el corazón. Detectaron que tenía presión baja en la sangre y falta de oxígeno en la sangre. Finalmente, encontraron una toxina llamada neurotoxina B producida por una bacteria llamada Clostridium botulinum en sus heces. Esta bacteria puede causar botulismo, una enfermedad grave que afecta los nervios y los músculos. Creen que la paciente se enfermó por comer una conserva casera de alubias contaminada.\n\n**Qué significa este diagnóstico**  \nEl botulismo es una enfermedad rara pero peligrosa que puede causar debilidad muscular grave y problemas para respirar. En este caso, la enfermedad afectó varios nervios importantes y causó síntomas como dificultad para tragar y hablar. Los médicos descartaron otras causas posibles antes de confirmar el botulismo. Gracias al tratamiento y cuidados, la paciente mejoró poco a poco y se recuperó completamente en unas semanas.\n\n**Resumen final**  \nEste caso muestra cómo el botulismo puede aparecer después de comer alimentos contaminados y causar síntomas graves. Es importante diagnosticarlo rápido para dar el tratamiento adecuado y evitar complicaciones. También se destacó que, durante la pandemia, fue necesario descartar COVID-19 antes de llegar a este diagnóstico.",
+                "fh_score": 59.12
+            },
+            "B3": {
+                "text": "**Contexto**  \nSe presenta el caso de una mujer de 71 años que ingresó en el Hospital de Mataró (Barcelona) en septiembre de 2020 con debilidad progresiva y síntomas neurológicos graves. Inicialmente, había experimentado diarrea leve y dolor abdominal, seguidos de dificultad para respirar (disnea), dificultad para tragar (disfagia), y alteraciones en el habla (disartria). La evolución clínica incluyó afectación bilateral de varios nervios craneales y debilidad en las cuatro extremidades.\n\n**Hallazgos Clave**  \nLa paciente mostró signos característicos de afectación neurológica severa: caída de los párpados (ptosis) en ambos ojos, parálisis facial bilateral, pupilas dilatadas que no respondían a la luz ni a la acomodación (midriasis arreactiva), y parálisis de los movimientos oculares en varias direcciones (oftalmoparesia). Además, presentaba debilidad moderada en brazos y piernas (tetraparesia), voz ronca (disfonía) y dificultad grave para tragar. A pesar de estos síntomas, estaba consciente y mantenía un lenguaje coherente, con reflejos y sensibilidad normales. La prueba del hielo, que consiste en aplicar frío sobre los párpados para evaluar la mejora temporal de la ptosis, fue positiva, lo que orientó hacia un trastorno neuromuscular.\n\nSe descartó repetidamente la infección por SARS-CoV-2 mediante pruebas PCR, dada la pandemia vigente en ese momento. Otros estudios complementarios, como radiografía de tórax, análisis de sangre y electrocardiograma, no mostraron alteraciones relevantes. La gasometría arterial reveló hipoxemia moderada, indicando un nivel bajo de oxígeno en sangre.\n\n**Interpretación Clínica**  \nEl cuadro clínico y la evolución sugirieron un botulismo alimentario, una enfermedad causada por la neurotoxina producida por la bacteria *Clostridium botulinum*, que afecta la función nerviosa y muscular. La confirmación diagnóstica se obtuvo al detectar la neurotoxina tipo B en las heces de la paciente. Se estableció que la fuente probable de la intoxicación fue la ingesta de una conserva casera de alubias. Además, la paciente presentó disautonomía, manifestada por hipotensión arterial, que requirió manejo con fluidos intravenosos.\n\nSe realizó un diagnóstico diferencial exhaustivo para descartar otras causas neurológicas que pudieran explicar los síntomas, asegurando así la precisión del diagnóstico.\n\n**Próximos Pasos y Evolución**  \nLa paciente recibió tratamiento de soporte, incluyendo oxígeno, nutrición por sonda nasogástrica y cuidados para prevenir complicaciones. Su condición se estabilizó en los primeros días y comenzó a mejorar lentamente a partir del octavo día, tolerando progresivamente la alimentación adaptada a su disfagia. Posteriormente, inició rehabilitación física, con buena respuesta, y fue trasladada a un centro especializado para continuar su recuperación. Seis semanas después, en la consulta de seguimiento neurológico, la paciente había recuperado completamente su función neuromuscular y capacidad para caminar con ayuda.\n\nEste caso destaca la importancia de considerar el botulismo alimentario en pacientes con debilidad neuromuscular progresiva y afectación de nervios craneales, especialmente cuando se descartan infecciones virales prevalentes como el SARS-CoV-2. Además, resalta la necesidad de un diagnóstico rápido y un manejo multidisciplinario para lograr una recuperación completa.",
+                "fh_score": 36.43
+            }
+        }
+    },
+    {
+        "article": "Un hombre de 52 años presentó pérdida de agudeza visual en su ojo derecho (OD) dos días después de una inyección intravenosa no complicada de ranibizumab con una aguja de 30 G. Su historial médico incluía PE, miopía alta y vitrectomía pars plana en el OD debido a desprendimiento de retina. Recibía tratamiento mensual con ranibizumab debido a neovascularización coroidea secundaria a estrías angioides, con 78 inyecciones previas en el OD. En el momento de la presentación, su BCVA era de 6/18 y la presión intraocular (IOP) era de 3 mmHg. El examen con lámpara de hendidura del segmento anterior no mostró nada de particular. El examen de fondo de ojo y los escaneos OCT revelaron pliegues corio-retinianos posteriores. En conjunto, la baja presión intraocular y los hallazgos del fondo de ojo llevaron al diagnóstico de hipotensión maculopatía. Se prescribió dexametasona tópica y atropina para mejorar la función del cuerpo ciliar. La IOP se normalizó en tres días con recuperación de la agudeza visual y resolución de los pliegues corio-retinianos. Cuatro meses después, se realizó una nueva inyección intravenosa anti-VEGF en el cuadrante inferolateral y el paciente informó disminución de la agudeza visual en el día siguiente a la inyección. La BCVA era contar los dedos y la IOP era de 2 mmHg. Los pliegues corio-retinianos en el polo posterior estaban presentes, incluso más prominentemente esta vez. El examen con lámpara de hendidura reveló una herida abierta en la esclerótica en el sitio de la inyección. La herida se suturó con monofilamento 10-0 y se prescribió dexametasona tópica y atropina. El paciente se recuperó bien y presentó una BCVA de 6/12 y una IOP de 12 mmHg.\n",
+        "gold_summary": "Un hombre de 52 años se quejó de pérdida de visión en el ojo derecho (OD) dos días después de un IVI anti-VEGF sin complicaciones para el tratamiento de la neovascularización coroidea secundaria a estrías angioides. Su historial médico incluía PE, miopía patológica y una vitrectomía pars plana (PPV) previa debido a un desprendimiento de retina. La agudeza visual mejor corregida (BCVA) en el OD disminuyó de 6/12 a 6/18 después del IVI. La presión intraocular (IOP) era de 3 mmHg y se observaron pliegues corio-retinianos en el polo posterior. Se prescribió dexametasona tópica y atropina, y se observó una recuperación completa después de tres días. Cuatro meses después, el paciente desarrolló un nuevo episodio de pérdida de visión después de otro IVI. Su BCVA era contar los dedos, la IOP era de 2 mmHg, y se observaron pliegues corio-retinianos más evidentes. Esta vez, una herida escleral abierta en el sitio de inyección era evidente y fue necesaria una sutura escleral. Una vez más, el paciente se recuperó bien.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un hombre tuvo problemas para ver con su ojo derecho. Esto pasó después de que le pusieron una medicina en el ojo. Su ojo estaba un poco débil y la presión dentro del ojo era baja. El doctor le dio unas gotas para ayudar. Después de tres días, su vista mejoró.\n\nCuatro meses después, le pusieron otra vez la medicina. Otra vez, su vista se puso muy mala. Esta vez, el ojo tenía una pequeña herida. El doctor la cerró con puntitos. Después, el hombre volvió a ver mejor.",
+                "fh_score": 92.59
+            },
+            "B2": {
+                "text": "### Lo que le pasó al paciente\n\nUn hombre de 52 años perdió visión en su ojo derecho dos días después de recibir una inyección en la vena para tratar un problema en la parte trasera del ojo llamado neovascularización coroidea, que es cuando crecen vasos sanguíneos anormales. Él tenía antecedentes de miopía fuerte, una cirugía previa en el ojo por desprendimiento de retina y otros problemas oculares.\n\n### Qué encontraron los doctores\n\nDespués de la inyección, su visión empeoró y la presión dentro del ojo bajó mucho, a solo 3 mmHg (lo normal es más alta). Al examinar el ojo, vieron pliegues en la capa del ojo llamada coroides y retina, que son señales de que el ojo estaba muy débil por la baja presión. Le dieron medicamentos en gotas para ayudar a que el ojo se recuperara, y en tres días su visión y presión volvieron a la normalidad.\n\n### Qué pasó después\n\nCuatro meses más tarde, el hombre recibió otra inyección similar y volvió a perder visión al día siguiente. Esta vez, la presión en el ojo bajó aún más, y los pliegues en la retina eran más visibles. Además, los doctores encontraron una herida abierta en la pared del ojo donde pusieron la inyección. Para arreglarla, tuvieron que coser esa herida. Después del tratamiento, el paciente mejoró y recuperó buena visión y presión normal en el ojo.\n\n### Qué significa esto\n\nEste caso muestra que, aunque las inyecciones en el ojo suelen ser seguras, pueden causar problemas como baja presión ocular y daño temporal en la retina. Es importante revisar bien el ojo después de cada inyección para detectar heridas o complicaciones y tratarlas rápido para evitar pérdida permanente de visión.",
+                "fh_score": 66.8
+            },
+            "B3": {
+                "text": "**Contexto:**  \nUn hombre de 52 años con antecedentes de preeclampsia (PE), miopía alta y una cirugía previa llamada vitrectomía pars plana (PPV) en su ojo derecho debido a un desprendimiento de retina, recibía tratamiento mensual con inyecciones intravenosas (IVI) de ranibizumab, un medicamento anti-VEGF (factor de crecimiento endotelial vascular), para tratar una neovascularización coroidea secundaria a estrías angioides (formación anormal de vasos sanguíneos en la capa vascular del ojo).\n\n**Hallazgos Clave:**  \nDos días después de una inyección intravenosa que inicialmente parecía no presentar complicaciones, el paciente notó una disminución de la agudeza visual en su ojo derecho. La agudeza visual mejor corregida (BCVA) bajó de 6/12 a 6/18, y la presión intraocular (IOP) estaba muy baja, en 3 mmHg (el rango normal es aproximadamente 10-21 mmHg). El examen con lámpara de hendidura no mostró alteraciones en la parte frontal del ojo, pero el examen del fondo de ojo y las imágenes por tomografía de coherencia óptica (OCT) revelaron pliegues en las capas coroideas y retinianas en la parte posterior del ojo. Estos hallazgos, junto con la baja presión intraocular, llevaron al diagnóstico de hipotensión maculopatía, una condición en la que la baja presión dentro del ojo causa cambios estructurales que afectan la visión.\n\nSe inició tratamiento con dexametasona tópica (un corticosteroide para reducir la inflamación) y atropina (un medicamento que ayuda a relajar el cuerpo ciliar, facilitando la producción de humor acuoso y aumentando la presión intraocular). En tres días, la presión intraocular volvió a la normalidad y la visión mejoró, con desaparición de los pliegues corio-retinianos.\n\nCuatro meses después, tras una nueva inyección intravenosa anti-VEGF aplicada en la zona inferolateral del ojo, el paciente presentó nuevamente una disminución significativa de la visión al día siguiente, con una BCVA reducida a “contar los dedos” (una medida de visión muy pobre) y una presión intraocular aún más baja, de 2 mmHg. Esta vez, los pliegues corio-retinianos eran más evidentes. El examen con lámpara de hendidura detectó una herida abierta en la esclerótica (la capa externa blanca del ojo) en el sitio de la inyección, lo que indicaba una filtración o fuga de líquido ocular. Esta herida fue reparada mediante sutura con un hilo muy fino (monofilamento 10-0). Se repitió el tratamiento con dexametasona tópica y atropina, y el paciente se recuperó satisfactoriamente, alcanzando una BCVA de 6/12 y una presión intraocular de 12 mmHg.\n\n**Interpretación Clínica:**  \nEste caso muestra que, aunque las inyecciones intravenosas de anti-VEGF son generalmente seguras, pueden presentarse complicaciones poco comunes como la hipotensión maculopatía causada por una baja presión intraocular. La presencia de pliegues corio-retinianos y la disminución de la visión son signos importantes que deben alertar al médico. Además, la aparición de una herida escleral abierta en el sitio de la inyección puede causar una fuga de líquido y empeorar la hipotensión ocular, requiriendo reparación quirúrgica.\n\n**Próximos Pasos:**  \nEs fundamental monitorizar cuidadosamente la presión intraocular y la integridad de la esclera después de las inyecciones anti-VEGF, especialmente en pacientes con antecedentes de cirugía ocular previa o miopía alta, que pueden tener mayor riesgo de complicaciones. El tratamiento temprano con corticosteroides tópicos y atropina puede ayudar a restaurar la presión intraocular y la función visual. En casos de filtración escleral, la reparación quirúrgica es necesaria para evitar daños permanentes. Además, se recomienda evaluar la técnica de inyección para minimizar el riesgo de heridas escleral abiertas en futuras aplicaciones.",
+                "fh_score": 42.57
+            }
+        }
+    },
+    {
+        "article": "Una mujer de 82 años acudió al servicio de urgencias por dolor abdominal, diarrea, confusión y deterioro de su estado general de varios días de evolución. Entre sus antecedentes médicos destacaban hipertensión arterial tratada e hipotiroidismo en tratamiento sustitutivo. No se recogieron antecedentes quirúrgicos ni hábitos tóxicos de interés. A la exploración física, la frecuencia cardíaca era de 84 lpm, tensión arterial de 105/82 mmHg, temperatura de 38 °C y saturación de oxígeno de 95% en aire ambiente. Las mucosas estaban secas y el abdomen era difusamente doloroso a la palpación sin masas palpables ni reacción peritoneal. La analítica realizada mostró una hemoglobina de 13.1 g/dL, proteína C reactiva a 122.9 mg/L sin leucocitosis (8.9 × 10^9/L), hiponatremia (130 mmol/L), hipopotasemia (2.9 mmol/L), pruebas de función renal, hepáticas, lipasa y enzimas cardiacas normales. El frotis para SARSCoV-2 fue negativo. La orina era maloliente con presencia de nitritos positivos, hematíes (+++) y leucocitos (+) por lo que se envió la muestra para cultivo microbiológico. Ante estos hallazgos se inició antibioticoterapia probabilista con ceftriaxona ante la sospecha de una posible infección urinaria y se decidió realizar una tomografía tóraco-abdomino-pélvica para descartar la presencia de un foco infeccioso profundo. Este examen reveló la presencia de signos de broncopatía crónica y una neumatosis vesical parietal a nivel abdominal compatible con una cistitis enfisematosa. El cultivo de orina reveló la presencia de Escherichia coli (> 100 000 UFC/m) sensible a la antibioticoterapia prescrita empíricamente y los hemocultivos fueron positivos al mismo germen. Se decidió el ingreso de la paciente en servicio de medicina interna y se continuó el tratamiento antibiótico durante 7 días con una evolución favorable desde el punto de vista clínico y analítico, permitiendo el alta hospitalaria.",
+        "gold_summary": "Una mujer de 82 años con antecedentes de hipertensión arterial e hipotiroidismo acudió al servicio de urgencias por dolor abdominal, diarrea, confusión y deterioro de su estado general de varios días de evolución. A su admisión, la paciente se encontraba febril y la analítica mostró una elevación de la proteína C reactiva sin leucocitosis (8.9 × 10^9/L). En ese contexto se realizó exudado nasofaríngeo para SARS-CoV-2 que fue negativo. Con estos resultados, la sospecha inicial era la de un cuadro infeccioso de origen digestivo. La muestra de orina era maloliente con presencia de leucocitos y nitritos enviándose a cultivo microbiológico. Se inició tratamiento antibiótico empírico con una cefalosporina de tercera generación ante la sospecha de une posible infección urinaria. Se decidió la realización de una tomografía tóraco-abdomino-pélvica con el objetivo de evaluar la presencia de otros focos infecciosos en una paciente de edad avanzada. Este estudio mostró una cistitis enfisematosa, una enfermedad poco frecuente en una paciente sin ninguno de los factores de riesgo clásicos para esta entidad. Los cultivos de orina y sangre fueron positivos para Escherichia coli sensible al antibiótico empírico por lo que se continuó para completar 7 días de tratamiento. La evolución clínica fue favorable.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una señora de 82 años se sentía muy mal. Tenía dolor en la barriga y estaba confundida. \n\nLos doctores le hicieron pruebas y vieron que tenía una infección en la orina. Le dieron medicina para ayudarla. \n\nTambién hicieron una foto especial de su cuerpo. Vieron que su vejiga estaba un poco dañada por la infección. \n\nLa medicina funcionó y la señora mejoró mucho. Después de una semana, pudo irse a su casa feliz.",
+                "fh_score": 80.0
+            },
+            "B2": {
+                "text": "**Lo que Encontraron**  \nUna mujer de 82 años llegó al hospital porque tenía dolor en el abdomen, diarrea, estaba confundida y se sentía muy mal desde hacía varios días. Tenía fiebre y algunos análisis de sangre mostraron que tenía inflamación, pero no un aumento en los glóbulos blancos, que son células que ayudan a combatir infecciones. También le hicieron una prueba para detectar COVID-19, que salió negativa.\n\n**Qué Significa la Orina y el Tratamiento**  \nLa orina de la paciente olía mal y tenía señales de infección, como leucocitos (células blancas) y nitritos. Por eso, enviaron una muestra para ver qué bacteria causaba la infección. Mientras esperaban, comenzaron a darle un antibiótico llamado ceftriaxona, que es fuerte y puede combatir muchas bacterias.\n\n**Descubrimiento Importante con la Tomografía**  \nPara asegurarse de que no hubiera una infección más grave en el cuerpo, le hicieron una tomografía, que es una imagen especial del cuerpo. Esta prueba mostró que tenía una cistitis enfisematosa, que es una infección rara en la vejiga donde se forman burbujas de gas en la pared de este órgano. Esto es inusual porque la paciente no tenía los factores de riesgo típicos para esta enfermedad.\n\n**Resultados del Cultivo y Evolución**  \nLos cultivos de la orina y la sangre mostraron que la bacteria causante era Escherichia coli, que respondía bien al antibiótico que ya le estaban dando. Por eso, continuaron con el tratamiento durante 7 días. La paciente mejoró mucho y pudo salir del hospital.  \n\nEn resumen, esta mujer tuvo una infección urinaria grave y poco común que se detectó a tiempo y se trató con éxito gracias a los exámenes y al antibiótico adecuado.",
+                "fh_score": 62.28
+            },
+            "B3": {
+                "text": "**Contexto**  \nUna mujer de 82 años con antecedentes médicos de hipertensión arterial e hipotiroidismo acudió al servicio de urgencias debido a varios días de dolor abdominal, diarrea, confusión y un deterioro general de su estado de salud. Al examen físico, presentaba fiebre y signos de deshidratación, con un abdomen doloroso a la palpación pero sin signos de irritación peritoneal.  \n\n**Hallazgos Clave**  \nLos análisis de sangre revelaron una elevación significativa de la proteína C reactiva (un marcador de inflamación) sin aumento en el número de glóbulos blancos (leucocitosis), lo que sugiere una respuesta inflamatoria sin infección bacteriana evidente en sangre. La prueba para detectar infección por SARS-CoV-2 fue negativa. La orina presentaba mal olor, nitritos positivos y presencia de leucocitos y glóbulos rojos, indicativos de infección urinaria.  \n\nSe inició tratamiento antibiótico empírico con ceftriaxona, una cefalosporina de tercera generación, ante la sospecha de infección urinaria. Para descartar la existencia de infecciones profundas o complicaciones, se realizó una tomografía computarizada (TC) del tórax, abdomen y pelvis. Este estudio identificó una neumatosis vesical parietal, es decir, presencia de gas en la pared de la vejiga, compatible con cistitis enfisematosa, una infección urinaria grave y poco frecuente caracterizada por la acumulación de gas en la vejiga.  \n\nLos cultivos microbiológicos confirmaron la presencia de Escherichia coli, una bacteria comúnmente responsable de infecciones urinarias, tanto en la orina como en la sangre, y que resultó sensible al antibiótico administrado.  \n\n**Interpretación Clínica**  \nLa cistitis enfisematosa es una infección poco común que suele presentarse en pacientes con factores de riesgo como diabetes o inmunosupresión, pero en este caso la paciente no presentaba estos antecedentes clásicos, lo que hace el diagnóstico más inusual. La detección temprana mediante imagen y el inicio rápido de tratamiento antibiótico adecuado fueron fundamentales para la evolución favorable del cuadro.  \n\n**Próximos Pasos**  \nLa paciente fue ingresada en el servicio de medicina interna para continuar el tratamiento antibiótico durante siete días. Durante su hospitalización, mostró mejoría clínica y analítica, lo que permitió su alta hospitalaria sin complicaciones. Se recomienda seguimiento médico para controlar posibles recurrencias o complicaciones y mantener el control de sus condiciones crónicas.",
+                "fh_score": 34.94
+            }
+        }
+    },
+    {
+        "article": "Varón nacido a las 38 semanas de gestación y sin controles obstétricos prenatales, producto de un parto eutócico sin complicaciones con un peso de 2.678 g y Apgar 7 y 8 al minuto y a los cinco minutos de vida, respectivamente; derivado por sospecha de enterocolitis necrotizante a los siete días de vida. Al nacimiento, en su hospital de origen, se descartaron malformaciones congénitas externas y se colocó una sonda orogástrica para verificar la permeabilidad esofágica, obteniendo 200 mL de líquido amniótico. Posteriormente inició alimentación vía oral pero debido a succión débil y vómitos biliosos fue ingresado en la unidad de cuidados intensivos neonatales. A las 4 horas de vida se realizó radiografía abdominal observando una imagen de doble burbuja atípica, por lo cual realizaron un control radiológico 48 horas después identificando gas intestinal aparentemente distal, y presentó meconiorrexis a las 50 horas de vida. Dos días después reinició la alimentación oral, tras lo cual presentó nuevamente vómitos de aspecto biliar y distensión abdominal que mejoró con el ayuno y sonda orogástrica; por lo cual se sospechó enterocolitis necrotizante indicándose dieta absoluta, nutrición parenteral total y antibioterapia con ampicilina y amikacina. A los siete días de vida y debido a la persistencia de los síntomas pese al tratamiento instaurado, fue derivado a nuestro centro. A su llegada presentaba distensión abdominal, sin ruidos intestinales ni signos de irritación peritoneal, por lo que se realizó tránsito intestinal sin progresión distal y colon por enema con hallazgo de microcolon, todo ello sugestivo de atresia intestinal yeyunoileal. Tras la realización de los estudios de imagen y con la sospecha de atresia intestinal se realizó una laparotomía exploradora mediante abordaje supraumbilical transverso, observando adherencias hepatoileales, una hernia interna a través de un defecto mesentérico con incarceración de un asa yeyunal y atresia yeyunoileal tipo IV. Se identificaron dos sitios de atresia a 56 cm del ángulo de Treitz y a 36 cm de la válvula ileocecal, con un segmento interatrésico de 10 cm con meconio intraluminal y cambios de coloración con aspecto violáceo pero sin perforación; la diferencia de diámetros intestinales proximal a distal tenía una relación 3:1. Se decidió disecar el mesenterio y resecar el asa ciega (10 cm) para realizar una anastomosis término-oblicua yeyunoileal, corroborando la permeabilidad distal con sonda intraluminal y administración de solución fisiológica hasta que presentó evacuación rectal. El reporte de histopatología confirmó una atresia yeyunoileal tipo IV con enteritis crónica leve. El paciente evolucionó favorablemente y al 5º día postoperatorio inició alimentación oral con adecuada tolerancia progresiva y descenso paulatino de la nutrición parenteral total con retirada al 8º día postoperatorio. Al 6° día de la intervención presentó deposiciones espontáneas y a los 20 días de vida fue dado de alta sin complicaciones. Doce meses después el paciente continúa asintomático con adecuada ganancia ponderal y tolerancia a la alimentación complementaria con deposiciones diarias de características normales.",
+        "gold_summary": "Recién nacido de sexo masculino, nacido a término, derivado por vómitos, evacuaciones escasas y distensión abdominal. A los 8 días de vida y tras excluir diversas causas de distensión abdominal se sometió a laparotomía exploradora, identificando una hernia transmesentérica y dos sitios de atresia intestinal. Se realizó resección del segmento atrésico y anastomosis primaria, con buena evolución.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un bebé nació sin problemas. Tenía dolor en la barriga y no podía hacer popó bien. Los doctores buscaron qué pasaba y lo operaron. Encontraron dos partes del intestino que estaban tapadas. Quitaron las partes malas y unieron el intestino bueno. El bebé mejoró mucho después de la operación.",
+                "fh_score": 78.51
+            },
+            "B2": {
+                "text": "**Lo que pasó con el bebé:**  \nUn bebé varón nació a término y, durante su primera semana de vida, tuvo problemas como vómitos, pocas evacuaciones y el abdomen hinchado. Estos síntomas indicaban que algo no estaba funcionando bien en su intestino.\n\n**Qué encontraron los médicos:**  \nDespués de hacer varios estudios para entender la causa de la hinchazón abdominal, los doctores decidieron hacer una cirugía llamada laparotomía exploradora. En esta operación, descubrieron que el bebé tenía una hernia transmesentérica, que es cuando una parte del intestino queda atrapada en un defecto del tejido que lo sostiene. Además, encontraron dos lugares donde el intestino estaba bloqueado, lo que se llama atresia intestinal.\n\n**Qué hicieron para ayudar:**  \nLos médicos quitaron la parte del intestino que estaba bloqueada (resección del segmento atrésico) y unieron las partes sanas del intestino (anastomosis primaria) para que el alimento pudiera pasar normalmente.\n\n**Cómo le fue al bebé:**  \nDespués de la cirugía, el bebé mejoró bien, comenzó a alimentarse por vía oral y pudo irse a casa sin complicaciones. Un año después, sigue sano, come bien y tiene evacuaciones normales.",
+                "fh_score": 52.16
+            },
+            "B3": {
+                "text": "Resumen detallado para público general universitario\n\n**Contexto:**  \nSe trata de un recién nacido varón, nacido a término (38 semanas de gestación) mediante un parto normal sin complicaciones, con un peso al nacer de 2.678 gramos. No contó con controles prenatales durante el embarazo. En las primeras horas de vida presentó dificultad para alimentarse debido a una succión débil y vómitos con contenido biliar (color verde), lo que motivó su ingreso a la unidad de cuidados intensivos neonatales. Las primeras radiografías abdominales mostraron una imagen sugestiva de obstrucción intestinal, pero con presencia de gas en intestino distal. A los pocos días presentó distensión abdominal y vómitos persistentes, lo que llevó a sospechar una enterocolitis necrotizante (una inflamación grave del intestino en recién nacidos), por lo que se inició tratamiento con ayuno, nutrición intravenosa y antibióticos.\n\n**Hallazgos clave:**  \nA pesar del tratamiento, los síntomas no mejoraron, por lo que fue trasladado a un centro especializado. Allí se realizaron estudios radiológicos que evidenciaron un colon muy pequeño (microcolon) y ausencia de progresión del tránsito intestinal, lo que sugirió la presencia de una atresia intestinal (una obstrucción causada por la ausencia o cierre de una parte del intestino). Durante la cirugía exploratoria se encontró una hernia interna a través de un defecto en el mesenterio (tejido que sostiene los intestinos) con atrapamiento de un segmento del intestino delgado (asa yeyunal), además de dos áreas de atresia en el intestino delgado (tipo IV, que implica múltiples segmentos afectados). Se observó un segmento intermedio con meconio (primera materia fecal) y cambios de coloración, pero sin perforación. La relación entre el diámetro del intestino proximal y distal era de 3 a 1, indicando una diferencia significativa en tamaño.\n\n**Interpretación clínica:**  \nSe realizó la resección del segmento intestinal afectado y una anastomosis término-oblicua yeyunoileal (unión quirúrgica entre dos partes del intestino delgado), asegurando la permeabilidad del intestino distal. El análisis histopatológico confirmó la atresia múltiple con inflamación crónica leve del intestino. El paciente mostró una evolución favorable tras la cirugía, iniciando alimentación oral progresivamente desde el quinto día postoperatorio y retirando la nutrición parenteral al octavo día. Presentó deposiciones normales y fue dado de alta a los 20 días de vida sin complicaciones.\n\n**Próximos pasos y seguimiento:**  \nA los doce meses de edad, el niño continúa asintomático, con un adecuado aumento de peso y tolerancia normal a la alimentación complementaria, manteniendo deposiciones diarias de características normales. Este caso resalta la importancia de un diagnóstico oportuno y tratamiento quirúrgico adecuado en atresias intestinales múltiples para lograr una recuperación exitosa en recién nacidos.",
+                "fh_score": 38.75
+            }
+        }
+    },
+    {
+        "article": "Se remitió a un hombre de 86 años para que se le implantara una válvula aórtica transfemoral.\n\nLa historia significativa incluyó el hecho de fumar 40 cajetillas al año (hasta fines de la década de 1980) y la fibrilación auricular paroxística que requería anticoagulación con Coumadin desde 1999, seguida poco después por la implantación de un marcapasos ventricular debido a bradicardia. Fue admitido por síncope en mayo de 2011 y se le diagnosticó una estenosis aórtica calcificada severa. Era eupneico y no mostraba signos de insuficiencia cardiaca o retención de líquidos. La ecocardiografía transtorácica reveló una estenosis aórtica severa (gradiente medio: 58 mmHg, área de la válvula aórtica: 0,4 cm2) con hipertrofia ventricular izquierda, fracción de eyección ventricular izquierda deteriorada (29%), acinesia inferior apical y obstrucción septal subvalvular (septum: 18 mm) con dilatación biauricular e hipertensión pulmonar con dilatación de la vena cava.\n\nLa angiografía coronaria mostró una estenosis del 75% de la arteria descendente anterior izquierda. El examen de eco-Doppler encontró vasos normales en el cuello. Se agregó aspirina 80 mg diariamente a su tratamiento; el paciente fue programado para un reemplazo de la válvula aórtica, pero no llegó hasta agosto, cuando fue readmitido en urgencias por disnea aguda y confusión. Había ganado 6 kg de peso, con edemas en las piernas y signos clínicos de derrame pleural. En ese momento, su SpO2 era del 92% y la proteína B-natriurética estaba elevada a 2336 pg·mL−1 (normal < 100 pg·mL−1).\n\nTras la terapia diurética y la eliminación de 850 ml de derrame pleural, se realizó una valvuloplastia de balón percutáneo aórtico de emergencia (Cristal Balloon, 23 mm) e inmediatamente después se le implantó un stent de metal desnudo (Biotronik-Pro-Kinetic 2.74 × 10.0) en la arteria descendente anterior izquierda. El gradiente medio transvalvular disminuyó de 59 a 38 mmHg. Se observaron algunas torsades de pointe el día 6 después de la intervención, que desaparecieron cuando la frecuencia más baja del marcapasos se aceleró a 80 latidos/min. Su estado mejoró drásticamente y se le dio el alta con furosemida, aldactazina y clopidogrel. Tras una revisión cuidadosa del expediente del paciente por parte del equipo cardiaco, se consideró que el riesgo de una cirugía valvular era demasiado alto (Euroscore logístico: 51%), y se propuso al paciente un implante de válvula aórtica transfemoral.\n\nLas notas de las enfermeras mencionan la hiperventilación nocturna y las crisis de ansiedad. El paciente era semiautónomo y vivía con su hija.\n\nLa implantación de la válvula aórtica transfemoral se programó para octubre de 2011. En el ingreso, 2 días antes del procedimiento, el paciente se describió como «ansioso e hiperventilante»; su peso era de 67 kg para una altura de 168 cm; el volumen espiratorio forzado en 1 s (FEV1) era de 1,1 L (50% del valor previsto) y la capacidad vital forzada de 1,7 L (55%); la presión arterial sistémica era de 120/60 mmHg; la concentración de hemoglobina era de 167 g·L−1; la creatinina era de 12,7 g·L−1; la tasa de filtración glomerular se calculó en 54 ml·min−1·m−2; el potasio era de 3,7 mEq·L−1; el sodio era de 141 mEq·L−1; el bicarbonato era de 22 mEq·L−1; y la proteína B natriurética era de 2.073 pg·mL−1. La ecografía describió un área de superficie de la válvula aórtica de 0,5 cm2 con un gradiente aórtico medio de 55 mmHg y acinesia inferoapical en el ventrículo izquierdo. La fracción de eyección se midió en 27% por el método Simpson biplano con regurgitación mitral moderada con dilatación biauricular y se estimó la presión pulmonar sistólica en >69 mmHg. La radiografía de tórax no mostró derrame pleural significativo. El paciente era totalmente dependiente del marcapasos.\n\nDos horas antes de la intervención, el paciente recibió 1 g de acetaminofeno por vía oral. Al llegar al quirófano, el paciente, plenamente consciente, presentaba respiración de Cheyne-Stokes periódica; cada ciclo duraba unos 85 s, con apneas de entre 15 y 20 s y grandes oscilaciones de la SpO2 entre el 88 % y el 99 %. Se le colocó dos catéteres intravenosos periféricos y uno arterial. El trazado arterial también mostraba oscilaciones de 85 s y una presión sistólica de 130 a 150 mmHg. Se le aplicó una máscara facial de oxígeno al 40 % con ventilación no invasiva; la SpO2 alcanzó un rango más estable (92 %-99 %). Diez minutos después, los análisis de gases en sangre mostraron un pH de 7,39, Pao2 de 108 mmHg, Paco2 de 40 mmHg, SaO2 del 97 %, y oscilaciones de lactato de 1,2 mEq·L−1. Se instaló una línea de muestreo capnógrafo dentro de la máscara facial para monitorizar la frecuencia respiratoria (Carescape Monitor B650, GE Healthcare, Helsinki, Finlandia). La monitorización también incluía un ECG de 12 derivaciones, oximetría de pulso, y oximetría cerebral regional (rSO2) mediante espectroscopia infrarroja cercana en el frente (INVOS, Somanetics). La capnografía reveló que las oscilaciones de la presión arterial eran sincrónicas con el ritmo de la respiración y que la presión disminuía durante los períodos apneicos e hipopneicos y aumentaba durante la hiperventilación; la rSO2 seguía el mismo patrón, a pesar de que la SpO2 del dedo permanecía a un nivel constante de 99 %. Se inició una infusión de propofol a una concentración objetivo de 0,2 µg·mL−1; se administraron 2,5 µg de sufentanilo antes de que los operadores infiltraran cada ingle con 200 mg de mepivacaína; el paciente se quedó dormido pero se mantuvo despierto al menor contacto con su cara o cuando su nombre se susurraba al oído; se administraron otros 2,5 µg de sufentanilo antes de la dilatación femoral de la arteria, un procedimiento requerido antes del reemplazo de la válvula. Los ciclos de ventilación se desaceleraron a un máximo de 120 s con 24 s de apneas centrales. Cuando la angiografía y los catéteres operativos estaban en su lugar en la aorta ascendente y se introdujo un marcapasos temporal en el ventrículo derecho, se indujo un ritmo rápido de 200 latidos/min para permitir una nueva dilatación de la válvula calcificada. Este procedimiento duró <25 s, durante el cual el paciente permaneció consciente y continuó respirando de la forma habitual, el ritmo se indujo justo después del final de un período apneico. Se preparó una válvula de 26 mm (SAPIEN, Edwards Lifesciences) y se introdujo en el orificio aórtico. Se dio una señal a los operadores una vez que la respiración se reanudó al final de un período apneico; se inició un ritmo ventricular rápido que llevó a la asistolia a una presión arterial media de 45 mmHg, y la válvula se expandió con balón y la angiografía confirmó la ausencia de fuga paravalvular. El balón se desinfló justo antes de que se detuviera el ritmo rápido, y el corazón volvió a latir a 80 latidos/min bajo la estimulación del marcapasos implantado. La secuencia completa se filmó; duró 31 s, durante los cuales el paciente siguió respirando regularmente (8 veces durante la detención circulatoria, es decir, una tasa de 16 veces por minuto) y no se despertó. Las expulsiones de sangre se reanudaron inmediatamente después de la deflación del balón, con una presión sistólica de 80 mmHg. Después de unas respiraciones profundas, la respiración se hizo regular; no se produjeron nuevos períodos apneicos ni oscilaciones de la presión arterial o rSO2. La hipertensión sistémica se desarrolló rápidamente, culminando después de 1 min a 190 mmHg y se controló con 40 mg de urapidil intravenoso durante los siguientes 15 min. La ecografía transtorácica midió el área valvular a 1,6 cm2 y el gradiente transvalvular máximo a 15 mmHg. La estimación de la presión arterial pulmonar mediante ecografía transtorácica mostró un gradiente sistólico de la presión ventricular derecha-aurícula derecha de 69 mmHg 1 día antes del procedimiento y 45 mmHg 2 días después. Un mes después, era de 28 mmHg. La evolución posterior no tuvo incidentes, y el paciente fue dado de alta 72 h después sin haber vuelto a la respiración periódica.\n\nMH - Edad 80 años y más\nMH - Cirugía de la válvula aórtica\nMH - *Estenosis/cirugía de la válvula aórtica\nMH - *Respiración de Cheyne-Stokes\nMH - Ecocardiografía\nMH - *Insuficiencia cardiaca\nMH - *Implantación de prótesis valvulares cardíacas\nMH - Hemodinámica\nMH - Humanos\nMH - Hombre\nMH - Resultado del tratamiento\n",
+        "gold_summary": "Se remitió a un hombre de 86 años para la implantación de una válvula aórtica transfemoral. La ecocardiografía transtorácica reveló una estenosis grave (gradiente medio: 58 mmHg, área de la válvula aórtica: 0,4 cm2), y después de una discusión multidisciplinaria, se consideró que el riesgo de la cirugía era demasiado alto (Euroscore logístico: 51%), y se propuso al paciente para la implantación de una válvula aórtica transfemoral (TAVI). Al llegar al quirófano, se observó que el paciente, completamente consciente, tenía respiración de Cheyne-Stokes (CSB), que persistió después de la administración de oxígeno al 40%. El procedimiento TAVI fue exitoso, y el patrón CSB se interrumpió en 8 s.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había un señor de 86 años que tenía un problema en su corazón. Su corazón tenía una puerta muy pequeña y difícil para que la sangre pasara.\n\nLos doctores dijeron que una operación grande era muy peligrosa para él. Entonces, decidieron ponerle una válvula nueva con un tubo pequeño por la pierna.\n\nCuando llegó al lugar para la operación, el señor respiraba de una forma rara que subía y bajaba. Le dieron aire para ayudar, pero seguía igual.\n\nLa operación salió muy bien. Después, su forma de respirar rara se detuvo rápido. El señor se sintió mejor y todo salió bien.",
+                "fh_score": 80.15
+            },
+            "B2": {
+                "text": "**Lo que le pasaba al paciente:**  \nUn hombre de 86 años tenía un problema grave en su corazón llamado estenosis aórtica, que significa que la válvula que controla el flujo de sangre desde el corazón hacia el cuerpo estaba muy estrecha. Esto hacía que su corazón trabajara mucho más duro para bombear la sangre. Los médicos usaron una ecografía especial para ver que la válvula estaba muy dañada y que el área por donde pasa la sangre era muy pequeña.\n\n**Por qué eligieron un tratamiento especial:**  \nDebido a que el paciente era mayor y tenía otros problemas de salud, los médicos pensaron que una cirugía tradicional para cambiar la válvula era demasiado riesgosa. En lugar de eso, decidieron hacer un procedimiento menos invasivo llamado TAVI, que consiste en implantar una nueva válvula a través de una arteria en la pierna, sin abrir el pecho.\n\n**Lo que ocurrió durante el procedimiento:**  \nCuando el paciente llegó al quirófano, estaba despierto y mostraba un tipo de respiración llamada Cheyne-Stokes. Esta respiración es irregular y se caracteriza por períodos en los que la persona respira muy rápido y otros en los que casi no respira. Aunque le dieron oxígeno, esta respiración continuó. Durante el procedimiento para poner la nueva válvula, todo salió bien y, justo después, la respiración irregular desapareció en pocos segundos.\n\n**Qué significa esto:**  \nEl éxito del procedimiento no solo mejoró la función de la válvula del corazón, sino que también ayudó a normalizar la respiración del paciente. Esto muestra que tratar la estenosis aórtica puede mejorar otros problemas relacionados con el corazón y la forma en que el cuerpo respira.",
+                "fh_score": 57.58
+            },
+            "B3": {
+                "text": "**Contexto**\n\nUn hombre de 86 años con antecedentes importantes, incluyendo tabaquismo intenso en el pasado, fibrilación auricular paroxística tratada con anticoagulación y marcapasos por bradicardia, fue diagnosticado con estenosis aórtica severa calcificada. Presentaba síntomas de insuficiencia cardíaca, como disnea y edemas, además de deterioro significativo de la función ventricular izquierda (fracción de eyección del 27-29%) y hipertensión pulmonar. Debido a su alto riesgo quirúrgico (Euroscore logístico del 51%), se decidió realizar un reemplazo valvular aórtico mediante un procedimiento menos invasivo conocido como implantación de válvula aórtica transfemoral (TAVI).\n\n**Hallazgos Clave**\n\n- La ecocardiografía mostró una estenosis aórtica severa con un área valvular muy reducida (0,4-0,5 cm²) y un gradiente medio elevado (55-58 mmHg), junto con disfunción ventricular izquierda y dilatación de las aurículas.\n- El paciente presentaba un patrón respiratorio anormal llamado respiración de Cheyne-Stokes (CSB), caracterizado por ciclos periódicos de respiración rápida seguidos de pausas (apneas), que persistió incluso tras la administración de oxígeno al 40%.\n- Durante el procedimiento TAVI, que se realizó bajo sedación consciente, se monitorizaron cuidadosamente la función cardíaca, la saturación de oxígeno y la respiración.\n- El procedimiento incluyó la valvuloplastia con balón y la implantación de una válvula protésica de 26 mm, con inducción temporal de ritmo cardíaco rápido para facilitar la expansión valvular.\n- El paciente mantuvo la respiración espontánea durante todo el procedimiento, sin despertar ni presentar complicaciones respiratorias.\n- Tras la implantación, se observó una interrupción inmediata del patrón de respiración de Cheyne-Stokes, con estabilización de la presión arterial y mejora hemodinámica.\n- La función valvular mejoró notablemente, con aumento del área valvular a 1,6 cm² y reducción del gradiente a 15 mmHg. La presión pulmonar también disminuyó progresivamente en el seguimiento.\n\n**Interpretación Clínica**\n\nEste caso ilustra la complejidad del manejo de un paciente anciano con estenosis aórtica severa y disfunción ventricular avanzada, en quien la cirugía convencional representaba un riesgo muy alto. La elección del TAVI permitió una intervención efectiva y menos invasiva. La presencia de respiración de Cheyne-Stokes, un patrón respiratorio asociado a insuficiencia cardíaca avanzada y alteraciones en el control respiratorio, fue un hallazgo relevante que se resolvió tras la mejora hemodinámica conseguida con la corrección valvular. Esto sugiere que la disfunción cardíaca contribuye directamente a la aparición de este patrón respiratorio anormal.\n\n**Próximos Pasos**\n\n- Continuar con el seguimiento clínico y ecocardiográfico para evaluar la función valvular y ventricular a largo plazo.\n- Monitorizar la presión arterial pulmonar y la función respiratoria, dado que la mejoría observada puede influir favorablemente en la calidad de vida y pronóstico.\n- Mantener el control de factores de riesgo cardiovascular y la anticoagulación adecuada, considerando la historia de fibrilación auricular y la implantación del marcapasos.\n- Evaluar y manejar cualquier síntoma residual o complicación relacionada con la insuficiencia cardíaca o el patrón respiratorio, aunque la desaparición de la respiración de Cheyne-Stokes tras el procedimiento es un signo alentador.\n\nEn resumen, la implantación de la válvula aórtica transfemoral en este paciente de alto riesgo fue exitosa y produjo una mejora significativa tanto en la función cardíaca como en la estabilidad respiratoria, evidenciando la importancia de un enfoque multidisciplinario y personalizado en casos complejos.",
+                "fh_score": 33.67
+            }
+        }
+    },
+    {
+        "article": "Una mujer árabe tunecina de 62 años, diagnosticada con la enfermedad de Von Hippel-Lindau en 2021, presentó varias manifestaciones relacionadas con la enfermedad. Tenía antecedentes de múltiples cirugías, principalmente por tumores renales, suprarrenales y pancreáticos, con hallazgos incidentales de masas ováricas.\n\nLa paciente no presentaba síntomas desde el punto de vista ginecológico, pero se quejaba principalmente de dolores de cabeza antes de someterse a una cirugía cerebral. No tenía antecedentes familiares o psicosociales significativos.\n\nSu historial quirúrgico incluye\n2021: Un tumor no operable (6 cm) del saco endolinfático del hueso petroso izquierdo, tratado con radioterapia.\n\n2021: Adrenalectomía izquierda por un feocromocitoma de 6 cm. El examen patológico reveló un feocromocitoma.\n\n2021: Nefrectomía izquierda por un tumor renal izquierdo roto. La microscopía mostró un carcinoma renal multifocal de células claras de grado nuclear 2.\n\n2022: Duodenopancreatectomía cefálica por una masa en el páncreas. El examen histológico confirmó tres cistadenomas serosos y dos tumores neuroendocrinos bien diferenciados.\n\nEn enero de 2021, durante la vigilancia posoperatoria con una tomografía computarizada (TC) abdominal-pélvica, se descubrió incidentalmente una masa anexial izquierda sólida de 4 cm, lo que levantó sospechas de malignidad. La masa se confirmó mediante ultrasonido transvaginal e IRM pélvica, clasificada como Sistema de Reporte y Datos Ováricos-Anexiales (O-RADS) 5 (alta sospecha de malignidad).\n\nExamen ginecológico e historial quirúrgico\nExamen físico: No se detectó masa abdominal-pélvica.\n\nExamen con espéculo: cuello uterino sano.\n\nSe observaron cicatrices quirúrgicas de una nefrectomía izquierda y una duodenopancreatectomía cefálica anteriores.\n\nUna reunión multidisciplinaria del personal concluyó que era necesaria la cirugía. Se realizó una laparotomía a través de una incisión en la línea media por debajo del ombligo, que reveló una masa quística sólida bien definida en el anexo izquierdo. No había ascitis ni signos de carcinomatosis peritoneal, y el anexo derecho parecía normal, sin signos macroscópicos de malignidad observados intraoperatoriamente, incluida la ausencia de vegetaciones exocísticas.\n\nSe realizó una citología junto con una anexectomía izquierda y la muestra se envió para un examen de sección congelada. Los resultados no fueron concluyentes, lo que planteó la posibilidad de tumores de margen o específicos del síndrome de Von Hippel-Lindau. Teniendo en cuenta el estado posmenopáusico de la paciente, se realizó una anexectomía derecha y una histerectomía total.\n\nEl examen histológico posterior reveló cistadenomas papilares de células claras bilaterales de las trompas de Falopio y el ligamento ancho, característicos de la enfermedad de Von Hippel-Lindau (0,5 cm en el lado derecho y 4 cm en el lado izquierdo). Los tumores consistían en papilas densamente compactadas con núcleos fibrosos, cubiertos por un epitelio monocapa.\n\nEl período postoperatorio inmediato transcurrió sin incidentes y, en el seguimiento de 1 mes, no se detectaron anomalías. Desde entonces, se ha hecho un seguimiento al paciente cada 4 meses con ecografías pélvicas normales. Durante estos 2 años de seguimiento, no han surgido complicaciones, pero el paciente fue readmitido recientemente en el departamento de neurocirugía por la recurrencia de un tumor cerebral.\n",
+        "gold_summary": "Una mujer blanca norteafricana de 62 años de edad, diagnosticada con la enfermedad de Von Hippel-Lindau en 2021, presentó múltiples manifestaciones, entre ellas, un tumor del hueso petroso izquierdo, feocromocitoma izquierdo, carcinoma de células renales izquierdo, riñón derecho con múltiples quistes y masas pancreáticas. Se sometió a varios tratamientos, entre ellos, radioterapia, adrenalectomía, nefrectomía y duodenopancreatectomía cefálica. Los exámenes de ultrasonografía y resonancia magnética revelaron una masa quística sólida en la región anexial izquierda. La laparoscopia identificó tumores quísticos en la mesosalpinx derecha e izquierda. Después de una histerectomía con anexectomía bilateral, el examen histológico reveló cistadenomas papilares de células claras bilaterales de la mesosalpinx y el ligamento ancho, compatibles con la enfermedad de Von Hippel-Lindau.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había una señora que tenía una enfermedad llamada Von Hippel-Lindau. Esta enfermedad le hizo tener bultos en partes de su cuerpo. Los doctores le hicieron varias operaciones para quitar esos bultos. \n\nUn día, los doctores encontraron otro bulto cerca de su barriga. Le hicieron una cirugía para quitarlo. Cuando miraron el bulto con el microscopio, vieron que era un tipo de bulto que pasa con su enfermedad. \n\nDespués de la operación, la señora se sintió bien y los doctores la cuidaron mucho para que siga sana.",
+                "fh_score": 76.92
+            },
+            "B2": {
+                "text": "**Lo que le Pasó a la Paciente**  \nUna mujer de 62 años fue diagnosticada con la enfermedad de Von Hippel-Lindau, que es una condición genética que causa tumores en diferentes partes del cuerpo. Ella tuvo varios tumores en lugares como el hueso cerca del oído, las glándulas suprarrenales, los riñones y el páncreas. Para tratar estos tumores, se sometió a diferentes cirugías y radioterapia.\n\n**Descubrimiento de una Nueva Masa**  \nDurante un control médico, los doctores encontraron una masa sólida y con líquido (quística) en la zona de los órganos reproductores femeninos, específicamente cerca del ovario izquierdo. Usaron ultrasonido y resonancia magnética para verla mejor.\n\n**Cirugía y Resultados**  \nLos médicos hicieron una cirugía para quitar la masa y también extirparon el útero y ambos anexos (que incluyen las trompas de Falopio y los ovarios). Al analizar el tejido, encontraron que la masa era un tipo de tumor llamado cistadenoma papilar de células claras. Este tumor es raro y está relacionado con la enfermedad de Von Hippel-Lindau.\n\n**Qué Significa Esto**  \nEstos tumores no eran cancerosos, pero están asociados con la enfermedad genética que tiene la paciente. Después de la cirugía, la mujer se recuperó bien y no tuvo problemas durante los dos años siguientes, aunque tuvo que regresar para tratar un tumor cerebral que volvió a aparecer.\n\nEn resumen, esta paciente con una enfermedad genética complicada tuvo varios tumores en diferentes órganos. Gracias a los controles y cirugías, los médicos pudieron identificar y tratar un tumor nuevo en su sistema reproductor, ayudándola a mantenerse estable por un tiempo.",
+                "fh_score": 54.91
+            },
+            "B3": {
+                "text": "**Contexto**  \nUna mujer tunecina de 62 años fue diagnosticada en 2021 con la enfermedad de Von Hippel-Lindau, un trastorno genético que predispone al desarrollo de múltiples tumores en diferentes órganos. A lo largo de su evolución clínica, presentó diversas manifestaciones relacionadas con esta enfermedad, incluyendo tumores en el hueso petroso (una parte del cráneo cerca del oído), glándula suprarrenal, riñón y páncreas. Su tratamiento incluyó radioterapia y varias cirugías importantes para extirpar estos tumores.\n\n**Hallazgos Clave**  \nDurante el seguimiento posoperatorio, se detectó de forma incidental mediante tomografía computarizada una masa sólida y quística de 4 cm en la región anexial izquierda (área ovárica y estructuras cercanas). Esta masa fue confirmada por ultrasonido transvaginal y resonancia magnética, clasificándose como de alta sospecha de malignidad según el sistema O-RADS. Sin embargo, la paciente no presentaba síntomas ginecológicos ni signos físicos evidentes de masa pélvica.\n\nSe decidió realizar una cirugía mediante laparotomía para evaluar y tratar la masa. Durante la intervención, se encontró una masa quística sólida bien delimitada en el anexo izquierdo, sin evidencia de diseminación tumoral en la cavidad abdominal. Se realizó la extirpación del anexo izquierdo y, debido a la edad posmenopáusica de la paciente y la sospecha de enfermedad bilateral, también se llevó a cabo la anexectomía derecha y la histerectomía total.\n\nEl análisis histológico posterior mostró la presencia de cistadenomas papilares de células claras en ambas trompas de Falopio y en el ligamento ancho (estructuras que sostienen el útero y las trompas), con tamaños de 4 cm en el lado izquierdo y 0,5 cm en el derecho. Estos tumores, caracterizados por papilas densamente agrupadas cubiertas por una capa única de células epiteliales, son una manifestación típica de la enfermedad de Von Hippel-Lindau.\n\n**Interpretación Clínica**  \nLos cistadenomas papilares de células claras bilaterales en las trompas de Falopio y el ligamento ancho representan una manifestación poco común pero reconocida de la enfermedad de Von Hippel-Lindau. La ausencia de síntomas ginecológicos y la detección incidental subrayan la importancia de un seguimiento cuidadoso en pacientes con esta enfermedad multisistémica. La cirugía fue necesaria para confirmar el diagnóstico y prevenir posibles complicaciones asociadas a estas masas.\n\n**Próximos Pasos**  \nEl postoperatorio inmediato fue favorable y, durante un seguimiento de dos años con controles ecográficos pélvicos regulares, no se observaron recurrencias ni nuevas lesiones en la región pélvica. No obstante, la paciente fue recientemente readmitida en neurocirugía debido a la recurrencia de un tumor cerebral, lo que refleja la naturaleza crónica y multisistémica de la enfermedad de Von Hippel-Lindau. Se recomienda continuar con un seguimiento multidisciplinario riguroso para manejar las diferentes manifestaciones de esta condición.",
+                "fh_score": 37.15
+            }
+        }
+    },
+    {
+        "article": "Una mujer embarazada de 31 años que había sido sometida a una cesárea fue derivada a la unidad de ultrasonido de nuestro departamento para un examen de ultrasonido morfológico de segundo trimestre. La paciente no tenía antecedentes familiares destacables y no había tomado medicamentos ni había estado expuesta a teratógenos durante el primer trimestre del embarazo. Los exámenes serológicos para diversas enfermedades infecciosas fueron negativos y un examen de ultrasonido previo a las 14 semanas fue normal. El triple examen para anomalías fetales también fue negativo a las 16 semanas.\n\nDurante la ecografía de la semana 20, se observó un feto masculino con una edad sonográfica compuesta de 20 semanas y 2 días que presentaba un edema significativo de las extremidades inferiores y líquido amniótico normal. Se recomendó un examen de seguimiento en 2 semanas, junto con pruebas de TORCH y pruebas de Coombs indirectas.\n\nSin embargo, se observó nuevamente edema subcutáneo en ambas extremidades inferiores durante la ecografía morfológica de la semana 23, lo que sugiere un posible diagnóstico de EM. Debido al linfedema persistente en las extremidades inferiores, se realizó una amniocentesis.\n\nLos exámenes posteriores revelaron que el cariotipo masculino era normal (46, XY), y el análisis molecular para el síndrome de Noonan fue negativo. Se realizó la secuenciación de nucleótidos del líquido amniótico con la secuenciación Illumina de 150 bases. Se aplicó el sistema de bioinformática (North-Oehler Aligarh, GATX) mientras se verificaba adicionalmente la existencia de deleciones/duplicaciones/CNV (Copy Number Variations) en el gen FLT4. El análisis identificó una mutación c.3116C>A p. (Ala1039Asp), que es una variante patogénica no conocida en el gen FLT4, lo que confirma el diagnóstico de linfedema hereditario tipo 1A – enfermedad de Milroy. El análisis de sangre materno confirmó la mutación materna y se realizó el asesoramiento genético.\n\nLa cesárea se realizó a las 38 semanas y 6 días de gestación y nació un neonato de sexo masculino que pesaba 3850 g y medía 46 cm con una puntuación de Apgar de 9/10. Después del parto se reconoció un edema en la extremidad inferior. El examen histopatológico de la placenta, el cordón umbilical y el saco amniótico no mostró signos de corioamnionitis u otra patología.\n",
+        "gold_summary": "Presentamos un informe de caso de una primera mutación descrita de un feto masculino diagnosticado prenatalmente con síndrome de Milroy a través de amniocentesis. El feto tenía edema bilateral de miembros inferiores, y las pruebas genéticas confirmaron el diagnóstico de síndrome de Milroy. La paciente fue monitoreada de cerca durante todo el embarazo, y después del parto, el lactante fue tratado con terapias apropiadas, incluyendo prendas de compresión y drenaje linfático manual. Los padres recibieron asesoramiento y apoyo apropiados.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un bebé niño tenía sus piernas un poco hinchadas cuando estaba en la barriga de su mamá. Los doctores hicieron pruebas para entender por qué. Descubrieron que el bebé tenía una condición llamada síndrome de Milroy. La mamá fue cuidada con mucho cariño durante todo el embarazo. Cuando el bebé nació, los doctores le ayudaron para que sus piernas estuvieran mejor. Los papás también recibieron ayuda para cuidar bien al bebé. Todo está hecho para que el bebé crezca fuerte y feliz.",
+                "fh_score": 77.82
+            },
+            "B2": {
+                "text": "**Lo que Encontraron**\n\nEn este caso, una mujer embarazada fue examinada con ultrasonido y se descubrió que su bebé tenía hinchazón (edema) en ambas piernas antes de nacer. Para entender mejor qué pasaba, los médicos hicieron una amniocentesis, que es cuando se toma un poco del líquido que rodea al bebé para estudiar sus genes. Encontraron una mutación, que es un cambio en un gen llamado FLT4, que causa una enfermedad llamada síndrome de Milroy. Esta enfermedad hace que el sistema que ayuda a drenar el líquido del cuerpo no funcione bien, causando hinchazón.\n\n**Qué Significa**\n\nEl diagnóstico se confirmó antes del nacimiento, lo que permitió a los médicos seguir de cerca el embarazo y prepararse para cuidar al bebé después del parto. El bebé nació con hinchazón en las piernas, pero recibió tratamientos especiales, como usar prendas que aprietan suavemente y masajes para ayudar a mover el líquido acumulado. Además, los padres recibieron información y apoyo para entender la enfermedad y cómo cuidar a su hijo.\n\nEste caso muestra la importancia de las pruebas genéticas y el seguimiento durante el embarazo para detectar y manejar enfermedades raras como el síndrome de Milroy.",
+                "fh_score": 56.95
+            },
+            "B3": {
+                "text": "**Contexto**  \nEste informe describe el caso de una mujer embarazada de 31 años cuyo feto masculino fue diagnosticado antes del nacimiento con síndrome de Milroy, una forma hereditaria de linfedema (acumulación anormal de líquido linfático que causa hinchazón). La paciente no presentaba antecedentes familiares relevantes ni factores de riesgo conocidos, y las pruebas iniciales durante el embarazo no mostraron anomalías.\n\n**Hallazgos Clave**  \nDurante la ecografía morfológica realizada en la semana 20 de gestación, se detectó un edema significativo en ambas extremidades inferiores del feto, aunque el líquido amniótico estaba dentro de los parámetros normales. Un seguimiento a las 23 semanas confirmó la persistencia de este edema subcutáneo. Ante estos hallazgos, se realizó una amniocentesis para obtener líquido amniótico y realizar estudios genéticos detallados.  \n\nEl análisis cromosómico mostró un cariotipo normal (46, XY), y se descartó el síndrome de Noonan mediante pruebas moleculares. Sin embargo, la secuenciación genética identificó una mutación patogénica inédita en el gen FLT4 (c.3116C>A p. (Ala1039Asp)), responsable del desarrollo del sistema linfático. Esta mutación confirmó el diagnóstico prenatal de linfedema hereditario tipo 1A, conocido como enfermedad de Milroy. Además, el análisis de sangre materno reveló que la madre también portaba esta mutación, lo que permitió realizar un asesoramiento genético adecuado a la familia.\n\nEl parto se llevó a cabo mediante cesárea a las 38 semanas y 6 días, naciendo un niño con buen peso y condición general (puntuación de Apgar 9/10). Tras el nacimiento, se observó edema en las extremidades inferiores, consistente con el diagnóstico prenatal. Los estudios histopatológicos de la placenta y membranas no mostraron infecciones ni otras patologías.\n\n**Interpretación Clínica**  \nEl síndrome de Milroy es una enfermedad genética que afecta el desarrollo y funcionamiento del sistema linfático, provocando linfedema desde etapas tempranas de la vida. La detección prenatal mediante ecografía y pruebas genéticas permite un diagnóstico temprano, lo que facilita la planificación del manejo clínico y el apoyo familiar. La identificación de una mutación previamente no descrita en el gen FLT4 amplía el conocimiento sobre la variabilidad genética de esta enfermedad.\n\n**Próximos Pasos**  \nDespués del nacimiento, el lactante recibió tratamiento especializado para el linfedema, que incluyó el uso de prendas de compresión y drenaje linfático manual, con el objetivo de controlar la hinchazón y mejorar la calidad de vida. La familia recibió asesoramiento genético para comprender el origen hereditario de la enfermedad, las implicaciones para futuros embarazos y las opciones disponibles. El seguimiento clínico continuo es esencial para monitorizar la evolución del linfedema y adaptar el tratamiento según sea necesario.",
+                "fh_score": 40.98
+            }
+        }
+    },
+    {
+        "article": "Un paciente de 50 años con antecedentes médicos conocidos de diabetes mellitus (DM) e hipertensión (HTN), que se manejaba de manera irregular, se presentó en nuestro hospital en la ciudad de Sana’a, Yemen, el 25 de mayo de 2022, a las 5:30 p. m. El paciente fue derivado a otro hospital y manifestó un dolor abdominal agudo que había durado una semana antes del ingreso. El dolor se localizaba en la región epigástrica, de inicio repentino, empeoramiento progresivo y radiación hacia la espalda. Además, el paciente experimentó distensión abdominal generalizada, náuseas, vómitos y fatiga significativa. También se informó un historial de melena y vómitos relacionados con los alimentos durante el mes pasado. Dos días antes del ingreso, el paciente había recibido una transfusión de sangre de 2 unidades. No había antecedentes de cirugías previas ni antecedentes familiares de neoplasias.\n\nAl examinar al paciente, se constató que estaba consciente y alerta, pero que presentaba un aspecto pálido. La presión arterial era de 90/60 mmHg y el pulso de 120 latidos por minuto. Se observó distensión abdominal generalizada, particularmente prominente en la región supraumbilical con desplazamiento hacia abajo del ombligo. Se constató una leve sensibilidad en la zona epigástrica, junto con sonidos intestinales positivos, el examen rectal digital reveló un tono normal del esfínter anal y no se detectó ninguna masa palpable.\n\nLos exámenes hematológicos y bioquímicos revelaron anemia microcítica hipocrómica con un nivel de hemoglobina de 6 g/dL (rango normal: 12-15.5 g/dL), un recuento de glóbulos blancos de 16,000 (rango normal: 4-10,000), y un recuento de plaquetas de 303. El nivel de nitrógeno ureico en sangre fue de 7 mg/dL (rango normal: 10-20 mg/dL), la creatinina fue de 0.49 mg/dL (rango normal: 0.7-1.5% / dL), el índice internacional normalizado fue de 1.34 (rango normal: 0.62-1.3), el tiempo de protrombina (PT) fue de 16.9, el tiempo de tromboplastina parcial (PTT) fue de 30, el calcio fue de 8.0 mg/dL (rango normal: 8.5-10.1 mg / dL) y el ácido láctico fue de 1.9 mmol/L (rango normal: 0.5-2.2% / L). Los niveles de enzimas hepáticas y amilasa estuvieron dentro de los límites normales.\n\nSe realizaron estudios de diagnóstico por imágenes, que incluyeron una radiografía de tórax y una ecografía abdominal. La radiografía de tórax no reveló aire subdiafragmático, pero se observó una elevación en el diafragma izquierdo. La ecografía abdominal demostró la presencia de una acumulación de líquido intraabdominal. Posteriormente, se realizó una angiografía por TC abdominal, que reveló un hematoma de aproximadamente 14,3 × 8,8 cm en la región paraumbilical. En el interior del hematoma, se identificó un aneurisma arterial de 3,4 × 2,2 cm conectado a la arteria gastroduodenal, acompañado de cambios edematosos circundantes. Estos hallazgos sugieren la presencia de un aneurisma trombosado grande en la arteria gastroduodenal. Además, se observó la evisceración del diafragma izquierdo, que contiene el bazo y parte del estómago, junto con una acumulación de líquido intraperitoneal leve a moderada. No se detectó evidencia de un aneurisma aórtico.\n\nPara estabilizar al paciente, se inició la reanimación con 1000 ml de lactato de Ringer y se transfundieron tres unidades de sangre fresca. Se obtuvo el consentimiento informado para la intervención de alto riesgo y el paciente fue llevado inmediatamente al quirófano. Bajo anestesia general, en posición supina y con estricta adhesión a las técnicas asépticas, se realizó una incisión de laparotomía en la línea media. Cuando se abrió el peritoneo, se evacuó aproximadamente 2000 ml de sangre, revelando una masa pulsátil ocluida en el duodeno. Se logró una exposición adecuada utilizando un retractor auto-reforzado. La flexión del hígado y el colon transverso se movilizaron inferiormente desde la cabeza del páncreas y se eliminó la sangre coagulada del intestino delgado. Se realizó una disección meticulosa sobre el gran aneurisma ocluido pulsátil en la arteria gastroduodenal abriendo el ligamento gastrohepático. La movilización del píloro y el duodeno lejos de la cabeza del páncreas expuso una fístula que conectaba el duodeno y el aneurisma, sin contenido digestivo. Después de la heparinización, se realizó un pinzamiento proximal y distal de la arteria gastroduodenal. Posteriormente, se abrió el pseudoaneurisma y se evacuó una cantidad significativa de trombo. Se realizó una aneurismorrafía utilizando suturas de prolina 7.0. La perforación en la primera parte del duodeno se reparó en dos capas y se insertó una sonda nasogástrica más allá de la perforación. Se logró una irrigación exhaustiva con solución salina normal y una hemostasia meticulosa. Se colocó un drenaje abdominal y se cerró la incisión abdominal en capas. El paciente fue trasladado a la unidad de cuidados intensivos (UCI) para una estrecha monitorización y observación.\n\nDurante el período postoperatorio, el drenaje abdominal recolectó aproximadamente 100 ml de fluido seroso, que se eliminó el tercer día después de la operación. La recuperación de la paciente progresó sin complicaciones. Diez días después de la cirugía, la paciente fue dada de alta en condiciones favorables. Se programaron citas de seguimiento en el departamento ambulatorio y se mantuvo una comunicación regular por teléfono, con la condición de la paciente reportada como satisfactoria.\n",
+        "gold_summary": "Un hombre de 50 años se presentó con dolor abdominal agudo, anemia y signos de inestabilidad hemodinámica. Las imágenes de diagnóstico, incluida la CTA, revelaron un aneurisma de la arteria gastroduodenal grande y trombosado con evidencia de ruptura. El paciente se sometió a exploración y reparación quirúrgica abierta para abordar tanto el aneurisma como la perforación duodenal. La recuperación del paciente fue satisfactoria y fue dado de alta en condiciones estables.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un hombre tenía mucho dolor en su barriga. Estaba muy cansado y débil. Los doctores vieron que tenía un bulto grande en una de sus venas. Ese bulto estaba lastimado y había sangre. Los doctores hicieron una operación para arreglar el bulto y la herida. Después, el hombre se sintió mejor y pudo ir a su casa.",
+                "fh_score": 86.62
+            },
+            "B2": {
+                "text": "### Lo que le pasó al paciente\n\nUn hombre de 50 años llegó al hospital con un dolor fuerte en el abdomen que había durado una semana. También estaba muy cansado y tenía anemia, que es cuando la sangre no tiene suficientes glóbulos rojos para llevar oxígeno al cuerpo. Su presión arterial estaba baja y su pulso rápido, lo que indicaba que su cuerpo estaba débil.\n\n### Lo que encontraron los médicos\n\nLos médicos hicieron varias pruebas, incluyendo imágenes especiales llamadas tomografía computarizada (CTA). Estas mostraron que tenía un aneurisma grande en una arteria llamada gastroduodenal. Un aneurisma es una zona donde la pared de un vaso sanguíneo está débil y se hincha, como un globo. Además, había coágulos de sangre dentro del aneurisma y parecía que se había roto, lo que es muy peligroso.\n\n### Qué hicieron los médicos\n\nPara salvarlo, los médicos hicieron una cirugía abierta. Abrieron el abdomen para encontrar y reparar el aneurisma. También encontraron una pequeña herida (perforación) en el duodeno, que es la primera parte del intestino delgado, y la repararon. Durante la cirugía, limpiaron la sangre acumulada y cerraron cuidadosamente las heridas.\n\n### Cómo fue la recuperación\n\nDespués de la operación, el paciente estuvo en cuidados intensivos para que lo vigilaran bien. Su recuperación fue buena, sin problemas importantes. Diez días después, pudo salir del hospital en buen estado y continuó con controles médicos para asegurarse de que siguiera mejorando.",
+                "fh_score": 61.88
+            },
+            "B3": {
+                "text": "**Contexto:**  \nUn hombre de 50 años con antecedentes de diabetes e hipertensión, que no seguía un tratamiento constante, acudió al hospital tras una semana de dolor abdominal intenso en la parte superior del abdomen, que se irradiaba hacia la espalda. Además, presentaba distensión abdominal, náuseas, vómitos, fatiga y antecedentes recientes de sangrado digestivo (melena). Dos días antes había recibido una transfusión de sangre debido a anemia.\n\n**Hallazgos Clave:**  \nEn la evaluación inicial, el paciente estaba consciente pero pálido, con presión arterial baja (90/60 mmHg) y pulso acelerado (120 latidos/minuto), signos que indicaban inestabilidad hemodinámica. El examen físico mostró distensión abdominal y sensibilidad leve en la zona del dolor. Los análisis de sangre revelaron anemia severa (hemoglobina de 6 g/dL), aumento de glóbulos blancos (16,000), y otros parámetros dentro de límites aceptables. Las imágenes diagnósticas, incluyendo una tomografía computarizada con angiografía (CTA), identificaron un hematoma grande en la región abdominal paraumbilical y un aneurisma (una dilatación anormal de un vaso sanguíneo) de la arteria gastroduodenal, con signos de trombosis (coágulos) y posible ruptura. También se observó una hernia diafragmática con desplazamiento de órganos abdominales hacia el tórax y acumulación de líquido en la cavidad abdominal.\n\n**Interpretación Clínica:**  \nEl diagnóstico principal fue un aneurisma gigante y trombosado de la arteria gastroduodenal con ruptura, que causaba hemorragia interna y perforación en la primera parte del duodeno (segmento inicial del intestino delgado). Esta situación representaba una emergencia quirúrgica debido al riesgo de sangrado masivo y complicaciones graves.\n\n**Próximos Pasos y Tratamiento:**  \nEl paciente fue estabilizado con líquidos intravenosos y transfusiones sanguíneas antes de ser llevado a cirugía de urgencia. Durante la operación, se evacuaron aproximadamente dos litros de sangre acumulada, se identificó y reparó el aneurisma mediante suturas, y se cerró la perforación duodenal en dos capas. Se colocó un drenaje abdominal para controlar posibles fugas y se monitorizó estrechamente en la unidad de cuidados intensivos. La recuperación fue favorable, sin complicaciones postoperatorias, y el paciente fue dado de alta diez días después en condiciones estables, con seguimiento ambulatorio programado.\n\nEn resumen, este caso ilustra la importancia de un diagnóstico rápido y un manejo quirúrgico oportuno en pacientes con aneurisma roto de la arteria gastroduodenal, una condición rara pero potencialmente mortal.",
+                "fh_score": 36.22
+            }
+        }
+    },
+    {
+        "article": "Una mujer de 60 años fue admitida en el departamento de nefrología con dolor epigástrico, hematemesis y edema en la pierna. La presión arterial era de 90/50 mmHg, dentro del rango normal para esta paciente.\nLos resultados de laboratorio fueron notables para las enzimas hepáticas alteradas con un patrón colestático: los niveles de alanina amino transferasa (ALT) y aspartato amino transferasa (AST) fueron ligeramente elevados a 28 U/L y 61 U/L, respectivamente, mientras que los niveles de fosfatasa alcalina (388 U/L) y gamma glutamiltransferasa (291 U/L) fueron muy elevados. Los niveles de albúmina en suero fueron de 24 g/L y el índice internacional normalizado fue normal a 1.02.\nOtros resultados de laboratorio, incluidos la bilirrubina total (0,32 mg/dL), la bilirrubina directa (0,26 mg/dL), el recuento total de plaquetas (176 000 plaquetas por microlitro) y el recuento de glóbulos blancos (8400 células por microlitro), se encontraban dentro de los valores normales.\nEl paciente tenía un extenso historial de enfermedades cardiacas y renales. A los 11 años, se le diagnosticó estenosis congénita de la válvula pulmonar, por lo que se le practicó una valvulotomía. Más adelante, desarrolló fibrilación auricular y aleteo auricular, que no toleró bien y para los que se intentó, sin éxito, la ablación del aleteo. Como el paciente seguía teniendo síntomas, se le practicó una ablación del nódulo auriculoventricular con colocación de un marcapasos.\nSe inició anticoagulación oral con fenprocoumon debido a una puntuación CHA2DS2-Vasc de 3 (mujer, insuficiencia cardiaca y enfermedad vascular periférica). A la edad de 55 años, se desarrolló una insuficiencia cardiaca derecha manifiesta y la paciente continuó luchando con ascitis y edemas periféricos que requerían múltiples ingresos hospitalarios. Además, también desarrolló un problema de efusiones pleurales transudativas recurrentes de etiología poco clara.\nLa ecocardiografía en ese momento mostró una severa regurgitación pulmonar y tricuspídea con un ventrículo derecho moderadamente dilatado y una aurícula derecha. El ventrículo izquierdo estaba ligeramente dilatado con una regurgitación mitral moderada. El cateterismo cardiaco derecho demostró presiones arteriales pulmonares de 74/30 mmHg con una presión venosa central de 28 mmHg. Se colocó un homotransplante pulmonar cuando el paciente tenía 57 años y se realizó una anuloplastia tricuspídea concomitante. A pesar de una presión venosa central más baja de 13 mmHg, el paciente seguía siendo readmitido varias veces por signos y síntomas de insuficiencia cardiaca derecha. La congestión venosa sistémica persistente finalmente dio lugar a una enfermedad renal en fase terminal para la que se inició una terapia de reemplazo renal a través de hemodiálisis intermitente. El caso se complicó por hemorragias gastrointestinales graves recurrentes, que requerían transfusiones de sangre frecuentes con hasta 60 unidades de glóbulos rojos por año. A pesar de esto, en combinación con la sustitución intravenosa de hierro, los niveles de hemoglobina variaron entre 5.3-8.8 g/dL. Debido a estos problemas de sangrado intratables, la anticoagulación oral con fenprocoumon se detuvo a la edad de 59 años.\nUna gastroscopia mostró una gastropatía erosiva con una mucosa difusa congestiva y friable. Como prevención de primera línea de las hemorragias gástricas recurrentes en el marco de la cirrosis, se inició el propranolol a una dosis de 5 mg por vía oral dos veces al día (el paciente no toleró una dosificación superior debido a la presión arterial baja). Además, se realizó una coagulación endoscópica de un angioma fúndico y un recorte de una lesión de Dieulafoy.\nSe creía que estas lesiones eran causadas por una gastropatía hipertensiva. Sin embargo, las hemorragias intractables persistieron.\nEl gradiente de presión venosa hepática se midió a 16 mmHg (27 mmHg-11 mmHg). Aunque hubo cierta reticencia debido al temor de empeorar la insuficiencia cardiaca derecha, se tomó la decisión de crear un TIPS. El procedimiento fue sin incidentes. Después de la colocación del TIPS, el gradiente de presión venosa hepática disminuyó a 4 mmHg (14 mmHg-10 mmHg). Por lo tanto, aunque el TIPS redujo considerablemente el gradiente venoso hepático, la presión portal se mantuvo alta debido a la elevada presión venosa central.\nDespués de la colocación del TIPS, el paciente desarrolló signos de encefalopatía hepática y se midieron niveles de amoniaco de 77 umol/L. Se inició el tratamiento con lactulosa oral y enemas, con poca mejora. En ese momento, se produjo otro episodio de sangrado gástrico.\nLa ecografía abdominal mostró buena permeabilidad del TIPS con flujo Doppler normal. Se detectó sangrado gástrico de una úlcera antral con endoscopia, a pesar de que la hiperemia gástrica disminuyó visualmente en comparación con la situación antes del TIPS. Se realizó una biopsia que mostró una mucosa foveolar edematosa, lo que sugiere isquemia de la mucosa. El sangrado fue demasiado difuso para una ligadura endoscópica adicional. No se encontró empeoramiento de la función hepática en los resultados de laboratorio, con el índice internacional normalizado 1.01 en este momento. La ecocardiografía no mostró cambios significativos en comparación con la situación antes de la colocación del TIPS. El ventrículo derecho permaneció moderadamente dilatado con una función longitudinal deficiente y una regurgitación tricuspídea severa persistente. Sin embargo, el estado general del paciente se deterioró y se desarrolló fiebre con consolidaciones pulmonares bilaterales.\nSe produjo una falla multiorgánica y, en ese momento, la familia del paciente decidió retirar el tratamiento. El paciente falleció finalmente 43 días después del procedimiento TIPS.\n\nMH - Resultado fatal\nMH - Mujer\nMH - Insuficiencia cardiaca/*complicaciones/fisiopatología\nMH - Encefalopatía hepática/etiología\nMH - Humanos\nMH - Hipertensión, Portal/etiología/fisiopatología/*cirugía\nMH - Cirrosis hepática/*complicaciones\nMH - Edad Media\nMH - Presión del portal\nMH - *Derivación portosistémica, intrahepática transyugular\nMH - Fracaso del tratamiento\n",
+        "gold_summary": "Una mujer de 60 años con antecedentes de estenosis congénita de la válvula pulmonar desarrolló insuficiencia cardíaca derecha, cirrosis hepática y enfermedad renal en fase terminal que requería terapia de reemplazo renal. La cirrosis hepática se complicó con hipertensión portal, lo que provocó hemorragias gastrointestinales intratables a pesar del tratamiento óptimo con betabloqueantes y la ligadura endoscópica de la banda. Debido al temor de que empeorara la insuficiencia cardíaca derecha, inicialmente se rechazó la colocación de una derivación intrahepática transyugular (TIPS). Sin embargo, como los problemas de hemorragia intratables persistieron y causaron grandes necesidades de transfusión, la TIPS se realizó finalmente como un procedimiento de rescate. Aunque la TIPS redujo con éxito el gradiente de presión venosa hepática de 16 mmHg a 4 mmHg, la presión portal se mantuvo alta a 14 mmHg debido a la persistencia de la insuficiencia cardíaca derecha con presión venosa central elevada. La encefalopatía hepática se desarrolló poco después de la colocación de la TIPS y culminó en una falla multiorgánica después de otro episodio de hemorragia gastrointestinal. En este punto, la familia del paciente decidió retirar la atención y el paciente falleció posteriormente.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había una señora de 60 años que tenía problemas en el corazón y en el hígado. Su hígado estaba muy enfermo y le dolía mucho la barriga. También tenía problemas para que la sangre no sangrara mucho por dentro.\n\nLos doctores intentaron ayudarla con medicinas y tratamientos, pero la sangre seguía saliendo. Entonces, hicieron una operación para ayudar a que la sangre pasara mejor por el hígado.\n\nDespués de la operación, la señora se sintió peor y tuvo más problemas en su cuerpo. Al final, su familia decidió que ya no la trataran más y la señora se fue al cielo.",
+                "fh_score": 79.25
+            },
+            "B2": {
+                "text": "**Historia Clínica y Problemas Principales**  \nUna mujer de 60 años tenía varios problemas de salud desde joven, incluyendo una enfermedad del corazón llamada estenosis congénita de la válvula pulmonar. Con el tiempo, desarrolló insuficiencia cardíaca derecha, que significa que el lado derecho de su corazón no funcionaba bien. También tenía cirrosis hepática, una enfermedad del hígado que causa daño y cicatrices, y enfermedad renal en etapa terminal, por lo que necesitaba diálisis para limpiar su sangre.\n\n**Complicaciones y Tratamientos**  \nLa cirrosis causó hipertensión portal, que es una presión alta en las venas del hígado. Esto provocó sangrados graves en su estómago y esófago que no se podían controlar fácilmente. A pesar de usar medicamentos llamados betabloqueantes, que ayudan a bajar la presión, y hacer tratamientos endoscópicos para detener el sangrado, las hemorragias continuaron. Por miedo a que un procedimiento llamado TIPS (una derivación que ayuda a bajar la presión en el hígado) empeorara su insuficiencia cardíaca, inicialmente no se realizó.\n\n**Procedimiento TIPS y Resultados**  \nFinalmente, debido a que las hemorragias seguían siendo muy graves y necesitaba muchas transfusiones de sangre, se decidió hacer el TIPS como último recurso. Este procedimiento logró bajar la presión en las venas del hígado de 16 a 4 mmHg, lo que es una mejora importante. Sin embargo, la presión en la vena principal del hígado siguió siendo alta porque su corazón derecho seguía funcionando mal.\n\n**Complicaciones Finales y Desenlace**  \nDespués del TIPS, la paciente desarrolló encefalopatía hepática, que es un problema en el cerebro causado por la acumulación de toxinas cuando el hígado no funciona bien. También tuvo otro sangrado en el estómago y su estado general empeoró, con fallas en varios órganos. Finalmente, la familia decidió suspender el tratamiento y la paciente falleció 43 días después del procedimiento.\n\n**Qué Significa Este Caso**  \nEste caso muestra lo difícil que es tratar a pacientes con problemas graves en el corazón, hígado y riñones al mismo tiempo. Aunque el TIPS puede ayudar a bajar la presión en el hígado y controlar el sangrado, no siempre es suficiente si el corazón no puede manejar los cambios. Además, el procedimiento puede causar complicaciones como la encefalopatía hepática. Por eso, cada caso necesita un cuidado muy cuidadoso y personalizado.",
+                "fh_score": 53.64
+            },
+            "B3": {
+                "text": "**Contexto**  \nSe presenta el caso de una mujer de 60 años con un complejo historial médico que incluye una estenosis congénita de la válvula pulmonar diagnosticada en la infancia, seguida de múltiples complicaciones cardíacas como fibrilación auricular, insuficiencia cardíaca derecha y regurgitación valvular severa. Estas condiciones condujeron a una congestión venosa sistémica persistente, que a su vez provocó cirrosis hepática y enfermedad renal en etapa terminal, requiriendo hemodiálisis. Además, la paciente sufrió hemorragias gastrointestinales graves y recurrentes, difíciles de controlar, que demandaron numerosas transfusiones sanguíneas.\n\n**Hallazgos Clave**  \n- La cirrosis hepática se acompañó de hipertensión portal, evidenciada por un gradiente de presión venosa hepática elevado (16 mmHg).  \n- A pesar del tratamiento con betabloqueantes (propranolol) y procedimientos endoscópicos para controlar las hemorragias gástricas, estas continuaron siendo incontrolables.  \n- Inicialmente, se evitó la colocación de una derivación portosistémica intrahepática transyugular (TIPS) debido al riesgo de empeoramiento de la insuficiencia cardíaca derecha.  \n- Finalmente, se realizó el procedimiento TIPS como medida de rescate, logrando reducir el gradiente de presión venosa hepática a 4 mmHg; sin embargo, la presión portal permaneció elevada (14 mmHg) debido a la presión venosa central alta secundaria a la insuficiencia cardíaca derecha persistente.  \n- Posterior a la colocación del TIPS, la paciente desarrolló encefalopatía hepática (una alteración cerebral causada por la acumulación de toxinas debido a la insuficiencia hepática), con niveles elevados de amoníaco en sangre y síntomas neurológicos.  \n- Se presentó un nuevo episodio de sangrado gástrico, con evidencia endoscópica de úlcera antral y cambios isquémicos en la mucosa gástrica.  \n- La función hepática no mostró deterioro significativo en los análisis de laboratorio tras el TIPS, y la ecocardiografía reveló que la función cardíaca derecha permaneció comprometida.  \n- Finalmente, la paciente desarrolló una falla multiorgánica acompañada de infección pulmonar, lo que llevó a la decisión familiar de retirar el soporte terapéutico.\n\n**Interpretación Clínica**  \nEste caso ilustra la compleja interacción entre la insuficiencia cardíaca derecha crónica y sus consecuencias sistémicas, incluyendo la hipertensión portal secundaria y la cirrosis hepática. La hipertensión portal generó hemorragias gastrointestinales difíciles de controlar, que agravaron el estado general de la paciente. La colocación del TIPS, aunque efectiva para reducir el gradiente hepático, no logró normalizar la presión portal debido a la persistente congestión venosa por insuficiencia cardíaca. Además, el procedimiento desencadenó encefalopatía hepática, complicación frecuente en estos casos, y no previno nuevos episodios hemorrágicos. La evolución desfavorable culminó en falla multiorgánica y muerte.\n\n**Próximos Pasos y Reflexiones**  \nEste caso subraya la dificultad de manejar la hipertensión portal y sus complicaciones en pacientes con insuficiencia cardíaca derecha avanzada. La decisión de realizar un TIPS debe sopesar cuidadosamente los riesgos de empeoramiento cardíaco y encefalopatía hepática. En situaciones similares, se requiere un enfoque multidisciplinario que incluya cardiología, hepatología y nefrología para optimizar el tratamiento y considerar alternativas terapéuticas. Además, es fundamental el diálogo con la familia para establecer objetivos realistas y respetar las decisiones sobre el cuidado al final de la vida.",
+                "fh_score": 27.34
+            }
+        }
+    },
+    {
+        "article": "Una mujer tailandesa de 62 años presentó pérdida visual bilateral súbita y cefalea durante 5 días. Negó antecedentes de traumatismo craneal. Su historia clínica era significativa por presentar hipertensión mal controlada.\n\nLos signos vitales fueron normales, excepto por la presión arterial de 200/105 mmHg. La agudeza visual fue de no percepción de luz (NLP) con pupilas fijas en ambos ojos. La motilidad ocular de ambos ojos fue limitada en todas las direcciones. Ambas párpados fueron difíciles de abrir. Las medidas del exoftalmómetro de Hertel fueron de 16 mm en el ojo derecho y 14 mm en el ojo izquierdo. Había quemosis significativa y vasos de sacacorchos episclerales en ambos ojos. Ambas córneas mostraron un edema estromal leve y difuso sin infiltración. Las cámaras anteriores fueron profundas y tranquilas en ambos ojos. Las presiones intraoculares fueron de 45 mmHg y 48 mmHg en los ojos derecho e izquierdo, respectivamente. La gonioscopia reveló sangre en el canal de Schlemm en el ángulo nasal del ojo derecho. El examen del fondo de ojo mostró venas de la retina ligeramente dilatadas y tortuosas con discos ópticos de apariencia normal en ambos ojos. La relación taza-disco fue de 0.3 bilateralmente. La tomografía de coherencia óptica demostró un espesor normal de la mácula en cada ojo. No hubo ruido audible. Otros exámenes neurológicos fueron normales.\n\nLa resonancia magnética (MRI) con gadolinio del cerebro y las órbitas demostró la dilatación de las venas oftálmicas superiores bilaterales (SOVs) y un grado marcado de congestión orbital y periorbital bilateralmente. Sin embargo, no se observó ni compresión ni estiramiento de los nervios ópticos bilaterales. Es interesante destacar que la restricción de la difusión, con la correspondiente reducción del coeficiente de difusión aparente (ADC), en todo el segmento orbital de los nervios ópticos bilateralmente se reveló en la resonancia magnética ponderada en difusión (DWI). Esto es consistente con el PION bilateral. La angiografía por resonancia magnética (MRA) del cerebro y las órbitas reveló arterialización de los senos cavernosos bilaterales y de las SOVs.\n\nLa angiografía cerebral confirmó el diagnóstico de CCF durales bilaterales de drenaje anterior. La CCF dural derecha se alimentaba de las ramas durales de la ICA (tronco meningo-hipofisario derecho). La CCF dural izquierda se alimentaba de las ramas durales de la ECA (arteria meningo-hipofisaria izquierda y la arteria izquierda del foramen redondo y las ramas durales de la ICA (tronco meningo-hipofisario izquierdo). Cada lado de la CCF dural contribuía con flujo sanguíneo arterial a los SOV bilaterales (SOV contralateral a través de la comunicación inter-cavernosa). No se observó reflujo venoso cortical del flujo sanguíneo arterial. Basándose en estos hallazgos, se realizó una embolización transvenosa de la bobina. Los senos cavernosos bilaterales se embolizaron utilizando bobinas para ocluir los vasos de alimentación de las ramas durales de la ICA y la ECA. La angiografía cerebral inmediata posterior a la embolización mostró el cierre completo de las fístulas.\n\nTres meses después de la embolización, el examen oftálmico demostró una mejora progresiva de los signos oftálmicos antes mencionados; no obstante, la agudeza visual del paciente se mantuvo en NLP en ambos ojos.\n",
+        "gold_summary": "Reportamos el caso de una mujer de 62 años de edad con antecedentes de hipertensión arterial mal controlada que presentó pérdida visual bilateral súbita y cefalea durante 5 días. Negó antecedentes de traumatismo craneal. En el examen, sus agudezas visuales eran de no percepción de luz (NLP) con pupilas fijas en ambos ojos. La motilidad ocular de ambos ojos era limitada en todas las direcciones. Era difícil abrir ambos párpados. El examen del segmento anterior reveló quemosis bilateral y vasos del sacacorchos episclerales. La presión intraocular era de 45 y 48 mmHg en los ojos derecho e izquierdo, respectivamente. La gonioscopia reveló sangre en el canal de Schlemm en el ángulo nasal del ojo derecho. El examen del fondo de ojo mostró venas retinianas ligeramente dilatadas y tortuosas con discos ópticos de apariencia normal en ambos ojos. Las relaciones entre la copa y el disco eran de 0,3 bilateralmente. Otros exámenes neurológicos no presentaron anormalidades. La resonancia magnética demostró dilatación de las venas oftálmicas superiores bilaterales (SOV) y congestión orbital y periorbital bilateral marcada. Sin embargo, no hubo compresión o estiramiento de los nervios ópticos bilaterales. Se reveló una restricción de la difusión en la difusión ponderada por la difusión, con la correspondiente reducción del coeficiente de difusión aparente, en todo el segmento orbital bilateral de los nervios ópticos, consistente con PION bilateral. La angiografía por resonancia magnética reveló arterialización de los senos cavernosos bilaterales y las SOV. La angiografía cerebral confirmó el diagnóstico de CCF bilaterales de drenaje anterior. El tratamiento con embolización de bobina transvenosa fue exitoso. Tres meses después de la embolización, el examen oftálmico demostró una mejora progresiva de los signos oftálmicos antes mencionados; sin embargo, sus agudezas visuales permanecieron como NLP en ambos ojos.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una señora mayor se enfermó y no pudo ver con sus ojos. Tenía dolor en la cabeza. Sus ojos estaban muy cansados y no se movían bien. Abrir los ojos era difícil. Los ojos estaban hinchados y con vasos raros. Tenía mucha presión dentro de los ojos. Los doctores hicieron fotos especiales de su cabeza y ojos. Vieron que las venas de sus ojos estaban muy grandes y llenas de sangre. También vieron que los nervios de sus ojos estaban dañados. Encontraron un problema con las venas que llevaba sangre en su cabeza. Los doctores hicieron una operación para arreglar las venas. Después de la operación, sus ojos se veían mejor, pero ella no pudo recuperar la vista. Los doctores la cuidaron mucho y trataron de ayudarla.",
+                "fh_score": 85.85
+            },
+            "B2": {
+                "text": "**Caso de una Mujer con Pérdida Súbita de la Vista**\n\nUna mujer de 62 años, que tenía presión arterial alta sin control, comenzó a perder la vista en ambos ojos de forma repentina y también tenía dolor de cabeza durante cinco días. No había sufrido golpes en la cabeza antes.\n\n**Lo que Encontraron en el Examen**\n\nCuando la revisaron, no podía ver nada con ninguno de sus ojos y sus pupilas no reaccionaban a la luz. Además, no podía mover bien los ojos y le costaba abrir los párpados. En sus ojos había hinchazón y vasos sanguíneos con forma torcida. La presión dentro de sus ojos estaba muy alta, mucho más de lo normal. También encontraron sangre en un canal especial dentro del ojo derecho. Al mirar el fondo del ojo, las venas estaban un poco dilatadas, pero el nervio óptico parecía normal. Otros exámenes del cerebro y nervios no mostraron problemas.\n\n**Lo que Mostraron las Imágenes Médicas**\n\nUna resonancia magnética (una imagen del cerebro y ojos) mostró que las venas grandes que drenan la sangre de los ojos estaban muy dilatadas y había mucha congestión alrededor de los ojos. No había daño visible en los nervios ópticos, pero una prueba especial mostró que esos nervios tenían daño por falta de oxígeno, llamado neuropatía óptica isquémica posterior (PION), en ambos ojos. Otra imagen mostró que unas venas en el cerebro estaban recibiendo sangre de arterias, lo que no es normal.\n\n**Diagnóstico y Tratamiento**\n\nCon una angiografía cerebral (un estudio para ver los vasos sanguíneos), confirmaron que tenía fístulas carotídeo-cavernosas durales bilaterales. Esto significa que había conexiones anormales entre arterias y venas en una parte del cerebro llamada seno cavernoso, lo que causaba que la sangre fluyera mal y afectara los ojos. Para tratarlo, hicieron una embolización con bobinas, que es un procedimiento para cerrar esas conexiones anormales.\n\n**Resultado Después del Tratamiento**\n\nTres meses después, los signos de hinchazón y congestión en los ojos mejoraron, pero la mujer no recuperó la visión y seguía sin poder percibir luz en ambos ojos. Esto indica que el daño en los nervios ópticos fue muy grave y no se pudo revertir.",
+                "fh_score": 65.7
+            },
+            "B3": {
+                "text": "**Contexto**  \nSe presentó el caso de una mujer tailandesa de 62 años con antecedentes de hipertensión arterial mal controlada, quien experimentó una pérdida súbita de la visión en ambos ojos acompañada de cefalea durante cinco días. No reportó antecedentes de traumatismo craneal ni otros síntomas neurológicos adicionales.\n\n**Hallazgos Clave**  \nEn la evaluación oftalmológica inicial, la paciente tenía una agudeza visual de no percepción de luz (NLP) en ambos ojos, con pupilas fijas y motilidad ocular limitada en todas las direcciones. La apertura de ambos párpados fue dificultosa. El examen del segmento anterior mostró quemosis (hinchazón de la conjuntiva) bilateral y vasos episclerales con aspecto de “sacacorchos”, indicativos de congestión vascular. La presión intraocular estaba elevada, con valores de 45 mmHg en el ojo derecho y 48 mmHg en el izquierdo. La gonioscopia (evaluación del ángulo de drenaje ocular) reveló presencia de sangre en el canal de Schlemm del ojo derecho, lo que sugiere hemorragia en el sistema de drenaje ocular. El fondo de ojo mostró venas retinianas levemente dilatadas y tortuosas, pero los discos ópticos tenían una apariencia normal, con una relación copa-disco de 0.3 en ambos ojos, lo que indica ausencia de daño glaucomatoso avanzado. Otros exámenes neurológicos no mostraron alteraciones.\n\nLa resonancia magnética (MRI) con contraste evidenció dilatación de las venas oftálmicas superiores (SOV) en ambos ojos, junto con congestión marcada en las regiones orbital y periorbital. No se observaron signos de compresión o estiramiento de los nervios ópticos. Sin embargo, la resonancia ponderada en difusión (DWI) mostró restricción en la difusión con reducción del coeficiente de difusión aparente (ADC) en el segmento orbital bilateral de los nervios ópticos, hallazgo compatible con neuropatía isquémica óptica posterior (PION) bilateral, una lesión causada por falta de flujo sanguíneo en los nervios ópticos. La angiografía por resonancia magnética (MRA) reveló arterialización (flujo arterial anormal) de los senos cavernosos y las venas oftálmicas superiores bilaterales.\n\nLa angiografía cerebral confirmó la presencia de fístulas carotídeo-cavernosas (CCF) durales bilaterales con drenaje anterior. Estas fístulas eran alimentadas por ramas durales de la arteria carótida interna (ICA) y externa (ECA) en ambos lados, y contribuían al flujo arterial anómalo en las venas oftálmicas superiores, incluyendo comunicación entre ambos senos cavernosos. No se detectó reflujo venoso cortical, lo que indica que no había afectación directa de la circulación cerebral superficial.\n\n**Interpretación Clínica**  \nLa paciente presentó una forma rara y grave de fístulas carotídeo-cavernosas durales bilaterales que causaron congestión venosa orbital severa, elevación de la presión intraocular y daño isquémico bilateral en los nervios ópticos, manifestado como neuropatía isquémica óptica posterior. Esta condición explicó la pérdida visual súbita e irreversible, a pesar de la ausencia de compresión directa de los nervios ópticos.\n\n**Próximos Pasos y Evolución**  \nSe realizó una embolización transvenosa mediante colocación de bobinas para ocluir las fístulas en ambos senos cavernosos, logrando el cierre completo de las comunicaciones anómalas según la angiografía postprocedimiento. Tres meses después, la congestión y los signos oftálmicos mejoraron progresivamente, incluyendo la reducción del edema y la congestión vascular; sin embargo, la agudeza visual permaneció sin recuperación, con no percepción de luz en ambos ojos, reflejando daño irreversible en los nervios ópticos.\n\nEste caso destaca la importancia de un diagnóstico temprano y tratamiento oportuno en fístulas carotídeo-cavernosas para prevenir complicaciones graves como la pérdida visual irreversible por neuropatía isquémica óptica.",
+                "fh_score": 38.74
+            }
+        }
+    },
+    {
+        "article": "Un paciente de 15 años de edad (altura = 161 cm; peso = 66 kg; superficie corporal = 1,70; grupo sanguíneo = B positivo) con cardiomiopatía dilatada fue derivado a la Universidad de Ankara con pérdida de conciencia y shock cardiogénico en julio de 2016. El apoyo de oxigenación de membrana extracorpórea venosa arterial se realizó aproximadamente 1 semana después. Su fracción de eyección ventricular izquierda fue del 22%. Ocho días después, el paciente recibió un implante de corazón artificial total SynCardia (50 ml; SynCardia Systems, Inc., Tucson, AZ, EE. UU.). En el día 131 postoperatorio después de la cirugía TAH, el paciente se quejó de pérdida de audición bilateral y fue derivado al departamento de oído, nariz y garganta.\n\nLos antecedentes médicos previos no revelaron evidencia de pérdida auditiva, antecedentes familiares de sordera o cualquier anomalía adicional en su niñez. Sus registros médicos no revelaron evidencia de meningitis. Sin embargo, había recibido amikacina (15 mg/kg), un antibiótico ototóxico, contra patógenos gramnegativos importantes durante su estancia en la unidad de cuidados intensivos. El paciente fue incluido en la lista de espera de trasplantes de corazón de alta urgencia y era móvil en el Freedom Driver portátil (SynCardia).\n\nEl examen otoscópico del paciente fue normal. La audiometría de tonos puros y la respuesta auditiva del tronco encefálico revelaron una pérdida auditiva profunda bilateral. La timpanometría mostró timpanogramas normales de tipo A bilaterales. Tanto la tomografía computarizada como la resonancia magnética confirmaron la morfología normal del laberinto y nervios cocleares intactos.\n\nFue examinado por un equipo multidisciplinario (cirugía cardiovascular, cuidados intensivos pediátricos, cardiología pediátrica, psiquiatría de consulta y enlace, fisioterapia y rehabilitación, enfermedades infecciosas y microbiología clínica, anestesiología, audiología y otorrinolaringología) para realizar un implante coclear. Después de analizar las posibles opciones con el paciente y sus padres, se decidió que se beneficiaría de un implante coclear debido a la pérdida auditiva y la reducción de la función cognitiva y la adaptación necesaria para el trasplante de corazón. Después de analizar su caso con el equipo multidisciplinario, se decidió un implante coclear del lado derecho (Nucleus CI24RE con Contour Advance Electrode; Cochlear, Macquarie University, Australia).\n\nEl paciente tomaba warfarina (10 mg/día), que se interrumpió tres días antes de la cirugía, y se inició la heparinización (dosis de carga de 50 U/kg y dosis de mantenimiento de 20 U/kg/h) cuando el tiempo de protrombina (cociente internacional normalizado [INR]) era inferior a 1,5. Dos horas antes de la cirugía, se interrumpió la heparinización. En el quirófano, se disponía de un dispositivo de reserva para un posible fallo del dispositivo TAH. El equipo de anestesia y el perfusionista controlaron de cerca los resultados del flujo para el TAH. El flujo sanguíneo no pulsátil afecta de forma negativa al control de los signos vitales, y la presión arterial no invasiva no fue suficiente en nuestro paciente. Bajo anestesia local, se realizó un cateterismo radial arterial invasivo. Además, se dejó la vena yugular interna izquierda en su lugar, lo que permitió el control de la presión venosa central y su uso como reemplazo de fluidos de gran volumen cuando fue necesario. Después de iniciar el control, se administraron con precaución 2 mg/kg de propofol, 1 mg/kg de bromuro de rocuronio y 1 µg/kg de fentanilo, y se intubió al paciente por vía oral. Se utilizó sevoflurano con una concentración alveolar mínima de 1 a 1,5 en oxígeno al 40 % para el mantenimiento. El óxido nítrico inhalado también estaba listo para usarse en caso de una posible crisis hipertensiva pulmonar.\n\nEl día 250 después del implante TAH, se realizó la cirugía de implante coclear con abordaje de ventana redonda sin complicaciones perioperatorias; el paciente tuvo una pérdida de sangre mínima (solo 50 ml). La duración de la operación fue de 120 minutos. El paciente fue extubado en el quirófano sin problemas circulatorios y respiratorios. La heparinización se inició a la hora 6 posoperatoria. Comenzamos con la warfarina el día 1 posoperatorio, y la heparinización se detuvo después de alcanzar un INR de 2.0. No se observaron complicaciones (infecciones, hematoma) en el seguimiento posoperatorio.\n\nEl implante coclear se activó en la semana 4 después de la operación. El equipo de audiología lo revisó 4 y 8 semanas después; mostró una mejora continua en su audición, con impedancias normales. Sus resultados de percepción del habla mejoraron significativamente 3 meses después del implante coclear.\n\nMH - Adolescente\nMH - Niño\nMH - *Implantación coclear\nMH - *Insuficiencia cardiaca/diagnóstico/etiología/cirugía\nMH - *Efectos adversos del trasplante de corazón\nMH - *Corazón, Artificial\nMH - Humanos\nMH - Hombre\nMH - Resultado del tratamiento\n",
+        "gold_summary": "Describimos el caso de un niño de 15 años con pérdida auditiva total bilateral postlingual tras la administración de medicamentos ototóxicos durante su estancia en la unidad de cuidados intensivos pediátricos. El paciente recibió el implante de corazón artificial total SynCardia (50 ml; SynCardia Systems, Inc., Tucson, AZ, EE. UU.) para la insuficiencia cardiaca biventricular en fase terminal como puente para el trasplante cardiaco. Durante su estancia en la lista de espera de trasplantes cardiacos urgentes, se sometió a una implantación coclear satisfactoria tras optimizar el estado de coagulación y hemostasis y una preparación anestésica adecuada.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un niño de 15 años tuvo problemas para oír después de tomar medicinas en el hospital. Su corazón estaba muy enfermo y le pusieron un corazón artificial para ayudarlo. Mientras esperaba un nuevo corazón, le pusieron un aparato especial en el oído para que pudiera oír mejor. Los doctores cuidaron mucho que todo saliera bien en la operación. Ahora puede oír mejor y está más feliz.",
+                "fh_score": 73.38
+            },
+            "B2": {
+                "text": "**Caso de un Adolescente con Problemas del Corazón y Pérdida de Audición**\n\nUn joven de 15 años tenía un problema grave en su corazón llamado insuficiencia cardiaca biventricular, que significa que ambos lados de su corazón no funcionaban bien. Para ayudarlo mientras esperaba un trasplante de corazón, le pusieron un corazón artificial llamado SynCardia. \n\nDurante su tratamiento en cuidados intensivos, recibió un medicamento llamado amikacina, que puede dañar el oído y causar pérdida de audición. Después de un tiempo, el paciente empezó a perder la audición en ambos oídos. Los médicos hicieron varios exámenes y confirmaron que tenía una pérdida auditiva profunda en los dos oídos, aunque sus oídos y nervios estaban físicamente normales.\n\nPara mejorar su audición y ayudarlo a comunicarse mejor, el equipo médico decidió ponerle un implante coclear en el oído derecho. Un implante coclear es un dispositivo que ayuda a las personas con pérdida auditiva severa a escuchar sonidos. Antes de la cirugía, ajustaron cuidadosamente sus medicamentos para evitar problemas con la coagulación de la sangre, ya que él tomaba medicinas para el corazón que afectan esto.\n\nLa operación para colocar el implante coclear fue exitosa y sin complicaciones. Después de la cirugía, el paciente mejoró su capacidad para oír y entender el habla, lo que es muy importante para su calidad de vida y para prepararse para el futuro trasplante de corazón.\n\nEn resumen, este caso muestra cómo un adolescente con un corazón artificial y pérdida auditiva causada por medicamentos pudo recibir un implante coclear con buenos resultados, gracias al trabajo de un equipo médico especializado y una cuidadosa preparación.",
+                "fh_score": 48.68
+            },
+            "B3": {
+                "text": "**Contexto**  \nPresentamos el caso de un adolescente de 15 años con insuficiencia cardiaca biventricular avanzada, que requirió el implante de un corazón artificial total SynCardia como medida temporal mientras esperaba un trasplante de corazón. Durante su hospitalización en cuidados intensivos, recibió amikacina, un antibiótico conocido por su potencial daño al oído (ototoxicidad). Posteriormente, desarrolló una pérdida auditiva profunda bilateral, detectada aproximadamente 131 días después de la implantación del corazón artificial.\n\n**Hallazgos Clave**  \n- El paciente no tenía antecedentes previos de pérdida auditiva ni factores familiares que sugirieran sordera.  \n- Las pruebas audiológicas confirmaron una pérdida auditiva profunda en ambos oídos, mientras que los estudios de imagen mostraron estructuras normales del oído interno y nervios cocleares intactos.  \n- La evaluación multidisciplinaria concluyó que un implante coclear era la mejor opción para mejorar su audición y facilitar su adaptación cognitiva y funcional en el contexto del trasplante cardíaco.  \n- La cirugía de implante coclear se realizó con éxito, tras una cuidadosa preparación para manejar los riesgos relacionados con la anticoagulación y la función del corazón artificial.  \n- No hubo complicaciones perioperatorias significativas, y la activación del implante coclear mostró una mejora progresiva en la audición y la percepción del habla en los meses siguientes.\n\n**Interpretación Clínica**  \nEste caso ilustra cómo la ototoxicidad inducida por medicamentos puede causar una pérdida auditiva severa en pacientes críticos, incluso en adolescentes sin antecedentes previos. La coordinación entre múltiples especialidades fue fundamental para manejar los riesgos asociados a la anticoagulación y la anestesia en un paciente con un dispositivo cardíaco artificial, permitiendo una intervención auditiva efectiva que mejoró significativamente su calidad de vida y capacidad de comunicación.\n\n**Próximos Pasos**  \nSe recomienda continuar con el seguimiento audiológico y rehabilitación auditiva para maximizar los beneficios del implante coclear. Además, se debe mantener una vigilancia estrecha de la función cardíaca y del estado anticoagulante, especialmente en el contexto del trasplante cardíaco futuro. Este caso destaca la importancia de la detección temprana y el manejo multidisciplinario de las complicaciones auditivas en pacientes con enfermedades cardíacas complejas.",
+                "fh_score": 27.49
+            }
+        }
+    },
+    {
+        "article": "Se encontró a un hombre de 25 años de edad recostado por familiares después de una noche de fiesta, con vómitos, agresión y dolor localizado en la región glútea e inferior derecha. La evaluación inicial en el departamento de urgencias no reveló lesiones traumáticas; sin embargo, el empeoramiento de los síntomas llevó a una nueva evaluación al día siguiente. Los resultados de laboratorio revelaron un recuento sanguíneo completo sin alteraciones, niveles elevados de CPK sérica (42 527 IU/l), creatinina sérica (735 µmol/l), urea (44,3 mmol/l) y potasio (5,7 mmol/l). El análisis de orina reveló orina de color rojo-marrón sin glóbulos rojos, proteinuria (+1), glucosuria (+1) y WBC (9-10/hpf). Estos resultados confirmaron la RM y la IRA. La toxicología estableció la administración de 1796 µg/l de heroína (> 5 veces el nivel basal) sin detección de ninguna otra sustancia. Aunque inicialmente negó haber tomado medicamentos, después del análisis toxicológico, el paciente admitió que había administrado heroína una vez por vía intramuscular en la región glútea derecha la noche del incidente.\n\nUna tomografía computarizada demostró edema muscular glúteo y miositis localizada en la región glútea derecha. Al comenzar el tratamiento convencional con resucitación de fluidos intravenosos (IV), el tratamiento de la IRA fracasó, lo que hizo necesario el TRR con hemodiálisis debido a la progresión de la azotemia con un aumento de la creatinina sérica a 1052 µmol/l. La función renal mejoró tras el cese del TRR con una duración total de la estancia (LOS) de 9 días. El seguimiento posterior del paciente fue incompleto debido a la falta de asistencia.\n",
+        "gold_summary": "Este informe de caso describe a un hombre de 25 años que desarrolló una RM grave y lesión renal aguda (LRA) después de la administración intramuscular (IM) de heroína como usuario por primera vez. El uso de la heroína IM puede inducir niveles más altos de CPK debido a la toxicidad directa de los miocitos y el trauma mecánico. Los músculos glúteos altamente vascularizados con fibras tipo 1 en el sitio de la inyección probablemente exacerbaron la gravedad. Los factores adicionales incluyeron una menor densidad mitocondrial en los hombres y la exposición al alcohol. A pesar de la reanimación agresiva con líquidos, se requirió la terapia de reemplazo renal (RRT) y el paciente respondió bien a la hemodiálisis.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Un hombre joven se lastimó el músculo de su nalga. Esto pasó porque se puso una medicina mala llamada heroína en esa parte. Su cuerpo se enfermó mucho y sus riñones también se lastimaron. \n\nLos doctores le dieron muchos líquidos para ayudarlo. Pero su riñón no mejoró solo. Entonces, usaron una máquina especial para limpiar su sangre. Después, el hombre empezó a sentirse mejor.",
+                "fh_score": 75.64
+            },
+            "B2": {
+                "text": "**Lo que pasó con el paciente**  \nUn hombre de 25 años usó heroína por primera vez y se la inyectó en el músculo de la nalga derecha. Después de eso, empezó a sentirse muy mal, con dolor, vómitos y agresividad. Cuando llegó al hospital, no encontraron heridas, pero sus síntomas empeoraron al día siguiente.\n\n**Qué encontraron los médicos**  \nLos análisis de sangre mostraron que tenía niveles muy altos de una enzima llamada CPK, que indica daño en los músculos. También tenía problemas en los riñones, con niveles altos de creatinina y urea, que son sustancias que el riñón normalmente limpia. La orina estaba de color rojo-marrón, pero sin sangre visible, lo que es un signo de daño muscular y renal. La tomografía mostró inflamación en el músculo de la nalga donde se inyectó la droga.\n\n**Qué significa todo esto**  \nEl hombre sufrió una condición llamada rabdomiólisis, que es cuando los músculos se dañan mucho y liberan sustancias que pueden dañar los riñones. Esto ocurrió por la inyección directa de heroína en el músculo, que causó daño tanto por la droga como por el trauma de la aguja. Además, factores como el alcohol y diferencias en el cuerpo de los hombres pueden haber empeorado la situación.\n\n**Cómo lo trataron**  \nLe dieron líquidos por vía intravenosa para ayudar a limpiar sus riñones, pero esto no fue suficiente. Por eso, tuvo que recibir un tratamiento especial llamado hemodiálisis, que es una máquina que hace el trabajo de los riñones cuando están muy dañados. Después de varios días, su función renal mejoró y pudo dejar el tratamiento.\n\n**Conclusión**  \nEste caso muestra que inyectarse heroína en el músculo puede causar un daño muscular grave y problemas serios en los riñones, incluso en personas que la usan por primera vez. Es importante buscar ayuda médica rápido si alguien presenta síntomas después de usar drogas de esta forma.",
+                "fh_score": 68.32
+            },
+            "B3": {
+                "text": "**Contexto**  \nEste caso clínico presenta a un hombre de 25 años que sufrió una lesión muscular grave conocida como rabdomiólisis (RM) y una lesión renal aguda (LRA) tras administrarse heroína por primera vez mediante una inyección intramuscular (IM) en la región glútea derecha. La rabdomiólisis es una condición en la que el daño muscular libera sustancias tóxicas en la sangre, lo que puede afectar negativamente a los riñones.\n\n**Hallazgos Clave**  \nEl paciente fue encontrado después de una noche de consumo de sustancias, con síntomas de vómitos, agresividad y dolor intenso en la zona glútea derecha. Inicialmente, no se detectaron lesiones traumáticas, pero al empeorar sus síntomas, se realizaron análisis que mostraron niveles extremadamente elevados de creatina fosfoquinasa (CPK) sérica (42,527 IU/l), un marcador que indica daño muscular severo. Además, presentó alteraciones en la función renal, evidenciadas por un aumento significativo de creatinina y urea en sangre, así como cambios en el análisis de orina, que mostraba orina de color rojo-marrón sin glóbulos rojos, proteinuria (presencia de proteínas) y glucosuria (presencia de glucosa), signos compatibles con daño renal. La toxicología confirmó una concentración elevada de heroína en sangre, y el paciente finalmente admitió haberse inyectado heroína en el glúteo la noche previa.\n\nUna tomografía computarizada reveló inflamación y edema (hinchazón) muscular en la región glútea derecha, confirmando la miositis (inflamación muscular) localizada.\n\n**Interpretación Clínica**  \nLa administración intramuscular de heroína puede causar daño muscular directo debido a la toxicidad de la droga sobre las células musculares (miocitos) y al trauma mecánico producido por la inyección. La región glútea, por su alta vascularización y predominancia de fibras musculares tipo 1 (que tienen características metabólicas específicas), probablemente contribuyó a la gravedad del daño. Además, factores como una menor densidad mitocondrial en hombres (las mitocondrias son las \"centrales energéticas\" de las células) y la exposición al alcohol podrían haber exacerbado la lesión muscular y renal.\n\nA pesar de iniciar un tratamiento convencional con líquidos intravenosos para intentar revertir la lesión renal, el daño progresó, requiriendo la implementación de terapia de reemplazo renal mediante hemodiálisis. Tras este tratamiento, la función renal del paciente mejoró, permitiendo su alta hospitalaria después de nueve días.\n\n**Próximos Pasos**  \nEl seguimiento posterior del paciente fue limitado debido a su falta de asistencia a controles médicos, lo que dificulta evaluar su recuperación a largo plazo y la prevención de complicaciones futuras. Este caso resalta la importancia de la detección temprana y el manejo adecuado de la rabdomiólisis inducida por drogas, así como la necesidad de apoyo y seguimiento continuo en pacientes con consumo de sustancias para evitar daños graves y mejorar los resultados clínicos.",
+                "fh_score": 35.29
+            }
+        }
+    },
+    {
+        "article": "Una mujer de 63 años con antecedentes de obesidad e hipertensión arterial acudió a la sala de urgencias de un hospital de nivel secundario con un historial de siete días de fiebre, tos seca, hiposmia y mialgia. Al momento del ingreso, se encontraba alerta, con una frecuencia respiratoria de 22 ciclos por minuto, pulso de 90 latidos por minuto y saturación de oxígeno de 90 %. Los análisis de laboratorio revelaron linfopenia (1,55 x 109) y niveles elevados de proteína C reactiva (10,62 mg/dL). Se realizó una prueba de reacción en cadena de la polimerasa para COVID-19 a partir de un hisopado nasofaríngeo y de la garganta, que resultó positivo para el coronavirus del síndrome respiratorio agudo severo 2 (SARS-CoV-2).\n\nLa situación evolucionó rápidamente con fiebre, postración y empeoramiento de la disnea. La gasometría arterial reveló una insuficiencia respiratoria grave, mientras que la radiografía de tórax evidenció infiltrados pulmonares bilaterales. La paciente fue intubada y sometida a ventilación mecánica, pero su condición respiratoria continuó deteriorándose, a pesar de los mejores cuidados críticos, incluyendo ventilación en posición prona y bloqueo neuromuscular. Su examen de tomografía computarizada del tórax, tras la intubación, reveló extensas opacificaciones multifocales bilaterales en vidrio molido, sin signos de embolia pulmonar. Los ajustes iniciales del ventilador fueron: ventilación controlada por volumen con volumen corriente de 360 ml (6 ml/kg de peso corporal ideal), frecuencia respiratoria de 14 respiraciones por minuto, presión espiratoria positiva final (PEEP) de 14 cmH2O y complacencia estática de 44 cmH2O.\n\nEn el segundo día de internación, la gasometría arterial mostró pH de 7,34, presión parcial de dióxido de carbono (PaCO2) de 53 mmHg, presión parcial de oxígeno (PaO2) de 102 mmHg y bicarbonato (HCO3) de 29,7 mmol/L, con una proporción presión parcial de oxígeno/fracción inspirada de oxígeno (PaO2/FiO2) de 98. Ella cumplía los criterios para indicación de VV-ECMO y fue transferida a la unidad de terapia intensiva (UTI), que disponía de un programa establecido para VV-ECMO. El procedimiento fue realizado con seguridad, no habiendo ocurrido complicaciones. El análisis de la gasometría arterial 3 horas después del inicio de la VV-ECMO mostró pH de 7,386, PaCO2 de 43 mmHg, PaO2 de 94,3 mmHg y HCO3 de 25,4 mmol/L, sin cualquier variación abruta de la PaCO2. Tuvieron inicio la nutrición y la rehabilitación precoces tras la introducción de la VV-ECMO. En el 14º día de internación, la paciente desarrolló neumonía asociada al ventilador causada por Pseudomonas aeruginosa, siendo sometida a 7 días de antibioticoterapia con ceftazidima y vancomicina, con respuesta favorable. En el 20º día de internación, su radiografía del tórax y la complacencia mejoraron, y la paciente fue retirada de la VV-ECMO con éxito tras 455 horas de soporte, siendo traqueostomizada 7 días después. La paciente mantuvo buena función renal durante toda la internación.\n\nEn el día 34 de internación, luego de 7 días de destete de la sedación, con evolución positiva de su cuadro neurológico, ocurrió una crisis epiléptica generalizada limitada, que llevó a la investigación diagnóstica.\n\nInvestigación\nLos análisis de sangre de laboratorio revelaron una disminución de los niveles de proteína C reactiva (6,11 mg/dL), procalcitonina (0,07 ng/mL), fibrinógeno (307 ng/mL) y ferritina (2802 ng/mL), pero un aumento en los niveles de dímero D (18021 ng/mL) e interleucina 6 (10,4 pg/mL) en el día anterior al inicio de los síntomas. No se asoció ninguno de los fármacos administrados a la paciente con el SEPR, es decir, fármacos inmunosupresores, inmunomoduladores y quimioterápicos.\n\nSe realizó una resonancia magnética (RM) del cerebro y las imágenes de recuperación de inversión atenuada por fluidos (FLAIR) demostraron una hiperintensidad simétrica y confluente que afectaba a la sustancia blanca justa y subcortical, principalmente en las regiones occipital y parietal, pero también en la región frontal, temporal y cerebelosa izquierda. Los núcleos grises profundos se conservaron y no había presencia de ninguna área con restricción del contraste. Las imágenes ponderadas por susceptibilidad mostraron múltiples microhemorragias puntiformes que afectaban a la sustancia blanca superficial y profunda, pero que no afectaban al área con hiperintensidad en FLAIR. Las microhemorragias puntiformes involucraban predominantemente a la sustancia blanca justacortical y al cuerpo calloso (especialmente el codo y el esplenio). Además, había tres hemorragias subagudas de menos de 1 cm en las cápsulas externas, con hiperintensidad en T1.\n\nLa muestra de líquido cefalorraquídeo dio negativo para SARS-CoV-2 y los niveles de proteínas (31 mg/dL), glucosa (74 mg/dL) y lactato (1,89 mmol/L) se encontraban dentro de los parámetros normales.\n\nDesvelado\nLa paciente logró una recuperación casi total de los déficits neurológicos, a pesar de la miopatía de la enfermedad crítica, y fue dada de alta después de 44 días en el hospital. Se la derivó a un hospital secundario para su rehabilitación y prácticamente recuperó su estado mental previo.\n",
+        "gold_summary": "Una mujer de 63 años de edad acudió a la sala de urgencias con un historial de fiebre aguda, postración y disnea. Se le diagnosticó un caso grave de COVID-19 y síndrome de dificultad respiratoria aguda. A pesar de recibir atención médica intensiva, cumplía con los requisitos para someterse a una oxigenación por membrana extracorpórea. El día 34, luego de siete días de haber suspendido la sedación y de que su cuadro neurológico hubiera evolucionado de manera positiva, presentó una crisis tónico-clónica generalizada limitada, que no guardaba relación con un desequilibrio hidroelectrolítico o metabólico, lo que hizo necesario realizar una investigación diagnóstica. Los estudios de imágenes cerebrales revelaron un síndrome de encefalopatía posterior reversible.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una señora muy enferma tenía fiebre y le costaba respirar. Tenía un virus que le hizo mucho daño en los pulmones. Los doctores le pusieron una máquina para ayudarla a respirar mejor.\n\nDespués de muchos días, la señora empezó a mejorar. Pero un día tuvo un problema en su cabeza que la asustó. Los doctores hicieron unas fotos especiales de su cerebro. Vieron que su cerebro estaba un poco dañado, pero podía mejorar.\n\nLa señora se puso mejor y los doctores la cuidaron mucho para que se sintiera bien otra vez.",
+                "fh_score": 79.85
+            },
+            "B2": {
+                "text": "**Lo que le pasó a la paciente**  \nUna mujer de 63 años llegó al hospital con fiebre alta, mucho cansancio y dificultad para respirar. Los médicos descubrieron que tenía COVID-19 muy grave y un problema llamado síndrome de dificultad respiratoria aguda, que afecta los pulmones y dificulta la respiración. Aunque recibió cuidados intensivos, su condición empeoró y necesitó un tratamiento especial llamado oxigenación por membrana extracorpórea (VV-ECMO). Este tratamiento ayuda a oxigenar la sangre cuando los pulmones no funcionan bien.\n\n**Qué pasó después**  \nDespués de 34 días en el hospital y tras dejar la sedación (medicamentos para dormirla) durante una semana, la paciente tuvo una crisis convulsiva, que es un movimiento fuerte y descontrolado del cuerpo. Esta crisis no se debió a problemas con líquidos o sustancias en su cuerpo, por lo que los médicos hicieron más estudios para entender la causa.\n\n**Lo que mostraron los estudios**  \nLas imágenes del cerebro mostraron un problema llamado síndrome de encefalopatía posterior reversible. Esto significa que algunas partes del cerebro estaban inflamadas o dañadas temporalmente, pero que esta condición puede mejorar con tratamiento. Gracias a la atención médica y la rehabilitación, la paciente casi recuperó completamente sus funciones cerebrales y fue dada de alta después de 44 días en el hospital.",
+                "fh_score": 53.04
+            },
+            "B3": {
+                "text": "**Contexto**  \nUna mujer de 63 años con antecedentes de obesidad e hipertensión presentó un cuadro de siete días con fiebre, tos seca, pérdida del olfato (hiposmia) y dolores musculares. Al ingresar al hospital, mostró signos de insuficiencia respiratoria leve y fue diagnosticada con COVID-19 mediante una prueba PCR. Su condición respiratoria empeoró rápidamente, desarrollando un síndrome de dificultad respiratoria aguda (SDRA) que requirió intubación y ventilación mecánica. Debido a la gravedad del compromiso pulmonar, fue sometida a oxigenación por membrana extracorpórea venovenosa (VV-ECMO), un soporte avanzado para mantener la oxigenación cuando los pulmones no funcionan adecuadamente.\n\n**Hallazgos Clave**  \nTras 34 días de hospitalización y después de haber suspendido la sedación durante una semana con mejoría neurológica, la paciente sufrió una crisis epiléptica generalizada limitada. Esta convulsión no se relacionó con alteraciones metabólicas o desequilibrios hidroelectrolíticos, por lo que se inició una investigación neurológica. La resonancia magnética cerebral mostró un patrón característico de síndrome de encefalopatía posterior reversible (SEPR), que se manifiesta por áreas de inflamación y edema en la sustancia blanca del cerebro, especialmente en regiones occipitales y parietales, sin daño permanente. Además, se detectaron microhemorragias puntiformes en la sustancia blanca, pero el líquido cefalorraquídeo no mostró infección ni inflamación activa.\n\n**Interpretación Clínica**  \nEl SEPR es una condición neurológica que puede presentarse en pacientes críticos y se caracteriza por síntomas como convulsiones, alteraciones visuales y cefalea, acompañados de cambios reversibles en el cerebro. En este caso, la aparición del SEPR después de una infección grave por COVID-19 y soporte con VV-ECMO sugiere una relación con la inflamación sistémica y posibles alteraciones vasculares inducidas por el virus o el tratamiento intensivo. La ausencia de infección directa del virus en el sistema nervioso central y la normalidad del líquido cefalorraquídeo apoyan esta hipótesis.\n\n**Próximos Pasos y Evolución**  \nLa paciente recibió tratamiento adecuado para la crisis epiléptica y cuidados de soporte neurológico. A pesar de la miopatía asociada a la enfermedad crítica, logró una recuperación casi completa de sus funciones neurológicas. Fue dada de alta tras 44 días de hospitalización y remitida a un centro de rehabilitación, donde continuó mejorando hasta recuperar prácticamente su estado mental previo al ingreso.\n\nEste caso resalta la importancia de la vigilancia neurológica en pacientes con COVID-19 grave, especialmente aquellos sometidos a terapias avanzadas como la VV-ECMO, para detectar y tratar complicaciones como el síndrome de encefalopatía posterior reversible.",
+                "fh_score": 32.34
+            }
+        }
+    },
+    {
+        "article": "Mujer de 65 años, originaria y residente de la Ciudad de México, con antecedente de infección por VIH de 20 años de diagnóstico con carga viral indetectable desde 2020 y con cuenta de CD4 de 1220 células por mililitro en febrero de 2022, hipotiroidismo de 29 años, cardiopatía isquémica de 9 años de diagnóstico, osteoporosis y dislipidemia, en tratamiento y bajo control médico.\n\nSu dermatosis problema se inició 10 años atrás, después de un cuadro de herpes zóster localizado en la extremidad inferior derecha y se complicó con una infección de tejidos blandos, referida como celulitis. Como secuela de este evento la paciente desarrolló úlcera, la cual ameritó corrección del defecto con 4 injertos cutáneos en diferentes tiempos quirúrgicos por cirugía plástica, con acompañamiento por parte de la clínica de heridas. Durante el seguimiento y a pesar de las medidas tomadas, no logró resolución completa y persistió con una úlcera asociada a dolor local, motivo de su envío a nuestro servicio.\n\nA la exploración física presentaba una dermatosis localizada en la extremidad inferior derecha, en la cara lateral del muslo, caracterizada por una neoformación aplanada sobre la que se asentaba una úlcera de 1.5 cm de diámetro, con fondo limpio, con costra sero-amarillenta, bordes sobreelevados, piel perilesional hiperpigmentada y queratósica, una cicatriz atrófica e hiperpigmentada. Se inició abordaje de la dermatosis mediante biopsia de piel, con reporte histopatológico de carcinoma verrugoso, por lo que se concluyó como úlcera de Marjolin asociada a carcinoma verrugoso en paciente portadora de VIH. Se canalizó al hospital de oncología para manejo con radioterapia.",
+        "gold_summary": "mujer de 65 años con el antecedente de ser portadora de infección por virus de inmunodeficiencia humana (VIH), que presentó un carcinoma verrugoso asociado a una úlcera de Marjolin secundaria a herpes zóster e infección de tejidos blandos en pierna derecha, con un periodo de latencia de 10 años desde el proceso infeccioso inicial hasta la confirmación histopatológica.",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Una señora de 65 años tuvo una herida en su pierna. La herida empezó hace mucho tiempo por una infección. La herida no sanó bien y cambió. Los doctores vieron que la herida tenía una enfermedad que puede crecer. Ella recibe ayuda para mejorar.",
+                "fh_score": 79.23
+            },
+            "B2": {
+                "text": "### Lo que pasó con la paciente\n\nUna mujer de 65 años, que vive en la Ciudad de México y tiene VIH controlado desde hace varios años, desarrolló un problema en la piel de su pierna derecha. Hace 10 años, tuvo una infección llamada herpes zóster, que afectó esa zona. Después, sufrió una infección en los tejidos blandos (la parte blanda bajo la piel), llamada celulitis. Esto causó una herida o úlcera que no sanaba bien.\n\n### Lo que encontraron\n\nA pesar de varios tratamientos, incluyendo cirugías para poner injertos de piel, la úlcera siguió abierta y le causaba dolor. Cuando la revisaron, vieron una lesión con una herida de 1.5 cm en el muslo derecho. Tomaron una biopsia, que es cuando se extrae un pequeño pedazo de piel para examinarlo bajo el microscopio. El examen mostró que la úlcera tenía un tipo de cáncer llamado carcinoma verrugoso, que es un tumor que crece lentamente y parece una verruga.\n\n### Qué significa\n\nEsta úlcera se llama úlcera de Marjolin, que es una herida crónica que puede convertirse en cáncer después de muchos años. En este caso, la úlcera apareció después de la infección por herpes zóster y la celulitis, y tardó 10 años en transformarse en cáncer. Debido a esto, la paciente fue enviada a un hospital especializado para recibir tratamiento con radioterapia, que usa rayos para destruir las células cancerosas.\n\nEn resumen, una infección antigua en la pierna causó una herida que no sanó y, con el tiempo, se convirtió en un tipo de cáncer en la piel. Por eso es importante cuidar bien las heridas que no se curan y revisarlas con el médico.",
+                "fh_score": 70.6
+            },
+            "B3": {
+                "text": "Contexto  \nSe trata de una mujer de 65 años con diagnóstico de infección por VIH desde hace 20 años, con carga viral indetectable y buen conteo de células CD4, además de otras condiciones crónicas como hipotiroidismo, cardiopatía isquémica, osteoporosis y dislipidemia, todas bajo control médico. Hace 10 años, tras un episodio de herpes zóster en la pierna derecha que se complicó con una infección de tejidos blandos (celulitis), desarrolló una úlcera en esa zona. A pesar de múltiples intervenciones quirúrgicas con injertos cutáneos y seguimiento especializado, la úlcera persistió y causó dolor local.\n\nHallazgos Clave  \nDurante la evaluación clínica, se observó una lesión en la cara lateral del muslo derecho consistente en una neoformación aplanada con una úlcera de 1.5 cm de diámetro, bordes elevados, piel circundante oscura y engrosada, y una cicatriz atrófica. La biopsia de piel reveló la presencia de un carcinoma verrugoso, que es un tipo de cáncer de piel de crecimiento lento y aspecto verrugoso (similar a una verruga). Este hallazgo confirmó que la úlcera crónica correspondía a una úlcera de Marjolin, que es una lesión maligna que puede desarrollarse en cicatrices o heridas crónicas.\n\nInterpretación Clínica  \nLa paciente presentó un carcinoma verrugoso asociado a una úlcera de Marjolin que se originó como secuela de una infección previa por herpes zóster y celulitis en la pierna derecha. El periodo de latencia entre el evento infeccioso inicial y la aparición del cáncer fue de aproximadamente 10 años. Esta condición es poco frecuente pero importante, ya que las úlceras crónicas pueden transformarse en lesiones malignas, especialmente en pacientes con factores de riesgo como el VIH.\n\nPróximos Pasos  \nLa paciente fue referida al hospital de oncología para recibir tratamiento con radioterapia, que es una modalidad adecuada para este tipo de carcinoma. Se requiere un seguimiento estrecho para evaluar la respuesta al tratamiento y prevenir complicaciones adicionales. Además, es fundamental mantener un control riguroso de sus condiciones crónicas y del estado inmunológico para optimizar su recuperación.",
+                "fh_score": 44.85
+            }
+        }
+    },
+    {
+        "article": "Una mujer de 90 años con hepatitis C y un historial de tabaquismo de 60 años proveniente de una zona rural presentó una hinchazón en la cara posteromedial del muslo izquierdo justo por encima de la rodilla. La hinchazón se notó por primera vez hace 3 años y aumentó gradualmente de tamaño durante este período. Ella sintió un leve malestar, pero niega cualquier síntoma asociado de dolor, picazón, secreción, fiebre o inmovilidad articular. Como provenía de una zona rural, también tenía un historial de exposición a animales.\nEn el examen físico, la hinchazón tenía una forma esférica de 14 × 10, era firme, fija y no sensible, con márgenes bien definidos en el aspecto posteromedial del muslo izquierdo, justo por encima de la rodilla. La piel que la recubría era pellizcable y mostraba venas prominentes, y la temperatura era comparable a la de la piel circundante.\nLa ecografía reveló una lesión quística grande con varios quistes pequeños en su interior, que medían 13,2 × 11 × 13,6 cm y un volumen de 1046 ml. Se originaba en la articulación de la rodilla izquierda y se extendía hasta la mitad del muslo. La ecografía Doppler en color no mostró vascularización en su interior. Se realizó una resonancia magnética que mostró una lesión quística grande (21 × 9,9 × 8,1 cm) con múltiples lesiones pequeñas dispersas, con extensión intramuscular e intermuscular que afectaban al aductor largo y al gracilis de manera medial y al bíceps femoral de manera posterior. Todas estas características eran indicativas de un quiste hidatídico. El diagnóstico se confirmó mediante una prueba de hemaglutinación para Echinococcus. La radiografía de tórax y la ecografía abdominal fueron normales.\nSe planificó la escisión quirúrgica de la tumefacción quística y se realizó una incisión en forma de S en la piel, seguida de una disección cuidadosa a través del tejido subcutáneo para acceder al quiste. La lesión estaba bien definida dentro de los planos intermuscular e intramuscular. Se realizó una disección meticulosa para aislar y extraer el quiste intacto, asegurando que no se derramara su contenido. Para minimizar el riesgo de contaminación, se irrigó a fondo el sitio quirúrgico con solución salina normal después de la escisión.\nLos hallazgos intraoperatorios revelaron una gran hinchazón quística intermuscular de 22 × 14 cm, que involucraba los compartimentos posterior y medial del muslo izquierdo. El quiste demostró extensión intramuscular hacia el aductor largo y el gracilis medialmente y hacia el bíceps femoral posteriormente, extendiéndose hasta la fosa poplítea. Cabe destacar que no había comunicación entre el quiste y la articulación de la rodilla. Una biopsia enviada al laboratorio confirmó aún más el diagnóstico. El examen histopatológico de la muestra extirpada reveló una pared quística fibrocondrogénica revestida por epitelio atenuado con infiltración inflamatoria. La presencia de material queratinoso focal caracterizó aún más la lesión. Estos hallazgos, junto con las características macroscópicas, favorecieron el diagnóstico de un quiste hidatídico. El curso postoperatorio fue sin complicaciones y el paciente fue dado de alta con una terapia antihelmíntica durante seis semanas. Se programaron visitas de seguimiento a la semana, tres semanas, seis semanas, nueve semanas y doce semanas. Durante estas visitas, el paciente no mostró signos de recurrencia o complicaciones.\n",
+        "gold_summary": "Una mujer de 90 años de edad, proveniente de una zona rural, presentó una hinchazón de crecimiento lento en el muslo posteromedial durante tres años. No tenía antecedentes de traumatismos ni síntomas sistémicos. El examen clínico reveló una masa firme y no dolorosa. Las imágenes sugieren una lesión quística, y la serología confirmó la infección por Echinococcus. Se realizó la extirpación quirúrgica, y la histopatología confirmó un quiste hidatídico. La paciente recibió un tratamiento posoperatorio de albendazol durante seis semanas. Su recuperación fue sin incidentes, sin recurrencia en el seguimiento.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Había una abuela de 90 años con una bola en su muslo. La bola creció muy despacito por tres años. No le dolía ni tenía fiebre. El doctor vio que la bola era dura y no hacía daño. Hicieron unas fotos especiales y encontraron que había un bichito dentro. El doctor sacó la bola con una operación. Luego, la abuela tomó medicina para quitar el bichito. Ella se puso bien y no volvió a salir la bola.",
+                "fh_score": 90.27
+            },
+            "B2": {
+                "text": "**Lo que Encontraron**  \nUna mujer de 90 años que vivía en una zona rural notó una hinchazón en la parte trasera y media de su muslo izquierdo, justo encima de la rodilla. Esta hinchazón creció lentamente durante tres años. No tenía dolor ni otros síntomas como fiebre o enrojecimiento. Al examinarla, los médicos encontraron una masa firme y que no dolía al tocarla.\n\n**Qué Significan las Pruebas**  \nLas imágenes por ecografía y resonancia mostraron que la hinchazón era un quiste grande, que es una bolsa llena de líquido. Además, la prueba de sangre confirmó que estaba infectada por un parásito llamado Echinococcus, que puede causar un quiste hidatídico. Este tipo de quiste se forma cuando el parásito crea una bolsa en el cuerpo.\n\n**El Tratamiento y Resultado**  \nLos médicos operaron para quitar el quiste completo, con mucho cuidado para no romperlo y evitar que el parásito se esparciera. Después de la cirugía, la muestra del quiste fue analizada y confirmó el diagnóstico. La paciente tomó un medicamento llamado albendazol durante seis semanas para eliminar cualquier parásito restante. Su recuperación fue buena y no tuvo problemas ni volvió a aparecer la hinchazón en las revisiones posteriores.\n\nEn resumen, esta mujer tuvo un quiste causado por un parásito, que fue tratado con cirugía y medicina, y se recuperó sin complicaciones.",
+                "fh_score": 61.98
+            },
+            "B3": {
+                "text": "**Contexto**  \nUna mujer de 90 años, originaria de una zona rural y con antecedentes de hepatitis C y tabaquismo prolongado, consultó por una hinchazón en la parte posterior y medial del muslo izquierdo, justo por encima de la rodilla. Esta masa había aparecido hace tres años y había ido aumentando de tamaño de forma gradual. La paciente no presentaba dolor, fiebre, picazón ni otros síntomas asociados, y no refería antecedentes de traumatismos recientes. Además, tenía historial de contacto con animales debido a su entorno rural.\n\n**Hallazgos Clave**  \nEn el examen físico, se detectó una masa esférica, firme, fija y no dolorosa, de aproximadamente 14 × 10 cm, con bordes bien definidos y piel sobre la lesión que se podía pellizcar, mostrando venas prominentes pero sin aumento de temperatura local. La ecografía reveló una lesión quística grande con múltiples quistes pequeños en su interior, originada en la articulación de la rodilla y extendiéndose hacia la mitad del muslo, sin vascularización interna. La resonancia magnética confirmó estas características, mostrando además extensión intramuscular e intermuscular en músculos específicos del muslo. Estos hallazgos fueron altamente sugestivos de un quiste hidatídico (una infección parasitaria causada por el Echinococcus). La confirmación diagnóstica se realizó mediante una prueba serológica de hemaglutinación para Echinococcus. Estudios adicionales, como radiografía de tórax y ecografía abdominal, no mostraron afectación en otros órganos.\n\n**Interpretación Clínica**  \nEl diagnóstico de quiste hidatídico en el muslo, aunque poco común, fue confirmado mediante imágenes, pruebas serológicas y análisis histopatológico. La lesión representaba una masa quística con múltiples compartimentos, infiltrando tejidos musculares pero sin comunicación con la articulación de la rodilla. La histología mostró una pared quística con infiltración inflamatoria y material característico del parásito, confirmando la naturaleza hidatídica de la lesión.\n\n**Próximos Pasos y Tratamiento**  \nSe planificó y llevó a cabo la extirpación quirúrgica completa del quiste mediante una incisión en forma de S, con una disección cuidadosa para evitar la ruptura y contaminación del área. El sitio quirúrgico fue irrigado con solución salina para minimizar riesgos de diseminación. El postoperatorio transcurrió sin complicaciones, y la paciente recibió tratamiento antiparasitario con albendazol durante seis semanas para asegurar la erradicación del parásito. Se realizaron controles periódicos a las 1, 3, 6, 9 y 12 semanas posteriores a la cirugía, durante los cuales no se evidenció recurrencia ni complicaciones.\n\nEn resumen, este caso ilustra la importancia de considerar infecciones parasitarias como causa de masas quísticas en pacientes de zonas rurales, y demuestra que un abordaje quirúrgico cuidadoso combinado con terapia antiparasitaria puede conducir a una recuperación exitosa sin recurrencia.",
+                "fh_score": 35.61
+            }
+        }
+    },
+    {
+        "article": "Una paciente de 21 años de edad, soltera, con antecedentes de hipertensión y feocromocitoma metastásico, se presentó en nuestro hospital. Su cáncer se ha metastatizado en la vejiga, los huesos y los pulmones. También tiene un fuerte historial familiar de neoplasias, en particular de feocromocitoma. La paciente fue admitida debido a la hipertensión no controlada y los síntomas crónicos relacionados con su enfermedad.\n\nEn el ingreso (09/06/2024), la paciente era normotensa (PA: 104/66 mmHg), su frecuencia cardiaca era de aproximadamente 90 latidos por minuto, afebril a 36.9°C, y tenía una saturación de oxígeno de 99% en aire ambiente. El examen físico indicó un estado de desempeño del Grupo Cooperativo de Oncología del Este (ECOG) de 2, palidez consistente con anemia crónica, latido cardiaco regular sin murmullos o sonidos adicionales. El examen abdominal no fue notable, y no se observó edema o equimosis en las extremidades inferiores.\n\nLa paciente tiene antecedentes de hipertensión y paraganglioma, su medicación incluye (Doxazosin 2 mg, Labetalol 100 mg, Oxibutinina 5 mg, Aceite de parafina, Nifedipina 30 mg). Su historial quirúrgico incluye una adrenalectomía derecha a los diez años, y ha recibido varios tratamientos, incluidos análogos de somatostatina y radioterapia paliativa. El historial familiar revela una mutación familiar de la subunidad B de la deshidrogenasa del succinato (mutación SDBH) con un importante historial de tumores malignos endocrinos, incluidos feocromocitomas en su padre y hermana y cáncer de páncreas en su abuela.\n\nLas investigaciones de laboratorio, incluido el recuento sanguíneo completo, revelaron anemia significativa, con un nivel de hemoglobina de 7.5 g/dl. Había evidencia de hemólisis, como lo indican el alto recuento de reticulocitos, la bilirrubina indirecta y la lactato deshidrogenasa. La haptoglobina era baja. Los resultados de laboratorio se muestran en. El perfil de coagulación excluyó la coagulación intravascular diseminada (DIC), que muestra (PT: 15.6, PTT: 23.3, fibrinógeno: 489, dímero D: 0.63). La prueba de Coombs directa para excluir la anemia hemolítica autoinmune fue negativa. Los frotis de sangre periférica mostraron la presencia de esquistocitos, equinocitos y algunas células en forma de lágrima, además de trombocitopenia, todo lo cual apuntaba a la anemia hemolítica microangiopática (MAHA). Dado el contexto del cáncer metastásico, el paciente fue diagnosticado con anemia hemolítica microangiopática paraneoplásica en marzo/2024.\n\nEl paciente fue programado para el protocolo CVD (ciclofosfamida, vincristina y doxorrubicina), pero sin ciclofosfamida debido al efecto inductor de anemia de los agentes alquilantes. El paciente recibió un total de 5 ciclos. Como indicador de respuesta clínica, el paciente ya no experimentó anemia o trombocitopenia. Un nuevo frotis de sangre periférica reveló células normales, lo que sugiere una respuesta clínica al MAHA que coincide con la mejora de la neoplasia subyacente. Esto se alinea con la definición de MAHA como un síndrome paraneoplásico.\n\nLos medicamentos que se le suministran al paciente al momento del alta son: comprimidos de dexametasona de 2 mg, 4 mg por vía oral (PO) una vez al día (OD) durante 3 días, comprimidos de ondansetrón de 8 mg por vía oral (PO) una vez al día (OD) durante 3 días, comprimidos de metoclopramida de 10 mg por vía oral (PO) tres veces al día durante 3 días, calcio de 600 mg con vitamina D por vía oral (PO) una vez al día (OD) durante 1 día, comprimidos de labetalol de 100 mg por vía oral (PO) dos veces al día durante 1 día, comprimidos de doxazocina de 2 mg por vía oral (PO) dos veces al día durante 1 día, comprimidos de citalopram de 20 mg por vía oral (PO) durante 1 día, comprimidos de omeprazol de 20 mg, 40 mg por vía oral (PO) durante 1 día, comprimidos de paracetamol de 500 mg, 1000 mg por vía oral (PO) dos veces al día durante 1 día, cápsulas de aprepitant de 125 mg/80 mg, 1 cápsula por vía oral (PO) dos veces al día durante 3 días (con prescripción médica).\n\nEl paciente fue objeto de seguimiento el 01/07/2024, y su aspecto clínico era bueno y activo. El paciente se sometió a exámenes de laboratorio que incluían un recuento sanguíneo completo (WBC 6.59 10e3/ul, RBC 4.47 × 10^6/ul, HGB 13.2 g/dl, 40.0%, MCV 89.4 fL, PLT 41.5 10e3/ul), nitrógeno ureico en sangre 33.8 mg/dl, creatina cinasa-MB 36.1 u/l, creatinina sérica 0.97 mg/dl, cloruro 101.5 mmol/l, potasio 4.52 mmol/l, sodio 135 mmol/l.\n",
+        "gold_summary": "En este informe de caso, presentamos a una mujer soltera de 21 años con un fuerte historial familiar de neoplasia endocrina. Fue derivada a nuestro hospital para quimioterapia debido a un diagnóstico de feocromocitoma maligno, que había hecho metástasis en la vejiga urinaria, los huesos y los pulmones. Además, desarrolló anemia hemolítica microangiopática como un síndrome paraneoplásico.\n",
+        "synthetic_summary": {
+            "B1": {
+                "text": "Esta es la historia de una joven de 21 años. Ella tiene un tipo de enfermedad que hace que su cuerpo tenga bultos malos. Estos bultos están en partes como la vejiga, los huesos y los pulmones. También, su sangre estaba muy débil y no estaba bien. Los doctores le dieron medicinas para ayudarla a mejorar. Ahora, ella está más fuerte y se siente mejor.",
+                "fh_score": 86.87
+            },
+            "B2": {
+                "text": "### Caso de una joven con cáncer y anemia especial\n\nPresentamos la historia de una mujer de 21 años que tiene un tipo de tumor llamado feocromocitoma maligno. Este tumor se originó en sus glándulas suprarrenales y se ha extendido a otros órganos, como la vejiga, los huesos y los pulmones. Además, su familia tiene antecedentes de tumores similares, lo que indica que puede haber una causa genética.\n\n### Qué le pasó a la paciente\n\nLa paciente también desarrolló un problema en la sangre llamado anemia hemolítica microangiopática. Esto significa que sus glóbulos rojos se destruyen más rápido de lo normal debido a pequeños daños en los vasos sanguíneos. Esta anemia está relacionada con su cáncer y se llama síndrome paraneoplásico, porque ocurre como una consecuencia del tumor, aunque no sea directamente causado por él.\n\n### Tratamiento y evolución\n\nElla recibió quimioterapia adaptada para evitar empeorar la anemia. Después de varios ciclos, su sangre mejoró y ya no tenía signos de anemia ni problemas en las células sanguíneas. Esto muestra que el tratamiento ayudó tanto al cáncer como a la anemia causada por él.\n\nEn resumen, este caso muestra cómo un cáncer puede afectar otras partes del cuerpo, como la sangre, y cómo un tratamiento adecuado puede mejorar la salud general de la paciente.",
+                "fh_score": 58.49
+            },
+            "B3": {
+                "text": "**Contexto**  \nSe trata de una mujer joven de 21 años con antecedentes familiares significativos de tumores endocrinos malignos, en particular feocromocitomas (tumores que producen hormonas y se originan en las glándulas suprarrenales o tejidos relacionados). La paciente fue ingresada en el hospital debido a un feocromocitoma metastásico, es decir, un tumor maligno que se ha extendido a otros órganos, incluyendo la vejiga, los huesos y los pulmones. Además, presentaba hipertensión arterial difícil de controlar y síntomas relacionados con su enfermedad avanzada.\n\n**Hallazgos Clave**  \nDurante su hospitalización, se detectó que la paciente tenía anemia severa causada por un proceso llamado anemia hemolítica microangiopática (MAHA). Esta condición implica la destrucción acelerada de glóbulos rojos debido a daños en los pequeños vasos sanguíneos, y en este caso se relaciona directamente con su cáncer avanzado, constituyendo un síndrome paraneoplásico (un efecto indirecto del tumor sobre el organismo). Los análisis de sangre mostraron anemia significativa, signos de destrucción de glóbulos rojos (como aumento de reticulocitos y bilirrubina indirecta), y alteraciones en el frotis sanguíneo que confirmaron la presencia de células fragmentadas características de MAHA.\n\n**Interpretación Clínica**  \nLa anemia hemolítica microangiopática en esta paciente se considera una complicación secundaria al feocromocitoma metastásico, reflejando la gravedad y la actividad del tumor. El tratamiento con quimioterapia adaptada (excluyendo ciertos fármacos que podrían empeorar la anemia) logró controlar tanto la anemia como la progresión del cáncer, evidenciado por la normalización de los parámetros sanguíneos y la desaparición de las células anormales en el frotis. Esto confirma la relación directa entre la actividad tumoral y la anemia hemolítica.\n\n**Próximos Pasos**  \nLa paciente fue dada de alta con un régimen farmacológico para manejar sus síntomas y prevenir complicaciones, incluyendo corticosteroides, medicamentos para controlar la presión arterial, antieméticos y suplementos. En el seguimiento posterior, mostró una mejoría clínica significativa, con parámetros sanguíneos dentro de rangos normales y un estado general activo y estable. Continuará bajo vigilancia estrecha para monitorear la evolución de su enfermedad y ajustar el tratamiento según sea necesario.",
+                "fh_score": 27.87
+            }
+        }
+    }
+]
\ No newline at end of file
diff --git a/generating_data/score/output.json b/generating_data/score/output.json
new file mode 100644
index 0000000000000000000000000000000000000000..2de9506855df0300e79ac3ce352f8a7737e4efee
--- /dev/null
+++ b/generating_data/score/output.json
@@ -0,0 +1,4202 @@
+[
+  {
+    "article": "Información para el paciente\nUn hombre de 27 años y fumador estuvo involucrado en un accidente de tráfico; se cayó de su motocicleta sin casco. El hombre llevó la motocicleta al hospital e informó de un dolor de cabeza y heridas hemorrágicas en la frente.\n\nEl paciente no tiene antecedentes patológicos y trabaja en una zona rural.\n\nHallazgos clínicos\nTras su ingreso en urgencias, perdió el conocimiento y sufrió dos convulsiones. En la exploración física, la escala de coma de Glasgow fue de 6/15 (no abrió los ojos, se retiró al sentir dolor, no respondió verbalmente) con midriasis bilateral, dificultad hemodinámica y buena saturación. Se identificó una lesión craneal penetrante con una profusa hemorragia intracraneal.\n\nLínea de tiempo\nTras caerse de la motocicleta, el paciente volvió a montarse en ella e inmediatamente fue al hospital, quejándose de dolores de cabeza y de una herida en la frente por la que sangraba. Recibió tratamiento de urgencia para estabilizar sus funciones respiratorias y hemodinámicas. Ese mismo día, fue trasladado inconsciente a un centro mejor equipado, donde se le realizó un TAC y se sometió a una operación quirúrgica con éxito.\n\nEvaluación diagnóstica\nSu nivel de hemoglobina era de 6 g/dL y su grupo sanguíneo era O positivo. El hospital no tenía ni una unidad de cuidados intensivos ni un escáner. El único diagnóstico sugerido fue el de traumatismo agudo en la cabeza, complicado por hemorragia intracraneal que provocó shock y convulsiones. El pronóstico vital, basado en la presentación clínica, era malo.\n\nIntervención terapéutica\nUna intervención inicial consiste en un relleno intracraneal a través de la fractura craneal, seguido de un vendaje cefálico que ayuda a detener el sangrado. El tratamiento involucró la estabilización de la columna cervical, intubación orotraqueal con oxígeno a 6 L por minuto y la inserción de un catéter Foley. Se usaron dos puertos venosos periféricos para administrar NaCl 0.9 % 1000 CC, Geloplasma* 500 CC, Manitol 20 % 250 CC; Phenobarbital inj 40 mg/2 ml: 100 mg, luego Thiopental 250 mg: bolo de 100 mg × 2 debido a otras convulsiones; Amoxicillin + Clavulanic Acid injection 2 g; Gentamycin 160 mg intramuscularmente. Se realizó un suero antitetánico de 1500 IU y una transfusión de 450 CC de sangre.\n\nEl paciente fue trasladado inconsciente a un equipo en un hospital de primera categoría, sin intubación y en un estado hemodinámico estable.\n\nEl primer día después de la transferencia, el paciente evolucionó bien; estaba consciente y podía caminar, sin problemas neurológicos, hemodinámicos o respiratorios. La tomografía computarizada reveló un edema bifrontal agudo, una contusión hemorrágica del parénquima predominantemente en el lado derecho, una capa de hematoma subdural agudo (3 mm) en la región fronto-parieto-temporo-occipital izquierda, una hernia subfalcular izquierda de 5 mm, una compresión discreta del ventrículo lateral derecho, una hemorragia subaracnoidea superior bifrontal aguda, una fractura frontal deprimida con rotura osteomeníngea y una fractura de la tercera vértebra cervical con compresión de la médula espinal. El paciente se sometió a una operación exitosa en el hospital de primera categoría.\n\nSeguimiento y resultados\nEl período postoperatorio estuvo marcado por convulsiones, para las cuales se le administró anticonvulsivos al paciente, con un buen resultado.\n",
+    "gold_summary": "Un hombre de 27 años, fumador sin antecedentes patológicos, estuvo involucrado en un accidente de tráfico, al caerse de una motocicleta sin casco. En el ingreso al hospital de nuestro distrito rural, la escala de coma de Glasgow durante el examen físico fue de 6/15 con midriasis bilateral, distrés hemodinámico y buena saturación. Se identificó una lesión penetrante en la cabeza con profusa hemorragia intracraneal. Se usó el relleno intracraneal conocido en la neurocirugía de control de daños para taponar la hemorragia intracraneal grave y que es una maniobra neuroquirúrgica que salva vidas. El paciente fue trasladado inconsciente a un hospital de primera categoría, libre de intubación y en un estado hemodinámico estable. El período postoperatorio estuvo marcado por convulsiones, por lo que el paciente fue puesto en anticonvulsivos con un buen resultado.\n",
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+        "text": "Un hombre se cayó de su moto y se lastimó la cabeza. No llevaba casco y se hizo una herida que sangraba mucho. Cuando llegó al hospital, estaba muy dormido y no podía hablar ni abrir los ojos. \n\nLos doctores pusieron algo para parar la sangre dentro de su cabeza. Luego lo llevaron a otro hospital donde lo cuidaron mejor. Después de la operación, tuvo algunos temblores, pero le dieron medicina y se mejoró.",
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+        "text": "**Lo que pasó con el paciente**  \nUn hombre de 27 años que fuma tuvo un accidente al caerse de su motocicleta sin usar casco. Cuando llegó al hospital en una zona rural, estaba muy grave. No respondía bien, tenía las pupilas dilatadas en ambos ojos y sangraba mucho dentro de su cabeza por una herida penetrante.\n\n**Qué hicieron los médicos**  \nPara detener la hemorragia dentro de su cráneo, los médicos usaron una técnica llamada relleno intracraneal. Esto significa que colocaron un material especial para tapar la herida y controlar el sangrado, lo cual es una cirugía que puede salvar vidas en casos graves. Luego, lo trasladaron a un hospital mejor equipado, donde estaba inconsciente pero estable en cuanto a su circulación y respiración.\n\n**Qué pasó después de la operación**  \nDespués de la cirugía, el paciente tuvo convulsiones, que son movimientos involuntarios causados por problemas en el cerebro. Por eso, le dieron medicamentos llamados anticonvulsivos para controlar estas convulsiones. Gracias a este tratamiento, el paciente mejoró y tuvo una buena recuperación.",
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+        "text": "Resumen detallado para público general universitario\n\nContexto  \nUn hombre de 27 años, fumador y sin antecedentes médicos previos, sufrió un accidente de tráfico al caerse de una motocicleta sin usar casco. Tras la caída, presentó dolor de cabeza y una herida sangrante en la frente, por lo que acudió al hospital local en una zona rural.\n\nHallazgos clínicos y evaluación inicial  \nAl llegar al hospital, el paciente perdió el conocimiento y tuvo dos convulsiones. La evaluación neurológica mostró una escala de coma de Glasgow de 6 sobre 15, lo que indica un estado de coma profundo (no abría los ojos, respondía solo con movimientos para evitar el dolor y no hablaba). Además, presentaba midriasis bilateral (dilatación anormal de ambas pupilas), dificultad para mantener la presión arterial (distrés hemodinámico) y buena saturación de oxígeno. Se detectó una lesión penetrante en el cráneo con una hemorragia intracraneal abundante, lo que significa que la sangre estaba acumulándose dentro del cerebro debido a la lesión.\n\nIntervención inicial y traslado  \nEn el hospital rural, donde no había unidad de cuidados intensivos ni tomografía computarizada (TAC), se aplicó un tratamiento de emergencia para controlar el sangrado intracraneal mediante una técnica quirúrgica llamada relleno intracraneal, que consiste en taponar la fractura del cráneo para detener la hemorragia y estabilizar al paciente. Además, se estabilizó la columna cervical, se realizó intubación orotraqueal para asegurar la respiración, se administraron líquidos intravenosos, medicamentos anticonvulsivos para controlar las convulsiones, antibióticos para prevenir infecciones y una transfusión sanguínea debido a la anemia severa (hemoglobina de 6 g/dL). Posteriormente, el paciente fue trasladado inconsciente pero hemodinámicamente estable a un hospital de mayor nivel con mejores recursos.\n\nDiagnóstico y tratamiento avanzado  \nEn el hospital de referencia, se realizó una tomografía computarizada que reveló múltiples lesiones cerebrales graves: edema cerebral (hinchazón del cerebro) en ambas áreas frontales, contusión hemorrágica (moretón con sangrado) en el tejido cerebral del lado derecho, un hematoma subdural agudo (acumulación de sangre entre el cerebro y la membrana que lo cubre) en el lado izquierdo, una hernia subfalcular (desplazamiento del cerebro hacia un lado), compresión ventricular leve, hemorragia subaracnoidea (sangrado en el espacio que rodea el cerebro), fractura deprimida del hueso frontal con ruptura de las membranas que cubren el cerebro, y fractura de la tercera vértebra cervical con compresión de la médula espinal. El paciente fue sometido a una cirugía exitosa para tratar estas lesiones.\n\nEvolución y seguimiento  \nDurante el postoperatorio, el paciente presentó convulsiones que fueron controladas con medicamentos anticonvulsivos, logrando una buena respuesta clínica. Al día siguiente de la cirugía, el paciente estaba consciente, podía caminar y no mostraba problemas neurológicos, respiratorios ni circulatorios.\n\nInterpretación clínica  \nEste caso ilustra la gravedad de los traumatismos craneoencefálicos penetrantes y la importancia de una intervención rápida y adecuada, incluso en entornos con recursos limitados. La técnica de relleno intracraneal utilizada inicialmente fue fundamental para controlar la hemorragia y estabilizar al paciente antes del traslado. La atención especializada posterior y el manejo multidisciplinario permitieron una recuperación favorable a pesar de las múltiples lesiones cerebrales y de la médula espinal.\n\nPróximos pasos  \nSe recomienda continuar con el seguimiento neurológico y rehabilitación para evaluar y tratar posibles secuelas a largo plazo, así como mantener el control de las convulsiones con medicación adecuada. Además, es fundamental promover el uso de casco y medidas de seguridad vial para prevenir este tipo de accidentes.",
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+    "article": "La paciente era una madre de 54 años que provenía de una zona rural y que llegó al Hospital Especializado de Compresión de Nekemte con la queja de una masa en su vagina de 3 años de duración. Hace tres años, encontró una protuberancia de masa a través de su vagina, que gradualmente creció en tamaño con el tiempo. Había tenido dos bebés, el último hace 12 años. Ambos partos fueron en casa, ya que el centro de salud está demasiado lejos de su área de residencia, y fue asistida por una comadrona tradicional. Ella afirmó que todo había sido sin problemas. Inicialmente, hace tres años, hubo sangrado y una descarga ofensiva de la masa, pero eso se detuvo en el último año. Desarrolló laceraciones en la masa hace seis meses. Por esta razón, se divorció y se aisló de toda la vida social durante este largo período de tiempo. Ahora, su hermana mayor y otro familiar la trajeron al hospital específicamente por la laceración de la masa. No tenía ninguna otra enfermedad médica crónica conocida.\n\nHallazgo pertinente del PE\nSigno vital: PA = 100/60 mm hg, FC = 84 lpm, FR = 20 lpm, T° = 36.5°C, peso = 47 kg.\n\nGUS: hay una masa rosada en la vagina que se encuentra a unos 7 cm del anillo del himen.\n\nEl fondo uterino es la parte principal de la masa.\n\nHabía una laceración longitudinal de unos 5 cm en el lado derecho de la masa.\n\nNo hubo sangrado ni secreción de la masa ni del área de la laceración.\n\nLaboratorio\nCBC: hemoglobina = 12 g/dl, PLT = 285 mil, neutrófilos = 74%.\n\nAnálisis de orina: resultado normal.\n\nGrupo sanguíneo = A, RH = positivo.\n\nPrueba de VIH = negativa.\n\nHBSAg = negativo.\n\nEcografía: vejiga parcialmente llena visible en el abdomen, útero no visible en el abdomen. Por lo demás, no se observaron otros hallazgos pertinentes.\n\nRadiografía de tórax: radiografía de tórax normal.\n\nPor este motivo, se le diagnosticó una inversión uterina crónica. Se tomaron imágenes preoperatorias y postoperatorias, el fondo uterino era el punto principal de la masa que sobresalía completamente a través de la vagina y había una laceración crónica desarrollada en la superficie endometrial. Después de la operación, se observó un canal vaginal normal. Después de revisar las opciones de tratamiento con ella y su familia, se programó una cirugía y se realizó una histerectomía abdominal al día siguiente. Era una cirugía abdominal y era fácil introducir el útero en el abdomen. Como el tejido era redundante y distorsionado, es difícil identificar la referencia anatómica y los puntos de referencia quirúrgicos. Debido a esto, la cirugía fue difícil y hubo una lesión ureteral derecha transaccional intraoperatoria y se realizó una anastomosis de extremo a extremo. Se dio de alta el décimo día de la operación y se encontró que estaba mejorando. Se le dio una cita de seguimiento dos semanas después y cuando se evaluó se encontró que estaba bien.\n",
+    "gold_summary": "Una mujer de 54 años de edad acudió a nuestro hospital con la queja de una masa indolora en su vagina de 3 años de duración. Hace tres años, encontró una protuberancia de masa a través de su vagina, que gradualmente creció en tamaño con el tiempo. En el examen físico, el fondo uterino fue el punto principal de la masa y sobresalía 7 cm por debajo del anillo del himen. Como resultado, se le diagnosticó inversión uterina crónica y se le sometió a una histerectomía abdominal. Fue dada de alta en casa mejorada. Presentamos este caso debido a un factor no identificado que provocó la inversión uterina, la presentación tardía de la enfermedad y la dificultad en el tratamiento quirúrgico.\n",
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+        "text": "Había una señora que tenía una bolita en su cuerpo. Esa bolita estaba en un lugar muy especial dentro de ella. La bolita creció poco a poco durante mucho tiempo. Los doctores vieron que esa bolita era parte de un órgano que estaba fuera de su lugar. Ella tuvo que ir al hospital para que los doctores la ayudaran con una operación. Después de la operación, la señora se sintió mejor y pudo ir a su casa. Los doctores contaron esta historia para que otros puedan aprender.",
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+        "text": "**Lo que le Pasó a la Paciente**  \nUna mujer de 54 años notó hace tres años una masa o bulto que salía de su vagina. Esta masa fue creciendo poco a poco y no le causaba dolor. Al principio, tuvo sangrado y mal olor, pero eso paró hace un año. También se lastimó la masa hace seis meses, lo que la hizo sentirse mal y alejarse de su familia y amigos.\n\n**Qué Encontraron los Médicos**  \nCuando la examinaron, vieron que la masa era parte del útero que había salido hacia afuera por la vagina. Esto se llama inversión uterina crónica, que es cuando el útero se da vuelta y sale fuera del cuerpo. Había una herida larga en la masa, pero no estaba sangrando en ese momento. Los exámenes de sangre y orina estaban normales, y no tenía infecciones como VIH o hepatitis.\n\n**Cómo la Ayudaron**  \nLos médicos decidieron hacer una cirugía para quitar el útero, llamada histerectomía abdominal. La operación fue complicada porque el tejido estaba muy cambiado y era difícil saber dónde estaban las partes normales. Durante la cirugía, se lastimó un conducto que lleva la orina desde el riñón a la vejiga, pero lo repararon en el mismo momento. Después de la operación, la paciente mejoró y pudo volver a casa. En el control dos semanas después, estaba bien y sin problemas.\n\n**Por Qué es Importante Este Caso**  \nEste caso es especial porque la inversión uterina es rara y no se sabe exactamente qué la causó en esta mujer. Además, ella llegó al hospital muy tarde, cuando la situación ya era difícil de tratar. La cirugía fue complicada, pero al final tuvo un buen resultado. Esto muestra la importancia de buscar ayuda médica a tiempo cuando se tiene una masa o bulto en el cuerpo.",
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+        "text": "Resumen para Público General Educado\n\nContexto  \nUna mujer de 54 años, originaria de una zona rural, acudió al hospital tras presentar durante tres años una masa que sobresalía por su vagina. Esta masa fue creciendo lentamente y, en sus primeros años, estuvo acompañada de sangrado y secreción con mal olor, aunque estos síntomas desaparecieron en el último año. La paciente había tenido dos partos en casa, asistida por una comadrona tradicional, sin complicaciones aparentes. Debido a la masa y a una herida (laceración) que apareció en ella hace seis meses, la paciente sufrió aislamiento social y divorcio. Finalmente, fue llevada al hospital por familiares para recibir atención médica.\n\nHallazgos Clínicos  \nAl examen físico, se encontró una masa de color rosado ubicada aproximadamente a 7 centímetros del borde del himen (la membrana que rodea la entrada de la vagina). La parte principal de esta masa correspondía al fondo uterino, que es la parte superior del útero. En la masa había una herida longitudinal de unos 5 centímetros, pero no se observó sangrado ni secreción en ese momento. Los signos vitales de la paciente estaban dentro de rangos normales y los análisis de sangre y orina no mostraron alteraciones significativas. La ecografía abdominal no logró visualizar el útero en su posición habitual, lo que apoyó el diagnóstico.\n\nDiagnóstico e Interpretación Clínica  \nSe diagnosticó a la paciente con inversión uterina crónica, una condición poco común en la que el útero se voltea hacia adentro y puede protruir a través de la vagina. En este caso, la inversión era completa y prolongada, lo que causó la formación de la masa visible y la laceración en su superficie. La causa exacta que originó esta inversión uterina no pudo ser identificada, lo que hace este caso especialmente relevante.\n\nTratamiento y Evolución  \nDespués de discutir las opciones con la paciente y su familia, se decidió realizar una histerectomía abdominal, que consiste en la extirpación quirúrgica del útero a través del abdomen. Durante la cirugía, se encontró que el tejido estaba muy distorsionado y redundante, lo que dificultó la identificación de las estructuras anatómicas normales. Esto llevó a una complicación quirúrgica: una lesión en el uréter derecho (el conducto que conecta el riñón con la vejiga), que fue reparada mediante una anastomosis (unión quirúrgica) de extremo a extremo. La paciente fue dada de alta diez días después de la operación, con mejoría clínica, y en el control posterior mostró una recuperación satisfactoria, con un canal vaginal normal.\n\nImportancia del Caso  \nEste caso destaca la presentación tardía y poco común de una inversión uterina crónica en una mujer rural, así como las dificultades quirúrgicas asociadas a esta condición. La ausencia de atención médica temprana y la falta de acceso a centros de salud contribuyeron a la evolución prolongada y compleja del caso. La experiencia subraya la necesidad de mejorar el acceso a servicios médicos y la educación sanitaria en áreas rurales para prevenir complicaciones graves.",
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+    "article": "Varón de 20 años, HIV negativo, con TB pulmonar y tratamiento irregular en 2020-2021. Se internó por síndrome de impregnación bacilar, dolor e impotencia funcional del hombro derecho. Presentaba mal estado general, adelgazado, hipotrofia muscular grave, lesiones tumorales frías fluctuantes fistulizadas en dorso, calota craneana y tórax anterior con secreción caseosa, sin presentar déficits motores ni sensitivos. El examen molecular rápido (GeneXpert Mtb/Rif) de secreción del tórax fue positivo para Mycobacterium tuberculosis, sensible a rifampicina (el antibiograma fenotípico mostró una cepa pansensible). La TC demostró consolidaciones pulmonares y árbol en brote, junto con el compromiso óseo de columna cervical, dorsal y lumbar con imágenes líticas y colecciones pre y paraespinales. En la RMN se observaron imágenes infiltrativas desde C4 a C6; D4 a D6, D9 a D12; fractura patológica de D6 y D10 e infiltración en L1, L2 y L3. Inició tratamiento anti-TB con esquema estándar de primera línea (isoniacida, rifampicina, pirazinamida, etambutol). Dada la extensa destrucción y el peligro de cuadriplejía/paraplejía por el compromiso cervical y/o dorsal, se indicó posición decúbito dorsal permanente, collar de Filadelfia, asistencia kinésica y conducta neuroquirúrgica en forma programada en los niveles cervicales, D6 y D10. Previo a la cirugía programada presentó un cuadro agudo de paraplejía con nivel sensitivo D8, con compromiso vesical. Se interpretó como nivel de compresión aguda en D6. Se indicó neurocirugía de urgencia con descompresión medular vía posterior con laminectomía dorsal 6 y parcialmente D5 y 7 y evacuación de una colección epidural. Fue recuperando la función motora y sensitiva en forma progresiva. Posteriormente se realizó la cirugía programada cervical vía anterior con corporectomía de C4, C5, C6 y C7 más artrodesis de C3 a D1 con reemplazo de cuerpo vertebral más injerto autólogo, placa y tornillos. En la TC de control se evidenció luxación posterior de D6 con compresión del canal espinal y deterioro neurológico por compresión medular. Se reconsideró la táctica quirúrgica debido a la inestabilidad mecánica y neurológica. Se realizó descompresión y alineación del nivel luxado con artrodesis posterior de los tres niveles espinales no adyacentes, cervical, dorsal 6 y dorsal 10 en un solo tiempo quirúrgico. Se fijó desde  C3 hasta D12 con tornillos poliaxiales y barra de transición cervicodorsal. En cada tiempo quirúrgico se evidenció evacuación espontánea de material caseoso, BAAR positivo, y se realizaron lavados profusos.  Presentó mejoría clínica, bacteriológica y resolución de las lesiones pulmonares. Recuperó movilidad con rehabilitación kinésica sumada al tratamiento específico (3 meses de primera fase e indicación de continuación con isoniacida y rifampicina hasta completar los 12 meses). Egresó caminando por sus propios medios, luego de una prolongada internación de 5 meses.",
+    "gold_summary": "Se presenta el caso de un varón de 20 años con espondilitis tuberculosa multinivel no contigua (cervical, dorsal 6, dorsal 10 y lumbar). Se trata de un paciente HIV negativo con tuberculosis diseminada con grave compromiso de su estado general y múltiples localizaciones de la enfermedad. Algunas tenían fistulas que secretaban caseum. El paciente presentó paraplejía aguda que requirió, teniendo en cuenta el nivel sensitivo a nivel dorsal 6, una primera cirugía urgente de descompresión por vía posterior. Luego se efectuó la cirugía programada. En primera instancia, la región cervical por vía anterior, con corporectomía, colocación de reemplazo de cuerpo vertebral más injerto autólogo y placa con tornillos. Posteriormente se evidenció luxación del nivel dorsal 6 hacia atrás comprimiendo la médula espinal y, dada la inestabilidad mecánica, se indicó un tercer tiempo quirúrgico por vía posterior que comprendió reducción, descompresión y fijación, resolviendo los tres niveles por vía posterior con barras y tornillos. El tratamiento quirúrgico, médico y kinésico de esta forma poco frecuente del mal de Pott fue exitoso, con recuperación de su estabilidad mecánica y progresiva recuperación de su estado neurológico.",
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+        "text": "Había un joven de 20 años muy enfermo con un hueso del cuello y la espalda roto por una infección. Esta infección era muy fuerte y estaba en muchos lugares de su cuerpo. A veces, de sus heridas salía una cosa blanda y fea. \n\nUn día, el joven no pudo mover sus piernas. Los doctores hicieron una operación rápida para ayudar a su espalda y que pudiera sentir y mover mejor. Después, le hicieron otra operación para arreglar los huesos del cuello con partes nuevas y tornillos. \n\nLuego, vieron que un hueso de su espalda estaba fuera de lugar y apretaba la parte que mueve y siente el cuerpo. Entonces, hicieron otra operación para poner todo en su lugar con barras y tornillos. \n\nCon medicinas, ejercicios y las operaciones, el joven mejoró mucho. Ahora puede caminar y está más fuerte. Los doctores están contentos porque él está mejor.",
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+        "text": "**Caso de Tuberculosis en la Columna Vertebral**\n\nEste es el caso de un joven de 20 años que tenía tuberculosis, una infección causada por una bacteria llamada Mycobacterium tuberculosis. Aunque no tenía VIH, la infección estaba muy extendida y afectaba varias partes de su columna vertebral: el cuello (cervical), la parte media de la espalda (dorsal) y la zona baja (lumbar). Algunas áreas tenían heridas abiertas que soltaban una sustancia llamada caseum, que es un material parecido a queso que se forma por la infección.\n\n**Problemas y Tratamiento Inicial**\n\nEl paciente sufrió una pérdida súbita de movimiento y sensibilidad en las piernas, llamada paraplejía, debido a que la médula espinal estaba comprimida en la zona dorsal 6 (parte media de la espalda). Por eso, tuvo que someterse a una cirugía urgente para aliviar la presión en la médula, llamada descompresión, realizada por la parte trasera de la columna.\n\nDespués, se hizo una cirugía programada en el cuello, por la parte delantera, donde se removieron varios cuerpos vertebrales dañados (corporectomía). Para reemplazarlos, se usaron injertos, que son partes de hueso tomadas del propio paciente, junto con placas y tornillos para estabilizar la columna.\n\n**Complicación y Cirugía Final**\n\nMás adelante, se descubrió que una vértebra en la zona dorsal 6 se había desplazado hacia atrás, presionando otra vez la médula espinal y causando inestabilidad en la columna. Por esta razón, se realizó una tercera cirugía por la parte trasera para corregir el desplazamiento, aliviar la presión y fijar la columna con barras y tornillos desde el cuello hasta la parte media de la espalda.\n\n**Resultado**\n\nCon el tratamiento combinado de medicamentos para la tuberculosis, cirugías y rehabilitación física, el paciente mejoró mucho. Recuperó la estabilidad de su columna y la función de sus piernas, pudiendo caminar por sí mismo después de una larga hospitalización de cinco meses. Este caso muestra cómo, aunque la tuberculosis en la columna puede ser grave y complicada, un tratamiento adecuado puede llevar a una buena recuperación.",
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+        "text": "**Contexto**  \nSe describe el caso de un joven de 20 años, sin infección por VIH, que presentó tuberculosis pulmonar y ósea diseminada, con afectación de múltiples niveles de la columna vertebral (cervical, dorsal y lumbar) en forma no contigua. El paciente tenía un estado general muy deteriorado, con pérdida de peso, atrofia muscular severa y lesiones tumorales en la piel que secretaban material caseoso (una sustancia similar a queso, típica de la tuberculosis). Estas lesiones estaban fistulizadas, es decir, comunicadas con el exterior, en regiones como el dorso, el cráneo y el tórax anterior.\n\n**Hallazgos Clave**  \n- Confirmación microbiológica de Mycobacterium tuberculosis sensible a rifampicina y otros antibióticos habituales.  \n- Imágenes de tomografía computarizada y resonancia magnética que mostraron consolidaciones pulmonares, lesiones óseas líticas (áreas de destrucción ósea) en varios niveles vertebrales y colecciones (acumulaciones de líquido o pus) pre y paraespinales.  \n- Fracturas patológicas en las vértebras dorsales D6 y D10, con infiltración tumoral desde C4 a C6, D4 a D6, D9 a D12 y L1 a L3.  \n- Episodio agudo de paraplejía (pérdida de movimiento y sensibilidad en las piernas) con nivel sensitivo en D8 y compromiso vesical, atribuible a compresión medular aguda en D6.\n\n**Interpretación Clínica**  \nEl paciente presentó una forma grave y poco común de tuberculosis ósea conocida como mal de Pott, con afectación de múltiples niveles vertebrales no contiguos. La destrucción ósea extensa y la presencia de colecciones pusieron en riesgo la integridad neurológica, con riesgo de parálisis permanente. La paraplejía aguda requirió una intervención quirúrgica urgente para descomprimir la médula espinal mediante laminectomía (extirpación de parte de la vértebra) y evacuación de la colección epidural. Posteriormente, se realizó una cirugía programada en la región cervical por vía anterior, que incluyó la extracción de varios cuerpos vertebrales afectados (corporectomía), reconstrucción con injerto óseo autólogo y fijación con placa y tornillos. Sin embargo, se detectó una luxación posterior en D6 que comprimía nuevamente la médula, causando inestabilidad mecánica y deterioro neurológico. Esto motivó una tercera cirugía por vía posterior para reducir la luxación, descomprimir la médula y fijar los niveles cervical y dorsales afectados con tornillos y barras, estabilizando la columna desde C3 hasta D12.\n\n**Próximos Pasos y Evolución**  \nEl tratamiento combinado, que incluyó terapia antituberculosa estándar de primera línea durante al menos 12 meses, intervenciones quirúrgicas escalonadas y rehabilitación kinésica intensiva, permitió la recuperación progresiva de la función motora y sensitiva del paciente. Además, se logró la resolución de las lesiones pulmonares y la estabilidad mecánica de la columna vertebral. Tras una prolongada hospitalización de cinco meses, el paciente egresó caminando por sus propios medios, evidenciando una evolución favorable en un caso complejo y de alta gravedad.",
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+    "article": "Un hombre japonés de 23 años fue admitido en nuestro hospital debido al empeoramiento de la disnea de esfuerzo. Había mostrado dificultad para correr a los dos años y se le diagnosticó EDMD con una mutación genética de LMNA (Lamin A/C) en el exón 1 de leucina 102 a prolina. De acuerdo con las manifestaciones típicas de EDMD, sus codos, rodillas y tendones de Aquiles se habían contraído a los cinco años, y sus músculos cervicales posteriores se habían vuelto rígidos; sin embargo, continuó con su vida diaria habitual, aunque con una leve restricción de ejercicio. Su padre también había sido diagnosticado con EDMD y murió repentinamente a los 40 años.\n\nCuando el paciente tenía 19 años, fue admitido en un hospital por primera vez debido a una insuficiencia cardiaca congestiva. Los signos de insuficiencia de la RV, tales como edema de las piernas y congestión hepática, fueron prominentes, como lo indica el alto nivel de bilirrubina en sangre (2,5 mg/dL). La ecocardiografía mostró que la excursión sistólica del plano anular tricúspide (TAPSE) era de 5,7 mm, la velocidad de la RV de 5,1 cm/s y el cambio del área fraccional de la RV (RVFAC) del 19 %, lo que indica una marcada disfunción de la RV. Se introdujeron diuréticos de alta dosis además de carvedilol (10 mg/día) y enalapril (2,5 mg/día). A pesar de esos medicamentos, fue readmitido debido al empeoramiento de la insuficiencia de la RV.\n\nA los 22 años, se le implantó un desfibrilador cardioversor implantable (ICD) debido a su taquicardia ventricular no sostenida (VT) y a la historia familiar de muerte súbita cardiaca. En este momento, el cateterismo cardiaco derecho (RHC) mostró una presión de la cuña de la arteria pulmonar (PAWP) de 22 mmHg, presión auricular derecha (RAP) de 17 mmHg, e índice de trabajo de accidente cerebrovascular ventricular derecho (RVSWI) de 6.47, lo que sugiere una disfunción severa sostenida del RV. Como tal, el fallo del RV probablemente fue la principal condición patológica a lo largo de su curso clínico.\n\nTenía insuficiencia cardiaca sintomática con la clasificación III de la New York Heart Association con dosis máximas de medicación guiada por directrices, y su electrocardiograma mostraba un ritmo sinusal regular y bloqueo de rama izquierda con ancho QRS (150 ms). Su fracción de eyección del ventrículo izquierdo (LVEF) era ≤35 % en la ecocardiografía. Por lo tanto, se consideró que estaba indicado para CRT y se le actualizó a ICD a los 23 años.\n\nAl ingreso, su presión arterial era de 106/65 mmHg y su frecuencia cardíaca de 60 latidos/min con un ritmo regular. El examen físico reveló un tercer sonido cardíaco y un soplo pan sistólico (Levine II/VI) en la región apical. Los sonidos respiratorios eran claros, mientras que una vena yugular distendida y un edema de miembros inferiores eran evidentes. La radiografía de tórax indicó un aumento de la relación cardiotorácica (59%) sin congestión pulmonar.\n\nEl electrocardiograma mostró un ritmo biventricular debido a la TRC. La ecocardiografía reveló una ligera dilatación en ambos ventrículos (diámetro final diastólico del LV: 54 mm, diámetro del RV: 50 mm) con una reducción de la LVEF (30%). La función del RV también se redujo, como lo indican una reducción de la RVFAC (11%) y un bajo TAPSE (8 mm). Ambos ventrículos agrandados causaron una pérdida de sujeción y coaptación de las valvas que resultó en una regurgitación mitral moderada y una regurgitación tricuspídea severa. La vena cava inferior se dilató a 23 mm con una reducción de la fluctuación respiratoria.\n\nEn los hallazgos histológicos de los músculos cervicales posteriores realizados más tarde en la autopsia, se observó un aumento en la variación del tamaño de la fibra muscular con una infiltración moderada de tejido conectivo, lo que fue compatible con la EDMD. Los análisis de sangre revelaron péptido natriurético cerebral (BNP) 196.1 pg/mL, bilirrubina total 1.4 mg/dL, aspartato aminotransferasa (AST) 39 U/L, alanina aminotransferasa (ALT) 43 U/L, y gamma glutamil transpeptidasa (gamma-GTP) 451 U/L, lo que sugirió una disfunción hepática. Aunque las arterias coronarias estaban intactas en la angiografía, una biopsia endocárdica del VD reveló una hipertrofia cardiaca con un aumento de la magnitud del núcleo y el miocardio.\n\nLa microscopía electrónica demostró hallazgos típicos de la EDMD: un número reducido de miofibrillas, necrosis y la formación de pseudo- o verdaderas inclusiones. Dado que se descartaron otras cardiomiopatías secundarias mediante estos hallazgos clínicos e histológicos, diagnosticamos una cardiomiopatía relacionada con la EDMD.\n\n\nEl curso clínico del paciente. El cateterismo cardiaco derecho (RHC) en el día 11 mostró disfunción y congestión severa del LV/RV, y se iniciaron algunos inótropos. Aunque la hemodinámica del paciente mejoró, su función renal empeoró progresivamente en el día 38. Preocupados por el empeoramiento de su función renal debido a la disminución de la presión arterial, se iniciaron la dopamina y el soporte mecánico (IABP y CRRT), y la función renal y la hemodinámica del paciente mejoraron. Sin embargo, desarrolló insuficiencia hepática aguda junto con insuficiencia severa del RV indicada por los datos del RHC en el día 68. Aunque se introdujo ECMO veno-atrial en el día 71, la disfunción hepática y la DIC causaron diátesis hemorrágica sistémica, y el paciente falleció por fallo multiorgánico en el día 100. CRRT: terapia de reemplazo renal continua, DIC: coagulación intravascular diseminada, ECMO: oxigenación por membrana extracorpórea, IABP: bombeo de globo intraaórtico, LV: ventrículo izquierdo, RV: ventrículo derecho\n\nEl RHC en el día 11 mostró que el índice cardiaco (IC) era de 2,0 L/min/m2 (método de Fick), y la PAP era de 15 mmHg, lo que indicaba un subgrupo IV de Forrester. La presión arterial pulmonar (PAP) era de 29/12 (18) mmHg, y la RAP era de 15 mmHg. El RVSWI, uno de los parámetros hemodinámicos para la función del RV, se calculó con la siguiente fórmula: RVSWI (g·m/m2/latido)=[presión arterial pulmonar media (mPAP)-presión atrial derecha media (mRAP)]×índice de volumen de latido (SVI)×0.0136. Su RVSWI era de 1.36 g·m/m2/latido, lo que indicaba una disfunción severa del RV. Para compensar el síndrome de baja producción del paciente y la congestión, comenzamos una infusión continua de dobutamina (3.0 μg/kg/min) y añadimos milrinona (0.125 μg/kg/min) en el día 16.\n\n\nEn el día 32, los datos de RHC mejoraron, con un aumento del IC (2,48 L/min/m2), una reducción de la PAWP (13 mmHg) y un aumento de la RVSWI (2,8 g·m/m2/latido). Sin embargo, en el día 38, la función renal del paciente empeoró progresivamente, posiblemente debido a una presión venosa central alta (CVP) e hipotensión, ya que la presión arterial había sido de alrededor de 70/40 mmHg varios días antes del empeoramiento de la función renal. Para aumentar su presión arterial, se inició una infusión continua de dopamina (2,0 μg/kg/min); se redujo la milrinona y se interrumpieron el enalapril y la eplerenona. Además, se necesitaron temporalmente el bombeo de globo intraaórtico (IABP) y la terapia de reemplazo renal continuo (CRRT). A medida que la hemodinámica del paciente mejoró en respuesta al aumento de la saturación de oxígeno venoso mixto (SvO2, 70-80%) y el IC (3,0-3,5 L/min/m2), se retiraron el IABP y la CRRT en el día 45.\n\nSin embargo, el día 68, el IC volvió a disminuir a 1,25 l/min/m2 y la congestión pulmonar y la retención de fluidos del paciente se deterioraron; la PAWP era tan alta como la RAP, a 22 mmHg. Además, los niveles de bilirrubina en suero y las transaminasas hepáticas del paciente aumentaron drásticamente, lo que sugiere el desarrollo de insuficiencia hepática. El día 71, se inició la ECMO VA a través de una vena femoral a la arteria subclavia, pero debido a la diátesis hemorrágica sistémica acompañada por la coagulación intravascular diseminada (CID), el paciente falleció de insuficiencia multiorgánica el día 100.\n\nUna autopsia realizada con el consentimiento informado de la familia del paciente reveló un agrandamiento eferente en ambos ventrículos con un espesor de pared delgado. El examen histopatológico reveló que la hipertrofia miocárdica leve a moderada y la fibrosis severa eran evidentes en el RV y el LV. El peso del hígado aumentó significativamente a 2298 g, y se detectaron congestión hepática macroscópica y colestasis. En las imágenes microscópicas, el área de la vena porta apenas cambió, y se observó atrofia o pérdida de hepatocitos alrededor de las venas centrales, lo que indica un «hígado de shock». En los pulmones, se observó una hemorragia alveolar extensa, y se observó una colección de macrófagos que habían ingerido hemosiderina, lo que refleja una diátesis hemorrágica sistémica.\n\nMH - Adulto\nMH - Insuficiencia cardiaca/*etiología/fisiopatología/terapia\nMH - Humanos\nMH - Lamin tipo A/genética\nMH - Hombre\nMH - Distrofia muscular, Emery-Dreifuss/*complicaciones/diagnóstico/genética/terapia\nMH - Mutación\n",
+    "gold_summary": "Un hombre de 23 años tenía debilidad muscular progresiva y distrofia muscular de Emery-Dreifuss (EDMD) debido a una mutación de LMNA (lamina A/C). Insuficiencia cardiaca congestiva diagnosticada a los 19 años de edad. El tratamiento farmacológico máximo/resincronización cardiaca no logró mejorar la función cardiaca. Por lo tanto, fue hospitalizado debido a insuficiencia cardiaca. A pesar de la oxigenación por membrana extracorpórea, desarrolló una disfunción cardiaca derecha grave y falleció (fallo multiorgánico).\n",
+    "synthetic_summary_eval": {
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+        "text": "Había un hombre joven con músculos muy débiles. Tenía una enfermedad que hace que los músculos se pongan muy rígidos y duros. Su corazón también se puso muy cansado y no podía trabajar bien. Los doctores le dieron medicinas y una máquina para ayudar su corazón. Pero su corazón se puso peor y se enfermó mucho. Al final, su cuerpo no pudo seguir y él murió.",
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+        "text": "**Lo que le pasaba al paciente:**  \nUn joven japonés de 23 años tenía una enfermedad llamada distrofia muscular de Emery-Dreifuss (EDMD). Esta enfermedad afecta los músculos y está causada por un cambio en un gen llamado LMNA, que produce una proteína importante para las células. Desde pequeño, él tenía problemas para moverse bien y sus músculos se ponían rígidos. A los 19 años, comenzó a tener problemas graves en su corazón, especialmente en la parte derecha, lo que causaba insuficiencia cardiaca, es decir, que el corazón no podía bombear sangre correctamente.\n\n**Tratamientos y evolución:**  \nEl paciente recibió varios medicamentos para mejorar su corazón y un dispositivo llamado desfibrilador para prevenir ritmos cardiacos peligrosos. Más tarde, le pusieron un tratamiento llamado terapia de resincronización cardiaca, que ayuda a que las partes del corazón trabajen juntas mejor. Sin embargo, ninguno de estos tratamientos logró mejorar suficientemente la función de su corazón.\n\n**Lo que ocurrió en el hospital:**  \nFue ingresado en el hospital por empeoramiento de su insuficiencia cardiaca. Los médicos usaron máquinas especiales para ayudar a su corazón y a sus órganos, como la oxigenación por membrana extracorpórea (ECMO), que es un sistema que ayuda a oxigenar la sangre cuando el corazón y los pulmones no funcionan bien. A pesar de estos esfuerzos, su corazón derecho siguió fallando gravemente, lo que provocó que otros órganos también dejaran de funcionar, y lamentablemente falleció.\n\n**Qué significa este caso:**  \nEste caso muestra cómo la distrofia muscular de Emery-Dreifuss puede afectar no solo los músculos, sino también el corazón, causando insuficiencia cardiaca severa que es difícil de tratar. La mutación genética en LMNA juega un papel importante en esta enfermedad. Aunque existen tratamientos avanzados, en algunos casos la enfermedad puede progresar y causar complicaciones graves que llevan a la muerte.",
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+        "text": "**Contexto**  \nSe presenta el caso de un hombre japonés de 23 años con distrofia muscular de Emery-Dreifuss (EDMD), una enfermedad genética causada por una mutación en el gen LMNA que codifica la proteína lamina A/C. Esta mutación específica (leucina 102 a prolina en el exón 1) provocó debilidad muscular progresiva desde la infancia, contracturas articulares y rigidez muscular, manifestaciones típicas de esta enfermedad. Además, existía un antecedente familiar importante, ya que su padre también padeció EDMD y falleció súbitamente a los 40 años.\n\n**Hallazgos Clave**  \nA los 19 años, el paciente desarrolló insuficiencia cardíaca congestiva, principalmente por disfunción severa del ventrículo derecho (RV), evidenciada por síntomas como edema en las piernas y congestión hepática, así como por estudios ecocardiográficos y cateterismo cardíaco que mostraron una función ventricular deteriorada. A pesar de recibir tratamiento farmacológico intensivo con diuréticos, betabloqueantes y inhibidores de la enzima convertidora de angiotensina, la función cardíaca no mejoró. A los 22 años se le implantó un desfibrilador cardioversor implantable (ICD) debido a episodios de taquicardia ventricular y riesgo de muerte súbita.\n\nCuando la insuficiencia cardíaca progresó a una etapa avanzada (clasificación funcional III de la New York Heart Association), se le realizó una terapia de resincronización cardíaca (CRT) para mejorar la función del corazón. Sin embargo, al ingreso hospitalario a los 23 años, persistían signos de insuficiencia cardíaca derecha grave, con dilatación de ambos ventrículos, reducción significativa de la fracción de eyección del ventrículo izquierdo (LVEF 30%) y disfunción severa del ventrículo derecho, acompañada de insuficiencia valvular mitral y tricuspídea.\n\nDurante su hospitalización, el paciente presentó empeoramiento progresivo de la función renal y hepática, complicaciones que reflejaban la insuficiencia multiorgánica secundaria a la falla cardíaca avanzada. Se implementaron tratamientos de soporte hemodinámico, incluyendo infusiones de medicamentos inotrópicos, bombeo de globo intraaórtico (IABP), terapia de reemplazo renal continua (CRRT) y finalmente oxigenación por membrana extracorpórea (ECMO) veno-arterial. A pesar de estas intervenciones, desarrolló coagulación intravascular diseminada (CID) y una diátesis hemorrágica sistémica, que culminaron en su fallecimiento por fallo multiorgánico al día 100 de hospitalización.\n\n**Interpretación Clínica**  \nEste caso ilustra la evolución grave y progresiva de la insuficiencia cardíaca en un paciente con EDMD causada por una mutación en LMNA, destacando la predominancia de la disfunción del ventrículo derecho como factor principal en su deterioro clínico. La resistencia a los tratamientos convencionales y avanzados, como la terapia farmacológica máxima, resincronización cardíaca y soporte mecánico, refleja la complejidad y severidad de la cardiomiopatía asociada a esta enfermedad genética. Los hallazgos histopatológicos post mortem confirmaron la presencia de hipertrofia miocárdica, fibrosis severa en ambos ventrículos y daño hepático compatible con congestión crónica y “hígado de shock”.\n\n**Próximos Pasos y Consideraciones**  \nEste caso subraya la necesidad de un diagnóstico temprano y un seguimiento riguroso en pacientes con EDMD, especialmente aquellos con mutaciones en LMNA, dado el alto riesgo de insuficiencia cardíaca progresiva y muerte súbita. La identificación de disfunción ventricular derecha precoz podría orientar intervenciones más agresivas o la consideración temprana de trasplante cardíaco. Además, se requiere investigación continua para desarrollar terapias específicas que puedan modificar el curso de la cardiomiopatía en EDMD y mejorar la supervivencia y calidad de vida de estos pacientes.",
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+  {
+    "article": "Mujer de 65 años sin antecedentes patológicos destacables que en 2004 inició paroxismos lancinantes en los territorios V2 y V3 derechos, con desencadenantes clásicos, por lo que se le diagnosticó una neuralgia del trigémino derecho. En las resonancias magnéticas cerebrales hasta 2021 no se habían realizado las secuencias que permiten identificar si hay un cruce neurovascular. Desde el inicio, el control del dolor con carboxamidas fue difícil. En 2021 presentó exacerbación de los paroxismos previos que aparecieron en V1. La neuralgia se volvió refractaria, sin respuesta a las carboxamidas y la lamotrigina, y muy escasa al clonacepam, por lo que requirió perfusiones de fenitoína y/o lidocaína en las exacerbaciones graves. Simultáneamente inició paroxismos lancinantes en la parte posterior de la lengua y la pared lateral derecha de la orofaringe, que se exacerbaron con la deglución y que aumentaron progresivamente en intensidad y frecuencia. Se orientó como el inicio de una neuralgia del nervio glosofaríngeo derecho. Se repitió la resonancia magnética cerebral con secuencia CISS (del inglés, constructive interference in steady state), que mostró un contacto arterial significativo entre la arteria cerebelosa superior derecha y el origen del V par craneal derecho, y de la arteria cerebelosa anteroinferior con el origen de los pares craneales bajos derechos. Ante un caso de neuralgia del nervio trigémino y neuralgia del nervio glosofaríngeo clásicas, concomitantes y refractarias, se planteó una doble descompresión microvascular en un tiempo como mejor opción terapéutica.\n\nEn marzo de 2021 se realizó una craniectomía retrosigmoidea derecha con exposición de la cisterna perimesencefálica y las cisternas basales. Se procedió a la liberación del V par craneal, y se apreció un íntimo contacto con la arteria cerebelosa superior en su parte sensitiva y adelgazamiento en la zona de entrada de la raíz nerviosa. Se procedió a la colocación de teflón entre la arteria cerebelosa superior y el V par craneal en todo su trayecto. Posteriormente, se exploró la cisterna basal y se apreció loop vascular de la arteria cerebelosa anteroinferior en íntimo contacto con el IX par craneal, donde se colocó teflón y sellante dural encima. El postoperatorio cursó sin incidencias, con resolución completa de la neuralgia del nervio trigémino y reducción >50% de la intensidad de los paroxismos en el territorio glosofaríngeo. A los dos años continúa sin paroxismos trigeminales y presenta <1 paroxismo/mes de intensidad tolerable en el territorio glosofaríngeo desencadenado con la deglución. El tratamiento farmacológico continúa en pauta descendente sin que ello haya supuesto la reaparición de los paroxismos.",
+    "gold_summary": "Mujer de 65 años con NT derecho (inicialmente en V2-V3) desde 2004 con control regular con carboxamidas. Diecisiete años después empeoraron los paroxismos en V2-V3, aparecieron también en V1 y en el territorio del nervio glosofaríngeo derecho (oído derecho y fosa amigdalar al hablar y deglutir). La resonancia magnética cerebral mostró contacto arterial significativo entre arteria cerebelosa superior (ACS) con origen del V par craneal derecho y de la arteria cerebelosa antero-inferior (AICA) con el origen de pares craneales bajos derechos. Se realizó DMV de ambos pares craneales en un mismo tiempo quirúrgico mediante craniectomía retrosigmoidea, y se procedió a la liberación del V par craneal, en contacto íntimo con la ACS, y del IX par craneal en contacto con la AICA derecha, para lo que se puso teflón entre ellas. La paciente tuvo una resolución inmediata de los paroxismos trigeminales y una mejoría considerable en intensidad y frecuencia de los glosofaríngeos. A los 2 años de la intervención continúa la desescalada de tratamiento neuromodulador con buena respuesta.",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Había una señora de 65 años que tenía dolor fuerte en la cara desde hace mucho tiempo. El dolor estaba en un lado de su cara y a veces se hacía más fuerte. También empezó a dolerle la garganta y el oído cuando comía o hablaba.\n\nLos doctores le hicieron una foto especial de su cabeza. Vieron que unas partes de su cuerpo, que son como tubitos, estaban tocando nervios que causaban el dolor.\n\nEntonces, los doctores hicieron una operación para poner un pedacito suave entre los tubitos y los nervios. Esto ayudó mucho a que el dolor se fuera.\n\nDespués de la operación, la señora se sintió mucho mejor. El dolor casi no volvió y pudo tomar menos medicina. Está feliz y tranquila.",
+        "scores": {
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+          "ROUGE-2": 0.04953560371517028,
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
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+      "B2": {
+        "text": "**Lo que le Pasó a la Paciente**  \nUna mujer de 65 años tuvo un dolor muy fuerte y repentino en la cara desde 2004. Este dolor afectaba principalmente dos zonas de su cara, llamadas V2 y V3, que son partes del nervio trigémino, un nervio que ayuda a sentir la cara. A pesar de tomar medicamentos llamados carboxamidas para controlar el dolor, este empeoró después de muchos años. Además, el dolor apareció en otra zona llamada V1 y también en el área de la garganta y oído derecho, que están conectados con otro nervio llamado glosofaríngeo.\n\n**Lo que Encontraron en las Pruebas**  \nSe le hizo una resonancia magnética especial que mostró que dos arterias (vasos sanguíneos) estaban presionando los nervios afectados. Una arteria llamada cerebelosa superior estaba tocando el nervio trigémino, y otra llamada cerebelosa antero-inferior estaba en contacto con el nervio glosofaríngeo. Esta presión puede causar los dolores intensos que ella sentía.\n\n**Qué Hicieron para Ayudarla**  \nLos médicos realizaron una cirugía llamada descompresión microvascular. En esta operación, hicieron una pequeña apertura en el cráneo para llegar a los nervios y separar las arterias que los estaban presionando. Para evitar que las arterias volvieran a tocar los nervios, colocaron un material llamado teflón entre ellos.\n\n**Resultados Después de la Cirugía**  \nDespués de la operación, el dolor en la cara (del nervio trigémino) desapareció completamente. El dolor en la garganta y oído (del nervio glosofaríngeo) mejoró mucho, con menos intensidad y frecuencia. Dos años después, la paciente sigue mejor, con muy pocos episodios de dolor que puede controlar fácilmente y ha podido reducir los medicamentos que tomaba.\n\n**En Resumen**  \nEsta paciente tenía dolores fuertes causados por arterias que presionaban nervios en su cabeza. La cirugía para separar esas arterias de los nervios fue exitosa y mejoró mucho su calidad de vida.",
+        "scores": {
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
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+      "B3": {
+        "text": "**Contexto**  \nSe trata de una mujer de 65 años que desde 2004 presentaba episodios de dolor intenso y punzante en las ramas V2 y V3 del nervio trigémino derecho (que corresponden a zonas de la cara como el maxilar y la mandíbula). Estos episodios, conocidos como neuralgia del trigémino, inicialmente se controlaban con medicamentos llamados carboxamidas. Sin embargo, diecisiete años después, el dolor empeoró, extendiéndose también a la rama V1 (zona de la frente) y aparecieron nuevos episodios dolorosos en el territorio del nervio glosofaríngeo derecho, afectando áreas como el oído y la parte lateral de la garganta, especialmente al hablar y tragar.\n\n**Hallazgos Clave**  \nUna resonancia magnética cerebral con una técnica especial (secuencia CISS) reveló que dos arterias cerebrales —la arteria cerebelosa superior (ACS) y la arteria cerebelosa anteroinferior (AICA)— estaban en contacto directo y presionando los orígenes de los nervios afectados: la ACS sobre el nervio trigémino derecho y la AICA sobre los nervios craneales inferiores, incluido el nervio glosofaríngeo derecho.\n\n**Interpretación Clínica**  \nEsta compresión vascular es una causa conocida de neuralgias craneales, ya que la presión constante puede irritar los nervios y provocar los episodios de dolor intenso. En este caso, la paciente presentaba neuralgia del trigémino y neuralgia del glosofaríngeo simultáneamente, ambas resistentes al tratamiento farmacológico habitual.\n\n**Próximos Pasos y Tratamiento**  \nSe decidió realizar una cirugía llamada descompresión microvascular (DMV) en un solo procedimiento, mediante una craniectomía retrosigmoidea (una apertura quirúrgica en la parte posterior del cráneo). Durante la intervención, se liberaron ambos nervios de la presión arterial colocando pequeñas almohadillas de teflón entre las arterias y los nervios para evitar el contacto directo.  \n\n**Resultados y Seguimiento**  \nLa paciente experimentó una resolución inmediata de los episodios dolorosos relacionados con el nervio trigémino y una reducción significativa en la frecuencia e intensidad del dolor en el territorio del nervio glosofaríngeo. Dos años después de la cirugía, continúa con un tratamiento farmacológico en disminución y mantiene un control satisfactorio del dolor, con episodios muy esporádicos y tolerables en la zona glosofaríngea, especialmente al tragar.\n\nEste caso ilustra la importancia de identificar la compresión vascular en neuralgias craneales refractarias y la eficacia de la descompresión microvascular como tratamiento para mejorar la calidad de vida en pacientes con neuralgia del trigémino y del glosofaríngeo.",
+        "scores": {
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+          "ROUGE-2": 0.18390804597701146,
+          "ROUGE-L-Sum": 0.4058919803600654,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
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+        }
+      }
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+  },
+  {
+    "article": "Hombre de 36 años, bisexual, en profilaxis antirretroviral de pre-exposición al HIV, sin antecedentes de viaje, que refirió haber asistido a un evento donde tuvo contactos con parejas ocasionales cuya identidad y antecedentes se desconocen. Diez días después comenzó con fiebre, odinofagia y dolor cervical por lo que consultó en varias oportunidades, hasta que a los siete días del inicio de los síntomas se internó por persistencia de los mismos a pesar del tratamiento antibiótico indicado. Al ingreso presentó exudado faríngeo, adenopatías cervicales bilaterales dolorosas y pápulas umbilicadas en escroto y pene y pústulas en cara de cinco días de evolución. Se realizó tomografía computarizada de cuello con contraste endovenoso que descartó colección, ecografía abdominal con leve hepatoesplenomegalia, e inició tratamiento empírico con ceftriaxona y azitromicina. Se tomaron muestras para cultivo, para serologías, y escarificación de dos lesiones de la cara que se enviaron al Laboratorio Nacional de Referencia, INEI-ANLIS Dr. Carlos G. Malbrán, para PCR de punto final para Orthopoxvirus, con resultado DETECTABLE, confirmando así el diagnóstico de viruela símica. La secuenciación arrojó un alto porcentaje de homología con secuencias del clado de África Occidental (MPV-ARG003-2022, Genbank_ID ON800897). Otros diagnósticos diferenciales fueron descartados. El paciente evolucionó con aparición de una úlcera en lengua y nuevas lesiones asincrónicas en glúteos, región perianal, inguinal derecha, umbilical, frontal, cuello, mano derecha y dorso de pie en un total de no más de 25. En el laboratorio se constató un aumento de transaminasas en 2.2 veces el valor normal, sin otros datos significativos.  Por persistencia del dolor cervical se solicitó nueva tomografía computarizada a los 14 días del inicio de los síntomas que evidenció adenomegalias con centro hipodenso de aspecto necrótico, que no requirieron drenaje quirúrgico. Al día 17 se realizó PCR en muestras de exudado de fauces y semen las que también resultaron positivas para virus de viruela símica. Se externó con franca mejoría clínica dos días después. El paciente dio su consentimiento informado escrito para la publicación de este informe de caso y las imágenes que lo acompañan.",
+    "gold_summary": "Se trata de un hombre joven, bisexual, en profilaxis antirretroviral de pre-exposición al HIV, cuya forma de presentación fue faringitis exudativa sin otra etiología documentada y adenopatías que evolucionaron a la necrosis, presencia de lesiones asincrónicas características en cara, cuello, abdomen, extremidades y genitales. El diagnóstico fue por detección de ADN viral por reacción en cadena de la polimerasa en lesiones de piel, exudado de fauces y semen. El compromiso faríngeo con presencia de exudado luego del descarte de otras infecciones, podría ser una rareza para la forma epidémica de la enfermedad. El hallazgo del virus en semen ya reportado en otras publicaciones no es suficiente aún para confirmar la vía sexual como forma de trasmisión.",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Un hombre joven se enfermó con dolor de garganta y bultos en el cuello. También tuvo manchitas en la cara, cuello, barriga, brazos y partes íntimas. Los doctores encontraron un virus en su piel, en la garganta y en otra parte del cuerpo. Este virus es raro y puede causar estas manchas y dolor. Los doctores no están seguros si el virus se pasa por el contacto en el cuerpo. El hombre mejoró con ayuda de los doctores.",
+        "scores": {
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
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+          "BERTScore_R": NaN,
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+        }
+      },
+      "B2": {
+        "text": "**Caso de un Hombre Joven con Viruela Símica**\n\nEste informe habla de un hombre de 36 años que es bisexual y estaba tomando medicamentos para prevenir el VIH antes de enfermarse. Él empezó con dolor de garganta, fiebre y dolor en el cuello. Además, tenía ganglios inflamados y dolorosos en el cuello. También aparecieron pequeñas lesiones en la cara, el pene y el escroto, que son áreas del cuerpo donde se pueden ver bultos o manchas.\n\nPara saber qué tenía, los médicos hicieron varios estudios. Tomaron muestras de las lesiones en la piel y las analizaron con una prueba llamada PCR, que busca el ADN del virus. Encontraron que tenía el virus de la viruela símica, una enfermedad causada por un virus parecido a la viruela común, pero menos grave. También encontraron el virus en la garganta y en el semen del paciente.\n\nDurante su enfermedad, el hombre desarrolló más lesiones en diferentes partes del cuerpo, como los glúteos, la zona alrededor del ano, el cuello y las manos. Además, tuvo un aumento en algunas enzimas del hígado, lo que indica que el virus afectó un poco este órgano. En el cuello, los ganglios inflamados mostraron signos de daño, pero no fue necesario hacer cirugía.\n\nAunque el virus se encontró en el semen, todavía no está claro si la viruela símica se transmite por contacto sexual. El dolor y la inflamación en la garganta con pus (exudado) que tuvo este paciente no es común en los casos que se han visto en la epidemia actual, por lo que es un detalle importante para los médicos.\n\nDespués de recibir tratamiento, el paciente mejoró y pudo salir del hospital. Este caso ayuda a entender mejor cómo puede presentarse la viruela símica y qué síntomas buscar para hacer un diagnóstico correcto.",
+        "scores": {
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+          "BERTScore_R": NaN,
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+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe presenta el caso de un hombre de 36 años, bisexual, que utiliza profilaxis antirretroviral de pre-exposición (PrEP) para prevenir la infección por VIH. Sin antecedentes de viajes recientes, asistió a un evento donde tuvo contacto con parejas sexuales ocasionales de identidad y antecedentes desconocidos. Diez días después comenzó con fiebre, dolor de garganta (odinofagia) y dolor en el cuello, síntomas que persistieron a pesar de tratamiento antibiótico inicial, lo que motivó su hospitalización.\n\n**Hallazgos Clave**  \nAl ingreso, el paciente mostró inflamación y exudado en la garganta, ganglios linfáticos cervicales inflamados y dolorosos en ambos lados, además de lesiones cutáneas características: pápulas umbilicadas (con un centro hundido) en el escroto y pene, y pústulas en la cara con cinco días de evolución. Se realizaron estudios de imagen, incluyendo tomografía computarizada (TC) de cuello con contraste, que descartó abscesos, y ecografía abdominal que evidenció un leve aumento del tamaño del hígado y bazo (hepatoesplenomegalia). Se inició tratamiento empírico con antibióticos ceftriaxona y azitromicina.\n\nSe tomaron muestras para cultivos, serologías y escarificación (raspado) de lesiones cutáneas, las cuales fueron enviadas a un laboratorio de referencia para realizar una prueba de reacción en cadena de la polimerasa (PCR) específica para Orthopoxvirus, confirmando la presencia de ADN viral de viruela símica (monkeypox). La secuenciación genética mostró alta similitud con cepas del clado de África Occidental, que es menos virulento que otros clados. Se descartaron otras posibles infecciones que podrían explicar los síntomas.\n\nDurante la evolución clínica, aparecieron nuevas lesiones en diferentes partes del cuerpo (glúteos, región perianal, ingle derecha, abdomen, frente, cuello, mano derecha y dorso del pie), sumando un total de aproximadamente 25 lesiones. Además, desarrolló una úlcera en la lengua. En análisis de laboratorio se detectó un aumento moderado de las enzimas hepáticas (transaminasas), sin otros hallazgos relevantes. Debido a la persistencia del dolor cervical, se realizó una nueva TC a los 14 días que mostró ganglios linfáticos agrandados con áreas centrales de necrosis (muerte del tejido), pero sin necesidad de intervención quirúrgica.\n\nAl día 17, se confirmó la presencia del virus mediante PCR en muestras de exudado faríngeo y semen. Dos días después, el paciente fue dado de alta con una mejoría clínica notable.\n\n**Interpretación Clínica**  \nEste caso destaca una presentación atípica de viruela símica en un adulto joven que utiliza profilaxis antirretroviral para VIH. La enfermedad se manifestó inicialmente como una faringitis exudativa (inflamación de la garganta con pus), acompañada de adenopatías cervicales que evolucionaron a necrosis, un cuadro poco común en la epidemia actual. Las lesiones cutáneas asincrónicas (que aparecen en diferentes momentos) en múltiples regiones del cuerpo son características de esta infección.\n\nLa confirmación diagnóstica se realizó mediante detección del ADN viral en las lesiones de piel, así como en muestras de exudado faríngeo y semen. Aunque la presencia del virus en el semen ha sido reportada en otros estudios, todavía no es suficiente para afirmar que la transmisión sexual sea la vía principal de contagio.\n\n**Próximos Pasos**  \nEl seguimiento clínico debe incluir la vigilancia de la evolución de las lesiones y la resolución de la inflamación ganglionar. Es importante continuar investigando las vías de transmisión del virus para mejorar las estrategias de prevención, especialmente en poblaciones con riesgo elevado. Además, este caso resalta la necesidad de considerar la viruela símica en el diagnóstico diferencial de faringitis exudativa persistente en contextos epidemiológicos compatibles.",
+        "scores": {
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+  },
+  {
+    "article": "Paciente de sexo masculino de 23 años, natural de Itagüí - Colombia, antecedente familiar de muerte súbita de etiología no clara en abuelo a los 50 años, sin otros antecedentes familiares o personales de importancia. Venía en seguimiento externo por episodios sincopales a repetición con diagnóstico desde la infancia de disfunción del nodo sinusal sintomática por lo que se le implantó un marcapaso.\n\nDurante controles posteriores no hay reporte de deterioro de clase funcional hasta el año 2012 en Guayaquil-Ecuador. Durante su hospitalización se realiza el cambio de generador; en el primer mes postoperatorio presenta como complicación temprana una infección de bolsillo de marcapaso por lo que requirió el explante de la unidad generadora con posterior abandono de electrodo ventricular previamente implantado. Se realiza un nuevo implante de marcapaso en el lado contralateral sin complicaciones ni registro de nuevos eventos sincopales en los siguientes 10 años de seguimiento.\n\nSeis meses antes del ingreso presentaba deterioro de clase funcional NYHA III, sin otros síntomas y sin reportes de evaluaciones por servicio de electrofisiología desde el último implante de generador de marcapaso en 2012. Durante controles ambulatorios se reportó la suspensión del tratamiento con beta bloqueador debido a la pobre tolerancia.\n\nAl examen físico se encontró soplo sistólico en foco aórtico II/VI sin irradiación, no presentó signos de congestión central o periférica. Dentro de los laboratorios no se evidenció alteración en función renal, electrolítica ni del perfil hematológico. Se programó el marcapaso con evidencia de agotamiento de la batería de generador. Se realizó un ecocardiograma transtorácico donde se encontró hipertrofia concéntrica severa del septum interventricular a nivel medio ventricular, de 26 mm con gradiente intracavitario pico de 117 mmHg y movimiento sistólico anterior del velo mitral (SAM) el cual generaba una regurgitación mitral leve.\n\nFue evaluado por Heart Team, debido al score de riesgo de muerte súbita (16,8%) además de tener antecedentes familiares de muerte súbita considerando EUROSCORE II 0,67%; en cuanto a los electrodos abandonados previamente y la contraindicación de realización de resonancia magnética cardiaca, dado a la incompatibilidad del marcapaso, se realiza un estudio tomográfico y se consideró la realización de miectomía por sintomatología y variante documentada.\n\nFue programado para realización de miectomía medio ventricular por abordaje transapical con retiro de electrodos; se realizó la ventriculotomía izquierda en el ápex, con posterior resección del septum desde el parte medio ventricular hasta la base, con posterior retiro de electrodos adheridos a velo septal tricúspideo. No hubo complicaciones intraoperatorias y posteriormente se presentó disminución del gradiente intracavitario sin presencia del fenómeno SAM. Durante su estancia en Unidad de Cuidados Intensivos el paciente cursó con dos episodios documentados de taquicardia ventricular con inestabilidad hemodinámica por lo cual se le colocó un cardiodesfibrilador implantable (CDI) compatible con resonancia magnética (MRI) ST Jude sin presentar nuevos episodios de TV. El paciente cursó sin nuevas intercurrencias y se iniciaron los estudios ambulatorios de estudio genético debido a sus antecedente familiares.\n\nEl paciente presentó una evolución posoperatoria favorable luego del implante de CDI. En los estudios genéticos se encontró una variante, probablemente patogénica, en heterocigosis del FLNC, c 4636G>A consistente con miocardiopatía familiar hipertrófica tipo 26 autosómica dominante.\n\nActualmente, el paciente se encuentra en clase funcional I, sin arritmias evidenciadas en la telemetría y en tratamiento regular con Bisoprolol 5 mg. Se inició ampliación de estudio genético a familiares directos, sin embargo, debido al difícil acceso a servicios de salud su ejecución fue limitada.",
+    "gold_summary": "A continuación, se presenta el caso de un paciente sexo masculino de 23 años con diagnóstico de cardiomiopatía hipertrófica variante medio apical, en quien se documenta variante de la filamina C, ante la inadecuada respuesta y persistencia de sintomatología frente al manejo médico, se realizó el procedimiento de miectomía con abordaje transapical, con posterior mejoría de sintomatología clínica y obstrucción al tracto de salida.",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Un joven de 23 años tenía un problema en su corazón. Su corazón era más grueso en una parte. Esto le hacía sentir mal y cansado.\n\nLos doctores le hicieron una operación para quitar un poco de ese corazón grueso. Después de la operación, se sintió mejor y su corazón pudo trabajar mejor.",
+        "scores": {
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+      },
+      "B2": {
+        "text": "**Caso de un joven con problema en el corazón**\n\nEste es el caso de un joven de 23 años que tiene una enfermedad llamada cardiomiopatía hipertrófica. Esto significa que una parte de su corazón, especialmente en la zona media y hacia el ápice (la punta), está más gruesa de lo normal. Esta enfermedad puede dificultar que la sangre salga bien del corazón.\n\n**Qué encontraron en sus genes**\n\nAl hacerle un estudio genético, descubrieron que tiene un cambio en un gen llamado filamina C. Este cambio puede causar problemas en el corazón y es una forma hereditaria de la enfermedad.\n\n**Tratamiento y resultados**\n\nEl joven no mejoraba con los medicamentos que le daban, así que los doctores decidieron hacer una cirugía llamada miectomía. En esta operación, quitaron parte del músculo grueso del corazón para que la sangre pueda salir mejor. La cirugía se hizo por la punta del corazón (abordaje transapical).\n\nDespués de la operación, el paciente mejoró mucho. Su corazón ya no tenía tanta obstrucción y sus síntomas disminuyeron. Actualmente, está en buen estado y sigue un tratamiento con medicamentos para cuidar su corazón.",
+        "scores": {
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+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
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+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe trata de un paciente masculino de 23 años, originario de Itagüí, Colombia, con antecedentes familiares relevantes de muerte súbita en su abuelo a los 50 años, sin otras enfermedades familiares o personales significativas. Desde la infancia, el paciente presentaba episodios repetidos de síncope (pérdida temporal del conocimiento) atribuibles a una disfunción del nodo sinusal (una alteración en el sistema eléctrico del corazón), por lo que se le implantó un marcapasos. Durante años, su condición se mantuvo estable hasta que en 2012, en Guayaquil, Ecuador, presentó una infección relacionada con el marcapasos que requirió la extracción del generador y el implante de uno nuevo en el lado opuesto, sin complicaciones posteriores ni nuevos episodios de síncope durante una década.\n\nSeis meses antes del ingreso actual, el paciente comenzó a mostrar un deterioro en su capacidad funcional (clasificación NYHA III, que indica limitación marcada en la actividad física), aunque sin otros síntomas adicionales. Se suspendió el tratamiento con betabloqueadores debido a mala tolerancia. En el examen físico se detectó un soplo cardíaco leve, sin signos de insuficiencia cardíaca. Los análisis de laboratorio fueron normales. El marcapasos mostró agotamiento de la batería, y el ecocardiograma reveló una hipertrofia severa y concéntrica del septum interventricular (pared que separa las cámaras del corazón), con un grosor de 26 mm y un gradiente de presión muy alto (117 mmHg) dentro del ventrículo, además de un movimiento anormal del velo mitral que causaba una regurgitación leve (retorno de sangre hacia la aurícula).\n\n**Hallazgos Clave**  \n- Hipertrofia severa del septum interventricular medio ventricular con obstrucción significativa al flujo sanguíneo dentro del ventrículo izquierdo.  \n- Movimiento sistólico anterior del velo mitral (SAM), que contribuye a la obstrucción y regurgitación mitral leve.  \n- Antecedentes familiares de muerte súbita y un riesgo calculado de muerte súbita del 16,8%, lo que indica un riesgo elevado.  \n- Imposibilidad de realizar resonancia magnética cardíaca debido a la incompatibilidad con el marcapasos y la presencia de electrodos abandonados.  \n- Confirmación genética de una variante probablemente patogénica en el gen FLNC (filamina C), asociada a miocardiopatía hipertrófica familiar tipo 26, que se hereda de forma autosómica dominante.\n\n**Interpretación Clínica**  \nEl paciente presenta una forma de miocardiopatía hipertrófica con predominio medio apical, caracterizada por un engrosamiento anormal del músculo cardíaco que obstruye el flujo de salida del ventrículo izquierdo y genera síntomas significativos. La variante genética encontrada en filamina C explica la naturaleza hereditaria y progresiva de su enfermedad. La persistencia de síntomas y la obstrucción significativa a pesar del tratamiento médico justificaron la realización de una miectomía medio ventricular (cirugía para remover parte del músculo engrosado), realizada mediante un abordaje transapical (a través del ápex del corazón). La cirugía fue exitosa, con reducción del gradiente de presión y desaparición del movimiento anormal del velo mitral.\n\nPosteriormente, el paciente presentó episodios de taquicardia ventricular (arritmias peligrosas) que requirieron la implantación de un cardiodesfibrilador implantable (CDI) compatible con resonancia magnética, para prevenir muerte súbita. Tras el implante, no se registraron nuevos episodios arrítmicos y el paciente evolucionó favorablemente.\n\n**Próximos Pasos**  \nActualmente, el paciente se encuentra en clase funcional I (sin limitaciones en la actividad física), sin arritmias detectadas en monitoreo continuo, y en tratamiento con bisoprolol (un betabloqueador) a dosis de 5 mg. Se ha iniciado un estudio genético ampliado en familiares directos para identificar portadores de la variante genética, aunque el acceso limitado a servicios de salud ha dificultado la realización completa de este estudio. El seguimiento continuo y la evaluación genética son fundamentales para el manejo integral del paciente y su familia, con el fin de prevenir complicaciones graves como la muerte súbita.",
+        "scores": {
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
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+  },
+  {
+    "article": "Varón de 32 años, con antecedentes de infección por VIH en terapia anti-retroviral (carga viral indetectable y recuento de CD4 de 454 céls/mm3) y consumo de tabaco y drogas (marihuana, éxtasis y ketamina). Consultó en nuestra unidad de salud sexual por una historia de dos semanas de secreción uretral de aspecto mucoso con escaso ardor local, asociado a una úlcera eritematosa indurada en el surco balanoprepucial de 1,5 cm de diámetro, dolorosa y exudativa. Al examen físico presentaba una adenopatía inguinal izquierda de 2 cm, sensible a palpación, blanda, no adherida a planos profundos ni asociada a signos inflamatorios cutáneos. No presentaba fiebre ni otros síntomas asociados. En la anamnesis dirigida, refirió 20 parejas sexuales hombres en el último año, con relaciones sexuales orales y anales insertivas y receptivas, con uso ocasional de preservativo. No tenía antecedente de viajes fuera de Chile. Cuatro semanas antes del inicio de los síntomas, había tenido un contacto sexual de riesgo sin preservativo con una pareja contactada mediante una aplicación de telefonía móvil. Con el diagnóstico presuntivo de una sífilis primaria y uretritis en estudio, se tomaron muestras de sangre y secreción uretral para estudio microbiológico. Por la conducta sexual de alto riesgo, se tomó también un hisopado anorrectal para tinción de Gram y cultivo. De acuerdo con la norma vigente en Chile, se administraron tres dosis de 2,4 millones de UI de penicilina benzatina intramuscular separadas por una semana, además de 250 mg de ceftriaxona intramuscular y 1 g de azitromicina oral, ambas por una vez. El estudio de laboratorio confirmó el diagnóstico de sífilis, con un VDRL (Venereal disease research laboratory) reactivo con dilución de 1:2 y MHA-TP (Microhemagglutination assay for antibody to Treponema pallidum) reactivo. La tinción de Gram y los cultivos de secreción uretral (agar sangre y Thayer Martin) fueron negativos. La muestra anorrectal mostró escasos diplococos gramnegativos en la tinción de Gram, con desarrollo abundante de N. meningitidis y microbiota comensal en el cultivo corriente. La identificación bacteriana se realizó a través de espectrometría de masas MALDI-TOF MS. El paciente evolucionó favorablemente, sin secreción uretral y con regresión de la lesión ulcerada genital y la adenopatía inguinal a las dos semanas de seguimiento. Las tinciones de Gram y los cultivos de control de secreción uretral, faríngea y anorrectal resultaron negativos. Se citó al contacto sexual reciente para estudio y tratamiento. Sin embargo, éste se encontraba asintomático y los cultivos faríngeo, anorrectal y uretral realizados fueron negativos.",
+    "gold_summary": "Presentamos el caso de un HSH con infección por VIH, que consultó por un cuadro de uretritis y sifilis primaria, en el cual se aisló N. meningitidis en una muestra anorectal. Fue tratado en forma empírica con ceftriaxona y azitromicina, realizándose un cultivo de control post-tratamiento que fue negativo.",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Un hombre con VIH tenía una herida y dolor al orinar. Los doctores encontraron una bacteria en su cuerpo. Le dieron medicinas para curarlo. Después, la bacteria ya no estaba. Él mejoró mucho.",
+        "scores": {
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+          "ROUGE-2": 0.0,
+          "ROUGE-L-Sum": 0.11363636363636365,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
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+      "B2": {
+        "text": "Caso de un hombre de 32 años con VIH que tuvo una infección en la uretra y una úlcera en el pene. Los médicos encontraron que tenía sífilis primaria, que es una infección de transmisión sexual. Además, en una muestra tomada del ano, detectaron una bacteria llamada Neisseria meningitidis, que normalmente no causa infecciones en esa zona. \n\nEl paciente recibió tratamiento con antibióticos llamados ceftriaxona y azitromicina para combatir las infecciones. Después del tratamiento, se hicieron pruebas de control y no encontraron más bacterias en las muestras tomadas de la uretra, la garganta y el ano. El paciente mejoró bien y la lesión en el pene y la inflamación en la ingle desaparecieron en dos semanas. \n\nEste caso muestra la importancia de revisar diferentes áreas del cuerpo en personas con conductas sexuales de riesgo y de usar tratamientos adecuados para varias posibles infecciones.",
+        "scores": {
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+          "ROUGE-2": 0.0966183574879227,
+          "ROUGE-L-Sum": 0.21052631578947364,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
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+      },
+      "B3": {
+        "text": "**Contexto**  \nSe trata de un hombre de 32 años que vive con infección por VIH controlada mediante tratamiento antirretroviral, con carga viral indetectable y un recuento adecuado de células CD4. Además, tiene antecedentes de consumo de tabaco y drogas recreativas. Consultó en una unidad de salud sexual debido a una secreción mucosa por la uretra y una úlcera dolorosa en el pene, acompañadas de inflamación en los ganglios linfáticos inguinales del lado izquierdo. No presentaba fiebre ni otros síntomas sistémicos. En la entrevista, refirió múltiples parejas sexuales masculinas en el último año, con prácticas sexuales orales y anales, y uso irregular de preservativos. Cuatro semanas antes, tuvo una relación sexual sin protección con una persona conocida a través de una aplicación móvil.\n\n**Hallazgos Clave**  \nSe sospechó inicialmente una sífilis primaria y una uretritis de origen incierto. Se tomaron muestras de sangre y secreción uretral para análisis microbiológicos, así como un hisopado anorrectal debido al alto riesgo sexual. El diagnóstico serológico confirmó sífilis, con pruebas VDRL y MHA-TP positivas. Los cultivos de secreción uretral fueron negativos para bacterias comunes causantes de uretritis. Sin embargo, en la muestra anorrectal se identificó la presencia de Neisseria meningitidis (una bacteria que normalmente habita en la garganta y que en este caso se encontró en el recto), confirmada mediante espectrometría de masas MALDI-TOF MS.  \n\n**Interpretación Clínica**  \nEl paciente fue tratado empíricamente con penicilina benzatina para la sífilis, además de una dosis única de ceftriaxona y azitromicina para cubrir posibles infecciones bacterianas de transmisión sexual. La detección de N. meningitidis en la muestra anorrectal es relevante, ya que esta bacteria no es un patógeno típico en uretritis, pero puede colonizar el tracto genital o anal, especialmente en personas con conductas sexuales de riesgo. El tratamiento fue efectivo, ya que a las dos semanas el paciente mostró resolución de la secreción uretral, cicatrización de la úlcera y desaparición de la inflamación ganglionar. Los cultivos posteriores fueron negativos, confirmando la erradicación de las infecciones.  \n\n**Próximos Pasos**  \nSe realizó el estudio y tratamiento del contacto sexual reciente para prevenir la transmisión y reinfección, aunque este contacto no presentó síntomas ni cultivos positivos. Este caso subraya la importancia de considerar agentes menos comunes como N. meningitidis en infecciones del tracto genital y anorrectal en personas con alto riesgo sexual, y la necesidad de un abordaje diagnóstico y terapéutico integral en estos pacientes.",
+        "scores": {
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
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+        }
+      }
+    }
+  },
+  {
+    "article": "Un paciente hispanoparlante de 63 años de edad se presentó en el hospital como una emergencia con inicio repentino de dificultad respiratoria severa, palpitaciones y sudoración profusa. Estaba en su estado habitual de salud y podía deambular con actividades independientes de la vida diaria hasta 30 minutos antes de su llegada a la sala de urgencias. Tenía un historial de 20 años de hipertensión, un historial de 15 años de diabetes mellitus, enfermedad de la arteria coronaria que requería la inserción de un stent de la arteria coronaria cinco años antes, un historial de diez años de insuficiencia cardiaca de la clase II de la New York Heart Association (NYHA) con una fracción de eyección reducida (EF) del 35 %, enfermedad renal crónica (CKD) en estadio 3B. Al ingresar en el hospital, sus medicamentos incluían carvedilol (25 mg dos veces al día), lisinopril (20 mg diario), espironolactona (25 mg diario), furosemida (20 mg diario), insulina glargina (20 unidades al acostarse), inyección de insulina lispro (7 unidades tres veces al día), atorvastatina (40 mg diario), y aspirina (81 mg diario), sin alergias a medicamentos conocidas.\n\nAl examen, su presión arterial era de 205/110 mmHg, su frecuencia respiratoria de 29 respiraciones/min, su frecuencia cardíaca de 118 latidos/min, la oximetría de pulso era de 82% (en aire ambiente) y su temperatura de 36.2°C. Su peso era de 72 kg y su estatura de 68 pulgadas, lo que resultó en un índice de masa corporal (IMC) de 24.13 kg/m2. Al examen físico, el paciente estaba en grave dificultad respiratoria, sudaba y no podía hablar con claridad. Su presión venosa yugular era elevada, como se muestra por la distensión de la vena yugular (3+). Al auscultar el tórax, se observaron crepitaciones bilaterales en todos los campos pulmonares. La auscultación cardíaca fue notable por un galope con una frecuencia regular y un murmullo sistólico 3/6 que se oía en la línea medioclavicular izquierda, al nivel del quinto espacio intercostal. El punto de impulso cardíaco máximo se desplazó hacia la izquierda (en la línea medioaxilar anterior) y no se observó distensión abdominal ni ascitis, con edema de los miembros inferiores (1+) hasta el nivel de la mitad de la pantorrilla.\n\nEl paciente fue trasladado a la zona de reanimación cardiopulmonar (RCP), donde se midieron los gases sanguíneos en el aire y se solicitaron pruebas de laboratorio. El paciente fue tratado con oxígeno al 100% utilizando una máscara no reanadora y se le colocó en posición de 90°, lo que produjo una mejora en la oximetría de pulso, que aumentó hasta el 90%. Un electrocardiograma (ECG) mostró taquicardia sinusal, depresión del ST del conductor lateral (de 1 mV), desviación del eje izquierdo e hipertrofia del ventrículo izquierdo. Se obtuvo una radiografía de tórax portátil que fue notable por una silueta cardiaca agrandada, señal de asta de ciervo de desviación venosa pulmonar del lóbulo superior (cefalización), y líneas B de Kerley, que indican edema intersticial.\n\nAunque se solicitaron pruebas de laboratorio, debido a que el paciente estaba gravemente enfermo y no se podía demorar el tratamiento, se inició un tratamiento inicial basado en los hallazgos clínicos, el historial clínico, el ECG, los gases arteriales en sangre y los hallazgos de rayos X. En vista de los hallazgos de las investigaciones iniciales y la ausencia de fiebre, se descartó la neumonía y se realizó un diagnóstico de edema pulmonar cardiogénico hipertensivo. Se inició un tratamiento intravenoso (IV) con nitroglicerina, comenzando a 30 mcg/min y aumentando en 15 mcg/min cada 3 minutos, con oximetría de pulso continua y monitoreo de los signos vitales cada 3 minutos. Después de 18 minutos, se tituló la nitroglicerina hasta 120 mcg/min y su presión arterial disminuyó a 148/82 mmHg, su presión arterial sistólica se redujo en un 29%, su presión arterial diastólica se redujo en un 25%, y su frecuencia cardíaca disminuyó a 87 latidos por minuto. Se hizo una rápida mejora clínica y el paciente pudo comunicarse con oraciones completas y pudo respirar sin el uso de músculos accesorios. La oximetría de pulso mostró una saturación de oxígeno >97%, y la suplementación de oxígeno continuó con el uso de una cánula nasal a 3 L/min y la medición de la oximetría de pulso del paciente fue >96%.\n\nDespués de 25 minutos, el paciente fue tratado con enalapril (2,5 mg IV) combinado con furosemida (20 mg IV). La nitroglicerina se redujo a una tasa de 10 mcg/min cada 5 minutos hasta que se interrumpió, seguido de una dosis oral de isosorbida dinitrato (30 mg). Después de la estabilización clínica completa, los resultados de los laboratorios mostraron un recuento de glóbulos blancos (WBC) de 11,43 × 109/uL, hemoglobina de 10,9 g/dl, hematocrito de 31,8%, plaquetas de 74 × 109/L, sodio de 144 mmol/L, potasio de 3,9 mmol/L, cloruro de 107 mmol/L, dióxido de carbono (CO2) de 25 mmol/L, nitrógeno ureico en sangre (BUN) de 27 mg/dL, creatinina de 1,4 mg/dL, péptido natriurético cerebral (BNP) de 3,452 pg/ml, y troponina I <0,05 ng/ml. Las mediciones de gases en sangre en aire incluyeron pH de 7,381, pCO2 de 44,8 mmHg, pO2 de 57 mmHg, HCO3 de 25,8 mmol/L, y saturación de oxígeno de 84%.\n\nSe evaluó al paciente para detectar la presencia de una posible embolia pulmonar (EP) subyacente, utilizando los criterios de estratificación de riesgo de EP de Wells, y se lo estratificó como de bajo riesgo, con una evaluación posterior con un nivel de dímero D de 340 ng/ml, que se interpretó como negativo. La evaluación para detectar hipertiroidismo mostró un valor normal de la medición ultrasensible del ensayo de la hormona estimulante de la tiroides en plasma (usTSH) de 2,56 μU/mL y tiroxina libre (T4) de 6,87 μU/mL.\n\nEl paciente fue admitido en la sala de hospital de medicina interna con un diagnóstico de edema pulmonar cardiogénico hipertensivo y fue dado de alta 48 horas después. Al momento del alta hospitalaria, su medicación incluía furosemida (40 mg diarios), carvedilol (12.5 mg dos veces al día), sacubitril/valsartan (24 mg/26 mg dos veces al día), espironolactona (25 mg diarios) e isosorbida mononitrato (60 mg diarios). El paciente fue sometido a seguimiento semanal por su cardiólogo, quien optimizó la terapia medicinal. No se registraron visitas a urgencias ni hospitalizaciones, al menos durante los siguientes 60 días.\n\nMH - Insuficiencia cardiaca/*complicaciones\nMH - Humanos\nMH - Hipertensión/*complicaciones\nMH - Infusiones, intravenosas\nMH - Hombre\nMH - Edad Media\nMH - Nitroglicerina/*administración y dosificación\nMH - Edema pulmonar/*terapia farmacológica/etiología\nMH - Insuficiencia respiratoria/*terapia farmacológica/etiología\nMH - Agentes vasodilatadores/*administración y dosificación\n",
+    "gold_summary": "Paciente: Hombre, 63 años\n\nDiagnóstico final: Edema pulmonar cardiovenoso hipertensivo\n\nSíntomas: falta de aire\n\nMedicación: —\n\nProcedimiento clínico: —\n\nEspecialidad: Medicina general e interna\n\nUn hombre hispano de 63 años con antecedentes de hipertensión, enfermedad de las arterias coronarias, insuficiencia cardiaca con una fracción de eyección reducida del 35 %, enfermedad renal crónica (ERC) y diabetes mellitus, se presentó como una emergencia con disnea aguda y grave. El paciente fue tratado inicialmente con 100 % de oxígeno suplementario y nitroglicerina intravenosa (IV) en dosis altas (30 mcg/min), que se ajustó cada 3 minutos, aumentando en 15 mcg/min hasta que se alcanzó una dosis de 120 mcg/min. Después de 18 minutos de terapia agresiva, la condición del paciente mejoró y ya no necesitaba ventilación mecánica.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Había un hombre de 63 años que se sentía muy mal. Le costaba mucho respirar y estaba muy cansado. Tenía problemas en el corazón y en los riñones desde hace tiempo.\n\nCuando llegó al hospital, le dieron aire con una máscara para ayudarlo a respirar mejor. También le pusieron un medicamento por la vena para que su corazón y su cuerpo se sintieran mejor.\n\nDespués de un rato, el hombre empezó a respirar mejor y se sintió más tranquilo. Los doctores cuidaron mucho de él y lo ayudaron a mejorar.",
+        "scores": {
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+      "B2": {
+        "text": "**Caso de un Hombre de 63 Años con Problemas del Corazón y Dificultad para Respirar**\n\n**Lo que Pasó:**  \nUn hombre de 63 años, que hablaba español y tenía varias enfermedades como presión alta (hipertensión), diabetes, problemas en las arterias del corazón y una enfermedad llamada insuficiencia cardíaca (que significa que su corazón no bombeaba bien la sangre), llegó al hospital muy enfermo. De repente, empezó a tener mucha dificultad para respirar, su corazón latía rápido y sudaba mucho. Antes de esto, estaba bien y podía hacer sus actividades normales.\n\n**Lo que Encontraron:**  \nAl examinarlo, su presión arterial estaba muy alta y tenía signos claros de que su corazón estaba trabajando mal. También tenía líquido en los pulmones, lo que se llama edema pulmonar, y eso dificultaba que el oxígeno llegara a su cuerpo. Las pruebas mostraron que su corazón estaba agrandado y que había problemas en la circulación de la sangre en sus pulmones.\n\n**Qué Hicieron para Ayudarlo:**  \nLe dieron oxígeno puro para que pudiera respirar mejor y empezaron a darle un medicamento llamado nitroglicerina por vía intravenosa (directamente en la vena). La nitroglicerina ayuda a bajar la presión arterial y a que el corazón trabaje menos. Comenzaron con una dosis baja y la aumentaron poco a poco cada pocos minutos. Después de 18 minutos, el paciente mejoró mucho: su presión bajó, su corazón latía más despacio y pudo respirar sin tanta dificultad. Ya no necesitó una máquina para ayudarlo a respirar.\n\n**Después del Tratamiento:**  \nLuego le dieron otros medicamentos para el corazón y para eliminar el exceso de líquido. El paciente se quedó en el hospital dos días y después pudo irse a casa. Continuó con controles médicos semanales y no volvió a tener problemas graves en los siguientes dos meses.\n\n**Resumen:**  \nEste caso muestra cómo un hombre con varias enfermedades del corazón y otros problemas puede sufrir una emergencia grave llamada edema pulmonar, que es cuando se acumula líquido en los pulmones por problemas del corazón. Con un tratamiento rápido y adecuado, que incluye oxígeno y medicamentos para bajar la presión y ayudar al corazón, el paciente pudo recuperarse sin complicaciones mayores.",
+        "scores": {
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+      "B3": {
+        "text": "**Contexto**  \nUn hombre hispanoparlante de 63 años con antecedentes médicos complejos, incluyendo hipertensión arterial de larga evolución, diabetes mellitus, enfermedad coronaria con colocación previa de stent, insuficiencia cardíaca crónica con función del corazón reducida (fracción de eyección del 35 %) y enfermedad renal crónica en estadio avanzado, acudió al hospital en estado de emergencia debido a un inicio súbito de dificultad respiratoria severa, palpitaciones y sudoración intensa. Hasta poco antes de su ingreso, el paciente se encontraba en su estado habitual de salud y realizaba actividades cotidianas de forma independiente.\n\n**Hallazgos Clave**  \nAl examen físico, el paciente presentaba signos evidentes de insuficiencia cardíaca descompensada: presión arterial muy elevada (205/110 mmHg), frecuencia cardíaca rápida (118 latidos por minuto), dificultad respiratoria grave con saturación de oxígeno baja (82 % en aire ambiente), distensión venosa yugular marcada, crepitaciones pulmonares bilaterales, y un galope cardíaco junto con un soplo sistólico. La radiografía de tórax mostró cardiomegalia (aumento del tamaño del corazón), signos de congestión pulmonar y edema intersticial, confirmando la sospecha clínica de edema pulmonar cardiogénico hipertensivo. El electrocardiograma evidenció taquicardia sinusal, hipertrofia ventricular izquierda y cambios isquémicos.\n\nLos análisis de laboratorio posteriores revelaron un péptido natriurético cerebral (BNP) muy elevado (3,452 pg/ml), indicador de insuficiencia cardíaca descompensada, y una troponina normal, descartando daño cardíaco agudo. Se descartaron otras causas de dificultad respiratoria aguda, como embolia pulmonar e infecciones pulmonares, mediante pruebas específicas y criterios clínicos.\n\n**Interpretación Clínica**  \nEl cuadro clínico y los estudios complementarios fueron consistentes con un episodio agudo de edema pulmonar cardiogénico hipertensivo, una condición en la que la presión arterial muy alta y la insuficiencia cardíaca provocan acumulación rápida de líquido en los pulmones, dificultando la respiración. La rápida identificación y tratamiento de esta emergencia fueron cruciales para evitar complicaciones mayores.\n\n**Tratamiento y Evolución**  \nEl manejo inicial incluyó la administración de oxígeno al 100 % mediante máscara no reanimadora y la colocación del paciente en posición sentada para facilitar la respiración. Se inició tratamiento intravenoso con nitroglicerina, un vasodilatador que reduce la presión arterial y la carga sobre el corazón, comenzando con una dosis de 30 microgramos por minuto y aumentando progresivamente hasta 120 microgramos por minuto en 18 minutos. Esta terapia permitió una reducción significativa de la presión arterial y de la frecuencia cardíaca, con una mejora clínica rápida: el paciente pudo respirar sin dificultad y comunicarse con normalidad, y su saturación de oxígeno superó el 97 % con oxígeno suplementario.\n\nPosteriormente, se administraron enalapril (un inhibidor de la enzima convertidora de angiotensina) y furosemida (un diurético) por vía intravenosa para continuar el control de la presión arterial y eliminar el exceso de líquido. La nitroglicerina se fue disminuyendo hasta suspenderla, y se inició tratamiento oral con isosorbida dinitrato para mantener la vasodilatación.\n\nEl paciente fue hospitalizado en la unidad de medicina interna, donde se ajustó su tratamiento con medicamentos para insuficiencia cardíaca, incluyendo furosemida, carvedilol (un betabloqueador), sacubitril/valsartán (un inhibidor de la neprilisina combinado con un bloqueador del receptor de angiotensina), espironolactona (un antagonista de la aldosterona) e isosorbida mononitrato. Tras 48 horas de hospitalización, se dio de alta en condiciones estables y con seguimiento cardiológico programado.\n\n**Próximos Pasos y Seguimiento**  \nDurante al menos 60 días posteriores al alta, el paciente no requirió nuevas hospitalizaciones ni visitas a urgencias, lo que indica una adecuada respuesta al tratamiento y control de su enfermedad cardíaca. El seguimiento semanal con su cardiólogo permitió optimizar la terapia médica para prevenir futuras descompensaciones.\n\n---\n\nEste caso ilustra la importancia de un diagnóstico rápido y un manejo agresivo en pacientes con edema pulmonar cardiogénico hipertensivo, especialmente en aquellos con múltiples comorbilidades cardiovasculares y renales, para mejorar la supervivencia y la calidad de vida.",
+        "scores": {
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+          "ROUGE-2": 0.07932692307692307,
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
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+  },
+  {
+    "article": "Historial clínico\nUn niño de 12 años se presentó en nuestro hospital con un mes de historia de sensación de cuerpo extraño y una masa conjuntival pedunculada carnosa que creció con el tiempo. No había historia de trauma o lesiones similares en el otro lado del cuerpo. Se descubrió una masa pedunculada carnosa rosácea de 15 mm de la conjuntiva palpebral derecha durante un examen oftalmológico. La agudeza visual estaba dentro de los límites normales. Se diagnosticó al niño como papiloma de células escamosas pedunculadas y se le realizó una biopsia excisional de la lesión.\n\nHallazgos macroscópicos y microscópicos\nRecibimos un fragmento de tejido blanco grisáceo, pequeño, firme, ovoide, fijado en formalina, de 1,5 x 1 cm, para su análisis patológico. En las secciones microscópicas se encontró una lesión poliopóidea hiperplásica con múltiples quistes globulares en la submucosa conjuntival, junto con una importante infiltración inflamatoria constituida por linfocitos, células plasmáticas y neutrófilos, así como enormes esporangios de paredes gruesas con numerosas endosporas. Las endosporas se liberaron después de que algunos de los esporangios maduros se rompieran. La rinosporidiosis conjuntival se diagnosticó histopatológicamente. No hubo recurrencia ni signo de rinosporidiosis en el ojo ni en ninguna otra área del cuerpo en el último examen del paciente, que fue 7 meses después de la escisión quirúrgica.\n",
+    "gold_summary": "Un niño de 12 años con una masa conjuntival pedunculada carnosa fue llevado al Centro Médico de la Universidad de Jimma con un historial de un mes de sensación de cuerpo extraño. Al paciente se le diagnosticó un papiloma pedunculado de células escamosas y se le realizó una biopsia excisional de la lesión. Se encontró que la masa era una lesión polipoide hiperplásica con numerosos quistes globulares dentro de la submucosa conjuntival, rodeados por un infiltrado inflamatorio pesado de linfocitos, células plasmáticas y neutrófilos, así como grandes esporas de paredes gruesas con numerosas endosporas en secciones microscópicas. Se diagnosticó histopatológicamente rinosporidiosis conjuntival.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Un niño tenía una bolita en el ojo que le molestaba. Los doctores le quitaron la bolita para verla mejor. \n\nAl mirar la bolita con un microscopio, vieron que tenía muchas cositas pequeñas dentro. Estas cositas eran como unas semillas que no son buenas. \n\nLos doctores dijeron que el niño tenía una infección en el ojo llamada rinosporidiosis. Después de quitar la bolita, el niño estuvo bien y no volvió a tener problema.",
+        "scores": {
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B2": {
+        "text": "**Lo que pasó con el niño**  \nUn niño de 12 años tenía una sensación rara en el ojo y una masa blanda y rosada que crecía en la parte interna del párpado derecho. No había sufrido golpes ni tenía problemas similares en el otro ojo. Cuando lo revisaron, su vista estaba normal, pero encontraron esta masa que parecía un papiloma, que es un tipo de bulto benigno hecho de células de la piel.\n\n**Qué hicieron los médicos**  \nLe quitaron la masa para analizarla mejor. Esto se llama biopsia, que es cuando se saca un pedacito de tejido para estudiar qué es exactamente. En el laboratorio, vieron que la masa tenía muchas células inflamatorias, que son células que el cuerpo usa para defenderse cuando hay una infección o irritación. También encontraron estructuras llamadas esporangios, que son como pequeñas bolsas con esporas dentro. Las esporas son formas de reproducción de ciertos microorganismos.\n\n**Qué significa el diagnóstico**  \nEl análisis mostró que el niño tenía rinosporidiosis conjuntival, que es una infección causada por un microorganismo que forma esas esporas. Esta infección afecta la conjuntiva, que es la membrana que cubre el ojo y el interior del párpado. Después de quitar la masa, el niño no tuvo problemas ni volvió a tener la infección en el ojo ni en otras partes del cuerpo durante al menos siete meses.\n\n**En resumen**  \nEl niño tenía una infección poco común en el ojo que causó una masa. Gracias a la biopsia, los médicos pudieron identificar la infección y tratarla con cirugía, evitando que regresara.",
+        "scores": {
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nUn niño de 12 años acudió al hospital tras presentar durante un mes una sensación persistente de cuerpo extraño en el ojo derecho, acompañada de una masa carnosa y pedunculada (con un tallo que la une a la superficie) en la conjuntiva palpebral (la membrana que recubre el párpado). No había antecedentes de trauma ni lesiones similares en el otro ojo. La agudeza visual del niño era normal. Inicialmente, se sospechó que la lesión correspondía a un papiloma de células escamosas pedunculado, por lo que se decidió realizar una biopsia excisional para su análisis.\n\n**Hallazgos Clave**  \nEl tejido extraído, de aproximadamente 1,5 x 1 cm, fue examinado bajo el microscopio. Se observó una lesión polipoide hiperplásica (un crecimiento en forma de pólipo con aumento en el número de células) que contenía múltiples quistes globulares en la submucosa conjuntival (la capa debajo de la superficie de la conjuntiva). Además, había una intensa infiltración inflamatoria compuesta por linfocitos, células plasmáticas y neutrófilos, que son tipos de células del sistema inmunitario. De manera destacada, se identificaron grandes esporangios (estructuras que contienen esporas) con paredes gruesas, dentro de los cuales se encontraban numerosas endosporas (esporas internas). Algunas de estas esporas se liberaban tras la ruptura de los esporangios maduros.\n\n**Interpretación Clínica**  \nEl examen histopatológico confirmó que la masa no era un papiloma, sino que correspondía a una infección por rinosporidiosis conjuntival, una enfermedad causada por el microorganismo Rhinosporidium seeberi que afecta principalmente las mucosas y puede formar masas polipoides. Esta infección es poco común y se caracteriza por la presencia de esporangios con endosporas en el tejido afectado.\n\n**Próximos Pasos y Seguimiento**  \nTras la escisión quirúrgica completa de la lesión, el paciente fue monitoreado durante al menos siete meses, sin presentar recurrencia de la lesión ni signos de infección en el ojo ni en otras partes del cuerpo. Este seguimiento indica un buen pronóstico tras el tratamiento quirúrgico. Se recomienda continuar con controles periódicos para detectar cualquier posible reaparición.",
+        "scores": {
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+          "ROUGE-L-Sum": 0.3326488706365503,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
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+  {
+    "article": "Presentamos el caso clínico de un varón de quince años, sin antecedentes médicos ni intervenciones previas, que acude al servicio de urgencias de pediatría con clínica de vómitos y dolor abdominal epigástrico de cuatro días de evolución, manteniéndose afebril durante la evolución del cuadro.\n\nInicialmente fue manejado como gastroenteritis, pero ante la ausencia de mejoría, con persistencia del dolor abdominal de tipo cólico a nivel epigástrico y de los vómitos de aspecto bilioso, acude a urgencias para nueva valoración.\n\nA la exploración física el paciente presentaba aceptable estado general, se encontraba afebril, con signos leves de deshidratación. El abdomen se encontraba distendido, sin datos de peritonismo y con ruidos hidroaéreos disminuidos. La analítica no presentaba hallazgos significativos, realizándose una radiografía de abdomen con hallazgos sugestivos de obstrucción intestinal.\n\nDada la evolución se decide realizar una tomografía computarizada urgente, en la que se observó presencia de ascitis e importante dilatación de asas de intestino delgado, sugiriendo la interposición de un asa de intestino delgado en el inicio de la transcavidad de los epiplones, con cambio de calibre a nivel del hiato de Winslow.\n\nSe realizó intervención quirúrgica urgente, realizando inicialmente una laparoscopia exploradora. Se observaban asas de intestino delgado dilatadas, e íleon terminal, ciego y colon ascendente de calibre normal pero localizados en hipocondrio derecho, con el ciego muy móvil y sin presentar adherencias al espacio parietocólico derecho. Siguiendo proximalmente el íleon terminal, se observaron asas de intestino delgado de distinto calibre desde la profundidad de la teórica localización del hiato de Winslow. Se consiguió traccionar de ciego e íleon terminal hasta desplazarlos a fosa iliaca derecha, pero sin llegar a identificar correctamente el punto de cambio de calibre, ya que la interposición del borde inferior del hígado y la distensión de asas de intestino delgado dificultaban la técnica. Se intentó mejorar la visualización mediante punción percutánea de un asa dilatada para vaciar el gas, sin mejoría. Para asegurar la resolución del cuadro obstructivo se decidió realizar una laparotomía media supraumbilical. Al acceder a cavidad se evidenciaba el cambio de calibre en íleon, a unos 40 centímetros de la válvula ileocecal, con signos compatibles con herniación de un tramo de unos cinco centímetros de íleon a través de hiato de Winslow. En ambos extremos del asa herniada observamos la impronta congestiva del hiato sobre el asa (Fig. 3). Se identificó el hiato de Winslow, de calibre normal, por lo que no se realizó ninguna técnica preventiva para disminuir el riesgo de recidiva.\n\nDurante los primeros días del postoperatorio el paciente presentó un íleo paralítico, pudiendo retirar la sonda nasogástrica a los cinco días de la cirugía e iniciando tolerancia oral con buena respuesta. Simultáneamente desarrolló una colección pélvica que se manejó de forma conservadora con antibióticos, con buena evolución. Finalmente, el paciente fue dado de alta a los diez días de la intervención, con tránsito conservado, manteniéndose afebril y con buen estado general.\n\nActualmente el paciente está en seguimiento en consultas externas de cirugía pediátrica.",
+    "gold_summary": "Presentamos el caso clínico de un varón adolescente de 15 años sin antecedentes quirúrgicos previos, con clínica de dolor abdominal y vómitos, en el que la tomografía computarizada sugería un cuadro de obstrucción intestinal a causa de hernia interna a nivel del hiato de Winslow. Precisó de intervención quirúrgica mediante laparoscopia exploradora, reconvertida por mala visualización a laparotomía media supraumbilical, para reducción del asa de íleon herniada. Esta presentaba buen aspecto y no fue necesaria la resección intestinal. No se realizó ninguna técnica preventiva para disminuir el riesgo de recidiva. Postoperatoriamente, el paciente presentó una colección pélvica manejada de manera conservadora con antibióticos. Actualmente se encuentra en seguimiento en consultas externas de cirugía pediátrica.",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Un niño de 15 años tenía dolor en la barriga y vomitaba. Los doctores vieron que su intestino estaba tapado por un lugar raro. Hicieron una operación para ayudarlo. Sacaron el intestino que estaba atrapado y estaba bien. No cortaron nada. Después, el niño tuvo un poco de líquido en la barriga, pero con medicinas mejoró. Ahora está bien y los doctores lo revisan para que siga sano.",
+        "scores": {
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
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+      },
+      "B2": {
+        "text": "**Caso Clínico de un Adolescente con Dolor Abdominal y Vómitos**\n\nUn chico de 15 años, sin problemas médicos anteriores, llegó al hospital con dolor en la parte superior del abdomen y vómitos que duraban cuatro días. Al principio, pensaron que tenía gastroenteritis, una infección del estómago, pero como no mejoraba, le hicieron más pruebas.\n\n**Lo que Encontraron**\n\nUna radiografía y una tomografía computarizada (una imagen detallada del cuerpo) mostraron que tenía una obstrucción en el intestino delgado. Esto ocurrió porque una parte del intestino se había metido por un espacio llamado hiato de Winslow, causando una hernia interna. Una hernia interna es cuando un órgano se mueve a un lugar donde no debería estar dentro del cuerpo.\n\n**Qué Hicieron**\n\nEl equipo médico decidió operar para arreglar la obstrucción. Comenzaron con una cirugía por laparoscopia, que es una operación con pequeñas incisiones y una cámara, pero tuvieron que cambiar a una cirugía abierta para ver mejor. Encontraron el intestino atrapado, pero estaba sano, así que no fue necesario cortar ninguna parte. No hicieron ninguna técnica para evitar que la hernia volviera a aparecer porque el espacio por donde se metió el intestino tenía un tamaño normal.\n\n**Después de la Cirugía**\n\nDespués de la operación, el chico tuvo un problema llamado íleo paralítico, que significa que el intestino tardó en empezar a funcionar normalmente. También desarrolló una acumulación de líquido en la pelvis, llamada colección pélvica, que trataron con antibióticos sin necesidad de otra cirugía. Finalmente, el paciente mejoró y fue dado de alta después de diez días.\n\n**Situación Actual**\n\nAhora, el adolescente sigue en control con el equipo de cirugía pediátrica para asegurarse de que se recupere bien y no tenga problemas futuros.",
+        "scores": {
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+          "ROUGE-2": 0.1572052401746725,
+          "ROUGE-L-Sum": 0.34782608695652173,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
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+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe describe el caso de un adolescente de 15 años, sin antecedentes médicos ni quirúrgicos previos, que presentó durante cuatro días dolor abdominal en la parte superior del abdomen (epigastrio) acompañado de vómitos biliosos (con contenido similar a bilis), sin fiebre. Inicialmente fue tratado como una gastroenteritis, pero al no mejorar y mantener los síntomas, acudió nuevamente a urgencias.\n\n**Hallazgos Clave**  \nEn la evaluación física, el paciente estaba en buen estado general, afebril, con signos leves de deshidratación y abdomen distendido, pero sin signos de inflamación grave (peritonismo). Los ruidos intestinales estaban disminuidos. Los análisis de sangre no mostraron alteraciones significativas. Una radiografía abdominal sugirió la presencia de una obstrucción intestinal. Posteriormente, una tomografía computarizada (TC) reveló ascitis (líquido en la cavidad abdominal) y dilatación importante de las asas del intestino delgado, con una posible herniación interna a través del hiato de Winslow, un orificio natural en la cavidad abdominal.\n\n**Interpretación Clínica**  \nEl diagnóstico fue una hernia interna del intestino delgado a través del hiato de Winslow, una causa poco frecuente de obstrucción intestinal. Debido a la gravedad y persistencia de los síntomas, se decidió realizar una cirugía urgente. Inicialmente se intentó una laparoscopia exploradora (cirugía mínimamente invasiva), pero la visualización limitada y la distensión intestinal dificultaron la intervención, por lo que se convirtió a una laparotomía (cirugía abierta) supraumbilical media. Durante la cirugía se identificó un asa de íleon (parte final del intestino delgado) herniada a través del hiato de Winslow, con signos de congestión por la presión del hiato, pero sin daño irreversible, por lo que no fue necesaria la resección intestinal. El asa herniada fue reducida (devuelta a su posición normal). El hiato de Winslow tenía un tamaño normal, por lo que no se realizó ninguna maniobra para prevenir la recurrencia de la hernia.\n\nEn el postoperatorio, el paciente presentó un íleo paralítico (falta temporal de movimiento intestinal), que mejoró progresivamente, permitiendo retirar la sonda nasogástrica a los cinco días y comenzar la alimentación oral con buena tolerancia. Además, desarrolló una colección pélvica (acumulación localizada de líquido o pus) que se trató con antibióticos de forma conservadora, sin necesidad de intervención quirúrgica adicional. El paciente evolucionó favorablemente y fue dado de alta al décimo día después de la cirugía, manteniendo un buen estado general y sin fiebre.\n\n**Próximos Pasos**  \nActualmente, el paciente se encuentra en seguimiento ambulatorio en consultas de cirugía pediátrica para monitorizar su recuperación y detectar posibles complicaciones o recurrencias. Se mantiene estable y con tránsito intestinal conservado.",
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
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+          "BERTScore_R": NaN,
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+  {
+    "article": "Un niño de 23 meses de edad con encefalopatía isquémica hipóxica al nacer, con buen potencial motor cerebral y desarrollo psicomotor normal. Tenía antecedentes personales de miocardiopatía restrictiva y fue incluido en un programa de trasplante cardiaco cuando tenía 16 meses de edad. También fue necesario implantarle un dispositivo de asistencia biventricular Berlin Heart externo. Para evitar eventos embólicos, se le administró un tratamiento antiplaquetario doble y anticoagulante. Cuando tenía 23 meses de edad, presentó desconexión y hemiparesia derecha. Una tomografía computarizada (TC) mostró una arteria cerebral media (ACM) izquierda hiperdensa, así como un infarto parietotemporal derecho crónico. Su análisis de sangre mostró: glóbulos rojos 4.16 × 106 µ/L; hemoglobina 11.4 g/gL; tiempo de tromboplastina parcial activada (TTPA) 93 segundos y relación internacional normalizada (INR) 1.08.\n\nEl tratamiento trombolítico intravenoso estaba contraindicado debido al doble tratamiento antiplaquetario y anticoagulante a la dosis completa con heparina, por lo que se realizó una trombectomía intraarterial. Aunque el paciente tenía 23 meses de edad, se encontraba en el tercer percentil de la curva de peso (10 kg). Bajo anestesia general, se perforó la arteria femoral derecha y se colocó una funda 4F de 11 cm de largo (Cordis, Irlanda). Se usó un catéter vertebral Radiofocus 4F (Glidecath de Terumo, Bélgica) para confirmar la oclusión del segmento M1 de la MCA izquierda. La arteria se recanalizó mediante trombectomía mecánica con un stentriever utilizando el catéter vertebral 4F como tutor, colocándolo en el segmento petroso de la arteria carótida. Se usó un dispositivo Trevo XP Pro Vue de 3 mm x 20 mm (Stryker, Países Bajos), con un microcatéter Rapid Transit recto (Codman Neurovascular, Reino Unido), abriendo la arteria en una sola pasada. Se retiró todo el sistema (catéter tutor, microcatéter y stentriever) simultáneamente. En la prueba de control, se detectó una disección iatrogénica de la arteria carótida interna izquierda, que no tuvo importancia clínica, ya que el hemisferio izquierdo se irrigaba a través de la arteria comunicante anterior.\n\nUn mes después, se realizó con éxito el trasplante de corazón. La única secuela neurológica a largo plazo que surgió como resultado del accidente cerebrovascular fue la espasticidad del miembro superior derecho.\n\nMH - Cardiomiopatía, Dilatada/complicaciones/cirugía\nMH - Cardiomiopatía, restrictiva/complicaciones/cirugía\nMH - Angiografía cerebral\nMH - Procedimientos/métodos endovasculares\nMH - Mujer\nMH - Estudios de seguimiento\nMH - Insuficiencia cardiaca/*complicaciones/tratamiento\nMH - Trasplante de corazón\nMH - *Dispositivos de asistencia cardíaca\nMH - Humanos\nMH - Infantil\nMH - Hombre\nMH - Arteria cerebral media/imágenes diagnósticas\nMH - Estudios Retrospectivos\nMH - Ictus/complicaciones/diagnóstico por imágenes/cirugía\nMH - Resultado del tratamiento\n",
+    "gold_summary": "Un niño de 16 meses de edad con cardiomiopatía restrictiva que fue incluido en una lista para un trasplante cardiaco. A los 20 meses de edad, requirió un implante de un dispositivo de asistencia biventricular externo (Berlin Heart) y tuvo un accidente cerebrovascular en el hemisferio izquierdo a los 23 meses. Se utilizó un enfoque intraarterial y produjo buenos resultados clínicos. Un mes después, se realizó con éxito un trasplante cardiaco.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Había un niño que tenía un problema en su corazón. Tenía que esperar para recibir un corazón nuevo. Le pusieron una máquina para ayudar a su corazón a latir. Un día, su cerebro se enfermó un poco. Los doctores usaron una medicina especial para ayudar a su cerebro. Después, el niño recibió un corazón nuevo y se puso mejor.",
+        "scores": {
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+        "text": "**Lo que pasó con el niño**\n\nUn niño de 16 meses tenía un problema en el corazón llamado cardiomiopatía restrictiva, que hace que el corazón no funcione bien. Por eso, lo pusieron en una lista para recibir un trasplante de corazón. A los 20 meses, le pusieron un dispositivo especial llamado Berlin Heart, que ayuda al corazón a bombear sangre mientras espera el trasplante.\n\n**El problema del accidente cerebrovascular**\n\nCuando tenía 23 meses, el niño sufrió un accidente cerebrovascular, que es cuando una parte del cerebro no recibe suficiente sangre y se daña. En su caso, el problema ocurrió en el lado izquierdo del cerebro. Debido a que ya estaba tomando medicamentos para evitar coágulos, no se pudo usar un tratamiento común para este tipo de accidente.\n\n**El tratamiento que recibieron**\n\nLos médicos usaron una técnica llamada trombectomía intraarterial. Esto significa que, con anestesia, introdujeron un pequeño tubo por una arteria en la pierna para llegar hasta el cerebro y quitar el coágulo que bloqueaba la arteria. Lograron abrir la arteria en una sola vez y restaurar el flujo de sangre.\n\n**Qué pasó después**\n\nUn mes después del accidente, el niño recibió el trasplante de corazón que necesitaba. Como consecuencia del accidente cerebrovascular, quedó con un poco de rigidez en el brazo derecho, pero en general tuvo buenos resultados y pudo continuar con su tratamiento.\n\n**Por qué es importante este caso**\n\nEste caso muestra que, incluso en niños muy pequeños con problemas graves del corazón, es posible usar técnicas avanzadas para tratar accidentes cerebrovasculares y mejorar su salud antes de un trasplante.",
+        "scores": {
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+      "B3": {
+        "text": "**Contexto:**  \nSe presenta el caso de un niño de 23 meses con antecedentes complejos, incluyendo encefalopatía isquémica hipóxica al nacer con desarrollo psicomotor normal, y una cardiomiopatía restrictiva diagnosticada en la infancia. Debido a la gravedad de su insuficiencia cardíaca, fue incluido en un programa de trasplante cardiaco a los 16 meses. Posteriormente, a los 20 meses, se le implantó un dispositivo de asistencia ventricular biventricular externo (Berlin Heart) para apoyar la función cardíaca mientras esperaba el trasplante. Para prevenir la formación de coágulos, recibió tratamiento combinado con anticoagulantes y antiplaquetarios.\n\n**Hallazgos Clave:**  \nA los 23 meses, el niño presentó síntomas neurológicos agudos, incluyendo desconexión y hemiparesia (debilidad) en el lado derecho del cuerpo. Una tomografía computarizada reveló una obstrucción en la arteria cerebral media izquierda, responsable del suministro sanguíneo a una parte importante del cerebro, junto con un infarto crónico en el hemisferio derecho. Debido a que el tratamiento trombolítico intravenoso (que disuelve coágulos) estaba contraindicado por su régimen anticoagulante, se optó por una trombectomía mecánica intraarterial, un procedimiento endovascular que consiste en extraer el coágulo directamente desde la arteria afectada.\n\nDurante la intervención, realizada bajo anestesia general, se accedió a la arteria femoral derecha para introducir un catéter que permitió llegar hasta la arteria cerebral afectada. Se utilizó un dispositivo llamado stentriever para recuperar el flujo sanguíneo en una sola maniobra. Aunque se detectó una disección (una lesión en la pared arterial causada por el procedimiento), esta no tuvo consecuencias clínicas importantes debido a la circulación colateral cerebral. El procedimiento fue exitoso y permitió la recuperación del flujo en la arteria ocluida.\n\n**Interpretación Clínica:**  \nEste caso destaca la viabilidad y eficacia de la trombectomía mecánica en pacientes pediátricos con ictus isquémico, incluso en niños muy pequeños y con condiciones cardíacas complejas que contraindican el tratamiento trombolítico convencional. La intervención permitió minimizar el daño cerebral y preservar la función neurológica, limitando la secuela a una espasticidad en el brazo derecho.\n\n**Próximos Pasos:**  \nUn mes después de la recuperación del accidente cerebrovascular, el niño fue sometido con éxito a un trasplante de corazón, mejorando su pronóstico a largo plazo. El seguimiento neurológico y cardiológico continúa siendo fundamental para monitorizar la evolución y manejar posibles complicaciones futuras. Este caso aporta evidencia sobre el manejo multidisciplinario y personalizado en pacientes pediátricos con enfermedades cardíacas graves y complicaciones neurológicas.",
+        "scores": {
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+    "article": "Una mujer de 23 años de edad se presentó al departamento de urgencias con pérdida de conciencia y exceso de secreciones orales 2 horas después de la ingestión de un veneno no especificado. No tenía movimientos corporales anormales, fiebre, diarrea, vómitos o sudoración. Inicialmente la habían llevado a un hospital primario cercano, donde fue tratada por posible intoxicación por OP con atropina y cimetidina durante 3 días, antes de ser trasladada al hospital Saint Peter. Después de un interrogatorio exhaustivo, se descubrió que la paciente había consumido unos 30 ml de 2,4-D en un intento de suicidio, precipitado por problemas financieros. No tenía antecedentes conocidos de enfermedad psiquiátrica, intentos de suicidio, episodios depresivos o abuso de sustancias. No se observaron trastornos cardíacos, renales o metabólicos previos.\n\nAl llegar al departamento de urgencias, la paciente estaba inconsciente. Sus constantes vitales eran PR 110/min, BP 120/70 mmHg, RR 21/min, y SPO2 96% en aire ambiente. Los resultados del examen físico fueron notables: un GCS de 6 sobre 15, pupilas dilatadas y reactivas, extremidades inferiores hipertónicas e hiperreflexivas, y reflejo plantar ascendente. Tras la investigación inicial, el recuento completo de células sanguíneas, la prueba de la función renal, la prueba de la función hepática, y la glucosa en sangre aleatoria fueron normales. Su electrocardiograma mostró taquicardia sinusal, mientras que la radiografía de tórax no fue notable. El análisis de gases en sangre arterial y el nivel sérico de la toxina no pudieron determinarse, ya que ninguno de los medios de prueba estaba disponible en el hospital.\n\nLa paciente fue trasladada a la unidad de cuidados intensivos (UCI), se le introdujo una sonda para proteger las vías respiratorias y se le inició inmediatamente una diuresis alcalina forzada. Su evolución en la UCI fue notable por el desarrollo de una insuficiencia renal (creatinina 3,1 ml/dL [intervalo de referencia 0,5-1,2 mg/dL], BUN 133 mg/dL [intervalo de referencia 16,6-48,5 mg/dL], análisis de orina 3+ hemoglobina y muchos glóbulos rojos), debido a una rabdomiolisis inducida por toxinas (nivel de creatina fosfocinasa de 1330 µg/L). Posteriormente, la paciente se volvió hipotensa y se le inició un tratamiento con vasopresores. La ecocardiografía y la ecografía abdominal no fueron significativas. A pesar de estos esfuerzos, falleció por colapso circulatorio el tercer día de estancia en la UCI.\n",
+    "gold_summary": "Aquí se informa sobre el caso de una joven granjera de la zona rural de Etiopía que fue internada en un hospital local tras perder el conocimiento y presentar exceso de secreciones orales 2 horas después de haber ingerido, de manera suicida, un agente tóxico desconocido. Originalmente, se la trató por intoxicación con organofosforados y luego se la trasladó al Hospital Saint Peter's en Addis Abeba para recibir atención médica más intensiva. Allí, se confirmó la ingesta de 2,4-D y se le brindó atención médica de apoyo, ventilación mecánica y diuresis alcalina forzada. A pesar de estas intervenciones, falleció varios días después.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Una joven tomó un veneno para hacerse daño. Se puso muy mal y perdió el conocimiento. La llevaron al hospital para ayudarla. \n\nLos doctores le dieron medicinas y la cuidaron mucho. Pero su cuerpo no pudo mejorar. Después de unos días, ella murió. \n\nLos doctores hicieron todo lo que pudieron para ayudarla.",
+        "scores": {
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
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+      "B2": {
+        "text": "Caso de Intoxicación Grave en una Joven\n\nUna mujer de 23 años de una zona rural de Etiopía tomó un veneno llamado 2,4-D con la intención de suicidarse. Dos horas después, perdió el conocimiento y tenía mucha saliva. Al principio, pensaron que había tomado otro tipo de veneno y la trataron en un hospital pequeño. Luego, la llevaron a un hospital más grande llamado Saint Peter para recibir mejor atención.\n\nLo que Encontraron en el Hospital\n\nCuando llegó, la paciente estaba inconsciente y tenía signos de daño en sus nervios y músculos. Los exámenes de sangre y orina mostraron que sus riñones no funcionaban bien y que había daño muscular grave, causado por el veneno. Los médicos intentaron ayudarla con tratamientos para limpiar el veneno y proteger sus órganos, incluyendo ponerle un tubo para ayudarla a respirar.\n\nQué Pasó Después\n\nA pesar de los esfuerzos médicos, la paciente empeoró. Su presión sanguínea bajó mucho y los médicos tuvieron que usar medicamentos para mantenerla estable. Finalmente, después de tres días en cuidados intensivos, falleció debido a un fallo en su circulación sanguínea.\n\nImportancia del Caso\n\nEste caso muestra lo peligroso que puede ser el veneno 2,4-D y cómo puede afectar seriamente el cuerpo, especialmente los riñones y los músculos. También destaca la importancia de un diagnóstico correcto y tratamiento rápido en casos de intoxicación para intentar salvar vidas.",
+        "scores": {
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+          "ROUGE-2": 0.1364829396325459,
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+          "BERTScore_R": NaN,
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+      "B3": {
+        "text": "**Contexto**\n\nSe presenta el caso de una mujer joven de 23 años, proveniente de una zona rural de Etiopía, que ingresó al hospital tras perder el conocimiento y mostrar un exceso de secreciones orales aproximadamente dos horas después de ingerir intencionalmente una sustancia tóxica. Inicialmente fue atendida en un hospital local donde se sospechó intoxicación por organofosforados (un tipo común de pesticida) y recibió tratamiento con atropina y cimetidina durante tres días. Posteriormente, fue trasladada al Hospital Saint Peter en Addis Abeba para recibir cuidados más especializados.\n\n**Hallazgos Clave**\n\nEn el hospital de referencia se confirmó que la sustancia ingerida era 2,4-D, un herbicida tóxico. Al ingreso, la paciente estaba inconsciente con un nivel de conciencia muy bajo (Glasgow Coma Scale de 6/15), presentaba pupilas dilatadas pero reactivas, hipertonicidad (aumento anormal del tono muscular) y reflejos exagerados en las extremidades inferiores, así como un reflejo plantar anormal (reflejo de Babinski positivo). Sus signos vitales mostraban taquicardia (frecuencia cardíaca rápida), presión arterial y saturación de oxígeno dentro de rangos aceptables. Los análisis iniciales de sangre, función renal y hepática, así como glucosa, fueron normales. Sin embargo, no se pudieron medir niveles específicos de la toxina ni gases en sangre debido a limitaciones del hospital.\n\nDurante su estancia en la unidad de cuidados intensivos (UCI), la paciente fue intubada para proteger sus vías respiratorias y se inició diuresis alcalina forzada, una técnica para ayudar a eliminar la toxina a través de la orina. A pesar de esto, desarrolló insuficiencia renal aguda, evidenciada por un aumento significativo de creatinina y nitrógeno ureico en sangre, así como presencia de hemoglobina y glóbulos rojos en la orina. Además, presentó rabdomiólisis (descomposición del tejido muscular) inducida por la toxina, confirmada por niveles elevados de creatina fosfocinasa, una enzima muscular. Posteriormente, la paciente sufrió hipotensión (presión arterial baja) que requirió el uso de medicamentos vasopresores para mantener la presión arterial. Estudios de ecocardiografía y ecografía abdominal no mostraron alteraciones significativas.\n\n**Interpretación Clínica**\n\nLa intoxicación por 2,4-D es poco común pero grave, y puede causar daño multisistémico, incluyendo alteraciones neurológicas, musculares y renales. En este caso, la rápida progresión hacia insuficiencia renal y colapso circulatorio refleja la alta toxicidad de esta sustancia y la dificultad para manejar sus complicaciones, incluso con tratamiento intensivo y medidas de soporte avanzadas.\n\n**Próximos Pasos**\n\nEste caso subraya la importancia de un diagnóstico preciso y rápido en intoxicaciones, especialmente en regiones con recursos limitados. La disponibilidad de pruebas específicas para identificar toxinas y la implementación temprana de tratamientos dirigidos podrían mejorar el pronóstico. Además, es fundamental fortalecer la atención en salud mental y los servicios de prevención del suicidio para evitar intentos con sustancias altamente tóxicas.",
+        "scores": {
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
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+  {
+    "article": "Una paciente etíope de 35 años de edad se presentó en el departamento de urgencias del Colegio Médico del Hospital Yekatitit 12 con síntomas de falta de aire en reposo, ortopnea, disnea paroxística nocturna significativa, dolor torácico, tos productiva teñida de sangre y vómitos de materia ingerida (2-3 episodios por día) durante 2 semanas. Presentaba una hinchazón progresiva del cuerpo que comenzó en las extremidades inferiores y luego afectó a todo el cuerpo, fatigabilidad fácil, pérdida de apetito, fiebre intermitente de alto grado y sensación de ardor epigástrico durante la misma semana y con la misma duración. La paciente también experimentó una pérdida de peso y fatiga no especificadas durante los últimos 2 meses. Por lo demás, no tenía comorbilidades conocidas, ni comportamientos de riesgo, como fumar o beber alcohol, medicamentos o antecedentes familiares de neoplasia. Estaba casada, tenía cuatro hijos y no tenía antecedentes obstétricos negativos. Su ocupación era la agricultura y había vivido en una zona rural. Nunca había sido admitida por una queja similar.\n\nLa escala de coma de Glasgow (GCS) de la paciente fue de 15 sobre 15, y no había anormalidades de memoria, potencia o tono. La paciente estaba en grave dificultad respiratoria con saturación de oxígeno del 70% con aire atmosférico, frecuencia respiratoria de 30-35 latidos/minuto, y frecuencia del pulso de 120 por minuto. Tenía registros de fiebre de alto grado hasta el nivel de 39.5 0C y puede mantener su presión arterial. El examen de mama con ultrasonido y mamografía fue supuestamente normal. No se detectó linfadenopatía en áreas accesibles.\n\nEl examen del tórax reveló signos de derrame pleural que también se observaron en las imágenes y se analizaron. Una tomografía computarizada (TC) del tórax con contraste mostró derrame pericárdico y neumonía multifocal. La angiografía por TC mostró un defecto de llenado arterial pulmonar segmentario del lóbulo inferior en ambos lados, lo que sugiere embolia pulmonar y derrame pleural en ambos lados. Los frotis citológicos se informaron con láminas de células mesoteliales, neutrófilos y grupos dispersos de células grandes atípicas con nucleolos prominentes que sugieren derrame maligno. El análisis del líquido pleural mostró un líquido con predominio linfocítico con glucosa normal (82 mg/dl), proteínas (2,2 g/dl) y lactato deshidrogenasa (LDH) de 592 mg/dl.\n\nLa presión venosa yugular aumentó con los sonidos cardiacos apagados. La ecocardiografía mostró derrame pericárdico masivo con características de taponamiento cardiaco, fracción de eyección preservada (65%), y excursión sistólica del plano anular tricuspídeo (TAPSE) mayor a 18 mm. Un electrocardiograma (ECG) reveló solo taquicardia sinusal y desviación del eje. Se realizó una pericardiocentesis inmediata, se extrajo un drenaje de aproximadamente 250 ml de fluido hemorrágico y se aseguró la ventana pericárdica. La repetida ecocardiografía reveló una reducción del tamaño. El informe de citología del fluido pericárdico mostró numerosos linfocitos junto con células malignas atípicas que tenían prominentes nucleolos, lo que sugería un derrame maligno.\n\nEn el examen abdominal, mostró signos positivos de acumulación de fluidos sin órgano hinchable. La tomografía computarizada abdominal y pélvica mostró un aumento en el tamaño del hígado con múltiples lesiones hepáticas hipointensas que sugerían metástasis. Los órganos pélvicos, incluidos los ovarios y el útero, no presentaron lesiones identificadas. Se realizó una biopsia con aguja de la lesión hepática y los resultados revelaron un adenocarcinoma secundario.\n\nSe realizó un diagnóstico de insuficiencia cardíaca causada por una efusión pericárdica masiva maligna secundaria a un adenocarcinoma diseminado y un carcinoma de origen primario desconocido que afectaba al pulmón, la pleura, el pericardio y el tracto gastrointestinal. Se le diagnosticó a la paciente una trombosis venosa profunda extensa en la extremidad superior izquierda, una embolia pulmonar bilateral y segmentaria, posiblemente debido a la CUP diseminada. Los hallazgos también mostraron una neumonía multifocal superpuesta y una anemia leve de enfermedad crónica.\n\nEl recuento sanguíneo completo inicial reveló leucocitosis con un recuento de glóbulos blancos de 24 × 103 por ml, neutrófilos predominantes (91%), recuento de glóbulos rojos de 3.7 × 106 por µl, anemia normocítica leve (hemoglobina (Hgb) 11.2 mg/dl), volumen corpuscular medio (MCV) de 81.2 fl, y trombocitopenia severa (66 × 103/µl). Después del tratamiento antibiótico para neumonía, el recuento sanguíneo completo volvió a la normalidad (excepto para Hgb). Con niveles normales de bilirrubina, la aspartato aminotransferasa (AST) aumentó más de siete veces (263 U/L), mientras que la alanina transaminasa (ALT) aumentó más de nueve veces (332 U/L). Los electrolitos séricos (excepto para Na + con hiponatremia leve, 129 mEq/L) y las pruebas de función renal fueron normales. La albúmina era baja (2.12 g/dl). Los niveles de lactato deshidrogenasa (LDH) aumentaron casi dos veces desde el inicio (592 U/L). Los virus del virus de inmunodeficiencia humana, hepatitis B y hepatitis C no fueron reactivos. La sangre y el cultivo del líquido pleural no tuvieron crecimiento. Un antígeno carcinoembrionario (CEA) aumentó más de 400 veces (1000 µg/L) del inicio.\n\nLa paciente fue admitida en la sala general. Se realizó una ventana pericárdica y una inserción de un tubo torácico derecho con un cirujano cardiotorácico junto con un cardiólogo (ver la cantidad de aspirado antes). Se realizó una aspiración pleural terapéutica intermitente para el derrame pleural maligno. Una vez que la dosis de carga (60 mg) de frusemida produjo suficiente producción de orina, esta dosis se mantuvo tres veces (TID) al día. Esto se redujo y se dio de alta a la paciente con una dosis oral de 20 mg dos veces al día (BID). Se inició una dosis estándar de enoxaparina para el tromboembolismo pulmonar y la trombosis venosa profunda aguda extensa en la extremidad superior izquierda. Se administró enoxaparina por vía subcutánea 40 mg BID durante la hospitalización, que se cambió a 5 mg de warfarina oral diaria durante el alta debido a problemas financieros. La neumonía multifocal se trató con ceftazidima (1 g intravenoso TID) y vancomicina (1 g intravenoso BID) según el protocolo de tratamiento estándar nacional. El dolor se controló con un potente medicamento contra el dolor (morfina 5 mg intravenosa TID) y se redujo y suspendió. También estaba en la profilaxis de la úlcera. La paciente fue dada de alta de la sala médica con una mejora significativa después de 14 días de hospitalización y fue asignada a la unidad de oncología del hospital. Por lo tanto, para el cáncer de origen primario desconocido, se le dio un ciclo de quimioterapia (carboplatino/paclitaxel). Se perdió el seguimiento debido a problemas financieros, y la paciente murió en su casa cuatro meses después del alta.\n\nMH - Humanos\nMH - Mujer\nMH - *Insuficiencia cardiaca/etiología\nMH - Adulto\nMH - *Neoplasias, complicaciones/primaria desconocida",
+    "gold_summary": "Una mujer negra de 35 años se presentó con falta de aire en reposo, ortopnea, disnea paroxística nocturna, dolor torácico, tos productiva teñida de sangre y fiebre durante 2 semanas. También tenía hinchazón progresiva del cuerpo, fatigabilidad fácil, pérdida de apetito y dolor abdominal durante la misma semana. La imagen corporal reveló grandes derrames pleurales y pericárdicos, lesiones hepáticas metastásicas y defectos de llenado segmentarios y subsegmentarios vasculares pulmonares bilaterales. La citología de los fluidos pericardio y pleural sugieren derrame maligno. Las lesiones hepáticas y la biopsia con aguja indicaron adenocarcinoma de origen desconocido, y el nivel de antígeno carcinoembriónico también aumentó significativamente.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Había una mujer que se sentía muy cansada y con dificultad para respirar. Su cuerpo se hinchó mucho y tenía dolor en el pecho. Los doctores vieron que tenía líquido en el pecho y alrededor del corazón. También encontraron que tenía un problema en el hígado y en los pulmones. El líquido que sacaron mostró que tenía células que no son buenas. Los doctores dijeron que tenía un tipo de cáncer que empezó en un lugar que no pudieron encontrar.",
+        "scores": {
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+          "ROUGE-2": 0.02830188679245283,
+          "ROUGE-L-Sum": 0.17757009345794392,
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+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
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+      },
+      "B2": {
+        "text": "**Lo que le Pasó a la Paciente**\n\nUna mujer de 35 años llegó al hospital porque tenía mucha dificultad para respirar, incluso cuando estaba en reposo. También tenía dolor en el pecho, tos con sangre, fiebre y una hinchazón que comenzó en sus piernas y se extendió por todo el cuerpo. Además, se sentía muy cansada, había perdido el apetito y tenía dolor en la parte superior del abdomen.\n\n**Lo que Encontraron en los Exámenes**\n\nLas imágenes médicas mostraron que tenía acumulación de líquido en los pulmones (llamado derrame pleural) y alrededor del corazón (derrame pericárdico). También encontraron lesiones en el hígado que parecían ser metástasis, es decir, que el cáncer se había extendido allí. En los vasos sanguíneos de sus pulmones había bloqueos que indicaban embolias pulmonares, que son coágulos que dificultan la circulación.\n\nAl analizar el líquido que rodeaba el corazón y los pulmones, los médicos encontraron células anormales que indicaban que el líquido estaba causado por un cáncer (derrame maligno). La biopsia del hígado confirmó que tenía un tipo de cáncer llamado adenocarcinoma, pero no pudieron encontrar dónde comenzó el cáncer originalmente.\n\nAdemás, un examen de sangre mostró que tenía un nivel muy alto de una sustancia llamada antígeno carcinoembrionario, que suele aumentar cuando hay ciertos tipos de cáncer.\n\n**Qué Significa Todo Esto**\n\nLa paciente tenía un cáncer avanzado que se había extendido a varias partes del cuerpo, incluyendo los pulmones, el corazón y el hígado. Esto causó problemas graves como dificultad para respirar, acumulación de líquidos y coágulos en la sangre. Aunque recibieron tratamiento para aliviar sus síntomas y para el cáncer, la enfermedad estaba muy avanzada y el origen del tumor principal no se pudo identificar.",
+        "scores": {
+          "ROUGE-1": 0.27814569536423844,
+          "ROUGE-2": 0.08869179600886919,
+          "ROUGE-L-Sum": 0.2560706401766004,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nUna mujer etíope de 35 años acudió al hospital presentando dificultad grave para respirar en reposo, dificultad para respirar al estar acostada (ortopnea), episodios repentinos de dificultad respiratoria nocturna (disnea paroxística nocturna), dolor en el pecho, tos con expectoración de sangre y vómitos de contenido alimenticio durante dos semanas. Además, manifestó una hinchazón progresiva que comenzó en las piernas y se extendió a todo el cuerpo, cansancio fácil, pérdida de apetito, fiebre alta intermitente y ardor en la parte superior del abdomen. También había experimentado pérdida de peso y fatiga durante los dos meses previos. No tenía antecedentes médicos relevantes ni factores de riesgo conocidos.\n\n**Hallazgos Clave**  \nEl examen físico y las pruebas de imagen revelaron derrames significativos de líquido tanto en la cavidad pleural (alrededor de los pulmones) como en el pericardio (la membrana que rodea el corazón). La tomografía computarizada mostró lesiones en el hígado compatibles con metástasis (diseminación del cáncer) y defectos en la circulación sanguínea pulmonar que indicaban embolias pulmonares bilaterales. El análisis del líquido extraído del pericardio y la pleura mostró células malignas, lo que sugiere que el líquido se debía a un derrame maligno. La biopsia hepática confirmó la presencia de un adenocarcinoma (un tipo de cáncer que se origina en células glandulares) de origen primario desconocido. Además, el nivel en sangre del antígeno carcinoembrionario (CEA), un marcador tumoral, estaba muy elevado, apoyando la presencia de un cáncer avanzado.\n\n**Interpretación Clínica**  \nLa paciente fue diagnosticada con insuficiencia cardíaca causada por un derrame pericárdico masivo de origen maligno, secundario a un adenocarcinoma diseminado que afectaba múltiples órganos, incluyendo pulmón, pleura, pericardio y tracto gastrointestinal. También se identificaron complicaciones como trombosis venosa profunda en el brazo izquierdo y embolia pulmonar, probablemente relacionadas con la enfermedad tumoral avanzada. Se detectó además una neumonía multifocal superpuesta y anemia leve asociada a enfermedad crónica.\n\n**Próximos Pasos y Tratamiento**  \nLa paciente recibió tratamiento urgente para aliviar el derrame pericárdico mediante pericardiocentesis y ventana pericárdica, así como drenaje del líquido pleural. Se inició tratamiento anticoagulante para la trombosis y embolia pulmonar, y antibióticos para la neumonía. Posteriormente, se administró quimioterapia con carboplatino y paclitaxel dirigida al cáncer de origen desconocido. A pesar de la mejoría inicial y el alta hospitalaria, la paciente falleció cuatro meses después debido a la progresión de la enfermedad.\n\nEste caso ilustra la complejidad del diagnóstico y manejo de un cáncer avanzado con origen primario desconocido, que se manifestó inicialmente con síntomas respiratorios y signos de insuficiencia cardíaca por derrame pericárdico maligno.",
+        "scores": {
+          "ROUGE-1": 0.2814070351758794,
+          "ROUGE-2": 0.11764705882352941,
+          "ROUGE-L-Sum": 0.271356783919598,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
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+  },
+  {
+    "article": "Paciente del sexo femenino de 17 años con diagnóstico de enfermedad de Graves con bocio difuso, la cual negó otros antecedentes de importancia.\n\nSu cuadro comenzó seis meses antes con pérdida de peso progresiva, episodios de ansiedad y agitación, temperaturas de 37.4 a 37.9 ºC, palpitaciones, dolor abdominal y diarrea intermitente. A los dos meses se agregó como síntoma el crecimiento de la cara anterior del cuello; al tercer mes presentó taquicardia de hasta 130 latidos por minuto. Al ser valorada por Endocrinología se le administró tiamazol de 15 mg cada 8 horas, el cual fue suspendido por cuadro de agranulocitosis. Por lo tanto, se le comenzó a administrar lugol y propanol de 20 mg cada 8 horas, sin respuesta adecuada. Por ende, se decidió aplicar una dosis terapéutica de yodo 131 (I-131) 10 mcU.\n\n\nExploración física\nA la exploración física, la paciente presentó como signos basales una presión arterial no invasiva (PANI) 137/75 mmHg, frecuencia cardiaca (FC) 105 lpm, frecuencia respiratoria (FR) 16 rpm, SpO2 95%, temperatura 37.4ºC. La paciente ingresó deambulando, con agitación leve, con actitud cooperadora; estaba hidratada y sin datos clínicos de vía aérea difícil, pero no se valoró movilidad de tráquea por crecimiento tiroideo de aproximadamente 7.5 x 7 x 10 cm). La superficie del cuello era regular y su movilidad tenía una adecuada extensión. A la auscultación cardiopulmonar no hubo ruidos agregados y la paciente tenía ruidos cardiacos aumentados en frecuencia; asimismo, abdomen blando, depresible, no doloroso, con peristalsis presente. Extremidades integras, sensibilidad con aumento de la percepción del calor, hiperhidrosis palmar, fuerza 5/5, y temblor fino.\n\nSe empleó la escala de Burch y Wartofsky y se obtuvieron 40 puntos con elevada probabilidad de tormenta tiroidea, por lo cual se decidió manejo con anestesia multimodal.\n\nEn la monitorización tipo 2 la paciente presentó signos vitales iniciales PANI 137/75 mmHg, frecuencia cardiaca 96 latidos por minuto, frecuencia respiratoria 16 respiraciones por minuto, 95% Spo2, monitoreo invasivo de tensión arterial.\n\nPor inducción endovenosa se le administraron a la paciente 2 mg de midazolam; 150 mcg de fentanilo; 5 mg de cisatracurio y 50 mg de propofol.\n\nEl abordaje de la vía aérea se hizo con videolaringoscopía Glide Scope con hoja hiperangular 3 sin complicaciones. La ventilación mecánica invasiva modo volumen presentó flujos bajos FIO2 (40%).\n\nSe llevó a cabo bloqueo cervical superficial bilateral ecoguiado con 4 mL de ropivacaina al 0.2% en cada lado (16 mg en total).\n\nPara el mantenimiento se empleó sevoflorano CAM 0.8, infusión de dexmedetomedina 0.7 a 0.4 mcg/kg/hora, infusión de lidocaína 25 mcg/kg/hora, concentración plasmática de fentanilo 0.001 mcg/mL.\n\nEn cuanto a los adyuvantes se empleó paracetamol 750 mg + parecoxib 40 mg + ketorolaco intravenoso 30 + sulfato de magnesio 1250 g en infusión para una hora. El balance de líquidos fue negativo. El tiempo anestésico fue de 215 minutos. En el transoperatorio, la paciente estuvo hemodinámicamente estable, con presión arterial media de 67 a 75 mmHg, que se considera adecuada para la perfusión de órganos.\n\nEn el postoperatorio la paciente presentó analgesia durante 12 horas. Rescate con 1 g de metamizol por razón necesaria, utilizando un solo rescate. Disfonía postoperatoria persistente, sin presencia de odinofagia.",
+    "gold_summary": "Adolescente de 17 años con enfermedad de Graves con manifestaciones clínicas descontroladas, la cual no respondió a tratamiento médico y se programó para tiroidectomia radical. Se obtuvieron 35 puntos en la Escala de Burch y Wartofsky. Se manejó con anestesia general y fueron disminuyendo los estímulos para control de vía aérea y regional a fin de disminuir los estímulos quirúrgicos. Se usaron medicamentos adyuvantes como sulfato de magnesio para la estabilidad transoperatoria.",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Una niña de 17 años tenía un problema en su cuello llamado enfermedad de Graves. Su cuerpo estaba muy acelerado y no mejoró con medicinas. Por eso, los doctores decidieron hacerle una operación para quitarle una parte del cuello. Durante la operación, los doctores usaron medicinas para que ella no sintiera dolor y para que su cuerpo estuviera tranquilo. También cuidaron mucho su respiración para que todo saliera bien.",
+        "scores": {
+          "ROUGE-1": 0.2692307692307693,
+          "ROUGE-2": 0.06493506493506494,
+          "ROUGE-L-Sum": 0.25641025641025644,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B2": {
+        "text": "**Caso de una Adolescente con Enfermedad de Graves**\n\nUna joven de 17 años tenía una enfermedad llamada Graves, que afecta la tiroides, una glándula en el cuello que controla muchas funciones del cuerpo. Su enfermedad estaba muy activa y no mejoró con los medicamentos que le dieron.\n\n**Lo que Pasó Antes de la Cirugía**\n\nLa paciente tenía síntomas como pérdida de peso, ansiedad, latidos rápidos del corazón y un aumento visible en el tamaño de su cuello debido al crecimiento de la tiroides. Los médicos usaron una escala llamada Burch y Wartofsky para medir qué tan grave estaba su condición, y obtuvo 35 puntos, lo que indica un problema serio.\n\n**Cómo Se Realizó la Cirugía**\n\nPara operarla, le pusieron anestesia general, que es un medicamento que la hizo dormir y no sentir dolor durante la cirugía. Los médicos cuidaron mucho la forma de manejar su respiración y usaron técnicas para reducir las molestias causadas por la operación. Además, le dieron medicamentos especiales, como sulfato de magnesio, para mantener su cuerpo estable mientras duraba la cirugía.\n\n**Por Qué Es Importante**\n\nEste caso muestra cómo se trata una enfermedad de Graves muy avanzada cuando los medicamentos no funcionan. La cirugía y el cuidado durante la operación son muy importantes para que la paciente esté segura y se recupere bien.",
+        "scores": {
+          "ROUGE-1": 0.3177570093457944,
+          "ROUGE-2": 0.10031347962382445,
+          "ROUGE-L-Sum": 0.29906542056074764,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe trata de una paciente femenina de 17 años diagnosticada con enfermedad de Graves, una condición autoinmune que provoca un aumento en la actividad de la glándula tiroides (hipertiroidismo) y crecimiento difuso del tiroides (bocio). Desde hace seis meses, presentó síntomas progresivos como pérdida de peso, ansiedad, fiebre leve, palpitaciones, dolor abdominal y diarrea. Posteriormente, desarrolló un aumento visible en la parte frontal del cuello y taquicardia (frecuencia cardíaca acelerada). El tratamiento inicial con tiamazol (un medicamento antitiroideo) fue suspendido debido a una complicación grave llamada agranulocitosis (disminución severa de glóbulos blancos). Se intentaron otros tratamientos sin éxito, por lo que se decidió administrar yodo radioactivo (I-131) para reducir la función tiroidea.\n\n**Hallazgos Clave**  \nEn la evaluación física, la paciente mostraba signos de hipertiroidismo activo: frecuencia cardíaca elevada (105 latidos por minuto), temperatura corporal ligeramente elevada (37.4 ºC), temblor fino, sudoración excesiva en las palmas y aumento de la sensibilidad al calor. Se observó un bocio grande (aproximadamente 7.5 x 7 x 10 cm) sin signos de dificultad respiratoria, aunque no se pudo evaluar completamente la movilidad de la tráquea debido al tamaño del tiroides. La escala de Burch y Wartofsky, que evalúa el riesgo de una crisis tiroidea grave llamada tormenta tiroidea, arrojó un puntaje de 40, indicando alta probabilidad de esta complicación.\n\nDurante la cirugía programada para extirpar la glándula tiroides (tiroidectomía radical), se utilizó anestesia general con técnicas avanzadas para asegurar la vía aérea, incluyendo videolaringoscopía, y ventilación mecánica controlada. Se aplicó un bloqueo nervioso cervical superficial guiado por ultrasonido para reducir el dolor y la respuesta al estímulo quirúrgico. Además, se emplearon varios medicamentos adyuvantes, como sulfato de magnesio, para mantener la estabilidad cardiovascular y mejorar el control del dolor durante la operación. La paciente se mantuvo estable durante todo el procedimiento, que duró aproximadamente 3 horas y 35 minutos.\n\n**Interpretación Clínica**  \nLa paciente presentaba un cuadro de enfermedad de Graves descontrolada, con signos y síntomas que indicaban un alto riesgo de tormenta tiroidea, una emergencia médica que puede ser potencialmente mortal. La falta de respuesta a tratamientos convencionales y la contraindicación del tiamazol por agranulocitosis hicieron necesaria la intervención quirúrgica. El manejo anestésico fue cuidadosamente planificado para minimizar los riesgos asociados a la hiperactividad tiroidea y al tamaño del bocio, utilizando técnicas que redujeron la estimulación del sistema nervioso y mantuvieron la estabilidad hemodinámica.\n\n**Próximos Pasos**  \nDespués de la cirugía, la paciente presentó analgesia efectiva durante 12 horas y requirió un solo rescate analgésico. Se observó disfonía (alteración de la voz) persistente, probablemente relacionada con la manipulación quirúrgica de los nervios laríngeos, pero sin dolor al tragar. Será importante realizar un seguimiento para evaluar la función vocal y ajustar el tratamiento hormonal tiroideo según sea necesario para evitar complicaciones a largo plazo. Además, se debe monitorizar la recuperación general y prevenir posibles efectos secundarios derivados de la cirugía y la enfermedad de base.",
+        "scores": {
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+          "ROUGE-2": 0.0972447325769854,
+          "ROUGE-L-Sum": 0.18739903069466882,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
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+  {
+    "article": "Una mujer de 30 años de edad, embarazada de 3, para 3, se presentó con disminución de la micción, dolor en el flanco izquierdo y fiebre durante 2 días después de una cesárea de emergencia por primera vez, indicada debido a la angustia materna y fetal secundaria al trabajo de parto prolongado y sangrado vaginal prolongado en el hospital Al-Thora, Ibb, Yemen. A pesar de los esfuerzos de reanimación, su recién nacido falleció después de 45 minutos. Durante la cesárea, se identificaron severas adherencias uterinas (ya que había lesiones de endometriosis y adherencias entre la pared posterior del útero y el colon sigmoide), y una pérdida de sangre estimada de 1500 cc, según el informe del ginecólogo. La paciente no recibió atención prenatal durante su embarazo. No es fumadora y negó condiciones médicas crónicas, abuso de drogas, intoxicación accidental o antecedentes quirúrgicos previos.\n\nEn el examen físico, el paciente se veía pálido, enfermo y febril durante la evaluación inicial, con una temperatura oral de 38 °C, pulso de 80 latidos por minuto y presión arterial de 95/70 mm Hg. El abdomen del paciente estaba levemente distendido, con sensibilidad moderada, principalmente en el cuadrante inferior izquierdo.\n\nLos datos de laboratorio fueron los siguientes: el recuento de glóbulos blancos (WBC) fue de 15,3 × 103/mL, con 90% de neutrófilos polimórficos (leucocitosis con predominio neutrofílico), la hemoglobina fue de 7,5 g/dL, el recuento de plaquetas fue de 200 × 103/µL, el nitrógeno ureico en sangre (BUN) fue de 23 mg/dl y la creatinina fue de 3,8 mg/dl. Otros análisis de sangre, como los de la función hepática y los de coagulación, estuvieron dentro de los rangos normales. La ecografía (US) mostró una hidronefrosis izquierda grave y un fluido libre moderado en la cavidad abdominal. Se realizó la aspiración de la punción abdominal y la creatinina en el punto fue de 52 mg/dL, lo que indica que el fluido era orina.\n\nLa paciente fue resucitada con glóbulos rojos concentrados y una amplia cobertura antibiótica. Después de esto, se le realizó una ureteroscopia urgente que mostró una oclusión total del uréter izquierdo. Se tomó la decisión de realizar una exploración quirúrgica, dada la inestabilidad hemodinámica, la falta de equipos de nefrostomía percutánea y la evidencia de contaminación intraabdominal. Durante la operación, se encontró fluido libre moderado en la cavidad abdominal. El uréter izquierdo fue aplastado y ligado con una sutura Vicryl (5 agujas) a unos 5 cm de su parte distal. Después de evacuar el fluido, se extirpó el segmento lesionado del uréter y se realizó una ureteroneocistostomía de forma refluyente tras distender la vejiga con solución salina a través del catéter. Además, diseccionamos el uréter, con cuidado, de los tejidos circundantes en dirección cefálica, espatulamos el extremo distal del uréter e insertamos un stent doble. Se implantó el uréter en la cúpula posterior de la vejiga urinaria con anastomosis sin tensión y se suturó con Vicryl 4-0 a través del uréter de espesor completo, luego la capa mucosa de la vejiga y la capa detrusora. Se insertó un drenaje Jackson-Pratt (JP) cerca de la anastomosis y se cerró la pared abdominal tras evaluar el contenido intraperitoneal.\n\n\nSeguimiento y resultado\nSe iniciaron líquidos transparentes el segundo día postoperatorio. La paciente tenía distensión abdominal leve, dolor y náuseas. El tercer día postoperatorio, tenía una distensión abdominal creciente y dejó de expulsar flatos. La ecografía abdominal mostró una gran cantidad de acumulación en la cavidad peritoneal. Los datos de laboratorio de sangre mostraron una leucocitosis (WBC de 22 × 103/mL con un cambio a la izquierda).\n\nUna tomografía computarizada (TC) del abdomen y la pelvis con contraste reveló una cantidad significativa de aire libre y líquido en todo el abdomen y la pelvis adyacente a la pared abdominal anterior. También se observaron múltiples localizaciones de gas libre en el mesenterio, con realce de contraste de múltiples bucles intestinales pequeños, sin evidencia de extravasación de contraste. Los hallazgos sugirieron una víscera perforada. Después de consultar al equipo de cirugía general, la paciente fue llevada inmediatamente al quirófano para una laparotomía exploratoria, que reveló una pequeña perforación en la parte rectosigmoidea con algo de derrame, peritonitis con edema del asa intestinal y alteración de la anastomosis ureteral. La complejidad de este caso nos obligó a realizar intervenciones en varias etapas de manera multidisciplinaria. En primer lugar, el ginecólogo realizó una histerectomía debido a endometritis (confirmada histopatológicamente), supuración severa y alteración de la sutura del útero. En segundo lugar, un urólogo realizó una derivación ureterocutánea del uréter izquierdo y se creó una urostomía en el lado izquierdo. Por último, el cirujano general realizó el procedimiento de colostomía después de reparar la lesión del colon y se creó una colostomía en el lado izquierdo. En el quinto día postoperatorio, se produjo retracción de la colostomía con infección de la herida y se observó comunicación entre la colostomía y la urostomía. Se decidió realizar una reexploración para reubicar la colostomía sigmoidea y se realizó una colostomía transversal derecha. Una semana después de la operación, la paciente experimentó una infección superficial de la pared abdominal complicada con dehiscencia de la herida e hipoalbuminemia (albúmina: 2 g/dL) que requirió tratamiento con varios desbridamientos, irrigación de la herida, antibióticos y terapia de apoyo. Los antibióticos recomendados fueron linezolid (600 mg IV cada 12 horas durante 7 días), luego cambiaron a ceftriaxona (1 g IV cada 12 horas durante 5 días) más metronidazol (500 mg IV cada 12 horas durante 5 días) y cambiaron a ciprofloxacina oral (500 mg cada 12 horas por vía oral durante 7 días). Gradualmente, reanudó su dieta normal y fue dada de alta 30 días después en condiciones estables. Requería atención domiciliaria para ayudarla con la colostomía, la ureterostomía y la deambulación.\n\nSeis meses después, se cerró la colostomía y se anastomosó el uréter mediante el procedimiento de colgajo de vejiga tabular de Boari (la vejiga se abrió en su superficie anterior y se volteó un colgajo de vejiga de espesor completo caudalmente y se tabularizó para anastomosis al segmento ureteral proximal después de la inserción de la endoprótesis doble J). Después de una recuperación postoperatoria sin incidentes, se dio de alta a la paciente el séptimo día postoperatorio. El seguimiento de un mes mediante ecografía y cistouretrografía miccional mostró un aspecto normal de la vejiga con capacidad vesical adecuada y un sistema del tracto urinario superior normal. Tres meses después, la ureteroscopia retrógrada mostró un calibre adecuado del uréter. Se hizo un seguimiento regular de la paciente con ecografía durante 3 meses durante un año. La paciente no tuvo síntomas irritativos o gastrointestinales en los 2 años de seguimiento.\n",
+    "gold_summary": "Una mujer de 30 años presentó disminución de la micción durante 2 días después de una cesárea. La ecografía mostró una hidronefrosis izquierda grave y un fluido abdominal libre moderado. Una ureteroscopia reveló una oclusión total del uréter izquierdo y, posteriormente, se realizó una ureteroneocistostomía. Dos días después, la paciente presentó complicaciones con distensión abdominal que requirieron una nueva exploración. La exploración reveló lesiones en el colon (recto-sigmoide), peritonitis, endometritis y alteración de la anastomosis ureteral. Se realizó una colostomía, reparación de lesiones en el colon, histerectomía y derivación ureterocutánea. La estancia hospitalaria de la paciente fue complicada, con retracción estomal que requirió revisión quirúrgica y dehiscencia de la herida, que se trató de forma conservadora. Después de 6 meses, se cerró la colostomía y se anastomosó el uréter mediante el procedimiento de colgajo de Boari.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Una mujer tuvo un bebé con una operación. Después, le dolía y no podía hacer pipí bien. Los doctores vieron que un tubito que lleva la pipí estaba tapado. Hicieron una operación para arreglarlo.\n\nDespués, la mujer se sintió peor y su pancita se hizo grande. Los doctores encontraron que tenía heridas en su pancita y en otros lugares. Hicieron más operaciones para ayudarla y poner todo bien.\n\nLa mujer estuvo en el hospital mucho tiempo. Poco a poco, se fue mejorando. Después de seis meses, los doctores cerraron una abertura que le habían hecho y arreglaron el tubito de la pipí otra vez. Ahora está bien y sin dolor.",
+        "scores": {
+          "ROUGE-1": 0.30985915492957744,
+          "ROUGE-2": 0.06382978723404256,
+          "ROUGE-L-Sum": 0.29577464788732394,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B2": {
+        "text": "**Lo que pasó con la paciente**  \nUna mujer de 30 años tuvo problemas para orinar durante dos días después de una cesárea, que es una operación para sacar al bebé. Al hacerle una ecografía, los médicos vieron que tenía una hinchazón grave en el riñón izquierdo llamada hidronefrosis, causada por la acumulación de orina, y también encontraron líquido libre en su abdomen. Luego, con un examen llamado ureteroscopia, descubrieron que el tubo que lleva la orina desde el riñón a la vejiga (el uréter izquierdo) estaba completamente bloqueado.\n\n**Tratamiento inicial**  \nPara arreglar este problema, los médicos hicieron una cirugía llamada ureteroneocistostomía, que consiste en conectar el uréter a la vejiga de nuevo para que la orina pueda salir. Sin embargo, dos días después, la paciente tuvo dolor y su abdomen se hinchó más, lo que indicaba que algo no estaba bien.\n\n**Complicaciones y nuevas cirugías**  \nAl revisarla otra vez, encontraron que tenía una infección grave en el abdomen (peritonitis), una herida en el colon (parte del intestino) y una inflamación en el útero (endometritis). También la conexión del uréter que habían hecho estaba dañada. Por eso, los médicos tuvieron que hacer varias cirugías: quitaron el útero (histerectomía), repararon el colon y crearon una abertura en la piel para que la orina y las heces pudieran salir por separado (derivación ureterocutánea y colostomía).\n\n**Recuperación y seguimiento**  \nLa recuperación fue difícil porque la paciente tuvo problemas con las heridas y la abertura del colon se contrajo, lo que necesitó otra cirugía. También tuvo infecciones que se trataron con antibióticos y cuidados especiales. Después de seis meses, los médicos cerraron la abertura del colon y volvieron a conectar el uréter usando una técnica llamada colgajo de Boari, que usa parte de la vejiga para reparar el uréter.\n\n**Resultado final**  \nTras esta última cirugía, la paciente se recuperó bien. Los controles con ecografías y otros estudios mostraron que su vejiga y riñones funcionaban normalmente. Durante dos años de seguimiento, no tuvo problemas ni síntomas molestos.",
+        "scores": {
+          "ROUGE-1": 0.4051094890510949,
+          "ROUGE-2": 0.1575091575091575,
+          "ROUGE-L-Sum": 0.37591240875912413,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nUna mujer de 30 años, embarazada por tercera vez, fue sometida a una cesárea de emergencia debido a complicaciones durante el trabajo de parto, incluyendo sangrado prolongado y sufrimiento fetal. Tras la cesárea, presentó disminución en la cantidad de orina, dolor en el costado izquierdo y fiebre. Durante la cirugía se detectaron adherencias severas en el útero y lesiones compatibles con endometriosis, además de una pérdida significativa de sangre. La paciente no había recibido atención prenatal y no presentaba antecedentes médicos relevantes.\n\n**Hallazgos Clave**  \n- Exámenes iniciales mostraron leucocitosis con predominio neutrofílico (indicativo de infección), anemia moderada y deterioro de la función renal (elevación de creatinina).  \n- La ecografía evidenció una hidronefrosis grave (dilatación del riñón por obstrucción) en el lado izquierdo y presencia de líquido libre en la cavidad abdominal, que resultó ser orina al analizarse.  \n- La ureteroscopia urgente identificó una obstrucción completa del uréter izquierdo.  \n- Se realizó una cirugía para extirpar el segmento dañado del uréter y se reconstruyó la conexión entre el uréter y la vejiga (ureteroneocistostomía), con colocación de un stent para mantener el flujo urinario.\n\n**Interpretación Clínica**  \nPocos días después de la cirugía, la paciente desarrolló distensión abdominal progresiva, dolor y ausencia de expulsión de gases, signos sugestivos de complicaciones intraabdominales. Estudios por imagen mostraron aire y líquido libre en el abdomen, lo que indicaba una posible perforación intestinal. La laparotomía exploratoria confirmó perforación en el colon rectosigmoide, peritonitis (inflamación del revestimiento abdominal), infección del útero (endometritis) y problemas en la reparación del uréter. Debido a la complejidad y gravedad del cuadro, se realizaron múltiples intervenciones: histerectomía para controlar la infección uterina, derivación urinaria mediante ureterostomía para proteger el tracto urinario, y reparación del colon con creación de colostomía para desviar las heces.\n\nDurante la hospitalización, la paciente presentó complicaciones adicionales como retracción de la colostomía con infección y dehiscencia (apertura) de la herida abdominal, que requirieron revisiones quirúrgicas y tratamiento con antibióticos y cuidados locales. La recuperación fue gradual, y la paciente fue dada de alta en condiciones estables tras un mes de hospitalización.\n\n**Próximos Pasos y Seguimiento**  \nSeis meses después, se realizó el cierre de la colostomía y la reconstrucción definitiva del uréter mediante el procedimiento de colgajo de Boari, que utiliza un segmento de la vejiga para reemplazar la parte dañada del uréter. La recuperación postoperatoria fue satisfactoria, con estudios de imagen que mostraron una vejiga y tracto urinario superiores normales, y ureteroscopias que confirmaron un calibre adecuado del uréter. Durante dos años de seguimiento, la paciente no presentó síntomas urinarios ni gastrointestinales, evidenciando una recuperación completa y funcional.\n\n---\n\nEste caso ilustra la complejidad y gravedad de las complicaciones postoperatorias tras una cesárea en un contexto de falta de atención prenatal y lesiones previas, así como la importancia de un manejo multidisciplinario para resolver complicaciones urológicas, ginecológicas y gastrointestinales simultáneas.",
+        "scores": {
+          "ROUGE-1": 0.3672316384180791,
+          "ROUGE-2": 0.19830028328611898,
+          "ROUGE-L-Sum": 0.3389830508474576,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      }
+    }
+  },
+  {
+    "article": "Mujer de 43 años, con antecedente de hipertensión arterial con tratamiento con losartán, dos cesáreas y oclusión tubaria bilateral. Ingresó a nuestro hospital y refirió dolor de 24 horas de evolución, tipo cólico en hipogastrio e irradiación a fosa iliaca izquierda, además de náusea y vómito en dos ocasiones. Se agregaron evacuaciones semilíquidas en forma inicial y posteriormente cese en las evacuaciones y en la canalización de gases. A la exploración física, la paciente presentó dolor en el abdomen, así como distensión, especialmente hacia el flanco izquierdo. En el mesogastrio y el flanco izquierdo hubo la presencia de timpanismo. La peristalsis estaba presente, mínima, abolida en flanco izquierdo y mesogastrio. La irritación peritoneal estuvo ausente. Se colocó sonda nasogástrica, con gasto mínimo gástrico y sin mejoría en la sintomatología. Los estudios de laboratorio demostraron: 9700 leucocitos con un 87% de neutrófilos, creatinina de 0.7 mg/dL, urea de 22 mg/dL y proteína C reactiva de 5.0 mg/L. En la radiografía simple de abdomen presentó dilatación importante del lado izquierdo del colon, con niveles hidroaéreos. La tomografía muestra la dilatación del colon del lado izquierdo, con imagen que simula grano de café en el corte coronal.\n\nAnte estos hallazgos clínicos y de imagen, se decidió hacer laparotomía de urgencia ante la sospecha de la presencia de vólvulo de sigmoides o de síndrome adherencial complicado. Durante la cirugía se evidenció un ciego flexionado hacia adelante y a la izquierda, carente de fijación retroperitoneal. El punto de flexión fue producido por una banda de adherencia colocada sobre el colon ascendente. Se realizó liberación de la adherencia y se corroboró continuidad adecuada hacia el colon distal. No se evidenció la presencia de isquemia, necrosis o perforación del ciego. Se realizó apendicectomía con descompresión del ciego a través de base apendicular y posteriormente ligadura de esta. Se llevó a cabo cecopexia hacia pared de fosa iliaca derecha. Después de la cirugía, hubo mejoría clínica de la paciente, que tuvo evacuaciones presentes normales. La paciente siguió controles correctos en consulta externa de cirugía y se mantuvo asintomática.",
+    "gold_summary": "Mujer de 43 años que ingresó a un servicio de urgencias con datos de obstrucción intestinal. Se realizó tomografía simple de abdomen donde se identificó dilatación del colon e imagen que semejaba un grano de café invertido. Se hizo laparotomía exploradora y se identificó vólvulo cecal del tipo báscula, sin compromiso vascular. Se realizó desvolvulación, descompresión a través de apendicectomía, y cecopexia. Posterior a evento quirúrgico, la paciente se recuperó sin incidentes y fue dada de alta con controles adecuados por consulta externa.",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Una señora tenía dolor en su barriga y no podía ir al baño bien. Los doctores le hicieron una foto especial para ver su barriga. Vieron que un pedazo de su barriga estaba doblado y tapado. La señora tuvo una operación para arreglar ese problema. Los doctores quitaron la parte que estaba doblada y la dejaron bien. Después de la operación, la señora se sintió mejor y pudo ir al baño normalmente. Ahora está bien y los doctores la revisan para cuidar que siga sana.",
+        "scores": {
+          "ROUGE-1": 0.18947368421052632,
+          "ROUGE-2": 0.010638297872340425,
+          "ROUGE-L-Sum": 0.18947368421052632,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B2": {
+        "text": "**Lo que pasó con la paciente**\n\nUna mujer de 43 años llegó al hospital porque tenía dolor en el abdomen, vómitos y problemas para evacuar. Los médicos hicieron estudios y vieron que una parte del intestino grueso, llamada colon, estaba muy inflamada y bloqueada. En la tomografía, que es una imagen especial del cuerpo, notaron una forma que parecía un \"grano de café\" invertido, lo que les hizo sospechar que había un problema llamado vólvulo, que es cuando el intestino se gira y se tapa.\n\n**Lo que hicieron los médicos**\n\nDecidieron hacer una cirugía urgente para ver qué pasaba. Durante la operación, encontraron que una parte del intestino llamada ciego estaba doblada y no estaba bien sujeta en su lugar. Esto causaba que el intestino se girara (vólvulo), pero sin dañar el flujo de sangre. Para arreglarlo, quitaron una banda de tejido que estaba causando el problema, hicieron una apendicectomía (que es sacar el apéndice) para descomprimir el intestino, y fijaron el ciego a la pared del abdomen para que no se moviera otra vez.\n\n**Qué pasó después**\n\nDespués de la cirugía, la paciente mejoró mucho. Empezó a evacuar normalmente y no tuvo más síntomas. Fue dada de alta y siguió controles médicos para asegurarse de que todo estuviera bien.",
+        "scores": {
+          "ROUGE-1": 0.3128834355828221,
+          "ROUGE-2": 0.11111111111111112,
+          "ROUGE-L-Sum": 0.3006134969325153,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B3": {
+        "text": "**Contexto:**  \nUna mujer de 43 años con antecedentes de hipertensión arterial, dos cesáreas previas y oclusión tubaria bilateral, ingresó al hospital presentando dolor abdominal intenso de tipo cólico en la parte baja del abdomen (hipogastrio), que se irradiaba hacia el lado izquierdo, acompañado de náuseas, vómitos y cambios en sus evacuaciones intestinales, incluyendo inicialmente heces semilíquidas y luego ausencia de evacuaciones y gases. En la exploración física, se detectó distensión abdominal y dolor localizado, especialmente en el lado izquierdo, con presencia de sonidos intestinales reducidos o ausentes en esa zona, pero sin signos de irritación peritoneal (inflamación de la membrana que recubre los órganos abdominales). Los análisis de sangre mostraron un aumento moderado de glóbulos blancos y proteína C reactiva, indicadores de inflamación o infección. La radiografía y la tomografía computarizada del abdomen revelaron una dilatación significativa del colon izquierdo y una imagen característica en forma de “grano de café”, que sugiere torsión intestinal.\n\n**Hallazgos Clave:**  \nAnte la sospecha de una obstrucción intestinal grave, posiblemente causada por torsión del colon (vólvulo de sigmoides) o adherencias (bandas de tejido cicatricial que pueden causar obstrucción), se decidió realizar una cirugía de emergencia (laparotomía). Durante la operación, se encontró que el ciego (la primera parte del colon) estaba anormalmente desplazado y flexionado hacia adelante y hacia la izquierda, sin estar fijado a la pared abdominal como es habitual. Esta torsión fue causada por una banda de adherencia sobre el colon ascendente. No se observaron signos de daño grave como falta de riego sanguíneo (isquemia), muerte del tejido (necrosis) o perforación. Se liberó la adherencia que causaba la torsión, se descomprimió el ciego mediante la extracción del apéndice (apendicectomía) y se fijó el ciego a la pared abdominal (cecopexia) para evitar futuras torsiones.\n\n**Interpretación Clínica:**  \nEl diagnóstico final fue un vólvulo cecal del tipo “báscula”, una torsión del ciego que puede provocar obstrucción intestinal pero que en este caso no comprometió la circulación sanguínea ni causó daño irreversible. La intervención quirúrgica oportuna permitió resolver la obstrucción, evitar complicaciones mayores y preservar la integridad del colon.\n\n**Próximos Pasos:**  \nTras la cirugía, la paciente mostró una recuperación favorable, con retorno normal de las evacuaciones intestinales y ausencia de síntomas. Fue dada de alta y se mantuvo en seguimiento ambulatorio con controles periódicos en consulta externa de cirugía, donde continuó asintomática y sin complicaciones. Este caso resalta la importancia del diagnóstico temprano y tratamiento quirúrgico adecuado en pacientes con obstrucción intestinal por vólvulo cecal.",
+        "scores": {
+          "ROUGE-1": 0.25840707964601767,
+          "ROUGE-2": 0.10301953818827707,
+          "ROUGE-L-Sum": 0.25132743362831855,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      }
+    }
+  },
+  {
+    "article": "Paciente de sexo femenino de 10 años, sin historia familiar de enfermedad tiroidea, portadora de bocio diagnosticado a los 9 años (ecografía tiroidea con sig nos compatibles de tiroiditis crónica) con presencia de anticuerpos antitiroideos positivos. Sin tratamiento al momento del ingreso hospitalario. Consultó por orina de aspecto espumoso de 5 días de evolución, asociado a dolor abdominal, vómitos profusos y diarrea. Evo lucionó con edema palpebral y de extremidades, disminución de la diuresis, decaimiento y fiebre de 38° C el día previo a su ingreso. Al momento de su eva luación en el servicio de urgencia destacó una pacien te con edema palpebral bilateral y pretibial, con bocio evidente (indoloro y sin nódulos palpables) y presen cia de soplo sistólico eyectivo en foco pulmonar IV/VI sin irradiación. Resto del examen sin alteraciones de significancia. Presión arterial 120/78 mmHg (percentil 95), temperatura 38,1°C, peso: 33.9 Kg, talla: 131,5 cm (p7), IMC 19,8 (p83).\n\nDentro de sus exámenes de admisión destacaron examen de orina completa con proteinuria +++, sin bacterias, sin nitritos, leucocitos 7 cel/uL (VN: 0-10 cel/uL), eritrocitos 4 cel/uL (VN: 0-15 cel/uL), índice proteinuria/creatininuria (IPC) 2 mg/mg, proteínas totales de 3.8 g/dL, hipoalbuminemia de 2,1 g/dL, hipercolesterolemia de 416 mg/dL, hipertrigliceridemia de 127 mg/dL y creatinina plasmática de 0,46 mg/dL (aclaramiento de creatinina calculado por fórmula de Schwartz: 125 ml/min/1,73 m2). Gases venosos, elec trolitos plasmáticos y hemograma dentro de rangos normales. En cuanto al estudio inmunológico destacó: inmunoglobulina A 181 mg/dL (VN 45-236), inmunoglobulina M 131 mg/dL (VN 52-242), inmunoglobulina G 208 (VN 608-1572) mg/dL, C3 125 mg/dL (VN 80-150), C4 37,3 mg/dL (VN 12-36). Ecografía renal normal. Se ingresó a la paciente con diagnóstico de SN y tiroiditis autoinmune.\n\nEn el contexto de SN se inició tratamiento con prednisona (60 mg/m2/día), con buena respuesta, logrando fundir edema y disminuir progresivamente la proteinuria hasta alcanzar rangos normales previo al egreso (IPC de egreso: 0.09, a los 6 días).\n\nDel punto de vista de función tiroidea su estudio mostró hormona tiroestimulante (TSH) 4,4 UI/ml (VN: 0,67-4,16 UI/ml), tiroxina (T4) libre 0,80 ng/ dL (VN: 0,86-1,4 ng/dL), anticuerpos antiperoxidasa (Anti Tpo) 120 U/ml (VN: 0-60 U/ml), anticuerpos antitiroglobulina (Anti-Tg) 82 U/ml (VN: 0-60 U/ ml), por lo que se inició terapia de sustitución con levotiroxina (25 mcg/día). La ecografía tiroidea descri bió tiroides de tamaño normal con leve aumento de vascularización difusa al Doppler, sin lesiones focales sólidas ni quísticas, siendo estos hallazgos sugerentes de tiroiditis. Resto del estudio (PCR para SARS CoV-2, anticuerpos anti citoplasma de neutrófilos, anticuer pos anti nucleares, anticuerpos anti DNA, anticuerpos anti estreptolisina O, anticuerpos anticardiolipinas, anticuerpos anti mieloperoxidasa y anticuerpos anti proteinasa 3) resultó negativo.\n\nA los 6 días de ingresada la paciente se encontraba en buenas condiciones, siendo dada de alta con prednisona (60 mg al día) y levotiroxina (25 ucg al día). En el seguimiento a los 12 meses la paciente se encontraba asintomática, con su patología tiroidea bajo control (TSH 1,11 UI/ml) con tratamiento de sustitución. No ha presentado recaídas del SN (examen de orina sin proteinuria y creatinina 0,44 mg/dL).",
+    "gold_summary": "Paciente de 10 años que se presenta con síndrome nefrótico y bocio. Se pesquisa antecedente de tiroiditis autoinmu ne e hipotiroidismo no tratado. Se inicia terapia corticoidal y hormonal de sustitución (levotiroxina), logrando buena respuesta clínica y de laboratorio.",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Niña de 10 años con hinchazón en el cuerpo y cuello grande. Tenía un problema en la tiroides que no se había tratado. Le dieron medicinas para ayudar su cuerpo y se puso mejor.",
+        "scores": {
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+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
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+      "B2": {
+        "text": "**Lo que le Pasó a la Paciente**  \nUna niña de 10 años llegó al hospital con hinchazón en los ojos y las piernas, además de orina con espuma. Ella tenía un bocio, que es cuando la glándula tiroides en el cuello está agrandada. También se sabía que tenía tiroiditis autoinmune, una enfermedad donde el cuerpo ataca su propia tiroides, y no estaba tomando ningún medicamento para eso.\n\n**Qué Encontraron en los Exámenes**  \nLos análisis de orina mostraron mucha proteína, lo que indica que los riñones no estaban funcionando bien. Esto se llama síndrome nefrótico, una condición que causa que el cuerpo pierda proteínas importantes. Además, sus niveles de algunas hormonas de la tiroides estaban bajos y tenía anticuerpos que confirmaban la tiroiditis. La ecografía del cuello mostró inflamación en la tiroides, pero sin tumores.\n\n**Cómo la Trataron y Qué Pasó Después**  \nLe dieron un medicamento llamado prednisona, que es un corticoide para reducir la inflamación, y levotiroxina, que es una hormona para ayudar a su tiroides a funcionar mejor. Con este tratamiento, la hinchazón bajó y los análisis mejoraron rápidamente. Después de un año, la niña estaba bien, sin síntomas y con su tiroides controlada gracias a la medicación. No tuvo problemas nuevos en los riñones.",
+        "scores": {
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+          "ROUGE-2": 0.0425531914893617,
+          "ROUGE-L-Sum": 0.16901408450704225,
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+      "B3": {
+        "text": "**Contexto:**  \nSe trata de una niña de 10 años con diagnóstico previo de bocio (aumento visible de la glándula tiroides) y tiroiditis autoinmune (una inflamación de la tiroides causada por el propio sistema inmunológico), sin tratamiento para su hipotiroidismo (función tiroidea disminuida) al momento de su ingreso hospitalario. Consultó por síntomas relacionados con síndrome nefrótico, que incluyen orina espumosa, edema (hinchazón) en párpados y extremidades, disminución de la cantidad de orina, dolor abdominal, vómitos y fiebre.\n\n**Hallazgos Clave:**  \n- En la evaluación inicial, se observó edema palpebral bilateral y en las piernas, así como un bocio evidente pero sin nódulos dolorosos. Además, presentó un soplo cardíaco leve.  \n- La presión arterial estaba en el límite superior normal para su edad.  \n- Los análisis de orina mostraron una proteinuria significativa (pérdida elevada de proteínas en la orina), sin signos de infección.  \n- En sangre, se detectó hipoalbuminemia (niveles bajos de albúmina, una proteína importante), hipercolesterolemia y niveles normales de creatinina, indicando función renal preservada.  \n- Los estudios inmunológicos confirmaron la presencia de anticuerpos antitiroideos elevados, compatibles con tiroiditis autoinmune, y niveles normales de otros marcadores inflamatorios y autoinmunes.  \n- La ecografía tiroidea mostró un tamaño normal de la glándula pero con aumento difuso de la vascularización, típico de tiroiditis.  \n- No se encontraron otras enfermedades autoinmunes o infecciones asociadas.\n\n**Interpretación Clínica:**  \nLa paciente presentó un síndrome nefrótico (una enfermedad renal caracterizada por pérdida excesiva de proteínas en la orina y edema) asociado a una tiroiditis autoinmune con hipotiroidismo no tratado. La coexistencia de estas dos condiciones autoinmunes sugiere un trastorno inmunológico subyacente que afecta tanto la tiroides como el riñón.\n\n**Próximos Pasos y Tratamiento:**  \nSe inició tratamiento con prednisona (un corticosteroide) para controlar el síndrome nefrótico, logrando una rápida mejoría clínica y normalización de la proteinuria en pocos días. Paralelamente, se comenzó terapia de reemplazo hormonal con levotiroxina para corregir el hipotiroidismo. La paciente fue dada de alta en buenas condiciones y, tras un seguimiento de 12 meses, se mantuvo asintomática, con función tiroidea controlada y sin recaídas del síndrome nefrótico.\n\nEste caso destaca la importancia de identificar y tratar de manera integral las enfermedades autoinmunes coexistentes para lograr una recuperación óptima y prevenir complicaciones a largo plazo.",
+        "scores": {
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+          "ROUGE-2": 0.0525164113785558,
+          "ROUGE-L-Sum": 0.13943355119825707,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
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+  {
+    "article": "La exploración neurológica exhaustiva puso de manifiesto una apariencia facial característica: mirada fija con los ojos muy abiertos, fruncimiento de la frente con una expresión de ceño fruncido (signo del procerus) y expresión fija de la parte inferior de la cara. La paciente presentaba hipocinesia-rigidez simétrica de predominio axial con postura retrocólica del tronco y el cuello. El examen de la deambulación reveló un patrón de la marcha del nivel superior caracterizado por una llamativa vacilación inicial que requería ayuda de objetos/personas cercanas. Una vez que comenzaba a caminar, los pasos mejoraban relativamente, pero volvía a aparecer una marcha inefectiva cuando intentaba girar. Exhibía zancadas cortas, congelación, base amplia de sustentación, desequilibrio, movimiento lento de los miembros inferiores, arrastre de los pies y pérdida de la fluidez normal del tronco y las extremidades. Los reflejos posturales estaban alterados. Asimismo, existía una dificultad grave para la bipedestación tras la sedestación y dificultad para darse la vuelta en la cama. Sin embargo, los signos frontales, como la rigidez paratónica, los reflejos de prensión, la incontinencia urinaria y las características de los déficits cognitivos frontales (por ejemplo, cambios disejecutivos y de personalidad e impulsividad) estaban ausentes, excepto por un estado apático progresivo. Los movimientos oculares sacádicos verticales estaban alterados, con amplitudes relativamente normales y movimientos sacádicos horizontales. Se evidenciaron sacadas de onda cuadrada y una oftalmoplejía supranuclear. La resonancia magnética del cerebro reveló atrofia del mesencéfalo, dilatación del acueducto de Silvio y del III ventrículo y atrofia de los lóbulos frontales, y los signos típicos del colibrí y de la gloria de la mañana. Finalmente, la paciente fue diagnosticada de una PSP probable.",
+    "gold_summary": "Mujer de 58 años sana que consultó por un trastorno de la marcha con caídas. La exploración neurológica mostró una apariencia facial característica (mirada fija, ojos muy abiertos, ceño fruncido y expresión fija hemifacial inferior), e hipocinesia-rigidez simétrica de predominio axial (postura retrocólica del tronco y el cuello). La exploración de la marcha reveló un trastorno de la marcha del nivel superior, caracterizado por una significativa vacilación inicial, que precisaba ayuda de objetos/personas cercanos. Al iniciar la marcha, los pasos mejoraban relativamente, pero reaparecía una deambulación inefectiva al girar. Presentaba zancadas cortas, congelación, base amplia de sustentación, desequilibrio, movimiento lento de las piernas, arrastre de los pies, y pérdida de la cadencia normal del tronco y las extremidades. Los reflejos posturales estaban alterados. La resonancia magnética cerebral desveló atrofia mesencefálica, dilatación de acueducto de Silvio y III ventrículo, atrofia frontal bilateral y el signo típico del colibrí. Finalmente, la paciente fue diagnosticada de una PSP probable.",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Había una señora que tenía problemas para caminar. Sus ojos se veían muy abiertos y su cara parecía quieta. Caminaba con pasos cortos y a veces se paraba sin poder seguir. Le costaba mucho girar y mantener el equilibrio. Su cuerpo estaba un poco rígido y lento. En el doctor, vieron que su cerebro estaba un poco cambiado. Por eso, dijeron que tenía una enfermedad que hace difícil caminar y moverse bien.",
+        "scores": {
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+        "text": "**Lo que Encontraron en la Paciente**\n\nUna mujer de 58 años, que antes estaba sana, empezó a tener problemas para caminar y se caía con frecuencia. Al examinarla, los médicos notaron que su cara tenía una expresión especial: sus ojos estaban muy abiertos y fijos, tenía el ceño fruncido y la parte baja de su cara parecía inmóvil. También tenía rigidez y movimientos lentos en el tronco y el cuello, con una postura inclinada hacia atrás.\n\nCuando caminaba, al principio dudaba mucho y necesitaba ayuda para no caerse. Después de unos pasos, mejoraba un poco, pero al girar volvía a tener problemas para caminar bien. Sus pasos eran cortos, a veces se quedaba paralizada (congelación), mantenía los pies separados para no perder el equilibrio, y arrastraba los pies. Además, sus movimientos eran lentos y perdía la forma normal de mover el cuerpo y las piernas. Los reflejos que ayudan a mantener el equilibrio también estaban afectados.\n\n**Lo que Vieron en el Cerebro**\n\nUna resonancia magnética, que es una imagen detallada del cerebro, mostró que algunas partes importantes estaban más pequeñas de lo normal. En especial, el mesencéfalo (una parte del cerebro que controla movimientos), el acueducto de Silvio y el tercer ventrículo (espacios llenos de líquido en el cerebro) estaban dilatados o agrandados. También había pérdida de tejido en los lóbulos frontales, que son áreas importantes para pensar y controlar movimientos. Además, apareció un signo especial llamado \"signo del colibrí\", que ayuda a los médicos a identificar esta enfermedad.\n\n**Qué Significa Todo Esto**\n\nCon estos síntomas y los resultados del examen, los médicos concluyeron que la paciente probablemente tiene una enfermedad llamada parálisis supranuclear progresiva (PSP). Esta enfermedad afecta el control de los movimientos, el equilibrio y la expresión facial, y suele empeorar con el tiempo. Aunque no tiene algunos síntomas típicos como problemas graves en la vejiga o cambios fuertes en la personalidad, sí muestra apatía, que es una falta de interés o motivación. Este diagnóstico ayudará a los médicos a planear el mejor cuidado para ella.",
+        "scores": {
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+          "ROUGE-2": 0.11849192100538601,
+          "ROUGE-L-Sum": 0.3220035778175313,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
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+      "B3": {
+        "text": "**Contexto**\n\nUna mujer de 58 años, previamente sana, acudió a consulta debido a problemas para caminar acompañados de caídas frecuentes. La evaluación neurológica detallada reveló signos característicos en su rostro y movimientos, así como alteraciones específicas en su forma de caminar y en estudios de imagen cerebral.\n\n**Hallazgos Clave**\n\n- **Apariencia facial característica:** La paciente mostraba una mirada fija con los ojos muy abiertos, fruncimiento de la frente que generaba una expresión de ceño fruncido (conocido como signo del procerus) y una expresión fija en la parte inferior de la cara.\n\n- **Alteraciones motoras:** Presentaba hipocinesia (movimientos lentos) y rigidez simétrica, principalmente en la zona axial, es decir, en el tronco y cuello, con una postura inclinada hacia atrás (retrocolis).\n\n- **Trastorno de la marcha:** La forma de caminar mostraba un patrón típico de afectación del nivel superior del sistema nervioso. Inicialmente, la paciente vacilaba notablemente y necesitaba apoyo de objetos o personas para comenzar a caminar. Al avanzar, sus pasos mejoraban algo, pero al intentar girar reaparecía una marcha ineficaz. Además, caminaba con pasos cortos, episodios de congelación (parálisis temporal de la marcha), base amplia para mantener el equilibrio, desequilibrio general, movimientos lentos de las piernas, arrastre de los pies y pérdida de la fluidez normal del tronco y extremidades. Los reflejos posturales, que ayudan a mantener la estabilidad, estaban alterados.\n\n- **Movimientos oculares:** Se observaron alteraciones en los movimientos sacádicos (movimientos rápidos del ojo para cambiar la mirada), especialmente en la dirección vertical, con una oftalmoplejía supranuclear, que implica dificultad para mover los ojos hacia arriba o abajo debido a un problema en el cerebro.\n\n- **Ausencia de otros signos frontales:** No se detectaron rigidez paratónica (una rigidez muscular variable), reflejos de prensión (agarre involuntario), incontinencia urinaria ni déficits cognitivos frontales típicos (como problemas en la planificación, cambios de personalidad o impulsividad), salvo un estado de apatía progresiva.\n\n- **Imágenes cerebrales:** La resonancia magnética mostró atrofia (pérdida de volumen) del mesencéfalo (una parte del tronco cerebral), dilatación del acueducto de Silvio y del tercer ventrículo (estructuras por donde circula el líquido cefalorraquídeo), atrofia bilateral de los lóbulos frontales y la presencia de signos característicos conocidos como el “signo del colibrí” y la “gloria de la mañana”, que son patrones específicos de daño cerebral en esta enfermedad.\n\n**Interpretación Clínica**\n\nEl conjunto de síntomas, signos neurológicos y hallazgos en la resonancia magnética son compatibles con un diagnóstico probable de parálisis supranuclear progresiva (PSP), una enfermedad neurodegenerativa que afecta principalmente el control del movimiento, el equilibrio y los movimientos oculares, con daño en áreas profundas del cerebro.\n\n**Próximos Pasos**\n\nEl diagnóstico de PSP implica un seguimiento neurológico continuo para manejar los síntomas, prevenir caídas y mejorar la calidad de vida. Aunque actualmente no existe una cura, el tratamiento puede incluir terapias físicas, medicamentos para controlar la rigidez y la lentitud de movimientos, y apoyo multidisciplinario para abordar las dificultades motoras y cognitivas que puedan surgir.",
+        "scores": {
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
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+    "article": "Una mujer de 36 años, previamente sana, fue picada una vez por un insecto Hymenoptera desconocido, lo que le provocó hinchazón y eritema en la parte dorsal de la mano derecha. La fiebre punzante apareció en un plazo de 6 horas, a pesar de que el sitio de la picadura se volvió irreconocible gradualmente. Acudió a una clínica local donde le recetaron esteroides orales (prednisolona 20 mg/día) y antibióticos. Tres días después, acudió a nuestro departamento de urgencias por una fiebre intermitente. Presentaba una temperatura elevada (38,9°C), taquicardia e hipotensión (presión arterial 80/52 mmHg) en el momento de la clasificación. La electrocardiografía mostró fibrilación auricular con una frecuencia ventricular rápida de alrededor de 130 latidos por minuto y elevación difusa del ST. La radiografía de tórax mostró una relación cardiotorácica normal sin signos de infiltración o congestión. El hemograma no mostró eosinofilia, leucocitosis, leucopenia o desviación a la izquierda. La isoenzima MB de creatina cinasa (CK-MB) y la troponina cardíaca I se elevaron a 96,0 ng/mL y 8,0 ng/mL, respectivamente. La proteína C reactiva fue de 10,5 mg/L y la procalcitonina fue de 0,32 ng/mL. El NT-proBNP fue de 20 700 pg/mL. La ecocardiografía mostró una hipocinesia global del ventrículo izquierdo con una fracción de eyección del 30,6% y sin derrame pericárdico. El cateterismo cardíaco emergente no reveló lesiones de las arterias coronarias o vasospasmo. Se insertó un globo intraaórtico durante el procedimiento para el shock cardiogénico. La hipotensión progresó acompañada de taquicardia ventricular y fibrilación ventricular, y luego se produjo un paro cardíaco intrahospitalario. La reanimación cardiopulmonar manual no tuvo éxito durante 25 minutos y se usó el soporte cardiopulmonar percutáneo (PCPS, CAPIOX® Centrifugal Pump Controller SP-200, Terumo). La circulación espontánea se estableció 25 minutos después con una recuperación total de la conciencia.\n\nLa prueba rápida de antígeno de influenza (Directigen EZ Flu A+B; BD, Franklin Lakes, NJ, EE. UU.), los cultivos de esputo, los cultivos de sangre y los exámenes serológicos para los virus respiratorios recolectados al ingreso fueron negativos. En el día 2 del ingreso, los niveles séricos de CK-MB y troponina I alcanzaron un máximo de >303 ng/ml y >81 ng/ml, respectivamente. La ecocardiografía de seguimiento 24 horas después del inicio del PCPS mostró deterioro de la función ventricular izquierda, cierre persistente de las válvulas aórticas y trombos intracardiacos en la aurícula izquierda y el ventrículo izquierdo, aproximadamente 24 horas después del inicio del soporte mecánico. En el día 3, el shock progresó con falla multiorgánica. Se aplicó hemodiálisis venovenosa continua debido a la acidosis metabólica y oliguria. En el día 4, la función ventricular derecha también se deterioró gravemente y la actividad eléctrica del corazón desapareció gradualmente. El PCPS se cambió a soportes mecánicos bi-ventriculares a través de canalizaciones hacia la aurícula derecha, el tronco pulmonar, el ápex del ventrículo izquierdo y la aorta ascendente. Ambos sistemas se establecieron utilizando bombas de sangre centrífugas MEDTRONIC Affinity CP. Debido a la hemorragia pulmonar con consolidación bilateral severa de los pulmones, se usó un oxigenador de membrana para lograr una oxigenación adecuada. El flujo sanguíneo se estableció a 3.5 L/minuto, lo que podría mantener la presión arterial media en torno a 65 mmHg. Se realizó una biopsia endomiocárdica del ventrículo izquierdo y la patología reveló una inflamación significativa compuesta principalmente por linfocitos y algunos eosinófilos. El daño miocárdico con necrosis estuvo presente, pero no extenso. En términos de ajustes de ventilador, la presión de conducción y la presión de meseta se establecieron en torno a 15 y 30 cmH2O respectivamente para la protección pulmonar. Se usó la fibra broncoscopia repetidamente para eliminar los coágulos de sangre que obstruían las vías respiratorias principales. En el día 13 del ingreso, la actividad eléctrica del corazón del paciente permaneció ausente y ambas bombas de sangre se cambiaron a los sistemas de asistencia ventricular Levitronix Centri-Mag (Levitronix LLC, Waltham, MA, EE. UU.) para un mejor soporte. El paciente fue trasladado a un centro de trasplantes y se registró como candidato para un trasplante de corazón. En el día 14 se insertó otra cánula en la vena femoral común izquierda para aumentar el flujo de entrada del VAD derecho. Desde el día 14 hasta el día 48, el paciente sufrió episodios de sangrado masivo del mediastino y la vagina, infección de la herida esternal con formación de abscesos, infecciones por úlceras de presión y progresiva hiperbilirrubinemia. Su condición se estabilizó después de desbridamiento, hemostasia quirúrgica y uso de antibióticos fuertes. Se sometió a 5 cursos de intercambio de plasma terapéutico para evitar el rechazo mediado por anticuerpos y recibió un trasplante de corazón ortotópico el día 49. El estudio patológico del corazón del paciente mostró pancarditis de ambos ventrículos y ninguna alteración específica de las 3 arterias coronarias. La ECMO de VA se mantuvo hasta el día 58 para el apoyo postoperatorio del fallo cardiaco. La biopsia endomiocárdica repetida después del trasplante no mostró evidencia de rechazo celular o humoral. La paciente experimentó episodios de shock séptico bajo inmunosupresión y se sometió a una laparoscopia exploratoria y apendicectomía el día 93. La extubación se realizó el día 96 y se dio de alta el día 101. La paciente permaneció clínicamente estable en el seguimiento de 3 meses.\n\nMH - Adulto\nMH - Animales\nMH - Abejas\nMH - Picaduras y mordeduras/*complicaciones\nMH - Oxigenación por membrana extracorpórea\nMH - Mujer\nMH - Paro cardiaco/*etiología/tratamiento\nMH - Insuficiencia cardiaca/*etiología/terapia\nMH - *Trasplante de corazón\nMH - Dispositivos de asistencia cardiaca\nMH - Humanos\nMH - Hipersensibilidad/*diagnóstico\nMH - Miocarditis/*diagnóstico\nMH - Shock, Cardiogénico/*etiología/terapia\n",
+    "gold_summary": "Paciente: Mujer, 36 años\n\nDiagnóstico final: Shock cardiogénico • miocarditis\n\nSíntomas: Fiebre\n\nMedicación: —\n\nProcedimiento clínico: soporte circulatorio mecánico\n\nEspecialidad: Cirugía\n\n\nInforme del caso:\n\nReportamos el caso de una mujer de 36 años que desarrolló fiebre y shock cardiogénico 3 días después de una picadura de abeja. La angiografía cardíaca mostró arterias coronarias permeables y una función ventricular izquierda gravemente comprometida. Su hemodinámica permaneció inestable bajo una dosis alta de agentes inotrópicos y apoyo con un balón intraaórtico. El paro cardíaco intrahospitalario ocurrió 4 horas después del ingreso y recibió reanimación cardiopulmonar extracorpórea. Su oxigenación de membrana extracorpórea venosa periférica (VA ECMO) se cambió a dispositivos de asistencia ventricular bilateral (VAD) debido a una insuficiencia cardíaca derecha progresiva. El resultado de la biopsia endomiocárdica fue compatible con el cuadro de miocarditis por hipersensibilidad. Su corazón entró en paro persistente bajo apoyo circulatorio mecánico. Se sometió a un trasplante de corazón el día 49 del ingreso y permaneció clínicamente estable 6 meses después del alta.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Una mujer de 36 años fue picada por una abeja. Tres días después, tuvo fiebre y su corazón se puso muy débil. Los doctores le ayudaron con máquinas para que su corazón pudiera latir. Su corazón no mejoró y se detuvo. Entonces, le pusieron un corazón nuevo. Después de eso, ella estuvo bien y fuerte.",
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+        "text": "Caso de una mujer de 36 años con problemas graves en el corazón tras una picadura de abeja\n\nLo que pasó:  \nUna mujer sana de 36 años fue picada por un insecto parecido a una abeja. Tres días después, empezó a tener fiebre y problemas serios en el corazón, llamados shock cardiogénico, que significa que el corazón no podía bombear suficiente sangre. Cuando la revisaron, sus arterias del corazón estaban normales, pero el ventrículo izquierdo (una parte importante del corazón) no funcionaba bien.\n\nQué hicieron los médicos:  \nIntentaron ayudarla con medicamentos para mejorar la fuerza del corazón y usaron un balón intraaórtico, que es un dispositivo que ayuda a que el corazón trabaje mejor. Sin embargo, su estado empeoró y sufrió un paro cardíaco, que es cuando el corazón deja de latir. La reanimaron usando una máquina especial que hace el trabajo del corazón y los pulmones (oxigenación por membrana extracorpórea o ECMO). Más tarde, cambiaron esta máquina por dispositivos que ayudan a ambos lados del corazón (asistencia ventricular bilateral), porque la parte derecha del corazón también empezó a fallar.\n\nQué encontraron:  \nTomaron una pequeña muestra del músculo del corazón (biopsia endomiocárdica) y vieron que tenía inflamación causada por una reacción alérgica, llamada miocarditis por hipersensibilidad. Esto significa que el corazón estaba dañado por la respuesta del cuerpo a la picadura.\n\nQué pasó después:  \nEl corazón dejó de funcionar completamente a pesar de las máquinas que lo ayudaban. Por eso, le hicieron un trasplante de corazón el día 49 después de entrar al hospital. Se recuperó bien y estuvo estable durante al menos seis meses después de salir del hospital.\n\nEn resumen:  \nUna picadura de abeja causó una inflamación grave en el corazón de esta mujer, que llevó a una falla cardíaca muy seria. Gracias a tratamientos avanzados y un trasplante de corazón, pudo recuperarse. Este caso muestra lo importante que es tratar rápido y con cuidado las reacciones alérgicas que afectan al corazón.",
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+        "text": "**Contexto**  \nSe presenta el caso de una mujer de 36 años, previamente sana, que desarrolló un cuadro grave de insuficiencia cardíaca tras una picadura de abeja. Inicialmente, la paciente presentó hinchazón y enrojecimiento en la mano derecha, seguidos de fiebre en menos de 6 horas. A pesar del tratamiento inicial con esteroides y antibióticos, evolucionó con fiebre intermitente, taquicardia, hipotensión y alteraciones electrocardiográficas que indicaban compromiso cardíaco.\n\n**Hallazgos Clave**  \nAl ingreso, la paciente mostró signos de shock cardiogénico (presión arterial baja y ritmo cardíaco acelerado con fibrilación auricular), elevación significativa de marcadores cardíacos (troponina I y CK-MB), y una función ventricular izquierda gravemente reducida (fracción de eyección del 30,6%) sin evidencia de enfermedad coronaria obstructiva en el cateterismo. La ecocardiografía reveló además la presencia de trombos dentro del corazón. A pesar del soporte con balón intraaórtico y medicamentos para mejorar la función cardíaca, la paciente sufrió un paro cardíaco intrahospitalario que requirió reanimación cardiopulmonar asistida con soporte mecánico extracorpóreo (PCPS).\n\nDurante su evolución, la función cardíaca se deterioró progresivamente, afectando ambos ventrículos, y se desarrolló falla multiorgánica que requirió hemodiálisis y soporte ventilatorio avanzado. La biopsia endomiocárdica evidenció inflamación significativa con predominio de linfocitos y algunos eosinófilos, compatible con miocarditis por hipersensibilidad (una inflamación del músculo cardíaco probablemente desencadenada por una reacción alérgica o inmunológica). La paciente presentó complicaciones graves como hemorragias, infecciones y problemas en la cicatrización, que fueron manejados con intervenciones quirúrgicas y tratamientos antibióticos.\n\n**Interpretación Clínica**  \nEl cuadro clínico y los estudios realizados indican que la paciente desarrolló una miocarditis severa secundaria a una reacción de hipersensibilidad tras la picadura de abeja, que llevó a un shock cardiogénico refractario y paro cardíaco. La ausencia de enfermedad coronaria y la inflamación observada en la biopsia apoyan este diagnóstico. El soporte mecánico avanzado, incluyendo dispositivos de asistencia ventricular bilateral y oxigenación por membrana extracorpórea, fue fundamental para mantener la circulación y oxigenación mientras se evaluaba la posibilidad de trasplante cardíaco.\n\n**Próximos Pasos y Evolución**  \nDada la persistencia del fallo cardíaco y la ausencia de recuperación, la paciente fue registrada como candidata para trasplante de corazón y recibió el trasplante ortotópico en el día 49 de hospitalización. Posteriormente, se mantuvo bajo soporte postoperatorio con ECMO y fue monitoreada para detectar rechazo cardíaco, sin evidencia de este. A pesar de episodios de shock séptico y la necesidad de cirugía abdominal, la paciente logró estabilizarse, fue extubada y dada de alta al día 101. En el seguimiento a tres meses, se mantuvo clínicamente estable.\n\n**Resumen Final**  \nEste caso ilustra una forma grave y poco común de miocarditis por hipersensibilidad desencadenada por una picadura de abeja, que evolucionó rápidamente hacia un shock cardiogénico y paro cardíaco. El manejo multidisciplinario con soporte circulatorio mecánico avanzado y trasplante cardíaco fue esencial para la supervivencia y recuperación de la paciente.",
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+    "article": "Un hombre de 24 años con complicaciones cardiovasculares relacionadas con MFS fue admitido en nuestro departamento de medicina interna debido a 3 episodios consecutivos de insuficiencia cardiaca aguda descompensada con fracción de eyección reducida (ADHFrEF) de 2014 a 2017. Su historia médica restante incluye hipertensión arterial, dislipidemia, hipertiroidismo, shock anafiláctico debido a flecainida y hábito tabágico previo.\n\nEl diagnóstico de MFS se realizó en 2010, cuando se llevó a cabo la sustitución de la aorta ascendente y la válvula aórtica con prótesis mecánica debido a una disección aórtica aguda tipo A en presencia de antecedentes familiares (madre, padre y 3 hijos con MFS). Durante el período intraoperatorio, se produjo un síndrome coronario agudo inferior y se trató con cirugía de injerto de derivación de la arteria coronaria.\n\nEn mayo de 2014, se realizó la implantación de una prótesis mecánica de aorta descendente y arco aórtico debido a un aneurisma disecante crónico. El hematoma peri-aórtico y la isquemia medular complicaron la cirugía y causaron paraplejia de las extremidades inferiores, dolor y hipoestesia térmica, e incontinencia rectal. Después de 2 meses, durante su primera admisión por ADHFrEF, las pruebas de laboratorio fueron notables para N-terminal pro-BNP (NT-proBNP) de 12,000 pg/mL y el ecocardiograma transtorácico mostró una función de la prótesis normal, dilatación de todas las cámaras cardiacas (principalmente las izquierdas) con insuficiencia mitral y tricuspídea moderada, hipertrofia ventricular izquierda, acinesia de la pared inferior, discinesia septal e hipocinesia de las paredes restantes con reducción severa de la fracción de eyección ventricular izquierda (LVEF) −20%. Se le trató con diuréticos intravenosos y desfibrilador cardiaco interno (St. Jude Ellipse DR, modo DDD) sin terapia de resincronización cardiaca (criterios de electrocardiograma no cumplidos) y se le dio de alta con la máxima terapia médica (furosemida, carvedilol, ramipril, espironolactona, digoxina y amlodipina).\n\nEn agosto de 2017, se produjo un nuevo episodio de ADHFrEF. Los valores de laboratorio de admisión notables incluían NT-proBNP de 2719 pg/mL y midregional-proadrenomedullin (MR-proADM) de 1.61 nmol/L, mientras que el ecocardiograma transtorácico y transesofágico mostró un LVEF de 35%, función de prótesis normal, severa regurgitación tricuspídea, y ruptura de la valva anterior de la chorda tendineae con severa regurgitación mitral. Los pacientes fueron tratados con diuréticos intravenosos y digoxina y dados de alta con una terapia médica óptima (furosemida, carvedilol, ramipril, espironolactona, digoxina, y amlodipina).\n\nPor último, volvió a ser admitido en nuestro departamento de medicina interna en noviembre de 2017 debido a un tercer episodio de ADHFrEF y una acumulación de líquido mediastinal infectado secundaria a una corrección quirúrgica de insuficiencia valvular severa un mes antes con implantación de prótesis mecánica mitral (31 mm ST Jude) y anuloplastia tricúspide De Vega.\n\nEl examen físico reveló una presión arterial de 120/80 mm Hg, pulso de 82 bpm, frecuencia respiratoria de 26 apm, saturación de O2 de 87% en aire ambiente con posición ortopneica obligatoria, y un habitus marfanoide (peso de 147 kg, altura de 2.2 m). La evaluación cardiopulmonar reveló un segundo sonido cardíaco metálico, percusión opaca con reducción del frémito vocal táctil y crepitaciones en la base de los pulmones, disminución amplia de los sonidos respiratorios vesiculares, presencia de ascitis abundante e hinchazón de las piernas.\n\nLos valores de laboratorio notables incluyeron NT-proBNP de 10,132 pg/mL y MR-proADM de 2,36 nmoL/mL.\n\nEl análisis de gases arteriales reveló una hipoxemia grave con alcalosis respiratoria y metabólica (pH 7,56, pO2 46 mm Hg, pCO2 24,8 mm Hg, HCO3− 21,9 mm mol/L, gradiente alveolar-arterial 31 mm Hg). Aunque el electrocardiograma resaltó fibrilación auricular con frecuencia ventricular de 80 bpm, hipertrofia ventricular izquierda e isquemia subepicárdica infralateral, el ecocardiograma transtorácico mostró las mismas características que el anterior, excepto por una FEVI de 30 %, presencia de prótesis mecánicas mitrales con fuga paravalvular y gradiente medio de 9 mm Hg, e insuficiencia tricuspídea leve.\n\n\nEn la radiografía de tórax y en la tomografía computarizada de alta resolución se observa una congestión hilar con cardiomegalia, consolidación pulmonar en el lóbulo superior derecho y acumulación de líquido mediastínico infectado.\n\nEl paciente fue tratado con 250 mg de furosemida intravenosa por día, 100 mg de canrenona por día, 4,5 g de piperacilina/tazobactam cada 6 horas y 12 mg/kg de teicoplanina por día, y luego 12 mg/kg por día. El día 9, una vez alcanzada la estabilización hemodinámica, se agregó una dosis intermedia de sacubitril/valsartan de 49/51 mg por día a 3,125 mg de carvedilol por día, 100 mg de espironolactona por día, 250 mg de furosemida por día y 0,25 mg de digoxina por día.\n\nEn el seguimiento de 1 mes, sacubitril/valsartan se aumentó a 97/103 mg b.i.d. para la buena condición clínica del paciente, lo que permitió una reducción persistente y progresiva de los parámetros clínicos, de laboratorio (reducción de NT-proBNP e incremento de MR-proADM), de los parámetros ecocardiográficos (aumento del EFV final del ventrículo izquierdo (42 % vs 30 %), del diámetro final del ventrículo izquierdo, del diámetro diastólico final del ventrículo izquierdo, de la masa del ventrículo izquierdo y del índice de masa del ventrículo izquierdo) y una mejora de la calidad de vida sin nuevos episodios de ADHFrEF hasta el seguimiento de 9 meses (Fig. (Fig.1B1B y D; Tabla 1).1). Debido a la falta de un régimen de dosificación específico para sacubitril/valsartan en la miocardiopatía relacionada con la EM, utilizamos el esquema terapéutico recomendado.\n\nMH - Aminobutiratos/uso terapéutico\nMH - Antagonistas de los receptores de la angiotensina/*uso terapéutico\nMH - Compuestos de bifenilo\nMH - Combinaciones de fármacos\nMH - Insuficiencia cardiaca/*terapia farmacológica/*etiología\nMH - Humanos\nMH - Hombre\nMH - Síndrome de Marfan/*complicaciones\nMH - Tetrazoles/uso terapéutico\nMH - Resultado del tratamiento\nMH - Valsartán\nMH - Adultos jóvenes\n",
+    "gold_summary": "Preocupaciones de los pacientes:\nUn hombre de 24 años fue admitido en nuestro departamento de medicina interna debido a disnea, ascitis e hinchazón de las piernas. El análisis de gases en sangre arterial reveló una hipoxemia grave con alcalosis respiratoria y metabólica. La radiografía de tórax mostró una congestión hilar.\n\nDiagnósticos:\nInsuficiencia cardíaca aguda descompensada recurrente con fracción de eyección reducida a pesar de la terapia médica óptima en la cardiomiopatía relacionada con el síndrome de Marfan.\n\nIntervenciones y resultados:\nSe agregó sacubitril/valsartan a la terapia médica óptima después de la estabilización hemodinámica, lo que permitió una mejora clínica, de laboratorio y ecocardiográfica progresiva. El paciente mantuvo una supervivencia libre de insuficiencia cardiaca y una buena calidad de vida hasta el seguimiento de 9 meses.\n",
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+        "text": "Un hombre joven estaba muy cansado y con las piernas hinchadas. Tenía problemas para respirar y mucho líquido en su barriga. Los doctores hicieron pruebas y vieron que su corazón no estaba funcionando bien.\n\nÉl tiene una enfermedad que hace que su corazón sea débil. Los doctores le dieron medicinas para ayudarlo. Luego, le dieron una medicina nueva llamada sacubitril/valsartan.\n\nDespués de tomar la medicina nueva, el hombre se sintió mejor. Su corazón empezó a trabajar mejor y pudo vivir sin problemas por mucho tiempo. Los doctores están contentos porque está más sano y feliz.",
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+        "text": "**Lo que le Pasó al Paciente**  \nUn joven de 24 años con síndrome de Marfan, una enfermedad que afecta el corazón y los vasos sanguíneos, fue llevado al hospital porque tenía dificultad para respirar, líquido en el abdomen (ascitis) y piernas hinchadas. Al hacerle un análisis de sangre, encontraron que tenía poco oxígeno en la sangre y un desequilibrio en los ácidos y bases de su cuerpo. La radiografía de su pecho mostró que sus pulmones estaban congestionados.\n\n**Qué Diagnosticaron**  \nEl paciente tenía insuficiencia cardíaca aguda descompensada, lo que significa que su corazón no podía bombear sangre correctamente y esto empeoraba de forma repetida. Además, su corazón tenía una fracción de eyección reducida, que es una medida de qué tan bien el corazón bombea la sangre. Esto ocurrió a pesar de que ya estaba recibiendo el mejor tratamiento médico disponible para su condición relacionada con el síndrome de Marfan.\n\n**Cómo lo Trataron y Qué Resultó**  \nDespués de estabilizar su estado, los médicos añadieron un medicamento llamado sacubitril/valsartán a su tratamiento. Este medicamento ayuda al corazón a funcionar mejor. Gracias a esto, el paciente mejoró poco a poco en su salud general, en los resultados de sus análisis de sangre y en los exámenes del corazón por ecocardiograma. Durante los siguientes nueve meses, el joven no tuvo nuevos episodios graves de insuficiencia cardíaca y pudo mantener una buena calidad de vida.",
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+        "text": "**Contexto:**  \nUn hombre joven de 24 años con diagnóstico previo de síndrome de Marfan (una enfermedad genética que afecta el tejido conectivo y puede causar problemas cardiovasculares graves) fue ingresado en el hospital debido a dificultad para respirar, acumulación de líquido en el abdomen (ascitis) y edema en las piernas. Este paciente presentaba antecedentes complejos, incluyendo múltiples cirugías aórticas y valvulares, episodios repetidos de insuficiencia cardíaca aguda con función del corazón gravemente reducida, así como complicaciones neurológicas y respiratorias.\n\n**Hallazgos Clave:**  \nAl ingreso, el análisis de gases en sangre mostró una hipoxemia severa (bajo nivel de oxígeno en la sangre) acompañada de alcalosis respiratoria y metabólica, lo que indica un desequilibrio en el pH sanguíneo debido a problemas respiratorios y metabólicos. La radiografía de tórax reveló congestión en la zona hilar (área central del pulmón), cardiomegalia (aumento del tamaño del corazón) y consolidación pulmonar, además de una acumulación de líquido infectado en el mediastino (espacio entre los pulmones). El ecocardiograma evidenció una fracción de eyección ventricular izquierda (FEVI) reducida al 30%, presencia de prótesis valvulares mecánicas con fugas y regurgitación valvular, reflejando un deterioro significativo de la función cardíaca a pesar del tratamiento previo.\n\n**Interpretación Clínica:**  \nEl paciente sufría de insuficiencia cardíaca aguda descompensada recurrente con fracción de eyección reducida, a pesar de recibir la mejor terapia médica disponible hasta ese momento. Esta condición estaba relacionada con la miocardiopatía (enfermedad del músculo cardíaco) secundaria al síndrome de Marfan, que había provocado daños estructurales severos en el corazón y los vasos sanguíneos. La infección mediastínica y las complicaciones pulmonares añadían un riesgo significativo para su pronóstico.\n\n**Intervenciones y Resultados:**  \nTras estabilizar su condición hemodinámica, se incorporó a su tratamiento sacubitril/valsartán, un medicamento que combina un inhibidor de la neprilisina y un antagonista del receptor de angiotensina, conocido por mejorar la función cardíaca en insuficiencia cardíaca con fracción de eyección reducida. La introducción de este fármaco, junto con la terapia médica óptima previa (incluyendo diuréticos, betabloqueantes, inhibidores de la enzima convertidora de angiotensina, espironolactona y digoxina), permitió una mejora progresiva en sus síntomas clínicos, parámetros de laboratorio (disminución de marcadores como NT-proBNP, que indican estrés cardíaco) y en los estudios ecocardiográficos (aumento de la fracción de eyección y mejoría en las dimensiones y masa ventricular). Durante un seguimiento de nueve meses, el paciente no presentó nuevos episodios de insuficiencia cardíaca aguda y experimentó una mejora significativa en su calidad de vida.\n\n**Próximos Pasos:**  \nDado el éxito observado con sacubitril/valsartán en este caso, se sugiere considerar este tratamiento como una opción terapéutica en pacientes jóvenes con miocardiopatía asociada al síndrome de Marfan y fracción de eyección reducida, aunque se requiere más investigación para establecer pautas específicas de dosificación y manejo en esta población particular. Además, es fundamental continuar con un seguimiento estrecho para monitorear la función cardíaca, controlar las complicaciones infecciosas y ajustar la terapia según la evolución clínica.",
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+    "article": "Paciente masculino de 41 años de edad quien ingresó en 2016 al servicio de urgencia con politraumatismo producto de accidente de tránsito; con trauma en miembros inferioA B res, en los rayos X se observa fractura de platillos tibiales izquierdos y fractura subtrocanteriana derecha, trauma toracoabdominal y trauma craneoencefálico leve.\nSe le practica osteosíntesis de fémur con clavo cefalomedular largo a foco cerrado corrigiendo la fractura subtrocanteriana y se le aplica tutor externo transarticular de rodilla como medida de control de daño local provisional; 15 días después se realiza osteosíntesis definitiva de su fractura de platillos tibiales. Evolución adecuada y satisfactoria de platillos tibiales.\nEntre 2016 y 2019 tuvo episodios esporádicos de dolor en cadera derecha que cedían fácilmente al manejo con antiinflamatorios y analgésicos sin limitar las actividades de la vida diaria y en la toma de rayos X se observaba fatiga de los bloqueos distales con dudas de la consolidación de la fractura.\nEn 2020 se incrementa el dolor en la cadera que no cede con el tratamiento médico y se acompaña de limitación funcional. En los rayos X de control se evidencia ruptura del clavo cefalomedular en su tercio proximal y no unión de la fractura subtrocantérica.\nEn Febrero de 2020 intento fallido de extracción de material de osteosíntesis (extrainstitucional), por lo que es remitido a nuestra institución. Se lleva a cirugía el 8 de Febrero, se realiza retiro de material de osteosíntesis, curetaje y toma de cultivo de foco de no unión. Cultivo positivo para Klebsiella pneumoniae recibiendo tratamiento con meropenem intravenoso por 10 días. Posteriormente se le realizó un lavado quirúrgico con drenaje de hematoma para el 20 de Febrero realizar nueva osteosíntesis con clavo cefalomedular + injerto óseo autólogo (tomado de ambas crestas iliacas) en foco de no unión.\nReactivación de la infección en Marzo de 2020, requiriendo nuevamente cirugía para lavados y desbridamiento quirúrgicos seriados (#5). Se aísla nueva bacteria Enterobacter que es manejada con vancomicina y meropenem. A f inales de Abril completa tratamiento médico y se le da salida en condiciones estables.\nEn Mayo de 2020 por persistencia de la infección se retira el material de osteosíntesis, se deja un clavo TENS endomedular recubierto de cemento con antibióticos (gentamicina).\nA finales de Mayo después de dos lavados quirúrgicos se retiró el clavo TENS, resección de bordes de fractura (hasta hueso sano) injerto óseo endomedular con un segmento de 10 cm de peroné no vascularizado (autólogo) y fijación de la fractura con una placa de soporte condíleo de fémur distal; colocación de sistema VAC y cierre definitivo de la herida en un segundo tiempo el 28 de Mayo de 2020. El paciente evolucionó adecuadamente, la herida quirúrgica cicatrizó por completo hasta el día de hoy con infección en remisión y evidencia radiológica de consolidación de la fractura, además paciente asintomático con función preservada de la extremidad.",
+    "gold_summary": "Masculino de 41 años de edad que sufre fractura subtrocantérica derecha producto de un accidente de tránsito que requirió manejo de osteosíntesis. Con posterior ruptura del clavo cefalomedular en su tercio proximal, no unión de la fractura e infecciones en sitio de la fractura. Fue tratado con múltiples lavados quirúrgicos, antibioticoterapia y un procedimiento ortopédico y quirúrgico poco convencional como el uso de una placa de soporte condíleo de fémur distal y un injerto óseo endomedular con un segmento de 10 cm de peroné no vascularizado. Paciente con evolución satisfactoria y favorable.",
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+        "text": "Un hombre se lastimó mucho la pierna en un accidente. Su hueso del muslo se rompió y tuvo que ir al doctor para arreglarlo. El doctor puso un palo especial para que el hueso se pegara. \n\nPero el palo se rompió y el hueso no sanaba bien. También tuvo una infección que le dolía mucho. Los doctores limpiaron muchas veces la herida y le dieron medicinas para la infección. \n\nDespués, hicieron una operación especial para poner un hueso nuevo y un soporte para ayudar a que su pierna sanara. Ahora, el hombre está mejor y su pierna está sanando bien.",
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+        "text": "**Lo que le pasó al paciente:**  \nUn hombre de 41 años tuvo un accidente de tránsito que le causó una fractura en la parte superior del fémur derecho, llamada fractura subtrocantérica. Para arreglarla, los doctores usaron un clavo especial dentro del hueso (osteosíntesis).  \n\n**Problemas que surgieron:**  \nCon el tiempo, el clavo se rompió y la fractura no sanó bien, lo que se llama \"no unión\". Además, la zona se infectó con bacterias, lo que complicó la recuperación.  \n\n**Tratamientos realizados:**  \nEl paciente necesitó varias cirugías para limpiar la infección y quitar el material roto. También recibió antibióticos fuertes para combatir las bacterias. Para ayudar a que el hueso sanara, los médicos usaron un método especial que incluyó colocar una placa metálica para sostener el hueso y un injerto óseo. Este injerto fue un pedazo de hueso tomado de su propia pierna (del peroné) que se colocó dentro del hueso fracturado para ayudar a que creciera y se uniera.  \n\n**Resultado final:**  \nDespués de todo este tratamiento, el paciente mejoró mucho. La herida sanó bien, la infección desapareció y la fractura se unió correctamente. Ahora puede usar su pierna sin dolor y con buena función.",
+        "scores": {
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+      "B3": {
+        "text": "**Contexto**  \nSe trata de un hombre de 41 años que sufrió un accidente de tránsito en 2016, el cual le provocó múltiples lesiones, entre ellas fracturas en ambas piernas: una fractura subtrocantérica (zona proximal del fémur) en la cadera derecha y fracturas en los platillos tibiales izquierdos. Inicialmente, se le realizó una cirugía para estabilizar la fractura de cadera mediante un clavo cefalomedular largo, y posteriormente se corrigió la fractura de la tibia. Durante los primeros años, el paciente tuvo episodios esporádicos de dolor en la cadera derecha, pero sin limitación importante en sus actividades diarias.\n\n**Hallazgos Clave**  \nEn 2020, el dolor en la cadera derecha empeoró y se acompañó de dificultad para mover la pierna. Las radiografías mostraron que el clavo utilizado para fijar la fractura se había roto en su parte proximal y que la fractura no había sanado correctamente (no unión). Se intentó retirar el material de osteosíntesis en otro centro sin éxito, por lo que fue referido a un hospital especializado. Allí se realizó la extracción del material, limpieza quirúrgica de la zona afectada y se identificó una infección causada por la bacteria Klebsiella pneumoniae, que fue tratada con antibióticos intravenosos.  \n\nA pesar del tratamiento, la infección reapareció en marzo de 2020, detectándose otra bacteria llamada Enterobacter, lo que requirió múltiples cirugías adicionales para limpiar y desbridar (eliminar tejido infectado) la zona afectada, junto con un tratamiento combinado de antibióticos. Debido a la persistencia de la infección, en mayo se retiró nuevamente el material de fijación y se colocó un clavo recubierto con cemento impregnado con antibióticos para controlar la infección localmente.  \n\nFinalmente, se realizó una cirugía más compleja que incluyó la resección de los bordes de la fractura hasta llegar a hueso sano, la colocación de un injerto óseo endomedular (un segmento de 10 cm de hueso peroné tomado del mismo paciente, sin conexión vascular directa), y la fijación definitiva con una placa metálica especial para soportar la zona distal del fémur. Se utilizó además un sistema de vacío para favorecer la cicatrización de la herida.  \n\n**Interpretación Clínica**  \nEste caso representa una fractura compleja con complicaciones importantes como la no unión ósea y la infección crónica, que dificultaron la consolidación normal del hueso. La ruptura del clavo de fijación y la persistencia de bacterias resistentes requirieron un manejo multidisciplinario que combinó cirugía ortopédica avanzada, técnicas de control de infecciones y uso de injertos óseos autólogos (del propio paciente). El uso de un injerto no vascularizado de peroné y una placa de soporte condíleo fue una estrategia poco convencional pero necesaria para lograr la estabilidad y promover la curación ósea.  \n\n**Próximos Pasos**  \nTras la última cirugía y el tratamiento antibiótico, el paciente mostró una evolución favorable con cicatrización completa de la herida, remisión de la infección y evidencia radiológica de consolidación de la fractura. Actualmente se encuentra asintomático y conserva la función de la extremidad afectada. Se recomienda continuar con seguimiento clínico y radiológico para asegurar la estabilidad a largo plazo y prevenir posibles recaídas infecciosas o problemas mecánicos.",
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+    "article": "Una adolescente de 17 años se presentó en nuestra clínica con una historia de dos meses de dolor torácico en el lado izquierdo y una historia de una semana de dolor en la espalda en el nivel de T7. El dolor torácico se acompañaba de palpitaciones y disnea que ocurrían de tres a cuatro días por semana. Una semana antes de la primera visita, las palpitaciones y la disnea se hicieron menos frecuentes, y desarrolló un dolor sordo diario intermitente en el lado izquierdo del pecho y la parte media de la espalda sin radiación, en la mayoría de los casos. El dolor ocurría tanto con el ejercicio como en reposo, y duraba horas, sin factores agravantes o atenuantes. Informó una intensidad del dolor de 2 a 6 en una escala de 10 puntos. La intensidad cambiaba durante un ataque, y el promedio era 4. Estaba sana por lo demás. No había limitación en la vida diaria. Visitó a un médico local un mes antes de visitar nuestra clínica. Los resultados de los exámenes electrocardiográficos y de laboratorio de Holter fueron normales. Su historial médico incluía migraña durante tres años. Sus medicamentos regulares eran lomerizina, loxoprofen y naratriptan para la prevención y el tratamiento agudo de la migraña. Su migraña estaba bien controlada, y rara vez experimentaba ataques. Negó trauma o cirugías previas. Negó síntomas sospechosos o antecedentes familiares de afecciones autoinmunes o inflamatorias.\n\nSu presión arterial era de 107/60 mmHg y su pulso de 62 latidos/min. Medía 162 cm de altura y pesaba 43 kg, con un índice de masa corporal de 16,4 kg/m2. No se escuchaba ningún murmullo ni arritmia en su examen cardiovascular. Los pulmones estaban limpios a la auscultación bilateral. La palpación del tórax provocó un dolor local no reproducible en las articulaciones inferiores esterno-costales; la maniobra de tracción del brazo horizontal y la maniobra del gallo cantando no provocaron dolor. No había sensibilidad en los músculos y huesos de la parte superior del cuerpo.\n\nLos hallazgos electrocardiográficos y de laboratorio, incluida la función tiroidea, fueron normales. El examen radiográfico torácico y torácico mostró el enderezamiento de la columna torácica superior y una pérdida de la curvatura cifótica normal. Las radiografías de las costillas inferiores no revelaron fractura ni neumotórax. Sospechamos un síndrome de la espalda recta, de acuerdo con los dos criterios diagnósticos diferentes propuestos por Davies et al. y DeLeon et al. La distancia entre la mitad del borde anterior de T8 y una línea vertical que conecta T4 a T12 fue de 0.91 cm. El diámetro anteroposterior fue de 74.0 cm, y el diámetro transversal fue de 243.2 cm. Le aconsejamos que comenzara y continuara la terapia quiropráctica para aumentar la cifosis torácica. Procedimos con una espera vigilante durante un mes en atención ambulatoria.\n\nDespués de esta primera visita, el dolor de pecho y de espalda se alivió gradualmente. Las palpitaciones y la disnea apenas se produjeron. Todos los síntomas desaparecieron en tres semanas. En la visita de seguimiento de un mes, se realizó una ecocardiografía, que reveló una regurgitación mitral trivial sin prolapso. Confirmamos el diagnóstico de síndrome de espalda recta. Reaseguramos a la paciente de que la enfermedad es benigna y le aconsejamos que continuara con la terapia quiropráctica. No ha tenido recaída de síntomas graves ni necesidad de visitar el hospital. Nunca volvió a visitar nuestra clínica en el año siguiente.\n",
+    "gold_summary": "Una adolescente de 17 años se presentó con su madre en nuestra clínica con un historial de dos meses de dolor en el pecho izquierdo y un historial de una semana de dolor en la parte media de la espalda. Diagnosticamos el síndrome de la columna vertebral basado en los hallazgos radiográficos del pecho y la columna vertebral y los síntomas de dolor en el pecho, palpitaciones y disnea. Tranquilizamos a la paciente de que la enfermedad era benigna y le aconsejamos que iniciara y continuara con la terapia quiropráctica. Todos los síntomas, incluido el dolor de espalda, desaparecieron en tres semanas.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Había una niña de 17 años que tenía dolor en el pecho y en la espalda. Ella fue al doctor para que la ayudara. El doctor miró sus huesos con una foto especial. El doctor dijo que sus huesos estaban un poco rectos y eso le dolía. Le dijo que no era algo peligroso. Le dio un tratamiento para ayudar a que su espalda se sintiera mejor. Después de unas semanas, la niña ya no tenía dolor. Ahora está bien y feliz.",
+        "scores": {
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+      "B2": {
+        "text": "**Lo que le pasaba a la paciente**  \nUna chica de 17 años llegó a la clínica porque tenía dolor en el lado izquierdo del pecho durante dos meses y dolor en la parte media de la espalda desde hacía una semana. Además, sentía palpitaciones (cuando el corazón late rápido o irregular) y dificultad para respirar algunas veces.\n\n**Qué encontraron los médicos**  \nDespués de hacerle varios estudios, como radiografías del pecho y la columna, vieron que su columna torácica (la parte media de la espalda) estaba más recta de lo normal. Esto se llama \"síndrome de la espalda recta\". No encontraron problemas en el corazón ni en los pulmones que explicaran el dolor y los otros síntomas.\n\n**Qué hicieron y qué pasó después**  \nLos médicos le dijeron que esta condición no era peligrosa. Le recomendaron hacer terapia quiropráctica, que es un tratamiento donde un especialista ayuda a mejorar la postura y la movilidad de la columna. Después de seguir este tratamiento, todos sus síntomas, incluyendo el dolor y las palpitaciones, desaparecieron en tres semanas.\n\n**Qué significa esto**  \nEl síndrome de la espalda recta puede causar dolor en el pecho y la espalda, pero no es una enfermedad grave. Con el tratamiento adecuado, como la terapia quiropráctica, los síntomas pueden mejorar y desaparecer. Es importante consultar al médico para recibir el diagnóstico correcto y el tratamiento adecuado.",
+        "scores": {
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+      "B3": {
+        "text": "**Contexto**  \nUna joven de 17 años acudió a nuestra clínica acompañada por su madre, presentando un cuadro de dos meses con dolor en el lado izquierdo del pecho y una semana con dolor en la parte media de la espalda, específicamente a nivel de la séptima vértebra torácica (T7). Además, experimentaba episodios de palpitaciones (sensación de latidos cardíacos acelerados o irregulares) y dificultad para respirar (disnea) varias veces por semana. Estos síntomas comenzaron a mejorar una semana antes de la consulta, aunque persistía un dolor sordo e intermitente en la zona afectada, que podía durar horas y ocurría tanto en reposo como durante la actividad física.\n\n**Hallazgos Clave**  \nEl examen físico no mostró signos de enfermedad cardíaca ni pulmonar: la presión arterial y el pulso estaban dentro de rangos normales, no se detectaron ruidos anormales en el corazón ni en los pulmones, y no había sensibilidad en músculos o huesos que sugiriera inflamación o lesión. Los estudios electrocardiográficos y de laboratorio, incluyendo pruebas de función tiroidea, fueron normales. Las radiografías del tórax revelaron una alteración en la curvatura normal de la columna torácica superior, conocida como pérdida de la cifosis (curvatura hacia adelante), y se descartaron fracturas o neumotórax (colapso pulmonar).\n\nCon base en estos hallazgos y los criterios diagnósticos establecidos en la literatura médica, se identificó un síndrome conocido como “síndrome de la espalda recta” o “síndrome de la columna vertebral rectificada”, que se caracteriza por la pérdida de la curvatura normal de la columna torácica y puede asociarse a dolor torácico y dorsal.\n\n**Interpretación Clínica**  \nEl síndrome de la espalda recta es una condición benigna, es decir, que no pone en riesgo la vida ni causa daño grave a largo plazo. En este caso, se relacionó con los síntomas de dolor en el pecho y la espalda, así como con las palpitaciones y la disnea, que probablemente estaban vinculados a la alteración postural y mecánica de la columna vertebral.\n\n**Próximos Pasos y Evolución**  \nSe recomendó iniciar y mantener un tratamiento quiropráctico, que consiste en técnicas manuales para mejorar la movilidad y la postura de la columna, con el objetivo de restaurar la curvatura torácica normal. Durante el seguimiento ambulatorio, los síntomas fueron mejorando progresivamente hasta desaparecer completamente en tres semanas. Una ecocardiografía (ultrasonido del corazón) realizada un mes después mostró una regurgitación mitral trivial (un leve retorno de sangre en una válvula cardíaca) sin prolapso (sin desplazamiento anormal), lo cual no requería tratamiento. La paciente fue tranquilizada sobre la naturaleza benigna de su condición y se le aconsejó continuar con la terapia quiropráctica. No presentó recaídas ni necesidad de atención médica adicional en el año siguiente.\n\n**Resumen Final**  \nUna adolescente con dolor torácico y dorsal, acompañado de palpitaciones y dificultad para respirar, fue diagnosticada con síndrome de la espalda recta tras estudios clínicos y radiográficos. Con tratamiento quiropráctico y seguimiento, sus síntomas desaparecieron completamente en pocas semanas, confirmando que se trataba de una condición benigna y manejable.",
+        "scores": {
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+    "article": "Una mujer de 59 años con urolitiasis bilateral recurrente se presentó con dolor en el flanco derecho, fiebre y fatiga. Se le había colocado un stent doble J derecho un año antes para una piedra pélvica sintomática, pero no se le dio seguimiento. Tenía insuficiencia cardíaca derecha, diabetes tipo 2 mal controlada y enfermedad renal crónica (nadir de creatinina: 18 mg/L).\nEstable clínicamente, tenía una escala de coma de Glasgow de 14/15 (respuesta verbal ligeramente alterada), fiebre (38,3 °C), sensibilidad en el flanco derecho y una producción de orina de 800 cc en 24 horas.\nLos resultados de laboratorio revelaron una lesión renal aguda, con un nivel de creatinina sérica de 107 mg/L (normal: 6-12 mg/L) y urea sanguínea de 3 g/L (normal: 0.15-0.45 g/L). Los marcadores inflamatorios estaban elevados, con un nivel de proteína C reactiva de 300 mg/L (normal: <5 mg/L) y un recuento de glóbulos blancos de 17,000/mm3 (normal: 4000-10,000/mm3). Además, el paciente exhibió anemia normocítica (hemoglobina: 7.6 g/dL; normal: 12-16 g/dL) e hipercalemia leve (potasio sérico: 5.4 mEq/L; normal: 3.5-5.1 mEq/L). El análisis de orina y el cultivo de orina fueron negativos para infección bacteriana.\nUna tomografía computarizada abdominal y pélvica sin contraste reveló una hidronefrosis del lado derecho, un stent de doble J calcificado en espiral en ambos extremos y una piedra en la pelvis derecha de 35 × 28 mm (588 UH). El riñón izquierdo está reducido en tamaño, con hidronefrosis y una piedra en la pelvis de 12 × 7 mm (531 UH).\n\nDebido a la obstructiva severa de la pielonefritis, en particular causada por la endoprótesis incrustada, se realizó una nefrostomía percutánea bilateral urgente, lo que produjo una importante mejora clínica y normalización de los marcadores inflamatorios y la función renal.\nTres días después, la paciente experimentó una convulsión generalizada asociada con disartria. Una tomografía computarizada urgente del cerebro mostró lesiones isquémicas en los lóbulos occipitales izquierdo y frontal derecho, lo que indicaba un accidente cerebrovascular embólico. Se le inició un tratamiento con enoxaparina (0,4 cc diarios) y Kardegic (160 mg diarios) para la prevención de accidentes cerebrovasculares.\nA pesar de la mejora neurológica, cuatro días después, la paciente desarrolló palidez mucocutánea progresiva, taquicardia (110 latidos por minuto), hipotensión (80/50 mmHg) y hematuria macroscópica por el catéter urinario. Los niveles de hemoglobina descendieron de 7,5 g/dL a 4,4 g/dL, lo que levantó sospechas de hemorragia activa. Se administró fluidoterapia, vasopresores intravenosos y transfusiones de sangre, estabilizando su estado para una exploración de angiografía por TAC con contraste.\nLa tomografía computarizada reveló una colección polar media heterogénea de 17 mm de espesor con extravasación de contraste en las fases arterial y portal, lo que indica una hemorragia activa de las arterias del polo superior y medio. También había coágulos intraluminales en la pelvis renal y la vejiga. Se hizo un diagnóstico de fístula arteriovenosa postnefrostomía, exacerbada por la terapia anticoagulante para el accidente cerebrovascular.\nSe realizó una arteriografía renal urgente a través del acceso a la arteria femoral derecha, utilizando un catéter de diagnóstico de calibre 5. La angiografía selectiva reveló una FAV en el polo inferior del riñón con drenaje venoso temprano hacia la vena cava inferior, junto con un pequeño pseudoaneurisma. La embolización superselectiva con microespirales de 3 mm y 5 mm logró ocluir con éxito la fístula, y se usaron partículas de Gelfoam para evitar el sangrado retrógrado. Una inyección final de contraste confirmó la oclusión completa de la fístula, restaurando la integridad arterial y deteniendo la hemorragia.\n\nDespués de la embolización, se vigiló de cerca al paciente en la UCI. La hemodinámica se mantuvo estable y se tomó la decisión colegiada de reintroducir la anticoagulación con monitorización del INR para controlar el accidente cerebrovascular isquémico mientras se equilibraba el riesgo de hemorragia. La hematuria se resolvió, la función renal se normalizó y la nefrostomía siguió siendo funcional.\nSe adoptó un enfoque multidisciplinario para el tratamiento definitivo. La primera etapa involucró la litotripsia endoscópica con láser del bucle inferior calcificado del stent de JJ, la inserción de un segundo stent de JJ en paralelo con el incrustado y la extracción de la nefrostomía, que se completó con éxito. La segunda etapa, programada seis semanas después, incluyó una ureteroscopia derecha flexible para liberar el bucle superior del stent de JJ calcificado, la fragmentación de la piedra pélvica derecha mediante litotripsia con láser y la extracción completa del stent incrustado. Lamentablemente, la salud del paciente se deterioró debido a múltiples factores, entre ellos, insuficiencia cardíaca, diabetes mal controlada, enfermedad renal crónica y un accidente cerebrovascular previo, lo que demoró la finalización de la segunda etapa del tratamiento planificado.\n",
+    "gold_summary": "Una mujer de 59 años con urolitiasis bilateral recurrente, insuficiencia cardiaca derecha, diabetes tipo 2 mal controlada y enfermedad renal crónica se presentó con dolor en el flanco derecho, fiebre y fatiga. Previamente se le había colocado un stent doble J derecho, pero se perdió su seguimiento. Una tomografía computarizada reveló una hidronefrosis, un stent calcificado y una piedra pélvica de 22 mm, lo que llevó a la realización de una nefrostomía percutánea. La paciente desarrolló un accidente cerebrovascular embólico tres días después y posteriormente presentó hematuria, hipotensión y anemia significativa. La angiografía por TC confirmó una FAV con sangrado activo, que se trató con éxito con embolización.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Una señora tenía dolor y fiebre. Tenía piedras en sus dos riñones. También tenía problemas con su corazón y azúcar alta. Le pusieron un tubito en el riñón, pero no fue al doctor para revisarlo. \n\nEl doctor vio que su riñón estaba muy hinchado y había una piedra grande. Le pusieron un tubito para sacar el líquido. \n\nDespués, la señora tuvo un problema en su cabeza y se cayó. Luego, empezó a tener sangre en la orina y se puso muy débil. \n\nLos doctores encontraron que estaba sangrando dentro del riñón. Hicieron un tratamiento para parar la sangre y la ayudaron mucho.",
+        "scores": {
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+        "text": "**Lo que le pasó a la paciente**  \nUna mujer de 59 años tenía piedras en ambos riñones que volvían a aparecer, además de problemas graves del corazón, diabetes mal controlada y enfermedad en los riñones. Ella sentía dolor en el lado derecho de su cuerpo, tenía fiebre y estaba cansada. Un año antes, le habían puesto un tubo llamado stent doble J en el riñón derecho para ayudar a que la orina pasara, pero no fue revisado después.  \n\n**Lo que encontraron en sus estudios**  \nUna tomografía (una especie de radiografía especial) mostró que su riñón derecho estaba inflamado por la acumulación de orina (hidronefrosis), que el stent estaba cubierto de calcio y que tenía una piedra grande en la pelvis del riñón. Por esto, le hicieron una nefrostomía, que es un procedimiento para drenar la orina directamente del riñón usando un tubo.  \n\n**Problemas que surgieron después**  \nTres días después, la mujer tuvo una convulsión y se descubrió que había sufrido un accidente cerebrovascular, que es cuando falta sangre en una parte del cerebro. Le dieron medicamentos para evitar más problemas en el cerebro.  \n\nLuego, presentó sangrado en la orina, presión baja y anemia (menos glóbulos rojos), lo que indicaba que estaba perdiendo mucha sangre. Un estudio con contraste mostró que tenía una fístula arteriovenosa (FAV), que es una conexión anormal entre una arteria y una vena en el riñón, causando sangrado.  \n\n**Cómo la trataron**  \nPara detener el sangrado, hicieron una embolización, que consiste en bloquear la fístula usando pequeños dispositivos llamados microespirales. Esto funcionó bien y la paciente se estabilizó.  \n\n**Seguimiento y tratamiento final**  \nDespués, continuaron con un tratamiento para eliminar el stent calcificado y las piedras en dos etapas, usando láser y endoscopios (instrumentos para ver y tratar dentro del cuerpo). Sin embargo, la salud de la paciente empeoró debido a sus otras enfermedades, lo que complicó completar el tratamiento.  \n\n**Qué significa todo esto**  \nEste caso muestra que cuando un stent se deja mucho tiempo sin control, puede causar problemas graves como infecciones, sangrados y daño renal. También destaca la importancia de un seguimiento médico cuidadoso para evitar complicaciones serias.",
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+      "B3": {
+        "text": "**Contexto**  \nUna mujer de 59 años con antecedentes complejos, incluyendo cálculos renales recurrentes en ambos riñones (urolitiasis bilateral), insuficiencia cardíaca del lado derecho, diabetes tipo 2 mal controlada y enfermedad renal crónica, acudió al hospital por dolor intenso en el costado derecho, fiebre y cansancio. Un año antes, se le había colocado un stent doble J (un tubo delgado que ayuda a drenar la orina desde el riñón hacia la vejiga) en el riñón derecho debido a una piedra renal, pero no se realizó un seguimiento adecuado de este dispositivo.\n\n**Hallazgos Clave**  \nAl realizar una tomografía computarizada (una exploración detallada con rayos X), se detectó que el riñón derecho presentaba hidronefrosis (acumulación de orina debido a una obstrucción), un stent doble J calcificado (con depósitos de calcio que dificultan su función) y una piedra renal grande de aproximadamente 35 × 28 mm. El riñón izquierdo también mostraba signos de daño, con una piedra más pequeña y reducción de tamaño. Debido a la obstrucción severa y el riesgo de infección, se realizó una nefrostomía percutánea bilateral urgente, que consiste en colocar tubos para drenar la orina directamente desde los riñones hacia el exterior, lo que mejoró significativamente su estado y normalizó los marcadores de inflamación y función renal.\n\nSin embargo, tres días después, la paciente sufrió una convulsión generalizada y dificultad para hablar. Un escáner cerebral mostró lesiones isquémicas (áreas con falta de riego sanguíneo) en diferentes partes del cerebro, confirmando un accidente cerebrovascular embólico (causado por un coágulo que bloqueó una arteria cerebral). Se inició tratamiento anticoagulante para prevenir nuevos eventos.\n\nPosteriormente, la paciente desarrolló signos de hemorragia activa: palidez, taquicardia, presión arterial baja y sangre visible en la orina. La hemoglobina, que mide la cantidad de glóbulos rojos, cayó drásticamente, indicando una pérdida significativa de sangre. Una tomografía con contraste evidenció una colección de sangre en el riñón con extravasación de contraste, señal clara de sangrado activo, y coágulos en la pelvis renal y vejiga. Se diagnosticó una fístula arteriovenosa (FAV), una conexión anormal entre una arteria y una vena en el riñón, probablemente causada por la nefrostomía y agravada por la anticoagulación.\n\n**Interpretación Clínica**  \nLa fístula arteriovenosa renal es una complicación rara pero grave que puede provocar hemorragias importantes. En este caso, la combinación de la lesión vascular por la nefrostomía y el tratamiento anticoagulante para el accidente cerebrovascular aumentó el riesgo de sangrado. La angiografía selectiva (una técnica que visualiza los vasos sanguíneos) confirmó la presencia de la FAV y un pequeño pseudoaneurisma (una dilatación anormal de la arteria).\n\n**Próximos Pasos y Tratamiento**  \nSe realizó una embolización superselectiva, un procedimiento mínimamente invasivo en el que se introdujeron microespirales y partículas especiales para bloquear la fístula y detener el sangrado. El procedimiento fue exitoso, restaurando la integridad vascular y estabilizando a la paciente. Posteriormente, se reintrodujo cuidadosamente la anticoagulación para tratar el accidente cerebrovascular, equilibrando el riesgo de hemorragia.\n\nEl manejo definitivo incluyó un enfoque multidisciplinario para tratar las piedras y el stent calcificado. En una primera etapa, se realizó una litotripsia endoscópica con láser para fragmentar el stent incrustado y se colocó un segundo stent para facilitar el drenaje, retirando la nefrostomía. Se planificó una segunda etapa para fragmentar la piedra pélvica y extraer completamente el stent calcificado, pero la salud general de la paciente, afectada por sus múltiples enfermedades crónicas y el accidente cerebrovascular, retrasó este procedimiento.\n\n**Resumen Final**  \nEsta paciente presentó una compleja combinación de problemas renales y vasculares, incluyendo obstrucción urinaria grave, infección, accidente cerebrovascular y una complicación hemorrágica por fístula arteriovenosa renal. El manejo requirió intervenciones urgentes y coordinadas para controlar la infección, detener el sangrado y tratar las piedras y el stent calcificado, destacando la importancia del seguimiento adecuado en pacientes con dispositivos urológicos y múltiples comorbilidades.",
+        "scores": {
+          "ROUGE-1": 0.25240384615384615,
+          "ROUGE-2": 0.14216867469879516,
+          "ROUGE-L-Sum": 0.23557692307692307,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
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+  },
+  {
+    "article": "Un hombre de 52 años fue admitido en un hospital debido a palpitaciones repentinas y fatiga general. La electrocardiografía reveló taquicardia ventricular con una frecuencia cardíaca de 180 lpm. Su ritmo cardíaco volvió a un ritmo sinusal después de una cardioversión inmediata y luego fue derivado a nuestra institución para una investigación adicional. Su historial médico pasado incluía reconstrucción del tracto de salida del ventrículo derecho utilizando un injerto homólogo y cierre de un defecto septal ventricular para TOF, que se realizó 47 años antes. Sin embargo, se perdió su seguimiento posterior. Tras ser derivado a nuestra institución, su presión arterial era de 116/70 mmHg, frecuencia cardíaca de 80 lpm, y saturación de oxígeno del 99% (con aire ambiente). Al inspeccionar la pulsación de la vena yugular, se observaron claramente una onda prominente y un descenso profundo, que eran consistentes con el aumento de la presión de llenado del ventrículo derecho y la compensación del aumento de la contracción de la RA. Cabe destacar que la auscultación reveló un murmullo diastólico regurgitante agudo en el tercer espacio intercostal izquierdo, un primer sonido cardíaco ampliamente dividido (S1) y un segundo sonido cardíaco (S2), lo que indicaba un ventrículo derecho severamente dilatado debido a la liberación de PR libre y la presencia de una válvula pulmonar no funcional. Además, se auscultó un tercer sonido cardíaco (S3) en el cuarto borde paraesternal, que era consistente con un S3 derecho. El electrocardiograma reveló bloqueo completo del haz de rama derecha, con una duración de QRS de 200 lpm. La radiografía de tórax mostró cardiomegalia con dilatación de las arterias pulmonares bilaterales. La ecocardiografía transtorácica reveló una regresión completa de la válvula pulmonar, que resultó en PR libre y una dilatación prominente del ventrículo derecho. La evaluación volumétrica del ventrículo derecho se realizó utilizando una resonancia magnética cardíaca, que reveló un volumen final diastólico del ventrículo derecho de 428 ml (índice de volumen final diastólico del ventrículo derecho de 240 ml/m2), una fracción de eyección del ventrículo derecho del 36% y una fracción de eyección de PR del 74%. Además, la tomografía computarizada multidetector mostró claramente una regresión completa de la válvula pulmonar del injerto homólogo.\n\nEl paciente se sometió a un examen con catéter para investigar más a fondo su estado hemodinámico. Su forma de onda de presión RA fue particularmente notable, ya que consistía en una onda a prominente y un descenso y, que coincidían con el cuarto sonido cardiaco (S4) y S3 en un fonocardiograma, respectivamente. Además, se reveló que la presión arterial pulmonar final diastólica y la presión final diastólica del VD eran casi idénticas debido al PR libre. Por lo tanto, la evaluación clínica del «quinteto de sonidos cardiacos», que incluye un murmullo diastólico regurgitante agudo, un S1 ampliamente dividido, un S2 único y la presencia de un S3 y un S4 derechos, se confirmó mediante una evaluación hemodinámica y anatómica multimodal como insuficiencia cardiaca derecha grave concomitante con un VD significativamente dilatado debido a la regresión completa de la válvula pulmonar y el PR libre resultante.\n\nDespués del reemplazo de la válvula pulmonar, el «quinteto de sonidos del corazón» se resolvió por completo.\n\nMH - Insuficiencia cardiaca/*etiología\nMH - Murmullos cardiacos/*diagnóstico\nMH - *Sonidos del corazón\nMH - Humanos\nMH - Hombre\nMH - Edad Media\nMH - Insuficiencia de la válvula pulmonar/*complicaciones/diagnóstico\nMH - Taquicardia, ventricular/etiología\nMH - Tetralogía de Fallot/*cirugía\nMH - Disfunción ventricular, derecha/etiología\n",
+    "gold_summary": "Un hombre de 52 años fue derivado a nuestra institución para la evaluación de una taquicardia ventricular de inicio súbito. Su historia clínica incluía una reconstrucción del tracto de salida del ventrículo derecho a los 5 años de edad. La auscultación reveló un murmullo diastólico regurgitante agudo, un primer sonido cardiaco (S1) ampliamente dividido y un segundo sonido cardiaco (S2) único, lo que indicaba un ventrículo derecho severamente dilatado debido a una regurgitación pulmonar (RP) grave y la presencia de una válvula pulmonar no funcional. Además, el tercer sonido cardiaco (S3) y el cuarto sonido cardiaco (S4) del lado derecho estaban presentes, lo que era coherente con una presión de llenado del ventrículo derecho elevada y la presencia de un ventrículo derecho no conforme. Finalmente, el mencionado «quinteto de sonidos cardiacos» se confirmó mediante una evaluación multimodal como insuficiencia cardiaca del lado derecho con un ventrículo derecho concomitantemente severamente dilatado debido a la regresión completa de la válvula pulmonar y la consiguiente RP libre.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Un hombre tenía problemas con su corazón. Su corazón latía muy rápido y se cansaba mucho. Cuando el doctor escuchó su corazón, oyó sonidos raros. Estos sonidos decían que una parte del corazón estaba muy grande y no funcionaba bien. La válvula del corazón que ayuda a la sangre a salir no estaba trabajando. Esto hizo que el corazón se llenara mucho y se hiciera más grande. Los doctores usaron muchas pruebas para entenderlo mejor. Al final, vieron que el corazón tenía problemas para trabajar bien porque la válvula estaba rota.",
+        "scores": {
+          "ROUGE-1": 0.2876712328767123,
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+          "ROUGE-L-Sum": 0.28082191780821913,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
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+      "B2": {
+        "text": "**Lo que le pasó al paciente**  \nUn hombre de 52 años llegó al hospital porque tenía palpitaciones rápidas y se sentía muy cansado. Cuando era niño, a los 5 años, había tenido una operación en el corazón para corregir un problema llamado Tetralogía de Fallot, que afecta cómo la sangre sale del corazón. En esa operación, le reconstruyeron una parte del ventrículo derecho, que es una de las cámaras del corazón que envía sangre a los pulmones.\n\n**Lo que encontraron al examinarlo**  \nAl escuchar su corazón con un estetoscopio, los médicos notaron varios sonidos anormales. Había un murmullo que indicaba que la sangre estaba regresando por la válvula pulmonar, que no funcionaba bien. Además, escucharon sonidos llamados S1 y S2 que estaban cambiados, y también sonidos llamados S3 y S4 en el lado derecho del corazón. Estos sonidos indican que el ventrículo derecho estaba muy agrandado y tenía problemas para llenarse y bombear la sangre correctamente.\n\n**Qué significa todo esto**  \nEstos signos juntos, que los médicos llamaron el «quinteto de sonidos cardiacos», mostraron que el paciente tenía insuficiencia cardíaca en el lado derecho del corazón. Esto pasó porque la válvula pulmonar que le habían reconstruido cuando era niño ya no funcionaba y la sangre regresaba libremente hacia el ventrículo derecho, causando que este se agrandara mucho y trabajara mal.\n\n**Qué hicieron después**  \nPara confirmar todo, usaron varios estudios, como ecocardiogramas y resonancias magnéticas, que mostraron claramente el daño en la válvula y el agrandamiento del ventrículo derecho. Finalmente, el paciente recibió un reemplazo de la válvula pulmonar, y después de la operación, los sonidos anormales del corazón desaparecieron, lo que indica que su corazón mejoró.",
+        "scores": {
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+          "ROUGE-2": 0.16699801192842942,
+          "ROUGE-L-Sum": 0.40396039603960393,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nUn hombre de 52 años, con antecedentes de cirugía cardíaca infantil para corregir la tetralogía de Fallot (una malformación congénita del corazón), fue ingresado tras presentar palpitaciones repentinas y fatiga. En su niñez, se le realizó una reconstrucción del tracto de salida del ventrículo derecho y cierre de un defecto septal ventricular, pero no tuvo seguimiento médico posterior. En el hospital, se detectó una taquicardia ventricular (ritmo cardíaco acelerado originado en el ventrículo) que se corrigió mediante cardioversión eléctrica.\n\n**Hallazgos Clave**  \nAl examen físico, se identificaron varios sonidos cardíacos anormales: un murmullo diastólico regurgitante agudo (sonido producido por el flujo anormal de sangre hacia atrás durante la diástole), un primer sonido cardíaco (S1) ampliamente dividido, un segundo sonido cardíaco (S2) único, y la presencia de un tercer (S3) y cuarto sonido cardíaco (S4) en el lado derecho del corazón. Estos hallazgos indicaban un ventrículo derecho severamente dilatado y con función alterada.  \n\nLas pruebas complementarias confirmaron estos hallazgos:  \n- El electrocardiograma mostró bloqueo completo del haz de rama derecha y un complejo QRS prolongado, reflejando alteraciones en la conducción eléctrica ventricular.  \n- La radiografía de tórax evidenció cardiomegalia (aumento del tamaño del corazón) y dilatación de las arterias pulmonares.  \n- La ecocardiografía y la resonancia magnética cardíaca demostraron una regresión completa de la válvula pulmonar (una estructura que normalmente evita el reflujo de sangre hacia el ventrículo derecho), lo que causaba una regurgitación pulmonar libre y una dilatación importante del ventrículo derecho con disminución de su capacidad de bombeo (fracción de eyección del 36%).  \n- La evaluación hemodinámica mediante cateterismo cardíaco mostró presiones elevadas en la aurícula derecha y ventrículo derecho, con formas de onda características que correspondían a los sonidos cardíacos S3 y S4 detectados en la auscultación.\n\n**Interpretación Clínica**  \nEl conjunto de sonidos cardíacos anormales —denominado aquí como el «quinteto de sonidos cardíacos»— reflejaba una insuficiencia cardíaca derecha grave causada por la dilatación y disfunción del ventrículo derecho, secundaria a la ausencia funcional de la válvula pulmonar y la regurgitación pulmonar libre resultante. La presencia simultánea de estos cinco sonidos (murmullo diastólico regurgitante, S1 ampliamente dividido, S2 único, S3 y S4 derechos) fue confirmada mediante una evaluación clínica, hemodinámica y anatómica exhaustiva.\n\n**Próximos Pasos y Resultado**  \nEl paciente fue sometido a un reemplazo de la válvula pulmonar, procedimiento que restauró la función valvular y eliminó la regurgitación pulmonar. Posteriormente, el «quinteto de sonidos cardíacos» desapareció por completo, indicando una mejora significativa en la función y la dinámica del ventrículo derecho.\n\n---\n\nEste caso ilustra cómo una alteración valvular congénita corregida en la infancia puede evolucionar décadas después hacia una insuficiencia cardíaca derecha severa, y cómo la evaluación detallada de los sonidos cardíacos, junto con estudios de imagen y hemodinámicos, es fundamental para un diagnóstico preciso y un tratamiento efectivo.",
+        "scores": {
+          "ROUGE-1": 0.3967168262653899,
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+          "ROUGE-L-Sum": 0.3693570451436389,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
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+      }
+    }
+  },
+  {
+    "article": "Un hombre de 62 años con antecedentes médicos de cardiopatía no isquémica que derivó en insuficiencia cardíaca, en estado postoperatorio de un dispositivo de asistencia ventricular izquierdo, se sometió a un trasplante cardíaco ortotópico. Mientras se recuperaba en la UCI quirúrgica, desarrolló un empeoramiento de la distensión abdominal, sensibilidad y leucocitosis, lo que motivó la evaluación por el equipo de cirugía general 6 días después del trasplante. El paciente no había evacuado ni expulsado gases desde su cirugía y no había respondido a los enemas administrados ni a la metoclopramida oral por un presunto íleo posoperatorio. Se realizó una tomografía computarizada del abdomen y la pelvis, que reveló múltiples bucles intestinales dilatados con niveles de aire-líquido y un punto de transición en el intestino delgado proximal en el cuadrante superior izquierdo, lo que generó preocupación por una obstrucción. En función de estos hallazgos y del hecho de que el paciente no había sido sometido a cirugías abdominales previas, lo que hacía que la obstrucción intestinal fuera secundaria a las adherencias, se llevó al paciente al quirófano para una laparotomía exploratoria. En el quirófano, se encontró que el intestino estaba dilatado de forma difusa sin ninguna área de isquemia aparente. Se encontró que una porción del intestino delgado estaba adherida a la pared abdominal anterior en el cuadrante superior izquierdo. Tras una exploración adicional, se encontró que una línea motriz de LVAD retenida estaba tunelizada en la cavidad peritoneal, estrangulando un bucle de intestino delgado en el cuadrante superior izquierdo. La línea motriz se liberó de la pared abdominal y se retiró, y se liberó el bucle de intestino afectado. Se encontró que era viable después de unos minutos de reperfusión. Se examinó el intestino delgado en su totalidad, desde el ligamento de Trietz distalmente hasta el intestino ciego, y se encontró que estaba dilatado pero en general era normal. Se reparó una pequeña área de desgarro seroso en el punto de adhesión a la línea motriz, principalmente. Se devolvió el intestino a la cavidad abdominal y se cerró la fascia y la piel con suturas corrientes y grapas cutáneas.\n\nMH - *Eliminación de dispositivo\nMH - Migración de cuerpos extraños/*complicaciones\nMH - Insuficiencia cardiaca/*terapia\nMH - *Trasplante de corazón\nMH - Dispositivos de asistencia cardíaca/*efectos adversos\nMH - Humanos\nMH - Obstrucción intestinal/diagnóstico por imágenes/*etiología\nMH - Laparotomía\nMH - Hombre\nMH - Edad Media\nMH - Tomografía computarizada por rayos X\nMH - Estados Unidos\n",
+    "gold_summary": "Un hombre de 62 años con antecedentes de insuficiencia cardiaca inducida por cardiomiopatía no isquémica, post-puente de asistencia ventricular izquierda y trasplante cardiaco ortotópico, presentó distensión abdominal, dolor y leucocitosis seis días después del trasplante. La TAC de abdomen y pelvis reveló bucles intestinales dilatados, niveles de aire-líquido y un punto de transición en el intestino delgado proximal. Se diagnosticó al paciente una obstrucción intestinal y se le realizó una laparotomía exploratoria. Se encontró que tenía un conducto de LVAD intraabdominal retenido que estrangulaba un bucle de intestino delgado en el cuadrante superior izquierdo. Se retiró el conducto y se liberó la sección de intestino con el retorno de la perfusión.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Un hombre de 62 años se sentía mal en su barriga después de una operación en su corazón. Su barriga estaba hinchada y le dolía. Los doctores le hicieron una foto especial para ver dentro de su barriga. Vieron que su intestino estaba muy grande y apretado en un lugar. Los doctores hicieron una operación para mirar dentro. Encontraron un tubito que estaba apretando su intestino. Quitaron el tubito y el intestino volvió a estar bien. Ahora el hombre puede sentirse mejor.",
+        "scores": {
+          "ROUGE-1": 0.32407407407407407,
+          "ROUGE-2": 0.07476635514018691,
+          "ROUGE-L-Sum": 0.3055555555555555,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
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+      "B2": {
+        "text": "**Lo que pasó con el paciente**  \nUn hombre de 62 años, que tenía problemas graves del corazón y había recibido un trasplante de corazón, comenzó a tener dolor y hinchazón en el abdomen seis días después de la operación. También tenía más glóbulos blancos en la sangre, lo que puede indicar infección o inflamación.\n\n**Qué encontraron los médicos**  \nLe hicieron una tomografía, que es un tipo de radiografía especial, y vieron que partes de su intestino estaban muy hinchadas y había señales de que algo bloqueaba el paso en el intestino delgado, que es la parte del intestino donde se absorben los nutrientes.\n\n**Qué hicieron para ayudarlo**  \nLos médicos lo operaron para ver qué causaba la obstrucción. Durante la cirugía, descubrieron que un tubo que se usaba para ayudar a su corazón (llamado LVAD) se había movido dentro del abdomen y estaba apretando un pedazo del intestino, bloqueando el paso.\n\n**Resultado de la cirugía**  \nQuitaron ese tubo que estaba causando el problema y liberaron el intestino. Después de unos minutos, el intestino volvió a funcionar bien y no había daño grave. Finalmente, cerraron la herida y el paciente pudo continuar con su recuperación.\n\n**Por qué es importante**  \nEste caso muestra que los dispositivos para ayudar al corazón pueden, en raras ocasiones, causar problemas en otras partes del cuerpo, como el intestino. Por eso, los médicos deben estar atentos a síntomas como dolor abdominal después de cirugías complejas.",
+        "scores": {
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+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nUn hombre de 62 años con antecedentes de insuficiencia cardíaca causada por una enfermedad del músculo cardíaco no relacionada con problemas de circulación (cardiomiopatía no isquémica), que había sido tratado previamente con un dispositivo de asistencia ventricular izquierdo (LVAD, un aparato que ayuda al corazón a bombear sangre), recibió un trasplante de corazón ortotópico (reemplazo del corazón en su posición normal). Durante su recuperación en la unidad de cuidados intensivos, seis días después de la cirugía, presentó un aumento progresivo de la distensión abdominal (hinchazón), dolor abdominal y un aumento en el número de glóbulos blancos (leucocitosis), indicativo de inflamación o infección.\n\n**Hallazgos Clave**  \nUna tomografía computarizada (TAC) del abdomen y la pelvis mostró múltiples segmentos del intestino delgado dilatados con niveles de aire y líquido, además de un punto de transición en el intestino delgado proximal en el cuadrante superior izquierdo del abdomen. Estos hallazgos sugirieron la presencia de una obstrucción intestinal. Dado que el paciente no tenía antecedentes de cirugías abdominales previas, lo que reduce la probabilidad de adherencias (bandas de tejido cicatricial que pueden causar obstrucción), se decidió realizar una laparotomía exploratoria (cirugía para abrir el abdomen y examinar los órganos).\n\nDurante la cirugía, se observó que el intestino estaba dilatado pero sin signos de daño irreversible (isquemia). Se identificó que una porción del intestino delgado estaba adherida a la pared abdominal anterior. Al investigar más a fondo, se descubrió que una línea motriz del LVAD, que había migrado y estaba dentro de la cavidad abdominal, estaba causando una estrangulación (compresión que impide el flujo sanguíneo) de un segmento del intestino delgado en el cuadrante superior izquierdo. Esta línea motriz fue liberada y retirada, y el segmento intestinal afectado recuperó su circulación sanguínea tras unos minutos.\n\nSe inspeccionó todo el intestino delgado desde el ligamento de Treitz (punto donde el duodeno se une al yeyuno) hasta el intestino ciego, encontrándose dilatado pero sin daño significativo. Se reparó una pequeña lesión en la capa externa del intestino (desgarro seroso) en el sitio donde estaba adherido a la línea motriz. Finalmente, el intestino fue reposicionado en la cavidad abdominal y se cerró la incisión quirúrgica.\n\n**Interpretación Clínica**  \nEste caso ilustra una complicación poco común pero grave en pacientes con dispositivos de asistencia ventricular izquierda: la migración intraabdominal de una línea motriz que puede causar obstrucción intestinal por estrangulación. La presentación clínica con distensión abdominal, dolor y leucocitosis, junto con los hallazgos radiológicos, orientaron hacia una obstrucción intestinal que requirió intervención quirúrgica urgente para evitar daño intestinal irreversible.\n\n**Próximos Pasos**  \nSe recomienda un seguimiento cuidadoso para detectar posibles complicaciones posteriores, como infecciones o recurrencia de obstrucción. Además, es importante evaluar la correcta colocación y manejo de los dispositivos de asistencia ventricular para prevenir migraciones similares. Este caso destaca la necesidad de un abordaje multidisciplinario en pacientes complejos post-trasplante cardíaco con dispositivos implantados.",
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+    "article": "Un paciente de 13 años de edad, del sexo masculino, fue admitido en el Hospital de Niños de Damasco tras notar una masa palpable agrandada en la región inguinal izquierda. Su historial médico no fue notable, excepto por una intervención quirúrgica en su columna vertebral 6 años atrás, debido a un accidente, que resultó en la pérdida de la función motora y la sensación en ambas extremidades inferiores.\n\nDebido al largo período que había pasado en la cama, el paciente desarrolló úlceras de decúbito en su pie izquierdo. El único hallazgo en el examen clínico fue una masa en el área inguinal izquierda, que era móvil en las estructuras profundas y también lo era la piel que la cubría. La masa no era sensible a la palpación y no se observaron signos de inflamación local.\n\nLos exámenes de laboratorio revelaron una ESR elevada (119 mm/h en la primera hora). Se solicitaron otros exámenes básicos de laboratorio, que incluían (recuento sanguíneo completo, pruebas de función hepática, electrolitos, urea, creatinina y LDH) y estaban dentro de los rangos normales para la edad. La realización de estos exámenes fue esencial para descartar enfermedades sistémicas. Dada la ausencia de hallazgos físicos indicativos de trastornos sistémicos o inmunodeficiencias, se consideró innecesario realizar exámenes adicionales como los de VIH o antiglobulina directa.\n\nLa tomografía computarizada del abdomen, el tórax y la pelvis mostró ganglios linfáticos agrandados por debajo del ligamento inguinal, el más grande de aproximadamente 3,5 por 2,4 cm. Otros órganos y ganglios estaban dentro de los límites normales.\n\nTodas las investigaciones mencionadas fueron esenciales para descartar otros diagnósticos de alto riesgo, como linfoma y leucemia. Sin embargo, no fueron suficientes para llegar al diagnóstico definitivo, por lo que se tomó la decisión de realizar una resección quirúrgica de los ganglios.\n\nPara confirmar los diagnósticos y descartar otras posibles diferencias que pudieran presentarse con ganglios linfáticos agrandados, se realizó la extirpación quirúrgica de todos estos ganglios agrandados bajo anestesia general y se enviaron biopsias para su estudio microscópico.\n\nLa biopsia mostró una arquitectura ganglionar hiperplásica con proliferación de histiocitos y células plasmáticas con proliferación vascular, lo que es compatible con el subtipo de enfermedad de Castleman de células plasmáticas.\n\nEl paciente fue dado de alta del hospital después de 14 días, tras comprobar que no había ganglios linfáticos agrandados. La única recomendación fue prednisolona oral. El paciente se sometió a un seguimiento mediante TAC de cuerpo entero cada tres meses. Durante cada visita al hospital, se realizó un examen clínico exhaustivo y pruebas de laboratorio (por ejemplo, análisis de sangre completo, VSG, proteína C reactiva, pruebas de función hepática, pruebas de función renal), además del TAC. Después de un período de seguimiento de 12 meses, el paciente no informó de nuevos síntomas o ganglios linfáticos agrandados. Además, no se observaron anomalías durante el examen clínico o en las pruebas de laboratorio.\n",
+    "gold_summary": "Reportamos un caso único de un niño de 13 años que presentó una masa palpable agrandada en la región inguinal izquierda sin ningún síntoma constitucional. La extirpación quirúrgica de esta masa fue esencial para descartar causas preocupantes. El examen patológico reveló cambios proliferativos consistentes con el tipo de célula plasmática de la enfermedad de Castleman, que es una de las formas más raras de la enfermedad en niños. Hasta donde sabemos, este caso es el primer caso reportado de enfermedad de Castleman unicéntrica (UCD) en el área inguinal. Durante un período de seguimiento de 12 meses, no se reportaron agrandamientos adicionales de los ganglios linfáticos u otros síntomas.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Había un niño de 13 años con una bolita en la ingle. La bolita no le dolía ni le hacía sentir mal. Los doctores sacaron la bolita con una operación para ver qué era. \n\nDespués, miraron la bolita con un microscopio y vieron que era una cosa rara que a veces pasa en niños. Es muy poco común. \n\nEl niño estuvo bien y no tuvo más bolitas ni se enfermó en un año. Los doctores lo cuidaron mucho y él está contento.",
+        "scores": {
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+          "ROUGE-2": 0.09259259259259259,
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
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+      },
+      "B2": {
+        "text": "Caso de un niño con una masa en la ingle\n\nUn niño de 13 años notó una masa o bulto en la parte izquierda de su ingle (la zona donde la pierna se une al cuerpo). No tenía otros síntomas como fiebre o pérdida de peso. Para entender qué era esa masa, los médicos decidieron quitarla con cirugía.\n\nQué encontraron en la biopsia\n\nDespués de la cirugía, examinaron la masa bajo el microscopio. Vieron que había un crecimiento anormal de ciertas células llamadas células plasmáticas, que forman parte del sistema inmunológico. Este hallazgo mostró que el niño tenía una enfermedad llamada enfermedad de Castleman, que es muy rara en niños y afecta los ganglios linfáticos.\n\nImportancia del caso y seguimiento\n\nEste es el primer caso conocido de esta enfermedad en un ganglio linfático de la ingle en un niño. Después de la cirugía, el niño recibió un medicamento llamado prednisolona para ayudar a controlar la enfermedad. Durante un año, los médicos lo revisaron regularmente con exámenes físicos y pruebas de imagen para asegurarse de que no aparecieran nuevos ganglios agrandados ni otros problemas. El niño se mantuvo sin síntomas y sin nuevos bultos durante todo ese tiempo.\n\nEn resumen, este caso muestra la importancia de investigar y tratar las masas en los ganglios linfáticos para encontrar enfermedades raras y cuidar bien la salud.",
+        "scores": {
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+          "ROUGE-2": 0.18085106382978725,
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
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+      "B3": {
+        "text": "**Contexto**  \nPresentamos el caso de un niño de 13 años que acudió al hospital debido a la presencia de una masa palpable en la región inguinal izquierda, sin presentar síntomas generales como fiebre, pérdida de peso o fatiga. Su historial médico previo incluía una cirugía en la columna vertebral tras un accidente, que le ocasionó parálisis y pérdida de sensibilidad en las piernas, lo que llevó a complicaciones como úlceras por presión en el pie izquierdo. No se identificaron otros signos clínicos relevantes ni indicios de infecciones o enfermedades sistémicas.\n\n**Hallazgos Clave**  \nLos análisis de laboratorio mostraron una velocidad de sedimentación globular (VSG) elevada, un marcador de inflamación, mientras que otros parámetros sanguíneos y pruebas de función orgánica se mantuvieron dentro de rangos normales. La tomografía computarizada (TAC) evidenció ganglios linfáticos aumentados de tamaño debajo del ligamento inguinal, siendo el mayor de aproximadamente 3,5 x 2,4 cm, sin afectación de otros órganos o ganglios. Para descartar enfermedades graves como linfoma o leucemia, se decidió realizar una cirugía para extirpar los ganglios afectados y analizarlos bajo el microscopio.\n\nEl examen histopatológico (microscópico) de los ganglios mostró una proliferación aumentada de células plasmáticas (un tipo de célula del sistema inmunitario) y células llamadas histiocitos, junto con un aumento en la formación de vasos sanguíneos, características compatibles con la forma de células plasmáticas de la enfermedad de Castleman. Esta enfermedad es una condición poco común que causa crecimiento anormal de ganglios linfáticos y puede presentarse en una única área (unicéntrica) o en múltiples regiones del cuerpo.\n\n**Interpretación Clínica**  \nEste caso representa una presentación rara de la enfermedad de Castleman unicéntrica en la región inguinal, un sitio poco frecuente para esta patología, especialmente en niños. La ausencia de síntomas sistémicos y la localización única de los ganglios afectados apoyan el diagnóstico de esta forma localizada de la enfermedad. La extirpación quirúrgica completa fue fundamental tanto para confirmar el diagnóstico como para tratar la condición.\n\n**Próximos Pasos y Seguimiento**  \nTras la cirugía, el paciente recibió tratamiento con prednisolona oral (un corticosteroide) y fue dado de alta después de 14 días sin complicaciones. Se estableció un seguimiento riguroso que incluyó evaluaciones clínicas, análisis de laboratorio y tomografías computarizadas cada tres meses para detectar cualquier recurrencia o aparición de nuevos ganglios agrandados. Durante un año de seguimiento, el paciente no presentó nuevos síntomas ni evidencia de enfermedad activa, lo que indica un buen pronóstico tras el tratamiento quirúrgico.\n\nEn resumen, este caso destaca la importancia de considerar la enfermedad de Castleman en el diagnóstico diferencial de masas ganglionares inguinales en niños, y demuestra que la resección quirúrgica puede ser curativa en la forma unicéntrica de esta enfermedad.",
+        "scores": {
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
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+  },
+  {
+    "article": "Un hombre asiático de 55 años de edad, que había estado recibiendo tratamiento irregularmente (el paciente no cumplía con el tratamiento) para DCMP durante los últimos 6 meses, acudió con quejas de disnea al hacer ejercicio durante 1 semana y disminución de la producción de orina durante 2 días. El paciente aparentemente estaba bien hace 1 semana cuando empezó a desarrollar disnea, inicio insidioso, gradualmente progresiva, inicialmente de grado II de la New York Heart Association (NYHA) pero progresó a grado IV de la NYHA asociada con pesadez en el pecho. La historia de ortopnea y disnea nocturna paroxística estuvo presente. Esto estuvo asociado con tos con una cantidad moderada de expectoración espumosa, no purulenta. El paciente también se quejó de hinchazón de las extremidades inferiores bilaterales. No hubo historia de hinchazón periorbital, orina espumosa o hematuria. No hubo historia de palpitación, síncope, dolor de pecho o hemoptisis. El paciente también dio una historia de una sensación de hormigueo en ambas manos y pies durante 1 mes.\n\nEl paciente había tenido un episodio similar 6 meses atrás, por el que fue hospitalizado y tratado de manera conservadora como un caso de DCMP. Se le había practicado una cirugía de cataratas en ambos ojos 15 años atrás.\n\nEn el examen físico general, el paciente estaba consciente y orientado en cuanto al tiempo, el lugar y la persona, y afebril con una presión arterial de 90/60 mmHg en el brazo derecho en posición supina y una frecuencia de pulso de 110/min, que era de bajo volumen y todos los pulsos periféricos eran palpables. Presentaba taquipnea con una frecuencia respiratoria de 28/min y palidez. Tenía un edema de pedal B/L, que era de tipo lento con presión venosa yugular elevada (JVP). No se observó ictericia, cianosis, clubbing ni linfadenopatía. Mientras se medía la presión arterial, el paciente empezó a tener espasmos en la muñeca, lo que nos dio una pista para examinar más a fondo y revelar un signo de Chvostek positivo. El signo de Trousseau también fue positivo a los 10 segundos.\n\nEl examen del sistema cardiovascular reveló un latido apical localizado en el sexto espacio intercostal izquierdo, a 1 cm fuera de la línea medioclavicular, de carácter hiperdinámico. Se escucharon S1 y S2 con normalidad en todas las áreas.\n\nEl examen del sistema respiratorio reveló una reducción de la entrada de aire en las bases pulmonares bilaterales con crepitación fina al final de la inspiración bilateral. El examen del sistema nervioso abdominal y central no reveló nada de interés.\n\n\nInvestigaciones\n\nEn el momento del ingreso, el ECG mostró bloqueo completo de rama izquierda (B-R) con un intervalo QT prolongado. La hemoglobina era de 58 g/l (133-162) con un cuadro dimórfico. El volumen corpuscular medio era de 110 fL (80,0-100,0 fL), la hemoglobina corpuscular media era de 34 pg/mL (27,0-32,0 pg/mL), la concentración media de hemoglobina corpuscular era de 36,2 g/dL (32,0-35,0 g/dL). Otros análisis revelaron niveles séricos de vitamina B12 de 135 pg/mL (211-911 pg/mL). El nivel sérico de ácido fólico era de 5,40 ng/mL (>5,38 ng/mL). El nitrógeno ureico en sangre era de 53 mg/dL (10-50) con creatinina de 0,8 mg/dL (0,7-1,3). Los resultados de las pruebas de función hepática (LFT) estaban dentro de los límites normales. El perfil de calcio mostró 4,3 mg/dL de S.calcium (8,5-10,5), fosfato 7,1 mg/dL (2,5-4,5), 3,06 g/dL de S.albumin (3,5-5,5). En vista de la hipocalcemia e hiperfosfatemia, se realizó un estudio del nivel de hormona paratiroidea intacta, que resultó ser <0,23 ng/mL (14-72). El S.magnesium era de 2,0 mg/dL (1,7-2,2). El análisis de gases en sangre arterial (ABG) fue sugestivo de una acidosis metabólica leve. El perfil tiroideo y los niveles de IgAtTG estaban dentro de los límites normales. Los niveles de ferritina y ceruloplasmina séricos estaban dentro de los límites normales. El ultrasonido abdominal y torácico mostró derrame pleural bilateral en posición supina. La vena cava inferior (IVC) y las venas hepáticas eran prominentes. El reposo dentro de los límites normales. La radiografía de tórax mostró un aplanamiento de los ángulos costofrénicos bilaterales que sugería derrame pleural bilateral. La ecocardiografía reveló un ventrículo izquierdo dilatado (LV) con una fracción de eyección del ventrículo izquierdo del 15 %, que sugería DCMP con disfunción severa del LV. Se realizó un arteriograma coronario basal que fue normal. La TC sin contraste de la cabeza mostró calcificación simétrica bilateral (B/L) en el hemisferio cerebeloso B/L, ganglios basales B/L y calcificación cortical/subcortical en la región B/L fronto-parieto-occipital. El reposo dentro de los límites normales.\n\n\nTratamiento\n\nPara el CHF, se inició al paciente con dobutamina intravenosa a una dosis de 6 µg/kg y furosemida intravenosa 20 mg BD para la descongestión. Sin embargo, el paciente no mostró una mejora significativa con el tratamiento anterior. En vista de la hipocalcemia con hiperfosfatemia y bajos niveles de hormona paratiroidea, se consideró un diagnóstico de cardiomiopatía hipocalcemica con hipoparatiroidismo y se inició al paciente con inyección de gluconato de calcio 1 g (90 mg de calcio elemental) administrado por vía intravenosa seguido de infusión de gluconato de calcio en 500 ml de dextrosa al 5% a una velocidad de 37,5 mg/hora de calcio elemental. El paciente mostró una mejora significativa después de iniciar el gluconato de calcio. El paciente fue dado de alta en condiciones estables con comprimidos de calcio por vía oral 3 g/día junto con calcitriol 0,5 µg/día. También se inició con benzotiazida con triamtereno (25/50 mg) OD, ramipril 5 mg una vez al día y carvedilol 3,125 mg dos veces al día. Para la anemia megaloblástica, se administraron inyecciones de cianocobalamina según el protocolo.\n\n\nResultado y seguimiento\n\nAl cabo de tres meses, el paciente había mejorado notablemente.\n\nLas investigaciones mostraron S.calcium 7.7, S.phosphate 6.0 y albúmina 3.6. La hemoglobina fue de 10.1 g/dL. El eco mostró una mejora en la función del LV con una fracción de eyección del 25%. Se planificó una biopsia endomiocardial, pero el paciente se negó, por lo que no pudo realizarse.\n\nMH - Gluconato de calcio/administración y dosificación/uso terapéutico\nMH - Cardiomiopatía, Dilatada/*complicaciones/diagnóstico\nMH - Ecocardiografía/métodos\nMH - Insuficiencia cardiaca/terapia farmacológica/*etiología/fisiopatología\nMH - Humanos\nMH - Hipocalcemia/*complicaciones/diagnóstico/terapia farmacológica/fisiopatología\nMH - Hipoparatiroidismo/*complicaciones/terapia farmacológica\nMH - Hombre\nMH - Edad Media\nMH - Volumen de carrera\nMH - Resultado del tratamiento\nMH - Disfunción ventricular izquierda/diagnóstico por imágenes\n",
+    "gold_summary": "Presentamos el caso de un hombre asiático de 55 años que había tenido un caso conocido de miocardiopatía dilatada durante 6 meses, que se presentó con las principales quejas de falta de aire al hacer ejercicio y disminución de la producción de orina. En el examen físico general, se observaron características que sugerían una ICC. El signo de Chvostek y Trousseau fue positivo. El paciente tenía antecedentes de cirugía de cataratas en ambos ojos 15 años atrás. Otras investigaciones revelaron una hipocalcemia. La ecografía mostró una grave hipocinesia global del ventrículo izquierdo con una fracción de eyección del ventrículo izquierdo del 15%. Esta ICC fue refractaria al tratamiento convencional, aunque, con la suplementación de calcio, el paciente mejoró sintomáticamente. En el seguimiento después de 3 meses, se observó una mejora en los parámetros ecocardiográficos con una fracción de eyección que mejoró al 25%.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Había un hombre que se sentía muy cansado y le costaba respirar cuando caminaba. También hacía menos pipí. El doctor vio que su corazón estaba muy débil. El hombre tenía señales en sus manos que mostraban que le faltaba calcio. Le dieron calcio para ayudarlo. Después de un tiempo, el corazón del hombre se puso un poco mejor y él se sintió mejor también.",
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+        "text": "**Caso de un Hombre con Problemas del Corazón y Bajos Niveles de Calcio**\n\nUn hombre de 55 años, que ya tenía un diagnóstico de miocardiopatía dilatada (una enfermedad del corazón donde el músculo del ventrículo izquierdo se debilita y agranda), llegó al hospital porque tenía dificultad para respirar al hacer ejercicio y producía menos orina de lo normal.\n\n**Lo que Encontraron en el Examen**\n\nAl revisarlo, los médicos notaron signos de insuficiencia cardíaca congestiva (cuando el corazón no bombea bien y se acumula líquido). También detectaron dos signos especiales llamados Chvostek y Trousseau, que indican que el cuerpo tiene poco calcio en la sangre. Además, el paciente había tenido cirugía de cataratas en ambos ojos hace 15 años.\n\n**Resultados de las Pruebas**\n\nLas pruebas mostraron que tenía hipocalcemia, es decir, niveles bajos de calcio en la sangre. El ultrasonido del corazón (ecocardiografía) reveló que su ventrículo izquierdo estaba muy debilitado, con una fracción de eyección del 15%, lo que significa que el corazón bombeaba muy poco sangre.\n\n**Tratamiento y Mejoría**\n\nEl paciente no mejoró con el tratamiento habitual para la insuficiencia cardíaca. Sin embargo, cuando le dieron calcio por vía intravenosa, su condición mejoró notablemente. Después de tres meses, su corazón funcionaba mejor, con una fracción de eyección aumentada al 25%.\n\n**Qué Significa Esto**\n\nEste caso muestra que la falta de calcio en la sangre, causada por un problema llamado hipoparatiroidismo (cuando una glándula llamada paratiroides no produce suficiente hormona para controlar el calcio), puede empeorar la función del corazón. Al corregir el calcio, se puede mejorar la salud del corazón en pacientes con miocardiopatía dilatada.",
+        "scores": {
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+      },
+      "B3": {
+        "text": "**Contexto**  \nSe presenta el caso de un hombre asiático de 55 años con diagnóstico previo de miocardiopatía dilatada (una enfermedad del músculo cardíaco que provoca su debilitamiento y agrandamiento) durante los últimos 6 meses. El paciente acudió al hospital debido a dificultad para respirar al realizar ejercicio (disnea) y una reducción en la cantidad de orina durante los últimos dos días. Su dificultad respiratoria había empeorado progresivamente, llegando a un grado severo según la clasificación de la Asociación del Corazón de Nueva York (NYHA). Además, presentaba hinchazón en ambas piernas y tos con expectoración espumosa, síntomas compatibles con insuficiencia cardíaca congestiva (ICC).\n\n**Hallazgos Clave**  \nEn el examen físico, el paciente mostraba signos típicos de insuficiencia cardíaca, como edema en las extremidades inferiores y aumento de la presión venosa yugular. Además, durante la toma de la presión arterial, se evidenciaron espasmos musculares en la muñeca, lo que llevó a descubrir signos positivos de Chvostek y Trousseau, indicativos de hipocalcemia (niveles bajos de calcio en sangre). El paciente también tenía antecedentes de cirugía de cataratas bilateral realizada 15 años antes.\n\nLos análisis de laboratorio confirmaron hipocalcemia severa junto con niveles elevados de fosfato y una hormona paratiroidea (PTH) muy baja, lo que sugiere hipoparatiroidismo (una condición en la que las glándulas paratiroides no producen suficiente hormona para regular el calcio). La ecocardiografía mostró un ventrículo izquierdo dilatado con una fracción de eyección muy baja (15%), reflejando una función cardíaca gravemente comprometida. Otras pruebas descartaron enfermedad coronaria y evidenciaron calcificaciones cerebrales simétricas.\n\n**Interpretación Clínica**  \nEl cuadro clínico y los resultados sugieren que la insuficiencia cardíaca del paciente no solo se debía a la miocardiopatía dilatada conocida, sino que estaba agravada por una cardiomiopatía secundaria a hipocalcemia causada por hipoparatiroidismo. La hipocalcemia puede afectar la contracción del músculo cardíaco, empeorando la función ventricular. Esto explica la falta de respuesta a los tratamientos convencionales para insuficiencia cardíaca.\n\n**Tratamiento y Evolución**  \nSe inició tratamiento estándar para insuficiencia cardíaca, incluyendo dobutamina y diuréticos, sin mejoría significativa. Al identificar la hipocalcemia e hipoparatiroidismo, se administró gluconato de calcio por vía intravenosa, seguido de calcio oral y calcitriol (una forma activa de vitamina D) para corregir el déficit de calcio. Tras esta intervención, el paciente mostró una mejoría clínica notable. También se trató la anemia megaloblástica con vitamina B12.\n\nEn el seguimiento a los tres meses, el paciente presentó mejoría en los niveles de calcio y en la función cardíaca, con una fracción de eyección que aumentó al 25%, lo que indica una recuperación parcial de la capacidad de bombeo del corazón. Sin embargo, el paciente rechazó realizar una biopsia endomiocárdica que podría haber ayudado a confirmar el diagnóstico definitivo.\n\n**Próximos Pasos**  \nSe recomienda continuar con el tratamiento de calcio y calcitriol para mantener niveles adecuados de calcio en sangre y prevenir complicaciones. Además, es fundamental el seguimiento cardiológico para monitorizar la función ventricular y ajustar la terapia para la insuficiencia cardíaca. La educación del paciente sobre la importancia de la adherencia al tratamiento es clave para evitar recaídas. En caso de que el paciente acepte, una biopsia cardíaca podría aportar información adicional para el manejo a largo plazo.",
+        "scores": {
+          "ROUGE-1": 0.3268482490272374,
+          "ROUGE-2": 0.1612483745123537,
+          "ROUGE-L-Sum": 0.30869001297016857,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      }
+    }
+  },
+  {
+    "article": "Una mujer de 54 años de edad, libanesa, en hemodiálisis (HD) de mantenimiento tres veces por semana para glomeruloesclerosis segmentaria focal (GSF) fue admitida en el departamento de urgencias, luego de haber sido sometida a su HD programada la noche anterior, debido al inicio repentino de un dolor lumbar agudo en el lado izquierdo, náuseas y vómitos. El dolor había comenzado repentinamente cerca de 12 horas antes de su presentación y se agravó rápidamente. En una nota al margen, un hiperparatiroidismo secundario grave con calcificación cutánea vascular fue tratado con cinacalcet durante 3 años sin respuesta, lo que demandó una paratiroidectomía (hiperplasia de cuatro glándulas) 8 meses antes de su presentación actual. Cinco días antes de su presentación, fue admitida en el hospital debido a anemia grave y rectorragia. Su evaluación por ultrasonido renal mostró riñones bilaterales pequeños con parénquima delgado que contenía quistes de hasta 3 cm y calcificaciones vasculares sin hidronefrosis. Cuatro días antes de su presentación, la colonoscopia a través del íleo terminal reveló un pólipo de 7 mm en el colon descendente izquierdo, que fue removido por mucosectomía. La microscopía volvió como adenoma tubular sésil con displasia de bajo grado. La paciente negó fiebre o antecedentes de trauma. No hubo antecedentes previos de uso de antiplaquetarios. En la emergencia, su presión arterial y pulso fueron de 112/65 mmHg y 96 bpm, su temperatura fue de 36.8°C y presentaba abdomen levemente distendido, con dolor importante en el ángulo costovertebral izquierdo. Los hallazgos de laboratorio mostraron hemoglobina de 9.0 g/dL mientras que el hematocrito fue de 29.7%, recuento total de leucocitos 12.2 × 1000/microlitro, creatinina de 6.06 mg/dL, y nivel de proteína C reactiva de 6 mg/L. Además, el TP fue de 83% y el INR fue de 1.13. En el día de la presentación (es decir, 4 días después de la colonoscopia), se realizó una tomografía computarizada (TC) multifásica del tórax, abdomen y pelvis con y sin contraste intravenoso. El examen reveló un gran quiste y enormes hematomas intraparenquimatosos perirrenales izquierdos con una colección subcapsular de hasta 1,8 cm de espesor con colección hemática en todo el compartimiento renal que alcanzaba un diámetro de más de 9 × 4 cm, hidronefrosis izquierda y edema alrededor de la grasa en todo el flanco y calcificaciones en el hilo. Para la descompresión del sistema pélvico renal y drenaje, optamos por tratarla con inserción retrógrada de doble stent ureteral a la izquierda, que identificó un coágulo en la parte media del uréter izquierdo. Se realizaron cultivo de orina y citología y los resultados fueron negativos. Una simple radiografía del abdomen mostró el doble J en su lugar. La paciente permaneció hemodinámicamente estable, pero presentó una nueva caída en la hemoglobina (6.1 g/dL) la misma noche, lo que exigió una transfusión de una unidad de concentrado de eritrocitos leucodepleados para estabilización. Se tomó la decisión de explorar quirúrgicamente con diagnóstico presuntivo de hematoma perirrenal izquierdo subagudo y para excluir una malignidad subyacente. Se sometió a una sesión de HD sin heparina. En el tercer día, se sometió a una nefrectomía radical abierta a la izquierda con conservación de la glándula suprarrenal. Recibió 2 unidades más de concentrado de eritrocitos leucodepleados durante la intervención. El parénquima renal fue casi totalmente reemplazado por un hematoma que medía 9 × 9 × 7 cm y se extendía hasta la grasa perirrenal. Una pequeña masa papilar fue enviada por separado para análisis. La evaluación histopatológica detallada reveló un parénquima renal con lesiones de nefritis crónica mutilada por grandes áreas hemorrágicas que se extendían hasta la grasa perirrenal. Además, había una proliferación neoplásica de 2 mm, con arquitectura papilar cubierta por pequeñas células cúbicas atípicas y macrófagos espumosos en el eje, compatibles con adenoma papilar. Al día siguiente de la operación, la paciente fue sometida a HD y recibió un paquete de eritrocitos leucodepleados. El período postoperatorio fue sin intercorrerencias. El nivel de hemoglobina se mantuvo alrededor de 10 g/dL. La paciente se recuperó sin signos o síntomas de sangrado. La paciente permanece bien y asintomática y actualmente se encuentra en HD de mantenimiento regular.\n",
+    "gold_summary": "A continuación, se describe un caso inusual de una paciente con HD de 54 años de edad que presentó HPE pocos días después de una colonoscopia. La causa de la HPE fue la ruptura de un quiste de DRCA. Consideramos que la colonoscopia fue un factor desencadenante y planteamos hipótesis sobre su etiopatogenia. La paciente se sometió a una nefrectomía izquierda exitosa.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Una señora de 54 años tenía un problema en sus riñones. Ella se hacía un tratamiento para limpiar su sangre. Unos días después de un examen en su barriga, empezó a sentir mucho dolor en un lado. Un quiste en su riñón se rompió y eso le dolió mucho. Los doctores le hicieron una operación para quitar ese riñón. Ahora ella está mejor y sigue con su tratamiento para limpiar su sangre.",
+        "scores": {
+          "ROUGE-1": 0.32,
+          "ROUGE-2": 0.13513513513513511,
+          "ROUGE-L-Sum": 0.3066666666666667,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B2": {
+        "text": "**Caso de una mujer con sangrado en el riñón después de una colonoscopia**\n\nUna mujer de 54 años que estaba en hemodiálisis, un tratamiento para personas con problemas graves en los riñones, tuvo un problema raro. Pocos días después de hacerse una colonoscopia (un examen para revisar el colon), comenzó a sentir un dolor fuerte en la parte baja de la espalda, del lado izquierdo, junto con náuseas y vómitos.\n\nLos médicos descubrieron que tenía un sangrado grande alrededor de su riñón izquierdo. Este sangrado ocurrió porque se rompió un quiste, que es una bolsa llena de líquido que se forma en el riñón. La ruptura del quiste causó un hematoma, que es una acumulación de sangre fuera de los vasos sanguíneos.\n\nCreen que la colonoscopia pudo haber sido la causa que desencadenó este problema, aunque no es común que esto pase. Para tratar la situación, los médicos le hicieron una cirugía para quitarle el riñón izquierdo, llamada nefrectomía. La operación fue exitosa y la paciente se recuperó bien, sin más sangrados.\n\nEste caso es importante porque muestra una complicación poco común después de una colonoscopia en una persona con enfermedad renal avanzada y hemodiálisis. Los médicos aprendieron que hay que estar atentos a síntomas como dolor intenso y sangrado después de estos procedimientos en pacientes con problemas renales.",
+        "scores": {
+          "ROUGE-1": 0.3018867924528302,
+          "ROUGE-2": 0.13291139240506328,
+          "ROUGE-L-Sum": 0.29559748427672955,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B3": {
+        "text": "**Contexto:**  \nSe presenta el caso poco común de una mujer de 54 años que se encuentra en hemodiálisis (HD) debido a una enfermedad renal crónica avanzada llamada glomeruloesclerosis segmentaria focal. Esta paciente desarrolló un hematoma perirrenal espontáneo (HPE), que es una acumulación de sangre alrededor del riñón, pocos días después de haberse sometido a una colonoscopia, un procedimiento para examinar el colon.\n\n**Hallazgos Clave:**  \nEl hematoma perirrenal se originó por la ruptura de un quiste renal asociado a una enfermedad renal crónica avanzada (DRCA). La tomografía computarizada mostró un gran hematoma intraparenquimatoso (dentro del tejido renal) y perirrenal (alrededor del riñón) en el riñón izquierdo, con signos de sangrado activo y compresión del sistema urinario. La paciente presentó dolor lumbar intenso, anemia progresiva y requerimientos de transfusión sanguínea. Durante la intervención quirúrgica, se confirmó que el parénquima renal estaba casi completamente reemplazado por el hematoma. Además, se identificó una pequeña lesión benigna llamada adenoma papilar.\n\n**Interpretación Clínica:**  \nSe considera que la colonoscopia, realizada días antes, pudo haber sido un factor desencadenante que contribuyó a la ruptura del quiste renal y la formación del hematoma. Aunque la relación causal no es completamente clara, la manipulación abdominal y los cambios en la presión intraabdominal durante la colonoscopia podrían haber favorecido este evento hemorrágico en un riñón ya debilitado por la enfermedad crónica y la presencia de quistes. La situación requirió una nefrectomía radical (extirpación completa del riñón afectado) para controlar el sangrado y evitar complicaciones mayores.\n\n**Próximos Pasos y Seguimiento:**  \nTras la cirugía, la paciente continuó con su tratamiento de hemodiálisis sin complicaciones adicionales y se mantuvo estable, sin signos de sangrado recurrente. Este caso resalta la importancia de considerar posibles complicaciones renales en pacientes con enfermedad renal crónica avanzada que se someten a procedimientos invasivos, y la necesidad de un manejo multidisciplinario para asegurar una recuperación adecuada.",
+        "scores": {
+          "ROUGE-1": 0.24519230769230765,
+          "ROUGE-2": 0.1111111111111111,
+          "ROUGE-L-Sum": 0.23076923076923078,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      }
+    }
+  },
+  {
+    "article": "Se evaluó a una mujer de 30 años de edad con antecedentes de dos meses de dolor progresivo y disminución de la visión OD. Dos semanas antes del desarrollo de los síntomas oculares, la paciente comenzó a disminuir la prednisona como tratamiento para sus síntomas inflamatorios sistémicos. Los antecedentes médicos incluyen artritis inflamatoria, síntomas gastrointestinales que sugieren enfermedad intestinal inflamatoria y pérdida de peso de 20 libras antes de la presentación. Los detalles completos del caso de la paciente se informaron previamente y se resumen aquí junto con análisis adicionales de quimiocina y citoquina de fluido ocular.13\n\nEn el examen, las BCVAs fueron 20/40 OD y 20/20 OS, y las pupilas fueron 9 mm y akinéticas OD y 5 mm con una rápida reactividad a la luz OS. Las presiones intraoculares fueron 65 mmHg OD y 21 mmHg OS. El examen con lámpara de hendidura mostró precipitados queráticos granulomatosos pigmentados (KP) dentro de la córnea inferior, 3+ células de la cámara anterior, atrofia difusa del iris con pigmento en las zónulas, y ectropion uvea OD, y OS fue normal. La gonioscopia mostró 3+ células pigmentadas dentro del ángulo inferior OD. El examen del fondo fue normal en ambos ojos. Una paracentesis anterior diagnóstica fue positiva para ADN de VZV mediante pruebas de PCR, y las pruebas serológicas fueron positivas para anticuerpos IgG de VZV. Posteriormente, se le diagnosticó uveítis anterior hipertensiva asociada a VZV, lo que provocó el inicio de acetazolamida oral y timolol oftálmico, dorzolamida, y brimonidina para la hipertensión ocular, así como valaciclovir 1 g TID y acetato de prednisolona 1% cada 2 horas. El curso de la enfermedad de la paciente y otros detalles de su tratamiento se describieron previamente.13\n\nLa paciente fue diagnosticada con un accidente cerebrovascular (ACV), que se cree que se debe a una vasculopatía del SNC asociada al VVZ, y fue hospitalizada durante 2 semanas, durante las cuales sus síntomas oculares mejoraron gradualmente. Sin embargo, dos meses después de su ACV, desarrolló un empeoramiento del dolor y la visión en el ojo derecho, y su BCVA disminuyó a 20/100 con una PIO elevada de 39 mmHg OD. El examen reveló una inyección ciliar 1+ y 3+ células de la cámara anterior, y se cambió de prednisolona a difluprednato con una mejora mínima. Posteriormente, se sometió a un procedimiento de filtración de glaucoma con una derivación de Ahmed debido a su PIO elevada persistente a pesar de la máxima tolerancia de la terapia ocular hipertensiva. Se obtuvo una muestra de humor acuoso del ojo derecho durante la cirugía de filtración para un análisis de perfil de quimiocina/citoquina. Se estimaron los niveles de 22 citoquinas y quimioquinas, incluidos IFN-Y, IL-10, IL-12p70, IL-17A, IL-1B, IL-2, IL-5, IL-6, IL-8, TNF-a, IL-18, IL-1RA, IL-1a, IL-1a, IP-10, MCP-1, MIP-1a, MIP-1B, SDF-1a, IL-21, IL-22, IL-23 e IL-27, utilizando la técnica de inmunoensayo de perlas múltiplex. Se detectaron niveles de concentración de 7 citoquinas/quimioquinas, incluidos IL-6, IL-8, IL-18, MIP-1b, IP-10, MCP-1, e IL-1RA. La IL-1RA fue la citoquina más abundante (1000 pg/mL), mientras que IP-10 y MCP-1 fueron las segundas citoquinas más abundantes (150–200 pg/mL). Se detectaron niveles de 10–20 pg/mL de IL-18 y MCP-1b, pero a niveles mínimos en esta muestra de AqH. Se detectaron niveles de IL-6 e IL-8, pero se encontró que eran las citoquinas menos abundantes, cada una con niveles de <10 pg/mL.\n\n",
+    "gold_summary": "El caso 2 fue el de una mujer de 30 años con antecedentes de dos meses de dolor progresivo y disminución de la visión en el ojo derecho. Se le diagnosticó uveítis anterior hipertensiva tras una paracentesis diagnóstica de la cámara anterior. A pesar de la terapia exitosa para la uveítis anterior, su presión intraocular se mantuvo elevada y requirió un procedimiento de filtración de glaucoma. Se recolectó una muestra de fluido ocular en el momento de la cirugía para el análisis de perfiles de citoquinas/quimioquinas, y se detectaron niveles de 7 citoquinas/quimioquinas, entre ellas, IL-6, IL-8, IL-18, MIP-1B, IP-10, MCP-1 e IL-1RA, siendo IL-1RA la citoquina más abundante.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Había una mujer que tenía dolor y no veía bien con un ojo. Los doctores encontraron que su ojo estaba inflamado y tenía mucha presión. Ella necesitó una operación para ayudar a que la presión bajara. Durante la operación, los doctores tomaron un poquito de líquido del ojo para ver qué había dentro. Encontraron unas cosas llamadas citoquinas, que son como mensajeros que dicen al cuerpo qué hacer. Una de estas citoquinas estaba más que las otras. Esto ayuda a los doctores a entender mejor qué pasa en el ojo.",
+        "scores": {
+          "ROUGE-1": 0.2758620689655172,
+          "ROUGE-2": 0.043478260869565216,
+          "ROUGE-L-Sum": 0.22413793103448276,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B2": {
+        "text": "**Caso de una Mujer con Problemas en el Ojo Derecho**\n\nUna mujer de 30 años tuvo dolor y pérdida de visión en su ojo derecho durante dos meses. Los médicos le diagnosticaron una inflamación llamada uveítis anterior hipertensiva, que significa que había inflamación en la parte frontal del ojo y la presión dentro del ojo estaba alta. Para confirmar esto, tomaron una pequeña muestra del líquido dentro del ojo, llamado fluido ocular.\n\nAunque recibió tratamiento para la inflamación, la presión en su ojo siguió siendo alta. Por eso, necesitó una cirugía llamada filtración de glaucoma, que ayuda a bajar la presión del ojo para evitar daños.\n\nDurante la cirugía, los médicos tomaron otra muestra del fluido ocular para estudiar unas sustancias llamadas citoquinas y quimioquinas. Estas sustancias son como señales que usan las células para comunicarse y controlar la inflamación. Encontraron siete de estas sustancias, entre ellas IL-6, IL-8, IL-18, MIP-1B, IP-10, MCP-1 y IL-1RA. La más abundante fue IL-1RA, que ayuda a reducir la inflamación en el cuerpo.\n\nEste análisis ayuda a entender mejor qué está pasando en el ojo durante la enfermedad y podría ayudar a mejorar los tratamientos en el futuro.",
+        "scores": {
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+          "ROUGE-L-Sum": 0.4122562674094708,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
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+      },
+      "B3": {
+        "text": "**Contexto**  \nSe evaluó a una mujer de 30 años que presentaba un cuadro de dos meses con dolor progresivo y disminución de la visión en su ojo derecho. Dos semanas antes del inicio de estos síntomas oculares, había comenzado a reducir la dosis de prednisona, un corticosteroide que utilizaba para tratar síntomas inflamatorios sistémicos relacionados con artritis inflamatoria y posibles enfermedades intestinales inflamatorias. Además, había experimentado una pérdida de peso significativa antes de la consulta.\n\n**Hallazgos Clave**  \nEn el examen ocular inicial, la agudeza visual era de 20/40 en el ojo derecho y 20/20 en el izquierdo. Se observaron pupilas anormalmente dilatadas y sin respuesta en el ojo derecho, con una presión intraocular (PIO) muy elevada de 65 mmHg (normalmente debe estar entre 10 y 21 mmHg), mientras que el ojo izquierdo estaba dentro de los parámetros normales. El examen con lámpara de hendidura reveló signos de inflamación en la parte frontal del ojo derecho, incluyendo células inflamatorias en la cámara anterior y depósitos granulomatosos pigmentados en la córnea. También se detectó atrofia del iris y otras alteraciones estructurales. La gonioscopia, que examina el ángulo donde drena el humor acuoso, mostró células pigmentadas inflamatorias. El fondo de ojo estaba normal en ambos ojos.\n\nUna prueba diagnóstica mediante paracentesis (extracción de fluido del ojo) confirmó la presencia de ADN del virus varicela-zóster (VVZ), responsable de la culebrilla, y los análisis serológicos indicaron anticuerpos contra este virus, confirmando la infección ocular. Se diagnosticó uveítis anterior hipertensiva asociada a VVZ, una inflamación del segmento anterior del ojo que causa aumento de la presión ocular. El tratamiento incluyó medicamentos para reducir la presión intraocular (acetazolamida, timolol, dorzolamida, brimonidina), un antiviral oral (valaciclovir) y corticosteroides tópicos (prednisolona).\n\nPosteriormente, la paciente sufrió un accidente cerebrovascular atribuido a una vasculopatía (enfermedad de los vasos sanguíneos) del sistema nervioso central relacionada con el VVZ, lo que requirió hospitalización. Durante su recuperación, los síntomas oculares mejoraron, pero dos meses después presentó un nuevo empeoramiento con aumento del dolor, disminución de la visión a 20/100 y presión intraocular elevada (39 mmHg). Se intensificó el tratamiento antiinflamatorio con difluprednato, pero la respuesta fue mínima, por lo que se realizó una cirugía de filtración para controlar la presión ocular, colocando una derivación de Ahmed.\n\n**Análisis de Citoquinas y Quimioquinas**  \nDurante la cirugía, se obtuvo una muestra del humor acuoso (fluido dentro del ojo) para analizar el perfil de citoquinas y quimioquinas, que son proteínas que regulan la inflamación y la respuesta inmune. Se evaluaron 22 de estas moléculas mediante una técnica avanzada llamada inmunoensayo de perlas múltiplex. Se detectaron niveles significativos de siete citoquinas/quimioquinas: interleucina-6 (IL-6), interleucina-8 (IL-8), interleucina-18 (IL-18), proteína quimioatrayente de macrófagos 1 beta (MIP-1b), proteína inducible por interferón gamma 10 (IP-10), proteína quimioatrayente de monocitos 1 (MCP-1) y antagonista del receptor de interleucina 1 (IL-1RA).\n\nDe estas, la IL-1RA fue la más abundante, con una concentración alrededor de 1000 pg/mL. Esta molécula actúa como un regulador que bloquea la acción de la interleucina 1, una citoquina proinflamatoria, y su presencia elevada sugiere un intento del organismo por controlar la inflamación ocular. IP-10 y MCP-1 fueron las segundas más abundantes, con niveles entre 150 y 200 pg/mL, y están involucradas en la atracción de células inmunitarias al sitio inflamado. Las otras citoquinas, incluyendo IL-6 e IL-8, estuvieron presentes en concentraciones más bajas (<10 pg/mL).\n\n**Interpretación Clínica**  \nEste caso ilustra una uveítis anterior hipertensiva causada por infección activa por VVZ, que además se complicó con un accidente cerebrovascular relacionado con la misma infección viral. La persistencia de la presión intraocular elevada a pesar del tratamiento médico requirió intervención quirúrgica. El análisis detallado del perfil inflamatorio en el humor acuoso reveló una respuesta inmunitaria compleja, con predominio de moléculas reguladoras como IL-1RA, lo que podría reflejar mecanismos de control de la inflamación en el ojo afectados por el virus.\n\n**Próximos Pasos**  \nEl manejo de esta paciente requiere un seguimiento estrecho para controlar la inflamación ocular y la presión intraocular, prevenir daños permanentes en la visión y vigilar posibles complicaciones neurológicas asociadas al VVZ. El análisis de citoquinas puede ofrecer información valiosa para ajustar terapias inmunomoduladoras y antivirales en casos similares.",
+        "scores": {
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+          "ROUGE-2": 0.13748657357679916,
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
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+  },
+  {
+    "article": "Un varón negro de 2021 g de peso nació a las 35 semanas y tres días de edad gestacional estimada por repetición de cesárea debido a la preocupación por la disminución del movimiento fetal en el contexto de una puntuación de perfil biofísico baja (basada en el tono muscular, la frecuencia cardíaca, el movimiento, la respiración y el volumen de líquido amniótico). La historia materna fue notable por el rasgo de células falciformes, la edad materna avanzada y la obesidad. La historia del embarazo fue notable por oligohidramnios observados por ultrasonografía a las 31 semanas. La ecografía fetal también mostró distensión de la vejiga, hidroceles bilaterales, dilatación de la uretra y ascitis abdominal preocupantes por la obstrucción del tracto urinario inferior y la posible ruptura de la vejiga. La ruptura de membranas ocurrió al momento del parto.\n\nAl nacer, el bebé experimentó dificultad respiratoria y fue tratado con ventilación con presión positiva, oxígeno suplementario e intubación. Las puntuaciones de Apgar fueron de dos y siete a un minuto y cinco minutos de vida, respectivamente. El examen mostró hematomas sustanciales y oscurecimiento de la extremidad superior izquierda. El bebé fue trasladado a la unidad de cuidados intensivos neonatales para el tratamiento de la dificultad respiratoria y sospecha de obstrucción del tracto urinario inferior. En la evaluación realizada dentro de la hora posterior al nacimiento por especialistas en ortopedia y cirugía plástica, el tercio distal del antebrazo y la mano estaban cianóticos, y una gran ampolla y área circundante de descamación eran evidentes en el dorso de la mano. No se observó movimiento espontáneo de la extremidad superior izquierda, y no se provocó la retirada o respuesta a los estímulos. La ecografía Doppler mostró flujo arterial al nivel de la fosa antecubital, pero no se detectaron pulsos radiales o cubitales. Los hallazgos del examen físico fueron consistentes con NCS, probablemente debido a la compresión de la pared uterina debido a oligohidramnios durante el embarazo.\n\nDespués de aproximadamente 5 horas de exámenes en serie, así como una amplia discusión con los equipos de ortopedia, cirugía plástica, neonatología y anestesia pediátrica, así como con los padres del bebé, se tomó la decisión de realizar una fasciotomía descompresiva del antebrazo, la mano y el túnel carpiano para permitir el rescate de la extremidad. La fasciotomía se realizó aproximadamente 6 horas después del nacimiento. El bebé fue monitoreado de cerca durante los siguientes días. La apariencia de la extremidad superior izquierda mejoró gradualmente. Al tercer día de vida, el antebrazo y la mano habían mejorado notablemente en color y parecían bien vascularizados. Las señales Doppler estaban presentes en todo momento, desde la arteria braquial hasta cada dedo. Se permitió que las heridas de la fasciotomía se curaran por intención secundaria, y se aplicó una férula personalizada con la muñeca en posición neutra y los dedos extendidos. No hubo signos de infección o isquemia en curso. Las heridas se curaron bien a las seis semanas de edad. En la visita de seguimiento a los cuatro meses de edad, las heridas se curaron por completo. El paciente tenía un rango de movimiento pasivo completo de la muñeca y los dedos. Se observó que tenía una ligera flexión y extensión del dedo anular y meñique, pero por lo demás, un movimiento activo mínimo de la muñeca o la mano en este momento. Tenía un movimiento activo del hombro y el codo. El paciente continuará recibiendo terapia ocupacional, así como férulas y masaje de cicatrices para prevenir/minimizar las contracturas. Los equipos multidisciplinarios continuarán siguiendo su progreso y recuperación de cerca.\n",
+    "gold_summary": "Presentamos un caso de NCS diagnosticado y tratado en base a los hallazgos del examen físico. La ecografía fetal mostró distensión de la vejiga, hidroceles bilaterales, dilatación de la uretra y ascitis abdominal que preocupaban por la obstrucción del tracto urinario inferior y posible ruptura de la vejiga. Una hora después del nacimiento, el examen de la extremidad superior izquierda del lactante no mostró movimiento espontáneo, la mano y el antebrazo parecían oscuros y la mano tenía una gran ampolla con descamación. No se detectó pulso distal a la fosa antecubital mediante ecografía Doppler. Se diagnosticó al lactante con NCS y se le practicó una fasciotomía urgente. La apariencia clínica y la perfusión de la extremidad superior izquierda mejoraron gradualmente. A los cuatro meses de edad, las heridas se habían curado y el paciente tenía un rango de movimiento pasivo completo de la extremidad superior izquierda. La recuperación del movimiento activo está en curso.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Un bebé nació y tenía problemas en su brazo izquierdo. El brazo estaba muy oscuro y no se movía solo. Tenía una burbuja grande en la mano. Los doctores no sentían el pulso en el brazo. Ellos hicieron una operación para ayudar al brazo. Poco a poco, el brazo se puso mejor. A los cuatro meses, las heridas estaban sanas. El bebé puede mover el brazo con ayuda. Los doctores siguen cuidando para que mejore más.",
+        "scores": {
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+          "ROUGE-2": 0.0796812749003984,
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
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+      "B2": {
+        "text": "**Lo que Encontraron al Nacer**  \nUn bebé nació con problemas en su brazo izquierdo. Su mano y antebrazo estaban oscuros y tenían una ampolla grande con piel que se estaba cayendo. Además, no movía esa parte del cuerpo y los médicos no pudieron sentir el pulso en la muñeca usando un examen especial llamado ecografía Doppler, que sirve para ver el flujo de sangre.\n\n**Qué Significa el Diagnóstico**  \nLos doctores dijeron que el bebé tenía un problema llamado Síndrome de Compartment Neonatal (NCS). Esto ocurre cuando hay mucha presión dentro de los músculos, lo que puede dañar la sangre y los nervios. En este caso, probablemente fue causado por la presión dentro del útero antes de nacer.\n\n**Cómo lo Trataron**  \nPara ayudar, los médicos hicieron una cirugía llamada fasciotomía. Esta operación abre la piel y los músculos para bajar la presión y salvar el brazo. La cirugía se hizo unas seis horas después del nacimiento.\n\n**Resultados y Seguimiento**  \nDespués de la operación, el brazo del bebé mejoró poco a poco. A los tres días, el color y la circulación de la sangre en el brazo y la mano eran normales. Las heridas sanaron bien y, a los cuatro meses, el bebé podía mover pasivamente (con ayuda) su muñeca y dedos. Aunque todavía tiene poco movimiento activo (por sí mismo), especialmente en algunos dedos, puede mover el hombro y el codo. El bebé seguirá recibiendo terapia para mejorar su movimiento y evitar que las cicatrices causen problemas. Los médicos continuarán observando su recuperación con cuidado.",
+        "scores": {
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+          "ROUGE-2": 0.1142857142857143,
+          "ROUGE-L-Sum": 0.3719912472647702,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
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+      "B3": {
+        "text": "**Contexto**  \nSe presenta el caso de un recién nacido prematuro (35 semanas y 3 días de gestación) que pesó 2021 gramos al nacer. La madre tenía antecedentes relevantes, incluyendo rasgo de células falciformes, edad avanzada y obesidad. Durante el embarazo se detectó oligohidramnios (disminución del líquido amniótico) y signos ecográficos preocupantes como distensión de la vejiga, hidroceles bilaterales (acumulación de líquido en las bolsas testiculares), dilatación de la uretra y ascitis abdominal, lo que sugería una posible obstrucción del tracto urinario inferior y ruptura de la vejiga. Debido a la disminución del movimiento fetal y un perfil biofísico bajo, se realizó una cesárea programada.\n\n**Hallazgos Clave**  \nAl nacer, el bebé presentó dificultad respiratoria y signos evidentes de compromiso en la extremidad superior izquierda: la mano y el antebrazo estaban oscuros (cianóticos), con una gran ampolla y descamación en el dorso de la mano, además de ausencia de movimiento espontáneo y falta de respuesta a estímulos. La ecografía Doppler mostró flujo arterial hasta la fosa antecubital, pero no se detectaron pulsos en las arterias radiales o cubitales, lo que indicaba compromiso circulatorio distal. Estos hallazgos fueron compatibles con un síndrome de compresión neuromuscular (NCS), probablemente causado por la presión ejercida sobre la extremidad dentro del útero debido al oligohidramnios.\n\n**Interpretación Clínica**  \nEl diagnóstico de NCS se basó en la combinación de los hallazgos físicos y ecográficos, que indicaban una isquemia (falta de flujo sanguíneo adecuado) en la extremidad superior izquierda. Para evitar daños permanentes, se decidió realizar una fasciotomía descompresiva urgente (una cirugía que libera la presión dentro de los compartimentos musculares del antebrazo y la mano, incluyendo el túnel carpiano) aproximadamente seis horas después del nacimiento. Esta intervención permitió restaurar la circulación y prevenir la necrosis (muerte del tejido).\n\n**Próximos Pasos y Evolución**  \nTras la cirugía, la apariencia y la perfusión de la extremidad mejoraron progresivamente. A los tres días de vida, el antebrazo y la mano mostraban una coloración normal y señales Doppler positivas en toda la extremidad, desde la arteria braquial hasta los dedos. Las heridas de la fasciotomía se dejaron curar de forma natural y se protegieron con una férula personalizada para mantener la muñeca y los dedos en posición adecuada. No se presentaron infecciones ni signos de isquemia persistente. A las seis semanas, las heridas estaban completamente cicatrizadas.\n\nEn la consulta de seguimiento a los cuatro meses, el bebé tenía un rango completo de movimiento pasivo en la muñeca y los dedos, aunque el movimiento activo era limitado, con ligera flexión y extensión en algunos dedos y buen movimiento activo en el hombro y codo. Se continúa con terapia ocupacional, uso de férulas y masaje de cicatrices para prevenir contracturas (rigidez anormal) y mejorar la función. Un equipo multidisciplinario sigue monitorizando su recuperación para optimizar los resultados funcionales a largo plazo.",
+        "scores": {
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
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+    "article": "Una mujer de 38 años de edad fue admitida en la sala de cirugía en noviembre de 2022 con la principal queja de una hinchazón abdominal progresiva que se asoció con un dolor abdominal leve y una saciedad precoz durante cinco meses. No tenía síntomas sistémicos como pérdida de peso, estreñimiento, diarrea, deseo de alimentos salados, fatigabilidad fácil o dolor de cabeza.\nEn el examen, parecía estar bien alimentada, pero presentaba una gran distensión abdominal, un leve palidez, afebril y con un tinte de ictericia en la esclerótica.\nLa palpación abdominal reveló una gran masa intraabdominal, no dolorosa, que ocupaba todo el abdomen inferior y se extendía hacia el superior, sin signos de irritación peritoneal u organomegalia.\nLos análisis de sangre mostraron un recuento de glóbulos blancos (5,7 × 109/l), hemoglobina (9,8 g/dl), bilirrubina (103 mg/dl) con recuentos normales de plaquetas (393 × 109/l). Las enzimas hepáticas, AST (24,0 U/l), ALT (21,0 U/l), albúmina 42,7 g/l. Creatinina sérica (53 μmol/l) y ESR (80 mm/h). Todos los demás análisis de sangre fueron normales. Una ecografía abdominal reveló un complejo quiste abdominal, ambos riñones eran de tamaño normal y con una ecografía normal, el hígado parecía normal. La TC abdominal y pélvica de contraste, vistas axiales y coronales, demostraron un gran quiste suprarrenal de paredes delgadas (flechas azules) que medía aproximadamente 23,5 cm (AP) x 20,3 cm (T) x 32,2 cm (CC) con un volumen de 8 l. El gran quiste desplaza el riñón derecho (flechas rojas) inferomedial a través de la línea media y ejerce presión sobre el hígado, la vesícula biliar, el páncreas y los intestinos delgados. Se extiende hasta la fosa ilíaca derecha. Como había un tinte de esclerosis ictérica, pero la masa era separada del hígado, el páncreas, los conductos biliares y el riñón derecho. Dado el tamaño del quiste y sus efectos compresivos, se planificó una intervención quirúrgica. Se eligió un enfoque quirúrgico abierto.\n\nSe le practicó una laparotomía al paciente. Se le hizo una incisión abdominal en la línea media, bajo anestesia general, y tras abrir las capas de la pared abdominal, se identificó un enorme quiste retroperitoneal que ocupaba toda la cavidad abdominal.\n\nSe abrió el quiste para acceder al fluido que se aspiraba, como se demostró en la cistectomía que se realizó con éxito. Se aspiraron unos 8 l de fluido de color marrón de la masa. Se enviaron muestras de la pared quística y del fluido para su análisis histológico.\n\nLa paciente se recuperó sin incidentes y fue dada de alta el día 7 después de la operación. El seguimiento a los 6 y 12 meses no mostró recurrencia ni complicaciones. El examen citológico de la muestra informó la presencia de material amorfo, no hubo evidencia de malignidad. Los resultados histológicos indicaron que la pared quística contenía tejido suprarrenal sin atipia, había infiltración de la pared quística por células inflamatorias mononucleares. La superficie interna de la pared no estaba revestida por células específicas reconocibles. En cuanto a los hallazgos clínicos intraoperativos, donde el origen del quiste era incierto, los hallazgos fueron más sugerentes de un quiste gigante idiopático retroperitoneal.\n\n",
+    "gold_summary": "Una mujer de 38 años se presentó con distensión abdominal progresiva. Las imágenes revelaron un quiste retroperitoneal gigante. Debido a los recursos limitados, se realizó una laparotomía abierta y se extirpó completamente un quiste de 33 cm que contenía 8 l de líquido transparente. La histopatología confirmó un quiste retroperitoneal idiopático gigante.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Una mujer tenía una barriga muy grande y le dolía un poco. Los doctores vieron que había una bolsa grande llena de líquido dentro de su barriga. La doctora hizo una operación para sacar la bolsa. La bolsa era muy grande y tenía mucho líquido adentro. Después de la operación, la mujer se sintió mejor y no volvió a tener la bolsa.",
+        "scores": {
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
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+      "B2": {
+        "text": "**Lo que le pasó a la paciente**  \nUna mujer de 38 años notó que su abdomen (la parte del cuerpo donde están el estómago y otros órganos) se hinchaba poco a poco durante cinco meses. También sentía un dolor leve y se llenaba rápido al comer. Al examinarla, los médicos encontraron una gran masa dentro de su abdomen, pero no tenía fiebre ni otros síntomas graves.\n\n**Qué encontraron los médicos**  \nLas pruebas de imagen, como la tomografía computarizada (una especie de radiografía avanzada), mostraron un quiste muy grande en la zona llamada retroperitoneo, que está detrás de los órganos principales del abdomen. Un quiste es una bolsa llena de líquido. Este quiste medía más de 30 centímetros y contenía alrededor de 8 litros de líquido. Debido a su tamaño, estaba presionando otros órganos importantes.\n\n**Cómo la trataron**  \nLos médicos decidieron hacer una cirugía abierta para quitar el quiste. Durante la operación, hicieron una incisión en el abdomen y sacaron el quiste, aspirando el líquido que tenía dentro. Luego, enviaron muestras del quiste para analizarlas y asegurarse de que no fuera canceroso.\n\n**Qué significan los resultados**  \nEl análisis mostró que el quiste no tenía células cancerosas y que estaba formado por tejido normal con algunas células inflamatorias. No encontraron una causa clara para el quiste, por lo que lo llamaron \"idiopático\", que significa que no se sabe exactamente por qué apareció.\n\n**Después de la cirugía**  \nLa paciente se recuperó bien y fue dada de alta una semana después. En los controles a los 6 y 12 meses no hubo problemas ni volvió a aparecer el quiste. Esto indica que la cirugía fue exitosa y que la paciente está en buen estado.",
+        "scores": {
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+          "ROUGE-2": 0.0802139037433155,
+          "ROUGE-L-Sum": 0.19148936170212763,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
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+      "B3": {
+        "text": "**Contexto:**  \nUna mujer de 38 años acudió al hospital debido a una hinchazón abdominal que había ido aumentando progresivamente durante cinco meses. Además, presentaba dolor abdominal leve y sensación de llenura rápida al comer. No tenía otros síntomas generales como pérdida de peso, problemas digestivos, fatiga o fiebre. En la exploración física, se observó una gran distensión del abdomen con una masa palpable que ocupaba gran parte de la cavidad abdominal, sin dolor ni signos de inflamación. También se detectó una leve palidez y un tinte amarillento en la parte blanca de los ojos (ictericia).\n\n**Hallazgos Clave:**  \nLos análisis de sangre mostraron anemia leve, bilirrubina elevada (lo que explica la ictericia), pero funciones hepáticas y renales normales. La ecografía y la tomografía computarizada (TC) con contraste revelaron un enorme quiste con paredes delgadas ubicado en la región retroperitoneal (la zona detrás del abdomen), que medía aproximadamente 33 cm en su mayor dimensión y contenía alrededor de 8 litros de líquido. Este quiste desplazaba órganos cercanos como el riñón derecho, el hígado, la vesícula biliar, el páncreas y los intestinos, pero no parecía originarse en ninguno de ellos.\n\n**Interpretación Clínica:**  \nDado el tamaño considerable del quiste y su efecto compresivo sobre órganos abdominales importantes, se decidió realizar una cirugía abierta (laparotomía) para extirparlo completamente. Durante la operación, se aspiraron 8 litros de líquido marrón del quiste y se removió la masa sin complicaciones. El análisis microscópico del tejido del quiste mostró que estaba formado por tejido suprarrenal (glándulas que se encuentran encima de los riñones) sin signos de células anormales o malignas, aunque había inflamación leve. La superficie interna del quiste no presentaba un revestimiento celular definido. Estos hallazgos sugieren que se trataba de un quiste retroperitoneal gigante idiopático, es decir, de origen desconocido y sin causa aparente.\n\n**Próximos Pasos:**  \nLa paciente tuvo una recuperación sin complicaciones y fue dada de alta siete días después de la cirugía. En los controles realizados a los 6 y 12 meses posteriores, no se detectó recurrencia del quiste ni problemas relacionados. Se recomienda continuar con seguimiento clínico periódico para asegurar que no aparezcan nuevas complicaciones o recidivas.",
+        "scores": {
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+    "article": "Un hombre de 71 años con diabetes y enfermedad de Chagas había perdido recientemente mucho peso (60 kg). La investigación clínica dio lugar a un diagnóstico de megaesófago asociado a una obstrucción significativa a nivel del cardias. Se realizó una dilatación esofágica con balón, recuperando con éxito el tránsito digestivo. Mientras tanto, durante la evaluación del riesgo quirúrgico, el paciente también presentó dolor torácico con el mínimo esfuerzo. La angiografía por tomografía computarizada coronaria realizada tres años antes mostró una enfermedad multivascular muy calcificada que afectaba a la arteria coronaria izquierda; en ese momento no se había realizado ninguna otra investigación. Esta vez, se lo derivó a nosotros para un cateterismo cardíaco.\nEl examen realizado el 16 de febrero de 2016 mostró: arteria coronaria derecha (RCA) con importante calcificación y una lesión del 50% en el tercio medio; arteria descendente posterior (PDA) y arteria posterolateral derecha (RPLA), con severa calcificación y lesiones del 80% y 70%, respectivamente; LM con 80% de lesiones calcificadas en el tercio distal; arteria descendente anterior izquierda (LAD) con significativa calcificación y 90% de lesión en el tercio medio; ramas diagonales (DG1 y DG2) con lesiones calcificadas del 70% y 80%, en el origen y en el tercio proximal, respectivamente; y arteria circunfleja izquierda (LCx) ocluida y calcificada, recibiendo colaterales grado II de múltiples orígenes. El volumen ventricular izquierdo y la contractilidad se conservaron.\n\nCon esta imagen angiográfica, una puntuación de riesgo de la Society of Thoracic Surgeons del 15,8 % para morbilidad o mortalidad, una puntuación EuroSCORE II del 4,67 %, y una debilidad significativa debido a una pérdida de peso importante y reciente, el equipo cardiaco decidió realizar una intervención coronaria percutánea (ICP) de la LM, LAD, DG1 y DG2 inicialmente y, en un segundo procedimiento después de 30 días, una ICP de las ramas de la RCA. En ambos procedimientos, también se indicó una RA debido a una calcificación significativa. No se abordaría la LCx, ya que angiográficamente el vaso no estaba tan gravemente afectado y también considerando la dificultad técnica de la recanalización, debido a la longitud del CTO y también a las paredes muy calcificadas (puntuación J-CTO 4). La LCx ya estaba recibiendo una circulación collateral de grado II.\nEl 19 de febrero de 2016, tras comenzar una terapia antiplaquetaria dual con aspirina y clopidogrel, el paciente se sometió a una angioplastia de la arteria descendente anterior, la arteria circunfleja y la arteria descendente derecha con una fresa de 1,5 mm, seguida de una predilatación con un balón de 3,0 mm x 20 mm a 14 atm y la implantación de stents liberadores de fármacos en la arteria descendente derecha y la arteria circunfleja, utilizando una técnica de mini-aplastamiento y un balón de contacto al final. Se realizó un balón de contacto en la bifurcación de la arteria descendente derecha/arteria circunfleja y, finalmente, se implantó el tercer stent liberador de fármacos desde el origen de la arteria descendente derecha para superponerse con el stent de la arteria descendente derecha. Se logró un éxito procedimental con un flujo TIMI de 3 y sin complicaciones clínicas o angiográficas.\nEl 22 de marzo de 2016, el paciente volvió para una PCI con un RotaWire PCI en el PDA y RPLA con una fresa de 1,5 mm, seguido por la implantación de dos DES de 2,75 mm x 20 mm y 2,75 mm x 16 mm a 12 atm en el PDA y RPLA, respectivamente, sin ninguna predilatación adicional. También observamos la presencia de una disección larga y severa en el tercio medio del RCA, sin duda causada por un manejo excesivo e intentos de remover la fresa, lo que causó una penetración profunda por el catéter guía 7F. Esta disección se corrigió rápidamente con la implantación de un tercer DES de 4,0 mm x 32 mm, y se obtuvo un flujo TIMI 3 final sin complicaciones clínicas o electrocardiográficas. Los dos sitios de punción femoral se ocluyeron con dispositivos AngioSeal 8F y 6F, respectivamente. El paciente permaneció en la unidad de cuidados intensivos durante 48 horas, la única anormalidad fue la elevación de CK-MB (el doble del valor de referencia). Fue dado de alta el día 3 en excelentes condiciones generales. El ecocardiograma de control mostró una contractilidad ventricular izquierda normal.\n",
+    "gold_summary": "Un hombre de 71 años con enfermedad de Chagas y angina estable en esfuerzo mínimo se sometió a una angiografía por tomografía computarizada y cineangiografía que reveló una enfermedad multivascular muy calcificada que afectaba a la arteria descendente anterior izquierda (LM). Debido al grado de calcificación, se decidió realizar una rotablation. La primera etapa de la intervención coronaria percutánea (ICP) con rotablation se realizó en la arteria descendente anterior izquierda (LM), la arteria descendente anterior izquierda y la segunda rama diagonal sin complicaciones. Casi 30 días después, volvió para una ICP de la arteria coronaria derecha (RCA). La estrategia propuesta fue la aterectomía rotativa en la arteria descendente anterior posterior (PDA) y la arteria posterolateral derecha (RPLA) con una fresa de 1,5 mm, seguida por la implantación de dos stents liberadores de fármacos (DES). A través del acceso a la arteria femoral derecha, la lesión de la RPLA se extirpó con éxito. Como no había signos de disección y se mantuvo el flujo TIMI 3, se reposicionó el RotaWire de 0,009″ para cruzar la lesión de la PDA y se realizó la extirpación de la lesión. Después de dos intentos, logramos cruzar la lesión con la fresa de 1,5 mm, sin embargo, se produjo el atrapamiento de la misma. El sistema se retiró hasta que el catéter guía penetró profundamente en la RCA, y se hicieron intentos para liberar el Rotablator moviéndolo hacia adelante y hacia atrás, pero la fresa ni siquiera giró. La arteria femoral contralateral se perforó y se insertó un catéter guía 6F JR, con el fin de mover un alambre guía y un pequeño globo de angioplastia tangencialmente a la fresa, pero sin éxito. Finalmente, avanzamos el alambre guía utilizando la técnica de «nudillo», aprovechando la torsión de la porción distal del alambre guía PT2, realizando una disección subintimal y reentrada, y pudimos cruzar fácilmente el globo, inflarlo y liberar la fresa atrapada. A través del sistema 6F, se implantaron dos DES programados y uno de rescate con éxito en la PDA, RPLA y RCA, obteniendo un flujo TIMI 3 final sin complicaciones.\n",
+    "synthetic_summary_eval": {
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+        "text": "Había un señor de 71 años con problemas en su corazón. Su corazón tenía partes muy duras y tapadas. Los doctores usaron una máquina especial para ver su corazón. \n\nPrimero, limpiaron unas partes del corazón con una herramienta que gira rápido. Esto ayudó a que la sangre pudiera pasar mejor. Después de un mes, volvieron a limpiar otras partes del corazón. \n\nEn una parte, la herramienta se quedó atrapada. Los doctores usaron un truco con un hilo para ayudar a que la herramienta se moviera otra vez. Al final, pusieron unos tubos pequeñitos para que la sangre siga fluyendo bien. \n\nEl señor quedó bien y sin problemas después de la ayuda.",
+        "scores": {
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+        "text": "**Lo que le pasó al paciente:**  \nUn hombre de 71 años con una enfermedad llamada Chagas y problemas en el corazón tuvo dolor en el pecho al hacer poco esfuerzo. Los médicos le hicieron estudios que mostraron que varias arterias del corazón estaban muy dañadas y tenían muchas calcificaciones, que son depósitos duros que bloquean el paso de la sangre.\n\n**Qué hicieron los médicos:**  \nPara ayudarlo, los doctores usaron una técnica llamada intervención coronaria percutánea (ICP). Esta técnica consiste en abrir las arterias del corazón usando pequeños tubos llamados stents, que ayudan a mantenerlas abiertas. Debido a que las arterias estaban muy duras por la calcificación, usaron una herramienta especial llamada rotablación. Esta herramienta tiene una pequeña fresa que gira rápido para eliminar la parte dura y permitir que el stent se coloque mejor.\n\n**Cómo fue el tratamiento:**  \nPrimero, trataron las arterias principales del lado izquierdo del corazón sin problemas. Después de casi un mes, regresó para tratar las arterias del lado derecho. Durante este segundo procedimiento, usaron la fresa para limpiar las arterias bloqueadas y pusieron stents para mantenerlas abiertas. Sin embargo, la fresa se quedó atrapada en una de las arterias, lo que complicó el procedimiento.\n\n**Cómo resolvieron el problema:**  \nPara liberar la fresa atrapada, los médicos usaron una técnica especial con un alambre guía que creó un nuevo camino dentro de la pared de la arteria para pasar un globo y liberar la fresa. Luego, colocaron los stents necesarios y lograron que la sangre fluyera bien por las arterias sin complicaciones.\n\n**Qué significa esto:**  \nEste caso muestra cómo los médicos pueden tratar arterias muy dañadas y duras usando herramientas avanzadas. Aunque hubo una complicación, pudieron solucionarla con éxito. El paciente salió en buen estado y con su corazón funcionando normalmente.",
+        "scores": {
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+        "text": "**Contexto**  \nUn hombre de 71 años con antecedentes de enfermedad de Chagas y diabetes presentó una pérdida de peso significativa y un diagnóstico de megaesófago con obstrucción en el cardias. Durante la evaluación prequirúrgica, manifestó dolor torácico con mínimo esfuerzo. Estudios previos mostraron una enfermedad coronaria multivascular severamente calcificada, especialmente en la arteria coronaria izquierda. Se decidió realizar una intervención coronaria percutánea (ICP) debido al alto riesgo quirúrgico y la complejidad de las lesiones.\n\n**Hallazgos Clave**  \nLa angiografía coronaria reveló múltiples lesiones calcificadas: una estenosis del 90% en la arteria descendente anterior izquierda (LAD), lesiones severas en ramas diagonales, y oclusión de la arteria circunfleja izquierda (LCx) con circulación colateral. La arteria coronaria derecha (RCA) también presentaba lesiones significativas y calcificación. La función ventricular izquierda se mantenía conservada.\n\n**Intervención y Procedimientos**  \nSe planificó la ICP en dos etapas debido a la extensión y severidad de las lesiones. La primera intervención, realizada el 19 de febrero de 2016, incluyó la rotablation (una técnica que utiliza una fresa rotatoria para eliminar la calcificación) en la arteria descendente anterior, seguida de la implantación de stents liberadores de fármacos (DES) en la arteria descendente derecha y la circunfleja, logrando un flujo sanguíneo óptimo sin complicaciones.\n\nCasi un mes después, el 22 de marzo de 2016, se realizó la segunda ICP en las ramas de la arteria coronaria derecha (PDA y RPLA) también con rotablation y colocación de DES. Durante este procedimiento, se produjo una disección severa en la arteria coronaria derecha, causada por la manipulación del catéter, que fue rápidamente corregida con la implantación de un stent adicional. Se presentó un incidente de atrapamiento de la fresa rotatoria dentro de la arteria, que fue resuelto mediante una técnica avanzada que permitió liberar el dispositivo sin daños adicionales.\n\n**Interpretación Clínica**  \nEste caso ilustra la complejidad del manejo de enfermedad coronaria multivascular severamente calcificada en un paciente con comorbilidades importantes y alto riesgo quirúrgico. La utilización de rotablation permitió tratar las lesiones calcificadas que dificultan la expansión de los stents, mejorando el flujo sanguíneo coronario. La estrategia en dos tiempos y la cuidadosa planificación fueron fundamentales para minimizar riesgos y lograr un resultado exitoso.\n\n**Próximos Pasos**  \nEl paciente fue dado de alta en buenas condiciones tras una estancia corta en cuidados intensivos, con función ventricular preservada y sin complicaciones clínicas significativas. Se recomienda seguimiento cardiológico estrecho, control de factores de riesgo cardiovascular y terapia antiplaquetaria dual para prevenir eventos trombóticos. La arteria circunfleja, ocluida pero con circulación colateral, no fue intervenida debido a la dificultad técnica y el riesgo asociado.",
+        "scores": {
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+    "article": "Una paciente de 29 años se presentó al departamento de urología con dolor intermittent en el flanco derecho durante un año y sensación de ardor urinaria ocasional sin hematuria; su estado general era estable. La paciente no mostró signos de tos, fatiga, pérdida de peso, no había tenido cirugías previas, pero había estado expuesta frecuentemente a ovejas. A pesar de los exámenes de laboratorio normales, el examen de anticuerpos de equinococos arrojó un resultado positivo. El ultrasonido abdominal posterior reveló una lesión quística grande en el riñón derecho, que medía aproximadamente 63 mm con paredes gruesas y sin flujo de doppler significativo. La tomografía computarizada con contraste, tanto en vista transversal como coronal, reveló una masa quística con septos en el lado lateral del riñón derecho, que presentaba una pared gruesa y regular que se intensificaba con el contraste. Esta lesión se clasificó como categoría 4 de Bosniak, con imágenes de tomografía computarizada en vista coronal que mostraban la participación del sistema colector y el contacto con el hígado. Se sospechó de HC en base a las evaluaciones clínicas y radiológicas. Los hallazgos de la radiografía de tórax no fueron significativos, sin evidencia de quistes pulmonares. Después de un régimen de tres meses de albendazol 400 mg administrado dos veces al día, la paciente se sometió a una intervención quirúrgica. Se realizó un procedimiento abierto a través de una incisión subcostal derecha de Kocher, lo que resultó en una nefrectomía derecha y una resección hepática parcial debido a las adherencias. El espécimen, que pesaba 372 g y medía 13 × 8 × 6 cm, mostró un gran quiste blanco con paredes delgadas que contenían una membrana desprendida, que afectaba los cálices renales y la pelvis. El diagnóstico final fue HC del riñón acompañado de pielonefritis crónica. Los exámenes de laboratorio posteriores al procedimiento mostraron resultados normales, con una producción urinaria estable y signos vitales. El catéter urinario se retiró después de 24 horas debido a una producción urinaria adecuada (2 L). El drenaje renal se retiró después de 3 días, con volúmenes de drenaje de 200 ml, 100 ml y ninguno en días consecutivos. La paciente volvió a sus actividades normales sin complicaciones.\n",
+    "gold_summary": "Se diagnosticó a una mujer de 29 años con dolor intermitente en el flanco derecho y ardor urinario un quiste hidatídico (HC) de categoría 4 de Bosniak, tras dar positivo en anticuerpos de equinococo. Las imágenes confirmaron el diagnóstico, lo que derivó en un tratamiento de tres meses con albendazol, seguido de una nefrectomía derecha y una resección hepática parcial. El análisis histopatológico confirmó un HC y una pielonefritis crónica. La paciente se recuperó sin incidentes y volvió a sus actividades normales.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Una mujer tenía dolor en un lado de su cuerpo y ardor al hacer pipí. Los doctores encontraron un quiste grande en su riñón. Le dieron medicina por tres meses para ayudarla. Luego, le hicieron una operación para quitar el riñón y un poco del hígado. Después, ella se sintió bien y pudo hacer sus cosas normales otra vez.",
+        "scores": {
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+        "text": "**Lo que Encontraron**  \nUna mujer de 29 años tenía dolor en el lado derecho de su espalda y a veces sentía ardor al orinar. Los médicos hicieron pruebas y encontraron que tenía anticuerpos contra un parásito llamado equinococo, que puede causar quistes en órganos. Las imágenes del riñón mostraron un quiste grande y complicado, clasificado como categoría 4 de Bosniak, lo que significa que podría ser peligroso.\n\n**Qué Hicieron**  \nPara tratarla, primero le dieron un medicamento llamado albendazol durante tres meses. Este medicamento ayuda a matar el parásito. Después, le hicieron una cirugía para quitar el riñón derecho y parte del hígado, porque el quiste estaba pegado a esos órganos.\n\n**Qué Significa el Diagnóstico**  \nAl analizar el quiste, confirmaron que era un quiste hidatídico, que es una bolsa llena de líquido causada por el parásito. También encontraron inflamación crónica en el riñón, llamada pielonefritis.  \n\n**Recuperación**  \nDespués de la operación, la paciente se recuperó bien, sin problemas. Su orina y signos vitales estaban normales. Pudo volver a sus actividades normales sin complicaciones.  \n\nEste caso muestra cómo una infección por parásitos puede afectar órganos importantes y cómo se puede tratar con medicamentos y cirugía.",
+        "scores": {
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+      "B3": {
+        "text": "**Contexto**  \nUna mujer de 29 años consultó por dolor intermitente en el flanco derecho y episodios ocasionales de ardor al orinar, sin presencia de sangre en la orina. No presentaba síntomas sistémicos como tos, fatiga o pérdida de peso, y su estado general era estable. Destacaba una exposición frecuente a ovejas, factor de riesgo para infecciones parasitarias. Los análisis de laboratorio fueron normales, pero la prueba serológica detectó anticuerpos contra equinococos, un parásito causante de quistes hidatídicos.\n\n**Hallazgos Clave**  \nEl ultrasonido abdominal reveló una lesión quística grande en el riñón derecho, con paredes gruesas y sin flujo sanguíneo significativo. La tomografía computarizada con contraste mostró una masa quística con tabiques internos y una pared engrosada que se realzaba con el contraste, clasificada como categoría 4 en la escala de Bosniak, lo que indica una alta probabilidad de lesión compleja y potencialmente maligna o infecciosa. Además, la lesión involucraba el sistema colector renal y estaba en contacto con el hígado. La radiografía de tórax no mostró quistes pulmonares, descartando afectación pulmonar.\n\n**Interpretación Clínica**  \nEl diagnóstico presuntivo fue un quiste hidatídico renal (HC), una infección parasitaria causada por el equinococo, con posible extensión hepática. El tratamiento inicial consistió en albendazol, un medicamento antiparasitario, administrado durante tres meses para reducir la carga parasitaria y minimizar riesgos quirúrgicos. Posteriormente, se realizó una cirugía abierta mediante una incisión subcostal derecha (incisión de Kocher), que incluyó la extracción completa del riñón derecho (nefrectomía) y una resección parcial del hígado debido a adherencias entre ambos órganos. El estudio histopatológico confirmó la presencia del quiste hidatídico y evidenció pielonefritis crónica, una inflamación prolongada del tejido renal.\n\n**Próximos Pasos y Evolución**  \nTras la cirugía, la paciente mostró una recuperación favorable, con parámetros vitales estables y función urinaria adecuada. El catéter urinario se retiró a las 24 horas, y el drenaje renal se retiró en los días siguientes sin complicaciones. Finalmente, la paciente pudo retomar sus actividades habituales sin presentar efectos adversos ni recurrencias. Este caso destaca la importancia de considerar infecciones parasitarias en pacientes con lesiones quísticas renales, especialmente en contextos de exposición a animales de riesgo.",
+        "scores": {
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+  {
+    "article": "Una paciente de 46 años de edad fue admitida en nuestro hospital debido a opresión en el pecho y falta de aire que había durado más de un mes. Su historial médico incluía una tiroidectomía parcial, y no tenía antecedentes de tabaquismo o consumo de alcohol. Fue tratada con medicamentos regulares (comprimidos de liberación prolongada de succinato de metoprolol, comprimidos de sacubitril valsartán sodio, espironolactona, comprimidos de dapagliflozina) para la IC, pero la respuesta fue pobre. Durante el examen físico, la paciente estaba consciente y bien orientada. Su frecuencia cardíaca era de 68 latidos por minuto, la presión arterial era de 150/98 mm Hg, la frecuencia respiratoria era de 20 latidos por minuto. No había signos de sangrado o ictericia en la piel o membranas mucosas, y no se observó distensión de la vena yugular. La glándula tiroides no estaba agrandada. Los sonidos respiratorios eran gruesos en ambos pulmones, con roncus húmedos presentes en las bases pulmonares. La frecuencia cardíaca era de 68 lpm con un ritmo regular. El abdomen era suave, sin sensibilidad o sensibilidad de rebote, y el hígado y el bazo no eran palpables por debajo de la caja torácica. El signo de reflujo hepatoyugular fue negativo, pero había edema en ambas extremidades inferiores.\n\nLa paciente fue hospitalizada y se le realizaron los exámenes pertinentes. Los análisis bioquímicos mostraron una hormona estimulante de la tiroides (TSH) de 7,190 uIU/mL, triglicéridos de 0,81 mmol/L, colesterol de lipoproteínas de baja densidad (LDL-C) de 2,61 mmol/L, lipoproteína (a) de suero de 435 mg/L y NT-proBNP de 6245 pg/mL. Un examen de electrocardiograma (ECG) mostró bradicardia sinusal, anomalías de la onda T-U y duración del QRS de 90 ms. Un examen ecocardiográfico transtorácico posterior reveló un diámetro de la aurícula izquierda (LA) (anteroposterior) de 41 mm, un diámetro del ventrículo izquierdo (LVD) (anteroposterior) de 54 mm, un espesor del tabique interventricular en diástole (IVSD) de 9 mm, un espesor de la pared posterior del ventrículo izquierdo en la fase final de la diástole (LVPWd) de 9 mm, una fracción de eyección del ventrículo izquierdo (LVEF) del 28% (M-mode), una fracción de acortamiento (FS) del 13% y una presión de la arteria pulmonar de 29 mm Hg. No se observaron lesiones coronarias significativas en la angiografía coronaria computarizada (CCA). Se diagnosticó a la paciente con cardiomiopatía dilatada, insuficiencia cardiaca de clase III con LVEF reducida según la New York Heart Association (NYHA). En combinación con los parámetros, se puede observar que los volúmenes de la aurícula izquierda y el ventrículo izquierdo se reducen gradualmente, lo que indica que la función diastólica del ventrículo izquierdo está mejorando. El tratamiento con CCM revierte la remodelación miocárdica. Además, E/e′ refleja la presión de llenado ventricular izquierdo. El valor normal debe ser inferior a 8. Se puede observar que en este caso, E/e′ vuelve al valor normal tres meses después de la implantación de CCM. Estos dos puntos reflejan el papel de CCM en la mejora de la función diastólica miocárdica en el tratamiento de la insuficiencia cardiaca. En resumen, la paciente tenía las siguientes características: (1) LVEF mejoró pero se mantuvo tan bajo como el 30% después de la terapia óptima para la insuficiencia cardiaca; (2) opresión en el pecho y malestar con ligera actividad, grado de función cardiaca III; (3) ECG muestra QRS estrecho. Teniendo en cuenta el resultado positivo de la prueba preoperatoria de levosimendan, después de una discusión general y una comunicación completa con el paciente y su familia, se decidió realizar el tratamiento con CCM.\n\nEl procedimiento de implantación del CCM fue similar al de la implantación de un marcapasos tradicional. El paciente se colocó en posición supina, se desinfectó con una toalla y se perforó la vena subclavia izquierda dos veces bajo anestesia local, y se hizo la bolsa capsular después de insertar el alambre guía. Bajo la guía del alambre guía, se introdujeron dos vainas de desprendimiento, y se introdujeron dos cables de estimulación ventricular (Medtronic 3830-69) a través de la vaina, y se ajustó la posición de los cables a la superficie del tabique ventricular derecho con una distancia de 3 cm. Durante la operación, se probó el electrodo de campo cercano (RV), que mostró un umbral de estimulación de 0,5 V, una amplitud de la onda R detectada mayor de 10 mV, y una impedancia del cable de 1080 Ω; el electrodo de campo lejano (LS) mostró un umbral de estimulación de 0,5 V, una amplitud de la onda R detectada mayor de 15 mV, y una impedancia del cable de 900 Ω. Estas mediciones cumplieron los criterios para una implantación exitosa del electrodo. Ambos cables se anclaron de forma segura en el tabique ventricular derecho. Después de asegurarse de que no había estimulación diafragmática palpable con un pulso de estimulación de 10 V y una anchura de pulso de 0,4 ms, se conectaron los cables al generador de impulsos Optimizer Smart. Posteriormente, se ajustaron los impulsos de salida y se programaron y optimizaron los parámetros.\n\nLa monitorización del ECG postoperatorio inmediato indicó un suministro normal de impulsos CCM (Figura 1C). Observamos la respuesta de los pacientes al CCM al adherirnos a un protocolo de seguimiento estandarizado. Utilizando una amplia variedad de herramientas de evaluación, que incluían ultrasonografía Doppler cardiaca a color, análisis de sangre NT-ProBNP, pruebas de caminata de seis minutos (6MW) y el Cuestionario de Minnesota para Vivir con Insuficiencia Cardiaca (MLHFQ), evaluamos sistemáticamente el estado clínico de los pacientes. El paciente no experimentó opresión en el pecho ni falta de aire, y hubo una marcada mejora en la tolerancia al ejercicio y la calidad de vida.\n",
+    "gold_summary": "Presentamos a una paciente de 46 años que fue admitida en nuestro hospital debido a opresión torácica y falta de aire que duró más de un mes. La ecocardiografía reveló un diámetro del ventrículo izquierdo (anteroposterior) de 54 mm, el electrocardiograma mostró bradicardia sinusal y duración del QRS de 90 ms. La paciente no experimentó opresión torácica o falta de aire, y hubo una marcada mejora en la tolerancia al ejercicio y calidad de vida después de la implantación de la modulación de la contractilidad cardiaca.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Una señora tenía dolor en el pecho y le costaba respirar mucho tiempo. Los doctores miraron su corazón con máquinas. Después de un tratamiento especial, ella se sintió mucho mejor. Ya no tenía dolor ni dificultad para respirar. Ahora puede jugar y caminar sin problema.",
+        "scores": {
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
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+        "text": "**Caso de una Paciente con Problemas del Corazón**\n\nUna mujer de 46 años llegó al hospital porque sentía opresión en el pecho y le costaba respirar desde hacía más de un mes. Para entender qué le pasaba, los médicos le hicieron varios estudios.\n\n**Lo que Encontraron**\n\nUn examen llamado ecocardiografía mostró que una parte de su corazón, llamada ventrículo izquierdo, estaba un poco agrandada (medía 54 mm). Otro examen, el electrocardiograma, mostró que su corazón latía más lento de lo normal (bradicardia sinusal) y que la señal eléctrica que controla el latido tenía una duración normal (QRS de 90 ms).\n\n**Qué Hicieron y Qué Pasó Después**\n\nPara ayudarla, los médicos le implantaron un dispositivo llamado modulador de la contractilidad cardiaca (CCM). Este aparato envía pequeñas señales eléctricas al corazón para mejorar su fuerza al latir. Después de la implantación, la paciente ya no tuvo opresión en el pecho ni dificultad para respirar. Además, pudo hacer ejercicio con más facilidad y su calidad de vida mejoró mucho.\n\nEn resumen, el tratamiento con CCM ayudó a mejorar la función de su corazón y su bienestar general.",
+        "scores": {
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+        "text": "**Contexto**\n\nUna mujer de 46 años fue hospitalizada por presentar opresión en el pecho y dificultad para respirar que persistían desde hacía más de un mes. Su historial incluía una cirugía parcial de tiroides y no tenía antecedentes de tabaquismo ni consumo de alcohol. A pesar de recibir tratamiento médico estándar para insuficiencia cardiaca, sus síntomas y función cardíaca no mejoraron adecuadamente. Los exámenes iniciales mostraron una fracción de eyección del ventrículo izquierdo (LVEF) muy reducida (28%), indicativa de una función cardíaca comprometida, y un electrocardiograma (ECG) con bradicardia sinusal y un complejo QRS estrecho (90 ms).\n\n**Hallazgos Clave**\n\n- Ecocardiografía: El ventrículo izquierdo tenía un diámetro anteroposterior de 54 mm, con una fracción de eyección del 28%, confirmando una cardiomiopatía dilatada con función cardíaca severamente reducida.\n- ECG: Bradicardia sinusal (ritmo cardíaco lento pero regular) y duración del QRS de 90 ms, lo que indica que la conducción eléctrica del corazón estaba relativamente normal.\n- Laboratorio: Elevación significativa del NT-proBNP (6245 pg/mL), marcador que refleja estrés y daño cardíaco.\n- Sintomatología: Opresión en el pecho y dificultad para realizar actividades físicas leves, clasificada como insuficiencia cardíaca clase III según la New York Heart Association (NYHA).\n\n**Interpretación Clínica**\n\nLa paciente presentaba insuficiencia cardíaca con función ventricular izquierda gravemente disminuida, a pesar del tratamiento médico óptimo. La cardiomiopatía dilatada y los síntomas persistentes indicaban la necesidad de una intervención adicional. Se decidió implantar un dispositivo de modulación de la contractilidad cardíaca (CCM), que es un tipo de terapia eléctrica que mejora la fuerza de contracción del corazón sin alterar el ritmo cardíaco normal.\n\nEl procedimiento de implantación fue similar al de un marcapasos tradicional, con cables colocados en el tabique del ventrículo derecho y un generador de impulsos programado para optimizar la función cardíaca. La implantación fue exitosa, sin complicaciones inmediatas.\n\n**Próximos Pasos y Resultados**\n\nTras la implantación del dispositivo CCM, la paciente fue monitoreada mediante ecocardiografía, análisis sanguíneos, pruebas de caminata y cuestionarios de calidad de vida. A los tres meses, se observó una mejora significativa en la función diastólica del ventrículo izquierdo, reducción de la presión de llenado ventricular y una disminución en los síntomas clínicos.\n\nLa paciente dejó de experimentar opresión en el pecho y dificultad para respirar, mostró una notable mejoría en la capacidad para realizar ejercicio y reportó una mejor calidad de vida. Estos resultados sugieren que la terapia con CCM puede ser una opción efectiva para pacientes con insuficiencia cardíaca avanzada que no responden adecuadamente al tratamiento médico convencional.",
+        "scores": {
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+  {
+    "article": "Paciente de sexo femenino, 61 años, caucásica, casada, dos hijos, informó empeoramiento de los síntomas de la psoriasis tras el inicio de L-metilfolato 15 mg al día para tratamiento coadyuvante de la depresión. Informó depresión y psoriasis desde los 20 años. Desde los 41 años, la paciente no había tenido recidivas de las lesiones psoriáticas.\n\nPor su historial de depresiones, se le indicó carbonato de litio, pero no lo tomó debido a la psoriasis. En 2000, su cuadro depresivo mejoró con venlafaxina 225 mg al día. En 2016, debido a las oscilaciones de humor, se le agregó lamotrigina 100 mg al día y, para mejorar el sueño, se le sumó quetiapina 50 mg al día.\n\nEstas fueron las dosis actuales, con una mejora en la depresión, la calidad de vida y sin efectos adversos significativos.\n\nEn enero de 2019, se detectó polimorfismo en el gen MTHFR, con una mutación heterozigótica en C677T, y se le recetó a la paciente 15 mg diarios de L-metilfolato. Antes de que finalizara la primera semana de uso de L-metilfolato, aparecieron lesiones psoriáticas que no se habían manifestado en 20 años. Se informó lo ocurrido al psiquiatra, quien retiró la medicación y, 4 días después, las lesiones psoriáticas comenzaron a remitir, desapareciendo por completo al cabo de unas semanas. La paciente no volvió a registrar manifestaciones hasta principios de 2020.\n",
+    "gold_summary": "Paciente de sexo femenino, de 61 años, que había estado en remisión de psoriasis durante 20 años. Sufrió una recaída de psoriasis en forma de placa pocos días después de comenzar el tratamiento con L-metilfolato a una dosis diaria de 15 mg.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Una señora de 61 años tuvo la piel con manchas hace mucho tiempo. Ella no tuvo esas manchas por 20 años. Pero cuando empezó a tomar una medicina nueva, las manchas volvieron rápido. Luego, dejó de tomar esa medicina y las manchas se fueron.",
+        "scores": {
+          "ROUGE-1": 0.24489795918367346,
+          "ROUGE-2": 0.10416666666666667,
+          "ROUGE-L-Sum": 0.24489795918367346,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
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+      },
+      "B2": {
+        "text": "**Lo que pasó con la paciente**  \nUna mujer de 61 años había tenido psoriasis, que es una enfermedad de la piel que causa manchas rojas y escamosas. Sin embargo, no había tenido problemas con la psoriasis durante 20 años.  \n\n**Qué tratamiento recibió y qué pasó después**  \nElla empezó a tomar un medicamento llamado L-metilfolato, que es una forma de vitamina B9 que ayuda en el tratamiento de la depresión. Tomaba 15 mg al día. Pero pocos días después de comenzar este medicamento, la psoriasis volvió a aparecer en su piel.  \n\n**Qué hicieron los médicos**  \nAl ver que la psoriasis regresó, el doctor decidió quitarle el L-metilfolato. Cuatro días después de dejar el medicamento, las manchas en la piel comenzaron a mejorar y desaparecieron completamente en unas semanas.  \n\n**Qué significa esto**  \nEste caso muestra que, en esta paciente, el L-metilfolato pudo haber causado que la psoriasis regresara después de muchos años sin síntomas. Por eso, es importante que los médicos revisen bien los tratamientos y los posibles efectos en cada persona.",
+        "scores": {
+          "ROUGE-1": 0.33472803347280333,
+          "ROUGE-2": 0.15189873417721517,
+          "ROUGE-L-Sum": 0.30125523012552297,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
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+      "B3": {
+        "text": "**Contexto**  \nSe trata de una mujer de 61 años con antecedentes de psoriasis y depresión desde los 20 años. Durante dos décadas, desde los 41 años, no presentó brotes de psoriasis. Su tratamiento psiquiátrico actual incluía venlafaxina, lamotrigina y quetiapina, con buena respuesta y sin efectos adversos importantes. En 2019, se identificó que tenía una mutación genética heterozigótica en el gen MTHFR (C677T), lo que llevó a prescribirle L-metilfolato, un suplemento que puede ayudar en ciertos trastornos depresivos.\n\n**Hallazgos Clave**  \nPocos días después de iniciar el L-metilfolato a una dosis diaria de 15 mg, la paciente presentó una recaída de psoriasis en forma de placas, una manifestación cutánea que no había experimentado en 20 años. Al suspender el L-metilfolato, las lesiones comenzaron a mejorar en cuatro días y desaparecieron completamente en unas semanas. No se registraron nuevos brotes hasta casi un año después.\n\n**Interpretación Clínica**  \nEl caso sugiere una posible relación entre la administración de L-metilfolato y la reactivación de la psoriasis en esta paciente. Aunque el L-metilfolato es utilizado para mejorar la depresión, en este caso pudo haber desencadenado una respuesta inflamatoria cutánea, posiblemente relacionada con su predisposición genética y su historial de psoriasis. Este hallazgo es relevante para considerar el impacto de tratamientos coadyuvantes en enfermedades autoinmunes o inflamatorias crónicas.\n\n**Próximos Pasos**  \nSe recomienda un seguimiento cuidadoso en pacientes con antecedentes de psoriasis cuando se prescriben suplementos como el L-metilfolato. Además, es importante evaluar alternativas terapéuticas para la depresión que no exacerben enfermedades cutáneas. La comunicación estrecha entre dermatólogos y psiquiatras es fundamental para manejar casos similares y evitar recaídas.",
+        "scores": {
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
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+  {
+    "article": "Se diagnosticó osteoartritis bilateral de las articulaciones de la cadera en un paciente de 61 años de edad con tratamiento con esteroides para la artritis reumatoide y dolencias en la ingle bilateral. [9] Recibió una inyección intraarticular bilateral de ácido hialurónico y se presentó doce semanas después en nuestro departamento de urgencias con fiebre, un estado general reducido y un dolor cada vez más incapacitante. Las radiografías de la pelvis mostraron una destrucción progresiva y rápida de ambas articulaciones de la cadera con una osteólisis extensa, subluxación concomitante y un defecto óseo acetabular del lado izquierdo. La aspiración de la articulación mostró pus en ambas articulaciones de la cadera y se hizo el diagnóstico de artritis séptica bilateral progresiva rápida. Se realizó una resección bilateral de ambas cabezas femorales con desbridamiento de la articulación de la cadera y la implantación de espaciadores de PMMA cargados con antibióticos a través de un enfoque anterolateral mínimamente invasivo.\n\nSe inició un tratamiento antibiótico sistémico empírico con vancomicina y ampicilina por vía intravenosa. Se detectó E. coli en muestras de tejido de ambas articulaciones de la cadera y se adaptó el tratamiento antibiótico sistémico a meropenem por vía intravenosa. Se realizaron dos procedimientos quirúrgicos de seguimiento con intercambio de los espaciadores de PMMA cargados con antibiótico para controlar la infección debido al drenaje persistente.\n\nDoce semanas después de la resección de la cabeza femoral y el control exitoso de la infección, el paciente recibió una artroplastia total de cadera con el uso adicional de un revestimiento multicapa de plata (HyProtect®, Bio-Gate, Nürnberg, Alemania). Este revestimiento consiste en una capa de siloxano ultrafina directamente sobre la superficie del implante (10 a 30 nm), de la que se liberan iones de plata.\n\n12 semanas después de la resección de la cabeza femoral, se realizó una artroplastia total de cadera en el lado derecho con una copa estándar sin cemento (Allofit®, ZimmerBiomet, Varsovia, EE. UU.) y un vástago femoral sin cemento (Avenir®, ZimmerBiomet, Varsovia, EE. UU.) a través del enfoque anterolateral mínimamente invasivo previamente utilizado con este revestimiento multicapa de plata ultrafino. Tanto la superficie posterior de la copa como todo el eje femoral se revistieron con plata.\n\nLa cadera izquierda se trató 18 semanas después de la resección de la cabeza femoral con una jaula de refuerzo recubierta de plata (Burch-Schneider®, ZimmerBiomet, Varsovia, EE. UU.) para un defecto acetabular tipo IIB de Paprosky y una copa de polietileno cementada (Durasul®, ZimmerBiomet, Varsovia, EE. UU.). El vástago femoral sin cemento (Avenir®, ZimmerBiomet, Varsovia, EE. UU.) también se recubrió de plata en toda su parte intramedular. Esta intervención también se realizó mediante el enfoque anterolateral mínimamente invasivo utilizado previamente. El paciente se sometió a una terapia antibiótica sistémica durante un período de tratamiento total de 18 semanas después de la implantación del lado derecho. Se aplicó ertapenem 1 g por vía intravenosa durante este período de tiempo una vez al día, después de la descarga en un entorno ambulatorio. Esto permitió una cobertura antibiótica del lado derecho de 18 semanas y del lado izquierdo de 12 semanas de tratamiento antibiótico.\n\nSe recomendó el uso parcial de peso con 20 kg en el lado operado y el uso de muletas durante 6 semanas después de las intervenciones.\n\nLas heridas de ambos lados se curaron sin incidentes. El paciente fue visto regularmente para un seguimiento clínico y radiológico. Se logró el apoyo total del peso sin el uso de muletas 7 semanas después de la operación en ambos lados. No hubo signos de PIJ y no fue necesaria una cirugía de revisión adicional.\n\nEn un seguimiento final tres años después de la implantación de las prótesis recubiertas de plata, la paciente mostró un aspecto normal de la piel con mínimas cicatrices después de enfoques antero-laterales mínimamente invasivos en ambos lados sin signos de argiria. Hubo un excelente resultado funcional de ambas caderas con marcha normal y una puntuación WOMAC de 6 en ambos lados (dolor: 0, rigidez: 0, función física: 6). El recuento de leucocitos en sangre fue de 7,29/nl (referencia: 4,23-9,1) y el nivel de proteína C reactiva (PCR) fue de 12,4 mg/l (referencia: <5 mg/l). El nivel ligeramente elevado de PCR es atribuible a la artritis reumatoide subyacente de la paciente. Las radiografías revelaron componentes protésicos de cadera bien integrados y no sueltos en ambos lados tres años después de la implantación con una articulación correcta.\n",
+    "gold_summary": "Este informe de caso se refiere a un paciente de 61 años con destrucción rápida de ambas articulaciones de la cadera debido a una artritis séptica que se trató con éxito con una implantación por etapas de prótesis de cadera recubiertas con plata con un recubrimiento ultrafino multicapa de plata. En un seguimiento de tres años, no hubo signos de infección, se observó un buen estado de todos los componentes protésicos y el resultado funcional fue excelente.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Había un señor con mucho dolor en sus dos caderas. Sus caderas se dañaron rápido por una infección. Los doctores le pusieron unas piezas nuevas en sus caderas. Estas piezas tenían una capa especial de plata para ayudar. Después de tres años, el señor está bien y sin dolor. Sus caderas funcionan muy bien y no hay infección.",
+        "scores": {
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
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+      "B2": {
+        "text": "**Lo que pasó con el paciente:**  \nUn hombre de 61 años tenía un problema grave en ambas caderas. Tenía una infección llamada artritis séptica, que hizo que sus articulaciones se dañaran muy rápido. Esta infección causó mucho dolor y dificultad para moverse.\n\n**Cómo lo trataron:**  \nPrimero, le quitaron las partes dañadas de las caderas y limpiaron bien las áreas infectadas. Luego, le pusieron unos espaciadores especiales con antibióticos para controlar la infección. Después de varias semanas y tratamientos con antibióticos fuertes, la infección mejoró.\n\nMás tarde, le pusieron prótesis nuevas en ambas caderas. Estas prótesis tenían un recubrimiento muy delgado de plata. La plata ayuda a evitar que las bacterias vuelvan a causar infección. Las cirugías se hicieron con técnicas que dañan poco los tejidos, para que la recuperación fuera mejor.\n\n**Qué pasó después:**  \nTres años después de las cirugías, el paciente estaba muy bien. No había señales de que la infección regresara. Las prótesis estaban firmes y funcionando bien. El paciente podía caminar normalmente y no sentía dolor ni rigidez en las caderas.\n\n**Por qué es importante:**  \nEste caso muestra que usar prótesis con un recubrimiento especial de plata puede ayudar a tratar infecciones graves en las articulaciones y mejorar la recuperación. Además, el seguimiento a largo plazo confirmó que el tratamiento fue exitoso y seguro.",
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+      },
+      "B3": {
+        "text": "**Contexto**  \nSe trató a un paciente de 61 años con antecedentes de artritis reumatoide, que recibía tratamiento con esteroides, y que presentaba osteoartritis en ambas caderas junto con dolor en la ingle. Después de una inyección de ácido hialurónico en ambas articulaciones, el paciente desarrolló fiebre, deterioro general y un dolor intenso y progresivo en las caderas. Las radiografías mostraron una rápida destrucción ósea en ambas articulaciones, y la aspiración reveló pus, confirmando una infección grave llamada artritis séptica bilateral.\n\n**Hallazgos Clave**  \nSe realizó la extracción quirúrgica de las cabezas femorales (la parte superior del hueso del muslo que forma la articulación de la cadera) y se limpiaron las articulaciones, implantando espaciadores temporales cargados con antibióticos para controlar la infección. Inicialmente se administraron antibióticos de amplio espectro, pero al identificar la bacteria Escherichia coli, el tratamiento se ajustó a un antibiótico específico (meropenem). Debido a la persistencia del drenaje, se llevaron a cabo dos cirugías adicionales para cambiar los espaciadores antibióticos.\n\nTras controlar la infección, se realizaron reemplazos definitivos de ambas caderas mediante prótesis recubiertas con un revestimiento ultrafino multicapa de plata. Este recubrimiento libera iones de plata, conocidos por sus propiedades antimicrobianas, con el objetivo de prevenir nuevas infecciones. La cirugía se realizó mediante un abordaje mínimamente invasivo para reducir el daño a los tejidos.\n\nEl lado derecho se operó primero, con una prótesis sin cemento y recubierta de plata en las superficies clave. La cadera izquierda se intervino semanas después, utilizando una jaula de refuerzo también recubierta de plata para reparar un defecto óseo importante, junto con una copa de polietileno cementada y un vástago femoral sin cemento igualmente recubierto. El paciente recibió un tratamiento antibiótico prolongado (hasta 18 semanas) para asegurar la erradicación completa de la infección.\n\n**Interpretación Clínica**  \nEl uso de prótesis recubiertas con plata en este caso permitió un control efectivo de la infección y una recuperación funcional excelente. Las heridas cicatrizaron sin complicaciones, y el paciente pudo caminar sin muletas en pocas semanas. Tres años después de la cirugía, no se observaron signos de infección recurrente ni efectos secundarios relacionados con la plata, como la argiria (una pigmentación anormal de la piel). Las radiografías mostraron que las prótesis estaban bien integradas y estables, y la función de las caderas era casi normal, con muy poco dolor y rigidez.\n\n**Próximos Pasos**  \nEl seguimiento clínico y radiológico continuado es fundamental para detectar cualquier posible complicación a largo plazo. En este caso, el éxito del tratamiento sugiere que las prótesis con recubrimiento de plata pueden ser una opción valiosa para pacientes con infecciones severas en las articulaciones, especialmente cuando se requiere una reconstrucción compleja. Además, el abordaje mínimamente invasivo contribuyó a una recuperación más rápida y con menos cicatrices visibles.\n\nEn resumen, este caso demuestra que un tratamiento escalonado que combina cirugía, antibióticos específicos y prótesis con recubrimiento antimicrobiano puede lograr resultados excelentes en infecciones articulares graves, mejorando la calidad de vida del paciente a largo plazo.",
+        "scores": {
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+  {
+    "article": "Una niña africana de raza negra, con 1000 g de peso, nacida a las 32 semanas de gestación, de madre viva, fue derivada a nuestra unidad de cuidados intensivos neonatales debido a múltiples anomalías congénitas y dificultad respiratoria moderada. La madre tiene 32 años y está en un matrimonio no consanguíneo. La madre no buscó atención médica hasta el inicio del tercer trimestre de embarazo, debido a un desprendimiento de placenta. El primer ultrasonido prenatal reveló oligohidramnios severos. No era diabética (la glucosa en sangre aleatoria fue de 5.1 mmol/L) y no recibió suplementos de ácido fólico durante el embarazo.\n\nAl ingreso, la bebé estaba alerta con características leves del síndrome de dificultad respiratoria. Presentaba múltiples rasgos dismórficos, entre ellos, microcefalia (circunferencia de la cabeza < 10%), occipucio prominente, orejas bajas, paladar hendido y labio derecho, micrognatia, contractura bilateral de los codos e inferiores más cortos.\n\n\nEl peso al nacer fue de 1000 g, la longitud del bebé fue de 40 cm y la circunferencia occipitofrontal fue de 30 cm.\n\nInvestigaciones\nLa radiografía esquelética mostró aplanamiento de las costillas, aplasia del fémur derecho e hipoplasia del fémur izquierdo. Los análisis de laboratorio incluyeron: hemograma completo, proteína C reactiva, creatinina, urea en sangre y electrolitos, todos dentro de los valores normales. La ecografía craneal fue normal, pero la ecocardiografía reveló un pequeño conducto arterioso permeable.\n\nDiagnóstico diferencial\nLa paciente presentaba aplasia femoral bilateral y facies inusuales. Estas características clínicas llevaron al diagnóstico de síndrome femoro-facial.\n\nLa similitud en la etiopatogénesis hace que el síndrome de regresión caudal sea el diagnóstico diferencial común. Ambos pueden ser causados por una hiperglucemia materna mal controlada. Sin embargo, los defectos faciales están ausentes en el síndrome de regresión caudal, la característica diagnóstica clave.\n\nLa hipoplasia femoral focal proximal y las anomalías craneofaciales suelen estar ausentes.\n\nEntre las condiciones que pueden provocar el labio leporino se incluye el síndrome de banda amniótica grave.\n\nTratamiento\nEl bebé recibió asistencia respiratoria y antibióticos empíricos. Participaron un cirujano ortopédico, un otorrinolaringólogo y un fisioterapeuta. Está previsto reparar quirúrgicamente el paladar hendido a los 6 meses de edad. La rehabilitación funcional está prevista antes de que el paciente comience a deambular. La cirugía de alargamiento de extremidades no se realiza actualmente en nuestro entorno.\n\nResultado y seguimiento\nEl paciente falleció a la edad de un mes por complicaciones de una sepsis neonatal grave de inicio tardío.\n",
+    "gold_summary": "Una niña africana de raza negra bantú de 1 día de vida fue admitida en la unidad neonatal debido a múltiples anomalías congénitas. La madre no buscó atención médica hasta el inicio del tercer trimestre, cuando tuvo un desprendimiento de placenta. La madre nunca recibió suplementos de ácido fólico prenatal. La niña tenía microcefalia, orejas bajas, paladar hendido derecho y labio, micrognatia, contractura y extremidades más cortas. Una radiografía esquelética mostró hipoplasia femoral. Presentamos este caso poco habitual y destacamos los retos en el diagnóstico y el tratamiento.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Una bebé nació con problemas en su cuerpo. Su mamá no fue al doctor mucho cuando estaba embarazada. La bebé tenía la cabeza pequeña y orejas bajitas. También tenía un huequito en la boca y su labio estaba partido. Sus brazos y piernas eran más cortos y un hueso de la pierna estaba pequeño. Los doctores cuidaron mucho a la bebé, pero fue difícil ayudarla.",
+        "scores": {
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+      "B2": {
+        "text": "**Lo que pasó con la bebé**  \nUna niña africana nació prematura, con solo 32 semanas de gestación y pesando 1000 gramos. Fue llevada a una unidad especial para bebés recién nacidos porque tenía varios problemas desde el nacimiento. Su mamá no recibió atención médica durante la mayor parte del embarazo y no tomó ácido fólico, una vitamina importante para evitar defectos al nacer. Además, la mamá tuvo un problema llamado desprendimiento de placenta, que puede afectar al bebé.\n\n**Lo que encontraron en la bebé**  \nLa niña tenía la cabeza más pequeña de lo normal (microcefalia), orejas bajas, un paladar y labio hendidos (como un corte en el labio y el techo de la boca), mandíbula pequeña (micrognatia), y sus brazos y piernas eran más cortos y rígidos. Las radiografías mostraron que sus huesos de las piernas, especialmente los fémures, estaban subdesarrollados o faltaban partes. También tenía dificultad para respirar leve y un pequeño problema en el corazón.\n\n**Qué significa el diagnóstico**  \nLos médicos diagnosticaron a la bebé con un síndrome llamado femoro-facial. Esto significa que tiene problemas en los huesos de las piernas (fémur) y en la cara. Este síndrome es raro y puede parecerse a otro llamado síndrome de regresión caudal, pero en ese último no hay problemas en la cara, lo que ayuda a diferenciarlos. Además, algunas de sus características podrían estar relacionadas con problemas durante el embarazo, como la falta de control de azúcar en la mamá, aunque en este caso no se encontró diabetes.\n\n**Cómo trataron a la bebé y qué pasó después**  \nLa bebé recibió ayuda para respirar y antibióticos para prevenir infecciones. También la atendieron varios especialistas para planear cirugías y terapias que la ayudaran a mejorar su movilidad y corregir el paladar hendido. Sin embargo, a pesar de los cuidados, la bebé falleció a los 30 días de vida debido a una infección grave.\n\n**Resumen final**  \nEste caso muestra lo difícil que es diagnosticar y tratar a bebés con problemas congénitos raros, especialmente cuando la atención prenatal no es adecuada. Es importante que las mamás reciban cuidado médico temprano y tomen vitaminas como el ácido fólico para prevenir algunos defectos al nacer.",
+        "scores": {
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+      "B3": {
+        "text": "**Contexto**  \nSe presentó el caso de una recién nacida africana de raza negra, con un peso bajo al nacer (1000 gramos) y prematura (32 semanas de gestación), que fue ingresada en la unidad de cuidados intensivos neonatales debido a múltiples anomalías congénitas y dificultad respiratoria moderada. La madre, de 32 años, no recibió atención prenatal adecuada hasta el tercer trimestre, cuando sufrió un desprendimiento de placenta, y no tomó suplementos de ácido fólico durante el embarazo. El embarazo se caracterizó por oligohidramnios severo (disminución del líquido amniótico).\n\n**Hallazgos Clave**  \nAl momento del ingreso, la bebé estaba alerta pero presentaba signos leves de síndrome de dificultad respiratoria. Se observaron varias malformaciones físicas: microcefalia (cabeza pequeña), occipucio prominente (parte posterior de la cabeza sobresaliente), orejas bajas, paladar hendido y labio leporino en el lado derecho, micrognatia (mandíbula pequeña), contracturas en ambos codos y extremidades inferiores más cortas.  \n\nLas radiografías mostraron aplanamiento de las costillas, ausencia completa del fémur derecho (aplasia) y desarrollo insuficiente del fémur izquierdo (hipoplasia). Los análisis de laboratorio básicos fueron normales, la ecografía cerebral no mostró alteraciones, pero el ecocardiograma detectó un pequeño conducto arterioso permeable (una conexión anormal entre dos vasos sanguíneos del corazón).\n\n**Interpretación Clínica**  \nEl conjunto de características clínicas llevó al diagnóstico de síndrome femoro-facial, una condición poco común que se caracteriza por anomalías en los huesos del muslo (fémur) y rasgos faciales inusuales. Este diagnóstico se diferencia del síndrome de regresión caudal, que también afecta la parte inferior del cuerpo pero no presenta malformaciones faciales. Además, se consideraron otras causas posibles del labio leporino, como el síndrome de banda amniótica, pero la combinación de hallazgos apuntó al síndrome femoro-facial.  \n\nEs importante destacar que, aunque la hiperglucemia materna mal controlada (niveles altos de azúcar en sangre durante el embarazo) puede causar ambas condiciones, en este caso la madre no tenía diabetes diagnosticada.\n\n**Tratamiento y Manejo**  \nLa bebé recibió soporte respiratorio y tratamiento antibiótico preventivo. Se contó con la participación de un equipo multidisciplinario que incluyó cirujano ortopédico, otorrinolaringólogo y fisioterapeuta. Se planificó la reparación quirúrgica del paladar hendido a los seis meses de edad y la rehabilitación funcional antes de que la niña comenzara a caminar. Sin embargo, la cirugía para alargar las extremidades no está disponible en el centro donde fue atendida.\n\n**Resultado y Seguimiento**  \nLamentablemente, la paciente falleció a la edad de un mes debido a complicaciones derivadas de una sepsis neonatal grave (infección generalizada en el recién nacido) de inicio tardío, lo que refleja la gravedad y complejidad del cuadro clínico.\n\n---\n\nEste caso resalta los desafíos en el diagnóstico y manejo de anomalías congénitas complejas en un contexto con recursos limitados, así como la importancia de la atención prenatal temprana y adecuada para prevenir y detectar estas condiciones.",
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+    "article": "Paciente de sexo masculino de 18 años, con diag nóstico clínico de Neurofibromatosis tipo 1 desde el primer año de vida. Entre sus antecedentes destaca que tiene educación completa, sus padres no son consan guíneos, y no tiene antecedentes familiares de manchas café con leche. Desde el punto de vista neurológico desarrolló durante la infancia retraso del desarrollo psicomotor fino y grueso, trastorno del lenguaje de predominio expresivo, con alteración fonológica y semántica del lenguaje, por lo que fue manejado con fonoaudiología en Escuela de Lenguaje, además de ki- nesioterapia y terapia ocupacional durante la infancia. Durante la adolescencia se le diagnosticó Trastorno por Déficit Atencional e Hiperactividad, que fue manejado con metilfenidato, manteniendo regular rendimiento escolar. Tuvo desarrollo puberal normal. Oftalmológi camente presentó nódulos de Lisch desde los 4 años de edad, euriblefaron y astigmatismo. Se mantuvo en control anual en Oftalmología y Neuropediatría. Su última Resonancia Magnética de cerebro fue realiza da 6 meses previo a la consulta en Dermatología, sin hallazgos patológicos y en la Resonancia Magnética de columna se evidenció discopatía L5-S1 y realce perifacetario en T11-T12 y T12-L1. A los 16 años se reali zó estudio genético que demostró deleción de exones 5-47 del gen NF1.\n\nA los 18 años consultó en servicio de Dermatología del Centro de Referencia en Salud Peñalolén Cordille ra Oriente por aparición de nueva mancha en muslo izquierdo de 1 año evolución, asintomática. Además, refirió aparición de nódulos en muñeca derecha, su praciliar derecho y cuero cabelludo, de unos meses de evolución, asintomáticos.\n\nAl examen físico destacaba presión arterial normal, macrocefalia (CC: 60 cm) y múltiples manchas café con leche generalizadas, efélides en axilas, y en zona supraciliar derecha, occipital y muñeca derecha nódulos subcutáneos ovalados de 0,5 cm, bien delimitados, móviles. En muslo izquierdo lateral pre sentaba placa de 25 mm algo rosada, con pérdida de anexos, y de consistencia blanda. Por último, en zona lumbar y pectoral, múltiples máculas rojo- azuladas pequeñas, de menos de 5 mm cada una, algu nas levemente deprimidas.\n\nSe realizó biopsia cutánea de máculas azuladas en pecho y de placa muslo, resultando ambas compatibles con NF. Se realizó una ecografía de nódulos supraciliar y occipital que resultó compatible con NF nodular subcutáneo.\n\nUsando la clasificación clínica de García-Martínez et al.1 se diagnosticó al paciente con NF superficial sub cutáneo nodular en zona supraciliar derecha, occipital y muñeca derecha, NF superficial cutáneo pseudoatró fico en muslo izquierdo lateral y NF superficial cutáneo rojo azulado en zona lumbar y pectoral.",
+    "gold_summary": "Paciente masculino de 18 años con diagnóstico desde la infancia de NF-1 que presenta múltiples nodulos ovalados en cara, zona occipital y muñeca, máculas rojo-azuladas en dorso y placa rosada atrófica en muslo. El estudio ecográfico de los nódulos fue compatible con neurofibromas y el estudio histopatológico de las lesiones de dorso y muslo compatibles con neurofibromas cutáneos.",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Un niño que ahora tiene 18 años tiene una enfermedad llamada NF-1 desde que era muy pequeño. En su piel hay bolitas redondas en la cara, la cabeza y la muñeca. También tiene manchas rojas y azules en la espalda. En el muslo tiene una mancha rosada y suave. Los doctores hicieron pruebas y vieron que esas bolitas y manchas son parte de su enfermedad. Todo está bien cuidado y los doctores lo están ayudando.",
+        "scores": {
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+      "B2": {
+        "text": "**Lo que encontraron en el paciente**  \nUn joven de 18 años, que desde pequeño tiene una enfermedad llamada Neurofibromatosis tipo 1 (NF-1), presentó varios bultos pequeños y redondeados en la cara, la parte de atrás de la cabeza (zona occipital) y la muñeca. También tenía manchas de color rojo-azulado en la espalda y una zona rosada y delgada en el muslo izquierdo.\n\n**Qué significan los estudios realizados**  \nSe usó una ecografía, que es una prueba con ondas sonoras para ver el interior de los bultos, y mostró que esos nódulos eran neurofibromas. Los neurofibromas son tumores benignos, es decir, no cancerosos, que crecen en los nervios. Además, se tomó una biopsia, que consiste en sacar un pequeño pedazo de piel para examinarlo bajo el microscopio. Esta prueba confirmó que las manchas en la espalda y la placa en el muslo también eran neurofibromas en la piel.\n\n**Importancia del diagnóstico**  \nEstos hallazgos ayudan a entender mejor cómo afecta la NF-1 a este paciente, mostrando que tiene diferentes tipos de neurofibromas en varias partes del cuerpo. Esto es importante para su seguimiento médico y para decidir el mejor tratamiento si fuera necesario.",
+        "scores": {
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+        "text": "**Contexto**\n\nSe trata de un joven de 18 años con diagnóstico clínico confirmado desde la infancia de Neurofibromatosis tipo 1 (NF1), una enfermedad genética que afecta el desarrollo de tejidos nerviosos y cutáneos. Su historia médica incluye retrasos en el desarrollo psicomotor y del lenguaje durante la infancia, así como un diagnóstico de Trastorno por Déficit de Atención e Hiperactividad en la adolescencia. Presenta además características típicas de NF1, como múltiples manchas café con leche en la piel, nódulos oculares llamados nódulos de Lisch, y una macrocefalia (cabeza de tamaño mayor al promedio).\n\n**Hallazgos Clínicos y Diagnósticos**\n\nA los 18 años, el paciente consultó por la aparición de una nueva mancha en el muslo izquierdo que llevaba un año, además de varios nódulos en la muñeca derecha, la zona supraciliar derecha (por encima de la ceja) y el cuero cabelludo, todos asintomáticos. En el examen físico se observaron:\n\n- Múltiples manchas café con leche distribuidas por todo el cuerpo.\n- Nódulos subcutáneos ovalados, bien delimitados y móviles, de aproximadamente 0,5 cm en la zona supraciliar derecha, occipital y muñeca derecha.\n- Una placa rosada de 25 mm en el muslo izquierdo, con pérdida de anexos cutáneos (como folículos pilosos) y consistencia blanda.\n- Múltiples máculas rojo-azuladas pequeñas, algunas ligeramente deprimidas, en la zona lumbar y pectoral.\n\nSe realizaron estudios complementarios:\n\n- Ecografía de los nódulos supraciliares y occipitales, que mostró características compatibles con neurofibromas nodulares subcutáneos (tumores benignos derivados de las células nerviosas).\n- Biopsias de las máculas rojo-azuladas del pecho y de la placa del muslo, cuyos resultados confirmaron la presencia de neurofibromas cutáneos.\n\n**Interpretación Clínica**\n\nEl diagnóstico se basó en la clasificación clínica propuesta por García-Martínez y colaboradores, identificando tres tipos de manifestaciones cutáneas en este paciente:\n\n1. Neurofibromas superficiales subcutáneos nodulares en la zona supraciliar derecha, occipital y muñeca derecha.\n2. Neurofibroma superficial cutáneo con aspecto pseudoatrófico (que simula una pérdida de tejido) en el muslo izquierdo.\n3. Neurofibromas superficiales cutáneos de color rojo-azulado en la zona lumbar y pectoral.\n\nEstos hallazgos son consistentes con la variedad de lesiones cutáneas que pueden presentarse en pacientes con NF1, reflejando la heterogeneidad clínica de la enfermedad.\n\n**Próximos Pasos**\n\nEl paciente debe continuar con seguimiento multidisciplinario, incluyendo dermatología, neurología y oftalmología, para monitorear la evolución de las lesiones cutáneas y detectar posibles complicaciones neurológicas o malignización de los neurofibromas. Además, es importante mantener el control de su desarrollo cognitivo y conductual, así como realizar evaluaciones periódicas mediante imágenes para descartar nuevas alteraciones. La educación y el apoyo psicosocial también son fundamentales para mejorar su calidad de vida.",
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
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+  {
+    "article": "Un hombre de 38 años de edad fue ingresado en el hospital por traumatismo torácico contundente. El paciente estaba generalmente sano y no tenía factores de riesgo de enfermedad coronaria. Fue golpeado en el pecho por un tornillo de alta velocidad que tenía aproximadamente 6 cm de diámetro mientras trabajaba en una fábrica. Voló aproximadamente 4 metros de distancia debido a la fuerza y presión del tornillo de alta velocidad. Perdió el conocimiento de inmediato, pero recuperó la conciencia varios minutos después. Fue trasladado inmediatamente a la sala de urgencias de un hospital local. Su puntaje en la escala de coma de Glasgow fue de 15. Se quejó de dolor torácico intenso y persistente, opresión y disnea. La tomografía computarizada del tórax mostró derrame pleural bilateral y fracturas de esternón y costillas. Por lo tanto, se insertó un tubo torácico durante varios días. Luego, fue dado de alta sin someterse a un electrocardiograma (ECG) u otros exámenes cardiovasculares.\n\nTres meses después del alta hospitalaria, durante un chequeo de seguimiento de rutina, todavía había presencia de derrame pleural con síntomas acompañantes de opresión en el pecho, falta de aire después de la actividad física, e incluso disnea por la noche, lo que motivó su ingreso en nuestro hospital. Sus constantes vitales durante el ingreso fueron las siguientes: frecuencia cardíaca regular de 98 latidos/min, presión arterial de 110/70 mmHg, y frecuencia respiratoria de 20 respiraciones/min. El examen físico mostró una pulsación carotídea y yugular normal. El movimiento respiratorio torácico bilateral y la actividad fueron normales, la fibrilación del lenguaje táctil del pulmón derecho disminuyó, la percusión del pulmón derecho presentó un sonido sordo, y los sonidos respiratorios disminuyeron. No hubo roncus ni estertores evidentes durante la auscultación pulmonar. No hubo murmullos en la auscultación cardíaca. Los exámenes del abdomen y las extremidades revelaron hallazgos normales. El primer ECG mostró evaluación ST e inversión de la onda T en las derivaciones I, aVL y V2-V5 y en el bloqueo de rama anterior izquierdo. La prueba de troponina-I fue negativa, y el nivel de NT-proBNP fue de 706 pg/ml (rango normal: 0-104 pg/ml), lo que sugiere un infarto de miocardio anterior antiguo. La ecocardiografía transtorácica mostró una aurícula izquierda de 26,4 mm, un ventrículo izquierdo de 51,8 mm, y una fracción de eyección ventricular izquierda (EF) del 32% (modo M). La pared anterior del LV e interventricular septum mostraron adelgazamiento a 6,6 mm, con un eco de movimiento notablemente reducido.\n\nAl examinar las arterias carótidas, intracraneales y de las extremidades inferiores del paciente, no se encontraron placas ateroscleróticas evidentes. Todos los hallazgos apoyaron el diagnóstico de infarto de miocardio antiguo (OMI), en lugar de arteriosclerosis. Sin embargo, el paciente era hemodinámicamente estable. Después de someterse a una terapia diurética, se le administraron bloqueadores beta, estatinas y estimulantes cardíacos, lo que alivió su malestar. La angiografía por tomografía computarizada coronaria mostró una estenosis moderada en la arteria LAD proximal. Para confirmar la estenosis y examinar el estado de la íntima coronaria, se realizó CAG 3 meses después del traumatismo torácico, que mostró un estrechamiento aproximado del 70% del lumen en la LAD proximal y el segmento coronario tenía una lesión curva. La arteria circunfleja izquierda (LCX) y la arteria coronaria derecha (RCA) eran normales. Los resultados de CAG confirmaron el diagnóstico de OMI, pero debido a la carga de costos, el paciente rechazó el examen IVUS. El paciente se sometió a una terapia conservadora y fue dado de alta del hospital varios días después.\n\nUn mes después, el 9 de diciembre de 2014, volvió al hospital para someterse a una intervención coronaria percutánea (ICP). Después de someterse a una terapia con fármacos, sus condiciones habían mejorado ligeramente. El examen físico y el ECG revelaron resultados casi normales. La ecocardiografía transtorácica mostró una mejora en la función sistólica del LV y EF del 45%. Se sometió a otra CAG 4 meses después del traumatismo torácico, que mostró una ligera mejora de la estenosis. Había aproximadamente un 60% de estrechamiento del lumen. Se realizó un IVUS y reveló que la gravedad de la lesión era del 55.9%, y la placa de bajo eco apareció antes de la formación de trombos después de la rotura subintimal. Completamos el examen sin más intervención porque solo se encontró un 55.9% de estrechamiento del lumen y el paciente tenía una hemodinámica estable sin evidencia de isquemia miocárdica constante. Se le recetó al paciente la medicación óptima, y su incomodidad se alivió gradualmente. El 17 de julio de 2018, 4 años después del traumatismo, la evaluación de seguimiento reveló que el paciente todavía experimentaba dificultad para respirar después de trabajar, pero se alivió poco después de descansar. El examen físico mostró los siguientes resultados: presión arterial de 114/80 mmHg, frecuencia cardíaca de 66 latidos/min, ausencia de anomalías obvias en la auscultación pulmonar y cardíaca; y ausencia de edema obvio en ambas extremidades inferiores. El ECG de seguimiento reveló los siguientes hallazgos: rS en las derivaciones V2-V4, inversión de la onda T en las derivaciones I, AVL y V2-V5 y bloqueo de rama izquierda. La ecocardiografía transtorácica mostró agrandamiento del ventrículo izquierdo con una aurícula izquierda de 39 mm, un ventrículo izquierdo de 54.7 mm y una EF del LV del 41% (Simpson's). También se observó adelgazamiento de la pared anterior del LV y del tabique interventricular, con la parte más delgada de 4.7 mm; el movimiento casi había desaparecido y el eco se había mejorado. Sin embargo, las arterias carótidas, intracraneales y de las extremidades inferiores seguían siendo normales. Además, descubrimos que los medicamentos recetados para tratar la insuficiencia cardíaca no se tomaron religiosamente después del alta; por lo tanto, recetamos 23.75 mg de metoprolol, 2.5 mg de benazepril y 20 mg de espironolactona para tomar una vez al día, y coenzima para tomar cada 10 horas.\n\nMH - Adulto\nMH - Errores de diagnóstico\nMH - Insuficiencia cardiaca/etiología\nMH - Humanos\nMH - Hombre\nMH - Infarto de miocardio/complicaciones/*etiología\nMH - Lesiones torácicas/*complicaciones\nMH - Tiempo hasta el tratamiento\nMH - Heridas, no penetrantes/complicaciones\n",
+    "gold_summary": "Preocupaciones de los pacientes:\nUn hombre de 38 años, previamente sano, fue admitido en nuestro hospital con una queja de disnea. Tenía un historial de haber sido golpeado en el pecho por un tornillo de alta velocidad mientras trabajaba en una fábrica 3 meses antes de ser admitido en el hospital.\n\nDiagnóstico:\nLuego de realizarse una angiografía coronaria y una ecocardiografía, finalmente se le diagnosticó un infarto de miocardio.\n\nIntervenciones:\nRecibió medicamentos optimizados, entre ellos, diuréticos, bloqueadores beta y estimulantes cardíacos.\n\nResultados:\nAl cabo de cuatro años de seguimiento, se le diagnosticó al paciente una insuficiencia cardíaca crónica con una fracción de eyección reducida.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Un hombre se lastimó el pecho con un tornillo grande. Tres meses después, le costaba mucho respirar. Los doctores le hicieron pruebas y vieron que su corazón estaba dañado. Le dieron medicinas para ayudar a su corazón a trabajar mejor. Cuatro años después, su corazón seguía un poco débil, pero los doctores siguen cuidándolo.",
+        "scores": {
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+      "B2": {
+        "text": "**Lo que le pasó al paciente**  \nUn hombre de 38 años, que estaba sano antes, sufrió un fuerte golpe en el pecho cuando un tornillo de alta velocidad lo alcanzó mientras trabajaba. Tres meses después, empezó a sentir dificultad para respirar y dolor en el pecho, por lo que fue llevado al hospital.\n\n**Qué encontraron los médicos**  \nDespués de hacerle varios exámenes, como una ecografía del corazón y una angiografía (que es una prueba para ver las arterias del corazón), descubrieron que había tenido un infarto de miocardio. Esto significa que una parte de su corazón no recibió suficiente sangre y se dañó.\n\n**Cómo lo trataron**  \nEl paciente recibió varios medicamentos para ayudar a su corazón a funcionar mejor. Entre ellos estaban diuréticos (que ayudan a eliminar el exceso de líquido), bloqueadores beta (que reducen la carga del corazón) y estimulantes cardíacos (que mejoran la fuerza del latido).\n\n**Qué pasó después**  \nDurante los siguientes cuatro años, los médicos lo siguieron controlando. Descubrieron que desarrolló insuficiencia cardíaca crónica, que es cuando el corazón no puede bombear sangre tan bien como antes. Esto se confirmó porque su fracción de eyección, que mide qué tan bien el corazón bombea, estaba baja.\n\nEn resumen, un golpe fuerte en el pecho causó daño en el corazón que llevó a un infarto y, con el tiempo, a problemas para que el corazón funcione correctamente. El paciente recibió tratamiento para mejorar su condición y sigue siendo monitoreado por los médicos.",
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+        "text": "**Contexto:**  \nUn hombre de 38 años, previamente sano y sin factores de riesgo conocidos para enfermedad coronaria, sufrió un traumatismo torácico grave al ser impactado en el pecho por un tornillo de alta velocidad mientras trabajaba en una fábrica. Tras perder el conocimiento brevemente, fue atendido inicialmente en un hospital local donde se identificaron fracturas en el esternón y costillas, además de derrame pleural bilateral. Fue tratado con drenaje torácico y dado de alta sin realizar estudios cardíacos. Sin embargo, tres meses después, presentó síntomas persistentes como dolor y opresión en el pecho, dificultad para respirar al realizar esfuerzos y disnea nocturna, lo que motivó su ingreso en un hospital especializado para una evaluación más profunda.\n\n**Hallazgos Clave:**  \n- El examen físico reveló signos compatibles con derrame pleural residual en el pulmón derecho, pero sin alteraciones cardíacas evidentes a la auscultación.  \n- El electrocardiograma mostró alteraciones sugestivas de un infarto de miocardio antiguo en la región anterior del corazón, incluyendo inversión de ondas T y bloqueo de rama izquierda anterior.  \n- Los niveles de troponina (marcador de daño cardíaco agudo) fueron negativos, pero el NT-proBNP (marcador de insuficiencia cardíaca) estaba elevado, indicando estrés cardíaco.  \n- La ecocardiografía evidenció una función ventricular izquierda reducida (fracción de eyección del 32%), con adelgazamiento y disminución del movimiento en la pared anterior del ventrículo izquierdo y el tabique interventricular.  \n- La angiografía coronaria mostró una estenosis (estrechamiento) significativa del 70% en la arteria coronaria descendente anterior (LAD), confirmando la presencia de una lesión coronaria importante.  \n- No se encontraron signos de aterosclerosis en otras arterias principales, lo que sugiere que el infarto fue consecuencia directa del traumatismo torácico y no de enfermedad arterial previa.\n\n**Interpretación Clínica:**  \nEl paciente desarrolló un infarto de miocardio antiguo como complicación tardía del traumatismo torácico contundente. La lesión en la arteria coronaria descendente anterior, probablemente causada por el impacto, condujo a daño en el músculo cardíaco y a una reducción significativa de la función del ventrículo izquierdo. A pesar de la gravedad inicial, el paciente se mantuvo hemodinámicamente estable y respondió favorablemente a la terapia médica. Sin embargo, con el tiempo evolucionó hacia una insuficiencia cardíaca crónica con función ventricular reducida, condición que requiere manejo continuo y seguimiento.\n\n**Próximos Pasos y Manejo:**  \n- Se inició tratamiento médico optimizado que incluyó diuréticos para controlar la retención de líquidos, bloqueadores beta para reducir la carga cardíaca y mejorar la función, estatinas para protección vascular y estimulantes cardíacos.  \n- Posteriormente, el paciente se sometió a una intervención coronaria percutánea (ICP) para mejorar el flujo sanguíneo en la arteria afectada.  \n- Durante el seguimiento a largo plazo, se observó una mejoría parcial en la función cardíaca, aunque persistió una insuficiencia cardíaca leve a moderada.  \n- Se enfatizó la importancia de la adherencia estricta a la medicación para prevenir la progresión de la insuficiencia cardíaca y mejorar la calidad de vida.  \n- En controles posteriores, se mantuvo la función cardíaca reducida y síntomas leves de disnea tras esfuerzos, requiriendo ajuste y continuidad en el tratamiento farmacológico.\n\n**Resumen Final:**  \nEste caso ilustra cómo un traumatismo torácico severo puede ocasionar una lesión coronaria significativa que conduce a un infarto de miocardio y, eventualmente, a insuficiencia cardíaca crónica. La evaluación cuidadosa, el diagnóstico oportuno mediante imágenes cardíacas y la terapia médica adecuada son fundamentales para mejorar el pronóstico en estos pacientes. Además, la adherencia al tratamiento y el seguimiento a largo plazo son esenciales para controlar los síntomas y evitar complicaciones mayores.",
+        "scores": {
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+  {
+    "article": "La paciente era una recién nacida de 0 días de edad, de etnia Han, que nació a las 36 semanas de gestación de una mujer embarazada de 3, para 2, con un peso de 2650 g. Se le practicó una cesárea de urgencia debido a la angustia fetal, con puntuaciones de Apgar de 6 a 1 min y 5 min. Su grupo sanguíneo era O y RhD positivo. Al nacer, presentaba palidez, equimosis dispersas en múltiples áreas del cuerpo, sangrado de las mucosas e insuficiencia respiratoria, con un leve flujo de sangre hemorrágica también observado en los sitios de punción venosa. El análisis de gases en sangre de la arteria umbilical mostró un hematocrito de 0.08 y una hemoglobina de 23 g/L. La paciente requirió intubación endotraqueal y ventilación mecánica. Después de la transfusión de una suspensión de glóbulos rojos, los recuentos sanguíneos iniciales revelaron una trombocitopenia severa (recuento de plaquetas de 12 × 109/L), anemia (hemoglobina de 46 g/L) y leucopenia (recuento de leucocitos de 1.11 × 109/L).\n\nLa paciente fue ingresada en la unidad de cuidados intensivos neonatales a las 3 horas de vida para recibir tratamiento adicional. Durante la hospitalización, se le diagnosticó coagulación intravascular diseminada (CID), con tiempo de tromboplastina parcial activada (TTPA) de 73,10 segundos, tiempo de protrombina (TP) de 25,4 segundos, fibrinógeno (FIB) de 1,01 g/L, razón internacional normalizada (INR) de 2,26 y dímero D > 20 mg/L. Se le administró ventilación mecánica, corrección de la acidosis y transfusión de plasma fresco congelado. A pesar de múltiples transfusiones de glóbulos rojos y plaquetas, los niveles de hemoglobina y plaquetas permanecieron por debajo de lo normal (hemoglobina 106 g/L y plaquetas 11 × 109/L el día 3). También recibió tratamiento antiinfeccioso, cardiotónico, vasopresor y otro tratamiento sintomático. Un frotis periférico mostró áreas de tinción pálida agrandadas de glóbulos rojos, con una proporción de reticulocitos del 1,5% y un resultado negativo en la prueba directa de Coombs. No se realizó aspiración de médula ósea debido a su grave estado. No hubo evidencia clínica o de laboratorio de sepsis neonatal, y las pruebas para toxoplasma, rubéola, citomegalovirus y virus del herpes simple (TORCH); virus de hepatitis; y Treponema pallidum fueron negativas. El examen físico de admisión reveló un estado mental deficiente, disminución del tono muscular en las extremidades y reflejo pupilar lento a la luz. Todos los demás hallazgos fueron normales. El ultrasonido craneal y electroencefalograma de cabecera revelaron hemorragia intracraneal grave y bajo voltaje, respectivamente. Los hallazgos del ecocardiograma sugirieron un conducto arterioso patente, foramen oval permeable e hipertensión pulmonar. El ultrasonido abdominal indicó hemorragia gastrointestinal. A pesar de todos los esfuerzos, la paciente falleció el tercer día de vida debido a falla multiorgánica y hemorragia intracraneal masiva (la información detallada se puede encontrar en el Informe Suplementario).\n\nLos padres de la paciente no eran consanguíneos y ambos tenían talasemia. La madre, que compartía el mismo tipo de sangre que la paciente, tuvo una anemia leve durante el embarazo (nivel de hemoglobina de 97 g/L) y un historial de aborto inducido. Los exámenes prenatales no mostraron anomalías, ni tampoco hidrops fetal, y no recibió ninguna medicación durante el embarazo que pudiera provocar una enfermedad hemorrágica de inicio temprano en el recién nacido. La paciente también tenía un hermano de 1 año que gozaba de buena salud. Su abuelo tenía un historial de anemia leve (detalles desconocidos).\n\nSe obtuvo el consentimiento informado de los padres del paciente y se realizó un secuenciamiento de Sanger para descubrir la causa de la enfermedad. Se detectó una nueva mutación de MECOM de desplazamiento de marco heterocigótica [NM_001105078: c.157_158del (p.Met53Glyfs*2)] en el probando. Esta variante cambió el aminoácido 53 de metionina (codón ATG) a glicina (codón GGT), seguido de una terminación temprana. La mutación no se encontró en los padres o en el hermano mayor. La variante se clasificó como patogénica según las directrices del Colegio Americano de Genética Médica (ACMG) [14]. El algoritmo “AutoPVS1” brindó un fuerte apoyo para la interpretación de PVS1 de p.Met53Glyfs*2, lo que indica patogenicidad. La variante no se ha informado previamente en la Base de Datos de Mutación Genética Humana (HGMD) o en Clinvar. El análisis de conservación mostró que el residuo Met53 está altamente conservado en todas las especies de mamíferos (incluidos humanos, ratones, ratas, chimpancés y bovinos) utilizando Clustal Omega. Se generaron modelos de estructura de proteínas tridimensionales de las proteínas MECOM de tipo salvaje y mutantes utilizando SWISS-MODEL, lo que indica que la mutación de desplazamiento de marco causó una terminación temprana de la síntesis de aminoácidos, alterando significativamente la estructura de la proteína.\n",
+    "gold_summary": "Reportamos el caso de una neonata Han china de 0 días de vida que presentó trombocitopenia grave y hemorragia intracraneal, y que finalmente falleció por fallo multiorgánico e intracraneal el tercer día después del nacimiento. La secuenciación genética identificó una variante de cambio de marco heterocigótica, c.157_158del, dentro del gen MECOM. Esta variante condujo a una sustitución del 53.º aminoácido de metionina a glicina, terminando en el 54.º aminoácido. Una revisión exhaustiva de la literatura indicó que las mutaciones del gen MECOM incluían mutaciones sin sentido (68.3%), deleción (8.5%), sitio de empalme (8.5%), cambio de marco (7.3%) y sin sentido (7.3%). Las pacientes con mutaciones sin sentido frecuentemente presentaban sinostosis radiocubital, mientras que el fallo de la médula ósea se asociaba más comúnmente con los otros cuatro tipos de mutaciones.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Una bebé nació muy pequeñita y se puso muy enferma. Tenía problemas para que su sangre funcionara bien y sangraba en la cabeza. Los doctores buscaron en sus genes y encontraron un cambio que no estaba bien. Ese cambio hizo que su cuerpo no pudiera hacer una parte importante para estar sano. Por eso, la bebé se enfermó mucho y no pudo mejorar.",
+        "scores": {
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+        "text": "**Caso de una recién nacida con un problema genético grave**\n\nPresentamos el caso de una bebé recién nacida de origen Han en China, que tenía un conteo muy bajo de plaquetas en la sangre, llamado trombocitopenia grave. Esto causó que tuviera sangrados dentro de su cabeza (hemorragia intracraneal). Lamentablemente, falleció al tercer día de vida debido a que varios órganos dejaron de funcionar correctamente.\n\n**Qué encontraron en sus genes**\n\nLos médicos analizaron el ADN de la bebé y encontraron un cambio en un gen llamado MECOM. Este cambio es una mutación que afecta cómo se produce una proteína importante. En concreto, la mutación cambió el aminoácido número 53 de metionina a glicina y provocó que la proteína se terminara de fabricar muy rápido, antes de tiempo. Esto afecta la función normal de la proteína.\n\n**Importancia de esta mutación**\n\nAl revisar otros casos en la literatura científica, se sabe que el gen MECOM puede tener diferentes tipos de mutaciones. La mayoría son mutaciones que detienen la producción normal de la proteína (llamadas mutaciones sin sentido), pero también hay otros tipos como deleciones o cambios en el marco de lectura del gen. Cada tipo de mutación puede causar distintos problemas. Por ejemplo, las mutaciones sin sentido suelen relacionarse con un problema en los huesos del brazo (sinostosis radiocubital), mientras que otras mutaciones, como la que tuvo esta bebé, están más asociadas con fallos en la médula ósea, que es donde se producen las células de la sangre.\n\n**Qué significa este caso**\n\nEste caso muestra cómo una mutación nueva en el gen MECOM puede causar una enfermedad muy grave desde el nacimiento. Entender estas mutaciones ayuda a los médicos a diagnosticar y estudiar mejor estas condiciones raras, aunque en este caso no fue posible salvar a la bebé.",
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+      "B3": {
+        "text": "**Contexto del Caso**  \nSe trató de una recién nacida de origen Han, nacida a las 36 semanas de gestación mediante cesárea de urgencia debido a sufrimiento fetal. Al nacer, presentó signos graves como palidez, sangrado en mucosas, equimosis (moretones) dispersos y dificultad respiratoria que requirió ventilación mecánica. Los análisis iniciales mostraron anemia severa, trombocitopenia (bajo recuento de plaquetas) y leucopenia (bajo recuento de glóbulos blancos). Durante su ingreso en la unidad de cuidados intensivos neonatales, se diagnosticó coagulación intravascular diseminada (una alteración grave de la coagulación sanguínea) y hemorragias múltiples, incluyendo una hemorragia intracraneal masiva. A pesar de tratamientos intensivos, la paciente falleció al tercer día de vida por falla multiorgánica y hemorragia cerebral.\n\n**Hallazgos Genéticos**  \nSe realizó un estudio genético mediante secuenciación Sanger para identificar la causa subyacente de su enfermedad. Se detectó una mutación nueva y heterocigótica (presente en una sola copia del gen) en el gen MECOM, específicamente una deleción de dos nucleótidos (c.157_158del) que provocó un cambio en el marco de lectura del gen (mutación de cambio de marco). Esta alteración causó que el aminoácido número 53, metionina, fuera sustituido por glicina, seguida de una terminación prematura en la síntesis proteica, lo que probablemente afecta gravemente la función de la proteína MECOM. Esta mutación no se encontró en los padres ni en el hermano mayor, indicando que fue una mutación de novo (nueva en la paciente). Además, el residuo afectado está altamente conservado en mamíferos, lo que sugiere su importancia funcional.\n\n**Interpretación Clínica y Revisión Bibliográfica**  \nEl gen MECOM está implicado en la regulación del desarrollo de la médula ósea y la formación de células sanguíneas. Mutaciones en este gen se han asociado con síndromes que incluyen fallo medular y anomalías óseas. Una revisión exhaustiva de la literatura mostró que las mutaciones en MECOM pueden ser de varios tipos: mutaciones sin sentido (que generan una proteína truncada), deleciones, alteraciones en sitios de empalme (que afectan el procesamiento del ARN), cambios de marco y otras mutaciones sin sentido. Se observó que las mutaciones sin sentido se relacionan frecuentemente con sinostosis radiocubital (fusión anormal de huesos del antebrazo), mientras que el fallo de la médula ósea es más común en los otros tipos de mutaciones, incluyendo la de cambio de marco que presentó esta paciente.\n\n**Conclusiones y Relevancia**  \nEste caso ilustra la gravedad clínica que puede tener una mutación de novo en el gen MECOM, manifestada por una trombocitopenia severa, hemorragias masivas y fallo multiorgánico en un recién nacido. La identificación precisa de la mutación permitió confirmar el diagnóstico genético y ampliar el conocimiento sobre la diversidad de mutaciones en MECOM y sus manifestaciones clínicas. Este hallazgo es importante para el diagnóstico prenatal y el asesoramiento genético en familias con antecedentes similares.",
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+    "article": "La paciente es una mujer de 74 años de edad, físicamente activa, que practica senderismo y equitación. Un mes después del tratamiento con inyección de cortisona de la tendinopatía insercional de Aquiles, sufrió una rotura total del tendón de Aquiles insercional al intentar dar un paso mientras montaba en bicicleta. Esta rotura se trató de forma conservadora con una bota de Walker durante 8 semanas. Después, mientras montaba a caballo, un intento de dar un paso provocó una nueva rotura total del tendón de Aquiles en la inserción. La rotura se trató quirúrgicamente con reinserción del tendón de Aquiles en el calcáneo, utilizando anclajes de sutura. Esto fue seguido por inmovilización en un yeso. Después de la operación, la paciente sufrió una infección profunda que no respondía a los antibióticos, signos de sepsis, y se indicó exploración quirúrgica. Durante la cirugía, se encontró que todo el tendón de Aquiles estaba gravemente afectado por la infección, más o menos destruido, y hubo que retirar el tendón de Aquiles distal de 7 cm (todo el tendón libre de Aquiles). Esto dejó una gran herida sin tejido tendinoso, y la piel se suturó sobre la herida. Después de este procedimiento, la inmovilización y el tratamiento con antibióticos de cloxacilina curaron la infección y la herida se curó adecuadamente. El pie se inmovilizó en un yeso durante las primeras 10 semanas, desde la máxima flexión plantar inicialmente, y luego la flexión plantar disminuyó gradualmente hasta alcanzar la posición neutra. Esto fue seguido por inmovilización en un yeso dorsal, evitando la extensión del tendón de Aquiles en flexión plantar, durante otros 3 meses. Se le dijo que aumentara gradualmente la carga al caminar, pero que evitara la extensión durante un total de 6 meses. Después de 6 meses se le ofreció reconstrucción quirúrgica con un injerto de flexor hallucis longus, pero como entonces tenía una función satisfactoria, decidió esperar y ver. Su función mejoró gradualmente, y un año después de la operación, cuando buscó ayuda por el dolor en el otro tendón de Aquiles, se notó la buena función en el lado operado. La exploración por ultrasonido mostró sorprendentemente un tendón que se parecía mucho a un tendón de Aquiles ligeramente tendinopático.\n",
+    "gold_summary": "Esta señora de 74 años padecía tendinopatía insercional de Aquiles. Después del tratamiento con una inyección local de cortisona, sufrió una rotura total del tendón de Aquiles insercional. Esta rotura se trató de forma conservadora y, después del tratamiento, el tendón de Aquiles volvió a romperse en la zona de inserción. La rotura se trató entonces con reinserción en la zona de inserción calcánea. Al poco tiempo del postoperatorio, la paciente sufrió una infección de herida quirúrgica profunda y sepsis. Debido al pobre efecto del tratamiento con antibióticos y a la destrucción total del tendón, se extirpó todo el tendón de Aquiles. Después de la extirpación, se inmovilizó en un yeso, seguido de movilización y aumento gradual de la carga. En un seguimiento de un año, la paciente caminaba sin cojera, podía levantar el talón hasta la mitad mientras estaba de pie sobre una pierna, había un tendón de Aquiles palpable y el escaneado por ultrasonido mostró una estructura muy similar a un tendón de Aquiles tendinopático y ligeramente engrosado. Había una regeneración evidente de todo el tendón de Aquiles y la función del tendón era sorprendentemente buena.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Había una señora de 74 años con un problema en el hueso del talón y el hueso del muslo. Se lastimó el hueso del muslo cerca del talón después de una inyección. Primero, usó una bota especial para sanar. Pero se volvió a lastimar el mismo hueso. Entonces, los doctores hicieron una operación para arreglarlo. Después, tuvo una infección que no se quitaba con medicina. Por eso, los doctores tuvieron que quitar todo el hueso del muslo que estaba lastimado. Luego, la señora usó un yeso para que su pie sanara. Poco a poco, pudo mover el pie y caminar sin dolor. Un año después, su hueso del muslo estaba casi como nuevo y ella podía caminar bien y levantar el talón.",
+        "scores": {
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+        "text": "**Lo que le Pasó a la Paciente**  \nUna mujer de 74 años tenía un problema llamado tendinopatía insercional de Aquiles. Esto significa que el tendón de Aquiles, que conecta el músculo de la pantorrilla con el hueso del talón, estaba dañado cerca de donde se une al hueso. Para tratarlo, le pusieron una inyección de cortisona, que es un medicamento para reducir la inflamación. Sin embargo, después de esto, el tendón se rompió completamente en esa zona.\n\n**Tratamientos y Complicaciones**  \nPrimero intentaron curar la rotura sin cirugía, usando una bota especial para inmovilizar el pie. Pero luego, el tendón se rompió otra vez. Esta vez, hicieron una operación para volver a unir el tendón al hueso usando anclajes, que son pequeños dispositivos para sujetar el tendón. Poco después de la cirugía, la paciente tuvo una infección grave en la herida que no mejoró con antibióticos y causó sepsis, una infección que afecta todo el cuerpo.\n\n**Cirugía y Recuperación**  \nDurante otra operación para tratar la infección, los médicos vieron que el tendón estaba muy dañado y tuvieron que quitarlo completamente, dejando una gran herida. La piel se cerró sobre esa zona y la paciente usó un yeso para inmovilizar el pie durante varias semanas. También recibió antibióticos para curar la infección. Luego, poco a poco, empezó a mover el pie y a cargar peso al caminar, pero evitando estirar demasiado el tendón.\n\n**Resultados Después de un Año**  \nUn año después, la paciente podía caminar sin cojear y levantar el talón mientras estaba de pie sobre una pierna, lo que muestra que el tendón funcionaba bien. Un examen con ultrasonido, que es una imagen que muestra los tejidos, mostró que el tendón de Aquiles había crecido de nuevo y parecía casi normal, aunque un poco engrosado y con signos de daño leve. Esto indica que el tendón se regeneró sorprendentemente bien y que la función del pie mejoró mucho, a pesar de que el tendón original fue removido.",
+        "scores": {
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+      "B3": {
+        "text": "**Contexto**  \nLa paciente es una mujer de 74 años, físicamente activa, que desarrolló una tendinopatía insercional del tendón de Aquiles (una lesión en la zona donde el tendón se une al hueso del talón). Tras recibir una inyección local de cortisona para tratar esta lesión, sufrió una rotura completa del tendón en la zona de inserción. Inicialmente, esta rotura se manejó con tratamiento conservador, pero posteriormente el tendón volvió a romperse en el mismo lugar. Esta segunda rotura se trató mediante cirugía para reinsertar el tendón en el hueso del talón.\n\n**Hallazgos Clave**  \nPoco después de la cirugía, la paciente desarrolló una infección profunda en la herida quirúrgica que evolucionó a sepsis (una infección grave que afecta a todo el organismo). Debido a que los antibióticos no controlaron la infección y el tendón estaba gravemente dañado, fue necesario extirpar completamente el tendón de Aquiles distal (aproximadamente 7 cm). Tras la extirpación, la herida se cerró y la paciente fue inmovilizada con yesos durante varios meses, con un protocolo gradual para permitir la recuperación y evitar movimientos que pudieran dañar la zona.\n\n**Interpretación Clínica**  \nA pesar de la pérdida total del tendón de Aquiles, la paciente mostró una recuperación funcional sorprendentemente buena. Un año después, caminaba sin cojera, podía levantar el talón mientras se apoyaba sobre una pierna y se palpaba un tendón en la zona afectada. El ultrasonido reveló que el tendón había regenerado una estructura similar a un tendón de Aquiles, aunque con signos leves de tendinopatía (engrosamiento y alteraciones en la textura). Esto indica que, incluso tras la extirpación completa del tendón, el organismo fue capaz de formar un nuevo tejido tendinoso funcional.\n\n**Próximos Pasos**  \nSe ofreció a la paciente la opción de una reconstrucción quirúrgica con un injerto de otro tendón (flexor hallucis longus) para mejorar aún más la función, pero ella decidió esperar debido a la buena recuperación que presentaba. Se recomienda continuar con seguimiento clínico y funcional para monitorizar la evolución, especialmente considerando que la regeneración espontánea del tendón de Aquiles es poco común y puede ofrecer información valiosa para futuros tratamientos.",
+        "scores": {
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+  {
+    "article": "Una mujer de 47 años con antecedentes de CHB congénita se presentó con quejas de dolor en el cuello del lado izquierdo y dolor en el oído izquierdo. Aproximadamente 30 meses antes de la presentación, la paciente había notado una pequeña masa en el lado izquierdo de su cuello, que había aumentado gradualmente de tamaño. El dolor se localizó inicialmente en la región del cuello, pero se intensificó con el tiempo y se extendió al área del oído izquierdo.\nInicialmente, debido al dolor en el oído izquierdo, el paciente consultó a varios otorrinolaringólogos y fue tratado por un diagnóstico preliminar de otitis media. Sin embargo, a pesar de los tratamientos, el dolor persistió. Finalmente, un otorrinolaringólogo derivó al paciente para una ecografía, que reveló una masa en el lado izquierdo del cuello, lo que llevó a una derivación quirúrgica. Después de las evaluaciones iniciales, se solicitó una angiografía por TC, que reveló una masa de forma ovalada que medía 30 por 50 mm en la bifurcación de la arteria carótida izquierda, lo que sugiere un CBT tipo II de Shamblin.\n\nEvaluaciones cardiovasculares preoperatorias\nDada la historia del paciente de CHB congénita, se realizó una evaluación cardiovascular preoperatoria exhaustiva. Esto incluyó un electrocardiograma (ECG) de 12 derivaciones, que confirmó la presencia de CHB con un ritmo de escape ventricular estable. Se realizó una ecocardiografía transtorácica para evaluar la estructura y función cardiaca, revelando una función sistólica ventricular normal sin evidencia de anormalidades estructurales. Además, se obtuvo una consulta de cardiología para evaluar la aptitud del paciente para la cirugía y optimizar el manejo perioperatorio.\n\nConsideraciones anestésicas\nDebido a la CHB congénita del paciente y al potencial de inestabilidad hemodinámica durante la cirugía, se formuló un plan anestésico detallado. El paciente fue clasificado como estado físico III de la Sociedad Estadounidense de Anestesiología (ASA). Preoperativamente, se le colocó un marcapasos externo temporal para garantizar un control adecuado de la frecuencia cardíaca y se le insertó un catéter arterial para el monitoreo continuo de la presión arterial. La inducción de la anestesia se realizó utilizando una combinación de etomidato (0,3 mg/kg) y fentanilo (2 μg/kg) para minimizar las fluctuaciones hemodinámicas. El mantenimiento se logró con sevoflurano (1-2 %) y rocuronio (0,6 mg/kg) para la relajación muscular. Los parámetros hemodinámicos, incluida la frecuencia cardíaca, la presión arterial y la saturación de oxígeno, se controlaron de forma continua. Además, se le colocó un catéter venoso central para monitorear la presión venosa central y administrar medicamentos vasoactivos si fuera necesario. El equipo de anestesia mantuvo una comunicación estrecha con el equipo quirúrgico para abordar de forma inmediata cualquier cambio hemodinámico intraoperatorio.\n\nEnfoque quirúrgico\nEl paciente fue sometido a cirugía el 19 de mayo de 2024, después de la localización precisa de la TCC mediante angiografía por TC. El enfoque quirúrgico se eligió en base a la clasificación de Shamblin tipo II, que indica un encasamiento parcial de las arterias carótidas. Dada la proximidad del tumor a estructuras neurovasculares críticas, incluidos los nervios vago e hipogloso, se consideró que el enfoque quirúrgico abierto era el más apropiado para garantizar una resección completa y minimizar las complicaciones.\nTras la inducción de la anestesia general, se colocó al paciente en posición supina con el cuello extendido y rotado hacia la derecha. Se realizó una incisión oblicua paralela al músculo esternocleidomastoideo izquierdo, que se extendía desde la apófisis mastoidea hasta la escotadura esternal. Tras la incisión de la piel y la disección del platisma, se expuso con cuidado la vaina carotídea. Se identificaron la arteria carótida común y su bifurcación en las arterias carótidas internas y externas. Se observó el tumor, de 30 × 50 mm, en la bifurcación carotídea y se diseccionó con cuidado de los tejidos circundantes.\n\nManobras y precauciones específicas\n1.\nSe aplicaron pinzas vasculares temporales en las arterias carótidas internas y externas para controlar el flujo sanguíneo durante la disección del tumor. Esto minimizó el sangrado y proporcionó un campo quirúrgico despejado.\n2.\nSe utilizó neuromonitorización intraoperativa para evaluar la integridad de los nervios vago e hipogloso. La retroalimentación continua garantizó que las estructuras neurales se preservaran durante la disección.\n3.\nEl tumor se separó cuidadosamente de las arterias carótidas y las estructuras neurales circundantes, mediante una combinación de disección aguda y roma. Se logró la hemostasis mediante cauterización bipolar y pinzas quirúrgicas para minimizar el sangrado.\n4.\nEl marcapasos externo se monitoreó activamente durante todo el procedimiento para garantizar un ritmo cardíaco estable. El equipo de anestesia estaba preparado para administrar atropina o epinefrina si se producía una bradicardia o hipotensión significativas.\n2.5. Manejo postoperatorio\nTras asegurarse de que no había hemorragia activa y restablecer el flujo sanguíneo, se devolvieron los tejidos a su posición original y se cerró la herida en múltiples capas. Se aplicó un vendaje apropiado. La cirugía se completó sin complicaciones y con un sangrado mínimo en 2 h y 10 min. El paciente fue trasladado a la UCI vascular para una estrecha monitorización.\nDespués de la operación, se controló al paciente en la UCI durante 24 horas y, más tarde, se le trasladó a la planta general tras mejorar su estado clínico. El marcapasos externo se retiró el día 1 después de la operación, ya que el paciente mantenía un ritmo de escape ventricular estable. El paciente fue dado de alta en buenas condiciones generales el día 3 después de la operación, sin quejas específicas.\n2.6. Seguimiento y resultados a largo plazo\nEl examen histopatológico confirmó el diagnóstico definitivo de TCC en la paciente. Se realizaron evaluaciones de seguimiento a las 2 semanas, 1 mes, 6 meses y 1 año posteriores a la cirugía para evaluar los resultados quirúrgicos y cardíacos. En cada visita, la paciente se sometió a un ECG de 12 derivaciones para monitorear el CHB congénito, que permaneció sin cambios durante todo el período de seguimiento. Se repitió la ecocardiografía transtorácica a los 6 meses y un año, sin deterioro de la función cardíaca y con una función sistólica ventricular estable.\n\nPara evaluar el impacto de la extirpación del tumor en la función cardiaca, se realizó un análisis de la variabilidad de la frecuencia cardiaca (VFC) antes de la operación y a los 6 meses después de la misma. El análisis de la VFC antes de la operación demostró una reducción de la actividad parasimpática, probablemente debido a la compresión del nervio vago por el tumor. El análisis de la VFC después de la operación mostró una mejora significativa del tono parasimpático, lo que sugiere que la extirpación del tumor alivió la compresión del nervio vago y restauró la función autónoma normal.\nAsimismo, el paciente manifestó que el dolor en el cuello y en el oído había desaparecido por completo después de la cirugía, sin que se produjera una reaparición de los síntomas durante el período de seguimiento. Se realizaron estudios de imagen, que incluyeron ultrasonido Doppler y angiografía por TAC, a los 6 meses y al año, que no mostraron evidencia de reaparición del tumor o complicaciones vasculares.\n",
+    "gold_summary": "Describimos el caso de una mujer de 47 años con antecedentes de dolor en el cuello izquierdo y en el oído, acompañado por una masa en el cuello que había ido aumentando gradualmente durante 2,5 años. Después de las evaluaciones iniciales y de múltiples diagnósticos diferenciales, la angiografía por TC reveló una masa ovalada de 30 × 50 mm en la bifurcación carotídea izquierda, lo que confirmó un CCT tipo II de Shamblin. Las evaluaciones preoperatorias demostraron CHB congénita en el electrocardiograma y la ecocardiografía. La paciente se sometió a una resección completa del tumor con todas las precauciones necesarias, incluida la colocación temporal de un marcapasos y un cuidadoso seguimiento.\n",
+    "synthetic_summary_eval": {
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+        "text": "Había una señora con dolor en su cuello y oído. Tenía una bolita en el cuello que creció poco a poco. Los doctores hicieron muchas pruebas y vieron la bolita en su cuello con una máquina especial. La bolita estaba cerca de unos tubos importantes del cuello. \n\nAntes de la operación, los doctores revisaron su corazón y vieron que tenía un problema que nació con ella. Para la operación, usaron un aparato para ayudar a su corazón a latir bien. Los doctores sacaron la bolita con mucho cuidado. Después, la señora se sintió mejor y no le dolió más.",
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+        "text": "**Lo que le pasó a la paciente**  \nUna mujer de 47 años tenía dolor en el lado izquierdo del cuello y en el oído izquierdo. También notó una bolita (masa) en el cuello que fue creciendo poco a poco durante más de dos años. Al principio, pensaron que tenía una infección en el oído, pero el dolor no mejoró con el tratamiento.\n\n**Lo que encontraron los médicos**  \nDespués de hacer varios estudios, usaron una tomografía computarizada (una especie de radiografía especial) para ver mejor el cuello. Descubrieron una masa ovalada de 3 por 5 centímetros en un lugar donde una arteria importante del cuello se divide. Esto confirmó que tenía un tumor llamado paraganglioma carotídeo, que es un tumor raro que crece cerca de las arterias del cuello.\n\nAdemás, al revisar su corazón, encontraron que tenía un bloqueo cardíaco congénito, que significa que su corazón late más lento de lo normal desde que nació. Por eso, antes de la cirugía, hicieron varios exámenes para asegurarse de que su corazón estaba estable.\n\n**Cómo la operaron y qué cuidados tuvieron**  \nPara quitar el tumor, los médicos planearon la cirugía con mucho cuidado. Le pusieron un marcapasos temporal, que es un dispositivo que ayuda a controlar el ritmo del corazón durante la operación. También usaron anestesia especial para que no tuviera problemas con la presión o el ritmo cardíaco.\n\nDurante la cirugía, hicieron una incisión en el cuello para llegar al tumor. Usaron pinzas para controlar el sangrado y monitorearon los nervios importantes para evitar dañarlos. El tumor fue separado cuidadosamente de las arterias y nervios cercanos. La operación duró poco más de dos horas y no hubo complicaciones graves.\n\n**Después de la cirugía y resultados**  \nLa paciente estuvo en cuidados intensivos un día para vigilar su estado. El marcapasos temporal se retiró al día siguiente porque su corazón mantenía un ritmo estable. Fue dada de alta tres días después, sin dolor ni problemas.\n\nEn los controles posteriores, los médicos vieron que el tumor no había vuelto a aparecer y que su corazón seguía funcionando bien. Además, el análisis mostró que la función de un nervio llamado nervio vago mejoró después de quitar el tumor, lo que ayudó a que su sistema nervioso autónomo trabajara mejor. La paciente también dijo que el dolor en el cuello y oído desapareció completamente.\n\n**Qué significa este caso**  \nEste caso muestra la importancia de hacer un diagnóstico correcto cuando hay dolor persistente y masas en el cuello. También destaca cómo los médicos deben planear cuidadosamente la cirugía en pacientes con problemas cardíacos para evitar riesgos. La operación fue exitosa y mejoró la calidad de vida de la paciente.",
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+      },
+      "B3": {
+        "text": "**Contexto del Caso**  \nSe presenta el caso de una mujer de 47 años que experimentaba dolor en el lado izquierdo del cuello y en el oído izquierdo, acompañado por la presencia de una masa en el mismo lado del cuello. Esta masa había sido detectada aproximadamente 30 meses antes y había ido aumentando de tamaño de forma progresiva. Inicialmente, el dolor se atribuyó a una infección del oído medio (otitis media), pero ante la persistencia de los síntomas, se realizaron estudios de imagen que identificaron una masa en la bifurcación de la arteria carótida izquierda.\n\n**Hallazgos Clave**  \nLa angiografía por tomografía computarizada (TC) mostró una masa ovalada de 30 × 50 mm ubicada en la bifurcación carotídea izquierda, característica de un tumor del cuerpo carotídeo (TCC) clasificado como tipo II según Shamblin, lo que indica un compromiso parcial de las arterias carótidas. Además, las evaluaciones cardiovasculares preoperatorias confirmaron que la paciente tenía un bloqueo auriculoventricular completo congénito (CHB), detectado mediante electrocardiograma (ECG) y corroborado por ecocardiografía, que mostró función ventricular normal sin anomalías estructurales.\n\n**Interpretación Clínica y Manejo**  \nDado el diagnóstico de TCC y la condición cardíaca de la paciente, se diseñó un plan quirúrgico y anestésico cuidadoso para minimizar riesgos. Se colocó un marcapasos temporal externo para mantener un ritmo cardíaco estable durante la cirugía y se monitorizó de forma continua la presión arterial y otros parámetros vitales. La cirugía se realizó mediante un abordaje abierto, con una incisión paralela al músculo esternocleidomastoideo para exponer la bifurcación carotídea y permitir la disección cuidadosa del tumor, preservando nervios importantes como el vago e hipogloso mediante neuromonitorización intraoperatoria.\n\nDurante la intervención, se aplicaron pinzas vasculares para controlar el flujo sanguíneo y evitar hemorragias, y se mantuvo una comunicación estrecha entre los equipos quirúrgico y anestésico para manejar cualquier cambio hemodinámico. La cirugía se completó exitosamente en poco más de dos horas, con sangrado mínimo y sin complicaciones inmediatas.\n\n**Próximos Pasos y Resultados a Largo Plazo**  \nDespués de la operación, la paciente fue vigilada en la unidad de cuidados intensivos y luego trasladada a planta general. El marcapasos temporal se retiró al día siguiente, ya que el ritmo cardíaco se mantuvo estable. La paciente fue dada de alta en buenas condiciones al tercer día postoperatorio, sin dolor ni otros síntomas. El examen histopatológico confirmó el diagnóstico de tumor del cuerpo carotídeo.\n\nEn el seguimiento a corto y largo plazo, que incluyó evaluaciones clínicas, electrocardiogramas y ecocardiografías, se observó que la función cardíaca permaneció estable y que el bloqueo cardíaco congénito no empeoró. Además, un análisis de la variabilidad de la frecuencia cardíaca mostró una mejora significativa en la actividad parasimpática después de la cirugía, lo que sugiere que la extirpación del tumor alivió la compresión del nervio vago y restauró la función autónoma normal. Los estudios de imagen realizados a los 6 meses y un año no evidenciaron recurrencia tumoral ni complicaciones vasculares. La paciente reportó la desaparición completa del dolor en cuello y oído, sin reaparición de síntomas durante el seguimiento.\n\nEn resumen, este caso ilustra la importancia de un diagnóstico preciso y un manejo multidisciplinario cuidadoso en pacientes con tumores carotídeos y condiciones cardíacas preexistentes, logrando una resección segura y resultados clínicos favorables a largo plazo.",
+        "scores": {
+          "ROUGE-1": 0.2830440587449934,
+          "ROUGE-2": 0.15796519410977242,
+          "ROUGE-L-Sum": 0.253671562082777,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      }
+    }
+  },
+  {
+    "article": "Una mujer de 19 años de edad acudió al servicio de urgencias de nuestro hospital con una queja principal de dos días de historia de cefalea, acompañada de náuseas recurrentes, vómitos y fiebre de un día. En el ingreso, su examen físico reveló una fiebre alta de 39.1°C, presión arterial elevada de 189/120 mmHg y una frecuencia cardíaca de 148 latidos por minuto. Los resultados de laboratorio indicaron un recuento de glóbulos blancos elevado de 14.77×10^9/L y un recuento de neutrófilos de 13.55×10^9/L, lo que sugiere una posible infección o respuesta inflamatoria. Se administró un tratamiento empírico inicial con antibióticos debido a la sospecha de infección, pero sus síntomas persistieron. Dados sus signos vitales anormales, marcadores inflamatorios elevados y falta de mejora de los síntomas, la paciente fue admitida para una evaluación diagnóstica adicional y transferida a la unidad de cuidados intensivos para una estrecha monitorización. Un año antes, la paciente había presentado síntomas similares y se le diagnosticó miocarditis en un hospital local en base a los hallazgos clínicos en ese momento. Durante esa hospitalización, también se le diagnosticó hipertensión y se le prescribieron medicamentos antihipertensivos. Sin embargo, después del alta, la paciente no se adhirió al tratamiento antihipertensivo prescrito y no controló regularmente su presión arterial. Además, es notable que su padre tenía antecedentes de muerte súbita inexplicable.\n\nPara investigar la etiología subyacente de los síntomas del paciente, se realizó una tomografía computarizada (TC) de tórax. De forma incidental, esta exploración reveló una masa suprarrenal izquierda con densidad de tejido blando, que medía 43 mm × 36 mm. No se observaron hallazgos patológicos en las exploraciones de TC de cabeza y tórax. El electrocardiograma demostró taquicardia sinusal con un intervalo PR acortado y ondas P altas y puntiagudas en las derivaciones II, III y aVF. La ecocardiografía transtorácica no reveló ninguna anomalía significativa.\n\nEn el segundo día de ingreso, el paciente mostró niveles crecientes de péptido natriurético cerebral (BNP) y troponina I (TnI). El cardiólogo diagnosticó provisionalmente al paciente con miocarditis de etiología incierta, basándose en la presentación clínica, los biomarcadores cardiacos elevados (BNP y TnI) y los hallazgos del electrocardiograma de apoyo. Se inició el tratamiento con metilprednisolona (0,25 g diarios) para abordar la posible inflamación miocárdica debida a la sospecha de miocarditis. Se administraron furosemida (20 mg cada 12 horas) y espironolactona (20 mg cada 12 horas) como diuréticos para controlar la retención de líquidos y reducir la carga de trabajo cardiaco. Se prescribió perindopril amlodipina (10 mg: 5 mg diarios) como inhibidor de la enzima convertidora de la angiotensina y bloqueador del canal del calcio para controlar la presión arterial y reducir la poscarga. Se usó tartrato de metoprolol (25 mg cada 12 horas) para controlar la frecuencia cardiaca y disminuir la demanda de oxígeno miocárdico, mientras que se administró esmolol (0,2 g/hora por infusión intravenosa), un bloqueador beta de acción corta, para controlar la frecuencia cardiaca aguda adicional debido a la taquicardia sinusal. Debido a la preocupación por una posible infección, se agregó moxifloxacina como terapia antibiótica empírica.\n\nDada la presentación del paciente con una masa suprarrenal e hipertensión, el endocrinólogo recomendó una evaluación de la relación aldosterona/renina, cortisol plasmático, catecolaminas plasmáticas y catecolaminas urinarias de 24 horas, junto con sus metabolitos. En posición supina, los niveles de catecolaminas plasmáticas y urinarias estaban marcadamente elevados (Tabla 1), incluyendo dopamina plasmática a 524,5 pmol/L, norepinefrina a 83975 pmol/L y epinefrina a 10579,3 pmol/L. Además, los niveles urinarios de 24 horas mostraron adrenalina libre a 4368,89 nmol/24 horas, norepinefrina libre superior a 12697,60 nmol/24 horas, normetaneprina a 8312 nmol/24 horas, metaneprinas a 4078 nmol/24 horas y ácido vanilmandélico a 58,1 mg/24 horas. Estos hallazgos apoyaron un diagnóstico clínico de feocromocitoma. En el quinto día posterior al ingreso, se interrumpió la terapia glucocorticoide y se sustituyó perindopril amlodipina con terazosin para un control más dirigido de la presión arterial.\n\nUna tomografía computarizada abdominal mejorada confirmó una masa suprarrenal izquierda, muy sugestiva de feocromocitoma. Además, después de obtener el consentimiento informado, se realizó una secuenciación del exoma completo, que reveló una mutación sin sentido heterocigótica, c.1900T > C: p. Cys634Arg, en el gen RET, que conduce a una sustitución de cisteína por arginina en el codón 634. Esta mutación levantó sospechas de un síndrome de neoplasia endocrina múltiple, lo que impulsó una evaluación adicional de las glándulas tiroides y paratiroides. La ecografía Doppler en color de la tiroides identificó una masa hipoecoica que medía 6 mm × 4 mm en el lóbulo tiroideo izquierdo, y se observó una leve elevación en los niveles de calcitonina. No se detectaron anormalidades significativas adicionales.\n\nA medida que la condición del paciente mejoró gradualmente, los niveles de cortisol en plasma y ACTH volvieron a la normalidad. El paciente fue dado de alta con una prescripción de tartrato de metoprolol (100 mg cada 12 horas) e hidrocloruro de ivabradina (5 mg cada 12 horas) para el tratamiento en el hogar. Tres meses después, después de lograr un estado clínico estable, el paciente se sometió a una resección del tumor suprarrenal izquierdo, que medía 50 mm × 40 mm × 30 mm. El análisis inmunohistoquímico confirmó una tinción positiva para Vim, CD56, Syn, CgA y NSE, con S-100 positivo en las células de Sertoli, mientras que CKpan, CD10, MART-1/Melan-A y Melan-A fueron negativos. El índice Ki67 fue del 1 %, lo que llevó a un diagnóstico definitivo de feocromocitoma suprarrenal. El paciente fue dado de alta sin más medicamentos y desde entonces se le ha dado seguimiento regular postoperatorio sin recurrencia de síntomas. Durante un seguimiento postoperatorio de 15 meses, el paciente exhibió hipercalcinotemia persistente leve con un tamaño de nódulo tiroideo estable, mientras que los niveles de PTH y calcio en suero mostraron un aumento progresivo (Tabla 2). Se realizó una gammagrafía paratiroidea adicional utilizando 99mTc-MIBI, y la conclusión fue un resultado negativo para el adenoma paratiroideo.\n",
+    "gold_summary": "Reportamos el caso de una mujer de 19 años que presentó feocromocitoma sin experimentar una crisis, a pesar de tener una masa suprarrenal significativa y someterse a un tratamiento glucocorticoide de alta dosis. Las pruebas genéticas revelaron una mutación de sentido erróneo heterocigótica en el gen RET (c.1900T > C: p. Cys634Arg), asociada con MEN2A. La evaluación endocrina adicional identificó un nódulo tiroideo con niveles de calcitonina levemente elevados, pero niveles normales de electrolitos y hormona paratiroidea. Durante un seguimiento postoperatorio de 15 meses, la paciente exhibió hipercalcitonemia persistente leve con tamaño de nódulo tiroideo estable, mientras que la PTH y los niveles de calcio sérico mostraron un aumento progresivo. Se realizó una gammagrafía paratiroidea adicional utilizando 99mTc-MIBI, que arrojó un resultado negativo para el adenoma paratiroideo.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Había una chica de 19 años que tenía un bulto en una parte de su cuerpo llamada glándula suprarrenal. Este bulto no le causó un problema muy grande de repente. Los doctores le hicieron un examen especial y encontraron un cambio en sus genes. Este cambio puede causar problemas en algunas partes del cuerpo que hacen hormonas.\n\nTambién encontraron un pequeño bulto en su cuello, en una parte llamada tiroides. Ella tenía un poco más de una sustancia llamada calcitonina, pero otras cosas en su cuerpo estaban normales. Después de que le sacaron el bulto del cuerpo, los doctores la cuidaron por mucho tiempo. Vieron que la calcitonina seguía un poco alta y que otras cosas en su sangre subían poco a poco. Hicieron otro examen para buscar otro bulto, pero no encontraron nada malo. Los doctores siguen cuidándola para que esté bien.",
+        "scores": {
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
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+      "B2": {
+        "text": "**Caso de una joven con tumor suprarrenal y mutación genética**\n\nUna mujer de 19 años llegó al hospital con dolor de cabeza, náuseas, vómitos y fiebre. Tenía la presión arterial muy alta y signos de inflamación en su cuerpo. Los médicos encontraron una masa (un bulto) en su glándula suprarrenal izquierda, que está encima del riñón y produce hormonas importantes. Esta masa causaba que su cuerpo liberara muchas sustancias llamadas catecolaminas, que pueden subir mucho la presión arterial.\n\nSe hizo un análisis genético y descubrieron que tenía un cambio en un gen llamado RET. Este cambio puede causar un síndrome llamado MEN2A, que hace que se formen tumores en varias glándulas del cuerpo. Por eso, también revisaron su tiroides y encontraron un pequeño nódulo (una bolita) con niveles un poco altos de calcitonina, una hormona relacionada con la tiroides.\n\nDespués de tratarla con medicamentos para controlar su presión y frecuencia cardíaca, la paciente se sometió a una cirugía para quitar la masa suprarrenal. El examen del tumor confirmó que era un feocromocitoma, un tipo de tumor que produce muchas hormonas. Tras la operación, la paciente mejoró y no tuvo más síntomas.\n\nDurante los siguientes 15 meses, los médicos siguieron revisando su tiroides y sus niveles de calcio en sangre. Aunque el nódulo en la tiroides no creció, los niveles de calcitonina y calcio en sangre aumentaron un poco, lo que puede indicar cambios en las glándulas paratiroides, que ayudan a controlar el calcio en el cuerpo. Sin embargo, una prueba especial llamada gammagrafía no mostró tumores en esas glándulas.\n\n**¿Qué significa esto?**\n\nEste caso muestra cómo un tumor en la glándula suprarrenal puede causar problemas graves, pero también cómo una mutación genética puede afectar varias glándulas del cuerpo. Es importante hacer un seguimiento cuidadoso para detectar y tratar cualquier cambio en otras glándulas, como la tiroides o las paratiroides, que pueden estar relacionadas con esta mutación.",
+        "scores": {
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+          "ROUGE-2": 0.10526315789473684,
+          "ROUGE-L-Sum": 0.30241935483870963,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
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+      },
+      "B3": {
+        "text": "**Contexto**  \nPresentamos el caso de una mujer joven de 19 años que acudió al hospital con síntomas de cefalea, náuseas, vómitos y fiebre, acompañados de hipertensión severa y taquicardia. Durante la evaluación, se detectó incidentalmente una masa en la glándula suprarrenal izquierda. Los análisis de sangre y orina mostraron niveles muy elevados de catecolaminas (sustancias químicas producidas por la médula suprarrenal), lo que sugirió la presencia de un feocromocitoma, un tumor poco común que produce estas hormonas y puede causar hipertensión y otros síntomas.\n\n**Hallazgos Clave**  \n- La paciente tenía una masa suprarrenal de aproximadamente 4 cm detectada por tomografía computarizada.  \n- Los niveles plasmáticos y urinarios de catecolaminas y sus metabolitos estaban marcadamente elevados, confirmando la sospecha de feocromocitoma.  \n- Se identificó una mutación genética heterocigótica en el gen RET (c.1900T > C: p. Cys634Arg), conocida por estar asociada con el síndrome de neoplasia endocrina múltiple tipo 2A (MEN2A), una condición que predispone a tumores endocrinos múltiples.  \n- La evaluación adicional mostró un pequeño nódulo en la glándula tiroides con leves elevaciones en los niveles de calcitonina, una hormona que puede indicar la presencia de carcinoma medular de tiroides, común en MEN2A.  \n- Durante el seguimiento postoperatorio de 15 meses, la paciente mantuvo niveles ligeramente elevados de calcitonina y un nódulo tiroideo estable, pero los niveles de hormona paratiroidea (PTH) y calcio en sangre aumentaron progresivamente.  \n- Una gammagrafía paratiroidea con 99mTc-MIBI no mostró evidencia de adenoma paratiroideo (tumor benigno de la glándula paratiroides).\n\n**Interpretación Clínica**  \nEste caso destaca la presentación atípica de un feocromocitoma sin crisis hipertensiva grave, a pesar de la masa suprarrenal significativa y el uso de glucocorticoides de alta dosis, que normalmente podrían desencadenar una crisis. La mutación en el gen RET confirma la asociación con MEN2A, un síndrome que requiere vigilancia cuidadosa por el riesgo de tumores endocrinos múltiples, incluyendo carcinoma medular de tiroides y alteraciones paratiroideas. La persistencia de hipercalcitoninemia y el aumento progresivo de PTH y calcio sugieren la necesidad de un seguimiento continuo para detectar posibles complicaciones o desarrollo de hiperparatiroidismo.\n\n**Próximos Pasos**  \n- Continuar con el seguimiento endocrinológico regular para monitorizar el nódulo tiroideo y los niveles hormonales, especialmente calcitonina, PTH y calcio sérico.  \n- Realizar evaluaciones periódicas para detectar signos tempranos de carcinoma medular de tiroides o hiperparatiroidismo.  \n- Considerar intervenciones quirúrgicas o terapéuticas adicionales si se evidencian cambios significativos en el nódulo tiroideo o en la función paratiroidea.  \n- Mantener un control estricto de la presión arterial y la función cardiaca, dado el antecedente de feocromocitoma y miocarditis.  \n- Brindar asesoramiento genético y seguimiento familiar, dado el componente hereditario asociado a la mutación RET y el antecedente de muerte súbita en el padre.\n\nEste caso subraya la importancia de una evaluación multidisciplinaria y un seguimiento prolongado en pacientes jóvenes con feocromocitoma y mutaciones genéticas relacionadas con síndromes endocrinos múltiples.",
+        "scores": {
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+          "ROUGE-L-Sum": 0.3212121212121213,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
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+  },
+  {
+    "article": "Una refugiada etíope embarazada de 39 años (Gravida 3 Para 2+0) fue derivada a nuestro departamento de urgencias de medicina interna en el Hospital Universitario de Gadarif, Gadarif State, Sudán, con hinchazón generalizada progresiva, falta de aire y fatiga durante 6 semanas y una revisión sistémica sin importancia. La paciente fue admitida en el sitio de admisión de casos críticos y su historia, tomada con la ayuda de un intérprete de idiomas más tarde en la admisión, reveló un episodio remoto inicialmente no revelado de tres convulsiones tónico-clónicas generalizadas no provocadas hace 21 años que se trataron tradicionalmente. Sin embargo, no había antecedentes de traumatismo craneal o antecedentes familiares de convulsiones. El examen general de la paciente reveló un PWS del lado izquierdo que involucraba la división oftálmica del nervio trigémino. Sin embargo, este hallazgo se perdió inicialmente en la inspección pero luego fue confirmado por el cónyuge de la paciente para estar presente desde el nacimiento. La paciente también estaba muy pálida y tenía derrames pleurales bilaterales, hepatomegalia blanda e hinchazón bilateral de las extremidades inferiores.\n\nLas investigaciones iniciales revelaron un nivel de hemoglobina de 8,84 g/dl. Por lo tanto, se diagnosticó insuficiencia cardíaca debido a anemia y se trató a la paciente en consecuencia. Sin embargo, ocho días después de su ingreso, la paciente había desarrollado aproximadamente seis episodios de convulsiones tónico-clónicas focales a bilaterales que respondieron bien a la fenitoína, pero que dejaron a la paciente en un estado comatoso profundo con un GCS de tres. Fue posteriormente admitida en la unidad de cuidados intensivos (UCI) y se le insertó un tubo nasogástrico para ayudarla con su nutrición y administración de fármacos. Además, para evitar más convulsiones, se le inició un tratamiento con comprimidos de carbamazepina de 200 mg administrados a través del tubo nasogástrico.\n\nSe retrasó una tomografía computarizada (TC) sin contraste del cerebro para el día posterior a la estabilización, ya que solo había una máquina de tomografía computarizada en el estado de Gadarif y funcionaba de forma intermitente debido a la falta de un número suficiente de técnicos radiólogos. La tomografía computarizada reveló calcificaciones corticales en la parte posterior del área parietal izquierda, lo que planteó el diagnóstico diferencial de SWS. En consecuencia, se realizó un examen físico de repetición, que mostró la presencia de una lesión plana de color rojo púrpura en la frente y el ojo. Al interrogar al cónyuge, se confirmó la presencia de esta lesión y que no había cambiado desde el nacimiento, lo que nos ayudó a descartar el diagnóstico de una mancha salmón, ya que esta lesión no se desvaneció, por lo que se diagnosticó como PWS. Además, no tenía características de megalencefalia, síndrome de malformación capilar que por lo general incluye un gran tamaño de la cabeza o del cerebro, problemas en las articulaciones y malformaciones capilares en la piel. Tampoco tenía hipertrofia de extremidades, anomalías del drenaje linfático o excrecencias óseas o de tejidos blandos que sugieran el síndrome de Klippel-Trenaunay-Weber. Por lo tanto, en función de los hallazgos de la tomografía computarizada y la presentación típica, llegamos a la conclusión del diagnóstico de SWS.\n\nDos días después de ingresar en la UCI, la paciente experimentó un cambio fluctuante en su estado de conciencia y una nueva aparición de hemiparesia contralateral (contralateral al SPW), así como afasia y labilidad emocional. Desafortunadamente, cuatro días después de ingresar en la UCI, la paciente empezó a experimentar sangrado vaginal; por ello, se consultó al departamento de obstetricia y ginecología y se descubrió que la paciente tenía un embarazo no viable (28 semanas + 1 día) y se realizó una inducción sin incidentes. Durante el mismo período, la paciente se volvió combativa y poco cooperativa, lo que llevó a que se la inmovilizara físicamente. Tres días después, la paciente desarrolló nuevos ataques focales bilaterales que comenzaron como episodios mioclónicos faciales y, tras consultar con el departamento de neurología, se aumentó la dosis de carbamazepina de la paciente a 1000 mg diarios, lo que ayudó a prevenir la recurrencia de los ataques. Cabe mencionar que, en su segundo trimestre y antes de recibir el resultado de la tomografía computarizada, se exploró un diagnóstico de eclampsia, pero sus constantes lecturas de presión arterial con una presión sistólica superior a la normal de 139 la mayoría de los días y una presión diastólica con un máximo de 97 mmHg y un rango bajo de proteinuria, así como la ausencia de características sistémicas como deterioro renal o hepático, excluyeron este diagnóstico. Después de alcanzar el diagnóstico de SW, se puso en juego un enfoque multidisciplinario; por ello, se realizó una consulta oftalmológica para descartar glaucoma. Sin embargo, la paciente estaba muy irritable y era difícil realizar un examen de fondo de ojo. Además, la paciente fue trasladada a la sala de medicina interna tras la estabilización.\n",
+    "gold_summary": "Presentamos el caso de una refugiada de 39 años, no diabética y no hipertensa, que inicialmente presentó insuficiencia cardiaca debido a anemia, por lo que recibió transfusiones de sangre. Más adelante, al ingresar, desarrolló convulsiones múltiples focales bilaterales, irritabilidad severa, afasia y hemiplejía derecha, lo que motivó su ingreso a la UCI. Un examen y un historial médico repetidos revelaron una mancha de vino de Oporto ocular izquierda leve que inicialmente pasó desapercibida y un historial remoto de convulsiones no provocadas 20 años atrás. Las imágenes revelaron calcificaciones parietales y confirmaron el diagnóstico de SWS. Por lo tanto, se adoptó un enfoque multidisciplinario para comprender plenamente el diagnóstico de la paciente y determinar una estrategia de tratamiento, que incluyó consultas con los departamentos de neurología, oftalmología, otorrinolaringología y fisioterapia. Se logró un control exitoso de las convulsiones mediante la administración de fenitoína IV durante 3 días y el aumento gradual de la carbamazepina oral a 1 g diario a través de una sonda nasogástrica. Lamentablemente, debido a la falta de personal o recursos, no se pudieron realizar otras evaluaciones importantes para pacientes con SWS, como evaluaciones avanzadas de neuroimagen, psiquiátricas, de cirugía plástica y neurocirugía, así como revisiones dentales.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Había una señora que estaba muy cansada y con el cuerpo hinchado. Ella tenía una manchita roja en la cara desde que nació. También tuvo muchos ataques donde se movía sin querer. Los doctores vieron que tenía un problema en el cerebro y en la cara. Le dieron medicinas para que los ataques pararan. Muchos doctores la ayudaron para que se sintiera mejor. A veces, no pudieron hacer todas las pruebas porque faltaban cosas en el hospital. Pero todos cuidaron mucho de ella para que estuviera tranquila.",
+        "scores": {
+          "ROUGE-1": 0.20952380952380953,
+          "ROUGE-2": 0.0,
+          "ROUGE-L-Sum": 0.19682539682539682,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
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+      "B2": {
+        "text": "**Caso de una mujer con Síndrome de Sturge-Weber (SWS)**\n\nPresentamos la historia de una mujer de 39 años que llegó al hospital con problemas de salud graves. Al principio, tenía insuficiencia cardíaca causada por anemia, que es cuando hay pocas células rojas en la sangre. Por eso, le dieron transfusiones de sangre para mejorar su condición.\n\nDespués, comenzó a tener varias convulsiones, que son movimientos involuntarios del cuerpo causados por actividad anormal en el cerebro. También mostró irritabilidad, dificultad para hablar (afasia) y debilidad en el lado derecho del cuerpo (hemiplejía). Debido a esto, fue ingresada en la unidad de cuidados intensivos (UCI) para recibir atención especial.\n\nAl revisar su historia médica y hacer un examen más detallado, los médicos notaron una mancha roja en el ojo izquierdo llamada mancha de vino de Oporto. Esta mancha estaba presente desde su nacimiento, pero no se había detectado antes. Además, la paciente había tenido convulsiones hace 20 años, aunque no se había tratado formalmente.\n\nUna tomografía computarizada (una imagen del cerebro) mostró calcificaciones en una parte del cerebro llamada área parietal. Estos hallazgos ayudaron a confirmar que la paciente tenía Síndrome de Sturge-Weber (SWS), una enfermedad rara que afecta la piel, el cerebro y a veces los ojos.\n\nPara tratarla, un equipo de diferentes especialistas trabajó junto: neurólogos (que cuidan del cerebro), oftalmólogos (que cuidan los ojos), otorrinolaringólogos (que cuidan oídos y garganta) y fisioterapeutas (que ayudan con la movilidad). Las convulsiones se controlaron con medicamentos llamados fenitoína y carbamazepina, administrados por vía intravenosa y a través de un tubo en la nariz.\n\nSin embargo, debido a la falta de personal y recursos en el hospital, no se pudieron hacer otros estudios importantes para pacientes con SWS, como imágenes más detalladas del cerebro, evaluaciones psicológicas, consultas para cirugía plástica o neurocirugía, ni revisiones dentales.\n\nEste caso muestra la importancia de un diagnóstico cuidadoso y un tratamiento multidisciplinario para manejar enfermedades complejas como el Síndrome de Sturge-Weber.",
+        "scores": {
+          "ROUGE-1": 0.4752136752136752,
+          "ROUGE-2": 0.1646655231560892,
+          "ROUGE-L-Sum": 0.4512820512820513,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B3": {
+        "text": "**Contexto del Caso**  \nSe trata de una mujer refugiada de 39 años, embarazada, sin antecedentes de diabetes o hipertensión, que acudió al hospital con síntomas iniciales de insuficiencia cardíaca secundaria a anemia severa. Inicialmente recibió transfusiones sanguíneas para tratar esta condición. Sin embargo, durante su hospitalización, desarrolló múltiples convulsiones focales que se extendieron a ambos hemisferios cerebrales, acompañadas de irritabilidad intensa, dificultad para hablar (afasia) y parálisis parcial en el lado derecho del cuerpo (hemiplejía). Estos signos neurológicos graves motivaron su ingreso a la unidad de cuidados intensivos (UCI).\n\n**Hallazgos Clave**  \nUna revisión detallada de su historia clínica, junto con un examen físico repetido, reveló la presencia de una mancha de vino de Oporto (una lesión vascular congénita de color rojo púrpura) en la región ocular izquierda, que inicialmente no se había detectado. Además, se confirmó un antecedente remoto de convulsiones no provocadas ocurridas hace aproximadamente 20 años, que no había sido reportado inicialmente. La tomografía computarizada del cerebro mostró calcificaciones en la región parietal izquierda, hallazgo característico que, junto con la mancha cutánea y el cuadro clínico, permitió establecer el diagnóstico de síndrome de Sturge-Weber (SWS), una enfermedad neurocutánea rara que afecta vasos sanguíneos del cerebro y la piel.\n\n**Interpretación Clínica**  \nEl síndrome de Sturge-Weber se caracteriza por la presencia de malformaciones vasculares en la piel y el cerebro, que pueden provocar convulsiones, déficits neurológicos y problemas oftalmológicos. En este caso, la combinación de convulsiones recurrentes, hemiplejía, afasia y la mancha facial típica apoyaron el diagnóstico. La anemia y la insuficiencia cardíaca iniciales complicaron el cuadro clínico, pero el manejo neurológico fue prioritario tras la aparición de las convulsiones y el deterioro neurológico.\n\n**Estrategia de Tratamiento y Manejo Multidisciplinario**  \nSe implementó un enfoque integral que involucró a varios especialistas: neurología para el control de las convulsiones, oftalmología para evaluar posibles complicaciones oculares como el glaucoma (aunque la paciente estaba muy irritable y dificultó el examen), otorrinolaringología y fisioterapia para abordar las secuelas neurológicas. El control de las convulsiones se logró con éxito mediante la administración intravenosa de fenitoína durante tres días, seguida de un aumento progresivo de la dosis de carbamazepina oral hasta 1000 mg diarios, administrada a través de una sonda nasogástrica debido al estado de coma profundo de la paciente.\n\n**Limitaciones y Próximos Pasos**  \nDebido a limitaciones en recursos humanos y técnicos en el hospital, no fue posible realizar evaluaciones adicionales importantes para pacientes con SWS, como estudios avanzados de neuroimagen, evaluaciones psiquiátricas, consultas de cirugía plástica y neurocirugía, ni revisiones dentales, que suelen ser necesarias para un manejo completo de esta enfermedad. Se recomienda continuar con un seguimiento multidisciplinario para optimizar el tratamiento y mejorar la calidad de vida de la paciente.",
+        "scores": {
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
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+  },
+  {
+    "article": "Una paciente de 69 años se quejaba de una pérdida progresiva de la visión. Sus padres eran primos hermanos. Le habían diagnosticado retinitis pigmentosa 27 años antes. La paciente había fumado durante 15 años. Tenía antecedentes de hiperlipidemia e hipotiroidismo.\n\nTras una evaluación oftalmológica completa, se determinó que el paciente tenía una agudeza visual corregida (AVC) de contar los dedos a 5’ y 3’ en los ojos derecho e izquierdo, respectivamente. La retinoscopia mostró una refracción de –1.00 + 0.50×70 y –2.00 + 1.00×5 en los ojos derecho e izquierdo, respectivamente. El paciente tenía discos ópticos pálidos con una atrofia profunda extensa de la mácula central, hiperplasia del pigmento epitelial y otras áreas de atrofia multifocal en el ojo derecho. Además, el paciente tenía atrofia macular en el ojo izquierdo. En la imagen de autofluorescencia del fondo del ojo (FAF) del paciente, había evidencia de una hipoautofluorescencia central de la mácula, con una extensión centrífuga difusa desde su centro hasta su periferia.\n\nLa tomografía de coherencia óptica macular (OCT) determinó que el espesor macular promedio era de 191 µM y 193 µM en los ojos derecho e izquierdo, respectivamente. El volumen macular era de 6.9 mm3 y 7.0 mm3 en los ojos derecho e izquierdo, respectivamente. No se encontró edema macular, quistes o fluido subretinal en ninguno de los ojos.\n\nUna prueba de campo visual reveló que el paciente tenía desviaciones medias de –23.75 dB y –24.56 dB en los ojos derecho e izquierdo, respectivamente. Las desviaciones estándar de patrón fueron de +3.69 dB y +4.69 dB en los ojos derecho e izquierdo, respectivamente. Los resultados de un electrorretinograma de campo completo (ERG) mostraron una respuesta normal de bastones y una respuesta de conos disminuida, bilateralmente. Por estas razones, se realizó un diagnóstico clínico de enfermedad STGD1.\n\nSe encontró una variante patogénica homocigótica intrónica c.5714+5G>A del gen ABCA4 tras el análisis de secuenciación y eliminación/duplicación utilizando secuenciación de próxima generación (Invitae Corporation, San Francisco, California). Tenía seis variantes adicionales de significación incierta (VUS) en los genes CACNA1F, EYS, KCNV2, KLHL7, MKKS y USH2A.\n",
+    "gold_summary": "Una paciente de 69 años de edad se presentó en la clínica quejándose de una pérdida progresiva de la visión. La evaluación oftálmica fue notable para una mejor agudeza visual corregida de contar los dedos a 5' en el ojo derecho y 3' en el ojo izquierdo. Las imágenes revelaron una atrofia profunda y extensa de la mácula central, una hiperplasia del pigmento epitelial y otras áreas de atrofia multifocal en el ojo derecho. Además, las imágenes de autofluorescencia del fondo de la mácula mostraron una hipoautofluorescencia central con expansión bilateral a la periferia en ambos ojos. Un electrorretinograma de campo completo mostró una respuesta normal de los bastones, con una respuesta disminuida de los conos, bilateralmente. Las pruebas genéticas fueron positivas para una mutación inotrópica homocigótica en el gen ABCA4 de la variante c.5714+5G>A.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Una señora de 69 años veía cada vez menos con sus ojos. El doctor le hizo muchas pruebas para mirar sus ojos. Vio que la parte del ojo que ayuda a ver bien estaba muy dañada. También encontró que algunas partes del ojo no funcionaban bien. El doctor hizo un examen especial y vio que unas células del ojo estaban normales y otras no. Luego, hicieron un examen de su sangre y encontraron un cambio en un gen que puede causar problemas en la vista.",
+        "scores": {
+          "ROUGE-1": 0.2764227642276423,
+          "ROUGE-2": 0.040983606557377046,
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B2": {
+        "text": "**Lo que le pasaba a la paciente**  \nUna mujer de 69 años empezó a perder la vista poco a poco. Cuando la examinaron, pudo ver solo lo suficiente para contar los dedos a una distancia muy corta: 5 pies en un ojo y 3 pies en el otro. Esto muestra que su visión estaba bastante afectada.\n\n**Qué encontraron en sus ojos**  \nAl mirar dentro de sus ojos con imágenes especiales, los médicos vieron que la parte central de la retina llamada mácula estaba muy dañada. Había zonas donde las células que ayudan a la vista estaban muertas o muy débiles. También notaron un aumento anormal de unas células llamadas pigmento epitelial. Las imágenes que muestran la luz que emite la retina (autofluorescencia) indicaron que la parte central de la mácula tenía menos luz de lo normal, lo que significa daño, y este daño se extendía hacia los lados en ambos ojos.\n\n**Cómo funcionaban sus células de la vista**  \nSe hizo un examen llamado electrorretinograma, que mide la actividad eléctrica de las células de la retina. Los resultados mostraron que las células llamadas bastones, que ayudan a ver en la oscuridad, funcionaban bien. Pero las células llamadas conos, que permiten ver colores y detalles, estaban debilitadas en ambos ojos.\n\n**Qué encontraron en sus genes**  \nAl analizar su ADN, descubrieron que tenía una mutación específica en un gen llamado ABCA4. Este gen es importante para la salud de la retina. La mutación encontrada puede causar problemas en la función de las células de la retina y explicar la pérdida de visión de la paciente.\n\n**En resumen**  \nLa paciente tiene una enfermedad llamada STGD1, que afecta la mácula y causa pérdida progresiva de la visión. Los exámenes clínicos y genéticos ayudaron a confirmar este diagnóstico.",
+        "scores": {
+          "ROUGE-1": 0.3917525773195876,
+          "ROUGE-2": 0.13250517598343686,
+          "ROUGE-L-Sum": 0.3628865979381443,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nUna mujer de 69 años acudió a consulta debido a una pérdida progresiva de la visión que había experimentado durante años. Su historia médica incluía un diagnóstico previo de retinitis pigmentosa desde hacía 27 años, antecedentes familiares de consanguinidad (sus padres eran primos hermanos), así como hiperlipidemia e hipotiroidismo. Además, había fumado durante 15 años.\n\n**Hallazgos Clave**  \nLa evaluación oftalmológica reveló una agudeza visual corregida muy reducida, con la paciente capaz solo de contar los dedos a 5 pies (aproximadamente 1.5 metros) con el ojo derecho y a 3 pies (menos de un metro) con el ojo izquierdo. La refracción mostró leves defectos de visión en ambos ojos. El examen del fondo de ojo evidenció una atrofia profunda y extensa de la mácula central (la zona responsable de la visión detallada), acompañada de hiperplasia (aumento) del pigmento epitelial y múltiples áreas de atrofia en el ojo derecho, mientras que el ojo izquierdo presentaba también atrofia macular. Las imágenes de autofluorescencia del fondo del ojo mostraron una zona central con baja autofluorescencia (hipoautofluorescencia), que se extendía desde el centro hacia la periferia en ambos ojos.\n\nLa tomografía de coherencia óptica (OCT), que permite visualizar las capas de la retina, indicó un grosor macular disminuido en ambos ojos, sin presencia de edema, quistes o líquido subretinal. Las pruebas de campo visual mostraron una pérdida significativa de sensibilidad en ambos ojos. El electrorretinograma (ERG), que mide la función de las células fotorreceptoras de la retina, evidenció una respuesta normal de los bastones (células responsables de la visión en condiciones de poca luz) pero una respuesta disminuida de los conos (células responsables de la visión en condiciones de luz y la percepción del color), de forma bilateral.\n\n**Interpretación Clínica**  \nCon base en estos hallazgos clínicos y funcionales, se estableció un diagnóstico de enfermedad de Stargardt tipo 1 (STGD1), una forma hereditaria de degeneración macular juvenil que afecta la visión central. El análisis genético confirmó la presencia de una mutación patogénica homocigótica (es decir, la misma alteración en ambas copias del gen) en el gen ABCA4, específicamente la variante intrónica c.5714+5G>A, conocida por estar asociada con esta enfermedad. Además, se identificaron seis variantes genéticas adicionales de significado incierto en otros genes relacionados con enfermedades retinianas, aunque su relevancia clínica no pudo ser determinada en este caso.\n\n**Próximos Pasos**  \nEl diagnóstico genético y clínico permite orientar el manejo y seguimiento de la paciente, que debe incluir controles oftalmológicos periódicos para evaluar la progresión de la enfermedad y la función visual. Aunque actualmente no existe una cura definitiva para la enfermedad de Stargardt, se pueden considerar opciones de apoyo visual y asesoramiento genético para la paciente y su familia. Asimismo, la identificación de la mutación específica puede facilitar la inclusión en estudios clínicos o terapias emergentes dirigidas a esta patología genética.",
+        "scores": {
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
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+  {
+    "article": "Un niño de 19 meses de edad fue admitido en el departamento de urgencias porque se cayó de la trona en la que comía. Esta caída ocurrió en un aparente bienestar, sin la presencia de signos o síntomas anticipados. Primero, se cayó sobre su glúteo y luego se golpeó la cabeza (occipucio) contra el suelo. Vomitó (tres episodios) y estaba muy irritable. Su frecuencia respiratoria y cardíaca eran >60 respiraciones y >150 latidos por minuto, mientras que la saturación de oxígeno era <80%. Tras el examen físico, el niño estaba hidratado y consciente, pero irritable. Más importante aún, observamos retracciones subcostal y, al auscultar, disminución de los sonidos respiratorios en la parte basal izquierda del tórax. El paciente fue ventilado con un balón de AMBU conectado a una fuente de oxígeno y monitorizado con un oxímetro de pulso. A pesar de nuestra intervención, la saturación de oxígeno cayó por debajo del 70% y cuanto más ventilábamos, más caía la saturación. La ecografía pulmonar mostró la ausencia de las típicas líneas A y la consolidación del pulmón, que se visualizó directamente como un parénquima sólido. Sobre la base del mal estado clínico, el paciente se sometió a intubación orotraqueal con un tubo endotraqueal con manguito. Después de que el bebé se estabilizó, se sometió a una tomografía computarizada (TC) de tórax que mostró una atelectasia completa del pulmón izquierdo con una interrupción del bronquio izquierdo principal a 12 cm de la bifurcación bronquial. Se sospechó un FBA ya que la madre también declaró que el bebé en los días anteriores había tenido un ataque de tos intenso y desapareció en 24 h sin ningún tratamiento. Por lo tanto, se realizó una broncoscopia rígida y se encontró y se eliminó rápidamente una almendra de 2 cm de diámetro en el bronquio izquierdo principal.\n\nEl paciente nunca había consumido antes almendras u otros frutos secos y, en esta ocasión, ingirió la almendra por accidente.\n\nEl bebé mostró una mejora clínica progresiva y, después de 24 horas, se le retiró la sonda y se le dio de alta de la unidad de cuidados intensivos para ser ingresado en la sala de pediatría general durante unos días, con una recuperación gradual y total de la función respiratoria.\n",
+    "gold_summary": "Describimos el caso de un niño de 19 meses que llegó a la sala de urgencias por un traumatismo en la cabeza. La evaluación clínica, sin embargo, reveló una dificultad respiratoria grave inexplicable que requería intubación traqueal. Después de nuestra evaluación, planteamos la hipótesis de que la dificultad respiratoria grave determinó un estado alterado de conciencia con el consiguiente traumatismo en la cabeza. Los hallazgos radiológicos levantaron la sospecha de aspiración de cuerpo extraño por la presencia de una atelectasia de todo el pulmón izquierdo. La tomografía computarizada mostró una interrupción abrupta del bronquio principal a 12 mm del casco. La siguiente broncoscopia identificó una amígdala de 2 cm.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Un niño pequeño se cayó y se lastimó la cabeza. Pero lo más importante es que no podía respirar bien. Los doctores pusieron un tubo para ayudarlo a respirar. Vieron que un huesito en su pulmón estaba tapado. Buscaron y sacaron una almendra que estaba en su pulmón. Después, el niño mejoró y pudo respirar bien otra vez.",
+        "scores": {
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+          "ROUGE-2": 0.05319148936170213,
+          "ROUGE-L-Sum": 0.24210526315789474,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B2": {
+        "text": "Caso de un niño con dificultad para respirar y caída en la cabeza\n\nUn niño de 19 meses llegó a urgencias después de caerse de la trona donde comía. Aunque parecía estar bien al principio, tenía problemas para respirar y vomitó varias veces. Su ritmo de respiración y corazón estaba muy rápido, y el nivel de oxígeno en su sangre era muy bajo. Al examinarlo, notaron que tenía dificultad para respirar y menos sonidos en el pulmón izquierdo.\n\nLo que encontraron\n\nUsaron una máquina para ayudarlo a respirar, pero el nivel de oxígeno seguía bajando. Una ecografía del pulmón mostró que una parte del pulmón estaba sólida, lo que no es normal. Luego, una tomografía (una imagen detallada del pecho) mostró que el pulmón izquierdo estaba colapsado y que el tubo principal que lleva aire a ese pulmón estaba bloqueado.\n\nQué significaba esto\n\nPensaron que algo estaba bloqueando la vía aérea, posiblemente un objeto que el niño había inhalado sin querer. La madre recordó que el niño había tenido una tos fuerte días antes. Al hacer una broncoscopia, que es cuando se usa un tubo con cámara para mirar dentro de los pulmones, encontraron y sacaron una almendra de 2 cm que estaba bloqueando el bronquio izquierdo.\n\nRecuperación\n\nEl niño nunca había comido almendras antes y la había tragado por accidente. Después de quitar la almendra, mejoró rápidamente. Lo mantuvieron en observación y finalmente se recuperó completamente de sus problemas para respirar.",
+        "scores": {
+          "ROUGE-1": 0.34653465346534656,
+          "ROUGE-2": 0.08955223880597016,
+          "ROUGE-L-Sum": 0.3069306930693069,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe presenta el caso de un niño de 19 meses que fue llevado a urgencias tras una caída desde la trona mientras comía. Inicialmente, se pensó que el motivo principal era el traumatismo craneal provocado por la caída. Sin embargo, durante la evaluación clínica se detectó una dificultad respiratoria grave que no podía explicarse únicamente por el golpe.\n\n**Hallazgos Clave**  \nEl niño mostraba signos de insuficiencia respiratoria severa, con frecuencia respiratoria y cardíaca elevadas, saturación de oxígeno muy baja (menos del 80%) y dificultad para respirar evidenciada por retracciones subcostales y disminución de los sonidos respiratorios en la base del pulmón izquierdo. La saturación de oxígeno empeoraba incluso con ventilación asistida. La ecografía pulmonar reveló ausencia de las líneas A típicas y consolidación pulmonar, indicando que el tejido pulmonar estaba sólido en lugar de aireado. La tomografía computarizada (TC) de tórax mostró una atelectasia completa (colapso) del pulmón izquierdo y una interrupción abrupta del bronquio principal izquierdo a 12 mm de la bifurcación bronquial.\n\n**Interpretación Clínica**  \nEstos hallazgos sugirieron que la dificultad respiratoria grave fue la causa principal del estado alterado de conciencia y, por ende, del traumatismo craneal secundario a la caída. La interrupción del bronquio principal y la atelectasia indicaron la presencia de un cuerpo extraño que obstruía la vía aérea. La madre confirmó que el niño había tenido un episodio previo de tos intensa, lo que apoyó la sospecha de aspiración de un objeto. La broncoscopia rígida permitió identificar y extraer una almendra de 2 cm alojada en el bronquio izquierdo principal, que el niño había ingerido accidentalmente, siendo su primera exposición a frutos secos.\n\n**Próximos Pasos y Evolución**  \nTras la extracción del cuerpo extraño, el niño mostró una mejoría clínica progresiva. Se retiró la intubación después de 24 horas y fue trasladado de la unidad de cuidados intensivos a la sala de pediatría general, donde continuó su recuperación hasta la normalización completa de la función respiratoria. Este caso resalta la importancia de considerar la aspiración de cuerpos extraños en niños pequeños con dificultad respiratoria grave y síntomas atípicos, incluso cuando se presenta un traumatismo asociado.",
+        "scores": {
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+          "ROUGE-L-Sum": 0.3595505617977528,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
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+        }
+      }
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+  },
+  {
+    "article": "Una mujer nulípara de 35 años con antecedentes de infertilidad se presentó en la consulta externa. Informó de un antecedente de tres años de dolor sordo cíclico en el ombligo. El dolor se asoció a un nódulo umbilical que sangraba durante la menstruación. Cabe destacar que el dolor empeoraba durante la menstruación y se aliviaba con analgésicos. La paciente también informó de dismenorrea, menorragia y dispareunia. La paciente se había insertado un DIU de cobre 3 años antes y había estado usando Zinnia P (levonorgestrel y etinilestradiol) durante los últimos 3-4 meses para intentar aliviar el dolor. Su historial ginecológico previo no fue notable y tenía un ciclo menstrual regular. No había antecedentes médicos, quirúrgicos o sociales de importancia.\nAl examinarla, sus constantes vitales eran estables. Se observó una hinchazón hiperpigmentada (3 × 2 cm) en el ombligo al examinar el abdomen. La hinchazón era firme, inmóvil, no dolorosa, no reductible y no estaba ligada a estructuras subyacentes. Una resonancia magnética abdominal reveló una masa de mejora mal definida que medía 3 × 4 × 6 cm ubicada a lo largo de la pared abdominal anterior derecha y estaba conectada a un tracto sinusal que se extendía hacia la región suprapúbica, pero no se comunicaba con la cavidad peritoneal, hallazgos que sugieren endometriosis. El diagnóstico diferencial fue amplio, incluida una hernia umbilical, granuloma, cicatriz queloide, neoplasias malignas nodulares y anomalías embriológicas. Además, se observaron lesiones anexiales bilaterales, eran hiperintensas con áreas hipointensas focales y restricciones variables, la lesión del lado derecho medía 1,6 × 1,7 cm y la lesión del lado izquierdo medía 2,0 × 0,8 cm, hallazgos consistentes con endometriosis ovárica bilateral.\n\nSe programó al paciente para la extirpación quirúrgica del nódulo umbilical. La muestra se envió para un examen histopatológico. Los resultados revelaron una epidermis normal con glándulas endometriales dispersas y estroma dentro de la dermis. La fotomicroscopía resaltó la presencia de estroma endometrial y tejido graso subcutáneo. Esta morfología es consistente con la endometriosis. La recuperación postoperatoria de la paciente fue sin incidentes, y se la consideró apta para el alta el día 2 postoperatorio. Recibió asesoramiento sobre su fertilidad futura y la posibilidad de FIV, riesgo de recurrencia y se programó una visita de seguimiento en dos semanas. Se le inició con Dienogest, Visanne y un anticonceptivo oral combinado para el tratamiento de la endometriosis. Se la ha monitoreado clínicamente cada cuatro semanas, y no se han observado síntomas o signos de recurrencia local durante el período de seguimiento de 8 meses. Cabe destacar que, a pesar de que su condición permaneció estable después del tratamiento, no concibió en el transcurso del año siguiente.\n",
+    "gold_summary": "Presentamos el caso de una mujer nulípara de 35 años de edad del norte de Tanzania con un historial de infertilidad de 10 años. Al presentarse, la paciente informó de un historial de tres años de dolor cíclico asociado a una masa umbilical. Una resonancia magnética abdominal reveló una masa mal definida que se intensificaba y medía 3 × 4 × 6 cm, localizada a lo largo de la pared abdominal anterior derecha. La masa estaba conectada a un tracto sinusal que se extendía hacia la región suprapúbica, pero no mostraba comunicación con la cavidad peritoneal, lo que sugería endometriosis. Además, las lesiones anexiales bilaterales demostraron señales hiperintensas con áreas hipointensas focales y restricciones variables, consistentes con endometriomas ováricos bilaterales. La paciente se sometió a la extirpación de la masa umbilical y el examen histopatológico confirmó el diagnóstico de endometriosis umbilical primaria. A pesar de su condición estable después del tratamiento, no concibió durante el año siguiente.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Había una mujer que tenía dolor en su pancita cerca del ombligo. El dolor venía y se iba, y a veces el ombligo sangraba. Los doctores vieron que tenía un bultito en el ombligo. Le sacaron el bultito con una operación. Cuando miraron el bultito, encontraron que era un problema llamado endometriosis. Ella se sintió mejor después de la operación. Pero todavía no pudo tener un bebé.",
+        "scores": {
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+          "ROUGE-2": 0.040160642570281124,
+          "ROUGE-L-Sum": 0.25498007968127495,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B2": {
+        "text": "**Caso de una mujer con dolor y un bulto en el ombligo**\n\nUna mujer de 35 años, que nunca ha tenido hijos y ha tenido problemas para quedar embarazada durante 10 años, acudió al médico porque tenía dolor en el ombligo desde hace tres años. Este dolor aparecía de forma cíclica, es decir, se repetía cada mes, y estaba relacionado con un bulto en esa zona.\n\n**Lo que encontraron en las pruebas**\n\nSe le hizo una resonancia magnética, que es un tipo de imagen que muestra el interior del cuerpo. Esta prueba mostró una masa o bulto de 3 × 4 × 6 centímetros en la pared del abdomen, cerca del ombligo. La masa estaba conectada a un pequeño canal que llegaba hacia la parte baja del abdomen, pero no estaba unida a la cavidad donde están los órganos internos. Esto hizo pensar que podría tratarse de endometriosis, que es cuando un tejido parecido al que recubre el interior del útero crece en otros lugares del cuerpo.\n\nAdemás, se encontraron lesiones en ambos ovarios que también parecían ser endometriomas, que son quistes causados por la endometriosis en los ovarios.\n\n**Qué hicieron y qué pasó después**\n\nLa mujer se sometió a una cirugía para quitar el bulto del ombligo. El tejido extraído se analizó bajo el microscopio y confirmó que era endometriosis en el ombligo, algo poco común. Después de la operación, la paciente se recuperó bien y comenzó un tratamiento con medicamentos para controlar la endometriosis.\n\nDurante los siguientes ocho meses, no tuvo nuevos síntomas ni signos de que la enfermedad regresara. Sin embargo, aunque su salud mejoró, no logró quedar embarazada en el año siguiente.\n\nEste caso muestra cómo la endometriosis puede afectar diferentes partes del cuerpo y la importancia de un diagnóstico y tratamiento adecuados para mejorar la calidad de vida y la fertilidad.",
+        "scores": {
+          "ROUGE-1": 0.42687747035573126,
+          "ROUGE-2": 0.16666666666666666,
+          "ROUGE-L-Sum": 0.41501976284584974,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe presenta el caso de una mujer de 35 años, sin hijos y con un historial de infertilidad de una década, que acudió a consulta por un dolor cíclico y persistente en el ombligo durante tres años. Este dolor se asociaba a la presencia de un nódulo umbilical que sangraba coincidiendo con su menstruación. Además, refería síntomas ginecológicos como dolor menstrual intenso (dismenorrea), sangrado menstrual abundante (menorragia) y dolor durante las relaciones sexuales (dispareunia). La paciente había utilizado un dispositivo intrauterino (DIU) de cobre desde hacía tres años y recientemente había iniciado tratamiento hormonal combinado para aliviar el dolor.\n\n**Hallazgos Clave**  \nEl examen físico reveló una masa firme, hiperpigmentada, inmóvil y no dolorosa en el ombligo, sin conexión palpable con estructuras internas. La resonancia magnética mostró una masa mal definida de 3 × 4 × 6 cm en la pared abdominal anterior derecha, conectada a un tracto sinusal que se extendía hacia la región suprapúbica, pero sin comunicación con la cavidad peritoneal, lo que orientó hacia un diagnóstico de endometriosis umbilical primaria. Además, se identificaron lesiones en ambos ovarios con características compatibles con endometriomas (quistes ováricos formados por tejido endometrial), confirmando la afectación bilateral.\n\n**Interpretación Clínica**  \nEl diagnóstico diferencial incluyó diversas condiciones como hernia umbilical, granuloma, cicatriz queloide, tumores malignos y anomalías congénitas, pero la combinación de síntomas, hallazgos de imagen y la confirmación histopatológica establecieron la endometriosis umbilical primaria. La biopsia del nódulo extirpado mostró tejido endometrial (glándulas y estroma) dentro de la dermis, confirmando la presencia de endometriosis fuera del útero. Este tipo de endometriosis es poco frecuente y puede causar dolor cíclico y sangrado en la piel del ombligo.\n\n**Próximos Pasos y Seguimiento**  \nTras la cirugía, la paciente tuvo una recuperación sin complicaciones y fue dada de alta al segundo día postoperatorio. Se le indicó tratamiento hormonal con dienogest y anticonceptivos orales combinados para controlar la endometriosis y reducir el riesgo de recurrencia. Se le brindó asesoramiento sobre su fertilidad futura, incluyendo la posibilidad de recurrir a técnicas de reproducción asistida como la fertilización in vitro (FIV). Durante un seguimiento clínico de ocho meses no se observaron signos de recurrencia local, aunque la paciente no logró concebir en el año posterior al tratamiento.\n\nEste caso destaca la importancia de considerar la endometriosis umbilical en mujeres con dolor cíclico y nódulos en el ombligo, especialmente en el contexto de infertilidad, y subraya la necesidad de un manejo multidisciplinario para optimizar el control de los síntomas y la fertilidad.",
+        "scores": {
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+          "ROUGE-2": 0.22397476340694003,
+          "ROUGE-L-Sum": 0.40566037735849053,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      }
+    }
+  },
+  {
+    "article": "Presentamos a un recién nacido de 15 minutos de edad, hijo de una madre para-cuatro que no recordaba su LNMP pero que afirmaba haber estado amenorreica durante los últimos nueve meses. Su madre había recibido atención prenatal en el centro de salud cercano dos veces y no había tenido incidentes. Sin embargo, no se le había realizado un ultrasonido obstétrico temprano. Por lo demás, no tiene antecedentes de enfermedades crónicas como diabetes mellitus e hipertensión. Durante su embarazo actual, no tuvo fiebre, dolor de cabeza o visión borrosa. Nunca había usado ninguna droga aparte de sulfato ferroso durante este embarazo. Sus hijos anteriores están todos sanos y vivos. A su llegada a nuestro hospital, tuvo una hemorragia vaginal de dos horas de duración. Posteriormente, fue admitida con un diagnóstico de embarazo de tercer trimestre más multigravida más hemorragia anteparto secundaria a desprendimiento de placenta más oligohidramnios severo más presentación de nalgas.\n\nEn el examen pélvico, tenía un sangrado vaginal activo. Se le realizó una ecografía obstétrica al llegar. En consecuencia, la edad gestacional era de 34 semanas, la placenta estaba en el fondo con un coágulo retroplacentario y el líquido amniótico había disminuido significativamente con un único bolsillo más profundo de 1,5 cm. El peso fetal estimado era de 2,4 kg y presentación de nalgas. Otras investigaciones de la madre son grupo sanguíneo AB+, VDRL=negativo, RBS=120 mg/dL, en CBC, glóbulos blancos=9000, hemoglobina=11 gm/dL, plaqueta=180,000 y neutrófilo=60%.\n\nTras obtener el consentimiento informado por escrito, se realizó una cesárea de urgencia por las indicaciones ya mencionadas para extraer un neonato vivo de 2,01 kg de peso con puntuaciones de 5 y 6 en las pruebas de Apgar en el primer y el quinto minuto, respectivamente.\n\nEl neonato no lloró y fue reanimado durante cinco minutos. Luego fue trasladado a la unidad de cuidados intensivos neonatales para recibir atención e investigaciones adicionales. Al llegar, el neonato estaba en dificultad respiratoria. Sus signos vitales eran de 160 latidos por minuto, 70 respiraciones por minuto, temperatura de 33,4 grados centígrados y saturación de oxígeno del 60%. La fontanela anterior del neonato medía 2 cm por 2 cm y tenía micrognatia y cuello corto. En el sistema respiratorio, había retracciones intercostales y subcostales, respiración trabajosa y gruñidos. En el examen precordial, se escucharon bien los sonidos s1 y s2, no había murmullo ni ritmo de galope. En el sistema musculoesquelético, había acortamiento bilateral de las extremidades superiores, la extremidad inferior derecha estaba normal en posición y estructura, la pierna izquierda giraba hacia adentro (flexión mediolateral) en la articulación de la rodilla y la estructura del pie era normal. En el examen neurológico, estaba letárgico, el tono era normotónico en la extremidad inferior derecha y el reflejo de Moro era difícil de evaluar. La investigación de laboratorio mostró grupo sanguíneo = A+, CRP = reactivo, WBC = 30,000, neutrófilos = 54%, linfocitos = 21.1%, HGB = 8 gm/dL y plaquetas = 150,000. Se realizó una radiografía que mostró un acortamiento extremo de las extremidades superiores. La extremidad inferior izquierda estaba internamente girada. La ecocardiografía fue normal. Con una evaluación de prematuro tardío (34-36 semanas por puntaje de Ballard) más bajo peso al nacer más apropiado para la edad gestacional más focomelia más asfixia perinatal más sepsis neonatal temprana, se manejó con apoyo de oxígeno, fluido de mantenimiento e antibióticos intravenosos. El neonato murió después de tres días de hospitalización.\n",
+    "gold_summary": "Presentamos a un neonato de 15 minutos de vida, hijo de una madre para-cuatro que no recordaba su LNMP pero que afirmaba estar amenorreica desde hacía nueve meses. El modo de parto fue por cesárea para extraer al neonato vivo, que pesaba 2,01 kg y tenía puntuaciones APGAR de 5 y 6 en el primer y quinto minutos, respectivamente. El neonato no lloró y fue reanimado durante cinco minutos. Después se lo trasladó a la unidad de cuidados intensivos neonatales para continuar con el tratamiento y las investigaciones. Sus signos vitales eran: pulso de 160 latidos por minuto, frecuencia respiratoria de 70 respiraciones por minuto, temperatura de 33,4 grados centígrados y saturación de oxígeno del 60%. La fontanela anterior del neonato medía 2 cm por 2 cm y tenía micrognatia y cuello corto. En el sistema respiratorio había retracciones intercostales y subcostales, respiración trabajosa y gruñidos. En el sistema musculoesquelético había acortamiento bilateral de la extremidad superior, la pierna derecha tenía una posición y estructura normales, la pierna izquierda giraba hacia adentro (se doblaba hacia la parte media) en la articulación de la rodilla y el pie tenía una estructura normal.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Un bebé nació hace muy poquito tiempo. Su mamá tuvo que ir al hospital para que lo sacaran con una operación especial. El bebé pesaba poquito y no pudo llorar al nacer. Los doctores lo ayudaron a respirar y lo llevaron a un lugar para cuidarlo mucho.\n\nEl bebé respiraba rápido y su corazón latía rápido también. Tenía frío y le faltaba un poco de aire. Su cabeza tenía una parte blanda y su cuello era cortito. Sus brazos eran más cortos de lo normal. Una pierna estaba normal, pero la otra estaba doblada hacia adentro. Sus pies estaban bien. Los doctores lo cuidaron mucho para que se sintiera mejor.",
+        "scores": {
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+          "ROUGE-2": 0.030303030303030304,
+          "ROUGE-L-Sum": 0.2831325301204819,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
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+      "B2": {
+        "text": "**Lo que pasó con el bebé al nacer**  \nUn bebé nació por cesárea después de que su mamá tuvo problemas en el embarazo. El bebé pesó 2,01 kg y sus primeras pruebas para saber cómo estaba (llamadas puntuaciones Apgar) fueron 5 y 6, lo que indica que necesitó ayuda para respirar. De hecho, el bebé no lloró al nacer y tuvo que ser reanimado durante cinco minutos para ayudarlo a respirar mejor.\n\n**Estado del bebé en la unidad de cuidados intensivos**  \nDespués de nacer, el bebé fue llevado a una unidad especial para recién nacidos que necesitan cuidados extra. Allí, los médicos notaron que su corazón latía rápido (160 latidos por minuto) y respiraba muy rápido (70 respiraciones por minuto). Además, tenía la temperatura baja (33,4 grados Celsius) y poca cantidad de oxígeno en la sangre (60%). La parte blanda en la cabeza del bebé (llamada fontanela anterior) medía 2 cm por 2 cm. También tenía micrognatia, que significa que la mandíbula era más pequeña de lo normal, y un cuello corto.\n\n**Problemas en la respiración y los huesos**  \nEl bebé tenía dificultad para respirar, con movimientos fuertes entre las costillas y sonidos de gruñidos al respirar. En cuanto a sus brazos, ambos eran más cortos de lo normal. La pierna derecha estaba normal, pero la pierna izquierda estaba doblada hacia adentro en la rodilla, aunque el pie tenía una forma normal.\n\n**Qué significa todo esto**  \nEstos signos muestran que el bebé tenía problemas para respirar y algunas malformaciones en sus extremidades. Estas condiciones pueden ser causadas por complicaciones durante el embarazo o problemas en el desarrollo del bebé. Los médicos le dieron oxígeno y otros tratamientos para ayudarlo, pero lamentablemente el bebé murió después de tres días en el hospital.",
+        "scores": {
+          "ROUGE-1": 0.5243445692883895,
+          "ROUGE-2": 0.2330827067669173,
+          "ROUGE-L-Sum": 0.5093632958801498,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
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+      "B3": {
+        "text": "**Contexto**  \nSe presentó un recién nacido de apenas 15 minutos de vida, hijo de una mujer con antecedentes obstétricos de cuatro partos previos (para-cuatro). La madre no recordaba la fecha de su última menstruación, pero aseguró haber estado sin menstruar durante nueve meses, lo que indicaba un embarazo avanzado. Durante el embarazo, la madre recibió atención prenatal limitada y no se realizó una ecografía temprana. Al momento del ingreso hospitalario, la madre presentaba hemorragia vaginal prolongada, diagnóstico de desprendimiento prematuro de placenta, oligohidramnios severo (disminución del líquido amniótico) y presentación fetal de nalgas.\n\n**Hallazgos Clave del Neonato**  \nEl bebé nació mediante cesárea de urgencia con un peso de 2,01 kg y puntuaciones de Apgar de 5 y 6 al primer y quinto minuto, respectivamente, lo que indica una adaptación inicial comprometida. No lloró al nacer y requirió reanimación durante cinco minutos. Fue trasladado a la unidad de cuidados intensivos neonatales debido a dificultad respiratoria grave, con signos vitales alterados: frecuencia cardíaca elevada (160 latidos por minuto), respiración rápida (70 respiraciones por minuto), temperatura corporal baja (33,4 °C) y saturación de oxígeno muy baja (60%).\n\nEn el examen físico, se observaron características faciales anómalas como micrognatia (mandíbula inferior pequeña) y cuello corto. En el sistema respiratorio, el neonato presentaba retracciones intercostales y subcostales (movimientos visibles de los músculos entre las costillas y debajo de ellas al respirar), respiración dificultosa y sonidos respiratorios anormales (gruñidos). En el sistema musculoesquelético, había un acortamiento marcado de ambas extremidades superiores (brazo y antebrazo), mientras que la pierna derecha tenía una estructura y posición normales. La pierna izquierda estaba girada hacia adentro en la articulación de la rodilla (flexión mediolateral), aunque el pie mantenía una estructura normal.\n\nLos estudios complementarios revelaron una elevación significativa de los glóbulos blancos (30,000), indicando posible infección, con una proteína C reactiva positiva (marcador de inflamación), anemia moderada (hemoglobina de 8 g/dL) y plaquetas dentro de rango normal. La radiografía confirmó el acortamiento extremo de las extremidades superiores y la rotación interna de la pierna izquierda. La ecocardiografía fue normal, descartando malformaciones cardíacas.\n\n**Interpretación Clínica**  \nEl diagnóstico principal incluyó un neonato prematuro tardío (34 semanas de gestación), con bajo peso al nacer pero adecuado para su edad gestacional, que presentaba focomelia (una malformación congénita caracterizada por extremidades muy cortas o ausentes), asfixia perinatal (falta de oxígeno al nacer) y sepsis neonatal temprana (infección grave en los primeros días de vida). Estas condiciones explican la dificultad respiratoria, el compromiso hemodinámico y las anomalías físicas observadas.\n\n**Próximos Pasos y Evolución**  \nEl manejo incluyó soporte respiratorio con oxígeno, administración de líquidos por vía intravenosa y tratamiento antibiótico para la infección. A pesar de estas intervenciones, el neonato falleció a los tres días de hospitalización debido a la gravedad de sus condiciones clínicas y malformaciones congénitas asociadas. Este caso resalta la importancia de un control prenatal adecuado, diagnóstico temprano y manejo multidisciplinario para mejorar el pronóstico en embarazos complicados y neonatos con malformaciones severas.",
+        "scores": {
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
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+  },
+  {
+    "article": "Mujer de 61 años con antecedente de carcinoma escamocelular de cuello uterino estadio FIGO IIB, diagnosticado en febrero de 2019, tratada en un hospital privado de cuarto nivel de atención, donde se ofrece cuidado ambulatorio y hospitalario para pacientes con condiciones complejas oncológicas y no oncológicas. Al momento del diagnóstico se realizó histerectomía radical con linfadenectomía pélvica, que descartó compromiso nodal. El tratamiento complementario de primera línea incluyó seis ciclos de quimioterapia con cisplatino, y braquiterapia y radioterapia, alcanzando una respuesta tumoral completa. En 2021, tras detectarse una recaída aislada en la región ilíaca, mediante tomografía, se administró cisplatino y 30 sesiones de radioterapia, logrando una nueva respuesta completa. En septiembre de 2022, una tomografía reveló otra recaída con compromiso del parametrio izquierdo, el uréter y la cadena ilíaca ipsilateral, por lo que se decidió primera línea para enfermedad recurrente con carboplatino, paclitaxel y pembrolizumab. Durante este régimen, la paciente presentó hipersensibilidad al platino en el quinto ciclo, gestionada con un protocolo de desensibilización, continuando con el pembrolizumab. En septiembre de 2023, ante la progresión en imágenes de una masa retroperitoneal única, debido a la falta de respuesta óptima, se inició gemcitabina, según guías de manejo, segunda línea de enfermedad recurrente, recibiendo una dosis acumulada de 8.544 mg/m2 hasta enero de 2024. Sin embargo, desarrolló síntomas de isquemia digital en manos, por lo que el tratamiento fue suspendido tras la segunda dosis del tercer ciclo, acumulando 11.744 mg/m2 de gemcitabina.\n\nEn febrero de 2024, la paciente ingresó al servicio de urgencias del mismo hospital donde era valorada de forma ambulatoria, remitida por oncología debido a progresión de los síntomas en sus extremidades. La paciente refería dolor lancinante y coloración azulada en dedos de manos; al examen físico se evidencia necrosis en el segundo dedo de la mano derecha, coloración ocre y fenómeno de Raynaud en los dedos de la mano izquierda. Las extremidades inferiores mostraban edema grado II en el miembro inferior izquierdo y pulsos presentes. Los estudios para autoinmunidad y vasculitis resultaron negativos, incluyendo anticuerpos anticitoplasma de neutrófilos (ANCAS), anticuerpos antinucleares (ANAS), anticuerpos antidesoxirribonucleicos (anti-DNA), cardiolipinas, prueba confirmatoria de anticoagulante lúpico, perfil de anticuerpos contra antígenos nucleares extraíbles (ENAS), anticuerpos contra proteinasa 3, anticuerpos antimieloperoxidasa y anticuerpos dirigidos contra la ADN topoisomerasa I (antiSCL). Además, el factor reumatoide y los niveles de complemento 3 (C3) y complemento 4 (C4) también fueron normales. Prueba serológica para sífilis (VDRL - Venereal Disease Research Laboratory) negativa, ecocardiograma transtorácico sin hallazgos de un foco cardioembólico.\n\nSe inició anticoagulación con heparina de bajo peso molecular, junto con ácido acetilsalicílico, estatina y un calcioantagonista. El equipo de cirugía de mano realizó amputación del segundo dedo de la mano derecha, confirmando necrosis por licuefacción en el estudio histopatológico.\n\nDurante el posoperatorio se agregó sildenafil al tratamiento, logrando una mejoría progresiva en los signos de isquemia de los dedos restantes. Durante la hospitalización, la paciente presenta complicación por sangrado vaginal masivo, requiriendo embolización de arterias uterinas.\n\nEl servicio de reumatología aplicó la escala de causalidad de Naranjo para determinar el papel de la gemcitabina en la vasculitis, con un puntaje de 8, lo que indicó que el medicamento probablemente provocó la necrosis.\n\nPosteriormente, a los 20 días de ingreso a hospitalización desarrolló deterioro neurológico, sin hallazgos significativos en la tomografía de cráneo. Evaluada por cuidados paliativos, su estado funcional se clasificó con un Barthel de 0/30, ECOG de 4 y Karnofsky de 10 %, con pronóstico de vida inferior a tres semanas según el Índice Pronóstico de Paciente (PPI: + 6 puntos). En consenso con la familia, se suspendieron estudios adicionales y se implementó un manejo paliativo integral. La paciente falleció tras el alta hospitalaria.",
+    "gold_summary": "Oaciente de 61 años tratada con gemcitabina (11.744 mg/m² acumulados) por enfermedad metastásica, en un hospital general de cuarto nivel, privado, no oncológico, donde venía siendo manejada de forma ambulatoria. Presentó necrosis distal del segundo dedo de la mano derecha, por lo que se suspendió el tratamiento y se requirió amputación de este dedo. Se realizó una búsqueda en Embase, Medline y Lilacs. Se buscaron estudios de reporte y series de casos sobre necrosis distal inducida por gemcitabina. Se extrajeron datos de dosis, diagnóstico y tratamiento.",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Una señora de 61 años estaba muy enferma y recibió medicina para el cáncer. Esta medicina le hizo daño en un dedo de su mano derecha. El dedo se puso muy mal y tuvieron que cortarlo para que no le doliera más. Los doctores buscaron información para entender mejor este problema y cómo ayudar.",
+        "scores": {
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+      "B2": {
+        "text": "**Caso de una Mujer con Cáncer y Problemas en las Manos**\n\nUna mujer de 61 años estaba recibiendo un medicamento llamado gemcitabina para tratar su cáncer que se había extendido. Este medicamento se usó en un hospital privado que atiende casos complejos. Después de recibir una dosis acumulada bastante alta (11.744 mg/m²), comenzó a tener problemas graves en su mano derecha. El segundo dedo se puso negro y murió (necrosis), lo que hizo necesario suspender el medicamento y amputar ese dedo.\n\n**Búsqueda de Información sobre el Problema**\n\nLos médicos buscaron en varias bases de datos científicas (Embase, Medline y Lilacs) para encontrar otros casos similares donde la gemcitabina causara necrosis en los dedos. Revisaron estudios y reportes para entender mejor las dosis usadas, cómo se diagnosticó el problema y qué tratamientos se aplicaron.\n\n**Qué Significa Esto**\n\nEste caso muestra que, aunque la gemcitabina es útil para tratar ciertos tipos de cáncer, puede causar efectos secundarios graves en las manos, como la muerte de tejido en los dedos. Por eso, los médicos deben vigilar muy bien a los pacientes que reciben este medicamento para detectar cualquier señal temprana de daño y actuar rápido para evitar complicaciones mayores.",
+        "scores": {
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+      "B3": {
+        "text": "Resumen detallado para público no médico universitario\n\nContexto  \nSe trata de una mujer de 61 años con un historial complejo de cáncer de cuello uterino (carcinoma escamocelular), inicialmente diagnosticado en 2019 y tratado con cirugía, quimioterapia y radioterapia, logrando respuestas completas. Sin embargo, presentó varias recaídas localizadas y regionales entre 2021 y 2023, que requirieron diferentes líneas de tratamiento con quimioterapia y terapia inmunológica. En 2023, ante la progresión tumoral, se inició gemcitabina como segunda línea de tratamiento para la enfermedad recurrente.\n\nHallazgos clave  \nDurante el tratamiento con gemcitabina, acumuló una dosis total de 11.744 mg/m², pero desarrolló síntomas de isquemia digital, es decir, falta de flujo sanguíneo en los dedos de las manos, que se manifestó con dolor intenso, coloración azulada y necrosis (muerte del tejido) en el segundo dedo de la mano derecha. Esto llevó a la suspensión inmediata del medicamento y a la amputación quirúrgica de dicho dedo, confirmándose la necrosis mediante análisis histopatológico (examen microscópico del tejido).\n\nSe descartaron otras causas comunes de daño vascular o inflamación de los vasos sanguíneos (vasculitis) mediante pruebas serológicas y de autoinmunidad, todas negativas. Tampoco se encontraron problemas cardíacos que pudieran explicar la formación de coágulos o embolias. El equipo médico inició tratamiento con anticoagulantes, antiinflamatorios, vasodilatadores y medicamentos para mejorar la circulación, logrando cierta mejoría en los dedos restantes.\n\nInterpretación clínica  \nEl análisis de causalidad mediante la escala de Naranjo, una herramienta que ayuda a determinar si un medicamento es responsable de un efecto adverso, indicó que la gemcitabina fue probablemente la causa de la necrosis digital. Este efecto adverso es poco frecuente pero grave, y se relaciona con daño vascular inducido por el fármaco.\n\nPróximos pasos y evolución  \nPosteriormente, la paciente presentó complicaciones adicionales, incluyendo un sangrado vaginal masivo que requirió embolización (procedimiento para detener el sangrado) y un deterioro neurológico sin causa clara en estudios de imagen. Su estado general empeoró significativamente, con pérdida total de autonomía y un pronóstico de vida inferior a tres semanas. En consenso con la familia, se decidió suspender estudios invasivos y se implementó un manejo paliativo integral para mejorar su calidad de vida en el tiempo restante. Finalmente, la paciente falleció tras el alta hospitalaria.\n\nResumen de la revisión bibliográfica  \nSe realizó una búsqueda en bases de datos médicas (Embase, Medline y Lilacs) para identificar reportes y series de casos sobre necrosis distal inducida por gemcitabina, recopilando información sobre dosis, diagnóstico y manejo de esta complicación, con el fin de contextualizar y comparar el caso presentado.\n\nEste caso resalta la importancia de la vigilancia estrecha de efectos adversos vasculares graves en pacientes tratados con gemcitabina, especialmente en contextos de enfermedad avanzada y tratamientos prolongados.",
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+  {
+    "article": "Mujer de 53 años, con antecedente de AR de 15 años de diagnóstico en tratamiento con metotrexato, resto de antecedentes sin datos de importancia, la cual presentó cuadro clínico 8 meses antes (de acudir a nuestro servicio) con astenia y adinamia de forma progresiva, palidez de tegumentos, alzas térmicas no cuantificadas de predominio nocturno, pérdida de peso no intencionada de 15 kg en 6 meses aproximadamente, sin valoración ni seguimiento médico, a lo que se agregó 3 meses después disnea de grandes a medianos esfuerzos, y cuya sintomatología se agudizó 5 días antes (de acudir a nuestro servicio), aunada a sangrado de tubo digestivo alto (STDA), caracterizado por evacuaciones melénicas abundantes, 3 evacuaciones en 24 horas, hematemesis en 2 ocasiones, escasas, sin causa aparente. La paciente negó consumo de analgésicos no esteroideos (AINE) y tuvo aumento de volumen en la pierna izquierda, la cual le dolía y tenía la presencia de edema y eritema, con limitación a la movilidad, motivo por el cual acudió a (nuestro) Servicio de Urgencias.\n\nDurante su hospitalización con anemia severa sin repercusión hemodinámica, se transfundieron 3 concentrados eritrocitarios sin complicaciones aparentes. Después de su estabilización, se inició abordaje diagnóstico para síndrome consuntivo. Por el cuadro clínico de miembro inferior izquierdo se hizo US Doppler que evidenció trombosis venosa profunda. Se realizó ultrasonido de abdomen por probable hepatopatía por metotrexato, el cual reportó infartos esplénicos y hepáticos, así como presencia de cambios crónicos hepáticos. Se llevó a cabo endoscopía con evidencia de varices pequeñas, sin sangrado activo. Debido a la sospecha de neoplasia por los antecedentes y el cuadro clínico de la paciente, se llevó a cabo tomografía axial simple y contrastada de tórax y abdomen y se encontró hepatoesplenomegalia y múltiples conglomerados ganglionares axilares, mediastinales y paraaórticos que sugerían actividad infiltrativa. Esto se valoró por el Servicio de Cirugía General para la realización de biopsia de ganglio axilar derecho, donde se reportó proliferación neoplásica de células linfoides. Posteriormente se valoró por el Servicio de Hematología de la unidad, se solicitaron estudios de laboratorio (cuadro I) y se realizó aspirado de médula ósea en el que se evidenciaron células plasmáticas displásicas y células reticulares, por lo cual se concluyó que había la presencia de infiltración linfoplasmocitaria. Con los antecedentes, el cuadro clínico y los estudios complementarios se diagnosticó LNH estadio IV y la paciente fue enviada a hospital de tercer nivel para realización de inmunohistoquímica, estadificación e inicio de tratamiento. En tercer nivel se identificó linfoma difuso de células B con inmunofenotipo B CD20 con sobrecrecimiento de células dendríticas, y la paciente fue valorada para inicio de tratamiento con quimioterapia.",
+    "gold_summary": "Mujer de 55 años con antecedente de AR que ingresó a un servicio de medicina interna por sangrado de tubo digestivo; presentó datos clínicos de trombosis venosa profunda en miembro pélvico izquierdo y síndrome consuntivo en estudio. Durante su abordaje se identificó con infartos esplénicos y hepáticos, así como múltiples conglomerados ganglionares, por lo que se practicó biopsia de ganglio axilar que reportó proliferación neoplásica de células linfoides y aspirado de médula ósea con presencia de infiltración linfoplasmocitaria, con lo que se determinó diagnóstico de linfoma no Hodgkin estadio IV. La paciente fue enviada a un hospital de tercer nivel para inicio de tratamiento.",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Había una señora que se sentía muy cansada y tenía dolor en una pierna. También tenía sangre en su pancita. Los doctores le hicieron muchas pruebas. Encontraron que tenía unos bultitos en su cuerpo que no estaban bien. Le hicieron una prueba en un lugar con bultitos y otra en su hueso. Vieron que tenía un tipo de enfermedad llamada linfoma. La señora fue a un hospital especial para que la cuiden y le den medicina para mejorar.",
+        "scores": {
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+        "text": "**Lo que le pasó a la paciente**  \nUna mujer de 53 años, que tenía artritis reumatoide (una enfermedad que afecta las articulaciones), llegó al hospital porque estaba sangrando por el tubo digestivo (el camino que va desde la boca hasta el estómago y los intestinos). Además, tenía dolor y hinchazón en la pierna izquierda, y estaba muy cansada y pálida. También había perdido mucho peso sin querer.\n\n**Lo que encontraron en los exámenes**  \nLos médicos descubrieron que tenía una trombosis venosa profunda, que es un coágulo de sangre en una vena grande de la pierna. También encontraron daños en el bazo y el hígado, llamados infartos, que son áreas donde no llegó suficiente sangre. Al hacer una tomografía (una imagen especial del cuerpo), vieron que sus ganglios linfáticos (pequeñas glándulas que ayudan a combatir infecciones) estaban muy grandes y agrupados en varias partes del cuerpo.\n\nPara entender mejor qué pasaba, le hicieron una biopsia, que es cuando se toma un pequeño pedazo de tejido para analizarlo. La biopsia del ganglio linfático mostró que había un crecimiento anormal de células llamadas linfocitos, que son parte del sistema inmunológico. También examinaron su médula ósea (donde se producen las células de la sangre) y encontraron células anormales que indicaban que el problema estaba afectando varias partes del cuerpo.\n\n**Qué significa el diagnóstico**  \nCon toda esta información, los médicos diagnosticaron un linfoma no Hodgkin en estadio IV. El linfoma no Hodgkin es un tipo de cáncer que afecta a los linfocitos. El estadio IV significa que el cáncer está avanzado y se ha extendido a varias áreas del cuerpo.\n\n**Próximos pasos**  \nLa paciente fue enviada a un hospital especializado para hacer más estudios y comenzar un tratamiento con quimioterapia, que es un tipo de medicina para combatir el cáncer.",
+        "scores": {
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+      "B3": {
+        "text": "**Contexto**  \nSe trata de una mujer de 53 años con diagnóstico previo de artritis reumatoide (AR) desde hace 15 años, en tratamiento con metotrexato. Ocho meses antes de su ingreso al hospital, comenzó a presentar síntomas progresivos como fatiga intensa (astenia), debilidad generalizada (adinamia), palidez en la piel, fiebre nocturna no cuantificada y una pérdida de peso no intencionada de aproximadamente 15 kg en seis meses. Tres meses después, desarrolló dificultad para respirar al realizar esfuerzos moderados. Cinco días antes de su ingreso, su condición empeoró con sangrado digestivo alto, manifestado por evacuaciones negras abundantes (melena) y vómitos con sangre (hematemesis), sin causa aparente. Además, presentó aumento de volumen, dolor, enrojecimiento y limitación de movimiento en la pierna izquierda, signos compatibles con trombosis venosa profunda (coágulo en una vena profunda).\n\n**Hallazgos Clave**  \nDurante la hospitalización, se confirmó anemia severa que requirió transfusión de glóbulos rojos. Un ultrasonido Doppler de la pierna izquierda confirmó la presencia de trombosis venosa profunda. El ultrasonido abdominal mostró infartos (áreas de tejido muerto por falta de riego sanguíneo) en el bazo y el hígado, junto con cambios hepáticos crónicos probablemente relacionados con el uso de metotrexato. La endoscopía digestiva evidenció varices pequeñas sin sangrado activo. La tomografía computarizada (TAC) de tórax y abdomen reveló agrandamiento del hígado y bazo (hepatoesplenomegalia) y múltiples conglomerados de ganglios linfáticos en axilas, mediastino y alrededor de la aorta, lo que sugirió una posible infiltración tumoral.  \n\nLa biopsia de un ganglio axilar derecho mostró proliferación anormal de células linfoides (células del sistema inmunitario). El aspirado de médula ósea evidenció infiltración por células plasmáticas anormales y células reticulares, confirmando la afectación linfoplasmocitaria. Estos hallazgos permitieron establecer el diagnóstico de linfoma no Hodgkin (LNH) en estadio IV, que indica una enfermedad avanzada con compromiso de múltiples órganos y tejidos.\n\n**Interpretación Clínica**  \nEl cuadro clínico y los estudios realizados indican que la paciente presenta un linfoma no Hodgkin difuso de células B, un tipo de cáncer que afecta a las células del sistema inmunitario. La enfermedad se encuentra en una etapa avanzada y ha provocado complicaciones como trombosis venosa profunda, infartos en órganos abdominales y sangrado digestivo. La asociación con su antecedente de artritis reumatoide y el tratamiento con metotrexato puede haber influido en la evolución y presentación clínica.\n\n**Próximos Pasos**  \nLa paciente fue referida a un hospital de tercer nivel para realizar estudios adicionales de inmunohistoquímica (técnicas que permiten caracterizar con precisión el tipo de células tumorales), completar la estadificación de la enfermedad y comenzar el tratamiento específico con quimioterapia. El manejo multidisciplinario es fundamental para optimizar el pronóstico y controlar tanto la enfermedad linfoproliferativa como las complicaciones asociadas.",
+        "scores": {
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+  {
+    "article": "Un hombre de 56 años se presentó en el departamento de urgencias de nuestro hospital debido a una falta de aire repentina y un episodio de síncope mientras caminaba dentro de su casa. Se sometió a una prostatectomía laparoscópica asistida por robot para el carcinoma de próstata, 5 días antes de su presentación en el departamento de urgencias. Su curso postoperatorio en el hospital fue sin incidentes. En el departamento de urgencias, su presión arterial era de 94/54 mmHg, frecuencia cardiaca de 121 latidos por minuto, frecuencia respiratoria de 20 respiraciones por minuto, no tenía fiebre y su saturación de oxígeno era de 92% con 6 L por minuto de oxígeno a través de una cánula nasal. El examen cardiaco reveló S1S2, regular, taquicardia, sin murmullos/galopes/ruidos respiratorios. El examen respiratorio reveló ruidos respiratorios vesiculares normales bilaterales. Se observó que tenía edema de extremidad inferior izquierdo asimétrico. El electrocardiograma (ECG) reveló taquicardia sinusal, sin cambios en la onda ST-T. La troponina estaba levemente elevada a 0.120 ng/mL (rango de referencia: 0 a 0.020). La angiografía por tomografía computarizada (CTA) del tórax mostró embolia pulmonar bilateral extensa, con una gran carga de coágulos en ambas arterias pulmonares principales, evidencia de insuficiencia ventricular derecha aguda. El examen dúplex venoso mostró trombosis venosa profunda izquierda aguda. El ecocardiograma mostró fracción de eyección ventricular izquierda normal del 60% al 65%, movimiento septal anormal y aplanamiento del tabique interventricular, presión sistólica ventricular derecha de 49.7 mmHg, ventrículo derecho moderadamente dilatado, función ventricular derecha disminuida, excursión sistólica tricuspídea de 12.1 mm (normal 15 a 20 mm). Como la mayoría de la carga de coágulos era distal, no se consideró susceptible de extracción quirúrgica, ya que la cirugía reciente era una contraindicación importante para la trombólisis. El paciente comenzó con un goteo de heparina e inhaló óxido nítrico a 20 ppm junto con 40 mg de sildenafil oral cada 8 horas. Al día siguiente, el paciente estaba hemodinámicamente estable y su óxido nítrico inhalado se redujo. Repetir el ecocardiograma 48 horas desde la presentación inicial mostró un tamaño y función del ventrículo derecho mejorados. Su presión sistólica ventricular derecha disminuyó a 22.4 mmHg y su excursión sistólica tricuspídea mejoró a 17.8 mm. Recomendamos que continuara con sildenafil durante el mes siguiente después del alta junto con anticoagulación oral con un plan de seguimiento como paciente ambulatorio. El paciente dio su consentimiento por escrito para el tratamiento durante su hospitalización. El paciente y sus familiares estaban bien informados sobre el plan de atención completo y estuvieron de acuerdo con el plan de atención.\n\nMH - Insuficiencia cardiaca/*terapia farmacológica/etiología\nMH - Humanos\nMH - Hombre\nMH - Edad Media\nMH - Inhibidores de la fosfodiesterasa 5/*uso terapéutico\nMH - Embolismo pulmonar/*complicaciones\nMH - Agentes vasodilatadores/*uso terapéutico\nMH - Disfunción ventricular, derecha/terapia/etiología\n",
+    "gold_summary": "Paciente: Hombre, 56 años\n\nDiagnóstico final: Insuficiencia cardíaca derecha por embolia pulmonar\n\nSíntomas: síncope\n\nMedicación: —\n\nProcedimiento clínico: —\n\nEspecialidad: Cardiología\n\nSe trata de un informe de caso en el que se utilizó sildenafil como agente de rescate para lograr una mejora en el tamaño y la función del ventrículo derecho en un caso de inicio agudo de embolia pulmonar masiva con insuficiencia aguda del ventrículo derecho en el escenario en el que la terapia trombolítica sistémica estaba contraindicada.\n",
+    "synthetic_summary_eval": {
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+        "text": "Un hombre de 56 años se sintió muy cansado y se desmayó. Tenía problemas para respirar. Esto pasó porque tenía unos tapones en sus pulmones. Estos tapones hicieron que su corazón derecho se pusiera muy cansado. Los doctores no le pudieron dar una medicina fuerte para quitar los tapones porque él había tenido una operación hace poco. Entonces, le dieron otra medicina llamada sildenafil. Esta medicina ayudó a que su corazón mejorara y se hiciera más fuerte. Después de un tiempo, el hombre se sintió mejor y su corazón trabajó mejor. Los doctores cuidaron mucho de él y le explicaron todo a él y a su familia.",
+        "scores": {
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+        "text": "**Lo que le pasó al paciente**  \nUn hombre de 56 años tuvo problemas para respirar de repente y se desmayó mientras caminaba en su casa. Cinco días antes, había tenido una cirugía para tratar un cáncer de próstata. Después de la cirugía, parecía estar bien, pero luego presentó estos síntomas.\n\n**Qué encontraron los médicos**  \nEn el hospital, su presión arterial estaba baja y su corazón latía muy rápido. Tenía hinchazón en una pierna, lo que puede indicar un coágulo de sangre. Un examen especial llamado tomografía mostró que tenía coágulos grandes en las arterias de los pulmones, lo que se llama embolia pulmonar. Estos coágulos estaban afectando el lado derecho del corazón, que se encargaba de enviar sangre a los pulmones. También confirmaron que había un coágulo en la pierna.\n\n**Cómo lo trataron**  \nNo pudieron hacer una cirugía para quitar los coágulos porque la cirugía reciente del paciente era un riesgo. En lugar de eso, le dieron un medicamento llamado heparina para evitar que se formen más coágulos. Además, usaron óxido nítrico inhalado y un medicamento llamado sildenafil, que ayuda a relajar los vasos sanguíneos y mejora la función del corazón derecho.\n\n**Qué pasó después**  \nDespués de un día, el paciente estaba más estable. Dos días después, los exámenes mostraron que el corazón derecho había mejorado en tamaño y función. La presión en el corazón derecho bajó y su capacidad para bombear sangre mejoró. Los médicos recomendaron que siguiera tomando sildenafil y medicamentos para evitar coágulos durante un mes después de salir del hospital.\n\n**Por qué es importante este caso**  \nEste caso muestra que el sildenafil puede ayudar a mejorar la función del corazón derecho en personas con embolia pulmonar grave cuando no se puede usar la cirugía o medicamentos para disolver coágulos. Es una opción útil para tratar problemas del corazón causados por coágulos en los pulmones.",
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+        "text": "**Contexto**\n\nUn hombre de 56 años fue atendido en urgencias tras presentar una dificultad respiratoria súbita y un episodio de desmayo mientras caminaba en su casa. Cinco días antes, había sido sometido a una prostatectomía laparoscópica asistida por robot para tratar un cáncer de próstata, y su recuperación inicial había sido sin complicaciones. Al llegar al hospital, mostraba signos de inestabilidad hemodinámica, con presión arterial baja y frecuencia cardíaca elevada. Además, se detectó hinchazón en su pierna izquierda.\n\n**Hallazgos Clave**\n\n- El electrocardiograma mostró taquicardia sinusal sin alteraciones isquémicas.\n- La troponina, un marcador de daño cardíaco, estaba ligeramente elevada.\n- La tomografía computarizada del tórax reveló una embolia pulmonar bilateral extensa, es decir, coágulos grandes en ambas arterias pulmonares principales, causando insuficiencia aguda del ventrículo derecho (la cámara del corazón que bombea sangre hacia los pulmones).\n- Un estudio de ultrasonido vascular confirmó la presencia de un coágulo en la vena profunda de la pierna izquierda (trombosis venosa profunda).\n- El ecocardiograma evidenció que el ventrículo izquierdo funcionaba normalmente, pero el ventrículo derecho estaba dilatado y con función reducida, con signos de presión elevada en esta cavidad.\n\n**Interpretación Clínica**\n\nEl paciente presentaba insuficiencia cardíaca derecha aguda secundaria a una embolia pulmonar masiva. Debido a que la mayoría de los coágulos estaban en áreas distales y que la cirugía reciente representaba una contraindicación para tratamientos trombolíticos (medicamentos que disuelven coágulos), no se consideró adecuada la extracción quirúrgica ni la trombólisis sistémica.\n\nEn este contexto, se inició tratamiento con heparina para anticoagulación, óxido nítrico inhalado para mejorar la oxigenación y sildenafil oral (un inhibidor de la fosfodiesterasa tipo 5, que actúa como vasodilatador pulmonar) para reducir la presión en el ventrículo derecho y mejorar su función.\n\n**Evolución y Próximos Pasos**\n\nAl día siguiente, el paciente mostró estabilidad hemodinámica y mejoría en la función del ventrículo derecho, confirmada mediante ecocardiografía realizada 48 horas después del ingreso. La presión en el ventrículo derecho disminuyó significativamente y la capacidad de contracción mejoró.\n\nSe recomendó continuar con sildenafil durante un mes tras el alta hospitalaria, junto con anticoagulación oral, y realizar seguimiento ambulatorio para monitorear su recuperación. El paciente y su familia fueron informados detalladamente y dieron su consentimiento para el plan terapéutico.\n\n**Resumen**\n\nEste caso ilustra el uso exitoso de sildenafil como tratamiento complementario para mejorar la función del ventrículo derecho en un paciente con embolia pulmonar masiva y disfunción ventricular derecha aguda, en un escenario donde la trombólisis estaba contraindicada debido a una cirugía reciente. El manejo combinado permitió la estabilización clínica y la recuperación funcional sin necesidad de intervenciones quirúrgicas o trombolíticas.",
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+    "article": "Presentamos el caso de un hombre de 78 años con antecedentes conocidos de fibrilación auricular crónica, cardiopatía hipertensiva y miocardiopatía no isquémica. Tenía una reducción global de la fracción de eyección del ventrículo izquierdo del 40-45 %, y su ecocardiograma no mostraba anomalías significativas. El paciente había sido seguido en la clínica de cardiología ambulatoria, donde fue tratado por insuficiencia cardiaca crónica en estadio C del Colegio Americano de Cardiología (ACC) con síntomas de clase III de la Asociación del Corazón de Nueva York (NYHA). A pesar de varios cambios en sus diuréticos e intentos de controlar su estado de líquidos, ganó 40 libras de peso en un período de 3 meses, con un aumento significativo de la falta de aire. A medida que su descompensación de la insuficiencia cardiaca progresó, fue hospitalizado durante 8 días y tratado con furosemida intravenosa (IV). Debido a su clasificación de la NYHA y su ingreso al hospital por exacerbación de la insuficiencia cardiaca, se indicó y se realizó un monitoreo hemodinámico invasivo con implantación de CardioMEMS. La implantación de su CardioMEMS se realizó en Grand Blanc, Michigan, a una altitud de 837 pies con una presión atmosférica de 731.2 el 9 de abril de 2019. Las mediciones hemodinámicas iniciales del cateterismo cardiaco mostraron una presión sistólica PA de 45 mmHg, presión diastólica PA de 16 mmHg y una presión PA media de 30 mmHg. La presión auricular derecha fue de 21 mmHg, presión ventricular derecha de 44/17 mmHg y la presión media de la cuña pulmonar fue de 24 mmHg. El procedimiento se completó sin complicaciones y el paciente fue dado de alta el mismo día.\n\nTras la implantación de CardioMEMS, el paciente permaneció estable durante 4 semanas sin empeoramiento de los síntomas de insuficiencia cardiaca. Cumplió con las lecturas diarias de CardioMEMS con una PA media que osciló entre 27 y 31 mmHg, y una presión diastólica de PA de 17 a 21 mmHg. Estos hallazgos hemodinámicos globales fueron estables en comparación con los del momento de la implantación.\n\nEl paciente viajó a Denver, Colorado, durante cuatro días a una altitud de 5280 pies con una presión atmosférica de 596.8 atm el 5 de mayo de 2019. Las grabaciones del primer día de su visita mostraron un aumento de la presión sistólica de 44 mmHg a 73 mmHg, un aumento de la presión media de 30 mmHg a 53 mmHg y un aumento de la presión diastólica de 20 mmHg a 40 mmHg. Al mismo tiempo, notó un aumento significativo de la falta de aire y la hinchazón de las extremidades inferiores. No buscó atención médica, sino que se contactó con su cardiólogo primario en Michigan. Su oxígeno nasal de referencia se incrementó de 1 litro a 2 litros y su dosis de furosemida se duplicó de 40 mg diarios a dos veces al día. Afortunadamente, este tratamiento mejoró los síntomas del paciente y evitó la admisión hospitalaria. Debido a que se evitó la admisión hospitalaria, no se dispuso de valores de laboratorio, imágenes de diagnóstico y signos vitales clínicos.\n\nDurante su estancia hospitalaria de 4 días, sus presiones invasivas se mantuvieron altas, pero disminuyeron lentamente y se estabilizaron con una PA sistólica de 72 mmHg, una PA media de 49 mmHg y una PA diastólica de 35 mmHg el día previo a su regreso a Michigan. El quinto día, volvió a Michigan y sus mediciones de presión invasiva se normalizaron rápidamente, con una presión PA media de 29 mmHg y una presión PA diastólica de 20 mmHg. Ha seguido estando bien mientras estuvo en Michigan con diuréticos de mantenimiento continuos y un control diario de las presiones PA con su dispositivo CardioMEMS.\n\nMH - Envejecido\nMH - *Altitud\nMH - Monitoreo de presión arterial, ambulatorio\nMH - *Insuficiencia cardiaca/diagnóstico/etiología\nMH - Hospitalización\nMH - Humanos\nMH - Hombre\nMH - Arteria Pulmonar\n",
+    "gold_summary": "Presentamos el caso de un hombre de 78 años con una exacerbación de la insuficiencia cardiaca mientras viajaba a gran altitud. Se detectó un aumento de sus presiones arteriales pulmonares (PA) mediante su dispositivo CardioMEMS implantado. La comprensión del cambio esperado en los registros de presión de la PA ayudó a identificar una verdadera exacerbación de la insuficiencia cardiaca en nuestro paciente. Esto llevó a un cambio rápido en la terapia médica, que en última instancia evitó la hospitalización.\n",
+    "synthetic_summary_eval": {
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+        "text": "Había un hombre de 78 años que tenía problemas en su corazón. Él usaba un aparato especial para medir la presión en su corazón. Cuando viajó a un lugar muy alto, su corazón trabajó más fuerte y se sintió mal. El aparato mostró que su corazón estaba con mucha presión. Los doctores cambiaron sus medicinas rápido. Así, él no tuvo que ir al hospital y se mejoró.",
+        "scores": {
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+        "text": "**Lo que pasó con el paciente**  \nUn hombre de 78 años tenía problemas graves del corazón llamados insuficiencia cardiaca, que significa que su corazón no bombeaba la sangre tan bien como debería. Para ayudar a controlar su enfermedad, le pusieron un dispositivo llamado CardioMEMS, que mide la presión en una arteria del pulmón. Esto ayuda a los doctores a saber cómo está funcionando su corazón sin que él tenga que ir al hospital.\n\n**Qué sucedió durante su viaje**  \nEl paciente viajó a una ciudad alta llamada Denver, que está a mucha altura sobre el nivel del mar. Allí, las mediciones del CardioMEMS mostraron que la presión en su arteria pulmonar subió mucho. Esto fue un problema porque también empezó a sentir más dificultad para respirar y sus piernas se hincharon. Estas señales indicaron que su insuficiencia cardiaca empeoró.\n\n**Cómo ayudaron los doctores**  \nAunque no fue al hospital, el paciente llamó a su cardiólogo, quien le cambió el tratamiento aumentando la cantidad de un medicamento llamado diurético, que ayuda a eliminar el exceso de líquido del cuerpo. Gracias a este cambio rápido, sus síntomas mejoraron y evitó tener que ser hospitalizado.\n\n**Qué aprendimos de este caso**  \nEste caso muestra que el dispositivo CardioMEMS es muy útil para detectar cambios importantes en la presión del corazón, especialmente cuando una persona viaja a lugares con altitudes altas. Saber cómo cambian las presiones en estas situaciones ayuda a los médicos a actuar rápido y evitar complicaciones graves.",
+        "scores": {
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+      "B3": {
+        "text": "**Contexto**\n\nSe describe el caso de un hombre de 78 años con antecedentes de fibrilación auricular crónica, cardiopatía hipertensiva y miocardiopatía no isquémica, que presentaba insuficiencia cardiaca crónica en estadio C (según el Colegio Americano de Cardiología) con síntomas moderados a severos (clase III de la Asociación del Corazón de Nueva York). A pesar del tratamiento ambulatorio, experimentó un aumento significativo de peso y empeoramiento de la falta de aire, lo que llevó a una hospitalización y al implante de un dispositivo CardioMEMS para monitoreo invasivo de las presiones en la arteria pulmonar.\n\n**Hallazgos Clave**\n\nTras la implantación del CardioMEMS, el paciente mostró presiones pulmonares estables durante cuatro semanas en su entorno habitual en Michigan (a una altitud de 837 pies). Sin embargo, durante un viaje de cuatro días a Denver, Colorado (a 5280 pies de altitud), se registró un aumento marcado y sostenido de las presiones sistólica, media y diastólica en la arteria pulmonar. Paralelamente, el paciente experimentó un empeoramiento de sus síntomas de insuficiencia cardiaca, como aumento de la falta de aire y edema (hinchazón) en las extremidades inferiores.\n\n**Interpretación Clínica**\n\nEl aumento de las presiones pulmonares detectado por el CardioMEMS durante la estancia en altitud elevada reflejó una verdadera exacerbación de la insuficiencia cardiaca, más allá del efecto esperado por el cambio de altitud. Este monitoreo permitió diferenciar entre las variaciones fisiológicas normales y un deterioro clínico significativo. La rápida comunicación con el equipo médico facilitó la intensificación del tratamiento, incluyendo el aumento de la dosis de diuréticos y oxígeno suplementario, lo que mejoró los síntomas y evitó la necesidad de hospitalización.\n\n**Próximos Pasos**\n\nEl paciente continuó con un seguimiento estrecho mediante el dispositivo CardioMEMS tras su regreso a Michigan, donde las presiones pulmonares se normalizaron rápidamente. Se mantuvo con tratamiento diurético de mantenimiento y control diario de las presiones arteriales pulmonares para prevenir futuras descompensaciones. Este caso resalta la utilidad del monitoreo hemodinámico invasivo en pacientes con insuficiencia cardiaca, especialmente en situaciones que pueden alterar la fisiología cardiovascular, como los viajes a gran altitud.",
+        "scores": {
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+  {
+    "article": "Un hombre de 55 años, previamente sano, fue derivado al servicio de urgencias por su médico de cabecera, quejándose de una fiebre de 3 semanas de evolución, tos productiva, disnea y sibilancias. Tenía un historial de 80 paquetes-año de consumo de tabaco y un historial familiar positivo de cáncer de pulmón. Había sido tratado por su médico de cabecera con un ciclo de amoxicilina oral y prednisona oral, pero sus síntomas empeoraron. Cuando llegó al servicio de urgencias, su recuento de glóbulos blancos era de 16,4 × 109/L (rango normal: 4,0-10,0 × 109/L), el recuento de neutrófilos de 13,8 × 109/L (rango normal: 2,0-7,0 × 109/L), la proteína C reactiva era de 118 mg/L (normal: 0-5 mg/L) y el sodio sérico era de 112 mmol/L (rango normal: 136-145 mmol/L). Otros marcadores bioquímicos estaban dentro de los límites normales. Una radiografía de tórax mostró consolidación del lóbulo medio e inferior derecho con derrame pleural moderado asociado. Fue admitido y tratado como neumonía adquirida en la comunidad y el estudio confirmó el diagnóstico de SIADH.\n\nEl paciente empeoró a pesar de la administración intravenosa de piperacilina-tazobactam y de claritromicina oral, con empeoramiento de la consolidación en la repetición de la radiografía de tórax. El paciente fue trasladado a la unidad de cuidados intensivos y, posteriormente, se le realizó una intubación y ventilación. Una tomografía computarizada (TC) de su tórax reveló una masa hilar derecha con afectación mediastinal y adenopatía hilar derecha con consolidación de espacio aéreo extenso superpuesta. Una biopsia realizada durante la broncoscopia reveló células pequeñas, histológicamente monótonas, con núcleos ovoides oscuros. No se observaron nucleolos, y varias figuras mitóticas estaban presentes. Las células tienen un citoplasma estrecho y mal definido. La inmunohistoquímica realizada en las células tumorales mostró negatividad a CD45, AE1/AE3, positividad a TTF1. También se observaron sinapsina mínima focal y positividad a cromogranina A. Este perfil inmunohistoquímico fue consistente con un diagnóstico de cáncer de pulmón de células pequeñas.\n\nLa estadificación completa, que consistió en una tomografía computarizada del cerebro y tórax-abdomen-pelvis, confirmó una enfermedad en estadio extenso con metástasis suprarrenales. El estado funcional ECOG de la paciente era deficiente debido a una combinación de SCLC y dificultad respiratoria que requería ventilación artificial. Como las tasas de respuesta con quimioterapia en SCLC son generalmente altas, se inició un tratamiento quimioterápico doble en forma de carboplatino y etopósido mientras la paciente estaba intubada en la UCI.\n\nEl paciente respondió bien al tratamiento y fue extubado y trasladado a la sala de ventilación no invasiva. Una nueva tomografía computarizada de tórax después de 1 ciclo mostró una buena respuesta parcial al tratamiento.\n\nEn el día 3 del ciclo 2 de quimioterapia, la paciente desarrolló dolor en la parte inferior de la espalda y debilidad bilateral en las extremidades inferiores. El examen identificó paresia motora bilateral en las extremidades inferiores (grado 3 del Consejo de Investigación Médica [MRC]) y paresia sensorial. El examen sensorial reveló ausencia de tacto ligero, pinchazo, coordinación y propiocepción en las extremidades inferiores. El día 3 de etopósido se retrasó como resultado de los nuevos hallazgos neurológicos.\n\nSe realizaron un TAC cerebral, resonancia magnética (RM) cerebral y resonancia magnética (RM) de la columna para investigar los nuevos hallazgos neurológicos. Todos los resultados radiológicos fueron normales, sin evidencia de metástasis intracerebrales, accidente cerebrovascular, mielitis o enfermedad leptomeníngea. Además, no hubo evidencia radiográfica obvia de compresión de la médula espinal, ya sea por compresión extrínseca por depósito metastásico óseo o depósitos intramedulares o leptomeníngeos.\n\nDos días después, un examen neurológico de seguimiento reveló tetraplejía, MRC grado 0 en las extremidades superiores e inferiores. Todos los reflejos tendinosos profundos estaban ausentes. Los músculos de la cabeza y el cuello, la cognición y el habla no se vieron afectados, y el examen de los nervios craneales fue normal.\n\nLos análisis de sangre de rutina, incluida la proteína C reactiva y la velocidad de sedimentación de eritrocitos, fueron normales. Los análisis de sangre específicos, incluidos los de vitamina B12 en suero, folato, serología del VIH, serología de la enfermedad de Lyme, serología del virus de Epstein-Barr, serología de Brucella, anticuerpos tiroideos, pruebas de función tiroidea, ANCA, ENA, ANA y electroforesis de proteínas séricas, fueron negativos o normales. Se enviaron anticuerpos para las pruebas de sangre Hu, Ri y Yo, y todos fueron negativos. En este momento, se sospechó un diagnóstico de polineuropatía simétrica ascendente aguda motora y sensorial y se realizó una punción lumbar. Los resultados del líquido cefalorraquídeo (LCR) revelaron una proteína total elevada de 3.32 g/L (normal 0.15–0.45), y otros parámetros fueron normales, con una repetición 3 días después que mostró resultados similares. La citología del LCR fue negativa para la malignidad y el cultivo del LCR también fue negativo.\n\nLa electromiografía fue consistente con una polineuropatía difusa predominantemente motora; los potenciales sensoriales se conservaron, pero fueron de pequeña amplitud. Las conducciones motoras mostraron características axonales/desmielinizantes mixtas, que no eran típicas del síndrome de Guillain-Barré.\n\nSe realizaron estudios de electromiografía y conducción nerviosa para investigar la polineuropatía motora y sensorial aguda del paciente. Los estudios de conducción nerviosa revelaron lo siguiente:\n\n•Nervios motores:\n◦Las amplitudes del potencial de acción muscular compuesto (CMAP) se redujeron notablemente en los nervios tibial y cubital de forma bilateral (tibial: 1,2 mV; normal > 4 mV; cubital: 0,8 mV; normal > 3 mV).\n◦Las velocidades de conducción motora (MCV) se desaceleraron en los nervios tibial y cubital (tibial: 30 m/s; normal > 40 m/s; cubital: 34 m/s; normal > 50 m/s), lo que es coherente con la desmielinización.\n◦Las latencias motoras distales se prolongaron, con un patrón mixto axonal y desmielinizante.\n•Nervios sensoriales:\n◦Las amplitudes del potencial de acción nerviosa sensorial (SNAP) se conservaron, pero fueron de poca amplitud en los nervios surales y medianos (sural: 4 μV; normal > 10 μV; mediano: 6 μV; normal > 15 μV).\n◦Las velocidades de conducción sensorial (VCS) se encontraban dentro de los límites normales.\nLos hallazgos electrofisiológicos revelaron una polineuropatía predominantemente motora con características axonales y desmielinizantes mixtas, atípicas para los síndromes paraneoplásicos clásicos, que generalmente son predominantemente sensoriales y se caracterizan por la ausencia de SNAP.\n\nMientras tanto, mientras estas investigaciones estaban en curso, se inició al paciente con dexametasona intravenosa y 0.4 g/kg/día de inmunoglobulina intravenosa sin ninguna mejora sintomática.\n\n3. Resultados y seguimiento\nA pesar de una importante respuesta oncológica inicial a la quimioterapia, el estado neurológico del paciente se deterioró rápidamente. Después de 1 ciclo de carboplatino y etopósido, las imágenes confirmaron una respuesta parcial con una reducción en el tamaño del tumor. Sin embargo, el inicio de una polineuropatía motora y sensorial grave y ascendente condujo a un compromiso respiratorio. Esta disociación entre las respuestas oncológicas y neurológicas destaca la naturaleza agresiva y refractaria del SNP, incluso cuando el tratamiento del cáncer es efectivo. Aunque la dexametasona intravenosa y la inmunoglobulina intravenosa se administraron rápidamente, no lograron mejorar los resultados neurológicos.\n\nSe llevaron a cabo largas y repetidas discusiones multidisciplinares con el paciente y su familia sobre la admisión en la unidad de cuidados intensivos para recibir apoyo ventilatorio. El paciente estaba bien informado y consciente de que era poco probable que sus síntomas neurológicos fueran reversibles y, por lo tanto, optó por el mejor tratamiento de apoyo. El paciente falleció 3 semanas después de los síntomas iniciales. La decisión del paciente de rechazar el apoyo ventilatorio invasivo en favor de los cuidados paliativos pone de relieve las consideraciones éticas que rodean la calidad de vida en los síndromes paraneoplásicos de progresión rápida.\n",
+    "gold_summary": "Preocupaciones del paciente: Un hombre de 55 años con un historial de 80 años fumando presenta al hospital con un historial de 3 semanas de fiebres, tos productiva, disnea y sibilancias. No tenía comorbilidades significativas.\n\nDiagnóstico: Extensas investigaciones radiológicas revelaron una gran masa en el hilum derecho que comprimía el bronquio inferior derecho con depósitos suprarrenales metastásicos. Las investigaciones bioquímicas confirmaron el síndrome de secreción inadecuada de la hormona antidiurética, y la histología identificó un CPCP.\n\nIntervenciones: A pesar de iniciar una quimioterapia combinada con carboplatino y etopósido, el paciente desarrolló parálisis motora progresiva y pérdida sensorial en el transcurso de 4 días, lo que derivó en un diagnóstico de polineuropatía motora y sensorial aguda paraneoplásica.\n\nResultados: Su estado empeoró rápidamente y falleció 14 días después de la aparición de los síntomas debido a una insuficiencia respiratoria, lo que pone de relieve la agresividad de los síndromes paraneoplásicos.\n",
+    "synthetic_summary_eval": {
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+        "text": "Había un hombre que estaba muy enfermo. Tenía tos, fiebre y le costaba respirar. \n\nLos doctores encontraron un bulto grande en su pulmón. También tenía un problema en otras partes de su cuerpo. \n\nLe dieron medicinas para el cáncer, pero empezó a perder fuerza en sus piernas y brazos. No podía sentir bien ni moverlos. \n\nMuy rápido, se puso muy mal y no pudo respirar bien. Después de unos días, se fue al cielo. \n\nLos doctores dijeron que su enfermedad fue muy fuerte y difícil de curar.",
+        "scores": {
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+      },
+      "B2": {
+        "text": "**Lo que le pasó al paciente**  \nUn hombre de 55 años que había fumado mucho durante muchos años llegó al hospital con fiebre, tos con flema, dificultad para respirar y silbidos al respirar. Estos síntomas habían durado tres semanas. Antes de esto, estaba sano y no tenía otras enfermedades importantes.\n\n**Qué encontraron los médicos**  \nLas pruebas de imagen mostraron una masa grande en una parte del pulmón derecho que estaba bloqueando una vía respiratoria importante. También encontraron que el cáncer se había extendido a las glándulas suprarrenales, que están encima de los riñones. Un análisis de sangre mostró que tenía un problema llamado síndrome de secreción inadecuada de hormona antidiurética, que afecta el equilibrio de líquidos en el cuerpo. Al analizar una muestra del tumor, confirmaron que tenía un tipo de cáncer de pulmón llamado cáncer de pulmón de células pequeñas (CPCP).\n\n**Tratamiento y complicaciones**  \nEl paciente comenzó a recibir quimioterapia con dos medicamentos, carboplatino y etopósido, que son comunes para tratar este tipo de cáncer. Sin embargo, en pocos días, empezó a perder fuerza en las piernas y luego en los brazos, además de perder sensibilidad. Los médicos diagnosticaron una polineuropatía motora y sensorial aguda paraneoplásica, que es una enfermedad nerviosa grave relacionada con el cáncer, donde los nervios dejan de funcionar correctamente.\n\n**Qué pasó al final**  \nA pesar de que el tratamiento contra el cáncer estaba funcionando y el tumor había disminuido de tamaño, la enfermedad nerviosa empeoró rápidamente. El paciente tuvo problemas para respirar y falleció dos semanas después de que aparecieron los síntomas nerviosos. Este caso muestra lo agresivos y difíciles de tratar que pueden ser los síndromes paraneoplásicos, que son enfermedades causadas por la reacción del cuerpo al cáncer.",
+        "scores": {
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+          "ROUGE-2": 0.19841269841269843,
+          "ROUGE-L-Sum": 0.4189723320158103,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
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+      "B3": {
+        "text": "**Contexto**  \nUn hombre de 55 años, con un historial muy extenso de tabaquismo (equivalente a 80 paquetes-año) y sin enfermedades previas relevantes, acudió al hospital tras presentar durante tres semanas fiebre persistente, tos con expectoración, dificultad para respirar y sibilancias. Inicialmente fue tratado con antibióticos y corticoides, pero sus síntomas empeoraron, lo que motivó su ingreso hospitalario.\n\n**Hallazgos Clave**  \nLas pruebas radiológicas, incluyendo radiografía y tomografía computarizada (TC) de tórax, revelaron una masa grande en la región del hilio derecho del pulmón, que comprimía el bronquio inferior derecho, además de metástasis en las glándulas suprarrenales. Los análisis de sangre mostraron un síndrome de secreción inadecuada de hormona antidiurética (SIADH), que explica un nivel muy bajo de sodio en sangre. La biopsia pulmonar confirmó el diagnóstico de cáncer de pulmón de células pequeñas (CPCP), un tipo agresivo de tumor pulmonar.\n\n**Interpretación Clínica**  \nA pesar de iniciar un tratamiento estándar con quimioterapia combinada de carboplatino y etopósido, el paciente desarrolló rápidamente una polineuropatía aguda, es decir, un daño progresivo en múltiples nervios que afectó tanto la función motora (movimiento) como sensorial (sensaciones). En pocos días, presentó debilidad grave en las extremidades inferiores que progresó a parálisis completa de brazos y piernas, acompañada de pérdida sensorial. Las pruebas de imágenes cerebrales y de la médula espinal no mostraron metástasis ni compresión nerviosa, y los análisis de líquido cefalorraquídeo descartaron infección o infiltración tumoral directa. Los estudios electrofisiológicos indicaron una combinación de daño axonal (afectación de las fibras nerviosas) y desmielinizante (pérdida de la cubierta protectora de los nervios), un patrón atípico para síndromes paraneoplásicos clásicos, que suelen afectar principalmente la sensibilidad.\n\nSe inició tratamiento inmunomodulador con dexametasona (un corticoide) e inmunoglobulina intravenosa, pero no se observó mejoría neurológica. La rápida progresión de la debilidad llevó a insuficiencia respiratoria, requiriendo soporte ventilatorio.\n\n**Próximos Pasos y Resultado Final**  \nTras una cuidadosa discusión multidisciplinaria y con el paciente plenamente informado, se decidió no continuar con soporte ventilatorio invasivo debido a la baja probabilidad de recuperación neurológica y la mala calidad de vida esperada. El paciente falleció tres semanas después del inicio de los síntomas neurológicos.\n\nEste caso ilustra la agresividad y complejidad de los síndromes paraneoplásicos asociados al cáncer de pulmón de células pequeñas, donde la respuesta favorable al tratamiento oncológico puede contrastar con un deterioro neurológico rápido e irreversible. Además, resalta la importancia de abordar las decisiones éticas y de calidad de vida en el manejo de estas complicaciones graves.",
+        "scores": {
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
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+  {
+    "article": "El paciente presentado firmó el Consentimiento Informado y se cumplieron los demás principios éticos, respetando la Resolución 466/12 del Consejo Nacional de Ética en Investigación. Este informe de caso fue aprobado por el Comité de Ética en Investigación de la Universidad Federal de São Paulo (UNIFESP), bajo el dictamen número 4.455.365.\n\nEl paciente, de 66 años de edad y sexo masculino, acudió a una consulta de otorrinolaringología por presentar disfagia tipo atragantamiento con sólidos y reflujo nasal de alimentos desde hacía un año. Había sufrido un accidente automovilístico 13 años atrás y era diabético. Se le realizó una videoendoscopia de la deglución (VED), en la que se observó, en la evaluación estructural, una protuberancia de la pared posterior de la hipofaringe con residuo salival sobre la lesión. En la evaluación funcional, tras la ingesta de alimentos sólidos, se observó una restricción de la retroflexión de la epiglotis, una limitación de la elevación de la laringe y un reflujo nasal de alimentos, con gran cantidad de residuo alimentario por encima de la lesión, en la pared posterior de la faringe. En la prueba de maniobras posturales, empeoró la disfagia al extender el cuello y mejoró la eliminación al flexionar la cabeza. Se le realizó una tomografía computarizada (TC) de la columna cervical, solicitada para evaluar la naturaleza de la lesión, que mostró la presencia de osteofitos cervicales anteriores entre las vértebras C3 y C6, el mayor de 12 milímetros (mm) de longitud, que estrechaba la columna aérea al nivel de la orofaringe e hipofaringe. Se descartaron otras causas de disfagia y se trató al paciente con terapia de deglución y omeprazol, dirigido al reflujo faringolaríngeo. Se realizaron 6 sesiones de terapia de deglución individualizada, con el objetivo de compensar el mecanismo de deglución ante un obstáculo mecánico en la región faríngea. Los principales aspectos trabajados fueron: modificación de la textura de la dieta, evitando alimentos sólidos y secos; maniobras posturales de deglución, probadas durante la VED, especialmente el chin tuck (“cabeza hacia abajo” o “flexión de la cabeza”), que aumenta el espacio de la válvula (“abre la válvula”) y mejora la presión de transferencia faríngea del alimento; y ejercicios de fortalecimiento de la lengua, para superar la barrera mecánica de la orofaringe durante la expulsión del alimento. Se recomendó, si fuera necesario, alternar la ingesta de alimentos sólidos con líquidos, ante la percepción de alimentos estancados en la faringe. Se le indicó que repitiera los ejercicios de lengua en el hogar, 2 a 3 veces al día. Después de las sesiones iniciales, el paciente presentó una respuesta satisfactoria, y se lo controló trimestralmente durante el primer año y semestralmente a partir del segundo año. Se lo derivó para una evaluación ortopédica para analizar la viabilidad quirúrgica, y se optó por un tratamiento conservador debido a la buena compensación con medidas clínicas. Sigue en seguimiento ambulatorio desde hace 2 años, y mantiene una deglución eficiente, sin incidencia de complicaciones relacionadas con la disfagia. Se optó por mantener reevaluaciones periódicas, al menos una vez al año, para detectar precozmente un posible nuevo desequilibrio de la homeostasis de la deglución relacionado con el deterioro gradual de las funciones en el contexto de la presbifagia o el surgimiento de un nuevo factor agresor.\n",
+    "gold_summary": "Se describió el caso de un paciente de 66 años con disfagia por atragantamiento con sólidos y reflujo nasal de alimentos desde hacía un año. La videoendoscopia de la deglución mostró una protuberancia en la pared posterior de la faringe y, al ofrecer alimentos sólidos, una restricción de la retroflexión de la epiglotis, reflujo nasal de alimentos y una gran cantidad de residuos de alimentos sobre la lesión. La tomografía computarizada de la columna cervical identificó la presencia de osteofitos cervicales anteriores entre las vértebras C3 y C6, el más grande con una longitud anteroposterior de 12 milímetros, que estrechaba la columna aérea a nivel de la orofaringe e hipofaringe. El paciente fue tratado adecuadamente con fonoterapia para la deglución.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Un señor de 66 años tenía problemas para tragar comida dura. A veces, la comida se le iba por la nariz. Los doctores vieron que tenía un bulto en la garganta. También había huesos grandes que apretaban su garganta. Para ayudarlo, le enseñaron ejercicios para tragar mejor. Ahora puede comer sin problemas y está bien cuidado.",
+        "scores": {
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
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+      },
+      "B2": {
+        "text": "**Lo que Encontraron**\n\nUn hombre de 66 años tenía problemas para tragar alimentos sólidos y notaba que la comida a veces regresaba por la nariz desde hacía un año. Al hacerle un examen llamado videoendoscopia de la deglución, que consiste en usar una cámara pequeña para ver cómo traga, se vio una protuberancia (una especie de bulto) en la parte de atrás de su garganta. Cuando comía alimentos sólidos, su epiglotis (una parte que ayuda a que la comida no vaya a los pulmones) no se movía bien, y parte de la comida subía hacia la nariz, quedando residuos sobre el bulto.\n\n**Qué Significa**\n\nPara entender mejor la causa, le hicieron una tomografía computarizada, que es un tipo de radiografía especial que muestra imágenes detalladas de los huesos y tejidos. En esta imagen, encontraron que tenía unos crecimientos óseos llamados osteofitos en su columna cervical (el cuello), entre las vértebras C3 y C6. El más grande medía 12 milímetros y estaba presionando la vía aérea en la garganta, dificultando el paso normal de la comida.\n\n**Cómo lo Trataron**\n\nEl paciente recibió terapia para mejorar la forma en que traga, llamada fonoterapia. Esta terapia incluyó ejercicios para la lengua y cambios en la postura al comer, como inclinar la cabeza hacia adelante para facilitar el paso de la comida. También modificaron su dieta para evitar alimentos muy duros o secos. Gracias a este tratamiento, pudo mejorar su capacidad para tragar sin necesidad de cirugía y sigue siendo controlado regularmente para asegurarse de que no tenga problemas nuevos.",
+        "scores": {
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+          "ROUGE-L-Sum": 0.3923444976076555,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe presentó el caso de un hombre de 66 años que acudió a consulta por dificultad para tragar alimentos sólidos, acompañada de sensación de atragantamiento y reflujo nasal de alimentos, síntomas que persistían desde hacía un año. Entre sus antecedentes médicos destacaba un accidente automovilístico ocurrido 13 años antes y diabetes.  \n\n**Hallazgos Clave**  \nMediante una videoendoscopia de la deglución, se identificó una protuberancia en la pared posterior de la hipofaringe (parte baja de la garganta), con acumulación de saliva sobre esta lesión. Al ofrecer alimentos sólidos, se observó que la epiglotis (estructura que ayuda a proteger las vías respiratorias durante la deglución) tenía dificultad para doblarse hacia atrás, además de reflujo nasal de alimentos y una gran cantidad de restos alimentarios acumulados por encima de la protuberancia.  \n\nUna tomografía computarizada (TC) de la columna cervical reveló la presencia de osteofitos (crecimientos óseos anormales) en la parte anterior de las vértebras cervicales C3 a C6, siendo el más grande de 12 milímetros. Estos osteofitos comprimían la vía aérea en la región de la orofaringe e hipofaringe, lo que explicaba la dificultad para tragar.  \n\n**Interpretación Clínica**  \nEl diagnóstico principal fue disfagia mecánica causada por osteofitos cervicales que estrechaban la vía aérea y alteraban el mecanismo normal de la deglución. Se descartaron otras posibles causas de disfagia.  \n\n**Tratamiento y Seguimiento**  \nEl paciente recibió terapia de deglución personalizada, que incluyó:  \n- Modificación de la dieta para evitar alimentos sólidos y secos, facilitando la ingesta.  \n- Maniobras posturales durante la deglución, especialmente la flexión de la cabeza hacia adelante (chin tuck), que mejora el paso del alimento y reduce el reflujo nasal.  \n- Ejercicios de fortalecimiento de la lengua para superar la obstrucción mecánica y facilitar la expulsión del alimento.  \n\nAdemás, se prescribió omeprazol para tratar el reflujo faringolaríngeo (reflujo de ácido hacia la garganta). El paciente mostró una respuesta favorable tras seis sesiones de terapia y se mantuvo bajo seguimiento regular durante dos años, con controles trimestrales en el primer año y semestrales posteriormente.  \n\nSe evaluó la posibilidad de tratamiento quirúrgico para eliminar los osteofitos, pero se decidió continuar con un manejo conservador debido a la buena compensación clínica. Se recomendó continuar con ejercicios en casa y mantener evaluaciones periódicas al menos una vez al año, para detectar a tiempo cualquier deterioro en la función de la deglución asociado al envejecimiento o a nuevos factores.  \n\n**Conclusión**  \nEste caso ilustra cómo los osteofitos cervicales pueden causar disfagia mecánica significativa, y cómo un tratamiento integral basado en terapia de deglución y modificaciones dietéticas puede lograr una adecuada compensación funcional, evitando la necesidad de cirugía y mejorando la calidad de vida del paciente.",
+        "scores": {
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+  {
+    "article": "Una paciente caucásica de 18 años de edad se presentó en nuestra clínica con quejas de múltiples bultos palpables en sus senos bilateralmente. En el examen físico, la paciente tenía múltiples lesiones pigmentadas lentigosas en su cara, cuerpo y esclerótica bilateralmente, nevos azules en su tronco y extremidades superiores y una cara redonda con forma de luna.\n\nTras la evaluación ultrasonográfica, se encontraron múltiples nódulos compactos (fibroadenomas) en ambos senos, siendo el más grande en el cuadrante superior externo del seno izquierdo, con un diámetro de 7,8 cm.\n\nEn 2018, se le había practicado una tiroidectomía total con el diagnóstico de adenoma folicular y la extirpación de un nódulo grande del seno izquierdo, debido a su gran tamaño y al dolor que causaba, con un informe de histopatología que sugería un fibroadenoma con estroma mixóide.\n\nSe realizó una biopsia por escisión de dos nódulos de la mama derecha con diagnóstico de fibroadenoma mixto, lo que respaldó nuestro diagnóstico de complejo de Carney.\n\nEn la resonancia magnética se encontraron múltiples fibroadenomas compactos en ambos senos, con alta intensidad de señal en las imágenes T2 y T2/FS, con tabiques internos sin restricción de difusión, compatibles con múltiples fibroadenomas mixoides.\n\nAdemás, había un par de ganglios linfáticos axilares y prominentes ganglios linfáticos mamarios internos bilaterales.\n\nAdemás, se observó una anomalía en la densidad de los tejidos blandos en el mediastino anterior, que medía 11 mm de espesor máximo, lo que sugería un timo prominente.\n\nTodos los hallazgos anteriores sugerían la posibilidad de un complejo de Carney. Se realizó una evaluación adicional en el laboratorio. Los análisis hormonales no mostraron anomalías en los niveles de testosterona, prolactina, PTH y DHEA-S.\n\nLuego se realizó un análisis genético que arrojó como resultado la mutación del gen PRHAR1A, heterocigótico para una variante sin sentido de significancia incierta en el exón 3 de este gen. Esta mutación nunca se había informado en la base de datos gnomAD.\n\nSe realizaron pruebas genéticas a los padres y se determinó que solo el padre era portador de la misma mutación genética.\n\nSe discutieron con la paciente varios planes de tratamiento conservadores, pero ninguno demostró proporcionar una solución/tratamiento definitivo. En el pasado se realizó la extirpación de los lóbulos grandes con alivio temporal de los síntomas de dolor de la paciente y las cirugías recurrentes estaban afectando su calidad de vida. La paciente también tuvo varias sesiones con la psicóloga de nuestra clínica y fue evaluada a fondo antes de decidir la solución final de una mastectomía bilateral.\n\nLa paciente se sometió a una mastectomía bilateral con conservación de la piel y colocación subcutánea de expansores de tejidos (suave, Motiva Flora®). La histopatología informó múltiples fibroadenomas mixóides en ambos senos, compatibles con el síndrome de Carney, con interrupción de la arquitectura normal del parénquima mamario. Las figuras muestran el fibroadenoma de forma macroscópica e histológica.\n\nEl cuidado de la herida fue mínimo, se le recomendó a la paciente usar un sujetador médico y visitas regulares a la clínica ambulatoria para seguimiento y rellenado adicional de los expansores de tejidos a intervalos regulares hasta que se alcanzó el tamaño deseado. Paciente antes y después de la mastectomía. Después de un año se realizó una segunda cirugía y los expansores se reemplazaron con implantes de silicona permanentes (suaves, Motiva Ergonomic®) submusculares, con los mismos requisitos mínimos de cuidado de la herida y colocación del sujetador.\n",
+    "gold_summary": "Una paciente de 18 años de edad se presentó en nuestra clínica con múltiples bultos palpables en sus senos bilateralmente. En el examen físico, la paciente también tenía múltiples lesiones pigmentadas lentigosas en su cara, cuerpo y esclerótica, nevos azules en su tronco y extremidades superiores y un rostro redondo con forma de luna. El diagnóstico del síndrome de Carney se decidió mediante imágenes, biopsias y análisis genético. La paciente se sometió a una mastectomía bilateral como plan de tratamiento profiláctico con colocación de expansores de tejidos.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Una niña de 18 años tenía muchos bultos en sus pechos. También tenía manchas de colores en su cara y cuerpo. Los doctores hicieron pruebas y encontraron una enfermedad llamada síndrome de Carney. Para ayudarla, le quitaron los pechos y pusieron cosas suaves para que su cuerpo se vea bien.",
+        "scores": {
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+      "B2": {
+        "text": "**Lo que Encontraron en la Paciente**  \nUna joven de 18 años llegó a la clínica porque tenía varios bultos en ambos senos. Al examinarla, también notaron manchas oscuras en su piel y ojos, así como lunares azules en su cuerpo. Su cara tenía una forma redonda, parecida a una luna llena. Estas señales indicaron que podría tener algo llamado síndrome de Carney, que es una enfermedad rara que causa tumores benignos (no cancerosos) en diferentes partes del cuerpo.\n\n**Cómo Confirmaron el Diagnóstico**  \nPara estar seguros, los médicos hicieron varias pruebas. Usaron imágenes especiales como ultrasonidos y resonancias magnéticas para ver los bultos en sus senos. Además, tomaron pequeñas muestras de esos bultos (biopsias) para analizarlas bajo el microscopio. También hicieron un examen genético y encontraron un cambio en un gen llamado PRHAR1A, que está relacionado con este síndrome.\n\n**Qué Tratamiento Eligieron**  \nDespués de discutir varias opciones, decidieron hacer una mastectomía bilateral. Esto significa que le quitaron ambos senos para evitar problemas futuros, ya que los bultos seguían creciendo y causaban dolor. Para ayudar a que la piel se mantuviera y poder reconstruir después, colocaron unos dispositivos llamados expansores de tejidos, que poco a poco estiran la piel. Más tarde, estos expansores se reemplazaron por implantes de silicona para que la paciente tuviera una apariencia natural.\n\n**Importancia del Caso**  \nEste caso muestra cómo es importante combinar diferentes pruebas para diagnosticar enfermedades raras como el síndrome de Carney. También destaca que, a veces, el tratamiento puede ser difícil y requiere decisiones importantes para mejorar la calidad de vida del paciente.",
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+      },
+      "B3": {
+        "text": "**Contexto**\n\nUna joven caucásica de 18 años acudió a la clínica debido a la presencia de múltiples bultos palpables en ambos senos. Durante el examen físico, se observaron varias lesiones pigmentadas llamadas lentigos (manchas oscuras) en la cara, el cuerpo y la esclerótica (parte blanca del ojo), además de nevos azules (manchas pigmentadas) en el tronco y extremidades superiores, y una característica forma redonda de su rostro, conocida como cara en forma de luna.\n\n**Hallazgos Clave**\n\n- Estudios por ultrasonido y resonancia magnética revelaron múltiples nódulos compactos en ambos senos, identificados como fibroadenomas mixoides, siendo el más grande de 7,8 cm en el seno izquierdo.\n- Se realizaron biopsias por escisión de algunos nódulos, confirmando el diagnóstico de fibroadenomas mixtos.\n- Se detectó una anomalía en el mediastino anterior (área entre los pulmones), consistente con un timo prominente, y ganglios linfáticos axilares e internos aumentados de tamaño.\n- Los análisis hormonales no mostraron alteraciones significativas.\n- Un estudio genético identificó una mutación en el gen PRKAR1A, asociada con el síndrome de Carney, una enfermedad rara que se caracteriza por la presencia de tumores benignos en diferentes órganos y lesiones pigmentadas en la piel.\n\n**Interpretación Clínica**\n\nEl conjunto de hallazgos clínicos, imagenológicos, histopatológicos y genéticos permitió establecer el diagnóstico del síndrome de Carney. Este síndrome explica la presencia simultánea de múltiples fibroadenomas mamarios, lesiones pigmentadas cutáneas y otras anomalías observadas en la paciente.\n\n**Próximos Pasos y Tratamiento**\n\nDado que las cirugías previas para extirpar los fibroadenomas grandes solo proporcionaron alivio temporal y afectaban negativamente la calidad de vida de la paciente, se consideraron opciones de tratamiento más definitivas. Tras una evaluación psicológica y médica exhaustiva, se decidió realizar una mastectomía bilateral (extirpación completa de ambos senos) con conservación de la piel, seguida de la colocación subcutánea de expansores de tejidos para permitir la reconstrucción mamaria gradual.\n\nEl cuidado postoperatorio incluyó el uso de un sujetador médico y visitas regulares para el llenado progresivo de los expansores. Un año después, se reemplazaron estos expansores por implantes permanentes de silicona colocados debajo del músculo, con un manejo mínimo de la herida y seguimiento ambulatorio.\n\nEste enfoque permitió controlar los síntomas, mejorar la calidad de vida de la paciente y manejar de manera efectiva las manifestaciones mamarias del síndrome de Carney.",
+        "scores": {
+          "ROUGE-1": 0.3245283018867925,
+          "ROUGE-2": 0.17045454545454547,
+          "ROUGE-L-Sum": 0.3132075471698113,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      }
+    }
+  },
+  {
+    "article": "Una adolescente femenino de 13 años sin antecedentes médico-quirúrgicos de interés acude a Urgencias por dolor e impotencia funcional en muñeca izquierda tras caída mientras patinaba. Diagnosticada de lesión en torus metafisaria con extensión fisaria de radio distal clasificada como lesión Peterson tipo I, es inmovilizada durante cuatro semanas con férula antebraquiopalmar. Dos semanas después de la retirada de la férula, acude nuevamente a Urgencias al sentir un crujido en la muñeca, sin sobreesfuerzo asociado e impotencia para movilizar el primer dedo de la mano izquierda. Clínicamente presenta déficit de extensión activa interfalángica, efecto tenodesis patológico, edema local y asimetría macroscópica a la comparación con la extremidad contralateral. Se estudia con resonancia magnética nuclear (RMN), identificando imagen de solución de continuidad del EPL. Con la paciente bajo anestesia general, se procede al tratamiento quirúrgico mediante transferencia tendinosa del extensor propio del índice (EPI) al remanente distal del EPL con sutura tipo Pulvertaft de monofilamento no absorbible. En el postoperatorio se inmovilizó la extremidad las cuatro primeras semanas.\n\nTras cuatro semanas, se autorizó movilidad evidenciando recuperación de extensión del primer dedo de la mano izquierda y cicatrices discretamente hipertróficas, sin dolor. El seguimiento a la sexta, duodécima semana y al año no reporta complicaciones, con una restitución completa de la función y una puntuación de 0 en la escala PRWE (Patient Rated Wrist Evaluation).",
+    "gold_summary": "Se presenta el caso de una paciente adolescente femenino que, tras tratamiento conservador con férula de una fractura fisaria Peterson tipo I en radio, sufre a las seis semanas déficit agudo de extensión del pulgar, diagnosticada mediante examen clínico radiológico de rotura espontánea del extensor pollicis longus. Es tratada por medio de transferencia del extensor propio del índice (EPI) con resultados satisfactorios y recuperación de su actividad habitual al mes postoperatorio.",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Una niña de 13 años se cayó y se lastimó la muñeca. Le pusieron una tablita para que su hueso sanara. \n\nDespués de quitarle la tablita, su dedo pulgar no podía moverse bien. Los doctores vieron que un hilo que mueve el dedo se había roto. \n\nElla tuvo una operación para arreglar ese hilo con otro hilo de su mano. \n\nDespués de un mes, su dedo volvió a moverse bien y pudo hacer todo como antes.",
+        "scores": {
+          "ROUGE-1": 0.19753086419753083,
+          "ROUGE-2": 0.0125,
+          "ROUGE-L-Sum": 0.13580246913580246,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B2": {
+        "text": "Caso de una adolescente de 13 años con fractura en la muñeca que fue tratada con una férula. Seis semanas después, comenzó a tener dificultad para estirar el pulgar de la mano izquierda. Los médicos descubrieron que uno de los tendones que mueve el pulgar, llamado extensor largo del pulgar, se había roto sin que ella hiciera un esfuerzo fuerte. Para arreglarlo, realizaron una cirugía donde usaron otro tendón del dedo índice para reemplazar el que estaba roto. Después de la operación y un periodo de inmovilización, la paciente recuperó completamente el movimiento del pulgar y pudo volver a sus actividades normales en un mes.",
+        "scores": {
+          "ROUGE-1": 0.36082474226804123,
+          "ROUGE-2": 0.0625,
+          "ROUGE-L-Sum": 0.268041237113402,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe trata de una adolescente de 13 años, sin antecedentes médicos relevantes, que sufrió una caída mientras patinaba, ocasionándole dolor e incapacidad para mover la muñeca izquierda. Fue diagnosticada con una fractura en la parte distal del radio (hueso del antebrazo), específicamente una lesión fisaria clasificada como Peterson tipo I, y se le inmovilizó la muñeca con una férula durante cuatro semanas.\n\n**Hallazgos Clave**  \nDos semanas después de retirar la férula, la paciente volvió a urgencias tras sentir un crujido en la muñeca sin haber realizado un esfuerzo adicional. Presentaba incapacidad para extender (levantar) el primer dedo de la mano izquierda, hinchazón local y asimetría visible en comparación con la mano contraria. La exploración clínica mostró un déficit en la extensión activa del dedo y un signo llamado tenodesis patológico, que indica alteración en la función tendinosa. La resonancia magnética confirmó la ruptura del tendón extensor largo del pulgar (EPL), que es el tendón responsable de estirar el pulgar.\n\n**Interpretación Clínica**  \nLa ruptura espontánea del tendón extensor largo del pulgar es una complicación poco frecuente pero grave que puede ocurrir después de fracturas en la muñeca, incluso cuando el tratamiento inicial es conservador. Debido a la pérdida de función del EPL, se decidió realizar una cirugía para restaurar la movilidad del pulgar. El procedimiento consistió en transferir el tendón extensor propio del índice (EPI), que normalmente mueve el dedo índice, para sustituir la función del tendón lesionado del pulgar. La sutura se realizó mediante una técnica llamada Pulvertaft, que asegura una unión firme entre los tendones.\n\n**Próximos Pasos y Resultados**  \nTras la cirugía, la muñeca se inmovilizó durante cuatro semanas para favorecer la cicatrización. Posteriormente, se permitió la movilidad y la paciente mostró una recuperación completa de la extensión del pulgar sin dolor ni limitaciones funcionales. En los controles realizados a las 6, 12 semanas y al año, no se observaron complicaciones, y la paciente recuperó completamente su actividad habitual, con una puntuación de 0 en la escala PRWE, que indica ausencia de dolor y discapacidad en la muñeca.\n\nEn resumen, este caso ilustra cómo una complicación inesperada tras una fractura en la muñeca puede ser tratada con éxito mediante una transferencia tendinosa, logrando una recuperación funcional completa en una paciente adolescente.",
+        "scores": {
+          "ROUGE-1": 0.24603174603174602,
+          "ROUGE-2": 0.08764940239043825,
+          "ROUGE-L-Sum": 0.1904761904761905,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      }
+    }
+  },
+  {
+    "article": "Se remitió a un hombre de 73 años para una SAVR para tratar la regurgitación valvular aórtica sintomática (AR). Dos años antes, había presentado múltiples lesiones exantématicas. Una biopsia de piel reveló infiltración de células plasmáticas, lo que motivó la derivación a un hematólogo. La tomografía computarizada reveló linfadenopatía sistémica y hepatoesplenomegalia. Una biopsia renal realizada por disfunción renal confirmó la amiloidosis AA; una biopsia de ganglios linfáticos mostró plasmocitosis interfolicular y un centro germinal hiperplásico, consistente con el subtipo plasmático de iMCD, apoyado por niveles elevados de IL-6 en plasma. Se administró al paciente TCZ intravenoso (640 mg cada 2 semanas), junto con prednisolona (10 mg diarios). La erupción cutánea y la linfadenopatía se resolvieron. La ecocardiografía reveló AR puro moderado y agrandamiento ventricular izquierdo. Dado que el paciente experimentó gradualmente disnea de esfuerzo con agrandamiento ventricular izquierdo progresivo, se consideró necesaria la SAVR.\n\nDebido al sangrado por hemorroides y a la hepatosplenomegalia, se consultó a un hepatólogo; se diagnosticó cirrosis hepática de Child-Pugh grado A y varices esofágicas. Se realizó una conferencia preoperatoria del equipo, en la que participaron un intensivista y un farmacéutico, en la que se revisaron los mecanismos de acción de TCZ, las posibles complicaciones y el tratamiento perioperatorio. La cirugía se realizó 26 días después de la última dosis de TCZ. Durante el período perioperatorio, se suspendió el tratamiento con TCZ, mientras que se continuó con los esteroides por vía oral o intravenosa. Las medidas preventivas para las infecciones del sitio quirúrgico (SSI) incluyeron la detección de portadores nasales de Staphylococcus aureus resistentes a la meticilina, la preparación antiséptica de la piel, la terapia antibiótica profiláctica y el control de la hiperglucemia. El cultivo nasal fue positivo para Staphylococcus coagulasa negativo. Se realizó el reemplazo de la válvula aórtica quirúrgica a través de una esternotomía media bajo circulación extracorpórea, con 65 minutos de tiempo de isquemia cardiaca y 128 minutos de tiempo de circulación extracorpórea. Se requirieron transfusiones de sangre, incluidos glóbulos rojos, plasma y plaquetas; el paciente fue extubado al día siguiente. Los hallazgos patológicos revelaron un espesamiento fibroso focal sin depósitos amiloides.\n\nLa herida quirúrgica no mostró signos de infección en el día 2 postoperatorio; se inició la terapia de presión negativa en la herida (NPWT) en la herida quirúrgica cerrada para evitar SSI. La terapia de presión negativa en la herida se interrumpió en el día 13 postoperatorio, sin aparente SSI. El paciente fue dado de alta en el día 17 postoperatorio sin ningún signo de infección.\n\nAunque los niveles de IL-6 aumentaron temporalmente los días 1 y 2 después de la operación, disminuyeron progresivamente hasta el día 24 después de la operación, y luego volvieron a aumentar al reanudarse el tratamiento con TCZ. Los niveles de proteína C reactiva (PCR) estaban ligeramente elevados, alcanzando un máximo de 0,56 mg/dL el día 2 después de la operación. Para el día 24 después de la operación, la PCR había aumentado a 1,06 mg/dL sin infección. Antes del aumento de la PCR, los niveles del factor de crecimiento endotelial vascular aumentaron el día 13 después de la operación.\n\nEl paciente no experimentó recurrencia de erupción cutánea o linfadenopatía durante el período perioperatorio. Los niveles de creatinina postoperatorios aumentaron temporalmente, pero volvieron a los niveles preoperatorios el día 24. Se reanudó el tratamiento con tocilizumab el día 30 postoperatorio tras confirmar la ausencia de infección, incluida la IFI.\n",
+    "gold_summary": "Un hombre de 73 años con enfermedad de Castleman, tratado con TCZ, se sometió a un reemplazo de la válvula aórtica por medio de esternotomía mediana para la regurgitación de la válvula aórtica con falta de aire al hacer ejercicio. Se implementaron medidas integrales para prevenir la infección del sitio quirúrgico junto con un examen minucioso durante el período perioperatorio. Tocilizumab se interrumpió 26 días antes de la cirugía y se reanudó 30 días después de la cirugía, durante los cuales los niveles de IL-6 en plasma disminuyeron. No hubo evidencia de infección o exacerbación de la enfermedad de Castleman. Los niveles del factor de crecimiento endotelial vascular aumentaron antes de un aumento en los niveles de proteína C reactiva después del alta hospitalaria y antes de la reanudación de TCZ.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Un hombre de 73 años estaba enfermo y tenía problemas en su corazón. Tenía dificultad para respirar cuando caminaba. Los doctores le hicieron una operación para cambiar una parte del corazón llamada válvula.\n\nAntes de la operación, dejaron de darle un medicamento llamado TCZ para que no tuviera problemas. También cuidaron mucho que no se le hiciera una infección en la herida.\n\nDespués de la operación, el hombre se fue mejorando. No tuvo infecciones ni se puso más enfermo. Cuando estuvo listo, le dieron otra vez el medicamento para ayudarlo.\n\nLos doctores vieron que su cuerpo estaba mejor y que el medicamento funcionaba bien. El hombre pudo salir del hospital sin problemas.",
+        "scores": {
+          "ROUGE-1": 0.3104693140794224,
+          "ROUGE-2": 0.08727272727272728,
+          "ROUGE-L-Sum": 0.3104693140794224,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B2": {
+        "text": "**Lo que le pasaba al paciente:**  \nUn hombre de 73 años tenía una enfermedad llamada enfermedad de Castleman, que afecta a los ganglios linfáticos y causa inflamación. También tenía un problema en el corazón llamado regurgitación de la válvula aórtica, que significa que la válvula no cerraba bien y eso le causaba dificultad para respirar al hacer ejercicio.\n\n**Qué tratamiento recibió:**  \nPara mejorar su corazón, los médicos le hicieron una cirugía para reemplazar la válvula aórtica. Antes de la operación, el paciente recibía un medicamento llamado tocilizumab (TCZ), que ayuda a controlar la inflamación en la enfermedad de Castleman. Este medicamento se detuvo 26 días antes de la cirugía para evitar problemas durante la operación y se volvió a empezar 30 días después, cuando ya estaba seguro.\n\n**Cómo cuidaron al paciente durante la cirugía:**  \nLos médicos tomaron muchas precauciones para evitar infecciones en la herida de la cirugía. Revisaron si tenía bacterias en la nariz, limpiaron bien la piel antes de operar, usaron antibióticos preventivos y controlaron su azúcar en sangre. Además, usaron una técnica especial llamada terapia de presión negativa en la herida para ayudar a que sanara sin infecciones.\n\n**Qué pasó después de la cirugía:**  \nEl paciente no tuvo infecciones ni empeoramiento de su enfermedad durante el tiempo que estuvo sin tomar el medicamento. Los niveles en sangre de una proteína llamada IL-6, que está relacionada con la inflamación, bajaron después de la cirugía y subieron nuevamente cuando volvió a tomar el medicamento. También observaron cambios en otras proteínas relacionadas con la inflamación, pero el paciente se recuperó bien y pudo salir del hospital sin problemas.\n\n**En resumen:**  \nEste caso muestra que es posible hacer una cirugía importante en un paciente con enfermedad de Castleman que usa tocilizumab, siempre que se tomen medidas cuidadosas para prevenir infecciones y se controle bien el tratamiento antes y después de la operación.",
+        "scores": {
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+          "ROUGE-2": 0.20866141732283464,
+          "ROUGE-L-Sum": 0.3803921568627451,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B3": {
+        "text": "**Contexto:**  \nUn hombre de 73 años con diagnóstico de enfermedad de Castleman idiopática multicéntrica (iMCD), un trastorno inflamatorio caracterizado por crecimiento anormal de ganglios linfáticos y producción elevada de interleucina-6 (IL-6), fue tratado con tocilizumab (TCZ), un medicamento que bloquea la acción de esta proteína inflamatoria. Además, presentaba regurgitación valvular aórtica (fuga en la válvula del corazón que permite el retorno de sangre), que causaba dificultad progresiva para respirar durante el esfuerzo, y se decidió realizar un reemplazo quirúrgico de la válvula aórtica (SAVR) mediante una incisión en el esternón (esternotomía media).\n\n**Hallazgos Clave y Manejo Perioperatorio:**  \nAntes de la cirugía, el paciente recibió cuidados especializados para minimizar el riesgo de infecciones en el sitio quirúrgico, incluyendo la detección y manejo de bacterias en la nariz, preparación cuidadosa de la piel, uso profiláctico de antibióticos y control estricto del azúcar en sangre. El tratamiento con tocilizumab se suspendió 26 días antes de la operación para reducir posibles complicaciones inmunológicas, mientras que la administración de esteroides continuó para controlar la inflamación. La cirugía se realizó con éxito bajo circulación extracorpórea (máquina que mantiene la circulación y oxigenación de la sangre durante la operación), requiriendo transfusiones de sangre, y el paciente fue extubado al día siguiente sin complicaciones inmediatas.\n\nDurante el postoperatorio, no se observaron signos de infección en la herida quirúrgica, y se utilizó terapia de presión negativa (una técnica para favorecer la cicatrización y prevenir infecciones) hasta el día 13 después de la cirugía. El paciente fue dado de alta el día 17 sin evidencia de infección ni recurrencia de los síntomas de la enfermedad de Castleman, como erupciones cutáneas o aumento de ganglios linfáticos.\n\n**Interpretación Clínica:**  \nLos niveles de IL-6 en plasma aumentaron temporalmente en los primeros días tras la cirugía, lo cual es esperado debido a la respuesta inflamatoria postoperatoria, pero luego disminuyeron progresivamente hasta el día 24. Posteriormente, al reanudarse el tratamiento con tocilizumab el día 30, los niveles de IL-6 volvieron a aumentar, reflejando la acción del medicamento. La proteína C reactiva (PCR), un marcador de inflamación, mostró un leve aumento sin evidencia de infección, y se observó un incremento previo en el factor de crecimiento endotelial vascular, una proteína relacionada con la reparación y formación de vasos sanguíneos, lo que podría indicar procesos de recuperación tisular.\n\nLa función renal mostró un aumento temporal en los niveles de creatinina después de la cirugía, pero volvió a los valores previos al alta, indicando una recuperación adecuada de la función renal.\n\n**Próximos Pasos y Conclusiones:**  \nEl manejo cuidadoso del tratamiento inmunosupresor y las medidas preventivas implementadas permitieron realizar con éxito el reemplazo valvular en un paciente con enfermedad de Castleman sin complicaciones infecciosas ni exacerbación de la enfermedad. La reanudación del tocilizumab se realizó de forma segura tras confirmar la ausencia de infección. Este caso resalta la importancia de una planificación multidisciplinaria y un seguimiento riguroso en pacientes con enfermedades inflamatorias complejas sometidos a cirugía mayor.",
+        "scores": {
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
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+      }
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+  },
+  {
+    "article": "Se trata de un paciente de sexo masculino de cuatro meses de edad, originario del centro de México y con dos hermanos hombres sanos. Durante el primer trimestre de gestación, su madre hipotiroidea consumió drogas. No obstante, el infante nació con peso y talla adecuados, fue alimentado con leche materna y recibió la vacuna del bacilo de Calmette-Guérin (BCG), sin desarrollo de cicatriz. La madre del paciente era prisionera en una cárcel y, junto con el bebé, compartían una celda insalubre con dos personas más.A los cuatro meses, el paciente fue valorado médicamente por un tumor doloroso en la región axilar izquierda. En la radiografía de tórax se observaron imágenes sugestivas de fracturas costales; se sospechó de maltrato infantil por parte de la madre, y el infante fue hospitalizado en un hospital pediátrico. Se determinó el peso (4.190 g) y la talla (58 cm) –por debajo del percentil tres–, saturación de oxígeno del 70 %, fiebre, tos, aumento de volumen en la región axilar izquierda, además de dolor, rubor y calor. En el cuadro hemático se encontró: hemoglobina de 8,8 g/dl (11,0 - 12,6), 29,3 × 109 leucocitos/L (6,0 - 17,5), 18,4 × 109 neutrófilos/L (1,0 - 8,5), 7,0 × 109 linfocitos/L (4,0 - 13,5), 3,5 × 109 monocitos/L, 459 × 109 plaquetas/L (150 - 350) y proteína C reactiva igual a 16 mg/L (< 3,0). En la primera tomografía toracoabdominal se observaron imágenes de un absceso en la región axilar izquierda, lesiones líticas en las costillas 3 a 6, neumonía apical izquierda, nódulos pulmonares en ambos pulmones y ganglios linfáticos cervicales y mediastinales incrementados de tamaño. En la biopsia del absceso axilar izquierdo se reportó miositis y paniculitis supurativa. Solo se hizo cultivo para bacterias del líquido broncoalveolar, el cual fue negativo, y la PCR para el complejo Mycobacterium tuberculosis fue negativa. Después de 41 días de hospitalización y de haber recibido dos esquemas de antimicrobianos –ceftriaxona-clindamicina y cefepima-vancomicina–, el paciente fue dado de alta.\n\nDos meses después, a los ocho meses de edad, reingresó al hospital por fiebre, irritabilidad y un absceso supurante en la escápula izquierda. En el cuadro hemático se encontró: hemoglobina de 10,8 g/dl (10,5 - 12), 21,2 × 109 leucocitos/L (6 - 17), 12,2 × 109 neutrófilos/L (1,5 - 8,5), 7,5 × 109 linfocitos/L (4 - 10,5), 1,2 × 109 monocitos/L (600), y 583 × 109 plaquetas/L (150 - 350); la prueba para la detección sérica de HIV fue negativa. En la tomografía de tórax se observó una consolidación apical izquierda, bronquiectasias, lesiones líticas en las costillas 2 a 7 y en las vértebras dorsales 2 a 7, además de una colección de líquido multiloculado; en el ultrasonido se encontró una fístula asociada con el absceso escapular. El paciente recibió piperacilina-tazobactam, que se sustituyó después por voriconazol al detectarse Aspergillus fumigatus en el cultivo de la muestra de secreción del absceso. Dada la recurrencia y la gravedad de la infección, se sospechó un error innato de la inmunidad. La prueba de dihidrorrodamina resultó sin producción de especies reactivas de oxígeno y la expresión de gp91phox en los neutrófilos fue nula, estableciéndose así el diagnóstico de enfermedad granulomatosa crónica ligada al cromosoma X. La variante patógena detectada por la secuenciación de nueva generación fue c.80_83del/Y (p.Val27Glyfs*33) en CYBB. La madre resultó portadora de la variante (c.80_83del/WT). No fue posible estudiar genéticamente a sus dos hermanos mayores, de sexo masculino, y aparentemente sanos. El paciente fue dado de alta después de 65 días de hospitalización y tratamiento con voriconazol por 28 días. Se inició profilaxis antibiótica diaria con trimetoprim-sulfametoxazol y profilaxis antifúngica con fluconazol dos veces a la semana. Dos meses después, al año de edad, el infante reingresó debido a una neumonía multifocal, por la cual requirió asistencia respiratoria mecánica. Se detectó el antígeno galactomanano en el suero y A. fumigatusen el cultivo del líquido del lavado broncoalveolar, por lo que se inició nuevamente tratamiento con voriconazol. El paciente sufrió una falla orgánica múltiple y falleció un mes después de su ingreso.\n",
+    "gold_summary": "Se presenta el caso de un infante con enfermedad granulomatosa crónica y aspergilosis invasiva. Se trata de un lactante de sexo masculino de cuatro meses de edad, de madre hipotiroidea y con quien convive en la celda de la cárcel. El infante presentó tumores en la región axilar izquierda y la radiografía de tórax sugirió fracturas costales; fue hospitalizado ante la sospecha de maltrato infantil. En la tomografía de tórax se observó un absceso axilar, osteólisis de costillas, neumonía y nódulos pulmonares; el paciente recibió antibióticos de amplio espectro y fue dado de alta. A los ocho meses, reingresó por fiebre y extensión del absceso purulento hacia la región escapular izquierda; en la tomografía se observaron imágenes de empeoramiento de la condición. Se aisló Aspergillus fumigatus de la secreción del absceso y se diagnosticó aspergilosis invasiva; se inició tratamiento con voriconazol por 28 días. Mediante la prueba de dihidrorrodamina, se diagnosticó enfermedad granulomatosa crónica causada por la variante patógena c.80_83del/Y del gen CYBB, portada por la madre (c.80_83del/WT). A los 12 meses, el paciente reingresó nuevamente por aspergilosis invasiva, resistente al tratamiento, con desenlace fatal.",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Había un bebé que estaba muy enfermo. Tenía un bulto doloroso en su brazo y problemas para respirar. Los doctores lo cuidaron mucho y le dieron medicinas para que mejorara.\n\nDespués, el bebé se volvió a enfermar. Tenía fiebre y otro bulto que dolía mucho. Los doctores encontraron un hongo que le hacía daño. Le dieron medicinas especiales para el hongo.\n\nLos doctores hicieron pruebas y vieron que el bebé tenía un problema en su cuerpo que no lo dejaba pelear bien contra las enfermedades. Su mamá también tenía ese problema, pero no estaba enferma.\n\nEl bebé estuvo en el hospital muchas veces. Aunque los doctores hicieron todo lo posible, el bebé se puso muy mal y no pudo mejorar. Los doctores y su familia lo cuidaron con mucho amor.",
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+      "B2": {
+        "text": "**Caso de un Bebé con Problemas en el Sistema Inmunológico y una Infección Grave**\n\nEste es el caso de un bebé de cuatro meses que vivía con su madre en una cárcel. Su madre tenía problemas de tiroides y durante el embarazo tomó medicamentos. El bebé nació con buen peso y tamaño, pero luego presentó un bulto doloroso en la axila izquierda. Al hacerle una radiografía, los médicos vieron posibles fracturas en sus costillas, por lo que pensaron que podría estar sufriendo maltrato. Fue hospitalizado para recibir atención.\n\nEn estudios más detallados, encontraron un absceso (una acumulación de pus) en la axila, daño en varias costillas, neumonía y nódulos en los pulmones. El bebé recibió antibióticos fuertes y fue dado de alta después de mejorar un poco.\n\nA los ocho meses, volvió al hospital con fiebre y un absceso que se extendió hacia la parte superior de la espalda. Nuevas imágenes mostraron que la infección había empeorado. En el pus del absceso encontraron un hongo llamado Aspergillus fumigatus, que puede causar infecciones graves, especialmente en personas con defensas bajas. Por eso, le dieron un medicamento antifúngico llamado voriconazol.\n\nLos médicos sospecharon que el bebé tenía un problema en su sistema inmunológico, que es el que nos protege de las infecciones. Hicieron una prueba llamada dihidrorrodamina, que mostró que sus células defensivas no podían producir sustancias necesarias para combatir gérmenes. Esto confirmó que tenía una enfermedad llamada enfermedad granulomatosa crónica, que afecta la capacidad del cuerpo para luchar contra ciertas infecciones. Esta enfermedad fue causada por un cambio en un gen llamado CYBB, que heredó de su madre.\n\nA pesar del tratamiento, a los 12 meses el bebé volvió a enfermar gravemente por la misma infección de Aspergillus. La infección no respondió bien a los medicamentos y, lamentablemente, el bebé falleció debido a una falla de varios órganos.\n\n**Qué Significa Este Caso**\n\nEste caso muestra cómo un problema genético en el sistema inmunológico puede hacer que un bebé sea muy vulnerable a infecciones graves, como las causadas por hongos. También resalta la importancia de diagnosticar estas enfermedades temprano para intentar proteger a los pacientes con tratamientos adecuados.",
+        "scores": {
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+      "B3": {
+        "text": "**Contexto**  \nSe describe el caso de un lactante varón de cuatro meses originario del centro de México, cuya madre presentaba hipotiroidismo y con quien vivía en condiciones precarias dentro de una cárcel. El bebé nació con peso y talla adecuados, pero a los cuatro meses desarrolló un tumor doloroso en la axila izquierda. Ante la sospecha inicial de maltrato infantil, debido a fracturas costales observadas en radiografías, fue hospitalizado para evaluación y tratamiento.\n\n**Hallazgos Clave**  \nDurante la hospitalización inicial, las imágenes de tomografía mostraron un absceso en la axila izquierda, lesiones destructivas en varias costillas (osteólisis), neumonía en el lóbulo superior del pulmón izquierdo y nódulos pulmonares bilaterales, además de ganglios linfáticos aumentados de tamaño. El análisis de sangre reveló anemia, elevación de leucocitos y marcadores inflamatorios, indicativos de infección activa. A pesar de recibir antibióticos de amplio espectro, el paciente presentó recurrencia de la infección a los ocho meses, manifestada por fiebre y un absceso supurante que se extendió hacia la región escapular izquierda. Nuevas imágenes mostraron empeoramiento con consolidación pulmonar, bronquiectasias (dilatación anormal de las vías respiratorias), lesiones óseas adicionales y formación de fístulas. En el cultivo de la secreción del absceso se aisló Aspergillus fumigatus, un hongo que causa infecciones invasivas en personas con alteraciones inmunológicas.\n\n**Interpretación Clínica**  \nLa recurrencia y gravedad de las infecciones, junto con la presencia de infecciones fúngicas invasivas, sugirieron un defecto en la inmunidad innata. La prueba funcional de dihidrorrodamina, que evalúa la capacidad de los neutrófilos (un tipo de glóbulo blanco) para producir especies reactivas de oxígeno necesarias para eliminar microorganismos, fue negativa. Además, no se detectó la proteína gp91^phox en neutrófilos, confirmando el diagnóstico de enfermedad granulomatosa crónica ligada al cromosoma X, una condición genética que afecta la capacidad del sistema inmunitario para combatir ciertas infecciones. La secuenciación genética identificó una mutación patógena específica (c.80_83del/Y) en el gen CYBB, responsable de esta enfermedad, y se confirmó que la madre era portadora de esta variante.\n\n**Próximos Pasos y Evolución**  \nTras el diagnóstico, el paciente recibió tratamiento antifúngico con voriconazol y profilaxis antibiótica y antifúngica para prevenir nuevas infecciones. Sin embargo, a la edad de un año, volvió a ingresar al hospital con neumonía multifocal grave causada nuevamente por Aspergillus fumigatus, que requirió soporte respiratorio avanzado. A pesar del tratamiento, el paciente desarrolló falla orgánica múltiple y falleció un mes después.\n\n**Resumen Final**  \nEste caso ilustra la presentación clínica y evolución de un lactante con enfermedad granulomatosa crónica ligada al cromosoma X, caracterizada por infecciones recurrentes graves, incluyendo aspergilosis invasiva. La identificación temprana de esta enfermedad genética es crucial para el manejo adecuado y la prevención de complicaciones fatales, aunque en este caso la gravedad y recurrencia de las infecciones condujeron a un desenlace fatal.",
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+    "article": "Se trata de un hombre de 66 años de edad que vive en la ciudad de Juan Bautista Alberdi de la provincia de Buenos Aires, con antecedentes de hipertensión arterial y trastorno obsesivo compulsivo. Su medicación habitual incluía amlodipina, quetiapina, venlafaxina y ácido valproico. Consultó por presentar fiebre de 39ºC de cuatro días de evolución sin síntomas asociados y se internó para estudio en sala general. Al examen de ingreso se constató un paciente lúcido, sin foco motor, sin trastorno sensitivo ni rigidez de nuca (escala de coma de Glasgow (GCS) 15/15). El resto del examen físico y el laboratorio general no presentaron particularidades. Los cultivos de sangre y orina resultaron negativos, y la tomografía computarizada de encéfalo, tórax, abdomen y pelvis no mostró afecciones. A las 24 horas agregó episodios de desorientación témporo-espacial que alternaban con otros de somnolencia (GCS 13/15). Al examen físico se constató temblor grueso distal en los cuatro miembros. El examen del LCR informó: líquido incoloro, límpido, y aspecto post centrifugado también límpido. Recuento de leucocitos 310/mm3 (mononucleares 54%, polimorfonucleares 46%), hematíes < de 1000/mm3, proteínas 0.76 g/l, glucosa 54 mg/dl (glucemia 120 mg/dl), y ácido láctico 21 mg/dl. Se inició tratamiento empírico con aciclovir 10 mg/kg endovenoso cada 8 horas. Se solicitaron en LCR: PCR para virus de herpes simple (VHS) y para virus de encefalopatía equina del oeste (VEEO) que resultaron no reactivas. Sin embargo, la IgM (ELISA) para EEO resultó positiva en suero y en LCR a los diez días. La RMN de encéfalo evidenció aumento en la intensidad en secuencias FLAIR y T2 a nivel de la región dorsal del tronco encefálico (tanto protuberancial, como también bulbar y mesencefálico), ambos pedúnculos cerebrales y ganglios de la base, con afectación bilateral y ligero predominio ganglio basal derecho. También se observaron múltiples imágenes focales hiperintensas en la sustancia blanca de ambos hemisferios cerebrales. El paciente evolucionó con deterioro del sensorio (GCS 8/15), sin protección de la vía aérea, por lo que ingresó a UTI. Requirió intubación y ventilación mecánica, con utilización de sedación y analgesia. Al ingreso a UTI presentaba: estado ácido-base (EAB) arterial: pH 7.11, pCO2 136 mmHg, pO2 75 mmHg, bicarbonato 43 mEq/l, exceso de base 11 mEq/l, saturación 88% (Con FIO2 21%), ácido láctico 11.5 mg/dl. Se inició la ventilación mecánica con un volumen minuto respiratorio (VMR) de 9.8 litros (volumen tidal 490 ml que corresponde a 6 ml/kg de peso teórico, frecuencia respiratoria 20 por minuto, presión positiva al final de espiración (PEEP) 5 cmH2 O, fracción inspirada de oxígeno 30%) se extrajo sangre para EAB arterial: pH 7.40, pCO2 41 mmHg, pO2 65 mmHg, bicarbonato 28 mEq/l, exceso de base 0 mEq/l, saturación 93%, PAFI 216. Evolucionó sin fiebre, estable hemodinámicamente, con adecuada oxigenación y ritmo diurético. Al suspender sedantes presentó GCS de 3 puntos sobre 10 (correspondiente con evaluación ocular 1 y motor 2 puntos), con rigidez generalizada y reflejos osteotendinosos adecuados, con movimientos rítmicos linguales y peribucales. El electroencefalograma de 12 canales no evidenció descargas patológicas. Al décimo día de inicio de los síntomas presentó apertura ocular y menor rigidez, pero no toleraba la modalidad respiratoria espontánea por hipoventilación e hipercapnia que lo llevaron a hipoxemia transitoria. En el EAB arterial presentó: pH 7.31, pCO2 70 mmHg, pO2 76 mmHg, bicarbonato 35 mEq/l, exceso de base 8 mEq/l bajo asistencia ventilatoria en modalidad espontánea de presión soporte de 5 cmH2 O, frecuencia respiratoria 6 por minuto, PEEP 5 cmH2 O y volumen tidal entre 120-150 ml. Los siguientes días el paciente se conectó, respondiendo órdenes simples y complejas, y movilizó simétricamente los miembros con cierta debilidad. Por intolerancia a las pruebas ventilatorias espontáneas fue traqueostomizado. En la evaluación funcional respiratoria presentaba presión inspiratoria máxima menor a -40 cm de H2 O, presión espiratoria máxima mayor a 80 cm de H2 O, pero continuaba con hipercapnia en la prueba ventilatoria espontánea, por lo que requirió soporte ventilatorio con modalidad controlada. Se realizó ecocardiograma transtorácico que informó cavidades derechas normales, sin signos de hipertensión pulmonar. En la nueva RMN de encéfalo se evidenció disminución de las áreas hiperintensas en secuencias FLAIR y T2 visibles previamente.\n\nEl enfermo evolucionó con requerimiento de menor soporte ventilatorio en forma progresiva al momento del desarrollo de este informe.",
+    "gold_summary": "Presentamos el caso de un varón de 66 años de edad oriundo de la ciudad Juan Bautista Alberdi de la provincia de Buenos Aires con antecedentes de hipertensión arterial y trastorno obsesivo compulsivo. Consultó por fiebre súbita de cuatro días de evolución, con desarrollo de encefalopatía durante su internación. La punción lumbar mostró un líquido cefalorraquídeo cristalino, aunque inflamatorio de predominio mononuclear. La RMN de encéfalo informó hiperintensidad en secuencias FLAIR y T2 en el dorso del tronco encefálico. Ingresó a terapia intensiva por deterioro neurológico y acidosis respiratoria grave, requiriendo asistencia ventilatoria mecánica. Luego de 10 días presentó mejoría neurológica, sin déficit motor pero con hipoventilación alveolar que dificultaron el destete del respirador.",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Un hombre de 66 años se puso muy enfermo. Tenía fiebre y estaba confundido. Los doctores le hicieron una prueba con líquido de su espalda. El líquido estaba un poco inflamado. Le hicieron fotos especiales a su cabeza y vieron partes que estaban diferentes. El hombre tuvo que ir a un lugar especial del hospital para que lo cuidaran mucho. No podía respirar bien solo y necesitó una máquina para ayudarlo a respirar. Después de 10 días, empezó a mejorar y podía moverse bien. Pero todavía le costaba respirar sin la máquina. Los doctores lo están cuidando para que se ponga mejor.",
+        "scores": {
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+      "B2": {
+        "text": "**Caso de un Hombre con Fiebre y Problemas Cerebrales**\n\nUn hombre de 66 años, que vivía en Juan Bautista Alberdi, Buenos Aires, tenía antecedentes de presión alta y un trastorno llamado obsesivo compulsivo. Él llegó al hospital porque tenía fiebre alta durante cuatro días. Al principio, estaba consciente y sin problemas en sus movimientos o sensibilidad.\n\n**Lo que Encontraron**\n\nDespués de un día, empezó a confundirse y a estar somnoliento. Le hicieron una punción lumbar, que es cuando se extrae un poco de líquido del cerebro para analizarlo. Este líquido estaba claro pero mostraba signos de inflamación, especialmente con células llamadas mononucleares, que son parte del sistema inmunológico. Una resonancia magnética (una imagen del cerebro) mostró zonas inflamadas en una parte del cerebro llamada tronco encefálico.\n\n**Qué Pasó Después**\n\nSu estado empeoró y tuvo problemas para respirar bien, por lo que fue llevado a la unidad de cuidados intensivos. Allí, necesitó un respirador para ayudarle a respirar porque su cuerpo no eliminaba bien el dióxido de carbono, lo que causaba un problema llamado acidosis respiratoria. Después de 10 días, mejoró en cuanto a la conciencia y no tenía problemas para mover sus brazos y piernas, pero seguía teniendo dificultades para respirar por sí solo, lo que complicó que pudiera dejar el respirador.\n\n**Resumen**\n\nEste caso muestra cómo una infección o inflamación en el cerebro puede causar fiebre, confusión y problemas graves para respirar. Aunque el paciente mejoró su estado mental y motor, la función respiratoria tardó más en recuperarse.",
+        "scores": {
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+      "B3": {
+        "text": "**Contexto**  \nSe trata de un hombre de 66 años con antecedentes de hipertensión arterial y trastorno obsesivo compulsivo, que residía en Juan Bautista Alberdi, provincia de Buenos Aires. Fue hospitalizado tras presentar fiebre alta (39ºC) durante cuatro días sin otros síntomas iniciales. En el ingreso, estaba consciente y sin signos neurológicos focales, pero a las 24 horas desarrolló episodios alternantes de desorientación y somnolencia, junto con temblor en las extremidades.\n\n**Hallazgos Clave**  \n- La punción lumbar reveló un líquido cefalorraquídeo (LCR) claro pero con signos de inflamación, mostrando un aumento de leucocitos con predominio mixto (mononucleares y polimorfonucleares), proteínas elevadas y glucosa normal.  \n- Los cultivos de sangre y orina fueron negativos, así como las pruebas PCR para virus herpes simple y encefalopatía equina del oeste en LCR. Sin embargo, la detección de anticuerpos IgM específicos para encefalopatía equina del este (EEO) fue positiva tanto en suero como en LCR, confirmando la infección viral.  \n- La resonancia magnética (RMN) cerebral mostró áreas de mayor intensidad en secuencias FLAIR y T2 localizadas en la región dorsal del tronco encefálico (incluyendo protuberancia, bulbo y mesencéfalo), ambos pedúnculos cerebrales y ganglios basales, con afectación bilateral y predominio en el ganglio basal derecho. También se observaron múltiples lesiones en la sustancia blanca de ambos hemisferios cerebrales.  \n- El paciente presentó deterioro neurológico progresivo con disminución del nivel de conciencia (escala de Glasgow reducida a 8/15), requiriendo ingreso a unidad de terapia intensiva (UTI), intubación y ventilación mecánica debido a insuficiencia respiratoria con acidosis respiratoria grave (pH 7.11, pCO2 136 mmHg).  \n- Posteriormente, mostró mejoría neurológica parcial, con apertura ocular y respuesta a órdenes simples, sin déficit motor significativo, pero persistió con hipoventilación alveolar (disminución de la capacidad para ventilar adecuadamente los pulmones), lo que dificultó el destete de la ventilación mecánica y motivó la realización de traqueostomía.  \n- La RMN de control evidenció reducción de las lesiones inflamatorias previamente observadas.\n\n**Interpretación Clínica**  \nEl cuadro clínico y los estudios complementarios son compatibles con una encefalitis viral causada por el virus de la encefalopatía equina del este, una infección poco frecuente en humanos pero con potencial severo. La inflamación del tronco encefálico y ganglios basales explica el deterioro neurológico y la afectación respiratoria, dado que estas áreas controlan funciones vitales como la respiración. La hipoventilación persistente refleja compromiso del centro respiratorio, dificultando la recuperación completa y la independencia ventilatoria.\n\n**Próximos Pasos**  \nEl manejo continuó con soporte ventilatorio adaptado a la capacidad respiratoria del paciente, monitorización neurológica estrecha y seguimiento por imágenes para evaluar la evolución de las lesiones cerebrales. Se recomienda rehabilitación neurológica y respiratoria para mejorar la función muscular y ventilatoria. Además, es fundamental mantener vigilancia para posibles complicaciones infecciosas o neurológicas asociadas. El pronóstico dependerá de la recuperación neurológica y la capacidad para mantener una ventilación adecuada sin soporte mecánico.",
+        "scores": {
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+    "article": "Mujer de 27 años de edad oriunda del interior de la Provincia de Buenos Aires sin antecedentes personales o familiares de relevancia, consultó por sangrado vaginal. El estudio colposcópico evidenció formación polipoide que protruía por el orificio cervical externo (OCE). Se arribó clínicamente al diagnóstico de mioma nascens y se tomó una muestra de biopsia para su evaluación. Ante el diagnóstico patológico de sarcoma, se instauró quimioterapia, con el fin de reducir la masa lesional. Una vez lograda la reducción del tamaño, se decidió derivarla a nuestra institución para realizar tratamiento quirúrgico. Se recibió una pieza de histerectomía total con anexos, f ijada en formol al 10%. Cuerpo de 5 × 5 × 3.2 cm, cuello de 3.5 × 3 × 2 cm, ambas trompas de 4.5 × 0.7 cm y ovarios de 4 × 2.5 × 2.5 cm. A la apertura de la pieza, se observó a nivel de la unión cérvico-ístmica una formación polipoide pediculada de 8.5 cm de diámetro, que emergía hacia el canal endocervical y se exteriorizaba por el OCE. La superficie externa era parda, lobulada, con sectores rojizos. Al corte, se observaba blanquecina, blanda, con sectores de aspecto gelatinoso y formaciones quísticas de hasta 0,6 cm de dimensión máxima. Luego del procesamiento de rutina, se efectuaron secciones histológicas y se colorearon con hematoxilina-eosina (H-E), las cuales evidenciaron sectores celulares alternados por áreas laxas, mixoides junto a glándulas ístmico-endometriales típicas. La proliferación, predominantemente fusocelular atípica se disponía en nidos, constituidos por células de amplio citoplasma eosinófilo y núcleos excéntricos con cromatina homogénea, algunos pleomórficos. Se apreciaron estriaciones citoplasmáticas transversales en dichas células. El estroma era ampliamente mixoide y ricamente vascularizado. Se destacaban focalmente áreas celulares densamente condensadas inmediatas y próximas al revestimiento epitelial intacto, pero separadas de él, por una fina capa de estroma laxo. Esto se conoce como cambium layer o capa cambial. Se realizaron técnicas de inmunohistoquímica para desmina, actina músculo específico (AME) y miogenina (MYF4), las cuales resultaron positivas, mientras que la actina músculo liso fue negativa. Esta inmunomarcación permitió comprobar la estirpe muscular estriada y en última instancia arribar al diagnóstico, junto al cuadro morfológico, de RMS embrionario. Asimismo, la presencia de rabdomioblastos agrupados constituyendo la capa cambial a nivel subepitelial resultó fundamental y necesario para tipificar al RMS embrionario como botrioide, independientemente de la presentación macroscópica en forma de racimos polipoides.",
+    "gold_summary": "Presentamos el caso de una mujer de 27 años que consultó por sangrado vaginal y en quien se evidenció en la colposcopia, una lesión polipoide blanquecina que se exteriorizaba a través del orificio cervical externo. El estudio histológico reveló sectores celulares alternados por áreas laxas, mixoides, junto a glándulas ístmico-endometriales típicas. La proliferación fusocelular atípica, se disponía en nidos, constituidos por células de amplio citoplasma eosinófilo con estriaciones citoplasmáticas transversales y núcleos excéntricos con cromatina homogénea. Se exhibían áreas de células densamente condensadas inmediatas y próximas al revestimiento epitelial intacto, pero separadas de él, por una fina capa de estroma laxo (capa cambial). El perfil de inmunomarcación resultó positivo para desmina, actina músculo específico y miogenina, y negativo para actina músculo liso. Se realizó diagnóstico de rabdomiosarcoma embrionario botroide de cuerpo uterino.",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Una mujer joven tenía sangrado y una bolita en su cuerpo. Los doctores miraron la bolita con cuidado. Vieron que estaba hecha de muchas células diferentes. Estas células eran especiales y venían de un músculo. Los doctores dijeron que la bolita era un tipo de enfermedad que necesita tratamiento. Ellos cuidarán mucho a la mujer para ayudarla a estar mejor.",
+        "scores": {
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+          "ROUGE-2": 0.03636363636363636,
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
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+      "B2": {
+        "text": "Caso de una mujer joven con sangrado vaginal\n\nUna mujer de 27 años fue al médico porque tenía sangrado vaginal. Al examinarla con un colposcopio (un instrumento que permite ver el cuello del útero), encontraron una lesión con forma de pólipo que salía por el orificio del cuello uterino. Esta lesión era de color blanquecino y tenía una superficie irregular.\n\nLo que encontraron en el laboratorio\n\nSe tomó una muestra de la lesión para analizarla bajo el microscopio. Los científicos vieron diferentes tipos de células: algunas estaban agrupadas en nidos y tenían un citoplasma (la parte de la célula fuera del núcleo) amplio y con un color rosado. Estas células también mostraban unas líneas transversales llamadas estriaciones, que indican que son células musculares especiales. Cerca de la superficie de la lesión, había una capa delgada de células muy densas, separadas del revestimiento normal por una capa de tejido blando llamada estroma laxo. Esta capa se llama “capa cambial” y es característica de ciertos tumores.\n\nCómo confirmaron el diagnóstico\n\nPara saber qué tipo de tumor era, usaron pruebas especiales que detectan proteínas en las células. Encontraron que las células tenían proteínas llamadas desmina, actina músculo específico y miogenina, que están presentes en músculos estriados (los músculos que usamos para movernos). No encontraron actina de músculo liso, que es otro tipo de músculo. Con esta información y la apariencia de las células, diagnosticaron un rabdomiosarcoma embrionario botrioide. Este es un tipo raro de tumor canceroso que se origina en células musculares jóvenes y se presenta en el cuerpo uterino.\n\nEn resumen, esta paciente tenía un tumor maligno muscular en el cuello del útero que se identificó gracias a la combinación de estudios visuales, microscópicos y de proteínas. El diagnóstico permitió iniciar un tratamiento adecuado para su condición.",
+        "scores": {
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+          "ROUGE-2": 0.12929292929292932,
+          "ROUGE-L-Sum": 0.32595573440643866,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
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+      "B3": {
+        "text": "**Contexto**  \nSe presenta el caso de una mujer joven de 27 años, sin antecedentes médicos relevantes, que consultó debido a sangrado vaginal. Durante la colposcopia (un examen visual del cuello uterino), se identificó una lesión con forma de pólipo blanquecino que sobresalía a través del orificio cervical externo (la abertura del cuello uterino hacia la vagina). Inicialmente, se sospechó un mioma nascens (un tipo de tumor benigno), pero la biopsia reveló un diagnóstico diferente.\n\n**Hallazgos Clave**  \nEl análisis microscópico del tejido mostró una combinación de áreas celulares densas y otras más laxas con características mixoides (tejido con apariencia gelatinosa), junto con glándulas típicas del istmo y endometrio (zonas del cuello y cuerpo uterino). La proliferación celular predominante estaba formada por células fusiformes (alargadas) atípicas organizadas en grupos o nidos. Estas células tenían un citoplasma amplio y rosado (eosinófilo), con estriaciones transversales visibles en el citoplasma, y núcleos excéntricos con cromatina homogénea, aunque algunos mostraban variabilidad en forma y tamaño (pleomorfismo).  \n\nAdemás, se observaron áreas específicas de células muy condensadas justo debajo del revestimiento epitelial intacto, separadas de este por una delgada capa de tejido conectivo laxo, conocida como “capa cambial”. Esta característica es importante para clasificar el tumor.  \n\nLas pruebas inmunohistoquímicas, que detectan proteínas específicas en las células, mostraron positividad para desmina, actina músculo específico y miogenina, marcadores que indican la presencia de células musculares estriadas (músculo esquelético). Por otro lado, la actina de músculo liso fue negativa, lo que ayudó a descartar otros tipos de tumores musculares.\n\n**Interpretación Clínica**  \nCon base en las características morfológicas y los resultados inmunohistoquímicos, se estableció el diagnóstico de rabdomiosarcoma embrionario botrioide, un tipo raro y agresivo de tumor maligno que se origina en células musculares estriadas y que en este caso afectaba el cuello uterino. La presencia de la capa cambial y la agrupación de rabdomioblastos (células tumorales características) fueron fundamentales para identificar esta variante específica.\n\n**Próximos Pasos**  \nTras el diagnóstico, la paciente recibió tratamiento con quimioterapia para reducir el tamaño del tumor. Posteriormente, se realizó una cirugía de histerectomía total con anexos (extirpación del útero, trompas y ovarios) para eliminar completamente la lesión. El seguimiento y manejo continuarán en función de la respuesta al tratamiento y la evolución clínica.  \n\nEste caso resalta la importancia de una evaluación cuidadosa y multidisciplinaria para diagnosticar correctamente tumores poco comunes que pueden presentarse con síntomas comunes como el sangrado vaginal.",
+        "scores": {
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
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+  {
+    "article": "Un hombre de 53 años de edad, que inició diálisis por disfunción renal en etapa terminal debido a nefropatía diabética o nefroesclerosis en nuestro departamento de nefrología 10 años antes, se sometió a una ecocardiografía de seguimiento anual para estenosis valvular aórtica progresiva (AVS) y regurgitación moderada con fracción de eyección ventricular izquierda (LVEF) normal. Un año antes, se observaron calcificaciones que sugerían MAC en el anillo mitral posterior, que no se habían visto dos años antes. En el último seguimiento, la ecocardiografía reveló una masa redonda de superficie lisa de 22 × 17 mm con alta ecogenicidad en el área circundante y un brillo interno ligeramente disminuido en el anillo mitral posterior del lado auricular izquierdo. El paciente no tenía síntomas significativos ni hallazgos físicos, excepto un soplo sistólico.\n\nLa ecocardiografía también reveló una VS moderada con un flujo de pico valvular transaórtico de 3,76 m/s y una regurgitación valvular aórtica moderada. Se observó una regurgitación mitral leve pero no estenosis. El patrón de velocidad de flujo de entrada del VI mostró un patrón pseudo-normal con un agrandamiento de la aurícula izquierda de 47 mm de diámetro. La ecocardiografía en serie durante dos años reveló un agrandamiento del VI y una disminución de la FEVI. El diámetro final diastólico/final sistólico del VI y la FEVI fueron de 50/33 mm y 64 %, respectivamente, hace dos años; 57/41 mm y 52 % hace un año; y 59/47 mm y 42 % en el último seguimiento.\n\nTeniendo en cuenta el estado de la hemodiálisis, predijimos la progresión a una AVS casi severa, con empeoramiento de la disfunción sistólica del LV, que se convertiría en una indicación para el reemplazo de la válvula aórtica (AVR) en un futuro cercano.\n\nLa tomografía computarizada (TC) reveló una masa de alta densidad sin realce de contraste. La resonancia magnética (MRI) mostró una masa bien definida de alta intensidad en el centro, con un borde hipointenso en la imagen T1 y una señal desprovista en T2. Se excluyeron los neoplasmas, incluidos los mixomas y los fibroelastomas papilares, en función de sus características de imagen. Los hallazgos de laboratorio no indicaron infección, y no se sospechó de vegetación con endocarditis infecciosa. Teniendo en cuenta la disfunción renal en etapa terminal en la hemodiálisis y los hallazgos de imagen, se sospechó CCMA. El rápido agrandamiento de la masa generó preocupación sobre una potencial embolia. En consecuencia, la masa se resecó con AVR.\n\nLa incisión del atrio izquierdo reveló una masa por debajo del endocardio auricular en el anillo de la válvula mitral (P1-2); se observaron sustancias cremosas en la incisión de la masa, lo que sugiere CCMA. Después de la extirpación y desbridamiento del tejido, el sitio de la incisión se suturó con prolina. Se realizó el reemplazo de la válvula aórtica utilizando una válvula SJM de 21 mm. La retirada del bypass cardiopulmonar fue relativamente suave. Al momento del alta, se prescribió warfarina y aspirina, junto con bisoprolol para la fibrilación auricular paroxística después de la cirugía.\n\nNo se observaron eventos embólicos antes o después de la cirugía.\n\nEl examen histopatológico reveló calcificaciones granulares y nodulares dispersas, que consistían principalmente en infiltración de células inflamatorias y proliferación vascular de neutrófilos, linfocitos, células espumosas, macrófagos tisulares y células plasmáticas, con osificación parcial compatible con CICM. La biopsia miocárdica LV para descartar cardiomiopatía secundaria y la válvula aórtica resecada mostraron células inflamatorias similares a las observadas en CICM. Por lo tanto, se diagnosticó CICM en base a la disminución del movimiento de la pared y la fibrosis miocárdica, con infiltración de células inflamatorias > 14 mm2, células T CD3 positivas > 7/mm2 y negatividad de tenascina C (4C8).7 Sin embargo, no se pudo determinar la causa de CICM.\n\nLa ecocardiografía 6 meses después de la resección no mostró recurrencia del tumor (ver material complementario en línea), ni progresión de la regurgitación mitral, función normal de la válvula aórtica protésica y ninguna mejora de la FEVI (41 %)\n\n",
+    "gold_summary": "Un hombre de 52 años con insuficiencia renal en fase terminal que requería hemodiálisis se sometió a una ecocardiografía anual de seguimiento para detectar una disfunción valvular aórtica. La ecocardiografía reveló una masa circular bien definida de 22 × 17 mm en el anillo de la valva mitral posterior que no se había detectado 2 años antes. En función de las características de la imagen, se sospechó que la masa era un CCMA. Se había agrandado rápidamente y suponía un riesgo potencial de embolia; por lo tanto, se extirpó al mismo tiempo que la sustitución de la válvula aórtica. Aunque se sospechó un CCMA en función de los hallazgos intraoperativos, el diagnóstico histopatológico fue un CAT. Tras el análisis histológico de la muestra de miocardio del ventrículo izquierdo y la válvula aórtica extirpada, se observó una infiltración de células inflamatorias crónicas; por lo tanto, se diagnosticó una cardiomiopatía inflamatoria crónica.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Había un hombre que tenía problemas en sus riñones. Tenía un huesito en su corazón que creció mucho y podía hacerle daño. Los doctores vieron el huesito con una máquina especial. Decidieron quitarlo para que el hombre estuviera mejor. También le pusieron una nueva parte en su corazón para que funcione bien. Cuando miraron el huesito con un microscopio, vieron que había muchas células que estaban peleando dentro. Eso les dijo que su corazón estaba un poco enfermo por dentro. Ahora el hombre está más seguro y los doctores lo cuidan mucho.",
+        "scores": {
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
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+          "BERTScore_F": NaN
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+      },
+      "B2": {
+        "text": "**Lo que pasó con el paciente**  \nUn hombre de 52 años tenía problemas graves en sus riñones y necesitaba hemodiálisis, que es un tratamiento para limpiar la sangre cuando los riñones no funcionan bien. Cada año, le hacían una ecocardiografía, que es un examen con ultrasonido para ver cómo está funcionando su corazón y sus válvulas.\n\n**Lo que encontraron en el corazón**  \nEn el último examen, vieron una masa redonda de 22 × 17 mm en una parte del corazón llamada anillo mitral posterior. Esta masa no estaba ahí dos años antes. Por las imágenes, pensaron que podía ser una calcificación caseosa del anillo mitral (CCMA), que es una acumulación dura y blanda de calcio en esa zona. La masa había crecido rápido y podía causar problemas si pedazos se soltaban y viajaban por la sangre (embolias).\n\n**Qué hicieron los médicos**  \nDecidieron quitar la masa y al mismo tiempo reemplazar la válvula aórtica, que también estaba dañada. Durante la cirugía, vieron que la masa tenía un aspecto cremoso, lo que apoyaba la idea de que era una CCMA.\n\n**Lo que mostraron los análisis después de la cirugía**  \nCuando examinaron la masa bajo el microscopio, encontraron que no era solo calcio, sino también muchas células inflamatorias, lo que indicaba una inflamación crónica en el corazón. Además, analizaron muestras del músculo del corazón y de la válvula aórtica y vieron signos similares de inflamación. Por eso, diagnosticaron al paciente con una cardiomiopatía inflamatoria crónica, que es una enfermedad donde el músculo del corazón está inflamado por mucho tiempo.\n\n**Estado después de la cirugía**  \nSeis meses después, el corazón no mostró que la masa hubiera vuelto, y la válvula nueva funcionaba bien. Sin embargo, la función del ventrículo izquierdo, que es la parte del corazón que bombea la sangre, no mejoró mucho.\n\n**Resumen final**  \nEste caso muestra cómo una masa en el corazón que parecía ser una calcificación pudo ser en realidad una inflamación crónica del músculo cardíaco. La cirugía ayudó a prevenir posibles problemas graves, pero la función del corazón seguía afectada.",
+        "scores": {
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+        "text": "**Contexto**  \nUn hombre de 53 años con insuficiencia renal terminal en hemodiálisis, causada por nefropatía diabética o nefroesclerosis, fue seguido durante 10 años en un servicio de nefrología. Presentaba estenosis valvular aórtica progresiva y regurgitación moderada, con función ventricular izquierda inicialmente normal. En controles ecocardiográficos anuales se detectó la aparición y rápido crecimiento de una masa en el anillo mitral posterior, que generó preocupación por riesgo de embolia.\n\n**Hallazgos Clave**  \nLa ecocardiografía mostró una masa redonda, bien delimitada, de 22 × 17 mm en el anillo mitral posterior, con características ecogénicas sugestivas de calcificación. La función del ventrículo izquierdo se deterioró progresivamente en dos años, con disminución de la fracción de eyección del 64 % al 42 %. La tomografía computarizada y la resonancia magnética descartaron tumores comunes como mixomas o fibroelastomas papilares, y no hubo evidencia de infección ni endocarditis. Por el contexto clínico y las imágenes, se sospechó una calcificación caseosa del anillo mitral (CCMA), una forma rara de calcificación valvular.\n\nDado el rápido crecimiento de la masa y el riesgo de embolia, se decidió extirparla quirúrgicamente junto con el reemplazo de la válvula aórtica. Durante la cirugía, se observó una masa con contenido cremoso típica de CCMA. Sin embargo, el análisis histopatológico reveló que la masa correspondía a un tumor calcificado atípico (CAT), caracterizado por calcificaciones nodulares y una infiltración inflamatoria crónica con células como neutrófilos, linfocitos, macrófagos y células plasmáticas. Además, la biopsia del músculo cardíaco del ventrículo izquierdo y la válvula aórtica resecada mostraron infiltración similar, lo que llevó al diagnóstico de una cardiomiopatía inflamatoria crónica (CICM). No se pudo determinar la causa exacta de esta inflamación.\n\n**Interpretación Clínica**  \nEste caso ilustra la complejidad diagnóstica de masas en el anillo mitral en pacientes con insuficiencia renal terminal y hemodiálisis, donde la calcificación caseosa puede simular tumores o lesiones inflamatorias. La progresión rápida y el riesgo embolígeno justificaron la cirugía. El diagnóstico definitivo mediante histología fue fundamental para identificar una cardiomiopatía inflamatoria crónica asociada, que podría explicar la disfunción ventricular progresiva observada.\n\n**Próximos Pasos**  \nSe realizó un seguimiento ecocardiográfico a los 6 meses postoperatorios que mostró ausencia de recurrencia de la masa, función normal de la válvula aórtica protésica y estabilidad de la regurgitación mitral, aunque sin mejoría en la función ventricular izquierda (fracción de eyección 41 %). El paciente recibió tratamiento anticoagulante y manejo para fibrilación auricular paroxística. Se recomienda continuar el seguimiento cardiológico para monitorizar la función ventricular y detectar posibles complicaciones asociadas a la cardiomiopatía inflamatoria crónica.",
+        "scores": {
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
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+  {
+    "article": "Paciente masculino de 28 años, sin antecedentes de importancia, acude a consulta de dermatología con un cuadro cutáneo de 48 horas de evolución caracterizado por dos placas eritematosas con ampollas centrales más ulceración superficial localizadas en cara flexora de brazo y antebrazo derecho equidistantes del pliegue del codo, acompañadas de una sensación de ardor y prurito en el lugar de las lesiones. No presentó síntomas sistémicos ni se automedicó. Como antecedente refiere que se encontraba de vacaciones en la región costera de Ecuador al momento de aparecer las lesiones. Se realizó una biopsia incisional que reportó epidermis con acantosis, paraqueratosis y espongiosis, neutrófilos en estrato córneo e infiltrado linfocitario perivascular en dermis superficial, media y profunda. Por las características clínicas, el antecedente de viaje a una región tropical y los hallazgos histológicos se diagnosticó como dermatitis por Paederus. Se indicó tratamiento con antihistamínicos, esteroides tópicos y compresas frías. Después de 8 días de tratamiento, las lesiones remitieron dejando una hiperpigmentación postinflamatoria.",
+    "gold_summary": "Se comunica el caso de un paciente masculino de 28 años, que acude a consulta de dermatología con cuadro de 48 horas de evolución de dos placas eritematosas con ampollas centrales más ulceración superficial localizadas en cara flexora de brazo y antebrazo derecho, acompañadas de una sensación de ardor y prurito en el lugar de las lesiones, sin síntomas acompañantes. Como antecedente refiere que se encontraba de vacaciones en la región costera de Ecuador al momento de aparecer las lesiones. Se realizó una biopsia incisional y por las características clínicas y el antecedente de viaje a una región tropical se diagnosticó como dermatitis por Paederus y se indicó tratamiento con antihistamínicos, esteroides tópicos y compresas frías. Después de 8 días de tratamiento, las lesiones remitieron dejando una hiperpigmentación postinflamatoria.",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Un hombre se lastimó la piel en su brazo. Tenía dos manchas rojas con ampollas y le picaban y quemaban. Esto pasó después de estar de vacaciones en un lugar con mucho calor y bichos. El doctor vio su piel y dijo que era una irritación por un bicho llamado Paederus. Le dieron medicinas para calmar la picazón y poner frío en su brazo. Después de unos días, la piel mejoró, pero quedó un poco de color diferente donde estaban las manchas.",
+        "scores": {
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
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+        }
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+      "B2": {
+        "text": "Caso de un joven de 28 años con lesiones en la piel\n\nUn hombre de 28 años fue al dermatólogo porque tenía dos manchas rojas en el brazo y antebrazo derecho. Estas manchas tenían ampollas (pequeñas burbujas llenas de líquido) en el centro y una pequeña herida superficial. Además, sentía ardor y picazón en esas áreas. No tenía otros síntomas ni había tomado medicamentos por su cuenta.\n\nLo que encontraron y cómo lo trataron\n\nEl paciente contó que estaba de vacaciones en la costa de Ecuador cuando aparecieron las lesiones. Para entender mejor qué pasaba, los médicos tomaron una biopsia, que es cuando se extrae un pequeño pedazo de piel para examinarlo bajo el microscopio. En el análisis, vieron cambios en las capas de la piel y células inflamatorias, lo que ayudó a confirmar que tenía dermatitis por Paederus. Esta dermatitis es una irritación causada por un insecto llamado Paederus, común en zonas tropicales.\n\nEl tratamiento incluyó medicamentos para reducir la picazón (antihistamínicos), cremas con esteroides para bajar la inflamación, y compresas frías para aliviar el ardor. Después de ocho días, las lesiones mejoraron, pero quedaron manchas oscuras en la piel, llamadas hiperpigmentación postinflamatoria, que suelen desaparecer con el tiempo.",
+        "scores": {
+          "ROUGE-1": 0.44562334217506633,
+          "ROUGE-2": 0.15466666666666667,
+          "ROUGE-L-Sum": 0.40848806366047746,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe presenta el caso de un hombre de 28 años, sin antecedentes médicos relevantes, que consultó en dermatología debido a la aparición de lesiones cutáneas durante las últimas 48 horas. Estas lesiones consistían en dos placas rojas (eritematosas) con ampollas en el centro y una ulceración superficial, localizadas en la parte interna del brazo y antebrazo derecho, equidistantes del pliegue del codo. El paciente describió sensación de ardor y picazón en las zonas afectadas, sin presentar otros síntomas generales ni haber tomado medicamentos por su cuenta. Como antecedente importante, refirió que se encontraba de vacaciones en una zona costera tropical de Ecuador cuando aparecieron las lesiones.\n\n**Hallazgos Clave**  \nSe realizó una biopsia incisional de la piel afectada, cuyo análisis microscópico mostró:  \n- Engrosamiento de la epidermis (acantosis)  \n- Presencia de células muertas con núcleo (paraqueratosis)  \n- Acumulación de líquido entre las células epidérmicas (espongiosis)  \n- Infiltración de neutrófilos (un tipo de glóbulo blanco) en la capa más superficial de la piel (estrato córneo)  \n- Presencia de un infiltrado inflamatorio linfocitario alrededor de los vasos sanguíneos en las capas superficiales, medias y profundas de la dermis (la capa intermedia de la piel).\n\n**Interpretación Clínica**  \nLa combinación de las características clínicas, el antecedente de exposición en una región tropical y los hallazgos histológicos permitió establecer el diagnóstico de dermatitis por Paederus. Esta condición es una inflamación cutánea causada por el contacto con un insecto del género Paederus, que libera una toxina irritante al ser aplastado sobre la piel.\n\n**Próximos Pasos y Tratamiento**  \nEl tratamiento indicado incluyó antihistamínicos para aliviar la picazón, esteroides tópicos para reducir la inflamación y la aplicación de compresas frías para calmar la zona afectada. Tras ocho días de tratamiento, las lesiones desaparecieron, aunque dejaron una hiperpigmentación postinflamatoria, es decir, una mancha oscura residual en la piel debido a la inflamación previa.\n\nEste caso resalta la importancia de considerar la dermatitis por Paederus en pacientes con lesiones cutáneas agudas tras viajes a regiones tropicales, y la efectividad del tratamiento tópico combinado para su resolución.",
+        "scores": {
+          "ROUGE-1": 0.44990548204158787,
+          "ROUGE-2": 0.24667931688804554,
+          "ROUGE-L-Sum": 0.41965973534971646,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
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+    }
+  },
+  {
+    "article": "Un hombre de 35 años de edad, herido en un accidente de tráfico, fue trasladado a nuestro hospital, que está equipado con un ER híbrido. Había sufrido una lesión potencialmente mortal, con su pierna derecha acortada y girada. Los signos vitales del paciente a su llegada fueron los siguientes: frecuencia respiratoria de 24 respiraciones/min, saturación de oxígeno del 99 % con 12 L de administración de oxígeno, frecuencia cardiaca de 143 latidos/min, presión arterial de 80/40 mmHg, y puntuación de Glasgow Coma Scale de E4V4M6. Intentamos realizar un TAC y resucitar al paciente. El TAC reveló un hemotórax izquierdo, ensanchamiento del mediastino, y fractura pélvica. Como la presión arterial del paciente cayó rápidamente antes del TAC, se administraron procedimientos de salvamento, como intubación de emergencia, preperitoneal pelvic packing, y transfusión masiva, con un cuidadoso control de la presión arterial en el ER híbrido. Después de la estabilización de los signos vitales con estos procedimientos, el TAC con contraste reveló una fractura de BTAI de grado IV que se extendía hacia la cavidad torácica izquierda. La embolización arterial transcatéter (TAE) para la fractura pélvica y la fijación esquelética externa de la fractura del fémur derecho se realizaron primero, ya que el radiólogo y el cirujano cardiovascular, que realizan TEVAR en nuestro centro médico, no estaban disponibles en ese momento. Posteriormente, se realizó TEVAR utilizando un injerto de stent (GORE C-TAG 26 × 150 mm; WL Gore & Associates, Flagstaff, Arizona, EE. UU.) en el ER híbrido sin transferir al paciente. Se desplegó un injerto de stent justo distal de la arteria carótida común izquierda (zona II) y el extremo distal del injerto de stent se posicionó en el nivel de Th 8. Decidimos sacrificar LSCA ya que el flujo sanguíneo de la arteria vertebral izquierda fue suficiente según lo evaluado por angiografía. El paciente no tuvo síntomas que sugirieran isquemia después de TEVER. Durante la cirugía, se administraron 50 unidades/kg (3000 unidades) de heparina. El paciente fue trasladado a un hospital de rehabilitación el día 41 postoperatorio.\n",
+    "gold_summary": "Un hombre de 35 años de edad sufrió múltiples lesiones tras un accidente de tráfico y fue trasladado a nuestro hospital en estado de shock. La tomografía computarizada reveló una fractura de TAI de grado IV que se extendía hasta la cavidad torácica y una fractura pélvica. Poco tiempo después de realizar un relleno pélvico preperitoneal y una embolización arterial transcatéter para la fractura pélvica, se realizó un TEVAR en el quirófano híbrido sin trasladar al paciente. El paciente fue trasladado a un hospital de rehabilitación el día 41 después de la operación.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Un hombre se lastimó mucho en un accidente. Su pierna estaba muy dañada y tenía huesos rotos en el cuerpo. Los doctores le hicieron muchas cosas para ayudarlo a estar mejor. Usaron una máquina para ver dentro de su cuerpo y encontraron problemas grandes. Luego, le pusieron un tubo especial para arreglar su corazón y sus huesos. El hombre se quedó en el hospital mucho tiempo. Después, fue a otro lugar para aprender a caminar y estar fuerte otra vez.",
+        "scores": {
+          "ROUGE-1": 0.29591836734693877,
+          "ROUGE-2": 0.05154639175257732,
+          "ROUGE-L-Sum": 0.2857142857142857,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B2": {
+        "text": "**Lo que pasó con el paciente**  \nUn hombre de 35 años tuvo un accidente de tráfico grave y llegó al hospital en estado muy delicado. Tenía varias heridas, incluyendo una fractura en la pelvis y una lesión grave en la arteria principal del pecho llamada aorta. Esta lesión se llama fractura de TAI de grado IV y puede ser muy peligrosa porque afecta el flujo de sangre al cuerpo.\n\n**Tratamientos que recibió**  \nPrimero, los médicos hicieron un procedimiento llamado relleno pélvico preperitoneal, que ayuda a controlar el sangrado en la pelvis. También realizaron una embolización arterial transcatéter, que es cuando se bloquea una arteria para detener una hemorragia. Después, sin mover al paciente a otro lugar, hicieron una cirugía llamada TEVAR en un quirófano especial que combina imagen y cirugía. En esta operación, colocaron un tubo especial llamado injerto de stent dentro de la arteria dañada para repararla y permitir que la sangre fluya bien.\n\n**Qué pasó después**  \nGracias a estos tratamientos, el paciente se estabilizó y pudo continuar su recuperación. Después de 41 días, fue enviado a un hospital de rehabilitación para seguir mejorando su salud.",
+        "scores": {
+          "ROUGE-1": 0.5078369905956113,
+          "ROUGE-2": 0.2523659305993691,
+          "ROUGE-L-Sum": 0.457680250783699,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B3": {
+        "text": "**Contexto:**  \nUn hombre de 35 años sufrió un grave accidente de tráfico que le provocó múltiples lesiones, incluyendo una fractura grave en la arteria aorta torácica (TAI, por sus siglas en inglés) y fracturas óseas en la pelvis y el fémur derecho. Fue trasladado a un hospital equipado con un quirófano híbrido, donde recibió atención de emergencia.\n\n**Hallazgos Clave:**  \nA su llegada, el paciente presentaba signos de shock, con presión arterial muy baja y frecuencia cardíaca elevada. La tomografía computarizada (TAC) mostró un hemotórax (acumulación de sangre en el tórax), ensanchamiento del mediastino (zona central del tórax que contiene el corazón y grandes vasos), una fractura pélvica y una lesión de grado IV en la arteria aorta torácica que se extendía hacia la cavidad torácica izquierda. Además, la pierna derecha estaba acortada y girada, indicando fractura del fémur.\n\n**Interpretación Clínica:**  \nDebido a la gravedad y la inestabilidad hemodinámica del paciente, se realizaron procedimientos de emergencia para controlar el sangrado y estabilizarlo, incluyendo intubación, relleno pélvico preperitoneal (una técnica para controlar hemorragias pélvicas) y transfusión masiva. Posteriormente, se realizó una embolización arterial transcatéter (TAE) para controlar el sangrado de la fractura pélvica y se fijó externamente la fractura del fémur. Finalmente, sin necesidad de trasladar al paciente, se llevó a cabo una reparación endovascular de la aorta torácica (TEVAR) en el quirófano híbrido, utilizando un injerto de stent que se colocó desde justo después de la arteria carótida común izquierda hasta la octava vértebra torácica. Para asegurar un flujo sanguíneo adecuado, se decidió sacrificar la arteria subclavia izquierda, ya que la circulación cerebral estaba garantizada por la arteria vertebral izquierda. Durante la cirugía se administró heparina para prevenir coágulos.\n\n**Próximos Pasos y Resultado:**  \nEl paciente evolucionó favorablemente sin signos de isquemia (falta de riego sanguíneo) tras la intervención. Fue dado de alta al hospital de rehabilitación 41 días después de la cirugía, donde continuó su recuperación.",
+        "scores": {
+          "ROUGE-1": 0.4223602484472049,
+          "ROUGE-2": 0.25363825363825365,
+          "ROUGE-L-Sum": 0.3768115942028985,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      }
+    }
+  },
+  {
+    "article": "Hombre de 31 años con antecedentes de consumo de alcohol, tabaco, cocaína inhalada, tuberculosis pulmonar tratada, nefrectomía izquierda y esplenectomía post-traumática. Consultó al servicio de urgencias por cuadro de una semana de evolución que inició inmediatamente posterior a la aplicación intramuscular de penicilina por contacto sexual con pareja con sífilis, caracterizado por dolor en región glútea derecha que irradiaba hasta pie, con posterior aparición de dermatosis purpúrica relacionada con sitio de inyección, siendo una lesión tipo placa configurada en forma anular, con bordes irregulares y distribución racemosa que medía 15 centímetros (cm), con piel sana en su interior. También presentaba una pequeña escara escrotal y una extensa lesión plantar derecha de aspecto livedoide desde la zona talar hasta la punta de los dedos que no respetaba margen estricto. Se realizó ecografía del glúteo mayor, que mostró pérdida del patrón fibrilar heterogéneo, aumento del espesor del mismo a nivel de su tercio medio de aspecto edematoso, además de edema del tejido celular subcutáneo (TCS); en región plantar homolateral y en escroto edema de TCS. En el laboratorio presentó leucocitosis de 13.7 × 109/L, proteína C reactiva de 3.2 mg/dL (normal hasta 0.5 mg/dL), que se interpretaron como reactantes de fase aguda, también aumento de transaminasas con aspartato aminotransferasa de 175 UI/L (normal hasta 32), alanino aminotransferasa de 245 UI/L (normal hasta 33), creatina kinasa con un valor de 2741 UI/L (normal hasta 170) y lactato deshidrogenasa de 2499 UI/L (normal hasta 250) representando compromiso muscular. Se realizaron serologías completas para sífilis, con venereal disease research laboratory (VDRL y anticuerpos treponémicos), virus de la inmunodeficiencia humana (HIV) hepatitis B, hepatitis C, con resultados negativos. La cronología, las manifestaciones clínicas y la posterior biopsia, respaldaron el diagnóstico de síndrome de Nicolau, para lo cual se inició anticoagulación con enoxaparina 1 mg/ kg c/12 hs vía subcutánea, cilostazol 100 mg cada 12 horas y tramadol, por 10 días. Se realizó biopsia de piel de glúteo que evidenció necrosis epidérmica y extensión a epitelio folicular, con formación de ampolla secundaria a reepitelización, sin vasculitis ni trombosis vascular, vinculable a embolia cutis medicamentosa en fase aguda, hubo franca mejoría con descenso de valores de transaminasas, con aspartato aminotransferasa de 39 UI/L, alanino aminotransferasa de 77 UI/L y creatin kinasa de 167 UI/L.  No se solicitó perfil inmunológico, basados en que nuestro diagnóstico presuntivo inicial no justificaba la búsqueda de otras etiologías. Se otorgó alta con cilostazol y analgésicos, control ambulatorio a los 3 meses con mejoría del dolor y de las lesiones, quedando en glúteo derecho cicatriz discrómica con presencia de descamación fina y en pie derecho cicatriz discrómica con zonas de descamación gruesas en región de apoyo tarso metatarsiano asociado a mínimas lesiones livedoides en planta del mismo pie.",
+    "gold_summary": "Se reporta el caso de un hombre de 31 años que presenta este síndrome luego de la aplicación de penicilina benzatínica intramuscular. La biopsia apoyó el diagnóstico. Recibió tratamiento con enoxaparina y cilostazol con posterior mejoría.",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Un hombre se puso una medicina en el glúteo. Después, le dolió mucho y le salió una mancha en la piel. El doctor vio que la piel estaba lastimada por la medicina. Le dieron medicinas para ayudar y se fue mejorando poco a poco. Ahora está mejor y la piel está sanando.",
+        "scores": {
+          "ROUGE-1": 0.2708333333333333,
+          "ROUGE-2": 0.02127659574468085,
+          "ROUGE-L-Sum": 0.20833333333333334,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B2": {
+        "text": "Caso de Síndrome de Nicolau tras Inyección de Penicilina\n\nUn hombre de 31 años recibió una inyección de penicilina para tratar una posible infección por sífilis, debido a que su pareja tenía esta enfermedad. Poco después, comenzó a sentir dolor en la nalga derecha que se extendía hasta el pie. Además, apareció una lesión en la piel cerca del lugar de la inyección, con forma de anillo y bordes irregulares, y otras heridas en el escroto y la planta del pie.\n\nPara entender qué pasaba, los médicos hicieron una ecografía que mostró inflamación en los músculos y tejidos cerca de la lesión. También se hicieron análisis de sangre que indicaron inflamación y daño muscular. Se descartaron otras infecciones como VIH y hepatitis.\n\nSe tomó una biopsia, que es cuando se extrae un pequeño pedazo de piel para examinarlo. Esta mostró que la piel estaba dañada por falta de sangre, pero sin inflamación de los vasos sanguíneos. Todo esto confirmó que el paciente tenía el síndrome de Nicolau, una reacción rara que puede ocurrir después de una inyección y que causa daño en la piel y músculos por bloqueo de vasos sanguíneos.\n\nEl tratamiento incluyó medicamentos para evitar coágulos (enoxaparina) y para mejorar la circulación (cilostazol), además de analgésicos para el dolor. Con este cuidado, el paciente mejoró, sus análisis de sangre volvieron casi a la normalidad y las lesiones en la piel sanaron, quedando solo algunas cicatrices leves.\n\nEste caso muestra la importancia de reconocer el síndrome de Nicolau para tratarlo rápido y evitar daños mayores.",
+        "scores": {
+          "ROUGE-1": 0.18289085545722714,
+          "ROUGE-2": 0.06528189910979229,
+          "ROUGE-L-Sum": 0.17109144542772858,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
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+      "B3": {
+        "text": "**Contexto**  \nSe trata de un hombre de 31 años con antecedentes de consumo de alcohol, tabaco y cocaína inhalada, además de haber tenido tuberculosis pulmonar tratada, y cirugías previas de nefrectomía izquierda y esplenectomía tras un trauma. Consultó en urgencias debido a un cuadro que comenzó una semana antes, inmediatamente después de recibir una inyección intramuscular de penicilina benzatínica, administrada por contacto sexual con una pareja diagnosticada con sífilis.\n\n**Hallazgos Clínicos y Diagnósticos**  \nEl paciente presentó dolor intenso en la región glútea derecha que se irradiaba hacia el pie, acompañado de una erupción cutánea purpúrica (manchas violáceas) en el sitio de la inyección. Esta lesión tenía forma de placa anular (con un borde en forma de anillo irregular) de aproximadamente 15 centímetros, con piel sana en el centro. Además, tenía una pequeña úlcera (escara) en el escroto y una lesión extensa en la planta del pie derecho con aspecto livedoide (patrón vascular irregular), que se extendía desde el talón hasta la punta de los dedos.\n\nLa ecografía del glúteo mostró alteraciones en el músculo mayor, con pérdida de su estructura normal, aumento de grosor y edema (hinchazón por acumulación de líquido) tanto en el músculo como en el tejido subcutáneo (debajo de la piel). Se observó edema también en la región plantar del pie y en el escroto.\n\nLos análisis de sangre revelaron leucocitosis (aumento de glóbulos blancos) y elevación de proteína C reactiva, indicadores de inflamación aguda. Además, hubo un aumento significativo de enzimas hepáticas (transaminasas) y de marcadores musculares como la creatina quinasa y la lactato deshidrogenasa, lo que sugiere daño muscular.\n\nLas pruebas serológicas para sífilis, VIH, hepatitis B y C fueron negativas.\n\nLa biopsia de piel del glúteo evidenció necrosis (muerte celular) epidérmica y afectación del epitelio folicular, con formación de ampollas debido a la reparación de la piel, pero sin signos de vasculitis (inflamación de vasos sanguíneos) ni trombosis (coágulos), lo que apoyó el diagnóstico de síndrome de Nicolau o embolia cutis medicamentosa en fase aguda. Este síndrome es una reacción adversa poco frecuente que ocurre tras la inyección intramuscular de ciertos medicamentos, causando daño vascular y necrosis en la piel y tejidos subyacentes.\n\n**Interpretación Clínica**  \nEl cuadro clínico, la historia temporal relacionada con la inyección de penicilina y los hallazgos histológicos confirmaron el diagnóstico de síndrome de Nicolau. Este diagnóstico explicó el dolor intenso, las lesiones cutáneas y el compromiso muscular observado.\n\n**Tratamiento y Evolución**  \nSe inició tratamiento con anticoagulación mediante enoxaparina (un anticoagulante) y cilostazol (un medicamento que mejora la circulación sanguínea), además de analgésicos para controlar el dolor. Durante la hospitalización, el paciente mostró una franca mejoría, con descenso progresivo de las enzimas hepáticas y musculares a valores cercanos a la normalidad.\n\nNo se realizaron estudios inmunológicos adicionales, dado que el diagnóstico clínico y patológico fue suficiente para explicar el cuadro.\n\nAl alta, el paciente continuó con cilostazol y analgésicos, y en el control ambulatorio a los tres meses presentó mejoría significativa del dolor y de las lesiones cutáneas. Quedaron secuelas en forma de cicatrices con alteraciones en la pigmentación y descamación fina en el glúteo derecho, así como cicatrices similares y mínimas lesiones livedoides en la planta del pie derecho.\n\n**Próximos Pasos**  \nSe recomienda seguimiento clínico para evaluar la evolución de las cicatrices y el manejo del dolor residual, así como evitar futuras inyecciones intramusculares en la zona afectada para prevenir recurrencias. Además, es importante la educación al paciente sobre los riesgos asociados a la administración de medicamentos por vía intramuscular y la vigilancia temprana de síntomas similares.",
+        "scores": {
+          "ROUGE-1": 0.0957592339261286,
+          "ROUGE-2": 0.05486968449931412,
+          "ROUGE-L-Sum": 0.0957592339261286,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
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+  },
+  {
+    "article": "Un varón de cuatro días de edad, nacido a las 39 semanas y 4 días de gestación, acude a un servicio de urgencias con un empeoramiento de la dificultad respiratoria y el estridor, que se ve agravado por la alimentación y la posición supina.\n\nNació de una madre de 31 años con serología significativa para una prueba de Coomb positiva indirecta, con un parto vaginal sin complicaciones y puntuaciones de APGAR de ocho y nueve en el primer y quinto minuto, respectivamente. Su peso al nacer fue de 3050 g. La ecografía fetal mostró preocupación por un foco intracardíaco, con un embarazo sin complicaciones. El curso de enfermería fue significativo solo por una prueba de audición bilateral fallida y un ecocardiograma normal. El bebé fue dado de alta en el día dos de vida. Se observó que tenía congestión nasal en el momento de la descarga. Se instruyó a la familia para que le aspirara la nariz y usara gotas salinas según fuera necesario.\n\nEn el día cuatro de vida, la madre del lactante notó estridor asociado con dificultad para alimentarse y el pediatra lo derivó al servicio de urgencias. El examen en el servicio de urgencias es significativo para el estridor inspiratorio agudo con tirones traqueales y retracciones subcostal. Además, se observa que tiene pectus excavatum. El estridor y el aumento del trabajo respiratorio mejoran con la posición prona o lateral. La evaluación de laboratorio es significativa para la acidosis respiratoria en el gas sanguíneo venoso [pH 7.18 y CO2 73 mmHg (9,732 Pa)] y el análisis de orina que revela bacterias moderadas y 11-20 glóbulos blancos sin la presencia de nitrito urinario o esterasa leucocitaria. Un recuento sanguíneo completo es tranquilizador. Se le coloca una cánula nasal de alto flujo y se inicia con ampicilina y gentamicina después de obtener cultivos de sangre.\n\nSe le aumentó la presión positiva continua en la vía aérea (CPAP) y se lo trasladó a una unidad de cuidados intensivos neonatales de nivel III para continuar con el tratamiento y la evaluación de otorrinolaringología. Se le introdujo un tubo nasogástrico por las dos fosas nasales sin dificultad. La laringoscopia flexible mostró una cuerda vocal izquierda inmóvil y cavidades nasales estrechas con edema de los cornetes nasales, aritenoides bilaterales y cuerdas vocales. La broncoscopia no reveló ninguna otra anormalidad. El examen físico posterior se caracterizó por rasgos dismórficos sutiles, que incluían orejas de implantación baja, retromicrognatia, microftalmia y clinodactilia de los dedos de los pies. Se interrumpió el tratamiento antibiótico empírico tras un examen infeccioso tranquilizador. Se consultó a un equipo multidisciplinario.\n\nEl paciente finalmente requirió intubación a las dos semanas de vida debido al empeoramiento del fallo respiratorio. Se administraron ciprofloxacina nasal y dexametasona para el edema de las vías respiratorias superiores. Una resonancia magnética del cerebro, cuello y tórax mostró un curso normal de los nervios laríngeos recurrentes. La evaluación genética incluyó un análisis de microarreglo cromosómico normal (CMA). La prueba adicional del panel genético fue positiva para la variante patogénica en el gen CHD7, consistente con el síndrome CHARGE. En este caso, el VFP se atribuyó a la asociación conocida con el síndrome CHARGE. La evaluación continua reveló otras características consistentes con el síndrome CHARGE, incluidos colobomas bilaterales, glaucoma, pérdida auditiva confirmada y anomalías genitales.\n\nLa repetición de la broncoscopia en el día 42 de vida demostró una mejora en el edema laríngeo general, pero continuó con un edema leve de las cuerdas vocales bilaterales. El paciente fue extubado después de la broncoscopia en el marco de un edema de las vías respiratorias mejorado. Sin embargo, fue re-intubado el día 46 de vida debido al empeoramiento de la insuficiencia respiratoria. La repetición de la laringoscopia ese día mostró un edema continuado. En este momento, el paciente ya había recibido múltiples ciclos cortos de Dexamethasone en un intento de disminuir el edema de las vías respiratorias. Debido a la necesidad de re-intubación, fue tratado con Tobramycin tópico y Dexamethasone aplicado directamente a las cuerdas vocales mediante laringoscopia directa durante cinco días. Después de este tratamiento, fue extubado con éxito a los dos meses de edad y se le colocó un tubo de gastrostomía a los tres meses.\n\nEn el momento de la colocación del tubo de gastrotomía, se le realizó una broncoscopia y una microlaringoscopia adicionales que demostraron que la cuerda vocal izquierda afectada originalmente era totalmente móvil, pero que mostraba una nueva inmovilidad de la cuerda derecha; la etiología de esto no está clara. Ambas cuerdas vocales seguían estando ligeramente edematosas, pero habían mejorado mucho desde la evaluación anterior. El paciente fue dado de alta en aire ambiente a los cuatro meses de edad y continúa siendo seguido de cerca por el otorrinolaringólogo. En la laringoscopia ambulatoria de repetición a los cuatro meses de edad, ambas cuerdas aparecían móviles con un edema de las vías respiratorias continuado.\n\n",
+    "gold_summary": "Un bebé de cuatro días de edad, a término, varón, nacido por parto vaginal sin complicaciones, con un curso de enfermería significativo para la falta de audición, se presentó en un departamento de emergencias (DE) con dificultad respiratoria y estridor en aumento. Fue trasladado a una unidad de cuidados intensivos neonatales (UCIN) de nivel III para una evaluación posterior y se le practicó una intubación debido a la hipercarbia progresiva. La laringoscopia reveló una parálisis unilateral de las cuerdas vocales (PCV) del lado izquierdo. Se le sometió a una evaluación posterior que incluyó un cerebro, cuello y tórax normales en una resonancia magnética. Se consultó a genética por la preocupación de los rasgos dismórficos en el examen físico. Después de las pruebas del panel de genes, la PCV se atribuyó a la asociación conocida con el síndrome CHARGE. Se observó un edema de las vías respiratorias en la laringoscopia que impidió la extubación hasta los dos meses de edad. Se identificaron otras características del síndrome CHARGE, incluidos los colobomas, el glaucoma, la pérdida auditiva neurosensorial y las anomalías genitales. Se le dio de alta con aire ambiente y después de la colocación de un tubo de gastrostomía con seguimiento de otorrinolaringología.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Un bebé de cuatro días tenía problemas para respirar y hacer ruido al respirar. Lo llevaron al hospital para que lo cuidaran mucho. Los doctores vieron que una cuerda en su garganta no se movía bien. Hicieron pruebas y encontraron que tenía un problema llamado síndrome CHARGE. Este problema puede hacer que los ojos, los oídos y otras partes del cuerpo no estén como deben. El bebé estuvo en el hospital hasta que pudo respirar mejor. Luego, le pusieron un tubito para ayudarlo a comer. Ahora, los doctores lo cuidan para que siga mejorando.",
+        "scores": {
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B2": {
+        "text": "**Lo que pasó con el bebé**  \nUn bebé de cuatro días, que nació sin problemas y a término, llegó al hospital porque tenía dificultad para respirar y un sonido extraño al inhalar llamado estridor. En el hospital, los médicos notaron que su respiración empeoraba y que tenía una cuerda vocal izquierda que no se movía, lo que se llama parálisis unilateral de las cuerdas vocales. Esto dificultaba que respirara bien.\n\n**Qué hicieron los médicos**  \nEl bebé fue llevado a una unidad especial para recién nacidos y le pusieron un tubo para ayudarlo a respirar mejor. Le hicieron varios estudios, incluyendo una resonancia magnética, que mostró que su cerebro, cuello y tórax estaban normales. También notaron que tenía algunas características físicas diferentes, como orejas bajas y ojos pequeños, por lo que pidieron ayuda a especialistas en genética.\n\n**El diagnóstico y su significado**  \nDespués de hacer pruebas genéticas, descubrieron que el bebé tenía una condición llamada síndrome CHARGE. Este síndrome puede causar problemas en varias partes del cuerpo, como los ojos (colobomas y glaucoma), pérdida de audición y problemas en los genitales. La parálisis de la cuerda vocal izquierda estaba relacionada con este síndrome.\n\n**El tratamiento y el seguimiento**  \nEl bebé tuvo inflamación en las vías respiratorias, lo que dificultó quitarle el tubo para respirar hasta que tenía dos meses. También le pusieron un tubo especial para alimentarse directamente al estómago (tubo de gastrostomía) a los tres meses. Finalmente, fue dado de alta para seguir en casa, pero continúa con controles médicos para vigilar su respiración y otros problemas relacionados con el síndrome CHARGE.",
+        "scores": {
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+          "ROUGE-2": 0.18903591682419657,
+          "ROUGE-L-Sum": 0.44067796610169485,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nUn recién nacido varón a término, sin complicaciones durante el parto, fue llevado al servicio de urgencias a los cuatro días de vida debido a un empeoramiento de la dificultad para respirar y la presencia de estridor (un sonido respiratorio agudo causado por la obstrucción de las vías aéreas). Estos síntomas se agravaban con la alimentación y al estar acostado boca arriba. En el examen inicial, se detectó también una deformidad torácica llamada pectus excavatum. La dificultad respiratoria mejoraba al colocarlo boca abajo o de lado.  \n\n**Hallazgos Clave**  \n- La evaluación inicial mostró acidosis respiratoria, lo que indica una acumulación de dióxido de carbono en la sangre por dificultad para respirar adecuadamente.  \n- Se inició soporte respiratorio con cánula nasal de alto flujo y posteriormente con presión positiva continua en la vía aérea (CPAP).  \n- La laringoscopia flexible (una exploración visual de la laringe) reveló parálisis unilateral de la cuerda vocal izquierda y edema (hinchazón) en varias estructuras de las vías respiratorias superiores.  \n- Se identificaron rasgos físicos sutiles que sugerían una posible condición genética, incluyendo orejas de implantación baja, mandíbula pequeña (retromicrognatia), ojos pequeños (microftalmia) y deformidades en los dedos de los pies.  \n- La resonancia magnética del cerebro, cuello y tórax fue normal, descartando lesiones estructurales en los nervios laríngeos recurrentes, que controlan las cuerdas vocales.  \n- El análisis genético confirmó la presencia de una mutación patogénica en el gen CHD7, diagnóstico que confirma el síndrome CHARGE, una enfermedad genética que afecta múltiples órganos y sistemas.  \n\n**Interpretación Clínica**  \nLa parálisis de la cuerda vocal izquierda se atribuyó a la asociación conocida con el síndrome CHARGE, que también explicó otros hallazgos clínicos como colobomas bilaterales (defectos en el ojo), glaucoma, pérdida auditiva neurosensorial y anomalías genitales. El edema persistente en las vías respiratorias superiores dificultó la extubación (retirar el tubo de respiración) hasta los dos meses de edad, requiriendo múltiples tratamientos con corticosteroides y antibióticos tópicos aplicados directamente sobre las cuerdas vocales. Posteriormente, se observó una nueva parálisis de la cuerda vocal derecha, cuya causa no está clara, aunque ambas cuerdas vocales mostraron mejoría progresiva.  \n\n**Próximos Pasos y Seguimiento**  \nEl paciente fue dado de alta respirando aire ambiente a los cuatro meses de edad, tras la colocación de un tubo de gastrostomía para alimentación directa al estómago, debido a las dificultades para alimentarse por vía oral. Continúa bajo seguimiento estrecho con otorrinolaringología para monitorizar la función de las cuerdas vocales y el estado de las vías respiratorias. Este caso resalta la importancia de una evaluación multidisciplinaria en recién nacidos con síntomas respiratorios y rasgos dismórficos, para identificar condiciones genéticas complejas como el síndrome CHARGE y manejar sus múltiples complicaciones.",
+        "scores": {
+          "ROUGE-1": 0.4790257104194858,
+          "ROUGE-2": 0.22523744911804613,
+          "ROUGE-L-Sum": 0.4438430311231394,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      }
+    }
+  },
+  {
+    "article": "Mujer de 17 años oriunda de Tucumán, acudió a la consulta por cuadro de vías aéreas superiores y hemoptisis leve. La tomografía computarizada de tórax informó, en lóbulo superior derecho, una imagen redondeada de paredes regulares y lisas de 25x24x24 mm, rodeado de un tenue halo periférico en vidrio esmerilado. No se observaba realce ante la administración de contraste endovenoso. Se sugirió un posible quiste broncogénico, por lo que se realizó una RMN de tórax que informó imagen redondeada de paredes regulares y lisas que alcanzó un diámetro anteroposterior de 25 x 24 x 24.5 mm con intensidad de señal líquida. Debido a la localización central de la lesión, se realizó una lobectomía superior derecha videoasistida. Dado que el estudio anatomopatológico intraoperatorio fue indeterminado, se complementó la resección pulmonar con un vaciamiento ganglionar mediastínico. La anatomía patológica definitiva informó neumocitoma esclerosante de 2 x 1.7 cm. La inmunomarcación fue positiva para TTF1, CK, CK7 y napsina.",
+    "gold_summary": "Describimos aquí el caso de una paciente de 17 años con diagnóstico de neumocitoma esclerosante con presentación infrecuente.",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Una niña de 17 años tenía un bulto en su pulmón. Los doctores lo sacaron con una operación para que ella esté mejor. El bulto no era peligroso.",
+        "scores": {
+          "ROUGE-1": 0.2962962962962963,
+          "ROUGE-2": 0.11538461538461538,
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B2": {
+        "text": "Caso de una joven con un tumor pulmonar poco común\n\nUna chica de 17 años de Tucumán fue al médico porque tenía síntomas en las vías respiratorias y tos con un poco de sangre. Se le hizo una tomografía, que es una imagen especial del pecho, y mostraba una bolita redonda en el pulmón derecho. Esta bolita tenía paredes lisas y un borde un poco borroso. Para entender mejor, le hicieron una resonancia magnética, que confirmó que la imagen parecía un líquido dentro de esa bolita.\n\nComo la lesión estaba en una zona difícil, los médicos decidieron sacar la parte superior del pulmón derecho usando una cirugía asistida por video, que es menos invasiva. Durante la operación, no pudieron saber exactamente qué era la lesión, así que también quitaron algunos ganglios cercanos para analizarlos.\n\nDespués de estudiar el tejido con un microscopio, los especialistas confirmaron que se trataba de un neumocitoma esclerosante. Este es un tipo raro de tumor en el pulmón que generalmente no es canceroso. Para asegurarse, usaron pruebas especiales que detectan ciertas proteínas en las células, y estas pruebas dieron resultados positivos para marcadores típicos de este tumor.\n\nEn resumen, este caso muestra cómo se identificó y trató un tumor pulmonar poco común en una paciente joven, usando diferentes estudios de imagen y cirugía para llegar a un diagnóstico claro.",
+        "scores": {
+          "ROUGE-1": 0.12408759124087591,
+          "ROUGE-2": 0.058823529411764705,
+          "ROUGE-L-Sum": 0.11678832116788321,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B3": {
+        "text": "**Contexto:**  \nSe presenta el caso de una joven de 17 años originaria de Tucumán que consultó por síntomas respiratorios superiores acompañados de hemoptisis leve (expectoración con sangre). Los estudios iniciales incluyeron una tomografía computarizada (TC) de tórax que reveló una lesión redondeada de aproximadamente 2.5 cm en el lóbulo superior derecho del pulmón, con bordes regulares y un halo periférico de vidrio esmerilado, sin captación de contraste. Posteriormente, una resonancia magnética (RMN) confirmó la presencia de esta lesión con características líquidas.\n\n**Hallazgos Clave:**  \nDebido a la ubicación central de la lesión, se decidió realizar una lobectomía superior derecha mediante cirugía videoasistida. Durante la operación, el estudio anatomopatológico preliminar no permitió un diagnóstico definitivo, por lo que se amplió la cirugía para incluir un vaciamiento ganglionar mediastínico (extirpación de ganglios linfáticos en el mediastino). El examen histológico final identificó la lesión como un neumocitoma esclerosante, un tumor pulmonar poco frecuente, de tamaño aproximado de 2 x 1.7 cm. Los marcadores inmunohistoquímicos fueron positivos para TTF1, CK, CK7 y napsina, proteínas que ayudan a confirmar el origen pulmonar y la naturaleza del tumor.\n\n**Interpretación Clínica:**  \nEl neumocitoma esclerosante es una neoplasia pulmonar rara que suele presentarse en adultos jóvenes y tiene un comportamiento generalmente benigno o de bajo grado maligno. En este caso, la presentación con hemoptisis y la localización central del tumor hicieron necesaria una intervención quirúrgica completa para su diagnóstico y tratamiento. La confirmación mediante inmunomarcadores es fundamental para diferenciarlo de otras lesiones pulmonares.\n\n**Próximos Pasos:**  \nSe recomienda un seguimiento clínico y radiológico periódico para vigilar la posible recurrencia o complicaciones postoperatorias. La cirugía completa y el vaciamiento ganglionar mediastínico realizados constituyen un manejo adecuado para este tipo de tumor, aunque su pronóstico suele ser favorable. En caso de aparición de nuevos síntomas o hallazgos, se deberá reevaluar para descartar progresión o complicaciones.",
+        "scores": {
+          "ROUGE-1": 0.09018567639257295,
+          "ROUGE-2": 0.047999999999999994,
+          "ROUGE-L-Sum": 0.07427055702917772,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      }
+    }
+  },
+  {
+    "article": "Una mujer asiática de 28 años fue admitida en el hospital para el tratamiento de «una masa pélvica durante 10 meses» el 11 de noviembre de 2018. La paciente solía tener menstruación regular, volumen menstrual moderado, dismenorrea y un G1P0L0A1. Examen ginecológico: la parte posterior del útero tenía aproximadamente 8 cm de diámetro con poca actividad y sensibilidad, pero no se observaron otras anomalías. La paciente no tenía una causa obvia de dolor abdominal durante los primeros 10 meses previos al ingreso. El examen de ultrasonido reveló una masa heterogénea en la parte superior derecha del útero con un diámetro de aproximadamente 4 cm, un nódulo del epiplón mayor con un diámetro de aproximadamente 2 cm y un nivel de CA125 sérico de 416 mU/mL. Se diagnosticó como «endometriosis, masas pélvicas inflamatorias». Se administró una terapia de rehidratación antiinfecciosa y se dio de alta a la paciente con alivio del dolor. Dos semanas después del alta, el nivel de CA125 sérico de la paciente disminuyó a 106 mU/mL y volvió a la normalidad después de 6 semanas. Sin embargo, la masa pélvica aumentó gradualmente. El reexamen de la ecografía pélvica realizada mostró una masa ecoica mixta de 7.7 cm x 7.4 cm x 8.2 cm en el lado derecho del útero con un límite claro, eco puntiforme fino en el quiste y derrame abdominal y pélvico. La ecografía de contraste mostró que la pared del quiste de la masa pélvica estaba significativamente mejorada, se sospechaba malignidad y se recomendó un tratamiento quirúrgico. El 14 de noviembre de 2018, la paciente se sometió a liberación de adherencias pélvicas e intestinales transabdominales, omento, ovarios bilaterales, peritoneo multipunto y múltiples adenomiosis y histerectomía. Durante la operación, se aspiraron aproximadamente 600 ml de ascitis hemorrágica. Tras la exploración, se observó una masa de color rojo grisáceo con un diámetro de aproximadamente 8 cm en la superficie del epiplón mayor, que era suave y se asemejaba a carne podrida. Se encontraron depósitos de celulosa marrón difusos en la superficie del útero, ovarios bilaterales, pared abdominal, tracto intestinal, surco lateral del recto y pared anterior del recto. Las lesiones no se eliminaron por completo y algunas áreas se electrocoagularon. El examen patológico de la muestra resecada mostró endometriosis del tejido retiniano con vasodilatación, ampollas, infiltración linfocítica difusa y focal, folículos ováricos císticos bilaterales, fibrosis peritoneal dentro de la necrosis del tejido adiposo, proliferación de fibroblastos, aumento de la infiltración de células espumosas y adenomiosis uterina. La patología de ascitis mostró muchos glóbulos rojos, un pequeño número de linfocitos y neutrófilos y ninguna célula tumoral. Después de la operación, la paciente se recuperó sin problemas y se trató con agonista de la hormona liberadora de gonadotropina (GnRH-α). Se inició leuprorelina una vez al mes durante 6 meses, seguido de dienogest oral (DNG) durante 3 años, después de lo cual se interrumpió la medicación durante 3 meses. La paciente concibió de forma natural y tuvo un embarazo normal. Se dio a luz a un bebé de 3300 g por vía vaginal a las 39 semanas + 3 días de gestación. Tanto la madre como el bebé estaban sanos, sin recurrencia ni reacciones adversas durante el seguimiento.\n\nMH - Humanos\nMH - Mujer\nMH - *Endometriosis/complicaciones/terapia\nMH - Adulto",
+    "gold_summary": "Preocupaciones de la paciente: Una mujer de 28 años de edad vino a nuestro hospital para recibir tratamiento debido al descubrimiento de una masa pélvica 10 meses antes. Después de la admisión, la paciente se sometió a tratamiento quirúrgico y fue dada de alta en 1 semana. Recibió tratamiento médico durante 3 años después del alta. Después de la retirada de la medicación, la paciente quedó embarazada y dio a luz a un niño sin recurrencia durante el seguimiento.\n\nDiagnósticos: Los diagnósticos iniciales al ingreso fueron «¿masa pelviana inflamatoria?» y «¿endometriosis?». Después de 10 meses, la paciente volvió a ser internada en el hospital debido a un aumento gradual de la masa, y se le diagnosticó endometriosis.\n\nIntervenciones: El paciente fue tratado con terapia antiinfecciosa de rehidratación por primera vez, y el paciente fue tratado quirúrgicamente por segunda vez, seguido de agonista de la hormona liberadora de gonadotropina (GnRH-α) y tratamiento con dienogest (DNG) después de la cirugía.\n\nResultados: Después de 6 ciclos de tratamiento con GnRH-α y 3 años de tratamiento con DNG, un hijo nació con éxito tras la interrupción de la medicación y, hasta ahora, no se han producido reacciones adversas ni recurrencias durante el período de seguimiento.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Había una mujer que tenía un bulto en su barriga por mucho tiempo. Los doctores la ayudaron con una operación y medicina para que se sintiera mejor. \n\nDespués de tomar la medicina por mucho tiempo, la mujer pudo tener un bebé sano. Ella y su bebé están bien y felices.",
+        "scores": {
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B2": {
+        "text": "**Lo que le pasó a la paciente:**  \nUna mujer de 28 años tenía una masa, que es una especie de bulto, en la parte baja de su abdomen desde hacía 10 meses. Fue al hospital para tratarse. Al principio, pensaron que podía ser una inflamación o una enfermedad llamada endometriosis, que ocurre cuando un tejido parecido al que está dentro del útero crece fuera de él y causa dolor o problemas.\n\n**Qué hicieron los médicos:**  \nPrimero, le dieron un tratamiento para la inflamación y la hidratación. Pero como la masa creció, la operaron para quitarla y examinarla mejor. Después de la cirugía, le dieron medicamentos especiales que ayudan a controlar la endometriosis. Estos medicamentos incluyen un tipo que afecta las hormonas del cuerpo (llamado agonista de GnRH) y otro llamado dienogest, que tomaba por varios años.\n\n**Qué pasó después:**  \nTras el tratamiento y la cirugía, la paciente pudo quedar embarazada de forma natural. Tuvo un bebé sano y no volvió a tener problemas ni síntomas de la enfermedad durante el tiempo que la siguieron en el hospital.\n\n**En resumen:**  \nEsta paciente con endometriosis y una masa pélvica recibió cirugía y tratamiento hormonal. Gracias a esto, pudo tener un embarazo normal y no tuvo complicaciones después del tratamiento.",
+        "scores": {
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+      "B3": {
+        "text": "Resumen detallado para público general universitario\n\n**Contexto y motivo de consulta**  \nUna mujer asiática de 28 años acudió al hospital tras haber detectado una masa en la pelvis que persistía desde hacía 10 meses. Antes de esto, su menstruación era regular, con un volumen moderado y dolor menstrual (dismenorrea). No presentaba antecedentes de embarazos exitosos, pero sí un aborto espontáneo. Durante el examen físico, se encontró que la parte posterior del útero estaba agrandada (aproximadamente 8 cm) y con poca movilidad, aunque sin otras anomalías evidentes. La paciente no había experimentado dolor abdominal significativo durante esos meses previos.\n\n**Hallazgos diagnósticos iniciales**  \nLa ecografía reveló una masa heterogénea de unos 4 cm en la parte superior derecha del útero y un pequeño nódulo en el epiplón mayor (una capa de tejido graso en el abdomen) de 2 cm. Además, el análisis sanguíneo mostró un nivel elevado de CA125 (416 mU/mL), una proteína que puede aumentar en enfermedades inflamatorias o tumorales del área pélvica. Se sospechó inicialmente que la masa correspondía a endometriosis (una condición en la que tejido similar al endometrio crece fuera del útero) o a una masa inflamatoria pélvica.\n\n**Evolución y revaluación**  \nTras un tratamiento inicial con líquidos y antibióticos, la paciente mejoró y fue dada de alta. Los niveles de CA125 disminuyeron progresivamente hasta normalizarse en 6 semanas. Sin embargo, la masa pélvica continuó creciendo, alcanzando dimensiones de aproximadamente 8 cm, con características ecográficas que sugerían posible malignidad, lo que llevó a recomendar cirugía.\n\n**Intervenciones quirúrgicas y hallazgos intraoperatorios**  \nEl 14 de noviembre de 2018, la paciente fue sometida a una cirugía abdominal para liberar adherencias (tejido cicatricial que une órganos) en la pelvis e intestinos, así como para extirpar tejido afectado en el epiplón, ovarios, peritoneo (membrana que recubre la cavidad abdominal) y el útero. Durante la operación se drenaron 600 ml de líquido abdominal con sangre (ascitis hemorrágica). Se observaron lesiones características de endometriosis, incluyendo depósitos marrones en múltiples superficies abdominales y uterinas, y una masa blanda en el epiplón que parecía tejido necrótico. No fue posible eliminar todas las lesiones, por lo que algunas áreas se trataron con electrocoagulación para reducir su actividad.\n\n**Resultados del análisis patológico**  \nEl examen microscópico confirmó la presencia de endometriosis en el tejido adiposo del epiplón, con inflamación crónica y cambios en el tejido uterino compatibles con adenomiosis (una forma de endometriosis dentro del músculo uterino). No se detectaron células tumorales malignas en el líquido ascítico. También se observaron fibrosis (formación de tejido cicatricial) y proliferación de fibroblastos (células que forman tejido conectivo).\n\n**Tratamiento posterior y seguimiento**  \nDespués de la cirugía, la paciente recibió terapia hormonal con un agonista de la hormona liberadora de gonadotropina (GnRH-α), específicamente leuprorelina, administrada mensualmente durante 6 meses para suprimir la actividad ovárica y reducir la endometriosis. Posteriormente, continuó con dienogest (un progestágeno oral) durante 3 años para mantener el control de la enfermedad. Tras suspender la medicación durante 3 meses, la paciente logró concebir de forma natural.\n\n**Resultados obstétricos y estado actual**  \nLa paciente tuvo un embarazo normal y dio a luz por vía vaginal a término (39 semanas y 3 días) a un bebé sano de 3300 gramos. Durante el seguimiento posterior, no se observaron recurrencias de la endometriosis ni efectos adversos relacionados con el tratamiento o el embarazo.\n\n---\n\n**Interpretación clínica**  \nEste caso ilustra la complejidad del diagnóstico y manejo de la endometriosis con masas pélvicas grandes y elevación del marcador CA125, que puede simular malignidad. La combinación de cirugía para el control de lesiones extensas y terapia hormonal prolongada fue efectiva para controlar la enfermedad y preservar la fertilidad, permitiendo un embarazo exitoso sin complicaciones.\n\n**Próximos pasos y recomendaciones**  \nEl seguimiento clínico continuo es fundamental para detectar posibles recurrencias. La terapia hormonal prolongada puede ser necesaria para mantener la remisión. Además, este caso destaca la importancia de un enfoque multidisciplinario para el manejo de endometriosis avanzada, especialmente en mujeres jóvenes que desean conservar la fertilidad.",
+        "scores": {
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+  {
+    "article": "Presentamos una paciente de 76 años de edad, que es traída al servicio de urgencias por bajo nivel de conciencia con tendencia al sueño.\n\nComo antecedentes médicos de interés destaca una enfermedad pulmonar intersticial difusa, dislipemia e hipertensión arterial.\n\nA la exploración física el paciente se encuentra estuporosa, arreactiva, con atonía de las 4 extremidades y desviación conjugada de la mirada hacia la derecha, sin fiebre y con una leve sequedad en piel y mucosas. La analítica sanguínea no muestra alteraciones significativas.\n\nEl paciente es valorado por el servicio de neurología que considera la realización de una TC cerebral urgente ante la sospecha de patología intracraneal de evolución aguda. Las pruebas de imagen ponen de manifiesto la presencia de numerosas burbujas aéreas que se disponen en los surcos cerebrales, cuerpo calloso y ambos tálamos así como áreas hipodensas cortico-subcorticales de distribución parcheada en hemisferio cerebeloso izquierdo y parietooccipitales bilaterales, todo ello compatible con isquemia cerebral subaguda secundaria a embolismo gaseoso.\n\nAnte los antecedentes personales de enfermedad pulmonar intersticial difusa se decide también realizar una placa de tórax en proyección anteroposterior y una TC torácica que objetivan un neumotórax apical izquierdo y aire ectópico en mediastino superior.\n\nSe decide el ingreso en la Unidad de Ictus del centro para control estrecho de constantes, sin embargo, la paciente presenta una evolución tórpida con el fallecimiento el segundo día de ingreso debido a fracaso multiorgánico.",
+    "gold_summary": "Paciente de 76 años con una enfermedad pulmonar intersticial difusa preexistente, que experimentó un ictus masivo debido a un neumomediastino espontáneo. Su presentación incluyó confusión, convulsiones y debilidad motora. Las pruebas de imagen revelaron burbujas de aire en los surcos cerebrales y áreas hipodensas en el cerebelo y parietooccipitales. Además, se observó neumotórax y aire en el mediastino superior en las radiografías de tórax y la tomografía torácica. A pesar de las medidas terapéuticas como el oxígeno hiperbárico, la paciente lamentablemente falleció debido al fallo multiorgánico.",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Había una señora de 76 años que estaba muy enferma y se sentía muy cansada. Ella tenía problemas en sus pulmones desde antes. Un día, su cerebro se enfermó mucho porque había aire donde no debía estar. Esto hizo que ella se confundiera y se sintiera muy débil. Los doctores vieron en sus fotos que había aire en su cabeza y en su pecho. Aunque trataron de ayudarla mucho, ella se puso muy mal y no pudo mejorar. Los doctores estaban tristes porque ella se fue al cielo.",
+        "scores": {
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+      "B2": {
+        "text": "Paciente de 76 años con una enfermedad pulmonar que afecta sus pulmones, llamada enfermedad pulmonar intersticial difusa. Ella llegó al hospital con confusión, somnolencia y debilidad en sus brazos y piernas. Los médicos hicieron una tomografía cerebral, que es una imagen detallada del cerebro, y encontraron burbujas de aire dentro de su cerebro y áreas dañadas en partes del cerebelo y otras zonas del cerebro. También hicieron radiografías y una tomografía del pecho, donde vieron que tenía un neumotórax, que es aire fuera del pulmón, y aire en una zona llamada mediastino, que está en el centro del pecho. Estos problemas causaron que el aire entrara en el cerebro, lo que provocó un tipo de accidente cerebrovascular llamado embolismo gaseoso. Aunque la paciente recibió tratamiento, incluyendo oxígeno especial para eliminar el aire, su estado empeoró y falleció por el fallo de varios órganos.",
+        "scores": {
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+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
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+      "B3": {
+        "text": "**Contexto**  \nSe presenta el caso de una mujer de 76 años con antecedentes de enfermedad pulmonar intersticial difusa, dislipemia e hipertensión arterial, que fue ingresada en urgencias debido a un estado de conciencia disminuido y tendencia al sueño. En la exploración física, la paciente estaba en estupor, sin respuesta a estímulos, con debilidad en las cuatro extremidades y desviación de la mirada hacia la derecha, sin fiebre y con signos leves de deshidratación.\n\n**Hallazgos Clave**  \nLa evaluación neurológica llevó a la realización urgente de una tomografía computarizada (TC) cerebral, que mostró múltiples burbujas de aire localizadas en los surcos cerebrales, el cuerpo calloso y ambos tálamos, además de áreas con menor densidad en la corteza y la sustancia subcortical del cerebelo izquierdo y regiones parietooccipitales bilaterales. Estas imágenes son compatibles con un daño cerebral por isquemia (falta de flujo sanguíneo) secundaria a embolismo gaseoso (bloqueo causado por burbujas de aire).  \n\nDado el antecedente pulmonar, se realizaron radiografías y una TC de tórax que evidenciaron un neumotórax apical izquierdo (colapso parcial del pulmón en la parte superior) y presencia de aire fuera de lugar en el mediastino superior (neumomediastino), lo que sugiere que el aire escapó desde el pulmón hacia estructuras cercanas.\n\n**Interpretación Clínica**  \nLa paciente sufrió un ictus masivo debido a la entrada de aire en la circulación cerebral, probablemente originado por el neumotórax y el neumomediastino espontáneos relacionados con su enfermedad pulmonar intersticial. Esta situación es grave porque las burbujas de aire pueden bloquear vasos sanguíneos y causar daño cerebral extenso. A pesar de la atención especializada y las medidas terapéuticas, incluyendo el soporte en la Unidad de Ictus, la evolución fue desfavorable.\n\n**Próximos Pasos y Resultado**  \nLa paciente falleció al segundo día de ingreso debido a un fallo multiorgánico, que es la incapacidad progresiva de varios órganos vitales. Este caso resalta la importancia de reconocer rápidamente el embolismo gaseoso cerebral como una complicación potencialmente mortal en pacientes con enfermedades pulmonares crónicas y neumotórax espontáneo.",
+        "scores": {
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
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+  {
+    "article": "Un hombre de 24 años de edad, de etnia persa, presentó una queja principal de mal olor bucal después de un período de recuperación de la enfermedad leve por coronavirus 2019 (COVID-19), que quería resolver lo antes posible. Su dentista notó pérdida ósea y sangrado al explorar el área interproximal de los dientes número 18 y 19 clínicamente. Se realizó un escalamiento y un aplanamiento radicular, y se ordenaron radiografías periapicales y panorámicas para la evaluación del paciente. Sin embargo, el paciente se negó a tomar radiografías. La halitosis del paciente disminuyó después de 1 semana de tratamiento. Después de 2 meses, el paciente volvió a su dentista con la queja principal de sensibilidad al frío en sus incisivos mandibulares. El dentista realizó una prueba de vitalidad, y los dientes eran vitales excepto los números 23 y 24. El dentista tomó una radiografía periapical, y una lesión radiolucente en la mandíbula anterior era evidente.\n\nEn la radiografía panorámica, se evidenció una lesión radiolúcida lítica grande y bien definida con bordes festoneados que se extendían desde el diente número 31 en el lado derecho hasta el ramus ascendente izquierdo. Un estudio posterior de tomografía computarizada de haz cónico (TCFC) reveló una lesión lítica multilocular grande, con un margen relativamente distinto, que causó adelgazamiento y perforación de los cortexes bucales y linguales y signos de festoneado.\n\nTras el examen, se remitió al paciente a un cirujano oral y maxilofacial. En la entrevista médica, el paciente explicó su prolapso de la válvula mitral; antecedentes de episodios recurrentes de otitis desde el primer año de vida; antecedentes de septicemia de origen desconocido cuando tenía un año de edad, tras episodios de diarrea y vómitos; antecedentes de uso de broncodilatadores para la alergia estacional; antecedentes de uso de levotiroxina, cabergolina, acetato de desmopresina (DDAVP) en spray y gel de testosterona durante 4 años tras el diagnóstico de síndrome de silla turca vacía, tras poliúria y polidipsia; y, por último, antecedentes de infección reciente por COVID-19 (3 meses antes). Su historia familiar reveló tiroiditis de Hashimoto en su familia materna; su abuelo, su madre y sus tres tías padecían este tipo de hipotiroidismo. El historial quirúrgico previo del paciente incluía una reparación de una hernia inguinal 10 años antes sin complicaciones. Además, el paciente era obeso, con un índice de masa corporal (IMC) de 34,5.\n\nEn el examen clínico, los hallazgos extraorales e intraorales no fueron relevantes. Los exámenes de laboratorio, incluido el recuento sanguíneo completo (CBC), fueron normales, excepto por un aumento en la velocidad de sedimentación globular (ESR) y los niveles de proteína C reactiva (CRP). Se realizó una biopsia incisional en la mandíbula anterior y la muestra se envió al departamento de patología oral y maxilofacial de la Universidad de Ciencias Médicas Shahid Beheshti. Las secciones mostraron una infiltración difusa de grandes células de tinción pálida, como los histiocitos, con eosinófilos dentados y numerosos en el fondo fibroso. Un examen de inmunohistoquímica (IHC) reveló un positivo disperso para el grupo de diferenciación 1a (CD-1a) (+ +), un positivo fuerte para Langerin (CD-207) (+ + +), y más del 50% positivo para S-100.\n\nDe acuerdo con los datos clínicos, radiológicos e histopatológicos, se llegó al diagnóstico de LCH. Los diagnósticos diferenciales fueron osteomielitis, granuloma eosinófilo y metástasis ósea. Sin embargo, debido a las pruebas de laboratorio, los datos radiológicos y el historial clínico, se confirmó el diagnóstico de LCH. Por lo tanto, para un examen más a fondo, el paciente fue derivado al departamento de medicina nuclear para una tomografía por emisión de positrones con fluor-2-desoxiglucosa y una tomografía computarizada (FDG PET/CT), que reveló lesiones líticas hipermetabólicas en la mandíbula, el parietal derecho, el frontal izquierdo y el esfenoidal izquierdo, y opacidad hipermetabólica en el seno etmoidal izquierdo. Además, se observó una actividad metabólica aumentada en la región sellar, hidrocefalia comunicante y amígdalas palatinas hipermetabólicas prominentes. Además, se evidenció una actividad metabólica heterogénea aumentada en las tibias y fémures bilaterales.\n\nUna resonancia magnética del cerebro reveló una notable ampliación de la intensidad del material del líquido cefalorraquídeo (LCR) que contiene la silla turca. La adenohipófisis apareció como una capa delgada en la base de la silla turca agrandada, y se observaron cambios homogéneos e inflamatorios en las células aéreas mastoideas izquierdas. Se observó la extensión de la inflamación hacia el oído medio izquierdo (es de destacar que el paciente había sufrido de otitis durante muchos años). De acuerdo con la implicación multifocal de la enfermedad y su pronóstico cuestionable, el paciente fue derivado al departamento de oncología para quimioterapia sistémica. Pruebas posteriores revelaron mutaciones en el oncogen BRAF y no se detectaron mutaciones en KRAS y NRAS. El oncólogo eligió un régimen de denosumab, vinblastina, etopósido, 6-mercaptopurina, metotrexato y pegfilgrastim; sin embargo, el seguimiento no fue posible ya que el paciente falleció tras un accidente.\n",
+    "gold_summary": "Un paciente de 24 años de edad, de etnia persa, se presentó con una queja principal de halitosis tras recuperarse de la enfermedad por coronavirus 2019 en el consultorio de su dentista general. Los exámenes intraorales y extraorales no revelaron ningún problema específico. En la sesión de seguimiento tras el tratamiento periodontal de fase I, la sensibilidad de los dientes al estímulo frío era evidente, y las radiografías revelaron una gran lesión intraósea lítica en la mandíbula. Una biopsia incisional reveló células de Langerhans y una reacción positiva a Langerina y al grupo de diferenciación 1a, por lo que se le diagnosticó histiocitosis de células de Langerhans. Después de realizar una tomografía por emisión de positrones con fluoro-2-desoxiglucosa y una tomografía computarizada, una resonancia magnética y una tomografía computarizada de haz cónico, debido a la implicación generalizada de la enfermedad, el paciente fue derivado a un oncólogo. En última instancia, se descubrió que los problemas de salud infantil del paciente, incluidos los problemas endocrinos, probablemente fueron causados por una histiocitosis de células de Langerhans no diagnosticada. El oncólogo eligió un régimen de denosumab, vinblastina, etopósido, 6-mercaptopurina, metotrexato y pegfilgrastim. El seguimiento no fue posible ya que el paciente falleció tras un accidente.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Había un hombre joven que tenía mal olor en la boca. Esto pasó después de que se enfermó con un virus. El dentista vio que algunos dientes le dolían con el frío. También encontró un hueco grande en el hueso de su mandíbula.\n\nEl doctor tomó un pedacito de ese hueso para mirar con un microscopio. Vieron unas células especiales llamadas células de Langerhans. Esto dijo que tenía una enfermedad llamada histiocitosis de células de Langerhans.\n\nEl hombre fue a ver a otro doctor que sabe de enfermedades graves. Le hicieron muchas pruebas para ver dónde estaba la enfermedad. Los doctores dijeron que la enfermedad estaba en muchas partes de su cuerpo.\n\nEl doctor le dio medicinas fuertes para ayudarlo. Pero el hombre tuvo un accidente y no pudo seguir con el tratamiento. Los doctores estaban muy tristes por eso.",
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+      "B2": {
+        "text": "**Lo que le pasó al paciente**  \nUn joven de 24 años, después de recuperarse de un caso leve de COVID-19, fue al dentista porque tenía mal olor en la boca. Al principio, no se encontraron problemas visibles en su boca ni en su cara. Sin embargo, después de un tratamiento para limpiar sus dientes, empezó a sentir sensibilidad al frío en algunos dientes. Las radiografías mostraron una lesión grande en el hueso de la mandíbula.\n\n**Qué encontraron los médicos**  \nPara entender mejor la lesión, los médicos tomaron una biopsia, que es cuando se extrae un pequeño pedazo de tejido para examinarlo bajo el microscopio. En esta muestra, vieron células especiales llamadas células de Langerhans. Estas células reaccionaron a ciertas pruebas que confirmaron que el paciente tenía una enfermedad llamada histiocitosis de células de Langerhans (LCH). Esta enfermedad puede afectar varios órganos y huesos.\n\n**Estudios adicionales y diagnóstico**  \nEl paciente se sometió a varios estudios, como tomografías y resonancias magnéticas, que mostraron que la enfermedad estaba en varias partes de su cuerpo, incluyendo huesos de la cabeza y las piernas, y también afectaba algunas áreas del cerebro. Además, descubrieron que algunos problemas de salud que tuvo cuando era niño, como problemas hormonales y frecuentes infecciones de oído, probablemente estaban relacionados con esta enfermedad que no se había detectado antes.\n\n**Tratamiento y resultado**  \nDebido a que la enfermedad estaba extendida, el paciente fue enviado a un especialista en cáncer para recibir quimioterapia, que es un tratamiento con medicamentos para combatir células enfermas. El médico eligió un plan con varios medicamentos para tratar la enfermedad. Lamentablemente, no se pudo hacer un seguimiento del tratamiento porque el paciente falleció debido a un accidente.  \n\nEste caso muestra la importancia de investigar a fondo cuando aparecen problemas inusuales en la boca, ya que pueden ser señales de enfermedades más serias en el cuerpo.",
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+      "B3": {
+        "text": "**Contexto**  \nUn hombre persa de 24 años acudió a su dentista quejándose de mal olor en la boca (halitosis) poco después de recuperarse de una infección leve por COVID-19. Inicialmente, no se encontraron problemas visibles en su boca ni en el examen externo. Sin embargo, tras un tratamiento periodontal inicial, el paciente comenzó a experimentar sensibilidad dental al frío, lo que llevó a la realización de radiografías que mostraron una lesión ósea anormal en la mandíbula.\n\n**Hallazgos Clave**  \nUna biopsia de la lesión reveló la presencia de células de Langerhans, un tipo específico de células inmunitarias, confirmada mediante pruebas inmunohistoquímicas positivas para marcadores como Langerina (CD-207) y CD1a. Estos hallazgos permitieron diagnosticar una enfermedad llamada histiocitosis de células de Langerhans (LCH), que es una condición poco común caracterizada por la proliferación anormal de estas células. Estudios de imagen adicionales, incluyendo tomografía computarizada de haz cónico (TCFC), tomografía por emisión de positrones con fluor-2-desoxiglucosa (FDG PET/CT) y resonancia magnética cerebral, revelaron que la enfermedad afectaba múltiples áreas óseas, incluyendo varias regiones del cráneo y huesos largos, así como inflamación en estructuras cercanas al oído y la hipófisis (glándula cerebral que regula varias funciones endocrinas).\n\n**Interpretación Clínica**  \nEl diagnóstico de LCH explicó no solo la lesión mandibular sino también varios problemas de salud que el paciente había tenido desde la infancia, como episodios recurrentes de otitis (infección del oído), alteraciones endocrinas relacionadas con un síndrome de silla turca vacía (una anomalía en la glándula hipófisis), y otros síntomas sistémicos. La enfermedad mostró un compromiso multifocal, lo que significa que afectaba varias áreas del cuerpo, complicando su pronóstico. Además, se detectó una mutación en el oncogen BRAF, un factor genético que puede influir en el comportamiento de la enfermedad y en las opciones de tratamiento.\n\n**Próximos Pasos y Tratamiento**  \nDebido a la extensión y gravedad de la enfermedad, el paciente fue remitido al departamento de oncología para recibir quimioterapia sistémica. El régimen elegido incluyó varios medicamentos: denosumab (que ayuda a inhibir la destrucción ósea), vinblastina, etopósido, 6-mercaptopurina, metotrexato y pegfilgrastim (que estimula la producción de células sanguíneas). Lamentablemente, no fue posible realizar un seguimiento del tratamiento porque el paciente falleció posteriormente a causa de un accidente.\n\n**Resumen Final**  \nEste caso ilustra cómo una enfermedad poco común como la histiocitosis de células de Langerhans puede manifestarse inicialmente con síntomas aparentemente leves, como mal aliento y sensibilidad dental, y estar relacionada con problemas médicos complejos desde la infancia. La detección temprana y el diagnóstico preciso mediante biopsia y estudios de imagen son fundamentales para orientar un tratamiento adecuado, aunque el pronóstico puede ser reservado cuando la enfermedad afecta múltiples órganos.",
+        "scores": {
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+    "article": "La paciente es una mujer de 66 años de edad que goza de buena salud. A mediados de la década de 1980, recibió varias sesiones de tratamiento con rayos grenz en el cuero cabelludo para aliviar el picor asociado con la psoriasis del cuero cabelludo. Con un tratamiento regular de aproximadamente una sesión al mes durante un período de 5 años, que se complementó de vez en cuando con alquitrán de hulla, ácido salicílico y prednisona, logró cierto alivio de su enfermedad. Con el tiempo, su cabello se adelgazó; la piel en toda el área del cuero cabelludo se volvió sensible al dolor y se produjo cicatrización. Los tratamientos con rayos grenz se habían administrado en una clínica privada; no se disponía de detalles del tratamiento, como la dosis única y acumulada. No había sufrido radiodermitis.\n\nEn un período muy breve en 2020, unos 35 años después de que cesara el tratamiento de radiación, aparecieron numerosos BCC y queratosis actínicas premalignas (AK) en su cuero cabelludo. Se inició un régimen de tratamiento de extirpación quirúrgica de BCC verificado por histología preoperatoria y crioterapia de AK por evaluación del médico. La terapia fotodinámica o los tratamientos tópicos no eran aplicables debido a la sensibilidad al dolor y las secuelas de la cirugía. De 2020 a 2022, recibió varios tratamientos de criocirugía y curetaje y un total de 13 extirpaciones quirúrgicas de BCC por cirugía de Mohs. Se estima que su número total de extirpaciones a lo largo del tiempo es de unos 30. Los BCC recalcitrantes y de novo en el cuero cabelludo cada vez más dañado, obviamente, son un desafío eterno; por lo tanto, los cirujanos plásticos y los dermatólogos buscaban otra modalidad de tratamiento con un mejor índice terapéutico.\n\nEn septiembre de 2022, aparecieron nuevos CCB confirmados histológicamente en el cuero cabelludo. La exploración por ultrasonido (DermaScan C, Cortex Technology ApS, Aalborg, Dinamarca) mostró tumores ecolucidos de 0,5-1,3 mm de espesor en ambos sitios analizados histológicamente, así como en algunas lesiones adicionales que pudieron identificarse en base al examen clínico y dermatoscópico. La paciente, tras ser informada, dio su consentimiento por escrito para el tratamiento con HIFU, con o sin biopsia de pretratamiento de las lesiones sospechosas.\n\nSe delinearon las lesiones elegibles para el tratamiento con un rotulador impermeable, incluyendo un margen perilesional de 2 mm. Se mapeó cada lesión seleccionada en una lámina transparente para ayudar a determinar la ubicación precisa en el seguimiento. Se usó el ultrasonido de 20 MHz para confirmar la profundidad de las lesiones identificadas al inicio y en las visitas de seguimiento posteriores. Debido al estado del cuero cabelludo conocido por ser sensible al dolor, se administró anestesia local (lidocaína 25 mg/ml + adrenalina 5 mg/ml, Amgros I/S, Copenhagen, Dinamarca) a todas las lesiones 10-15 minutos antes del tratamiento.\n\nLas lesiones fueron tratadas con HIFU utilizando la sonda de 1.3 mm; ajustes de 150 ms/dosis y energía acústica de 0.9 J/dosis. Se aplicaron 20-200 dosis a las lesiones, dependiendo de la extensión de la lesión. Las lesiones tratadas se curaron de forma espontánea sin complicaciones o necesidad de tratamiento especial. Se programaron visitas de seguimiento cada 3-6 meses para controlar la tasa de curación/recaída, tolerancia local y lesiones nuevas no identificadas anteriormente.\n\nDurante los 15 meses posteriores a la limpieza inicial con HIFU, se trataron con HIFU un total de 10 lesiones que, de acuerdo con las rutinas, hubieran requerido una biopsia seguida de una cirugía de escisión, en sesiones de unos 30 minutos. Las lesiones se curaron en unos pocos días sin complicaciones ni necesidad de intervención. Se observó una limpieza total en 7 de 8 lesiones de BCC tratadas y en ambas lesiones de AK. La única lesión recurrente de BCC de pequeño tamaño se observó después de 15 meses entre las primeras seis lesiones tratadas; la lesión se volvió a tratar con HIFU. Ejemplos de lesiones curadas 15 meses después del tratamiento con HIFU; el tumor con recurrencia.\n",
+    "gold_summary": "Una mujer de 66 años que en la década de 1980 había recibido varios tratamientos de rayos gamma en el cuero cabelludo desarrolló múltiples carcinomas basocelulares en la zona. Se le habían realizado más de 30 cirugías de escisión, incluida la cirugía de Mohs, en el pasado, con muchas complicaciones locales, pero, no obstante, los cánceres recurrentes. Los tratamientos con HIFU aplicados a ocho carcinomas basocelulares y dos lesiones precancerosas dieron como resultado una limpieza completa en el control a los 12 meses, pero una recurrencia después de 15 meses.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Había una señora de 66 años con problemas en su cabeza. Hace mucho tiempo, le dieron unos rayos para ayudar su piel que le picaba. Pero después, le salieron muchos bultitos malos en la cabeza.\n\nElla tuvo muchas operaciones para quitar esos bultitos. A veces, le dolía mucho y los bultitos volvían a salir. Luego, los doctores usaron un tratamiento especial con un aparato que usa calor para quitar los bultitos.\n\nDespués de un año, casi todos los bultitos se fueron. Pero después de un poco más de un año, uno volvió a salir. Los doctores la cuidaron y trataron otra vez. Ella está siendo cuidada con mucho cariño.",
+        "scores": {
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+      "B2": {
+        "text": "**Caso de una mujer con cáncer en el cuero cabelludo**\n\nUna mujer de 66 años recibió hace muchos años, en la década de 1980, un tratamiento con rayos especiales en su cuero cabelludo para aliviar una enfermedad llamada psoriasis, que causa picor y enrojecimiento. Después de ese tratamiento, su piel se volvió sensible y se dañó con el tiempo.\n\nAproximadamente 35 años después, empezaron a aparecer en su cuero cabelludo varios tumores llamados carcinomas basocelulares (que son un tipo de cáncer de piel) y lesiones que podrían volverse cancerosas. Para tratar estos tumores, le hicieron más de 30 cirugías, incluyendo una técnica especial llamada cirugía de Mohs, que busca eliminar el cáncer sin dañar mucho la piel sana. Sin embargo, los tumores seguían apareciendo y la piel estaba muy dañada y sensible.\n\n**Nuevo tratamiento con ultrasonido de alta intensidad (HIFU)**\n\nEn 2022, los médicos decidieron probar un nuevo tratamiento llamado HIFU, que usa ondas de ultrasonido para destruir los tumores sin necesidad de cirugía. Antes de aplicar el tratamiento, marcaron las lesiones y usaron anestesia local para evitar el dolor.\n\nDurante 15 meses, trataron con HIFU diez lesiones: ocho eran carcinomas basocelulares y dos eran lesiones precancerosas. Siete de los ocho tumores desaparecieron completamente después de un año. Solo uno volvió a aparecer después de 15 meses, y fue tratado nuevamente con HIFU. Las lesiones precancerosas también sanaron sin problemas.\n\n**Qué significa esto**\n\nEste caso muestra que el tratamiento con HIFU puede ser una opción efectiva para eliminar ciertos cánceres de piel y lesiones precancerosas en pacientes con piel sensible y dañada, evitando cirugías complicadas. Aunque algunos tumores pueden volver, el HIFU ofrece una alternativa menos invasiva y con buena tolerancia para controlar estos problemas.",
+        "scores": {
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
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+      "B3": {
+        "text": "**Contexto**  \nSe trata de una mujer de 66 años que, durante la década de 1980, recibió múltiples tratamientos con rayos grenz (una forma de radiación de baja energía) en el cuero cabelludo para aliviar la psoriasis, una enfermedad inflamatoria de la piel. Estos tratamientos, junto con otros medicamentos tópicos, lograron cierto alivio, pero con el tiempo provocaron adelgazamiento del cabello, sensibilidad dolorosa y cicatrización en la piel del cuero cabelludo. Aproximadamente 35 años después de finalizar la radioterapia, la paciente desarrolló numerosos carcinomas basocelulares (un tipo común de cáncer de piel) y queratosis actínicas (lesiones precancerosas) en la misma zona.\n\n**Hallazgos Clave**  \nEntre 2020 y 2022, la paciente fue sometida a múltiples tratamientos convencionales, incluyendo más de 30 cirugías para extirpar los carcinomas basocelulares, algunas de ellas mediante cirugía de Mohs, una técnica especializada para eliminar tumores de piel con precisión. También recibió crioterapia para las lesiones precancerosas. Sin embargo, los tumores continuaron apareciendo, y la sensibilidad y daño en el cuero cabelludo dificultaban la aplicación de otros tratamientos tópicos o fotodinámicos.\n\nEn septiembre de 2022, se detectaron nuevos carcinomas basocelulares confirmados mediante biopsia. Para evaluar la extensión y profundidad de las lesiones, se utilizó un ultrasonido especializado que mostró tumores de entre 0,5 y 1,3 mm de grosor. La paciente aceptó someterse a un tratamiento con ultrasonido focalizado de alta intensidad (HIFU, por sus siglas en inglés), una técnica que utiliza ondas de ultrasonido para destruir tejido tumoral sin cirugía.\n\nAntes del tratamiento, se aplicó anestesia local para minimizar el dolor, y las lesiones fueron cuidadosamente marcadas y mapeadas para su seguimiento. El HIFU se administró con parámetros específicos (dosis de 150 ms y energía de 0.9 julios por dosis), aplicando entre 20 y 200 dosis según el tamaño de cada lesión.\n\n**Interpretación Clínica**  \nDurante los 15 meses posteriores al tratamiento inicial con HIFU, se trataron un total de 10 lesiones (8 carcinomas basocelulares y 2 queratosis actínicas) que, según los protocolos habituales, habrían requerido biopsia y cirugía. Todas las lesiones sanaron espontáneamente en pocos días sin complicaciones ni necesidad de tratamientos adicionales.\n\nEn el seguimiento a 12 meses, se observó una eliminación completa de 7 de las 8 lesiones de carcinoma basocelular y de ambas lesiones precancerosas. Solo una lesión pequeña de carcinoma basocelular recidivó después de 15 meses y fue nuevamente tratada con HIFU con éxito.\n\n**Próximos Pasos**  \nEl uso de HIFU en esta paciente representa una alternativa prometedora para el manejo de carcinomas basocelulares recurrentes en un cuero cabelludo dañado y sensible, donde las opciones quirúrgicas y tópicas son limitadas o generan complicaciones. Se recomienda continuar con controles periódicos cada 3 a 6 meses para detectar nuevas lesiones o recurrencias y evaluar la tolerancia a largo plazo del tratamiento. Además, la experiencia obtenida sugiere que el HIFU podría ser una modalidad terapéutica eficaz y menos invasiva para casos similares en el futuro.",
+        "scores": {
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+    "article": "Se realizó un trasplante cardíaco ortotópico a una niña de 12 años con insuficiencia cardíaca en fase terminal debido a una miocardiopatía restrictiva. Durante la operación, se presentó una disfunción primaria grave del injerto, que requirió el uso de oxigenación por membrana extracorpórea venosa arterial. La función cardíaca se recuperó completamente después de 4 días, y su período postoperatorio se complicó por una insuficiencia renal aguda transitoria y un bloqueo auriculoventricular completo que duró >3 semanas después de la operación. Para evitar la disincronía del ventrículo izquierdo y el posible daño de la derivación del ventrículo derecho debido a las biopsias endomiocárdicas de vigilancia de rechazo múltiple, se indicó un marcapasos biventricular transvenoso que utiliza un marcapasos del ventrículo izquierdo aislado a través de la vena coronaria.\n\nBajo anestesia local y sedación suave, se cortó la vena cefálica izquierda y se introdujo un catéter guía en la vena subclavia y se colocó en el seno coronario inicialmente para realizar un venograma cardiaco. Se implantó un electrodo de estimulación endocárdica de elución de esteroides unipolar con mecanismo de fijación activa (Attain StarFix® 4195, Medtronic, Minneapolis, MN) en la rama de la vena interventricular anterior. Las medidas en el momento del implante fueron las siguientes: umbral 2 V a 0,4 ms, onda R 6 mV e impedancia 300 Ω a 4,8 mA. Se implantó un segundo electrodo de estimulación endocárdica de elución de esteroides bipolar con fijación activa (2088T®, St. Jude Medical, Minneapolis, MN) en la aurícula derecha.\n\nAmbos cables se aseguraron y se conectaron a un marcapasos adaptable a la frecuencia (Accent DR®, St. Jude Medical, Minneapolis, MN) que se colocó en una bolsa muscular infraclavicular izquierda y se programó a VDD. Las mediciones de los cables electrofisiológicos fueron estables después del implante: umbral ventricular 1.5 V a 0.7 ms, onda R 4.5 mV, onda P 4.3 mV (bipolar), impedancia ventricular 260 Ω y vida útil estimada de la batería de 5 años.\n\nEl electrocardiograma posterior al implante mostró complejos de morfología de bloqueo de rama derecha, y la evaluación ecocardiográfica mostró ausencia de disincronías auriculoventriculares, interventriculares e intraventriculares. En el seguimiento a 5 años, el paciente permaneció en Clase Funcional I con el mismo sistema de estimulación y conservó la función ventricular.\n\nMH - Bloqueo auriculoventricular/etiología/*terapia\nMH - Niño\nMH - Sinus coronario\nMH - Mujer\nMH - Insuficiencia cardiaca/cirugía\nMH - Trasplante de corazón/*efectos adversos\nMH - Ventrículos del corazón\nMH - Humanos\nMH - *Marcapasos, artificial\nMH - Disfunción/complicaciones/tratamiento del injerto primario\n",
+    "gold_summary": "Se sometió a un trasplante de corazón ortotópico a un niño de 12 años con insuficiencia cardiaca en fase terminal debido a una miocardiopatía restrictiva. La disfunción primaria del injerto precisó oxigenación con membrana extracorpórea venosa arterial. La función cardiaca se normalizó, pero el bloqueo auriculoventricular completo persistió después de 3 semanas. Se realizó un marcapaso bicameral con marcapaso transvenoso del ventrículo izquierdo a través del seno coronario. Tras 5 años de seguimiento, el paciente se encuentra estable con el mismo sistema de marcapaso y con la función ventricular preservada.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Un niño de 12 años recibió un nuevo corazón porque su corazón estaba muy enfermo. Al principio, su nuevo corazón tuvo problemas y necesitó ayuda para funcionar. Después de un tiempo, el corazón empezó a trabajar bien. Pero el niño tenía un problema con el ritmo del corazón. Por eso, los doctores le pusieron un pequeño aparato llamado marcapasos para ayudar a que su corazón latiera bien. Cinco años después, el niño está bien y su corazón funciona muy bien con el marcapasos.",
+        "scores": {
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+      "B2": {
+        "text": "**Trasplante de Corazón y Uso de Marcapasos en una Niña de 12 Años**\n\nUna niña de 12 años con un problema grave en el corazón llamado miocardiopatía restrictiva, que causa que el corazón no funcione bien, recibió un trasplante de corazón. Durante la operación, el nuevo corazón tuvo dificultades para funcionar correctamente, por lo que los médicos usaron una máquina especial llamada oxigenación por membrana extracorpórea. Esta máquina ayuda a oxigenar la sangre cuando el corazón está débil.\n\nDespués de cuatro días, el corazón trasplantado comenzó a funcionar bien. Sin embargo, la niña tuvo un problema llamado bloqueo auriculoventricular completo, que significa que las señales eléctricas entre las partes superiores e inferiores del corazón no se transmitían bien. Este problema duró más de tres semanas.\n\nPara ayudar a su corazón a latir de manera sincronizada y evitar daños, los médicos le implantaron un marcapasos especial. Un marcapasos es un dispositivo que envía señales eléctricas para controlar el ritmo del corazón. En este caso, colocaron un marcapasos que estimula ambos ventrículos del corazón (las partes inferiores) usando cables que pasan por las venas hasta llegar al corazón.\n\nEl procedimiento se hizo con anestesia local y sedación suave, y los cables se colocaron cuidadosamente en las venas del corazón. El marcapasos se programó para adaptarse a las necesidades del corazón de la niña. Después de la operación, los exámenes mostraron que el corazón latía de forma sincronizada y sin problemas.\n\nCinco años después, la niña está estable, con buena función del corazón y sigue usando el mismo marcapasos sin complicaciones. Esto muestra que el tratamiento fue exitoso para mejorar su calidad de vida.",
+        "scores": {
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+          "ROUGE-2": 0.11320754716981131,
+          "ROUGE-L-Sum": 0.29577464788732394,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
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+      "B3": {
+        "text": "**Contexto**  \nUna niña de 12 años con insuficiencia cardíaca avanzada causada por una miocardiopatía restrictiva (una enfermedad que limita la capacidad del corazón para llenarse de sangre) fue sometida a un trasplante cardíaco ortotópico, que consiste en reemplazar el corazón enfermo por uno sano en la misma posición anatómica. Durante la cirugía, presentó una disfunción grave del nuevo corazón (injerto), lo que requirió soporte temporal con oxigenación por membrana extracorpórea venosa arterial (una técnica que ayuda a oxigenar la sangre y mantener la circulación mientras el corazón se recupera).\n\n**Hallazgos Clave**  \n- La función cardíaca del injerto se recuperó completamente en 4 días.  \n- Posteriormente, la paciente desarrolló un bloqueo auriculoventricular completo (una interrupción total en la transmisión eléctrica entre las aurículas y los ventrículos del corazón) que persistió por más de tres semanas.  \n- Para evitar problemas relacionados con la descoordinación del ventrículo izquierdo y el daño potencial al ventrículo derecho por las biopsias repetidas que se realizan para vigilar el rechazo del trasplante, se decidió implantar un marcapasos biventricular transvenoso. Este dispositivo estimula eléctricamente ambos ventrículos para mantener un ritmo cardíaco sincronizado.  \n- El electrodo del ventrículo izquierdo se colocó a través de la vena coronaria (una vena del corazón) usando un catéter guiado, mientras que otro electrodo se implantó en la aurícula derecha.  \n- Ambos electrodos se conectaron a un marcapasos adaptable a la frecuencia, ubicado en una bolsa muscular debajo de la clavícula izquierda.  \n- Las mediciones eléctricas del marcapasos mostraron parámetros estables y adecuados para un funcionamiento óptimo.  \n- El electrocardiograma posterior mostró una morfología compatible con bloqueo de rama derecha, pero la ecocardiografía confirmó que no existían desincronías en la contracción de las cámaras cardíacas.\n\n**Interpretación Clínica**  \nEl uso de un marcapasos biventricular con estimulación del ventrículo izquierdo a través del seno coronario resultó ser una estrategia efectiva para manejar el bloqueo auriculoventricular prolongado en esta paciente trasplantada. Este enfoque permitió mantener la sincronía en la contracción del corazón, evitando complicaciones que podrían afectar la función ventricular. La estabilidad de los parámetros eléctricos y la ausencia de disincronías evidenciadas por ecocardiografía respaldan la eficacia del tratamiento.\n\n**Próximos Pasos y Seguimiento**  \nA cinco años del implante del marcapasos, la paciente se mantiene en clase funcional I (sin limitaciones para realizar actividades físicas normales), con función ventricular preservada y sin necesidad de cambios en el sistema de estimulación. Esto indica un pronóstico favorable y una buena calidad de vida a largo plazo. Se recomienda continuar con el seguimiento cardiológico regular para monitorear la función del marcapasos y del injerto cardíaco, así como para detectar cualquier posible complicación futura.",
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+  },
+  {
+    "article": "Una paciente de 20 años de edad se presentó con distensión abdominal progresiva asociada con calambres abdominales, incapacidad para expulsar flatos y heces, así como vómitos frecuentes de materia ingerida y biliar de un día de duración. El día anterior, dio a luz por cesárea por una indicación de bradicardia fetal severa. También tenía preeclampsia sin signos de gravedad y desnutrición de inicio en la edad adulta con un índice de masa corporal (IMC) de 16,5 kg/M2. No tenía antecedentes de cirugía abdominal previa. Negó cualquier queja similar en el pasado o antecedentes de cambio de hábitos intestinales o estreñimiento con paso de heces sanguinolentas. No tenía ninguna enfermedad médica crónica conocida.\n\nEn el examen físico, la paciente se veía enferma y con dolor. Su presión arterial era de 90/70 mmHg, su pulso oscilaba entre 116 y 120 latidos por minuto, y su frecuencia respiratoria era de 22 a 24 respiraciones por minuto. No se registró fiebre. Su abdomen estaba muy distendido y simétrico, con visibles movimientos intestinales peristálticos. Había una difusa sensibilidad directa en todo su abdomen, más en el cuadrante inferior derecho. Había un signo positivo de acumulación de fluido intraperitoneal con opacidad cambiante. Había una herida quirúrgica suprapúbica bien aproximada con un vendaje limpio. El examen rectal digital no mostró nada destacable. Tenía una herida superficial lineal de 3 cm de largo, orientada verticalmente, en su labio mayor izquierdo, que el equipo de obstetricia pensó inicialmente que era una quemadura de yodo en la piel.\n\nSe le introdujo un catéter y se le resucitó con dos bolsas de solución salina normal y produjo 200 ml de orina en una hora. Se le introdujo una sonda nasogástrica (NGT) pero no hubo una salida significativa. Se le realizó un hemograma completo y una radiografía abdominal simple. Su recuento de glóbulos blancos era de 1780 células/µl con predominio de neutrófilos del 88 %, hemoglobina de 12,7 mg/dl y un recuento de plaquetas de 78 x 103/ µl. Su prueba de función renal era normal y sus enzimas hepáticas estaban ligeramente elevadas por encima del rango normal pero no fue significativo. Su radiografía abdominal simple muestra múltiples niveles de aire-líquido ubicados centralmente con un bucle intestinal grande dilatado ubicado periféricamente y blanqueamiento del espacio pélvico que indica una acumulación de líquido. No se solicitó una tomografía computarizada abdominal (CT) porque trabajamos en un entorno con recursos limitados y para pacientes con obstrucción intestinal, solicitamos una tomografía computarizada cuando existe la posibilidad de un diagnóstico alternativo o cuando se sospecha una obstrucción tumoral.\n\nTras obtener el consentimiento informado por escrito, se exploró a la paciente bajo anestesia general con un diagnóstico de abdomen agudo secundario a obstrucción intestinal mixta secundaria a vólvulo del intestino delgado. El hallazgo intraoperatorio fue un íleon distal que rodeaba el ciego y el colon ascendente proximal, ambos móviles y no adheridos a la pared abdominal posterolateral derecha. Tanto el íleon como el ciego, así como el colon ascendente, eran viables. La punta del apéndice estaba enredada con el nudo ileal y estaba gangrenoso. El intestino delgado proximal y el intestino grueso distal estaban muy distendidos, pero en su ubicación normal. Había unos cuatro litros de líquido intraperitoneal seroso.\n\nDurante la operación, la paciente se mantuvo hipotensa (80/50 mmHg) desde que se le indujo la anestesia y se le administró un vasopresor. Debido a la inestabilidad de la paciente y a la viabilidad de los intestinos afectados por el nudo, se procedió a una hemicolectomía derecha. Se realizó una descompresión proximal y distal de los intestinos delgado y grueso distendidos, respectivamente. Se fijó el ciego y el colon ascendente a la pared abdominal posterolateral derecha con suturas seromusculares interrumpidas con hilo no absorbible (Silk 2-0).\n\nDespués del procedimiento, se le retiró la intubación y se le dio alimentación por vía oral (NPO) durante 24 horas y se le administró un fluido de mantenimiento con reposición de la pérdida. A pesar de la reanimación con fluidos y el apoyo con vasopresores, ella se encontraba persistentemente hipotensa, por lo que se le administró un tratamiento antibiótico doble con ceftriaxona 1 g, IV, BID y metronidazol 500 mg, IV, TID, en vista de un posible shock séptico de origen genitourinario. Su estado empeoró gradualmente y, tras una nueva evaluación el primer día postoperatorio, la herida superficial en su vulva se había extendido hacia la zona suprapúbica con signos clínicos de gangrena de Fournier. Por ello, revisamos su tratamiento antibiótico a meropenem 1 g, IV, BID, vancomicina 1 g, IV, BID y metronidazol 500 mg, IV, TID. Después de obtener el consentimiento informado por escrito, se la volvió a llevar al quirófano para un desbridamiento radical de la gangrena de Fournier y, posteriormente, se la trasladó a la unidad de cuidados intensivos quirúrgicos (ICU) intubada debido a un shock séptico persistente y un retraso en la recuperación de la anestesia. Lamentablemente, falleció con fallo multiorgánico debido a un shock séptico refractario en su segundo día postoperatorio, después de la exploración inicial.\n",
+    "gold_summary": "Presentamos un caso de nudos ileocecales en una paciente posparto con distensión abdominal, vómitos y ausencia de heces y flatos. La radiografía abdominal simple reveló bucles intestinales dilatados con múltiples niveles de aire y fluidos. Se realizó una laparotomía exploratoria con hallazgo intraoperatorio de nudos ileocecales con intestino viable, ciego móvil y colon ascendente y punta gangrenosa del apéndice. Deshicimos el nudo y realizamos una apendectomía. Debido a la inestabilidad intraoperatoria de los signos vitales de la paciente, se aplazó la hemicolectomía derecha y se fijaron el ciego y el colon ascendente a la pared abdominal posterolateral derecha.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Había una niña que acababa de tener un bebé. Su barriga estaba muy grande y le dolía mucho. No podía hacer popó ni tirar gases y vomitaba mucho.\n\nLos doctores le hicieron una radiografía y vieron que sus intestinos estaban muy hinchados. La niña fue al hospital y los doctores la operaron para ver qué pasaba.\n\nDentro, encontraron que sus intestinos estaban enredados como un nudo. También vieron que una parte pequeña llamada apéndice estaba dañada. Los doctores deshicieron el nudo y quitaron el apéndice malo.\n\nComo la niña estaba muy débil, los doctores hicieron algo para que sus intestinos no se movieran mucho y la cuidaron mucho después.",
+        "scores": {
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+      "B2": {
+        "text": "**Lo que le pasó a la paciente:**  \nUna joven de 20 años, que acababa de tener un bebé por cesárea, llegó al hospital con el abdomen muy hinchado, dolor y vómitos. Además, no podía expulsar gases ni hacer sus necesidades. Estos síntomas indicaban que algo estaba bloqueando su intestino.\n\n**Lo que encontraron en las pruebas:**  \nLa radiografía mostró que partes del intestino estaban muy dilatadas y había niveles de aire y líquido, lo que sugiere una obstrucción. Por eso, los médicos decidieron hacer una cirugía para ver qué estaba pasando.\n\n**Lo que vieron durante la operación:**  \nDescubrieron que una parte del intestino delgado (íleon) estaba enredada alrededor del ciego y el colon ascendente, formando un nudo llamado \"nudo ileocecal\". El intestino estaba en buen estado, pero la punta del apéndice estaba dañada (gangrenosa). Los médicos deshicieron el nudo y quitaron el apéndice enfermo (apendectomía).\n\n**Cómo continuó el tratamiento:**  \nLa paciente tuvo problemas con su presión arterial durante la cirugía, por lo que no pudieron hacer una cirugía más grande (hemicolectomía derecha) en ese momento. En cambio, fijaron el ciego y el colon a la pared abdominal para evitar que se movieran y causaran más problemas.\n\n**Qué significa esto:**  \nEl nudo ileocecal es una causa rara de bloqueo intestinal que puede ser grave. En este caso, la cirugía ayudó a liberar el intestino y a quitar la parte dañada. Sin embargo, la paciente tuvo complicaciones después, lo que muestra que este tipo de problemas necesita atención rápida y cuidadosa.",
+        "scores": {
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+        "text": "**Contexto:**  \nSe trató de una mujer joven de 20 años que, tras un parto por cesárea debido a problemas con el ritmo cardíaco fetal, comenzó a presentar una distensión abdominal progresiva acompañada de calambres, vómitos frecuentes y la incapacidad para expulsar gases y heces. No tenía antecedentes de cirugías abdominales ni enfermedades crónicas. Su estado general era grave, con signos de dolor abdominal intenso, presión arterial baja y taquicardia (latidos rápidos del corazón). Las pruebas iniciales mostraron una disminución en el número de glóbulos blancos y plaquetas, además de una radiografía abdominal que evidenció dilatación de los intestinos y acumulación de líquido en la cavidad abdominal.\n\n**Hallazgos Clave:**  \nDurante la cirugía exploratoria, se encontró que una parte del intestino delgado (íleon distal) estaba enredada alrededor del ciego y el colon ascendente, formando un nudo intestinal (nudo ileocecal). Aunque el intestino estaba viable (sin daño irreversible), la punta del apéndice estaba gangrenosa (tejido muerto por falta de circulación). Se observó también una gran cantidad de líquido seroso en la cavidad abdominal. La paciente presentó inestabilidad hemodinámica (presión arterial muy baja) durante la operación, lo que complicó el manejo quirúrgico.\n\n**Interpretación Clínica:**  \nEl nudo ileocecal es una causa rara pero grave de obstrucción intestinal que puede provocar compromiso vascular y gangrena si no se trata oportunamente. En este caso, la viabilidad del intestino permitió deshacer el nudo y realizar la extirpación del apéndice afectado (apendicectomía). Debido a la inestabilidad de la paciente, se decidió posponer la resección mayor (hemicolectomía derecha) y en su lugar se fijaron el ciego y el colon ascendente para evitar una nueva torsión.\n\n**Próximos Pasos y Evolución:**  \nA pesar de las intervenciones quirúrgicas y el soporte con líquidos y medicamentos para estabilizar la presión arterial, la paciente desarrolló una infección grave denominada gangrena de Fournier, que afectó la región genital y suprapúbica. Se requirió un desbridamiento quirúrgico radical y tratamiento antibiótico intensivo. Sin embargo, la paciente evolucionó hacia un shock séptico refractario (una infección generalizada que no responde al tratamiento) y finalmente falleció debido a un fallo multiorgánico en el segundo día postoperatorio.\n\nEste caso resalta la complejidad y gravedad de las complicaciones abdominales posparto, la importancia del diagnóstico temprano y la dificultad de manejo en pacientes con inestabilidad hemodinámica y recursos limitados.",
+        "scores": {
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+  {
+    "article": "Un hombre de 38 años se presentó en el hospital con opresión en el pecho y falta de aire. Tres años antes, había experimentado síntomas similares después de la actividad y recibió tratamiento en nuestro hospital. La ecocardiografía ambulatoria indicó una masa de eco del corazón izquierdo que sugería un mixoma, lo que llevó a su ingreso para una evaluación adicional. El examen físico reveló pigmentación de las orejas del paciente caracterizada por múltiples puntos pequeños de color café y negro. La tomografía computarizada abdominal (TC) mostró múltiples hígados y pequeños quistes en el riñón izquierdo. Las pruebas genéticas identificaron mutaciones en los genes TTN y PRKAR1A. El diagnóstico de CNC se confirmó mediante examen clínico, imágenes y pruebas genéticas. Después del tratamiento sintomático, la condición del paciente mejoró; sin embargo, rechazó la intervención quirúrgica. El 20 de septiembre de 2023, el paciente se presentó en nuestro hospital con opresión en el pecho y falta de aire exacerbadas. Informó dificultad para permanecer acostado boca arriba y necesidad de sentarse erguido para respirar. El examen físico reveló distensión de la vena yugular, desplazamiento hacia la izquierda y hacia abajo del límite del corazón, ritmo cardíaco irregular en la auscultación y un murmullo de la válvula mitral de intensidad 2/6-3/6 en el cuarto espacio intercostal a lo largo del margen izquierdo del esternón. Se escucharon estertores húmedos en ambos campos pulmonares medio e inferior. La palpación reveló un hígado firme que se extendía tres dedos por debajo del proceso xifoides y dos dedos por debajo de la caja torácica, junto con un edema de pitting leve en ambas extremidades inferiores. Las imágenes ecocardiográficas indicaron un agrandamiento global del corazón, dilatación del seno aórtico y arteria pulmonar, regurgitación mitral pequeña a moderada y una masa ecógena irregular que medía 54 mm × 43 mm en la cámara izquierda unida al tabique auricular. La fracción de eyección del ventrículo izquierdo (FEVI) fue del 23,1 %, con acortamiento fraccional (FS) del 10,9 %. La electrocardiografía demostró fibrilación auricular (frecuencia ventricular promedio, 150 latidos/min) y ondas Q anormales en las derivaciones V1-V3. Basándose en la historia del paciente, el diagnóstico incluyó DCM y CNC con mixoma cardíaco. Dada la presencia de insuficiencia cardíaca en etapa terminal y mixoma cardíaco concurrente, el paciente fue hospitalizado y se consideró el trasplante de corazón como una opción terapéutica viable para abordar ambas afecciones simultáneamente. Un corazón de donante adecuado estuvo disponible para su trasplante inmediato el 1 de octubre de 2024.\n\n\nProcedimiento quirúrgico\n\nLa piel y los tejidos subcutáneos se incisionaron cuidadosamente capa por capa a través de una esternotomía media. El esternón se abrió longitudinalmente y se controló el sangrado mediante electrocoagulación y cera ósea. La exploración extracardíaca reveló un agrandamiento global del corazón, más prominente en el ventrículo izquierdo. El corazón mostró una disminución de la fuerza contráctil. La aorta y la arteria pulmonar principal (AP) se diseccionaron desde la región supravalvular. Algunos tejidos se conservaron para suturarlos posteriormente, mientras que la mayor parte de la aurícula derecha enferma, la aurícula izquierda (AL), el ventrículo derecho y el ventrículo izquierdo se extirparon. La resección reveló una masa mucoide de color blanco grisáceo. Los tejidos de la aurícula izquierda del donante y del receptor se suturaron utilizando hilos Prolene 3/0 dobles continuos. La anastomosis se inspeccionó meticulosamente varias veces y no se observó sangrado significativo. De forma similar, la anastomosis término-terminal de la aorta ascendente del donante y la arteria pulmonar del receptor se realizó utilizando suturas Prolene 5/0 continuas, y una inspección cuidadosa no reveló sangrado.\n\nAdemás, la LA del donante y la PA del receptor se cerraron de forma segura utilizando suturas Prolene 5/0 dobles y continuas. Los tejidos de la vena cava inferior tanto del donante como del receptor se suturaron de forma similar con suturas Prolene 5/0, y se realizaron varias inspecciones para confirmar que no había presencia de sangrado significativo. El lado izquierdo del corazón se desinfló y, a medida que comenzó el recalentamiento, se restableció la oxigenación, se soltó la aorta ascendente y el corazón volvió espontáneamente al ritmo sinusal. Se aplicó sutura continua con Prolene 5/0 tanto a la vena cava superior del donante como del receptor y se inspeccionó de forma diligente para garantizar la ausencia de sangrado significativo. Después de la interrupción exitosa de la circulación asistida, se descanuló la cavidad venosa. Se recogieron muestras de tejido del corazón izquierdo y de la materia gris del paciente para un examen histopatológico, y se confirmó el diagnóstico de DCM y mixoma cardiaco.\n\n\nManejo postoperatorio\n\nEl primer día después del trasplante de corazón, el paciente produjo 1200 ml de orina. Los exámenes de laboratorio revelaron un nivel de troponina T hipersensible de 796.70 ng/L y un nivel de NT-proBNP de 10798 pg/ml. El recuento completo de sangre mostró un recuento de glóbulos blancos de 17.15 × 109/L, sin anomalías significativas en otros resultados de exámenes. El ecocardiógrafo mostró un EFV del 65 %, FS del 35 %, un espesor de la pared ventricular normal y ecogenicidad, y no se observaron anomalías discernibles en la morfología y estructura de la válvula. Después del trasplante de corazón, se administró una terapia hormonal intravenosa de succinato sódico de metilprednisolona (0.25 g) para mejorar la inmunidad, y se proporcionó un tratamiento intravenoso antiinfeccioso con cefoperazona y sulbactam sódico (2 g). El paciente recibió una solución nutriente y tiopronina en el primer día después de la cirugía. En el día tres postoperatorio, se reemplazó el succinato sódico de metilprednisolona con acetato de prednisona oral (25 mg). Se administraron cápsulas de micofenolato de mofetilo (0.5 g) por vía oral para minimizar el rechazo del corazón, y se administró acetato de carpofénico intravenoso (50 mg) para prevenir infecciones fúngicas. La producción de orina del paciente fue de 2000 ml, con niveles de troponina T hipersensible de 390 ng/L, niveles de NT-proBNP de 7877 pg/ml, y un recuento de leucocitos de 12.15 × 109/L. En el día siete postoperatorio, se introdujeron cápsulas de tacrolimus a una dosis oral de (1 mg) para minimizar el rechazo del paciente al corazón del donante, con un cuidadoso monitoreo de las concentraciones sanguíneas. Subsiguientemente, la dosis oral de acetato de prednisona se redujo gradualmente a (10 mg) mientras se ajustaba la concentración sanguínea de tacrolimus a 10.90 ng/L. La recuperación del paciente mejoró. El 20 de octubre de 2023, la ecocardiografía de seguimiento (Fig. 6) no mostró anomalías, con niveles de troponina T de 85 ng/L, NT-proBNP de 210 pg/ml, y todos los demás resultados de exámenes dentro de los rangos normales. El paciente exhibió una excelente recuperación postoperatoria y fue dado de alta. Las visitas regulares de seguimiento a nuestro departamento después del alta mostraron que el paciente permanece en buen estado.\n\nMH - Humanos\nMH - *Cardiomiopatía, Dilatada/cirugía/etiología/diagnóstico/diagnóstico por imágenes\nMH - Hombre\nMH - *Complejo de Carney/genética/diagnóstico/cirugía/complicaciones\nMH - Adulto\nMH - *Trasplante de corazón\nMH - *Mixoma/complicaciones/cirugía/diagnóstico por imágenes/diagnóstico/genética\nMH - *Insuficiencia cardiaca/etiología/diagnóstico/cirugía\nMH - *Neoplasias cardiacas/cirugía/complicaciones/diagnóstico por imágenes/diagnóstico/genética\nMH - Resultado del tratamiento\nMH - Subunidad/genética de la proteína quinasa Rlalpha dependiente de AMP cíclico\n",
+    "gold_summary": "Aquí, reportamos un caso de insuficiencia cardiaca debido al síndrome de Carney que resultó en mixoma cardiaco combinado con cardiomiopatía dilatada. Un hombre de 35 años de edad fue admitido en el hospital hace tres años debido a opresión torácica repentina y falta de aire. La ecocardiografía indicó mixoma, y una combinación de cribado genético y examen físico confirmó el síndrome de Carney con mixoma cardiaco. Después del tratamiento sintomático, fue dado de alta. Las intervenciones quirúrgicas no fueron consideradas en ese momento. Sin embargo, la opresión torácica y los síntomas de falta de aire del paciente empeoraron, y volvió al hospital. Se confirmó una función cardiaca de grado IV de la New York Heart Association, y la ecocardiografía indicó la presencia de cardiomiopatía dilatada acompañada de mixoma cardiaco. En última instancia, la insuficiencia cardiaca del paciente fue tratada con éxito con un trasplante cardiaco.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Había un hombre que se sentía muy cansado y le dolía el pecho. Tenía un bulto en su corazón que no era bueno. Los doctores le hicieron pruebas y encontraron que tenía una enfermedad llamada síndrome de Carney. Al principio, le dieron medicinas para sentirse mejor y se fue a su casa. Pero después, se sintió peor y volvió al hospital. Su corazón estaba muy débil y tenía el bulto grande. Los doctores le dieron un corazón nuevo con una operación. Ahora, el hombre está mejor y puede vivir feliz.",
+        "scores": {
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+        "text": "**Lo que le pasó al paciente**\n\nUn hombre de 35 años tuvo problemas en el corazón que le causaban dolor en el pecho y dificultad para respirar. Al principio, los médicos encontraron una masa en su corazón llamada mixoma, que es un tipo de tumor benigno, y también detectaron que tenía el síndrome de Carney, una enfermedad rara que puede causar tumores y otros problemas en el cuerpo. En ese momento, solo le dieron medicamentos para aliviar los síntomas y no le hicieron cirugía.\n\n**Cómo empeoró su condición**\n\nCon el tiempo, sus síntomas se hicieron más graves. Volvió al hospital porque le costaba mucho respirar y su corazón estaba muy débil. Los médicos descubrieron que tenía cardiomiopatía dilatada, que significa que su corazón estaba agrandado y no podía bombear la sangre bien. Además, el mixoma seguía presente en su corazón.\n\n**Qué hicieron los médicos**\n\nDebido a que su corazón estaba muy dañado y tenía insuficiencia cardíaca avanzada, los médicos decidieron hacerle un trasplante de corazón. Esto significa que le pusieron un corazón nuevo de un donante para reemplazar el suyo enfermo.\n\n**Cómo fue la cirugía y la recuperación**\n\nLa operación fue complicada, pero exitosa. Los médicos quitaron el corazón enfermo y el tumor, y pusieron el corazón nuevo. Después de la cirugía, el paciente recibió medicamentos para evitar que su cuerpo rechazara el nuevo corazón y para prevenir infecciones. Poco a poco, su corazón comenzó a funcionar bien y sus síntomas mejoraron mucho.\n\n**Qué significa este caso**\n\nEste caso muestra cómo el síndrome de Carney puede causar problemas graves en el corazón, como tumores y debilidad del músculo cardíaco. También enseña que, cuando el corazón está muy dañado, un trasplante puede ser la mejor opción para salvar la vida del paciente.",
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+        "text": "**Contexto**\n\nPresentamos el caso de un hombre de 38 años diagnosticado con el síndrome de Carney (CNC), una enfermedad genética rara caracterizada por tumores cardíacos benignos llamados mixomas, pigmentación cutánea y otras anomalías. Este paciente inicialmente se presentó hace tres años con síntomas de opresión en el pecho y dificultad para respirar, y fue diagnosticado con un mixoma en el corazón izquierdo mediante ecocardiografía. Además, el examen físico reveló manchas pigmentadas en las orejas, y estudios de imagen detectaron múltiples lesiones hepáticas y quistes renales. Las pruebas genéticas confirmaron mutaciones en los genes TTN y PRKAR1A, asociadas con CNC y cardiomiopatía dilatada (una enfermedad que afecta la capacidad del corazón para bombear sangre). En ese momento, recibió tratamiento para aliviar los síntomas y fue dado de alta, rechazando la cirugía.\n\n**Evolución y Hallazgos Clínicos**\n\nEn septiembre de 2023, el paciente regresó con empeoramiento de la opresión torácica y dificultad respiratoria, incluyendo intolerancia a la posición acostada. El examen físico evidenció signos de insuficiencia cardíaca avanzada, como distensión de la vena yugular, ritmo cardíaco irregular (fibrilación auricular), murmullo en la válvula mitral y estertores pulmonares. También se observaron un hígado aumentado de tamaño y edema en las piernas. La ecocardiografía mostró un corazón globalmente agrandado, dilatación de grandes vasos, regurgitación mitral moderada y una masa irregular de 54 × 43 mm en la aurícula izquierda, compatible con mixoma. La función del ventrículo izquierdo estaba gravemente reducida, con una fracción de eyección del 23,1 % (normalmente >55 %). La electrocardiografía confirmó fibrilación auricular y alteraciones en las derivaciones precordiales. El diagnóstico final incluyó cardiomiopatía dilatada (DCM) y síndrome de Carney con mixoma cardíaco, en contexto de insuficiencia cardíaca terminal.\n\n**Procedimiento Quirúrgico**\n\nDada la gravedad de la insuficiencia cardíaca y la presencia del mixoma, se decidió realizar un trasplante de corazón. Durante la cirugía, se realizó una esternotomía media para acceder al corazón agrandado y debilitado. Se extirparon las aurículas y ventrículos enfermos junto con la masa tumoral, y se implantó el corazón donante mediante suturas meticulosas para conectar las estructuras vasculares y auriculares. El corazón trasplantado recuperó el ritmo sinusal espontáneamente y sin complicaciones hemorrágicas. El examen histopatológico confirmó la presencia de mixoma y cardiomiopatía dilatada en el tejido removido.\n\n**Manejo Postoperatorio y Resultados**\n\nEn el postoperatorio inmediato, el paciente mostró una producción urinaria adecuada y niveles elevados pero decrecientes de marcadores cardíacos (troponina T y NT-proBNP), indicadores de daño y estrés cardíaco. La ecocardiografía evidenció una función ventricular normalizada con fracción de eyección del 65 % y estructura valvular sin anomalías. Se instauró un régimen inmunosupresor con metilprednisolona, prednisona, micofenolato de mofetilo y tacrolimus para prevenir el rechazo del trasplante, junto con tratamiento antibiótico y antifúngico para evitar infecciones. La recuperación fue favorable, con normalización progresiva de los parámetros clínicos y de laboratorio. En el seguimiento a largo plazo, el paciente mantuvo un buen estado general sin signos de rechazo ni complicaciones, y fue dado de alta con un pronóstico positivo.\n\n**Interpretación Clínica**\n\nEste caso ilustra la complejidad del síndrome de Carney cuando se asocia con mixoma cardíaco y cardiomiopatía dilatada, condiciones que pueden conducir a insuficiencia cardíaca grave. La identificación temprana mediante ecocardiografía, examen físico detallado y pruebas genéticas es fundamental para el diagnóstico. Aunque inicialmente se manejó de forma conservadora, el deterioro progresivo de la función cardíaca requirió un trasplante de corazón, que resultó ser una opción terapéutica eficaz para tratar simultáneamente la insuficiencia cardíaca terminal y la masa tumoral. La cirugía y el manejo postoperatorio cuidadoso permitieron una recuperación exitosa y mejoraron significativamente la calidad de vida del paciente.\n\n**Próximos Pasos**\n\nSe recomienda continuar con controles regulares para monitorear la función cardíaca y detectar posibles signos de rechazo o recurrencia de la enfermedad. Además, el seguimiento genético y clínico es importante para evaluar otras manifestaciones del síndrome de Carney y prevenir complicaciones asociadas. La educación del paciente sobre la adherencia al tratamiento inmunosupresor y la vigilancia de síntomas es esencial para mantener un resultado favorable a largo plazo.",
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+    "article": "Un paciente de 52 años de edad con un diagnóstico inicial de arteria pulmonar fue admitido en el departamento de cardiología para una evaluación médica y una decisión sobre el tratamiento posterior. El paciente tenía un historial de neumotórax espontáneo del lado derecho, tratado con toracocentesis y drenaje por vacío 35 años antes. El paciente sentía una disnea creciente al hacer ejercicio. También se quejaba de signos de insuficiencia ventricular derecha y cianosis. Cuatro años antes, el paciente fue hospitalizado tres veces por fibrilación auricular paroxística que se convirtió en ritmo sinusal por cardioversión eléctrica, además de que el examen electrocardiográfico era normal.\n\nEn ese mismo año, la angiografía coronaria indicó arterias coronarias normales. La ecocardiografía reveló una hipertensión pulmonar leve con una presión sistólica calculada en el ventrículo derecho de 36 mmHg sin dilatación de ese ventrículo.\n\nEn los años siguientes, se observó insuficiencia cardiaca progresiva con aumento de la presión arterial pulmonar en la ecocardiografía. Se realizó angio-CT en dos ocasiones y se excluyó la hipertensión pulmonar tromboembólica crónica en cada ocasión. La tomografía computarizada de alta resolución excluyó la patología pulmonar intersticial. La espirometría fue normal. La detección de enfermedades autoinmunes y la infección por VIH fue negativa.\n\n\nLínea de tiempo: historia, curso de la enfermedad, diagnóstico y tratamiento\n\n1976  neumotórax derecho\n2007 Hospitalizado tres veces por fibrilación auricular e insuficiencia cardiaca. Se le realizaron ecocardiografías, cardioversiones y coronografías. En cada ocasión, fue dado de alta de los servicios con diagnósticos de fibrilación auricular, insuficiencia cardiaca e insuficiencia cardiaca de clase II de la NYHA.\n2010-2011: Aumento de la falta de aire y síntomas de insuficiencia cardiaca. El paciente fue hospitalizado tres veces. Se detectaron características indirectas de hipertensión pulmonar en ecocardiografía. Se realizó tres veces un examen de tórax por TAC; se excluyó la embolia pulmonar o la hipertensión arterial pulmonar tromboembólica crónica (2 x angio-TAC) o la fibrosis pulmonar (tomografía computarizada de alta resolución).\nSe estableció el diagnóstico de hipertensión pulmonar, clase III de la OMS.\nDEC-2011 Admisión a la clínica de cardiología – ecocardiografía (TTE, TEE), prueba de caminata de 6 minutos, NT-proBNP, cateterización cardiaca derecha, prueba de vasoreactividad pulmonar.\nSe estableció el diagnóstico de hipertensión pulmonar arterial irreversible.\nSe ha iniciado el tratamiento con iloprost y sildenafil\nEn enero de 2012, visita de control: mejora en la clase de la OMS, disminución de la concentración de NT-proBNP e incremento de la distancia en la prueba de 6 minutos.\nMAY-2012. Control RHC. La SaO2 de las muestras de sangre obtenidas durante el RHC de la arteria del lóbulo superior del pulmón derecho fue del 87 %.\nEl diagnóstico angiográfico de las arterias pulmonares reveló fístulas de HAP entre las arterias subclavianas y el lóbulo superior del pulmón derecho.\nJUN 2012  angiografía por TC de las arterias sistémicas reveló la presencia adicional de fístulas arteriales bronquiales en el lóbulo superior de las arterias del pulmón derecho\nIII-2013 Embolización de fístulas\nVI-2013. Muerte como resultado del empeoramiento de la insuficiencia cardiaca, combinado con neumonía.\n\n\n\nEn el ingreso a nuestra clínica, la clase funcional del paciente fue evaluada como OMS III. En el examen físico, el segundo sonido cardiaco (S2) fue acentuado con S2 dividido ensanchado. Además, la auscultación cardiaca indicó un murmullo holosistólico de regurgitación tricuspídea. La auscultación del tórax no mostró un murmullo vascular. La cianosis periférica y central fue marcada. Se examinaron la hepatomegalia, el edema periférico y las venas varicosas bilateralmente.\n\nLa SaO2 obtenida por el método de oximetría de pulso se redujo al 88 %. La electrocardiografía reveló fibrilación auricular, desviación del eje derecho y onda T negativa en las derivaciones precordiales v1-v3. Las pruebas adicionales fueron las siguientes: concentración de NT-proBNP - 3383 pg/ml, distancia de la prueba de caminata de seis minutos - 373 m con 7/10 puntos en la escala de disnea de Borg.\n\nLa ecocardiografía mostró características de hipertensión pulmonar grave: agrandamiento del ventrículo derecho a 44 mm (cuatro cámaras), con función deprimida del TAPSE del ventrículo derecho de 9 mm, agrandamiento del área de la aurícula derecha a 40 cm2, regurgitación tricuspídea grave (++++), aumento del PSVR calculado a 112 mmHg, acortamiento del tiempo de aceleración de la arteria pulmonar a 60 ms y derrame pericárdico leve. No hubo defecto en el tabique interventricular. La ecocardiografía transesofágica tampoco mostró un defecto en el tabique auricular, lo que se confirmó más tarde con angio-TAC.\n\n\nLa SaO2 de la sangre obtenida de la arteria radial se redujo al 87,8%. Se realizó un cateterismo cardiaco derecho. La SaO2 de las muestras de sangre obtenidas durante el RHC de la vena cava superior, la vena cava inferior, la aurícula derecha, el tronco pulmonar, la arteria del lóbulo medio del pulmón derecho y la arteria pulmonar izquierda ascendieron respectivamente a: 64,8%; 77,4%; 73,2%; 70,2%; 69,3%; 71,2% y no indicaron la presencia de un shunt de izquierda a derecha.\n\nLas mediciones hemodinámicas mostraron una hipertensión pulmonar precapilar grave, irreversible en las pruebas de vasoreactividad con óxido nítrico inhalado (80 ppm) y una combinación de sildenafil oral (50 mg) y óxido nítrico inhalado (80 ppm).\n\nEn base a todos los datos clínicos y los resultados de la RHC, se estableció un diagnóstico de hipertensión pulmonar idiopática irreversible.\n\nSe inició el tratamiento con iloprost inhalado (Ventavis) 6 × 5 µg y sildenafil (Revatio) por vía oral 3 × 20 mg. Además, se administraron digoxina (0,1 mg diarios), warfarina (INR rango: 2-3), furosemida (40 mg por vía oral diarios) y espironolactona (100 mg diarios).\n\nUn mes después se realizó un seguimiento no invasivo. El paciente manifestó una mejoría en la capacidad física, clase II según la OMS, concentración de NT-proBNP: 1014 pg/ml. Distancia en la prueba de caminata de seis minutos: 471 m.\n\nCinco meses después se realizó una evaluación invasiva. La RHC mostró valores de PAP más elevados que en las mediciones iniciales [75,4/51,8 (59,7) mm Hg] y PVR (13,4 WU) (Tabla 22 – control RHC).\n\nLa saturación de oxígeno de las muestras de sangre obtenidas durante la RHC de la arteria lobular superior del pulmón derecho fue elevada y ascendió al 89.7%.\n\nEn la angiografía pulmonar se detectó la reducción del trazo vascular periférico típico de la hipertensión arterial pulmonar y la falta de contraste de la arteria del lóbulo superior derecho. Además, se encontró evidencia de flujo sanguíneo retrógrado visible como un contraste negativo en la arteria pulmonar derecha. Después, se realizó una arteriografía de la arteria subclavia derecha y se detectó una enorme malformación vascular que se comunicaba con la arteria del lóbulo superior derecho.\n\nLa angio-TC de las arterias sistémicas confirmó la presencia de las fístulas previamente descritas y reveló la presencia adicional de fístulas de la arteria bronquial en el lóbulo superior de las arterias del pulmón derecho.\n\nSe realizó embolización selectiva de las fístulas (mezcla al 50% de Lipiodol y pegamento monomérico de n-butil-2-cianoacrilato). La embolización no produjo ningún cambio clínico en el estado del paciente.\n\nMH - Fístula arterio-arterial/*complicaciones\nMH - *Cateterización cardiaca\nMH - Angiografía por tomografía computarizada\nMH - Hipertensión pulmonar primaria familiar/*diagnóstico/terapia farmacológica\nMH - Resultado fatal\nMH - Insuficiencia cardiaca/fisiopatología\nMH - Humanos",
+    "gold_summary": "Un paciente caucásico de 52 años de edad con hipertensión pulmonar (HP) confirmada por ecocardiografía fue admitido en el departamento de cardiología debido a disnea de esfuerzo y signos de insuficiencia ventricular derecha. La exploración rutinaria para detectar causas de HP secundaria fue negativa. El cateterismo cardiaco derecho (CCR) confirmó una HP arterial de alto grado [presión arterial pulmonar media (PAPm); 50,6 mmHg, presión de enclavamiento pulmonar (PWP); 11,3 mmHg, resistencia vascular pulmonar (PVR); 11,9 unidades de Wood (UW)] irreversible en la prueba con óxido nítrico inhalado. La saturación de oxígeno (SaO2) de las muestras de sangre obtenidas durante el primer CCR osciló entre 69,3 y 73,2%. Se diagnosticó hipertensión arterial pulmonar idiopática. Se inició el tratamiento con iloprost inhalado y sildenafil.\n\nEl control RHC, realizado 5 meses después, mostró valores de mPAP (59,7 mmHg) y PVR (13,4 WU) más altos en comparación con la medición inicial. El SaO2 de sangre obtenida durante el RHC de la arteria del lóbulo superior del pulmón derecho fue elevado y ascendió al 89,7 %.\n\nLuego se realizó una arteriografía pulmonar. Se encontró falta de contraste en la arteria del lóbulo superior derecho con evidencia de flujo sanguíneo retrógrado visible como contraste negativo en la arteria pulmonar derecha. Después, una arteriografía de la arteria subclavia derecha detectó una enorme malformación vascular que se comunicaba con la arteria del lóbulo superior derecho. Después, un angiograma por tomografía computarizada (angio-CT) reveló adicionalmente el agrandamiento de las arterias bronquiales que se originaban en las fístulas hacia la arteria pulmonar del lóbulo superior derecho.\n\nA pesar del tratamiento farmacológico intensivo, que incluyó la terapia de la hipertensión pulmonar y la embolización percutánea de las fístulas, el estado del paciente siguió deteriorándose. Falleció tres meses después de la embolización debido a una insuficiencia cardiaca grave complicada por neumonía.\n",
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+        "text": "Había un hombre de 52 años que tenía problemas para respirar. Su corazón y pulmones no funcionaban bien. Los doctores hicieron muchas pruebas para entender qué pasaba.\n\nEncontraron que la presión en sus pulmones era muy alta. Le dieron medicinas para ayudar, pero no mejoró mucho.\n\nLuego vieron que tenía unos tubos raros en sus pulmones que no estaban bien. Intentaron taparlos para ayudar, pero el hombre se puso más enfermo.\n\nAl final, el hombre murió porque su corazón se cansó mucho y tuvo una infección en los pulmones. Los doctores hicieron todo lo que pudieron para ayudarlo.",
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+        "text": "**Caso de un Paciente con Hipertensión Pulmonar y Problemas en las Arterias del Pulmón**\n\nUn hombre de 52 años tenía dificultad para respirar y problemas en el lado derecho de su corazón. Los médicos confirmaron que tenía hipertensión pulmonar, que es cuando la presión en las arterias de los pulmones está muy alta. Para entender mejor su enfermedad, le hicieron un examen llamado cateterismo cardiaco derecho, que mide la presión y el flujo de sangre en el corazón y los pulmones. Los resultados mostraron que su hipertensión pulmonar era grave y no mejoraba con el tratamiento con óxido nítrico inhalado. Además, la cantidad de oxígeno en su sangre estaba baja, entre 69% y 73%.\n\nLos médicos pensaron que tenía hipertensión arterial pulmonar idiopática, que significa que la causa es desconocida. Por eso, comenzaron un tratamiento con dos medicamentos: iloprost inhalado y sildenafil, que ayudan a bajar la presión en las arterias pulmonares.\n\nCinco meses después, hicieron otro cateterismo y encontraron que la presión en sus pulmones había aumentado aún más, y la resistencia al flujo sanguíneo también era mayor. Sin embargo, la cantidad de oxígeno en la sangre de una parte específica del pulmón derecho había subido a casi 90%, lo que era extraño.\n\nPara investigar esto, realizaron una arteriografía, que es una prueba que usa un contraste para ver las arterias con rayos X. Descubrieron que la arteria del lóbulo superior del pulmón derecho no se llenaba bien con el contraste y que la sangre estaba fluyendo en dirección contraria en esa arteria. Luego, hicieron otra arteriografía en la arteria subclavia derecha (una arteria cerca del hombro) y encontraron una gran malformación, que es una conexión anormal entre vasos sanguíneos, que se comunicaba con la arteria del pulmón derecho.\n\nTambién un estudio por tomografía computarizada mostró que las arterias bronquiales, que normalmente llevan sangre a los pulmones, estaban agrandadas y formaban fístulas. Las fístulas son conexiones anormales entre arterias que pueden causar problemas en el flujo sanguíneo.\n\nAunque el paciente recibió tratamiento médico y se intentó cerrar estas fístulas mediante un procedimiento llamado embolización (que bloquea estas conexiones anormales), su salud empeoró. Tres meses después de este procedimiento, falleció debido a insuficiencia cardiaca grave, que fue complicada por una infección pulmonar llamada neumonía.\n\n**Qué Significa Este Caso**\n\nEste caso muestra que en algunos pacientes con hipertensión pulmonar grave, pueden existir conexiones anormales entre arterias que afectan el flujo de sangre y el oxígeno en los pulmones. Aunque se usen medicamentos y procedimientos para tratar estas malformaciones, la enfermedad puede avanzar y causar complicaciones serias. Por eso, es importante hacer estudios detallados para entender todas las causas y buscar el mejor tratamiento posible.",
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+        "text": "**Contexto**  \nSe trata de un hombre caucásico de 52 años con hipertensión pulmonar (HP) grave, inicialmente diagnosticada mediante ecocardiografía, que presentaba dificultad para respirar al esfuerzo y signos de insuficiencia del ventrículo derecho del corazón. A lo largo de su evolución, se descartaron causas secundarias comunes de hipertensión pulmonar mediante estudios exhaustivos, incluyendo pruebas de imagen y análisis de laboratorio.\n\n**Hallazgos Clave**  \nEl cateterismo cardiaco derecho (CCR), una prueba invasiva que mide directamente las presiones y flujos en el corazón y pulmones, confirmó una hipertensión arterial pulmonar severa e irreversible, con una presión arterial pulmonar media elevada (50,6 mmHg), presión de enclavamiento pulmonar normal (11,3 mmHg) y resistencia vascular pulmonar alta (11,9 unidades de Wood). La saturación de oxígeno en la sangre obtenida durante este procedimiento fue moderadamente reducida (entre 69,3% y 73,2%), lo que indicaba un intercambio de oxígeno comprometido.\n\nCinco meses después, un nuevo cateterismo mostró un empeoramiento de las presiones pulmonares (presión media de 59,7 mmHg) y de la resistencia vascular (13,4 unidades de Wood). Sin embargo, la saturación de oxígeno en la arteria del lóbulo superior derecho del pulmón aumentó notablemente hasta 89,7%, lo que sugería la presencia de un flujo anormal de sangre.\n\nUna angiografía pulmonar (estudio de imagen con contraste para visualizar las arterias pulmonares) reveló ausencia de contraste en la arteria del lóbulo superior derecho y flujo sanguíneo retrógrado (en sentido contrario al habitual) en la arteria pulmonar derecha. Posteriormente, una arteriografía de la arteria subclavia derecha identificó una gran malformación vascular que conectaba esta arteria con la arteria del lóbulo superior derecho del pulmón. Un estudio adicional con angiografía por tomografía computarizada (angio-TC) mostró además un aumento del tamaño de las arterias bronquiales que formaban fístulas (conexiones anormales) hacia la arteria pulmonar del mismo lóbulo.\n\n**Interpretación Clínica**  \nEl diagnóstico final fue hipertensión arterial pulmonar idiopática (sin causa identificable) complicada por la presencia de fístulas arterio-arteriales entre las arterias sistémicas (subclavia y bronquiales) y las arterias pulmonares del lóbulo superior derecho. Estas conexiones anómalas alteraban el flujo sanguíneo normal, contribuyendo al empeoramiento de la insuficiencia cardiaca derecha y a la hipoxemia (bajo nivel de oxígeno en sangre).\n\nA pesar del tratamiento médico intensivo con vasodilatadores pulmonares (iloprost inhalado y sildenafil oral) y de la embolización percutánea (procedimiento para cerrar las fístulas mediante la introducción de materiales que bloquean el flujo anormal), la condición del paciente continuó deteriorándose.\n\n**Próximos Pasos y Resultado**  \nEl paciente falleció tres meses después de la embolización debido a insuficiencia cardiaca grave, agravada por una neumonía. Este caso resalta la complejidad y gravedad de la hipertensión pulmonar idiopática cuando se asocia a malformaciones vasculares, y la dificultad para controlar la progresión a pesar de las terapias disponibles.",
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+    "article": "Paciente de 73 años, diagnosticada de enfermedad pulmonar obstructiva crónica (EPOC), hipertensión arterial (HTA), trastorno bipolar, ansiedad, depresión, hipotiroidismo y artritis reumatoide, condiciones para las cuales tiene prescrito el tratamiento reflejado en el Anexo I.\n\nRealiza una llamada telefónica a la farmacia comunitaria para solicitar información sobre una nueva medicación prescrita para el tratamiento de una infección de orina y un déficit de vitamina D, diagnosticados tras la realización de una analítica completa en el servicio de urgencias de un hospital privado.\n\nLa paciente es totalmente dependiente y no sale de casa, siendo su cuidadora la persona que siempre va a retirar su medicación y elabora los pastilleros semanales.\n\nLos fármacos prescritos para el tratamiento de la infección de orina fueron cefuroxima 250 mg (1 comprimido cada 12 horas durante 5 días) y butilescopolamina 10 mg (1 comprimido en la mañana si presentaba molestias).\n\nPara el déficit de vitamina D se le prescribió colecalciferol 50.000 U.I. (1 cápsula una vez al mes durante dos meses) y colecalciferol 25.000 UI (1 cápsula una vez al mes tras finalizar el envase de 50.000 U.I.).\n\nESTUDIO Y EVALUACIÓN\nSe lleva a cabo el servicio de dispensación (SD) sin incidencias, siguiendo la metodología expuesta en la Guía práctica para los Servicios Profesionales Farmacéuticos Asistenciales en la Farmacia Comunitaria. Posteriormente, la paciente contacta con la farmacia comunitaria, preocupada porque la nueva medicación le ha generado confusión, ya que ella tomaba unas cápsulas naranjas para su déficit de vitamina D prescritas por su médico de Atención Primaria hace unos meses y en la parte del informe de urgencias en la que figura el tratamiento venía reflejado una medicación nueva para ese mismo problema de salud. Además, coincidió con que su cuidadora habitual ya no podrá trabajar más con ella y no la podrá ayudar con su medicación. Por ello, se le propone a la paciente el servicio de Revisión del Uso del Medicamento (RUM) con el objetivo de evaluar el grado de conocimiento que tienen la paciente con respecto a sus patologías y su tratamiento, a la par que poder resolver posibles errores en la administración de los distintos fármacos que forman parte del mismo. Se le explica en qué consiste todo el procedimiento y decide aceptar.\n\nTras esto, se procedió a citar a la cuidadora en la farmacia con la tarjeta sanitaria de la paciente, su bolsa de medicación para hacer una revisión exhaustiva de su botiquín y el último informe de urgencias con el objetivo de recopilar toda la información necesaria para realizar el servicio asistencial vía telefónica. Durante la llamada con la paciente, se procede a cumplimentar el formulario RUM, el cual se volcó posteriormente en la plataforma SEFAC e_XPERT ®. Además, para poder evaluar correctamente todo el tratamiento farmacológico, se emplearon herramientas como el CIMA (donde se consultaron las fichas técnicas de los medicamentos) y el BotPlus (donde se consultaron las posibles interacciones farmacológicas).\n\nINTERVENCIÓN\nTras la primera toma de contacto a través de la entrevista telefónica y hacer revisión del botiquín, se pudo detectar que la paciente y su cuidadora no estaban haciendo una gestión apropiada de la medicación. Tras la revisión de su botiquín, se hallaron envases caducados y con anotaciones erróneas sobre su uso, blísteres con comprimidos partidos que no deberían de estarlo y acúmulo de varios envases de un mismo fármaco. Al tratarse de una paciente dependiente, polimedicada y con problemas para gestionar correctamente su tratamiento antes y durante la ausencia de su cuidadora habitual se decidió con el fin de garantizar la seguridad farmacoterapéutica y mejorar la adherencia al tratamiento derivar al servicio de sistema personalizado de dosificación (SPD). A través de la plataforma de SEFAC e_XPERT ® se procedió a redactar un informe de derivación a su médico de Atención Primaria (MAP) del Sistema Nacional de Salud (SNS) (ver Anexo II), donde se detallaba la inclusión de la paciente en el servicio de Revisión del Uso de la Medicación y su posterior derivación al servicio de SPD. Además, quedaron recogidas las siguientes propuestas de intervención:\n\nRevisión de la pauta posológica de tramadol 50 mg de liberación retardada por la existencia de un posible error en la prescripción.\n\nRevisión del tratamiento prescrito para el déficit de vitamina D por la existencia de una duplicidad terapéutica.\n\nCambio del absorbente de incontinencia de tipo pants a elástico alegando la situación de dependencia de la paciente y las dificultades para realizar una correcta colocación por parte de la cuidadora al pasar encamada la mayor parte del tiempo. Se aportaron los Códigos Nacionales (CN) correspondientes.\n\nRevisión del tratamiento para la EPOC por dificultades de empleo del inhalador y falta de adherencia terapéutica.\n\nRESULTADOS\nDurante la cita médica, la médico de atención primaria recibe el informe de derivación entregado a la cuidadora donde, además, se solicita contacto con la farmacia comunitaria para poder iniciar de forma correcta el servicio de SPD. Tras hablar con ella vía telefónica, se realizaron los siguientes cambios en su tratamiento:\n\nDéficit de vitamina D: anulación de calcifediol y sustitución por colecalciferol prescrito en el Servicio de Urgencias.\n\nArtritis reumatoide: modificación de pauta de tramadol de liberación prolongada a 1-0-1 y empleo de paracetamol 1000 mg 1-1-1 si precisa.\n\nIncontinencia urinaria: sustitución de absorbente tipo pants por elástico.\n\nEPOC: no se realizó un cambio de tratamiento. La médico de atención primaria consideró oportuno llevar a cabo una supervisión diaria por parte de la cuidadora en cada una de las tomas del inhalador.",
+    "gold_summary": "Paciente 73 años, dependiente, polimedicada y pluripatológica contacta telefónicamente con la farmacia comunitaria para solicitar información sobre un tratamiento de nueva prescripción para una infección de orina y un déficit de vitamina D. La dispensación de la medicación a su cuidadora deriva en mayores dudas a la paciente, por lo que se le ofrece el servicio de revisión del uso del medicamento (RUM). Durante la prestación del servicio se detectan varias incidencias en su tratamiento, por lo que se decide realizar un informe de derivación al médico de atención primaria para una revisión completa del tratamiento y poder así derivar a la paciente al servicio de Sistema Personalizado de Dosificación (SPD) con el fin de garantizar la seguridad farmacoterapéutica de la paciente y mejorar su adherencia al tratamiento.",
+    "synthetic_summary_eval": {
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+        "text": "Una señora de 73 años se siente confundida con sus medicinas nuevas. Ella no puede salir de casa y su cuidadora siempre le ayuda con sus pastillas. La señora llamó a la farmacia para preguntar. \n\nLa farmacia revisó todas sus medicinas y vio que había problemas. Algunas pastillas estaban mal guardadas y había medicinas repetidas. \n\nPor eso, la farmacia habló con su doctor para ayudarla mejor. El doctor cambió algunas medicinas y pidió que la señora tenga un organizador especial para sus pastillas. Así, será más fácil y seguro tomar sus medicinas.",
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+        "text": "**Información sobre la Paciente y su Situación**\n\nUna mujer de 73 años, que depende totalmente de otras personas para su cuidado y toma muchos medicamentos por varias enfermedades, llamó a la farmacia para preguntar sobre un nuevo tratamiento. Este tratamiento era para una infección de orina y para un problema de falta de vitamina D, que le habían diagnosticado en un hospital.\n\n**Problemas Detectados con la Medicación**\n\nAunque su cuidadora recogió los medicamentos, la paciente se confundió porque ya tomaba otras pastillas para la vitamina D y no entendía bien los cambios. Además, su cuidadora habitual ya no podía ayudarla, lo que complicaba más la situación. Por eso, la farmacia le ofreció un servicio llamado Revisión del Uso del Medicamento (RUM). Este servicio ayuda a revisar si la paciente entiende bien sus medicinas y si las está tomando correctamente.\n\nAl revisar los medicamentos, encontraron varios problemas: había medicinas vencidas, instrucciones equivocadas, pastillas partidas que no debían estar así y varios envases del mismo medicamento. Como la paciente no podía manejar bien su tratamiento y estaba sin su cuidadora, se decidió que necesitaba un Sistema Personalizado de Dosificación (SPD). Este sistema organiza las medicinas en pastilleros para que sea más fácil y seguro tomarlas.\n\n**Acciones y Cambios Realizados**\n\nSe preparó un informe para el médico de atención primaria explicando la situación y recomendando la revisión completa del tratamiento. El médico hizo algunos cambios importantes, como:\n\n- Cambiar la vitamina D para evitar tomar dos tipos diferentes al mismo tiempo.\n\n- Ajustar la dosis de un analgésico llamado tramadol.\n\n- Cambiar el tipo de pañales para facilitar su uso debido a la dependencia de la paciente.\n\n- Mantener el tratamiento para la enfermedad pulmonar, pero con supervisión diaria para asegurar que la paciente use bien el inhalador.\n\n**Conclusión**\n\nGracias a la revisión y coordinación entre la farmacia y el médico, se mejoró la seguridad y el manejo del tratamiento de la paciente. Además, se implementó un sistema que facilitará que tome sus medicamentos correctamente, lo cual es muy importante para su salud y bienestar.",
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+        "text": "**Contexto**  \nSe trata de una paciente de 73 años con múltiples enfermedades crónicas, incluyendo enfermedad pulmonar obstructiva crónica (EPOC), hipertensión arterial, trastorno bipolar, ansiedad, depresión, hipotiroidismo y artritis reumatoide. Es totalmente dependiente para sus actividades diarias y no sale de casa; su cuidadora habitual se encargaba de gestionar y recoger su medicación. Recientemente, tras una analítica en urgencias, se le diagnosticó una infección de orina y un déficit de vitamina D, para los cuales se le prescribió un nuevo tratamiento.\n\n**Hallazgos Clave**  \nLa paciente contactó con la farmacia comunitaria para aclarar dudas sobre la nueva medicación, ya que existía confusión debido a la coexistencia de tratamientos previos para el déficit de vitamina D y la reciente prescripción. Además, la cuidadora habitual informó que ya no podría continuar asistiendo a la paciente, lo que generó preocupación sobre la correcta administración de los medicamentos. Se ofreció entonces el servicio de Revisión del Uso del Medicamento (RUM) para evaluar el conocimiento de la paciente y su cuidadora sobre las patologías y tratamientos, y para identificar posibles errores en la gestión farmacológica.\n\nDurante la revisión, se detectaron múltiples problemas: medicamentos caducados, instrucciones incorrectas, comprimidos partidos indebidamente y acumulación de envases duplicados. También se identificaron errores potenciales en la prescripción, como duplicidad en el tratamiento para la vitamina D y una pauta inadecuada para tramadol. Además, se observaron dificultades en el manejo del inhalador para la EPOC y problemas relacionados con la elección del absorbente para la incontinencia urinaria, que complicaban la correcta atención de la paciente.\n\n**Interpretación Clínica**  \nDada la complejidad del caso, la dependencia de la paciente y la ausencia de su cuidadora habitual, se consideró necesario derivar a la paciente al servicio de Sistema Personalizado de Dosificación (SPD), que facilita la organización y administración segura de la medicación. Se elaboró un informe detallado para el médico de Atención Primaria, incluyendo recomendaciones específicas para ajustar el tratamiento, como la sustitución del calcifediol por colecalciferol para el déficit de vitamina D, la modificación de la pauta de tramadol y el cambio del tipo de absorbente para mejorar la comodidad y manejo.\n\nEn cuanto al tratamiento para la EPOC, el médico decidió mantener la medicación actual pero reforzar la supervisión diaria por parte de la cuidadora para asegurar la correcta utilización del inhalador.\n\n**Próximos Pasos**  \nEl médico de Atención Primaria recibió el informe y coordinó con la farmacia comunitaria la implementación del Sistema Personalizado de Dosificación. Este enfoque busca mejorar la seguridad en la administración de los medicamentos, evitar errores y aumentar la adherencia al tratamiento, aspectos fundamentales para el bienestar y la calidad de vida de la paciente. Además, se estableció un seguimiento estrecho para supervisar la evolución clínica y la correcta gestión terapéutica en el contexto de la nueva situación de dependencia y ausencia de la cuidadora habitual.",
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+    "article": "Nuestra paciente era una mujer japonesa de 83 años con insuficiencia cardiaca crónica (fracción de eyección: aproximadamente 30 %) que inició un tratamiento con empagliflozina 10 mg diarios unos 8 meses antes de su ingreso. Nunca se le había diagnosticado diabetes mellitus (HbA1c 5.9 % antes de iniciar el tratamiento con empagliflozina). Unos 6 meses antes de su ingreso, su tratamiento se cambió a dapagliflozina 5 mg. Sus diuréticos y otros medicamentos cardiacos no se ajustaron durante ese tiempo. Dos semanas antes de su ingreso, tropezó y cayó, sufriendo fracturas vertebrales y de costillas. La paciente se debilitó significativamente por el dolor de las fracturas, lo que le causó dificultad para caminar y anorexia. Solo podía comer el 50-70 % de su ingesta dietética habitual. Esto empeoró en la semana siguiente, cuando también desarrolló náuseas y vómitos y redujo aún más su ingesta de alimentos a solo el 10-20 % de la cantidad habitual. Durante este período, continuó tomando dapagliflozina. Fue ingresada en el hospital.\nAl ingreso, la paciente estaba consciente con una temperatura corporal de 37.4°C, presión arterial de 124/68 mmHg, frecuencia cardiaca de 91 bpm y saturación de oxígeno de 98% en aire ambiente. Los análisis de sangre revelaron un nivel de glucosa en sangre de 124 mg/dL, pH de 7.3, concentración de HCO3– de 14 mmol/L, exceso de base de -10 mEq/L, brecha aniónica de 20 mEq/L y concentración de b-hidroxibutirato de 5150 umol/L (Tabla 1). Estos hallazgos fueron consistentes con el diagnóstico de cetoacidosis normoglucémica. La paciente no tenía antecedentes de consumo de alcohol, tabaquismo o uso de drogas.\nSe descartaron otras causas de acidosis con alto déficit aniónico. Su nivel de péptido C era coherente con los niveles de glucosa en sangre en el ingreso, lo que indicaba que tenía una secreción de insulina adecuada; por lo tanto, no se inició la administración de insulina. Se interrumpió el uso de inhibidores de SGLT2 y la paciente se trató inicialmente con solución salina isotónica y una infusión de mantenimiento de aproximadamente 170 g de glucosa diarios.\nA pesar de no haber iniciado la insulina, su pH (7.418), concentración de HCO3– (20.7 mmol/L) y brecha aniónica (13.3 mEq/L) mejoraron al día siguiente de su ingreso. Se inició la dieta Carb 60, pero se continuaron las infusiones intravenosas de glucosa porque la ingesta de alimentos de la paciente era escasa. La cantidad de infusión de glucosa administrada se ajustó según su ingesta de alimentos. En el cuarto día de hospitalización, las cetonas urinarias desaparecieron.\nLa infusión de glucosa se interrumpió el día 12 de la hospitalización, una vez que el paciente pudo comer comidas completas. Aunque el nivel de glucosa en sangre del paciente estaba dentro del rango normal, la excreción de glucosa en la orina fue de 3+ (>500 mg/dL) durante 8 días después de la última dosis de dapagliflozina.\nAl ingreso, la paciente no podía caminar debido al dolor de la fractura, la fatiga general y el síndrome de desuso, pero después de la rehabilitación pudo hacerlo de forma independiente. Fue dada de alta el día 19 de hospitalización, tras someterse a rehabilitación.\nLos inhibidores de SGLT2 no se reiniciaron.\n\nMH - Humanos\nMH - Mujer\nMH - *Insuficiencia cardiaca/inducida químicamente\nMH - *Inhibidores del transportador de glucosa y sodio 2/efectos adversos\nMH - Edad 80 años y más\nMH - Cetosis/químicamente inducida\nMH - glucósidos/efectos adversos\nMH - Cetoacidosis diabética/inducida químicamente\n",
+    "gold_summary": "A continuación, describimos un caso de cetoacidosis en una mujer japonesa de 83 años sin diabetes a la que se le administraron inhibidores de SGLT2 para la insuficiencia cardiaca (fracción de eyección: aproximadamente 30 %). Dos semanas antes de su ingreso, había sufrido una fractura vertebral y una fractura de costilla debido a una caída, a la que siguió una anorexia, pero continuó tomando inhibidores de SGLT2. En el momento del ingreso, los resultados de los análisis de sangre revelaron un nivel de glucosa en sangre de 124 mg/dL, un nivel de hemoglobina A1C del 5,9 %, un pH de 7,329, una concentración de HCO₃⁻ de 14,3 mmol/L y una concentración de β-hidroxibutirato de 5150 μmol/L, lo que condujo a un diagnóstico de cetoacidosis euglucémica. El nivel de péptido C de la paciente coincidía con los niveles de glucosa en sangre en el momento del ingreso, lo que indicaba que tenía una secreción de insulina adecuada. La paciente fue tratada únicamente con administración de glucosa sin insulina y fue dada de alta tras la interrupción del inhibidor de SGLT2.\n",
+    "synthetic_summary_eval": {
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+        "text": "Había una señora de 83 años que no tenía diabetes. Ella tenía un problema en el corazón. Tomaba una medicina para ayudar su corazón. \n\nUn día, se cayó y se lastimó mucho. Le dolían los huesos y no quería comer. Pero siguió tomando su medicina. \n\nCuando llegó al hospital, los doctores le hicieron pruebas. Vieron que su sangre estaba un poco rara, pero no tenía mucha azúcar. \n\nElla tenía un problema llamado cetoacidosis, que pasa cuando el cuerpo usa mucha energía y se cansa. Los doctores le dieron agua con azúcar para ayudarla. No le dieron insulina porque su cuerpo todavía hacía insulina sola. \n\nDespués de un tiempo, ella se sintió mejor y pudo irse a su casa. Ya no tomó esa medicina para el corazón.",
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+        "text": "Caso de una mujer mayor con problemas del corazón y un medicamento especial\n\nUna mujer japonesa de 83 años tenía insuficiencia cardíaca, que significa que su corazón no bombeaba sangre tan bien como debería. Para ayudarla, le dieron un medicamento llamado inhibidor de SGLT2, que normalmente se usa para la diabetes, pero ella no tenía diabetes. Este medicamento ayuda al corazón, pero puede causar un problema llamado cetoacidosis, que es cuando el cuerpo produce sustancias ácidas llamadas cetonas.\n\nLo que pasó antes de ir al hospital\n\nDos semanas antes de entrar al hospital, la mujer se cayó y se fracturó una vértebra y una costilla. Por el dolor, dejó de comer bien y se debilitó mucho. A pesar de esto, siguió tomando el medicamento inhibidor de SGLT2.\n\nLo que encontraron en el hospital\n\nCuando llegó al hospital, sus análisis de sangre mostraron que tenía niveles normales de azúcar en la sangre (124 mg/dL), pero su cuerpo estaba en cetoacidosis, porque el pH de su sangre estaba bajo (7.3), el bicarbonato (HCO3–) estaba bajo (14 mmol/L) y tenía muchas cetonas (β-hidroxibutirato alto). Esto significa que su cuerpo estaba produciendo ácidos, aunque el azúcar en sangre no estaba alto, por eso se llama cetoacidosis euglucémica. Además, su cuerpo todavía producía insulina, la hormona que controla el azúcar en sangre, lo que se confirmó con un análisis llamado péptido C.\n\nCómo la trataron y qué pasó después\n\nLos médicos dejaron de darle el medicamento inhibidor de SGLT2 y no le pusieron insulina porque su cuerpo seguía produciéndola. En cambio, le dieron líquidos con glucosa (azúcar) para ayudar a su cuerpo a recuperarse. Poco a poco, sus análisis mejoraron y las cetonas desaparecieron. Cuando pudo volver a comer bien, dejaron de darle glucosa por vía intravenosa. Aunque su azúcar en sangre se mantuvo normal, todavía eliminaba glucosa por la orina durante varios días después de dejar el medicamento. Después de rehabilitación para recuperarse de las fracturas y el cansancio, pudo caminar sola y fue dada de alta del hospital. No volvieron a darle el medicamento inhibidor de SGLT2.\n\nResumen\n\nEste caso muestra que los inhibidores de SGLT2 pueden causar cetoacidosis en personas sin diabetes, especialmente si están débiles o comen poco. Es importante vigilar a los pacientes que usan este medicamento y suspenderlo si aparecen síntomas como náuseas, vómitos o debilidad.",
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+      "B3": {
+        "text": "**Contexto:**  \nSe presenta el caso de una mujer japonesa de 83 años con insuficiencia cardíaca crónica, caracterizada por una fracción de eyección del 30 %, que recibió tratamiento con inhibidores del cotransportador sodio-glucosa tipo 2 (SGLT2), medicamentos usados para mejorar la función cardíaca y controlar la glucosa en sangre. La paciente no tenía diagnóstico previo de diabetes, con una hemoglobina A1c del 5.9 % antes de iniciar el tratamiento. Aproximadamente dos semanas antes de su ingreso hospitalario, sufrió fracturas vertebrales y de costillas tras una caída, lo que le provocó dolor intenso, dificultad para caminar y una marcada disminución en su ingesta alimentaria, aunque continuó tomando dapagliflozina, un inhibidor de SGLT2.\n\n**Hallazgos Clave:**  \nAl ingresar al hospital, la paciente estaba consciente y estable en signos vitales, pero los análisis de sangre mostraron:  \n- Glucosa en sangre de 124 mg/dL (dentro del rango normal).  \n- pH sanguíneo de 7.3, indicando acidosis (un aumento en la acidez de la sangre).  \n- Bicarbonato (HCO₃⁻) de 14 mmol/L, bajo, lo que confirma acidosis metabólica.  \n- Brecha aniónica elevada (20 mEq/L), que sugiere la presencia de ácidos en la sangre.  \n- Elevada concentración de β-hidroxibutirato (5150 μmol/L), una cetona que indica cetosis.  \nEstos resultados permitieron diagnosticar una cetoacidosis euglucémica, una condición en la que hay acumulación de ácidos cetónicos en sangre sin hiperglucemia significativa. Además, el nivel de péptido C, un marcador de producción de insulina, era adecuado, lo que indicaba que la paciente seguía produciendo insulina de forma suficiente.\n\n**Interpretación Clínica:**  \nLa cetoacidosis euglucémica en esta paciente fue probablemente inducida por el uso de inhibidores de SGLT2 en el contexto de una ingesta alimentaria muy reducida y estrés físico debido a las fracturas. Estos medicamentos pueden aumentar la producción de cuerpos cetónicos al promover la eliminación de glucosa por la orina y reducir la insulina circulante, favoreciendo la cetosis incluso cuando los niveles de glucosa en sangre no están elevados. La secreción adecuada de insulina descartó la necesidad de administrar insulina exógena.\n\n**Próximos Pasos y Evolución:**  \nSe suspendió el tratamiento con inhibidores de SGLT2 y se inició terapia con infusión intravenosa de glucosa y líquidos para corregir la acidosis y mantener la ingesta energética, sin administrar insulina. La paciente mostró mejoría rápida en los parámetros ácido-base al día siguiente y la cetosis desapareció en cuatro días. La infusión de glucosa se ajustó según su capacidad para alimentarse y se suspendió una vez que pudo consumir comidas completas. Durante ocho días posteriores a la suspensión del medicamento, la paciente continuó excretando glucosa en la orina, un efecto residual conocido de la dapagliflozina. Tras rehabilitación para recuperar la movilidad afectada por las fracturas y el desuso, la paciente fue dada de alta en buen estado y sin reiniciar los inhibidores de SGLT2.\n\n---\n\nEste caso ilustra la importancia de reconocer la cetoacidosis euglucémica como una complicación potencial de los inhibidores de SGLT2, especialmente en pacientes sin diabetes que presentan factores de riesgo como ingesta insuficiente y estrés físico. La intervención temprana con suspensión del medicamento y soporte nutricional adecuado puede conducir a una recuperación favorable sin necesidad de insulina.",
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+    "article": "Una recién nacida fue evaluada en la sala de neonatos poco tiempo después del parto debido a la presencia de extensas lesiones similares a cicatrices en sus flancos y muslos superiores. La bebé, nacida de una madre asiática de 28 años a las 39 semanas de gestación, formaba parte de un embarazo gemelar espontáneo. Su madre, que ya había tenido cinco hijos, había tenido un aborto espontáneo en el primer trimestre durante su segundo embarazo.\n\nLos padres eran primos hermanos y no habían tenido problemas de salud en sus tres hijos vivos. La ecografía a las 13 semanas confirmó un embarazo bicorial y diacítico y la ausencia de actividad cardíaca en uno de los gemelos. Las ecografías posteriores mostraron un feto que se desarrollaba con normalidad junto a un gemelo no viable.\n\nDurante el embarazo, la madre no informó sobre el uso de medicamentos o síntomas como fiebre y erupción cutánea. Dio negativo para estreptococo del grupo B y fue admitida en el departamento de urgencias obstétricas con dolores de parto. La niña fue entregada por vía vaginal, pesando 2,83 kg, y fue vigorosa al nacer. A la placenta se le unió un remanente fetal no viable comprimido que medía 6 × 2 cm. La placenta pesaba 460 g y parecía normal al examen.\n\nLa niña presentaba lesiones cutáneas extensas e irregulares, que se caracterizaban por un aspecto estrellado en ambos flancos, que se extendían lateralmente sobre la zona glútea y el muslo superior. Las lesiones eran simétricas en ambos flancos. No obstante, las lesiones en los muslos eran notablemente más leves en el lado izquierdo. Sus constantes vitales eran estables y no presentaba otras anomalías externas. El examen clínico de sus sistemas respiratorio, cardiovascular, gastrointestinal y neurológico reveló resultados normales, y no se observaron otras anomalías cutáneas, incluida la ausencia de lesiones ampollosas.\n\nDada la naturaleza simétrica de las anomalías cutáneas y el contexto de embarazo de mellizos con FP, se realizó un diagnóstico de aplasia cutis congénita grupo V. Los exámenes de laboratorio, que incluían hemograma completo, electrolitos y pruebas de función renal e hepática, arrojaron resultados normales. Los exámenes de detección de toxoplasmosis, rubéola, citomegalovirus, herpes simple y VIH (TORCH) arrojaron resultados negativos. La ecografía del cerebro, abdomen y corazón no reveló anomalías.\n\nDado que las lesiones se curaron en el útero, solo se prescribieron emolientes locales. Después de 48 horas de observación, el bebé fue dado de alta en su casa, con derivaciones a clínicas de dermatología pediátrica y cirugía plástica. En el seguimiento de 2 semanas, no se observaron cambios en las lesiones de la piel ni nuevos síntomas. Su análisis de microarreglo cromosómico fue reportado como normal.\n",
+    "gold_summary": "Informamos sobre un neonato al que se le diagnosticó ACC de grupo G-V asociado con fetus papyraceus de un embarazo gemelar di-coriónico y di-amniótico. Nacida de una madre asiática de 28 años, esta niña presentaba lesiones extensas, cicatrizadas, similares a las cicatrices en sus flancos y muslos superiores. Estas lesiones eran consistentes con la distribución en forma de «H» comúnmente descrita en ACC ligada a fetus papyraceus. A pesar de las manifestaciones dermatológicas significativas, la niña no mostró otras anormalidades externas o implicación sistémica, y las evaluaciones exhaustivas, incluidos los ultrasonidos y el microarray cromosómico, fueron normales.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Una bebé nació con marcas en la piel que parecían cicatrices. Estas marcas estaban en sus lados y muslos. La mamá tuvo dos bebés, pero uno no creció bien en la barriga. \n\nLa bebé con las marcas está sana y fuerte. Los doctores revisaron su cuerpo y todo está bien. No tiene otras partes malas en su cuerpo. \n\nLas marcas en su piel se hicieron mientras estaba en la barriga. Los doctores solo le pusieron crema para cuidar su piel. La bebé está bien y seguirá creciendo feliz.",
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+      "B2": {
+        "text": "**Caso de una recién nacida con lesiones en la piel**\n\nLes presentamos el caso de una bebé que nació con unas marcas especiales en la piel, llamadas aplasia cutis congénita (ACC) grupo V. Estas marcas aparecieron porque tuvo un gemelo que no sobrevivió durante el embarazo, lo que se conoce como fetus papyraceus (un gemelo aplastado y no viable).\n\n**Lo que encontraron en la bebé**\n\nLa niña, nacida de una madre asiática de 28 años, tenía lesiones en la piel que parecían cicatrices en forma de “H” en sus costados y muslos superiores. Estas marcas son típicas en casos de ACC cuando hay un fetus papyraceus. A pesar de estas lesiones, la bebé estaba saludable en general. No tenía otros problemas visibles ni síntomas en su cuerpo. Las pruebas médicas, como ecografías del cerebro, corazón y abdomen, y un análisis genético llamado microarreglo cromosómico, mostraron resultados normales.\n\n**Qué significa este diagnóstico**\n\nLa ACC grupo V es una condición rara que afecta la piel y está relacionada con la pérdida de un gemelo durante el embarazo. Aunque las marcas en la piel pueden ser grandes, no siempre causan otros problemas de salud. En este caso, la bebé solo necesitó cuidados para mantener la piel hidratada y fue seguida por especialistas en dermatología y cirugía plástica para asegurar una buena recuperación.\n\nEn resumen, esta niña nació con lesiones en la piel causadas por la pérdida de su gemelo, pero su salud general es buena y no presenta otras complicaciones.",
+        "scores": {
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+          "BERTScore_R": NaN,
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+      "B3": {
+        "text": "**Contexto**  \nSe presenta el caso de una recién nacida diagnosticada con aplasia cutis congénita (ACC) del grupo V, una condición caracterizada por la ausencia localizada de piel, en asociación con fetus papyraceus (un gemelo fetal muerto y comprimido) en un embarazo gemelar bicorial y biamniótico. La bebé nació de una madre asiática de 28 años, producto de un embarazo espontáneo gemelar, en el que uno de los fetos no sobrevivió desde etapas tempranas.\n\n**Hallazgos Clave**  \nAl momento del nacimiento, la niña mostró lesiones cutáneas extensas, con un patrón simétrico en forma de «H» en ambos flancos y muslos superiores, que se asemejaban a cicatrices. Estas lesiones son típicas de la ACC grupo V cuando se asocia con fetus papyraceus. A pesar de la apariencia notable de la piel, la bebé no presentó otras anomalías externas ni signos de afectación en órganos o sistemas. Los exámenes clínicos y de laboratorio, incluyendo ecografías cerebrales, abdominales y cardíacas, así como pruebas para infecciones congénitas (TORCH) y análisis cromosómicos mediante microarreglo, no mostraron alteraciones.\n\n**Interpretación Clínica**  \nLa distribución y características de las lesiones cutáneas, junto con la historia del embarazo gemelar con un gemelo no viable, apoyan el diagnóstico de aplasia cutis congénita grupo V. Esta forma de ACC se relaciona con la presencia de fetus papyraceus y suele manifestarse con lesiones simétricas en la piel, pero sin compromiso sistémico. La ausencia de otras anomalías y la normalidad de las pruebas complementarias indican un pronóstico favorable.\n\n**Próximos Pasos**  \nEl tratamiento consistió en cuidados locales con emolientes para favorecer la hidratación y cicatrización de la piel. La bebé fue dada de alta tras 48 horas de observación y se programaron controles en dermatología pediátrica y cirugía plástica para seguimiento y manejo de las lesiones cutáneas. A las dos semanas, no se observaron cambios ni aparición de nuevos síntomas, confirmando la estabilidad clínica del caso.",
+        "scores": {
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
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+  {
+    "article": "Información para el paciente\nUn hombre de 44 años de edad fue ingresado en nuestro hospital con quejas principales de neumaturia y cistitis repetida. El paciente también tenía antecedentes de hipotiroidismo.\n\nLa tomografía computarizada con contraste mejorado reveló múltiples divertículos del colon sigmoide, y el límite entre el divertículo y la vejiga no estaba claro. La endoscopia gastrointestinal inferior reveló una fístula en el colon rectosigmoide aproximadamente a 15 cm del borde anal. La cistoscopia reveló una fístula en la pared posterior izquierda de la vejiga. Se diagnosticó una fístula vesicovaginal y se planificó una cirugía laparoscópica. Los hallazgos intraoperatorios revelaron una inflamación severa alrededor de la fístula vesicovaginal, y también se habían formado adhesiones severas entre el íleon y la vejiga. El íleon y la vejiga eran difíciles de exfoliar debido a las adhesiones severas. Por lo tanto, decidimos realizar una resección intestinal combinada. El colon rectosigmoide, incluida la fístula, se movilizó y se resecó. La fístula vesical se seccionó y se cerró con una sutura de púas sin nudos (V-LocTM 180, Covidien, Mansfield). La anastomosis sigmoide-rectal se reconstruyó utilizando la técnica de doble grapado. La resección parcial del íleon se reconstruyó con una anastomosis funcional de extremo a extremo (FEEA). Además de la presencia de una anastomosis de 2 sitios, había una inflamación severa en el área circundante, y considerando el riesgo de fuga anastomótica, se creó una ileostomía de derivación 30 cm proximal a la anastomosis ileo-ileal.\n\nLos procedimientos quirúrgicos incluyeron resección anterior alta laparoscópica, resección parcial del intestino delgado, cistectomía parcial y derivación en forma de asa. La operación duró 236 minutos y la pérdida de sangre fue de 50 ml. El curso postoperatorio fue sin incidentes y el cierre de la ileostomía se planificó 1 mes después de la cirugía inicial. Con ayuda laparoscópica, se eliminaron las adherencias entre el omento y la pared abdominal alrededor del estoma. Se realizó una movilización completa alrededor del estoma y el intestino se sacó hacia afuera. El íleon se reconstruyó utilizando FEEA. El procedimiento quirúrgico implicó el cierre de la ileostomía asistida por laparoscopia. La operación duró 100 minutos y la pérdida de sangre fue de 30 ml.\n\nHallazgos clínicos\nAl día siguiente de la cirugía, se produjo un shock sintomático debido a la presión arterial baja (<80 mm Hg) y la taquicardia. Los análisis de sangre mostraron que la hemoglobina disminuyó de 15.3 antes de la cirugía a 8.6 g/dL después de la cirugía.\n\nEvaluación diagnóstica\nLa tomografía computarizada abdominal (TC) reveló una gran cantidad de fluido de alta densidad en la cavidad abdominal. El diagnóstico fue sangrado posoperatorio y shock hemorrágico. Se insertó un catéter venoso central y se administraron 8 unidades de glóbulos rojos y 8 unidades de plasma fresco congelado para estabilizar los signos vitales. Los signos vitales se estabilizaron y no se observó progresión de la anemia después de eso. Aunque se logró la hemostasia, la distensión abdominal severa y los altos niveles de respuesta inflamatoria (proteína C reactiva [CRP] a 42.9 mg/dL y recuento de glóbulos blancos [WBC] de 18,500/uL) persistieron 7 días después de la cirugía.\n\nLa TC con contraste reveló que el hematoma intraabdominal se localizaba en el abdomen inferior izquierdo y derecho, y se consideró posible el drenaje percutáneo. En el día 8 posoperatorio, se insertaron tubos de drenaje de 18 Fr en el abdomen inferior izquierdo y derecho a través de una punción guiada por TC, y se drenó una gran cantidad de sangre antigua. Después del drenaje, la reacción inflamatoria y la distensión abdominal causadas por la infección del hematoma residual mejoraron (CRP a 1,9 mg/dL y WBC de 5000/μL). No se observó progresión de la anemia. En el día 14 posoperatorio, el drenaje en el abdomen inferior derecho cambió de sangre antigua a jugo intestinal. Una angiografía de drenaje reveló fuga anastomótica tardía en el sitio de cierre de la ileostomía. No hubo signos de peritonitis con buen drenaje, pero el drenaje fue de aproximadamente 100 a 200 ml, y el flato del drenaje continuó. No se observó disminución del drenaje durante los siguientes 14 días.\n\nIntervención terapéutica\nAunque se consideró la posibilidad de una nueva operación, se esperaban adhesiones intraabdominales severas debido a la historia de cirugías anteriores, sangrado postoperatorio y fuga anastomótica. Por lo tanto, se consideró que la nueva operación era un procedimiento de alto riesgo. La tomografía computarizada con contraste mostró que un hematoma organizado permanecía en el mesenterio del intestino delgado y el íleon en el lado distal de 10 cm de la anastomosis estaba comprimido cerca del hematoma restante. Teniendo en cuenta la estenosis del íleon en el lado anal de la anastomosis debido a un hematoma residual como la causa de fuga anastomótica, se intentó la dilatación radioscópica del área de estenosis a través del drenaje en el día 24 postoperatorio. Se colocó un introductor de funda Cordis BRITE TIP® (8 Fr × 23 cm) en la fístula donde ocurrió la fuga anastomótica después del drenaje angiográfico. Se usó un hilo radioscópico GT (0.016 pulgadas, 180 cm, 90°) (Terumo, Tokio, Japón) y un microcatéter Renegade HI-FLO (135 × 20 cm) (Boston Scientific, Tokio, Japón) para alcanzar el íleon terminal. Usando el catéter Selecon MP II (6 Fr, 80 cm, φ20 mm) (Terumo), se identificó el área de estenosis en el íleon debido a la compresión del hematoma donde el globo no podía pasar.\n\nSe realizó dilatación con globo fluoroscópica en la estenosis del íleo utilizando un globo guiado por alambre CRE PRO GI (180 cm, 15-18 mm) (Boston Scientific), inflado a 16,5 mm de diámetro a 4,5 atm durante 3 minutos.\n\nSeguimiento y resultados\nDesde el día posterior a la dilatación con globo, la cantidad de drenaje disminuyó notablemente, y se observaron flatos y defecaciones desde el ano. Una semana después de la dilatación con globo, el drenaje fue casi nulo, y se determinó que la fuga anastomótica se había resuelto. El drenaje se eliminó gradualmente. La ingesta oral fue buena, y tuvo movimientos intestinales regulares. Fue dado de alta el día 45 posterior a la operación. Desde entonces, no se ha informado de ninguna recurrencia de la estenosis o fuga anastomótica.\n",
+    "gold_summary": "Preocupaciones del paciente: Presentamos el caso de un hombre de 44 años con fuga anastomótica tardía después del cierre de la ileostomía, causada por la compresión de un hematoma intraabdominal que se curó rápidamente después de la dilatación fluoroscópica con globo del área de la estenosis intestinal.\n\nDiagnósticos: Se produjo sangrado postoperatorio y shock hemorrágico el día 1 postoperatorio tras el cierre de la ileostomía. Los signos vitales se estabilizaron tras la transfusión de sangre, y se realizó con éxito un drenaje guiado por tomografía computarizada para reducir el volumen del hematoma. Sin embargo, el hematoma residual comprimió el íleon en el lado anal de la anastomosis, lo que provocó una fuga anastomótica tardía.\n\nIntervenciones/resultados: Se realizó con éxito la dilatación con balón fluoroscópico del área estenótica a través del drenaje y la fuga anastomótica se curó rápidamente.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Había un hombre que se lastimó su tripita después de una operación. Tenía un bulto con sangre que apretaba su intestino y eso hizo que se hiciera un agujero pequeño. \n\nLos doctores le pusieron una bolsita con aire para hacer más grande el lugar apretado. Así, el agujero se cerró y el hombre empezó a sentirse mejor. \n\nDespués, pudo comer y hacer popó sin problema. Los doctores cuidaron mucho de él y se fue a su casa feliz.",
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+        "text": "Caso del paciente  \nUn hombre de 44 años tuvo una complicación después de una cirugía para cerrar una ileostomía, que es una abertura temporal en el abdomen para sacar los desechos del intestino. Esta complicación se llamó fuga anastomótica tardía, que significa que la unión hecha entre partes del intestino empezó a tener una filtración de líquidos.\n\nQué pasó después de la cirugía  \nAl día siguiente de cerrar la ileostomía, el paciente sufrió una hemorragia interna que causó un shock, una condición grave donde la presión de la sangre baja mucho. Los médicos le transfundieron sangre y drenaron un hematoma, que es una acumulación de sangre fuera de los vasos sanguíneos dentro del abdomen. Aunque esto ayudó, quedó un hematoma pequeño que presionaba una parte del intestino llamada íleon, causando que la unión intestinal se filtrara.\n\nTratamiento y resultados  \nPara solucionar la fuga, los médicos usaron una técnica llamada dilatación con balón fluoroscópico. Esto consiste en insertar un pequeño globo dentro del área estrecha del intestino y luego inflarlo para abrir el paso. Esta intervención se hizo a través del drenaje ya colocado y ayudó a aliviar la presión causada por el hematoma. Después del tratamiento, la fuga se cerró rápidamente, el drenaje disminuyó y el paciente pudo volver a comer y tener movimientos intestinales normales. Fue dado de alta sin más problemas y no ha tenido recurrencias.",
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+      },
+      "B3": {
+        "text": "**Contexto del Caso**  \nSe presenta el caso de un hombre de 44 años que inicialmente fue hospitalizado por síntomas de neumaturia (presencia de aire en la orina) y episodios repetidos de cistitis (infección de la vejiga). Tenía antecedentes de hipotiroidismo. Estudios de imagen y endoscopía revelaron una fístula (una conexión anormal) entre el colon sigmoide y la vejiga, acompañada de múltiples divertículos (pequeñas bolsas) en el colon. Debido a la inflamación severa y adherencias entre intestino y vejiga, se realizó una cirugía laparoscópica compleja que incluyó la resección del colon afectado, cierre de la fístula vesical, resección parcial del intestino delgado y creación temporal de una ileostomía (una abertura en el abdomen para desviar las heces).\n\n**Hallazgos y Complicaciones Postoperatorias**  \nAl día siguiente del cierre de la ileostomía, el paciente presentó un shock hemorrágico debido a una hemorragia interna, evidenciada por una caída significativa de hemoglobina y acumulación de líquido denso en la cavidad abdominal detectada por tomografía computarizada (TC). Se estabilizó con transfusiones y drenaje guiado por TC de un hematoma (acumulación de sangre) intraabdominal. A pesar de la hemostasia, persistió una inflamación intensa y distensión abdominal. Posteriormente, el drenaje mostró presencia de jugo intestinal, lo que indicó una fuga en la anastomosis (la unión quirúrgica entre segmentos intestinales) en el sitio del cierre de la ileostomía. Esta fuga anastomótica tardía se atribuyó a la compresión del íleon (parte final del intestino delgado) por un hematoma residual que causaba estenosis (estrechamiento) en esa zona.\n\n**Intervención Terapéutica**  \nDado el alto riesgo de una nueva cirugía debido a las adherencias y complicaciones previas, se optó por un tratamiento menos invasivo. Se realizó una dilatación con balón guiada por fluoroscopía (una técnica de imagen en tiempo real) a través del drenaje existente para ampliar el área estenótica del íleon comprimido. Este procedimiento consistió en introducir un catéter y un globo inflable en el sitio estrechado y expandirlo cuidadosamente para aliviar la compresión.\n\n**Resultados y Seguimiento**  \nTras la dilatación con balón, la cantidad de drenaje intestinal disminuyó notablemente y el paciente recuperó la función intestinal normal, con evacuaciones por vía natural. Una semana después, la fuga anastomótica se resolvió completamente, permitiendo la retirada progresiva del drenaje. El paciente mantuvo una buena ingesta oral y movimientos intestinales regulares, y fue dado de alta 45 días después de la cirugía inicial. Hasta la fecha, no se ha reportado recurrencia de la estenosis ni de la fuga anastomótica.\n\n---\n\nEste caso ilustra cómo una complicación grave tras cirugía intestinal, como una fuga anastomótica causada por compresión de un hematoma residual, puede ser tratada eficazmente mediante una dilatación endovascular guiada por imágenes, evitando una cirugía adicional de alto riesgo.",
+        "scores": {
+          "ROUGE-1": 0.3796711509715994,
+          "ROUGE-2": 0.2128935532233883,
+          "ROUGE-L-Sum": 0.3408071748878924,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
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+  },
+  {
+    "article": "Paciente femenino de 23 años, ASA I, acude al Centro de Salud de la Universidad Peruana de Ciencias Aplicadas (CUS-UPC) para colocarle un implante en la zona edéntula de la pieza 1.6. Durante la evaluación, la paciente refiere que hace unos meses se le fracturó la primera molar superior derecha y, como consecuencia, le realizaron la exodoncia atraumática de dicha pieza dentaria.\n\nTras la inspección clínica, se observó la ausencia de la pieza dentaria 1.6, fenotipo gingival delgado y disminución en altura de reborde edéntulo Seibert tipo II 13. Tomográficamente, se registraron medidas de la altura del reborde óseo residual en relación con el piso del seno maxilar (6 mm) y el ancho de la cresta ósea a nivel cervical (11,20 mm), medio (11,80 mm) y apical (12,40 mm), con lo que se identifica la presencia de un seno maxilar ovoide, según Nie et al. Se realizó la planificación quirúrgica para la realización de una elevación del seno maxilar con abordaje transcrestal y la colocación de un implante dental de 4,8 x 8 mm.\n\nSe inició el procedimiento quirúrgico, que consistió en lo siguiente:\n\n• Asepsia y antisepsia\n\n• Técnica anestesia infiltrativa por vestibular y palatino de la zona edéntula 1.6 utilizando 2 cartuchos de lidocaína al 2% con epinefrina 1:80.000.\n\n• Incisión supracrestal en la zona edéntula 1.6 e incisiones sulculares en mesial de la pieza dentaria 1.7 y en distal de la pieza dentaria 1.5.\n\n• Decolado del colgajo a espesor parcial y, luego, se procedió a probar la guía quirúrgica para realizar la secuencia de fresado hasta una longitud de 6 mm, dejando 1 mm de distancia al piso del seno maxilar, el cual fue comprobado con los calibradores de profundidad, según el diámetro de la fresa que se utilizó durante la osteotomía. La secuencia de fresado se realizó hasta la fresa 3,5 mm de diámetro y luego se procedió a realizar el levantamiento de 2 mm del seno maxilar con la técnica de abordaje transcrestal mediante el uso de un osteótomo, hasta llegar a una longitud de 8 mm.\n\n• Colocación del implante φ 4,8 x 8 mm (Bone Level tapered, Straumann®) y tornillo de cierre, ambos con un torque de inserción de 20 N.\n\n• Sutura con puntos interrumpidos con ácido poliglicólico 5/0 y lavado de la zona quirúrgica con suero fisiológico al 0,09%.\n\n• Radiografía posquirúrgica del implante en zona edéntula 1.6.\n\n• Indicación de tomar amoxicilina de 500 mg + ácido clavulánico 125 mg cada 8 horas durante 7 días, ketorolaco de 10 mg cada 8 horas por 3 días, cetirizina de 10 mg cada 24 horas por 3 días y clorhexidina al 0,12%, 2 veces al día, por 10 días. Entre las indicaciones posquirúrgicas se le indicó a la paciente reposo absoluto, sin esfuerzo físico, dieta blanda, no sonarse la nariz, no succionar líquidos por dos semanas, no sumergir la cabeza en agua, tampoco estornudar o toser con la boca abierta, mantener la cabeza elevada y aplicarse compresas de hielo durante las primeras 4 horas.\n\nSe realizó un control posquirúrgico a los 7 días, el cual evidenció tejidos blandos en proceso de cicatrización, por lo que se procedió al retiro de puntos y lavado con suero fisiológico al 0,9%, y se realizó una tomografía de control que evidenció la elevación de seno maxilar, con 2,83 mm aproximadamente. Asimismo, se realizaron controles posquirúrgicos a los 35 y 56 días, en los cueles se hallaron tejidos blandos en completo proceso de cicatrización.",
+    "gold_summary": "Se realizó un levantamiento de seno maxilar sin injerto óseo en una paciente de sexo femenino de 23 años que requería la colocación de un implante dental en la zona edéntula de la pieza 16. La evaluación clínica y tomográfica permitieron planificar y realizar la elevación de seno maxilar mediante el abordaje transcrestal y sin la necesidad de injerto óseo. El reborde residual de 6 mm permitió la colocación de un implante dental simultáneo. Luego de 6 meses de seguimiento tomográfico, antes de la carga protésica, se consiguió una altura ósea vertical de 8,83 mm, lo que dio como resultado una ganancia ósea vertical de 2,83 mm. Adicionalmente, se observa una adecuada integración del implante dental sin complicaciones posoperatorias.",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Una joven de 23 años necesitaba un diente nuevo. El doctor hizo un pequeño espacio en su hueso cerca de la nariz. No usó nada más para llenar ese espacio. Puso un tornillo especial para el diente. Después de un tiempo, el hueso creció un poquito más. El diente nuevo quedó bien y sin problemas. Todo está sanando muy bien.",
+        "scores": {
+          "ROUGE-1": 0.16080402010050251,
+          "ROUGE-2": 0.06091370558375634,
+          "ROUGE-L-Sum": 0.16080402010050251,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B2": {
+        "text": "**Lo que hicieron y encontraron**\n\nUna joven de 23 años necesitaba un implante dental porque le faltaba un molar superior derecho. Los doctores revisaron su boca y tomaron imágenes para medir el hueso donde se colocaría el implante. Vieron que había 6 mm de hueso en esa zona, lo que era suficiente para poner un implante, pero necesitaban levantar un poco el seno maxilar. El seno maxilar es un espacio lleno de aire dentro del hueso de la cara, cerca de los dientes superiores. Para hacer espacio para el implante, realizaron una cirugía llamada elevación de seno maxilar usando un método que no requiere poner hueso nuevo (injerto).\n\n**Cómo fue la cirugía**\n\nDurante la operación, anestesiaron la zona para que no sintiera dolor. Hicieron una pequeña incisión y usaron herramientas especiales para levantar el suelo del seno maxilar unos 2 mm. Luego colocaron un implante dental de 8 mm de largo en el hueso existente. Después, cerraron la herida con puntos y le dieron medicamentos para evitar infecciones y controlar el dolor. También le indicaron cuidados para que la zona sanara bien.\n\n**Qué pasó después**\n\nA los 7 días, la herida estaba sanando bien y retiraron los puntos. Después de 6 meses, las imágenes mostraron que el hueso había crecido 2,83 mm más en altura, alcanzando un total de 8,83 mm. Esto significa que el implante estaba bien integrado y estable, sin problemas después de la cirugía.\n\n**Por qué es importante**\n\nEste caso muestra que es posible levantar el seno maxilar y colocar un implante al mismo tiempo sin usar hueso extra. Esto puede hacer que el tratamiento sea más rápido y menos complicado para pacientes que necesitan implantes en esa zona.",
+        "scores": {
+          "ROUGE-1": 0.330316742081448,
+          "ROUGE-2": 0.10909090909090909,
+          "ROUGE-L-Sum": 0.3257918552036199,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nUna mujer de 23 años, sin antecedentes médicos relevantes (clasificación ASA I), acudió a un centro de salud para la colocación de un implante dental en el espacio dejado por la extracción previa de su primer molar superior derecho (pieza 1.6). La paciente había perdido este diente debido a una fractura y se le realizó una exodoncia atraumática. Durante la evaluación clínica se observó la ausencia del diente, un tipo de encía delgada y una reducción en la altura del reborde óseo (zona del hueso donde se apoya el diente), clasificada como Seibert tipo II. Las imágenes tomográficas mostraron que el reborde óseo residual tenía una altura de 6 mm desde el piso del seno maxilar, con un ancho adecuado para la colocación del implante, y se identificó un seno maxilar de forma ovoide.\n\n**Hallazgos Clave y Procedimiento Realizado**  \nSe planificó una elevación del seno maxilar mediante un abordaje transcrestal (acceso a través de la cresta ósea donde se colocará el implante) sin necesidad de utilizar injerto óseo. Durante la cirugía, se realizó anestesia local, incisiones precisas para levantar un colgajo de encía, y se preparó el sitio para el implante con fresas de diferentes diámetros, respetando una distancia segura de 1 mm al piso del seno maxilar. Se elevó la membrana del seno maxilar 2 mm con un osteótomo (instrumento para levantar el seno), permitiendo colocar un implante dental de 4,8 mm de diámetro por 8 mm de longitud. La inserción se realizó con un torque adecuado (20 N), y se cerró la zona con suturas. Se indicó un tratamiento antibiótico, antiinflamatorio, antihistamínico y enjuagues con clorhexidina, además de recomendaciones estrictas para evitar complicaciones, como reposo absoluto y evitar esfuerzos que puedan afectar la zona quirúrgica.\n\n**Interpretación Clínica**  \nEl procedimiento permitió aumentar la altura ósea vertical disponible para el implante sin necesidad de injerto óseo, aprovechando el reborde óseo residual de 6 mm para colocar el implante simultáneamente con la elevación del seno maxilar. El seguimiento tomográfico realizado a los 7 días mostró una elevación de la membrana del seno de aproximadamente 2,83 mm, y controles posteriores a los 35 y 56 días confirmaron una adecuada cicatrización de los tejidos blandos sin complicaciones. Se logró una ganancia ósea vertical total de 2,83 mm, alcanzando una altura ósea de 8,83 mm antes de la colocación de la prótesis dental.\n\n**Próximos Pasos**  \nCon la adecuada integración del implante y la ganancia ósea confirmada, el siguiente paso será la carga protésica, es decir, la colocación de la corona o diente artificial sobre el implante para restaurar la función masticatoria y estética. Se continuará con controles periódicos para asegurar la estabilidad del implante y la salud de los tejidos circundantes.",
+        "scores": {
+          "ROUGE-1": 0.3607594936708861,
+          "ROUGE-2": 0.20634920634920634,
+          "ROUGE-L-Sum": 0.32594936708860756,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      }
+    }
+  },
+  {
+    "article": "Una paciente de 42 años de edad fue remitida a nuestro centro terciario de cáncer con antecedentes de seroma recurrente del seno izquierdo. La paciente se había sometido a una extracción bilateral de implantes mamarios con una capsulotomía parcial 11 meses antes de su primera visita a nuestro centro. La paciente no presentaba ninguna comorbilidad notable y tenía antecedentes de aumento bilateral de senos con implantes mamarios en el plano submuscular en 2003, a la edad de 21 años. No se pudo localizar ninguna información sobre el tipo de implantes que había recibido originalmente. La paciente volvió a consultar al mismo cirujano en 2008, quejándose de seroma bilateral, para someterse a un primer reemplazo bilateral de implantes mamarios con implantes mamarios anatómicos texturados de 425 cc (Sebbin LSA TF 425). En 2013, se sometió a un segundo procedimiento de reemplazo de implantes para aumentar el tamaño con implantes mamarios de 480 cc del mismo fabricante (Sebbin LSA TF 480). En 2017, la paciente volvió para una revisión en la que se quejaba de dolor y aumento del volumen del seno bilateralmente. En ese momento, se le realizó una exploración por ultrasonido que identificó efusiones periprostéticas bilaterales sin linfadenopatía o masas palpables en las regiones mamarias. Las efusiones se drenaron sin análisis, pero reaparecieron a lo largo de los años, cuando la paciente buscó ayuda del mismo cirujano y se sometió a un tercer procedimiento de revisión en 2022, con un reemplazo bilateral de implantes mamarios y una toma de muestras de la cápsula anterior. El cirujano envió dos especímenes desde el lado derecho (9 x 1 cm y 3 x 3 cm) y uno desde el lado izquierdo (2 x 1 cm). El informe histopatológico del espécimen encontró «material proteico amorfo celular acellular» en el lado derecho y «tejido fibroso escleroso con inflamación de linfocitos-monocitos, que requiere correlación con la presentación clínica» en el lado izquierdo. A pesar de la extracción, el seroma reapareció en el lado izquierdo, y se envió para pruebas citopatológicas que identificaron «una población de células pleomórficas atípicas irregulares con contornos irregulares que sugieren un proceso linfoproliferativo con CD30+ elementos» para los que se recomendaron pruebas diagnósticas adicionales. Por esta razón, la paciente buscó tratamiento en nuestra institución, donde el caso fue gestionado por un equipo multidisciplinario (MDT) que incluía a un cirujano plástico, un hematopatólogo, un hematólogo, un oncólogo, un radioterapeuta, un oncólogo quirúrgico y un radiólogo de mama. El espécimen histopatológico original de la toma de la cápsula se revisó por un hematopatólogo de nuestro centro de referencia, que identificó células CD30+ grandes y escasas atípicas con contornos irregulares que se consideraron compatibles con el diagnóstico de BIA-ALCL. Las células presentaron el siguiente fenotipo: CD30+, CD3-, CD7-, CD5-, CD4-, CD8-, Granzima B+/-, TIA1-, ALK1-, PAX5-, CD79a-, CD68-, CD15-/+. La paciente recibió una exploración por ultrasonido con aspiración por aguja fina y citopatología de la efusión recurrente que confirmó un proceso CD30+ linfoproliferativo atípico con captación de 18F-FDG (fluorodeoxiglucosa) (SUV máx. 1,8). No se pudieron localizar otras áreas de captación en todos los demás segmentos corporales explorados. La paciente también recibió una exploración por resonancia magnética de ambos senos con medio de contraste para completar la estadificación preoperativa, confirmando el seroma del lado izquierdo. Los portaobjetos del espécimen de la cirugía anterior se revisaron por el hematopatólogo que consideró los hallazgos suficientes para identificar BIA-ALCL con infiltración temprana de la cápsula periprostética (pT2 según el sistema de estadificación MD Anderson-TNM). Tres semanas después de la visita inicial, la paciente se sometió a cirugía radical con capsulotomía en bloque que contenía solo 150 cc de efusión serosa sin implante. El contenido líquido se envió para cultivo y citopatología, mientras que el espécimen sólido se envió para examen histopatológico. Además, la paciente se sometió a biopsia de ganglio linfático centinela de 2 ganglios axilares identificados preoperativamente a través de linfografía segmentaria. Los ganglios linfáticos presentaron una linfadenopatía silicona-asociada reactiva crónica sin signos de linfadenopatía metastásica. El informe histopatológico de la cápsula reveló agregados celulares infiltrantes en la cápsula periprostética, pero márgenes de resección claros y sin signos de infiltración más allá de la cápsula. Como tal, la paciente recibió un estadio IC (pT3pN0M0). El curso postoperatorio fue sin incidentes, y no se consideraron necesarios más tratamientos adyuvantes por el MDT. La paciente continuó su estricto protocolo de seguimiento, con PET/CT de 6, 12 y 18 meses posteriores a la cirugía que no mostró signos de recurrencia de enfermedad local o distante. Como está, la paciente continúa sus visitas de seguimiento y exploraciones, con supervivencia libre de enfermedad más allá de 18 meses.\n",
+    "gold_summary": "Describimos el caso de una mujer de 42 años con antecedentes de aumento de senos bilateral con fines cosméticos 21 años antes, que desarrolló seroma recurrente del lado izquierdo. Buscó ayuda de su primer cirujano, quien realizó 2 procedimientos de intercambio de implantes mamarios, colocando dispositivos texturados y, finalmente, una extracción bilateral de implantes mamarios en el transcurso de dos décadas. La paciente no recibió capsulectomías en los intercambios de implantes anteriores y recibió una muestra de la cápsula anterior en el último procedimiento, donde se diagnosticó BIA-ALCL en el lado izquierdo. Fue derivada a un centro de cáncer terciario donde el examen preoperatorio confirmó la presencia de enfermedad residual local. Después de la gestión del equipo multidisciplinario, se sometió a una revisión de capsulectomía en bloque del lado izquierdo sin necesidad de tratamientos adicionales. El curso postoperatorio fue sin incidentes y sin signos de recurrencias locales a los 18 meses de seguimiento.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Había una mujer que se puso pechos nuevos hace mucho tiempo. Con el tiempo, su pecho izquierdo se llenó de líquido muchas veces. Fue al doctor varias veces y le cambiaron los pechos dos veces. Al final, le quitaron los pechos nuevos. \n\nEl doctor vio que había unas células raras en el pecho izquierdo. La llevaron a un hospital especial para ayudarla. Allí le hicieron una operación para sacar todo lo raro. \n\nDespués de la operación, la mujer estuvo bien. Los doctores la revisaron muchas veces y no encontraron nada malo. Ahora está sana y sigue yendo al doctor para cuidarse.",
+        "scores": {
+          "ROUGE-1": 0.2773722627737226,
+          "ROUGE-2": 0.051470588235294115,
+          "ROUGE-L-Sum": 0.2700729927007299,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
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+      "B2": {
+        "text": "**Caso de una mujer con problemas en sus implantes mamarios**\n\nUna mujer de 42 años se hizo un aumento de senos cuando tenía 21 años. Con el tiempo, comenzó a tener un problema llamado seroma, que es cuando se acumula líquido alrededor del implante. Esto pasó especialmente en su seno izquierdo y volvió varias veces.\n\n**Tratamientos previos y diagnóstico**\n\nLa mujer visitó a su cirujano varias veces y se le cambiaron los implantes dos veces. En la última cirugía, le quitaron ambos implantes, pero no retiraron toda la cápsula, que es el tejido que se forma alrededor del implante. Al analizar una muestra de esta cápsula, los médicos encontraron células anormales que indicaban una enfermedad llamada linfoma anaplásico de células grandes asociado a implantes mamarios (BIA-ALCL). Este es un tipo raro de cáncer que puede aparecer en personas con implantes mamarios.\n\n**Atención en un centro especializado**\n\nDespués de este diagnóstico, la paciente fue enviada a un hospital especializado en cáncer. Allí, un equipo de diferentes especialistas revisó su caso y confirmó que todavía había enfermedad en la cápsula del seno izquierdo. La paciente se sometió a una cirugía para quitar toda la cápsula afectada y el líquido acumulado, sin necesidad de tratamientos como quimioterapia o radioterapia.\n\n**Resultado y seguimiento**\n\nLa operación fue exitosa y no hubo complicaciones. Durante 18 meses después de la cirugía, la mujer fue revisada varias veces y no se detectó que el cáncer regresara. Actualmente, sigue en control médico para asegurarse de que se mantenga sana.\n\nEn resumen, este caso muestra la importancia de detectar y tratar a tiempo un tipo raro de cáncer que puede aparecer en personas con implantes mamarios, y cómo un equipo médico especializado puede ayudar a manejarlo con éxito.",
+        "scores": {
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
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+      },
+      "B3": {
+        "text": "**Contexto**  \nPresentamos el caso de una mujer de 42 años que, tras haberse sometido a un aumento bilateral de senos con implantes mamarios hace 21 años, desarrolló un seroma (acumulación anormal de líquido) recurrente en el seno izquierdo. A lo largo de dos décadas, la paciente consultó repetidamente a su cirujano original, quien realizó dos procedimientos para reemplazar los implantes, utilizando dispositivos texturados (implantes con superficie rugosa), y finalmente llevó a cabo una extracción bilateral de los implantes. Durante estos procedimientos previos, no se realizaron capsulectomías completas (extirpación total de la cápsula fibrosa que se forma alrededor del implante). En el último procedimiento, se tomó una muestra de la cápsula del lado izquierdo que reveló la presencia de un linfoma anaplásico de células grandes asociado a implantes mamarios (BIA-ALCL, por sus siglas en inglés), un tipo raro de cáncer que afecta el tejido alrededor del implante.\n\n**Hallazgos Clave**  \nAl ser remitida a un centro terciario especializado en cáncer, se confirmó mediante estudios preoperatorios que la enfermedad persistía localmente en el seno izquierdo. El equipo multidisciplinario, compuesto por cirujanos plásticos, hematopatólogos, hematólogos, oncólogos, radiólogos y radioterapeutas, evaluó cuidadosamente el caso. Se realizó una capsulectomía en bloque (extirpación completa de la cápsula y el tejido circundante) en el lado afectado, sin encontrar necesidad de tratamientos adicionales como quimioterapia o radioterapia. El examen histopatológico mostró infiltración tumoral limitada a la cápsula periprostética, con márgenes quirúrgicos libres de enfermedad y sin afectación ganglionar.\n\n**Interpretación Clínica**  \nEste caso ilustra la importancia de la vigilancia y el diagnóstico temprano del BIA-ALCL, especialmente en pacientes con implantes texturados que presentan seromas persistentes o recurrentes. La ausencia de capsulectomías completas en procedimientos previos pudo haber contribuido a la persistencia de la enfermedad. La intervención quirúrgica radical, sin necesidad de tratamientos complementarios, fue suficiente para controlar la enfermedad en estadio temprano (IC según la clasificación MD Anderson-TNM).\n\n**Próximos Pasos**  \nLa paciente ha seguido un riguroso protocolo de seguimiento con estudios de imagen, incluyendo tomografías por emisión de positrones (PET/CT) a los 6, 12 y 18 meses postcirugía, sin evidencia de recurrencia local ni a distancia. Continúa bajo vigilancia médica estrecha para detectar cualquier signo de reaparición del linfoma, manteniendo hasta la fecha una supervivencia libre de enfermedad más allá de 18 meses. Este caso subraya la eficacia del manejo multidisciplinario y la cirugía completa en el tratamiento del BIA-ALCL en estadios iniciales.",
+        "scores": {
+          "ROUGE-1": 0.434640522875817,
+          "ROUGE-2": 0.22295081967213115,
+          "ROUGE-L-Sum": 0.39869281045751637,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      }
+    }
+  },
+  {
+    "article": "Se trata de un paciente de 50 años que se presentó con una queja de dolor e hinchazón de la lengua de tres días de duración. Asociado a esto, tenía dolor al tragar, dificultad para abrir la boca, falta de aire y babeo. Asimismo, tenía fiebre alta y un tipo de dolor de cabeza global. Por lo demás, no tenía traumatismo en la lengua, ni procedimientos dentales u orales recientes, ni antecedentes de tabaquismo ni de enfermedad médica crónica como diabetes mellitus, enfermedad cardiaca e hipertensión. Históricamente, había tenido un dolor dental agudo en los últimos seis meses antes de su queja actual. Había masticado khat desde su niñez y tenía una mala higiene oral.\n\nEn el examen físico, se veía muy enfermo y sus signos vitales eran: presión arterial 115 por 70 mmHg, pulso 120 latidos por minuto, frecuencia respiratoria 20, temperatura 39 grados centígrados y saturación de oxígeno 92% de oxígeno. En el examen HEENT, había una hinchazón significativa de la lengua en el área anterolateral izquierdo, fluctuante a la palpación, y tenía un borde eritematoso. Hay múltiples caries en las áreas maxilares y mandibulares. No hubo hallazgos pertinentes en los sistemas restantes.\n\nTras obtener el consentimiento informado, el paciente fue trasladado al quirófano con el diagnóstico de absceso lingual. Posteriormente, se realizó la incisión y el drenaje bajo anestesia general, y se drenaron unos 30 ml de pus espeso. La bolsa se lavó con solución salina normal y peróxido de hidrógeno al 2 %. El paciente fue trasladado a la sala de cirugía con signos vitales estables y había tomado ceftriaxona 1 g por vía intravenosa dos veces al día y metronidazol 500 mg por vía intravenosa tres veces al día durante dos días. Fue dado de alta después de dos días de estancia en el hospital con mejoría y Augmentin 625 mg por vía oral tres veces al día durante cinco días.\n",
+    "gold_summary": "Se trata de un paciente de 50 años que se presentó con una queja de dolor e hinchazón de la lengua de tres días de duración. Asociado a esto, tenía dolor al tragar, dificultad para abrir la boca, falta de aire y babeo. Asimismo, tenía fiebre alta y un tipo de dolor de cabeza global. En el examen físico, había una hinchazón significativa de la lengua en el área anterolateral izquierda, fluctuante a la palpación, y tenía un borde eritematoso. Después de que se tomó el consentimiento informado, el paciente fue trasladado al quirófano con el diagnóstico de absceso de la lengua. Posteriormente, se hizo una incisión y drenaje bajo anestesia general, y se drenaron unos 30 ml de pus espeso. El bolsillo se lavó con solución salina normal y peróxido de hidrógeno al 2%. El paciente fue trasladado a la sala de cirugía con signos vitales estables y había estado tomando antibióticos. Fue dado de alta después de dos días de estancia en el hospital.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Un hombre tenía la lengua muy hinchada y le dolía mucho. También le costaba abrir la boca y respirar bien. Tenía fiebre y dolor de cabeza. Los doctores vieron que su lengua estaba muy inflamada y con una bolita de pus. Lo llevaron al hospital para limpiar la lengua y sacar el pus. Le dieron medicinas para que no se enfermara más. Después de dos días, se sintió mejor y pudo ir a su casa.",
+        "scores": {
+          "ROUGE-1": 0.33210332103321033,
+          "ROUGE-2": 0.12639405204460968,
+          "ROUGE-L-Sum": 0.3247232472324723,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B2": {
+        "text": "**Lo que le Pasó al Paciente**  \nUn hombre de 50 años llegó al hospital porque tenía dolor e hinchazón en la lengua desde hacía tres días. También le dolía al tragar, le costaba abrir la boca, tenía dificultad para respirar y babeaba mucho. Además, tenía fiebre alta y un dolor de cabeza que sentía en toda la cabeza.\n\n**Lo que Encontraron en el Examen**  \nCuando lo examinaron, vieron que la parte izquierda de su lengua estaba muy hinchada y blanda al tocarla. La piel alrededor estaba roja. También tenía muchos dientes con caries, que son daños en los dientes causados por bacterias.\n\n**Qué Hicieron para Ayudarlo**  \nLos médicos decidieron que tenía un absceso en la lengua. Un absceso es una acumulación de pus, que es un líquido lleno de bacterias y células muertas, causado por una infección. Para tratarlo, lo llevaron al quirófano y, bajo anestesia general (cuando el paciente está dormido y no siente dolor), hicieron una pequeña abertura para sacar el pus, aproximadamente 30 mililitros. Luego limpiaron la zona con agua salada y peróxido de hidrógeno, que ayuda a eliminar las bacterias.\n\n**Recuperación y Tratamiento**  \nDespués de la operación, el paciente recibió antibióticos por vía intravenosa para combatir la infección. Su estado mejoró y, tras dos días en el hospital, pudo irse a su casa con medicamentos para seguir tomando y asegurar que la infección desapareciera completamente.",
+        "scores": {
+          "ROUGE-1": 0.48888888888888893,
+          "ROUGE-2": 0.21875,
+          "ROUGE-L-Sum": 0.4577777777777778,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B3": {
+        "text": "**Contexto**\n\nUn hombre de 50 años acudió al hospital debido a dolor e inflamación en la lengua que había persistido durante tres días. Además, presentaba dificultad para tragar, problemas para abrir la boca, sensación de falta de aire y babeo excesivo. También tenía fiebre alta y un dolor de cabeza generalizado. No reportaba antecedentes recientes de traumatismos en la boca, procedimientos dentales, tabaquismo ni enfermedades crónicas como diabetes o hipertensión. Sin embargo, había experimentado dolor dental agudo en los seis meses previos y tenía hábitos de masticar khat desde la niñez, junto con una higiene oral deficiente.\n\n**Hallazgos Clave**\n\nDurante el examen físico, el paciente se mostró visiblemente enfermo. Sus signos vitales indicaron fiebre (39 °C), pulso acelerado (120 latidos por minuto), presión arterial normal (115/70 mmHg), frecuencia respiratoria de 20 respiraciones por minuto y saturación de oxígeno ligeramente disminuida (92%). En la exploración de cabeza y cuello, se observó una inflamación notable en la parte anterolateral izquierda de la lengua, que al tacto era fluctuante (lo que sugiere acumulación de líquido) y presentaba un borde enrojecido (eritematoso). Además, se detectaron múltiples caries en los dientes superiores e inferiores.\n\n**Interpretación Clínica**\n\nEl cuadro clínico y los hallazgos físicos fueron compatibles con un absceso lingual, que es una acumulación de pus en la lengua debido a una infección. Esta condición puede ser grave porque la inflamación y el pus pueden dificultar la respiración y la deglución, como ocurrió en este paciente.\n\n**Próximos Pasos y Tratamiento**\n\nCon el consentimiento informado del paciente, se decidió realizar una intervención quirúrgica para drenar el absceso. Bajo anestesia general, se hizo una incisión en la lengua y se extrajeron aproximadamente 30 mililitros de pus espeso. La cavidad se limpió cuidadosamente con solución salina y peróxido de hidrógeno al 2% para eliminar restos de infección. Posteriormente, el paciente recibió tratamiento antibiótico intravenoso con ceftriaxona y metronidazol durante dos días. Su estado se mantuvo estable y, tras mejorar, fue dado de alta con indicaciones para continuar con antibióticos orales (Augmentin) durante cinco días más.\n\nEste manejo oportuno permitió controlar la infección y evitar complicaciones mayores, destacando la importancia de un diagnóstico rápido y un tratamiento adecuado en casos de abscesos en la lengua.",
+        "scores": {
+          "ROUGE-1": 0.49917355371900823,
+          "ROUGE-2": 0.24875621890547261,
+          "ROUGE-L-Sum": 0.46280991735537197,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      }
+    }
+  },
+  {
+    "article": "Hombre de 73 años de edad de origen latinoamericano, con antecedente de madre con diagnóstico de demencia tipo Alzheimer con panel genético negativo; hermano con diagnóstico de ELA; hermana con diagnóstico de enfermedad de Parkinson. La sintomatología progresiva comenzó desde el año 2016 y se caracterizó por síntomas progresivos de hiposmia, hipoacusia, estreñimiento e insomnio, los cuales ameritaron valoración por otorrinolaringología y audiología, sin conclusión diagnóstica. En el año 2020 los familiares notaron que el paciente presentaba problemas en la memoria episódica, olvidos de objetos de la vida cotidiana, problemas de ganancias en su negocio (de comercio). Estos síntomas fueron progresivos hasta que el paciente empezó a tener limitación en las tareas diarias, como al manejar y al cambiar las velocidades, además de al salir de su casa. A finales de ese año el paciente comenzó a presentar debilidad muscular distal, manifestada al abrir botellas, cepillarse los dientes, lo cual progresó de forma insidiosa, no fluctuante, sin predominio de horario.\n\nEn enero de 2021 el paciente comenzó con alteraciones de la marcha, las cuales condicionaron caídas frecuentes hasta más de 6 veces a la semana, esto debido a inestabilidad postural. El paciente acudió a valoración en mayo. Se le hizo test de MoCA de 16 puntos con alteraciones en la fluidez del lenguaje y repetición de oraciones; en la abstracción, recuerdo diferido y problemas visuoespaciales y disejecutivos. El test de Luria dio positivo. El paciente presentó facie hipomímica, emitió con hipofonía, entrecortado y lento, y presentó reflejo nauseoso disminuido, rigidez generalizada de predominio izquierdo, hipotrofia generalizada, bradicinesia de predominio izquierdo, fuerza 4/5 generalizada, reflejos de estiramientos musculares 3/4, reflejos abdominocutáneos abolidos, signos de Hoffmann y Trömner presentes de forma bilateral, respuesta plantar extensora bilateral, fasciculaciones en extremidades inferiores evocadas al tacto, marcha con pasos cortos, congelamiento de la marcha al giro, pull test positivo (inestabilidad postural). Se manejó con levodopa carbidopa a una dosis gradual. Al seguimiento a los 3 meses el paciente había presentado nula mejoría en cuanto a los síntomas parkinsónicos, aumento de la debilidad muscular y persistieron los datos de motoneurona inferior y superior. Con estos hallazgos se realizó resonancia magnética (RM) del encéfalo. La velocidad de neuroconducción (VCN) presentó neuropatía axonal motora de miembros torácicos en relación con atrofia y neuroconducción sensitiva sin alteraciones. La electromiografía (EMG) presentó datos de denervación activa (aumento de actividad insercional, potenciales de fibrilación, fasciculación) y reinervación crónica (potenciales de acción de la unidad motora polifásicos, y bajo reclutamiento a la contracción máxima) en los 5 segmentos corporales, lo cual es compatible con enfermedad de motoneurona.\n\n\nLa EMG mostró un aumento de actividad insercional en músculos deltoides, bíceps, tríceps, extensor digital común bilateral y músculos linguales de forma bilateral. Se observaron abundantes potenciales de fibrilación y predominó la fasciculación en los músculos de los miembros torácicos. Durante la contracción, se observó una activación del potencial de acción de la unidad motora (PAUM) de forma polifásica y de gran amplitud. Y a máxima contracción se observó una disminución del reclutamiento en la mayoría de los músculos evaluados.\n\nEl paciente perdió seguimiento un año. Al vover a valoración se encontraba con postración en cama, afásico, aumento de los datos de parkinsonismo y síndrome de motoneurona. Se decidió realizar panel genético que resultó negativo para C9ORF72, así como para 143 genes más involucrados en enfermedades neuromusculares y neurodegenerativas, incluidos los genes VCP, MAT3, asociados a ELA, NOTCH3, asociado a demencia frontotemporal, sin alteraciones. Se reportó resultado de variante patogénica para el gen POLG: C.2209G>C, p.(Gly737Arg), relacionado con síndrome de depleción mitocondrial autosómico dominante y recesivo. Se realizó sesión de asesoramiento genético y el paciente fue informado. En mayo de 2022, el paciente presentaba disfagia y acudió en silla de ruedas, por lo que fue enviado a que se le practicara una gastrostomía.",
+    "gold_summary": "Presentamos un caso de origen latinoamericano que inicialmente se manifestó con síntomas sistémicos de más de 6 años de evolución, con posteriores alteraciones cognitivas. Después presentó alteraciones de la marcha y síntomas motores sugestivos de parkinsonismo con datos atípicos y datos de enfermedad de motoneurona. Se hicieron estudios de extensión que confirmaron hallazgos compatibles con afectación en motoneurona superior e inferior. Observamos mutación en gen POLG, relacionada con síndrome de depleción mitocondrial.",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Un señor empezó a sentirse mal hace mucho tiempo. Primero, tenía problemas para oler, escuchar y dormir. Luego, se le olvidaban cosas y le costaba hacer tareas fáciles.\n\nDespués, le costaba caminar y se caía mucho. También tenía los músculos débiles y se movía lento. Los doctores hicieron pruebas y vieron que sus nervios y músculos no funcionaban bien.\n\nEncontraron un cambio en un gen que puede causar problemas en el cuerpo. Los doctores le explicaron todo con calma. Ahora, lo cuidan para que esté lo más cómodo posible.",
+        "scores": {
+          "ROUGE-1": 0.19251336898395724,
+          "ROUGE-2": 0.02162162162162162,
+          "ROUGE-L-Sum": 0.19251336898395724,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B2": {
+        "text": "**Lo que pasó con el paciente:**  \nUn hombre latinoamericano de 73 años tuvo síntomas durante más de seis años. Primero, presentó problemas en su cuerpo como dificultad para oler, escuchar y dormir. Luego, comenzó a tener problemas con la memoria y a olvidar cosas de su vida diaria. Más adelante, tuvo problemas para caminar y debilidad en sus músculos, lo que afectó sus movimientos y le causó caídas frecuentes.\n\n**Qué encontraron los médicos:**  \nAl hacerle pruebas, vieron que tenía signos de parkinsonismo, que es un conjunto de síntomas parecidos a los del Parkinson, pero con algunas diferencias. También encontraron que sus nervios y músculos estaban dañados, mostrando que tenía problemas en las motoneuronas. Las motoneuronas son células nerviosas que controlan los músculos, y en su caso, tanto las motoneuronas superiores como las inferiores estaban afectadas.\n\n**Resultados genéticos importantes:**  \nSe le hizo un examen genético y encontraron una mutación en un gen llamado POLG. Este gen está relacionado con un problema llamado síndrome de depleción mitocondrial, que afecta la energía que producen las células. Esta mutación puede causar enfermedades que afectan los músculos y el sistema nervioso.\n\n**Qué significa todo esto:**  \nEl caso es complejo porque el paciente tiene síntomas que involucran tanto problemas de memoria como de movimiento y debilidad muscular. La combinación de parkinsonismo atípico y enfermedad de motoneurona, junto con la mutación genética, ayuda a entender mejor su enfermedad y a buscar tratamientos adecuados.",
+        "scores": {
+          "ROUGE-1": 0.31908831908831903,
+          "ROUGE-2": 0.10315186246418338,
+          "ROUGE-L-Sum": 0.3076923076923077,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe trata de un hombre latinoamericano de 73 años con antecedentes familiares de enfermedades neurodegenerativas, incluyendo Alzheimer, esclerosis lateral amiotrófica (ELA) y Parkinson. Su cuadro clínico comenzó en 2016 con síntomas no específicos como disminución del olfato (hiposmia), pérdida auditiva leve (hipoacusia), estreñimiento e insomnio. En 2020, aparecieron problemas de memoria, dificultades en actividades cotidianas y debilidad muscular progresiva, especialmente en manos. En 2021, desarrolló alteraciones de la marcha con caídas frecuentes, rigidez y lentitud de movimientos, además de signos neurológicos que sugerían afectación tanto de la motoneurona superior como inferior.\n\n**Hallazgos Clave**  \n- Evaluación cognitiva mostró deterioro en funciones ejecutivas, memoria y habilidades visuoespaciales.  \n- Examen neurológico reveló rigidez, bradicinesia (lentitud de movimientos), reflejos anormales, fasciculaciones musculares (contracciones involuntarias) y alteraciones en la marcha con congelamiento.  \n- Estudios electromiográficos (EMG) y de velocidad de conducción nerviosa confirmaron daño en las motoneuronas superiores e inferiores, compatible con enfermedad de motoneurona.  \n- La resonancia magnética cerebral no mostró hallazgos específicos que expliquen el cuadro.  \n- Un panel genético amplio fue negativo para mutaciones comunes en enfermedades neurodegenerativas, pero identificó una variante patogénica en el gen POLG, asociado a síndromes de depleción mitocondrial, que afectan la función celular energética.  \n- En etapas avanzadas, el paciente presentó afasia (pérdida del lenguaje), disfagia (dificultad para tragar) y dependencia para movilizarse, requiriendo gastrostomía para alimentación.\n\n**Interpretación Clínica**  \nEste caso ilustra una enfermedad neurodegenerativa compleja con síntomas iniciales sistémicos y progresión hacia un síndrome mixto que combina características de parkinsonismo atípico y enfermedad de motoneurona. La presencia de la mutación en POLG sugiere un trastorno mitocondrial subyacente que podría estar contribuyendo a la degeneración neuronal. La afectación simultánea de motoneuronas superiores e inferiores y la falta de respuesta a levodopa apoyan un diagnóstico fuera del parkinsonismo típico. La evolución rápida hacia discapacidad severa y alteraciones del lenguaje y la deglución reflejan la gravedad del proceso.\n\n**Próximos Pasos**  \n- Continuar con manejo multidisciplinario que incluya neurología, rehabilitación, nutrición y apoyo psicológico.  \n- Monitorizar complicaciones respiratorias y nutricionales, dado el compromiso neuromuscular avanzado.  \n- Realizar asesoramiento genético familiar para evaluar riesgos y orientar a los parientes.  \n- Considerar terapias sintomáticas y soporte paliativo conforme avance la enfermedad, dado que no existen tratamientos curativos para esta condición.  \n\nEste caso destaca la importancia de una evaluación integral en pacientes con síntomas neurológicos progresivos y la utilidad de estudios genéticos para identificar causas poco frecuentes que pueden influir en el pronóstico y manejo.",
+        "scores": {
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+          "ROUGE-2": 0.1119402985074627,
+          "ROUGE-L-Sum": 0.24907063197026025,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      }
+    }
+  },
+  {
+    "article": "Mujer de 33 años, previamente sana, presentó disnea progresiva, fiebre alta, sudores nocturnos y pérdida de peso en diciembre de 2017. Después de un mes de evolución, fue ingresada en un hospital general con insuficiencia respiratoria aguda y shock séptico con infiltrados alveolares difusos, ictericia, hemoptisis y petequias en las extremidades inferiores. Fue intubada y necesitó soporte hemodinámico. Se detectó un soplo sistólico mitral a la ausculta del precordio. Había leucocitosis acentuada con desviación a la izquierda, plaquetopenia, disfunción hepática y renal asociada a proteinuria subnefrótica y consumo de complemento. El resultado de los anticuerpos antinucleares fue de 1/80, a pesar de los niveles normales de anti-DNA de doble cadena, anti-SM y anti-PR3. Después de la administración de ceftriaxona, mejoró clínicamente. Fiebre amarilla, dengue, chikungunya, leptospirosis, VIH y hepatitis virales fueron descartados. Las hemoculturas fueron positivas para Haemophilus spp. en las seis muestras recolectadas. El ecocardiograma transtorácico (ETT) demostró una masa ecogénica amorfa con superficie irregular y algunos elementos móviles que envolvían ambos folletos de la válvula mitral, midiendo 20x17 mm en el folleto anterior y 19 mm en su mayor diámetro en los folletos posteriores, resultando en regurgitación grave por flail mitral y perforación. La resonancia magnética mostró pequeños abscesos esplénicos, tratados de manera conservadora. Un aneurisma micótico no complicado de la arteria cerebral media izquierda fue tratado por embolización percutánea. Treinta días después de la hospitalización, se sometió a un reemplazo de la válvula mitral con éxito por una prótesis valvular biológica de tamaño 29 mm y después de una extensa resección del tumor. Se evidenció regurgitación aórtica moderada debido a lesión de la fibrosa intervalvar mitroaórtica y retracción de la cúspide no coronaria, tratada de manera conservadora. El examen patológico confirmó la presencia de un mixoma valvular mitral infectado. La paciente completó 28 días de ceftriaxona y gentamicina, recibiendo el alta hospitalaria asintomática. En el seguimiento de un año, no hubo evidencia de recurrencia y se constató solamente regurgitación aórtica leve. Los mixomas infectados presentan mayor riesgo de eventos embólicos, aunque las manifestaciones clínicas son indistinguibles de tumores no infectados.2 El presente caso parece ser el sexto de mixoma valvular mitral infectado relatado en la literatura, llenando criterios definitivos para el diagnóstico, y el tercero causado por un microorganismo del grupo HACEK.3 - 8 De los 64 mixomas valvulares mitrales publicados de 2006 a 2012, los síntomas eran cardiovasculares en 36,7%; 9,5 a 21,6% de los mixomas de la válvula mitral fueron sometidos al cambio de válvula y el tiempo del diagnóstico hasta la cirugía varió de algunas horas a 42 días.2 , 9 La mortalidad operatoria y general fue relatada como siendo, respectivamente, 2,6 a 3% y 5,1 a 21%.2 , 10 En la presente serie, la mayoría de los pacientes presentó insuficiencia cardiaca sintomática, fueron sometidos al cambio de válvula mitral y todos presentaron buenos resultados en el seguimiento.\n",
+    "gold_summary": "Una mujer de 33 años de edad, con antecedentes de fiebre y disnea de unos pocos días de evolución, fue hospitalizada con un síndrome lupoide, con hemocultivos positivos para Haemophilus spp. El ecocardiograma reveló una masa gigante que involucraba ambas valvas mitrales, con una severa regurgitación mitral que requería un reemplazo valvular mitral biológico. La microscopía reveló un mixoma infectado y la paciente fue dada de alta asintomática tras finalizar la terapia con antibióticos. Ella tuvo un buen seguimiento.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Había una mujer que se sentía muy mal. Tenía fiebre y le costaba mucho respirar. \n\nLos doctores la llevaron al hospital. Le encontraron una bolita grande en el corazón. Esa bolita hacía que su corazón no funcionara bien. \n\nLos doctores le pusieron una nueva parte en el corazón para ayudarla. También le dieron medicinas para que se mejorara. \n\nDespués de un tiempo, ella se sintió bien y pudo irse a su casa. Los doctores la cuidaron mucho y ella estuvo sana.",
+        "scores": {
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+          "ROUGE-2": 0.022598870056497175,
+          "ROUGE-L-Sum": 0.2122905027932961,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B2": {
+        "text": "**Lo que le pasó a la paciente**  \nUna mujer de 33 años comenzó con dificultad para respirar, fiebre alta y otros síntomas graves. Fue hospitalizada porque tenía una infección en la sangre causada por una bacteria llamada Haemophilus. Además, su corazón tenía un problema: una masa grande creció en la válvula mitral, que es una parte importante para que la sangre fluya bien en el corazón.\n\n**Qué encontraron los médicos**  \nUn examen llamado ecocardiograma mostró que esta masa afectaba ambas partes de la válvula mitral y causaba que la sangre regresara hacia el corazón, lo que se llama regurgitación mitral grave. Por eso, fue necesario reemplazar esa válvula por una nueva hecha de material biológico. Cuando analizaron la masa con un microscopio, descubrieron que era un mixoma infectado, que es un tumor benigno pero que en este caso tenía infección.\n\n**Cómo terminó el caso**  \nDespués de la cirugía y de recibir antibióticos durante varias semanas, la paciente mejoró mucho y pudo salir del hospital sin síntomas. En el seguimiento durante un año, no hubo problemas ni regreso del tumor. Este caso es muy raro y muestra la importancia de un diagnóstico rápido y un tratamiento adecuado para este tipo de infecciones en el corazón.",
+        "scores": {
+          "ROUGE-1": 0.3385579937304075,
+          "ROUGE-2": 0.10725552050473187,
+          "ROUGE-L-Sum": 0.2884012539184953,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
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+        }
+      },
+      "B3": {
+        "text": "**Contexto**\n\nUna mujer de 33 años, previamente sana, comenzó a experimentar dificultad para respirar progresiva, fiebre alta, sudores nocturnos y pérdida de peso durante un mes. Fue ingresada en un hospital con insuficiencia respiratoria aguda, shock séptico, sangrado pulmonar (hemoptisis), ictericia (coloración amarillenta de piel y mucosas) y petequias (pequeñas manchas rojas) en las piernas. Presentaba además un soplo cardíaco en la válvula mitral, leucocitosis (aumento de glóbulos blancos), plaquetopenia (disminución de plaquetas), disfunción hepática y renal, y alteraciones en pruebas inmunológicas.\n\n**Hallazgos Clave**\n\n- Se descartaron infecciones virales comunes en la región (fiebre amarilla, dengue, chikungunya, VIH, hepatitis).\n- Hemocultivos confirmaron infección por Haemophilus spp., un tipo de bacteria del grupo HACEK, conocida por afectar las válvulas cardíacas.\n- Ecocardiograma mostró una masa grande y irregular que afectaba ambas valvas de la válvula mitral, causando una regurgitación grave (flujo sanguíneo anormal hacia atrás) debido a daño estructural.\n- Resonancia magnética detectó pequeños abscesos en el bazo y un aneurisma micótico (una dilatación arterial causada por infección) en una arteria cerebral, tratado con embolización (bloqueo del vaso).\n- La paciente fue sometida a reemplazo exitoso de la válvula mitral por una prótesis biológica tras resección completa del tumor.\n- El examen patológico confirmó que la masa era un mixoma valvular mitral infectado, un tumor cardíaco benigno pero con infección bacteriana.\n- Se observó además regurgitación aórtica moderada por lesión en la estructura entre la válvula mitral y la aórtica, manejada sin cirugía.\n- Recibió tratamiento antibiótico con ceftriaxona y gentamicina durante 28 días.\n\n**Interpretación Clínica**\n\nEste caso representa una forma rara y grave de mixoma valvular mitral infectado, que es poco frecuente en la literatura médica y con alto riesgo de complicaciones embólicas (formación de coágulos que pueden viajar a otros órganos). La infección por Haemophilus spp. del grupo HACEK es especialmente relevante por su asociación con endocarditis (infección de las válvulas cardíacas). La presentación clínica puede ser similar a la de tumores no infectados, pero el riesgo de complicaciones es mayor.\n\nEl manejo combinado de cirugía para remover el tumor y reemplazar la válvula dañada, junto con terapia antibiótica prolongada, permitió una recuperación exitosa. La paciente mostró buena evolución clínica y no presentó recurrencia ni complicaciones significativas durante un seguimiento de un año.\n\n**Próximos Pasos**\n\n- Continuar con controles cardiológicos periódicos para monitorear la función valvular y detectar posibles complicaciones tardías.\n- Mantener vigilancia clínica para signos de infección o embolias.\n- Considerar la importancia de un diagnóstico precoz en casos similares para reducir la mortalidad y mejorar los resultados quirúrgicos.\n- Difundir el conocimiento sobre esta entidad rara para facilitar su reconocimiento y tratamiento oportuno en la práctica clínica.",
+        "scores": {
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+          "ROUGE-2": 0.05743243243243243,
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
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+        }
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+  },
+  {
+    "article": "Mujer de 71 años, que fue atendida en urgencias del Hospital de Mataró (Barcelona, España) el 9 de septiembre de 2020 con debilidad progresiva, por lo que se decidió su ingreso en neurología. Como antecedentes patológicos destacaban hipertensión arterial, temblor esencial, artrosis y trastorno de ansiedad leve, en tratamiento con gabapentina, sertralina y tramadol. La paciente había consultado a su médico de cabecera el 1 de septiembre de 2020 por dolor abdominal, junto con diarrea leve que duró 24 horas. Al día siguiente comenzó a sentirse débil y, a lo largo de los días siguientes, apareció disnea y disfagia, por lo que se sospechó laringitis y se le recetó prednisona. El 8 de septiembre de 2020 fue visitada nuevamente por su médico de cabecera por empeoramiento global de la debilidad; presentaba, además, disartria, disfagia y ptosis bilateral, por lo que fue derivada a urgencias del hospital.\n\nA su llegada no presentaba fiebre, la presión arterial y la frecuencia cardíaca eran normales, y la exploración física era normal, a excepción de taquipnea moderada. El examen neurológico mostró ptosis palpebral bilateral, parálisis facial bilateral, midriasis bilateral arreactiva a la luz y a la acomodación, oftalmoparesia bilateral tanto para la suprainfraversión como para la mirada horizontal bilateral, tetraparesia moderada en las extremidades (3/5), y disfonía y disfagia graves. Ella estaba consciente y el contenido del lenguaje era normal, al igual que los reflejos miotáticos, la sensibilidad y la coordinación. Las maniobras de fatigabilidad no fueron concluyentes y se realizó la prueba del hielo, que resultó positiva, mejorando –transitoriamente– la ptosis.\n\nLa reacción en cadena de la polimerasa (PCR) para el SARS-CoV-2 fue repetidamente negativa (en su ambulatorio y en el hospital). La gasometría arterial mostró hipoxemia: 75, con SO2 al 95%, y el resto de las exploraciones realizadas en urgencias resultaron normales (radiografía de tórax, análisis de sangre de rutina, electrocardiograma).\n\nSe inició tratamiento de soporte con oxígeno, sueroterapia, nutrición por sonda nasogástrica y medidas encaminadas a la prevención de complicaciones. El cuadro se estabilizó el tercer día del ingreso en planta, sin requerir soporte ventilatorio avanzado, y comenzó una mejoría lenta a partir del octavo día, iniciando tolerancia a la dieta adaptada de disfagia. Durante la primera semana presentaba hipotensión arterial, que fue corrigiéndose con la sueroterapia. A partir de la segunda semana, pudo iniciar rehabilitación física, con buena evolución, por lo que fue trasladada a un centro específico de rehabilitación al 19.º día, y entonces fue capaz de deambular con ayuda bilateral. En la visita de control en consultas externas de neurología seis semanas después, la paciente estaba completamente recuperada.",
+    "gold_summary": "Describimos el caso confirmado de botulismo alimentario en una paciente atendida en nuestro hospital en septiembre de 2020. La instauración en pocos días de una afectación bilateral de pares craneales, incluyendo disfagia, disnea y disartria, junto con midriasis y tetraparesia graves, precedida de diarrea, constituyó la presentación clínica en el primer caso; mientras que en su familiar cursó con síntomas inespecíficos y transitorios. Constatamos disautonomía consistente en hipotensión arterial. Teniendo en cuenta la situación pandémica en aquel momento, se descartó repetidamente la infección por SARS-CoV-2 antes de plantear alternativas diagnósticas. La neurotoxina B de C. botulinum fue detectada en las heces de la paciente, confirmando el diagnóstico de botulismo, que relacionamos con la ingesta de una conserva casera de alubias. Se completó el diagnóstico diferencial del cuadro descartando otras posibles etiologías.",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Una señora se enfermó después de comer unas alubias hechas en casa. Ella se puso muy débil y le costaba hablar, tragar y respirar. También tenía los ojos muy abiertos y los músculos muy flojos. Los doctores buscaron otras enfermedades, pero no encontró ninguna. Por eso, supieron que tenía una enfermedad llamada botulismo. Ella recibió ayuda en el hospital y poco a poco se fue mejorando hasta poder caminar con ayuda.",
+        "scores": {
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+          "ROUGE-L-Sum": 0.19383259911894274,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B2": {
+        "text": "**Lo que pasó con la paciente**  \nUna mujer de 71 años llegó al hospital con debilidad que empeoraba rápidamente. Antes, había tenido diarrea leve y dolor de barriga. Luego, empezó a tener problemas para respirar, tragar y hablar. En el examen, los médicos vieron que tenía caída de los párpados, parálisis en la cara, pupilas que no reaccionaban a la luz, debilidad en brazos y piernas, y dificultad para mover los ojos. A pesar de estos síntomas, estaba consciente y sus reflejos y sensibilidad estaban normales.\n\n**Qué descubrieron los médicos**  \nBuscaron si tenía COVID-19, pero las pruebas fueron negativas varias veces. También hicieron otros estudios que no mostraron problemas en el pecho ni en el corazón. Detectaron que tenía presión baja en la sangre y falta de oxígeno en la sangre. Finalmente, encontraron una toxina llamada neurotoxina B producida por una bacteria llamada Clostridium botulinum en sus heces. Esta bacteria puede causar botulismo, una enfermedad grave que afecta los nervios y los músculos. Creen que la paciente se enfermó por comer una conserva casera de alubias contaminada.\n\n**Qué significa este diagnóstico**  \nEl botulismo es una enfermedad rara pero peligrosa que puede causar debilidad muscular grave y problemas para respirar. En este caso, la enfermedad afectó varios nervios importantes y causó síntomas como dificultad para tragar y hablar. Los médicos descartaron otras causas posibles antes de confirmar el botulismo. Gracias al tratamiento y cuidados, la paciente mejoró poco a poco y se recuperó completamente en unas semanas.\n\n**Resumen final**  \nEste caso muestra cómo el botulismo puede aparecer después de comer alimentos contaminados y causar síntomas graves. Es importante diagnosticarlo rápido para dar el tratamiento adecuado y evitar complicaciones. También se destacó que, durante la pandemia, fue necesario descartar COVID-19 antes de llegar a este diagnóstico.",
+        "scores": {
+          "ROUGE-1": 0.326963906581741,
+          "ROUGE-2": 0.05543710021321962,
+          "ROUGE-L-Sum": 0.30997876857749473,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe presenta el caso de una mujer de 71 años que ingresó en el Hospital de Mataró (Barcelona) en septiembre de 2020 con debilidad progresiva y síntomas neurológicos graves. Inicialmente, había experimentado diarrea leve y dolor abdominal, seguidos de dificultad para respirar (disnea), dificultad para tragar (disfagia), y alteraciones en el habla (disartria). La evolución clínica incluyó afectación bilateral de varios nervios craneales y debilidad en las cuatro extremidades.\n\n**Hallazgos Clave**  \nLa paciente mostró signos característicos de afectación neurológica severa: caída de los párpados (ptosis) en ambos ojos, parálisis facial bilateral, pupilas dilatadas que no respondían a la luz ni a la acomodación (midriasis arreactiva), y parálisis de los movimientos oculares en varias direcciones (oftalmoparesia). Además, presentaba debilidad moderada en brazos y piernas (tetraparesia), voz ronca (disfonía) y dificultad grave para tragar. A pesar de estos síntomas, estaba consciente y mantenía un lenguaje coherente, con reflejos y sensibilidad normales. La prueba del hielo, que consiste en aplicar frío sobre los párpados para evaluar la mejora temporal de la ptosis, fue positiva, lo que orientó hacia un trastorno neuromuscular.\n\nSe descartó repetidamente la infección por SARS-CoV-2 mediante pruebas PCR, dada la pandemia vigente en ese momento. Otros estudios complementarios, como radiografía de tórax, análisis de sangre y electrocardiograma, no mostraron alteraciones relevantes. La gasometría arterial reveló hipoxemia moderada, indicando un nivel bajo de oxígeno en sangre.\n\n**Interpretación Clínica**  \nEl cuadro clínico y la evolución sugirieron un botulismo alimentario, una enfermedad causada por la neurotoxina producida por la bacteria *Clostridium botulinum*, que afecta la función nerviosa y muscular. La confirmación diagnóstica se obtuvo al detectar la neurotoxina tipo B en las heces de la paciente. Se estableció que la fuente probable de la intoxicación fue la ingesta de una conserva casera de alubias. Además, la paciente presentó disautonomía, manifestada por hipotensión arterial, que requirió manejo con fluidos intravenosos.\n\nSe realizó un diagnóstico diferencial exhaustivo para descartar otras causas neurológicas que pudieran explicar los síntomas, asegurando así la precisión del diagnóstico.\n\n**Próximos Pasos y Evolución**  \nLa paciente recibió tratamiento de soporte, incluyendo oxígeno, nutrición por sonda nasogástrica y cuidados para prevenir complicaciones. Su condición se estabilizó en los primeros días y comenzó a mejorar lentamente a partir del octavo día, tolerando progresivamente la alimentación adaptada a su disfagia. Posteriormente, inició rehabilitación física, con buena respuesta, y fue trasladada a un centro especializado para continuar su recuperación. Seis semanas después, en la consulta de seguimiento neurológico, la paciente había recuperado completamente su función neuromuscular y capacidad para caminar con ayuda.\n\nEste caso destaca la importancia de considerar el botulismo alimentario en pacientes con debilidad neuromuscular progresiva y afectación de nervios craneales, especialmente cuando se descartan infecciones virales prevalentes como el SARS-CoV-2. Además, resalta la necesidad de un diagnóstico rápido y un manejo multidisciplinario para lograr una recuperación completa.",
+        "scores": {
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+          "ROUGE-2": 0.13215859030837004,
+          "ROUGE-L-Sum": 0.3045387994143484,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
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+  {
+    "article": "Un hombre de 52 años presentó pérdida de agudeza visual en su ojo derecho (OD) dos días después de una inyección intravenosa no complicada de ranibizumab con una aguja de 30 G. Su historial médico incluía PE, miopía alta y vitrectomía pars plana en el OD debido a desprendimiento de retina. Recibía tratamiento mensual con ranibizumab debido a neovascularización coroidea secundaria a estrías angioides, con 78 inyecciones previas en el OD. En el momento de la presentación, su BCVA era de 6/18 y la presión intraocular (IOP) era de 3 mmHg. El examen con lámpara de hendidura del segmento anterior no mostró nada de particular. El examen de fondo de ojo y los escaneos OCT revelaron pliegues corio-retinianos posteriores. En conjunto, la baja presión intraocular y los hallazgos del fondo de ojo llevaron al diagnóstico de hipotensión maculopatía. Se prescribió dexametasona tópica y atropina para mejorar la función del cuerpo ciliar. La IOP se normalizó en tres días con recuperación de la agudeza visual y resolución de los pliegues corio-retinianos. Cuatro meses después, se realizó una nueva inyección intravenosa anti-VEGF en el cuadrante inferolateral y el paciente informó disminución de la agudeza visual en el día siguiente a la inyección. La BCVA era contar los dedos y la IOP era de 2 mmHg. Los pliegues corio-retinianos en el polo posterior estaban presentes, incluso más prominentemente esta vez. El examen con lámpara de hendidura reveló una herida abierta en la esclerótica en el sitio de la inyección. La herida se suturó con monofilamento 10-0 y se prescribió dexametasona tópica y atropina. El paciente se recuperó bien y presentó una BCVA de 6/12 y una IOP de 12 mmHg.\n",
+    "gold_summary": "Un hombre de 52 años se quejó de pérdida de visión en el ojo derecho (OD) dos días después de un IVI anti-VEGF sin complicaciones para el tratamiento de la neovascularización coroidea secundaria a estrías angioides. Su historial médico incluía PE, miopía patológica y una vitrectomía pars plana (PPV) previa debido a un desprendimiento de retina. La agudeza visual mejor corregida (BCVA) en el OD disminuyó de 6/12 a 6/18 después del IVI. La presión intraocular (IOP) era de 3 mmHg y se observaron pliegues corio-retinianos en el polo posterior. Se prescribió dexametasona tópica y atropina, y se observó una recuperación completa después de tres días. Cuatro meses después, el paciente desarrolló un nuevo episodio de pérdida de visión después de otro IVI. Su BCVA era contar los dedos, la IOP era de 2 mmHg, y se observaron pliegues corio-retinianos más evidentes. Esta vez, una herida escleral abierta en el sitio de inyección era evidente y fue necesaria una sutura escleral. Una vez más, el paciente se recuperó bien.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Un hombre tuvo problemas para ver con su ojo derecho. Esto pasó después de que le pusieron una medicina en el ojo. Su ojo estaba un poco débil y la presión dentro del ojo era baja. El doctor le dio unas gotas para ayudar. Después de tres días, su vista mejoró.\n\nCuatro meses después, le pusieron otra vez la medicina. Otra vez, su vista se puso muy mala. Esta vez, el ojo tenía una pequeña herida. El doctor la cerró con puntitos. Después, el hombre volvió a ver mejor.",
+        "scores": {
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
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+      },
+      "B2": {
+        "text": "### Lo que le pasó al paciente\n\nUn hombre de 52 años perdió visión en su ojo derecho dos días después de recibir una inyección en la vena para tratar un problema en la parte trasera del ojo llamado neovascularización coroidea, que es cuando crecen vasos sanguíneos anormales. Él tenía antecedentes de miopía fuerte, una cirugía previa en el ojo por desprendimiento de retina y otros problemas oculares.\n\n### Qué encontraron los doctores\n\nDespués de la inyección, su visión empeoró y la presión dentro del ojo bajó mucho, a solo 3 mmHg (lo normal es más alta). Al examinar el ojo, vieron pliegues en la capa del ojo llamada coroides y retina, que son señales de que el ojo estaba muy débil por la baja presión. Le dieron medicamentos en gotas para ayudar a que el ojo se recuperara, y en tres días su visión y presión volvieron a la normalidad.\n\n### Qué pasó después\n\nCuatro meses más tarde, el hombre recibió otra inyección similar y volvió a perder visión al día siguiente. Esta vez, la presión en el ojo bajó aún más, y los pliegues en la retina eran más visibles. Además, los doctores encontraron una herida abierta en la pared del ojo donde pusieron la inyección. Para arreglarla, tuvieron que coser esa herida. Después del tratamiento, el paciente mejoró y recuperó buena visión y presión normal en el ojo.\n\n### Qué significa esto\n\nEste caso muestra que, aunque las inyecciones en el ojo suelen ser seguras, pueden causar problemas como baja presión ocular y daño temporal en la retina. Es importante revisar bien el ojo después de cada inyección para detectar heridas o complicaciones y tratarlas rápido para evitar pérdida permanente de visión.",
+        "scores": {
+          "ROUGE-1": 0.421455938697318,
+          "ROUGE-2": 0.1807692307692308,
+          "ROUGE-L-Sum": 0.40996168582375475,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B3": {
+        "text": "**Contexto:**  \nUn hombre de 52 años con antecedentes de preeclampsia (PE), miopía alta y una cirugía previa llamada vitrectomía pars plana (PPV) en su ojo derecho debido a un desprendimiento de retina, recibía tratamiento mensual con inyecciones intravenosas (IVI) de ranibizumab, un medicamento anti-VEGF (factor de crecimiento endotelial vascular), para tratar una neovascularización coroidea secundaria a estrías angioides (formación anormal de vasos sanguíneos en la capa vascular del ojo).\n\n**Hallazgos Clave:**  \nDos días después de una inyección intravenosa que inicialmente parecía no presentar complicaciones, el paciente notó una disminución de la agudeza visual en su ojo derecho. La agudeza visual mejor corregida (BCVA) bajó de 6/12 a 6/18, y la presión intraocular (IOP) estaba muy baja, en 3 mmHg (el rango normal es aproximadamente 10-21 mmHg). El examen con lámpara de hendidura no mostró alteraciones en la parte frontal del ojo, pero el examen del fondo de ojo y las imágenes por tomografía de coherencia óptica (OCT) revelaron pliegues en las capas coroideas y retinianas en la parte posterior del ojo. Estos hallazgos, junto con la baja presión intraocular, llevaron al diagnóstico de hipotensión maculopatía, una condición en la que la baja presión dentro del ojo causa cambios estructurales que afectan la visión.\n\nSe inició tratamiento con dexametasona tópica (un corticosteroide para reducir la inflamación) y atropina (un medicamento que ayuda a relajar el cuerpo ciliar, facilitando la producción de humor acuoso y aumentando la presión intraocular). En tres días, la presión intraocular volvió a la normalidad y la visión mejoró, con desaparición de los pliegues corio-retinianos.\n\nCuatro meses después, tras una nueva inyección intravenosa anti-VEGF aplicada en la zona inferolateral del ojo, el paciente presentó nuevamente una disminución significativa de la visión al día siguiente, con una BCVA reducida a “contar los dedos” (una medida de visión muy pobre) y una presión intraocular aún más baja, de 2 mmHg. Esta vez, los pliegues corio-retinianos eran más evidentes. El examen con lámpara de hendidura detectó una herida abierta en la esclerótica (la capa externa blanca del ojo) en el sitio de la inyección, lo que indicaba una filtración o fuga de líquido ocular. Esta herida fue reparada mediante sutura con un hilo muy fino (monofilamento 10-0). Se repitió el tratamiento con dexametasona tópica y atropina, y el paciente se recuperó satisfactoriamente, alcanzando una BCVA de 6/12 y una presión intraocular de 12 mmHg.\n\n**Interpretación Clínica:**  \nEste caso muestra que, aunque las inyecciones intravenosas de anti-VEGF son generalmente seguras, pueden presentarse complicaciones poco comunes como la hipotensión maculopatía causada por una baja presión intraocular. La presencia de pliegues corio-retinianos y la disminución de la visión son signos importantes que deben alertar al médico. Además, la aparición de una herida escleral abierta en el sitio de la inyección puede causar una fuga de líquido y empeorar la hipotensión ocular, requiriendo reparación quirúrgica.\n\n**Próximos Pasos:**  \nEs fundamental monitorizar cuidadosamente la presión intraocular y la integridad de la esclera después de las inyecciones anti-VEGF, especialmente en pacientes con antecedentes de cirugía ocular previa o miopía alta, que pueden tener mayor riesgo de complicaciones. El tratamiento temprano con corticosteroides tópicos y atropina puede ayudar a restaurar la presión intraocular y la función visual. En casos de filtración escleral, la reparación quirúrgica es necesaria para evitar daños permanentes. Además, se recomienda evaluar la técnica de inyección para minimizar el riesgo de heridas escleral abiertas en futuras aplicaciones.",
+        "scores": {
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+          "ROUGE-2": 0.21411764705882352,
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
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+  },
+  {
+    "article": "Una mujer de 82 años acudió al servicio de urgencias por dolor abdominal, diarrea, confusión y deterioro de su estado general de varios días de evolución. Entre sus antecedentes médicos destacaban hipertensión arterial tratada e hipotiroidismo en tratamiento sustitutivo. No se recogieron antecedentes quirúrgicos ni hábitos tóxicos de interés. A la exploración física, la frecuencia cardíaca era de 84 lpm, tensión arterial de 105/82 mmHg, temperatura de 38 °C y saturación de oxígeno de 95% en aire ambiente. Las mucosas estaban secas y el abdomen era difusamente doloroso a la palpación sin masas palpables ni reacción peritoneal. La analítica realizada mostró una hemoglobina de 13.1 g/dL, proteína C reactiva a 122.9 mg/L sin leucocitosis (8.9 × 10^9/L), hiponatremia (130 mmol/L), hipopotasemia (2.9 mmol/L), pruebas de función renal, hepáticas, lipasa y enzimas cardiacas normales. El frotis para SARSCoV-2 fue negativo. La orina era maloliente con presencia de nitritos positivos, hematíes (+++) y leucocitos (+) por lo que se envió la muestra para cultivo microbiológico. Ante estos hallazgos se inició antibioticoterapia probabilista con ceftriaxona ante la sospecha de una posible infección urinaria y se decidió realizar una tomografía tóraco-abdomino-pélvica para descartar la presencia de un foco infeccioso profundo. Este examen reveló la presencia de signos de broncopatía crónica y una neumatosis vesical parietal a nivel abdominal compatible con una cistitis enfisematosa. El cultivo de orina reveló la presencia de Escherichia coli (> 100 000 UFC/m) sensible a la antibioticoterapia prescrita empíricamente y los hemocultivos fueron positivos al mismo germen. Se decidió el ingreso de la paciente en servicio de medicina interna y se continuó el tratamiento antibiótico durante 7 días con una evolución favorable desde el punto de vista clínico y analítico, permitiendo el alta hospitalaria.",
+    "gold_summary": "Una mujer de 82 años con antecedentes de hipertensión arterial e hipotiroidismo acudió al servicio de urgencias por dolor abdominal, diarrea, confusión y deterioro de su estado general de varios días de evolución. A su admisión, la paciente se encontraba febril y la analítica mostró una elevación de la proteína C reactiva sin leucocitosis (8.9 × 10^9/L). En ese contexto se realizó exudado nasofaríngeo para SARS-CoV-2 que fue negativo. Con estos resultados, la sospecha inicial era la de un cuadro infeccioso de origen digestivo. La muestra de orina era maloliente con presencia de leucocitos y nitritos enviándose a cultivo microbiológico. Se inició tratamiento antibiótico empírico con una cefalosporina de tercera generación ante la sospecha de une posible infección urinaria. Se decidió la realización de una tomografía tóraco-abdomino-pélvica con el objetivo de evaluar la presencia de otros focos infecciosos en una paciente de edad avanzada. Este estudio mostró una cistitis enfisematosa, una enfermedad poco frecuente en una paciente sin ninguno de los factores de riesgo clásicos para esta entidad. Los cultivos de orina y sangre fueron positivos para Escherichia coli sensible al antibiótico empírico por lo que se continuó para completar 7 días de tratamiento. La evolución clínica fue favorable.",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Una señora de 82 años se sentía muy mal. Tenía dolor en la barriga y estaba confundida. \n\nLos doctores le hicieron pruebas y vieron que tenía una infección en la orina. Le dieron medicina para ayudarla. \n\nTambién hicieron una foto especial de su cuerpo. Vieron que su vejiga estaba un poco dañada por la infección. \n\nLa medicina funcionó y la señora mejoró mucho. Después de una semana, pudo irse a su casa feliz.",
+        "scores": {
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+          "ROUGE-2": 0.05750798722044729,
+          "ROUGE-L-Sum": 0.25396825396825395,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
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+      },
+      "B2": {
+        "text": "**Lo que Encontraron**  \nUna mujer de 82 años llegó al hospital porque tenía dolor en el abdomen, diarrea, estaba confundida y se sentía muy mal desde hacía varios días. Tenía fiebre y algunos análisis de sangre mostraron que tenía inflamación, pero no un aumento en los glóbulos blancos, que son células que ayudan a combatir infecciones. También le hicieron una prueba para detectar COVID-19, que salió negativa.\n\n**Qué Significa la Orina y el Tratamiento**  \nLa orina de la paciente olía mal y tenía señales de infección, como leucocitos (células blancas) y nitritos. Por eso, enviaron una muestra para ver qué bacteria causaba la infección. Mientras esperaban, comenzaron a darle un antibiótico llamado ceftriaxona, que es fuerte y puede combatir muchas bacterias.\n\n**Descubrimiento Importante con la Tomografía**  \nPara asegurarse de que no hubiera una infección más grave en el cuerpo, le hicieron una tomografía, que es una imagen especial del cuerpo. Esta prueba mostró que tenía una cistitis enfisematosa, que es una infección rara en la vejiga donde se forman burbujas de gas en la pared de este órgano. Esto es inusual porque la paciente no tenía los factores de riesgo típicos para esta enfermedad.\n\n**Resultados del Cultivo y Evolución**  \nLos cultivos de la orina y la sangre mostraron que la bacteria causante era Escherichia coli, que respondía bien al antibiótico que ya le estaban dando. Por eso, continuaron con el tratamiento durante 7 días. La paciente mejoró mucho y pudo salir del hospital.  \n\nEn resumen, esta mujer tuvo una infección urinaria grave y poco común que se detectó a tiempo y se trató con éxito gracias a los exámenes y al antibiótico adecuado.",
+        "scores": {
+          "ROUGE-1": 0.43703703703703706,
+          "ROUGE-2": 0.13011152416356878,
+          "ROUGE-L-Sum": 0.4148148148148148,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nUna mujer de 82 años con antecedentes médicos de hipertensión arterial e hipotiroidismo acudió al servicio de urgencias debido a varios días de dolor abdominal, diarrea, confusión y un deterioro general de su estado de salud. Al examen físico, presentaba fiebre y signos de deshidratación, con un abdomen doloroso a la palpación pero sin signos de irritación peritoneal.  \n\n**Hallazgos Clave**  \nLos análisis de sangre revelaron una elevación significativa de la proteína C reactiva (un marcador de inflamación) sin aumento en el número de glóbulos blancos (leucocitosis), lo que sugiere una respuesta inflamatoria sin infección bacteriana evidente en sangre. La prueba para detectar infección por SARS-CoV-2 fue negativa. La orina presentaba mal olor, nitritos positivos y presencia de leucocitos y glóbulos rojos, indicativos de infección urinaria.  \n\nSe inició tratamiento antibiótico empírico con ceftriaxona, una cefalosporina de tercera generación, ante la sospecha de infección urinaria. Para descartar la existencia de infecciones profundas o complicaciones, se realizó una tomografía computarizada (TC) del tórax, abdomen y pelvis. Este estudio identificó una neumatosis vesical parietal, es decir, presencia de gas en la pared de la vejiga, compatible con cistitis enfisematosa, una infección urinaria grave y poco frecuente caracterizada por la acumulación de gas en la vejiga.  \n\nLos cultivos microbiológicos confirmaron la presencia de Escherichia coli, una bacteria comúnmente responsable de infecciones urinarias, tanto en la orina como en la sangre, y que resultó sensible al antibiótico administrado.  \n\n**Interpretación Clínica**  \nLa cistitis enfisematosa es una infección poco común que suele presentarse en pacientes con factores de riesgo como diabetes o inmunosupresión, pero en este caso la paciente no presentaba estos antecedentes clásicos, lo que hace el diagnóstico más inusual. La detección temprana mediante imagen y el inicio rápido de tratamiento antibiótico adecuado fueron fundamentales para la evolución favorable del cuadro.  \n\n**Próximos Pasos**  \nLa paciente fue ingresada en el servicio de medicina interna para continuar el tratamiento antibiótico durante siete días. Durante su hospitalización, mostró mejoría clínica y analítica, lo que permitió su alta hospitalaria sin complicaciones. Se recomienda seguimiento médico para controlar posibles recurrencias o complicaciones y mantener el control de sus condiciones crónicas.",
+        "scores": {
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+          "ROUGE-L-Sum": 0.5181674565560821,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
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+  },
+  {
+    "article": "Varón nacido a las 38 semanas de gestación y sin controles obstétricos prenatales, producto de un parto eutócico sin complicaciones con un peso de 2.678 g y Apgar 7 y 8 al minuto y a los cinco minutos de vida, respectivamente; derivado por sospecha de enterocolitis necrotizante a los siete días de vida. Al nacimiento, en su hospital de origen, se descartaron malformaciones congénitas externas y se colocó una sonda orogástrica para verificar la permeabilidad esofágica, obteniendo 200 mL de líquido amniótico. Posteriormente inició alimentación vía oral pero debido a succión débil y vómitos biliosos fue ingresado en la unidad de cuidados intensivos neonatales. A las 4 horas de vida se realizó radiografía abdominal observando una imagen de doble burbuja atípica, por lo cual realizaron un control radiológico 48 horas después identificando gas intestinal aparentemente distal, y presentó meconiorrexis a las 50 horas de vida. Dos días después reinició la alimentación oral, tras lo cual presentó nuevamente vómitos de aspecto biliar y distensión abdominal que mejoró con el ayuno y sonda orogástrica; por lo cual se sospechó enterocolitis necrotizante indicándose dieta absoluta, nutrición parenteral total y antibioterapia con ampicilina y amikacina. A los siete días de vida y debido a la persistencia de los síntomas pese al tratamiento instaurado, fue derivado a nuestro centro. A su llegada presentaba distensión abdominal, sin ruidos intestinales ni signos de irritación peritoneal, por lo que se realizó tránsito intestinal sin progresión distal y colon por enema con hallazgo de microcolon, todo ello sugestivo de atresia intestinal yeyunoileal. Tras la realización de los estudios de imagen y con la sospecha de atresia intestinal se realizó una laparotomía exploradora mediante abordaje supraumbilical transverso, observando adherencias hepatoileales, una hernia interna a través de un defecto mesentérico con incarceración de un asa yeyunal y atresia yeyunoileal tipo IV. Se identificaron dos sitios de atresia a 56 cm del ángulo de Treitz y a 36 cm de la válvula ileocecal, con un segmento interatrésico de 10 cm con meconio intraluminal y cambios de coloración con aspecto violáceo pero sin perforación; la diferencia de diámetros intestinales proximal a distal tenía una relación 3:1. Se decidió disecar el mesenterio y resecar el asa ciega (10 cm) para realizar una anastomosis término-oblicua yeyunoileal, corroborando la permeabilidad distal con sonda intraluminal y administración de solución fisiológica hasta que presentó evacuación rectal. El reporte de histopatología confirmó una atresia yeyunoileal tipo IV con enteritis crónica leve. El paciente evolucionó favorablemente y al 5º día postoperatorio inició alimentación oral con adecuada tolerancia progresiva y descenso paulatino de la nutrición parenteral total con retirada al 8º día postoperatorio. Al 6° día de la intervención presentó deposiciones espontáneas y a los 20 días de vida fue dado de alta sin complicaciones. Doce meses después el paciente continúa asintomático con adecuada ganancia ponderal y tolerancia a la alimentación complementaria con deposiciones diarias de características normales.",
+    "gold_summary": "Recién nacido de sexo masculino, nacido a término, derivado por vómitos, evacuaciones escasas y distensión abdominal. A los 8 días de vida y tras excluir diversas causas de distensión abdominal se sometió a laparotomía exploradora, identificando una hernia transmesentérica y dos sitios de atresia intestinal. Se realizó resección del segmento atrésico y anastomosis primaria, con buena evolución.",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Un bebé nació sin problemas. Tenía dolor en la barriga y no podía hacer popó bien. Los doctores buscaron qué pasaba y lo operaron. Encontraron dos partes del intestino que estaban tapadas. Quitaron las partes malas y unieron el intestino bueno. El bebé mejoró mucho después de la operación.",
+        "scores": {
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+          "ROUGE-2": 0.0,
+          "ROUGE-L-Sum": 0.16528925619834714,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
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+      "B2": {
+        "text": "**Lo que pasó con el bebé:**  \nUn bebé varón nació a término y, durante su primera semana de vida, tuvo problemas como vómitos, pocas evacuaciones y el abdomen hinchado. Estos síntomas indicaban que algo no estaba funcionando bien en su intestino.\n\n**Qué encontraron los médicos:**  \nDespués de hacer varios estudios para entender la causa de la hinchazón abdominal, los doctores decidieron hacer una cirugía llamada laparotomía exploradora. En esta operación, descubrieron que el bebé tenía una hernia transmesentérica, que es cuando una parte del intestino queda atrapada en un defecto del tejido que lo sostiene. Además, encontraron dos lugares donde el intestino estaba bloqueado, lo que se llama atresia intestinal.\n\n**Qué hicieron para ayudar:**  \nLos médicos quitaron la parte del intestino que estaba bloqueada (resección del segmento atrésico) y unieron las partes sanas del intestino (anastomosis primaria) para que el alimento pudiera pasar normalmente.\n\n**Cómo le fue al bebé:**  \nDespués de la cirugía, el bebé mejoró bien, comenzó a alimentarse por vía oral y pudo irse a casa sin complicaciones. Un año después, sigue sano, come bien y tiene evacuaciones normales.",
+        "scores": {
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
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+      "B3": {
+        "text": "Resumen detallado para público general universitario\n\n**Contexto:**  \nSe trata de un recién nacido varón, nacido a término (38 semanas de gestación) mediante un parto normal sin complicaciones, con un peso al nacer de 2.678 gramos. No contó con controles prenatales durante el embarazo. En las primeras horas de vida presentó dificultad para alimentarse debido a una succión débil y vómitos con contenido biliar (color verde), lo que motivó su ingreso a la unidad de cuidados intensivos neonatales. Las primeras radiografías abdominales mostraron una imagen sugestiva de obstrucción intestinal, pero con presencia de gas en intestino distal. A los pocos días presentó distensión abdominal y vómitos persistentes, lo que llevó a sospechar una enterocolitis necrotizante (una inflamación grave del intestino en recién nacidos), por lo que se inició tratamiento con ayuno, nutrición intravenosa y antibióticos.\n\n**Hallazgos clave:**  \nA pesar del tratamiento, los síntomas no mejoraron, por lo que fue trasladado a un centro especializado. Allí se realizaron estudios radiológicos que evidenciaron un colon muy pequeño (microcolon) y ausencia de progresión del tránsito intestinal, lo que sugirió la presencia de una atresia intestinal (una obstrucción causada por la ausencia o cierre de una parte del intestino). Durante la cirugía exploratoria se encontró una hernia interna a través de un defecto en el mesenterio (tejido que sostiene los intestinos) con atrapamiento de un segmento del intestino delgado (asa yeyunal), además de dos áreas de atresia en el intestino delgado (tipo IV, que implica múltiples segmentos afectados). Se observó un segmento intermedio con meconio (primera materia fecal) y cambios de coloración, pero sin perforación. La relación entre el diámetro del intestino proximal y distal era de 3 a 1, indicando una diferencia significativa en tamaño.\n\n**Interpretación clínica:**  \nSe realizó la resección del segmento intestinal afectado y una anastomosis término-oblicua yeyunoileal (unión quirúrgica entre dos partes del intestino delgado), asegurando la permeabilidad del intestino distal. El análisis histopatológico confirmó la atresia múltiple con inflamación crónica leve del intestino. El paciente mostró una evolución favorable tras la cirugía, iniciando alimentación oral progresivamente desde el quinto día postoperatorio y retirando la nutrición parenteral al octavo día. Presentó deposiciones normales y fue dado de alta a los 20 días de vida sin complicaciones.\n\n**Próximos pasos y seguimiento:**  \nA los doce meses de edad, el niño continúa asintomático, con un adecuado aumento de peso y tolerancia normal a la alimentación complementaria, manteniendo deposiciones diarias de características normales. Este caso resalta la importancia de un diagnóstico oportuno y tratamiento quirúrgico adecuado en atresias intestinales múltiples para lograr una recuperación exitosa en recién nacidos.",
+        "scores": {
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+          "ROUGE-L-Sum": 0.1516245487364621,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
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+  {
+    "article": "Se remitió a un hombre de 86 años para que se le implantara una válvula aórtica transfemoral.\n\nLa historia significativa incluyó el hecho de fumar 40 cajetillas al año (hasta fines de la década de 1980) y la fibrilación auricular paroxística que requería anticoagulación con Coumadin desde 1999, seguida poco después por la implantación de un marcapasos ventricular debido a bradicardia. Fue admitido por síncope en mayo de 2011 y se le diagnosticó una estenosis aórtica calcificada severa. Era eupneico y no mostraba signos de insuficiencia cardiaca o retención de líquidos. La ecocardiografía transtorácica reveló una estenosis aórtica severa (gradiente medio: 58 mmHg, área de la válvula aórtica: 0,4 cm2) con hipertrofia ventricular izquierda, fracción de eyección ventricular izquierda deteriorada (29%), acinesia inferior apical y obstrucción septal subvalvular (septum: 18 mm) con dilatación biauricular e hipertensión pulmonar con dilatación de la vena cava.\n\nLa angiografía coronaria mostró una estenosis del 75% de la arteria descendente anterior izquierda. El examen de eco-Doppler encontró vasos normales en el cuello. Se agregó aspirina 80 mg diariamente a su tratamiento; el paciente fue programado para un reemplazo de la válvula aórtica, pero no llegó hasta agosto, cuando fue readmitido en urgencias por disnea aguda y confusión. Había ganado 6 kg de peso, con edemas en las piernas y signos clínicos de derrame pleural. En ese momento, su SpO2 era del 92% y la proteína B-natriurética estaba elevada a 2336 pg·mL−1 (normal < 100 pg·mL−1).\n\nTras la terapia diurética y la eliminación de 850 ml de derrame pleural, se realizó una valvuloplastia de balón percutáneo aórtico de emergencia (Cristal Balloon, 23 mm) e inmediatamente después se le implantó un stent de metal desnudo (Biotronik-Pro-Kinetic 2.74 × 10.0) en la arteria descendente anterior izquierda. El gradiente medio transvalvular disminuyó de 59 a 38 mmHg. Se observaron algunas torsades de pointe el día 6 después de la intervención, que desaparecieron cuando la frecuencia más baja del marcapasos se aceleró a 80 latidos/min. Su estado mejoró drásticamente y se le dio el alta con furosemida, aldactazina y clopidogrel. Tras una revisión cuidadosa del expediente del paciente por parte del equipo cardiaco, se consideró que el riesgo de una cirugía valvular era demasiado alto (Euroscore logístico: 51%), y se propuso al paciente un implante de válvula aórtica transfemoral.\n\nLas notas de las enfermeras mencionan la hiperventilación nocturna y las crisis de ansiedad. El paciente era semiautónomo y vivía con su hija.\n\nLa implantación de la válvula aórtica transfemoral se programó para octubre de 2011. En el ingreso, 2 días antes del procedimiento, el paciente se describió como «ansioso e hiperventilante»; su peso era de 67 kg para una altura de 168 cm; el volumen espiratorio forzado en 1 s (FEV1) era de 1,1 L (50% del valor previsto) y la capacidad vital forzada de 1,7 L (55%); la presión arterial sistémica era de 120/60 mmHg; la concentración de hemoglobina era de 167 g·L−1; la creatinina era de 12,7 g·L−1; la tasa de filtración glomerular se calculó en 54 ml·min−1·m−2; el potasio era de 3,7 mEq·L−1; el sodio era de 141 mEq·L−1; el bicarbonato era de 22 mEq·L−1; y la proteína B natriurética era de 2.073 pg·mL−1. La ecografía describió un área de superficie de la válvula aórtica de 0,5 cm2 con un gradiente aórtico medio de 55 mmHg y acinesia inferoapical en el ventrículo izquierdo. La fracción de eyección se midió en 27% por el método Simpson biplano con regurgitación mitral moderada con dilatación biauricular y se estimó la presión pulmonar sistólica en >69 mmHg. La radiografía de tórax no mostró derrame pleural significativo. El paciente era totalmente dependiente del marcapasos.\n\nDos horas antes de la intervención, el paciente recibió 1 g de acetaminofeno por vía oral. Al llegar al quirófano, el paciente, plenamente consciente, presentaba respiración de Cheyne-Stokes periódica; cada ciclo duraba unos 85 s, con apneas de entre 15 y 20 s y grandes oscilaciones de la SpO2 entre el 88 % y el 99 %. Se le colocó dos catéteres intravenosos periféricos y uno arterial. El trazado arterial también mostraba oscilaciones de 85 s y una presión sistólica de 130 a 150 mmHg. Se le aplicó una máscara facial de oxígeno al 40 % con ventilación no invasiva; la SpO2 alcanzó un rango más estable (92 %-99 %). Diez minutos después, los análisis de gases en sangre mostraron un pH de 7,39, Pao2 de 108 mmHg, Paco2 de 40 mmHg, SaO2 del 97 %, y oscilaciones de lactato de 1,2 mEq·L−1. Se instaló una línea de muestreo capnógrafo dentro de la máscara facial para monitorizar la frecuencia respiratoria (Carescape Monitor B650, GE Healthcare, Helsinki, Finlandia). La monitorización también incluía un ECG de 12 derivaciones, oximetría de pulso, y oximetría cerebral regional (rSO2) mediante espectroscopia infrarroja cercana en el frente (INVOS, Somanetics). La capnografía reveló que las oscilaciones de la presión arterial eran sincrónicas con el ritmo de la respiración y que la presión disminuía durante los períodos apneicos e hipopneicos y aumentaba durante la hiperventilación; la rSO2 seguía el mismo patrón, a pesar de que la SpO2 del dedo permanecía a un nivel constante de 99 %. Se inició una infusión de propofol a una concentración objetivo de 0,2 µg·mL−1; se administraron 2,5 µg de sufentanilo antes de que los operadores infiltraran cada ingle con 200 mg de mepivacaína; el paciente se quedó dormido pero se mantuvo despierto al menor contacto con su cara o cuando su nombre se susurraba al oído; se administraron otros 2,5 µg de sufentanilo antes de la dilatación femoral de la arteria, un procedimiento requerido antes del reemplazo de la válvula. Los ciclos de ventilación se desaceleraron a un máximo de 120 s con 24 s de apneas centrales. Cuando la angiografía y los catéteres operativos estaban en su lugar en la aorta ascendente y se introdujo un marcapasos temporal en el ventrículo derecho, se indujo un ritmo rápido de 200 latidos/min para permitir una nueva dilatación de la válvula calcificada. Este procedimiento duró <25 s, durante el cual el paciente permaneció consciente y continuó respirando de la forma habitual, el ritmo se indujo justo después del final de un período apneico. Se preparó una válvula de 26 mm (SAPIEN, Edwards Lifesciences) y se introdujo en el orificio aórtico. Se dio una señal a los operadores una vez que la respiración se reanudó al final de un período apneico; se inició un ritmo ventricular rápido que llevó a la asistolia a una presión arterial media de 45 mmHg, y la válvula se expandió con balón y la angiografía confirmó la ausencia de fuga paravalvular. El balón se desinfló justo antes de que se detuviera el ritmo rápido, y el corazón volvió a latir a 80 latidos/min bajo la estimulación del marcapasos implantado. La secuencia completa se filmó; duró 31 s, durante los cuales el paciente siguió respirando regularmente (8 veces durante la detención circulatoria, es decir, una tasa de 16 veces por minuto) y no se despertó. Las expulsiones de sangre se reanudaron inmediatamente después de la deflación del balón, con una presión sistólica de 80 mmHg. Después de unas respiraciones profundas, la respiración se hizo regular; no se produjeron nuevos períodos apneicos ni oscilaciones de la presión arterial o rSO2. La hipertensión sistémica se desarrolló rápidamente, culminando después de 1 min a 190 mmHg y se controló con 40 mg de urapidil intravenoso durante los siguientes 15 min. La ecografía transtorácica midió el área valvular a 1,6 cm2 y el gradiente transvalvular máximo a 15 mmHg. La estimación de la presión arterial pulmonar mediante ecografía transtorácica mostró un gradiente sistólico de la presión ventricular derecha-aurícula derecha de 69 mmHg 1 día antes del procedimiento y 45 mmHg 2 días después. Un mes después, era de 28 mmHg. La evolución posterior no tuvo incidentes, y el paciente fue dado de alta 72 h después sin haber vuelto a la respiración periódica.\n\nMH - Edad 80 años y más\nMH - Cirugía de la válvula aórtica\nMH - *Estenosis/cirugía de la válvula aórtica\nMH - *Respiración de Cheyne-Stokes\nMH - Ecocardiografía\nMH - *Insuficiencia cardiaca\nMH - *Implantación de prótesis valvulares cardíacas\nMH - Hemodinámica\nMH - Humanos\nMH - Hombre\nMH - Resultado del tratamiento\n",
+    "gold_summary": "Se remitió a un hombre de 86 años para la implantación de una válvula aórtica transfemoral. La ecocardiografía transtorácica reveló una estenosis grave (gradiente medio: 58 mmHg, área de la válvula aórtica: 0,4 cm2), y después de una discusión multidisciplinaria, se consideró que el riesgo de la cirugía era demasiado alto (Euroscore logístico: 51%), y se propuso al paciente para la implantación de una válvula aórtica transfemoral (TAVI). Al llegar al quirófano, se observó que el paciente, completamente consciente, tenía respiración de Cheyne-Stokes (CSB), que persistió después de la administración de oxígeno al 40%. El procedimiento TAVI fue exitoso, y el patrón CSB se interrumpió en 8 s.\n",
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+        "text": "Había un señor de 86 años que tenía un problema en su corazón. Su corazón tenía una puerta muy pequeña y difícil para que la sangre pasara.\n\nLos doctores dijeron que una operación grande era muy peligrosa para él. Entonces, decidieron ponerle una válvula nueva con un tubo pequeño por la pierna.\n\nCuando llegó al lugar para la operación, el señor respiraba de una forma rara que subía y bajaba. Le dieron aire para ayudar, pero seguía igual.\n\nLa operación salió muy bien. Después, su forma de respirar rara se detuvo rápido. El señor se sintió mejor y todo salió bien.",
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+        "text": "**Lo que le pasaba al paciente:**  \nUn hombre de 86 años tenía un problema grave en su corazón llamado estenosis aórtica, que significa que la válvula que controla el flujo de sangre desde el corazón hacia el cuerpo estaba muy estrecha. Esto hacía que su corazón trabajara mucho más duro para bombear la sangre. Los médicos usaron una ecografía especial para ver que la válvula estaba muy dañada y que el área por donde pasa la sangre era muy pequeña.\n\n**Por qué eligieron un tratamiento especial:**  \nDebido a que el paciente era mayor y tenía otros problemas de salud, los médicos pensaron que una cirugía tradicional para cambiar la válvula era demasiado riesgosa. En lugar de eso, decidieron hacer un procedimiento menos invasivo llamado TAVI, que consiste en implantar una nueva válvula a través de una arteria en la pierna, sin abrir el pecho.\n\n**Lo que ocurrió durante el procedimiento:**  \nCuando el paciente llegó al quirófano, estaba despierto y mostraba un tipo de respiración llamada Cheyne-Stokes. Esta respiración es irregular y se caracteriza por períodos en los que la persona respira muy rápido y otros en los que casi no respira. Aunque le dieron oxígeno, esta respiración continuó. Durante el procedimiento para poner la nueva válvula, todo salió bien y, justo después, la respiración irregular desapareció en pocos segundos.\n\n**Qué significa esto:**  \nEl éxito del procedimiento no solo mejoró la función de la válvula del corazón, sino que también ayudó a normalizar la respiración del paciente. Esto muestra que tratar la estenosis aórtica puede mejorar otros problemas relacionados con el corazón y la forma en que el cuerpo respira.",
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+        "text": "**Contexto**\n\nUn hombre de 86 años con antecedentes importantes, incluyendo tabaquismo intenso en el pasado, fibrilación auricular paroxística tratada con anticoagulación y marcapasos por bradicardia, fue diagnosticado con estenosis aórtica severa calcificada. Presentaba síntomas de insuficiencia cardíaca, como disnea y edemas, además de deterioro significativo de la función ventricular izquierda (fracción de eyección del 27-29%) y hipertensión pulmonar. Debido a su alto riesgo quirúrgico (Euroscore logístico del 51%), se decidió realizar un reemplazo valvular aórtico mediante un procedimiento menos invasivo conocido como implantación de válvula aórtica transfemoral (TAVI).\n\n**Hallazgos Clave**\n\n- La ecocardiografía mostró una estenosis aórtica severa con un área valvular muy reducida (0,4-0,5 cm²) y un gradiente medio elevado (55-58 mmHg), junto con disfunción ventricular izquierda y dilatación de las aurículas.\n- El paciente presentaba un patrón respiratorio anormal llamado respiración de Cheyne-Stokes (CSB), caracterizado por ciclos periódicos de respiración rápida seguidos de pausas (apneas), que persistió incluso tras la administración de oxígeno al 40%.\n- Durante el procedimiento TAVI, que se realizó bajo sedación consciente, se monitorizaron cuidadosamente la función cardíaca, la saturación de oxígeno y la respiración.\n- El procedimiento incluyó la valvuloplastia con balón y la implantación de una válvula protésica de 26 mm, con inducción temporal de ritmo cardíaco rápido para facilitar la expansión valvular.\n- El paciente mantuvo la respiración espontánea durante todo el procedimiento, sin despertar ni presentar complicaciones respiratorias.\n- Tras la implantación, se observó una interrupción inmediata del patrón de respiración de Cheyne-Stokes, con estabilización de la presión arterial y mejora hemodinámica.\n- La función valvular mejoró notablemente, con aumento del área valvular a 1,6 cm² y reducción del gradiente a 15 mmHg. La presión pulmonar también disminuyó progresivamente en el seguimiento.\n\n**Interpretación Clínica**\n\nEste caso ilustra la complejidad del manejo de un paciente anciano con estenosis aórtica severa y disfunción ventricular avanzada, en quien la cirugía convencional representaba un riesgo muy alto. La elección del TAVI permitió una intervención efectiva y menos invasiva. La presencia de respiración de Cheyne-Stokes, un patrón respiratorio asociado a insuficiencia cardíaca avanzada y alteraciones en el control respiratorio, fue un hallazgo relevante que se resolvió tras la mejora hemodinámica conseguida con la corrección valvular. Esto sugiere que la disfunción cardíaca contribuye directamente a la aparición de este patrón respiratorio anormal.\n\n**Próximos Pasos**\n\n- Continuar con el seguimiento clínico y ecocardiográfico para evaluar la función valvular y ventricular a largo plazo.\n- Monitorizar la presión arterial pulmonar y la función respiratoria, dado que la mejoría observada puede influir favorablemente en la calidad de vida y pronóstico.\n- Mantener el control de factores de riesgo cardiovascular y la anticoagulación adecuada, considerando la historia de fibrilación auricular y la implantación del marcapasos.\n- Evaluar y manejar cualquier síntoma residual o complicación relacionada con la insuficiencia cardíaca o el patrón respiratorio, aunque la desaparición de la respiración de Cheyne-Stokes tras el procedimiento es un signo alentador.\n\nEn resumen, la implantación de la válvula aórtica transfemoral en este paciente de alto riesgo fue exitosa y produjo una mejora significativa tanto en la función cardíaca como en la estabilidad respiratoria, evidenciando la importancia de un enfoque multidisciplinario y personalizado en casos complejos.",
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+    "article": "Una mujer árabe tunecina de 62 años, diagnosticada con la enfermedad de Von Hippel-Lindau en 2021, presentó varias manifestaciones relacionadas con la enfermedad. Tenía antecedentes de múltiples cirugías, principalmente por tumores renales, suprarrenales y pancreáticos, con hallazgos incidentales de masas ováricas.\n\nLa paciente no presentaba síntomas desde el punto de vista ginecológico, pero se quejaba principalmente de dolores de cabeza antes de someterse a una cirugía cerebral. No tenía antecedentes familiares o psicosociales significativos.\n\nSu historial quirúrgico incluye\n2021: Un tumor no operable (6 cm) del saco endolinfático del hueso petroso izquierdo, tratado con radioterapia.\n\n2021: Adrenalectomía izquierda por un feocromocitoma de 6 cm. El examen patológico reveló un feocromocitoma.\n\n2021: Nefrectomía izquierda por un tumor renal izquierdo roto. La microscopía mostró un carcinoma renal multifocal de células claras de grado nuclear 2.\n\n2022: Duodenopancreatectomía cefálica por una masa en el páncreas. El examen histológico confirmó tres cistadenomas serosos y dos tumores neuroendocrinos bien diferenciados.\n\nEn enero de 2021, durante la vigilancia posoperatoria con una tomografía computarizada (TC) abdominal-pélvica, se descubrió incidentalmente una masa anexial izquierda sólida de 4 cm, lo que levantó sospechas de malignidad. La masa se confirmó mediante ultrasonido transvaginal e IRM pélvica, clasificada como Sistema de Reporte y Datos Ováricos-Anexiales (O-RADS) 5 (alta sospecha de malignidad).\n\nExamen ginecológico e historial quirúrgico\nExamen físico: No se detectó masa abdominal-pélvica.\n\nExamen con espéculo: cuello uterino sano.\n\nSe observaron cicatrices quirúrgicas de una nefrectomía izquierda y una duodenopancreatectomía cefálica anteriores.\n\nUna reunión multidisciplinaria del personal concluyó que era necesaria la cirugía. Se realizó una laparotomía a través de una incisión en la línea media por debajo del ombligo, que reveló una masa quística sólida bien definida en el anexo izquierdo. No había ascitis ni signos de carcinomatosis peritoneal, y el anexo derecho parecía normal, sin signos macroscópicos de malignidad observados intraoperatoriamente, incluida la ausencia de vegetaciones exocísticas.\n\nSe realizó una citología junto con una anexectomía izquierda y la muestra se envió para un examen de sección congelada. Los resultados no fueron concluyentes, lo que planteó la posibilidad de tumores de margen o específicos del síndrome de Von Hippel-Lindau. Teniendo en cuenta el estado posmenopáusico de la paciente, se realizó una anexectomía derecha y una histerectomía total.\n\nEl examen histológico posterior reveló cistadenomas papilares de células claras bilaterales de las trompas de Falopio y el ligamento ancho, característicos de la enfermedad de Von Hippel-Lindau (0,5 cm en el lado derecho y 4 cm en el lado izquierdo). Los tumores consistían en papilas densamente compactadas con núcleos fibrosos, cubiertos por un epitelio monocapa.\n\nEl período postoperatorio inmediato transcurrió sin incidentes y, en el seguimiento de 1 mes, no se detectaron anomalías. Desde entonces, se ha hecho un seguimiento al paciente cada 4 meses con ecografías pélvicas normales. Durante estos 2 años de seguimiento, no han surgido complicaciones, pero el paciente fue readmitido recientemente en el departamento de neurocirugía por la recurrencia de un tumor cerebral.\n",
+    "gold_summary": "Una mujer blanca norteafricana de 62 años de edad, diagnosticada con la enfermedad de Von Hippel-Lindau en 2021, presentó múltiples manifestaciones, entre ellas, un tumor del hueso petroso izquierdo, feocromocitoma izquierdo, carcinoma de células renales izquierdo, riñón derecho con múltiples quistes y masas pancreáticas. Se sometió a varios tratamientos, entre ellos, radioterapia, adrenalectomía, nefrectomía y duodenopancreatectomía cefálica. Los exámenes de ultrasonografía y resonancia magnética revelaron una masa quística sólida en la región anexial izquierda. La laparoscopia identificó tumores quísticos en la mesosalpinx derecha e izquierda. Después de una histerectomía con anexectomía bilateral, el examen histológico reveló cistadenomas papilares de células claras bilaterales de la mesosalpinx y el ligamento ancho, compatibles con la enfermedad de Von Hippel-Lindau.\n",
+    "synthetic_summary_eval": {
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+        "text": "Había una señora que tenía una enfermedad llamada Von Hippel-Lindau. Esta enfermedad le hizo tener bultos en partes de su cuerpo. Los doctores le hicieron varias operaciones para quitar esos bultos. \n\nUn día, los doctores encontraron otro bulto cerca de su barriga. Le hicieron una cirugía para quitarlo. Cuando miraron el bulto con el microscopio, vieron que era un tipo de bulto que pasa con su enfermedad. \n\nDespués de la operación, la señora se sintió bien y los doctores la cuidaron mucho para que siga sana.",
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+        "text": "**Lo que le Pasó a la Paciente**  \nUna mujer de 62 años fue diagnosticada con la enfermedad de Von Hippel-Lindau, que es una condición genética que causa tumores en diferentes partes del cuerpo. Ella tuvo varios tumores en lugares como el hueso cerca del oído, las glándulas suprarrenales, los riñones y el páncreas. Para tratar estos tumores, se sometió a diferentes cirugías y radioterapia.\n\n**Descubrimiento de una Nueva Masa**  \nDurante un control médico, los doctores encontraron una masa sólida y con líquido (quística) en la zona de los órganos reproductores femeninos, específicamente cerca del ovario izquierdo. Usaron ultrasonido y resonancia magnética para verla mejor.\n\n**Cirugía y Resultados**  \nLos médicos hicieron una cirugía para quitar la masa y también extirparon el útero y ambos anexos (que incluyen las trompas de Falopio y los ovarios). Al analizar el tejido, encontraron que la masa era un tipo de tumor llamado cistadenoma papilar de células claras. Este tumor es raro y está relacionado con la enfermedad de Von Hippel-Lindau.\n\n**Qué Significa Esto**  \nEstos tumores no eran cancerosos, pero están asociados con la enfermedad genética que tiene la paciente. Después de la cirugía, la mujer se recuperó bien y no tuvo problemas durante los dos años siguientes, aunque tuvo que regresar para tratar un tumor cerebral que volvió a aparecer.\n\nEn resumen, esta paciente con una enfermedad genética complicada tuvo varios tumores en diferentes órganos. Gracias a los controles y cirugías, los médicos pudieron identificar y tratar un tumor nuevo en su sistema reproductor, ayudándola a mantenerse estable por un tiempo.",
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+        "text": "**Contexto**  \nUna mujer tunecina de 62 años fue diagnosticada en 2021 con la enfermedad de Von Hippel-Lindau, un trastorno genético que predispone al desarrollo de múltiples tumores en diferentes órganos. A lo largo de su evolución clínica, presentó diversas manifestaciones relacionadas con esta enfermedad, incluyendo tumores en el hueso petroso (una parte del cráneo cerca del oído), glándula suprarrenal, riñón y páncreas. Su tratamiento incluyó radioterapia y varias cirugías importantes para extirpar estos tumores.\n\n**Hallazgos Clave**  \nDurante el seguimiento posoperatorio, se detectó de forma incidental mediante tomografía computarizada una masa sólida y quística de 4 cm en la región anexial izquierda (área ovárica y estructuras cercanas). Esta masa fue confirmada por ultrasonido transvaginal y resonancia magnética, clasificándose como de alta sospecha de malignidad según el sistema O-RADS. Sin embargo, la paciente no presentaba síntomas ginecológicos ni signos físicos evidentes de masa pélvica.\n\nSe decidió realizar una cirugía mediante laparotomía para evaluar y tratar la masa. Durante la intervención, se encontró una masa quística sólida bien delimitada en el anexo izquierdo, sin evidencia de diseminación tumoral en la cavidad abdominal. Se realizó la extirpación del anexo izquierdo y, debido a la edad posmenopáusica de la paciente y la sospecha de enfermedad bilateral, también se llevó a cabo la anexectomía derecha y la histerectomía total.\n\nEl análisis histológico posterior mostró la presencia de cistadenomas papilares de células claras en ambas trompas de Falopio y en el ligamento ancho (estructuras que sostienen el útero y las trompas), con tamaños de 4 cm en el lado izquierdo y 0,5 cm en el derecho. Estos tumores, caracterizados por papilas densamente agrupadas cubiertas por una capa única de células epiteliales, son una manifestación típica de la enfermedad de Von Hippel-Lindau.\n\n**Interpretación Clínica**  \nLos cistadenomas papilares de células claras bilaterales en las trompas de Falopio y el ligamento ancho representan una manifestación poco común pero reconocida de la enfermedad de Von Hippel-Lindau. La ausencia de síntomas ginecológicos y la detección incidental subrayan la importancia de un seguimiento cuidadoso en pacientes con esta enfermedad multisistémica. La cirugía fue necesaria para confirmar el diagnóstico y prevenir posibles complicaciones asociadas a estas masas.\n\n**Próximos Pasos**  \nEl postoperatorio inmediato fue favorable y, durante un seguimiento de dos años con controles ecográficos pélvicos regulares, no se observaron recurrencias ni nuevas lesiones en la región pélvica. No obstante, la paciente fue recientemente readmitida en neurocirugía debido a la recurrencia de un tumor cerebral, lo que refleja la naturaleza crónica y multisistémica de la enfermedad de Von Hippel-Lindau. Se recomienda continuar con un seguimiento multidisciplinario riguroso para manejar las diferentes manifestaciones de esta condición.",
+        "scores": {
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+          "ROUGE-2": 0.15723270440251574,
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
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+  },
+  {
+    "article": "Una mujer embarazada de 31 años que había sido sometida a una cesárea fue derivada a la unidad de ultrasonido de nuestro departamento para un examen de ultrasonido morfológico de segundo trimestre. La paciente no tenía antecedentes familiares destacables y no había tomado medicamentos ni había estado expuesta a teratógenos durante el primer trimestre del embarazo. Los exámenes serológicos para diversas enfermedades infecciosas fueron negativos y un examen de ultrasonido previo a las 14 semanas fue normal. El triple examen para anomalías fetales también fue negativo a las 16 semanas.\n\nDurante la ecografía de la semana 20, se observó un feto masculino con una edad sonográfica compuesta de 20 semanas y 2 días que presentaba un edema significativo de las extremidades inferiores y líquido amniótico normal. Se recomendó un examen de seguimiento en 2 semanas, junto con pruebas de TORCH y pruebas de Coombs indirectas.\n\nSin embargo, se observó nuevamente edema subcutáneo en ambas extremidades inferiores durante la ecografía morfológica de la semana 23, lo que sugiere un posible diagnóstico de EM. Debido al linfedema persistente en las extremidades inferiores, se realizó una amniocentesis.\n\nLos exámenes posteriores revelaron que el cariotipo masculino era normal (46, XY), y el análisis molecular para el síndrome de Noonan fue negativo. Se realizó la secuenciación de nucleótidos del líquido amniótico con la secuenciación Illumina de 150 bases. Se aplicó el sistema de bioinformática (North-Oehler Aligarh, GATX) mientras se verificaba adicionalmente la existencia de deleciones/duplicaciones/CNV (Copy Number Variations) en el gen FLT4. El análisis identificó una mutación c.3116C>A p. (Ala1039Asp), que es una variante patogénica no conocida en el gen FLT4, lo que confirma el diagnóstico de linfedema hereditario tipo 1A – enfermedad de Milroy. El análisis de sangre materno confirmó la mutación materna y se realizó el asesoramiento genético.\n\nLa cesárea se realizó a las 38 semanas y 6 días de gestación y nació un neonato de sexo masculino que pesaba 3850 g y medía 46 cm con una puntuación de Apgar de 9/10. Después del parto se reconoció un edema en la extremidad inferior. El examen histopatológico de la placenta, el cordón umbilical y el saco amniótico no mostró signos de corioamnionitis u otra patología.\n",
+    "gold_summary": "Presentamos un informe de caso de una primera mutación descrita de un feto masculino diagnosticado prenatalmente con síndrome de Milroy a través de amniocentesis. El feto tenía edema bilateral de miembros inferiores, y las pruebas genéticas confirmaron el diagnóstico de síndrome de Milroy. La paciente fue monitoreada de cerca durante todo el embarazo, y después del parto, el lactante fue tratado con terapias apropiadas, incluyendo prendas de compresión y drenaje linfático manual. Los padres recibieron asesoramiento y apoyo apropiados.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Un bebé niño tenía sus piernas un poco hinchadas cuando estaba en la barriga de su mamá. Los doctores hicieron pruebas para entender por qué. Descubrieron que el bebé tenía una condición llamada síndrome de Milroy. La mamá fue cuidada con mucho cariño durante todo el embarazo. Cuando el bebé nació, los doctores le ayudaron para que sus piernas estuvieran mejor. Los papás también recibieron ayuda para cuidar bien al bebé. Todo está hecho para que el bebé crezca fuerte y feliz.",
+        "scores": {
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
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+      "B2": {
+        "text": "**Lo que Encontraron**\n\nEn este caso, una mujer embarazada fue examinada con ultrasonido y se descubrió que su bebé tenía hinchazón (edema) en ambas piernas antes de nacer. Para entender mejor qué pasaba, los médicos hicieron una amniocentesis, que es cuando se toma un poco del líquido que rodea al bebé para estudiar sus genes. Encontraron una mutación, que es un cambio en un gen llamado FLT4, que causa una enfermedad llamada síndrome de Milroy. Esta enfermedad hace que el sistema que ayuda a drenar el líquido del cuerpo no funcione bien, causando hinchazón.\n\n**Qué Significa**\n\nEl diagnóstico se confirmó antes del nacimiento, lo que permitió a los médicos seguir de cerca el embarazo y prepararse para cuidar al bebé después del parto. El bebé nació con hinchazón en las piernas, pero recibió tratamientos especiales, como usar prendas que aprietan suavemente y masajes para ayudar a mover el líquido acumulado. Además, los padres recibieron información y apoyo para entender la enfermedad y cómo cuidar a su hijo.\n\nEste caso muestra la importancia de las pruebas genéticas y el seguimiento durante el embarazo para detectar y manejar enfermedades raras como el síndrome de Milroy.",
+        "scores": {
+          "ROUGE-1": 0.36,
+          "ROUGE-2": 0.1610738255033557,
+          "ROUGE-L-Sum": 0.31999999999999995,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
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+      },
+      "B3": {
+        "text": "**Contexto**  \nEste informe describe el caso de una mujer embarazada de 31 años cuyo feto masculino fue diagnosticado antes del nacimiento con síndrome de Milroy, una forma hereditaria de linfedema (acumulación anormal de líquido linfático que causa hinchazón). La paciente no presentaba antecedentes familiares relevantes ni factores de riesgo conocidos, y las pruebas iniciales durante el embarazo no mostraron anomalías.\n\n**Hallazgos Clave**  \nDurante la ecografía morfológica realizada en la semana 20 de gestación, se detectó un edema significativo en ambas extremidades inferiores del feto, aunque el líquido amniótico estaba dentro de los parámetros normales. Un seguimiento a las 23 semanas confirmó la persistencia de este edema subcutáneo. Ante estos hallazgos, se realizó una amniocentesis para obtener líquido amniótico y realizar estudios genéticos detallados.  \n\nEl análisis cromosómico mostró un cariotipo normal (46, XY), y se descartó el síndrome de Noonan mediante pruebas moleculares. Sin embargo, la secuenciación genética identificó una mutación patogénica inédita en el gen FLT4 (c.3116C>A p. (Ala1039Asp)), responsable del desarrollo del sistema linfático. Esta mutación confirmó el diagnóstico prenatal de linfedema hereditario tipo 1A, conocido como enfermedad de Milroy. Además, el análisis de sangre materno reveló que la madre también portaba esta mutación, lo que permitió realizar un asesoramiento genético adecuado a la familia.\n\nEl parto se llevó a cabo mediante cesárea a las 38 semanas y 6 días, naciendo un niño con buen peso y condición general (puntuación de Apgar 9/10). Tras el nacimiento, se observó edema en las extremidades inferiores, consistente con el diagnóstico prenatal. Los estudios histopatológicos de la placenta y membranas no mostraron infecciones ni otras patologías.\n\n**Interpretación Clínica**  \nEl síndrome de Milroy es una enfermedad genética que afecta el desarrollo y funcionamiento del sistema linfático, provocando linfedema desde etapas tempranas de la vida. La detección prenatal mediante ecografía y pruebas genéticas permite un diagnóstico temprano, lo que facilita la planificación del manejo clínico y el apoyo familiar. La identificación de una mutación previamente no descrita en el gen FLT4 amplía el conocimiento sobre la variabilidad genética de esta enfermedad.\n\n**Próximos Pasos**  \nDespués del nacimiento, el lactante recibió tratamiento especializado para el linfedema, que incluyó el uso de prendas de compresión y drenaje linfático manual, con el objetivo de controlar la hinchazón y mejorar la calidad de vida. La familia recibió asesoramiento genético para comprender el origen hereditario de la enfermedad, las implicaciones para futuros embarazos y las opciones disponibles. El seguimiento clínico continuo es esencial para monitorizar la evolución del linfedema y adaptar el tratamiento según sea necesario.",
+        "scores": {
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+          "ROUGE-2": 0.1087719298245614,
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
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+  {
+    "article": "Un paciente de 50 años con antecedentes médicos conocidos de diabetes mellitus (DM) e hipertensión (HTN), que se manejaba de manera irregular, se presentó en nuestro hospital en la ciudad de Sana’a, Yemen, el 25 de mayo de 2022, a las 5:30 p. m. El paciente fue derivado a otro hospital y manifestó un dolor abdominal agudo que había durado una semana antes del ingreso. El dolor se localizaba en la región epigástrica, de inicio repentino, empeoramiento progresivo y radiación hacia la espalda. Además, el paciente experimentó distensión abdominal generalizada, náuseas, vómitos y fatiga significativa. También se informó un historial de melena y vómitos relacionados con los alimentos durante el mes pasado. Dos días antes del ingreso, el paciente había recibido una transfusión de sangre de 2 unidades. No había antecedentes de cirugías previas ni antecedentes familiares de neoplasias.\n\nAl examinar al paciente, se constató que estaba consciente y alerta, pero que presentaba un aspecto pálido. La presión arterial era de 90/60 mmHg y el pulso de 120 latidos por minuto. Se observó distensión abdominal generalizada, particularmente prominente en la región supraumbilical con desplazamiento hacia abajo del ombligo. Se constató una leve sensibilidad en la zona epigástrica, junto con sonidos intestinales positivos, el examen rectal digital reveló un tono normal del esfínter anal y no se detectó ninguna masa palpable.\n\nLos exámenes hematológicos y bioquímicos revelaron anemia microcítica hipocrómica con un nivel de hemoglobina de 6 g/dL (rango normal: 12-15.5 g/dL), un recuento de glóbulos blancos de 16,000 (rango normal: 4-10,000), y un recuento de plaquetas de 303. El nivel de nitrógeno ureico en sangre fue de 7 mg/dL (rango normal: 10-20 mg/dL), la creatinina fue de 0.49 mg/dL (rango normal: 0.7-1.5% / dL), el índice internacional normalizado fue de 1.34 (rango normal: 0.62-1.3), el tiempo de protrombina (PT) fue de 16.9, el tiempo de tromboplastina parcial (PTT) fue de 30, el calcio fue de 8.0 mg/dL (rango normal: 8.5-10.1 mg / dL) y el ácido láctico fue de 1.9 mmol/L (rango normal: 0.5-2.2% / L). Los niveles de enzimas hepáticas y amilasa estuvieron dentro de los límites normales.\n\nSe realizaron estudios de diagnóstico por imágenes, que incluyeron una radiografía de tórax y una ecografía abdominal. La radiografía de tórax no reveló aire subdiafragmático, pero se observó una elevación en el diafragma izquierdo. La ecografía abdominal demostró la presencia de una acumulación de líquido intraabdominal. Posteriormente, se realizó una angiografía por TC abdominal, que reveló un hematoma de aproximadamente 14,3 × 8,8 cm en la región paraumbilical. En el interior del hematoma, se identificó un aneurisma arterial de 3,4 × 2,2 cm conectado a la arteria gastroduodenal, acompañado de cambios edematosos circundantes. Estos hallazgos sugieren la presencia de un aneurisma trombosado grande en la arteria gastroduodenal. Además, se observó la evisceración del diafragma izquierdo, que contiene el bazo y parte del estómago, junto con una acumulación de líquido intraperitoneal leve a moderada. No se detectó evidencia de un aneurisma aórtico.\n\nPara estabilizar al paciente, se inició la reanimación con 1000 ml de lactato de Ringer y se transfundieron tres unidades de sangre fresca. Se obtuvo el consentimiento informado para la intervención de alto riesgo y el paciente fue llevado inmediatamente al quirófano. Bajo anestesia general, en posición supina y con estricta adhesión a las técnicas asépticas, se realizó una incisión de laparotomía en la línea media. Cuando se abrió el peritoneo, se evacuó aproximadamente 2000 ml de sangre, revelando una masa pulsátil ocluida en el duodeno. Se logró una exposición adecuada utilizando un retractor auto-reforzado. La flexión del hígado y el colon transverso se movilizaron inferiormente desde la cabeza del páncreas y se eliminó la sangre coagulada del intestino delgado. Se realizó una disección meticulosa sobre el gran aneurisma ocluido pulsátil en la arteria gastroduodenal abriendo el ligamento gastrohepático. La movilización del píloro y el duodeno lejos de la cabeza del páncreas expuso una fístula que conectaba el duodeno y el aneurisma, sin contenido digestivo. Después de la heparinización, se realizó un pinzamiento proximal y distal de la arteria gastroduodenal. Posteriormente, se abrió el pseudoaneurisma y se evacuó una cantidad significativa de trombo. Se realizó una aneurismorrafía utilizando suturas de prolina 7.0. La perforación en la primera parte del duodeno se reparó en dos capas y se insertó una sonda nasogástrica más allá de la perforación. Se logró una irrigación exhaustiva con solución salina normal y una hemostasia meticulosa. Se colocó un drenaje abdominal y se cerró la incisión abdominal en capas. El paciente fue trasladado a la unidad de cuidados intensivos (UCI) para una estrecha monitorización y observación.\n\nDurante el período postoperatorio, el drenaje abdominal recolectó aproximadamente 100 ml de fluido seroso, que se eliminó el tercer día después de la operación. La recuperación de la paciente progresó sin complicaciones. Diez días después de la cirugía, la paciente fue dada de alta en condiciones favorables. Se programaron citas de seguimiento en el departamento ambulatorio y se mantuvo una comunicación regular por teléfono, con la condición de la paciente reportada como satisfactoria.\n",
+    "gold_summary": "Un hombre de 50 años se presentó con dolor abdominal agudo, anemia y signos de inestabilidad hemodinámica. Las imágenes de diagnóstico, incluida la CTA, revelaron un aneurisma de la arteria gastroduodenal grande y trombosado con evidencia de ruptura. El paciente se sometió a exploración y reparación quirúrgica abierta para abordar tanto el aneurisma como la perforación duodenal. La recuperación del paciente fue satisfactoria y fue dado de alta en condiciones estables.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Un hombre tenía mucho dolor en su barriga. Estaba muy cansado y débil. Los doctores vieron que tenía un bulto grande en una de sus venas. Ese bulto estaba lastimado y había sangre. Los doctores hicieron una operación para arreglar el bulto y la herida. Después, el hombre se sintió mejor y pudo ir a su casa.",
+        "scores": {
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+          "ROUGE-2": 0.014184397163120567,
+          "ROUGE-L-Sum": 0.26573426573426573,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
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+      "B2": {
+        "text": "### Lo que le pasó al paciente\n\nUn hombre de 50 años llegó al hospital con un dolor fuerte en el abdomen que había durado una semana. También estaba muy cansado y tenía anemia, que es cuando la sangre no tiene suficientes glóbulos rojos para llevar oxígeno al cuerpo. Su presión arterial estaba baja y su pulso rápido, lo que indicaba que su cuerpo estaba débil.\n\n### Lo que encontraron los médicos\n\nLos médicos hicieron varias pruebas, incluyendo imágenes especiales llamadas tomografía computarizada (CTA). Estas mostraron que tenía un aneurisma grande en una arteria llamada gastroduodenal. Un aneurisma es una zona donde la pared de un vaso sanguíneo está débil y se hincha, como un globo. Además, había coágulos de sangre dentro del aneurisma y parecía que se había roto, lo que es muy peligroso.\n\n### Qué hicieron los médicos\n\nPara salvarlo, los médicos hicieron una cirugía abierta. Abrieron el abdomen para encontrar y reparar el aneurisma. También encontraron una pequeña herida (perforación) en el duodeno, que es la primera parte del intestino delgado, y la repararon. Durante la cirugía, limpiaron la sangre acumulada y cerraron cuidadosamente las heridas.\n\n### Cómo fue la recuperación\n\nDespués de la operación, el paciente estuvo en cuidados intensivos para que lo vigilaran bien. Su recuperación fue buena, sin problemas importantes. Diez días después, pudo salir del hospital en buen estado y continuó con controles médicos para asegurarse de que siguiera mejorando.",
+        "scores": {
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
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+      "B3": {
+        "text": "**Contexto:**  \nUn hombre de 50 años con antecedentes de diabetes e hipertensión, que no seguía un tratamiento constante, acudió al hospital tras una semana de dolor abdominal intenso en la parte superior del abdomen, que se irradiaba hacia la espalda. Además, presentaba distensión abdominal, náuseas, vómitos, fatiga y antecedentes recientes de sangrado digestivo (melena). Dos días antes había recibido una transfusión de sangre debido a anemia.\n\n**Hallazgos Clave:**  \nEn la evaluación inicial, el paciente estaba consciente pero pálido, con presión arterial baja (90/60 mmHg) y pulso acelerado (120 latidos/minuto), signos que indicaban inestabilidad hemodinámica. El examen físico mostró distensión abdominal y sensibilidad leve en la zona del dolor. Los análisis de sangre revelaron anemia severa (hemoglobina de 6 g/dL), aumento de glóbulos blancos (16,000), y otros parámetros dentro de límites aceptables. Las imágenes diagnósticas, incluyendo una tomografía computarizada con angiografía (CTA), identificaron un hematoma grande en la región abdominal paraumbilical y un aneurisma (una dilatación anormal de un vaso sanguíneo) de la arteria gastroduodenal, con signos de trombosis (coágulos) y posible ruptura. También se observó una hernia diafragmática con desplazamiento de órganos abdominales hacia el tórax y acumulación de líquido en la cavidad abdominal.\n\n**Interpretación Clínica:**  \nEl diagnóstico principal fue un aneurisma gigante y trombosado de la arteria gastroduodenal con ruptura, que causaba hemorragia interna y perforación en la primera parte del duodeno (segmento inicial del intestino delgado). Esta situación representaba una emergencia quirúrgica debido al riesgo de sangrado masivo y complicaciones graves.\n\n**Próximos Pasos y Tratamiento:**  \nEl paciente fue estabilizado con líquidos intravenosos y transfusiones sanguíneas antes de ser llevado a cirugía de urgencia. Durante la operación, se evacuaron aproximadamente dos litros de sangre acumulada, se identificó y reparó el aneurisma mediante suturas, y se cerró la perforación duodenal en dos capas. Se colocó un drenaje abdominal para controlar posibles fugas y se monitorizó estrechamente en la unidad de cuidados intensivos. La recuperación fue favorable, sin complicaciones postoperatorias, y el paciente fue dado de alta diez días después en condiciones estables, con seguimiento ambulatorio programado.\n\nEn resumen, este caso ilustra la importancia de un diagnóstico rápido y un manejo quirúrgico oportuno en pacientes con aneurisma roto de la arteria gastroduodenal, una condición rara pero potencialmente mortal.",
+        "scores": {
+          "ROUGE-1": 0.2703777335984096,
+          "ROUGE-2": 0.12375249500998003,
+          "ROUGE-L-Sum": 0.2504970178926441,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
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+  {
+    "article": "Una mujer de 60 años fue admitida en el departamento de nefrología con dolor epigástrico, hematemesis y edema en la pierna. La presión arterial era de 90/50 mmHg, dentro del rango normal para esta paciente.\nLos resultados de laboratorio fueron notables para las enzimas hepáticas alteradas con un patrón colestático: los niveles de alanina amino transferasa (ALT) y aspartato amino transferasa (AST) fueron ligeramente elevados a 28 U/L y 61 U/L, respectivamente, mientras que los niveles de fosfatasa alcalina (388 U/L) y gamma glutamiltransferasa (291 U/L) fueron muy elevados. Los niveles de albúmina en suero fueron de 24 g/L y el índice internacional normalizado fue normal a 1.02.\nOtros resultados de laboratorio, incluidos la bilirrubina total (0,32 mg/dL), la bilirrubina directa (0,26 mg/dL), el recuento total de plaquetas (176 000 plaquetas por microlitro) y el recuento de glóbulos blancos (8400 células por microlitro), se encontraban dentro de los valores normales.\nEl paciente tenía un extenso historial de enfermedades cardiacas y renales. A los 11 años, se le diagnosticó estenosis congénita de la válvula pulmonar, por lo que se le practicó una valvulotomía. Más adelante, desarrolló fibrilación auricular y aleteo auricular, que no toleró bien y para los que se intentó, sin éxito, la ablación del aleteo. Como el paciente seguía teniendo síntomas, se le practicó una ablación del nódulo auriculoventricular con colocación de un marcapasos.\nSe inició anticoagulación oral con fenprocoumon debido a una puntuación CHA2DS2-Vasc de 3 (mujer, insuficiencia cardiaca y enfermedad vascular periférica). A la edad de 55 años, se desarrolló una insuficiencia cardiaca derecha manifiesta y la paciente continuó luchando con ascitis y edemas periféricos que requerían múltiples ingresos hospitalarios. Además, también desarrolló un problema de efusiones pleurales transudativas recurrentes de etiología poco clara.\nLa ecocardiografía en ese momento mostró una severa regurgitación pulmonar y tricuspídea con un ventrículo derecho moderadamente dilatado y una aurícula derecha. El ventrículo izquierdo estaba ligeramente dilatado con una regurgitación mitral moderada. El cateterismo cardiaco derecho demostró presiones arteriales pulmonares de 74/30 mmHg con una presión venosa central de 28 mmHg. Se colocó un homotransplante pulmonar cuando el paciente tenía 57 años y se realizó una anuloplastia tricuspídea concomitante. A pesar de una presión venosa central más baja de 13 mmHg, el paciente seguía siendo readmitido varias veces por signos y síntomas de insuficiencia cardiaca derecha. La congestión venosa sistémica persistente finalmente dio lugar a una enfermedad renal en fase terminal para la que se inició una terapia de reemplazo renal a través de hemodiálisis intermitente. El caso se complicó por hemorragias gastrointestinales graves recurrentes, que requerían transfusiones de sangre frecuentes con hasta 60 unidades de glóbulos rojos por año. A pesar de esto, en combinación con la sustitución intravenosa de hierro, los niveles de hemoglobina variaron entre 5.3-8.8 g/dL. Debido a estos problemas de sangrado intratables, la anticoagulación oral con fenprocoumon se detuvo a la edad de 59 años.\nUna gastroscopia mostró una gastropatía erosiva con una mucosa difusa congestiva y friable. Como prevención de primera línea de las hemorragias gástricas recurrentes en el marco de la cirrosis, se inició el propranolol a una dosis de 5 mg por vía oral dos veces al día (el paciente no toleró una dosificación superior debido a la presión arterial baja). Además, se realizó una coagulación endoscópica de un angioma fúndico y un recorte de una lesión de Dieulafoy.\nSe creía que estas lesiones eran causadas por una gastropatía hipertensiva. Sin embargo, las hemorragias intractables persistieron.\nEl gradiente de presión venosa hepática se midió a 16 mmHg (27 mmHg-11 mmHg). Aunque hubo cierta reticencia debido al temor de empeorar la insuficiencia cardiaca derecha, se tomó la decisión de crear un TIPS. El procedimiento fue sin incidentes. Después de la colocación del TIPS, el gradiente de presión venosa hepática disminuyó a 4 mmHg (14 mmHg-10 mmHg). Por lo tanto, aunque el TIPS redujo considerablemente el gradiente venoso hepático, la presión portal se mantuvo alta debido a la elevada presión venosa central.\nDespués de la colocación del TIPS, el paciente desarrolló signos de encefalopatía hepática y se midieron niveles de amoniaco de 77 umol/L. Se inició el tratamiento con lactulosa oral y enemas, con poca mejora. En ese momento, se produjo otro episodio de sangrado gástrico.\nLa ecografía abdominal mostró buena permeabilidad del TIPS con flujo Doppler normal. Se detectó sangrado gástrico de una úlcera antral con endoscopia, a pesar de que la hiperemia gástrica disminuyó visualmente en comparación con la situación antes del TIPS. Se realizó una biopsia que mostró una mucosa foveolar edematosa, lo que sugiere isquemia de la mucosa. El sangrado fue demasiado difuso para una ligadura endoscópica adicional. No se encontró empeoramiento de la función hepática en los resultados de laboratorio, con el índice internacional normalizado 1.01 en este momento. La ecocardiografía no mostró cambios significativos en comparación con la situación antes de la colocación del TIPS. El ventrículo derecho permaneció moderadamente dilatado con una función longitudinal deficiente y una regurgitación tricuspídea severa persistente. Sin embargo, el estado general del paciente se deterioró y se desarrolló fiebre con consolidaciones pulmonares bilaterales.\nSe produjo una falla multiorgánica y, en ese momento, la familia del paciente decidió retirar el tratamiento. El paciente falleció finalmente 43 días después del procedimiento TIPS.\n\nMH - Resultado fatal\nMH - Mujer\nMH - Insuficiencia cardiaca/*complicaciones/fisiopatología\nMH - Encefalopatía hepática/etiología\nMH - Humanos\nMH - Hipertensión, Portal/etiología/fisiopatología/*cirugía\nMH - Cirrosis hepática/*complicaciones\nMH - Edad Media\nMH - Presión del portal\nMH - *Derivación portosistémica, intrahepática transyugular\nMH - Fracaso del tratamiento\n",
+    "gold_summary": "Una mujer de 60 años con antecedentes de estenosis congénita de la válvula pulmonar desarrolló insuficiencia cardíaca derecha, cirrosis hepática y enfermedad renal en fase terminal que requería terapia de reemplazo renal. La cirrosis hepática se complicó con hipertensión portal, lo que provocó hemorragias gastrointestinales intratables a pesar del tratamiento óptimo con betabloqueantes y la ligadura endoscópica de la banda. Debido al temor de que empeorara la insuficiencia cardíaca derecha, inicialmente se rechazó la colocación de una derivación intrahepática transyugular (TIPS). Sin embargo, como los problemas de hemorragia intratables persistieron y causaron grandes necesidades de transfusión, la TIPS se realizó finalmente como un procedimiento de rescate. Aunque la TIPS redujo con éxito el gradiente de presión venosa hepática de 16 mmHg a 4 mmHg, la presión portal se mantuvo alta a 14 mmHg debido a la persistencia de la insuficiencia cardíaca derecha con presión venosa central elevada. La encefalopatía hepática se desarrolló poco después de la colocación de la TIPS y culminó en una falla multiorgánica después de otro episodio de hemorragia gastrointestinal. En este punto, la familia del paciente decidió retirar la atención y el paciente falleció posteriormente.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Había una señora de 60 años que tenía problemas en el corazón y en el hígado. Su hígado estaba muy enfermo y le dolía mucho la barriga. También tenía problemas para que la sangre no sangrara mucho por dentro.\n\nLos doctores intentaron ayudarla con medicinas y tratamientos, pero la sangre seguía saliendo. Entonces, hicieron una operación para ayudar a que la sangre pasara mejor por el hígado.\n\nDespués de la operación, la señora se sintió peor y tuvo más problemas en su cuerpo. Al final, su familia decidió que ya no la trataran más y la señora se fue al cielo.",
+        "scores": {
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+      "B2": {
+        "text": "**Historia Clínica y Problemas Principales**  \nUna mujer de 60 años tenía varios problemas de salud desde joven, incluyendo una enfermedad del corazón llamada estenosis congénita de la válvula pulmonar. Con el tiempo, desarrolló insuficiencia cardíaca derecha, que significa que el lado derecho de su corazón no funcionaba bien. También tenía cirrosis hepática, una enfermedad del hígado que causa daño y cicatrices, y enfermedad renal en etapa terminal, por lo que necesitaba diálisis para limpiar su sangre.\n\n**Complicaciones y Tratamientos**  \nLa cirrosis causó hipertensión portal, que es una presión alta en las venas del hígado. Esto provocó sangrados graves en su estómago y esófago que no se podían controlar fácilmente. A pesar de usar medicamentos llamados betabloqueantes, que ayudan a bajar la presión, y hacer tratamientos endoscópicos para detener el sangrado, las hemorragias continuaron. Por miedo a que un procedimiento llamado TIPS (una derivación que ayuda a bajar la presión en el hígado) empeorara su insuficiencia cardíaca, inicialmente no se realizó.\n\n**Procedimiento TIPS y Resultados**  \nFinalmente, debido a que las hemorragias seguían siendo muy graves y necesitaba muchas transfusiones de sangre, se decidió hacer el TIPS como último recurso. Este procedimiento logró bajar la presión en las venas del hígado de 16 a 4 mmHg, lo que es una mejora importante. Sin embargo, la presión en la vena principal del hígado siguió siendo alta porque su corazón derecho seguía funcionando mal.\n\n**Complicaciones Finales y Desenlace**  \nDespués del TIPS, la paciente desarrolló encefalopatía hepática, que es un problema en el cerebro causado por la acumulación de toxinas cuando el hígado no funciona bien. También tuvo otro sangrado en el estómago y su estado general empeoró, con fallas en varios órganos. Finalmente, la familia decidió suspender el tratamiento y la paciente falleció 43 días después del procedimiento.\n\n**Qué Significa Este Caso**  \nEste caso muestra lo difícil que es tratar a pacientes con problemas graves en el corazón, hígado y riñones al mismo tiempo. Aunque el TIPS puede ayudar a bajar la presión en el hígado y controlar el sangrado, no siempre es suficiente si el corazón no puede manejar los cambios. Además, el procedimiento puede causar complicaciones como la encefalopatía hepática. Por eso, cada caso necesita un cuidado muy cuidadoso y personalizado.",
+        "scores": {
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+      "B3": {
+        "text": "**Contexto**  \nSe presenta el caso de una mujer de 60 años con un complejo historial médico que incluye una estenosis congénita de la válvula pulmonar diagnosticada en la infancia, seguida de múltiples complicaciones cardíacas como fibrilación auricular, insuficiencia cardíaca derecha y regurgitación valvular severa. Estas condiciones condujeron a una congestión venosa sistémica persistente, que a su vez provocó cirrosis hepática y enfermedad renal en etapa terminal, requiriendo hemodiálisis. Además, la paciente sufrió hemorragias gastrointestinales graves y recurrentes, difíciles de controlar, que demandaron numerosas transfusiones sanguíneas.\n\n**Hallazgos Clave**  \n- La cirrosis hepática se acompañó de hipertensión portal, evidenciada por un gradiente de presión venosa hepática elevado (16 mmHg).  \n- A pesar del tratamiento con betabloqueantes (propranolol) y procedimientos endoscópicos para controlar las hemorragias gástricas, estas continuaron siendo incontrolables.  \n- Inicialmente, se evitó la colocación de una derivación portosistémica intrahepática transyugular (TIPS) debido al riesgo de empeoramiento de la insuficiencia cardíaca derecha.  \n- Finalmente, se realizó el procedimiento TIPS como medida de rescate, logrando reducir el gradiente de presión venosa hepática a 4 mmHg; sin embargo, la presión portal permaneció elevada (14 mmHg) debido a la presión venosa central alta secundaria a la insuficiencia cardíaca derecha persistente.  \n- Posterior a la colocación del TIPS, la paciente desarrolló encefalopatía hepática (una alteración cerebral causada por la acumulación de toxinas debido a la insuficiencia hepática), con niveles elevados de amoníaco en sangre y síntomas neurológicos.  \n- Se presentó un nuevo episodio de sangrado gástrico, con evidencia endoscópica de úlcera antral y cambios isquémicos en la mucosa gástrica.  \n- La función hepática no mostró deterioro significativo en los análisis de laboratorio tras el TIPS, y la ecocardiografía reveló que la función cardíaca derecha permaneció comprometida.  \n- Finalmente, la paciente desarrolló una falla multiorgánica acompañada de infección pulmonar, lo que llevó a la decisión familiar de retirar el soporte terapéutico.\n\n**Interpretación Clínica**  \nEste caso ilustra la compleja interacción entre la insuficiencia cardíaca derecha crónica y sus consecuencias sistémicas, incluyendo la hipertensión portal secundaria y la cirrosis hepática. La hipertensión portal generó hemorragias gastrointestinales difíciles de controlar, que agravaron el estado general de la paciente. La colocación del TIPS, aunque efectiva para reducir el gradiente hepático, no logró normalizar la presión portal debido a la persistente congestión venosa por insuficiencia cardíaca. Además, el procedimiento desencadenó encefalopatía hepática, complicación frecuente en estos casos, y no previno nuevos episodios hemorrágicos. La evolución desfavorable culminó en falla multiorgánica y muerte.\n\n**Próximos Pasos y Reflexiones**  \nEste caso subraya la dificultad de manejar la hipertensión portal y sus complicaciones en pacientes con insuficiencia cardíaca derecha avanzada. La decisión de realizar un TIPS debe sopesar cuidadosamente los riesgos de empeoramiento cardíaco y encefalopatía hepática. En situaciones similares, se requiere un enfoque multidisciplinario que incluya cardiología, hepatología y nefrología para optimizar el tratamiento y considerar alternativas terapéuticas. Además, es fundamental el diálogo con la familia para establecer objetivos realistas y respetar las decisiones sobre el cuidado al final de la vida.",
+        "scores": {
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
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+  {
+    "article": "Una mujer tailandesa de 62 años presentó pérdida visual bilateral súbita y cefalea durante 5 días. Negó antecedentes de traumatismo craneal. Su historia clínica era significativa por presentar hipertensión mal controlada.\n\nLos signos vitales fueron normales, excepto por la presión arterial de 200/105 mmHg. La agudeza visual fue de no percepción de luz (NLP) con pupilas fijas en ambos ojos. La motilidad ocular de ambos ojos fue limitada en todas las direcciones. Ambas párpados fueron difíciles de abrir. Las medidas del exoftalmómetro de Hertel fueron de 16 mm en el ojo derecho y 14 mm en el ojo izquierdo. Había quemosis significativa y vasos de sacacorchos episclerales en ambos ojos. Ambas córneas mostraron un edema estromal leve y difuso sin infiltración. Las cámaras anteriores fueron profundas y tranquilas en ambos ojos. Las presiones intraoculares fueron de 45 mmHg y 48 mmHg en los ojos derecho e izquierdo, respectivamente. La gonioscopia reveló sangre en el canal de Schlemm en el ángulo nasal del ojo derecho. El examen del fondo de ojo mostró venas de la retina ligeramente dilatadas y tortuosas con discos ópticos de apariencia normal en ambos ojos. La relación taza-disco fue de 0.3 bilateralmente. La tomografía de coherencia óptica demostró un espesor normal de la mácula en cada ojo. No hubo ruido audible. Otros exámenes neurológicos fueron normales.\n\nLa resonancia magnética (MRI) con gadolinio del cerebro y las órbitas demostró la dilatación de las venas oftálmicas superiores bilaterales (SOVs) y un grado marcado de congestión orbital y periorbital bilateralmente. Sin embargo, no se observó ni compresión ni estiramiento de los nervios ópticos bilaterales. Es interesante destacar que la restricción de la difusión, con la correspondiente reducción del coeficiente de difusión aparente (ADC), en todo el segmento orbital de los nervios ópticos bilateralmente se reveló en la resonancia magnética ponderada en difusión (DWI). Esto es consistente con el PION bilateral. La angiografía por resonancia magnética (MRA) del cerebro y las órbitas reveló arterialización de los senos cavernosos bilaterales y de las SOVs.\n\nLa angiografía cerebral confirmó el diagnóstico de CCF durales bilaterales de drenaje anterior. La CCF dural derecha se alimentaba de las ramas durales de la ICA (tronco meningo-hipofisario derecho). La CCF dural izquierda se alimentaba de las ramas durales de la ECA (arteria meningo-hipofisaria izquierda y la arteria izquierda del foramen redondo y las ramas durales de la ICA (tronco meningo-hipofisario izquierdo). Cada lado de la CCF dural contribuía con flujo sanguíneo arterial a los SOV bilaterales (SOV contralateral a través de la comunicación inter-cavernosa). No se observó reflujo venoso cortical del flujo sanguíneo arterial. Basándose en estos hallazgos, se realizó una embolización transvenosa de la bobina. Los senos cavernosos bilaterales se embolizaron utilizando bobinas para ocluir los vasos de alimentación de las ramas durales de la ICA y la ECA. La angiografía cerebral inmediata posterior a la embolización mostró el cierre completo de las fístulas.\n\nTres meses después de la embolización, el examen oftálmico demostró una mejora progresiva de los signos oftálmicos antes mencionados; no obstante, la agudeza visual del paciente se mantuvo en NLP en ambos ojos.\n",
+    "gold_summary": "Reportamos el caso de una mujer de 62 años de edad con antecedentes de hipertensión arterial mal controlada que presentó pérdida visual bilateral súbita y cefalea durante 5 días. Negó antecedentes de traumatismo craneal. En el examen, sus agudezas visuales eran de no percepción de luz (NLP) con pupilas fijas en ambos ojos. La motilidad ocular de ambos ojos era limitada en todas las direcciones. Era difícil abrir ambos párpados. El examen del segmento anterior reveló quemosis bilateral y vasos del sacacorchos episclerales. La presión intraocular era de 45 y 48 mmHg en los ojos derecho e izquierdo, respectivamente. La gonioscopia reveló sangre en el canal de Schlemm en el ángulo nasal del ojo derecho. El examen del fondo de ojo mostró venas retinianas ligeramente dilatadas y tortuosas con discos ópticos de apariencia normal en ambos ojos. Las relaciones entre la copa y el disco eran de 0,3 bilateralmente. Otros exámenes neurológicos no presentaron anormalidades. La resonancia magnética demostró dilatación de las venas oftálmicas superiores bilaterales (SOV) y congestión orbital y periorbital bilateral marcada. Sin embargo, no hubo compresión o estiramiento de los nervios ópticos bilaterales. Se reveló una restricción de la difusión en la difusión ponderada por la difusión, con la correspondiente reducción del coeficiente de difusión aparente, en todo el segmento orbital bilateral de los nervios ópticos, consistente con PION bilateral. La angiografía por resonancia magnética reveló arterialización de los senos cavernosos bilaterales y las SOV. La angiografía cerebral confirmó el diagnóstico de CCF bilaterales de drenaje anterior. El tratamiento con embolización de bobina transvenosa fue exitoso. Tres meses después de la embolización, el examen oftálmico demostró una mejora progresiva de los signos oftálmicos antes mencionados; sin embargo, sus agudezas visuales permanecieron como NLP en ambos ojos.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Una señora mayor se enfermó y no pudo ver con sus ojos. Tenía dolor en la cabeza. Sus ojos estaban muy cansados y no se movían bien. Abrir los ojos era difícil. Los ojos estaban hinchados y con vasos raros. Tenía mucha presión dentro de los ojos. Los doctores hicieron fotos especiales de su cabeza y ojos. Vieron que las venas de sus ojos estaban muy grandes y llenas de sangre. También vieron que los nervios de sus ojos estaban dañados. Encontraron un problema con las venas que llevaba sangre en su cabeza. Los doctores hicieron una operación para arreglar las venas. Después de la operación, sus ojos se veían mejor, pero ella no pudo recuperar la vista. Los doctores la cuidaron mucho y trataron de ayudarla.",
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+        "text": "**Caso de una Mujer con Pérdida Súbita de la Vista**\n\nUna mujer de 62 años, que tenía presión arterial alta sin control, comenzó a perder la vista en ambos ojos de forma repentina y también tenía dolor de cabeza durante cinco días. No había sufrido golpes en la cabeza antes.\n\n**Lo que Encontraron en el Examen**\n\nCuando la revisaron, no podía ver nada con ninguno de sus ojos y sus pupilas no reaccionaban a la luz. Además, no podía mover bien los ojos y le costaba abrir los párpados. En sus ojos había hinchazón y vasos sanguíneos con forma torcida. La presión dentro de sus ojos estaba muy alta, mucho más de lo normal. También encontraron sangre en un canal especial dentro del ojo derecho. Al mirar el fondo del ojo, las venas estaban un poco dilatadas, pero el nervio óptico parecía normal. Otros exámenes del cerebro y nervios no mostraron problemas.\n\n**Lo que Mostraron las Imágenes Médicas**\n\nUna resonancia magnética (una imagen del cerebro y ojos) mostró que las venas grandes que drenan la sangre de los ojos estaban muy dilatadas y había mucha congestión alrededor de los ojos. No había daño visible en los nervios ópticos, pero una prueba especial mostró que esos nervios tenían daño por falta de oxígeno, llamado neuropatía óptica isquémica posterior (PION), en ambos ojos. Otra imagen mostró que unas venas en el cerebro estaban recibiendo sangre de arterias, lo que no es normal.\n\n**Diagnóstico y Tratamiento**\n\nCon una angiografía cerebral (un estudio para ver los vasos sanguíneos), confirmaron que tenía fístulas carotídeo-cavernosas durales bilaterales. Esto significa que había conexiones anormales entre arterias y venas en una parte del cerebro llamada seno cavernoso, lo que causaba que la sangre fluyera mal y afectara los ojos. Para tratarlo, hicieron una embolización con bobinas, que es un procedimiento para cerrar esas conexiones anormales.\n\n**Resultado Después del Tratamiento**\n\nTres meses después, los signos de hinchazón y congestión en los ojos mejoraron, pero la mujer no recuperó la visión y seguía sin poder percibir luz en ambos ojos. Esto indica que el daño en los nervios ópticos fue muy grave y no se pudo revertir.",
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+      },
+      "B3": {
+        "text": "**Contexto**  \nSe presentó el caso de una mujer tailandesa de 62 años con antecedentes de hipertensión arterial mal controlada, quien experimentó una pérdida súbita de la visión en ambos ojos acompañada de cefalea durante cinco días. No reportó antecedentes de traumatismo craneal ni otros síntomas neurológicos adicionales.\n\n**Hallazgos Clave**  \nEn la evaluación oftalmológica inicial, la paciente tenía una agudeza visual de no percepción de luz (NLP) en ambos ojos, con pupilas fijas y motilidad ocular limitada en todas las direcciones. La apertura de ambos párpados fue dificultosa. El examen del segmento anterior mostró quemosis (hinchazón de la conjuntiva) bilateral y vasos episclerales con aspecto de “sacacorchos”, indicativos de congestión vascular. La presión intraocular estaba elevada, con valores de 45 mmHg en el ojo derecho y 48 mmHg en el izquierdo. La gonioscopia (evaluación del ángulo de drenaje ocular) reveló presencia de sangre en el canal de Schlemm del ojo derecho, lo que sugiere hemorragia en el sistema de drenaje ocular. El fondo de ojo mostró venas retinianas levemente dilatadas y tortuosas, pero los discos ópticos tenían una apariencia normal, con una relación copa-disco de 0.3 en ambos ojos, lo que indica ausencia de daño glaucomatoso avanzado. Otros exámenes neurológicos no mostraron alteraciones.\n\nLa resonancia magnética (MRI) con contraste evidenció dilatación de las venas oftálmicas superiores (SOV) en ambos ojos, junto con congestión marcada en las regiones orbital y periorbital. No se observaron signos de compresión o estiramiento de los nervios ópticos. Sin embargo, la resonancia ponderada en difusión (DWI) mostró restricción en la difusión con reducción del coeficiente de difusión aparente (ADC) en el segmento orbital bilateral de los nervios ópticos, hallazgo compatible con neuropatía isquémica óptica posterior (PION) bilateral, una lesión causada por falta de flujo sanguíneo en los nervios ópticos. La angiografía por resonancia magnética (MRA) reveló arterialización (flujo arterial anormal) de los senos cavernosos y las venas oftálmicas superiores bilaterales.\n\nLa angiografía cerebral confirmó la presencia de fístulas carotídeo-cavernosas (CCF) durales bilaterales con drenaje anterior. Estas fístulas eran alimentadas por ramas durales de la arteria carótida interna (ICA) y externa (ECA) en ambos lados, y contribuían al flujo arterial anómalo en las venas oftálmicas superiores, incluyendo comunicación entre ambos senos cavernosos. No se detectó reflujo venoso cortical, lo que indica que no había afectación directa de la circulación cerebral superficial.\n\n**Interpretación Clínica**  \nLa paciente presentó una forma rara y grave de fístulas carotídeo-cavernosas durales bilaterales que causaron congestión venosa orbital severa, elevación de la presión intraocular y daño isquémico bilateral en los nervios ópticos, manifestado como neuropatía isquémica óptica posterior. Esta condición explicó la pérdida visual súbita e irreversible, a pesar de la ausencia de compresión directa de los nervios ópticos.\n\n**Próximos Pasos y Evolución**  \nSe realizó una embolización transvenosa mediante colocación de bobinas para ocluir las fístulas en ambos senos cavernosos, logrando el cierre completo de las comunicaciones anómalas según la angiografía postprocedimiento. Tres meses después, la congestión y los signos oftálmicos mejoraron progresivamente, incluyendo la reducción del edema y la congestión vascular; sin embargo, la agudeza visual permaneció sin recuperación, con no percepción de luz en ambos ojos, reflejando daño irreversible en los nervios ópticos.\n\nEste caso destaca la importancia de un diagnóstico temprano y tratamiento oportuno en fístulas carotídeo-cavernosas para prevenir complicaciones graves como la pérdida visual irreversible por neuropatía isquémica óptica.",
+        "scores": {
+          "ROUGE-1": 0.5720207253886009,
+          "ROUGE-2": 0.3468328141225337,
+          "ROUGE-L-Sum": 0.5492227979274612,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
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+  },
+  {
+    "article": "Un paciente de 15 años de edad (altura = 161 cm; peso = 66 kg; superficie corporal = 1,70; grupo sanguíneo = B positivo) con cardiomiopatía dilatada fue derivado a la Universidad de Ankara con pérdida de conciencia y shock cardiogénico en julio de 2016. El apoyo de oxigenación de membrana extracorpórea venosa arterial se realizó aproximadamente 1 semana después. Su fracción de eyección ventricular izquierda fue del 22%. Ocho días después, el paciente recibió un implante de corazón artificial total SynCardia (50 ml; SynCardia Systems, Inc., Tucson, AZ, EE. UU.). En el día 131 postoperatorio después de la cirugía TAH, el paciente se quejó de pérdida de audición bilateral y fue derivado al departamento de oído, nariz y garganta.\n\nLos antecedentes médicos previos no revelaron evidencia de pérdida auditiva, antecedentes familiares de sordera o cualquier anomalía adicional en su niñez. Sus registros médicos no revelaron evidencia de meningitis. Sin embargo, había recibido amikacina (15 mg/kg), un antibiótico ototóxico, contra patógenos gramnegativos importantes durante su estancia en la unidad de cuidados intensivos. El paciente fue incluido en la lista de espera de trasplantes de corazón de alta urgencia y era móvil en el Freedom Driver portátil (SynCardia).\n\nEl examen otoscópico del paciente fue normal. La audiometría de tonos puros y la respuesta auditiva del tronco encefálico revelaron una pérdida auditiva profunda bilateral. La timpanometría mostró timpanogramas normales de tipo A bilaterales. Tanto la tomografía computarizada como la resonancia magnética confirmaron la morfología normal del laberinto y nervios cocleares intactos.\n\nFue examinado por un equipo multidisciplinario (cirugía cardiovascular, cuidados intensivos pediátricos, cardiología pediátrica, psiquiatría de consulta y enlace, fisioterapia y rehabilitación, enfermedades infecciosas y microbiología clínica, anestesiología, audiología y otorrinolaringología) para realizar un implante coclear. Después de analizar las posibles opciones con el paciente y sus padres, se decidió que se beneficiaría de un implante coclear debido a la pérdida auditiva y la reducción de la función cognitiva y la adaptación necesaria para el trasplante de corazón. Después de analizar su caso con el equipo multidisciplinario, se decidió un implante coclear del lado derecho (Nucleus CI24RE con Contour Advance Electrode; Cochlear, Macquarie University, Australia).\n\nEl paciente tomaba warfarina (10 mg/día), que se interrumpió tres días antes de la cirugía, y se inició la heparinización (dosis de carga de 50 U/kg y dosis de mantenimiento de 20 U/kg/h) cuando el tiempo de protrombina (cociente internacional normalizado [INR]) era inferior a 1,5. Dos horas antes de la cirugía, se interrumpió la heparinización. En el quirófano, se disponía de un dispositivo de reserva para un posible fallo del dispositivo TAH. El equipo de anestesia y el perfusionista controlaron de cerca los resultados del flujo para el TAH. El flujo sanguíneo no pulsátil afecta de forma negativa al control de los signos vitales, y la presión arterial no invasiva no fue suficiente en nuestro paciente. Bajo anestesia local, se realizó un cateterismo radial arterial invasivo. Además, se dejó la vena yugular interna izquierda en su lugar, lo que permitió el control de la presión venosa central y su uso como reemplazo de fluidos de gran volumen cuando fue necesario. Después de iniciar el control, se administraron con precaución 2 mg/kg de propofol, 1 mg/kg de bromuro de rocuronio y 1 µg/kg de fentanilo, y se intubió al paciente por vía oral. Se utilizó sevoflurano con una concentración alveolar mínima de 1 a 1,5 en oxígeno al 40 % para el mantenimiento. El óxido nítrico inhalado también estaba listo para usarse en caso de una posible crisis hipertensiva pulmonar.\n\nEl día 250 después del implante TAH, se realizó la cirugía de implante coclear con abordaje de ventana redonda sin complicaciones perioperatorias; el paciente tuvo una pérdida de sangre mínima (solo 50 ml). La duración de la operación fue de 120 minutos. El paciente fue extubado en el quirófano sin problemas circulatorios y respiratorios. La heparinización se inició a la hora 6 posoperatoria. Comenzamos con la warfarina el día 1 posoperatorio, y la heparinización se detuvo después de alcanzar un INR de 2.0. No se observaron complicaciones (infecciones, hematoma) en el seguimiento posoperatorio.\n\nEl implante coclear se activó en la semana 4 después de la operación. El equipo de audiología lo revisó 4 y 8 semanas después; mostró una mejora continua en su audición, con impedancias normales. Sus resultados de percepción del habla mejoraron significativamente 3 meses después del implante coclear.\n\nMH - Adolescente\nMH - Niño\nMH - *Implantación coclear\nMH - *Insuficiencia cardiaca/diagnóstico/etiología/cirugía\nMH - *Efectos adversos del trasplante de corazón\nMH - *Corazón, Artificial\nMH - Humanos\nMH - Hombre\nMH - Resultado del tratamiento\n",
+    "gold_summary": "Describimos el caso de un niño de 15 años con pérdida auditiva total bilateral postlingual tras la administración de medicamentos ototóxicos durante su estancia en la unidad de cuidados intensivos pediátricos. El paciente recibió el implante de corazón artificial total SynCardia (50 ml; SynCardia Systems, Inc., Tucson, AZ, EE. UU.) para la insuficiencia cardiaca biventricular en fase terminal como puente para el trasplante cardiaco. Durante su estancia en la lista de espera de trasplantes cardiacos urgentes, se sometió a una implantación coclear satisfactoria tras optimizar el estado de coagulación y hemostasis y una preparación anestésica adecuada.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Un niño de 15 años tuvo problemas para oír después de tomar medicinas en el hospital. Su corazón estaba muy enfermo y le pusieron un corazón artificial para ayudarlo. Mientras esperaba un nuevo corazón, le pusieron un aparato especial en el oído para que pudiera oír mejor. Los doctores cuidaron mucho que todo saliera bien en la operación. Ahora puede oír mejor y está más feliz.",
+        "scores": {
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+          "ROUGE-2": 0.09836065573770492,
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+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B2": {
+        "text": "**Caso de un Adolescente con Problemas del Corazón y Pérdida de Audición**\n\nUn joven de 15 años tenía un problema grave en su corazón llamado insuficiencia cardiaca biventricular, que significa que ambos lados de su corazón no funcionaban bien. Para ayudarlo mientras esperaba un trasplante de corazón, le pusieron un corazón artificial llamado SynCardia. \n\nDurante su tratamiento en cuidados intensivos, recibió un medicamento llamado amikacina, que puede dañar el oído y causar pérdida de audición. Después de un tiempo, el paciente empezó a perder la audición en ambos oídos. Los médicos hicieron varios exámenes y confirmaron que tenía una pérdida auditiva profunda en los dos oídos, aunque sus oídos y nervios estaban físicamente normales.\n\nPara mejorar su audición y ayudarlo a comunicarse mejor, el equipo médico decidió ponerle un implante coclear en el oído derecho. Un implante coclear es un dispositivo que ayuda a las personas con pérdida auditiva severa a escuchar sonidos. Antes de la cirugía, ajustaron cuidadosamente sus medicamentos para evitar problemas con la coagulación de la sangre, ya que él tomaba medicinas para el corazón que afectan esto.\n\nLa operación para colocar el implante coclear fue exitosa y sin complicaciones. Después de la cirugía, el paciente mejoró su capacidad para oír y entender el habla, lo que es muy importante para su calidad de vida y para prepararse para el futuro trasplante de corazón.\n\nEn resumen, este caso muestra cómo un adolescente con un corazón artificial y pérdida auditiva causada por medicamentos pudo recibir un implante coclear con buenos resultados, gracias al trabajo de un equipo médico especializado y una cuidadosa preparación.",
+        "scores": {
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+          "ROUGE-2": 0.11707317073170731,
+          "ROUGE-L-Sum": 0.2815533980582524,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
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+      },
+      "B3": {
+        "text": "**Contexto**  \nPresentamos el caso de un adolescente de 15 años con insuficiencia cardiaca biventricular avanzada, que requirió el implante de un corazón artificial total SynCardia como medida temporal mientras esperaba un trasplante de corazón. Durante su hospitalización en cuidados intensivos, recibió amikacina, un antibiótico conocido por su potencial daño al oído (ototoxicidad). Posteriormente, desarrolló una pérdida auditiva profunda bilateral, detectada aproximadamente 131 días después de la implantación del corazón artificial.\n\n**Hallazgos Clave**  \n- El paciente no tenía antecedentes previos de pérdida auditiva ni factores familiares que sugirieran sordera.  \n- Las pruebas audiológicas confirmaron una pérdida auditiva profunda en ambos oídos, mientras que los estudios de imagen mostraron estructuras normales del oído interno y nervios cocleares intactos.  \n- La evaluación multidisciplinaria concluyó que un implante coclear era la mejor opción para mejorar su audición y facilitar su adaptación cognitiva y funcional en el contexto del trasplante cardíaco.  \n- La cirugía de implante coclear se realizó con éxito, tras una cuidadosa preparación para manejar los riesgos relacionados con la anticoagulación y la función del corazón artificial.  \n- No hubo complicaciones perioperatorias significativas, y la activación del implante coclear mostró una mejora progresiva en la audición y la percepción del habla en los meses siguientes.\n\n**Interpretación Clínica**  \nEste caso ilustra cómo la ototoxicidad inducida por medicamentos puede causar una pérdida auditiva severa en pacientes críticos, incluso en adolescentes sin antecedentes previos. La coordinación entre múltiples especialidades fue fundamental para manejar los riesgos asociados a la anticoagulación y la anestesia en un paciente con un dispositivo cardíaco artificial, permitiendo una intervención auditiva efectiva que mejoró significativamente su calidad de vida y capacidad de comunicación.\n\n**Próximos Pasos**  \nSe recomienda continuar con el seguimiento audiológico y rehabilitación auditiva para maximizar los beneficios del implante coclear. Además, se debe mantener una vigilancia estrecha de la función cardíaca y del estado anticoagulante, especialmente en el contexto del trasplante cardíaco futuro. Este caso destaca la importancia de la detección temprana y el manejo multidisciplinario de las complicaciones auditivas en pacientes con enfermedades cardíacas complejas.",
+        "scores": {
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+          "ROUGE-2": 0.10288065843621398,
+          "ROUGE-L-Sum": 0.25,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      }
+    }
+  },
+  {
+    "article": "Se encontró a un hombre de 25 años de edad recostado por familiares después de una noche de fiesta, con vómitos, agresión y dolor localizado en la región glútea e inferior derecha. La evaluación inicial en el departamento de urgencias no reveló lesiones traumáticas; sin embargo, el empeoramiento de los síntomas llevó a una nueva evaluación al día siguiente. Los resultados de laboratorio revelaron un recuento sanguíneo completo sin alteraciones, niveles elevados de CPK sérica (42 527 IU/l), creatinina sérica (735 µmol/l), urea (44,3 mmol/l) y potasio (5,7 mmol/l). El análisis de orina reveló orina de color rojo-marrón sin glóbulos rojos, proteinuria (+1), glucosuria (+1) y WBC (9-10/hpf). Estos resultados confirmaron la RM y la IRA. La toxicología estableció la administración de 1796 µg/l de heroína (> 5 veces el nivel basal) sin detección de ninguna otra sustancia. Aunque inicialmente negó haber tomado medicamentos, después del análisis toxicológico, el paciente admitió que había administrado heroína una vez por vía intramuscular en la región glútea derecha la noche del incidente.\n\nUna tomografía computarizada demostró edema muscular glúteo y miositis localizada en la región glútea derecha. Al comenzar el tratamiento convencional con resucitación de fluidos intravenosos (IV), el tratamiento de la IRA fracasó, lo que hizo necesario el TRR con hemodiálisis debido a la progresión de la azotemia con un aumento de la creatinina sérica a 1052 µmol/l. La función renal mejoró tras el cese del TRR con una duración total de la estancia (LOS) de 9 días. El seguimiento posterior del paciente fue incompleto debido a la falta de asistencia.\n",
+    "gold_summary": "Este informe de caso describe a un hombre de 25 años que desarrolló una RM grave y lesión renal aguda (LRA) después de la administración intramuscular (IM) de heroína como usuario por primera vez. El uso de la heroína IM puede inducir niveles más altos de CPK debido a la toxicidad directa de los miocitos y el trauma mecánico. Los músculos glúteos altamente vascularizados con fibras tipo 1 en el sitio de la inyección probablemente exacerbaron la gravedad. Los factores adicionales incluyeron una menor densidad mitocondrial en los hombres y la exposición al alcohol. A pesar de la reanimación agresiva con líquidos, se requirió la terapia de reemplazo renal (RRT) y el paciente respondió bien a la hemodiálisis.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Un hombre joven se lastimó el músculo de su nalga. Esto pasó porque se puso una medicina mala llamada heroína en esa parte. Su cuerpo se enfermó mucho y sus riñones también se lastimaron. \n\nLos doctores le dieron muchos líquidos para ayudarlo. Pero su riñón no mejoró solo. Entonces, usaron una máquina especial para limpiar su sangre. Después, el hombre empezó a sentirse mejor.",
+        "scores": {
+          "ROUGE-1": 0.23414634146341465,
+          "ROUGE-2": 0.04926108374384237,
+          "ROUGE-L-Sum": 0.21463414634146344,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
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+      "B2": {
+        "text": "**Lo que pasó con el paciente**  \nUn hombre de 25 años usó heroína por primera vez y se la inyectó en el músculo de la nalga derecha. Después de eso, empezó a sentirse muy mal, con dolor, vómitos y agresividad. Cuando llegó al hospital, no encontraron heridas, pero sus síntomas empeoraron al día siguiente.\n\n**Qué encontraron los médicos**  \nLos análisis de sangre mostraron que tenía niveles muy altos de una enzima llamada CPK, que indica daño en los músculos. También tenía problemas en los riñones, con niveles altos de creatinina y urea, que son sustancias que el riñón normalmente limpia. La orina estaba de color rojo-marrón, pero sin sangre visible, lo que es un signo de daño muscular y renal. La tomografía mostró inflamación en el músculo de la nalga donde se inyectó la droga.\n\n**Qué significa todo esto**  \nEl hombre sufrió una condición llamada rabdomiólisis, que es cuando los músculos se dañan mucho y liberan sustancias que pueden dañar los riñones. Esto ocurrió por la inyección directa de heroína en el músculo, que causó daño tanto por la droga como por el trauma de la aguja. Además, factores como el alcohol y diferencias en el cuerpo de los hombres pueden haber empeorado la situación.\n\n**Cómo lo trataron**  \nLe dieron líquidos por vía intravenosa para ayudar a limpiar sus riñones, pero esto no fue suficiente. Por eso, tuvo que recibir un tratamiento especial llamado hemodiálisis, que es una máquina que hace el trabajo de los riñones cuando están muy dañados. Después de varios días, su función renal mejoró y pudo dejar el tratamiento.\n\n**Conclusión**  \nEste caso muestra que inyectarse heroína en el músculo puede causar un daño muscular grave y problemas serios en los riñones, incluso en personas que la usan por primera vez. Es importante buscar ayuda médica rápido si alguien presenta síntomas después de usar drogas de esta forma.",
+        "scores": {
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+          "ROUGE-2": 0.12474849094567406,
+          "ROUGE-L-Sum": 0.3326653306613226,
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+      "B3": {
+        "text": "**Contexto**  \nEste caso clínico presenta a un hombre de 25 años que sufrió una lesión muscular grave conocida como rabdomiólisis (RM) y una lesión renal aguda (LRA) tras administrarse heroína por primera vez mediante una inyección intramuscular (IM) en la región glútea derecha. La rabdomiólisis es una condición en la que el daño muscular libera sustancias tóxicas en la sangre, lo que puede afectar negativamente a los riñones.\n\n**Hallazgos Clave**  \nEl paciente fue encontrado después de una noche de consumo de sustancias, con síntomas de vómitos, agresividad y dolor intenso en la zona glútea derecha. Inicialmente, no se detectaron lesiones traumáticas, pero al empeorar sus síntomas, se realizaron análisis que mostraron niveles extremadamente elevados de creatina fosfoquinasa (CPK) sérica (42,527 IU/l), un marcador que indica daño muscular severo. Además, presentó alteraciones en la función renal, evidenciadas por un aumento significativo de creatinina y urea en sangre, así como cambios en el análisis de orina, que mostraba orina de color rojo-marrón sin glóbulos rojos, proteinuria (presencia de proteínas) y glucosuria (presencia de glucosa), signos compatibles con daño renal. La toxicología confirmó una concentración elevada de heroína en sangre, y el paciente finalmente admitió haberse inyectado heroína en el glúteo la noche previa.\n\nUna tomografía computarizada reveló inflamación y edema (hinchazón) muscular en la región glútea derecha, confirmando la miositis (inflamación muscular) localizada.\n\n**Interpretación Clínica**  \nLa administración intramuscular de heroína puede causar daño muscular directo debido a la toxicidad de la droga sobre las células musculares (miocitos) y al trauma mecánico producido por la inyección. La región glútea, por su alta vascularización y predominancia de fibras musculares tipo 1 (que tienen características metabólicas específicas), probablemente contribuyó a la gravedad del daño. Además, factores como una menor densidad mitocondrial en hombres (las mitocondrias son las \"centrales energéticas\" de las células) y la exposición al alcohol podrían haber exacerbado la lesión muscular y renal.\n\nA pesar de iniciar un tratamiento convencional con líquidos intravenosos para intentar revertir la lesión renal, el daño progresó, requiriendo la implementación de terapia de reemplazo renal mediante hemodiálisis. Tras este tratamiento, la función renal del paciente mejoró, permitiendo su alta hospitalaria después de nueve días.\n\n**Próximos Pasos**  \nEl seguimiento posterior del paciente fue limitado debido a su falta de asistencia a controles médicos, lo que dificulta evaluar su recuperación a largo plazo y la prevención de complicaciones futuras. Este caso resalta la importancia de la detección temprana y el manejo adecuado de la rabdomiólisis inducida por drogas, así como la necesidad de apoyo y seguimiento continuo en pacientes con consumo de sustancias para evitar daños graves y mejorar los resultados clínicos.",
+        "scores": {
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+          "ROUGE-2": 0.18322981366459626,
+          "ROUGE-L-Sum": 0.3250773993808049,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
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+  {
+    "article": "Una mujer de 63 años con antecedentes de obesidad e hipertensión arterial acudió a la sala de urgencias de un hospital de nivel secundario con un historial de siete días de fiebre, tos seca, hiposmia y mialgia. Al momento del ingreso, se encontraba alerta, con una frecuencia respiratoria de 22 ciclos por minuto, pulso de 90 latidos por minuto y saturación de oxígeno de 90 %. Los análisis de laboratorio revelaron linfopenia (1,55 x 109) y niveles elevados de proteína C reactiva (10,62 mg/dL). Se realizó una prueba de reacción en cadena de la polimerasa para COVID-19 a partir de un hisopado nasofaríngeo y de la garganta, que resultó positivo para el coronavirus del síndrome respiratorio agudo severo 2 (SARS-CoV-2).\n\nLa situación evolucionó rápidamente con fiebre, postración y empeoramiento de la disnea. La gasometría arterial reveló una insuficiencia respiratoria grave, mientras que la radiografía de tórax evidenció infiltrados pulmonares bilaterales. La paciente fue intubada y sometida a ventilación mecánica, pero su condición respiratoria continuó deteriorándose, a pesar de los mejores cuidados críticos, incluyendo ventilación en posición prona y bloqueo neuromuscular. Su examen de tomografía computarizada del tórax, tras la intubación, reveló extensas opacificaciones multifocales bilaterales en vidrio molido, sin signos de embolia pulmonar. Los ajustes iniciales del ventilador fueron: ventilación controlada por volumen con volumen corriente de 360 ml (6 ml/kg de peso corporal ideal), frecuencia respiratoria de 14 respiraciones por minuto, presión espiratoria positiva final (PEEP) de 14 cmH2O y complacencia estática de 44 cmH2O.\n\nEn el segundo día de internación, la gasometría arterial mostró pH de 7,34, presión parcial de dióxido de carbono (PaCO2) de 53 mmHg, presión parcial de oxígeno (PaO2) de 102 mmHg y bicarbonato (HCO3) de 29,7 mmol/L, con una proporción presión parcial de oxígeno/fracción inspirada de oxígeno (PaO2/FiO2) de 98. Ella cumplía los criterios para indicación de VV-ECMO y fue transferida a la unidad de terapia intensiva (UTI), que disponía de un programa establecido para VV-ECMO. El procedimiento fue realizado con seguridad, no habiendo ocurrido complicaciones. El análisis de la gasometría arterial 3 horas después del inicio de la VV-ECMO mostró pH de 7,386, PaCO2 de 43 mmHg, PaO2 de 94,3 mmHg y HCO3 de 25,4 mmol/L, sin cualquier variación abruta de la PaCO2. Tuvieron inicio la nutrición y la rehabilitación precoces tras la introducción de la VV-ECMO. En el 14º día de internación, la paciente desarrolló neumonía asociada al ventilador causada por Pseudomonas aeruginosa, siendo sometida a 7 días de antibioticoterapia con ceftazidima y vancomicina, con respuesta favorable. En el 20º día de internación, su radiografía del tórax y la complacencia mejoraron, y la paciente fue retirada de la VV-ECMO con éxito tras 455 horas de soporte, siendo traqueostomizada 7 días después. La paciente mantuvo buena función renal durante toda la internación.\n\nEn el día 34 de internación, luego de 7 días de destete de la sedación, con evolución positiva de su cuadro neurológico, ocurrió una crisis epiléptica generalizada limitada, que llevó a la investigación diagnóstica.\n\nInvestigación\nLos análisis de sangre de laboratorio revelaron una disminución de los niveles de proteína C reactiva (6,11 mg/dL), procalcitonina (0,07 ng/mL), fibrinógeno (307 ng/mL) y ferritina (2802 ng/mL), pero un aumento en los niveles de dímero D (18021 ng/mL) e interleucina 6 (10,4 pg/mL) en el día anterior al inicio de los síntomas. No se asoció ninguno de los fármacos administrados a la paciente con el SEPR, es decir, fármacos inmunosupresores, inmunomoduladores y quimioterápicos.\n\nSe realizó una resonancia magnética (RM) del cerebro y las imágenes de recuperación de inversión atenuada por fluidos (FLAIR) demostraron una hiperintensidad simétrica y confluente que afectaba a la sustancia blanca justa y subcortical, principalmente en las regiones occipital y parietal, pero también en la región frontal, temporal y cerebelosa izquierda. Los núcleos grises profundos se conservaron y no había presencia de ninguna área con restricción del contraste. Las imágenes ponderadas por susceptibilidad mostraron múltiples microhemorragias puntiformes que afectaban a la sustancia blanca superficial y profunda, pero que no afectaban al área con hiperintensidad en FLAIR. Las microhemorragias puntiformes involucraban predominantemente a la sustancia blanca justacortical y al cuerpo calloso (especialmente el codo y el esplenio). Además, había tres hemorragias subagudas de menos de 1 cm en las cápsulas externas, con hiperintensidad en T1.\n\nLa muestra de líquido cefalorraquídeo dio negativo para SARS-CoV-2 y los niveles de proteínas (31 mg/dL), glucosa (74 mg/dL) y lactato (1,89 mmol/L) se encontraban dentro de los parámetros normales.\n\nDesvelado\nLa paciente logró una recuperación casi total de los déficits neurológicos, a pesar de la miopatía de la enfermedad crítica, y fue dada de alta después de 44 días en el hospital. Se la derivó a un hospital secundario para su rehabilitación y prácticamente recuperó su estado mental previo.\n",
+    "gold_summary": "Una mujer de 63 años de edad acudió a la sala de urgencias con un historial de fiebre aguda, postración y disnea. Se le diagnosticó un caso grave de COVID-19 y síndrome de dificultad respiratoria aguda. A pesar de recibir atención médica intensiva, cumplía con los requisitos para someterse a una oxigenación por membrana extracorpórea. El día 34, luego de siete días de haber suspendido la sedación y de que su cuadro neurológico hubiera evolucionado de manera positiva, presentó una crisis tónico-clónica generalizada limitada, que no guardaba relación con un desequilibrio hidroelectrolítico o metabólico, lo que hizo necesario realizar una investigación diagnóstica. Los estudios de imágenes cerebrales revelaron un síndrome de encefalopatía posterior reversible.\n",
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+        "text": "Una señora muy enferma tenía fiebre y le costaba respirar. Tenía un virus que le hizo mucho daño en los pulmones. Los doctores le pusieron una máquina para ayudarla a respirar mejor.\n\nDespués de muchos días, la señora empezó a mejorar. Pero un día tuvo un problema en su cabeza que la asustó. Los doctores hicieron unas fotos especiales de su cerebro. Vieron que su cerebro estaba un poco dañado, pero podía mejorar.\n\nLa señora se puso mejor y los doctores la cuidaron mucho para que se sintiera bien otra vez.",
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+        "text": "**Lo que le pasó a la paciente**  \nUna mujer de 63 años llegó al hospital con fiebre alta, mucho cansancio y dificultad para respirar. Los médicos descubrieron que tenía COVID-19 muy grave y un problema llamado síndrome de dificultad respiratoria aguda, que afecta los pulmones y dificulta la respiración. Aunque recibió cuidados intensivos, su condición empeoró y necesitó un tratamiento especial llamado oxigenación por membrana extracorpórea (VV-ECMO). Este tratamiento ayuda a oxigenar la sangre cuando los pulmones no funcionan bien.\n\n**Qué pasó después**  \nDespués de 34 días en el hospital y tras dejar la sedación (medicamentos para dormirla) durante una semana, la paciente tuvo una crisis convulsiva, que es un movimiento fuerte y descontrolado del cuerpo. Esta crisis no se debió a problemas con líquidos o sustancias en su cuerpo, por lo que los médicos hicieron más estudios para entender la causa.\n\n**Lo que mostraron los estudios**  \nLas imágenes del cerebro mostraron un problema llamado síndrome de encefalopatía posterior reversible. Esto significa que algunas partes del cerebro estaban inflamadas o dañadas temporalmente, pero que esta condición puede mejorar con tratamiento. Gracias a la atención médica y la rehabilitación, la paciente casi recuperó completamente sus funciones cerebrales y fue dada de alta después de 44 días en el hospital.",
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+        "text": "**Contexto**  \nUna mujer de 63 años con antecedentes de obesidad e hipertensión presentó un cuadro de siete días con fiebre, tos seca, pérdida del olfato (hiposmia) y dolores musculares. Al ingresar al hospital, mostró signos de insuficiencia respiratoria leve y fue diagnosticada con COVID-19 mediante una prueba PCR. Su condición respiratoria empeoró rápidamente, desarrollando un síndrome de dificultad respiratoria aguda (SDRA) que requirió intubación y ventilación mecánica. Debido a la gravedad del compromiso pulmonar, fue sometida a oxigenación por membrana extracorpórea venovenosa (VV-ECMO), un soporte avanzado para mantener la oxigenación cuando los pulmones no funcionan adecuadamente.\n\n**Hallazgos Clave**  \nTras 34 días de hospitalización y después de haber suspendido la sedación durante una semana con mejoría neurológica, la paciente sufrió una crisis epiléptica generalizada limitada. Esta convulsión no se relacionó con alteraciones metabólicas o desequilibrios hidroelectrolíticos, por lo que se inició una investigación neurológica. La resonancia magnética cerebral mostró un patrón característico de síndrome de encefalopatía posterior reversible (SEPR), que se manifiesta por áreas de inflamación y edema en la sustancia blanca del cerebro, especialmente en regiones occipitales y parietales, sin daño permanente. Además, se detectaron microhemorragias puntiformes en la sustancia blanca, pero el líquido cefalorraquídeo no mostró infección ni inflamación activa.\n\n**Interpretación Clínica**  \nEl SEPR es una condición neurológica que puede presentarse en pacientes críticos y se caracteriza por síntomas como convulsiones, alteraciones visuales y cefalea, acompañados de cambios reversibles en el cerebro. En este caso, la aparición del SEPR después de una infección grave por COVID-19 y soporte con VV-ECMO sugiere una relación con la inflamación sistémica y posibles alteraciones vasculares inducidas por el virus o el tratamiento intensivo. La ausencia de infección directa del virus en el sistema nervioso central y la normalidad del líquido cefalorraquídeo apoyan esta hipótesis.\n\n**Próximos Pasos y Evolución**  \nLa paciente recibió tratamiento adecuado para la crisis epiléptica y cuidados de soporte neurológico. A pesar de la miopatía asociada a la enfermedad crítica, logró una recuperación casi completa de sus funciones neurológicas. Fue dada de alta tras 44 días de hospitalización y remitida a un centro de rehabilitación, donde continuó mejorando hasta recuperar prácticamente su estado mental previo al ingreso.\n\nEste caso resalta la importancia de la vigilancia neurológica en pacientes con COVID-19 grave, especialmente aquellos sometidos a terapias avanzadas como la VV-ECMO, para detectar y tratar complicaciones como el síndrome de encefalopatía posterior reversible.",
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+    "article": "Mujer de 65 años, originaria y residente de la Ciudad de México, con antecedente de infección por VIH de 20 años de diagnóstico con carga viral indetectable desde 2020 y con cuenta de CD4 de 1220 células por mililitro en febrero de 2022, hipotiroidismo de 29 años, cardiopatía isquémica de 9 años de diagnóstico, osteoporosis y dislipidemia, en tratamiento y bajo control médico.\n\nSu dermatosis problema se inició 10 años atrás, después de un cuadro de herpes zóster localizado en la extremidad inferior derecha y se complicó con una infección de tejidos blandos, referida como celulitis. Como secuela de este evento la paciente desarrolló úlcera, la cual ameritó corrección del defecto con 4 injertos cutáneos en diferentes tiempos quirúrgicos por cirugía plástica, con acompañamiento por parte de la clínica de heridas. Durante el seguimiento y a pesar de las medidas tomadas, no logró resolución completa y persistió con una úlcera asociada a dolor local, motivo de su envío a nuestro servicio.\n\nA la exploración física presentaba una dermatosis localizada en la extremidad inferior derecha, en la cara lateral del muslo, caracterizada por una neoformación aplanada sobre la que se asentaba una úlcera de 1.5 cm de diámetro, con fondo limpio, con costra sero-amarillenta, bordes sobreelevados, piel perilesional hiperpigmentada y queratósica, una cicatriz atrófica e hiperpigmentada. Se inició abordaje de la dermatosis mediante biopsia de piel, con reporte histopatológico de carcinoma verrugoso, por lo que se concluyó como úlcera de Marjolin asociada a carcinoma verrugoso en paciente portadora de VIH. Se canalizó al hospital de oncología para manejo con radioterapia.",
+    "gold_summary": "mujer de 65 años con el antecedente de ser portadora de infección por virus de inmunodeficiencia humana (VIH), que presentó un carcinoma verrugoso asociado a una úlcera de Marjolin secundaria a herpes zóster e infección de tejidos blandos en pierna derecha, con un periodo de latencia de 10 años desde el proceso infeccioso inicial hasta la confirmación histopatológica.",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Una señora de 65 años tuvo una herida en su pierna. La herida empezó hace mucho tiempo por una infección. La herida no sanó bien y cambió. Los doctores vieron que la herida tenía una enfermedad que puede crecer. Ella recibe ayuda para mejorar.",
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+        "text": "### Lo que pasó con la paciente\n\nUna mujer de 65 años, que vive en la Ciudad de México y tiene VIH controlado desde hace varios años, desarrolló un problema en la piel de su pierna derecha. Hace 10 años, tuvo una infección llamada herpes zóster, que afectó esa zona. Después, sufrió una infección en los tejidos blandos (la parte blanda bajo la piel), llamada celulitis. Esto causó una herida o úlcera que no sanaba bien.\n\n### Lo que encontraron\n\nA pesar de varios tratamientos, incluyendo cirugías para poner injertos de piel, la úlcera siguió abierta y le causaba dolor. Cuando la revisaron, vieron una lesión con una herida de 1.5 cm en el muslo derecho. Tomaron una biopsia, que es cuando se extrae un pequeño pedazo de piel para examinarlo bajo el microscopio. El examen mostró que la úlcera tenía un tipo de cáncer llamado carcinoma verrugoso, que es un tumor que crece lentamente y parece una verruga.\n\n### Qué significa\n\nEsta úlcera se llama úlcera de Marjolin, que es una herida crónica que puede convertirse en cáncer después de muchos años. En este caso, la úlcera apareció después de la infección por herpes zóster y la celulitis, y tardó 10 años en transformarse en cáncer. Debido a esto, la paciente fue enviada a un hospital especializado para recibir tratamiento con radioterapia, que usa rayos para destruir las células cancerosas.\n\nEn resumen, una infección antigua en la pierna causó una herida que no sanó y, con el tiempo, se convirtió en un tipo de cáncer en la piel. Por eso es importante cuidar bien las heridas que no se curan y revisarlas con el médico.",
+        "scores": {
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+      "B3": {
+        "text": "Contexto  \nSe trata de una mujer de 65 años con diagnóstico de infección por VIH desde hace 20 años, con carga viral indetectable y buen conteo de células CD4, además de otras condiciones crónicas como hipotiroidismo, cardiopatía isquémica, osteoporosis y dislipidemia, todas bajo control médico. Hace 10 años, tras un episodio de herpes zóster en la pierna derecha que se complicó con una infección de tejidos blandos (celulitis), desarrolló una úlcera en esa zona. A pesar de múltiples intervenciones quirúrgicas con injertos cutáneos y seguimiento especializado, la úlcera persistió y causó dolor local.\n\nHallazgos Clave  \nDurante la evaluación clínica, se observó una lesión en la cara lateral del muslo derecho consistente en una neoformación aplanada con una úlcera de 1.5 cm de diámetro, bordes elevados, piel circundante oscura y engrosada, y una cicatriz atrófica. La biopsia de piel reveló la presencia de un carcinoma verrugoso, que es un tipo de cáncer de piel de crecimiento lento y aspecto verrugoso (similar a una verruga). Este hallazgo confirmó que la úlcera crónica correspondía a una úlcera de Marjolin, que es una lesión maligna que puede desarrollarse en cicatrices o heridas crónicas.\n\nInterpretación Clínica  \nLa paciente presentó un carcinoma verrugoso asociado a una úlcera de Marjolin que se originó como secuela de una infección previa por herpes zóster y celulitis en la pierna derecha. El periodo de latencia entre el evento infeccioso inicial y la aparición del cáncer fue de aproximadamente 10 años. Esta condición es poco frecuente pero importante, ya que las úlceras crónicas pueden transformarse en lesiones malignas, especialmente en pacientes con factores de riesgo como el VIH.\n\nPróximos Pasos  \nLa paciente fue referida al hospital de oncología para recibir tratamiento con radioterapia, que es una modalidad adecuada para este tipo de carcinoma. Se requiere un seguimiento estrecho para evaluar la respuesta al tratamiento y prevenir complicaciones adicionales. Además, es fundamental mantener un control riguroso de sus condiciones crónicas y del estado inmunológico para optimizar su recuperación.",
+        "scores": {
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+    "article": "Una mujer de 90 años con hepatitis C y un historial de tabaquismo de 60 años proveniente de una zona rural presentó una hinchazón en la cara posteromedial del muslo izquierdo justo por encima de la rodilla. La hinchazón se notó por primera vez hace 3 años y aumentó gradualmente de tamaño durante este período. Ella sintió un leve malestar, pero niega cualquier síntoma asociado de dolor, picazón, secreción, fiebre o inmovilidad articular. Como provenía de una zona rural, también tenía un historial de exposición a animales.\nEn el examen físico, la hinchazón tenía una forma esférica de 14 × 10, era firme, fija y no sensible, con márgenes bien definidos en el aspecto posteromedial del muslo izquierdo, justo por encima de la rodilla. La piel que la recubría era pellizcable y mostraba venas prominentes, y la temperatura era comparable a la de la piel circundante.\nLa ecografía reveló una lesión quística grande con varios quistes pequeños en su interior, que medían 13,2 × 11 × 13,6 cm y un volumen de 1046 ml. Se originaba en la articulación de la rodilla izquierda y se extendía hasta la mitad del muslo. La ecografía Doppler en color no mostró vascularización en su interior. Se realizó una resonancia magnética que mostró una lesión quística grande (21 × 9,9 × 8,1 cm) con múltiples lesiones pequeñas dispersas, con extensión intramuscular e intermuscular que afectaban al aductor largo y al gracilis de manera medial y al bíceps femoral de manera posterior. Todas estas características eran indicativas de un quiste hidatídico. El diagnóstico se confirmó mediante una prueba de hemaglutinación para Echinococcus. La radiografía de tórax y la ecografía abdominal fueron normales.\nSe planificó la escisión quirúrgica de la tumefacción quística y se realizó una incisión en forma de S en la piel, seguida de una disección cuidadosa a través del tejido subcutáneo para acceder al quiste. La lesión estaba bien definida dentro de los planos intermuscular e intramuscular. Se realizó una disección meticulosa para aislar y extraer el quiste intacto, asegurando que no se derramara su contenido. Para minimizar el riesgo de contaminación, se irrigó a fondo el sitio quirúrgico con solución salina normal después de la escisión.\nLos hallazgos intraoperatorios revelaron una gran hinchazón quística intermuscular de 22 × 14 cm, que involucraba los compartimentos posterior y medial del muslo izquierdo. El quiste demostró extensión intramuscular hacia el aductor largo y el gracilis medialmente y hacia el bíceps femoral posteriormente, extendiéndose hasta la fosa poplítea. Cabe destacar que no había comunicación entre el quiste y la articulación de la rodilla. Una biopsia enviada al laboratorio confirmó aún más el diagnóstico. El examen histopatológico de la muestra extirpada reveló una pared quística fibrocondrogénica revestida por epitelio atenuado con infiltración inflamatoria. La presencia de material queratinoso focal caracterizó aún más la lesión. Estos hallazgos, junto con las características macroscópicas, favorecieron el diagnóstico de un quiste hidatídico. El curso postoperatorio fue sin complicaciones y el paciente fue dado de alta con una terapia antihelmíntica durante seis semanas. Se programaron visitas de seguimiento a la semana, tres semanas, seis semanas, nueve semanas y doce semanas. Durante estas visitas, el paciente no mostró signos de recurrencia o complicaciones.\n",
+    "gold_summary": "Una mujer de 90 años de edad, proveniente de una zona rural, presentó una hinchazón de crecimiento lento en el muslo posteromedial durante tres años. No tenía antecedentes de traumatismos ni síntomas sistémicos. El examen clínico reveló una masa firme y no dolorosa. Las imágenes sugieren una lesión quística, y la serología confirmó la infección por Echinococcus. Se realizó la extirpación quirúrgica, y la histopatología confirmó un quiste hidatídico. La paciente recibió un tratamiento posoperatorio de albendazol durante seis semanas. Su recuperación fue sin incidentes, sin recurrencia en el seguimiento.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Había una abuela de 90 años con una bola en su muslo. La bola creció muy despacito por tres años. No le dolía ni tenía fiebre. El doctor vio que la bola era dura y no hacía daño. Hicieron unas fotos especiales y encontraron que había un bichito dentro. El doctor sacó la bola con una operación. Luego, la abuela tomó medicina para quitar el bichito. Ella se puso bien y no volvió a salir la bola.",
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+      },
+      "B2": {
+        "text": "**Lo que Encontraron**  \nUna mujer de 90 años que vivía en una zona rural notó una hinchazón en la parte trasera y media de su muslo izquierdo, justo encima de la rodilla. Esta hinchazón creció lentamente durante tres años. No tenía dolor ni otros síntomas como fiebre o enrojecimiento. Al examinarla, los médicos encontraron una masa firme y que no dolía al tocarla.\n\n**Qué Significan las Pruebas**  \nLas imágenes por ecografía y resonancia mostraron que la hinchazón era un quiste grande, que es una bolsa llena de líquido. Además, la prueba de sangre confirmó que estaba infectada por un parásito llamado Echinococcus, que puede causar un quiste hidatídico. Este tipo de quiste se forma cuando el parásito crea una bolsa en el cuerpo.\n\n**El Tratamiento y Resultado**  \nLos médicos operaron para quitar el quiste completo, con mucho cuidado para no romperlo y evitar que el parásito se esparciera. Después de la cirugía, la muestra del quiste fue analizada y confirmó el diagnóstico. La paciente tomó un medicamento llamado albendazol durante seis semanas para eliminar cualquier parásito restante. Su recuperación fue buena y no tuvo problemas ni volvió a aparecer la hinchazón en las revisiones posteriores.\n\nEn resumen, esta mujer tuvo un quiste causado por un parásito, que fue tratado con cirugía y medicina, y se recuperó sin complicaciones.",
+        "scores": {
+          "ROUGE-1": 0.43181818181818177,
+          "ROUGE-2": 0.18857142857142856,
+          "ROUGE-L-Sum": 0.4147727272727273,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nUna mujer de 90 años, originaria de una zona rural y con antecedentes de hepatitis C y tabaquismo prolongado, consultó por una hinchazón en la parte posterior y medial del muslo izquierdo, justo por encima de la rodilla. Esta masa había aparecido hace tres años y había ido aumentando de tamaño de forma gradual. La paciente no presentaba dolor, fiebre, picazón ni otros síntomas asociados, y no refería antecedentes de traumatismos recientes. Además, tenía historial de contacto con animales debido a su entorno rural.\n\n**Hallazgos Clave**  \nEn el examen físico, se detectó una masa esférica, firme, fija y no dolorosa, de aproximadamente 14 × 10 cm, con bordes bien definidos y piel sobre la lesión que se podía pellizcar, mostrando venas prominentes pero sin aumento de temperatura local. La ecografía reveló una lesión quística grande con múltiples quistes pequeños en su interior, originada en la articulación de la rodilla y extendiéndose hacia la mitad del muslo, sin vascularización interna. La resonancia magnética confirmó estas características, mostrando además extensión intramuscular e intermuscular en músculos específicos del muslo. Estos hallazgos fueron altamente sugestivos de un quiste hidatídico (una infección parasitaria causada por el Echinococcus). La confirmación diagnóstica se realizó mediante una prueba serológica de hemaglutinación para Echinococcus. Estudios adicionales, como radiografía de tórax y ecografía abdominal, no mostraron afectación en otros órganos.\n\n**Interpretación Clínica**  \nEl diagnóstico de quiste hidatídico en el muslo, aunque poco común, fue confirmado mediante imágenes, pruebas serológicas y análisis histopatológico. La lesión representaba una masa quística con múltiples compartimentos, infiltrando tejidos musculares pero sin comunicación con la articulación de la rodilla. La histología mostró una pared quística con infiltración inflamatoria y material característico del parásito, confirmando la naturaleza hidatídica de la lesión.\n\n**Próximos Pasos y Tratamiento**  \nSe planificó y llevó a cabo la extirpación quirúrgica completa del quiste mediante una incisión en forma de S, con una disección cuidadosa para evitar la ruptura y contaminación del área. El sitio quirúrgico fue irrigado con solución salina para minimizar riesgos de diseminación. El postoperatorio transcurrió sin complicaciones, y la paciente recibió tratamiento antiparasitario con albendazol durante seis semanas para asegurar la erradicación del parásito. Se realizaron controles periódicos a las 1, 3, 6, 9 y 12 semanas posteriores a la cirugía, durante los cuales no se evidenció recurrencia ni complicaciones.\n\nEn resumen, este caso ilustra la importancia de considerar infecciones parasitarias como causa de masas quísticas en pacientes de zonas rurales, y demuestra que un abordaje quirúrgico cuidadoso combinado con terapia antiparasitaria puede conducir a una recuperación exitosa sin recurrencia.",
+        "scores": {
+          "ROUGE-1": 0.3018242122719734,
+          "ROUGE-2": 0.16306156405990016,
+          "ROUGE-L-Sum": 0.2885572139303483,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      }
+    }
+  },
+  {
+    "article": "Una paciente de 21 años de edad, soltera, con antecedentes de hipertensión y feocromocitoma metastásico, se presentó en nuestro hospital. Su cáncer se ha metastatizado en la vejiga, los huesos y los pulmones. También tiene un fuerte historial familiar de neoplasias, en particular de feocromocitoma. La paciente fue admitida debido a la hipertensión no controlada y los síntomas crónicos relacionados con su enfermedad.\n\nEn el ingreso (09/06/2024), la paciente era normotensa (PA: 104/66 mmHg), su frecuencia cardiaca era de aproximadamente 90 latidos por minuto, afebril a 36.9°C, y tenía una saturación de oxígeno de 99% en aire ambiente. El examen físico indicó un estado de desempeño del Grupo Cooperativo de Oncología del Este (ECOG) de 2, palidez consistente con anemia crónica, latido cardiaco regular sin murmullos o sonidos adicionales. El examen abdominal no fue notable, y no se observó edema o equimosis en las extremidades inferiores.\n\nLa paciente tiene antecedentes de hipertensión y paraganglioma, su medicación incluye (Doxazosin 2 mg, Labetalol 100 mg, Oxibutinina 5 mg, Aceite de parafina, Nifedipina 30 mg). Su historial quirúrgico incluye una adrenalectomía derecha a los diez años, y ha recibido varios tratamientos, incluidos análogos de somatostatina y radioterapia paliativa. El historial familiar revela una mutación familiar de la subunidad B de la deshidrogenasa del succinato (mutación SDBH) con un importante historial de tumores malignos endocrinos, incluidos feocromocitomas en su padre y hermana y cáncer de páncreas en su abuela.\n\nLas investigaciones de laboratorio, incluido el recuento sanguíneo completo, revelaron anemia significativa, con un nivel de hemoglobina de 7.5 g/dl. Había evidencia de hemólisis, como lo indican el alto recuento de reticulocitos, la bilirrubina indirecta y la lactato deshidrogenasa. La haptoglobina era baja. Los resultados de laboratorio se muestran en. El perfil de coagulación excluyó la coagulación intravascular diseminada (DIC), que muestra (PT: 15.6, PTT: 23.3, fibrinógeno: 489, dímero D: 0.63). La prueba de Coombs directa para excluir la anemia hemolítica autoinmune fue negativa. Los frotis de sangre periférica mostraron la presencia de esquistocitos, equinocitos y algunas células en forma de lágrima, además de trombocitopenia, todo lo cual apuntaba a la anemia hemolítica microangiopática (MAHA). Dado el contexto del cáncer metastásico, el paciente fue diagnosticado con anemia hemolítica microangiopática paraneoplásica en marzo/2024.\n\nEl paciente fue programado para el protocolo CVD (ciclofosfamida, vincristina y doxorrubicina), pero sin ciclofosfamida debido al efecto inductor de anemia de los agentes alquilantes. El paciente recibió un total de 5 ciclos. Como indicador de respuesta clínica, el paciente ya no experimentó anemia o trombocitopenia. Un nuevo frotis de sangre periférica reveló células normales, lo que sugiere una respuesta clínica al MAHA que coincide con la mejora de la neoplasia subyacente. Esto se alinea con la definición de MAHA como un síndrome paraneoplásico.\n\nLos medicamentos que se le suministran al paciente al momento del alta son: comprimidos de dexametasona de 2 mg, 4 mg por vía oral (PO) una vez al día (OD) durante 3 días, comprimidos de ondansetrón de 8 mg por vía oral (PO) una vez al día (OD) durante 3 días, comprimidos de metoclopramida de 10 mg por vía oral (PO) tres veces al día durante 3 días, calcio de 600 mg con vitamina D por vía oral (PO) una vez al día (OD) durante 1 día, comprimidos de labetalol de 100 mg por vía oral (PO) dos veces al día durante 1 día, comprimidos de doxazocina de 2 mg por vía oral (PO) dos veces al día durante 1 día, comprimidos de citalopram de 20 mg por vía oral (PO) durante 1 día, comprimidos de omeprazol de 20 mg, 40 mg por vía oral (PO) durante 1 día, comprimidos de paracetamol de 500 mg, 1000 mg por vía oral (PO) dos veces al día durante 1 día, cápsulas de aprepitant de 125 mg/80 mg, 1 cápsula por vía oral (PO) dos veces al día durante 3 días (con prescripción médica).\n\nEl paciente fue objeto de seguimiento el 01/07/2024, y su aspecto clínico era bueno y activo. El paciente se sometió a exámenes de laboratorio que incluían un recuento sanguíneo completo (WBC 6.59 10e3/ul, RBC 4.47 × 10^6/ul, HGB 13.2 g/dl, 40.0%, MCV 89.4 fL, PLT 41.5 10e3/ul), nitrógeno ureico en sangre 33.8 mg/dl, creatina cinasa-MB 36.1 u/l, creatinina sérica 0.97 mg/dl, cloruro 101.5 mmol/l, potasio 4.52 mmol/l, sodio 135 mmol/l.\n",
+    "gold_summary": "En este informe de caso, presentamos a una mujer soltera de 21 años con un fuerte historial familiar de neoplasia endocrina. Fue derivada a nuestro hospital para quimioterapia debido a un diagnóstico de feocromocitoma maligno, que había hecho metástasis en la vejiga urinaria, los huesos y los pulmones. Además, desarrolló anemia hemolítica microangiopática como un síndrome paraneoplásico.\n",
+    "synthetic_summary_eval": {
+      "B1": {
+        "text": "Esta es la historia de una joven de 21 años. Ella tiene un tipo de enfermedad que hace que su cuerpo tenga bultos malos. Estos bultos están en partes como la vejiga, los huesos y los pulmones. También, su sangre estaba muy débil y no estaba bien. Los doctores le dieron medicinas para ayudarla a mejorar. Ahora, ella está más fuerte y se siente mejor.",
+        "scores": {
+          "ROUGE-1": 0.338235294117647,
+          "ROUGE-2": 0.11940298507462686,
+          "ROUGE-L-Sum": 0.338235294117647,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B2": {
+        "text": "### Caso de una joven con cáncer y anemia especial\n\nPresentamos la historia de una mujer de 21 años que tiene un tipo de tumor llamado feocromocitoma maligno. Este tumor se originó en sus glándulas suprarrenales y se ha extendido a otros órganos, como la vejiga, los huesos y los pulmones. Además, su familia tiene antecedentes de tumores similares, lo que indica que puede haber una causa genética.\n\n### Qué le pasó a la paciente\n\nLa paciente también desarrolló un problema en la sangre llamado anemia hemolítica microangiopática. Esto significa que sus glóbulos rojos se destruyen más rápido de lo normal debido a pequeños daños en los vasos sanguíneos. Esta anemia está relacionada con su cáncer y se llama síndrome paraneoplásico, porque ocurre como una consecuencia del tumor, aunque no sea directamente causado por él.\n\n### Tratamiento y evolución\n\nElla recibió quimioterapia adaptada para evitar empeorar la anemia. Después de varios ciclos, su sangre mejoró y ya no tenía signos de anemia ni problemas en las células sanguíneas. Esto muestra que el tratamiento ayudó tanto al cáncer como a la anemia causada por él.\n\nEn resumen, este caso muestra cómo un cáncer puede afectar otras partes del cuerpo, como la sangre, y cómo un tratamiento adecuado puede mejorar la salud general de la paciente.",
+        "scores": {
+          "ROUGE-1": 0.31683168316831684,
+          "ROUGE-2": 0.13953488372093023,
+          "ROUGE-L-Sum": 0.3036303630363036,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      },
+      "B3": {
+        "text": "**Contexto**  \nSe trata de una mujer joven de 21 años con antecedentes familiares significativos de tumores endocrinos malignos, en particular feocromocitomas (tumores que producen hormonas y se originan en las glándulas suprarrenales o tejidos relacionados). La paciente fue ingresada en el hospital debido a un feocromocitoma metastásico, es decir, un tumor maligno que se ha extendido a otros órganos, incluyendo la vejiga, los huesos y los pulmones. Además, presentaba hipertensión arterial difícil de controlar y síntomas relacionados con su enfermedad avanzada.\n\n**Hallazgos Clave**  \nDurante su hospitalización, se detectó que la paciente tenía anemia severa causada por un proceso llamado anemia hemolítica microangiopática (MAHA). Esta condición implica la destrucción acelerada de glóbulos rojos debido a daños en los pequeños vasos sanguíneos, y en este caso se relaciona directamente con su cáncer avanzado, constituyendo un síndrome paraneoplásico (un efecto indirecto del tumor sobre el organismo). Los análisis de sangre mostraron anemia significativa, signos de destrucción de glóbulos rojos (como aumento de reticulocitos y bilirrubina indirecta), y alteraciones en el frotis sanguíneo que confirmaron la presencia de células fragmentadas características de MAHA.\n\n**Interpretación Clínica**  \nLa anemia hemolítica microangiopática en esta paciente se considera una complicación secundaria al feocromocitoma metastásico, reflejando la gravedad y la actividad del tumor. El tratamiento con quimioterapia adaptada (excluyendo ciertos fármacos que podrían empeorar la anemia) logró controlar tanto la anemia como la progresión del cáncer, evidenciado por la normalización de los parámetros sanguíneos y la desaparición de las células anormales en el frotis. Esto confirma la relación directa entre la actividad tumoral y la anemia hemolítica.\n\n**Próximos Pasos**  \nLa paciente fue dada de alta con un régimen farmacológico para manejar sus síntomas y prevenir complicaciones, incluyendo corticosteroides, medicamentos para controlar la presión arterial, antieméticos y suplementos. En el seguimiento posterior, mostró una mejoría clínica significativa, con parámetros sanguíneos dentro de rangos normales y un estado general activo y estable. Continuará bajo vigilancia estrecha para monitorear la evolución de su enfermedad y ajustar el tratamiento según sea necesario.",
+        "scores": {
+          "ROUGE-1": 0.2177777777777778,
+          "ROUGE-2": 0.11160714285714286,
+          "ROUGE-L-Sum": 0.2177777777777778,
+          "BERTScore_Model": "emilyalsentzer/Bio_ClinicalBERT",
+          "BERTScore_P": NaN,
+          "BERTScore_R": NaN,
+          "BERTScore_F": NaN
+        }
+      }
+    }
+  }
+]
\ No newline at end of file
diff --git a/generating_data/score/synthetic.json b/generating_data/score/synthetic.json
new file mode 100644
index 0000000000000000000000000000000000000000..def4711e79e962865246e42bea5e0bffc0a5650e
--- /dev/null
+++ b/generating_data/score/synthetic.json
@@ -0,0 +1,758 @@
+[
+    {
+        "original_text_language": "es",
+        "source_topic": "Traumatismo craneoencefálico grave",
+        "synthetic_summary": {
+            "easy": {
+                "text": "Un hombre de 27 años tuvo un accidente con su moto. No llevaba casco y se golpeó la cabeza. Fue él mismo al hospital con dolor de cabeza y sangre en la frente. Al llegar, perdió el conocimiento y tuvo convulsiones. Los médicos vieron que tenía una herida grave en la cabeza y sangraba mucho por dentro. Lo trasladaron a otro hospital mejor equipado. Le hicieron una operación y luego despertó bien. Ahora está estable, puede caminar y no tiene problemas importantes. Después de la operación, tuvo más convulsiones, pero le dieron medicina y mejoró.",
+                "fh_score": 75.59
+            },
+            "intermediate": {
+                "text": "Un hombre de 27 años que fumaba sufrió un accidente en moto sin llevar casco. Se presentó en el hospital por su cuenta, con dolor de cabeza y una herida sangrante en la frente. Luego perdió el conocimiento y tuvo dos convulsiones. Su estado al llegar era crítico, con hemorragia interna en el cráneo y midriasis bilateral. Fue estabilizado e intubado, recibió varios medicamentos para detener las convulsiones y prevenir infecciones. Fue trasladado a un hospital de mayor nivel donde se le realizó una tomografía que mostró múltiples lesiones cerebrales, incluyendo contusiones, hemorragias y fracturas. Fue operado con éxito y, al día siguiente, estaba consciente y caminaba. Durante el posoperatorio tuvo algunas convulsiones más, que fueron controladas con medicamentos.",
+                "fh_score": 55.6
+            },
+            "hard": {
+                "text": "Paciente masculino de 27 años, fumador, sufre traumatismo craneoencefálico severo tras caída en motocicleta sin casco. Se presenta consciente al hospital inicial con cefalea y herida frontal hemorrágica, pero posteriormente pierde el conocimiento y experimenta crisis convulsivas tónico-clónicas. Glasgow 6/15 con midriasis bilateral y compromiso hemodinámico. La evaluación identifica fractura craneal penetrante con hemorragia intracraneal profusa. Recibe estabilización inicial que incluye intubación orotraqueal, uso de manitol, barbitúricos, antibióticos de amplio espectro y transfusión de sangre. Es derivado a hospital terciario, donde se confirma mediante TAC edema bifrontal, contusión hemorrágica parenquimatosa, hematoma subdural, hernia subfalcina izquierda y fractura de C3 con compresión medular. Se realiza intervención neuroquirúrgica con desenlace quirúrgico exitoso. En el postoperatorio desarrolla convulsiones tratadas farmacológicamente con evolución clínica favorable.",
+                "fh_score": 14.54
+            }
+        }
+    },
+    {
+        "original_text_language": "es",
+        "source_topic": "Inversión uterina crónica y tratamiento quirúrgico",
+        "synthetic_summary": {
+            "easy": {
+                "text": "Una mujer de 54 años vino al hospital con un bulto en su vagina que tenía desde hace 3 años. El bulto fue creciendo poco a poco. Ella había tenido dos hijos y todos nacieron en casa. Hace un año el bulto dejó de sangrar, pero hace seis meses le salió una herida. Por eso, su familia la trajo al hospital. En el examen, los doctores vieron que la masa era una parte del útero (el fondo uterino) que había salido por la vagina. Tenía una herida en un lado. No había sangre ni pus. Después de hacerle varios exámenes, le dijeron que tenía una inversión uterina, una condición en la que el útero se voltea. Le hicieron una operación llamada histerectomía (le sacaron el útero). Aunque la cirugía fue difícil, los médicos la lograron hacer. Después de 10 días, salió del hospital y mejoró bien. Dos semanas después, fue al control y seguía bien.",
+                "fh_score": 81.35
+            },
+            "intermediate": {
+                "text": "Una paciente de 54 años, de una zona rural, acudió al hospital con una masa vaginal que había notado hacía 3 años. Esta masa fue creciendo y presentaba sangrado y mal olor al inicio. Hace seis meses tuvo una laceración (herida) en la masa, lo que afectó su vida personal y social. No tenía otras enfermedades conocidas. En el examen, los doctores encontraron una masa que salía de la vagina, identificando como fondo uterino; la masa no sangraba, pero tenía una laceración de 5 cm. Los análisis de sangre y orina fueron normales. Con base en los hallazgos clínicos y estudios, se diagnosticó una inversión uterina crónica. Se decidió realizar una histerectomía abdominal. Durante la cirugía, el útero estaba distorsionado y hubo dificultad para identificar las estructuras internas; hubo una complicación: se lesionó el uréter derecho, y se realizó una reparación especial. La paciente fue dada de alta después de 10 días y, en su cita de control a las dos semanas, se encontraba estable y en buen estado general.",
+                "fh_score": 62.95
+            },
+            "hard": {
+                "text": "Paciente femenina de 54 años, procedente de zona rural, se presenta con queja de masa vaginal de evolución crónica (3 años). Refiere inicio con sangrado y secreción fétida, con resolución espontánea en el último año, aunque presentó laceraciones recientes en la superficie tumoral. Antecedentes obstétricos de dos partos domiciliarios, sin complicaciones reportadas. Exploración física revela masa rosada protruyendo aproximadamente 7 cm desde el anillo himenal, identificada como el fondo uterino, con laceración longitudinal de 5 cm en el flanco derecho. No se evidencian sangrado activo ni secreción. Estudios paraclínicos sin alteraciones relevantes. Ecografía muestra vejiga parcialmente llena, sin visualización uterina intraabdominal. Diagnóstico de inversión uterina crónica. Se realizó histerectomía abdominal, encontrándose tejido redundante y distorsionado, lo cual dificultó la anatomía quirúrgica. Se produjo lesión ureteral derecha intraoperatoria que fue resuelta con anastomosis término-terminal. Evolución favorable, alta médica al décimo día posoperatorio y seguimiento ambulatorio satisfactorio a las dos semanas.",
+                "fh_score": 27.03
+            }
+        }
+    },
+    {
+        "original_text_language": "es",
+        "source_topic": "Tuberculosis vertebral complicada con compromiso neurológico severo",
+        "synthetic_summary": {
+            "easy": {
+                "text": "Un joven de 20 años fue internado en el hospital con mucho dolor. Tenía tuberculosis y no había seguido bien su tratamiento. Estaba muy débil y delgado. Tenía bultos en la espalda que soltaban pus. Los doctores descubrieron que la bacteria de la tuberculosis seguía en su cuerpo. Además, su columna estaba muy dañada. Al inicio, le dieron medicinas y lo pusieron a descansar en cama con un collar especial. Antes de su operación, dejó de mover las piernas. Entonces, los médicos hicieron una cirugía urgente para ayudarlo. Más tarde, tuvo otras operaciones en el cuello y la espalda para fortalecer sus huesos. Con los tratamientos y ejercicios, el joven comenzó a moverse de nuevo. Estuvo cinco meses en el hospital. Al final, pudo caminar y seguir tomando sus medicinas en casa.",
+                "fh_score": 75.36
+            },
+            "intermediate": {
+                "text": "Un joven de 20 años fue ingresado al hospital con tuberculosis mal tratada. Llegó con dolor en el hombro, debilidad general y bultos con pus en el cuerpo. Los análisis confirmaron que tenía tuberculosis activa. También se encontró daño en varias partes de su columna vertebral. Inició tratamiento con medicamentos y reposo. Usó un collar para proteger su cuello. Antes de una cirugía programada, perdió la movilidad en sus piernas. Lo operaron de urgencia para descomprimir la médula espinal. Más adelante, tuvo otras cirugías en el cuello y la espalda para alinear y fijar los huesos con tornillos. En esas operaciones encontraron más pus causado por la infección. Gracias al tratamiento completo y la rehabilitación, logró volver a caminar. Estuvo cinco meses internado, y fue dado de alta en buen estado, con indicación de seguir tomando sus medicamentos por 12 meses.",
+                "fh_score": 67.83
+            },
+            "hard": {
+                "text": "Paciente masculino de 20 años, HIV negativo, antecedente de tuberculosis pulmonar con tratamiento irregular (2020–2021), ingresa con síndrome de impregnación bacilar, dorsalgia, impotencia funcional del hombro derecho, caquexia y múltiples masas fistulizadas con secreción caseosa. GeneXpert positivo para Mycobacterium tuberculosis sensible a rifampicina. Imagenología (TC y RMN) evidenció compromiso óseo multisegmentario (C4-C6, D4-D6, D9-D12, L1-L3) con fracturas patológicas D6 y D10, colecciones pre y paraespinales y colapso de estructuras vertebrales. Inició tratamiento de primera línea. Ante riesgo inminente de deterioro neurológico, se indicó reposo absoluto en decúbito dorsal, uso de collar de Filadelfia, apoyo kinésico y cirugía cervical programada. Sin embargo, desarrolló paraplejía aguda con nivel D8 y retención urinaria, lo que motivó neurocirugía urgente con laminectomía descompresiva (D5–D7) y drenaje epidural. Mejoró progresivamente. Posteriormente, se realizó corporectomía cervical (C4–C7), artrodesis anterior (C3–D1) y estabilización cervicodorsal extendida hasta D12. Procedimientos revelaron materiales caseosos BAAR positivos; se realizaron lavados profusos. Evolución favorable bacteriológica, radiológica y funcional, con egreso tras 5 meses de internación. Completará 12 meses de esquema antituberculoso.",
+                "fh_score": 30.98
+            }
+        }
+    },
+    {
+        "original_text_language": "es",
+        "source_topic": "Distrofia muscular tipo Emery-Dreifuss con insuficiencia cardíaca severa",
+        "synthetic_summary": {
+            "easy": {
+                "text": "Un joven japonés de 23 años fue hospitalizado porque le costaba mucho respirar al hacer esfuerzo. Desde niño tenía una enfermedad muscular llamada EDMD. Su padre también la tuvo y murió joven. A los 19 años, su corazón empezó a fallar. Le pusieron un aparato especial en el pecho para ayudar con los latidos. Tomó muchas medicinas, pero seguía empeorando. Tenía los pies hinchados y le costaba mover sus músculos. A los 22 años, volvieron a internarlo y le cambiaron el aparato porque su corazón seguía débil. Le daban medicinas por las venas. Su riñón y su hígado comenzaron a fallar. Luego, le pusieron una máquina llamada ECMO para ayudar con la sangre y el oxígeno. Aunque al principio mejoró, luego su cuerpo ya no pudo más. Después de 100 días en el hospital, él falleció. En la autopsia vieron que su corazón, hígado y pulmones estaban muy dañados por la enfermedad y por la falta de oxígeno.",
+                "fh_score": 74.42
+            },
+            "intermediate": {
+                "text": "Este caso trata de un hombre japonés de 23 años con una enfermedad genética llamada distrofia muscular de Emery-Dreifuss (EDMD), que afectó su movimiento desde niño y que también dañó su corazón progresivamente. A los 19 años fue hospitalizado por insuficiencia cardíaca. A pesar del tratamiento con medicamentos, su corazón se debilitó aún más. Se le instaló un desfibrilador y más adelante se le cambió por un dispositivo más avanzado llamado terapia de resincronización cardíaca. También tuvo acumulación de líquidos, hinchazón de piernas y problemas respiratorios. Su función cardíaca y luego renal se deterioraron a pesar de los tratamientos. Más adelante, desarrolló insuficiencia hepática grave y fue conectado a una máquina ECMO. A pesar de todos los esfuerzos médicos, falleció por falla multiorgánica al día 100 de internación. En la autopsia encontraron fibrosis y daño severo en su corazón e hígado, resultado de su enfermedad de base.",
+                "fh_score": 55.4
+            },
+            "hard": {
+                "text": "Varón japonés de 23 años con distrofia muscular de Emery-Dreifuss (EDMD) ligada a mutación LMNA (exón 1, Leu102Pro), admitido por disnea progresiva de esfuerzo. Antecedentes de rigidez articular desde la infancia y muerte súbita paterna a los 40 años. A los 19 años presentó insuficiencia cardíaca con predominio derecho e hiperbilirrubinemia (2,5 mg/dL), TAPSE: 5,7 mm, RVFAC: 19 %. Evolucionó a disfunción biventricular severa pese a tratamiento con carvedilol y enalapril. A los 22 años, por taquicardia ventricular no sostenida e historia familiar, se implantó un desfibrilador. Posteriormente se indicó terapia de resincronización (CRT) asociada al empeoramiento hemodinámico con FEVI ≤35 %, LVEF 30 %, RVFAC reducido (11 %), TAPSE 8 mm. RHC mostró IC = 2,0 L/min/m², PAWP = 22 mmHg, RVSWI = 1,36. Se instauró soporte inotrópico (dobutamina, milrinona), IABP, CRRT y finalmente ECMO VA. El paciente falleció por insuficiencia multiorgánica en el día 100. Autopsia: miopatía severa con fibrosis miocárdica avanzada, congestión hepática (hígado de shock, 2298 g), CID masiva, hemorragia alveolar significativa. Diagnóstico final: cardiomiopatía por EDMD con disfunción biventricular refractaria.",
+                "fh_score": 41.19
+            }
+        }
+    },
+    {
+        "original_text_language": "es",
+        "source_topic": "Neuralgia del trigémino y glosofaríngeo con tratamiento quirúrgico",
+        "synthetic_summary": {
+            "easy": {
+                "text": "Una mujer de 65 años empezó a sentir dolores muy fuertes en la cara en 2004. Los doctores dijeron que era un problema con un nervio llamado trigémino. Las medicinas no le quitaban el dolor. En 2021, también le dolía la lengua y la garganta del lado derecho, sobre todo cuando tragaba. Descubrieron que otro nervio, el glosofaríngeo, también tenía un problema. La operaron para separar los nervios de unas arterias que los apretaban. Después de la operación, el dolor de la cara se fue y el de la garganta mejoró mucho. Dos años después, casi no tiene dolor y toma menos medicina.",
+                "fh_score": 76.49
+            },
+            "intermediate": {
+                "text": "Una mujer de 65 años comenzó a sufrir, en 2004, episodios de dolor intenso y punzante en la cara, relacionados con el nervio trigémino derecho. Los tratamientos con medicinas como carboxamidas y lamotrigina no fueron efectivos. En 2021, el dolor se extendió a otras áreas de la cara y aparecieron nuevos dolores al tragar, afectando también el nervio glosofaríngeo. Tras nuevas pruebas que revelaron presión de arterias sobre los nervios, los médicos decidieron hacer una cirugía para separar los vasos sanguíneos de los nervios. Durante la operación colocaron teflón para evitar el contacto directo. Después de operarse, la paciente mejoró notablemente: el dolor trigeminal desapareció y el del glosofaríngeo se redujo más del 50%. Dos años después, casi no presenta molestias y ya necesita menos medicina.",
+                "fh_score": 53.29
+            },
+            "hard": {
+                "text": "Paciente femenina de 65 años, sin antecedentes médicos relevantes, con inicio en 2004 de paroxismos lancinantes en las ramas V2 y V3 derechas, compatibles con neuralgia del trigémino derecho clásica. A pesar de tratamiento con carboxamidas, el control del dolor fue subóptimo. En 2021, presentó exacerbación con extensión a V1 y refractariedad al tratamiento farmacológico, incluyendo lamotrigina y clonacepam. Precisó perfusiones endovenosas de fenitoína/lidocaína en crisis agudas. De forma concomitante, desarrolló paroxismos dolorosos en localizaciones compatibles con la neuralgia del glosofaríngeo derecho. La RM cerebral con secuencia CISS evidenció conflicto neurovascular: contacto arterial significativo entre la A. cerebelosa superior derecha y el V par, y entre la AICA derecha y el conjunto de pares craneales bajos. Se realizó descompresión microvascular única mediante craniectomía retrosigmoidea derecha. Se identificaron contactos vasculonerviosos en ambos territorios, con colocación de teflón y sellante dural. Postoperatorio sin complicaciones, con resolución completa de la neuralgia trigeminal y mejoría clínica >50% en el glosofaríngeo. A los 24 meses, la paciente se mantiene asintomática del trigémino y presenta menos de un paroxismo mensual en el glosofaríngeo, con tratamiento farmacológico en retirada progresiva sin recurrencias.",
+                "fh_score": 33.06
+            }
+        }
+    },
+    {
+        "original_text_language": "es",
+        "source_topic": "Caso clínico de viruela símica (monkeypox)",
+        "synthetic_summary": {
+            "easy": {
+                "text": "Un hombre de 36 años fue al hospital porque tenía fiebre, dolor de garganta y en el cuello. Dijo que había ido a una fiesta y tuvo contacto con personas que no conocía. Después de varios días y sin mejorar con medicinas, lo internaron. Tenía granitos en la cara, el pene y el escroto. También le dolían unos ganglios del cuello. Le hicieron estudios y descubrieron que tenía viruela símica, un virus parecido al de la viruela común. Le salieron más heridas en varias partes del cuerpo, como la lengua, el glúteo y las manos. No necesitó operaciones y se sintió mejor después de algunos días en el hospital. Se fue a su casa cuando ya estaba mucho mejor.",
+                "fh_score": 80.07
+            },
+            "intermediate": {
+                "text": "Un hombre de 36 años, que estaba tomando medicamentos para prevenir el VIH, fue al médico tras presentar fiebre, dolor de garganta y cuello, diez días después de tener relaciones con personas desconocidas en un evento. A pesar de recibir antibióticos, los síntomas no mejoraron, por lo que fue internado. Tenía ganglios dolorosos en el cuello, granos en la cara, pene y escroto. Se le hicieron varios estudios, incluyendo una tomografía y análisis de laboratorio. El diagnóstico fue viruela símica, confirmado por PCR. El virus se relacionó con una cepa del oeste de África. Le aparecieron nuevas lesiones en distintas partes del cuerpo, como lengua, glúteos y manos. También presentaba ciertas alteraciones en las pruebas de laboratorio. No necesitó cirugías y fue dado de alta tras mejorar clínicamente. El paciente autorizó la publicación de su caso.",
+                "fh_score": 63.47
+            },
+            "hard": {
+                "text": "Varón de 36 años, bisexual, en esquema de profilaxis preexposición (PrEP) al HIV, sin antecedentes de viaje, que refirió contacto sexual con múltiples parejas ocasionales en un evento reciente. Diez días post-exposición inició fiebre, odinofagia y cervicalgia, con ingreso hospitalario al séptimo día por persistencia sintomática pese a tratamiento antibiótico ambulatorio. Se constató exudado faríngeo, adenopatías cervicales bilaterales dolorosas y lesiones dérmicas: pápulas umbilicadas en escroto y pene, y pústulas faciales de cinco días de evolución. TC de cuello con contraste descartó colección; ecografía abdominal evidenció hepatoesplenomegalia leve. Se inició tratamiento empírico con ceftriaxona y azitromicina. Se enviaron muestras de exudado y escarificación de lesiones al INEI-ANLIS Dr. Carlos G. Malbrán, confirmándose Orthopoxvirus por PCR (positivo), consistente con viruela símica. Secuenciación genómica reveló alta homología con MPV clado África Occidental (GenBank ON800897). Evolucionó con úlcera lingual y lesiones asincrónicas en múltiples localizaciones cutáneas, totalizando ≤25. Laboratorio con elevación de transaminasas x2.2. A los 14 días, nueva TC cervical evidenció adenomegalias necróticas sin requerimiento quirúrgico. PCR en fauces y semen positiva el día 17. Alta clínica al día 19 con mejoría franca. Consentimiento informado otorgado para publicación del caso e imágenes.",
+                "fh_score": 38.35
+            }
+        }
+    },
+    {
+        "original_text_language": "es",
+        "source_topic": "Caso clínico de miocardiopatía hipertrófica y manejo con cirugía y CDI",
+        "synthetic_summary": {
+            "easy": {
+                "text": "Un joven de 23 años se desmayaba desde niño. Por eso, le pusieron un marcapaso para ayudar a su corazón. Con el tiempo se sintió más cansado, y el marcapaso ya no funcionaba bien. Le hicieron exámenes y vieron que una parte del corazón estaba muy gruesa y bloqueaba el paso de la sangre. Lo operaron para quitar esa parte y sacaron unos cables viejos del marcapaso. Después tuvo dos problemas graves con los latidos del corazón, así que le pusieron otro aparato especial (desfibrilador) para cuidarlo. También le revisaron su ADN y encontraron un problema del corazón que podía venir de su familia. Ahora él está bien, toma su medicina y también quieren revisar a sus familiares.",
+                "fh_score": 76.11
+            },
+            "intermediate": {
+                "text": "Un joven de 23 años tenía desmayos desde pequeño y usaba un marcapaso. Después de varios años, empezó a sentirse más cansado al hacer actividades. Los estudios mostraron que una parte del corazón estaba muy engrosada y no dejaba pasar bien la sangre. Como tenía antecedentes en su familia y riesgo alto, decidieron operarlo para quitar esa parte. También le sacaron unos cables viejos del marcapaso. Luego de la cirugía, tuvo dos arritmias graves, así que le pusieron un desfibrilador moderno para protegerlo. Se recuperó bien. Un estudio genético mostró un problema hereditario en el corazón. Ahora está estable, toma su medicina y su familia también será evaluada.",
+                "fh_score": 62.11
+            },
+            "hard": {
+                "text": "Varón de 23 años, oriundo de Itagüí (Colombia), con antecedente de muerte súbita en abuelo paterno a los 50 años. Diagnóstico de disfunción sintomática del nodo sinusal desde la infancia en seguimiento, con implante de marcapaso bicameral. En 2012, presentó infección de bolsillo posoperatoria requiriendo explante del generador y abandono de electrodo ventricular. Se reimplanta nuevo sistema contralateral sin eventos sincopales por 10 años. Seis meses previo al ingreso presentó progresivo deterioro funcional (NYHA III). Examen físico con soplo sistólico aórtico II/VI; ecocardiograma mostró hipertrofia septal media severa (26 mm), gradiente intracavitario pico 117 mmHg y SAM con insuficiencia mitral leve. Ante contraindicación para RM cardíaca por marcapaso no compatible, se realizó TC y fue evaluado por Heart Team, decidiéndose miectomía medio-ventricular por vía transapical con resección septal extendida y retiro de electrodos adheridos al velo septal tricuspídeo. En el posoperatorio, presentó dos episodios de TV sostenida con repercusión hemodinámica, requiriendo implante de CDI MRI compatible (St. Jude). Sin nuevas arritmias en seguimiento. Estudio genético reveló variante probablemente patogénica en heterocigosis en FLNC c.4636G>A, compatible con miocardiopatía hipertrófica tipo 26 autosómica dominante. Actualmente en clase funcional I sin recurrencia de TV y tratamiento de mantenimiento con bisoprolol. Estudio genético familiar iniciado, limitado por dificultades de acceso al sistema de salud.",
+                "fh_score": 42.58
+            }
+        }
+    },
+    {
+        "original_text_language": "es",
+        "source_topic": "Caso clínico de sífilis primaria y detección de Neisseria meningitidis en paciente con VIH",
+        "synthetic_summary": {
+            "easy": {
+                "text": "Un hombre de 32 años fue al médico porque tenía una llaga en el pene y un poco de secreción por la uretra. También tenía un ganglio inflamado en la ingle que dolía al tocarlo. No tenía fiebre ni otros síntomas. Él tiene VIH, pero está controlado con medicamentos. Contó que tuvo relaciones sexuales sin condón con varios hombres. Los doctores pensaron que podía tener sífilis, una enfermedad que se transmite por contacto sexual. Le hicieron exámenes y le dieron antibióticos. Las pruebas confirmaron que tenía sífilis. También encontraron una bacteria llamada Neisseria meningitidis en una muestra del ano. Después del tratamiento, el hombre mejoró: la llaga desapareció y ya no tenía secreción. Se llamó a su última pareja sexual para que también se hiciera los estudios, pero esa persona no tenía síntomas ni infecciones en las pruebas.",
+                "fh_score": 72.19
+            },
+            "intermediate": {
+                "text": "Un hombre de 32 años, con VIH controlado y antecedentes de consumo de drogas, acudió a una unidad de salud sexual por presentar secreción por la uretra y una úlcera dolorosa en el pene de dos semanas de evolución. También tenía un ganglio inflamado en la ingle. En total, había tenido 20 parejas sexuales hombres durante el último año, con uso ocasional de preservativo. No tenía fiebre ni otros síntomas generales. Los médicos sospecharon sífilis primaria y le realizaron varios exámenes, incluyendo muestras de sangre y cultivos. Mientras tanto, se le administró tratamiento antibiótico según las normas del país. Los análisis confirmaron sífilis y también detectaron la presencia de la bacteria Neisseria meningitidis en una muestra anorrectal. El paciente mejoró completamente tras el tratamiento. Se contactó a su última pareja sexual para su evaluación, pero no se detectaron infecciones en sus análisis.",
+                "fh_score": 56.57
+            },
+            "hard": {
+                "text": "Varón de 32 años con antecedente de infección por VIH en tratamiento antirretroviral (carga viral indetectable, 454 CD4 céls/mm³) y consumo de sustancias psicoactivas, consultó por cuadro de dos semanas de evolución consistente en uretritis mucosa leve, acompañada de úlcera genital indurada, eritematosa y dolorosa de 1,5 cm en el surco balanoprepucial, sin fiebre ni síntomas sistémicos. Al examen físico se evidenció adenopatía inguinal izquierda palpable, dolorosa y móvil. Refería múltiples parejas sexuales masculinas en el último año, con uso ocasional de preservativo. Se presuncionó sífilis primaria con uretritis, indicándose tratamiento empírico con penicilina benzatina (3 dosis IM semanales), ceftriaxona IM única dosis y azitromicina VO. Estudios confirmaron sífilis (VDRL 1:2 y MHA-TP reactivo). Cultivos de secreción uretral fueron negativos, mientras que el hisopado anorrectal evidenció diplococos gramnegativos escasos y cultivo con desarrollo abundante de *Neisseria meningitidis* (identificación vía MALDI-TOF MS). El paciente evolucionó favorablemente con resolución de lesiones y cultivos de control negativos. Se contactó al último compañero sexual, quien se encontraba asintomático y con cultivos negativos.",
+                "fh_score": 37.75
+            }
+        }
+    },
+    {
+        "original_text_language": "es",
+        "source_topic": "Edema pulmonar cardiogénico hipertensivo en paciente con comorbilidades crónicas",
+        "synthetic_summary": {
+            "easy": {
+                "text": "Un hombre de 63 años fue al hospital porque de repente le costaba mucho respirar, tenía palpitaciones y sudaba mucho. Antes se sentía bien. Tenía problemas del corazón, presión alta, diabetes y riñones. Usaba varios medicamentos. Cuando llegó, tenía la presión muy alta, respiraba rápido y tenía el corazón acelerado. No podía hablar bien y tenía los pulmones llenos de líquido. Los doctores le pusieron oxígeno, lo acostaron sentado y le dieron una medicina por la vena llamada nitroglicerina. Esto ayudó a bajarle la presión y a que respirara mejor. Luego le dieron otras medicinas para ayudar al corazón. Los exámenes mostraron que su corazón estaba muy débil. Después de mejorar, fue internado y luego dado de alta del hospital en buen estado. Le cambiaron algunos medicamentos y lo revisó su cardiólogo cada semana. No volvió a tener problemas en los siguientes dos meses.",
+                "fh_score": 68.42
+            },
+            "intermediate": {
+                "text": "Un hombre de 63 años llegó a urgencias con dificultad para respirar, palpitaciones y sudoración. Hasta poco antes se encontraba bien. Tenía antecedentes de hipertensión, diabetes, insuficiencia cardíaca con fracción de eyección del 35%, enfermedad del corazón y problemas renales. Al examen tenía la presión muy alta, baja oxigenación y signos de líquido en los pulmones. Se descartó neumonía y se diagnosticó edema pulmonar cardiogénico por hipertensión. Se le administró oxígeno y nitroglicerina por vena, lo que ayudó a bajar la presión y mejorar su respiración. Luego se agregaron enalapril y furosemida. También tomó otras medicinas para ayudar al corazón. Los exámenes mostraron un corazón sobrecargado, pero sin signos de ataque cardíaco ni embolia pulmonar. Después de estabilizarse, fue internado y dado de alta en 48 horas con tratamiento optimizado. Tuvo controles semanales y no necesitó volver al hospital en los siguientes 60 días.",
+                "fh_score": 53.46
+            },
+            "hard": {
+                "text": "Paciente varón hispanohablante de 63 años, con antecedentes de hipertensión arterial de 20 años, diabetes mellitus tipo 2 de 15 años, enfermedad coronaria con colocación previa de stent, insuficiencia cardíaca con fracción de eyección del 35% (NYHA II) y enfermedad renal crónica estadio 3B, se presentó en servicios de urgencia con disnea súbita severa, palpitaciones y diaforesis. A su llegada, presentaba hipertensión severa (205/110 mmHg), taquicardia e hipoxemia (SpO2 82%). La exploración reveló signos claros de edema pulmonar, crepitantes bilaterales, galope S3, soplo sistólico y elevación de la presión venosa yugular. El EKG mostró hipertrofia ventricular izquierda, taquicardia sinusal y depresión del ST. La radiografía indicó cardiomegalia y edema intersticial. Se inició tratamiento inmediato con nitroglicerina IV en dosis tituladas progresivas, alcanzando 120 mcg/min, logrando disminución de la TA y mejora clínica rápida. Se añadieron enalapril y furosemida IV. Luego se cambió a nitrato oral (isosorbida). Los gases arteriales confirmaron hipoxia severa (pO2 57 mmHg, SatO2 84%). El BNP estaba elevado (3,452 pg/ml), sin elevación de troponina. Se descartó TEP y disfunción tiroidea. Fue ingresado con diagnóstico de edema pulmonar cardiogénico hipertensivo, con estabilización clínica completa en 48 horas. Al alta, se ajustó tratamiento con furosemida, carvedilol, sacubitrilo/valsartán, espironolactona e isosorbida. Evolución ambulatoria sin eventos en los siguientes 60 días.",
+                "fh_score": 41.97
+            }
+        }
+    },
+    {
+        "original_text_language": "es",
+        "source_topic": "Rinosporidiosis conjuntival en un niño",
+        "synthetic_summary": {
+            "easy": {
+                "text": "Un niño de 12 años fue al hospital porque tenía una bolita rosada que salía del párpado derecho y que le molestaba como si tuviera algo en el ojo. La bolita fue creciendo durante un mes. Su vista era buena y no tenía heridas ni golpes. Los doctores pensaron que podía ser un tipo de papiloma, así que le hicieron una cirugía para quitar la bolita y analizarla. Al mirar el tejido con el microscopio, vieron signos de una infección rara llamada rinosporidiosis, que afecta la parte interna del ojo. Después de la operación, el niño se recuperó bien y en los siguientes 7 meses no tuvo más problemas ni volvió a salirle la bolita.",
+                "fh_score": 68.83
+            },
+            "intermediate": {
+                "text": "Un niño de 12 años llegó al hospital con una masa rosada y blanda en el párpado derecho que había crecido durante un mes y le causaba sensación de tener algo en el ojo. No presentaba pérdida de visión ni antecedentes de trauma. Se le diagnosticó inicialmente un papiloma escamoso pedunculado y se decidió realizar una cirugía para extraer la lesión y analizarla. En el estudio microscópico, los médicos encontraron inflamación con muchas células del sistema inmune, además de estructuras grandes llamadas esporangios, típicas de una infección llamada rinosporidiosis. Esta enfermedad es poco frecuente y afecta la mucosa, en este caso, la conjuntiva. A los 7 meses del procedimiento, el paciente seguía sin signos de que la infección hubiera regresado.",
+                "fh_score": 50.58
+            },
+            "hard": {
+                "text": "Paciente masculino de 12 años con historia de un mes de sensación de cuerpo extraño ocular y masa conjuntival pedunculada de crecimiento progresivo en conjuntiva palpebral derecha. Sin antecedentes traumáticos ni lesiones similares contralaterales. Al examen oftalmológico se evidenció masa rosácea de 15 mm, con agudeza visual conservada. Se realizó escisión quirúrgica diagnóstica por sospecha de papiloma escamoso pedunculado. Macroscópicamente se recibió lesión ovoide, firme, blanquecina, de 1,5 × 1 cm. En el análisis histopatológico se observó lesión poliopóidea hiperplásica con múltiples quistes submucosos, infiltrado inflamatorio mixto (linfocitos, células plasmáticas, neutrófilos) y abundantes esporangios con endosporas, algunas de las cuales se liberaban por rotura de esporangios maduros. Diagnóstico concluyente de rinosporidiosis conjuntival. No se evidenció recurrencia ni afectación sistémica durante el seguimiento de 7 meses posteriores a la cirugía.",
+                "fh_score": 26.29
+            }
+        }
+    },
+    {
+        "original_text_language": "es",
+        "source_topic": "Hernia interna a través del hiato de Winslow en adolescente",
+        "synthetic_summary": {
+            "easy": {
+                "text": "Un joven de 15 años fue al hospital porque tenía dolor en el estómago y muchos vómitos por varios días. Al principio pensaron que era una infección del estómago, pero no mejoraba. Le hicieron exámenes y vieron que algo bloqueaba su intestino. Le hicieron una operación y descubrieron que una parte del intestino estaba atrapada en un pequeño espacio del abdomen llamado hiato de Winslow. Lo sacaron de ahí y lo colocaron en su lugar. Después de la operación, el joven tardó unos días en volver a comer, pero se recuperó bien. Estuvo diez días en el hospital y ahora lo siguen controlando en consultas externas.",
+                "fh_score": 69.74
+            },
+            "intermediate": {
+                "text": "Un adolescente de 15 años acudió a urgencias por vómitos biliosos y dolor abdominal en la parte alta del abdomen durante cuatro días. Al no mejorar con el tratamiento inicial para gastroenteritis, se le realizaron estudios que mostraron signos de obstrucción intestinal. En una tomografía se sospechó una hernia interna a través del hiato de Winslow. Fue operado de urgencia. Primero se intentó una cirugía por laparoscopia, pero debido a la mala visibilidad por la distensión intestinal, se realizó una laparotomía. Se encontró un segmento de intestino delgado herniado a través del hiato, que fue recolocado. No se hizo ninguna técnica para evitar que volviera a ocurrir porque el orificio era normal. Tras la cirugía, tuvo recuperación lenta con un íleo paralítico y una colección pélvica que se trató con antibióticos. Fue dado de alta tras diez días, en buen estado general.",
+                "fh_score": 57.06
+            },
+            "hard": {
+                "text": "Varón de 15 años, sin antecedentes personales, consultó por cuadro de vómitos biliosos y dolor abdominal epigástrico de 4 días de evolución, afebril. Exploración física con distensión abdominal, ruidos hidroaéreos disminuidos y signos leves de deshidratación. Analítica sin hallazgos relevantes. Radiografía abdominal sugestiva de obstrucción intestinal; TC urgente evidenció ascitis y dilatación de intestino delgado con sospecha de herniación a través del hiato de Winslow. Se realizó laparoscopia exploradora donde se observaron asas de delgado dilatadas, con ciego e íleon terminal en hipocondrio derecho sin adherencias. Dificultad en la identificación del punto de obstrucción motivó conversión a laparotomía. Se descubrió segmento de íleon (~5 cm) herniado a través del hiato de Winslow a ~40 cm de la válvula ileocecal, con impronta congestiva en ambos extremos. El hiato presentaba calibre normal, por lo que no se realizó cierre profiláctico. Postoperatorio complicado con íleo paralítico y colección pélvica manejada conservadoramente. Alta hospitalaria al décimo día en buen estado general y actualmente en seguimiento ambulatorio por cirugía pediátrica.",
+                "fh_score": 40.01
+            }
+        }
+    },
+    {
+        "original_text_language": "es",
+        "source_topic": "Trombectomía mecánica en lactante con miocardiopatía restrictiva y asistencia ventricular",
+        "synthetic_summary": {
+            "easy": {
+                "text": "Un niño de casi 2 años tenía una enfermedad del corazón desde que nació y estaba esperando un trasplante. Mientras tanto, usaba una máquina para ayudar a su corazón. Como tenía riesgo de que se le formaran coágulos, tomaba varias medicinas para evitarlos. Un día, el niño se desconectó y no podía mover bien su lado derecho. Le hicieron una tomografía y vieron que tenía un coágulo en una arteria del cerebro. No podían darle medicinas para disolverlo, así que los doctores usaron un pequeño tubo por la pierna para llegar al cerebro y sacar el coágulo. Lo hicieron en un solo intento. Aunque dañaron una arteria, no le causó problemas. Un mes después, el niño recibió su nuevo corazón. Después del problema en el cerebro, solo le quedó un poco de rigidez en el brazo derecho.",
+                "fh_score": 70.57
+            },
+            "intermediate": {
+                "text": "Un niño de 23 meses tenía una enfermedad del corazón y estaba esperando un trasplante. Usaba un dispositivo externo que ayudaba a su corazón a bombear sangre y tomaba medicinas para evitar coágulos. Un día dejó de reaccionar y no podía mover el lado derecho del cuerpo. Una tomografía mostró que una arteria del cerebro estaba tapada por un coágulo. Como no podía recibir medicinas para disolverlo, los médicos hicieron una trombectomía: entraron por la pierna con un tubo especial y sacaron el coágulo del cerebro. Lo lograron en un solo intento. Aunque hubo una pequeña lesión en una arteria, no causó problemas. Un mes después, recibió el trasplante de corazón. Lo único que le quedó como secuela fue cierta rigidez en el brazo derecho.",
+                "fh_score": 65.19
+            },
+            "hard": {
+                "text": "Paciente masculino de 23 meses con antecedentes de encefalopatía hipóxico-isquémica leve, desarrollo psicomotor normal y miocardiopatía restrictiva avanzada en lista de espera para trasplante cardíaco. Portador de asistencia biventricular externa tipo Berlin Heart, con anticoagulación plena (heparina) y doble antiagregación. Presentó cuadro agudo de hemiparesia derecha y desconexión. TC craneal evidenció ACM izquierda hiperdensa e infarto antiguo parietotemporal derecho. La trombólisis IV fue contraindicación absoluta, por lo que se condujo trombectomía mecánica intraarterial bajo anestesia general. Se accedió por arteria femoral derecha con catéter vertebral 4F, confirmando oclusión de M1. Se utilizó stentriever Trevo XP Pro Vue 3x20 mm con microcatéter Rapid Transit, logrando recanalización completa en una pasada. Se observó disección iatrogénica de carótida interna izquierda sin repercusión clínica gracias al flujo compensador por la comunicante anterior. Posteriormente, se realizó exitosamente el trasplante cardiaco. A largo plazo, el único déficit neurológico observado fue espasticidad en miembro superior derecho.",
+                "fh_score": 32.17
+            }
+        }
+    },
+    {
+        "original_text_language": "es",
+        "source_topic": "Intoxicación aguda por herbicida 2,4-D en paciente joven",
+        "synthetic_summary": {
+            "easy": {
+                "text": "Una mujer de 23 años llegó al hospital después de desmayarse. Tenía mucha saliva en la boca y no respondía. Tres días antes, había tomado un veneno usado en plantas, llamado 2,4-D, porque tenía problemas de dinero. No tenía otras enfermedades conocidas. Al llegar, su presión y respiración eran normales, pero no estaba despierta. Le pusieron una sonda para ayudarla a respirar y la trasladaron a cuidados intensivos. Le hicieron pruebas que mostraron daño en los riñones y en los músculos. Le dieron medicinas para subir la presión, pero su cuerpo no respondió bien. Después de tres días, su corazón y su circulación dejaron de funcionar y murió.",
+                "fh_score": 70.51
+            },
+            "intermediate": {
+                "text": "Una mujer de 23 años fue llevada al hospital después de perder el conocimiento y tener mucha saliva en la boca. No tenía fiebre ni vómitos. Antes había sido tratada por posible intoxicación con pesticida, pero luego se supo que tomó unos 30 ml de un herbicida llamado 2,4-D, en un intento de suicidio motivado por dificultades económicas. No tenía enfermedades previas ni problemas de salud mental conocidos. Al ingresar, estaba inconsciente, con pupilas reactivas y reflejos aumentados. Fue llevada a cuidados intensivos donde empezó a mostrar daño en los riñones y músculos (rabdomiolisis). A pesar del tratamiento con líquidos y medicinas para subirle la presión, su salud empeoró rápidamente. Murió al tercer día en terapia intensiva por falla circulatoria.",
+                "fh_score": 57.87
+            },
+            "hard": {
+                "text": "Paciente femenina de 23 años presentó pérdida de conciencia y sialorrea 2 horas post-ingestión de sustancia tóxica inicialmente no especificada. Recibió tratamiento por presunta intoxicación por organofosforados con atropina y cimetidina durante 3 días en centro primario. Posteriormente, se confirma ingestión intencional de ~30 ml de herbicida 2,4-diclorofenoxiacético (2,4-D), motivada por factores socioeconómicos. Sin antecedentes psiquiátricos, neurológicos ni cardiovasculares. A su llegada, GCS 6/15, reflejos exaltados y plantares ascendentes. Exámenes iniciales de laboratorio no revelaron alteraciones, salvo estudio cardíaco con taquicardia sinusal. Sin disponibilidad local para estudios toxicológicos ni gases arteriales. En UCI, se inició diuresis alcalina y soporte avanzado. Evolucionó con fallo renal agudo (Cr: 3.1 mg/dL, BUN: 133 mg/dL) y rabdomiolisis severa (CPK: 1330 µg/L). Se instauró soporte con vasopresores tras hipotensión refractaria. El desenlace fue fatal por colapso circulatorio en el tercer día de internación. La intoxicación por 2,4-D puede inducir miotoxicidad severa, acidosis metabólica, y falla multiorgánica sin antídoto específico disponible.",
+                "fh_score": 33.31
+            }
+        }
+    },
+    {
+        "original_text_language": "es",
+        "source_topic": "Carcinoma de origen primario desconocido con diseminación sistémica en paciente joven",
+        "synthetic_summary": {
+            "easy": {
+                "text": "Una mujer de 35 años fue al hospital porque le costaba respirar, tenía dolor en el pecho, tos con sangre, fiebre y vómitos. También dijo que estaba débil, sin apetito y bajando de peso. Vivía en una zona rural y no tenía enfermedades conocidas. Los exámenes mostraron líquido alrededor del corazón y los pulmones, y una infección en los pulmones. También tenía un coágulo en los pulmones y una hinchazón en el brazo por un nuevo coágulo de sangre. Se encontraron células de cáncer en el líquido del corazón y los pulmones, además de lesiones en el hígado. Le hicieron una cirugía para quitar el líquido, se le dio medicina para los coágulos, antibióticos y se le inició quimioterapia. Mejoró en el hospital, pero no pudo continuar con el tratamiento por falta de dinero. Murió en su casa cuatro meses después.",
+                "fh_score": 70.37
+            },
+            "intermediate": {
+                "text": "Una mujer de 35 años acudió a urgencias con dificultad respiratoria, dolor de pecho, tos con sangre, fiebre y vómitos. También sufría debilidad, pérdida de apetito y bajó de peso en los últimos meses. No tenía enfermedades previas ni hábitos de riesgo. Los exámenes mostraron líquido en el corazón y en los pulmones, signos de infección pulmonar, y coágulos de sangre en los pulmones y en un brazo. El análisis del líquido reveló células malignas, y estudios posteriores mostraron que el hígado tenía metástasis. No se encontró el origen del cáncer. La paciente fue tratada con antibióticos, anticoagulantes, drenaje del líquido y quimioterapia. Se le dio de alta tras 14 días con mejoría, pero perdió el seguimiento por razones económicas, y murió en casa cuatro meses después.",
+                "fh_score": 62.51
+            },
+            "hard": {
+                "text": "Paciente etíope de 35 años sin antecedentes clínicos relevantes presentó disnea en reposo, ortopnea, DPN, hemoptisis, vómitos, fiebre alta, edema generalizado y pérdida ponderal progresiva. A la evaluación mostró hipoxemia (SpO2 70%), taquicardia, signos de derrame pleural y pericárdico con compromiso hemodinámico. TC de tórax y abdomen revelaron neumonía multifocal, derrames pleural y pericárdico, embolismo pulmonar bilateral, hepatoesplenomegalia y múltiples lesiones hepáticas sugestivas de metástasis. Exámenes del líquido pleural y pericárdico confirmaron células malignas atípicas. Biopsia hepática compatible con adenocarcinoma metastásico con origen primario desconocido (CUP). EC transthorácico evidenció taponamiento cardiaco, tratado con pericardiocentesis e instauración de ventana pericárdica. Se instauró anticoagulación con enoxaparina y posteriormente warfarina; antibióticos por neumonía; frusemida IV por sobrecarga de volumen; y de forma paliativa, carboplatino-paclitaxel. Fue dada de alta tras 14 días en mejoría clínica, pero falleció 4 meses después sin seguimiento oncológico debido a barreras económicas.",
+                "fh_score": 21.44
+            }
+        }
+    },
+    {
+        "original_text_language": "es",
+        "source_topic": "Tormenta tiroidea en paciente con enfermedad de Graves tratada con yodo radiactivo y anestesia multimodal",
+        "synthetic_summary": {
+            "easy": {
+                "text": "Una chica de 17 años tenía una enfermedad en la tiroides llamada Graves. Durante varios meses, perdió peso, se sentía nerviosa, tenía palpitaciones, diarrea, fiebre leve y dolor de estómago. Su cuello empezó a crecer por un bulto. Le dieron medicina, pero una le causó problemas en la sangre y la otra no ayudó. Luego le dieron un tratamiento con yodo. Como estaba en riesgo de una crisis grave de tiroides, la operaron con cuidados especiales. Le pusieron anestesia y medicinas para el dolor. Todo salió bien en la cirugía. Después, tuvo buen control del dolor y solo necesitó una medicina más. Quedó un poco ronca, pero sin dolor al tragar.",
+                "fh_score": 74.42
+            },
+            "intermediate": {
+                "text": "Una joven de 17 años con enfermedad de Graves presentaba síntomas como pérdida de peso, palpitaciones, ansiedad, fiebre leve, diarrea y crecimiento del cuello por agrandamiento de la tiroides. Primero recibió tiamazol, pero tuvo que dejarlo por efectos secundarios graves. Luego tomó lugol y propranolol, pero no mejoró. Le aplicaron yodo radiactivo y, debido a signos de tormenta tiroidea, fue operada con anestesia especial. La cirugía fue estable y sin problemas. Después, estuvo bien controlada del dolor por 12 horas y solo necesitó una medicina más. Lo único que presentó fue ronquera, pero sin dolor al tragar.",
+                "fh_score": 59.2
+            },
+            "hard": {
+                "text": "Paciente femenina de 17 años con diagnóstico confirmado de enfermedad de Graves con bocio difuso, en evolución de 6 meses con síntomas de hipertiroidismo severo y signos compatibles con tormenta tiroidea. Presentó agranulocitosis secundaria al uso de tiamazol, por lo que fue manejada con lugol y propranolol sin respuesta adecuada. Se indicó ablación con radioyodo (I-131, dosis 10 mCi). A su ingreso, obtuvo una puntuación de 40 en la escala de Burch-Wartofsky, lo que indicó alta probabilidad de tormenta tiroidea. Se realizó manejo anestésico multimodal, incluyendo inducción endovenosa con fentanilo, propofol, midazolam y cisatracurio, videolaringoscopia GlideScope sin complicaciones, mantenimiento con sevoflurano, dexmedetomidina, lidocaína y monitoreo invasivo. Se realizó bloqueo cervical superficial bilateral guiado por ecografía. Se administraron múltiples adyuvantes analgésicos y antiinflamatorios. El procedimiento fue hemodinámicamente estable; el postoperatorio cursó con analgesia adecuada por 12 horas, único rescate con metamizol, y como única complicación persistente, disfonía sin odinofagia.",
+                "fh_score": 22.95
+            }
+        }
+    },
+    {
+        "original_text_language": "es",
+        "source_topic": "Lesión ureteral y complicaciones postoperatorias tras cesárea de emergencia",
+        "synthetic_summary": {
+            "easy": {
+                "text": "Una mujer de 30 años tuvo una cesárea de emergencia porque el parto fue difícil y hubo mucho sangrado. Su bebé murió a los pocos minutos de nacer. Después de la operación, la mujer tuvo fiebre y dolor. Descubrieron que uno de los tubos que llevan la orina (uréter) se había cerrado y que había orina dentro del abdomen. Le hicieron una cirugía para arreglarlo. Más tarde, tuvo otra operación porque parte del intestino se rompió. Los doctores le quitaron el útero, pusieron una salida para la orina en la piel y una bolsita para las heces. Se enfermó, pero fue mejorando con medicinas y cuidados. Unos meses después, los doctores le volvieron a operar para cerrar las salidas temporales. Después de dos años, la mujer estaba bien y sin problemas.",
+                "fh_score": 76.99
+            },
+            "intermediate": {
+                "text": "Una mujer de 30 años tuvo una cesárea de emergencia por complicaciones en el parto y mucha pérdida de sangre. Su bebé murió poco después. Días después, la mujer empezó con fiebre, dolor y problemas para orinar. Los exámenes mostraron que uno de sus uréteres estaba dañado y que había orina en el abdomen. La operaron para arreglarlo. Luego tuvo una infección abdominal por ruptura de una parte del intestino y hubo que hacerle varias cirugías: le quitaron el útero, hicieron una abertura para orinar y otra para defecar. Tuvo infecciones y heridas, pero mejoró con tratamiento. Meses después, le realizaron otra cirugía para cerrar esas aberturas. Dos años después, seguía sin molestias y en buen estado de salud.",
+                "fh_score": 65.2
+            },
+            "hard": {
+                "text": "Paciente femenina de 30 años, G3P3, sin atención prenatal, ingresó para cesárea de emergencia por sufrimiento fetal y trabajo de parto prolongado, con desenlace neonatal fatal. Intraoperatoriamente se identificaron adherencias pélvicas severas y sangrado estimado de 1500 cc. Evolucionó con oliguria, fiebre y dolor en flanco izquierdo. Hidronefrosis izquierda severa con urinoma intraabdominal confirmada por US y creatinina elevada en líquido aspirado. Se detectó obstrucción completa del uréter izquierdo; se realizó ureteroneocistostomía con stent doble J. Posteriormente, presentó perforación de colon, peritonitis, dehiscencia de anastomosis ureteral e infección severa; se practicaron histerectomía, colostomía izquierda y ureterostomía izquierda en contexto multidisciplinario. Complicaciones posteriores incluyeron retracción de colostomía, infección de herida quirúrgica, y desnutrición. Fue tratada con cirugía correctiva, antibioterapia escalonada y soporte nutricional. Se realizó cierre de colostomía y reconstrucción ureteral mediante colgajo vesical tipo Boari con adecuada evolución. Seguimiento ecográfico y cistográfico durante 2 años mostró función urinaria y digestiva normal sin recurrencias.",
+                "fh_score": 16.49
+            }
+        }
+    },
+    {
+        "original_text_language": "es",
+        "source_topic": "Vólvulo cecal con malrotación y adherencias en mujer con antecedente quirúrgico",
+        "synthetic_summary": {
+            "easy": {
+                "text": "Una mujer de 43 años fue al hospital con dolor en la parte baja del abdomen, náuseas y vómitos. También dejó de ir al baño y de expulsar gases. Los doctores pensaron que podía tener el intestino torcido. En los exámenes vieron que el colon izquierdo estaba muy dilatado. Durante la cirugía, encontraron que una parte del intestino (el ciego) estaba doblada por una banda interna. Le quitaron esa banda, el apéndice y fijaron el ciego en su lugar. La paciente se recuperó bien, empezó a evacuar normalmente y siguió en control sin problemas.",
+                "fh_score": 76.9
+            },
+            "intermediate": {
+                "text": "Una mujer de 43 años llegó al hospital con dolor abdominal tipo cólico, vómitos y dificultad para evacuar y eliminar gases. En los estudios se observó dilatación del colon izquierdo, y la tomografía mostró una imagen típica de vólvulo (torsión del intestino). En la cirugía encontraron que el ciego estaba doblado hacia adelante por una banda de adherencias sin estar correctamente fijado al retroperitoneo. Se liberó la banda, se hizo descompresión a través del apéndice, se retiró el apéndice y se fijó el ciego a la pared abdominal (cecopexia). Después de la operación, la paciente mejoró, volvió a evacuar normalmente y en el seguimiento no tuvo más síntomas.",
+                "fh_score": 59.24
+            },
+            "hard": {
+                "text": "Paciente femenina de 43 años con antecedentes de hipertensión arterial controlada, dos cesáreas previas y oclusión tubaria bilateral, ingresó con cuadro de 24 h de evolución con dolor cólico en hipogastrio irradiado a FII, náuseas, vómito y posteriormente ausencia de evacuaciones y eliminación de gases. Exploración con distensión abdominal predominante en flanco izquierdo, timpanismo en mesogastrio y FII, y peristalsis abolida en esas zonas. Laboratorio mostró leucocitosis con neutrofilia y PCR levemente elevada. Radiografía de abdomen con dilatación del colon izquierdo y niveles hidroaéreos; TAC con imagen en “grano de café” sugerente de vólvulo. Se realizó laparotomía exploradora urgente. Se identificó ciego con movilidad aumentada y flexión anterior provocada por una brida sobre colon ascendente. Se liberó la adherencia, se realizó apendicectomía con descompresión cecal por base apendicular y posterior cecopexia. No se evidenció isquemia ni perforación. Evolución postoperatoria favorable con reanudación del tránsito intestinal y controles ambulatorios sin complicaciones clínicas.",
+                "fh_score": 33.84
+            }
+        }
+    },
+    {
+        "original_text_language": "es",
+        "source_topic": "Caso clínico de tiroiditis autoinmune y síndrome nefrótico en una niña de 10 años",
+        "synthetic_summary": {
+            "easy": {
+                "text": "Una niña de 10 años no tenía familia con problemas de tiroides. A los 9 años le encontraron un bocio, que es cuando la tiroides se hincha. Un examen mostró que tenía tiroiditis crónica, una inflamación de la tiroides. Tenía anticuerpos que atacan la tiroides. No tomaba medicinas cuando entró al hospital. Vino porque su orina salía con espuma desde hace 5 días. También tenía dolor de barriga, vómitos y diarrea. Luego le salieron hinchazones en los ojos y las piernas. Orinaba menos, se sentía débil y tuvo fiebre de 38 grados el día antes de entrar. En la urgencia, vieron que tenía hinchazón en los ojos y en las piernas. Tenía el bocio visible, pero no dolía ni tenía bultos. Escucharon un ruido en el corazón, como un soplo. Lo demás estaba bien. Su presión era 120/78, que es alta para su edad. Temperatura 38,1 grados. Pesaba 33,9 kilos, medía 131,5 cm y su IMC era 19,8. En los exámenes, la orina tenía mucha proteína, pero no bacterias. El índice de proteína era 2. Las proteínas en sangre eran bajas, 3,8 g/dL, albúmina 2,1. Colesterol alto, 416, triglicéridos 127. Creatinina 0,46. Los gases y la sangre normal. Inmunoglobulinas: A 181, M 131, G 208 baja. C3 y C4 normales. Ecografía de riñones normal. La ingresaron con síndrome nefrótico y tiroiditis autoinmune. Le dieron prednisona, 60 mg por metro cuadrado al día. Mejoró, se le fue la hinchazón y la proteína en orina bajó a normal en 6 días. Para la tiroides, TSH 4,4 alta, T4 libre 0,80 baja. Anticuerpos anti TPO 120, anti Tg 82. Le dieron levotiroxina 25 mcg al día. Ecografía de tiroides normal, con más sangre pero sin lesiones. Otros exámenes negativos. A los 6 días salió bien, con prednisona y levotiroxina. A los 12 meses estaba sin síntomas, tiroides controlada con TSH 1,11. No volvió el síndrome nefrótico.",
+                "fh_score": 70.56
+            },
+            "intermediate": {
+                "text": "Paciente femenina de 10 años, sin antecedentes familiares de patología tiroidea, diagnosticada con bocio a los 9 años mediante ecografía que mostró signos de tiroiditis crónica, y con anticuerpos antitiroideos positivos. No recibía tratamiento al ingreso. Consultó por orina espumosa de 5 días de evolución, acompañada de dolor abdominal, vómitos abundantes y diarrea. Evolucionó con edema en párpados y extremidades, oliguria, astenia y fiebre de 38°C el día previo. En urgencias, se observó edema palpebral bilateral y pretibial, bocio evidente sin dolor ni nódulos, y soplo sistólico eyectivo IV/VI en foco pulmonar sin irradiación. Examen físico restante normal. Presión arterial 120/78 mmHg (percentil 95), temperatura 38,1°C, peso 33,9 kg, talla 131,5 cm (p7), IMC 19,8 (p83). Exámenes de ingreso: orina con proteinuria +++, sin bacterias ni nitritos, leucocitos 7 cel/µL (VN 0-10), eritrocitos 4 cel/µL (VN 0-15), IPC 2 mg/mg, proteínas totales 3,8 g/dL, albúmina 2,1 g/dL, colesterol 416 mg/dL, triglicéridos 127 mg/dL, creatinina 0,46 mg/dL (aclaramiento por Schwartz: 125 ml/min/1,73 m²). Gases venosos, electrolitos y hemograma normales. Estudio inmunológico: IgA 181 mg/dL (VN 45-236), IgM 131 mg/dL (VN 52-242), IgG 208 mg/dL (VN 608-1572), C3 125 mg/dL (VN 80-150), C4 37,3 mg/dL (VN 12-36). Ecografía renal normal. Diagnosticada con síndrome nefrótico (SN) y tiroiditis autoinmune, se inició prednisona 60 mg/m²/día, con respuesta favorable: resolución de edema y proteinuria normal (IPC 0,09) a los 6 días. Función tiroidea: TSH 4,4 UI/ml (VN 0,67-4,16), T4 libre 0,80 ng/dL (VN 0,86-1,4), anti-TPO 120 U/ml (VN 0-60), anti-Tg 82 U/ml (VN 0-60). Iniciada levotiroxina 25 mcg/día. Ecografía tiroidea: tamaño normal, aumento vascular difuso al Doppler, sin lesiones, sugestivo de tiroiditis. Resto de estudios negativos (PCR SARS-CoV-2, ANCA, ANA, anti-DNA, ASLO, anticardiolipinas, anti-MPO, anti-PR3). Alta a los 6 días con prednisona 60 mg/día y levotiroxina 25 mcg/día. Seguimiento a 12 meses: asintomática, tiroides controlada (TSH 1,11 UI/ml), sin recaídas de SN (orina sin proteinuria, creatinina 0,44 mg/dL).",
+                "fh_score": 54.71
+            },
+            "hard": {
+                "text": "Paciente pediátrica de género femenino, 10 años de edad, ausente de anamnesis familiar de endocrinopatía tiroidea, portadora de bocio eutiroideo diagnosticado a los 9 años mediante ultrasonografía tiroidea que evidenció patrones ecográficos compatibles con tiroiditis linfocítica crónica, concomitantemente con positividad para autoanticuerpos antitiroideos. Ausencia de terapia farmacológica al momento de la hospitalización. Motivo de consulta: hematuria espumosa de 5 días de progresión, asociada a cólico abdominal, emesis profusa y evacuaciones diarreicas. Evolución clínica caracterizada por edema periorbitario y en miembros inferiores, oligoanuria, astenia marcada y episodio febril de 38°C en las 24 horas precedentes al ingreso. Evaluación en servicio de emergencias reveló paciente con edema bipalpebral simétrico y pretibial, estruma palpable indoloro sin nodularidad, y presencia de soplo sistólico eyectivo grado IV/VI en foco pulmonar sin propagación. Exploración física remanente sin hallazgos patológicos relevantes. Tensión arterial 120/78 mmHg (percentil 95 para edad y estatura), temperatura axilar 38,1°C, masa corporal 33,9 kg, estatura 131,5 cm (percentil 7), índice de masa corporal 19,8 (percentil 83). Paraclínicos de ingreso destacaron: uroanálisis con proteinuria cualitativa +++ , ausente de bacteriuria y nitrituria, leucocituria 7 células/µL (valor normal: 0-10), eritrocituria 4 células/µL (valor normal: 0-15), ratio proteinuria/creatininuria 2 mg/mg, proteinemia total 3,8 g/dL, hipoalbuminemia severa 2,1 g/dL, hipercolesterolemia 416 mg/dL, hipertrigliceridemia moderada 127 mg/dL, creatininemia 0,46 mg/dL (filtrado glomerular estimado por ecuación de Schwartz: 125 ml/min/1,73 m²). Gasometría venosa, ionograma plasmático y hemoleucograma dentro de límites fisiológicos. Perfil inmunológico: inmunoglobulina A sérica 181 mg/dL (rango normal 45-236), inmunoglobulina M 131 mg/dL (rango normal 52-242), inmunoglobulina G 208 mg/dL (rango normal 608-1572) denotando hipogammaglobulinemia selectiva, complemento C3 125 mg/dL (rango normal 80-150), C4 37,3 mg/dL (rango normal 12-36). Ecografía renal sin alteraciones morfológicas. Ingreso hospitalario bajo diagnóstico de síndrome nefrótico idiopático y tiroiditis autoinmune crónica. Institución terapéutica con corticosteroides orales (prednisona 60 mg/m²/día), evolutivamente favorable con resolución edematosa y remisión progresiva de la proteinuria hasta normoalbuminuria pre-alta (ratio proteinuria/creatininuria 0,09 mg/mg al día 6). Evaluación tireoidea: hormona tirotropina (TSH) 4,4 µUI/ml (rango normal 0,67-4,16), tiroxina libre (FT4) 0,80 ng/dL (rango normal 0,86-1,4), autoanticuerpos anti-tiroperoxidasa 120 U/ml (rango normal 0-60), anti-tiroglobulina 82 U/ml (rango normal 0-60), configurando hipotiroidismo subclínico. Inicio de reposición hormonal con levotiroxina sódica 25 µg/día. Ultrasonido tiroideo: glándula de volumen preservado con hipervascularización difusa en modo Doppler color, ausente de focos sólidos o quísticos, hallazgos sugestivos de proceso inflamatorio autoinmune. Estudios complementarios negativos: reacción en cadena de la polimerasa para SARS-CoV-2, anticuerpos anticitoplasma de neutrófilos, anticuerpos antinucleares, anti-ADN bicatenario, anti-estreptolisina O, anticardiolipinas, anti-mieloperoxidasa y anti-proteinasa 3. Egreso hospitalario al día 6 en condiciones hemodinámicas estables, prescribiendo prednisona 60 mg/día y levotiroxina 25 µg/día. Control ambulatorio a 12 meses: asintomatología completa, eutiroidismo farmacológico (TSH 1,11 µUI/ml), ausencia de recidivas nefróticas (uroanálisis sin proteinuria, creatininemia 0,44 mg/dL).",
+                "fh_score": 17.72
+            }
+        }
+    },
+    {
+        "original_text_language": "es",
+        "source_topic": "Caso clínico de parálisis supranuclear progresiva (PSP)",
+        "synthetic_summary": {
+            "easy": {
+                "text": "Una doctora revisó a una paciente y notó que su cara se veía diferente. Sus ojos estaban muy abiertos, su frente arrugada y su boca no se movía mucho. La paciente caminaba con dificultad, como si se quedara pegada al empezar a caminar. Necesitaba ayuda para moverse. Cuando caminaba, sus pasos eran cortos y lentos, y a veces arrastraba los pies. No podía girar bien ni levantarse fácilmente de una silla. También le costaba moverse en la cama. No tenía problemas para controlar la orina ni mostraba cambios raros en su forma de pensar, pero parecía estar muy apagada y sin ánimos. Sus ojos no se movían bien hacia arriba o abajo, y a veces hacía movimientos extraños con ellos. Un examen del cerebro mostró que una parte estaba más pequeña y había espacios más grandes de lo normal. Los doctores vieron señales claras en las imágenes, como formas que llamaron 'colibrí' y 'gloria de la mañana'. Al final, le diagnosticaron una enfermedad llamada parálisis supranuclear progresiva.",
+                "fh_score": 68.44
+            },
+            "intermediate": {
+                "text": "La evaluación neurológica mostró que la paciente tenía una expresión facial peculiar: ojos muy abiertos, frente arrugada (signo del procerus) y la parte inferior de la cara rígida. Presentaba movimientos lentos y rigidez, especialmente en el tronco y el cuello, con una postura inclinada hacia atrás. Al caminar, tenía problemas para empezar, necesitando apoyo de objetos o personas cercanas. Aunque mejoraba un poco al avanzar, al intentar girar volvía a tener dificultades. Sus pasos eran cortos, con congelación, base amplia, desequilibrio, movimientos lentos en las piernas, arrastre de pies y falta de fluidez en el cuerpo. Los reflejos que ayudan a mantener el equilibrio estaban alterados. Le costaba levantarse de una silla y girarse en la cama. No mostraba signos como rigidez paratónica, reflejos de prensión, incontinencia urinaria ni problemas cognitivos graves, salvo un estado de apatía que empeoraba. Los movimientos de sus ojos hacia arriba y abajo estaban limitados, con movimientos horizontales normales, pero con sacadas de onda cuadrada y oftalmoplejía supranuclear. La resonancia magnética mostró atrofia en el mesencéfalo, dilatación del acueducto de Silvio y del tercer ventrículo, y atrofia en los lóbulos frontales, con signos característicos como el del colibrí y la gloria de la mañana. Fue diagnosticada con parálisis supranuclear progresiva (PSP) probable.",
+                "fh_score": 54.44
+            },
+            "hard": {
+                "text": "La exploración neurológica exhaustiva reveló un fenotipo facial distintivo: facies de mirada fija con marcada midriasis bilateral, contracción persistente del músculo procerus (signo del procerus) y rigidez de la musculatura facial inferior. Se constató hipocinesia con rigidez simétrica de predominio axial, acompañado de una postura retrocólica del tronco y el cuello. La evaluación de la deambulación evidenció un patrón de marcha de nivel superior, caracterizado por una notable vacilación inicial que requería soporte físico externo. Tras la iniciación de la marcha, se observaba una relativa mejoría en la cadencia, aunque con recidiva de ineficiencia al intentar giros corporales. La paciente presentaba pasos cortos, episodios de congelación, base de sustentación ensanchada, inestabilidad postural, bradiquinesia de miembros inferiores, arrastre podal y pérdida de la fluidez cinética troncoapendicular. Los reflejos posturales estaban significativamente comprometidos. Asimismo, se documentó una severa dificultad para la transición de sedestación a bipedestación y para la rotación en decúbito. No se constataron signos de liberación frontal, como rigidez paratónica, reflejos de prensión, incontinencia urinaria o déficits cognitivos frontales (alteraciones disejecutivas, cambios de personalidad o impulsividad), salvo una apatía progresiva de intensidad moderada. Los movimientos sacádicos verticales mostraban marcada restricción, con amplitudes horizontales preservadas, acompañados de sacadas de onda cuadrada y oftalmoplejía supranuclear confirmada. La resonancia magnética cerebral reveló atrofia mesencefálica, dilatación del acueducto de Silvio y del tercer ventrículo, así como atrofia frontocortical, con signos radiológicos patognomónicos del colibrí y de la gloria de la mañana. El diagnóstico final fue de parálisis supranuclear progresiva (PSP) probable.",
+                "fh_score": 31.45
+            }
+        }
+    },
+    {
+        "original_text_language": "es",
+        "source_topic": "Caso clínico de miocarditis y shock cardiogénico tras picadura de insecto",
+        "synthetic_summary": {
+            "easy": {
+                "text": "Una mujer de 36 años, que estaba sana, fue picada por un insecto en la mano. Se le hinchó y se puso roja. A las pocas horas tuvo fiebre. Fue a una clínica y le dieron medicinas para la inflamación y antibióticos. Tres días después, fue al hospital porque seguía con fiebre. Tenía la temperatura alta (38,9°C), el corazón muy rápido y la presión baja. Un examen mostró que su corazón latía mal y estaba débil. Los análisis de sangre mostraron problemas en el corazón, pero no infección. Una ecografía mostró que el corazón no bombeaba bien. En el hospital, intentaron ayudarla con máquinas para el corazón, pero tuvo un paro cardíaco. Lograron salvarla con una máquina especial. Al día siguiente, el corazón estaba peor y tenía coágulos. También tuvo problemas en los riñones y necesitó otra máquina para limpiarle la sangre. Los pulmones también se enfermaron, y usaron otra máquina para ayudarla a respirar. Un examen del corazón mostró inflamación. Cambiaron las máquinas para ayudar más al corazón. La mujer tuvo sangrados y otras complicaciones, pero la estabilizaron. La pusieron en lista para un trasplante de corazón. Después de 49 días, le hicieron el trasplante. Tuvo más problemas, como infecciones, pero se mejoró. La dieron de alta después de 101 días y estaba bien tres meses después.",
+                "fh_score": 73.7
+            },
+            "intermediate": {
+                "text": "Una mujer de 36 años, sin problemas de salud previos, fue picada por un insecto en la mano derecha, lo que le causó hinchazón y enrojecimiento. A las 6 horas tuvo fiebre, aunque la marca de la picadura desapareció. En una clínica le dieron prednisolona (20 mg/día) y antibióticos. Tres días después, llegó a urgencias con fiebre intermitente, temperatura de 38,9°C, corazón acelerado y presión baja (80/52 mmHg). Un electrocardiograma mostró que el corazón latía de forma irregular y con problemas. La radiografía de tórax estaba normal. Los análisis de sangre mostraron daño cardíaco (CK-MB 96 ng/mL, troponina I 8 ng/mL), pero no infección. Una ecografía mostró que el corazón bombeaba mal (fracción de eyección 30,6%). Un examen de las arterias del corazón no encontró bloqueos. Usaron una máquina para ayudar al corazón, pero tuvo un paro cardíaco. Tras 25 minutos, una máquina especial (PCPS) la estabilizó. Las pruebas de infecciones fueron negativas. Al día 2, los marcadores de daño cardíaco subieron más. La ecografía mostró coágulos en el corazón y función aún peor. Al día 3, tuvo fallo en varios órganos y necesitó hemodiálisis por problemas renales. Al día 4, el lado derecho del corazón también falló, y usaron máquinas para ambos lados del corazón. Los pulmones se complicaron, requiriendo una máquina para oxigenar la sangre. Un examen del corazón mostró inflamación. Cambiaron a máquinas más fuertes el día 13. La paciente tuvo un trasplante de corazón el día 49. Hubo sangrados e infecciones, pero se controlaron con cirugía y medicinas. La dieron de alta el día 101, y estaba estable a los 3 meses.",
+                "fh_score": 66.77
+            },
+            "hard": {
+                "text": "Mujer de 36 años, previamente sana, sufrió una única picadura por un insecto Hymenoptera no identificado en el dorso de la mano derecha, desencadenando edema localizado y eritema. A las 6 horas se manifestó fiebre punzante, con resolución progresiva del sitio de la picadura. Atendida en un centro local, se le prescribió prednisolona oral (20 mg/día) y antibioticoterapia empírica. A los 3 días, ingresó al servicio de urgencias por fiebre intermitente, presentando temperatura de 38,9°C, taquicardia sinusal e hipotensión severa (80/52 mmHg). La electrocardiografía evidenció fibrilación auricular con respuesta ventricular rápida (130 lpm) y elevación difusa del segmento ST. La radiografía torácica mostró relación cardiotorácica normal, sin infiltrados ni congestión. El hemograma descartó eosinofilia, leucocitosis, leucopenia o desviación izquierda. Los biomarcadores cardíacos revelaron CK-MB de 96,0 ng/mL, troponina I de 8,0 ng/mL, proteína C reactiva de 10,5 mg/L, procalcitonina de 0,32 ng/mL y NT-proBNP de 20 700 pg/mL. La ecocardiografía transtorácica demostró hipocinesia global del ventrículo izquierdo (fracción de eyección 30,6%) sin derrame pericárdico. El cateterismo cardíaco urgente descartó obstrucciones coronarias o vasospasmo. Se implantó un balón de contrapulsación intraaórtico ante shock cardiogénico, pero la paciente progresó a taquicardia ventricular, fibrilación ventricular y paro cardíaco intrahospitalario. La reanimación cardiopulmonar manual fue ineficaz tras 25 minutos, requiriendo soporte cardiopulmonar percutáneo (PCPS, CAPIOX®). La circulación espontánea se restableció tras 25 minutos, con recuperación neurológica completa. Las pruebas microbiológicas (antígeno de influenza, cultivos de esputo y sangre, serologías virales) resultaron negativas. Al día 2, CK-MB y troponina I alcanzaron picos de >303 ng/mL y >81 ng/mL, respectivamente. La ecocardiografía de control mostró deterioro de la función ventricular izquierda, trombos intracardiacos en aurícula y ventrículo izquierdos, y cierre persistente de válvulas aórticas. Al día 3, se instauró fallo multiorgánico, requiriendo hemodiálisis venovenosa continua por acidosis metabólica y oliguria. Al día 4, la disfunción ventricular derecha se agravó, con pérdida progresiva de actividad eléctrica cardíaca, requiriendo transición a soporte mecánico biventricular (cánulas en aurícula derecha, tronco pulmonar, ápex ventricular izquierdo y aorta ascendente, utilizando bombas centrífugas MEDTRONIC Affinity CP). La hemorragia pulmonar con consolidación bilateral severa obligó al uso de un oxigenador de membrana, manteniendo un flujo de 3,5 L/min y presión arterial media de 65 mmHg. La biopsia endomiocárdica reveló inflamación linfocítica predominante con eosinófilos y necrosis miocárdica focal. Los ajustes ventilatorios priorizaron protección pulmonar (presión de conducción 15 cmH2O, meseta 30 cmH2O), con broncoscopias repetidas para desobstrucción traqueobronquial. En el día 13, ante ausencia de actividad eléctrica, se migró a dispositivos Levitronix Centri-Mag. La paciente fue transferida a un centro de trasplantes, recibiendo trasplante cardíaco ortotópico el día 49. La evolución postrasplante incluyó hemorragias mediastínicas y vaginales, infecciones de herida esternal, úlceras de presión e hiperbilirrubinemia, estabilizadas mediante desbridamiento, hemostasia y antibioticoterapia intensiva. Cinco sesiones de plasmaféresis previnieron rechazo humoral. La ECMO venoarterial se mantuvo hasta el día 58 por insuficiencia cardíaca postoperatoria. La biopsia postrasplante descartó rechazo celular o humoral. Un episodio de shock séptico llevó a laparoscopia exploratoria y apendicectomía el día 93. La extubación ocurrió el día 96, con alta hospitalaria el día 101. A los 3 meses de seguimiento, la paciente permanecía clínicamente estable.",
+                "fh_score": 30.05
+            }
+        }
+    },
+    {
+        "original_text_language": "es",
+        "source_topic": "Caso clínico de insuficiencia cardíaca en un paciente con síndrome de Marfan",
+        "synthetic_summary": {
+            "easy": {
+                "text": "Un hombre joven de 24 años tenía una enfermedad llamada síndrome de Marfan, que daña el corazón. Fue al hospital tres veces entre 2014 y 2017 porque su corazón no trabajaba bien. También tenía presión alta y otros problemas de salud. En 2010, le operaron para arreglar un problema en un vaso grande del corazón y le pusieron una válvula nueva. Durante esa cirugía, tuvo un problema grave en el corazón y necesitó otra operación. En 2014, le pusieron otra pieza en el corazón, pero la cirugía le causó parálisis en las piernas. Su corazón estaba muy débil. Le dieron medicinas y una máquina para ayudar al corazón. En 2017, tuvo más problemas cardíacos y una infección después de otra cirugía. Estaba muy cansado, con las piernas hinchadas y le costaba respirar. Le dieron medicinas fuertes y una máquina para ayudarlo. Con un nuevo medicamento, mejoró y no tuvo más problemas graves en 9 meses.",
+                "fh_score": 67.66
+            },
+            "intermediate": {
+                "text": "Un hombre de 24 años con síndrome de Marfan (MFS) fue internado por tres episodios de insuficiencia cardíaca entre 2014 y 2017. Tenía presión alta, colesterol alto, problemas de tiroides, una alergia grave a un medicamento y antes fumaba. En 2010, le diagnosticaron MFS tras un problema grave en la aorta, con antecedentes familiares. Le operaron para poner una válvula y aorta artificiales, pero tuvo un infarto durante la cirugía, tratado con otra operación. En 2014, le pusieron otra prótesis en la aorta por un aneurisma, pero la cirugía causó parálisis en las piernas y problemas para ir al baño. Su corazón estaba muy débil (fracción de eyección 20%). Le dieron medicinas y un desfibrilador. En 2017, tuvo otro episodio cardíaco y una infección tras una cirugía para arreglar válvulas del corazón. Tenía hinchazón en las piernas, líquido en el abdomen y problemas para respirar. Los exámenes mostraron el corazón débil y una infección. Lo trataron con diuréticos, antibióticos y un nuevo medicamento (sacubitril/valsartan). En un mes, mejoró, y a los 9 meses, su corazón estaba más fuerte (fracción de eyección 42%) sin más problemas.",
+                "fh_score": 63.01
+            },
+            "hard": {
+                "text": "Varón de 24 años con síndrome de Marfan (MFS) ingresó al departamento de medicina interna por tres episodios consecutivos de insuficiencia cardíaca aguda descompensada con fracción de eyección reducida (ADHFrEF) entre 2014 y 2017. Antecedentes: hipertensión arterial, dislipidemia, hipertiroidismo, anafilaxia por flecainida y tabaquismo previo. El diagnóstico de MFS se estableció en 2010 tras disección aórtica aguda tipo A, con antecedentes familiares (padres y tres hermanos con MFS). Se realizó reemplazo de aorta ascendente y válvula aórtica con prótesis mecánica, complicado intraoperatoriamente por síndrome coronario agudo inferior, tratado con injerto de derivación coronaria. En mayo de 2014, se implantó prótesis mecánica en aorta descendente y arco aórtico por aneurisma disecante crónico, resultando en hematoma periaórtico, isquemia medular, paraplejia, hipoestesia térmica, dolor neuropático e incontinencia rectal. Durante el primer episodio de ADHFrEF (2014), se documentó NT-proBNP de 12,000 pg/mL y ecocardiograma transtorácico con dilatación bicameral izquierda, insuficiencia mitral y tricuspídea moderada, hipertrofia ventricular izquierda, acinesia inferior, discinesia septal, hipocinesia global y fracción de eyección ventricular izquierda (FEVI) del 20%. Se instauró tratamiento con diuréticos intravenosos, implante de desfibrilador (St. Jude Ellipse DR, modo DDD) y terapia médica optimizada (furosemida, carvedilol, ramipril, espironolactona, digoxina, amlodipina). En agosto de 2017, nuevo episodio de ADHFrEF mostró NT-proBNP de 2,719 pg/mL, MR-proADM de 1.61 nmol/L, FEVI de 35%, regurgitación tricuspídea severa y ruptura de cuerdas tendinosas mitraales, tratado con diuréticos y terapia médica. En noviembre de 2017, reingresó por ADHFrEF y acumulación de líquido mediastinal infectado post-corrección quirúrgica de insuficiencia valvular (prótesis mitral 31 mm St. Jude y anuloplastia tricuspídea De Vega). Examen físico: presión arterial 120/80 mmHg, pulso 82 lpm, frecuencia respiratoria 26 apm, saturación de oxígeno 87% en aire ambiente, ortopnea, habitus marfanoide (147 kg, 2.2 m), ascitis, edema periférico, crepitaciones pulmonares y disminución de sonidos respiratorios. Laboratorio: NT-proBNP 10,132 pg/mL, MR-proADM 2.36 nmol/L, hipoxemia grave (pO2 46 mmHg), alcalosis mixta (pH 7.56, pCO2 24.8 mmHg, HCO3− 21.9 mmol/L). Electrocardiograma: fibrilación auricular (80 lpm), hipertrofia ventricular izquierda, isquemia subepicárdica. Ecocardiograma: FEVI 30%, fuga paravalvular mitral (gradiente medio 9 mmHg), insuficiencia tricuspídea leve. Radiografía y TAC torácica: congestión hilar, cardiomegalia, consolidación pulmonar y líquido mediastinal infectado. Tratamiento: furosemida 250 mg/día IV, canrenona 100 mg/día, piperacilina/tazobactam 4.5 g/6h, teicoplanina 12 mg/kg/día, seguido de sacubitril/valsartan 49/51 mg/día, carvedilol 3.125 mg/día, espironolactona 100 mg/día, digoxina 0.25 mg/día. A los 9 días, estabilización hemodinámica permitió escalar sacubitril/valsartan a 97/103 mg b.i.d. Seguimiento a 9 meses: FEVI 42%, reducción de NT-proBNP, mejora ecocardiográfica (diámetros y masa ventricular) y calidad de vida sin nuevos episodios de ADHFrEF.",
+                "fh_score": 33.41
+            }
+        }
+    },
+    {
+        "original_text_language": "es",
+        "source_topic": "Caso clínico de politraumatismo y complicaciones por fractura subtrocanteriana",
+        "synthetic_summary": {
+            "easy": {
+                "text": "Un hombre de 41 años tuvo un accidente de auto en 2016. Se lastimó las piernas, el pecho, el abdomen y la cabeza, pero la cabeza no mucho. Los rayos X mostraron que se rompió un hueso de la pierna izquierda y otro en la cadera derecha. Los doctores le pusieron un clavo en el hueso de la cadera y un aparato en la rodilla para ayudar a sanar. Dos semanas después, arreglaron el hueso de la pierna izquierda. Todo iba bien. Entre 2016 y 2019, a veces le dolía la cadera, pero se le quitaba con medicinas. En 2020, el dolor empeoró y no podía moverse bien. Los rayos X mostraron que el clavo se rompió y el hueso no sanó. Intentaron sacarle el clavo, pero no pudieron. En nuestra clínica, en febrero de 2020, le quitaron el clavo roto, limpiaron el hueso y encontraron una infección. Le dieron medicinas fuertes por 10 días. Luego, limpiaron otra vez y pusieron un nuevo clavo con un pedazo de hueso de su cuerpo. En marzo, la infección volvió, así que limpiaron varias veces y dieron más medicinas. En mayo, quitaron el clavo, pusieron otro con antibióticos y después usaron un hueso de su pierna para arreglar la cadera con una placa. Cerraron la herida bien. Ahora, el hombre está bien, sin dolor, la infección se fue y el hueso sanó.",
+                "fh_score": 81.92
+            },
+            "intermediate": {
+                "text": "Un hombre de 41 años ingresó en 2016 a urgencias tras un accidente de tránsito con múltiples lesiones: fractura de platillos tibiales izquierdos, fractura subtrocanteriana derecha, trauma toracoabdominal y trauma craneoencefálico leve. Le realizaron cirugía para colocar un clavo cefalomedular en el fémur derecho y un tutor externo en la rodilla izquierda como medida temporal. A los 15 días, arreglaron la fractura tibial con cirugía definitiva, con buena recuperación. Entre 2016 y 2019, tuvo dolores ocasionales en la cadera derecha que mejoraban con analgésicos y antiinflamatorios, pero los rayos X mostraban problemas en el clavo y dudas sobre la unión del hueso. En 2020, el dolor aumentó, limitando su movimiento. Los rayos X confirmaron que el clavo se rompió y el hueso no había sanado. En otro hospital intentaron sin éxito retirar el clavo. En febrero de 2020, en nuestra institución, le quitaron el clavo, limpiaron el hueso y encontraron una infección por Klebsiella pneumoniae, tratada con meropenem por 10 días. Luego, hicieron otro lavado quirúrgico y colocaron un nuevo clavo con injerto óseo de sus crestas iliacas. En marzo, la infección volvió, con una nueva bacteria (Enterobacter), tratada con vancomicina y meropenem tras varias limpiezas quirúrgicas. En abril, terminó el tratamiento y salió estable. En mayo, por persistencia de la infección, retiraron el clavo, pusieron uno con antibióticos (gentamicina) y luego usaron un hueso de su peroné con una placa para fijar la fractura. Usaron un sistema para cerrar la herida. La infección desapareció, el hueso sanó y el paciente recuperó la movilidad sin dolor.",
+                "fh_score": 56.73
+            },
+            "hard": {
+                "text": "Paciente masculino de 41 años ingresó en 2016 al servicio de urgencias por politraumatismo secundario a colisión vehicular, presentando fractura de platillos tibiales izquierdos, fractura subtrocanteriana derecha, trauma toracoabdominal y traumatismo craneoencefálico leve. La radiografía inicial confirmó las fracturas. Se realizó osteosíntesis de fémur derecho con clavo cefalomedular largo a foco cerrado y colocación de tutor externo transarticular de rodilla como control de daño provisional. A los 15 días, se procedió a osteosíntesis definitiva de platillos tibiales, con evolución radiológica y clínica favorable. Entre 2016 y 2019, refirió episodios intermitentes de dolor coxofemoral derecho, controlados con antiinflamatorios no esteroideos y analgésicos, sin limitación funcional significativa; las radiografías seriadas sugerían fatiga de los bloqueos distales y cuestionable consolidación ósea. En 2020, el dolor coxofemoral se exacerbó, acompañado de limitación funcional. La radiografía de control evidenció fractura del clavo cefalomedular en su tercio proximal y pseudoartrosis subtrocanteriana. Un intento extrainstitucional de extracción del material de osteosíntesis fue infructuoso, derivando al paciente a nuestra institución. El 8 de febrero de 2020, se realizó extracción del material, curetaje del foco de no unión y toma de cultivo, que resultó positivo para Klebsiella pneumoniae, tratado con meropenem intravenoso durante 10 días. El 20 de febrero, tras lavado quirúrgico y drenaje de hematoma, se procedió a nueva osteosíntesis con clavo cefalomedular y autoinjerto óseo de crestas iliacas. En marzo de 2020, se reactivó la infección, requiriendo cinco intervenciones de desbridamiento y lavado quirúrgico, identificándose Enterobacter spp., manejado con vancomicina y meropenem. A finales de abril, completó el tratamiento antibiótico con estabilidad clínica. En mayo, ante persistencia infecciosa, se retiró el material de osteosíntesis, colocando un clavo TENS endomedular recubierto de cemento con gentamicina. Tras dos lavados quirúrgicos adicionales, se procedió a resección de bordes óseos hasta tejido viable, injerto óseo autólogo peroneal no vascularizado (10 cm) y fijación con placa condílea de fémur distal. Se empleó un sistema de cierre asistido por vacío (VAC), con cierre definitivo el 28 de mayo. La evolución postoperatoria fue favorable, con cicatrización completa, remisión de la infección, consolidación radiológica confirmada y preservación funcional de la extremidad, manteniendo al paciente asintomático.",
+                "fh_score": 29.21
+            }
+        }
+    },
+    {
+        "original_text_language": "es",
+        "source_topic": "Caso clínico de síndrome de espalda recta en una adolescente",
+        "synthetic_summary": {
+            "easy": {
+                "text": "Una chica de 17 años fue al doctor porque le dolía el pecho y la espalda. El dolor empezó hace dos meses y se sentía unos días por semana. También sentía el corazón rápido y le faltaba el aire. El dolor no era muy fuerte y no cambiaba si hacía ejercicio o descansaba. Estaba sana, pero tenía migrañas que controlaba con pastillas. Un doctor ya le había hecho pruebas del corazón y todo estaba bien. En la clínica, su presión y pulso estaban normales. Era alta, delgada y no tenía ruidos raros en el corazón ni pulmones. Las pruebas de sangre y corazón salieron bien. Una radiografía mostró que su espalda estaba muy recta, sin la curva normal. Los doctores dijeron que tenía síndrome de espalda recta. Le recomendaron ejercicios con un especialista para arreglar la espalda. Un mes después, casi no tenía dolor ni otros problemas. Una prueba mostró un pequeño problema en el corazón, pero no era grave. Le explicaron que no era peligroso y debía seguir los ejercicios. No volvió a tener problemas en un año.",
+                "fh_score": 79.1
+            },
+            "intermediate": {
+                "text": "Una adolescente de 17 años visitó la clínica por dolor en el pecho izquierdo y en la espalda (a nivel de T7) durante dos meses. También sentía palpitaciones y dificultad para respirar algunos días. El dolor, que era leve (2-6/10), aparecía tanto en reposo como con ejercicio. Estaba sana, salvo por migrañas controladas con medicamentos (lomerizina, loxoprofen, naratriptan). Un mes antes, un médico hizo pruebas de corazón que salieron normales. No tenía antecedentes de lesiones ni enfermedades autoinmunes. En el examen, su presión era 107/60 mmHg, pulso 62 lpm, altura 162 cm, peso 43 kg (IMC 16,4). El corazón y los pulmones estaban normales, y el dolor no aumentaba al tocar el pecho. Las pruebas de sangre y corazón fueron normales. Las radiografías mostraron que su espalda estaba recta, sin la curva normal. Se sospechó síndrome de espalda recta y le indicaron ejercicios quiroprácticos para mejorar la curva de la espalda. Un mes después, el dolor y los síntomas casi desaparecieron. Una ecografía mostró un leve problema en una válvula del corazón, pero no era grave. Le confirmaron que tenía síndrome de espalda recta, le explicaron que no era peligroso y le recomendaron seguir los ejercicios. No tuvo más problemas ni visitó el hospital en un año.",
+                "fh_score": 68.13
+            },
+            "hard": {
+                "text": "Adolescente femenina de 17 años consultó por un cuadro de dos meses de evolución caracterizado por dolor torácico izquierdo y una semana de dolor dorsal a nivel de T7. El dolor torácico se asociaba a palpitaciones y disnea episódica (3-4 días/semana). Una semana previa a la consulta, la frecuencia de palpitaciones y disnea disminuyó, pero persistía un dolor sordo intermitente en hemitórax izquierdo y región dorsal media, sin irradiación, con intensidad fluctuante (2-6/10, promedio 4/10), independiente de la actividad física o el reposo, sin factores desencadenantes ni atenuantes. La paciente, por lo demás sana, presentaba antecedentes de migraña controlada con lomerizina, loxoprofen y naratriptan, sin ataques recientes. Un mes antes, un médico local realizó electrocardiograma y monitoreo Holter, con resultados dentro de rangos normales. Negaba traumatismos, intervenciones quirúrgicas o antecedentes familiares de patologías autoinmunes/inflamatorias. Al examen físico: presión arterial 107/60 mmHg, frecuencia cardíaca 62 lpm, estatura 162 cm, peso 43 kg (IMC 16,4 kg/m²). La auscultación cardiopulmonar no reveló soplos, arritmias ni ruidos patológicos. La palpación torácica mostró dolor localizado no reproducible en articulaciones esternocostales inferiores; las maniobras de tracción de brazo horizontal y del gallo cantando fueron negativas. No se detectó hiperestesia musculoesquelética. Los estudios paraclínicos, incluyendo función tiroidea, fueron normales. La radiografía torácica evidenció rectificación de la columna torácica superior con pérdida de la cifosis fisiológica, sin fracturas costales ni neumotórax. Se sospechó síndrome de espalda recta, corroborado por criterios diagnósticos de Davies et al. y DeLeon et al., con una distancia T8-línea T4-T12 de 0,91 cm, diámetro anteroposterior de 74 cm y transversal de 243,2 cm. Se indicó terapia quiropráctica para restaurar la cifosis torácica y seguimiento ambulatorio por un mes. Postconsulta, los síntomas (dolor torácico/dorsal, palpitaciones, disnea) remitieron progresivamente, desapareciendo a las tres semanas. En el control al mes, la ecocardiografía reveló regurgitación mitral trivial sin prolapso valvular. Se confirmó el diagnóstico de síndrome de espalda recta, se reaseguró a la paciente sobre su carácter benigno y se recomendó continuar la terapia quiropráctica. No se reportaron recaídas ni consultas hospitalarias en el año posterior.",
+                "fh_score": 41.74
+            }
+        }
+    },
+    {
+        "original_text_language": "es",
+        "source_topic": "Caso clínico de urolitiasis bilateral complicada con pielonefritis obstructiva y hemorragia post-nefrostomía",
+        "synthetic_summary": {
+            "easy": {
+                "text": "Una mujer de 59 años fue al hospital con dolor en el lado derecho, fiebre y cansancio. Tenía piedras en los riñones y un tubo en el riñón derecho desde hace un año, pero no lo revisaron. También tenía problemas de corazón y diabetes. Estaba un poco confundida, con fiebre y dolor al tocar el lado derecho. Orinaba poco. Los exámenes mostraron que sus riñones no funcionaban bien y tenía inflamación. Una tomografía mostró el riñón derecho hinchado, el tubo bloqueado y una piedra grande. El riñón izquierdo tenía una piedra pequeña. Le pusieron tubos en los riñones para ayudar a la orina, y mejoró. Días después, tuvo una convulsión y problemas para hablar. Una prueba mostró un problema en el cerebro. Le dieron medicinas para evitar más problemas. Luego, se puso pálida, con el corazón rápido y sangre en la orina. Le dieron líquidos y sangre. Encontraron una hemorragia en el riñón derecho y la arreglaron con un procedimiento. En la UCI, mejoró. Luego, usaron un láser para romper la piedra y el tubo bloqueado, y pusieron otro tubo. Querían hacer otro procedimiento, pero su salud empeoró por el corazón y la diabetes, y no pudieron terminar.",
+                "fh_score": 75.68
+            },
+            "intermediate": {
+                "text": "Una mujer de 59 años con piedras en ambos riñones llegó al hospital con dolor en el flanco derecho, fiebre (38,3°C) y fatiga. Tenía un stent doble J en el riñón derecho desde hace un año sin seguimiento, además de insuficiencia cardíaca, diabetes tipo 2 mal controlada y enfermedad renal crónica. Estaba estable, pero un poco confundida (Glasgow 14/15), con dolor en el flanco y orina de 800 cc/día. Los exámenes mostraron daño renal (creatinina 107 mg/L, urea 3 g/L), inflamación (proteína C reactiva 300 mg/L, glóbulos blancos 17,000/mm³), anemia (hemoglobina 7.6 g/dL) y potasio alto (5.4 mEq/L). No había infección en la orina. Una tomografía mostró hinchazón en el riñón derecho, un stent calcificado y una piedra de 35x28 mm, y en el riñón izquierdo, una piedra de 12x7 mm. Le pusieron tubos (nefrostomía) en ambos riñones, mejorando los síntomas y los exámenes. Tres días después, tuvo una convulsión y dificultad para hablar. Una tomografía cerebral mostró un derrame cerebral, y le dieron enoxaparina y Kardegic. Cuatro días después, tuvo palidez, taquicardia (110 lpm), presión baja (80/50 mmHg) y sangre en la orina. Su hemoglobina cayó a 4.4 g/dL. Le dieron líquidos, vasopresores y transfusiones. Una tomografía encontró una hemorragia en el riñón derecho. En un procedimiento, cerraron un vaso que sangraba con éxito. En la UCI, se estabilizó y reiniciaron las medicinas para el cerebro con cuidado. Luego, rompieron parte del stent calcificado con láser y pusieron otro tubo. Planearon otro procedimiento para quitar el stent y la piedra, pero su salud empeoró por el corazón, la diabetes y los riñones, retrasando el tratamiento.",
+                "fh_score": 69.45
+            },
+            "hard": {
+                "text": "Mujer de 59 años con antecedentes de urolitiasis bilateral recurrente presentó dolor en flanco derecho, fiebre (38,3°C) y astenia. Portadora de stent doble J derecho colocado un año antes por litiasis pélvica sintomática, sin seguimiento. Comorbilidades: insuficiencia cardíaca derecha, diabetes mellitus tipo 2 mal controlada y enfermedad renal crónica (creatinina nadir 18 mg/L). Clínicamente estable, con escala de Glasgow 14/15 (respuesta verbal levemente alterada), sensibilidad en flanco derecho y diuresis de 800 cc/24h. Laboratorio: lesión renal aguda (creatinina sérica 107 mg/L, normal 6-12 mg/L; urea 3 g/L, normal 0.15-0.45 g/L), marcadores inflamatorios elevados (PCR 300 mg/L, normal <5 mg/L; leucocitos 17,000/mm³, normal 4000-10,000/mm³), anemia normocítica (hemoglobina 7.6 g/dL, normal 12-16 g/dL) e hiperkalemia leve (potasio 5.4 mEq/L, normal 3.5-5.1 mEq/L). Uroanálisis y urocultivo negativos para infección bacteriana. Tomografía abdominopélvica sin contraste: hidronefrosis derecha, stent doble J calcificado en ambos extremos, litiasis pélvica derecha (35x28 mm, 588 UH); riñón izquierdo atrófico con hidronefrosis y litiasis pélvica (12x7 mm, 531 UH). Ante pielonefritis obstructiva severa por stent incrustado, se realizó nefrostomía percutánea bilateral, con mejoría clínica y normalización de marcadores inflamatorios y función renal. A los tres días, presentó convulsión generalizada con disartria; tomografía cerebral urgente reveló lesiones isquémicas en lóbulos occipital izquierdo y frontal derecho, sugestivas de accidente cerebrovascular embólico. Inició enoxaparina (0.4 cc/día) y ácido acetilsalicílico (160 mg/día). Cuatro días después, desarrolló palidez mucocutánea, taquicardia (110 lpm), hipotensión (80/50 mmHg) y hematuria macroscópica por catéter urinario, con caída de hemoglobina (7.5 a 4.4 g/dL), sugiriendo hemorragia activa. Se administró fluidoterapia, vasopresores y transfusiones, estabilizando para angiografía por TAC. Esta mostró colección polar media heterogénea (17 mm) con extravasación de contraste en fases arterial y portal, indicando hemorragia activa de arterias polares superior y media, con coágulos intraluminales en pelvis renal y vejiga, diagnosticándose fístula arteriovenosa (FAV) post-nefrostomía, exacerbada por anticoagulación. Arteriografía renal urgente vía femoral derecha con catéter 5F reveló FAV en polo inferior renal con drenaje venoso temprano a vena cava inferior y pseudoaneurisma. Embolización superselectiva con microespirales (3-5 mm) y partículas de Gelfoam logró oclusión completa, confirmada por inyección de contraste. En UCI, la hemodinámica se estabilizó; se reintrodujo anticoagulación con monitorización de INR. La hematuria cesó y la función renal se normalizó. La primera etapa del tratamiento incluyó litotripsia endoscópica láser del bucle inferior calcificado del stent, inserción de un segundo stent doble J y extracción de nefrostomía. La segunda etapa, planificada a las seis semanas, incluyó ureteroscopia flexible derecha para liberar el bucle superior calcificado, fragmentación de litiasis pélvica y extracción del stent incrustado. Sin embargo, la deterioración por insuficiencia cardíaca, diabetes descontrolada, enfermedad renal crónica y accidente cerebrovascular previo impidió completar la segunda etapa.",
+                "fh_score": 35.79
+            }
+        }
+    },
+    {
+        "original_text_language": "es",
+        "source_topic": "Caso clínico de insuficiencia cardíaca derecha por insuficiencia de válvula pulmonar en paciente con tetralogía de Fallot corregida",
+        "synthetic_summary": {
+            "easy": {
+                "text": "Un hombre de 52 años fue al hospital porque su corazón latía muy rápido y estaba cansado. Los doctores arreglaron su corazón con un choque eléctrico. Hace muchos años, le operaron el corazón por un problema desde que nació, pero no fue a revisiones después. En la clínica, vieron que una válvula del corazón no funcionaba y una parte del corazón estaba muy grande. Las pruebas confirmaron el problema. Le operaron para cambiar la válvula, y después se sintió mucho mejor.",
+                "fh_score": 73.84
+            },
+            "intermediate": {
+                "text": "Un hombre de 52 años llegó al hospital por palpitaciones y cansancio. Un examen mostró que su corazón latía muy rápido (180 lpm). Lo estabilizaron con un choque eléctrico y lo enviaron a nuestra clínica. A los 5 años, le operaron por tetralogía de Fallot, pero no tuvo seguimiento. Su presión era 116/70 mmHg, pulso 80 lpm y oxígeno 99%. Los doctores notaron venas del cuello hinchadas y ruidos extraños en el corazón, indicando que una válvula no funcionaba y el corazón estaba agrandado. Los rayos X y una ecografía confirmaron que la válvula pulmonar estaba dañada, causando problemas en el corazón derecho. Un examen especial mostró que el corazón no bombeaba bien. Le cambiaron la válvula pulmonar en una cirugía, y los ruidos del corazón se fueron. El paciente mejoró.",
+                "fh_score": 67.45
+            },
+            "hard": {
+                "text": "Varón de 52 años ingresó por palpitaciones súbitas y astenia generalizada. La electrocardiografía inicial reveló taquicardia ventricular sostenida (180 lpm), revertida a ritmo sinusal mediante cardioversión eléctrica inmediata. Fue derivado a nuestra institución para evaluación exhaustiva. Antecedentes: corrección quirúrgica de tetralogía de Fallot (TOF) a los 5 años con reconstrucción del tracto de salida del ventrículo derecho (VD) mediante injerto homólogo y cierre de defecto septal ventricular, sin seguimiento posterior. Al ingreso, presentaba presión arterial 116/70 mmHg, frecuencia cardíaca 80 lpm y saturación de oxígeno 99% en aire ambiente. La inspección de pulsos yugulares mostró onda a prominente y descenso profundo, sugestivos de elevada presión de llenado del VD y compensación por hipercontracción auricular derecha. La auscultación identificó un murmullo diastólico regurgitante agudo en el tercer espacio intercostal izquierdo, primer sonido cardíaco (S1) ampliamente dividido, segundo sonido (S2) único y tercer sonido (S3) derecho en el cuarto borde paraesternal, compatibles con dilatación severa del VD secundaria a insuficiencia pulmonar (PR) libre por disfunción valvular. El electrocardiograma evidenció bloqueo completo de rama derecha (QRS 200 ms). La radiografía torácica mostró cardiomegalia con dilatación de arterias pulmonares bilaterales. La ecocardiografía transtorácica confirmó regresión completa de la válvula pulmonar, PR libre y dilatación significativa del VD. La resonancia magnética cardíaca cuantificó un volumen diastólico final del VD de 428 ml (índice 240 ml/m²), fracción de eyección del VD del 36% y fracción de regurgitación pulmonar del 74%. La tomografía computarizada multidetector corroboró la ausencia funcional de la válvula pulmonar del injerto homólogo. La cateterización cardíaca reveló una onda de presión auricular derecha con morfología característica (onda a prominente, descenso y asociado a S4 y S3 en fonocardiograma) y presiones diastólicas finales pulmonar y del VD prácticamente idénticas debido a PR libre. La evaluación multimodal confirmó insuficiencia cardíaca derecha severa por dilatación significativa del VD secundaria a regresión valvular pulmonar. Tras reemplazo valvular pulmonar, el «quinteto de sonidos cardíacos» (murmullo diastólico, S1 dividido, S2 único, S3 y S4 derechos) se resolvió completamente, con mejoría clínica significativa.",
+                "fh_score": 40.17
+            }
+        }
+    },
+    {
+        "original_text_language": "es",
+        "source_topic": "Caso clínico de obstrucción intestinal post-trasplante cardíaco por línea motriz de dispositivo de asistencia ventricular",
+        "synthetic_summary": {
+            "easy": {
+                "text": "Un hombre de 62 años con problemas de corazón tuvo un trasplante. Días después, su barriga se hinchó y le dolía. No podía ir al baño, aunque le dieron medicinas. Una prueba mostró que su intestino estaba bloqueado. Lo operaron y encontraron un cable de una máquina vieja del corazón que apretaba el intestino. Quitaron el cable, arreglaron el intestino y cerraron la barriga. Después, el hombre se sintió mejor.",
+                "fh_score": 74.98
+            },
+            "intermediate": {
+                "text": "Un hombre de 62 años con insuficiencia cardíaca, tras usar una máquina para ayudar a su corazón, recibió un trasplante de corazón. Seis días después, en la UCI, tuvo hinchazón abdominal, dolor y fiebre. No evacuaba ni expulsaba gases, y las medicinas no ayudaron. Una tomografía mostró un bloqueo en el intestino delgado. Lo operaron y encontraron un cable de la máquina cardíaca atrapando el intestino. Liberaron el intestino, quitaron el cable y repararon una pequeña herida. Cerraron la barriga, y el paciente mejoró.",
+                "fh_score": 60.34
+            },
+            "hard": {
+                "text": "Varón de 62 años con antecedentes de cardiopatía no isquémica evolucionada a insuficiencia cardíaca, portador de dispositivo de asistencia ventricular izquierda (LVAD), fue sometido a trasplante cardíaco ortotópico. A los 6 días postoperatorios, en la UCI quirúrgica, desarrolló distensión abdominal progresiva, sensibilidad y leucocitosis, motivando evaluación por cirugía general. El paciente no presentaba evacuaciones ni eliminación de gases, sin respuesta a enemas ni metoclopramida oral, inicialmente atribuido a íleo postoperatorio. La tomografía computarizada abdominopélvica reveló múltiples asas intestinales dilatadas con niveles hidroaéreos y un punto de transición en el intestino delgado proximal en el cuadrante superior izquierdo, sugiriendo obstrucción mecánica. Dado que no había antecedentes de cirugías abdominales que justificaran adherencias, se procedió a laparotomía exploratoria. Intraoperatoriamente, se observó dilatación difusa del intestino delgado sin isquemia. Una porción del intestino delgado estaba adherida a la pared abdominal anterior en el cuadrante superior izquierdo, estrangulada por una línea motriz de LVAD retenida, tunelizada en la cavidad peritoneal. Se liberó la línea motriz, se extrajo y se desadhirió el asa intestinal, que resultó viable tras reperfusión. La exploración completa del intestino delgado, desde el ligamento de Treitz hasta el ciego, confirmó dilatación sin otras anomalías. Se reparó un desgarro seroso menor en el punto de adhesión y se restituyó el intestino a la cavidad abdominal, cerrando la fascia con suturas corrientes y la piel con grapas. La evolución postoperatoria fue favorable, con resolución de la obstrucción y mejoría clínica.",
+                "fh_score": 30.6
+            }
+        }
+    },
+    {
+        "original_text_language": "es",
+        "source_topic": "Caso clínico de enfermedad de Castleman en un adolescente",
+        "synthetic_summary": {
+            "easy": {
+                "text": "Un chico de 13 años fue al hospital porque sintió un bulto en la ingle izquierda. Hace 6 años, tuvo un accidente y una operación en la espalda que le hizo perder el movimiento y la sensibilidad en las piernas. Como estuvo mucho tiempo en cama, le salió una llaga en el pie. En el examen, los doctores encontraron un bulto que se movía, pero no dolía ni estaba rojo. Un análisis de sangre mostró algo de inflamación, pero otras pruebas salieron normales. Una tomografía mostró ganglios grandes en la ingle, pero no en otras partes. Para saber qué era, operaron al chico y quitaron los ganglios. Los examinaron y encontraron que tenía una enfermedad rara llamada enfermedad de Castleman. Le dieron pastillas para la inflamación y salió del hospital después de 14 días. Lo revisaron cada 3 meses con pruebas y tomografías, y durante un año no tuvo más bultos ni problemas.",
+                "fh_score": 72.84
+            },
+            "intermediate": {
+                "text": "Un adolescente de 13 años ingresó al hospital por un bulto en la ingle izquierda. Tenía antecedentes de una cirugía en la columna hace 6 años por un accidente, lo que le causó parálisis en las piernas. Por estar mucho tiempo en cama, desarrolló una úlcera en el pie izquierdo. El examen mostró una masa móvil en la ingle, sin dolor ni inflamación. Los análisis de sangre indicaron inflamación (ESR 119 mm/h), pero otras pruebas (sangre, hígado, riñones) fueron normales. Una tomografía de abdomen, tórax y pelvis mostró ganglios agrandados en la ingle (el mayor de 3,5x2,4 cm), sin otros hallazgos. Para descartar enfermedades graves como linfoma, operaron al paciente bajo anestesia general, extirpando los ganglios para biopsia. El análisis mostró enfermedad de Castleman tipo células plasmáticas. Le dieron prednisolona oral y salió del hospital a los 14 días. Lo revisaron cada 3 meses con tomografías, exámenes clínicos y pruebas de sangre. Durante un año, no tuvo más bultos ni síntomas.",
+                "fh_score": 69.62
+            },
+            "hard": {
+                "text": "Adolescente masculino de 13 años ingresó al Hospital de Niños de Damasco por una masa palpable en la región inguinal izquierda. Antecedentes: cirugía vertebral 6 años atrás por traumatismo, resultando en paraplejia y pérdida sensorial en extremidades inferiores. La inmovilización prolongada derivó en úlceras de decúbito en el pie izquierdo. El examen clínico reveló una masa inguinal izquierda móvil, no dolorosa, sin signos inflamatorios locales. Laboratorio: velocidad de sedimentación globular elevada (119 mm/h); hemograma completo, función hepática, electrolitos, urea, creatinina y LDH dentro de rangos normales, descartando enfermedades sistémicas. No se justificaron pruebas adicionales (VIH, antiglobulina directa) ante la ausencia de signos de inmunodeficiencia o trastornos sistémicos. La tomografía computarizada abdominotorácica-pélvica mostró adenopatías infralinguinales, la mayor de 3,5x2,4 cm, sin compromiso de otros órganos o ganglios. Para descartar diagnósticos diferenciales (linfoma, leucemia), se realizó escisión quirúrgica de los ganglios afectados bajo anestesia general, enviándose a estudio histopatológico. La biopsia reveló hiperplasia ganglionar con proliferación de histiocitos, células plasmáticas y vascularización, compatible con enfermedad de Castleman, subtipo de células plasmáticas. El paciente fue dado de alta a los 14 días con prednisolona oral. Se instauró seguimiento trimestral con tomografía de cuerpo entero, examen clínico exhaustivo y pruebas de laboratorio (hemograma, VSG, proteína C reactiva, función hepática y renal). Tras 12 meses, no se reportaron síntomas nuevos, adenopatías ni alteraciones clínicas o de laboratorio, indicando remisión.",
+                "fh_score": 34.11
+            }
+        }
+    },
+    {
+        "original_text_language": "es",
+        "source_topic": "Caso clínico de cardiomiopatía dilatada con hipocalcemia e hipoparatiroidismo",
+        "synthetic_summary": {
+            "easy": {
+                "text": "Un hombre de 55 años fue al hospital porque le costaba respirar al hacer ejercicio y orinaba poco. Tenía un problema en el corazón desde hace 6 meses, pero no tomaba sus medicinas como debía. También sentía pesadez en el pecho, tos con flema espumosa y las piernas hinchadas. Los doctores vieron que estaba pálido, con presión baja y respiración rápida. Su corazón y pulmones no sonaban bien. Las pruebas mostraron que su corazón estaba débil, con poco calcio en la sangre y anemia. También tenía líquido en los pulmones. Le dieron medicinas para el corazón y calcio por vena. Mejoró mucho y le dieron pastillas para el calcio y el corazón. También le pusieron inyecciones para la anemia. Tres meses después, estaba mucho mejor, con el corazón más fuerte.",
+                "fh_score": 75.57
+            },
+            "intermediate": {
+                "text": "Un hombre de 55 años con cardiomiopatía dilatada (DCMP), que no seguía bien su tratamiento, llegó al hospital con dificultad para respirar al hacer ejercicio (NYHA grado IV), menos orina y tos con flema espumosa. También tenía hinchazón en las piernas y hormigueo en manos y pies. Seis meses antes había sido tratado por DCMP. En el examen, tenía presión baja (90/60 mmHg), pulso rápido (110 lpm), respiración acelerada (28/min), palidez y edema en las piernas. Mostró signos de hipocalcemia (Chvostek y Trousseau positivos). Las pruebas revelaron anemia (hemoglobina 5,8 g/dL), calcio bajo (4,3 mg/dL), fosfato alto (7,1 mg/dL), y niveles bajos de hormona paratiroidea. Una ecografía mostró un corazón débil (fracción de eyección 15%) y líquido en los pulmones. Le dieron dobutamina y furosemida, pero no mejoró hasta que recibió calcio intravenoso. Fue dado de alta con pastillas de calcio, calcitriol y medicinas para el corazón, además de inyecciones para la anemia. A los 3 meses, su corazón mejoró (fracción de eyección 25%) y los niveles de calcio y hemoglobina subieron.",
+                "fh_score": 68.78
+            },
+            "hard": {
+                "text": "Varón asiático de 55 años con antecedentes de cardiomiopatía dilatada (DCMP) y adherencia irregular al tratamiento durante 6 meses presentó disnea de esfuerzo (progresión de NYHA II a IV), oliguria de 2 días, tos con expectoración espumosa, edema bilateral en extremidades inferiores y parestesias en manos/pies durante 1 mes. Antecedente de episodio similar tratado conservadoramente 6 meses atrás y cirugía de cataratas 15 años antes. Examen físico: consciente, orientado, afebril, presión arterial 90/60 mmHg, pulso 110 lpm (bajo volumen), frecuencia respiratoria 28/min, palidez, edema pedal bilateral, presión venosa yugular elevada. Signos de Chvostek y Trousseau positivos (hipocalcemia). Cardiovascular: latido apical hiperdinámico en sexto espacio intercostal izquierdo, S1 y S2 normales. Respiratorio: hipoventilación basal bilateral con crepitaciones finas inspiratorias. Laboratorio: hemoglobina 58 g/L (dimórfica), VCM 110 fL, HCM 34 pg/mL, CHCM 36,2 g/dL, vitamina B12 135 pg/mL, ácido fólico 5,4 ng/mL, urea 53 mg/dL, creatinina 0,8 mg/dL, calcio sérico 4,3 mg/dL, fosfato 7,1 mg/dL, albúmina 3,06 g/dL, hormona paratiroidea <0,23 ng/mL, magnesio 2,0 mg/dL. Gasometría arterial: acidosis metabólica leve. ECG: bloqueo completo de rama izquierda, QT prolongado. Radiografía torácica: derrame pleural bilateral. Ecocardiografía: ventrículo izquierdo dilatado, fracción de eyección 15%, compatible con DCMP severa. Tomografía cerebral sin contraste: calcificaciones simétricas bilaterales en cerebelo, ganglios basales y regiones fronto-parieto-occipitales. Tratamiento inicial: dobutamina (6 µg/kg) y furosemida (20 mg IV BID) sin mejoría significativa. Ante hipocalcemia, hiperfosfatemia y hipoparatiroidismo, se diagnosticó cardiomiopatía hipocalcémica; se administró gluconato de calcio IV (1 g inicial, seguido de infusión 37,5 mg/h) con mejoría notable. Alta con calcio oral (3 g/día), calcitriol (0,5 µg/día), benzotiazida/triamtereno (25/50 mg OD), ramipril (5 mg OD), carvedilol (3,125 mg BID) y cianocobalamina para anemia megaloblástica. A los 3 meses: calcio sérico 7,7 mg/dL, fosfato 6,0 mg/dL, hemoglobina 10,1 g/dL, fracción de eyección 25%. Biopsia endomiocárdica planificada, rechazada por el paciente.",
+                "fh_score": 34.65
+            }
+        }
+    },
+    {
+        "original_text_language": "es",
+        "source_topic": "Caso clínico de hematoma perirrenal y adenoma papilar en paciente con glomeruloesclerosis segmentaria focal",
+        "synthetic_summary": {
+            "easy": {
+                "text": "Una mujer de 54 años fue al hospital con mucho dolor en la espalda izquierda, náuseas y vómitos. Sus riñones no funcionaban bien, por lo que estaba en diálisis. Días antes, tuvo anemia y sangre en las heces, y le quitaron un pólipo en el colon. En urgencias, su barriga estaba hinchada y le dolía mucho. Las pruebas mostraron anemia. Una tomografía encontró sangre y un quiste grande en el riñón izquierdo. Le pusieron un tubo para ayudar al riñón, pero necesitó sangre porque la anemia empeoró. La operaron para quitar el riñón izquierdo, donde hallaron un hematoma y una pequeña masa no peligrosa. Después de la cirugía, siguió en diálisis y se recuperó bien, sin más sangrado.",
+                "fh_score": 74.78
+            },
+            "intermediate": {
+                "text": "Una mujer de 54 años, en hemodiálisis por una enfermedad renal, llegó a urgencias con dolor lumbar izquierdo, náuseas y vómitos tras su diálisis. Tenía antecedentes de una operación para quitar glándulas paratiroides y, días antes, anemia y sangrado rectal. Le habían removido un pólipo en el colon. En urgencias, tenía presión 112/65 mmHg, pulso 96 lpm, abdomen hinchado y dolor al tocarlo. Los exámenes mostraron hemoglobina baja (9,0 g/dL) y creatinina alta (6,06 mg/dL). Una tomografía encontró un hematoma grande y un quiste en el riñón izquierdo, con obstrucción. Le pusieron un stent ureteral, pero la hemoglobina cayó a 6,1 g/dL, necesitando transfusión. La operaron, quitando el riñón izquierdo, donde hallaron un hematoma y una pequeña masa benigna. Tras diálisis y transfusiones, se recuperó sin más sangrado y sigue en diálisis.",
+                "fh_score": 60.28
+            },
+            "hard": {
+                "text": "Mujer libanesa de 54 años, en hemodiálisis (HD) de mantenimiento tres veces por semana por glomeruloesclerosis segmentaria focal (GSF), ingresó a urgencias tras HD por dolor lumbar izquierdo agudo, náuseas y vómitos de inicio súbito 12 horas antes. Antecedentes: hiperparatiroidismo secundario severo con calcificación vascular cutánea, tratado sin éxito con cinacalcet durante 3 años, requiriendo paratiroidectomía (hiperplasia de cuatro glándulas) 8 meses previos. Cinco días antes, ingresó por anemia severa y rectorragia; ultrasonido renal mostró riñones pequeños con quistes (hasta 3 cm) y calcificaciones sin hidronefrosis. Cuatro días antes, colonoscopia reveló un pólipo de 7 mm en colon descendente izquierdo, resecado por mucosectomía (adenoma tubular sésil con displasia de bajo grado). Sin fiebre ni traumatismos previos, negaba uso de antiplaquetarios. En urgencias: presión arterial 112/65 mmHg, pulso 96 lpm, temperatura 36,8°C, abdomen distendido con dolor severo en ángulo costovertebral izquierdo. Laboratorio: hemoglobina 9,0 g/dL, hematocrito 29,7%, leucocitos 12,2 x 1000/µL, creatinina 6,06 mg/dL, proteína C reactiva 6 mg/L, TP 83%, INR 1,13. Tomografía multifásica toracoabdominopélvica mostró hematoma perirrenal izquierdo (9x4 cm), colección subcapsular (1,8 cm), quiste grande, hidronefrosis izquierda y calcificaciones hiliares. Se colocó stent ureteral doble J retrógrado, identificando un coágulo ureteral; cultivos y citología de orina negativos. Radiografía abdominal confirmó correcta colocación del stent. Persistió caída de hemoglobina (6,1 g/dL), requiriendo transfusión de eritrocitos leucodepleados. Ante sospecha de hematoma perirrenal subagudo y para descartar malignidad, se realizó nefrectomía radical izquierda tras HD sin heparina, hallando un hematoma (9x9x7 cm) que reemplazaba el parénquima renal y una masa papilar de 2 mm (adenoma papilar en histopatología). Recibió 2 unidades adicionales de eritrocitos intraoperatoriamente. Postoperatorio sin complicaciones, con hemoglobina estabilizada en 10 g/dL tras HD y transfusión adicional. La paciente se recuperó sin evidencia de sangrado, manteniéndose asintomática en HD regular.",
+                "fh_score": 30.23
+            }
+        }
+    },
+    {
+        "original_text_language": "es",
+        "source_topic": "Caso clínico de uveítis anterior hipertensiva asociada a virus varicela-zóster (VZV) y accidente cerebrovascular",
+        "synthetic_summary": {
+            "easy": {
+                "text": "Una mujer de 30 años fue al hospital porque le dolía el ojo derecho y veía menos. También tenía problemas en las articulaciones, el estómago y había perdido mucho peso. Dos semanas antes, dejó de tomar una medicina que ayudaba con la inflamación. Los doctores vieron que su ojo derecho estaba muy inflamado y tenía mucha presión (como si estuviera muy apretado). Las pruebas mostraron que tenía un virus llamado varicela-zóster en el ojo. Le dieron pastillas y gotas para bajar la inflamación y la presión. Mejoró un poco, pero luego tuvo un problema en el cerebro (un derrame). Estuvo dos semanas en el hospital y su ojo mejoró. Sin embargo, dos meses después, el dolor y la mala visión volvieron. La operaron para poner un tubo en el ojo y controlar la presión. Durante la cirugía, tomaron un líquido del ojo y encontraron sustancias que mostraban inflamación. La operación ayudó, y la paciente siguió en tratamiento.",
+                "fh_score": 73.01
+            },
+            "intermediate": {
+                "text": "Una mujer de 30 años llegó al hospital con dolor y pérdida de visión en el ojo derecho durante dos meses. Tenía antecedentes de artritis, problemas gastrointestinales y pérdida de 20 libras. Había reducido la prednisona, un medicamento para la inflamación, antes de los síntomas. El examen mostró visión de 20/40 en el ojo derecho, presión ocular alta (65 mmHg) y signos de inflamación. Las pruebas confirmaron el virus varicela-zóster (VZV) en el ojo. Le dieron acetazolamida, gotas para la presión ocular y valaciclovir. Después, tuvo un accidente cerebrovascular (ACV) por el virus, estuvo hospitalizada dos semanas y mejoró. Dos meses después, el dolor y la visión empeoraron (20/100, presión 39 mmHg). Cambiaron el tratamiento, pero no mejoró mucho, así que le pusieron un tubo (derivación de Ahmed) en el ojo para controlar la presión. Durante la cirugía, analizaron el líquido del ojo y encontraron niveles altos de sustancias inflamatorias como IL-1RA, IP-10 y MCP-1. La cirugía ayudó, y siguió en tratamiento.",
+                "fh_score": 66.78
+            },
+            "hard": {
+                "text": "Mujer de 30 años con antecedentes de artritis inflamatoria, síntomas gastrointestinales sugestivos de enfermedad inflamatoria intestinal y pérdida de peso de 20 libras presentó dolor ocular derecho progresivo y disminución visual de dos meses. Dos semanas antes, redujo prednisona para síntomas inflamatorios sistémicos. Examen oftalmológico: agudeza visual corregida 20/40 OD, 20/20 OS; pupilas 9 mm akinéticas OD, 5 mm reactivas OS; presión intraocular 65 mmHg OD, 21 mmHg OS. Lámpara de hendidura: precipitados queráticos granulomatosos, 3+ células en cámara anterior, atrofia iridiana difusa, ectropion uvea OD; OS normal. Gonioscopia: 3+ células pigmentadas en ángulo inferior OD. Fondo de ojo normal bilateral. Paracentesis anterior: ADN de VZV positivo por PCR; serología IgG VZV positiva. Diagnóstico: uveítis anterior hipertensiva asociada a VZV. Tratamiento: acetazolamida oral, timolol, dorzolamida, brimonidina oftálmicos, valaciclovir 1 g TID, prednisolona 1% cada 2 horas. Posteriormente, presentó accidente cerebrovascular (ACV) por vasculopatía del SNC asociada a VZV, requiriendo hospitalización de 2 semanas con mejoría ocular. A los dos meses, recrudescencia de dolor y visión (BCVA 20/100, PIO 39 mmHg OD), con inyección ciliar 1+ y 3+ células en cámara anterior. Cambio a difluprednato con mínima mejoría. Persistencia de hipertensión ocular llevó a cirugía de filtración con derivación de Ahmed. Durante el procedimiento, se obtuvo humor acuoso para análisis de 22 citoquinas/quimiocinas mediante inmunoensayo de perlas múltiplex, detectando niveles elevados de IL-1RA (1000 pg/mL), IP-10, MCP-1 (150-200 pg/mL), IL-18, MIP-1b (10-20 pg/mL), IL-6 e IL-8 (<10 pg/mL). La intervención quirúrgica estabilizó la presión intraocular, y la paciente continuó en tratamiento.",
+                "fh_score": 39.41
+            }
+        }
+    },
+    {
+        "original_text_language": "es",
+        "source_topic": "Complicaciones neonatales y manejo de fasciotomía",
+        "synthetic_summary": {
+            "easy": {
+                "text": "Un bebé nació antes de tiempo, a las 35 semanas, porque los doctores vieron que se movía poco en el vientre. La mamá tenía algunos problemas de salud, como obesidad y un rasgo en la sangre llamado células falciformes. Durante el embarazo, la bolsa de agua tenía poca cantidad de líquido y el bebé tenía la vejiga y el estómago hinchados. Al nacer, el bebé tuvo problemas para respirar y necesitó oxígeno y tubos para ayudarlo. También tenía el brazo izquierdo muy morado y con ampollas. Los doctores vieron que no se movía y no respondía con ese brazo. Decidieron hacerle una cirugía llamada fasciotomía para liberar la presión en el brazo y salvarlo. Con los días, el brazo mejoró de color y circulación. Las heridas fueron sanando poco a poco y no hubo infecciones. A los 4 meses, las heridas estaban cerradas, y aunque el bebé aún movía poco la mano, podía mover el hombro y el codo. Sigue con terapias y cuidados para mejorar sus movimientos.",
+                "fh_score": 70.25
+            },
+            "intermediate": {
+                "text": "Un bebé nació a las 35 semanas por cesárea porque se movía poco en el vientre y tenía un puntaje bajo en los estudios de control. La madre tenía obesidad, era mayor y presentaba un rasgo de células falciformes. Durante el embarazo se encontró poco líquido amniótico y señales de que la orina del bebé no salía bien. Al nacer, el bebé tuvo problemas para respirar y necesitó intubación y oxígeno. Su brazo izquierdo estaba muy morado, con ampollas y sin movimiento. Los doctores pensaron en un síndrome compartimental, causado por la presión dentro del útero. A las 6 horas de vida, se realizó una cirugía llamada fasciotomía para liberar la presión del brazo y la mano. Con los días, la circulación y el color del brazo mejoraron. Las heridas sanaron bien y no hubo infecciones. Al cumplir 4 meses, el bebé tenía buena movilidad en el hombro y el codo, pero movimientos limitados en la mano. Sigue en tratamiento con terapias y controles médicos para recuperar la función.",
+                "fh_score": 67.85
+            },
+            "hard": {
+                "text": "Se reporta el caso de un neonato masculino de 2021 g, nacido a las 35+3 semanas por cesárea repetida debido a disminución de movimientos fetales y perfil biofísico anómalo. Antecedentes maternos: rasgo falciforme, obesidad y edad materna avanzada. Durante la gestación se documentó oligohidramnios con ecografía que mostró distensión vesical, hidroceles bilaterales, dilatación uretral y ascitis, hallazgos sugestivos de obstrucción del tracto urinario inferior con posible ruptura vesical. Al nacimiento, el neonato cursó con dificultad respiratoria, precisando intubación y ventilación asistida. Se evidenció compromiso vascular severo del miembro superior izquierdo: cianosis distal, flictenas dorsales, descamación y ausencia de respuesta motora espontánea o a estímulos. El Doppler reveló flujo arterial en fosa antecubital sin pulsos radiales o cubitales, compatible con síndrome compartimental neonatal secundario a compresión intrauterina por oligohidramnios. Tras evaluación multidisciplinaria, se efectuó fasciotomía descompresiva de antebrazo, mano y túnel carpiano a las 6 horas de vida. Evolutivamente, la extremidad mostró reperfusión progresiva, con pulsos Doppler mantenidos hasta el nivel digital. Las heridas cicatrizaron por segunda intención, sin complicaciones infecciosas, con uso de férula en posición funcional. A las 6 semanas, cicatrización completa; al seguimiento a 4 meses, movilidad pasiva completa de muñeca y dedos, movilidad activa limitada de la mano pero preservada en hombro y codo. Se mantiene terapia ocupacional intensiva y vigilancia por equipos de ortopedia, cirugía plástica y neonatología para prevenir contracturas y optimizar la recuperación funcional.",
+                "fh_score": 29.05
+            }
+        }
+    },
+    {
+        "original_text_language": "es",
+        "source_topic": "Quiste suprarrenal gigante retroperitoneal",
+        "synthetic_summary": {
+            "easy": {
+                "text": "Una mujer de 38 años fue al hospital porque tenía la barriga cada vez más hinchada durante cinco meses. También sentía dolor leve y se llenaba rápido al comer. Los doctores vieron que estaba un poco pálida y con un tono amarillo en los ojos. Al revisarla, notaron una gran masa en el abdomen. Los análisis de sangre mostraron anemia y bilirrubina alta. En los estudios de imagen, como la ecografía y la tomografía, encontraron un quiste gigante cerca de la glándula suprarrenal, que medía más de 30 cm y tenía 8 litros de líquido. El quiste empujaba órganos como el riñón, hígado e intestinos. Por el tamaño, los médicos decidieron operarla. Le hicieron una cirugía en la barriga, abrieron el quiste y sacaron 8 litros de líquido marrón. Después retiraron la pared del quiste y la mandaron a analizar. La paciente se recuperó bien y salió del hospital a la semana. En los controles de 6 y 12 meses no hubo complicaciones ni regreso del quiste. El análisis mostró que no era cáncer, sino un quiste gigante sin causa clara.",
+                "fh_score": 70.11
+            },
+            "intermediate": {
+                "text": "Una mujer de 38 años ingresó en cirugía en 2022 por una hinchazón abdominal progresiva de cinco meses, con dolor leve y sensación de llenura rápida. No tenía otros síntomas generales. En el examen se encontró un abdomen muy distendido y una gran masa abdominal, con leve palidez e ictericia en los ojos. Los análisis mostraron anemia y bilirrubina elevada, pero el resto de los valores eran normales. La ecografía y la tomografía revelaron un quiste gigante de la glándula suprarrenal derecha, de más de 30 cm y con un volumen aproximado de 8 litros, que desplazaba órganos vecinos como el riñón, hígado, páncreas e intestinos. Se decidió realizar cirugía abierta. Durante la operación se abrió el abdomen y se encontró un enorme quiste retroperitoneal, del cual se extrajeron 8 litros de líquido marrón. Luego se retiró la pared del quiste para su análisis. La paciente evolucionó sin complicaciones y fue dada de alta al séptimo día. En los seguimientos a 6 y 12 meses no hubo recurrencia. El estudio histológico confirmó que no había malignidad y que se trataba de un quiste gigante retroperitoneal idiopático.",
+                "fh_score": 55.84
+            },
+            "hard": {
+                "text": "Paciente femenina de 38 años ingresó en noviembre de 2022 con antecedente de distensión abdominal progresiva de 5 meses, asociada a dolor abdominal leve y saciedad precoz, sin síntomas sistémicos. El examen físico mostró buen estado nutricional, abdomen severamente distendido, palidez leve e ictericia escleral. Se palpó una gran masa abdominal no dolorosa que ocupaba la totalidad del hemiabdomen inferior con extensión superior. Laboratorios: Hb 9,8 g/dl, leucocitos 5,7×10^9/l, plaquetas 393×10^9/l, bilirrubina 103 mg/dl, enzimas hepáticas normales, creatinina 53 μmol/l, VSG 80 mm/h. Ultrasonido: quiste abdominal complejo con órganos renales e hígado normales. TC contrastada abdomen-pelvis: quiste suprarrenal derecho de paredes finas de 23,5×20,3×32,2 cm (~8 l), desplazando riñón derecho inferomedialmente y comprimiendo hígado, vesícula, páncreas e intestinos. Se realizó laparotomía exploradora bajo anestesia general, hallándose un quiste retroperitoneal gigante. Se practicó aspiración de ~8 l de líquido marrón y cistectomía. Postoperatorio sin complicaciones, egreso a los 7 días. Seguimientos a 6 y 12 meses sin recurrencia. Citología: material amorfo sin atipia. Histología: pared quística con tejido suprarrenal, infiltrado inflamatorio mononuclear, sin revestimiento epitelial reconocible. Con base en los hallazgos, se diagnosticó quiste retroperitoneal suprarrenal idiopático gigante.",
+                "fh_score": 28.51
+            }
+        }
+    },
+    {
+        "original_text_language": "es",
+        "source_topic": "Reporte médico de un paciente con diabetes, enfermedad de Chagas y enfermedad coronaria",
+        "synthetic_summary": {
+            "easy": {
+                "text": "Un hombre mayor con diabetes y una enfermedad llamada Chagas perdió mucho peso. Los médicos encontraron un problema en su esófago que le dificultaba comer. Le hicieron un tratamiento con un balón para abrir el esófago y ayudarlo a comer mejor. También tenía dolor en el pecho al hacer esfuerzo. Los doctores revisaron su corazón y vieron que las arterias estaban bloqueadas. Le hicieron un procedimiento para abrir las arterias del corazón con pequeños tubos llamados stents. Todo salió bien, y el hombre se recuperó en el hospital. Después de unos días, estaba mucho mejor y pudo volver a casa.",
+                "fh_score": 71.69
+            },
+            "intermediate": {
+                "text": "Un hombre de 71 años con diabetes y enfermedad de Chagas había perdido 60 kg recientemente. Los médicos descubrieron que tenía un megaesófago, un problema que bloqueaba el paso de la comida por el esófago. Le realizaron una dilatación con un balón para solucionar este problema, lo que mejoró su digestión. Además, el hombre sentía dolor torácico al hacer pequeños esfuerzos. Exámenes previos mostraron que tenía arterias coronarias con calcificaciones y bloqueos. En un procedimiento, los médicos colocaron stents en varias arterias del corazón para mejorar el flujo de sangre. Un mes después, realizaron otro procedimiento para tratar otras arterias. Todo salió bien, aunque hubo una complicación menor que se corrigió rápidamente. El paciente se recuperó en pocos días y fue dado de alta en buen estado.",
+                "fh_score": 58.87
+            },
+            "hard": {
+                "text": "Paciente masculino de 71 años con antecedentes de diabetes mellitus y enfermedad de Chagas presentó una pérdida de peso significativa (60 kg). La evaluación clínica reveló megaesófago secundario a obstrucción cardial, tratado mediante dilatación esofágica con balón, logrando restablecer el tránsito digestivo. Concomitantemente, el paciente refirió angina de esfuerzo mínima. Una angiografía por tomografía computarizada coronaria previa (2013) evidenció enfermedad coronaria multivascular calcificada, sin intervenciones previas. El cateterismo cardíaco (16/02/2016) mostró: RCA con calcificación severa y lesión del 50% en el tercio medio; PDA y RPLA con lesiones calcificadas del 80% y 70%, respectivamente; LM con estenosis del 80% en el tercio distal; LAD con estenosis del 90% y calcificación significativa; DG1 y DG2 con lesiones del 70% y 80%; y LCx ocluida con colaterales grado II. Con una puntuación STS de 15,8% y EuroSCORE II de 4,67%, se optó por una intervención coronaria percutánea (ICP) en dos etapas: la primera (19/02/2016) abordó LM, LAD, DG1 y DG2 con aterectomía rotacional (RA) y stents liberadores de fármacos (DES), logrando flujo TIMI 3. La segunda (22/03/2016) incluyó RA en PDA y RPLA, con implantación de DES adicionales. Una disección en RCA, secundaria a manipulación del catéter, fue corregida con un DES de 4,0 mm x 32 mm. El paciente, tras 48 horas en UCI con elevación leve de CK-MB, fue dado de alta al tercer día con función ventricular preservada.",
+                "fh_score": 55.29
+            }
+        }
+    },
+    {
+        "original_text_language": "es",
+        "source_topic": "Reporte médico de una paciente con quiste hidatídico renal",
+        "synthetic_summary": {
+            "easy": {
+                "text": "Una mujer de 29 años sentía dolor en el lado derecho de su cuerpo. A veces le ardía al orinar. Los doctores encontraron una bolsa grande con líquido en su riñón derecho. Como había estado cerca de ovejas, pensaron que un parásito causó el problema. Le dieron medicinas por tres meses y luego le quitaron el riñón derecho en una operación. También sacaron un pedacito de su hígado. Después, la mujer se sintió bien y volvió a su vida normal.",
+                "fh_score": 80.12
+            },
+            "intermediate": {
+                "text": "Una mujer de 29 años fue al hospital porque tenía dolor en el lado derecho por un año y a veces sentía ardor al orinar. No tenía fiebre ni pérdida de peso, y nunca la habían operado, pero había estado cerca de ovejas. Los exámenes mostraron que tenía un parásito. Un ultrasonido y una tomografía encontraron un quiste grande en su riñón derecho. Los médicos le dieron albendazol por tres meses y luego hicieron una cirugía para quitar el riñón y un poco del hígado. Todo salió bien, y la paciente se recuperó rápido, volviendo a sus actividades normales.",
+                "fh_score": 67.78
+            },
+            "hard": {
+                "text": "Mujer de 29 años acudió al servicio de urología con dolor intermitente en el flanco derecho de un año de evolución y disuria ocasional sin hematuria. Su estado general era estable, sin fiebre, pérdida de peso ni antecedentes quirúrgicos, pero con exposición recurrente a ovinos. Los análisis de laboratorio fueron normales, salvo un resultado positivo para anticuerpos anti-equinococos. El ultrasonido abdominal identificó una lesión quística de 63 mm en el riñón derecho, con paredes gruesas y ausencia de flujo Doppler. La tomografía computarizada con contraste confirmó una masa quística con septos, pared gruesa realzada y compromiso del sistema colector, clasificada como Bosniak 4, con contacto hepático en vistas coronales. La radiografía torácica descartó quistes pulmonares. Tras un tratamiento de tres meses con albendazol (400 mg bid), se realizó una nefrectomía derecha y resección hepática parcial mediante incisión subcostal de Kocher, debido a adherencias. El espécimen (372 g, 13 × 8 × 6 cm) reveló un quiste hidatídico con membrana desprendida, afectando cálices y pelvis renales, acompañado de pielonefritis crónica. Postoperatoriamente, los parámetros de laboratorio fueron normales, con diuresis adecuada (2 L/día). El catéter urinario se retiró a las 24 horas, y el drenaje renal tras tres días (200 ml, 100 ml, 0 ml). La paciente reanudó actividades normales sin complicaciones.",
+                "fh_score": 44.42
+            }
+        }
+    },
+    {
+        "original_text_language": "es",
+        "source_topic": "Reporte médico de una paciente con insuficiencia cardíaca y tratamiento con modulación por contractilidad cardíaca",
+        "synthetic_summary": {
+            "easy": {
+                "text": "Una mujer de 46 años llegó al hospital porque sentía presión en el pecho y le faltaba el aire. Los doctores descubrieron que su corazón no funcionaba bien. Le dieron medicinas, pero no mejoró mucho. Su corazón latía normal, pero tenía las piernas hinchadas. Los exámenes mostraron que su corazón estaba débil y más grande de lo normal. Los médicos decidieron ponerle un dispositivo especial, como un marcapasos, para ayudar a su corazón a trabajar mejor. La operación salió bien, y después la mujer se sintió mucho mejor, sin presión en el pecho y con más energía para moverse.",
+                "fh_score": 73.76
+            },
+            "intermediate": {
+                "text": "Una mujer de 46 años ingresó al hospital por sentir opresión en el pecho y dificultad para respirar durante más de un mes. Había tenido una cirugía parcial de tiroides, pero no fumaba ni bebía alcohol. Tomaba medicamentos para la insuficiencia cardíaca, pero no mejoraba mucho. Los exámenes mostraron que su corazón estaba débil, con una fracción de eyección baja (28%), y tenía las piernas hinchadas. Un ultrasonido mostró que su corazón estaba agrandado. Los médicos le diagnosticaron insuficiencia cardíaca clase III y decidieron implantarle un dispositivo de modulación por contractilidad cardíaca (CCM), similar a un marcapasos. La operación fue exitosa, y la paciente mejoró, con menos síntomas y mejor calidad de vida.",
+                "fh_score": 59.15
+            },
+            "hard": {
+                "text": "Paciente femenina de 46 años ingresó por disnea y opresión torácica de más de un mes de evolución. Antecedente de tiroidectomía parcial, sin tabaquismo ni etilismo. Tratada con metoprolol de liberación prolongada, sacubitril/valsartán, espironolactona y dapagliflozina para insuficiencia cardíaca (IC), con respuesta subóptima. Al examen físico: consciente, FC 68 lpm, PA 150/98 mm Hg, FR 20 rpm, sin ictericia ni distensión yugular, roncus húmedos en bases pulmonares, edema bilateral en extremidades inferiores. Laboratorio: TSH 7,19 uIU/mL, triglicéridos 0,81 mmol/L, LDL-C 2,61 mmol/L, lipoproteína (a) 435 mg/L, NT-proBNP 6245 pg/mL. ECG: bradicardia sinusal, anomalías T-U, QRS 90 ms. Ecocardiograma transtorácico: diámetro auricular izquierdo 41 mm, ventricular izquierdo 54 mm, IVSD 9 mm, LVPWd 9 mm, FEVI 28%, FS 13%, presión arterial pulmonar 29 mm Hg. Angiografía coronaria computarizada sin lesiones significativas. Diagnóstico: cardiomiopatía dilatada, IC NYHA clase III con FEVI reducida. Se implantó un dispositivo de modulación por contractilidad cardíaca (CCM) mediante punción de vena subclavia izquierda, con dos cables de estimulación ventricular (Medtronic 3830-69) anclados en el tabique ventricular derecho (umbral 0,5 V, onda R >10 mV, impedancia 1080 Ω y 900 Ω). Postoperatoriamente, ECG confirmó entrega normal de impulsos CCM. Seguimiento con Doppler cardíaco, NT-proBNP, prueba de caminata de 6 minutos y cuestionario MLHFQ mostró mejoría en síntomas, tolerancia al ejercicio y calidad de vida, con normalización de E/e′ a los tres meses, indicando mejora en la función diastólica.",
+                "fh_score": 47.09
+            }
+        }
+    },
+    {
+        "original_text_language": "es",
+        "source_topic": "Reporte médico de una paciente con psoriasis y depresión relacionada con L-metilfolato",
+        "synthetic_summary": {
+            "easy": {
+                "text": "Una mujer de 61 años tenía depresión y psoriasis, una enfermedad que causa manchas en la piel. Durante muchos años, no tuvo problemas con la piel. Tomaba medicinas para la depresión que le ayudaban a sentirse mejor. En 2019, los doctores le dieron una nueva medicina llamada L-metilfolato. Pero, en pocos días, le salieron manchas en la piel otra vez. Cuando dejó de tomar esa medicina, las manchas desaparecieron en unas semanas. Desde entonces, no ha tenido más problemas con la piel.",
+                "fh_score": 74.44
+            },
+            "intermediate": {
+                "text": "Una mujer de 61 años, con antecedentes de depresión y psoriasis desde los 20 años, no había tenido brotes de psoriasis desde los 41. Tomaba venlafaxina, lamotrigina y quetiapina para tratar su depresión, lo que mejoró su estado de ánimo y calidad de vida. En 2019, tras detectar una mutación en un gen, le recetaron L-metilfolato. A los pocos días de empezar este medicamento,出现了 lesiones psoriáticas que no había tenido en 20 años. Al suspender el L-metilfolato, las lesiones comenzaron a desaparecer en 4 días y se resolvieron completamente en unas semanas. No tuvo más brotes hasta 2020.",
+                "fh_score": 58.26
+            },
+            "hard": {
+                "text": "Paciente femenina, caucásica, de 61 años, con antecedentes de depresión y psoriasis desde los 20 años, sin recidivas psoriáticas desde los 41. Tratada previamente con venlafaxina 225 mg/día desde 2000, con mejoría significativa del cuadro depresivo. En 2016, se adicionaron lamotrigina 100 mg/día para estabilización del estado de ánimo y quetiapina 50 mg/día para insomnio, con buena respuesta y sin efectos adversos relevantes. En enero de 2019, se identificó un polimorfismo heterozigótico C677T en el gen MTHFR, iniciándose L-metilfolato 15 mg/día como coadyuvante. A los pocos días, la paciente presentó recrudecimiento de lesiones psoriáticas, ausentes por 20 años. Tras notificar al psiquiatra, se suspendió el L-metilfolato, observando remisión inicial de las lesiones a los 4 días y resolución completa en semanas. No se registraron nuevas manifestaciones psoriáticas hasta inicios de 2020.",
+                "fh_score": 34.58
+            }
+        }
+    },
+    {
+        "original_text_language": "es",
+        "source_topic": "Reporte médico de un paciente con osteoartritis y artritis séptica bilateral de cadera",
+        "synthetic_summary": {
+            "easy": {
+                "text": "Un hombre de 61 años tenía dolor fuerte en las dos caderas. Después de una inyección se enfermó con fiebre e infección. Los doctores limpiaron las caderas y pusieron piezas temporales con medicina. Más tarde le colocaron prótesis nuevas cubiertas de plata para evitar infecciones. Usó muletas por un tiempo y luego volvió a caminar. Tres años después seguía bien y sin problemas.",
+                "fh_score": 76.3
+            },
+            "intermediate": {
+                "text": "Un hombre de 61 años con dolor en las caderas por osteoartritis, tratado con medicinas para artritis reumatoide, llegó al hospital con fiebre y mucho dolor. Los rayos X mostraron que sus caderas estaban muy dañadas. Los médicos encontraron una infección y operaron para limpiar las articulaciones, poniendo piezas con antibióticos. Más tarde, le colocaron prótesis de cadera con un recubrimiento especial para evitar infecciones. Tomó antibióticos por semanas y usó muletas. A las siete semanas, caminaba sin ayuda. Tres años después, sus caderas estaban bien y no tuvo más infecciones.",
+                "fh_score": 60.52
+            },
+            "hard": {
+                "text": "Paciente masculino de 61 años, con osteoartritis bilateral de cadera y tratamiento con corticosteroides por artritis reumatoide, presentó fiebre, deterioro general y dolor incapacitante en ambas caderas doce semanas tras inyección intraarticular de ácido hialurónico. Radiografías pélvicas revelaron osteólisis extensa, subluxación y defecto acetabular izquierdo. La aspiración articular confirmó artritis séptica bilateral por E. coli, iniciándose vancomicina y ampicilina IV, ajustándose a meropenem tras cultivos. Se realizó resección bilateral de cabezas femorales, desbridamiento y colocación de espaciadores de PMMA con antibióticos vía enfoque anterolateral mínimamente invasivo, con dos recambios posteriores por drenaje persistente. A las 12 semanas, se implantó una artroplastia total de cadera derecha con copa (Allofit®) y vástago femoral (Avenir®) sin cemento, recubiertos con plata (HyProtect®). A las 18 semanas, la cadera izquierda recibió una jaula de refuerzo (Burch-Schneider®) para defecto acetabular tipo IIB de Paprosky y vástago femoral sin cemento, ambos recubiertos de plata. Se administró ertapenem IV (1 g/día) por 18 semanas. La carga parcial con muletas se indicó por 6 semanas. A las 7 semanas, el paciente logró carga total. A tres años, la evaluación clínica (puntuación WOMAC 6) y radiológica mostró prótesis bien integradas, marcha normal, leucocitos 7,29/nl y PCR 12,4 mg/l (elevada por artritis reumatoide), sin signos de infección protésica ni argiria.",
+                "fh_score": 44.01
+            }
+        }
+    },
+    {
+        "original_text_language": "es",
+        "source_topic": "Reporte médico de un paciente con osteoartritis y artritis séptica bilateral de cadera",
+        "synthetic_summary": {
+            "easy": {
+                "text": "Un hombre de 61 años sentía dolor en las caderas. Tomaba medicinas para otra enfermedad, pero luego tuvo fiebre y más dolor. Los doctores vieron que sus caderas tenían una infección. Lo operaron para limpiarlas y pusieron piezas con medicinas. Después, le pusieron caderas nuevas para evitar más infecciones. Tomó medicinas y usó muletas por un tiempo. Luego, pudo caminar bien y se sintió mucho mejor.",
+                "fh_score": 70.76
+            },
+            "intermediate": {
+                "text": "Un hombre de 61 años con osteoartritis en ambas caderas, tratado con medicinas para artritis reumatoide, llegó al hospital con fiebre y dolor fuerte. Los rayos X mostraron daño en las articulaciones de las caderas. Los médicos hallaron una infección y operaron para limpiarlas, colocando piezas con antibióticos. Luego, le pusieron prótesis de cadera con un recubrimiento especial para evitar infecciones. Tomó antibióticos por varias semanas y usó muletas. Siete semanas después, caminaba sin ayuda. Tres años después, sus caderas estaban bien y no tuvo más infecciones.",
+                "fh_score": 58.1
+            },
+            "hard": {
+                "text": "Paciente masculino de 61 años, con osteoartritis bilateral de cadera y tratamiento con corticosteroides por artritis reumatoide, presentó fiebre, deterioro general y dolor incapacitante en ambas caderas doce semanas tras inyección intraarticular de ácido hialurónico. Radiografías pélvicas evidenciaron osteólisis extensa, subluxación y defecto acetabular izquierdo. La aspiración articular confirmó artritis séptica bilateral por E. coli, iniciándose vancomicina y ampicilina IV, ajustándose a meropenem tras cultivos. Se realizó resección bilateral de cabezas femorales, desbridamiento y colocación de espaciadores de PMMA con antibióticos vía enfoque anterolateral mínimamente invasivo, con dos recambios posteriores por drenaje persistente. A las 12 semanas, se implantó una artroplastia total de cadera derecha con copa (Allofit®) y vástago femoral (Avenir®) sin cemento, recubiertos con plata (HyProtect®). A las 18 semanas, la cadera izquierda recibió una jaula de refuerzo (Burch-Schneider®) para defecto acetabular tipo IIB de Paprosky y vástago femoral sin cemento, ambos recubiertos de plata. Se administró ertapenem IV (1 g/día) por 18 semanas. La carga parcial con muletas se indicó por 6 semanas. A las 7 semanas, el paciente logró carga total. A tres años, la evaluación clínica (puntuación WOMAC 6) y radiológica mostró prótesis bien integradas, marcha normal, leucocitos 7,29/nl y PCR 12,4 mg/l (elevada por artritis reumatoide), sin signos de infección protésica ni argiria.",
+                "fh_score": 43.41
+            }
+        }
+    },
+    {
+        "original_text_language": "es",
+        "source_topic": "Reporte médico de una neonata con síndrome femoro-facial",
+        "synthetic_summary": {
+            "easy": {
+                "text": "Una bebé nació muy pequeña y antes de tiempo. Le costaba respirar y tenía la cabeza pequeña y un labio abierto. Sus piernas no estaban bien formadas. Los doctores le ayudaron a respirar y le dieron medicinas para infecciones. Planearon una operación para su labio más adelante. Pero la bebé murió por una infección fuerte.",
+                "fh_score": 74.49
+            },
+            "intermediate": {
+                "text": "Una bebé nació a las 32 semanas pesando 1000 gramos y fue llevada a cuidados intensivos por problemas respiratorios y anomalías físicas. Su madre, de 32 años, tuvo un problema en el embarazo y no tomó ácido fólico. La bebé tenía la cabeza pequeña, labio y paladar hendido, y las piernas mal formadas. Los exámenes mostraron que los huesos de sus piernas no estaban bien y tenía un pequeño problema en el corazón. Los médicos diagnosticaron síndrome femoro-facial. Le dieron ayuda para respirar y antibióticos, y planearon una cirugía para el labio. Sin embargo, la bebé falleció al mes por una infección grave.",
+                "fh_score": 64.92
+            },
+            "hard": {
+                "text": "Neonata de raza negra, nacida a las 32 semanas de gestación con 1000 g, derivada a la unidad de cuidados intensivos neonatales por distress respiratorio moderado y múltiples anomalías congénitas. La madre, de 32 años, en matrimonio no consanguíneo, presentó desprendimiento placentario en el tercer trimestre, con oligohidramnios severo detectado en el primer ultrasonido prenatal, sin suplementación de ácido fólico ni diabetes materna (glucosa 5.1 mmol/L). La paciente exhibía microcefalia (circunferencia occipitofrontal <10%), occipucio prominente, orejas bajas, paladar y labio hendido derecho, micrognatia, contracturas bilaterales de codos y extremidades inferiores acortadas. La radiografía esquelética reveló aplanamiento costal, aplasia del fémur derecho e hipoplasia del fémur izquierdo. Los análisis de laboratorio (hemograma, PCR, creatinina, urea, electrolitos) fueron normales; la ecografía craneal no mostró alteraciones, pero la ecocardiografía identificó un conducto arterioso permeable. El diagnóstico de síndrome femoro-facial se estableció por aplasia femoral bilateral y facies dismórficas, diferenciándose del síndrome de regresión caudal por la presencia de defectos craneofaciales. Se instauró soporte respiratorio y antibioticoterapia empírica, con participación de ortopedia, otorrinolaringología y fisioterapia, planificando reparación del paladar hendido a los 6 meses. La paciente falleció al mes por sepsis neonatal tardía grave.",
+                "fh_score": 24.99
+            }
+        }
+    },
+    {
+        "original_text_language": "es",
+        "source_topic": "Reporte médico de un paciente con Neurofibromatosis tipo 1",
+        "synthetic_summary": {
+            "easy": {
+                "text": "Un joven de 18 años tiene una enfermedad llamada Neurofibromatosis tipo 1 desde que era bebé. Tiene manchas en la piel y algunos bultos. También le costaba hablar y moverse bien cuando era pequeño, pero lo ayudaron con terapias. En la escuela, a veces le costaba concentrarse, pero tomó medicinas para eso. Sus ojos también tienen problemas desde pequeño. Hace poco, notó una nueva mancha en la pierna y unos bultos en la cabeza y la muñeca. Los doctores revisaron y confirmaron que todo es parte de su enfermedad. Sigue en control con los médicos.",
+                "fh_score": 73.79
+            },
+            "intermediate": {
+                "text": "Un joven de 18 años con Neurofibromatosis tipo 1, diagnosticada desde su primer año, consultó por una nueva mancha en la pierna y bultos en la muñeca, cabeza y ceja. Desde niño tuvo retrasos en el habla y el movimiento, tratados con terapias de lenguaje, kinesioterapia y terapia ocupacional. En la adolescencia le diagnosticaron déficit de atención e hiperactividad, tratado con metilfenidato, logrando un rendimiento escolar regular. También tiene problemas en los ojos desde los 4 años. Una resonancia magnética reciente no mostró problemas graves, pero sí cambios en la columna. Los exámenes de piel confirmaron que las manchas y bultos son parte de la enfermedad. Sigue en control médico regular.",
+                "fh_score": 59.1
+            },
+            "hard": {
+                "text": "Paciente masculino de 18 años con diagnóstico de Neurofibromatosis tipo 1 (NF1) desde el primer año de vida, sin antecedentes familiares de manchas café con leche, en matrimonio no consanguíneo. Presentó retraso psicomotor fino y grueso en la infancia, trastorno expresivo del lenguaje con alteraciones fonológicas y semánticas, manejado con fonoaudiología, kinesioterapia y terapia ocupacional. En la adolescencia se diagnosticó TDAH, tratado con metilfenidato, con rendimiento escolar regular. Oftalmológicamente, nódulos de Lisch desde los 4 años, euriblefaron y astigmatismo. Resonancia magnética cerebral reciente sin hallazgos patológicos; en columna, discopatía L5-S1 y realce perifacetario T11-L1. Estudio genético a los 16 años confirmó deleción de exones 5-47 del gen NF1. A los 18 años, consultó en Dermatología por una placa asintomática de 25 mm en muslo izquierdo (1 año de evolución) y nódulos subcutáneos en muñeca derecha, supraciliar derecha y occipital. Examen físico: macrocefalia (CC 60 cm), múltiples manchas café con leche, efélides axilares, nódulos subcutáneos (0,5 cm) y máculas rojo-azuladas (<5 mm) en zona lumbar y pectoral. Biopsias cutáneas y ecografía confirmaron NF superficial subcutáneo nodular (supraciliar, occipital, muñeca), NF superficial cutáneo pseudoatrófico (muslo) y NF superficial cutáneo rojo-azulado (lumbar, pectoral), según clasificación de García-Martínez et al. Se mantiene en seguimiento multidisciplinario.",
+                "fh_score": 39.54
+            }
+        }
+    },
+    {
+        "original_text_language": "es",
+        "source_topic": "Reporte médico de un paciente con infarto de miocardio secundario a traumatismo torácico",
+        "synthetic_summary": {
+            "easy": {
+                "text": "Un hombre de 38 años tuvo un accidente en el trabajo cuando un objeto lo golpeó en el pecho. Se desmayó, pero despertó rápido. En el hospital, le encontraron líquido en los pulmones y huesos rotos. Le pusieron un tubo para ayudar a respirar y lo mandaron a casa. Meses después, seguía con dificultad para respirar y dolor. Los doctores descubrieron que había tenido un problema en el corazón. Le dieron medicinas y más tarde una operación para abrir una arteria. Con el tiempo, se sintió mejor, pero aún tiene algo de dificultad para respirar después de trabajar.",
+                "fh_score": 73.88
+            },
+            "intermediate": {
+                "text": "Un hombre de 38 años ingresó al hospital tras un golpe fuerte en el pecho por un tornillo en una fábrica. Perdió el conocimiento brevemente y sintió dolor torácico y dificultad para respirar. Una tomografía mostró líquido en los pulmones y fracturas en el esternón y costillas. Le colocaron un tubo torácico y fue dado de alta. Tres meses después, seguía con opresión torácica y falta de aire. Exámenes mostraron que había tenido un infarto de miocardio antiguo. Le dieron medicinas y, meses después, una intervención para abrir una arteria del corazón. Su estado mejoró, aunque aún tiene síntomas leves tras esfuerzo físico.",
+                "fh_score": 66.64
+            },
+            "hard": {
+                "text": "Varón de 38 años, previamente sano, ingresó por traumatismo torácico contundente tras impacto de un tornillo de 6 cm en una fábrica, proyectándolo 4 metros. Perdió el conocimiento transitoriamente, recuperándolo minutos después. En urgencias, con escala de coma de Glasgow 15, refirió dolor torácico severo, opresión y disnea. La TC torácica reveló derrame pleural bilateral y fracturas esternal y costales, requiriendo drenaje torácico. Fue dado de alta sin evaluación cardiovascular. A los tres meses, en seguimiento, persistían disnea, opresión y disnea paroxística nocturna. Signos vitales: FC 98 lpm, PA 110/70 mmHg, FR 20 rpm. Examen físico: disminución de murmullo pulmonar derecho, sin estertores ni soplos. ECG: elevación ST, inversión de onda T (I, aVL, V2-V5), bloqueo de rama anterior izquierda. Troponina-I negativa, NT-proBNP 706 pg/ml. Ecocardiograma: aurícula izquierda 26,4 mm, ventrículo izquierdo 51,8 mm, FEVI 32%, adelgazamiento de pared anterior y septum (6,6 mm). Sin placas ateroscleróticas en carótidas ni arterias periféricas. Diagnóstico: infarto de miocardio antiguo (OMI). Tratado con diuréticos, betabloqueantes, estatinas y estimulantes cardíacos, mejoró parcialmente. La TC coronaria mostró estenosis moderada en LAD proximal; la angiografía (CAG) confirmó estenosis del 70%. Sin IVUS por costos, optó por manejo conservador. A los 4 meses, nueva CAG mostró estenosis del 60%; IVUS reveló placa de bajo eco (55,9%) sin isquemia significativa. A los 4 años, persistía disnea de esfuerzo leve, con FEVI 41%, agrandamiento ventricular y adelgazamiento parietal. Se optimizó tratamiento con metoprolol 23,75 mg, benazepril 2,5 mg, espironolactona 20 mg y coenzima, debido a adherencia irregular previa.",
+                "fh_score": 46.28
+            }
+        }
+    },
+    {
+        "original_text_language": "es",
+        "source_topic": "Reporte médico de una neonata con coagulación intravascular diseminada y mutación MECOM",
+        "synthetic_summary": {
+            "easy": {
+                "text": "Una bebé nació antes de tiempo, muy pequeña y débil. Estaba pálida, con moretones y sangrados. Le costaba respirar, así que los doctores la ayudaron con máquinas y le dieron sangre y medicinas. Descubrieron que tenía un problema grave de coagulación y sangrados en el cerebro y el estómago. Aunque intentaron salvarla, la bebé murió a los tres días. Los doctores encontraron un cambio en un gen que causó su enfermedad, algo que no tenían sus padres ni su hermano.",
+                "fh_score": 76.24
+            },
+            "intermediate": {
+                "text": "Una bebé nació a las 36 semanas con 2650 g por cesárea de urgencia debido a sufrimiento fetal. Mostró palidez, moretones, sangrado y problemas para respirar. La llevaron a cuidados intensivos, donde diagnosticaron un problema grave de coagulación en la sangre. Le dieron ventilación mecánica, transfusiones de sangre y medicinas para infecciones. Los exámenes mostraron sangrados en el cerebro y el estómago. A pesar del tratamiento, murió a los tres días por fallos en varios órganos. Un estudio genético encontró una mutación en un gen, no presente en sus padres ni hermano, que causó su enfermedad.",
+                "fh_score": 63.54
+            },
+            "hard": {
+                "text": "Neonata de etnia Han, nacida a las 36 semanas (2650 g) vía cesárea de urgencia por distress fetal, con Apgar 6 y 6 a 1 y 5 minutos, presentó palidez, equimosis, sangrado mucosal, insuficiencia respiratoria y hemorragia en sitios de punción. Análisis inicial: hematocrito 0.08, hemoglobina 23 g/L, plaquetas 12 × 109/L, leucocitos 1.11 × 109/L. Requirió intubación y ventilación mecánica. En la UCIN, se diagnosticó coagulación intravascular diseminada (TTPA 73,10 s, TP 25,4 s, INR 2,26, fibrinógeno 1,01 g/L, dímero D >20 mg/L). Se administraron transfusiones de plasma fresco congelado, glóbulos rojos, plaquetas, antiinfecciosos, cardiotónicos y vasopresores, sin normalización de hemoglobina (106 g/L) ni plaquetas (11 × 109/L). Ecocardiograma: conducto arterioso patente, foramen oval permeable, hipertensión pulmonar. Ultrasonido craneal: hemorragia intracraneal grave; abdominal: hemorragia gastrointestinal. Electroencefalograma: bajo voltaje. Frotis periférico: reticulocitos 1,5%, Coombs negativa. Sin evidencia de sepsis neonatal ni infecciones TORCH, hepatitis o sífilis. Falleció al tercer día por falla multiorgánica y hemorragia intracraneal masiva. Padres no consanguíneos, ambos con talasemia; madre con anemia leve gestacional (hemoglobina 97 g/L). Secuenciamiento de Sanger identificó una mutación heterocigótica de desplazamiento de marco en MECOM [NM_001105078: c.157_158del (p.Met53Glyfs*2)], no presente en padres ni hermano, clasificada como patogénica (ACMG). Modelos SWISS-MODEL confirmaron alteración estructural proteica por terminación temprana, no reportada en HGMD ni Clinvar.",
+                "fh_score": 31.58
+            }
+        }
+    }
+]
\ No newline at end of file
diff --git a/generating_data/tik_ache/es_syntheticV3.json b/generating_data/tik_ache/es_syntheticV3.json
new file mode 100644
index 0000000000000000000000000000000000000000..ca803eaa3dac4a3f01d4d4112b0ddb15e6f7b1ed
--- /dev/null
+++ b/generating_data/tik_ache/es_syntheticV3.json
@@ -0,0 +1,902 @@
+[
+    {
+        "article": "Información para el paciente\nUn hombre de 27 años y fumador estuvo involucrado en un accidente de tráfico; se cayó de su motocicleta sin casco. El hombre llevó la motocicleta al hospital e informó de un dolor de cabeza y heridas hemorrágicas en la frente.\n\nEl paciente no tiene antecedentes patológicos y trabaja en una zona rural.\n\nHallazgos clínicos\nTras su ingreso en urgencias, perdió el conocimiento y sufrió dos convulsiones. En la exploración física, la escala de coma de Glasgow fue de 6/15 (no abrió los ojos, se retiró al sentir dolor, no respondió verbalmente) con midriasis bilateral, dificultad hemodinámica y buena saturación. Se identificó una lesión craneal penetrante con una profusa hemorragia intracraneal.\n\nLínea de tiempo\nTras caerse de la motocicleta, el paciente volvió a montarse en ella e inmediatamente fue al hospital, quejándose de dolores de cabeza y de una herida en la frente por la que sangraba. Recibió tratamiento de urgencia para estabilizar sus funciones respiratorias y hemodinámicas. Ese mismo día, fue trasladado inconsciente a un centro mejor equipado, donde se le realizó un TAC y se sometió a una operación quirúrgica con éxito.\n\nEvaluación diagnóstica\nSu nivel de hemoglobina era de 6 g/dL y su grupo sanguíneo era O positivo. El hospital no tenía ni una unidad de cuidados intensivos ni un escáner. El único diagnóstico sugerido fue el de traumatismo agudo en la cabeza, complicado por hemorragia intracraneal que provocó shock y convulsiones. El pronóstico vital, basado en la presentación clínica, era malo.\n\nIntervención terapéutica\nUna intervención inicial consiste en un relleno intracraneal a través de la fractura craneal, seguido de un vendaje cefálico que ayuda a detener el sangrado. El tratamiento involucró la estabilización de la columna cervical, intubación orotraqueal con oxígeno a 6 L por minuto y la inserción de un catéter Foley. Se usaron dos puertos venosos periféricos para administrar NaCl 0.9 % 1000 CC, Geloplasma* 500 CC, Manitol 20 % 250 CC; Phenobarbital inj 40 mg/2 ml: 100 mg, luego Thiopental 250 mg: bolo de 100 mg × 2 debido a otras convulsiones; Amoxicillin + Clavulanic Acid injection 2 g; Gentamycin 160 mg intramuscularmente. Se realizó un suero antitetánico de 1500 IU y una transfusión de 450 CC de sangre.\n\nEl paciente fue trasladado inconsciente a un equipo en un hospital de primera categoría, sin intubación y en un estado hemodinámico estable.\n\nEl primer día después de la transferencia, el paciente evolucionó bien; estaba consciente y podía caminar, sin problemas neurológicos, hemodinámicos o respiratorios. La tomografía computarizada reveló un edema bifrontal agudo, una contusión hemorrágica del parénquima predominantemente en el lado derecho, una capa de hematoma subdural agudo (3 mm) en la región fronto-parieto-temporo-occipital izquierda, una hernia subfalcular izquierda de 5 mm, una compresión discreta del ventrículo lateral derecho, una hemorragia subaracnoidea superior bifrontal aguda, una fractura frontal deprimida con rotura osteomeníngea y una fractura de la tercera vértebra cervical con compresión de la médula espinal. El paciente se sometió a una operación exitosa en el hospital de primera categoría.\n\nSeguimiento y resultados\nEl período postoperatorio estuvo marcado por convulsiones, para las cuales se le administró anticonvulsivos al paciente, con un buen resultado.\n",
+        "gold_summary": "Un hombre de 27 años, fumador sin antecedentes patológicos, estuvo involucrado en un accidente de tráfico, al caerse de una motocicleta sin casco. En el ingreso al hospital de nuestro distrito rural, la escala de coma de Glasgow durante el examen físico fue de 6/15 con midriasis bilateral, distrés hemodinámico y buena saturación. Se identificó una lesión penetrante en la cabeza con profusa hemorragia intracraneal. Se usó el relleno intracraneal conocido en la neurocirugía de control de daños para taponar la hemorragia intracraneal grave y que es una maniobra neuroquirúrgica que salva vidas. El paciente fue trasladado inconsciente a un hospital de primera categoría, libre de intubación y en un estado hemodinámico estable. El período postoperatorio estuvo marcado por convulsiones, por lo que el paciente fue puesto en anticonvulsivos con un buen resultado.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre se cayó de su moto y se lastimó la cabeza. No llevaba casco y se hizo una herida que sangraba mucho. Cuando llegó al hospital, estaba muy dormido y no podía hablar ni abrir los ojos. \n\nLos doctores pusieron algo para parar la sangre dentro de su cabeza. Luego lo llevaron a otro hospital donde lo cuidaron mejor. Después de la operación, tuvo algunos temblores, pero le dieron medicina y se mejoró.",
+            "B2": "**Lo que pasó con el paciente**  \nUn hombre de 27 años que fuma tuvo un accidente al caerse de su motocicleta sin usar casco. Cuando llegó al hospital en una zona rural, estaba muy grave. No respondía bien, tenía las pupilas dilatadas en ambos ojos y sangraba mucho dentro de su cabeza por una herida penetrante.\n\n**Qué hicieron los médicos**  \nPara detener la hemorragia dentro de su cráneo, los médicos usaron una técnica llamada relleno intracraneal. Esto significa que colocaron un material especial para tapar la herida y controlar el sangrado, lo cual es una cirugía que puede salvar vidas en casos graves. Luego, lo trasladaron a un hospital mejor equipado, donde estaba inconsciente pero estable en cuanto a su circulación y respiración.\n\n**Qué pasó después de la operación**  \nDespués de la cirugía, el paciente tuvo convulsiones, que son movimientos involuntarios causados por problemas en el cerebro. Por eso, le dieron medicamentos llamados anticonvulsivos para controlar estas convulsiones. Gracias a este tratamiento, el paciente mejoró y tuvo una buena recuperación.",
+            "B3": "Resumen detallado para público general universitario\n\nContexto  \nUn hombre de 27 años, fumador y sin antecedentes médicos previos, sufrió un accidente de tráfico al caerse de una motocicleta sin usar casco. Tras la caída, presentó dolor de cabeza y una herida sangrante en la frente, por lo que acudió al hospital local en una zona rural.\n\nHallazgos clínicos y evaluación inicial  \nAl llegar al hospital, el paciente perdió el conocimiento y tuvo dos convulsiones. La evaluación neurológica mostró una escala de coma de Glasgow de 6 sobre 15, lo que indica un estado de coma profundo (no abría los ojos, respondía solo con movimientos para evitar el dolor y no hablaba). Además, presentaba midriasis bilateral (dilatación anormal de ambas pupilas), dificultad para mantener la presión arterial (distrés hemodinámico) y buena saturación de oxígeno. Se detectó una lesión penetrante en el cráneo con una hemorragia intracraneal abundante, lo que significa que la sangre estaba acumulándose dentro del cerebro debido a la lesión.\n\nIntervención inicial y traslado  \nEn el hospital rural, donde no había unidad de cuidados intensivos ni tomografía computarizada (TAC), se aplicó un tratamiento de emergencia para controlar el sangrado intracraneal mediante una técnica quirúrgica llamada relleno intracraneal, que consiste en taponar la fractura del cráneo para detener la hemorragia y estabilizar al paciente. Además, se estabilizó la columna cervical, se realizó intubación orotraqueal para asegurar la respiración, se administraron líquidos intravenosos, medicamentos anticonvulsivos para controlar las convulsiones, antibióticos para prevenir infecciones y una transfusión sanguínea debido a la anemia severa (hemoglobina de 6 g/dL). Posteriormente, el paciente fue trasladado inconsciente pero hemodinámicamente estable a un hospital de mayor nivel con mejores recursos.\n\nDiagnóstico y tratamiento avanzado  \nEn el hospital de referencia, se realizó una tomografía computarizada que reveló múltiples lesiones cerebrales graves: edema cerebral (hinchazón del cerebro) en ambas áreas frontales, contusión hemorrágica (moretón con sangrado) en el tejido cerebral del lado derecho, un hematoma subdural agudo (acumulación de sangre entre el cerebro y la membrana que lo cubre) en el lado izquierdo, una hernia subfalcular (desplazamiento del cerebro hacia un lado), compresión ventricular leve, hemorragia subaracnoidea (sangrado en el espacio que rodea el cerebro), fractura deprimida del hueso frontal con ruptura de las membranas que cubren el cerebro, y fractura de la tercera vértebra cervical con compresión de la médula espinal. El paciente fue sometido a una cirugía exitosa para tratar estas lesiones.\n\nEvolución y seguimiento  \nDurante el postoperatorio, el paciente presentó convulsiones que fueron controladas con medicamentos anticonvulsivos, logrando una buena respuesta clínica. Al día siguiente de la cirugía, el paciente estaba consciente, podía caminar y no mostraba problemas neurológicos, respiratorios ni circulatorios.\n\nInterpretación clínica  \nEste caso ilustra la gravedad de los traumatismos craneoencefálicos penetrantes y la importancia de una intervención rápida y adecuada, incluso en entornos con recursos limitados. La técnica de relleno intracraneal utilizada inicialmente fue fundamental para controlar la hemorragia y estabilizar al paciente antes del traslado. La atención especializada posterior y el manejo multidisciplinario permitieron una recuperación favorable a pesar de las múltiples lesiones cerebrales y de la médula espinal.\n\nPróximos pasos  \nSe recomienda continuar con el seguimiento neurológico y rehabilitación para evaluar y tratar posibles secuelas a largo plazo, así como mantener el control de las convulsiones con medicación adecuada. Además, es fundamental promover el uso de casco y medidas de seguridad vial para prevenir este tipo de accidentes."
+        }
+    },
+    {
+        "article": "La paciente era una madre de 54 años que provenía de una zona rural y que llegó al Hospital Especializado de Compresión de Nekemte con la queja de una masa en su vagina de 3 años de duración. Hace tres años, encontró una protuberancia de masa a través de su vagina, que gradualmente creció en tamaño con el tiempo. Había tenido dos bebés, el último hace 12 años. Ambos partos fueron en casa, ya que el centro de salud está demasiado lejos de su área de residencia, y fue asistida por una comadrona tradicional. Ella afirmó que todo había sido sin problemas. Inicialmente, hace tres años, hubo sangrado y una descarga ofensiva de la masa, pero eso se detuvo en el último año. Desarrolló laceraciones en la masa hace seis meses. Por esta razón, se divorció y se aisló de toda la vida social durante este largo período de tiempo. Ahora, su hermana mayor y otro familiar la trajeron al hospital específicamente por la laceración de la masa. No tenía ninguna otra enfermedad médica crónica conocida.\n\nHallazgo pertinente del PE\nSigno vital: PA = 100/60 mm hg, FC = 84 lpm, FR = 20 lpm, T° = 36.5°C, peso = 47 kg.\n\nGUS: hay una masa rosada en la vagina que se encuentra a unos 7 cm del anillo del himen.\n\nEl fondo uterino es la parte principal de la masa.\n\nHabía una laceración longitudinal de unos 5 cm en el lado derecho de la masa.\n\nNo hubo sangrado ni secreción de la masa ni del área de la laceración.\n\nLaboratorio\nCBC: hemoglobina = 12 g/dl, PLT = 285 mil, neutrófilos = 74%.\n\nAnálisis de orina: resultado normal.\n\nGrupo sanguíneo = A, RH = positivo.\n\nPrueba de VIH = negativa.\n\nHBSAg = negativo.\n\nEcografía: vejiga parcialmente llena visible en el abdomen, útero no visible en el abdomen. Por lo demás, no se observaron otros hallazgos pertinentes.\n\nRadiografía de tórax: radiografía de tórax normal.\n\nPor este motivo, se le diagnosticó una inversión uterina crónica. Se tomaron imágenes preoperatorias y postoperatorias, el fondo uterino era el punto principal de la masa que sobresalía completamente a través de la vagina y había una laceración crónica desarrollada en la superficie endometrial. Después de la operación, se observó un canal vaginal normal. Después de revisar las opciones de tratamiento con ella y su familia, se programó una cirugía y se realizó una histerectomía abdominal al día siguiente. Era una cirugía abdominal y era fácil introducir el útero en el abdomen. Como el tejido era redundante y distorsionado, es difícil identificar la referencia anatómica y los puntos de referencia quirúrgicos. Debido a esto, la cirugía fue difícil y hubo una lesión ureteral derecha transaccional intraoperatoria y se realizó una anastomosis de extremo a extremo. Se dio de alta el décimo día de la operación y se encontró que estaba mejorando. Se le dio una cita de seguimiento dos semanas después y cuando se evaluó se encontró que estaba bien.\n",
+        "gold_summary": "Una mujer de 54 años de edad acudió a nuestro hospital con la queja de una masa indolora en su vagina de 3 años de duración. Hace tres años, encontró una protuberancia de masa a través de su vagina, que gradualmente creció en tamaño con el tiempo. En el examen físico, el fondo uterino fue el punto principal de la masa y sobresalía 7 cm por debajo del anillo del himen. Como resultado, se le diagnosticó inversión uterina crónica y se le sometió a una histerectomía abdominal. Fue dada de alta en casa mejorada. Presentamos este caso debido a un factor no identificado que provocó la inversión uterina, la presentación tardía de la enfermedad y la dificultad en el tratamiento quirúrgico.\n",
+        "synthetic_summary": {
+            "B1": "Había una señora que tenía una bolita en su cuerpo. Esa bolita estaba en un lugar muy especial dentro de ella. La bolita creció poco a poco durante mucho tiempo. Los doctores vieron que esa bolita era parte de un órgano que estaba fuera de su lugar. Ella tuvo que ir al hospital para que los doctores la ayudaran con una operación. Después de la operación, la señora se sintió mejor y pudo ir a su casa. Los doctores contaron esta historia para que otros puedan aprender.",
+            "B2": "**Lo que le Pasó a la Paciente**  \nUna mujer de 54 años notó hace tres años una masa o bulto que salía de su vagina. Esta masa fue creciendo poco a poco y no le causaba dolor. Al principio, tuvo sangrado y mal olor, pero eso paró hace un año. También se lastimó la masa hace seis meses, lo que la hizo sentirse mal y alejarse de su familia y amigos.\n\n**Qué Encontraron los Médicos**  \nCuando la examinaron, vieron que la masa era parte del útero que había salido hacia afuera por la vagina. Esto se llama inversión uterina crónica, que es cuando el útero se da vuelta y sale fuera del cuerpo. Había una herida larga en la masa, pero no estaba sangrando en ese momento. Los exámenes de sangre y orina estaban normales, y no tenía infecciones como VIH o hepatitis.\n\n**Cómo la Ayudaron**  \nLos médicos decidieron hacer una cirugía para quitar el útero, llamada histerectomía abdominal. La operación fue complicada porque el tejido estaba muy cambiado y era difícil saber dónde estaban las partes normales. Durante la cirugía, se lastimó un conducto que lleva la orina desde el riñón a la vejiga, pero lo repararon en el mismo momento. Después de la operación, la paciente mejoró y pudo volver a casa. En el control dos semanas después, estaba bien y sin problemas.\n\n**Por Qué es Importante Este Caso**  \nEste caso es especial porque la inversión uterina es rara y no se sabe exactamente qué la causó en esta mujer. Además, ella llegó al hospital muy tarde, cuando la situación ya era difícil de tratar. La cirugía fue complicada, pero al final tuvo un buen resultado. Esto muestra la importancia de buscar ayuda médica a tiempo cuando se tiene una masa o bulto en el cuerpo.",
+            "B3": "Resumen para Público General Educado\n\nContexto  \nUna mujer de 54 años, originaria de una zona rural, acudió al hospital tras presentar durante tres años una masa que sobresalía por su vagina. Esta masa fue creciendo lentamente y, en sus primeros años, estuvo acompañada de sangrado y secreción con mal olor, aunque estos síntomas desaparecieron en el último año. La paciente había tenido dos partos en casa, asistida por una comadrona tradicional, sin complicaciones aparentes. Debido a la masa y a una herida (laceración) que apareció en ella hace seis meses, la paciente sufrió aislamiento social y divorcio. Finalmente, fue llevada al hospital por familiares para recibir atención médica.\n\nHallazgos Clínicos  \nAl examen físico, se encontró una masa de color rosado ubicada aproximadamente a 7 centímetros del borde del himen (la membrana que rodea la entrada de la vagina). La parte principal de esta masa correspondía al fondo uterino, que es la parte superior del útero. En la masa había una herida longitudinal de unos 5 centímetros, pero no se observó sangrado ni secreción en ese momento. Los signos vitales de la paciente estaban dentro de rangos normales y los análisis de sangre y orina no mostraron alteraciones significativas. La ecografía abdominal no logró visualizar el útero en su posición habitual, lo que apoyó el diagnóstico.\n\nDiagnóstico e Interpretación Clínica  \nSe diagnosticó a la paciente con inversión uterina crónica, una condición poco común en la que el útero se voltea hacia adentro y puede protruir a través de la vagina. En este caso, la inversión era completa y prolongada, lo que causó la formación de la masa visible y la laceración en su superficie. La causa exacta que originó esta inversión uterina no pudo ser identificada, lo que hace este caso especialmente relevante.\n\nTratamiento y Evolución  \nDespués de discutir las opciones con la paciente y su familia, se decidió realizar una histerectomía abdominal, que consiste en la extirpación quirúrgica del útero a través del abdomen. Durante la cirugía, se encontró que el tejido estaba muy distorsionado y redundante, lo que dificultó la identificación de las estructuras anatómicas normales. Esto llevó a una complicación quirúrgica: una lesión en el uréter derecho (el conducto que conecta el riñón con la vejiga), que fue reparada mediante una anastomosis (unión quirúrgica) de extremo a extremo. La paciente fue dada de alta diez días después de la operación, con mejoría clínica, y en el control posterior mostró una recuperación satisfactoria, con un canal vaginal normal.\n\nImportancia del Caso  \nEste caso destaca la presentación tardía y poco común de una inversión uterina crónica en una mujer rural, así como las dificultades quirúrgicas asociadas a esta condición. La ausencia de atención médica temprana y la falta de acceso a centros de salud contribuyeron a la evolución prolongada y compleja del caso. La experiencia subraya la necesidad de mejorar el acceso a servicios médicos y la educación sanitaria en áreas rurales para prevenir complicaciones graves."
+        }
+    },
+    {
+        "article": "Varón de 20 años, HIV negativo, con TB pulmonar y tratamiento irregular en 2020-2021. Se internó por síndrome de impregnación bacilar, dolor e impotencia funcional del hombro derecho. Presentaba mal estado general, adelgazado, hipotrofia muscular grave, lesiones tumorales frías fluctuantes fistulizadas en dorso, calota craneana y tórax anterior con secreción caseosa, sin presentar déficits motores ni sensitivos. El examen molecular rápido (GeneXpert Mtb/Rif) de secreción del tórax fue positivo para Mycobacterium tuberculosis, sensible a rifampicina (el antibiograma fenotípico mostró una cepa pansensible). La TC demostró consolidaciones pulmonares y árbol en brote, junto con el compromiso óseo de columna cervical, dorsal y lumbar con imágenes líticas y colecciones pre y paraespinales. En la RMN se observaron imágenes infiltrativas desde C4 a C6; D4 a D6, D9 a D12; fractura patológica de D6 y D10 e infiltración en L1, L2 y L3. Inició tratamiento anti-TB con esquema estándar de primera línea (isoniacida, rifampicina, pirazinamida, etambutol). Dada la extensa destrucción y el peligro de cuadriplejía/paraplejía por el compromiso cervical y/o dorsal, se indicó posición decúbito dorsal permanente, collar de Filadelfia, asistencia kinésica y conducta neuroquirúrgica en forma programada en los niveles cervicales, D6 y D10. Previo a la cirugía programada presentó un cuadro agudo de paraplejía con nivel sensitivo D8, con compromiso vesical. Se interpretó como nivel de compresión aguda en D6. Se indicó neurocirugía de urgencia con descompresión medular vía posterior con laminectomía dorsal 6 y parcialmente D5 y 7 y evacuación de una colección epidural. Fue recuperando la función motora y sensitiva en forma progresiva. Posteriormente se realizó la cirugía programada cervical vía anterior con corporectomía de C4, C5, C6 y C7 más artrodesis de C3 a D1 con reemplazo de cuerpo vertebral más injerto autólogo, placa y tornillos. En la TC de control se evidenció luxación posterior de D6 con compresión del canal espinal y deterioro neurológico por compresión medular. Se reconsideró la táctica quirúrgica debido a la inestabilidad mecánica y neurológica. Se realizó descompresión y alineación del nivel luxado con artrodesis posterior de los tres niveles espinales no adyacentes, cervical, dorsal 6 y dorsal 10 en un solo tiempo quirúrgico. Se fijó desde  C3 hasta D12 con tornillos poliaxiales y barra de transición cervicodorsal. En cada tiempo quirúrgico se evidenció evacuación espontánea de material caseoso, BAAR positivo, y se realizaron lavados profusos.  Presentó mejoría clínica, bacteriológica y resolución de las lesiones pulmonares. Recuperó movilidad con rehabilitación kinésica sumada al tratamiento específico (3 meses de primera fase e indicación de continuación con isoniacida y rifampicina hasta completar los 12 meses). Egresó caminando por sus propios medios, luego de una prolongada internación de 5 meses.",
+        "gold_summary": "Se presenta el caso de un varón de 20 años con espondilitis tuberculosa multinivel no contigua (cervical, dorsal 6, dorsal 10 y lumbar). Se trata de un paciente HIV negativo con tuberculosis diseminada con grave compromiso de su estado general y múltiples localizaciones de la enfermedad. Algunas tenían fistulas que secretaban caseum. El paciente presentó paraplejía aguda que requirió, teniendo en cuenta el nivel sensitivo a nivel dorsal 6, una primera cirugía urgente de descompresión por vía posterior. Luego se efectuó la cirugía programada. En primera instancia, la región cervical por vía anterior, con corporectomía, colocación de reemplazo de cuerpo vertebral más injerto autólogo y placa con tornillos. Posteriormente se evidenció luxación del nivel dorsal 6 hacia atrás comprimiendo la médula espinal y, dada la inestabilidad mecánica, se indicó un tercer tiempo quirúrgico por vía posterior que comprendió reducción, descompresión y fijación, resolviendo los tres niveles por vía posterior con barras y tornillos. El tratamiento quirúrgico, médico y kinésico de esta forma poco frecuente del mal de Pott fue exitoso, con recuperación de su estabilidad mecánica y progresiva recuperación de su estado neurológico.",
+        "synthetic_summary": {
+            "B1": "Había un joven de 20 años muy enfermo con un hueso del cuello y la espalda roto por una infección. Esta infección era muy fuerte y estaba en muchos lugares de su cuerpo. A veces, de sus heridas salía una cosa blanda y fea. \n\nUn día, el joven no pudo mover sus piernas. Los doctores hicieron una operación rápida para ayudar a su espalda y que pudiera sentir y mover mejor. Después, le hicieron otra operación para arreglar los huesos del cuello con partes nuevas y tornillos. \n\nLuego, vieron que un hueso de su espalda estaba fuera de lugar y apretaba la parte que mueve y siente el cuerpo. Entonces, hicieron otra operación para poner todo en su lugar con barras y tornillos. \n\nCon medicinas, ejercicios y las operaciones, el joven mejoró mucho. Ahora puede caminar y está más fuerte. Los doctores están contentos porque él está mejor.",
+            "B2": "**Caso de Tuberculosis en la Columna Vertebral**\n\nEste es el caso de un joven de 20 años que tenía tuberculosis, una infección causada por una bacteria llamada Mycobacterium tuberculosis. Aunque no tenía VIH, la infección estaba muy extendida y afectaba varias partes de su columna vertebral: el cuello (cervical), la parte media de la espalda (dorsal) y la zona baja (lumbar). Algunas áreas tenían heridas abiertas que soltaban una sustancia llamada caseum, que es un material parecido a queso que se forma por la infección.\n\n**Problemas y Tratamiento Inicial**\n\nEl paciente sufrió una pérdida súbita de movimiento y sensibilidad en las piernas, llamada paraplejía, debido a que la médula espinal estaba comprimida en la zona dorsal 6 (parte media de la espalda). Por eso, tuvo que someterse a una cirugía urgente para aliviar la presión en la médula, llamada descompresión, realizada por la parte trasera de la columna.\n\nDespués, se hizo una cirugía programada en el cuello, por la parte delantera, donde se removieron varios cuerpos vertebrales dañados (corporectomía). Para reemplazarlos, se usaron injertos, que son partes de hueso tomadas del propio paciente, junto con placas y tornillos para estabilizar la columna.\n\n**Complicación y Cirugía Final**\n\nMás adelante, se descubrió que una vértebra en la zona dorsal 6 se había desplazado hacia atrás, presionando otra vez la médula espinal y causando inestabilidad en la columna. Por esta razón, se realizó una tercera cirugía por la parte trasera para corregir el desplazamiento, aliviar la presión y fijar la columna con barras y tornillos desde el cuello hasta la parte media de la espalda.\n\n**Resultado**\n\nCon el tratamiento combinado de medicamentos para la tuberculosis, cirugías y rehabilitación física, el paciente mejoró mucho. Recuperó la estabilidad de su columna y la función de sus piernas, pudiendo caminar por sí mismo después de una larga hospitalización de cinco meses. Este caso muestra cómo, aunque la tuberculosis en la columna puede ser grave y complicada, un tratamiento adecuado puede llevar a una buena recuperación.",
+            "B3": "**Contexto**  \nSe describe el caso de un joven de 20 años, sin infección por VIH, que presentó tuberculosis pulmonar y ósea diseminada, con afectación de múltiples niveles de la columna vertebral (cervical, dorsal y lumbar) en forma no contigua. El paciente tenía un estado general muy deteriorado, con pérdida de peso, atrofia muscular severa y lesiones tumorales en la piel que secretaban material caseoso (una sustancia similar a queso, típica de la tuberculosis). Estas lesiones estaban fistulizadas, es decir, comunicadas con el exterior, en regiones como el dorso, el cráneo y el tórax anterior.\n\n**Hallazgos Clave**  \n- Confirmación microbiológica de Mycobacterium tuberculosis sensible a rifampicina y otros antibióticos habituales.  \n- Imágenes de tomografía computarizada y resonancia magnética que mostraron consolidaciones pulmonares, lesiones óseas líticas (áreas de destrucción ósea) en varios niveles vertebrales y colecciones (acumulaciones de líquido o pus) pre y paraespinales.  \n- Fracturas patológicas en las vértebras dorsales D6 y D10, con infiltración tumoral desde C4 a C6, D4 a D6, D9 a D12 y L1 a L3.  \n- Episodio agudo de paraplejía (pérdida de movimiento y sensibilidad en las piernas) con nivel sensitivo en D8 y compromiso vesical, atribuible a compresión medular aguda en D6.\n\n**Interpretación Clínica**  \nEl paciente presentó una forma grave y poco común de tuberculosis ósea conocida como mal de Pott, con afectación de múltiples niveles vertebrales no contiguos. La destrucción ósea extensa y la presencia de colecciones pusieron en riesgo la integridad neurológica, con riesgo de parálisis permanente. La paraplejía aguda requirió una intervención quirúrgica urgente para descomprimir la médula espinal mediante laminectomía (extirpación de parte de la vértebra) y evacuación de la colección epidural. Posteriormente, se realizó una cirugía programada en la región cervical por vía anterior, que incluyó la extracción de varios cuerpos vertebrales afectados (corporectomía), reconstrucción con injerto óseo autólogo y fijación con placa y tornillos. Sin embargo, se detectó una luxación posterior en D6 que comprimía nuevamente la médula, causando inestabilidad mecánica y deterioro neurológico. Esto motivó una tercera cirugía por vía posterior para reducir la luxación, descomprimir la médula y fijar los niveles cervical y dorsales afectados con tornillos y barras, estabilizando la columna desde C3 hasta D12.\n\n**Próximos Pasos y Evolución**  \nEl tratamiento combinado, que incluyó terapia antituberculosa estándar de primera línea durante al menos 12 meses, intervenciones quirúrgicas escalonadas y rehabilitación kinésica intensiva, permitió la recuperación progresiva de la función motora y sensitiva del paciente. Además, se logró la resolución de las lesiones pulmonares y la estabilidad mecánica de la columna vertebral. Tras una prolongada hospitalización de cinco meses, el paciente egresó caminando por sus propios medios, evidenciando una evolución favorable en un caso complejo y de alta gravedad."
+        }
+    },
+    {
+        "article": "Un hombre japonés de 23 años fue admitido en nuestro hospital debido al empeoramiento de la disnea de esfuerzo. Había mostrado dificultad para correr a los dos años y se le diagnosticó EDMD con una mutación genética de LMNA (Lamin A/C) en el exón 1 de leucina 102 a prolina. De acuerdo con las manifestaciones típicas de EDMD, sus codos, rodillas y tendones de Aquiles se habían contraído a los cinco años, y sus músculos cervicales posteriores se habían vuelto rígidos; sin embargo, continuó con su vida diaria habitual, aunque con una leve restricción de ejercicio. Su padre también había sido diagnosticado con EDMD y murió repentinamente a los 40 años.\n\nCuando el paciente tenía 19 años, fue admitido en un hospital por primera vez debido a una insuficiencia cardiaca congestiva. Los signos de insuficiencia de la RV, tales como edema de las piernas y congestión hepática, fueron prominentes, como lo indica el alto nivel de bilirrubina en sangre (2,5 mg/dL). La ecocardiografía mostró que la excursión sistólica del plano anular tricúspide (TAPSE) era de 5,7 mm, la velocidad de la RV de 5,1 cm/s y el cambio del área fraccional de la RV (RVFAC) del 19 %, lo que indica una marcada disfunción de la RV. Se introdujeron diuréticos de alta dosis además de carvedilol (10 mg/día) y enalapril (2,5 mg/día). A pesar de esos medicamentos, fue readmitido debido al empeoramiento de la insuficiencia de la RV.\n\nA los 22 años, se le implantó un desfibrilador cardioversor implantable (ICD) debido a su taquicardia ventricular no sostenida (VT) y a la historia familiar de muerte súbita cardiaca. En este momento, el cateterismo cardiaco derecho (RHC) mostró una presión de la cuña de la arteria pulmonar (PAWP) de 22 mmHg, presión auricular derecha (RAP) de 17 mmHg, e índice de trabajo de accidente cerebrovascular ventricular derecho (RVSWI) de 6.47, lo que sugiere una disfunción severa sostenida del RV. Como tal, el fallo del RV probablemente fue la principal condición patológica a lo largo de su curso clínico.\n\nTenía insuficiencia cardiaca sintomática con la clasificación III de la New York Heart Association con dosis máximas de medicación guiada por directrices, y su electrocardiograma mostraba un ritmo sinusal regular y bloqueo de rama izquierda con ancho QRS (150 ms). Su fracción de eyección del ventrículo izquierdo (LVEF) era ≤35 % en la ecocardiografía. Por lo tanto, se consideró que estaba indicado para CRT y se le actualizó a ICD a los 23 años.\n\nAl ingreso, su presión arterial era de 106/65 mmHg y su frecuencia cardíaca de 60 latidos/min con un ritmo regular. El examen físico reveló un tercer sonido cardíaco y un soplo pan sistólico (Levine II/VI) en la región apical. Los sonidos respiratorios eran claros, mientras que una vena yugular distendida y un edema de miembros inferiores eran evidentes. La radiografía de tórax indicó un aumento de la relación cardiotorácica (59%) sin congestión pulmonar.\n\nEl electrocardiograma mostró un ritmo biventricular debido a la TRC. La ecocardiografía reveló una ligera dilatación en ambos ventrículos (diámetro final diastólico del LV: 54 mm, diámetro del RV: 50 mm) con una reducción de la LVEF (30%). La función del RV también se redujo, como lo indican una reducción de la RVFAC (11%) y un bajo TAPSE (8 mm). Ambos ventrículos agrandados causaron una pérdida de sujeción y coaptación de las valvas que resultó en una regurgitación mitral moderada y una regurgitación tricuspídea severa. La vena cava inferior se dilató a 23 mm con una reducción de la fluctuación respiratoria.\n\nEn los hallazgos histológicos de los músculos cervicales posteriores realizados más tarde en la autopsia, se observó un aumento en la variación del tamaño de la fibra muscular con una infiltración moderada de tejido conectivo, lo que fue compatible con la EDMD. Los análisis de sangre revelaron péptido natriurético cerebral (BNP) 196.1 pg/mL, bilirrubina total 1.4 mg/dL, aspartato aminotransferasa (AST) 39 U/L, alanina aminotransferasa (ALT) 43 U/L, y gamma glutamil transpeptidasa (gamma-GTP) 451 U/L, lo que sugirió una disfunción hepática. Aunque las arterias coronarias estaban intactas en la angiografía, una biopsia endocárdica del VD reveló una hipertrofia cardiaca con un aumento de la magnitud del núcleo y el miocardio.\n\nLa microscopía electrónica demostró hallazgos típicos de la EDMD: un número reducido de miofibrillas, necrosis y la formación de pseudo- o verdaderas inclusiones. Dado que se descartaron otras cardiomiopatías secundarias mediante estos hallazgos clínicos e histológicos, diagnosticamos una cardiomiopatía relacionada con la EDMD.\n\n\nEl curso clínico del paciente. El cateterismo cardiaco derecho (RHC) en el día 11 mostró disfunción y congestión severa del LV/RV, y se iniciaron algunos inótropos. Aunque la hemodinámica del paciente mejoró, su función renal empeoró progresivamente en el día 38. Preocupados por el empeoramiento de su función renal debido a la disminución de la presión arterial, se iniciaron la dopamina y el soporte mecánico (IABP y CRRT), y la función renal y la hemodinámica del paciente mejoraron. Sin embargo, desarrolló insuficiencia hepática aguda junto con insuficiencia severa del RV indicada por los datos del RHC en el día 68. Aunque se introdujo ECMO veno-atrial en el día 71, la disfunción hepática y la DIC causaron diátesis hemorrágica sistémica, y el paciente falleció por fallo multiorgánico en el día 100. CRRT: terapia de reemplazo renal continua, DIC: coagulación intravascular diseminada, ECMO: oxigenación por membrana extracorpórea, IABP: bombeo de globo intraaórtico, LV: ventrículo izquierdo, RV: ventrículo derecho\n\nEl RHC en el día 11 mostró que el índice cardiaco (IC) era de 2,0 L/min/m2 (método de Fick), y la PAP era de 15 mmHg, lo que indicaba un subgrupo IV de Forrester. La presión arterial pulmonar (PAP) era de 29/12 (18) mmHg, y la RAP era de 15 mmHg. El RVSWI, uno de los parámetros hemodinámicos para la función del RV, se calculó con la siguiente fórmula: RVSWI (g·m/m2/latido)=[presión arterial pulmonar media (mPAP)-presión atrial derecha media (mRAP)]×índice de volumen de latido (SVI)×0.0136. Su RVSWI era de 1.36 g·m/m2/latido, lo que indicaba una disfunción severa del RV. Para compensar el síndrome de baja producción del paciente y la congestión, comenzamos una infusión continua de dobutamina (3.0 μg/kg/min) y añadimos milrinona (0.125 μg/kg/min) en el día 16.\n\n\nEn el día 32, los datos de RHC mejoraron, con un aumento del IC (2,48 L/min/m2), una reducción de la PAWP (13 mmHg) y un aumento de la RVSWI (2,8 g·m/m2/latido). Sin embargo, en el día 38, la función renal del paciente empeoró progresivamente, posiblemente debido a una presión venosa central alta (CVP) e hipotensión, ya que la presión arterial había sido de alrededor de 70/40 mmHg varios días antes del empeoramiento de la función renal. Para aumentar su presión arterial, se inició una infusión continua de dopamina (2,0 μg/kg/min); se redujo la milrinona y se interrumpieron el enalapril y la eplerenona. Además, se necesitaron temporalmente el bombeo de globo intraaórtico (IABP) y la terapia de reemplazo renal continuo (CRRT). A medida que la hemodinámica del paciente mejoró en respuesta al aumento de la saturación de oxígeno venoso mixto (SvO2, 70-80%) y el IC (3,0-3,5 L/min/m2), se retiraron el IABP y la CRRT en el día 45.\n\nSin embargo, el día 68, el IC volvió a disminuir a 1,25 l/min/m2 y la congestión pulmonar y la retención de fluidos del paciente se deterioraron; la PAWP era tan alta como la RAP, a 22 mmHg. Además, los niveles de bilirrubina en suero y las transaminasas hepáticas del paciente aumentaron drásticamente, lo que sugiere el desarrollo de insuficiencia hepática. El día 71, se inició la ECMO VA a través de una vena femoral a la arteria subclavia, pero debido a la diátesis hemorrágica sistémica acompañada por la coagulación intravascular diseminada (CID), el paciente falleció de insuficiencia multiorgánica el día 100.\n\nUna autopsia realizada con el consentimiento informado de la familia del paciente reveló un agrandamiento eferente en ambos ventrículos con un espesor de pared delgado. El examen histopatológico reveló que la hipertrofia miocárdica leve a moderada y la fibrosis severa eran evidentes en el RV y el LV. El peso del hígado aumentó significativamente a 2298 g, y se detectaron congestión hepática macroscópica y colestasis. En las imágenes microscópicas, el área de la vena porta apenas cambió, y se observó atrofia o pérdida de hepatocitos alrededor de las venas centrales, lo que indica un «hígado de shock». En los pulmones, se observó una hemorragia alveolar extensa, y se observó una colección de macrófagos que habían ingerido hemosiderina, lo que refleja una diátesis hemorrágica sistémica.\n\nMH - Adulto\nMH - Insuficiencia cardiaca/*etiología/fisiopatología/terapia\nMH - Humanos\nMH - Lamin tipo A/genética\nMH - Hombre\nMH - Distrofia muscular, Emery-Dreifuss/*complicaciones/diagnóstico/genética/terapia\nMH - Mutación\n",
+        "gold_summary": "Un hombre de 23 años tenía debilidad muscular progresiva y distrofia muscular de Emery-Dreifuss (EDMD) debido a una mutación de LMNA (lamina A/C). Insuficiencia cardiaca congestiva diagnosticada a los 19 años de edad. El tratamiento farmacológico máximo/resincronización cardiaca no logró mejorar la función cardiaca. Por lo tanto, fue hospitalizado debido a insuficiencia cardiaca. A pesar de la oxigenación por membrana extracorpórea, desarrolló una disfunción cardiaca derecha grave y falleció (fallo multiorgánico).\n",
+        "synthetic_summary": {
+            "B1": "Había un hombre joven con músculos muy débiles. Tenía una enfermedad que hace que los músculos se pongan muy rígidos y duros. Su corazón también se puso muy cansado y no podía trabajar bien. Los doctores le dieron medicinas y una máquina para ayudar su corazón. Pero su corazón se puso peor y se enfermó mucho. Al final, su cuerpo no pudo seguir y él murió.",
+            "B2": "**Lo que le pasaba al paciente:**  \nUn joven japonés de 23 años tenía una enfermedad llamada distrofia muscular de Emery-Dreifuss (EDMD). Esta enfermedad afecta los músculos y está causada por un cambio en un gen llamado LMNA, que produce una proteína importante para las células. Desde pequeño, él tenía problemas para moverse bien y sus músculos se ponían rígidos. A los 19 años, comenzó a tener problemas graves en su corazón, especialmente en la parte derecha, lo que causaba insuficiencia cardiaca, es decir, que el corazón no podía bombear sangre correctamente.\n\n**Tratamientos y evolución:**  \nEl paciente recibió varios medicamentos para mejorar su corazón y un dispositivo llamado desfibrilador para prevenir ritmos cardiacos peligrosos. Más tarde, le pusieron un tratamiento llamado terapia de resincronización cardiaca, que ayuda a que las partes del corazón trabajen juntas mejor. Sin embargo, ninguno de estos tratamientos logró mejorar suficientemente la función de su corazón.\n\n**Lo que ocurrió en el hospital:**  \nFue ingresado en el hospital por empeoramiento de su insuficiencia cardiaca. Los médicos usaron máquinas especiales para ayudar a su corazón y a sus órganos, como la oxigenación por membrana extracorpórea (ECMO), que es un sistema que ayuda a oxigenar la sangre cuando el corazón y los pulmones no funcionan bien. A pesar de estos esfuerzos, su corazón derecho siguió fallando gravemente, lo que provocó que otros órganos también dejaran de funcionar, y lamentablemente falleció.\n\n**Qué significa este caso:**  \nEste caso muestra cómo la distrofia muscular de Emery-Dreifuss puede afectar no solo los músculos, sino también el corazón, causando insuficiencia cardiaca severa que es difícil de tratar. La mutación genética en LMNA juega un papel importante en esta enfermedad. Aunque existen tratamientos avanzados, en algunos casos la enfermedad puede progresar y causar complicaciones graves que llevan a la muerte.",
+            "B3": "**Contexto**  \nSe presenta el caso de un hombre japonés de 23 años con distrofia muscular de Emery-Dreifuss (EDMD), una enfermedad genética causada por una mutación en el gen LMNA que codifica la proteína lamina A/C. Esta mutación específica (leucina 102 a prolina en el exón 1) provocó debilidad muscular progresiva desde la infancia, contracturas articulares y rigidez muscular, manifestaciones típicas de esta enfermedad. Además, existía un antecedente familiar importante, ya que su padre también padeció EDMD y falleció súbitamente a los 40 años.\n\n**Hallazgos Clave**  \nA los 19 años, el paciente desarrolló insuficiencia cardíaca congestiva, principalmente por disfunción severa del ventrículo derecho (RV), evidenciada por síntomas como edema en las piernas y congestión hepática, así como por estudios ecocardiográficos y cateterismo cardíaco que mostraron una función ventricular deteriorada. A pesar de recibir tratamiento farmacológico intensivo con diuréticos, betabloqueantes y inhibidores de la enzima convertidora de angiotensina, la función cardíaca no mejoró. A los 22 años se le implantó un desfibrilador cardioversor implantable (ICD) debido a episodios de taquicardia ventricular y riesgo de muerte súbita.\n\nCuando la insuficiencia cardíaca progresó a una etapa avanzada (clasificación funcional III de la New York Heart Association), se le realizó una terapia de resincronización cardíaca (CRT) para mejorar la función del corazón. Sin embargo, al ingreso hospitalario a los 23 años, persistían signos de insuficiencia cardíaca derecha grave, con dilatación de ambos ventrículos, reducción significativa de la fracción de eyección del ventrículo izquierdo (LVEF 30%) y disfunción severa del ventrículo derecho, acompañada de insuficiencia valvular mitral y tricuspídea.\n\nDurante su hospitalización, el paciente presentó empeoramiento progresivo de la función renal y hepática, complicaciones que reflejaban la insuficiencia multiorgánica secundaria a la falla cardíaca avanzada. Se implementaron tratamientos de soporte hemodinámico, incluyendo infusiones de medicamentos inotrópicos, bombeo de globo intraaórtico (IABP), terapia de reemplazo renal continua (CRRT) y finalmente oxigenación por membrana extracorpórea (ECMO) veno-arterial. A pesar de estas intervenciones, desarrolló coagulación intravascular diseminada (CID) y una diátesis hemorrágica sistémica, que culminaron en su fallecimiento por fallo multiorgánico al día 100 de hospitalización.\n\n**Interpretación Clínica**  \nEste caso ilustra la evolución grave y progresiva de la insuficiencia cardíaca en un paciente con EDMD causada por una mutación en LMNA, destacando la predominancia de la disfunción del ventrículo derecho como factor principal en su deterioro clínico. La resistencia a los tratamientos convencionales y avanzados, como la terapia farmacológica máxima, resincronización cardíaca y soporte mecánico, refleja la complejidad y severidad de la cardiomiopatía asociada a esta enfermedad genética. Los hallazgos histopatológicos post mortem confirmaron la presencia de hipertrofia miocárdica, fibrosis severa en ambos ventrículos y daño hepático compatible con congestión crónica y “hígado de shock”.\n\n**Próximos Pasos y Consideraciones**  \nEste caso subraya la necesidad de un diagnóstico temprano y un seguimiento riguroso en pacientes con EDMD, especialmente aquellos con mutaciones en LMNA, dado el alto riesgo de insuficiencia cardíaca progresiva y muerte súbita. La identificación de disfunción ventricular derecha precoz podría orientar intervenciones más agresivas o la consideración temprana de trasplante cardíaco. Además, se requiere investigación continua para desarrollar terapias específicas que puedan modificar el curso de la cardiomiopatía en EDMD y mejorar la supervivencia y calidad de vida de estos pacientes."
+        }
+    },
+    {
+        "article": "Mujer de 65 años sin antecedentes patológicos destacables que en 2004 inició paroxismos lancinantes en los territorios V2 y V3 derechos, con desencadenantes clásicos, por lo que se le diagnosticó una neuralgia del trigémino derecho. En las resonancias magnéticas cerebrales hasta 2021 no se habían realizado las secuencias que permiten identificar si hay un cruce neurovascular. Desde el inicio, el control del dolor con carboxamidas fue difícil. En 2021 presentó exacerbación de los paroxismos previos que aparecieron en V1. La neuralgia se volvió refractaria, sin respuesta a las carboxamidas y la lamotrigina, y muy escasa al clonacepam, por lo que requirió perfusiones de fenitoína y/o lidocaína en las exacerbaciones graves. Simultáneamente inició paroxismos lancinantes en la parte posterior de la lengua y la pared lateral derecha de la orofaringe, que se exacerbaron con la deglución y que aumentaron progresivamente en intensidad y frecuencia. Se orientó como el inicio de una neuralgia del nervio glosofaríngeo derecho. Se repitió la resonancia magnética cerebral con secuencia CISS (del inglés, constructive interference in steady state), que mostró un contacto arterial significativo entre la arteria cerebelosa superior derecha y el origen del V par craneal derecho, y de la arteria cerebelosa anteroinferior con el origen de los pares craneales bajos derechos. Ante un caso de neuralgia del nervio trigémino y neuralgia del nervio glosofaríngeo clásicas, concomitantes y refractarias, se planteó una doble descompresión microvascular en un tiempo como mejor opción terapéutica.\n\nEn marzo de 2021 se realizó una craniectomía retrosigmoidea derecha con exposición de la cisterna perimesencefálica y las cisternas basales. Se procedió a la liberación del V par craneal, y se apreció un íntimo contacto con la arteria cerebelosa superior en su parte sensitiva y adelgazamiento en la zona de entrada de la raíz nerviosa. Se procedió a la colocación de teflón entre la arteria cerebelosa superior y el V par craneal en todo su trayecto. Posteriormente, se exploró la cisterna basal y se apreció loop vascular de la arteria cerebelosa anteroinferior en íntimo contacto con el IX par craneal, donde se colocó teflón y sellante dural encima. El postoperatorio cursó sin incidencias, con resolución completa de la neuralgia del nervio trigémino y reducción >50% de la intensidad de los paroxismos en el territorio glosofaríngeo. A los dos años continúa sin paroxismos trigeminales y presenta <1 paroxismo/mes de intensidad tolerable en el territorio glosofaríngeo desencadenado con la deglución. El tratamiento farmacológico continúa en pauta descendente sin que ello haya supuesto la reaparición de los paroxismos.",
+        "gold_summary": "Mujer de 65 años con NT derecho (inicialmente en V2-V3) desde 2004 con control regular con carboxamidas. Diecisiete años después empeoraron los paroxismos en V2-V3, aparecieron también en V1 y en el territorio del nervio glosofaríngeo derecho (oído derecho y fosa amigdalar al hablar y deglutir). La resonancia magnética cerebral mostró contacto arterial significativo entre arteria cerebelosa superior (ACS) con origen del V par craneal derecho y de la arteria cerebelosa antero-inferior (AICA) con el origen de pares craneales bajos derechos. Se realizó DMV de ambos pares craneales en un mismo tiempo quirúrgico mediante craniectomía retrosigmoidea, y se procedió a la liberación del V par craneal, en contacto íntimo con la ACS, y del IX par craneal en contacto con la AICA derecha, para lo que se puso teflón entre ellas. La paciente tuvo una resolución inmediata de los paroxismos trigeminales y una mejoría considerable en intensidad y frecuencia de los glosofaríngeos. A los 2 años de la intervención continúa la desescalada de tratamiento neuromodulador con buena respuesta.",
+        "synthetic_summary": {
+            "B1": "Había una señora de 65 años que tenía dolor fuerte en la cara desde hace mucho tiempo. El dolor estaba en un lado de su cara y a veces se hacía más fuerte. También empezó a dolerle la garganta y el oído cuando comía o hablaba.\n\nLos doctores le hicieron una foto especial de su cabeza. Vieron que unas partes de su cuerpo, que son como tubitos, estaban tocando nervios que causaban el dolor.\n\nEntonces, los doctores hicieron una operación para poner un pedacito suave entre los tubitos y los nervios. Esto ayudó mucho a que el dolor se fuera.\n\nDespués de la operación, la señora se sintió mucho mejor. El dolor casi no volvió y pudo tomar menos medicina. Está feliz y tranquila.",
+            "B2": "**Lo que le Pasó a la Paciente**  \nUna mujer de 65 años tuvo un dolor muy fuerte y repentino en la cara desde 2004. Este dolor afectaba principalmente dos zonas de su cara, llamadas V2 y V3, que son partes del nervio trigémino, un nervio que ayuda a sentir la cara. A pesar de tomar medicamentos llamados carboxamidas para controlar el dolor, este empeoró después de muchos años. Además, el dolor apareció en otra zona llamada V1 y también en el área de la garganta y oído derecho, que están conectados con otro nervio llamado glosofaríngeo.\n\n**Lo que Encontraron en las Pruebas**  \nSe le hizo una resonancia magnética especial que mostró que dos arterias (vasos sanguíneos) estaban presionando los nervios afectados. Una arteria llamada cerebelosa superior estaba tocando el nervio trigémino, y otra llamada cerebelosa antero-inferior estaba en contacto con el nervio glosofaríngeo. Esta presión puede causar los dolores intensos que ella sentía.\n\n**Qué Hicieron para Ayudarla**  \nLos médicos realizaron una cirugía llamada descompresión microvascular. En esta operación, hicieron una pequeña apertura en el cráneo para llegar a los nervios y separar las arterias que los estaban presionando. Para evitar que las arterias volvieran a tocar los nervios, colocaron un material llamado teflón entre ellos.\n\n**Resultados Después de la Cirugía**  \nDespués de la operación, el dolor en la cara (del nervio trigémino) desapareció completamente. El dolor en la garganta y oído (del nervio glosofaríngeo) mejoró mucho, con menos intensidad y frecuencia. Dos años después, la paciente sigue mejor, con muy pocos episodios de dolor que puede controlar fácilmente y ha podido reducir los medicamentos que tomaba.\n\n**En Resumen**  \nEsta paciente tenía dolores fuertes causados por arterias que presionaban nervios en su cabeza. La cirugía para separar esas arterias de los nervios fue exitosa y mejoró mucho su calidad de vida.",
+            "B3": "**Contexto**  \nSe trata de una mujer de 65 años que desde 2004 presentaba episodios de dolor intenso y punzante en las ramas V2 y V3 del nervio trigémino derecho (que corresponden a zonas de la cara como el maxilar y la mandíbula). Estos episodios, conocidos como neuralgia del trigémino, inicialmente se controlaban con medicamentos llamados carboxamidas. Sin embargo, diecisiete años después, el dolor empeoró, extendiéndose también a la rama V1 (zona de la frente) y aparecieron nuevos episodios dolorosos en el territorio del nervio glosofaríngeo derecho, afectando áreas como el oído y la parte lateral de la garganta, especialmente al hablar y tragar.\n\n**Hallazgos Clave**  \nUna resonancia magnética cerebral con una técnica especial (secuencia CISS) reveló que dos arterias cerebrales —la arteria cerebelosa superior (ACS) y la arteria cerebelosa anteroinferior (AICA)— estaban en contacto directo y presionando los orígenes de los nervios afectados: la ACS sobre el nervio trigémino derecho y la AICA sobre los nervios craneales inferiores, incluido el nervio glosofaríngeo derecho.\n\n**Interpretación Clínica**  \nEsta compresión vascular es una causa conocida de neuralgias craneales, ya que la presión constante puede irritar los nervios y provocar los episodios de dolor intenso. En este caso, la paciente presentaba neuralgia del trigémino y neuralgia del glosofaríngeo simultáneamente, ambas resistentes al tratamiento farmacológico habitual.\n\n**Próximos Pasos y Tratamiento**  \nSe decidió realizar una cirugía llamada descompresión microvascular (DMV) en un solo procedimiento, mediante una craniectomía retrosigmoidea (una apertura quirúrgica en la parte posterior del cráneo). Durante la intervención, se liberaron ambos nervios de la presión arterial colocando pequeñas almohadillas de teflón entre las arterias y los nervios para evitar el contacto directo.  \n\n**Resultados y Seguimiento**  \nLa paciente experimentó una resolución inmediata de los episodios dolorosos relacionados con el nervio trigémino y una reducción significativa en la frecuencia e intensidad del dolor en el territorio del nervio glosofaríngeo. Dos años después de la cirugía, continúa con un tratamiento farmacológico en disminución y mantiene un control satisfactorio del dolor, con episodios muy esporádicos y tolerables en la zona glosofaríngea, especialmente al tragar.\n\nEste caso ilustra la importancia de identificar la compresión vascular en neuralgias craneales refractarias y la eficacia de la descompresión microvascular como tratamiento para mejorar la calidad de vida en pacientes con neuralgia del trigémino y del glosofaríngeo."
+        }
+    },
+    {
+        "article": "Hombre de 36 años, bisexual, en profilaxis antirretroviral de pre-exposición al HIV, sin antecedentes de viaje, que refirió haber asistido a un evento donde tuvo contactos con parejas ocasionales cuya identidad y antecedentes se desconocen. Diez días después comenzó con fiebre, odinofagia y dolor cervical por lo que consultó en varias oportunidades, hasta que a los siete días del inicio de los síntomas se internó por persistencia de los mismos a pesar del tratamiento antibiótico indicado. Al ingreso presentó exudado faríngeo, adenopatías cervicales bilaterales dolorosas y pápulas umbilicadas en escroto y pene y pústulas en cara de cinco días de evolución. Se realizó tomografía computarizada de cuello con contraste endovenoso que descartó colección, ecografía abdominal con leve hepatoesplenomegalia, e inició tratamiento empírico con ceftriaxona y azitromicina. Se tomaron muestras para cultivo, para serologías, y escarificación de dos lesiones de la cara que se enviaron al Laboratorio Nacional de Referencia, INEI-ANLIS Dr. Carlos G. Malbrán, para PCR de punto final para Orthopoxvirus, con resultado DETECTABLE, confirmando así el diagnóstico de viruela símica. La secuenciación arrojó un alto porcentaje de homología con secuencias del clado de África Occidental (MPV-ARG003-2022, Genbank_ID ON800897). Otros diagnósticos diferenciales fueron descartados. El paciente evolucionó con aparición de una úlcera en lengua y nuevas lesiones asincrónicas en glúteos, región perianal, inguinal derecha, umbilical, frontal, cuello, mano derecha y dorso de pie en un total de no más de 25. En el laboratorio se constató un aumento de transaminasas en 2.2 veces el valor normal, sin otros datos significativos.  Por persistencia del dolor cervical se solicitó nueva tomografía computarizada a los 14 días del inicio de los síntomas que evidenció adenomegalias con centro hipodenso de aspecto necrótico, que no requirieron drenaje quirúrgico. Al día 17 se realizó PCR en muestras de exudado de fauces y semen las que también resultaron positivas para virus de viruela símica. Se externó con franca mejoría clínica dos días después. El paciente dio su consentimiento informado escrito para la publicación de este informe de caso y las imágenes que lo acompañan.",
+        "gold_summary": "Se trata de un hombre joven, bisexual, en profilaxis antirretroviral de pre-exposición al HIV, cuya forma de presentación fue faringitis exudativa sin otra etiología documentada y adenopatías que evolucionaron a la necrosis, presencia de lesiones asincrónicas características en cara, cuello, abdomen, extremidades y genitales. El diagnóstico fue por detección de ADN viral por reacción en cadena de la polimerasa en lesiones de piel, exudado de fauces y semen. El compromiso faríngeo con presencia de exudado luego del descarte de otras infecciones, podría ser una rareza para la forma epidémica de la enfermedad. El hallazgo del virus en semen ya reportado en otras publicaciones no es suficiente aún para confirmar la vía sexual como forma de trasmisión.",
+        "synthetic_summary": {
+            "B1": "Un hombre joven se enfermó con dolor de garganta y bultos en el cuello. También tuvo manchitas en la cara, cuello, barriga, brazos y partes íntimas. Los doctores encontraron un virus en su piel, en la garganta y en otra parte del cuerpo. Este virus es raro y puede causar estas manchas y dolor. Los doctores no están seguros si el virus se pasa por el contacto en el cuerpo. El hombre mejoró con ayuda de los doctores.",
+            "B2": "**Caso de un Hombre Joven con Viruela Símica**\n\nEste informe habla de un hombre de 36 años que es bisexual y estaba tomando medicamentos para prevenir el VIH antes de enfermarse. Él empezó con dolor de garganta, fiebre y dolor en el cuello. Además, tenía ganglios inflamados y dolorosos en el cuello. También aparecieron pequeñas lesiones en la cara, el pene y el escroto, que son áreas del cuerpo donde se pueden ver bultos o manchas.\n\nPara saber qué tenía, los médicos hicieron varios estudios. Tomaron muestras de las lesiones en la piel y las analizaron con una prueba llamada PCR, que busca el ADN del virus. Encontraron que tenía el virus de la viruela símica, una enfermedad causada por un virus parecido a la viruela común, pero menos grave. También encontraron el virus en la garganta y en el semen del paciente.\n\nDurante su enfermedad, el hombre desarrolló más lesiones en diferentes partes del cuerpo, como los glúteos, la zona alrededor del ano, el cuello y las manos. Además, tuvo un aumento en algunas enzimas del hígado, lo que indica que el virus afectó un poco este órgano. En el cuello, los ganglios inflamados mostraron signos de daño, pero no fue necesario hacer cirugía.\n\nAunque el virus se encontró en el semen, todavía no está claro si la viruela símica se transmite por contacto sexual. El dolor y la inflamación en la garganta con pus (exudado) que tuvo este paciente no es común en los casos que se han visto en la epidemia actual, por lo que es un detalle importante para los médicos.\n\nDespués de recibir tratamiento, el paciente mejoró y pudo salir del hospital. Este caso ayuda a entender mejor cómo puede presentarse la viruela símica y qué síntomas buscar para hacer un diagnóstico correcto.",
+            "B3": "**Contexto**  \nSe presenta el caso de un hombre de 36 años, bisexual, que utiliza profilaxis antirretroviral de pre-exposición (PrEP) para prevenir la infección por VIH. Sin antecedentes de viajes recientes, asistió a un evento donde tuvo contacto con parejas sexuales ocasionales de identidad y antecedentes desconocidos. Diez días después comenzó con fiebre, dolor de garganta (odinofagia) y dolor en el cuello, síntomas que persistieron a pesar de tratamiento antibiótico inicial, lo que motivó su hospitalización.\n\n**Hallazgos Clave**  \nAl ingreso, el paciente mostró inflamación y exudado en la garganta, ganglios linfáticos cervicales inflamados y dolorosos en ambos lados, además de lesiones cutáneas características: pápulas umbilicadas (con un centro hundido) en el escroto y pene, y pústulas en la cara con cinco días de evolución. Se realizaron estudios de imagen, incluyendo tomografía computarizada (TC) de cuello con contraste, que descartó abscesos, y ecografía abdominal que evidenció un leve aumento del tamaño del hígado y bazo (hepatoesplenomegalia). Se inició tratamiento empírico con antibióticos ceftriaxona y azitromicina.\n\nSe tomaron muestras para cultivos, serologías y escarificación (raspado) de lesiones cutáneas, las cuales fueron enviadas a un laboratorio de referencia para realizar una prueba de reacción en cadena de la polimerasa (PCR) específica para Orthopoxvirus, confirmando la presencia de ADN viral de viruela símica (monkeypox). La secuenciación genética mostró alta similitud con cepas del clado de África Occidental, que es menos virulento que otros clados. Se descartaron otras posibles infecciones que podrían explicar los síntomas.\n\nDurante la evolución clínica, aparecieron nuevas lesiones en diferentes partes del cuerpo (glúteos, región perianal, ingle derecha, abdomen, frente, cuello, mano derecha y dorso del pie), sumando un total de aproximadamente 25 lesiones. Además, desarrolló una úlcera en la lengua. En análisis de laboratorio se detectó un aumento moderado de las enzimas hepáticas (transaminasas), sin otros hallazgos relevantes. Debido a la persistencia del dolor cervical, se realizó una nueva TC a los 14 días que mostró ganglios linfáticos agrandados con áreas centrales de necrosis (muerte del tejido), pero sin necesidad de intervención quirúrgica.\n\nAl día 17, se confirmó la presencia del virus mediante PCR en muestras de exudado faríngeo y semen. Dos días después, el paciente fue dado de alta con una mejoría clínica notable.\n\n**Interpretación Clínica**  \nEste caso destaca una presentación atípica de viruela símica en un adulto joven que utiliza profilaxis antirretroviral para VIH. La enfermedad se manifestó inicialmente como una faringitis exudativa (inflamación de la garganta con pus), acompañada de adenopatías cervicales que evolucionaron a necrosis, un cuadro poco común en la epidemia actual. Las lesiones cutáneas asincrónicas (que aparecen en diferentes momentos) en múltiples regiones del cuerpo son características de esta infección.\n\nLa confirmación diagnóstica se realizó mediante detección del ADN viral en las lesiones de piel, así como en muestras de exudado faríngeo y semen. Aunque la presencia del virus en el semen ha sido reportada en otros estudios, todavía no es suficiente para afirmar que la transmisión sexual sea la vía principal de contagio.\n\n**Próximos Pasos**  \nEl seguimiento clínico debe incluir la vigilancia de la evolución de las lesiones y la resolución de la inflamación ganglionar. Es importante continuar investigando las vías de transmisión del virus para mejorar las estrategias de prevención, especialmente en poblaciones con riesgo elevado. Además, este caso resalta la necesidad de considerar la viruela símica en el diagnóstico diferencial de faringitis exudativa persistente en contextos epidemiológicos compatibles."
+        }
+    },
+    {
+        "article": "Paciente de sexo masculino de 23 años, natural de Itagüí - Colombia, antecedente familiar de muerte súbita de etiología no clara en abuelo a los 50 años, sin otros antecedentes familiares o personales de importancia. Venía en seguimiento externo por episodios sincopales a repetición con diagnóstico desde la infancia de disfunción del nodo sinusal sintomática por lo que se le implantó un marcapaso.\n\nDurante controles posteriores no hay reporte de deterioro de clase funcional hasta el año 2012 en Guayaquil-Ecuador. Durante su hospitalización se realiza el cambio de generador; en el primer mes postoperatorio presenta como complicación temprana una infección de bolsillo de marcapaso por lo que requirió el explante de la unidad generadora con posterior abandono de electrodo ventricular previamente implantado. Se realiza un nuevo implante de marcapaso en el lado contralateral sin complicaciones ni registro de nuevos eventos sincopales en los siguientes 10 años de seguimiento.\n\nSeis meses antes del ingreso presentaba deterioro de clase funcional NYHA III, sin otros síntomas y sin reportes de evaluaciones por servicio de electrofisiología desde el último implante de generador de marcapaso en 2012. Durante controles ambulatorios se reportó la suspensión del tratamiento con beta bloqueador debido a la pobre tolerancia.\n\nAl examen físico se encontró soplo sistólico en foco aórtico II/VI sin irradiación, no presentó signos de congestión central o periférica. Dentro de los laboratorios no se evidenció alteración en función renal, electrolítica ni del perfil hematológico. Se programó el marcapaso con evidencia de agotamiento de la batería de generador. Se realizó un ecocardiograma transtorácico donde se encontró hipertrofia concéntrica severa del septum interventricular a nivel medio ventricular, de 26 mm con gradiente intracavitario pico de 117 mmHg y movimiento sistólico anterior del velo mitral (SAM) el cual generaba una regurgitación mitral leve.\n\nFue evaluado por Heart Team, debido al score de riesgo de muerte súbita (16,8%) además de tener antecedentes familiares de muerte súbita considerando EUROSCORE II 0,67%; en cuanto a los electrodos abandonados previamente y la contraindicación de realización de resonancia magnética cardiaca, dado a la incompatibilidad del marcapaso, se realiza un estudio tomográfico y se consideró la realización de miectomía por sintomatología y variante documentada.\n\nFue programado para realización de miectomía medio ventricular por abordaje transapical con retiro de electrodos; se realizó la ventriculotomía izquierda en el ápex, con posterior resección del septum desde el parte medio ventricular hasta la base, con posterior retiro de electrodos adheridos a velo septal tricúspideo. No hubo complicaciones intraoperatorias y posteriormente se presentó disminución del gradiente intracavitario sin presencia del fenómeno SAM. Durante su estancia en Unidad de Cuidados Intensivos el paciente cursó con dos episodios documentados de taquicardia ventricular con inestabilidad hemodinámica por lo cual se le colocó un cardiodesfibrilador implantable (CDI) compatible con resonancia magnética (MRI) ST Jude sin presentar nuevos episodios de TV. El paciente cursó sin nuevas intercurrencias y se iniciaron los estudios ambulatorios de estudio genético debido a sus antecedente familiares.\n\nEl paciente presentó una evolución posoperatoria favorable luego del implante de CDI. En los estudios genéticos se encontró una variante, probablemente patogénica, en heterocigosis del FLNC, c 4636G>A consistente con miocardiopatía familiar hipertrófica tipo 26 autosómica dominante.\n\nActualmente, el paciente se encuentra en clase funcional I, sin arritmias evidenciadas en la telemetría y en tratamiento regular con Bisoprolol 5 mg. Se inició ampliación de estudio genético a familiares directos, sin embargo, debido al difícil acceso a servicios de salud su ejecución fue limitada.",
+        "gold_summary": "A continuación, se presenta el caso de un paciente sexo masculino de 23 años con diagnóstico de cardiomiopatía hipertrófica variante medio apical, en quien se documenta variante de la filamina C, ante la inadecuada respuesta y persistencia de sintomatología frente al manejo médico, se realizó el procedimiento de miectomía con abordaje transapical, con posterior mejoría de sintomatología clínica y obstrucción al tracto de salida.",
+        "synthetic_summary": {
+            "B1": "Un joven de 23 años tenía un problema en su corazón. Su corazón era más grueso en una parte. Esto le hacía sentir mal y cansado.\n\nLos doctores le hicieron una operación para quitar un poco de ese corazón grueso. Después de la operación, se sintió mejor y su corazón pudo trabajar mejor.",
+            "B2": "**Caso de un joven con problema en el corazón**\n\nEste es el caso de un joven de 23 años que tiene una enfermedad llamada cardiomiopatía hipertrófica. Esto significa que una parte de su corazón, especialmente en la zona media y hacia el ápice (la punta), está más gruesa de lo normal. Esta enfermedad puede dificultar que la sangre salga bien del corazón.\n\n**Qué encontraron en sus genes**\n\nAl hacerle un estudio genético, descubrieron que tiene un cambio en un gen llamado filamina C. Este cambio puede causar problemas en el corazón y es una forma hereditaria de la enfermedad.\n\n**Tratamiento y resultados**\n\nEl joven no mejoraba con los medicamentos que le daban, así que los doctores decidieron hacer una cirugía llamada miectomía. En esta operación, quitaron parte del músculo grueso del corazón para que la sangre pueda salir mejor. La cirugía se hizo por la punta del corazón (abordaje transapical).\n\nDespués de la operación, el paciente mejoró mucho. Su corazón ya no tenía tanta obstrucción y sus síntomas disminuyeron. Actualmente, está en buen estado y sigue un tratamiento con medicamentos para cuidar su corazón.",
+            "B3": "**Contexto**  \nSe trata de un paciente masculino de 23 años, originario de Itagüí, Colombia, con antecedentes familiares relevantes de muerte súbita en su abuelo a los 50 años, sin otras enfermedades familiares o personales significativas. Desde la infancia, el paciente presentaba episodios repetidos de síncope (pérdida temporal del conocimiento) atribuibles a una disfunción del nodo sinusal (una alteración en el sistema eléctrico del corazón), por lo que se le implantó un marcapasos. Durante años, su condición se mantuvo estable hasta que en 2012, en Guayaquil, Ecuador, presentó una infección relacionada con el marcapasos que requirió la extracción del generador y el implante de uno nuevo en el lado opuesto, sin complicaciones posteriores ni nuevos episodios de síncope durante una década.\n\nSeis meses antes del ingreso actual, el paciente comenzó a mostrar un deterioro en su capacidad funcional (clasificación NYHA III, que indica limitación marcada en la actividad física), aunque sin otros síntomas adicionales. Se suspendió el tratamiento con betabloqueadores debido a mala tolerancia. En el examen físico se detectó un soplo cardíaco leve, sin signos de insuficiencia cardíaca. Los análisis de laboratorio fueron normales. El marcapasos mostró agotamiento de la batería, y el ecocardiograma reveló una hipertrofia severa y concéntrica del septum interventricular (pared que separa las cámaras del corazón), con un grosor de 26 mm y un gradiente de presión muy alto (117 mmHg) dentro del ventrículo, además de un movimiento anormal del velo mitral que causaba una regurgitación leve (retorno de sangre hacia la aurícula).\n\n**Hallazgos Clave**  \n- Hipertrofia severa del septum interventricular medio ventricular con obstrucción significativa al flujo sanguíneo dentro del ventrículo izquierdo.  \n- Movimiento sistólico anterior del velo mitral (SAM), que contribuye a la obstrucción y regurgitación mitral leve.  \n- Antecedentes familiares de muerte súbita y un riesgo calculado de muerte súbita del 16,8%, lo que indica un riesgo elevado.  \n- Imposibilidad de realizar resonancia magnética cardíaca debido a la incompatibilidad con el marcapasos y la presencia de electrodos abandonados.  \n- Confirmación genética de una variante probablemente patogénica en el gen FLNC (filamina C), asociada a miocardiopatía hipertrófica familiar tipo 26, que se hereda de forma autosómica dominante.\n\n**Interpretación Clínica**  \nEl paciente presenta una forma de miocardiopatía hipertrófica con predominio medio apical, caracterizada por un engrosamiento anormal del músculo cardíaco que obstruye el flujo de salida del ventrículo izquierdo y genera síntomas significativos. La variante genética encontrada en filamina C explica la naturaleza hereditaria y progresiva de su enfermedad. La persistencia de síntomas y la obstrucción significativa a pesar del tratamiento médico justificaron la realización de una miectomía medio ventricular (cirugía para remover parte del músculo engrosado), realizada mediante un abordaje transapical (a través del ápex del corazón). La cirugía fue exitosa, con reducción del gradiente de presión y desaparición del movimiento anormal del velo mitral.\n\nPosteriormente, el paciente presentó episodios de taquicardia ventricular (arritmias peligrosas) que requirieron la implantación de un cardiodesfibrilador implantable (CDI) compatible con resonancia magnética, para prevenir muerte súbita. Tras el implante, no se registraron nuevos episodios arrítmicos y el paciente evolucionó favorablemente.\n\n**Próximos Pasos**  \nActualmente, el paciente se encuentra en clase funcional I (sin limitaciones en la actividad física), sin arritmias detectadas en monitoreo continuo, y en tratamiento con bisoprolol (un betabloqueador) a dosis de 5 mg. Se ha iniciado un estudio genético ampliado en familiares directos para identificar portadores de la variante genética, aunque el acceso limitado a servicios de salud ha dificultado la realización completa de este estudio. El seguimiento continuo y la evaluación genética son fundamentales para el manejo integral del paciente y su familia, con el fin de prevenir complicaciones graves como la muerte súbita."
+        }
+    },
+    {
+        "article": "Varón de 32 años, con antecedentes de infección por VIH en terapia anti-retroviral (carga viral indetectable y recuento de CD4 de 454 céls/mm3) y consumo de tabaco y drogas (marihuana, éxtasis y ketamina). Consultó en nuestra unidad de salud sexual por una historia de dos semanas de secreción uretral de aspecto mucoso con escaso ardor local, asociado a una úlcera eritematosa indurada en el surco balanoprepucial de 1,5 cm de diámetro, dolorosa y exudativa. Al examen físico presentaba una adenopatía inguinal izquierda de 2 cm, sensible a palpación, blanda, no adherida a planos profundos ni asociada a signos inflamatorios cutáneos. No presentaba fiebre ni otros síntomas asociados. En la anamnesis dirigida, refirió 20 parejas sexuales hombres en el último año, con relaciones sexuales orales y anales insertivas y receptivas, con uso ocasional de preservativo. No tenía antecedente de viajes fuera de Chile. Cuatro semanas antes del inicio de los síntomas, había tenido un contacto sexual de riesgo sin preservativo con una pareja contactada mediante una aplicación de telefonía móvil. Con el diagnóstico presuntivo de una sífilis primaria y uretritis en estudio, se tomaron muestras de sangre y secreción uretral para estudio microbiológico. Por la conducta sexual de alto riesgo, se tomó también un hisopado anorrectal para tinción de Gram y cultivo. De acuerdo con la norma vigente en Chile, se administraron tres dosis de 2,4 millones de UI de penicilina benzatina intramuscular separadas por una semana, además de 250 mg de ceftriaxona intramuscular y 1 g de azitromicina oral, ambas por una vez. El estudio de laboratorio confirmó el diagnóstico de sífilis, con un VDRL (Venereal disease research laboratory) reactivo con dilución de 1:2 y MHA-TP (Microhemagglutination assay for antibody to Treponema pallidum) reactivo. La tinción de Gram y los cultivos de secreción uretral (agar sangre y Thayer Martin) fueron negativos. La muestra anorrectal mostró escasos diplococos gramnegativos en la tinción de Gram, con desarrollo abundante de N. meningitidis y microbiota comensal en el cultivo corriente. La identificación bacteriana se realizó a través de espectrometría de masas MALDI-TOF MS. El paciente evolucionó favorablemente, sin secreción uretral y con regresión de la lesión ulcerada genital y la adenopatía inguinal a las dos semanas de seguimiento. Las tinciones de Gram y los cultivos de control de secreción uretral, faríngea y anorrectal resultaron negativos. Se citó al contacto sexual reciente para estudio y tratamiento. Sin embargo, éste se encontraba asintomático y los cultivos faríngeo, anorrectal y uretral realizados fueron negativos.",
+        "gold_summary": "Presentamos el caso de un HSH con infección por VIH, que consultó por un cuadro de uretritis y sifilis primaria, en el cual se aisló N. meningitidis en una muestra anorectal. Fue tratado en forma empírica con ceftriaxona y azitromicina, realizándose un cultivo de control post-tratamiento que fue negativo.",
+        "synthetic_summary": {
+            "B1": "Un hombre con VIH tenía una herida y dolor al orinar. Los doctores encontraron una bacteria en su cuerpo. Le dieron medicinas para curarlo. Después, la bacteria ya no estaba. Él mejoró mucho.",
+            "B2": "Caso de un hombre de 32 años con VIH que tuvo una infección en la uretra y una úlcera en el pene. Los médicos encontraron que tenía sífilis primaria, que es una infección de transmisión sexual. Además, en una muestra tomada del ano, detectaron una bacteria llamada Neisseria meningitidis, que normalmente no causa infecciones en esa zona. \n\nEl paciente recibió tratamiento con antibióticos llamados ceftriaxona y azitromicina para combatir las infecciones. Después del tratamiento, se hicieron pruebas de control y no encontraron más bacterias en las muestras tomadas de la uretra, la garganta y el ano. El paciente mejoró bien y la lesión en el pene y la inflamación en la ingle desaparecieron en dos semanas. \n\nEste caso muestra la importancia de revisar diferentes áreas del cuerpo en personas con conductas sexuales de riesgo y de usar tratamientos adecuados para varias posibles infecciones.",
+            "B3": "**Contexto**  \nSe trata de un hombre de 32 años que vive con infección por VIH controlada mediante tratamiento antirretroviral, con carga viral indetectable y un recuento adecuado de células CD4. Además, tiene antecedentes de consumo de tabaco y drogas recreativas. Consultó en una unidad de salud sexual debido a una secreción mucosa por la uretra y una úlcera dolorosa en el pene, acompañadas de inflamación en los ganglios linfáticos inguinales del lado izquierdo. No presentaba fiebre ni otros síntomas sistémicos. En la entrevista, refirió múltiples parejas sexuales masculinas en el último año, con prácticas sexuales orales y anales, y uso irregular de preservativos. Cuatro semanas antes, tuvo una relación sexual sin protección con una persona conocida a través de una aplicación móvil.\n\n**Hallazgos Clave**  \nSe sospechó inicialmente una sífilis primaria y una uretritis de origen incierto. Se tomaron muestras de sangre y secreción uretral para análisis microbiológicos, así como un hisopado anorrectal debido al alto riesgo sexual. El diagnóstico serológico confirmó sífilis, con pruebas VDRL y MHA-TP positivas. Los cultivos de secreción uretral fueron negativos para bacterias comunes causantes de uretritis. Sin embargo, en la muestra anorrectal se identificó la presencia de Neisseria meningitidis (una bacteria que normalmente habita en la garganta y que en este caso se encontró en el recto), confirmada mediante espectrometría de masas MALDI-TOF MS.  \n\n**Interpretación Clínica**  \nEl paciente fue tratado empíricamente con penicilina benzatina para la sífilis, además de una dosis única de ceftriaxona y azitromicina para cubrir posibles infecciones bacterianas de transmisión sexual. La detección de N. meningitidis en la muestra anorrectal es relevante, ya que esta bacteria no es un patógeno típico en uretritis, pero puede colonizar el tracto genital o anal, especialmente en personas con conductas sexuales de riesgo. El tratamiento fue efectivo, ya que a las dos semanas el paciente mostró resolución de la secreción uretral, cicatrización de la úlcera y desaparición de la inflamación ganglionar. Los cultivos posteriores fueron negativos, confirmando la erradicación de las infecciones.  \n\n**Próximos Pasos**  \nSe realizó el estudio y tratamiento del contacto sexual reciente para prevenir la transmisión y reinfección, aunque este contacto no presentó síntomas ni cultivos positivos. Este caso subraya la importancia de considerar agentes menos comunes como N. meningitidis en infecciones del tracto genital y anorrectal en personas con alto riesgo sexual, y la necesidad de un abordaje diagnóstico y terapéutico integral en estos pacientes."
+        }
+    },
+    {
+        "article": "Un paciente hispanoparlante de 63 años de edad se presentó en el hospital como una emergencia con inicio repentino de dificultad respiratoria severa, palpitaciones y sudoración profusa. Estaba en su estado habitual de salud y podía deambular con actividades independientes de la vida diaria hasta 30 minutos antes de su llegada a la sala de urgencias. Tenía un historial de 20 años de hipertensión, un historial de 15 años de diabetes mellitus, enfermedad de la arteria coronaria que requería la inserción de un stent de la arteria coronaria cinco años antes, un historial de diez años de insuficiencia cardiaca de la clase II de la New York Heart Association (NYHA) con una fracción de eyección reducida (EF) del 35 %, enfermedad renal crónica (CKD) en estadio 3B. Al ingresar en el hospital, sus medicamentos incluían carvedilol (25 mg dos veces al día), lisinopril (20 mg diario), espironolactona (25 mg diario), furosemida (20 mg diario), insulina glargina (20 unidades al acostarse), inyección de insulina lispro (7 unidades tres veces al día), atorvastatina (40 mg diario), y aspirina (81 mg diario), sin alergias a medicamentos conocidas.\n\nAl examen, su presión arterial era de 205/110 mmHg, su frecuencia respiratoria de 29 respiraciones/min, su frecuencia cardíaca de 118 latidos/min, la oximetría de pulso era de 82% (en aire ambiente) y su temperatura de 36.2°C. Su peso era de 72 kg y su estatura de 68 pulgadas, lo que resultó en un índice de masa corporal (IMC) de 24.13 kg/m2. Al examen físico, el paciente estaba en grave dificultad respiratoria, sudaba y no podía hablar con claridad. Su presión venosa yugular era elevada, como se muestra por la distensión de la vena yugular (3+). Al auscultar el tórax, se observaron crepitaciones bilaterales en todos los campos pulmonares. La auscultación cardíaca fue notable por un galope con una frecuencia regular y un murmullo sistólico 3/6 que se oía en la línea medioclavicular izquierda, al nivel del quinto espacio intercostal. El punto de impulso cardíaco máximo se desplazó hacia la izquierda (en la línea medioaxilar anterior) y no se observó distensión abdominal ni ascitis, con edema de los miembros inferiores (1+) hasta el nivel de la mitad de la pantorrilla.\n\nEl paciente fue trasladado a la zona de reanimación cardiopulmonar (RCP), donde se midieron los gases sanguíneos en el aire y se solicitaron pruebas de laboratorio. El paciente fue tratado con oxígeno al 100% utilizando una máscara no reanadora y se le colocó en posición de 90°, lo que produjo una mejora en la oximetría de pulso, que aumentó hasta el 90%. Un electrocardiograma (ECG) mostró taquicardia sinusal, depresión del ST del conductor lateral (de 1 mV), desviación del eje izquierdo e hipertrofia del ventrículo izquierdo. Se obtuvo una radiografía de tórax portátil que fue notable por una silueta cardiaca agrandada, señal de asta de ciervo de desviación venosa pulmonar del lóbulo superior (cefalización), y líneas B de Kerley, que indican edema intersticial.\n\nAunque se solicitaron pruebas de laboratorio, debido a que el paciente estaba gravemente enfermo y no se podía demorar el tratamiento, se inició un tratamiento inicial basado en los hallazgos clínicos, el historial clínico, el ECG, los gases arteriales en sangre y los hallazgos de rayos X. En vista de los hallazgos de las investigaciones iniciales y la ausencia de fiebre, se descartó la neumonía y se realizó un diagnóstico de edema pulmonar cardiogénico hipertensivo. Se inició un tratamiento intravenoso (IV) con nitroglicerina, comenzando a 30 mcg/min y aumentando en 15 mcg/min cada 3 minutos, con oximetría de pulso continua y monitoreo de los signos vitales cada 3 minutos. Después de 18 minutos, se tituló la nitroglicerina hasta 120 mcg/min y su presión arterial disminuyó a 148/82 mmHg, su presión arterial sistólica se redujo en un 29%, su presión arterial diastólica se redujo en un 25%, y su frecuencia cardíaca disminuyó a 87 latidos por minuto. Se hizo una rápida mejora clínica y el paciente pudo comunicarse con oraciones completas y pudo respirar sin el uso de músculos accesorios. La oximetría de pulso mostró una saturación de oxígeno >97%, y la suplementación de oxígeno continuó con el uso de una cánula nasal a 3 L/min y la medición de la oximetría de pulso del paciente fue >96%.\n\nDespués de 25 minutos, el paciente fue tratado con enalapril (2,5 mg IV) combinado con furosemida (20 mg IV). La nitroglicerina se redujo a una tasa de 10 mcg/min cada 5 minutos hasta que se interrumpió, seguido de una dosis oral de isosorbida dinitrato (30 mg). Después de la estabilización clínica completa, los resultados de los laboratorios mostraron un recuento de glóbulos blancos (WBC) de 11,43 × 109/uL, hemoglobina de 10,9 g/dl, hematocrito de 31,8%, plaquetas de 74 × 109/L, sodio de 144 mmol/L, potasio de 3,9 mmol/L, cloruro de 107 mmol/L, dióxido de carbono (CO2) de 25 mmol/L, nitrógeno ureico en sangre (BUN) de 27 mg/dL, creatinina de 1,4 mg/dL, péptido natriurético cerebral (BNP) de 3,452 pg/ml, y troponina I <0,05 ng/ml. Las mediciones de gases en sangre en aire incluyeron pH de 7,381, pCO2 de 44,8 mmHg, pO2 de 57 mmHg, HCO3 de 25,8 mmol/L, y saturación de oxígeno de 84%.\n\nSe evaluó al paciente para detectar la presencia de una posible embolia pulmonar (EP) subyacente, utilizando los criterios de estratificación de riesgo de EP de Wells, y se lo estratificó como de bajo riesgo, con una evaluación posterior con un nivel de dímero D de 340 ng/ml, que se interpretó como negativo. La evaluación para detectar hipertiroidismo mostró un valor normal de la medición ultrasensible del ensayo de la hormona estimulante de la tiroides en plasma (usTSH) de 2,56 μU/mL y tiroxina libre (T4) de 6,87 μU/mL.\n\nEl paciente fue admitido en la sala de hospital de medicina interna con un diagnóstico de edema pulmonar cardiogénico hipertensivo y fue dado de alta 48 horas después. Al momento del alta hospitalaria, su medicación incluía furosemida (40 mg diarios), carvedilol (12.5 mg dos veces al día), sacubitril/valsartan (24 mg/26 mg dos veces al día), espironolactona (25 mg diarios) e isosorbida mononitrato (60 mg diarios). El paciente fue sometido a seguimiento semanal por su cardiólogo, quien optimizó la terapia medicinal. No se registraron visitas a urgencias ni hospitalizaciones, al menos durante los siguientes 60 días.\n\nMH - Insuficiencia cardiaca/*complicaciones\nMH - Humanos\nMH - Hipertensión/*complicaciones\nMH - Infusiones, intravenosas\nMH - Hombre\nMH - Edad Media\nMH - Nitroglicerina/*administración y dosificación\nMH - Edema pulmonar/*terapia farmacológica/etiología\nMH - Insuficiencia respiratoria/*terapia farmacológica/etiología\nMH - Agentes vasodilatadores/*administración y dosificación\n",
+        "gold_summary": "Paciente: Hombre, 63 años\n\nDiagnóstico final: Edema pulmonar cardiovenoso hipertensivo\n\nSíntomas: falta de aire\n\nMedicación: —\n\nProcedimiento clínico: —\n\nEspecialidad: Medicina general e interna\n\nUn hombre hispano de 63 años con antecedentes de hipertensión, enfermedad de las arterias coronarias, insuficiencia cardiaca con una fracción de eyección reducida del 35 %, enfermedad renal crónica (ERC) y diabetes mellitus, se presentó como una emergencia con disnea aguda y grave. El paciente fue tratado inicialmente con 100 % de oxígeno suplementario y nitroglicerina intravenosa (IV) en dosis altas (30 mcg/min), que se ajustó cada 3 minutos, aumentando en 15 mcg/min hasta que se alcanzó una dosis de 120 mcg/min. Después de 18 minutos de terapia agresiva, la condición del paciente mejoró y ya no necesitaba ventilación mecánica.\n",
+        "synthetic_summary": {
+            "B1": "Había un hombre de 63 años que se sentía muy mal. Le costaba mucho respirar y estaba muy cansado. Tenía problemas en el corazón y en los riñones desde hace tiempo.\n\nCuando llegó al hospital, le dieron aire con una máscara para ayudarlo a respirar mejor. También le pusieron un medicamento por la vena para que su corazón y su cuerpo se sintieran mejor.\n\nDespués de un rato, el hombre empezó a respirar mejor y se sintió más tranquilo. Los doctores cuidaron mucho de él y lo ayudaron a mejorar.",
+            "B2": "**Caso de un Hombre de 63 Años con Problemas del Corazón y Dificultad para Respirar**\n\n**Lo que Pasó:**  \nUn hombre de 63 años, que hablaba español y tenía varias enfermedades como presión alta (hipertensión), diabetes, problemas en las arterias del corazón y una enfermedad llamada insuficiencia cardíaca (que significa que su corazón no bombeaba bien la sangre), llegó al hospital muy enfermo. De repente, empezó a tener mucha dificultad para respirar, su corazón latía rápido y sudaba mucho. Antes de esto, estaba bien y podía hacer sus actividades normales.\n\n**Lo que Encontraron:**  \nAl examinarlo, su presión arterial estaba muy alta y tenía signos claros de que su corazón estaba trabajando mal. También tenía líquido en los pulmones, lo que se llama edema pulmonar, y eso dificultaba que el oxígeno llegara a su cuerpo. Las pruebas mostraron que su corazón estaba agrandado y que había problemas en la circulación de la sangre en sus pulmones.\n\n**Qué Hicieron para Ayudarlo:**  \nLe dieron oxígeno puro para que pudiera respirar mejor y empezaron a darle un medicamento llamado nitroglicerina por vía intravenosa (directamente en la vena). La nitroglicerina ayuda a bajar la presión arterial y a que el corazón trabaje menos. Comenzaron con una dosis baja y la aumentaron poco a poco cada pocos minutos. Después de 18 minutos, el paciente mejoró mucho: su presión bajó, su corazón latía más despacio y pudo respirar sin tanta dificultad. Ya no necesitó una máquina para ayudarlo a respirar.\n\n**Después del Tratamiento:**  \nLuego le dieron otros medicamentos para el corazón y para eliminar el exceso de líquido. El paciente se quedó en el hospital dos días y después pudo irse a casa. Continuó con controles médicos semanales y no volvió a tener problemas graves en los siguientes dos meses.\n\n**Resumen:**  \nEste caso muestra cómo un hombre con varias enfermedades del corazón y otros problemas puede sufrir una emergencia grave llamada edema pulmonar, que es cuando se acumula líquido en los pulmones por problemas del corazón. Con un tratamiento rápido y adecuado, que incluye oxígeno y medicamentos para bajar la presión y ayudar al corazón, el paciente pudo recuperarse sin complicaciones mayores.",
+            "B3": "**Contexto**  \nUn hombre hispanoparlante de 63 años con antecedentes médicos complejos, incluyendo hipertensión arterial de larga evolución, diabetes mellitus, enfermedad coronaria con colocación previa de stent, insuficiencia cardíaca crónica con función del corazón reducida (fracción de eyección del 35 %) y enfermedad renal crónica en estadio avanzado, acudió al hospital en estado de emergencia debido a un inicio súbito de dificultad respiratoria severa, palpitaciones y sudoración intensa. Hasta poco antes de su ingreso, el paciente se encontraba en su estado habitual de salud y realizaba actividades cotidianas de forma independiente.\n\n**Hallazgos Clave**  \nAl examen físico, el paciente presentaba signos evidentes de insuficiencia cardíaca descompensada: presión arterial muy elevada (205/110 mmHg), frecuencia cardíaca rápida (118 latidos por minuto), dificultad respiratoria grave con saturación de oxígeno baja (82 % en aire ambiente), distensión venosa yugular marcada, crepitaciones pulmonares bilaterales, y un galope cardíaco junto con un soplo sistólico. La radiografía de tórax mostró cardiomegalia (aumento del tamaño del corazón), signos de congestión pulmonar y edema intersticial, confirmando la sospecha clínica de edema pulmonar cardiogénico hipertensivo. El electrocardiograma evidenció taquicardia sinusal, hipertrofia ventricular izquierda y cambios isquémicos.\n\nLos análisis de laboratorio posteriores revelaron un péptido natriurético cerebral (BNP) muy elevado (3,452 pg/ml), indicador de insuficiencia cardíaca descompensada, y una troponina normal, descartando daño cardíaco agudo. Se descartaron otras causas de dificultad respiratoria aguda, como embolia pulmonar e infecciones pulmonares, mediante pruebas específicas y criterios clínicos.\n\n**Interpretación Clínica**  \nEl cuadro clínico y los estudios complementarios fueron consistentes con un episodio agudo de edema pulmonar cardiogénico hipertensivo, una condición en la que la presión arterial muy alta y la insuficiencia cardíaca provocan acumulación rápida de líquido en los pulmones, dificultando la respiración. La rápida identificación y tratamiento de esta emergencia fueron cruciales para evitar complicaciones mayores.\n\n**Tratamiento y Evolución**  \nEl manejo inicial incluyó la administración de oxígeno al 100 % mediante máscara no reanimadora y la colocación del paciente en posición sentada para facilitar la respiración. Se inició tratamiento intravenoso con nitroglicerina, un vasodilatador que reduce la presión arterial y la carga sobre el corazón, comenzando con una dosis de 30 microgramos por minuto y aumentando progresivamente hasta 120 microgramos por minuto en 18 minutos. Esta terapia permitió una reducción significativa de la presión arterial y de la frecuencia cardíaca, con una mejora clínica rápida: el paciente pudo respirar sin dificultad y comunicarse con normalidad, y su saturación de oxígeno superó el 97 % con oxígeno suplementario.\n\nPosteriormente, se administraron enalapril (un inhibidor de la enzima convertidora de angiotensina) y furosemida (un diurético) por vía intravenosa para continuar el control de la presión arterial y eliminar el exceso de líquido. La nitroglicerina se fue disminuyendo hasta suspenderla, y se inició tratamiento oral con isosorbida dinitrato para mantener la vasodilatación.\n\nEl paciente fue hospitalizado en la unidad de medicina interna, donde se ajustó su tratamiento con medicamentos para insuficiencia cardíaca, incluyendo furosemida, carvedilol (un betabloqueador), sacubitril/valsartán (un inhibidor de la neprilisina combinado con un bloqueador del receptor de angiotensina), espironolactona (un antagonista de la aldosterona) e isosorbida mononitrato. Tras 48 horas de hospitalización, se dio de alta en condiciones estables y con seguimiento cardiológico programado.\n\n**Próximos Pasos y Seguimiento**  \nDurante al menos 60 días posteriores al alta, el paciente no requirió nuevas hospitalizaciones ni visitas a urgencias, lo que indica una adecuada respuesta al tratamiento y control de su enfermedad cardíaca. El seguimiento semanal con su cardiólogo permitió optimizar la terapia médica para prevenir futuras descompensaciones.\n\n---\n\nEste caso ilustra la importancia de un diagnóstico rápido y un manejo agresivo en pacientes con edema pulmonar cardiogénico hipertensivo, especialmente en aquellos con múltiples comorbilidades cardiovasculares y renales, para mejorar la supervivencia y la calidad de vida."
+        }
+    },
+    {
+        "article": "Historial clínico\nUn niño de 12 años se presentó en nuestro hospital con un mes de historia de sensación de cuerpo extraño y una masa conjuntival pedunculada carnosa que creció con el tiempo. No había historia de trauma o lesiones similares en el otro lado del cuerpo. Se descubrió una masa pedunculada carnosa rosácea de 15 mm de la conjuntiva palpebral derecha durante un examen oftalmológico. La agudeza visual estaba dentro de los límites normales. Se diagnosticó al niño como papiloma de células escamosas pedunculadas y se le realizó una biopsia excisional de la lesión.\n\nHallazgos macroscópicos y microscópicos\nRecibimos un fragmento de tejido blanco grisáceo, pequeño, firme, ovoide, fijado en formalina, de 1,5 x 1 cm, para su análisis patológico. En las secciones microscópicas se encontró una lesión poliopóidea hiperplásica con múltiples quistes globulares en la submucosa conjuntival, junto con una importante infiltración inflamatoria constituida por linfocitos, células plasmáticas y neutrófilos, así como enormes esporangios de paredes gruesas con numerosas endosporas. Las endosporas se liberaron después de que algunos de los esporangios maduros se rompieran. La rinosporidiosis conjuntival se diagnosticó histopatológicamente. No hubo recurrencia ni signo de rinosporidiosis en el ojo ni en ninguna otra área del cuerpo en el último examen del paciente, que fue 7 meses después de la escisión quirúrgica.\n",
+        "gold_summary": "Un niño de 12 años con una masa conjuntival pedunculada carnosa fue llevado al Centro Médico de la Universidad de Jimma con un historial de un mes de sensación de cuerpo extraño. Al paciente se le diagnosticó un papiloma pedunculado de células escamosas y se le realizó una biopsia excisional de la lesión. Se encontró que la masa era una lesión polipoide hiperplásica con numerosos quistes globulares dentro de la submucosa conjuntival, rodeados por un infiltrado inflamatorio pesado de linfocitos, células plasmáticas y neutrófilos, así como grandes esporas de paredes gruesas con numerosas endosporas en secciones microscópicas. Se diagnosticó histopatológicamente rinosporidiosis conjuntival.\n",
+        "synthetic_summary": {
+            "B1": "Un niño tenía una bolita en el ojo que le molestaba. Los doctores le quitaron la bolita para verla mejor. \n\nAl mirar la bolita con un microscopio, vieron que tenía muchas cositas pequeñas dentro. Estas cositas eran como unas semillas que no son buenas. \n\nLos doctores dijeron que el niño tenía una infección en el ojo llamada rinosporidiosis. Después de quitar la bolita, el niño estuvo bien y no volvió a tener problema.",
+            "B2": "**Lo que pasó con el niño**  \nUn niño de 12 años tenía una sensación rara en el ojo y una masa blanda y rosada que crecía en la parte interna del párpado derecho. No había sufrido golpes ni tenía problemas similares en el otro ojo. Cuando lo revisaron, su vista estaba normal, pero encontraron esta masa que parecía un papiloma, que es un tipo de bulto benigno hecho de células de la piel.\n\n**Qué hicieron los médicos**  \nLe quitaron la masa para analizarla mejor. Esto se llama biopsia, que es cuando se saca un pedacito de tejido para estudiar qué es exactamente. En el laboratorio, vieron que la masa tenía muchas células inflamatorias, que son células que el cuerpo usa para defenderse cuando hay una infección o irritación. También encontraron estructuras llamadas esporangios, que son como pequeñas bolsas con esporas dentro. Las esporas son formas de reproducción de ciertos microorganismos.\n\n**Qué significa el diagnóstico**  \nEl análisis mostró que el niño tenía rinosporidiosis conjuntival, que es una infección causada por un microorganismo que forma esas esporas. Esta infección afecta la conjuntiva, que es la membrana que cubre el ojo y el interior del párpado. Después de quitar la masa, el niño no tuvo problemas ni volvió a tener la infección en el ojo ni en otras partes del cuerpo durante al menos siete meses.\n\n**En resumen**  \nEl niño tenía una infección poco común en el ojo que causó una masa. Gracias a la biopsia, los médicos pudieron identificar la infección y tratarla con cirugía, evitando que regresara.",
+            "B3": "**Contexto**  \nUn niño de 12 años acudió al hospital tras presentar durante un mes una sensación persistente de cuerpo extraño en el ojo derecho, acompañada de una masa carnosa y pedunculada (con un tallo que la une a la superficie) en la conjuntiva palpebral (la membrana que recubre el párpado). No había antecedentes de trauma ni lesiones similares en el otro ojo. La agudeza visual del niño era normal. Inicialmente, se sospechó que la lesión correspondía a un papiloma de células escamosas pedunculado, por lo que se decidió realizar una biopsia excisional para su análisis.\n\n**Hallazgos Clave**  \nEl tejido extraído, de aproximadamente 1,5 x 1 cm, fue examinado bajo el microscopio. Se observó una lesión polipoide hiperplásica (un crecimiento en forma de pólipo con aumento en el número de células) que contenía múltiples quistes globulares en la submucosa conjuntival (la capa debajo de la superficie de la conjuntiva). Además, había una intensa infiltración inflamatoria compuesta por linfocitos, células plasmáticas y neutrófilos, que son tipos de células del sistema inmunitario. De manera destacada, se identificaron grandes esporangios (estructuras que contienen esporas) con paredes gruesas, dentro de los cuales se encontraban numerosas endosporas (esporas internas). Algunas de estas esporas se liberaban tras la ruptura de los esporangios maduros.\n\n**Interpretación Clínica**  \nEl examen histopatológico confirmó que la masa no era un papiloma, sino que correspondía a una infección por rinosporidiosis conjuntival, una enfermedad causada por el microorganismo Rhinosporidium seeberi que afecta principalmente las mucosas y puede formar masas polipoides. Esta infección es poco común y se caracteriza por la presencia de esporangios con endosporas en el tejido afectado.\n\n**Próximos Pasos y Seguimiento**  \nTras la escisión quirúrgica completa de la lesión, el paciente fue monitoreado durante al menos siete meses, sin presentar recurrencia de la lesión ni signos de infección en el ojo ni en otras partes del cuerpo. Este seguimiento indica un buen pronóstico tras el tratamiento quirúrgico. Se recomienda continuar con controles periódicos para detectar cualquier posible reaparición."
+        }
+    },
+    {
+        "article": "Presentamos el caso clínico de un varón de quince años, sin antecedentes médicos ni intervenciones previas, que acude al servicio de urgencias de pediatría con clínica de vómitos y dolor abdominal epigástrico de cuatro días de evolución, manteniéndose afebril durante la evolución del cuadro.\n\nInicialmente fue manejado como gastroenteritis, pero ante la ausencia de mejoría, con persistencia del dolor abdominal de tipo cólico a nivel epigástrico y de los vómitos de aspecto bilioso, acude a urgencias para nueva valoración.\n\nA la exploración física el paciente presentaba aceptable estado general, se encontraba afebril, con signos leves de deshidratación. El abdomen se encontraba distendido, sin datos de peritonismo y con ruidos hidroaéreos disminuidos. La analítica no presentaba hallazgos significativos, realizándose una radiografía de abdomen con hallazgos sugestivos de obstrucción intestinal.\n\nDada la evolución se decide realizar una tomografía computarizada urgente, en la que se observó presencia de ascitis e importante dilatación de asas de intestino delgado, sugiriendo la interposición de un asa de intestino delgado en el inicio de la transcavidad de los epiplones, con cambio de calibre a nivel del hiato de Winslow.\n\nSe realizó intervención quirúrgica urgente, realizando inicialmente una laparoscopia exploradora. Se observaban asas de intestino delgado dilatadas, e íleon terminal, ciego y colon ascendente de calibre normal pero localizados en hipocondrio derecho, con el ciego muy móvil y sin presentar adherencias al espacio parietocólico derecho. Siguiendo proximalmente el íleon terminal, se observaron asas de intestino delgado de distinto calibre desde la profundidad de la teórica localización del hiato de Winslow. Se consiguió traccionar de ciego e íleon terminal hasta desplazarlos a fosa iliaca derecha, pero sin llegar a identificar correctamente el punto de cambio de calibre, ya que la interposición del borde inferior del hígado y la distensión de asas de intestino delgado dificultaban la técnica. Se intentó mejorar la visualización mediante punción percutánea de un asa dilatada para vaciar el gas, sin mejoría. Para asegurar la resolución del cuadro obstructivo se decidió realizar una laparotomía media supraumbilical. Al acceder a cavidad se evidenciaba el cambio de calibre en íleon, a unos 40 centímetros de la válvula ileocecal, con signos compatibles con herniación de un tramo de unos cinco centímetros de íleon a través de hiato de Winslow. En ambos extremos del asa herniada observamos la impronta congestiva del hiato sobre el asa (Fig. 3). Se identificó el hiato de Winslow, de calibre normal, por lo que no se realizó ninguna técnica preventiva para disminuir el riesgo de recidiva.\n\nDurante los primeros días del postoperatorio el paciente presentó un íleo paralítico, pudiendo retirar la sonda nasogástrica a los cinco días de la cirugía e iniciando tolerancia oral con buena respuesta. Simultáneamente desarrolló una colección pélvica que se manejó de forma conservadora con antibióticos, con buena evolución. Finalmente, el paciente fue dado de alta a los diez días de la intervención, con tránsito conservado, manteniéndose afebril y con buen estado general.\n\nActualmente el paciente está en seguimiento en consultas externas de cirugía pediátrica.",
+        "gold_summary": "Presentamos el caso clínico de un varón adolescente de 15 años sin antecedentes quirúrgicos previos, con clínica de dolor abdominal y vómitos, en el que la tomografía computarizada sugería un cuadro de obstrucción intestinal a causa de hernia interna a nivel del hiato de Winslow. Precisó de intervención quirúrgica mediante laparoscopia exploradora, reconvertida por mala visualización a laparotomía media supraumbilical, para reducción del asa de íleon herniada. Esta presentaba buen aspecto y no fue necesaria la resección intestinal. No se realizó ninguna técnica preventiva para disminuir el riesgo de recidiva. Postoperatoriamente, el paciente presentó una colección pélvica manejada de manera conservadora con antibióticos. Actualmente se encuentra en seguimiento en consultas externas de cirugía pediátrica.",
+        "synthetic_summary": {
+            "B1": "Un niño de 15 años tenía dolor en la barriga y vomitaba. Los doctores vieron que su intestino estaba tapado por un lugar raro. Hicieron una operación para ayudarlo. Sacaron el intestino que estaba atrapado y estaba bien. No cortaron nada. Después, el niño tuvo un poco de líquido en la barriga, pero con medicinas mejoró. Ahora está bien y los doctores lo revisan para que siga sano.",
+            "B2": "**Caso Clínico de un Adolescente con Dolor Abdominal y Vómitos**\n\nUn chico de 15 años, sin problemas médicos anteriores, llegó al hospital con dolor en la parte superior del abdomen y vómitos que duraban cuatro días. Al principio, pensaron que tenía gastroenteritis, una infección del estómago, pero como no mejoraba, le hicieron más pruebas.\n\n**Lo que Encontraron**\n\nUna radiografía y una tomografía computarizada (una imagen detallada del cuerpo) mostraron que tenía una obstrucción en el intestino delgado. Esto ocurrió porque una parte del intestino se había metido por un espacio llamado hiato de Winslow, causando una hernia interna. Una hernia interna es cuando un órgano se mueve a un lugar donde no debería estar dentro del cuerpo.\n\n**Qué Hicieron**\n\nEl equipo médico decidió operar para arreglar la obstrucción. Comenzaron con una cirugía por laparoscopia, que es una operación con pequeñas incisiones y una cámara, pero tuvieron que cambiar a una cirugía abierta para ver mejor. Encontraron el intestino atrapado, pero estaba sano, así que no fue necesario cortar ninguna parte. No hicieron ninguna técnica para evitar que la hernia volviera a aparecer porque el espacio por donde se metió el intestino tenía un tamaño normal.\n\n**Después de la Cirugía**\n\nDespués de la operación, el chico tuvo un problema llamado íleo paralítico, que significa que el intestino tardó en empezar a funcionar normalmente. También desarrolló una acumulación de líquido en la pelvis, llamada colección pélvica, que trataron con antibióticos sin necesidad de otra cirugía. Finalmente, el paciente mejoró y fue dado de alta después de diez días.\n\n**Situación Actual**\n\nAhora, el adolescente sigue en control con el equipo de cirugía pediátrica para asegurarse de que se recupere bien y no tenga problemas futuros.",
+            "B3": "**Contexto**  \nSe describe el caso de un adolescente de 15 años, sin antecedentes médicos ni quirúrgicos previos, que presentó durante cuatro días dolor abdominal en la parte superior del abdomen (epigastrio) acompañado de vómitos biliosos (con contenido similar a bilis), sin fiebre. Inicialmente fue tratado como una gastroenteritis, pero al no mejorar y mantener los síntomas, acudió nuevamente a urgencias.\n\n**Hallazgos Clave**  \nEn la evaluación física, el paciente estaba en buen estado general, afebril, con signos leves de deshidratación y abdomen distendido, pero sin signos de inflamación grave (peritonismo). Los ruidos intestinales estaban disminuidos. Los análisis de sangre no mostraron alteraciones significativas. Una radiografía abdominal sugirió la presencia de una obstrucción intestinal. Posteriormente, una tomografía computarizada (TC) reveló ascitis (líquido en la cavidad abdominal) y dilatación importante de las asas del intestino delgado, con una posible herniación interna a través del hiato de Winslow, un orificio natural en la cavidad abdominal.\n\n**Interpretación Clínica**  \nEl diagnóstico fue una hernia interna del intestino delgado a través del hiato de Winslow, una causa poco frecuente de obstrucción intestinal. Debido a la gravedad y persistencia de los síntomas, se decidió realizar una cirugía urgente. Inicialmente se intentó una laparoscopia exploradora (cirugía mínimamente invasiva), pero la visualización limitada y la distensión intestinal dificultaron la intervención, por lo que se convirtió a una laparotomía (cirugía abierta) supraumbilical media. Durante la cirugía se identificó un asa de íleon (parte final del intestino delgado) herniada a través del hiato de Winslow, con signos de congestión por la presión del hiato, pero sin daño irreversible, por lo que no fue necesaria la resección intestinal. El asa herniada fue reducida (devuelta a su posición normal). El hiato de Winslow tenía un tamaño normal, por lo que no se realizó ninguna maniobra para prevenir la recurrencia de la hernia.\n\nEn el postoperatorio, el paciente presentó un íleo paralítico (falta temporal de movimiento intestinal), que mejoró progresivamente, permitiendo retirar la sonda nasogástrica a los cinco días y comenzar la alimentación oral con buena tolerancia. Además, desarrolló una colección pélvica (acumulación localizada de líquido o pus) que se trató con antibióticos de forma conservadora, sin necesidad de intervención quirúrgica adicional. El paciente evolucionó favorablemente y fue dado de alta al décimo día después de la cirugía, manteniendo un buen estado general y sin fiebre.\n\n**Próximos Pasos**  \nActualmente, el paciente se encuentra en seguimiento ambulatorio en consultas de cirugía pediátrica para monitorizar su recuperación y detectar posibles complicaciones o recurrencias. Se mantiene estable y con tránsito intestinal conservado."
+        }
+    },
+    {
+        "article": "Un niño de 23 meses de edad con encefalopatía isquémica hipóxica al nacer, con buen potencial motor cerebral y desarrollo psicomotor normal. Tenía antecedentes personales de miocardiopatía restrictiva y fue incluido en un programa de trasplante cardiaco cuando tenía 16 meses de edad. También fue necesario implantarle un dispositivo de asistencia biventricular Berlin Heart externo. Para evitar eventos embólicos, se le administró un tratamiento antiplaquetario doble y anticoagulante. Cuando tenía 23 meses de edad, presentó desconexión y hemiparesia derecha. Una tomografía computarizada (TC) mostró una arteria cerebral media (ACM) izquierda hiperdensa, así como un infarto parietotemporal derecho crónico. Su análisis de sangre mostró: glóbulos rojos 4.16 × 106 µ/L; hemoglobina 11.4 g/gL; tiempo de tromboplastina parcial activada (TTPA) 93 segundos y relación internacional normalizada (INR) 1.08.\n\nEl tratamiento trombolítico intravenoso estaba contraindicado debido al doble tratamiento antiplaquetario y anticoagulante a la dosis completa con heparina, por lo que se realizó una trombectomía intraarterial. Aunque el paciente tenía 23 meses de edad, se encontraba en el tercer percentil de la curva de peso (10 kg). Bajo anestesia general, se perforó la arteria femoral derecha y se colocó una funda 4F de 11 cm de largo (Cordis, Irlanda). Se usó un catéter vertebral Radiofocus 4F (Glidecath de Terumo, Bélgica) para confirmar la oclusión del segmento M1 de la MCA izquierda. La arteria se recanalizó mediante trombectomía mecánica con un stentriever utilizando el catéter vertebral 4F como tutor, colocándolo en el segmento petroso de la arteria carótida. Se usó un dispositivo Trevo XP Pro Vue de 3 mm x 20 mm (Stryker, Países Bajos), con un microcatéter Rapid Transit recto (Codman Neurovascular, Reino Unido), abriendo la arteria en una sola pasada. Se retiró todo el sistema (catéter tutor, microcatéter y stentriever) simultáneamente. En la prueba de control, se detectó una disección iatrogénica de la arteria carótida interna izquierda, que no tuvo importancia clínica, ya que el hemisferio izquierdo se irrigaba a través de la arteria comunicante anterior.\n\nUn mes después, se realizó con éxito el trasplante de corazón. La única secuela neurológica a largo plazo que surgió como resultado del accidente cerebrovascular fue la espasticidad del miembro superior derecho.\n\nMH - Cardiomiopatía, Dilatada/complicaciones/cirugía\nMH - Cardiomiopatía, restrictiva/complicaciones/cirugía\nMH - Angiografía cerebral\nMH - Procedimientos/métodos endovasculares\nMH - Mujer\nMH - Estudios de seguimiento\nMH - Insuficiencia cardiaca/*complicaciones/tratamiento\nMH - Trasplante de corazón\nMH - *Dispositivos de asistencia cardíaca\nMH - Humanos\nMH - Infantil\nMH - Hombre\nMH - Arteria cerebral media/imágenes diagnósticas\nMH - Estudios Retrospectivos\nMH - Ictus/complicaciones/diagnóstico por imágenes/cirugía\nMH - Resultado del tratamiento\n",
+        "gold_summary": "Un niño de 16 meses de edad con cardiomiopatía restrictiva que fue incluido en una lista para un trasplante cardiaco. A los 20 meses de edad, requirió un implante de un dispositivo de asistencia biventricular externo (Berlin Heart) y tuvo un accidente cerebrovascular en el hemisferio izquierdo a los 23 meses. Se utilizó un enfoque intraarterial y produjo buenos resultados clínicos. Un mes después, se realizó con éxito un trasplante cardiaco.\n",
+        "synthetic_summary": {
+            "B1": "Había un niño que tenía un problema en su corazón. Tenía que esperar para recibir un corazón nuevo. Le pusieron una máquina para ayudar a su corazón a latir. Un día, su cerebro se enfermó un poco. Los doctores usaron una medicina especial para ayudar a su cerebro. Después, el niño recibió un corazón nuevo y se puso mejor.",
+            "B2": "**Lo que pasó con el niño**\n\nUn niño de 16 meses tenía un problema en el corazón llamado cardiomiopatía restrictiva, que hace que el corazón no funcione bien. Por eso, lo pusieron en una lista para recibir un trasplante de corazón. A los 20 meses, le pusieron un dispositivo especial llamado Berlin Heart, que ayuda al corazón a bombear sangre mientras espera el trasplante.\n\n**El problema del accidente cerebrovascular**\n\nCuando tenía 23 meses, el niño sufrió un accidente cerebrovascular, que es cuando una parte del cerebro no recibe suficiente sangre y se daña. En su caso, el problema ocurrió en el lado izquierdo del cerebro. Debido a que ya estaba tomando medicamentos para evitar coágulos, no se pudo usar un tratamiento común para este tipo de accidente.\n\n**El tratamiento que recibieron**\n\nLos médicos usaron una técnica llamada trombectomía intraarterial. Esto significa que, con anestesia, introdujeron un pequeño tubo por una arteria en la pierna para llegar hasta el cerebro y quitar el coágulo que bloqueaba la arteria. Lograron abrir la arteria en una sola vez y restaurar el flujo de sangre.\n\n**Qué pasó después**\n\nUn mes después del accidente, el niño recibió el trasplante de corazón que necesitaba. Como consecuencia del accidente cerebrovascular, quedó con un poco de rigidez en el brazo derecho, pero en general tuvo buenos resultados y pudo continuar con su tratamiento.\n\n**Por qué es importante este caso**\n\nEste caso muestra que, incluso en niños muy pequeños con problemas graves del corazón, es posible usar técnicas avanzadas para tratar accidentes cerebrovasculares y mejorar su salud antes de un trasplante.",
+            "B3": "**Contexto:**  \nSe presenta el caso de un niño de 23 meses con antecedentes complejos, incluyendo encefalopatía isquémica hipóxica al nacer con desarrollo psicomotor normal, y una cardiomiopatía restrictiva diagnosticada en la infancia. Debido a la gravedad de su insuficiencia cardíaca, fue incluido en un programa de trasplante cardiaco a los 16 meses. Posteriormente, a los 20 meses, se le implantó un dispositivo de asistencia ventricular biventricular externo (Berlin Heart) para apoyar la función cardíaca mientras esperaba el trasplante. Para prevenir la formación de coágulos, recibió tratamiento combinado con anticoagulantes y antiplaquetarios.\n\n**Hallazgos Clave:**  \nA los 23 meses, el niño presentó síntomas neurológicos agudos, incluyendo desconexión y hemiparesia (debilidad) en el lado derecho del cuerpo. Una tomografía computarizada reveló una obstrucción en la arteria cerebral media izquierda, responsable del suministro sanguíneo a una parte importante del cerebro, junto con un infarto crónico en el hemisferio derecho. Debido a que el tratamiento trombolítico intravenoso (que disuelve coágulos) estaba contraindicado por su régimen anticoagulante, se optó por una trombectomía mecánica intraarterial, un procedimiento endovascular que consiste en extraer el coágulo directamente desde la arteria afectada.\n\nDurante la intervención, realizada bajo anestesia general, se accedió a la arteria femoral derecha para introducir un catéter que permitió llegar hasta la arteria cerebral afectada. Se utilizó un dispositivo llamado stentriever para recuperar el flujo sanguíneo en una sola maniobra. Aunque se detectó una disección (una lesión en la pared arterial causada por el procedimiento), esta no tuvo consecuencias clínicas importantes debido a la circulación colateral cerebral. El procedimiento fue exitoso y permitió la recuperación del flujo en la arteria ocluida.\n\n**Interpretación Clínica:**  \nEste caso destaca la viabilidad y eficacia de la trombectomía mecánica en pacientes pediátricos con ictus isquémico, incluso en niños muy pequeños y con condiciones cardíacas complejas que contraindican el tratamiento trombolítico convencional. La intervención permitió minimizar el daño cerebral y preservar la función neurológica, limitando la secuela a una espasticidad en el brazo derecho.\n\n**Próximos Pasos:**  \nUn mes después de la recuperación del accidente cerebrovascular, el niño fue sometido con éxito a un trasplante de corazón, mejorando su pronóstico a largo plazo. El seguimiento neurológico y cardiológico continúa siendo fundamental para monitorizar la evolución y manejar posibles complicaciones futuras. Este caso aporta evidencia sobre el manejo multidisciplinario y personalizado en pacientes pediátricos con enfermedades cardíacas graves y complicaciones neurológicas."
+        }
+    },
+    {
+        "article": "Una mujer de 23 años de edad se presentó al departamento de urgencias con pérdida de conciencia y exceso de secreciones orales 2 horas después de la ingestión de un veneno no especificado. No tenía movimientos corporales anormales, fiebre, diarrea, vómitos o sudoración. Inicialmente la habían llevado a un hospital primario cercano, donde fue tratada por posible intoxicación por OP con atropina y cimetidina durante 3 días, antes de ser trasladada al hospital Saint Peter. Después de un interrogatorio exhaustivo, se descubrió que la paciente había consumido unos 30 ml de 2,4-D en un intento de suicidio, precipitado por problemas financieros. No tenía antecedentes conocidos de enfermedad psiquiátrica, intentos de suicidio, episodios depresivos o abuso de sustancias. No se observaron trastornos cardíacos, renales o metabólicos previos.\n\nAl llegar al departamento de urgencias, la paciente estaba inconsciente. Sus constantes vitales eran PR 110/min, BP 120/70 mmHg, RR 21/min, y SPO2 96% en aire ambiente. Los resultados del examen físico fueron notables: un GCS de 6 sobre 15, pupilas dilatadas y reactivas, extremidades inferiores hipertónicas e hiperreflexivas, y reflejo plantar ascendente. Tras la investigación inicial, el recuento completo de células sanguíneas, la prueba de la función renal, la prueba de la función hepática, y la glucosa en sangre aleatoria fueron normales. Su electrocardiograma mostró taquicardia sinusal, mientras que la radiografía de tórax no fue notable. El análisis de gases en sangre arterial y el nivel sérico de la toxina no pudieron determinarse, ya que ninguno de los medios de prueba estaba disponible en el hospital.\n\nLa paciente fue trasladada a la unidad de cuidados intensivos (UCI), se le introdujo una sonda para proteger las vías respiratorias y se le inició inmediatamente una diuresis alcalina forzada. Su evolución en la UCI fue notable por el desarrollo de una insuficiencia renal (creatinina 3,1 ml/dL [intervalo de referencia 0,5-1,2 mg/dL], BUN 133 mg/dL [intervalo de referencia 16,6-48,5 mg/dL], análisis de orina 3+ hemoglobina y muchos glóbulos rojos), debido a una rabdomiolisis inducida por toxinas (nivel de creatina fosfocinasa de 1330 µg/L). Posteriormente, la paciente se volvió hipotensa y se le inició un tratamiento con vasopresores. La ecocardiografía y la ecografía abdominal no fueron significativas. A pesar de estos esfuerzos, falleció por colapso circulatorio el tercer día de estancia en la UCI.\n",
+        "gold_summary": "Aquí se informa sobre el caso de una joven granjera de la zona rural de Etiopía que fue internada en un hospital local tras perder el conocimiento y presentar exceso de secreciones orales 2 horas después de haber ingerido, de manera suicida, un agente tóxico desconocido. Originalmente, se la trató por intoxicación con organofosforados y luego se la trasladó al Hospital Saint Peter's en Addis Abeba para recibir atención médica más intensiva. Allí, se confirmó la ingesta de 2,4-D y se le brindó atención médica de apoyo, ventilación mecánica y diuresis alcalina forzada. A pesar de estas intervenciones, falleció varios días después.\n",
+        "synthetic_summary": {
+            "B1": "Una joven tomó un veneno para hacerse daño. Se puso muy mal y perdió el conocimiento. La llevaron al hospital para ayudarla. \n\nLos doctores le dieron medicinas y la cuidaron mucho. Pero su cuerpo no pudo mejorar. Después de unos días, ella murió. \n\nLos doctores hicieron todo lo que pudieron para ayudarla.",
+            "B2": "Caso de Intoxicación Grave en una Joven\n\nUna mujer de 23 años de una zona rural de Etiopía tomó un veneno llamado 2,4-D con la intención de suicidarse. Dos horas después, perdió el conocimiento y tenía mucha saliva. Al principio, pensaron que había tomado otro tipo de veneno y la trataron en un hospital pequeño. Luego, la llevaron a un hospital más grande llamado Saint Peter para recibir mejor atención.\n\nLo que Encontraron en el Hospital\n\nCuando llegó, la paciente estaba inconsciente y tenía signos de daño en sus nervios y músculos. Los exámenes de sangre y orina mostraron que sus riñones no funcionaban bien y que había daño muscular grave, causado por el veneno. Los médicos intentaron ayudarla con tratamientos para limpiar el veneno y proteger sus órganos, incluyendo ponerle un tubo para ayudarla a respirar.\n\nQué Pasó Después\n\nA pesar de los esfuerzos médicos, la paciente empeoró. Su presión sanguínea bajó mucho y los médicos tuvieron que usar medicamentos para mantenerla estable. Finalmente, después de tres días en cuidados intensivos, falleció debido a un fallo en su circulación sanguínea.\n\nImportancia del Caso\n\nEste caso muestra lo peligroso que puede ser el veneno 2,4-D y cómo puede afectar seriamente el cuerpo, especialmente los riñones y los músculos. También destaca la importancia de un diagnóstico correcto y tratamiento rápido en casos de intoxicación para intentar salvar vidas.",
+            "B3": "**Contexto**\n\nSe presenta el caso de una mujer joven de 23 años, proveniente de una zona rural de Etiopía, que ingresó al hospital tras perder el conocimiento y mostrar un exceso de secreciones orales aproximadamente dos horas después de ingerir intencionalmente una sustancia tóxica. Inicialmente fue atendida en un hospital local donde se sospechó intoxicación por organofosforados (un tipo común de pesticida) y recibió tratamiento con atropina y cimetidina durante tres días. Posteriormente, fue trasladada al Hospital Saint Peter en Addis Abeba para recibir cuidados más especializados.\n\n**Hallazgos Clave**\n\nEn el hospital de referencia se confirmó que la sustancia ingerida era 2,4-D, un herbicida tóxico. Al ingreso, la paciente estaba inconsciente con un nivel de conciencia muy bajo (Glasgow Coma Scale de 6/15), presentaba pupilas dilatadas pero reactivas, hipertonicidad (aumento anormal del tono muscular) y reflejos exagerados en las extremidades inferiores, así como un reflejo plantar anormal (reflejo de Babinski positivo). Sus signos vitales mostraban taquicardia (frecuencia cardíaca rápida), presión arterial y saturación de oxígeno dentro de rangos aceptables. Los análisis iniciales de sangre, función renal y hepática, así como glucosa, fueron normales. Sin embargo, no se pudieron medir niveles específicos de la toxina ni gases en sangre debido a limitaciones del hospital.\n\nDurante su estancia en la unidad de cuidados intensivos (UCI), la paciente fue intubada para proteger sus vías respiratorias y se inició diuresis alcalina forzada, una técnica para ayudar a eliminar la toxina a través de la orina. A pesar de esto, desarrolló insuficiencia renal aguda, evidenciada por un aumento significativo de creatinina y nitrógeno ureico en sangre, así como presencia de hemoglobina y glóbulos rojos en la orina. Además, presentó rabdomiólisis (descomposición del tejido muscular) inducida por la toxina, confirmada por niveles elevados de creatina fosfocinasa, una enzima muscular. Posteriormente, la paciente sufrió hipotensión (presión arterial baja) que requirió el uso de medicamentos vasopresores para mantener la presión arterial. Estudios de ecocardiografía y ecografía abdominal no mostraron alteraciones significativas.\n\n**Interpretación Clínica**\n\nLa intoxicación por 2,4-D es poco común pero grave, y puede causar daño multisistémico, incluyendo alteraciones neurológicas, musculares y renales. En este caso, la rápida progresión hacia insuficiencia renal y colapso circulatorio refleja la alta toxicidad de esta sustancia y la dificultad para manejar sus complicaciones, incluso con tratamiento intensivo y medidas de soporte avanzadas.\n\n**Próximos Pasos**\n\nEste caso subraya la importancia de un diagnóstico preciso y rápido en intoxicaciones, especialmente en regiones con recursos limitados. La disponibilidad de pruebas específicas para identificar toxinas y la implementación temprana de tratamientos dirigidos podrían mejorar el pronóstico. Además, es fundamental fortalecer la atención en salud mental y los servicios de prevención del suicidio para evitar intentos con sustancias altamente tóxicas."
+        }
+    },
+    {
+        "article": "Una paciente etíope de 35 años de edad se presentó en el departamento de urgencias del Colegio Médico del Hospital Yekatitit 12 con síntomas de falta de aire en reposo, ortopnea, disnea paroxística nocturna significativa, dolor torácico, tos productiva teñida de sangre y vómitos de materia ingerida (2-3 episodios por día) durante 2 semanas. Presentaba una hinchazón progresiva del cuerpo que comenzó en las extremidades inferiores y luego afectó a todo el cuerpo, fatigabilidad fácil, pérdida de apetito, fiebre intermitente de alto grado y sensación de ardor epigástrico durante la misma semana y con la misma duración. La paciente también experimentó una pérdida de peso y fatiga no especificadas durante los últimos 2 meses. Por lo demás, no tenía comorbilidades conocidas, ni comportamientos de riesgo, como fumar o beber alcohol, medicamentos o antecedentes familiares de neoplasia. Estaba casada, tenía cuatro hijos y no tenía antecedentes obstétricos negativos. Su ocupación era la agricultura y había vivido en una zona rural. Nunca había sido admitida por una queja similar.\n\nLa escala de coma de Glasgow (GCS) de la paciente fue de 15 sobre 15, y no había anormalidades de memoria, potencia o tono. La paciente estaba en grave dificultad respiratoria con saturación de oxígeno del 70% con aire atmosférico, frecuencia respiratoria de 30-35 latidos/minuto, y frecuencia del pulso de 120 por minuto. Tenía registros de fiebre de alto grado hasta el nivel de 39.5 0C y puede mantener su presión arterial. El examen de mama con ultrasonido y mamografía fue supuestamente normal. No se detectó linfadenopatía en áreas accesibles.\n\nEl examen del tórax reveló signos de derrame pleural que también se observaron en las imágenes y se analizaron. Una tomografía computarizada (TC) del tórax con contraste mostró derrame pericárdico y neumonía multifocal. La angiografía por TC mostró un defecto de llenado arterial pulmonar segmentario del lóbulo inferior en ambos lados, lo que sugiere embolia pulmonar y derrame pleural en ambos lados. Los frotis citológicos se informaron con láminas de células mesoteliales, neutrófilos y grupos dispersos de células grandes atípicas con nucleolos prominentes que sugieren derrame maligno. El análisis del líquido pleural mostró un líquido con predominio linfocítico con glucosa normal (82 mg/dl), proteínas (2,2 g/dl) y lactato deshidrogenasa (LDH) de 592 mg/dl.\n\nLa presión venosa yugular aumentó con los sonidos cardiacos apagados. La ecocardiografía mostró derrame pericárdico masivo con características de taponamiento cardiaco, fracción de eyección preservada (65%), y excursión sistólica del plano anular tricuspídeo (TAPSE) mayor a 18 mm. Un electrocardiograma (ECG) reveló solo taquicardia sinusal y desviación del eje. Se realizó una pericardiocentesis inmediata, se extrajo un drenaje de aproximadamente 250 ml de fluido hemorrágico y se aseguró la ventana pericárdica. La repetida ecocardiografía reveló una reducción del tamaño. El informe de citología del fluido pericárdico mostró numerosos linfocitos junto con células malignas atípicas que tenían prominentes nucleolos, lo que sugería un derrame maligno.\n\nEn el examen abdominal, mostró signos positivos de acumulación de fluidos sin órgano hinchable. La tomografía computarizada abdominal y pélvica mostró un aumento en el tamaño del hígado con múltiples lesiones hepáticas hipointensas que sugerían metástasis. Los órganos pélvicos, incluidos los ovarios y el útero, no presentaron lesiones identificadas. Se realizó una biopsia con aguja de la lesión hepática y los resultados revelaron un adenocarcinoma secundario.\n\nSe realizó un diagnóstico de insuficiencia cardíaca causada por una efusión pericárdica masiva maligna secundaria a un adenocarcinoma diseminado y un carcinoma de origen primario desconocido que afectaba al pulmón, la pleura, el pericardio y el tracto gastrointestinal. Se le diagnosticó a la paciente una trombosis venosa profunda extensa en la extremidad superior izquierda, una embolia pulmonar bilateral y segmentaria, posiblemente debido a la CUP diseminada. Los hallazgos también mostraron una neumonía multifocal superpuesta y una anemia leve de enfermedad crónica.\n\nEl recuento sanguíneo completo inicial reveló leucocitosis con un recuento de glóbulos blancos de 24 × 103 por ml, neutrófilos predominantes (91%), recuento de glóbulos rojos de 3.7 × 106 por µl, anemia normocítica leve (hemoglobina (Hgb) 11.2 mg/dl), volumen corpuscular medio (MCV) de 81.2 fl, y trombocitopenia severa (66 × 103/µl). Después del tratamiento antibiótico para neumonía, el recuento sanguíneo completo volvió a la normalidad (excepto para Hgb). Con niveles normales de bilirrubina, la aspartato aminotransferasa (AST) aumentó más de siete veces (263 U/L), mientras que la alanina transaminasa (ALT) aumentó más de nueve veces (332 U/L). Los electrolitos séricos (excepto para Na + con hiponatremia leve, 129 mEq/L) y las pruebas de función renal fueron normales. La albúmina era baja (2.12 g/dl). Los niveles de lactato deshidrogenasa (LDH) aumentaron casi dos veces desde el inicio (592 U/L). Los virus del virus de inmunodeficiencia humana, hepatitis B y hepatitis C no fueron reactivos. La sangre y el cultivo del líquido pleural no tuvieron crecimiento. Un antígeno carcinoembrionario (CEA) aumentó más de 400 veces (1000 µg/L) del inicio.\n\nLa paciente fue admitida en la sala general. Se realizó una ventana pericárdica y una inserción de un tubo torácico derecho con un cirujano cardiotorácico junto con un cardiólogo (ver la cantidad de aspirado antes). Se realizó una aspiración pleural terapéutica intermitente para el derrame pleural maligno. Una vez que la dosis de carga (60 mg) de frusemida produjo suficiente producción de orina, esta dosis se mantuvo tres veces (TID) al día. Esto se redujo y se dio de alta a la paciente con una dosis oral de 20 mg dos veces al día (BID). Se inició una dosis estándar de enoxaparina para el tromboembolismo pulmonar y la trombosis venosa profunda aguda extensa en la extremidad superior izquierda. Se administró enoxaparina por vía subcutánea 40 mg BID durante la hospitalización, que se cambió a 5 mg de warfarina oral diaria durante el alta debido a problemas financieros. La neumonía multifocal se trató con ceftazidima (1 g intravenoso TID) y vancomicina (1 g intravenoso BID) según el protocolo de tratamiento estándar nacional. El dolor se controló con un potente medicamento contra el dolor (morfina 5 mg intravenosa TID) y se redujo y suspendió. También estaba en la profilaxis de la úlcera. La paciente fue dada de alta de la sala médica con una mejora significativa después de 14 días de hospitalización y fue asignada a la unidad de oncología del hospital. Por lo tanto, para el cáncer de origen primario desconocido, se le dio un ciclo de quimioterapia (carboplatino/paclitaxel). Se perdió el seguimiento debido a problemas financieros, y la paciente murió en su casa cuatro meses después del alta.\n\nMH - Humanos\nMH - Mujer\nMH - *Insuficiencia cardiaca/etiología\nMH - Adulto\nMH - *Neoplasias, complicaciones/primaria desconocida",
+        "gold_summary": "Una mujer negra de 35 años se presentó con falta de aire en reposo, ortopnea, disnea paroxística nocturna, dolor torácico, tos productiva teñida de sangre y fiebre durante 2 semanas. También tenía hinchazón progresiva del cuerpo, fatigabilidad fácil, pérdida de apetito y dolor abdominal durante la misma semana. La imagen corporal reveló grandes derrames pleurales y pericárdicos, lesiones hepáticas metastásicas y defectos de llenado segmentarios y subsegmentarios vasculares pulmonares bilaterales. La citología de los fluidos pericardio y pleural sugieren derrame maligno. Las lesiones hepáticas y la biopsia con aguja indicaron adenocarcinoma de origen desconocido, y el nivel de antígeno carcinoembriónico también aumentó significativamente.\n",
+        "synthetic_summary": {
+            "B1": "Había una mujer que se sentía muy cansada y con dificultad para respirar. Su cuerpo se hinchó mucho y tenía dolor en el pecho. Los doctores vieron que tenía líquido en el pecho y alrededor del corazón. También encontraron que tenía un problema en el hígado y en los pulmones. El líquido que sacaron mostró que tenía células que no son buenas. Los doctores dijeron que tenía un tipo de cáncer que empezó en un lugar que no pudieron encontrar.",
+            "B2": "**Lo que le Pasó a la Paciente**\n\nUna mujer de 35 años llegó al hospital porque tenía mucha dificultad para respirar, incluso cuando estaba en reposo. También tenía dolor en el pecho, tos con sangre, fiebre y una hinchazón que comenzó en sus piernas y se extendió por todo el cuerpo. Además, se sentía muy cansada, había perdido el apetito y tenía dolor en la parte superior del abdomen.\n\n**Lo que Encontraron en los Exámenes**\n\nLas imágenes médicas mostraron que tenía acumulación de líquido en los pulmones (llamado derrame pleural) y alrededor del corazón (derrame pericárdico). También encontraron lesiones en el hígado que parecían ser metástasis, es decir, que el cáncer se había extendido allí. En los vasos sanguíneos de sus pulmones había bloqueos que indicaban embolias pulmonares, que son coágulos que dificultan la circulación.\n\nAl analizar el líquido que rodeaba el corazón y los pulmones, los médicos encontraron células anormales que indicaban que el líquido estaba causado por un cáncer (derrame maligno). La biopsia del hígado confirmó que tenía un tipo de cáncer llamado adenocarcinoma, pero no pudieron encontrar dónde comenzó el cáncer originalmente.\n\nAdemás, un examen de sangre mostró que tenía un nivel muy alto de una sustancia llamada antígeno carcinoembrionario, que suele aumentar cuando hay ciertos tipos de cáncer.\n\n**Qué Significa Todo Esto**\n\nLa paciente tenía un cáncer avanzado que se había extendido a varias partes del cuerpo, incluyendo los pulmones, el corazón y el hígado. Esto causó problemas graves como dificultad para respirar, acumulación de líquidos y coágulos en la sangre. Aunque recibieron tratamiento para aliviar sus síntomas y para el cáncer, la enfermedad estaba muy avanzada y el origen del tumor principal no se pudo identificar.",
+            "B3": "**Contexto**  \nUna mujer etíope de 35 años acudió al hospital presentando dificultad grave para respirar en reposo, dificultad para respirar al estar acostada (ortopnea), episodios repentinos de dificultad respiratoria nocturna (disnea paroxística nocturna), dolor en el pecho, tos con expectoración de sangre y vómitos de contenido alimenticio durante dos semanas. Además, manifestó una hinchazón progresiva que comenzó en las piernas y se extendió a todo el cuerpo, cansancio fácil, pérdida de apetito, fiebre alta intermitente y ardor en la parte superior del abdomen. También había experimentado pérdida de peso y fatiga durante los dos meses previos. No tenía antecedentes médicos relevantes ni factores de riesgo conocidos.\n\n**Hallazgos Clave**  \nEl examen físico y las pruebas de imagen revelaron derrames significativos de líquido tanto en la cavidad pleural (alrededor de los pulmones) como en el pericardio (la membrana que rodea el corazón). La tomografía computarizada mostró lesiones en el hígado compatibles con metástasis (diseminación del cáncer) y defectos en la circulación sanguínea pulmonar que indicaban embolias pulmonares bilaterales. El análisis del líquido extraído del pericardio y la pleura mostró células malignas, lo que sugiere que el líquido se debía a un derrame maligno. La biopsia hepática confirmó la presencia de un adenocarcinoma (un tipo de cáncer que se origina en células glandulares) de origen primario desconocido. Además, el nivel en sangre del antígeno carcinoembrionario (CEA), un marcador tumoral, estaba muy elevado, apoyando la presencia de un cáncer avanzado.\n\n**Interpretación Clínica**  \nLa paciente fue diagnosticada con insuficiencia cardíaca causada por un derrame pericárdico masivo de origen maligno, secundario a un adenocarcinoma diseminado que afectaba múltiples órganos, incluyendo pulmón, pleura, pericardio y tracto gastrointestinal. También se identificaron complicaciones como trombosis venosa profunda en el brazo izquierdo y embolia pulmonar, probablemente relacionadas con la enfermedad tumoral avanzada. Se detectó además una neumonía multifocal superpuesta y anemia leve asociada a enfermedad crónica.\n\n**Próximos Pasos y Tratamiento**  \nLa paciente recibió tratamiento urgente para aliviar el derrame pericárdico mediante pericardiocentesis y ventana pericárdica, así como drenaje del líquido pleural. Se inició tratamiento anticoagulante para la trombosis y embolia pulmonar, y antibióticos para la neumonía. Posteriormente, se administró quimioterapia con carboplatino y paclitaxel dirigida al cáncer de origen desconocido. A pesar de la mejoría inicial y el alta hospitalaria, la paciente falleció cuatro meses después debido a la progresión de la enfermedad.\n\nEste caso ilustra la complejidad del diagnóstico y manejo de un cáncer avanzado con origen primario desconocido, que se manifestó inicialmente con síntomas respiratorios y signos de insuficiencia cardíaca por derrame pericárdico maligno."
+        }
+    },
+    {
+        "article": "Paciente del sexo femenino de 17 años con diagnóstico de enfermedad de Graves con bocio difuso, la cual negó otros antecedentes de importancia.\n\nSu cuadro comenzó seis meses antes con pérdida de peso progresiva, episodios de ansiedad y agitación, temperaturas de 37.4 a 37.9 ºC, palpitaciones, dolor abdominal y diarrea intermitente. A los dos meses se agregó como síntoma el crecimiento de la cara anterior del cuello; al tercer mes presentó taquicardia de hasta 130 latidos por minuto. Al ser valorada por Endocrinología se le administró tiamazol de 15 mg cada 8 horas, el cual fue suspendido por cuadro de agranulocitosis. Por lo tanto, se le comenzó a administrar lugol y propanol de 20 mg cada 8 horas, sin respuesta adecuada. Por ende, se decidió aplicar una dosis terapéutica de yodo 131 (I-131) 10 mcU.\n\n\nExploración física\nA la exploración física, la paciente presentó como signos basales una presión arterial no invasiva (PANI) 137/75 mmHg, frecuencia cardiaca (FC) 105 lpm, frecuencia respiratoria (FR) 16 rpm, SpO2 95%, temperatura 37.4ºC. La paciente ingresó deambulando, con agitación leve, con actitud cooperadora; estaba hidratada y sin datos clínicos de vía aérea difícil, pero no se valoró movilidad de tráquea por crecimiento tiroideo de aproximadamente 7.5 x 7 x 10 cm). La superficie del cuello era regular y su movilidad tenía una adecuada extensión. A la auscultación cardiopulmonar no hubo ruidos agregados y la paciente tenía ruidos cardiacos aumentados en frecuencia; asimismo, abdomen blando, depresible, no doloroso, con peristalsis presente. Extremidades integras, sensibilidad con aumento de la percepción del calor, hiperhidrosis palmar, fuerza 5/5, y temblor fino.\n\nSe empleó la escala de Burch y Wartofsky y se obtuvieron 40 puntos con elevada probabilidad de tormenta tiroidea, por lo cual se decidió manejo con anestesia multimodal.\n\nEn la monitorización tipo 2 la paciente presentó signos vitales iniciales PANI 137/75 mmHg, frecuencia cardiaca 96 latidos por minuto, frecuencia respiratoria 16 respiraciones por minuto, 95% Spo2, monitoreo invasivo de tensión arterial.\n\nPor inducción endovenosa se le administraron a la paciente 2 mg de midazolam; 150 mcg de fentanilo; 5 mg de cisatracurio y 50 mg de propofol.\n\nEl abordaje de la vía aérea se hizo con videolaringoscopía Glide Scope con hoja hiperangular 3 sin complicaciones. La ventilación mecánica invasiva modo volumen presentó flujos bajos FIO2 (40%).\n\nSe llevó a cabo bloqueo cervical superficial bilateral ecoguiado con 4 mL de ropivacaina al 0.2% en cada lado (16 mg en total).\n\nPara el mantenimiento se empleó sevoflorano CAM 0.8, infusión de dexmedetomedina 0.7 a 0.4 mcg/kg/hora, infusión de lidocaína 25 mcg/kg/hora, concentración plasmática de fentanilo 0.001 mcg/mL.\n\nEn cuanto a los adyuvantes se empleó paracetamol 750 mg + parecoxib 40 mg + ketorolaco intravenoso 30 + sulfato de magnesio 1250 g en infusión para una hora. El balance de líquidos fue negativo. El tiempo anestésico fue de 215 minutos. En el transoperatorio, la paciente estuvo hemodinámicamente estable, con presión arterial media de 67 a 75 mmHg, que se considera adecuada para la perfusión de órganos.\n\nEn el postoperatorio la paciente presentó analgesia durante 12 horas. Rescate con 1 g de metamizol por razón necesaria, utilizando un solo rescate. Disfonía postoperatoria persistente, sin presencia de odinofagia.",
+        "gold_summary": "Adolescente de 17 años con enfermedad de Graves con manifestaciones clínicas descontroladas, la cual no respondió a tratamiento médico y se programó para tiroidectomia radical. Se obtuvieron 35 puntos en la Escala de Burch y Wartofsky. Se manejó con anestesia general y fueron disminuyendo los estímulos para control de vía aérea y regional a fin de disminuir los estímulos quirúrgicos. Se usaron medicamentos adyuvantes como sulfato de magnesio para la estabilidad transoperatoria.",
+        "synthetic_summary": {
+            "B1": "Una niña de 17 años tenía un problema en su cuello llamado enfermedad de Graves. Su cuerpo estaba muy acelerado y no mejoró con medicinas. Por eso, los doctores decidieron hacerle una operación para quitarle una parte del cuello. Durante la operación, los doctores usaron medicinas para que ella no sintiera dolor y para que su cuerpo estuviera tranquilo. También cuidaron mucho su respiración para que todo saliera bien.",
+            "B2": "**Caso de una Adolescente con Enfermedad de Graves**\n\nUna joven de 17 años tenía una enfermedad llamada Graves, que afecta la tiroides, una glándula en el cuello que controla muchas funciones del cuerpo. Su enfermedad estaba muy activa y no mejoró con los medicamentos que le dieron.\n\n**Lo que Pasó Antes de la Cirugía**\n\nLa paciente tenía síntomas como pérdida de peso, ansiedad, latidos rápidos del corazón y un aumento visible en el tamaño de su cuello debido al crecimiento de la tiroides. Los médicos usaron una escala llamada Burch y Wartofsky para medir qué tan grave estaba su condición, y obtuvo 35 puntos, lo que indica un problema serio.\n\n**Cómo Se Realizó la Cirugía**\n\nPara operarla, le pusieron anestesia general, que es un medicamento que la hizo dormir y no sentir dolor durante la cirugía. Los médicos cuidaron mucho la forma de manejar su respiración y usaron técnicas para reducir las molestias causadas por la operación. Además, le dieron medicamentos especiales, como sulfato de magnesio, para mantener su cuerpo estable mientras duraba la cirugía.\n\n**Por Qué Es Importante**\n\nEste caso muestra cómo se trata una enfermedad de Graves muy avanzada cuando los medicamentos no funcionan. La cirugía y el cuidado durante la operación son muy importantes para que la paciente esté segura y se recupere bien.",
+            "B3": "**Contexto**  \nSe trata de una paciente femenina de 17 años diagnosticada con enfermedad de Graves, una condición autoinmune que provoca un aumento en la actividad de la glándula tiroides (hipertiroidismo) y crecimiento difuso del tiroides (bocio). Desde hace seis meses, presentó síntomas progresivos como pérdida de peso, ansiedad, fiebre leve, palpitaciones, dolor abdominal y diarrea. Posteriormente, desarrolló un aumento visible en la parte frontal del cuello y taquicardia (frecuencia cardíaca acelerada). El tratamiento inicial con tiamazol (un medicamento antitiroideo) fue suspendido debido a una complicación grave llamada agranulocitosis (disminución severa de glóbulos blancos). Se intentaron otros tratamientos sin éxito, por lo que se decidió administrar yodo radioactivo (I-131) para reducir la función tiroidea.\n\n**Hallazgos Clave**  \nEn la evaluación física, la paciente mostraba signos de hipertiroidismo activo: frecuencia cardíaca elevada (105 latidos por minuto), temperatura corporal ligeramente elevada (37.4 ºC), temblor fino, sudoración excesiva en las palmas y aumento de la sensibilidad al calor. Se observó un bocio grande (aproximadamente 7.5 x 7 x 10 cm) sin signos de dificultad respiratoria, aunque no se pudo evaluar completamente la movilidad de la tráquea debido al tamaño del tiroides. La escala de Burch y Wartofsky, que evalúa el riesgo de una crisis tiroidea grave llamada tormenta tiroidea, arrojó un puntaje de 40, indicando alta probabilidad de esta complicación.\n\nDurante la cirugía programada para extirpar la glándula tiroides (tiroidectomía radical), se utilizó anestesia general con técnicas avanzadas para asegurar la vía aérea, incluyendo videolaringoscopía, y ventilación mecánica controlada. Se aplicó un bloqueo nervioso cervical superficial guiado por ultrasonido para reducir el dolor y la respuesta al estímulo quirúrgico. Además, se emplearon varios medicamentos adyuvantes, como sulfato de magnesio, para mantener la estabilidad cardiovascular y mejorar el control del dolor durante la operación. La paciente se mantuvo estable durante todo el procedimiento, que duró aproximadamente 3 horas y 35 minutos.\n\n**Interpretación Clínica**  \nLa paciente presentaba un cuadro de enfermedad de Graves descontrolada, con signos y síntomas que indicaban un alto riesgo de tormenta tiroidea, una emergencia médica que puede ser potencialmente mortal. La falta de respuesta a tratamientos convencionales y la contraindicación del tiamazol por agranulocitosis hicieron necesaria la intervención quirúrgica. El manejo anestésico fue cuidadosamente planificado para minimizar los riesgos asociados a la hiperactividad tiroidea y al tamaño del bocio, utilizando técnicas que redujeron la estimulación del sistema nervioso y mantuvieron la estabilidad hemodinámica.\n\n**Próximos Pasos**  \nDespués de la cirugía, la paciente presentó analgesia efectiva durante 12 horas y requirió un solo rescate analgésico. Se observó disfonía (alteración de la voz) persistente, probablemente relacionada con la manipulación quirúrgica de los nervios laríngeos, pero sin dolor al tragar. Será importante realizar un seguimiento para evaluar la función vocal y ajustar el tratamiento hormonal tiroideo según sea necesario para evitar complicaciones a largo plazo. Además, se debe monitorizar la recuperación general y prevenir posibles efectos secundarios derivados de la cirugía y la enfermedad de base."
+        }
+    },
+    {
+        "article": "Una mujer de 30 años de edad, embarazada de 3, para 3, se presentó con disminución de la micción, dolor en el flanco izquierdo y fiebre durante 2 días después de una cesárea de emergencia por primera vez, indicada debido a la angustia materna y fetal secundaria al trabajo de parto prolongado y sangrado vaginal prolongado en el hospital Al-Thora, Ibb, Yemen. A pesar de los esfuerzos de reanimación, su recién nacido falleció después de 45 minutos. Durante la cesárea, se identificaron severas adherencias uterinas (ya que había lesiones de endometriosis y adherencias entre la pared posterior del útero y el colon sigmoide), y una pérdida de sangre estimada de 1500 cc, según el informe del ginecólogo. La paciente no recibió atención prenatal durante su embarazo. No es fumadora y negó condiciones médicas crónicas, abuso de drogas, intoxicación accidental o antecedentes quirúrgicos previos.\n\nEn el examen físico, el paciente se veía pálido, enfermo y febril durante la evaluación inicial, con una temperatura oral de 38 °C, pulso de 80 latidos por minuto y presión arterial de 95/70 mm Hg. El abdomen del paciente estaba levemente distendido, con sensibilidad moderada, principalmente en el cuadrante inferior izquierdo.\n\nLos datos de laboratorio fueron los siguientes: el recuento de glóbulos blancos (WBC) fue de 15,3 × 103/mL, con 90% de neutrófilos polimórficos (leucocitosis con predominio neutrofílico), la hemoglobina fue de 7,5 g/dL, el recuento de plaquetas fue de 200 × 103/µL, el nitrógeno ureico en sangre (BUN) fue de 23 mg/dl y la creatinina fue de 3,8 mg/dl. Otros análisis de sangre, como los de la función hepática y los de coagulación, estuvieron dentro de los rangos normales. La ecografía (US) mostró una hidronefrosis izquierda grave y un fluido libre moderado en la cavidad abdominal. Se realizó la aspiración de la punción abdominal y la creatinina en el punto fue de 52 mg/dL, lo que indica que el fluido era orina.\n\nLa paciente fue resucitada con glóbulos rojos concentrados y una amplia cobertura antibiótica. Después de esto, se le realizó una ureteroscopia urgente que mostró una oclusión total del uréter izquierdo. Se tomó la decisión de realizar una exploración quirúrgica, dada la inestabilidad hemodinámica, la falta de equipos de nefrostomía percutánea y la evidencia de contaminación intraabdominal. Durante la operación, se encontró fluido libre moderado en la cavidad abdominal. El uréter izquierdo fue aplastado y ligado con una sutura Vicryl (5 agujas) a unos 5 cm de su parte distal. Después de evacuar el fluido, se extirpó el segmento lesionado del uréter y se realizó una ureteroneocistostomía de forma refluyente tras distender la vejiga con solución salina a través del catéter. Además, diseccionamos el uréter, con cuidado, de los tejidos circundantes en dirección cefálica, espatulamos el extremo distal del uréter e insertamos un stent doble. Se implantó el uréter en la cúpula posterior de la vejiga urinaria con anastomosis sin tensión y se suturó con Vicryl 4-0 a través del uréter de espesor completo, luego la capa mucosa de la vejiga y la capa detrusora. Se insertó un drenaje Jackson-Pratt (JP) cerca de la anastomosis y se cerró la pared abdominal tras evaluar el contenido intraperitoneal.\n\n\nSeguimiento y resultado\nSe iniciaron líquidos transparentes el segundo día postoperatorio. La paciente tenía distensión abdominal leve, dolor y náuseas. El tercer día postoperatorio, tenía una distensión abdominal creciente y dejó de expulsar flatos. La ecografía abdominal mostró una gran cantidad de acumulación en la cavidad peritoneal. Los datos de laboratorio de sangre mostraron una leucocitosis (WBC de 22 × 103/mL con un cambio a la izquierda).\n\nUna tomografía computarizada (TC) del abdomen y la pelvis con contraste reveló una cantidad significativa de aire libre y líquido en todo el abdomen y la pelvis adyacente a la pared abdominal anterior. También se observaron múltiples localizaciones de gas libre en el mesenterio, con realce de contraste de múltiples bucles intestinales pequeños, sin evidencia de extravasación de contraste. Los hallazgos sugirieron una víscera perforada. Después de consultar al equipo de cirugía general, la paciente fue llevada inmediatamente al quirófano para una laparotomía exploratoria, que reveló una pequeña perforación en la parte rectosigmoidea con algo de derrame, peritonitis con edema del asa intestinal y alteración de la anastomosis ureteral. La complejidad de este caso nos obligó a realizar intervenciones en varias etapas de manera multidisciplinaria. En primer lugar, el ginecólogo realizó una histerectomía debido a endometritis (confirmada histopatológicamente), supuración severa y alteración de la sutura del útero. En segundo lugar, un urólogo realizó una derivación ureterocutánea del uréter izquierdo y se creó una urostomía en el lado izquierdo. Por último, el cirujano general realizó el procedimiento de colostomía después de reparar la lesión del colon y se creó una colostomía en el lado izquierdo. En el quinto día postoperatorio, se produjo retracción de la colostomía con infección de la herida y se observó comunicación entre la colostomía y la urostomía. Se decidió realizar una reexploración para reubicar la colostomía sigmoidea y se realizó una colostomía transversal derecha. Una semana después de la operación, la paciente experimentó una infección superficial de la pared abdominal complicada con dehiscencia de la herida e hipoalbuminemia (albúmina: 2 g/dL) que requirió tratamiento con varios desbridamientos, irrigación de la herida, antibióticos y terapia de apoyo. Los antibióticos recomendados fueron linezolid (600 mg IV cada 12 horas durante 7 días), luego cambiaron a ceftriaxona (1 g IV cada 12 horas durante 5 días) más metronidazol (500 mg IV cada 12 horas durante 5 días) y cambiaron a ciprofloxacina oral (500 mg cada 12 horas por vía oral durante 7 días). Gradualmente, reanudó su dieta normal y fue dada de alta 30 días después en condiciones estables. Requería atención domiciliaria para ayudarla con la colostomía, la ureterostomía y la deambulación.\n\nSeis meses después, se cerró la colostomía y se anastomosó el uréter mediante el procedimiento de colgajo de vejiga tabular de Boari (la vejiga se abrió en su superficie anterior y se volteó un colgajo de vejiga de espesor completo caudalmente y se tabularizó para anastomosis al segmento ureteral proximal después de la inserción de la endoprótesis doble J). Después de una recuperación postoperatoria sin incidentes, se dio de alta a la paciente el séptimo día postoperatorio. El seguimiento de un mes mediante ecografía y cistouretrografía miccional mostró un aspecto normal de la vejiga con capacidad vesical adecuada y un sistema del tracto urinario superior normal. Tres meses después, la ureteroscopia retrógrada mostró un calibre adecuado del uréter. Se hizo un seguimiento regular de la paciente con ecografía durante 3 meses durante un año. La paciente no tuvo síntomas irritativos o gastrointestinales en los 2 años de seguimiento.\n",
+        "gold_summary": "Una mujer de 30 años presentó disminución de la micción durante 2 días después de una cesárea. La ecografía mostró una hidronefrosis izquierda grave y un fluido abdominal libre moderado. Una ureteroscopia reveló una oclusión total del uréter izquierdo y, posteriormente, se realizó una ureteroneocistostomía. Dos días después, la paciente presentó complicaciones con distensión abdominal que requirieron una nueva exploración. La exploración reveló lesiones en el colon (recto-sigmoide), peritonitis, endometritis y alteración de la anastomosis ureteral. Se realizó una colostomía, reparación de lesiones en el colon, histerectomía y derivación ureterocutánea. La estancia hospitalaria de la paciente fue complicada, con retracción estomal que requirió revisión quirúrgica y dehiscencia de la herida, que se trató de forma conservadora. Después de 6 meses, se cerró la colostomía y se anastomosó el uréter mediante el procedimiento de colgajo de Boari.\n",
+        "synthetic_summary": {
+            "B1": "Una mujer tuvo un bebé con una operación. Después, le dolía y no podía hacer pipí bien. Los doctores vieron que un tubito que lleva la pipí estaba tapado. Hicieron una operación para arreglarlo.\n\nDespués, la mujer se sintió peor y su pancita se hizo grande. Los doctores encontraron que tenía heridas en su pancita y en otros lugares. Hicieron más operaciones para ayudarla y poner todo bien.\n\nLa mujer estuvo en el hospital mucho tiempo. Poco a poco, se fue mejorando. Después de seis meses, los doctores cerraron una abertura que le habían hecho y arreglaron el tubito de la pipí otra vez. Ahora está bien y sin dolor.",
+            "B2": "**Lo que pasó con la paciente**  \nUna mujer de 30 años tuvo problemas para orinar durante dos días después de una cesárea, que es una operación para sacar al bebé. Al hacerle una ecografía, los médicos vieron que tenía una hinchazón grave en el riñón izquierdo llamada hidronefrosis, causada por la acumulación de orina, y también encontraron líquido libre en su abdomen. Luego, con un examen llamado ureteroscopia, descubrieron que el tubo que lleva la orina desde el riñón a la vejiga (el uréter izquierdo) estaba completamente bloqueado.\n\n**Tratamiento inicial**  \nPara arreglar este problema, los médicos hicieron una cirugía llamada ureteroneocistostomía, que consiste en conectar el uréter a la vejiga de nuevo para que la orina pueda salir. Sin embargo, dos días después, la paciente tuvo dolor y su abdomen se hinchó más, lo que indicaba que algo no estaba bien.\n\n**Complicaciones y nuevas cirugías**  \nAl revisarla otra vez, encontraron que tenía una infección grave en el abdomen (peritonitis), una herida en el colon (parte del intestino) y una inflamación en el útero (endometritis). También la conexión del uréter que habían hecho estaba dañada. Por eso, los médicos tuvieron que hacer varias cirugías: quitaron el útero (histerectomía), repararon el colon y crearon una abertura en la piel para que la orina y las heces pudieran salir por separado (derivación ureterocutánea y colostomía).\n\n**Recuperación y seguimiento**  \nLa recuperación fue difícil porque la paciente tuvo problemas con las heridas y la abertura del colon se contrajo, lo que necesitó otra cirugía. También tuvo infecciones que se trataron con antibióticos y cuidados especiales. Después de seis meses, los médicos cerraron la abertura del colon y volvieron a conectar el uréter usando una técnica llamada colgajo de Boari, que usa parte de la vejiga para reparar el uréter.\n\n**Resultado final**  \nTras esta última cirugía, la paciente se recuperó bien. Los controles con ecografías y otros estudios mostraron que su vejiga y riñones funcionaban normalmente. Durante dos años de seguimiento, no tuvo problemas ni síntomas molestos.",
+            "B3": "**Contexto**  \nUna mujer de 30 años, embarazada por tercera vez, fue sometida a una cesárea de emergencia debido a complicaciones durante el trabajo de parto, incluyendo sangrado prolongado y sufrimiento fetal. Tras la cesárea, presentó disminución en la cantidad de orina, dolor en el costado izquierdo y fiebre. Durante la cirugía se detectaron adherencias severas en el útero y lesiones compatibles con endometriosis, además de una pérdida significativa de sangre. La paciente no había recibido atención prenatal y no presentaba antecedentes médicos relevantes.\n\n**Hallazgos Clave**  \n- Exámenes iniciales mostraron leucocitosis con predominio neutrofílico (indicativo de infección), anemia moderada y deterioro de la función renal (elevación de creatinina).  \n- La ecografía evidenció una hidronefrosis grave (dilatación del riñón por obstrucción) en el lado izquierdo y presencia de líquido libre en la cavidad abdominal, que resultó ser orina al analizarse.  \n- La ureteroscopia urgente identificó una obstrucción completa del uréter izquierdo.  \n- Se realizó una cirugía para extirpar el segmento dañado del uréter y se reconstruyó la conexión entre el uréter y la vejiga (ureteroneocistostomía), con colocación de un stent para mantener el flujo urinario.\n\n**Interpretación Clínica**  \nPocos días después de la cirugía, la paciente desarrolló distensión abdominal progresiva, dolor y ausencia de expulsión de gases, signos sugestivos de complicaciones intraabdominales. Estudios por imagen mostraron aire y líquido libre en el abdomen, lo que indicaba una posible perforación intestinal. La laparotomía exploratoria confirmó perforación en el colon rectosigmoide, peritonitis (inflamación del revestimiento abdominal), infección del útero (endometritis) y problemas en la reparación del uréter. Debido a la complejidad y gravedad del cuadro, se realizaron múltiples intervenciones: histerectomía para controlar la infección uterina, derivación urinaria mediante ureterostomía para proteger el tracto urinario, y reparación del colon con creación de colostomía para desviar las heces.\n\nDurante la hospitalización, la paciente presentó complicaciones adicionales como retracción de la colostomía con infección y dehiscencia (apertura) de la herida abdominal, que requirieron revisiones quirúrgicas y tratamiento con antibióticos y cuidados locales. La recuperación fue gradual, y la paciente fue dada de alta en condiciones estables tras un mes de hospitalización.\n\n**Próximos Pasos y Seguimiento**  \nSeis meses después, se realizó el cierre de la colostomía y la reconstrucción definitiva del uréter mediante el procedimiento de colgajo de Boari, que utiliza un segmento de la vejiga para reemplazar la parte dañada del uréter. La recuperación postoperatoria fue satisfactoria, con estudios de imagen que mostraron una vejiga y tracto urinario superiores normales, y ureteroscopias que confirmaron un calibre adecuado del uréter. Durante dos años de seguimiento, la paciente no presentó síntomas urinarios ni gastrointestinales, evidenciando una recuperación completa y funcional.\n\n---\n\nEste caso ilustra la complejidad y gravedad de las complicaciones postoperatorias tras una cesárea en un contexto de falta de atención prenatal y lesiones previas, así como la importancia de un manejo multidisciplinario para resolver complicaciones urológicas, ginecológicas y gastrointestinales simultáneas."
+        }
+    },
+    {
+        "article": "Mujer de 43 años, con antecedente de hipertensión arterial con tratamiento con losartán, dos cesáreas y oclusión tubaria bilateral. Ingresó a nuestro hospital y refirió dolor de 24 horas de evolución, tipo cólico en hipogastrio e irradiación a fosa iliaca izquierda, además de náusea y vómito en dos ocasiones. Se agregaron evacuaciones semilíquidas en forma inicial y posteriormente cese en las evacuaciones y en la canalización de gases. A la exploración física, la paciente presentó dolor en el abdomen, así como distensión, especialmente hacia el flanco izquierdo. En el mesogastrio y el flanco izquierdo hubo la presencia de timpanismo. La peristalsis estaba presente, mínima, abolida en flanco izquierdo y mesogastrio. La irritación peritoneal estuvo ausente. Se colocó sonda nasogástrica, con gasto mínimo gástrico y sin mejoría en la sintomatología. Los estudios de laboratorio demostraron: 9700 leucocitos con un 87% de neutrófilos, creatinina de 0.7 mg/dL, urea de 22 mg/dL y proteína C reactiva de 5.0 mg/L. En la radiografía simple de abdomen presentó dilatación importante del lado izquierdo del colon, con niveles hidroaéreos. La tomografía muestra la dilatación del colon del lado izquierdo, con imagen que simula grano de café en el corte coronal.\n\nAnte estos hallazgos clínicos y de imagen, se decidió hacer laparotomía de urgencia ante la sospecha de la presencia de vólvulo de sigmoides o de síndrome adherencial complicado. Durante la cirugía se evidenció un ciego flexionado hacia adelante y a la izquierda, carente de fijación retroperitoneal. El punto de flexión fue producido por una banda de adherencia colocada sobre el colon ascendente. Se realizó liberación de la adherencia y se corroboró continuidad adecuada hacia el colon distal. No se evidenció la presencia de isquemia, necrosis o perforación del ciego. Se realizó apendicectomía con descompresión del ciego a través de base apendicular y posteriormente ligadura de esta. Se llevó a cabo cecopexia hacia pared de fosa iliaca derecha. Después de la cirugía, hubo mejoría clínica de la paciente, que tuvo evacuaciones presentes normales. La paciente siguió controles correctos en consulta externa de cirugía y se mantuvo asintomática.",
+        "gold_summary": "Mujer de 43 años que ingresó a un servicio de urgencias con datos de obstrucción intestinal. Se realizó tomografía simple de abdomen donde se identificó dilatación del colon e imagen que semejaba un grano de café invertido. Se hizo laparotomía exploradora y se identificó vólvulo cecal del tipo báscula, sin compromiso vascular. Se realizó desvolvulación, descompresión a través de apendicectomía, y cecopexia. Posterior a evento quirúrgico, la paciente se recuperó sin incidentes y fue dada de alta con controles adecuados por consulta externa.",
+        "synthetic_summary": {
+            "B1": "Una señora tenía dolor en su barriga y no podía ir al baño bien. Los doctores le hicieron una foto especial para ver su barriga. Vieron que un pedazo de su barriga estaba doblado y tapado. La señora tuvo una operación para arreglar ese problema. Los doctores quitaron la parte que estaba doblada y la dejaron bien. Después de la operación, la señora se sintió mejor y pudo ir al baño normalmente. Ahora está bien y los doctores la revisan para cuidar que siga sana.",
+            "B2": "**Lo que pasó con la paciente**\n\nUna mujer de 43 años llegó al hospital porque tenía dolor en el abdomen, vómitos y problemas para evacuar. Los médicos hicieron estudios y vieron que una parte del intestino grueso, llamada colon, estaba muy inflamada y bloqueada. En la tomografía, que es una imagen especial del cuerpo, notaron una forma que parecía un \"grano de café\" invertido, lo que les hizo sospechar que había un problema llamado vólvulo, que es cuando el intestino se gira y se tapa.\n\n**Lo que hicieron los médicos**\n\nDecidieron hacer una cirugía urgente para ver qué pasaba. Durante la operación, encontraron que una parte del intestino llamada ciego estaba doblada y no estaba bien sujeta en su lugar. Esto causaba que el intestino se girara (vólvulo), pero sin dañar el flujo de sangre. Para arreglarlo, quitaron una banda de tejido que estaba causando el problema, hicieron una apendicectomía (que es sacar el apéndice) para descomprimir el intestino, y fijaron el ciego a la pared del abdomen para que no se moviera otra vez.\n\n**Qué pasó después**\n\nDespués de la cirugía, la paciente mejoró mucho. Empezó a evacuar normalmente y no tuvo más síntomas. Fue dada de alta y siguió controles médicos para asegurarse de que todo estuviera bien.",
+            "B3": "**Contexto:**  \nUna mujer de 43 años con antecedentes de hipertensión arterial, dos cesáreas previas y oclusión tubaria bilateral, ingresó al hospital presentando dolor abdominal intenso de tipo cólico en la parte baja del abdomen (hipogastrio), que se irradiaba hacia el lado izquierdo, acompañado de náuseas, vómitos y cambios en sus evacuaciones intestinales, incluyendo inicialmente heces semilíquidas y luego ausencia de evacuaciones y gases. En la exploración física, se detectó distensión abdominal y dolor localizado, especialmente en el lado izquierdo, con presencia de sonidos intestinales reducidos o ausentes en esa zona, pero sin signos de irritación peritoneal (inflamación de la membrana que recubre los órganos abdominales). Los análisis de sangre mostraron un aumento moderado de glóbulos blancos y proteína C reactiva, indicadores de inflamación o infección. La radiografía y la tomografía computarizada del abdomen revelaron una dilatación significativa del colon izquierdo y una imagen característica en forma de “grano de café”, que sugiere torsión intestinal.\n\n**Hallazgos Clave:**  \nAnte la sospecha de una obstrucción intestinal grave, posiblemente causada por torsión del colon (vólvulo de sigmoides) o adherencias (bandas de tejido cicatricial que pueden causar obstrucción), se decidió realizar una cirugía de emergencia (laparotomía). Durante la operación, se encontró que el ciego (la primera parte del colon) estaba anormalmente desplazado y flexionado hacia adelante y hacia la izquierda, sin estar fijado a la pared abdominal como es habitual. Esta torsión fue causada por una banda de adherencia sobre el colon ascendente. No se observaron signos de daño grave como falta de riego sanguíneo (isquemia), muerte del tejido (necrosis) o perforación. Se liberó la adherencia que causaba la torsión, se descomprimió el ciego mediante la extracción del apéndice (apendicectomía) y se fijó el ciego a la pared abdominal (cecopexia) para evitar futuras torsiones.\n\n**Interpretación Clínica:**  \nEl diagnóstico final fue un vólvulo cecal del tipo “báscula”, una torsión del ciego que puede provocar obstrucción intestinal pero que en este caso no comprometió la circulación sanguínea ni causó daño irreversible. La intervención quirúrgica oportuna permitió resolver la obstrucción, evitar complicaciones mayores y preservar la integridad del colon.\n\n**Próximos Pasos:**  \nTras la cirugía, la paciente mostró una recuperación favorable, con retorno normal de las evacuaciones intestinales y ausencia de síntomas. Fue dada de alta y se mantuvo en seguimiento ambulatorio con controles periódicos en consulta externa de cirugía, donde continuó asintomática y sin complicaciones. Este caso resalta la importancia del diagnóstico temprano y tratamiento quirúrgico adecuado en pacientes con obstrucción intestinal por vólvulo cecal."
+        }
+    },
+    {
+        "article": "Paciente de sexo femenino de 10 años, sin historia familiar de enfermedad tiroidea, portadora de bocio diagnosticado a los 9 años (ecografía tiroidea con sig nos compatibles de tiroiditis crónica) con presencia de anticuerpos antitiroideos positivos. Sin tratamiento al momento del ingreso hospitalario. Consultó por orina de aspecto espumoso de 5 días de evolución, asociado a dolor abdominal, vómitos profusos y diarrea. Evo lucionó con edema palpebral y de extremidades, disminución de la diuresis, decaimiento y fiebre de 38° C el día previo a su ingreso. Al momento de su eva luación en el servicio de urgencia destacó una pacien te con edema palpebral bilateral y pretibial, con bocio evidente (indoloro y sin nódulos palpables) y presen cia de soplo sistólico eyectivo en foco pulmonar IV/VI sin irradiación. Resto del examen sin alteraciones de significancia. Presión arterial 120/78 mmHg (percentil 95), temperatura 38,1°C, peso: 33.9 Kg, talla: 131,5 cm (p7), IMC 19,8 (p83).\n\nDentro de sus exámenes de admisión destacaron examen de orina completa con proteinuria +++, sin bacterias, sin nitritos, leucocitos 7 cel/uL (VN: 0-10 cel/uL), eritrocitos 4 cel/uL (VN: 0-15 cel/uL), índice proteinuria/creatininuria (IPC) 2 mg/mg, proteínas totales de 3.8 g/dL, hipoalbuminemia de 2,1 g/dL, hipercolesterolemia de 416 mg/dL, hipertrigliceridemia de 127 mg/dL y creatinina plasmática de 0,46 mg/dL (aclaramiento de creatinina calculado por fórmula de Schwartz: 125 ml/min/1,73 m2). Gases venosos, elec trolitos plasmáticos y hemograma dentro de rangos normales. En cuanto al estudio inmunológico destacó: inmunoglobulina A 181 mg/dL (VN 45-236), inmunoglobulina M 131 mg/dL (VN 52-242), inmunoglobulina G 208 (VN 608-1572) mg/dL, C3 125 mg/dL (VN 80-150), C4 37,3 mg/dL (VN 12-36). Ecografía renal normal. Se ingresó a la paciente con diagnóstico de SN y tiroiditis autoinmune.\n\nEn el contexto de SN se inició tratamiento con prednisona (60 mg/m2/día), con buena respuesta, logrando fundir edema y disminuir progresivamente la proteinuria hasta alcanzar rangos normales previo al egreso (IPC de egreso: 0.09, a los 6 días).\n\nDel punto de vista de función tiroidea su estudio mostró hormona tiroestimulante (TSH) 4,4 UI/ml (VN: 0,67-4,16 UI/ml), tiroxina (T4) libre 0,80 ng/ dL (VN: 0,86-1,4 ng/dL), anticuerpos antiperoxidasa (Anti Tpo) 120 U/ml (VN: 0-60 U/ml), anticuerpos antitiroglobulina (Anti-Tg) 82 U/ml (VN: 0-60 U/ ml), por lo que se inició terapia de sustitución con levotiroxina (25 mcg/día). La ecografía tiroidea descri bió tiroides de tamaño normal con leve aumento de vascularización difusa al Doppler, sin lesiones focales sólidas ni quísticas, siendo estos hallazgos sugerentes de tiroiditis. Resto del estudio (PCR para SARS CoV-2, anticuerpos anti citoplasma de neutrófilos, anticuer pos anti nucleares, anticuerpos anti DNA, anticuerpos anti estreptolisina O, anticuerpos anticardiolipinas, anticuerpos anti mieloperoxidasa y anticuerpos anti proteinasa 3) resultó negativo.\n\nA los 6 días de ingresada la paciente se encontraba en buenas condiciones, siendo dada de alta con prednisona (60 mg al día) y levotiroxina (25 ucg al día). En el seguimiento a los 12 meses la paciente se encontraba asintomática, con su patología tiroidea bajo control (TSH 1,11 UI/ml) con tratamiento de sustitución. No ha presentado recaídas del SN (examen de orina sin proteinuria y creatinina 0,44 mg/dL).",
+        "gold_summary": "Paciente de 10 años que se presenta con síndrome nefrótico y bocio. Se pesquisa antecedente de tiroiditis autoinmu ne e hipotiroidismo no tratado. Se inicia terapia corticoidal y hormonal de sustitución (levotiroxina), logrando buena respuesta clínica y de laboratorio.",
+        "synthetic_summary": {
+            "B1": "Niña de 10 años con hinchazón en el cuerpo y cuello grande. Tenía un problema en la tiroides que no se había tratado. Le dieron medicinas para ayudar su cuerpo y se puso mejor.",
+            "B2": "**Lo que le Pasó a la Paciente**  \nUna niña de 10 años llegó al hospital con hinchazón en los ojos y las piernas, además de orina con espuma. Ella tenía un bocio, que es cuando la glándula tiroides en el cuello está agrandada. También se sabía que tenía tiroiditis autoinmune, una enfermedad donde el cuerpo ataca su propia tiroides, y no estaba tomando ningún medicamento para eso.\n\n**Qué Encontraron en los Exámenes**  \nLos análisis de orina mostraron mucha proteína, lo que indica que los riñones no estaban funcionando bien. Esto se llama síndrome nefrótico, una condición que causa que el cuerpo pierda proteínas importantes. Además, sus niveles de algunas hormonas de la tiroides estaban bajos y tenía anticuerpos que confirmaban la tiroiditis. La ecografía del cuello mostró inflamación en la tiroides, pero sin tumores.\n\n**Cómo la Trataron y Qué Pasó Después**  \nLe dieron un medicamento llamado prednisona, que es un corticoide para reducir la inflamación, y levotiroxina, que es una hormona para ayudar a su tiroides a funcionar mejor. Con este tratamiento, la hinchazón bajó y los análisis mejoraron rápidamente. Después de un año, la niña estaba bien, sin síntomas y con su tiroides controlada gracias a la medicación. No tuvo problemas nuevos en los riñones.",
+            "B3": "**Contexto:**  \nSe trata de una niña de 10 años con diagnóstico previo de bocio (aumento visible de la glándula tiroides) y tiroiditis autoinmune (una inflamación de la tiroides causada por el propio sistema inmunológico), sin tratamiento para su hipotiroidismo (función tiroidea disminuida) al momento de su ingreso hospitalario. Consultó por síntomas relacionados con síndrome nefrótico, que incluyen orina espumosa, edema (hinchazón) en párpados y extremidades, disminución de la cantidad de orina, dolor abdominal, vómitos y fiebre.\n\n**Hallazgos Clave:**  \n- En la evaluación inicial, se observó edema palpebral bilateral y en las piernas, así como un bocio evidente pero sin nódulos dolorosos. Además, presentó un soplo cardíaco leve.  \n- La presión arterial estaba en el límite superior normal para su edad.  \n- Los análisis de orina mostraron una proteinuria significativa (pérdida elevada de proteínas en la orina), sin signos de infección.  \n- En sangre, se detectó hipoalbuminemia (niveles bajos de albúmina, una proteína importante), hipercolesterolemia y niveles normales de creatinina, indicando función renal preservada.  \n- Los estudios inmunológicos confirmaron la presencia de anticuerpos antitiroideos elevados, compatibles con tiroiditis autoinmune, y niveles normales de otros marcadores inflamatorios y autoinmunes.  \n- La ecografía tiroidea mostró un tamaño normal de la glándula pero con aumento difuso de la vascularización, típico de tiroiditis.  \n- No se encontraron otras enfermedades autoinmunes o infecciones asociadas.\n\n**Interpretación Clínica:**  \nLa paciente presentó un síndrome nefrótico (una enfermedad renal caracterizada por pérdida excesiva de proteínas en la orina y edema) asociado a una tiroiditis autoinmune con hipotiroidismo no tratado. La coexistencia de estas dos condiciones autoinmunes sugiere un trastorno inmunológico subyacente que afecta tanto la tiroides como el riñón.\n\n**Próximos Pasos y Tratamiento:**  \nSe inició tratamiento con prednisona (un corticosteroide) para controlar el síndrome nefrótico, logrando una rápida mejoría clínica y normalización de la proteinuria en pocos días. Paralelamente, se comenzó terapia de reemplazo hormonal con levotiroxina para corregir el hipotiroidismo. La paciente fue dada de alta en buenas condiciones y, tras un seguimiento de 12 meses, se mantuvo asintomática, con función tiroidea controlada y sin recaídas del síndrome nefrótico.\n\nEste caso destaca la importancia de identificar y tratar de manera integral las enfermedades autoinmunes coexistentes para lograr una recuperación óptima y prevenir complicaciones a largo plazo."
+        }
+    },
+    {
+        "article": "La exploración neurológica exhaustiva puso de manifiesto una apariencia facial característica: mirada fija con los ojos muy abiertos, fruncimiento de la frente con una expresión de ceño fruncido (signo del procerus) y expresión fija de la parte inferior de la cara. La paciente presentaba hipocinesia-rigidez simétrica de predominio axial con postura retrocólica del tronco y el cuello. El examen de la deambulación reveló un patrón de la marcha del nivel superior caracterizado por una llamativa vacilación inicial que requería ayuda de objetos/personas cercanas. Una vez que comenzaba a caminar, los pasos mejoraban relativamente, pero volvía a aparecer una marcha inefectiva cuando intentaba girar. Exhibía zancadas cortas, congelación, base amplia de sustentación, desequilibrio, movimiento lento de los miembros inferiores, arrastre de los pies y pérdida de la fluidez normal del tronco y las extremidades. Los reflejos posturales estaban alterados. Asimismo, existía una dificultad grave para la bipedestación tras la sedestación y dificultad para darse la vuelta en la cama. Sin embargo, los signos frontales, como la rigidez paratónica, los reflejos de prensión, la incontinencia urinaria y las características de los déficits cognitivos frontales (por ejemplo, cambios disejecutivos y de personalidad e impulsividad) estaban ausentes, excepto por un estado apático progresivo. Los movimientos oculares sacádicos verticales estaban alterados, con amplitudes relativamente normales y movimientos sacádicos horizontales. Se evidenciaron sacadas de onda cuadrada y una oftalmoplejía supranuclear. La resonancia magnética del cerebro reveló atrofia del mesencéfalo, dilatación del acueducto de Silvio y del III ventrículo y atrofia de los lóbulos frontales, y los signos típicos del colibrí y de la gloria de la mañana. Finalmente, la paciente fue diagnosticada de una PSP probable.",
+        "gold_summary": "Mujer de 58 años sana que consultó por un trastorno de la marcha con caídas. La exploración neurológica mostró una apariencia facial característica (mirada fija, ojos muy abiertos, ceño fruncido y expresión fija hemifacial inferior), e hipocinesia-rigidez simétrica de predominio axial (postura retrocólica del tronco y el cuello). La exploración de la marcha reveló un trastorno de la marcha del nivel superior, caracterizado por una significativa vacilación inicial, que precisaba ayuda de objetos/personas cercanos. Al iniciar la marcha, los pasos mejoraban relativamente, pero reaparecía una deambulación inefectiva al girar. Presentaba zancadas cortas, congelación, base amplia de sustentación, desequilibrio, movimiento lento de las piernas, arrastre de los pies, y pérdida de la cadencia normal del tronco y las extremidades. Los reflejos posturales estaban alterados. La resonancia magnética cerebral desveló atrofia mesencefálica, dilatación de acueducto de Silvio y III ventrículo, atrofia frontal bilateral y el signo típico del colibrí. Finalmente, la paciente fue diagnosticada de una PSP probable.",
+        "synthetic_summary": {
+            "B1": "Había una señora que tenía problemas para caminar. Sus ojos se veían muy abiertos y su cara parecía quieta. Caminaba con pasos cortos y a veces se paraba sin poder seguir. Le costaba mucho girar y mantener el equilibrio. Su cuerpo estaba un poco rígido y lento. En el doctor, vieron que su cerebro estaba un poco cambiado. Por eso, dijeron que tenía una enfermedad que hace difícil caminar y moverse bien.",
+            "B2": "**Lo que Encontraron en la Paciente**\n\nUna mujer de 58 años, que antes estaba sana, empezó a tener problemas para caminar y se caía con frecuencia. Al examinarla, los médicos notaron que su cara tenía una expresión especial: sus ojos estaban muy abiertos y fijos, tenía el ceño fruncido y la parte baja de su cara parecía inmóvil. También tenía rigidez y movimientos lentos en el tronco y el cuello, con una postura inclinada hacia atrás.\n\nCuando caminaba, al principio dudaba mucho y necesitaba ayuda para no caerse. Después de unos pasos, mejoraba un poco, pero al girar volvía a tener problemas para caminar bien. Sus pasos eran cortos, a veces se quedaba paralizada (congelación), mantenía los pies separados para no perder el equilibrio, y arrastraba los pies. Además, sus movimientos eran lentos y perdía la forma normal de mover el cuerpo y las piernas. Los reflejos que ayudan a mantener el equilibrio también estaban afectados.\n\n**Lo que Vieron en el Cerebro**\n\nUna resonancia magnética, que es una imagen detallada del cerebro, mostró que algunas partes importantes estaban más pequeñas de lo normal. En especial, el mesencéfalo (una parte del cerebro que controla movimientos), el acueducto de Silvio y el tercer ventrículo (espacios llenos de líquido en el cerebro) estaban dilatados o agrandados. También había pérdida de tejido en los lóbulos frontales, que son áreas importantes para pensar y controlar movimientos. Además, apareció un signo especial llamado \"signo del colibrí\", que ayuda a los médicos a identificar esta enfermedad.\n\n**Qué Significa Todo Esto**\n\nCon estos síntomas y los resultados del examen, los médicos concluyeron que la paciente probablemente tiene una enfermedad llamada parálisis supranuclear progresiva (PSP). Esta enfermedad afecta el control de los movimientos, el equilibrio y la expresión facial, y suele empeorar con el tiempo. Aunque no tiene algunos síntomas típicos como problemas graves en la vejiga o cambios fuertes en la personalidad, sí muestra apatía, que es una falta de interés o motivación. Este diagnóstico ayudará a los médicos a planear el mejor cuidado para ella.",
+            "B3": "**Contexto**\n\nUna mujer de 58 años, previamente sana, acudió a consulta debido a problemas para caminar acompañados de caídas frecuentes. La evaluación neurológica detallada reveló signos característicos en su rostro y movimientos, así como alteraciones específicas en su forma de caminar y en estudios de imagen cerebral.\n\n**Hallazgos Clave**\n\n- **Apariencia facial característica:** La paciente mostraba una mirada fija con los ojos muy abiertos, fruncimiento de la frente que generaba una expresión de ceño fruncido (conocido como signo del procerus) y una expresión fija en la parte inferior de la cara.\n\n- **Alteraciones motoras:** Presentaba hipocinesia (movimientos lentos) y rigidez simétrica, principalmente en la zona axial, es decir, en el tronco y cuello, con una postura inclinada hacia atrás (retrocolis).\n\n- **Trastorno de la marcha:** La forma de caminar mostraba un patrón típico de afectación del nivel superior del sistema nervioso. Inicialmente, la paciente vacilaba notablemente y necesitaba apoyo de objetos o personas para comenzar a caminar. Al avanzar, sus pasos mejoraban algo, pero al intentar girar reaparecía una marcha ineficaz. Además, caminaba con pasos cortos, episodios de congelación (parálisis temporal de la marcha), base amplia para mantener el equilibrio, desequilibrio general, movimientos lentos de las piernas, arrastre de los pies y pérdida de la fluidez normal del tronco y extremidades. Los reflejos posturales, que ayudan a mantener la estabilidad, estaban alterados.\n\n- **Movimientos oculares:** Se observaron alteraciones en los movimientos sacádicos (movimientos rápidos del ojo para cambiar la mirada), especialmente en la dirección vertical, con una oftalmoplejía supranuclear, que implica dificultad para mover los ojos hacia arriba o abajo debido a un problema en el cerebro.\n\n- **Ausencia de otros signos frontales:** No se detectaron rigidez paratónica (una rigidez muscular variable), reflejos de prensión (agarre involuntario), incontinencia urinaria ni déficits cognitivos frontales típicos (como problemas en la planificación, cambios de personalidad o impulsividad), salvo un estado de apatía progresiva.\n\n- **Imágenes cerebrales:** La resonancia magnética mostró atrofia (pérdida de volumen) del mesencéfalo (una parte del tronco cerebral), dilatación del acueducto de Silvio y del tercer ventrículo (estructuras por donde circula el líquido cefalorraquídeo), atrofia bilateral de los lóbulos frontales y la presencia de signos característicos conocidos como el “signo del colibrí” y la “gloria de la mañana”, que son patrones específicos de daño cerebral en esta enfermedad.\n\n**Interpretación Clínica**\n\nEl conjunto de síntomas, signos neurológicos y hallazgos en la resonancia magnética son compatibles con un diagnóstico probable de parálisis supranuclear progresiva (PSP), una enfermedad neurodegenerativa que afecta principalmente el control del movimiento, el equilibrio y los movimientos oculares, con daño en áreas profundas del cerebro.\n\n**Próximos Pasos**\n\nEl diagnóstico de PSP implica un seguimiento neurológico continuo para manejar los síntomas, prevenir caídas y mejorar la calidad de vida. Aunque actualmente no existe una cura, el tratamiento puede incluir terapias físicas, medicamentos para controlar la rigidez y la lentitud de movimientos, y apoyo multidisciplinario para abordar las dificultades motoras y cognitivas que puedan surgir."
+        }
+    },
+    {
+        "article": "Una mujer de 36 años, previamente sana, fue picada una vez por un insecto Hymenoptera desconocido, lo que le provocó hinchazón y eritema en la parte dorsal de la mano derecha. La fiebre punzante apareció en un plazo de 6 horas, a pesar de que el sitio de la picadura se volvió irreconocible gradualmente. Acudió a una clínica local donde le recetaron esteroides orales (prednisolona 20 mg/día) y antibióticos. Tres días después, acudió a nuestro departamento de urgencias por una fiebre intermitente. Presentaba una temperatura elevada (38,9°C), taquicardia e hipotensión (presión arterial 80/52 mmHg) en el momento de la clasificación. La electrocardiografía mostró fibrilación auricular con una frecuencia ventricular rápida de alrededor de 130 latidos por minuto y elevación difusa del ST. La radiografía de tórax mostró una relación cardiotorácica normal sin signos de infiltración o congestión. El hemograma no mostró eosinofilia, leucocitosis, leucopenia o desviación a la izquierda. La isoenzima MB de creatina cinasa (CK-MB) y la troponina cardíaca I se elevaron a 96,0 ng/mL y 8,0 ng/mL, respectivamente. La proteína C reactiva fue de 10,5 mg/L y la procalcitonina fue de 0,32 ng/mL. El NT-proBNP fue de 20 700 pg/mL. La ecocardiografía mostró una hipocinesia global del ventrículo izquierdo con una fracción de eyección del 30,6% y sin derrame pericárdico. El cateterismo cardíaco emergente no reveló lesiones de las arterias coronarias o vasospasmo. Se insertó un globo intraaórtico durante el procedimiento para el shock cardiogénico. La hipotensión progresó acompañada de taquicardia ventricular y fibrilación ventricular, y luego se produjo un paro cardíaco intrahospitalario. La reanimación cardiopulmonar manual no tuvo éxito durante 25 minutos y se usó el soporte cardiopulmonar percutáneo (PCPS, CAPIOX® Centrifugal Pump Controller SP-200, Terumo). La circulación espontánea se estableció 25 minutos después con una recuperación total de la conciencia.\n\nLa prueba rápida de antígeno de influenza (Directigen EZ Flu A+B; BD, Franklin Lakes, NJ, EE. UU.), los cultivos de esputo, los cultivos de sangre y los exámenes serológicos para los virus respiratorios recolectados al ingreso fueron negativos. En el día 2 del ingreso, los niveles séricos de CK-MB y troponina I alcanzaron un máximo de >303 ng/ml y >81 ng/ml, respectivamente. La ecocardiografía de seguimiento 24 horas después del inicio del PCPS mostró deterioro de la función ventricular izquierda, cierre persistente de las válvulas aórticas y trombos intracardiacos en la aurícula izquierda y el ventrículo izquierdo, aproximadamente 24 horas después del inicio del soporte mecánico. En el día 3, el shock progresó con falla multiorgánica. Se aplicó hemodiálisis venovenosa continua debido a la acidosis metabólica y oliguria. En el día 4, la función ventricular derecha también se deterioró gravemente y la actividad eléctrica del corazón desapareció gradualmente. El PCPS se cambió a soportes mecánicos bi-ventriculares a través de canalizaciones hacia la aurícula derecha, el tronco pulmonar, el ápex del ventrículo izquierdo y la aorta ascendente. Ambos sistemas se establecieron utilizando bombas de sangre centrífugas MEDTRONIC Affinity CP. Debido a la hemorragia pulmonar con consolidación bilateral severa de los pulmones, se usó un oxigenador de membrana para lograr una oxigenación adecuada. El flujo sanguíneo se estableció a 3.5 L/minuto, lo que podría mantener la presión arterial media en torno a 65 mmHg. Se realizó una biopsia endomiocárdica del ventrículo izquierdo y la patología reveló una inflamación significativa compuesta principalmente por linfocitos y algunos eosinófilos. El daño miocárdico con necrosis estuvo presente, pero no extenso. En términos de ajustes de ventilador, la presión de conducción y la presión de meseta se establecieron en torno a 15 y 30 cmH2O respectivamente para la protección pulmonar. Se usó la fibra broncoscopia repetidamente para eliminar los coágulos de sangre que obstruían las vías respiratorias principales. En el día 13 del ingreso, la actividad eléctrica del corazón del paciente permaneció ausente y ambas bombas de sangre se cambiaron a los sistemas de asistencia ventricular Levitronix Centri-Mag (Levitronix LLC, Waltham, MA, EE. UU.) para un mejor soporte. El paciente fue trasladado a un centro de trasplantes y se registró como candidato para un trasplante de corazón. En el día 14 se insertó otra cánula en la vena femoral común izquierda para aumentar el flujo de entrada del VAD derecho. Desde el día 14 hasta el día 48, el paciente sufrió episodios de sangrado masivo del mediastino y la vagina, infección de la herida esternal con formación de abscesos, infecciones por úlceras de presión y progresiva hiperbilirrubinemia. Su condición se estabilizó después de desbridamiento, hemostasia quirúrgica y uso de antibióticos fuertes. Se sometió a 5 cursos de intercambio de plasma terapéutico para evitar el rechazo mediado por anticuerpos y recibió un trasplante de corazón ortotópico el día 49. El estudio patológico del corazón del paciente mostró pancarditis de ambos ventrículos y ninguna alteración específica de las 3 arterias coronarias. La ECMO de VA se mantuvo hasta el día 58 para el apoyo postoperatorio del fallo cardiaco. La biopsia endomiocárdica repetida después del trasplante no mostró evidencia de rechazo celular o humoral. La paciente experimentó episodios de shock séptico bajo inmunosupresión y se sometió a una laparoscopia exploratoria y apendicectomía el día 93. La extubación se realizó el día 96 y se dio de alta el día 101. La paciente permaneció clínicamente estable en el seguimiento de 3 meses.\n\nMH - Adulto\nMH - Animales\nMH - Abejas\nMH - Picaduras y mordeduras/*complicaciones\nMH - Oxigenación por membrana extracorpórea\nMH - Mujer\nMH - Paro cardiaco/*etiología/tratamiento\nMH - Insuficiencia cardiaca/*etiología/terapia\nMH - *Trasplante de corazón\nMH - Dispositivos de asistencia cardiaca\nMH - Humanos\nMH - Hipersensibilidad/*diagnóstico\nMH - Miocarditis/*diagnóstico\nMH - Shock, Cardiogénico/*etiología/terapia\n",
+        "gold_summary": "Paciente: Mujer, 36 años\n\nDiagnóstico final: Shock cardiogénico • miocarditis\n\nSíntomas: Fiebre\n\nMedicación: —\n\nProcedimiento clínico: soporte circulatorio mecánico\n\nEspecialidad: Cirugía\n\n\nInforme del caso:\n\nReportamos el caso de una mujer de 36 años que desarrolló fiebre y shock cardiogénico 3 días después de una picadura de abeja. La angiografía cardíaca mostró arterias coronarias permeables y una función ventricular izquierda gravemente comprometida. Su hemodinámica permaneció inestable bajo una dosis alta de agentes inotrópicos y apoyo con un balón intraaórtico. El paro cardíaco intrahospitalario ocurrió 4 horas después del ingreso y recibió reanimación cardiopulmonar extracorpórea. Su oxigenación de membrana extracorpórea venosa periférica (VA ECMO) se cambió a dispositivos de asistencia ventricular bilateral (VAD) debido a una insuficiencia cardíaca derecha progresiva. El resultado de la biopsia endomiocárdica fue compatible con el cuadro de miocarditis por hipersensibilidad. Su corazón entró en paro persistente bajo apoyo circulatorio mecánico. Se sometió a un trasplante de corazón el día 49 del ingreso y permaneció clínicamente estable 6 meses después del alta.\n",
+        "synthetic_summary": {
+            "B1": "Una mujer de 36 años fue picada por una abeja. Tres días después, tuvo fiebre y su corazón se puso muy débil. Los doctores le ayudaron con máquinas para que su corazón pudiera latir. Su corazón no mejoró y se detuvo. Entonces, le pusieron un corazón nuevo. Después de eso, ella estuvo bien y fuerte.",
+            "B2": "Caso de una mujer de 36 años con problemas graves en el corazón tras una picadura de abeja\n\nLo que pasó:  \nUna mujer sana de 36 años fue picada por un insecto parecido a una abeja. Tres días después, empezó a tener fiebre y problemas serios en el corazón, llamados shock cardiogénico, que significa que el corazón no podía bombear suficiente sangre. Cuando la revisaron, sus arterias del corazón estaban normales, pero el ventrículo izquierdo (una parte importante del corazón) no funcionaba bien.\n\nQué hicieron los médicos:  \nIntentaron ayudarla con medicamentos para mejorar la fuerza del corazón y usaron un balón intraaórtico, que es un dispositivo que ayuda a que el corazón trabaje mejor. Sin embargo, su estado empeoró y sufrió un paro cardíaco, que es cuando el corazón deja de latir. La reanimaron usando una máquina especial que hace el trabajo del corazón y los pulmones (oxigenación por membrana extracorpórea o ECMO). Más tarde, cambiaron esta máquina por dispositivos que ayudan a ambos lados del corazón (asistencia ventricular bilateral), porque la parte derecha del corazón también empezó a fallar.\n\nQué encontraron:  \nTomaron una pequeña muestra del músculo del corazón (biopsia endomiocárdica) y vieron que tenía inflamación causada por una reacción alérgica, llamada miocarditis por hipersensibilidad. Esto significa que el corazón estaba dañado por la respuesta del cuerpo a la picadura.\n\nQué pasó después:  \nEl corazón dejó de funcionar completamente a pesar de las máquinas que lo ayudaban. Por eso, le hicieron un trasplante de corazón el día 49 después de entrar al hospital. Se recuperó bien y estuvo estable durante al menos seis meses después de salir del hospital.\n\nEn resumen:  \nUna picadura de abeja causó una inflamación grave en el corazón de esta mujer, que llevó a una falla cardíaca muy seria. Gracias a tratamientos avanzados y un trasplante de corazón, pudo recuperarse. Este caso muestra lo importante que es tratar rápido y con cuidado las reacciones alérgicas que afectan al corazón.",
+            "B3": "**Contexto**  \nSe presenta el caso de una mujer de 36 años, previamente sana, que desarrolló un cuadro grave de insuficiencia cardíaca tras una picadura de abeja. Inicialmente, la paciente presentó hinchazón y enrojecimiento en la mano derecha, seguidos de fiebre en menos de 6 horas. A pesar del tratamiento inicial con esteroides y antibióticos, evolucionó con fiebre intermitente, taquicardia, hipotensión y alteraciones electrocardiográficas que indicaban compromiso cardíaco.\n\n**Hallazgos Clave**  \nAl ingreso, la paciente mostró signos de shock cardiogénico (presión arterial baja y ritmo cardíaco acelerado con fibrilación auricular), elevación significativa de marcadores cardíacos (troponina I y CK-MB), y una función ventricular izquierda gravemente reducida (fracción de eyección del 30,6%) sin evidencia de enfermedad coronaria obstructiva en el cateterismo. La ecocardiografía reveló además la presencia de trombos dentro del corazón. A pesar del soporte con balón intraaórtico y medicamentos para mejorar la función cardíaca, la paciente sufrió un paro cardíaco intrahospitalario que requirió reanimación cardiopulmonar asistida con soporte mecánico extracorpóreo (PCPS).\n\nDurante su evolución, la función cardíaca se deterioró progresivamente, afectando ambos ventrículos, y se desarrolló falla multiorgánica que requirió hemodiálisis y soporte ventilatorio avanzado. La biopsia endomiocárdica evidenció inflamación significativa con predominio de linfocitos y algunos eosinófilos, compatible con miocarditis por hipersensibilidad (una inflamación del músculo cardíaco probablemente desencadenada por una reacción alérgica o inmunológica). La paciente presentó complicaciones graves como hemorragias, infecciones y problemas en la cicatrización, que fueron manejados con intervenciones quirúrgicas y tratamientos antibióticos.\n\n**Interpretación Clínica**  \nEl cuadro clínico y los estudios realizados indican que la paciente desarrolló una miocarditis severa secundaria a una reacción de hipersensibilidad tras la picadura de abeja, que llevó a un shock cardiogénico refractario y paro cardíaco. La ausencia de enfermedad coronaria y la inflamación observada en la biopsia apoyan este diagnóstico. El soporte mecánico avanzado, incluyendo dispositivos de asistencia ventricular bilateral y oxigenación por membrana extracorpórea, fue fundamental para mantener la circulación y oxigenación mientras se evaluaba la posibilidad de trasplante cardíaco.\n\n**Próximos Pasos y Evolución**  \nDada la persistencia del fallo cardíaco y la ausencia de recuperación, la paciente fue registrada como candidata para trasplante de corazón y recibió el trasplante ortotópico en el día 49 de hospitalización. Posteriormente, se mantuvo bajo soporte postoperatorio con ECMO y fue monitoreada para detectar rechazo cardíaco, sin evidencia de este. A pesar de episodios de shock séptico y la necesidad de cirugía abdominal, la paciente logró estabilizarse, fue extubada y dada de alta al día 101. En el seguimiento a tres meses, se mantuvo clínicamente estable.\n\n**Resumen Final**  \nEste caso ilustra una forma grave y poco común de miocarditis por hipersensibilidad desencadenada por una picadura de abeja, que evolucionó rápidamente hacia un shock cardiogénico y paro cardíaco. El manejo multidisciplinario con soporte circulatorio mecánico avanzado y trasplante cardíaco fue esencial para la supervivencia y recuperación de la paciente."
+        }
+    },
+    {
+        "article": "Un hombre de 24 años con complicaciones cardiovasculares relacionadas con MFS fue admitido en nuestro departamento de medicina interna debido a 3 episodios consecutivos de insuficiencia cardiaca aguda descompensada con fracción de eyección reducida (ADHFrEF) de 2014 a 2017. Su historia médica restante incluye hipertensión arterial, dislipidemia, hipertiroidismo, shock anafiláctico debido a flecainida y hábito tabágico previo.\n\nEl diagnóstico de MFS se realizó en 2010, cuando se llevó a cabo la sustitución de la aorta ascendente y la válvula aórtica con prótesis mecánica debido a una disección aórtica aguda tipo A en presencia de antecedentes familiares (madre, padre y 3 hijos con MFS). Durante el período intraoperatorio, se produjo un síndrome coronario agudo inferior y se trató con cirugía de injerto de derivación de la arteria coronaria.\n\nEn mayo de 2014, se realizó la implantación de una prótesis mecánica de aorta descendente y arco aórtico debido a un aneurisma disecante crónico. El hematoma peri-aórtico y la isquemia medular complicaron la cirugía y causaron paraplejia de las extremidades inferiores, dolor y hipoestesia térmica, e incontinencia rectal. Después de 2 meses, durante su primera admisión por ADHFrEF, las pruebas de laboratorio fueron notables para N-terminal pro-BNP (NT-proBNP) de 12,000 pg/mL y el ecocardiograma transtorácico mostró una función de la prótesis normal, dilatación de todas las cámaras cardiacas (principalmente las izquierdas) con insuficiencia mitral y tricuspídea moderada, hipertrofia ventricular izquierda, acinesia de la pared inferior, discinesia septal e hipocinesia de las paredes restantes con reducción severa de la fracción de eyección ventricular izquierda (LVEF) −20%. Se le trató con diuréticos intravenosos y desfibrilador cardiaco interno (St. Jude Ellipse DR, modo DDD) sin terapia de resincronización cardiaca (criterios de electrocardiograma no cumplidos) y se le dio de alta con la máxima terapia médica (furosemida, carvedilol, ramipril, espironolactona, digoxina y amlodipina).\n\nEn agosto de 2017, se produjo un nuevo episodio de ADHFrEF. Los valores de laboratorio de admisión notables incluían NT-proBNP de 2719 pg/mL y midregional-proadrenomedullin (MR-proADM) de 1.61 nmol/L, mientras que el ecocardiograma transtorácico y transesofágico mostró un LVEF de 35%, función de prótesis normal, severa regurgitación tricuspídea, y ruptura de la valva anterior de la chorda tendineae con severa regurgitación mitral. Los pacientes fueron tratados con diuréticos intravenosos y digoxina y dados de alta con una terapia médica óptima (furosemida, carvedilol, ramipril, espironolactona, digoxina, y amlodipina).\n\nPor último, volvió a ser admitido en nuestro departamento de medicina interna en noviembre de 2017 debido a un tercer episodio de ADHFrEF y una acumulación de líquido mediastinal infectado secundaria a una corrección quirúrgica de insuficiencia valvular severa un mes antes con implantación de prótesis mecánica mitral (31 mm ST Jude) y anuloplastia tricúspide De Vega.\n\nEl examen físico reveló una presión arterial de 120/80 mm Hg, pulso de 82 bpm, frecuencia respiratoria de 26 apm, saturación de O2 de 87% en aire ambiente con posición ortopneica obligatoria, y un habitus marfanoide (peso de 147 kg, altura de 2.2 m). La evaluación cardiopulmonar reveló un segundo sonido cardíaco metálico, percusión opaca con reducción del frémito vocal táctil y crepitaciones en la base de los pulmones, disminución amplia de los sonidos respiratorios vesiculares, presencia de ascitis abundante e hinchazón de las piernas.\n\nLos valores de laboratorio notables incluyeron NT-proBNP de 10,132 pg/mL y MR-proADM de 2,36 nmoL/mL.\n\nEl análisis de gases arteriales reveló una hipoxemia grave con alcalosis respiratoria y metabólica (pH 7,56, pO2 46 mm Hg, pCO2 24,8 mm Hg, HCO3− 21,9 mm mol/L, gradiente alveolar-arterial 31 mm Hg). Aunque el electrocardiograma resaltó fibrilación auricular con frecuencia ventricular de 80 bpm, hipertrofia ventricular izquierda e isquemia subepicárdica infralateral, el ecocardiograma transtorácico mostró las mismas características que el anterior, excepto por una FEVI de 30 %, presencia de prótesis mecánicas mitrales con fuga paravalvular y gradiente medio de 9 mm Hg, e insuficiencia tricuspídea leve.\n\n\nEn la radiografía de tórax y en la tomografía computarizada de alta resolución se observa una congestión hilar con cardiomegalia, consolidación pulmonar en el lóbulo superior derecho y acumulación de líquido mediastínico infectado.\n\nEl paciente fue tratado con 250 mg de furosemida intravenosa por día, 100 mg de canrenona por día, 4,5 g de piperacilina/tazobactam cada 6 horas y 12 mg/kg de teicoplanina por día, y luego 12 mg/kg por día. El día 9, una vez alcanzada la estabilización hemodinámica, se agregó una dosis intermedia de sacubitril/valsartan de 49/51 mg por día a 3,125 mg de carvedilol por día, 100 mg de espironolactona por día, 250 mg de furosemida por día y 0,25 mg de digoxina por día.\n\nEn el seguimiento de 1 mes, sacubitril/valsartan se aumentó a 97/103 mg b.i.d. para la buena condición clínica del paciente, lo que permitió una reducción persistente y progresiva de los parámetros clínicos, de laboratorio (reducción de NT-proBNP e incremento de MR-proADM), de los parámetros ecocardiográficos (aumento del EFV final del ventrículo izquierdo (42 % vs 30 %), del diámetro final del ventrículo izquierdo, del diámetro diastólico final del ventrículo izquierdo, de la masa del ventrículo izquierdo y del índice de masa del ventrículo izquierdo) y una mejora de la calidad de vida sin nuevos episodios de ADHFrEF hasta el seguimiento de 9 meses (Fig. (Fig.1B1B y D; Tabla 1).1). Debido a la falta de un régimen de dosificación específico para sacubitril/valsartan en la miocardiopatía relacionada con la EM, utilizamos el esquema terapéutico recomendado.\n\nMH - Aminobutiratos/uso terapéutico\nMH - Antagonistas de los receptores de la angiotensina/*uso terapéutico\nMH - Compuestos de bifenilo\nMH - Combinaciones de fármacos\nMH - Insuficiencia cardiaca/*terapia farmacológica/*etiología\nMH - Humanos\nMH - Hombre\nMH - Síndrome de Marfan/*complicaciones\nMH - Tetrazoles/uso terapéutico\nMH - Resultado del tratamiento\nMH - Valsartán\nMH - Adultos jóvenes\n",
+        "gold_summary": "Preocupaciones de los pacientes:\nUn hombre de 24 años fue admitido en nuestro departamento de medicina interna debido a disnea, ascitis e hinchazón de las piernas. El análisis de gases en sangre arterial reveló una hipoxemia grave con alcalosis respiratoria y metabólica. La radiografía de tórax mostró una congestión hilar.\n\nDiagnósticos:\nInsuficiencia cardíaca aguda descompensada recurrente con fracción de eyección reducida a pesar de la terapia médica óptima en la cardiomiopatía relacionada con el síndrome de Marfan.\n\nIntervenciones y resultados:\nSe agregó sacubitril/valsartan a la terapia médica óptima después de la estabilización hemodinámica, lo que permitió una mejora clínica, de laboratorio y ecocardiográfica progresiva. El paciente mantuvo una supervivencia libre de insuficiencia cardiaca y una buena calidad de vida hasta el seguimiento de 9 meses.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre joven estaba muy cansado y con las piernas hinchadas. Tenía problemas para respirar y mucho líquido en su barriga. Los doctores hicieron pruebas y vieron que su corazón no estaba funcionando bien.\n\nÉl tiene una enfermedad que hace que su corazón sea débil. Los doctores le dieron medicinas para ayudarlo. Luego, le dieron una medicina nueva llamada sacubitril/valsartan.\n\nDespués de tomar la medicina nueva, el hombre se sintió mejor. Su corazón empezó a trabajar mejor y pudo vivir sin problemas por mucho tiempo. Los doctores están contentos porque está más sano y feliz.",
+            "B2": "**Lo que le Pasó al Paciente**  \nUn joven de 24 años con síndrome de Marfan, una enfermedad que afecta el corazón y los vasos sanguíneos, fue llevado al hospital porque tenía dificultad para respirar, líquido en el abdomen (ascitis) y piernas hinchadas. Al hacerle un análisis de sangre, encontraron que tenía poco oxígeno en la sangre y un desequilibrio en los ácidos y bases de su cuerpo. La radiografía de su pecho mostró que sus pulmones estaban congestionados.\n\n**Qué Diagnosticaron**  \nEl paciente tenía insuficiencia cardíaca aguda descompensada, lo que significa que su corazón no podía bombear sangre correctamente y esto empeoraba de forma repetida. Además, su corazón tenía una fracción de eyección reducida, que es una medida de qué tan bien el corazón bombea la sangre. Esto ocurrió a pesar de que ya estaba recibiendo el mejor tratamiento médico disponible para su condición relacionada con el síndrome de Marfan.\n\n**Cómo lo Trataron y Qué Resultó**  \nDespués de estabilizar su estado, los médicos añadieron un medicamento llamado sacubitril/valsartán a su tratamiento. Este medicamento ayuda al corazón a funcionar mejor. Gracias a esto, el paciente mejoró poco a poco en su salud general, en los resultados de sus análisis de sangre y en los exámenes del corazón por ecocardiograma. Durante los siguientes nueve meses, el joven no tuvo nuevos episodios graves de insuficiencia cardíaca y pudo mantener una buena calidad de vida.",
+            "B3": "**Contexto:**  \nUn hombre joven de 24 años con diagnóstico previo de síndrome de Marfan (una enfermedad genética que afecta el tejido conectivo y puede causar problemas cardiovasculares graves) fue ingresado en el hospital debido a dificultad para respirar, acumulación de líquido en el abdomen (ascitis) y edema en las piernas. Este paciente presentaba antecedentes complejos, incluyendo múltiples cirugías aórticas y valvulares, episodios repetidos de insuficiencia cardíaca aguda con función del corazón gravemente reducida, así como complicaciones neurológicas y respiratorias.\n\n**Hallazgos Clave:**  \nAl ingreso, el análisis de gases en sangre mostró una hipoxemia severa (bajo nivel de oxígeno en la sangre) acompañada de alcalosis respiratoria y metabólica, lo que indica un desequilibrio en el pH sanguíneo debido a problemas respiratorios y metabólicos. La radiografía de tórax reveló congestión en la zona hilar (área central del pulmón), cardiomegalia (aumento del tamaño del corazón) y consolidación pulmonar, además de una acumulación de líquido infectado en el mediastino (espacio entre los pulmones). El ecocardiograma evidenció una fracción de eyección ventricular izquierda (FEVI) reducida al 30%, presencia de prótesis valvulares mecánicas con fugas y regurgitación valvular, reflejando un deterioro significativo de la función cardíaca a pesar del tratamiento previo.\n\n**Interpretación Clínica:**  \nEl paciente sufría de insuficiencia cardíaca aguda descompensada recurrente con fracción de eyección reducida, a pesar de recibir la mejor terapia médica disponible hasta ese momento. Esta condición estaba relacionada con la miocardiopatía (enfermedad del músculo cardíaco) secundaria al síndrome de Marfan, que había provocado daños estructurales severos en el corazón y los vasos sanguíneos. La infección mediastínica y las complicaciones pulmonares añadían un riesgo significativo para su pronóstico.\n\n**Intervenciones y Resultados:**  \nTras estabilizar su condición hemodinámica, se incorporó a su tratamiento sacubitril/valsartán, un medicamento que combina un inhibidor de la neprilisina y un antagonista del receptor de angiotensina, conocido por mejorar la función cardíaca en insuficiencia cardíaca con fracción de eyección reducida. La introducción de este fármaco, junto con la terapia médica óptima previa (incluyendo diuréticos, betabloqueantes, inhibidores de la enzima convertidora de angiotensina, espironolactona y digoxina), permitió una mejora progresiva en sus síntomas clínicos, parámetros de laboratorio (disminución de marcadores como NT-proBNP, que indican estrés cardíaco) y en los estudios ecocardiográficos (aumento de la fracción de eyección y mejoría en las dimensiones y masa ventricular). Durante un seguimiento de nueve meses, el paciente no presentó nuevos episodios de insuficiencia cardíaca aguda y experimentó una mejora significativa en su calidad de vida.\n\n**Próximos Pasos:**  \nDado el éxito observado con sacubitril/valsartán en este caso, se sugiere considerar este tratamiento como una opción terapéutica en pacientes jóvenes con miocardiopatía asociada al síndrome de Marfan y fracción de eyección reducida, aunque se requiere más investigación para establecer pautas específicas de dosificación y manejo en esta población particular. Además, es fundamental continuar con un seguimiento estrecho para monitorear la función cardíaca, controlar las complicaciones infecciosas y ajustar la terapia según la evolución clínica."
+        }
+    },
+    {
+        "article": "Paciente masculino de 41 años de edad quien ingresó en 2016 al servicio de urgencia con politraumatismo producto de accidente de tránsito; con trauma en miembros inferioA B res, en los rayos X se observa fractura de platillos tibiales izquierdos y fractura subtrocanteriana derecha, trauma toracoabdominal y trauma craneoencefálico leve.\nSe le practica osteosíntesis de fémur con clavo cefalomedular largo a foco cerrado corrigiendo la fractura subtrocanteriana y se le aplica tutor externo transarticular de rodilla como medida de control de daño local provisional; 15 días después se realiza osteosíntesis definitiva de su fractura de platillos tibiales. Evolución adecuada y satisfactoria de platillos tibiales.\nEntre 2016 y 2019 tuvo episodios esporádicos de dolor en cadera derecha que cedían fácilmente al manejo con antiinflamatorios y analgésicos sin limitar las actividades de la vida diaria y en la toma de rayos X se observaba fatiga de los bloqueos distales con dudas de la consolidación de la fractura.\nEn 2020 se incrementa el dolor en la cadera que no cede con el tratamiento médico y se acompaña de limitación funcional. En los rayos X de control se evidencia ruptura del clavo cefalomedular en su tercio proximal y no unión de la fractura subtrocantérica.\nEn Febrero de 2020 intento fallido de extracción de material de osteosíntesis (extrainstitucional), por lo que es remitido a nuestra institución. Se lleva a cirugía el 8 de Febrero, se realiza retiro de material de osteosíntesis, curetaje y toma de cultivo de foco de no unión. Cultivo positivo para Klebsiella pneumoniae recibiendo tratamiento con meropenem intravenoso por 10 días. Posteriormente se le realizó un lavado quirúrgico con drenaje de hematoma para el 20 de Febrero realizar nueva osteosíntesis con clavo cefalomedular + injerto óseo autólogo (tomado de ambas crestas iliacas) en foco de no unión.\nReactivación de la infección en Marzo de 2020, requiriendo nuevamente cirugía para lavados y desbridamiento quirúrgicos seriados (#5). Se aísla nueva bacteria Enterobacter que es manejada con vancomicina y meropenem. A f inales de Abril completa tratamiento médico y se le da salida en condiciones estables.\nEn Mayo de 2020 por persistencia de la infección se retira el material de osteosíntesis, se deja un clavo TENS endomedular recubierto de cemento con antibióticos (gentamicina).\nA finales de Mayo después de dos lavados quirúrgicos se retiró el clavo TENS, resección de bordes de fractura (hasta hueso sano) injerto óseo endomedular con un segmento de 10 cm de peroné no vascularizado (autólogo) y fijación de la fractura con una placa de soporte condíleo de fémur distal; colocación de sistema VAC y cierre definitivo de la herida en un segundo tiempo el 28 de Mayo de 2020. El paciente evolucionó adecuadamente, la herida quirúrgica cicatrizó por completo hasta el día de hoy con infección en remisión y evidencia radiológica de consolidación de la fractura, además paciente asintomático con función preservada de la extremidad.",
+        "gold_summary": "Masculino de 41 años de edad que sufre fractura subtrocantérica derecha producto de un accidente de tránsito que requirió manejo de osteosíntesis. Con posterior ruptura del clavo cefalomedular en su tercio proximal, no unión de la fractura e infecciones en sitio de la fractura. Fue tratado con múltiples lavados quirúrgicos, antibioticoterapia y un procedimiento ortopédico y quirúrgico poco convencional como el uso de una placa de soporte condíleo de fémur distal y un injerto óseo endomedular con un segmento de 10 cm de peroné no vascularizado. Paciente con evolución satisfactoria y favorable.",
+        "synthetic_summary": {
+            "B1": "Un hombre se lastimó mucho la pierna en un accidente. Su hueso del muslo se rompió y tuvo que ir al doctor para arreglarlo. El doctor puso un palo especial para que el hueso se pegara. \n\nPero el palo se rompió y el hueso no sanaba bien. También tuvo una infección que le dolía mucho. Los doctores limpiaron muchas veces la herida y le dieron medicinas para la infección. \n\nDespués, hicieron una operación especial para poner un hueso nuevo y un soporte para ayudar a que su pierna sanara. Ahora, el hombre está mejor y su pierna está sanando bien.",
+            "B2": "**Lo que le pasó al paciente:**  \nUn hombre de 41 años tuvo un accidente de tránsito que le causó una fractura en la parte superior del fémur derecho, llamada fractura subtrocantérica. Para arreglarla, los doctores usaron un clavo especial dentro del hueso (osteosíntesis).  \n\n**Problemas que surgieron:**  \nCon el tiempo, el clavo se rompió y la fractura no sanó bien, lo que se llama \"no unión\". Además, la zona se infectó con bacterias, lo que complicó la recuperación.  \n\n**Tratamientos realizados:**  \nEl paciente necesitó varias cirugías para limpiar la infección y quitar el material roto. También recibió antibióticos fuertes para combatir las bacterias. Para ayudar a que el hueso sanara, los médicos usaron un método especial que incluyó colocar una placa metálica para sostener el hueso y un injerto óseo. Este injerto fue un pedazo de hueso tomado de su propia pierna (del peroné) que se colocó dentro del hueso fracturado para ayudar a que creciera y se uniera.  \n\n**Resultado final:**  \nDespués de todo este tratamiento, el paciente mejoró mucho. La herida sanó bien, la infección desapareció y la fractura se unió correctamente. Ahora puede usar su pierna sin dolor y con buena función.",
+            "B3": "**Contexto**  \nSe trata de un hombre de 41 años que sufrió un accidente de tránsito en 2016, el cual le provocó múltiples lesiones, entre ellas fracturas en ambas piernas: una fractura subtrocantérica (zona proximal del fémur) en la cadera derecha y fracturas en los platillos tibiales izquierdos. Inicialmente, se le realizó una cirugía para estabilizar la fractura de cadera mediante un clavo cefalomedular largo, y posteriormente se corrigió la fractura de la tibia. Durante los primeros años, el paciente tuvo episodios esporádicos de dolor en la cadera derecha, pero sin limitación importante en sus actividades diarias.\n\n**Hallazgos Clave**  \nEn 2020, el dolor en la cadera derecha empeoró y se acompañó de dificultad para mover la pierna. Las radiografías mostraron que el clavo utilizado para fijar la fractura se había roto en su parte proximal y que la fractura no había sanado correctamente (no unión). Se intentó retirar el material de osteosíntesis en otro centro sin éxito, por lo que fue referido a un hospital especializado. Allí se realizó la extracción del material, limpieza quirúrgica de la zona afectada y se identificó una infección causada por la bacteria Klebsiella pneumoniae, que fue tratada con antibióticos intravenosos.  \n\nA pesar del tratamiento, la infección reapareció en marzo de 2020, detectándose otra bacteria llamada Enterobacter, lo que requirió múltiples cirugías adicionales para limpiar y desbridar (eliminar tejido infectado) la zona afectada, junto con un tratamiento combinado de antibióticos. Debido a la persistencia de la infección, en mayo se retiró nuevamente el material de fijación y se colocó un clavo recubierto con cemento impregnado con antibióticos para controlar la infección localmente.  \n\nFinalmente, se realizó una cirugía más compleja que incluyó la resección de los bordes de la fractura hasta llegar a hueso sano, la colocación de un injerto óseo endomedular (un segmento de 10 cm de hueso peroné tomado del mismo paciente, sin conexión vascular directa), y la fijación definitiva con una placa metálica especial para soportar la zona distal del fémur. Se utilizó además un sistema de vacío para favorecer la cicatrización de la herida.  \n\n**Interpretación Clínica**  \nEste caso representa una fractura compleja con complicaciones importantes como la no unión ósea y la infección crónica, que dificultaron la consolidación normal del hueso. La ruptura del clavo de fijación y la persistencia de bacterias resistentes requirieron un manejo multidisciplinario que combinó cirugía ortopédica avanzada, técnicas de control de infecciones y uso de injertos óseos autólogos (del propio paciente). El uso de un injerto no vascularizado de peroné y una placa de soporte condíleo fue una estrategia poco convencional pero necesaria para lograr la estabilidad y promover la curación ósea.  \n\n**Próximos Pasos**  \nTras la última cirugía y el tratamiento antibiótico, el paciente mostró una evolución favorable con cicatrización completa de la herida, remisión de la infección y evidencia radiológica de consolidación de la fractura. Actualmente se encuentra asintomático y conserva la función de la extremidad afectada. Se recomienda continuar con seguimiento clínico y radiológico para asegurar la estabilidad a largo plazo y prevenir posibles recaídas infecciosas o problemas mecánicos."
+        }
+    },
+    {
+        "article": "Una adolescente de 17 años se presentó en nuestra clínica con una historia de dos meses de dolor torácico en el lado izquierdo y una historia de una semana de dolor en la espalda en el nivel de T7. El dolor torácico se acompañaba de palpitaciones y disnea que ocurrían de tres a cuatro días por semana. Una semana antes de la primera visita, las palpitaciones y la disnea se hicieron menos frecuentes, y desarrolló un dolor sordo diario intermitente en el lado izquierdo del pecho y la parte media de la espalda sin radiación, en la mayoría de los casos. El dolor ocurría tanto con el ejercicio como en reposo, y duraba horas, sin factores agravantes o atenuantes. Informó una intensidad del dolor de 2 a 6 en una escala de 10 puntos. La intensidad cambiaba durante un ataque, y el promedio era 4. Estaba sana por lo demás. No había limitación en la vida diaria. Visitó a un médico local un mes antes de visitar nuestra clínica. Los resultados de los exámenes electrocardiográficos y de laboratorio de Holter fueron normales. Su historial médico incluía migraña durante tres años. Sus medicamentos regulares eran lomerizina, loxoprofen y naratriptan para la prevención y el tratamiento agudo de la migraña. Su migraña estaba bien controlada, y rara vez experimentaba ataques. Negó trauma o cirugías previas. Negó síntomas sospechosos o antecedentes familiares de afecciones autoinmunes o inflamatorias.\n\nSu presión arterial era de 107/60 mmHg y su pulso de 62 latidos/min. Medía 162 cm de altura y pesaba 43 kg, con un índice de masa corporal de 16,4 kg/m2. No se escuchaba ningún murmullo ni arritmia en su examen cardiovascular. Los pulmones estaban limpios a la auscultación bilateral. La palpación del tórax provocó un dolor local no reproducible en las articulaciones inferiores esterno-costales; la maniobra de tracción del brazo horizontal y la maniobra del gallo cantando no provocaron dolor. No había sensibilidad en los músculos y huesos de la parte superior del cuerpo.\n\nLos hallazgos electrocardiográficos y de laboratorio, incluida la función tiroidea, fueron normales. El examen radiográfico torácico y torácico mostró el enderezamiento de la columna torácica superior y una pérdida de la curvatura cifótica normal. Las radiografías de las costillas inferiores no revelaron fractura ni neumotórax. Sospechamos un síndrome de la espalda recta, de acuerdo con los dos criterios diagnósticos diferentes propuestos por Davies et al. y DeLeon et al. La distancia entre la mitad del borde anterior de T8 y una línea vertical que conecta T4 a T12 fue de 0.91 cm. El diámetro anteroposterior fue de 74.0 cm, y el diámetro transversal fue de 243.2 cm. Le aconsejamos que comenzara y continuara la terapia quiropráctica para aumentar la cifosis torácica. Procedimos con una espera vigilante durante un mes en atención ambulatoria.\n\nDespués de esta primera visita, el dolor de pecho y de espalda se alivió gradualmente. Las palpitaciones y la disnea apenas se produjeron. Todos los síntomas desaparecieron en tres semanas. En la visita de seguimiento de un mes, se realizó una ecocardiografía, que reveló una regurgitación mitral trivial sin prolapso. Confirmamos el diagnóstico de síndrome de espalda recta. Reaseguramos a la paciente de que la enfermedad es benigna y le aconsejamos que continuara con la terapia quiropráctica. No ha tenido recaída de síntomas graves ni necesidad de visitar el hospital. Nunca volvió a visitar nuestra clínica en el año siguiente.\n",
+        "gold_summary": "Una adolescente de 17 años se presentó con su madre en nuestra clínica con un historial de dos meses de dolor en el pecho izquierdo y un historial de una semana de dolor en la parte media de la espalda. Diagnosticamos el síndrome de la columna vertebral basado en los hallazgos radiográficos del pecho y la columna vertebral y los síntomas de dolor en el pecho, palpitaciones y disnea. Tranquilizamos a la paciente de que la enfermedad era benigna y le aconsejamos que iniciara y continuara con la terapia quiropráctica. Todos los síntomas, incluido el dolor de espalda, desaparecieron en tres semanas.\n",
+        "synthetic_summary": {
+            "B1": "Había una niña de 17 años que tenía dolor en el pecho y en la espalda. Ella fue al doctor para que la ayudara. El doctor miró sus huesos con una foto especial. El doctor dijo que sus huesos estaban un poco rectos y eso le dolía. Le dijo que no era algo peligroso. Le dio un tratamiento para ayudar a que su espalda se sintiera mejor. Después de unas semanas, la niña ya no tenía dolor. Ahora está bien y feliz.",
+            "B2": "**Lo que le pasaba a la paciente**  \nUna chica de 17 años llegó a la clínica porque tenía dolor en el lado izquierdo del pecho durante dos meses y dolor en la parte media de la espalda desde hacía una semana. Además, sentía palpitaciones (cuando el corazón late rápido o irregular) y dificultad para respirar algunas veces.\n\n**Qué encontraron los médicos**  \nDespués de hacerle varios estudios, como radiografías del pecho y la columna, vieron que su columna torácica (la parte media de la espalda) estaba más recta de lo normal. Esto se llama \"síndrome de la espalda recta\". No encontraron problemas en el corazón ni en los pulmones que explicaran el dolor y los otros síntomas.\n\n**Qué hicieron y qué pasó después**  \nLos médicos le dijeron que esta condición no era peligrosa. Le recomendaron hacer terapia quiropráctica, que es un tratamiento donde un especialista ayuda a mejorar la postura y la movilidad de la columna. Después de seguir este tratamiento, todos sus síntomas, incluyendo el dolor y las palpitaciones, desaparecieron en tres semanas.\n\n**Qué significa esto**  \nEl síndrome de la espalda recta puede causar dolor en el pecho y la espalda, pero no es una enfermedad grave. Con el tratamiento adecuado, como la terapia quiropráctica, los síntomas pueden mejorar y desaparecer. Es importante consultar al médico para recibir el diagnóstico correcto y el tratamiento adecuado.",
+            "B3": "**Contexto**  \nUna joven de 17 años acudió a nuestra clínica acompañada por su madre, presentando un cuadro de dos meses con dolor en el lado izquierdo del pecho y una semana con dolor en la parte media de la espalda, específicamente a nivel de la séptima vértebra torácica (T7). Además, experimentaba episodios de palpitaciones (sensación de latidos cardíacos acelerados o irregulares) y dificultad para respirar (disnea) varias veces por semana. Estos síntomas comenzaron a mejorar una semana antes de la consulta, aunque persistía un dolor sordo e intermitente en la zona afectada, que podía durar horas y ocurría tanto en reposo como durante la actividad física.\n\n**Hallazgos Clave**  \nEl examen físico no mostró signos de enfermedad cardíaca ni pulmonar: la presión arterial y el pulso estaban dentro de rangos normales, no se detectaron ruidos anormales en el corazón ni en los pulmones, y no había sensibilidad en músculos o huesos que sugiriera inflamación o lesión. Los estudios electrocardiográficos y de laboratorio, incluyendo pruebas de función tiroidea, fueron normales. Las radiografías del tórax revelaron una alteración en la curvatura normal de la columna torácica superior, conocida como pérdida de la cifosis (curvatura hacia adelante), y se descartaron fracturas o neumotórax (colapso pulmonar).\n\nCon base en estos hallazgos y los criterios diagnósticos establecidos en la literatura médica, se identificó un síndrome conocido como “síndrome de la espalda recta” o “síndrome de la columna vertebral rectificada”, que se caracteriza por la pérdida de la curvatura normal de la columna torácica y puede asociarse a dolor torácico y dorsal.\n\n**Interpretación Clínica**  \nEl síndrome de la espalda recta es una condición benigna, es decir, que no pone en riesgo la vida ni causa daño grave a largo plazo. En este caso, se relacionó con los síntomas de dolor en el pecho y la espalda, así como con las palpitaciones y la disnea, que probablemente estaban vinculados a la alteración postural y mecánica de la columna vertebral.\n\n**Próximos Pasos y Evolución**  \nSe recomendó iniciar y mantener un tratamiento quiropráctico, que consiste en técnicas manuales para mejorar la movilidad y la postura de la columna, con el objetivo de restaurar la curvatura torácica normal. Durante el seguimiento ambulatorio, los síntomas fueron mejorando progresivamente hasta desaparecer completamente en tres semanas. Una ecocardiografía (ultrasonido del corazón) realizada un mes después mostró una regurgitación mitral trivial (un leve retorno de sangre en una válvula cardíaca) sin prolapso (sin desplazamiento anormal), lo cual no requería tratamiento. La paciente fue tranquilizada sobre la naturaleza benigna de su condición y se le aconsejó continuar con la terapia quiropráctica. No presentó recaídas ni necesidad de atención médica adicional en el año siguiente.\n\n**Resumen Final**  \nUna adolescente con dolor torácico y dorsal, acompañado de palpitaciones y dificultad para respirar, fue diagnosticada con síndrome de la espalda recta tras estudios clínicos y radiográficos. Con tratamiento quiropráctico y seguimiento, sus síntomas desaparecieron completamente en pocas semanas, confirmando que se trataba de una condición benigna y manejable."
+        }
+    },
+    {
+        "article": "Una mujer de 59 años con urolitiasis bilateral recurrente se presentó con dolor en el flanco derecho, fiebre y fatiga. Se le había colocado un stent doble J derecho un año antes para una piedra pélvica sintomática, pero no se le dio seguimiento. Tenía insuficiencia cardíaca derecha, diabetes tipo 2 mal controlada y enfermedad renal crónica (nadir de creatinina: 18 mg/L).\nEstable clínicamente, tenía una escala de coma de Glasgow de 14/15 (respuesta verbal ligeramente alterada), fiebre (38,3 °C), sensibilidad en el flanco derecho y una producción de orina de 800 cc en 24 horas.\nLos resultados de laboratorio revelaron una lesión renal aguda, con un nivel de creatinina sérica de 107 mg/L (normal: 6-12 mg/L) y urea sanguínea de 3 g/L (normal: 0.15-0.45 g/L). Los marcadores inflamatorios estaban elevados, con un nivel de proteína C reactiva de 300 mg/L (normal: <5 mg/L) y un recuento de glóbulos blancos de 17,000/mm3 (normal: 4000-10,000/mm3). Además, el paciente exhibió anemia normocítica (hemoglobina: 7.6 g/dL; normal: 12-16 g/dL) e hipercalemia leve (potasio sérico: 5.4 mEq/L; normal: 3.5-5.1 mEq/L). El análisis de orina y el cultivo de orina fueron negativos para infección bacteriana.\nUna tomografía computarizada abdominal y pélvica sin contraste reveló una hidronefrosis del lado derecho, un stent de doble J calcificado en espiral en ambos extremos y una piedra en la pelvis derecha de 35 × 28 mm (588 UH). El riñón izquierdo está reducido en tamaño, con hidronefrosis y una piedra en la pelvis de 12 × 7 mm (531 UH).\n\nDebido a la obstructiva severa de la pielonefritis, en particular causada por la endoprótesis incrustada, se realizó una nefrostomía percutánea bilateral urgente, lo que produjo una importante mejora clínica y normalización de los marcadores inflamatorios y la función renal.\nTres días después, la paciente experimentó una convulsión generalizada asociada con disartria. Una tomografía computarizada urgente del cerebro mostró lesiones isquémicas en los lóbulos occipitales izquierdo y frontal derecho, lo que indicaba un accidente cerebrovascular embólico. Se le inició un tratamiento con enoxaparina (0,4 cc diarios) y Kardegic (160 mg diarios) para la prevención de accidentes cerebrovasculares.\nA pesar de la mejora neurológica, cuatro días después, la paciente desarrolló palidez mucocutánea progresiva, taquicardia (110 latidos por minuto), hipotensión (80/50 mmHg) y hematuria macroscópica por el catéter urinario. Los niveles de hemoglobina descendieron de 7,5 g/dL a 4,4 g/dL, lo que levantó sospechas de hemorragia activa. Se administró fluidoterapia, vasopresores intravenosos y transfusiones de sangre, estabilizando su estado para una exploración de angiografía por TAC con contraste.\nLa tomografía computarizada reveló una colección polar media heterogénea de 17 mm de espesor con extravasación de contraste en las fases arterial y portal, lo que indica una hemorragia activa de las arterias del polo superior y medio. También había coágulos intraluminales en la pelvis renal y la vejiga. Se hizo un diagnóstico de fístula arteriovenosa postnefrostomía, exacerbada por la terapia anticoagulante para el accidente cerebrovascular.\nSe realizó una arteriografía renal urgente a través del acceso a la arteria femoral derecha, utilizando un catéter de diagnóstico de calibre 5. La angiografía selectiva reveló una FAV en el polo inferior del riñón con drenaje venoso temprano hacia la vena cava inferior, junto con un pequeño pseudoaneurisma. La embolización superselectiva con microespirales de 3 mm y 5 mm logró ocluir con éxito la fístula, y se usaron partículas de Gelfoam para evitar el sangrado retrógrado. Una inyección final de contraste confirmó la oclusión completa de la fístula, restaurando la integridad arterial y deteniendo la hemorragia.\n\nDespués de la embolización, se vigiló de cerca al paciente en la UCI. La hemodinámica se mantuvo estable y se tomó la decisión colegiada de reintroducir la anticoagulación con monitorización del INR para controlar el accidente cerebrovascular isquémico mientras se equilibraba el riesgo de hemorragia. La hematuria se resolvió, la función renal se normalizó y la nefrostomía siguió siendo funcional.\nSe adoptó un enfoque multidisciplinario para el tratamiento definitivo. La primera etapa involucró la litotripsia endoscópica con láser del bucle inferior calcificado del stent de JJ, la inserción de un segundo stent de JJ en paralelo con el incrustado y la extracción de la nefrostomía, que se completó con éxito. La segunda etapa, programada seis semanas después, incluyó una ureteroscopia derecha flexible para liberar el bucle superior del stent de JJ calcificado, la fragmentación de la piedra pélvica derecha mediante litotripsia con láser y la extracción completa del stent incrustado. Lamentablemente, la salud del paciente se deterioró debido a múltiples factores, entre ellos, insuficiencia cardíaca, diabetes mal controlada, enfermedad renal crónica y un accidente cerebrovascular previo, lo que demoró la finalización de la segunda etapa del tratamiento planificado.\n",
+        "gold_summary": "Una mujer de 59 años con urolitiasis bilateral recurrente, insuficiencia cardiaca derecha, diabetes tipo 2 mal controlada y enfermedad renal crónica se presentó con dolor en el flanco derecho, fiebre y fatiga. Previamente se le había colocado un stent doble J derecho, pero se perdió su seguimiento. Una tomografía computarizada reveló una hidronefrosis, un stent calcificado y una piedra pélvica de 22 mm, lo que llevó a la realización de una nefrostomía percutánea. La paciente desarrolló un accidente cerebrovascular embólico tres días después y posteriormente presentó hematuria, hipotensión y anemia significativa. La angiografía por TC confirmó una FAV con sangrado activo, que se trató con éxito con embolización.\n",
+        "synthetic_summary": {
+            "B1": "Una señora tenía dolor y fiebre. Tenía piedras en sus dos riñones. También tenía problemas con su corazón y azúcar alta. Le pusieron un tubito en el riñón, pero no fue al doctor para revisarlo. \n\nEl doctor vio que su riñón estaba muy hinchado y había una piedra grande. Le pusieron un tubito para sacar el líquido. \n\nDespués, la señora tuvo un problema en su cabeza y se cayó. Luego, empezó a tener sangre en la orina y se puso muy débil. \n\nLos doctores encontraron que estaba sangrando dentro del riñón. Hicieron un tratamiento para parar la sangre y la ayudaron mucho.",
+            "B2": "**Lo que le pasó a la paciente**  \nUna mujer de 59 años tenía piedras en ambos riñones que volvían a aparecer, además de problemas graves del corazón, diabetes mal controlada y enfermedad en los riñones. Ella sentía dolor en el lado derecho de su cuerpo, tenía fiebre y estaba cansada. Un año antes, le habían puesto un tubo llamado stent doble J en el riñón derecho para ayudar a que la orina pasara, pero no fue revisado después.  \n\n**Lo que encontraron en sus estudios**  \nUna tomografía (una especie de radiografía especial) mostró que su riñón derecho estaba inflamado por la acumulación de orina (hidronefrosis), que el stent estaba cubierto de calcio y que tenía una piedra grande en la pelvis del riñón. Por esto, le hicieron una nefrostomía, que es un procedimiento para drenar la orina directamente del riñón usando un tubo.  \n\n**Problemas que surgieron después**  \nTres días después, la mujer tuvo una convulsión y se descubrió que había sufrido un accidente cerebrovascular, que es cuando falta sangre en una parte del cerebro. Le dieron medicamentos para evitar más problemas en el cerebro.  \n\nLuego, presentó sangrado en la orina, presión baja y anemia (menos glóbulos rojos), lo que indicaba que estaba perdiendo mucha sangre. Un estudio con contraste mostró que tenía una fístula arteriovenosa (FAV), que es una conexión anormal entre una arteria y una vena en el riñón, causando sangrado.  \n\n**Cómo la trataron**  \nPara detener el sangrado, hicieron una embolización, que consiste en bloquear la fístula usando pequeños dispositivos llamados microespirales. Esto funcionó bien y la paciente se estabilizó.  \n\n**Seguimiento y tratamiento final**  \nDespués, continuaron con un tratamiento para eliminar el stent calcificado y las piedras en dos etapas, usando láser y endoscopios (instrumentos para ver y tratar dentro del cuerpo). Sin embargo, la salud de la paciente empeoró debido a sus otras enfermedades, lo que complicó completar el tratamiento.  \n\n**Qué significa todo esto**  \nEste caso muestra que cuando un stent se deja mucho tiempo sin control, puede causar problemas graves como infecciones, sangrados y daño renal. También destaca la importancia de un seguimiento médico cuidadoso para evitar complicaciones serias.",
+            "B3": "**Contexto**  \nUna mujer de 59 años con antecedentes complejos, incluyendo cálculos renales recurrentes en ambos riñones (urolitiasis bilateral), insuficiencia cardíaca del lado derecho, diabetes tipo 2 mal controlada y enfermedad renal crónica, acudió al hospital por dolor intenso en el costado derecho, fiebre y cansancio. Un año antes, se le había colocado un stent doble J (un tubo delgado que ayuda a drenar la orina desde el riñón hacia la vejiga) en el riñón derecho debido a una piedra renal, pero no se realizó un seguimiento adecuado de este dispositivo.\n\n**Hallazgos Clave**  \nAl realizar una tomografía computarizada (una exploración detallada con rayos X), se detectó que el riñón derecho presentaba hidronefrosis (acumulación de orina debido a una obstrucción), un stent doble J calcificado (con depósitos de calcio que dificultan su función) y una piedra renal grande de aproximadamente 35 × 28 mm. El riñón izquierdo también mostraba signos de daño, con una piedra más pequeña y reducción de tamaño. Debido a la obstrucción severa y el riesgo de infección, se realizó una nefrostomía percutánea bilateral urgente, que consiste en colocar tubos para drenar la orina directamente desde los riñones hacia el exterior, lo que mejoró significativamente su estado y normalizó los marcadores de inflamación y función renal.\n\nSin embargo, tres días después, la paciente sufrió una convulsión generalizada y dificultad para hablar. Un escáner cerebral mostró lesiones isquémicas (áreas con falta de riego sanguíneo) en diferentes partes del cerebro, confirmando un accidente cerebrovascular embólico (causado por un coágulo que bloqueó una arteria cerebral). Se inició tratamiento anticoagulante para prevenir nuevos eventos.\n\nPosteriormente, la paciente desarrolló signos de hemorragia activa: palidez, taquicardia, presión arterial baja y sangre visible en la orina. La hemoglobina, que mide la cantidad de glóbulos rojos, cayó drásticamente, indicando una pérdida significativa de sangre. Una tomografía con contraste evidenció una colección de sangre en el riñón con extravasación de contraste, señal clara de sangrado activo, y coágulos en la pelvis renal y vejiga. Se diagnosticó una fístula arteriovenosa (FAV), una conexión anormal entre una arteria y una vena en el riñón, probablemente causada por la nefrostomía y agravada por la anticoagulación.\n\n**Interpretación Clínica**  \nLa fístula arteriovenosa renal es una complicación rara pero grave que puede provocar hemorragias importantes. En este caso, la combinación de la lesión vascular por la nefrostomía y el tratamiento anticoagulante para el accidente cerebrovascular aumentó el riesgo de sangrado. La angiografía selectiva (una técnica que visualiza los vasos sanguíneos) confirmó la presencia de la FAV y un pequeño pseudoaneurisma (una dilatación anormal de la arteria).\n\n**Próximos Pasos y Tratamiento**  \nSe realizó una embolización superselectiva, un procedimiento mínimamente invasivo en el que se introdujeron microespirales y partículas especiales para bloquear la fístula y detener el sangrado. El procedimiento fue exitoso, restaurando la integridad vascular y estabilizando a la paciente. Posteriormente, se reintrodujo cuidadosamente la anticoagulación para tratar el accidente cerebrovascular, equilibrando el riesgo de hemorragia.\n\nEl manejo definitivo incluyó un enfoque multidisciplinario para tratar las piedras y el stent calcificado. En una primera etapa, se realizó una litotripsia endoscópica con láser para fragmentar el stent incrustado y se colocó un segundo stent para facilitar el drenaje, retirando la nefrostomía. Se planificó una segunda etapa para fragmentar la piedra pélvica y extraer completamente el stent calcificado, pero la salud general de la paciente, afectada por sus múltiples enfermedades crónicas y el accidente cerebrovascular, retrasó este procedimiento.\n\n**Resumen Final**  \nEsta paciente presentó una compleja combinación de problemas renales y vasculares, incluyendo obstrucción urinaria grave, infección, accidente cerebrovascular y una complicación hemorrágica por fístula arteriovenosa renal. El manejo requirió intervenciones urgentes y coordinadas para controlar la infección, detener el sangrado y tratar las piedras y el stent calcificado, destacando la importancia del seguimiento adecuado en pacientes con dispositivos urológicos y múltiples comorbilidades."
+        }
+    },
+    {
+        "article": "Un hombre de 52 años fue admitido en un hospital debido a palpitaciones repentinas y fatiga general. La electrocardiografía reveló taquicardia ventricular con una frecuencia cardíaca de 180 lpm. Su ritmo cardíaco volvió a un ritmo sinusal después de una cardioversión inmediata y luego fue derivado a nuestra institución para una investigación adicional. Su historial médico pasado incluía reconstrucción del tracto de salida del ventrículo derecho utilizando un injerto homólogo y cierre de un defecto septal ventricular para TOF, que se realizó 47 años antes. Sin embargo, se perdió su seguimiento posterior. Tras ser derivado a nuestra institución, su presión arterial era de 116/70 mmHg, frecuencia cardíaca de 80 lpm, y saturación de oxígeno del 99% (con aire ambiente). Al inspeccionar la pulsación de la vena yugular, se observaron claramente una onda prominente y un descenso profundo, que eran consistentes con el aumento de la presión de llenado del ventrículo derecho y la compensación del aumento de la contracción de la RA. Cabe destacar que la auscultación reveló un murmullo diastólico regurgitante agudo en el tercer espacio intercostal izquierdo, un primer sonido cardíaco ampliamente dividido (S1) y un segundo sonido cardíaco (S2), lo que indicaba un ventrículo derecho severamente dilatado debido a la liberación de PR libre y la presencia de una válvula pulmonar no funcional. Además, se auscultó un tercer sonido cardíaco (S3) en el cuarto borde paraesternal, que era consistente con un S3 derecho. El electrocardiograma reveló bloqueo completo del haz de rama derecha, con una duración de QRS de 200 lpm. La radiografía de tórax mostró cardiomegalia con dilatación de las arterias pulmonares bilaterales. La ecocardiografía transtorácica reveló una regresión completa de la válvula pulmonar, que resultó en PR libre y una dilatación prominente del ventrículo derecho. La evaluación volumétrica del ventrículo derecho se realizó utilizando una resonancia magnética cardíaca, que reveló un volumen final diastólico del ventrículo derecho de 428 ml (índice de volumen final diastólico del ventrículo derecho de 240 ml/m2), una fracción de eyección del ventrículo derecho del 36% y una fracción de eyección de PR del 74%. Además, la tomografía computarizada multidetector mostró claramente una regresión completa de la válvula pulmonar del injerto homólogo.\n\nEl paciente se sometió a un examen con catéter para investigar más a fondo su estado hemodinámico. Su forma de onda de presión RA fue particularmente notable, ya que consistía en una onda a prominente y un descenso y, que coincidían con el cuarto sonido cardiaco (S4) y S3 en un fonocardiograma, respectivamente. Además, se reveló que la presión arterial pulmonar final diastólica y la presión final diastólica del VD eran casi idénticas debido al PR libre. Por lo tanto, la evaluación clínica del «quinteto de sonidos cardiacos», que incluye un murmullo diastólico regurgitante agudo, un S1 ampliamente dividido, un S2 único y la presencia de un S3 y un S4 derechos, se confirmó mediante una evaluación hemodinámica y anatómica multimodal como insuficiencia cardiaca derecha grave concomitante con un VD significativamente dilatado debido a la regresión completa de la válvula pulmonar y el PR libre resultante.\n\nDespués del reemplazo de la válvula pulmonar, el «quinteto de sonidos del corazón» se resolvió por completo.\n\nMH - Insuficiencia cardiaca/*etiología\nMH - Murmullos cardiacos/*diagnóstico\nMH - *Sonidos del corazón\nMH - Humanos\nMH - Hombre\nMH - Edad Media\nMH - Insuficiencia de la válvula pulmonar/*complicaciones/diagnóstico\nMH - Taquicardia, ventricular/etiología\nMH - Tetralogía de Fallot/*cirugía\nMH - Disfunción ventricular, derecha/etiología\n",
+        "gold_summary": "Un hombre de 52 años fue derivado a nuestra institución para la evaluación de una taquicardia ventricular de inicio súbito. Su historia clínica incluía una reconstrucción del tracto de salida del ventrículo derecho a los 5 años de edad. La auscultación reveló un murmullo diastólico regurgitante agudo, un primer sonido cardiaco (S1) ampliamente dividido y un segundo sonido cardiaco (S2) único, lo que indicaba un ventrículo derecho severamente dilatado debido a una regurgitación pulmonar (RP) grave y la presencia de una válvula pulmonar no funcional. Además, el tercer sonido cardiaco (S3) y el cuarto sonido cardiaco (S4) del lado derecho estaban presentes, lo que era coherente con una presión de llenado del ventrículo derecho elevada y la presencia de un ventrículo derecho no conforme. Finalmente, el mencionado «quinteto de sonidos cardiacos» se confirmó mediante una evaluación multimodal como insuficiencia cardiaca del lado derecho con un ventrículo derecho concomitantemente severamente dilatado debido a la regresión completa de la válvula pulmonar y la consiguiente RP libre.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre tenía problemas con su corazón. Su corazón latía muy rápido y se cansaba mucho. Cuando el doctor escuchó su corazón, oyó sonidos raros. Estos sonidos decían que una parte del corazón estaba muy grande y no funcionaba bien. La válvula del corazón que ayuda a la sangre a salir no estaba trabajando. Esto hizo que el corazón se llenara mucho y se hiciera más grande. Los doctores usaron muchas pruebas para entenderlo mejor. Al final, vieron que el corazón tenía problemas para trabajar bien porque la válvula estaba rota.",
+            "B2": "**Lo que le pasó al paciente**  \nUn hombre de 52 años llegó al hospital porque tenía palpitaciones rápidas y se sentía muy cansado. Cuando era niño, a los 5 años, había tenido una operación en el corazón para corregir un problema llamado Tetralogía de Fallot, que afecta cómo la sangre sale del corazón. En esa operación, le reconstruyeron una parte del ventrículo derecho, que es una de las cámaras del corazón que envía sangre a los pulmones.\n\n**Lo que encontraron al examinarlo**  \nAl escuchar su corazón con un estetoscopio, los médicos notaron varios sonidos anormales. Había un murmullo que indicaba que la sangre estaba regresando por la válvula pulmonar, que no funcionaba bien. Además, escucharon sonidos llamados S1 y S2 que estaban cambiados, y también sonidos llamados S3 y S4 en el lado derecho del corazón. Estos sonidos indican que el ventrículo derecho estaba muy agrandado y tenía problemas para llenarse y bombear la sangre correctamente.\n\n**Qué significa todo esto**  \nEstos signos juntos, que los médicos llamaron el «quinteto de sonidos cardiacos», mostraron que el paciente tenía insuficiencia cardíaca en el lado derecho del corazón. Esto pasó porque la válvula pulmonar que le habían reconstruido cuando era niño ya no funcionaba y la sangre regresaba libremente hacia el ventrículo derecho, causando que este se agrandara mucho y trabajara mal.\n\n**Qué hicieron después**  \nPara confirmar todo, usaron varios estudios, como ecocardiogramas y resonancias magnéticas, que mostraron claramente el daño en la válvula y el agrandamiento del ventrículo derecho. Finalmente, el paciente recibió un reemplazo de la válvula pulmonar, y después de la operación, los sonidos anormales del corazón desaparecieron, lo que indica que su corazón mejoró.",
+            "B3": "**Contexto**  \nUn hombre de 52 años, con antecedentes de cirugía cardíaca infantil para corregir la tetralogía de Fallot (una malformación congénita del corazón), fue ingresado tras presentar palpitaciones repentinas y fatiga. En su niñez, se le realizó una reconstrucción del tracto de salida del ventrículo derecho y cierre de un defecto septal ventricular, pero no tuvo seguimiento médico posterior. En el hospital, se detectó una taquicardia ventricular (ritmo cardíaco acelerado originado en el ventrículo) que se corrigió mediante cardioversión eléctrica.\n\n**Hallazgos Clave**  \nAl examen físico, se identificaron varios sonidos cardíacos anormales: un murmullo diastólico regurgitante agudo (sonido producido por el flujo anormal de sangre hacia atrás durante la diástole), un primer sonido cardíaco (S1) ampliamente dividido, un segundo sonido cardíaco (S2) único, y la presencia de un tercer (S3) y cuarto sonido cardíaco (S4) en el lado derecho del corazón. Estos hallazgos indicaban un ventrículo derecho severamente dilatado y con función alterada.  \n\nLas pruebas complementarias confirmaron estos hallazgos:  \n- El electrocardiograma mostró bloqueo completo del haz de rama derecha y un complejo QRS prolongado, reflejando alteraciones en la conducción eléctrica ventricular.  \n- La radiografía de tórax evidenció cardiomegalia (aumento del tamaño del corazón) y dilatación de las arterias pulmonares.  \n- La ecocardiografía y la resonancia magnética cardíaca demostraron una regresión completa de la válvula pulmonar (una estructura que normalmente evita el reflujo de sangre hacia el ventrículo derecho), lo que causaba una regurgitación pulmonar libre y una dilatación importante del ventrículo derecho con disminución de su capacidad de bombeo (fracción de eyección del 36%).  \n- La evaluación hemodinámica mediante cateterismo cardíaco mostró presiones elevadas en la aurícula derecha y ventrículo derecho, con formas de onda características que correspondían a los sonidos cardíacos S3 y S4 detectados en la auscultación.\n\n**Interpretación Clínica**  \nEl conjunto de sonidos cardíacos anormales —denominado aquí como el «quinteto de sonidos cardíacos»— reflejaba una insuficiencia cardíaca derecha grave causada por la dilatación y disfunción del ventrículo derecho, secundaria a la ausencia funcional de la válvula pulmonar y la regurgitación pulmonar libre resultante. La presencia simultánea de estos cinco sonidos (murmullo diastólico regurgitante, S1 ampliamente dividido, S2 único, S3 y S4 derechos) fue confirmada mediante una evaluación clínica, hemodinámica y anatómica exhaustiva.\n\n**Próximos Pasos y Resultado**  \nEl paciente fue sometido a un reemplazo de la válvula pulmonar, procedimiento que restauró la función valvular y eliminó la regurgitación pulmonar. Posteriormente, el «quinteto de sonidos cardíacos» desapareció por completo, indicando una mejora significativa en la función y la dinámica del ventrículo derecho.\n\n---\n\nEste caso ilustra cómo una alteración valvular congénita corregida en la infancia puede evolucionar décadas después hacia una insuficiencia cardíaca derecha severa, y cómo la evaluación detallada de los sonidos cardíacos, junto con estudios de imagen y hemodinámicos, es fundamental para un diagnóstico preciso y un tratamiento efectivo."
+        }
+    },
+    {
+        "article": "Un hombre de 62 años con antecedentes médicos de cardiopatía no isquémica que derivó en insuficiencia cardíaca, en estado postoperatorio de un dispositivo de asistencia ventricular izquierdo, se sometió a un trasplante cardíaco ortotópico. Mientras se recuperaba en la UCI quirúrgica, desarrolló un empeoramiento de la distensión abdominal, sensibilidad y leucocitosis, lo que motivó la evaluación por el equipo de cirugía general 6 días después del trasplante. El paciente no había evacuado ni expulsado gases desde su cirugía y no había respondido a los enemas administrados ni a la metoclopramida oral por un presunto íleo posoperatorio. Se realizó una tomografía computarizada del abdomen y la pelvis, que reveló múltiples bucles intestinales dilatados con niveles de aire-líquido y un punto de transición en el intestino delgado proximal en el cuadrante superior izquierdo, lo que generó preocupación por una obstrucción. En función de estos hallazgos y del hecho de que el paciente no había sido sometido a cirugías abdominales previas, lo que hacía que la obstrucción intestinal fuera secundaria a las adherencias, se llevó al paciente al quirófano para una laparotomía exploratoria. En el quirófano, se encontró que el intestino estaba dilatado de forma difusa sin ninguna área de isquemia aparente. Se encontró que una porción del intestino delgado estaba adherida a la pared abdominal anterior en el cuadrante superior izquierdo. Tras una exploración adicional, se encontró que una línea motriz de LVAD retenida estaba tunelizada en la cavidad peritoneal, estrangulando un bucle de intestino delgado en el cuadrante superior izquierdo. La línea motriz se liberó de la pared abdominal y se retiró, y se liberó el bucle de intestino afectado. Se encontró que era viable después de unos minutos de reperfusión. Se examinó el intestino delgado en su totalidad, desde el ligamento de Trietz distalmente hasta el intestino ciego, y se encontró que estaba dilatado pero en general era normal. Se reparó una pequeña área de desgarro seroso en el punto de adhesión a la línea motriz, principalmente. Se devolvió el intestino a la cavidad abdominal y se cerró la fascia y la piel con suturas corrientes y grapas cutáneas.\n\nMH - *Eliminación de dispositivo\nMH - Migración de cuerpos extraños/*complicaciones\nMH - Insuficiencia cardiaca/*terapia\nMH - *Trasplante de corazón\nMH - Dispositivos de asistencia cardíaca/*efectos adversos\nMH - Humanos\nMH - Obstrucción intestinal/diagnóstico por imágenes/*etiología\nMH - Laparotomía\nMH - Hombre\nMH - Edad Media\nMH - Tomografía computarizada por rayos X\nMH - Estados Unidos\n",
+        "gold_summary": "Un hombre de 62 años con antecedentes de insuficiencia cardiaca inducida por cardiomiopatía no isquémica, post-puente de asistencia ventricular izquierda y trasplante cardiaco ortotópico, presentó distensión abdominal, dolor y leucocitosis seis días después del trasplante. La TAC de abdomen y pelvis reveló bucles intestinales dilatados, niveles de aire-líquido y un punto de transición en el intestino delgado proximal. Se diagnosticó al paciente una obstrucción intestinal y se le realizó una laparotomía exploratoria. Se encontró que tenía un conducto de LVAD intraabdominal retenido que estrangulaba un bucle de intestino delgado en el cuadrante superior izquierdo. Se retiró el conducto y se liberó la sección de intestino con el retorno de la perfusión.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre de 62 años se sentía mal en su barriga después de una operación en su corazón. Su barriga estaba hinchada y le dolía. Los doctores le hicieron una foto especial para ver dentro de su barriga. Vieron que su intestino estaba muy grande y apretado en un lugar. Los doctores hicieron una operación para mirar dentro. Encontraron un tubito que estaba apretando su intestino. Quitaron el tubito y el intestino volvió a estar bien. Ahora el hombre puede sentirse mejor.",
+            "B2": "**Lo que pasó con el paciente**  \nUn hombre de 62 años, que tenía problemas graves del corazón y había recibido un trasplante de corazón, comenzó a tener dolor y hinchazón en el abdomen seis días después de la operación. También tenía más glóbulos blancos en la sangre, lo que puede indicar infección o inflamación.\n\n**Qué encontraron los médicos**  \nLe hicieron una tomografía, que es un tipo de radiografía especial, y vieron que partes de su intestino estaban muy hinchadas y había señales de que algo bloqueaba el paso en el intestino delgado, que es la parte del intestino donde se absorben los nutrientes.\n\n**Qué hicieron para ayudarlo**  \nLos médicos lo operaron para ver qué causaba la obstrucción. Durante la cirugía, descubrieron que un tubo que se usaba para ayudar a su corazón (llamado LVAD) se había movido dentro del abdomen y estaba apretando un pedazo del intestino, bloqueando el paso.\n\n**Resultado de la cirugía**  \nQuitaron ese tubo que estaba causando el problema y liberaron el intestino. Después de unos minutos, el intestino volvió a funcionar bien y no había daño grave. Finalmente, cerraron la herida y el paciente pudo continuar con su recuperación.\n\n**Por qué es importante**  \nEste caso muestra que los dispositivos para ayudar al corazón pueden, en raras ocasiones, causar problemas en otras partes del cuerpo, como el intestino. Por eso, los médicos deben estar atentos a síntomas como dolor abdominal después de cirugías complejas.",
+            "B3": "**Contexto**  \nUn hombre de 62 años con antecedentes de insuficiencia cardíaca causada por una enfermedad del músculo cardíaco no relacionada con problemas de circulación (cardiomiopatía no isquémica), que había sido tratado previamente con un dispositivo de asistencia ventricular izquierdo (LVAD, un aparato que ayuda al corazón a bombear sangre), recibió un trasplante de corazón ortotópico (reemplazo del corazón en su posición normal). Durante su recuperación en la unidad de cuidados intensivos, seis días después de la cirugía, presentó un aumento progresivo de la distensión abdominal (hinchazón), dolor abdominal y un aumento en el número de glóbulos blancos (leucocitosis), indicativo de inflamación o infección.\n\n**Hallazgos Clave**  \nUna tomografía computarizada (TAC) del abdomen y la pelvis mostró múltiples segmentos del intestino delgado dilatados con niveles de aire y líquido, además de un punto de transición en el intestino delgado proximal en el cuadrante superior izquierdo del abdomen. Estos hallazgos sugirieron la presencia de una obstrucción intestinal. Dado que el paciente no tenía antecedentes de cirugías abdominales previas, lo que reduce la probabilidad de adherencias (bandas de tejido cicatricial que pueden causar obstrucción), se decidió realizar una laparotomía exploratoria (cirugía para abrir el abdomen y examinar los órganos).\n\nDurante la cirugía, se observó que el intestino estaba dilatado pero sin signos de daño irreversible (isquemia). Se identificó que una porción del intestino delgado estaba adherida a la pared abdominal anterior. Al investigar más a fondo, se descubrió que una línea motriz del LVAD, que había migrado y estaba dentro de la cavidad abdominal, estaba causando una estrangulación (compresión que impide el flujo sanguíneo) de un segmento del intestino delgado en el cuadrante superior izquierdo. Esta línea motriz fue liberada y retirada, y el segmento intestinal afectado recuperó su circulación sanguínea tras unos minutos.\n\nSe inspeccionó todo el intestino delgado desde el ligamento de Treitz (punto donde el duodeno se une al yeyuno) hasta el intestino ciego, encontrándose dilatado pero sin daño significativo. Se reparó una pequeña lesión en la capa externa del intestino (desgarro seroso) en el sitio donde estaba adherido a la línea motriz. Finalmente, el intestino fue reposicionado en la cavidad abdominal y se cerró la incisión quirúrgica.\n\n**Interpretación Clínica**  \nEste caso ilustra una complicación poco común pero grave en pacientes con dispositivos de asistencia ventricular izquierda: la migración intraabdominal de una línea motriz que puede causar obstrucción intestinal por estrangulación. La presentación clínica con distensión abdominal, dolor y leucocitosis, junto con los hallazgos radiológicos, orientaron hacia una obstrucción intestinal que requirió intervención quirúrgica urgente para evitar daño intestinal irreversible.\n\n**Próximos Pasos**  \nSe recomienda un seguimiento cuidadoso para detectar posibles complicaciones posteriores, como infecciones o recurrencia de obstrucción. Además, es importante evaluar la correcta colocación y manejo de los dispositivos de asistencia ventricular para prevenir migraciones similares. Este caso destaca la necesidad de un abordaje multidisciplinario en pacientes complejos post-trasplante cardíaco con dispositivos implantados."
+        }
+    },
+    {
+        "article": "Un paciente de 13 años de edad, del sexo masculino, fue admitido en el Hospital de Niños de Damasco tras notar una masa palpable agrandada en la región inguinal izquierda. Su historial médico no fue notable, excepto por una intervención quirúrgica en su columna vertebral 6 años atrás, debido a un accidente, que resultó en la pérdida de la función motora y la sensación en ambas extremidades inferiores.\n\nDebido al largo período que había pasado en la cama, el paciente desarrolló úlceras de decúbito en su pie izquierdo. El único hallazgo en el examen clínico fue una masa en el área inguinal izquierda, que era móvil en las estructuras profundas y también lo era la piel que la cubría. La masa no era sensible a la palpación y no se observaron signos de inflamación local.\n\nLos exámenes de laboratorio revelaron una ESR elevada (119 mm/h en la primera hora). Se solicitaron otros exámenes básicos de laboratorio, que incluían (recuento sanguíneo completo, pruebas de función hepática, electrolitos, urea, creatinina y LDH) y estaban dentro de los rangos normales para la edad. La realización de estos exámenes fue esencial para descartar enfermedades sistémicas. Dada la ausencia de hallazgos físicos indicativos de trastornos sistémicos o inmunodeficiencias, se consideró innecesario realizar exámenes adicionales como los de VIH o antiglobulina directa.\n\nLa tomografía computarizada del abdomen, el tórax y la pelvis mostró ganglios linfáticos agrandados por debajo del ligamento inguinal, el más grande de aproximadamente 3,5 por 2,4 cm. Otros órganos y ganglios estaban dentro de los límites normales.\n\nTodas las investigaciones mencionadas fueron esenciales para descartar otros diagnósticos de alto riesgo, como linfoma y leucemia. Sin embargo, no fueron suficientes para llegar al diagnóstico definitivo, por lo que se tomó la decisión de realizar una resección quirúrgica de los ganglios.\n\nPara confirmar los diagnósticos y descartar otras posibles diferencias que pudieran presentarse con ganglios linfáticos agrandados, se realizó la extirpación quirúrgica de todos estos ganglios agrandados bajo anestesia general y se enviaron biopsias para su estudio microscópico.\n\nLa biopsia mostró una arquitectura ganglionar hiperplásica con proliferación de histiocitos y células plasmáticas con proliferación vascular, lo que es compatible con el subtipo de enfermedad de Castleman de células plasmáticas.\n\nEl paciente fue dado de alta del hospital después de 14 días, tras comprobar que no había ganglios linfáticos agrandados. La única recomendación fue prednisolona oral. El paciente se sometió a un seguimiento mediante TAC de cuerpo entero cada tres meses. Durante cada visita al hospital, se realizó un examen clínico exhaustivo y pruebas de laboratorio (por ejemplo, análisis de sangre completo, VSG, proteína C reactiva, pruebas de función hepática, pruebas de función renal), además del TAC. Después de un período de seguimiento de 12 meses, el paciente no informó de nuevos síntomas o ganglios linfáticos agrandados. Además, no se observaron anomalías durante el examen clínico o en las pruebas de laboratorio.\n",
+        "gold_summary": "Reportamos un caso único de un niño de 13 años que presentó una masa palpable agrandada en la región inguinal izquierda sin ningún síntoma constitucional. La extirpación quirúrgica de esta masa fue esencial para descartar causas preocupantes. El examen patológico reveló cambios proliferativos consistentes con el tipo de célula plasmática de la enfermedad de Castleman, que es una de las formas más raras de la enfermedad en niños. Hasta donde sabemos, este caso es el primer caso reportado de enfermedad de Castleman unicéntrica (UCD) en el área inguinal. Durante un período de seguimiento de 12 meses, no se reportaron agrandamientos adicionales de los ganglios linfáticos u otros síntomas.\n",
+        "synthetic_summary": {
+            "B1": "Había un niño de 13 años con una bolita en la ingle. La bolita no le dolía ni le hacía sentir mal. Los doctores sacaron la bolita con una operación para ver qué era. \n\nDespués, miraron la bolita con un microscopio y vieron que era una cosa rara que a veces pasa en niños. Es muy poco común. \n\nEl niño estuvo bien y no tuvo más bolitas ni se enfermó en un año. Los doctores lo cuidaron mucho y él está contento.",
+            "B2": "Caso de un niño con una masa en la ingle\n\nUn niño de 13 años notó una masa o bulto en la parte izquierda de su ingle (la zona donde la pierna se une al cuerpo). No tenía otros síntomas como fiebre o pérdida de peso. Para entender qué era esa masa, los médicos decidieron quitarla con cirugía.\n\nQué encontraron en la biopsia\n\nDespués de la cirugía, examinaron la masa bajo el microscopio. Vieron que había un crecimiento anormal de ciertas células llamadas células plasmáticas, que forman parte del sistema inmunológico. Este hallazgo mostró que el niño tenía una enfermedad llamada enfermedad de Castleman, que es muy rara en niños y afecta los ganglios linfáticos.\n\nImportancia del caso y seguimiento\n\nEste es el primer caso conocido de esta enfermedad en un ganglio linfático de la ingle en un niño. Después de la cirugía, el niño recibió un medicamento llamado prednisolona para ayudar a controlar la enfermedad. Durante un año, los médicos lo revisaron regularmente con exámenes físicos y pruebas de imagen para asegurarse de que no aparecieran nuevos ganglios agrandados ni otros problemas. El niño se mantuvo sin síntomas y sin nuevos bultos durante todo ese tiempo.\n\nEn resumen, este caso muestra la importancia de investigar y tratar las masas en los ganglios linfáticos para encontrar enfermedades raras y cuidar bien la salud.",
+            "B3": "**Contexto**  \nPresentamos el caso de un niño de 13 años que acudió al hospital debido a la presencia de una masa palpable en la región inguinal izquierda, sin presentar síntomas generales como fiebre, pérdida de peso o fatiga. Su historial médico previo incluía una cirugía en la columna vertebral tras un accidente, que le ocasionó parálisis y pérdida de sensibilidad en las piernas, lo que llevó a complicaciones como úlceras por presión en el pie izquierdo. No se identificaron otros signos clínicos relevantes ni indicios de infecciones o enfermedades sistémicas.\n\n**Hallazgos Clave**  \nLos análisis de laboratorio mostraron una velocidad de sedimentación globular (VSG) elevada, un marcador de inflamación, mientras que otros parámetros sanguíneos y pruebas de función orgánica se mantuvieron dentro de rangos normales. La tomografía computarizada (TAC) evidenció ganglios linfáticos aumentados de tamaño debajo del ligamento inguinal, siendo el mayor de aproximadamente 3,5 x 2,4 cm, sin afectación de otros órganos o ganglios. Para descartar enfermedades graves como linfoma o leucemia, se decidió realizar una cirugía para extirpar los ganglios afectados y analizarlos bajo el microscopio.\n\nEl examen histopatológico (microscópico) de los ganglios mostró una proliferación aumentada de células plasmáticas (un tipo de célula del sistema inmunitario) y células llamadas histiocitos, junto con un aumento en la formación de vasos sanguíneos, características compatibles con la forma de células plasmáticas de la enfermedad de Castleman. Esta enfermedad es una condición poco común que causa crecimiento anormal de ganglios linfáticos y puede presentarse en una única área (unicéntrica) o en múltiples regiones del cuerpo.\n\n**Interpretación Clínica**  \nEste caso representa una presentación rara de la enfermedad de Castleman unicéntrica en la región inguinal, un sitio poco frecuente para esta patología, especialmente en niños. La ausencia de síntomas sistémicos y la localización única de los ganglios afectados apoyan el diagnóstico de esta forma localizada de la enfermedad. La extirpación quirúrgica completa fue fundamental tanto para confirmar el diagnóstico como para tratar la condición.\n\n**Próximos Pasos y Seguimiento**  \nTras la cirugía, el paciente recibió tratamiento con prednisolona oral (un corticosteroide) y fue dado de alta después de 14 días sin complicaciones. Se estableció un seguimiento riguroso que incluyó evaluaciones clínicas, análisis de laboratorio y tomografías computarizadas cada tres meses para detectar cualquier recurrencia o aparición de nuevos ganglios agrandados. Durante un año de seguimiento, el paciente no presentó nuevos síntomas ni evidencia de enfermedad activa, lo que indica un buen pronóstico tras el tratamiento quirúrgico.\n\nEn resumen, este caso destaca la importancia de considerar la enfermedad de Castleman en el diagnóstico diferencial de masas ganglionares inguinales en niños, y demuestra que la resección quirúrgica puede ser curativa en la forma unicéntrica de esta enfermedad."
+        }
+    },
+    {
+        "article": "Un hombre asiático de 55 años de edad, que había estado recibiendo tratamiento irregularmente (el paciente no cumplía con el tratamiento) para DCMP durante los últimos 6 meses, acudió con quejas de disnea al hacer ejercicio durante 1 semana y disminución de la producción de orina durante 2 días. El paciente aparentemente estaba bien hace 1 semana cuando empezó a desarrollar disnea, inicio insidioso, gradualmente progresiva, inicialmente de grado II de la New York Heart Association (NYHA) pero progresó a grado IV de la NYHA asociada con pesadez en el pecho. La historia de ortopnea y disnea nocturna paroxística estuvo presente. Esto estuvo asociado con tos con una cantidad moderada de expectoración espumosa, no purulenta. El paciente también se quejó de hinchazón de las extremidades inferiores bilaterales. No hubo historia de hinchazón periorbital, orina espumosa o hematuria. No hubo historia de palpitación, síncope, dolor de pecho o hemoptisis. El paciente también dio una historia de una sensación de hormigueo en ambas manos y pies durante 1 mes.\n\nEl paciente había tenido un episodio similar 6 meses atrás, por el que fue hospitalizado y tratado de manera conservadora como un caso de DCMP. Se le había practicado una cirugía de cataratas en ambos ojos 15 años atrás.\n\nEn el examen físico general, el paciente estaba consciente y orientado en cuanto al tiempo, el lugar y la persona, y afebril con una presión arterial de 90/60 mmHg en el brazo derecho en posición supina y una frecuencia de pulso de 110/min, que era de bajo volumen y todos los pulsos periféricos eran palpables. Presentaba taquipnea con una frecuencia respiratoria de 28/min y palidez. Tenía un edema de pedal B/L, que era de tipo lento con presión venosa yugular elevada (JVP). No se observó ictericia, cianosis, clubbing ni linfadenopatía. Mientras se medía la presión arterial, el paciente empezó a tener espasmos en la muñeca, lo que nos dio una pista para examinar más a fondo y revelar un signo de Chvostek positivo. El signo de Trousseau también fue positivo a los 10 segundos.\n\nEl examen del sistema cardiovascular reveló un latido apical localizado en el sexto espacio intercostal izquierdo, a 1 cm fuera de la línea medioclavicular, de carácter hiperdinámico. Se escucharon S1 y S2 con normalidad en todas las áreas.\n\nEl examen del sistema respiratorio reveló una reducción de la entrada de aire en las bases pulmonares bilaterales con crepitación fina al final de la inspiración bilateral. El examen del sistema nervioso abdominal y central no reveló nada de interés.\n\n\nInvestigaciones\n\nEn el momento del ingreso, el ECG mostró bloqueo completo de rama izquierda (B-R) con un intervalo QT prolongado. La hemoglobina era de 58 g/l (133-162) con un cuadro dimórfico. El volumen corpuscular medio era de 110 fL (80,0-100,0 fL), la hemoglobina corpuscular media era de 34 pg/mL (27,0-32,0 pg/mL), la concentración media de hemoglobina corpuscular era de 36,2 g/dL (32,0-35,0 g/dL). Otros análisis revelaron niveles séricos de vitamina B12 de 135 pg/mL (211-911 pg/mL). El nivel sérico de ácido fólico era de 5,40 ng/mL (>5,38 ng/mL). El nitrógeno ureico en sangre era de 53 mg/dL (10-50) con creatinina de 0,8 mg/dL (0,7-1,3). Los resultados de las pruebas de función hepática (LFT) estaban dentro de los límites normales. El perfil de calcio mostró 4,3 mg/dL de S.calcium (8,5-10,5), fosfato 7,1 mg/dL (2,5-4,5), 3,06 g/dL de S.albumin (3,5-5,5). En vista de la hipocalcemia e hiperfosfatemia, se realizó un estudio del nivel de hormona paratiroidea intacta, que resultó ser <0,23 ng/mL (14-72). El S.magnesium era de 2,0 mg/dL (1,7-2,2). El análisis de gases en sangre arterial (ABG) fue sugestivo de una acidosis metabólica leve. El perfil tiroideo y los niveles de IgAtTG estaban dentro de los límites normales. Los niveles de ferritina y ceruloplasmina séricos estaban dentro de los límites normales. El ultrasonido abdominal y torácico mostró derrame pleural bilateral en posición supina. La vena cava inferior (IVC) y las venas hepáticas eran prominentes. El reposo dentro de los límites normales. La radiografía de tórax mostró un aplanamiento de los ángulos costofrénicos bilaterales que sugería derrame pleural bilateral. La ecocardiografía reveló un ventrículo izquierdo dilatado (LV) con una fracción de eyección del ventrículo izquierdo del 15 %, que sugería DCMP con disfunción severa del LV. Se realizó un arteriograma coronario basal que fue normal. La TC sin contraste de la cabeza mostró calcificación simétrica bilateral (B/L) en el hemisferio cerebeloso B/L, ganglios basales B/L y calcificación cortical/subcortical en la región B/L fronto-parieto-occipital. El reposo dentro de los límites normales.\n\n\nTratamiento\n\nPara el CHF, se inició al paciente con dobutamina intravenosa a una dosis de 6 µg/kg y furosemida intravenosa 20 mg BD para la descongestión. Sin embargo, el paciente no mostró una mejora significativa con el tratamiento anterior. En vista de la hipocalcemia con hiperfosfatemia y bajos niveles de hormona paratiroidea, se consideró un diagnóstico de cardiomiopatía hipocalcemica con hipoparatiroidismo y se inició al paciente con inyección de gluconato de calcio 1 g (90 mg de calcio elemental) administrado por vía intravenosa seguido de infusión de gluconato de calcio en 500 ml de dextrosa al 5% a una velocidad de 37,5 mg/hora de calcio elemental. El paciente mostró una mejora significativa después de iniciar el gluconato de calcio. El paciente fue dado de alta en condiciones estables con comprimidos de calcio por vía oral 3 g/día junto con calcitriol 0,5 µg/día. También se inició con benzotiazida con triamtereno (25/50 mg) OD, ramipril 5 mg una vez al día y carvedilol 3,125 mg dos veces al día. Para la anemia megaloblástica, se administraron inyecciones de cianocobalamina según el protocolo.\n\n\nResultado y seguimiento\n\nAl cabo de tres meses, el paciente había mejorado notablemente.\n\nLas investigaciones mostraron S.calcium 7.7, S.phosphate 6.0 y albúmina 3.6. La hemoglobina fue de 10.1 g/dL. El eco mostró una mejora en la función del LV con una fracción de eyección del 25%. Se planificó una biopsia endomiocardial, pero el paciente se negó, por lo que no pudo realizarse.\n\nMH - Gluconato de calcio/administración y dosificación/uso terapéutico\nMH - Cardiomiopatía, Dilatada/*complicaciones/diagnóstico\nMH - Ecocardiografía/métodos\nMH - Insuficiencia cardiaca/terapia farmacológica/*etiología/fisiopatología\nMH - Humanos\nMH - Hipocalcemia/*complicaciones/diagnóstico/terapia farmacológica/fisiopatología\nMH - Hipoparatiroidismo/*complicaciones/terapia farmacológica\nMH - Hombre\nMH - Edad Media\nMH - Volumen de carrera\nMH - Resultado del tratamiento\nMH - Disfunción ventricular izquierda/diagnóstico por imágenes\n",
+        "gold_summary": "Presentamos el caso de un hombre asiático de 55 años que había tenido un caso conocido de miocardiopatía dilatada durante 6 meses, que se presentó con las principales quejas de falta de aire al hacer ejercicio y disminución de la producción de orina. En el examen físico general, se observaron características que sugerían una ICC. El signo de Chvostek y Trousseau fue positivo. El paciente tenía antecedentes de cirugía de cataratas en ambos ojos 15 años atrás. Otras investigaciones revelaron una hipocalcemia. La ecografía mostró una grave hipocinesia global del ventrículo izquierdo con una fracción de eyección del ventrículo izquierdo del 15%. Esta ICC fue refractaria al tratamiento convencional, aunque, con la suplementación de calcio, el paciente mejoró sintomáticamente. En el seguimiento después de 3 meses, se observó una mejora en los parámetros ecocardiográficos con una fracción de eyección que mejoró al 25%.\n",
+        "synthetic_summary": {
+            "B1": "Había un hombre que se sentía muy cansado y le costaba respirar cuando caminaba. También hacía menos pipí. El doctor vio que su corazón estaba muy débil. El hombre tenía señales en sus manos que mostraban que le faltaba calcio. Le dieron calcio para ayudarlo. Después de un tiempo, el corazón del hombre se puso un poco mejor y él se sintió mejor también.",
+            "B2": "**Caso de un Hombre con Problemas del Corazón y Bajos Niveles de Calcio**\n\nUn hombre de 55 años, que ya tenía un diagnóstico de miocardiopatía dilatada (una enfermedad del corazón donde el músculo del ventrículo izquierdo se debilita y agranda), llegó al hospital porque tenía dificultad para respirar al hacer ejercicio y producía menos orina de lo normal.\n\n**Lo que Encontraron en el Examen**\n\nAl revisarlo, los médicos notaron signos de insuficiencia cardíaca congestiva (cuando el corazón no bombea bien y se acumula líquido). También detectaron dos signos especiales llamados Chvostek y Trousseau, que indican que el cuerpo tiene poco calcio en la sangre. Además, el paciente había tenido cirugía de cataratas en ambos ojos hace 15 años.\n\n**Resultados de las Pruebas**\n\nLas pruebas mostraron que tenía hipocalcemia, es decir, niveles bajos de calcio en la sangre. El ultrasonido del corazón (ecocardiografía) reveló que su ventrículo izquierdo estaba muy debilitado, con una fracción de eyección del 15%, lo que significa que el corazón bombeaba muy poco sangre.\n\n**Tratamiento y Mejoría**\n\nEl paciente no mejoró con el tratamiento habitual para la insuficiencia cardíaca. Sin embargo, cuando le dieron calcio por vía intravenosa, su condición mejoró notablemente. Después de tres meses, su corazón funcionaba mejor, con una fracción de eyección aumentada al 25%.\n\n**Qué Significa Esto**\n\nEste caso muestra que la falta de calcio en la sangre, causada por un problema llamado hipoparatiroidismo (cuando una glándula llamada paratiroides no produce suficiente hormona para controlar el calcio), puede empeorar la función del corazón. Al corregir el calcio, se puede mejorar la salud del corazón en pacientes con miocardiopatía dilatada.",
+            "B3": "**Contexto**  \nSe presenta el caso de un hombre asiático de 55 años con diagnóstico previo de miocardiopatía dilatada (una enfermedad del músculo cardíaco que provoca su debilitamiento y agrandamiento) durante los últimos 6 meses. El paciente acudió al hospital debido a dificultad para respirar al realizar ejercicio (disnea) y una reducción en la cantidad de orina durante los últimos dos días. Su dificultad respiratoria había empeorado progresivamente, llegando a un grado severo según la clasificación de la Asociación del Corazón de Nueva York (NYHA). Además, presentaba hinchazón en ambas piernas y tos con expectoración espumosa, síntomas compatibles con insuficiencia cardíaca congestiva (ICC).\n\n**Hallazgos Clave**  \nEn el examen físico, el paciente mostraba signos típicos de insuficiencia cardíaca, como edema en las extremidades inferiores y aumento de la presión venosa yugular. Además, durante la toma de la presión arterial, se evidenciaron espasmos musculares en la muñeca, lo que llevó a descubrir signos positivos de Chvostek y Trousseau, indicativos de hipocalcemia (niveles bajos de calcio en sangre). El paciente también tenía antecedentes de cirugía de cataratas bilateral realizada 15 años antes.\n\nLos análisis de laboratorio confirmaron hipocalcemia severa junto con niveles elevados de fosfato y una hormona paratiroidea (PTH) muy baja, lo que sugiere hipoparatiroidismo (una condición en la que las glándulas paratiroides no producen suficiente hormona para regular el calcio). La ecocardiografía mostró un ventrículo izquierdo dilatado con una fracción de eyección muy baja (15%), reflejando una función cardíaca gravemente comprometida. Otras pruebas descartaron enfermedad coronaria y evidenciaron calcificaciones cerebrales simétricas.\n\n**Interpretación Clínica**  \nEl cuadro clínico y los resultados sugieren que la insuficiencia cardíaca del paciente no solo se debía a la miocardiopatía dilatada conocida, sino que estaba agravada por una cardiomiopatía secundaria a hipocalcemia causada por hipoparatiroidismo. La hipocalcemia puede afectar la contracción del músculo cardíaco, empeorando la función ventricular. Esto explica la falta de respuesta a los tratamientos convencionales para insuficiencia cardíaca.\n\n**Tratamiento y Evolución**  \nSe inició tratamiento estándar para insuficiencia cardíaca, incluyendo dobutamina y diuréticos, sin mejoría significativa. Al identificar la hipocalcemia e hipoparatiroidismo, se administró gluconato de calcio por vía intravenosa, seguido de calcio oral y calcitriol (una forma activa de vitamina D) para corregir el déficit de calcio. Tras esta intervención, el paciente mostró una mejoría clínica notable. También se trató la anemia megaloblástica con vitamina B12.\n\nEn el seguimiento a los tres meses, el paciente presentó mejoría en los niveles de calcio y en la función cardíaca, con una fracción de eyección que aumentó al 25%, lo que indica una recuperación parcial de la capacidad de bombeo del corazón. Sin embargo, el paciente rechazó realizar una biopsia endomiocárdica que podría haber ayudado a confirmar el diagnóstico definitivo.\n\n**Próximos Pasos**  \nSe recomienda continuar con el tratamiento de calcio y calcitriol para mantener niveles adecuados de calcio en sangre y prevenir complicaciones. Además, es fundamental el seguimiento cardiológico para monitorizar la función ventricular y ajustar la terapia para la insuficiencia cardíaca. La educación del paciente sobre la importancia de la adherencia al tratamiento es clave para evitar recaídas. En caso de que el paciente acepte, una biopsia cardíaca podría aportar información adicional para el manejo a largo plazo."
+        }
+    },
+    {
+        "article": "Una mujer de 54 años de edad, libanesa, en hemodiálisis (HD) de mantenimiento tres veces por semana para glomeruloesclerosis segmentaria focal (GSF) fue admitida en el departamento de urgencias, luego de haber sido sometida a su HD programada la noche anterior, debido al inicio repentino de un dolor lumbar agudo en el lado izquierdo, náuseas y vómitos. El dolor había comenzado repentinamente cerca de 12 horas antes de su presentación y se agravó rápidamente. En una nota al margen, un hiperparatiroidismo secundario grave con calcificación cutánea vascular fue tratado con cinacalcet durante 3 años sin respuesta, lo que demandó una paratiroidectomía (hiperplasia de cuatro glándulas) 8 meses antes de su presentación actual. Cinco días antes de su presentación, fue admitida en el hospital debido a anemia grave y rectorragia. Su evaluación por ultrasonido renal mostró riñones bilaterales pequeños con parénquima delgado que contenía quistes de hasta 3 cm y calcificaciones vasculares sin hidronefrosis. Cuatro días antes de su presentación, la colonoscopia a través del íleo terminal reveló un pólipo de 7 mm en el colon descendente izquierdo, que fue removido por mucosectomía. La microscopía volvió como adenoma tubular sésil con displasia de bajo grado. La paciente negó fiebre o antecedentes de trauma. No hubo antecedentes previos de uso de antiplaquetarios. En la emergencia, su presión arterial y pulso fueron de 112/65 mmHg y 96 bpm, su temperatura fue de 36.8°C y presentaba abdomen levemente distendido, con dolor importante en el ángulo costovertebral izquierdo. Los hallazgos de laboratorio mostraron hemoglobina de 9.0 g/dL mientras que el hematocrito fue de 29.7%, recuento total de leucocitos 12.2 × 1000/microlitro, creatinina de 6.06 mg/dL, y nivel de proteína C reactiva de 6 mg/L. Además, el TP fue de 83% y el INR fue de 1.13. En el día de la presentación (es decir, 4 días después de la colonoscopia), se realizó una tomografía computarizada (TC) multifásica del tórax, abdomen y pelvis con y sin contraste intravenoso. El examen reveló un gran quiste y enormes hematomas intraparenquimatosos perirrenales izquierdos con una colección subcapsular de hasta 1,8 cm de espesor con colección hemática en todo el compartimiento renal que alcanzaba un diámetro de más de 9 × 4 cm, hidronefrosis izquierda y edema alrededor de la grasa en todo el flanco y calcificaciones en el hilo. Para la descompresión del sistema pélvico renal y drenaje, optamos por tratarla con inserción retrógrada de doble stent ureteral a la izquierda, que identificó un coágulo en la parte media del uréter izquierdo. Se realizaron cultivo de orina y citología y los resultados fueron negativos. Una simple radiografía del abdomen mostró el doble J en su lugar. La paciente permaneció hemodinámicamente estable, pero presentó una nueva caída en la hemoglobina (6.1 g/dL) la misma noche, lo que exigió una transfusión de una unidad de concentrado de eritrocitos leucodepleados para estabilización. Se tomó la decisión de explorar quirúrgicamente con diagnóstico presuntivo de hematoma perirrenal izquierdo subagudo y para excluir una malignidad subyacente. Se sometió a una sesión de HD sin heparina. En el tercer día, se sometió a una nefrectomía radical abierta a la izquierda con conservación de la glándula suprarrenal. Recibió 2 unidades más de concentrado de eritrocitos leucodepleados durante la intervención. El parénquima renal fue casi totalmente reemplazado por un hematoma que medía 9 × 9 × 7 cm y se extendía hasta la grasa perirrenal. Una pequeña masa papilar fue enviada por separado para análisis. La evaluación histopatológica detallada reveló un parénquima renal con lesiones de nefritis crónica mutilada por grandes áreas hemorrágicas que se extendían hasta la grasa perirrenal. Además, había una proliferación neoplásica de 2 mm, con arquitectura papilar cubierta por pequeñas células cúbicas atípicas y macrófagos espumosos en el eje, compatibles con adenoma papilar. Al día siguiente de la operación, la paciente fue sometida a HD y recibió un paquete de eritrocitos leucodepleados. El período postoperatorio fue sin intercorrerencias. El nivel de hemoglobina se mantuvo alrededor de 10 g/dL. La paciente se recuperó sin signos o síntomas de sangrado. La paciente permanece bien y asintomática y actualmente se encuentra en HD de mantenimiento regular.\n",
+        "gold_summary": "A continuación, se describe un caso inusual de una paciente con HD de 54 años de edad que presentó HPE pocos días después de una colonoscopia. La causa de la HPE fue la ruptura de un quiste de DRCA. Consideramos que la colonoscopia fue un factor desencadenante y planteamos hipótesis sobre su etiopatogenia. La paciente se sometió a una nefrectomía izquierda exitosa.\n",
+        "synthetic_summary": {
+            "B1": "Una señora de 54 años tenía un problema en sus riñones. Ella se hacía un tratamiento para limpiar su sangre. Unos días después de un examen en su barriga, empezó a sentir mucho dolor en un lado. Un quiste en su riñón se rompió y eso le dolió mucho. Los doctores le hicieron una operación para quitar ese riñón. Ahora ella está mejor y sigue con su tratamiento para limpiar su sangre.",
+            "B2": "**Caso de una mujer con sangrado en el riñón después de una colonoscopia**\n\nUna mujer de 54 años que estaba en hemodiálisis, un tratamiento para personas con problemas graves en los riñones, tuvo un problema raro. Pocos días después de hacerse una colonoscopia (un examen para revisar el colon), comenzó a sentir un dolor fuerte en la parte baja de la espalda, del lado izquierdo, junto con náuseas y vómitos.\n\nLos médicos descubrieron que tenía un sangrado grande alrededor de su riñón izquierdo. Este sangrado ocurrió porque se rompió un quiste, que es una bolsa llena de líquido que se forma en el riñón. La ruptura del quiste causó un hematoma, que es una acumulación de sangre fuera de los vasos sanguíneos.\n\nCreen que la colonoscopia pudo haber sido la causa que desencadenó este problema, aunque no es común que esto pase. Para tratar la situación, los médicos le hicieron una cirugía para quitarle el riñón izquierdo, llamada nefrectomía. La operación fue exitosa y la paciente se recuperó bien, sin más sangrados.\n\nEste caso es importante porque muestra una complicación poco común después de una colonoscopia en una persona con enfermedad renal avanzada y hemodiálisis. Los médicos aprendieron que hay que estar atentos a síntomas como dolor intenso y sangrado después de estos procedimientos en pacientes con problemas renales.",
+            "B3": "**Contexto:**  \nSe presenta el caso poco común de una mujer de 54 años que se encuentra en hemodiálisis (HD) debido a una enfermedad renal crónica avanzada llamada glomeruloesclerosis segmentaria focal. Esta paciente desarrolló un hematoma perirrenal espontáneo (HPE), que es una acumulación de sangre alrededor del riñón, pocos días después de haberse sometido a una colonoscopia, un procedimiento para examinar el colon.\n\n**Hallazgos Clave:**  \nEl hematoma perirrenal se originó por la ruptura de un quiste renal asociado a una enfermedad renal crónica avanzada (DRCA). La tomografía computarizada mostró un gran hematoma intraparenquimatoso (dentro del tejido renal) y perirrenal (alrededor del riñón) en el riñón izquierdo, con signos de sangrado activo y compresión del sistema urinario. La paciente presentó dolor lumbar intenso, anemia progresiva y requerimientos de transfusión sanguínea. Durante la intervención quirúrgica, se confirmó que el parénquima renal estaba casi completamente reemplazado por el hematoma. Además, se identificó una pequeña lesión benigna llamada adenoma papilar.\n\n**Interpretación Clínica:**  \nSe considera que la colonoscopia, realizada días antes, pudo haber sido un factor desencadenante que contribuyó a la ruptura del quiste renal y la formación del hematoma. Aunque la relación causal no es completamente clara, la manipulación abdominal y los cambios en la presión intraabdominal durante la colonoscopia podrían haber favorecido este evento hemorrágico en un riñón ya debilitado por la enfermedad crónica y la presencia de quistes. La situación requirió una nefrectomía radical (extirpación completa del riñón afectado) para controlar el sangrado y evitar complicaciones mayores.\n\n**Próximos Pasos y Seguimiento:**  \nTras la cirugía, la paciente continuó con su tratamiento de hemodiálisis sin complicaciones adicionales y se mantuvo estable, sin signos de sangrado recurrente. Este caso resalta la importancia de considerar posibles complicaciones renales en pacientes con enfermedad renal crónica avanzada que se someten a procedimientos invasivos, y la necesidad de un manejo multidisciplinario para asegurar una recuperación adecuada."
+        }
+    },
+    {
+        "article": "Se evaluó a una mujer de 30 años de edad con antecedentes de dos meses de dolor progresivo y disminución de la visión OD. Dos semanas antes del desarrollo de los síntomas oculares, la paciente comenzó a disminuir la prednisona como tratamiento para sus síntomas inflamatorios sistémicos. Los antecedentes médicos incluyen artritis inflamatoria, síntomas gastrointestinales que sugieren enfermedad intestinal inflamatoria y pérdida de peso de 20 libras antes de la presentación. Los detalles completos del caso de la paciente se informaron previamente y se resumen aquí junto con análisis adicionales de quimiocina y citoquina de fluido ocular.13\n\nEn el examen, las BCVAs fueron 20/40 OD y 20/20 OS, y las pupilas fueron 9 mm y akinéticas OD y 5 mm con una rápida reactividad a la luz OS. Las presiones intraoculares fueron 65 mmHg OD y 21 mmHg OS. El examen con lámpara de hendidura mostró precipitados queráticos granulomatosos pigmentados (KP) dentro de la córnea inferior, 3+ células de la cámara anterior, atrofia difusa del iris con pigmento en las zónulas, y ectropion uvea OD, y OS fue normal. La gonioscopia mostró 3+ células pigmentadas dentro del ángulo inferior OD. El examen del fondo fue normal en ambos ojos. Una paracentesis anterior diagnóstica fue positiva para ADN de VZV mediante pruebas de PCR, y las pruebas serológicas fueron positivas para anticuerpos IgG de VZV. Posteriormente, se le diagnosticó uveítis anterior hipertensiva asociada a VZV, lo que provocó el inicio de acetazolamida oral y timolol oftálmico, dorzolamida, y brimonidina para la hipertensión ocular, así como valaciclovir 1 g TID y acetato de prednisolona 1% cada 2 horas. El curso de la enfermedad de la paciente y otros detalles de su tratamiento se describieron previamente.13\n\nLa paciente fue diagnosticada con un accidente cerebrovascular (ACV), que se cree que se debe a una vasculopatía del SNC asociada al VVZ, y fue hospitalizada durante 2 semanas, durante las cuales sus síntomas oculares mejoraron gradualmente. Sin embargo, dos meses después de su ACV, desarrolló un empeoramiento del dolor y la visión en el ojo derecho, y su BCVA disminuyó a 20/100 con una PIO elevada de 39 mmHg OD. El examen reveló una inyección ciliar 1+ y 3+ células de la cámara anterior, y se cambió de prednisolona a difluprednato con una mejora mínima. Posteriormente, se sometió a un procedimiento de filtración de glaucoma con una derivación de Ahmed debido a su PIO elevada persistente a pesar de la máxima tolerancia de la terapia ocular hipertensiva. Se obtuvo una muestra de humor acuoso del ojo derecho durante la cirugía de filtración para un análisis de perfil de quimiocina/citoquina. Se estimaron los niveles de 22 citoquinas y quimioquinas, incluidos IFN-Y, IL-10, IL-12p70, IL-17A, IL-1B, IL-2, IL-5, IL-6, IL-8, TNF-a, IL-18, IL-1RA, IL-1a, IL-1a, IP-10, MCP-1, MIP-1a, MIP-1B, SDF-1a, IL-21, IL-22, IL-23 e IL-27, utilizando la técnica de inmunoensayo de perlas múltiplex. Se detectaron niveles de concentración de 7 citoquinas/quimioquinas, incluidos IL-6, IL-8, IL-18, MIP-1b, IP-10, MCP-1, e IL-1RA. La IL-1RA fue la citoquina más abundante (1000 pg/mL), mientras que IP-10 y MCP-1 fueron las segundas citoquinas más abundantes (150–200 pg/mL). Se detectaron niveles de 10–20 pg/mL de IL-18 y MCP-1b, pero a niveles mínimos en esta muestra de AqH. Se detectaron niveles de IL-6 e IL-8, pero se encontró que eran las citoquinas menos abundantes, cada una con niveles de <10 pg/mL.\n\n",
+        "gold_summary": "El caso 2 fue el de una mujer de 30 años con antecedentes de dos meses de dolor progresivo y disminución de la visión en el ojo derecho. Se le diagnosticó uveítis anterior hipertensiva tras una paracentesis diagnóstica de la cámara anterior. A pesar de la terapia exitosa para la uveítis anterior, su presión intraocular se mantuvo elevada y requirió un procedimiento de filtración de glaucoma. Se recolectó una muestra de fluido ocular en el momento de la cirugía para el análisis de perfiles de citoquinas/quimioquinas, y se detectaron niveles de 7 citoquinas/quimioquinas, entre ellas, IL-6, IL-8, IL-18, MIP-1B, IP-10, MCP-1 e IL-1RA, siendo IL-1RA la citoquina más abundante.\n",
+        "synthetic_summary": {
+            "B1": "Había una mujer que tenía dolor y no veía bien con un ojo. Los doctores encontraron que su ojo estaba inflamado y tenía mucha presión. Ella necesitó una operación para ayudar a que la presión bajara. Durante la operación, los doctores tomaron un poquito de líquido del ojo para ver qué había dentro. Encontraron unas cosas llamadas citoquinas, que son como mensajeros que dicen al cuerpo qué hacer. Una de estas citoquinas estaba más que las otras. Esto ayuda a los doctores a entender mejor qué pasa en el ojo.",
+            "B2": "**Caso de una Mujer con Problemas en el Ojo Derecho**\n\nUna mujer de 30 años tuvo dolor y pérdida de visión en su ojo derecho durante dos meses. Los médicos le diagnosticaron una inflamación llamada uveítis anterior hipertensiva, que significa que había inflamación en la parte frontal del ojo y la presión dentro del ojo estaba alta. Para confirmar esto, tomaron una pequeña muestra del líquido dentro del ojo, llamado fluido ocular.\n\nAunque recibió tratamiento para la inflamación, la presión en su ojo siguió siendo alta. Por eso, necesitó una cirugía llamada filtración de glaucoma, que ayuda a bajar la presión del ojo para evitar daños.\n\nDurante la cirugía, los médicos tomaron otra muestra del fluido ocular para estudiar unas sustancias llamadas citoquinas y quimioquinas. Estas sustancias son como señales que usan las células para comunicarse y controlar la inflamación. Encontraron siete de estas sustancias, entre ellas IL-6, IL-8, IL-18, MIP-1B, IP-10, MCP-1 y IL-1RA. La más abundante fue IL-1RA, que ayuda a reducir la inflamación en el cuerpo.\n\nEste análisis ayuda a entender mejor qué está pasando en el ojo durante la enfermedad y podría ayudar a mejorar los tratamientos en el futuro.",
+            "B3": "**Contexto**  \nSe evaluó a una mujer de 30 años que presentaba un cuadro de dos meses con dolor progresivo y disminución de la visión en su ojo derecho. Dos semanas antes del inicio de estos síntomas oculares, había comenzado a reducir la dosis de prednisona, un corticosteroide que utilizaba para tratar síntomas inflamatorios sistémicos relacionados con artritis inflamatoria y posibles enfermedades intestinales inflamatorias. Además, había experimentado una pérdida de peso significativa antes de la consulta.\n\n**Hallazgos Clave**  \nEn el examen ocular inicial, la agudeza visual era de 20/40 en el ojo derecho y 20/20 en el izquierdo. Se observaron pupilas anormalmente dilatadas y sin respuesta en el ojo derecho, con una presión intraocular (PIO) muy elevada de 65 mmHg (normalmente debe estar entre 10 y 21 mmHg), mientras que el ojo izquierdo estaba dentro de los parámetros normales. El examen con lámpara de hendidura reveló signos de inflamación en la parte frontal del ojo derecho, incluyendo células inflamatorias en la cámara anterior y depósitos granulomatosos pigmentados en la córnea. También se detectó atrofia del iris y otras alteraciones estructurales. La gonioscopia, que examina el ángulo donde drena el humor acuoso, mostró células pigmentadas inflamatorias. El fondo de ojo estaba normal en ambos ojos.\n\nUna prueba diagnóstica mediante paracentesis (extracción de fluido del ojo) confirmó la presencia de ADN del virus varicela-zóster (VVZ), responsable de la culebrilla, y los análisis serológicos indicaron anticuerpos contra este virus, confirmando la infección ocular. Se diagnosticó uveítis anterior hipertensiva asociada a VVZ, una inflamación del segmento anterior del ojo que causa aumento de la presión ocular. El tratamiento incluyó medicamentos para reducir la presión intraocular (acetazolamida, timolol, dorzolamida, brimonidina), un antiviral oral (valaciclovir) y corticosteroides tópicos (prednisolona).\n\nPosteriormente, la paciente sufrió un accidente cerebrovascular atribuido a una vasculopatía (enfermedad de los vasos sanguíneos) del sistema nervioso central relacionada con el VVZ, lo que requirió hospitalización. Durante su recuperación, los síntomas oculares mejoraron, pero dos meses después presentó un nuevo empeoramiento con aumento del dolor, disminución de la visión a 20/100 y presión intraocular elevada (39 mmHg). Se intensificó el tratamiento antiinflamatorio con difluprednato, pero la respuesta fue mínima, por lo que se realizó una cirugía de filtración para controlar la presión ocular, colocando una derivación de Ahmed.\n\n**Análisis de Citoquinas y Quimioquinas**  \nDurante la cirugía, se obtuvo una muestra del humor acuoso (fluido dentro del ojo) para analizar el perfil de citoquinas y quimioquinas, que son proteínas que regulan la inflamación y la respuesta inmune. Se evaluaron 22 de estas moléculas mediante una técnica avanzada llamada inmunoensayo de perlas múltiplex. Se detectaron niveles significativos de siete citoquinas/quimioquinas: interleucina-6 (IL-6), interleucina-8 (IL-8), interleucina-18 (IL-18), proteína quimioatrayente de macrófagos 1 beta (MIP-1b), proteína inducible por interferón gamma 10 (IP-10), proteína quimioatrayente de monocitos 1 (MCP-1) y antagonista del receptor de interleucina 1 (IL-1RA).\n\nDe estas, la IL-1RA fue la más abundante, con una concentración alrededor de 1000 pg/mL. Esta molécula actúa como un regulador que bloquea la acción de la interleucina 1, una citoquina proinflamatoria, y su presencia elevada sugiere un intento del organismo por controlar la inflamación ocular. IP-10 y MCP-1 fueron las segundas más abundantes, con niveles entre 150 y 200 pg/mL, y están involucradas en la atracción de células inmunitarias al sitio inflamado. Las otras citoquinas, incluyendo IL-6 e IL-8, estuvieron presentes en concentraciones más bajas (<10 pg/mL).\n\n**Interpretación Clínica**  \nEste caso ilustra una uveítis anterior hipertensiva causada por infección activa por VVZ, que además se complicó con un accidente cerebrovascular relacionado con la misma infección viral. La persistencia de la presión intraocular elevada a pesar del tratamiento médico requirió intervención quirúrgica. El análisis detallado del perfil inflamatorio en el humor acuoso reveló una respuesta inmunitaria compleja, con predominio de moléculas reguladoras como IL-1RA, lo que podría reflejar mecanismos de control de la inflamación en el ojo afectados por el virus.\n\n**Próximos Pasos**  \nEl manejo de esta paciente requiere un seguimiento estrecho para controlar la inflamación ocular y la presión intraocular, prevenir daños permanentes en la visión y vigilar posibles complicaciones neurológicas asociadas al VVZ. El análisis de citoquinas puede ofrecer información valiosa para ajustar terapias inmunomoduladoras y antivirales en casos similares."
+        }
+    },
+    {
+        "article": "Un varón negro de 2021 g de peso nació a las 35 semanas y tres días de edad gestacional estimada por repetición de cesárea debido a la preocupación por la disminución del movimiento fetal en el contexto de una puntuación de perfil biofísico baja (basada en el tono muscular, la frecuencia cardíaca, el movimiento, la respiración y el volumen de líquido amniótico). La historia materna fue notable por el rasgo de células falciformes, la edad materna avanzada y la obesidad. La historia del embarazo fue notable por oligohidramnios observados por ultrasonografía a las 31 semanas. La ecografía fetal también mostró distensión de la vejiga, hidroceles bilaterales, dilatación de la uretra y ascitis abdominal preocupantes por la obstrucción del tracto urinario inferior y la posible ruptura de la vejiga. La ruptura de membranas ocurrió al momento del parto.\n\nAl nacer, el bebé experimentó dificultad respiratoria y fue tratado con ventilación con presión positiva, oxígeno suplementario e intubación. Las puntuaciones de Apgar fueron de dos y siete a un minuto y cinco minutos de vida, respectivamente. El examen mostró hematomas sustanciales y oscurecimiento de la extremidad superior izquierda. El bebé fue trasladado a la unidad de cuidados intensivos neonatales para el tratamiento de la dificultad respiratoria y sospecha de obstrucción del tracto urinario inferior. En la evaluación realizada dentro de la hora posterior al nacimiento por especialistas en ortopedia y cirugía plástica, el tercio distal del antebrazo y la mano estaban cianóticos, y una gran ampolla y área circundante de descamación eran evidentes en el dorso de la mano. No se observó movimiento espontáneo de la extremidad superior izquierda, y no se provocó la retirada o respuesta a los estímulos. La ecografía Doppler mostró flujo arterial al nivel de la fosa antecubital, pero no se detectaron pulsos radiales o cubitales. Los hallazgos del examen físico fueron consistentes con NCS, probablemente debido a la compresión de la pared uterina debido a oligohidramnios durante el embarazo.\n\nDespués de aproximadamente 5 horas de exámenes en serie, así como una amplia discusión con los equipos de ortopedia, cirugía plástica, neonatología y anestesia pediátrica, así como con los padres del bebé, se tomó la decisión de realizar una fasciotomía descompresiva del antebrazo, la mano y el túnel carpiano para permitir el rescate de la extremidad. La fasciotomía se realizó aproximadamente 6 horas después del nacimiento. El bebé fue monitoreado de cerca durante los siguientes días. La apariencia de la extremidad superior izquierda mejoró gradualmente. Al tercer día de vida, el antebrazo y la mano habían mejorado notablemente en color y parecían bien vascularizados. Las señales Doppler estaban presentes en todo momento, desde la arteria braquial hasta cada dedo. Se permitió que las heridas de la fasciotomía se curaran por intención secundaria, y se aplicó una férula personalizada con la muñeca en posición neutra y los dedos extendidos. No hubo signos de infección o isquemia en curso. Las heridas se curaron bien a las seis semanas de edad. En la visita de seguimiento a los cuatro meses de edad, las heridas se curaron por completo. El paciente tenía un rango de movimiento pasivo completo de la muñeca y los dedos. Se observó que tenía una ligera flexión y extensión del dedo anular y meñique, pero por lo demás, un movimiento activo mínimo de la muñeca o la mano en este momento. Tenía un movimiento activo del hombro y el codo. El paciente continuará recibiendo terapia ocupacional, así como férulas y masaje de cicatrices para prevenir/minimizar las contracturas. Los equipos multidisciplinarios continuarán siguiendo su progreso y recuperación de cerca.\n",
+        "gold_summary": "Presentamos un caso de NCS diagnosticado y tratado en base a los hallazgos del examen físico. La ecografía fetal mostró distensión de la vejiga, hidroceles bilaterales, dilatación de la uretra y ascitis abdominal que preocupaban por la obstrucción del tracto urinario inferior y posible ruptura de la vejiga. Una hora después del nacimiento, el examen de la extremidad superior izquierda del lactante no mostró movimiento espontáneo, la mano y el antebrazo parecían oscuros y la mano tenía una gran ampolla con descamación. No se detectó pulso distal a la fosa antecubital mediante ecografía Doppler. Se diagnosticó al lactante con NCS y se le practicó una fasciotomía urgente. La apariencia clínica y la perfusión de la extremidad superior izquierda mejoraron gradualmente. A los cuatro meses de edad, las heridas se habían curado y el paciente tenía un rango de movimiento pasivo completo de la extremidad superior izquierda. La recuperación del movimiento activo está en curso.\n",
+        "synthetic_summary": {
+            "B1": "Un bebé nació y tenía problemas en su brazo izquierdo. El brazo estaba muy oscuro y no se movía solo. Tenía una burbuja grande en la mano. Los doctores no sentían el pulso en el brazo. Ellos hicieron una operación para ayudar al brazo. Poco a poco, el brazo se puso mejor. A los cuatro meses, las heridas estaban sanas. El bebé puede mover el brazo con ayuda. Los doctores siguen cuidando para que mejore más.",
+            "B2": "**Lo que Encontraron al Nacer**  \nUn bebé nació con problemas en su brazo izquierdo. Su mano y antebrazo estaban oscuros y tenían una ampolla grande con piel que se estaba cayendo. Además, no movía esa parte del cuerpo y los médicos no pudieron sentir el pulso en la muñeca usando un examen especial llamado ecografía Doppler, que sirve para ver el flujo de sangre.\n\n**Qué Significa el Diagnóstico**  \nLos doctores dijeron que el bebé tenía un problema llamado Síndrome de Compartment Neonatal (NCS). Esto ocurre cuando hay mucha presión dentro de los músculos, lo que puede dañar la sangre y los nervios. En este caso, probablemente fue causado por la presión dentro del útero antes de nacer.\n\n**Cómo lo Trataron**  \nPara ayudar, los médicos hicieron una cirugía llamada fasciotomía. Esta operación abre la piel y los músculos para bajar la presión y salvar el brazo. La cirugía se hizo unas seis horas después del nacimiento.\n\n**Resultados y Seguimiento**  \nDespués de la operación, el brazo del bebé mejoró poco a poco. A los tres días, el color y la circulación de la sangre en el brazo y la mano eran normales. Las heridas sanaron bien y, a los cuatro meses, el bebé podía mover pasivamente (con ayuda) su muñeca y dedos. Aunque todavía tiene poco movimiento activo (por sí mismo), especialmente en algunos dedos, puede mover el hombro y el codo. El bebé seguirá recibiendo terapia para mejorar su movimiento y evitar que las cicatrices causen problemas. Los médicos continuarán observando su recuperación con cuidado.",
+            "B3": "**Contexto**  \nSe presenta el caso de un recién nacido prematuro (35 semanas y 3 días de gestación) que pesó 2021 gramos al nacer. La madre tenía antecedentes relevantes, incluyendo rasgo de células falciformes, edad avanzada y obesidad. Durante el embarazo se detectó oligohidramnios (disminución del líquido amniótico) y signos ecográficos preocupantes como distensión de la vejiga, hidroceles bilaterales (acumulación de líquido en las bolsas testiculares), dilatación de la uretra y ascitis abdominal, lo que sugería una posible obstrucción del tracto urinario inferior y ruptura de la vejiga. Debido a la disminución del movimiento fetal y un perfil biofísico bajo, se realizó una cesárea programada.\n\n**Hallazgos Clave**  \nAl nacer, el bebé presentó dificultad respiratoria y signos evidentes de compromiso en la extremidad superior izquierda: la mano y el antebrazo estaban oscuros (cianóticos), con una gran ampolla y descamación en el dorso de la mano, además de ausencia de movimiento espontáneo y falta de respuesta a estímulos. La ecografía Doppler mostró flujo arterial hasta la fosa antecubital, pero no se detectaron pulsos en las arterias radiales o cubitales, lo que indicaba compromiso circulatorio distal. Estos hallazgos fueron compatibles con un síndrome de compresión neuromuscular (NCS), probablemente causado por la presión ejercida sobre la extremidad dentro del útero debido al oligohidramnios.\n\n**Interpretación Clínica**  \nEl diagnóstico de NCS se basó en la combinación de los hallazgos físicos y ecográficos, que indicaban una isquemia (falta de flujo sanguíneo adecuado) en la extremidad superior izquierda. Para evitar daños permanentes, se decidió realizar una fasciotomía descompresiva urgente (una cirugía que libera la presión dentro de los compartimentos musculares del antebrazo y la mano, incluyendo el túnel carpiano) aproximadamente seis horas después del nacimiento. Esta intervención permitió restaurar la circulación y prevenir la necrosis (muerte del tejido).\n\n**Próximos Pasos y Evolución**  \nTras la cirugía, la apariencia y la perfusión de la extremidad mejoraron progresivamente. A los tres días de vida, el antebrazo y la mano mostraban una coloración normal y señales Doppler positivas en toda la extremidad, desde la arteria braquial hasta los dedos. Las heridas de la fasciotomía se dejaron curar de forma natural y se protegieron con una férula personalizada para mantener la muñeca y los dedos en posición adecuada. No se presentaron infecciones ni signos de isquemia persistente. A las seis semanas, las heridas estaban completamente cicatrizadas.\n\nEn la consulta de seguimiento a los cuatro meses, el bebé tenía un rango completo de movimiento pasivo en la muñeca y los dedos, aunque el movimiento activo era limitado, con ligera flexión y extensión en algunos dedos y buen movimiento activo en el hombro y codo. Se continúa con terapia ocupacional, uso de férulas y masaje de cicatrices para prevenir contracturas (rigidez anormal) y mejorar la función. Un equipo multidisciplinario sigue monitorizando su recuperación para optimizar los resultados funcionales a largo plazo."
+        }
+    },
+    {
+        "article": "Una mujer de 38 años de edad fue admitida en la sala de cirugía en noviembre de 2022 con la principal queja de una hinchazón abdominal progresiva que se asoció con un dolor abdominal leve y una saciedad precoz durante cinco meses. No tenía síntomas sistémicos como pérdida de peso, estreñimiento, diarrea, deseo de alimentos salados, fatigabilidad fácil o dolor de cabeza.\nEn el examen, parecía estar bien alimentada, pero presentaba una gran distensión abdominal, un leve palidez, afebril y con un tinte de ictericia en la esclerótica.\nLa palpación abdominal reveló una gran masa intraabdominal, no dolorosa, que ocupaba todo el abdomen inferior y se extendía hacia el superior, sin signos de irritación peritoneal u organomegalia.\nLos análisis de sangre mostraron un recuento de glóbulos blancos (5,7 × 109/l), hemoglobina (9,8 g/dl), bilirrubina (103 mg/dl) con recuentos normales de plaquetas (393 × 109/l). Las enzimas hepáticas, AST (24,0 U/l), ALT (21,0 U/l), albúmina 42,7 g/l. Creatinina sérica (53 μmol/l) y ESR (80 mm/h). Todos los demás análisis de sangre fueron normales. Una ecografía abdominal reveló un complejo quiste abdominal, ambos riñones eran de tamaño normal y con una ecografía normal, el hígado parecía normal. La TC abdominal y pélvica de contraste, vistas axiales y coronales, demostraron un gran quiste suprarrenal de paredes delgadas (flechas azules) que medía aproximadamente 23,5 cm (AP) x 20,3 cm (T) x 32,2 cm (CC) con un volumen de 8 l. El gran quiste desplaza el riñón derecho (flechas rojas) inferomedial a través de la línea media y ejerce presión sobre el hígado, la vesícula biliar, el páncreas y los intestinos delgados. Se extiende hasta la fosa ilíaca derecha. Como había un tinte de esclerosis ictérica, pero la masa era separada del hígado, el páncreas, los conductos biliares y el riñón derecho. Dado el tamaño del quiste y sus efectos compresivos, se planificó una intervención quirúrgica. Se eligió un enfoque quirúrgico abierto.\n\nSe le practicó una laparotomía al paciente. Se le hizo una incisión abdominal en la línea media, bajo anestesia general, y tras abrir las capas de la pared abdominal, se identificó un enorme quiste retroperitoneal que ocupaba toda la cavidad abdominal.\n\nSe abrió el quiste para acceder al fluido que se aspiraba, como se demostró en la cistectomía que se realizó con éxito. Se aspiraron unos 8 l de fluido de color marrón de la masa. Se enviaron muestras de la pared quística y del fluido para su análisis histológico.\n\nLa paciente se recuperó sin incidentes y fue dada de alta el día 7 después de la operación. El seguimiento a los 6 y 12 meses no mostró recurrencia ni complicaciones. El examen citológico de la muestra informó la presencia de material amorfo, no hubo evidencia de malignidad. Los resultados histológicos indicaron que la pared quística contenía tejido suprarrenal sin atipia, había infiltración de la pared quística por células inflamatorias mononucleares. La superficie interna de la pared no estaba revestida por células específicas reconocibles. En cuanto a los hallazgos clínicos intraoperativos, donde el origen del quiste era incierto, los hallazgos fueron más sugerentes de un quiste gigante idiopático retroperitoneal.\n\n",
+        "gold_summary": "Una mujer de 38 años se presentó con distensión abdominal progresiva. Las imágenes revelaron un quiste retroperitoneal gigante. Debido a los recursos limitados, se realizó una laparotomía abierta y se extirpó completamente un quiste de 33 cm que contenía 8 l de líquido transparente. La histopatología confirmó un quiste retroperitoneal idiopático gigante.\n",
+        "synthetic_summary": {
+            "B1": "Una mujer tenía una barriga muy grande y le dolía un poco. Los doctores vieron que había una bolsa grande llena de líquido dentro de su barriga. La doctora hizo una operación para sacar la bolsa. La bolsa era muy grande y tenía mucho líquido adentro. Después de la operación, la mujer se sintió mejor y no volvió a tener la bolsa.",
+            "B2": "**Lo que le pasó a la paciente**  \nUna mujer de 38 años notó que su abdomen (la parte del cuerpo donde están el estómago y otros órganos) se hinchaba poco a poco durante cinco meses. También sentía un dolor leve y se llenaba rápido al comer. Al examinarla, los médicos encontraron una gran masa dentro de su abdomen, pero no tenía fiebre ni otros síntomas graves.\n\n**Qué encontraron los médicos**  \nLas pruebas de imagen, como la tomografía computarizada (una especie de radiografía avanzada), mostraron un quiste muy grande en la zona llamada retroperitoneo, que está detrás de los órganos principales del abdomen. Un quiste es una bolsa llena de líquido. Este quiste medía más de 30 centímetros y contenía alrededor de 8 litros de líquido. Debido a su tamaño, estaba presionando otros órganos importantes.\n\n**Cómo la trataron**  \nLos médicos decidieron hacer una cirugía abierta para quitar el quiste. Durante la operación, hicieron una incisión en el abdomen y sacaron el quiste, aspirando el líquido que tenía dentro. Luego, enviaron muestras del quiste para analizarlas y asegurarse de que no fuera canceroso.\n\n**Qué significan los resultados**  \nEl análisis mostró que el quiste no tenía células cancerosas y que estaba formado por tejido normal con algunas células inflamatorias. No encontraron una causa clara para el quiste, por lo que lo llamaron \"idiopático\", que significa que no se sabe exactamente por qué apareció.\n\n**Después de la cirugía**  \nLa paciente se recuperó bien y fue dada de alta una semana después. En los controles a los 6 y 12 meses no hubo problemas ni volvió a aparecer el quiste. Esto indica que la cirugía fue exitosa y que la paciente está en buen estado.",
+            "B3": "**Contexto:**  \nUna mujer de 38 años acudió al hospital debido a una hinchazón abdominal que había ido aumentando progresivamente durante cinco meses. Además, presentaba dolor abdominal leve y sensación de llenura rápida al comer. No tenía otros síntomas generales como pérdida de peso, problemas digestivos, fatiga o fiebre. En la exploración física, se observó una gran distensión del abdomen con una masa palpable que ocupaba gran parte de la cavidad abdominal, sin dolor ni signos de inflamación. También se detectó una leve palidez y un tinte amarillento en la parte blanca de los ojos (ictericia).\n\n**Hallazgos Clave:**  \nLos análisis de sangre mostraron anemia leve, bilirrubina elevada (lo que explica la ictericia), pero funciones hepáticas y renales normales. La ecografía y la tomografía computarizada (TC) con contraste revelaron un enorme quiste con paredes delgadas ubicado en la región retroperitoneal (la zona detrás del abdomen), que medía aproximadamente 33 cm en su mayor dimensión y contenía alrededor de 8 litros de líquido. Este quiste desplazaba órganos cercanos como el riñón derecho, el hígado, la vesícula biliar, el páncreas y los intestinos, pero no parecía originarse en ninguno de ellos.\n\n**Interpretación Clínica:**  \nDado el tamaño considerable del quiste y su efecto compresivo sobre órganos abdominales importantes, se decidió realizar una cirugía abierta (laparotomía) para extirparlo completamente. Durante la operación, se aspiraron 8 litros de líquido marrón del quiste y se removió la masa sin complicaciones. El análisis microscópico del tejido del quiste mostró que estaba formado por tejido suprarrenal (glándulas que se encuentran encima de los riñones) sin signos de células anormales o malignas, aunque había inflamación leve. La superficie interna del quiste no presentaba un revestimiento celular definido. Estos hallazgos sugieren que se trataba de un quiste retroperitoneal gigante idiopático, es decir, de origen desconocido y sin causa aparente.\n\n**Próximos Pasos:**  \nLa paciente tuvo una recuperación sin complicaciones y fue dada de alta siete días después de la cirugía. En los controles realizados a los 6 y 12 meses posteriores, no se detectó recurrencia del quiste ni problemas relacionados. Se recomienda continuar con seguimiento clínico periódico para asegurar que no aparezcan nuevas complicaciones o recidivas."
+        }
+    },
+    {
+        "article": "Un hombre de 71 años con diabetes y enfermedad de Chagas había perdido recientemente mucho peso (60 kg). La investigación clínica dio lugar a un diagnóstico de megaesófago asociado a una obstrucción significativa a nivel del cardias. Se realizó una dilatación esofágica con balón, recuperando con éxito el tránsito digestivo. Mientras tanto, durante la evaluación del riesgo quirúrgico, el paciente también presentó dolor torácico con el mínimo esfuerzo. La angiografía por tomografía computarizada coronaria realizada tres años antes mostró una enfermedad multivascular muy calcificada que afectaba a la arteria coronaria izquierda; en ese momento no se había realizado ninguna otra investigación. Esta vez, se lo derivó a nosotros para un cateterismo cardíaco.\nEl examen realizado el 16 de febrero de 2016 mostró: arteria coronaria derecha (RCA) con importante calcificación y una lesión del 50% en el tercio medio; arteria descendente posterior (PDA) y arteria posterolateral derecha (RPLA), con severa calcificación y lesiones del 80% y 70%, respectivamente; LM con 80% de lesiones calcificadas en el tercio distal; arteria descendente anterior izquierda (LAD) con significativa calcificación y 90% de lesión en el tercio medio; ramas diagonales (DG1 y DG2) con lesiones calcificadas del 70% y 80%, en el origen y en el tercio proximal, respectivamente; y arteria circunfleja izquierda (LCx) ocluida y calcificada, recibiendo colaterales grado II de múltiples orígenes. El volumen ventricular izquierdo y la contractilidad se conservaron.\n\nCon esta imagen angiográfica, una puntuación de riesgo de la Society of Thoracic Surgeons del 15,8 % para morbilidad o mortalidad, una puntuación EuroSCORE II del 4,67 %, y una debilidad significativa debido a una pérdida de peso importante y reciente, el equipo cardiaco decidió realizar una intervención coronaria percutánea (ICP) de la LM, LAD, DG1 y DG2 inicialmente y, en un segundo procedimiento después de 30 días, una ICP de las ramas de la RCA. En ambos procedimientos, también se indicó una RA debido a una calcificación significativa. No se abordaría la LCx, ya que angiográficamente el vaso no estaba tan gravemente afectado y también considerando la dificultad técnica de la recanalización, debido a la longitud del CTO y también a las paredes muy calcificadas (puntuación J-CTO 4). La LCx ya estaba recibiendo una circulación collateral de grado II.\nEl 19 de febrero de 2016, tras comenzar una terapia antiplaquetaria dual con aspirina y clopidogrel, el paciente se sometió a una angioplastia de la arteria descendente anterior, la arteria circunfleja y la arteria descendente derecha con una fresa de 1,5 mm, seguida de una predilatación con un balón de 3,0 mm x 20 mm a 14 atm y la implantación de stents liberadores de fármacos en la arteria descendente derecha y la arteria circunfleja, utilizando una técnica de mini-aplastamiento y un balón de contacto al final. Se realizó un balón de contacto en la bifurcación de la arteria descendente derecha/arteria circunfleja y, finalmente, se implantó el tercer stent liberador de fármacos desde el origen de la arteria descendente derecha para superponerse con el stent de la arteria descendente derecha. Se logró un éxito procedimental con un flujo TIMI de 3 y sin complicaciones clínicas o angiográficas.\nEl 22 de marzo de 2016, el paciente volvió para una PCI con un RotaWire PCI en el PDA y RPLA con una fresa de 1,5 mm, seguido por la implantación de dos DES de 2,75 mm x 20 mm y 2,75 mm x 16 mm a 12 atm en el PDA y RPLA, respectivamente, sin ninguna predilatación adicional. También observamos la presencia de una disección larga y severa en el tercio medio del RCA, sin duda causada por un manejo excesivo e intentos de remover la fresa, lo que causó una penetración profunda por el catéter guía 7F. Esta disección se corrigió rápidamente con la implantación de un tercer DES de 4,0 mm x 32 mm, y se obtuvo un flujo TIMI 3 final sin complicaciones clínicas o electrocardiográficas. Los dos sitios de punción femoral se ocluyeron con dispositivos AngioSeal 8F y 6F, respectivamente. El paciente permaneció en la unidad de cuidados intensivos durante 48 horas, la única anormalidad fue la elevación de CK-MB (el doble del valor de referencia). Fue dado de alta el día 3 en excelentes condiciones generales. El ecocardiograma de control mostró una contractilidad ventricular izquierda normal.\n",
+        "gold_summary": "Un hombre de 71 años con enfermedad de Chagas y angina estable en esfuerzo mínimo se sometió a una angiografía por tomografía computarizada y cineangiografía que reveló una enfermedad multivascular muy calcificada que afectaba a la arteria descendente anterior izquierda (LM). Debido al grado de calcificación, se decidió realizar una rotablation. La primera etapa de la intervención coronaria percutánea (ICP) con rotablation se realizó en la arteria descendente anterior izquierda (LM), la arteria descendente anterior izquierda y la segunda rama diagonal sin complicaciones. Casi 30 días después, volvió para una ICP de la arteria coronaria derecha (RCA). La estrategia propuesta fue la aterectomía rotativa en la arteria descendente anterior posterior (PDA) y la arteria posterolateral derecha (RPLA) con una fresa de 1,5 mm, seguida por la implantación de dos stents liberadores de fármacos (DES). A través del acceso a la arteria femoral derecha, la lesión de la RPLA se extirpó con éxito. Como no había signos de disección y se mantuvo el flujo TIMI 3, se reposicionó el RotaWire de 0,009″ para cruzar la lesión de la PDA y se realizó la extirpación de la lesión. Después de dos intentos, logramos cruzar la lesión con la fresa de 1,5 mm, sin embargo, se produjo el atrapamiento de la misma. El sistema se retiró hasta que el catéter guía penetró profundamente en la RCA, y se hicieron intentos para liberar el Rotablator moviéndolo hacia adelante y hacia atrás, pero la fresa ni siquiera giró. La arteria femoral contralateral se perforó y se insertó un catéter guía 6F JR, con el fin de mover un alambre guía y un pequeño globo de angioplastia tangencialmente a la fresa, pero sin éxito. Finalmente, avanzamos el alambre guía utilizando la técnica de «nudillo», aprovechando la torsión de la porción distal del alambre guía PT2, realizando una disección subintimal y reentrada, y pudimos cruzar fácilmente el globo, inflarlo y liberar la fresa atrapada. A través del sistema 6F, se implantaron dos DES programados y uno de rescate con éxito en la PDA, RPLA y RCA, obteniendo un flujo TIMI 3 final sin complicaciones.\n",
+        "synthetic_summary": {
+            "B1": "Había un señor de 71 años con problemas en su corazón. Su corazón tenía partes muy duras y tapadas. Los doctores usaron una máquina especial para ver su corazón. \n\nPrimero, limpiaron unas partes del corazón con una herramienta que gira rápido. Esto ayudó a que la sangre pudiera pasar mejor. Después de un mes, volvieron a limpiar otras partes del corazón. \n\nEn una parte, la herramienta se quedó atrapada. Los doctores usaron un truco con un hilo para ayudar a que la herramienta se moviera otra vez. Al final, pusieron unos tubos pequeñitos para que la sangre siga fluyendo bien. \n\nEl señor quedó bien y sin problemas después de la ayuda.",
+            "B2": "**Lo que le pasó al paciente:**  \nUn hombre de 71 años con una enfermedad llamada Chagas y problemas en el corazón tuvo dolor en el pecho al hacer poco esfuerzo. Los médicos le hicieron estudios que mostraron que varias arterias del corazón estaban muy dañadas y tenían muchas calcificaciones, que son depósitos duros que bloquean el paso de la sangre.\n\n**Qué hicieron los médicos:**  \nPara ayudarlo, los doctores usaron una técnica llamada intervención coronaria percutánea (ICP). Esta técnica consiste en abrir las arterias del corazón usando pequeños tubos llamados stents, que ayudan a mantenerlas abiertas. Debido a que las arterias estaban muy duras por la calcificación, usaron una herramienta especial llamada rotablación. Esta herramienta tiene una pequeña fresa que gira rápido para eliminar la parte dura y permitir que el stent se coloque mejor.\n\n**Cómo fue el tratamiento:**  \nPrimero, trataron las arterias principales del lado izquierdo del corazón sin problemas. Después de casi un mes, regresó para tratar las arterias del lado derecho. Durante este segundo procedimiento, usaron la fresa para limpiar las arterias bloqueadas y pusieron stents para mantenerlas abiertas. Sin embargo, la fresa se quedó atrapada en una de las arterias, lo que complicó el procedimiento.\n\n**Cómo resolvieron el problema:**  \nPara liberar la fresa atrapada, los médicos usaron una técnica especial con un alambre guía que creó un nuevo camino dentro de la pared de la arteria para pasar un globo y liberar la fresa. Luego, colocaron los stents necesarios y lograron que la sangre fluyera bien por las arterias sin complicaciones.\n\n**Qué significa esto:**  \nEste caso muestra cómo los médicos pueden tratar arterias muy dañadas y duras usando herramientas avanzadas. Aunque hubo una complicación, pudieron solucionarla con éxito. El paciente salió en buen estado y con su corazón funcionando normalmente.",
+            "B3": "**Contexto**  \nUn hombre de 71 años con antecedentes de enfermedad de Chagas y diabetes presentó una pérdida de peso significativa y un diagnóstico de megaesófago con obstrucción en el cardias. Durante la evaluación prequirúrgica, manifestó dolor torácico con mínimo esfuerzo. Estudios previos mostraron una enfermedad coronaria multivascular severamente calcificada, especialmente en la arteria coronaria izquierda. Se decidió realizar una intervención coronaria percutánea (ICP) debido al alto riesgo quirúrgico y la complejidad de las lesiones.\n\n**Hallazgos Clave**  \nLa angiografía coronaria reveló múltiples lesiones calcificadas: una estenosis del 90% en la arteria descendente anterior izquierda (LAD), lesiones severas en ramas diagonales, y oclusión de la arteria circunfleja izquierda (LCx) con circulación colateral. La arteria coronaria derecha (RCA) también presentaba lesiones significativas y calcificación. La función ventricular izquierda se mantenía conservada.\n\n**Intervención y Procedimientos**  \nSe planificó la ICP en dos etapas debido a la extensión y severidad de las lesiones. La primera intervención, realizada el 19 de febrero de 2016, incluyó la rotablation (una técnica que utiliza una fresa rotatoria para eliminar la calcificación) en la arteria descendente anterior, seguida de la implantación de stents liberadores de fármacos (DES) en la arteria descendente derecha y la circunfleja, logrando un flujo sanguíneo óptimo sin complicaciones.\n\nCasi un mes después, el 22 de marzo de 2016, se realizó la segunda ICP en las ramas de la arteria coronaria derecha (PDA y RPLA) también con rotablation y colocación de DES. Durante este procedimiento, se produjo una disección severa en la arteria coronaria derecha, causada por la manipulación del catéter, que fue rápidamente corregida con la implantación de un stent adicional. Se presentó un incidente de atrapamiento de la fresa rotatoria dentro de la arteria, que fue resuelto mediante una técnica avanzada que permitió liberar el dispositivo sin daños adicionales.\n\n**Interpretación Clínica**  \nEste caso ilustra la complejidad del manejo de enfermedad coronaria multivascular severamente calcificada en un paciente con comorbilidades importantes y alto riesgo quirúrgico. La utilización de rotablation permitió tratar las lesiones calcificadas que dificultan la expansión de los stents, mejorando el flujo sanguíneo coronario. La estrategia en dos tiempos y la cuidadosa planificación fueron fundamentales para minimizar riesgos y lograr un resultado exitoso.\n\n**Próximos Pasos**  \nEl paciente fue dado de alta en buenas condiciones tras una estancia corta en cuidados intensivos, con función ventricular preservada y sin complicaciones clínicas significativas. Se recomienda seguimiento cardiológico estrecho, control de factores de riesgo cardiovascular y terapia antiplaquetaria dual para prevenir eventos trombóticos. La arteria circunfleja, ocluida pero con circulación colateral, no fue intervenida debido a la dificultad técnica y el riesgo asociado."
+        }
+    },
+    {
+        "article": "Una paciente de 29 años se presentó al departamento de urología con dolor intermittent en el flanco derecho durante un año y sensación de ardor urinaria ocasional sin hematuria; su estado general era estable. La paciente no mostró signos de tos, fatiga, pérdida de peso, no había tenido cirugías previas, pero había estado expuesta frecuentemente a ovejas. A pesar de los exámenes de laboratorio normales, el examen de anticuerpos de equinococos arrojó un resultado positivo. El ultrasonido abdominal posterior reveló una lesión quística grande en el riñón derecho, que medía aproximadamente 63 mm con paredes gruesas y sin flujo de doppler significativo. La tomografía computarizada con contraste, tanto en vista transversal como coronal, reveló una masa quística con septos en el lado lateral del riñón derecho, que presentaba una pared gruesa y regular que se intensificaba con el contraste. Esta lesión se clasificó como categoría 4 de Bosniak, con imágenes de tomografía computarizada en vista coronal que mostraban la participación del sistema colector y el contacto con el hígado. Se sospechó de HC en base a las evaluaciones clínicas y radiológicas. Los hallazgos de la radiografía de tórax no fueron significativos, sin evidencia de quistes pulmonares. Después de un régimen de tres meses de albendazol 400 mg administrado dos veces al día, la paciente se sometió a una intervención quirúrgica. Se realizó un procedimiento abierto a través de una incisión subcostal derecha de Kocher, lo que resultó en una nefrectomía derecha y una resección hepática parcial debido a las adherencias. El espécimen, que pesaba 372 g y medía 13 × 8 × 6 cm, mostró un gran quiste blanco con paredes delgadas que contenían una membrana desprendida, que afectaba los cálices renales y la pelvis. El diagnóstico final fue HC del riñón acompañado de pielonefritis crónica. Los exámenes de laboratorio posteriores al procedimiento mostraron resultados normales, con una producción urinaria estable y signos vitales. El catéter urinario se retiró después de 24 horas debido a una producción urinaria adecuada (2 L). El drenaje renal se retiró después de 3 días, con volúmenes de drenaje de 200 ml, 100 ml y ninguno en días consecutivos. La paciente volvió a sus actividades normales sin complicaciones.\n",
+        "gold_summary": "Se diagnosticó a una mujer de 29 años con dolor intermitente en el flanco derecho y ardor urinario un quiste hidatídico (HC) de categoría 4 de Bosniak, tras dar positivo en anticuerpos de equinococo. Las imágenes confirmaron el diagnóstico, lo que derivó en un tratamiento de tres meses con albendazol, seguido de una nefrectomía derecha y una resección hepática parcial. El análisis histopatológico confirmó un HC y una pielonefritis crónica. La paciente se recuperó sin incidentes y volvió a sus actividades normales.\n",
+        "synthetic_summary": {
+            "B1": "Una mujer tenía dolor en un lado de su cuerpo y ardor al hacer pipí. Los doctores encontraron un quiste grande en su riñón. Le dieron medicina por tres meses para ayudarla. Luego, le hicieron una operación para quitar el riñón y un poco del hígado. Después, ella se sintió bien y pudo hacer sus cosas normales otra vez.",
+            "B2": "**Lo que Encontraron**  \nUna mujer de 29 años tenía dolor en el lado derecho de su espalda y a veces sentía ardor al orinar. Los médicos hicieron pruebas y encontraron que tenía anticuerpos contra un parásito llamado equinococo, que puede causar quistes en órganos. Las imágenes del riñón mostraron un quiste grande y complicado, clasificado como categoría 4 de Bosniak, lo que significa que podría ser peligroso.\n\n**Qué Hicieron**  \nPara tratarla, primero le dieron un medicamento llamado albendazol durante tres meses. Este medicamento ayuda a matar el parásito. Después, le hicieron una cirugía para quitar el riñón derecho y parte del hígado, porque el quiste estaba pegado a esos órganos.\n\n**Qué Significa el Diagnóstico**  \nAl analizar el quiste, confirmaron que era un quiste hidatídico, que es una bolsa llena de líquido causada por el parásito. También encontraron inflamación crónica en el riñón, llamada pielonefritis.  \n\n**Recuperación**  \nDespués de la operación, la paciente se recuperó bien, sin problemas. Su orina y signos vitales estaban normales. Pudo volver a sus actividades normales sin complicaciones.  \n\nEste caso muestra cómo una infección por parásitos puede afectar órganos importantes y cómo se puede tratar con medicamentos y cirugía.",
+            "B3": "**Contexto**  \nUna mujer de 29 años consultó por dolor intermitente en el flanco derecho y episodios ocasionales de ardor al orinar, sin presencia de sangre en la orina. No presentaba síntomas sistémicos como tos, fatiga o pérdida de peso, y su estado general era estable. Destacaba una exposición frecuente a ovejas, factor de riesgo para infecciones parasitarias. Los análisis de laboratorio fueron normales, pero la prueba serológica detectó anticuerpos contra equinococos, un parásito causante de quistes hidatídicos.\n\n**Hallazgos Clave**  \nEl ultrasonido abdominal reveló una lesión quística grande en el riñón derecho, con paredes gruesas y sin flujo sanguíneo significativo. La tomografía computarizada con contraste mostró una masa quística con tabiques internos y una pared engrosada que se realzaba con el contraste, clasificada como categoría 4 en la escala de Bosniak, lo que indica una alta probabilidad de lesión compleja y potencialmente maligna o infecciosa. Además, la lesión involucraba el sistema colector renal y estaba en contacto con el hígado. La radiografía de tórax no mostró quistes pulmonares, descartando afectación pulmonar.\n\n**Interpretación Clínica**  \nEl diagnóstico presuntivo fue un quiste hidatídico renal (HC), una infección parasitaria causada por el equinococo, con posible extensión hepática. El tratamiento inicial consistió en albendazol, un medicamento antiparasitario, administrado durante tres meses para reducir la carga parasitaria y minimizar riesgos quirúrgicos. Posteriormente, se realizó una cirugía abierta mediante una incisión subcostal derecha (incisión de Kocher), que incluyó la extracción completa del riñón derecho (nefrectomía) y una resección parcial del hígado debido a adherencias entre ambos órganos. El estudio histopatológico confirmó la presencia del quiste hidatídico y evidenció pielonefritis crónica, una inflamación prolongada del tejido renal.\n\n**Próximos Pasos y Evolución**  \nTras la cirugía, la paciente mostró una recuperación favorable, con parámetros vitales estables y función urinaria adecuada. El catéter urinario se retiró a las 24 horas, y el drenaje renal se retiró en los días siguientes sin complicaciones. Finalmente, la paciente pudo retomar sus actividades habituales sin presentar efectos adversos ni recurrencias. Este caso destaca la importancia de considerar infecciones parasitarias en pacientes con lesiones quísticas renales, especialmente en contextos de exposición a animales de riesgo."
+        }
+    },
+    {
+        "article": "Una paciente de 46 años de edad fue admitida en nuestro hospital debido a opresión en el pecho y falta de aire que había durado más de un mes. Su historial médico incluía una tiroidectomía parcial, y no tenía antecedentes de tabaquismo o consumo de alcohol. Fue tratada con medicamentos regulares (comprimidos de liberación prolongada de succinato de metoprolol, comprimidos de sacubitril valsartán sodio, espironolactona, comprimidos de dapagliflozina) para la IC, pero la respuesta fue pobre. Durante el examen físico, la paciente estaba consciente y bien orientada. Su frecuencia cardíaca era de 68 latidos por minuto, la presión arterial era de 150/98 mm Hg, la frecuencia respiratoria era de 20 latidos por minuto. No había signos de sangrado o ictericia en la piel o membranas mucosas, y no se observó distensión de la vena yugular. La glándula tiroides no estaba agrandada. Los sonidos respiratorios eran gruesos en ambos pulmones, con roncus húmedos presentes en las bases pulmonares. La frecuencia cardíaca era de 68 lpm con un ritmo regular. El abdomen era suave, sin sensibilidad o sensibilidad de rebote, y el hígado y el bazo no eran palpables por debajo de la caja torácica. El signo de reflujo hepatoyugular fue negativo, pero había edema en ambas extremidades inferiores.\n\nLa paciente fue hospitalizada y se le realizaron los exámenes pertinentes. Los análisis bioquímicos mostraron una hormona estimulante de la tiroides (TSH) de 7,190 uIU/mL, triglicéridos de 0,81 mmol/L, colesterol de lipoproteínas de baja densidad (LDL-C) de 2,61 mmol/L, lipoproteína (a) de suero de 435 mg/L y NT-proBNP de 6245 pg/mL. Un examen de electrocardiograma (ECG) mostró bradicardia sinusal, anomalías de la onda T-U y duración del QRS de 90 ms. Un examen ecocardiográfico transtorácico posterior reveló un diámetro de la aurícula izquierda (LA) (anteroposterior) de 41 mm, un diámetro del ventrículo izquierdo (LVD) (anteroposterior) de 54 mm, un espesor del tabique interventricular en diástole (IVSD) de 9 mm, un espesor de la pared posterior del ventrículo izquierdo en la fase final de la diástole (LVPWd) de 9 mm, una fracción de eyección del ventrículo izquierdo (LVEF) del 28% (M-mode), una fracción de acortamiento (FS) del 13% y una presión de la arteria pulmonar de 29 mm Hg. No se observaron lesiones coronarias significativas en la angiografía coronaria computarizada (CCA). Se diagnosticó a la paciente con cardiomiopatía dilatada, insuficiencia cardiaca de clase III con LVEF reducida según la New York Heart Association (NYHA). En combinación con los parámetros, se puede observar que los volúmenes de la aurícula izquierda y el ventrículo izquierdo se reducen gradualmente, lo que indica que la función diastólica del ventrículo izquierdo está mejorando. El tratamiento con CCM revierte la remodelación miocárdica. Además, E/e′ refleja la presión de llenado ventricular izquierdo. El valor normal debe ser inferior a 8. Se puede observar que en este caso, E/e′ vuelve al valor normal tres meses después de la implantación de CCM. Estos dos puntos reflejan el papel de CCM en la mejora de la función diastólica miocárdica en el tratamiento de la insuficiencia cardiaca. En resumen, la paciente tenía las siguientes características: (1) LVEF mejoró pero se mantuvo tan bajo como el 30% después de la terapia óptima para la insuficiencia cardiaca; (2) opresión en el pecho y malestar con ligera actividad, grado de función cardiaca III; (3) ECG muestra QRS estrecho. Teniendo en cuenta el resultado positivo de la prueba preoperatoria de levosimendan, después de una discusión general y una comunicación completa con el paciente y su familia, se decidió realizar el tratamiento con CCM.\n\nEl procedimiento de implantación del CCM fue similar al de la implantación de un marcapasos tradicional. El paciente se colocó en posición supina, se desinfectó con una toalla y se perforó la vena subclavia izquierda dos veces bajo anestesia local, y se hizo la bolsa capsular después de insertar el alambre guía. Bajo la guía del alambre guía, se introdujeron dos vainas de desprendimiento, y se introdujeron dos cables de estimulación ventricular (Medtronic 3830-69) a través de la vaina, y se ajustó la posición de los cables a la superficie del tabique ventricular derecho con una distancia de 3 cm. Durante la operación, se probó el electrodo de campo cercano (RV), que mostró un umbral de estimulación de 0,5 V, una amplitud de la onda R detectada mayor de 10 mV, y una impedancia del cable de 1080 Ω; el electrodo de campo lejano (LS) mostró un umbral de estimulación de 0,5 V, una amplitud de la onda R detectada mayor de 15 mV, y una impedancia del cable de 900 Ω. Estas mediciones cumplieron los criterios para una implantación exitosa del electrodo. Ambos cables se anclaron de forma segura en el tabique ventricular derecho. Después de asegurarse de que no había estimulación diafragmática palpable con un pulso de estimulación de 10 V y una anchura de pulso de 0,4 ms, se conectaron los cables al generador de impulsos Optimizer Smart. Posteriormente, se ajustaron los impulsos de salida y se programaron y optimizaron los parámetros.\n\nLa monitorización del ECG postoperatorio inmediato indicó un suministro normal de impulsos CCM (Figura 1C). Observamos la respuesta de los pacientes al CCM al adherirnos a un protocolo de seguimiento estandarizado. Utilizando una amplia variedad de herramientas de evaluación, que incluían ultrasonografía Doppler cardiaca a color, análisis de sangre NT-ProBNP, pruebas de caminata de seis minutos (6MW) y el Cuestionario de Minnesota para Vivir con Insuficiencia Cardiaca (MLHFQ), evaluamos sistemáticamente el estado clínico de los pacientes. El paciente no experimentó opresión en el pecho ni falta de aire, y hubo una marcada mejora en la tolerancia al ejercicio y la calidad de vida.\n",
+        "gold_summary": "Presentamos a una paciente de 46 años que fue admitida en nuestro hospital debido a opresión torácica y falta de aire que duró más de un mes. La ecocardiografía reveló un diámetro del ventrículo izquierdo (anteroposterior) de 54 mm, el electrocardiograma mostró bradicardia sinusal y duración del QRS de 90 ms. La paciente no experimentó opresión torácica o falta de aire, y hubo una marcada mejora en la tolerancia al ejercicio y calidad de vida después de la implantación de la modulación de la contractilidad cardiaca.\n",
+        "synthetic_summary": {
+            "B1": "Una señora tenía dolor en el pecho y le costaba respirar mucho tiempo. Los doctores miraron su corazón con máquinas. Después de un tratamiento especial, ella se sintió mucho mejor. Ya no tenía dolor ni dificultad para respirar. Ahora puede jugar y caminar sin problema.",
+            "B2": "**Caso de una Paciente con Problemas del Corazón**\n\nUna mujer de 46 años llegó al hospital porque sentía opresión en el pecho y le costaba respirar desde hacía más de un mes. Para entender qué le pasaba, los médicos le hicieron varios estudios.\n\n**Lo que Encontraron**\n\nUn examen llamado ecocardiografía mostró que una parte de su corazón, llamada ventrículo izquierdo, estaba un poco agrandada (medía 54 mm). Otro examen, el electrocardiograma, mostró que su corazón latía más lento de lo normal (bradicardia sinusal) y que la señal eléctrica que controla el latido tenía una duración normal (QRS de 90 ms).\n\n**Qué Hicieron y Qué Pasó Después**\n\nPara ayudarla, los médicos le implantaron un dispositivo llamado modulador de la contractilidad cardiaca (CCM). Este aparato envía pequeñas señales eléctricas al corazón para mejorar su fuerza al latir. Después de la implantación, la paciente ya no tuvo opresión en el pecho ni dificultad para respirar. Además, pudo hacer ejercicio con más facilidad y su calidad de vida mejoró mucho.\n\nEn resumen, el tratamiento con CCM ayudó a mejorar la función de su corazón y su bienestar general.",
+            "B3": "**Contexto**\n\nUna mujer de 46 años fue hospitalizada por presentar opresión en el pecho y dificultad para respirar que persistían desde hacía más de un mes. Su historial incluía una cirugía parcial de tiroides y no tenía antecedentes de tabaquismo ni consumo de alcohol. A pesar de recibir tratamiento médico estándar para insuficiencia cardiaca, sus síntomas y función cardíaca no mejoraron adecuadamente. Los exámenes iniciales mostraron una fracción de eyección del ventrículo izquierdo (LVEF) muy reducida (28%), indicativa de una función cardíaca comprometida, y un electrocardiograma (ECG) con bradicardia sinusal y un complejo QRS estrecho (90 ms).\n\n**Hallazgos Clave**\n\n- Ecocardiografía: El ventrículo izquierdo tenía un diámetro anteroposterior de 54 mm, con una fracción de eyección del 28%, confirmando una cardiomiopatía dilatada con función cardíaca severamente reducida.\n- ECG: Bradicardia sinusal (ritmo cardíaco lento pero regular) y duración del QRS de 90 ms, lo que indica que la conducción eléctrica del corazón estaba relativamente normal.\n- Laboratorio: Elevación significativa del NT-proBNP (6245 pg/mL), marcador que refleja estrés y daño cardíaco.\n- Sintomatología: Opresión en el pecho y dificultad para realizar actividades físicas leves, clasificada como insuficiencia cardíaca clase III según la New York Heart Association (NYHA).\n\n**Interpretación Clínica**\n\nLa paciente presentaba insuficiencia cardíaca con función ventricular izquierda gravemente disminuida, a pesar del tratamiento médico óptimo. La cardiomiopatía dilatada y los síntomas persistentes indicaban la necesidad de una intervención adicional. Se decidió implantar un dispositivo de modulación de la contractilidad cardíaca (CCM), que es un tipo de terapia eléctrica que mejora la fuerza de contracción del corazón sin alterar el ritmo cardíaco normal.\n\nEl procedimiento de implantación fue similar al de un marcapasos tradicional, con cables colocados en el tabique del ventrículo derecho y un generador de impulsos programado para optimizar la función cardíaca. La implantación fue exitosa, sin complicaciones inmediatas.\n\n**Próximos Pasos y Resultados**\n\nTras la implantación del dispositivo CCM, la paciente fue monitoreada mediante ecocardiografía, análisis sanguíneos, pruebas de caminata y cuestionarios de calidad de vida. A los tres meses, se observó una mejora significativa en la función diastólica del ventrículo izquierdo, reducción de la presión de llenado ventricular y una disminución en los síntomas clínicos.\n\nLa paciente dejó de experimentar opresión en el pecho y dificultad para respirar, mostró una notable mejoría en la capacidad para realizar ejercicio y reportó una mejor calidad de vida. Estos resultados sugieren que la terapia con CCM puede ser una opción efectiva para pacientes con insuficiencia cardíaca avanzada que no responden adecuadamente al tratamiento médico convencional."
+        }
+    },
+    {
+        "article": "Paciente de sexo femenino, 61 años, caucásica, casada, dos hijos, informó empeoramiento de los síntomas de la psoriasis tras el inicio de L-metilfolato 15 mg al día para tratamiento coadyuvante de la depresión. Informó depresión y psoriasis desde los 20 años. Desde los 41 años, la paciente no había tenido recidivas de las lesiones psoriáticas.\n\nPor su historial de depresiones, se le indicó carbonato de litio, pero no lo tomó debido a la psoriasis. En 2000, su cuadro depresivo mejoró con venlafaxina 225 mg al día. En 2016, debido a las oscilaciones de humor, se le agregó lamotrigina 100 mg al día y, para mejorar el sueño, se le sumó quetiapina 50 mg al día.\n\nEstas fueron las dosis actuales, con una mejora en la depresión, la calidad de vida y sin efectos adversos significativos.\n\nEn enero de 2019, se detectó polimorfismo en el gen MTHFR, con una mutación heterozigótica en C677T, y se le recetó a la paciente 15 mg diarios de L-metilfolato. Antes de que finalizara la primera semana de uso de L-metilfolato, aparecieron lesiones psoriáticas que no se habían manifestado en 20 años. Se informó lo ocurrido al psiquiatra, quien retiró la medicación y, 4 días después, las lesiones psoriáticas comenzaron a remitir, desapareciendo por completo al cabo de unas semanas. La paciente no volvió a registrar manifestaciones hasta principios de 2020.\n",
+        "gold_summary": "Paciente de sexo femenino, de 61 años, que había estado en remisión de psoriasis durante 20 años. Sufrió una recaída de psoriasis en forma de placa pocos días después de comenzar el tratamiento con L-metilfolato a una dosis diaria de 15 mg.\n",
+        "synthetic_summary": {
+            "B1": "Una señora de 61 años tuvo la piel con manchas hace mucho tiempo. Ella no tuvo esas manchas por 20 años. Pero cuando empezó a tomar una medicina nueva, las manchas volvieron rápido. Luego, dejó de tomar esa medicina y las manchas se fueron.",
+            "B2": "**Lo que pasó con la paciente**  \nUna mujer de 61 años había tenido psoriasis, que es una enfermedad de la piel que causa manchas rojas y escamosas. Sin embargo, no había tenido problemas con la psoriasis durante 20 años.  \n\n**Qué tratamiento recibió y qué pasó después**  \nElla empezó a tomar un medicamento llamado L-metilfolato, que es una forma de vitamina B9 que ayuda en el tratamiento de la depresión. Tomaba 15 mg al día. Pero pocos días después de comenzar este medicamento, la psoriasis volvió a aparecer en su piel.  \n\n**Qué hicieron los médicos**  \nAl ver que la psoriasis regresó, el doctor decidió quitarle el L-metilfolato. Cuatro días después de dejar el medicamento, las manchas en la piel comenzaron a mejorar y desaparecieron completamente en unas semanas.  \n\n**Qué significa esto**  \nEste caso muestra que, en esta paciente, el L-metilfolato pudo haber causado que la psoriasis regresara después de muchos años sin síntomas. Por eso, es importante que los médicos revisen bien los tratamientos y los posibles efectos en cada persona.",
+            "B3": "**Contexto**  \nSe trata de una mujer de 61 años con antecedentes de psoriasis y depresión desde los 20 años. Durante dos décadas, desde los 41 años, no presentó brotes de psoriasis. Su tratamiento psiquiátrico actual incluía venlafaxina, lamotrigina y quetiapina, con buena respuesta y sin efectos adversos importantes. En 2019, se identificó que tenía una mutación genética heterozigótica en el gen MTHFR (C677T), lo que llevó a prescribirle L-metilfolato, un suplemento que puede ayudar en ciertos trastornos depresivos.\n\n**Hallazgos Clave**  \nPocos días después de iniciar el L-metilfolato a una dosis diaria de 15 mg, la paciente presentó una recaída de psoriasis en forma de placas, una manifestación cutánea que no había experimentado en 20 años. Al suspender el L-metilfolato, las lesiones comenzaron a mejorar en cuatro días y desaparecieron completamente en unas semanas. No se registraron nuevos brotes hasta casi un año después.\n\n**Interpretación Clínica**  \nEl caso sugiere una posible relación entre la administración de L-metilfolato y la reactivación de la psoriasis en esta paciente. Aunque el L-metilfolato es utilizado para mejorar la depresión, en este caso pudo haber desencadenado una respuesta inflamatoria cutánea, posiblemente relacionada con su predisposición genética y su historial de psoriasis. Este hallazgo es relevante para considerar el impacto de tratamientos coadyuvantes en enfermedades autoinmunes o inflamatorias crónicas.\n\n**Próximos Pasos**  \nSe recomienda un seguimiento cuidadoso en pacientes con antecedentes de psoriasis cuando se prescriben suplementos como el L-metilfolato. Además, es importante evaluar alternativas terapéuticas para la depresión que no exacerben enfermedades cutáneas. La comunicación estrecha entre dermatólogos y psiquiatras es fundamental para manejar casos similares y evitar recaídas."
+        }
+    },
+    {
+        "article": "Se diagnosticó osteoartritis bilateral de las articulaciones de la cadera en un paciente de 61 años de edad con tratamiento con esteroides para la artritis reumatoide y dolencias en la ingle bilateral. [9] Recibió una inyección intraarticular bilateral de ácido hialurónico y se presentó doce semanas después en nuestro departamento de urgencias con fiebre, un estado general reducido y un dolor cada vez más incapacitante. Las radiografías de la pelvis mostraron una destrucción progresiva y rápida de ambas articulaciones de la cadera con una osteólisis extensa, subluxación concomitante y un defecto óseo acetabular del lado izquierdo. La aspiración de la articulación mostró pus en ambas articulaciones de la cadera y se hizo el diagnóstico de artritis séptica bilateral progresiva rápida. Se realizó una resección bilateral de ambas cabezas femorales con desbridamiento de la articulación de la cadera y la implantación de espaciadores de PMMA cargados con antibióticos a través de un enfoque anterolateral mínimamente invasivo.\n\nSe inició un tratamiento antibiótico sistémico empírico con vancomicina y ampicilina por vía intravenosa. Se detectó E. coli en muestras de tejido de ambas articulaciones de la cadera y se adaptó el tratamiento antibiótico sistémico a meropenem por vía intravenosa. Se realizaron dos procedimientos quirúrgicos de seguimiento con intercambio de los espaciadores de PMMA cargados con antibiótico para controlar la infección debido al drenaje persistente.\n\nDoce semanas después de la resección de la cabeza femoral y el control exitoso de la infección, el paciente recibió una artroplastia total de cadera con el uso adicional de un revestimiento multicapa de plata (HyProtect®, Bio-Gate, Nürnberg, Alemania). Este revestimiento consiste en una capa de siloxano ultrafina directamente sobre la superficie del implante (10 a 30 nm), de la que se liberan iones de plata.\n\n12 semanas después de la resección de la cabeza femoral, se realizó una artroplastia total de cadera en el lado derecho con una copa estándar sin cemento (Allofit®, ZimmerBiomet, Varsovia, EE. UU.) y un vástago femoral sin cemento (Avenir®, ZimmerBiomet, Varsovia, EE. UU.) a través del enfoque anterolateral mínimamente invasivo previamente utilizado con este revestimiento multicapa de plata ultrafino. Tanto la superficie posterior de la copa como todo el eje femoral se revistieron con plata.\n\nLa cadera izquierda se trató 18 semanas después de la resección de la cabeza femoral con una jaula de refuerzo recubierta de plata (Burch-Schneider®, ZimmerBiomet, Varsovia, EE. UU.) para un defecto acetabular tipo IIB de Paprosky y una copa de polietileno cementada (Durasul®, ZimmerBiomet, Varsovia, EE. UU.). El vástago femoral sin cemento (Avenir®, ZimmerBiomet, Varsovia, EE. UU.) también se recubrió de plata en toda su parte intramedular. Esta intervención también se realizó mediante el enfoque anterolateral mínimamente invasivo utilizado previamente. El paciente se sometió a una terapia antibiótica sistémica durante un período de tratamiento total de 18 semanas después de la implantación del lado derecho. Se aplicó ertapenem 1 g por vía intravenosa durante este período de tiempo una vez al día, después de la descarga en un entorno ambulatorio. Esto permitió una cobertura antibiótica del lado derecho de 18 semanas y del lado izquierdo de 12 semanas de tratamiento antibiótico.\n\nSe recomendó el uso parcial de peso con 20 kg en el lado operado y el uso de muletas durante 6 semanas después de las intervenciones.\n\nLas heridas de ambos lados se curaron sin incidentes. El paciente fue visto regularmente para un seguimiento clínico y radiológico. Se logró el apoyo total del peso sin el uso de muletas 7 semanas después de la operación en ambos lados. No hubo signos de PIJ y no fue necesaria una cirugía de revisión adicional.\n\nEn un seguimiento final tres años después de la implantación de las prótesis recubiertas de plata, la paciente mostró un aspecto normal de la piel con mínimas cicatrices después de enfoques antero-laterales mínimamente invasivos en ambos lados sin signos de argiria. Hubo un excelente resultado funcional de ambas caderas con marcha normal y una puntuación WOMAC de 6 en ambos lados (dolor: 0, rigidez: 0, función física: 6). El recuento de leucocitos en sangre fue de 7,29/nl (referencia: 4,23-9,1) y el nivel de proteína C reactiva (PCR) fue de 12,4 mg/l (referencia: <5 mg/l). El nivel ligeramente elevado de PCR es atribuible a la artritis reumatoide subyacente de la paciente. Las radiografías revelaron componentes protésicos de cadera bien integrados y no sueltos en ambos lados tres años después de la implantación con una articulación correcta.\n",
+        "gold_summary": "Este informe de caso se refiere a un paciente de 61 años con destrucción rápida de ambas articulaciones de la cadera debido a una artritis séptica que se trató con éxito con una implantación por etapas de prótesis de cadera recubiertas con plata con un recubrimiento ultrafino multicapa de plata. En un seguimiento de tres años, no hubo signos de infección, se observó un buen estado de todos los componentes protésicos y el resultado funcional fue excelente.\n",
+        "synthetic_summary": {
+            "B1": "Había un señor con mucho dolor en sus dos caderas. Sus caderas se dañaron rápido por una infección. Los doctores le pusieron unas piezas nuevas en sus caderas. Estas piezas tenían una capa especial de plata para ayudar. Después de tres años, el señor está bien y sin dolor. Sus caderas funcionan muy bien y no hay infección.",
+            "B2": "**Lo que pasó con el paciente:**  \nUn hombre de 61 años tenía un problema grave en ambas caderas. Tenía una infección llamada artritis séptica, que hizo que sus articulaciones se dañaran muy rápido. Esta infección causó mucho dolor y dificultad para moverse.\n\n**Cómo lo trataron:**  \nPrimero, le quitaron las partes dañadas de las caderas y limpiaron bien las áreas infectadas. Luego, le pusieron unos espaciadores especiales con antibióticos para controlar la infección. Después de varias semanas y tratamientos con antibióticos fuertes, la infección mejoró.\n\nMás tarde, le pusieron prótesis nuevas en ambas caderas. Estas prótesis tenían un recubrimiento muy delgado de plata. La plata ayuda a evitar que las bacterias vuelvan a causar infección. Las cirugías se hicieron con técnicas que dañan poco los tejidos, para que la recuperación fuera mejor.\n\n**Qué pasó después:**  \nTres años después de las cirugías, el paciente estaba muy bien. No había señales de que la infección regresara. Las prótesis estaban firmes y funcionando bien. El paciente podía caminar normalmente y no sentía dolor ni rigidez en las caderas.\n\n**Por qué es importante:**  \nEste caso muestra que usar prótesis con un recubrimiento especial de plata puede ayudar a tratar infecciones graves en las articulaciones y mejorar la recuperación. Además, el seguimiento a largo plazo confirmó que el tratamiento fue exitoso y seguro.",
+            "B3": "**Contexto**  \nSe trató a un paciente de 61 años con antecedentes de artritis reumatoide, que recibía tratamiento con esteroides, y que presentaba osteoartritis en ambas caderas junto con dolor en la ingle. Después de una inyección de ácido hialurónico en ambas articulaciones, el paciente desarrolló fiebre, deterioro general y un dolor intenso y progresivo en las caderas. Las radiografías mostraron una rápida destrucción ósea en ambas articulaciones, y la aspiración reveló pus, confirmando una infección grave llamada artritis séptica bilateral.\n\n**Hallazgos Clave**  \nSe realizó la extracción quirúrgica de las cabezas femorales (la parte superior del hueso del muslo que forma la articulación de la cadera) y se limpiaron las articulaciones, implantando espaciadores temporales cargados con antibióticos para controlar la infección. Inicialmente se administraron antibióticos de amplio espectro, pero al identificar la bacteria Escherichia coli, el tratamiento se ajustó a un antibiótico específico (meropenem). Debido a la persistencia del drenaje, se llevaron a cabo dos cirugías adicionales para cambiar los espaciadores antibióticos.\n\nTras controlar la infección, se realizaron reemplazos definitivos de ambas caderas mediante prótesis recubiertas con un revestimiento ultrafino multicapa de plata. Este recubrimiento libera iones de plata, conocidos por sus propiedades antimicrobianas, con el objetivo de prevenir nuevas infecciones. La cirugía se realizó mediante un abordaje mínimamente invasivo para reducir el daño a los tejidos.\n\nEl lado derecho se operó primero, con una prótesis sin cemento y recubierta de plata en las superficies clave. La cadera izquierda se intervino semanas después, utilizando una jaula de refuerzo también recubierta de plata para reparar un defecto óseo importante, junto con una copa de polietileno cementada y un vástago femoral sin cemento igualmente recubierto. El paciente recibió un tratamiento antibiótico prolongado (hasta 18 semanas) para asegurar la erradicación completa de la infección.\n\n**Interpretación Clínica**  \nEl uso de prótesis recubiertas con plata en este caso permitió un control efectivo de la infección y una recuperación funcional excelente. Las heridas cicatrizaron sin complicaciones, y el paciente pudo caminar sin muletas en pocas semanas. Tres años después de la cirugía, no se observaron signos de infección recurrente ni efectos secundarios relacionados con la plata, como la argiria (una pigmentación anormal de la piel). Las radiografías mostraron que las prótesis estaban bien integradas y estables, y la función de las caderas era casi normal, con muy poco dolor y rigidez.\n\n**Próximos Pasos**  \nEl seguimiento clínico y radiológico continuado es fundamental para detectar cualquier posible complicación a largo plazo. En este caso, el éxito del tratamiento sugiere que las prótesis con recubrimiento de plata pueden ser una opción valiosa para pacientes con infecciones severas en las articulaciones, especialmente cuando se requiere una reconstrucción compleja. Además, el abordaje mínimamente invasivo contribuyó a una recuperación más rápida y con menos cicatrices visibles.\n\nEn resumen, este caso demuestra que un tratamiento escalonado que combina cirugía, antibióticos específicos y prótesis con recubrimiento antimicrobiano puede lograr resultados excelentes en infecciones articulares graves, mejorando la calidad de vida del paciente a largo plazo."
+        }
+    },
+    {
+        "article": "Una niña africana de raza negra, con 1000 g de peso, nacida a las 32 semanas de gestación, de madre viva, fue derivada a nuestra unidad de cuidados intensivos neonatales debido a múltiples anomalías congénitas y dificultad respiratoria moderada. La madre tiene 32 años y está en un matrimonio no consanguíneo. La madre no buscó atención médica hasta el inicio del tercer trimestre de embarazo, debido a un desprendimiento de placenta. El primer ultrasonido prenatal reveló oligohidramnios severos. No era diabética (la glucosa en sangre aleatoria fue de 5.1 mmol/L) y no recibió suplementos de ácido fólico durante el embarazo.\n\nAl ingreso, la bebé estaba alerta con características leves del síndrome de dificultad respiratoria. Presentaba múltiples rasgos dismórficos, entre ellos, microcefalia (circunferencia de la cabeza < 10%), occipucio prominente, orejas bajas, paladar hendido y labio derecho, micrognatia, contractura bilateral de los codos e inferiores más cortos.\n\n\nEl peso al nacer fue de 1000 g, la longitud del bebé fue de 40 cm y la circunferencia occipitofrontal fue de 30 cm.\n\nInvestigaciones\nLa radiografía esquelética mostró aplanamiento de las costillas, aplasia del fémur derecho e hipoplasia del fémur izquierdo. Los análisis de laboratorio incluyeron: hemograma completo, proteína C reactiva, creatinina, urea en sangre y electrolitos, todos dentro de los valores normales. La ecografía craneal fue normal, pero la ecocardiografía reveló un pequeño conducto arterioso permeable.\n\nDiagnóstico diferencial\nLa paciente presentaba aplasia femoral bilateral y facies inusuales. Estas características clínicas llevaron al diagnóstico de síndrome femoro-facial.\n\nLa similitud en la etiopatogénesis hace que el síndrome de regresión caudal sea el diagnóstico diferencial común. Ambos pueden ser causados por una hiperglucemia materna mal controlada. Sin embargo, los defectos faciales están ausentes en el síndrome de regresión caudal, la característica diagnóstica clave.\n\nLa hipoplasia femoral focal proximal y las anomalías craneofaciales suelen estar ausentes.\n\nEntre las condiciones que pueden provocar el labio leporino se incluye el síndrome de banda amniótica grave.\n\nTratamiento\nEl bebé recibió asistencia respiratoria y antibióticos empíricos. Participaron un cirujano ortopédico, un otorrinolaringólogo y un fisioterapeuta. Está previsto reparar quirúrgicamente el paladar hendido a los 6 meses de edad. La rehabilitación funcional está prevista antes de que el paciente comience a deambular. La cirugía de alargamiento de extremidades no se realiza actualmente en nuestro entorno.\n\nResultado y seguimiento\nEl paciente falleció a la edad de un mes por complicaciones de una sepsis neonatal grave de inicio tardío.\n",
+        "gold_summary": "Una niña africana de raza negra bantú de 1 día de vida fue admitida en la unidad neonatal debido a múltiples anomalías congénitas. La madre no buscó atención médica hasta el inicio del tercer trimestre, cuando tuvo un desprendimiento de placenta. La madre nunca recibió suplementos de ácido fólico prenatal. La niña tenía microcefalia, orejas bajas, paladar hendido derecho y labio, micrognatia, contractura y extremidades más cortas. Una radiografía esquelética mostró hipoplasia femoral. Presentamos este caso poco habitual y destacamos los retos en el diagnóstico y el tratamiento.\n",
+        "synthetic_summary": {
+            "B1": "Una bebé nació con problemas en su cuerpo. Su mamá no fue al doctor mucho cuando estaba embarazada. La bebé tenía la cabeza pequeña y orejas bajitas. También tenía un huequito en la boca y su labio estaba partido. Sus brazos y piernas eran más cortos y un hueso de la pierna estaba pequeño. Los doctores cuidaron mucho a la bebé, pero fue difícil ayudarla.",
+            "B2": "**Lo que pasó con la bebé**  \nUna niña africana nació prematura, con solo 32 semanas de gestación y pesando 1000 gramos. Fue llevada a una unidad especial para bebés recién nacidos porque tenía varios problemas desde el nacimiento. Su mamá no recibió atención médica durante la mayor parte del embarazo y no tomó ácido fólico, una vitamina importante para evitar defectos al nacer. Además, la mamá tuvo un problema llamado desprendimiento de placenta, que puede afectar al bebé.\n\n**Lo que encontraron en la bebé**  \nLa niña tenía la cabeza más pequeña de lo normal (microcefalia), orejas bajas, un paladar y labio hendidos (como un corte en el labio y el techo de la boca), mandíbula pequeña (micrognatia), y sus brazos y piernas eran más cortos y rígidos. Las radiografías mostraron que sus huesos de las piernas, especialmente los fémures, estaban subdesarrollados o faltaban partes. También tenía dificultad para respirar leve y un pequeño problema en el corazón.\n\n**Qué significa el diagnóstico**  \nLos médicos diagnosticaron a la bebé con un síndrome llamado femoro-facial. Esto significa que tiene problemas en los huesos de las piernas (fémur) y en la cara. Este síndrome es raro y puede parecerse a otro llamado síndrome de regresión caudal, pero en ese último no hay problemas en la cara, lo que ayuda a diferenciarlos. Además, algunas de sus características podrían estar relacionadas con problemas durante el embarazo, como la falta de control de azúcar en la mamá, aunque en este caso no se encontró diabetes.\n\n**Cómo trataron a la bebé y qué pasó después**  \nLa bebé recibió ayuda para respirar y antibióticos para prevenir infecciones. También la atendieron varios especialistas para planear cirugías y terapias que la ayudaran a mejorar su movilidad y corregir el paladar hendido. Sin embargo, a pesar de los cuidados, la bebé falleció a los 30 días de vida debido a una infección grave.\n\n**Resumen final**  \nEste caso muestra lo difícil que es diagnosticar y tratar a bebés con problemas congénitos raros, especialmente cuando la atención prenatal no es adecuada. Es importante que las mamás reciban cuidado médico temprano y tomen vitaminas como el ácido fólico para prevenir algunos defectos al nacer.",
+            "B3": "**Contexto**  \nSe presentó el caso de una recién nacida africana de raza negra, con un peso bajo al nacer (1000 gramos) y prematura (32 semanas de gestación), que fue ingresada en la unidad de cuidados intensivos neonatales debido a múltiples anomalías congénitas y dificultad respiratoria moderada. La madre, de 32 años, no recibió atención prenatal adecuada hasta el tercer trimestre, cuando sufrió un desprendimiento de placenta, y no tomó suplementos de ácido fólico durante el embarazo. El embarazo se caracterizó por oligohidramnios severo (disminución del líquido amniótico).\n\n**Hallazgos Clave**  \nAl momento del ingreso, la bebé estaba alerta pero presentaba signos leves de síndrome de dificultad respiratoria. Se observaron varias malformaciones físicas: microcefalia (cabeza pequeña), occipucio prominente (parte posterior de la cabeza sobresaliente), orejas bajas, paladar hendido y labio leporino en el lado derecho, micrognatia (mandíbula pequeña), contracturas en ambos codos y extremidades inferiores más cortas.  \n\nLas radiografías mostraron aplanamiento de las costillas, ausencia completa del fémur derecho (aplasia) y desarrollo insuficiente del fémur izquierdo (hipoplasia). Los análisis de laboratorio básicos fueron normales, la ecografía cerebral no mostró alteraciones, pero el ecocardiograma detectó un pequeño conducto arterioso permeable (una conexión anormal entre dos vasos sanguíneos del corazón).\n\n**Interpretación Clínica**  \nEl conjunto de características clínicas llevó al diagnóstico de síndrome femoro-facial, una condición poco común que se caracteriza por anomalías en los huesos del muslo (fémur) y rasgos faciales inusuales. Este diagnóstico se diferencia del síndrome de regresión caudal, que también afecta la parte inferior del cuerpo pero no presenta malformaciones faciales. Además, se consideraron otras causas posibles del labio leporino, como el síndrome de banda amniótica, pero la combinación de hallazgos apuntó al síndrome femoro-facial.  \n\nEs importante destacar que, aunque la hiperglucemia materna mal controlada (niveles altos de azúcar en sangre durante el embarazo) puede causar ambas condiciones, en este caso la madre no tenía diabetes diagnosticada.\n\n**Tratamiento y Manejo**  \nLa bebé recibió soporte respiratorio y tratamiento antibiótico preventivo. Se contó con la participación de un equipo multidisciplinario que incluyó cirujano ortopédico, otorrinolaringólogo y fisioterapeuta. Se planificó la reparación quirúrgica del paladar hendido a los seis meses de edad y la rehabilitación funcional antes de que la niña comenzara a caminar. Sin embargo, la cirugía para alargar las extremidades no está disponible en el centro donde fue atendida.\n\n**Resultado y Seguimiento**  \nLamentablemente, la paciente falleció a la edad de un mes debido a complicaciones derivadas de una sepsis neonatal grave (infección generalizada en el recién nacido) de inicio tardío, lo que refleja la gravedad y complejidad del cuadro clínico.\n\n---\n\nEste caso resalta los desafíos en el diagnóstico y manejo de anomalías congénitas complejas en un contexto con recursos limitados, así como la importancia de la atención prenatal temprana y adecuada para prevenir y detectar estas condiciones."
+        }
+    },
+    {
+        "article": "Paciente de sexo masculino de 18 años, con diag nóstico clínico de Neurofibromatosis tipo 1 desde el primer año de vida. Entre sus antecedentes destaca que tiene educación completa, sus padres no son consan guíneos, y no tiene antecedentes familiares de manchas café con leche. Desde el punto de vista neurológico desarrolló durante la infancia retraso del desarrollo psicomotor fino y grueso, trastorno del lenguaje de predominio expresivo, con alteración fonológica y semántica del lenguaje, por lo que fue manejado con fonoaudiología en Escuela de Lenguaje, además de ki- nesioterapia y terapia ocupacional durante la infancia. Durante la adolescencia se le diagnosticó Trastorno por Déficit Atencional e Hiperactividad, que fue manejado con metilfenidato, manteniendo regular rendimiento escolar. Tuvo desarrollo puberal normal. Oftalmológi camente presentó nódulos de Lisch desde los 4 años de edad, euriblefaron y astigmatismo. Se mantuvo en control anual en Oftalmología y Neuropediatría. Su última Resonancia Magnética de cerebro fue realiza da 6 meses previo a la consulta en Dermatología, sin hallazgos patológicos y en la Resonancia Magnética de columna se evidenció discopatía L5-S1 y realce perifacetario en T11-T12 y T12-L1. A los 16 años se reali zó estudio genético que demostró deleción de exones 5-47 del gen NF1.\n\nA los 18 años consultó en servicio de Dermatología del Centro de Referencia en Salud Peñalolén Cordille ra Oriente por aparición de nueva mancha en muslo izquierdo de 1 año evolución, asintomática. Además, refirió aparición de nódulos en muñeca derecha, su praciliar derecho y cuero cabelludo, de unos meses de evolución, asintomáticos.\n\nAl examen físico destacaba presión arterial normal, macrocefalia (CC: 60 cm) y múltiples manchas café con leche generalizadas, efélides en axilas, y en zona supraciliar derecha, occipital y muñeca derecha nódulos subcutáneos ovalados de 0,5 cm, bien delimitados, móviles. En muslo izquierdo lateral pre sentaba placa de 25 mm algo rosada, con pérdida de anexos, y de consistencia blanda. Por último, en zona lumbar y pectoral, múltiples máculas rojo- azuladas pequeñas, de menos de 5 mm cada una, algu nas levemente deprimidas.\n\nSe realizó biopsia cutánea de máculas azuladas en pecho y de placa muslo, resultando ambas compatibles con NF. Se realizó una ecografía de nódulos supraciliar y occipital que resultó compatible con NF nodular subcutáneo.\n\nUsando la clasificación clínica de García-Martínez et al.1 se diagnosticó al paciente con NF superficial sub cutáneo nodular en zona supraciliar derecha, occipital y muñeca derecha, NF superficial cutáneo pseudoatró fico en muslo izquierdo lateral y NF superficial cutáneo rojo azulado en zona lumbar y pectoral.",
+        "gold_summary": "Paciente masculino de 18 años con diagnóstico desde la infancia de NF-1 que presenta múltiples nodulos ovalados en cara, zona occipital y muñeca, máculas rojo-azuladas en dorso y placa rosada atrófica en muslo. El estudio ecográfico de los nódulos fue compatible con neurofibromas y el estudio histopatológico de las lesiones de dorso y muslo compatibles con neurofibromas cutáneos.",
+        "synthetic_summary": {
+            "B1": "Un niño que ahora tiene 18 años tiene una enfermedad llamada NF-1 desde que era muy pequeño. En su piel hay bolitas redondas en la cara, la cabeza y la muñeca. También tiene manchas rojas y azules en la espalda. En el muslo tiene una mancha rosada y suave. Los doctores hicieron pruebas y vieron que esas bolitas y manchas son parte de su enfermedad. Todo está bien cuidado y los doctores lo están ayudando.",
+            "B2": "**Lo que encontraron en el paciente**  \nUn joven de 18 años, que desde pequeño tiene una enfermedad llamada Neurofibromatosis tipo 1 (NF-1), presentó varios bultos pequeños y redondeados en la cara, la parte de atrás de la cabeza (zona occipital) y la muñeca. También tenía manchas de color rojo-azulado en la espalda y una zona rosada y delgada en el muslo izquierdo.\n\n**Qué significan los estudios realizados**  \nSe usó una ecografía, que es una prueba con ondas sonoras para ver el interior de los bultos, y mostró que esos nódulos eran neurofibromas. Los neurofibromas son tumores benignos, es decir, no cancerosos, que crecen en los nervios. Además, se tomó una biopsia, que consiste en sacar un pequeño pedazo de piel para examinarlo bajo el microscopio. Esta prueba confirmó que las manchas en la espalda y la placa en el muslo también eran neurofibromas en la piel.\n\n**Importancia del diagnóstico**  \nEstos hallazgos ayudan a entender mejor cómo afecta la NF-1 a este paciente, mostrando que tiene diferentes tipos de neurofibromas en varias partes del cuerpo. Esto es importante para su seguimiento médico y para decidir el mejor tratamiento si fuera necesario.",
+            "B3": "**Contexto**\n\nSe trata de un joven de 18 años con diagnóstico clínico confirmado desde la infancia de Neurofibromatosis tipo 1 (NF1), una enfermedad genética que afecta el desarrollo de tejidos nerviosos y cutáneos. Su historia médica incluye retrasos en el desarrollo psicomotor y del lenguaje durante la infancia, así como un diagnóstico de Trastorno por Déficit de Atención e Hiperactividad en la adolescencia. Presenta además características típicas de NF1, como múltiples manchas café con leche en la piel, nódulos oculares llamados nódulos de Lisch, y una macrocefalia (cabeza de tamaño mayor al promedio).\n\n**Hallazgos Clínicos y Diagnósticos**\n\nA los 18 años, el paciente consultó por la aparición de una nueva mancha en el muslo izquierdo que llevaba un año, además de varios nódulos en la muñeca derecha, la zona supraciliar derecha (por encima de la ceja) y el cuero cabelludo, todos asintomáticos. En el examen físico se observaron:\n\n- Múltiples manchas café con leche distribuidas por todo el cuerpo.\n- Nódulos subcutáneos ovalados, bien delimitados y móviles, de aproximadamente 0,5 cm en la zona supraciliar derecha, occipital y muñeca derecha.\n- Una placa rosada de 25 mm en el muslo izquierdo, con pérdida de anexos cutáneos (como folículos pilosos) y consistencia blanda.\n- Múltiples máculas rojo-azuladas pequeñas, algunas ligeramente deprimidas, en la zona lumbar y pectoral.\n\nSe realizaron estudios complementarios:\n\n- Ecografía de los nódulos supraciliares y occipitales, que mostró características compatibles con neurofibromas nodulares subcutáneos (tumores benignos derivados de las células nerviosas).\n- Biopsias de las máculas rojo-azuladas del pecho y de la placa del muslo, cuyos resultados confirmaron la presencia de neurofibromas cutáneos.\n\n**Interpretación Clínica**\n\nEl diagnóstico se basó en la clasificación clínica propuesta por García-Martínez y colaboradores, identificando tres tipos de manifestaciones cutáneas en este paciente:\n\n1. Neurofibromas superficiales subcutáneos nodulares en la zona supraciliar derecha, occipital y muñeca derecha.\n2. Neurofibroma superficial cutáneo con aspecto pseudoatrófico (que simula una pérdida de tejido) en el muslo izquierdo.\n3. Neurofibromas superficiales cutáneos de color rojo-azulado en la zona lumbar y pectoral.\n\nEstos hallazgos son consistentes con la variedad de lesiones cutáneas que pueden presentarse en pacientes con NF1, reflejando la heterogeneidad clínica de la enfermedad.\n\n**Próximos Pasos**\n\nEl paciente debe continuar con seguimiento multidisciplinario, incluyendo dermatología, neurología y oftalmología, para monitorear la evolución de las lesiones cutáneas y detectar posibles complicaciones neurológicas o malignización de los neurofibromas. Además, es importante mantener el control de su desarrollo cognitivo y conductual, así como realizar evaluaciones periódicas mediante imágenes para descartar nuevas alteraciones. La educación y el apoyo psicosocial también son fundamentales para mejorar su calidad de vida."
+        }
+    },
+    {
+        "article": "Un hombre de 38 años de edad fue ingresado en el hospital por traumatismo torácico contundente. El paciente estaba generalmente sano y no tenía factores de riesgo de enfermedad coronaria. Fue golpeado en el pecho por un tornillo de alta velocidad que tenía aproximadamente 6 cm de diámetro mientras trabajaba en una fábrica. Voló aproximadamente 4 metros de distancia debido a la fuerza y presión del tornillo de alta velocidad. Perdió el conocimiento de inmediato, pero recuperó la conciencia varios minutos después. Fue trasladado inmediatamente a la sala de urgencias de un hospital local. Su puntaje en la escala de coma de Glasgow fue de 15. Se quejó de dolor torácico intenso y persistente, opresión y disnea. La tomografía computarizada del tórax mostró derrame pleural bilateral y fracturas de esternón y costillas. Por lo tanto, se insertó un tubo torácico durante varios días. Luego, fue dado de alta sin someterse a un electrocardiograma (ECG) u otros exámenes cardiovasculares.\n\nTres meses después del alta hospitalaria, durante un chequeo de seguimiento de rutina, todavía había presencia de derrame pleural con síntomas acompañantes de opresión en el pecho, falta de aire después de la actividad física, e incluso disnea por la noche, lo que motivó su ingreso en nuestro hospital. Sus constantes vitales durante el ingreso fueron las siguientes: frecuencia cardíaca regular de 98 latidos/min, presión arterial de 110/70 mmHg, y frecuencia respiratoria de 20 respiraciones/min. El examen físico mostró una pulsación carotídea y yugular normal. El movimiento respiratorio torácico bilateral y la actividad fueron normales, la fibrilación del lenguaje táctil del pulmón derecho disminuyó, la percusión del pulmón derecho presentó un sonido sordo, y los sonidos respiratorios disminuyeron. No hubo roncus ni estertores evidentes durante la auscultación pulmonar. No hubo murmullos en la auscultación cardíaca. Los exámenes del abdomen y las extremidades revelaron hallazgos normales. El primer ECG mostró evaluación ST e inversión de la onda T en las derivaciones I, aVL y V2-V5 y en el bloqueo de rama anterior izquierdo. La prueba de troponina-I fue negativa, y el nivel de NT-proBNP fue de 706 pg/ml (rango normal: 0-104 pg/ml), lo que sugiere un infarto de miocardio anterior antiguo. La ecocardiografía transtorácica mostró una aurícula izquierda de 26,4 mm, un ventrículo izquierdo de 51,8 mm, y una fracción de eyección ventricular izquierda (EF) del 32% (modo M). La pared anterior del LV e interventricular septum mostraron adelgazamiento a 6,6 mm, con un eco de movimiento notablemente reducido.\n\nAl examinar las arterias carótidas, intracraneales y de las extremidades inferiores del paciente, no se encontraron placas ateroscleróticas evidentes. Todos los hallazgos apoyaron el diagnóstico de infarto de miocardio antiguo (OMI), en lugar de arteriosclerosis. Sin embargo, el paciente era hemodinámicamente estable. Después de someterse a una terapia diurética, se le administraron bloqueadores beta, estatinas y estimulantes cardíacos, lo que alivió su malestar. La angiografía por tomografía computarizada coronaria mostró una estenosis moderada en la arteria LAD proximal. Para confirmar la estenosis y examinar el estado de la íntima coronaria, se realizó CAG 3 meses después del traumatismo torácico, que mostró un estrechamiento aproximado del 70% del lumen en la LAD proximal y el segmento coronario tenía una lesión curva. La arteria circunfleja izquierda (LCX) y la arteria coronaria derecha (RCA) eran normales. Los resultados de CAG confirmaron el diagnóstico de OMI, pero debido a la carga de costos, el paciente rechazó el examen IVUS. El paciente se sometió a una terapia conservadora y fue dado de alta del hospital varios días después.\n\nUn mes después, el 9 de diciembre de 2014, volvió al hospital para someterse a una intervención coronaria percutánea (ICP). Después de someterse a una terapia con fármacos, sus condiciones habían mejorado ligeramente. El examen físico y el ECG revelaron resultados casi normales. La ecocardiografía transtorácica mostró una mejora en la función sistólica del LV y EF del 45%. Se sometió a otra CAG 4 meses después del traumatismo torácico, que mostró una ligera mejora de la estenosis. Había aproximadamente un 60% de estrechamiento del lumen. Se realizó un IVUS y reveló que la gravedad de la lesión era del 55.9%, y la placa de bajo eco apareció antes de la formación de trombos después de la rotura subintimal. Completamos el examen sin más intervención porque solo se encontró un 55.9% de estrechamiento del lumen y el paciente tenía una hemodinámica estable sin evidencia de isquemia miocárdica constante. Se le recetó al paciente la medicación óptima, y su incomodidad se alivió gradualmente. El 17 de julio de 2018, 4 años después del traumatismo, la evaluación de seguimiento reveló que el paciente todavía experimentaba dificultad para respirar después de trabajar, pero se alivió poco después de descansar. El examen físico mostró los siguientes resultados: presión arterial de 114/80 mmHg, frecuencia cardíaca de 66 latidos/min, ausencia de anomalías obvias en la auscultación pulmonar y cardíaca; y ausencia de edema obvio en ambas extremidades inferiores. El ECG de seguimiento reveló los siguientes hallazgos: rS en las derivaciones V2-V4, inversión de la onda T en las derivaciones I, AVL y V2-V5 y bloqueo de rama izquierda. La ecocardiografía transtorácica mostró agrandamiento del ventrículo izquierdo con una aurícula izquierda de 39 mm, un ventrículo izquierdo de 54.7 mm y una EF del LV del 41% (Simpson's). También se observó adelgazamiento de la pared anterior del LV y del tabique interventricular, con la parte más delgada de 4.7 mm; el movimiento casi había desaparecido y el eco se había mejorado. Sin embargo, las arterias carótidas, intracraneales y de las extremidades inferiores seguían siendo normales. Además, descubrimos que los medicamentos recetados para tratar la insuficiencia cardíaca no se tomaron religiosamente después del alta; por lo tanto, recetamos 23.75 mg de metoprolol, 2.5 mg de benazepril y 20 mg de espironolactona para tomar una vez al día, y coenzima para tomar cada 10 horas.\n\nMH - Adulto\nMH - Errores de diagnóstico\nMH - Insuficiencia cardiaca/etiología\nMH - Humanos\nMH - Hombre\nMH - Infarto de miocardio/complicaciones/*etiología\nMH - Lesiones torácicas/*complicaciones\nMH - Tiempo hasta el tratamiento\nMH - Heridas, no penetrantes/complicaciones\n",
+        "gold_summary": "Preocupaciones de los pacientes:\nUn hombre de 38 años, previamente sano, fue admitido en nuestro hospital con una queja de disnea. Tenía un historial de haber sido golpeado en el pecho por un tornillo de alta velocidad mientras trabajaba en una fábrica 3 meses antes de ser admitido en el hospital.\n\nDiagnóstico:\nLuego de realizarse una angiografía coronaria y una ecocardiografía, finalmente se le diagnosticó un infarto de miocardio.\n\nIntervenciones:\nRecibió medicamentos optimizados, entre ellos, diuréticos, bloqueadores beta y estimulantes cardíacos.\n\nResultados:\nAl cabo de cuatro años de seguimiento, se le diagnosticó al paciente una insuficiencia cardíaca crónica con una fracción de eyección reducida.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre se lastimó el pecho con un tornillo grande. Tres meses después, le costaba mucho respirar. Los doctores le hicieron pruebas y vieron que su corazón estaba dañado. Le dieron medicinas para ayudar a su corazón a trabajar mejor. Cuatro años después, su corazón seguía un poco débil, pero los doctores siguen cuidándolo.",
+            "B2": "**Lo que le pasó al paciente**  \nUn hombre de 38 años, que estaba sano antes, sufrió un fuerte golpe en el pecho cuando un tornillo de alta velocidad lo alcanzó mientras trabajaba. Tres meses después, empezó a sentir dificultad para respirar y dolor en el pecho, por lo que fue llevado al hospital.\n\n**Qué encontraron los médicos**  \nDespués de hacerle varios exámenes, como una ecografía del corazón y una angiografía (que es una prueba para ver las arterias del corazón), descubrieron que había tenido un infarto de miocardio. Esto significa que una parte de su corazón no recibió suficiente sangre y se dañó.\n\n**Cómo lo trataron**  \nEl paciente recibió varios medicamentos para ayudar a su corazón a funcionar mejor. Entre ellos estaban diuréticos (que ayudan a eliminar el exceso de líquido), bloqueadores beta (que reducen la carga del corazón) y estimulantes cardíacos (que mejoran la fuerza del latido).\n\n**Qué pasó después**  \nDurante los siguientes cuatro años, los médicos lo siguieron controlando. Descubrieron que desarrolló insuficiencia cardíaca crónica, que es cuando el corazón no puede bombear sangre tan bien como antes. Esto se confirmó porque su fracción de eyección, que mide qué tan bien el corazón bombea, estaba baja.\n\nEn resumen, un golpe fuerte en el pecho causó daño en el corazón que llevó a un infarto y, con el tiempo, a problemas para que el corazón funcione correctamente. El paciente recibió tratamiento para mejorar su condición y sigue siendo monitoreado por los médicos.",
+            "B3": "**Contexto:**  \nUn hombre de 38 años, previamente sano y sin factores de riesgo conocidos para enfermedad coronaria, sufrió un traumatismo torácico grave al ser impactado en el pecho por un tornillo de alta velocidad mientras trabajaba en una fábrica. Tras perder el conocimiento brevemente, fue atendido inicialmente en un hospital local donde se identificaron fracturas en el esternón y costillas, además de derrame pleural bilateral. Fue tratado con drenaje torácico y dado de alta sin realizar estudios cardíacos. Sin embargo, tres meses después, presentó síntomas persistentes como dolor y opresión en el pecho, dificultad para respirar al realizar esfuerzos y disnea nocturna, lo que motivó su ingreso en un hospital especializado para una evaluación más profunda.\n\n**Hallazgos Clave:**  \n- El examen físico reveló signos compatibles con derrame pleural residual en el pulmón derecho, pero sin alteraciones cardíacas evidentes a la auscultación.  \n- El electrocardiograma mostró alteraciones sugestivas de un infarto de miocardio antiguo en la región anterior del corazón, incluyendo inversión de ondas T y bloqueo de rama izquierda anterior.  \n- Los niveles de troponina (marcador de daño cardíaco agudo) fueron negativos, pero el NT-proBNP (marcador de insuficiencia cardíaca) estaba elevado, indicando estrés cardíaco.  \n- La ecocardiografía evidenció una función ventricular izquierda reducida (fracción de eyección del 32%), con adelgazamiento y disminución del movimiento en la pared anterior del ventrículo izquierdo y el tabique interventricular.  \n- La angiografía coronaria mostró una estenosis (estrechamiento) significativa del 70% en la arteria coronaria descendente anterior (LAD), confirmando la presencia de una lesión coronaria importante.  \n- No se encontraron signos de aterosclerosis en otras arterias principales, lo que sugiere que el infarto fue consecuencia directa del traumatismo torácico y no de enfermedad arterial previa.\n\n**Interpretación Clínica:**  \nEl paciente desarrolló un infarto de miocardio antiguo como complicación tardía del traumatismo torácico contundente. La lesión en la arteria coronaria descendente anterior, probablemente causada por el impacto, condujo a daño en el músculo cardíaco y a una reducción significativa de la función del ventrículo izquierdo. A pesar de la gravedad inicial, el paciente se mantuvo hemodinámicamente estable y respondió favorablemente a la terapia médica. Sin embargo, con el tiempo evolucionó hacia una insuficiencia cardíaca crónica con función ventricular reducida, condición que requiere manejo continuo y seguimiento.\n\n**Próximos Pasos y Manejo:**  \n- Se inició tratamiento médico optimizado que incluyó diuréticos para controlar la retención de líquidos, bloqueadores beta para reducir la carga cardíaca y mejorar la función, estatinas para protección vascular y estimulantes cardíacos.  \n- Posteriormente, el paciente se sometió a una intervención coronaria percutánea (ICP) para mejorar el flujo sanguíneo en la arteria afectada.  \n- Durante el seguimiento a largo plazo, se observó una mejoría parcial en la función cardíaca, aunque persistió una insuficiencia cardíaca leve a moderada.  \n- Se enfatizó la importancia de la adherencia estricta a la medicación para prevenir la progresión de la insuficiencia cardíaca y mejorar la calidad de vida.  \n- En controles posteriores, se mantuvo la función cardíaca reducida y síntomas leves de disnea tras esfuerzos, requiriendo ajuste y continuidad en el tratamiento farmacológico.\n\n**Resumen Final:**  \nEste caso ilustra cómo un traumatismo torácico severo puede ocasionar una lesión coronaria significativa que conduce a un infarto de miocardio y, eventualmente, a insuficiencia cardíaca crónica. La evaluación cuidadosa, el diagnóstico oportuno mediante imágenes cardíacas y la terapia médica adecuada son fundamentales para mejorar el pronóstico en estos pacientes. Además, la adherencia al tratamiento y el seguimiento a largo plazo son esenciales para controlar los síntomas y evitar complicaciones mayores."
+        }
+    },
+    {
+        "article": "La paciente era una recién nacida de 0 días de edad, de etnia Han, que nació a las 36 semanas de gestación de una mujer embarazada de 3, para 2, con un peso de 2650 g. Se le practicó una cesárea de urgencia debido a la angustia fetal, con puntuaciones de Apgar de 6 a 1 min y 5 min. Su grupo sanguíneo era O y RhD positivo. Al nacer, presentaba palidez, equimosis dispersas en múltiples áreas del cuerpo, sangrado de las mucosas e insuficiencia respiratoria, con un leve flujo de sangre hemorrágica también observado en los sitios de punción venosa. El análisis de gases en sangre de la arteria umbilical mostró un hematocrito de 0.08 y una hemoglobina de 23 g/L. La paciente requirió intubación endotraqueal y ventilación mecánica. Después de la transfusión de una suspensión de glóbulos rojos, los recuentos sanguíneos iniciales revelaron una trombocitopenia severa (recuento de plaquetas de 12 × 109/L), anemia (hemoglobina de 46 g/L) y leucopenia (recuento de leucocitos de 1.11 × 109/L).\n\nLa paciente fue ingresada en la unidad de cuidados intensivos neonatales a las 3 horas de vida para recibir tratamiento adicional. Durante la hospitalización, se le diagnosticó coagulación intravascular diseminada (CID), con tiempo de tromboplastina parcial activada (TTPA) de 73,10 segundos, tiempo de protrombina (TP) de 25,4 segundos, fibrinógeno (FIB) de 1,01 g/L, razón internacional normalizada (INR) de 2,26 y dímero D > 20 mg/L. Se le administró ventilación mecánica, corrección de la acidosis y transfusión de plasma fresco congelado. A pesar de múltiples transfusiones de glóbulos rojos y plaquetas, los niveles de hemoglobina y plaquetas permanecieron por debajo de lo normal (hemoglobina 106 g/L y plaquetas 11 × 109/L el día 3). También recibió tratamiento antiinfeccioso, cardiotónico, vasopresor y otro tratamiento sintomático. Un frotis periférico mostró áreas de tinción pálida agrandadas de glóbulos rojos, con una proporción de reticulocitos del 1,5% y un resultado negativo en la prueba directa de Coombs. No se realizó aspiración de médula ósea debido a su grave estado. No hubo evidencia clínica o de laboratorio de sepsis neonatal, y las pruebas para toxoplasma, rubéola, citomegalovirus y virus del herpes simple (TORCH); virus de hepatitis; y Treponema pallidum fueron negativas. El examen físico de admisión reveló un estado mental deficiente, disminución del tono muscular en las extremidades y reflejo pupilar lento a la luz. Todos los demás hallazgos fueron normales. El ultrasonido craneal y electroencefalograma de cabecera revelaron hemorragia intracraneal grave y bajo voltaje, respectivamente. Los hallazgos del ecocardiograma sugirieron un conducto arterioso patente, foramen oval permeable e hipertensión pulmonar. El ultrasonido abdominal indicó hemorragia gastrointestinal. A pesar de todos los esfuerzos, la paciente falleció el tercer día de vida debido a falla multiorgánica y hemorragia intracraneal masiva (la información detallada se puede encontrar en el Informe Suplementario).\n\nLos padres de la paciente no eran consanguíneos y ambos tenían talasemia. La madre, que compartía el mismo tipo de sangre que la paciente, tuvo una anemia leve durante el embarazo (nivel de hemoglobina de 97 g/L) y un historial de aborto inducido. Los exámenes prenatales no mostraron anomalías, ni tampoco hidrops fetal, y no recibió ninguna medicación durante el embarazo que pudiera provocar una enfermedad hemorrágica de inicio temprano en el recién nacido. La paciente también tenía un hermano de 1 año que gozaba de buena salud. Su abuelo tenía un historial de anemia leve (detalles desconocidos).\n\nSe obtuvo el consentimiento informado de los padres del paciente y se realizó un secuenciamiento de Sanger para descubrir la causa de la enfermedad. Se detectó una nueva mutación de MECOM de desplazamiento de marco heterocigótica [NM_001105078: c.157_158del (p.Met53Glyfs*2)] en el probando. Esta variante cambió el aminoácido 53 de metionina (codón ATG) a glicina (codón GGT), seguido de una terminación temprana. La mutación no se encontró en los padres o en el hermano mayor. La variante se clasificó como patogénica según las directrices del Colegio Americano de Genética Médica (ACMG) [14]. El algoritmo “AutoPVS1” brindó un fuerte apoyo para la interpretación de PVS1 de p.Met53Glyfs*2, lo que indica patogenicidad. La variante no se ha informado previamente en la Base de Datos de Mutación Genética Humana (HGMD) o en Clinvar. El análisis de conservación mostró que el residuo Met53 está altamente conservado en todas las especies de mamíferos (incluidos humanos, ratones, ratas, chimpancés y bovinos) utilizando Clustal Omega. Se generaron modelos de estructura de proteínas tridimensionales de las proteínas MECOM de tipo salvaje y mutantes utilizando SWISS-MODEL, lo que indica que la mutación de desplazamiento de marco causó una terminación temprana de la síntesis de aminoácidos, alterando significativamente la estructura de la proteína.\n",
+        "gold_summary": "Reportamos el caso de una neonata Han china de 0 días de vida que presentó trombocitopenia grave y hemorragia intracraneal, y que finalmente falleció por fallo multiorgánico e intracraneal el tercer día después del nacimiento. La secuenciación genética identificó una variante de cambio de marco heterocigótica, c.157_158del, dentro del gen MECOM. Esta variante condujo a una sustitución del 53.º aminoácido de metionina a glicina, terminando en el 54.º aminoácido. Una revisión exhaustiva de la literatura indicó que las mutaciones del gen MECOM incluían mutaciones sin sentido (68.3%), deleción (8.5%), sitio de empalme (8.5%), cambio de marco (7.3%) y sin sentido (7.3%). Las pacientes con mutaciones sin sentido frecuentemente presentaban sinostosis radiocubital, mientras que el fallo de la médula ósea se asociaba más comúnmente con los otros cuatro tipos de mutaciones.\n",
+        "synthetic_summary": {
+            "B1": "Una bebé nació muy pequeñita y se puso muy enferma. Tenía problemas para que su sangre funcionara bien y sangraba en la cabeza. Los doctores buscaron en sus genes y encontraron un cambio que no estaba bien. Ese cambio hizo que su cuerpo no pudiera hacer una parte importante para estar sano. Por eso, la bebé se enfermó mucho y no pudo mejorar.",
+            "B2": "**Caso de una recién nacida con un problema genético grave**\n\nPresentamos el caso de una bebé recién nacida de origen Han en China, que tenía un conteo muy bajo de plaquetas en la sangre, llamado trombocitopenia grave. Esto causó que tuviera sangrados dentro de su cabeza (hemorragia intracraneal). Lamentablemente, falleció al tercer día de vida debido a que varios órganos dejaron de funcionar correctamente.\n\n**Qué encontraron en sus genes**\n\nLos médicos analizaron el ADN de la bebé y encontraron un cambio en un gen llamado MECOM. Este cambio es una mutación que afecta cómo se produce una proteína importante. En concreto, la mutación cambió el aminoácido número 53 de metionina a glicina y provocó que la proteína se terminara de fabricar muy rápido, antes de tiempo. Esto afecta la función normal de la proteína.\n\n**Importancia de esta mutación**\n\nAl revisar otros casos en la literatura científica, se sabe que el gen MECOM puede tener diferentes tipos de mutaciones. La mayoría son mutaciones que detienen la producción normal de la proteína (llamadas mutaciones sin sentido), pero también hay otros tipos como deleciones o cambios en el marco de lectura del gen. Cada tipo de mutación puede causar distintos problemas. Por ejemplo, las mutaciones sin sentido suelen relacionarse con un problema en los huesos del brazo (sinostosis radiocubital), mientras que otras mutaciones, como la que tuvo esta bebé, están más asociadas con fallos en la médula ósea, que es donde se producen las células de la sangre.\n\n**Qué significa este caso**\n\nEste caso muestra cómo una mutación nueva en el gen MECOM puede causar una enfermedad muy grave desde el nacimiento. Entender estas mutaciones ayuda a los médicos a diagnosticar y estudiar mejor estas condiciones raras, aunque en este caso no fue posible salvar a la bebé.",
+            "B3": "**Contexto del Caso**  \nSe trató de una recién nacida de origen Han, nacida a las 36 semanas de gestación mediante cesárea de urgencia debido a sufrimiento fetal. Al nacer, presentó signos graves como palidez, sangrado en mucosas, equimosis (moretones) dispersos y dificultad respiratoria que requirió ventilación mecánica. Los análisis iniciales mostraron anemia severa, trombocitopenia (bajo recuento de plaquetas) y leucopenia (bajo recuento de glóbulos blancos). Durante su ingreso en la unidad de cuidados intensivos neonatales, se diagnosticó coagulación intravascular diseminada (una alteración grave de la coagulación sanguínea) y hemorragias múltiples, incluyendo una hemorragia intracraneal masiva. A pesar de tratamientos intensivos, la paciente falleció al tercer día de vida por falla multiorgánica y hemorragia cerebral.\n\n**Hallazgos Genéticos**  \nSe realizó un estudio genético mediante secuenciación Sanger para identificar la causa subyacente de su enfermedad. Se detectó una mutación nueva y heterocigótica (presente en una sola copia del gen) en el gen MECOM, específicamente una deleción de dos nucleótidos (c.157_158del) que provocó un cambio en el marco de lectura del gen (mutación de cambio de marco). Esta alteración causó que el aminoácido número 53, metionina, fuera sustituido por glicina, seguida de una terminación prematura en la síntesis proteica, lo que probablemente afecta gravemente la función de la proteína MECOM. Esta mutación no se encontró en los padres ni en el hermano mayor, indicando que fue una mutación de novo (nueva en la paciente). Además, el residuo afectado está altamente conservado en mamíferos, lo que sugiere su importancia funcional.\n\n**Interpretación Clínica y Revisión Bibliográfica**  \nEl gen MECOM está implicado en la regulación del desarrollo de la médula ósea y la formación de células sanguíneas. Mutaciones en este gen se han asociado con síndromes que incluyen fallo medular y anomalías óseas. Una revisión exhaustiva de la literatura mostró que las mutaciones en MECOM pueden ser de varios tipos: mutaciones sin sentido (que generan una proteína truncada), deleciones, alteraciones en sitios de empalme (que afectan el procesamiento del ARN), cambios de marco y otras mutaciones sin sentido. Se observó que las mutaciones sin sentido se relacionan frecuentemente con sinostosis radiocubital (fusión anormal de huesos del antebrazo), mientras que el fallo de la médula ósea es más común en los otros tipos de mutaciones, incluyendo la de cambio de marco que presentó esta paciente.\n\n**Conclusiones y Relevancia**  \nEste caso ilustra la gravedad clínica que puede tener una mutación de novo en el gen MECOM, manifestada por una trombocitopenia severa, hemorragias masivas y fallo multiorgánico en un recién nacido. La identificación precisa de la mutación permitió confirmar el diagnóstico genético y ampliar el conocimiento sobre la diversidad de mutaciones en MECOM y sus manifestaciones clínicas. Este hallazgo es importante para el diagnóstico prenatal y el asesoramiento genético en familias con antecedentes similares."
+        }
+    },
+    {
+        "article": "La paciente es una mujer de 74 años de edad, físicamente activa, que practica senderismo y equitación. Un mes después del tratamiento con inyección de cortisona de la tendinopatía insercional de Aquiles, sufrió una rotura total del tendón de Aquiles insercional al intentar dar un paso mientras montaba en bicicleta. Esta rotura se trató de forma conservadora con una bota de Walker durante 8 semanas. Después, mientras montaba a caballo, un intento de dar un paso provocó una nueva rotura total del tendón de Aquiles en la inserción. La rotura se trató quirúrgicamente con reinserción del tendón de Aquiles en el calcáneo, utilizando anclajes de sutura. Esto fue seguido por inmovilización en un yeso. Después de la operación, la paciente sufrió una infección profunda que no respondía a los antibióticos, signos de sepsis, y se indicó exploración quirúrgica. Durante la cirugía, se encontró que todo el tendón de Aquiles estaba gravemente afectado por la infección, más o menos destruido, y hubo que retirar el tendón de Aquiles distal de 7 cm (todo el tendón libre de Aquiles). Esto dejó una gran herida sin tejido tendinoso, y la piel se suturó sobre la herida. Después de este procedimiento, la inmovilización y el tratamiento con antibióticos de cloxacilina curaron la infección y la herida se curó adecuadamente. El pie se inmovilizó en un yeso durante las primeras 10 semanas, desde la máxima flexión plantar inicialmente, y luego la flexión plantar disminuyó gradualmente hasta alcanzar la posición neutra. Esto fue seguido por inmovilización en un yeso dorsal, evitando la extensión del tendón de Aquiles en flexión plantar, durante otros 3 meses. Se le dijo que aumentara gradualmente la carga al caminar, pero que evitara la extensión durante un total de 6 meses. Después de 6 meses se le ofreció reconstrucción quirúrgica con un injerto de flexor hallucis longus, pero como entonces tenía una función satisfactoria, decidió esperar y ver. Su función mejoró gradualmente, y un año después de la operación, cuando buscó ayuda por el dolor en el otro tendón de Aquiles, se notó la buena función en el lado operado. La exploración por ultrasonido mostró sorprendentemente un tendón que se parecía mucho a un tendón de Aquiles ligeramente tendinopático.\n",
+        "gold_summary": "Esta señora de 74 años padecía tendinopatía insercional de Aquiles. Después del tratamiento con una inyección local de cortisona, sufrió una rotura total del tendón de Aquiles insercional. Esta rotura se trató de forma conservadora y, después del tratamiento, el tendón de Aquiles volvió a romperse en la zona de inserción. La rotura se trató entonces con reinserción en la zona de inserción calcánea. Al poco tiempo del postoperatorio, la paciente sufrió una infección de herida quirúrgica profunda y sepsis. Debido al pobre efecto del tratamiento con antibióticos y a la destrucción total del tendón, se extirpó todo el tendón de Aquiles. Después de la extirpación, se inmovilizó en un yeso, seguido de movilización y aumento gradual de la carga. En un seguimiento de un año, la paciente caminaba sin cojera, podía levantar el talón hasta la mitad mientras estaba de pie sobre una pierna, había un tendón de Aquiles palpable y el escaneado por ultrasonido mostró una estructura muy similar a un tendón de Aquiles tendinopático y ligeramente engrosado. Había una regeneración evidente de todo el tendón de Aquiles y la función del tendón era sorprendentemente buena.\n",
+        "synthetic_summary": {
+            "B1": "Había una señora de 74 años con un problema en el hueso del talón y el hueso del muslo. Se lastimó el hueso del muslo cerca del talón después de una inyección. Primero, usó una bota especial para sanar. Pero se volvió a lastimar el mismo hueso. Entonces, los doctores hicieron una operación para arreglarlo. Después, tuvo una infección que no se quitaba con medicina. Por eso, los doctores tuvieron que quitar todo el hueso del muslo que estaba lastimado. Luego, la señora usó un yeso para que su pie sanara. Poco a poco, pudo mover el pie y caminar sin dolor. Un año después, su hueso del muslo estaba casi como nuevo y ella podía caminar bien y levantar el talón.",
+            "B2": "**Lo que le Pasó a la Paciente**  \nUna mujer de 74 años tenía un problema llamado tendinopatía insercional de Aquiles. Esto significa que el tendón de Aquiles, que conecta el músculo de la pantorrilla con el hueso del talón, estaba dañado cerca de donde se une al hueso. Para tratarlo, le pusieron una inyección de cortisona, que es un medicamento para reducir la inflamación. Sin embargo, después de esto, el tendón se rompió completamente en esa zona.\n\n**Tratamientos y Complicaciones**  \nPrimero intentaron curar la rotura sin cirugía, usando una bota especial para inmovilizar el pie. Pero luego, el tendón se rompió otra vez. Esta vez, hicieron una operación para volver a unir el tendón al hueso usando anclajes, que son pequeños dispositivos para sujetar el tendón. Poco después de la cirugía, la paciente tuvo una infección grave en la herida que no mejoró con antibióticos y causó sepsis, una infección que afecta todo el cuerpo.\n\n**Cirugía y Recuperación**  \nDurante otra operación para tratar la infección, los médicos vieron que el tendón estaba muy dañado y tuvieron que quitarlo completamente, dejando una gran herida. La piel se cerró sobre esa zona y la paciente usó un yeso para inmovilizar el pie durante varias semanas. También recibió antibióticos para curar la infección. Luego, poco a poco, empezó a mover el pie y a cargar peso al caminar, pero evitando estirar demasiado el tendón.\n\n**Resultados Después de un Año**  \nUn año después, la paciente podía caminar sin cojear y levantar el talón mientras estaba de pie sobre una pierna, lo que muestra que el tendón funcionaba bien. Un examen con ultrasonido, que es una imagen que muestra los tejidos, mostró que el tendón de Aquiles había crecido de nuevo y parecía casi normal, aunque un poco engrosado y con signos de daño leve. Esto indica que el tendón se regeneró sorprendentemente bien y que la función del pie mejoró mucho, a pesar de que el tendón original fue removido.",
+            "B3": "**Contexto**  \nLa paciente es una mujer de 74 años, físicamente activa, que desarrolló una tendinopatía insercional del tendón de Aquiles (una lesión en la zona donde el tendón se une al hueso del talón). Tras recibir una inyección local de cortisona para tratar esta lesión, sufrió una rotura completa del tendón en la zona de inserción. Inicialmente, esta rotura se manejó con tratamiento conservador, pero posteriormente el tendón volvió a romperse en el mismo lugar. Esta segunda rotura se trató mediante cirugía para reinsertar el tendón en el hueso del talón.\n\n**Hallazgos Clave**  \nPoco después de la cirugía, la paciente desarrolló una infección profunda en la herida quirúrgica que evolucionó a sepsis (una infección grave que afecta a todo el organismo). Debido a que los antibióticos no controlaron la infección y el tendón estaba gravemente dañado, fue necesario extirpar completamente el tendón de Aquiles distal (aproximadamente 7 cm). Tras la extirpación, la herida se cerró y la paciente fue inmovilizada con yesos durante varios meses, con un protocolo gradual para permitir la recuperación y evitar movimientos que pudieran dañar la zona.\n\n**Interpretación Clínica**  \nA pesar de la pérdida total del tendón de Aquiles, la paciente mostró una recuperación funcional sorprendentemente buena. Un año después, caminaba sin cojera, podía levantar el talón mientras se apoyaba sobre una pierna y se palpaba un tendón en la zona afectada. El ultrasonido reveló que el tendón había regenerado una estructura similar a un tendón de Aquiles, aunque con signos leves de tendinopatía (engrosamiento y alteraciones en la textura). Esto indica que, incluso tras la extirpación completa del tendón, el organismo fue capaz de formar un nuevo tejido tendinoso funcional.\n\n**Próximos Pasos**  \nSe ofreció a la paciente la opción de una reconstrucción quirúrgica con un injerto de otro tendón (flexor hallucis longus) para mejorar aún más la función, pero ella decidió esperar debido a la buena recuperación que presentaba. Se recomienda continuar con seguimiento clínico y funcional para monitorizar la evolución, especialmente considerando que la regeneración espontánea del tendón de Aquiles es poco común y puede ofrecer información valiosa para futuros tratamientos."
+        }
+    },
+    {
+        "article": "Una mujer de 47 años con antecedentes de CHB congénita se presentó con quejas de dolor en el cuello del lado izquierdo y dolor en el oído izquierdo. Aproximadamente 30 meses antes de la presentación, la paciente había notado una pequeña masa en el lado izquierdo de su cuello, que había aumentado gradualmente de tamaño. El dolor se localizó inicialmente en la región del cuello, pero se intensificó con el tiempo y se extendió al área del oído izquierdo.\nInicialmente, debido al dolor en el oído izquierdo, el paciente consultó a varios otorrinolaringólogos y fue tratado por un diagnóstico preliminar de otitis media. Sin embargo, a pesar de los tratamientos, el dolor persistió. Finalmente, un otorrinolaringólogo derivó al paciente para una ecografía, que reveló una masa en el lado izquierdo del cuello, lo que llevó a una derivación quirúrgica. Después de las evaluaciones iniciales, se solicitó una angiografía por TC, que reveló una masa de forma ovalada que medía 30 por 50 mm en la bifurcación de la arteria carótida izquierda, lo que sugiere un CBT tipo II de Shamblin.\n\nEvaluaciones cardiovasculares preoperatorias\nDada la historia del paciente de CHB congénita, se realizó una evaluación cardiovascular preoperatoria exhaustiva. Esto incluyó un electrocardiograma (ECG) de 12 derivaciones, que confirmó la presencia de CHB con un ritmo de escape ventricular estable. Se realizó una ecocardiografía transtorácica para evaluar la estructura y función cardiaca, revelando una función sistólica ventricular normal sin evidencia de anormalidades estructurales. Además, se obtuvo una consulta de cardiología para evaluar la aptitud del paciente para la cirugía y optimizar el manejo perioperatorio.\n\nConsideraciones anestésicas\nDebido a la CHB congénita del paciente y al potencial de inestabilidad hemodinámica durante la cirugía, se formuló un plan anestésico detallado. El paciente fue clasificado como estado físico III de la Sociedad Estadounidense de Anestesiología (ASA). Preoperativamente, se le colocó un marcapasos externo temporal para garantizar un control adecuado de la frecuencia cardíaca y se le insertó un catéter arterial para el monitoreo continuo de la presión arterial. La inducción de la anestesia se realizó utilizando una combinación de etomidato (0,3 mg/kg) y fentanilo (2 μg/kg) para minimizar las fluctuaciones hemodinámicas. El mantenimiento se logró con sevoflurano (1-2 %) y rocuronio (0,6 mg/kg) para la relajación muscular. Los parámetros hemodinámicos, incluida la frecuencia cardíaca, la presión arterial y la saturación de oxígeno, se controlaron de forma continua. Además, se le colocó un catéter venoso central para monitorear la presión venosa central y administrar medicamentos vasoactivos si fuera necesario. El equipo de anestesia mantuvo una comunicación estrecha con el equipo quirúrgico para abordar de forma inmediata cualquier cambio hemodinámico intraoperatorio.\n\nEnfoque quirúrgico\nEl paciente fue sometido a cirugía el 19 de mayo de 2024, después de la localización precisa de la TCC mediante angiografía por TC. El enfoque quirúrgico se eligió en base a la clasificación de Shamblin tipo II, que indica un encasamiento parcial de las arterias carótidas. Dada la proximidad del tumor a estructuras neurovasculares críticas, incluidos los nervios vago e hipogloso, se consideró que el enfoque quirúrgico abierto era el más apropiado para garantizar una resección completa y minimizar las complicaciones.\nTras la inducción de la anestesia general, se colocó al paciente en posición supina con el cuello extendido y rotado hacia la derecha. Se realizó una incisión oblicua paralela al músculo esternocleidomastoideo izquierdo, que se extendía desde la apófisis mastoidea hasta la escotadura esternal. Tras la incisión de la piel y la disección del platisma, se expuso con cuidado la vaina carotídea. Se identificaron la arteria carótida común y su bifurcación en las arterias carótidas internas y externas. Se observó el tumor, de 30 × 50 mm, en la bifurcación carotídea y se diseccionó con cuidado de los tejidos circundantes.\n\nManobras y precauciones específicas\n1.\nSe aplicaron pinzas vasculares temporales en las arterias carótidas internas y externas para controlar el flujo sanguíneo durante la disección del tumor. Esto minimizó el sangrado y proporcionó un campo quirúrgico despejado.\n2.\nSe utilizó neuromonitorización intraoperativa para evaluar la integridad de los nervios vago e hipogloso. La retroalimentación continua garantizó que las estructuras neurales se preservaran durante la disección.\n3.\nEl tumor se separó cuidadosamente de las arterias carótidas y las estructuras neurales circundantes, mediante una combinación de disección aguda y roma. Se logró la hemostasis mediante cauterización bipolar y pinzas quirúrgicas para minimizar el sangrado.\n4.\nEl marcapasos externo se monitoreó activamente durante todo el procedimiento para garantizar un ritmo cardíaco estable. El equipo de anestesia estaba preparado para administrar atropina o epinefrina si se producía una bradicardia o hipotensión significativas.\n2.5. Manejo postoperatorio\nTras asegurarse de que no había hemorragia activa y restablecer el flujo sanguíneo, se devolvieron los tejidos a su posición original y se cerró la herida en múltiples capas. Se aplicó un vendaje apropiado. La cirugía se completó sin complicaciones y con un sangrado mínimo en 2 h y 10 min. El paciente fue trasladado a la UCI vascular para una estrecha monitorización.\nDespués de la operación, se controló al paciente en la UCI durante 24 horas y, más tarde, se le trasladó a la planta general tras mejorar su estado clínico. El marcapasos externo se retiró el día 1 después de la operación, ya que el paciente mantenía un ritmo de escape ventricular estable. El paciente fue dado de alta en buenas condiciones generales el día 3 después de la operación, sin quejas específicas.\n2.6. Seguimiento y resultados a largo plazo\nEl examen histopatológico confirmó el diagnóstico definitivo de TCC en la paciente. Se realizaron evaluaciones de seguimiento a las 2 semanas, 1 mes, 6 meses y 1 año posteriores a la cirugía para evaluar los resultados quirúrgicos y cardíacos. En cada visita, la paciente se sometió a un ECG de 12 derivaciones para monitorear el CHB congénito, que permaneció sin cambios durante todo el período de seguimiento. Se repitió la ecocardiografía transtorácica a los 6 meses y un año, sin deterioro de la función cardíaca y con una función sistólica ventricular estable.\n\nPara evaluar el impacto de la extirpación del tumor en la función cardiaca, se realizó un análisis de la variabilidad de la frecuencia cardiaca (VFC) antes de la operación y a los 6 meses después de la misma. El análisis de la VFC antes de la operación demostró una reducción de la actividad parasimpática, probablemente debido a la compresión del nervio vago por el tumor. El análisis de la VFC después de la operación mostró una mejora significativa del tono parasimpático, lo que sugiere que la extirpación del tumor alivió la compresión del nervio vago y restauró la función autónoma normal.\nAsimismo, el paciente manifestó que el dolor en el cuello y en el oído había desaparecido por completo después de la cirugía, sin que se produjera una reaparición de los síntomas durante el período de seguimiento. Se realizaron estudios de imagen, que incluyeron ultrasonido Doppler y angiografía por TAC, a los 6 meses y al año, que no mostraron evidencia de reaparición del tumor o complicaciones vasculares.\n",
+        "gold_summary": "Describimos el caso de una mujer de 47 años con antecedentes de dolor en el cuello izquierdo y en el oído, acompañado por una masa en el cuello que había ido aumentando gradualmente durante 2,5 años. Después de las evaluaciones iniciales y de múltiples diagnósticos diferenciales, la angiografía por TC reveló una masa ovalada de 30 × 50 mm en la bifurcación carotídea izquierda, lo que confirmó un CCT tipo II de Shamblin. Las evaluaciones preoperatorias demostraron CHB congénita en el electrocardiograma y la ecocardiografía. La paciente se sometió a una resección completa del tumor con todas las precauciones necesarias, incluida la colocación temporal de un marcapasos y un cuidadoso seguimiento.\n",
+        "synthetic_summary": {
+            "B1": "Había una señora con dolor en su cuello y oído. Tenía una bolita en el cuello que creció poco a poco. Los doctores hicieron muchas pruebas y vieron la bolita en su cuello con una máquina especial. La bolita estaba cerca de unos tubos importantes del cuello. \n\nAntes de la operación, los doctores revisaron su corazón y vieron que tenía un problema que nació con ella. Para la operación, usaron un aparato para ayudar a su corazón a latir bien. Los doctores sacaron la bolita con mucho cuidado. Después, la señora se sintió mejor y no le dolió más.",
+            "B2": "**Lo que le pasó a la paciente**  \nUna mujer de 47 años tenía dolor en el lado izquierdo del cuello y en el oído izquierdo. También notó una bolita (masa) en el cuello que fue creciendo poco a poco durante más de dos años. Al principio, pensaron que tenía una infección en el oído, pero el dolor no mejoró con el tratamiento.\n\n**Lo que encontraron los médicos**  \nDespués de hacer varios estudios, usaron una tomografía computarizada (una especie de radiografía especial) para ver mejor el cuello. Descubrieron una masa ovalada de 3 por 5 centímetros en un lugar donde una arteria importante del cuello se divide. Esto confirmó que tenía un tumor llamado paraganglioma carotídeo, que es un tumor raro que crece cerca de las arterias del cuello.\n\nAdemás, al revisar su corazón, encontraron que tenía un bloqueo cardíaco congénito, que significa que su corazón late más lento de lo normal desde que nació. Por eso, antes de la cirugía, hicieron varios exámenes para asegurarse de que su corazón estaba estable.\n\n**Cómo la operaron y qué cuidados tuvieron**  \nPara quitar el tumor, los médicos planearon la cirugía con mucho cuidado. Le pusieron un marcapasos temporal, que es un dispositivo que ayuda a controlar el ritmo del corazón durante la operación. También usaron anestesia especial para que no tuviera problemas con la presión o el ritmo cardíaco.\n\nDurante la cirugía, hicieron una incisión en el cuello para llegar al tumor. Usaron pinzas para controlar el sangrado y monitorearon los nervios importantes para evitar dañarlos. El tumor fue separado cuidadosamente de las arterias y nervios cercanos. La operación duró poco más de dos horas y no hubo complicaciones graves.\n\n**Después de la cirugía y resultados**  \nLa paciente estuvo en cuidados intensivos un día para vigilar su estado. El marcapasos temporal se retiró al día siguiente porque su corazón mantenía un ritmo estable. Fue dada de alta tres días después, sin dolor ni problemas.\n\nEn los controles posteriores, los médicos vieron que el tumor no había vuelto a aparecer y que su corazón seguía funcionando bien. Además, el análisis mostró que la función de un nervio llamado nervio vago mejoró después de quitar el tumor, lo que ayudó a que su sistema nervioso autónomo trabajara mejor. La paciente también dijo que el dolor en el cuello y oído desapareció completamente.\n\n**Qué significa este caso**  \nEste caso muestra la importancia de hacer un diagnóstico correcto cuando hay dolor persistente y masas en el cuello. También destaca cómo los médicos deben planear cuidadosamente la cirugía en pacientes con problemas cardíacos para evitar riesgos. La operación fue exitosa y mejoró la calidad de vida de la paciente.",
+            "B3": "**Contexto del Caso**  \nSe presenta el caso de una mujer de 47 años que experimentaba dolor en el lado izquierdo del cuello y en el oído izquierdo, acompañado por la presencia de una masa en el mismo lado del cuello. Esta masa había sido detectada aproximadamente 30 meses antes y había ido aumentando de tamaño de forma progresiva. Inicialmente, el dolor se atribuyó a una infección del oído medio (otitis media), pero ante la persistencia de los síntomas, se realizaron estudios de imagen que identificaron una masa en la bifurcación de la arteria carótida izquierda.\n\n**Hallazgos Clave**  \nLa angiografía por tomografía computarizada (TC) mostró una masa ovalada de 30 × 50 mm ubicada en la bifurcación carotídea izquierda, característica de un tumor del cuerpo carotídeo (TCC) clasificado como tipo II según Shamblin, lo que indica un compromiso parcial de las arterias carótidas. Además, las evaluaciones cardiovasculares preoperatorias confirmaron que la paciente tenía un bloqueo auriculoventricular completo congénito (CHB), detectado mediante electrocardiograma (ECG) y corroborado por ecocardiografía, que mostró función ventricular normal sin anomalías estructurales.\n\n**Interpretación Clínica y Manejo**  \nDado el diagnóstico de TCC y la condición cardíaca de la paciente, se diseñó un plan quirúrgico y anestésico cuidadoso para minimizar riesgos. Se colocó un marcapasos temporal externo para mantener un ritmo cardíaco estable durante la cirugía y se monitorizó de forma continua la presión arterial y otros parámetros vitales. La cirugía se realizó mediante un abordaje abierto, con una incisión paralela al músculo esternocleidomastoideo para exponer la bifurcación carotídea y permitir la disección cuidadosa del tumor, preservando nervios importantes como el vago e hipogloso mediante neuromonitorización intraoperatoria.\n\nDurante la intervención, se aplicaron pinzas vasculares para controlar el flujo sanguíneo y evitar hemorragias, y se mantuvo una comunicación estrecha entre los equipos quirúrgico y anestésico para manejar cualquier cambio hemodinámico. La cirugía se completó exitosamente en poco más de dos horas, con sangrado mínimo y sin complicaciones inmediatas.\n\n**Próximos Pasos y Resultados a Largo Plazo**  \nDespués de la operación, la paciente fue vigilada en la unidad de cuidados intensivos y luego trasladada a planta general. El marcapasos temporal se retiró al día siguiente, ya que el ritmo cardíaco se mantuvo estable. La paciente fue dada de alta en buenas condiciones al tercer día postoperatorio, sin dolor ni otros síntomas. El examen histopatológico confirmó el diagnóstico de tumor del cuerpo carotídeo.\n\nEn el seguimiento a corto y largo plazo, que incluyó evaluaciones clínicas, electrocardiogramas y ecocardiografías, se observó que la función cardíaca permaneció estable y que el bloqueo cardíaco congénito no empeoró. Además, un análisis de la variabilidad de la frecuencia cardíaca mostró una mejora significativa en la actividad parasimpática después de la cirugía, lo que sugiere que la extirpación del tumor alivió la compresión del nervio vago y restauró la función autónoma normal. Los estudios de imagen realizados a los 6 meses y un año no evidenciaron recurrencia tumoral ni complicaciones vasculares. La paciente reportó la desaparición completa del dolor en cuello y oído, sin reaparición de síntomas durante el seguimiento.\n\nEn resumen, este caso ilustra la importancia de un diagnóstico preciso y un manejo multidisciplinario cuidadoso en pacientes con tumores carotídeos y condiciones cardíacas preexistentes, logrando una resección segura y resultados clínicos favorables a largo plazo."
+        }
+    },
+    {
+        "article": "Una mujer de 19 años de edad acudió al servicio de urgencias de nuestro hospital con una queja principal de dos días de historia de cefalea, acompañada de náuseas recurrentes, vómitos y fiebre de un día. En el ingreso, su examen físico reveló una fiebre alta de 39.1°C, presión arterial elevada de 189/120 mmHg y una frecuencia cardíaca de 148 latidos por minuto. Los resultados de laboratorio indicaron un recuento de glóbulos blancos elevado de 14.77×10^9/L y un recuento de neutrófilos de 13.55×10^9/L, lo que sugiere una posible infección o respuesta inflamatoria. Se administró un tratamiento empírico inicial con antibióticos debido a la sospecha de infección, pero sus síntomas persistieron. Dados sus signos vitales anormales, marcadores inflamatorios elevados y falta de mejora de los síntomas, la paciente fue admitida para una evaluación diagnóstica adicional y transferida a la unidad de cuidados intensivos para una estrecha monitorización. Un año antes, la paciente había presentado síntomas similares y se le diagnosticó miocarditis en un hospital local en base a los hallazgos clínicos en ese momento. Durante esa hospitalización, también se le diagnosticó hipertensión y se le prescribieron medicamentos antihipertensivos. Sin embargo, después del alta, la paciente no se adhirió al tratamiento antihipertensivo prescrito y no controló regularmente su presión arterial. Además, es notable que su padre tenía antecedentes de muerte súbita inexplicable.\n\nPara investigar la etiología subyacente de los síntomas del paciente, se realizó una tomografía computarizada (TC) de tórax. De forma incidental, esta exploración reveló una masa suprarrenal izquierda con densidad de tejido blando, que medía 43 mm × 36 mm. No se observaron hallazgos patológicos en las exploraciones de TC de cabeza y tórax. El electrocardiograma demostró taquicardia sinusal con un intervalo PR acortado y ondas P altas y puntiagudas en las derivaciones II, III y aVF. La ecocardiografía transtorácica no reveló ninguna anomalía significativa.\n\nEn el segundo día de ingreso, el paciente mostró niveles crecientes de péptido natriurético cerebral (BNP) y troponina I (TnI). El cardiólogo diagnosticó provisionalmente al paciente con miocarditis de etiología incierta, basándose en la presentación clínica, los biomarcadores cardiacos elevados (BNP y TnI) y los hallazgos del electrocardiograma de apoyo. Se inició el tratamiento con metilprednisolona (0,25 g diarios) para abordar la posible inflamación miocárdica debida a la sospecha de miocarditis. Se administraron furosemida (20 mg cada 12 horas) y espironolactona (20 mg cada 12 horas) como diuréticos para controlar la retención de líquidos y reducir la carga de trabajo cardiaco. Se prescribió perindopril amlodipina (10 mg: 5 mg diarios) como inhibidor de la enzima convertidora de la angiotensina y bloqueador del canal del calcio para controlar la presión arterial y reducir la poscarga. Se usó tartrato de metoprolol (25 mg cada 12 horas) para controlar la frecuencia cardiaca y disminuir la demanda de oxígeno miocárdico, mientras que se administró esmolol (0,2 g/hora por infusión intravenosa), un bloqueador beta de acción corta, para controlar la frecuencia cardiaca aguda adicional debido a la taquicardia sinusal. Debido a la preocupación por una posible infección, se agregó moxifloxacina como terapia antibiótica empírica.\n\nDada la presentación del paciente con una masa suprarrenal e hipertensión, el endocrinólogo recomendó una evaluación de la relación aldosterona/renina, cortisol plasmático, catecolaminas plasmáticas y catecolaminas urinarias de 24 horas, junto con sus metabolitos. En posición supina, los niveles de catecolaminas plasmáticas y urinarias estaban marcadamente elevados (Tabla 1), incluyendo dopamina plasmática a 524,5 pmol/L, norepinefrina a 83975 pmol/L y epinefrina a 10579,3 pmol/L. Además, los niveles urinarios de 24 horas mostraron adrenalina libre a 4368,89 nmol/24 horas, norepinefrina libre superior a 12697,60 nmol/24 horas, normetaneprina a 8312 nmol/24 horas, metaneprinas a 4078 nmol/24 horas y ácido vanilmandélico a 58,1 mg/24 horas. Estos hallazgos apoyaron un diagnóstico clínico de feocromocitoma. En el quinto día posterior al ingreso, se interrumpió la terapia glucocorticoide y se sustituyó perindopril amlodipina con terazosin para un control más dirigido de la presión arterial.\n\nUna tomografía computarizada abdominal mejorada confirmó una masa suprarrenal izquierda, muy sugestiva de feocromocitoma. Además, después de obtener el consentimiento informado, se realizó una secuenciación del exoma completo, que reveló una mutación sin sentido heterocigótica, c.1900T > C: p. Cys634Arg, en el gen RET, que conduce a una sustitución de cisteína por arginina en el codón 634. Esta mutación levantó sospechas de un síndrome de neoplasia endocrina múltiple, lo que impulsó una evaluación adicional de las glándulas tiroides y paratiroides. La ecografía Doppler en color de la tiroides identificó una masa hipoecoica que medía 6 mm × 4 mm en el lóbulo tiroideo izquierdo, y se observó una leve elevación en los niveles de calcitonina. No se detectaron anormalidades significativas adicionales.\n\nA medida que la condición del paciente mejoró gradualmente, los niveles de cortisol en plasma y ACTH volvieron a la normalidad. El paciente fue dado de alta con una prescripción de tartrato de metoprolol (100 mg cada 12 horas) e hidrocloruro de ivabradina (5 mg cada 12 horas) para el tratamiento en el hogar. Tres meses después, después de lograr un estado clínico estable, el paciente se sometió a una resección del tumor suprarrenal izquierdo, que medía 50 mm × 40 mm × 30 mm. El análisis inmunohistoquímico confirmó una tinción positiva para Vim, CD56, Syn, CgA y NSE, con S-100 positivo en las células de Sertoli, mientras que CKpan, CD10, MART-1/Melan-A y Melan-A fueron negativos. El índice Ki67 fue del 1 %, lo que llevó a un diagnóstico definitivo de feocromocitoma suprarrenal. El paciente fue dado de alta sin más medicamentos y desde entonces se le ha dado seguimiento regular postoperatorio sin recurrencia de síntomas. Durante un seguimiento postoperatorio de 15 meses, el paciente exhibió hipercalcinotemia persistente leve con un tamaño de nódulo tiroideo estable, mientras que los niveles de PTH y calcio en suero mostraron un aumento progresivo (Tabla 2). Se realizó una gammagrafía paratiroidea adicional utilizando 99mTc-MIBI, y la conclusión fue un resultado negativo para el adenoma paratiroideo.\n",
+        "gold_summary": "Reportamos el caso de una mujer de 19 años que presentó feocromocitoma sin experimentar una crisis, a pesar de tener una masa suprarrenal significativa y someterse a un tratamiento glucocorticoide de alta dosis. Las pruebas genéticas revelaron una mutación de sentido erróneo heterocigótica en el gen RET (c.1900T > C: p. Cys634Arg), asociada con MEN2A. La evaluación endocrina adicional identificó un nódulo tiroideo con niveles de calcitonina levemente elevados, pero niveles normales de electrolitos y hormona paratiroidea. Durante un seguimiento postoperatorio de 15 meses, la paciente exhibió hipercalcitonemia persistente leve con tamaño de nódulo tiroideo estable, mientras que la PTH y los niveles de calcio sérico mostraron un aumento progresivo. Se realizó una gammagrafía paratiroidea adicional utilizando 99mTc-MIBI, que arrojó un resultado negativo para el adenoma paratiroideo.\n",
+        "synthetic_summary": {
+            "B1": "Había una chica de 19 años que tenía un bulto en una parte de su cuerpo llamada glándula suprarrenal. Este bulto no le causó un problema muy grande de repente. Los doctores le hicieron un examen especial y encontraron un cambio en sus genes. Este cambio puede causar problemas en algunas partes del cuerpo que hacen hormonas.\n\nTambién encontraron un pequeño bulto en su cuello, en una parte llamada tiroides. Ella tenía un poco más de una sustancia llamada calcitonina, pero otras cosas en su cuerpo estaban normales. Después de que le sacaron el bulto del cuerpo, los doctores la cuidaron por mucho tiempo. Vieron que la calcitonina seguía un poco alta y que otras cosas en su sangre subían poco a poco. Hicieron otro examen para buscar otro bulto, pero no encontraron nada malo. Los doctores siguen cuidándola para que esté bien.",
+            "B2": "**Caso de una joven con tumor suprarrenal y mutación genética**\n\nUna mujer de 19 años llegó al hospital con dolor de cabeza, náuseas, vómitos y fiebre. Tenía la presión arterial muy alta y signos de inflamación en su cuerpo. Los médicos encontraron una masa (un bulto) en su glándula suprarrenal izquierda, que está encima del riñón y produce hormonas importantes. Esta masa causaba que su cuerpo liberara muchas sustancias llamadas catecolaminas, que pueden subir mucho la presión arterial.\n\nSe hizo un análisis genético y descubrieron que tenía un cambio en un gen llamado RET. Este cambio puede causar un síndrome llamado MEN2A, que hace que se formen tumores en varias glándulas del cuerpo. Por eso, también revisaron su tiroides y encontraron un pequeño nódulo (una bolita) con niveles un poco altos de calcitonina, una hormona relacionada con la tiroides.\n\nDespués de tratarla con medicamentos para controlar su presión y frecuencia cardíaca, la paciente se sometió a una cirugía para quitar la masa suprarrenal. El examen del tumor confirmó que era un feocromocitoma, un tipo de tumor que produce muchas hormonas. Tras la operación, la paciente mejoró y no tuvo más síntomas.\n\nDurante los siguientes 15 meses, los médicos siguieron revisando su tiroides y sus niveles de calcio en sangre. Aunque el nódulo en la tiroides no creció, los niveles de calcitonina y calcio en sangre aumentaron un poco, lo que puede indicar cambios en las glándulas paratiroides, que ayudan a controlar el calcio en el cuerpo. Sin embargo, una prueba especial llamada gammagrafía no mostró tumores en esas glándulas.\n\n**¿Qué significa esto?**\n\nEste caso muestra cómo un tumor en la glándula suprarrenal puede causar problemas graves, pero también cómo una mutación genética puede afectar varias glándulas del cuerpo. Es importante hacer un seguimiento cuidadoso para detectar y tratar cualquier cambio en otras glándulas, como la tiroides o las paratiroides, que pueden estar relacionadas con esta mutación.",
+            "B3": "**Contexto**  \nPresentamos el caso de una mujer joven de 19 años que acudió al hospital con síntomas de cefalea, náuseas, vómitos y fiebre, acompañados de hipertensión severa y taquicardia. Durante la evaluación, se detectó incidentalmente una masa en la glándula suprarrenal izquierda. Los análisis de sangre y orina mostraron niveles muy elevados de catecolaminas (sustancias químicas producidas por la médula suprarrenal), lo que sugirió la presencia de un feocromocitoma, un tumor poco común que produce estas hormonas y puede causar hipertensión y otros síntomas.\n\n**Hallazgos Clave**  \n- La paciente tenía una masa suprarrenal de aproximadamente 4 cm detectada por tomografía computarizada.  \n- Los niveles plasmáticos y urinarios de catecolaminas y sus metabolitos estaban marcadamente elevados, confirmando la sospecha de feocromocitoma.  \n- Se identificó una mutación genética heterocigótica en el gen RET (c.1900T > C: p. Cys634Arg), conocida por estar asociada con el síndrome de neoplasia endocrina múltiple tipo 2A (MEN2A), una condición que predispone a tumores endocrinos múltiples.  \n- La evaluación adicional mostró un pequeño nódulo en la glándula tiroides con leves elevaciones en los niveles de calcitonina, una hormona que puede indicar la presencia de carcinoma medular de tiroides, común en MEN2A.  \n- Durante el seguimiento postoperatorio de 15 meses, la paciente mantuvo niveles ligeramente elevados de calcitonina y un nódulo tiroideo estable, pero los niveles de hormona paratiroidea (PTH) y calcio en sangre aumentaron progresivamente.  \n- Una gammagrafía paratiroidea con 99mTc-MIBI no mostró evidencia de adenoma paratiroideo (tumor benigno de la glándula paratiroides).\n\n**Interpretación Clínica**  \nEste caso destaca la presentación atípica de un feocromocitoma sin crisis hipertensiva grave, a pesar de la masa suprarrenal significativa y el uso de glucocorticoides de alta dosis, que normalmente podrían desencadenar una crisis. La mutación en el gen RET confirma la asociación con MEN2A, un síndrome que requiere vigilancia cuidadosa por el riesgo de tumores endocrinos múltiples, incluyendo carcinoma medular de tiroides y alteraciones paratiroideas. La persistencia de hipercalcitoninemia y el aumento progresivo de PTH y calcio sugieren la necesidad de un seguimiento continuo para detectar posibles complicaciones o desarrollo de hiperparatiroidismo.\n\n**Próximos Pasos**  \n- Continuar con el seguimiento endocrinológico regular para monitorizar el nódulo tiroideo y los niveles hormonales, especialmente calcitonina, PTH y calcio sérico.  \n- Realizar evaluaciones periódicas para detectar signos tempranos de carcinoma medular de tiroides o hiperparatiroidismo.  \n- Considerar intervenciones quirúrgicas o terapéuticas adicionales si se evidencian cambios significativos en el nódulo tiroideo o en la función paratiroidea.  \n- Mantener un control estricto de la presión arterial y la función cardiaca, dado el antecedente de feocromocitoma y miocarditis.  \n- Brindar asesoramiento genético y seguimiento familiar, dado el componente hereditario asociado a la mutación RET y el antecedente de muerte súbita en el padre.\n\nEste caso subraya la importancia de una evaluación multidisciplinaria y un seguimiento prolongado en pacientes jóvenes con feocromocitoma y mutaciones genéticas relacionadas con síndromes endocrinos múltiples."
+        }
+    },
+    {
+        "article": "Una refugiada etíope embarazada de 39 años (Gravida 3 Para 2+0) fue derivada a nuestro departamento de urgencias de medicina interna en el Hospital Universitario de Gadarif, Gadarif State, Sudán, con hinchazón generalizada progresiva, falta de aire y fatiga durante 6 semanas y una revisión sistémica sin importancia. La paciente fue admitida en el sitio de admisión de casos críticos y su historia, tomada con la ayuda de un intérprete de idiomas más tarde en la admisión, reveló un episodio remoto inicialmente no revelado de tres convulsiones tónico-clónicas generalizadas no provocadas hace 21 años que se trataron tradicionalmente. Sin embargo, no había antecedentes de traumatismo craneal o antecedentes familiares de convulsiones. El examen general de la paciente reveló un PWS del lado izquierdo que involucraba la división oftálmica del nervio trigémino. Sin embargo, este hallazgo se perdió inicialmente en la inspección pero luego fue confirmado por el cónyuge de la paciente para estar presente desde el nacimiento. La paciente también estaba muy pálida y tenía derrames pleurales bilaterales, hepatomegalia blanda e hinchazón bilateral de las extremidades inferiores.\n\nLas investigaciones iniciales revelaron un nivel de hemoglobina de 8,84 g/dl. Por lo tanto, se diagnosticó insuficiencia cardíaca debido a anemia y se trató a la paciente en consecuencia. Sin embargo, ocho días después de su ingreso, la paciente había desarrollado aproximadamente seis episodios de convulsiones tónico-clónicas focales a bilaterales que respondieron bien a la fenitoína, pero que dejaron a la paciente en un estado comatoso profundo con un GCS de tres. Fue posteriormente admitida en la unidad de cuidados intensivos (UCI) y se le insertó un tubo nasogástrico para ayudarla con su nutrición y administración de fármacos. Además, para evitar más convulsiones, se le inició un tratamiento con comprimidos de carbamazepina de 200 mg administrados a través del tubo nasogástrico.\n\nSe retrasó una tomografía computarizada (TC) sin contraste del cerebro para el día posterior a la estabilización, ya que solo había una máquina de tomografía computarizada en el estado de Gadarif y funcionaba de forma intermitente debido a la falta de un número suficiente de técnicos radiólogos. La tomografía computarizada reveló calcificaciones corticales en la parte posterior del área parietal izquierda, lo que planteó el diagnóstico diferencial de SWS. En consecuencia, se realizó un examen físico de repetición, que mostró la presencia de una lesión plana de color rojo púrpura en la frente y el ojo. Al interrogar al cónyuge, se confirmó la presencia de esta lesión y que no había cambiado desde el nacimiento, lo que nos ayudó a descartar el diagnóstico de una mancha salmón, ya que esta lesión no se desvaneció, por lo que se diagnosticó como PWS. Además, no tenía características de megalencefalia, síndrome de malformación capilar que por lo general incluye un gran tamaño de la cabeza o del cerebro, problemas en las articulaciones y malformaciones capilares en la piel. Tampoco tenía hipertrofia de extremidades, anomalías del drenaje linfático o excrecencias óseas o de tejidos blandos que sugieran el síndrome de Klippel-Trenaunay-Weber. Por lo tanto, en función de los hallazgos de la tomografía computarizada y la presentación típica, llegamos a la conclusión del diagnóstico de SWS.\n\nDos días después de ingresar en la UCI, la paciente experimentó un cambio fluctuante en su estado de conciencia y una nueva aparición de hemiparesia contralateral (contralateral al SPW), así como afasia y labilidad emocional. Desafortunadamente, cuatro días después de ingresar en la UCI, la paciente empezó a experimentar sangrado vaginal; por ello, se consultó al departamento de obstetricia y ginecología y se descubrió que la paciente tenía un embarazo no viable (28 semanas + 1 día) y se realizó una inducción sin incidentes. Durante el mismo período, la paciente se volvió combativa y poco cooperativa, lo que llevó a que se la inmovilizara físicamente. Tres días después, la paciente desarrolló nuevos ataques focales bilaterales que comenzaron como episodios mioclónicos faciales y, tras consultar con el departamento de neurología, se aumentó la dosis de carbamazepina de la paciente a 1000 mg diarios, lo que ayudó a prevenir la recurrencia de los ataques. Cabe mencionar que, en su segundo trimestre y antes de recibir el resultado de la tomografía computarizada, se exploró un diagnóstico de eclampsia, pero sus constantes lecturas de presión arterial con una presión sistólica superior a la normal de 139 la mayoría de los días y una presión diastólica con un máximo de 97 mmHg y un rango bajo de proteinuria, así como la ausencia de características sistémicas como deterioro renal o hepático, excluyeron este diagnóstico. Después de alcanzar el diagnóstico de SW, se puso en juego un enfoque multidisciplinario; por ello, se realizó una consulta oftalmológica para descartar glaucoma. Sin embargo, la paciente estaba muy irritable y era difícil realizar un examen de fondo de ojo. Además, la paciente fue trasladada a la sala de medicina interna tras la estabilización.\n",
+        "gold_summary": "Presentamos el caso de una refugiada de 39 años, no diabética y no hipertensa, que inicialmente presentó insuficiencia cardiaca debido a anemia, por lo que recibió transfusiones de sangre. Más adelante, al ingresar, desarrolló convulsiones múltiples focales bilaterales, irritabilidad severa, afasia y hemiplejía derecha, lo que motivó su ingreso a la UCI. Un examen y un historial médico repetidos revelaron una mancha de vino de Oporto ocular izquierda leve que inicialmente pasó desapercibida y un historial remoto de convulsiones no provocadas 20 años atrás. Las imágenes revelaron calcificaciones parietales y confirmaron el diagnóstico de SWS. Por lo tanto, se adoptó un enfoque multidisciplinario para comprender plenamente el diagnóstico de la paciente y determinar una estrategia de tratamiento, que incluyó consultas con los departamentos de neurología, oftalmología, otorrinolaringología y fisioterapia. Se logró un control exitoso de las convulsiones mediante la administración de fenitoína IV durante 3 días y el aumento gradual de la carbamazepina oral a 1 g diario a través de una sonda nasogástrica. Lamentablemente, debido a la falta de personal o recursos, no se pudieron realizar otras evaluaciones importantes para pacientes con SWS, como evaluaciones avanzadas de neuroimagen, psiquiátricas, de cirugía plástica y neurocirugía, así como revisiones dentales.\n",
+        "synthetic_summary": {
+            "B1": "Había una señora que estaba muy cansada y con el cuerpo hinchado. Ella tenía una manchita roja en la cara desde que nació. También tuvo muchos ataques donde se movía sin querer. Los doctores vieron que tenía un problema en el cerebro y en la cara. Le dieron medicinas para que los ataques pararan. Muchos doctores la ayudaron para que se sintiera mejor. A veces, no pudieron hacer todas las pruebas porque faltaban cosas en el hospital. Pero todos cuidaron mucho de ella para que estuviera tranquila.",
+            "B2": "**Caso de una mujer con Síndrome de Sturge-Weber (SWS)**\n\nPresentamos la historia de una mujer de 39 años que llegó al hospital con problemas de salud graves. Al principio, tenía insuficiencia cardíaca causada por anemia, que es cuando hay pocas células rojas en la sangre. Por eso, le dieron transfusiones de sangre para mejorar su condición.\n\nDespués, comenzó a tener varias convulsiones, que son movimientos involuntarios del cuerpo causados por actividad anormal en el cerebro. También mostró irritabilidad, dificultad para hablar (afasia) y debilidad en el lado derecho del cuerpo (hemiplejía). Debido a esto, fue ingresada en la unidad de cuidados intensivos (UCI) para recibir atención especial.\n\nAl revisar su historia médica y hacer un examen más detallado, los médicos notaron una mancha roja en el ojo izquierdo llamada mancha de vino de Oporto. Esta mancha estaba presente desde su nacimiento, pero no se había detectado antes. Además, la paciente había tenido convulsiones hace 20 años, aunque no se había tratado formalmente.\n\nUna tomografía computarizada (una imagen del cerebro) mostró calcificaciones en una parte del cerebro llamada área parietal. Estos hallazgos ayudaron a confirmar que la paciente tenía Síndrome de Sturge-Weber (SWS), una enfermedad rara que afecta la piel, el cerebro y a veces los ojos.\n\nPara tratarla, un equipo de diferentes especialistas trabajó junto: neurólogos (que cuidan del cerebro), oftalmólogos (que cuidan los ojos), otorrinolaringólogos (que cuidan oídos y garganta) y fisioterapeutas (que ayudan con la movilidad). Las convulsiones se controlaron con medicamentos llamados fenitoína y carbamazepina, administrados por vía intravenosa y a través de un tubo en la nariz.\n\nSin embargo, debido a la falta de personal y recursos en el hospital, no se pudieron hacer otros estudios importantes para pacientes con SWS, como imágenes más detalladas del cerebro, evaluaciones psicológicas, consultas para cirugía plástica o neurocirugía, ni revisiones dentales.\n\nEste caso muestra la importancia de un diagnóstico cuidadoso y un tratamiento multidisciplinario para manejar enfermedades complejas como el Síndrome de Sturge-Weber.",
+            "B3": "**Contexto del Caso**  \nSe trata de una mujer refugiada de 39 años, embarazada, sin antecedentes de diabetes o hipertensión, que acudió al hospital con síntomas iniciales de insuficiencia cardíaca secundaria a anemia severa. Inicialmente recibió transfusiones sanguíneas para tratar esta condición. Sin embargo, durante su hospitalización, desarrolló múltiples convulsiones focales que se extendieron a ambos hemisferios cerebrales, acompañadas de irritabilidad intensa, dificultad para hablar (afasia) y parálisis parcial en el lado derecho del cuerpo (hemiplejía). Estos signos neurológicos graves motivaron su ingreso a la unidad de cuidados intensivos (UCI).\n\n**Hallazgos Clave**  \nUna revisión detallada de su historia clínica, junto con un examen físico repetido, reveló la presencia de una mancha de vino de Oporto (una lesión vascular congénita de color rojo púrpura) en la región ocular izquierda, que inicialmente no se había detectado. Además, se confirmó un antecedente remoto de convulsiones no provocadas ocurridas hace aproximadamente 20 años, que no había sido reportado inicialmente. La tomografía computarizada del cerebro mostró calcificaciones en la región parietal izquierda, hallazgo característico que, junto con la mancha cutánea y el cuadro clínico, permitió establecer el diagnóstico de síndrome de Sturge-Weber (SWS), una enfermedad neurocutánea rara que afecta vasos sanguíneos del cerebro y la piel.\n\n**Interpretación Clínica**  \nEl síndrome de Sturge-Weber se caracteriza por la presencia de malformaciones vasculares en la piel y el cerebro, que pueden provocar convulsiones, déficits neurológicos y problemas oftalmológicos. En este caso, la combinación de convulsiones recurrentes, hemiplejía, afasia y la mancha facial típica apoyaron el diagnóstico. La anemia y la insuficiencia cardíaca iniciales complicaron el cuadro clínico, pero el manejo neurológico fue prioritario tras la aparición de las convulsiones y el deterioro neurológico.\n\n**Estrategia de Tratamiento y Manejo Multidisciplinario**  \nSe implementó un enfoque integral que involucró a varios especialistas: neurología para el control de las convulsiones, oftalmología para evaluar posibles complicaciones oculares como el glaucoma (aunque la paciente estaba muy irritable y dificultó el examen), otorrinolaringología y fisioterapia para abordar las secuelas neurológicas. El control de las convulsiones se logró con éxito mediante la administración intravenosa de fenitoína durante tres días, seguida de un aumento progresivo de la dosis de carbamazepina oral hasta 1000 mg diarios, administrada a través de una sonda nasogástrica debido al estado de coma profundo de la paciente.\n\n**Limitaciones y Próximos Pasos**  \nDebido a limitaciones en recursos humanos y técnicos en el hospital, no fue posible realizar evaluaciones adicionales importantes para pacientes con SWS, como estudios avanzados de neuroimagen, evaluaciones psiquiátricas, consultas de cirugía plástica y neurocirugía, ni revisiones dentales, que suelen ser necesarias para un manejo completo de esta enfermedad. Se recomienda continuar con un seguimiento multidisciplinario para optimizar el tratamiento y mejorar la calidad de vida de la paciente."
+        }
+    },
+    {
+        "article": "Una paciente de 69 años se quejaba de una pérdida progresiva de la visión. Sus padres eran primos hermanos. Le habían diagnosticado retinitis pigmentosa 27 años antes. La paciente había fumado durante 15 años. Tenía antecedentes de hiperlipidemia e hipotiroidismo.\n\nTras una evaluación oftalmológica completa, se determinó que el paciente tenía una agudeza visual corregida (AVC) de contar los dedos a 5’ y 3’ en los ojos derecho e izquierdo, respectivamente. La retinoscopia mostró una refracción de –1.00 + 0.50×70 y –2.00 + 1.00×5 en los ojos derecho e izquierdo, respectivamente. El paciente tenía discos ópticos pálidos con una atrofia profunda extensa de la mácula central, hiperplasia del pigmento epitelial y otras áreas de atrofia multifocal en el ojo derecho. Además, el paciente tenía atrofia macular en el ojo izquierdo. En la imagen de autofluorescencia del fondo del ojo (FAF) del paciente, había evidencia de una hipoautofluorescencia central de la mácula, con una extensión centrífuga difusa desde su centro hasta su periferia.\n\nLa tomografía de coherencia óptica macular (OCT) determinó que el espesor macular promedio era de 191 µM y 193 µM en los ojos derecho e izquierdo, respectivamente. El volumen macular era de 6.9 mm3 y 7.0 mm3 en los ojos derecho e izquierdo, respectivamente. No se encontró edema macular, quistes o fluido subretinal en ninguno de los ojos.\n\nUna prueba de campo visual reveló que el paciente tenía desviaciones medias de –23.75 dB y –24.56 dB en los ojos derecho e izquierdo, respectivamente. Las desviaciones estándar de patrón fueron de +3.69 dB y +4.69 dB en los ojos derecho e izquierdo, respectivamente. Los resultados de un electrorretinograma de campo completo (ERG) mostraron una respuesta normal de bastones y una respuesta de conos disminuida, bilateralmente. Por estas razones, se realizó un diagnóstico clínico de enfermedad STGD1.\n\nSe encontró una variante patogénica homocigótica intrónica c.5714+5G>A del gen ABCA4 tras el análisis de secuenciación y eliminación/duplicación utilizando secuenciación de próxima generación (Invitae Corporation, San Francisco, California). Tenía seis variantes adicionales de significación incierta (VUS) en los genes CACNA1F, EYS, KCNV2, KLHL7, MKKS y USH2A.\n",
+        "gold_summary": "Una paciente de 69 años de edad se presentó en la clínica quejándose de una pérdida progresiva de la visión. La evaluación oftálmica fue notable para una mejor agudeza visual corregida de contar los dedos a 5' en el ojo derecho y 3' en el ojo izquierdo. Las imágenes revelaron una atrofia profunda y extensa de la mácula central, una hiperplasia del pigmento epitelial y otras áreas de atrofia multifocal en el ojo derecho. Además, las imágenes de autofluorescencia del fondo de la mácula mostraron una hipoautofluorescencia central con expansión bilateral a la periferia en ambos ojos. Un electrorretinograma de campo completo mostró una respuesta normal de los bastones, con una respuesta disminuida de los conos, bilateralmente. Las pruebas genéticas fueron positivas para una mutación inotrópica homocigótica en el gen ABCA4 de la variante c.5714+5G>A.\n",
+        "synthetic_summary": {
+            "B1": "Una señora de 69 años veía cada vez menos con sus ojos. El doctor le hizo muchas pruebas para mirar sus ojos. Vio que la parte del ojo que ayuda a ver bien estaba muy dañada. También encontró que algunas partes del ojo no funcionaban bien. El doctor hizo un examen especial y vio que unas células del ojo estaban normales y otras no. Luego, hicieron un examen de su sangre y encontraron un cambio en un gen que puede causar problemas en la vista.",
+            "B2": "**Lo que le pasaba a la paciente**  \nUna mujer de 69 años empezó a perder la vista poco a poco. Cuando la examinaron, pudo ver solo lo suficiente para contar los dedos a una distancia muy corta: 5 pies en un ojo y 3 pies en el otro. Esto muestra que su visión estaba bastante afectada.\n\n**Qué encontraron en sus ojos**  \nAl mirar dentro de sus ojos con imágenes especiales, los médicos vieron que la parte central de la retina llamada mácula estaba muy dañada. Había zonas donde las células que ayudan a la vista estaban muertas o muy débiles. También notaron un aumento anormal de unas células llamadas pigmento epitelial. Las imágenes que muestran la luz que emite la retina (autofluorescencia) indicaron que la parte central de la mácula tenía menos luz de lo normal, lo que significa daño, y este daño se extendía hacia los lados en ambos ojos.\n\n**Cómo funcionaban sus células de la vista**  \nSe hizo un examen llamado electrorretinograma, que mide la actividad eléctrica de las células de la retina. Los resultados mostraron que las células llamadas bastones, que ayudan a ver en la oscuridad, funcionaban bien. Pero las células llamadas conos, que permiten ver colores y detalles, estaban debilitadas en ambos ojos.\n\n**Qué encontraron en sus genes**  \nAl analizar su ADN, descubrieron que tenía una mutación específica en un gen llamado ABCA4. Este gen es importante para la salud de la retina. La mutación encontrada puede causar problemas en la función de las células de la retina y explicar la pérdida de visión de la paciente.\n\n**En resumen**  \nLa paciente tiene una enfermedad llamada STGD1, que afecta la mácula y causa pérdida progresiva de la visión. Los exámenes clínicos y genéticos ayudaron a confirmar este diagnóstico.",
+            "B3": "**Contexto**  \nUna mujer de 69 años acudió a consulta debido a una pérdida progresiva de la visión que había experimentado durante años. Su historia médica incluía un diagnóstico previo de retinitis pigmentosa desde hacía 27 años, antecedentes familiares de consanguinidad (sus padres eran primos hermanos), así como hiperlipidemia e hipotiroidismo. Además, había fumado durante 15 años.\n\n**Hallazgos Clave**  \nLa evaluación oftalmológica reveló una agudeza visual corregida muy reducida, con la paciente capaz solo de contar los dedos a 5 pies (aproximadamente 1.5 metros) con el ojo derecho y a 3 pies (menos de un metro) con el ojo izquierdo. La refracción mostró leves defectos de visión en ambos ojos. El examen del fondo de ojo evidenció una atrofia profunda y extensa de la mácula central (la zona responsable de la visión detallada), acompañada de hiperplasia (aumento) del pigmento epitelial y múltiples áreas de atrofia en el ojo derecho, mientras que el ojo izquierdo presentaba también atrofia macular. Las imágenes de autofluorescencia del fondo del ojo mostraron una zona central con baja autofluorescencia (hipoautofluorescencia), que se extendía desde el centro hacia la periferia en ambos ojos.\n\nLa tomografía de coherencia óptica (OCT), que permite visualizar las capas de la retina, indicó un grosor macular disminuido en ambos ojos, sin presencia de edema, quistes o líquido subretinal. Las pruebas de campo visual mostraron una pérdida significativa de sensibilidad en ambos ojos. El electrorretinograma (ERG), que mide la función de las células fotorreceptoras de la retina, evidenció una respuesta normal de los bastones (células responsables de la visión en condiciones de poca luz) pero una respuesta disminuida de los conos (células responsables de la visión en condiciones de luz y la percepción del color), de forma bilateral.\n\n**Interpretación Clínica**  \nCon base en estos hallazgos clínicos y funcionales, se estableció un diagnóstico de enfermedad de Stargardt tipo 1 (STGD1), una forma hereditaria de degeneración macular juvenil que afecta la visión central. El análisis genético confirmó la presencia de una mutación patogénica homocigótica (es decir, la misma alteración en ambas copias del gen) en el gen ABCA4, específicamente la variante intrónica c.5714+5G>A, conocida por estar asociada con esta enfermedad. Además, se identificaron seis variantes genéticas adicionales de significado incierto en otros genes relacionados con enfermedades retinianas, aunque su relevancia clínica no pudo ser determinada en este caso.\n\n**Próximos Pasos**  \nEl diagnóstico genético y clínico permite orientar el manejo y seguimiento de la paciente, que debe incluir controles oftalmológicos periódicos para evaluar la progresión de la enfermedad y la función visual. Aunque actualmente no existe una cura definitiva para la enfermedad de Stargardt, se pueden considerar opciones de apoyo visual y asesoramiento genético para la paciente y su familia. Asimismo, la identificación de la mutación específica puede facilitar la inclusión en estudios clínicos o terapias emergentes dirigidas a esta patología genética."
+        }
+    },
+    {
+        "article": "Un niño de 19 meses de edad fue admitido en el departamento de urgencias porque se cayó de la trona en la que comía. Esta caída ocurrió en un aparente bienestar, sin la presencia de signos o síntomas anticipados. Primero, se cayó sobre su glúteo y luego se golpeó la cabeza (occipucio) contra el suelo. Vomitó (tres episodios) y estaba muy irritable. Su frecuencia respiratoria y cardíaca eran >60 respiraciones y >150 latidos por minuto, mientras que la saturación de oxígeno era <80%. Tras el examen físico, el niño estaba hidratado y consciente, pero irritable. Más importante aún, observamos retracciones subcostal y, al auscultar, disminución de los sonidos respiratorios en la parte basal izquierda del tórax. El paciente fue ventilado con un balón de AMBU conectado a una fuente de oxígeno y monitorizado con un oxímetro de pulso. A pesar de nuestra intervención, la saturación de oxígeno cayó por debajo del 70% y cuanto más ventilábamos, más caía la saturación. La ecografía pulmonar mostró la ausencia de las típicas líneas A y la consolidación del pulmón, que se visualizó directamente como un parénquima sólido. Sobre la base del mal estado clínico, el paciente se sometió a intubación orotraqueal con un tubo endotraqueal con manguito. Después de que el bebé se estabilizó, se sometió a una tomografía computarizada (TC) de tórax que mostró una atelectasia completa del pulmón izquierdo con una interrupción del bronquio izquierdo principal a 12 cm de la bifurcación bronquial. Se sospechó un FBA ya que la madre también declaró que el bebé en los días anteriores había tenido un ataque de tos intenso y desapareció en 24 h sin ningún tratamiento. Por lo tanto, se realizó una broncoscopia rígida y se encontró y se eliminó rápidamente una almendra de 2 cm de diámetro en el bronquio izquierdo principal.\n\nEl paciente nunca había consumido antes almendras u otros frutos secos y, en esta ocasión, ingirió la almendra por accidente.\n\nEl bebé mostró una mejora clínica progresiva y, después de 24 horas, se le retiró la sonda y se le dio de alta de la unidad de cuidados intensivos para ser ingresado en la sala de pediatría general durante unos días, con una recuperación gradual y total de la función respiratoria.\n",
+        "gold_summary": "Describimos el caso de un niño de 19 meses que llegó a la sala de urgencias por un traumatismo en la cabeza. La evaluación clínica, sin embargo, reveló una dificultad respiratoria grave inexplicable que requería intubación traqueal. Después de nuestra evaluación, planteamos la hipótesis de que la dificultad respiratoria grave determinó un estado alterado de conciencia con el consiguiente traumatismo en la cabeza. Los hallazgos radiológicos levantaron la sospecha de aspiración de cuerpo extraño por la presencia de una atelectasia de todo el pulmón izquierdo. La tomografía computarizada mostró una interrupción abrupta del bronquio principal a 12 mm del casco. La siguiente broncoscopia identificó una amígdala de 2 cm.\n",
+        "synthetic_summary": {
+            "B1": "Un niño pequeño se cayó y se lastimó la cabeza. Pero lo más importante es que no podía respirar bien. Los doctores pusieron un tubo para ayudarlo a respirar. Vieron que un huesito en su pulmón estaba tapado. Buscaron y sacaron una almendra que estaba en su pulmón. Después, el niño mejoró y pudo respirar bien otra vez.",
+            "B2": "Caso de un niño con dificultad para respirar y caída en la cabeza\n\nUn niño de 19 meses llegó a urgencias después de caerse de la trona donde comía. Aunque parecía estar bien al principio, tenía problemas para respirar y vomitó varias veces. Su ritmo de respiración y corazón estaba muy rápido, y el nivel de oxígeno en su sangre era muy bajo. Al examinarlo, notaron que tenía dificultad para respirar y menos sonidos en el pulmón izquierdo.\n\nLo que encontraron\n\nUsaron una máquina para ayudarlo a respirar, pero el nivel de oxígeno seguía bajando. Una ecografía del pulmón mostró que una parte del pulmón estaba sólida, lo que no es normal. Luego, una tomografía (una imagen detallada del pecho) mostró que el pulmón izquierdo estaba colapsado y que el tubo principal que lleva aire a ese pulmón estaba bloqueado.\n\nQué significaba esto\n\nPensaron que algo estaba bloqueando la vía aérea, posiblemente un objeto que el niño había inhalado sin querer. La madre recordó que el niño había tenido una tos fuerte días antes. Al hacer una broncoscopia, que es cuando se usa un tubo con cámara para mirar dentro de los pulmones, encontraron y sacaron una almendra de 2 cm que estaba bloqueando el bronquio izquierdo.\n\nRecuperación\n\nEl niño nunca había comido almendras antes y la había tragado por accidente. Después de quitar la almendra, mejoró rápidamente. Lo mantuvieron en observación y finalmente se recuperó completamente de sus problemas para respirar.",
+            "B3": "**Contexto**  \nSe presenta el caso de un niño de 19 meses que fue llevado a urgencias tras una caída desde la trona mientras comía. Inicialmente, se pensó que el motivo principal era el traumatismo craneal provocado por la caída. Sin embargo, durante la evaluación clínica se detectó una dificultad respiratoria grave que no podía explicarse únicamente por el golpe.\n\n**Hallazgos Clave**  \nEl niño mostraba signos de insuficiencia respiratoria severa, con frecuencia respiratoria y cardíaca elevadas, saturación de oxígeno muy baja (menos del 80%) y dificultad para respirar evidenciada por retracciones subcostales y disminución de los sonidos respiratorios en la base del pulmón izquierdo. La saturación de oxígeno empeoraba incluso con ventilación asistida. La ecografía pulmonar reveló ausencia de las líneas A típicas y consolidación pulmonar, indicando que el tejido pulmonar estaba sólido en lugar de aireado. La tomografía computarizada (TC) de tórax mostró una atelectasia completa (colapso) del pulmón izquierdo y una interrupción abrupta del bronquio principal izquierdo a 12 mm de la bifurcación bronquial.\n\n**Interpretación Clínica**  \nEstos hallazgos sugirieron que la dificultad respiratoria grave fue la causa principal del estado alterado de conciencia y, por ende, del traumatismo craneal secundario a la caída. La interrupción del bronquio principal y la atelectasia indicaron la presencia de un cuerpo extraño que obstruía la vía aérea. La madre confirmó que el niño había tenido un episodio previo de tos intensa, lo que apoyó la sospecha de aspiración de un objeto. La broncoscopia rígida permitió identificar y extraer una almendra de 2 cm alojada en el bronquio izquierdo principal, que el niño había ingerido accidentalmente, siendo su primera exposición a frutos secos.\n\n**Próximos Pasos y Evolución**  \nTras la extracción del cuerpo extraño, el niño mostró una mejoría clínica progresiva. Se retiró la intubación después de 24 horas y fue trasladado de la unidad de cuidados intensivos a la sala de pediatría general, donde continuó su recuperación hasta la normalización completa de la función respiratoria. Este caso resalta la importancia de considerar la aspiración de cuerpos extraños en niños pequeños con dificultad respiratoria grave y síntomas atípicos, incluso cuando se presenta un traumatismo asociado."
+        }
+    },
+    {
+        "article": "Una mujer nulípara de 35 años con antecedentes de infertilidad se presentó en la consulta externa. Informó de un antecedente de tres años de dolor sordo cíclico en el ombligo. El dolor se asoció a un nódulo umbilical que sangraba durante la menstruación. Cabe destacar que el dolor empeoraba durante la menstruación y se aliviaba con analgésicos. La paciente también informó de dismenorrea, menorragia y dispareunia. La paciente se había insertado un DIU de cobre 3 años antes y había estado usando Zinnia P (levonorgestrel y etinilestradiol) durante los últimos 3-4 meses para intentar aliviar el dolor. Su historial ginecológico previo no fue notable y tenía un ciclo menstrual regular. No había antecedentes médicos, quirúrgicos o sociales de importancia.\nAl examinarla, sus constantes vitales eran estables. Se observó una hinchazón hiperpigmentada (3 × 2 cm) en el ombligo al examinar el abdomen. La hinchazón era firme, inmóvil, no dolorosa, no reductible y no estaba ligada a estructuras subyacentes. Una resonancia magnética abdominal reveló una masa de mejora mal definida que medía 3 × 4 × 6 cm ubicada a lo largo de la pared abdominal anterior derecha y estaba conectada a un tracto sinusal que se extendía hacia la región suprapúbica, pero no se comunicaba con la cavidad peritoneal, hallazgos que sugieren endometriosis. El diagnóstico diferencial fue amplio, incluida una hernia umbilical, granuloma, cicatriz queloide, neoplasias malignas nodulares y anomalías embriológicas. Además, se observaron lesiones anexiales bilaterales, eran hiperintensas con áreas hipointensas focales y restricciones variables, la lesión del lado derecho medía 1,6 × 1,7 cm y la lesión del lado izquierdo medía 2,0 × 0,8 cm, hallazgos consistentes con endometriosis ovárica bilateral.\n\nSe programó al paciente para la extirpación quirúrgica del nódulo umbilical. La muestra se envió para un examen histopatológico. Los resultados revelaron una epidermis normal con glándulas endometriales dispersas y estroma dentro de la dermis. La fotomicroscopía resaltó la presencia de estroma endometrial y tejido graso subcutáneo. Esta morfología es consistente con la endometriosis. La recuperación postoperatoria de la paciente fue sin incidentes, y se la consideró apta para el alta el día 2 postoperatorio. Recibió asesoramiento sobre su fertilidad futura y la posibilidad de FIV, riesgo de recurrencia y se programó una visita de seguimiento en dos semanas. Se le inició con Dienogest, Visanne y un anticonceptivo oral combinado para el tratamiento de la endometriosis. Se la ha monitoreado clínicamente cada cuatro semanas, y no se han observado síntomas o signos de recurrencia local durante el período de seguimiento de 8 meses. Cabe destacar que, a pesar de que su condición permaneció estable después del tratamiento, no concibió en el transcurso del año siguiente.\n",
+        "gold_summary": "Presentamos el caso de una mujer nulípara de 35 años de edad del norte de Tanzania con un historial de infertilidad de 10 años. Al presentarse, la paciente informó de un historial de tres años de dolor cíclico asociado a una masa umbilical. Una resonancia magnética abdominal reveló una masa mal definida que se intensificaba y medía 3 × 4 × 6 cm, localizada a lo largo de la pared abdominal anterior derecha. La masa estaba conectada a un tracto sinusal que se extendía hacia la región suprapúbica, pero no mostraba comunicación con la cavidad peritoneal, lo que sugería endometriosis. Además, las lesiones anexiales bilaterales demostraron señales hiperintensas con áreas hipointensas focales y restricciones variables, consistentes con endometriomas ováricos bilaterales. La paciente se sometió a la extirpación de la masa umbilical y el examen histopatológico confirmó el diagnóstico de endometriosis umbilical primaria. A pesar de su condición estable después del tratamiento, no concibió durante el año siguiente.\n",
+        "synthetic_summary": {
+            "B1": "Había una mujer que tenía dolor en su pancita cerca del ombligo. El dolor venía y se iba, y a veces el ombligo sangraba. Los doctores vieron que tenía un bultito en el ombligo. Le sacaron el bultito con una operación. Cuando miraron el bultito, encontraron que era un problema llamado endometriosis. Ella se sintió mejor después de la operación. Pero todavía no pudo tener un bebé.",
+            "B2": "**Caso de una mujer con dolor y un bulto en el ombligo**\n\nUna mujer de 35 años, que nunca ha tenido hijos y ha tenido problemas para quedar embarazada durante 10 años, acudió al médico porque tenía dolor en el ombligo desde hace tres años. Este dolor aparecía de forma cíclica, es decir, se repetía cada mes, y estaba relacionado con un bulto en esa zona.\n\n**Lo que encontraron en las pruebas**\n\nSe le hizo una resonancia magnética, que es un tipo de imagen que muestra el interior del cuerpo. Esta prueba mostró una masa o bulto de 3 × 4 × 6 centímetros en la pared del abdomen, cerca del ombligo. La masa estaba conectada a un pequeño canal que llegaba hacia la parte baja del abdomen, pero no estaba unida a la cavidad donde están los órganos internos. Esto hizo pensar que podría tratarse de endometriosis, que es cuando un tejido parecido al que recubre el interior del útero crece en otros lugares del cuerpo.\n\nAdemás, se encontraron lesiones en ambos ovarios que también parecían ser endometriomas, que son quistes causados por la endometriosis en los ovarios.\n\n**Qué hicieron y qué pasó después**\n\nLa mujer se sometió a una cirugía para quitar el bulto del ombligo. El tejido extraído se analizó bajo el microscopio y confirmó que era endometriosis en el ombligo, algo poco común. Después de la operación, la paciente se recuperó bien y comenzó un tratamiento con medicamentos para controlar la endometriosis.\n\nDurante los siguientes ocho meses, no tuvo nuevos síntomas ni signos de que la enfermedad regresara. Sin embargo, aunque su salud mejoró, no logró quedar embarazada en el año siguiente.\n\nEste caso muestra cómo la endometriosis puede afectar diferentes partes del cuerpo y la importancia de un diagnóstico y tratamiento adecuados para mejorar la calidad de vida y la fertilidad.",
+            "B3": "**Contexto**  \nSe presenta el caso de una mujer de 35 años, sin hijos y con un historial de infertilidad de una década, que acudió a consulta por un dolor cíclico y persistente en el ombligo durante tres años. Este dolor se asociaba a la presencia de un nódulo umbilical que sangraba coincidiendo con su menstruación. Además, refería síntomas ginecológicos como dolor menstrual intenso (dismenorrea), sangrado menstrual abundante (menorragia) y dolor durante las relaciones sexuales (dispareunia). La paciente había utilizado un dispositivo intrauterino (DIU) de cobre desde hacía tres años y recientemente había iniciado tratamiento hormonal combinado para aliviar el dolor.\n\n**Hallazgos Clave**  \nEl examen físico reveló una masa firme, hiperpigmentada, inmóvil y no dolorosa en el ombligo, sin conexión palpable con estructuras internas. La resonancia magnética mostró una masa mal definida de 3 × 4 × 6 cm en la pared abdominal anterior derecha, conectada a un tracto sinusal que se extendía hacia la región suprapúbica, pero sin comunicación con la cavidad peritoneal, lo que orientó hacia un diagnóstico de endometriosis umbilical primaria. Además, se identificaron lesiones en ambos ovarios con características compatibles con endometriomas (quistes ováricos formados por tejido endometrial), confirmando la afectación bilateral.\n\n**Interpretación Clínica**  \nEl diagnóstico diferencial incluyó diversas condiciones como hernia umbilical, granuloma, cicatriz queloide, tumores malignos y anomalías congénitas, pero la combinación de síntomas, hallazgos de imagen y la confirmación histopatológica establecieron la endometriosis umbilical primaria. La biopsia del nódulo extirpado mostró tejido endometrial (glándulas y estroma) dentro de la dermis, confirmando la presencia de endometriosis fuera del útero. Este tipo de endometriosis es poco frecuente y puede causar dolor cíclico y sangrado en la piel del ombligo.\n\n**Próximos Pasos y Seguimiento**  \nTras la cirugía, la paciente tuvo una recuperación sin complicaciones y fue dada de alta al segundo día postoperatorio. Se le indicó tratamiento hormonal con dienogest y anticonceptivos orales combinados para controlar la endometriosis y reducir el riesgo de recurrencia. Se le brindó asesoramiento sobre su fertilidad futura, incluyendo la posibilidad de recurrir a técnicas de reproducción asistida como la fertilización in vitro (FIV). Durante un seguimiento clínico de ocho meses no se observaron signos de recurrencia local, aunque la paciente no logró concebir en el año posterior al tratamiento.\n\nEste caso destaca la importancia de considerar la endometriosis umbilical en mujeres con dolor cíclico y nódulos en el ombligo, especialmente en el contexto de infertilidad, y subraya la necesidad de un manejo multidisciplinario para optimizar el control de los síntomas y la fertilidad."
+        }
+    },
+    {
+        "article": "Presentamos a un recién nacido de 15 minutos de edad, hijo de una madre para-cuatro que no recordaba su LNMP pero que afirmaba haber estado amenorreica durante los últimos nueve meses. Su madre había recibido atención prenatal en el centro de salud cercano dos veces y no había tenido incidentes. Sin embargo, no se le había realizado un ultrasonido obstétrico temprano. Por lo demás, no tiene antecedentes de enfermedades crónicas como diabetes mellitus e hipertensión. Durante su embarazo actual, no tuvo fiebre, dolor de cabeza o visión borrosa. Nunca había usado ninguna droga aparte de sulfato ferroso durante este embarazo. Sus hijos anteriores están todos sanos y vivos. A su llegada a nuestro hospital, tuvo una hemorragia vaginal de dos horas de duración. Posteriormente, fue admitida con un diagnóstico de embarazo de tercer trimestre más multigravida más hemorragia anteparto secundaria a desprendimiento de placenta más oligohidramnios severo más presentación de nalgas.\n\nEn el examen pélvico, tenía un sangrado vaginal activo. Se le realizó una ecografía obstétrica al llegar. En consecuencia, la edad gestacional era de 34 semanas, la placenta estaba en el fondo con un coágulo retroplacentario y el líquido amniótico había disminuido significativamente con un único bolsillo más profundo de 1,5 cm. El peso fetal estimado era de 2,4 kg y presentación de nalgas. Otras investigaciones de la madre son grupo sanguíneo AB+, VDRL=negativo, RBS=120 mg/dL, en CBC, glóbulos blancos=9000, hemoglobina=11 gm/dL, plaqueta=180,000 y neutrófilo=60%.\n\nTras obtener el consentimiento informado por escrito, se realizó una cesárea de urgencia por las indicaciones ya mencionadas para extraer un neonato vivo de 2,01 kg de peso con puntuaciones de 5 y 6 en las pruebas de Apgar en el primer y el quinto minuto, respectivamente.\n\nEl neonato no lloró y fue reanimado durante cinco minutos. Luego fue trasladado a la unidad de cuidados intensivos neonatales para recibir atención e investigaciones adicionales. Al llegar, el neonato estaba en dificultad respiratoria. Sus signos vitales eran de 160 latidos por minuto, 70 respiraciones por minuto, temperatura de 33,4 grados centígrados y saturación de oxígeno del 60%. La fontanela anterior del neonato medía 2 cm por 2 cm y tenía micrognatia y cuello corto. En el sistema respiratorio, había retracciones intercostales y subcostales, respiración trabajosa y gruñidos. En el examen precordial, se escucharon bien los sonidos s1 y s2, no había murmullo ni ritmo de galope. En el sistema musculoesquelético, había acortamiento bilateral de las extremidades superiores, la extremidad inferior derecha estaba normal en posición y estructura, la pierna izquierda giraba hacia adentro (flexión mediolateral) en la articulación de la rodilla y la estructura del pie era normal. En el examen neurológico, estaba letárgico, el tono era normotónico en la extremidad inferior derecha y el reflejo de Moro era difícil de evaluar. La investigación de laboratorio mostró grupo sanguíneo = A+, CRP = reactivo, WBC = 30,000, neutrófilos = 54%, linfocitos = 21.1%, HGB = 8 gm/dL y plaquetas = 150,000. Se realizó una radiografía que mostró un acortamiento extremo de las extremidades superiores. La extremidad inferior izquierda estaba internamente girada. La ecocardiografía fue normal. Con una evaluación de prematuro tardío (34-36 semanas por puntaje de Ballard) más bajo peso al nacer más apropiado para la edad gestacional más focomelia más asfixia perinatal más sepsis neonatal temprana, se manejó con apoyo de oxígeno, fluido de mantenimiento e antibióticos intravenosos. El neonato murió después de tres días de hospitalización.\n",
+        "gold_summary": "Presentamos a un neonato de 15 minutos de vida, hijo de una madre para-cuatro que no recordaba su LNMP pero que afirmaba estar amenorreica desde hacía nueve meses. El modo de parto fue por cesárea para extraer al neonato vivo, que pesaba 2,01 kg y tenía puntuaciones APGAR de 5 y 6 en el primer y quinto minutos, respectivamente. El neonato no lloró y fue reanimado durante cinco minutos. Después se lo trasladó a la unidad de cuidados intensivos neonatales para continuar con el tratamiento y las investigaciones. Sus signos vitales eran: pulso de 160 latidos por minuto, frecuencia respiratoria de 70 respiraciones por minuto, temperatura de 33,4 grados centígrados y saturación de oxígeno del 60%. La fontanela anterior del neonato medía 2 cm por 2 cm y tenía micrognatia y cuello corto. En el sistema respiratorio había retracciones intercostales y subcostales, respiración trabajosa y gruñidos. En el sistema musculoesquelético había acortamiento bilateral de la extremidad superior, la pierna derecha tenía una posición y estructura normales, la pierna izquierda giraba hacia adentro (se doblaba hacia la parte media) en la articulación de la rodilla y el pie tenía una estructura normal.\n",
+        "synthetic_summary": {
+            "B1": "Un bebé nació hace muy poquito tiempo. Su mamá tuvo que ir al hospital para que lo sacaran con una operación especial. El bebé pesaba poquito y no pudo llorar al nacer. Los doctores lo ayudaron a respirar y lo llevaron a un lugar para cuidarlo mucho.\n\nEl bebé respiraba rápido y su corazón latía rápido también. Tenía frío y le faltaba un poco de aire. Su cabeza tenía una parte blanda y su cuello era cortito. Sus brazos eran más cortos de lo normal. Una pierna estaba normal, pero la otra estaba doblada hacia adentro. Sus pies estaban bien. Los doctores lo cuidaron mucho para que se sintiera mejor.",
+            "B2": "**Lo que pasó con el bebé al nacer**  \nUn bebé nació por cesárea después de que su mamá tuvo problemas en el embarazo. El bebé pesó 2,01 kg y sus primeras pruebas para saber cómo estaba (llamadas puntuaciones Apgar) fueron 5 y 6, lo que indica que necesitó ayuda para respirar. De hecho, el bebé no lloró al nacer y tuvo que ser reanimado durante cinco minutos para ayudarlo a respirar mejor.\n\n**Estado del bebé en la unidad de cuidados intensivos**  \nDespués de nacer, el bebé fue llevado a una unidad especial para recién nacidos que necesitan cuidados extra. Allí, los médicos notaron que su corazón latía rápido (160 latidos por minuto) y respiraba muy rápido (70 respiraciones por minuto). Además, tenía la temperatura baja (33,4 grados Celsius) y poca cantidad de oxígeno en la sangre (60%). La parte blanda en la cabeza del bebé (llamada fontanela anterior) medía 2 cm por 2 cm. También tenía micrognatia, que significa que la mandíbula era más pequeña de lo normal, y un cuello corto.\n\n**Problemas en la respiración y los huesos**  \nEl bebé tenía dificultad para respirar, con movimientos fuertes entre las costillas y sonidos de gruñidos al respirar. En cuanto a sus brazos, ambos eran más cortos de lo normal. La pierna derecha estaba normal, pero la pierna izquierda estaba doblada hacia adentro en la rodilla, aunque el pie tenía una forma normal.\n\n**Qué significa todo esto**  \nEstos signos muestran que el bebé tenía problemas para respirar y algunas malformaciones en sus extremidades. Estas condiciones pueden ser causadas por complicaciones durante el embarazo o problemas en el desarrollo del bebé. Los médicos le dieron oxígeno y otros tratamientos para ayudarlo, pero lamentablemente el bebé murió después de tres días en el hospital.",
+            "B3": "**Contexto**  \nSe presentó un recién nacido de apenas 15 minutos de vida, hijo de una mujer con antecedentes obstétricos de cuatro partos previos (para-cuatro). La madre no recordaba la fecha de su última menstruación, pero aseguró haber estado sin menstruar durante nueve meses, lo que indicaba un embarazo avanzado. Durante el embarazo, la madre recibió atención prenatal limitada y no se realizó una ecografía temprana. Al momento del ingreso hospitalario, la madre presentaba hemorragia vaginal prolongada, diagnóstico de desprendimiento prematuro de placenta, oligohidramnios severo (disminución del líquido amniótico) y presentación fetal de nalgas.\n\n**Hallazgos Clave del Neonato**  \nEl bebé nació mediante cesárea de urgencia con un peso de 2,01 kg y puntuaciones de Apgar de 5 y 6 al primer y quinto minuto, respectivamente, lo que indica una adaptación inicial comprometida. No lloró al nacer y requirió reanimación durante cinco minutos. Fue trasladado a la unidad de cuidados intensivos neonatales debido a dificultad respiratoria grave, con signos vitales alterados: frecuencia cardíaca elevada (160 latidos por minuto), respiración rápida (70 respiraciones por minuto), temperatura corporal baja (33,4 °C) y saturación de oxígeno muy baja (60%).\n\nEn el examen físico, se observaron características faciales anómalas como micrognatia (mandíbula inferior pequeña) y cuello corto. En el sistema respiratorio, el neonato presentaba retracciones intercostales y subcostales (movimientos visibles de los músculos entre las costillas y debajo de ellas al respirar), respiración dificultosa y sonidos respiratorios anormales (gruñidos). En el sistema musculoesquelético, había un acortamiento marcado de ambas extremidades superiores (brazo y antebrazo), mientras que la pierna derecha tenía una estructura y posición normales. La pierna izquierda estaba girada hacia adentro en la articulación de la rodilla (flexión mediolateral), aunque el pie mantenía una estructura normal.\n\nLos estudios complementarios revelaron una elevación significativa de los glóbulos blancos (30,000), indicando posible infección, con una proteína C reactiva positiva (marcador de inflamación), anemia moderada (hemoglobina de 8 g/dL) y plaquetas dentro de rango normal. La radiografía confirmó el acortamiento extremo de las extremidades superiores y la rotación interna de la pierna izquierda. La ecocardiografía fue normal, descartando malformaciones cardíacas.\n\n**Interpretación Clínica**  \nEl diagnóstico principal incluyó un neonato prematuro tardío (34 semanas de gestación), con bajo peso al nacer pero adecuado para su edad gestacional, que presentaba focomelia (una malformación congénita caracterizada por extremidades muy cortas o ausentes), asfixia perinatal (falta de oxígeno al nacer) y sepsis neonatal temprana (infección grave en los primeros días de vida). Estas condiciones explican la dificultad respiratoria, el compromiso hemodinámico y las anomalías físicas observadas.\n\n**Próximos Pasos y Evolución**  \nEl manejo incluyó soporte respiratorio con oxígeno, administración de líquidos por vía intravenosa y tratamiento antibiótico para la infección. A pesar de estas intervenciones, el neonato falleció a los tres días de hospitalización debido a la gravedad de sus condiciones clínicas y malformaciones congénitas asociadas. Este caso resalta la importancia de un control prenatal adecuado, diagnóstico temprano y manejo multidisciplinario para mejorar el pronóstico en embarazos complicados y neonatos con malformaciones severas."
+        }
+    },
+    {
+        "article": "Mujer de 61 años con antecedente de carcinoma escamocelular de cuello uterino estadio FIGO IIB, diagnosticado en febrero de 2019, tratada en un hospital privado de cuarto nivel de atención, donde se ofrece cuidado ambulatorio y hospitalario para pacientes con condiciones complejas oncológicas y no oncológicas. Al momento del diagnóstico se realizó histerectomía radical con linfadenectomía pélvica, que descartó compromiso nodal. El tratamiento complementario de primera línea incluyó seis ciclos de quimioterapia con cisplatino, y braquiterapia y radioterapia, alcanzando una respuesta tumoral completa. En 2021, tras detectarse una recaída aislada en la región ilíaca, mediante tomografía, se administró cisplatino y 30 sesiones de radioterapia, logrando una nueva respuesta completa. En septiembre de 2022, una tomografía reveló otra recaída con compromiso del parametrio izquierdo, el uréter y la cadena ilíaca ipsilateral, por lo que se decidió primera línea para enfermedad recurrente con carboplatino, paclitaxel y pembrolizumab. Durante este régimen, la paciente presentó hipersensibilidad al platino en el quinto ciclo, gestionada con un protocolo de desensibilización, continuando con el pembrolizumab. En septiembre de 2023, ante la progresión en imágenes de una masa retroperitoneal única, debido a la falta de respuesta óptima, se inició gemcitabina, según guías de manejo, segunda línea de enfermedad recurrente, recibiendo una dosis acumulada de 8.544 mg/m2 hasta enero de 2024. Sin embargo, desarrolló síntomas de isquemia digital en manos, por lo que el tratamiento fue suspendido tras la segunda dosis del tercer ciclo, acumulando 11.744 mg/m2 de gemcitabina.\n\nEn febrero de 2024, la paciente ingresó al servicio de urgencias del mismo hospital donde era valorada de forma ambulatoria, remitida por oncología debido a progresión de los síntomas en sus extremidades. La paciente refería dolor lancinante y coloración azulada en dedos de manos; al examen físico se evidencia necrosis en el segundo dedo de la mano derecha, coloración ocre y fenómeno de Raynaud en los dedos de la mano izquierda. Las extremidades inferiores mostraban edema grado II en el miembro inferior izquierdo y pulsos presentes. Los estudios para autoinmunidad y vasculitis resultaron negativos, incluyendo anticuerpos anticitoplasma de neutrófilos (ANCAS), anticuerpos antinucleares (ANAS), anticuerpos antidesoxirribonucleicos (anti-DNA), cardiolipinas, prueba confirmatoria de anticoagulante lúpico, perfil de anticuerpos contra antígenos nucleares extraíbles (ENAS), anticuerpos contra proteinasa 3, anticuerpos antimieloperoxidasa y anticuerpos dirigidos contra la ADN topoisomerasa I (antiSCL). Además, el factor reumatoide y los niveles de complemento 3 (C3) y complemento 4 (C4) también fueron normales. Prueba serológica para sífilis (VDRL - Venereal Disease Research Laboratory) negativa, ecocardiograma transtorácico sin hallazgos de un foco cardioembólico.\n\nSe inició anticoagulación con heparina de bajo peso molecular, junto con ácido acetilsalicílico, estatina y un calcioantagonista. El equipo de cirugía de mano realizó amputación del segundo dedo de la mano derecha, confirmando necrosis por licuefacción en el estudio histopatológico.\n\nDurante el posoperatorio se agregó sildenafil al tratamiento, logrando una mejoría progresiva en los signos de isquemia de los dedos restantes. Durante la hospitalización, la paciente presenta complicación por sangrado vaginal masivo, requiriendo embolización de arterias uterinas.\n\nEl servicio de reumatología aplicó la escala de causalidad de Naranjo para determinar el papel de la gemcitabina en la vasculitis, con un puntaje de 8, lo que indicó que el medicamento probablemente provocó la necrosis.\n\nPosteriormente, a los 20 días de ingreso a hospitalización desarrolló deterioro neurológico, sin hallazgos significativos en la tomografía de cráneo. Evaluada por cuidados paliativos, su estado funcional se clasificó con un Barthel de 0/30, ECOG de 4 y Karnofsky de 10 %, con pronóstico de vida inferior a tres semanas según el Índice Pronóstico de Paciente (PPI: + 6 puntos). En consenso con la familia, se suspendieron estudios adicionales y se implementó un manejo paliativo integral. La paciente falleció tras el alta hospitalaria.",
+        "gold_summary": "Oaciente de 61 años tratada con gemcitabina (11.744 mg/m² acumulados) por enfermedad metastásica, en un hospital general de cuarto nivel, privado, no oncológico, donde venía siendo manejada de forma ambulatoria. Presentó necrosis distal del segundo dedo de la mano derecha, por lo que se suspendió el tratamiento y se requirió amputación de este dedo. Se realizó una búsqueda en Embase, Medline y Lilacs. Se buscaron estudios de reporte y series de casos sobre necrosis distal inducida por gemcitabina. Se extrajeron datos de dosis, diagnóstico y tratamiento.",
+        "synthetic_summary": {
+            "B1": "Una señora de 61 años estaba muy enferma y recibió medicina para el cáncer. Esta medicina le hizo daño en un dedo de su mano derecha. El dedo se puso muy mal y tuvieron que cortarlo para que no le doliera más. Los doctores buscaron información para entender mejor este problema y cómo ayudar.",
+            "B2": "**Caso de una Mujer con Cáncer y Problemas en las Manos**\n\nUna mujer de 61 años estaba recibiendo un medicamento llamado gemcitabina para tratar su cáncer que se había extendido. Este medicamento se usó en un hospital privado que atiende casos complejos. Después de recibir una dosis acumulada bastante alta (11.744 mg/m²), comenzó a tener problemas graves en su mano derecha. El segundo dedo se puso negro y murió (necrosis), lo que hizo necesario suspender el medicamento y amputar ese dedo.\n\n**Búsqueda de Información sobre el Problema**\n\nLos médicos buscaron en varias bases de datos científicas (Embase, Medline y Lilacs) para encontrar otros casos similares donde la gemcitabina causara necrosis en los dedos. Revisaron estudios y reportes para entender mejor las dosis usadas, cómo se diagnosticó el problema y qué tratamientos se aplicaron.\n\n**Qué Significa Esto**\n\nEste caso muestra que, aunque la gemcitabina es útil para tratar ciertos tipos de cáncer, puede causar efectos secundarios graves en las manos, como la muerte de tejido en los dedos. Por eso, los médicos deben vigilar muy bien a los pacientes que reciben este medicamento para detectar cualquier señal temprana de daño y actuar rápido para evitar complicaciones mayores.",
+            "B3": "Resumen detallado para público no médico universitario\n\nContexto  \nSe trata de una mujer de 61 años con un historial complejo de cáncer de cuello uterino (carcinoma escamocelular), inicialmente diagnosticado en 2019 y tratado con cirugía, quimioterapia y radioterapia, logrando respuestas completas. Sin embargo, presentó varias recaídas localizadas y regionales entre 2021 y 2023, que requirieron diferentes líneas de tratamiento con quimioterapia y terapia inmunológica. En 2023, ante la progresión tumoral, se inició gemcitabina como segunda línea de tratamiento para la enfermedad recurrente.\n\nHallazgos clave  \nDurante el tratamiento con gemcitabina, acumuló una dosis total de 11.744 mg/m², pero desarrolló síntomas de isquemia digital, es decir, falta de flujo sanguíneo en los dedos de las manos, que se manifestó con dolor intenso, coloración azulada y necrosis (muerte del tejido) en el segundo dedo de la mano derecha. Esto llevó a la suspensión inmediata del medicamento y a la amputación quirúrgica de dicho dedo, confirmándose la necrosis mediante análisis histopatológico (examen microscópico del tejido).\n\nSe descartaron otras causas comunes de daño vascular o inflamación de los vasos sanguíneos (vasculitis) mediante pruebas serológicas y de autoinmunidad, todas negativas. Tampoco se encontraron problemas cardíacos que pudieran explicar la formación de coágulos o embolias. El equipo médico inició tratamiento con anticoagulantes, antiinflamatorios, vasodilatadores y medicamentos para mejorar la circulación, logrando cierta mejoría en los dedos restantes.\n\nInterpretación clínica  \nEl análisis de causalidad mediante la escala de Naranjo, una herramienta que ayuda a determinar si un medicamento es responsable de un efecto adverso, indicó que la gemcitabina fue probablemente la causa de la necrosis digital. Este efecto adverso es poco frecuente pero grave, y se relaciona con daño vascular inducido por el fármaco.\n\nPróximos pasos y evolución  \nPosteriormente, la paciente presentó complicaciones adicionales, incluyendo un sangrado vaginal masivo que requirió embolización (procedimiento para detener el sangrado) y un deterioro neurológico sin causa clara en estudios de imagen. Su estado general empeoró significativamente, con pérdida total de autonomía y un pronóstico de vida inferior a tres semanas. En consenso con la familia, se decidió suspender estudios invasivos y se implementó un manejo paliativo integral para mejorar su calidad de vida en el tiempo restante. Finalmente, la paciente falleció tras el alta hospitalaria.\n\nResumen de la revisión bibliográfica  \nSe realizó una búsqueda en bases de datos médicas (Embase, Medline y Lilacs) para identificar reportes y series de casos sobre necrosis distal inducida por gemcitabina, recopilando información sobre dosis, diagnóstico y manejo de esta complicación, con el fin de contextualizar y comparar el caso presentado.\n\nEste caso resalta la importancia de la vigilancia estrecha de efectos adversos vasculares graves en pacientes tratados con gemcitabina, especialmente en contextos de enfermedad avanzada y tratamientos prolongados."
+        }
+    },
+    {
+        "article": "Mujer de 53 años, con antecedente de AR de 15 años de diagnóstico en tratamiento con metotrexato, resto de antecedentes sin datos de importancia, la cual presentó cuadro clínico 8 meses antes (de acudir a nuestro servicio) con astenia y adinamia de forma progresiva, palidez de tegumentos, alzas térmicas no cuantificadas de predominio nocturno, pérdida de peso no intencionada de 15 kg en 6 meses aproximadamente, sin valoración ni seguimiento médico, a lo que se agregó 3 meses después disnea de grandes a medianos esfuerzos, y cuya sintomatología se agudizó 5 días antes (de acudir a nuestro servicio), aunada a sangrado de tubo digestivo alto (STDA), caracterizado por evacuaciones melénicas abundantes, 3 evacuaciones en 24 horas, hematemesis en 2 ocasiones, escasas, sin causa aparente. La paciente negó consumo de analgésicos no esteroideos (AINE) y tuvo aumento de volumen en la pierna izquierda, la cual le dolía y tenía la presencia de edema y eritema, con limitación a la movilidad, motivo por el cual acudió a (nuestro) Servicio de Urgencias.\n\nDurante su hospitalización con anemia severa sin repercusión hemodinámica, se transfundieron 3 concentrados eritrocitarios sin complicaciones aparentes. Después de su estabilización, se inició abordaje diagnóstico para síndrome consuntivo. Por el cuadro clínico de miembro inferior izquierdo se hizo US Doppler que evidenció trombosis venosa profunda. Se realizó ultrasonido de abdomen por probable hepatopatía por metotrexato, el cual reportó infartos esplénicos y hepáticos, así como presencia de cambios crónicos hepáticos. Se llevó a cabo endoscopía con evidencia de varices pequeñas, sin sangrado activo. Debido a la sospecha de neoplasia por los antecedentes y el cuadro clínico de la paciente, se llevó a cabo tomografía axial simple y contrastada de tórax y abdomen y se encontró hepatoesplenomegalia y múltiples conglomerados ganglionares axilares, mediastinales y paraaórticos que sugerían actividad infiltrativa. Esto se valoró por el Servicio de Cirugía General para la realización de biopsia de ganglio axilar derecho, donde se reportó proliferación neoplásica de células linfoides. Posteriormente se valoró por el Servicio de Hematología de la unidad, se solicitaron estudios de laboratorio (cuadro I) y se realizó aspirado de médula ósea en el que se evidenciaron células plasmáticas displásicas y células reticulares, por lo cual se concluyó que había la presencia de infiltración linfoplasmocitaria. Con los antecedentes, el cuadro clínico y los estudios complementarios se diagnosticó LNH estadio IV y la paciente fue enviada a hospital de tercer nivel para realización de inmunohistoquímica, estadificación e inicio de tratamiento. En tercer nivel se identificó linfoma difuso de células B con inmunofenotipo B CD20 con sobrecrecimiento de células dendríticas, y la paciente fue valorada para inicio de tratamiento con quimioterapia.",
+        "gold_summary": "Mujer de 55 años con antecedente de AR que ingresó a un servicio de medicina interna por sangrado de tubo digestivo; presentó datos clínicos de trombosis venosa profunda en miembro pélvico izquierdo y síndrome consuntivo en estudio. Durante su abordaje se identificó con infartos esplénicos y hepáticos, así como múltiples conglomerados ganglionares, por lo que se practicó biopsia de ganglio axilar que reportó proliferación neoplásica de células linfoides y aspirado de médula ósea con presencia de infiltración linfoplasmocitaria, con lo que se determinó diagnóstico de linfoma no Hodgkin estadio IV. La paciente fue enviada a un hospital de tercer nivel para inicio de tratamiento.",
+        "synthetic_summary": {
+            "B1": "Había una señora que se sentía muy cansada y tenía dolor en una pierna. También tenía sangre en su pancita. Los doctores le hicieron muchas pruebas. Encontraron que tenía unos bultitos en su cuerpo que no estaban bien. Le hicieron una prueba en un lugar con bultitos y otra en su hueso. Vieron que tenía un tipo de enfermedad llamada linfoma. La señora fue a un hospital especial para que la cuiden y le den medicina para mejorar.",
+            "B2": "**Lo que le pasó a la paciente**  \nUna mujer de 53 años, que tenía artritis reumatoide (una enfermedad que afecta las articulaciones), llegó al hospital porque estaba sangrando por el tubo digestivo (el camino que va desde la boca hasta el estómago y los intestinos). Además, tenía dolor y hinchazón en la pierna izquierda, y estaba muy cansada y pálida. También había perdido mucho peso sin querer.\n\n**Lo que encontraron en los exámenes**  \nLos médicos descubrieron que tenía una trombosis venosa profunda, que es un coágulo de sangre en una vena grande de la pierna. También encontraron daños en el bazo y el hígado, llamados infartos, que son áreas donde no llegó suficiente sangre. Al hacer una tomografía (una imagen especial del cuerpo), vieron que sus ganglios linfáticos (pequeñas glándulas que ayudan a combatir infecciones) estaban muy grandes y agrupados en varias partes del cuerpo.\n\nPara entender mejor qué pasaba, le hicieron una biopsia, que es cuando se toma un pequeño pedazo de tejido para analizarlo. La biopsia del ganglio linfático mostró que había un crecimiento anormal de células llamadas linfocitos, que son parte del sistema inmunológico. También examinaron su médula ósea (donde se producen las células de la sangre) y encontraron células anormales que indicaban que el problema estaba afectando varias partes del cuerpo.\n\n**Qué significa el diagnóstico**  \nCon toda esta información, los médicos diagnosticaron un linfoma no Hodgkin en estadio IV. El linfoma no Hodgkin es un tipo de cáncer que afecta a los linfocitos. El estadio IV significa que el cáncer está avanzado y se ha extendido a varias áreas del cuerpo.\n\n**Próximos pasos**  \nLa paciente fue enviada a un hospital especializado para hacer más estudios y comenzar un tratamiento con quimioterapia, que es un tipo de medicina para combatir el cáncer.",
+            "B3": "**Contexto**  \nSe trata de una mujer de 53 años con diagnóstico previo de artritis reumatoide (AR) desde hace 15 años, en tratamiento con metotrexato. Ocho meses antes de su ingreso al hospital, comenzó a presentar síntomas progresivos como fatiga intensa (astenia), debilidad generalizada (adinamia), palidez en la piel, fiebre nocturna no cuantificada y una pérdida de peso no intencionada de aproximadamente 15 kg en seis meses. Tres meses después, desarrolló dificultad para respirar al realizar esfuerzos moderados. Cinco días antes de su ingreso, su condición empeoró con sangrado digestivo alto, manifestado por evacuaciones negras abundantes (melena) y vómitos con sangre (hematemesis), sin causa aparente. Además, presentó aumento de volumen, dolor, enrojecimiento y limitación de movimiento en la pierna izquierda, signos compatibles con trombosis venosa profunda (coágulo en una vena profunda).\n\n**Hallazgos Clave**  \nDurante la hospitalización, se confirmó anemia severa que requirió transfusión de glóbulos rojos. Un ultrasonido Doppler de la pierna izquierda confirmó la presencia de trombosis venosa profunda. El ultrasonido abdominal mostró infartos (áreas de tejido muerto por falta de riego sanguíneo) en el bazo y el hígado, junto con cambios hepáticos crónicos probablemente relacionados con el uso de metotrexato. La endoscopía digestiva evidenció varices pequeñas sin sangrado activo. La tomografía computarizada (TAC) de tórax y abdomen reveló agrandamiento del hígado y bazo (hepatoesplenomegalia) y múltiples conglomerados de ganglios linfáticos en axilas, mediastino y alrededor de la aorta, lo que sugirió una posible infiltración tumoral.  \n\nLa biopsia de un ganglio axilar derecho mostró proliferación anormal de células linfoides (células del sistema inmunitario). El aspirado de médula ósea evidenció infiltración por células plasmáticas anormales y células reticulares, confirmando la afectación linfoplasmocitaria. Estos hallazgos permitieron establecer el diagnóstico de linfoma no Hodgkin (LNH) en estadio IV, que indica una enfermedad avanzada con compromiso de múltiples órganos y tejidos.\n\n**Interpretación Clínica**  \nEl cuadro clínico y los estudios realizados indican que la paciente presenta un linfoma no Hodgkin difuso de células B, un tipo de cáncer que afecta a las células del sistema inmunitario. La enfermedad se encuentra en una etapa avanzada y ha provocado complicaciones como trombosis venosa profunda, infartos en órganos abdominales y sangrado digestivo. La asociación con su antecedente de artritis reumatoide y el tratamiento con metotrexato puede haber influido en la evolución y presentación clínica.\n\n**Próximos Pasos**  \nLa paciente fue referida a un hospital de tercer nivel para realizar estudios adicionales de inmunohistoquímica (técnicas que permiten caracterizar con precisión el tipo de células tumorales), completar la estadificación de la enfermedad y comenzar el tratamiento específico con quimioterapia. El manejo multidisciplinario es fundamental para optimizar el pronóstico y controlar tanto la enfermedad linfoproliferativa como las complicaciones asociadas."
+        }
+    },
+    {
+        "article": "Un hombre de 56 años se presentó en el departamento de urgencias de nuestro hospital debido a una falta de aire repentina y un episodio de síncope mientras caminaba dentro de su casa. Se sometió a una prostatectomía laparoscópica asistida por robot para el carcinoma de próstata, 5 días antes de su presentación en el departamento de urgencias. Su curso postoperatorio en el hospital fue sin incidentes. En el departamento de urgencias, su presión arterial era de 94/54 mmHg, frecuencia cardiaca de 121 latidos por minuto, frecuencia respiratoria de 20 respiraciones por minuto, no tenía fiebre y su saturación de oxígeno era de 92% con 6 L por minuto de oxígeno a través de una cánula nasal. El examen cardiaco reveló S1S2, regular, taquicardia, sin murmullos/galopes/ruidos respiratorios. El examen respiratorio reveló ruidos respiratorios vesiculares normales bilaterales. Se observó que tenía edema de extremidad inferior izquierdo asimétrico. El electrocardiograma (ECG) reveló taquicardia sinusal, sin cambios en la onda ST-T. La troponina estaba levemente elevada a 0.120 ng/mL (rango de referencia: 0 a 0.020). La angiografía por tomografía computarizada (CTA) del tórax mostró embolia pulmonar bilateral extensa, con una gran carga de coágulos en ambas arterias pulmonares principales, evidencia de insuficiencia ventricular derecha aguda. El examen dúplex venoso mostró trombosis venosa profunda izquierda aguda. El ecocardiograma mostró fracción de eyección ventricular izquierda normal del 60% al 65%, movimiento septal anormal y aplanamiento del tabique interventricular, presión sistólica ventricular derecha de 49.7 mmHg, ventrículo derecho moderadamente dilatado, función ventricular derecha disminuida, excursión sistólica tricuspídea de 12.1 mm (normal 15 a 20 mm). Como la mayoría de la carga de coágulos era distal, no se consideró susceptible de extracción quirúrgica, ya que la cirugía reciente era una contraindicación importante para la trombólisis. El paciente comenzó con un goteo de heparina e inhaló óxido nítrico a 20 ppm junto con 40 mg de sildenafil oral cada 8 horas. Al día siguiente, el paciente estaba hemodinámicamente estable y su óxido nítrico inhalado se redujo. Repetir el ecocardiograma 48 horas desde la presentación inicial mostró un tamaño y función del ventrículo derecho mejorados. Su presión sistólica ventricular derecha disminuyó a 22.4 mmHg y su excursión sistólica tricuspídea mejoró a 17.8 mm. Recomendamos que continuara con sildenafil durante el mes siguiente después del alta junto con anticoagulación oral con un plan de seguimiento como paciente ambulatorio. El paciente dio su consentimiento por escrito para el tratamiento durante su hospitalización. El paciente y sus familiares estaban bien informados sobre el plan de atención completo y estuvieron de acuerdo con el plan de atención.\n\nMH - Insuficiencia cardiaca/*terapia farmacológica/etiología\nMH - Humanos\nMH - Hombre\nMH - Edad Media\nMH - Inhibidores de la fosfodiesterasa 5/*uso terapéutico\nMH - Embolismo pulmonar/*complicaciones\nMH - Agentes vasodilatadores/*uso terapéutico\nMH - Disfunción ventricular, derecha/terapia/etiología\n",
+        "gold_summary": "Paciente: Hombre, 56 años\n\nDiagnóstico final: Insuficiencia cardíaca derecha por embolia pulmonar\n\nSíntomas: síncope\n\nMedicación: —\n\nProcedimiento clínico: —\n\nEspecialidad: Cardiología\n\nSe trata de un informe de caso en el que se utilizó sildenafil como agente de rescate para lograr una mejora en el tamaño y la función del ventrículo derecho en un caso de inicio agudo de embolia pulmonar masiva con insuficiencia aguda del ventrículo derecho en el escenario en el que la terapia trombolítica sistémica estaba contraindicada.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre de 56 años se sintió muy cansado y se desmayó. Tenía problemas para respirar. Esto pasó porque tenía unos tapones en sus pulmones. Estos tapones hicieron que su corazón derecho se pusiera muy cansado. Los doctores no le pudieron dar una medicina fuerte para quitar los tapones porque él había tenido una operación hace poco. Entonces, le dieron otra medicina llamada sildenafil. Esta medicina ayudó a que su corazón mejorara y se hiciera más fuerte. Después de un tiempo, el hombre se sintió mejor y su corazón trabajó mejor. Los doctores cuidaron mucho de él y le explicaron todo a él y a su familia.",
+            "B2": "**Lo que le pasó al paciente**  \nUn hombre de 56 años tuvo problemas para respirar de repente y se desmayó mientras caminaba en su casa. Cinco días antes, había tenido una cirugía para tratar un cáncer de próstata. Después de la cirugía, parecía estar bien, pero luego presentó estos síntomas.\n\n**Qué encontraron los médicos**  \nEn el hospital, su presión arterial estaba baja y su corazón latía muy rápido. Tenía hinchazón en una pierna, lo que puede indicar un coágulo de sangre. Un examen especial llamado tomografía mostró que tenía coágulos grandes en las arterias de los pulmones, lo que se llama embolia pulmonar. Estos coágulos estaban afectando el lado derecho del corazón, que se encargaba de enviar sangre a los pulmones. También confirmaron que había un coágulo en la pierna.\n\n**Cómo lo trataron**  \nNo pudieron hacer una cirugía para quitar los coágulos porque la cirugía reciente del paciente era un riesgo. En lugar de eso, le dieron un medicamento llamado heparina para evitar que se formen más coágulos. Además, usaron óxido nítrico inhalado y un medicamento llamado sildenafil, que ayuda a relajar los vasos sanguíneos y mejora la función del corazón derecho.\n\n**Qué pasó después**  \nDespués de un día, el paciente estaba más estable. Dos días después, los exámenes mostraron que el corazón derecho había mejorado en tamaño y función. La presión en el corazón derecho bajó y su capacidad para bombear sangre mejoró. Los médicos recomendaron que siguiera tomando sildenafil y medicamentos para evitar coágulos durante un mes después de salir del hospital.\n\n**Por qué es importante este caso**  \nEste caso muestra que el sildenafil puede ayudar a mejorar la función del corazón derecho en personas con embolia pulmonar grave cuando no se puede usar la cirugía o medicamentos para disolver coágulos. Es una opción útil para tratar problemas del corazón causados por coágulos en los pulmones.",
+            "B3": "**Contexto**\n\nUn hombre de 56 años fue atendido en urgencias tras presentar una dificultad respiratoria súbita y un episodio de desmayo mientras caminaba en su casa. Cinco días antes, había sido sometido a una prostatectomía laparoscópica asistida por robot para tratar un cáncer de próstata, y su recuperación inicial había sido sin complicaciones. Al llegar al hospital, mostraba signos de inestabilidad hemodinámica, con presión arterial baja y frecuencia cardíaca elevada. Además, se detectó hinchazón en su pierna izquierda.\n\n**Hallazgos Clave**\n\n- El electrocardiograma mostró taquicardia sinusal sin alteraciones isquémicas.\n- La troponina, un marcador de daño cardíaco, estaba ligeramente elevada.\n- La tomografía computarizada del tórax reveló una embolia pulmonar bilateral extensa, es decir, coágulos grandes en ambas arterias pulmonares principales, causando insuficiencia aguda del ventrículo derecho (la cámara del corazón que bombea sangre hacia los pulmones).\n- Un estudio de ultrasonido vascular confirmó la presencia de un coágulo en la vena profunda de la pierna izquierda (trombosis venosa profunda).\n- El ecocardiograma evidenció que el ventrículo izquierdo funcionaba normalmente, pero el ventrículo derecho estaba dilatado y con función reducida, con signos de presión elevada en esta cavidad.\n\n**Interpretación Clínica**\n\nEl paciente presentaba insuficiencia cardíaca derecha aguda secundaria a una embolia pulmonar masiva. Debido a que la mayoría de los coágulos estaban en áreas distales y que la cirugía reciente representaba una contraindicación para tratamientos trombolíticos (medicamentos que disuelven coágulos), no se consideró adecuada la extracción quirúrgica ni la trombólisis sistémica.\n\nEn este contexto, se inició tratamiento con heparina para anticoagulación, óxido nítrico inhalado para mejorar la oxigenación y sildenafil oral (un inhibidor de la fosfodiesterasa tipo 5, que actúa como vasodilatador pulmonar) para reducir la presión en el ventrículo derecho y mejorar su función.\n\n**Evolución y Próximos Pasos**\n\nAl día siguiente, el paciente mostró estabilidad hemodinámica y mejoría en la función del ventrículo derecho, confirmada mediante ecocardiografía realizada 48 horas después del ingreso. La presión en el ventrículo derecho disminuyó significativamente y la capacidad de contracción mejoró.\n\nSe recomendó continuar con sildenafil durante un mes tras el alta hospitalaria, junto con anticoagulación oral, y realizar seguimiento ambulatorio para monitorear su recuperación. El paciente y su familia fueron informados detalladamente y dieron su consentimiento para el plan terapéutico.\n\n**Resumen**\n\nEste caso ilustra el uso exitoso de sildenafil como tratamiento complementario para mejorar la función del ventrículo derecho en un paciente con embolia pulmonar masiva y disfunción ventricular derecha aguda, en un escenario donde la trombólisis estaba contraindicada debido a una cirugía reciente. El manejo combinado permitió la estabilización clínica y la recuperación funcional sin necesidad de intervenciones quirúrgicas o trombolíticas."
+        }
+    },
+    {
+        "article": "Presentamos el caso de un hombre de 78 años con antecedentes conocidos de fibrilación auricular crónica, cardiopatía hipertensiva y miocardiopatía no isquémica. Tenía una reducción global de la fracción de eyección del ventrículo izquierdo del 40-45 %, y su ecocardiograma no mostraba anomalías significativas. El paciente había sido seguido en la clínica de cardiología ambulatoria, donde fue tratado por insuficiencia cardiaca crónica en estadio C del Colegio Americano de Cardiología (ACC) con síntomas de clase III de la Asociación del Corazón de Nueva York (NYHA). A pesar de varios cambios en sus diuréticos e intentos de controlar su estado de líquidos, ganó 40 libras de peso en un período de 3 meses, con un aumento significativo de la falta de aire. A medida que su descompensación de la insuficiencia cardiaca progresó, fue hospitalizado durante 8 días y tratado con furosemida intravenosa (IV). Debido a su clasificación de la NYHA y su ingreso al hospital por exacerbación de la insuficiencia cardiaca, se indicó y se realizó un monitoreo hemodinámico invasivo con implantación de CardioMEMS. La implantación de su CardioMEMS se realizó en Grand Blanc, Michigan, a una altitud de 837 pies con una presión atmosférica de 731.2 el 9 de abril de 2019. Las mediciones hemodinámicas iniciales del cateterismo cardiaco mostraron una presión sistólica PA de 45 mmHg, presión diastólica PA de 16 mmHg y una presión PA media de 30 mmHg. La presión auricular derecha fue de 21 mmHg, presión ventricular derecha de 44/17 mmHg y la presión media de la cuña pulmonar fue de 24 mmHg. El procedimiento se completó sin complicaciones y el paciente fue dado de alta el mismo día.\n\nTras la implantación de CardioMEMS, el paciente permaneció estable durante 4 semanas sin empeoramiento de los síntomas de insuficiencia cardiaca. Cumplió con las lecturas diarias de CardioMEMS con una PA media que osciló entre 27 y 31 mmHg, y una presión diastólica de PA de 17 a 21 mmHg. Estos hallazgos hemodinámicos globales fueron estables en comparación con los del momento de la implantación.\n\nEl paciente viajó a Denver, Colorado, durante cuatro días a una altitud de 5280 pies con una presión atmosférica de 596.8 atm el 5 de mayo de 2019. Las grabaciones del primer día de su visita mostraron un aumento de la presión sistólica de 44 mmHg a 73 mmHg, un aumento de la presión media de 30 mmHg a 53 mmHg y un aumento de la presión diastólica de 20 mmHg a 40 mmHg. Al mismo tiempo, notó un aumento significativo de la falta de aire y la hinchazón de las extremidades inferiores. No buscó atención médica, sino que se contactó con su cardiólogo primario en Michigan. Su oxígeno nasal de referencia se incrementó de 1 litro a 2 litros y su dosis de furosemida se duplicó de 40 mg diarios a dos veces al día. Afortunadamente, este tratamiento mejoró los síntomas del paciente y evitó la admisión hospitalaria. Debido a que se evitó la admisión hospitalaria, no se dispuso de valores de laboratorio, imágenes de diagnóstico y signos vitales clínicos.\n\nDurante su estancia hospitalaria de 4 días, sus presiones invasivas se mantuvieron altas, pero disminuyeron lentamente y se estabilizaron con una PA sistólica de 72 mmHg, una PA media de 49 mmHg y una PA diastólica de 35 mmHg el día previo a su regreso a Michigan. El quinto día, volvió a Michigan y sus mediciones de presión invasiva se normalizaron rápidamente, con una presión PA media de 29 mmHg y una presión PA diastólica de 20 mmHg. Ha seguido estando bien mientras estuvo en Michigan con diuréticos de mantenimiento continuos y un control diario de las presiones PA con su dispositivo CardioMEMS.\n\nMH - Envejecido\nMH - *Altitud\nMH - Monitoreo de presión arterial, ambulatorio\nMH - *Insuficiencia cardiaca/diagnóstico/etiología\nMH - Hospitalización\nMH - Humanos\nMH - Hombre\nMH - Arteria Pulmonar\n",
+        "gold_summary": "Presentamos el caso de un hombre de 78 años con una exacerbación de la insuficiencia cardiaca mientras viajaba a gran altitud. Se detectó un aumento de sus presiones arteriales pulmonares (PA) mediante su dispositivo CardioMEMS implantado. La comprensión del cambio esperado en los registros de presión de la PA ayudó a identificar una verdadera exacerbación de la insuficiencia cardiaca en nuestro paciente. Esto llevó a un cambio rápido en la terapia médica, que en última instancia evitó la hospitalización.\n",
+        "synthetic_summary": {
+            "B1": "Había un hombre de 78 años que tenía problemas en su corazón. Él usaba un aparato especial para medir la presión en su corazón. Cuando viajó a un lugar muy alto, su corazón trabajó más fuerte y se sintió mal. El aparato mostró que su corazón estaba con mucha presión. Los doctores cambiaron sus medicinas rápido. Así, él no tuvo que ir al hospital y se mejoró.",
+            "B2": "**Lo que pasó con el paciente**  \nUn hombre de 78 años tenía problemas graves del corazón llamados insuficiencia cardiaca, que significa que su corazón no bombeaba la sangre tan bien como debería. Para ayudar a controlar su enfermedad, le pusieron un dispositivo llamado CardioMEMS, que mide la presión en una arteria del pulmón. Esto ayuda a los doctores a saber cómo está funcionando su corazón sin que él tenga que ir al hospital.\n\n**Qué sucedió durante su viaje**  \nEl paciente viajó a una ciudad alta llamada Denver, que está a mucha altura sobre el nivel del mar. Allí, las mediciones del CardioMEMS mostraron que la presión en su arteria pulmonar subió mucho. Esto fue un problema porque también empezó a sentir más dificultad para respirar y sus piernas se hincharon. Estas señales indicaron que su insuficiencia cardiaca empeoró.\n\n**Cómo ayudaron los doctores**  \nAunque no fue al hospital, el paciente llamó a su cardiólogo, quien le cambió el tratamiento aumentando la cantidad de un medicamento llamado diurético, que ayuda a eliminar el exceso de líquido del cuerpo. Gracias a este cambio rápido, sus síntomas mejoraron y evitó tener que ser hospitalizado.\n\n**Qué aprendimos de este caso**  \nEste caso muestra que el dispositivo CardioMEMS es muy útil para detectar cambios importantes en la presión del corazón, especialmente cuando una persona viaja a lugares con altitudes altas. Saber cómo cambian las presiones en estas situaciones ayuda a los médicos a actuar rápido y evitar complicaciones graves.",
+            "B3": "**Contexto**\n\nSe describe el caso de un hombre de 78 años con antecedentes de fibrilación auricular crónica, cardiopatía hipertensiva y miocardiopatía no isquémica, que presentaba insuficiencia cardiaca crónica en estadio C (según el Colegio Americano de Cardiología) con síntomas moderados a severos (clase III de la Asociación del Corazón de Nueva York). A pesar del tratamiento ambulatorio, experimentó un aumento significativo de peso y empeoramiento de la falta de aire, lo que llevó a una hospitalización y al implante de un dispositivo CardioMEMS para monitoreo invasivo de las presiones en la arteria pulmonar.\n\n**Hallazgos Clave**\n\nTras la implantación del CardioMEMS, el paciente mostró presiones pulmonares estables durante cuatro semanas en su entorno habitual en Michigan (a una altitud de 837 pies). Sin embargo, durante un viaje de cuatro días a Denver, Colorado (a 5280 pies de altitud), se registró un aumento marcado y sostenido de las presiones sistólica, media y diastólica en la arteria pulmonar. Paralelamente, el paciente experimentó un empeoramiento de sus síntomas de insuficiencia cardiaca, como aumento de la falta de aire y edema (hinchazón) en las extremidades inferiores.\n\n**Interpretación Clínica**\n\nEl aumento de las presiones pulmonares detectado por el CardioMEMS durante la estancia en altitud elevada reflejó una verdadera exacerbación de la insuficiencia cardiaca, más allá del efecto esperado por el cambio de altitud. Este monitoreo permitió diferenciar entre las variaciones fisiológicas normales y un deterioro clínico significativo. La rápida comunicación con el equipo médico facilitó la intensificación del tratamiento, incluyendo el aumento de la dosis de diuréticos y oxígeno suplementario, lo que mejoró los síntomas y evitó la necesidad de hospitalización.\n\n**Próximos Pasos**\n\nEl paciente continuó con un seguimiento estrecho mediante el dispositivo CardioMEMS tras su regreso a Michigan, donde las presiones pulmonares se normalizaron rápidamente. Se mantuvo con tratamiento diurético de mantenimiento y control diario de las presiones arteriales pulmonares para prevenir futuras descompensaciones. Este caso resalta la utilidad del monitoreo hemodinámico invasivo en pacientes con insuficiencia cardiaca, especialmente en situaciones que pueden alterar la fisiología cardiovascular, como los viajes a gran altitud."
+        }
+    },
+    {
+        "article": "Un hombre de 55 años, previamente sano, fue derivado al servicio de urgencias por su médico de cabecera, quejándose de una fiebre de 3 semanas de evolución, tos productiva, disnea y sibilancias. Tenía un historial de 80 paquetes-año de consumo de tabaco y un historial familiar positivo de cáncer de pulmón. Había sido tratado por su médico de cabecera con un ciclo de amoxicilina oral y prednisona oral, pero sus síntomas empeoraron. Cuando llegó al servicio de urgencias, su recuento de glóbulos blancos era de 16,4 × 109/L (rango normal: 4,0-10,0 × 109/L), el recuento de neutrófilos de 13,8 × 109/L (rango normal: 2,0-7,0 × 109/L), la proteína C reactiva era de 118 mg/L (normal: 0-5 mg/L) y el sodio sérico era de 112 mmol/L (rango normal: 136-145 mmol/L). Otros marcadores bioquímicos estaban dentro de los límites normales. Una radiografía de tórax mostró consolidación del lóbulo medio e inferior derecho con derrame pleural moderado asociado. Fue admitido y tratado como neumonía adquirida en la comunidad y el estudio confirmó el diagnóstico de SIADH.\n\nEl paciente empeoró a pesar de la administración intravenosa de piperacilina-tazobactam y de claritromicina oral, con empeoramiento de la consolidación en la repetición de la radiografía de tórax. El paciente fue trasladado a la unidad de cuidados intensivos y, posteriormente, se le realizó una intubación y ventilación. Una tomografía computarizada (TC) de su tórax reveló una masa hilar derecha con afectación mediastinal y adenopatía hilar derecha con consolidación de espacio aéreo extenso superpuesta. Una biopsia realizada durante la broncoscopia reveló células pequeñas, histológicamente monótonas, con núcleos ovoides oscuros. No se observaron nucleolos, y varias figuras mitóticas estaban presentes. Las células tienen un citoplasma estrecho y mal definido. La inmunohistoquímica realizada en las células tumorales mostró negatividad a CD45, AE1/AE3, positividad a TTF1. También se observaron sinapsina mínima focal y positividad a cromogranina A. Este perfil inmunohistoquímico fue consistente con un diagnóstico de cáncer de pulmón de células pequeñas.\n\nLa estadificación completa, que consistió en una tomografía computarizada del cerebro y tórax-abdomen-pelvis, confirmó una enfermedad en estadio extenso con metástasis suprarrenales. El estado funcional ECOG de la paciente era deficiente debido a una combinación de SCLC y dificultad respiratoria que requería ventilación artificial. Como las tasas de respuesta con quimioterapia en SCLC son generalmente altas, se inició un tratamiento quimioterápico doble en forma de carboplatino y etopósido mientras la paciente estaba intubada en la UCI.\n\nEl paciente respondió bien al tratamiento y fue extubado y trasladado a la sala de ventilación no invasiva. Una nueva tomografía computarizada de tórax después de 1 ciclo mostró una buena respuesta parcial al tratamiento.\n\nEn el día 3 del ciclo 2 de quimioterapia, la paciente desarrolló dolor en la parte inferior de la espalda y debilidad bilateral en las extremidades inferiores. El examen identificó paresia motora bilateral en las extremidades inferiores (grado 3 del Consejo de Investigación Médica [MRC]) y paresia sensorial. El examen sensorial reveló ausencia de tacto ligero, pinchazo, coordinación y propiocepción en las extremidades inferiores. El día 3 de etopósido se retrasó como resultado de los nuevos hallazgos neurológicos.\n\nSe realizaron un TAC cerebral, resonancia magnética (RM) cerebral y resonancia magnética (RM) de la columna para investigar los nuevos hallazgos neurológicos. Todos los resultados radiológicos fueron normales, sin evidencia de metástasis intracerebrales, accidente cerebrovascular, mielitis o enfermedad leptomeníngea. Además, no hubo evidencia radiográfica obvia de compresión de la médula espinal, ya sea por compresión extrínseca por depósito metastásico óseo o depósitos intramedulares o leptomeníngeos.\n\nDos días después, un examen neurológico de seguimiento reveló tetraplejía, MRC grado 0 en las extremidades superiores e inferiores. Todos los reflejos tendinosos profundos estaban ausentes. Los músculos de la cabeza y el cuello, la cognición y el habla no se vieron afectados, y el examen de los nervios craneales fue normal.\n\nLos análisis de sangre de rutina, incluida la proteína C reactiva y la velocidad de sedimentación de eritrocitos, fueron normales. Los análisis de sangre específicos, incluidos los de vitamina B12 en suero, folato, serología del VIH, serología de la enfermedad de Lyme, serología del virus de Epstein-Barr, serología de Brucella, anticuerpos tiroideos, pruebas de función tiroidea, ANCA, ENA, ANA y electroforesis de proteínas séricas, fueron negativos o normales. Se enviaron anticuerpos para las pruebas de sangre Hu, Ri y Yo, y todos fueron negativos. En este momento, se sospechó un diagnóstico de polineuropatía simétrica ascendente aguda motora y sensorial y se realizó una punción lumbar. Los resultados del líquido cefalorraquídeo (LCR) revelaron una proteína total elevada de 3.32 g/L (normal 0.15–0.45), y otros parámetros fueron normales, con una repetición 3 días después que mostró resultados similares. La citología del LCR fue negativa para la malignidad y el cultivo del LCR también fue negativo.\n\nLa electromiografía fue consistente con una polineuropatía difusa predominantemente motora; los potenciales sensoriales se conservaron, pero fueron de pequeña amplitud. Las conducciones motoras mostraron características axonales/desmielinizantes mixtas, que no eran típicas del síndrome de Guillain-Barré.\n\nSe realizaron estudios de electromiografía y conducción nerviosa para investigar la polineuropatía motora y sensorial aguda del paciente. Los estudios de conducción nerviosa revelaron lo siguiente:\n\n•Nervios motores:\n◦Las amplitudes del potencial de acción muscular compuesto (CMAP) se redujeron notablemente en los nervios tibial y cubital de forma bilateral (tibial: 1,2 mV; normal > 4 mV; cubital: 0,8 mV; normal > 3 mV).\n◦Las velocidades de conducción motora (MCV) se desaceleraron en los nervios tibial y cubital (tibial: 30 m/s; normal > 40 m/s; cubital: 34 m/s; normal > 50 m/s), lo que es coherente con la desmielinización.\n◦Las latencias motoras distales se prolongaron, con un patrón mixto axonal y desmielinizante.\n•Nervios sensoriales:\n◦Las amplitudes del potencial de acción nerviosa sensorial (SNAP) se conservaron, pero fueron de poca amplitud en los nervios surales y medianos (sural: 4 μV; normal > 10 μV; mediano: 6 μV; normal > 15 μV).\n◦Las velocidades de conducción sensorial (VCS) se encontraban dentro de los límites normales.\nLos hallazgos electrofisiológicos revelaron una polineuropatía predominantemente motora con características axonales y desmielinizantes mixtas, atípicas para los síndromes paraneoplásicos clásicos, que generalmente son predominantemente sensoriales y se caracterizan por la ausencia de SNAP.\n\nMientras tanto, mientras estas investigaciones estaban en curso, se inició al paciente con dexametasona intravenosa y 0.4 g/kg/día de inmunoglobulina intravenosa sin ninguna mejora sintomática.\n\n3. Resultados y seguimiento\nA pesar de una importante respuesta oncológica inicial a la quimioterapia, el estado neurológico del paciente se deterioró rápidamente. Después de 1 ciclo de carboplatino y etopósido, las imágenes confirmaron una respuesta parcial con una reducción en el tamaño del tumor. Sin embargo, el inicio de una polineuropatía motora y sensorial grave y ascendente condujo a un compromiso respiratorio. Esta disociación entre las respuestas oncológicas y neurológicas destaca la naturaleza agresiva y refractaria del SNP, incluso cuando el tratamiento del cáncer es efectivo. Aunque la dexametasona intravenosa y la inmunoglobulina intravenosa se administraron rápidamente, no lograron mejorar los resultados neurológicos.\n\nSe llevaron a cabo largas y repetidas discusiones multidisciplinares con el paciente y su familia sobre la admisión en la unidad de cuidados intensivos para recibir apoyo ventilatorio. El paciente estaba bien informado y consciente de que era poco probable que sus síntomas neurológicos fueran reversibles y, por lo tanto, optó por el mejor tratamiento de apoyo. El paciente falleció 3 semanas después de los síntomas iniciales. La decisión del paciente de rechazar el apoyo ventilatorio invasivo en favor de los cuidados paliativos pone de relieve las consideraciones éticas que rodean la calidad de vida en los síndromes paraneoplásicos de progresión rápida.\n",
+        "gold_summary": "Preocupaciones del paciente: Un hombre de 55 años con un historial de 80 años fumando presenta al hospital con un historial de 3 semanas de fiebres, tos productiva, disnea y sibilancias. No tenía comorbilidades significativas.\n\nDiagnóstico: Extensas investigaciones radiológicas revelaron una gran masa en el hilum derecho que comprimía el bronquio inferior derecho con depósitos suprarrenales metastásicos. Las investigaciones bioquímicas confirmaron el síndrome de secreción inadecuada de la hormona antidiurética, y la histología identificó un CPCP.\n\nIntervenciones: A pesar de iniciar una quimioterapia combinada con carboplatino y etopósido, el paciente desarrolló parálisis motora progresiva y pérdida sensorial en el transcurso de 4 días, lo que derivó en un diagnóstico de polineuropatía motora y sensorial aguda paraneoplásica.\n\nResultados: Su estado empeoró rápidamente y falleció 14 días después de la aparición de los síntomas debido a una insuficiencia respiratoria, lo que pone de relieve la agresividad de los síndromes paraneoplásicos.\n",
+        "synthetic_summary": {
+            "B1": "Había un hombre que estaba muy enfermo. Tenía tos, fiebre y le costaba respirar. \n\nLos doctores encontraron un bulto grande en su pulmón. También tenía un problema en otras partes de su cuerpo. \n\nLe dieron medicinas para el cáncer, pero empezó a perder fuerza en sus piernas y brazos. No podía sentir bien ni moverlos. \n\nMuy rápido, se puso muy mal y no pudo respirar bien. Después de unos días, se fue al cielo. \n\nLos doctores dijeron que su enfermedad fue muy fuerte y difícil de curar.",
+            "B2": "**Lo que le pasó al paciente**  \nUn hombre de 55 años que había fumado mucho durante muchos años llegó al hospital con fiebre, tos con flema, dificultad para respirar y silbidos al respirar. Estos síntomas habían durado tres semanas. Antes de esto, estaba sano y no tenía otras enfermedades importantes.\n\n**Qué encontraron los médicos**  \nLas pruebas de imagen mostraron una masa grande en una parte del pulmón derecho que estaba bloqueando una vía respiratoria importante. También encontraron que el cáncer se había extendido a las glándulas suprarrenales, que están encima de los riñones. Un análisis de sangre mostró que tenía un problema llamado síndrome de secreción inadecuada de hormona antidiurética, que afecta el equilibrio de líquidos en el cuerpo. Al analizar una muestra del tumor, confirmaron que tenía un tipo de cáncer de pulmón llamado cáncer de pulmón de células pequeñas (CPCP).\n\n**Tratamiento y complicaciones**  \nEl paciente comenzó a recibir quimioterapia con dos medicamentos, carboplatino y etopósido, que son comunes para tratar este tipo de cáncer. Sin embargo, en pocos días, empezó a perder fuerza en las piernas y luego en los brazos, además de perder sensibilidad. Los médicos diagnosticaron una polineuropatía motora y sensorial aguda paraneoplásica, que es una enfermedad nerviosa grave relacionada con el cáncer, donde los nervios dejan de funcionar correctamente.\n\n**Qué pasó al final**  \nA pesar de que el tratamiento contra el cáncer estaba funcionando y el tumor había disminuido de tamaño, la enfermedad nerviosa empeoró rápidamente. El paciente tuvo problemas para respirar y falleció dos semanas después de que aparecieron los síntomas nerviosos. Este caso muestra lo agresivos y difíciles de tratar que pueden ser los síndromes paraneoplásicos, que son enfermedades causadas por la reacción del cuerpo al cáncer.",
+            "B3": "**Contexto**  \nUn hombre de 55 años, con un historial muy extenso de tabaquismo (equivalente a 80 paquetes-año) y sin enfermedades previas relevantes, acudió al hospital tras presentar durante tres semanas fiebre persistente, tos con expectoración, dificultad para respirar y sibilancias. Inicialmente fue tratado con antibióticos y corticoides, pero sus síntomas empeoraron, lo que motivó su ingreso hospitalario.\n\n**Hallazgos Clave**  \nLas pruebas radiológicas, incluyendo radiografía y tomografía computarizada (TC) de tórax, revelaron una masa grande en la región del hilio derecho del pulmón, que comprimía el bronquio inferior derecho, además de metástasis en las glándulas suprarrenales. Los análisis de sangre mostraron un síndrome de secreción inadecuada de hormona antidiurética (SIADH), que explica un nivel muy bajo de sodio en sangre. La biopsia pulmonar confirmó el diagnóstico de cáncer de pulmón de células pequeñas (CPCP), un tipo agresivo de tumor pulmonar.\n\n**Interpretación Clínica**  \nA pesar de iniciar un tratamiento estándar con quimioterapia combinada de carboplatino y etopósido, el paciente desarrolló rápidamente una polineuropatía aguda, es decir, un daño progresivo en múltiples nervios que afectó tanto la función motora (movimiento) como sensorial (sensaciones). En pocos días, presentó debilidad grave en las extremidades inferiores que progresó a parálisis completa de brazos y piernas, acompañada de pérdida sensorial. Las pruebas de imágenes cerebrales y de la médula espinal no mostraron metástasis ni compresión nerviosa, y los análisis de líquido cefalorraquídeo descartaron infección o infiltración tumoral directa. Los estudios electrofisiológicos indicaron una combinación de daño axonal (afectación de las fibras nerviosas) y desmielinizante (pérdida de la cubierta protectora de los nervios), un patrón atípico para síndromes paraneoplásicos clásicos, que suelen afectar principalmente la sensibilidad.\n\nSe inició tratamiento inmunomodulador con dexametasona (un corticoide) e inmunoglobulina intravenosa, pero no se observó mejoría neurológica. La rápida progresión de la debilidad llevó a insuficiencia respiratoria, requiriendo soporte ventilatorio.\n\n**Próximos Pasos y Resultado Final**  \nTras una cuidadosa discusión multidisciplinaria y con el paciente plenamente informado, se decidió no continuar con soporte ventilatorio invasivo debido a la baja probabilidad de recuperación neurológica y la mala calidad de vida esperada. El paciente falleció tres semanas después del inicio de los síntomas neurológicos.\n\nEste caso ilustra la agresividad y complejidad de los síndromes paraneoplásicos asociados al cáncer de pulmón de células pequeñas, donde la respuesta favorable al tratamiento oncológico puede contrastar con un deterioro neurológico rápido e irreversible. Además, resalta la importancia de abordar las decisiones éticas y de calidad de vida en el manejo de estas complicaciones graves."
+        }
+    },
+    {
+        "article": "El paciente presentado firmó el Consentimiento Informado y se cumplieron los demás principios éticos, respetando la Resolución 466/12 del Consejo Nacional de Ética en Investigación. Este informe de caso fue aprobado por el Comité de Ética en Investigación de la Universidad Federal de São Paulo (UNIFESP), bajo el dictamen número 4.455.365.\n\nEl paciente, de 66 años de edad y sexo masculino, acudió a una consulta de otorrinolaringología por presentar disfagia tipo atragantamiento con sólidos y reflujo nasal de alimentos desde hacía un año. Había sufrido un accidente automovilístico 13 años atrás y era diabético. Se le realizó una videoendoscopia de la deglución (VED), en la que se observó, en la evaluación estructural, una protuberancia de la pared posterior de la hipofaringe con residuo salival sobre la lesión. En la evaluación funcional, tras la ingesta de alimentos sólidos, se observó una restricción de la retroflexión de la epiglotis, una limitación de la elevación de la laringe y un reflujo nasal de alimentos, con gran cantidad de residuo alimentario por encima de la lesión, en la pared posterior de la faringe. En la prueba de maniobras posturales, empeoró la disfagia al extender el cuello y mejoró la eliminación al flexionar la cabeza. Se le realizó una tomografía computarizada (TC) de la columna cervical, solicitada para evaluar la naturaleza de la lesión, que mostró la presencia de osteofitos cervicales anteriores entre las vértebras C3 y C6, el mayor de 12 milímetros (mm) de longitud, que estrechaba la columna aérea al nivel de la orofaringe e hipofaringe. Se descartaron otras causas de disfagia y se trató al paciente con terapia de deglución y omeprazol, dirigido al reflujo faringolaríngeo. Se realizaron 6 sesiones de terapia de deglución individualizada, con el objetivo de compensar el mecanismo de deglución ante un obstáculo mecánico en la región faríngea. Los principales aspectos trabajados fueron: modificación de la textura de la dieta, evitando alimentos sólidos y secos; maniobras posturales de deglución, probadas durante la VED, especialmente el chin tuck (“cabeza hacia abajo” o “flexión de la cabeza”), que aumenta el espacio de la válvula (“abre la válvula”) y mejora la presión de transferencia faríngea del alimento; y ejercicios de fortalecimiento de la lengua, para superar la barrera mecánica de la orofaringe durante la expulsión del alimento. Se recomendó, si fuera necesario, alternar la ingesta de alimentos sólidos con líquidos, ante la percepción de alimentos estancados en la faringe. Se le indicó que repitiera los ejercicios de lengua en el hogar, 2 a 3 veces al día. Después de las sesiones iniciales, el paciente presentó una respuesta satisfactoria, y se lo controló trimestralmente durante el primer año y semestralmente a partir del segundo año. Se lo derivó para una evaluación ortopédica para analizar la viabilidad quirúrgica, y se optó por un tratamiento conservador debido a la buena compensación con medidas clínicas. Sigue en seguimiento ambulatorio desde hace 2 años, y mantiene una deglución eficiente, sin incidencia de complicaciones relacionadas con la disfagia. Se optó por mantener reevaluaciones periódicas, al menos una vez al año, para detectar precozmente un posible nuevo desequilibrio de la homeostasis de la deglución relacionado con el deterioro gradual de las funciones en el contexto de la presbifagia o el surgimiento de un nuevo factor agresor.\n",
+        "gold_summary": "Se describió el caso de un paciente de 66 años con disfagia por atragantamiento con sólidos y reflujo nasal de alimentos desde hacía un año. La videoendoscopia de la deglución mostró una protuberancia en la pared posterior de la faringe y, al ofrecer alimentos sólidos, una restricción de la retroflexión de la epiglotis, reflujo nasal de alimentos y una gran cantidad de residuos de alimentos sobre la lesión. La tomografía computarizada de la columna cervical identificó la presencia de osteofitos cervicales anteriores entre las vértebras C3 y C6, el más grande con una longitud anteroposterior de 12 milímetros, que estrechaba la columna aérea a nivel de la orofaringe e hipofaringe. El paciente fue tratado adecuadamente con fonoterapia para la deglución.\n",
+        "synthetic_summary": {
+            "B1": "Un señor de 66 años tenía problemas para tragar comida dura. A veces, la comida se le iba por la nariz. Los doctores vieron que tenía un bulto en la garganta. También había huesos grandes que apretaban su garganta. Para ayudarlo, le enseñaron ejercicios para tragar mejor. Ahora puede comer sin problemas y está bien cuidado.",
+            "B2": "**Lo que Encontraron**\n\nUn hombre de 66 años tenía problemas para tragar alimentos sólidos y notaba que la comida a veces regresaba por la nariz desde hacía un año. Al hacerle un examen llamado videoendoscopia de la deglución, que consiste en usar una cámara pequeña para ver cómo traga, se vio una protuberancia (una especie de bulto) en la parte de atrás de su garganta. Cuando comía alimentos sólidos, su epiglotis (una parte que ayuda a que la comida no vaya a los pulmones) no se movía bien, y parte de la comida subía hacia la nariz, quedando residuos sobre el bulto.\n\n**Qué Significa**\n\nPara entender mejor la causa, le hicieron una tomografía computarizada, que es un tipo de radiografía especial que muestra imágenes detalladas de los huesos y tejidos. En esta imagen, encontraron que tenía unos crecimientos óseos llamados osteofitos en su columna cervical (el cuello), entre las vértebras C3 y C6. El más grande medía 12 milímetros y estaba presionando la vía aérea en la garganta, dificultando el paso normal de la comida.\n\n**Cómo lo Trataron**\n\nEl paciente recibió terapia para mejorar la forma en que traga, llamada fonoterapia. Esta terapia incluyó ejercicios para la lengua y cambios en la postura al comer, como inclinar la cabeza hacia adelante para facilitar el paso de la comida. También modificaron su dieta para evitar alimentos muy duros o secos. Gracias a este tratamiento, pudo mejorar su capacidad para tragar sin necesidad de cirugía y sigue siendo controlado regularmente para asegurarse de que no tenga problemas nuevos.",
+            "B3": "**Contexto**  \nSe presentó el caso de un hombre de 66 años que acudió a consulta por dificultad para tragar alimentos sólidos, acompañada de sensación de atragantamiento y reflujo nasal de alimentos, síntomas que persistían desde hacía un año. Entre sus antecedentes médicos destacaba un accidente automovilístico ocurrido 13 años antes y diabetes.  \n\n**Hallazgos Clave**  \nMediante una videoendoscopia de la deglución, se identificó una protuberancia en la pared posterior de la hipofaringe (parte baja de la garganta), con acumulación de saliva sobre esta lesión. Al ofrecer alimentos sólidos, se observó que la epiglotis (estructura que ayuda a proteger las vías respiratorias durante la deglución) tenía dificultad para doblarse hacia atrás, además de reflujo nasal de alimentos y una gran cantidad de restos alimentarios acumulados por encima de la protuberancia.  \n\nUna tomografía computarizada (TC) de la columna cervical reveló la presencia de osteofitos (crecimientos óseos anormales) en la parte anterior de las vértebras cervicales C3 a C6, siendo el más grande de 12 milímetros. Estos osteofitos comprimían la vía aérea en la región de la orofaringe e hipofaringe, lo que explicaba la dificultad para tragar.  \n\n**Interpretación Clínica**  \nEl diagnóstico principal fue disfagia mecánica causada por osteofitos cervicales que estrechaban la vía aérea y alteraban el mecanismo normal de la deglución. Se descartaron otras posibles causas de disfagia.  \n\n**Tratamiento y Seguimiento**  \nEl paciente recibió terapia de deglución personalizada, que incluyó:  \n- Modificación de la dieta para evitar alimentos sólidos y secos, facilitando la ingesta.  \n- Maniobras posturales durante la deglución, especialmente la flexión de la cabeza hacia adelante (chin tuck), que mejora el paso del alimento y reduce el reflujo nasal.  \n- Ejercicios de fortalecimiento de la lengua para superar la obstrucción mecánica y facilitar la expulsión del alimento.  \n\nAdemás, se prescribió omeprazol para tratar el reflujo faringolaríngeo (reflujo de ácido hacia la garganta). El paciente mostró una respuesta favorable tras seis sesiones de terapia y se mantuvo bajo seguimiento regular durante dos años, con controles trimestrales en el primer año y semestrales posteriormente.  \n\nSe evaluó la posibilidad de tratamiento quirúrgico para eliminar los osteofitos, pero se decidió continuar con un manejo conservador debido a la buena compensación clínica. Se recomendó continuar con ejercicios en casa y mantener evaluaciones periódicas al menos una vez al año, para detectar a tiempo cualquier deterioro en la función de la deglución asociado al envejecimiento o a nuevos factores.  \n\n**Conclusión**  \nEste caso ilustra cómo los osteofitos cervicales pueden causar disfagia mecánica significativa, y cómo un tratamiento integral basado en terapia de deglución y modificaciones dietéticas puede lograr una adecuada compensación funcional, evitando la necesidad de cirugía y mejorando la calidad de vida del paciente."
+        }
+    },
+    {
+        "article": "Una paciente caucásica de 18 años de edad se presentó en nuestra clínica con quejas de múltiples bultos palpables en sus senos bilateralmente. En el examen físico, la paciente tenía múltiples lesiones pigmentadas lentigosas en su cara, cuerpo y esclerótica bilateralmente, nevos azules en su tronco y extremidades superiores y una cara redonda con forma de luna.\n\nTras la evaluación ultrasonográfica, se encontraron múltiples nódulos compactos (fibroadenomas) en ambos senos, siendo el más grande en el cuadrante superior externo del seno izquierdo, con un diámetro de 7,8 cm.\n\nEn 2018, se le había practicado una tiroidectomía total con el diagnóstico de adenoma folicular y la extirpación de un nódulo grande del seno izquierdo, debido a su gran tamaño y al dolor que causaba, con un informe de histopatología que sugería un fibroadenoma con estroma mixóide.\n\nSe realizó una biopsia por escisión de dos nódulos de la mama derecha con diagnóstico de fibroadenoma mixto, lo que respaldó nuestro diagnóstico de complejo de Carney.\n\nEn la resonancia magnética se encontraron múltiples fibroadenomas compactos en ambos senos, con alta intensidad de señal en las imágenes T2 y T2/FS, con tabiques internos sin restricción de difusión, compatibles con múltiples fibroadenomas mixoides.\n\nAdemás, había un par de ganglios linfáticos axilares y prominentes ganglios linfáticos mamarios internos bilaterales.\n\nAdemás, se observó una anomalía en la densidad de los tejidos blandos en el mediastino anterior, que medía 11 mm de espesor máximo, lo que sugería un timo prominente.\n\nTodos los hallazgos anteriores sugerían la posibilidad de un complejo de Carney. Se realizó una evaluación adicional en el laboratorio. Los análisis hormonales no mostraron anomalías en los niveles de testosterona, prolactina, PTH y DHEA-S.\n\nLuego se realizó un análisis genético que arrojó como resultado la mutación del gen PRHAR1A, heterocigótico para una variante sin sentido de significancia incierta en el exón 3 de este gen. Esta mutación nunca se había informado en la base de datos gnomAD.\n\nSe realizaron pruebas genéticas a los padres y se determinó que solo el padre era portador de la misma mutación genética.\n\nSe discutieron con la paciente varios planes de tratamiento conservadores, pero ninguno demostró proporcionar una solución/tratamiento definitivo. En el pasado se realizó la extirpación de los lóbulos grandes con alivio temporal de los síntomas de dolor de la paciente y las cirugías recurrentes estaban afectando su calidad de vida. La paciente también tuvo varias sesiones con la psicóloga de nuestra clínica y fue evaluada a fondo antes de decidir la solución final de una mastectomía bilateral.\n\nLa paciente se sometió a una mastectomía bilateral con conservación de la piel y colocación subcutánea de expansores de tejidos (suave, Motiva Flora®). La histopatología informó múltiples fibroadenomas mixóides en ambos senos, compatibles con el síndrome de Carney, con interrupción de la arquitectura normal del parénquima mamario. Las figuras muestran el fibroadenoma de forma macroscópica e histológica.\n\nEl cuidado de la herida fue mínimo, se le recomendó a la paciente usar un sujetador médico y visitas regulares a la clínica ambulatoria para seguimiento y rellenado adicional de los expansores de tejidos a intervalos regulares hasta que se alcanzó el tamaño deseado. Paciente antes y después de la mastectomía. Después de un año se realizó una segunda cirugía y los expansores se reemplazaron con implantes de silicona permanentes (suaves, Motiva Ergonomic®) submusculares, con los mismos requisitos mínimos de cuidado de la herida y colocación del sujetador.\n",
+        "gold_summary": "Una paciente de 18 años de edad se presentó en nuestra clínica con múltiples bultos palpables en sus senos bilateralmente. En el examen físico, la paciente también tenía múltiples lesiones pigmentadas lentigosas en su cara, cuerpo y esclerótica, nevos azules en su tronco y extremidades superiores y un rostro redondo con forma de luna. El diagnóstico del síndrome de Carney se decidió mediante imágenes, biopsias y análisis genético. La paciente se sometió a una mastectomía bilateral como plan de tratamiento profiláctico con colocación de expansores de tejidos.\n",
+        "synthetic_summary": {
+            "B1": "Una niña de 18 años tenía muchos bultos en sus pechos. También tenía manchas de colores en su cara y cuerpo. Los doctores hicieron pruebas y encontraron una enfermedad llamada síndrome de Carney. Para ayudarla, le quitaron los pechos y pusieron cosas suaves para que su cuerpo se vea bien.",
+            "B2": "**Lo que Encontraron en la Paciente**  \nUna joven de 18 años llegó a la clínica porque tenía varios bultos en ambos senos. Al examinarla, también notaron manchas oscuras en su piel y ojos, así como lunares azules en su cuerpo. Su cara tenía una forma redonda, parecida a una luna llena. Estas señales indicaron que podría tener algo llamado síndrome de Carney, que es una enfermedad rara que causa tumores benignos (no cancerosos) en diferentes partes del cuerpo.\n\n**Cómo Confirmaron el Diagnóstico**  \nPara estar seguros, los médicos hicieron varias pruebas. Usaron imágenes especiales como ultrasonidos y resonancias magnéticas para ver los bultos en sus senos. Además, tomaron pequeñas muestras de esos bultos (biopsias) para analizarlas bajo el microscopio. También hicieron un examen genético y encontraron un cambio en un gen llamado PRHAR1A, que está relacionado con este síndrome.\n\n**Qué Tratamiento Eligieron**  \nDespués de discutir varias opciones, decidieron hacer una mastectomía bilateral. Esto significa que le quitaron ambos senos para evitar problemas futuros, ya que los bultos seguían creciendo y causaban dolor. Para ayudar a que la piel se mantuviera y poder reconstruir después, colocaron unos dispositivos llamados expansores de tejidos, que poco a poco estiran la piel. Más tarde, estos expansores se reemplazaron por implantes de silicona para que la paciente tuviera una apariencia natural.\n\n**Importancia del Caso**  \nEste caso muestra cómo es importante combinar diferentes pruebas para diagnosticar enfermedades raras como el síndrome de Carney. También destaca que, a veces, el tratamiento puede ser difícil y requiere decisiones importantes para mejorar la calidad de vida del paciente.",
+            "B3": "**Contexto**\n\nUna joven caucásica de 18 años acudió a la clínica debido a la presencia de múltiples bultos palpables en ambos senos. Durante el examen físico, se observaron varias lesiones pigmentadas llamadas lentigos (manchas oscuras) en la cara, el cuerpo y la esclerótica (parte blanca del ojo), además de nevos azules (manchas pigmentadas) en el tronco y extremidades superiores, y una característica forma redonda de su rostro, conocida como cara en forma de luna.\n\n**Hallazgos Clave**\n\n- Estudios por ultrasonido y resonancia magnética revelaron múltiples nódulos compactos en ambos senos, identificados como fibroadenomas mixoides, siendo el más grande de 7,8 cm en el seno izquierdo.\n- Se realizaron biopsias por escisión de algunos nódulos, confirmando el diagnóstico de fibroadenomas mixtos.\n- Se detectó una anomalía en el mediastino anterior (área entre los pulmones), consistente con un timo prominente, y ganglios linfáticos axilares e internos aumentados de tamaño.\n- Los análisis hormonales no mostraron alteraciones significativas.\n- Un estudio genético identificó una mutación en el gen PRKAR1A, asociada con el síndrome de Carney, una enfermedad rara que se caracteriza por la presencia de tumores benignos en diferentes órganos y lesiones pigmentadas en la piel.\n\n**Interpretación Clínica**\n\nEl conjunto de hallazgos clínicos, imagenológicos, histopatológicos y genéticos permitió establecer el diagnóstico del síndrome de Carney. Este síndrome explica la presencia simultánea de múltiples fibroadenomas mamarios, lesiones pigmentadas cutáneas y otras anomalías observadas en la paciente.\n\n**Próximos Pasos y Tratamiento**\n\nDado que las cirugías previas para extirpar los fibroadenomas grandes solo proporcionaron alivio temporal y afectaban negativamente la calidad de vida de la paciente, se consideraron opciones de tratamiento más definitivas. Tras una evaluación psicológica y médica exhaustiva, se decidió realizar una mastectomía bilateral (extirpación completa de ambos senos) con conservación de la piel, seguida de la colocación subcutánea de expansores de tejidos para permitir la reconstrucción mamaria gradual.\n\nEl cuidado postoperatorio incluyó el uso de un sujetador médico y visitas regulares para el llenado progresivo de los expansores. Un año después, se reemplazaron estos expansores por implantes permanentes de silicona colocados debajo del músculo, con un manejo mínimo de la herida y seguimiento ambulatorio.\n\nEste enfoque permitió controlar los síntomas, mejorar la calidad de vida de la paciente y manejar de manera efectiva las manifestaciones mamarias del síndrome de Carney."
+        }
+    },
+    {
+        "article": "Una adolescente femenino de 13 años sin antecedentes médico-quirúrgicos de interés acude a Urgencias por dolor e impotencia funcional en muñeca izquierda tras caída mientras patinaba. Diagnosticada de lesión en torus metafisaria con extensión fisaria de radio distal clasificada como lesión Peterson tipo I, es inmovilizada durante cuatro semanas con férula antebraquiopalmar. Dos semanas después de la retirada de la férula, acude nuevamente a Urgencias al sentir un crujido en la muñeca, sin sobreesfuerzo asociado e impotencia para movilizar el primer dedo de la mano izquierda. Clínicamente presenta déficit de extensión activa interfalángica, efecto tenodesis patológico, edema local y asimetría macroscópica a la comparación con la extremidad contralateral. Se estudia con resonancia magnética nuclear (RMN), identificando imagen de solución de continuidad del EPL. Con la paciente bajo anestesia general, se procede al tratamiento quirúrgico mediante transferencia tendinosa del extensor propio del índice (EPI) al remanente distal del EPL con sutura tipo Pulvertaft de monofilamento no absorbible. En el postoperatorio se inmovilizó la extremidad las cuatro primeras semanas.\n\nTras cuatro semanas, se autorizó movilidad evidenciando recuperación de extensión del primer dedo de la mano izquierda y cicatrices discretamente hipertróficas, sin dolor. El seguimiento a la sexta, duodécima semana y al año no reporta complicaciones, con una restitución completa de la función y una puntuación de 0 en la escala PRWE (Patient Rated Wrist Evaluation).",
+        "gold_summary": "Se presenta el caso de una paciente adolescente femenino que, tras tratamiento conservador con férula de una fractura fisaria Peterson tipo I en radio, sufre a las seis semanas déficit agudo de extensión del pulgar, diagnosticada mediante examen clínico radiológico de rotura espontánea del extensor pollicis longus. Es tratada por medio de transferencia del extensor propio del índice (EPI) con resultados satisfactorios y recuperación de su actividad habitual al mes postoperatorio.",
+        "synthetic_summary": {
+            "B1": "Una niña de 13 años se cayó y se lastimó la muñeca. Le pusieron una tablita para que su hueso sanara. \n\nDespués de quitarle la tablita, su dedo pulgar no podía moverse bien. Los doctores vieron que un hilo que mueve el dedo se había roto. \n\nElla tuvo una operación para arreglar ese hilo con otro hilo de su mano. \n\nDespués de un mes, su dedo volvió a moverse bien y pudo hacer todo como antes.",
+            "B2": "Caso de una adolescente de 13 años con fractura en la muñeca que fue tratada con una férula. Seis semanas después, comenzó a tener dificultad para estirar el pulgar de la mano izquierda. Los médicos descubrieron que uno de los tendones que mueve el pulgar, llamado extensor largo del pulgar, se había roto sin que ella hiciera un esfuerzo fuerte. Para arreglarlo, realizaron una cirugía donde usaron otro tendón del dedo índice para reemplazar el que estaba roto. Después de la operación y un periodo de inmovilización, la paciente recuperó completamente el movimiento del pulgar y pudo volver a sus actividades normales en un mes.",
+            "B3": "**Contexto**  \nSe trata de una adolescente de 13 años, sin antecedentes médicos relevantes, que sufrió una caída mientras patinaba, ocasionándole dolor e incapacidad para mover la muñeca izquierda. Fue diagnosticada con una fractura en la parte distal del radio (hueso del antebrazo), específicamente una lesión fisaria clasificada como Peterson tipo I, y se le inmovilizó la muñeca con una férula durante cuatro semanas.\n\n**Hallazgos Clave**  \nDos semanas después de retirar la férula, la paciente volvió a urgencias tras sentir un crujido en la muñeca sin haber realizado un esfuerzo adicional. Presentaba incapacidad para extender (levantar) el primer dedo de la mano izquierda, hinchazón local y asimetría visible en comparación con la mano contraria. La exploración clínica mostró un déficit en la extensión activa del dedo y un signo llamado tenodesis patológico, que indica alteración en la función tendinosa. La resonancia magnética confirmó la ruptura del tendón extensor largo del pulgar (EPL), que es el tendón responsable de estirar el pulgar.\n\n**Interpretación Clínica**  \nLa ruptura espontánea del tendón extensor largo del pulgar es una complicación poco frecuente pero grave que puede ocurrir después de fracturas en la muñeca, incluso cuando el tratamiento inicial es conservador. Debido a la pérdida de función del EPL, se decidió realizar una cirugía para restaurar la movilidad del pulgar. El procedimiento consistió en transferir el tendón extensor propio del índice (EPI), que normalmente mueve el dedo índice, para sustituir la función del tendón lesionado del pulgar. La sutura se realizó mediante una técnica llamada Pulvertaft, que asegura una unión firme entre los tendones.\n\n**Próximos Pasos y Resultados**  \nTras la cirugía, la muñeca se inmovilizó durante cuatro semanas para favorecer la cicatrización. Posteriormente, se permitió la movilidad y la paciente mostró una recuperación completa de la extensión del pulgar sin dolor ni limitaciones funcionales. En los controles realizados a las 6, 12 semanas y al año, no se observaron complicaciones, y la paciente recuperó completamente su actividad habitual, con una puntuación de 0 en la escala PRWE, que indica ausencia de dolor y discapacidad en la muñeca.\n\nEn resumen, este caso ilustra cómo una complicación inesperada tras una fractura en la muñeca puede ser tratada con éxito mediante una transferencia tendinosa, logrando una recuperación funcional completa en una paciente adolescente."
+        }
+    },
+    {
+        "article": "Se remitió a un hombre de 73 años para una SAVR para tratar la regurgitación valvular aórtica sintomática (AR). Dos años antes, había presentado múltiples lesiones exantématicas. Una biopsia de piel reveló infiltración de células plasmáticas, lo que motivó la derivación a un hematólogo. La tomografía computarizada reveló linfadenopatía sistémica y hepatoesplenomegalia. Una biopsia renal realizada por disfunción renal confirmó la amiloidosis AA; una biopsia de ganglios linfáticos mostró plasmocitosis interfolicular y un centro germinal hiperplásico, consistente con el subtipo plasmático de iMCD, apoyado por niveles elevados de IL-6 en plasma. Se administró al paciente TCZ intravenoso (640 mg cada 2 semanas), junto con prednisolona (10 mg diarios). La erupción cutánea y la linfadenopatía se resolvieron. La ecocardiografía reveló AR puro moderado y agrandamiento ventricular izquierdo. Dado que el paciente experimentó gradualmente disnea de esfuerzo con agrandamiento ventricular izquierdo progresivo, se consideró necesaria la SAVR.\n\nDebido al sangrado por hemorroides y a la hepatosplenomegalia, se consultó a un hepatólogo; se diagnosticó cirrosis hepática de Child-Pugh grado A y varices esofágicas. Se realizó una conferencia preoperatoria del equipo, en la que participaron un intensivista y un farmacéutico, en la que se revisaron los mecanismos de acción de TCZ, las posibles complicaciones y el tratamiento perioperatorio. La cirugía se realizó 26 días después de la última dosis de TCZ. Durante el período perioperatorio, se suspendió el tratamiento con TCZ, mientras que se continuó con los esteroides por vía oral o intravenosa. Las medidas preventivas para las infecciones del sitio quirúrgico (SSI) incluyeron la detección de portadores nasales de Staphylococcus aureus resistentes a la meticilina, la preparación antiséptica de la piel, la terapia antibiótica profiláctica y el control de la hiperglucemia. El cultivo nasal fue positivo para Staphylococcus coagulasa negativo. Se realizó el reemplazo de la válvula aórtica quirúrgica a través de una esternotomía media bajo circulación extracorpórea, con 65 minutos de tiempo de isquemia cardiaca y 128 minutos de tiempo de circulación extracorpórea. Se requirieron transfusiones de sangre, incluidos glóbulos rojos, plasma y plaquetas; el paciente fue extubado al día siguiente. Los hallazgos patológicos revelaron un espesamiento fibroso focal sin depósitos amiloides.\n\nLa herida quirúrgica no mostró signos de infección en el día 2 postoperatorio; se inició la terapia de presión negativa en la herida (NPWT) en la herida quirúrgica cerrada para evitar SSI. La terapia de presión negativa en la herida se interrumpió en el día 13 postoperatorio, sin aparente SSI. El paciente fue dado de alta en el día 17 postoperatorio sin ningún signo de infección.\n\nAunque los niveles de IL-6 aumentaron temporalmente los días 1 y 2 después de la operación, disminuyeron progresivamente hasta el día 24 después de la operación, y luego volvieron a aumentar al reanudarse el tratamiento con TCZ. Los niveles de proteína C reactiva (PCR) estaban ligeramente elevados, alcanzando un máximo de 0,56 mg/dL el día 2 después de la operación. Para el día 24 después de la operación, la PCR había aumentado a 1,06 mg/dL sin infección. Antes del aumento de la PCR, los niveles del factor de crecimiento endotelial vascular aumentaron el día 13 después de la operación.\n\nEl paciente no experimentó recurrencia de erupción cutánea o linfadenopatía durante el período perioperatorio. Los niveles de creatinina postoperatorios aumentaron temporalmente, pero volvieron a los niveles preoperatorios el día 24. Se reanudó el tratamiento con tocilizumab el día 30 postoperatorio tras confirmar la ausencia de infección, incluida la IFI.\n",
+        "gold_summary": "Un hombre de 73 años con enfermedad de Castleman, tratado con TCZ, se sometió a un reemplazo de la válvula aórtica por medio de esternotomía mediana para la regurgitación de la válvula aórtica con falta de aire al hacer ejercicio. Se implementaron medidas integrales para prevenir la infección del sitio quirúrgico junto con un examen minucioso durante el período perioperatorio. Tocilizumab se interrumpió 26 días antes de la cirugía y se reanudó 30 días después de la cirugía, durante los cuales los niveles de IL-6 en plasma disminuyeron. No hubo evidencia de infección o exacerbación de la enfermedad de Castleman. Los niveles del factor de crecimiento endotelial vascular aumentaron antes de un aumento en los niveles de proteína C reactiva después del alta hospitalaria y antes de la reanudación de TCZ.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre de 73 años estaba enfermo y tenía problemas en su corazón. Tenía dificultad para respirar cuando caminaba. Los doctores le hicieron una operación para cambiar una parte del corazón llamada válvula.\n\nAntes de la operación, dejaron de darle un medicamento llamado TCZ para que no tuviera problemas. También cuidaron mucho que no se le hiciera una infección en la herida.\n\nDespués de la operación, el hombre se fue mejorando. No tuvo infecciones ni se puso más enfermo. Cuando estuvo listo, le dieron otra vez el medicamento para ayudarlo.\n\nLos doctores vieron que su cuerpo estaba mejor y que el medicamento funcionaba bien. El hombre pudo salir del hospital sin problemas.",
+            "B2": "**Lo que le pasaba al paciente:**  \nUn hombre de 73 años tenía una enfermedad llamada enfermedad de Castleman, que afecta a los ganglios linfáticos y causa inflamación. También tenía un problema en el corazón llamado regurgitación de la válvula aórtica, que significa que la válvula no cerraba bien y eso le causaba dificultad para respirar al hacer ejercicio.\n\n**Qué tratamiento recibió:**  \nPara mejorar su corazón, los médicos le hicieron una cirugía para reemplazar la válvula aórtica. Antes de la operación, el paciente recibía un medicamento llamado tocilizumab (TCZ), que ayuda a controlar la inflamación en la enfermedad de Castleman. Este medicamento se detuvo 26 días antes de la cirugía para evitar problemas durante la operación y se volvió a empezar 30 días después, cuando ya estaba seguro.\n\n**Cómo cuidaron al paciente durante la cirugía:**  \nLos médicos tomaron muchas precauciones para evitar infecciones en la herida de la cirugía. Revisaron si tenía bacterias en la nariz, limpiaron bien la piel antes de operar, usaron antibióticos preventivos y controlaron su azúcar en sangre. Además, usaron una técnica especial llamada terapia de presión negativa en la herida para ayudar a que sanara sin infecciones.\n\n**Qué pasó después de la cirugía:**  \nEl paciente no tuvo infecciones ni empeoramiento de su enfermedad durante el tiempo que estuvo sin tomar el medicamento. Los niveles en sangre de una proteína llamada IL-6, que está relacionada con la inflamación, bajaron después de la cirugía y subieron nuevamente cuando volvió a tomar el medicamento. También observaron cambios en otras proteínas relacionadas con la inflamación, pero el paciente se recuperó bien y pudo salir del hospital sin problemas.\n\n**En resumen:**  \nEste caso muestra que es posible hacer una cirugía importante en un paciente con enfermedad de Castleman que usa tocilizumab, siempre que se tomen medidas cuidadosas para prevenir infecciones y se controle bien el tratamiento antes y después de la operación.",
+            "B3": "**Contexto:**  \nUn hombre de 73 años con diagnóstico de enfermedad de Castleman idiopática multicéntrica (iMCD), un trastorno inflamatorio caracterizado por crecimiento anormal de ganglios linfáticos y producción elevada de interleucina-6 (IL-6), fue tratado con tocilizumab (TCZ), un medicamento que bloquea la acción de esta proteína inflamatoria. Además, presentaba regurgitación valvular aórtica (fuga en la válvula del corazón que permite el retorno de sangre), que causaba dificultad progresiva para respirar durante el esfuerzo, y se decidió realizar un reemplazo quirúrgico de la válvula aórtica (SAVR) mediante una incisión en el esternón (esternotomía media).\n\n**Hallazgos Clave y Manejo Perioperatorio:**  \nAntes de la cirugía, el paciente recibió cuidados especializados para minimizar el riesgo de infecciones en el sitio quirúrgico, incluyendo la detección y manejo de bacterias en la nariz, preparación cuidadosa de la piel, uso profiláctico de antibióticos y control estricto del azúcar en sangre. El tratamiento con tocilizumab se suspendió 26 días antes de la operación para reducir posibles complicaciones inmunológicas, mientras que la administración de esteroides continuó para controlar la inflamación. La cirugía se realizó con éxito bajo circulación extracorpórea (máquina que mantiene la circulación y oxigenación de la sangre durante la operación), requiriendo transfusiones de sangre, y el paciente fue extubado al día siguiente sin complicaciones inmediatas.\n\nDurante el postoperatorio, no se observaron signos de infección en la herida quirúrgica, y se utilizó terapia de presión negativa (una técnica para favorecer la cicatrización y prevenir infecciones) hasta el día 13 después de la cirugía. El paciente fue dado de alta el día 17 sin evidencia de infección ni recurrencia de los síntomas de la enfermedad de Castleman, como erupciones cutáneas o aumento de ganglios linfáticos.\n\n**Interpretación Clínica:**  \nLos niveles de IL-6 en plasma aumentaron temporalmente en los primeros días tras la cirugía, lo cual es esperado debido a la respuesta inflamatoria postoperatoria, pero luego disminuyeron progresivamente hasta el día 24. Posteriormente, al reanudarse el tratamiento con tocilizumab el día 30, los niveles de IL-6 volvieron a aumentar, reflejando la acción del medicamento. La proteína C reactiva (PCR), un marcador de inflamación, mostró un leve aumento sin evidencia de infección, y se observó un incremento previo en el factor de crecimiento endotelial vascular, una proteína relacionada con la reparación y formación de vasos sanguíneos, lo que podría indicar procesos de recuperación tisular.\n\nLa función renal mostró un aumento temporal en los niveles de creatinina después de la cirugía, pero volvió a los valores previos al alta, indicando una recuperación adecuada de la función renal.\n\n**Próximos Pasos y Conclusiones:**  \nEl manejo cuidadoso del tratamiento inmunosupresor y las medidas preventivas implementadas permitieron realizar con éxito el reemplazo valvular en un paciente con enfermedad de Castleman sin complicaciones infecciosas ni exacerbación de la enfermedad. La reanudación del tocilizumab se realizó de forma segura tras confirmar la ausencia de infección. Este caso resalta la importancia de una planificación multidisciplinaria y un seguimiento riguroso en pacientes con enfermedades inflamatorias complejas sometidos a cirugía mayor."
+        }
+    },
+    {
+        "article": "Se trata de un paciente de sexo masculino de cuatro meses de edad, originario del centro de México y con dos hermanos hombres sanos. Durante el primer trimestre de gestación, su madre hipotiroidea consumió drogas. No obstante, el infante nació con peso y talla adecuados, fue alimentado con leche materna y recibió la vacuna del bacilo de Calmette-Guérin (BCG), sin desarrollo de cicatriz. La madre del paciente era prisionera en una cárcel y, junto con el bebé, compartían una celda insalubre con dos personas más.A los cuatro meses, el paciente fue valorado médicamente por un tumor doloroso en la región axilar izquierda. En la radiografía de tórax se observaron imágenes sugestivas de fracturas costales; se sospechó de maltrato infantil por parte de la madre, y el infante fue hospitalizado en un hospital pediátrico. Se determinó el peso (4.190 g) y la talla (58 cm) –por debajo del percentil tres–, saturación de oxígeno del 70 %, fiebre, tos, aumento de volumen en la región axilar izquierda, además de dolor, rubor y calor. En el cuadro hemático se encontró: hemoglobina de 8,8 g/dl (11,0 - 12,6), 29,3 × 109 leucocitos/L (6,0 - 17,5), 18,4 × 109 neutrófilos/L (1,0 - 8,5), 7,0 × 109 linfocitos/L (4,0 - 13,5), 3,5 × 109 monocitos/L, 459 × 109 plaquetas/L (150 - 350) y proteína C reactiva igual a 16 mg/L (< 3,0). En la primera tomografía toracoabdominal se observaron imágenes de un absceso en la región axilar izquierda, lesiones líticas en las costillas 3 a 6, neumonía apical izquierda, nódulos pulmonares en ambos pulmones y ganglios linfáticos cervicales y mediastinales incrementados de tamaño. En la biopsia del absceso axilar izquierdo se reportó miositis y paniculitis supurativa. Solo se hizo cultivo para bacterias del líquido broncoalveolar, el cual fue negativo, y la PCR para el complejo Mycobacterium tuberculosis fue negativa. Después de 41 días de hospitalización y de haber recibido dos esquemas de antimicrobianos –ceftriaxona-clindamicina y cefepima-vancomicina–, el paciente fue dado de alta.\n\nDos meses después, a los ocho meses de edad, reingresó al hospital por fiebre, irritabilidad y un absceso supurante en la escápula izquierda. En el cuadro hemático se encontró: hemoglobina de 10,8 g/dl (10,5 - 12), 21,2 × 109 leucocitos/L (6 - 17), 12,2 × 109 neutrófilos/L (1,5 - 8,5), 7,5 × 109 linfocitos/L (4 - 10,5), 1,2 × 109 monocitos/L (600), y 583 × 109 plaquetas/L (150 - 350); la prueba para la detección sérica de HIV fue negativa. En la tomografía de tórax se observó una consolidación apical izquierda, bronquiectasias, lesiones líticas en las costillas 2 a 7 y en las vértebras dorsales 2 a 7, además de una colección de líquido multiloculado; en el ultrasonido se encontró una fístula asociada con el absceso escapular. El paciente recibió piperacilina-tazobactam, que se sustituyó después por voriconazol al detectarse Aspergillus fumigatus en el cultivo de la muestra de secreción del absceso. Dada la recurrencia y la gravedad de la infección, se sospechó un error innato de la inmunidad. La prueba de dihidrorrodamina resultó sin producción de especies reactivas de oxígeno y la expresión de gp91phox en los neutrófilos fue nula, estableciéndose así el diagnóstico de enfermedad granulomatosa crónica ligada al cromosoma X. La variante patógena detectada por la secuenciación de nueva generación fue c.80_83del/Y (p.Val27Glyfs*33) en CYBB. La madre resultó portadora de la variante (c.80_83del/WT). No fue posible estudiar genéticamente a sus dos hermanos mayores, de sexo masculino, y aparentemente sanos. El paciente fue dado de alta después de 65 días de hospitalización y tratamiento con voriconazol por 28 días. Se inició profilaxis antibiótica diaria con trimetoprim-sulfametoxazol y profilaxis antifúngica con fluconazol dos veces a la semana. Dos meses después, al año de edad, el infante reingresó debido a una neumonía multifocal, por la cual requirió asistencia respiratoria mecánica. Se detectó el antígeno galactomanano en el suero y A. fumigatusen el cultivo del líquido del lavado broncoalveolar, por lo que se inició nuevamente tratamiento con voriconazol. El paciente sufrió una falla orgánica múltiple y falleció un mes después de su ingreso.\n",
+        "gold_summary": "Se presenta el caso de un infante con enfermedad granulomatosa crónica y aspergilosis invasiva. Se trata de un lactante de sexo masculino de cuatro meses de edad, de madre hipotiroidea y con quien convive en la celda de la cárcel. El infante presentó tumores en la región axilar izquierda y la radiografía de tórax sugirió fracturas costales; fue hospitalizado ante la sospecha de maltrato infantil. En la tomografía de tórax se observó un absceso axilar, osteólisis de costillas, neumonía y nódulos pulmonares; el paciente recibió antibióticos de amplio espectro y fue dado de alta. A los ocho meses, reingresó por fiebre y extensión del absceso purulento hacia la región escapular izquierda; en la tomografía se observaron imágenes de empeoramiento de la condición. Se aisló Aspergillus fumigatus de la secreción del absceso y se diagnosticó aspergilosis invasiva; se inició tratamiento con voriconazol por 28 días. Mediante la prueba de dihidrorrodamina, se diagnosticó enfermedad granulomatosa crónica causada por la variante patógena c.80_83del/Y del gen CYBB, portada por la madre (c.80_83del/WT). A los 12 meses, el paciente reingresó nuevamente por aspergilosis invasiva, resistente al tratamiento, con desenlace fatal.",
+        "synthetic_summary": {
+            "B1": "Había un bebé que estaba muy enfermo. Tenía un bulto doloroso en su brazo y problemas para respirar. Los doctores lo cuidaron mucho y le dieron medicinas para que mejorara.\n\nDespués, el bebé se volvió a enfermar. Tenía fiebre y otro bulto que dolía mucho. Los doctores encontraron un hongo que le hacía daño. Le dieron medicinas especiales para el hongo.\n\nLos doctores hicieron pruebas y vieron que el bebé tenía un problema en su cuerpo que no lo dejaba pelear bien contra las enfermedades. Su mamá también tenía ese problema, pero no estaba enferma.\n\nEl bebé estuvo en el hospital muchas veces. Aunque los doctores hicieron todo lo posible, el bebé se puso muy mal y no pudo mejorar. Los doctores y su familia lo cuidaron con mucho amor.",
+            "B2": "**Caso de un Bebé con Problemas en el Sistema Inmunológico y una Infección Grave**\n\nEste es el caso de un bebé de cuatro meses que vivía con su madre en una cárcel. Su madre tenía problemas de tiroides y durante el embarazo tomó medicamentos. El bebé nació con buen peso y tamaño, pero luego presentó un bulto doloroso en la axila izquierda. Al hacerle una radiografía, los médicos vieron posibles fracturas en sus costillas, por lo que pensaron que podría estar sufriendo maltrato. Fue hospitalizado para recibir atención.\n\nEn estudios más detallados, encontraron un absceso (una acumulación de pus) en la axila, daño en varias costillas, neumonía y nódulos en los pulmones. El bebé recibió antibióticos fuertes y fue dado de alta después de mejorar un poco.\n\nA los ocho meses, volvió al hospital con fiebre y un absceso que se extendió hacia la parte superior de la espalda. Nuevas imágenes mostraron que la infección había empeorado. En el pus del absceso encontraron un hongo llamado Aspergillus fumigatus, que puede causar infecciones graves, especialmente en personas con defensas bajas. Por eso, le dieron un medicamento antifúngico llamado voriconazol.\n\nLos médicos sospecharon que el bebé tenía un problema en su sistema inmunológico, que es el que nos protege de las infecciones. Hicieron una prueba llamada dihidrorrodamina, que mostró que sus células defensivas no podían producir sustancias necesarias para combatir gérmenes. Esto confirmó que tenía una enfermedad llamada enfermedad granulomatosa crónica, que afecta la capacidad del cuerpo para luchar contra ciertas infecciones. Esta enfermedad fue causada por un cambio en un gen llamado CYBB, que heredó de su madre.\n\nA pesar del tratamiento, a los 12 meses el bebé volvió a enfermar gravemente por la misma infección de Aspergillus. La infección no respondió bien a los medicamentos y, lamentablemente, el bebé falleció debido a una falla de varios órganos.\n\n**Qué Significa Este Caso**\n\nEste caso muestra cómo un problema genético en el sistema inmunológico puede hacer que un bebé sea muy vulnerable a infecciones graves, como las causadas por hongos. También resalta la importancia de diagnosticar estas enfermedades temprano para intentar proteger a los pacientes con tratamientos adecuados.",
+            "B3": "**Contexto**  \nSe describe el caso de un lactante varón de cuatro meses originario del centro de México, cuya madre presentaba hipotiroidismo y con quien vivía en condiciones precarias dentro de una cárcel. El bebé nació con peso y talla adecuados, pero a los cuatro meses desarrolló un tumor doloroso en la axila izquierda. Ante la sospecha inicial de maltrato infantil, debido a fracturas costales observadas en radiografías, fue hospitalizado para evaluación y tratamiento.\n\n**Hallazgos Clave**  \nDurante la hospitalización inicial, las imágenes de tomografía mostraron un absceso en la axila izquierda, lesiones destructivas en varias costillas (osteólisis), neumonía en el lóbulo superior del pulmón izquierdo y nódulos pulmonares bilaterales, además de ganglios linfáticos aumentados de tamaño. El análisis de sangre reveló anemia, elevación de leucocitos y marcadores inflamatorios, indicativos de infección activa. A pesar de recibir antibióticos de amplio espectro, el paciente presentó recurrencia de la infección a los ocho meses, manifestada por fiebre y un absceso supurante que se extendió hacia la región escapular izquierda. Nuevas imágenes mostraron empeoramiento con consolidación pulmonar, bronquiectasias (dilatación anormal de las vías respiratorias), lesiones óseas adicionales y formación de fístulas. En el cultivo de la secreción del absceso se aisló Aspergillus fumigatus, un hongo que causa infecciones invasivas en personas con alteraciones inmunológicas.\n\n**Interpretación Clínica**  \nLa recurrencia y gravedad de las infecciones, junto con la presencia de infecciones fúngicas invasivas, sugirieron un defecto en la inmunidad innata. La prueba funcional de dihidrorrodamina, que evalúa la capacidad de los neutrófilos (un tipo de glóbulo blanco) para producir especies reactivas de oxígeno necesarias para eliminar microorganismos, fue negativa. Además, no se detectó la proteína gp91^phox en neutrófilos, confirmando el diagnóstico de enfermedad granulomatosa crónica ligada al cromosoma X, una condición genética que afecta la capacidad del sistema inmunitario para combatir ciertas infecciones. La secuenciación genética identificó una mutación patógena específica (c.80_83del/Y) en el gen CYBB, responsable de esta enfermedad, y se confirmó que la madre era portadora de esta variante.\n\n**Próximos Pasos y Evolución**  \nTras el diagnóstico, el paciente recibió tratamiento antifúngico con voriconazol y profilaxis antibiótica y antifúngica para prevenir nuevas infecciones. Sin embargo, a la edad de un año, volvió a ingresar al hospital con neumonía multifocal grave causada nuevamente por Aspergillus fumigatus, que requirió soporte respiratorio avanzado. A pesar del tratamiento, el paciente desarrolló falla orgánica múltiple y falleció un mes después.\n\n**Resumen Final**  \nEste caso ilustra la presentación clínica y evolución de un lactante con enfermedad granulomatosa crónica ligada al cromosoma X, caracterizada por infecciones recurrentes graves, incluyendo aspergilosis invasiva. La identificación temprana de esta enfermedad genética es crucial para el manejo adecuado y la prevención de complicaciones fatales, aunque en este caso la gravedad y recurrencia de las infecciones condujeron a un desenlace fatal."
+        }
+    },
+    {
+        "article": "Se trata de un hombre de 66 años de edad que vive en la ciudad de Juan Bautista Alberdi de la provincia de Buenos Aires, con antecedentes de hipertensión arterial y trastorno obsesivo compulsivo. Su medicación habitual incluía amlodipina, quetiapina, venlafaxina y ácido valproico. Consultó por presentar fiebre de 39ºC de cuatro días de evolución sin síntomas asociados y se internó para estudio en sala general. Al examen de ingreso se constató un paciente lúcido, sin foco motor, sin trastorno sensitivo ni rigidez de nuca (escala de coma de Glasgow (GCS) 15/15). El resto del examen físico y el laboratorio general no presentaron particularidades. Los cultivos de sangre y orina resultaron negativos, y la tomografía computarizada de encéfalo, tórax, abdomen y pelvis no mostró afecciones. A las 24 horas agregó episodios de desorientación témporo-espacial que alternaban con otros de somnolencia (GCS 13/15). Al examen físico se constató temblor grueso distal en los cuatro miembros. El examen del LCR informó: líquido incoloro, límpido, y aspecto post centrifugado también límpido. Recuento de leucocitos 310/mm3 (mononucleares 54%, polimorfonucleares 46%), hematíes < de 1000/mm3, proteínas 0.76 g/l, glucosa 54 mg/dl (glucemia 120 mg/dl), y ácido láctico 21 mg/dl. Se inició tratamiento empírico con aciclovir 10 mg/kg endovenoso cada 8 horas. Se solicitaron en LCR: PCR para virus de herpes simple (VHS) y para virus de encefalopatía equina del oeste (VEEO) que resultaron no reactivas. Sin embargo, la IgM (ELISA) para EEO resultó positiva en suero y en LCR a los diez días. La RMN de encéfalo evidenció aumento en la intensidad en secuencias FLAIR y T2 a nivel de la región dorsal del tronco encefálico (tanto protuberancial, como también bulbar y mesencefálico), ambos pedúnculos cerebrales y ganglios de la base, con afectación bilateral y ligero predominio ganglio basal derecho. También se observaron múltiples imágenes focales hiperintensas en la sustancia blanca de ambos hemisferios cerebrales. El paciente evolucionó con deterioro del sensorio (GCS 8/15), sin protección de la vía aérea, por lo que ingresó a UTI. Requirió intubación y ventilación mecánica, con utilización de sedación y analgesia. Al ingreso a UTI presentaba: estado ácido-base (EAB) arterial: pH 7.11, pCO2 136 mmHg, pO2 75 mmHg, bicarbonato 43 mEq/l, exceso de base 11 mEq/l, saturación 88% (Con FIO2 21%), ácido láctico 11.5 mg/dl. Se inició la ventilación mecánica con un volumen minuto respiratorio (VMR) de 9.8 litros (volumen tidal 490 ml que corresponde a 6 ml/kg de peso teórico, frecuencia respiratoria 20 por minuto, presión positiva al final de espiración (PEEP) 5 cmH2 O, fracción inspirada de oxígeno 30%) se extrajo sangre para EAB arterial: pH 7.40, pCO2 41 mmHg, pO2 65 mmHg, bicarbonato 28 mEq/l, exceso de base 0 mEq/l, saturación 93%, PAFI 216. Evolucionó sin fiebre, estable hemodinámicamente, con adecuada oxigenación y ritmo diurético. Al suspender sedantes presentó GCS de 3 puntos sobre 10 (correspondiente con evaluación ocular 1 y motor 2 puntos), con rigidez generalizada y reflejos osteotendinosos adecuados, con movimientos rítmicos linguales y peribucales. El electroencefalograma de 12 canales no evidenció descargas patológicas. Al décimo día de inicio de los síntomas presentó apertura ocular y menor rigidez, pero no toleraba la modalidad respiratoria espontánea por hipoventilación e hipercapnia que lo llevaron a hipoxemia transitoria. En el EAB arterial presentó: pH 7.31, pCO2 70 mmHg, pO2 76 mmHg, bicarbonato 35 mEq/l, exceso de base 8 mEq/l bajo asistencia ventilatoria en modalidad espontánea de presión soporte de 5 cmH2 O, frecuencia respiratoria 6 por minuto, PEEP 5 cmH2 O y volumen tidal entre 120-150 ml. Los siguientes días el paciente se conectó, respondiendo órdenes simples y complejas, y movilizó simétricamente los miembros con cierta debilidad. Por intolerancia a las pruebas ventilatorias espontáneas fue traqueostomizado. En la evaluación funcional respiratoria presentaba presión inspiratoria máxima menor a -40 cm de H2 O, presión espiratoria máxima mayor a 80 cm de H2 O, pero continuaba con hipercapnia en la prueba ventilatoria espontánea, por lo que requirió soporte ventilatorio con modalidad controlada. Se realizó ecocardiograma transtorácico que informó cavidades derechas normales, sin signos de hipertensión pulmonar. En la nueva RMN de encéfalo se evidenció disminución de las áreas hiperintensas en secuencias FLAIR y T2 visibles previamente.\n\nEl enfermo evolucionó con requerimiento de menor soporte ventilatorio en forma progresiva al momento del desarrollo de este informe.",
+        "gold_summary": "Presentamos el caso de un varón de 66 años de edad oriundo de la ciudad Juan Bautista Alberdi de la provincia de Buenos Aires con antecedentes de hipertensión arterial y trastorno obsesivo compulsivo. Consultó por fiebre súbita de cuatro días de evolución, con desarrollo de encefalopatía durante su internación. La punción lumbar mostró un líquido cefalorraquídeo cristalino, aunque inflamatorio de predominio mononuclear. La RMN de encéfalo informó hiperintensidad en secuencias FLAIR y T2 en el dorso del tronco encefálico. Ingresó a terapia intensiva por deterioro neurológico y acidosis respiratoria grave, requiriendo asistencia ventilatoria mecánica. Luego de 10 días presentó mejoría neurológica, sin déficit motor pero con hipoventilación alveolar que dificultaron el destete del respirador.",
+        "synthetic_summary": {
+            "B1": "Un hombre de 66 años se puso muy enfermo. Tenía fiebre y estaba confundido. Los doctores le hicieron una prueba con líquido de su espalda. El líquido estaba un poco inflamado. Le hicieron fotos especiales a su cabeza y vieron partes que estaban diferentes. El hombre tuvo que ir a un lugar especial del hospital para que lo cuidaran mucho. No podía respirar bien solo y necesitó una máquina para ayudarlo a respirar. Después de 10 días, empezó a mejorar y podía moverse bien. Pero todavía le costaba respirar sin la máquina. Los doctores lo están cuidando para que se ponga mejor.",
+            "B2": "**Caso de un Hombre con Fiebre y Problemas Cerebrales**\n\nUn hombre de 66 años, que vivía en Juan Bautista Alberdi, Buenos Aires, tenía antecedentes de presión alta y un trastorno llamado obsesivo compulsivo. Él llegó al hospital porque tenía fiebre alta durante cuatro días. Al principio, estaba consciente y sin problemas en sus movimientos o sensibilidad.\n\n**Lo que Encontraron**\n\nDespués de un día, empezó a confundirse y a estar somnoliento. Le hicieron una punción lumbar, que es cuando se extrae un poco de líquido del cerebro para analizarlo. Este líquido estaba claro pero mostraba signos de inflamación, especialmente con células llamadas mononucleares, que son parte del sistema inmunológico. Una resonancia magnética (una imagen del cerebro) mostró zonas inflamadas en una parte del cerebro llamada tronco encefálico.\n\n**Qué Pasó Después**\n\nSu estado empeoró y tuvo problemas para respirar bien, por lo que fue llevado a la unidad de cuidados intensivos. Allí, necesitó un respirador para ayudarle a respirar porque su cuerpo no eliminaba bien el dióxido de carbono, lo que causaba un problema llamado acidosis respiratoria. Después de 10 días, mejoró en cuanto a la conciencia y no tenía problemas para mover sus brazos y piernas, pero seguía teniendo dificultades para respirar por sí solo, lo que complicó que pudiera dejar el respirador.\n\n**Resumen**\n\nEste caso muestra cómo una infección o inflamación en el cerebro puede causar fiebre, confusión y problemas graves para respirar. Aunque el paciente mejoró su estado mental y motor, la función respiratoria tardó más en recuperarse.",
+            "B3": "**Contexto**  \nSe trata de un hombre de 66 años con antecedentes de hipertensión arterial y trastorno obsesivo compulsivo, que residía en Juan Bautista Alberdi, provincia de Buenos Aires. Fue hospitalizado tras presentar fiebre alta (39ºC) durante cuatro días sin otros síntomas iniciales. En el ingreso, estaba consciente y sin signos neurológicos focales, pero a las 24 horas desarrolló episodios alternantes de desorientación y somnolencia, junto con temblor en las extremidades.\n\n**Hallazgos Clave**  \n- La punción lumbar reveló un líquido cefalorraquídeo (LCR) claro pero con signos de inflamación, mostrando un aumento de leucocitos con predominio mixto (mononucleares y polimorfonucleares), proteínas elevadas y glucosa normal.  \n- Los cultivos de sangre y orina fueron negativos, así como las pruebas PCR para virus herpes simple y encefalopatía equina del oeste en LCR. Sin embargo, la detección de anticuerpos IgM específicos para encefalopatía equina del este (EEO) fue positiva tanto en suero como en LCR, confirmando la infección viral.  \n- La resonancia magnética (RMN) cerebral mostró áreas de mayor intensidad en secuencias FLAIR y T2 localizadas en la región dorsal del tronco encefálico (incluyendo protuberancia, bulbo y mesencéfalo), ambos pedúnculos cerebrales y ganglios basales, con afectación bilateral y predominio en el ganglio basal derecho. También se observaron múltiples lesiones en la sustancia blanca de ambos hemisferios cerebrales.  \n- El paciente presentó deterioro neurológico progresivo con disminución del nivel de conciencia (escala de Glasgow reducida a 8/15), requiriendo ingreso a unidad de terapia intensiva (UTI), intubación y ventilación mecánica debido a insuficiencia respiratoria con acidosis respiratoria grave (pH 7.11, pCO2 136 mmHg).  \n- Posteriormente, mostró mejoría neurológica parcial, con apertura ocular y respuesta a órdenes simples, sin déficit motor significativo, pero persistió con hipoventilación alveolar (disminución de la capacidad para ventilar adecuadamente los pulmones), lo que dificultó el destete de la ventilación mecánica y motivó la realización de traqueostomía.  \n- La RMN de control evidenció reducción de las lesiones inflamatorias previamente observadas.\n\n**Interpretación Clínica**  \nEl cuadro clínico y los estudios complementarios son compatibles con una encefalitis viral causada por el virus de la encefalopatía equina del este, una infección poco frecuente en humanos pero con potencial severo. La inflamación del tronco encefálico y ganglios basales explica el deterioro neurológico y la afectación respiratoria, dado que estas áreas controlan funciones vitales como la respiración. La hipoventilación persistente refleja compromiso del centro respiratorio, dificultando la recuperación completa y la independencia ventilatoria.\n\n**Próximos Pasos**  \nEl manejo continuó con soporte ventilatorio adaptado a la capacidad respiratoria del paciente, monitorización neurológica estrecha y seguimiento por imágenes para evaluar la evolución de las lesiones cerebrales. Se recomienda rehabilitación neurológica y respiratoria para mejorar la función muscular y ventilatoria. Además, es fundamental mantener vigilancia para posibles complicaciones infecciosas o neurológicas asociadas. El pronóstico dependerá de la recuperación neurológica y la capacidad para mantener una ventilación adecuada sin soporte mecánico."
+        }
+    },
+    {
+        "article": "Mujer de 27 años de edad oriunda del interior de la Provincia de Buenos Aires sin antecedentes personales o familiares de relevancia, consultó por sangrado vaginal. El estudio colposcópico evidenció formación polipoide que protruía por el orificio cervical externo (OCE). Se arribó clínicamente al diagnóstico de mioma nascens y se tomó una muestra de biopsia para su evaluación. Ante el diagnóstico patológico de sarcoma, se instauró quimioterapia, con el fin de reducir la masa lesional. Una vez lograda la reducción del tamaño, se decidió derivarla a nuestra institución para realizar tratamiento quirúrgico. Se recibió una pieza de histerectomía total con anexos, f ijada en formol al 10%. Cuerpo de 5 × 5 × 3.2 cm, cuello de 3.5 × 3 × 2 cm, ambas trompas de 4.5 × 0.7 cm y ovarios de 4 × 2.5 × 2.5 cm. A la apertura de la pieza, se observó a nivel de la unión cérvico-ístmica una formación polipoide pediculada de 8.5 cm de diámetro, que emergía hacia el canal endocervical y se exteriorizaba por el OCE. La superficie externa era parda, lobulada, con sectores rojizos. Al corte, se observaba blanquecina, blanda, con sectores de aspecto gelatinoso y formaciones quísticas de hasta 0,6 cm de dimensión máxima. Luego del procesamiento de rutina, se efectuaron secciones histológicas y se colorearon con hematoxilina-eosina (H-E), las cuales evidenciaron sectores celulares alternados por áreas laxas, mixoides junto a glándulas ístmico-endometriales típicas. La proliferación, predominantemente fusocelular atípica se disponía en nidos, constituidos por células de amplio citoplasma eosinófilo y núcleos excéntricos con cromatina homogénea, algunos pleomórficos. Se apreciaron estriaciones citoplasmáticas transversales en dichas células. El estroma era ampliamente mixoide y ricamente vascularizado. Se destacaban focalmente áreas celulares densamente condensadas inmediatas y próximas al revestimiento epitelial intacto, pero separadas de él, por una fina capa de estroma laxo. Esto se conoce como cambium layer o capa cambial. Se realizaron técnicas de inmunohistoquímica para desmina, actina músculo específico (AME) y miogenina (MYF4), las cuales resultaron positivas, mientras que la actina músculo liso fue negativa. Esta inmunomarcación permitió comprobar la estirpe muscular estriada y en última instancia arribar al diagnóstico, junto al cuadro morfológico, de RMS embrionario. Asimismo, la presencia de rabdomioblastos agrupados constituyendo la capa cambial a nivel subepitelial resultó fundamental y necesario para tipificar al RMS embrionario como botrioide, independientemente de la presentación macroscópica en forma de racimos polipoides.",
+        "gold_summary": "Presentamos el caso de una mujer de 27 años que consultó por sangrado vaginal y en quien se evidenció en la colposcopia, una lesión polipoide blanquecina que se exteriorizaba a través del orificio cervical externo. El estudio histológico reveló sectores celulares alternados por áreas laxas, mixoides, junto a glándulas ístmico-endometriales típicas. La proliferación fusocelular atípica, se disponía en nidos, constituidos por células de amplio citoplasma eosinófilo con estriaciones citoplasmáticas transversales y núcleos excéntricos con cromatina homogénea. Se exhibían áreas de células densamente condensadas inmediatas y próximas al revestimiento epitelial intacto, pero separadas de él, por una fina capa de estroma laxo (capa cambial). El perfil de inmunomarcación resultó positivo para desmina, actina músculo específico y miogenina, y negativo para actina músculo liso. Se realizó diagnóstico de rabdomiosarcoma embrionario botroide de cuerpo uterino.",
+        "synthetic_summary": {
+            "B1": "Una mujer joven tenía sangrado y una bolita en su cuerpo. Los doctores miraron la bolita con cuidado. Vieron que estaba hecha de muchas células diferentes. Estas células eran especiales y venían de un músculo. Los doctores dijeron que la bolita era un tipo de enfermedad que necesita tratamiento. Ellos cuidarán mucho a la mujer para ayudarla a estar mejor.",
+            "B2": "Caso de una mujer joven con sangrado vaginal\n\nUna mujer de 27 años fue al médico porque tenía sangrado vaginal. Al examinarla con un colposcopio (un instrumento que permite ver el cuello del útero), encontraron una lesión con forma de pólipo que salía por el orificio del cuello uterino. Esta lesión era de color blanquecino y tenía una superficie irregular.\n\nLo que encontraron en el laboratorio\n\nSe tomó una muestra de la lesión para analizarla bajo el microscopio. Los científicos vieron diferentes tipos de células: algunas estaban agrupadas en nidos y tenían un citoplasma (la parte de la célula fuera del núcleo) amplio y con un color rosado. Estas células también mostraban unas líneas transversales llamadas estriaciones, que indican que son células musculares especiales. Cerca de la superficie de la lesión, había una capa delgada de células muy densas, separadas del revestimiento normal por una capa de tejido blando llamada estroma laxo. Esta capa se llama “capa cambial” y es característica de ciertos tumores.\n\nCómo confirmaron el diagnóstico\n\nPara saber qué tipo de tumor era, usaron pruebas especiales que detectan proteínas en las células. Encontraron que las células tenían proteínas llamadas desmina, actina músculo específico y miogenina, que están presentes en músculos estriados (los músculos que usamos para movernos). No encontraron actina de músculo liso, que es otro tipo de músculo. Con esta información y la apariencia de las células, diagnosticaron un rabdomiosarcoma embrionario botrioide. Este es un tipo raro de tumor canceroso que se origina en células musculares jóvenes y se presenta en el cuerpo uterino.\n\nEn resumen, esta paciente tenía un tumor maligno muscular en el cuello del útero que se identificó gracias a la combinación de estudios visuales, microscópicos y de proteínas. El diagnóstico permitió iniciar un tratamiento adecuado para su condición.",
+            "B3": "**Contexto**  \nSe presenta el caso de una mujer joven de 27 años, sin antecedentes médicos relevantes, que consultó debido a sangrado vaginal. Durante la colposcopia (un examen visual del cuello uterino), se identificó una lesión con forma de pólipo blanquecino que sobresalía a través del orificio cervical externo (la abertura del cuello uterino hacia la vagina). Inicialmente, se sospechó un mioma nascens (un tipo de tumor benigno), pero la biopsia reveló un diagnóstico diferente.\n\n**Hallazgos Clave**  \nEl análisis microscópico del tejido mostró una combinación de áreas celulares densas y otras más laxas con características mixoides (tejido con apariencia gelatinosa), junto con glándulas típicas del istmo y endometrio (zonas del cuello y cuerpo uterino). La proliferación celular predominante estaba formada por células fusiformes (alargadas) atípicas organizadas en grupos o nidos. Estas células tenían un citoplasma amplio y rosado (eosinófilo), con estriaciones transversales visibles en el citoplasma, y núcleos excéntricos con cromatina homogénea, aunque algunos mostraban variabilidad en forma y tamaño (pleomorfismo).  \n\nAdemás, se observaron áreas específicas de células muy condensadas justo debajo del revestimiento epitelial intacto, separadas de este por una delgada capa de tejido conectivo laxo, conocida como “capa cambial”. Esta característica es importante para clasificar el tumor.  \n\nLas pruebas inmunohistoquímicas, que detectan proteínas específicas en las células, mostraron positividad para desmina, actina músculo específico y miogenina, marcadores que indican la presencia de células musculares estriadas (músculo esquelético). Por otro lado, la actina de músculo liso fue negativa, lo que ayudó a descartar otros tipos de tumores musculares.\n\n**Interpretación Clínica**  \nCon base en las características morfológicas y los resultados inmunohistoquímicos, se estableció el diagnóstico de rabdomiosarcoma embrionario botrioide, un tipo raro y agresivo de tumor maligno que se origina en células musculares estriadas y que en este caso afectaba el cuello uterino. La presencia de la capa cambial y la agrupación de rabdomioblastos (células tumorales características) fueron fundamentales para identificar esta variante específica.\n\n**Próximos Pasos**  \nTras el diagnóstico, la paciente recibió tratamiento con quimioterapia para reducir el tamaño del tumor. Posteriormente, se realizó una cirugía de histerectomía total con anexos (extirpación del útero, trompas y ovarios) para eliminar completamente la lesión. El seguimiento y manejo continuarán en función de la respuesta al tratamiento y la evolución clínica.  \n\nEste caso resalta la importancia de una evaluación cuidadosa y multidisciplinaria para diagnosticar correctamente tumores poco comunes que pueden presentarse con síntomas comunes como el sangrado vaginal."
+        }
+    },
+    {
+        "article": "Un hombre de 53 años de edad, que inició diálisis por disfunción renal en etapa terminal debido a nefropatía diabética o nefroesclerosis en nuestro departamento de nefrología 10 años antes, se sometió a una ecocardiografía de seguimiento anual para estenosis valvular aórtica progresiva (AVS) y regurgitación moderada con fracción de eyección ventricular izquierda (LVEF) normal. Un año antes, se observaron calcificaciones que sugerían MAC en el anillo mitral posterior, que no se habían visto dos años antes. En el último seguimiento, la ecocardiografía reveló una masa redonda de superficie lisa de 22 × 17 mm con alta ecogenicidad en el área circundante y un brillo interno ligeramente disminuido en el anillo mitral posterior del lado auricular izquierdo. El paciente no tenía síntomas significativos ni hallazgos físicos, excepto un soplo sistólico.\n\nLa ecocardiografía también reveló una VS moderada con un flujo de pico valvular transaórtico de 3,76 m/s y una regurgitación valvular aórtica moderada. Se observó una regurgitación mitral leve pero no estenosis. El patrón de velocidad de flujo de entrada del VI mostró un patrón pseudo-normal con un agrandamiento de la aurícula izquierda de 47 mm de diámetro. La ecocardiografía en serie durante dos años reveló un agrandamiento del VI y una disminución de la FEVI. El diámetro final diastólico/final sistólico del VI y la FEVI fueron de 50/33 mm y 64 %, respectivamente, hace dos años; 57/41 mm y 52 % hace un año; y 59/47 mm y 42 % en el último seguimiento.\n\nTeniendo en cuenta el estado de la hemodiálisis, predijimos la progresión a una AVS casi severa, con empeoramiento de la disfunción sistólica del LV, que se convertiría en una indicación para el reemplazo de la válvula aórtica (AVR) en un futuro cercano.\n\nLa tomografía computarizada (TC) reveló una masa de alta densidad sin realce de contraste. La resonancia magnética (MRI) mostró una masa bien definida de alta intensidad en el centro, con un borde hipointenso en la imagen T1 y una señal desprovista en T2. Se excluyeron los neoplasmas, incluidos los mixomas y los fibroelastomas papilares, en función de sus características de imagen. Los hallazgos de laboratorio no indicaron infección, y no se sospechó de vegetación con endocarditis infecciosa. Teniendo en cuenta la disfunción renal en etapa terminal en la hemodiálisis y los hallazgos de imagen, se sospechó CCMA. El rápido agrandamiento de la masa generó preocupación sobre una potencial embolia. En consecuencia, la masa se resecó con AVR.\n\nLa incisión del atrio izquierdo reveló una masa por debajo del endocardio auricular en el anillo de la válvula mitral (P1-2); se observaron sustancias cremosas en la incisión de la masa, lo que sugiere CCMA. Después de la extirpación y desbridamiento del tejido, el sitio de la incisión se suturó con prolina. Se realizó el reemplazo de la válvula aórtica utilizando una válvula SJM de 21 mm. La retirada del bypass cardiopulmonar fue relativamente suave. Al momento del alta, se prescribió warfarina y aspirina, junto con bisoprolol para la fibrilación auricular paroxística después de la cirugía.\n\nNo se observaron eventos embólicos antes o después de la cirugía.\n\nEl examen histopatológico reveló calcificaciones granulares y nodulares dispersas, que consistían principalmente en infiltración de células inflamatorias y proliferación vascular de neutrófilos, linfocitos, células espumosas, macrófagos tisulares y células plasmáticas, con osificación parcial compatible con CICM. La biopsia miocárdica LV para descartar cardiomiopatía secundaria y la válvula aórtica resecada mostraron células inflamatorias similares a las observadas en CICM. Por lo tanto, se diagnosticó CICM en base a la disminución del movimiento de la pared y la fibrosis miocárdica, con infiltración de células inflamatorias > 14 mm2, células T CD3 positivas > 7/mm2 y negatividad de tenascina C (4C8).7 Sin embargo, no se pudo determinar la causa de CICM.\n\nLa ecocardiografía 6 meses después de la resección no mostró recurrencia del tumor (ver material complementario en línea), ni progresión de la regurgitación mitral, función normal de la válvula aórtica protésica y ninguna mejora de la FEVI (41 %)\n\n",
+        "gold_summary": "Un hombre de 52 años con insuficiencia renal en fase terminal que requería hemodiálisis se sometió a una ecocardiografía anual de seguimiento para detectar una disfunción valvular aórtica. La ecocardiografía reveló una masa circular bien definida de 22 × 17 mm en el anillo de la valva mitral posterior que no se había detectado 2 años antes. En función de las características de la imagen, se sospechó que la masa era un CCMA. Se había agrandado rápidamente y suponía un riesgo potencial de embolia; por lo tanto, se extirpó al mismo tiempo que la sustitución de la válvula aórtica. Aunque se sospechó un CCMA en función de los hallazgos intraoperativos, el diagnóstico histopatológico fue un CAT. Tras el análisis histológico de la muestra de miocardio del ventrículo izquierdo y la válvula aórtica extirpada, se observó una infiltración de células inflamatorias crónicas; por lo tanto, se diagnosticó una cardiomiopatía inflamatoria crónica.\n",
+        "synthetic_summary": {
+            "B1": "Había un hombre que tenía problemas en sus riñones. Tenía un huesito en su corazón que creció mucho y podía hacerle daño. Los doctores vieron el huesito con una máquina especial. Decidieron quitarlo para que el hombre estuviera mejor. También le pusieron una nueva parte en su corazón para que funcione bien. Cuando miraron el huesito con un microscopio, vieron que había muchas células que estaban peleando dentro. Eso les dijo que su corazón estaba un poco enfermo por dentro. Ahora el hombre está más seguro y los doctores lo cuidan mucho.",
+            "B2": "**Lo que pasó con el paciente**  \nUn hombre de 52 años tenía problemas graves en sus riñones y necesitaba hemodiálisis, que es un tratamiento para limpiar la sangre cuando los riñones no funcionan bien. Cada año, le hacían una ecocardiografía, que es un examen con ultrasonido para ver cómo está funcionando su corazón y sus válvulas.\n\n**Lo que encontraron en el corazón**  \nEn el último examen, vieron una masa redonda de 22 × 17 mm en una parte del corazón llamada anillo mitral posterior. Esta masa no estaba ahí dos años antes. Por las imágenes, pensaron que podía ser una calcificación caseosa del anillo mitral (CCMA), que es una acumulación dura y blanda de calcio en esa zona. La masa había crecido rápido y podía causar problemas si pedazos se soltaban y viajaban por la sangre (embolias).\n\n**Qué hicieron los médicos**  \nDecidieron quitar la masa y al mismo tiempo reemplazar la válvula aórtica, que también estaba dañada. Durante la cirugía, vieron que la masa tenía un aspecto cremoso, lo que apoyaba la idea de que era una CCMA.\n\n**Lo que mostraron los análisis después de la cirugía**  \nCuando examinaron la masa bajo el microscopio, encontraron que no era solo calcio, sino también muchas células inflamatorias, lo que indicaba una inflamación crónica en el corazón. Además, analizaron muestras del músculo del corazón y de la válvula aórtica y vieron signos similares de inflamación. Por eso, diagnosticaron al paciente con una cardiomiopatía inflamatoria crónica, que es una enfermedad donde el músculo del corazón está inflamado por mucho tiempo.\n\n**Estado después de la cirugía**  \nSeis meses después, el corazón no mostró que la masa hubiera vuelto, y la válvula nueva funcionaba bien. Sin embargo, la función del ventrículo izquierdo, que es la parte del corazón que bombea la sangre, no mejoró mucho.\n\n**Resumen final**  \nEste caso muestra cómo una masa en el corazón que parecía ser una calcificación pudo ser en realidad una inflamación crónica del músculo cardíaco. La cirugía ayudó a prevenir posibles problemas graves, pero la función del corazón seguía afectada.",
+            "B3": "**Contexto**  \nUn hombre de 53 años con insuficiencia renal terminal en hemodiálisis, causada por nefropatía diabética o nefroesclerosis, fue seguido durante 10 años en un servicio de nefrología. Presentaba estenosis valvular aórtica progresiva y regurgitación moderada, con función ventricular izquierda inicialmente normal. En controles ecocardiográficos anuales se detectó la aparición y rápido crecimiento de una masa en el anillo mitral posterior, que generó preocupación por riesgo de embolia.\n\n**Hallazgos Clave**  \nLa ecocardiografía mostró una masa redonda, bien delimitada, de 22 × 17 mm en el anillo mitral posterior, con características ecogénicas sugestivas de calcificación. La función del ventrículo izquierdo se deterioró progresivamente en dos años, con disminución de la fracción de eyección del 64 % al 42 %. La tomografía computarizada y la resonancia magnética descartaron tumores comunes como mixomas o fibroelastomas papilares, y no hubo evidencia de infección ni endocarditis. Por el contexto clínico y las imágenes, se sospechó una calcificación caseosa del anillo mitral (CCMA), una forma rara de calcificación valvular.\n\nDado el rápido crecimiento de la masa y el riesgo de embolia, se decidió extirparla quirúrgicamente junto con el reemplazo de la válvula aórtica. Durante la cirugía, se observó una masa con contenido cremoso típica de CCMA. Sin embargo, el análisis histopatológico reveló que la masa correspondía a un tumor calcificado atípico (CAT), caracterizado por calcificaciones nodulares y una infiltración inflamatoria crónica con células como neutrófilos, linfocitos, macrófagos y células plasmáticas. Además, la biopsia del músculo cardíaco del ventrículo izquierdo y la válvula aórtica resecada mostraron infiltración similar, lo que llevó al diagnóstico de una cardiomiopatía inflamatoria crónica (CICM). No se pudo determinar la causa exacta de esta inflamación.\n\n**Interpretación Clínica**  \nEste caso ilustra la complejidad diagnóstica de masas en el anillo mitral en pacientes con insuficiencia renal terminal y hemodiálisis, donde la calcificación caseosa puede simular tumores o lesiones inflamatorias. La progresión rápida y el riesgo embolígeno justificaron la cirugía. El diagnóstico definitivo mediante histología fue fundamental para identificar una cardiomiopatía inflamatoria crónica asociada, que podría explicar la disfunción ventricular progresiva observada.\n\n**Próximos Pasos**  \nSe realizó un seguimiento ecocardiográfico a los 6 meses postoperatorios que mostró ausencia de recurrencia de la masa, función normal de la válvula aórtica protésica y estabilidad de la regurgitación mitral, aunque sin mejoría en la función ventricular izquierda (fracción de eyección 41 %). El paciente recibió tratamiento anticoagulante y manejo para fibrilación auricular paroxística. Se recomienda continuar el seguimiento cardiológico para monitorizar la función ventricular y detectar posibles complicaciones asociadas a la cardiomiopatía inflamatoria crónica."
+        }
+    },
+    {
+        "article": "Paciente masculino de 28 años, sin antecedentes de importancia, acude a consulta de dermatología con un cuadro cutáneo de 48 horas de evolución caracterizado por dos placas eritematosas con ampollas centrales más ulceración superficial localizadas en cara flexora de brazo y antebrazo derecho equidistantes del pliegue del codo, acompañadas de una sensación de ardor y prurito en el lugar de las lesiones. No presentó síntomas sistémicos ni se automedicó. Como antecedente refiere que se encontraba de vacaciones en la región costera de Ecuador al momento de aparecer las lesiones. Se realizó una biopsia incisional que reportó epidermis con acantosis, paraqueratosis y espongiosis, neutrófilos en estrato córneo e infiltrado linfocitario perivascular en dermis superficial, media y profunda. Por las características clínicas, el antecedente de viaje a una región tropical y los hallazgos histológicos se diagnosticó como dermatitis por Paederus. Se indicó tratamiento con antihistamínicos, esteroides tópicos y compresas frías. Después de 8 días de tratamiento, las lesiones remitieron dejando una hiperpigmentación postinflamatoria.",
+        "gold_summary": "Se comunica el caso de un paciente masculino de 28 años, que acude a consulta de dermatología con cuadro de 48 horas de evolución de dos placas eritematosas con ampollas centrales más ulceración superficial localizadas en cara flexora de brazo y antebrazo derecho, acompañadas de una sensación de ardor y prurito en el lugar de las lesiones, sin síntomas acompañantes. Como antecedente refiere que se encontraba de vacaciones en la región costera de Ecuador al momento de aparecer las lesiones. Se realizó una biopsia incisional y por las características clínicas y el antecedente de viaje a una región tropical se diagnosticó como dermatitis por Paederus y se indicó tratamiento con antihistamínicos, esteroides tópicos y compresas frías. Después de 8 días de tratamiento, las lesiones remitieron dejando una hiperpigmentación postinflamatoria.",
+        "synthetic_summary": {
+            "B1": "Un hombre se lastimó la piel en su brazo. Tenía dos manchas rojas con ampollas y le picaban y quemaban. Esto pasó después de estar de vacaciones en un lugar con mucho calor y bichos. El doctor vio su piel y dijo que era una irritación por un bicho llamado Paederus. Le dieron medicinas para calmar la picazón y poner frío en su brazo. Después de unos días, la piel mejoró, pero quedó un poco de color diferente donde estaban las manchas.",
+            "B2": "Caso de un joven de 28 años con lesiones en la piel\n\nUn hombre de 28 años fue al dermatólogo porque tenía dos manchas rojas en el brazo y antebrazo derecho. Estas manchas tenían ampollas (pequeñas burbujas llenas de líquido) en el centro y una pequeña herida superficial. Además, sentía ardor y picazón en esas áreas. No tenía otros síntomas ni había tomado medicamentos por su cuenta.\n\nLo que encontraron y cómo lo trataron\n\nEl paciente contó que estaba de vacaciones en la costa de Ecuador cuando aparecieron las lesiones. Para entender mejor qué pasaba, los médicos tomaron una biopsia, que es cuando se extrae un pequeño pedazo de piel para examinarlo bajo el microscopio. En el análisis, vieron cambios en las capas de la piel y células inflamatorias, lo que ayudó a confirmar que tenía dermatitis por Paederus. Esta dermatitis es una irritación causada por un insecto llamado Paederus, común en zonas tropicales.\n\nEl tratamiento incluyó medicamentos para reducir la picazón (antihistamínicos), cremas con esteroides para bajar la inflamación, y compresas frías para aliviar el ardor. Después de ocho días, las lesiones mejoraron, pero quedaron manchas oscuras en la piel, llamadas hiperpigmentación postinflamatoria, que suelen desaparecer con el tiempo.",
+            "B3": "**Contexto**  \nSe presenta el caso de un hombre de 28 años, sin antecedentes médicos relevantes, que consultó en dermatología debido a la aparición de lesiones cutáneas durante las últimas 48 horas. Estas lesiones consistían en dos placas rojas (eritematosas) con ampollas en el centro y una ulceración superficial, localizadas en la parte interna del brazo y antebrazo derecho, equidistantes del pliegue del codo. El paciente describió sensación de ardor y picazón en las zonas afectadas, sin presentar otros síntomas generales ni haber tomado medicamentos por su cuenta. Como antecedente importante, refirió que se encontraba de vacaciones en una zona costera tropical de Ecuador cuando aparecieron las lesiones.\n\n**Hallazgos Clave**  \nSe realizó una biopsia incisional de la piel afectada, cuyo análisis microscópico mostró:  \n- Engrosamiento de la epidermis (acantosis)  \n- Presencia de células muertas con núcleo (paraqueratosis)  \n- Acumulación de líquido entre las células epidérmicas (espongiosis)  \n- Infiltración de neutrófilos (un tipo de glóbulo blanco) en la capa más superficial de la piel (estrato córneo)  \n- Presencia de un infiltrado inflamatorio linfocitario alrededor de los vasos sanguíneos en las capas superficiales, medias y profundas de la dermis (la capa intermedia de la piel).\n\n**Interpretación Clínica**  \nLa combinación de las características clínicas, el antecedente de exposición en una región tropical y los hallazgos histológicos permitió establecer el diagnóstico de dermatitis por Paederus. Esta condición es una inflamación cutánea causada por el contacto con un insecto del género Paederus, que libera una toxina irritante al ser aplastado sobre la piel.\n\n**Próximos Pasos y Tratamiento**  \nEl tratamiento indicado incluyó antihistamínicos para aliviar la picazón, esteroides tópicos para reducir la inflamación y la aplicación de compresas frías para calmar la zona afectada. Tras ocho días de tratamiento, las lesiones desaparecieron, aunque dejaron una hiperpigmentación postinflamatoria, es decir, una mancha oscura residual en la piel debido a la inflamación previa.\n\nEste caso resalta la importancia de considerar la dermatitis por Paederus en pacientes con lesiones cutáneas agudas tras viajes a regiones tropicales, y la efectividad del tratamiento tópico combinado para su resolución."
+        }
+    },
+    {
+        "article": "Un hombre de 35 años de edad, herido en un accidente de tráfico, fue trasladado a nuestro hospital, que está equipado con un ER híbrido. Había sufrido una lesión potencialmente mortal, con su pierna derecha acortada y girada. Los signos vitales del paciente a su llegada fueron los siguientes: frecuencia respiratoria de 24 respiraciones/min, saturación de oxígeno del 99 % con 12 L de administración de oxígeno, frecuencia cardiaca de 143 latidos/min, presión arterial de 80/40 mmHg, y puntuación de Glasgow Coma Scale de E4V4M6. Intentamos realizar un TAC y resucitar al paciente. El TAC reveló un hemotórax izquierdo, ensanchamiento del mediastino, y fractura pélvica. Como la presión arterial del paciente cayó rápidamente antes del TAC, se administraron procedimientos de salvamento, como intubación de emergencia, preperitoneal pelvic packing, y transfusión masiva, con un cuidadoso control de la presión arterial en el ER híbrido. Después de la estabilización de los signos vitales con estos procedimientos, el TAC con contraste reveló una fractura de BTAI de grado IV que se extendía hacia la cavidad torácica izquierda. La embolización arterial transcatéter (TAE) para la fractura pélvica y la fijación esquelética externa de la fractura del fémur derecho se realizaron primero, ya que el radiólogo y el cirujano cardiovascular, que realizan TEVAR en nuestro centro médico, no estaban disponibles en ese momento. Posteriormente, se realizó TEVAR utilizando un injerto de stent (GORE C-TAG 26 × 150 mm; WL Gore & Associates, Flagstaff, Arizona, EE. UU.) en el ER híbrido sin transferir al paciente. Se desplegó un injerto de stent justo distal de la arteria carótida común izquierda (zona II) y el extremo distal del injerto de stent se posicionó en el nivel de Th 8. Decidimos sacrificar LSCA ya que el flujo sanguíneo de la arteria vertebral izquierda fue suficiente según lo evaluado por angiografía. El paciente no tuvo síntomas que sugirieran isquemia después de TEVER. Durante la cirugía, se administraron 50 unidades/kg (3000 unidades) de heparina. El paciente fue trasladado a un hospital de rehabilitación el día 41 postoperatorio.\n",
+        "gold_summary": "Un hombre de 35 años de edad sufrió múltiples lesiones tras un accidente de tráfico y fue trasladado a nuestro hospital en estado de shock. La tomografía computarizada reveló una fractura de TAI de grado IV que se extendía hasta la cavidad torácica y una fractura pélvica. Poco tiempo después de realizar un relleno pélvico preperitoneal y una embolización arterial transcatéter para la fractura pélvica, se realizó un TEVAR en el quirófano híbrido sin trasladar al paciente. El paciente fue trasladado a un hospital de rehabilitación el día 41 después de la operación.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre se lastimó mucho en un accidente. Su pierna estaba muy dañada y tenía huesos rotos en el cuerpo. Los doctores le hicieron muchas cosas para ayudarlo a estar mejor. Usaron una máquina para ver dentro de su cuerpo y encontraron problemas grandes. Luego, le pusieron un tubo especial para arreglar su corazón y sus huesos. El hombre se quedó en el hospital mucho tiempo. Después, fue a otro lugar para aprender a caminar y estar fuerte otra vez.",
+            "B2": "**Lo que pasó con el paciente**  \nUn hombre de 35 años tuvo un accidente de tráfico grave y llegó al hospital en estado muy delicado. Tenía varias heridas, incluyendo una fractura en la pelvis y una lesión grave en la arteria principal del pecho llamada aorta. Esta lesión se llama fractura de TAI de grado IV y puede ser muy peligrosa porque afecta el flujo de sangre al cuerpo.\n\n**Tratamientos que recibió**  \nPrimero, los médicos hicieron un procedimiento llamado relleno pélvico preperitoneal, que ayuda a controlar el sangrado en la pelvis. También realizaron una embolización arterial transcatéter, que es cuando se bloquea una arteria para detener una hemorragia. Después, sin mover al paciente a otro lugar, hicieron una cirugía llamada TEVAR en un quirófano especial que combina imagen y cirugía. En esta operación, colocaron un tubo especial llamado injerto de stent dentro de la arteria dañada para repararla y permitir que la sangre fluya bien.\n\n**Qué pasó después**  \nGracias a estos tratamientos, el paciente se estabilizó y pudo continuar su recuperación. Después de 41 días, fue enviado a un hospital de rehabilitación para seguir mejorando su salud.",
+            "B3": "**Contexto:**  \nUn hombre de 35 años sufrió un grave accidente de tráfico que le provocó múltiples lesiones, incluyendo una fractura grave en la arteria aorta torácica (TAI, por sus siglas en inglés) y fracturas óseas en la pelvis y el fémur derecho. Fue trasladado a un hospital equipado con un quirófano híbrido, donde recibió atención de emergencia.\n\n**Hallazgos Clave:**  \nA su llegada, el paciente presentaba signos de shock, con presión arterial muy baja y frecuencia cardíaca elevada. La tomografía computarizada (TAC) mostró un hemotórax (acumulación de sangre en el tórax), ensanchamiento del mediastino (zona central del tórax que contiene el corazón y grandes vasos), una fractura pélvica y una lesión de grado IV en la arteria aorta torácica que se extendía hacia la cavidad torácica izquierda. Además, la pierna derecha estaba acortada y girada, indicando fractura del fémur.\n\n**Interpretación Clínica:**  \nDebido a la gravedad y la inestabilidad hemodinámica del paciente, se realizaron procedimientos de emergencia para controlar el sangrado y estabilizarlo, incluyendo intubación, relleno pélvico preperitoneal (una técnica para controlar hemorragias pélvicas) y transfusión masiva. Posteriormente, se realizó una embolización arterial transcatéter (TAE) para controlar el sangrado de la fractura pélvica y se fijó externamente la fractura del fémur. Finalmente, sin necesidad de trasladar al paciente, se llevó a cabo una reparación endovascular de la aorta torácica (TEVAR) en el quirófano híbrido, utilizando un injerto de stent que se colocó desde justo después de la arteria carótida común izquierda hasta la octava vértebra torácica. Para asegurar un flujo sanguíneo adecuado, se decidió sacrificar la arteria subclavia izquierda, ya que la circulación cerebral estaba garantizada por la arteria vertebral izquierda. Durante la cirugía se administró heparina para prevenir coágulos.\n\n**Próximos Pasos y Resultado:**  \nEl paciente evolucionó favorablemente sin signos de isquemia (falta de riego sanguíneo) tras la intervención. Fue dado de alta al hospital de rehabilitación 41 días después de la cirugía, donde continuó su recuperación."
+        }
+    },
+    {
+        "article": "Hombre de 31 años con antecedentes de consumo de alcohol, tabaco, cocaína inhalada, tuberculosis pulmonar tratada, nefrectomía izquierda y esplenectomía post-traumática. Consultó al servicio de urgencias por cuadro de una semana de evolución que inició inmediatamente posterior a la aplicación intramuscular de penicilina por contacto sexual con pareja con sífilis, caracterizado por dolor en región glútea derecha que irradiaba hasta pie, con posterior aparición de dermatosis purpúrica relacionada con sitio de inyección, siendo una lesión tipo placa configurada en forma anular, con bordes irregulares y distribución racemosa que medía 15 centímetros (cm), con piel sana en su interior. También presentaba una pequeña escara escrotal y una extensa lesión plantar derecha de aspecto livedoide desde la zona talar hasta la punta de los dedos que no respetaba margen estricto. Se realizó ecografía del glúteo mayor, que mostró pérdida del patrón fibrilar heterogéneo, aumento del espesor del mismo a nivel de su tercio medio de aspecto edematoso, además de edema del tejido celular subcutáneo (TCS); en región plantar homolateral y en escroto edema de TCS. En el laboratorio presentó leucocitosis de 13.7 × 109/L, proteína C reactiva de 3.2 mg/dL (normal hasta 0.5 mg/dL), que se interpretaron como reactantes de fase aguda, también aumento de transaminasas con aspartato aminotransferasa de 175 UI/L (normal hasta 32), alanino aminotransferasa de 245 UI/L (normal hasta 33), creatina kinasa con un valor de 2741 UI/L (normal hasta 170) y lactato deshidrogenasa de 2499 UI/L (normal hasta 250) representando compromiso muscular. Se realizaron serologías completas para sífilis, con venereal disease research laboratory (VDRL y anticuerpos treponémicos), virus de la inmunodeficiencia humana (HIV) hepatitis B, hepatitis C, con resultados negativos. La cronología, las manifestaciones clínicas y la posterior biopsia, respaldaron el diagnóstico de síndrome de Nicolau, para lo cual se inició anticoagulación con enoxaparina 1 mg/ kg c/12 hs vía subcutánea, cilostazol 100 mg cada 12 horas y tramadol, por 10 días. Se realizó biopsia de piel de glúteo que evidenció necrosis epidérmica y extensión a epitelio folicular, con formación de ampolla secundaria a reepitelización, sin vasculitis ni trombosis vascular, vinculable a embolia cutis medicamentosa en fase aguda, hubo franca mejoría con descenso de valores de transaminasas, con aspartato aminotransferasa de 39 UI/L, alanino aminotransferasa de 77 UI/L y creatin kinasa de 167 UI/L.  No se solicitó perfil inmunológico, basados en que nuestro diagnóstico presuntivo inicial no justificaba la búsqueda de otras etiologías. Se otorgó alta con cilostazol y analgésicos, control ambulatorio a los 3 meses con mejoría del dolor y de las lesiones, quedando en glúteo derecho cicatriz discrómica con presencia de descamación fina y en pie derecho cicatriz discrómica con zonas de descamación gruesas en región de apoyo tarso metatarsiano asociado a mínimas lesiones livedoides en planta del mismo pie.",
+        "gold_summary": "Se reporta el caso de un hombre de 31 años que presenta este síndrome luego de la aplicación de penicilina benzatínica intramuscular. La biopsia apoyó el diagnóstico. Recibió tratamiento con enoxaparina y cilostazol con posterior mejoría.",
+        "synthetic_summary": {
+            "B1": "Un hombre se puso una medicina en el glúteo. Después, le dolió mucho y le salió una mancha en la piel. El doctor vio que la piel estaba lastimada por la medicina. Le dieron medicinas para ayudar y se fue mejorando poco a poco. Ahora está mejor y la piel está sanando.",
+            "B2": "Caso de Síndrome de Nicolau tras Inyección de Penicilina\n\nUn hombre de 31 años recibió una inyección de penicilina para tratar una posible infección por sífilis, debido a que su pareja tenía esta enfermedad. Poco después, comenzó a sentir dolor en la nalga derecha que se extendía hasta el pie. Además, apareció una lesión en la piel cerca del lugar de la inyección, con forma de anillo y bordes irregulares, y otras heridas en el escroto y la planta del pie.\n\nPara entender qué pasaba, los médicos hicieron una ecografía que mostró inflamación en los músculos y tejidos cerca de la lesión. También se hicieron análisis de sangre que indicaron inflamación y daño muscular. Se descartaron otras infecciones como VIH y hepatitis.\n\nSe tomó una biopsia, que es cuando se extrae un pequeño pedazo de piel para examinarlo. Esta mostró que la piel estaba dañada por falta de sangre, pero sin inflamación de los vasos sanguíneos. Todo esto confirmó que el paciente tenía el síndrome de Nicolau, una reacción rara que puede ocurrir después de una inyección y que causa daño en la piel y músculos por bloqueo de vasos sanguíneos.\n\nEl tratamiento incluyó medicamentos para evitar coágulos (enoxaparina) y para mejorar la circulación (cilostazol), además de analgésicos para el dolor. Con este cuidado, el paciente mejoró, sus análisis de sangre volvieron casi a la normalidad y las lesiones en la piel sanaron, quedando solo algunas cicatrices leves.\n\nEste caso muestra la importancia de reconocer el síndrome de Nicolau para tratarlo rápido y evitar daños mayores.",
+            "B3": "**Contexto**  \nSe trata de un hombre de 31 años con antecedentes de consumo de alcohol, tabaco y cocaína inhalada, además de haber tenido tuberculosis pulmonar tratada, y cirugías previas de nefrectomía izquierda y esplenectomía tras un trauma. Consultó en urgencias debido a un cuadro que comenzó una semana antes, inmediatamente después de recibir una inyección intramuscular de penicilina benzatínica, administrada por contacto sexual con una pareja diagnosticada con sífilis.\n\n**Hallazgos Clínicos y Diagnósticos**  \nEl paciente presentó dolor intenso en la región glútea derecha que se irradiaba hacia el pie, acompañado de una erupción cutánea purpúrica (manchas violáceas) en el sitio de la inyección. Esta lesión tenía forma de placa anular (con un borde en forma de anillo irregular) de aproximadamente 15 centímetros, con piel sana en el centro. Además, tenía una pequeña úlcera (escara) en el escroto y una lesión extensa en la planta del pie derecho con aspecto livedoide (patrón vascular irregular), que se extendía desde el talón hasta la punta de los dedos.\n\nLa ecografía del glúteo mostró alteraciones en el músculo mayor, con pérdida de su estructura normal, aumento de grosor y edema (hinchazón por acumulación de líquido) tanto en el músculo como en el tejido subcutáneo (debajo de la piel). Se observó edema también en la región plantar del pie y en el escroto.\n\nLos análisis de sangre revelaron leucocitosis (aumento de glóbulos blancos) y elevación de proteína C reactiva, indicadores de inflamación aguda. Además, hubo un aumento significativo de enzimas hepáticas (transaminasas) y de marcadores musculares como la creatina quinasa y la lactato deshidrogenasa, lo que sugiere daño muscular.\n\nLas pruebas serológicas para sífilis, VIH, hepatitis B y C fueron negativas.\n\nLa biopsia de piel del glúteo evidenció necrosis (muerte celular) epidérmica y afectación del epitelio folicular, con formación de ampollas debido a la reparación de la piel, pero sin signos de vasculitis (inflamación de vasos sanguíneos) ni trombosis (coágulos), lo que apoyó el diagnóstico de síndrome de Nicolau o embolia cutis medicamentosa en fase aguda. Este síndrome es una reacción adversa poco frecuente que ocurre tras la inyección intramuscular de ciertos medicamentos, causando daño vascular y necrosis en la piel y tejidos subyacentes.\n\n**Interpretación Clínica**  \nEl cuadro clínico, la historia temporal relacionada con la inyección de penicilina y los hallazgos histológicos confirmaron el diagnóstico de síndrome de Nicolau. Este diagnóstico explicó el dolor intenso, las lesiones cutáneas y el compromiso muscular observado.\n\n**Tratamiento y Evolución**  \nSe inició tratamiento con anticoagulación mediante enoxaparina (un anticoagulante) y cilostazol (un medicamento que mejora la circulación sanguínea), además de analgésicos para controlar el dolor. Durante la hospitalización, el paciente mostró una franca mejoría, con descenso progresivo de las enzimas hepáticas y musculares a valores cercanos a la normalidad.\n\nNo se realizaron estudios inmunológicos adicionales, dado que el diagnóstico clínico y patológico fue suficiente para explicar el cuadro.\n\nAl alta, el paciente continuó con cilostazol y analgésicos, y en el control ambulatorio a los tres meses presentó mejoría significativa del dolor y de las lesiones cutáneas. Quedaron secuelas en forma de cicatrices con alteraciones en la pigmentación y descamación fina en el glúteo derecho, así como cicatrices similares y mínimas lesiones livedoides en la planta del pie derecho.\n\n**Próximos Pasos**  \nSe recomienda seguimiento clínico para evaluar la evolución de las cicatrices y el manejo del dolor residual, así como evitar futuras inyecciones intramusculares en la zona afectada para prevenir recurrencias. Además, es importante la educación al paciente sobre los riesgos asociados a la administración de medicamentos por vía intramuscular y la vigilancia temprana de síntomas similares."
+        }
+    },
+    {
+        "article": "Un varón de cuatro días de edad, nacido a las 39 semanas y 4 días de gestación, acude a un servicio de urgencias con un empeoramiento de la dificultad respiratoria y el estridor, que se ve agravado por la alimentación y la posición supina.\n\nNació de una madre de 31 años con serología significativa para una prueba de Coomb positiva indirecta, con un parto vaginal sin complicaciones y puntuaciones de APGAR de ocho y nueve en el primer y quinto minuto, respectivamente. Su peso al nacer fue de 3050 g. La ecografía fetal mostró preocupación por un foco intracardíaco, con un embarazo sin complicaciones. El curso de enfermería fue significativo solo por una prueba de audición bilateral fallida y un ecocardiograma normal. El bebé fue dado de alta en el día dos de vida. Se observó que tenía congestión nasal en el momento de la descarga. Se instruyó a la familia para que le aspirara la nariz y usara gotas salinas según fuera necesario.\n\nEn el día cuatro de vida, la madre del lactante notó estridor asociado con dificultad para alimentarse y el pediatra lo derivó al servicio de urgencias. El examen en el servicio de urgencias es significativo para el estridor inspiratorio agudo con tirones traqueales y retracciones subcostal. Además, se observa que tiene pectus excavatum. El estridor y el aumento del trabajo respiratorio mejoran con la posición prona o lateral. La evaluación de laboratorio es significativa para la acidosis respiratoria en el gas sanguíneo venoso [pH 7.18 y CO2 73 mmHg (9,732 Pa)] y el análisis de orina que revela bacterias moderadas y 11-20 glóbulos blancos sin la presencia de nitrito urinario o esterasa leucocitaria. Un recuento sanguíneo completo es tranquilizador. Se le coloca una cánula nasal de alto flujo y se inicia con ampicilina y gentamicina después de obtener cultivos de sangre.\n\nSe le aumentó la presión positiva continua en la vía aérea (CPAP) y se lo trasladó a una unidad de cuidados intensivos neonatales de nivel III para continuar con el tratamiento y la evaluación de otorrinolaringología. Se le introdujo un tubo nasogástrico por las dos fosas nasales sin dificultad. La laringoscopia flexible mostró una cuerda vocal izquierda inmóvil y cavidades nasales estrechas con edema de los cornetes nasales, aritenoides bilaterales y cuerdas vocales. La broncoscopia no reveló ninguna otra anormalidad. El examen físico posterior se caracterizó por rasgos dismórficos sutiles, que incluían orejas de implantación baja, retromicrognatia, microftalmia y clinodactilia de los dedos de los pies. Se interrumpió el tratamiento antibiótico empírico tras un examen infeccioso tranquilizador. Se consultó a un equipo multidisciplinario.\n\nEl paciente finalmente requirió intubación a las dos semanas de vida debido al empeoramiento del fallo respiratorio. Se administraron ciprofloxacina nasal y dexametasona para el edema de las vías respiratorias superiores. Una resonancia magnética del cerebro, cuello y tórax mostró un curso normal de los nervios laríngeos recurrentes. La evaluación genética incluyó un análisis de microarreglo cromosómico normal (CMA). La prueba adicional del panel genético fue positiva para la variante patogénica en el gen CHD7, consistente con el síndrome CHARGE. En este caso, el VFP se atribuyó a la asociación conocida con el síndrome CHARGE. La evaluación continua reveló otras características consistentes con el síndrome CHARGE, incluidos colobomas bilaterales, glaucoma, pérdida auditiva confirmada y anomalías genitales.\n\nLa repetición de la broncoscopia en el día 42 de vida demostró una mejora en el edema laríngeo general, pero continuó con un edema leve de las cuerdas vocales bilaterales. El paciente fue extubado después de la broncoscopia en el marco de un edema de las vías respiratorias mejorado. Sin embargo, fue re-intubado el día 46 de vida debido al empeoramiento de la insuficiencia respiratoria. La repetición de la laringoscopia ese día mostró un edema continuado. En este momento, el paciente ya había recibido múltiples ciclos cortos de Dexamethasone en un intento de disminuir el edema de las vías respiratorias. Debido a la necesidad de re-intubación, fue tratado con Tobramycin tópico y Dexamethasone aplicado directamente a las cuerdas vocales mediante laringoscopia directa durante cinco días. Después de este tratamiento, fue extubado con éxito a los dos meses de edad y se le colocó un tubo de gastrostomía a los tres meses.\n\nEn el momento de la colocación del tubo de gastrotomía, se le realizó una broncoscopia y una microlaringoscopia adicionales que demostraron que la cuerda vocal izquierda afectada originalmente era totalmente móvil, pero que mostraba una nueva inmovilidad de la cuerda derecha; la etiología de esto no está clara. Ambas cuerdas vocales seguían estando ligeramente edematosas, pero habían mejorado mucho desde la evaluación anterior. El paciente fue dado de alta en aire ambiente a los cuatro meses de edad y continúa siendo seguido de cerca por el otorrinolaringólogo. En la laringoscopia ambulatoria de repetición a los cuatro meses de edad, ambas cuerdas aparecían móviles con un edema de las vías respiratorias continuado.\n\n",
+        "gold_summary": "Un bebé de cuatro días de edad, a término, varón, nacido por parto vaginal sin complicaciones, con un curso de enfermería significativo para la falta de audición, se presentó en un departamento de emergencias (DE) con dificultad respiratoria y estridor en aumento. Fue trasladado a una unidad de cuidados intensivos neonatales (UCIN) de nivel III para una evaluación posterior y se le practicó una intubación debido a la hipercarbia progresiva. La laringoscopia reveló una parálisis unilateral de las cuerdas vocales (PCV) del lado izquierdo. Se le sometió a una evaluación posterior que incluyó un cerebro, cuello y tórax normales en una resonancia magnética. Se consultó a genética por la preocupación de los rasgos dismórficos en el examen físico. Después de las pruebas del panel de genes, la PCV se atribuyó a la asociación conocida con el síndrome CHARGE. Se observó un edema de las vías respiratorias en la laringoscopia que impidió la extubación hasta los dos meses de edad. Se identificaron otras características del síndrome CHARGE, incluidos los colobomas, el glaucoma, la pérdida auditiva neurosensorial y las anomalías genitales. Se le dio de alta con aire ambiente y después de la colocación de un tubo de gastrostomía con seguimiento de otorrinolaringología.\n",
+        "synthetic_summary": {
+            "B1": "Un bebé de cuatro días tenía problemas para respirar y hacer ruido al respirar. Lo llevaron al hospital para que lo cuidaran mucho. Los doctores vieron que una cuerda en su garganta no se movía bien. Hicieron pruebas y encontraron que tenía un problema llamado síndrome CHARGE. Este problema puede hacer que los ojos, los oídos y otras partes del cuerpo no estén como deben. El bebé estuvo en el hospital hasta que pudo respirar mejor. Luego, le pusieron un tubito para ayudarlo a comer. Ahora, los doctores lo cuidan para que siga mejorando.",
+            "B2": "**Lo que pasó con el bebé**  \nUn bebé de cuatro días, que nació sin problemas y a término, llegó al hospital porque tenía dificultad para respirar y un sonido extraño al inhalar llamado estridor. En el hospital, los médicos notaron que su respiración empeoraba y que tenía una cuerda vocal izquierda que no se movía, lo que se llama parálisis unilateral de las cuerdas vocales. Esto dificultaba que respirara bien.\n\n**Qué hicieron los médicos**  \nEl bebé fue llevado a una unidad especial para recién nacidos y le pusieron un tubo para ayudarlo a respirar mejor. Le hicieron varios estudios, incluyendo una resonancia magnética, que mostró que su cerebro, cuello y tórax estaban normales. También notaron que tenía algunas características físicas diferentes, como orejas bajas y ojos pequeños, por lo que pidieron ayuda a especialistas en genética.\n\n**El diagnóstico y su significado**  \nDespués de hacer pruebas genéticas, descubrieron que el bebé tenía una condición llamada síndrome CHARGE. Este síndrome puede causar problemas en varias partes del cuerpo, como los ojos (colobomas y glaucoma), pérdida de audición y problemas en los genitales. La parálisis de la cuerda vocal izquierda estaba relacionada con este síndrome.\n\n**El tratamiento y el seguimiento**  \nEl bebé tuvo inflamación en las vías respiratorias, lo que dificultó quitarle el tubo para respirar hasta que tenía dos meses. También le pusieron un tubo especial para alimentarse directamente al estómago (tubo de gastrostomía) a los tres meses. Finalmente, fue dado de alta para seguir en casa, pero continúa con controles médicos para vigilar su respiración y otros problemas relacionados con el síndrome CHARGE.",
+            "B3": "**Contexto**  \nUn recién nacido varón a término, sin complicaciones durante el parto, fue llevado al servicio de urgencias a los cuatro días de vida debido a un empeoramiento de la dificultad para respirar y la presencia de estridor (un sonido respiratorio agudo causado por la obstrucción de las vías aéreas). Estos síntomas se agravaban con la alimentación y al estar acostado boca arriba. En el examen inicial, se detectó también una deformidad torácica llamada pectus excavatum. La dificultad respiratoria mejoraba al colocarlo boca abajo o de lado.  \n\n**Hallazgos Clave**  \n- La evaluación inicial mostró acidosis respiratoria, lo que indica una acumulación de dióxido de carbono en la sangre por dificultad para respirar adecuadamente.  \n- Se inició soporte respiratorio con cánula nasal de alto flujo y posteriormente con presión positiva continua en la vía aérea (CPAP).  \n- La laringoscopia flexible (una exploración visual de la laringe) reveló parálisis unilateral de la cuerda vocal izquierda y edema (hinchazón) en varias estructuras de las vías respiratorias superiores.  \n- Se identificaron rasgos físicos sutiles que sugerían una posible condición genética, incluyendo orejas de implantación baja, mandíbula pequeña (retromicrognatia), ojos pequeños (microftalmia) y deformidades en los dedos de los pies.  \n- La resonancia magnética del cerebro, cuello y tórax fue normal, descartando lesiones estructurales en los nervios laríngeos recurrentes, que controlan las cuerdas vocales.  \n- El análisis genético confirmó la presencia de una mutación patogénica en el gen CHD7, diagnóstico que confirma el síndrome CHARGE, una enfermedad genética que afecta múltiples órganos y sistemas.  \n\n**Interpretación Clínica**  \nLa parálisis de la cuerda vocal izquierda se atribuyó a la asociación conocida con el síndrome CHARGE, que también explicó otros hallazgos clínicos como colobomas bilaterales (defectos en el ojo), glaucoma, pérdida auditiva neurosensorial y anomalías genitales. El edema persistente en las vías respiratorias superiores dificultó la extubación (retirar el tubo de respiración) hasta los dos meses de edad, requiriendo múltiples tratamientos con corticosteroides y antibióticos tópicos aplicados directamente sobre las cuerdas vocales. Posteriormente, se observó una nueva parálisis de la cuerda vocal derecha, cuya causa no está clara, aunque ambas cuerdas vocales mostraron mejoría progresiva.  \n\n**Próximos Pasos y Seguimiento**  \nEl paciente fue dado de alta respirando aire ambiente a los cuatro meses de edad, tras la colocación de un tubo de gastrostomía para alimentación directa al estómago, debido a las dificultades para alimentarse por vía oral. Continúa bajo seguimiento estrecho con otorrinolaringología para monitorizar la función de las cuerdas vocales y el estado de las vías respiratorias. Este caso resalta la importancia de una evaluación multidisciplinaria en recién nacidos con síntomas respiratorios y rasgos dismórficos, para identificar condiciones genéticas complejas como el síndrome CHARGE y manejar sus múltiples complicaciones."
+        }
+    },
+    {
+        "article": "Mujer de 17 años oriunda de Tucumán, acudió a la consulta por cuadro de vías aéreas superiores y hemoptisis leve. La tomografía computarizada de tórax informó, en lóbulo superior derecho, una imagen redondeada de paredes regulares y lisas de 25x24x24 mm, rodeado de un tenue halo periférico en vidrio esmerilado. No se observaba realce ante la administración de contraste endovenoso. Se sugirió un posible quiste broncogénico, por lo que se realizó una RMN de tórax que informó imagen redondeada de paredes regulares y lisas que alcanzó un diámetro anteroposterior de 25 x 24 x 24.5 mm con intensidad de señal líquida. Debido a la localización central de la lesión, se realizó una lobectomía superior derecha videoasistida. Dado que el estudio anatomopatológico intraoperatorio fue indeterminado, se complementó la resección pulmonar con un vaciamiento ganglionar mediastínico. La anatomía patológica definitiva informó neumocitoma esclerosante de 2 x 1.7 cm. La inmunomarcación fue positiva para TTF1, CK, CK7 y napsina.",
+        "gold_summary": "Describimos aquí el caso de una paciente de 17 años con diagnóstico de neumocitoma esclerosante con presentación infrecuente.",
+        "synthetic_summary": {
+            "B1": "Una niña de 17 años tenía un bulto en su pulmón. Los doctores lo sacaron con una operación para que ella esté mejor. El bulto no era peligroso.",
+            "B2": "Caso de una joven con un tumor pulmonar poco común\n\nUna chica de 17 años de Tucumán fue al médico porque tenía síntomas en las vías respiratorias y tos con un poco de sangre. Se le hizo una tomografía, que es una imagen especial del pecho, y mostraba una bolita redonda en el pulmón derecho. Esta bolita tenía paredes lisas y un borde un poco borroso. Para entender mejor, le hicieron una resonancia magnética, que confirmó que la imagen parecía un líquido dentro de esa bolita.\n\nComo la lesión estaba en una zona difícil, los médicos decidieron sacar la parte superior del pulmón derecho usando una cirugía asistida por video, que es menos invasiva. Durante la operación, no pudieron saber exactamente qué era la lesión, así que también quitaron algunos ganglios cercanos para analizarlos.\n\nDespués de estudiar el tejido con un microscopio, los especialistas confirmaron que se trataba de un neumocitoma esclerosante. Este es un tipo raro de tumor en el pulmón que generalmente no es canceroso. Para asegurarse, usaron pruebas especiales que detectan ciertas proteínas en las células, y estas pruebas dieron resultados positivos para marcadores típicos de este tumor.\n\nEn resumen, este caso muestra cómo se identificó y trató un tumor pulmonar poco común en una paciente joven, usando diferentes estudios de imagen y cirugía para llegar a un diagnóstico claro.",
+            "B3": "**Contexto:**  \nSe presenta el caso de una joven de 17 años originaria de Tucumán que consultó por síntomas respiratorios superiores acompañados de hemoptisis leve (expectoración con sangre). Los estudios iniciales incluyeron una tomografía computarizada (TC) de tórax que reveló una lesión redondeada de aproximadamente 2.5 cm en el lóbulo superior derecho del pulmón, con bordes regulares y un halo periférico de vidrio esmerilado, sin captación de contraste. Posteriormente, una resonancia magnética (RMN) confirmó la presencia de esta lesión con características líquidas.\n\n**Hallazgos Clave:**  \nDebido a la ubicación central de la lesión, se decidió realizar una lobectomía superior derecha mediante cirugía videoasistida. Durante la operación, el estudio anatomopatológico preliminar no permitió un diagnóstico definitivo, por lo que se amplió la cirugía para incluir un vaciamiento ganglionar mediastínico (extirpación de ganglios linfáticos en el mediastino). El examen histológico final identificó la lesión como un neumocitoma esclerosante, un tumor pulmonar poco frecuente, de tamaño aproximado de 2 x 1.7 cm. Los marcadores inmunohistoquímicos fueron positivos para TTF1, CK, CK7 y napsina, proteínas que ayudan a confirmar el origen pulmonar y la naturaleza del tumor.\n\n**Interpretación Clínica:**  \nEl neumocitoma esclerosante es una neoplasia pulmonar rara que suele presentarse en adultos jóvenes y tiene un comportamiento generalmente benigno o de bajo grado maligno. En este caso, la presentación con hemoptisis y la localización central del tumor hicieron necesaria una intervención quirúrgica completa para su diagnóstico y tratamiento. La confirmación mediante inmunomarcadores es fundamental para diferenciarlo de otras lesiones pulmonares.\n\n**Próximos Pasos:**  \nSe recomienda un seguimiento clínico y radiológico periódico para vigilar la posible recurrencia o complicaciones postoperatorias. La cirugía completa y el vaciamiento ganglionar mediastínico realizados constituyen un manejo adecuado para este tipo de tumor, aunque su pronóstico suele ser favorable. En caso de aparición de nuevos síntomas o hallazgos, se deberá reevaluar para descartar progresión o complicaciones."
+        }
+    },
+    {
+        "article": "Una mujer asiática de 28 años fue admitida en el hospital para el tratamiento de «una masa pélvica durante 10 meses» el 11 de noviembre de 2018. La paciente solía tener menstruación regular, volumen menstrual moderado, dismenorrea y un G1P0L0A1. Examen ginecológico: la parte posterior del útero tenía aproximadamente 8 cm de diámetro con poca actividad y sensibilidad, pero no se observaron otras anomalías. La paciente no tenía una causa obvia de dolor abdominal durante los primeros 10 meses previos al ingreso. El examen de ultrasonido reveló una masa heterogénea en la parte superior derecha del útero con un diámetro de aproximadamente 4 cm, un nódulo del epiplón mayor con un diámetro de aproximadamente 2 cm y un nivel de CA125 sérico de 416 mU/mL. Se diagnosticó como «endometriosis, masas pélvicas inflamatorias». Se administró una terapia de rehidratación antiinfecciosa y se dio de alta a la paciente con alivio del dolor. Dos semanas después del alta, el nivel de CA125 sérico de la paciente disminuyó a 106 mU/mL y volvió a la normalidad después de 6 semanas. Sin embargo, la masa pélvica aumentó gradualmente. El reexamen de la ecografía pélvica realizada mostró una masa ecoica mixta de 7.7 cm x 7.4 cm x 8.2 cm en el lado derecho del útero con un límite claro, eco puntiforme fino en el quiste y derrame abdominal y pélvico. La ecografía de contraste mostró que la pared del quiste de la masa pélvica estaba significativamente mejorada, se sospechaba malignidad y se recomendó un tratamiento quirúrgico. El 14 de noviembre de 2018, la paciente se sometió a liberación de adherencias pélvicas e intestinales transabdominales, omento, ovarios bilaterales, peritoneo multipunto y múltiples adenomiosis y histerectomía. Durante la operación, se aspiraron aproximadamente 600 ml de ascitis hemorrágica. Tras la exploración, se observó una masa de color rojo grisáceo con un diámetro de aproximadamente 8 cm en la superficie del epiplón mayor, que era suave y se asemejaba a carne podrida. Se encontraron depósitos de celulosa marrón difusos en la superficie del útero, ovarios bilaterales, pared abdominal, tracto intestinal, surco lateral del recto y pared anterior del recto. Las lesiones no se eliminaron por completo y algunas áreas se electrocoagularon. El examen patológico de la muestra resecada mostró endometriosis del tejido retiniano con vasodilatación, ampollas, infiltración linfocítica difusa y focal, folículos ováricos císticos bilaterales, fibrosis peritoneal dentro de la necrosis del tejido adiposo, proliferación de fibroblastos, aumento de la infiltración de células espumosas y adenomiosis uterina. La patología de ascitis mostró muchos glóbulos rojos, un pequeño número de linfocitos y neutrófilos y ninguna célula tumoral. Después de la operación, la paciente se recuperó sin problemas y se trató con agonista de la hormona liberadora de gonadotropina (GnRH-α). Se inició leuprorelina una vez al mes durante 6 meses, seguido de dienogest oral (DNG) durante 3 años, después de lo cual se interrumpió la medicación durante 3 meses. La paciente concibió de forma natural y tuvo un embarazo normal. Se dio a luz a un bebé de 3300 g por vía vaginal a las 39 semanas + 3 días de gestación. Tanto la madre como el bebé estaban sanos, sin recurrencia ni reacciones adversas durante el seguimiento.\n\nMH - Humanos\nMH - Mujer\nMH - *Endometriosis/complicaciones/terapia\nMH - Adulto",
+        "gold_summary": "Preocupaciones de la paciente: Una mujer de 28 años de edad vino a nuestro hospital para recibir tratamiento debido al descubrimiento de una masa pélvica 10 meses antes. Después de la admisión, la paciente se sometió a tratamiento quirúrgico y fue dada de alta en 1 semana. Recibió tratamiento médico durante 3 años después del alta. Después de la retirada de la medicación, la paciente quedó embarazada y dio a luz a un niño sin recurrencia durante el seguimiento.\n\nDiagnósticos: Los diagnósticos iniciales al ingreso fueron «¿masa pelviana inflamatoria?» y «¿endometriosis?». Después de 10 meses, la paciente volvió a ser internada en el hospital debido a un aumento gradual de la masa, y se le diagnosticó endometriosis.\n\nIntervenciones: El paciente fue tratado con terapia antiinfecciosa de rehidratación por primera vez, y el paciente fue tratado quirúrgicamente por segunda vez, seguido de agonista de la hormona liberadora de gonadotropina (GnRH-α) y tratamiento con dienogest (DNG) después de la cirugía.\n\nResultados: Después de 6 ciclos de tratamiento con GnRH-α y 3 años de tratamiento con DNG, un hijo nació con éxito tras la interrupción de la medicación y, hasta ahora, no se han producido reacciones adversas ni recurrencias durante el período de seguimiento.\n",
+        "synthetic_summary": {
+            "B1": "Había una mujer que tenía un bulto en su barriga por mucho tiempo. Los doctores la ayudaron con una operación y medicina para que se sintiera mejor. \n\nDespués de tomar la medicina por mucho tiempo, la mujer pudo tener un bebé sano. Ella y su bebé están bien y felices.",
+            "B2": "**Lo que le pasó a la paciente:**  \nUna mujer de 28 años tenía una masa, que es una especie de bulto, en la parte baja de su abdomen desde hacía 10 meses. Fue al hospital para tratarse. Al principio, pensaron que podía ser una inflamación o una enfermedad llamada endometriosis, que ocurre cuando un tejido parecido al que está dentro del útero crece fuera de él y causa dolor o problemas.\n\n**Qué hicieron los médicos:**  \nPrimero, le dieron un tratamiento para la inflamación y la hidratación. Pero como la masa creció, la operaron para quitarla y examinarla mejor. Después de la cirugía, le dieron medicamentos especiales que ayudan a controlar la endometriosis. Estos medicamentos incluyen un tipo que afecta las hormonas del cuerpo (llamado agonista de GnRH) y otro llamado dienogest, que tomaba por varios años.\n\n**Qué pasó después:**  \nTras el tratamiento y la cirugía, la paciente pudo quedar embarazada de forma natural. Tuvo un bebé sano y no volvió a tener problemas ni síntomas de la enfermedad durante el tiempo que la siguieron en el hospital.\n\n**En resumen:**  \nEsta paciente con endometriosis y una masa pélvica recibió cirugía y tratamiento hormonal. Gracias a esto, pudo tener un embarazo normal y no tuvo complicaciones después del tratamiento.",
+            "B3": "Resumen detallado para público general universitario\n\n**Contexto y motivo de consulta**  \nUna mujer asiática de 28 años acudió al hospital tras haber detectado una masa en la pelvis que persistía desde hacía 10 meses. Antes de esto, su menstruación era regular, con un volumen moderado y dolor menstrual (dismenorrea). No presentaba antecedentes de embarazos exitosos, pero sí un aborto espontáneo. Durante el examen físico, se encontró que la parte posterior del útero estaba agrandada (aproximadamente 8 cm) y con poca movilidad, aunque sin otras anomalías evidentes. La paciente no había experimentado dolor abdominal significativo durante esos meses previos.\n\n**Hallazgos diagnósticos iniciales**  \nLa ecografía reveló una masa heterogénea de unos 4 cm en la parte superior derecha del útero y un pequeño nódulo en el epiplón mayor (una capa de tejido graso en el abdomen) de 2 cm. Además, el análisis sanguíneo mostró un nivel elevado de CA125 (416 mU/mL), una proteína que puede aumentar en enfermedades inflamatorias o tumorales del área pélvica. Se sospechó inicialmente que la masa correspondía a endometriosis (una condición en la que tejido similar al endometrio crece fuera del útero) o a una masa inflamatoria pélvica.\n\n**Evolución y revaluación**  \nTras un tratamiento inicial con líquidos y antibióticos, la paciente mejoró y fue dada de alta. Los niveles de CA125 disminuyeron progresivamente hasta normalizarse en 6 semanas. Sin embargo, la masa pélvica continuó creciendo, alcanzando dimensiones de aproximadamente 8 cm, con características ecográficas que sugerían posible malignidad, lo que llevó a recomendar cirugía.\n\n**Intervenciones quirúrgicas y hallazgos intraoperatorios**  \nEl 14 de noviembre de 2018, la paciente fue sometida a una cirugía abdominal para liberar adherencias (tejido cicatricial que une órganos) en la pelvis e intestinos, así como para extirpar tejido afectado en el epiplón, ovarios, peritoneo (membrana que recubre la cavidad abdominal) y el útero. Durante la operación se drenaron 600 ml de líquido abdominal con sangre (ascitis hemorrágica). Se observaron lesiones características de endometriosis, incluyendo depósitos marrones en múltiples superficies abdominales y uterinas, y una masa blanda en el epiplón que parecía tejido necrótico. No fue posible eliminar todas las lesiones, por lo que algunas áreas se trataron con electrocoagulación para reducir su actividad.\n\n**Resultados del análisis patológico**  \nEl examen microscópico confirmó la presencia de endometriosis en el tejido adiposo del epiplón, con inflamación crónica y cambios en el tejido uterino compatibles con adenomiosis (una forma de endometriosis dentro del músculo uterino). No se detectaron células tumorales malignas en el líquido ascítico. También se observaron fibrosis (formación de tejido cicatricial) y proliferación de fibroblastos (células que forman tejido conectivo).\n\n**Tratamiento posterior y seguimiento**  \nDespués de la cirugía, la paciente recibió terapia hormonal con un agonista de la hormona liberadora de gonadotropina (GnRH-α), específicamente leuprorelina, administrada mensualmente durante 6 meses para suprimir la actividad ovárica y reducir la endometriosis. Posteriormente, continuó con dienogest (un progestágeno oral) durante 3 años para mantener el control de la enfermedad. Tras suspender la medicación durante 3 meses, la paciente logró concebir de forma natural.\n\n**Resultados obstétricos y estado actual**  \nLa paciente tuvo un embarazo normal y dio a luz por vía vaginal a término (39 semanas y 3 días) a un bebé sano de 3300 gramos. Durante el seguimiento posterior, no se observaron recurrencias de la endometriosis ni efectos adversos relacionados con el tratamiento o el embarazo.\n\n---\n\n**Interpretación clínica**  \nEste caso ilustra la complejidad del diagnóstico y manejo de la endometriosis con masas pélvicas grandes y elevación del marcador CA125, que puede simular malignidad. La combinación de cirugía para el control de lesiones extensas y terapia hormonal prolongada fue efectiva para controlar la enfermedad y preservar la fertilidad, permitiendo un embarazo exitoso sin complicaciones.\n\n**Próximos pasos y recomendaciones**  \nEl seguimiento clínico continuo es fundamental para detectar posibles recurrencias. La terapia hormonal prolongada puede ser necesaria para mantener la remisión. Además, este caso destaca la importancia de un enfoque multidisciplinario para el manejo de endometriosis avanzada, especialmente en mujeres jóvenes que desean conservar la fertilidad."
+        }
+    },
+    {
+        "article": "Presentamos una paciente de 76 años de edad, que es traída al servicio de urgencias por bajo nivel de conciencia con tendencia al sueño.\n\nComo antecedentes médicos de interés destaca una enfermedad pulmonar intersticial difusa, dislipemia e hipertensión arterial.\n\nA la exploración física el paciente se encuentra estuporosa, arreactiva, con atonía de las 4 extremidades y desviación conjugada de la mirada hacia la derecha, sin fiebre y con una leve sequedad en piel y mucosas. La analítica sanguínea no muestra alteraciones significativas.\n\nEl paciente es valorado por el servicio de neurología que considera la realización de una TC cerebral urgente ante la sospecha de patología intracraneal de evolución aguda. Las pruebas de imagen ponen de manifiesto la presencia de numerosas burbujas aéreas que se disponen en los surcos cerebrales, cuerpo calloso y ambos tálamos así como áreas hipodensas cortico-subcorticales de distribución parcheada en hemisferio cerebeloso izquierdo y parietooccipitales bilaterales, todo ello compatible con isquemia cerebral subaguda secundaria a embolismo gaseoso.\n\nAnte los antecedentes personales de enfermedad pulmonar intersticial difusa se decide también realizar una placa de tórax en proyección anteroposterior y una TC torácica que objetivan un neumotórax apical izquierdo y aire ectópico en mediastino superior.\n\nSe decide el ingreso en la Unidad de Ictus del centro para control estrecho de constantes, sin embargo, la paciente presenta una evolución tórpida con el fallecimiento el segundo día de ingreso debido a fracaso multiorgánico.",
+        "gold_summary": "Paciente de 76 años con una enfermedad pulmonar intersticial difusa preexistente, que experimentó un ictus masivo debido a un neumomediastino espontáneo. Su presentación incluyó confusión, convulsiones y debilidad motora. Las pruebas de imagen revelaron burbujas de aire en los surcos cerebrales y áreas hipodensas en el cerebelo y parietooccipitales. Además, se observó neumotórax y aire en el mediastino superior en las radiografías de tórax y la tomografía torácica. A pesar de las medidas terapéuticas como el oxígeno hiperbárico, la paciente lamentablemente falleció debido al fallo multiorgánico.",
+        "synthetic_summary": {
+            "B1": "Había una señora de 76 años que estaba muy enferma y se sentía muy cansada. Ella tenía problemas en sus pulmones desde antes. Un día, su cerebro se enfermó mucho porque había aire donde no debía estar. Esto hizo que ella se confundiera y se sintiera muy débil. Los doctores vieron en sus fotos que había aire en su cabeza y en su pecho. Aunque trataron de ayudarla mucho, ella se puso muy mal y no pudo mejorar. Los doctores estaban tristes porque ella se fue al cielo.",
+            "B2": "Paciente de 76 años con una enfermedad pulmonar que afecta sus pulmones, llamada enfermedad pulmonar intersticial difusa. Ella llegó al hospital con confusión, somnolencia y debilidad en sus brazos y piernas. Los médicos hicieron una tomografía cerebral, que es una imagen detallada del cerebro, y encontraron burbujas de aire dentro de su cerebro y áreas dañadas en partes del cerebelo y otras zonas del cerebro. También hicieron radiografías y una tomografía del pecho, donde vieron que tenía un neumotórax, que es aire fuera del pulmón, y aire en una zona llamada mediastino, que está en el centro del pecho. Estos problemas causaron que el aire entrara en el cerebro, lo que provocó un tipo de accidente cerebrovascular llamado embolismo gaseoso. Aunque la paciente recibió tratamiento, incluyendo oxígeno especial para eliminar el aire, su estado empeoró y falleció por el fallo de varios órganos.",
+            "B3": "**Contexto**  \nSe presenta el caso de una mujer de 76 años con antecedentes de enfermedad pulmonar intersticial difusa, dislipemia e hipertensión arterial, que fue ingresada en urgencias debido a un estado de conciencia disminuido y tendencia al sueño. En la exploración física, la paciente estaba en estupor, sin respuesta a estímulos, con debilidad en las cuatro extremidades y desviación de la mirada hacia la derecha, sin fiebre y con signos leves de deshidratación.\n\n**Hallazgos Clave**  \nLa evaluación neurológica llevó a la realización urgente de una tomografía computarizada (TC) cerebral, que mostró múltiples burbujas de aire localizadas en los surcos cerebrales, el cuerpo calloso y ambos tálamos, además de áreas con menor densidad en la corteza y la sustancia subcortical del cerebelo izquierdo y regiones parietooccipitales bilaterales. Estas imágenes son compatibles con un daño cerebral por isquemia (falta de flujo sanguíneo) secundaria a embolismo gaseoso (bloqueo causado por burbujas de aire).  \n\nDado el antecedente pulmonar, se realizaron radiografías y una TC de tórax que evidenciaron un neumotórax apical izquierdo (colapso parcial del pulmón en la parte superior) y presencia de aire fuera de lugar en el mediastino superior (neumomediastino), lo que sugiere que el aire escapó desde el pulmón hacia estructuras cercanas.\n\n**Interpretación Clínica**  \nLa paciente sufrió un ictus masivo debido a la entrada de aire en la circulación cerebral, probablemente originado por el neumotórax y el neumomediastino espontáneos relacionados con su enfermedad pulmonar intersticial. Esta situación es grave porque las burbujas de aire pueden bloquear vasos sanguíneos y causar daño cerebral extenso. A pesar de la atención especializada y las medidas terapéuticas, incluyendo el soporte en la Unidad de Ictus, la evolución fue desfavorable.\n\n**Próximos Pasos y Resultado**  \nLa paciente falleció al segundo día de ingreso debido a un fallo multiorgánico, que es la incapacidad progresiva de varios órganos vitales. Este caso resalta la importancia de reconocer rápidamente el embolismo gaseoso cerebral como una complicación potencialmente mortal en pacientes con enfermedades pulmonares crónicas y neumotórax espontáneo."
+        }
+    },
+    {
+        "article": "Un hombre de 24 años de edad, de etnia persa, presentó una queja principal de mal olor bucal después de un período de recuperación de la enfermedad leve por coronavirus 2019 (COVID-19), que quería resolver lo antes posible. Su dentista notó pérdida ósea y sangrado al explorar el área interproximal de los dientes número 18 y 19 clínicamente. Se realizó un escalamiento y un aplanamiento radicular, y se ordenaron radiografías periapicales y panorámicas para la evaluación del paciente. Sin embargo, el paciente se negó a tomar radiografías. La halitosis del paciente disminuyó después de 1 semana de tratamiento. Después de 2 meses, el paciente volvió a su dentista con la queja principal de sensibilidad al frío en sus incisivos mandibulares. El dentista realizó una prueba de vitalidad, y los dientes eran vitales excepto los números 23 y 24. El dentista tomó una radiografía periapical, y una lesión radiolucente en la mandíbula anterior era evidente.\n\nEn la radiografía panorámica, se evidenció una lesión radiolúcida lítica grande y bien definida con bordes festoneados que se extendían desde el diente número 31 en el lado derecho hasta el ramus ascendente izquierdo. Un estudio posterior de tomografía computarizada de haz cónico (TCFC) reveló una lesión lítica multilocular grande, con un margen relativamente distinto, que causó adelgazamiento y perforación de los cortexes bucales y linguales y signos de festoneado.\n\nTras el examen, se remitió al paciente a un cirujano oral y maxilofacial. En la entrevista médica, el paciente explicó su prolapso de la válvula mitral; antecedentes de episodios recurrentes de otitis desde el primer año de vida; antecedentes de septicemia de origen desconocido cuando tenía un año de edad, tras episodios de diarrea y vómitos; antecedentes de uso de broncodilatadores para la alergia estacional; antecedentes de uso de levotiroxina, cabergolina, acetato de desmopresina (DDAVP) en spray y gel de testosterona durante 4 años tras el diagnóstico de síndrome de silla turca vacía, tras poliúria y polidipsia; y, por último, antecedentes de infección reciente por COVID-19 (3 meses antes). Su historia familiar reveló tiroiditis de Hashimoto en su familia materna; su abuelo, su madre y sus tres tías padecían este tipo de hipotiroidismo. El historial quirúrgico previo del paciente incluía una reparación de una hernia inguinal 10 años antes sin complicaciones. Además, el paciente era obeso, con un índice de masa corporal (IMC) de 34,5.\n\nEn el examen clínico, los hallazgos extraorales e intraorales no fueron relevantes. Los exámenes de laboratorio, incluido el recuento sanguíneo completo (CBC), fueron normales, excepto por un aumento en la velocidad de sedimentación globular (ESR) y los niveles de proteína C reactiva (CRP). Se realizó una biopsia incisional en la mandíbula anterior y la muestra se envió al departamento de patología oral y maxilofacial de la Universidad de Ciencias Médicas Shahid Beheshti. Las secciones mostraron una infiltración difusa de grandes células de tinción pálida, como los histiocitos, con eosinófilos dentados y numerosos en el fondo fibroso. Un examen de inmunohistoquímica (IHC) reveló un positivo disperso para el grupo de diferenciación 1a (CD-1a) (+ +), un positivo fuerte para Langerin (CD-207) (+ + +), y más del 50% positivo para S-100.\n\nDe acuerdo con los datos clínicos, radiológicos e histopatológicos, se llegó al diagnóstico de LCH. Los diagnósticos diferenciales fueron osteomielitis, granuloma eosinófilo y metástasis ósea. Sin embargo, debido a las pruebas de laboratorio, los datos radiológicos y el historial clínico, se confirmó el diagnóstico de LCH. Por lo tanto, para un examen más a fondo, el paciente fue derivado al departamento de medicina nuclear para una tomografía por emisión de positrones con fluor-2-desoxiglucosa y una tomografía computarizada (FDG PET/CT), que reveló lesiones líticas hipermetabólicas en la mandíbula, el parietal derecho, el frontal izquierdo y el esfenoidal izquierdo, y opacidad hipermetabólica en el seno etmoidal izquierdo. Además, se observó una actividad metabólica aumentada en la región sellar, hidrocefalia comunicante y amígdalas palatinas hipermetabólicas prominentes. Además, se evidenció una actividad metabólica heterogénea aumentada en las tibias y fémures bilaterales.\n\nUna resonancia magnética del cerebro reveló una notable ampliación de la intensidad del material del líquido cefalorraquídeo (LCR) que contiene la silla turca. La adenohipófisis apareció como una capa delgada en la base de la silla turca agrandada, y se observaron cambios homogéneos e inflamatorios en las células aéreas mastoideas izquierdas. Se observó la extensión de la inflamación hacia el oído medio izquierdo (es de destacar que el paciente había sufrido de otitis durante muchos años). De acuerdo con la implicación multifocal de la enfermedad y su pronóstico cuestionable, el paciente fue derivado al departamento de oncología para quimioterapia sistémica. Pruebas posteriores revelaron mutaciones en el oncogen BRAF y no se detectaron mutaciones en KRAS y NRAS. El oncólogo eligió un régimen de denosumab, vinblastina, etopósido, 6-mercaptopurina, metotrexato y pegfilgrastim; sin embargo, el seguimiento no fue posible ya que el paciente falleció tras un accidente.\n",
+        "gold_summary": "Un paciente de 24 años de edad, de etnia persa, se presentó con una queja principal de halitosis tras recuperarse de la enfermedad por coronavirus 2019 en el consultorio de su dentista general. Los exámenes intraorales y extraorales no revelaron ningún problema específico. En la sesión de seguimiento tras el tratamiento periodontal de fase I, la sensibilidad de los dientes al estímulo frío era evidente, y las radiografías revelaron una gran lesión intraósea lítica en la mandíbula. Una biopsia incisional reveló células de Langerhans y una reacción positiva a Langerina y al grupo de diferenciación 1a, por lo que se le diagnosticó histiocitosis de células de Langerhans. Después de realizar una tomografía por emisión de positrones con fluoro-2-desoxiglucosa y una tomografía computarizada, una resonancia magnética y una tomografía computarizada de haz cónico, debido a la implicación generalizada de la enfermedad, el paciente fue derivado a un oncólogo. En última instancia, se descubrió que los problemas de salud infantil del paciente, incluidos los problemas endocrinos, probablemente fueron causados por una histiocitosis de células de Langerhans no diagnosticada. El oncólogo eligió un régimen de denosumab, vinblastina, etopósido, 6-mercaptopurina, metotrexato y pegfilgrastim. El seguimiento no fue posible ya que el paciente falleció tras un accidente.\n",
+        "synthetic_summary": {
+            "B1": "Había un hombre joven que tenía mal olor en la boca. Esto pasó después de que se enfermó con un virus. El dentista vio que algunos dientes le dolían con el frío. También encontró un hueco grande en el hueso de su mandíbula.\n\nEl doctor tomó un pedacito de ese hueso para mirar con un microscopio. Vieron unas células especiales llamadas células de Langerhans. Esto dijo que tenía una enfermedad llamada histiocitosis de células de Langerhans.\n\nEl hombre fue a ver a otro doctor que sabe de enfermedades graves. Le hicieron muchas pruebas para ver dónde estaba la enfermedad. Los doctores dijeron que la enfermedad estaba en muchas partes de su cuerpo.\n\nEl doctor le dio medicinas fuertes para ayudarlo. Pero el hombre tuvo un accidente y no pudo seguir con el tratamiento. Los doctores estaban muy tristes por eso.",
+            "B2": "**Lo que le pasó al paciente**  \nUn joven de 24 años, después de recuperarse de un caso leve de COVID-19, fue al dentista porque tenía mal olor en la boca. Al principio, no se encontraron problemas visibles en su boca ni en su cara. Sin embargo, después de un tratamiento para limpiar sus dientes, empezó a sentir sensibilidad al frío en algunos dientes. Las radiografías mostraron una lesión grande en el hueso de la mandíbula.\n\n**Qué encontraron los médicos**  \nPara entender mejor la lesión, los médicos tomaron una biopsia, que es cuando se extrae un pequeño pedazo de tejido para examinarlo bajo el microscopio. En esta muestra, vieron células especiales llamadas células de Langerhans. Estas células reaccionaron a ciertas pruebas que confirmaron que el paciente tenía una enfermedad llamada histiocitosis de células de Langerhans (LCH). Esta enfermedad puede afectar varios órganos y huesos.\n\n**Estudios adicionales y diagnóstico**  \nEl paciente se sometió a varios estudios, como tomografías y resonancias magnéticas, que mostraron que la enfermedad estaba en varias partes de su cuerpo, incluyendo huesos de la cabeza y las piernas, y también afectaba algunas áreas del cerebro. Además, descubrieron que algunos problemas de salud que tuvo cuando era niño, como problemas hormonales y frecuentes infecciones de oído, probablemente estaban relacionados con esta enfermedad que no se había detectado antes.\n\n**Tratamiento y resultado**  \nDebido a que la enfermedad estaba extendida, el paciente fue enviado a un especialista en cáncer para recibir quimioterapia, que es un tratamiento con medicamentos para combatir células enfermas. El médico eligió un plan con varios medicamentos para tratar la enfermedad. Lamentablemente, no se pudo hacer un seguimiento del tratamiento porque el paciente falleció debido a un accidente.  \n\nEste caso muestra la importancia de investigar a fondo cuando aparecen problemas inusuales en la boca, ya que pueden ser señales de enfermedades más serias en el cuerpo.",
+            "B3": "**Contexto**  \nUn hombre persa de 24 años acudió a su dentista quejándose de mal olor en la boca (halitosis) poco después de recuperarse de una infección leve por COVID-19. Inicialmente, no se encontraron problemas visibles en su boca ni en el examen externo. Sin embargo, tras un tratamiento periodontal inicial, el paciente comenzó a experimentar sensibilidad dental al frío, lo que llevó a la realización de radiografías que mostraron una lesión ósea anormal en la mandíbula.\n\n**Hallazgos Clave**  \nUna biopsia de la lesión reveló la presencia de células de Langerhans, un tipo específico de células inmunitarias, confirmada mediante pruebas inmunohistoquímicas positivas para marcadores como Langerina (CD-207) y CD1a. Estos hallazgos permitieron diagnosticar una enfermedad llamada histiocitosis de células de Langerhans (LCH), que es una condición poco común caracterizada por la proliferación anormal de estas células. Estudios de imagen adicionales, incluyendo tomografía computarizada de haz cónico (TCFC), tomografía por emisión de positrones con fluor-2-desoxiglucosa (FDG PET/CT) y resonancia magnética cerebral, revelaron que la enfermedad afectaba múltiples áreas óseas, incluyendo varias regiones del cráneo y huesos largos, así como inflamación en estructuras cercanas al oído y la hipófisis (glándula cerebral que regula varias funciones endocrinas).\n\n**Interpretación Clínica**  \nEl diagnóstico de LCH explicó no solo la lesión mandibular sino también varios problemas de salud que el paciente había tenido desde la infancia, como episodios recurrentes de otitis (infección del oído), alteraciones endocrinas relacionadas con un síndrome de silla turca vacía (una anomalía en la glándula hipófisis), y otros síntomas sistémicos. La enfermedad mostró un compromiso multifocal, lo que significa que afectaba varias áreas del cuerpo, complicando su pronóstico. Además, se detectó una mutación en el oncogen BRAF, un factor genético que puede influir en el comportamiento de la enfermedad y en las opciones de tratamiento.\n\n**Próximos Pasos y Tratamiento**  \nDebido a la extensión y gravedad de la enfermedad, el paciente fue remitido al departamento de oncología para recibir quimioterapia sistémica. El régimen elegido incluyó varios medicamentos: denosumab (que ayuda a inhibir la destrucción ósea), vinblastina, etopósido, 6-mercaptopurina, metotrexato y pegfilgrastim (que estimula la producción de células sanguíneas). Lamentablemente, no fue posible realizar un seguimiento del tratamiento porque el paciente falleció posteriormente a causa de un accidente.\n\n**Resumen Final**  \nEste caso ilustra cómo una enfermedad poco común como la histiocitosis de células de Langerhans puede manifestarse inicialmente con síntomas aparentemente leves, como mal aliento y sensibilidad dental, y estar relacionada con problemas médicos complejos desde la infancia. La detección temprana y el diagnóstico preciso mediante biopsia y estudios de imagen son fundamentales para orientar un tratamiento adecuado, aunque el pronóstico puede ser reservado cuando la enfermedad afecta múltiples órganos."
+        }
+    },
+    {
+        "article": "La paciente es una mujer de 66 años de edad que goza de buena salud. A mediados de la década de 1980, recibió varias sesiones de tratamiento con rayos grenz en el cuero cabelludo para aliviar el picor asociado con la psoriasis del cuero cabelludo. Con un tratamiento regular de aproximadamente una sesión al mes durante un período de 5 años, que se complementó de vez en cuando con alquitrán de hulla, ácido salicílico y prednisona, logró cierto alivio de su enfermedad. Con el tiempo, su cabello se adelgazó; la piel en toda el área del cuero cabelludo se volvió sensible al dolor y se produjo cicatrización. Los tratamientos con rayos grenz se habían administrado en una clínica privada; no se disponía de detalles del tratamiento, como la dosis única y acumulada. No había sufrido radiodermitis.\n\nEn un período muy breve en 2020, unos 35 años después de que cesara el tratamiento de radiación, aparecieron numerosos BCC y queratosis actínicas premalignas (AK) en su cuero cabelludo. Se inició un régimen de tratamiento de extirpación quirúrgica de BCC verificado por histología preoperatoria y crioterapia de AK por evaluación del médico. La terapia fotodinámica o los tratamientos tópicos no eran aplicables debido a la sensibilidad al dolor y las secuelas de la cirugía. De 2020 a 2022, recibió varios tratamientos de criocirugía y curetaje y un total de 13 extirpaciones quirúrgicas de BCC por cirugía de Mohs. Se estima que su número total de extirpaciones a lo largo del tiempo es de unos 30. Los BCC recalcitrantes y de novo en el cuero cabelludo cada vez más dañado, obviamente, son un desafío eterno; por lo tanto, los cirujanos plásticos y los dermatólogos buscaban otra modalidad de tratamiento con un mejor índice terapéutico.\n\nEn septiembre de 2022, aparecieron nuevos CCB confirmados histológicamente en el cuero cabelludo. La exploración por ultrasonido (DermaScan C, Cortex Technology ApS, Aalborg, Dinamarca) mostró tumores ecolucidos de 0,5-1,3 mm de espesor en ambos sitios analizados histológicamente, así como en algunas lesiones adicionales que pudieron identificarse en base al examen clínico y dermatoscópico. La paciente, tras ser informada, dio su consentimiento por escrito para el tratamiento con HIFU, con o sin biopsia de pretratamiento de las lesiones sospechosas.\n\nSe delinearon las lesiones elegibles para el tratamiento con un rotulador impermeable, incluyendo un margen perilesional de 2 mm. Se mapeó cada lesión seleccionada en una lámina transparente para ayudar a determinar la ubicación precisa en el seguimiento. Se usó el ultrasonido de 20 MHz para confirmar la profundidad de las lesiones identificadas al inicio y en las visitas de seguimiento posteriores. Debido al estado del cuero cabelludo conocido por ser sensible al dolor, se administró anestesia local (lidocaína 25 mg/ml + adrenalina 5 mg/ml, Amgros I/S, Copenhagen, Dinamarca) a todas las lesiones 10-15 minutos antes del tratamiento.\n\nLas lesiones fueron tratadas con HIFU utilizando la sonda de 1.3 mm; ajustes de 150 ms/dosis y energía acústica de 0.9 J/dosis. Se aplicaron 20-200 dosis a las lesiones, dependiendo de la extensión de la lesión. Las lesiones tratadas se curaron de forma espontánea sin complicaciones o necesidad de tratamiento especial. Se programaron visitas de seguimiento cada 3-6 meses para controlar la tasa de curación/recaída, tolerancia local y lesiones nuevas no identificadas anteriormente.\n\nDurante los 15 meses posteriores a la limpieza inicial con HIFU, se trataron con HIFU un total de 10 lesiones que, de acuerdo con las rutinas, hubieran requerido una biopsia seguida de una cirugía de escisión, en sesiones de unos 30 minutos. Las lesiones se curaron en unos pocos días sin complicaciones ni necesidad de intervención. Se observó una limpieza total en 7 de 8 lesiones de BCC tratadas y en ambas lesiones de AK. La única lesión recurrente de BCC de pequeño tamaño se observó después de 15 meses entre las primeras seis lesiones tratadas; la lesión se volvió a tratar con HIFU. Ejemplos de lesiones curadas 15 meses después del tratamiento con HIFU; el tumor con recurrencia.\n",
+        "gold_summary": "Una mujer de 66 años que en la década de 1980 había recibido varios tratamientos de rayos gamma en el cuero cabelludo desarrolló múltiples carcinomas basocelulares en la zona. Se le habían realizado más de 30 cirugías de escisión, incluida la cirugía de Mohs, en el pasado, con muchas complicaciones locales, pero, no obstante, los cánceres recurrentes. Los tratamientos con HIFU aplicados a ocho carcinomas basocelulares y dos lesiones precancerosas dieron como resultado una limpieza completa en el control a los 12 meses, pero una recurrencia después de 15 meses.\n",
+        "synthetic_summary": {
+            "B1": "Había una señora de 66 años con problemas en su cabeza. Hace mucho tiempo, le dieron unos rayos para ayudar su piel que le picaba. Pero después, le salieron muchos bultitos malos en la cabeza.\n\nElla tuvo muchas operaciones para quitar esos bultitos. A veces, le dolía mucho y los bultitos volvían a salir. Luego, los doctores usaron un tratamiento especial con un aparato que usa calor para quitar los bultitos.\n\nDespués de un año, casi todos los bultitos se fueron. Pero después de un poco más de un año, uno volvió a salir. Los doctores la cuidaron y trataron otra vez. Ella está siendo cuidada con mucho cariño.",
+            "B2": "**Caso de una mujer con cáncer en el cuero cabelludo**\n\nUna mujer de 66 años recibió hace muchos años, en la década de 1980, un tratamiento con rayos especiales en su cuero cabelludo para aliviar una enfermedad llamada psoriasis, que causa picor y enrojecimiento. Después de ese tratamiento, su piel se volvió sensible y se dañó con el tiempo.\n\nAproximadamente 35 años después, empezaron a aparecer en su cuero cabelludo varios tumores llamados carcinomas basocelulares (que son un tipo de cáncer de piel) y lesiones que podrían volverse cancerosas. Para tratar estos tumores, le hicieron más de 30 cirugías, incluyendo una técnica especial llamada cirugía de Mohs, que busca eliminar el cáncer sin dañar mucho la piel sana. Sin embargo, los tumores seguían apareciendo y la piel estaba muy dañada y sensible.\n\n**Nuevo tratamiento con ultrasonido de alta intensidad (HIFU)**\n\nEn 2022, los médicos decidieron probar un nuevo tratamiento llamado HIFU, que usa ondas de ultrasonido para destruir los tumores sin necesidad de cirugía. Antes de aplicar el tratamiento, marcaron las lesiones y usaron anestesia local para evitar el dolor.\n\nDurante 15 meses, trataron con HIFU diez lesiones: ocho eran carcinomas basocelulares y dos eran lesiones precancerosas. Siete de los ocho tumores desaparecieron completamente después de un año. Solo uno volvió a aparecer después de 15 meses, y fue tratado nuevamente con HIFU. Las lesiones precancerosas también sanaron sin problemas.\n\n**Qué significa esto**\n\nEste caso muestra que el tratamiento con HIFU puede ser una opción efectiva para eliminar ciertos cánceres de piel y lesiones precancerosas en pacientes con piel sensible y dañada, evitando cirugías complicadas. Aunque algunos tumores pueden volver, el HIFU ofrece una alternativa menos invasiva y con buena tolerancia para controlar estos problemas.",
+            "B3": "**Contexto**  \nSe trata de una mujer de 66 años que, durante la década de 1980, recibió múltiples tratamientos con rayos grenz (una forma de radiación de baja energía) en el cuero cabelludo para aliviar la psoriasis, una enfermedad inflamatoria de la piel. Estos tratamientos, junto con otros medicamentos tópicos, lograron cierto alivio, pero con el tiempo provocaron adelgazamiento del cabello, sensibilidad dolorosa y cicatrización en la piel del cuero cabelludo. Aproximadamente 35 años después de finalizar la radioterapia, la paciente desarrolló numerosos carcinomas basocelulares (un tipo común de cáncer de piel) y queratosis actínicas (lesiones precancerosas) en la misma zona.\n\n**Hallazgos Clave**  \nEntre 2020 y 2022, la paciente fue sometida a múltiples tratamientos convencionales, incluyendo más de 30 cirugías para extirpar los carcinomas basocelulares, algunas de ellas mediante cirugía de Mohs, una técnica especializada para eliminar tumores de piel con precisión. También recibió crioterapia para las lesiones precancerosas. Sin embargo, los tumores continuaron apareciendo, y la sensibilidad y daño en el cuero cabelludo dificultaban la aplicación de otros tratamientos tópicos o fotodinámicos.\n\nEn septiembre de 2022, se detectaron nuevos carcinomas basocelulares confirmados mediante biopsia. Para evaluar la extensión y profundidad de las lesiones, se utilizó un ultrasonido especializado que mostró tumores de entre 0,5 y 1,3 mm de grosor. La paciente aceptó someterse a un tratamiento con ultrasonido focalizado de alta intensidad (HIFU, por sus siglas en inglés), una técnica que utiliza ondas de ultrasonido para destruir tejido tumoral sin cirugía.\n\nAntes del tratamiento, se aplicó anestesia local para minimizar el dolor, y las lesiones fueron cuidadosamente marcadas y mapeadas para su seguimiento. El HIFU se administró con parámetros específicos (dosis de 150 ms y energía de 0.9 julios por dosis), aplicando entre 20 y 200 dosis según el tamaño de cada lesión.\n\n**Interpretación Clínica**  \nDurante los 15 meses posteriores al tratamiento inicial con HIFU, se trataron un total de 10 lesiones (8 carcinomas basocelulares y 2 queratosis actínicas) que, según los protocolos habituales, habrían requerido biopsia y cirugía. Todas las lesiones sanaron espontáneamente en pocos días sin complicaciones ni necesidad de tratamientos adicionales.\n\nEn el seguimiento a 12 meses, se observó una eliminación completa de 7 de las 8 lesiones de carcinoma basocelular y de ambas lesiones precancerosas. Solo una lesión pequeña de carcinoma basocelular recidivó después de 15 meses y fue nuevamente tratada con HIFU con éxito.\n\n**Próximos Pasos**  \nEl uso de HIFU en esta paciente representa una alternativa prometedora para el manejo de carcinomas basocelulares recurrentes en un cuero cabelludo dañado y sensible, donde las opciones quirúrgicas y tópicas son limitadas o generan complicaciones. Se recomienda continuar con controles periódicos cada 3 a 6 meses para detectar nuevas lesiones o recurrencias y evaluar la tolerancia a largo plazo del tratamiento. Además, la experiencia obtenida sugiere que el HIFU podría ser una modalidad terapéutica eficaz y menos invasiva para casos similares en el futuro."
+        }
+    },
+    {
+        "article": "Se realizó un trasplante cardíaco ortotópico a una niña de 12 años con insuficiencia cardíaca en fase terminal debido a una miocardiopatía restrictiva. Durante la operación, se presentó una disfunción primaria grave del injerto, que requirió el uso de oxigenación por membrana extracorpórea venosa arterial. La función cardíaca se recuperó completamente después de 4 días, y su período postoperatorio se complicó por una insuficiencia renal aguda transitoria y un bloqueo auriculoventricular completo que duró >3 semanas después de la operación. Para evitar la disincronía del ventrículo izquierdo y el posible daño de la derivación del ventrículo derecho debido a las biopsias endomiocárdicas de vigilancia de rechazo múltiple, se indicó un marcapasos biventricular transvenoso que utiliza un marcapasos del ventrículo izquierdo aislado a través de la vena coronaria.\n\nBajo anestesia local y sedación suave, se cortó la vena cefálica izquierda y se introdujo un catéter guía en la vena subclavia y se colocó en el seno coronario inicialmente para realizar un venograma cardiaco. Se implantó un electrodo de estimulación endocárdica de elución de esteroides unipolar con mecanismo de fijación activa (Attain StarFix® 4195, Medtronic, Minneapolis, MN) en la rama de la vena interventricular anterior. Las medidas en el momento del implante fueron las siguientes: umbral 2 V a 0,4 ms, onda R 6 mV e impedancia 300 Ω a 4,8 mA. Se implantó un segundo electrodo de estimulación endocárdica de elución de esteroides bipolar con fijación activa (2088T®, St. Jude Medical, Minneapolis, MN) en la aurícula derecha.\n\nAmbos cables se aseguraron y se conectaron a un marcapasos adaptable a la frecuencia (Accent DR®, St. Jude Medical, Minneapolis, MN) que se colocó en una bolsa muscular infraclavicular izquierda y se programó a VDD. Las mediciones de los cables electrofisiológicos fueron estables después del implante: umbral ventricular 1.5 V a 0.7 ms, onda R 4.5 mV, onda P 4.3 mV (bipolar), impedancia ventricular 260 Ω y vida útil estimada de la batería de 5 años.\n\nEl electrocardiograma posterior al implante mostró complejos de morfología de bloqueo de rama derecha, y la evaluación ecocardiográfica mostró ausencia de disincronías auriculoventriculares, interventriculares e intraventriculares. En el seguimiento a 5 años, el paciente permaneció en Clase Funcional I con el mismo sistema de estimulación y conservó la función ventricular.\n\nMH - Bloqueo auriculoventricular/etiología/*terapia\nMH - Niño\nMH - Sinus coronario\nMH - Mujer\nMH - Insuficiencia cardiaca/cirugía\nMH - Trasplante de corazón/*efectos adversos\nMH - Ventrículos del corazón\nMH - Humanos\nMH - *Marcapasos, artificial\nMH - Disfunción/complicaciones/tratamiento del injerto primario\n",
+        "gold_summary": "Se sometió a un trasplante de corazón ortotópico a un niño de 12 años con insuficiencia cardiaca en fase terminal debido a una miocardiopatía restrictiva. La disfunción primaria del injerto precisó oxigenación con membrana extracorpórea venosa arterial. La función cardiaca se normalizó, pero el bloqueo auriculoventricular completo persistió después de 3 semanas. Se realizó un marcapaso bicameral con marcapaso transvenoso del ventrículo izquierdo a través del seno coronario. Tras 5 años de seguimiento, el paciente se encuentra estable con el mismo sistema de marcapaso y con la función ventricular preservada.\n",
+        "synthetic_summary": {
+            "B1": "Un niño de 12 años recibió un nuevo corazón porque su corazón estaba muy enfermo. Al principio, su nuevo corazón tuvo problemas y necesitó ayuda para funcionar. Después de un tiempo, el corazón empezó a trabajar bien. Pero el niño tenía un problema con el ritmo del corazón. Por eso, los doctores le pusieron un pequeño aparato llamado marcapasos para ayudar a que su corazón latiera bien. Cinco años después, el niño está bien y su corazón funciona muy bien con el marcapasos.",
+            "B2": "**Trasplante de Corazón y Uso de Marcapasos en una Niña de 12 Años**\n\nUna niña de 12 años con un problema grave en el corazón llamado miocardiopatía restrictiva, que causa que el corazón no funcione bien, recibió un trasplante de corazón. Durante la operación, el nuevo corazón tuvo dificultades para funcionar correctamente, por lo que los médicos usaron una máquina especial llamada oxigenación por membrana extracorpórea. Esta máquina ayuda a oxigenar la sangre cuando el corazón está débil.\n\nDespués de cuatro días, el corazón trasplantado comenzó a funcionar bien. Sin embargo, la niña tuvo un problema llamado bloqueo auriculoventricular completo, que significa que las señales eléctricas entre las partes superiores e inferiores del corazón no se transmitían bien. Este problema duró más de tres semanas.\n\nPara ayudar a su corazón a latir de manera sincronizada y evitar daños, los médicos le implantaron un marcapasos especial. Un marcapasos es un dispositivo que envía señales eléctricas para controlar el ritmo del corazón. En este caso, colocaron un marcapasos que estimula ambos ventrículos del corazón (las partes inferiores) usando cables que pasan por las venas hasta llegar al corazón.\n\nEl procedimiento se hizo con anestesia local y sedación suave, y los cables se colocaron cuidadosamente en las venas del corazón. El marcapasos se programó para adaptarse a las necesidades del corazón de la niña. Después de la operación, los exámenes mostraron que el corazón latía de forma sincronizada y sin problemas.\n\nCinco años después, la niña está estable, con buena función del corazón y sigue usando el mismo marcapasos sin complicaciones. Esto muestra que el tratamiento fue exitoso para mejorar su calidad de vida.",
+            "B3": "**Contexto**  \nUna niña de 12 años con insuficiencia cardíaca avanzada causada por una miocardiopatía restrictiva (una enfermedad que limita la capacidad del corazón para llenarse de sangre) fue sometida a un trasplante cardíaco ortotópico, que consiste en reemplazar el corazón enfermo por uno sano en la misma posición anatómica. Durante la cirugía, presentó una disfunción grave del nuevo corazón (injerto), lo que requirió soporte temporal con oxigenación por membrana extracorpórea venosa arterial (una técnica que ayuda a oxigenar la sangre y mantener la circulación mientras el corazón se recupera).\n\n**Hallazgos Clave**  \n- La función cardíaca del injerto se recuperó completamente en 4 días.  \n- Posteriormente, la paciente desarrolló un bloqueo auriculoventricular completo (una interrupción total en la transmisión eléctrica entre las aurículas y los ventrículos del corazón) que persistió por más de tres semanas.  \n- Para evitar problemas relacionados con la descoordinación del ventrículo izquierdo y el daño potencial al ventrículo derecho por las biopsias repetidas que se realizan para vigilar el rechazo del trasplante, se decidió implantar un marcapasos biventricular transvenoso. Este dispositivo estimula eléctricamente ambos ventrículos para mantener un ritmo cardíaco sincronizado.  \n- El electrodo del ventrículo izquierdo se colocó a través de la vena coronaria (una vena del corazón) usando un catéter guiado, mientras que otro electrodo se implantó en la aurícula derecha.  \n- Ambos electrodos se conectaron a un marcapasos adaptable a la frecuencia, ubicado en una bolsa muscular debajo de la clavícula izquierda.  \n- Las mediciones eléctricas del marcapasos mostraron parámetros estables y adecuados para un funcionamiento óptimo.  \n- El electrocardiograma posterior mostró una morfología compatible con bloqueo de rama derecha, pero la ecocardiografía confirmó que no existían desincronías en la contracción de las cámaras cardíacas.\n\n**Interpretación Clínica**  \nEl uso de un marcapasos biventricular con estimulación del ventrículo izquierdo a través del seno coronario resultó ser una estrategia efectiva para manejar el bloqueo auriculoventricular prolongado en esta paciente trasplantada. Este enfoque permitió mantener la sincronía en la contracción del corazón, evitando complicaciones que podrían afectar la función ventricular. La estabilidad de los parámetros eléctricos y la ausencia de disincronías evidenciadas por ecocardiografía respaldan la eficacia del tratamiento.\n\n**Próximos Pasos y Seguimiento**  \nA cinco años del implante del marcapasos, la paciente se mantiene en clase funcional I (sin limitaciones para realizar actividades físicas normales), con función ventricular preservada y sin necesidad de cambios en el sistema de estimulación. Esto indica un pronóstico favorable y una buena calidad de vida a largo plazo. Se recomienda continuar con el seguimiento cardiológico regular para monitorear la función del marcapasos y del injerto cardíaco, así como para detectar cualquier posible complicación futura."
+        }
+    },
+    {
+        "article": "Una paciente de 20 años de edad se presentó con distensión abdominal progresiva asociada con calambres abdominales, incapacidad para expulsar flatos y heces, así como vómitos frecuentes de materia ingerida y biliar de un día de duración. El día anterior, dio a luz por cesárea por una indicación de bradicardia fetal severa. También tenía preeclampsia sin signos de gravedad y desnutrición de inicio en la edad adulta con un índice de masa corporal (IMC) de 16,5 kg/M2. No tenía antecedentes de cirugía abdominal previa. Negó cualquier queja similar en el pasado o antecedentes de cambio de hábitos intestinales o estreñimiento con paso de heces sanguinolentas. No tenía ninguna enfermedad médica crónica conocida.\n\nEn el examen físico, la paciente se veía enferma y con dolor. Su presión arterial era de 90/70 mmHg, su pulso oscilaba entre 116 y 120 latidos por minuto, y su frecuencia respiratoria era de 22 a 24 respiraciones por minuto. No se registró fiebre. Su abdomen estaba muy distendido y simétrico, con visibles movimientos intestinales peristálticos. Había una difusa sensibilidad directa en todo su abdomen, más en el cuadrante inferior derecho. Había un signo positivo de acumulación de fluido intraperitoneal con opacidad cambiante. Había una herida quirúrgica suprapúbica bien aproximada con un vendaje limpio. El examen rectal digital no mostró nada destacable. Tenía una herida superficial lineal de 3 cm de largo, orientada verticalmente, en su labio mayor izquierdo, que el equipo de obstetricia pensó inicialmente que era una quemadura de yodo en la piel.\n\nSe le introdujo un catéter y se le resucitó con dos bolsas de solución salina normal y produjo 200 ml de orina en una hora. Se le introdujo una sonda nasogástrica (NGT) pero no hubo una salida significativa. Se le realizó un hemograma completo y una radiografía abdominal simple. Su recuento de glóbulos blancos era de 1780 células/µl con predominio de neutrófilos del 88 %, hemoglobina de 12,7 mg/dl y un recuento de plaquetas de 78 x 103/ µl. Su prueba de función renal era normal y sus enzimas hepáticas estaban ligeramente elevadas por encima del rango normal pero no fue significativo. Su radiografía abdominal simple muestra múltiples niveles de aire-líquido ubicados centralmente con un bucle intestinal grande dilatado ubicado periféricamente y blanqueamiento del espacio pélvico que indica una acumulación de líquido. No se solicitó una tomografía computarizada abdominal (CT) porque trabajamos en un entorno con recursos limitados y para pacientes con obstrucción intestinal, solicitamos una tomografía computarizada cuando existe la posibilidad de un diagnóstico alternativo o cuando se sospecha una obstrucción tumoral.\n\nTras obtener el consentimiento informado por escrito, se exploró a la paciente bajo anestesia general con un diagnóstico de abdomen agudo secundario a obstrucción intestinal mixta secundaria a vólvulo del intestino delgado. El hallazgo intraoperatorio fue un íleon distal que rodeaba el ciego y el colon ascendente proximal, ambos móviles y no adheridos a la pared abdominal posterolateral derecha. Tanto el íleon como el ciego, así como el colon ascendente, eran viables. La punta del apéndice estaba enredada con el nudo ileal y estaba gangrenoso. El intestino delgado proximal y el intestino grueso distal estaban muy distendidos, pero en su ubicación normal. Había unos cuatro litros de líquido intraperitoneal seroso.\n\nDurante la operación, la paciente se mantuvo hipotensa (80/50 mmHg) desde que se le indujo la anestesia y se le administró un vasopresor. Debido a la inestabilidad de la paciente y a la viabilidad de los intestinos afectados por el nudo, se procedió a una hemicolectomía derecha. Se realizó una descompresión proximal y distal de los intestinos delgado y grueso distendidos, respectivamente. Se fijó el ciego y el colon ascendente a la pared abdominal posterolateral derecha con suturas seromusculares interrumpidas con hilo no absorbible (Silk 2-0).\n\nDespués del procedimiento, se le retiró la intubación y se le dio alimentación por vía oral (NPO) durante 24 horas y se le administró un fluido de mantenimiento con reposición de la pérdida. A pesar de la reanimación con fluidos y el apoyo con vasopresores, ella se encontraba persistentemente hipotensa, por lo que se le administró un tratamiento antibiótico doble con ceftriaxona 1 g, IV, BID y metronidazol 500 mg, IV, TID, en vista de un posible shock séptico de origen genitourinario. Su estado empeoró gradualmente y, tras una nueva evaluación el primer día postoperatorio, la herida superficial en su vulva se había extendido hacia la zona suprapúbica con signos clínicos de gangrena de Fournier. Por ello, revisamos su tratamiento antibiótico a meropenem 1 g, IV, BID, vancomicina 1 g, IV, BID y metronidazol 500 mg, IV, TID. Después de obtener el consentimiento informado por escrito, se la volvió a llevar al quirófano para un desbridamiento radical de la gangrena de Fournier y, posteriormente, se la trasladó a la unidad de cuidados intensivos quirúrgicos (ICU) intubada debido a un shock séptico persistente y un retraso en la recuperación de la anestesia. Lamentablemente, falleció con fallo multiorgánico debido a un shock séptico refractario en su segundo día postoperatorio, después de la exploración inicial.\n",
+        "gold_summary": "Presentamos un caso de nudos ileocecales en una paciente posparto con distensión abdominal, vómitos y ausencia de heces y flatos. La radiografía abdominal simple reveló bucles intestinales dilatados con múltiples niveles de aire y fluidos. Se realizó una laparotomía exploratoria con hallazgo intraoperatorio de nudos ileocecales con intestino viable, ciego móvil y colon ascendente y punta gangrenosa del apéndice. Deshicimos el nudo y realizamos una apendectomía. Debido a la inestabilidad intraoperatoria de los signos vitales de la paciente, se aplazó la hemicolectomía derecha y se fijaron el ciego y el colon ascendente a la pared abdominal posterolateral derecha.\n",
+        "synthetic_summary": {
+            "B1": "Había una niña que acababa de tener un bebé. Su barriga estaba muy grande y le dolía mucho. No podía hacer popó ni tirar gases y vomitaba mucho.\n\nLos doctores le hicieron una radiografía y vieron que sus intestinos estaban muy hinchados. La niña fue al hospital y los doctores la operaron para ver qué pasaba.\n\nDentro, encontraron que sus intestinos estaban enredados como un nudo. También vieron que una parte pequeña llamada apéndice estaba dañada. Los doctores deshicieron el nudo y quitaron el apéndice malo.\n\nComo la niña estaba muy débil, los doctores hicieron algo para que sus intestinos no se movieran mucho y la cuidaron mucho después.",
+            "B2": "**Lo que le pasó a la paciente:**  \nUna joven de 20 años, que acababa de tener un bebé por cesárea, llegó al hospital con el abdomen muy hinchado, dolor y vómitos. Además, no podía expulsar gases ni hacer sus necesidades. Estos síntomas indicaban que algo estaba bloqueando su intestino.\n\n**Lo que encontraron en las pruebas:**  \nLa radiografía mostró que partes del intestino estaban muy dilatadas y había niveles de aire y líquido, lo que sugiere una obstrucción. Por eso, los médicos decidieron hacer una cirugía para ver qué estaba pasando.\n\n**Lo que vieron durante la operación:**  \nDescubrieron que una parte del intestino delgado (íleon) estaba enredada alrededor del ciego y el colon ascendente, formando un nudo llamado \"nudo ileocecal\". El intestino estaba en buen estado, pero la punta del apéndice estaba dañada (gangrenosa). Los médicos deshicieron el nudo y quitaron el apéndice enfermo (apendectomía).\n\n**Cómo continuó el tratamiento:**  \nLa paciente tuvo problemas con su presión arterial durante la cirugía, por lo que no pudieron hacer una cirugía más grande (hemicolectomía derecha) en ese momento. En cambio, fijaron el ciego y el colon a la pared abdominal para evitar que se movieran y causaran más problemas.\n\n**Qué significa esto:**  \nEl nudo ileocecal es una causa rara de bloqueo intestinal que puede ser grave. En este caso, la cirugía ayudó a liberar el intestino y a quitar la parte dañada. Sin embargo, la paciente tuvo complicaciones después, lo que muestra que este tipo de problemas necesita atención rápida y cuidadosa.",
+            "B3": "**Contexto:**  \nSe trató de una mujer joven de 20 años que, tras un parto por cesárea debido a problemas con el ritmo cardíaco fetal, comenzó a presentar una distensión abdominal progresiva acompañada de calambres, vómitos frecuentes y la incapacidad para expulsar gases y heces. No tenía antecedentes de cirugías abdominales ni enfermedades crónicas. Su estado general era grave, con signos de dolor abdominal intenso, presión arterial baja y taquicardia (latidos rápidos del corazón). Las pruebas iniciales mostraron una disminución en el número de glóbulos blancos y plaquetas, además de una radiografía abdominal que evidenció dilatación de los intestinos y acumulación de líquido en la cavidad abdominal.\n\n**Hallazgos Clave:**  \nDurante la cirugía exploratoria, se encontró que una parte del intestino delgado (íleon distal) estaba enredada alrededor del ciego y el colon ascendente, formando un nudo intestinal (nudo ileocecal). Aunque el intestino estaba viable (sin daño irreversible), la punta del apéndice estaba gangrenosa (tejido muerto por falta de circulación). Se observó también una gran cantidad de líquido seroso en la cavidad abdominal. La paciente presentó inestabilidad hemodinámica (presión arterial muy baja) durante la operación, lo que complicó el manejo quirúrgico.\n\n**Interpretación Clínica:**  \nEl nudo ileocecal es una causa rara pero grave de obstrucción intestinal que puede provocar compromiso vascular y gangrena si no se trata oportunamente. En este caso, la viabilidad del intestino permitió deshacer el nudo y realizar la extirpación del apéndice afectado (apendicectomía). Debido a la inestabilidad de la paciente, se decidió posponer la resección mayor (hemicolectomía derecha) y en su lugar se fijaron el ciego y el colon ascendente para evitar una nueva torsión.\n\n**Próximos Pasos y Evolución:**  \nA pesar de las intervenciones quirúrgicas y el soporte con líquidos y medicamentos para estabilizar la presión arterial, la paciente desarrolló una infección grave denominada gangrena de Fournier, que afectó la región genital y suprapúbica. Se requirió un desbridamiento quirúrgico radical y tratamiento antibiótico intensivo. Sin embargo, la paciente evolucionó hacia un shock séptico refractario (una infección generalizada que no responde al tratamiento) y finalmente falleció debido a un fallo multiorgánico en el segundo día postoperatorio.\n\nEste caso resalta la complejidad y gravedad de las complicaciones abdominales posparto, la importancia del diagnóstico temprano y la dificultad de manejo en pacientes con inestabilidad hemodinámica y recursos limitados."
+        }
+    },
+    {
+        "article": "Un hombre de 38 años se presentó en el hospital con opresión en el pecho y falta de aire. Tres años antes, había experimentado síntomas similares después de la actividad y recibió tratamiento en nuestro hospital. La ecocardiografía ambulatoria indicó una masa de eco del corazón izquierdo que sugería un mixoma, lo que llevó a su ingreso para una evaluación adicional. El examen físico reveló pigmentación de las orejas del paciente caracterizada por múltiples puntos pequeños de color café y negro. La tomografía computarizada abdominal (TC) mostró múltiples hígados y pequeños quistes en el riñón izquierdo. Las pruebas genéticas identificaron mutaciones en los genes TTN y PRKAR1A. El diagnóstico de CNC se confirmó mediante examen clínico, imágenes y pruebas genéticas. Después del tratamiento sintomático, la condición del paciente mejoró; sin embargo, rechazó la intervención quirúrgica. El 20 de septiembre de 2023, el paciente se presentó en nuestro hospital con opresión en el pecho y falta de aire exacerbadas. Informó dificultad para permanecer acostado boca arriba y necesidad de sentarse erguido para respirar. El examen físico reveló distensión de la vena yugular, desplazamiento hacia la izquierda y hacia abajo del límite del corazón, ritmo cardíaco irregular en la auscultación y un murmullo de la válvula mitral de intensidad 2/6-3/6 en el cuarto espacio intercostal a lo largo del margen izquierdo del esternón. Se escucharon estertores húmedos en ambos campos pulmonares medio e inferior. La palpación reveló un hígado firme que se extendía tres dedos por debajo del proceso xifoides y dos dedos por debajo de la caja torácica, junto con un edema de pitting leve en ambas extremidades inferiores. Las imágenes ecocardiográficas indicaron un agrandamiento global del corazón, dilatación del seno aórtico y arteria pulmonar, regurgitación mitral pequeña a moderada y una masa ecógena irregular que medía 54 mm × 43 mm en la cámara izquierda unida al tabique auricular. La fracción de eyección del ventrículo izquierdo (FEVI) fue del 23,1 %, con acortamiento fraccional (FS) del 10,9 %. La electrocardiografía demostró fibrilación auricular (frecuencia ventricular promedio, 150 latidos/min) y ondas Q anormales en las derivaciones V1-V3. Basándose en la historia del paciente, el diagnóstico incluyó DCM y CNC con mixoma cardíaco. Dada la presencia de insuficiencia cardíaca en etapa terminal y mixoma cardíaco concurrente, el paciente fue hospitalizado y se consideró el trasplante de corazón como una opción terapéutica viable para abordar ambas afecciones simultáneamente. Un corazón de donante adecuado estuvo disponible para su trasplante inmediato el 1 de octubre de 2024.\n\n\nProcedimiento quirúrgico\n\nLa piel y los tejidos subcutáneos se incisionaron cuidadosamente capa por capa a través de una esternotomía media. El esternón se abrió longitudinalmente y se controló el sangrado mediante electrocoagulación y cera ósea. La exploración extracardíaca reveló un agrandamiento global del corazón, más prominente en el ventrículo izquierdo. El corazón mostró una disminución de la fuerza contráctil. La aorta y la arteria pulmonar principal (AP) se diseccionaron desde la región supravalvular. Algunos tejidos se conservaron para suturarlos posteriormente, mientras que la mayor parte de la aurícula derecha enferma, la aurícula izquierda (AL), el ventrículo derecho y el ventrículo izquierdo se extirparon. La resección reveló una masa mucoide de color blanco grisáceo. Los tejidos de la aurícula izquierda del donante y del receptor se suturaron utilizando hilos Prolene 3/0 dobles continuos. La anastomosis se inspeccionó meticulosamente varias veces y no se observó sangrado significativo. De forma similar, la anastomosis término-terminal de la aorta ascendente del donante y la arteria pulmonar del receptor se realizó utilizando suturas Prolene 5/0 continuas, y una inspección cuidadosa no reveló sangrado.\n\nAdemás, la LA del donante y la PA del receptor se cerraron de forma segura utilizando suturas Prolene 5/0 dobles y continuas. Los tejidos de la vena cava inferior tanto del donante como del receptor se suturaron de forma similar con suturas Prolene 5/0, y se realizaron varias inspecciones para confirmar que no había presencia de sangrado significativo. El lado izquierdo del corazón se desinfló y, a medida que comenzó el recalentamiento, se restableció la oxigenación, se soltó la aorta ascendente y el corazón volvió espontáneamente al ritmo sinusal. Se aplicó sutura continua con Prolene 5/0 tanto a la vena cava superior del donante como del receptor y se inspeccionó de forma diligente para garantizar la ausencia de sangrado significativo. Después de la interrupción exitosa de la circulación asistida, se descanuló la cavidad venosa. Se recogieron muestras de tejido del corazón izquierdo y de la materia gris del paciente para un examen histopatológico, y se confirmó el diagnóstico de DCM y mixoma cardiaco.\n\n\nManejo postoperatorio\n\nEl primer día después del trasplante de corazón, el paciente produjo 1200 ml de orina. Los exámenes de laboratorio revelaron un nivel de troponina T hipersensible de 796.70 ng/L y un nivel de NT-proBNP de 10798 pg/ml. El recuento completo de sangre mostró un recuento de glóbulos blancos de 17.15 × 109/L, sin anomalías significativas en otros resultados de exámenes. El ecocardiógrafo mostró un EFV del 65 %, FS del 35 %, un espesor de la pared ventricular normal y ecogenicidad, y no se observaron anomalías discernibles en la morfología y estructura de la válvula. Después del trasplante de corazón, se administró una terapia hormonal intravenosa de succinato sódico de metilprednisolona (0.25 g) para mejorar la inmunidad, y se proporcionó un tratamiento intravenoso antiinfeccioso con cefoperazona y sulbactam sódico (2 g). El paciente recibió una solución nutriente y tiopronina en el primer día después de la cirugía. En el día tres postoperatorio, se reemplazó el succinato sódico de metilprednisolona con acetato de prednisona oral (25 mg). Se administraron cápsulas de micofenolato de mofetilo (0.5 g) por vía oral para minimizar el rechazo del corazón, y se administró acetato de carpofénico intravenoso (50 mg) para prevenir infecciones fúngicas. La producción de orina del paciente fue de 2000 ml, con niveles de troponina T hipersensible de 390 ng/L, niveles de NT-proBNP de 7877 pg/ml, y un recuento de leucocitos de 12.15 × 109/L. En el día siete postoperatorio, se introdujeron cápsulas de tacrolimus a una dosis oral de (1 mg) para minimizar el rechazo del paciente al corazón del donante, con un cuidadoso monitoreo de las concentraciones sanguíneas. Subsiguientemente, la dosis oral de acetato de prednisona se redujo gradualmente a (10 mg) mientras se ajustaba la concentración sanguínea de tacrolimus a 10.90 ng/L. La recuperación del paciente mejoró. El 20 de octubre de 2023, la ecocardiografía de seguimiento (Fig. 6) no mostró anomalías, con niveles de troponina T de 85 ng/L, NT-proBNP de 210 pg/ml, y todos los demás resultados de exámenes dentro de los rangos normales. El paciente exhibió una excelente recuperación postoperatoria y fue dado de alta. Las visitas regulares de seguimiento a nuestro departamento después del alta mostraron que el paciente permanece en buen estado.\n\nMH - Humanos\nMH - *Cardiomiopatía, Dilatada/cirugía/etiología/diagnóstico/diagnóstico por imágenes\nMH - Hombre\nMH - *Complejo de Carney/genética/diagnóstico/cirugía/complicaciones\nMH - Adulto\nMH - *Trasplante de corazón\nMH - *Mixoma/complicaciones/cirugía/diagnóstico por imágenes/diagnóstico/genética\nMH - *Insuficiencia cardiaca/etiología/diagnóstico/cirugía\nMH - *Neoplasias cardiacas/cirugía/complicaciones/diagnóstico por imágenes/diagnóstico/genética\nMH - Resultado del tratamiento\nMH - Subunidad/genética de la proteína quinasa Rlalpha dependiente de AMP cíclico\n",
+        "gold_summary": "Aquí, reportamos un caso de insuficiencia cardiaca debido al síndrome de Carney que resultó en mixoma cardiaco combinado con cardiomiopatía dilatada. Un hombre de 35 años de edad fue admitido en el hospital hace tres años debido a opresión torácica repentina y falta de aire. La ecocardiografía indicó mixoma, y una combinación de cribado genético y examen físico confirmó el síndrome de Carney con mixoma cardiaco. Después del tratamiento sintomático, fue dado de alta. Las intervenciones quirúrgicas no fueron consideradas en ese momento. Sin embargo, la opresión torácica y los síntomas de falta de aire del paciente empeoraron, y volvió al hospital. Se confirmó una función cardiaca de grado IV de la New York Heart Association, y la ecocardiografía indicó la presencia de cardiomiopatía dilatada acompañada de mixoma cardiaco. En última instancia, la insuficiencia cardiaca del paciente fue tratada con éxito con un trasplante cardiaco.\n",
+        "synthetic_summary": {
+            "B1": "Había un hombre que se sentía muy cansado y le dolía el pecho. Tenía un bulto en su corazón que no era bueno. Los doctores le hicieron pruebas y encontraron que tenía una enfermedad llamada síndrome de Carney. Al principio, le dieron medicinas para sentirse mejor y se fue a su casa. Pero después, se sintió peor y volvió al hospital. Su corazón estaba muy débil y tenía el bulto grande. Los doctores le dieron un corazón nuevo con una operación. Ahora, el hombre está mejor y puede vivir feliz.",
+            "B2": "**Lo que le pasó al paciente**\n\nUn hombre de 35 años tuvo problemas en el corazón que le causaban dolor en el pecho y dificultad para respirar. Al principio, los médicos encontraron una masa en su corazón llamada mixoma, que es un tipo de tumor benigno, y también detectaron que tenía el síndrome de Carney, una enfermedad rara que puede causar tumores y otros problemas en el cuerpo. En ese momento, solo le dieron medicamentos para aliviar los síntomas y no le hicieron cirugía.\n\n**Cómo empeoró su condición**\n\nCon el tiempo, sus síntomas se hicieron más graves. Volvió al hospital porque le costaba mucho respirar y su corazón estaba muy débil. Los médicos descubrieron que tenía cardiomiopatía dilatada, que significa que su corazón estaba agrandado y no podía bombear la sangre bien. Además, el mixoma seguía presente en su corazón.\n\n**Qué hicieron los médicos**\n\nDebido a que su corazón estaba muy dañado y tenía insuficiencia cardíaca avanzada, los médicos decidieron hacerle un trasplante de corazón. Esto significa que le pusieron un corazón nuevo de un donante para reemplazar el suyo enfermo.\n\n**Cómo fue la cirugía y la recuperación**\n\nLa operación fue complicada, pero exitosa. Los médicos quitaron el corazón enfermo y el tumor, y pusieron el corazón nuevo. Después de la cirugía, el paciente recibió medicamentos para evitar que su cuerpo rechazara el nuevo corazón y para prevenir infecciones. Poco a poco, su corazón comenzó a funcionar bien y sus síntomas mejoraron mucho.\n\n**Qué significa este caso**\n\nEste caso muestra cómo el síndrome de Carney puede causar problemas graves en el corazón, como tumores y debilidad del músculo cardíaco. También enseña que, cuando el corazón está muy dañado, un trasplante puede ser la mejor opción para salvar la vida del paciente.",
+            "B3": "**Contexto**\n\nPresentamos el caso de un hombre de 38 años diagnosticado con el síndrome de Carney (CNC), una enfermedad genética rara caracterizada por tumores cardíacos benignos llamados mixomas, pigmentación cutánea y otras anomalías. Este paciente inicialmente se presentó hace tres años con síntomas de opresión en el pecho y dificultad para respirar, y fue diagnosticado con un mixoma en el corazón izquierdo mediante ecocardiografía. Además, el examen físico reveló manchas pigmentadas en las orejas, y estudios de imagen detectaron múltiples lesiones hepáticas y quistes renales. Las pruebas genéticas confirmaron mutaciones en los genes TTN y PRKAR1A, asociadas con CNC y cardiomiopatía dilatada (una enfermedad que afecta la capacidad del corazón para bombear sangre). En ese momento, recibió tratamiento para aliviar los síntomas y fue dado de alta, rechazando la cirugía.\n\n**Evolución y Hallazgos Clínicos**\n\nEn septiembre de 2023, el paciente regresó con empeoramiento de la opresión torácica y dificultad respiratoria, incluyendo intolerancia a la posición acostada. El examen físico evidenció signos de insuficiencia cardíaca avanzada, como distensión de la vena yugular, ritmo cardíaco irregular (fibrilación auricular), murmullo en la válvula mitral y estertores pulmonares. También se observaron un hígado aumentado de tamaño y edema en las piernas. La ecocardiografía mostró un corazón globalmente agrandado, dilatación de grandes vasos, regurgitación mitral moderada y una masa irregular de 54 × 43 mm en la aurícula izquierda, compatible con mixoma. La función del ventrículo izquierdo estaba gravemente reducida, con una fracción de eyección del 23,1 % (normalmente >55 %). La electrocardiografía confirmó fibrilación auricular y alteraciones en las derivaciones precordiales. El diagnóstico final incluyó cardiomiopatía dilatada (DCM) y síndrome de Carney con mixoma cardíaco, en contexto de insuficiencia cardíaca terminal.\n\n**Procedimiento Quirúrgico**\n\nDada la gravedad de la insuficiencia cardíaca y la presencia del mixoma, se decidió realizar un trasplante de corazón. Durante la cirugía, se realizó una esternotomía media para acceder al corazón agrandado y debilitado. Se extirparon las aurículas y ventrículos enfermos junto con la masa tumoral, y se implantó el corazón donante mediante suturas meticulosas para conectar las estructuras vasculares y auriculares. El corazón trasplantado recuperó el ritmo sinusal espontáneamente y sin complicaciones hemorrágicas. El examen histopatológico confirmó la presencia de mixoma y cardiomiopatía dilatada en el tejido removido.\n\n**Manejo Postoperatorio y Resultados**\n\nEn el postoperatorio inmediato, el paciente mostró una producción urinaria adecuada y niveles elevados pero decrecientes de marcadores cardíacos (troponina T y NT-proBNP), indicadores de daño y estrés cardíaco. La ecocardiografía evidenció una función ventricular normalizada con fracción de eyección del 65 % y estructura valvular sin anomalías. Se instauró un régimen inmunosupresor con metilprednisolona, prednisona, micofenolato de mofetilo y tacrolimus para prevenir el rechazo del trasplante, junto con tratamiento antibiótico y antifúngico para evitar infecciones. La recuperación fue favorable, con normalización progresiva de los parámetros clínicos y de laboratorio. En el seguimiento a largo plazo, el paciente mantuvo un buen estado general sin signos de rechazo ni complicaciones, y fue dado de alta con un pronóstico positivo.\n\n**Interpretación Clínica**\n\nEste caso ilustra la complejidad del síndrome de Carney cuando se asocia con mixoma cardíaco y cardiomiopatía dilatada, condiciones que pueden conducir a insuficiencia cardíaca grave. La identificación temprana mediante ecocardiografía, examen físico detallado y pruebas genéticas es fundamental para el diagnóstico. Aunque inicialmente se manejó de forma conservadora, el deterioro progresivo de la función cardíaca requirió un trasplante de corazón, que resultó ser una opción terapéutica eficaz para tratar simultáneamente la insuficiencia cardíaca terminal y la masa tumoral. La cirugía y el manejo postoperatorio cuidadoso permitieron una recuperación exitosa y mejoraron significativamente la calidad de vida del paciente.\n\n**Próximos Pasos**\n\nSe recomienda continuar con controles regulares para monitorear la función cardíaca y detectar posibles signos de rechazo o recurrencia de la enfermedad. Además, el seguimiento genético y clínico es importante para evaluar otras manifestaciones del síndrome de Carney y prevenir complicaciones asociadas. La educación del paciente sobre la adherencia al tratamiento inmunosupresor y la vigilancia de síntomas es esencial para mantener un resultado favorable a largo plazo."
+        }
+    },
+    {
+        "article": "Un paciente de 52 años de edad con un diagnóstico inicial de arteria pulmonar fue admitido en el departamento de cardiología para una evaluación médica y una decisión sobre el tratamiento posterior. El paciente tenía un historial de neumotórax espontáneo del lado derecho, tratado con toracocentesis y drenaje por vacío 35 años antes. El paciente sentía una disnea creciente al hacer ejercicio. También se quejaba de signos de insuficiencia ventricular derecha y cianosis. Cuatro años antes, el paciente fue hospitalizado tres veces por fibrilación auricular paroxística que se convirtió en ritmo sinusal por cardioversión eléctrica, además de que el examen electrocardiográfico era normal.\n\nEn ese mismo año, la angiografía coronaria indicó arterias coronarias normales. La ecocardiografía reveló una hipertensión pulmonar leve con una presión sistólica calculada en el ventrículo derecho de 36 mmHg sin dilatación de ese ventrículo.\n\nEn los años siguientes, se observó insuficiencia cardiaca progresiva con aumento de la presión arterial pulmonar en la ecocardiografía. Se realizó angio-CT en dos ocasiones y se excluyó la hipertensión pulmonar tromboembólica crónica en cada ocasión. La tomografía computarizada de alta resolución excluyó la patología pulmonar intersticial. La espirometría fue normal. La detección de enfermedades autoinmunes y la infección por VIH fue negativa.\n\n\nLínea de tiempo: historia, curso de la enfermedad, diagnóstico y tratamiento\n\n1976  neumotórax derecho\n2007 Hospitalizado tres veces por fibrilación auricular e insuficiencia cardiaca. Se le realizaron ecocardiografías, cardioversiones y coronografías. En cada ocasión, fue dado de alta de los servicios con diagnósticos de fibrilación auricular, insuficiencia cardiaca e insuficiencia cardiaca de clase II de la NYHA.\n2010-2011: Aumento de la falta de aire y síntomas de insuficiencia cardiaca. El paciente fue hospitalizado tres veces. Se detectaron características indirectas de hipertensión pulmonar en ecocardiografía. Se realizó tres veces un examen de tórax por TAC; se excluyó la embolia pulmonar o la hipertensión arterial pulmonar tromboembólica crónica (2 x angio-TAC) o la fibrosis pulmonar (tomografía computarizada de alta resolución).\nSe estableció el diagnóstico de hipertensión pulmonar, clase III de la OMS.\nDEC-2011 Admisión a la clínica de cardiología – ecocardiografía (TTE, TEE), prueba de caminata de 6 minutos, NT-proBNP, cateterización cardiaca derecha, prueba de vasoreactividad pulmonar.\nSe estableció el diagnóstico de hipertensión pulmonar arterial irreversible.\nSe ha iniciado el tratamiento con iloprost y sildenafil\nEn enero de 2012, visita de control: mejora en la clase de la OMS, disminución de la concentración de NT-proBNP e incremento de la distancia en la prueba de 6 minutos.\nMAY-2012. Control RHC. La SaO2 de las muestras de sangre obtenidas durante el RHC de la arteria del lóbulo superior del pulmón derecho fue del 87 %.\nEl diagnóstico angiográfico de las arterias pulmonares reveló fístulas de HAP entre las arterias subclavianas y el lóbulo superior del pulmón derecho.\nJUN 2012  angiografía por TC de las arterias sistémicas reveló la presencia adicional de fístulas arteriales bronquiales en el lóbulo superior de las arterias del pulmón derecho\nIII-2013 Embolización de fístulas\nVI-2013. Muerte como resultado del empeoramiento de la insuficiencia cardiaca, combinado con neumonía.\n\n\n\nEn el ingreso a nuestra clínica, la clase funcional del paciente fue evaluada como OMS III. En el examen físico, el segundo sonido cardiaco (S2) fue acentuado con S2 dividido ensanchado. Además, la auscultación cardiaca indicó un murmullo holosistólico de regurgitación tricuspídea. La auscultación del tórax no mostró un murmullo vascular. La cianosis periférica y central fue marcada. Se examinaron la hepatomegalia, el edema periférico y las venas varicosas bilateralmente.\n\nLa SaO2 obtenida por el método de oximetría de pulso se redujo al 88 %. La electrocardiografía reveló fibrilación auricular, desviación del eje derecho y onda T negativa en las derivaciones precordiales v1-v3. Las pruebas adicionales fueron las siguientes: concentración de NT-proBNP - 3383 pg/ml, distancia de la prueba de caminata de seis minutos - 373 m con 7/10 puntos en la escala de disnea de Borg.\n\nLa ecocardiografía mostró características de hipertensión pulmonar grave: agrandamiento del ventrículo derecho a 44 mm (cuatro cámaras), con función deprimida del TAPSE del ventrículo derecho de 9 mm, agrandamiento del área de la aurícula derecha a 40 cm2, regurgitación tricuspídea grave (++++), aumento del PSVR calculado a 112 mmHg, acortamiento del tiempo de aceleración de la arteria pulmonar a 60 ms y derrame pericárdico leve. No hubo defecto en el tabique interventricular. La ecocardiografía transesofágica tampoco mostró un defecto en el tabique auricular, lo que se confirmó más tarde con angio-TAC.\n\n\nLa SaO2 de la sangre obtenida de la arteria radial se redujo al 87,8%. Se realizó un cateterismo cardiaco derecho. La SaO2 de las muestras de sangre obtenidas durante el RHC de la vena cava superior, la vena cava inferior, la aurícula derecha, el tronco pulmonar, la arteria del lóbulo medio del pulmón derecho y la arteria pulmonar izquierda ascendieron respectivamente a: 64,8%; 77,4%; 73,2%; 70,2%; 69,3%; 71,2% y no indicaron la presencia de un shunt de izquierda a derecha.\n\nLas mediciones hemodinámicas mostraron una hipertensión pulmonar precapilar grave, irreversible en las pruebas de vasoreactividad con óxido nítrico inhalado (80 ppm) y una combinación de sildenafil oral (50 mg) y óxido nítrico inhalado (80 ppm).\n\nEn base a todos los datos clínicos y los resultados de la RHC, se estableció un diagnóstico de hipertensión pulmonar idiopática irreversible.\n\nSe inició el tratamiento con iloprost inhalado (Ventavis) 6 × 5 µg y sildenafil (Revatio) por vía oral 3 × 20 mg. Además, se administraron digoxina (0,1 mg diarios), warfarina (INR rango: 2-3), furosemida (40 mg por vía oral diarios) y espironolactona (100 mg diarios).\n\nUn mes después se realizó un seguimiento no invasivo. El paciente manifestó una mejoría en la capacidad física, clase II según la OMS, concentración de NT-proBNP: 1014 pg/ml. Distancia en la prueba de caminata de seis minutos: 471 m.\n\nCinco meses después se realizó una evaluación invasiva. La RHC mostró valores de PAP más elevados que en las mediciones iniciales [75,4/51,8 (59,7) mm Hg] y PVR (13,4 WU) (Tabla 22 – control RHC).\n\nLa saturación de oxígeno de las muestras de sangre obtenidas durante la RHC de la arteria lobular superior del pulmón derecho fue elevada y ascendió al 89.7%.\n\nEn la angiografía pulmonar se detectó la reducción del trazo vascular periférico típico de la hipertensión arterial pulmonar y la falta de contraste de la arteria del lóbulo superior derecho. Además, se encontró evidencia de flujo sanguíneo retrógrado visible como un contraste negativo en la arteria pulmonar derecha. Después, se realizó una arteriografía de la arteria subclavia derecha y se detectó una enorme malformación vascular que se comunicaba con la arteria del lóbulo superior derecho.\n\nLa angio-TC de las arterias sistémicas confirmó la presencia de las fístulas previamente descritas y reveló la presencia adicional de fístulas de la arteria bronquial en el lóbulo superior de las arterias del pulmón derecho.\n\nSe realizó embolización selectiva de las fístulas (mezcla al 50% de Lipiodol y pegamento monomérico de n-butil-2-cianoacrilato). La embolización no produjo ningún cambio clínico en el estado del paciente.\n\nMH - Fístula arterio-arterial/*complicaciones\nMH - *Cateterización cardiaca\nMH - Angiografía por tomografía computarizada\nMH - Hipertensión pulmonar primaria familiar/*diagnóstico/terapia farmacológica\nMH - Resultado fatal\nMH - Insuficiencia cardiaca/fisiopatología\nMH - Humanos",
+        "gold_summary": "Un paciente caucásico de 52 años de edad con hipertensión pulmonar (HP) confirmada por ecocardiografía fue admitido en el departamento de cardiología debido a disnea de esfuerzo y signos de insuficiencia ventricular derecha. La exploración rutinaria para detectar causas de HP secundaria fue negativa. El cateterismo cardiaco derecho (CCR) confirmó una HP arterial de alto grado [presión arterial pulmonar media (PAPm); 50,6 mmHg, presión de enclavamiento pulmonar (PWP); 11,3 mmHg, resistencia vascular pulmonar (PVR); 11,9 unidades de Wood (UW)] irreversible en la prueba con óxido nítrico inhalado. La saturación de oxígeno (SaO2) de las muestras de sangre obtenidas durante el primer CCR osciló entre 69,3 y 73,2%. Se diagnosticó hipertensión arterial pulmonar idiopática. Se inició el tratamiento con iloprost inhalado y sildenafil.\n\nEl control RHC, realizado 5 meses después, mostró valores de mPAP (59,7 mmHg) y PVR (13,4 WU) más altos en comparación con la medición inicial. El SaO2 de sangre obtenida durante el RHC de la arteria del lóbulo superior del pulmón derecho fue elevado y ascendió al 89,7 %.\n\nLuego se realizó una arteriografía pulmonar. Se encontró falta de contraste en la arteria del lóbulo superior derecho con evidencia de flujo sanguíneo retrógrado visible como contraste negativo en la arteria pulmonar derecha. Después, una arteriografía de la arteria subclavia derecha detectó una enorme malformación vascular que se comunicaba con la arteria del lóbulo superior derecho. Después, un angiograma por tomografía computarizada (angio-CT) reveló adicionalmente el agrandamiento de las arterias bronquiales que se originaban en las fístulas hacia la arteria pulmonar del lóbulo superior derecho.\n\nA pesar del tratamiento farmacológico intensivo, que incluyó la terapia de la hipertensión pulmonar y la embolización percutánea de las fístulas, el estado del paciente siguió deteriorándose. Falleció tres meses después de la embolización debido a una insuficiencia cardiaca grave complicada por neumonía.\n",
+        "synthetic_summary": {
+            "B1": "Había un hombre de 52 años que tenía problemas para respirar. Su corazón y pulmones no funcionaban bien. Los doctores hicieron muchas pruebas para entender qué pasaba.\n\nEncontraron que la presión en sus pulmones era muy alta. Le dieron medicinas para ayudar, pero no mejoró mucho.\n\nLuego vieron que tenía unos tubos raros en sus pulmones que no estaban bien. Intentaron taparlos para ayudar, pero el hombre se puso más enfermo.\n\nAl final, el hombre murió porque su corazón se cansó mucho y tuvo una infección en los pulmones. Los doctores hicieron todo lo que pudieron para ayudarlo.",
+            "B2": "**Caso de un Paciente con Hipertensión Pulmonar y Problemas en las Arterias del Pulmón**\n\nUn hombre de 52 años tenía dificultad para respirar y problemas en el lado derecho de su corazón. Los médicos confirmaron que tenía hipertensión pulmonar, que es cuando la presión en las arterias de los pulmones está muy alta. Para entender mejor su enfermedad, le hicieron un examen llamado cateterismo cardiaco derecho, que mide la presión y el flujo de sangre en el corazón y los pulmones. Los resultados mostraron que su hipertensión pulmonar era grave y no mejoraba con el tratamiento con óxido nítrico inhalado. Además, la cantidad de oxígeno en su sangre estaba baja, entre 69% y 73%.\n\nLos médicos pensaron que tenía hipertensión arterial pulmonar idiopática, que significa que la causa es desconocida. Por eso, comenzaron un tratamiento con dos medicamentos: iloprost inhalado y sildenafil, que ayudan a bajar la presión en las arterias pulmonares.\n\nCinco meses después, hicieron otro cateterismo y encontraron que la presión en sus pulmones había aumentado aún más, y la resistencia al flujo sanguíneo también era mayor. Sin embargo, la cantidad de oxígeno en la sangre de una parte específica del pulmón derecho había subido a casi 90%, lo que era extraño.\n\nPara investigar esto, realizaron una arteriografía, que es una prueba que usa un contraste para ver las arterias con rayos X. Descubrieron que la arteria del lóbulo superior del pulmón derecho no se llenaba bien con el contraste y que la sangre estaba fluyendo en dirección contraria en esa arteria. Luego, hicieron otra arteriografía en la arteria subclavia derecha (una arteria cerca del hombro) y encontraron una gran malformación, que es una conexión anormal entre vasos sanguíneos, que se comunicaba con la arteria del pulmón derecho.\n\nTambién un estudio por tomografía computarizada mostró que las arterias bronquiales, que normalmente llevan sangre a los pulmones, estaban agrandadas y formaban fístulas. Las fístulas son conexiones anormales entre arterias que pueden causar problemas en el flujo sanguíneo.\n\nAunque el paciente recibió tratamiento médico y se intentó cerrar estas fístulas mediante un procedimiento llamado embolización (que bloquea estas conexiones anormales), su salud empeoró. Tres meses después de este procedimiento, falleció debido a insuficiencia cardiaca grave, que fue complicada por una infección pulmonar llamada neumonía.\n\n**Qué Significa Este Caso**\n\nEste caso muestra que en algunos pacientes con hipertensión pulmonar grave, pueden existir conexiones anormales entre arterias que afectan el flujo de sangre y el oxígeno en los pulmones. Aunque se usen medicamentos y procedimientos para tratar estas malformaciones, la enfermedad puede avanzar y causar complicaciones serias. Por eso, es importante hacer estudios detallados para entender todas las causas y buscar el mejor tratamiento posible.",
+            "B3": "**Contexto**  \nSe trata de un hombre caucásico de 52 años con hipertensión pulmonar (HP) grave, inicialmente diagnosticada mediante ecocardiografía, que presentaba dificultad para respirar al esfuerzo y signos de insuficiencia del ventrículo derecho del corazón. A lo largo de su evolución, se descartaron causas secundarias comunes de hipertensión pulmonar mediante estudios exhaustivos, incluyendo pruebas de imagen y análisis de laboratorio.\n\n**Hallazgos Clave**  \nEl cateterismo cardiaco derecho (CCR), una prueba invasiva que mide directamente las presiones y flujos en el corazón y pulmones, confirmó una hipertensión arterial pulmonar severa e irreversible, con una presión arterial pulmonar media elevada (50,6 mmHg), presión de enclavamiento pulmonar normal (11,3 mmHg) y resistencia vascular pulmonar alta (11,9 unidades de Wood). La saturación de oxígeno en la sangre obtenida durante este procedimiento fue moderadamente reducida (entre 69,3% y 73,2%), lo que indicaba un intercambio de oxígeno comprometido.\n\nCinco meses después, un nuevo cateterismo mostró un empeoramiento de las presiones pulmonares (presión media de 59,7 mmHg) y de la resistencia vascular (13,4 unidades de Wood). Sin embargo, la saturación de oxígeno en la arteria del lóbulo superior derecho del pulmón aumentó notablemente hasta 89,7%, lo que sugería la presencia de un flujo anormal de sangre.\n\nUna angiografía pulmonar (estudio de imagen con contraste para visualizar las arterias pulmonares) reveló ausencia de contraste en la arteria del lóbulo superior derecho y flujo sanguíneo retrógrado (en sentido contrario al habitual) en la arteria pulmonar derecha. Posteriormente, una arteriografía de la arteria subclavia derecha identificó una gran malformación vascular que conectaba esta arteria con la arteria del lóbulo superior derecho del pulmón. Un estudio adicional con angiografía por tomografía computarizada (angio-TC) mostró además un aumento del tamaño de las arterias bronquiales que formaban fístulas (conexiones anormales) hacia la arteria pulmonar del mismo lóbulo.\n\n**Interpretación Clínica**  \nEl diagnóstico final fue hipertensión arterial pulmonar idiopática (sin causa identificable) complicada por la presencia de fístulas arterio-arteriales entre las arterias sistémicas (subclavia y bronquiales) y las arterias pulmonares del lóbulo superior derecho. Estas conexiones anómalas alteraban el flujo sanguíneo normal, contribuyendo al empeoramiento de la insuficiencia cardiaca derecha y a la hipoxemia (bajo nivel de oxígeno en sangre).\n\nA pesar del tratamiento médico intensivo con vasodilatadores pulmonares (iloprost inhalado y sildenafil oral) y de la embolización percutánea (procedimiento para cerrar las fístulas mediante la introducción de materiales que bloquean el flujo anormal), la condición del paciente continuó deteriorándose.\n\n**Próximos Pasos y Resultado**  \nEl paciente falleció tres meses después de la embolización debido a insuficiencia cardiaca grave, agravada por una neumonía. Este caso resalta la complejidad y gravedad de la hipertensión pulmonar idiopática cuando se asocia a malformaciones vasculares, y la dificultad para controlar la progresión a pesar de las terapias disponibles."
+        }
+    },
+    {
+        "article": "Paciente de 73 años, diagnosticada de enfermedad pulmonar obstructiva crónica (EPOC), hipertensión arterial (HTA), trastorno bipolar, ansiedad, depresión, hipotiroidismo y artritis reumatoide, condiciones para las cuales tiene prescrito el tratamiento reflejado en el Anexo I.\n\nRealiza una llamada telefónica a la farmacia comunitaria para solicitar información sobre una nueva medicación prescrita para el tratamiento de una infección de orina y un déficit de vitamina D, diagnosticados tras la realización de una analítica completa en el servicio de urgencias de un hospital privado.\n\nLa paciente es totalmente dependiente y no sale de casa, siendo su cuidadora la persona que siempre va a retirar su medicación y elabora los pastilleros semanales.\n\nLos fármacos prescritos para el tratamiento de la infección de orina fueron cefuroxima 250 mg (1 comprimido cada 12 horas durante 5 días) y butilescopolamina 10 mg (1 comprimido en la mañana si presentaba molestias).\n\nPara el déficit de vitamina D se le prescribió colecalciferol 50.000 U.I. (1 cápsula una vez al mes durante dos meses) y colecalciferol 25.000 UI (1 cápsula una vez al mes tras finalizar el envase de 50.000 U.I.).\n\nESTUDIO Y EVALUACIÓN\nSe lleva a cabo el servicio de dispensación (SD) sin incidencias, siguiendo la metodología expuesta en la Guía práctica para los Servicios Profesionales Farmacéuticos Asistenciales en la Farmacia Comunitaria. Posteriormente, la paciente contacta con la farmacia comunitaria, preocupada porque la nueva medicación le ha generado confusión, ya que ella tomaba unas cápsulas naranjas para su déficit de vitamina D prescritas por su médico de Atención Primaria hace unos meses y en la parte del informe de urgencias en la que figura el tratamiento venía reflejado una medicación nueva para ese mismo problema de salud. Además, coincidió con que su cuidadora habitual ya no podrá trabajar más con ella y no la podrá ayudar con su medicación. Por ello, se le propone a la paciente el servicio de Revisión del Uso del Medicamento (RUM) con el objetivo de evaluar el grado de conocimiento que tienen la paciente con respecto a sus patologías y su tratamiento, a la par que poder resolver posibles errores en la administración de los distintos fármacos que forman parte del mismo. Se le explica en qué consiste todo el procedimiento y decide aceptar.\n\nTras esto, se procedió a citar a la cuidadora en la farmacia con la tarjeta sanitaria de la paciente, su bolsa de medicación para hacer una revisión exhaustiva de su botiquín y el último informe de urgencias con el objetivo de recopilar toda la información necesaria para realizar el servicio asistencial vía telefónica. Durante la llamada con la paciente, se procede a cumplimentar el formulario RUM, el cual se volcó posteriormente en la plataforma SEFAC e_XPERT ®. Además, para poder evaluar correctamente todo el tratamiento farmacológico, se emplearon herramientas como el CIMA (donde se consultaron las fichas técnicas de los medicamentos) y el BotPlus (donde se consultaron las posibles interacciones farmacológicas).\n\nINTERVENCIÓN\nTras la primera toma de contacto a través de la entrevista telefónica y hacer revisión del botiquín, se pudo detectar que la paciente y su cuidadora no estaban haciendo una gestión apropiada de la medicación. Tras la revisión de su botiquín, se hallaron envases caducados y con anotaciones erróneas sobre su uso, blísteres con comprimidos partidos que no deberían de estarlo y acúmulo de varios envases de un mismo fármaco. Al tratarse de una paciente dependiente, polimedicada y con problemas para gestionar correctamente su tratamiento antes y durante la ausencia de su cuidadora habitual se decidió con el fin de garantizar la seguridad farmacoterapéutica y mejorar la adherencia al tratamiento derivar al servicio de sistema personalizado de dosificación (SPD). A través de la plataforma de SEFAC e_XPERT ® se procedió a redactar un informe de derivación a su médico de Atención Primaria (MAP) del Sistema Nacional de Salud (SNS) (ver Anexo II), donde se detallaba la inclusión de la paciente en el servicio de Revisión del Uso de la Medicación y su posterior derivación al servicio de SPD. Además, quedaron recogidas las siguientes propuestas de intervención:\n\nRevisión de la pauta posológica de tramadol 50 mg de liberación retardada por la existencia de un posible error en la prescripción.\n\nRevisión del tratamiento prescrito para el déficit de vitamina D por la existencia de una duplicidad terapéutica.\n\nCambio del absorbente de incontinencia de tipo pants a elástico alegando la situación de dependencia de la paciente y las dificultades para realizar una correcta colocación por parte de la cuidadora al pasar encamada la mayor parte del tiempo. Se aportaron los Códigos Nacionales (CN) correspondientes.\n\nRevisión del tratamiento para la EPOC por dificultades de empleo del inhalador y falta de adherencia terapéutica.\n\nRESULTADOS\nDurante la cita médica, la médico de atención primaria recibe el informe de derivación entregado a la cuidadora donde, además, se solicita contacto con la farmacia comunitaria para poder iniciar de forma correcta el servicio de SPD. Tras hablar con ella vía telefónica, se realizaron los siguientes cambios en su tratamiento:\n\nDéficit de vitamina D: anulación de calcifediol y sustitución por colecalciferol prescrito en el Servicio de Urgencias.\n\nArtritis reumatoide: modificación de pauta de tramadol de liberación prolongada a 1-0-1 y empleo de paracetamol 1000 mg 1-1-1 si precisa.\n\nIncontinencia urinaria: sustitución de absorbente tipo pants por elástico.\n\nEPOC: no se realizó un cambio de tratamiento. La médico de atención primaria consideró oportuno llevar a cabo una supervisión diaria por parte de la cuidadora en cada una de las tomas del inhalador.",
+        "gold_summary": "Paciente 73 años, dependiente, polimedicada y pluripatológica contacta telefónicamente con la farmacia comunitaria para solicitar información sobre un tratamiento de nueva prescripción para una infección de orina y un déficit de vitamina D. La dispensación de la medicación a su cuidadora deriva en mayores dudas a la paciente, por lo que se le ofrece el servicio de revisión del uso del medicamento (RUM). Durante la prestación del servicio se detectan varias incidencias en su tratamiento, por lo que se decide realizar un informe de derivación al médico de atención primaria para una revisión completa del tratamiento y poder así derivar a la paciente al servicio de Sistema Personalizado de Dosificación (SPD) con el fin de garantizar la seguridad farmacoterapéutica de la paciente y mejorar su adherencia al tratamiento.",
+        "synthetic_summary": {
+            "B1": "Una señora de 73 años se siente confundida con sus medicinas nuevas. Ella no puede salir de casa y su cuidadora siempre le ayuda con sus pastillas. La señora llamó a la farmacia para preguntar. \n\nLa farmacia revisó todas sus medicinas y vio que había problemas. Algunas pastillas estaban mal guardadas y había medicinas repetidas. \n\nPor eso, la farmacia habló con su doctor para ayudarla mejor. El doctor cambió algunas medicinas y pidió que la señora tenga un organizador especial para sus pastillas. Así, será más fácil y seguro tomar sus medicinas.",
+            "B2": "**Información sobre la Paciente y su Situación**\n\nUna mujer de 73 años, que depende totalmente de otras personas para su cuidado y toma muchos medicamentos por varias enfermedades, llamó a la farmacia para preguntar sobre un nuevo tratamiento. Este tratamiento era para una infección de orina y para un problema de falta de vitamina D, que le habían diagnosticado en un hospital.\n\n**Problemas Detectados con la Medicación**\n\nAunque su cuidadora recogió los medicamentos, la paciente se confundió porque ya tomaba otras pastillas para la vitamina D y no entendía bien los cambios. Además, su cuidadora habitual ya no podía ayudarla, lo que complicaba más la situación. Por eso, la farmacia le ofreció un servicio llamado Revisión del Uso del Medicamento (RUM). Este servicio ayuda a revisar si la paciente entiende bien sus medicinas y si las está tomando correctamente.\n\nAl revisar los medicamentos, encontraron varios problemas: había medicinas vencidas, instrucciones equivocadas, pastillas partidas que no debían estar así y varios envases del mismo medicamento. Como la paciente no podía manejar bien su tratamiento y estaba sin su cuidadora, se decidió que necesitaba un Sistema Personalizado de Dosificación (SPD). Este sistema organiza las medicinas en pastilleros para que sea más fácil y seguro tomarlas.\n\n**Acciones y Cambios Realizados**\n\nSe preparó un informe para el médico de atención primaria explicando la situación y recomendando la revisión completa del tratamiento. El médico hizo algunos cambios importantes, como:\n\n- Cambiar la vitamina D para evitar tomar dos tipos diferentes al mismo tiempo.\n\n- Ajustar la dosis de un analgésico llamado tramadol.\n\n- Cambiar el tipo de pañales para facilitar su uso debido a la dependencia de la paciente.\n\n- Mantener el tratamiento para la enfermedad pulmonar, pero con supervisión diaria para asegurar que la paciente use bien el inhalador.\n\n**Conclusión**\n\nGracias a la revisión y coordinación entre la farmacia y el médico, se mejoró la seguridad y el manejo del tratamiento de la paciente. Además, se implementó un sistema que facilitará que tome sus medicamentos correctamente, lo cual es muy importante para su salud y bienestar.",
+            "B3": "**Contexto**  \nSe trata de una paciente de 73 años con múltiples enfermedades crónicas, incluyendo enfermedad pulmonar obstructiva crónica (EPOC), hipertensión arterial, trastorno bipolar, ansiedad, depresión, hipotiroidismo y artritis reumatoide. Es totalmente dependiente para sus actividades diarias y no sale de casa; su cuidadora habitual se encargaba de gestionar y recoger su medicación. Recientemente, tras una analítica en urgencias, se le diagnosticó una infección de orina y un déficit de vitamina D, para los cuales se le prescribió un nuevo tratamiento.\n\n**Hallazgos Clave**  \nLa paciente contactó con la farmacia comunitaria para aclarar dudas sobre la nueva medicación, ya que existía confusión debido a la coexistencia de tratamientos previos para el déficit de vitamina D y la reciente prescripción. Además, la cuidadora habitual informó que ya no podría continuar asistiendo a la paciente, lo que generó preocupación sobre la correcta administración de los medicamentos. Se ofreció entonces el servicio de Revisión del Uso del Medicamento (RUM) para evaluar el conocimiento de la paciente y su cuidadora sobre las patologías y tratamientos, y para identificar posibles errores en la gestión farmacológica.\n\nDurante la revisión, se detectaron múltiples problemas: medicamentos caducados, instrucciones incorrectas, comprimidos partidos indebidamente y acumulación de envases duplicados. También se identificaron errores potenciales en la prescripción, como duplicidad en el tratamiento para la vitamina D y una pauta inadecuada para tramadol. Además, se observaron dificultades en el manejo del inhalador para la EPOC y problemas relacionados con la elección del absorbente para la incontinencia urinaria, que complicaban la correcta atención de la paciente.\n\n**Interpretación Clínica**  \nDada la complejidad del caso, la dependencia de la paciente y la ausencia de su cuidadora habitual, se consideró necesario derivar a la paciente al servicio de Sistema Personalizado de Dosificación (SPD), que facilita la organización y administración segura de la medicación. Se elaboró un informe detallado para el médico de Atención Primaria, incluyendo recomendaciones específicas para ajustar el tratamiento, como la sustitución del calcifediol por colecalciferol para el déficit de vitamina D, la modificación de la pauta de tramadol y el cambio del tipo de absorbente para mejorar la comodidad y manejo.\n\nEn cuanto al tratamiento para la EPOC, el médico decidió mantener la medicación actual pero reforzar la supervisión diaria por parte de la cuidadora para asegurar la correcta utilización del inhalador.\n\n**Próximos Pasos**  \nEl médico de Atención Primaria recibió el informe y coordinó con la farmacia comunitaria la implementación del Sistema Personalizado de Dosificación. Este enfoque busca mejorar la seguridad en la administración de los medicamentos, evitar errores y aumentar la adherencia al tratamiento, aspectos fundamentales para el bienestar y la calidad de vida de la paciente. Además, se estableció un seguimiento estrecho para supervisar la evolución clínica y la correcta gestión terapéutica en el contexto de la nueva situación de dependencia y ausencia de la cuidadora habitual."
+        }
+    },
+    {
+        "article": "Nuestra paciente era una mujer japonesa de 83 años con insuficiencia cardiaca crónica (fracción de eyección: aproximadamente 30 %) que inició un tratamiento con empagliflozina 10 mg diarios unos 8 meses antes de su ingreso. Nunca se le había diagnosticado diabetes mellitus (HbA1c 5.9 % antes de iniciar el tratamiento con empagliflozina). Unos 6 meses antes de su ingreso, su tratamiento se cambió a dapagliflozina 5 mg. Sus diuréticos y otros medicamentos cardiacos no se ajustaron durante ese tiempo. Dos semanas antes de su ingreso, tropezó y cayó, sufriendo fracturas vertebrales y de costillas. La paciente se debilitó significativamente por el dolor de las fracturas, lo que le causó dificultad para caminar y anorexia. Solo podía comer el 50-70 % de su ingesta dietética habitual. Esto empeoró en la semana siguiente, cuando también desarrolló náuseas y vómitos y redujo aún más su ingesta de alimentos a solo el 10-20 % de la cantidad habitual. Durante este período, continuó tomando dapagliflozina. Fue ingresada en el hospital.\nAl ingreso, la paciente estaba consciente con una temperatura corporal de 37.4°C, presión arterial de 124/68 mmHg, frecuencia cardiaca de 91 bpm y saturación de oxígeno de 98% en aire ambiente. Los análisis de sangre revelaron un nivel de glucosa en sangre de 124 mg/dL, pH de 7.3, concentración de HCO3– de 14 mmol/L, exceso de base de -10 mEq/L, brecha aniónica de 20 mEq/L y concentración de b-hidroxibutirato de 5150 umol/L (Tabla 1). Estos hallazgos fueron consistentes con el diagnóstico de cetoacidosis normoglucémica. La paciente no tenía antecedentes de consumo de alcohol, tabaquismo o uso de drogas.\nSe descartaron otras causas de acidosis con alto déficit aniónico. Su nivel de péptido C era coherente con los niveles de glucosa en sangre en el ingreso, lo que indicaba que tenía una secreción de insulina adecuada; por lo tanto, no se inició la administración de insulina. Se interrumpió el uso de inhibidores de SGLT2 y la paciente se trató inicialmente con solución salina isotónica y una infusión de mantenimiento de aproximadamente 170 g de glucosa diarios.\nA pesar de no haber iniciado la insulina, su pH (7.418), concentración de HCO3– (20.7 mmol/L) y brecha aniónica (13.3 mEq/L) mejoraron al día siguiente de su ingreso. Se inició la dieta Carb 60, pero se continuaron las infusiones intravenosas de glucosa porque la ingesta de alimentos de la paciente era escasa. La cantidad de infusión de glucosa administrada se ajustó según su ingesta de alimentos. En el cuarto día de hospitalización, las cetonas urinarias desaparecieron.\nLa infusión de glucosa se interrumpió el día 12 de la hospitalización, una vez que el paciente pudo comer comidas completas. Aunque el nivel de glucosa en sangre del paciente estaba dentro del rango normal, la excreción de glucosa en la orina fue de 3+ (>500 mg/dL) durante 8 días después de la última dosis de dapagliflozina.\nAl ingreso, la paciente no podía caminar debido al dolor de la fractura, la fatiga general y el síndrome de desuso, pero después de la rehabilitación pudo hacerlo de forma independiente. Fue dada de alta el día 19 de hospitalización, tras someterse a rehabilitación.\nLos inhibidores de SGLT2 no se reiniciaron.\n\nMH - Humanos\nMH - Mujer\nMH - *Insuficiencia cardiaca/inducida químicamente\nMH - *Inhibidores del transportador de glucosa y sodio 2/efectos adversos\nMH - Edad 80 años y más\nMH - Cetosis/químicamente inducida\nMH - glucósidos/efectos adversos\nMH - Cetoacidosis diabética/inducida químicamente\n",
+        "gold_summary": "A continuación, describimos un caso de cetoacidosis en una mujer japonesa de 83 años sin diabetes a la que se le administraron inhibidores de SGLT2 para la insuficiencia cardiaca (fracción de eyección: aproximadamente 30 %). Dos semanas antes de su ingreso, había sufrido una fractura vertebral y una fractura de costilla debido a una caída, a la que siguió una anorexia, pero continuó tomando inhibidores de SGLT2. En el momento del ingreso, los resultados de los análisis de sangre revelaron un nivel de glucosa en sangre de 124 mg/dL, un nivel de hemoglobina A1C del 5,9 %, un pH de 7,329, una concentración de HCO₃⁻ de 14,3 mmol/L y una concentración de β-hidroxibutirato de 5150 μmol/L, lo que condujo a un diagnóstico de cetoacidosis euglucémica. El nivel de péptido C de la paciente coincidía con los niveles de glucosa en sangre en el momento del ingreso, lo que indicaba que tenía una secreción de insulina adecuada. La paciente fue tratada únicamente con administración de glucosa sin insulina y fue dada de alta tras la interrupción del inhibidor de SGLT2.\n",
+        "synthetic_summary": {
+            "B1": "Había una señora de 83 años que no tenía diabetes. Ella tenía un problema en el corazón. Tomaba una medicina para ayudar su corazón. \n\nUn día, se cayó y se lastimó mucho. Le dolían los huesos y no quería comer. Pero siguió tomando su medicina. \n\nCuando llegó al hospital, los doctores le hicieron pruebas. Vieron que su sangre estaba un poco rara, pero no tenía mucha azúcar. \n\nElla tenía un problema llamado cetoacidosis, que pasa cuando el cuerpo usa mucha energía y se cansa. Los doctores le dieron agua con azúcar para ayudarla. No le dieron insulina porque su cuerpo todavía hacía insulina sola. \n\nDespués de un tiempo, ella se sintió mejor y pudo irse a su casa. Ya no tomó esa medicina para el corazón.",
+            "B2": "Caso de una mujer mayor con problemas del corazón y un medicamento especial\n\nUna mujer japonesa de 83 años tenía insuficiencia cardíaca, que significa que su corazón no bombeaba sangre tan bien como debería. Para ayudarla, le dieron un medicamento llamado inhibidor de SGLT2, que normalmente se usa para la diabetes, pero ella no tenía diabetes. Este medicamento ayuda al corazón, pero puede causar un problema llamado cetoacidosis, que es cuando el cuerpo produce sustancias ácidas llamadas cetonas.\n\nLo que pasó antes de ir al hospital\n\nDos semanas antes de entrar al hospital, la mujer se cayó y se fracturó una vértebra y una costilla. Por el dolor, dejó de comer bien y se debilitó mucho. A pesar de esto, siguió tomando el medicamento inhibidor de SGLT2.\n\nLo que encontraron en el hospital\n\nCuando llegó al hospital, sus análisis de sangre mostraron que tenía niveles normales de azúcar en la sangre (124 mg/dL), pero su cuerpo estaba en cetoacidosis, porque el pH de su sangre estaba bajo (7.3), el bicarbonato (HCO3–) estaba bajo (14 mmol/L) y tenía muchas cetonas (β-hidroxibutirato alto). Esto significa que su cuerpo estaba produciendo ácidos, aunque el azúcar en sangre no estaba alto, por eso se llama cetoacidosis euglucémica. Además, su cuerpo todavía producía insulina, la hormona que controla el azúcar en sangre, lo que se confirmó con un análisis llamado péptido C.\n\nCómo la trataron y qué pasó después\n\nLos médicos dejaron de darle el medicamento inhibidor de SGLT2 y no le pusieron insulina porque su cuerpo seguía produciéndola. En cambio, le dieron líquidos con glucosa (azúcar) para ayudar a su cuerpo a recuperarse. Poco a poco, sus análisis mejoraron y las cetonas desaparecieron. Cuando pudo volver a comer bien, dejaron de darle glucosa por vía intravenosa. Aunque su azúcar en sangre se mantuvo normal, todavía eliminaba glucosa por la orina durante varios días después de dejar el medicamento. Después de rehabilitación para recuperarse de las fracturas y el cansancio, pudo caminar sola y fue dada de alta del hospital. No volvieron a darle el medicamento inhibidor de SGLT2.\n\nResumen\n\nEste caso muestra que los inhibidores de SGLT2 pueden causar cetoacidosis en personas sin diabetes, especialmente si están débiles o comen poco. Es importante vigilar a los pacientes que usan este medicamento y suspenderlo si aparecen síntomas como náuseas, vómitos o debilidad.",
+            "B3": "**Contexto:**  \nSe presenta el caso de una mujer japonesa de 83 años con insuficiencia cardíaca crónica, caracterizada por una fracción de eyección del 30 %, que recibió tratamiento con inhibidores del cotransportador sodio-glucosa tipo 2 (SGLT2), medicamentos usados para mejorar la función cardíaca y controlar la glucosa en sangre. La paciente no tenía diagnóstico previo de diabetes, con una hemoglobina A1c del 5.9 % antes de iniciar el tratamiento. Aproximadamente dos semanas antes de su ingreso hospitalario, sufrió fracturas vertebrales y de costillas tras una caída, lo que le provocó dolor intenso, dificultad para caminar y una marcada disminución en su ingesta alimentaria, aunque continuó tomando dapagliflozina, un inhibidor de SGLT2.\n\n**Hallazgos Clave:**  \nAl ingresar al hospital, la paciente estaba consciente y estable en signos vitales, pero los análisis de sangre mostraron:  \n- Glucosa en sangre de 124 mg/dL (dentro del rango normal).  \n- pH sanguíneo de 7.3, indicando acidosis (un aumento en la acidez de la sangre).  \n- Bicarbonato (HCO₃⁻) de 14 mmol/L, bajo, lo que confirma acidosis metabólica.  \n- Brecha aniónica elevada (20 mEq/L), que sugiere la presencia de ácidos en la sangre.  \n- Elevada concentración de β-hidroxibutirato (5150 μmol/L), una cetona que indica cetosis.  \nEstos resultados permitieron diagnosticar una cetoacidosis euglucémica, una condición en la que hay acumulación de ácidos cetónicos en sangre sin hiperglucemia significativa. Además, el nivel de péptido C, un marcador de producción de insulina, era adecuado, lo que indicaba que la paciente seguía produciendo insulina de forma suficiente.\n\n**Interpretación Clínica:**  \nLa cetoacidosis euglucémica en esta paciente fue probablemente inducida por el uso de inhibidores de SGLT2 en el contexto de una ingesta alimentaria muy reducida y estrés físico debido a las fracturas. Estos medicamentos pueden aumentar la producción de cuerpos cetónicos al promover la eliminación de glucosa por la orina y reducir la insulina circulante, favoreciendo la cetosis incluso cuando los niveles de glucosa en sangre no están elevados. La secreción adecuada de insulina descartó la necesidad de administrar insulina exógena.\n\n**Próximos Pasos y Evolución:**  \nSe suspendió el tratamiento con inhibidores de SGLT2 y se inició terapia con infusión intravenosa de glucosa y líquidos para corregir la acidosis y mantener la ingesta energética, sin administrar insulina. La paciente mostró mejoría rápida en los parámetros ácido-base al día siguiente y la cetosis desapareció en cuatro días. La infusión de glucosa se ajustó según su capacidad para alimentarse y se suspendió una vez que pudo consumir comidas completas. Durante ocho días posteriores a la suspensión del medicamento, la paciente continuó excretando glucosa en la orina, un efecto residual conocido de la dapagliflozina. Tras rehabilitación para recuperar la movilidad afectada por las fracturas y el desuso, la paciente fue dada de alta en buen estado y sin reiniciar los inhibidores de SGLT2.\n\n---\n\nEste caso ilustra la importancia de reconocer la cetoacidosis euglucémica como una complicación potencial de los inhibidores de SGLT2, especialmente en pacientes sin diabetes que presentan factores de riesgo como ingesta insuficiente y estrés físico. La intervención temprana con suspensión del medicamento y soporte nutricional adecuado puede conducir a una recuperación favorable sin necesidad de insulina."
+        }
+    },
+    {
+        "article": "Una recién nacida fue evaluada en la sala de neonatos poco tiempo después del parto debido a la presencia de extensas lesiones similares a cicatrices en sus flancos y muslos superiores. La bebé, nacida de una madre asiática de 28 años a las 39 semanas de gestación, formaba parte de un embarazo gemelar espontáneo. Su madre, que ya había tenido cinco hijos, había tenido un aborto espontáneo en el primer trimestre durante su segundo embarazo.\n\nLos padres eran primos hermanos y no habían tenido problemas de salud en sus tres hijos vivos. La ecografía a las 13 semanas confirmó un embarazo bicorial y diacítico y la ausencia de actividad cardíaca en uno de los gemelos. Las ecografías posteriores mostraron un feto que se desarrollaba con normalidad junto a un gemelo no viable.\n\nDurante el embarazo, la madre no informó sobre el uso de medicamentos o síntomas como fiebre y erupción cutánea. Dio negativo para estreptococo del grupo B y fue admitida en el departamento de urgencias obstétricas con dolores de parto. La niña fue entregada por vía vaginal, pesando 2,83 kg, y fue vigorosa al nacer. A la placenta se le unió un remanente fetal no viable comprimido que medía 6 × 2 cm. La placenta pesaba 460 g y parecía normal al examen.\n\nLa niña presentaba lesiones cutáneas extensas e irregulares, que se caracterizaban por un aspecto estrellado en ambos flancos, que se extendían lateralmente sobre la zona glútea y el muslo superior. Las lesiones eran simétricas en ambos flancos. No obstante, las lesiones en los muslos eran notablemente más leves en el lado izquierdo. Sus constantes vitales eran estables y no presentaba otras anomalías externas. El examen clínico de sus sistemas respiratorio, cardiovascular, gastrointestinal y neurológico reveló resultados normales, y no se observaron otras anomalías cutáneas, incluida la ausencia de lesiones ampollosas.\n\nDada la naturaleza simétrica de las anomalías cutáneas y el contexto de embarazo de mellizos con FP, se realizó un diagnóstico de aplasia cutis congénita grupo V. Los exámenes de laboratorio, que incluían hemograma completo, electrolitos y pruebas de función renal e hepática, arrojaron resultados normales. Los exámenes de detección de toxoplasmosis, rubéola, citomegalovirus, herpes simple y VIH (TORCH) arrojaron resultados negativos. La ecografía del cerebro, abdomen y corazón no reveló anomalías.\n\nDado que las lesiones se curaron en el útero, solo se prescribieron emolientes locales. Después de 48 horas de observación, el bebé fue dado de alta en su casa, con derivaciones a clínicas de dermatología pediátrica y cirugía plástica. En el seguimiento de 2 semanas, no se observaron cambios en las lesiones de la piel ni nuevos síntomas. Su análisis de microarreglo cromosómico fue reportado como normal.\n",
+        "gold_summary": "Informamos sobre un neonato al que se le diagnosticó ACC de grupo G-V asociado con fetus papyraceus de un embarazo gemelar di-coriónico y di-amniótico. Nacida de una madre asiática de 28 años, esta niña presentaba lesiones extensas, cicatrizadas, similares a las cicatrices en sus flancos y muslos superiores. Estas lesiones eran consistentes con la distribución en forma de «H» comúnmente descrita en ACC ligada a fetus papyraceus. A pesar de las manifestaciones dermatológicas significativas, la niña no mostró otras anormalidades externas o implicación sistémica, y las evaluaciones exhaustivas, incluidos los ultrasonidos y el microarray cromosómico, fueron normales.\n",
+        "synthetic_summary": {
+            "B1": "Una bebé nació con marcas en la piel que parecían cicatrices. Estas marcas estaban en sus lados y muslos. La mamá tuvo dos bebés, pero uno no creció bien en la barriga. \n\nLa bebé con las marcas está sana y fuerte. Los doctores revisaron su cuerpo y todo está bien. No tiene otras partes malas en su cuerpo. \n\nLas marcas en su piel se hicieron mientras estaba en la barriga. Los doctores solo le pusieron crema para cuidar su piel. La bebé está bien y seguirá creciendo feliz.",
+            "B2": "**Caso de una recién nacida con lesiones en la piel**\n\nLes presentamos el caso de una bebé que nació con unas marcas especiales en la piel, llamadas aplasia cutis congénita (ACC) grupo V. Estas marcas aparecieron porque tuvo un gemelo que no sobrevivió durante el embarazo, lo que se conoce como fetus papyraceus (un gemelo aplastado y no viable).\n\n**Lo que encontraron en la bebé**\n\nLa niña, nacida de una madre asiática de 28 años, tenía lesiones en la piel que parecían cicatrices en forma de “H” en sus costados y muslos superiores. Estas marcas son típicas en casos de ACC cuando hay un fetus papyraceus. A pesar de estas lesiones, la bebé estaba saludable en general. No tenía otros problemas visibles ni síntomas en su cuerpo. Las pruebas médicas, como ecografías del cerebro, corazón y abdomen, y un análisis genético llamado microarreglo cromosómico, mostraron resultados normales.\n\n**Qué significa este diagnóstico**\n\nLa ACC grupo V es una condición rara que afecta la piel y está relacionada con la pérdida de un gemelo durante el embarazo. Aunque las marcas en la piel pueden ser grandes, no siempre causan otros problemas de salud. En este caso, la bebé solo necesitó cuidados para mantener la piel hidratada y fue seguida por especialistas en dermatología y cirugía plástica para asegurar una buena recuperación.\n\nEn resumen, esta niña nació con lesiones en la piel causadas por la pérdida de su gemelo, pero su salud general es buena y no presenta otras complicaciones.",
+            "B3": "**Contexto**  \nSe presenta el caso de una recién nacida diagnosticada con aplasia cutis congénita (ACC) del grupo V, una condición caracterizada por la ausencia localizada de piel, en asociación con fetus papyraceus (un gemelo fetal muerto y comprimido) en un embarazo gemelar bicorial y biamniótico. La bebé nació de una madre asiática de 28 años, producto de un embarazo espontáneo gemelar, en el que uno de los fetos no sobrevivió desde etapas tempranas.\n\n**Hallazgos Clave**  \nAl momento del nacimiento, la niña mostró lesiones cutáneas extensas, con un patrón simétrico en forma de «H» en ambos flancos y muslos superiores, que se asemejaban a cicatrices. Estas lesiones son típicas de la ACC grupo V cuando se asocia con fetus papyraceus. A pesar de la apariencia notable de la piel, la bebé no presentó otras anomalías externas ni signos de afectación en órganos o sistemas. Los exámenes clínicos y de laboratorio, incluyendo ecografías cerebrales, abdominales y cardíacas, así como pruebas para infecciones congénitas (TORCH) y análisis cromosómicos mediante microarreglo, no mostraron alteraciones.\n\n**Interpretación Clínica**  \nLa distribución y características de las lesiones cutáneas, junto con la historia del embarazo gemelar con un gemelo no viable, apoyan el diagnóstico de aplasia cutis congénita grupo V. Esta forma de ACC se relaciona con la presencia de fetus papyraceus y suele manifestarse con lesiones simétricas en la piel, pero sin compromiso sistémico. La ausencia de otras anomalías y la normalidad de las pruebas complementarias indican un pronóstico favorable.\n\n**Próximos Pasos**  \nEl tratamiento consistió en cuidados locales con emolientes para favorecer la hidratación y cicatrización de la piel. La bebé fue dada de alta tras 48 horas de observación y se programaron controles en dermatología pediátrica y cirugía plástica para seguimiento y manejo de las lesiones cutáneas. A las dos semanas, no se observaron cambios ni aparición de nuevos síntomas, confirmando la estabilidad clínica del caso."
+        }
+    },
+    {
+        "article": "Información para el paciente\nUn hombre de 44 años de edad fue ingresado en nuestro hospital con quejas principales de neumaturia y cistitis repetida. El paciente también tenía antecedentes de hipotiroidismo.\n\nLa tomografía computarizada con contraste mejorado reveló múltiples divertículos del colon sigmoide, y el límite entre el divertículo y la vejiga no estaba claro. La endoscopia gastrointestinal inferior reveló una fístula en el colon rectosigmoide aproximadamente a 15 cm del borde anal. La cistoscopia reveló una fístula en la pared posterior izquierda de la vejiga. Se diagnosticó una fístula vesicovaginal y se planificó una cirugía laparoscópica. Los hallazgos intraoperatorios revelaron una inflamación severa alrededor de la fístula vesicovaginal, y también se habían formado adhesiones severas entre el íleon y la vejiga. El íleon y la vejiga eran difíciles de exfoliar debido a las adhesiones severas. Por lo tanto, decidimos realizar una resección intestinal combinada. El colon rectosigmoide, incluida la fístula, se movilizó y se resecó. La fístula vesical se seccionó y se cerró con una sutura de púas sin nudos (V-LocTM 180, Covidien, Mansfield). La anastomosis sigmoide-rectal se reconstruyó utilizando la técnica de doble grapado. La resección parcial del íleon se reconstruyó con una anastomosis funcional de extremo a extremo (FEEA). Además de la presencia de una anastomosis de 2 sitios, había una inflamación severa en el área circundante, y considerando el riesgo de fuga anastomótica, se creó una ileostomía de derivación 30 cm proximal a la anastomosis ileo-ileal.\n\nLos procedimientos quirúrgicos incluyeron resección anterior alta laparoscópica, resección parcial del intestino delgado, cistectomía parcial y derivación en forma de asa. La operación duró 236 minutos y la pérdida de sangre fue de 50 ml. El curso postoperatorio fue sin incidentes y el cierre de la ileostomía se planificó 1 mes después de la cirugía inicial. Con ayuda laparoscópica, se eliminaron las adherencias entre el omento y la pared abdominal alrededor del estoma. Se realizó una movilización completa alrededor del estoma y el intestino se sacó hacia afuera. El íleon se reconstruyó utilizando FEEA. El procedimiento quirúrgico implicó el cierre de la ileostomía asistida por laparoscopia. La operación duró 100 minutos y la pérdida de sangre fue de 30 ml.\n\nHallazgos clínicos\nAl día siguiente de la cirugía, se produjo un shock sintomático debido a la presión arterial baja (<80 mm Hg) y la taquicardia. Los análisis de sangre mostraron que la hemoglobina disminuyó de 15.3 antes de la cirugía a 8.6 g/dL después de la cirugía.\n\nEvaluación diagnóstica\nLa tomografía computarizada abdominal (TC) reveló una gran cantidad de fluido de alta densidad en la cavidad abdominal. El diagnóstico fue sangrado posoperatorio y shock hemorrágico. Se insertó un catéter venoso central y se administraron 8 unidades de glóbulos rojos y 8 unidades de plasma fresco congelado para estabilizar los signos vitales. Los signos vitales se estabilizaron y no se observó progresión de la anemia después de eso. Aunque se logró la hemostasia, la distensión abdominal severa y los altos niveles de respuesta inflamatoria (proteína C reactiva [CRP] a 42.9 mg/dL y recuento de glóbulos blancos [WBC] de 18,500/uL) persistieron 7 días después de la cirugía.\n\nLa TC con contraste reveló que el hematoma intraabdominal se localizaba en el abdomen inferior izquierdo y derecho, y se consideró posible el drenaje percutáneo. En el día 8 posoperatorio, se insertaron tubos de drenaje de 18 Fr en el abdomen inferior izquierdo y derecho a través de una punción guiada por TC, y se drenó una gran cantidad de sangre antigua. Después del drenaje, la reacción inflamatoria y la distensión abdominal causadas por la infección del hematoma residual mejoraron (CRP a 1,9 mg/dL y WBC de 5000/μL). No se observó progresión de la anemia. En el día 14 posoperatorio, el drenaje en el abdomen inferior derecho cambió de sangre antigua a jugo intestinal. Una angiografía de drenaje reveló fuga anastomótica tardía en el sitio de cierre de la ileostomía. No hubo signos de peritonitis con buen drenaje, pero el drenaje fue de aproximadamente 100 a 200 ml, y el flato del drenaje continuó. No se observó disminución del drenaje durante los siguientes 14 días.\n\nIntervención terapéutica\nAunque se consideró la posibilidad de una nueva operación, se esperaban adhesiones intraabdominales severas debido a la historia de cirugías anteriores, sangrado postoperatorio y fuga anastomótica. Por lo tanto, se consideró que la nueva operación era un procedimiento de alto riesgo. La tomografía computarizada con contraste mostró que un hematoma organizado permanecía en el mesenterio del intestino delgado y el íleon en el lado distal de 10 cm de la anastomosis estaba comprimido cerca del hematoma restante. Teniendo en cuenta la estenosis del íleon en el lado anal de la anastomosis debido a un hematoma residual como la causa de fuga anastomótica, se intentó la dilatación radioscópica del área de estenosis a través del drenaje en el día 24 postoperatorio. Se colocó un introductor de funda Cordis BRITE TIP® (8 Fr × 23 cm) en la fístula donde ocurrió la fuga anastomótica después del drenaje angiográfico. Se usó un hilo radioscópico GT (0.016 pulgadas, 180 cm, 90°) (Terumo, Tokio, Japón) y un microcatéter Renegade HI-FLO (135 × 20 cm) (Boston Scientific, Tokio, Japón) para alcanzar el íleon terminal. Usando el catéter Selecon MP II (6 Fr, 80 cm, φ20 mm) (Terumo), se identificó el área de estenosis en el íleon debido a la compresión del hematoma donde el globo no podía pasar.\n\nSe realizó dilatación con globo fluoroscópica en la estenosis del íleo utilizando un globo guiado por alambre CRE PRO GI (180 cm, 15-18 mm) (Boston Scientific), inflado a 16,5 mm de diámetro a 4,5 atm durante 3 minutos.\n\nSeguimiento y resultados\nDesde el día posterior a la dilatación con globo, la cantidad de drenaje disminuyó notablemente, y se observaron flatos y defecaciones desde el ano. Una semana después de la dilatación con globo, el drenaje fue casi nulo, y se determinó que la fuga anastomótica se había resuelto. El drenaje se eliminó gradualmente. La ingesta oral fue buena, y tuvo movimientos intestinales regulares. Fue dado de alta el día 45 posterior a la operación. Desde entonces, no se ha informado de ninguna recurrencia de la estenosis o fuga anastomótica.\n",
+        "gold_summary": "Preocupaciones del paciente: Presentamos el caso de un hombre de 44 años con fuga anastomótica tardía después del cierre de la ileostomía, causada por la compresión de un hematoma intraabdominal que se curó rápidamente después de la dilatación fluoroscópica con globo del área de la estenosis intestinal.\n\nDiagnósticos: Se produjo sangrado postoperatorio y shock hemorrágico el día 1 postoperatorio tras el cierre de la ileostomía. Los signos vitales se estabilizaron tras la transfusión de sangre, y se realizó con éxito un drenaje guiado por tomografía computarizada para reducir el volumen del hematoma. Sin embargo, el hematoma residual comprimió el íleon en el lado anal de la anastomosis, lo que provocó una fuga anastomótica tardía.\n\nIntervenciones/resultados: Se realizó con éxito la dilatación con balón fluoroscópico del área estenótica a través del drenaje y la fuga anastomótica se curó rápidamente.\n",
+        "synthetic_summary": {
+            "B1": "Había un hombre que se lastimó su tripita después de una operación. Tenía un bulto con sangre que apretaba su intestino y eso hizo que se hiciera un agujero pequeño. \n\nLos doctores le pusieron una bolsita con aire para hacer más grande el lugar apretado. Así, el agujero se cerró y el hombre empezó a sentirse mejor. \n\nDespués, pudo comer y hacer popó sin problema. Los doctores cuidaron mucho de él y se fue a su casa feliz.",
+            "B2": "Caso del paciente  \nUn hombre de 44 años tuvo una complicación después de una cirugía para cerrar una ileostomía, que es una abertura temporal en el abdomen para sacar los desechos del intestino. Esta complicación se llamó fuga anastomótica tardía, que significa que la unión hecha entre partes del intestino empezó a tener una filtración de líquidos.\n\nQué pasó después de la cirugía  \nAl día siguiente de cerrar la ileostomía, el paciente sufrió una hemorragia interna que causó un shock, una condición grave donde la presión de la sangre baja mucho. Los médicos le transfundieron sangre y drenaron un hematoma, que es una acumulación de sangre fuera de los vasos sanguíneos dentro del abdomen. Aunque esto ayudó, quedó un hematoma pequeño que presionaba una parte del intestino llamada íleon, causando que la unión intestinal se filtrara.\n\nTratamiento y resultados  \nPara solucionar la fuga, los médicos usaron una técnica llamada dilatación con balón fluoroscópico. Esto consiste en insertar un pequeño globo dentro del área estrecha del intestino y luego inflarlo para abrir el paso. Esta intervención se hizo a través del drenaje ya colocado y ayudó a aliviar la presión causada por el hematoma. Después del tratamiento, la fuga se cerró rápidamente, el drenaje disminuyó y el paciente pudo volver a comer y tener movimientos intestinales normales. Fue dado de alta sin más problemas y no ha tenido recurrencias.",
+            "B3": "**Contexto del Caso**  \nSe presenta el caso de un hombre de 44 años que inicialmente fue hospitalizado por síntomas de neumaturia (presencia de aire en la orina) y episodios repetidos de cistitis (infección de la vejiga). Tenía antecedentes de hipotiroidismo. Estudios de imagen y endoscopía revelaron una fístula (una conexión anormal) entre el colon sigmoide y la vejiga, acompañada de múltiples divertículos (pequeñas bolsas) en el colon. Debido a la inflamación severa y adherencias entre intestino y vejiga, se realizó una cirugía laparoscópica compleja que incluyó la resección del colon afectado, cierre de la fístula vesical, resección parcial del intestino delgado y creación temporal de una ileostomía (una abertura en el abdomen para desviar las heces).\n\n**Hallazgos y Complicaciones Postoperatorias**  \nAl día siguiente del cierre de la ileostomía, el paciente presentó un shock hemorrágico debido a una hemorragia interna, evidenciada por una caída significativa de hemoglobina y acumulación de líquido denso en la cavidad abdominal detectada por tomografía computarizada (TC). Se estabilizó con transfusiones y drenaje guiado por TC de un hematoma (acumulación de sangre) intraabdominal. A pesar de la hemostasia, persistió una inflamación intensa y distensión abdominal. Posteriormente, el drenaje mostró presencia de jugo intestinal, lo que indicó una fuga en la anastomosis (la unión quirúrgica entre segmentos intestinales) en el sitio del cierre de la ileostomía. Esta fuga anastomótica tardía se atribuyó a la compresión del íleon (parte final del intestino delgado) por un hematoma residual que causaba estenosis (estrechamiento) en esa zona.\n\n**Intervención Terapéutica**  \nDado el alto riesgo de una nueva cirugía debido a las adherencias y complicaciones previas, se optó por un tratamiento menos invasivo. Se realizó una dilatación con balón guiada por fluoroscopía (una técnica de imagen en tiempo real) a través del drenaje existente para ampliar el área estenótica del íleon comprimido. Este procedimiento consistió en introducir un catéter y un globo inflable en el sitio estrechado y expandirlo cuidadosamente para aliviar la compresión.\n\n**Resultados y Seguimiento**  \nTras la dilatación con balón, la cantidad de drenaje intestinal disminuyó notablemente y el paciente recuperó la función intestinal normal, con evacuaciones por vía natural. Una semana después, la fuga anastomótica se resolvió completamente, permitiendo la retirada progresiva del drenaje. El paciente mantuvo una buena ingesta oral y movimientos intestinales regulares, y fue dado de alta 45 días después de la cirugía inicial. Hasta la fecha, no se ha reportado recurrencia de la estenosis ni de la fuga anastomótica.\n\n---\n\nEste caso ilustra cómo una complicación grave tras cirugía intestinal, como una fuga anastomótica causada por compresión de un hematoma residual, puede ser tratada eficazmente mediante una dilatación endovascular guiada por imágenes, evitando una cirugía adicional de alto riesgo."
+        }
+    },
+    {
+        "article": "Paciente femenino de 23 años, ASA I, acude al Centro de Salud de la Universidad Peruana de Ciencias Aplicadas (CUS-UPC) para colocarle un implante en la zona edéntula de la pieza 1.6. Durante la evaluación, la paciente refiere que hace unos meses se le fracturó la primera molar superior derecha y, como consecuencia, le realizaron la exodoncia atraumática de dicha pieza dentaria.\n\nTras la inspección clínica, se observó la ausencia de la pieza dentaria 1.6, fenotipo gingival delgado y disminución en altura de reborde edéntulo Seibert tipo II 13. Tomográficamente, se registraron medidas de la altura del reborde óseo residual en relación con el piso del seno maxilar (6 mm) y el ancho de la cresta ósea a nivel cervical (11,20 mm), medio (11,80 mm) y apical (12,40 mm), con lo que se identifica la presencia de un seno maxilar ovoide, según Nie et al. Se realizó la planificación quirúrgica para la realización de una elevación del seno maxilar con abordaje transcrestal y la colocación de un implante dental de 4,8 x 8 mm.\n\nSe inició el procedimiento quirúrgico, que consistió en lo siguiente:\n\n• Asepsia y antisepsia\n\n• Técnica anestesia infiltrativa por vestibular y palatino de la zona edéntula 1.6 utilizando 2 cartuchos de lidocaína al 2% con epinefrina 1:80.000.\n\n• Incisión supracrestal en la zona edéntula 1.6 e incisiones sulculares en mesial de la pieza dentaria 1.7 y en distal de la pieza dentaria 1.5.\n\n• Decolado del colgajo a espesor parcial y, luego, se procedió a probar la guía quirúrgica para realizar la secuencia de fresado hasta una longitud de 6 mm, dejando 1 mm de distancia al piso del seno maxilar, el cual fue comprobado con los calibradores de profundidad, según el diámetro de la fresa que se utilizó durante la osteotomía. La secuencia de fresado se realizó hasta la fresa 3,5 mm de diámetro y luego se procedió a realizar el levantamiento de 2 mm del seno maxilar con la técnica de abordaje transcrestal mediante el uso de un osteótomo, hasta llegar a una longitud de 8 mm.\n\n• Colocación del implante φ 4,8 x 8 mm (Bone Level tapered, Straumann®) y tornillo de cierre, ambos con un torque de inserción de 20 N.\n\n• Sutura con puntos interrumpidos con ácido poliglicólico 5/0 y lavado de la zona quirúrgica con suero fisiológico al 0,09%.\n\n• Radiografía posquirúrgica del implante en zona edéntula 1.6.\n\n• Indicación de tomar amoxicilina de 500 mg + ácido clavulánico 125 mg cada 8 horas durante 7 días, ketorolaco de 10 mg cada 8 horas por 3 días, cetirizina de 10 mg cada 24 horas por 3 días y clorhexidina al 0,12%, 2 veces al día, por 10 días. Entre las indicaciones posquirúrgicas se le indicó a la paciente reposo absoluto, sin esfuerzo físico, dieta blanda, no sonarse la nariz, no succionar líquidos por dos semanas, no sumergir la cabeza en agua, tampoco estornudar o toser con la boca abierta, mantener la cabeza elevada y aplicarse compresas de hielo durante las primeras 4 horas.\n\nSe realizó un control posquirúrgico a los 7 días, el cual evidenció tejidos blandos en proceso de cicatrización, por lo que se procedió al retiro de puntos y lavado con suero fisiológico al 0,9%, y se realizó una tomografía de control que evidenció la elevación de seno maxilar, con 2,83 mm aproximadamente. Asimismo, se realizaron controles posquirúrgicos a los 35 y 56 días, en los cueles se hallaron tejidos blandos en completo proceso de cicatrización.",
+        "gold_summary": "Se realizó un levantamiento de seno maxilar sin injerto óseo en una paciente de sexo femenino de 23 años que requería la colocación de un implante dental en la zona edéntula de la pieza 16. La evaluación clínica y tomográfica permitieron planificar y realizar la elevación de seno maxilar mediante el abordaje transcrestal y sin la necesidad de injerto óseo. El reborde residual de 6 mm permitió la colocación de un implante dental simultáneo. Luego de 6 meses de seguimiento tomográfico, antes de la carga protésica, se consiguió una altura ósea vertical de 8,83 mm, lo que dio como resultado una ganancia ósea vertical de 2,83 mm. Adicionalmente, se observa una adecuada integración del implante dental sin complicaciones posoperatorias.",
+        "synthetic_summary": {
+            "B1": "Una joven de 23 años necesitaba un diente nuevo. El doctor hizo un pequeño espacio en su hueso cerca de la nariz. No usó nada más para llenar ese espacio. Puso un tornillo especial para el diente. Después de un tiempo, el hueso creció un poquito más. El diente nuevo quedó bien y sin problemas. Todo está sanando muy bien.",
+            "B2": "**Lo que hicieron y encontraron**\n\nUna joven de 23 años necesitaba un implante dental porque le faltaba un molar superior derecho. Los doctores revisaron su boca y tomaron imágenes para medir el hueso donde se colocaría el implante. Vieron que había 6 mm de hueso en esa zona, lo que era suficiente para poner un implante, pero necesitaban levantar un poco el seno maxilar. El seno maxilar es un espacio lleno de aire dentro del hueso de la cara, cerca de los dientes superiores. Para hacer espacio para el implante, realizaron una cirugía llamada elevación de seno maxilar usando un método que no requiere poner hueso nuevo (injerto).\n\n**Cómo fue la cirugía**\n\nDurante la operación, anestesiaron la zona para que no sintiera dolor. Hicieron una pequeña incisión y usaron herramientas especiales para levantar el suelo del seno maxilar unos 2 mm. Luego colocaron un implante dental de 8 mm de largo en el hueso existente. Después, cerraron la herida con puntos y le dieron medicamentos para evitar infecciones y controlar el dolor. También le indicaron cuidados para que la zona sanara bien.\n\n**Qué pasó después**\n\nA los 7 días, la herida estaba sanando bien y retiraron los puntos. Después de 6 meses, las imágenes mostraron que el hueso había crecido 2,83 mm más en altura, alcanzando un total de 8,83 mm. Esto significa que el implante estaba bien integrado y estable, sin problemas después de la cirugía.\n\n**Por qué es importante**\n\nEste caso muestra que es posible levantar el seno maxilar y colocar un implante al mismo tiempo sin usar hueso extra. Esto puede hacer que el tratamiento sea más rápido y menos complicado para pacientes que necesitan implantes en esa zona.",
+            "B3": "**Contexto**  \nUna mujer de 23 años, sin antecedentes médicos relevantes (clasificación ASA I), acudió a un centro de salud para la colocación de un implante dental en el espacio dejado por la extracción previa de su primer molar superior derecho (pieza 1.6). La paciente había perdido este diente debido a una fractura y se le realizó una exodoncia atraumática. Durante la evaluación clínica se observó la ausencia del diente, un tipo de encía delgada y una reducción en la altura del reborde óseo (zona del hueso donde se apoya el diente), clasificada como Seibert tipo II. Las imágenes tomográficas mostraron que el reborde óseo residual tenía una altura de 6 mm desde el piso del seno maxilar, con un ancho adecuado para la colocación del implante, y se identificó un seno maxilar de forma ovoide.\n\n**Hallazgos Clave y Procedimiento Realizado**  \nSe planificó una elevación del seno maxilar mediante un abordaje transcrestal (acceso a través de la cresta ósea donde se colocará el implante) sin necesidad de utilizar injerto óseo. Durante la cirugía, se realizó anestesia local, incisiones precisas para levantar un colgajo de encía, y se preparó el sitio para el implante con fresas de diferentes diámetros, respetando una distancia segura de 1 mm al piso del seno maxilar. Se elevó la membrana del seno maxilar 2 mm con un osteótomo (instrumento para levantar el seno), permitiendo colocar un implante dental de 4,8 mm de diámetro por 8 mm de longitud. La inserción se realizó con un torque adecuado (20 N), y se cerró la zona con suturas. Se indicó un tratamiento antibiótico, antiinflamatorio, antihistamínico y enjuagues con clorhexidina, además de recomendaciones estrictas para evitar complicaciones, como reposo absoluto y evitar esfuerzos que puedan afectar la zona quirúrgica.\n\n**Interpretación Clínica**  \nEl procedimiento permitió aumentar la altura ósea vertical disponible para el implante sin necesidad de injerto óseo, aprovechando el reborde óseo residual de 6 mm para colocar el implante simultáneamente con la elevación del seno maxilar. El seguimiento tomográfico realizado a los 7 días mostró una elevación de la membrana del seno de aproximadamente 2,83 mm, y controles posteriores a los 35 y 56 días confirmaron una adecuada cicatrización de los tejidos blandos sin complicaciones. Se logró una ganancia ósea vertical total de 2,83 mm, alcanzando una altura ósea de 8,83 mm antes de la colocación de la prótesis dental.\n\n**Próximos Pasos**  \nCon la adecuada integración del implante y la ganancia ósea confirmada, el siguiente paso será la carga protésica, es decir, la colocación de la corona o diente artificial sobre el implante para restaurar la función masticatoria y estética. Se continuará con controles periódicos para asegurar la estabilidad del implante y la salud de los tejidos circundantes."
+        }
+    },
+    {
+        "article": "Una paciente de 42 años de edad fue remitida a nuestro centro terciario de cáncer con antecedentes de seroma recurrente del seno izquierdo. La paciente se había sometido a una extracción bilateral de implantes mamarios con una capsulotomía parcial 11 meses antes de su primera visita a nuestro centro. La paciente no presentaba ninguna comorbilidad notable y tenía antecedentes de aumento bilateral de senos con implantes mamarios en el plano submuscular en 2003, a la edad de 21 años. No se pudo localizar ninguna información sobre el tipo de implantes que había recibido originalmente. La paciente volvió a consultar al mismo cirujano en 2008, quejándose de seroma bilateral, para someterse a un primer reemplazo bilateral de implantes mamarios con implantes mamarios anatómicos texturados de 425 cc (Sebbin LSA TF 425). En 2013, se sometió a un segundo procedimiento de reemplazo de implantes para aumentar el tamaño con implantes mamarios de 480 cc del mismo fabricante (Sebbin LSA TF 480). En 2017, la paciente volvió para una revisión en la que se quejaba de dolor y aumento del volumen del seno bilateralmente. En ese momento, se le realizó una exploración por ultrasonido que identificó efusiones periprostéticas bilaterales sin linfadenopatía o masas palpables en las regiones mamarias. Las efusiones se drenaron sin análisis, pero reaparecieron a lo largo de los años, cuando la paciente buscó ayuda del mismo cirujano y se sometió a un tercer procedimiento de revisión en 2022, con un reemplazo bilateral de implantes mamarios y una toma de muestras de la cápsula anterior. El cirujano envió dos especímenes desde el lado derecho (9 x 1 cm y 3 x 3 cm) y uno desde el lado izquierdo (2 x 1 cm). El informe histopatológico del espécimen encontró «material proteico amorfo celular acellular» en el lado derecho y «tejido fibroso escleroso con inflamación de linfocitos-monocitos, que requiere correlación con la presentación clínica» en el lado izquierdo. A pesar de la extracción, el seroma reapareció en el lado izquierdo, y se envió para pruebas citopatológicas que identificaron «una población de células pleomórficas atípicas irregulares con contornos irregulares que sugieren un proceso linfoproliferativo con CD30+ elementos» para los que se recomendaron pruebas diagnósticas adicionales. Por esta razón, la paciente buscó tratamiento en nuestra institución, donde el caso fue gestionado por un equipo multidisciplinario (MDT) que incluía a un cirujano plástico, un hematopatólogo, un hematólogo, un oncólogo, un radioterapeuta, un oncólogo quirúrgico y un radiólogo de mama. El espécimen histopatológico original de la toma de la cápsula se revisó por un hematopatólogo de nuestro centro de referencia, que identificó células CD30+ grandes y escasas atípicas con contornos irregulares que se consideraron compatibles con el diagnóstico de BIA-ALCL. Las células presentaron el siguiente fenotipo: CD30+, CD3-, CD7-, CD5-, CD4-, CD8-, Granzima B+/-, TIA1-, ALK1-, PAX5-, CD79a-, CD68-, CD15-/+. La paciente recibió una exploración por ultrasonido con aspiración por aguja fina y citopatología de la efusión recurrente que confirmó un proceso CD30+ linfoproliferativo atípico con captación de 18F-FDG (fluorodeoxiglucosa) (SUV máx. 1,8). No se pudieron localizar otras áreas de captación en todos los demás segmentos corporales explorados. La paciente también recibió una exploración por resonancia magnética de ambos senos con medio de contraste para completar la estadificación preoperativa, confirmando el seroma del lado izquierdo. Los portaobjetos del espécimen de la cirugía anterior se revisaron por el hematopatólogo que consideró los hallazgos suficientes para identificar BIA-ALCL con infiltración temprana de la cápsula periprostética (pT2 según el sistema de estadificación MD Anderson-TNM). Tres semanas después de la visita inicial, la paciente se sometió a cirugía radical con capsulotomía en bloque que contenía solo 150 cc de efusión serosa sin implante. El contenido líquido se envió para cultivo y citopatología, mientras que el espécimen sólido se envió para examen histopatológico. Además, la paciente se sometió a biopsia de ganglio linfático centinela de 2 ganglios axilares identificados preoperativamente a través de linfografía segmentaria. Los ganglios linfáticos presentaron una linfadenopatía silicona-asociada reactiva crónica sin signos de linfadenopatía metastásica. El informe histopatológico de la cápsula reveló agregados celulares infiltrantes en la cápsula periprostética, pero márgenes de resección claros y sin signos de infiltración más allá de la cápsula. Como tal, la paciente recibió un estadio IC (pT3pN0M0). El curso postoperatorio fue sin incidentes, y no se consideraron necesarios más tratamientos adyuvantes por el MDT. La paciente continuó su estricto protocolo de seguimiento, con PET/CT de 6, 12 y 18 meses posteriores a la cirugía que no mostró signos de recurrencia de enfermedad local o distante. Como está, la paciente continúa sus visitas de seguimiento y exploraciones, con supervivencia libre de enfermedad más allá de 18 meses.\n",
+        "gold_summary": "Describimos el caso de una mujer de 42 años con antecedentes de aumento de senos bilateral con fines cosméticos 21 años antes, que desarrolló seroma recurrente del lado izquierdo. Buscó ayuda de su primer cirujano, quien realizó 2 procedimientos de intercambio de implantes mamarios, colocando dispositivos texturados y, finalmente, una extracción bilateral de implantes mamarios en el transcurso de dos décadas. La paciente no recibió capsulectomías en los intercambios de implantes anteriores y recibió una muestra de la cápsula anterior en el último procedimiento, donde se diagnosticó BIA-ALCL en el lado izquierdo. Fue derivada a un centro de cáncer terciario donde el examen preoperatorio confirmó la presencia de enfermedad residual local. Después de la gestión del equipo multidisciplinario, se sometió a una revisión de capsulectomía en bloque del lado izquierdo sin necesidad de tratamientos adicionales. El curso postoperatorio fue sin incidentes y sin signos de recurrencias locales a los 18 meses de seguimiento.\n",
+        "synthetic_summary": {
+            "B1": "Había una mujer que se puso pechos nuevos hace mucho tiempo. Con el tiempo, su pecho izquierdo se llenó de líquido muchas veces. Fue al doctor varias veces y le cambiaron los pechos dos veces. Al final, le quitaron los pechos nuevos. \n\nEl doctor vio que había unas células raras en el pecho izquierdo. La llevaron a un hospital especial para ayudarla. Allí le hicieron una operación para sacar todo lo raro. \n\nDespués de la operación, la mujer estuvo bien. Los doctores la revisaron muchas veces y no encontraron nada malo. Ahora está sana y sigue yendo al doctor para cuidarse.",
+            "B2": "**Caso de una mujer con problemas en sus implantes mamarios**\n\nUna mujer de 42 años se hizo un aumento de senos cuando tenía 21 años. Con el tiempo, comenzó a tener un problema llamado seroma, que es cuando se acumula líquido alrededor del implante. Esto pasó especialmente en su seno izquierdo y volvió varias veces.\n\n**Tratamientos previos y diagnóstico**\n\nLa mujer visitó a su cirujano varias veces y se le cambiaron los implantes dos veces. En la última cirugía, le quitaron ambos implantes, pero no retiraron toda la cápsula, que es el tejido que se forma alrededor del implante. Al analizar una muestra de esta cápsula, los médicos encontraron células anormales que indicaban una enfermedad llamada linfoma anaplásico de células grandes asociado a implantes mamarios (BIA-ALCL). Este es un tipo raro de cáncer que puede aparecer en personas con implantes mamarios.\n\n**Atención en un centro especializado**\n\nDespués de este diagnóstico, la paciente fue enviada a un hospital especializado en cáncer. Allí, un equipo de diferentes especialistas revisó su caso y confirmó que todavía había enfermedad en la cápsula del seno izquierdo. La paciente se sometió a una cirugía para quitar toda la cápsula afectada y el líquido acumulado, sin necesidad de tratamientos como quimioterapia o radioterapia.\n\n**Resultado y seguimiento**\n\nLa operación fue exitosa y no hubo complicaciones. Durante 18 meses después de la cirugía, la mujer fue revisada varias veces y no se detectó que el cáncer regresara. Actualmente, sigue en control médico para asegurarse de que se mantenga sana.\n\nEn resumen, este caso muestra la importancia de detectar y tratar a tiempo un tipo raro de cáncer que puede aparecer en personas con implantes mamarios, y cómo un equipo médico especializado puede ayudar a manejarlo con éxito.",
+            "B3": "**Contexto**  \nPresentamos el caso de una mujer de 42 años que, tras haberse sometido a un aumento bilateral de senos con implantes mamarios hace 21 años, desarrolló un seroma (acumulación anormal de líquido) recurrente en el seno izquierdo. A lo largo de dos décadas, la paciente consultó repetidamente a su cirujano original, quien realizó dos procedimientos para reemplazar los implantes, utilizando dispositivos texturados (implantes con superficie rugosa), y finalmente llevó a cabo una extracción bilateral de los implantes. Durante estos procedimientos previos, no se realizaron capsulectomías completas (extirpación total de la cápsula fibrosa que se forma alrededor del implante). En el último procedimiento, se tomó una muestra de la cápsula del lado izquierdo que reveló la presencia de un linfoma anaplásico de células grandes asociado a implantes mamarios (BIA-ALCL, por sus siglas en inglés), un tipo raro de cáncer que afecta el tejido alrededor del implante.\n\n**Hallazgos Clave**  \nAl ser remitida a un centro terciario especializado en cáncer, se confirmó mediante estudios preoperatorios que la enfermedad persistía localmente en el seno izquierdo. El equipo multidisciplinario, compuesto por cirujanos plásticos, hematopatólogos, hematólogos, oncólogos, radiólogos y radioterapeutas, evaluó cuidadosamente el caso. Se realizó una capsulectomía en bloque (extirpación completa de la cápsula y el tejido circundante) en el lado afectado, sin encontrar necesidad de tratamientos adicionales como quimioterapia o radioterapia. El examen histopatológico mostró infiltración tumoral limitada a la cápsula periprostética, con márgenes quirúrgicos libres de enfermedad y sin afectación ganglionar.\n\n**Interpretación Clínica**  \nEste caso ilustra la importancia de la vigilancia y el diagnóstico temprano del BIA-ALCL, especialmente en pacientes con implantes texturados que presentan seromas persistentes o recurrentes. La ausencia de capsulectomías completas en procedimientos previos pudo haber contribuido a la persistencia de la enfermedad. La intervención quirúrgica radical, sin necesidad de tratamientos complementarios, fue suficiente para controlar la enfermedad en estadio temprano (IC según la clasificación MD Anderson-TNM).\n\n**Próximos Pasos**  \nLa paciente ha seguido un riguroso protocolo de seguimiento con estudios de imagen, incluyendo tomografías por emisión de positrones (PET/CT) a los 6, 12 y 18 meses postcirugía, sin evidencia de recurrencia local ni a distancia. Continúa bajo vigilancia médica estrecha para detectar cualquier signo de reaparición del linfoma, manteniendo hasta la fecha una supervivencia libre de enfermedad más allá de 18 meses. Este caso subraya la eficacia del manejo multidisciplinario y la cirugía completa en el tratamiento del BIA-ALCL en estadios iniciales."
+        }
+    },
+    {
+        "article": "Se trata de un paciente de 50 años que se presentó con una queja de dolor e hinchazón de la lengua de tres días de duración. Asociado a esto, tenía dolor al tragar, dificultad para abrir la boca, falta de aire y babeo. Asimismo, tenía fiebre alta y un tipo de dolor de cabeza global. Por lo demás, no tenía traumatismo en la lengua, ni procedimientos dentales u orales recientes, ni antecedentes de tabaquismo ni de enfermedad médica crónica como diabetes mellitus, enfermedad cardiaca e hipertensión. Históricamente, había tenido un dolor dental agudo en los últimos seis meses antes de su queja actual. Había masticado khat desde su niñez y tenía una mala higiene oral.\n\nEn el examen físico, se veía muy enfermo y sus signos vitales eran: presión arterial 115 por 70 mmHg, pulso 120 latidos por minuto, frecuencia respiratoria 20, temperatura 39 grados centígrados y saturación de oxígeno 92% de oxígeno. En el examen HEENT, había una hinchazón significativa de la lengua en el área anterolateral izquierdo, fluctuante a la palpación, y tenía un borde eritematoso. Hay múltiples caries en las áreas maxilares y mandibulares. No hubo hallazgos pertinentes en los sistemas restantes.\n\nTras obtener el consentimiento informado, el paciente fue trasladado al quirófano con el diagnóstico de absceso lingual. Posteriormente, se realizó la incisión y el drenaje bajo anestesia general, y se drenaron unos 30 ml de pus espeso. La bolsa se lavó con solución salina normal y peróxido de hidrógeno al 2 %. El paciente fue trasladado a la sala de cirugía con signos vitales estables y había tomado ceftriaxona 1 g por vía intravenosa dos veces al día y metronidazol 500 mg por vía intravenosa tres veces al día durante dos días. Fue dado de alta después de dos días de estancia en el hospital con mejoría y Augmentin 625 mg por vía oral tres veces al día durante cinco días.\n",
+        "gold_summary": "Se trata de un paciente de 50 años que se presentó con una queja de dolor e hinchazón de la lengua de tres días de duración. Asociado a esto, tenía dolor al tragar, dificultad para abrir la boca, falta de aire y babeo. Asimismo, tenía fiebre alta y un tipo de dolor de cabeza global. En el examen físico, había una hinchazón significativa de la lengua en el área anterolateral izquierda, fluctuante a la palpación, y tenía un borde eritematoso. Después de que se tomó el consentimiento informado, el paciente fue trasladado al quirófano con el diagnóstico de absceso de la lengua. Posteriormente, se hizo una incisión y drenaje bajo anestesia general, y se drenaron unos 30 ml de pus espeso. El bolsillo se lavó con solución salina normal y peróxido de hidrógeno al 2%. El paciente fue trasladado a la sala de cirugía con signos vitales estables y había estado tomando antibióticos. Fue dado de alta después de dos días de estancia en el hospital.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre tenía la lengua muy hinchada y le dolía mucho. También le costaba abrir la boca y respirar bien. Tenía fiebre y dolor de cabeza. Los doctores vieron que su lengua estaba muy inflamada y con una bolita de pus. Lo llevaron al hospital para limpiar la lengua y sacar el pus. Le dieron medicinas para que no se enfermara más. Después de dos días, se sintió mejor y pudo ir a su casa.",
+            "B2": "**Lo que le Pasó al Paciente**  \nUn hombre de 50 años llegó al hospital porque tenía dolor e hinchazón en la lengua desde hacía tres días. También le dolía al tragar, le costaba abrir la boca, tenía dificultad para respirar y babeaba mucho. Además, tenía fiebre alta y un dolor de cabeza que sentía en toda la cabeza.\n\n**Lo que Encontraron en el Examen**  \nCuando lo examinaron, vieron que la parte izquierda de su lengua estaba muy hinchada y blanda al tocarla. La piel alrededor estaba roja. También tenía muchos dientes con caries, que son daños en los dientes causados por bacterias.\n\n**Qué Hicieron para Ayudarlo**  \nLos médicos decidieron que tenía un absceso en la lengua. Un absceso es una acumulación de pus, que es un líquido lleno de bacterias y células muertas, causado por una infección. Para tratarlo, lo llevaron al quirófano y, bajo anestesia general (cuando el paciente está dormido y no siente dolor), hicieron una pequeña abertura para sacar el pus, aproximadamente 30 mililitros. Luego limpiaron la zona con agua salada y peróxido de hidrógeno, que ayuda a eliminar las bacterias.\n\n**Recuperación y Tratamiento**  \nDespués de la operación, el paciente recibió antibióticos por vía intravenosa para combatir la infección. Su estado mejoró y, tras dos días en el hospital, pudo irse a su casa con medicamentos para seguir tomando y asegurar que la infección desapareciera completamente.",
+            "B3": "**Contexto**\n\nUn hombre de 50 años acudió al hospital debido a dolor e inflamación en la lengua que había persistido durante tres días. Además, presentaba dificultad para tragar, problemas para abrir la boca, sensación de falta de aire y babeo excesivo. También tenía fiebre alta y un dolor de cabeza generalizado. No reportaba antecedentes recientes de traumatismos en la boca, procedimientos dentales, tabaquismo ni enfermedades crónicas como diabetes o hipertensión. Sin embargo, había experimentado dolor dental agudo en los seis meses previos y tenía hábitos de masticar khat desde la niñez, junto con una higiene oral deficiente.\n\n**Hallazgos Clave**\n\nDurante el examen físico, el paciente se mostró visiblemente enfermo. Sus signos vitales indicaron fiebre (39 °C), pulso acelerado (120 latidos por minuto), presión arterial normal (115/70 mmHg), frecuencia respiratoria de 20 respiraciones por minuto y saturación de oxígeno ligeramente disminuida (92%). En la exploración de cabeza y cuello, se observó una inflamación notable en la parte anterolateral izquierda de la lengua, que al tacto era fluctuante (lo que sugiere acumulación de líquido) y presentaba un borde enrojecido (eritematoso). Además, se detectaron múltiples caries en los dientes superiores e inferiores.\n\n**Interpretación Clínica**\n\nEl cuadro clínico y los hallazgos físicos fueron compatibles con un absceso lingual, que es una acumulación de pus en la lengua debido a una infección. Esta condición puede ser grave porque la inflamación y el pus pueden dificultar la respiración y la deglución, como ocurrió en este paciente.\n\n**Próximos Pasos y Tratamiento**\n\nCon el consentimiento informado del paciente, se decidió realizar una intervención quirúrgica para drenar el absceso. Bajo anestesia general, se hizo una incisión en la lengua y se extrajeron aproximadamente 30 mililitros de pus espeso. La cavidad se limpió cuidadosamente con solución salina y peróxido de hidrógeno al 2% para eliminar restos de infección. Posteriormente, el paciente recibió tratamiento antibiótico intravenoso con ceftriaxona y metronidazol durante dos días. Su estado se mantuvo estable y, tras mejorar, fue dado de alta con indicaciones para continuar con antibióticos orales (Augmentin) durante cinco días más.\n\nEste manejo oportuno permitió controlar la infección y evitar complicaciones mayores, destacando la importancia de un diagnóstico rápido y un tratamiento adecuado en casos de abscesos en la lengua."
+        }
+    },
+    {
+        "article": "Hombre de 73 años de edad de origen latinoamericano, con antecedente de madre con diagnóstico de demencia tipo Alzheimer con panel genético negativo; hermano con diagnóstico de ELA; hermana con diagnóstico de enfermedad de Parkinson. La sintomatología progresiva comenzó desde el año 2016 y se caracterizó por síntomas progresivos de hiposmia, hipoacusia, estreñimiento e insomnio, los cuales ameritaron valoración por otorrinolaringología y audiología, sin conclusión diagnóstica. En el año 2020 los familiares notaron que el paciente presentaba problemas en la memoria episódica, olvidos de objetos de la vida cotidiana, problemas de ganancias en su negocio (de comercio). Estos síntomas fueron progresivos hasta que el paciente empezó a tener limitación en las tareas diarias, como al manejar y al cambiar las velocidades, además de al salir de su casa. A finales de ese año el paciente comenzó a presentar debilidad muscular distal, manifestada al abrir botellas, cepillarse los dientes, lo cual progresó de forma insidiosa, no fluctuante, sin predominio de horario.\n\nEn enero de 2021 el paciente comenzó con alteraciones de la marcha, las cuales condicionaron caídas frecuentes hasta más de 6 veces a la semana, esto debido a inestabilidad postural. El paciente acudió a valoración en mayo. Se le hizo test de MoCA de 16 puntos con alteraciones en la fluidez del lenguaje y repetición de oraciones; en la abstracción, recuerdo diferido y problemas visuoespaciales y disejecutivos. El test de Luria dio positivo. El paciente presentó facie hipomímica, emitió con hipofonía, entrecortado y lento, y presentó reflejo nauseoso disminuido, rigidez generalizada de predominio izquierdo, hipotrofia generalizada, bradicinesia de predominio izquierdo, fuerza 4/5 generalizada, reflejos de estiramientos musculares 3/4, reflejos abdominocutáneos abolidos, signos de Hoffmann y Trömner presentes de forma bilateral, respuesta plantar extensora bilateral, fasciculaciones en extremidades inferiores evocadas al tacto, marcha con pasos cortos, congelamiento de la marcha al giro, pull test positivo (inestabilidad postural). Se manejó con levodopa carbidopa a una dosis gradual. Al seguimiento a los 3 meses el paciente había presentado nula mejoría en cuanto a los síntomas parkinsónicos, aumento de la debilidad muscular y persistieron los datos de motoneurona inferior y superior. Con estos hallazgos se realizó resonancia magnética (RM) del encéfalo. La velocidad de neuroconducción (VCN) presentó neuropatía axonal motora de miembros torácicos en relación con atrofia y neuroconducción sensitiva sin alteraciones. La electromiografía (EMG) presentó datos de denervación activa (aumento de actividad insercional, potenciales de fibrilación, fasciculación) y reinervación crónica (potenciales de acción de la unidad motora polifásicos, y bajo reclutamiento a la contracción máxima) en los 5 segmentos corporales, lo cual es compatible con enfermedad de motoneurona.\n\n\nLa EMG mostró un aumento de actividad insercional en músculos deltoides, bíceps, tríceps, extensor digital común bilateral y músculos linguales de forma bilateral. Se observaron abundantes potenciales de fibrilación y predominó la fasciculación en los músculos de los miembros torácicos. Durante la contracción, se observó una activación del potencial de acción de la unidad motora (PAUM) de forma polifásica y de gran amplitud. Y a máxima contracción se observó una disminución del reclutamiento en la mayoría de los músculos evaluados.\n\nEl paciente perdió seguimiento un año. Al vover a valoración se encontraba con postración en cama, afásico, aumento de los datos de parkinsonismo y síndrome de motoneurona. Se decidió realizar panel genético que resultó negativo para C9ORF72, así como para 143 genes más involucrados en enfermedades neuromusculares y neurodegenerativas, incluidos los genes VCP, MAT3, asociados a ELA, NOTCH3, asociado a demencia frontotemporal, sin alteraciones. Se reportó resultado de variante patogénica para el gen POLG: C.2209G>C, p.(Gly737Arg), relacionado con síndrome de depleción mitocondrial autosómico dominante y recesivo. Se realizó sesión de asesoramiento genético y el paciente fue informado. En mayo de 2022, el paciente presentaba disfagia y acudió en silla de ruedas, por lo que fue enviado a que se le practicara una gastrostomía.",
+        "gold_summary": "Presentamos un caso de origen latinoamericano que inicialmente se manifestó con síntomas sistémicos de más de 6 años de evolución, con posteriores alteraciones cognitivas. Después presentó alteraciones de la marcha y síntomas motores sugestivos de parkinsonismo con datos atípicos y datos de enfermedad de motoneurona. Se hicieron estudios de extensión que confirmaron hallazgos compatibles con afectación en motoneurona superior e inferior. Observamos mutación en gen POLG, relacionada con síndrome de depleción mitocondrial.",
+        "synthetic_summary": {
+            "B1": "Un señor empezó a sentirse mal hace mucho tiempo. Primero, tenía problemas para oler, escuchar y dormir. Luego, se le olvidaban cosas y le costaba hacer tareas fáciles.\n\nDespués, le costaba caminar y se caía mucho. También tenía los músculos débiles y se movía lento. Los doctores hicieron pruebas y vieron que sus nervios y músculos no funcionaban bien.\n\nEncontraron un cambio en un gen que puede causar problemas en el cuerpo. Los doctores le explicaron todo con calma. Ahora, lo cuidan para que esté lo más cómodo posible.",
+            "B2": "**Lo que pasó con el paciente:**  \nUn hombre latinoamericano de 73 años tuvo síntomas durante más de seis años. Primero, presentó problemas en su cuerpo como dificultad para oler, escuchar y dormir. Luego, comenzó a tener problemas con la memoria y a olvidar cosas de su vida diaria. Más adelante, tuvo problemas para caminar y debilidad en sus músculos, lo que afectó sus movimientos y le causó caídas frecuentes.\n\n**Qué encontraron los médicos:**  \nAl hacerle pruebas, vieron que tenía signos de parkinsonismo, que es un conjunto de síntomas parecidos a los del Parkinson, pero con algunas diferencias. También encontraron que sus nervios y músculos estaban dañados, mostrando que tenía problemas en las motoneuronas. Las motoneuronas son células nerviosas que controlan los músculos, y en su caso, tanto las motoneuronas superiores como las inferiores estaban afectadas.\n\n**Resultados genéticos importantes:**  \nSe le hizo un examen genético y encontraron una mutación en un gen llamado POLG. Este gen está relacionado con un problema llamado síndrome de depleción mitocondrial, que afecta la energía que producen las células. Esta mutación puede causar enfermedades que afectan los músculos y el sistema nervioso.\n\n**Qué significa todo esto:**  \nEl caso es complejo porque el paciente tiene síntomas que involucran tanto problemas de memoria como de movimiento y debilidad muscular. La combinación de parkinsonismo atípico y enfermedad de motoneurona, junto con la mutación genética, ayuda a entender mejor su enfermedad y a buscar tratamientos adecuados.",
+            "B3": "**Contexto**  \nSe trata de un hombre latinoamericano de 73 años con antecedentes familiares de enfermedades neurodegenerativas, incluyendo Alzheimer, esclerosis lateral amiotrófica (ELA) y Parkinson. Su cuadro clínico comenzó en 2016 con síntomas no específicos como disminución del olfato (hiposmia), pérdida auditiva leve (hipoacusia), estreñimiento e insomnio. En 2020, aparecieron problemas de memoria, dificultades en actividades cotidianas y debilidad muscular progresiva, especialmente en manos. En 2021, desarrolló alteraciones de la marcha con caídas frecuentes, rigidez y lentitud de movimientos, además de signos neurológicos que sugerían afectación tanto de la motoneurona superior como inferior.\n\n**Hallazgos Clave**  \n- Evaluación cognitiva mostró deterioro en funciones ejecutivas, memoria y habilidades visuoespaciales.  \n- Examen neurológico reveló rigidez, bradicinesia (lentitud de movimientos), reflejos anormales, fasciculaciones musculares (contracciones involuntarias) y alteraciones en la marcha con congelamiento.  \n- Estudios electromiográficos (EMG) y de velocidad de conducción nerviosa confirmaron daño en las motoneuronas superiores e inferiores, compatible con enfermedad de motoneurona.  \n- La resonancia magnética cerebral no mostró hallazgos específicos que expliquen el cuadro.  \n- Un panel genético amplio fue negativo para mutaciones comunes en enfermedades neurodegenerativas, pero identificó una variante patogénica en el gen POLG, asociado a síndromes de depleción mitocondrial, que afectan la función celular energética.  \n- En etapas avanzadas, el paciente presentó afasia (pérdida del lenguaje), disfagia (dificultad para tragar) y dependencia para movilizarse, requiriendo gastrostomía para alimentación.\n\n**Interpretación Clínica**  \nEste caso ilustra una enfermedad neurodegenerativa compleja con síntomas iniciales sistémicos y progresión hacia un síndrome mixto que combina características de parkinsonismo atípico y enfermedad de motoneurona. La presencia de la mutación en POLG sugiere un trastorno mitocondrial subyacente que podría estar contribuyendo a la degeneración neuronal. La afectación simultánea de motoneuronas superiores e inferiores y la falta de respuesta a levodopa apoyan un diagnóstico fuera del parkinsonismo típico. La evolución rápida hacia discapacidad severa y alteraciones del lenguaje y la deglución reflejan la gravedad del proceso.\n\n**Próximos Pasos**  \n- Continuar con manejo multidisciplinario que incluya neurología, rehabilitación, nutrición y apoyo psicológico.  \n- Monitorizar complicaciones respiratorias y nutricionales, dado el compromiso neuromuscular avanzado.  \n- Realizar asesoramiento genético familiar para evaluar riesgos y orientar a los parientes.  \n- Considerar terapias sintomáticas y soporte paliativo conforme avance la enfermedad, dado que no existen tratamientos curativos para esta condición.  \n\nEste caso destaca la importancia de una evaluación integral en pacientes con síntomas neurológicos progresivos y la utilidad de estudios genéticos para identificar causas poco frecuentes que pueden influir en el pronóstico y manejo."
+        }
+    },
+    {
+        "article": "Mujer de 33 años, previamente sana, presentó disnea progresiva, fiebre alta, sudores nocturnos y pérdida de peso en diciembre de 2017. Después de un mes de evolución, fue ingresada en un hospital general con insuficiencia respiratoria aguda y shock séptico con infiltrados alveolares difusos, ictericia, hemoptisis y petequias en las extremidades inferiores. Fue intubada y necesitó soporte hemodinámico. Se detectó un soplo sistólico mitral a la ausculta del precordio. Había leucocitosis acentuada con desviación a la izquierda, plaquetopenia, disfunción hepática y renal asociada a proteinuria subnefrótica y consumo de complemento. El resultado de los anticuerpos antinucleares fue de 1/80, a pesar de los niveles normales de anti-DNA de doble cadena, anti-SM y anti-PR3. Después de la administración de ceftriaxona, mejoró clínicamente. Fiebre amarilla, dengue, chikungunya, leptospirosis, VIH y hepatitis virales fueron descartados. Las hemoculturas fueron positivas para Haemophilus spp. en las seis muestras recolectadas. El ecocardiograma transtorácico (ETT) demostró una masa ecogénica amorfa con superficie irregular y algunos elementos móviles que envolvían ambos folletos de la válvula mitral, midiendo 20x17 mm en el folleto anterior y 19 mm en su mayor diámetro en los folletos posteriores, resultando en regurgitación grave por flail mitral y perforación. La resonancia magnética mostró pequeños abscesos esplénicos, tratados de manera conservadora. Un aneurisma micótico no complicado de la arteria cerebral media izquierda fue tratado por embolización percutánea. Treinta días después de la hospitalización, se sometió a un reemplazo de la válvula mitral con éxito por una prótesis valvular biológica de tamaño 29 mm y después de una extensa resección del tumor. Se evidenció regurgitación aórtica moderada debido a lesión de la fibrosa intervalvar mitroaórtica y retracción de la cúspide no coronaria, tratada de manera conservadora. El examen patológico confirmó la presencia de un mixoma valvular mitral infectado. La paciente completó 28 días de ceftriaxona y gentamicina, recibiendo el alta hospitalaria asintomática. En el seguimiento de un año, no hubo evidencia de recurrencia y se constató solamente regurgitación aórtica leve. Los mixomas infectados presentan mayor riesgo de eventos embólicos, aunque las manifestaciones clínicas son indistinguibles de tumores no infectados.2 El presente caso parece ser el sexto de mixoma valvular mitral infectado relatado en la literatura, llenando criterios definitivos para el diagnóstico, y el tercero causado por un microorganismo del grupo HACEK.3 - 8 De los 64 mixomas valvulares mitrales publicados de 2006 a 2012, los síntomas eran cardiovasculares en 36,7%; 9,5 a 21,6% de los mixomas de la válvula mitral fueron sometidos al cambio de válvula y el tiempo del diagnóstico hasta la cirugía varió de algunas horas a 42 días.2 , 9 La mortalidad operatoria y general fue relatada como siendo, respectivamente, 2,6 a 3% y 5,1 a 21%.2 , 10 En la presente serie, la mayoría de los pacientes presentó insuficiencia cardiaca sintomática, fueron sometidos al cambio de válvula mitral y todos presentaron buenos resultados en el seguimiento.\n",
+        "gold_summary": "Una mujer de 33 años de edad, con antecedentes de fiebre y disnea de unos pocos días de evolución, fue hospitalizada con un síndrome lupoide, con hemocultivos positivos para Haemophilus spp. El ecocardiograma reveló una masa gigante que involucraba ambas valvas mitrales, con una severa regurgitación mitral que requería un reemplazo valvular mitral biológico. La microscopía reveló un mixoma infectado y la paciente fue dada de alta asintomática tras finalizar la terapia con antibióticos. Ella tuvo un buen seguimiento.\n",
+        "synthetic_summary": {
+            "B1": "Había una mujer que se sentía muy mal. Tenía fiebre y le costaba mucho respirar. \n\nLos doctores la llevaron al hospital. Le encontraron una bolita grande en el corazón. Esa bolita hacía que su corazón no funcionara bien. \n\nLos doctores le pusieron una nueva parte en el corazón para ayudarla. También le dieron medicinas para que se mejorara. \n\nDespués de un tiempo, ella se sintió bien y pudo irse a su casa. Los doctores la cuidaron mucho y ella estuvo sana.",
+            "B2": "**Lo que le pasó a la paciente**  \nUna mujer de 33 años comenzó con dificultad para respirar, fiebre alta y otros síntomas graves. Fue hospitalizada porque tenía una infección en la sangre causada por una bacteria llamada Haemophilus. Además, su corazón tenía un problema: una masa grande creció en la válvula mitral, que es una parte importante para que la sangre fluya bien en el corazón.\n\n**Qué encontraron los médicos**  \nUn examen llamado ecocardiograma mostró que esta masa afectaba ambas partes de la válvula mitral y causaba que la sangre regresara hacia el corazón, lo que se llama regurgitación mitral grave. Por eso, fue necesario reemplazar esa válvula por una nueva hecha de material biológico. Cuando analizaron la masa con un microscopio, descubrieron que era un mixoma infectado, que es un tumor benigno pero que en este caso tenía infección.\n\n**Cómo terminó el caso**  \nDespués de la cirugía y de recibir antibióticos durante varias semanas, la paciente mejoró mucho y pudo salir del hospital sin síntomas. En el seguimiento durante un año, no hubo problemas ni regreso del tumor. Este caso es muy raro y muestra la importancia de un diagnóstico rápido y un tratamiento adecuado para este tipo de infecciones en el corazón.",
+            "B3": "**Contexto**\n\nUna mujer de 33 años, previamente sana, comenzó a experimentar dificultad para respirar progresiva, fiebre alta, sudores nocturnos y pérdida de peso durante un mes. Fue ingresada en un hospital con insuficiencia respiratoria aguda, shock séptico, sangrado pulmonar (hemoptisis), ictericia (coloración amarillenta de piel y mucosas) y petequias (pequeñas manchas rojas) en las piernas. Presentaba además un soplo cardíaco en la válvula mitral, leucocitosis (aumento de glóbulos blancos), plaquetopenia (disminución de plaquetas), disfunción hepática y renal, y alteraciones en pruebas inmunológicas.\n\n**Hallazgos Clave**\n\n- Se descartaron infecciones virales comunes en la región (fiebre amarilla, dengue, chikungunya, VIH, hepatitis).\n- Hemocultivos confirmaron infección por Haemophilus spp., un tipo de bacteria del grupo HACEK, conocida por afectar las válvulas cardíacas.\n- Ecocardiograma mostró una masa grande y irregular que afectaba ambas valvas de la válvula mitral, causando una regurgitación grave (flujo sanguíneo anormal hacia atrás) debido a daño estructural.\n- Resonancia magnética detectó pequeños abscesos en el bazo y un aneurisma micótico (una dilatación arterial causada por infección) en una arteria cerebral, tratado con embolización (bloqueo del vaso).\n- La paciente fue sometida a reemplazo exitoso de la válvula mitral por una prótesis biológica tras resección completa del tumor.\n- El examen patológico confirmó que la masa era un mixoma valvular mitral infectado, un tumor cardíaco benigno pero con infección bacteriana.\n- Se observó además regurgitación aórtica moderada por lesión en la estructura entre la válvula mitral y la aórtica, manejada sin cirugía.\n- Recibió tratamiento antibiótico con ceftriaxona y gentamicina durante 28 días.\n\n**Interpretación Clínica**\n\nEste caso representa una forma rara y grave de mixoma valvular mitral infectado, que es poco frecuente en la literatura médica y con alto riesgo de complicaciones embólicas (formación de coágulos que pueden viajar a otros órganos). La infección por Haemophilus spp. del grupo HACEK es especialmente relevante por su asociación con endocarditis (infección de las válvulas cardíacas). La presentación clínica puede ser similar a la de tumores no infectados, pero el riesgo de complicaciones es mayor.\n\nEl manejo combinado de cirugía para remover el tumor y reemplazar la válvula dañada, junto con terapia antibiótica prolongada, permitió una recuperación exitosa. La paciente mostró buena evolución clínica y no presentó recurrencia ni complicaciones significativas durante un seguimiento de un año.\n\n**Próximos Pasos**\n\n- Continuar con controles cardiológicos periódicos para monitorear la función valvular y detectar posibles complicaciones tardías.\n- Mantener vigilancia clínica para signos de infección o embolias.\n- Considerar la importancia de un diagnóstico precoz en casos similares para reducir la mortalidad y mejorar los resultados quirúrgicos.\n- Difundir el conocimiento sobre esta entidad rara para facilitar su reconocimiento y tratamiento oportuno en la práctica clínica."
+        }
+    },
+    {
+        "article": "Mujer de 71 años, que fue atendida en urgencias del Hospital de Mataró (Barcelona, España) el 9 de septiembre de 2020 con debilidad progresiva, por lo que se decidió su ingreso en neurología. Como antecedentes patológicos destacaban hipertensión arterial, temblor esencial, artrosis y trastorno de ansiedad leve, en tratamiento con gabapentina, sertralina y tramadol. La paciente había consultado a su médico de cabecera el 1 de septiembre de 2020 por dolor abdominal, junto con diarrea leve que duró 24 horas. Al día siguiente comenzó a sentirse débil y, a lo largo de los días siguientes, apareció disnea y disfagia, por lo que se sospechó laringitis y se le recetó prednisona. El 8 de septiembre de 2020 fue visitada nuevamente por su médico de cabecera por empeoramiento global de la debilidad; presentaba, además, disartria, disfagia y ptosis bilateral, por lo que fue derivada a urgencias del hospital.\n\nA su llegada no presentaba fiebre, la presión arterial y la frecuencia cardíaca eran normales, y la exploración física era normal, a excepción de taquipnea moderada. El examen neurológico mostró ptosis palpebral bilateral, parálisis facial bilateral, midriasis bilateral arreactiva a la luz y a la acomodación, oftalmoparesia bilateral tanto para la suprainfraversión como para la mirada horizontal bilateral, tetraparesia moderada en las extremidades (3/5), y disfonía y disfagia graves. Ella estaba consciente y el contenido del lenguaje era normal, al igual que los reflejos miotáticos, la sensibilidad y la coordinación. Las maniobras de fatigabilidad no fueron concluyentes y se realizó la prueba del hielo, que resultó positiva, mejorando –transitoriamente– la ptosis.\n\nLa reacción en cadena de la polimerasa (PCR) para el SARS-CoV-2 fue repetidamente negativa (en su ambulatorio y en el hospital). La gasometría arterial mostró hipoxemia: 75, con SO2 al 95%, y el resto de las exploraciones realizadas en urgencias resultaron normales (radiografía de tórax, análisis de sangre de rutina, electrocardiograma).\n\nSe inició tratamiento de soporte con oxígeno, sueroterapia, nutrición por sonda nasogástrica y medidas encaminadas a la prevención de complicaciones. El cuadro se estabilizó el tercer día del ingreso en planta, sin requerir soporte ventilatorio avanzado, y comenzó una mejoría lenta a partir del octavo día, iniciando tolerancia a la dieta adaptada de disfagia. Durante la primera semana presentaba hipotensión arterial, que fue corrigiéndose con la sueroterapia. A partir de la segunda semana, pudo iniciar rehabilitación física, con buena evolución, por lo que fue trasladada a un centro específico de rehabilitación al 19.º día, y entonces fue capaz de deambular con ayuda bilateral. En la visita de control en consultas externas de neurología seis semanas después, la paciente estaba completamente recuperada.",
+        "gold_summary": "Describimos el caso confirmado de botulismo alimentario en una paciente atendida en nuestro hospital en septiembre de 2020. La instauración en pocos días de una afectación bilateral de pares craneales, incluyendo disfagia, disnea y disartria, junto con midriasis y tetraparesia graves, precedida de diarrea, constituyó la presentación clínica en el primer caso; mientras que en su familiar cursó con síntomas inespecíficos y transitorios. Constatamos disautonomía consistente en hipotensión arterial. Teniendo en cuenta la situación pandémica en aquel momento, se descartó repetidamente la infección por SARS-CoV-2 antes de plantear alternativas diagnósticas. La neurotoxina B de C. botulinum fue detectada en las heces de la paciente, confirmando el diagnóstico de botulismo, que relacionamos con la ingesta de una conserva casera de alubias. Se completó el diagnóstico diferencial del cuadro descartando otras posibles etiologías.",
+        "synthetic_summary": {
+            "B1": "Una señora se enfermó después de comer unas alubias hechas en casa. Ella se puso muy débil y le costaba hablar, tragar y respirar. También tenía los ojos muy abiertos y los músculos muy flojos. Los doctores buscaron otras enfermedades, pero no encontró ninguna. Por eso, supieron que tenía una enfermedad llamada botulismo. Ella recibió ayuda en el hospital y poco a poco se fue mejorando hasta poder caminar con ayuda.",
+            "B2": "**Lo que pasó con la paciente**  \nUna mujer de 71 años llegó al hospital con debilidad que empeoraba rápidamente. Antes, había tenido diarrea leve y dolor de barriga. Luego, empezó a tener problemas para respirar, tragar y hablar. En el examen, los médicos vieron que tenía caída de los párpados, parálisis en la cara, pupilas que no reaccionaban a la luz, debilidad en brazos y piernas, y dificultad para mover los ojos. A pesar de estos síntomas, estaba consciente y sus reflejos y sensibilidad estaban normales.\n\n**Qué descubrieron los médicos**  \nBuscaron si tenía COVID-19, pero las pruebas fueron negativas varias veces. También hicieron otros estudios que no mostraron problemas en el pecho ni en el corazón. Detectaron que tenía presión baja en la sangre y falta de oxígeno en la sangre. Finalmente, encontraron una toxina llamada neurotoxina B producida por una bacteria llamada Clostridium botulinum en sus heces. Esta bacteria puede causar botulismo, una enfermedad grave que afecta los nervios y los músculos. Creen que la paciente se enfermó por comer una conserva casera de alubias contaminada.\n\n**Qué significa este diagnóstico**  \nEl botulismo es una enfermedad rara pero peligrosa que puede causar debilidad muscular grave y problemas para respirar. En este caso, la enfermedad afectó varios nervios importantes y causó síntomas como dificultad para tragar y hablar. Los médicos descartaron otras causas posibles antes de confirmar el botulismo. Gracias al tratamiento y cuidados, la paciente mejoró poco a poco y se recuperó completamente en unas semanas.\n\n**Resumen final**  \nEste caso muestra cómo el botulismo puede aparecer después de comer alimentos contaminados y causar síntomas graves. Es importante diagnosticarlo rápido para dar el tratamiento adecuado y evitar complicaciones. También se destacó que, durante la pandemia, fue necesario descartar COVID-19 antes de llegar a este diagnóstico.",
+            "B3": "**Contexto**  \nSe presenta el caso de una mujer de 71 años que ingresó en el Hospital de Mataró (Barcelona) en septiembre de 2020 con debilidad progresiva y síntomas neurológicos graves. Inicialmente, había experimentado diarrea leve y dolor abdominal, seguidos de dificultad para respirar (disnea), dificultad para tragar (disfagia), y alteraciones en el habla (disartria). La evolución clínica incluyó afectación bilateral de varios nervios craneales y debilidad en las cuatro extremidades.\n\n**Hallazgos Clave**  \nLa paciente mostró signos característicos de afectación neurológica severa: caída de los párpados (ptosis) en ambos ojos, parálisis facial bilateral, pupilas dilatadas que no respondían a la luz ni a la acomodación (midriasis arreactiva), y parálisis de los movimientos oculares en varias direcciones (oftalmoparesia). Además, presentaba debilidad moderada en brazos y piernas (tetraparesia), voz ronca (disfonía) y dificultad grave para tragar. A pesar de estos síntomas, estaba consciente y mantenía un lenguaje coherente, con reflejos y sensibilidad normales. La prueba del hielo, que consiste en aplicar frío sobre los párpados para evaluar la mejora temporal de la ptosis, fue positiva, lo que orientó hacia un trastorno neuromuscular.\n\nSe descartó repetidamente la infección por SARS-CoV-2 mediante pruebas PCR, dada la pandemia vigente en ese momento. Otros estudios complementarios, como radiografía de tórax, análisis de sangre y electrocardiograma, no mostraron alteraciones relevantes. La gasometría arterial reveló hipoxemia moderada, indicando un nivel bajo de oxígeno en sangre.\n\n**Interpretación Clínica**  \nEl cuadro clínico y la evolución sugirieron un botulismo alimentario, una enfermedad causada por la neurotoxina producida por la bacteria *Clostridium botulinum*, que afecta la función nerviosa y muscular. La confirmación diagnóstica se obtuvo al detectar la neurotoxina tipo B en las heces de la paciente. Se estableció que la fuente probable de la intoxicación fue la ingesta de una conserva casera de alubias. Además, la paciente presentó disautonomía, manifestada por hipotensión arterial, que requirió manejo con fluidos intravenosos.\n\nSe realizó un diagnóstico diferencial exhaustivo para descartar otras causas neurológicas que pudieran explicar los síntomas, asegurando así la precisión del diagnóstico.\n\n**Próximos Pasos y Evolución**  \nLa paciente recibió tratamiento de soporte, incluyendo oxígeno, nutrición por sonda nasogástrica y cuidados para prevenir complicaciones. Su condición se estabilizó en los primeros días y comenzó a mejorar lentamente a partir del octavo día, tolerando progresivamente la alimentación adaptada a su disfagia. Posteriormente, inició rehabilitación física, con buena respuesta, y fue trasladada a un centro especializado para continuar su recuperación. Seis semanas después, en la consulta de seguimiento neurológico, la paciente había recuperado completamente su función neuromuscular y capacidad para caminar con ayuda.\n\nEste caso destaca la importancia de considerar el botulismo alimentario en pacientes con debilidad neuromuscular progresiva y afectación de nervios craneales, especialmente cuando se descartan infecciones virales prevalentes como el SARS-CoV-2. Además, resalta la necesidad de un diagnóstico rápido y un manejo multidisciplinario para lograr una recuperación completa."
+        }
+    },
+    {
+        "article": "Un hombre de 52 años presentó pérdida de agudeza visual en su ojo derecho (OD) dos días después de una inyección intravenosa no complicada de ranibizumab con una aguja de 30 G. Su historial médico incluía PE, miopía alta y vitrectomía pars plana en el OD debido a desprendimiento de retina. Recibía tratamiento mensual con ranibizumab debido a neovascularización coroidea secundaria a estrías angioides, con 78 inyecciones previas en el OD. En el momento de la presentación, su BCVA era de 6/18 y la presión intraocular (IOP) era de 3 mmHg. El examen con lámpara de hendidura del segmento anterior no mostró nada de particular. El examen de fondo de ojo y los escaneos OCT revelaron pliegues corio-retinianos posteriores. En conjunto, la baja presión intraocular y los hallazgos del fondo de ojo llevaron al diagnóstico de hipotensión maculopatía. Se prescribió dexametasona tópica y atropina para mejorar la función del cuerpo ciliar. La IOP se normalizó en tres días con recuperación de la agudeza visual y resolución de los pliegues corio-retinianos. Cuatro meses después, se realizó una nueva inyección intravenosa anti-VEGF en el cuadrante inferolateral y el paciente informó disminución de la agudeza visual en el día siguiente a la inyección. La BCVA era contar los dedos y la IOP era de 2 mmHg. Los pliegues corio-retinianos en el polo posterior estaban presentes, incluso más prominentemente esta vez. El examen con lámpara de hendidura reveló una herida abierta en la esclerótica en el sitio de la inyección. La herida se suturó con monofilamento 10-0 y se prescribió dexametasona tópica y atropina. El paciente se recuperó bien y presentó una BCVA de 6/12 y una IOP de 12 mmHg.\n",
+        "gold_summary": "Un hombre de 52 años se quejó de pérdida de visión en el ojo derecho (OD) dos días después de un IVI anti-VEGF sin complicaciones para el tratamiento de la neovascularización coroidea secundaria a estrías angioides. Su historial médico incluía PE, miopía patológica y una vitrectomía pars plana (PPV) previa debido a un desprendimiento de retina. La agudeza visual mejor corregida (BCVA) en el OD disminuyó de 6/12 a 6/18 después del IVI. La presión intraocular (IOP) era de 3 mmHg y se observaron pliegues corio-retinianos en el polo posterior. Se prescribió dexametasona tópica y atropina, y se observó una recuperación completa después de tres días. Cuatro meses después, el paciente desarrolló un nuevo episodio de pérdida de visión después de otro IVI. Su BCVA era contar los dedos, la IOP era de 2 mmHg, y se observaron pliegues corio-retinianos más evidentes. Esta vez, una herida escleral abierta en el sitio de inyección era evidente y fue necesaria una sutura escleral. Una vez más, el paciente se recuperó bien.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre tuvo problemas para ver con su ojo derecho. Esto pasó después de que le pusieron una medicina en el ojo. Su ojo estaba un poco débil y la presión dentro del ojo era baja. El doctor le dio unas gotas para ayudar. Después de tres días, su vista mejoró.\n\nCuatro meses después, le pusieron otra vez la medicina. Otra vez, su vista se puso muy mala. Esta vez, el ojo tenía una pequeña herida. El doctor la cerró con puntitos. Después, el hombre volvió a ver mejor.",
+            "B2": "### Lo que le pasó al paciente\n\nUn hombre de 52 años perdió visión en su ojo derecho dos días después de recibir una inyección en la vena para tratar un problema en la parte trasera del ojo llamado neovascularización coroidea, que es cuando crecen vasos sanguíneos anormales. Él tenía antecedentes de miopía fuerte, una cirugía previa en el ojo por desprendimiento de retina y otros problemas oculares.\n\n### Qué encontraron los doctores\n\nDespués de la inyección, su visión empeoró y la presión dentro del ojo bajó mucho, a solo 3 mmHg (lo normal es más alta). Al examinar el ojo, vieron pliegues en la capa del ojo llamada coroides y retina, que son señales de que el ojo estaba muy débil por la baja presión. Le dieron medicamentos en gotas para ayudar a que el ojo se recuperara, y en tres días su visión y presión volvieron a la normalidad.\n\n### Qué pasó después\n\nCuatro meses más tarde, el hombre recibió otra inyección similar y volvió a perder visión al día siguiente. Esta vez, la presión en el ojo bajó aún más, y los pliegues en la retina eran más visibles. Además, los doctores encontraron una herida abierta en la pared del ojo donde pusieron la inyección. Para arreglarla, tuvieron que coser esa herida. Después del tratamiento, el paciente mejoró y recuperó buena visión y presión normal en el ojo.\n\n### Qué significa esto\n\nEste caso muestra que, aunque las inyecciones en el ojo suelen ser seguras, pueden causar problemas como baja presión ocular y daño temporal en la retina. Es importante revisar bien el ojo después de cada inyección para detectar heridas o complicaciones y tratarlas rápido para evitar pérdida permanente de visión.",
+            "B3": "**Contexto:**  \nUn hombre de 52 años con antecedentes de preeclampsia (PE), miopía alta y una cirugía previa llamada vitrectomía pars plana (PPV) en su ojo derecho debido a un desprendimiento de retina, recibía tratamiento mensual con inyecciones intravenosas (IVI) de ranibizumab, un medicamento anti-VEGF (factor de crecimiento endotelial vascular), para tratar una neovascularización coroidea secundaria a estrías angioides (formación anormal de vasos sanguíneos en la capa vascular del ojo).\n\n**Hallazgos Clave:**  \nDos días después de una inyección intravenosa que inicialmente parecía no presentar complicaciones, el paciente notó una disminución de la agudeza visual en su ojo derecho. La agudeza visual mejor corregida (BCVA) bajó de 6/12 a 6/18, y la presión intraocular (IOP) estaba muy baja, en 3 mmHg (el rango normal es aproximadamente 10-21 mmHg). El examen con lámpara de hendidura no mostró alteraciones en la parte frontal del ojo, pero el examen del fondo de ojo y las imágenes por tomografía de coherencia óptica (OCT) revelaron pliegues en las capas coroideas y retinianas en la parte posterior del ojo. Estos hallazgos, junto con la baja presión intraocular, llevaron al diagnóstico de hipotensión maculopatía, una condición en la que la baja presión dentro del ojo causa cambios estructurales que afectan la visión.\n\nSe inició tratamiento con dexametasona tópica (un corticosteroide para reducir la inflamación) y atropina (un medicamento que ayuda a relajar el cuerpo ciliar, facilitando la producción de humor acuoso y aumentando la presión intraocular). En tres días, la presión intraocular volvió a la normalidad y la visión mejoró, con desaparición de los pliegues corio-retinianos.\n\nCuatro meses después, tras una nueva inyección intravenosa anti-VEGF aplicada en la zona inferolateral del ojo, el paciente presentó nuevamente una disminución significativa de la visión al día siguiente, con una BCVA reducida a “contar los dedos” (una medida de visión muy pobre) y una presión intraocular aún más baja, de 2 mmHg. Esta vez, los pliegues corio-retinianos eran más evidentes. El examen con lámpara de hendidura detectó una herida abierta en la esclerótica (la capa externa blanca del ojo) en el sitio de la inyección, lo que indicaba una filtración o fuga de líquido ocular. Esta herida fue reparada mediante sutura con un hilo muy fino (monofilamento 10-0). Se repitió el tratamiento con dexametasona tópica y atropina, y el paciente se recuperó satisfactoriamente, alcanzando una BCVA de 6/12 y una presión intraocular de 12 mmHg.\n\n**Interpretación Clínica:**  \nEste caso muestra que, aunque las inyecciones intravenosas de anti-VEGF son generalmente seguras, pueden presentarse complicaciones poco comunes como la hipotensión maculopatía causada por una baja presión intraocular. La presencia de pliegues corio-retinianos y la disminución de la visión son signos importantes que deben alertar al médico. Además, la aparición de una herida escleral abierta en el sitio de la inyección puede causar una fuga de líquido y empeorar la hipotensión ocular, requiriendo reparación quirúrgica.\n\n**Próximos Pasos:**  \nEs fundamental monitorizar cuidadosamente la presión intraocular y la integridad de la esclera después de las inyecciones anti-VEGF, especialmente en pacientes con antecedentes de cirugía ocular previa o miopía alta, que pueden tener mayor riesgo de complicaciones. El tratamiento temprano con corticosteroides tópicos y atropina puede ayudar a restaurar la presión intraocular y la función visual. En casos de filtración escleral, la reparación quirúrgica es necesaria para evitar daños permanentes. Además, se recomienda evaluar la técnica de inyección para minimizar el riesgo de heridas escleral abiertas en futuras aplicaciones."
+        }
+    },
+    {
+        "article": "Una mujer de 82 años acudió al servicio de urgencias por dolor abdominal, diarrea, confusión y deterioro de su estado general de varios días de evolución. Entre sus antecedentes médicos destacaban hipertensión arterial tratada e hipotiroidismo en tratamiento sustitutivo. No se recogieron antecedentes quirúrgicos ni hábitos tóxicos de interés. A la exploración física, la frecuencia cardíaca era de 84 lpm, tensión arterial de 105/82 mmHg, temperatura de 38 °C y saturación de oxígeno de 95% en aire ambiente. Las mucosas estaban secas y el abdomen era difusamente doloroso a la palpación sin masas palpables ni reacción peritoneal. La analítica realizada mostró una hemoglobina de 13.1 g/dL, proteína C reactiva a 122.9 mg/L sin leucocitosis (8.9 × 10^9/L), hiponatremia (130 mmol/L), hipopotasemia (2.9 mmol/L), pruebas de función renal, hepáticas, lipasa y enzimas cardiacas normales. El frotis para SARSCoV-2 fue negativo. La orina era maloliente con presencia de nitritos positivos, hematíes (+++) y leucocitos (+) por lo que se envió la muestra para cultivo microbiológico. Ante estos hallazgos se inició antibioticoterapia probabilista con ceftriaxona ante la sospecha de una posible infección urinaria y se decidió realizar una tomografía tóraco-abdomino-pélvica para descartar la presencia de un foco infeccioso profundo. Este examen reveló la presencia de signos de broncopatía crónica y una neumatosis vesical parietal a nivel abdominal compatible con una cistitis enfisematosa. El cultivo de orina reveló la presencia de Escherichia coli (> 100 000 UFC/m) sensible a la antibioticoterapia prescrita empíricamente y los hemocultivos fueron positivos al mismo germen. Se decidió el ingreso de la paciente en servicio de medicina interna y se continuó el tratamiento antibiótico durante 7 días con una evolución favorable desde el punto de vista clínico y analítico, permitiendo el alta hospitalaria.",
+        "gold_summary": "Una mujer de 82 años con antecedentes de hipertensión arterial e hipotiroidismo acudió al servicio de urgencias por dolor abdominal, diarrea, confusión y deterioro de su estado general de varios días de evolución. A su admisión, la paciente se encontraba febril y la analítica mostró una elevación de la proteína C reactiva sin leucocitosis (8.9 × 10^9/L). En ese contexto se realizó exudado nasofaríngeo para SARS-CoV-2 que fue negativo. Con estos resultados, la sospecha inicial era la de un cuadro infeccioso de origen digestivo. La muestra de orina era maloliente con presencia de leucocitos y nitritos enviándose a cultivo microbiológico. Se inició tratamiento antibiótico empírico con una cefalosporina de tercera generación ante la sospecha de une posible infección urinaria. Se decidió la realización de una tomografía tóraco-abdomino-pélvica con el objetivo de evaluar la presencia de otros focos infecciosos en una paciente de edad avanzada. Este estudio mostró una cistitis enfisematosa, una enfermedad poco frecuente en una paciente sin ninguno de los factores de riesgo clásicos para esta entidad. Los cultivos de orina y sangre fueron positivos para Escherichia coli sensible al antibiótico empírico por lo que se continuó para completar 7 días de tratamiento. La evolución clínica fue favorable.",
+        "synthetic_summary": {
+            "B1": "Una señora de 82 años se sentía muy mal. Tenía dolor en la barriga y estaba confundida. \n\nLos doctores le hicieron pruebas y vieron que tenía una infección en la orina. Le dieron medicina para ayudarla. \n\nTambién hicieron una foto especial de su cuerpo. Vieron que su vejiga estaba un poco dañada por la infección. \n\nLa medicina funcionó y la señora mejoró mucho. Después de una semana, pudo irse a su casa feliz.",
+            "B2": "**Lo que Encontraron**  \nUna mujer de 82 años llegó al hospital porque tenía dolor en el abdomen, diarrea, estaba confundida y se sentía muy mal desde hacía varios días. Tenía fiebre y algunos análisis de sangre mostraron que tenía inflamación, pero no un aumento en los glóbulos blancos, que son células que ayudan a combatir infecciones. También le hicieron una prueba para detectar COVID-19, que salió negativa.\n\n**Qué Significa la Orina y el Tratamiento**  \nLa orina de la paciente olía mal y tenía señales de infección, como leucocitos (células blancas) y nitritos. Por eso, enviaron una muestra para ver qué bacteria causaba la infección. Mientras esperaban, comenzaron a darle un antibiótico llamado ceftriaxona, que es fuerte y puede combatir muchas bacterias.\n\n**Descubrimiento Importante con la Tomografía**  \nPara asegurarse de que no hubiera una infección más grave en el cuerpo, le hicieron una tomografía, que es una imagen especial del cuerpo. Esta prueba mostró que tenía una cistitis enfisematosa, que es una infección rara en la vejiga donde se forman burbujas de gas en la pared de este órgano. Esto es inusual porque la paciente no tenía los factores de riesgo típicos para esta enfermedad.\n\n**Resultados del Cultivo y Evolución**  \nLos cultivos de la orina y la sangre mostraron que la bacteria causante era Escherichia coli, que respondía bien al antibiótico que ya le estaban dando. Por eso, continuaron con el tratamiento durante 7 días. La paciente mejoró mucho y pudo salir del hospital.  \n\nEn resumen, esta mujer tuvo una infección urinaria grave y poco común que se detectó a tiempo y se trató con éxito gracias a los exámenes y al antibiótico adecuado.",
+            "B3": "**Contexto**  \nUna mujer de 82 años con antecedentes médicos de hipertensión arterial e hipotiroidismo acudió al servicio de urgencias debido a varios días de dolor abdominal, diarrea, confusión y un deterioro general de su estado de salud. Al examen físico, presentaba fiebre y signos de deshidratación, con un abdomen doloroso a la palpación pero sin signos de irritación peritoneal.  \n\n**Hallazgos Clave**  \nLos análisis de sangre revelaron una elevación significativa de la proteína C reactiva (un marcador de inflamación) sin aumento en el número de glóbulos blancos (leucocitosis), lo que sugiere una respuesta inflamatoria sin infección bacteriana evidente en sangre. La prueba para detectar infección por SARS-CoV-2 fue negativa. La orina presentaba mal olor, nitritos positivos y presencia de leucocitos y glóbulos rojos, indicativos de infección urinaria.  \n\nSe inició tratamiento antibiótico empírico con ceftriaxona, una cefalosporina de tercera generación, ante la sospecha de infección urinaria. Para descartar la existencia de infecciones profundas o complicaciones, se realizó una tomografía computarizada (TC) del tórax, abdomen y pelvis. Este estudio identificó una neumatosis vesical parietal, es decir, presencia de gas en la pared de la vejiga, compatible con cistitis enfisematosa, una infección urinaria grave y poco frecuente caracterizada por la acumulación de gas en la vejiga.  \n\nLos cultivos microbiológicos confirmaron la presencia de Escherichia coli, una bacteria comúnmente responsable de infecciones urinarias, tanto en la orina como en la sangre, y que resultó sensible al antibiótico administrado.  \n\n**Interpretación Clínica**  \nLa cistitis enfisematosa es una infección poco común que suele presentarse en pacientes con factores de riesgo como diabetes o inmunosupresión, pero en este caso la paciente no presentaba estos antecedentes clásicos, lo que hace el diagnóstico más inusual. La detección temprana mediante imagen y el inicio rápido de tratamiento antibiótico adecuado fueron fundamentales para la evolución favorable del cuadro.  \n\n**Próximos Pasos**  \nLa paciente fue ingresada en el servicio de medicina interna para continuar el tratamiento antibiótico durante siete días. Durante su hospitalización, mostró mejoría clínica y analítica, lo que permitió su alta hospitalaria sin complicaciones. Se recomienda seguimiento médico para controlar posibles recurrencias o complicaciones y mantener el control de sus condiciones crónicas."
+        }
+    },
+    {
+        "article": "Varón nacido a las 38 semanas de gestación y sin controles obstétricos prenatales, producto de un parto eutócico sin complicaciones con un peso de 2.678 g y Apgar 7 y 8 al minuto y a los cinco minutos de vida, respectivamente; derivado por sospecha de enterocolitis necrotizante a los siete días de vida. Al nacimiento, en su hospital de origen, se descartaron malformaciones congénitas externas y se colocó una sonda orogástrica para verificar la permeabilidad esofágica, obteniendo 200 mL de líquido amniótico. Posteriormente inició alimentación vía oral pero debido a succión débil y vómitos biliosos fue ingresado en la unidad de cuidados intensivos neonatales. A las 4 horas de vida se realizó radiografía abdominal observando una imagen de doble burbuja atípica, por lo cual realizaron un control radiológico 48 horas después identificando gas intestinal aparentemente distal, y presentó meconiorrexis a las 50 horas de vida. Dos días después reinició la alimentación oral, tras lo cual presentó nuevamente vómitos de aspecto biliar y distensión abdominal que mejoró con el ayuno y sonda orogástrica; por lo cual se sospechó enterocolitis necrotizante indicándose dieta absoluta, nutrición parenteral total y antibioterapia con ampicilina y amikacina. A los siete días de vida y debido a la persistencia de los síntomas pese al tratamiento instaurado, fue derivado a nuestro centro. A su llegada presentaba distensión abdominal, sin ruidos intestinales ni signos de irritación peritoneal, por lo que se realizó tránsito intestinal sin progresión distal y colon por enema con hallazgo de microcolon, todo ello sugestivo de atresia intestinal yeyunoileal. Tras la realización de los estudios de imagen y con la sospecha de atresia intestinal se realizó una laparotomía exploradora mediante abordaje supraumbilical transverso, observando adherencias hepatoileales, una hernia interna a través de un defecto mesentérico con incarceración de un asa yeyunal y atresia yeyunoileal tipo IV. Se identificaron dos sitios de atresia a 56 cm del ángulo de Treitz y a 36 cm de la válvula ileocecal, con un segmento interatrésico de 10 cm con meconio intraluminal y cambios de coloración con aspecto violáceo pero sin perforación; la diferencia de diámetros intestinales proximal a distal tenía una relación 3:1. Se decidió disecar el mesenterio y resecar el asa ciega (10 cm) para realizar una anastomosis término-oblicua yeyunoileal, corroborando la permeabilidad distal con sonda intraluminal y administración de solución fisiológica hasta que presentó evacuación rectal. El reporte de histopatología confirmó una atresia yeyunoileal tipo IV con enteritis crónica leve. El paciente evolucionó favorablemente y al 5º día postoperatorio inició alimentación oral con adecuada tolerancia progresiva y descenso paulatino de la nutrición parenteral total con retirada al 8º día postoperatorio. Al 6° día de la intervención presentó deposiciones espontáneas y a los 20 días de vida fue dado de alta sin complicaciones. Doce meses después el paciente continúa asintomático con adecuada ganancia ponderal y tolerancia a la alimentación complementaria con deposiciones diarias de características normales.",
+        "gold_summary": "Recién nacido de sexo masculino, nacido a término, derivado por vómitos, evacuaciones escasas y distensión abdominal. A los 8 días de vida y tras excluir diversas causas de distensión abdominal se sometió a laparotomía exploradora, identificando una hernia transmesentérica y dos sitios de atresia intestinal. Se realizó resección del segmento atrésico y anastomosis primaria, con buena evolución.",
+        "synthetic_summary": {
+            "B1": "Un bebé nació sin problemas. Tenía dolor en la barriga y no podía hacer popó bien. Los doctores buscaron qué pasaba y lo operaron. Encontraron dos partes del intestino que estaban tapadas. Quitaron las partes malas y unieron el intestino bueno. El bebé mejoró mucho después de la operación.",
+            "B2": "**Lo que pasó con el bebé:**  \nUn bebé varón nació a término y, durante su primera semana de vida, tuvo problemas como vómitos, pocas evacuaciones y el abdomen hinchado. Estos síntomas indicaban que algo no estaba funcionando bien en su intestino.\n\n**Qué encontraron los médicos:**  \nDespués de hacer varios estudios para entender la causa de la hinchazón abdominal, los doctores decidieron hacer una cirugía llamada laparotomía exploradora. En esta operación, descubrieron que el bebé tenía una hernia transmesentérica, que es cuando una parte del intestino queda atrapada en un defecto del tejido que lo sostiene. Además, encontraron dos lugares donde el intestino estaba bloqueado, lo que se llama atresia intestinal.\n\n**Qué hicieron para ayudar:**  \nLos médicos quitaron la parte del intestino que estaba bloqueada (resección del segmento atrésico) y unieron las partes sanas del intestino (anastomosis primaria) para que el alimento pudiera pasar normalmente.\n\n**Cómo le fue al bebé:**  \nDespués de la cirugía, el bebé mejoró bien, comenzó a alimentarse por vía oral y pudo irse a casa sin complicaciones. Un año después, sigue sano, come bien y tiene evacuaciones normales.",
+            "B3": "Resumen detallado para público general universitario\n\n**Contexto:**  \nSe trata de un recién nacido varón, nacido a término (38 semanas de gestación) mediante un parto normal sin complicaciones, con un peso al nacer de 2.678 gramos. No contó con controles prenatales durante el embarazo. En las primeras horas de vida presentó dificultad para alimentarse debido a una succión débil y vómitos con contenido biliar (color verde), lo que motivó su ingreso a la unidad de cuidados intensivos neonatales. Las primeras radiografías abdominales mostraron una imagen sugestiva de obstrucción intestinal, pero con presencia de gas en intestino distal. A los pocos días presentó distensión abdominal y vómitos persistentes, lo que llevó a sospechar una enterocolitis necrotizante (una inflamación grave del intestino en recién nacidos), por lo que se inició tratamiento con ayuno, nutrición intravenosa y antibióticos.\n\n**Hallazgos clave:**  \nA pesar del tratamiento, los síntomas no mejoraron, por lo que fue trasladado a un centro especializado. Allí se realizaron estudios radiológicos que evidenciaron un colon muy pequeño (microcolon) y ausencia de progresión del tránsito intestinal, lo que sugirió la presencia de una atresia intestinal (una obstrucción causada por la ausencia o cierre de una parte del intestino). Durante la cirugía exploratoria se encontró una hernia interna a través de un defecto en el mesenterio (tejido que sostiene los intestinos) con atrapamiento de un segmento del intestino delgado (asa yeyunal), además de dos áreas de atresia en el intestino delgado (tipo IV, que implica múltiples segmentos afectados). Se observó un segmento intermedio con meconio (primera materia fecal) y cambios de coloración, pero sin perforación. La relación entre el diámetro del intestino proximal y distal era de 3 a 1, indicando una diferencia significativa en tamaño.\n\n**Interpretación clínica:**  \nSe realizó la resección del segmento intestinal afectado y una anastomosis término-oblicua yeyunoileal (unión quirúrgica entre dos partes del intestino delgado), asegurando la permeabilidad del intestino distal. El análisis histopatológico confirmó la atresia múltiple con inflamación crónica leve del intestino. El paciente mostró una evolución favorable tras la cirugía, iniciando alimentación oral progresivamente desde el quinto día postoperatorio y retirando la nutrición parenteral al octavo día. Presentó deposiciones normales y fue dado de alta a los 20 días de vida sin complicaciones.\n\n**Próximos pasos y seguimiento:**  \nA los doce meses de edad, el niño continúa asintomático, con un adecuado aumento de peso y tolerancia normal a la alimentación complementaria, manteniendo deposiciones diarias de características normales. Este caso resalta la importancia de un diagnóstico oportuno y tratamiento quirúrgico adecuado en atresias intestinales múltiples para lograr una recuperación exitosa en recién nacidos."
+        }
+    },
+    {
+        "article": "Se remitió a un hombre de 86 años para que se le implantara una válvula aórtica transfemoral.\n\nLa historia significativa incluyó el hecho de fumar 40 cajetillas al año (hasta fines de la década de 1980) y la fibrilación auricular paroxística que requería anticoagulación con Coumadin desde 1999, seguida poco después por la implantación de un marcapasos ventricular debido a bradicardia. Fue admitido por síncope en mayo de 2011 y se le diagnosticó una estenosis aórtica calcificada severa. Era eupneico y no mostraba signos de insuficiencia cardiaca o retención de líquidos. La ecocardiografía transtorácica reveló una estenosis aórtica severa (gradiente medio: 58 mmHg, área de la válvula aórtica: 0,4 cm2) con hipertrofia ventricular izquierda, fracción de eyección ventricular izquierda deteriorada (29%), acinesia inferior apical y obstrucción septal subvalvular (septum: 18 mm) con dilatación biauricular e hipertensión pulmonar con dilatación de la vena cava.\n\nLa angiografía coronaria mostró una estenosis del 75% de la arteria descendente anterior izquierda. El examen de eco-Doppler encontró vasos normales en el cuello. Se agregó aspirina 80 mg diariamente a su tratamiento; el paciente fue programado para un reemplazo de la válvula aórtica, pero no llegó hasta agosto, cuando fue readmitido en urgencias por disnea aguda y confusión. Había ganado 6 kg de peso, con edemas en las piernas y signos clínicos de derrame pleural. En ese momento, su SpO2 era del 92% y la proteína B-natriurética estaba elevada a 2336 pg·mL−1 (normal < 100 pg·mL−1).\n\nTras la terapia diurética y la eliminación de 850 ml de derrame pleural, se realizó una valvuloplastia de balón percutáneo aórtico de emergencia (Cristal Balloon, 23 mm) e inmediatamente después se le implantó un stent de metal desnudo (Biotronik-Pro-Kinetic 2.74 × 10.0) en la arteria descendente anterior izquierda. El gradiente medio transvalvular disminuyó de 59 a 38 mmHg. Se observaron algunas torsades de pointe el día 6 después de la intervención, que desaparecieron cuando la frecuencia más baja del marcapasos se aceleró a 80 latidos/min. Su estado mejoró drásticamente y se le dio el alta con furosemida, aldactazina y clopidogrel. Tras una revisión cuidadosa del expediente del paciente por parte del equipo cardiaco, se consideró que el riesgo de una cirugía valvular era demasiado alto (Euroscore logístico: 51%), y se propuso al paciente un implante de válvula aórtica transfemoral.\n\nLas notas de las enfermeras mencionan la hiperventilación nocturna y las crisis de ansiedad. El paciente era semiautónomo y vivía con su hija.\n\nLa implantación de la válvula aórtica transfemoral se programó para octubre de 2011. En el ingreso, 2 días antes del procedimiento, el paciente se describió como «ansioso e hiperventilante»; su peso era de 67 kg para una altura de 168 cm; el volumen espiratorio forzado en 1 s (FEV1) era de 1,1 L (50% del valor previsto) y la capacidad vital forzada de 1,7 L (55%); la presión arterial sistémica era de 120/60 mmHg; la concentración de hemoglobina era de 167 g·L−1; la creatinina era de 12,7 g·L−1; la tasa de filtración glomerular se calculó en 54 ml·min−1·m−2; el potasio era de 3,7 mEq·L−1; el sodio era de 141 mEq·L−1; el bicarbonato era de 22 mEq·L−1; y la proteína B natriurética era de 2.073 pg·mL−1. La ecografía describió un área de superficie de la válvula aórtica de 0,5 cm2 con un gradiente aórtico medio de 55 mmHg y acinesia inferoapical en el ventrículo izquierdo. La fracción de eyección se midió en 27% por el método Simpson biplano con regurgitación mitral moderada con dilatación biauricular y se estimó la presión pulmonar sistólica en >69 mmHg. La radiografía de tórax no mostró derrame pleural significativo. El paciente era totalmente dependiente del marcapasos.\n\nDos horas antes de la intervención, el paciente recibió 1 g de acetaminofeno por vía oral. Al llegar al quirófano, el paciente, plenamente consciente, presentaba respiración de Cheyne-Stokes periódica; cada ciclo duraba unos 85 s, con apneas de entre 15 y 20 s y grandes oscilaciones de la SpO2 entre el 88 % y el 99 %. Se le colocó dos catéteres intravenosos periféricos y uno arterial. El trazado arterial también mostraba oscilaciones de 85 s y una presión sistólica de 130 a 150 mmHg. Se le aplicó una máscara facial de oxígeno al 40 % con ventilación no invasiva; la SpO2 alcanzó un rango más estable (92 %-99 %). Diez minutos después, los análisis de gases en sangre mostraron un pH de 7,39, Pao2 de 108 mmHg, Paco2 de 40 mmHg, SaO2 del 97 %, y oscilaciones de lactato de 1,2 mEq·L−1. Se instaló una línea de muestreo capnógrafo dentro de la máscara facial para monitorizar la frecuencia respiratoria (Carescape Monitor B650, GE Healthcare, Helsinki, Finlandia). La monitorización también incluía un ECG de 12 derivaciones, oximetría de pulso, y oximetría cerebral regional (rSO2) mediante espectroscopia infrarroja cercana en el frente (INVOS, Somanetics). La capnografía reveló que las oscilaciones de la presión arterial eran sincrónicas con el ritmo de la respiración y que la presión disminuía durante los períodos apneicos e hipopneicos y aumentaba durante la hiperventilación; la rSO2 seguía el mismo patrón, a pesar de que la SpO2 del dedo permanecía a un nivel constante de 99 %. Se inició una infusión de propofol a una concentración objetivo de 0,2 µg·mL−1; se administraron 2,5 µg de sufentanilo antes de que los operadores infiltraran cada ingle con 200 mg de mepivacaína; el paciente se quedó dormido pero se mantuvo despierto al menor contacto con su cara o cuando su nombre se susurraba al oído; se administraron otros 2,5 µg de sufentanilo antes de la dilatación femoral de la arteria, un procedimiento requerido antes del reemplazo de la válvula. Los ciclos de ventilación se desaceleraron a un máximo de 120 s con 24 s de apneas centrales. Cuando la angiografía y los catéteres operativos estaban en su lugar en la aorta ascendente y se introdujo un marcapasos temporal en el ventrículo derecho, se indujo un ritmo rápido de 200 latidos/min para permitir una nueva dilatación de la válvula calcificada. Este procedimiento duró <25 s, durante el cual el paciente permaneció consciente y continuó respirando de la forma habitual, el ritmo se indujo justo después del final de un período apneico. Se preparó una válvula de 26 mm (SAPIEN, Edwards Lifesciences) y se introdujo en el orificio aórtico. Se dio una señal a los operadores una vez que la respiración se reanudó al final de un período apneico; se inició un ritmo ventricular rápido que llevó a la asistolia a una presión arterial media de 45 mmHg, y la válvula se expandió con balón y la angiografía confirmó la ausencia de fuga paravalvular. El balón se desinfló justo antes de que se detuviera el ritmo rápido, y el corazón volvió a latir a 80 latidos/min bajo la estimulación del marcapasos implantado. La secuencia completa se filmó; duró 31 s, durante los cuales el paciente siguió respirando regularmente (8 veces durante la detención circulatoria, es decir, una tasa de 16 veces por minuto) y no se despertó. Las expulsiones de sangre se reanudaron inmediatamente después de la deflación del balón, con una presión sistólica de 80 mmHg. Después de unas respiraciones profundas, la respiración se hizo regular; no se produjeron nuevos períodos apneicos ni oscilaciones de la presión arterial o rSO2. La hipertensión sistémica se desarrolló rápidamente, culminando después de 1 min a 190 mmHg y se controló con 40 mg de urapidil intravenoso durante los siguientes 15 min. La ecografía transtorácica midió el área valvular a 1,6 cm2 y el gradiente transvalvular máximo a 15 mmHg. La estimación de la presión arterial pulmonar mediante ecografía transtorácica mostró un gradiente sistólico de la presión ventricular derecha-aurícula derecha de 69 mmHg 1 día antes del procedimiento y 45 mmHg 2 días después. Un mes después, era de 28 mmHg. La evolución posterior no tuvo incidentes, y el paciente fue dado de alta 72 h después sin haber vuelto a la respiración periódica.\n\nMH - Edad 80 años y más\nMH - Cirugía de la válvula aórtica\nMH - *Estenosis/cirugía de la válvula aórtica\nMH - *Respiración de Cheyne-Stokes\nMH - Ecocardiografía\nMH - *Insuficiencia cardiaca\nMH - *Implantación de prótesis valvulares cardíacas\nMH - Hemodinámica\nMH - Humanos\nMH - Hombre\nMH - Resultado del tratamiento\n",
+        "gold_summary": "Se remitió a un hombre de 86 años para la implantación de una válvula aórtica transfemoral. La ecocardiografía transtorácica reveló una estenosis grave (gradiente medio: 58 mmHg, área de la válvula aórtica: 0,4 cm2), y después de una discusión multidisciplinaria, se consideró que el riesgo de la cirugía era demasiado alto (Euroscore logístico: 51%), y se propuso al paciente para la implantación de una válvula aórtica transfemoral (TAVI). Al llegar al quirófano, se observó que el paciente, completamente consciente, tenía respiración de Cheyne-Stokes (CSB), que persistió después de la administración de oxígeno al 40%. El procedimiento TAVI fue exitoso, y el patrón CSB se interrumpió en 8 s.\n",
+        "synthetic_summary": {
+            "B1": "Había un señor de 86 años que tenía un problema en su corazón. Su corazón tenía una puerta muy pequeña y difícil para que la sangre pasara.\n\nLos doctores dijeron que una operación grande era muy peligrosa para él. Entonces, decidieron ponerle una válvula nueva con un tubo pequeño por la pierna.\n\nCuando llegó al lugar para la operación, el señor respiraba de una forma rara que subía y bajaba. Le dieron aire para ayudar, pero seguía igual.\n\nLa operación salió muy bien. Después, su forma de respirar rara se detuvo rápido. El señor se sintió mejor y todo salió bien.",
+            "B2": "**Lo que le pasaba al paciente:**  \nUn hombre de 86 años tenía un problema grave en su corazón llamado estenosis aórtica, que significa que la válvula que controla el flujo de sangre desde el corazón hacia el cuerpo estaba muy estrecha. Esto hacía que su corazón trabajara mucho más duro para bombear la sangre. Los médicos usaron una ecografía especial para ver que la válvula estaba muy dañada y que el área por donde pasa la sangre era muy pequeña.\n\n**Por qué eligieron un tratamiento especial:**  \nDebido a que el paciente era mayor y tenía otros problemas de salud, los médicos pensaron que una cirugía tradicional para cambiar la válvula era demasiado riesgosa. En lugar de eso, decidieron hacer un procedimiento menos invasivo llamado TAVI, que consiste en implantar una nueva válvula a través de una arteria en la pierna, sin abrir el pecho.\n\n**Lo que ocurrió durante el procedimiento:**  \nCuando el paciente llegó al quirófano, estaba despierto y mostraba un tipo de respiración llamada Cheyne-Stokes. Esta respiración es irregular y se caracteriza por períodos en los que la persona respira muy rápido y otros en los que casi no respira. Aunque le dieron oxígeno, esta respiración continuó. Durante el procedimiento para poner la nueva válvula, todo salió bien y, justo después, la respiración irregular desapareció en pocos segundos.\n\n**Qué significa esto:**  \nEl éxito del procedimiento no solo mejoró la función de la válvula del corazón, sino que también ayudó a normalizar la respiración del paciente. Esto muestra que tratar la estenosis aórtica puede mejorar otros problemas relacionados con el corazón y la forma en que el cuerpo respira.",
+            "B3": "**Contexto**\n\nUn hombre de 86 años con antecedentes importantes, incluyendo tabaquismo intenso en el pasado, fibrilación auricular paroxística tratada con anticoagulación y marcapasos por bradicardia, fue diagnosticado con estenosis aórtica severa calcificada. Presentaba síntomas de insuficiencia cardíaca, como disnea y edemas, además de deterioro significativo de la función ventricular izquierda (fracción de eyección del 27-29%) y hipertensión pulmonar. Debido a su alto riesgo quirúrgico (Euroscore logístico del 51%), se decidió realizar un reemplazo valvular aórtico mediante un procedimiento menos invasivo conocido como implantación de válvula aórtica transfemoral (TAVI).\n\n**Hallazgos Clave**\n\n- La ecocardiografía mostró una estenosis aórtica severa con un área valvular muy reducida (0,4-0,5 cm²) y un gradiente medio elevado (55-58 mmHg), junto con disfunción ventricular izquierda y dilatación de las aurículas.\n- El paciente presentaba un patrón respiratorio anormal llamado respiración de Cheyne-Stokes (CSB), caracterizado por ciclos periódicos de respiración rápida seguidos de pausas (apneas), que persistió incluso tras la administración de oxígeno al 40%.\n- Durante el procedimiento TAVI, que se realizó bajo sedación consciente, se monitorizaron cuidadosamente la función cardíaca, la saturación de oxígeno y la respiración.\n- El procedimiento incluyó la valvuloplastia con balón y la implantación de una válvula protésica de 26 mm, con inducción temporal de ritmo cardíaco rápido para facilitar la expansión valvular.\n- El paciente mantuvo la respiración espontánea durante todo el procedimiento, sin despertar ni presentar complicaciones respiratorias.\n- Tras la implantación, se observó una interrupción inmediata del patrón de respiración de Cheyne-Stokes, con estabilización de la presión arterial y mejora hemodinámica.\n- La función valvular mejoró notablemente, con aumento del área valvular a 1,6 cm² y reducción del gradiente a 15 mmHg. La presión pulmonar también disminuyó progresivamente en el seguimiento.\n\n**Interpretación Clínica**\n\nEste caso ilustra la complejidad del manejo de un paciente anciano con estenosis aórtica severa y disfunción ventricular avanzada, en quien la cirugía convencional representaba un riesgo muy alto. La elección del TAVI permitió una intervención efectiva y menos invasiva. La presencia de respiración de Cheyne-Stokes, un patrón respiratorio asociado a insuficiencia cardíaca avanzada y alteraciones en el control respiratorio, fue un hallazgo relevante que se resolvió tras la mejora hemodinámica conseguida con la corrección valvular. Esto sugiere que la disfunción cardíaca contribuye directamente a la aparición de este patrón respiratorio anormal.\n\n**Próximos Pasos**\n\n- Continuar con el seguimiento clínico y ecocardiográfico para evaluar la función valvular y ventricular a largo plazo.\n- Monitorizar la presión arterial pulmonar y la función respiratoria, dado que la mejoría observada puede influir favorablemente en la calidad de vida y pronóstico.\n- Mantener el control de factores de riesgo cardiovascular y la anticoagulación adecuada, considerando la historia de fibrilación auricular y la implantación del marcapasos.\n- Evaluar y manejar cualquier síntoma residual o complicación relacionada con la insuficiencia cardíaca o el patrón respiratorio, aunque la desaparición de la respiración de Cheyne-Stokes tras el procedimiento es un signo alentador.\n\nEn resumen, la implantación de la válvula aórtica transfemoral en este paciente de alto riesgo fue exitosa y produjo una mejora significativa tanto en la función cardíaca como en la estabilidad respiratoria, evidenciando la importancia de un enfoque multidisciplinario y personalizado en casos complejos."
+        }
+    },
+    {
+        "article": "Una mujer árabe tunecina de 62 años, diagnosticada con la enfermedad de Von Hippel-Lindau en 2021, presentó varias manifestaciones relacionadas con la enfermedad. Tenía antecedentes de múltiples cirugías, principalmente por tumores renales, suprarrenales y pancreáticos, con hallazgos incidentales de masas ováricas.\n\nLa paciente no presentaba síntomas desde el punto de vista ginecológico, pero se quejaba principalmente de dolores de cabeza antes de someterse a una cirugía cerebral. No tenía antecedentes familiares o psicosociales significativos.\n\nSu historial quirúrgico incluye\n2021: Un tumor no operable (6 cm) del saco endolinfático del hueso petroso izquierdo, tratado con radioterapia.\n\n2021: Adrenalectomía izquierda por un feocromocitoma de 6 cm. El examen patológico reveló un feocromocitoma.\n\n2021: Nefrectomía izquierda por un tumor renal izquierdo roto. La microscopía mostró un carcinoma renal multifocal de células claras de grado nuclear 2.\n\n2022: Duodenopancreatectomía cefálica por una masa en el páncreas. El examen histológico confirmó tres cistadenomas serosos y dos tumores neuroendocrinos bien diferenciados.\n\nEn enero de 2021, durante la vigilancia posoperatoria con una tomografía computarizada (TC) abdominal-pélvica, se descubrió incidentalmente una masa anexial izquierda sólida de 4 cm, lo que levantó sospechas de malignidad. La masa se confirmó mediante ultrasonido transvaginal e IRM pélvica, clasificada como Sistema de Reporte y Datos Ováricos-Anexiales (O-RADS) 5 (alta sospecha de malignidad).\n\nExamen ginecológico e historial quirúrgico\nExamen físico: No se detectó masa abdominal-pélvica.\n\nExamen con espéculo: cuello uterino sano.\n\nSe observaron cicatrices quirúrgicas de una nefrectomía izquierda y una duodenopancreatectomía cefálica anteriores.\n\nUna reunión multidisciplinaria del personal concluyó que era necesaria la cirugía. Se realizó una laparotomía a través de una incisión en la línea media por debajo del ombligo, que reveló una masa quística sólida bien definida en el anexo izquierdo. No había ascitis ni signos de carcinomatosis peritoneal, y el anexo derecho parecía normal, sin signos macroscópicos de malignidad observados intraoperatoriamente, incluida la ausencia de vegetaciones exocísticas.\n\nSe realizó una citología junto con una anexectomía izquierda y la muestra se envió para un examen de sección congelada. Los resultados no fueron concluyentes, lo que planteó la posibilidad de tumores de margen o específicos del síndrome de Von Hippel-Lindau. Teniendo en cuenta el estado posmenopáusico de la paciente, se realizó una anexectomía derecha y una histerectomía total.\n\nEl examen histológico posterior reveló cistadenomas papilares de células claras bilaterales de las trompas de Falopio y el ligamento ancho, característicos de la enfermedad de Von Hippel-Lindau (0,5 cm en el lado derecho y 4 cm en el lado izquierdo). Los tumores consistían en papilas densamente compactadas con núcleos fibrosos, cubiertos por un epitelio monocapa.\n\nEl período postoperatorio inmediato transcurrió sin incidentes y, en el seguimiento de 1 mes, no se detectaron anomalías. Desde entonces, se ha hecho un seguimiento al paciente cada 4 meses con ecografías pélvicas normales. Durante estos 2 años de seguimiento, no han surgido complicaciones, pero el paciente fue readmitido recientemente en el departamento de neurocirugía por la recurrencia de un tumor cerebral.\n",
+        "gold_summary": "Una mujer blanca norteafricana de 62 años de edad, diagnosticada con la enfermedad de Von Hippel-Lindau en 2021, presentó múltiples manifestaciones, entre ellas, un tumor del hueso petroso izquierdo, feocromocitoma izquierdo, carcinoma de células renales izquierdo, riñón derecho con múltiples quistes y masas pancreáticas. Se sometió a varios tratamientos, entre ellos, radioterapia, adrenalectomía, nefrectomía y duodenopancreatectomía cefálica. Los exámenes de ultrasonografía y resonancia magnética revelaron una masa quística sólida en la región anexial izquierda. La laparoscopia identificó tumores quísticos en la mesosalpinx derecha e izquierda. Después de una histerectomía con anexectomía bilateral, el examen histológico reveló cistadenomas papilares de células claras bilaterales de la mesosalpinx y el ligamento ancho, compatibles con la enfermedad de Von Hippel-Lindau.\n",
+        "synthetic_summary": {
+            "B1": "Había una señora que tenía una enfermedad llamada Von Hippel-Lindau. Esta enfermedad le hizo tener bultos en partes de su cuerpo. Los doctores le hicieron varias operaciones para quitar esos bultos. \n\nUn día, los doctores encontraron otro bulto cerca de su barriga. Le hicieron una cirugía para quitarlo. Cuando miraron el bulto con el microscopio, vieron que era un tipo de bulto que pasa con su enfermedad. \n\nDespués de la operación, la señora se sintió bien y los doctores la cuidaron mucho para que siga sana.",
+            "B2": "**Lo que le Pasó a la Paciente**  \nUna mujer de 62 años fue diagnosticada con la enfermedad de Von Hippel-Lindau, que es una condición genética que causa tumores en diferentes partes del cuerpo. Ella tuvo varios tumores en lugares como el hueso cerca del oído, las glándulas suprarrenales, los riñones y el páncreas. Para tratar estos tumores, se sometió a diferentes cirugías y radioterapia.\n\n**Descubrimiento de una Nueva Masa**  \nDurante un control médico, los doctores encontraron una masa sólida y con líquido (quística) en la zona de los órganos reproductores femeninos, específicamente cerca del ovario izquierdo. Usaron ultrasonido y resonancia magnética para verla mejor.\n\n**Cirugía y Resultados**  \nLos médicos hicieron una cirugía para quitar la masa y también extirparon el útero y ambos anexos (que incluyen las trompas de Falopio y los ovarios). Al analizar el tejido, encontraron que la masa era un tipo de tumor llamado cistadenoma papilar de células claras. Este tumor es raro y está relacionado con la enfermedad de Von Hippel-Lindau.\n\n**Qué Significa Esto**  \nEstos tumores no eran cancerosos, pero están asociados con la enfermedad genética que tiene la paciente. Después de la cirugía, la mujer se recuperó bien y no tuvo problemas durante los dos años siguientes, aunque tuvo que regresar para tratar un tumor cerebral que volvió a aparecer.\n\nEn resumen, esta paciente con una enfermedad genética complicada tuvo varios tumores en diferentes órganos. Gracias a los controles y cirugías, los médicos pudieron identificar y tratar un tumor nuevo en su sistema reproductor, ayudándola a mantenerse estable por un tiempo.",
+            "B3": "**Contexto**  \nUna mujer tunecina de 62 años fue diagnosticada en 2021 con la enfermedad de Von Hippel-Lindau, un trastorno genético que predispone al desarrollo de múltiples tumores en diferentes órganos. A lo largo de su evolución clínica, presentó diversas manifestaciones relacionadas con esta enfermedad, incluyendo tumores en el hueso petroso (una parte del cráneo cerca del oído), glándula suprarrenal, riñón y páncreas. Su tratamiento incluyó radioterapia y varias cirugías importantes para extirpar estos tumores.\n\n**Hallazgos Clave**  \nDurante el seguimiento posoperatorio, se detectó de forma incidental mediante tomografía computarizada una masa sólida y quística de 4 cm en la región anexial izquierda (área ovárica y estructuras cercanas). Esta masa fue confirmada por ultrasonido transvaginal y resonancia magnética, clasificándose como de alta sospecha de malignidad según el sistema O-RADS. Sin embargo, la paciente no presentaba síntomas ginecológicos ni signos físicos evidentes de masa pélvica.\n\nSe decidió realizar una cirugía mediante laparotomía para evaluar y tratar la masa. Durante la intervención, se encontró una masa quística sólida bien delimitada en el anexo izquierdo, sin evidencia de diseminación tumoral en la cavidad abdominal. Se realizó la extirpación del anexo izquierdo y, debido a la edad posmenopáusica de la paciente y la sospecha de enfermedad bilateral, también se llevó a cabo la anexectomía derecha y la histerectomía total.\n\nEl análisis histológico posterior mostró la presencia de cistadenomas papilares de células claras en ambas trompas de Falopio y en el ligamento ancho (estructuras que sostienen el útero y las trompas), con tamaños de 4 cm en el lado izquierdo y 0,5 cm en el derecho. Estos tumores, caracterizados por papilas densamente agrupadas cubiertas por una capa única de células epiteliales, son una manifestación típica de la enfermedad de Von Hippel-Lindau.\n\n**Interpretación Clínica**  \nLos cistadenomas papilares de células claras bilaterales en las trompas de Falopio y el ligamento ancho representan una manifestación poco común pero reconocida de la enfermedad de Von Hippel-Lindau. La ausencia de síntomas ginecológicos y la detección incidental subrayan la importancia de un seguimiento cuidadoso en pacientes con esta enfermedad multisistémica. La cirugía fue necesaria para confirmar el diagnóstico y prevenir posibles complicaciones asociadas a estas masas.\n\n**Próximos Pasos**  \nEl postoperatorio inmediato fue favorable y, durante un seguimiento de dos años con controles ecográficos pélvicos regulares, no se observaron recurrencias ni nuevas lesiones en la región pélvica. No obstante, la paciente fue recientemente readmitida en neurocirugía debido a la recurrencia de un tumor cerebral, lo que refleja la naturaleza crónica y multisistémica de la enfermedad de Von Hippel-Lindau. Se recomienda continuar con un seguimiento multidisciplinario riguroso para manejar las diferentes manifestaciones de esta condición."
+        }
+    },
+    {
+        "article": "Una mujer embarazada de 31 años que había sido sometida a una cesárea fue derivada a la unidad de ultrasonido de nuestro departamento para un examen de ultrasonido morfológico de segundo trimestre. La paciente no tenía antecedentes familiares destacables y no había tomado medicamentos ni había estado expuesta a teratógenos durante el primer trimestre del embarazo. Los exámenes serológicos para diversas enfermedades infecciosas fueron negativos y un examen de ultrasonido previo a las 14 semanas fue normal. El triple examen para anomalías fetales también fue negativo a las 16 semanas.\n\nDurante la ecografía de la semana 20, se observó un feto masculino con una edad sonográfica compuesta de 20 semanas y 2 días que presentaba un edema significativo de las extremidades inferiores y líquido amniótico normal. Se recomendó un examen de seguimiento en 2 semanas, junto con pruebas de TORCH y pruebas de Coombs indirectas.\n\nSin embargo, se observó nuevamente edema subcutáneo en ambas extremidades inferiores durante la ecografía morfológica de la semana 23, lo que sugiere un posible diagnóstico de EM. Debido al linfedema persistente en las extremidades inferiores, se realizó una amniocentesis.\n\nLos exámenes posteriores revelaron que el cariotipo masculino era normal (46, XY), y el análisis molecular para el síndrome de Noonan fue negativo. Se realizó la secuenciación de nucleótidos del líquido amniótico con la secuenciación Illumina de 150 bases. Se aplicó el sistema de bioinformática (North-Oehler Aligarh, GATX) mientras se verificaba adicionalmente la existencia de deleciones/duplicaciones/CNV (Copy Number Variations) en el gen FLT4. El análisis identificó una mutación c.3116C>A p. (Ala1039Asp), que es una variante patogénica no conocida en el gen FLT4, lo que confirma el diagnóstico de linfedema hereditario tipo 1A – enfermedad de Milroy. El análisis de sangre materno confirmó la mutación materna y se realizó el asesoramiento genético.\n\nLa cesárea se realizó a las 38 semanas y 6 días de gestación y nació un neonato de sexo masculino que pesaba 3850 g y medía 46 cm con una puntuación de Apgar de 9/10. Después del parto se reconoció un edema en la extremidad inferior. El examen histopatológico de la placenta, el cordón umbilical y el saco amniótico no mostró signos de corioamnionitis u otra patología.\n",
+        "gold_summary": "Presentamos un informe de caso de una primera mutación descrita de un feto masculino diagnosticado prenatalmente con síndrome de Milroy a través de amniocentesis. El feto tenía edema bilateral de miembros inferiores, y las pruebas genéticas confirmaron el diagnóstico de síndrome de Milroy. La paciente fue monitoreada de cerca durante todo el embarazo, y después del parto, el lactante fue tratado con terapias apropiadas, incluyendo prendas de compresión y drenaje linfático manual. Los padres recibieron asesoramiento y apoyo apropiados.\n",
+        "synthetic_summary": {
+            "B1": "Un bebé niño tenía sus piernas un poco hinchadas cuando estaba en la barriga de su mamá. Los doctores hicieron pruebas para entender por qué. Descubrieron que el bebé tenía una condición llamada síndrome de Milroy. La mamá fue cuidada con mucho cariño durante todo el embarazo. Cuando el bebé nació, los doctores le ayudaron para que sus piernas estuvieran mejor. Los papás también recibieron ayuda para cuidar bien al bebé. Todo está hecho para que el bebé crezca fuerte y feliz.",
+            "B2": "**Lo que Encontraron**\n\nEn este caso, una mujer embarazada fue examinada con ultrasonido y se descubrió que su bebé tenía hinchazón (edema) en ambas piernas antes de nacer. Para entender mejor qué pasaba, los médicos hicieron una amniocentesis, que es cuando se toma un poco del líquido que rodea al bebé para estudiar sus genes. Encontraron una mutación, que es un cambio en un gen llamado FLT4, que causa una enfermedad llamada síndrome de Milroy. Esta enfermedad hace que el sistema que ayuda a drenar el líquido del cuerpo no funcione bien, causando hinchazón.\n\n**Qué Significa**\n\nEl diagnóstico se confirmó antes del nacimiento, lo que permitió a los médicos seguir de cerca el embarazo y prepararse para cuidar al bebé después del parto. El bebé nació con hinchazón en las piernas, pero recibió tratamientos especiales, como usar prendas que aprietan suavemente y masajes para ayudar a mover el líquido acumulado. Además, los padres recibieron información y apoyo para entender la enfermedad y cómo cuidar a su hijo.\n\nEste caso muestra la importancia de las pruebas genéticas y el seguimiento durante el embarazo para detectar y manejar enfermedades raras como el síndrome de Milroy.",
+            "B3": "**Contexto**  \nEste informe describe el caso de una mujer embarazada de 31 años cuyo feto masculino fue diagnosticado antes del nacimiento con síndrome de Milroy, una forma hereditaria de linfedema (acumulación anormal de líquido linfático que causa hinchazón). La paciente no presentaba antecedentes familiares relevantes ni factores de riesgo conocidos, y las pruebas iniciales durante el embarazo no mostraron anomalías.\n\n**Hallazgos Clave**  \nDurante la ecografía morfológica realizada en la semana 20 de gestación, se detectó un edema significativo en ambas extremidades inferiores del feto, aunque el líquido amniótico estaba dentro de los parámetros normales. Un seguimiento a las 23 semanas confirmó la persistencia de este edema subcutáneo. Ante estos hallazgos, se realizó una amniocentesis para obtener líquido amniótico y realizar estudios genéticos detallados.  \n\nEl análisis cromosómico mostró un cariotipo normal (46, XY), y se descartó el síndrome de Noonan mediante pruebas moleculares. Sin embargo, la secuenciación genética identificó una mutación patogénica inédita en el gen FLT4 (c.3116C>A p. (Ala1039Asp)), responsable del desarrollo del sistema linfático. Esta mutación confirmó el diagnóstico prenatal de linfedema hereditario tipo 1A, conocido como enfermedad de Milroy. Además, el análisis de sangre materno reveló que la madre también portaba esta mutación, lo que permitió realizar un asesoramiento genético adecuado a la familia.\n\nEl parto se llevó a cabo mediante cesárea a las 38 semanas y 6 días, naciendo un niño con buen peso y condición general (puntuación de Apgar 9/10). Tras el nacimiento, se observó edema en las extremidades inferiores, consistente con el diagnóstico prenatal. Los estudios histopatológicos de la placenta y membranas no mostraron infecciones ni otras patologías.\n\n**Interpretación Clínica**  \nEl síndrome de Milroy es una enfermedad genética que afecta el desarrollo y funcionamiento del sistema linfático, provocando linfedema desde etapas tempranas de la vida. La detección prenatal mediante ecografía y pruebas genéticas permite un diagnóstico temprano, lo que facilita la planificación del manejo clínico y el apoyo familiar. La identificación de una mutación previamente no descrita en el gen FLT4 amplía el conocimiento sobre la variabilidad genética de esta enfermedad.\n\n**Próximos Pasos**  \nDespués del nacimiento, el lactante recibió tratamiento especializado para el linfedema, que incluyó el uso de prendas de compresión y drenaje linfático manual, con el objetivo de controlar la hinchazón y mejorar la calidad de vida. La familia recibió asesoramiento genético para comprender el origen hereditario de la enfermedad, las implicaciones para futuros embarazos y las opciones disponibles. El seguimiento clínico continuo es esencial para monitorizar la evolución del linfedema y adaptar el tratamiento según sea necesario."
+        }
+    },
+    {
+        "article": "Un paciente de 50 años con antecedentes médicos conocidos de diabetes mellitus (DM) e hipertensión (HTN), que se manejaba de manera irregular, se presentó en nuestro hospital en la ciudad de Sana’a, Yemen, el 25 de mayo de 2022, a las 5:30 p. m. El paciente fue derivado a otro hospital y manifestó un dolor abdominal agudo que había durado una semana antes del ingreso. El dolor se localizaba en la región epigástrica, de inicio repentino, empeoramiento progresivo y radiación hacia la espalda. Además, el paciente experimentó distensión abdominal generalizada, náuseas, vómitos y fatiga significativa. También se informó un historial de melena y vómitos relacionados con los alimentos durante el mes pasado. Dos días antes del ingreso, el paciente había recibido una transfusión de sangre de 2 unidades. No había antecedentes de cirugías previas ni antecedentes familiares de neoplasias.\n\nAl examinar al paciente, se constató que estaba consciente y alerta, pero que presentaba un aspecto pálido. La presión arterial era de 90/60 mmHg y el pulso de 120 latidos por minuto. Se observó distensión abdominal generalizada, particularmente prominente en la región supraumbilical con desplazamiento hacia abajo del ombligo. Se constató una leve sensibilidad en la zona epigástrica, junto con sonidos intestinales positivos, el examen rectal digital reveló un tono normal del esfínter anal y no se detectó ninguna masa palpable.\n\nLos exámenes hematológicos y bioquímicos revelaron anemia microcítica hipocrómica con un nivel de hemoglobina de 6 g/dL (rango normal: 12-15.5 g/dL), un recuento de glóbulos blancos de 16,000 (rango normal: 4-10,000), y un recuento de plaquetas de 303. El nivel de nitrógeno ureico en sangre fue de 7 mg/dL (rango normal: 10-20 mg/dL), la creatinina fue de 0.49 mg/dL (rango normal: 0.7-1.5% / dL), el índice internacional normalizado fue de 1.34 (rango normal: 0.62-1.3), el tiempo de protrombina (PT) fue de 16.9, el tiempo de tromboplastina parcial (PTT) fue de 30, el calcio fue de 8.0 mg/dL (rango normal: 8.5-10.1 mg / dL) y el ácido láctico fue de 1.9 mmol/L (rango normal: 0.5-2.2% / L). Los niveles de enzimas hepáticas y amilasa estuvieron dentro de los límites normales.\n\nSe realizaron estudios de diagnóstico por imágenes, que incluyeron una radiografía de tórax y una ecografía abdominal. La radiografía de tórax no reveló aire subdiafragmático, pero se observó una elevación en el diafragma izquierdo. La ecografía abdominal demostró la presencia de una acumulación de líquido intraabdominal. Posteriormente, se realizó una angiografía por TC abdominal, que reveló un hematoma de aproximadamente 14,3 × 8,8 cm en la región paraumbilical. En el interior del hematoma, se identificó un aneurisma arterial de 3,4 × 2,2 cm conectado a la arteria gastroduodenal, acompañado de cambios edematosos circundantes. Estos hallazgos sugieren la presencia de un aneurisma trombosado grande en la arteria gastroduodenal. Además, se observó la evisceración del diafragma izquierdo, que contiene el bazo y parte del estómago, junto con una acumulación de líquido intraperitoneal leve a moderada. No se detectó evidencia de un aneurisma aórtico.\n\nPara estabilizar al paciente, se inició la reanimación con 1000 ml de lactato de Ringer y se transfundieron tres unidades de sangre fresca. Se obtuvo el consentimiento informado para la intervención de alto riesgo y el paciente fue llevado inmediatamente al quirófano. Bajo anestesia general, en posición supina y con estricta adhesión a las técnicas asépticas, se realizó una incisión de laparotomía en la línea media. Cuando se abrió el peritoneo, se evacuó aproximadamente 2000 ml de sangre, revelando una masa pulsátil ocluida en el duodeno. Se logró una exposición adecuada utilizando un retractor auto-reforzado. La flexión del hígado y el colon transverso se movilizaron inferiormente desde la cabeza del páncreas y se eliminó la sangre coagulada del intestino delgado. Se realizó una disección meticulosa sobre el gran aneurisma ocluido pulsátil en la arteria gastroduodenal abriendo el ligamento gastrohepático. La movilización del píloro y el duodeno lejos de la cabeza del páncreas expuso una fístula que conectaba el duodeno y el aneurisma, sin contenido digestivo. Después de la heparinización, se realizó un pinzamiento proximal y distal de la arteria gastroduodenal. Posteriormente, se abrió el pseudoaneurisma y se evacuó una cantidad significativa de trombo. Se realizó una aneurismorrafía utilizando suturas de prolina 7.0. La perforación en la primera parte del duodeno se reparó en dos capas y se insertó una sonda nasogástrica más allá de la perforación. Se logró una irrigación exhaustiva con solución salina normal y una hemostasia meticulosa. Se colocó un drenaje abdominal y se cerró la incisión abdominal en capas. El paciente fue trasladado a la unidad de cuidados intensivos (UCI) para una estrecha monitorización y observación.\n\nDurante el período postoperatorio, el drenaje abdominal recolectó aproximadamente 100 ml de fluido seroso, que se eliminó el tercer día después de la operación. La recuperación de la paciente progresó sin complicaciones. Diez días después de la cirugía, la paciente fue dada de alta en condiciones favorables. Se programaron citas de seguimiento en el departamento ambulatorio y se mantuvo una comunicación regular por teléfono, con la condición de la paciente reportada como satisfactoria.\n",
+        "gold_summary": "Un hombre de 50 años se presentó con dolor abdominal agudo, anemia y signos de inestabilidad hemodinámica. Las imágenes de diagnóstico, incluida la CTA, revelaron un aneurisma de la arteria gastroduodenal grande y trombosado con evidencia de ruptura. El paciente se sometió a exploración y reparación quirúrgica abierta para abordar tanto el aneurisma como la perforación duodenal. La recuperación del paciente fue satisfactoria y fue dado de alta en condiciones estables.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre tenía mucho dolor en su barriga. Estaba muy cansado y débil. Los doctores vieron que tenía un bulto grande en una de sus venas. Ese bulto estaba lastimado y había sangre. Los doctores hicieron una operación para arreglar el bulto y la herida. Después, el hombre se sintió mejor y pudo ir a su casa.",
+            "B2": "### Lo que le pasó al paciente\n\nUn hombre de 50 años llegó al hospital con un dolor fuerte en el abdomen que había durado una semana. También estaba muy cansado y tenía anemia, que es cuando la sangre no tiene suficientes glóbulos rojos para llevar oxígeno al cuerpo. Su presión arterial estaba baja y su pulso rápido, lo que indicaba que su cuerpo estaba débil.\n\n### Lo que encontraron los médicos\n\nLos médicos hicieron varias pruebas, incluyendo imágenes especiales llamadas tomografía computarizada (CTA). Estas mostraron que tenía un aneurisma grande en una arteria llamada gastroduodenal. Un aneurisma es una zona donde la pared de un vaso sanguíneo está débil y se hincha, como un globo. Además, había coágulos de sangre dentro del aneurisma y parecía que se había roto, lo que es muy peligroso.\n\n### Qué hicieron los médicos\n\nPara salvarlo, los médicos hicieron una cirugía abierta. Abrieron el abdomen para encontrar y reparar el aneurisma. También encontraron una pequeña herida (perforación) en el duodeno, que es la primera parte del intestino delgado, y la repararon. Durante la cirugía, limpiaron la sangre acumulada y cerraron cuidadosamente las heridas.\n\n### Cómo fue la recuperación\n\nDespués de la operación, el paciente estuvo en cuidados intensivos para que lo vigilaran bien. Su recuperación fue buena, sin problemas importantes. Diez días después, pudo salir del hospital en buen estado y continuó con controles médicos para asegurarse de que siguiera mejorando.",
+            "B3": "**Contexto:**  \nUn hombre de 50 años con antecedentes de diabetes e hipertensión, que no seguía un tratamiento constante, acudió al hospital tras una semana de dolor abdominal intenso en la parte superior del abdomen, que se irradiaba hacia la espalda. Además, presentaba distensión abdominal, náuseas, vómitos, fatiga y antecedentes recientes de sangrado digestivo (melena). Dos días antes había recibido una transfusión de sangre debido a anemia.\n\n**Hallazgos Clave:**  \nEn la evaluación inicial, el paciente estaba consciente pero pálido, con presión arterial baja (90/60 mmHg) y pulso acelerado (120 latidos/minuto), signos que indicaban inestabilidad hemodinámica. El examen físico mostró distensión abdominal y sensibilidad leve en la zona del dolor. Los análisis de sangre revelaron anemia severa (hemoglobina de 6 g/dL), aumento de glóbulos blancos (16,000), y otros parámetros dentro de límites aceptables. Las imágenes diagnósticas, incluyendo una tomografía computarizada con angiografía (CTA), identificaron un hematoma grande en la región abdominal paraumbilical y un aneurisma (una dilatación anormal de un vaso sanguíneo) de la arteria gastroduodenal, con signos de trombosis (coágulos) y posible ruptura. También se observó una hernia diafragmática con desplazamiento de órganos abdominales hacia el tórax y acumulación de líquido en la cavidad abdominal.\n\n**Interpretación Clínica:**  \nEl diagnóstico principal fue un aneurisma gigante y trombosado de la arteria gastroduodenal con ruptura, que causaba hemorragia interna y perforación en la primera parte del duodeno (segmento inicial del intestino delgado). Esta situación representaba una emergencia quirúrgica debido al riesgo de sangrado masivo y complicaciones graves.\n\n**Próximos Pasos y Tratamiento:**  \nEl paciente fue estabilizado con líquidos intravenosos y transfusiones sanguíneas antes de ser llevado a cirugía de urgencia. Durante la operación, se evacuaron aproximadamente dos litros de sangre acumulada, se identificó y reparó el aneurisma mediante suturas, y se cerró la perforación duodenal en dos capas. Se colocó un drenaje abdominal para controlar posibles fugas y se monitorizó estrechamente en la unidad de cuidados intensivos. La recuperación fue favorable, sin complicaciones postoperatorias, y el paciente fue dado de alta diez días después en condiciones estables, con seguimiento ambulatorio programado.\n\nEn resumen, este caso ilustra la importancia de un diagnóstico rápido y un manejo quirúrgico oportuno en pacientes con aneurisma roto de la arteria gastroduodenal, una condición rara pero potencialmente mortal."
+        }
+    },
+    {
+        "article": "Una mujer de 60 años fue admitida en el departamento de nefrología con dolor epigástrico, hematemesis y edema en la pierna. La presión arterial era de 90/50 mmHg, dentro del rango normal para esta paciente.\nLos resultados de laboratorio fueron notables para las enzimas hepáticas alteradas con un patrón colestático: los niveles de alanina amino transferasa (ALT) y aspartato amino transferasa (AST) fueron ligeramente elevados a 28 U/L y 61 U/L, respectivamente, mientras que los niveles de fosfatasa alcalina (388 U/L) y gamma glutamiltransferasa (291 U/L) fueron muy elevados. Los niveles de albúmina en suero fueron de 24 g/L y el índice internacional normalizado fue normal a 1.02.\nOtros resultados de laboratorio, incluidos la bilirrubina total (0,32 mg/dL), la bilirrubina directa (0,26 mg/dL), el recuento total de plaquetas (176 000 plaquetas por microlitro) y el recuento de glóbulos blancos (8400 células por microlitro), se encontraban dentro de los valores normales.\nEl paciente tenía un extenso historial de enfermedades cardiacas y renales. A los 11 años, se le diagnosticó estenosis congénita de la válvula pulmonar, por lo que se le practicó una valvulotomía. Más adelante, desarrolló fibrilación auricular y aleteo auricular, que no toleró bien y para los que se intentó, sin éxito, la ablación del aleteo. Como el paciente seguía teniendo síntomas, se le practicó una ablación del nódulo auriculoventricular con colocación de un marcapasos.\nSe inició anticoagulación oral con fenprocoumon debido a una puntuación CHA2DS2-Vasc de 3 (mujer, insuficiencia cardiaca y enfermedad vascular periférica). A la edad de 55 años, se desarrolló una insuficiencia cardiaca derecha manifiesta y la paciente continuó luchando con ascitis y edemas periféricos que requerían múltiples ingresos hospitalarios. Además, también desarrolló un problema de efusiones pleurales transudativas recurrentes de etiología poco clara.\nLa ecocardiografía en ese momento mostró una severa regurgitación pulmonar y tricuspídea con un ventrículo derecho moderadamente dilatado y una aurícula derecha. El ventrículo izquierdo estaba ligeramente dilatado con una regurgitación mitral moderada. El cateterismo cardiaco derecho demostró presiones arteriales pulmonares de 74/30 mmHg con una presión venosa central de 28 mmHg. Se colocó un homotransplante pulmonar cuando el paciente tenía 57 años y se realizó una anuloplastia tricuspídea concomitante. A pesar de una presión venosa central más baja de 13 mmHg, el paciente seguía siendo readmitido varias veces por signos y síntomas de insuficiencia cardiaca derecha. La congestión venosa sistémica persistente finalmente dio lugar a una enfermedad renal en fase terminal para la que se inició una terapia de reemplazo renal a través de hemodiálisis intermitente. El caso se complicó por hemorragias gastrointestinales graves recurrentes, que requerían transfusiones de sangre frecuentes con hasta 60 unidades de glóbulos rojos por año. A pesar de esto, en combinación con la sustitución intravenosa de hierro, los niveles de hemoglobina variaron entre 5.3-8.8 g/dL. Debido a estos problemas de sangrado intratables, la anticoagulación oral con fenprocoumon se detuvo a la edad de 59 años.\nUna gastroscopia mostró una gastropatía erosiva con una mucosa difusa congestiva y friable. Como prevención de primera línea de las hemorragias gástricas recurrentes en el marco de la cirrosis, se inició el propranolol a una dosis de 5 mg por vía oral dos veces al día (el paciente no toleró una dosificación superior debido a la presión arterial baja). Además, se realizó una coagulación endoscópica de un angioma fúndico y un recorte de una lesión de Dieulafoy.\nSe creía que estas lesiones eran causadas por una gastropatía hipertensiva. Sin embargo, las hemorragias intractables persistieron.\nEl gradiente de presión venosa hepática se midió a 16 mmHg (27 mmHg-11 mmHg). Aunque hubo cierta reticencia debido al temor de empeorar la insuficiencia cardiaca derecha, se tomó la decisión de crear un TIPS. El procedimiento fue sin incidentes. Después de la colocación del TIPS, el gradiente de presión venosa hepática disminuyó a 4 mmHg (14 mmHg-10 mmHg). Por lo tanto, aunque el TIPS redujo considerablemente el gradiente venoso hepático, la presión portal se mantuvo alta debido a la elevada presión venosa central.\nDespués de la colocación del TIPS, el paciente desarrolló signos de encefalopatía hepática y se midieron niveles de amoniaco de 77 umol/L. Se inició el tratamiento con lactulosa oral y enemas, con poca mejora. En ese momento, se produjo otro episodio de sangrado gástrico.\nLa ecografía abdominal mostró buena permeabilidad del TIPS con flujo Doppler normal. Se detectó sangrado gástrico de una úlcera antral con endoscopia, a pesar de que la hiperemia gástrica disminuyó visualmente en comparación con la situación antes del TIPS. Se realizó una biopsia que mostró una mucosa foveolar edematosa, lo que sugiere isquemia de la mucosa. El sangrado fue demasiado difuso para una ligadura endoscópica adicional. No se encontró empeoramiento de la función hepática en los resultados de laboratorio, con el índice internacional normalizado 1.01 en este momento. La ecocardiografía no mostró cambios significativos en comparación con la situación antes de la colocación del TIPS. El ventrículo derecho permaneció moderadamente dilatado con una función longitudinal deficiente y una regurgitación tricuspídea severa persistente. Sin embargo, el estado general del paciente se deterioró y se desarrolló fiebre con consolidaciones pulmonares bilaterales.\nSe produjo una falla multiorgánica y, en ese momento, la familia del paciente decidió retirar el tratamiento. El paciente falleció finalmente 43 días después del procedimiento TIPS.\n\nMH - Resultado fatal\nMH - Mujer\nMH - Insuficiencia cardiaca/*complicaciones/fisiopatología\nMH - Encefalopatía hepática/etiología\nMH - Humanos\nMH - Hipertensión, Portal/etiología/fisiopatología/*cirugía\nMH - Cirrosis hepática/*complicaciones\nMH - Edad Media\nMH - Presión del portal\nMH - *Derivación portosistémica, intrahepática transyugular\nMH - Fracaso del tratamiento\n",
+        "gold_summary": "Una mujer de 60 años con antecedentes de estenosis congénita de la válvula pulmonar desarrolló insuficiencia cardíaca derecha, cirrosis hepática y enfermedad renal en fase terminal que requería terapia de reemplazo renal. La cirrosis hepática se complicó con hipertensión portal, lo que provocó hemorragias gastrointestinales intratables a pesar del tratamiento óptimo con betabloqueantes y la ligadura endoscópica de la banda. Debido al temor de que empeorara la insuficiencia cardíaca derecha, inicialmente se rechazó la colocación de una derivación intrahepática transyugular (TIPS). Sin embargo, como los problemas de hemorragia intratables persistieron y causaron grandes necesidades de transfusión, la TIPS se realizó finalmente como un procedimiento de rescate. Aunque la TIPS redujo con éxito el gradiente de presión venosa hepática de 16 mmHg a 4 mmHg, la presión portal se mantuvo alta a 14 mmHg debido a la persistencia de la insuficiencia cardíaca derecha con presión venosa central elevada. La encefalopatía hepática se desarrolló poco después de la colocación de la TIPS y culminó en una falla multiorgánica después de otro episodio de hemorragia gastrointestinal. En este punto, la familia del paciente decidió retirar la atención y el paciente falleció posteriormente.\n",
+        "synthetic_summary": {
+            "B1": "Había una señora de 60 años que tenía problemas en el corazón y en el hígado. Su hígado estaba muy enfermo y le dolía mucho la barriga. También tenía problemas para que la sangre no sangrara mucho por dentro.\n\nLos doctores intentaron ayudarla con medicinas y tratamientos, pero la sangre seguía saliendo. Entonces, hicieron una operación para ayudar a que la sangre pasara mejor por el hígado.\n\nDespués de la operación, la señora se sintió peor y tuvo más problemas en su cuerpo. Al final, su familia decidió que ya no la trataran más y la señora se fue al cielo.",
+            "B2": "**Historia Clínica y Problemas Principales**  \nUna mujer de 60 años tenía varios problemas de salud desde joven, incluyendo una enfermedad del corazón llamada estenosis congénita de la válvula pulmonar. Con el tiempo, desarrolló insuficiencia cardíaca derecha, que significa que el lado derecho de su corazón no funcionaba bien. También tenía cirrosis hepática, una enfermedad del hígado que causa daño y cicatrices, y enfermedad renal en etapa terminal, por lo que necesitaba diálisis para limpiar su sangre.\n\n**Complicaciones y Tratamientos**  \nLa cirrosis causó hipertensión portal, que es una presión alta en las venas del hígado. Esto provocó sangrados graves en su estómago y esófago que no se podían controlar fácilmente. A pesar de usar medicamentos llamados betabloqueantes, que ayudan a bajar la presión, y hacer tratamientos endoscópicos para detener el sangrado, las hemorragias continuaron. Por miedo a que un procedimiento llamado TIPS (una derivación que ayuda a bajar la presión en el hígado) empeorara su insuficiencia cardíaca, inicialmente no se realizó.\n\n**Procedimiento TIPS y Resultados**  \nFinalmente, debido a que las hemorragias seguían siendo muy graves y necesitaba muchas transfusiones de sangre, se decidió hacer el TIPS como último recurso. Este procedimiento logró bajar la presión en las venas del hígado de 16 a 4 mmHg, lo que es una mejora importante. Sin embargo, la presión en la vena principal del hígado siguió siendo alta porque su corazón derecho seguía funcionando mal.\n\n**Complicaciones Finales y Desenlace**  \nDespués del TIPS, la paciente desarrolló encefalopatía hepática, que es un problema en el cerebro causado por la acumulación de toxinas cuando el hígado no funciona bien. También tuvo otro sangrado en el estómago y su estado general empeoró, con fallas en varios órganos. Finalmente, la familia decidió suspender el tratamiento y la paciente falleció 43 días después del procedimiento.\n\n**Qué Significa Este Caso**  \nEste caso muestra lo difícil que es tratar a pacientes con problemas graves en el corazón, hígado y riñones al mismo tiempo. Aunque el TIPS puede ayudar a bajar la presión en el hígado y controlar el sangrado, no siempre es suficiente si el corazón no puede manejar los cambios. Además, el procedimiento puede causar complicaciones como la encefalopatía hepática. Por eso, cada caso necesita un cuidado muy cuidadoso y personalizado.",
+            "B3": "**Contexto**  \nSe presenta el caso de una mujer de 60 años con un complejo historial médico que incluye una estenosis congénita de la válvula pulmonar diagnosticada en la infancia, seguida de múltiples complicaciones cardíacas como fibrilación auricular, insuficiencia cardíaca derecha y regurgitación valvular severa. Estas condiciones condujeron a una congestión venosa sistémica persistente, que a su vez provocó cirrosis hepática y enfermedad renal en etapa terminal, requiriendo hemodiálisis. Además, la paciente sufrió hemorragias gastrointestinales graves y recurrentes, difíciles de controlar, que demandaron numerosas transfusiones sanguíneas.\n\n**Hallazgos Clave**  \n- La cirrosis hepática se acompañó de hipertensión portal, evidenciada por un gradiente de presión venosa hepática elevado (16 mmHg).  \n- A pesar del tratamiento con betabloqueantes (propranolol) y procedimientos endoscópicos para controlar las hemorragias gástricas, estas continuaron siendo incontrolables.  \n- Inicialmente, se evitó la colocación de una derivación portosistémica intrahepática transyugular (TIPS) debido al riesgo de empeoramiento de la insuficiencia cardíaca derecha.  \n- Finalmente, se realizó el procedimiento TIPS como medida de rescate, logrando reducir el gradiente de presión venosa hepática a 4 mmHg; sin embargo, la presión portal permaneció elevada (14 mmHg) debido a la presión venosa central alta secundaria a la insuficiencia cardíaca derecha persistente.  \n- Posterior a la colocación del TIPS, la paciente desarrolló encefalopatía hepática (una alteración cerebral causada por la acumulación de toxinas debido a la insuficiencia hepática), con niveles elevados de amoníaco en sangre y síntomas neurológicos.  \n- Se presentó un nuevo episodio de sangrado gástrico, con evidencia endoscópica de úlcera antral y cambios isquémicos en la mucosa gástrica.  \n- La función hepática no mostró deterioro significativo en los análisis de laboratorio tras el TIPS, y la ecocardiografía reveló que la función cardíaca derecha permaneció comprometida.  \n- Finalmente, la paciente desarrolló una falla multiorgánica acompañada de infección pulmonar, lo que llevó a la decisión familiar de retirar el soporte terapéutico.\n\n**Interpretación Clínica**  \nEste caso ilustra la compleja interacción entre la insuficiencia cardíaca derecha crónica y sus consecuencias sistémicas, incluyendo la hipertensión portal secundaria y la cirrosis hepática. La hipertensión portal generó hemorragias gastrointestinales difíciles de controlar, que agravaron el estado general de la paciente. La colocación del TIPS, aunque efectiva para reducir el gradiente hepático, no logró normalizar la presión portal debido a la persistente congestión venosa por insuficiencia cardíaca. Además, el procedimiento desencadenó encefalopatía hepática, complicación frecuente en estos casos, y no previno nuevos episodios hemorrágicos. La evolución desfavorable culminó en falla multiorgánica y muerte.\n\n**Próximos Pasos y Reflexiones**  \nEste caso subraya la dificultad de manejar la hipertensión portal y sus complicaciones en pacientes con insuficiencia cardíaca derecha avanzada. La decisión de realizar un TIPS debe sopesar cuidadosamente los riesgos de empeoramiento cardíaco y encefalopatía hepática. En situaciones similares, se requiere un enfoque multidisciplinario que incluya cardiología, hepatología y nefrología para optimizar el tratamiento y considerar alternativas terapéuticas. Además, es fundamental el diálogo con la familia para establecer objetivos realistas y respetar las decisiones sobre el cuidado al final de la vida."
+        }
+    },
+    {
+        "article": "Una mujer tailandesa de 62 años presentó pérdida visual bilateral súbita y cefalea durante 5 días. Negó antecedentes de traumatismo craneal. Su historia clínica era significativa por presentar hipertensión mal controlada.\n\nLos signos vitales fueron normales, excepto por la presión arterial de 200/105 mmHg. La agudeza visual fue de no percepción de luz (NLP) con pupilas fijas en ambos ojos. La motilidad ocular de ambos ojos fue limitada en todas las direcciones. Ambas párpados fueron difíciles de abrir. Las medidas del exoftalmómetro de Hertel fueron de 16 mm en el ojo derecho y 14 mm en el ojo izquierdo. Había quemosis significativa y vasos de sacacorchos episclerales en ambos ojos. Ambas córneas mostraron un edema estromal leve y difuso sin infiltración. Las cámaras anteriores fueron profundas y tranquilas en ambos ojos. Las presiones intraoculares fueron de 45 mmHg y 48 mmHg en los ojos derecho e izquierdo, respectivamente. La gonioscopia reveló sangre en el canal de Schlemm en el ángulo nasal del ojo derecho. El examen del fondo de ojo mostró venas de la retina ligeramente dilatadas y tortuosas con discos ópticos de apariencia normal en ambos ojos. La relación taza-disco fue de 0.3 bilateralmente. La tomografía de coherencia óptica demostró un espesor normal de la mácula en cada ojo. No hubo ruido audible. Otros exámenes neurológicos fueron normales.\n\nLa resonancia magnética (MRI) con gadolinio del cerebro y las órbitas demostró la dilatación de las venas oftálmicas superiores bilaterales (SOVs) y un grado marcado de congestión orbital y periorbital bilateralmente. Sin embargo, no se observó ni compresión ni estiramiento de los nervios ópticos bilaterales. Es interesante destacar que la restricción de la difusión, con la correspondiente reducción del coeficiente de difusión aparente (ADC), en todo el segmento orbital de los nervios ópticos bilateralmente se reveló en la resonancia magnética ponderada en difusión (DWI). Esto es consistente con el PION bilateral. La angiografía por resonancia magnética (MRA) del cerebro y las órbitas reveló arterialización de los senos cavernosos bilaterales y de las SOVs.\n\nLa angiografía cerebral confirmó el diagnóstico de CCF durales bilaterales de drenaje anterior. La CCF dural derecha se alimentaba de las ramas durales de la ICA (tronco meningo-hipofisario derecho). La CCF dural izquierda se alimentaba de las ramas durales de la ECA (arteria meningo-hipofisaria izquierda y la arteria izquierda del foramen redondo y las ramas durales de la ICA (tronco meningo-hipofisario izquierdo). Cada lado de la CCF dural contribuía con flujo sanguíneo arterial a los SOV bilaterales (SOV contralateral a través de la comunicación inter-cavernosa). No se observó reflujo venoso cortical del flujo sanguíneo arterial. Basándose en estos hallazgos, se realizó una embolización transvenosa de la bobina. Los senos cavernosos bilaterales se embolizaron utilizando bobinas para ocluir los vasos de alimentación de las ramas durales de la ICA y la ECA. La angiografía cerebral inmediata posterior a la embolización mostró el cierre completo de las fístulas.\n\nTres meses después de la embolización, el examen oftálmico demostró una mejora progresiva de los signos oftálmicos antes mencionados; no obstante, la agudeza visual del paciente se mantuvo en NLP en ambos ojos.\n",
+        "gold_summary": "Reportamos el caso de una mujer de 62 años de edad con antecedentes de hipertensión arterial mal controlada que presentó pérdida visual bilateral súbita y cefalea durante 5 días. Negó antecedentes de traumatismo craneal. En el examen, sus agudezas visuales eran de no percepción de luz (NLP) con pupilas fijas en ambos ojos. La motilidad ocular de ambos ojos era limitada en todas las direcciones. Era difícil abrir ambos párpados. El examen del segmento anterior reveló quemosis bilateral y vasos del sacacorchos episclerales. La presión intraocular era de 45 y 48 mmHg en los ojos derecho e izquierdo, respectivamente. La gonioscopia reveló sangre en el canal de Schlemm en el ángulo nasal del ojo derecho. El examen del fondo de ojo mostró venas retinianas ligeramente dilatadas y tortuosas con discos ópticos de apariencia normal en ambos ojos. Las relaciones entre la copa y el disco eran de 0,3 bilateralmente. Otros exámenes neurológicos no presentaron anormalidades. La resonancia magnética demostró dilatación de las venas oftálmicas superiores bilaterales (SOV) y congestión orbital y periorbital bilateral marcada. Sin embargo, no hubo compresión o estiramiento de los nervios ópticos bilaterales. Se reveló una restricción de la difusión en la difusión ponderada por la difusión, con la correspondiente reducción del coeficiente de difusión aparente, en todo el segmento orbital bilateral de los nervios ópticos, consistente con PION bilateral. La angiografía por resonancia magnética reveló arterialización de los senos cavernosos bilaterales y las SOV. La angiografía cerebral confirmó el diagnóstico de CCF bilaterales de drenaje anterior. El tratamiento con embolización de bobina transvenosa fue exitoso. Tres meses después de la embolización, el examen oftálmico demostró una mejora progresiva de los signos oftálmicos antes mencionados; sin embargo, sus agudezas visuales permanecieron como NLP en ambos ojos.\n",
+        "synthetic_summary": {
+            "B1": "Una señora mayor se enfermó y no pudo ver con sus ojos. Tenía dolor en la cabeza. Sus ojos estaban muy cansados y no se movían bien. Abrir los ojos era difícil. Los ojos estaban hinchados y con vasos raros. Tenía mucha presión dentro de los ojos. Los doctores hicieron fotos especiales de su cabeza y ojos. Vieron que las venas de sus ojos estaban muy grandes y llenas de sangre. También vieron que los nervios de sus ojos estaban dañados. Encontraron un problema con las venas que llevaba sangre en su cabeza. Los doctores hicieron una operación para arreglar las venas. Después de la operación, sus ojos se veían mejor, pero ella no pudo recuperar la vista. Los doctores la cuidaron mucho y trataron de ayudarla.",
+            "B2": "**Caso de una Mujer con Pérdida Súbita de la Vista**\n\nUna mujer de 62 años, que tenía presión arterial alta sin control, comenzó a perder la vista en ambos ojos de forma repentina y también tenía dolor de cabeza durante cinco días. No había sufrido golpes en la cabeza antes.\n\n**Lo que Encontraron en el Examen**\n\nCuando la revisaron, no podía ver nada con ninguno de sus ojos y sus pupilas no reaccionaban a la luz. Además, no podía mover bien los ojos y le costaba abrir los párpados. En sus ojos había hinchazón y vasos sanguíneos con forma torcida. La presión dentro de sus ojos estaba muy alta, mucho más de lo normal. También encontraron sangre en un canal especial dentro del ojo derecho. Al mirar el fondo del ojo, las venas estaban un poco dilatadas, pero el nervio óptico parecía normal. Otros exámenes del cerebro y nervios no mostraron problemas.\n\n**Lo que Mostraron las Imágenes Médicas**\n\nUna resonancia magnética (una imagen del cerebro y ojos) mostró que las venas grandes que drenan la sangre de los ojos estaban muy dilatadas y había mucha congestión alrededor de los ojos. No había daño visible en los nervios ópticos, pero una prueba especial mostró que esos nervios tenían daño por falta de oxígeno, llamado neuropatía óptica isquémica posterior (PION), en ambos ojos. Otra imagen mostró que unas venas en el cerebro estaban recibiendo sangre de arterias, lo que no es normal.\n\n**Diagnóstico y Tratamiento**\n\nCon una angiografía cerebral (un estudio para ver los vasos sanguíneos), confirmaron que tenía fístulas carotídeo-cavernosas durales bilaterales. Esto significa que había conexiones anormales entre arterias y venas en una parte del cerebro llamada seno cavernoso, lo que causaba que la sangre fluyera mal y afectara los ojos. Para tratarlo, hicieron una embolización con bobinas, que es un procedimiento para cerrar esas conexiones anormales.\n\n**Resultado Después del Tratamiento**\n\nTres meses después, los signos de hinchazón y congestión en los ojos mejoraron, pero la mujer no recuperó la visión y seguía sin poder percibir luz en ambos ojos. Esto indica que el daño en los nervios ópticos fue muy grave y no se pudo revertir.",
+            "B3": "**Contexto**  \nSe presentó el caso de una mujer tailandesa de 62 años con antecedentes de hipertensión arterial mal controlada, quien experimentó una pérdida súbita de la visión en ambos ojos acompañada de cefalea durante cinco días. No reportó antecedentes de traumatismo craneal ni otros síntomas neurológicos adicionales.\n\n**Hallazgos Clave**  \nEn la evaluación oftalmológica inicial, la paciente tenía una agudeza visual de no percepción de luz (NLP) en ambos ojos, con pupilas fijas y motilidad ocular limitada en todas las direcciones. La apertura de ambos párpados fue dificultosa. El examen del segmento anterior mostró quemosis (hinchazón de la conjuntiva) bilateral y vasos episclerales con aspecto de “sacacorchos”, indicativos de congestión vascular. La presión intraocular estaba elevada, con valores de 45 mmHg en el ojo derecho y 48 mmHg en el izquierdo. La gonioscopia (evaluación del ángulo de drenaje ocular) reveló presencia de sangre en el canal de Schlemm del ojo derecho, lo que sugiere hemorragia en el sistema de drenaje ocular. El fondo de ojo mostró venas retinianas levemente dilatadas y tortuosas, pero los discos ópticos tenían una apariencia normal, con una relación copa-disco de 0.3 en ambos ojos, lo que indica ausencia de daño glaucomatoso avanzado. Otros exámenes neurológicos no mostraron alteraciones.\n\nLa resonancia magnética (MRI) con contraste evidenció dilatación de las venas oftálmicas superiores (SOV) en ambos ojos, junto con congestión marcada en las regiones orbital y periorbital. No se observaron signos de compresión o estiramiento de los nervios ópticos. Sin embargo, la resonancia ponderada en difusión (DWI) mostró restricción en la difusión con reducción del coeficiente de difusión aparente (ADC) en el segmento orbital bilateral de los nervios ópticos, hallazgo compatible con neuropatía isquémica óptica posterior (PION) bilateral, una lesión causada por falta de flujo sanguíneo en los nervios ópticos. La angiografía por resonancia magnética (MRA) reveló arterialización (flujo arterial anormal) de los senos cavernosos y las venas oftálmicas superiores bilaterales.\n\nLa angiografía cerebral confirmó la presencia de fístulas carotídeo-cavernosas (CCF) durales bilaterales con drenaje anterior. Estas fístulas eran alimentadas por ramas durales de la arteria carótida interna (ICA) y externa (ECA) en ambos lados, y contribuían al flujo arterial anómalo en las venas oftálmicas superiores, incluyendo comunicación entre ambos senos cavernosos. No se detectó reflujo venoso cortical, lo que indica que no había afectación directa de la circulación cerebral superficial.\n\n**Interpretación Clínica**  \nLa paciente presentó una forma rara y grave de fístulas carotídeo-cavernosas durales bilaterales que causaron congestión venosa orbital severa, elevación de la presión intraocular y daño isquémico bilateral en los nervios ópticos, manifestado como neuropatía isquémica óptica posterior. Esta condición explicó la pérdida visual súbita e irreversible, a pesar de la ausencia de compresión directa de los nervios ópticos.\n\n**Próximos Pasos y Evolución**  \nSe realizó una embolización transvenosa mediante colocación de bobinas para ocluir las fístulas en ambos senos cavernosos, logrando el cierre completo de las comunicaciones anómalas según la angiografía postprocedimiento. Tres meses después, la congestión y los signos oftálmicos mejoraron progresivamente, incluyendo la reducción del edema y la congestión vascular; sin embargo, la agudeza visual permaneció sin recuperación, con no percepción de luz en ambos ojos, reflejando daño irreversible en los nervios ópticos.\n\nEste caso destaca la importancia de un diagnóstico temprano y tratamiento oportuno en fístulas carotídeo-cavernosas para prevenir complicaciones graves como la pérdida visual irreversible por neuropatía isquémica óptica."
+        }
+    },
+    {
+        "article": "Un paciente de 15 años de edad (altura = 161 cm; peso = 66 kg; superficie corporal = 1,70; grupo sanguíneo = B positivo) con cardiomiopatía dilatada fue derivado a la Universidad de Ankara con pérdida de conciencia y shock cardiogénico en julio de 2016. El apoyo de oxigenación de membrana extracorpórea venosa arterial se realizó aproximadamente 1 semana después. Su fracción de eyección ventricular izquierda fue del 22%. Ocho días después, el paciente recibió un implante de corazón artificial total SynCardia (50 ml; SynCardia Systems, Inc., Tucson, AZ, EE. UU.). En el día 131 postoperatorio después de la cirugía TAH, el paciente se quejó de pérdida de audición bilateral y fue derivado al departamento de oído, nariz y garganta.\n\nLos antecedentes médicos previos no revelaron evidencia de pérdida auditiva, antecedentes familiares de sordera o cualquier anomalía adicional en su niñez. Sus registros médicos no revelaron evidencia de meningitis. Sin embargo, había recibido amikacina (15 mg/kg), un antibiótico ototóxico, contra patógenos gramnegativos importantes durante su estancia en la unidad de cuidados intensivos. El paciente fue incluido en la lista de espera de trasplantes de corazón de alta urgencia y era móvil en el Freedom Driver portátil (SynCardia).\n\nEl examen otoscópico del paciente fue normal. La audiometría de tonos puros y la respuesta auditiva del tronco encefálico revelaron una pérdida auditiva profunda bilateral. La timpanometría mostró timpanogramas normales de tipo A bilaterales. Tanto la tomografía computarizada como la resonancia magnética confirmaron la morfología normal del laberinto y nervios cocleares intactos.\n\nFue examinado por un equipo multidisciplinario (cirugía cardiovascular, cuidados intensivos pediátricos, cardiología pediátrica, psiquiatría de consulta y enlace, fisioterapia y rehabilitación, enfermedades infecciosas y microbiología clínica, anestesiología, audiología y otorrinolaringología) para realizar un implante coclear. Después de analizar las posibles opciones con el paciente y sus padres, se decidió que se beneficiaría de un implante coclear debido a la pérdida auditiva y la reducción de la función cognitiva y la adaptación necesaria para el trasplante de corazón. Después de analizar su caso con el equipo multidisciplinario, se decidió un implante coclear del lado derecho (Nucleus CI24RE con Contour Advance Electrode; Cochlear, Macquarie University, Australia).\n\nEl paciente tomaba warfarina (10 mg/día), que se interrumpió tres días antes de la cirugía, y se inició la heparinización (dosis de carga de 50 U/kg y dosis de mantenimiento de 20 U/kg/h) cuando el tiempo de protrombina (cociente internacional normalizado [INR]) era inferior a 1,5. Dos horas antes de la cirugía, se interrumpió la heparinización. En el quirófano, se disponía de un dispositivo de reserva para un posible fallo del dispositivo TAH. El equipo de anestesia y el perfusionista controlaron de cerca los resultados del flujo para el TAH. El flujo sanguíneo no pulsátil afecta de forma negativa al control de los signos vitales, y la presión arterial no invasiva no fue suficiente en nuestro paciente. Bajo anestesia local, se realizó un cateterismo radial arterial invasivo. Además, se dejó la vena yugular interna izquierda en su lugar, lo que permitió el control de la presión venosa central y su uso como reemplazo de fluidos de gran volumen cuando fue necesario. Después de iniciar el control, se administraron con precaución 2 mg/kg de propofol, 1 mg/kg de bromuro de rocuronio y 1 µg/kg de fentanilo, y se intubió al paciente por vía oral. Se utilizó sevoflurano con una concentración alveolar mínima de 1 a 1,5 en oxígeno al 40 % para el mantenimiento. El óxido nítrico inhalado también estaba listo para usarse en caso de una posible crisis hipertensiva pulmonar.\n\nEl día 250 después del implante TAH, se realizó la cirugía de implante coclear con abordaje de ventana redonda sin complicaciones perioperatorias; el paciente tuvo una pérdida de sangre mínima (solo 50 ml). La duración de la operación fue de 120 minutos. El paciente fue extubado en el quirófano sin problemas circulatorios y respiratorios. La heparinización se inició a la hora 6 posoperatoria. Comenzamos con la warfarina el día 1 posoperatorio, y la heparinización se detuvo después de alcanzar un INR de 2.0. No se observaron complicaciones (infecciones, hematoma) en el seguimiento posoperatorio.\n\nEl implante coclear se activó en la semana 4 después de la operación. El equipo de audiología lo revisó 4 y 8 semanas después; mostró una mejora continua en su audición, con impedancias normales. Sus resultados de percepción del habla mejoraron significativamente 3 meses después del implante coclear.\n\nMH - Adolescente\nMH - Niño\nMH - *Implantación coclear\nMH - *Insuficiencia cardiaca/diagnóstico/etiología/cirugía\nMH - *Efectos adversos del trasplante de corazón\nMH - *Corazón, Artificial\nMH - Humanos\nMH - Hombre\nMH - Resultado del tratamiento\n",
+        "gold_summary": "Describimos el caso de un niño de 15 años con pérdida auditiva total bilateral postlingual tras la administración de medicamentos ototóxicos durante su estancia en la unidad de cuidados intensivos pediátricos. El paciente recibió el implante de corazón artificial total SynCardia (50 ml; SynCardia Systems, Inc., Tucson, AZ, EE. UU.) para la insuficiencia cardiaca biventricular en fase terminal como puente para el trasplante cardiaco. Durante su estancia en la lista de espera de trasplantes cardiacos urgentes, se sometió a una implantación coclear satisfactoria tras optimizar el estado de coagulación y hemostasis y una preparación anestésica adecuada.\n",
+        "synthetic_summary": {
+            "B1": "Un niño de 15 años tuvo problemas para oír después de tomar medicinas en el hospital. Su corazón estaba muy enfermo y le pusieron un corazón artificial para ayudarlo. Mientras esperaba un nuevo corazón, le pusieron un aparato especial en el oído para que pudiera oír mejor. Los doctores cuidaron mucho que todo saliera bien en la operación. Ahora puede oír mejor y está más feliz.",
+            "B2": "**Caso de un Adolescente con Problemas del Corazón y Pérdida de Audición**\n\nUn joven de 15 años tenía un problema grave en su corazón llamado insuficiencia cardiaca biventricular, que significa que ambos lados de su corazón no funcionaban bien. Para ayudarlo mientras esperaba un trasplante de corazón, le pusieron un corazón artificial llamado SynCardia. \n\nDurante su tratamiento en cuidados intensivos, recibió un medicamento llamado amikacina, que puede dañar el oído y causar pérdida de audición. Después de un tiempo, el paciente empezó a perder la audición en ambos oídos. Los médicos hicieron varios exámenes y confirmaron que tenía una pérdida auditiva profunda en los dos oídos, aunque sus oídos y nervios estaban físicamente normales.\n\nPara mejorar su audición y ayudarlo a comunicarse mejor, el equipo médico decidió ponerle un implante coclear en el oído derecho. Un implante coclear es un dispositivo que ayuda a las personas con pérdida auditiva severa a escuchar sonidos. Antes de la cirugía, ajustaron cuidadosamente sus medicamentos para evitar problemas con la coagulación de la sangre, ya que él tomaba medicinas para el corazón que afectan esto.\n\nLa operación para colocar el implante coclear fue exitosa y sin complicaciones. Después de la cirugía, el paciente mejoró su capacidad para oír y entender el habla, lo que es muy importante para su calidad de vida y para prepararse para el futuro trasplante de corazón.\n\nEn resumen, este caso muestra cómo un adolescente con un corazón artificial y pérdida auditiva causada por medicamentos pudo recibir un implante coclear con buenos resultados, gracias al trabajo de un equipo médico especializado y una cuidadosa preparación.",
+            "B3": "**Contexto**  \nPresentamos el caso de un adolescente de 15 años con insuficiencia cardiaca biventricular avanzada, que requirió el implante de un corazón artificial total SynCardia como medida temporal mientras esperaba un trasplante de corazón. Durante su hospitalización en cuidados intensivos, recibió amikacina, un antibiótico conocido por su potencial daño al oído (ototoxicidad). Posteriormente, desarrolló una pérdida auditiva profunda bilateral, detectada aproximadamente 131 días después de la implantación del corazón artificial.\n\n**Hallazgos Clave**  \n- El paciente no tenía antecedentes previos de pérdida auditiva ni factores familiares que sugirieran sordera.  \n- Las pruebas audiológicas confirmaron una pérdida auditiva profunda en ambos oídos, mientras que los estudios de imagen mostraron estructuras normales del oído interno y nervios cocleares intactos.  \n- La evaluación multidisciplinaria concluyó que un implante coclear era la mejor opción para mejorar su audición y facilitar su adaptación cognitiva y funcional en el contexto del trasplante cardíaco.  \n- La cirugía de implante coclear se realizó con éxito, tras una cuidadosa preparación para manejar los riesgos relacionados con la anticoagulación y la función del corazón artificial.  \n- No hubo complicaciones perioperatorias significativas, y la activación del implante coclear mostró una mejora progresiva en la audición y la percepción del habla en los meses siguientes.\n\n**Interpretación Clínica**  \nEste caso ilustra cómo la ototoxicidad inducida por medicamentos puede causar una pérdida auditiva severa en pacientes críticos, incluso en adolescentes sin antecedentes previos. La coordinación entre múltiples especialidades fue fundamental para manejar los riesgos asociados a la anticoagulación y la anestesia en un paciente con un dispositivo cardíaco artificial, permitiendo una intervención auditiva efectiva que mejoró significativamente su calidad de vida y capacidad de comunicación.\n\n**Próximos Pasos**  \nSe recomienda continuar con el seguimiento audiológico y rehabilitación auditiva para maximizar los beneficios del implante coclear. Además, se debe mantener una vigilancia estrecha de la función cardíaca y del estado anticoagulante, especialmente en el contexto del trasplante cardíaco futuro. Este caso destaca la importancia de la detección temprana y el manejo multidisciplinario de las complicaciones auditivas en pacientes con enfermedades cardíacas complejas."
+        }
+    },
+    {
+        "article": "Se encontró a un hombre de 25 años de edad recostado por familiares después de una noche de fiesta, con vómitos, agresión y dolor localizado en la región glútea e inferior derecha. La evaluación inicial en el departamento de urgencias no reveló lesiones traumáticas; sin embargo, el empeoramiento de los síntomas llevó a una nueva evaluación al día siguiente. Los resultados de laboratorio revelaron un recuento sanguíneo completo sin alteraciones, niveles elevados de CPK sérica (42 527 IU/l), creatinina sérica (735 µmol/l), urea (44,3 mmol/l) y potasio (5,7 mmol/l). El análisis de orina reveló orina de color rojo-marrón sin glóbulos rojos, proteinuria (+1), glucosuria (+1) y WBC (9-10/hpf). Estos resultados confirmaron la RM y la IRA. La toxicología estableció la administración de 1796 µg/l de heroína (> 5 veces el nivel basal) sin detección de ninguna otra sustancia. Aunque inicialmente negó haber tomado medicamentos, después del análisis toxicológico, el paciente admitió que había administrado heroína una vez por vía intramuscular en la región glútea derecha la noche del incidente.\n\nUna tomografía computarizada demostró edema muscular glúteo y miositis localizada en la región glútea derecha. Al comenzar el tratamiento convencional con resucitación de fluidos intravenosos (IV), el tratamiento de la IRA fracasó, lo que hizo necesario el TRR con hemodiálisis debido a la progresión de la azotemia con un aumento de la creatinina sérica a 1052 µmol/l. La función renal mejoró tras el cese del TRR con una duración total de la estancia (LOS) de 9 días. El seguimiento posterior del paciente fue incompleto debido a la falta de asistencia.\n",
+        "gold_summary": "Este informe de caso describe a un hombre de 25 años que desarrolló una RM grave y lesión renal aguda (LRA) después de la administración intramuscular (IM) de heroína como usuario por primera vez. El uso de la heroína IM puede inducir niveles más altos de CPK debido a la toxicidad directa de los miocitos y el trauma mecánico. Los músculos glúteos altamente vascularizados con fibras tipo 1 en el sitio de la inyección probablemente exacerbaron la gravedad. Los factores adicionales incluyeron una menor densidad mitocondrial en los hombres y la exposición al alcohol. A pesar de la reanimación agresiva con líquidos, se requirió la terapia de reemplazo renal (RRT) y el paciente respondió bien a la hemodiálisis.\n",
+        "synthetic_summary": {
+            "B1": "Un hombre joven se lastimó el músculo de su nalga. Esto pasó porque se puso una medicina mala llamada heroína en esa parte. Su cuerpo se enfermó mucho y sus riñones también se lastimaron. \n\nLos doctores le dieron muchos líquidos para ayudarlo. Pero su riñón no mejoró solo. Entonces, usaron una máquina especial para limpiar su sangre. Después, el hombre empezó a sentirse mejor.",
+            "B2": "**Lo que pasó con el paciente**  \nUn hombre de 25 años usó heroína por primera vez y se la inyectó en el músculo de la nalga derecha. Después de eso, empezó a sentirse muy mal, con dolor, vómitos y agresividad. Cuando llegó al hospital, no encontraron heridas, pero sus síntomas empeoraron al día siguiente.\n\n**Qué encontraron los médicos**  \nLos análisis de sangre mostraron que tenía niveles muy altos de una enzima llamada CPK, que indica daño en los músculos. También tenía problemas en los riñones, con niveles altos de creatinina y urea, que son sustancias que el riñón normalmente limpia. La orina estaba de color rojo-marrón, pero sin sangre visible, lo que es un signo de daño muscular y renal. La tomografía mostró inflamación en el músculo de la nalga donde se inyectó la droga.\n\n**Qué significa todo esto**  \nEl hombre sufrió una condición llamada rabdomiólisis, que es cuando los músculos se dañan mucho y liberan sustancias que pueden dañar los riñones. Esto ocurrió por la inyección directa de heroína en el músculo, que causó daño tanto por la droga como por el trauma de la aguja. Además, factores como el alcohol y diferencias en el cuerpo de los hombres pueden haber empeorado la situación.\n\n**Cómo lo trataron**  \nLe dieron líquidos por vía intravenosa para ayudar a limpiar sus riñones, pero esto no fue suficiente. Por eso, tuvo que recibir un tratamiento especial llamado hemodiálisis, que es una máquina que hace el trabajo de los riñones cuando están muy dañados. Después de varios días, su función renal mejoró y pudo dejar el tratamiento.\n\n**Conclusión**  \nEste caso muestra que inyectarse heroína en el músculo puede causar un daño muscular grave y problemas serios en los riñones, incluso en personas que la usan por primera vez. Es importante buscar ayuda médica rápido si alguien presenta síntomas después de usar drogas de esta forma.",
+            "B3": "**Contexto**  \nEste caso clínico presenta a un hombre de 25 años que sufrió una lesión muscular grave conocida como rabdomiólisis (RM) y una lesión renal aguda (LRA) tras administrarse heroína por primera vez mediante una inyección intramuscular (IM) en la región glútea derecha. La rabdomiólisis es una condición en la que el daño muscular libera sustancias tóxicas en la sangre, lo que puede afectar negativamente a los riñones.\n\n**Hallazgos Clave**  \nEl paciente fue encontrado después de una noche de consumo de sustancias, con síntomas de vómitos, agresividad y dolor intenso en la zona glútea derecha. Inicialmente, no se detectaron lesiones traumáticas, pero al empeorar sus síntomas, se realizaron análisis que mostraron niveles extremadamente elevados de creatina fosfoquinasa (CPK) sérica (42,527 IU/l), un marcador que indica daño muscular severo. Además, presentó alteraciones en la función renal, evidenciadas por un aumento significativo de creatinina y urea en sangre, así como cambios en el análisis de orina, que mostraba orina de color rojo-marrón sin glóbulos rojos, proteinuria (presencia de proteínas) y glucosuria (presencia de glucosa), signos compatibles con daño renal. La toxicología confirmó una concentración elevada de heroína en sangre, y el paciente finalmente admitió haberse inyectado heroína en el glúteo la noche previa.\n\nUna tomografía computarizada reveló inflamación y edema (hinchazón) muscular en la región glútea derecha, confirmando la miositis (inflamación muscular) localizada.\n\n**Interpretación Clínica**  \nLa administración intramuscular de heroína puede causar daño muscular directo debido a la toxicidad de la droga sobre las células musculares (miocitos) y al trauma mecánico producido por la inyección. La región glútea, por su alta vascularización y predominancia de fibras musculares tipo 1 (que tienen características metabólicas específicas), probablemente contribuyó a la gravedad del daño. Además, factores como una menor densidad mitocondrial en hombres (las mitocondrias son las \"centrales energéticas\" de las células) y la exposición al alcohol podrían haber exacerbado la lesión muscular y renal.\n\nA pesar de iniciar un tratamiento convencional con líquidos intravenosos para intentar revertir la lesión renal, el daño progresó, requiriendo la implementación de terapia de reemplazo renal mediante hemodiálisis. Tras este tratamiento, la función renal del paciente mejoró, permitiendo su alta hospitalaria después de nueve días.\n\n**Próximos Pasos**  \nEl seguimiento posterior del paciente fue limitado debido a su falta de asistencia a controles médicos, lo que dificulta evaluar su recuperación a largo plazo y la prevención de complicaciones futuras. Este caso resalta la importancia de la detección temprana y el manejo adecuado de la rabdomiólisis inducida por drogas, así como la necesidad de apoyo y seguimiento continuo en pacientes con consumo de sustancias para evitar daños graves y mejorar los resultados clínicos."
+        }
+    },
+    {
+        "article": "Una mujer de 63 años con antecedentes de obesidad e hipertensión arterial acudió a la sala de urgencias de un hospital de nivel secundario con un historial de siete días de fiebre, tos seca, hiposmia y mialgia. Al momento del ingreso, se encontraba alerta, con una frecuencia respiratoria de 22 ciclos por minuto, pulso de 90 latidos por minuto y saturación de oxígeno de 90 %. Los análisis de laboratorio revelaron linfopenia (1,55 x 109) y niveles elevados de proteína C reactiva (10,62 mg/dL). Se realizó una prueba de reacción en cadena de la polimerasa para COVID-19 a partir de un hisopado nasofaríngeo y de la garganta, que resultó positivo para el coronavirus del síndrome respiratorio agudo severo 2 (SARS-CoV-2).\n\nLa situación evolucionó rápidamente con fiebre, postración y empeoramiento de la disnea. La gasometría arterial reveló una insuficiencia respiratoria grave, mientras que la radiografía de tórax evidenció infiltrados pulmonares bilaterales. La paciente fue intubada y sometida a ventilación mecánica, pero su condición respiratoria continuó deteriorándose, a pesar de los mejores cuidados críticos, incluyendo ventilación en posición prona y bloqueo neuromuscular. Su examen de tomografía computarizada del tórax, tras la intubación, reveló extensas opacificaciones multifocales bilaterales en vidrio molido, sin signos de embolia pulmonar. Los ajustes iniciales del ventilador fueron: ventilación controlada por volumen con volumen corriente de 360 ml (6 ml/kg de peso corporal ideal), frecuencia respiratoria de 14 respiraciones por minuto, presión espiratoria positiva final (PEEP) de 14 cmH2O y complacencia estática de 44 cmH2O.\n\nEn el segundo día de internación, la gasometría arterial mostró pH de 7,34, presión parcial de dióxido de carbono (PaCO2) de 53 mmHg, presión parcial de oxígeno (PaO2) de 102 mmHg y bicarbonato (HCO3) de 29,7 mmol/L, con una proporción presión parcial de oxígeno/fracción inspirada de oxígeno (PaO2/FiO2) de 98. Ella cumplía los criterios para indicación de VV-ECMO y fue transferida a la unidad de terapia intensiva (UTI), que disponía de un programa establecido para VV-ECMO. El procedimiento fue realizado con seguridad, no habiendo ocurrido complicaciones. El análisis de la gasometría arterial 3 horas después del inicio de la VV-ECMO mostró pH de 7,386, PaCO2 de 43 mmHg, PaO2 de 94,3 mmHg y HCO3 de 25,4 mmol/L, sin cualquier variación abruta de la PaCO2. Tuvieron inicio la nutrición y la rehabilitación precoces tras la introducción de la VV-ECMO. En el 14º día de internación, la paciente desarrolló neumonía asociada al ventilador causada por Pseudomonas aeruginosa, siendo sometida a 7 días de antibioticoterapia con ceftazidima y vancomicina, con respuesta favorable. En el 20º día de internación, su radiografía del tórax y la complacencia mejoraron, y la paciente fue retirada de la VV-ECMO con éxito tras 455 horas de soporte, siendo traqueostomizada 7 días después. La paciente mantuvo buena función renal durante toda la internación.\n\nEn el día 34 de internación, luego de 7 días de destete de la sedación, con evolución positiva de su cuadro neurológico, ocurrió una crisis epiléptica generalizada limitada, que llevó a la investigación diagnóstica.\n\nInvestigación\nLos análisis de sangre de laboratorio revelaron una disminución de los niveles de proteína C reactiva (6,11 mg/dL), procalcitonina (0,07 ng/mL), fibrinógeno (307 ng/mL) y ferritina (2802 ng/mL), pero un aumento en los niveles de dímero D (18021 ng/mL) e interleucina 6 (10,4 pg/mL) en el día anterior al inicio de los síntomas. No se asoció ninguno de los fármacos administrados a la paciente con el SEPR, es decir, fármacos inmunosupresores, inmunomoduladores y quimioterápicos.\n\nSe realizó una resonancia magnética (RM) del cerebro y las imágenes de recuperación de inversión atenuada por fluidos (FLAIR) demostraron una hiperintensidad simétrica y confluente que afectaba a la sustancia blanca justa y subcortical, principalmente en las regiones occipital y parietal, pero también en la región frontal, temporal y cerebelosa izquierda. Los núcleos grises profundos se conservaron y no había presencia de ninguna área con restricción del contraste. Las imágenes ponderadas por susceptibilidad mostraron múltiples microhemorragias puntiformes que afectaban a la sustancia blanca superficial y profunda, pero que no afectaban al área con hiperintensidad en FLAIR. Las microhemorragias puntiformes involucraban predominantemente a la sustancia blanca justacortical y al cuerpo calloso (especialmente el codo y el esplenio). Además, había tres hemorragias subagudas de menos de 1 cm en las cápsulas externas, con hiperintensidad en T1.\n\nLa muestra de líquido cefalorraquídeo dio negativo para SARS-CoV-2 y los niveles de proteínas (31 mg/dL), glucosa (74 mg/dL) y lactato (1,89 mmol/L) se encontraban dentro de los parámetros normales.\n\nDesvelado\nLa paciente logró una recuperación casi total de los déficits neurológicos, a pesar de la miopatía de la enfermedad crítica, y fue dada de alta después de 44 días en el hospital. Se la derivó a un hospital secundario para su rehabilitación y prácticamente recuperó su estado mental previo.\n",
+        "gold_summary": "Una mujer de 63 años de edad acudió a la sala de urgencias con un historial de fiebre aguda, postración y disnea. Se le diagnosticó un caso grave de COVID-19 y síndrome de dificultad respiratoria aguda. A pesar de recibir atención médica intensiva, cumplía con los requisitos para someterse a una oxigenación por membrana extracorpórea. El día 34, luego de siete días de haber suspendido la sedación y de que su cuadro neurológico hubiera evolucionado de manera positiva, presentó una crisis tónico-clónica generalizada limitada, que no guardaba relación con un desequilibrio hidroelectrolítico o metabólico, lo que hizo necesario realizar una investigación diagnóstica. Los estudios de imágenes cerebrales revelaron un síndrome de encefalopatía posterior reversible.\n",
+        "synthetic_summary": {
+            "B1": "Una señora muy enferma tenía fiebre y le costaba respirar. Tenía un virus que le hizo mucho daño en los pulmones. Los doctores le pusieron una máquina para ayudarla a respirar mejor.\n\nDespués de muchos días, la señora empezó a mejorar. Pero un día tuvo un problema en su cabeza que la asustó. Los doctores hicieron unas fotos especiales de su cerebro. Vieron que su cerebro estaba un poco dañado, pero podía mejorar.\n\nLa señora se puso mejor y los doctores la cuidaron mucho para que se sintiera bien otra vez.",
+            "B2": "**Lo que le pasó a la paciente**  \nUna mujer de 63 años llegó al hospital con fiebre alta, mucho cansancio y dificultad para respirar. Los médicos descubrieron que tenía COVID-19 muy grave y un problema llamado síndrome de dificultad respiratoria aguda, que afecta los pulmones y dificulta la respiración. Aunque recibió cuidados intensivos, su condición empeoró y necesitó un tratamiento especial llamado oxigenación por membrana extracorpórea (VV-ECMO). Este tratamiento ayuda a oxigenar la sangre cuando los pulmones no funcionan bien.\n\n**Qué pasó después**  \nDespués de 34 días en el hospital y tras dejar la sedación (medicamentos para dormirla) durante una semana, la paciente tuvo una crisis convulsiva, que es un movimiento fuerte y descontrolado del cuerpo. Esta crisis no se debió a problemas con líquidos o sustancias en su cuerpo, por lo que los médicos hicieron más estudios para entender la causa.\n\n**Lo que mostraron los estudios**  \nLas imágenes del cerebro mostraron un problema llamado síndrome de encefalopatía posterior reversible. Esto significa que algunas partes del cerebro estaban inflamadas o dañadas temporalmente, pero que esta condición puede mejorar con tratamiento. Gracias a la atención médica y la rehabilitación, la paciente casi recuperó completamente sus funciones cerebrales y fue dada de alta después de 44 días en el hospital.",
+            "B3": "**Contexto**  \nUna mujer de 63 años con antecedentes de obesidad e hipertensión presentó un cuadro de siete días con fiebre, tos seca, pérdida del olfato (hiposmia) y dolores musculares. Al ingresar al hospital, mostró signos de insuficiencia respiratoria leve y fue diagnosticada con COVID-19 mediante una prueba PCR. Su condición respiratoria empeoró rápidamente, desarrollando un síndrome de dificultad respiratoria aguda (SDRA) que requirió intubación y ventilación mecánica. Debido a la gravedad del compromiso pulmonar, fue sometida a oxigenación por membrana extracorpórea venovenosa (VV-ECMO), un soporte avanzado para mantener la oxigenación cuando los pulmones no funcionan adecuadamente.\n\n**Hallazgos Clave**  \nTras 34 días de hospitalización y después de haber suspendido la sedación durante una semana con mejoría neurológica, la paciente sufrió una crisis epiléptica generalizada limitada. Esta convulsión no se relacionó con alteraciones metabólicas o desequilibrios hidroelectrolíticos, por lo que se inició una investigación neurológica. La resonancia magnética cerebral mostró un patrón característico de síndrome de encefalopatía posterior reversible (SEPR), que se manifiesta por áreas de inflamación y edema en la sustancia blanca del cerebro, especialmente en regiones occipitales y parietales, sin daño permanente. Además, se detectaron microhemorragias puntiformes en la sustancia blanca, pero el líquido cefalorraquídeo no mostró infección ni inflamación activa.\n\n**Interpretación Clínica**  \nEl SEPR es una condición neurológica que puede presentarse en pacientes críticos y se caracteriza por síntomas como convulsiones, alteraciones visuales y cefalea, acompañados de cambios reversibles en el cerebro. En este caso, la aparición del SEPR después de una infección grave por COVID-19 y soporte con VV-ECMO sugiere una relación con la inflamación sistémica y posibles alteraciones vasculares inducidas por el virus o el tratamiento intensivo. La ausencia de infección directa del virus en el sistema nervioso central y la normalidad del líquido cefalorraquídeo apoyan esta hipótesis.\n\n**Próximos Pasos y Evolución**  \nLa paciente recibió tratamiento adecuado para la crisis epiléptica y cuidados de soporte neurológico. A pesar de la miopatía asociada a la enfermedad crítica, logró una recuperación casi completa de sus funciones neurológicas. Fue dada de alta tras 44 días de hospitalización y remitida a un centro de rehabilitación, donde continuó mejorando hasta recuperar prácticamente su estado mental previo al ingreso.\n\nEste caso resalta la importancia de la vigilancia neurológica en pacientes con COVID-19 grave, especialmente aquellos sometidos a terapias avanzadas como la VV-ECMO, para detectar y tratar complicaciones como el síndrome de encefalopatía posterior reversible."
+        }
+    },
+    {
+        "article": "Mujer de 65 años, originaria y residente de la Ciudad de México, con antecedente de infección por VIH de 20 años de diagnóstico con carga viral indetectable desde 2020 y con cuenta de CD4 de 1220 células por mililitro en febrero de 2022, hipotiroidismo de 29 años, cardiopatía isquémica de 9 años de diagnóstico, osteoporosis y dislipidemia, en tratamiento y bajo control médico.\n\nSu dermatosis problema se inició 10 años atrás, después de un cuadro de herpes zóster localizado en la extremidad inferior derecha y se complicó con una infección de tejidos blandos, referida como celulitis. Como secuela de este evento la paciente desarrolló úlcera, la cual ameritó corrección del defecto con 4 injertos cutáneos en diferentes tiempos quirúrgicos por cirugía plástica, con acompañamiento por parte de la clínica de heridas. Durante el seguimiento y a pesar de las medidas tomadas, no logró resolución completa y persistió con una úlcera asociada a dolor local, motivo de su envío a nuestro servicio.\n\nA la exploración física presentaba una dermatosis localizada en la extremidad inferior derecha, en la cara lateral del muslo, caracterizada por una neoformación aplanada sobre la que se asentaba una úlcera de 1.5 cm de diámetro, con fondo limpio, con costra sero-amarillenta, bordes sobreelevados, piel perilesional hiperpigmentada y queratósica, una cicatriz atrófica e hiperpigmentada. Se inició abordaje de la dermatosis mediante biopsia de piel, con reporte histopatológico de carcinoma verrugoso, por lo que se concluyó como úlcera de Marjolin asociada a carcinoma verrugoso en paciente portadora de VIH. Se canalizó al hospital de oncología para manejo con radioterapia.",
+        "gold_summary": "mujer de 65 años con el antecedente de ser portadora de infección por virus de inmunodeficiencia humana (VIH), que presentó un carcinoma verrugoso asociado a una úlcera de Marjolin secundaria a herpes zóster e infección de tejidos blandos en pierna derecha, con un periodo de latencia de 10 años desde el proceso infeccioso inicial hasta la confirmación histopatológica.",
+        "synthetic_summary": {
+            "B1": "Una señora de 65 años tuvo una herida en su pierna. La herida empezó hace mucho tiempo por una infección. La herida no sanó bien y cambió. Los doctores vieron que la herida tenía una enfermedad que puede crecer. Ella recibe ayuda para mejorar.",
+            "B2": "### Lo que pasó con la paciente\n\nUna mujer de 65 años, que vive en la Ciudad de México y tiene VIH controlado desde hace varios años, desarrolló un problema en la piel de su pierna derecha. Hace 10 años, tuvo una infección llamada herpes zóster, que afectó esa zona. Después, sufrió una infección en los tejidos blandos (la parte blanda bajo la piel), llamada celulitis. Esto causó una herida o úlcera que no sanaba bien.\n\n### Lo que encontraron\n\nA pesar de varios tratamientos, incluyendo cirugías para poner injertos de piel, la úlcera siguió abierta y le causaba dolor. Cuando la revisaron, vieron una lesión con una herida de 1.5 cm en el muslo derecho. Tomaron una biopsia, que es cuando se extrae un pequeño pedazo de piel para examinarlo bajo el microscopio. El examen mostró que la úlcera tenía un tipo de cáncer llamado carcinoma verrugoso, que es un tumor que crece lentamente y parece una verruga.\n\n### Qué significa\n\nEsta úlcera se llama úlcera de Marjolin, que es una herida crónica que puede convertirse en cáncer después de muchos años. En este caso, la úlcera apareció después de la infección por herpes zóster y la celulitis, y tardó 10 años en transformarse en cáncer. Debido a esto, la paciente fue enviada a un hospital especializado para recibir tratamiento con radioterapia, que usa rayos para destruir las células cancerosas.\n\nEn resumen, una infección antigua en la pierna causó una herida que no sanó y, con el tiempo, se convirtió en un tipo de cáncer en la piel. Por eso es importante cuidar bien las heridas que no se curan y revisarlas con el médico.",
+            "B3": "Contexto  \nSe trata de una mujer de 65 años con diagnóstico de infección por VIH desde hace 20 años, con carga viral indetectable y buen conteo de células CD4, además de otras condiciones crónicas como hipotiroidismo, cardiopatía isquémica, osteoporosis y dislipidemia, todas bajo control médico. Hace 10 años, tras un episodio de herpes zóster en la pierna derecha que se complicó con una infección de tejidos blandos (celulitis), desarrolló una úlcera en esa zona. A pesar de múltiples intervenciones quirúrgicas con injertos cutáneos y seguimiento especializado, la úlcera persistió y causó dolor local.\n\nHallazgos Clave  \nDurante la evaluación clínica, se observó una lesión en la cara lateral del muslo derecho consistente en una neoformación aplanada con una úlcera de 1.5 cm de diámetro, bordes elevados, piel circundante oscura y engrosada, y una cicatriz atrófica. La biopsia de piel reveló la presencia de un carcinoma verrugoso, que es un tipo de cáncer de piel de crecimiento lento y aspecto verrugoso (similar a una verruga). Este hallazgo confirmó que la úlcera crónica correspondía a una úlcera de Marjolin, que es una lesión maligna que puede desarrollarse en cicatrices o heridas crónicas.\n\nInterpretación Clínica  \nLa paciente presentó un carcinoma verrugoso asociado a una úlcera de Marjolin que se originó como secuela de una infección previa por herpes zóster y celulitis en la pierna derecha. El periodo de latencia entre el evento infeccioso inicial y la aparición del cáncer fue de aproximadamente 10 años. Esta condición es poco frecuente pero importante, ya que las úlceras crónicas pueden transformarse en lesiones malignas, especialmente en pacientes con factores de riesgo como el VIH.\n\nPróximos Pasos  \nLa paciente fue referida al hospital de oncología para recibir tratamiento con radioterapia, que es una modalidad adecuada para este tipo de carcinoma. Se requiere un seguimiento estrecho para evaluar la respuesta al tratamiento y prevenir complicaciones adicionales. Además, es fundamental mantener un control riguroso de sus condiciones crónicas y del estado inmunológico para optimizar su recuperación."
+        }
+    },
+    {
+        "article": "Una mujer de 90 años con hepatitis C y un historial de tabaquismo de 60 años proveniente de una zona rural presentó una hinchazón en la cara posteromedial del muslo izquierdo justo por encima de la rodilla. La hinchazón se notó por primera vez hace 3 años y aumentó gradualmente de tamaño durante este período. Ella sintió un leve malestar, pero niega cualquier síntoma asociado de dolor, picazón, secreción, fiebre o inmovilidad articular. Como provenía de una zona rural, también tenía un historial de exposición a animales.\nEn el examen físico, la hinchazón tenía una forma esférica de 14 × 10, era firme, fija y no sensible, con márgenes bien definidos en el aspecto posteromedial del muslo izquierdo, justo por encima de la rodilla. La piel que la recubría era pellizcable y mostraba venas prominentes, y la temperatura era comparable a la de la piel circundante.\nLa ecografía reveló una lesión quística grande con varios quistes pequeños en su interior, que medían 13,2 × 11 × 13,6 cm y un volumen de 1046 ml. Se originaba en la articulación de la rodilla izquierda y se extendía hasta la mitad del muslo. La ecografía Doppler en color no mostró vascularización en su interior. Se realizó una resonancia magnética que mostró una lesión quística grande (21 × 9,9 × 8,1 cm) con múltiples lesiones pequeñas dispersas, con extensión intramuscular e intermuscular que afectaban al aductor largo y al gracilis de manera medial y al bíceps femoral de manera posterior. Todas estas características eran indicativas de un quiste hidatídico. El diagnóstico se confirmó mediante una prueba de hemaglutinación para Echinococcus. La radiografía de tórax y la ecografía abdominal fueron normales.\nSe planificó la escisión quirúrgica de la tumefacción quística y se realizó una incisión en forma de S en la piel, seguida de una disección cuidadosa a través del tejido subcutáneo para acceder al quiste. La lesión estaba bien definida dentro de los planos intermuscular e intramuscular. Se realizó una disección meticulosa para aislar y extraer el quiste intacto, asegurando que no se derramara su contenido. Para minimizar el riesgo de contaminación, se irrigó a fondo el sitio quirúrgico con solución salina normal después de la escisión.\nLos hallazgos intraoperatorios revelaron una gran hinchazón quística intermuscular de 22 × 14 cm, que involucraba los compartimentos posterior y medial del muslo izquierdo. El quiste demostró extensión intramuscular hacia el aductor largo y el gracilis medialmente y hacia el bíceps femoral posteriormente, extendiéndose hasta la fosa poplítea. Cabe destacar que no había comunicación entre el quiste y la articulación de la rodilla. Una biopsia enviada al laboratorio confirmó aún más el diagnóstico. El examen histopatológico de la muestra extirpada reveló una pared quística fibrocondrogénica revestida por epitelio atenuado con infiltración inflamatoria. La presencia de material queratinoso focal caracterizó aún más la lesión. Estos hallazgos, junto con las características macroscópicas, favorecieron el diagnóstico de un quiste hidatídico. El curso postoperatorio fue sin complicaciones y el paciente fue dado de alta con una terapia antihelmíntica durante seis semanas. Se programaron visitas de seguimiento a la semana, tres semanas, seis semanas, nueve semanas y doce semanas. Durante estas visitas, el paciente no mostró signos de recurrencia o complicaciones.\n",
+        "gold_summary": "Una mujer de 90 años de edad, proveniente de una zona rural, presentó una hinchazón de crecimiento lento en el muslo posteromedial durante tres años. No tenía antecedentes de traumatismos ni síntomas sistémicos. El examen clínico reveló una masa firme y no dolorosa. Las imágenes sugieren una lesión quística, y la serología confirmó la infección por Echinococcus. Se realizó la extirpación quirúrgica, y la histopatología confirmó un quiste hidatídico. La paciente recibió un tratamiento posoperatorio de albendazol durante seis semanas. Su recuperación fue sin incidentes, sin recurrencia en el seguimiento.\n",
+        "synthetic_summary": {
+            "B1": "Había una abuela de 90 años con una bola en su muslo. La bola creció muy despacito por tres años. No le dolía ni tenía fiebre. El doctor vio que la bola era dura y no hacía daño. Hicieron unas fotos especiales y encontraron que había un bichito dentro. El doctor sacó la bola con una operación. Luego, la abuela tomó medicina para quitar el bichito. Ella se puso bien y no volvió a salir la bola.",
+            "B2": "**Lo que Encontraron**  \nUna mujer de 90 años que vivía en una zona rural notó una hinchazón en la parte trasera y media de su muslo izquierdo, justo encima de la rodilla. Esta hinchazón creció lentamente durante tres años. No tenía dolor ni otros síntomas como fiebre o enrojecimiento. Al examinarla, los médicos encontraron una masa firme y que no dolía al tocarla.\n\n**Qué Significan las Pruebas**  \nLas imágenes por ecografía y resonancia mostraron que la hinchazón era un quiste grande, que es una bolsa llena de líquido. Además, la prueba de sangre confirmó que estaba infectada por un parásito llamado Echinococcus, que puede causar un quiste hidatídico. Este tipo de quiste se forma cuando el parásito crea una bolsa en el cuerpo.\n\n**El Tratamiento y Resultado**  \nLos médicos operaron para quitar el quiste completo, con mucho cuidado para no romperlo y evitar que el parásito se esparciera. Después de la cirugía, la muestra del quiste fue analizada y confirmó el diagnóstico. La paciente tomó un medicamento llamado albendazol durante seis semanas para eliminar cualquier parásito restante. Su recuperación fue buena y no tuvo problemas ni volvió a aparecer la hinchazón en las revisiones posteriores.\n\nEn resumen, esta mujer tuvo un quiste causado por un parásito, que fue tratado con cirugía y medicina, y se recuperó sin complicaciones.",
+            "B3": "**Contexto**  \nUna mujer de 90 años, originaria de una zona rural y con antecedentes de hepatitis C y tabaquismo prolongado, consultó por una hinchazón en la parte posterior y medial del muslo izquierdo, justo por encima de la rodilla. Esta masa había aparecido hace tres años y había ido aumentando de tamaño de forma gradual. La paciente no presentaba dolor, fiebre, picazón ni otros síntomas asociados, y no refería antecedentes de traumatismos recientes. Además, tenía historial de contacto con animales debido a su entorno rural.\n\n**Hallazgos Clave**  \nEn el examen físico, se detectó una masa esférica, firme, fija y no dolorosa, de aproximadamente 14 × 10 cm, con bordes bien definidos y piel sobre la lesión que se podía pellizcar, mostrando venas prominentes pero sin aumento de temperatura local. La ecografía reveló una lesión quística grande con múltiples quistes pequeños en su interior, originada en la articulación de la rodilla y extendiéndose hacia la mitad del muslo, sin vascularización interna. La resonancia magnética confirmó estas características, mostrando además extensión intramuscular e intermuscular en músculos específicos del muslo. Estos hallazgos fueron altamente sugestivos de un quiste hidatídico (una infección parasitaria causada por el Echinococcus). La confirmación diagnóstica se realizó mediante una prueba serológica de hemaglutinación para Echinococcus. Estudios adicionales, como radiografía de tórax y ecografía abdominal, no mostraron afectación en otros órganos.\n\n**Interpretación Clínica**  \nEl diagnóstico de quiste hidatídico en el muslo, aunque poco común, fue confirmado mediante imágenes, pruebas serológicas y análisis histopatológico. La lesión representaba una masa quística con múltiples compartimentos, infiltrando tejidos musculares pero sin comunicación con la articulación de la rodilla. La histología mostró una pared quística con infiltración inflamatoria y material característico del parásito, confirmando la naturaleza hidatídica de la lesión.\n\n**Próximos Pasos y Tratamiento**  \nSe planificó y llevó a cabo la extirpación quirúrgica completa del quiste mediante una incisión en forma de S, con una disección cuidadosa para evitar la ruptura y contaminación del área. El sitio quirúrgico fue irrigado con solución salina para minimizar riesgos de diseminación. El postoperatorio transcurrió sin complicaciones, y la paciente recibió tratamiento antiparasitario con albendazol durante seis semanas para asegurar la erradicación del parásito. Se realizaron controles periódicos a las 1, 3, 6, 9 y 12 semanas posteriores a la cirugía, durante los cuales no se evidenció recurrencia ni complicaciones.\n\nEn resumen, este caso ilustra la importancia de considerar infecciones parasitarias como causa de masas quísticas en pacientes de zonas rurales, y demuestra que un abordaje quirúrgico cuidadoso combinado con terapia antiparasitaria puede conducir a una recuperación exitosa sin recurrencia."
+        }
+    },
+    {
+        "article": "Una paciente de 21 años de edad, soltera, con antecedentes de hipertensión y feocromocitoma metastásico, se presentó en nuestro hospital. Su cáncer se ha metastatizado en la vejiga, los huesos y los pulmones. También tiene un fuerte historial familiar de neoplasias, en particular de feocromocitoma. La paciente fue admitida debido a la hipertensión no controlada y los síntomas crónicos relacionados con su enfermedad.\n\nEn el ingreso (09/06/2024), la paciente era normotensa (PA: 104/66 mmHg), su frecuencia cardiaca era de aproximadamente 90 latidos por minuto, afebril a 36.9°C, y tenía una saturación de oxígeno de 99% en aire ambiente. El examen físico indicó un estado de desempeño del Grupo Cooperativo de Oncología del Este (ECOG) de 2, palidez consistente con anemia crónica, latido cardiaco regular sin murmullos o sonidos adicionales. El examen abdominal no fue notable, y no se observó edema o equimosis en las extremidades inferiores.\n\nLa paciente tiene antecedentes de hipertensión y paraganglioma, su medicación incluye (Doxazosin 2 mg, Labetalol 100 mg, Oxibutinina 5 mg, Aceite de parafina, Nifedipina 30 mg). Su historial quirúrgico incluye una adrenalectomía derecha a los diez años, y ha recibido varios tratamientos, incluidos análogos de somatostatina y radioterapia paliativa. El historial familiar revela una mutación familiar de la subunidad B de la deshidrogenasa del succinato (mutación SDBH) con un importante historial de tumores malignos endocrinos, incluidos feocromocitomas en su padre y hermana y cáncer de páncreas en su abuela.\n\nLas investigaciones de laboratorio, incluido el recuento sanguíneo completo, revelaron anemia significativa, con un nivel de hemoglobina de 7.5 g/dl. Había evidencia de hemólisis, como lo indican el alto recuento de reticulocitos, la bilirrubina indirecta y la lactato deshidrogenasa. La haptoglobina era baja. Los resultados de laboratorio se muestran en. El perfil de coagulación excluyó la coagulación intravascular diseminada (DIC), que muestra (PT: 15.6, PTT: 23.3, fibrinógeno: 489, dímero D: 0.63). La prueba de Coombs directa para excluir la anemia hemolítica autoinmune fue negativa. Los frotis de sangre periférica mostraron la presencia de esquistocitos, equinocitos y algunas células en forma de lágrima, además de trombocitopenia, todo lo cual apuntaba a la anemia hemolítica microangiopática (MAHA). Dado el contexto del cáncer metastásico, el paciente fue diagnosticado con anemia hemolítica microangiopática paraneoplásica en marzo/2024.\n\nEl paciente fue programado para el protocolo CVD (ciclofosfamida, vincristina y doxorrubicina), pero sin ciclofosfamida debido al efecto inductor de anemia de los agentes alquilantes. El paciente recibió un total de 5 ciclos. Como indicador de respuesta clínica, el paciente ya no experimentó anemia o trombocitopenia. Un nuevo frotis de sangre periférica reveló células normales, lo que sugiere una respuesta clínica al MAHA que coincide con la mejora de la neoplasia subyacente. Esto se alinea con la definición de MAHA como un síndrome paraneoplásico.\n\nLos medicamentos que se le suministran al paciente al momento del alta son: comprimidos de dexametasona de 2 mg, 4 mg por vía oral (PO) una vez al día (OD) durante 3 días, comprimidos de ondansetrón de 8 mg por vía oral (PO) una vez al día (OD) durante 3 días, comprimidos de metoclopramida de 10 mg por vía oral (PO) tres veces al día durante 3 días, calcio de 600 mg con vitamina D por vía oral (PO) una vez al día (OD) durante 1 día, comprimidos de labetalol de 100 mg por vía oral (PO) dos veces al día durante 1 día, comprimidos de doxazocina de 2 mg por vía oral (PO) dos veces al día durante 1 día, comprimidos de citalopram de 20 mg por vía oral (PO) durante 1 día, comprimidos de omeprazol de 20 mg, 40 mg por vía oral (PO) durante 1 día, comprimidos de paracetamol de 500 mg, 1000 mg por vía oral (PO) dos veces al día durante 1 día, cápsulas de aprepitant de 125 mg/80 mg, 1 cápsula por vía oral (PO) dos veces al día durante 3 días (con prescripción médica).\n\nEl paciente fue objeto de seguimiento el 01/07/2024, y su aspecto clínico era bueno y activo. El paciente se sometió a exámenes de laboratorio que incluían un recuento sanguíneo completo (WBC 6.59 10e3/ul, RBC 4.47 × 10^6/ul, HGB 13.2 g/dl, 40.0%, MCV 89.4 fL, PLT 41.5 10e3/ul), nitrógeno ureico en sangre 33.8 mg/dl, creatina cinasa-MB 36.1 u/l, creatinina sérica 0.97 mg/dl, cloruro 101.5 mmol/l, potasio 4.52 mmol/l, sodio 135 mmol/l.\n",
+        "gold_summary": "En este informe de caso, presentamos a una mujer soltera de 21 años con un fuerte historial familiar de neoplasia endocrina. Fue derivada a nuestro hospital para quimioterapia debido a un diagnóstico de feocromocitoma maligno, que había hecho metástasis en la vejiga urinaria, los huesos y los pulmones. Además, desarrolló anemia hemolítica microangiopática como un síndrome paraneoplásico.\n",
+        "synthetic_summary": {
+            "B1": "Esta es la historia de una joven de 21 años. Ella tiene un tipo de enfermedad que hace que su cuerpo tenga bultos malos. Estos bultos están en partes como la vejiga, los huesos y los pulmones. También, su sangre estaba muy débil y no estaba bien. Los doctores le dieron medicinas para ayudarla a mejorar. Ahora, ella está más fuerte y se siente mejor.",
+            "B2": "### Caso de una joven con cáncer y anemia especial\n\nPresentamos la historia de una mujer de 21 años que tiene un tipo de tumor llamado feocromocitoma maligno. Este tumor se originó en sus glándulas suprarrenales y se ha extendido a otros órganos, como la vejiga, los huesos y los pulmones. Además, su familia tiene antecedentes de tumores similares, lo que indica que puede haber una causa genética.\n\n### Qué le pasó a la paciente\n\nLa paciente también desarrolló un problema en la sangre llamado anemia hemolítica microangiopática. Esto significa que sus glóbulos rojos se destruyen más rápido de lo normal debido a pequeños daños en los vasos sanguíneos. Esta anemia está relacionada con su cáncer y se llama síndrome paraneoplásico, porque ocurre como una consecuencia del tumor, aunque no sea directamente causado por él.\n\n### Tratamiento y evolución\n\nElla recibió quimioterapia adaptada para evitar empeorar la anemia. Después de varios ciclos, su sangre mejoró y ya no tenía signos de anemia ni problemas en las células sanguíneas. Esto muestra que el tratamiento ayudó tanto al cáncer como a la anemia causada por él.\n\nEn resumen, este caso muestra cómo un cáncer puede afectar otras partes del cuerpo, como la sangre, y cómo un tratamiento adecuado puede mejorar la salud general de la paciente.",
+            "B3": "**Contexto**  \nSe trata de una mujer joven de 21 años con antecedentes familiares significativos de tumores endocrinos malignos, en particular feocromocitomas (tumores que producen hormonas y se originan en las glándulas suprarrenales o tejidos relacionados). La paciente fue ingresada en el hospital debido a un feocromocitoma metastásico, es decir, un tumor maligno que se ha extendido a otros órganos, incluyendo la vejiga, los huesos y los pulmones. Además, presentaba hipertensión arterial difícil de controlar y síntomas relacionados con su enfermedad avanzada.\n\n**Hallazgos Clave**  \nDurante su hospitalización, se detectó que la paciente tenía anemia severa causada por un proceso llamado anemia hemolítica microangiopática (MAHA). Esta condición implica la destrucción acelerada de glóbulos rojos debido a daños en los pequeños vasos sanguíneos, y en este caso se relaciona directamente con su cáncer avanzado, constituyendo un síndrome paraneoplásico (un efecto indirecto del tumor sobre el organismo). Los análisis de sangre mostraron anemia significativa, signos de destrucción de glóbulos rojos (como aumento de reticulocitos y bilirrubina indirecta), y alteraciones en el frotis sanguíneo que confirmaron la presencia de células fragmentadas características de MAHA.\n\n**Interpretación Clínica**  \nLa anemia hemolítica microangiopática en esta paciente se considera una complicación secundaria al feocromocitoma metastásico, reflejando la gravedad y la actividad del tumor. El tratamiento con quimioterapia adaptada (excluyendo ciertos fármacos que podrían empeorar la anemia) logró controlar tanto la anemia como la progresión del cáncer, evidenciado por la normalización de los parámetros sanguíneos y la desaparición de las células anormales en el frotis. Esto confirma la relación directa entre la actividad tumoral y la anemia hemolítica.\n\n**Próximos Pasos**  \nLa paciente fue dada de alta con un régimen farmacológico para manejar sus síntomas y prevenir complicaciones, incluyendo corticosteroides, medicamentos para controlar la presión arterial, antieméticos y suplementos. En el seguimiento posterior, mostró una mejoría clínica significativa, con parámetros sanguíneos dentro de rangos normales y un estado general activo y estable. Continuará bajo vigilancia estrecha para monitorear la evolución de su enfermedad y ajustar el tratamiento según sea necesario."
+        }
+    }
+]
\ No newline at end of file
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new file mode 100644
index 0000000000000000000000000000000000000000..9efe8be8fe322336f3412cd0370a89620e6c100a
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@@ -0,0 +1,902 @@
+[
+    {
+        "article": "Une femme de 80 ans, qui était évaluée pour une perte de poids involontaire importante, a été admise au service des urgences en raison de vomissements et de l'apparition soudaine de douleurs aiguës dans sa cuisse droite. Les douleurs étaient constantes et s'aggravaient avec le mouvement. L'examen clinique a révélé un point très sensible dans la région médiale proximale de sa cuisse droite. Il n'y avait aucune indication de traumatisme.\n\nLa patiente a été envoyée pour une radiographie de la hanche droite afin d'examiner une éventuelle fracture pathologique. Aucune fracture ou désalignement n'a été observé, et elle a été admise au service d'orthopédie pour la gestion de la douleur et la mobilisation. Elle a été renvoyée le jour suivant malgré une douleur persistante et des vomissements. Le troisième jour, la patiente a été réadmise au service des urgences avec les mêmes symptômes. Elle était apyrexique, mais en raison de marqueurs d'infection légèrement élevés, de leucocytes à 13,5 × 109/L (fourchette de référence 4,1–9,8 × 109/L) et de CRP à 60 mg/L (< 5 mg/L), une radiographie thoracique a été réalisée, révélant des consolidations confluentes basales dans le poumon droit, soulevant des soupçons d'infiltration pneumonique. La patiente a été transférée au service médical pour observation. Les antibiotiques n'ont pas été initiés en raison de symptômes respiratoires minimes.\n\nLe quatrième jour, l'état de la femme s'est détérioré, avec une tachycardie (rythme cardiaque de 119 bpm), une fréquence respiratoire de 28 respirations par minute (plage normale : 12-16), et une fièvre de 38,1 °C. Son taux de CRP a également augmenté de 50 à 250 mg/L. La pipéracilline-tazobactam a été initiée par voie intraveineuse à une dose ajustée au poids de 2 g x 4, et elle a été envoyée pour une tomodensitométrie du thorax/abdomen/pelvis en raison d'une suspicion de septicémie d'origine abdominale. La tomodensitométrie a révélé une boucle intestinale emprisonnée qui dépassait le canal obturateur droit et une dilatation intestinale pré-obstructive, compatible avec une hernie obturatrice aiguë irréductible. Le chirurgien de garde a été rapidement consulté, et la patiente a été programmée pour une chirurgie d'urgence.\n\nPendant la laparoscopie sous anesthésie générale, une petite boucle intestinale emprisonnée a été découverte dans le canal obturateur, ce qui correspond aux résultats de la tomodensitométrie. L'intestin a été réduit avec précaution, sans signe de nécrose ou de perforation. Après la réduction de la hernie, la patiente a présenté une hypotension, avec une tension artérielle de 98/37 mmHg. L'analyse des gaz artériels intraopérative a montré un pH de 7,22 (7,36-7,44), une PCO2 (a) de 7,0 (4,7-6,0 kPa), une PO2 (a) de 15,0 (> 8,7 kPa), un HCO3 de 19 (22-26 mmol/L), un excès de base de -6,6 (1,9-4,5 mmol/L), un Cl de 104 (98-107 mmol/L), et un lactate de 1,0 (0,4-1,3 mmol/L), ce qui correspond à une acidose respiratoire et métabolique mixte. L'hypercapnie était présumée être causée par l'absorption périopérative de gaz CO2 insufflé du péritoine dans le réseau capillaire. Une perfusion de norépinéphrine a été initiée à 0,04 mcg/kg/min, et la ventilation minute a été augmentée pour corriger l'acidose. Le segment de l'intestin grêle réduit a été réévalué et a été considéré comme encore viable, sans besoin de résection. Le défaut de hernie a été fermé avec des sutures primaires en utilisant une suture barbelée non absorbable, sans noeud (V-Loc) pour minimiser le temps de chirurgie en raison de la détérioration de l'état du patient.\n\nLa patiente a été extubée immédiatement après l'opération et a été observée dans l'unité de soins intensifs jusqu'au jour suivant. Les vasopresseurs et un tube nasogastrique de décompression ont été retirés le premier jour postopératoire. Elle a ensuite été transférée dans le service de chirurgie. La fonction intestinale a repris le deuxième jour postopératoire. Les antibiotiques ont été arrêtés le troisième jour postopératoire. Le même jour, elle a également été transférée dans le service de médecine pour une évaluation plus approfondie de sa perte de poids.",
+        "gold_summary": "Une femme de 80 ans ayant des antécédents de perte de poids involontaire s'est présentée au service des urgences en raison de douleurs aiguës dans la cuisse droite, de nausées et de vomissements. À l'examen, la patiente a présenté une sensibilité à la palpation dans la partie proximale et médiale de la cuisse droite. La tomographie par ordinateur abdominale a révélé une boucle de l'intestin grêle saillie dans le canal obturateur droit, compatible avec une hernie obturatrice incarnée. Une laparoscopie d'urgence a été réalisée, révélant que le segment de l'intestin grêle affecté était viable après réduction de la hernie. En raison du développement d'une acidose respiratoire et d'une hypotension, le défaut obturateur a été principalement suturé pour réduire le temps d'opération. La patiente a bien récupéré et a été transférée au service médical pour une évaluation plus approfondie de sa perte de poids.\n",
+        "synthetic_summary": {
+            "B1": "Une dame de 80 ans avait très mal à la cuisse droite. Elle avait aussi envie de vomir. Le docteur a regardé sa cuisse et elle faisait très mal quand on touchait.\n\nLe docteur a fait une photo spéciale de son ventre. Il a vu que un petit bout de son ventre était coincé dans un trou. C’est ce qu’on appelle une hernie.\n\nElle a eu une petite opération pour remettre le ventre à sa place. Après, elle est allée mieux. Le docteur a fermé le trou vite pour que l’opération ne dure pas trop longtemps.\n\nAprès l’opération, elle a bien récupéré. Elle est allée dans un autre service pour qu’on regarde pourquoi elle avait perdu du poids. Tout va mieux maintenant.",
+            "B2": "Une femme de 80 ans a été amenée aux urgences parce qu’elle avait une douleur forte et soudaine dans la cuisse droite, ainsi que des nausées et des vomissements. Lors de l’examen, les médecins ont trouvé une zone très sensible à toucher sur la partie haute et intérieure de sa cuisse droite. Une tomodensitométrie (un examen qui utilise des rayons X pour voir à l’intérieur du corps) a montré qu’une petite partie de son intestin grêle était coincée dans un passage osseux appelé canal obturateur, ce qui correspond à une hernie obturatrice bloquée.\n\nLes médecins ont fait une opération appelée laparoscopie, qui consiste à utiliser une petite caméra pour réparer la hernie sans ouvrir complètement le ventre. Ils ont réussi à remettre l’intestin en place et ont vu qu’il n’était pas abîmé. Pendant l’opération, la patiente a eu des problèmes de respiration et une baisse de tension, alors les chirurgiens ont fermé la hernie rapidement avec des points pour que l’intervention soit courte. Après l’opération, elle s’est bien remise et a été transférée dans un service médical pour comprendre pourquoi elle avait perdu beaucoup de poids avant.",
+            "B3": "Contexte  \nUne femme de 80 ans, présentant une perte de poids involontaire importante, s’est présentée aux urgences avec des vomissements et une douleur aiguë soudaine au niveau de la cuisse droite, localisée principalement dans la région médiale proximale. Cette douleur était constante et s’aggravait lors des mouvements. Aucun traumatisme n’a été rapporté.  \n\nPrincipales Observations  \nL’examen clinique a révélé une sensibilité marquée à la palpation de la cuisse droite. Une radiographie initiale de la hanche droite n’a montré ni fracture ni anomalie osseuse. Malgré une prise en charge orthopédique, les symptômes ont persisté, accompagnés de vomissements. Lors d’une réadmission, des signes biologiques d’inflammation ont été notés, avec une augmentation des leucocytes et de la protéine C-réactive (CRP). Une radiographie thoracique a suggéré une possible infection pulmonaire, mais sans symptômes respiratoires majeurs, les antibiotiques n’ont pas été débutés.  \n\nLe quatrième jour, l’état général s’est aggravé avec apparition de fièvre, tachycardie et augmentation significative de la CRP. Une tomodensitométrie (TDM) thoraco-abdomino-pelvienne a révélé une hernie obturatrice aiguë irréductible, caractérisée par une boucle intestinale emprisonnée dans le canal obturateur droit, avec une dilatation intestinale en amont, signe d’obstruction.  \n\nIntervention et prise en charge  \nUne chirurgie d’urgence par laparoscopie a été réalisée. L’intestin grêle emprisonné a été réduit sans signe de nécrose ni perforation, confirmant la viabilité du segment intestinal. Pendant l’intervention, la patiente a développé une hypotension et une acidose mixte respiratoire et métabolique, probablement liée à l’absorption peropératoire de dioxyde de carbone insufflé dans la cavité péritonéale. Une perfusion de norépinéphrine a été mise en place et la ventilation ajustée pour corriger l’acidose.  \n\nLe défaut herniaire a été fermé rapidement par une suture primaire à l’aide d’un fil barbelé non résorbable, afin de limiter la durée opératoire compte tenu de la dégradation de l’état clinique.  \n\nÉvolution et suivi  \nLa patiente a été extubée immédiatement après l’opération et surveillée en unité de soins intensifs. Les vasopresseurs et la sonde nasogastrique ont été retirés dès le premier jour postopératoire. La reprise du transit intestinal a eu lieu au deuxième jour, et les antibiotiques ont été arrêtés au troisième jour. La patiente a ensuite été transférée en service de médecine pour poursuivre l’évaluation de sa perte de poids initiale.  \n\nRésumé  \nCette patiente âgée a présenté une hernie obturatrice aiguë, une pathologie rare et difficile à diagnostiquer, responsable d’une obstruction intestinale et de douleurs atypiques à la cuisse. Le diagnostic a été confirmé par tomodensitométrie, et la prise en charge chirurgicale urgente a permis la réduction de la hernie sans complication intestinale majeure. La gestion attentive des complications peropératoires a contribué à une récupération favorable. Une investigation complémentaire est en cours pour comprendre l’origine de sa perte de poids."
+        }
+    },
+    {
+        "article": "Février 2020, un homme de 36 ans sans antécédents médicaux significatifs a présenté une masse pénos-scrotale gauche datant de 5 ans. Il n'a pas de symptômes du tractus urinaire inférieur. Il n'a pas d'antécédents de traumatisme ou d'infections et a nié toute histoire de perte de poids, d'anorexie ou de fièvre. À l'examen, il y a une surface lisse, une lésion kystique tendre d'environ 20 mm * 20 mm attachée au côté gauche de l'urètre bulbaire à la jonction pénos-scrotale, elle était profonde sans aucune traction de la peau et n'était pas liée au cordon spermatique gauche et elle était partiellement mobile.\n\nL'échographie Doppler a montré une masse hypoéchogène bien définie mesurant 2,7 * 3,1 * 2,0 cm avec une vascularisation significativement accrue à gauche de la jonction péno-scrotale. L'imagerie par résonance magnétique du bassin a révélé une masse dans le côté inféro-latéral gauche de la base du pénis avec un plan de graisse clair, qui est isointense aux testicules dans l'imagerie pondérée en T2, l'imagerie pondérée en T1 et l'imagerie pondérée en diffusion et elle était reliée au canal déférent, aucune lymphadénopathie n'a été notée. Les taux d'alpha-foetoprotéine et de bêta-gonadotrophine humaine étaient tous dans la plage normale. Compte tenu des résultats de l'examen et de la douleur ressentie par le patient, il a été décidé de procéder à l'ablation chirurgicale de la masse à des fins diagnostiques et thérapeutiques. Au cours de l'opération, une masse a été vue dans le côté postéro-latéral gauche du scrotum et elle a été complètement réséquée et envoyée pour l'histopathologie.\n\nL'histopathologie de la masse a montré un tumeur à cellules fusiformes disposées en faisceaux interlacés, les cellules ont des noyaux vésiculaires fusiformes à chromatine uniformément dispersée et des nucléoles peu visibles. La tumeur a montré une activité mitotique élevée atteignant 3/champ de haute puissance. L'analyse immunohistochimique était cohérente avec un sarcome synovial, révélant un TLE-1, CD99, lymphome à cellules B 2 (BLC2), cytokératine focale et antigène membranaire épithélial focal (EMA) positifs. Le matériel a été envoyé pour une hybridation in situ par fluorescence (FISH) et a révélé un réarrangement du gène SS18 à 18q11.2, qui a été observé dans les sarcomes synoviales. Les marges de la masse étaient difficiles à évaluer par histopathologie, car l'échantillon avait des marges fragmentées.\n\nLe patient s'est présenté à la clinique après 2 semaines et, après avoir reçu le rapport d'histopathologie, une ré-excision avec une marge plus large a été discutée avec le patient et il a accepté. Une tomographie par émission de positrons - tomographie par ordinateur (PET/CT) a été réalisée pour la tête et le cou, la poitrine, l'abdomen, le pelvis et les structures musculo-squelettiques. Seul un nodule thyroïdien de 29 * 27 mm dans le pôle inférieur du lobe thyroïdien gauche avec un hypermétabolisme modéré à des valeurs d'absorption standardisées (SUV) de 4,9. L'échographie thyroïdienne a montré un nodule solide isoéchogène bien défini dans le pôle inférieur du lobe thyroïdien gauche sans foyers échogènes. Le rapport d'imagerie et de données du système de thyroïde (TIRADS) était TR3.\n\nUne deuxième résection a été réalisée 3 semaines après la première. L'échantillon entier a été résectionné des deux cordes bilatéralement, ce qui a été approfondi jusqu'à atteindre le corps spongieux, qui a été rasé en haut jusqu'à l'urètre. L'échantillon a été envoyé pour une histopathologie. La masse résectionnée mesurait 6,0 × 6,0 × 3,0 cm et était négative pour toute pathologie. Le patient a ensuite été placé sous surveillance active et après 16 mois de surveillance active, il a été trouvé porteur de lésions métastatiques dans le sixième segment du foie et le corps vertébral L1. L'équipe d'oncologie a commencé un régime de chimiothérapie d'ifosfamide et de doxorubicine pendant 6 cycles sans amélioration de la lésion du foie. Une résection chirurgicale a été réalisée pour les cinquième et sixième sections du foie avec cholécystectomie. Le patient a ensuite développé une nouvelle lésion pulmonaire et a commencé un traitement par pazopanib et une radiothérapie stéréotaxique du corps. Le patient a ensuite été soumis à une surveillance pendant 6 mois, puis a développé de nouvelles lésions du foie et des poumons, puis un régime de chimiothérapie de gemcitabine et de docétaxel pour 3 cycles et a progressé, puis a commencé 2 cycles de dacarbazine et a progressé, puis 2 cycles de pembrolizumab et a progressé. Le patient a ensuite été transféré en soins palliatifs et a cessé de suivre le traitement.\n",
+        "gold_summary": "Un homme de 36 ans a présenté une masse péno-scrotale tendre pendant 5 ans. Le patient a subi une résection chirurgicale de la masse. L'histopathologie a révélé une tumeur à cellules fusiformes organisées en faisceaux entrelacés. L'analyse immunohistochimique a révélé un TLE-1, CD99, lymphome à cellules B 2 (BLC2), cytokératine focale et antigène membranaire épithélial focal (EMA) positifs. Dans notre cas, le patient a été agressivement traité avec deux résections chirurgicales et a malgré tout progressé et a métastasé et a continué à progresser même après différents régimes de chimiothérapie.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur avait une grosse boule douce près de son pantalon depuis longtemps. Les docteurs ont enlevé cette boule avec une opération. Ils ont regardé la boule au microscope et ont vu que c’était une maladie avec des petites cellules. \n\nMême après deux opérations et plusieurs médicaments, la maladie n’est pas partie. Elle s’est même déplacée dans d’autres parties du corps. Les docteurs ont essayé beaucoup de traitements, mais la maladie a continué à grandir.",
+            "B2": "**Ce qu'ils ont trouvé**  \nUn homme de 36 ans avait une grosseur douloureuse entre le pénis et le scrotum depuis 5 ans. Les médecins ont enlevé cette masse grâce à une opération. En regardant la masse au microscope, ils ont vu qu’elle était faite de cellules allongées organisées en faisceaux. Pour mieux comprendre de quel type de tumeur il s’agissait, ils ont fait des tests spéciaux qui ont montré la présence de certaines protéines (comme TLE-1, CD99, BCL2, cytokératine et EMA). Ces résultats ont permis de diagnostiquer un sarcome synovial, un type rare de cancer des tissus mous.\n\n**Ce que cela signifie**  \nMalgré deux opérations pour enlever la tumeur, le cancer a continué à se développer et à se propager dans d’autres parties du corps, comme le foie et les poumons. Le patient a reçu plusieurs traitements de chimiothérapie différents, mais aucun n’a réussi à arrêter la progression de la maladie. Finalement, il a dû arrêter les traitements actifs et passer en soins palliatifs, qui visent à soulager les symptômes et améliorer la qualité de vie.\n\n**Résumé**  \nCe cas montre qu’un sarcome synovial peut être difficile à traiter, même avec des opérations et plusieurs chimiothérapies. Il est important de surveiller attentivement les patients après le traitement, car ce cancer peut revenir ou se propager rapidement.",
+            "B3": "Résumé détaillé et structuré\n\nContexte  \nUn homme de 36 ans, sans antécédents médicaux notables, a consulté pour une masse péno-scrotale gauche, présente depuis environ cinq ans. Cette masse était indolore au repos, mais sensible à la palpation, située à la jonction entre le pénis et le scrotum, sans symptômes urinaires associés ni signes généraux tels que fièvre ou perte de poids. Les examens cliniques et d’imagerie (échographie Doppler et IRM pelvienne) ont montré une masse bien délimitée, vascularisée, attachée au canal déférent, sans atteinte ganglionnaire ni anomalies biologiques tumorales.\n\nPrincipales observations  \nLa masse a été retirée chirurgicalement pour établir un diagnostic précis et soulager le patient. L’analyse histopathologique a révélé une tumeur composée de cellules fusiformes (allongées) organisées en faisceaux entrelacés, avec une activité mitotique élevée, signe d’une prolifération cellulaire rapide. L’étude immunohistochimique a montré la présence de marqueurs caractéristiques (TLE-1, CD99, BCL2, cytokératine focale et antigène membranaire épithélial focal) compatibles avec un sarcome synovial, une forme rare de cancer des tissus mous. Une analyse génétique par hybridation in situ (FISH) a confirmé la présence d’un réarrangement du gène SS18, typique de ce type de sarcome. Les marges chirurgicales initiales étaient fragmentées, rendant difficile l’évaluation complète de l’exérèse.\n\nInterprétation clinique  \nAprès discussion, une seconde intervention chirurgicale avec élargissement des marges a été réalisée. Un bilan d’extension par TEP-TDM a révélé un nodule thyroïdien sans signe évident de malignité. La résection secondaire a permis d’enlever la totalité de la masse sans tissu tumoral résiduel. Malgré ces interventions, le patient a développé, 16 mois plus tard, des métastases hépatiques et vertébrales. Plusieurs lignes de chimiothérapie ont été administrées (ifosfamide/doxorubicine, gemcitabine/docétaxel, dacarbazine) ainsi que des traitements ciblés (pazopanib) et une radiothérapie stéréotaxique, mais la maladie a continué à progresser. Une immunothérapie par pembrolizumab a également été tentée sans succès. Face à cette évolution défavorable, le patient a été orienté vers des soins palliatifs.\n\nProchaines étapes  \nCe cas illustre la nature agressive et la difficulté de prise en charge des sarcomes synoviaux localisés dans la région péno-scrotale, malgré une prise en charge chirurgicale complète et des traitements médicaux multiples. La surveillance attentive et la prise en charge multidisciplinaire restent essentielles. De nouvelles approches thérapeutiques sont nécessaires pour améliorer le pronostic de ce type de tumeur rare et agressive."
+        }
+    },
+    {
+        "article": "Une Chinoise de 30 ans a présenté une masse ovarienne gauche lors d'un examen physique de routine. Elle était asymptomatique et n'avait pas d'antécédents médicaux de tumeurs cérébrales ou de troubles neurologiques. La patiente souffrait d'ovaires polykystiques à l'âge de 19 ans sans aucun traitement. Les taux sériques de CEA, CA125 et CA19-9 étaient dans les limites normales.\n\nUne IRM a révélé une lésion hypointense pondérée en T1 et hyperintense pondérée en T2 mesurant 6,3 × 4,8 cm dans la région adnexale gauche, avec un nodule de fixation mural à signal légèrement inférieur. En outre, l'image pondérée en diffusion (DWI) a montré un signal isointense des nodules muraux. Par conséquent, il a été considéré comme une tumeur bénigne ou limite.\n\nLa patiente a subi une résection laparoscopique de l'ovaire gauche et de la trompe de Fallope. Au cours des 12 mois de suivi, elle a subi des examens d'échographie pelvienne et abdominale tous les trois mois, et aucune anomalie n'a été détectée. Elle est restée en bonne condition après la chirurgie sans chimiothérapie.\n\nConstatations pathologiques\nL'examen macroscopique a révélé une masse kystique de 5 × 3,5 × 1 cm dans l'ovaire gauche. Deux nodules muraux de 0,8 cm et 1,2 cm de diamètre ont été observés, de couleur rouge-gris et de texture molle. L'examen histologique a révélé un nodule bien défini sous faible grossissement. Les composants du tératome comprenaient l'épiderme, des appendices cutanés étaient visibles dans le nodule mural environnant et le tissu de la paroi du kyste. Sous fort grossissement, il a révélé des cellules gliales désordonnées et des ganglions proliférant dans le nodule mural. Des ganglions anormaux ont été agrégés, avec un noyau de grande taille et irrégulier, qui présentait également des nucléoles évidents, et des cellules binucléées ont été observées. Les figures mitotiques ont été difficilement identifiées.\n\nImmunohistochimiquement, les cellules gliales étaient positives pour GFAP et Olig2. Les cellules ganglionnaires étaient positives pour Neu-N, CgA, Nestin et CR. En outre, les cellules ganglionnaires exprimaient CD34 et mettaient en évidence les cellules tumorales ramifiées. Une faible expression de NSE et une expression de P53 de type sauvage ont été observées dans certaines cellules tumorales. En outre, les cellules tumorales étaient négatives pour IDH1 et BRAF V600E. L'indice Ki67 était d'environ 5 %. Sur la base de ces résultats, un diagnostic de gangliogliome résultant d'un tératome kystique mature ovarien a été établi.\n",
+        "gold_summary": "La patiente, une femme de 30 ans sans antécédents médicaux de tumeurs cérébrales ou de troubles neurologiques, a présenté une masse kystique dans l'ovaire gauche, accompagnée de deux nodules muraux. D'un point de vue histologique, le nodule mural du tératome présentait une combinaison de cellules ganglionnaires et gliales néoplasiques. Notamment, les cellules ganglionnaires présentaient une binucléation et une distribution focale, avec la présence occasionnelle de corps de Nissl. Immunohistochimiquement, GFAP et Olig2 étaient positifs dans les cellules gliales, la chromogranine A (CgA), Nestin, CD34, Neu-N et Calretinin (CR) étaient positifs dans les cellules ganglionnaires. Les cellules tumorales présentaient un faible indice Ki67, une expression de P53 de type sauvage et étaient négatives pour IDH1 et BRAF V600E. La patiente a subi une résection laparoscopique de l'ovaire gauche et de la trompe de Fallope et elle était en bonne condition à 12 mois de suivi.\n",
+        "synthetic_summary": {
+            "B1": "Une dame de 30 ans avait une grosseur dans son ventre, près de son os de la cuisse. Elle n’avait pas mal et ne se sentait pas malade. \n\nLes docteurs ont enlevé cette grosse boule avec une petite opération. Ils ont regardé la boule au microscope. Ils ont vu des petites cellules différentes à l’intérieur. \n\nAprès l’opération, la dame allait très bien. Elle n’avait plus de problème et elle était contente.",
+            "B2": "**Ce qu'ils ont trouvé**  \nUne femme de 30 ans, sans problème de santé lié au cerveau ou aux nerfs, avait une grosseur dans son ovaire gauche. Cette grosseur était un kyste (une sorte de poche remplie de liquide) avec deux petits nodules sur sa paroi. En regardant ces nodules au microscope, les médecins ont vu deux types de cellules : des cellules gliales (qui soutiennent les cellules nerveuses) et des cellules ganglionnaires (des cellules nerveuses importantes). Certaines cellules ganglionnaires avaient deux noyaux, ce qui est inhabituel, et on a aussi vu des structures appelées corps de Nissl, qui sont normales dans ces cellules.\n\n**Comment ils ont confirmé le diagnostic**  \nPour mieux comprendre ces cellules, ils ont utilisé une technique appelée immunohistochimie. Cela consiste à utiliser des marqueurs spéciaux qui collent à certaines protéines dans les cellules. Ils ont trouvé que les cellules gliales étaient positives pour GFAP et Olig2, des protéines spécifiques à ce type de cellules. Les cellules ganglionnaires montraient des protéines comme la chromogranine A, Nestin, CD34, Neu-N et Calrétinine, qui sont typiques des cellules nerveuses. De plus, les cellules tumorales avaient un faible taux de division (indiqué par un faible indice Ki67) et une expression normale de la protéine P53, ce qui est un bon signe. Elles ne présentaient pas certaines mutations souvent liées à des cancers (IDH1 et BRAF V600E étaient négatifs).\n\n**Ce que cela signifie pour la patiente**  \nLe diagnostic final était un gangliogliome, c’est-à-dire une tumeur composée de cellules nerveuses et gliales, qui s’est développée à partir d’un tératome kystique mature de l’ovaire. Un tératome est une tumeur qui peut contenir différents types de tissus, comme de la peau ou des cellules nerveuses. La patiente a subi une opération par laparoscopie pour enlever l’ovaire gauche et la trompe de Fallope. Après 12 mois de suivi avec des échographies régulières, elle allait bien et aucune récidive n’a été détectée.",
+            "B3": "Résumé détaillé et structuré :\n\n**Contexte**  \nUne femme chinoise de 30 ans, sans antécédents de tumeurs cérébrales ni de troubles neurologiques, a été découverte porteuse d’une masse au niveau de l’ovaire gauche lors d’un examen médical de routine. Elle avait des antécédents d’ovaires polykystiques diagnostiqués à 19 ans, non traités. Les marqueurs tumoraux sanguins (CEA, CA125, CA19-9) étaient normaux. Une IRM pelvienne a montré une lésion kystique de 6,3 × 4,8 cm avec des nodules muraux, suggérant une tumeur bénigne ou à potentiel limité de malignité.\n\n**Principales Observations**  \nLa patiente a subi une ablation laparoscopique de l’ovaire gauche et de la trompe de Fallope. L’examen macroscopique a révélé une masse kystique de 5 × 3,5 × 1 cm avec deux nodules muraux rouges-gris, mous, mesurant 0,8 et 1,2 cm. L’analyse histologique a montré que ces nodules contenaient des tissus caractéristiques d’un tératome mature (tissu d’origine embryonnaire comprenant notamment de l’épiderme et des annexes cutanées), ainsi qu’une prolifération de cellules gliales (cellules du système nerveux central) et de cellules ganglionnaires (neurones matures). Ces cellules ganglionnaires présentaient des anomalies telles que la présence de deux noyaux (binucléation) et des noyaux volumineux et irréguliers. Les figures de division cellulaire (mitoses) étaient rares.\n\nSur le plan immunohistochimique, les cellules gliales exprimaient les marqueurs GFAP et Olig2, typiques des cellules gliales. Les cellules ganglionnaires étaient positives pour plusieurs marqueurs neuronaux et neuroendocriniens : Neu-N, chromogranine A (CgA), Nestin, Calretinine (CR) et CD34, ce dernier marquant également des cellules tumorales ramifiées. L’expression de la protéine P53 était de type sauvage (absence de mutation), l’indice de prolifération Ki67 était faible (environ 5 %), et les mutations des gènes IDH1 et BRAF V600E, souvent impliquées dans certains cancers, étaient absentes.\n\n**Interprétation Clinique**  \nCes caractéristiques histologiques et immunohistochimiques ont permis de diagnostiquer un gangliogliome, une tumeur rare composée à la fois de cellules gliales et ganglionnaires, développée à partir d’un tératome kystique mature de l’ovaire. Ce type de tumeur est inhabituel dans cette localisation et généralement considéré comme bénin.\n\n**Prochaines Étapes et Évolution**  \nAprès la chirurgie, la patiente a été suivie pendant 12 mois par échographies pelviennes et abdominales tous les trois mois, sans détection de récidive ou d’anomalie. Elle est restée en bonne santé sans nécessiter de traitement complémentaire comme la chimiothérapie.\n\nEn résumé, cette observation illustre un cas rare de gangliogliome associé à un tératome ovarien mature, traité efficacement par chirurgie seule avec un bon pronostic à court terme."
+        }
+    },
+    {
+        "article": "Femme de 76 ans, de nationalité paraguayenne, résidant à Buenos Aires, sans antécédents de voyages récents, ayant des antécédents de sténose aortique et d’hypertension artérielle, traitement habituel : bisoprolol. Elle a commencé à présenter des symptômes 5 jours avant son admission, avec une fièvre, une toux avec expectoration mucopurulente et une dyspnée qui a progressé jusqu’à la classe fonctionnelle III-IV, des douleurs abdominales et des céphalées. Elle a été traitée en ambulatoire 48 heures avant son admission avec de l’amoxicilline-acide clavulanique ; un test SARS-CoV-2, un virus de la grippe A et B et un virus respiratoire syncytial ont été effectués par réaction en chaîne de la polymérase, qui s’est avéré négatif. Elle a consulté l’hôpital pour une dyspnée de classe fonctionnelle IV, des nausées et des douleurs abdominales, une tomographie axiale assistée par ordinateur (TAC) a été réalisée, qui a mis en évidence un infiltrat interstitiel bilatéral. Admise à l’unité de soins intensifs le 30 mars 2023, avec un choc septique secondaire à un foyer respiratoire, une fièvre de 38 °C, 120 battements par minute et une acidose, les scores de gravité SOFA (Sepsis Related Organ Failures Assesment) ont totalisé 7 points et APACHE II (Acute Physiology and Cronic Health Classification System II) 21 points. Une réanimation a été initiée avec des fluides, des analyses cliniques ont été effectuées, qui ont mis en évidence une hématocrite élevée, une hémoconcentration, une leucocytose et une insuffisance rénale aiguë, des échantillons ont été prélevés pour des hémocultures, des cultures d’urine et des cultures respiratoires. Des échantillons ont été envoyés au laboratoire de virologie sanguine pour les virus dengue et CHIKV. Une échocardiographie a été réalisée en mode point of care ultrasound (POCUS) qui a mis en évidence une sténose aortique modérée, avec une vitesse de pointe de 3,4 m/seconde, une fonction systolique du ventricule gauche préservée, sans altération de la mobilité segmentaire, sans signe d’insuffisance cardiaque aiguë, aucune végétation n’a été observée sur les valves par cette approche. Un traitement a été initié avec des antibiotiques à large spectre : ceftriaxone et vancomycine. Elle a évolué avec une progression des insuffisances respiratoires, hémodynamiques et rénales. Elle a nécessité une ventilation mécanique, des vasopresseurs à haute dose, une perfusion de furosémide pour oligurie, un choc réfractaire, et elle est décédée le 31 mars 2023. Les cultures bactériologiques de sang, d’urine et de sécrétions trachéales ont conclu sans développement bactérien, réaction en chaîne de la polymérase en temps réel et antigène NS1 non détectable pour virus dengue, et réaction en chaîne de la polymérase en temps réel pour CHIKV détectable dans le sérum.\n",
+        "gold_summary": "C'est le cas d'une femme de 76 ans, ayant des antécédents d'hypertension artérielle et de sténose aortique, admise en soins intensifs pour un choc septique avec foyer respiratoire, avec un modèle de pneumonie interstitielle, une évolution torpide et un décès dans les 24 heures suivant l'admission. Le résultat détectable du virus Chikungunya par réaction en chaîne de la polymérase en temps réel a été reçu post mortem.\n",
+        "synthetic_summary": {
+            "B1": "Une dame de 76 ans était très malade. Elle avait de la fièvre et du mal à respirer. Elle est allée à l'hôpital. Les docteurs ont trouvé un virus dans son sang. Ce virus s'appelle Chikungunya. Elle est restée très malade et elle est partie au ciel. Les docteurs ont fait tout leur possible pour l'aider.",
+            "B2": "Cas d'une femme de 76 ans avec des problèmes de santé connus : une tension artérielle élevée et un rétrécissement de la valve aortique du cœur (appelé sténose aortique). Elle a été admise en soins intensifs à cause d'une infection grave qui a causé un choc septique, c’est-à-dire que son corps était en état de défaillance à cause d’une infection. Cette infection venait des poumons, où une pneumonie interstitielle (une inflammation des tissus autour des alvéoles pulmonaires) a été observée.\n\nMalheureusement, son état s’est rapidement aggravé malgré les traitements, et elle est décédée moins de 24 heures après son admission. Après sa mort, les médecins ont découvert la présence du virus Chikungunya dans son sang grâce à un test appelé réaction en chaîne de la polymérase (PCR). Ce virus est transmis par des moustiques et peut provoquer de la fièvre, des douleurs et parfois des complications graves, surtout chez les personnes âgées ou fragiles.",
+            "B3": "Résumé détaillé et structuré du cas clinique\n\nContexte  \nIl s’agit d’une femme de 76 ans, originaire du Paraguay et résidant à Buenos Aires, présentant des antécédents médicaux importants, notamment une sténose aortique (rétrécissement de la valve aortique du cœur) et une hypertension artérielle, traitée par bisoprolol. Elle n’avait pas voyagé récemment. Cinq jours avant son admission à l’hôpital, elle a développé une fièvre, une toux avec expectoration mucopurulente (crachats contenant du mucus et du pus), une difficulté respiratoire progressive (dyspnée) jusqu’à un stade sévère (classe fonctionnelle III-IV), ainsi que des douleurs abdominales et des céphalées. Un traitement antibiotique ambulatoire par amoxicilline-acide clavulanique a été prescrit 48 heures avant son admission, sans amélioration. Les tests virologiques initiaux pour le SARS-CoV-2, les virus de la grippe A et B, ainsi que le virus respiratoire syncytial, étaient négatifs.\n\nPrincipales observations  \nÀ son admission, la patiente présentait une dyspnée sévère (classe fonctionnelle IV), des nausées et des douleurs abdominales. Une tomodensitométrie thoracique a révélé un infiltrat interstitiel bilatéral, signe d’une pneumonie touchant les tissus pulmonaires profonds. Elle a été admise en unité de soins intensifs le 30 mars 2023, dans un état de choc septique (une défaillance circulatoire grave liée à une infection) d’origine respiratoire, avec une fièvre à 38 °C, une fréquence cardiaque rapide (120 battements par minute) et une acidose métabolique (déséquilibre du pH sanguin). Les scores de gravité étaient élevés : SOFA à 7 points et APACHE II à 21 points, indiquant un pronostic sévère.  \n\nLes analyses sanguines ont montré une hémoconcentration (augmentation de la concentration des cellules sanguines), une leucocytose (augmentation des globules blancs) et une insuffisance rénale aiguë. Des prélèvements pour cultures bactériennes (sang, urine, sécrétions respiratoires) ont été réalisés, ainsi que des analyses virologiques pour les virus dengue et Chikungunya (CHIKV). Une échocardiographie réalisée au lit du patient a confirmé la sténose aortique modérée, une fonction normale du ventricule gauche, sans signes d’insuffisance cardiaque aiguë ni d’infection des valves cardiaques (endocardite).  \n\nUn traitement antibiotique à large spectre (ceftriaxone et vancomycine) a été instauré. Malgré cela, la patiente a présenté une aggravation rapide de ses insuffisances respiratoire, hémodynamique et rénale, nécessitant une ventilation mécanique, des vasopresseurs à haute dose pour maintenir la pression artérielle, ainsi qu’une perfusion de furosémide pour traiter une oligurie (diminution de la production d’urine). Elle a développé un choc réfractaire, c’est-à-dire un état de défaillance circulatoire non réversible, et est décédée le 31 mars 2023, moins de 24 heures après son admission en soins intensifs.\n\nInterprétation clinique  \nLes cultures bactériennes sont restées négatives, ce qui exclut une infection bactérienne détectable comme cause principale du choc septique. Les tests virologiques ont révélé la présence du virus Chikungunya dans le sérum par réaction en chaîne de la polymérase en temps réel, confirmée après le décès. Le virus dengue a été exclu. Ce cas illustre une forme grave et rapidement évolutive d’infection par le virus Chikungunya, responsable d’une pneumonie interstitielle sévère et d’un choc septique, compliquée par une défaillance multiviscérale chez une patiente âgée avec comorbidités cardiovasculaires.\n\nProchaines étapes  \nCe cas souligne l’importance de considérer les infections virales émergentes comme le Chikungunya dans le diagnostic différentiel des pneumonies sévères et des états de choc septique, surtout dans les zones endémiques ou chez des patients sans réponse aux traitements antibactériens classiques. Une surveillance accrue, un diagnostic rapide par biologie moléculaire et une prise en charge adaptée sont essentiels pour améliorer le pronostic. La recherche de traitements antiviraux spécifiques et la prévention par la lutte contre les vecteurs (moustiques) restent des priorités de santé publique."
+        }
+    },
+    {
+        "article": "Il s’agit d’un garçon de 16 ans qui, dans les mois précédant la consultation, souffre occasionnellement de paralysies du sommeil, quelques minutes après le début de la sieste postprandiale, qui lui causent beaucoup d’anxiété, principale raison pour laquelle il se rend à la consultation. Ces paralysies du sommeil sont parfois accompagnées d’hallucinations hypnopompiques (qu’il attribue à des rêves ou au fait de ne pas être complètement éveillé). Il a un horaire de sommeil nocturne d’environ sept heures, plus deux heures de sieste qui lui procurent beaucoup de repos. Il a de bonnes performances scolaires. Lorsqu’il a fait une anamnèse ciblée, il a déclaré qu’après avoir souffert de ces paralysies du sommeil pendant des mois, il a eu des épisodes de secousses des bras et des jambes, surtout quand il riait, qui l’ont presque fait tomber (il pensait que cela arrivait à tout le monde). Par la suite, ces symptômes ont été rejoints par environ trois réveils nocturnes de courte durée, avec une réconciliation immédiate et occasionnelle, et des attaques de sommeil le matin, qu’il relie aux cours de mathématiques (le professeur est très ennuyeux). Après la suspicion clinique, nous avons demandé un test de latences multiples du sommeil et une étude polysomnographique nocturne, qui sont concluants avec le diagnostic de narcolepsie (latence de sommeil très courte, latence de sommeil REM avancée, sommeil quelque peu fragmenté, moyenne dans le test de latences multiples du sommeil de 2,1 minutes et présence de quatre REM au début du sommeil). Étant donné que ces épisodes de somnolence lui arrivent tous les jours à la même heure, nous lui avons prescrit une sieste matinale brève qui, au début, l’a beaucoup rafraîchi et il a déclaré pouvoir continuer ses activités scolaires. Par la suite, nous avons ajouté modafinil à la même heure (200 mg). Nous lui avons recommandé la venlafaxine pour les cataplexies ou même un traitement à l’oxybate de sodium (ce dernier refuse de le prendre à cause de l’inconfort de la deuxième dose, et la venlafaxine refuse également à cause de la peur des effets secondaires). Nous avons convenu qu’il se conformerait à une bonne hygiène du sommeil, prendrait le modafinil et continuerait les siestes programmées (la sieste du soir qu’il faisait déjà et la sieste du matin). Et, s’il empire, nous ajouterons d’autres traitements. Il se porte bien avec cette routine, ne ressent pas beaucoup de fragmentation du sommeil nocturne (un ou deux réveils très brefs après lesquels il se rendort sans problème) ; en fait, il se réveille reposé, les cataplexies sont occasionnelles et ne le gênent pas dans son quotidien, et les crises de sommeil sont très contrôlées. Il se sent mieux et sans grandes limitations dans sa vie quotidienne (bon rendement scolaire, il ne boit pas d’alcool, mais cela ne l’affecte pas non plus, car il n’a jamais bu, il a des horaires de sommeil réguliers et fait de l’activité physique régulière).\n",
+        "gold_summary": "Homme de 16 ans consultant après avoir consulté différents spécialistes en raison de paralysies du sommeil pendant les siestes, qui lui causaient de la peur et occasionnellement la chute d'objets de ses mains (diagnostiquées comme possibles myoclonies). Dans l'anamnèse, nous avons été surpris par la présence de paralysies du sommeil immédiatement après le début des siestes et, dans l'anamnèse dirigée, ces mouvements brusques provoqués par des émotions étaient compatibles avec des cataplexies, nous avons donc réalisé une étude polysomnographique nocturne et un test de latences multiples du sommeil. Avec l'évolution, des hallucinations hypnopomphiques et un sommeil fragmenté nocturne sont apparus, ainsi qu'une somnolence diurne occasionnelle (la tétrade symptomatologique typique de la narcolepsie avec cataplexie de type 1 a été complétée).\n",
+        "synthetic_summary": {
+            "B1": "Il y a un garçon de 16 ans. Parfois, quand il fait une sieste, il ne peut pas bouger. Ça lui fait un peu peur. Parfois, ses bras ou ses jambes bougent tout seuls quand il rit.  \n\nLe docteur a fait des examens pour regarder son sommeil. Le garçon a un problème appelé narcolepsie. Cela veut dire qu’il est très fatigué et qu’il s’endort vite.  \n\nLe docteur lui a donné des conseils pour bien dormir. Il fait aussi des petites siestes pour se sentir mieux. Maintenant, il va mieux et peut faire ses devoirs sans problème.",
+            "B2": "**Ce qu’ils ont observé chez le garçon de 16 ans**\n\nCe garçon venait consulter parce qu’il avait des paralysies du sommeil, c’est-à-dire qu’il se réveillait sans pouvoir bouger pendant quelques minutes, surtout juste après avoir commencé sa sieste. Ces épisodes lui faisaient très peur. Parfois, il voyait aussi des choses qui n’étaient pas là, ce qu’on appelle des hallucinations hypnopompiques, qu’il pensait être des rêves ou le fait de ne pas être complètement réveillé. Il dormait environ sept heures la nuit et faisait deux heures de sieste, ce qui lui apportait du repos. Il réussissait bien à l’école.\n\nEn parlant plus avec lui, on a appris qu’il avait aussi des secousses soudaines dans les bras et les jambes, surtout quand il riait, ce qui le faisait presque tomber. Ces mouvements brusques sont appelés cataplexies, c’est un symptôme lié à une maladie du sommeil. Il avait aussi des réveils courts la nuit et des épisodes de sommeil soudain le matin, surtout en classe.\n\n**Ce que cela signifie**\n\nAprès ces observations, les médecins ont fait deux examens du sommeil. Ils ont mesuré le temps qu’il mettait à s’endormir et observé son sommeil pendant la nuit. Les résultats ont montré qu’il s’endormait très vite, qu’il entrait rapidement dans une phase de sommeil appelée REM (celle où l’on rêve), et que son sommeil était un peu interrompu. Ces signes, avec ses symptômes, ont permis de diagnostiquer une narcolepsie de type 1, une maladie où le cerveau ne contrôle pas bien le sommeil et les muscles.\n\n**Comment il est soigné**\n\nPour l’aider, on lui a conseillé de faire une sieste courte le matin, ce qui l’a beaucoup aidé au début. Ensuite, on lui a donné un médicament appelé modafinil pour l’aider à rester éveillé. On lui a aussi proposé d’autres traitements pour les cataplexies, mais il a préféré ne pas les prendre à cause des effets secondaires possibles. Il suit une bonne routine de sommeil, continue ses siestes, et se sent mieux. Ses réveils nocturnes sont rares et courts, il est reposé le matin, les cataplexies sont peu fréquentes et ne gênent pas sa vie. Il réussit bien à l’école, ne boit pas d’alcool, et fait du sport régulièrement.\n\nEn résumé, grâce à un diagnostic précis et un traitement adapté, ce garçon vit mieux avec sa maladie du sommeil et peut continuer ses activités normalement.",
+            "B3": "Résumé détaillé et structuré pour un public non médical mais éduqué :\n\n**Contexte**  \nUn adolescent de 16 ans consulte pour des épisodes répétés de paralysies du sommeil survenant quelques minutes après le début de ses siestes après le repas. Ces épisodes lui provoquent une grande anxiété. Il rapporte également des hallucinations hypnopompiques, c’est-à-dire des sensations visuelles ou auditives survenant au réveil, qu’il attribue à des rêves ou à un état de semi-éveil. Son sommeil nocturne dure environ sept heures, complété par deux heures de sieste, ce qui lui procure un repos satisfaisant. Il réussit bien à l’école et ne présente pas d’autres troubles majeurs au départ.\n\n**Principales observations**  \nAu fil du temps, il décrit des secousses involontaires des bras et des jambes, surtout lorsqu’il rit, qui ont failli le faire tomber. Ces mouvements brusques, initialement considérés comme des myoclonies (contractions musculaires involontaires), ont été réinterprétés comme des cataplexies, c’est-à-dire des pertes soudaines de tonus musculaire déclenchées par des émotions fortes, caractéristiques de la narcolepsie. Par ailleurs, il présente des réveils nocturnes brefs et une somnolence excessive le matin, notamment pendant les cours qu’il trouve ennuyeux.\n\n**Interprétation clinique**  \nDevant ce tableau symptomatique – paralysies du sommeil, hallucinations hypnopompiques, cataplexies et somnolence diurne excessive – une narcolepsie de type 1 a été suspectée. Cette forme de narcolepsie se caractérise par la présence de cataplexies associées à une somnolence diurne importante. Les examens complémentaires, comprenant une polysomnographie nocturne (enregistrement du sommeil) et un test de latences multiples du sommeil (évaluation de la rapidité d’endormissement et de l’apparition du sommeil paradoxal), ont confirmé ce diagnostic. Les résultats montraient un endormissement très rapide, une apparition précoce du sommeil paradoxal (phase du sommeil liée aux rêves), un sommeil nocturne fragmenté, et une moyenne de latence d’endormissement très courte (2,1 minutes), avec plusieurs épisodes de sommeil paradoxal dès le début du sommeil.\n\n**Prochaines étapes et prise en charge**  \nPour gérer la somnolence diurne survenant régulièrement à la même heure, une sieste matinale courte a été prescrite, ce qui a amélioré son état et son attention en classe. Un traitement médicamenteux par modafinil (200 mg) a été ajouté pour stimuler l’éveil. Des options thérapeutiques supplémentaires, comme la venlafaxine (un antidépresseur pouvant réduire les cataplexies) ou l’oxybate de sodium (médicament spécifique pour la narcolepsie), ont été proposées, mais le patient a refusé ces traitements en raison de craintes liées aux effets secondaires ou à la posologie. Il a été conseillé de maintenir une bonne hygiène du sommeil, de continuer les siestes programmées (matinale et vespérale), et de suivre le traitement par modafinil.  \n\nActuellement, le jeune patient se porte bien avec cette prise en charge : il présente peu de fragmentation du sommeil nocturne, se réveille reposé, les cataplexies sont rares et peu gênantes, et les épisodes de somnolence sont bien contrôlés. Son rendement scolaire reste bon, il ne consomme pas d’alcool, et il suit un rythme de vie régulier avec une activité physique régulière. En cas d’aggravation, d’autres traitements pourront être envisagés.  \n\nCe cas illustre l’importance d’une évaluation approfondie des symptômes liés au sommeil chez l’adolescent, notamment lorsque des signes évocateurs de narcolepsie apparaissent, afin d’instaurer une prise en charge adaptée et améliorer la qualité de vie."
+        }
+    },
+    {
+        "article": "Un nouveau-né de 3050 g à terme est né après une grossesse sans complication d'une femme primipare de 20 ans à 39 semaines de grossesse. La grossesse était sans complication. L'accouchement n'a pas été prolongé avec un accouchement vaginal spontané sans incident. Les scores d'Apgar étaient de 8 et 9 à 1 min et 5 min, respectivement, avec un score de grimace normal de 2. Son Apgar est resté à 9 à 10 et 20 minutes. Il était alerte avec un bon cri, une couleur rose, une fréquence cardiaque de 134 et une fréquence respiratoire de 56. Il a reçu de la vitamine K à la naissance. Il s'est présenté à notre hôpital avec un refus de téter pendant trois jours à l'âge de 29 jours. La famille a également déclaré qu'il avait eu des vomissements intermittents depuis la naissance. Sinon, il n'y avait pas d'antécédents de diathèse hémorragique, de fièvre, de raideur du cou ou de convulsions. À la présentation, il avait une fontanelle antérieure bombée. Moro était incomplet ; la succion n'a pas été soutenue mais un bon tonus musculaire a été noté dans toutes les extrémités. Son compte sanguin complet (CBC) et son profil de coagulation étaient normaux. L'IRM du cerveau a montré une convexité cérébrale bilatérale T1WI et T2WI hyperintense mesurant 2 cm avec une extension supracerebrale et péraciduculaire. En outre, l'obliteration du quatrième ventricule et la dilatation du troisième ventricule et du ventricule latéral ont également été notées. Sous anesthésie générale, le patient a été placé en position ventrale en utilisant une incision cutanée médiane, une craniostomie bilatérale a été réalisée. Après l'ouverture de la dure-mère dans une incision cruciforme, une membrane épaisse et bien définie ; avec du sang hémolysé sombre est sorti sous pression. En chirurgie, le patient a eu un arrêt cardiaque pour lequel un cycle de réanimation cardiopulmonaire (RCP) a été effectué et un retour de la circulation spontanée a été obtenu. Après cela, la peau a été fermée, un drain sous-dural a été placé et le patient a été extubé et transféré à l'unité de soins intensifs (USI). Le scanner CT de contrôle effectué le 3e jour postopératoire a montré une évacuation complète de l'hématome et une amélioration de l'hydrocéphalie. Le patient a été libéré le 7e jour postopératoire. Le premier mois de suivi postopératoire a été sans incident avec des jalons de développement normaux atteints pour son âge.\n",
+        "gold_summary": "Un nouveau-né de sexe masculin âgé de vingt-neuf jours a présenté un échec de la succion pendant trois jours associé à des vomissements. L'imagerie a montré un hématome sous-dural chronique bilatéral postérieur et une hydrocéphalie obstructive. Une craniostomie bilatérale et une évacuation de l'hématome ont été effectuées, ce qui a donné un excellent résultat.\n",
+        "synthetic_summary": {
+            "B1": "Un bébé de presque un mois avait du mal à boire et vomissait. Les docteurs ont vu du sang dans sa tête avec une photo spéciale. Ils ont fait une petite opération pour enlever le sang. Après, le bébé allait beaucoup mieux.",
+            "B2": "Un bébé garçon de 29 jours avait du mal à téter depuis trois jours et vomissait parfois. Une imagerie spéciale du cerveau a montré qu'il avait un hématome sous-dural chronique, c’est-à-dire une accumulation de sang entre le cerveau et la membrane qui le recouvre, des deux côtés à l’arrière de la tête. Cette accumulation bloquait aussi la circulation normale du liquide dans le cerveau, causant une hydrocéphalie, c’est-à-dire un gonflement des ventricules, qui sont des cavités remplies de liquide. Pour traiter cela, les médecins ont fait une opération appelée craniostomie bilatérale, où ils ont ouvert le crâne de chaque côté pour enlever le sang accumulé. Après cette intervention, le bébé s’est bien rétabli et a pu sortir de l’hôpital avec un bon développement un mois plus tard.",
+            "B3": "Résumé destiné à un adulte éduqué non-médecin\n\n**Contexte**  \nUn nouveau-né de sexe masculin, né à terme avec un poids normal (3050 g), a présenté à l’âge de 29 jours un refus de téter depuis trois jours, accompagné de vomissements intermittents signalés depuis la naissance. Sa grossesse et son accouchement s’étaient déroulés sans complication, et ses premiers examens à la naissance étaient normaux. À l’examen clinique, il montrait une fontanelle antérieure bombée (gonflée), un réflexe de Moro incomplet (réflexe de surprise), et une succion faible, bien que son tonus musculaire restait bon. Les analyses sanguines, y compris le bilan de coagulation, étaient normales.\n\n**Principales Observations**  \nL’imagerie par résonance magnétique (IRM) cérébrale a révélé la présence d’un hématome sous-dural chronique bilatéral (accumulation de sang entre le cerveau et la membrane qui le recouvre, des deux côtés à l’arrière du cerveau) mesurant environ 2 cm, ainsi qu’une hydrocéphalie obstructive (accumulation excessive de liquide cérébral due à un blocage), avec dilatation des ventricules cérébraux (espaces contenant le liquide cérébrospinal).  \n\n**Intervention et déroulement**  \nSous anesthésie générale, une intervention chirurgicale appelée craniostomie bilatérale a été réalisée. Cette opération consiste à ouvrir le crâne de chaque côté pour accéder à l’hématome. À l’ouverture de la dure-mère (membrane entourant le cerveau), une membrane épaisse contenant du sang ancien a été évacuée sous pression. Pendant l’intervention, le nouveau-né a présenté un arrêt cardiaque, mais une réanimation cardio-pulmonaire a permis de rétablir la circulation. Un drain a été placé pour évacuer les liquides résiduels, puis la peau a été refermée.  \n\n**Prochaines Étapes et suivi**  \nLe scanner cérébral réalisé trois jours après l’opération a montré une évacuation complète de l’hématome et une amélioration de l’hydrocéphalie. Le bébé a pu quitter l’hôpital au septième jour post-opératoire. Lors du suivi un mois plus tard, il présentait un développement normal adapté à son âge, sans complication apparente.\n\n**Conclusion**  \nCe cas illustre qu’un hématome sous-dural chronique chez un nouveau-né, responsable de troubles de la succion et de vomissements, peut être efficacement traité par chirurgie, avec un bon pronostic lorsque la prise en charge est rapide et adaptée."
+        }
+    },
+    {
+        "article": "Une femme enceinte de 32 ans atteinte du syndrome de Holt-Oram a été adressée à notre établissement pour une échographie d'anatomie de routine du deuxième trimestre. Elle avait des antécédents familiaux positifs du syndrome de Holt-Oram impliquant sa mère et sa sœur. Chez tous les membres de la famille concernés, la seule preuve clinique du syndrome concerne les défauts des membres supérieurs, avec une malformation de l'os carpien et une agenèse du pouce. L'échographie a rapporté une aplasie bilatérale des rayons, un ulna légèrement incurvé et une torsion bilatérale de la main avec quatre rayons digitaux. Une augmentation significative de l'oreillette droite sans régurgitation tricuspide a également été détectée. La patiente a refusé l'amniocentèse et a décidé de poursuivre la grossesse. Au moment de l'échographie de suivi à 30 semaines, l'élargissement de l'oreillette droite a été confirmé sans insuffisance tricuspide ou autres malformations cardiaques. La patiente a subi une césarienne d'urgence à 40 semaines de gestation en raison d'une bradycardie fœtale pendant le travail. Un nourrisson de sexe masculin a été livré avec un poids de naissance de 3 110 g et un score d'APGAR de 9 et 9 à 1′ et 5′ min. L'évaluation postnatale a confirmé la grave hypoplasie des rayons, un ulna légèrement incurvé et une agenèse du premier rayon. L'échocardiographie néonatale a constaté un élargissement de l'oreillette droite et a également constaté un défaut atrial et deux petits défects du septum ventriculaire non détectés prénatalement. L'analyse génétique a également été réalisée et une mutation TBX5 a été détectée.\n",
+        "gold_summary": "Nous présentons le cas d'une femme enceinte de 32 ans atteinte du syndrome de Holt-Oram, qui a été adressée à notre établissement pour une échographie d'anatomie de routine au deuxième trimestre. L'échographie a révélé une aplasie bilatérale du radius, un ulna légèrement incurvé et une main tordue bilatérale avec quatre rayons digitaux. Une augmentation significative de l'oreillette droite sans régurgitation tricuspidienne a également été détectée. La patiente a refusé l'amniocentèse et l'évaluation postnatale a confirmé le diagnostic du syndrome de Holt-Oram.\n",
+        "synthetic_summary": {
+            "B1": "Une maman avait un bébé dans son ventre. Les docteurs ont regardé le bébé avec une machine spéciale. Ils ont vu que les bras du bébé étaient un peu différents. Les mains avaient quatre doigts et étaient un peu tordues. Le cœur du bébé avait aussi une petite différence. La maman a choisi de ne pas faire un test spécial. Après la naissance, les docteurs ont vu que le bébé avait bien ces différences. Tout va bien, et les docteurs vont aider le bébé à grandir.",
+            "B2": "Cas d'une femme enceinte avec le syndrome de Holt-Oram\n\nUne femme de 32 ans, enceinte, a passé une échographie au deuxième trimestre de sa grossesse. Elle a ce qu'on appelle le syndrome de Holt-Oram, une maladie héréditaire qui affecte surtout les bras et le cœur. Dans sa famille, sa mère et sa sœur ont aussi ce syndrome, qui cause des malformations des os du bras et l'absence du pouce.\n\nCe qu'ils ont trouvé à l'échographie\n\nL'échographie a montré que les deux os du radius (un os de l'avant-bras) étaient absents. L'ulna, un autre os de l'avant-bras, était un peu courbé. Ses mains étaient tordues des deux côtés et avaient seulement quatre doigts au lieu de cinq. Ils ont aussi remarqué que la partie droite du cœur, appelée oreillette droite, était plus grande que la normale, mais sans problème de valve.\n\nCe qui s'est passé ensuite\n\nLa femme a refusé de faire une amniocentèse, un test où l'on prélève un peu de liquide autour du bébé pour chercher des anomalies génétiques. Elle a continué sa grossesse normalement. À la naissance, le bébé garçon est venu au monde par césarienne d'urgence à cause d'un rythme cardiaque lent pendant le travail. Le bébé pesait 3 110 grammes et avait un bon score de santé.\n\nAprès la naissance, les médecins ont confirmé les malformations des bras et ont découvert des problèmes cardiaques supplémentaires, comme des trous dans les parois du cœur, qui n'avaient pas été vus avant la naissance. Une analyse génétique a montré une mutation dans le gène TBX5, qui est liée au syndrome de Holt-Oram.\n\nEn résumé, ce cas montre comment le syndrome de Holt-Oram peut affecter les bras et le cœur, et l'importance de suivre la grossesse et le bébé de près.",
+            "B3": "Résumé détaillé et structuré du cas clinique\n\nContexte  \nUne femme enceinte de 32 ans, porteuse du syndrome de Holt-Oram, a été adressée pour une échographie d’anatomie de routine au deuxième trimestre de grossesse. Ce syndrome, transmis dans sa famille (sa mère et sa sœur en sont également atteintes), se manifeste principalement par des anomalies des membres supérieurs, notamment des malformations osseuses du carpe (les os du poignet) et l’absence congénitale du pouce.\n\nPrincipales observations  \nL’échographie prénatale a révélé plusieurs anomalies squelettiques : une aplasie bilatérale du radius (absence des deux os radius dans les avant-bras), un ulna (l’autre os de l’avant-bras) légèrement incurvé, ainsi qu’une torsion des deux mains, chacune présentant quatre rayons digitaux (doigts). Par ailleurs, une dilatation importante de l’oreillette droite du cœur a été détectée, sans signe de régurgitation de la valve tricuspide (pas de reflux sanguin anormal). La patiente a choisi de ne pas réaliser d’amniocentèse (prélèvement de liquide amniotique pour analyse génétique) et a poursuivi sa grossesse.\n\nÀ 30 semaines de gestation, une échographie de suivi a confirmé l’élargissement de l’oreillette droite, toujours sans insuffisance valvulaire ni autres malformations cardiaques visibles. La naissance a eu lieu par césarienne d’urgence à 40 semaines, motivée par une bradycardie fœtale (ralentissement du rythme cardiaque du bébé) lors du travail. Le nouveau-né, un garçon pesant 3 110 grammes, présentait un score d’Apgar (évaluation rapide de son état à la naissance) de 9 à 1 minute et 9 à 5 minutes, indiquant une bonne adaptation initiale.\n\nInterprétation clinique  \nL’examen postnatal a confirmé les anomalies des membres supérieurs observées in utero, avec une hypoplasie sévère des rayons digitaux, un ulna incurvé et une absence du premier rayon (pouce). L’échocardiographie néonatale a mis en évidence une dilatation de l’oreillette droite, ainsi que la présence d’un défaut atrial (trou dans la cloison entre les deux oreillettes) et de deux petits défauts du septum ventriculaire (trous dans la cloison entre les ventricules), qui n’avaient pas été détectés lors des échographies prénatales. Une analyse génétique a confirmé la présence d’une mutation du gène TBX5, responsable du syndrome de Holt-Oram.\n\nProchaines étapes  \nLe suivi médical devra inclure une surveillance cardiologique attentive pour évaluer l’impact des malformations cardiaques, ainsi qu’un accompagnement orthopédique et fonctionnel pour les anomalies des membres supérieurs. La confirmation génétique permettra également d’informer la famille sur les risques de transmission et les options de prise en charge future."
+        }
+    },
+    {
+        "article": "Une femme de 20 ans a été suivie depuis l'âge de huit ans pour une NS idiopathique inaugurée par une thrombose veineuse cérébrale étendue à la veine jugulaire droite avec une embolie pulmonaire massive. La patiente n'a eu aucune séquelle. Elle n'avait pas d'autre antécédent médical ou chirurgical. Il n'a pas été rapporté d'antécédent familial de thrombose. La patiente n'a pas eu de biopsie car elle n'avait pas d'insuffisance rénale ni d'hématurie brute, ni d'hypertension à la première présentation ; en outre, elle n'avait pas d'autre signe rénal évocateur d'un syndrome néphrotique secondaire. Elle a été mise en conséquence sous traitement anticoagulant (antagoniste de la vitamine K par voie orale) et sous traitement corticoïde oral avec une bonne évolution. Par la suite, la patiente a reçu plusieurs cures de corticoïdes à haute dose pour des rechutes de NS dépendantes des stéroïdes. Elle a donc été mise sous mycophenolate mofetil (MMF) comme traitement de fond pour éviter les corticoïdes et assurer une croissance normale. Une évaluation exhaustive de la thrombophilie a été réalisée et n'a pas montré d'anomalie. Le taux d'homocystéine, le taux de fibrinogène sanguin, la protéine C, la protéine S, l'antithrombine III, la mutation du facteur V Leiden, la mutation JAK-2, les cryoglobulines, les anticorps anti-cardiolipine, le lupus anticoagulant et les anticorps anti-bêta-1-glycoprotéine étaient normaux. Le traitement anticoagulant a été arrêté après neuf ans. L'évolution a été émaillée par la survenue de plusieurs rechutes de sa maladie contrôlées par un traitement corticoïde oral. La rémission de la NS a été notée depuis 2017, le MMF a donc été progressivement arrêté en 2019 et la patiente est restée asymptomatique et sans aucune rechute.\n\nUn an plus tard, le patient est venu à notre service des urgences pour une douleur abdominale diffuse aiguë intense sans irradiation particulière associée à des vomissements postprandiaux et un œdème des membres inférieurs bilatéral depuis les six dernières heures. L'examen physique a révélé une sensibilité épigastrique intense avec des signes vitaux normaux (pression artérielle de 120/70 mm Hg, fréquence cardiaque de 83 bpm et saturation en oxygène à 100 % sur l'air ambiant). Le patient était apyrétique avec une conscience normale. Le reste de l'examen physique était sans objet. L'analyse d'urine avec labstix a révélé une protéinurie. Les résultats de l'analyse de gaz sanguins ont montré une acidose métabolique avec compensation respiratoire. D'autres tests de laboratoire ont révélé une hypoalbuminémie, une hypercholestérolémie, un temps de prothrombine à 90 %, des taux élevés de D-dimères, de lactate déshydrogénase et de créatine phosphokinase ainsi qu'un syndrome inflammatoire biologique avec une CRP de 37 mg/L et une leucocytose à 26,4 x 103/µL. Les fonctions rénales et hépatiques étaient normales.\n\nLe patient a été hospitalisé dans une unité de soins intensifs avec une surveillance étroite des signes vitaux et l'initiation de mesures de réanimation. Une échographie abdominale a été réalisée d'urgence, montrant un épanchement intra-abdominal de faible à modérée abondance. Un scanner abdominal a révélé une thrombose aiguë de l'artère mésentérique supérieure avec une ischémie mésentérique aiguë. Le patient a été immédiatement dirigé vers la salle d'opération. L'exploration intra-opératoire a confirmé une ischémie mésentérique avec une nécrose étendue de presque la totalité de l'intestin grêle, rendant leurs résections incompatibles avec la vie, comme le montre la figure 3. Le patient est mort après 48 heures.\n",
+        "gold_summary": "Nous présentons le cas d'une femme de 20 ans ayant une histoire de 12 ans de NS idiopathique révélée par une thrombose veineuse cérébrale étendue avec embolie pulmonaire traitée par une thérapie anticoagulante et une thérapie orale par corticostéroïdes suivie par du mycophenolate mofetil (MMF). L'évaluation de la thrombophilie n'a pas montré d'anomalies. L'évolution a été marquée par la survenue de plusieurs rechutes de NS contrôlées par une thérapie orale par corticostéroïdes jusqu'en 2017. Par la suite, la patiente n'a pas présenté de rechute de sa maladie. Le traitement anticoagulant et le MMF ont été arrêtés. Un an plus tard, la patiente a présenté une douleur abdominale aiguë diffuse sévère associée à des vomissements postprandiaux et un oedème des membres inférieurs bilatéraux. Les résultats de laboratoire ont confirmé une rechute de NS. Une tomodensitométrie abdominale a révélé une thrombose aiguë de l'artère mésentérique supérieure avec une ischémie mésentérique aiguë. L'exploration intraopératoire a montré une ischémie mésentérique avec une nécrose étendue de l'intestin grêle rendant leurs résections incompatibles avec la vie. La patiente est morte après 48 heures.\n",
+        "synthetic_summary": {
+            "B1": "Il y a une jeune fille qui a eu très mal à la tête quand elle était petite. Les docteurs lui ont donné des médicaments pour l’aider. Elle a été soignée longtemps et elle allait mieux.\n\nUn jour, elle a eu très mal au ventre. Elle a aussi vomi et ses jambes étaient un peu gonflées. Les docteurs ont fait des examens et ont vu que son ventre était malade.\n\nIls ont essayé de l’aider, mais son ventre était trop malade. Elle est partie au ciel après deux jours. Les docteurs étaient très tristes.",
+            "B2": "Voici un résumé plus simple et clair pour un adolescent de 14 ans :\n\n**Histoire de la patiente**  \nCette jeune femme de 20 ans avait une maladie appelée syndrome néphrotique (SN) depuis qu’elle avait 8 ans. Le syndrome néphrotique est une maladie des reins qui fait perdre beaucoup de protéines dans l’urine. Au début, elle a eu un gros caillot de sang dans une veine du cerveau et une embolie pulmonaire, c’est-à-dire un caillot qui est allé dans ses poumons. Elle a été soignée avec des médicaments pour empêcher la formation de caillots (anticoagulants) et des corticoïdes, qui sont des médicaments pour calmer l’inflammation. Plus tard, elle a eu plusieurs rechutes (retours de la maladie) et a reçu un autre médicament appelé mycophénolate mofétil (MMF) pour éviter trop de corticoïdes et permettre une croissance normale.\n\n**Suivi et traitement**  \nLes médecins ont cherché si elle avait un problème qui favorise les caillots, mais ils n’ont rien trouvé. Après neuf ans, ils ont arrêté les anticoagulants. Sa maladie a continué à revenir parfois, mais elle était contrôlée par des corticoïdes. Depuis 2017, elle n’a plus eu de rechute, alors ils ont arrêté le MMF en 2019. Elle est restée sans symptôme pendant un an.\n\n**Nouvelle urgence et complications**  \nUn an après, elle est venue aux urgences avec une douleur très forte au ventre, des vomissements et un gonflement des jambes. Les analyses ont montré que son syndrome néphrotique était revenu. Un scanner a révélé un caillot dans une artère importante qui apporte le sang à l’intestin (artère mésentérique supérieure). Ce caillot a provoqué une mauvaise circulation sanguine et une mort des tissus de l’intestin grêle (ischémie et nécrose). Lors de l’opération, les médecins ont vu que l’intestin était trop abîmé pour être sauvé. Malheureusement, la patiente est décédée 48 heures plus tard.\n\n**Ce que cela signifie**  \nCe cas montre que même chez une jeune personne suivie depuis longtemps pour un syndrome néphrotique, des complications graves comme des caillots dans des artères importantes peuvent survenir. Ces complications peuvent être mortelles malgré les traitements. Il est donc important de surveiller attentivement les patients avec ce type de maladie.",
+            "B3": "Résumé détaillé et structuré\n\nContexte  \nNous rapportons le cas d’une femme de 20 ans suivie depuis l’âge de huit ans pour un syndrome néphrotique (NS) idiopathique, initialement révélé par une thrombose veineuse cérébrale étendue à la veine jugulaire droite, compliquée d’une embolie pulmonaire massive. Ce tableau a été traité par anticoagulants oraux (antagonistes de la vitamine K) et corticostéroïdes, avec une bonne évolution clinique. En l’absence de signes rénaux secondaires (pas d’insuffisance rénale, d’hématurie ou d’hypertension), aucune biopsie rénale n’a été réalisée. La patiente a présenté plusieurs rechutes de NS dépendantes des corticoïdes, conduisant à l’instauration d’un traitement de fond par mycophénolate mofétil (MMF) pour limiter les effets secondaires des corticoïdes et permettre une croissance normale. Une évaluation exhaustive de la thrombophilie n’a révélé aucune anomalie (homocystéine, facteurs de coagulation, mutations génétiques, anticorps antiphospholipides, etc.). Le traitement anticoagulant a été arrêté après neuf ans. La patiente est restée en rémission depuis 2017, ce qui a permis l’arrêt progressif du MMF en 2019.\n\nPrincipales observations  \nUn an après l’arrêt du traitement, la patiente s’est présentée aux urgences pour une douleur abdominale aiguë diffuse, intense, accompagnée de vomissements après les repas et d’un œdème bilatéral des membres inférieurs apparu depuis six heures. L’examen clinique a montré une sensibilité marquée de la région épigastrique, sans fièvre ni altération de l’état de conscience. Les constantes vitales étaient normales. Les analyses urinaires ont révélé une protéinurie, signe d’une rechute du syndrome néphrotique. Les bilans sanguins ont mis en évidence une acidose métabolique compensée, une hypoalbuminémie, une hypercholestérolémie, un syndrome inflammatoire (CRP élevée, leucocytose), ainsi qu’une élévation des D-dimères, de la lactate déshydrogénase et de la créatine phosphokinase. Les fonctions rénales et hépatiques étaient normales. L’échographie abdominale a montré un épanchement intra-abdominal modéré, tandis que la tomodensitométrie a confirmé la présence d’une thrombose aiguë de l’artère mésentérique supérieure, responsable d’une ischémie aiguë de l’intestin.\n\nInterprétation clinique  \nLa thrombose artérielle mésentérique a conduit à une ischémie sévère avec nécrose étendue de presque tout l’intestin grêle, constatée lors de l’exploration chirurgicale. La gravité des lésions a rendu impossible la résection intestinale compatible avec la survie. Cette complication aiguë, survenant dans le contexte d’une rechute de syndrome néphrotique, illustre le risque thrombotique majeur associé à cette maladie, même après une longue période de rémission et l’arrêt des traitements anticoagulants.\n\nProchaines étapes  \nMalheureusement, malgré la prise en charge chirurgicale urgente et les soins intensifs, la patiente est décédée 48 heures après son admission. Ce cas souligne l’importance d’une surveillance étroite des patients atteints de syndrome néphrotique, notamment en ce qui concerne les risques thromboemboliques, et la nécessité d’une prise en charge rapide devant toute douleur abdominale aiguë chez ces patients."
+        }
+    },
+    {
+        "article": "Un Chinois de 38 ans a été admis à notre hôpital pendant plus de deux ans avec une protéinurie modérée accompagnée d'une hématurie microscopique lors d'un examen de laboratoire. Le patient était asymptomatique. Il n'y avait pas d'antécédents d'autres maladies, et aucun membre de la famille du patient n'avait de maladies rénales ou auto-immunes. Il n'y avait pas d'antécédents de consommation de médicaments ou de plantes médicinales chinoises. À l'admission, sa tension artérielle était de 151/81 mmHg, et l'examen physique n'a révélé aucun signe spécifique de hyperlipidémie, tel que l'opacité cornéenne ou les xanthomes. Au moment de la présentation, il avait une protéinurie (0,94 g/24 h) et une hématurie, mais pas de leucocyturie. Son taux de filtration glomérulaire estimé (eGFR) était de 84 ml/min par 1,73 m2. Les taux de cholestérol total et de triglycérides étaient de 205 mg/dL et de 115 mg/dL, respectivement. Les indicateurs immunologiques, tels que les taux de C3, C4 et IgA sériques, étaient normaux. Les autres paramètres de laboratoire sont décrits dans le tableau 1. L'analyse par immunofluorescence a montré une forte coloration pour les IgA, C3 et ApoE, mais une coloration négative pour les IgG, IgM, C1q et C4. En outre, l'immunofluorescence double a montré que KM55 et IgA étaient tous deux colorés positivement dans la région mésangulaire. La biopsie rénale a révélé une dilatation marquée des capillaires remplis de substances thrombotiques et une prolifération mésangulaire. Environ 12 % de la fibrose interstitielle avec atrophie tubulaire a également été observée. Les substances thrombotiques ont été colorées positivement pour le Soudan III et ApoE. L'examen au microscope électronique a révélé un dépôt de granules lipidiques dans la lumière capillaire glomérulaire dilatée, une hyperplasie mésangulaire et un dépôt électronique dense dans la région mésangulaire. Ces caractéristiques pathologiques étaient compatibles avec celles de la LGP avec IgAN.\n\nL'analyse du gène ApoE a révélé une transition hétérozygote C→T dans l'exon 3, qui a modifié l'acide aminé en position 25 de l'arginine à la cystéine (mutation de Kyoto). Le génotypage familial a montré que cette mutation a été transmise du père à sa fille. L'ApoE sérique était de 14,4 mg/dL déterminé par immuno-essai enzymatique (LOT : 20210702, JianCheng Bioengineering Institute). Combiné avec les résultats ci-dessus, le patient a été diagnostiqué avec LPG accompagné d'IgAN.\n\nAprès la biopsie rénale, le patient a été suivi en consultation externe à l'hôpital de Daping. Le taux de lipides plasmatiques et la TFGe étaient dans les limites normales pendant 18 mois, même sans médicaments hypolipidémiants. La protéinurie s'est améliorée (fluctuant à + ~ ± ; rapport albumine urinaire/créatinine de 186,06 mg/g Cr à 111,72 mg/g Cr) après l'administration de 10 mg d'énalapril par jour. En outre, nous avons suivi sa fille et ses taux de protéines urinaires sont restés négatifs.\n",
+        "gold_summary": "Un homme de 38 ans a été admis à notre hôpital en raison de protéinurie et d'hématurie, qui ont été découvertes lors d'un examen urinaire. La fonction rénale et les taux de lipides et de lipoprotéines dans le sang étaient normaux. Après biopsie rénale, le patient a été diagnostiqué comme ayant une LPG avec IgAN. L'analyse du gène ApoE a montré une transition hétérozygote C→T dans l'exon 3, entraînant un changement du 25e acide aminé de l'arginine à la cystéine (mutation de Kyoto). L'analyse génétique de la famille a montré que cette mutation a été héritée de son père et transmise à sa fille. L'ApoE sérique était de 14,4 mg/dL. Combinée aux résultats ci-dessus, le patient a été diagnostiqué comme ayant une LPG accompagnée d'IgAN. Après 18 mois de traitement par enalapril sans thérapie hypolipidémiant, la fonction rénale et les taux de lipides dans le sang étaient stables et les taux de protéines dans l'urine ont été significativement améliorés.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 38 ans est venu à l’hôpital.  \nLes docteurs ont vu qu’il avait un peu de protéines et de sang dans son pipi.  \n\nSes reins fonctionnaient bien. Son sang était normal.  \nLes docteurs ont fait un petit examen avec un tout petit morceau de son rein.  \n\nIls ont trouvé un problème spécial dans ses reins.  \nCe problème venait d’un petit changement dans un gène, que son papa lui a donné.  \nCe gène, il l’a aussi donné à sa fille.  \n\nLe monsieur a pris un médicament doux.  \nAprès un moment, son pipi est devenu meilleur.  \nSes reins et son sang sont restés en bonne santé.  \n\nTout va bien maintenant, et les docteurs le surveillent doucement.",
+            "B2": "**Ce qu'ils ont trouvé chez le patient**  \nUn homme de 38 ans a été suivi pendant plus de deux ans parce qu’il avait des protéines et un peu de sang dans ses urines, détectés lors d’un examen. Il ne présentait pas de symptômes, et ses reins fonctionnaient presque normalement. Ses taux de graisses dans le sang étaient aussi normaux.  \n\nUne biopsie rénale, c’est-à-dire un prélèvement d’un petit morceau de rein pour l’étudier, a montré des signes de deux maladies : la lipoprotéinémie glomérulaire (LPG), où des dépôts gras bouchent certains petits vaisseaux du rein, et la néphropathie à IgA (IgAN), une maladie où des protéines du système immunitaire s’accumulent dans le rein.  \n\n**Ce que cela signifie au niveau génétique**  \nEn étudiant le gène ApoE, qui est important pour le transport des graisses dans le corps, les médecins ont découvert une mutation appelée « mutation de Kyoto ». Cette mutation change une partie de la protéine ApoE, ce qui peut causer la LPG. Cette mutation a été transmise dans la famille : le père du patient l’avait aussi, et elle est passée à sa fille.  \n\n**Le suivi et le traitement**  \nLe patient a reçu un médicament appelé énalapril, qui aide à protéger les reins et à réduire la quantité de protéines dans l’urine. Après 18 mois, ses reins fonctionnaient toujours bien, ses taux de graisses dans le sang restaient normaux, et la quantité de protéines dans ses urines avait beaucoup diminué. Sa fille, qui porte aussi la mutation, n’a pas montré de problème aux reins jusqu’à présent.  \n\n**En résumé**  \nCe cas montre qu’une mutation génétique peut causer une maladie rénale rare avec des dépôts gras et des protéines immunitaires dans le rein. Un traitement adapté peut stabiliser la maladie et améliorer les résultats, même sans médicaments pour réduire les graisses dans le sang.",
+            "B3": "**Contexte**  \nUn homme chinois de 38 ans a été suivi pendant plus de deux ans en raison d’une présence modérée de protéines dans les urines (protéinurie) et d’une hématurie microscopique (sang non visible à l’œil nu dans les urines), découvertes lors d’examens de laboratoire. Le patient ne présentait aucun symptôme, sans antécédents médicaux particuliers ni consommation de médicaments ou de plantes médicinales. Sa tension artérielle était légèrement élevée (151/81 mmHg), mais l’examen clinique ne montrait pas de signes visibles d’anomalies lipidiques, telles que des dépôts sur la cornée ou des xanthomes (amas de lipides sous la peau). Sa fonction rénale était proche de la normale, avec un débit de filtration glomérulaire estimé à 84 ml/min/1,73 m². Les taux sanguins de cholestérol total et de triglycérides étaient dans les limites normales, tout comme les marqueurs immunologiques (C3, C4, IgA).\n\n**Principales Observations**  \nLa biopsie rénale a révélé plusieurs anomalies caractéristiques : une dilatation importante des capillaires glomérulaires remplis de substances ressemblant à des caillots (thromboses), une prolifération des cellules mésangiales (cellules situées dans le glomérule, une structure filtrante du rein), ainsi qu’une fibrose interstitielle modérée avec atrophie tubulaire (lésions chroniques du rein). L’analyse immunofluorescente a montré une forte présence d’immunoglobuline A (IgA), de complément C3 et d’apolipoprotéine E (ApoE) dans la région mésangiale, tandis que d’autres immunoglobulines et composants du complément étaient absents. L’examen au microscope électronique a confirmé la présence de dépôts lipidiques dans les capillaires dilatés et des dépôts denses dans la région mésangiale. Ces caractéristiques sont compatibles avec une lipoprotéinose glomérulaire (LPG) associée à une néphropathie à IgA (IgAN).\n\nL’analyse génétique a identifié une mutation spécifique dans le gène codant pour l’ApoE : une substitution d’une base C par T dans l’exon 3, provoquant un changement d’acide aminé à la position 25, de l’arginine à la cystéine, appelée mutation de Kyoto. Cette mutation a été retrouvée chez le père du patient et transmise à sa fille. Le taux sérique d’ApoE était mesuré à 14,4 mg/dL.\n\n**Interprétation Clinique**  \nLe diagnostic retenu est une lipoprotéinose glomérulaire (LPG) associée à une néphropathie à IgA (IgAN). La LPG est une maladie rénale rare caractérisée par des dépôts lipidiques anormaux dans les glomérules, souvent liée à des mutations du gène ApoE. L’IgAN est une maladie immunologique fréquente du rein, caractérisée par des dépôts d’IgA dans les glomérules. La coexistence des deux pathologies est inhabituelle et a été confirmée par les analyses histologiques et génétiques.\n\n**Prochaines Étapes et Évolution**  \nAprès la biopsie, le patient a été suivi en consultation externe. Il a reçu un traitement par énalapril (un médicament inhibiteur de l’enzyme de conversion de l’angiotensine, utilisé pour protéger les reins) à la dose de 10 mg par jour. Pendant 18 mois de suivi, sans traitement hypolipidémiant, sa fonction rénale est restée stable, les taux lipidiques sanguins normaux, et la protéinurie s’est nettement améliorée, avec une réduction du rapport albumine/créatinine urinaire. Sa fille, porteuse de la même mutation génétique, n’a montré aucun signe de maladie rénale à ce jour.\n\nCe cas illustre l’importance de l’analyse génétique et histologique dans le diagnostic précis des maladies rénales rares, ainsi que l’efficacité d’un traitement ciblé pour stabiliser la fonction rénale et réduire les symptômes urinaires."
+        }
+    },
+    {
+        "article": "Chef des plaintes\nUne femme enceinte de 35 ans a été admise pour des douleurs abdominales 3 heures avant son admission.\n\nHistorique de la maladie actuelle\nElle est initialement venue à la sage-femme avec des douleurs de travail qui étaient de plus en plus fréquentes la veille de son admission. Après une observation de nuit, elle a ressenti des douleurs de travail de plus en plus fréquentes et plus fortes jusqu'à ce qu'elle ressente un inconfort abdominal, aucun mouvement fœtal n'a été ressenti et le rythme cardiaque fœtal était difficile à trouver par la sage-femme. Plus tard, elle a été dirigée vers l'hôpital Otto Iskandar Dinata en raison de la suspicion de mort fœtale intra-utérine. Après un entretien approfondi, elle a obtenu l'eau de la médecine à base de plantes bouillie que sa voisine lui a donnée, qui lui a suggéré de boire l'eau à base de plantes extraite pour l'aider lorsque le travail commencerait, ce qui est censé aider à améliorer le déroulement du travail. Elle a dit que l'eau était faite d'eau bouillie de rumput Fatimah de sa voisine. Pendant l'admission à l'hôpital, elle s'est plainte d'un inconfort abdominal qui ressemblait à une crampe musculaire et à une déchirure.\n\nHistorique personnel et historique familial\nSon antécédent obstétrical indiquait qu'elle était G2P1A0, sa dernière menstruation avait eu lieu le 31 septembre 2022, et l'âge gestationnel actuel était de 41 semaines. Il n'y avait eu aucune complication lors de sa précédente grossesse ; la sage-femme locale avait assisté son accouchement, et le bébé pesait 2600 grammes. Elle était mariée depuis l'âge de 21 ans avec son mari actuel, qui avait huit ans de plus qu'elle. Durant sa grossesse, elle avait eu un contrôle de routine avec la sage-femme tous les mois. Il n'y avait pas de antécédents familiaux pertinents.\n\nExamen physique\nLa tension artérielle de la patiente était de 80/60 mmHg, la fréquence cardiaque de 128 bpm, la fréquence respiratoire de 20 fois par minute, la taille du corps de 152 cm, le poids corporel de 58 kg, et avant la grossesse son poids corporel était de 58 kg. L'examen obstétrique a révélé que son abdomen était raide et tendu, la contraction était difficile d'accès, le son cardiaque fœtal était négatif, aucun signe d'anneau de faisceau, et la hauteur du fond était de 32 cm. De VT, la membrane était positive, et l'ouverture du col était de 3 cm.\n\nDiagnostic final\nLe diagnostic final de ce cas était G2P1A0 parturient aterm phase latente ; abdomen aigu en raison de la suspicion de décollement placentaire ; et décès foetal intra-utérin.\n\nTraitement\nUne laparotomie exploratoire a été décidée en raison de la douleur abdominale aiguë. Au cours de l'intervention, il n'y avait aucun signe de vie de la part du bébé, le bébé était une fille, son poids était de 2350 grammes et sa longueur était de 44 cm. L'opérateur a également constaté que le placenta était situé à l'extérieur et que son utérus était déjà rompu, environ 15-18 cm. L'opérateur a décidé de pratiquer une hystérectomie subtotale sur la patiente en raison du contexte éloigné et d'une transfusion sanguine non disponible, il est donc risqué de pratiquer une hystérotomie.\n\nRésultat et suivi\nLe bébé ne pouvait pas être sauvé en raison d'une mortinaissance. Son diagnostic final était rupture utérine spontanée > 15 cm en P2A0 post-terme ; mortinaissance. Plus tard, elle a été hospitalisée pendant quelques jours, puis son état s'est amélioré. La patiente était triste du résultat de la naissance, mais reconnaissante au médecin parce que l'équipe a pu la sauver. Elle a dit qu'elle serait plus prudente quant à ce qu'elle consomme, en particulier la médecine traditionnelle.\n",
+        "gold_summary": "Une femme enceinte de 35 ans a été envoyée à l'hôpital en raison de douleurs abdominales 3 heures avant son admission, en raison d'une suspicion de mort fœtale intra-utérine. Elle a bu l'eau aux herbes extraite pour l'aider à accoucher, qui était faite d'eau bouillie avec du rumput Fatimah de chez sa voisine. Elle a ensuite été diagnostiquée avec une phase latente de l'aterme parturient G2P1A0 ; abdomen aigu en raison d'une suspicion de décollement du placenta dd/ rupture de l'utérus ; et mort fœtale intra-utérine. Une laparotomie exploratoire a été décidée en raison de douleurs abdominales aiguës, et pendant la procédure, l'opérateur a décidé de faire une hystérectomie subtotale sur la patiente. L'opérateur a constaté que son utérus était déjà rompu, environ 15-18 cm et que le placenta était situé à l'extérieur de l'utérus.\n",
+        "synthetic_summary": {
+            "B1": "Une maman enceinte avait très mal au ventre. Elle a bu une eau aux plantes que sa voisine lui a donnée. Mais le bébé ne bougeait plus dans son ventre. \n\nLa maman est allée à l’hôpital. Les docteurs ont vu que le bébé était très fatigué et qu’il ne vivait plus. Le ventre de la maman était très dur et faisait très mal. \n\nLes docteurs ont fait une opération pour aider la maman. Ils ont vu que le ventre de la maman était cassé. Ils ont dû faire une grande opération pour la soigner. \n\nLa maman était triste, mais les docteurs ont fait tout pour la sauver. Maintenant, elle va mieux.",
+            "B2": "Une femme enceinte de 35 ans est venue à l’hôpital parce qu’elle avait de fortes douleurs au ventre depuis trois heures. On pensait que son bébé était mort dans son ventre. Avant cela, elle avait bu une infusion à base d’une plante appelée rumput Fatimah, donnée par sa voisine, pour aider le travail à commencer.\n\nÀ l’hôpital, les médecins ont découvert qu’elle était en début de travail, mais qu’elle avait un problème grave : le placenta, qui nourrit le bébé, semblait s’être détaché ou que son utérus s’était déchiré. Malheureusement, le bébé ne montrait plus de signes de vie.\n\nPour comprendre ce qui se passait, les médecins ont fait une opération appelée laparotomie, qui consiste à ouvrir le ventre. Pendant l’opération, ils ont vu que l’utérus de la femme était déchiré sur une grande longueur (15 à 18 cm) et que le placenta était en dehors de l’utérus. Le bébé, une fille, pesait 2350 grammes mais était malheureusement décédé.\n\nÀ cause de la gravité de la déchirure et du manque de sang disponible pour une transfusion, les médecins ont dû enlever une partie de l’utérus (hystérectomie subtotale) pour sauver la vie de la maman. Après quelques jours à l’hôpital, elle s’est remise. Elle était triste de la perte de son bébé, mais reconnaissante envers les médecins qui l’avaient sauvée. Elle a aussi dit qu’elle ferait plus attention à ce qu’elle boit pendant sa grossesse, notamment aux remèdes à base de plantes.",
+            "B3": "Résumé détaillé et structuré\n\nContexte  \nUne femme enceinte de 35 ans, en fin de grossesse (41 semaines d’aménorrhée), a été admise à l’hôpital après avoir ressenti des douleurs abdominales aiguës depuis environ trois heures. Elle avait initialement consulté une sage-femme la veille pour des contractions de plus en plus fréquentes et intenses. Par la suite, elle a signalé une absence de mouvements fœtaux et le rythme cardiaque du bébé était difficile à détecter, ce qui a conduit à une suspicion de mort fœtale intra-utérine. Elle avait également consommé une infusion à base de plantes (rumput Fatimah) recommandée par une voisine pour faciliter le travail.\n\nPrincipales observations  \nÀ l’examen, la patiente présentait une tension artérielle basse (80/60 mmHg), une fréquence cardiaque élevée (128 battements par minute) et un abdomen tendu et rigide. Le rythme cardiaque fœtal était absent, confirmant la mort du fœtus. L’examen gynécologique montrait une ouverture du col de l’utérus à 3 cm et des membranes rompues. L’état clinique évoquait un abdomen aigu, avec une suspicion de décollement placentaire ou de rupture utérine.\n\nInterprétation clinique  \nLe diagnostic retenu était celui d’une grossesse à terme (G2P1A0) en phase latente du travail, compliquée par un abdomen aigu lié à une probable rupture utérine ou un décollement placentaire, associée à une mort fœtale intra-utérine. La consommation d’une infusion traditionnelle à base de rumput Fatimah, bien que destinée à faciliter le travail, pourrait avoir contribué à ces complications.\n\nProchaines étapes et traitement  \nFace à la douleur abdominale aiguë et à la gravité de la situation, une laparotomie exploratoire (intervention chirurgicale pour examiner l’abdomen) a été réalisée. Au cours de l’opération, le fœtus, une fille pesant 2350 grammes, était décédé. L’équipe chirurgicale a découvert une rupture utérine importante, mesurant entre 15 et 18 cm, ainsi qu’un placenta situé en dehors de l’utérus. En raison de l’état avancé de la rupture et de l’absence de possibilité de transfusion sanguine, une hystérectomie subtotale (ablation partielle de l’utérus) a été pratiquée pour sauver la vie de la patiente.\n\nRésultat et suivi  \nLa patiente a survécu à l’intervention et a été hospitalisée plusieurs jours pour surveillance. Elle a exprimé sa tristesse face à la perte de son enfant, mais aussi sa gratitude envers l’équipe médicale qui a pu préserver sa vie. Elle a indiqué qu’elle serait désormais plus prudente quant à l’utilisation de médecines traditionnelles pendant la grossesse."
+        }
+    },
+    {
+        "article": "Une primigravide de 19 ans, à 35 semaines de gestation, sans antécédents médicaux ou familiaux, sans consanguinité, a été adressée pour évaluation d'une masse pelvienne fœtale découverte lors d'une échographie du troisième trimestre. À l'admission, les signes vitaux étaient dans les limites normales et les échographies fœtales antérieures étaient également dans la norme.\n\nLa patiente a été hospitalisée pour un examen de la malformation fœtale. L'échographie obstétrique transabdominale a montré un fœtus unique en position longitudinale, une présentation cul-de-sac complète et des données biométriques et un poids fœtal adéquats pour l'âge gestationnel. Les résultats anatomiques comprenaient une tête fœtale avec hypotélorisme et microphthalmie ; un abdomen fœtal avec une image hypogénique circulaire de 58 × 59 × 69 mm aux contours irréguliers et un volume de 124 centimètres cubes localisé postérieur à la vessie, sans absorption de doppler couleur ; un système urinaire fœtal non compromis, avec une impression diagnostique d'hydrométrorcolpos fœtal. L'imagerie par résonance magnétique fœtale complémentaire a confirmé la présence d'hypotélorisme, de microphthalmie et, dans le bassin fœtal, d'une lésion kystique de 74 × 64 × 52 mm de taille significative et de morphologie ronde s'étendant du bassin à l'abdomen, de haute intensité de signal en T2 et faible en T1, sans septations ou composants solides à l'intérieur. Elle a provoqué un déplacement antérieur de la vessie et un déplacement postérieur du rectum. Une petite formation sacculaire a été observée dans la partie supérieure, suggérant la présence de liquide dans l'utérus, compatible avec l'impression diagnostique d'hydrométrorcolpos fœtal.\n\nPendant l'hospitalisation, la patiente a eu une activité utérine prématurée ; l'infection a été écartée avec un hémogramme complet, une protéine C réactive et une analyse d'urine normale. Une maturation pulmonaire prématurée tardive a été instituée. La progression du travail prématuré et une présentation par le siège complète ont nécessité une césarienne immédiate à 36 semaines pour accoucher d'un seul fœtus avec un liquide amniotique normal, une nouveau-née de sexe féminin pesant 2 550 g, un APGAR de 2, 0, 0 à une, cinq et dix minutes, respectivement. La réanimation néonatale n'a pas été efficace, le résultat étant la mort périnatale.\n\nL'examen post mortem a révélé des oreilles basses, une micrognathie, un large pont nasal et une anoftalmie bilatérale ; le cou et la poitrine avaient une apparence normale ; l'abdomen était gonflé ; il y avait des syndactylie dans les membres supérieurs et inférieurs ; les organes génitaux externes féminins avaient un hymen imperforé. L'examen interne du crâne et des sections du cerveau n'a révélé aucune preuve de malformations graves ou de lésions focales. Le thorax, le cœur, les poumons et le diaphragme étaient normaux. L'abdomen, le foie, la rate, les reins et la vessie avaient une morphologie normale. L'utérus et le vagin avaient une apparence kystique et étaient nettement dilatés par le contenu de matériel jaunâtre associé à l'atrésie vaginale. Ces résultats ont confirmé un diagnostic définitif de FS.\n",
+        "gold_summary": "Une primigravide de 19 ans, enceinte de 35 semaines, présentant une hydrométrorrhée associée à un hypotélorisme et une microphtalmie. Une césarienne a été pratiquée en raison d'un travail de siège et d'une mort périnatale. L'autopsie a confirmé une hydrométrorrhée secondaire à une atrésie vaginale et un hymen imperforé, associés à un cryptophthalmos, des syndactylie, des malformations nasales et auriculaires, confirmant le diagnostic du syndrome de Fraser.\n",
+        "synthetic_summary": {
+            "B1": "Une jeune maman attendait un bébé. Le bébé avait un petit problème dans son ventre. Sa petite poche pour faire pipi était un peu gonflée.\n\nLe bébé avait aussi des petits yeux très petits et des doigts qui étaient collés. Le bébé ne pouvait pas sortir normalement, alors la maman a eu une opération pour aider.\n\nMalheureusement, le bébé est parti au ciel. Le docteur a regardé le bébé et a vu que certains petits morceaux du corps étaient différents. C’est une maladie très rare qui fait ça. Les docteurs sont là pour aider les mamans et les bébés.",
+            "B2": "**Ce qu'ils ont trouvé chez la maman et le bébé**\n\nUne jeune femme de 19 ans, enceinte pour la première fois et à 35 semaines de grossesse, a été suivie parce qu’on a découvert une masse anormale près du bébé lors d’une échographie. Cette masse était liée à une accumulation de liquide dans l’utérus et le vagin du bébé, appelée hydrométrorcolpos. Le bébé présentait aussi des anomalies au niveau des yeux (yeux très rapprochés et très petits) et d’autres malformations visibles.\n\n**Ce qui s’est passé pendant l’accouchement**\n\nLa maman a commencé un travail prématuré avec le bébé en position siège (les fesses en bas). Une césarienne a été faite à 36 semaines pour essayer de sauver le bébé. Malheureusement, le bébé est né sans signes de vie malgré les efforts pour le réanimer.\n\n**Ce que l’autopsie a montré**\n\nAprès la naissance, une autopsie a été réalisée. Elle a révélé plusieurs malformations : des oreilles basses, une mâchoire petite, un large nez, l’absence des yeux (anoftalmie), des doigts soudés (syndactylie), et un hymen qui ne s’ouvrait pas. À l’intérieur, l’utérus et le vagin étaient très dilatés à cause d’une obstruction (atrésie vaginale) qui expliquait l’accumulation de liquide. Le reste des organes était normal.\n\n**Ce que cela signifie**\n\nTous ces signes ensemble correspondent au syndrome de Fraser, une maladie rare qui cause plusieurs malformations congénitales. Ce diagnostic explique les problèmes observés chez le bébé et la difficulté à le sauver à la naissance.",
+            "B3": "Résumé destiné à un public adulte non-médecin\n\n**Contexte**  \nUne jeune femme de 19 ans, enceinte pour la première fois et à 35 semaines de grossesse, a été adressée pour l’évaluation d’une masse anormale détectée près du fœtus lors d’une échographie réalisée au troisième trimestre. Elle ne présentait aucun antécédent médical ou familial particulier, et les examens prénataux précédents étaient normaux.\n\n**Principales observations**  \nL’échographie a montré un fœtus unique avec un développement adapté à son âge gestationnel, mais présentant des anomalies faciales telles qu’un rapprochement anormal des yeux (hypotélorisme) et des yeux très petits (microphthalmie). Une masse kystique (remplie de liquide) importante a été identifiée dans la région pelvienne du fœtus, derrière la vessie, sans signe d’irrigation sanguine. Une imagerie par résonance magnétique (IRM) fœtale a confirmé cette masse kystique, qui correspondait à une accumulation de liquide dans l’utérus et le vagin du fœtus, une condition appelée hydrométrorcolpos. Cette masse déformait les organes pelviens voisins. Pendant l’hospitalisation, la mère a présenté un travail prématuré, nécessitant une césarienne à 36 semaines en raison de la position du bébé (présentation par le siège). La naissance a été compliquée par une absence d’activité vitale chez le nouveau-né, malgré les tentatives de réanimation.\n\n**Interprétation clinique**  \nL’examen post mortem du bébé a révélé plusieurs malformations congénitales : absence des globes oculaires (anoftalmie), malformations des oreilles et du nez, fusion anormale des doigts et des orteils (syndactylie), ainsi qu’un hymen imperforé (une membrane fermée empêchant l’écoulement normal des sécrétions vaginales). L’utérus et le vagin étaient dilatés par du liquide, confirmant une obstruction due à une atrésie vaginale (absence ou fermeture anormale du vagin). L’ensemble de ces anomalies correspond au syndrome de Fraser, une maladie génétique rare caractérisée par des malformations multiples affectant notamment les yeux, les organes génitaux et les membres.\n\n**Prochaines étapes**  \nCe cas souligne l’importance d’un diagnostic prénatal précis en cas de masse pelvienne fœtale et d’anomalies faciales, afin de préparer la prise en charge périnatale et d’informer les parents sur le pronostic et les implications génétiques. Une consultation en génétique médicale est recommandée pour évaluer le risque de récidive dans les grossesses futures et pour un accompagnement adapté."
+        }
+    },
+    {
+        "article": "Une femme de 67 ans atteinte d'une cardiomyopathie dilatée, diagnostiquée il y a 10 ans avec une fraction d'éjection ventriculaire gauche (FEVG) de 35 % (intervalle de référence : 50 % - 70 %) et une MR modérée, a été adressée pour dyspnée de classe II et III de la New York Heart Association (NYHA). Elle ne présentait pas de facteurs de risque cardiovasculaires significatifs ou d'autres comorbidités qui auraient pu affecter la stratégie de traitement. Ses symptômes persistaient malgré un traitement médical optimal avec 10 mg de carvedilol, 2,5 mg d'énalapril, 25 mg de spironolactone, 30 mg d'azosémide et 3,75 mg de tolvaptan par jour. À l'examen physique, la patiente mesurait 160 cm, pesait 57 kg, avait une tension artérielle de 123/71 mmHg et une fréquence cardiaque de 100/min. L'examen cardiaque a révélé un murmure d'éjection systolique de grade II/VI de Levine au troisième espace intercostal gauche et un oedème modéré des membres inférieurs.\n\nLes taux de peptide natriurétique de type B en ambulatoire allaient de 150 à 250 pg/mL (intervalle normal : < 125 pg/mL). L’échocardiographie transthoracique a révélé un diamètre de fin de diastole du ventricule gauche de 70 mm (intervalle normal : 35-52 mm), une fraction d’éjection du ventricule gauche de 31 %, et une MR fonctionnelle sévère entre les crêtes A2 et P2, caractérisée par une fraction régurgitante de 59 % (seuil pour une MR sévère : 50 %) et une surface effective de l’orifice régurgitant de 0,27 cm2 (seuil pour une MR sévère : 0,20 cm2). L’échocardiographie transœsophagienne (TEE) a confirmé un rétrécissement significatif de la veine contractée > 11 mm (seuil pour une MR sévère : 7 mm). Malgré un score de la Society of Thoracic Surgeons faible (1,89 %), notre équipe multidisciplinaire a choisi le M-TEER en utilisant deux dispositifs MitraClip de deuxième génération en raison du dysfonctionnement du ventricule gauche, de l’étiologie fonctionnelle de la MR et de la préférence du patient pour une mobilisation précoce.\n\nLa réparation transcathéter de la valve mitrale bord à bord a été réalisée sous anesthésie générale. Au cours de la préparation du clip, une légère résistance a été constatée lorsque l'introduction du clip glissait sur le clip. Bien que le clip ait semblé fonctionner normalement lors des contrôles, l'introduction n'a pas été inspectée de manière approfondie. Le clip a ensuite été avancé dans le système sans difficulté. Après la ponction transeptale et l'avancement vers la position de chevauchement, le clip a été positionné sur la valve mitrale sans problème. Cependant, lorsque le levier de verrouillage a été déverrouillé pour ouverture dans la LA, le clip a montré un mouvement limité et ne s'est pas ouvert au-delà de 30°.\n\nLes premières tentatives de fermeture et de récupération du clip ont échoué en raison de la résistance du positionneur de bras. Pour résoudre le problème, nous avons ramené le positionneur de bras à la position neutre et tiré la poignée de verrouillage vers l'arrière d'environ 5 mm. Nous avons ensuite légèrement tourné le positionneur de bras dans le sens de la fermeture, puis dans le sens de l'ouverture. Lorsque cette manœuvre a échoué, nous avons répété le processus en tournant davantage le positionneur de bras dans le sens de la fermeture, ce qui a engendré une résistance mécanique sans précédent. Au cours de la rotation suivante dans le sens de l'ouverture, le clip s'est soudainement ouvert à 180° et s'est détaché du système de distribution de clips (CDS), restant connecté uniquement par la ligne de préhension dans sa position par défaut.\n\nSous TEE et guidage fluoroscopique, nous avons effectué le retrait direct du clip. Bien que les pinces aient été temporairement déplacées vers le bas lors du détachement, elles sont revenues à leur position relevée lors d'une traction contrôlée vers le cathéter guide orientable (SGC). La position de la pince a été maintenue pour assurer une connexion sécurisée. En utilisant une traction douce et régulière sur le CDS, le clip a été progressivement guidé vers le SGC. Le clip s'est inversé au cours de ce processus et est partiellement entré dans le SGC, permettant un retrait sécurisé de l'ensemble du système dans l'oreillette droite. L'échocardiographie transœsophagienne a révélé un défaut septal auriculaire de 2 à 3 mm, mais aucune autre complication mécanique n'a été observée avec une hémodynamique stable. Le CDS et le SGC ont été récupérés par une incision fémorale. Une inspection minutieuse du système récupéré a révélé une déchirure de l'introducteur qui n'était pas visible lors de la préparation initiale.\n\nÀ la suite de la récupération du système, deux dispositifs MitraClip NT ont été implantés avec succès en utilisant de nouveaux CDS et SGC, ce qui a entraîné une MR résiduelle modérée. Les rayons X et TEE ont confirmé qu'aucun composant du dispositif n'était resté chez le patient.\n\nLa patiente a été déchargée le jour 4 sans complications. Au cours du suivi ambulatoire, la pharmacothérapie a été optimisée : le traitement par bêta-bloquant a été changé de carvedilol 10 mg à bisoprolol 3,75 mg quotidien, qui a ensuite été augmenté à 5 mg. L'inhibiteur de l'enzyme de conversion de l'angiotensine a été changé d'énalapril 2,5 mg à perindopril 4 mg quotidien, et a ensuite été remplacé par sacubitril/valsartan 200 mg quotidien. L'empagliflozine 10 mg quotidien a été ajoutée au régime après son approbation réglementaire. Ses symptômes s'étaient améliorés à la classe NYHA I et sont restés stables pendant 4,5 ans.\n",
+        "gold_summary": "Une femme de 67 ans atteinte de cardiomyopathie dilatée a subi une M-TEER pour une MR fonctionnelle sévère. Bien que la résistance ait été constatée lors de la préparation initiale et du chargement de l'appareil, les tests fonctionnels limités sont apparus normaux et la procédure a été poursuivie. Au cours de la manipulation du clip dans l'oreillette gauche, la résistance mécanique dans le bras de positionnement a conduit à un détachement inattendu du MitraClip, relié uniquement par la ligne de préhension. Grâce à une traction soigneuse sous guidage échocardiographique et fluoroscopique, nous avons récupéré le clip par voie percutanée avec succès. La procédure a été complétée avec de nouveaux systèmes MitraClip, obtenant une MR résiduelle modérée. Les symptômes de la patiente sont passés de New York Heart Association Classes II et III à I, avec une amélioration soutenue pendant 4,5 ans de suivi.\n",
+        "synthetic_summary": {
+            "B1": "Une dame de 67 ans avait un cœur un peu fatigué. Elle avait un problème avec une petite porte dans son cœur qui ne se fermait pas bien. \n\nLes médecins ont voulu réparer cette porte avec un petit clip spécial. Au début, le clip a eu un petit souci et s’est un peu décroché. \n\nLes médecins ont été très doux et ont réussi à enlever ce clip sans faire de mal. Puis, ils ont mis un nouveau clip qui a bien marché. \n\nAprès, la dame a eu moins de mal à respirer et elle s’est sentie mieux pendant longtemps.",
+            "B2": "### Ce qu'ils ont fait et ce qu'ils ont trouvé\n\nUne femme de 67 ans avait un problème au cœur appelé cardiomyopathie dilatée, ce qui signifie que son muscle cardiaque était affaibli et que son ventricule gauche (la partie qui pompe le sang) ne fonctionnait pas bien. Elle souffrait aussi d’une fuite importante de la valve mitrale, appelée régurgitation mitrale (MR), qui empêche le sang de circuler correctement. Ses symptômes, comme un essoufflement, étaient assez sérieux malgré un traitement médical.\n\nPour améliorer sa situation, les médecins ont décidé de faire une réparation de la valve mitrale sans ouvrir le cœur, en utilisant une technique appelée M-TEER avec un appareil nommé MitraClip. Cet appareil agit comme une petite pince pour rapprocher les feuillets de la valve et réduire la fuite.\n\n### Ce qui s’est passé pendant la procédure\n\nAu début, ils ont senti une résistance quand ils préparaient et chargeaient le clip, mais comme les tests semblaient normaux, ils ont continué. Plus tard, quand ils ont essayé d’ouvrir le clip dans une partie du cœur appelée l’oreillette gauche, le bras qui positionne le clip a rencontré une forte résistance. Cela a provoqué un détachement inattendu du clip : il s’est séparé du système qui le guide, restant attaché seulement par un fil.\n\n### Comment ils ont résolu le problème\n\nSous contrôle par échographie et rayons X, les médecins ont réussi à récupérer le clip cassé en le tirant doucement par la veine, sans causer de blessure. Après cela, ils ont utilisé un nouveau système MitraClip pour finir la réparation de la valve. La fuite mitrale est alors devenue modérée, ce qui est une amélioration importante.\n\n### Résultat pour la patiente\n\nAprès la procédure, la patiente a été surveillée et son traitement médical a été ajusté pour mieux contrôler sa maladie. Ses symptômes se sont nettement améliorés : elle est passée d’une difficulté à respirer modérée à presque normale. Cette amélioration est restée stable pendant plus de 4 ans.\n\n### En résumé\n\nCette histoire montre qu’une procédure complexe pour réparer une valve du cœur peut rencontrer des problèmes techniques, mais qu’avec de la prudence et de l’expérience, les médecins peuvent gérer ces situations difficiles et aider les patients à retrouver une meilleure qualité de vie.",
+            "B3": "**Contexte**  \nUne femme de 67 ans souffrant d’une cardiomyopathie dilatée depuis dix ans, avec une fonction ventriculaire gauche réduite (fraction d’éjection à 31-35 %) et une régurgitation mitrale (MR) fonctionnelle sévère, présentait une dyspnée persistante de classe II-III selon la classification de la New York Heart Association (NYHA) malgré un traitement médical optimal. L’échocardiographie avait confirmé une dilatation importante du ventricule gauche et une MR sévère justifiant une intervention. En raison de la dysfonction ventriculaire, de la nature fonctionnelle de la MR et de la préférence de la patiente pour une procédure moins invasive, une réparation mitrale transcathéter par MitraClip (M-TEER) a été décidée.\n\n**Principales Observations**  \nLors de la préparation du premier clip MitraClip, une résistance inhabituelle a été notée lors de son chargement, mais les contrôles fonctionnels initiaux semblaient normaux, ce qui a conduit à poursuivre la procédure. Cependant, lors de la manipulation du clip dans l’oreillette gauche, un blocage mécanique important au niveau du bras de positionnement a empêché l’ouverture complète du clip. Les tentatives de fermeture et de récupération ont échoué, et après des manœuvres répétées de rotation et de traction, le clip s’est détaché de son système de distribution, restant suspendu uniquement par la ligne de préhension. Sous guidage échocardiographique transœsophagien et fluoroscopique, une extraction percutanée prudente a été réalisée avec succès, sans complications hémodynamiques ni lésion septale significative.\n\nUne inspection du matériel récupéré a révélé une déchirure de l’introducteur, non détectée initialement, probablement responsable de la résistance mécanique rencontrée. La procédure a ensuite été poursuivie avec deux nouveaux dispositifs MitraClip, permettant une réduction efficace de la MR à un grade modéré.\n\n**Interprétation Clinique**  \nCe cas illustre une complication mécanique rare mais grave lors d’une réparation mitrale par MitraClip, liée à un défaut matériel invisible au départ. La gestion rapide et méthodique sous imagerie multimodale a permis de retirer le dispositif défectueux sans recours chirurgical, évitant ainsi un risque majeur pour la patiente. L’utilisation de nouveaux dispositifs a permis d’achever la procédure avec succès.\n\n**Prochaines Étapes et Suivi**  \nLa patiente a été hospitalisée quatre jours sans complications post-procédure. Son traitement médical a été ajusté et optimisé, notamment par un changement de bêta-bloquant, d’inhibiteur de l’enzyme de conversion vers un inhibiteur de la néprilysine (sacubitril/valsartan), et l’ajout d’empagliflozine. Ces modifications ont contribué à une amélioration clinique notable, avec une réduction des symptômes à la classe NYHA I, stable sur une période de suivi de 4,5 ans. Ce suivi prolongé souligne l’efficacité durable de la réparation mitrale combinée à une prise en charge médicale adaptée dans ce contexte de cardiomyopathie dilatée avec MR fonctionnelle sévère."
+        }
+    },
+    {
+        "article": "Femme de 65 ans, native et originaire de Mérida, au Venezuela, ayant une antécédent chirurgical d'appendicectomie ouverte, qui présente une maladie actuelle de 4 mois d'évolution caractérisée par une douleur abdominale d'apparition insidieuse, d'intensité modérée, lancinante, initialement généralisée, mais localisée dans la fosse iliaque droite après 3 mois, ce qui l'a amenée à consulter un médecin, qui lui a indiqué un traitement médical, avec une amélioration partielle du tableau. Étant donné que la symptomatologie persiste et qu'une masse palpable apparaît dans la fosse iliaque droite, elle se rend au service de gastroentérologie de notre établissement, où une coloscopie est réalisée, qui révèle une tumeur sous-épithéliale dans la région cecale.\n\nElle présente également une altération du schéma de défécation, alternant périodes de constipation et diarrhées, des élévations de température d'apparition récente (15 jours) et une intolérance à la voie orale (solides), raison pour laquelle elle a été adressée au service de chirurgie générale.\n\nL’examen physique a révélé un état clinique stable, une absence de fièvre, une hydratation adéquate, une bonne coloration cutanée et muqueuse ; à l’examen abdominal, un abdomen plat, des bruits hydroaéreux présents, un abdomen mou, dépressible, une masse palpable dans la fosse iliaque droite de 5 × 5 cm, mobile, douloureuse à la palpation et sans signe d’irritation péritonéale ; au toucher rectal, un anus sans altérations, un sphincter avec une tonicité conservée, une ampoule rectale aux parois lisses, sans tuméfaction palpable, et avec peu de selles molles à l’intérieur ; un examen gynécologique sans altérations ; le reste de l’examen physique, sans altérations.\n\nUne tomographie par ordinateur à double contraste (oral et intraveineux) est demandée, dans laquelle on observe une perte de la configuration habituelle dans la région iléo-cécale avec une augmentation importante du volume du côlon, et on observe l'incursion de l'iléon dans le côlon droit sur une longue distance allant du côlon transverse à l'angle splénique, où on observe une formation sacculaire remplie de contraste oral. Au cours de la phase artérielle, la région cæcale ne montre aucun changement de densité et les trajets vasculaires sont visibles dans tout l'intérieur du côlon, accompagnés de tissu adipeux, mais il existe un double renforcement dans la région de l'angle splénique du côlon transverse. On conclut que les résultats suggèrent une intussusception intestinale secondaire à une tumeur.\n\nAu vu des résultats de l’examen tomographique et de l’examen physique, la patiente a été emmenée au bloc opératoire, où on a constaté la présence d’un petit liquide jaunâtre libre dans la cavité abdominale. Une intussusception iléo-colique a été observée jusqu’à l’angle hépatique du côlon transverse. En réduisant l’intussusception, on a observé une tumeur de 10 cm dans la valve iléo-cécale et de 10 cm dans l’intestin grêle, qui envahit la séreuse, qui est indurée et qui compromet la lumière intestinale, et de multiples adénopathies de tailles variées (non > 2 cm) dans le mésentère du côlon droit, sans évidence de lésions dans le foie. On a effectué la manœuvre de Cattell-Braasch, une hémicolectomie droite jusqu’à l’émergence de l’artère colique droite, la fermeture du moignon du côlon transverse et la confection d’une anastomose iléo-transverse latérale, le lavage et le drainage de la cavité, et la fermeture par plans de la cavité abdominale. L’acte chirurgical s’est achevé sans complications et la patiente a eu une évolution clinique favorable. Au bout de 48 heures de postopératoire, elle a commencé à prendre des aliments par voie orale. Elle a été renvoyée à la maison cinq jours après l’opération, le drain a été retiré au bout de 10 jours et la patiente a été suivie par le service de chirurgie générale, sans évènements dans son évolution.\n\nL’échantillon étudié a révélé une lésion néoplasique caractérisée par la prolifération de structures tubulaires revêtues d’un revêtement endothélial présentant un cytoplasme éosinophile, des noyaux vésiculaires sans nucléole, des vacuoles intracytoplasmiques présentant des lumières endothéliales, quelques érythrocytes et des mitoses isolées (trois sur 40 champs de haute puissance). Cette zone présente une augmentation du tissu conjonctif fibreux. On observe à la périphérie un infiltrat inflammatoire polymorphonuclearnéutrophile et lymphocytaire important avec des zones de nécrose, des détritus cellulaires et des érythrocytes extravasés. Des colorations spéciales au PAS (acide périodique-Schiff) et au trichrome de Gomori ont révélé la présence de tissu conjonctif fibreux autour des zones de lésion néoplasique décrites ; les coupes de l’intestin grêle revêtu de muqueuse ne présentent pas de modifications significatives, tout comme le mésentère. Les résultats de l’examen de l’intestin grêle sont compatibles avec une HÉ de malignité intermédiaire.\n",
+        "gold_summary": "Femme de 65 ans se présentant avec des douleurs abdominales chroniques. Une tomographie par ordinateur a été réalisée et une incursion de l'iléon dans le côlon droit a été observée. Elle a été emmenée au bloc opératoire où on a découvert une intussusception intestinale iléo-colique due à une tumeur de l'intestin grêle, avec un résultat anatomopathologique d'hémangio-endothéliome épithélioïde.\n",
+        "synthetic_summary": {
+            "B1": "Une dame de 65 ans avait mal au ventre depuis longtemps. Les docteurs ont fait une grande photo de son ventre. Ils ont vu que une partie de son ventre était rentrée dans une autre. \n\nIls l'ont aidée avec une opération. Ils ont trouvé une grosse boule dans son ventre. Cette boule venait d’un petit bout de son ventre. \n\nAprès, ils ont regardé cette boule au microscope. Ils ont vu que ce n’était pas gentil, mais ils ont bien soigné la dame. Elle va mieux maintenant.",
+            "B2": "**Ce qu'ils ont trouvé**  \nUne femme de 65 ans avait mal au ventre depuis plusieurs mois. Les médecins ont fait un scanner (une sorte de photo détaillée à l’intérieur du corps) et ont vu que l’intestin grêle s’était glissé à l’intérieur du côlon droit, ce qui s’appelle une intussusception. Cette situation est souvent causée par une tumeur qui fait comme un obstacle.\n\n**Ce que cela signifie**  \nLors de l’opération, ils ont confirmé cette intussusception entre l’intestin grêle et le côlon. Ils ont enlevé la partie malade et ont découvert que la tumeur était un hémangio-endothéliome épithélioïde. C’est un type de tumeur qui vient des cellules des vaisseaux sanguins et qui peut être de gravité moyenne. Grâce à l’opération, la patiente a pu guérir et reprendre une vie normale.",
+            "B3": "Résumé détaillé et structuré\n\nContexte  \nUne femme de 65 ans, originaire du Venezuela, a consulté pour une douleur abdominale évoluant depuis quatre mois. Cette douleur, initialement diffuse et modérée, s’est progressivement localisée dans la fosse iliaque droite. Elle présentait également des troubles du transit intestinal alternant constipation et diarrhée, une fièvre récente et une difficulté à tolérer les aliments solides. Une masse palpable douloureuse de 5 × 5 cm a été détectée dans la fosse iliaque droite lors de l’examen clinique.\n\nPrincipales observations  \nUne coloscopie a révélé une tumeur sous-épithéliale dans la région cæcale. La tomodensitométrie (scanner) abdominale, réalisée avec double contraste, a montré une perte de la configuration normale de la région iléo-cæcale, une dilatation importante du côlon droit et une invagination (intussusception) de l’iléon dans le côlon droit sur une longue distance, suggérant une intussusception intestinale secondaire à une tumeur. L’examen physique et les images ont motivé une intervention chirurgicale.\n\nInterprétation clinique et intervention  \nAu bloc opératoire, une intussusception iléo-colique étendue jusqu’à l’angle hépatique du côlon transverse a été confirmée. La réduction de cette invagination a permis de mettre en évidence une tumeur de 10 cm au niveau de la valve iléo-cæcale et une autre de même taille dans l’intestin grêle, envahissant la séreuse et obstruant la lumière intestinale. Plusieurs ganglions lymphatiques mésentériques étaient également présents, sans signes de métastases hépatiques. Une hémicolectomie droite avec anastomose iléo-transverse a été réalisée sans complications, et la patiente a eu une récupération postopératoire favorable.\n\nRésultats anatomopathologiques  \nL’analyse microscopique a montré une prolifération néoplasique de structures tubulaires tapissées par des cellules endothéliales aux caractéristiques épithélioïdes, avec un faible taux de mitoses et un infiltrat inflammatoire périphérique important. Ces éléments sont compatibles avec un hémangio-endothéliome épithélioïde, une tumeur vasculaire de malignité intermédiaire. Les tissus adjacents, y compris la muqueuse intestinale et le mésentère, ne présentaient pas d’anomalies significatives.\n\nProchaines étapes  \nLa patiente a été suivie en consultation de chirurgie générale, avec une évolution clinique sans complications. Un suivi régulier est nécessaire pour surveiller une éventuelle récidive ou progression tumorale, compte tenu du caractère intermédiaire de malignité de la tumeur diagnostiquée. Une prise en charge multidisciplinaire incluant oncologie pourrait être envisagée selon l’évolution clinique et les résultats complémentaires."
+        }
+    },
+    {
+        "article": "Un garçon est né par césarienne d'urgence en raison d'une détresse fœtale à 40 semaines de grossesse. La mère avait 33 ans et était enceinte de 1 enfant et de 1 enfant en voie de naissance. Ni les parents ni le frère n'avaient des antécédents familiaux d'anomalies congénitales, de maladies liées à l'aorte ou de mort subite. D'après les résultats de l'échographie prénatale à la fin du deuxième trimestre, la longueur du fémur du fœtus était de 1 à 3 semaines plus longue que la longueur supposée de l'âge gestationnel réel. L'échocardiographie fœtale a montré une cardiomégalie avec un rapport de circonférence cardiaque-thoracique fœtale de 0,5 ou plus en fonction de la durée de vie du bébé. En outre, la taille du foramen ovale était plus grande que la normale et une constriction aortique gauche a été observée à côté du bassin de l'artère sous-clavière. En outre, aucune autre anomalie n'a été constatée lors de l'échographie prénatale.\n\nÀ la naissance, le poids était de 3560 g (75e percentile), la longueur de 56,5 cm (au-dessus du 90e percentile), et le tour de tête de 36 cm (au-dessus du 90e percentile). Les scores d'Apgar à 1 et 5 minutes étaient de 4 et 6 points, respectivement. Dans la salle d'accouchement, la patiente ne respirait pas spontanément et avait une bradycardie et une cyanose. Après avoir été admise à l'unité de soins intensifs néonatals, diverses malformations musculo-squelettiques ont été confirmées par examen physique. Une arachnodactylie sévère et une camptodactylie ont été observées dans les deux mains et les deux pieds, et la plante des pieds était plate. Les articulations du coude et du genou n'étaient pas complètement étendues. Le visage avait une hypoplasie malaire avec un aspect facial sénile. L'œil était profondément enfoncé avec une fissure palpebrale oblique vers le bas, et l'oreille avec un cartilage hypoplasique était mal positionnée et froissée. La patiente présentait une bouche tombante, une suture coronale proéminente et une brachycephalie. Un murmure systolique de grade V/VI a été entendu à la fois à la limite sternale supérieure et à la limite sternale inférieure gauche avec un parasternal de grade III. L'échocardiographie a montré une mauvaise contractilité cardiaque, une hypertension pulmonaire sévère, un sinus aortique dilaté (20,2 mm) (Z-score ; 8,08 par Boston, 6,37 par Detroit, ou 5,97 par Halifax), et une dysfonction valvulaire intracardiaque multiple avec prolapsus valvulaire (régurgitation aortique modérée, régurgitation mitrale sévère, régurgitation tricuspide modérée, et régurgitation valvulaire pulmonaire modérée). Les résultats de l'examen ophtalmologique ont montré une ectopie lentis dans les deux yeux ainsi qu'une subluxation du cristallin. Une hernie hépatique a été confirmée par une radiographie abdominale et une échographie. Le score systémique de la manifestation musculo-squelettique était de 11 points, selon les critères de Gand (critères diagnostiques internationaux pour la MFS).\n\nPour le diagnostic génétique, le séquençage de Sanger et la réaction en chaîne de la polymérase ont été effectués sur la séquence nucléotidique comme référence pour le gène FBN1. En conséquence, une mutation dans laquelle G, la première base du 32e intron sous la forme d'une mutation hétérogène, a été remplacée par T (c.3964 + 1G > T). Cela a été confirmé comme la variante pathogène probable sur la base de la directive ACMG/AMP de 2015. L'emplacement de la mutation a été inclus dans le site précédemment connu sous le nom de région néonatale de MFS (exons 24-32). Le patient a pu être diagnostiqué avec MFS néonatale avec une nouvelle mutation du gène FBN1 dans les 2 semaines de la vie.\n\nLe premier jour de la vie, une cyanose différentielle a été constatée, indiquant une hypoxémie réfractaire malgré un apport en oxygène supérieur à 60 % et des signes d'un faible débit cardiaque. La patiente a été prise en charge médicalement pour améliorer le faible débit cardiaque en fonction de la régurgitation mitrale sévère et de la régurgitation aortique. La réduction de la postcharge, y compris l'infusion continue de milrinone, la sédation complète avec l'infusion continue de fentanyl et l'utilisation de diurétiques ont été tentées pour améliorer l'oligurie et l'insuffisance cardiaque. Malgré la prise en charge médicale, la patiente a présenté une insuffisance respiratoire, une insuffisance cardiaque et une hypertension pulmonaire sévère nécessitant une ventilation mécanique invasive continue. La régurgitation aortique, la régurgitation mitrale, l'hypertension pulmonaire et la contractilité cardiaque se sont aggravées. Après plusieurs consultations avec la famille et le personnel médical de la patiente au sujet du plan de traitement, les soins palliatifs ont été poursuivis au lieu d'un traitement chirurgical. En conséquence, la congestion hépatique et pulmonaire accompagnée d'une hémorragie pulmonaire a progressé également. Elle a finalement progressé vers un syndrome de défaillance multiviscérale et la patiente est morte 32 jours après la naissance.\n\nMH - Anomalies/complications cardiovasculaires\nMH - Système cardiovasculaire/pathologie",
+        "gold_summary": "Inquiétudes des patients:\nUn nouveau-né atteint de MFS néonatale et d'une atteinte cardiaque sévère. Il présentait diverses caractéristiques cliniques sévères telles que l'arachnodactylie, la camptodactylie, la contracture des articulations du coude et du genou, un aspect facial sénile et une dépression profonde avec fissure palpérale inclinée vers le bas, un cartilage d'oreille hypoplasique, une bouche affaissée, une brachycephalie et une ectopie du cristallin.\n\nDiagnosis:\nL'analyse génétique a révélé une nouvelle mutation au nucléotide 3964 (c.3964 + 1 G > T) dans l'intron 32 du gène fibrillin-1. Cette mutation est identifiée dans la région dite néonatale de l'exon 24 à 32 de la fibrilline-1, comme indiqué précédemment.\n\nInterventions:\nLe patient a été traité médicalement pour améliorer la faible débit cardiaque en fonction de la régurgitation mitrale sévère et de la régurgitation aortique. La réduction de la précharge, la sédation complète et l'utilisation de diurétiques ont été tentées pour améliorer l'oligurie et l'insuffisance cardiaque.\n\nRésultats:\nMalgré la prise en charge médicale, la régurgitation aortique, la régurgitation mitrale, l'hypertension pulmonaire et la contractilité cardiaque se sont aggravées. Le traitement chirurgical est essentiel pour prolonger la vie du patient, cependant, les considérations relatives à la progression grave de la maladie font que les familles décident de poursuivre les soins palliatifs au lieu du traitement chirurgical. Quelques mois après la naissance, il a présenté une régurgitation aortique, une régurgitation mitrale et une insuffisance cardiaque congestive rapidement progressives, qui ont conduit à la mort.\n",
+        "synthetic_summary": {
+            "B1": "Un bébé est né avec un problème très rare qui touche son cœur et son corps. Ses doigts étaient très longs et pliés. Ses bras et jambes ne pouvaient pas bien bouger. Son visage avait une forme spéciale, un peu différente.\n\nLes docteurs ont trouvé un petit changement dans un de ses gènes. Ce changement cause ce problème.\n\nIls ont donné des médicaments pour aider son cœur à mieux marcher. Mais le cœur est devenu de plus en plus fatigué. Le bébé est resté très malade. Sa famille a choisi de le garder au calme et de le soigner doucement.\n\nLe bébé est parti au ciel après un mois, car son cœur ne pouvait plus tenir. Les docteurs et sa famille l'ont beaucoup aimé et pris soin de lui.",
+            "B2": "**Résumé pour un adolescent de 14 ans**\n\n**Ce qu’ils ont trouvé chez le bébé**  \nUn bébé est né avec une maladie appelée syndrome de Marfan (MFS) néonatal, qui affecte le tissu conjonctif, c’est-à-dire les parties du corps qui soutiennent les organes et les os. Ce bébé avait plusieurs problèmes visibles : des doigts très longs et pliés (arachnodactylie et camptodactylie), des articulations du coude et du genou qui ne pouvaient pas bien s’étendre, un visage qui paraissait plus vieux que son âge, des yeux enfoncés avec des paupières inclinées vers le bas, des oreilles mal formées, une bouche tombante, et une tête plus large que la normale. Il avait aussi un problème aux yeux appelé ectopie lentis, où le cristallin (la lentille à l’intérieur de l’œil) est mal placé.\n\n**Ce que cela signifie au niveau du cœur**  \nLe cœur du bébé ne fonctionnait pas bien. Il avait une dilatation du sinus aortique (une partie importante du cœur) et plusieurs valves cardiaques qui fuyaient, ce qui s’appelle une régurgitation. Ces problèmes empêchaient le cœur de pomper le sang correctement, causant une insuffisance cardiaque et une hypertension pulmonaire (pression élevée dans les poumons).\n\n**Comment ils ont confirmé la maladie**  \nLes médecins ont fait un test génétique pour chercher une mutation dans le gène FBN1, qui est souvent responsable du syndrome de Marfan. Ils ont trouvé une nouvelle mutation dans une région du gène connue pour causer des formes graves de la maladie chez les nouveau-nés.\n\n**Comment ils ont essayé de soigner le bébé**  \nLe bébé a reçu des médicaments pour aider le cœur à mieux fonctionner, réduire la charge sur le cœur, calmer la douleur et éliminer l’excès d’eau dans le corps. Malgré ces traitements, son état s’est aggravé : le cœur pompait de moins en moins bien et les problèmes de valves cardiaques sont devenus plus graves.\n\n**Ce qui s’est passé ensuite**  \nÀ cause de la gravité de la maladie, la famille et les médecins ont décidé de ne pas faire d’opération chirurgicale, mais de continuer les soins pour soulager la souffrance du bébé (soins palliatifs). Malheureusement, le bébé est décédé un mois après sa naissance à cause de l’insuffisance cardiaque et d’autres complications graves.\n\n---\n\nCe cas montre à quel point le syndrome de Marfan peut être sévère chez les nouveau-nés, surtout quand il touche le cœur. La découverte rapide de la mutation génétique a aidé à comprendre la maladie, mais malheureusement, les traitements médicaux n’ont pas suffi à sauver le bébé.",
+            "B3": "Résumé détaillé et structuré du cas clinique\n\nContexte  \nUn nouveau-né de sexe masculin est né par césarienne d’urgence à terme (40 semaines) en raison d’une souffrance fœtale. La mère, âgée de 33 ans, était enceinte pour la première fois. Aucun antécédent familial d’anomalies congénitales, de pathologies aortiques ou de mort subite n’était rapporté. L’échographie prénatale avait révélé une croissance fœtale légèrement avancée (longueur du fémur supérieure à la normale), une cardiomégalie (augmentation du volume cardiaque) avec un rapport circonférence cardiaque/thoracique élevé, un foramen ovale élargi et une constriction de l’aorte gauche. Aucune autre anomalie n’avait été détectée avant la naissance.\n\nPrincipales observations cliniques à la naissance  \nLe nouveau-né pesait 3560 g (75e percentile) et mesurait 56,5 cm (au-dessus du 90e percentile), avec un tour de tête également supérieur au 90e percentile. Les scores d’Apgar étaient faibles (4 à 1 minute, 6 à 5 minutes), indiquant une adaptation difficile. Il ne respirait pas spontanément, présentait une bradycardie et une cyanose. À l’examen physique, plusieurs malformations musculo-squelettiques sévères étaient visibles : arachnodactylie (doigts anormalement longs et fins), camptodactylie (doigts en flexion permanente), pieds plats, limitation de l’extension des articulations du coude et du genou. Le visage présentait une hypoplasie malaire (sous-développement des pommettes), un aspect vieilli, des yeux enfoncés avec des fissures palpébrales obliques vers le bas, des oreilles malformées et mal positionnées, une bouche tombante, une brachycéphalie (tête large) et une suture coronale proéminente.\n\nExamens complémentaires  \nL’auscultation cardiaque révélait un souffle systolique intense (grade V/VI) aux limites sternales supérieures et inférieures gauches. L’échocardiographie montrait une dysfonction cardiaque sévère avec mauvaise contractilité, hypertension pulmonaire importante, dilatation du sinus aortique (taille anormalement augmentée), et des régurgitations valvulaires multiples : modérée à sévère pour les valves aortique, mitrale, tricuspide et pulmonaire. L’examen ophtalmologique a confirmé une ectopie lentis bilatérale (déplacement du cristallin) avec subluxation. Une hernie hépatique a été identifiée par imagerie abdominale. Le score musculo-squelettique selon les critères internationaux de Gand était élevé (11 points), compatible avec un syndrome de Marfan (MFS) néonatal.\n\nDiagnostic génétique  \nLe séquençage du gène FBN1, codant pour la fibrilline-1, a mis en évidence une mutation hétérozygote nouvelle (c.3964 + 1G > T) au niveau de l’intron 32, dans la région dite « néonatale » (exons 24-32) associée à des formes sévères de MFS. Cette variante a été classée comme probablement pathogène selon les recommandations ACMG/AMP 2015. Le diagnostic de MFS néonatal a ainsi été confirmé dans les deux premières semaines de vie.\n\nPrise en charge et évolution  \nDès le premier jour, le nouveau-né présentait une cyanose différentielle et une hypoxémie réfractaire malgré un apport élevé en oxygène (>60 %), témoignant d’un faible débit cardiaque. Le traitement médical a visé à améliorer la fonction cardiaque en réduisant la postcharge (notamment par une perfusion continue de milrinone), en assurant une sédation complète (fentanyl) et en utilisant des diurétiques pour lutter contre l’oligurie et l’insuffisance cardiaque. Malgré ces mesures, la fonction cardiaque s’est détériorée, avec aggravation des régurgitations valvulaires, de l’hypertension pulmonaire et de la contractilité. La ventilation mécanique invasive a été nécessaire.\n\nAprès discussions approfondies avec la famille et l’équipe médicale, il a été décidé de privilégier les soins palliatifs plutôt qu’une intervention chirurgicale, compte tenu de la gravité et de la progression rapide de la maladie. La patiente a développé une congestion hépatique et pulmonaire, associée à une hémorragie pulmonaire, évoluant vers un syndrome de défaillance multiviscérale. Elle est décédée à l’âge de 32 jours.\n\nInterprétation clinique  \nCe cas illustre une forme néonatale sévère du syndrome de Marfan, caractérisée par une mutation spécifique du gène FBN1 dans une région associée à un pronostic défavorable. Les manifestations cliniques multisystémiques (musculo-squelettiques, cardiovasculaires, ophtalmologiques) sont très prononcées dès la naissance. La prise en charge médicale est complexe et souvent insuffisante pour stabiliser la fonction cardiaque, rendant le pronostic très réservé.\n\nProchaines étapes  \nCe cas souligne l’importance du diagnostic prénatal et génétique précoce pour orienter la prise en charge et les décisions thérapeutiques. La recherche de nouvelles stratégies thérapeutiques, y compris chirurgicales adaptées aux formes néonatales, reste un enjeu majeur pour améliorer la survie et la qualité de vie des patients atteints de MFS sévère. Un accompagnement psychologique des familles est également essentiel face à la gravité de cette pathologie."
+        }
+    },
+    {
+        "article": "La patiente était une Chinoise de 75 ans, une agricultrice de la ville de Yongzhou, dans la province du Hunan, en Chine. Deux mois auparavant, la patiente présentait des symptômes de vertiges, de manque d'appétit, de sommeil médiocre et de faiblesse des membres sans cause évidente. La patiente a progressivement empiré et a été diagnostiquée avec une gastrite atrophique chronique avec positivité Helicobacter pylori (Hp), une hypoproteinémie et une IDA. En outre, une hypertrophie de l'oreillette gauche et une dysfonction diastolique du ventricule gauche ont été diagnostiquées par échocardiographie.\n\nLes résultats des tests sanguins de routine étaient les suivants : un nombre de globules rouges (RBC) de 1,84 × 1012/L, un taux d’hématocrite de 13 %, un nombre de plaquettes de 500 × 109/L, un taux d’hémoglobine de 35 g/L (valeur critique), un volume corpusculaire moyen de 70,7 fL, un taux de protéines totales de 44,6 g/L, un taux d’éosinophiles de 5,3 %, un taux de sédimentation érythrocytaire de 25 mm/h, un taux d’immunoglobuline (Ig)E de 1282,2 IU/ml, un taux de fer sérique de 3,85 μmol/L et un résultat positif au test de sang occulte dans les selles. L’examen cytomorphologique de la moelle osseuse a révélé une prolifération active des granulocytes, des mégacaryocytes et des cellules myéloïdes. Un examen par cytométrie de flux n’a pas indiqué les immunophénotypes anormaux indicatifs d’une leucémie aiguë, d’un MDS, d’un lymphome ou de tumeurs myéloïdes. L’endoscopie gastro-intestinale a montré la présence de nématodes vivants dans la partie descendante du duodénum du patient. La patiente a été traitée avec des globules rouges à faible teneur en leucocytes pour corriger une anémie sévère et l’antihelminthique albendazole. Après le traitement, son taux d’hémoglobine a été confirmé à 77 g/L. Au cours des visites de suivi, la patiente a été traitée avec succès avec un antihelminthique et son anémie a été guérie.\n\nExamens d'imagerie et morphologiques\nPour exclure une maladie gastro-intestinale, le patient a subi une endoscopie gastro-intestinale. Des nématodes vivants ont été découverts se nourrissant de la muqueuse de la partie descendante du duodénum du patient. Des œufs d'ankylostomes ont été trouvés dans les selles par flottation en saumure saturée. Par conséquent, le patient a finalement été diagnostiqué avec une IDA sévère causée par une infection par ankylostomes.",
+        "gold_summary": "Une Chinoise de 75 ans qui présentait des vertiges, un manque d’appétit, des troubles du sommeil et une faiblesse des membres a été diagnostiquée avec une gastrite atrophique chronique et a été testée positive pour Helicobacter pylori, une anémie ferriprive avec une concentration en hémoglobine de 35 g/L et une hypertrophie de l’oreillette gauche. Cependant, après un traitement symptomatique, la patiente ne s’est pas améliorée. Une endoscopie gastro-intestinale supérieure a révélé la présence de nématodes vivants dans la partie descendante du duodénum de la patiente. Un examen fécal par flottation en saumure saturée a révélé des œufs d’ankylostomes. Une vérification supplémentaire par un test de réaction en chaîne de la polymérase par transcription inverse semi-nested a confirmé que l’espèce d’ankylostomes était Necator americanus. L’albendazole a été utilisé pour un traitement antihelminthique. Au cours des visites de suivi, nous avons constaté que le traitement antihelminthique était efficace et que son anémie avait été guérie.\n",
+        "synthetic_summary": {
+            "B1": "Une dame de 75 ans se sentait très fatiguée et avait mal au ventre. Elle ne mangeait pas bien et dormait mal. Les docteurs ont trouvé qu’elle avait un problème dans son ventre et qu’elle avait très peu de sang. \n\nIls ont regardé dans son ventre avec une petite caméra. Ils ont vu des petits vers vivants. Ces vers faisaient du mal à son ventre et lui prenaient du sang. \n\nLes docteurs lui ont donné un médicament pour tuer les vers. Après le médicament, elle est allée beaucoup mieux. Son sang est redevenu normal et elle n’était plus fatiguée.",
+            "B2": "**Ce qu’ils ont trouvé chez la patiente**\n\nUne femme chinoise de 75 ans avait des vertiges, elle ne mangeait pas bien, dormait mal et se sentait faible. Les médecins ont d’abord découvert qu’elle avait une inflammation chronique de l’estomac appelée gastrite atrophique, ainsi qu’une infection par une bactérie nommée Helicobacter pylori. Elle souffrait aussi d’une anémie très grave, c’est-à-dire qu’elle avait peu de globules rouges et une très faible quantité d’hémoglobine, une protéine qui transporte l’oxygène dans le sang. Son cœur montrait aussi des signes de fatigue avec une partie appelée oreillette gauche qui était plus grosse que la normale.\n\n**Ce qu’ils ont fait ensuite**\n\nMalgré un traitement pour ses symptômes, la patiente ne s’améliorait pas. Les médecins ont donc fait une endoscopie, c’est-à-dire qu’ils ont utilisé une petite caméra pour regarder à l’intérieur de son tube digestif. Ils ont alors vu des petits vers vivants, appelés nématodes, dans une partie de son intestin appelée le duodénum. En analysant ses selles, ils ont trouvé des œufs de ces vers, qui s’appellent ankylostomes. Un test spécial a confirmé que ces vers étaient de l’espèce Necator americanus.\n\n**Ce que cela signifie et le traitement**\n\nCes ankylostomes se nourrissaient du sang de la patiente, ce qui expliquait son anémie sévère. Pour la soigner, elle a reçu un médicament appelé albendazole, qui tue ces vers. Après ce traitement, son taux d’hémoglobine s’est amélioré et son anémie a disparu. Lors des contrôles suivants, la patiente allait mieux et les vers avaient disparu.\n\n**En résumé**\n\nCette patiente avait une anémie grave causée par une infection parasitaire dans son intestin. Grâce à un examen approfondi et un traitement adapté, elle a pu guérir. Cela montre l’importance de chercher des causes inhabituelles quand une maladie ne s’améliore pas avec les traitements habituels.",
+            "B3": "### Contexte  \nUne femme chinoise de 75 ans, agricultrice dans la province du Hunan, a présenté depuis deux mois des symptômes progressifs comprenant des vertiges, une perte d’appétit, des troubles du sommeil et une faiblesse musculaire sans cause évidente. Initialement, elle a été diagnostiquée avec une gastrite atrophique chronique associée à une infection par Helicobacter pylori, ainsi qu’une anémie ferriprive sévère (manque de fer entraînant une baisse importante de l’hémoglobine) avec un taux critique de 35 g/L. Par ailleurs, une hypertrophie (augmentation de taille) de l’oreillette gauche du cœur et une dysfonction diastolique du ventricule gauche ont été identifiées par échocardiographie.\n\n### Principales Observations  \nLes analyses sanguines ont montré une anémie très sévère, avec un nombre très bas de globules rouges (1,84 × 10^12/L), un taux d’hématocrite de 13 %, un volume corpusculaire moyen des globules rouges réduit (70,7 fL), ainsi qu’une hypoprotéinémie (faible taux de protéines totales à 44,6 g/L). Le test de sang occulte dans les selles était positif, suggérant une perte de sang digestive. L’examen de la moelle osseuse a révélé une activité accrue des cellules formant les globules blancs et les plaquettes, sans signe de cancer du sang.  \n\nL’endoscopie gastro-intestinale a mis en évidence la présence de nématodes vivants dans la partie descendante du duodénum (première partie de l’intestin grêle). L’analyse des selles par flottation en saumure saturée a confirmé la présence d’œufs d’ankylostomes, des parasites intestinaux connus pour provoquer des pertes sanguines digestives et donc une anémie ferriprive. Une analyse moléculaire (PCR semi-nested) a identifié spécifiquement l’espèce Necator americanus.\n\n### Interprétation Clinique  \nL’anémie sévère de la patiente était principalement due à une infection par des ankylostomes, parasites intestinaux qui se nourrissent du sang de la muqueuse duodénale, provoquant ainsi une perte chronique de fer. Cette cause parasitaire expliquait l’absence d’amélioration malgré le traitement initial centré sur la gastrite et l’infection à Helicobacter pylori. L’hypertrophie de l’oreillette gauche et la dysfonction cardiaque étaient probablement des complications secondaires liées à l’anémie sévère.\n\n### Prochaines Étapes et Résultats  \nLa patiente a reçu une transfusion de globules rouges à faible teneur en leucocytes pour corriger rapidement son anémie critique, ainsi qu’un traitement antihelminthique par albendazole pour éliminer les ankylostomes. Après traitement, son taux d’hémoglobine est remonté à 77 g/L, et lors des suivis ultérieurs, la patiente a montré une guérison complète de son anémie et une résolution de l’infection parasitaire.  \n\nCe cas souligne l’importance de rechercher une cause parasitaire en cas d’anémie ferriprive sévère, notamment dans les régions où les ankylostomes sont endémiques, et d’adapter le traitement en conséquence."
+        }
+    },
+    {
+        "article": "Un nourrisson de 5 mois a été admis au service d'urgence pédiatrique avec des antécédents de toux et d'obstruction nasale depuis trois jours. Son état général s'était détérioré au cours des 24 heures précédentes, avec de la fièvre, des efforts respiratoires, une perte d'appétit et des vomissements après les repas.\n\nIl s'agissait d'un nourrisson en bonne santé, ayant eu une grossesse à faible risque, avec des soins prénataux tardifs (3e trimestre), une échographie obstétrique normale (à 26 semaines de gestation), mais sans échographie morphologique. Il est né par voie vaginale, à terme, avec un poids adéquat pour l'âge gestationnel, sans complications.\n\nL'examen physique à l'admission a révélé un patient apyrétique (36,8 °C), tachycardique (158 bpm), tachypneique (50 bpm), avec hypoxémie (SpO2 92 %). L'auscultation pulmonaire a révélé une réduction des bruits respiratoires sur le côté gauche de l'hémithorax et la présence de râles fins, de ronflements et de respiration sifflante bilatérale diffuse. Une coryza hyaline et une détresse respiratoire ont été observées, avec une rétraction intercostale, sous-costale et sternale modérée à sévère. L'auscultation cardiaque a révélé des bruits cardiaques étouffés. Il y a eu une amélioration de la saturation en oxygène (98 %) et de l'effort respiratoire avec l'administration d'oxygène par un cathéter nasal.\n\nLe patient a été diagnostiqué avec une AVB et admis au service pédiatrique en raison de la nécessité d'oxygène supplémentaire et d'un effort respiratoire modéré à sévère. Des tests de laboratoire et d'imagerie ont été demandés.\n\nLe virus respiratoire syncytial a été détecté sur un écouvillon nasopharyngé. La formule leucocytaire était normale (8 000/μL), avec une prédominance de lymphocytes (72 % = 5 760/μL) et la présence de lymphocytes réactifs (2 % = 160/μL), en plus d'une thrombocytose modérée (487 000/μL). La protéine C-réactive (CRP) était normale (5,8 mg/L ; valeur de référence : moins de 10 mg/dL). La radiographie thoracique a montré un élargissement du contour cardiaque.\n\nEn raison des résultats radiographiques, une investigation cardiaque a été réalisée, qui a révélé des taux de troponine de 86,5 pg/mL (valeur de référence : jusqu'à 19,8 pg/mL) et de créatine phosphokinase-MB (CKMB) de 18 U/L (valeur de référence : jusqu'à 16U/L). L'électrocardiogramme a montré une altération de la repolarisation ventriculaire gauche. L'échocardiogramme a montré une masse hétérogène, mesurant 52 × 38 mm, sur la paroi latérale du ventricule gauche, avec des zones de calcification, préservant l'écoulement et le reflux du ventricule gauche.\n\nL'angiographie par TDM du thorax a montré une grande masse cardiaque intramurale dans le ventricule gauche avec une restriction significative du volume ventriculaire et une extension extra-cardiaque, de petits foyers de calcification centrale et un petit épanchement péricardique.\n\nL'IRM cardiaque a montré une masse dans le ventricule gauche, mesurant 5,5 × 5,3 cm, mobile avec le cycle cardiaque, s'étendant jusqu'à l'artère pulmonaire et dans le médiastin. Un effet de masse important a été noté dans le ventricule gauche, avec une réduction de la cavité ventriculaire, altérant modérément sa fonction globale (fraction d'éjection ventriculaire gauche [EF] = 46 %). Les images pondérées en T2 ont montré un hypersignal myocardique modéré et une absorption de contraste nettement retardée (> 10 minutes).\n\nL'extension extra-cardiaque de la lésion et l'épanchement péricardique suggéraient un comportement agressif. Cependant, la caractérisation du site et des tissus, c'est-à-dire les foyers de calcification et l'amélioration nettement ralentie, suggéraient des composants fibrotiques. Par conséquent, les hypothèses suggérées par les tests d'imagerie étaient le rhabdomyosarcome et le fibrome cardiaque.\n\nUn Holter a été effectué et a montré un bloc de branche droit complet et des extrasystoles supraventriculaires isolées. Une IRM abdominale totale et une échographie transfontanellaire ont été effectuées, en raison de la possibilité d'un rhabdomyosarcome cardiaque, les deux étant normaux.\n\nLe patient a subi une cathétérisation cardiaque pour biopsie, et des fragments ont été envoyés pour analyse histopathologique et immunohistochimique. La biopsie étant peu concluante, il a été décidé de commencer un traitement par sirolimus hors indication.\n\nPendant l'utilisation de sirolimus, des échocardiogrammes périodiques ont été réalisés, en plus des tests de laboratoire hebdomadaires, y compris la numération sanguine, la CRP, la dose de sirolimus sérique, la fonction rénale, la fonction hépatique et le profil lipidique. Pendant cette période, la dose de sirolimus sérique a été maintenue dans la plage thérapeutique, entre 5 et 10 ng/mL, sans modification des autres tests de laboratoire.\n\nL'échocardiogramme de la deuxième semaine d'utilisation du sirolimus a identifié un épanchement péricardique important, provoquant un dysfonctionnement du ventricule droit (VD), et une péricardiocentèse a été réalisée, drainant 48 ml de liquide séro-sanguinolent.\n\nAprès trois semaines d'utilisation de sirolimus, une IRM de contrôle a été réalisée et il n'y a pas eu de changements significatifs dans la taille ou les caractéristiques de la masse tumorale, par conséquent l'utilisation hors indication de sirolimus a été interrompue.\n\nUne nouvelle cathétérisation cardiaque avec biopsie a été réalisée. Deux fragments de tissus ont été envoyés pour analyse anatomopathologique, le plus grand mesurant 1,5 cm de longueur et 0,1 cm de diamètre. Cette fois, l'analyse histopathologique a été concluante pour un fibrome cardiaque.\n\nLa masse était une tumeur histologiquement bénigne, mais avec un comportement agressif en raison de sa taille, de son emplacement et de son infiltration dans le myocarde. La patiente a nécessité une hospitalisation prolongée, avec l'utilisation de médicaments vasoactifs en raison d'un compromis hémodynamique. La tumeur n'a pas répondu à l'utilisation hors indication de sirolimus, nécessitant une polypharmacie cardiologique, de multiples hospitalisations en raison d'une décompensation cardiaque, et la patiente a développé une insuffisance cardiaque congestive de classe fonctionnelle 3 (ICC), atteignant une EF de 35 %.\n\nEn raison de l'aggravation progressive de la EF et, par conséquent, de la classe fonctionnelle de l'ICC, il a été décidé d'inclure le patient dans la liste de transplantation cardiaque, car la résection de la tumeur était impossible en raison de son infiltration dans la paroi myocardique du ventricule gauche.\n\nSix mois après le diagnostic, la patiente a subi une transplantation cardiaque dans le même hôpital où le diagnostic a été posé, avec un bon déroulement postopératoire. L'anatomie et les résultats histopathologiques de l'échantillon chirurgical ont confirmé le diagnostic de fibrome cardiaque.",
+        "gold_summary": "Un nourrisson de 5 mois a été admis au service d'urgence pédiatrique avec une bronchiolite virale aiguë nécessitant une hospitalisation. Il présentait un virus respiratoire syncytial détectable dans un écouvillon oropharyngé, un test sanguin avec lymphocytose et une radiographie thoracique a révélé une cardiomégalie. Des tests cardiaques supplémentaires ont été effectués, détectant une élévation des biomarqueurs cardiaques, un électrocardiogramme avec une altération de la repolarisation ventriculaire gauche et une échocardiographie avec une masse hétérogène dans le ventricule gauche, avec des zones de calcification. Une angiotomographie thoracique suggérait un rhabdomyosarcome ou un fibrome cardiaque et une résonance magnétique a montré une masse, avec des caractéristiques suggérant un fibrome. Le diagnostic final a été fait après deux cathétérismes cardiaques pour biopsie de la lésion, confirmant un fibrome cardiaque par examen anatomo-pathologique. Le patient ayant une dysfonction systolique modérée à sévère, il a été soumis à une transplantation cardiaque.\n",
+        "synthetic_summary": {
+            "B1": "Un bébé de 5 mois était très malade. Il avait du mal à respirer et une grosse toux. \n\nLe docteur a trouvé un gros cœur avec une grosse boule dedans. Cette boule faisait mal au cœur. \n\nIls ont fait beaucoup de tests pour comprendre. La boule était un gros bouton dans le cœur. Ce bouton n’était pas dangereux, mais il était très gros. \n\nLe bébé était très fatigué parce que son cœur ne marchait pas bien. Les docteurs ont décidé de changer son cœur. \n\nLe bébé a eu un nouveau cœur. Maintenant, il va mieux et il est suivi par les docteurs.",
+            "B2": "Un bébé de 5 mois est arrivé aux urgences avec une infection virale des voies respiratoires, appelée bronchiolite, qui l’a rendu très malade. On a trouvé chez lui un virus appelé virus respiratoire syncytial, souvent responsable de ce type d’infection. Une radiographie du thorax a montré que son cœur était plus gros que la normale, ce qui a poussé les médecins à faire des examens plus approfondis du cœur.\n\nCes examens ont révélé des signes d’atteinte cardiaque : des analyses sanguines montraient des substances élevées qui indiquent un stress du muscle cardiaque. L’électrocardiogramme, qui enregistre l’activité électrique du cœur, montrait des anomalies. Une échographie du cœur a découvert une grosse masse anormale dans la paroi du ventricule gauche, une des cavités principales du cœur. Cette masse contenait aussi des zones calcifiées, c’est-à-dire durcies.\n\nPour mieux comprendre cette masse, les médecins ont réalisé un scanner et une IRM cardiaque. Ces images ont suggéré que la masse pouvait être soit un rhabdomyosarcome (une tumeur cancéreuse des muscles), soit un fibrome cardiaque (une tumeur bénigne faite de tissu fibreux). Pour confirmer le diagnostic, deux biopsies ont été faites : cela consiste à prélever un petit morceau de la masse pour l’étudier au microscope.\n\nL’analyse des tissus a finalement confirmé qu’il s’agissait d’un fibrome cardiaque, une tumeur non cancéreuse mais qui peut être dangereuse à cause de sa taille et de sa position dans le cœur. Cette masse a causé une mauvaise fonction du cœur, avec une diminution de la capacité du ventricule gauche à pomper le sang.\n\nComme la tumeur ne pouvait pas être enlevée par chirurgie à cause de son infiltration dans le muscle cardiaque, et que la fonction du cœur continuait à s’aggraver, les médecins ont décidé de proposer une transplantation cardiaque. Six mois après le diagnostic, le bébé a reçu un nouveau cœur, et l’opération s’est bien passée. L’étude du cœur enlevé a confirmé le diagnostic de fibrome cardiaque.",
+            "B3": "**Contexte**  \nUn nourrisson de 5 mois, initialement admis pour une bronchiolite aiguë causée par le virus respiratoire syncytial, présentait des symptômes respiratoires sévères, notamment une toux, une obstruction nasale, des efforts respiratoires importants, une hypoxémie et une détérioration de l’état général. L’examen clinique révélait une tachycardie, une tachypnée, des râles pulmonaires bilatéraux et une diminution des bruits respiratoires à gauche, ainsi qu’une saturation en oxygène améliorée sous oxygénothérapie. La radiographie thoracique montrait une cardiomégalie (augmentation de la taille du cœur), ce qui a motivé une exploration cardiaque approfondie.\n\n**Principales Observations**  \nLes analyses sanguines ont révélé une formule leucocytaire normale avec une prédominance lymphocytaire, une thrombocytose modérée et une protéine C-réactive normale, suggérant une inflammation virale sans infection bactérienne associée. Les biomarqueurs cardiaques, notamment la troponine et la créatine phosphokinase-MB (CKMB), étaient élevés, indiquant une atteinte myocardique. L’électrocardiogramme montrait une altération de la repolarisation du ventricule gauche, signe d’une souffrance cardiaque. L’échocardiographie a mis en évidence une masse hétérogène de grande taille (52 × 38 mm) localisée sur la paroi latérale du ventricule gauche, comportant des zones de calcification, sans obstruction du flux sanguin.\n\nL’angiographie par tomodensitométrie (TDM) et l’imagerie par résonance magnétique (IRM) cardiaque ont confirmé la présence d’une masse intramurale volumineuse, avec extension extra-cardiaque et épanchement péricardique, suggérant un comportement agressif. Les caractéristiques d’imagerie (calcifications, absorption tardive du contraste) orientaient vers un fibrome cardiaque ou un rhabdomyosarcome, deux types de tumeurs cardiaques rares chez l’enfant.\n\n**Interprétation Clinique**  \nLe diagnostic définitif a été établi après deux biopsies cardiaques réalisées par cathétérisme. La première biopsie était peu concluante, ce qui a conduit à un traitement expérimental par sirolimus, un médicament immunosuppresseur, sans amélioration notable de la masse tumorale. La seconde biopsie a confirmé un fibrome cardiaque, une tumeur bénigne mais agressive en raison de sa taille importante, de son infiltration myocardique et de son impact sur la fonction cardiaque. Le patient a développé une insuffisance cardiaque congestive modérée à sévère, avec une fraction d’éjection ventriculaire gauche diminuée à 35 %, malgré un traitement médical intensif.\n\n**Prochaines Étapes**  \nLa résection chirurgicale de la tumeur n’étant pas réalisable à cause de son infiltration profonde dans le muscle cardiaque, le nourrisson a été inscrit sur la liste de transplantation cardiaque. Six mois après le diagnostic initial, il a bénéficié d’une transplantation cardiaque avec un bon déroulement postopératoire. L’analyse histopathologique de la pièce opératoire a confirmé le diagnostic de fibrome cardiaque.\n\nCe cas illustre la complexité du diagnostic et de la prise en charge des masses cardiaques chez le nourrisson, notamment lorsqu’elles se manifestent dans un contexte infectieux aigu. La surveillance attentive, les investigations multimodales et la collaboration multidisciplinaire sont essentielles pour optimiser le pronostic dans ces situations rares et graves."
+        }
+    },
+    {
+        "article": "Patient de 15 mois, sexe féminin, première fille de parents en bonne santé, non consanguins. Sa grossesse a été contrôlée et s'est déroulée sans complications. Elle est née par accouchement vaginal à 40 semaines de gestation, avec un poids de 2635 grammes (percentile 2), une taille de 48 cm (percentile 8) et un périmètre crânien de 33 cm (percentile 5), selon les courbes d'Alarcón et Pittaluga4 avec un score d'APGAR de 9-10.\n\nElle a évolué avec un développement psychomoteur normal et n’a pas eu de maladies intercurrentes. À l’âge de 4 mois, un souffle cardiaque a été ausculté lors d’un contrôle pédiatrique, et elle a été référée en cardiologie. Un échocardiogramme a révélé une sténose des branches pulmonaires, ce qui, ajouté à la découverte d’un front proéminent lors de l’examen physique, a motivé son orientation vers la génétique clinique.\n\nL'évaluation génétique a révélé des caractéristiques telles qu'une implantation antérieure des cheveux élevée, des sourcils droits, des yeux enfoncés, des pavillons auriculaires proéminents, un pont nasal bas, un profil nasal convexe avec une pointe bulbeuse, une columelle courte et un menton pointu. En outre, un souffle systolique a été détecté au niveau du poumon lors de l'auscultation. Aucune altération de l'abdomen, des organes génitaux ou des extrémités n'a été observée.\n\nDes examens complémentaires ont été réalisés en raison du soupçon de SALG. Les radiographies de la colonne vertébrale ont révélé des vertèbres D4 et D6 avec une tendance morphologique en papillon et une ossification incomplète de l'arc postérieur de L5. Les radiographies des extrémités et du bassin, ainsi que les échographies abdominales et rénales, n'ont pas révélé d'anomalies. Les analyses des paramètres hormonaux, biochimiques, de la fonction hépatique et rénale n'ont révélé qu'une légère élévation de la LDH.\n\nL’hypothèse diagnostique principale a été confirmée par un panel commercial pour les anomalies cardiaques congénitales et l’hétérotaxie, qui comprenait les deux gènes associés à SALG (JAG1 et NOTCH2), permettant l’étude des variantes ponctuelles et des variantes du nombre de copies (CNV) des gènes analysés, un aspect important pour la pathologie étudiée. Cette analyse a identifié une microdélétion pathogénique hétérozygote couvrant la totalité de la séquence codante du gène JAG1 , ainsi que trois variantes hétérozygotes de signification incertaine dans les gènes DNAH11, NME8 et NEK8 (associés à la dyskinésie ciliaire primaire et à la néphronoptisis, toutes deux héréditaires autosomiques récessives).\n\nÉtant donné qu'une délétion complète du gène JAG1 a été identifiée et compte tenu des rapports de gènes contiguës associés à des pathologies qui pourraient nécessiter des interventions supplémentaires chez la patiente, il a été décidé de procéder à une étude plus approfondie au moyen d'un caryotype moléculaire (Affymetrix CytoScan 750K). L'array a confirmé la présence d'une microdélétion pathogénique, arr[GRCh37] 20p12.2(10414643_10792802)x1, d'environ 378 kb, qui comprenait 5 gènes : MKKS, SLX4IP, JAG1, MIR6870, LINC01752. Cela a confirmé moléculairement le SALG en raison de la délétion complète du gène JAG1.\n\nLa patiente remplissait trois des sept critères cliniques pour le diagnostic de SALG, avec une sténose des branches des artères pulmonaires, des vertèbres thoraciques en forme de papillon et des caractéristiques faciales typiques, y compris des yeux enfoncés, un bout du nez bulbeux et un menton pointu. Les contrôles ultérieurs n'ont pas révélé de modifications des tests de la fonction hépatique ou rénale, d'anomalies ophtalmologiques ou de xantomes. Son développement neurologique est conforme à son âge.\n\nIl a été suggéré aux parents de procéder à une étude du caryotype moléculaire pour déterminer la possibilité d’être porteur de CNV, ce qui les exposerait à un risque de récurrence de 50 % pour un autre enfant. Cependant, pour des raisons économiques, cette étude n’a pas été réalisée.\n\n",
+        "gold_summary": "Patient de sexe féminin, qui a été diagnostiquée avec un souffle cardiaque à l'âge de 4 mois. L'échocardiographie a révélé une sténose des branches pulmonaires, ce qui, avec le front proéminent observé à l'examen physique, a motivé son orientation vers la génétique clinique. En raison du soupçon de SALG, des études complémentaires ont été réalisées, qui ont révélé des vertèbres en papillon et un panel génétique qui a identifié une délétion pathogénique en hétérozygotie, couvrant toute la séquence codante du gène JAG1. Pour exclure une délétion plus étendue, un caryotype moléculaire a été réalisé, confirmant une microdélétion pathogénique sur le chromosome 20 de 378 kb (arr[GRCh37] 20p12.2(10414643_10792802)x1).\n",
+        "synthetic_summary": {
+            "B1": "Il y a une petite fille qui a un souffle dans son cœur. Ce souffle vient d’un petit problème dans ses tuyaux du cœur. Le docteur a vu aussi que son front est un peu différent.\n\nPour mieux comprendre, les docteurs ont fait des examens. Ils ont regardé ses os dans le dos. Certains os ont une forme spéciale, comme un papillon.\n\nIls ont aussi cherché dans ses gènes, qui sont comme des petits livres dans le corps. Ils ont trouvé qu’un petit morceau d’un de ces livres, appelé JAG1, manque.\n\nPour être sûrs, ils ont fait un autre test. Ce test a confirmé que ce petit morceau est bien absent.\n\nCe problème s’appelle SALG. Les docteurs vont bien s’occuper d’elle.",
+            "B2": "**Ce qu'ils ont trouvé chez la petite fille**\n\nUne fillette de 15 mois a été suivie depuis sa naissance. À 4 mois, les médecins ont entendu un bruit anormal au cœur appelé souffle cardiaque. Une échographie du cœur a montré que certaines artères pulmonaires, qui amènent le sang aux poumons, étaient rétrécies. En même temps, ils ont remarqué que son front était un peu plus en avant que la normale. Ces signes ont poussé les médecins à chercher une cause génétique, c’est-à-dire liée à ses gènes.\n\n**Les examens et analyses**\n\nLes médecins ont fait plusieurs examens. Des radiographies ont montré que certaines vertèbres de sa colonne vertébrale avaient une forme spéciale appelée « en papillon ». Ensuite, une analyse génétique a été faite pour chercher des anomalies dans des gènes connus pour causer des maladies cardiaques congénitales. Cette analyse a trouvé une perte (appelée délétion) d’une partie importante du gène JAG1, qui est lié à une maladie appelée syndrome d’Alagille (SALG). Pour vérifier si cette perte était plus grande, un test plus précis appelé caryotype moléculaire a été réalisé. Ce test a confirmé qu’une petite partie du chromosome 20, contenant plusieurs gènes dont JAG1, manquait.\n\n**Ce que cela signifie**\n\nLa perte du gène JAG1 explique certains des problèmes de la fillette, comme la sténose des artères pulmonaires et les particularités de son visage. Elle a aussi des vertèbres en papillon, un autre signe de ce syndrome. Pour l’instant, ses autres organes fonctionnent normalement, et son développement est adapté à son âge. Les médecins ont conseillé aux parents de faire des tests génétiques pour savoir s’ils portent eux aussi cette délétion, car cela pourrait augmenter le risque d’avoir un autre enfant avec la même maladie. Cependant, ils n’ont pas pu faire ces tests pour des raisons financières.\n\nEn résumé, cette petite fille a été diagnostiquée avec le syndrome d’Alagille grâce à des examens cliniques, radiologiques et génétiques qui ont montré une perte importante du gène JAG1. Ce diagnostic aidera à mieux suivre sa santé et à prévenir d’autres complications.",
+            "B3": "Résumé structuré destiné à un adulte éduqué non-médecin\n\n**Contexte**  \nUne fillette de 15 mois, née à terme sans complication notable, a présenté un souffle cardiaque détecté à l’âge de 4 mois lors d’un examen pédiatrique de routine. L’échocardiogramme a révélé une sténose (rétrécissement) des branches des artères pulmonaires. Par ailleurs, un examen physique a mis en évidence un front proéminent, ce qui a conduit à une orientation vers une consultation en génétique clinique.\n\n**Principales observations**  \nL’évaluation génétique a mis en lumière plusieurs caractéristiques faciales typiques, telles que des yeux enfoncés, un nez à pointe bulbeuse et un menton pointu. Des radiographies ont montré des vertèbres thoraciques présentant une forme dite « en papillon », signe radiologique évocateur. Les examens complémentaires, notamment des analyses sanguines et des échographies abdominales et rénales, n’ont pas révélé d’anomalies majeures, à l’exception d’une légère élévation de la LDH (enzyme pouvant indiquer une atteinte tissulaire).\n\nUn test génétique ciblé, conçu pour détecter des anomalies liées aux cardiopathies congénitales et à l’hétérotaxie (une anomalie de position des organes), a identifié une microdélétion pathogénique en hétérozygotie (perte d’une copie) englobant la totalité du gène JAG1. Ce gène est connu pour être impliqué dans le syndrome d’Alagille (SALG), une maladie génétique multisystémique. Pour préciser l’étendue de cette délétion, un caryotype moléculaire (analyse chromosomique fine) a été réalisé, confirmant une microdélétion d’environ 378 kilobases sur le chromosome 20, incluant cinq gènes dont JAG1.\n\n**Interprétation clinique**  \nLa patiente remplit trois des sept critères cliniques diagnostiques du syndrome d’Alagille : la sténose des branches pulmonaires, les vertèbres en papillon et les traits faciaux caractéristiques. Ce diagnostic génétique explique les manifestations observées et oriente le suivi médical. À ce jour, aucune atteinte hépatique, rénale ou ophtalmologique n’a été détectée, et le développement neurologique est normal.\n\n**Prochaines étapes**  \nIl a été recommandé aux parents de réaliser un caryotype moléculaire pour déterminer s’ils sont porteurs de la même anomalie génétique, ce qui impliquerait un risque de transmission de 50 % à un autre enfant. Cependant, cette étude n’a pas été effectuée pour des raisons financières. Un suivi régulier multidisciplinaire est nécessaire pour surveiller l’apparition éventuelle de complications liées au syndrome d’Alagille."
+        }
+    },
+    {
+        "article": "Une femme de 82 ans atteinte de diabète de type 2 et d'insuffisance rénale chronique a été admise à l'hôpital avec un antécédent de 7 jours de fièvre, de délire et de dyspnée. Elle avait subi une prothèse valvulaire aortique (prothèse valvulaire sans suture de Perceval) 18 mois auparavant en raison d'une sténose aortique. La période post-opératoire immédiate a été compliquée par un épisode de fibrillation auriculaire paroxystique, un épanchement pleural gauche transudatif et une oligoanurie rénale. Elle n'a présenté aucune infection compliquée et l'incision de la sternotomie médiane s'est normalement refermée. Entre 1 et 14 mois après une chirurgie aortique, elle a été admise à l'hôpital cinq fois en raison d'une insuffisance cardiaque sévère inexpliquée et d'un épisode de fibrillation auriculaire paroxystique. Elle n'a présenté aucune fièvre ou autre signe d'infection et n'a reçu aucun traitement antibiotique. Un échocardiogramme transoesophagien réalisé 3 mois après la chirurgie a montré une prothèse valvulaire aortique sans altération. Au cours de l'examen physique, sa température était de 39 °C, elle était confuse et tachypneique. Un murmure de la fonction cardiaque de 3/6 a été observé en position aortique et une crépitation pulmonaire basale a été observée. Elle présentait des ulcères de pression non infectés de grade II au niveau des talons et de la région sacrococcygienne. Les tests de laboratoire ont montré un nombre normal de cellules sanguines, une créatinine sérique de 2,14 mg/dL et une augmentation de la protéine C-réactive (13 mg/dL) et une hyperglycémie (628 mg/dL). Une radiographie thoracique a montré un épanchement pleural gauche et un oedème pulmonaire interstitiel bilatéral. Deux ensembles de bouteilles de culture sanguine aérobie et anaérobie ont été prélevés à l'admission, et une ceftriaxone empirique (2 mg/dL) et une levofloxacine ajustée à la fonction rénale (250 mg/dL) ont été démarrées. Après 26 à 80 heures d'incubation dans le système BACTEC FX (Becton, Dickinson and Company), les quatre bouteilles de culture sanguine étaient positives. La coloration Gram a montré des bacilles Gram positifs coryneformes avec des formes ramifiées occasionnelles. Après incubation sur de l'agar CNA et de l'agar chocolat, les colonies étaient inférieures à 2 mm, luisantes et jaunes. Les colonies pénétraient dans l'agar lors d'une incubation ultérieure. Le 5e jour d'admission, des cultures sanguines ont été obtenues à nouveau, et le même organisme a été cultivé dans 1 des 4 bouteilles. Les isolats ont été initialement identifiés par une matrice-assistée par laser-ionisation-temps de vol (MALDI-TOF MS, Bruker Daltonics) comme C. cellulans. Par la suite, l'identification a été confirmée par API Coryne strip (bioMérieux ; code numéro 7572767), qui était une « excellente identification » pour C. cellulans avec une fiabilité de 99,9 %, et par séquençage de l'ARN 16S (en utilisant l'outil d'analyse de séquence BLAST de la base de données GenBank), montrant une similitude de 100 % avec C. cellulans et 99,8 % avec C. funkei. Les tests de susceptibilité antimicrobienne ont été effectués en utilisant un panneau de microdilution microtitre MICroSTREP plus 6 (MicroScan Walk Away, Beckman Coulter). Après les critères d'Eucast pour Corynebacterium, l'isolate était sensible ou probablement sensible (pour les antibiotiques sans critères d'Eucast, mais avec une faible MIC) à l'amoxicilline-clavulanate (MIC = 2 mg/L), à la daptomycine (MIC = 0,5 mg/L), à la levofloxacin (MIC = 2 mg/L), à la linezolid (MIC≤1 mg/L), à la tétracycline (MIC = 0,5 mg/L), au trimethoprim-sulfamethoxazole (MIC = 0,006 mg/L) et à la vancomycine (MIC = 0,5 mg/L), et résistante ou probablement résistante à l'amikacine (MIC = 32 mg/L), à la cefotaxime (MIC> 2 mg/L), à la ciprofloxacine (MIC> 2 mg/L), à la clindamycine (MIC> 2 mg/L), à l'érythromycine (MIC = 1 mg/L), à la gentamycine (MIC = 4 mg/L), à l'imipenem (MIC = 4 mg/L), au meropenem (MIC = 8 mg/L) et à la rifampicine (MIC = 1 mg/L). Les MICs de l'amoxicilline-clavulanate, de la cefotaxime, du meropenem, du trimethoprim-sulfamethoxazole et de la vancomycine ont également été déterminés par Etest® (bioMérieux) en utilisant de l'agar Mueller-Hinton plus 5 % de sang, et des résultats similaires ont été trouvés.\n\nLe 7e jour, un échocardiogramme transthoracique n’a pas révélé de modifications. Le traitement a été changé pour de l’amoxicilline-clavulanate (1 g trois fois par jour, par voie intraveineuse), et de nouvelles cultures sanguines obtenues 24 heures plus tard étaient négatives. Un échocardiogramme transoesophagien réalisé le 9e jour de l’hospitalisation a révélé une végétation échogène et mobile de 6 × 9 mm sur la valve aortique prothétique fixée à la commissure entre la cuspide coronaire droite et la cuspide non coronaire. La fonction de la valve prothétique était par ailleurs normale. Le 11e jour, l’amoxicilline-clavulanate a été changé pour de la vancomycine ajustée à la fonction rénale (750 mg par jour) plus du linézolide (600 mg deux fois par jour, par voie intraveineuse). Le remplacement chirurgical a été considéré comme inapproprié chez cette patiente en raison de la comorbidité, de l’âge avancé, de la mobilité limitée et du rejet de la famille. Dans les jours suivants, elle a développé une anémie sévère, un état confusionnel aigu et une insuffisance cardiaque réfractaire. La prise de décision en fin de vie a été mise en œuvre, en donnant la priorité au contrôle des symptômes, et le traitement antibiotique a été changé en amoxicilline-clavulanate le 22e jour de l’admission. Le 28e jour, elle a été transférée dans un autre hôpital pour des soins palliatifs, et elle est morte 7 jours plus tard à cause d’une septicémie et d’une insuffisance cardiaque sévère. Une autopsie n’a pas été réalisée.",
+        "gold_summary": "Une femme de 82 ans avec une valve prothétique aortique a été admise à l'hôpital avec de la fièvre et une insuffisance cardiaque. Des examens complémentaires ont révélé le diagnostic d'endocardite infectieuse à C. cellulans (IE). La souche a été identifiée par MALDI-TOF MS, API Coryne et séquençage de l'ARNr 16S. La patiente a été jugée non opérable et est morte malgré la thérapie antibiotique 35 jours après son admission.\n",
+        "synthetic_summary": {
+            "B1": "Une dame de 82 ans avait une valve dans son cœur. Elle est venue à l’hôpital parce qu’elle avait de la fièvre et son cœur n’allait pas bien. Les docteurs ont trouvé une petite bête qui faisait du mal à sa valve. Ils ont donné des médicaments pour la soigner. Mais la dame était trop fatiguée et elle n’a pas guéri. Elle est morte après un mois à l’hôpital.",
+            "B2": "Une femme de 82 ans, qui avait une valve cardiaque artificielle, est arrivée à l’hôpital avec de la fièvre et des problèmes au cœur. Après plusieurs examens, les médecins ont découvert qu’elle avait une infection grave appelée endocardite infectieuse, causée par une bactérie nommée Corynebacterium cellulans. Pour identifier cette bactérie, ils ont utilisé des techniques spéciales, comme la spectrométrie de masse (MALDI-TOF MS), un test biochimique (API Coryne) et l’analyse de son matériel génétique (séquençage de l’ARN 16S). Malheureusement, à cause de son âge, de ses autres maladies et de son état général, elle n’a pas pu être opérée pour enlever la valve infectée. Malgré les traitements avec des antibiotiques, elle est décédée 35 jours après son admission à l’hôpital.",
+            "B3": "**Contexte**  \nUne femme de 82 ans, porteuse d’une valve aortique prothétique implantée 18 mois auparavant, souffrant de diabète de type 2 et d’insuffisance rénale chronique, a été hospitalisée après une semaine de fièvre, de confusion mentale (délire) et de difficultés respiratoires (dyspnée). Son suivi post-opératoire avait été marqué par plusieurs hospitalisations pour insuffisance cardiaque sévère inexpliquée et fibrillation auriculaire paroxystique, sans signes d’infection ni traitement antibiotique. À son admission actuelle, elle présentait une fièvre élevée (39 °C), une respiration rapide, une altération de l’état mental, ainsi que des signes cardiaques et pulmonaires évocateurs d’une infection.\n\n**Principales Observations**  \nLes analyses sanguines ont montré une inflammation importante (protéine C-réactive élevée), une hyperglycémie sévère et une fonction rénale altérée. Les radiographies thoraciques ont révélé un épanchement pleural gauche et un œdème pulmonaire bilatéral. Des cultures sanguines répétées ont permis d’isoler un bacille Gram positif corynéforme, identifié précisément comme Corynebacterium cellulans grâce à plusieurs méthodes complémentaires : spectrométrie de masse MALDI-TOF, test biochimique API Coryne et séquençage de l’ARN ribosomal 16S. Ce germe, rare et peu fréquent en pathologie humaine, était sensible à plusieurs antibiotiques, notamment l’amoxicilline-clavulanate et la vancomycine, mais résistant à d’autres.\n\nUn échocardiogramme transœsophagien réalisé au 9e jour a mis en évidence une végétation mobile de 6 × 9 mm fixée sur la valve aortique prothétique, confirmant le diagnostic d’endocardite infectieuse (infection de la valve cardiaque). La fonction de la valve prothétique restait par ailleurs normale.\n\n**Interprétation Clinique**  \nCette patiente présentait une endocardite infectieuse à C. cellulans sur valve prothétique aortique, une infection grave et rare, compliquée par son âge avancé, ses comorbidités (diabète, insuffisance rénale), et son état général fragile. Le traitement antibiotique initial empirique a été adapté en fonction des résultats microbiologiques, avec un passage à l’amoxicilline-clavulanate puis à une association vancomycine-linézolide. Cependant, en raison de son âge, de ses multiples pathologies, de sa mobilité réduite et du refus familial, une intervention chirurgicale pour remplacer la valve infectée n’a pas été envisagée.\n\n**Prochaines Étapes et Évolution**  \nMalgré la prise en charge médicale, la patiente a rapidement développé des complications sévères, notamment une anémie importante, une confusion accrue et une insuffisance cardiaque réfractaire. Une décision de soins palliatifs a été prise, centrée sur le confort et le contrôle des symptômes. Elle est décédée 35 jours après son admission à l’hôpital, des suites d’une septicémie (infection généralisée) et d’une insuffisance cardiaque sévère. Aucun examen post-mortem n’a été réalisé.\n\n---\n\nCe cas illustre la complexité du diagnostic et du traitement des infections sur prothèses valvulaires, en particulier lorsque des bactéries inhabituelles comme Corynebacterium cellulans sont impliquées, et souligne l’importance d’une approche multidisciplinaire adaptée aux caractéristiques individuelles du patient."
+        }
+    },
+    {
+        "article": "Patient et observation\nInformations relatives au patient: il s´agissait d´un patient âgé de 67 ans, sans antécédents pathologiques qui a consulté pour une gêne à la déglutition avec une dysphonie et une altération de l´état général.\n\nRésultats cliniques: l'examen clinique initial trouvait un patient conscient avec un score de Glasgow à 15/15, apyrétique, une tension artérielle de 12/07 cmHg, une saturation en oxygène de 100%, une fréquence cardiaque à 80/min, des conjonctives normocolorées avec la présence d´une volumineuse masse au niveau du cavum. Il n´y avait pas d´hépatomégalie ni de splénomégalie, les aires ganglionnaires étaient libres, le reste de l'examen somatique était normal.\n\nChronologie: le patient présentait depuis 6 mois une gêne à la déglutition avec une dysphonie, le tableau clinique s´est aggravé par l´installation d´une dysphagie aux solides avec une altération de l´état général (amaigrissement chiffré à 15kg/6 mois).\n\nDémarche diagnostique: la TDM cervico-thoraco-abdomino-pelvienne a objectivé une masse nasopharyngée de 70 mm x 40 mm étendue sur 60 mm. Le bilan biologique du patient était normal (la numération de formule sanguine, le bilan rénal et hépatique, la lacticodéshydrogénase et les sérologies VIH VHC VHB). L´étude histologique et immunohistochimique de la biopsie nasopharyngée était en faveur de LNH folliculaire B grade 1,2 CD20+; CD19+; CD79a+; CD10+ sur 2 lectures dans deux laboratoires différents. La biopsie ostéomédullaire était normale ainsi que le bilan préthérapeutique.\n\nIntervention thérapeutique: le patient a reçu 4 cures RCHOP 21 (rituximab 375mg/m2 en intraveineux (iv), cyclophosphamide 750 mg/m2 iv, oncovin 2 mg iv, prednisolone 100 mg par voie orale, et doxorubicine 50 mg/m2 (iv) sans réponse puis 3 cures RDHAOX (rituximab 375 mg/m2 en intraveineux (iv) à J1, aracytine haute dose 2 g/m2 x 2 iv à J2, dexamethasone 40 mg de J1 à J4, et oxalipatine 100 mg/m2 à J1) sans réponse clinique.\n\nSuivi et résultats des interventions thérapeutiques: la persistance et l´augmentation de la masse nasopharyngée a conduit à la réalisation de la trachéotomie, la biopsie de la masse nasopharyngée a objectivé la disparition de l´infiltration lymphoïde B avec présence des dépôts amyloïdes AL type kappa.\n\nL´immunoélectrophorèse des protéines plasmatiques a mis en évidence la présence de l´immunoglobuline M kappa, le dosage des chaines légères n´a pas été réalisé par manque de moyens, le myélogramme et une deuxième biopsie ostéomédullaire étaient normaux, la TEP scan a objectivé un processus nasopharyngé hypermétabolique sans autres anomalies, l´évaluation cardiaque (ECG, peptides natriurétiques, troponine, echocoeur) et rénale étaient sans particularités, le malade est actuellement sous protocole bortezomib, prednisone et bendamustine avec bonne évolution clinique après première cure.",
+        "gold_summary": "Nous rapportons le cas d´un patient âgé de 67 ans sans ATCDs pathologiques particuliers ayant présenté une altération de l´état général avec une dysphonie et dysphagie d´aggravation progressive avec une volumineuse masse du cavum dont la biopsie était en faveur d´un lymphome non hodgkinien folliculaire B grade 1 et 2. La tomodensitométrie (TDM) cervico-thoraco-abdomino-pelvienne a objectivé une masse nasopharyngée de 70 mm x 40 mm étendue sur 60 mm. La biopsie ostéomédullaire était normale ainsi que le bilan préthérapeutique. Le malade a reçu 4 cures de protocole Rituximab plus CHOP (cyclophosphamide, adriamycine, prednisone et oncovin) sans réponse puis 3 cures Rituximab plus DHAOX (dexamethasone, aracytine haute dose, et oxalipatine) avec persistance de la masse. La biopsie de cette dernière a objectivé la disparition de l´infiltration lymphoïde B avec présence des dépôts amyloïdes AL. L´immunoélectrophorèse des protéines plasmatiques a mis en évidence la présence de l´immunoglobuline M. La tomographie par émission de positons (TEP) scan a objectivé un processus nasopharyngé hypermétabolique. Le malade est actuellement sous protocole bortezomib, prednisone et bendamustine.",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 67 ans avait du mal à avaler et à parler. Il avait une grosse boule dans sa gorge. \n\nLes docteurs ont fait des examens et ont trouvé que cette boule était un problème dans ses cellules. Ils ont essayé plusieurs médicaments, mais la boule ne partait pas. \n\nAprès d’autres examens, ils ont vu que la boule avait changé un peu. Maintenant, ils donnent un nouveau traitement. Le monsieur va un peu mieux.",
+            "B2": "Cas d’un homme de 67 ans avec des difficultés à avaler et à parler\n\nUn homme de 67 ans, sans maladie connue avant, a commencé à avoir des problèmes pour avaler et une voix enrouée. Ces symptômes ont empiré pendant six mois, avec une perte de poids importante. Lors de l’examen, les médecins ont trouvé une grosse masse dans sa gorge, au niveau du cavum (une partie derrière le nez).\n\nCe qu’ils ont découvert\n\nUne analyse par scanner a montré que cette masse mesurait environ 7 cm sur 4 cm et s’étendait sur 6 cm. Une biopsie, c’est-à-dire un prélèvement d’un petit morceau de cette masse pour l’étudier, a révélé qu’il s’agissait d’un lymphome non hodgkinien folliculaire B de bas grade. C’est un type de cancer qui touche les cellules lymphatiques, des cellules du système immunitaire. D’autres examens, comme une biopsie de la moelle osseuse, étaient normaux.\n\nLes traitements essayés\n\nLe patient a d’abord reçu un traitement appelé R-CHOP, qui combine plusieurs médicaments pour combattre le cancer. Après quatre cycles, la masse n’a pas diminué. Ensuite, il a eu un autre traitement, le R-DHAOX, pendant trois cycles, mais la masse est restée. Une nouvelle biopsie a montré que les cellules cancéreuses avaient disparu, mais qu’il y avait maintenant des dépôts d’une substance appelée amyloïde, qui peut s’accumuler dans les tissus et causer des problèmes.\n\nLes examens complémentaires\n\nUne analyse du sang a détecté une protéine particulière, l’immunoglobuline M, liée à ces dépôts amyloïdes. D’autres tests, comme un scanner spécial appelé TEP, ont confirmé que la masse dans la gorge était toujours active, mais il n’y avait pas d’autres zones touchées. Le cœur et les reins du patient fonctionnaient normalement.\n\nSituation actuelle\n\nLe patient reçoit maintenant un nouveau traitement avec des médicaments nommés bortezomib, prednisone et bendamustine. Après la première cure, son état s’est amélioré. Les médecins continuent de le suivre pour surveiller l’évolution de la maladie.",
+            "B3": "Résumé détaillé et structuré\n\nContexte  \nNous présentons le cas d’un homme de 67 ans, sans antécédents médicaux notables, qui a consulté pour une gêne progressive à la déglutition accompagnée d’une dysphonie (modification de la voix) et d’une altération générale de son état de santé, notamment une perte de poids importante de 15 kg sur six mois. L’examen clinique a révélé une masse volumineuse au niveau du cavum (région nasopharyngée), sans autres anomalies majeures.\n\nPrincipales observations  \nUne tomodensitométrie (TDM) cervico-thoraco-abdomino-pelvienne a mis en évidence une masse nasopharyngée mesurant 70 mm sur 40 mm, s’étendant sur 60 mm. La biopsie de cette masse a confirmé la présence d’un lymphome non hodgkinien (LNH) folliculaire de type B, de grade 1 et 2, caractérisé par des marqueurs immunohistochimiques positifs (CD20+, CD19+, CD79a+, CD10+). Les examens complémentaires, notamment la biopsie ostéomédullaire et le bilan préthérapeutique, étaient normaux, indiquant l’absence d’extension médullaire ou d’autres atteintes systémiques.\n\nIntervention thérapeutique et évolution  \nLe patient a d’abord reçu quatre cycles de chimiothérapie selon le protocole R-CHOP (association de rituximab, cyclophosphamide, doxorubicine, vincristine et prednisone), sans amélioration clinique ni réduction de la masse. Une deuxième ligne de traitement, comprenant trois cycles de chimiothérapie R-DHAOX (rituximab, dexaméthasone, aracytine à haute dose et oxaliplatine), a également été inefficace. La persistance et l’augmentation de la masse ont conduit à une trachéotomie pour assurer la respiration.\n\nUne nouvelle biopsie de la masse nasopharyngée a montré la disparition des cellules lymphoïdes B malignes, mais a révélé la présence de dépôts amyloïdes de type AL (amylose liée à des chaînes légères d’immunoglobulines), de type kappa. L’immunoélectrophorèse des protéines plasmatiques a détecté une immunoglobuline M de type kappa, suggérant une production anormale de cette protéine. Les examens complémentaires, notamment un myélogramme, une seconde biopsie ostéomédullaire, ainsi qu’une évaluation cardiaque et rénale, étaient sans anomalies. La tomographie par émission de positons (TEP scan) a confirmé un processus hypermétabolique localisé au niveau nasopharyngé, sans autre localisation suspecte.\n\nProchaines étapes  \nFace à cette évolution, le patient a été mis sous un nouveau protocole associant bortezomib (un inhibiteur du protéasome utilisé dans le traitement des maladies à dépôts amyloïdes), prednisone et bendamustine (un agent alkylant). Après la première cure, une amélioration clinique a été observée, témoignant d’une bonne réponse initiale à ce traitement. Un suivi régulier est nécessaire pour évaluer l’évolution de la maladie et adapter la prise en charge."
+        }
+    },
+    {
+        "article": "Un homme africain de 53 ans ayant des antécédents médicaux d'hypertension diagnostiquée à la mi-vingtaine, d'ICS systolique et de cardiomyopathie non ischémique a présenté une aggravation de la dyspnée d'effort, un œdème des membres inférieurs, une dyspnée nocturne paroxystique et une orthopnée pendant environ une semaine. Le patient prenait six médicaments antihypertenseurs en ambulatoire, dont la clonidine, l'hydralazine, le mononitrate d'isosorbide, le valsartan et la furosémide. Malgré le respect des médicaments, il a été admis fréquemment pour des exacerbations de l'ICS. Il a nié avoir consommé du tabac, de la drogue ou de l'alcool. Bien qu'il ait été diagnostiqué d'hypertension à un jeune âge, le patient ne se rappelait pas avoir subi des tests supplémentaires pour des causes secondaires de l'HTN au moment du diagnostic. Il se rappelait un diagnostic d'hypokaliémie chronique, qui avait été attribué à l'utilisation de la furosémide, et il s'était vu prescrire des suppléments de potassium par intermittence dans le passé. Il a nié toute antécédent familial connu de PA ou d'HTN non contrôlée. Les signes vitaux ont révélé une tension artérielle de 163/103 mm Hg, une fréquence cardiaque de 74 battements par minute, une fréquence respiratoire de 17 et une saturation en oxygène de 95 % sur une canule nasale de 3 L. Les résultats pertinents de l'examen physique comprenaient une distension veineuse jugulaire, un œdème pitting bilatéral des membres inférieurs, des râles bilatéraux et un galop S3 proéminent.\n\n\nEnquêtes\n\nL'ECG ne révélait aucune modification ischémique aiguë, un rythme sinusal avec un bloc de branche gauche chronique. Les troponines étaient négatives à trois reprises consécutives. La radiographie thoracique révélait une congestion vasculaire pulmonaire bilatérale. L'échocardiographie transthoracique révélait une hypertrophie ventriculaire gauche modérée et une dilatation avec une hypokinésie globale et une fraction d'éjection de 10 % à 15 %. Aucune anomalie valvulaire n'a été notée. L'IRM cardiaque révélait des zones de fibrose myocardique probablement liées à une hypertrophie, atypique pour une maladie ischémique et atypique pour un infarctus antérieur ou une amyloïdose. Les études de laboratoire révélaient un potassium sérique de 2,6 mmol/L et un bicarbonate de 34 mmol/L. Une PA était suspectée, et des tests complémentaires ont révélé un taux plasmatique d'aldostérone élevé de 154 ng/dL (normal inférieur à 39,2 ng/dL), une activité rénine plasmatique (AR) diminuée de moins de 2,1 ng/mL/heure et un rapport de concentration plasmatique d'aldostérone/AR plasmatique (PAC/PRA) de 73,3 (ng/dL)/(ng/mL/heure).\n\nLes résultats d’un test de suppression de la dexaméthasone pendant la nuit, d’un test de la fonction thyroïdienne et des métanéphrines plasmatiques et urinaires étaient normaux. Un test de suppression de la dexaméthasone par surcharge saline orale n’a pas été effectué par crainte d’exacerber son œdème pulmonaire et son insuffisance cardiaque. La TDM de l’abdomen et du bassin avec injection de produit de contraste a montré un adénome de la glande surrénale gauche bien défini et homogène de 1,2 × 2,4 cm. L’échantillonnage ultérieur de la veine surrénale a confirmé une PA unilatérale avec latéralisation vers la glande surrénale gauche (tableau 1). Le rapport cortisol de la veine surrénale inférieure à cortisol de la veine cave inférieure pour les veines surrénales gauche et droite était supérieur à 3, ce qui correspond à une canulation réussie de la veine surrénale. Le rapport aldostérone de la veine surrénale à cortisol de la veine surrénale était de 14,8 et 2,2, respectivement. Un rapport de latéralisation supérieur à 4 est compatible avec une maladie unilatérale, tandis qu’un rapport de latéralisation inférieur à 3 est compatible avec une maladie bilatérale. Le rapport de latéralisation du patient de gauche à droite était de 6,7, ce qui correspond à une maladie unilatérale. Le patient a commencé un traitement par spironolactone avec une amélioration de sa tension artérielle et de son hypokaliémie et a été référé pour une adrénalectomie gauche.",
+        "gold_summary": "Un homme africain de 53 ans ayant des antécédents de 25 ans d’hypertension artérielle non contrôlée et d’insuffisance cardiaque systolique a présenté une exacerbation aiguë d’insuffisance cardiaque congestive. Il a été trouvé qu’il souffrait d’hypokaliémie sévère, des tests supplémentaires ont donc été effectués et l’aldostéronisme primaire a été confirmé. La tomographie par ordinateur a montré un adénome homogène bien défini de 1,2 × 2,4 cm de la glande surrénale gauche. L’échantillonnage de la veine surrénale a confirmé un aldostéronisme primaire unilatéral avec latéralisation vers la glande surrénale gauche. Le patient a commencé à prendre de la spironolactone et a été référé à une chirurgie pour une adrénalectomie gauche laparoscopique.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 53 ans avait le cœur fatigué depuis longtemps. Il avait aussi la tension très haute depuis beaucoup d’années. Un jour, il a eu beaucoup de mal à respirer et ses jambes ont gonflé.\n\nLes docteurs ont fait des examens. Ils ont vu que son corps manquait d’un petit sel important appelé potassium. Ils ont aussi trouvé une petite boule dans une glande près de ses reins.\n\nCette boule faisait que son corps gardait trop de sel et d’eau. Les docteurs lui ont donné un médicament pour l’aider. Ils ont aussi prévu une petite opération pour enlever cette boule. Cela va l’aider à se sentir mieux.",
+            "B2": "### Ce qu'ils ont trouvé\n\nUn homme de 53 ans souffrait depuis longtemps d'une tension artérielle très élevée et d'une maladie du cœur appelée insuffisance cardiaque. Récemment, ses symptômes se sont aggravés, avec des difficultés à respirer et des gonflements aux jambes. Lors des examens, on a découvert qu'il avait un taux très bas de potassium dans le sang, ce qui peut être dangereux.\n\n### Ce que cela signifie\n\nPour comprendre la cause de cette hypokaliémie, les médecins ont fait des tests qui ont montré qu'il avait une maladie appelée aldostéronisme primaire. Cela signifie que sa glande surrénale (une petite glande au-dessus du rein) produisait trop d’aldostérone, une hormone qui fait augmenter la tension artérielle et fait perdre du potassium.\n\n### Ce qu'ils ont fait\n\nUne tomographie (un scanner) a montré une petite tumeur bénigne (appelée adénome) sur la glande surrénale gauche. Un test spécial appelé prélèvement veineux surrénalien a confirmé que cette tumeur était responsable de la production excessive d’aldostérone. Le patient a alors commencé un traitement avec un médicament, la spironolactone, qui bloque l’effet de l’aldostérone. Il a aussi été orienté vers une chirurgie pour enlever cette tumeur afin d’améliorer sa santé.",
+            "B3": "Résumé détaillé et structuré\n\nContexte  \nUn homme africain de 53 ans, avec un historique de 25 ans d’hypertension artérielle (HTA) non contrôlée et d’insuffisance cardiaque systolique d’origine non ischémique, a présenté une aggravation récente de symptômes évocateurs d’insuffisance cardiaque congestive, notamment une dyspnée à l’effort, un œdème des jambes, une dyspnée nocturne paroxystique et une orthopnée. Malgré un traitement antihypertenseur intensif comprenant six médicaments, dont des diurétiques et des vasodilatateurs, il avait des hospitalisations fréquentes pour décompensation cardiaque. Il ne fumait pas, ne consommait ni alcool ni drogues, et ne rapportait pas d’antécédents familiaux d’HTA sévère ou non contrôlée. Il avait également une hypokaliémie chronique attribuée auparavant à son traitement diurétique.\n\nPrincipales observations  \nÀ l’examen clinique, le patient présentait une tension artérielle élevée (163/103 mm Hg), une distension des veines jugulaires, un œdème bilatéral des membres inférieurs, des râles pulmonaires et un galop S3, signes compatibles avec une insuffisance cardiaque congestive. Les examens complémentaires ont montré :  \n- Un électrocardiogramme avec un bloc de branche gauche chronique sans signe d’ischémie aiguë.  \n- Une radiographie thoracique révélant une congestion pulmonaire.  \n- Une échocardiographie mettant en évidence une hypertrophie ventriculaire gauche modérée, une dilatation ventriculaire avec une hypokinésie globale et une fraction d’éjection très basse (10-15 %), sans anomalie valvulaire.  \n- Une IRM cardiaque suggérant une fibrose myocardique liée à l’hypertrophie, sans signes d’infarctus ou d’amyloïdose.  \n- Des analyses sanguines révélant une hypokaliémie sévère (potassium à 2,6 mmol/L) et une alcalose métabolique (bicarbonate à 34 mmol/L).  \n\nDevant cette hypokaliémie associée à une HTA sévère, une hyperaldostéronisme primaire (PA) a été suspecté. Les dosages hormonaux ont confirmé un taux d’aldostérone plasmatique très élevé (154 ng/dL), une activité rénine plasmatique basse (< 2,1 ng/mL/h) et un rapport aldostérone/rénine plasmatique très élevé (73,3), ce qui est typique d’un aldostéronisme primaire. Les autres causes secondaires d’HTA (dysfonction thyroïdienne, phéochromocytome, syndrome de Cushing) ont été exclues par des tests normaux.  \n\nUne tomodensitométrie abdominale avec injection a identifié un adénome surrénalien gauche bien délimité et homogène de 1,2 × 2,4 cm. L’échantillonnage sélectif des veines surrénales a confirmé que la sécrétion excessive d’aldostérone provenait uniquement de la glande surrénale gauche, avec un rapport de latéralisation de 6,7 (supérieur au seuil de 4), indiquant une maladie unilatérale.\n\nInterprétation clinique  \nCe patient souffre d’un aldostéronisme primaire unilatéral causé par un adénome surrénalien gauche, responsable de son hypertension artérielle sévère, de son hypokaliémie chronique et probablement de son insuffisance cardiaque systolique aggravée. L’aldostéronisme primaire est une cause traitable d’HTA secondaire, souvent sous-diagnostiquée, qui peut entraîner des complications cardiovasculaires sévères si elle n’est pas prise en charge.\n\nProchaines étapes  \nLe patient a débuté un traitement médical par spironolactone, un antagoniste des récepteurs de l’aldostérone, qui a permis une amélioration de sa tension artérielle et de son taux de potassium. Il a été orienté vers une chirurgie pour une adrénalectomie laparoscopique gauche, qui vise à retirer l’adénome responsable de la sécrétion excessive d’aldostérone et ainsi potentiellement guérir son hypertension et prévenir la progression de son insuffisance cardiaque."
+        }
+    },
+    {
+        "article": "Une femme de 57 ans ayant suivi pendant 8 ans un traitement de cardiomyopathie dilatée idiopathique a présenté une aggravation de la classe fonctionnelle et des hospitalisations récurrentes pour insuffisance cardiaque. La classe fonctionnelle de la New York Heart Association était de 4 et l'Interagency Registry for Mechanically Assisted Circulatory Support était de 5. Elle avait été traitée avec une thérapie médicale guidée par les directives à des doses maximales tolérées, notamment avec de l'énalapril 10 mg b.i.d., du métoprolol 50 mg b.i.d., de la spironolactone 25 mg, de la furosémide 40 mg b.i.d. et de la digoxine 0,125 mg par jour, pendant au moins 5 ans. Les comorbidités comprenaient le tabagisme actif et l'obésité morbide (indice de masse corporelle de 37 kg/m2). Elle était principalement limitée par la fatigue d'effort et la dyspnée, malgré une euvolemie principalement non dépendante de doses élevées de diurétiques. L'électrocardiogramme de repos (ECG) a montré un rythme sinusal à une fréquence de 70 bpm et une durée de QRS de 80 ms. La fraction d'éjection ventriculaire gauche était de 23 %, avec un ventricule gauche dilaté (diamètre de fin de diastole de 6,7 cm) et une hypokinésie diffuse. Un test d'effort cardiopulmonaire (CPET) a démontré une capacité d'exercice sévèrement diminuée, avec une consommation maximale d'oxygène (VO2 de pointe) de 12 ml/kg/min (ou 16,46 ml/kg/min lorsque corrigée pour la masse corporelle maigre), ainsi que d'autres variables indiquant un pronostic défavorable d'insuffisance cardiaque, y compris la ventilation minute/production de dioxyde de carbone (VE/VCO2) de 42 et la respiration périodique. À la deuxième minute de l'exercice, à une fréquence cardiaque de 131 bpm, la patiente a développé une LBBB avec un élargissement du QRS à 200 ms. Cette constatation a persisté dans la phase de récupération. Il convient de noter que la réponse pressorostatique a également été observée pendant le CPET. Une échocardiographie d'effort a ensuite démontré une dyssynchronie intraventriculaire et interventriculaire induite par l'exercice, avec un retard électromécanique du début du QRS à l'onde S de plus de 65 ms et une différence entre les intervalles pré-éjection gauche et droite de plus de 40 ms, respectivement.\n\nLa patiente n’étant pas considérée comme éligible à une transplantation cardiaque, compte tenu de ses comorbidités actives, il a été décidé de lui implanter un CRT (Etrinsa 8 HF‐T, Biotronik, Berlin, Allemagne) pour tenter de corriger l’EI‐LBBB. L’imagerie par résonance magnétique cardiaque réalisée avant l’insertion du CRT n’a montré qu’une petite zone d’amélioration tardive du gadolinium au niveau du septum basilaire mésocardique, mais aucun motif suggérant une étiologie spécifique autre qu’une cardiomyopathie dilatée non ischémique n’a été noté. Initialement, la stimulation biventriculaire a été réglée à une fréquence cardiaque minimale de 75 bpm avec un retard atrioventriculaire de 105‐80 ms, et l’ECG a montré une durée de QRS de 145 ms.\n\nAprès l'implantation du CRT, l'état du patient s'est amélioré et il a été classé dans la catégorie II de la New York Heart Association. Il n'y a pas eu de récidive d'hospitalisation pour insuffisance cardiaque. Le traitement médical a été relativement inchangé après le CRT, à l'exception de l'introduction de l'amiodarone en raison d'arythmies ventriculaires et du changement de metoprolol à carvedilol et de l'introduction de l'hydralazine, tous deux pour améliorer la gestion de l'hypertension, car les niveaux de pression artérielle ont augmenté et la tolérance aux médicaments s'est améliorée après le CRT. L'interrogation du stimulateur cardiaque a montré une stimulation auriculaire à 94 % et une stimulation biventriculaire à 100 %. Quelques mois plus tard, un CPET répété à 6 et 12 mois a démontré une amélioration significative et soutenue de la capacité d'exercice. La stimulation biventriculaire a eu lieu à 100 % du temps d'exercice, et la respiration périodique était absente lors des deux examens. Une remodélisation cardiaque inverse et une amélioration de la fraction d'éjection ont également été observées.",
+        "gold_summary": "Une femme de 57 ans atteinte de cardiomyopathie dilatée idiopathique (fraction d'éjection de 23 %) a présenté une insuffisance cardiaque de classe IV selon la New York Heart Association et des hospitalisations récurrentes. Au cours de l'évaluation de la transplantation cardiaque, un nouveau début de bloc de branche gauche intermittent a été observé lors du test d'effort cardiopulmonaire. La CRT a été implantée et un taux de resynchronisation de 97 % a été atteint. Au cours du suivi de 12 mois, les paramètres d'exercice cliniques et pronostiques se sont améliorés.\n",
+        "synthetic_summary": {
+            "B1": "Une dame avait un cœur qui ne marchait pas bien. Elle était très fatiguée et avait du mal à respirer.\n\nLes docteurs ont fait un test où elle devait bouger un peu. Son cœur a eu un problème pendant ce test.\n\nIls lui ont mis un petit appareil pour aider son cœur à battre mieux. Après, elle allait beaucoup mieux.\n\nElle pouvait faire plus de choses sans être fatiguée. Son cœur est devenu plus fort.",
+            "B2": "Une femme de 57 ans souffrait d'une maladie du cœur appelée cardiomyopathie dilatée, où le muscle du cœur est affaibli et le ventricule gauche (la principale chambre qui pompe le sang) est dilaté. Sa capacité à pomper le sang était très faible, avec une fraction d'éjection de seulement 23 % (ce qui signifie que son cœur pompait moins d’un quart du sang normalement attendu). Elle avait aussi une insuffisance cardiaque sévère, ce qui la fatiguait beaucoup et la faisait souvent être hospitalisée.\n\nLors d’un test d’effort, qui mesure comment le cœur fonctionne pendant l’exercice, les médecins ont découvert qu’elle développait un problème appelé bloc de branche gauche intermittent. Ce bloc ralentit la façon dont les signaux électriques traversent le cœur, ce qui peut rendre le battement du cœur moins efficace.\n\nComme elle ne pouvait pas recevoir de greffe de cœur à cause d’autres problèmes de santé, les médecins ont décidé de lui implanter un appareil appelé resynchroniseur cardiaque (CRT). Cet appareil aide à coordonner les battements du cœur en envoyant des impulsions électriques aux deux côtés du cœur pour améliorer son fonctionnement.\n\nAprès l’implantation du CRT, sa condition s’est nettement améliorée. Elle a moins ressenti de fatigue, n’a plus été hospitalisée pour son insuffisance cardiaque, et sa capacité à faire de l’exercice a augmenté. Les examens réalisés jusqu’à un an après l’implantation ont montré que son cœur pompait mieux et que son rythme cardiaque était bien contrôlé grâce à l’appareil.",
+            "B3": "### Contexte  \nUne femme de 57 ans souffrant depuis huit ans d’une cardiomyopathie dilatée idiopathique, caractérisée par une fraction d’éjection ventriculaire gauche très basse (23 %) et un ventricule gauche dilaté, présentait une aggravation importante de son insuffisance cardiaque. Elle était classée en stade IV selon la classification fonctionnelle de la New York Heart Association (NYHA), ce qui signifie une limitation sévère des activités physiques, et avait subi plusieurs hospitalisations pour décompensation cardiaque. Malgré un traitement médical optimal comprenant plusieurs médicaments à doses maximales tolérées, ses symptômes principaux étaient une fatigue importante à l’effort et une difficulté respiratoire (dyspnée). Ses comorbidités comprenaient un tabagisme actif et une obésité morbide.\n\n### Principales observations  \nLors d’un test d’effort cardiopulmonaire (CPET), la patiente a développé un bloc de branche gauche (LBBB) intermittent, caractérisé par un élargissement marqué du complexe QRS à 200 ms, signe d’une conduction électrique retardée dans le ventricule gauche. Ce trouble de conduction, induit par l’exercice, a été confirmé par une échocardiographie d’effort montrant une dyssynchronie (désynchronisation) électrique et mécanique entre les ventricules droit et gauche, ce qui aggrave la fonction cardiaque. Ces anomalies étaient associées à une capacité d’exercice sévèrement réduite (VO2 max à 12 ml/kg/min) et à des signes pronostiques défavorables, tels qu’une ventilation inefficace et une respiration périodique.\n\n### Interprétation clinique  \nLa patiente n’était pas éligible à une transplantation cardiaque en raison de ses comorbidités actives. Il a donc été décidé d’implanter un dispositif de resynchronisation cardiaque (CRT), qui stimule simultanément les deux ventricules pour corriger la dyssynchronie induite par le bloc de branche gauche. Avant l’implantation, l’imagerie par résonance magnétique cardiaque n’a montré qu’une petite zone de fibrose sans cause ischémique évidente, confirmant le diagnostic de cardiomyopathie dilatée non ischémique. Après l’implantation du CRT, la stimulation biventriculaire a été réglée pour assurer une activation électrique optimale.\n\n### Prochaines étapes et résultats  \nSuite à la mise en place du CRT, l’état clinique de la patiente s’est nettement amélioré, avec un passage à la classe fonctionnelle II de la NYHA, indiquant une limitation modérée des activités physiques. Elle n’a plus nécessité d’hospitalisation pour insuffisance cardiaque. Le traitement médical a été ajusté, notamment par l’introduction de l’amiodarone pour contrôler des arythmies ventriculaires, le remplacement du métoprolol par le carvedilol, et l’ajout d’hydralazine pour mieux gérer son hypertension artérielle. Le suivi du stimulateur a montré une stimulation auriculaire à 94 % et une stimulation biventriculaire à 100 %, assurant une resynchronisation quasi complète.\n\nDes tests d’effort répétés à 6 et 12 mois ont confirmé une amélioration significative et durable de la capacité d’exercice, avec une disparition de la respiration périodique et une stimulation biventriculaire maintenue pendant tout l’effort. Par ailleurs, une remodélisation cardiaque inverse a été observée, traduite par une réduction de la dilatation ventriculaire et une amélioration de la fraction d’éjection, témoignant d’une récupération partielle de la fonction cardiaque.\n\n### Conclusion  \nChez cette patiente atteinte de cardiomyopathie dilatée sévère avec un bloc de branche gauche induit par l’exercice, l’implantation d’un dispositif de resynchronisation cardiaque a permis une amélioration clinique, fonctionnelle et pronostique notable sur une période de suivi d’un an. Cette prise en charge a constitué une alternative efficace à la transplantation cardiaque, contre-indiquée dans son cas."
+        }
+    },
+    {
+        "article": "Patient de dix mois, sexe féminin, hospitalisée à l'HCPA depuis neuf mois, a séjourné en unité de soins intensifs néonatale (UTIN) pendant quatre mois pour une recherche génétique, nécessitant une ventilation mécanique invasive (VMI) pour la stabilité du cadre respiratoire. Au cours de l'hospitalisation, elle a eu besoin d'une trachéotomie (TQT) et d'une VMI pour une utilisation à domicile. Pour cela, la patiente a été adaptée à l'UTIN au ventilateur mécanique Trilogy 100 (Philips Respironics, États-Unis), mode ventilatoire avec pression contrôlée, pression inspiratoire (IPAP) de 25 cmH2O, pression expiratoire (EPAP) de 6 cmH2O, fréquence respiratoire (FR) de 22 irpm, sensibilité auto-track et temps inspiratoire de 0,8 seconde.\n\nAprès son adaptation, il a été libéré dans l'unité de soins intensifs pédiatriques, où il était cliniquement stable, sans besoin d'oxygénothérapie, en attendant la libération judiciaire pour soins à domicile. Cependant, au neuvième mois d'hospitalisation, il a commencé à avoir de la fièvre et une hypoxémie (saturation partielle en oxygène (SpO2): 90%), nécessitant l'administration d'oxygène (2 L/min) et le transfert sur un lit d'isolement, où il a effectué le test de réaction en chaîne de la polymérase (PCR) pour COVID-19, dont le résultat a été positif.\n\nL’équipe de physiothérapie de l’unité, afin de prévenir la dispersion d’aérosols, a installé un circuit d’aspiration fermé, bien que peu efficace, car l’enfant était actif et déconnectait fréquemment le circuit de VMI. Elle a également inséré un filtre à haute efficacité de particules d’air (HEPA) à la sortie du respirateur, suivi d’un filtre échangeur de chaleur et d’humidité (HME) près de la TCT. Elle a utilisé un filtre échangeur de chaleur et d’humidité (HMEF) dans le réanimateur manuel pour la réalisation de techniques de décongestion bronchique et un filtre HEPA à la sortie de l’air comprimé, afin de réduire la dispersion d’aérosol pendant l’aspiration des voies aériennes.\n\nLa radiographie thoracique initiale ne révélait aucune anomalie. La gazométrie veineuse a indiqué une acidose respiratoire (pH = 7,27 ; pCO2 = 69,9 ; HCO3 = 31,7), nécessitant des ajustements des paramètres ventilatoires (IPAP = 28 cmH2O ; EPAP = 5 cmH2O ; FR = 25 irpm), et l'utilisation d'oxygénothérapie (1 L/min). Sept jours après le début des symptômes, une nouvelle radiographie thoracique a été réalisée, révélant la présence d'un infiltrat péri-hilar et une apparente consolidation dans le lobe moyen.\n\nPendant les séances de kinésithérapie, des techniques manuelles ont été utilisées pour maintenir l'expansion pulmonaire et promouvoir l'hygiène bronchique. Les techniques les plus utilisées étaient : la compression/décompression, l'expiration lente prolongée (ELPr), l'hyperinsufflation manuelle (HM) avec sac auto-gonflable et le bag squeezing. Afin de maintenir la patiente active et prévenir la régression du tableau moteur, l'encadrement familial a maintenu la stimulation motrice quotidienne.\n\n19 jours après le début des symptômes de COVID-19, la patiente a été autorisée à quitter l'hôpital, cliniquement stable, avec un résultat négatif au test SARS-CoV-2, une gazométrie sans modification et un retour aux paramètres ventilatoires utilisés avant l'infection. Quelques jours avant la sortie, l'enquête génétique a été menée à bien, confirmant le syndrome d'Ondine. Malgré une hospitalisation prolongée (300 jours), la patiente contrôlait sa tête, pouvait s'asseoir sans soutien, roulait et saisissait et atteignait des objets sans difficulté. En outre, l'évaluation fonctionnelle au moyen de l'échelle d'état fonctionnel (FSS-Brésil) a indiqué un degré modéré de dysfonctionnement (12 points), et les soins de physiothérapie motrice et respiratoire ont été poursuivis à domicile.\n",
+        "gold_summary": "sexe féminin, 10 mois, avec une maladie chronique préexistante, hospitalisée depuis la naissance, utilisant une ventilation mécanique par trachéotomie, a évolué avec une hypoxémie, nécessitant une oxygénothérapie et une augmentation des paramètres ventilatoires, confirmant la COVID-19. Des techniques de désobstruction bronchique et de maintien de l'expansion pulmonaire ont été réalisées. En outre, l'enfant a acquis, pendant l'hospitalisation, le contrôle de la tête, la position assise sans soutien, le roulement et la portée des objets et, pendant l'infection par le coronavirus, des instructions ont été données à la famille pour le maintien des repères moteurs acquis.\n",
+        "synthetic_summary": {
+            "B1": "Il y a une petite fille de 10 mois. Elle est restée longtemps à l’hôpital. Elle avait besoin d’un appareil pour l’aider à bien respirer. Un jour, elle est tombée malade avec un virus appelé coronavirus. Elle avait du mal à respirer. Les docteurs lui ont donné de l’oxygène pour l’aider. \n\nLes soignants ont fait des petits massages pour que ses poumons restent forts. Ils ont aussi aidé la petite fille à bouger un peu. Pendant qu’elle était malade, sa famille a appris comment continuer à l’aider à bouger et à grandir. \n\nMême si elle était malade, elle a appris à tenir sa tête, à s’asseoir toute seule, à se retourner et à attraper des objets. Les docteurs et sa famille ont travaillé ensemble pour qu’elle aille mieux.",
+            "B2": "Patiente de 10 mois, une fille, souffrant d’une maladie chronique, a été hospitalisée depuis sa naissance. Elle utilisait un appareil appelé ventilation mécanique par trachéotomie, qui aide à respirer grâce à un tube placé dans la gorge. Pendant son séjour, elle a développé une baisse de l’oxygène dans le sang (hypoxémie), ce qui a nécessité l’ajout d’oxygène et l’augmentation des réglages de la machine pour mieux l’aider à respirer. Un test a confirmé qu’elle avait la COVID-19.\n\nPour l’aider à mieux respirer, les kinésithérapeutes ont utilisé des techniques spéciales pour nettoyer ses poumons et garder ses poumons bien ouverts. Malgré la maladie, la petite fille a progressé dans ses capacités motrices : elle a appris à contrôler sa tête, à s’asseoir sans aide, à se retourner et à attraper des objets. Pendant sa maladie, la famille a reçu des conseils pour continuer à stimuler ses mouvements à la maison afin de ne pas perdre ces progrès.",
+            "B3": "Résumé détaillé et structuré\n\nContexte  \nIl s’agit d’une patiente de dix mois, hospitalisée depuis sa naissance en raison d’une maladie chronique rare, le syndrome d’Ondine, diagnostiqué tardivement par analyse génétique. Elle a nécessité une ventilation mécanique invasive via une trachéotomie pour assurer sa respiration, d’abord en unité de soins intensifs néonatale, puis en unité pédiatrique, avec un ventilateur adapté à domicile.\n\nPrincipales observations  \nAu neuvième mois d’hospitalisation, la patiente a présenté une infection à SARS-CoV-2 confirmée par test PCR, accompagnée de fièvre et d’une hypoxémie (diminution de la saturation en oxygène à 90 %). Cette situation a nécessité une oxygénothérapie supplémentaire et une augmentation des paramètres de ventilation mécanique (notamment une pression inspiratoire plus élevée et une fréquence respiratoire accrue). La radiographie thoracique initiale était normale, mais sept jours après l’apparition des symptômes, elle montrait un infiltrat péri-hilar et une consolidation pulmonaire, signes d’atteinte respiratoire liée à l’infection.\n\nInterventions thérapeutiques  \nPour limiter la dispersion des aérosols infectieux, l’équipe de physiothérapie a mis en place un circuit d’aspiration fermé et des filtres à haute efficacité (HEPA) sur le ventilateur et les dispositifs d’aspiration. Par ailleurs, des techniques manuelles de kinésithérapie respiratoire ont été utilisées pour maintenir l’expansion pulmonaire et faciliter le nettoyage des voies respiratoires, notamment la compression/décompression thoracique, l’expiration lente prolongée, l’hyperinsufflation manuelle et le bag squeezing. Ces interventions visaient à prévenir les complications pulmonaires et à améliorer la ventilation.\n\nÉvolution fonctionnelle  \nMalgré la longue hospitalisation (près d’un an), la patiente a acquis plusieurs compétences motrices importantes : contrôle de la tête, capacité à s’asseoir sans soutien, rouler sur le côté et saisir des objets. Pendant la phase aiguë de l’infection, la famille a été activement impliquée pour maintenir ces acquis moteurs grâce à une stimulation quotidienne. À la sortie, la patiente était cliniquement stable, avec un test COVID-19 négatif, une gazométrie normale et un retour aux paramètres ventilatoires antérieurs à l’infection. L’évaluation fonctionnelle a montré un dysfonctionnement modéré, justifiant la poursuite des soins de physiothérapie respiratoire et motrice à domicile.\n\nProchaines étapes  \nLa prise en charge doit continuer à domicile, avec un suivi étroit de la fonction respiratoire et motrice, ainsi qu’un accompagnement familial pour soutenir le développement moteur et prévenir les complications liées à la maladie chronique et aux séquelles de l’infection virale."
+        }
+    },
+    {
+        "article": "Une femme japonaise de 35 ans, pesant 42,7 kg (poids sec, 41,1 kg avant la grossesse), et mesurant 147 cm a été opérée par césarienne. Elle souffrait d'une insuffisance rénale due à une glomérulonéphrite chronique. Avant de devenir enceinte, elle avait été soumise à une hémodialyse trois fois par semaine. L'accès à l'hémodialyse (fistule artério-veineuse) se trouvait dans son bras supérieur gauche. Les symptômes et le déroulement du traitement jusqu'à la césarienne sont décrits dans le tableau 1. Lorsque la grossesse a été identifiée, elle a reçu une hémodialyse cinq fois par semaine. Bien qu'elle n'ait pas présenté de symptômes avant la grossesse, elle a déclaré avoir souffert d'une dyspnée à 12 semaines de gestation et a ensuite développé une toux sévère. L'échocardiographie transthoracique (TTE) a montré une fraction d'éjection ventriculaire gauche (FEVG) de 40 % et une hypertension pulmonaire modérée. Après l'hospitalisation, l'hémodialyse a été augmentée à six fois par semaine pour prévenir une insuffisance cardiaque. La FEVG a été améliorée à près de 50 % et les symptômes ont également été améliorés, de sorte que le plan était de reporter l'accouchement aussi longtemps que possible. Cependant, elle a de nouveau développé une toux et une dyspnée à 22 semaines de gestation.\n\nLa radiographie thoracique a montré une congestion importante. La TTE a montré une EFV de 20 %, une régurgitation mitrale modérée à modérée et une dilatation ventriculaire gauche. Elle a donc été admise à l'unité de soins intensifs (USI). La saturation en oxygène percutanée (SpO2) était de 92 % en air ambiant, de sorte que l'oxygène supplémentaire a été fourni à 1 l/minute par canule nasale. Après l'administration d'oxygène, la SpO2 était de 98 %. En outre, le volume d'eau a été éliminé par ultrafiltration extracorporelle. Bien que l'état respiratoire et la fonction cardiaque se soient légèrement améliorés avec les soins intensifs, une conférence clinique d'obstétriciens, de pédiatres, d'urologues, de cardiologues et d'anesthésiologistes a décidé qu'une césarienne devait être pratiquée à 24 semaines 0 jours de gestation. L'anticoagulant utilisé pour la dialyse a été changé de l'héparine au nafamostat mesylate (nafamostat) à 23 semaines de gestation pour la césarienne. Les tests sanguins ont montré une hémoglobine de 10,1 g/dl et des plaquettes de 12,1 × 104/μl. Le temps de prothrombine international normalisé était de 0,85 et le temps de thromboplastine partielle activée était de 25,6 secondes.\n\nLorsque la patiente est arrivée dans la salle d'opération, deux lignes veineuses périphériques intraveineuses ont été insérées avec une canule de calibre 22 et une canule de calibre 18 dans l'avant-bras droit pour une réanimation par fluides. Une ligne artérielle a été insérée par l'artère radiale droite avec une canule de calibre 22. Des lignes veineuses centrales ont été insérées par l'artère jugulaire. Nous avons inséré les lignes veineuses centrales en utilisant l'échographie tout en surveillant attentivement la pression artérielle. L'échographie a montré que l'artère jugulaire était claire et nous avons vérifié que la position légère de Trendelenburg ne modifiait pas la dynamique circulatoire. Dans l'ensemble, la procédure a été menée à bien sans changements significatifs dans l'hémodynamique. Des agents anesthésiques épidurales et rachidiens ont été administrés dans la position latérale droite aux espaces intervertébraux L3-L4 et Th10-Th11, respectivement. Après une infiltration locale de 1 % de mepivacaïne, une ligne épidurale a été insérée avec une aiguille Tuohy de calibre 18. L'espace épidural a été confirmé en utilisant la méthode conventionnelle de perte de résistance. Après un test d'aspiration, un résultat négatif a été obtenu, une dose d'essai de 1 % de mepivacaïne (3 ml) a été administrée par le biais du cathéter. La ponction lombaire a été réalisée avec succès et 5 mg de bupivacaïne hyperbare à 0,5 % et 10 μg de fentanyl ont été administrés par voie intrathécale avec une aiguille épidurale Quincke de calibre 25. Le montant et le type d'agents anesthésiques ont été décidés par les anesthésiologistes et les chirurgiens. L'administration continue de la phénylephrine a été immédiatement commencée à 1 mg/heure pour éviter une hypotension due à l'anesthésie. Cinq millilitres de 0,25 % de ropivacaïne ont été administrés par le biais du cathéter épidural.\n\nAprès confirmation du blocus sensoriel au niveau Th4, l'opération a été commencée. Avant l'accouchement, 0,1 mg de nitroglycérine a été administré pour détendre l'utérus. Le nouveau-né a été livré 4 minutes après le début de la césarienne. Les pressions artérielles veineuse centrale et périphérique ont été maintenues pendant la césarienne. La patiente n'a signalé aucune nausée, douleur ou dyspnée intraopérative. Après l'accouchement, 600 mg d'acétaminophène ont été administrés. Une fois l'opération terminée sans complications, 2 mg de morphine ont été administrés via le cathéter péridural, qui a ensuite été retiré. Les temps d'opération et d'anesthésie étaient respectivement de 49 minutes et 88 minutes. Les volumes de perfusion totale et de perte de sang étaient respectivement de 1050 ml et 1029 ml. Après l'opération, la patiente a été transférée à l'unité de soins intensifs et une hémodialyse a été effectuée. Elle a été transférée au service de gynécologie le jour postopératoire (POD) 5 et a été libérée le POD 10. La fonction cardiaque s'est améliorée après la césarienne. Au moment de la rédaction du présent rapport, la mère et l'enfant allaient bien.",
+        "gold_summary": "Nous avons rencontré un cas dans lequel une césarienne a été réalisée en utilisant une anesthésie rachidienne et épidurale combinée pour une femme enceinte souffrant d'insuffisance rénale et cardiaque chronique. La femme japonaise de 35 ans avait été soumise à une hémodialyse pendant plusieurs années. Les symptômes d'insuffisance cardiaque apparus pendant la grossesse se sont initialement améliorés avec des traitements tels que l'augmentation de l'hémodialyse, mais ont réapparu. Elle a été admise à l'unité de soins intensifs. Le plan initial était de livrer le bébé après quelques semaines, mais la progression de l'insuffisance cardiaque est devenue une préoccupation. Après une conférence clinique entre le personnel, une césarienne avec anesthésie rachidienne et épidurale combinée a été programmée pour 24 semaines, 0 jours de gestation. L'anticoagulant pour dialyse a également été changé de l'héparine au nafamostat en préparation pour la césarienne. La surveillance a été commencée avec des pressions veineuses centrales et radiales avant l'induction de l'anesthésie. Une anesthésie rachidienne et épidurale combinée a été induite et la césarienne a été complétée sans complications. La chirurgie a été initiée sous administration continue de phényléphrine, qui était destinée à éviter l'hypotension due à l'anesthésie. L'état hémodynamique et respiratoire du patient est resté stable après l'opération. Après la césarienne, la morphine a été administrée par voie épidurale et le cathéter épidural a été retiré.\n",
+        "synthetic_summary": {
+            "B1": "Une maman était très malade avec son cœur et ses reins. Elle devait faire un traitement spécial pour aider ses reins. Pendant qu'elle attendait un bébé, son cœur est devenu fatigué. Les docteurs ont essayé de la soigner pour que le bébé reste encore un peu dans son ventre. Mais le cœur de la maman est devenu trop faible. \n\nAlors, les docteurs ont décidé d’aider la maman à avoir son bébé par une opération appelée césarienne. Ils ont donné des médicaments pour que la maman ne sente pas de douleur. L’opération s’est bien passée. La maman et le bébé vont bien après. Les docteurs ont bien pris soin d’eux.",
+            "B2": "**Résumé adapté pour un adolescent de 14 ans**\n\nCette histoire parle d’une femme japonaise de 35 ans qui était enceinte et avait de graves problèmes de reins et de cœur. Avant sa grossesse, elle devait faire une hémodialyse, c’est-à-dire un traitement qui nettoie le sang quand les reins ne fonctionnent plus bien. Pendant sa grossesse, ses problèmes de cœur se sont aggravés, elle avait du mal à respirer et une toux forte. Les médecins ont essayé d’augmenter ses séances d’hémodialyse pour l’aider, mais ses symptômes sont revenus.\n\nElle a dû être admise en soins intensifs, un service spécial pour les malades très graves. Au début, ils voulaient attendre un peu avant de faire naître le bébé, mais comme son cœur s’est encore affaibli, ils ont décidé de faire une césarienne à 24 semaines de grossesse, ce qui est très tôt. Pour préparer cette opération, ils ont changé le médicament utilisé pendant l’hémodialyse pour éviter des problèmes de saignement.\n\nPendant la césarienne, les médecins ont utilisé deux types d’anesthésie, appelés anesthésie rachidienne et épidurale, qui engourdissent le bas du corps pour que la femme ne ressente pas la douleur. Ils ont aussi surveillé de près sa tension artérielle et son cœur grâce à des petits tubes placés dans ses veines et artères. Pour éviter que sa tension baisse trop à cause de l’anesthésie, ils ont donné un médicament appelé phényléphrine.\n\nL’opération s’est bien passée, sans problème. Le bébé est né rapidement et la maman n’a pas eu de douleur ni de difficulté à respirer pendant l’intervention. Après la naissance, elle a reçu un médicament contre la douleur par l’épidurale, puis le tube a été retiré. La maman a continué à être surveillée et a repris l’hémodialyse. Sa fonction cardiaque s’est améliorée après la césarienne. Au moment où ce rapport a été écrit, la maman et son bébé allaient bien.",
+            "B3": "Résumé réécrit pour un public adulte non spécialiste :\n\n**Contexte**  \nNous rapportons le cas d’une femme japonaise de 35 ans, atteinte d’une insuffisance rénale chronique liée à une glomérulonéphrite, qui était sous hémodialyse régulière avant sa grossesse. Pendant sa grossesse, elle a développé une insuffisance cardiaque progressive, caractérisée par une diminution importante de la fonction du ventricule gauche du cœur et une hypertension pulmonaire modérée. Malgré une augmentation de la fréquence des séances d’hémodialyse et des traitements intensifs, son état cardiaque s’est aggravé à 22 semaines de gestation, nécessitant une hospitalisation en unité de soins intensifs.\n\n**Principales observations**  \nÀ 24 semaines de grossesse, devant la dégradation de sa fonction cardiaque et la congestion pulmonaire importante, une équipe multidisciplinaire composée d’obstétriciens, de pédiatres, de cardiologues, d’urologues et d’anesthésistes a décidé de pratiquer une césarienne prématurée. Pour limiter les risques de saignement liés à la dialyse, l’anticoagulant utilisé a été changé de l’héparine au nafamostat, un médicament à action plus courte. Avant l’intervention, la patiente a été équipée de dispositifs de surveillance avancée, notamment des cathéters veineux centraux et artériels, afin de suivre précisément sa pression sanguine et son état circulatoire.\n\n**Intervention anesthésique et chirurgicale**  \nL’anesthésie a été réalisée par une combinaison de techniques rachidienne (injection d’anesthésique dans le liquide entourant la moelle épinière) et épidurale (injection dans l’espace situé autour de la moelle épinière), permettant un contrôle efficace de la douleur tout en maintenant la stabilité hémodynamique. Une perfusion continue de phényléphrine, un médicament qui maintient la pression artérielle, a été administrée pour prévenir une chute de tension liée à l’anesthésie. La césarienne s’est déroulée sans complications majeures, avec un accouchement rapide du nouveau-né quatre minutes après le début de l’intervention. La patiente n’a présenté ni douleur, ni nausée, ni difficulté respiratoire pendant l’opération.\n\n**Prochaines étapes et évolution**  \nAprès la chirurgie, la patiente a reçu un traitement antidouleur par morphine via le cathéter épidural, qui a ensuite été retiré. Elle a été transférée en soins intensifs pour poursuivre l’hémodialyse et la surveillance. Sa fonction cardiaque s’est améliorée après l’accouchement. La mère et l’enfant étaient en bonne santé au moment du suivi, avec une sortie hospitalière au dixième jour postopératoire.\n\n**Conclusion**  \nCe cas illustre la complexité de la prise en charge anesthésique et obstétricale d’une femme enceinte souffrant d’insuffisance rénale chronique et d’insuffisance cardiaque sévère. La coordination étroite entre les différentes spécialités médicales, l’adaptation des traitements dialytiques et le choix d’une anesthésie combinée ont permis une césarienne sécurisée et une amélioration de l’état cardiaque maternel après l’accouchement."
+        }
+    },
+    {
+        "article": "Une femme de 34 ans sans antécédents médicaux ou chirurgicaux a été présentée au service des urgences avec un historique de cinq jours de fatigue, d'intolérance à la chaleur, de transpiration et de palpitations qui s'aggravaient progressivement. Ses symptômes n'avaient pas de variation diurne. La patiente a décrit une fatigue et des palpitations présentes avec une intensité plus modérée au cours des deux dernières années, mais qui n'a jamais été suffisamment gênante pour qu'elle cherche une attention médicale. Après un interrogatoire plus approfondi, la patiente a déclaré avoir perdu cinq kilos de poids involontaire au cours des cinq derniers mois. Elle n'a pas signalé de diarrhée, de symptômes respiratoires ou de douleurs thoraciques. Ses menstruations étaient régulières. La patiente a arrêté de fumer trois mois avant sa présentation et n'a jamais consommé d'alcool. La patiente a nié toute consommation excessive de caféine dans son alimentation.\n\nUn examen physique a révélé une euthermie (36,6 °C), une tachycardie avec une fréquence cardiaque (FC) allant jusqu'à 120 battements par minute (BPM), une tension artérielle élevée (140/100 mmHg), une fréquence respiratoire de 20 respirations par minute, une saturation en oxygène de 99 % en air ambiant et un indice de masse corporelle (IMC) de 23,5 kg/m2. Un examen plus approfondi a révélé un goitre diffus, de fins tremblements bilatéraux sur les mains tendues, une proptose bilatérale, un retard et une rétraction des paupières bilatérales, plus marqués du côté droit. Un électrocardiogramme a montré une tachycardie sinusale (TS) sans changements ischémiques ou signes d'hypertension chronique. Une radiographie thoracique et un échocardiogramme transthoracique au lit n'ont révélé aucune pathologie. Un profil sanguin complet et des tests de la fonction rénale et hépatique n'ont pas révélé de pathologie.\n\nDe nouvelles analyses sanguines ont révélé une thyrotoxicose avec suppression totale de l'hormone stimulant la thyroïde (TSH) (<0,01 mUI/L, plage normale : 0,3-4,2), avec une augmentation de la T3 (17,8 pmol/L, plage normale : 3,7-6,4) et de la T4 (52,5 pmol/L, plage normale : 11-23,3). Son anticorps anti-récepteur de la TSH (TRAB) était positif (16,5 IU/L, seuil de 1,75 IU/L), confirmant ainsi un diagnostic de maladie de Basedow (GBD). La patiente a été informée de la maladie de Basedow et des effets et effets secondaires (en particulier l'agranulocytose) du CBZ. Elle a ensuite commencé à prendre du CBZ 20 mg une fois par jour (OD) et du propranolol 80 mg à libération prolongée (SR) OD avec un suivi ambulatoire pour une répétition du TFT et un ajustement supplémentaire de la dose. Cependant, après quatre semaines, la patiente a revisité le service des urgences avec une histoire de trois jours de palpitations associées à une gêne thoracique et des vertiges. L'examen physique a révélé un ST (HR 137 BPM) et un examen thyroïdien similaire à sa visite initiale. Un panel TFT répété a montré TSH <0,01, T3 : 17,5, et T4 : 64,1. Elle a nié le non-respect du traitement. Le CBZ a été augmenté à 20 mg deux fois par jour (BD), et le propranolol 80 mg SR a été poursuivi. La patiente a été vue à la clinique endocrinienne après deux semaines. Elle s'est toujours plainte de palpitations et d'intolérance à la chaleur ; cependant, le ST s'est stabilisé.\n\nDeux semaines après la visite en clinique, la patiente s'est rendue aux urgences pour la troisième fois avec des palpitations gênantes depuis un jour. L'examen a révélé un ST (HR140 BPM), et son IMC était passé à 24,5 kg/m2. Les TFT ont montré une hyperthyroïdie persistante (TSH <0,01, T3 : 12,1, T4 : 54,1). La patiente a été admise et a reçu du CBZ 20 mg trois fois par jour (TD) et du propranolol 160 mg SR OD sous surveillance. Ses TFT ont été répétés cinq jours plus tard, montrant une hyperthyroïdie persistante avec seulement une amélioration marginale de la T4 (39 pmol/L). La possibilité d'une non-observance du traitement a été discutée lors d'une entrevue détaillée avec la patiente. La patiente a insisté sur le respect strict du traitement. Elle était gênée par des symptômes persistants, sans stress ou dépression sous-jacents, et voulait que les symptômes soient traités. Elle avait pris du poids et avait une réduction de son nombre absolu de neutrophiles, ce qui suggérait une observance du traitement.\n\nEn outre, son TRAB a été réduit de 16,5 à 6,9. Elle a été libérée (sous CBZ 20 mg par voie orale et propranolol 160 mg par voie orale) avec un plan de suivi rapproché.\n\nLors de la visite de suivi après quatre semaines, elle restait hyperthyroïdienne (TSH : 0,01, T3 : 11,1, T4 : 43,9) avec un rythme cardiaque normal. La patiente a été invitée à apporter des bouteilles vides de son médicament pour vérifier son respect du traitement, ce qui a renforcé la possibilité de prendre les médicaments comme prescrit. La malabsorption a été écartée avec un dépistage négatif de la maladie cœliaque (anticorps anti-transglutaminase tissulaire négatifs) et des taux normaux de cyanocobalamine et d'albumine. La GD résistante à la CBZ a été considérée à ce stade et a été transférée à 100 mg de PTU par voie orale, avec 160 mg de propranolol SR OD et 20 mg de prednisolone par jour pendant deux mois avec un régime de réduction progressive. À la visite de suivi de quatre semaines, elle n'avait pas constaté d'amélioration de ses TFT (TSH : <0,01, T3 : 11,3, T4 : 40,1). Après une autre visite de suivi de quatre semaines, ses stéroïdes ont été arrêtés et la dose de PTU a été augmentée à 150 mg par voie orale, en raison de TFT persistants dérangés (TSH : <0,01, T3 : 12, T4 : 40,4). La patiente a eu une réponse partielle à la dose augmentée de PTU avec des TFT répétés après un mois, indiquant TSH <0,01, T3 : 7, T4 : 25,5. La tendance des TFT de la patiente depuis le diagnostic jusqu'à la dernière visite de suivi est représentée graphiquement.\n\nÉtant donné la réponse partielle aux doses croissantes de PTU, la patiente a été référée à l'équipe chirurgicale pour un traitement définitif par thyroïdectomie, évitant ainsi les éventuelles complications hépatotoxiques et hématologiques des doses plus élevées de PTU à long terme. La patiente a bien toléré la thyroïdectomie totale sans aucune complication. Son dernier profil thyroïdien était normal (TSH 3,42) avec une lévothyroxine de substitution à 75 mcg par jour.\n",
+        "gold_summary": "Une femme de 34 ans a présenté une fatigue, une intolérance à la chaleur, une transpiration et des palpitations qui s'aggravaient progressivement depuis 5 jours. Elle a été diagnostiquée avec une GD sur la base de ses tests de fonction thyroïdienne (TFT) et a commencé à prendre du CBZ et du propranolol. Malgré le fait qu'elle ait respecté les doses de CBZ de 20 mg une fois par jour puis deux fois par jour, ses TFT sont restés inchangés pendant 4 mois. Cependant, la patiente a de nouveau consulté les urgences en raison d'une thyrotoxicose persistante et de TFT inchangés. Sa dose a finalement été augmentée à 20 mg trois fois par jour, et l'administration sous surveillance n'a pas amélioré ses TFT. La patiente a finalement été transférée à PTU 150 mg trois fois par jour avec des stéroïdes, avec une amélioration minimale. La patiente a finalement subi une thyroïdectomie pour éviter l'utilisation à long terme de PTU.\n",
+        "synthetic_summary": {
+            "B1": "Une dame avait très chaud, elle était fatiguée et son cœur battait vite. Elle est allée voir le docteur. Le docteur a dit que sa glande dans le cou ne marchait pas bien. \n\nElle a pris des médicaments pour aider. Mais ça n’a pas beaucoup changé. Elle est allée plusieurs fois à l’hôpital. \n\nAlors, le docteur a donné d’autres médicaments. Ça a un peu aidé, mais pas assez. \n\nAprès, elle a eu une petite opération pour enlever la glande. Maintenant, elle va mieux et prend un médicament pour rester en bonne santé.",
+            "B2": "**Ce qu'ils ont trouvé**  \nUne femme de 34 ans est venue aux urgences parce qu'elle se sentait très fatiguée, avait chaud sans raison, transpirait beaucoup et avait des palpitations au cœur depuis cinq jours. Ces symptômes étaient déjà un peu présents depuis deux ans, mais moins forts. Elle avait aussi perdu du poids sans le vouloir. Lors de l’examen, les médecins ont remarqué que sa thyroïde (une glande dans le cou qui contrôle l’énergie du corps) était gonflée, et elle avait des signes typiques d’une maladie appelée maladie de Basedow. Cette maladie fait que la thyroïde produit trop d’hormones, ce qui explique ses symptômes.\n\n**Ce que cela signifie**  \nLes tests sanguins ont confirmé que sa thyroïde fonctionnait trop (on appelle cela une hyperthyroïdie). Elle a commencé un traitement avec un médicament appelé carbimazole (CBZ), qui aide à réduire la production d’hormones thyroïdiennes, et un autre médicament, le propranolol, pour calmer son cœur. Mais même en prenant bien ses médicaments, ses analyses sont restées mauvaises pendant plusieurs mois, et ses symptômes ne s’amélioraient pas.\n\n**Ce qu’ils ont fait ensuite**  \nLes médecins ont augmenté la dose de CBZ, puis ont ajouté des stéroïdes et ont changé le médicament principal pour un autre appelé propylthiouracile (PTU). Malgré cela, l’état de la patiente ne s’est amélioré que très peu. Pour éviter les effets secondaires graves liés à ces médicaments pris longtemps, ils ont décidé de lui enlever complètement la thyroïde par chirurgie (thyroïdectomie).\n\n**Résultat final**  \nAprès l’opération, la patiente a bien récupéré. Elle prend maintenant un médicament appelé lévothyroxine, qui remplace les hormones que sa thyroïde ne produit plus. Ses analyses sont revenues normales et ses symptômes ont disparu.  \n\nEn résumé, cette patiente avait une maladie de Basedow qui ne répondait pas bien aux médicaments habituels. La chirurgie a été la meilleure solution pour elle.",
+            "B3": "**Contexte**  \nUne femme de 34 ans, sans antécédents médicaux notables, s’est présentée aux urgences avec une fatigue progressive, une intolérance à la chaleur, des sueurs et des palpitations depuis cinq jours. Ces symptômes s’étaient déjà manifestés de façon modérée au cours des deux années précédentes, sans qu’elle ne consulte. Elle rapportait également une perte de poids involontaire de cinq kilogrammes sur les cinq derniers mois. L’examen clinique a révélé une tachycardie (jusqu’à 140 battements par minute), une tension artérielle élevée, un goitre diffus, des tremblements des mains, ainsi que des signes oculaires caractéristiques (proptose et rétraction palpébrale). Les analyses sanguines ont confirmé une thyrotoxicose avec une suppression totale de la TSH, une élévation marquée des hormones thyroïdiennes T3 et T4, et la présence d’anticorps anti-récepteurs de la TSH (TRAB), confirmant le diagnostic de maladie de Basedow (ou maladie de Graves).\n\n**Principales Observations**  \nLa patiente a débuté un traitement par carbimazole (CBZ) à faible dose (20 mg une fois par jour) et propranolol pour contrôler les symptômes cardiaques. Malgré une augmentation progressive de la dose de CBZ jusqu’à 60 mg par jour (20 mg trois fois par jour) et une surveillance stricte, ses tests de fonction thyroïdienne (TFT) sont restés anormaux pendant plusieurs mois, témoignant d’une hyperthyroïdie persistante. La patiente a rapporté une bonne observance du traitement, confirmée par des entretiens répétés et la vérification des médicaments. Une malabsorption digestive a été exclue par des tests appropriés. L’ajout de corticostéroïdes (prednisolone) associé au passage au propylthiouracile (PTU) n’a apporté qu’une amélioration marginale des paramètres thyroïdiens.\n\n**Interprétation Clinique**  \nCette présentation correspond à une maladie de Basedow résistante au traitement antithyroïdien classique par carbimazole, une situation rare où la thyroïde reste hyperactive malgré des doses adéquates et une bonne observance. La persistance des symptômes et des anomalies biologiques malgré un traitement intensif impose de considérer des alternatives thérapeutiques pour éviter les complications liées à une hyperthyroïdie prolongée et aux effets secondaires potentiels des médicaments à fortes doses.\n\n**Prochaines Étapes**  \nFace à cette résistance médicamenteuse, la patiente a été orientée vers une prise en charge chirurgicale. Elle a subi une thyroïdectomie totale, intervention qui a été bien tolérée sans complications. Après l’ablation de la thyroïde, elle a bénéficié d’un traitement substitutif par lévothyroxine, permettant une normalisation complète de ses hormones thyroïdiennes. Cette approche a permis de contrôler définitivement sa maladie tout en évitant les risques liés à un traitement antithyroïdien prolongé à fortes doses."
+        }
+    },
+    {
+        "article": "Une Japonaise de 71 ans ayant des antécédents de diabète de type 1, d’insuffisance rénale en phase terminale, de blocus auriculo-ventriculaire complet et d’infarctus antérieur du myocarde a été admise au service de gastroentérologie de notre hôpital pour évaluation et traitement d’une perte de conscience aiguë secondaire à une hypoglycémie. Au moment de son admission, elle portait un stimulateur cardiaque permanent et était en dialyse trois fois par semaine. Le service d’orthopédie a été contacté pour évaluer un gonflement, une chaleur et une rougeur de sa main gauche dus à une morsure au bout de son majeur gauche auto-infligée lors d’un épisode de démence. Un traitement standard par céfazoline intraveineuse (1 g par jour) a été prescrit pour traiter une suspicion de cellulite. L’infection n’a pas répondu et a progressé malgré deux jours complets de traitement antibiotique. Une culture bactérienne de la lésion a révélé une bactérie résistante à la méthicilline (MRSA). Après un examen physique, la patiente a présenté les quatre signes cardinaux de la tendinite du fléchisseur de Kanavel. Une perfusion de vancomycine (valeur minimale, 15-20 µg/mL) a été initiée pour traiter l’infection à MRSA, ainsi qu’un débridement de la plaie et une amputation partielle de l’articulation interphalangienne distale. Une décompression du nerf médian a été réalisée pour soulager la pression résultant d’un abcès purulent. Bien que la rougeur et le gonflement aient persisté après cette procédure, la progression de l’infection a semblé quelque peu réduite. Bien que le traitement antibiotique par vancomycine ait été poursuivi, la patiente s’est soudainement plainte de douleurs abdominales, de sang brun foncé dans les selles indiquant une hémorragie gastro-intestinale, et a développé des signes compatibles avec un choc systémique. Sa tension artérielle systolique initiale était de 60 mmHg, ce qui a réagi à l’administration aiguë de vasopresseurs. Les données de laboratoire comprenaient un nombre élevé de globules blancs (9890/mm3), ainsi qu’une augmentation des taux sériques de protéine C réactive (CRP ; 259,7 mg/L) et de créatinine (421,7 µmol/L) et une réduction des taux de sodium (132 mEq/L), de glucose sanguin (2,6 mmol/L) et d’hémoglobine (8,2 g/dL). Les résultats d’une tomographie par ordinateur (CT) ont abouti à un diagnostic d’ischémie mésentérique non occlusive ; une résection intestinale d’urgence a été effectuée. Des tubes d’alimentation ont été initiés et poursuivis pendant une semaine. La norépinephrine a été ajoutée à son traitement pour maintenir la tension artérielle à des niveaux nécessaires pour soutenir la perfusion des organes avec une pression artérielle moyenne cible de 70.\n\nPendant son séjour à l'hôpital, la patiente a été exposée au SARS-CoV-2 après avoir été en contact étroit prolongé avec une personne infectée pendant une dialyse. Son prélèvement nasal a été positif pour le COVID-19 en utilisant un test d'amplification isotherme induite par boucle. Quatre jours après le test positif, elle a développé des signes de pneumonie aiguë. Les résultats d'une radiographie thoracique et d'une tomodensitométrie ont confirmé ce diagnostic et ont révélé une consolidation des poumons ainsi que des épanchements pleuraux bilatéraux. Un traitement antiviral avec favipiravir (200 mg par voie orale deux fois par jour) a été initié et la patiente a été transférée à l'unité de soins intensifs. Cela était conforme aux recommandations au moment de l'administration. La patiente était hypervolémique avec une demande d'oxygène accrue. Une hémodiafiltration continue a été effectuée pour éviter une surcharge liquidienne.\n\nImmédiatement avant l’exposition au COVID-19, la patiente a développé des signes cliniques de fasciite nécrosante. L’infection s’était étendue au fascia et à la musculature environnante de sa main gauche. Bien qu’une amputation d’urgence de la main ait été jugée nécessaire, la patiente a développé un choc septique et a eu besoin d’une respiration artificielle en raison d’une augmentation soudaine de la demande en oxygène. L’oxygène à haut débit a été administré en continu par le tube endotrachéal, et son traitement antiviral a été changé pour du remdesivir (100 mg intraveineux une fois par jour) avec de l’hydrocortisone intraveineuse (200 mg/dose). Le remdesivir était encore en phase d’utilisation compassionnelle à ce moment-là. Alors qu’elle suivait un traitement pour des événements aigus potentiellement mortels, l’infection a progressé pour inclure les phalanges du troisième doigt gauche, avec une nécrose osseuse visible sur la radiographie. La vancomycine (500 mg) a été prescrite pour gérer l’ostéomyélite et prévenir sa propagation. La patiente a ensuite développé un syndrome de détresse respiratoire aiguë (ARDS). Bien que l’infection COVID-19 de la patiente ait été contrôlée après deux semaines, elle a développé une coagulation intravasculaire disséminée (DIC; score >4) qui a peut-être accéléré la croissance bactérienne. L’héparine étant contre-indiquée dans ce cas, l’ART-123, une forme recombinante et soluble de thrombomoduline alpha, a été administrée par voie intraveineuse (12 800 U une fois par jour pendant 3 jours) pour dissoudre les caillots systémiques. L’infection a progressé pour inclure la nécrose de l’ensemble du troisième doigt ainsi que la peau, le fascia et la musculature jusqu’à l’articulation radio-carpienne avec des signes d’invasion progressive dans l’avant-bras. Malheureusement, les restrictions et les fermetures d’hôpitaux liées à la COVID ont empêché tout traitement chirurgical supplémentaire à ce moment-là.\n\nLe patient a finalement récupéré de COVID-19. Deux semaines après le diagnostic initial, le patient a été sevré de la ventilation mécanique et le tube endotrachéal a été retiré. Deux semaines après l'extubation, le patient a terminé le traitement pour COVID-19 et a eu un test négatif pour l'antigène SARS-CoV-2. Une amputation majeure au tiers distal de l'avant-bras a ensuite été réalisée. Les tissus ont été débridés et lavés complètement pendant la procédure et tous les tissus infectés ont été enlevés. Étant donné que le site de l'amputation était proximal à sa sonde d'hémodialyse, son remplacement a été discuté avec des chirurgiens vasculaires et des néphrologues. La procédure a révélé une calcification importante des artères de son avant-bras gauche avec tortuosité et éventuelles occlusions, tant proximales que distales à la sonde. Le bruit et le frisson détectés dans la sonde ont également suggéré la possibilité d'un syndrome ischémique hypoperfusif distal. Une couverture adéquate du lambeau de peau a été obtenue et la souche a été fermée ; une étude radiographique de suivi n'a révélé aucune complication. La souche a semblé guérir bien, un mois plus tard, la patiente a succombé à un choc septique et à un arrêt cardiopulmonaire.\n",
+        "gold_summary": "Une femme de 71 ans a présenté une infection non contrôlée suite à une blessure auto-infligée au moyen de son index gauche. Une culture bactérienne de la lésion a révélé la présence de Staphylococcus aureus résistant à la méthicilline (MRSA). L'infection n'a pas pu être contrôlée par des antibiotiques ou des interventions supplémentaires, y compris un débridement et une amputation mineure. Elle a contracté une COVID-19 sévère à l'hôpital, ce qui a limité les options de traitement disponibles. Dans une tentative de contrôle de l'infection, la patiente a finalement subi une amputation majeure de l'avant-bras gauche distal. En se rétablissant de la procédure, la patiente a succombé à un choc septique et à un arrêt cardiopulmonaire.\n",
+        "synthetic_summary": {
+            "B1": "Une dame de 71 ans s’est fait très mal à la main gauche. Une vilaine bactérie est entrée dans sa blessure. Les médicaments n’ont pas réussi à guérir sa main. Elle a dû se faire couper un petit bout de doigt. Puis, elle a attrapé un gros rhume appelé COVID à l’hôpital. Ce rhume a rendu son corps très faible. Les docteurs ont dû couper une grande partie de son bras pour arrêter la maladie. Même après cela, elle est restée très malade. Elle est partie au ciel à cause de son corps trop fatigué.",
+            "B2": "Une femme japonaise de 71 ans, ayant plusieurs problèmes de santé comme le diabète et des problèmes rénaux, s’est blessée toute seule au bout de son doigt gauche. Cette blessure est devenue infectée par une bactérie appelée Staphylococcus aureus résistante à certains antibiotiques (on l’appelle MRSA). Malgré plusieurs traitements avec des antibiotiques et des opérations pour enlever les tissus malades, l’infection a continué à s’aggraver.\n\nPendant son séjour à l’hôpital, elle a aussi attrapé la COVID-19, une maladie qui a compliqué son état et limité les traitements possibles. L’infection dans sa main s’est étendue, obligeant les médecins à lui amputer une grande partie de son avant-bras gauche pour essayer de stopper la maladie.\n\nMalheureusement, même après cette opération, la patiente a développé un choc septique, une réaction grave du corps à l’infection, qui a provoqué un arrêt du cœur et des poumons. Elle est décédée malgré tous les soins reçus. Cette histoire montre à quel point certaines infections peuvent être difficiles à traiter, surtout quand elles surviennent chez des personnes déjà fragiles.",
+            "B3": "Résumé détaillé et structuré pour un public non médical éduqué\n\nContexte  \nUne femme japonaise de 71 ans, présentant plusieurs problèmes de santé chroniques graves, dont un diabète de type 1, une insuffisance rénale terminale nécessitant une dialyse régulière, un bloc cardiaque complet avec stimulateur cardiaque, et des antécédents d’infarctus du myocarde, a été hospitalisée pour une perte de conscience due à une hypoglycémie (baisse importante du taux de sucre dans le sang). Lors de son admission, elle présentait une infection de la main gauche causée par une morsure auto-infligée sur le bout de son majeur gauche, survenue pendant un épisode de confusion mentale.\n\nPrincipales observations  \nL’infection initiale, suspectée comme une cellulite (infection cutanée), a été traitée par un antibiotique standard (céfazoline), mais a rapidement progressé malgré ce traitement. Une analyse bactérienne a identifié un Staphylococcus aureus résistant à la méthicilline (MRSA), une bactérie difficile à traiter. La patiente a alors reçu un traitement antibiotique adapté (vancomycine), accompagné d’un débridement (nettoyage chirurgical) de la plaie et d’une amputation partielle de l’articulation du majeur. Une intervention chirurgicale supplémentaire a été nécessaire pour soulager la pression causée par un abcès purulent (accumulation de pus) comprimant un nerf important de la main.\n\nMalgré ces mesures, l’infection s’est étendue, provoquant une fasciite nécrosante, une infection grave qui détruit les tissus mous, incluant le fascia (membrane entourant les muscles) et les muscles de la main. Une amputation d’urgence de la main a été envisagée, mais la patiente a développé un choc septique (réaction inflammatoire sévère à l’infection) et une insuffisance respiratoire nécessitant une assistance ventilatoire. Parallèlement, elle a contracté une pneumonie sévère liée au COVID-19, confirmée par des examens radiologiques et un test positif au SARS-CoV-2, compliquant davantage sa prise en charge.\n\nLe traitement antiviral a été adapté en fonction de l’évolution, passant du favipiravir au remdesivir, associé à des corticostéroïdes pour réduire l’inflammation pulmonaire. La patiente a également développé un syndrome de détresse respiratoire aiguë (ARDS), une complication grave du COVID-19, ainsi qu’une coagulation intravasculaire disséminée (DIC), un trouble de la coagulation sanguine favorisant la formation de caillots dans les vaisseaux, ce qui a pu aggraver la progression bactérienne. Un traitement anticoagulant spécifique (ART-123) a été administré pour dissoudre ces caillots.\n\nL’infection s’est étendue jusqu’à l’avant-bras, avec une nécrose osseuse visible au niveau du troisième doigt gauche. En raison des restrictions liées à la pandémie, les interventions chirurgicales supplémentaires ont été retardées. Après la guérison de l’infection COVID-19, la patiente a finalement subi une amputation majeure au tiers distal de l’avant-bras gauche, avec un débridement complet des tissus infectés. L’examen chirurgical a révélé une calcification importante et des anomalies vasculaires dans l’avant-bras, compliquant la circulation sanguine locale.\n\nInterprétation clinique  \nCette patiente a présenté une infection bactérienne sévère et résistante, compliquée par des facteurs de risque majeurs tels que le diabète, l’insuffisance rénale et une immunodépression liée à la COVID-19. L’infection initiale, mal contrôlée, a évolué vers une fasciite nécrosante et une ostéomyélite (infection osseuse), nécessitant des amputations successives. La survenue d’une pneumonie COVID-19 sévère a limité les options thérapeutiques et retardé les interventions chirurgicales, aggravant la progression de l’infection. La coagulation intravasculaire disséminée a également contribué à la gravité de la situation.\n\nProchaines étapes et issue  \nMalgré un traitement antibiotique adapté, des interventions chirurgicales multiples et une prise en charge intensive incluant la ventilation mécanique et les traitements antiviraux, la patiente a finalement succombé à un choc septique et à un arrêt cardiopulmonaire environ un mois après l’amputation majeure. Ce cas illustre la complexité de la prise en charge des infections sévères chez des patients fragiles, particulièrement en contexte de pandémie, où les ressources et les interventions peuvent être limitées."
+        }
+    },
+    {
+        "article": "C’est le cas d’une femme de 36 ans de la région d’Oromia, zone d’Arsi occidentale, qui présentait une toux, une dysphonie et un ronflement depuis 6 mois, ainsi qu’une perte de poids importante mais non quantifiée, une fatigue et une fièvre modérée et intermittente, pour lesquels elle avait consulté différents établissements de santé sans amélioration notable de ses symptômes. Elle souffrait de diabète depuis 5 ans et prenait de la metformine 500 mg deux fois par jour avec un contrôle glycémique médiocre. Les résultats de l’examen physique à la présentation, y compris l’examen de la gorge, étaient anodins. Le taux de sucre dans le sang au hasard était de 300 mg/dl au moment de la présentation (élevé). La laryngoscopie a révélé une tumeur irrégulière sur le tiers antérieur du cordon vocal bilatéralement, impliquant la commissure antérieure. Le résultat de la biopsie a révélé des granulés actinomycosiques avec formation d’abcès. La patiente a ensuite été traitée par pénicilline G (pendant 1 mois), avec la résolution de ses symptômes au cours du suivi, puis par amoxicilline pendant les 6 mois suivants, qui a été arrêtée lorsqu’elle a été complètement rétablie de ses symptômes et que la masse a été éliminée lors du suivi laryngoscopique.\n\nLors de l'enquête, la formule sanguine complète, le taux de sédimentation érythrocytaire, les tests de la fonction rénale et les tests de la fonction hépatique étaient tous dans les limites normales. Les tests sérologiques pour le virus de l'immunodéficience humaine (VIH), l'antigène de surface de l'hépatite B (HbsAg) et l'ARN du virus de l'hépatite C (ARN HCV) ont révélé des résultats négatifs. Son taux de sucre dans le sang au hasard était de 300 mg/dl, ce qui est élevé, et son contrôle glycémique était également médiocre sur le tableau de suivi.\n\nSon examen d'oto-rhino-laryngologie était sans particularité, mais une laryngoscopie souple a révélé une masse irrégulière dans le tiers antérieur du cordon vocal des deux côtés, avec une atteinte de la commissure antérieure.\n",
+        "gold_summary": "Il s'agissait d'une femme de 36 ans de la région d'Oromia, dans la zone d'Arsi occidentale, qui présentait une toux, une dysphonie et un ronflement depuis 6 mois, ainsi qu'une perte de poids importante mais non quantifiée, une fatigue et une fièvre modérée et intermittente, pour laquelle elle avait consulté plusieurs établissements de santé sans amélioration notable de ses symptômes. Elle souffrait de diabète depuis 5 ans et prenait de la metformine 500 mg deux fois par jour avec un contrôle glycémique médiocre. Les résultats de l'examen physique à la présentation, y compris l'examen de la gorge, étaient anodins. Le taux de sucre dans le sang au hasard était de 300 mg/dl au moment de la présentation (élevé). La laryngoscopie a révélé une tumeur irrégulière sur le tiers antérieur du cordon vocal bilatéralement, impliquant la commissure antérieure. Le résultat de la biopsie a révélé des granulés actinomycosiques avec formation d'abcès. La patiente a ensuite commencé à prendre de la pénicilline G, et ses symptômes ont disparu au cours du suivi, puis elle a pris de l'amoxicilline pendant les 6 mois suivants, qui a été arrêtée lorsqu'elle a complètement récupéré de ses symptômes et que la masse a été éliminée lors du suivi laryngoscopique.\n",
+        "synthetic_summary": {
+            "B1": "Il y avait une dame qui toussait beaucoup depuis longtemps. Elle avait aussi mal à la gorge et elle était très fatiguée.\n\nElle avait du sucre dans le sang qui était trop haut. Cela la rendait malade.\n\nLe docteur a regardé sa gorge avec un petit appareil. Il a vu une petite boule qui ne devait pas être là.\n\nLe docteur a donné des médicaments pour faire partir la boule. La dame a pris ces médicaments longtemps.\n\nPetit à petit, la dame est allée mieux. La boule est partie et elle n’avait plus mal.",
+            "B2": "**Ce qu’ils ont observé chez la patiente**  \nUne femme de 36 ans de la région d’Oromia avait une toux, une voix enrouée (dysphonie) et un ronflement depuis six mois. Elle avait aussi perdu beaucoup de poids, se sentait fatiguée et avait de la fièvre qui revenait par moments. Malgré plusieurs visites chez le médecin, ses symptômes ne s’amélioraient pas. Elle souffrait de diabète depuis cinq ans et prenait un médicament appelé metformine, mais son taux de sucre dans le sang restait élevé (300 mg/dl), ce qui n’était pas bien contrôlé.\n\n**Ce qu’ils ont découvert lors des examens**  \nL’examen général et celui de sa gorge ne montraient rien d’anormal. Cependant, une laryngoscopie — c’est un examen où on regarde l’intérieur de la gorge avec une petite caméra — a montré une tumeur irrégulière sur la partie avant de ses cordes vocales, des deux côtés. Pour comprendre ce que c’était, les médecins ont fait une biopsie, c’est-à-dire qu’ils ont prélevé un petit morceau de cette tumeur pour l’analyser. Ils ont trouvé des granulés actinomycosiques, ce qui signifie qu’il y avait une infection causée par une bactérie appelée Actinomyces, et aussi la formation d’un abcès, une sorte de poche de pus.\n\n**Le traitement et le résultat**  \nLa patiente a reçu un traitement avec un antibiotique appelé pénicilline G pendant un mois. Ses symptômes ont alors commencé à disparaître. Ensuite, elle a continué avec un autre antibiotique, l’amoxicilline, pendant six mois. Après ce traitement, elle s’est complètement rétablie : ses symptômes ont disparu et la masse dans sa gorge a disparu aussi, comme l’a montré le suivi avec la laryngoscopie.\n\n**Ce que cela signifie**  \nCette histoire montre qu’une tumeur dans la gorge n’est pas toujours un cancer. Parfois, c’est une infection rare mais grave qui peut ressembler à une tumeur. Un bon diagnostic avec une biopsie est important pour choisir le bon traitement. De plus, un diabète mal contrôlé peut rendre les infections plus difficiles à guérir. Grâce à un traitement antibiotique adapté, cette patiente a pu guérir complètement.",
+            "B3": "**Contexte**  \nUne femme de 36 ans, originaire de la région d’Oromia (zone d’Arsi occidentale), a présenté pendant six mois une toux persistante, une dysphonie (modification de la voix) et un ronflement. Elle souffrait également d’une perte de poids importante (non quantifiée), d’une fatigue marquée et de fièvres modérées intermittentes. Malgré plusieurs consultations dans différents établissements de santé, ses symptômes ne s’étaient pas améliorés. Par ailleurs, elle était diabétique depuis cinq ans, traitée par metformine 500 mg deux fois par jour, mais avec un contrôle insuffisant de sa glycémie.\n\n**Principales Observations**  \nÀ l’examen physique initial, y compris l’inspection de la gorge, aucun signe anormal n’a été détecté. Cependant, une mesure aléatoire de la glycémie sanguine a révélé un taux élevé de 300 mg/dl. L’examen spécialisé par laryngoscopie souple a mis en évidence une masse irrégulière située sur le tiers antérieur des deux cordes vocales, avec atteinte de la commissure antérieure (zone où les deux cordes vocales se rejoignent). Une biopsie de cette masse a montré la présence de granulomes actinomycosiques, c’est-à-dire des amas de bactéries du genre Actinomyces, associés à la formation d’un abcès (collection de pus).\n\nLes analyses sanguines complémentaires, comprenant la formule sanguine complète, le taux de sédimentation érythrocytaire (marqueur d’inflammation), ainsi que les fonctions rénale et hépatique, étaient normales. Les tests sérologiques pour le VIH, l’hépatite B et l’hépatite C étaient négatifs.\n\n**Interprétation Clinique**  \nLe diagnostic retenu était une actinomycose laryngée, une infection bactérienne rare qui peut former des masses inflammatoires ressemblant à des tumeurs. Cette infection était probablement favorisée par le diabète mal contrôlé de la patiente, qui affaiblit le système immunitaire. La localisation bilatérale sur les cordes vocales et la présence d’un abcès expliquaient les symptômes de toux, de modification de la voix et de ronflement.\n\n**Prochaines Étapes et Évolution**  \nLa patiente a été traitée initialement par injection intraveineuse de pénicilline G pendant un mois, ce qui a permis une nette amélioration clinique. Par la suite, un traitement oral par amoxicilline a été poursuivi pendant six mois. Ce traitement prolongé est nécessaire pour éradiquer complètement l’infection. Lors du suivi, la patiente a retrouvé une santé normale, ses symptômes ont disparu et la masse laryngée a complètement disparu à la laryngoscopie de contrôle. Le traitement antibiotique a alors été arrêté.  \n\nCe cas illustre l’importance de considérer une infection bactérienne rare comme cause de masse laryngée, surtout chez les patients diabétiques, et la nécessité d’un traitement antibiotique prolongé pour obtenir une guérison complète."
+        }
+    },
+    {
+        "article": "Nous présentons un nouveau-né âgé de cinq jours admis à l'unité de soins intensifs néonatals avec une plainte d'absence de l'orifice anal. Le bébé n'a pas passé de méconium pendant 48 heures depuis la naissance et plus tard, les familles ont remarqué que le méconium passait par l'orifice urétral avec l'urine. Après une évaluation plus approfondie, ils ont constaté qu'il n'y avait pas de l'ouverture anale en dehors d'une légère fosse sur la zone qui était supposée être une ouverture anale. En outre, le nouveau-né avait un gonflement abdominal qui a progressivement augmenté depuis la naissance. Sinon, le nouveau-né n'avait pas de fièvre, une décoloration jaunâtre de la peau et des yeux, des vomissements et des mouvements corporels anormaux.\n\nLe bébé est né d'une mère para-quatre de 32 ans qui ne se souvient pas de sa dernière période menstruelle normale mais qui prétend être aménorrhéique depuis neuf mois. La mère a bénéficié de soins prénataux au centre de santé voisin et tout s'est bien passé. Elle a accouché au centre de santé voisin par accouchement vaginal spontané après avoir travaillé pendant 14 heures et le poids de naissance était de 3,2 kg. Le nouveau-né a pleuré immédiatement après la naissance avec des scores APGAR de 7 et 10 à la 1re et à la 10e minutes, respectivement. La mère n'a pas de maladies chroniques comme l'hypertension et le diabète sucré. Ses enfants précédents sont tous en bonne santé et vivants.\n\nL'examen physique a révélé une apparence générale alerte et des signes vitaux suivants : pouls = 152 battements par minute, respiration = 46 respirations par minute, température = 36 °C et saturation en oxygène veineux = 97 % dans l'air ambiant. L'examen de la tête a révélé une circonférence de 42 cm et une fontanelle antérieure de 2 cm. Les résultats physiques positifs pertinents ont été observés dans l'abdomen et le système génito-urinaire. L'abdomen était très distendu et il n'y avait pas d'ouverture anale autre qu'une fossette sur la région sacrococcygienne. L'examen du système génito-urinaire a révélé des organes génitaux externes féminins à l'inspection, avec des grandes lèvres bien développées et aucune fusion. Cependant, à la palpation, les petites lèvres étaient entièrement fusionnées à la base du clitoris et il n'y avait pas de vagin. Le phallus mesurait environ 0,8 cm avec une ouverture centrale par laquelle des selles liquides s'écoulait en pleurant. L'ouverture urétrale est une voie commune pour les voies urinaires, génitales et rectales. Il n'y a pas de gonades palpables dans les plis labio-scrotal et dans la région inguinale.\n\nDes tests de laboratoire et des images ont été réalisés pour explorer les résultats. Le compte total de globules blancs = 20 000, neutrophiles = 53 %, lymphocytes = 23 %, globules rouges = 5*106, hémoglobine = 15 g/dl, plaquettes = 272*103, le groupe sanguin était A+, et la glycémie aléatoire était de 120 g/dl. Une radiographie abdominale a été réalisée et elle a montré l'absence d'ombre d'air dans le gros intestin distal. L'échographie abdomino-pelvienne a été réalisée pour révéler les structures de Müller et l'état de l'intestin distal. Cependant, elle a seulement montré un rein surnuméraire unilatéral (côté gauche), un se trouvant dans la fosse rénale et l'autre se trouvant caudale sur le muscle psoas gauche, ayant tous deux des capsules distinctes et un apport sanguin avec un seul rein normal contralatéral. L'échographie n'a pas commenté les structures de Müller en raison de la vessie effondrée étant incapable de visualiser les structures.\n\nLa patiente a été admise avec un diagnostic de terme + Poids normal à la naissance + Approprié pour l'âge gestationnel + Anomalie du cloaque + Genitalia ambiguë + Rein surnuméraire + Sepsis néonatal précoce. Le nouveau-né a été géré avec des fluides de maintien calculés et des antibiotiques intraveineux, ampicillin 150 mg/kg/dose Iv deux fois par jour (BID) et gentamicine 3 mg/kg/dose iv quotidiennement. Le deuxième jour de l'admission, le bébé a été référé à l'hôpital spécialisé Black Lion pour une meilleure évaluation et gestion.\n",
+        "gold_summary": "Nous présentons un nouveau-né de cinq jours admis à l'unité de soins intensifs néonatals avec une plainte d'absence de l'orifice anal. Le bébé n'avait pas passé de méconium dans les 48 heures suivant l'accouchement, mais les familles ont ensuite réalisé que le méconium avait traversé l'orifice urétral avec l'urine. L'enfant est né d'une femme para-quatre de 32 ans qui prétend avoir été aménorrhéique au cours des neuf derniers mois, mais ne se souvenait pas de ses dernières règles régulières. À l'examen physique, l'abdomen était grossièrement distendu, et il n'y avait pas d'ouverture anale autre qu'une fossette sur la région sacrococcygienne, et les organes génitaux externes semblent féminins à l'inspection avec des grandes lèvres bien développées et aucune fusion.\n",
+        "synthetic_summary": {
+            "B1": "Un bébé de cinq jours est venu à l'hôpital. Il n'avait pas de petit trou pour faire caca. Sa famille a vu que le caca sortait avec la pipi. Le ventre du bébé était gros et dur. Le bébé a des parties du corps qui ressemblent à celles des filles. Mais il n'y avait pas de vrai trou pour faire caca. Les docteurs vont aider le bébé pour qu'il aille mieux.",
+            "B2": "Voici un résumé simple et clair pour un élève de 14 ans :\n\nUn bébé de cinq jours a été amené à l'hôpital parce qu'il n'avait pas d'ouverture pour l'anus, c’est-à-dire qu’il n’avait pas de trou normal pour évacuer les selles. Le bébé n’avait pas fait de méconium, qui est la première selle d’un nouveau-né, pendant les deux premiers jours. Plus tard, la famille a remarqué que les selles sortaient avec l’urine, par un autre orifice. \n\nLa maman, âgée de 32 ans, avait déjà eu quatre enfants et disait ne pas avoir eu ses règles pendant environ neuf mois avant la naissance. Lors de l’examen, le ventre du bébé était très gonflé. On a vu qu’il n’y avait pas de vrai trou pour l’anus, juste une petite dépression à l’endroit où il devrait être. Les organes génitaux semblaient être des organes féminins à première vue, avec des grandes lèvres bien formées, mais il y avait des particularités à l’intérieur, comme une fusion des petites lèvres et l’absence du vagin. \n\nCe cas est complexe car le bébé a une malformation appelée « anomalie du cloaque », où les voies urinaires, génitales et digestives sont mélangées. Le bébé a aussi un rein supplémentaire sur un côté. Il a reçu des soins avec des liquides et des antibiotiques, puis a été transféré dans un hôpital spécialisé pour des examens et un traitement plus approfondis.",
+            "B3": "Résumé détaillé et structuré\n\nContexte  \nNous rapportons le cas d’un nouveau-né âgé de cinq jours admis en unité de soins intensifs néonatals pour une malformation congénitale caractérisée par l’absence d’orifice anal visible. Le bébé n’a pas évacué de méconium (premières selles du nouveau-né) dans les 48 heures suivant la naissance. Par la suite, les parents ont observé que le méconium s’écoulait avec l’urine par l’orifice urétral, suggérant une anomalie des voies excrétrices.\n\nPrincipales observations  \nLa mère, âgée de 32 ans et ayant eu quatre enfants auparavant en bonne santé, rapporte une aménorrhée (absence de règles) de neuf mois, sans se souvenir de la date précise de ses dernières règles. La grossesse a été suivie de manière régulière, et l’accouchement s’est déroulé par voie basse avec un poids de naissance normal (3,2 kg). Le nouveau-né a présenté un score APGAR satisfaisant à la première et à la dixième minute.\n\nÀ l’examen clinique, l’enfant était alerte, avec des signes vitaux normaux pour son âge. L’abdomen était très distendu, sans ouverture anale visible, seulement une fossette au niveau sacrococcygien. L’inspection des organes génitaux externes montrait des caractéristiques féminines, notamment des grandes lèvres bien développées sans fusion apparente. Cependant, à la palpation, les petites lèvres étaient fusionnées à la base du clitoris, et aucune ouverture vaginale n’était détectée. Le phallus mesurait environ 0,8 cm et présentait une ouverture centrale par laquelle s’écoulait des selles liquides, indiquant une communication anormale entre les voies digestives, urinaires et génitales (anomalie du cloaque). Aucune gonade n’était palpable dans les plis labio-scrotaux ni en région inguinale.\n\nLes examens complémentaires ont révélé un taux élevé de globules blancs (20 000/mm³), suggérant une infection néonatale précoce. La radiographie abdominale a montré une absence d’air dans le gros intestin distal, compatible avec une obstruction ou une malformation. L’échographie abdomino-pelvienne a mis en évidence un rein surnuméraire gauche, avec deux reins distincts et vascularisés, mais n’a pas permis de visualiser clairement les structures génitales internes en raison d’une vessie effondrée.\n\nInterprétation clinique  \nLe diagnostic principal retenu est une anomalie complexe du cloaque, caractérisée par l’absence d’orifice anal, une fusion partielle des organes génitaux externes féminins et une communication anormale entre les voies urinaires, génitales et digestives. Cette malformation est associée à un rein surnuméraire et à un sepsis néonatal précoce, nécessitant une prise en charge urgente.\n\nProchaines étapes  \nLe nouveau-né a été traité initialement par des perfusions de maintien et une antibiothérapie intraveineuse combinant ampicilline et gentamicine pour contrôler l’infection. En raison de la complexité de la malformation et des besoins en soins spécialisés, l’enfant a été transféré au deuxième jour d’hospitalisation vers un centre hospitalier de référence (hôpital Black Lion) pour une évaluation approfondie et une prise en charge chirurgicale adaptée."
+        }
+    },
+    {
+        "article": "Ce patient était un homme blanc de 73 ans, hypertendu, qui a été admis en unité de soins intensifs avec une insuffisance respiratoire aiguë due à la COVID-19. Peu après son admission, il a été intubé orotrachéalement et placé en position couchée sur le dos pour améliorer l'hypoxie due au syndrome respiratoire aigu sévère (SRAS). Au troisième jour de son admission, il a développé une oligurie, une azotémie et une surcharge de volume. Le service de néphrologie a été activé pour effectuer un accès veineux profond pour la TSR. Le patient ne pouvait pas être placé en position couchée sur le dos en raison d'une hypoxémie importante. Un cathéter de dialyse de longue durée a été inséré dans la veine poplitée gauche. Il a été soumis à une hémodialyse intermittente conventionnelle quotidienne pendant 8 jours. Le flux sanguin pendant les séances est resté entre 300 et 400 ml/min. En raison de la gravité du tableau clinique, le patient a fini par décéder des suites d'une insuffisance respiratoire au 11e jour. Ce rapport de cas décrit une situation difficile pour obtenir un accès vasculaire en traitant des patients atteints de COVID-19 en position couchée sur le dos. Aspects techniques La veine poplitée gauche a été évaluée par ultrasons. Nous avons utilisé des coupes transversales et longitudinales pour éviter toute valve, en faisant attention à ne pas blesser le nerf tibial superficiel ou l'artère poplitée, la structure la plus profonde de la fosse poplitée. La veine poplitée a été perforée avec une aiguille 18GA x 7 cm, et un guide-fil de 0,035 pouces a été inséré sans aucune résistance. Une incision a été faite dans la peau au-dessus du fil, la veine a été dilatée et le permcath de 50 cm a été inséré par le néphrologue interventionnel, à l'aide d'un introducteur divisible 16F. Le brassard a été suturé sur le tissu sous-cutané. Les voies artérielle et veineuse ont été testées et salinisées avec succès. Une hémodialyse intermittente conventionnelle a été initiée sans difficulté.\n",
+        "gold_summary": "Le patient était un homme de 73 ans qui était venu initialement dans notre service avec une insuffisance respiratoire aiguë secondaire à la COVID-19. Peu après son admission, il a été intubé orotrachéalement et mis en position couchée pour améliorer l'hypoxie due au syndrome respiratoire aigu sévère (SARS). Au troisième jour de son admission, il a développé une lésion rénale aiguë oligurique et une surcharge de volume. Le service de néphrologie a été sollicité pour effectuer un accès veineux profond pour une thérapie de remplacement rénal (TRS). Le patient ne pouvait pas être mis en position couchée en raison d'une hypoxémie importante. Un Permcath de 50 cm (MAHURKARTM, Covidien, Massachusetts, États-Unis) a été inséré dans la veine poplitée gauche.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 73 ans était très malade à cause du virus COVID-19. Il avait du mal à bien respirer. Les docteurs l'ont aidé avec un tuyau pour qu'il puisse mieux respirer.\n\nAprès quelques jours, ses reins ont commencé à moins bien marcher. Les docteurs ont dû l'aider à nettoyer son sang. Mais il ne pouvait pas rester allongé sur le dos comme d'habitude.\n\nAlors, les docteurs ont mis un petit tuyau spécial dans une veine derrière son genou. Ce tuyau a aidé à faire le travail des reins.",
+            "B2": "Ce patient était un homme de 73 ans qui est arrivé à l'hôpital avec de graves problèmes pour respirer à cause de la COVID-19. Très vite, il a dû être intubé, c’est-à-dire qu’un tube a été placé dans sa gorge pour l’aider à respirer. Il a été couché sur le dos pour améliorer l’oxygène dans son sang, car il souffrait d’un syndrome respiratoire aigu sévère.\n\nAu troisième jour, ses reins ont commencé à mal fonctionner, ce qui a causé une baisse de la quantité d’urine et une accumulation de liquide dans son corps. Pour l’aider, les médecins spécialistes des reins (néphrologues) ont dû mettre en place un accès spécial dans une grosse veine pour faire une dialyse. La dialyse est un traitement qui remplace le travail des reins en filtrant le sang.\n\nCependant, le patient ne pouvait pas être couché sur le dos à cause de son manque d’oxygène. Les médecins ont donc choisi une veine située derrière le genou, appelée veine poplitée, pour insérer un cathéter long (un tube fin) de 50 cm. Ce cathéter a permis de faire la dialyse quotidienne sans problème. Malheureusement, malgré ces soins, le patient est décédé au 11e jour à cause de son insuffisance respiratoire. \n\nCe cas montre qu’il peut être difficile de trouver un bon endroit pour mettre un cathéter chez des patients très malades de la COVID-19, surtout quand ils ne peuvent pas rester couchés sur le dos.",
+            "B3": "Résumé destiné à un public adulte non spécialiste :\n\nContexte  \nUn homme blanc de 73 ans, souffrant d’hypertension artérielle, a été admis en unité de soins intensifs en raison d’une insuffisance respiratoire aiguë causée par une infection au virus SARS-CoV-2 (COVID-19). Peu après son arrivée, il a été intubé (un tube a été placé dans sa trachée pour l’aider à respirer) et positionné sur le dos afin d’améliorer son oxygénation, qui était gravement altérée par un syndrome respiratoire aigu sévère.\n\nPrincipales observations  \nAu troisième jour d’hospitalisation, le patient a présenté une diminution importante de la production d’urine (oligurie), une accumulation de déchets azotés dans le sang (azotémie) et un excès de liquide dans l’organisme (surcharge volémique), signes d’une insuffisance rénale aiguë. Le service de néphrologie a été consulté pour mettre en place une thérapie de remplacement rénal (TRR), une procédure qui remplace temporairement la fonction des reins. Cependant, en raison de son état respiratoire très fragile, il n’était pas possible de le positionner sur le dos pour réaliser un accès veineux central classique.\n\nIntervention technique  \nPour contourner cette difficulté, les médecins ont choisi d’insérer un cathéter de dialyse long (Permcath de 50 cm) dans la veine poplitée gauche, située derrière le genou. Cette veine a été soigneusement examinée par échographie pour éviter d’endommager les structures nerveuses et artérielles avoisinantes. L’insertion du cathéter a été réalisée sous guidage échographique, en utilisant une aiguille fine et un fil guide, puis le cathéter a été placé avec succès et fixé sous la peau. Les voies sanguines du cathéter ont été testées et nettoyées avec du sérum physiologique, permettant ainsi de débuter une hémodialyse intermittente quotidienne sans complication.\n\nÉvolution et conclusion  \nMalgré ces mesures, l’état du patient s’est aggravé, et il est décédé au onzième jour d’hospitalisation des suites de son insuffisance respiratoire. Ce cas illustre la complexité de la prise en charge des patients atteints de COVID-19 sévère, notamment les difficultés techniques liées à la mise en place d’un accès vasculaire pour la dialyse lorsque la position couchée sur le dos est impossible en raison d’une hypoxémie sévère. L’utilisation de la veine poplitée comme site d’accès veineux profond peut constituer une alternative viable dans ces situations exceptionnelles."
+        }
+    },
+    {
+        "article": "Homme, fils d'une mère de 28 ans au moment de la naissance et d'un père de 34 ans. Pas de consanguinité, pas d'antécédents familiaux, né de deuxième grossesse, contrôlée, de cours normal. Sérologies : toxoplasme, virus de l'immunodéficience humaine et HBsAg négatifs, et rubéole immunitaire. Dépistage combiné du premier trimestre à risque faible. Échographies prénatales normales. Pas de contact ou d'ingestion connue de toxiques et/ou de tératogènes. Accouchement eutopique à 40 semaines. Apgar : 9/10. Poids à la naissance : 3 780 g (p50-90, graphiques Fenton). Longueur : 52 cm (p50-90). Périmètre crânien : 37 cm (p90). Examen néonatal décrit comme normal. Dépistages néonataux métabolique et auditif sans altérations.\n\nIl était suivi par une neuropédiatre pour retard psychomoteur dans son évolution : marche autonome à 18 mois et retard de langage. Il a suivi un programme de prise en charge précoce à partir de la deuxième année de vie, avec des soutiens scolaires (audition et langage + pédagogie thérapeutique) dès le début de l'école maternelle et une adaptation du programme scolaire dès l'école primaire. Quotient intellectuel à 6 ans : 68. Il suit actuellement une formation fonctionnelle. Autres problèmes de santé : exotropie alternante décompensée en attente de chirurgie, obésité suivie par une endocrinologie infantile et diagnostic de bêtalasémie mineure.\n\nÉvalué lors d'une consultation en génétique clinique à l'âge de 8,5 ans : poids, 45 kg (p95 ; écart-type, DS) = 1,75 ; taille, 138 cm (p77 ; DS) = 0,77 ; indice de masse corporelle, 23,63 (p96 ; DS) = 1,85 ; et périmètre crânien, 57 cm (p99 ; DS) = 3,05). Phénotype avec macro-céphalie, obésité troncale avec adipomastie, front large et large, yeux enfoncés, nez bulbeux, pavillons auriculaires décollés légèrement non dysplasiques, menton effilé, uvula courte et large, voix nasale, phalanges distales des mains effilées, pieds plats laxés et pénis enfoui dans la graisse pré-pubienne.\n\nÉtude génétique. Array SNP/CNV 750K (plateforme GeneChipÒ System 3000, AffymetrixÒ, Cyto-Scan Assay P/N 703038 Rev.5. Analyse avec le programme Chromosome Analysis Suite, AffymetrixÒ v.3.3): une délétion de 586 kb est détectée dans la bande cytologique Xq21.1 arr[GRCh37]Xq21.1(79564583_80150138)x0. La délétion inclut un seul gène avec pathologie connue associée, BRWD3. Un array est ensuite réalisé sur la mère et la sœur, asymptomatiques, toutes deux porteuses de la délétion identifiée chez le patient, non présente chez la grand-mère maternelle.\n",
+        "gold_summary": "Homme sans antécédents familiaux ou périnataux d'intérêt avec un trouble du développement neurologique : retard psychomoteur, retard de langage et déficience cognitive, macro-céphalie (p > 99) et obésité. Phénotype avec dysmorphie faciale : front large, yeux enfoncés, nez bulbeux, oreilles décollées et menton pointu. Array d'hybridation génomique comparée avec délétion de 586 ko dans Xq21.1, qui inclut un seul gène associé à la pathologie, BRWD3. Une étude a ensuite été réalisée sur la mère et la sœur, asymptomatiques, et toutes deux porteuses de la délétion.\n",
+        "synthetic_summary": {
+            "B1": "Il y a un garçon qui a eu un peu de retard pour marcher et parler. Sa tête est un peu plus grande que celle des autres enfants. Il est aussi un peu gros.\n\nSon visage est un peu différent : son front est large, ses yeux sont un peu enfoncés, son nez est un peu rond, ses oreilles sont un peu décollées, et son menton est pointu.\n\nLes médecins ont cherché dans ses gènes. Ils ont trouvé un petit morceau qui manque dans un gène important. Sa maman et sa sœur ont aussi ce petit morceau qui manque, mais elles vont bien.",
+            "B2": "### Ce qu'ils ont observé chez le garçon\n\nCe garçon n’a pas d’antécédents familiaux ou problèmes à la naissance. Cependant, il a eu des difficultés à se développer normalement : il a marché tard, à 18 mois, a eu un retard pour parler, et a une intelligence un peu plus faible que la moyenne (quotient intellectuel de 68 à 6 ans). Il est aussi en surpoids et a une grosse tête (ce qu’on appelle une macro-céphalie). Son visage présente quelques particularités : un front large, des yeux enfoncés, un nez un peu arrondi, des oreilles un peu décollées, et un menton pointu.\n\n### Ce qu’ils ont découvert avec les tests génétiques\n\nLes médecins ont fait un test spécial appelé \"array d’hybridation génomique comparée\". Ce test cherche des morceaux manquants ou en trop dans les chromosomes, qui sont les structures contenant nos gènes. Ils ont trouvé qu’il manque un petit morceau d’ADN sur le chromosome X, dans une zone appelée Xq21.1. Ce morceau manquant fait environ 586 000 bases, ce qui est assez petit, mais important. Ce morceau contient un seul gène connu, appelé BRWD3, qui est lié à des problèmes de développement comme ceux du garçon.\n\n### Ce que cela signifie\n\nIls ont aussi testé la mère et la sœur du garçon. Elles ont toutes les deux ce même morceau manquant, mais elles ne présentent pas de symptômes. Cela peut arriver car les filles ont deux chromosomes X, donc celui qui est normal peut compenser. Ce résultat aide à comprendre que la délétion du gène BRWD3 est probablement la cause des difficultés du garçon. Cela explique ses retards et certains traits physiques. Cette information est importante pour mieux suivre sa santé et aider sa famille.",
+            "B3": "Résumé structuré pour un public adulte non spécialiste\n\n**Contexte**  \nIl s’agit d’un garçon né sans complication particulière, issu d’une grossesse normale et d’un accouchement à terme sans problème. Ses premiers examens médicaux à la naissance étaient normaux, et il n’y avait pas d’antécédents familiaux ni d’exposition à des substances toxiques pendant la grossesse. Cependant, au cours de son développement, il a présenté un retard dans l’acquisition de la marche (à 18 mois) et des difficultés de langage. Un suivi spécialisé a été mis en place dès ses deux ans, incluant un soutien pour l’audition, le langage et des adaptations scolaires. À six ans, son quotient intellectuel était de 68, indiquant une déficience intellectuelle légère à modérée. Par ailleurs, il présente une exotropie (déviation des yeux vers l’extérieur) nécessitant une chirurgie, une obésité suivie par un endocrinologue, ainsi qu’une bêta-thalassémie mineure (un trouble sanguin héréditaire).\n\n**Principales observations cliniques**  \nÀ l’âge de 8 ans et demi, lors d’une consultation en génétique, plusieurs caractéristiques physiques ont été notées : une tête anormalement grande (macro-céphalie), une obésité localisée au tronc avec un développement mammaire chez le garçon (adipomastie), un front large, des yeux enfoncés, un nez arrondi et volumineux (bulbeux), des oreilles légèrement décollées sans malformation, un menton fin, une uvule (petite structure au fond de la gorge) courte et large, une voix nasale, des doigts fins aux extrémités, des pieds plats avec une certaine laxité articulaire, ainsi qu’un pénis partiellement enfoui dans la graisse pré-pubienne.\n\n**Résultats génétiques**  \nUne analyse approfondie du génome a révélé une délétion (perte) d’une petite portion d’ADN, d’environ 586 000 bases, située sur le chromosome X dans la région appelée Xq21.1. Cette délétion affecte un seul gène connu pour être impliqué dans des troubles du développement, nommé BRWD3. Cette anomalie génétique est considérée comme la cause probable des difficultés neurologiques et des caractéristiques physiques observées. Des tests réalisés chez la mère et la sœur, qui ne présentent aucun symptôme, ont montré qu’elles portent également cette même délétion, ce qui suggère une transmission héréditaire avec une expression variable.\n\n**Interprétation clinique**  \nLe tableau clinique de ce patient, associant retard psychomoteur, déficience intellectuelle, macro-céphalie, obésité et particularités faciales, correspond à un syndrome lié à la mutation ou à la perte du gène BRWD3. Ce gène joue un rôle important dans le développement neurologique. La présence de la délétion chez des membres de la famille asymptomatiques indique que cette anomalie peut ne pas toujours entraîner de symptômes visibles, notamment chez les femmes porteuses, en raison de la nature du chromosome X.\n\n**Prochaines étapes**  \nUn suivi multidisciplinaire est recommandé pour accompagner l’évolution du patient, incluant des interventions en neurologie, endocrinologie, ophtalmologie et orthophonie. Un conseil génétique est également important pour informer la famille sur la transmission héréditaire de cette délétion et ses implications possibles. Une surveillance régulière permettra d’adapter la prise en charge en fonction des besoins évolutifs du patient."
+        }
+    },
+    {
+        "article": "Un patient de 86 ans s'est présenté aux urgences pour un priapisme non douloureux de 3 semaines. Notre patient, un ancien agent de nettoyage, n'a connu qu'un accident ischémique transitoire. Il n'a pas d'antécédents chirurgicaux. L'examen physique a révélé un pénis semi-erect non douloureux avec une légère déviation latérale et un gland lisse. Aucune lésion pénienne superficielle n'a été observée. Le patient a déclaré avoir perdu des érections normales il y a près de 20 ans. Tous les signes cliniques étaient en faveur d'un priapisme non ischémique. Le patient était un ancien fumeur et a également déclaré avoir des symptômes respiratoires supérieurs modérés. Les résultats des analyses de laboratoire et des analyses d'urine étaient remarquables ; par conséquent, la décision a été de poursuivre les investigations en ambulatoire en utilisant une échographie pénienne et une tomodensitométrie thoracoabdominale (CT) à la recherche d'une tumeur maligne.\n\nUne échographie Doppler du pénis a été réalisée, révélant des nodules hypoéchogènes circonscrits infiltrant l'albugée du corps caverneux, avec une prédominance à la base et du côté droit. Aucune anomalie n'a été détectée dans le corps spongieux. Un indice résistif normal avec une vitesse artérielle pénienne normale a été mesuré, en faveur d'une situation non ischémique.\n\nLa TDM thoraco-abdominale a révélé une masse au niveau du hilum gauche du poumon entourant les structures broncho-vasculaires. Plusieurs nodules bilatéraux et micronodules ont été observés. Les plus grands étaient situés à l'apex droit et à la base droite du poumon. Des ganglions lymphatiques médiastinaux élargis ont également été observés à la station paratrachéale inférieure. Le foie a également été affecté par plusieurs lésions ; la plus grande était située au segment 7, qui mesurait 96 mm. Des lésions de la glande surrénale gauche et du pancréas ont été notées. Enfin, deux lésions ostéolytiques ont été observées sur la première côte gauche et sur le processus transverse de la cinquième vertèbre lombaire (L5). Le patient a été référé au spécialiste du cancer du poumon pour de nouvelles investigations. Une biopsie pulmonaire a été réalisée, confirmant un adénocarcinome du poumon. L'analyse moléculaire des cellules a montré une variante pGly12Cys (G12C) du gène KRAS. PDL-1 a également été noté comme positif.\n\nAprès une discussion multidisciplinaire, la décision a été prise pour la patiente de poursuivre une chimiothérapie à quatre cycles et une immunothérapie par le cisplatine, le pemetrexed et le pembrolizumab. La patiente a mal toléré le premier cycle de chimiothérapie et a développé une pancytopénie fébrile. La décision a été prise d'arrêter la chimiothérapie et de poursuivre l'immunothérapie par le pembrolizumab.\n\nEn ce qui concerne les lésions du pénis, le patient ne ressentant aucune douleur, une surveillance a été adoptée.\n",
+        "gold_summary": "Nous rapportons le cas d'un patient de 86 ans qui a présenté un priapisme non douloureux de 3 semaines. Une échographie Doppler du pénis et une tomodensitométrie thoracique et abdominale ont été effectuées, révélant une masse pulmonaire hilaire gauche ainsi que des lésions dans le foie, les glandes surrénales, le pancréas, les structures osseuses et le pénis. Les métastases péniennes sont associées à un mauvais pronostic en raison des fréquentes lésions malignes disséminées dans d'autres sites.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 86 ans avait un problème avec son corps qui restait un peu dur sans faire mal. Les docteurs ont fait des images pour regarder dedans. Ils ont vu une grosse boule dans son poumon et aussi des petits problèmes dans son foie, ses os et une autre partie de son corps. Ces problèmes viennent d’une maladie qui peut être grave. Les docteurs vont l’aider avec des médicaments pour essayer de le soigner.",
+            "B2": "Cas d’un homme de 86 ans avec un priapisme non douloureux\n\nUn homme âgé de 86 ans est venu aux urgences parce que son pénis restait semi-erect sans douleur depuis trois semaines. Ce phénomène s’appelle un priapisme. Il avait perdu ses érections normales depuis environ 20 ans. Lors de l’examen, son pénis était légèrement dévié sur le côté, mais sans blessure visible.\n\nCe qu’ils ont découvert avec les examens\n\nUne échographie spéciale appelée Doppler a montré des nodules, c’est-à-dire des petites masses, dans le tissu du pénis. Une autre analyse, un scanner du thorax et de l’abdomen, a révélé une grosse masse dans le poumon gauche, ainsi que plusieurs petites tumeurs dans le foie, les glandes surrénales, le pancréas, et des zones osseuses. Ces résultats indiquent que le cancer s’est étendu à plusieurs endroits du corps, y compris le pénis.\n\nCe que cela signifie\n\nLe patient a reçu un diagnostic de cancer du poumon appelé adénocarcinome, confirmé par une biopsie, c’est-à-dire un prélèvement de tissu pour l’étude. Ce type de cancer peut se propager à d’autres organes, ce qui rend le pronostic plus sérieux. Le patient a commencé un traitement combiné de chimiothérapie et d’immunothérapie, mais a eu des effets secondaires importants. Le traitement a donc été ajusté pour continuer seulement l’immunothérapie.\n\nConcernant le priapisme et les nodules dans le pénis, comme il n’y avait pas de douleur, les médecins ont choisi de surveiller la situation sans traitement immédiat.\n\nEn résumé, ce cas montre qu’un priapisme non douloureux chez une personne âgée peut être un signe rare que le cancer s’est étendu au pénis, ce qui nécessite des examens approfondis et un suivi médical adapté.",
+            "B3": "Résumé détaillé et structuré pour un public non médical éduqué :\n\n**Contexte**  \nUn homme de 86 ans s’est présenté aux urgences avec un priapisme, c’est-à-dire une érection prolongée et non douloureuse, qui durait depuis trois semaines. Ce patient, ancien agent de nettoyage, n’avait pas d’antécédents chirurgicaux majeurs, mais avait souffert auparavant d’un accident ischémique transitoire (un épisode temporaire de réduction du flux sanguin au cerveau). Il avait également perdu ses érections normales depuis environ vingt ans. À l’examen, son pénis était semi-erect, légèrement dévié sur le côté, sans douleur ni lésion visible à la surface.\n\n**Principales observations**  \nDes examens complémentaires ont été réalisés pour comprendre l’origine de ce priapisme. Une échographie Doppler du pénis a montré la présence de nodules (petites masses) infiltrant une structure appelée l’albuginée, qui entoure les corps caverneux responsables de l’érection. Ces nodules étaient localisés surtout à la base et à droite du pénis. Les mesures du flux sanguin dans le pénis étaient normales, ce qui confirmait que le priapisme n’était pas dû à un problème d’obstruction du sang (non ischémique).\n\nPar ailleurs, une tomodensitométrie (scanner) du thorax et de l’abdomen a révélé une masse importante au niveau du hilum gauche du poumon (zone où les vaisseaux et bronches entrent dans le poumon), ainsi que plusieurs nodules dans les deux poumons. Des ganglions lymphatiques élargis ont été observés dans la région médiastinale (entre les poumons). De plus, plusieurs lésions ont été détectées dans le foie, la glande surrénale gauche, le pancréas, ainsi que des lésions osseuses sur une côte et une vertèbre lombaire.\n\nUne biopsie pulmonaire a confirmé qu’il s’agissait d’un adénocarcinome du poumon, un type fréquent de cancer pulmonaire. L’analyse génétique des cellules cancéreuses a identifié une mutation spécifique du gène KRAS (variante G12C), connue pour influencer le comportement de la tumeur. Le marqueur PDL-1, qui peut prédire la réponse à certains traitements immunothérapeutiques, était également positif.\n\n**Interprétation clinique**  \nLa présence de nodules dans le pénis correspond à des métastases, c’est-à-dire des extensions du cancer initial du poumon vers d’autres organes. Ces métastases péniennes sont rares mais indiquent une maladie avancée avec dissémination multiple. Ce contexte est généralement associé à un pronostic défavorable.\n\n**Prise en charge et prochaines étapes**  \nAprès discussion entre spécialistes, le patient a commencé un traitement combiné associant chimiothérapie (cisplatine et pemetrexed) et immunothérapie (pembrolizumab). Cependant, il a mal toléré la chimiothérapie, développant une pancytopénie fébrile (une diminution sévère des cellules sanguines avec fièvre), ce qui a conduit à l’arrêt de la chimiothérapie. Le traitement par immunothérapie a été poursuivi seul.\n\nConcernant les lésions péniennes, comme le patient ne ressentait aucune douleur, une surveillance régulière a été choisie plutôt qu’un traitement invasif.\n\n**Conclusion**  \nCe cas illustre une forme rare de métastases du cancer du poumon au pénis, révélée par un priapisme non douloureux. La dissémination étendue du cancer rend le pronostic réservé, et la prise en charge doit être adaptée à la tolérance du patient et à la progression de la maladie."
+        }
+    },
+    {
+        "article": "Une femme enceinte de 22 ans, gravida 5, para 1, ayant fait trois fausses couches à la 5e semaine de grossesse, a été admise au service d'endocrinologie pour évaluation d'une hypokaliémie sévère détectée lors d'un test de grossesse au service de gynécologie. 16 ans auparavant, à l'âge de 6 ans, elle avait commencé à avoir des crampes après avoir pleuré ou avoir perdu son sang-froid, sans étourdissements, convulsions ou autres symptômes. Les tests de laboratoire ont révélé une hypokaliémie (données manquantes), et les symptômes ont été soulagés après supplémentation en potassium. Par la suite, elle a connu des crampes récurrentes après avoir pleuré, avoir perdu son sang-froid ou être fatiguée. Les symptômes ont été soulagés sans aucun traitement et n'ont eu aucun effet sur sa vie quotidienne ; par conséquent, elle n'a pas porté attention à ces symptômes. Deux jours avant son admission, elle a subi un test de laboratoire pour la grossesse. Son résultat de test sanguin a révélé des troubles électrolytiques sévères : son taux de potassium sérique était de 2,42 mmol/L et son taux de magnésium était de 0,65 mmol/L, mais elle n'avait aucun symptôme. Après supplémentation en chlorure de potassium par voie intraveineuse et orale au service des urgences, la patiente a été admise au service d'endocrinologie pour enquête sur l'hypokaliémie.\n\nAu moment de la présentation, la patiente ne transpirait pas, ne vomissait pas, n'avait pas de diarrhée, ni d'anorexie. Elle a nié avoir abusé de laxatifs ou de diurétiques, avoir une hypokaliémie ou des crampes chez d'autres membres de la famille. L'examen physique a révélé une taille de 149 cm, un poids de 46,3 kg et une tension artérielle de 97/71 mmHg. Il n'y avait aucun signe positif à l'examen physique, à l'exception du signe de Trousseau. Des examens de laboratoire détaillés ont été effectués pour un diagnostic et un traitement ultérieurs. L'analyse de laboratoire a révélé une hypokaliémie, une alcalose métabolique, une perte de potassium rénale, une hypomagnésémie, une hypocalciurie, une hyperréninémie et un hyperaldostéronisme avec une tension artérielle normale, ce qui a indiqué un diagnostic clinique de GS. Le diagnostic a été confirmé lorsqu'une mutation hétérozygote c.1077C>G (p.Asn359Lys) et c.965-1_976delGCGGACATTTTTGinsACCGAAAATTTT dans SLC12A3 a été identifiée par séquençage de l'exome entier. Après que les niveaux d'électrolytes ont été maintenus dans une plage relativement optimale, le traitement intraveineux a été changé en supplémentation orale.\n",
+        "gold_summary": "La patiente ne présentait aucun symptôme spécifique, mais souffrait d'hypokaliémie, d'alcalose métabolique, d'hypomagnésémie, d'hypocalciurie, d'hyperréninémie, d'hyperaldostéronisme et avait une tension artérielle normale. L'ensemble de ces symptômes indiquait le diagnostic clinique du syndrome de Gitelman, qui a été confirmé par une analyse génétique. De nombreux médicaments ont des données de sécurité limitées en début de grossesse, et des taux optimaux de potassium et de magnésium sont nécessaires pour une grossesse réussie.\n",
+        "synthetic_summary": {
+            "B1": "La dame avait un problème avec son corps. Elle avait peu de potassium et de magnésium dans son sang. Son corps faisait aussi un peu trop de certaines choses, mais sa tension était normale.\n\nLes docteurs ont trouvé que c’était une maladie appelée syndrome de Gitelman. Ils ont vérifié cela avec un test spécial.\n\nPour que la dame et son bébé aillent bien, il faut que son corps ait assez de potassium et de magnésium. C’est très important pendant la grossesse.",
+            "B2": "### Ce qu'ils ont trouvé chez la patiente\n\nCette jeune femme enceinte ne montrait pas de symptômes évidents, mais ses analyses de sang ont révélé plusieurs problèmes importants. Elle avait un faible taux de potassium (hypokaliémie), un déséquilibre dans l’acidité de son sang (alcalose métabolique), un faible taux de magnésium (hypomagnésémie), et d’autres anomalies liées aux minéraux dans son corps. Malgré tout cela, sa tension artérielle était normale.\n\n### Ce que cela signifie\n\nCes signes ont permis aux médecins de diagnostiquer un syndrome appelé syndrome de Gitelman. Ce syndrome est une maladie génétique qui affecte la façon dont les reins gèrent certains minéraux, comme le potassium et le magnésium. Pour confirmer ce diagnostic, ils ont fait un test génétique qui a trouvé des mutations dans un gène appelé SLC12A3.\n\n### Pourquoi c’est important pour la grossesse\n\nAu début de la grossesse, beaucoup de médicaments ne sont pas toujours sûrs à utiliser. Il est donc très important de bien contrôler les niveaux de potassium et de magnésium dans le corps de la patiente pour que la grossesse se passe bien. Les médecins ont commencé par lui donner ces minéraux par perfusion, puis ils sont passés à des compléments oraux pour maintenir un bon équilibre.",
+            "B3": "Résumé détaillé et structuré pour un public non médical éduqué :\n\n**Contexte**  \nUne femme enceinte de 22 ans, avec un historique de plusieurs fausses couches précoces, a été admise en endocrinologie après la découverte d’un faible taux de potassium dans le sang (hypokaliémie) lors d’un test de grossesse. Depuis l’enfance, elle souffrait de crampes musculaires récurrentes, souvent déclenchées par des émotions fortes ou la fatigue, mais ces symptômes n’avaient jamais été suffisamment graves pour justifier une consultation médicale. Lors de son admission, elle ne présentait aucun symptôme aigu, malgré des anomalies électrolytiques importantes.\n\n**Principales observations**  \nLes analyses sanguines ont montré plusieurs anomalies : un taux bas de potassium (hypokaliémie), un déséquilibre du pH sanguin appelé alcalose métabolique, un faible taux de magnésium (hypomagnésémie), une faible concentration de calcium dans les urines (hypocalciurie), ainsi qu’une augmentation des hormones rénales rénine et aldostérone (hyperréninémie et hyperaldostéronisme). Malgré ces troubles, sa tension artérielle était normale. L’examen physique était par ailleurs peu révélateur, excepté un signe de Trousseau positif, qui indique une sensibilité musculaire accrue liée au déséquilibre électrolytique.\n\n**Interprétation clinique**  \nL’ensemble de ces résultats a orienté vers un diagnostic de syndrome de Gitelman, une maladie génétique rare qui affecte la capacité des reins à réabsorber certains sels, provoquant une perte excessive de potassium et de magnésium. Ce diagnostic a été confirmé par une analyse génétique qui a identifié des mutations spécifiques dans le gène SLC12A3, responsable de cette maladie.\n\n**Prochaines étapes et prise en charge**  \nLe traitement a consisté à corriger les déséquilibres électrolytiques, d’abord par voie intraveineuse, puis par supplémentation orale en potassium et magnésium. Il est important de maintenir ces niveaux dans une plage optimale, surtout en début de grossesse, car de nombreux médicaments ne sont pas sûrs à ce stade et un bon équilibre électrolytique est essentiel pour la santé de la mère et du fœtus. Cette prise en charge adaptée vise à prévenir les complications liées au syndrome de Gitelman et à favoriser une grossesse réussie."
+        }
+    },
+    {
+        "article": "Présentation et traitement initial\n\nUne femme de 67 ans s'est présentée à l'Institut de cardiologie de Varsovie, en Pologne, en juin 2016, avec un antécédent de trois semaines d'insuffisance cardiaque croissante. La patiente présentait des symptômes de la classe fonctionnelle IV de la New York Heart Association (NYHA) qui comprenaient une dyspnée, une faiblesse et une prise de poids. La patiente avait des antécédents d'insuffisance cardiaque chronique due à une cardiomyopathie dilatée. Elle avait une fraction d'éjection ventriculaire gauche (FEVG) de 25 % et une régurgitation mitrale sévère. En 2015, elle a été diagnostiquée avec une fibrillation auriculaire paroxystique et une hypothyroïdie. Elle avait été précédemment traitée avec le système d'annuloplastie percutanée Mitralign (Mitralign Inc., Tewksbury MA, USA) pour la régurgitation mitrale. Elle avait également été précédemment traitée avec un dispositif de thérapie de resynchronisation cardiaque (CRT-D). Cependant, elle a souffert d'un œdème pulmonaire récurrent avec des épisodes d'hypertension pulmonaire et a nécessité une intubation et une ventilation. La patiente a été admise à la clinique de thérapie cardiaque intensive pour un traitement médical immédiat. Un IABP avec accès par cathéter par artère fémorale a été utilisé initialement. À ce stade, parce qu'elle souffrait d'hypertension pulmonaire sévère, cela a été considéré comme une contre-indication pour une transplantation cardiaque. Au cours des 115 jours de séjour à l'hôpital, la patiente a souffert d'immobilité associée à la mise en place du cathéter IABP.\n\nEn décembre 2016, après plusieurs tentatives infructueuses pour retirer le cathéter IABP de l'artère fémorale, il a été décidé de changer l'accès IABP de l'artère fémorale vers l'artère iliaque externe. Après avoir réinstallé le cathéter IABP, l'objectif était de combiner une gestion pharmacologique optimale avec une rééducation physique active et passive.\n\nUne approche en quatre étapes utilisant l'artère iliaque externe pour le placement du cathéter IABP\n\nUne technique innovante a été récemment développée dans notre établissement pour répondre aux problèmes résultant du placement à long terme d'un IABP fémoral. La patiente a été informée de cette nouvelle procédure et a signé un consentement éclairé écrit pour ce traitement. L'artère iliaque externe gauche a été utilisée pour l'insertion du cathéter IABP et comprenait un conduit prothétique Gelsoft de 8 mm de diamètre (Vascutek, Inchinnan, Écosse, Royaume-Uni). Une greffe de Dacron biseautée de 8 mm a été anastomosée bout à bout à l'artère avec une suture en polypropylène 5-0. Le cathéter a été retiré sous-cutanément de l'espace rétropéritonéal gauche vers le quadrant inférieur droit de l'abdomen. Aucune complication n'est survenue pendant la procédure.\n\nLa procédure mise au point dans notre établissement comprenait quatre étapes principales. La première étape a commencé par une incision longitudinale du quadrant inférieur gauche depuis l’arcade costale inférieure jusqu’à la partie supérieure du ligament inguinal. La peau, le tissu sous-cutané et les muscles ont été incisés jusqu’à la membrane péritonéale pour exposer l’artère iliaque externe. À l’aide de rétracteurs, les organes intra-abdominaux ont été déplacés vers le médiastin pour exposer les artères iliaques. Une anastomose latérale a été réalisée entre l’artère iliaque externe et le greffon prothétique. La deuxième étape de la procédure a comporté une incision de 1 cm dans le côté droit de l’abdomen, à 5-6 cm de l’ombilic et 2 cm en dessous. Un tunnel a été créé dans le plan sous-cutané du côté droit de l’abdomen vers le côté gauche. La troisième étape de la procédure a consisté à faire avancer la partie proximale du cathéter de l’IABP du côté droit de l’abdomen à travers le tunnel sous-cutané vers le côté gauche. Le cathéter a été placé dans l’aorte thoracique descendante à travers le greffon prothétique, l’artère iliaque et l’aorte. Le cathéter a été noué et scellé au niveau du site de connexion avec le greffon à l’aide d’une suture prolène 2-0. La quatrième étape de la procédure a consisté à fermer la plaie rétropéritonéale. L’utilisation du conduit vasculaire a permis de retirer relativement facilement l’IABP d’une petite incision dans le quadrant inférieur gauche de l’abdomen, qui a été fermée à l’aide de deux points de suture.\n\n\nRésultats et suivi des patients\n\nAprès la procédure IABP, le patient a été autorisé à s'asseoir, à se tenir debout et à marcher avec assistance et aucune complication neurologique ne s'est produite. Il n'y a eu aucun épisode de septicémie lié au site d'insertion. Après la procédure IABP transiliaque, le patient a présenté une réduction des taux sériques de créatinine et de bilirubine totale. Le patient n'a pas eu d'ischémie des membres pendant la contre-pulsation IABP. Les améliorations constatées pendant la physiothérapie comprenaient la marche sur 290 mètres pendant un test de marche de six minutes. Le patient a connu une amélioration significative de la fonction cardiaque avec une réduction de l'hypertension pulmonaire et de la résistance vasculaire pulmonaire. 195 jours après le changement de l'accès IABP, le patient a subi une transplantation cardiaque réussie.",
+        "gold_summary": "Patient : Femme, 67 ans\n\nDiagnostic final : Insuffisance cardiaque\n\nSymptômes : douleur thoracique • dyspnée • faible tolérance à l'exercice\n\nMédication : —\n\nProcédure clinique : insertion intra-articulaire d'une pompe à ballonnet - nouvelle technique\n\nSpécialité : chirurgie cardiaque\n\nRapport de cas:\nUne femme de 67 ans se présentait avec des antécédents d'insuffisance cardiaque. Elle avait des symptômes de classe fonctionnelle IV de la New York Heart Association (NYHA). La patiente avait des antécédents d'insuffisance cardiaque chronique due à une cardiomyopathie dilatée avec une fraction d'éjection ventriculaire gauche de 25 %, une régurgitation mitrale sévère, une fibrillation auriculaire paroxystique et une hypothyroïdie. Un traitement pharmacologique immédiat a été initié et un cathéter IABP a été initialement inséré en utilisant l'accès par l'artère fémorale. Au cours des 115 jours de traitement hospitalier, plusieurs tentatives infructueuses ont été faites pour retirer le cathéter IABP. En raison de l'immobilité prolongée du patient, l'accès du cathéter IABP a été changé de l'artère fémorale à l'artère iliaque externe. Un greffon prothétique en Dacron et un canal sous-cutané ont été utilisés. Une pharmacothérapie optimale a été initiée et la patiente a subi une rééducation et une mobilisation avec une amélioration significative de la fonction cardiaque. 195 jours après le changement de l'accès du cathéter IABP, la patiente a subi une transplantation cardiaque réussie.\n",
+        "synthetic_summary": {
+            "B1": "Une dame de 67 ans avait un gros problème avec son cœur. Son cœur ne marchait pas bien. Elle avait du mal à respirer et à bouger.\n\nLes docteurs ont mis un petit tuyau spécial pour aider son cœur à battre. Au début, ils ont mis ce tuyau dans une grosse veine de sa jambe. Mais ça ne marchait pas bien longtemps.\n\nAlors, ils ont changé et mis le tuyau dans un autre endroit près du ventre. Cela a aidé la dame à bouger un peu et à se sentir mieux.\n\nAprès un long moment, les docteurs ont pu lui donner un nouveau cœur. Maintenant, elle va mieux.",
+            "B2": "**Résumé simplifié pour un élève de 14 ans**\n\n**Ce qu’ils ont trouvé**  \nUne femme de 67 ans souffrait d’une maladie grave du cœur appelée insuffisance cardiaque. Cela signifie que son cœur ne pompait pas bien le sang. Elle avait aussi d’autres problèmes comme une valve du cœur qui ne fermait pas bien (régurgitation mitrale), un rythme cardiaque irrégulier (fibrillation auriculaire) et une maladie de la thyroïde. Ses symptômes étaient très forts : elle avait du mal à respirer, se sentait très faible et ne pouvait presque plus faire d’efforts.\n\n**Le traitement initial**  \nPour l’aider, les médecins ont mis en place un petit appareil appelé pompe à ballonnet intra-aortique (IABP). Cette pompe aide le cœur à mieux fonctionner en poussant le sang dans les artères. Au début, ils ont inséré cette pompe par une grosse artère dans la cuisse (artère fémorale). Mais la patiente est restée très longtemps allongée à cause de cette pompe, ce qui a causé des problèmes.\n\n**La nouvelle technique utilisée**  \nPour éviter ces problèmes, les médecins ont changé la façon d’installer la pompe. Cette fois, ils ont utilisé une autre artère située plus haut dans le ventre, appelée artère iliaque externe. Ils ont aussi mis un petit tube spécial (greffon prothétique en Dacron) pour protéger l’artère et faire passer la pompe. Grâce à cette nouvelle méthode, la patiente a pu bouger, s’asseoir, se lever et même marcher un peu pendant son traitement.\n\n**Les résultats**  \nAprès ce changement, la santé de la patiente s’est améliorée : son cœur fonctionnait mieux, sa pression dans les poumons a diminué, et elle a pu faire de la rééducation. Finalement, environ six mois plus tard, elle a pu recevoir une greffe de cœur qui a réussi.\n\n**Ce que cela signifie**  \nCette nouvelle technique pour placer la pompe à ballonnet permet aux patients de rester plus actifs pendant leur traitement, ce qui aide à améliorer leur état avant une transplantation cardiaque. C’est une avancée importante pour les personnes souffrant d’insuffisance cardiaque grave.",
+            "B3": "Résumé détaillé destiné à un public non spécialiste mais instruit\n\n**Contexte**  \nUne femme de 67 ans souffrant d’une insuffisance cardiaque chronique sévère s’est présentée à l’Institut de cardiologie de Varsovie avec une aggravation progressive de ses symptômes sur trois semaines. Elle était classée en stade IV selon la classification de la New York Heart Association (NYHA), ce qui signifie une incapacité majeure à réaliser des activités physiques normales, accompagnée de difficultés respiratoires (dyspnée), de fatigue importante et d’une prise de poids. Ses antécédents médicaux comprenaient une cardiomyopathie dilatée (une maladie du muscle cardiaque entraînant une diminution de sa capacité à pomper le sang), une fraction d’éjection ventriculaire gauche très basse (25 %, alors que la normale est supérieure à 55 %), une régurgitation mitrale sévère (fuite importante de la valve mitrale du cœur), une fibrillation auriculaire paroxystique (trouble du rythme cardiaque) et une hypothyroïdie. Elle avait déjà été traitée par un dispositif de resynchronisation cardiaque (CRT-D) et par une technique percutanée d’annuloplastie mitrale pour réduire la fuite valvulaire.\n\n**Principales observations et interventions initiales**  \nÀ son admission, la patiente présentait un œdème pulmonaire récurrent et une hypertension pulmonaire sévère, compliquant son état et rendant la transplantation cardiaque initialement contre-indiquée. Un dispositif d’assistance circulatoire appelé ballonnet intra-aortique de contre-pulsation (IABP) a été mis en place via l’artère fémorale (au niveau de l’aine) pour soutenir la fonction cardiaque. Cependant, après 115 jours d’hospitalisation, plusieurs tentatives pour retirer ce cathéter ont échoué, et l’immobilité prolongée liée à la présence du cathéter a entraîné des complications.\n\n**Technique innovante de changement d’accès IABP**  \nFace à ces difficultés, une nouvelle procédure a été développée pour repositionner le cathéter IABP via l’artère iliaque externe (une artère plus haute dans l’abdomen), en utilisant un greffon vasculaire prothétique en Dacron de 8 mm de diamètre. Cette intervention s’est déroulée en quatre étapes principales :  \n1. Une incision abdominale a permis d’exposer l’artère iliaque externe et d’y anastomoser (relier) le greffon prothétique.  \n2. Une petite incision a été réalisée sur le côté droit de l’abdomen pour créer un tunnel sous-cutané permettant de faire passer le cathéter d’un côté à l’autre de l’abdomen.  \n3. Le cathéter IABP a été inséré à travers le greffon, l’artère iliaque et l’aorte thoracique descendante, puis fixé solidement.  \n4. La plaie abdominale a été refermée soigneusement.  \n\nCette technique a permis de retirer facilement le cathéter par une petite incision ultérieure, réduisant ainsi les risques liés à un accès fémoral prolongé.\n\n**Résultats cliniques et suivi**  \nAprès ce changement d’accès, la patiente a pu être mobilisée rapidement : elle a pu s’asseoir, se tenir debout et marcher avec assistance, sans complication neurologique ni infection liée au site d’insertion. Les paramètres biologiques se sont améliorés, notamment la fonction rénale et hépatique, sans signe d’ischémie (manque d’oxygène) des membres inférieurs. La rééducation a permis une progression notable, avec une capacité à marcher 290 mètres lors d’un test standard de six minutes. Sur le plan cardiaque, une amélioration significative a été observée, avec une réduction de l’hypertension pulmonaire et de la résistance vasculaire pulmonaire. Enfin, 195 jours après le changement de cathéter, la patiente a pu bénéficier d’une transplantation cardiaque réussie.\n\n**Interprétation clinique**  \nCe cas illustre l’intérêt d’une approche innovante pour le maintien à long terme d’un dispositif d’assistance circulatoire chez un patient en insuffisance cardiaque avancée. Le recours à un accès par l’artère iliaque externe via un greffon prothétique a permis d’éviter les complications liées à l’immobilité prolongée et à l’accès fémoral, tout en facilitant la rééducation et en améliorant la condition générale du patient en vue d’une transplantation.\n\n**Prochaines étapes**  \nCette technique pourrait représenter une alternative précieuse dans la prise en charge des patients nécessitant une assistance circulatoire prolongée, notamment ceux pour qui l’accès fémoral est problématique. Une surveillance attentive et une rééducation adaptée restent essentielles pour optimiser les résultats avant une éventuelle transplantation cardiaque."
+        }
+    },
+    {
+        "article": "Patient féminine caucasienne de 73 ans qui a consulté pour un trouble mammaire avec une anomalie rose de la peau du sein droit il y a environ 30 jours. La mammographie bilatérale 5 mois avant la consultation a montré des anomalies bénignes (rapport d'imagerie mammaire et système de données - BI-RADS™ 2). La patiente avait des antécédents de carcinome canalaire invasif du sein droit G3 sans type spécial, qui avait été traité par résection segmentaire et dissection des ganglions axillaires de niveaux I et II en décembre 2011. Au moment de la chirurgie, on a observé une tumeur de 3,0 cm et trois ganglions axillaires métastatiques (3/10). L'immunohistochimie a révélé que la tumeur était positive pour le récepteur des œstrogènes (90%), positive pour le récepteur de la progestérone (2%), négative pour HER-2, positive pour Ki-67 (60%) et du sous-type luminaire B. La thérapie adjuvante de la patiente comprenait six cycles de doxorubicine, cyclophosphamide et paclitaxel, suivis d'une radiothérapie (25 séances avec une dose de 50 Gy au sein droit et à la fossa supraclaviculaire, plus une dose de 10 Gy). La patiente suit actuellement un traitement endocrinologique avec le létrozole (6 ans de traitement). Au cours de l'examen physique, elle a présenté deux lésions roses au sein droit, dont une érythémateuse légère et presque imperceptible au niveau de la jonction quadrante supérieure (JQS) et une autre lésion violacée plus intense au niveau de la jonction quadrante inférieure (JQI) mesurant 0,5 cm.\n\nUne biopsie incisionnelle de la lésion a été réalisée au JQI, qui a révélé une lésion vasculaire atypique en coloration hématoxyline-éosine. Une étude immuno-histochimique complémentaire de l'angiosarcome a été suggérée pour compléter le diagnostic. Après le résultat de cette étude, la patiente a été soumise à une résection des deux lésions cutanées. Le rapport pathologique anatomique de l'échantillon résectionné a montré un angiosarcome bien différencié (G1), une néoplasie caractérisée par des anastomoses vasculaires alignées par des cellules endothéliales atypiques caractérisées par la présence d'hyperchromatisme et d'anisocaryose et, dans certains cas, contenant des érythrocytes, organisées dans le modèle de croissance infiltrée, pénétrant le parenchyme mammaire et le derme au JQI, mesurant 1,9x1,4 cm, et au JQI, constituant une néoplasie limitée au derme, mesurant 1,1x0,5 cm. L'examen immuno-histochimique a révélé une positivité pour l'expression du groupe de différenciation 31 (CD31) et de l'oncogène C-MYC, confirmant la malignité secondaire à la radiothérapie. La tomographie par ordinateur du thorax et de l'abdomen et la scintigraphie osseuse n'ont pas montré de signes de métastases à distance. La patiente a subi une mastectomie simple du côté droit, sans reconstruction, comme traitement complémentaire. Le rapport final histopathologique a montré un angiosarcome bien différencié (G1) et trois foyers microscopiques ont été trouvés dans le parenchyme mammaire, dont le plus grand mesurait 2 mm. Deux ans après la chirurgie, la patiente n'a pas développé de récidive.\n",
+        "gold_summary": "Nous rapportons le cas d'une femme de 73 ans ayant des antécédents de traitement conservateur d'un cancer du sein droit, présentant une modification rose discrète de la peau du sein homolatéral. La mammographie a montré un résultat compatible avec des modifications bénignes (BI-RADS 2). L'hématoxyline-éosine a montré une lésion vasculaire atypique et a suggéré une immunohistochimie pour une élucidation diagnostique. La patiente a subi une résection de la lésion et l'histologie a montré un angiosarcome radiogénique. Une mastectomie simple a ensuite été réalisée. L'immunohistochimie a montré une positivité pour les antigènes CD31 et CD34, et l'amplification de l'oncogène C-MYC a confirmé le diagnostic d'un angiosarcome induit par une radiothérapie mammaire. Le retard dans le diagnostic constitue un problème important. Étant donné que les modifications initiales de la peau de l'angiosarcome radiogénique sont subtiles et peuvent être confondues avec d'autres affections cutanées bénignes, telles que les télangiectasies, nous soulignons dans ce rapport les aspects cliniques, afin de mettre en garde contre la possibilité d'un angiosarcome du sein chez les patients ayant des antécédents de radiothérapie adjuvante pour le traitement du cancer du sein. La patiente est restée asymptomatique 16 mois après la chirurgie.\n",
+        "synthetic_summary": {
+            "B1": "Une dame de 73 ans avait un petit changement rose sur sa peau du sein droit. Elle avait déjà eu un cancer du sein et un traitement avec des rayons. Le docteur a regardé la peau et a fait un petit prélèvement. Ce prélèvement a montré un problème dans les petits vaisseaux du sein. \n\nLes docteurs ont enlevé cette partie de la peau malade. Puis, ils ont enlevé tout le sein droit pour que la dame aille mieux. Ce problème est rare et peut arriver après un traitement avec des rayons. \n\nIl faut bien regarder la peau quand on a eu un cancer du sein et des rayons. Même un petit changement peut être important. La dame va bien deux ans après l’opération.",
+            "B2": "**Ce qu'ils ont trouvé**  \nUne femme de 73 ans, qui avait déjà eu un cancer du sein droit traité sans enlever tout le sein, a remarqué une légère coloration rose sur la peau de ce même sein. Une mammographie récente n’avait montré que des anomalies bénignes, c’est-à-dire sans gravité apparente. Pour mieux comprendre la lésion rose, les médecins ont fait une biopsie, c’est-à-dire qu’ils ont prélevé un petit morceau de peau pour l’examiner au microscope. Cette analyse a montré une lésion anormale liée aux vaisseaux sanguins, mais il fallait des tests supplémentaires pour confirmer ce que c’était.\n\n**Ce que cela signifie**  \nAprès avoir retiré la lésion, les médecins ont découvert qu’il s’agissait d’un angiosarcome, un type rare de cancer qui se forme dans les cellules des vaisseaux sanguins. Ce cancer est apparu à cause de la radiothérapie que la patiente avait reçue plusieurs années auparavant pour son premier cancer du sein. Des tests spéciaux ont confirmé que cette tumeur était bien liée à la radiothérapie. Heureusement, aucun signe de propagation à d’autres parties du corps n’a été trouvé.\n\n**Le traitement et le suivi**  \nLa patiente a ensuite subi une mastectomie simple, c’est-à-dire l’ablation complète du sein droit sans reconstruction. Deux ans après cette opération, elle n’a pas eu de récidive, ce qui signifie que le cancer ne s’est pas reformé.\n\n**Pourquoi c’est important**  \nCe cas montre que les premiers signes d’un angiosarcome causé par la radiothérapie peuvent être très discrets, comme une simple coloration rose sur la peau. Ces signes peuvent facilement être confondus avec des problèmes bénins, ce qui peut retarder le diagnostic. Il est donc important que les médecins surveillent attentivement les patients ayant reçu une radiothérapie au sein pour détecter rapidement ce type de cancer rare.",
+            "B3": "Résumé détaillé et structuré :\n\nContexte  \nNous présentons le cas d’une femme caucasienne de 73 ans, avec des antécédents de cancer du sein droit traité de manière conservatrice en 2011 par chirurgie, chimiothérapie adjuvante, radiothérapie et traitement endocrinologique prolongé. Cinq mois avant la consultation actuelle, une mammographie bilatérale avait montré uniquement des anomalies bénignes (classification BI-RADS 2). La patiente s’est présentée avec une modification cutanée discrète, rose, au niveau du sein droit, apparue depuis environ un mois.\n\nPrincipales observations  \nÀ l’examen clinique, deux lésions cutanées ont été identifiées sur le sein droit : une lésion légèrement érythémateuse au quadrant supérieur et une autre, plus violacée et mesurant 0,5 cm, au quadrant inférieur. Une biopsie incisionnelle de la lésion du quadrant inférieur a révélé, à l’hématoxyline-éosine, une lésion vasculaire atypique. Pour préciser le diagnostic, une étude immunohistochimique complémentaire a été réalisée, mettant en évidence la positivité des marqueurs CD31 (un antigène exprimé par les cellules endothéliales) et l’amplification de l’oncogène C-MYC, ce qui a confirmé la nature maligne de la lésion et son caractère secondaire à la radiothérapie antérieure.\n\nSuite à ce diagnostic, une résection chirurgicale des deux lésions cutanées a été effectuée. L’analyse histopathologique a confirmé la présence d’un angiosarcome bien différencié (grade 1), une tumeur maligne des vaisseaux sanguins caractérisée par des structures vasculaires anastomosées tapissées de cellules endothéliales atypiques infiltrant le derme et le parenchyme mammaire. La plus grande tumeur mesurait 1,9 x 1,4 cm. Un bilan d’extension par tomodensitométrie thoraco-abdominale et scintigraphie osseuse n’a pas montré de métastases à distance.\n\nInterprétation clinique  \nL’angiosarcome radiogénique est une complication rare mais grave survenant après radiothérapie mammaire. Il se manifeste initialement par des modifications cutanées subtiles, souvent confondues avec des lésions bénignes comme des télangiectasies (dilatations vasculaires superficielles). Ce retard diagnostique est préoccupant, car un diagnostic précoce est essentiel pour améliorer le pronostic. L’immunohistochimie, notamment la détection de CD31 et de C-MYC, est cruciale pour confirmer la nature maligne et la relation avec la radiothérapie.\n\nProchaines étapes  \nLa patiente a subi une mastectomie simple du sein droit, sans reconstruction, en traitement complémentaire. L’examen histopathologique post-opératoire a montré la persistance de foyers microscopiques d’angiosarcome dans le parenchyme mammaire. Deux ans après la chirurgie, la patiente ne présente pas de récidive ni de métastases, témoignant d’un suivi favorable à moyen terme.\n\nConclusion  \nCe cas illustre l’importance d’une vigilance accrue face à toute modification cutanée chez les patientes ayant reçu une radiothérapie mammaire, même plusieurs années auparavant. La reconnaissance précoce d’un angiosarcome radiogénique repose sur une évaluation clinique attentive, une biopsie appropriée et des analyses immunohistochimiques ciblées. Une prise en charge chirurgicale rapide est indispensable pour limiter la progression de cette tumeur agressive."
+        }
+    },
+    {
+        "article": "Homme de 40 ans, admis aux urgences pour douleurs thoraciques. Ses antécédents comprenaient un surpoids, une stéatose hépatique non alcoolique, un syndrome d'apnée du sommeil sans besoin de pression positive continue des voies respiratoires et une coronaropathie chez son grand-père. Les symptômes ont débuté 6 jours avant la consultation, sous forme de douleurs thoraciques de classe fonctionnelle II (1000 mètres), intensité 5/10, brûlantes, non irradiées, d'une durée de 15 à 20 minutes, qui s'amélioraient avec le repos et sans association de dyspnée, palpitations ou transpiration. Des épisodes similaires ont été répétés les jours suivants avant la consultation, dans la même classe fonctionnelle, 2 heures avant l'admission, débutant la douleur dans la classe fonctionnelle IV, postprandial, d'intensité 8/10, associée à une dyspnée, ce qui a conduit le patient à consulter.À l'admission, les signes vitaux suivants ont été observés : TA 150/80 mmHg, FC 85 LPM, FR 16 RPM, saturation 98 % (0,21), non fébrile. Douleur thoracique résiduelle d'intensité 4/10, sans signes d'insuffisance cardiaque. Un électrocardiogramme a été réalisé, où des ondes T négatives, symétriques, ont été visualisées dans les dérivations précordiales et supradesnivel de ST de < 1 mm avec des ondes T bifasic en V3, sans ondes Q et bonne progression de R dans les précordiales (non observé dans l'électrocardiogramme préalable). Laboratoire : Hto 43 %, Cr 0,8 mg/dl, troponine ultrasensible de 132 pg/ml avec élévation ultérieure à 172 pg/ml. On a interprété infarctus aigu du myocarde sans élévation du ST, TIMI score de 3 points, GRACE score 66 points. On a administré une charge d'aspirine, des statines de haute intensité et une anticoagulation avec de l'héparine de faible poids moléculaire. Il a commencé un traitement avec de la nitroglycérine intraveineuse, avec une amélioration de la douleur. Un nouvel électrocardiogramme a été réalisé, où des ondes T négatives ont été visualisées dans les précordiales, mais persistance du supradesnivel avec une onde T bifasic en V2-V3. L'échocardiogramme a mis en évidence une bonne fonction ventriculaire et une hypokinésie antéroseptal, basale et médiale. L'angiographie a mis en évidence des lésions graves dans le tiers proximal, moyen de l'artère descendante antérieure et une lésion grave dans le tiers moyen de la première diagonale, ce qui a conduit à la pose de trois stents libérant des médicaments dans ces lésions. Un nouvel électrocardiogramme a été réalisé après la pose des stents, où l'absence de changements a été observée. Le patient a été libéré sans complications.\n",
+        "gold_summary": "Il s’agit d’un homme de 40 ans sans antécédents cardiovasculaires, qui a été admis à notre centre pour des douleurs précordiales. L’électrocardiogramme a révélé un schéma typique, déjà décrit, connu sous le nom de syndrome de Wellens de type 1 ou A, caractérisé par un supradesnivel du ST < 1 mm et une onde T biphasique dans la dérivation V3. On a diagnostiqué un infarctus aigu du myocarde sans élévation du ST, TIMI 3 et GRACE score 66 points. Ce schéma électrocardiographique est à haut risque, au-delà des scores stratifiants, étant donné qu’il est corrélé à une lésion grave de l’artère descendante antérieure au niveau proximal et nécessite une intervention percutanée sans délai. La coronarographie a révélé 3 lésions graves : tiers proximal et moyen de l’artère descendante antérieure et première diagonale.\n",
+        "synthetic_summary": {
+            "B1": "Un homme de 40 ans avait mal au cœur. Son cœur montrait un problème important. Les docteurs ont vu que son cœur avait des parties bouchées. Ils ont vite mis des petits tuyaux pour aider le sang à passer. Maintenant, il va mieux et il n’a plus mal.",
+            "B2": "**Ce qu'ils ont trouvé chez le patient**  \nUn homme de 40 ans est venu à l'hôpital parce qu'il avait des douleurs au niveau de la poitrine. Son électrocardiogramme (un examen qui enregistre l'activité électrique du cœur) montrait un signe spécial appelé syndrome de Wellens de type 1. Cela signifie qu'il y avait des petites anomalies dans certaines ondes, notamment une onde T qui changeait de forme dans une zone précise du cœur. Ce signe est important car il indique un problème sérieux dans une artère principale du cœur.\n\n**Ce que cela signifie**  \nLe patient avait un infarctus du myocarde sans élévation du segment ST, ce qui est un type d'attaque cardiaque. Les scores TIMI et GRACE, qui aident à mesurer le risque, étaient modérés, mais le signe sur l'électrocardiogramme montrait un risque élevé. En effet, ce syndrome est lié à une grave obstruction dans l'artère descendante antérieure, une artère qui nourrit une grande partie du muscle cardiaque.\n\n**Le traitement et le résultat**  \nUne angiographie, c’est-à-dire un examen qui utilise un produit spécial pour voir les artères du cœur, a montré trois blocages importants dans cette artère et une autre artère voisine. Pour les débloquer, les médecins ont posé trois stents, qui sont de petits tubes métalliques libérant un médicament pour garder les artères ouvertes. Après cette intervention, le patient s’est amélioré et a pu quitter l’hôpital sans problème.  \n\nEn résumé, ce cas montre l’importance de reconnaître rapidement certains signes sur l’électrocardiogramme, car ils indiquent des blocages graves qui doivent être traités rapidement pour éviter des complications graves.",
+            "B3": "### Contexte  \nUn homme de 40 ans, sans antécédents cardiovasculaires personnels mais avec des facteurs de risque tels que surpoids, stéatose hépatique non alcoolique et syndrome d’apnée du sommeil, a été admis aux urgences pour des douleurs thoraciques récurrentes évoluant depuis six jours. Ces douleurs, initialement modérées et soulagées par le repos, sont devenues plus intenses et associées à une difficulté respiratoire, ce qui a motivé la consultation.\n\n### Principales Observations  \nÀ l’admission, le patient présentait une tension artérielle élevée (150/80 mmHg) et une douleur thoracique persistante modérée. L’électrocardiogramme (ECG) montrait des anomalies spécifiques : des ondes T négatives symétriques et bifasiques dans les dérivations précordiales, notamment en V3, ainsi qu’un léger sus-décalage du segment ST inférieur à 1 mm. Ces modifications n’étaient pas présentes sur un ECG antérieur. Les analyses sanguines ont révélé une élévation progressive de la troponine ultrasensible, un marqueur de lésion cardiaque, confirmant un infarctus aigu du myocarde sans élévation du segment ST (NSTEMI). Les scores cliniques TIMI (3 points) et GRACE (66 points) indiquaient un risque modéré.\n\nL’échocardiogramme a montré une fonction ventriculaire globale préservée, mais une hypokinésie (diminution du mouvement) localisée dans la paroi antéroseptale du cœur. L’angiographie coronarienne a mis en évidence trois lésions sévères : dans le tiers proximal et moyen de l’artère descendante antérieure (une artère principale du cœur) ainsi que dans le tiers moyen de la première branche diagonale. Ces lésions ont été traitées par la pose de trois stents médicamenteux.\n\n### Interprétation Clinique  \nLe tableau électrocardiographique correspond au syndrome de Wellens de type 1 (ou type A), caractérisé par des ondes T biphasique en V3 et un sus-décalage du segment ST inférieur à 1 mm. Ce syndrome est un signe d’alerte majeur, indiquant une obstruction critique de l’artère descendante antérieure proximale, une situation à haut risque d’infarctus étendu si elle n’est pas prise en charge rapidement. Malgré des scores de risque modérés, la présence de ce syndrome justifie une intervention urgente.\n\n### Prochaines Étapes  \nLe patient a bénéficié d’une angioplastie avec pose de stents pour rétablir le flux sanguin dans les artères coronaires affectées. Après cette intervention, son état s’est amélioré sans complications immédiates, et il a pu être libéré avec un suivi cardiologique adapté. Ce cas souligne l’importance de reconnaître rapidement le syndrome de Wellens, car il guide la prise en charge urgente pour prévenir un infarctus majeur."
+        }
+    },
+    {
+        "article": "Un patient iranien de 38 ans s'est présenté au service des urgences de l'hôpital de Kowsar, à Semnan, le 2 octobre 2021, avec pour principaux symptômes une douleur abdominale sévère et un œdème des membres inférieurs. La douleur, qui provenait de la région ombilicale et se répandait dans tout l'abdomen, a motivé la visite. Les signes vitaux ont été enregistrés comme suit : tension artérielle (TA) = 130/90 mmHg, fréquence cardiaque (FC) = 80 bpm, et température (T) = 37 °C. L'examen abdominal a révélé des bruits intestinaux normaux, une légère sensibilité dans la région inguinale, et des bruits tympaniques. Il a également été noté qu'il souffrait d'une SBS congénitale avec une longueur totale mesurée de l'intestin grêle d'environ 185 cm, significativement plus courte que la normale, et une absence de l'épiploon.\n\nLe 10 août 2021, la patiente a subi une hémicolectomie droite et une iléostomie en raison de douleurs abdominales associées à un diagnostic d'obstruction intestinale. Par la suite, le 21 septembre 2021, la patiente a subi une colostomie et a été hospitalisée pendant 6 jours (dont 3 jours en unité de soins intensifs [USI]). Après la sortie, la patiente a présenté des douleurs abdominales et un œdème, avec une escalade des symptômes le 1er octobre 2021. Des nausées ont été signalées lors de l'admission, mais sans vomissements, et il n'y a pas eu de plaintes liées à la miction. En raison de douleurs postprandiales et d'un mauvais appétit, la prise alimentaire de la patiente a été compromise. Aucune fièvre, aucun frisson, ni aucune dyspnée n'ont été signalés. Un œdème des membres inférieurs a été constaté (2+), sans clubbing ou cyanose observée. Les autres signes vitaux étaient dans les limites normales (pouls 82 battements/minute, tension artérielle 110/70 mmHg, fréquence respiratoire 18 respirations/minute, température 37 °C). La sensibilité abdominale a entravé un examen complet en raison de douleurs sévères. L'examen de la tête, du cou et de la poitrine n'a révélé aucune constatation spécifique.\n\nLe compte sanguin complet a indiqué une leucocytose (hémoglobine 11,7 g/dL, nombre de globules blancs 19,23 × 103/µL, plaquettes 406 × 103/µL, RBC 4,30 × 106/µL, et hématocrite [HTC] 34,3%), tandis que l'analyse des gaz du sang artériel a montré une alcalose métabolique (pH 7,56, pression partielle d'oxygène [PO2] 204,5 mmHg, pression partielle de dioxyde de carbone [PCO2] 31,9 mmHg, excès de base [BE] 7,0 mmol/L, et bicarbonate [HCO3] 29,1 mmol/L).\n\nRadiographies abdominales et thoraciques d’un homme de 38 ans atteint du syndrome congénital de l’intestin court et d’absence de l’omentum. Radiographie abdominale couchée démontrant des boucles intestinales dilatées et l’absence de l’omentum, sans preuve de niveaux air-fluide. La radiographie thoracique ne montrait pas non plus de signes d’anomalies significatives, confirmant les résultats cardiopulmonaires normaux. La radiographie abdominale debout révélait des signes de distension gazeuse et de boucles compatibles avec le diagnostic du patient.\n\nUne tomographie par ordinateur (CT) à contraste amélioré de l'abdomen et du bassin a été recommandée. La sécrétion fécale des sutures du patient a soulevé des préoccupations concernant une péritonite postopératoire due à une fuite anastomotique, ce qui a nécessité une intervention chirurgicale immédiate. Le patient a subi une laparotomie d'urgence, un drainage et une jéjunostomie à double baril.\n\nLa récupération du patient s'est déroulée sans incident, avec une prise orale de liquides clairs autorisée le jour postopératoire 2 et une prise de liquides complète autorisée le jour postopératoire 4.\n\nPour l'absence congénitale d'omentum et le syndrome du petit intestin, les options de traitement comprennent un soutien nutritionnel, tel que la nutrition parentérale ou entérale totale. Les cas graves peuvent nécessiter une intervention chirurgicale pour allonger le reste de l'intestin ou effectuer une transplantation intestinale. Les stratégies pour le syndrome du petit intestin résultant de l'absence congénitale d'omentum peuvent impliquer un soutien nutritionnel, ainsi que l'amélioration de l'expression des protéines de transport (telles que les cotransporteurs Na+/glucose, les échangeurs Na+/H+) pour faciliter l'adaptation intestinale. Les interventions humaines comprennent le traitement par glutamine et par hormone de croissance ou l'administration de peptides glucagon-like, bien que des études multicentres soient nécessaires pour obtenir des preuves concluantes.\n",
+        "gold_summary": "Ce rapport de cas présente une convergence unique de ces conditions rares chez un homme iranien de 38 ans ayant des antécédents d'obstruction intestinale nécessitant une hémicolectomie droite et une iléostomie. Il s'est ensuite présenté au service des urgences en présentant une douleur abdominale intense et un gonflement de ses membres inférieurs. Les examens de laboratoire ont révélé une augmentation du nombre de globules blancs et une alcalose métabolique. Au cours de l'exploration chirurgicale provoquée par sa présentation aiguë, l'absence congénitale de l'omentum et le syndrome du petit intestin ont été confirmés. Une jéjunostomie a été réalisée, mais malheureusement, cette intervention a entraîné une malabsorption sévère et une cachexie ultérieure. Ce cas met en lumière la rare occurrence de fuite anastomotique et de péritonite ultérieure suite à une hémicolectomie droite et une iléostomie chez un patient présentant les conditions combinées d'intestin court congénital et d'absence congénitale de l'omentum.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 38 ans avait très mal au ventre. Ses jambes étaient aussi un peu gonflées. Il avait un petit ventre parce que son intestin était plus court que d’habitude. \n\nLes docteurs ont fait une opération pour l’aider. Après, il a eu encore mal et ils ont dû refaire une autre opération. \n\nCe monsieur est très spécial parce qu’il a deux choses rares dans son ventre. Les docteurs ont travaillé très fort pour le soigner.",
+            "B2": "**Résumé simple pour un élève de 14 ans**\n\nCe cas parle d’un homme iranien de 38 ans qui avait deux problèmes rares dans son intestin. D’abord, il avait un intestin beaucoup plus court que la normale, ce qu’on appelle le syndrome de l’intestin court. Ensuite, il lui manquait une partie spéciale du ventre appelée l’épiploon, qui aide normalement à protéger les organes.\n\nCet homme avait déjà eu une opération pour enlever une partie de son gros intestin à cause d’un blocage. Plus tard, il est venu à l’hôpital avec une forte douleur au ventre et des jambes enflées. Les médecins ont fait des analyses et ont vu qu’il avait beaucoup de globules blancs, ce qui montre une infection, et un problème avec l’équilibre de son sang.\n\nIls ont dû faire une autre opération d’urgence. Pendant cette intervention, ils ont confirmé qu’il n’avait pas d’épiploon et que son intestin était très court. Ils ont fait une ouverture spéciale dans son intestin appelée jéjunostomie pour aider à évacuer les déchets.\n\nMalheureusement, après cette opération, il a eu des difficultés à bien absorber les aliments, ce qui l’a rendu très faible. Ce cas est important car il montre que chez des patients avec ces deux problèmes rares, des complications graves comme des fuites au niveau des sutures et des infections peuvent arriver après une opération.\n\nPour aider des personnes avec un intestin court ou sans épiploon, les médecins utilisent souvent des traitements pour améliorer la nutrition, comme des perfusions spéciales ou des médicaments qui aident l’intestin à mieux fonctionner. Parfois, des opérations pour allonger l’intestin ou même une greffe sont nécessaires.",
+            "B3": "Résumé détaillé et structuré pour un lecteur non spécialiste\n\n**Contexte**  \nCe rapport décrit le cas d’un homme iranien de 38 ans présentant une combinaison très rare de deux anomalies congénitales : le syndrome de l’intestin court (SIC), caractérisé par une longueur anormalement réduite de l’intestin grêle, et l’absence congénitale de l’épiploon (omentum), une structure graisseuse normalement présente dans l’abdomen. Le patient avait des antécédents récents d’obstruction intestinale ayant nécessité une chirurgie majeure, comprenant une hémicolectomie droite (ablation d’une partie du côlon droit) et une iléostomie (dérivation de l’intestin grêle vers la peau).\n\n**Principales observations**  \nÀ son admission aux urgences, le patient présentait une douleur abdominale sévère localisée autour du nombril, irradiant dans tout l’abdomen, ainsi qu’un œdème (gonflement) des membres inférieurs. Ses signes vitaux étaient globalement stables. L’examen clinique montrait une sensibilité abdominale importante, empêchant un examen approfondi, mais sans autres anomalies notables. Les analyses sanguines révélaient une leucocytose (augmentation du nombre de globules blancs, signe d’inflammation ou d’infection) et une alcalose métabolique (déséquilibre du pH sanguin avec une augmentation du bicarbonate), suggérant un dérèglement métabolique. Les radiographies abdominales ont montré des boucles intestinales dilatées sans signes évidents d’obstruction complète, tandis que la radiographie thoracique était normale.\n\nUne tomodensitométrie (scanner) abdominale avec injection de produit de contraste a été réalisée pour mieux évaluer la situation. La présence de sécrétions fécales au niveau des sutures chirurgicales a soulevé la suspicion d’une fuite anastomotique (fuite au niveau de la jonction intestinale opérée), compliquée par une péritonite (infection de la cavité abdominale). Cette complication grave a conduit à une intervention chirurgicale d’urgence, consistant en une laparotomie (ouverture de l’abdomen), un drainage de la cavité abdominale et la réalisation d’une jéjunostomie à double baril (création de deux ouvertures dans le jéjunum, une partie de l’intestin grêle).\n\n**Interprétation clinique**  \nCe cas illustre la complexité de la prise en charge d’un patient présentant simultanément un syndrome de l’intestin court et une absence congénitale d’épiploon, deux conditions rares qui affectent la fonction intestinale et la protection de la cavité abdominale. La survenue d’une fuite anastomotique après une chirurgie intestinale majeure est une complication grave, particulièrement chez ce patient dont l’intestin est déjà raccourci et dont la capacité d’adaptation est limitée. La jéjunostomie réalisée vise à assurer une alimentation entérale, mais expose aussi à un risque accru de malabsorption et de dénutrition sévère (cachexie).\n\n**Prochaines étapes et prise en charge**  \nLe traitement du syndrome de l’intestin court, surtout lorsqu’il est associé à l’absence d’épiploon, repose principalement sur un soutien nutritionnel intensif, souvent par nutrition parentérale (apport direct de nutriments par voie intraveineuse) ou entérale (par sonde digestive). Dans certains cas sévères, des interventions chirurgicales visant à allonger l’intestin restant ou une transplantation intestinale peuvent être nécessaires. Des approches pharmacologiques, telles que l’administration de glutamine, d’hormone de croissance ou de peptides glucagon-like, sont en cours d’évaluation pour améliorer l’adaptation intestinale et la fonction de transport des nutriments. Cependant, ces traitements nécessitent encore des études cliniques approfondies pour confirmer leur efficacité.\n\nLa récupération postopératoire du patient a été favorable, avec une reprise progressive de l’alimentation orale. Ce cas souligne l’importance d’une surveillance étroite après chirurgie intestinale chez des patients présentant des anomalies congénitales rares, afin de détecter rapidement les complications et d’adapter la prise en charge nutritionnelle et chirurgicale."
+        }
+    },
+    {
+        "article": "Un homme de 20 ans travaillant comme fermier, sans antécédents médicaux et chirurgicaux, a été admis au service des urgences se plaignant de douleurs coliques sévères dans la région du flanc droit, irradiant la région environnante et l'aine. La douleur est associée à une fièvre élevée et à des vomissements récurrents. Il a signalé une hématurie indolore, une fièvre et des symptômes pseudo-grippaux 2 semaines avant son admission à l'hôpital. La fièvre et les symptômes pseudo-grippaux avaient été traités avec l'utilisation d'une analgésie. Il n'avait pas d'antécédents de maladie des calculs urinaires ou d'infections des voies urinaires. L'examen physique a révélé une sensibilité dans l'aine droite et une sensibilité positive de l'angle costovértebral droit, sinon, il était normal. Un test complet de numération sanguine, une analyse d'urine, une analyse des selles et une échographie abdominale ont été effectués. L'analyse de laboratoire a révélé une leucocytose modérée de 20 000/mm3 (intervalle normal : 4,5-11 × 103/mm3), une neutrophilie relative et une lymphopénie relative. La créatinine sérique était normale. L'analyse d'urine a révélé une hématurie +3 et des cristaux d'oxalate de calcium. L'analyse des selles a révélé la présence d'Entamoeba histolytica, sans œufs ou vers détectés, et le reste de l'analyse des selles était normal. L'échographie abdominale a révélé une structure cylindrique hyperechoïque de 6 mm de diamètre et de 6 cm de longueur dans la partie distale de l'uretère droit impliquant la jonction urétéro-vésicale (JUV) associée à une hydronéphrose droite minimale et une légère augmentation de l'échogénicité du rein droit. Il n'y a pas de calcul rénal définitif ; sinon, les deux reins sont normaux en taille, site et forme. L'imagerie Doppler n'a pas été réalisée.\n\nIl a été hospitalisé au service d'urologie ; un traitement conservateur a été initialement suivi. Une tomodensitométrie de contraste a été réalisée, qui a montré une structure tubulaire de 6 cm (un corps étranger) située à l'urètre distal environ 2,5 cm à l'intérieur de la vessie. La structure montre une densité de tissu mou dans la paroi et une densité de fluide dans la partie intérieure, ce qui provoque une hydrourénéphrose du côté droit minimale. Une image axiale au niveau de la partie distale de l'urètre droit montre un urètre dilaté et un défaut de remplissage arrondi représentant le parasite obstructeur. Image axiale de la tomodensitométrie au niveau de la jonction vésico-urétérale à 10 minutes de retard, montrant le parasite qui passe partiellement à travers la jonction vésico-urétérale. Sinon, le rein droit est normal en taille, écho-texture et épaisseur corticale, sans calculs ni masses. Il n'y a aucune preuve d'une fistule entre les voies gastro-intestinale et urinaire.\n\nUne urétéroscopie a été réalisée à l'hôpital. Au cours de l'intervention, une structure ressemblant à de la cire de 6 mm a été découverte dans le tiers distal de l'uretère droit, accompagnée d'une quantité importante de pus. En outre, une projection ressemblant à un polype a été observée dans la vue de l'urétéroscope. L'objet extrait mesurait 6 cm de longueur, avait une coloration brune, n'était pas une structure mobile et présentait une consistance élastique serrée. Pour faciliter le drainage du pus, un double J (stent urétéral) a été inséré. Par la suite, l'échantillon mort a été soumis à un examen pathologique, qui l'a identifié comme étant A lumbricoides. La patiente a reçu un comprimé d'albendazole de 400 mg une fois par jour pendant 3 jours et a connu une récupération sans incident.\n",
+        "gold_summary": "Dans ce rapport, nous présentons le cas d'un homme de 20 ans qui est arrivé aux urgences avec de graves douleurs au flanc droit, une forte fièvre et des vomissements récurrents. Des évaluations diagnostiques ont été menées, y compris un test de numération sanguine complète, une analyse d'urine, une analyse des selles, une échographie abdominale et un scanner. Le diagnostic final était A lumbricoides trouvé dans la partie distale de l'uretère. Une procédure d'urétéroscopie a confirmé le diagnostic et a extrait le ver, qui mesurait 6 cm de longueur, avait une couleur brune et présentait une consistance élastique serrée.\n",
+        "synthetic_summary": {
+            "B1": "Un jeune homme avait très mal sur le côté droit du ventre. Il avait aussi de la fièvre et il vomissait souvent. Les docteurs ont fait plusieurs examens pour comprendre ce qui n’allait pas. \n\nIls ont trouvé un gros ver dans un petit tuyau qui va du rein à la vessie. Les docteurs ont enlevé ce ver avec un petit appareil. Après, le jeune homme a pris un médicament et il est devenu mieux.",
+            "B2": "Cas d’un jeune homme de 20 ans avec une douleur sévère au côté droit\n\nUn homme de 20 ans, qui travaille comme fermier et n’avait jamais eu de problème de santé avant, est venu aux urgences. Il avait très mal au côté droit de son ventre, une forte fièvre et il vomissait souvent. Deux semaines avant, il avait eu de la fièvre et des symptômes ressemblant à une grippe, mais il n’avait pas consulté un médecin.\n\nCe qu’ils ont découvert\n\nLes médecins ont fait plusieurs examens : une prise de sang, une analyse d’urine, une analyse des selles, une échographie du ventre et un scanner. La prise de sang montrait une infection avec beaucoup de globules blancs. L’analyse d’urine montrait du sang et des cristaux. L’analyse des selles a trouvé un parasite appelé Entamoeba histolytica. L’échographie et le scanner ont montré une sorte de tube de 6 cm dans l’uretère droit, qui est le canal qui conduit l’urine du rein à la vessie. Ce tube bloquait un peu le passage de l’urine et causait un gonflement léger du rein.\n\nCe que cela signifie et ce qu’ils ont fait\n\nLes médecins ont fait une petite opération appelée urétéroscopie, qui consiste à regarder à l’intérieur de l’uretère avec une caméra. Ils ont trouvé un ver brun de 6 cm qui bloquait l’uretère et une grande quantité de pus. Ils ont retiré ce ver, qui s’appelait Ascaris lumbricoides, un parasite intestinal qui avait migré dans l’uretère. Pour aider à vider le pus et l’urine, ils ont mis un petit tube appelé stent. Ensuite, le patient a pris un médicament antiparasitaire pendant trois jours. Il s’est bien remis sans problème.\n\nEn résumé, ce cas montre qu’un parasite intestinal peut parfois se retrouver dans les voies urinaires et causer une infection grave. Grâce aux examens et à l’opération, le parasite a été enlevé et le patient a guéri.",
+            "B3": "Résumé structuré du cas clinique\n\nContexte  \nUn homme de 20 ans, fermier sans antécédents médicaux notables, a été admis aux urgences pour des douleurs intenses de type colique au flanc droit, irradiant vers l’aine, accompagnées de fièvre élevée et de vomissements répétés. Deux semaines avant son admission, il avait présenté une hématurie (présence de sang dans les urines) indolore, une fièvre et des symptômes pseudo-grippaux, traités uniquement par des analgésiques. Il ne rapportait pas d’antécédents de calculs urinaires ni d’infections urinaires.\n\nPrincipales observations  \nL’examen clinique a révélé une sensibilité marquée au niveau de l’aine droite et une douleur à la percussion de l’angle costovértebral droit, signe souvent associé à une atteinte rénale. Les analyses biologiques ont montré une leucocytose modérée (augmentation des globules blancs à 20 000/mm3), une neutrophilie relative (augmentation des neutrophiles, globules blancs impliqués dans l’inflammation) et une lymphopénie relative (diminution des lymphocytes). La fonction rénale était normale. L’analyse d’urine a confirmé une hématurie importante (+3) et la présence de cristaux d’oxalate de calcium. L’examen parasitologique des selles a détecté Entamoeba histolytica, un parasite intestinal, sans présence d’œufs ou vers. L’échographie abdominale a mis en évidence une structure cylindrique hyperechoïque (très visible à l’échographie) de 6 mm de diamètre et 6 cm de long dans la partie distale de l’uretère droit, au niveau de la jonction urétéro-vésicale (jonction entre l’uretère et la vessie), associée à une légère dilatation des voies urinaires (hydronéphrose) du rein droit et une augmentation modérée de l’échogénicité du rein, sans calcul rénal visible.\n\nInterprétation clinique  \nUne tomodensitométrie (scanner) avec injection de contraste a confirmé la présence d’une structure tubulaire de 6 cm dans l’uretère distal, partiellement située dans la vessie, provoquant une obstruction responsable de l’hydronéphrose. Cette structure présentait une densité de tissu mou en périphérie et une densité liquidienne en son centre, compatible avec un corps étranger. L’urétéroscopie (examen endoscopique de l’uretère) a permis de visualiser et d’extraire un objet brun, de consistance élastique, mesurant 6 cm, obstruant l’uretère distal et accompagné de pus. Une projection polypoïde (semblable à un polype) a également été observée. L’analyse anatomopathologique a identifié cet objet comme étant un ver parasite, Ascaris lumbricoides, un nématode intestinal rarement retrouvé dans les voies urinaires.\n\nProchaines étapes et traitement  \nAprès extraction du parasite, un stent urétéral double J a été placé pour assurer le drainage urinaire et prévenir une obstruction persistante. Le patient a reçu un traitement antiparasitaire par albendazole (400 mg par jour pendant 3 jours). L’évolution clinique a été favorable, avec une récupération complète sans complications.\n\nConclusion  \nCe cas illustre une localisation exceptionnelle d’Ascaris lumbricoides dans l’uretère distal, responsable d’une obstruction urinaire aiguë avec hydronéphrose et infection. Le diagnostic repose sur l’imagerie et la confirmation endoscopique, tandis que le traitement combine extraction mécanique et antiparasitaire. Cette observation souligne l’importance de considérer les causes parasitaires dans les douleurs urinaires obstructives, notamment dans les zones à risque."
+        }
+    },
+    {
+        "article": "Une patiente de 27 ans a présenté une rougeur, des démangeaisons et des brûlures de l’œil droit quatre heures après avoir reçu sa troisième dose totale de vaccin de rappel à ARN messager contre la COVID-19. Elle a utilisé des larmes artificielles, mais ses symptômes sont restés inchangés le jour suivant, ce qui l’a incitée à consulter un ophtalmologue. Elle a nié une photophobie, une vision floue, une vision double, une sensation de corps étranger, une épiphorie, des éclairs de lumière ou des corps flottants. Il n’y a pas eu d’épisodes similaires antérieurs avec le même vaccin avant les deux doses. L’œil gauche était asymptomatique et non affecté. Les antécédents médicaux de la patiente étaient importants pour l’astigmatisme myopique des deux yeux, la conjonctivite allergique bilatérale, la rhinite allergique, la maladie de Crohn et l’asthme intermittent modéré.\n\nL'examen ophtalmologique a révélé une acuité visuelle corrigée de 20/20 bilatéralement. Les pressions intraoculaires mesurées étaient de 15 mmHg dans l'œil droit et de 16 mmHg dans l'œil gauche. La conjonctive droite avait une injection 2+ qui blanchissait avec des gouttes de phényléphrine. Il n'y avait pas d'injection sclérale, pas de sensibilité sclérale, et pas d'irritation physique adjacente à la zone de l'épisclérite (par exemple, pas de trichiasis). La chambre antérieure de l'œil droit paraissait profonde et calme. L'épisclérite associée a été décrite. Le reste de l'examen clinique des segments antérieur et postérieur était sans importance. La patiente a continué à utiliser des larmes artificielles et a commencé à prendre de l'ibuprofène 200 mg trois fois par jour pendant une semaine. La patiente a respecté et toléré le régime décrit et une semaine plus tard, tous les symptômes oculaires et signes ont disparu.\n\nLa patiente était satisfaite des soins qu'elle a reçus. Elle était soulagée que ses symptômes aient disparu et que sa vision finale n'ait pas été affectée. Elle prévoit de vérifier auprès de son rhumatologue avant les prochaines doses de vaccin de rappel COVID-19. Le consentement éclairé écrit a été obtenu de la patiente pour publication et pour l'utilisation des données et des images.\n",
+        "gold_summary": "Une femme de 27 ans a présenté un œil rouge, des démangeaisons et des brûlures d'un jour. La patiente a déclaré avoir développé ces symptômes dans les 3 à 4 heures suivant la vaccination. Ses antécédents médicaux étaient pertinents pour la maladie de Crohn. L'examen ophtalmologique a révélé une injection conjonctivale droite 2+ qui blanchissait avec des gouttes de phényléphrine. Sinon, son examen ophtalmologique était sans importance. La patiente a commencé à utiliser des larmes artificielles et de l'ibuprofène 200 mg trois fois par jour pendant une semaine. Après une semaine, tous les symptômes ont disparu et l'examen ophtalmologique est revenu à la ligne de base.\n",
+        "synthetic_summary": {
+            "B1": "Une jeune femme avait un œil rouge qui piquait et brûlait. Cela est arrivé peu de temps après qu’elle a reçu un vaccin. \n\nLe docteur a regardé son œil. Il a vu que l’œil était un peu rouge, mais tout allait bien autrement. \n\nElle a pris des gouttes et un médicament pour aider. Après une semaine, son œil allait mieux. \n\nElle était contente parce que son œil n’avait plus mal et qu’elle voyait bien.",
+            "B2": "Une jeune femme de 27 ans a eu l’œil droit rouge, qui la démangeait et la brûlait, environ 3 à 4 heures après avoir reçu sa troisième dose de vaccin contre la COVID-19. Elle avait déjà des problèmes de santé comme la maladie de Crohn, mais n’avait jamais eu ce genre de symptômes avant. Lors de l’examen chez l’ophtalmologue, on a vu que la partie blanche de son œil droit était très rouge, mais cette rougeur pouvait s’atténuer avec des gouttes spéciales appelées phényléphrine. À part cela, son œil semblait normal et sa vue n’était pas affectée. \n\nPour la soigner, elle a utilisé des larmes artificielles, qui sont des gouttes pour hydrater l’œil, et elle a pris un médicament contre la douleur et l’inflammation appelé ibuprofène, trois fois par jour pendant une semaine. Une semaine plus tard, tous ses symptômes avaient disparu et son œil était redevenu normal. Elle était contente que sa vision ne soit pas touchée et prévoit de parler avec son médecin avant de recevoir une autre dose de vaccin.",
+            "B3": "Résumé détaillé et structuré pour un public non médical éduqué\n\n**Contexte**  \nUne femme âgée de 27 ans a présenté une rougeur, des démangeaisons et une sensation de brûlure au niveau de son œil droit, apparues environ quatre heures après avoir reçu sa troisième dose de vaccin à ARN messager contre la COVID-19. Ces symptômes sont survenus rapidement après la vaccination, alors qu’elle n’avait jamais eu de réaction similaire lors des deux premières injections. Ses antécédents médicaux comprenaient notamment une maladie de Crohn, un astigmatisme myopique (une anomalie de la vision), une conjonctivite allergique bilatérale, une rhinite allergique et un asthme intermittent modéré. Elle n’a pas rapporté de troubles visuels tels que vision floue ou double, ni de douleur intense ou de sensibilité à la lumière.\n\n**Principales observations cliniques**  \nL’examen ophtalmologique a montré que sa vision corrigée était normale (20/20) dans les deux yeux. La pression à l’intérieur de l’œil droit était de 15 mmHg, ce qui est dans la norme, et de 16 mmHg dans l’œil gauche. La conjonctive (la membrane qui recouvre l’œil) de l’œil droit présentait une rougeur modérée (notée 2+), qui diminuait après instillation de gouttes de phényléphrine, un médicament vasoconstricteur. Il n’y avait pas d’inflammation de la sclère (la partie blanche de l’œil), ni de sensibilité ou d’irritation locale. La chambre antérieure de l’œil (espace rempli de liquide entre la cornée et l’iris) était normale et calme. L’examen a permis d’identifier une épisclérite, une inflammation bénigne de la couche superficielle de la sclère, sans autre anomalie notable dans les segments antérieur et postérieur de l’œil.\n\n**Interprétation clinique**  \nLes symptômes et les signes observés sont compatibles avec une épisclérite aiguë, probablement déclenchée par la vaccination. Cette inflammation superficielle est généralement bénigne et réversible. L’absence de symptômes plus graves ou de complications visuelles a permis d’écarter d’autres diagnostics plus sévères.\n\n**Prise en charge et évolution**  \nLa patiente a poursuivi l’utilisation de larmes artificielles pour apaiser l’œil et a commencé un traitement anti-inflammatoire oral avec de l’ibuprofène à la dose de 200 mg, trois fois par jour, pendant une semaine. Ce traitement a été bien toléré et respecté. Une semaine plus tard, tous les symptômes oculaires avaient disparu et l’examen ophtalmologique était revenu à la normale.\n\n**Prochaines étapes**  \nLa patiente s’est déclarée satisfaite des soins reçus et soulagée de la disparition complète des symptômes sans atteinte de sa vision. Elle prévoit de consulter son rhumatologue avant de recevoir d’éventuelles futures doses de rappel du vaccin contre la COVID-19 afin d’évaluer les risques et les précautions à prendre. Un consentement éclairé a été obtenu pour la publication de ces données."
+        }
+    },
+    {
+        "article": "Nous décrivons une femme de 25 ans chez qui on a diagnostiqué une AD depuis l'enfance et une apparition ultérieure de vitiligo lentement progressif à l'âge de 16 ans. Au début de l'examen, la patiente présentait une xérose cutanée diffuse, des papules excoriées et des plaques sur le dos, et des lésions érythémateuses lichénifiées sur les membres supérieurs et le dos des mains avec un indice de gravité et de surface de l'eczéma (EASI) de 18. La patiente a rapporté des démangeaisons intenses (échelle de numérotation des démangeaisons [NRS] = 10). Des macules achromiques confluentes évoquant un vitiligo étaient également présentes sur les coudes et sur le visage, principalement dans la région des paupières, bilatéralement. La patiente présentait également de multiples macules achromiques de forme irrégulière sur le cou, le tronc et le dos des mains, et des manifestations hypopigmentées initiales dans la région axillaire gauche et le genou gauche avec un indice de gravité et de surface de l'eczéma (VASI) de 0,45. Les deux affections cutanées ont eu un impact sur sa qualité de vie, ce qui a entraîné un indice de qualité de vie dermatologique (DLQI) de 17.\n\nLes traitements antérieurs pour la DA comprenaient des corticostéroïdes topiques et systémiques, des inhibiteurs topiques de la calcineurine, des antihistaminiques et un court traitement par cyclosporine, qui a été abandonné en raison d'une intolérance. Les traitements antérieurs pour le vitiligo comprenaient un traitement à court terme par des corticostéroïdes topiques et systémiques au début de la maladie et, pendant les 2 premières années, sans résultats. Par la suite, le tacrolimus, un inhibiteur topique de la calcineurine, a été utilisé pendant plusieurs années suivant un régime d'entretien pulsé proactif après une période d'induction initiale, donnant des bénéfices thérapeutiques minimes. Des antioxydants et des produits à base de vitamines ont également été utilisés comme traitements adjuvants. Pour des raisons logistiques, le patient a refusé la photothérapie.\n\nÉtant donné la coexistence de la DA et du vitiligo, et compte tenu des avantages potentiels supplémentaires, une thérapie systémique avec 15 mg d'upadacitinib par jour a été initiée après des évaluations médicales et de laboratoire pour exclure la grossesse et d'autres contre-indications. Sur la base de l'indication approuvée de l'upadacitinib pour la DA, nous avons opté pour un début de traitement en vue d'atteindre la dose efficace la plus faible.\n\nUne amélioration progressive de la DA a été observée après les premières semaines de traitement avec une rémission clinique à la semaine 16 (EASI 0 ; NRS 0) associée à une amélioration de la qualité de vie (DLQI 0). Dans le même temps, une nette amélioration du vitiligo a été observée avec une repigmentation complète des zones acromiques du cou, du tronc, du dos des mains et des coudes (Fig. 1b), et une repigmentation partielle mais significative des patches acromiques de la région des paupières (Fig. 2b) (VASI = 0.25). Une rémission presque complète du vitiligo a été obtenue à la semaine 28 de traitement et a été maintenue jusqu'à 1 an de suivi, sans effets secondaires, à l'exception d'une légère aggravation de l'acné, facilement contrôlée par des traitements topiques.\n",
+        "gold_summary": "Nous décrivons une femme de 25 ans chez qui on a diagnostiqué une AD depuis l'enfance et une apparition ultérieure de vitiligo lentement progressif à l'âge de 16 ans. Une thérapie systémique avec l'inhibiteur de JAK1 upadacitinib 15 mg par jour a été commencée, après une évaluation médicale et de laboratoire pour exclure une grossesse et d'autres contre-indications. Une amélioration progressive de l'AD a été observée après les premières semaines de traitement avec une rémission clinique à la semaine 16. Dans le même temps, une nette amélioration du vitiligo a été observée avec une rémission presque complète atteinte à la semaine 28 de traitement.\n",
+        "synthetic_summary": {
+            "B1": "Il y a une dame qui avait la peau qui grattait beaucoup depuis qu'elle était petite. Elle avait aussi des taches blanches sur la peau qui sont venues quand elle avait 16 ans.\n\nLes docteurs lui ont donné un médicament pour aider sa peau. Ce médicament a commencé à faire du bien après quelques semaines.\n\nAprès un peu plus de trois mois, sa peau qui grattait était presque guérie. Et ses taches blanches ont aussi beaucoup disparu après environ six mois.\n\nElle a continué à aller mieux sans problème. Les docteurs étaient contents car elle se sentait mieux.",
+            "B2": "Voici un résumé adapté pour un adolescent de 14 ans en classe de biologie :\n\n**Ce qu'ils ont observé**  \nUne femme de 25 ans avait deux problèmes de peau : une dermatite atopique (AD), qui est une maladie causant des démangeaisons et des plaques rouges, depuis son enfance, et un vitiligo, qui fait disparaître la couleur de la peau en formant des taches blanches, apparu vers ses 16 ans.  \n\n**Le traitement utilisé**  \nLes médecins lui ont donné un médicament appelé upadacitinib, qui agit sur certaines protéines dans le corps pour réduire l’inflammation. Ce médicament se prend en comprimé, 15 mg par jour. Avant de commencer, ils ont fait des tests pour s’assurer qu’elle n’était pas enceinte et qu’elle pouvait prendre ce traitement sans danger.  \n\n**Les résultats du traitement**  \nAprès quelques semaines, la dermatite s’est beaucoup améliorée, et au bout de 16 semaines, elle avait presque complètement disparu. En même temps, le vitiligo s’est aussi amélioré : la couleur de la peau est revenue sur plusieurs zones blanches. Après 28 semaines, le vitiligo avait presque totalement disparu. Cette amélioration est restée stable pendant un an, avec seulement un léger problème d’acné qui a été facile à soigner.  \n\nEn résumé, ce médicament a aidé cette patiente à guérir ses deux maladies de peau en même temps, ce qui est une bonne nouvelle pour les personnes qui ont ces problèmes.",
+            "B3": "Résumé détaillé et structuré :\n\n**Contexte**  \nNous rapportons le cas d’une femme de 25 ans présentant une dermatite atopique (DA) diagnostiquée durant l’enfance, associée à un vitiligo d’apparition progressive à partir de l’âge de 16 ans. Lors de l’examen initial, la patiente présentait une sécheresse cutanée étendue, des lésions caractéristiques de la DA avec un score EASI (indice de gravité et de surface de l’eczéma) de 18, ainsi que des macules dépigmentées typiques du vitiligo, notamment sur le visage, les coudes, le cou et d’autres zones, avec un score VASI (indice de gravité et de surface du vitiligo) de 0,45. Ces deux affections cutanées avaient un impact significatif sur sa qualité de vie, évaluée par un score DLQI (indice de qualité de vie dermatologique) de 17.\n\n**Traitements antérieurs**  \nLa patiente avait reçu divers traitements pour sa dermatite atopique, incluant des corticostéroïdes topiques et systémiques, des inhibiteurs topiques de la calcineurine, des antihistaminiques, ainsi qu’un court traitement par cyclosporine interrompu en raison d’intolérance. Pour le vitiligo, des corticostéroïdes topiques et systémiques avaient été utilisés sans succès notable, suivis d’un traitement prolongé par tacrolimus topique avec des bénéfices minimes. Des antioxydants et des compléments vitaminiques avaient également été employés. La photothérapie a été refusée pour des raisons logistiques.\n\n**Intervention thérapeutique et résultats**  \nFace à la coexistence de la DA et du vitiligo, une thérapie systémique par upadacitinib, un inhibiteur sélectif de la Janus kinase 1 (JAK1), a été initiée à la dose de 15 mg par jour, après une évaluation médicale et biologique rigoureuse excluant la grossesse et d’autres contre-indications. Ce traitement est approuvé pour la DA, et la dose choisie visait à atteindre l’efficacité optimale avec le minimum d’exposition.\n\nUne amélioration progressive de la dermatite atopique a été observée dès les premières semaines, avec une rémission clinique complète à la semaine 16, confirmée par un score EASI à 0 et une disparition totale des démangeaisons (NRS = 0), ainsi qu’une amélioration totale de la qualité de vie (DLQI = 0). Parallèlement, une amélioration significative du vitiligo a été constatée, avec une repigmentation complète des zones dépigmentées du cou, du tronc, du dos des mains et des coudes, et une repigmentation partielle mais notable des paupières, réduisant le score VASI à 0,25. À la semaine 28, la patiente présentait une rémission quasi complète du vitiligo, qui a été maintenue jusqu’à un an de suivi.\n\n**Effets secondaires**  \nLe traitement a été bien toléré, sans effets indésirables majeurs. Une légère poussée d’acné est survenue, facilement contrôlée par des traitements topiques.\n\n**Prochaines étapes**  \nCe cas illustre le potentiel bénéfique de l’upadacitinib non seulement sur la dermatite atopique mais également sur le vitiligo, suggérant une voie thérapeutique prometteuse pour les patients présentant ces deux affections concomitantes. Un suivi à long terme est nécessaire pour confirmer la durabilité des résultats et la sécurité du traitement."
+        }
+    },
+    {
+        "article": "Patient et observation\nInformations relatives au patient (présentation du patient): il s'agit d'un jeune homme de 28 ans célibataire sans enfant, militaire en activité. Présente depuis 5 semaines, des douleurs abdominales d'installation progressive plus marquées à l'épigastre et l'hypochondre droite, suivi peu de temps après par une fièvre non chiffrée, des frissons, sueurs profuses dans un contexte d'anorexie et d'amaigrissement chiffré à 6kgs. Notons que le patient n'est pas alcoolo-tabagique, vacciné au BCG ne présentant aucun autre antécédent personnel ou familial contributif.\n\nRésultats cliniques: à l'admission, l'examen physique a retrouvé le patient dans un état général altéré, asthénique avec un amaigrissement chiffré à 6kgs sur un mois. Un syndrome inflammatoire à réponse systémique clinique était présent avec comme éléments: une fièvre à 39,1°C, une tachycardie (124 battements/min), une polypnée (22 cycles/min). L'examen pulmonaire et l'exploration des aires ganglionnaires superficielles étaient sans particularité. Au niveau abdominal, une sensibilité modérée à l'hypochondre droite avec une hépatomégalie a été retrouvée.\n\nChronologie: remonte à février 2022 par l'installation d'une douleur abdominale diffuse avec trouble du transite à type de diarrhée-constipation, le tout dans un contexte de conservation de l'état général avec fébricule à prédominance nocturne. Un traitement syntagmatique a été instauré sans succès. L'évolution est marquée par la persistance de la fébricule associée à une anorexie et un amaigrissement progressif chiffré à 12kgs sur trois mois. Devant ce trouble du transit avec fièvre inexpliquée et la dégradation de l'état général le patient sera admis aux urgences pour meilleure investigation.\n\nDémarche diagnostique: dès son admission, des bilans ont été réalisés rapportant un syndrome infectieux biologique une hyperleucocytose (17800 élts/mm3) à prédominance neutrophile (14000 élts/mm3) et une protéine C-réactive élevée à 323 mg/L.\n\nFace à sa douleur abdominale, la lipasémie et la troponine réalisées sont revenues normales respectivement 38 UI/L (VN: <3 78 UI/L) et 4 ng/L (VN: 2 à 16 ng/L). Le bilan hépatique stable avec des ALAT (Alanine amino-transférase) à 22 UI/L (VN: < 40UI/L), des ASAT (Aspartate amino-transférase) à 17 UI/L (VN: < 35UI/L), des GGT (Gamma glutamyl transférase) à 42 UI/L (VN: < 50UI/L), PAL (Phosphatases alcalines) à 115 UI/L (VN: 40- 150 UI/L) et une bilirubinémie normale. La fonction hépatique était normale avec un taux de prothrombine à 78% et une albuminémie à 39 g/L. L'ionogramme sanguin ainsi que la fonction rénale sont revenus normaux. La radiographie du thorax et l'échographie abdominale réalisés sans particularité.\n\nAvec une procalcitonine positive à 4,1ng/L, un bilan infectieux à la recherche du foyer infectieux a été initié entre autres un examen cytobactériologique des urines et des hémocultures lors des pics fébriles à 39°C qui sont tous deux revenus négatifs. Les sérologies hépatites virales B, C et VIH, ainsi que la sérologie de la syphilis réalisée en hospitalisation étaient toutes négatives. La lactate déshydrogénase (LDH) et la béta-2 microglobuline étaient normales respectivement 231 UI/L et 2,28 mg/L. Le GeneXpert à la recherche du Mycobactérium sur ces pièces biopsiques était négatif. Le quantiféron était revenu négatif. La recherche du Mycobactérium sur les expectorations matinales de 3 jours consécutifs était négative.\n\nSur le plan morphologique, un scanner thoraco-abdomino-pelvien a montré au niveau de l'étage abdominal, un foie augmenté de taille (flèche hépatique à 17cm), siège de multiples lésions hypodenses tissulaire, arrondies bien limitées, non rehaussées après injection du produit de contraste dont les plus volumineuses siègent au segment I (21 x 16mm) et au segment V (36 x 27mm). Au niveau des étages thoracique et pelvien, aucune lésion suspecte n'a été mise en évidence. Des premières biopsies hépatiques obtenues par ponction écho-guidée ont révélées à l'examen histologique des lésions hépatiques fibro-inflammatoires subaiguës, sans indice histologique de spécificité ou de malignité.\n\nUne IRM hépatique à la suite du scanner a objectivé un foie dysmorphique, siège de lésions en signal hétérogène T2 entourée d'une paroi en hypersignal T2, rehaussée en périphérie après injection du produit de contraste dont les plus volumineuses siègent au segment I (20 x 22mm) et au segment V (33 x 31mm). Aucune adénopathie profonde n'avait été objectivée, aussi bien au scanner qu'à l'IRM. Une cœlioscopie diagnostique réalisée sur les nodules hépatiques, l'examen histologique a retrouvé des granulomes épithélioides et gigantocellulaires de taille variable avec nécrose caséeuse en faveur d'une tuberculose hépatique.\n\nIntervention thérapeutique: le patient a été mis sous traitement antituberculeux selon le protocole standard pendant mois à savoir: Phase 1: quadrithérapie (Isoniazide + Rifampicine + Pyrazinamide + Ethambutol) en une seule prise orale chaque matin à jeun pendant 2 mois. Phase 2: bithérapie (Isoniazide + Rifampicine) en une seule prise orale chaque matin à jeun pendant 4 mois\n\nSuivi et résultats des interventions thérapeutiques: dès les premiers jours du traitement, une bonne réponse a été obtenue avec disparition du syndrome inflammatoire à réponse systémique tant sur le plan clinique que biologique. Au bout de trois mois de traitement, un scanner hépatique de contrôle a montré une diminution du nombre et du volume des lésions hépatiques.",
+        "gold_summary": "Ce cas clinique rapporté chez un jeune marocain, se présentant dans un tableau de colique hépatique évoluant depuis un mois associé à des signes frustres d'imprégnation tuberculeuse. Des lésions nodulaires hépatiques non spécifiques ont été révélées au scanner et à l'imagerie par résonance magnétique (IRM) hépatique. Le diagnostic de tuberculose hépatique focale a été confirmé après analyse anatomopathologique sur biopsies des nodules hépatiques obtenues au décours d'une cœlioscopie. Après début du traitement anti bacillaire bien conduit, une bonne amélioration clinico-biologique a été obtenue.",
+        "synthetic_summary": {
+            "B1": "Un jeune homme avait mal au ventre depuis longtemps. Il avait aussi de la fièvre et il perdait du poids. \n\nLe docteur a fait des images de son ventre. Il a vu des petites taches dans son foie. \n\nLe docteur a pris un petit bout du foie pour regarder de près. Il a trouvé une maladie appelée tuberculose. \n\nLe jeune homme a pris des médicaments pour guérir. Très vite, il s’est senti mieux. Les taches dans son foie ont diminué.",
+            "B2": "### Ce qu'ils ont trouvé chez le patient\n\nUn jeune homme de 28 ans a eu pendant plusieurs semaines des douleurs au ventre, surtout dans la partie droite sous les côtes, avec de la fièvre, des sueurs et une perte de poids importante. Les examens ont montré que son foie était plus gros que la normale et qu’il avait plusieurs petites lésions (zones anormales) à l’intérieur. Ces lésions n’étaient pas clairement identifiées par les premières analyses.\n\n### Ce que cela signifie\n\nPour comprendre ce qui causait ces problèmes, les médecins ont fait une biopsie, c’est-à-dire qu’ils ont prélevé un petit morceau de tissu du foie pour l’examiner au microscope. Ils ont découvert des granulomes, qui sont des groupes de cellules formés quand le corps essaie de combattre une infection. Ces granulomes avaient une nécrose caséeuse, une sorte de tissu mort typique de la tuberculose. Cela a confirmé que le patient avait une tuberculose dans le foie, appelée tuberculose hépatique focale.\n\n### Le traitement et les résultats\n\nLe patient a reçu un traitement spécial contre la tuberculose, avec plusieurs médicaments pris pendant six mois. Très rapidement, ses symptômes ont disparu et les analyses sont redevenues normales. Après trois mois, une nouvelle imagerie a montré que les lésions dans le foie avaient diminué en taille et en nombre. Cela montre que le traitement a bien fonctionné.",
+            "B3": "Résumé détaillé et structuré\n\nContexte  \nUn homme de 28 ans, militaire en activité, sans antécédents médicaux notables, a présenté depuis cinq semaines des douleurs abdominales progressives localisées principalement à l’épigastre et à l’hypochondre droit. Ces symptômes étaient accompagnés d’une fièvre élevée, de frissons, de sueurs abondantes, d’une perte d’appétit et d’un amaigrissement important de 6 kg en un mois. Le patient ne consommait ni alcool ni tabac et avait été vacciné contre la tuberculose (BCG).\n\nPrincipales observations  \nÀ l’admission, l’examen clinique a révélé un état général altéré avec une fièvre à 39,1 °C, une accélération du rythme cardiaque (tachycardie à 124 battements/min) et une respiration rapide (polypnée à 22 cycles/min). L’examen pulmonaire et ganglionnaire était normal, mais une sensibilité modérée à l’hypochondre droit ainsi qu’une augmentation de la taille du foie (hépatomégalie) étaient présentes.  \nLes analyses biologiques ont montré un syndrome inflammatoire marqué par une hyperleucocytose à prédominance neutrophile et une protéine C-réactive très élevée (323 mg/L). Les enzymes pancréatiques et cardiaques étaient normales, tout comme les tests hépatiques et la fonction rénale. La radiographie thoracique et l’échographie abdominale n’ont pas révélé d’anomalies.  \nUn bilan infectieux approfondi, incluant des hémocultures, des analyses d’urine, des sérologies virales (hépatites B et C, VIH) et une recherche de mycobactéries par différentes méthodes (GeneXpert, quantiféron, expectorations) est resté négatif.  \nL’imagerie par scanner a montré un foie augmenté de volume avec plusieurs lésions nodulaires hypodenses bien limitées, sans prise de contraste, localisées notamment aux segments I et V. L’IRM hépatique a confirmé ces lésions, qui apparaissaient hétérogènes en signal T2 avec une paroi périphérique rehaussée. Aucune adénopathie profonde n’a été détectée.  \nLes premières biopsies hépatiques par ponction ont révélé une inflammation fibro-inflammatoire subaiguë sans signes spécifiques ni malignité. Une cœlioscopie diagnostique a permis la biopsie des nodules hépatiques, dont l’analyse histologique a mis en évidence des granulomes épithélioïdes et gigantocellulaires avec nécrose caséeuse, caractéristique d’une tuberculose hépatique focale.\n\nInterprétation clinique  \nLe tableau clinique associant douleurs hépatiques, fièvre prolongée, amaigrissement et lésions nodulaires hépatiques a orienté vers une tuberculose hépatique, diagnostic confirmé par l’examen anatomopathologique des biopsies obtenues par cœlioscopie. L’absence de signes pulmonaires et la négativité des tests microbiologiques classiques soulignent la difficulté diagnostique de cette forme extrapulmonaire de tuberculose.\n\nProchaines étapes  \nLe patient a été traité selon le protocole antituberculeux standard, comprenant une phase initiale de quadrithérapie (isoniazide, rifampicine, pyrazinamide, éthambutol) pendant deux mois, suivie d’une bithérapie (isoniazide et rifampicine) pendant quatre mois. Dès les premiers jours, une amélioration clinique et biologique significative a été observée, avec disparition du syndrome inflammatoire systémique. Après trois mois de traitement, un scanner de contrôle a montré une réduction du nombre et de la taille des lésions hépatiques, témoignant de l’efficacité du traitement.\n\nEn résumé, ce cas illustre une tuberculose hépatique focale chez un jeune adulte, diagnostiquée grâce à une approche multidisciplinaire incluant imagerie avancée et biopsie cœlioscopique, et répondant favorablement à un traitement antituberculeux bien conduit."
+        }
+    },
+    {
+        "article": "Le patient était un Japonais de 59 ans ayant une histoire de diabète de type 1 de 28 ans. Il visitait notre hôpital tous les mois pour la gestion du diabète avec une thérapie intensive utilisant des injections d'insuline à doses multiples. Sa taille et son poids étaient de 168 cm et 52 kg (indice de masse corporelle : 18,4 kg/m2), respectivement. Il a présenté une sécrétion d'insuline déplétée (le niveau de C-peptide sérique était inférieur à la limite de détection), de sorte que ses taux de glycémie fluctuaient sévèrement, et son taux d'hémoglobine A1c (HbA1c) était d'environ 9,0 % malgré une thérapie intensive d'insuline. Il avait été diagnostiqué avec une régurgitation aortique sévère asymptomatique chronique (grade III) 16 ans avant la présentation actuelle, mais avait refusé un suivi pour la régurgitation aortique. Il n'avait jamais subi d'opération chirurgicale ni l'implantation de dispositifs prothétiques.\n\nHuit jours après sa visite régulière à l'hôpital, il a consulté une clinique d'urgence se plaignant de difficultés respiratoires et avait une fièvre supérieure à 38℃. Jusqu'à ce jour, il n'avait pas remarqué de fièvre, de frissons, de faiblesse ou d'autres symptômes. Sa tension artérielle et son pouls étaient de 192/82 mmHg et 118/min, respectivement. Il présentait une orthopnée et sa saturation en oxygène (SpO2) était de 80%. Il a été transporté au service des urgences de notre hôpital. Un examen physique a révélé un murmure systolique de Levine 3/6, bien que son murmure cardiaque n'ait pas été vérifié lors des visites régulières à l'hôpital. Aucune constatation physique suggérant une IE, telle que les nœuds d'Osler, les lésions de Janeway ou les pétéchies conjonctivales, n'a été reconnue. Son nombre de globules blancs (WBC) a été nettement augmenté à 20 800 /μL, et sa protéine C-réactive (CRP) a été élevée à 6,06 mg/dL. La créatine phosphokinase MB sérique était dans la plage normale, à 6,0 IU/L, et la troponine T était négative. La radiographie thoracique a montré une congestion pulmonaire avec un élargissement cardiaque (rapport cardiothoracique : 55%). L'électrocardiographie a révélé une élévation du ST sur V1-V4, mais l'échocardiographie d'urgence n'a révélé aucune dysfonction de la contractilité cardiaque. Il a été diagnostiqué avec une insuffisance cardiaque aiguë due à une maladie valvulaire, et un traitement par ventilation positive non invasive et nitrates a été initié.\n\nAprès admission à l'hôpital, un examen détaillé par échocardiographie transthoracique a montré une grave régurgitation aortique, une grave régurgitation mitrale et une végétation mobile sur la valve mitrale. L'échocardiographie transœsophagienne a révélé une végétation mobile de 16,5 × 6 mm sur la valve mitrale antérieure et une végétation non mobile de 11,2 × 5 mm sur la cuspide non coronaire de la valve aortique. Ces résultats ont soulevé de fortes suspicions de NVP. Dans ce cas, la tomographie par ordinateur (CT) et l'imagerie par résonance magnétique n'ont révélé aucun infarctus cérébral ou hémorragie, bien qu'une végétation mobile ait été détectée.\n\nEn examinant l'évolution clinique jusqu'à l'hospitalisation, nous avons noté que lors de la visite quatre mois avant l'admission, son nombre de globules blancs était légèrement élevé. Le mois suivant, son taux d'albumine (Alb) était tombé à 3,0 g/dL, et son taux d'hémoglobine (Hb) avait diminué progressivement au cours des 2 mois précédant l'admission. Au cours de cette période, il avait perdu 4 kg. Une oesophagogastroduodénoscopie et une tomodensitométrie du corps entier ont été effectuées, mais aucune anomalie n'a été détectée. Un mois plus tard, il avait regagné un peu de poids, et les résultats de laboratoire étaient presque normaux, à l'exception d'un taux de CRP légèrement élevé (0,54 mg/dL). À la dernière visite (8 jours avant l'admission), son nombre de globules blancs était de nouveau monté à 9 300 /μL, tandis que ses taux d'hémoglobine et d'albumine étaient de nouveau tombés à 13,1 g/dL et 3,0 g/dL, respectivement. En outre, son taux de CRP était passé à 4,18 mg/dL. À ce moment-là, sa tension artérielle diastolique avait manifesté une baisse évidente. Jusqu'à présent, il n'avait pas connu de fièvre ou de symptômes autres que la perte de poids. Nous avons soupçonné des maladies d'origine infectieuse et/ou maligne et avons initié des examens complets pour identifier la source de ses résultats cliniques.\n\nAprès le début du traitement de l'insuffisance cardiaque, ses symptômes cliniques ont rapidement diminué et sa stabilité hémodynamique a été maintenue pendant les six premières heures. Il a initialement reçu une antibiothérapie empirique intraveineuse consistant en 12 g/jour d'ampicilline sulbactam (ABPC/S) et 120 mg/jour de gentamycine (GM). Trois ensembles de cultures sanguines ont été obtenus à l'admission, et tous étaient positifs pour S. warneri [concentration inhibitrice minimale (CIM) à ABPC/S ≤8 μg/mL ; CIM à GM ≤1 μg/mL ; CIM à cefazolin (CEZ) ≤2 μg/mL]. Ainsi, l'IE causée par cet organisme a été diagnostiquée.\n\nSelon la directive clinique établie par la Japanese Circulation Society, la chirurgie d'urgence est généralement recommandée pour l'insuffisance cardiaque de NYHA III à IV ou la chirurgie urgente pour la végétation mobile de l'EVE dépassant 10 mm et le dysfonctionnement sévère de la valve. Dans ce cas, cependant, son insuffisance cardiaque a été améliorée avec succès. Sur la base de la directive, le risque d'embolie a été considéré comme ayant été réduit par l'administration d'une antibiothérapie appropriée. En outre, le patient avait un diabète de type 1, et son contrôle glycémique était si mauvais que nous craignions que la chirurgie à double valve ne soit une procédure à haut risque. Par conséquent, nous avons planifié une chirurgie élective après un contrôle suffisant de l'infection et du diabète.\n\nEn fonction des résultats de la culture sanguine, le régime antibiotique a été changé pour 6 g/jour de CEZ. Un examen dentaire détaillé n'a révélé aucune anomalie, telle que la parodontite. Après quatre semaines de traitement antibiotique, il a subi une intervention chirurgicale. Sa valve aortique s'est avérée bicuspide, et les anneaux aortiques et mitraux étaient intacts sans formation d'abcès. De grandes végétations ont été exentérées, et les valves aortiques et mitrales ont été remplacées par des valves mécaniques. Il n'a pas eu de complications postopératoires et a été renvoyé à la maison le 22e jour après l'opération sans embolie apparente. Il n'a pas eu de récidive depuis plus de deux ans après l'opération.",
+        "gold_summary": "Un homme de 59 ans atteint de diabète de type 1 a présenté une insuffisance cardiaque. L'échocardiographie a montré de grandes végétations sur les valves mitrale et aortique. La culture bactérienne sanguine était positive pour Staphylococcus warneri, un membre de la famille des staphylocoques coagulase-négatifs (CoNS). Il a été diagnostiqué avec une endocardite valvulaire native (NVE) induite par les bactéries résidentes et a finalement subi un double remplacement valvulaire. Rétrospectivement, de légères anomalies des données de laboratoire et une perte de poids débutant quatre mois auparavant ont peut-être été des signes de NVE. Il n'avait pas d'antécédents de thérapies immunosuppressives ou d'implantation de dispositifs médicaux.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 59 ans était très malade parce que son cœur ne marchait pas bien. Dans son cœur, il y avait des petites boules qui ne devraient pas être là. Ces boules étaient faites par des petites bêtes appelées bactéries.\n\nLe docteur a trouvé ces bactéries dans son sang. Elles venaient de son propre corps. Le monsieur a dû avoir une opération pour changer deux parties de son cœur. \n\nAvant d’être très malade, il avait perdu un peu de poids et ses analyses montraient que quelque chose n’allait pas. Mais il n’avait jamais eu d’autres maladies graves ou d’opérations avant. \n\nMaintenant, il va mieux après son opération.",
+            "B2": "**Ce qu'ils ont trouvé**  \nUn homme japonais de 59 ans, qui avait un diabète de type 1 depuis 28 ans, est venu à l’hôpital parce qu’il avait des problèmes au cœur. Des examens ont montré qu’il avait de grosses \"végétations\" sur deux valves importantes de son cœur, la valve mitrale et la valve aortique. Ces végétations sont des amas de bactéries et de cellules qui s’accrochent aux valves. Une analyse de son sang a révélé la présence d’une bactérie appelée Staphylococcus warneri, qui fait partie d’un groupe de bactéries souvent présentes sur la peau.\n\n**Ce que cela signifie**  \nCette infection des valves cardiaques s’appelle une endocardite valvulaire native (NVE). Cela veut dire que les valves naturelles du cœur sont infectées par des bactéries qui viennent du corps lui-même. Cette maladie peut être grave car elle empêche les valves de bien fonctionner, ce qui cause une insuffisance cardiaque, c’est-à-dire que le cœur ne pompe pas assez bien le sang.  \n\n**L’évolution de la maladie**  \nQuatre mois avant l’hospitalisation, le patient avait déjà des signes légers comme une perte de poids et des changements dans ses analyses de sang, mais il n’avait pas de fièvre ni de symptômes évidents. Ces signes auraient pu indiquer le début de l’infection. Il n’avait jamais reçu de traitement qui affaiblit le système immunitaire ni d’implant de matériel médical, ce qui rend cette infection plus rare.\n\n**Le traitement et le résultat**  \nAprès avoir commencé un traitement avec des antibiotiques pour combattre l’infection, son état s’est amélioré. Ensuite, il a subi une opération pour remplacer les deux valves infectées par des valves mécaniques. L’opération s’est bien passée, sans complications, et il n’a pas eu de récidive de l’infection depuis plus de deux ans.\n\n**En résumé**  \nCe cas montre qu’une infection grave du cœur peut se développer lentement, avec des signes discrets au début. Il est important de surveiller les patients à risque, surtout ceux avec des problèmes cardiaques et un diabète, même s’ils n’ont pas de symptômes évidents. Un diagnostic et un traitement rapides peuvent sauver la vie.",
+            "B3": "Résumé détaillé et structuré pour un public non médical éduqué\n\nContexte  \nUn homme japonais de 59 ans, souffrant depuis 28 ans d’un diabète de type 1 mal contrôlé malgré un traitement intensif à base d’insuline, a développé une insuffisance cardiaque aiguë. Il avait également une régurgitation aortique sévère chronique (fuite de la valve aortique) diagnostiquée 16 ans auparavant, mais non suivie régulièrement. Sa santé générale était fragile, avec un poids faible (52 kg pour 168 cm) et des fluctuations importantes de sa glycémie.\n\nPrincipales observations  \nÀ son admission en urgence, le patient présentait une fièvre élevée, des difficultés respiratoires sévères, une pression artérielle élevée et une saturation en oxygène très basse (80 %). Les examens ont révélé une insuffisance cardiaque aiguë liée à une maladie valvulaire. L’échocardiographie a montré de grandes végétations (amas de bactéries et de cellules inflammatoires) mobiles sur les valves mitrale et aortique, signes caractéristiques d’une endocardite infectieuse (infection de la paroi interne du cœur). Les analyses sanguines ont confirmé la présence de Staphylococcus warneri, une bactérie habituellement présente sur la peau mais pouvant causer des infections graves, notamment chez des patients fragiles. Cette bactérie appartient au groupe des staphylocoques coagulase-négatifs, souvent moins virulents mais capables d’infecter les valves cardiaques natives (non remplacées).\n\nInterprétation clinique  \nL’endocardite valvulaire native (NVE) a été diagnostiquée sur la base des signes cliniques, des images échographiques et des cultures sanguines positives. Rétrospectivement, des anomalies biologiques discrètes (élévation modérée des globules blancs et de la protéine C-réactive, baisse de l’albumine et de l’hémoglobine) ainsi qu’une perte de poids progressive sur plusieurs mois avaient probablement été les premiers signes avant-coureurs de cette infection. Le patient n’avait pas d’antécédents d’immunosuppression ni d’implantation de dispositifs cardiaques, ce qui rend ce cas particulier car l’infection est survenue sur des valves natives sans facteur déclenchant évident.\n\nProchaines étapes et prise en charge  \nInitialement, une antibiothérapie empirique a été mise en place, puis adaptée en fonction des résultats bactériologiques. Malgré la gravité de l’insuffisance cardiaque, la chirurgie d’urgence a été évitée grâce à une amélioration clinique sous traitement médical. Après quatre semaines d’antibiotiques, une intervention chirurgicale programmée a permis d’enlever les végétations et de remplacer les valves mitrale et aortique par des prothèses mécaniques. L’examen peropératoire a confirmé l’absence de complications telles que des abcès. Le patient a bien récupéré, sans embolie (migration de fragments infectieux) ni récidive de l’infection, et est resté en bonne santé plus de deux ans après l’opération.\n\nCe cas illustre l’importance d’une surveillance attentive des signes biologiques subtils et des symptômes non spécifiques, notamment chez les patients diabétiques à risque, afin de diagnostiquer précocement une endocardite infectieuse et d’adapter la prise en charge thérapeutique."
+        }
+    },
+    {
+        "article": "Il s’agit d’un patient de 8 mois né d’une mère para 3. La mère avait un suivi ANC, mais il était irrégulier, et il était dans un centre de santé rural avec une mauvaise installation où elle ne pouvait pas obtenir d’échographie obstétricale. L’accouchement a eu lieu à la maison avec une sage-femme traditionnelle. Après l’accouchement, les parents ont remarqué un gonflement sur la partie occipitale de la tête. Il a progressivement augmenté de taille pour atteindre la taille actuelle. Les parents sont allés au centre de santé, où ils ont été dirigés vers l’hôpital principal, qui les a ensuite dirigés vers notre centre. Le gonflement n’avait pas de décharge, et le patient n’avait pas de fièvre, de vomissements, de difficultés à téter, de pleurs aigus, de mouvements corporels anormaux ou de léthargie. Après l’examen du patient, il y avait un gonflement de 40 cm sur 35 cm, transilluminant la lumière, masse occipitale tendre, sur la zone des sinus frontaux. Il y avait un défaut osseux palpable à la base du sac. Les fontanelles antérieure et postérieure n’étaient pas ouvertes. Le bébé était joueur, alerte, bougeant toutes les extrémités, suçant bien, et avait des signes vitaux stables. Le patient a ensuite été examiné avec un CBC, un groupe sanguin, des tests de fonction rénale et hépatique qui étaient dans la plage normale, et une IRM du cerveau a révélé un énorme sac occipital hypointense et hyperintense T2 avec de multiples flux vides montrant le torcula, le sinus sagittal supérieur et le sinus transverse, et une partie du lobe occipital droit du cerveau avec un défaut osseux à la base du sac. Après avoir obtenu un consentement écrit informé, le patient a été placé sur la table d’opération avec la tête suspendue au-delà du bord de la table d’opération sur le côté de la machine d’anesthésie, avec un anesthésiste tenant la tête et le sac suspendu au-delà de la table, et a été intubé avec la première tentative. Après intubation, le patient a été placé en position couchée sur le côté avec l’aide d’une étrière Mayfield. Les cheveux ont été rasés et nettoyés avec de l’eau et du savon, et un assistant tenant la masse avec une main gantée stérile, la peau a ensuite été nettoyée et drapée. Initialement, nous avons fait une incision cutanée transversale, drainée le LCR, et le sac s’est effondré. Puis, le tissu cérébral dysplasique a été réséqué, et le sinus veineux, la tumeur, le torcula et d’autres tissus cérébraux viables ont été réduits doucement au crâne. La dure-mère a été disséquée, taillée, taillée et fermée comme une primaire étanche. Nous n’avons pas recommandé une cranioplastie dans un cas d’encéphalocèle occipital géant avec un risque élevé d’hydrocéphalie postopératoire ; par conséquent, nous n’avons pas fermé le défaut osseux. Après cela, la peau a été taillée et fermée en deux couches. Après l’opération, le patient est resté dans le service de neurochirurgie pendant sept jours sans hydrocéphalie et sans déficit neurologique. Le patient est ensuite suivi dans une clinique externe toutes les deux semaines sans complications chirurgicales ou neurologiques.\n",
+        "gold_summary": "Il s'agit d'un cas d'un nourrisson de 8 mois né d'une mère qui n'avait pas bénéficié de soins anténataux réguliers. Après que le bébé ait présenté une masse postérieure de la tête progressivement croissante, qui est cystique, transilluminante, tendre et de 40 cm x 35 cm, l'imagerie a démontré un petit tissu cérébral principalement partie du lobe occipital droit avec la majeure partie du sac occupé par le liquide cérébrospinal. La réparation a été effectuée et le tissu cérébral dysplasique a été résectionné, puis le tissu cérébral sain et les sinus durales ont été réduits au crâne, puis le patient est resté à l'hôpital et a été suivi de près pour l'hydrocéphalie pendant sept jours et a été renvoyé sans hydrocéphalie et sans déficit neurologique.\n",
+        "synthetic_summary": {
+            "B1": "Un bébé de 8 mois avait un gros gonflement à l’arrière de la tête. Ce gonflement était rempli d’un liquide doux et un peu de cerveau dedans. \n\nLes docteurs ont fait une opération pour enlever la partie qui ne va pas. Ils ont remis le reste du cerveau à sa place. \n\nAprès l’opération, le bébé est resté à l’hôpital. Il allait bien, il bougeait et ne faisait pas de problème. Les docteurs l’ont surveillé longtemps. Tout s’est bien passé.",
+            "B2": "Cas d’un bébé de 8 mois dont la maman n’a pas eu de suivi médical régulier pendant la grossesse. Après la naissance, les parents ont remarqué un gros gonflement à l’arrière de la tête qui a grandi avec le temps. Ce gonflement, qui mesurait environ 40 cm sur 35 cm, était rempli de liquide et un peu sensible au toucher.\n\nUne imagerie spéciale appelée IRM a montré que ce sac contenait surtout du liquide cérébral, avec seulement une petite partie du cerveau, surtout dans la région arrière droite de la tête. Lors de l’opération, les médecins ont enlevé le tissu cérébral anormal et replacé doucement le tissu sain et les veines importantes à l’intérieur du crâne. Ils n’ont pas fermé le trou dans l’os pour éviter des complications.\n\nAprès l’opération, le bébé est resté à l’hôpital pendant une semaine. Il n’a pas eu de problème de liquide dans le cerveau (appelé hydrocéphalie) ni de difficulté neurologique. Depuis, il est suivi régulièrement en consultation et se porte bien.",
+            "B3": "Résumé détaillé et structuré pour un public non médical éduqué\n\n**Contexte**  \nIl s’agit d’un nourrisson de 8 mois, né d’une mère ayant eu un suivi prénatal irrégulier dans un centre de santé rural dépourvu d’échographie obstétricale. L’accouchement a eu lieu à domicile, assisté par une sage-femme traditionnelle. Peu après la naissance, les parents ont observé un gonflement important à l’arrière de la tête de l’enfant, qui a progressivement augmenté de volume.\n\n**Principales observations cliniques et examens**  \nÀ l’examen, le bébé présentait une masse occipitale (à l’arrière du crâne) de grande taille, mesurant environ 40 cm sur 35 cm. Cette masse était tendre au toucher, translucide à la lumière (transilluminante), et un défaut osseux était palpable à sa base. Malgré cette masse, le bébé était en bon état général : éveillé, joueur, avec des mouvements normaux et une bonne succion. Les fontanelles (espaces mous entre les os du crâne) étaient fermées. Les analyses sanguines et les fonctions rénales et hépatiques étaient normales. Une imagerie par résonance magnétique (IRM) cérébrale a révélé que la masse contenait principalement du liquide cérébrospinal, avec une petite portion de tissu cérébral anormal (dysplasique) provenant du lobe occipital droit. Cette masse comprenait également des structures veineuses importantes (sinus veineux).\n\n**Intervention chirurgicale**  \nAprès consentement des parents, une intervention chirurgicale a été réalisée sous anesthésie générale. La tête du bébé a été soigneusement positionnée pour permettre l’accès à la masse. Une incision cutanée a permis de drainer le liquide contenu dans la masse, ce qui a fait s’effondrer le sac. Le tissu cérébral anormal a été retiré, tandis que les parties saines du cerveau et les sinus veineux ont été replacés avec précaution dans le crâne. La membrane protectrice du cerveau (dure-mère) a été refermée de manière étanche. Le défaut osseux à la base de la masse n’a pas été fermé par une prothèse osseuse (cranioplastie) en raison du risque élevé d’apparition d’hydrocéphalie (accumulation de liquide dans le cerveau) après l’opération. La peau a ensuite été suturée en deux couches.\n\n**Prochaines étapes et suivi**  \nLe bébé est resté hospitalisé en neurochirurgie pendant sept jours, période durant laquelle aucun signe d’hydrocéphalie ni de déficit neurologique n’a été observé. Par la suite, il a été suivi régulièrement en consultation externe toutes les deux semaines, sans complications chirurgicales ni neurologiques.\n\n**Conclusion**  \nCe cas illustre la prise en charge réussie d’une encéphalocèle occipitale géante (une malformation congénitale où une partie du cerveau et ses membranes sortent à travers un défaut du crâne) chez un nourrisson, malgré un suivi prénatal limité et des conditions initiales difficiles. La chirurgie a permis de retirer le tissu cérébral anormal et de préserver les structures saines, avec un bon résultat fonctionnel à court terme."
+        }
+    },
+    {
+        "article": "Cet homme de 53 ans a présenté initialement une gêne thoracique aiguë comme symptôme isolé. Il était auparavant un non-fumeur actif, en forme et en bonne santé, sans antécédents médicaux ni familiaux.\n\nLors de l'examen, il avait des bruits cardiaques normaux sans murmures. Sa pression veineuse jugulaire n'était pas élevée. Sa poitrine était claire et il n'y avait pas d'œdème de la cheville.\n\nSa tension artérielle était de 98/78 mm Hg et son rythme cardiaque de 62 battements par minute. Sa saturation en oxygène était de 100 % en air ambiant et son rythme respiratoire de 16 respirations par minute. Il était apyrexial avec une température de 37,1 °C.\n\n\nEnquêtes\n\nL'ECG a montré une hypertrophie ventriculaire gauche et des inversions de l'onde T généralisées. Les taux sériques de troponine cardiaque de haute sensibilité (hs-cTnI) sont passés de 28 ng/L (0 heure) à 77 ng/L (6 heures) (limite supérieure de référence pour cet essai : 34 ng/L). Il a été traité par une double antiagrégation plaquettaire pour un diagnostic de travail d'infarctus du myocarde sans élévation du segment ST.\n\nL'angiographie coronarienne CT a montré une plaque calcifiée dans deux artères coronaires. L'angiographie conventionnelle n'a confirmé aucune limitation du flux. L'échocardiographie transthoracique a montré une HVI modérée avec une obstruction significative du tractus de sortie. Il y avait une légère insuffisance systolique avec une akinésie localisée de la paroi inférieure. Une IRM cardiaque a été demandée en tant qu'investigation ambulatoire.\n\nUn mois plus tard, le patient a été réadmis avec de nouveaux malaises thoraciques. Quatre jours de télémétrie n’ont révélé aucune dysrythmie au cours de ces épisodes de malaise. L’ECG n’a montré aucune modification dynamique. Il y avait une augmentation statique de faible niveau de hs-cTnI à 37 ng/L, 30 ng/L et 33 ng/L, respectivement, prise quotidiennement en raison de multiples épisodes intermittents de douleurs thoraciques sur plusieurs jours. Le taux de protéine C réactive était inférieur à 3 mg/L et il était apyremique.\n\nL'IRM cardiaque a montré une hypertrophie ventriculaire gauche concentrique, une zone d'oedème inféro-latéral probable et un schéma inhabituel d'amélioration tardive du gadolinium (LGE) principalement endocardique avec une amélioration de la paroi médiane du septum et une amélioration sous-endocardique diffuse. Il avait des volumes de LV normaux et une fraction d'éjection (61%), mais une masse élevée à 221 g (101 g/m2) compatible avec une hypertrophie. Comme sa tension artérielle restait normale, nous étions réticents à attribuer l'hypertrophie ventriculaire gauche à une cardiopathie hypertensive.\n\n\nDiagnostic différentiel\n\nEn raison de la nature inhabituelle de l'affaire, elle a été discutée lors de la réunion de l'équipe multidisciplinaire régionale. L'IRM ne semblait pas être classique, ni de myocardite, ni d'amyloïde, mais le résultat de la réunion avait suggéré de dépister une cardiomyopathie amyloïde et une maladie d'Anderson-Fabry.\n\nLe taux d'alpha galactosidase était normal, ce qui excluait effectivement la maladie de Fabry.\n\nLa chaîne légère libre de sérum (SF) a montré une augmentation de la SF Kappa à 253,20 mg/L (plage de référence : 3,3-19,4) avec une normale de la SF Lambda 9,6 mg/L (plage de référence : 5,7-26,3). Le rapport kappa/lambda était de 26,375 (plage de référence : 0,26-1,65).\n\nL'aspirat de moelle osseuse a montré des particules largement masquées par des dépôts extracellulaires protéiniques bleus, nuageux et amorphes. Ces dépôts étaient teintés en rose saumon par la coloration au rouge Congo. Lorsqu'ils ont été visualisés au microscope à lumière polarisée, ils ont présenté une biréfringence verte caractéristique, compatible avec une accumulation d'amyloïdes. Il y avait un léger excès de cellules plasmatiques, insuffisant pour diagnostiquer une dyscrasie plasmatique.\n\nLa coloration de l'aspirat de la bourse graisseuse au rouge Congo n'a pas fourni de preuves convaincantes de la présence de dépôts amyloïdes.\n\nUne tomodensitométrie de l'abdomen et du bassin ne révélait rien d'autre qui puisse expliquer son amyloïdose. Les tests de dépistage de l'hépatite B, de l'hépatite C et du VIH étaient négatifs. L'électrophorèse du sérum ne révélait aucune bande monoclonale anormale et les immunoglobulines étaient normales.\n\n\nTraitement\n\nLe patient a été référé au National Amyloidosis Centre à Londres où le diagnostic a été confirmé. Sur leur recommandation, l'équipe d'hématologie locale a supervisé l'administration de chimiothérapie pour l'amylose primaire AL avec implication cardiaque. Il a reçu un cycle de 21 jours de VCD (bortezomib, cyclophosphamide et dexaméthasone).\n\nDes médicaments de soutien supplémentaires ont été fournis, notamment la doxycycline, l'aciclovir et l'allopurinol pour les 2 premiers cycles de chimiothérapie.\n\n\nRésultat et suivi\n\nLe suivi à 1 an du diagnostic a montré que le patient restait stable, que sa douleur thoracique avait complètement disparu et qu'il ne présentait toujours aucun symptôme d'insuffisance cardiaque.\n\nCependant, lorsque la pandémie de COVID-19 a frappé le pays, ses cliniciens du Centre national d'amylose ont arrêté sa chimiothérapie, compte tenu de ses bons progrès avec le traitement et des risques associés de COVID-19.\n\nDeux mois plus tard, il a présenté un autre épisode de douleurs thoraciques et une augmentation modérée de la hs-cTnI. Sa chimiothérapie a donc été réintroduite et ses douleurs thoraciques ont ensuite disparu.",
+        "gold_summary": "Un homme de 53 ans s'est présenté à un hôpital général de district avec des douleurs thoraciques, des modifications de l'ECG et une légère augmentation de la troponine cardiaque de haute sensibilité. Il n'y avait aucun symptôme d'insuffisance cardiaque. L'angiographie coronarienne par TDM a révélé une maladie calcifiante modérée et l'angiographie conventionnelle n'a confirmé aucune limitation du flux. L'échocardiographie a montré une hypertrophie ventriculaire gauche (HVG). Sa tension artérielle est restée normale tout au long de son admission. Le centre tertiaire a qualifié cela d'événement de « rupture de plaque », mais l'HVG est restée inexpliquée. L'IRM cardiaque a montré un modèle inhabituel de rehaussement tardif du gadolinium, qui n'était pas classique de l'amyloïde. Cependant, une augmentation de la chaîne légère kappa libre sérique ainsi que le dépôt d'amyloïde sur son aspirât de moelle osseuse ont confirmé le diagnostic d'amyloïdose primaire AL avec implication cardiaque. Le patient a ensuite suivi une chimiothérapie et est resté stable à 1 an de suivi.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 53 ans avait mal au cœur. Les docteurs ont fait des examens. Son cœur était un peu gros. Son sang montrait quelque chose d’inhabituel. \n\nLes docteurs ont trouvé des petites choses bizarres dans son corps. Cela s’appelle amyloïdose. C’est une maladie où des choses collantes se mettent dans le cœur. \n\nIl a pris des médicaments très forts pour guérir. Après un an, il allait mieux. Il n’avait plus mal au cœur. Les docteurs continuent de bien s’occuper de lui.",
+            "B2": "Un homme de 53 ans est venu à l’hôpital parce qu’il avait des douleurs dans la poitrine. Son électrocardiogramme (ECG), un test qui mesure l’activité électrique du cœur, montrait des changements, et un examen sanguin a révélé une légère augmentation d’une protéine appelée troponine, qui indique un petit dommage au muscle cardiaque. Il ne présentait pas de signes d’insuffisance cardiaque, c’est-à-dire que son cœur fonctionnait encore bien pour pomper le sang.\n\nUne tomodensitométrie (scanner) des artères du cœur a montré des plaques calcifiées, mais les artères n’étaient pas bloquées de façon importante. Une échographie du cœur a révélé que la paroi du ventricule gauche (la principale chambre qui pompe le sang) était épaissie, ce qu’on appelle une hypertrophie ventriculaire gauche (HVG). Sa tension artérielle est restée normale, ce qui rendait cette hypertrophie difficile à expliquer.\n\nUne IRM cardiaque, qui donne des images détaillées du cœur, a montré un motif inhabituel dans la paroi du cœur après injection d’un produit appelé gadolinium. Ce motif n’était pas typique d’une maladie appelée amyloïdose, où des protéines anormales s’accumulent dans les tissus.\n\nCependant, des analyses de sang ont montré une augmentation anormale d’une protéine appelée chaîne légère kappa libre. De plus, un examen de la moelle osseuse, où sont fabriquées les cellules sanguines, a révélé la présence de dépôts d’amyloïde, confirmant que le patient avait une amyloïdose primaire AL, une maladie où des protéines anormales s’accumulent dans le cœur.\n\nLe patient a reçu une chimiothérapie, un traitement qui aide à réduire ces protéines anormales, et un an plus tard, il était stable, sans douleur thoracique ni problème cardiaque grave.",
+            "B3": "Résumé structuré pour un public adulte non spécialiste\n\nContexte  \nUn homme de 53 ans, auparavant en bonne santé sans antécédents médicaux ni familiaux, s’est présenté avec une douleur thoracique aiguë isolée. À l’examen clinique, ses signes vitaux étaient normaux, sans signes d’insuffisance cardiaque ou d’autres anomalies évidentes.\n\nPrincipales observations  \nL’électrocardiogramme (ECG) a montré une hypertrophie du ventricule gauche (c’est-à-dire un épaississement de la paroi du cœur) et des modifications des ondes T, tandis que les taux sanguins de troponine cardiaque (un marqueur de lésion du muscle cardiaque) étaient légèrement élevés et en augmentation progressive. Une angiographie coronarienne par scanner a révélé des plaques calcifiées dans les artères du cœur, mais sans obstruction significative du flux sanguin. L’échocardiographie a confirmé une hypertrophie ventriculaire gauche modérée avec une obstruction importante du passage du sang vers l’aorte. La tension artérielle du patient est restée normale, ce qui rendait peu probable une cause hypertensive pour cette hypertrophie.\n\nUne réadmission un mois plus tard pour des douleurs thoraciques récurrentes a conduit à la réalisation d’une imagerie par résonance magnétique (IRM) cardiaque. Celle-ci a montré un épaississement concentrique du ventricule gauche, une zone probable d’œdème (inflammation) au niveau de la paroi inféro-latérale du cœur, et un schéma inhabituel de rehaussement tardif du gadolinium (un produit de contraste), principalement au niveau de la couche interne du muscle cardiaque. Ces images n’étaient pas typiques des formes classiques de myocardite (inflammation du muscle cardiaque) ou d’amyloïdose (accumulation anormale de protéines).\n\nInterprétation clinique  \nDevant ces résultats atypiques, une réunion multidisciplinaire a suggéré d’explorer la possibilité d’une amyloïdose cardiaque, une maladie caractérisée par le dépôt de protéines anormales dans le cœur. Les tests sanguins ont montré une augmentation très marquée des chaînes légères kappa libres (un type de protéine produite par certaines cellules immunitaires), ce qui orientait vers une amyloïdose de type AL (amylose primaire). L’analyse de l’aspirat de moelle osseuse a confirmé la présence de dépôts amyloïdes, caractérisés par une coloration spécifique (rouge Congo) et une biréfringence verte sous lumière polarisée, signe distinctif de cette maladie. Aucun autre signe d’atteinte systémique ou d’infection n’a été retrouvé.\n\nTraitement et suivi  \nLe diagnostic d’amyloïdose primaire AL avec atteinte cardiaque a été confirmé par un centre spécialisé. Le patient a reçu une chimiothérapie adaptée (association de bortezomib, cyclophosphamide et dexaméthasone) sous supervision hématologique, ainsi que des traitements de soutien pour prévenir les complications. Après un an de suivi, il est resté stable, sans douleur thoracique ni signes d’insuffisance cardiaque. Lors de la pandémie de COVID-19, la chimiothérapie a été temporairement interrompue en raison des risques infectieux, mais la réapparition de douleurs thoraciques et l’augmentation des marqueurs cardiaques ont conduit à la reprise du traitement, avec disparition ultérieure des symptômes.\n\nConclusion  \nCe cas illustre une présentation atypique d’amyloïdose cardiaque primaire AL, initialement confondue avec un infarctus du myocarde et une hypertrophie ventriculaire gauche inexpliquée. L’imagerie cardiaque avancée et les analyses biologiques spécifiques ont permis d’établir un diagnostic précis, essentiel pour orienter un traitement efficace et améliorer le pronostic du patient."
+        }
+    },
+    {
+        "article": "Une femme de 58 ans s'est présentée au service des urgences avec un antécédent de dyspnée qui s'aggravait depuis 6 mois. Au cours des 10 jours précédents, ses symptômes s'étaient gravement aggravés, accompagnés d'un léger inconfort thoracique et d'un gonflement des jambes bilatérales. Ses antécédents médicaux comprenaient l'asthme et l'hypertension. À son arrivée, elle a été trouvée hypoxémique avec une saturation en oxygène de 74 %, qui est passée à 94 % avec 5 litres d'oxygène supplémentaire. L'examen physique a révélé des crépitations inspiratoires bilatérales et un œdème pitting dans les membres inférieurs.\n\nLes examens de laboratoire ont révélé un taux élevé de NT-proBNP (peptide natriurétique cérébral) de 2110 ng/mL (intervalle <125 ng/mL) et des taux normaux de troponine. L'angiographie thoracique par tomodensitométrie (CT) a révélé des infiltrats modérés bilatéraux de verre dépoli, un tronc de l'artère pulmonaire (PA) élargi et une dilatation de l'oreillette droite (RA) et du ventricule droit (RV) sans preuve d'embolie pulmonaire. L'échocardiographie transthoracique (TTE) a montré une fraction d'éjection ventriculaire gauche (LVEF) de 75 % à 80 %, une dilatation modérée de la RA et de la RV, un aplati systolique et diastolique du septum intervéculaire, une fonction systolique réduite du RV et une pression systolique de la PA estimée de 55 à 60 mm Hg. Aucun shunt intracardiaque n'a été identifié par Doppler couleur ou injection de contraste saline agitée.\n\nLe patient a été initié à la furosémide intraveineuse. La cathétérisation cardiaque droite (RHC) a été réalisée le jour suivant, tandis que le patient recevait 3 litres d'oxygène supplémentaire par canule nasale. La procédure a confirmé la PH, avec une pression artérielle pulmonaire moyenne (mPAP) de 41 mm Hg et un débit cardiaque élevé de 8,46 L/min par la méthode de Fick. Un test de vasoreactivité utilisant le protocole standard d'adénosine a confirmé que le patient n'était pas vasoreactif, indiquant que la thérapie par inhibiteur des canaux calciques ne serait pas bénéfique. Les autres investigations, y compris la numération globulaire complète, l'hormone stimulant la thyroïde, le dépistage du VIH, le dépistage des anticorps antinucléaires, le facteur rhumatoïde et les taux de thiamine, n'ont pas été remarquables. Les études d'imagerie, y compris l'angiographie par CT du thorax et de l'abdomen et l'échographie Doppler du foie, ont exclu les shunts systémiques, les malformations artério-veineuses pulmonaires et la splénomégalie. Au moment de la sortie, l'hypoxémie du patient avait été résolue par la diurèse.\n\nL'évaluation en consultation externe comprenait un test de la fonction pulmonaire qui a montré un léger défaut ventilatoire obstructif. L'étude du sommeil et l'étude de la ventilation-perfusion n'ont pas été remarquées. Comme la RHC a démontré une pression d'occlusion de l'artère pulmonaire (pression de coin) de 11 mmHg (<15 mmHg) et un gradient transpulmonaire élevé de 26 mmHg (>12 mmHg), le PH de groupe II dû à une maladie cardiaque gauche a été exclu. On lui a prescrit un inhalateur corticostéroïde et on a continué à lui administrer de la furosémide par voie orale (20 mg par jour). La thérapie spécifique à l'hypertension pulmonaire n'a pas été initiée, étant donné que son PH a été classé dans le groupe III, attribué à une maladie pulmonaire obstructive. Au cours des rendez-vous de suivi, la patiente a signalé une amélioration initiale de sa dyspnée perçue, qui s'est ensuite stabilisée. Elle est restée systématiquement dans la catégorie intermédiaire à faible risque selon l'outil d'évaluation du risque à 4 niveaux pour le suivi de l'hypertension pulmonaire.\n\nDeux ans plus tard, elle est revenue avec une dyspnée et un gonflement des jambes qui s'aggravaient après avoir arrêté la furosémide. Une nouvelle angiographie pulmonaire par TDM a révélé des résultats similaires à ceux de l'imagerie initiale, mais a également identifié une veine pulmonaire gauche anormale qui se drainait dans le tronc brachio-céphalque gauche. Une révision rétrospective de son premier scanner a confirmé l'anomalie manquée. L'EEFT a montré une EFV de 60 %, une dilatation modérée de l'AR et de la RV, une fonction systolique réduite de la RV et une pression systolique artérielle pulmonaire estimée de 50 à 55 mmHg. Contrairement à la première RHC, l'évaluation du shunt a cette fois-ci démontré une augmentation de 6 % de la saturation en oxygène entre la veine cave supérieure (VCS) et l'AR, confirmant un shunt gauche-droit. Cette divergence était due à la mesure de la saturation de la VCS obtenue de manière appropriée au-dessus du drainage de la veine cave supérieure, guidée par la connaissance de la PAPVR issue des résultats de la TDM. La fraction de shunt (Qp/Qs) a été calculée à 1,52. En conséquence, son PH a été reclassé dans le groupe I en raison d'une cardiopathie congénitale de l'adulte.\n\nLa patiente a reçu un traitement par diurétiques intraveineux. En raison de son PH modéré et de sa classification à risque intermédiaire-faible basée sur l'outil d'évaluation du risque en 4 catégories (OMS-FC III, NT-proBNP 81 pg/mL, et une distance de marche de 460 m en 6 minutes), une thérapie spécifique à la PH n'a pas été conseillée. Elle a refusé des évaluations complémentaires, y compris une imagerie par résonance magnétique cardiaque (IRM) et une orientation vers un centre de cardiologie congénitale adulte, préférant poursuivre une surveillance ambulatoire étroite.\n",
+        "gold_summary": "Nous rapportons le cas d'une femme de 58 ans qui a présenté initialement une dyspnée progressive et a été diagnostiquée avec une hypertension pulmonaire de groupe III attribuée à une maladie pulmonaire obstructive. Deux ans plus tard, elle est revenue avec des symptômes similaires après avoir arrêté la thérapie diurétique. Une évaluation plus approfondie a révélé une anomalie antérieurement non détectée de la veine pulmonaire gauche drainant dans la veine innominata gauche.\n",
+        "synthetic_summary": {
+            "B1": "Une dame de 58 ans avait du mal à bien respirer. Au début, on a pensé que c’était à cause de ses poumons qui ne fonctionnaient pas bien.\n\nDeux ans plus tard, elle avait encore du mal à respirer. On a regardé de plus près et on a trouvé un petit problème dans une veine de ses poumons. Cette veine n’était pas à sa place comme il faut.",
+            "B2": "Cas d'une femme de 58 ans avec des difficultés à respirer\n\nUne femme de 58 ans a d'abord consulté à l'hôpital parce qu'elle avait de plus en plus de mal à respirer depuis six mois. Elle avait aussi un peu mal à la poitrine et ses jambes étaient enflées. Les médecins ont découvert qu'elle avait une pression trop élevée dans les artères de ses poumons, appelée hypertension pulmonaire. Au début, ils ont pensé que cela venait d'un problème de ses poumons, car elle avait une légère maladie pulmonaire.\n\nCe qu'ils ont trouvé plus tard\n\nDeux ans plus tard, elle est revenue avec les mêmes problèmes après avoir arrêté son traitement pour éliminer l'eau en excès dans son corps (les diurétiques). Cette fois, les médecins ont fait des examens plus poussés et ont découvert une anomalie dans une veine pulmonaire. Normalement, cette veine doit se connecter au cœur, mais chez elle, elle se connectait à une autre grosse veine, ce qui provoquait un mélange anormal du sang.\n\nCe que cela signifie\n\nCette anomalie, appelée drainage veineux pulmonaire partiellement anormal, peut causer une hypertension pulmonaire et expliquer ses symptômes. Au début, cette anomalie n'avait pas été détectée, ce qui a retardé le diagnostic correct. Grâce à cette découverte, les médecins ont pu mieux comprendre sa maladie et adapter son suivi médical.",
+            "B3": "Résumé structuré pour un lecteur non spécialiste mais instruit\n\n**Contexte**  \nUne femme de 58 ans s’est présentée avec une difficulté croissante à respirer (dyspnée) sur six mois, aggravée récemment, accompagnée d’un léger inconfort thoracique et d’un gonflement des jambes. Ses antécédents médicaux incluaient de l’asthme et de l’hypertension artérielle. À son admission, elle présentait une faible saturation en oxygène, des crépitements pulmonaires et un œdème des membres inférieurs.\n\n**Principales observations**  \nLes examens ont montré une élévation importante du NT-proBNP, un marqueur indiquant une surcharge cardiaque, mais des enzymes cardiaques normales. L’imagerie par scanner thoracique a révélé des infiltrats pulmonaires bilatéraux et une dilatation des cavités droites du cœur, sans embolie pulmonaire. L’échocardiographie a confirmé une fonction normale du ventricule gauche, mais une dilatation et un dysfonctionnement du ventricule droit, ainsi qu’une pression élevée dans l’artère pulmonaire. Aucun passage anormal de sang entre les cavités cardiaques n’a été détecté à ce stade.\n\nLa cathétérisation cardiaque droite a confirmé une hypertension pulmonaire avec une pression moyenne élevée dans l’artère pulmonaire et un débit cardiaque augmenté. Le test de vasoréactivité a montré que les inhibiteurs calciques ne seraient pas efficaces. Les investigations complémentaires ont exclu d’autres causes comme des maladies auto-immunes, infectieuses ou des malformations vasculaires visibles. Le diagnostic initial retenu était une hypertension pulmonaire secondaire à une maladie pulmonaire obstructive (groupe III).\n\n**Interprétation clinique**  \nLe traitement a consisté en une diurèse pour réduire la surcharge liquidienne et un traitement inhalé pour l’asthme. La patiente a connu une amélioration symptomatique et est restée stable pendant deux ans sous traitement. Cependant, après l’arrêt des diurétiques, ses symptômes ont récidivé.\n\nUne nouvelle imagerie a alors mis en évidence une anomalie vasculaire jusque-là non détectée : une veine pulmonaire gauche anormale drainant dans la veine innominée gauche (tronc brachio-céphalique), ce qui constitue une malformation congénitale appelée drainage veineux pulmonaire partiel anormal (PAPVR). Cette anomalie avait été manquée lors de l’examen initial. Une nouvelle cathétérisation a confirmé la présence d’un shunt gauche-droite (passage anormal de sang d’une circulation à haute pression vers une autre), expliquant en partie l’hypertension pulmonaire.\n\nCette découverte a conduit à reclasser son hypertension pulmonaire dans le groupe I, correspondant aux cardiopathies congénitales de l’adulte.\n\n**Prochaines étapes**  \nLa patiente a repris un traitement diurétique intraveineux. Étant donné la sévérité modérée de son hypertension pulmonaire et son risque intermédiaire-faible, aucun traitement spécifique de l’hypertension pulmonaire n’a été initié. La patiente a refusé des examens complémentaires, notamment une imagerie cardiaque par résonance magnétique et une consultation spécialisée en cardiologie congénitale adulte. Elle poursuit actuellement une surveillance étroite en ambulatoire.\n\n---\n\nCe cas illustre l’importance d’une évaluation complète et répétée en cas d’hypertension pulmonaire, notamment pour détecter des anomalies vasculaires congénitales pouvant être initialement méconnues, et ainsi adapter le diagnostic et la prise en charge thérapeutique."
+        }
+    },
+    {
+        "article": "Il s’agit d’un homme de 27 ans, originaire et résident de Mexico, dont les parents et trois frères sont apparemment en bonne santé. Il a reçu le vaccin BCG à la naissance, mais a présenté une réaction indésirable deux mois plus tard, avec une adénite aux deux aisselles et un défaut de cicatrisation au site d’injection du vaccin ; il a été amélioré par l’administration de rifampicine pendant huit mois, mais a conservé une cicatrice chéloïde. À neuf mois, il a développé une candidose buccale et dans la région de la couche. Bien que les deux aient régressé sous traitement, ils ont récidivé. La candidose buccale persiste à ce jour et affecte sa langue et ses gencives. À l’âge de sept ans, il a présenté une teigne du cuir chevelu, qui a été améliorée par un traitement non spécifié. Depuis l’âge de 10 ans, il a présenté une rosacée du visage, initialement avec des papules et un érythème de la peau des joues et du nez, et actuellement avec des changements chroniques. À l’âge de 15 ans, il a présenté une onychomycose, a reçu de multiples traitements antifongiques, sans amélioration et avec persistance à ce jour. Il a présenté une rosacée oculaire depuis l’enfance et souffre également d’asthme et de rhinite allergique.\n\nLes tests cutanés ont été positifs pour les acariens, les épithéliums animaux et le pollen. Des stéroïdes topiques et des bronchodilatateurs inhalés ont été administrés. En raison de la nature chronique de la candidose, une altération du système immunitaire a été considérée, une infection par le VIH a été écartée et le patient a été informé qu'il souffrait d'une maladie granulomateuse chronique (la base du diagnostic n'est pas connue). À 26 ans, il a présenté de la fièvre, une perte de poids, une asthénie, une adynamie, une hyporésie, une toux, une hémoptysie, une dyspnée et un abcès fessier. Au service des urgences, le patient était en mauvais état général, avec une malnutrition, une pâleur de la peau et des muqueuses, une détresse respiratoire, une saturation en oxygène de 87 %, une rosacée au visage, à la langue et aux muqueuses orales avec des plaques blanches, un érythème des gencives, une cicatrice de vaccination BCG de 5 cm de diamètre, une hypoventilation pulmonaire et une onychomycose des mains et des pieds.\n\nL’examen thoracique a révélé une image de pleurésie droite et de pneumonie multifocale. L’échographie du fessier a révélé un abcès profond. Les résultats de laboratoire ont révélé une anémie, une leucocytose avec neutrophilie et une élévation de la protéine C réactive. Le test de dihydrorhodamine était normal, ce qui a exclu le diagnostic précédent de maladie granulomateuse chronique. La culture de l’échantillon prélevé dans la cavité buccale et l’hémoculture ont révélé une croissance de Candida albicans ; la culture de l’expectoration a révélé une croissance de C. albicans et de C. krusei ; la culture du liquide broncho-alvéolaire était négative.\n\nLe patient a été traité par vancomycine pour l'abcès, ce qui a entraîné une amélioration. Le patient a reçu de la ceftriaxone, de la clarithromycine et du fluconazole, mais la fièvre a persisté. Une biopsie pleurale a été pratiquée, au cours de laquelle M. tuberculosis a été détecté par PCR. La phase intensive du schéma antituberculeux, ou antifimique, a été initiée avec de l'isoniazide, de la rifampicine, de la pyrazinamide et de l'étambutol, avec une amélioration adéquate. Au cours de cette hospitalisation, il a également développé un zona qui a disparu après 10 jours de valaciclovir. Actuellement, le patient termine son traitement antituberculeux.En réévaluant le cas, en raison des antécédents d'infection par le bacille de Calmette-Guérin, de tuberculose, de zona, de candidose mucocutané et de rosacée, le diagnostic a été orienté vers une augmentation de la fonction de STAT1 (figure 4). Un panel de gènes d'erreurs innées de l'immunité a été demandé par séquençage de nouvelle génération, et la variante pathogénique c.961A>G (p.Arg321Gly) a été trouvée dans le gène STAT1, associée à une augmentation de la fonction de STAT1. Ses parents et ses trois frères ne portent pas la mutation (WT/WT) du gène STAT1.\n",
+        "gold_summary": "Ce rapport concerne un patient qui a présenté une augmentation de la fonction du facteur STAT1 au cours de sa première année de vie. Il a maintenant 27 ans et a présenté une infection par le bacille de Calmette-Guérin et Mycobacterium tuberculosis, une candidose mucocutané chronique, une teigne de la tête (tinea capitis) et une rosacée faciale et oculaire. Une infection par le VIH a été écartée. Des manifestations cliniques ont fait suspecter une immunodéficience congénitale, en particulier une augmentation de la fonction ou de l'activité du STAT1. Le diagnostic a été confirmé par le séquençage de plusieurs gènes associés à des immunodéficiences congénitales. La variante pathogénique c.961A>G (p.Arg321Gly) du gène STAT1, précédemment rapportée comme une mutation augmentant la fonction, a été trouvée chez ce patient.\n",
+        "synthetic_summary": {
+            "B1": "Il y a un monsieur qui est malade depuis qu’il est bébé.  \n\nSon corps a du mal à se défendre contre certains microbes.  \n\nIl a eu des boutons rouges sur le visage et des champignons dans la bouche.  \n\nIl a aussi eu une grosse maladie dans les poumons.  \n\nLes docteurs ont fait des tests et ont trouvé un petit problème dans ses défenses.  \n\nCe problème vient d’un tout petit morceau dans ses gènes, qui sont comme des instructions dans le corps.  \n\nCe monsieur reçoit des médicaments pour l’aider à guérir.  \n\nLes docteurs sont là pour bien s’occuper de lui.",
+            "B2": "**Ce qu’ils ont découvert chez ce patient**\n\nCe résumé parle d’un homme de 27 ans qui a eu plusieurs problèmes de santé depuis tout petit. Il a reçu un vaccin appelé BCG à la naissance, mais il a eu une mauvaise réaction avec des infections aux aisselles et une cicatrice qui a mal guéri. Ensuite, il a souvent eu des infections à champignons, comme une candidose dans la bouche et sur la peau, qui revenaient malgré les traitements. Il a aussi eu une teigne sur la tête, une rosacée (une maladie de la peau du visage), et des infections des ongles. En plus, il souffre d’asthme et d’allergies.\n\n**Ce que cela signifie pour son système immunitaire**\n\nLes médecins ont pensé qu’il avait un problème avec son système immunitaire, car ces infections revenaient souvent et étaient difficiles à soigner. Ils ont vérifié s’il avait le VIH, ce qui n’était pas le cas. Plus tard, il a eu une tuberculose, une infection grave des poumons, et un abcès (une grosse infection avec du pus) à la fesse. Des analyses ont montré qu’il avait des champignons dans la bouche et les poumons. Il a reçu plusieurs médicaments pour combattre ces infections, y compris des antibiotiques et des antifongiques.\n\n**Le diagnostic précis**\n\nPour comprendre pourquoi il avait tous ces problèmes, les médecins ont fait un test génétique appelé séquençage. Ce test cherche des changements dans les gènes qui contrôlent le système immunitaire. Ils ont trouvé une mutation dans un gène appelé STAT1. Ce gène aide normalement le corps à combattre les infections, mais chez lui, cette mutation fait que le gène fonctionne trop, ce qui peut causer des infections répétées et des problèmes de peau. Cette mutation n’était pas présente chez ses parents ni ses frères, ce qui signifie qu’elle est apparue chez lui.\n\n**En résumé**\n\nCet homme a une maladie rare où un gène important du système immunitaire, STAT1, fonctionne trop. Cela explique pourquoi il a eu plusieurs infections graves et des problèmes de peau depuis l’enfance. Grâce à ce diagnostic, les médecins peuvent mieux comprendre sa maladie et adapter son traitement.",
+            "B3": "Résumé destiné à un public adulte non spécialiste\n\n**Contexte**  \nCe rapport décrit le cas d’un homme de 27 ans originaire de Mexico, présentant depuis sa petite enfance plusieurs infections et troubles cutanés récurrents. Dès ses premiers mois, il a eu une réaction anormale au vaccin BCG (vaccin contre la tuberculose), avec une inflammation des ganglions des aisselles et une mauvaise cicatrisation. Par la suite, il a souffert d’infections chroniques à levures (candidose) au niveau de la bouche et de la peau, d’une infection fongique du cuir chevelu (teigne), ainsi que de rosacée au visage et aux yeux. Il a également présenté une infection fongique persistante des ongles (onychomycose), un asthme et une rhinite allergique.  \n\n**Principales observations**  \nÀ 26 ans, le patient a développé une infection pulmonaire grave avec fièvre, toux, crachats de sang et difficultés respiratoires, ainsi qu’un abcès profond au niveau de la fesse. Les examens ont révélé une pneumonie multifocale, une pleurésie (inflammation de la membrane entourant les poumons) et une infection à Candida albicans (un champignon). Une biopsie a confirmé la présence de Mycobacterium tuberculosis, la bactérie responsable de la tuberculose. Le patient a reçu un traitement antibiotique et antifongique adapté, avec une amélioration progressive. Il a aussi présenté un zona (réactivation virale) durant son hospitalisation.  \n\nLes tests immunologiques ont exclu une infection par le VIH et une maladie granulomateuse chronique, une maladie génétique qui affecte normalement la capacité des globules blancs à combattre certaines infections.  \n\n**Interprétation clinique**  \nCompte tenu de ses antécédents d’infections récurrentes, notamment liées au vaccin BCG, à la tuberculose, aux champignons et au virus du zona, les médecins ont suspecté une anomalie génétique affectant le système immunitaire. Une analyse génétique approfondie a révélé une mutation spécifique dans le gène STAT1, appelée c.961A>G (p.Arg321Gly), connue pour augmenter l’activité de cette protéine. STAT1 est un facteur important dans la régulation de la réponse immunitaire. Cette mutation entraîne une hyperactivation du système immunitaire, ce qui paradoxalement peut favoriser certaines infections chroniques et inflammations cutanées. Cette mutation n’a pas été retrouvée chez ses parents ni chez ses frères, ce qui suggère qu’elle est apparue de novo (nouvelle chez ce patient).  \n\n**Prochaines étapes**  \nLe diagnostic d’une augmentation de la fonction de STAT1 permet d’expliquer les infections et troubles cutanés chroniques du patient. Ce diagnostic oriente vers une prise en charge spécialisée, notamment un suivi immunologique régulier et un traitement adapté pour prévenir et contrôler les infections. La connaissance précise de cette mutation génétique est essentielle pour adapter les traitements et envisager, si nécessaire, des thérapies ciblées.  \n\nEn résumé, ce cas illustre comment une mutation génétique affectant la régulation du système immunitaire peut entraîner des infections répétées et des manifestations cutanées chroniques, nécessitant une prise en charge médicale multidisciplinaire."
+        }
+    },
+    {
+        "article": "La patiente est une fille de 6 ans issue d'une famille d'agriculteurs dans une région non haute altitude. Elle a présenté une cyanose modérée des lèvres à la naissance et a été initialement diagnostiquée comme souffrant d'une cardiopathie congénitale. En raison de la cyanose progressive et de la dyspnée, la patiente a été amenée à notre clinique externe pour un diagnostic et un traitement ultérieurs. Elle a connu une croissance et un développement normaux sans retards physiques ou intellectuels importants. La famille a déclaré qu'elle était sujette à des pneumonies et qu'elle toussait fréquemment depuis sa naissance. L'examen physique a révélé des bruits cardiaques importants, des doigts clubbés et une cyanose des lèvres. L'électrocardiographie a montré un rythme sinusal avec une hypertrophie biventriculaire et une déviation de l'axe droit. L'échocardiographie transthoracique a révélé une hypertrophie importante des deux ventricules et de l'oreillette gauche, avec un écho absent entre la paroi gauche de l'aorte ascendante et la paroi droite de la principale artère pulmonaire (MPA), qui mesurait environ 18 mm. Il y avait un segment étroit dans l'isthme de l'arc aortique, mesurant environ 4 mm, et une interruption de l'arc aortique distale à l'artère sous-clavière gauche (LSA). L'artère pulmonaire droite (RPA) est issue de l'aorte ascendante, tandis que l'artère pulmonaire gauche (LPA) provient du tronc pulmonaire. Entre l'aorte descendante et l'artère pulmonaire gauche, il y avait un PDA proéminent d'un diamètre d'environ 6 mm. Les septes atrio-ventriculaires et ventriculaires étaient intacts, la fonction valvulaire était normale, et les origines des artères coronaires étaient normales. L'hypertension pulmonaire était de 50 mm Hg. La patiente n'a pas pris de traitement antihypertensif pulmonaire avant la chirurgie. Par la suite, la patiente a subi une angiographie par CT, qui a confirmé les résultats de l'échocardiographie. La reconstruction en 3 dimensions a clairement montré un APW de type I, un IAA de type A et un PDA. Quatre branches artérielles ont également été visualisées, à savoir l'artère carotide commune droite (RCCA), l'artère carotide commune gauche (LCCA), l'artère sous-clavière droite anormale (ARSA), et l'artère sous-clavière gauche, qui toutes sont issues de l'extrémité proximale de l'arc aortique interrompu.\n\nSur la base de l'historique médical du patient et des examens, un diagnostic définitif de syndrome de Berry a été établi, et une intervention chirurgicale a été indiquée. La famille du patient a demandé une intervention chirurgicale. Une approche standard de mi-sternotomie a été réalisée, révélant de nombreux vaisseaux collatéraux de l'artère pulmonaire principale. Au cours de la réparation de l'arc aortique interrompu, une arrêt circulatoire hypothermique conventionnelle profonde et une perfusion cérébrale sélective ont été utilisées. Tout d'abord, le canal artériel a été disséqué distalement et ligaturé, suivi d'une excision du tissu du canal. L'arc aortique et l'aorte descendante ont été soigneusement mobilisés, et une anastomose end-to-side a été réalisée entre l'aorte descendante et l'arc aortique. La paroi antérieure a été renforcée à l'aide d'un patch péricardique. Après la correction de l'IAA, le RPA a été déconnecté. L'APW a été observée, et le défaut était situé à environ 1 cm de l'annulus de la valve aortique. L'origine des artères coronaires était normale. Le long du bord de l'APW, l'aorte et le MPA ont été séparés, tandis que le RPA a été anastomosé en bout-à-bout au MPA. Un patch péricardique bovin a été utilisé, et l'incision dans l'aorte a été fermée avec des sutures prolène 6-0 de manière continue. L'échocardiographie transœsophagienne intraopérative a confirmé un flux continu à travers l'arc aortique et aucune dérivation entre le MPA et l'aorte. Le patient a reçu un traitement supplémentaire en unité de soins intensifs post-opératoire et a été transféré dans une salle de soins ordinaires après 5 jours. L'hypertension pulmonaire a été réduite à 26 mm Hg après la chirurgie et aucun médicament contre l'hypertension pulmonaire n'a été nécessaire. Le patient n'a pas eu besoin de soutien hémodynamique après la chirurgie. Une évaluation réussie a été réalisée, et le patient a été renvoyé 7 jours plus tard.\n",
+        "gold_summary": "Inquiétudes des patients : Dans cet article, nous rapportons le cas d'une fille de 6 ans atteinte du syndrome de Berry qui présentait des symptômes ischémiques et hypoxiques importants.\n\nDiagnostics : Sur la base des antécédents médicaux du patient et des examens, un diagnostic définitif du syndrome de Berry a été établi.\n\nInterventions : Elle a subi un traitement chirurgical en 1 étape et a été déchargée avec succès. Le processus chirurgical visait à préserver le potentiel de croissance de l'aorte et des artères pulmonaires tout en assurant un écoulement ventriculaire gauche non obstrué et la continuité de l'arc aortique, en évitant toute dérivation entre les principales artères pulmonaires.\n\nRésultats : L'échocardiographie transœsophagienne intraopératoire a confirmé un flux continu à travers l'arc aortique et l'absence de dérivation entre le MPA et l'aorte.\n",
+        "synthetic_summary": {
+            "B1": "Il y a une petite fille de 6 ans qui avait un problème avec son cœur. Ses lèvres étaient un peu bleues, et elle avait du mal à bien respirer.\n\nLes docteurs ont fait des examens et ont trouvé ce qui n’allait pas dans son cœur. Ils ont décidé de l’aider avec une opération.\n\nPendant l’opération, les docteurs ont réparé son cœur pour que le sang puisse bien passer. Après, la petite fille allait beaucoup mieux. Les docteurs ont vérifié que tout fonctionnait bien dans son cœur. Elle est rentrée à la maison en bonne santé.",
+            "B2": "**Ce qu'ils ont trouvé chez la patiente**  \nCette histoire concerne une fille de 6 ans qui souffrait d’un problème rare appelé syndrome de Berry. Ce syndrome affecte le cœur et les gros vaisseaux sanguins. Elle avait des symptômes sérieux, comme un manque d’oxygène dans le sang (hypoxie) et des signes d’un mauvais apport en sang aux organes (ischémie).\n\n**Comment ils ont diagnostiqué le problème**  \nLes médecins ont utilisé plusieurs examens, comme une échographie du cœur et un scanner spécial, pour bien comprendre son cœur et ses artères. Ils ont découvert que certaines grosses artères étaient mal formées ou interrompues, ce qui empêchait le sang de circuler normalement. Ces résultats ont permis de confirmer le diagnostic du syndrome de Berry.\n\n**Le traitement réalisé**  \nLa patiente a subi une opération chirurgicale en une seule fois. Pendant l’opération, les chirurgiens ont réparé l’arc aortique (une grosse artère qui sort du cœur) et les artères pulmonaires, en veillant à ce que ces vaisseaux puissent encore grandir avec elle. Ils ont aussi évité que du sang ne passe entre les artères pulmonaires et l’aorte de façon anormale, ce qui pourrait causer des problèmes.\n\n**Les résultats après l’opération**  \nPendant l’opération, une échographie spéciale a montré que le sang circulait bien dans l’arc aortique et qu’il n’y avait pas de fuite entre les artères pulmonaires et l’aorte. Après l’opération, la pression dans les poumons de la patiente a diminué, elle n’a pas eu besoin de médicaments pour cela, et elle a pu quitter l’hôpital en bonne santé.",
+            "B3": "Résumé détaillé et structuré du cas clinique\n\nContexte  \nNous présentons le cas d’une fille de 6 ans issue d’une famille d’agriculteurs, qui présentait dès la naissance une cyanose modérée des lèvres (coloration bleutée due à un manque d’oxygène dans le sang) et des épisodes fréquents de toux et de pneumonies. Initialement suspectée d’avoir une cardiopathie congénitale, elle a été adressée à notre clinique en raison d’une aggravation progressive de sa cyanose et de difficultés respiratoires (dyspnée). Sa croissance et son développement intellectuel étaient normaux.\n\nPrincipales observations  \nL’examen clinique a révélé des bruits cardiaques anormaux, des doigts en baguette de tambour (clubbing) et une cyanose labiale persistante. L’électrocardiogramme a montré un rythme cardiaque normal avec une hypertrophie (augmentation de taille) des deux ventricules du cœur et une déviation de l’axe électrique vers la droite. L’échocardiographie transthoracique a mis en évidence une hypertrophie importante des ventricules et de l’oreillette gauche, ainsi qu’une interruption de l’arc aortique distal à l’artère sous-clavière gauche (c’est-à-dire une discontinuité dans la grande artère principale qui sort du cœur). Par ailleurs, l’artère pulmonaire droite provenait anormalement de l’aorte ascendante, tandis que l’artère pulmonaire gauche émanait du tronc pulmonaire. Un canal artériel persistant (PDA) reliait l’aorte descendante à l’artère pulmonaire gauche. L’hypertension pulmonaire était modérée, avec une pression estimée à 50 mm Hg. Une angiographie par tomodensitométrie (CT) en 3D a confirmé ces anomalies, identifiant un défaut de communication aorto-pulmonaire (APW) de type I, une interruption de l’arc aortique (IAA) de type A, et un PDA. Quatre branches artérielles principales étaient visibles, dont une artère sous-clavière droite anormale.\n\nInterprétation clinique  \nCes anomalies complexes correspondent au syndrome de Berry, une malformation cardiaque congénitale rare associant interruption de l’arc aortique, communication anormale entre l’aorte et l’artère pulmonaire, et canal artériel persistant. Ce diagnostic explique la cyanose, la dyspnée et les infections pulmonaires récurrentes observées chez la patiente.\n\nIntervention chirurgicale  \nLa patiente a bénéficié d’une intervention chirurgicale en une seule étape, réalisée par une incision au milieu du sternum (mi-sternotomie). La chirurgie a inclus la ligature et l’excision du canal artériel, la réparation de l’interruption de l’arc aortique par une anastomose (raccord) entre l’aorte descendante et l’arc aortique, renforcée par un patch de péricarde (membrane entourant le cœur). L’artère pulmonaire droite a été déconnectée de l’aorte et rattachée au tronc pulmonaire, tandis que le défaut de communication aorto-pulmonaire a été fermé à l’aide d’un patch péricardique bovin. La fonction des valves cardiaques et des artères coronaires a été préservée. Une technique d’arrêt circulatoire hypothermique profonde avec perfusion cérébrale sélective a été utilisée pour protéger le cerveau pendant l’intervention.\n\nRésultats post-opératoires  \nL’échocardiographie transœsophagienne réalisée pendant la chirurgie a confirmé un flux sanguin continu et non obstrué à travers l’arc aortique, sans dérivation anormale entre l’aorte et l’artère pulmonaire principale. Après l’opération, la patiente a été prise en charge en unité de soins intensifs, puis transférée en service conventionnel au bout de cinq jours. La pression artérielle pulmonaire a diminué à 26 mm Hg sans nécessiter de traitement médicamenteux spécifique. Aucun soutien hémodynamique n’a été requis, et la patiente a pu quitter l’hôpital en bonne condition sept jours après l’intervention.\n\nProchaines étapes  \nUn suivi régulier est nécessaire pour surveiller la croissance et la fonction des vaisseaux réparés, ainsi que l’évolution de la pression pulmonaire. Cette prise en charge vise à assurer une qualité de vie optimale et prévenir d’éventuelles complications à long terme.\n\nEn résumé, ce cas illustre la complexité du syndrome de Berry et la réussite d’une réparation chirurgicale complète en une seule étape, permettant de restaurer une circulation sanguine normale et d’améliorer significativement l’état clinique de la patiente."
+        }
+    },
+    {
+        "article": "En décembre 2020, un homme de 43 ans ayant des antécédents d'hépatite B de 9 ans a subi une échographie lors d'un examen médical de routine à l'hôpital populaire de Ruian, qui a révélé plusieurs lésions hypoéchogènes dans son foie.\n\nLes tests de laboratoire ont montré une légère élévation des taux d'alpha-foetoprotéine (AFP) (AFP : 32,9 ng/ml), tandis que les autres marqueurs tumoraux tels que les antigènes glucidiques 19-9, 125 et 153, et l'antigène carcino-embryonnaire étaient dans les limites normales. Les lésions apparaissaient comme de faible densité avec des marges peu claires sur l'imagerie par tomographie par ordinateur (CT) et présentaient une intensification centripète de la phase artérielle à la phase portale sur l'imagerie par tomographie par ordinateur à contraste dynamique. Les tailles des lésions variaient, la plus grande étant une lésion de forme irrégulière mesurant 4,1 × 4,3 cm de diamètre.\n\nEn ce qui concerne l'imagerie par résonance magnétique (IRM) à contraste dynamique, la plus grande lésion a présenté une amélioration périphérique immédiate en forme d'anneau, suivie d'une amélioration continue progressive et d'une cicatrice d'amélioration centrale. Pendant ce temps, les lésions plus petites ont présenté une amélioration en forme d'anneau avec une amélioration centripète progressive pendant les phases veineuse portale et retardée. Pour un examen plus approfondi, le patient a été envoyé à l'hôpital Huashan de Shanghai le 30 décembre 2020.\n\nLe patient a rapidement subi une tomographie par émission de positrons (TEP) avec [18F]-FDG, qui n’a révélé aucune absorption évidente. Cependant, la TEP avec [11C] acétate a indiqué une faible absorption uniquement pour la plus grande lésion située dans le lobe VII (valeur de l’absorption standard maximale [VASmax] = 4,21, rapport tumeur-arrière-plan [RTAB] = 1,45), tandis que les autres plus petites n’ont pas montré d’absorption. Fait intéressant, la TEP avec [68Ga] Ga-FAPI-04 a non seulement montré une forte absorption élevée pour la plus grande lésion (VASmax = 1,94, RTAB = 3,08), mais aussi pour les plus petites lésions intrahépatiques (VASmax = 1,47, RTAB = 2,33).\n\nSur la base des examens existants, un diagnostic préliminaire de carcinome hépatocellulaire (CHC) a été établi. Le patient a ensuite bénéficié d'une hépatectomie partielle en 6 jours, et le diagnostic a été confirmé par une analyse pathologique. La plus grande lésion située dans le segment VII a été identifiée comme un CHC solitaire, tandis que les autres lésions plus petites ont été diagnostiquées comme des hémangioendothéliomes épithéliaux hépatiques (HEHE).\n\nMicroscopiquement, de plus petites lésions sont apparues sous forme de nids et de cordes de cellules endothéliales épithélioïdes, avec des lumières intracytoplasmiques réparties dans tout le stroma myxo-hyalinique. La coloration CD31 et ERG1 était fortement positive, confirmant le diagnostic de lésion hépatique de type HEHE (Fig. 4A-E). La lésion hépatique du segment VII a présenté une positivité pour Hep1 en immunohistochimie, confirmant le diagnostic de HCC.\n\nLe patient a été libéré le jour postopératoire 9 et aucune récidive n'a été détectée lors de son suivi jusqu'à présent.\n",
+        "gold_summary": "Nous présentons un cas de carcinome hépatocellulaire synchrone (CHC) et de HEHE chez un patient chinois de 43 ans. Des lésions hépatiques hypoéchogènes multiples ont été décrites, mais aucun résultat d'imagerie spécifique n'a été détecté sur une tomographie par ordinateur (CT) ou une imagerie par résonance magnétique (MRI) améliorée par contraste. Le patient a ensuite subi une TEP/CT avec [18F]-FDG, une TEP/CT avec acétate [11C] et une TEP/CT avec [68Ga]Ga-FAPI-04. Les lésions de HEHE n'ont pas présenté de prise sur les images TEP/CT avec 18F-FDG et 11C-acétate, mais ont présenté une visualisation claire dans la TEP/CT avec [68Ga]Ga-FAPI-04. La plus grande lésion située dans le segment VII a finalement été diagnostiquée comme CHC, tandis que les autres plus petites ont été diagnostiquées comme HEHE, ce qui a été confirmé par une coloration immunohistochimique pour CD31. À notre connaissance, seuls 2 cas ont été rapportés dans la littérature mondiale, et le premier cas a utilisé à la fois l'acétate [11C] et le [68Ga]Ga-FAPI-04 TEP/CT au lieu du 18F-FDG TEP/CT.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 43 ans avait des petits boutons dans son gros ventre. Ces boutons étaient dans son foie, un organe important. \n\nLes docteurs ont fait plusieurs photos spéciales pour voir ces boutons. Certaines photos montraient bien le plus gros bouton, mais pas les petits. \n\nIls ont utilisé une autre photo spéciale qui a bien montré tous les boutons. Après, ils ont enlevé le gros bouton avec une opération. \n\nLe gros bouton était un vilain bouton. Les petits boutons étaient des boutons pas dangereux. \n\nLe monsieur va bien maintenant et les docteurs continuent de le surveiller.",
+            "B2": "**Un cas rare de deux types de tumeurs du foie chez un homme de 43 ans**\n\nUn homme de 43 ans, qui avait une hépatite B depuis plusieurs années, a découvert plusieurs petites zones anormales dans son foie lors d’un examen médical. Ces zones, appelées lésions, étaient visibles grâce à différentes techniques d’imagerie, comme l’échographie, le scanner (CT) et l’IRM avec injection de produit de contraste. Cependant, ces examens ne montraient pas clairement de quel type de tumeur il s’agissait.\n\nPour mieux comprendre, les médecins ont utilisé une technique spéciale appelée TEP/CT, qui permet de voir l’activité des cellules dans le corps en utilisant différentes substances radioactives. Avec la première substance ([18F]-FDG), ils n’ont pas vu d’activité particulière. Avec une deuxième substance ([11C] acétate), seule la plus grande lésion montrait une faible activité. Mais avec une troisième substance ([68Ga]Ga-FAPI-04), toutes les lésions, même les plus petites, étaient bien visibles.\n\nAprès une opération pour enlever une partie du foie, les analyses au microscope ont montré que la plus grande tumeur était un carcinome hépatocellulaire (CHC), un type courant de cancer du foie. Les autres petites lésions étaient un type rare de tumeur appelée hémangioendothéliome épithélioïde hépatique (HEHE). Cette distinction a été confirmée grâce à des colorations spéciales qui détectent certaines protéines dans les cellules.\n\nCe cas est très rare car il montre la présence en même temps de ces deux types de tumeurs dans le foie. C’est aussi la première fois qu’on utilise à la fois les substances [11C] acétate et [68Ga]Ga-FAPI-04 pour mieux détecter ces lésions, alors que la substance classique [18F]-FDG ne montrait rien. Le patient s’est bien remis après l’opération et aucune nouvelle tumeur n’a été trouvée jusqu’à présent.",
+            "B3": "Résumé détaillé et structuré\n\nContexte  \nNous rapportons le cas d’un homme chinois de 43 ans, porteur d’une hépatite B chronique depuis neuf ans, chez qui plusieurs lésions hépatiques ont été découvertes de manière fortuite lors d’un examen médical de routine en décembre 2020. Ces lésions étaient hypoéchogènes (c’est-à-dire apparaissant plus sombres à l’échographie) et multiples, sans caractéristiques spécifiques évidentes à l’imagerie conventionnelle par tomodensitométrie (CT) ou imagerie par résonance magnétique (IRM) avec injection de produit de contraste.\n\nPrincipales observations  \nLes analyses sanguines ont révélé une élévation modérée de l’alpha-foetoprotéine (AFP), un marqueur souvent associé au cancer du foie, tandis que d’autres marqueurs tumoraux étaient normaux. L’imagerie CT dynamique a montré des lésions de densité faible avec un rehaussement (augmentation du contraste) progressif de la périphérie vers le centre, tandis que l’IRM dynamique a mis en évidence une amélioration périphérique en anneau suivie d’une progression centripète et d’une cicatrice centrale dans la plus grande lésion. Ces caractéristiques n’étaient pas spécifiques et ne permettaient pas de différencier clairement les types de lésions.\n\nPour affiner le diagnostic, le patient a subi plusieurs examens par tomographie par émission de positrons (TEP) utilisant différents traceurs radioactifs :  \n- La TEP avec [18F]-FDG, un traceur classique du métabolisme du glucose, n’a montré aucune absorption significative dans les lésions.  \n- La TEP avec [11C]-acétate a révélé une faible absorption uniquement dans la plus grande lésion située dans le segment VII du foie, suggérant une activité métabolique accrue compatible avec un carcinome hépatocellulaire (CHC).  \n- La TEP avec [68Ga]Ga-FAPI-04, un traceur ciblant les fibroblastes associés aux tumeurs (cellules du tissu conjonctif souvent activées dans les cancers), a montré une forte absorption non seulement dans la plus grande lésion mais aussi dans les lésions plus petites.\n\nInterprétation clinique  \nSur la base de ces examens, un diagnostic préliminaire de carcinome hépatocellulaire pour la plus grande lésion a été posé, tandis que la nature des autres lésions restait incertaine. Après une résection partielle du foie réalisée six jours plus tard, l’analyse histopathologique a confirmé que la plus grande lésion correspondait bien à un CHC. Les lésions plus petites ont été identifiées comme des hémangioendothéliomes épithélioïdes hépatiques (HEHE), une tumeur rare d’origine vasculaire. Cette distinction a été confirmée par des colorations immunohistochimiques spécifiques : les cellules des HEHE étaient fortement positives pour CD31 et ERG1 (marqueurs des cellules endothéliales), tandis que la lésion CHC exprimait HepPar-1, un marqueur hépatocytaire.\n\nProchaines étapes et conclusion  \nLe patient a été libéré neuf jours après l’intervention chirurgicale et aucun signe de récidive tumorale n’a été observé lors du suivi ultérieur. Ce cas est remarquable car la coexistence synchrone d’un CHC et d’HEHE est extrêmement rare, avec seulement deux cas similaires rapportés dans la littérature mondiale. De plus, c’est le premier cas documenté utilisant conjointement la TEP avec [11C]-acétate et [68Ga]Ga-FAPI-04, qui a permis une meilleure détection des lésions HEHE que la TEP classique au [18F]-FDG. Cette observation suggère que la TEP avec [68Ga]Ga-FAPI-04 pourrait constituer un outil précieux pour le diagnostic et la caractérisation des lésions hépatiques rares."
+        }
+    },
+    {
+        "article": "Un homme de 65 ans a présenté une enflure et une déformation boutonnière du doigt médian droit six mois après un accident de moto survenu le 1er janvier 2023. Au début, il a géré la blessure avec des analgésiques et n'a pas consulté un médecin. Après six mois de symptômes persistants, y compris une incapacité à étendre complètement le doigt et un œdème visible, il a demandé un traitement.\n\nConstatations cliniques\nL'inspection de la main droite a révélé la présence d'une déformation avec oedème. L'amplitude active du mouvement (ROM) était altérée dans l'articulation PIP du troisième doigt de la main droite. L'amplitude active du mouvement (ROM) de l'articulation PIP du troisième doigt de la main droite était de 45 à 110 degrés. L'amplitude passive du mouvement (ROM) de l'articulation PIP du troisième doigt de la main droite était normale.\n\nÉvaluation diagnostique\nNous avons effectué une radiographie de la main droite AP/Lateral qui a montré qu'il n'y avait aucune anomalie osseuse et nous avons diagnostiqué une déformation des tissus mous due à une blessure centrale par glissement.\n\nTechnique chirurgicale\nUne reconstruction du défaut de glissement central utilisant le côté ulnaire du tendon flexor digitorum superficiel a été réalisée. Sous anesthésie, le patient a été positionné en décubitus dorsal avec un garrot appliqué au bras supérieur. Une incision médiolatérale a été pratiquée sur le côté ulnaire de la phalange médiane droite, centrée sur l'articulation PIP. L'incision s'est étendue dorsalement de manière oblique. Une incision transversale a été pratiquée sur le pli de flexion de l'articulation MCP, juste proximal à la poulie A1. La procédure implique l'identification et la protection du faisceau neurovasculaire digital ulnaire, l'exposition du glissement central et du tendon extenseur à l'articulation PIPJ, les lambeaux dorsaux de pleine épaisseur sont élevés. Le tissu cicatriciel et le tissu pseudo-tendineux sont identifiés et excisés. Le glissement central ne peut pas être réparé en premier, donc le glissement ulnaire du tendon FDS est utilisé pour la reconstruction. Le faisceau neurovasculaire ulnaire est mobilisé pour visualiser l'insertion périostale de la poulie A3.\n\nLe tendon extenseur est mobilisé et tenolysé, suivi d'une incision de la capsule dorsale de l'articulation PIP et de l'ablation du tissu interposé. L'insertion périostée de la poulie A3 est incisée longitudinalement, et la capsule palmaire de l'articulation PIP est incisée longitudinalement. Le slip ulnaire du tendon FDS est identifié et une suture monofilament non résorbable 2-0 est placée autour de lui. Une incision transversale est faite au pli de flexion de l'articulation MCP, proximal à la poulie A1, révélant la gaine du tendon fléchisseur. La gaine du tendon et la poulie A1 sont incisées longitudinalement. Le tendon FDS est identifié. Le slip ulnaire du tendon FDS est isolé et tranché pour libérer le slip ulnaire, en évitant l'enchevêtrement ou la capture du slip radial. La suture 2-0 qui a été placée autour du slip ulnaire au niveau de l'articulation PIP est utilisée pour libérer le slip distal du tendon FDS et délivrer le slip ulnaire du tendon FDS distalement.\n\nUne perceuse de 2,8 mm est utilisée pour créer un tunnel osseux verticalement orienté dorsal à volar. Un élévateur est placé entre le tendon du flexor digitorum profundus, la plaque volar et l'aspect volar de la base de la phalange médiane, protégeant les structures anatomiques volar. Le tendon FDS passe à travers le tunnel tout en maintenant l'articulation PIP en extension et en position réduite. Le tendon FDS passe à travers la section proximale intacte du tendon central et du tendon extenseur. Un tisserand de tendon complète un tissage de Pulvertaft, confirmant la tension appropriée avec l'articulation PIPJ en position réduite, en pleine extension. Une suture non absorbable 3-0 sécurise le tissage de Pulvertaft. Les marges de la reconstruction de la capsule et du tunnel central sont approximées à travers l'articulation PIP, et les adhérences sont libérées et les bandes latérales mobilisées.\n\nLa posture générale, la stabilité et le mouvement avec la tenodèse sont évalués. Toutes les incisions sont abondamment irriguées. Le garrot est dégonflé et l'hémostase est obtenue. Le remplissage capillaire de tous les doigts est évalué. La peau est fermée à l'aide de points de suture horizontaux. Un pansement stérile est appliqué avec une attelle d'extension de l'articulation PIP appropriée pour permettre un mouvement précoce de l'articulation DIP et de l'articulation MCP.\n\nSuivi et résultats\nLe premier suivi a été effectué 4 jours plus tard pour le traitement de la plaie. Le patient a reçu du méloxicam oral à 7,5 mg deux fois par jour et de la doxycycline à 100 mg deux fois par jour pendant 3 jours. Le deuxième suivi a été effectué 3 jours plus tard pour le traitement de la plaie. Après 2 semaines, nous avons enlevé la plaque arrière, retiré la suture externe et commencé l'exercice de ROM active et passive. Après 3 semaines, la plaie a été guérie et nous avons constaté que la ROM de l'articulation PIP était de 0 à 90 degrés. Et après un mois, le patient est venu avec une ROM active et passive de l'articulation PIP de 0 à 100 degrés, et un résultat fonctionnel amélioré. Après 7 semaines de réadaptation physique, les patients sont déjà de retour au travail avec une ROM active et passive de l'articulation PIP de 0 à 110 degrés. La fonction de la main droite du patient est évaluée avec le score DASH, qui s'améliore significativement de 50 à 4,2.\n",
+        "gold_summary": "Un patient de 65 ans a présenté un gonflement et une déformation boutonnière du troisième doigt de la main droite. Le patient était tombé précédemment d'une moto et son pouce droit avait été écrasé par une moto six mois auparavant. Après l'incident, le pouce droit du patient ne pouvait plus être complètement étendu. La main droite du patient a présenté un oedème avec flexion de l'articulation interphalangienne (PIP) et hyperextension de l'articulation interphalangienne distale (DIP). L'amplitude de mouvement (ROM) du pouce droit était de 45 à 110 degrés. La radiographie de la main droite AP/oblique ne montrait aucune ossification de la déformation. Le patient a subi une reconstruction du défaut de glissement central en utilisant le côté ulnaire partiel du tendon superficiel du flexor digitorum. Une attelle de prolongation du pouce droit a été appliquée pendant 2 semaines. L'exercice actif et passif de l'amplitude de mouvement du pouce droit a commencé 2 semaines après l'attelle de prolongation du pouce droit. L'amplitude de mouvement du pouce droit (0 à 90 degrés) a été significativement améliorée 1 mois après l'intervention chirurgicale. L'amplitude de mouvement du pouce droit a été rétablie à la normale 2 mois après l'intervention chirurgicale. La fonction de la main droite du patient a été évaluée avec le score DASH, qui s'est amélioré significativement de 50 à 4,2.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 65 ans s’est fait mal au doigt de la main droite. Son doigt était tout gonflé et tordu. Il ne pouvait plus bien l’étirer.\n\nIl s’était fait mal en tombant de sa moto. Son doigt est resté bloqué comme ça pendant six mois.\n\nLe docteur a fait une petite opération pour réparer le doigt. Il a utilisé un petit bout de tendon pour aider à remettre le doigt droit.\n\nAprès l’opération, il a mis une attelle pour garder le doigt bien droit. Deux semaines plus tard, il a commencé à bouger doucement son doigt.\n\nUn mois après, il pouvait presque bien bouger son doigt. Deux mois après, son doigt allait presque comme avant.\n\nLe docteur a dit que sa main allait beaucoup mieux et qu’il pouvait faire plein de choses avec.",
+            "B2": "**Ce qu'ils ont trouvé**  \nUn homme de 65 ans a eu un accident de moto et, six mois plus tard, son troisième doigt de la main droite était gonflé et déformé. Il ne pouvait plus tendre complètement ce doigt. En regardant sa main, on a vu un gonflement et une position anormale : l’articulation du milieu du doigt (appelée PIP) était pliée, tandis que l’articulation la plus proche de l’ongle (DIP) était trop tendue. Quand il essayait de bouger son doigt, il pouvait l’étendre entre 45 et 110 degrés, ce qui est moins que la normale. Une radiographie a montré que ses os étaient normaux, donc le problème venait des tissus mous autour de l’articulation.\n\n**Ce qu’ils ont fait**  \nLes médecins ont réparé le tendon endommagé en utilisant une partie d’un autre tendon appelé tendon fléchisseur superficiel. Ce tendon aide normalement à plier les doigts. Ils ont fait une opération pour reconstruire la partie cassée du tendon extenseur, qui sert à tendre le doigt. Après l’opération, ils ont mis une attelle pour garder le doigt en extension pendant deux semaines.\n\n**La récupération**  \nDeux semaines après l’opération, le patient a commencé des exercices pour bouger doucement son doigt, à la fois activement (en le bougeant lui-même) et passivement (en aidant le doigt à bouger). Un mois après l’opération, il pouvait tendre son doigt de 0 à 90 degrés, ce qui est une nette amélioration. Après deux mois, il avait retrouvé presque toute sa mobilité normale, avec un mouvement de 0 à 110 degrés. Sa fonction de la main s’est aussi beaucoup améliorée, mesurée par un test appelé score DASH, qui est passé de 50 (beaucoup de difficulté) à 4,2 (presque normal).\n\n**En résumé**  \nCette opération a permis à cet homme de retrouver l’usage normal de son doigt après une blessure qui avait causé une déformation et une perte de mouvement. Grâce à la chirurgie et à la rééducation, il a pu reprendre ses activités habituelles.",
+            "B3": "Résumé réécrit pour un public adulte non-médecin :\n\n**Contexte**  \nUn homme de 65 ans a consulté pour un gonflement et une déformation en boutonnière (une position anormale où le doigt est plié au milieu et hyperétendu à l’extrémité) du troisième doigt de sa main droite. Ces symptômes sont apparus six mois après un accident de moto, au cours duquel il s’était blessé la main droite. Initialement, il n’avait pas consulté, mais l’incapacité à redresser complètement son doigt et l’œdème persistant l’ont amené à chercher un traitement.\n\n**Principales observations cliniques**  \nL’examen a montré un œdème et une déformation caractéristique du doigt médian droit. Le mouvement actif de l’articulation intermédiaire du doigt (appelée articulation interphalangienne proximale, ou PIP) était limité, avec une amplitude allant de 45 à 110 degrés, alors que le mouvement passif (lorsqu’on déplace le doigt sans effort du patient) était normal. La radiographie n’a révélé aucune anomalie osseuse, ce qui a orienté le diagnostic vers une lésion des tissus mous, plus précisément une rupture du tendon extenseur central du doigt.\n\n**Intervention chirurgicale**  \nLe patient a subi une reconstruction chirurgicale du tendon extenseur central, en utilisant une partie du tendon fléchisseur superficiel (un tendon fléchisseur du doigt) du même doigt, côté ulnaire (côté du petit doigt). L’opération a été réalisée sous anesthésie avec un garrot au bras pour limiter le saignement. Le chirurgien a fait plusieurs incisions autour de l’articulation PIP pour accéder au tendon endommagé, retirer le tissu cicatriciel, et préparer le site pour la reconstruction. Le segment du tendon fléchisseur a été isolé, détaché partiellement, puis passé à travers un tunnel osseux créé dans la phalange médiane du doigt. Ce tendon a été fixé solidement pour remplacer la partie rompue du tendon extenseur, permettant de restaurer la fonction d’extension du doigt. La stabilité et la tension ont été vérifiées avant de refermer les incisions. Une attelle maintenant le doigt en extension a été posée pour protéger la réparation.\n\n**Suivi et résultats**  \nLe patient a été vu en consultation plusieurs fois pour le soin des plaies et la gestion de la douleur avec des médicaments anti-inflammatoires et antibiotiques. Deux semaines après l’opération, l’attelle a été retirée et des exercices de mobilisation active et passive du doigt ont commencé. Après un mois, l’amplitude de mouvement de l’articulation PIP s’était améliorée, passant de 0 à 90 degrés, et à deux mois, elle était revenue à 0 à 110 degrés, proche de la normale. La fonction globale de la main droite, évaluée par le score DASH (un questionnaire mesurant la capacité fonctionnelle du membre supérieur), s’est nettement améliorée, passant de 50 (indiquant une incapacité importante) à 4,2 (presque normale). Après sept semaines de rééducation, le patient avait retrouvé une fonction suffisante pour reprendre son travail.\n\n**Conclusion**  \nCette reconstruction chirurgicale utilisant une partie du tendon fléchisseur superficiel a permis de restaurer efficacement la fonction d’extension du doigt médian chez un patient présentant une déformation boutonnière chronique due à une rupture du tendon extenseur central. La rééducation postopératoire précoce a contribué à l’amélioration fonctionnelle rapide et durable."
+        }
+    },
+    {
+        "article": "Une femme de 26 ans a été référée par un neurologue pour une perte de vision progressive, séquentielle et bilatérale et une vision floue survenues au cours d'un mois à partir de l'œil droit et plus prononcées dans cet œil, sans mouvements oculaires douloureux. Elle avait des antécédents médicaux de syndrome cliniquement isolé impliquant la moelle épinière. Ses symptômes sensoriels avaient débuté 7 ans avant la présentation, impliquant son pied gauche et se déplaçant sur une période de plusieurs semaines pour atteindre un niveau distal à la taille. Son imagerie par résonance magnétique (IRM) du cerveau et de la moelle épinière avait révélé une lésion dans la région infratentorielle et une autre dans la moelle épinière thoracique. Les IRM de suivi ont identifié de nouvelles lésions d'amélioration temporellement distinctes aux niveaux C4, C6-C7, T2 et T7-T8. Des examens complémentaires ont révélé des résultats négatifs pour les anticorps anti-aquaporine-4 et anti-protéine des oligodendrocytes myéliniques (MOG). Elle ne recevait aucune médication au moment de la présentation et son historique de tabagisme et de consommation d'alcool était insignifiant. Ses antécédents familiaux étaient insignifiants pour les causes héréditaires de la perte de vision, y compris la LHON.\n\nL'examen neuro-ophtalmologique a révélé une acuité visuelle corrigée (AV) de 20/100 OD et 20/30-2 OS. Son AV a progressivement amélioré lors des visites de suivi. Les plaques de couleur Ishihara ont révélé qu'elle était capable de lire seulement 1 sur 17 plaques de couleur dans l'œil droit et 14 sur 17 plaques de couleur dans l'œil gauche. Il n'y avait pas de défaut pupillaire afférent relatif. La tomographie en cohérence optique (OCT) a révélé une épaisseur moyenne de la couche de fibres nerveuses rétiniennes de 83 microns OD et 93 microns OS avec un léger amincissement temporel. L'examen du fond d'œil dilaté a révélé une pâleur des deux nerfs optiques avec un rapport de la coupole au disque de 0,2.\n\nLe diagnostic différentiel pour ses symptômes visuels comprenait des neuropathies optiques bilatérales, telles que la neurite optique ou la LHON. Les carences nutritionnelles ont été exclues en raison du nombre normal de globules rouges, de B12, de folate. Elle a ensuite pris 1 250 mg de prednisone par voie orale par jour pendant 3 jours, suivis de 60 mg et d'une réduction progressive de 10 mg tous les 5 jours ; toutefois, lors de la visite de suivi, elle n'a signalé aucune amélioration de ses symptômes. Des examens complémentaires ont révélé des hyperintensités T2 modérées du côté droit du chiasma optique et trois nouvelles lésions de la substance blanche cérébrale (splenium ; 2 lésions de la substance blanche pariétale péri-ventriculaire gauche) sur l'IRM. Les résultats de l'IRM et les bandes oligoclonales détectées par ponction lombaire ont confirmé le diagnostic de la sclérose en plaque. Au cours des visites de suivi ultérieures, son test de champ visuel Humphrey a révélé des scotomes centraux bilatéraux dans les deux yeux. La nature lentement progressive, l'implication séquentielle des yeux, les scotomes centraux symétriques, les symptômes non sensibles aux stéroïdes et les hyperintensités du chiasma optique détectées par IRM étaient suggestives de la LHON. L'examen du fond d'œil dilaté a révélé une pâleur temporelle. Les tests génétiques pour les trois mutations primaires ont été négatifs ; toutefois, elle était hétérozygote pour la variante c.152A>G du gène DNAJC30 associée à la sclérose en plaque latérale. Elle a également été testée positive pour la variante c.1239C>T dans le gène UQCRC1 avec un modèle d'héritage autosomique dominant. Elle a été diagnostiquée avec le syndrome de Harding et a commencé à prendre 300 mg d'idébénone par voie orale par TDS quotidiennement, ce qui a conduit à une amélioration de ses symptômes. Son AV a progressivement amélioré au fil des visites annuelles de suivi (son dernier AV corrigé était de 20/40-2 OD et 20/20-2 OS) et les métriques et examens OCT sont restés stables avec une pâleur temporelle bilatérale. Les champs visuels et les OCT 4 ans après le suivi sont présentés.\n",
+        "gold_summary": "Nous présentons une femme de 26 ans avec une perte visuelle progressive, séquentielle, indolore, bilatérale qui ne répond pas aux stéroïdes, et deux épisodes distincts de troubles neurologiques temporaires évoquant une démyélinisation du système nerveux central. Des investigations approfondies, y compris des tests sérologiques, ont exclu d'autres causes, y compris une neuromyélite optique négative et des anticorps anti-protéine oligodendrocytaire de myéline (MOG) et des carences nutritionnelles. L'IRM a détecté des zones de démyélinisation dans la moelle épinière et le cerveau (zones infratentoriales et périventriculaires). Après une analyse génétique révélant une mutation c.152A>G (p.Tyr51Cys) au niveau du gène DNAJC30, une LHON a été suggérée. Elle a été traitée par idébenone et son acuité visuelle a été résolue à 4 ans de suivi.\n",
+        "synthetic_summary": {
+            "B1": "Une jeune femme avait de plus en plus de mal à bien voir avec ses deux yeux. Ça ne faisait pas mal. \n\nLes docteurs ont fait beaucoup de tests pour comprendre pourquoi. Ils ont regardé dans sa tête et dans son dos avec une grosse machine. Ils ont vu des endroits qui ne marchaient pas bien. \n\nIls ont aussi cherché si elle avait des maladies qui se transmettent dans la famille. Ils ont trouvé un petit problème dans ses gènes. \n\nLes docteurs lui ont donné un médicament spécial. Avec ce médicament, elle a commencé à mieux voir. \n\nAprès plusieurs années, sa vue était beaucoup mieux. Les docteurs sont contents car elle va mieux.",
+            "B2": "### Ce qu'ils ont trouvé\n\nUne jeune femme de 26 ans a perdu progressivement la vue dans ses deux yeux, d'abord dans l'œil droit, sans douleur. Cette perte de vision est venue lentement, sur plusieurs semaines, et n’a pas répondu au traitement habituel par stéroïdes. Elle avait déjà eu des problèmes nerveux liés à la moelle épinière plusieurs années auparavant. Des examens d’imagerie (IRM) ont montré des zones anormales dans son cerveau et sa moelle épinière, ce qui suggère une maladie appelée sclérose en plaques, où la protection des nerfs est abîmée.\n\n### Ce que cela signifie\n\nLes médecins ont cherché d’autres causes possibles, comme des infections, des carences en vitamines, ou d’autres maladies des nerfs optiques, mais tous ces tests étaient négatifs. Une analyse génétique a trouvé une mutation dans un gène appelé DNAJC30, qui est liée à une maladie appelée LHON (neuropathie optique héréditaire de Leber). Cette maladie provoque une perte progressive de la vision à cause d’un problème dans les cellules nerveuses des yeux.\n\n### Le traitement et l’évolution\n\nElle a commencé un traitement avec un médicament nommé idébenone, qui aide à protéger les cellules nerveuses. Après quatre ans, sa vision s’est améliorée, même si certains signes de dommages aux nerfs optiques restent visibles. Ce cas montre qu’il est important de faire des examens complets, y compris des tests génétiques, quand une perte de vision progressive ne répond pas aux traitements habituels.",
+            "B3": "**Contexte**  \nNous rapportons le cas d’une femme de 26 ans présentant une perte progressive et séquentielle de la vision, touchant d’abord l’œil droit puis l’œil gauche, sans douleur lors des mouvements oculaires. Ses antécédents incluaient un syndrome cliniquement isolé avec des symptômes sensoriels liés à des lésions démyélinisantes de la moelle épinière survenues sept ans auparavant. Les examens d’imagerie par résonance magnétique (IRM) avaient montré plusieurs lésions cérébrales et médullaires caractéristiques d’une atteinte démyélinisante, sans présence d’anticorps spécifiques de neuromyélite optique (anti-aquaporine-4) ni d’anticorps anti-MOG. Aucun traitement n’était en cours au moment de la survenue des troubles visuels.\n\n**Principales observations**  \nL’examen neuro-ophtalmologique a révélé une baisse importante de l’acuité visuelle, plus marquée à droite (20/100) qu’à gauche (20/30), avec une altération notable de la perception des couleurs dans l’œil droit. L’examen du fond d’œil montrait une pâleur bilatérale des nerfs optiques, signe d’atrophie optique. La tomographie en cohérence optique (OCT) a mis en évidence un amincissement modéré de la couche des fibres nerveuses rétiniennes, plus prononcé dans la région temporale. Malgré un traitement par corticostéroïdes oraux, aucun bénéfice clinique n’a été observé. L’IRM cérébrale a révélé des lésions nouvelles au niveau du chiasma optique et de la substance blanche cérébrale, compatibles avec une sclérose en plaques (SEP), diagnostic confirmé par la présence de bandes oligoclonales dans le liquide céphalorachidien.\n\n**Interprétation clinique**  \nLa nature progressive et bilatérale des troubles visuels, l’absence de réponse aux stéroïdes, la présence de scotomes centraux symétriques au test du champ visuel, ainsi que les anomalies IRM du chiasma optique, ont orienté vers un diagnostic différentiel entre une neuropathie optique démyélinisante et la neuropathie optique héréditaire de Leber (LHON). Les tests génétiques ont exclu les mutations primaires classiques de la LHON, mais ont identifié une variante hétérozygote c.152A>G dans le gène DNAJC30, associée à une forme de LHON. Par ailleurs, une autre mutation dans le gène UQCRC1, avec un mode de transmission autosomique dominant, a été détectée. Ces résultats ont conduit au diagnostic final de syndrome de Harding, une forme de LHON.\n\n**Prochaines étapes et évolution**  \nLa patiente a débuté un traitement par idébenone (300 mg trois fois par jour), un médicament visant à améliorer la fonction mitochondriale. Ce traitement a permis une amélioration progressive de son acuité visuelle sur une période de quatre ans, avec une stabilisation des mesures OCT et une persistance de la pâleur optique bilatérale. Les examens de suivi ont confirmé la stabilisation des déficits visuels et l’absence de nouvelles lésions démyélinisantes. Ce cas illustre l’importance d’une évaluation multidisciplinaire approfondie, combinant imagerie, analyses biologiques et tests génétiques, pour différencier les neuropathies optiques démyélinisantes des neuropathies optiques héréditaires, et adapter le traitement en conséquence."
+        }
+    },
+    {
+        "article": "Nous décrivons le cas d'un patient de 18 ans atteint de DMD et en fauteuil roulant depuis l'âge de 11 ans, qui a toujours été suivi par une équipe multidisciplinaire au sein de notre établissement. Depuis l'âge de 6 ans, il a été traité par un médicament oral avec du déflazacort. Au cours de ces années, le patient a été régulièrement suivi par des pneumologues utilisant la spirométrie et par des neurologues qui ont surveillé l'évolution de la maladie neuromusculaire en termes de fonction thoraco‐abdominale et de scoliose. La capacité vitale forcée (CVF), le volume expiratoire forcé en 1 s (VEF1) et le débit expiratoire de pointe (PEF) étaient respectivement de 60 %, 70 % et 70 % des valeurs prévues (CVF, 2,24 l ; VEF1, 2,09 l ; PEF, 4,07 l). Le patient a également subi une cathétérisation cardiaque droite pour surveiller les résistances vasculaires pulmonaires avec des valeurs témoins dans la plage normale. Lorsqu'il a progressivement développé une cardiomyopathie dilatée en 2016, à l'âge de 14 ans, il a subi une implantation de LVAD HeartWare, en raison d'une insuffisance cardiaque réfractaire aiguë. L'option de transplantation cardiaque n'a pas été envisagée par les chirurgiens cardiaques pédiatriques, (i) en raison de l'urgence dans laquelle se trouvait le patient et (ii) en raison du scepticisme commun à l'égard de la transplantation cardiaque chez ces patients atteints de DMD. Le sevrage de la ventilation mécanique s'est produit de manière routinière, et aucune complication postopératoire n'a été rencontrée.\n\nAu cours des 47 mois suivants, le patient a été régulièrement suivi, et nous n'avons rapporté qu'une infection du site de sortie, traitée par antibiotiques et toilette chirurgicale, 30 mois après l'implantation du LVAD. Le débridement de la ligne de commande consistait en une incision de la peau suivant le trajet du câble, une extériorisation du câble plus proximalement, un nettoyage du trajet fistuleux et une nouvelle suture de la peau. Bien que la récupération ait été excellente, étant donné que la sortie de la ligne de commande était très proche de la plaie sternale, le patient a été suffisamment stressé psychologiquement pour demander spontanément une solution radicale au problème. La CVF, la VEMS et le PEF étaient respectivement de 1,66 l, 1,62 l et 4,41 l. Compte tenu des bonnes conditions générales du patient et de sa motivation personnelle, notre équipe multidisciplinaire a commencé à envisager une transplantation cardiaque comme option. Ainsi, le 12 février 2020, à l'âge de 18 ans, le patient a subi une transplantation cardiaque sans complications postopératoires. Le sevrage de la ventilation mécanique a eu lieu comme d'habitude une fois de plus. Le premier jour post-transplantation, il a été possible d'extuber le patient. La sortie de l'unité de soins intensifs a été possible le troisième jour postopératoire. En ce qui concerne la mobilisation, dans notre unité, les patients sont suivis par une équipe spécialisée de physiothérapeutes. Le patient a été formé par eux dès les premiers jours ; et dès qu'il a été transféré de l'unité de soins intensifs au service, la mobilisation a été commencée dès que possible. En ce qui concerne la stabilisation sternale, comme nous le faisons habituellement, nous avons suggéré d'utiliser une bande sternale en tissu. La mobilisation en fauteuil roulant a été possible le cinquième jour postopératoire. La durée totale de l'hospitalisation était de 3 semaines, le temps nécessaire pour effectuer les trois biopsies canoniques pour l'évaluation de tout rejet myocardique. Une thérapie immunosuppressive standard à trois agents a été administrée (cyclosporine, mycophenolate mofetil et stéroïdes). Au bout de 3 mois, la CVF, la VEMS et le PEF étaient inchangés par rapport à la période pré-transplantation.",
+        "gold_summary": "Nous décrivons le cas d'un patient de 18 ans, atteint de DMD et en fauteuil roulant depuis l'âge de 11 ans. Il a progressivement développé une cardiomyopathie dilatée et, en 2016, à l'âge de 14 ans, il a subi une implantation de LVAD HeartWare, en tant que traitement de destination, sans complications postopératoires. Il a été suivi pendant 47 mois consécutifs ; et 30 mois après l'implantation de LVAD, il a développé une infection du site de sortie, traitée par antibiotiques et toilette chirurgicale. À la suite de cet événement, sur la base des bonnes conditions générales du patient et de sa volonté, nous avons commencé à envisager la transplantation cardiaque comme option. Avant que le patient ne soit inscrit, il a subi un examen approfondi, et nous avons trouvé des valeurs plus élevées de capacité vitale forcée, de volume expiratoire forcé en 1 s, et de débit expiratoire de pointe, par rapport aux valeurs prévues des patients DMD du même âge. Le patient n'a ni scoliose ni besoin de ventilation mécanique non invasive, et enfin, il a toujours été traité avec des stéroïdes avec une fonction thoraco-abdominale stable au fil des ans. Conformément à ces considérations, le patient a été inscrit pour une transplantation cardiaque. Le 12 février 2020, à l'âge de 18 ans, le patient a subi une transplantation cardiaque sans complications postopératoires. La transplantation cardiaque n'est pas considérée comme une option valable pour les patients DMD, en raison du manque de disponibilité des donneurs et de la nature systémique de la maladie DMD. Considérant que ce patient avait déjà connu une complication liée au LVAD et qu'il avait une meilleure condition générale que ses pairs DMD, nous l'avons inscrit pour une transplantation cardiaque. Nous décrivons le cas d'un patient DMD qui a subi une transplantation cardiaque réussie après 47 mois d'assistance LVAD HeartWare. Le suivi de trois mois est sans incident.\n",
+        "synthetic_summary": {
+            "B1": "Il y a un garçon de 18 ans qui ne peut plus marcher. Il a une maladie qui rend ses muscles très faibles. Depuis qu’il a 14 ans, son cœur ne marche pas bien. Les docteurs lui ont mis une petite machine pour aider son cœur à battre.\n\nCette machine a bien marché pendant presque 4 ans. Mais un jour, il a eu une petite infection. Les docteurs ont soigné cette infection avec des médicaments et un petit soin.\n\nLe garçon était en bonne forme malgré tout. Il voulait un nouveau cœur pour aller mieux. Les docteurs ont regardé tout son corps et ont décidé de lui donner un nouveau cœur.\n\nLe 12 février 2020, il a eu une opération pour changer son cœur. Tout s’est bien passé. Après l’opération, il a bien récupéré et il va mieux. Les docteurs continuent de bien s’occuper de lui.",
+            "B2": "Cas d’un jeune patient atteint de DMD et suivi médical\n\nNous racontons l’histoire d’un garçon de 18 ans atteint de dystrophie musculaire de Duchenne (DMD), une maladie qui affaiblit les muscles. Il est en fauteuil roulant depuis l’âge de 11 ans. À 14 ans, il a développé un problème grave au cœur appelé cardiomyopathie dilatée, où le muscle cardiaque devient faible et dilaté. Pour l’aider, les médecins lui ont implanté un appareil appelé LVAD HeartWare. Ce dispositif aide le cœur à pomper le sang. L’opération s’est bien passée et il n’y a pas eu de complications après.\n\nSuivi et complication liée à l’appareil\n\nPendant presque 4 ans, le patient a été suivi régulièrement. Trente mois après la pose de l’appareil, il a eu une infection au niveau du câble qui sortait de sa peau. Cette infection a été soignée avec des antibiotiques et une petite opération pour nettoyer la zone. Malgré cette complication, le patient se portait bien et voulait une solution plus durable.\n\nDécision de faire une transplantation cardiaque\n\nLes médecins ont alors pensé à une transplantation cardiaque, c’est-à-dire remplacer son cœur malade par un cœur sain donné par un donneur. Avant cela, ils ont fait des examens pour vérifier sa capacité respiratoire et sa santé générale. Ils ont constaté que ses poumons fonctionnaient mieux que chez d’autres patients atteints de DMD du même âge. Il n’avait pas de scoliose (courbure de la colonne vertébrale) ni besoin d’aide pour respirer. Il suivait un traitement par stéroïdes qui aidait à stabiliser ses muscles thoraciques et abdominaux.\n\nTransplantation et suivi\n\nLe 12 février 2020, à 18 ans, il a reçu un nouveau cœur sans problème pendant ou après l’opération. Il a pu être retiré rapidement de la ventilation mécanique (appareil qui aide à respirer). Après l’opération, il a été aidé par des physiothérapeutes pour se mobiliser en fauteuil roulant dès que possible. Il est resté à l’hôpital trois semaines, le temps de vérifier que son corps acceptait bien le nouveau cœur. Un traitement spécial a été donné pour éviter que son corps rejette le cœur.\n\nConclusion\n\nLa transplantation cardiaque est rarement proposée aux patients atteints de DMD à cause de la maladie qui touche tout le corps et du manque de cœurs disponibles. Mais dans ce cas, grâce à la bonne condition générale du patient et à sa motivation, cette opération a réussi. Trois mois après la transplantation, son état respiratoire était stable et il n’y a pas eu de complications. Ce cas montre qu’une transplantation cardiaque peut être une option possible chez certains patients DMD bien suivis.",
+            "B3": "Résumé détaillé et structuré du cas clinique d’un patient atteint de dystrophie musculaire de Duchenne (DMD) ayant bénéficié d’une transplantation cardiaque après assistance ventriculaire gauche (LVAD) :\n\n**Contexte**  \nIl s’agit d’un patient de 18 ans atteint de dystrophie musculaire de Duchenne, une maladie neuromusculaire progressive, en fauteuil roulant depuis l’âge de 11 ans. Depuis son enfance, il a été suivi par une équipe multidisciplinaire comprenant pneumologues et neurologues, et traité par déflazacort, un corticostéroïde oral, depuis l’âge de 6 ans. Sa fonction respiratoire, évaluée par spirométrie, montrait une capacité vitale forcée (CVF) à 60 % des valeurs attendues, un volume expiratoire maximal en une seconde (VEF1) à 70 %, et un débit expiratoire de pointe (PEF) également à 70 %. Il ne présentait pas de scoliose ni de besoin de ventilation mécanique non invasive. Sur le plan cardiaque, il a développé une cardiomyopathie dilatée à l’âge de 14 ans, compliquée d’une insuffisance cardiaque aiguë réfractaire.\n\n**Principales Observations**  \nEn 2016, à 14 ans, le patient a bénéficié de l’implantation d’un dispositif d’assistance ventriculaire gauche (LVAD HeartWare) en traitement de destination, car la transplantation cardiaque n’était pas envisagée à ce stade, notamment en raison de l’urgence et des réserves habituelles concernant la transplantation chez les patients atteints de DMD. Le sevrage de la ventilation mécanique postopératoire s’est déroulé sans complication. Pendant les 47 mois suivants, le patient a été suivi régulièrement. Une seule complication majeure a été rapportée : une infection du site de sortie du câble de l’appareil survenue 30 mois après l’implantation, traitée efficacement par antibiotiques et débridement chirurgical local.\n\nSuite à cet épisode infectieux, et compte tenu de l’état général satisfaisant du patient ainsi que de sa motivation, l’équipe multidisciplinaire a réévalué la possibilité d’une transplantation cardiaque. Les examens prétransplantation ont montré une fonction respiratoire stable, avec des valeurs de CVF, VEF1 et PEF supérieures à celles habituellement observées chez des patients DMD du même âge. Le patient ne présentait pas de scoliose ni de ventilation non invasive, et sa fonction thoraco-abdominale était stable sous traitement corticoïde.\n\n**Interprétation Clinique**  \nLa transplantation cardiaque est généralement peu considérée chez les patients atteints de DMD en raison de la nature systémique de la maladie, de la rareté des donneurs et des complications associées. Cependant, dans ce cas particulier, la bonne condition générale du patient, son absence de complications respiratoires majeures, et la survenue d’une complication liée au LVAD ont motivé l’inscription sur liste de transplantation. Cette décision a été prise après une évaluation approfondie et en tenant compte de la volonté du patient.\n\n**Prochaines Étapes et Résultats**  \nLe 12 février 2020, à l’âge de 18 ans, le patient a subi une transplantation cardiaque sans complication postopératoire. Le sevrage de la ventilation mécanique a été réalisé rapidement, avec extubation dès le premier jour post-transplantation. La mobilisation a été initiée précocement grâce à une équipe spécialisée en physiothérapie, et la stabilisation sternale a été assurée par une bande sternale en tissu. La durée totale d’hospitalisation a été de trois semaines, incluant la surveillance par biopsies myocardiques pour détecter un éventuel rejet. Le traitement immunosuppresseur standard à trois agents a été administré. Au terme d’un suivi de trois mois, la fonction respiratoire du patient est restée stable, sans dégradation par rapport à la période pré-transplantation.\n\n**Conclusion**  \nCe cas illustre qu’une transplantation cardiaque peut être une option viable chez certains patients atteints de dystrophie musculaire de Duchenne présentant une bonne condition générale et une fonction respiratoire préservée, même après une longue période d’assistance ventriculaire gauche. Cette approche multidisciplinaire individualisée a permis une prise en charge réussie, avec un suivi postopératoire favorable à court terme."
+        }
+    },
+    {
+        "article": "M. S. était un patient de 88 ans, retraité, ouvrier du bâtiment, veuf, vivant seul dans un appartement au premier étage avec des escaliers. Il n’avait qu’une fille, sa principale personne de soutien. Il n’avait pas de services d’aide à domicile avant son hospitalisation.\n\nSon historique clinique était marqué par des arthrites répétées décrites comme de la goutte, une insuffisance cardiaque sur une sténose aortique serrée qui a ensuite bénéficié d'une TAVI, une insuffisance rénale chronique modérée (clairance 45 ml/min/1,73 m2), un stenting bi-fémoral aorto-bi-fémoral, une hypertension artérielle, un accident ischémique transitoire, un tremblement essentiel et une thrombose veineuse du droit. Il n'avait pas de mauvaises habitudes ou d'allergies.\n\nLe 7 novembre, ce patient a été admis au service des urgences pour décompensation cardio-rénale consécutive à une pneumopathie. Le patient s'est rétabli avec un traitement antibiotique associé à un traitement diurétique. Après cinq jours, il a été transféré dans une unité gériatrique pour une évaluation gériatrique standardisée et pour une rééducation en raison d'un déconditionnement physique.\n\nLes premiers prélèvements sanguins du 13 novembre ont révélé un taux de calcium de 2,55 mmol/L, corrigé à 2,84 mmol/L. Il y avait une dénutrition sévère avec une dose d'albumine mesurée à 28,3 mmol/L. Une PTH a été augmentée à 94 ng/L et une 25-hydroxy-vitamine D effondrée à 15 nmol/L. Cliniquement, il ne présentait aucun signe clinique évocateur d'hypercalcémie. La radiographie thoracique ne révélait aucune anomalie. En décembre, compte tenu du soupçon d'hyperparathyroïdie secondaire due à une hypovitaminose D et non conforme aux recommandations standard, une échographie parathyroïdienne n'a révélé aucun nodule suspect. Une supplémentation en cholécalciférol a été introduite. En outre, une gestion nutritionnelle a été initiée. M. S présentait en même temps une arthrite douloureuse des genoux avec épanchement articulaire associé à un syndrome inflammatoire biologique. Une chondrocalcinose était suspectée mais le taux d'acide urique était élevé à 478 µmol/L. Une ponction a été réalisée : 920 cellules nucléées par mm3 et des cristaux d'urate sodique ont été trouvés dans le liquide articulaire. Le traitement par la colchicine et ensuite l'ajout d'allopurinol ont amélioré les symptômes. L'état cardiaque et les améliorations physiques ont permis au patient de rentrer chez lui le 2 janvier.\n\nMalheureusement, une nouvelle décompensation cardiaque a nécessité une nouvelle hospitalisation le 23 janvier. Au cours de cette hospitalisation ultérieure, les taux de calcium sanguin sont restés légèrement élevés (2,64 mmol/L) et la PTH a été significativement augmentée (191 ng/L) malgré la supplémentation en vitamine D. En mars, un échantillon d’urine de 24 heures a été collecté pour la mesure de la calciurie, qui a révélé une diminution de la concentration de calcium urinaire de 1,23 mmol/L. L’excrétion fractionnée du calcium était de 1,2 %. En raison de ces résultats inhabituels, une scintigraphie parathyroïdienne MIBI n’a révélé aucune anomalie en faveur d’un adénome ou d’une hyperplasie parathyroïdienne. En avril, une analyse génétique pour détecter la mutation inhibitrice du gène CASR codant pour le récepteur sensible au calcium (gène 3q21.1) a révélé une variante pathogène classée comme FHH de type 1 selon les directives ACMG. La famille du patient a été informée et un dépistage génétique a été organisé pour éviter des tests supplémentaires inutiles. Le patient a finalement pu rentrer chez lui. Le patient et sa famille ont donné leur consentement éclairé pour ce rapport de cas. L’approbation éthique n’a pas été requise pour ce manuscrit. Consentement pour publication de la fille du patient obtenu.",
+        "gold_summary": "Nous rapportons le diagnostic de FHH chez un patient polypathologique de 88 ans présentant une hypercalcémie découverte lors d'un contrôle pour décompensation cardiaque. Malgré une présentation clinique confuse avec des symptômes de goutte, y compris des épisodes répétés d'arthrite du genou, une hypercalcémie persistante a conduit à des investigations complémentaires. Les tests biologiques ont exclu un hyperparathyroïdisme primaire ou hyperparathyroïdisme lié à une tumeur maligne, confirmant le diagnostic de FHH par la détection d'une mutation inhibitrice dans le gène du récepteur sensible au calcium.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 88 ans avait trop de calcium dans son sang. Les docteurs ont fait beaucoup de tests pour comprendre pourquoi. Ils ont trouvé que ce n’était pas une maladie grave.  \n\nCe monsieur avait aussi mal aux genoux, mais ce n’était pas lié au calcium.  \n\nLes docteurs ont découvert que son corps garde trop de calcium à cause d’un petit problème dans ses gènes. Ce problème ne fait pas de mal.  \n\nIls ont expliqué tout ça à sa famille pour qu’ils comprennent bien. Le monsieur a pu rentrer chez lui tranquille.",
+            "B2": "**Ce qu'ils ont découvert chez le patient**\n\nM. S., un homme de 88 ans avec plusieurs problèmes de santé, avait un taux de calcium dans le sang un peu trop élevé, appelé hypercalcémie. Cette situation a été remarquée pendant qu’il était soigné pour des problèmes cardiaques. Il souffrait aussi de douleurs aux genoux liées à la goutte, une maladie où des cristaux s’accumulent dans les articulations.\n\n**Les examens réalisés**\n\nLes médecins ont fait plusieurs analyses pour comprendre pourquoi son calcium était élevé. Ils ont vérifié si cela venait d’une maladie des glandes parathyroïdes, qui contrôlent le calcium dans le corps, ou d’un cancer. Ces causes ont été exclues grâce aux tests. Ensuite, une analyse génétique a montré que M. S. avait une mutation dans un gène important pour le contrôle du calcium, ce qui explique son hypercalcémie.\n\n**Ce que cela signifie**\n\nCette mutation provoque une maladie appelée « hypercalcémie familiale bénigne » (FHH). C’est une maladie rare où le corps garde un taux de calcium un peu élevé, mais qui n’est généralement pas dangereuse. Connaitre ce diagnostic est important pour éviter des examens inutiles et pour informer la famille, car cette maladie peut être héréditaire.\n\nEn résumé, même si M. S. avait plusieurs problèmes de santé compliqués, les médecins ont réussi à identifier la vraie cause de son taux de calcium élevé grâce à des tests précis, ce qui a aidé à mieux gérer sa santé.",
+            "B3": "Résumé détaillé et structuré :\n\n**Contexte**  \nM. S., un homme de 88 ans avec de multiples antécédents médicaux (notamment une insuffisance cardiaque, une insuffisance rénale chronique modérée, une hypertension artérielle, et des épisodes d’arthrite goutteuse), a été hospitalisé à plusieurs reprises pour des décompensations cardiaques et des complications associées. Lors de son suivi, une hypercalcémie (taux élevé de calcium dans le sang) a été détectée de manière persistante, sans signes cliniques évidents d’hypercalcémie.\n\n**Principales Observations**  \n- Le patient présentait une hypercalcémie modérée et persistante, avec des taux de calcium corrigés allant jusqu’à 2,84 mmol/L.  \n- La parathormone (PTH), hormone régulant le calcium, était augmentée de façon significative, ce qui a initialement orienté vers un hyperparathyroïdisme secondaire ou primaire.  \n- Une carence sévère en vitamine D a été identifiée, et une supplémentation a été mise en place.  \n- Les examens d’imagerie (échographie et scintigraphie parathyroïdienne) n’ont pas montré de nodules ou d’adénomes parathyroïdiens, excluant une cause tumorale classique.  \n- L’analyse du calcium dans les urines a révélé une excrétion calcique basse, ce qui est atypique dans l’hyperparathyroïdisme primaire.  \n- Une analyse génétique a identifié une mutation pathogène du gène CASR, codant pour le récepteur sensible au calcium, confirmant le diagnostic de « FHH » (hypercalcémie familiale bénigne, une maladie génétique rare caractérisée par une régulation anormale du calcium).\n\n**Interprétation Clinique**  \nLe diagnostic de FHH a été retenu chez ce patient âgé présentant une hypercalcémie persistante. Cette affection génétique provoque une élévation modérée du calcium sanguin sans conséquences graves, souvent confondue avec un hyperparathyroïdisme primaire. La distinction est essentielle car la FHH ne nécessite pas de traitement chirurgical et évite des interventions inutiles. La présence concomitante de goutte et d’autres pathologies a complexifié le tableau clinique, mais les investigations approfondies ont permis d’écarter d’autres causes plus fréquentes d’hypercalcémie.\n\n**Prochaines Étapes**  \n- Information et suivi du patient et de sa famille, avec un dépistage génétique proposé aux membres à risque afin d’éviter des examens invasifs ou inutiles.  \n- Poursuite de la gestion des autres comorbidités (goutte, insuffisance cardiaque, dénutrition) dans un cadre multidisciplinaire.  \n- Surveillance clinique régulière sans indication de traitement spécifique pour la FHH, compte tenu de son caractère bénin.  \n\nCe cas illustre l’importance d’une évaluation complète et rigoureuse des hypercalcémies, en particulier chez les patients âgés polypathologiques, afin d’identifier des causes rares comme la FHH et d’adapter la prise en charge en conséquence."
+        }
+    },
+    {
+        "article": "Une femme de 65 ans présentant une dyspnée a été admise dans un hôpital local et a été hospitalisée pour insuffisance cardiaque et pneumonie en octobre 2017. Une immunoélectrophorèse urinaire a révélé la présence de la protéine Bence Jones de type λ. Une analyse de l'urine immunoélectrophorèse a révélé une hématurie de 1,29 g/grammes de créatinine urinaire et < 1 globule rouge/champ de haute puissance. Les facteurs de complément du sérum 3 et 4 étaient normaux. Les anticorps antinucléaires, le facteur rhumatoïde et les anticorps cytoplasmiques antineutrophiles étaient négatifs. Son analyse d'urine a révélé une protéinurie de 1,29 g/grammes de créatinine urinaire et < 1 globule rouge/champ de haute puissance. La tomodensitométrie a révélé des épanchements pleuraux bilatéraux et des infiltrations pulmonaires indiquant une pneumonie dans les deux poumons. L'échocardiographie après admission a révélé les résultats suivants : diamètre de fin de diastole du ventricule gauche, 41,8 mm ; diamètre de fin de systole du ventricule gauche, 28,7 mm ; fraction d'éjection, 59,6 % ; épaisseur du septum interventriculaire, 14,8 mm ; épaisseur de la paroi postérieure du ventricule gauche, 14,5 mm ; rapport E/A, 1,14 ; et E/e' 14,75. L'épaississement étendu du ventricule gauche et du septum interventriculaire et la dysfonction diastolique (restrictive) ont été observés, et ces anomalies étaient compatibles avec une amyloïdose cardiaque. Après admission, elle a commencé un traitement avec des antimicrobiens, de la dobutamine, et une dialyse continue par hémodialyse (CHDF). Les paramètres de la CHDF étaient les suivants : débit sanguin de 60-80 ml/min, débit de dialysat de 100-300 ml/h, et débit de filtration de 100-300 ml/h. Son état général s'est stabilisé progressivement, et elle a été transférée à une hémodialyse intermittente (HD). La HD a été réalisée pendant 4 h avec un débit sanguin de 100-120 ml/min, en utilisant un dialyseur en polyéthersulfone (PES-15Eαeco, Nipro Corporation, Osaka, Japon). Cependant, elle a développé une thrombocytopénie, et des anticorps anti-héparine-facteur plaquettaire 4 (PF4) sont devenus positifs (1,1 U/mL ; valeur négative inférieure à 0,9 U/mL) le 14e jour après admission. Nous avons arrêté l'héparine en raison d'une suspicion de thrombocytopénie induite par l'héparine (TIH), et avons administré un régime de dialyse continue et un argatroban. En outre, elle a développé une hypotension intradialytique (IDH). Dans ces circonstances, il était difficile de poursuivre la HD, et nous avons donc changé la RRT en PD. Un cathéter de PD a été inséré sous anesthésie locale le 16e jour après admission. À partir du 2e jour postopératoire, une PD ambulatoire continue a été initiée, et nous avons ajusté le régime de PD en fonction du volume de la patiente. Le régime de PD a finalement été fixé à une dialyse péritonéale automatisée utilisant 4 L de tampon neutralisé à 1,35 % de glucose par dialyse péritonéale (Midpeliq 135L, Terumo Corporation, Tokyo, Japon) et une solution de 1 L de 7,5 % d'icodextrine par dialyse péritonéale (Nicopeliq, Terumo Corporation, Tokyo, Japon) par jour. L'élimination de fluide par la PD était d'environ 500 ml/jour, et nous avons pu gérer le volume de la patiente avec succès grâce à ce régime. Le volume d'urine était d'environ 1000 ml/jour avec l'administration de 160 mg/jour de furosémide, 50 mg/jour de spironolactone, et 15 mg/jour de tolvaptan, et n'a pas changé pendant l'hospitalisation, indiquant une bonne fonction rénale résiduelle. Elle a été renvoyée à la maison le 44e jour après admission. Les niveaux de BNP et de NT-proBNP étaient améliorés à 195,1 pg/mL et 12 922,0 pg/mL à la décharge, respectivement. Depuis lors, elle a été suivie en tant que patient externe, et elle continue la PD pendant 2 ans sans aucun symptôme ou complication grave. Elle a une bonne qualité de vie et aime voyager autour du Japon. Les résultats de l'échocardiographie après décharge étaient comme suit : diamètre de fin de diastole du ventricule gauche, 42,9 mm ; diamètre de fin de systole du ventricule gauche, 31,0 mm ; fraction d'éjection, 54,1 % ; épaisseur du septum interventriculaire, 16,4 mm ; épaisseur de la paroi postérieure du ventricule gauche, 11,4 mm ; rapport E/A, 0,71 ; et E/e' 8,57. Ces résultats étaient similaires à ceux pendant l'hospitalisation, bien que la dysfonction diastolique ait été légèrement améliorée.",
+        "gold_summary": "Une femme de 65 ans a été hospitalisée pour insuffisance cardiaque et pneumonie dans un hôpital voisin. Elle avait été précédemment diagnostiquée comme souffrant d'amylose à chaînes légères (AL) et traitée par mélphalan plus dexaméthasone (Mel-Dex) et lenalidomide plus dexaméthasone (Len-Dex). Elle a commencé un traitement comprenant des antimicrobiens et des diurétiques, mais sa fonction rénale s'est progressivement détériorée, et elle a été transférée dans notre hôpital pour des soins néphrologiques. Elle a été traitée par des antimicrobiens, de la noradrénaline, de la dobutamine et une hémodiafiltration continue. Son état général s'est progressivement stabilisé, et elle a été transférée à une hémodialyse intermittente (HD). Cependant, la HD a été interrompue en raison d'une hypotension intradialytique et du développement d'une thrombocytopénie induite par l'héparine. Son traitement de remplacement rénal a été transféré à une dialyse péritonéale (DP), ce qui a permis un bon contrôle du volume et une fonction cardiaque stable. Elle a été libérée et est toujours en bonne condition, sans complications graves et avec un pronostic considérablement meilleur que prévu.\n",
+        "synthetic_summary": {
+            "B1": "Une dame de 65 ans était très malade. Elle avait du mal à respirer et une infection aux poumons. Son cœur ne marchait pas bien. \n\nLes docteurs ont donné des médicaments pour l’aider. Mais ses reins ont commencé à moins bien marcher. Elle est venue dans un autre hôpital pour être soignée. \n\nIls ont utilisé une machine pour nettoyer son sang. Puis, ils ont essayé une autre machine, mais elle ne lui faisait pas du bien. \n\nAlors, ils ont mis un petit tuyau dans son ventre pour faire une autre sorte de nettoyage. Ça a très bien marché. \n\nLa dame est devenue plus forte. Elle est rentrée chez elle et elle va bien maintenant. Elle peut même voyager et s’amuser. Les docteurs sont contents.",
+            "B2": "Une femme de 65 ans a été hospitalisée à cause de problèmes au cœur (insuffisance cardiaque) et d’une infection aux poumons (pneumonie). Elle avait déjà une maladie appelée amylose à chaînes légères (AL), où des protéines anormales s’accumulent dans certains organes, ce qui peut causer des dégâts. Avant, elle avait reçu des traitements pour cette maladie.\n\nÀ l’hôpital, elle a reçu des médicaments pour combattre l’infection et aider son cœur, ainsi que des traitements pour ses reins qui ne fonctionnaient plus bien. D’abord, elle a eu une hémodiafiltration continue, une méthode pour nettoyer le sang quand les reins sont en panne. Son état s’est amélioré, alors on est passé à une hémodialyse intermittente, une autre technique pour filtrer le sang.\n\nCependant, elle a eu des problèmes pendant cette hémodialyse : sa tension artérielle baissait trop souvent, et elle a développé une baisse importante de ses plaquettes, les cellules qui aident à la coagulation du sang. Cette baisse était causée par une réaction à l’héparine, un médicament utilisé pour éviter les caillots pendant la dialyse.\n\nÀ cause de ces complications, les médecins ont changé son traitement rénal pour une dialyse péritonéale. Cette méthode utilise la membrane à l’intérieur de son ventre pour filtrer le sang, ce qui est plus doux et mieux toléré dans son cas. Grâce à cela, ils ont pu bien contrôler le volume de liquide dans son corps et maintenir une bonne fonction cardiaque.\n\nAprès sa sortie de l’hôpital, elle a continué la dialyse péritonéale chez elle pendant au moins deux ans, sans problème grave. Sa qualité de vie est bonne, elle se sent bien et peut même voyager. Ses examens cardiaques montrent que son cœur reste stable, avec une légère amélioration de sa fonction. En résumé, ce changement de traitement a beaucoup aidé sa santé et son bien-être.",
+            "B3": "Résumé destiné à un public non spécialiste mais instruit\n\n**Contexte**  \nUne femme de 65 ans a été admise initialement dans un hôpital local pour une insuffisance cardiaque associée à une pneumonie. Elle avait un antécédent d’amylose à chaînes légères (AL), une maladie rare caractérisée par le dépôt anormal de protéines dans les tissus, notamment le cœur et les reins. Elle avait déjà reçu des traitements spécifiques à base de mélphalan, dexaméthasone et lenalidomide. À son admission, elle présentait une détérioration progressive de la fonction rénale, nécessitant une prise en charge spécialisée.\n\n**Principales observations**  \nLes examens ont montré une atteinte cardiaque compatible avec une amylose, notamment un épaississement anormal des parois du ventricule gauche et du septum interventriculaire, ainsi qu’une dysfonction diastolique restrictive (difficulté du cœur à se remplir correctement). Une analyse d’urine a révélé une protéinurie modérée (présence de protéines dans les urines) et une hématurie légère (présence de sang dans les urines). Des examens sanguins ont exclu d’autres causes auto-immunes. Une tomodensitométrie a confirmé la présence d’épanchements pleuraux bilatéraux et d’infiltrats pulmonaires liés à la pneumonie.\n\nLe traitement initial comprenait des antimicrobiens, des médicaments pour soutenir la fonction cardiaque (dobutamine), et une dialyse continue par hémodialyse (CHDF) pour compenser la défaillance rénale. Après stabilisation, la patiente a été mise sous hémodialyse intermittente (HD). Cependant, elle a développé une thrombocytopénie (diminution du nombre de plaquettes sanguines) liée à une réaction immunitaire contre l’héparine, un médicament utilisé pour prévenir la coagulation pendant la dialyse. Par ailleurs, elle souffrait d’hypotension lors des séances de dialyse, rendant ce traitement difficile à poursuivre.\n\n**Interprétation clinique**  \nFace à ces complications, l’équipe médicale a décidé de remplacer l’hémodialyse par une dialyse péritonéale (DP), une technique de dialyse utilisant la membrane péritonéale de l’abdomen pour filtrer le sang. Un cathéter a été posé sous anesthésie locale, et un traitement de dialyse péritonéale automatisée a été instauré, combinant deux types de solutions de dialyse adaptées au contrôle du volume et à l’élimination des déchets. Ce régime a permis une gestion efficace du volume hydrique et une bonne fonction rénale résiduelle, avec un volume d’urine stable grâce à des médicaments diurétiques.\n\n**Prochaines étapes et évolution**  \nLa patiente a pu quitter l’hôpital au 44e jour après son admission initiale. À sa sortie, les marqueurs cardiaques (BNP et NT-proBNP), indicateurs de la charge sur le cœur, étaient améliorés. Elle a poursuivi la dialyse péritonéale en ambulatoire pendant au moins deux ans, sans complications majeures, avec une bonne qualité de vie et la possibilité de voyager. Les examens cardiaques réalisés après sa sortie ont montré une stabilité des anomalies structurelles, avec une légère amélioration de la fonction diastolique.\n\n**Conclusion**  \nCette prise en charge illustre la complexité du traitement d’une patiente atteinte d’amylose cardiaque et rénale, compliquée par une réaction indésirable à l’héparine et une hypotension liée à l’hémodialyse. Le passage à la dialyse péritonéale a permis un contrôle efficace de la maladie rénale et une stabilisation de la fonction cardiaque, contribuant à un pronostic favorable et à une bonne qualité de vie sur le long terme."
+        }
+    },
+    {
+        "article": "Un homme de 60 ans s'est effondré dans la salle de sauna d'un hôtel capsule, un établissement d'hébergement économique doté de petits dortoirs, où il résidait depuis deux ans. Le patient a déclaré avoir eu pendant une semaine un manque d'appétit, une diarrhée et une fièvre modérée, accompagnés d'une dyspnée qui s'aggravait progressivement au cours des trois jours précédant son admission. Son historique médical et ses médicaments étaient inconnus en raison d'un manque de contacts familiaux et d'une dyspnée sévère qui a empêché de recueillir des antécédents détaillés.\n\nLors de son admission, le patient présentait une tachycardie, une tachypnée et une hypoxémie. Ses signes vitaux étaient les suivants : tension artérielle 128/85 mmHg, fréquence cardiaque 120 battements par minute, fréquence respiratoire 40 respirations par minute, saturation en oxygène 88 % sur un masque non respiratoire de 15 L, et température corporelle 37,8 °C, correspondant à une fièvre modérée. L'examen physique a révélé une respiration rapide et peu profonde utilisant les muscles respiratoires accessoires. Son score sur l'échelle de Glasgow était E4V5M6.\n\nLes premiers résultats de laboratoire ont révélé une acidose métabolique sévère avec compensation respiratoire, comme en témoigne une analyse des gaz du sang artériel indiquant un pH de 7,067, une pression partielle de dioxyde de carbone (pCO₂) de 63,1 mmHg, une pression partielle d'oxygène (pO₂) de 126 mmHg, un bicarbonate (HCO₃⁻) de 17,3 mmol/L et un lactate de 11 mmol/L. Les résultats de laboratoire ont également indiqué une dysfonction rénale sévère avec une urée sanguine (BUN) de 147,2 mg/dL et une créatinine de 8,82 mg/dL. L'aspartate aminotransférase (AST) était élevée à 268 U/L et l'alanine aminotransférase (ALT) à 108 U/L, ainsi que la lactate déshydrogénase (LDH) à 1910 U/L et la créatine kinase (CK) à 1552 U/L. Une inflammation marquée était évidente, avec un nombre de globules blancs (WBC) de 64 × 10⁹/L et un taux de protéine C-réactive (CRP) de 17,13 mg/dL. La patiente avait également une thrombocytopénie, avec un nombre de plaquettes (PLT) de 8,6 × 10⁹/L (voir Tableau 1 pour les résultats de laboratoire complets). Les tests pour le VIH, COVID-19, et l'antigène urinaire de la légionnelle étaient négatifs. Une tomodensitométrie thoracique a révélé des consolidations bilatérales avec des lésions cavitaires, principalement dans le poumon gauche.\n\nDes échantillons d'expectorations obtenus par lavage bronchoalvéolaire ont révélé à la fois des cocci Gram-positifs et des bâtonnets Gram-négatifs. Le patient a été diagnostiqué comme souffrant d'une pneumonie sévère et d'un abcès pulmonaire causé par une infection polymicrobienne. Il a été intubé lors de son admission en USI. Des antibiotiques empiriques, dont la vancomycine, la pipéracilline-tazobactam et l'azithromycine, ont été initiés. De l'hydrocortisone à 200 mg/jour a également été administrée. Le rapport initial PaO₂/FiO₂ était de 110 lors de la ventilation mécanique, ce qui correspond à un ARDS modéré. En raison de l'aggravation de l'hypoxie, un blocus neuromusculaire a été initié et poursuivi pendant 48 heures, et une position couchée a été initiée. En raison de l'aggravation de la dysfonction rénale, une thérapie de remplacement rénal a été initiée. Une stratégie d'hypercapnie permissive a permis un pH aussi bas que 7,15.\n\nAu troisième jour, son rapport PaO₂/FiO₂ avait rapidement diminué à 65, ce qui témoignait d'une nouvelle détérioration. Une thérapie par l'oxyde nitrique inhalé a été initiée, mais elle n'a pas entraîné d'amélioration significative. Par conséquent, une oxygénation extracorporelle à membrane (OEC) a été initiée le soir du troisième jour.\n\nLes cultures d'expectorations n'ont donné que des résultats pour Moraxella catarrhalis, ce qui était en contradiction avec la première coloration de Gram, ce qui suggère une infection polymicrobienne. Les résultats de la culture étaient en contradiction avec les résultats de la première coloration de Gram. Compte tenu de cette contradiction et du fait que le patient résidait dans un hôtel capsule, la tuberculose a été suspectée comme cause sous-jacente de sa pneumonie réfractaire et de son SDRA. Au quatrième jour de l'admission, les bacilles acido-résistants étaient fortement positifs (>10 bacilles acido-résistants par champ d'huile), et la réaction en chaîne de la polymérase a détecté Mycobacterium tuberculosis, confirmant le diagnostic de tuberculose pulmonaire. Un traitement anti-tuberculeux avec isoniazide, rifampicine, pyrazinamide et éthambutol a été initié. 1 g de méthylprednisolone a été administré pendant trois jours pour traiter le SDRA associé à la tuberculose. Une bronchoscopie quotidienne a été effectuée pour gérer l'expectoration.\n\nEntre les jours 9 et 11, l'état clinique du patient s'est amélioré, comme en témoigne la résolution radiographique des infiltrats pulmonaires et une augmentation de la compliance respiratoire à 40 ml/cmH₂O, permettant un sevrage réussi de la MV-ECMO. Par la suite, une trachéotomie a été réalisée cinq jours plus tard pour faciliter un soutien ventilatoire prolongé.\n\nDeux jours après la trachéotomie, une lésion hépatique induite par les médicaments a nécessité l'ajustement de la thérapie anti-TB à l'étambutol, la streptomycine et la lévofloxacine. La cyclosérine a été ajoutée trois jours plus tard. Le patient est resté dépendant d'un ventilateur et a été transféré dans un hôpital spécialisé dans la tuberculose 29 jours après son admission. Étant donné que de nombreux professionnels de santé ont été exposés à la tuberculose avant sa confirmation, un programme de dépistage de l'exposition a été mis en place. Il comprenait une évaluation médicale, une radiographie thoracique et un test de libération d'interféron gamma sans identifier de cas de tuberculose active ou latente parmi le personnel.\n",
+        "gold_summary": "Nous rapportons le cas d'un homme de 60 ans qui a développé une insuffisance respiratoire sévère après s'être effondré dans une sauna. Initialement diagnostiqué avec une pneumonie communautaire sévère et un syndrome de détresse respiratoire aiguë (SDRA), son état s'est détérioré malgré un traitement standard, nécessitant une oxygénation extracorporelle à membrane (OECV) veino-veineuse. Les tests de bacilles acido-résistants ont confirmé une tuberculose pulmonaire (TB) au jour 4, ce qui a entraîné l'initiation d'une thérapie anti-TB. Après une amélioration clinique, le patient a été sevré avec succès de l'OECV et transféré dans un hôpital spécialisé en TB pour des soins continus.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 60 ans est tombé dans un sauna. Il avait beaucoup de mal à respirer. Les médecins ont d'abord pensé qu'il avait une grosse infection aux poumons. Ils lui ont donné des médicaments et de l'oxygène. Mais il n'allait pas mieux.\n\nAprès quelques jours, ils ont trouvé qu'il avait une maladie appelée tuberculose. C'est une maladie qui rend les poumons très malades. Ils ont commencé un autre traitement spécial pour cette maladie.\n\nPetit à petit, le monsieur a commencé à aller mieux. Il a pu arrêter l'oxygène spécial. Ensuite, il est allé dans un autre hôpital pour continuer ses soins. Les médecins ont bien pris soin de lui.",
+            "B2": "Cas d’un homme de 60 ans avec une grave infection pulmonaire\n\nUn homme de 60 ans s’est effondré dans un sauna d’un hôtel où il vivait. Avant cela, il avait eu pendant une semaine une perte d’appétit, de la diarrhée, de la fièvre modérée et des difficultés à respirer qui s’aggravaient. À son arrivée à l’hôpital, il avait une respiration très rapide, un rythme cardiaque élevé et un faible taux d’oxygène dans le sang.\n\nLes analyses ont montré qu’il avait une acidose métabolique (un problème d’équilibre acide-base dans le sang), une insuffisance rénale sévère (ses reins ne fonctionnaient pas bien), une forte inflammation et une baisse importante de ses plaquettes sanguines. Une radiographie du thorax a révélé des lésions dans ses poumons. Les premiers tests ont suggéré une infection par plusieurs types de bactéries.\n\nLe patient a été placé sous ventilation mécanique (un appareil pour l’aider à respirer) et a reçu des antibiotiques puissants. Malgré cela, son état s’est aggravé, avec une baisse importante de l’oxygène dans son sang. Une technique appelée oxygénation extracorporelle à membrane (OEC), qui aide à oxygéner le sang en dehors du corps, a été mise en place.\n\nAu quatrième jour, des tests spécifiques ont détecté la présence de bacilles acido-résistants, c’est-à-dire des bactéries responsables de la tuberculose pulmonaire. La tuberculose est une infection bactérienne qui attaque surtout les poumons. Un traitement spécial contre la tuberculose a alors été commencé, ainsi qu’un traitement pour réduire l’inflammation des poumons.\n\nAprès plusieurs jours, l’état du patient s’est amélioré : ses poumons ont commencé à guérir, et il a pu être sevré de l’oxygénation extracorporelle. Il a ensuite été transféré dans un hôpital spécialisé pour continuer son traitement contre la tuberculose. Un dépistage a été organisé pour le personnel soignant qui avait été en contact avec lui, mais aucune nouvelle infection n’a été détectée.\n\nCe cas montre qu’une tuberculose peut causer une pneumonie très grave et un syndrome de détresse respiratoire aiguë, nécessitant des soins intensifs et des traitements spécifiques. Il est important de penser à cette maladie, surtout chez des patients vivant dans des conditions particulières comme un hôtel capsule.",
+            "B3": "Résumé détaillé et structuré pour un public non médical éduqué\n\n**Contexte**  \nUn homme de 60 ans, résidant depuis deux ans dans un hôtel capsule (un type d’hébergement économique avec de petits dortoirs), s’est effondré dans la salle de sauna de l’établissement. Il présentait depuis une semaine des symptômes tels qu’une perte d’appétit, une diarrhée, une fièvre modérée, ainsi qu’une difficulté progressive à respirer (dyspnée) sur les trois jours précédant son admission à l’hôpital. Son historique médical était inconnu, car il n’avait pas de contacts familiaux et son état respiratoire sévère empêchait de recueillir des informations détaillées.\n\n**Principales observations cliniques et résultats**  \nÀ son arrivée, le patient était en détresse respiratoire sévère : sa fréquence cardiaque et respiratoire étaient très élevées, sa saturation en oxygène était basse malgré un apport important en oxygène, et il présentait une fièvre modérée. L’examen physique montrait une respiration rapide et superficielle utilisant les muscles accessoires, signe d’un effort respiratoire important. Son état neurologique était globalement conservé.\n\nLes analyses sanguines ont révélé une acidose métabolique sévère (un déséquilibre important du pH sanguin), une insuffisance rénale grave (avec des taux très élevés d’urée et de créatinine), des lésions hépatiques (élévation des enzymes hépatiques), une inflammation marquée (nombre très élevé de globules blancs et protéine C-réactive élevée) ainsi qu’une baisse importante du nombre de plaquettes sanguines. Les tests pour le VIH, la COVID-19 et la légionellose étaient négatifs. Une tomodensitométrie thoracique a montré des lésions pulmonaires étendues, avec des zones de consolidation (zones où le tissu pulmonaire est rempli de liquide ou de cellules inflammatoires) et des cavités, surtout dans le poumon gauche.\n\nL’examen des prélèvements pulmonaires a mis en évidence une infection bactérienne polymicrobienne (plusieurs types de bactéries), justifiant un traitement antibiotique large et l’intubation du patient en unité de soins intensifs. Malgré ces mesures, son état respiratoire s’est rapidement aggravé, nécessitant le recours à une ventilation mécanique avancée, à des médicaments pour faciliter la respiration, et à une thérapie de remplacement rénal.\n\n**Interprétation clinique**  \nAu troisième jour, la fonction respiratoire s’est encore détériorée, avec une hypoxie sévère (manque d’oxygène dans le sang), malgré l’utilisation d’oxygène inhalé. Une oxygénation extracorporelle à membrane (OEC), une technique de suppléance respiratoire très avancée qui oxygène le sang en dehors du corps, a alors été mise en place.\n\nLes cultures bactériennes ont montré uniquement la présence de Moraxella catarrhalis, ce qui ne correspondait pas aux résultats initiaux suggérant une infection polymicrobienne. Cette contradiction, associée au contexte de vie dans un hôtel capsule (facteur de risque pour certaines infections), a conduit les médecins à suspecter une tuberculose pulmonaire, une infection bactérienne chronique des poumons. Cette hypothèse a été confirmée au quatrième jour par la détection de bacilles acido-résistants (bactéries caractéristiques de la tuberculose) et par un test moléculaire spécifique.\n\nUn traitement antituberculeux standard, associant plusieurs médicaments (isoniazide, rifampicine, pyrazinamide et éthambutol), a alors été initié, ainsi qu’un traitement corticoïde pour réduire l’inflammation pulmonaire liée au syndrome de détresse respiratoire aiguë (SDRA) associé à la tuberculose. Des bronchoscopies quotidiennes ont été réalisées pour aider à éliminer les sécrétions pulmonaires.\n\n**Évolution et prise en charge ultérieure**  \nEntre les jours 9 et 11, l’état du patient s’est amélioré, avec une résolution partielle des lésions pulmonaires visibles à l’imagerie et une meilleure compliance (souplesse) pulmonaire, permettant le sevrage progressif de l’OEC. Une trachéotomie (ouverture chirurgicale dans la trachée) a été réalisée pour faciliter la ventilation prolongée.\n\nCependant, une toxicité hépatique liée aux médicaments antituberculeux est apparue, nécessitant un ajustement du traitement. Le patient est resté dépendant de la ventilation mécanique et a été transféré dans un centre spécialisé dans la prise en charge de la tuberculose pour poursuivre son traitement.\n\nPar mesure de précaution, un dépistage des professionnels de santé exposés a été organisé, sans identification de cas de tuberculose active ou latente parmi eux.\n\n**Conclusion**  \nCe cas illustre la complexité du diagnostic et de la prise en charge d’une pneumonie sévère et d’un SDRA chez un patient vivant dans un environnement à risque, avec une tuberculose pulmonaire initialement méconnue. Il souligne l’importance de considérer la tuberculose dans les diagnostics différentiels des pneumonies réfractaires, surtout en présence de signes cliniques et radiologiques atypiques, et la nécessité d’une prise en charge multidisciplinaire incluant des traitements spécifiques et un soutien respiratoire avancé."
+        }
+    },
+    {
+        "article": "Un garçon de 4 ans, chez qui on avait diagnostiqué une dilatation pyélo-calicielle droite prénatalement, a présenté de multiples microcystes hyperechogènes dans le groupe caliceal supérieur droit après la naissance. Les consultations régulières n'ont révélé aucune anomalie physique, mais les ultrasons de suivi ont indiqué un élargissement progressif de trois kystes polaires supérieurs.\n\nÀ la naissance, une échographie rénale a révélé une dilatation modérée du système calycéal supérieur et de multiples microcystes hyperechoïques dans le rein supérieur droit. Le rein gauche a présenté une légère dilatation des cavités pyélo-calycéales (7 mm de diamètre antéro-postérieur).\n\nÀ 2 mois, l'enfant a développé une infection fébrile des voies urinaires (IVU). L'échographie a montré le rein droit mesurant 58 mm, avec une lésion kystique de 24 mm et une formation hypèrechoïque (18 × 8 mm), qui était mobile. Le rein gauche mesurait 54 mm, avec une dilatation calycée globale modérée (10 mm de diamètre antéro-postérieur). Une cystourétrographie de miction à 5 mois a confirmé un reflux vésico-urétéral bilatéral (RVU), grade 2. La scintigraphie rénale DMSA a montré une fonction rénale symétrique sans cicatrisation. Un traitement antiseptique urinaire prophylactique a été démarré avec un suivi clinique et radiologique régulier.\n\nÀ 7 mois, une uro-CT a identifié des kystes corticaux simples, dont le plus grand mesurait 37 mm, et a révélé des cavités urétéro-pyélo-calciques bilatérales finement délimitées. À 11 mois, le rein droit mesurait 75 mm, avec trois kystes (39 × 29 × 25 mm, 17 × 14 × 11 mm, et 10 × 6 × 5 mm). Le rein gauche est resté normal, et aucune infection urinaire récurrente n'a été observée, ce qui a permis l'arrêt des antibiotiques prophylactiques à 1,5 ans.\n\nÀ 2 ans, le rein droit mesurait 100 mm, avec deux kystes polaires supérieurs (60 × 50 × 53 mm et 15 × 12 × 2 mm). Le rein gauche restait normal. À 3,5 ans, une échographie de suivi a montré un kyste polaire supérieur exophytique mesurant 70 × 47 mm, avec des parois minces et des septations incomplètes. Le rein gauche restait normal.\n\nUne aspiration de kyste percutanée guidée par tomodensitométrie a donné un fluide séreux. L'analyse cytologique a confirmé un fluide paucicellulaire dépourvu de caractéristiques anaplasiques. Cependant, l'échographie post-aspiration a révélé un kyste dans le sinus polaire supérieur du rein droit (81 × 78 × 64 mm). À la lumière de ces résultats, une intervention chirurgicale a été recommandée.\n\nUne néphrectomie droite haute a été réalisée par voie ouverte, par incision antérolatérale lombaire. L'examen anatomo-pathologique a révélé que l'échantillon de la néphrectomie hémi était occupé par un kyste de consistance scléreuse, de couleur blanchâtre. Ce kyste était recouvert par une demi-lune de tissu rénal de 0,6 cm d'épaisseur. L'examen en coupe séquentielle de la paroi de ce kyste a révélé un deuxième kyste dont la lumière était remplie d'une substance pâteuse de couleur blanc jaunâtre. Le kyste plus grand avait une surface interne tapissée d'un épithélium multicouche, souvent de type transitionnel et de type squameux kératinisé. Le reste de la paroi du kyste était composé de tissu fibreux riche en cellules musculaires lisses. Le plus petit kyste présentait des caractéristiques d'un kyste dermoïde, dont la lumière était remplie de kératine et de cellules squameuses desquamées. Sa paroi était tapissée d'un épithélium épidermique et contenait des follicules pileux et des glandes sébacées. On a observé autour de ces kystes des tissus conjonctifs et adipeux contenant un autre kyste tapissé d'épithélium squameux et des tubules entourés concentriquement par du tissu conjonctif cellulaire ressemblant à une dysplasie rénale. En outre, le tissu rénal identifié macroscopiquement ne présentait aucune lésion.\n\nLe suivi postopératoire sur trois ans n'a révélé aucune infection urinaire. La surveillance par ultrasons a démontré un rein droit réduit à 50 mm et un rein gauche normal, sans lésions kystiques ou solides et sans dilatation des cavités excrétoires.\n",
+        "gold_summary": "Nous rapportons le cas d'un garçon de 4 ans chez qui on a diagnostiqué une dilatation pyélo-calicielle droite in utero, confirmée après la naissance comme étant une MCDK. Les ultrasons de suivi ont révélé une croissance rapide de trois kystes du pôle supérieur, atteignant 8 cm. Une néphrectomie du pôle supérieur droit a été réalisée, et l'histopathologie a révélé un kyste dermoïde rénal dans le cadre d'une dysplasie rénale multicystique segmentaire.\n",
+        "synthetic_summary": {
+            "B1": "Un petit garçon avait un gros ballon d'eau dans son rein droit. Ce ballon a grandi vite. Les docteurs ont enlevé la partie du rein avec le ballon. Après, le garçon est allé mieux.",
+            "B2": "**Ce qu'ils ont trouvé**  \nUn garçon de 4 ans avait une dilatation de certaines parties de son rein droit détectée avant sa naissance. Après sa naissance, des échographies ont montré qu’il avait plusieurs petits kystes (des sortes de poches remplies de liquide) dans la partie supérieure de ce rein. Ces kystes ont grossi rapidement, atteignant jusqu’à 8 centimètres.\n\n**Ce qu’ils ont fait**  \nÀ cause de cette croissance, les médecins ont décidé d’enlever chirurgicalement la partie supérieure du rein droit. Après l’opération, ils ont étudié les tissus en détail.\n\n**Ce que cela signifie**  \nL’analyse a montré que le garçon avait un kyste dermoïde dans son rein. Un kyste dermoïde est une poche qui contient des cellules de la peau et parfois des éléments comme des poils ou des glandes. Ce kyste faisait partie d’une maladie appelée dysplasie rénale multicystique segmentaire, ce qui veut dire que certaines parties du rein se sont mal formées avec plusieurs kystes. Après l’opération, le garçon n’a plus eu d’infections urinaires, et son autre rein est resté normal.",
+            "B3": "Résumé détaillé et structuré du cas clinique\n\nContexte  \nUn garçon de 4 ans a été suivi dès la période prénatale pour une dilatation du système pyélo-caliciel (les cavités rénales qui collectent l’urine) du rein droit. Après la naissance, des échographies ont confirmé la présence de multiples microkystes (petites cavités remplies de liquide) dans la partie supérieure du rein droit, sans anomalie physique apparente. Au fil du temps, ces kystes ont augmenté de taille, suscitant une surveillance régulière.\n\nPrincipales observations  \n- À la naissance, le rein droit présentait une dilatation modérée des cavités supérieures et plusieurs microkystes hyperechogènes (zones brillantes à l’échographie). Le rein gauche montrait une légère dilatation.  \n- À 2 mois, l’enfant a eu une infection urinaire fébrile. L’échographie a montré une lésion kystique mobile dans le rein droit et une dilatation modérée du rein gauche.  \n- Une cystourétrographie (examen radiologique de la vessie et des uretères) réalisée à 5 mois a confirmé un reflux vésico-urétéral bilatéral de grade 2, c’est-à-dire un reflux modéré d’urine de la vessie vers les reins.  \n- Une scintigraphie rénale a montré une fonction rénale symétrique sans cicatrices. Un traitement antibiotique préventif a été instauré.  \n- À 7 mois, un scanner a identifié plusieurs kystes corticaux simples dans le rein droit, avec des cavités urétéro-pyélo-calciques bilatérales bien délimitées.  \n- À 11 mois, le rein droit avait augmenté de taille avec trois kystes de dimensions variables, tandis que le rein gauche restait normal. Aucun nouvel épisode infectieux n’a été noté, permettant l’arrêt des antibiotiques à 1,5 an.  \n- À 2 ans, le rein droit mesurait 100 mm avec deux kystes polaires supérieurs importants, le rein gauche restant normal.  \n- À 3,5 ans, une échographie a montré un kyste exophytique (qui dépasse la surface du rein) de grande taille avec des parois fines et des cloisons incomplètes.  \n- Une ponction aspirative guidée par scanner a prélevé un liquide clair, sans cellules anormales. Cependant, le kyste est resté volumineux après aspiration.  \n\nInterprétation clinique  \nDevant la croissance rapide des kystes et leur persistance, une intervention chirurgicale a été décidée. Une néphrectomie partielle (ablation du pôle supérieur du rein droit) a été réalisée par voie ouverte. L’analyse anatomopathologique a révélé :  \n- Un kyste principal à paroi scléreuse, tapissé d’un épithélium multicouche de type transitionnel (propre aux voies urinaires) et squameux kératinisé (similaire à la peau).  \n- Un second kyste plus petit de type dermoïde, contenant de la kératine, des cellules squameuses, des follicules pileux et des glandes sébacées, caractéristiques d’un tissu cutané ectopique.  \n- Des tissus conjonctifs et adipeux environnants avec un autre kyste et des tubules rénaux entourés de tissu conjonctif cellulaire évoquant une dysplasie rénale (développement anormal du rein).  \n- Le tissu rénal macroscopiquement visible ne présentait pas de lésion.  \n\nProchaines étapes et suivi  \nLe suivi postopératoire sur trois ans a été favorable, sans nouvelle infection urinaire. L’échographie a montré une réduction de la taille du rein droit (50 mm) et un rein gauche normal, sans kystes ni dilatation des cavités urinaires.\n\nConclusion  \nCe cas illustre une dilatation pyélo-calicielle droite diagnostiquée avant la naissance, évoluant vers une dysplasie rénale multicystique segmentaire avec présence d’un kyste dermoïde rénal. La croissance rapide des kystes a conduit à une néphrectomie partielle, permettant un bon contrôle clinique et radiologique à long terme."
+        }
+    },
+    {
+        "article": "Un homme syrien de 61 ans ayant des antécédents d’alcoolisme et de tabagisme lourd a été présenté au service de dermatologie avec des plaintes de lésions pigmentées prurigineuses sans télangiectasies, desquamation ou atrophie sur le côté droit de son tronc et de sa cuisse droite. Le patient a nié avoir été exposé antérieurement à des produits chimiques ou solvants, et il n’y avait pas de antécédents familiaux de cancers de la peau, de maladies de la peau ou de conditions systémiques pertinentes. Ces lésions étaient persistantes depuis 3 ans, et le patient avait précédemment reçu une crème topique à 0,1 % d’hydrocortisone par un dermatologue local pour soulager les démangeaisons ; le patient utilisait la crème par intermittence et seulement lorsque les démangeaisons étaient sévères. À l’examen clinique, des plaques hyperpigmentées étaient visibles sur le côté droit de son tronc et la surface latérale de sa cuisse droite, sans autres caractéristiques cliniques. Les tests sanguins du patient étaient dans les limites normales, à l’exception d’une légère augmentation du nombre de globules blancs. Compte tenu des caractéristiques non spécifiques, une biopsie de la peau a été réalisée pour une évaluation plus approfondie, et l’examen histopathologique de la biopsie a révélé une épiderme hyperkératosique parakeratosique avec une légère spongiose. Le derme papillaire était modérément infiltré par des lymphocytes atypiques avec un léger dépôt de mélanophages. L’infiltration lymphocytaire était située en grappes et en distribution basilaire linéaire le long de la jonction dermo-épidermique. L’immunochimie des lymphocytes atypiques était CD3+, CD8+, CD4−, CD20−. Une tomographie par ordinateur (CT) du thorax et de l’abdomen a été réalisée, mais n’a donné que des résultats normaux sans lymphadénopathie ou organomégalie. Le patient a été diagnostiqué comme étant atteint d’un HPMF au stade précoce et a été ensuite référé à un hôpital spécialisé pour recevoir le traitement. Notre patient a subi une thérapie par psoralène et lumière ultraviolette A (PUVA), avec 8-méthoxypsoralène oral deux fois par semaine, et a été prescrit une crème topique à 0,1 % de bétaméthasone dipropionate. Après 12 semaines de traitement, les démangeaisons ont été soulagées, et l’hyperpigmentation a régressé, mais n’a pas disparu. Le pronostic à long terme du patient est excellent, et il a été conseillé de lui appliquer une crème hydratante et d’éviter l’exposition au soleil, et il est évalué tous les 6 mois pour détecter toute rechute ou nouvelle lésion sur d’autres parties du corps.\n\n",
+        "gold_summary": "Un Syrien de 61 ans s'est présenté à la clinique de dermatologie se plaignant d'une lésion prurigineuse pigmentée persistante sur le côté droit du tronc et de la cuisse droite. L'examen histologique de la biopsie cutanée a montré une épiderme parakeratosique hyperkératosique avec une spongiose et un dépôt de mélanophages. L'immunohistochimie a montré CD3+, CD4-, CD8+ et CD20-, et notre patient a été diagnostiqué avec une mycose fongoïde hyperpigmentée, et a été ensuite traité avec du psoralène et une thérapie aux ultraviolets A. Une très bonne amélioration a été notée, et le pronostic était excellent.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 61 ans avait une tache qui grattait sur son ventre et sa cuisse. Cette tache était là depuis longtemps. \n\nLe docteur a pris un petit bout de peau pour regarder de plus près. Il a trouvé des choses spéciales qui expliquent pourquoi ça gratte. \n\nLe monsieur a reçu un traitement avec de la lumière spéciale et un médicament. Après, la tache a moins gratté et elle a un peu disparu. \n\nLe docteur dit que ça ira bien, mais il faut bien prendre soin de la peau et éviter le soleil.",
+            "B2": "Un homme syrien de 61 ans est venu à la clinique de dermatologie parce qu’il avait depuis trois ans des plaques sombres qui le démangeaient sur le côté droit de son torse et de sa cuisse. Pour mieux comprendre ce problème, les médecins ont prélevé un petit morceau de peau, appelé biopsie, et l’ont examiné au microscope. Ils ont vu que la couche supérieure de la peau était épaissie et qu’il y avait des cellules spéciales appelées lymphocytes qui semblaient anormales. Ces cellules montraient certains marqueurs particuliers (CD3+ et CD8+), ce qui a aidé à poser un diagnostic. Le patient souffrait d’une maladie appelée mycose fongoïde hyperpigmentée, un type rare de cancer de la peau qui évolue lentement.\n\nPour le traiter, il a reçu un médicament appelé psoralène, pris par la bouche, associé à une lumière spéciale appelée ultraviolets A (PUVA). Il a aussi utilisé une crème à base de corticoïdes pour calmer les démangeaisons. Après trois mois, ses démangeaisons avaient beaucoup diminué et les plaques sombres avaient commencé à s’estomper, même si elles n’avaient pas complètement disparu. Le pronostic, c’est-à-dire l’évolution attendue de la maladie, est très bon. Les médecins lui ont conseillé d’hydrater sa peau, d’éviter le soleil et de revenir tous les six mois pour vérifier que la maladie ne réapparaisse pas.",
+            "B3": "Résumé destiné à un adulte éduqué non-médecin\n\n**Contexte**  \nUn homme syrien de 61 ans, avec des antécédents importants d’alcoolisme et de tabagisme, a consulté en dermatologie pour des plaques pigmentées qui démangeaient sur le côté droit de son tronc et de sa cuisse. Ces lésions étaient présentes depuis environ trois ans. Il n’avait pas d’antécédents familiaux de maladies de la peau ou de cancers cutanés, ni d’exposition connue à des produits chimiques. Il avait utilisé occasionnellement une crème à base d’hydrocortisone pour soulager les démangeaisons, sans amélioration durable.\n\n**Principales observations**  \nÀ l’examen, les plaques étaient hyperpigmentées (plus foncées que la peau normale) sans signes d’inflammation visible comme des vaisseaux dilatés (télangiectasies), desquamation (peau qui pèle) ou atrophie (amincissement de la peau). Les analyses sanguines étaient normales, sauf une légère augmentation des globules blancs, signe possible d’une réaction immunitaire. Une biopsie cutanée a été réalisée pour mieux comprendre la nature des lésions.\n\nL’analyse microscopique de la peau a montré un épaississement de la couche superficielle de la peau (hyperkératose) avec une anomalie appelée parakératose (présence de cellules mortes non éliminées normalement), ainsi qu’une légère inflammation entre les cellules de l’épiderme (spongiose). Dans le derme, la couche sous-jacente, on a observé un infiltrat de lymphocytes (un type de globules blancs) atypiques, regroupés près de la jonction entre l’épiderme et le derme. Ces cellules immunitaires étaient positives pour certains marqueurs (CD3 et CD8) et négatives pour d’autres (CD4 et CD20), ce qui oriente vers un type particulier de lymphocytes T cytotoxiques.\n\nUn scanner thoraco-abdominal n’a pas révélé d’extension de la maladie à d’autres organes ou ganglions lymphatiques.\n\n**Interprétation clinique**  \nLe diagnostic retenu était celui d’une mycose fongoïde hyperpigmentée (MFH), une forme rare et précoce d’un lymphome cutané T, c’est-à-dire un cancer des lymphocytes qui se manifeste principalement par des lésions de la peau. Cette forme particulière se caractérise par une pigmentation foncée des plaques cutanées.\n\n**Prochaines étapes et traitement**  \nLe patient a été adressé à un centre spécialisé où il a reçu un traitement combiné associant un médicament appelé psoralène (qui sensibilise la peau à la lumière) et une exposition contrôlée à la lumière ultraviolette A (thérapie PUVA). Il a également utilisé une crème corticoïde puissante (bétaméthasone dipropionate) pour réduire l’inflammation. Après 12 semaines, les démangeaisons se sont nettement améliorées et la pigmentation des lésions a diminué, bien qu’elle n’ait pas complètement disparu.\n\nLe pronostic à long terme est considéré comme excellent, à condition d’un suivi régulier tous les six mois pour surveiller toute récidive ou apparition de nouvelles lésions. Il a également été conseillé au patient d’utiliser régulièrement une crème hydratante et d’éviter l’exposition excessive au soleil afin de protéger sa peau."
+        }
+    },
+    {
+        "article": "Nous présentons le cas d'un homme de 82 ans ayant un diagnostic confirmé par biopsie endoscopique d'un adénocarcinome du côlon ascendant. Les études de stadification préopératoire n'ont pas révélé de signes de maladie à distance et il avait un CEA de 2,8 ng/mL. Une hémicolectomie droite laparoscopique a été réalisée et il a eu un bon postopératoire. L'anatomie pathologique a rapporté un adénocarcinome modérément différencié de stade 1, T1 N0, qui n'a pas nécessité de traitement adjuvant.\n\nAu cours du suivi oncologique, une image d'aspect nodulaire en chaîne iliaque primitive gauche mesurant 22 mm sur son axe mineur a été identifiée par tomographie. En raison de cette découverte, une TEP-TDM avec 18F-FDG a été réalisée, qui a mis en évidence une lésion ovoïde, unique, au niveau rétropéritonéal, adjacente à la bifurcation aortique d'environ 34 mm de diamètre major avec un faible renforcement après administration de contraste iodé.\n\nCette image s’est avérée hypermétabolique (SUV : 6,7). Aucune autre image liée à la pathologie étudiée n’a été trouvée. Compte tenu des antécédents du patient, une biopsie percutanée guidée par imagerie a été programmée sous anesthésie locale. La procédure a été bien tolérée et n’a été associée à aucune complication. Cette étude a démontré que la découverte était un schwannome. Après un an de suivi, une augmentation de la taille de la lésion biopsiée a été constatée (44 mm de diamètre maximum), sans manifestations cliniques. En revanche, il n’y a eu aucune preuve de progression de la maladie oncologique.\n",
+        "gold_summary": "Nous présentons le cas d'un patient de 82 ans, récemment diagnostiqué d'un adénocarcinome du côlon modérément différencié et d'un nodule hypermétabolique périaortique comme découverte fortuite.\n\nRésultats : la biopsie percutanée du nodule périaortique a confirmé le diagnostic de schwannome. Au cours de l'année de suivi, la croissance du schwannome a été démontrée. Il n'y a pas de signe de progression de sa maladie oncologique.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 82 ans avait un petit problème dans son ventre. Les médecins ont trouvé une petite boule qui n’était pas dangereuse. \n\nIls ont fait un petit examen pour regarder cette boule de plus près. C’était une boule appelée schwannome. \n\nAprès un an, la boule a un peu grandi, mais le monsieur va bien. Son autre problème n’a pas bougé. Tout va bien pour lui.",
+            "B2": "Cas d’un homme de 82 ans avec un cancer du côlon\n\nUn homme de 82 ans a été diagnostiqué avec un cancer appelé adénocarcinome dans la partie droite de son côlon. Ce cancer était à un stade précoce et modérément différencié, ce qui signifie que les cellules cancéreuses ressemblaient encore assez aux cellules normales. Il a subi une opération pour enlever la partie malade du côlon, et tout s’est bien passé après l’intervention. Aucun traitement supplémentaire n’a été nécessaire.\n\nDécouverte d’une autre masse près de l’aorte\n\nLors des contrôles après l’opération, les médecins ont trouvé une petite masse près d’une grosse artère appelée l’aorte, dans la région du ventre. Cette masse mesurait environ 3 centimètres et semblait active, ce qui a poussé les médecins à faire une biopsie. Une biopsie, c’est quand on prélève un petit morceau de tissu pour l’étudier au microscope.\n\nRésultat et suivi\n\nL’analyse a montré que cette masse n’était pas un cancer, mais un schwannome. Un schwannome est une tumeur bénigne qui vient des cellules nerveuses. Après un an, cette tumeur a un peu grossi, mais le patient n’a pas eu de symptômes ni de signes que son cancer du côlon avait progressé. Les médecins continuent de le surveiller pour s’assurer que tout reste stable.",
+            "B3": "Résumé destiné à un public non médical mais éduqué\n\nContexte  \nNous rapportons le cas d’un homme de 82 ans chez qui un cancer du côlon ascendant, appelé adénocarcinome modérément différencié, a été diagnostiqué par biopsie. Avant l’opération, les examens n’ont pas montré de métastases (propagation du cancer à distance) et son taux sanguin de CEA, un marqueur tumoral, était normal. Il a subi une chirurgie laparoscopique pour retirer la partie droite du côlon, avec un bon rétablissement. L’analyse de la tumeur a indiqué un stade précoce (T1 N0), ne nécessitant pas de traitement complémentaire.\n\nPrincipales observations  \nLors du suivi après chirurgie, une image anormale en forme de nodule a été détectée près d’une artère importante dans la région pelvienne gauche, mesurant environ 22 mm. Une tomographie par émission de positons (TEP-TDM) utilisant un traceur radioactif (18F-FDG) a montré que cette masse, située près de la bifurcation de l’aorte dans la cavité abdominale, était hyperactive sur le plan métabolique, ce qui peut évoquer une tumeur. Sa taille était alors d’environ 34 mm. Aucune autre anomalie suspecte n’a été trouvée.\n\nInterprétation clinique  \nPour identifier la nature de cette masse, une biopsie guidée par imagerie a été réalisée sous anesthésie locale, sans complication. L’examen microscopique a révélé qu’il s’agissait d’un schwannome, une tumeur bénigne qui se développe à partir des cellules des nerfs périphériques. Au cours de l’année suivante, cette tumeur a augmenté de taille, atteignant 44 mm, mais le patient n’a présenté aucun symptôme lié à cette croissance. Par ailleurs, aucun signe de récidive ou d’évolution du cancer du côlon n’a été observé.\n\nProchaines étapes  \nLe cas illustre l’importance d’investiguer toute masse nouvelle chez un patient ayant un antécédent de cancer, afin d’en déterminer la nature exacte. Bien que le schwannome soit bénin, sa surveillance régulière est recommandée pour suivre son évolution et prévenir d’éventuelles complications. Le suivi oncologique doit également se poursuivre pour détecter toute récidive du cancer initial."
+        }
+    },
+    {
+        "article": "Un homme de 71 ans hospitalisé dans un autre hôpital pour insuffisance cardiaque, ayant déjà été admis plusieurs fois pour insuffisance cardiaque, a été transféré dans notre hôpital pour une évaluation et un traitement plus poussés de son insuffisance cardiaque réfractaire. Bien qu'il ait été soupçonné d'avoir une amyloïdose cardiaque dans l'hôpital précédent, un diagnostic n'a pas été établi.\n\nÀ son admission à notre hôpital, il a reçu des médicaments oraux, dont de nombreux types de diurétiques, mais il avait toujours une dyspnée avec une classe fonctionnelle IV de la NYHA. Sa tension artérielle était de 106/70 mmHg, et le troisième son de cœur était audible au sommet. Des veines jugulaires congestionnées ont été observées, mais aucun œdème périphérique n’a été trouvé. La radiographie thoracique a montré un rapport cardiothoracique élevé de 61 % avec un épanchement pleural bilatéral. Les résultats électrocardiographiques étaient une fréquence cardiaque de 65/min avec une fibrillation auriculaire, un retard de conduction intra-ventriculaire et une déviation de l’axe gauche. L’échocardiographie transthoracique a révélé une hypertrophie diffuse du ventricule gauche (VG) avec une augmentation de l’épaisseur de la paroi de 12 mm, un mouvement de la paroi du VG hypokinétique modéré (fraction d’éjection = 43 %), une augmentation de l’épaisseur de la paroi du ventricule droit de 7 mm avec une fonction systolique du VD réduite et une dilatation biatriale. L’échocardiographie par spectrométrie de diffusion a montré un modèle de contraction longitudinale « apical sparing ». Il avait des résultats anormaux aux tests de laboratoire, avec un taux élevé de peptide natriurétique cérébral (BNP) (1 186 pg/mL) et un taux élevé de troponine T cardiaque de haute sensibilité (0,057 ng/mL). La scintigraphie au pyrophosphate de 99mTechnetium (99mTc-PYP) a révélé une prise cardiaque de grade 3 sur l’imagerie de fusion SPECT/CT. La protéine de Bence-Jones n’était pas détectable, et le rapport de la chaîne légère libre κ/λ était normal. Plus tard, nous avons effectué une biopsie endomyocardique et une analyse génétique, et nous avons finalement posé un diagnostic de ATTRwt.\n\nEn ce qui concerne la gestion de l'insuffisance cardiaque, nous avons essayé de contrôler son insuffisance cardiaque avec une oxygénothérapie et une prise en charge médicale, y compris une injection intraveineuse de furosémide, mais il avait toujours une dyspnée avec une fatigue générale persistante, et son taux de bilirubine a augmenté. La cathétérisation cardiaque droite (RHC) a montré une pression de coin artérielle pulmonaire élevée et une hypertension pulmonaire et un faible indice cardiaque de 1,37 L/min/m2 (thermodilution) avec une pression moyenne auriculaire droite de 8 mmHg.\n\nSur la base de ces résultats, nous avons commencé une perfusion de dobutamine à 2 μg/kg/min pour son faible débit cardiaque. Ses symptômes ont considérablement amélioré avec l'amélioration des taux de créatinine et de bilirubine. Six jours plus tard, nous avons administré du pimobendan afin de réduire progressivement la perfusion de dobutamine. Au cours du traitement, il était fondamentalement stable, à l'exception d'une détérioration temporaire de l'insuffisance cardiaque due à la grippe. Après un mois de traitement médical et de rééducation cardiaque en hospitalisation, la perfusion de dobutamine a été arrêtée et le RHC a montré une amélioration spectaculaire de son état hémodynamique. Depuis sa sortie de l'hôpital, son état est resté stable sans détérioration de l'insuffisance cardiaque ou des arythmies pendant six mois.",
+        "gold_summary": "Nous avons traité un homme de 71 ans souffrant d'insuffisance cardiaque réfractaire due à l'ATTRwt. Il devait être dépendant d'une perfusion de dobutamine. Nous avons administré du pimobendan et avons réussi à améliorer ses symptômes et son état hémodynamique pour permettre sa sortie de l'hôpital. Une enquête rétrospective supplémentaire a révélé qu'il y avait huit patients atteints d'amyloïdose ATTR auxquels on avait administré du pimobendan. Bien que tous les patients au moment de l'administration du pimobendan étaient de classe III ou IV de la NYHA avec une hospitalisation répétée pour insuffisance cardiaque, le pimobendan semblait être efficace pour améliorer les symptômes et permettre aux patients d'être sortis et de recevoir des soins médicaux ambulatoires. En outre, en se concentrant sur les changements dans certains biomarqueurs, nous avons constaté que les valeurs du peptide natriurétique cérébral et du taux de filtration glomérulaire estimé s'étaient améliorées après l'administration du pimobendan chez 5 patients consécutifs pour lesquels les données étaient disponibles sans traitement supplémentaire (p = 0,018 et 0,051, respectivement).\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 71 ans avait un cœur très fatigué. Il avait du mal à respirer et se sentait très fatigué. Les médecins lui ont donné un médicament spécial appelé pimobendan. Ce médicament l’a beaucoup aidé. Il a pu sortir de l’hôpital et se sentir mieux.\n\nD’autres personnes avec le même problème ont aussi pris ce médicament. Ça les a aidées à se sentir mieux aussi. Ce médicament aide le cœur à mieux travailler. Les médecins sont contents car il aide les gens à vivre plus facilement.",
+            "B2": "### Ce qu'ils ont fait et observé\n\nLes médecins ont soigné un homme de 71 ans qui avait une insuffisance cardiaque très grave à cause d'une maladie appelée ATTRwt. Cette maladie fait que des protéines anormales s'accumulent dans le cœur, ce qui l'empêche de bien fonctionner. Au début, l’homme avait besoin d’un médicament appelé dobutamine, donné par perfusion, pour aider son cœur à pomper le sang.\n\nPour améliorer son état, ils ont ajouté un autre médicament appelé pimobendan. Ce traitement a aidé à réduire ses symptômes, comme la fatigue et la difficulté à respirer, et a amélioré la façon dont son cœur fonctionnait. Grâce à cela, il a pu quitter l’hôpital et rester stable pendant au moins six mois.\n\n### Ce qu’ils ont découvert en regardant d’autres cas\n\nLes médecins ont aussi regardé en arrière les dossiers de huit autres patients atteints de la même maladie ATTR qui avaient reçu le pimobendan. Tous ces patients étaient très malades, avec des symptômes sévères et plusieurs hospitalisations. Pourtant, le pimobendan a semblé les aider à se sentir mieux, à sortir de l’hôpital et à continuer leurs soins à la maison.\n\n### Ce que cela signifie\n\nEn plus des améliorations visibles, ils ont mesuré certains marqueurs dans le sang, comme le peptide natriurétique cérébral (BNP), qui indique la gravité de l’insuffisance cardiaque, et la fonction des reins. Chez cinq patients, ces marqueurs se sont améliorés après le traitement au pimobendan, ce qui suggère que ce médicament peut aider non seulement le cœur mais aussi la santé générale des patients.\n\n### Conclusion simple\n\nLe pimobendan pourrait être un traitement utile pour les personnes souffrant d’insuffisance cardiaque grave liée à l’ATTRwt. Il aide à améliorer les symptômes et la qualité de vie, permettant aux patients de sortir de l’hôpital et de mieux vivre au quotidien. Cependant, cette découverte vient d’un petit nombre de cas, donc il faudra plus d’études pour confirmer ces résultats.",
+            "B3": "Résumé destiné à un public adulte non spécialiste mais éduqué\n\n**Contexte**  \nUn homme de 71 ans souffrant d’une insuffisance cardiaque sévère, résistante aux traitements habituels, a été transféré pour une prise en charge spécialisée. Malgré des traitements médicamenteux oraux, il présentait une fatigue importante et une difficulté respiratoire majeure (classe IV selon la classification NYHA, qui mesure la gravité des symptômes cardiaques). Des examens approfondis ont révélé une amyloïdose cardiaque de type ATTRwt (amyloïdose à transthyrétine de type sauvage), une maladie où des protéines anormales s’accumulent dans le cœur, entraînant une défaillance progressive.\n\n**Principales observations**  \nÀ l’admission, le patient présentait une hypertrophie (épaississement) des parois cardiaques, une fonction cardiaque réduite, ainsi qu’une fibrillation auriculaire (un trouble du rythme cardiaque). Les analyses sanguines montraient des marqueurs élevés indiquant une souffrance du muscle cardiaque. Une scintigraphie spécifique a confirmé la présence d’amyloïdose cardiaque. Une biopsie du muscle cardiaque et des tests génétiques ont permis de confirmer le diagnostic d’ATTRwt. Malgré un traitement médical intensif, y compris des diurétiques et une oxygénothérapie, son état restait instable avec une faible capacité du cœur à pomper le sang (faible débit cardiaque) et une hypertension pulmonaire (pression élevée dans les artères des poumons).\n\n**Interprétation clinique**  \nPour améliorer la fonction cardiaque, une perfusion continue de dobutamine, un médicament stimulant le cœur, a été mise en place, ce qui a amélioré ses symptômes et ses paramètres biologiques. Afin de réduire progressivement cette perfusion, le pimobendan, un médicament qui augmente la force de contraction du cœur tout en dilatant les vaisseaux sanguins, a été introduit. Sous pimobendan, le patient est resté stable, avec une amélioration notable de son état hémodynamique (fonctionnement du cœur et circulation sanguine), ce qui a permis l’arrêt de la dobutamine et la sortie de l’hôpital. Six mois après, son état est resté stable sans aggravation de son insuffisance cardiaque ni apparition d’arythmies.\n\n**Prochaines étapes et observations complémentaires**  \nUne analyse rétrospective portant sur huit patients atteints d’amyloïdose ATTR traités avec le pimobendan a montré que, malgré une insuffisance cardiaque avancée (classe III ou IV) et des hospitalisations répétées, ce médicament semblait améliorer les symptômes et permettre aux patients de bénéficier de soins ambulatoires. Chez cinq patients pour lesquels des données biologiques étaient disponibles, on a observé une amélioration significative du peptide natriurétique cérébral (un marqueur de la gravité de l’insuffisance cardiaque) et une tendance à l’amélioration de la fonction rénale après traitement par pimobendan, sans autres modifications thérapeutiques.\n\n**Conclusion**  \nChez ce patient et dans un petit groupe de cas similaires, le pimobendan s’est révélé efficace pour améliorer les symptômes et la fonction cardiaque dans le cadre d’une amyloïdose cardiaque ATTRwt avancée, permettant une meilleure prise en charge ambulatoire. Ces résultats suggèrent que ce médicament pourrait être une option thérapeutique utile dans cette maladie difficile à traiter, mais des études plus larges sont nécessaires pour confirmer ces observations."
+        }
+    },
+    {
+        "article": "Femme de 76 ans, ayant des antécédents d'hypertension artérielle il y a 14 ans, en traitement avec candésartan, sans autre élément d'intérêt. Elle s'est présentée aux urgences, avec des antécédents d'AVC de 48 heures d'évolution, des signes cliniques de dysarthrie et d'hémiplégie droite qui ont disparu en quelques heures et ont récidivé 24 heures plus tard. À son arrivée aux urgences, avec 5 heures d'évolution. L'examen physique a révélé des signes vitaux normaux, somnolence, désorientation dans le temps et l'espace, regard préférentiel vers la gauche, hémianopsie homonyme droite, force musculaire 0 sur 5 dans l'hémicorps droit sur l'échelle de Daniels ; hyperréflexie dans les membres inférieurs 3/4 et hyporéflexie dans le membre supérieur droit 1/4, réponse plantaire extensora bilatérale, sans autre élément. Une tomographie par ordinateur (CT) cérébrale urgente a été réalisée immédiatement, qui a mis en évidence une image hyperdense extra-axiale en relation avec la face latérale gauche de la médulla oblongue qui s'étend jusqu'au pont, avec de multiples densités à ce niveau. L'étude urgente a été complétée par une angiotomographie cérébrale qui a mis en évidence une dolichocéphalie basilaire de 5,09 mm de diamètre et une anévrisme fusiforme au niveau de l'artère vertébrale gauche, d'environ 20 x 9 mm, partiellement oblitéré avec thrombus mural et calcifié, avec un passage adéquat du contraste. L'imagerie par résonance magnétique cérébrale dans les heures qui ont suivi a révélé une restriction de la diffusion dans le territoire de l'artère choroïde antérieure gauche et dans le territoire basilaire de la protubérance.\n",
+        "gold_summary": "Une femme de 76 ans a été admise aux urgences pour un accident vasculaire cérébral ischémique qui a touché le territoire de l'artère cérébrale antérieure gauche et basilaire. Les examens d'imagerie ont révélé une dolichocéphalie basilaire associée à un anévrisme fusiforme avec thrombus intra-anévrisme dans l'artère vertébrale gauche. Les deux anomalies anatomiques sont associées à un accident vasculaire cérébral ischémique.\n",
+        "synthetic_summary": {
+            "B1": "Une dame de 76 ans est venue à l'hôpital. Elle avait un problème dans son cerveau.  \n\nLes docteurs ont fait des images pour regarder dedans. Ils ont vu que des petits tuyaux dans sa tête étaient un peu bizarres.  \n\nCes choses bizarres ont fait que le sang n’a pas bien circulé. Cela a rendu son cerveau malade.  \n\nLes docteurs vont l’aider pour qu’elle aille mieux.",
+            "B2": "Une femme de 76 ans est venue aux urgences parce qu'elle avait des signes d'accident vasculaire cérébral (AVC). Un AVC, c'est quand une partie du cerveau ne reçoit plus assez de sang, ce qui peut causer des problèmes comme une faiblesse ou des difficultés à parler. Les examens ont montré qu'elle avait deux problèmes dans ses vaisseaux sanguins : une dolichocéphalie basilaire, c’est-à-dire que l'artère principale à la base du cerveau est plus longue et plus fine que d'habitude, et un anévrisme fusiforme, qui est une sorte de grosseur en forme de ballon sur une autre artère appelée l'artère vertébrale gauche. À l'intérieur de cet anévrisme, il y avait un caillot de sang. Ces deux anomalies ont empêché le sang de bien circuler dans certaines parties du cerveau, ce qui a causé l’AVC.",
+            "B3": "Contexte  \nUne femme de 76 ans, avec un antécédent d’hypertension artérielle traitée depuis 14 ans, s’est présentée aux urgences suite à un accident vasculaire cérébral (AVC) survenu depuis 48 heures. Elle avait initialement présenté des troubles de la parole (dysarthrie) et une paralysie complète du côté droit du corps (hémiplégie) qui s’étaient résorbés en quelques heures, mais ces symptômes sont réapparus 24 heures plus tard. À son arrivée, cinq heures après la récidive, l’examen clinique a montré une somnolence, une désorientation dans le temps et l’espace, un regard tourné vers la gauche, une perte de la vision dans la moitié droite du champ visuel (hémianopsie homonyme droite) et une paralysie complète du côté droit (force musculaire nulle). Les réflexes étaient anormaux, avec une hyperactivité dans les jambes et une diminution dans le bras droit, ainsi qu’une réponse anormale des pieds indiquant une atteinte neurologique centrale.\n\nPrincipales Observations  \nUne tomodensitométrie cérébrale urgente a révélé une image anormale dense à la face latérale gauche du bulbe rachidien (médulla oblongata) s’étendant jusqu’au pont, suggérant une lésion extra-axiale. Une angiotomodensitométrie (examen des vaisseaux sanguins cérébraux) a mis en évidence une dilatation anormale et allongée de l’artère basilaire (dolichocéphalie basilaire) mesurant 5,09 mm de diamètre, ainsi qu’un anévrisme fusiforme (dilatation en forme de fuseau) de l’artère vertébrale gauche, d’environ 20 x 9 mm, partiellement obstrué par un caillot (thrombus mural) et présentant des calcifications. L’imagerie par résonance magnétique (IRM) cérébrale a confirmé la présence d’une zone d’ischémie (manque d’oxygène) dans le territoire de l’artère choroïde antérieure gauche et dans la région du pont (protubérance), correspondant aux symptômes cliniques.\n\nInterprétation Clinique  \nLe diagnostic retenu est un accident vasculaire cérébral ischémique affectant à la fois les territoires de l’artère cérébrale antérieure gauche et de l’artère basilaire. Les anomalies vasculaires identifiées, à savoir la dolichocéphalie basilaire et l’anévrisme fusiforme thrombosé de l’artère vertébrale gauche, sont des facteurs anatomiques qui ont contribué à la survenue de cet AVC. Ces malformations vasculaires peuvent favoriser la formation de caillots et perturber le flux sanguin cérébral, entraînant ainsi une ischémie cérébrale.\n\nProchaines Étapes  \nLa prise en charge devra inclure une surveillance neurologique étroite, un traitement adapté pour prévenir la formation de nouveaux caillots, et une évaluation spécialisée pour envisager un traitement endovasculaire ou chirurgical de l’anévrisme si nécessaire. Une rééducation fonctionnelle sera également essentielle pour améliorer la récupération motrice et cognitive de la patiente."
+        }
+    },
+    {
+        "article": "Une femme de 31 ans de la République du Zimbabwe s'est présentée au service des urgences de notre hôpital avec une fièvre de 3 jours, des douleurs thoraciques, des vomissements et une diarrhée. La patiente n'avait pas d'antécédents médicaux de pneumonie, de maladies contagieuses ou de contacts malades connus et a nié l'utilisation de tabac ou d'alcool. De plus, elle n'avait pas d'antécédents d'hospitalisation. Au Zimbabwe, un sous-groupe de la population consomme habituellement de l'argile rouge, et la patiente faisait partie de ce groupe. En raison de l'indisponibilité de l'argile rouge, elle a eu recours à la consommation de terre de jardin une fois tous les deux mois, avec son ingestion la plus récente survenue six jours avant la présentation. Elle a développé une fièvre avec une température maximale de 38,8 ° C accompagnée de frissons, de toux non productive et de douleurs thoraciques du côté droit exacerbées par la respiration 3 jours après l'ingestion du sol. Elle a connu quatre épisodes de vomissements de liquide jaune-vert et une diarrhée sévère, avec des selles jaunes aqueuses survenant 3 à 6 fois par heure à son apogée. La patiente s'est auto-administrée de l'ibuprofène, mais ses symptômes ont persisté, ce qui a conduit à son renvoi à notre hôpital en raison de l'aggravation de la diarrhée et de la fatigue.\nL'examen physique du patient a révélé les signes vitaux suivants : température corporelle de 38 °C, tension artérielle de 100/60 mmHg, fréquence cardiaque de 83 battements/min, fréquence respiratoire de 18 respirations/min, et saturation en oxygène de 99 % en air ambiant. L'auscultation a révélé des bruits respiratoires bruyants bilatéraux. Les résultats de laboratoire ont indiqué un nombre de globules blancs de 28,65 × 109/L, avec des neutrophiles à 25,95 × 109/L et un pourcentage de neutrophiles de 90,6 %. La protéine C-réactive était élevée à 198,76 mg/L. En outre, le D-dimère (22,62 mg/L), la créatinine (276,0 μmol/L), l'azote uréique (14,27 mmol/L), la bilirubine totale (61,0 μmol/L), la bilirubine directe (18,3 μmol/L) et la bilirubine indirecte (42,7 μmol/L) étaient élevés. La tomographie par ordinateur thoracique (CT) a révélé deux lésions suspectes dans le lobe inférieur gauche, avec une cavitation observée dans la plus grande lésion.\nUne thérapie empirique avec de la pipéracline-tazobactam et de la moxifloxacine a été initiée. Pour identifier l'agent pathogène responsable, une bronchoscopie a été réalisée et une culture du liquide de lavage broncho-alvéolaire (BALF) a identifié P. aeruginosa et un test de sensibilité antimicrobienne a démontré que l'isolement de P. aeruginosa était pan-sensible à la cefoperazone-sulbactam, à la lévofloxacine, à la ceftazidime, à la ceftazidime-avibactam, au meropenem, à la pipéracline-tazobactam, à la ciprofloxacine, à la cefepime, à l'aztréonam et à l'imipénem. Une culture fécale a simultanément indiqué une infection avec P. aeruginosa, tandis qu'une culture microbienne sanguine et urinaire n'a montré aucune anomalie significative. Par conséquent, le régime antibactérien a été ajusté à la pipéracline-tazobactam et à la ciprofloxacine sur la base des résultats de sensibilité. Des traitements symptomatiques, y compris une inhibition de l'acidité, une protection gastrique, une protection hépatique, des agents antidiarrhéiques et une régulation de la flore intestinale, ont été administrés, ce qui a entraîné une amélioration significative des symptômes gastro-intestinaux.\n\nAprès 3 jours de traitement, la fièvre, les vomissements et la diarrhée de la patiente ont disparu, ne laissant qu'une toux modérée. Une nouvelle tomographie effectuée 11 jours plus tard a montré un élargissement et une fusion des lésions dans le lobe inférieur gauche avec un petit épanchement pleural du côté gauche. Malgré ces résultats radiologiques, les marqueurs d'infection de la patiente s'étaient considérablement améliorés, ce qui a conduit à sa sortie avec des instructions pour poursuivre la thérapie par moxifloxacine en ambulatoire. Un mois plus tard, une nouvelle tomographie a démontré une réduction significative des lésions du lobe inférieur gauche, et la patiente est restée asymptomatique.\n",
+        "gold_summary": "Nous présentons le cas d'une patiente de 31 ans en bonne santé, enseignante au collège, qui a développé une CAP due à P. aeruginosa après avoir ingéré de la terre de jardin pendant trois jours consécutifs. La patiente a été admise avec des symptômes incluant de la fièvre, des douleurs thoraciques, des vomissements et une diarrhée. La tomographie par ordinateur (CT) thoracique a révélé deux lésions suspectes dans le lobe inférieur gauche, dont une lésion présentant une cavitation. La culture microbiologique du liquide de lavage broncho-alvéolaire (BALF) et des selles a confirmé la présence d'une infection à P. aeruginosa. Les tests de sensibilité antimicrobienne ultérieurs ont révélé que l'isolement de P. aeruginosa était pan-sensible. Après 13 jours de traitement antimicrobien ciblé, les symptômes et les marqueurs de laboratoire de la patiente ont considérablement amélioré. Une tomographie par ordinateur de suivi un mois plus tard a démontré une résolution substantielle des lésions du lobe inférieur gauche, et la patiente est restée asymptomatique.\n",
+        "synthetic_summary": {
+            "B1": "Une dame est tombée malade après avoir mangé de la terre. Elle avait de la fièvre, mal à la poitrine, vomissait et avait la diarrhée. Le docteur a fait une photo spéciale de ses poumons. Il a vu des endroits malades dedans. Le docteur a trouvé des petits microbes dans ses poumons et dans ses selles. Ces microbes ont rendu la dame malade. Elle a pris des médicaments pour guérir. Après plusieurs jours, elle allait beaucoup mieux. Un mois plus tard, ses poumons étaient presque guéris. Elle n’avait plus mal ni de fièvre. Tout va bien maintenant.",
+            "B2": "**Ce qu’ils ont trouvé**  \nUne femme de 31 ans, enseignante, est venue à l’hôpital avec de la fièvre, des douleurs dans la poitrine, des vomissements et une diarrhée. Elle avait mangé de la terre de jardin pendant trois jours avant de tomber malade. Une radio spéciale appelée tomographie a montré deux zones anormales dans son poumon gauche, dont une avec un trou à l’intérieur, ce qui peut arriver quand une infection détruit une partie du tissu.  \n\n**Ce que cela signifie**  \nLes médecins ont prélevé un liquide dans ses poumons pour chercher des microbes. Ils ont trouvé une bactérie appelée *Pseudomonas aeruginosa*, qui est connue pour causer des infections. Cette bactérie était aussi présente dans ses selles. Heureusement, cette bactérie était sensible à plusieurs antibiotiques, ce qui veut dire que les médicaments pouvaient bien la combattre.  \n\n**Le traitement et l’évolution**  \nLa patiente a reçu des antibiotiques adaptés pendant 13 jours. Ses symptômes, comme la fièvre et la diarrhée, ont beaucoup diminué. Une nouvelle tomographie un mois plus tard a montré que les lésions dans son poumon avaient beaucoup rétréci. Elle n’avait plus de symptômes et allait bien.  \n\n**En résumé**  \nCette histoire montre qu’ingérer de la terre peut parfois causer une infection grave des poumons à cause de bactéries comme *Pseudomonas aeruginosa*. Avec un bon diagnostic et un traitement adapté, la maladie peut guérir complètement.",
+            "B3": "**Contexte**  \nUne femme de 31 ans, enseignante au Zimbabwe, sans antécédents médicaux particuliers, s’est présentée aux urgences avec une fièvre persistante depuis trois jours, des douleurs thoraciques à droite, des vomissements et une diarrhée sévère. Elle avait consommé occasionnellement de la terre de jardin, la dernière ingestion datant de six jours avant l’apparition des symptômes. Cette pratique est liée à une habitude locale de consommation d’argile rouge, remplacée temporairement par la terre de jardin en raison de son indisponibilité.\n\n**Principales Observations**  \nÀ l’examen clinique, la patiente présentait une fièvre modérée (38 °C), une tension artérielle basse normale, une fréquence cardiaque et respiratoire normales, ainsi qu’une bonne saturation en oxygène. L’auscultation pulmonaire montrait des bruits respiratoires anormaux des deux côtés. Les analyses sanguines révélaient une importante augmentation des globules blancs, en particulier des neutrophiles, ainsi qu’une élévation marquée de la protéine C-réactive, signe d’une inflammation aiguë. D’autres paramètres biologiques indiquaient une atteinte rénale et hépatique modérée. Une tomodensitométrie (CT) thoracique a mis en évidence deux lésions suspectes dans le lobe inférieur gauche du poumon, dont une avec cavitation (formation d’une cavité).\n\nPour identifier l’agent infectieux, une bronchoscopie a été réalisée, permettant de prélever un liquide de lavage broncho-alvéolaire (BALF). La culture de ce prélèvement a isolé la bactérie Pseudomonas aeruginosa, un micro-organisme opportuniste souvent responsable d’infections pulmonaires sévères. Cette bactérie était sensible à un large éventail d’antibiotiques. Parallèlement, une culture des selles a également confirmé la présence de cette bactérie, tandis que les cultures sanguines et urinaires étaient normales.\n\n**Interprétation Clinique**  \nLe diagnostic retenu était une pneumonie acquise en communauté (CAP) causée par Pseudomonas aeruginosa, probablement liée à l’ingestion de terre contaminée. Cette infection a provoqué une inflammation pulmonaire avec formation de lésions cavitaires. Le traitement initial empirique a été ajusté en fonction des résultats de sensibilité bactérienne, associant pipéracilline-tazobactam et ciprofloxacine. Des soins symptomatiques complémentaires ont été apportés pour contrôler les troubles digestifs et protéger les organes affectés.\n\n**Prochaines Étapes et Évolution**  \nAprès trois jours de traitement, la fièvre, les vomissements et la diarrhée ont disparu, ne laissant qu’une toux modérée. Une nouvelle tomodensitométrie réalisée onze jours plus tard a montré une progression radiologique avec fusion des lésions et un petit épanchement pleural, malgré une nette amélioration des marqueurs biologiques d’infection. La patiente a été autorisée à poursuivre son traitement en ambulatoire avec de la moxifloxacine. Un contrôle un mois plus tard a révélé une réduction significative des lésions pulmonaires et l’absence de symptômes, témoignant d’une guérison satisfaisante.\n\n**Résumé**  \nCe cas illustre une pneumonie sévère à Pseudomonas aeruginosa survenue chez une adulte jeune en bonne santé, liée à la consommation de terre contaminée. Le diagnostic a été confirmé par des prélèvements microbiologiques ciblés, et le traitement antibiotique adapté a permis une guérison complète malgré une évolution radiologique initialement défavorable. Cette observation souligne l’importance d’enquêter sur les habitudes environnementales et alimentaires dans les infections pulmonaires inhabituelles."
+        }
+    },
+    {
+        "article": "Un garçon de 15 ans a été présenté à notre clinique avec la plainte principale d'hypertrichose focale des cheveux blancs depuis 4 mois. Il avait des antécédents de vitiligo depuis l'âge de 10 ans. La lésion de vitiligo était située sur son cou droit et traitée avec une pommade topique de tacrolimus à 0,1 % environ deux fois par jour et une thérapie au laser excimer de 308 nm (500 mJ/cm2) et au laser CO2 fractionné (25 W, largeur d'impulsion 2 ms, pas 1,3 mm) toutes les 2 semaines au cours des dernières années, et il a remarqué les cheveux blancs anormaux il y a 4 mois. Les cheveux blancs anormaux sur la lésion de vitiligo poussent plus vite que les cheveux normaux sur d'autres parties du cou. Il a nié avoir jamais utilisé une autre pommade dans cette région. Après avoir arrêté le tacrolimus pendant un demi-mois, les cheveux blancs sur son cou droit ont cessé de pousser. Au suivi de 2 mois, aucune nouvelle croissance de cheveux blancs n'a été observée. Pendant cette période, le patient a continué à recevoir la thérapie au laser excimer de 308 nm et au laser CO2 fractionné toutes les 2 semaines. Nous proposons que l'hypertrichose focale ait été induite par le tacrolimus.\n",
+        "gold_summary": "Nous présentons un garçon de 15 ans avec une hypertrichose focale des cheveux blancs depuis 4 mois, après un traitement par tacrolimus topique 0,1 % pommade. Il a nié avoir jamais utilisé une autre pommade dans cette région. Après avoir arrêté le tacrolimus pendant un demi-mois, l'hypertrichose focale s'est améliorée.\n",
+        "synthetic_summary": {
+            "B1": "Un garçon de 15 ans avait des cheveux blancs qui poussaient vite sur son cou. Il utilisait une crème spéciale pour sa peau. Quand il a arrêté la crème, les cheveux blancs ont arrêté de pousser vite. Maintenant, tout va mieux.",
+            "B2": "Un garçon de 15 ans avait des cheveux blancs qui poussaient anormalement vite sur une petite zone de son cou depuis 4 mois. Cette zone était déjà touchée par le vitiligo, une maladie qui fait disparaître la couleur de la peau. Pour soigner son vitiligo, il utilisait une pommade appelée tacrolimus, appliquée deux fois par jour, ainsi que des traitements au laser toutes les deux semaines. Quand il a arrêté d’utiliser la pommade pendant environ deux semaines, la croissance rapide des cheveux blancs s’est arrêtée. Deux mois plus tard, aucun nouveau cheveu blanc ne poussait sur cette zone. Cela montre que la pommade tacrolimus a probablement causé cette croissance inhabituelle des cheveux blancs.",
+            "B3": "Résumé détaillé et structuré :\n\n**Contexte**  \nUn garçon de 15 ans, suivi pour un vitiligo localisé sur le cou droit depuis l’âge de 10 ans, a développé depuis 4 mois une hypertrichose focale, c’est-à-dire une croissance excessive de cheveux blancs, sur la même zone affectée par le vitiligo. Son traitement antérieur comprenait l’application d’une pommade topique de tacrolimus à 0,1 % environ deux fois par jour, ainsi qu’une thérapie combinée au laser excimer 308 nm et au laser CO2 fractionné toutes les deux semaines.\n\n**Principales Observations**  \nLes cheveux blancs anormaux sur la lésion de vitiligo poussaient plus rapidement que les cheveux normaux sur d’autres parties du cou. Le patient a clairement indiqué ne pas avoir utilisé d’autres pommades dans cette région. Lorsqu’il a interrompu l’application du tacrolimus pendant une quinzaine de jours, la croissance anormale des cheveux blancs s’est arrêtée. Au suivi deux mois plus tard, aucune nouvelle pousse de cheveux blancs n’a été constatée, malgré la poursuite des traitements au laser.\n\n**Interprétation Clinique**  \nL’apparition d’une hypertrichose focale (croissance excessive de poils ou cheveux) localisée sur la zone traitée suggère que le tacrolimus topique a probablement induit cet effet secondaire. Le fait que la croissance anormale ait cessé après l’arrêt du tacrolimus renforce cette hypothèse. La thérapie laser, poursuivie sans modification, ne semble pas être responsable de cette hypertrichose.\n\n**Prochaines Étapes**  \nIl est recommandé de surveiller attentivement la zone traitée pour détecter toute récidive de l’hypertrichose et d’évaluer la nécessité de poursuivre ou d’adapter le traitement par tacrolimus. Une attention particulière doit être portée aux effets secondaires potentiels lors de l’utilisation prolongée de ce médicament topique, notamment chez les patients atteints de vitiligo."
+        }
+    },
+    {
+        "article": "Une femme afro-américaine de 48 ans ayant des antécédents médicaux importants pour une hypertension essentielle non contrôlée s'est présentée au service des urgences avec une plainte principale de palpitations. Elle a également signalé une fatigue associée et un essoufflement. Au cours du mois dernier, elle a décrit une sensation intermittente de battements cardiaques irréguliers sans déclencheurs spécifiques. Ses symptômes ont progressé vers une gêne thoracique du côté gauche avec des picotements associés au membre supérieur gauche. En outre, elle a signalé des taches noires dans sa vision, ainsi qu'une dysphagie principalement aux solides, qui s'était également aggravée au cours des dernières semaines. Elle n'avait pas d'antécédents de symptômes similaires dans le passé. Elle ne prenait aucun médicament.\n\nLors de l'admission, les signes vitaux étaient significatifs pour une tension artérielle de 166/92 mmHg et une fréquence cardiaque de 109 battements/minute. Un examen physique était significatif pour une pâleur conjonctivale, sans preuve de glossite ou de koilonychia. Au service des urgences, un panel métabolique complet était normal, y compris une créatinine sérique de 0,56 mg/dL [0,60-1,20 mg/dL]. Un électrocardiogramme a montré une tachycardie sinusale avec complexes ventriculaires prématurés occasionnels. Les troponines étaient dans les limites normales. L'hémoglobine à l'admission était de 5,7 g/dL [11,9-15,1 g/dL] avec un volume corpusculaire moyen de 65,3 fL [80,0-96,0 fL]. La ferritine était de 3,1 ng/mL [11,0-306,8 ng/mL]. Le test immunochimique fécal (FIT) était négatif. Après un interrogatoire plus approfondi, la patiente a déclaré qu'elle avait encore ses règles, mais n'a pas décrit de ménorragie. Elle a nié avoir eu des hématèmesis, des hématochèses ou des mélénas. Elle a reçu 2 unités de globules rouges en poche au service des urgences et a commencé à recevoir des perfusions de complexes de fer déxtran par voie intraveineuse à 1400 mg.\n\nLa patiente était incapable de s'asseoir pour un esophagogramme afin d'évaluer une dysphagie secondaire à des nausées et des vomissements en essayant de boire l'agent de contraste. La gastroentérologie a été consultée, et la patiente a subi une endoscopie œsophagopancréatique (EOPC) et une coloscopie le jour 6 de son hospitalisation. Les résultats de la coloscopie étaient dans les limites normales. L'EOPC a révélé quelques sténoses intrinsèques dans l'œsophage supérieur, dont la plus étroite mesurait 9 millimètres. Des biopsies ont été obtenues à partir de l'œsophage proximal et distal avec des pinces à froid pour un soupçon d'œsophagite éosinophile par opposition au syndrome de Plummer-Vinson, en fonction de l'apparence macroscopique. Un examen pathologique de l'œsophage a montré une muqueuse uniquement squameuse, avec une inflammation chronique modérée. Aucune éosinophilie n'a été observée. Compte tenu des résultats cliniques, de laboratoire et endoscopiques, un diagnostic de syndrome de Plummer-Vinson a été posé. Sa dysphagie s'est améliorée au cours des 9 jours suivants à l'hôpital après des perfusions de fer et des transfusions sanguines, et elle a pu tolérer un régime alimentaire normal en mangeant lentement avec de petites bouchées.\n\nElle a subi un examen cardiaque pour évaluer les palpitations, y compris un échocardiogramme, qui a révélé une fraction d'éjection de 30 à 34 %, avec une hypokinésie globale et sans pathologie valvulaire ou hypertension pulmonaire. Un test de stress nucléaire a été négatif pour l'ischémie myocardique. Un nouveau diagnostic d'insuffisance cardiaque congestive avec fraction d'éjection réduite a été fait. La cardiologie a été consultée et elle a commencé un traitement par carvedilol, lisinopril, spironolactone et hydralazine. Elle a reçu un gilet de sauvetage à l'hôpital lors de la sortie.\n\nEnviron 6 mois après sa sortie, un appel téléphonique de suivi a été fait à la patiente. Elle a déclaré qu'elle avait respecté tous ses médicaments et que sa dysphagie avait été résolue. Au moment de l'appel téléphonique, elle tolérait une alimentation normale sans aucune restriction alimentaire.",
+        "gold_summary": "Patient : Femme, 48 ans\n\nDiagnostic final : syndrome de Plummer-Vinson\n\nSymptômes : douleur thoracique • fatigue • palpitation\n\nMédication : —\n\nProcédure clinique : oesophagogastroduodénoscopie (EGD) • coloscopie\n\nSpécialité : Médecine générale et interne\n\nNous présentons le cas d'une femme afro-américaine de 48 ans souffrant d'anémie symptomatique et d'une insuffisance cardiaque congestive secondaire à l'hypertension, qui présentait les symptômes classiques de la PVS.\n",
+        "synthetic_summary": {
+            "B1": "Une dame de 48 ans se sentait très fatiguée. Son cœur battait très vite et elle avait mal à la poitrine. Elle avait aussi du mal à avaler sa nourriture.\n\nLes docteurs ont fait des examens pour comprendre. Ils ont vu que son sang avait peu de fer. Son œsophage, le tube pour avaler, était un peu rétréci. Cela rendait la déglutition difficile.\n\nIls lui ont donné du fer et du sang pour l’aider. Après, elle a pu manger normalement. Son cœur aussi a reçu un traitement pour battre mieux.\n\nMaintenant, elle va mieux et peut manger sans problème. Les docteurs sont contents car elle se sent plus forte.",
+            "B2": "Présentation du cas  \nUne femme de 48 ans est venue aux urgences parce qu'elle avait des palpitations, c’est-à-dire qu’elle sentait son cœur battre très vite ou de façon irrégulière. Elle se sentait aussi très fatiguée et avait du mal à respirer. Depuis un mois, elle avait parfois des battements cardiaques bizarres sans raison claire. Ensuite, elle a ressenti une gêne du côté gauche de la poitrine avec des picotements dans son bras gauche. Elle voyait aussi des taches noires devant ses yeux et avait des difficultés à avaler surtout les aliments solides. Elle n’avait jamais eu ces problèmes auparavant et ne prenait aucun médicament.\n\nCe qu’ils ont trouvé  \nÀ son arrivée, sa tension artérielle était élevée (166/92) et son cœur battait vite (109 battements par minute). L’examen montrait qu’elle était pâle, ce qui peut indiquer une anémie, c’est-à-dire un manque de globules rouges. Les analyses ont confirmé une anémie sévère avec un taux d’hémoglobine très bas (5,7 g/dL, alors que la normale est autour de 12-15 g/dL). Son volume moyen des globules rouges était petit, ce qui suggère une carence en fer. En effet, son taux de ferritine, une protéine qui stocke le fer, était très bas. Un test pour chercher du sang dans les selles était négatif, et elle n’avait pas d’autres signes de saignement. Elle a reçu des transfusions de sang et des perfusions de fer pour corriger cette anémie.\n\nPour comprendre pourquoi elle avait du mal à avaler, les médecins ont fait une endoscopie, c’est-à-dire qu’ils ont regardé l’intérieur de son œsophage avec une caméra. Ils ont trouvé des rétrécissements dans la partie haute de l’œsophage. Des biopsies, c’est-à-dire des petits prélèvements de tissu, ont montré une inflammation mais pas d’éosinophiles, un type de cellule souvent présent dans certaines inflammations. Ces résultats, associés à son anémie et ses symptômes, ont permis de poser le diagnostic de syndrome de Plummer-Vinson. Ce syndrome est une maladie rare liée à une carence en fer qui provoque des difficultés à avaler à cause de rétrécissements dans l’œsophage.\n\nCe que cela signifie pour elle  \nAprès avoir reçu du fer et du sang, sa difficulté à avaler s’est améliorée en moins de deux semaines. Elle a pu manger normalement en prenant son temps. Par ailleurs, un examen du cœur a montré qu’elle avait une insuffisance cardiaque, c’est-à-dire que son cœur pompait moins bien le sang, probablement à cause de son hypertension non contrôlée. Elle a commencé un traitement pour son cœur avec plusieurs médicaments et a reçu un appareil de secours en cas de problème cardiaque grave.\n\nSix mois plus tard, lors d’un suivi par téléphone, elle a dit qu’elle prenait bien ses médicaments et que ses difficultés pour avaler avaient disparu. Elle mangeait normalement sans problème.\n\nEn résumé  \nCette patiente avait un syndrome de Plummer-Vinson causé par une carence en fer sévère, qui expliquait ses symptômes de fatigue, palpitations et difficulté à avaler. Son traitement par fer et transfusions a permis une amélioration rapide. Elle a aussi été prise en charge pour son insuffisance cardiaque liée à son hypertension. Ce cas montre l’importance de rechercher une cause de l’anémie et de surveiller les complications cardiaques chez les patients avec ce syndrome.",
+            "B3": "Résumé détaillé et structuré pour un public non-médecin éduqué\n\n**Contexte**  \nUne femme afro-américaine de 48 ans, avec un antécédent d’hypertension artérielle non contrôlée, s’est présentée aux urgences en raison de palpitations cardiaques, accompagnées de fatigue et d’essoufflement. Depuis un mois, elle ressentait des battements cardiaques irréguliers intermittents, sans facteur déclenchant évident. Ses symptômes ont évolué vers une gêne thoracique localisée à gauche, associée à des picotements dans le bras gauche. Elle a également rapporté des troubles visuels (apparition de taches noires) et une difficulté à avaler principalement les aliments solides (dysphagie), qui s’aggravait progressivement. Elle ne prenait aucun traitement au moment de son admission.\n\n**Principales observations cliniques et résultats d’examens**  \nÀ son arrivée, sa tension artérielle était élevée (166/92 mmHg) et sa fréquence cardiaque rapide (109 battements par minute). L’examen physique a révélé une pâleur des conjonctives (indiquant une possible anémie), sans signes spécifiques tels que l’inflammation de la langue ou des déformations des ongles. Les analyses sanguines ont montré une anémie sévère avec une hémoglobine très basse (5,7 g/dL, alors que la normale est autour de 12-15 g/dL) et un volume corpusculaire moyen réduit (indiquant des globules rouges plus petits que la normale). La ferritine, qui reflète les réserves en fer, était très faible, confirmant une carence en fer. Les tests cardiaques ont montré une tachycardie sinusale avec quelques battements prématurés, mais sans signe d’atteinte cardiaque aiguë (troponines normales). Un test de recherche de sang occulte dans les selles était négatif, et la patiente ne rapportait pas de saignements digestifs évidents.\n\nPour traiter l’anémie, elle a reçu des transfusions sanguines et un traitement intraveineux par fer.\n\n**Examens complémentaires**  \nLa patiente présentait une dysphagie, mais n’a pas pu réaliser un examen radiologique de l’œsophage (esophagogramme) à cause de nausées. Une consultation en gastroentérologie a conduit à la réalisation d’une endoscopie (examen visuel direct de l’œsophage, de l’estomac et du duodénum) et d’une coloscopie (examen du côlon). La coloscopie était normale. L’endoscopie a révélé plusieurs rétrécissements (sténoses) dans la partie supérieure de l’œsophage, la plus étroite mesurant 9 millimètres. Des biopsies ont été prélevées pour rechercher une inflammation spécifique appelée œsophagite éosinophile, mais l’analyse a montré seulement une inflammation chronique modérée sans présence d’éosinophiles (un type de globules blancs). Ces résultats, associés à l’anémie ferriprive et aux symptômes, ont conduit au diagnostic du syndrome de Plummer-Vinson (PVS), une maladie rare caractérisée par une triade : anémie ferriprive, dysphagie et sténoses œsophagiennes.\n\n**Interprétation clinique**  \nLe syndrome de Plummer-Vinson est une cause classique de dysphagie chez les patients présentant une carence en fer sévère. Dans ce cas, la correction de l’anémie par transfusions et perfusions de fer a permis une amélioration progressive de la dysphagie, la patiente retrouvant la capacité de s’alimenter normalement en mangeant lentement et par petites bouchées.\n\nPar ailleurs, l’évaluation cardiaque a révélé une insuffisance cardiaque congestive avec une fraction d’éjection réduite (mesure de la capacité du cœur à pomper le sang), probablement liée à son hypertension non contrôlée. Aucun signe d’ischémie (manque d’oxygène au muscle cardiaque) n’a été détecté. Un traitement médicamenteux adapté a été instauré, comprenant des bêta-bloquants, des inhibiteurs de l’enzyme de conversion, des diurétiques et des vasodilatateurs.\n\n**Prochaines étapes et suivi**  \nLa patiente a été suivie six mois après sa sortie de l’hôpital. Elle rapportait une bonne observance de son traitement, une disparition complète de la dysphagie et une alimentation normale sans restriction. Son état cardiaque était pris en charge par la cardiologie.\n\n**Conclusion**  \nCe cas illustre l’importance de reconnaître le syndrome de Plummer-Vinson chez une patiente présentant une anémie ferriprive sévère et une dysphagie, ainsi que la nécessité d’une prise en charge multidisciplinaire incluant gastroentérologie et cardiologie, notamment en présence de complications cardiaques associées. Le traitement de la carence en fer peut entraîner une amélioration significative des symptômes œsophagiens."
+        }
+    },
+    {
+        "article": "La patiente était une femme de 81 ans ayant des antécédents médicaux d’hypertension et d’hyperlipidémie. La patiente a été amenée à notre hôpital avec une hémiplégie droite sévère et une aphasie totale, et la note de l’échelle des accidents vasculaires cérébraux des National Institutes of Health (NIHSS) était de 16 à l’admission. Le dernier point de contrôle connu (LKW) était de 12 heures. Dans notre établissement, nous suivons un protocole d’imagerie basé sur le temps pour les cas d’AVC aigus : les cas dans les 4,5 heures suivant le début sont soumis à une CTA en premier, tandis que les cas au-delà de 4,5 heures sont évalués en premier avec une IRM. L’IRM a révélé un infarctus cérébral dans la région de l’artère cérébrale moyenne gauche, et le score de l’Alberta Stroke Program Early CT Score (DWI ASPECTS) était de 7. L’ARM a révélé une occlusion du segment M2 gauche. Cependant, les résultats de la radiographie thoracique ont indiqué une anomalie possible dans l’arc aortique, ce qui nous a conduit à effectuer une CTA supplémentaire pour évaluer la voie d’accès à la thrombectomie. La CTA a révélé une RAA avec une ramification en miroir. La patiente n’a pas reçu d’activateur de plasminogène de tissu recombinant par voie intraveineuse. Bien que les preuves soutenant la MT dans de tels scénarios soient limitées, nous avons soigneusement évalué l’état de la patiente en fonction de plusieurs facteurs : le score modifié de Rankin (mRS) avant l’AVC était de 0, le DWI ASPECTS était de 7, et la présentation était un AVC réveillant avec un DWI-FLAIR non conforme, ce qui suggère que le temps réel depuis le début de l’AVC pourrait ne pas être aussi long que le LKW l’indique. En outre, la patiente présentait des symptômes sévères avec un NIHSS de 16. Sur la base de ces facteurs, nous avons jugé que la MT était appropriée, car elle offrait une chance d’améliorer le résultat de la patiente.\n\nNous avons choisi le système de guidage habituel. Une gaine de 9 Fr a été insérée dans l'artère fémorale commune droite. Un fil-guide (Radifocus ; Terumo, Tokyo, Japon) et un cathéter JB2 de 6 Fr (Medikit, Tokyo, Japon) ont été avancés à l'aide d'un cathéter guide à ballon OPTIMO de 9 Fr (Tokai Medical Products, Aichi, Japon).\n\nLe cathéter guide a été avancé de l'aorte abdominale au milieu de la colonne vertébrale vers l'aorte thoracique du côté droit de la colonne vertébrale et a été facilement placé dans l'artère carotide interne gauche de la manière habituelle en se référant à l'ACP. L'angiographie de l'artère carotide interne gauche a révélé une occlusion du tronc inférieur gauche M2. La thrombolyse dans la réperfusion de l'infarctus cérébral 2B a été réalisée en utilisant Trevo NXT 3 × 32 mm (Stryker, Fremont, CA, USA) et Catalyst 6 (Stryker) après 3 passes. Le temps de la ponction à la recanalisation était de 61 minutes (10 minutes, de la ponction au placement du cathéter guide dans l'artère carotide interne gauche ; 51 minutes, du placement du cathéter guide à la recanalisation). La TDM post-procédurale a révélé une petite hémorragie sous-arachnoïdienne.\n\nLa fibrillation auriculaire n'a pas été détectée, et une TDM de contraste de l'ensemble du corps a été réalisée pour rechercher davantage la source de l'embolie. Une thrombose veineuse profonde (TVP) et une embolie pulmonaire (EP) ont été observées dans la veine fémorale profonde droite et dans les deux artères pulmonaires, respectivement. L'échocardiographie transœsophagienne a démontré un foramen ovale patent (FOP). Malgré les anticorps antinucléaires et la coagulabilité examinés à l'aide de tests sanguins, ceux-ci n'étaient pas la cause de l'infarctus cérébral. La pathogenèse de l'infarctus cérébral a été déterminée comme étant une embolie paradoxale, et l'apixaban a été administré après que la TVP et l'EP aient été révélées. Le thrombus dans la veine fémorale et l'artère pulmonaire a presque disparu, et l'infarctus cérébral n'a pas récidivé. L'hémiplégie droite et l'aphasie ont persisté, et à la sortie, le score mRS était de 5.\n",
+        "gold_summary": "Une femme de 81 ans a présenté une hémiplégie droite sévère et une aphasie. La note de l'échelle des accidents vasculaires cérébraux des National Institutes of Health était de 16, l'imagerie par résonance magnétique a révélé une valeur de 7 sur l'échelle de l'Alberta Stroke Program Early CT, et l'angiographie par résonance magnétique a révélé une occlusion de la M2 gauche. L'angiographie par résonance magnétique a révélé un arc aortique droit avec des branches en miroir. La thrombectomie mécanique a été réalisée en utilisant le système habituel, et une recanalisation efficace a été obtenue avec un stent retriever et un cathéter d'aspiration après 3 passes. L'angiographie par résonance magnétique a révélé une embolie pulmonaire et une thrombose veineuse profonde (TVP) dans la veine fémorale profonde droite, et l'échocardiographie transœsophagienne a révélé un foramen ovale patent. L'électrocardiographie n'a pas révélé de fibrillation auriculaire, et les autres examens n'ont pas révélé d'autre cause ; par conséquent, un embolisme cérébral paradoxal a été diagnostiqué. Après un traitement anticoagulant, aucune récidive d'infarctus, d'embolie pulmonaire ou de TVP n'a été observée. Une hémiplégie droite sévère et une aphasie totale ne se sont pas améliorées, et la patiente a été sortie le jour 37 après admission avec une note de 5 sur l'échelle de Rankin modifiée.\n",
+        "synthetic_summary": {
+            "B1": "Une dame de 81 ans a eu un gros problème au cerveau. Elle ne pouvait plus bouger son bras et sa jambe droite. Elle ne pouvait plus parler non plus.\n\nLes docteurs ont fait des images de son cerveau. Ils ont vu qu’un petit tuyau dans son cerveau était bouché. Ils ont utilisé des outils spéciaux pour enlever le bouchon. Ça a bien marché.\n\nIls ont aussi trouvé des caillots dans une grosse veine de sa jambe et dans ses poumons. Ils ont donné des médicaments pour que les caillots partent.\n\nLa dame n’a pas eu d’autres problèmes après. Mais elle ne pouvait toujours pas bien bouger ni parler quand elle est rentrée chez elle. Les docteurs vont continuer à l’aider.",
+            "B2": "**Ce qu'ils ont trouvé chez la patiente**  \nUne femme de 81 ans est arrivée à l’hôpital avec une paralysie sévère du côté droit de son corps (appelée hémiplégie) et une incapacité totale à parler (aphasie). Son état était grave, avec un score de 16 sur une échelle utilisée pour mesurer la gravité des accidents vasculaires cérébraux (AVC). Une IRM a montré une zone de cerveau touchée, et une autre imagerie a révélé qu’une artère importante dans son cerveau (appelée segment M2 de l’artère cérébrale moyenne gauche) était bloquée. De plus, une anomalie rare dans la forme de son aorte (le gros vaisseau qui sort du cœur) a été découverte : elle avait un arc aortique droit avec des branches en miroir.\n\n**Le traitement réalisé**  \nLes médecins ont décidé de faire une thrombectomie mécanique, c’est-à-dire qu’ils ont utilisé des petits instruments pour enlever le caillot qui bloquait l’artère dans le cerveau. Cette intervention a réussi après trois tentatives, permettant de rétablir le flux sanguin.\n\n**Ce qu’ils ont découvert après**  \nD’autres examens ont montré qu’elle avait aussi des caillots dans une grosse veine de sa jambe droite (thrombose veineuse profonde) et dans ses poumons (embolie pulmonaire). Une échographie spéciale du cœur a révélé un petit passage anormal appelé foramen ovale patent, qui peut laisser passer des caillots du côté droit vers le côté gauche du cœur, causant un AVC. Ils n’ont pas trouvé d’autres causes comme une fibrillation auriculaire (un trouble du rythme cardiaque). Les médecins ont donc conclu que son AVC était dû à un \"embolie paradoxale\", c’est-à-dire un caillot venant des veines qui a traversé ce passage anormal pour aller dans le cerveau.\n\n**Le suivi et l’évolution**  \nAprès avoir commencé un traitement anticoagulant (un médicament qui empêche la formation de nouveaux caillots), les caillots dans ses veines et ses poumons ont presque disparu, et elle n’a pas eu de nouvel AVC. Cependant, la paralysie et les difficultés à parler sont restées sévères. Elle est sortie de l’hôpital après 37 jours avec un score de 5 sur l’échelle de Rankin modifiée, ce qui signifie qu’elle avait besoin d’aide importante pour ses activités quotidiennes.",
+            "B3": "**Contexte**  \nUne femme de 81 ans, avec des antécédents d’hypertension et d’hyperlipidémie, a été admise suite à une hémiplégie droite sévère (paralysie d’un côté du corps) et une aphasie totale (incapacité à parler). À son arrivée, son score NIHSS (une échelle mesurant la gravité de l’accident vasculaire cérébral, AVC) était de 16, indiquant un AVC sévère. Le dernier moment où la patiente était connue sans symptômes (LKW) remontait à 12 heures. Selon le protocole de l’hôpital, une IRM a été réalisée en priorité, révélant un infarctus dans la région de l’artère cérébrale moyenne gauche avec un score DWI ASPECTS de 7 (indiquant une atteinte modérée du cerveau). L’angiographie par résonance magnétique (ARM) a montré une occlusion du segment M2 gauche de cette artère. Par ailleurs, une anomalie de l’arc aortique a été détectée à la radiographie thoracique, confirmée par une angiographie par tomodensitométrie (CTA) révélant un arc aortique droit avec une ramification en miroir, une variante anatomique rare.\n\n**Principales Observations**  \nLa patiente n’a pas reçu de traitement thrombolytique intraveineux en raison du délai depuis le début des symptômes. Cependant, en raison de son bon état fonctionnel avant l’AVC (score mRS de 0), du score DWI ASPECTS favorable, de la sévérité des symptômes et d’une discordance entre les images IRM DWI et FLAIR suggérant un AVC récent, une thrombectomie mécanique (MT) a été décidée. Cette intervention consiste à retirer mécaniquement le caillot obstruant l’artère. Le geste a été réalisé via une voie d’accès femorale droite, avec un cathéter guide et un stent retriever, permettant une recanalisation efficace après trois tentatives en 61 minutes. Une petite hémorragie sous-arachnoïdienne post-procédurale a été détectée, sans complication majeure.\n\nPar la suite, une recherche approfondie de la cause de l’AVC a été menée. Aucune fibrillation auriculaire (arythmie cardiaque fréquente responsable d’embolies) n’a été détectée. Une thrombose veineuse profonde (TVP) dans la veine fémorale droite et une embolie pulmonaire (obstruction des artères pulmonaires par un caillot) bilatérale ont été identifiées par tomodensitométrie. Une échocardiographie transœsophagienne a révélé un foramen ovale patent (FOP), une communication anormale entre les oreillettes cardiaques qui peut permettre à un caillot veineux d’accéder à la circulation artérielle cérébrale, provoquant un AVC dit « paradoxal ». Les tests sanguins n’ont pas montré d’autres causes thrombotiques ou auto-immunes.\n\n**Interprétation Clinique**  \nLe diagnostic retenu est celui d’un infarctus cérébral par embolie paradoxale, c’est-à-dire un caillot veineux migré vers le cerveau via le FOP. La thrombectomie mécanique a permis de rétablir la circulation cérébrale malgré la variante anatomique de l’arc aortique. Le traitement anticoagulant par apixaban a été initié pour prévenir la récidive, ce qui a conduit à la disparition quasi complète des thromboses veineuses et pulmonaires, sans nouvel AVC.\n\n**Prochaines Étapes et Évolution**  \nMalgré la prise en charge rapide et adaptée, la patiente a conservé une hémiplégie droite sévère et une aphasie totale. À sa sortie, 37 jours après l’admission, son score mRS était de 5, indiquant une dépendance sévère nécessitant une assistance pour les activités quotidiennes. Ce cas illustre l’importance d’une évaluation complète, y compris des anomalies anatomiques et des causes emboliques rares, pour guider le traitement des AVC complexes chez les personnes âgées."
+        }
+    },
+    {
+        "article": "Un homme de 37 ans s'est présenté à notre établissement de troisième niveau pour une uvéite en janvier 2020, suite à une référence pour une évaluation vitréorétinienne plus approfondie. Ses symptômes étaient des éclairs et des photoréactions, principalement dans l'œil droit. Il avait été diagnostiqué auparavant avec une probable BRCSCR bilatérale à l'été 2016. Les évaluations de laboratoire initiales, y compris le compte sanguin complet, le bilan métabolique complet, l'hémoglobine A1c et les études du fer, étaient toutes normales. Les évaluations de laboratoire pour les étiologies infectieuses, y compris les tests QuantiFERON-TB Gold (QFT), le réactif plasmatique rapide (RPR) et l'absorption des anticorps fluorescents (FTA-ABS), étaient toutes négatives ou non réactives. L'imagerie par résonance magnétique du cerveau en septembre 2016 était normale. En novembre 2016, le patient a été traité par corticostéroïde topique et bevacizumab intravitréen dans l'œil droit (OD), ainsi que 60 mg de prednisone orale quotidienne. En décembre 2016, il a commencé un traitement immunomodulateur (IMT) avec la cyclosporine et le méthotrexate, qui ont tous deux été arrêtés en 2017 en raison d'un manque d'efficacité possible. Le patient a ensuite commencé un traitement par adalimumab, au cours duquel ses symptômes (éclairs et corps flottants) se sont améliorés. Après environ 1 an de traitement, l'adalimumab a été arrêté en raison de la réduction des taux de fer sérique début 2019. En octobre 2019, il a reçu une injection intravitréenne de fluocinolone acétonide de 0,18 mg dans l'œil droit, mais n'a constaté aucune amélioration ultérieure des symptômes visuels.\n\nLors de l'examen initial en janvier 2020, le patient a noté un inconfort oculaire modéré (OD > OS), une vision trouble (OD > OS) et des corps flottants (OU). L'acuité visuelle était de 20/20 OU. Lors de l'évaluation initiale, l'examen des systèmes était négatif du point de vue systémique. Les pressions intraoculaires étaient de 13 mm Hg OD et 12 mm Hg OS. L'examen du segment antérieur était remarquable pour une éruption bilatérale de grade 1+, avec une cataracte sous-capsulaire postérieure modérée OD, mais était par ailleurs sans particularité. L'examen du fond d'œil dilaté était remarquable pour un œdème du disque optique (OD > OS) et des lésions choriorétinales hypopigmentées ovoïdes péripapillaires et périphériques (OU). L'œil droit présentait également une atrophie temporale péripapillaire, des cellules vitreuses 1+, des modifications pigmentaires du pigment rétinien maculaire et une petite hémorragie rétinienne dans la périphérie du quadrant supérotemporal. La tomographie par cohérence optique dans le domaine spectral (SD-OCT) a montré une élévation du disque optique dans le liquide intrarétinien péripapillaire avec une membrane épirétinienne modérée (ERM) OD > OS. L'angiographie à la fluorescéine grand angle (FA) (OPTOS Plc, Dunfermline, Royaume-Uni) a montré un média trouble, une fuite du disque et une coloration péripapillaire OD, et une fuite optique diffuse avec une coloration segmentaire modérée des veinules le long de l'arcade temporale inférieure OS. Il y avait une hyperfluorescence de plusieurs lésions dans la région péripapillaire et le long de l'arcade temporale inférieure sans aucun signe de fuite OU.\n\nDeux semaines plus tard, l'électrorétinographie de champ complet (ffERG) a montré une dysfonction rétinienne globale modérée à modérée, avec des régions géographiques claires de dépression maculaire (OD > OS). Les temps de clignotement implicites de 30 Hz ont révélé un retard significatif dans les deux yeux (OS > OD). Le potentiel évoqué visuel a montré un retard relativement symétrique pour les petits et les grands stimuli, suggérant une dysfonction modérée du nerf optique. Les champs visuels de Goldmann (GVF) et les champs visuels de Humphrey (HVF) ont montré un élargissement du point aveugle OD et un point aveugle normal sans constriction généralisée OS. Les évaluations de laboratoire n'étaient remarquables que pour la positivité de l'antigène leucocytaire humain (HLA) A29. Les résultats des tests de l'enzyme de conversion de l'angiotensine, de la lysozyme et du QFT répété étaient tous dans les limites normales.\n\nLors de la visite de suivi d'un mois en février 2020, le patient a noté une acuité visuelle stable, une certaine amélioration des corps flottants dans les deux yeux et une opacité persistante principalement dans l'OD. L'acuité visuelle est restée de 20/20 OU. La pression intraoculaire était de 15 mm Hg OD et 8 mm Hg OS. L'examen du segment antérieur a été remarquable pour un éclat OU de 1+. L'examen du fond d'œil dilaté a été remarquable pour 0,5+ cellules et 0,5+ opacité du vitré OU. Les résultats de l'examen global du pôle postérieur étaient stables. Les résultats de l'OCT SD et de la FA grand angle étaient relativement inchangés depuis la première visite. La coréoangiographie en indocyanine verte grand angle (ICG) a montré un médium clair, de multiples taches hypocyanescentes dans le pôle postérieur et la périphérie médiane dans la phase intermédiaire, et des taches hypocyanescentes ont disparu dans la phase tardive OU. L'autofluorescence du fond d'œil a montré une hypofluorescence autour du disque optique et de la rétine.\n\nLe patient a été diagnostiqué avec un BSCR sur la base de la positivité HLA-A29, de l’aspect typique du fond d’œil et de l’évaluation négative pour d’autres étiologies auto-immunes et infectieuses. Étant donné la maladie active du patient, comme en témoigne l’œdème du disque optique associé à des cellules vitreuses dans les deux yeux, ainsi que les résultats très suggestifs de la FA et de l’ICG, le patient a commencé un traitement par infliximab à une dose de 7,5 mg/kg par mois. Il a également reçu 3 jours de méthylprednisolone par voie intraveineuse (IV) à une dose de 1000 mg/jour, suivis d’un traitement par voie orale de prednisone.\n\nLe patient ne s'est pas présenté à la visite de suivi avant avril 2021 et a reçu huit cycles de 7,5 mg/kg d'infliximab en perfusion avec 1000 mg de prednisone pendant 3 jours au cours de cette période. La vision était réduite à 20/40 OD en raison de la formation de cataracte sous-capsulaire postérieure (PSC) et était de 20/20 OS. Aucune cellule AC et aucune éruption n'étaient présentes dans les deux yeux. Le vitré était trouble en OD en raison de la formation de cataracte. Le disque optique SD-OCT ne présentait pas de changements significatifs. Sur la FA, le média était flou au centre OD en raison de la formation de cataracte. La coloration partielle du disque optique était présente dans l'OU. Il n'y avait pas de coloration vasculaire rétinienne et de fuite capillaire dans l'OU. La coloration des lésions choroïdiennes péripapillaires dans les cadres précoce et tardif de la FA restait la même dans l'OU. Quatre mois plus tard, le patient a reçu quatre cycles supplémentaires d'infusions IFX en plus d'un jour de 1000 mg de méthylprednisolone. La vision a diminué à 20/70 OD en raison de la progression de la PSC et était de 20/20 OS. L'examen ophtalmologique, les résultats SD-OCT et FA sont restés inchangés. L'ICG a été effectué et les taches hypocyanescentes ont montré une nette amélioration avec quelques taches hypocyanescentes au pôle postérieur (OS>OD) dans les deux yeux sur ICG. Les tests électrophysiologiques, y compris ffERG, mfERG et VEP et les tests du champ visuel, y compris GVF et HVF, sont restés inchangés depuis la visite initiale. Bien qu'il y ait eu une amélioration significative des résultats oculaires à l'examen et à la fois dans la FA et dans l'ICG, le mycophenolate mofetil 2000 mg quotidien a été ajouté à son traitement en raison de la présence d'oedème du disque optique et il restait quelques taches hypocyanescentes au pôle postérieur dans l'ICG.\n",
+        "gold_summary": "Un homme de 37 ans s'est présenté à notre service d'uvéites tertiaires avec un inconfort oculaire bilatéral, une vision trouble et des corps flottants. L'examen oculaire a révélé une vitrite, un œdème du disque optique et des lésions choriorétinales hypopigmentées ovoïdes, visibles sur la choroangiographie au vert indocyanine sous forme de multiples taches hypocyanescentes dans la phase intermédiaire. L'électrorétinographie à champ complet et le potentiel évoqué visuel ont montré une dysfonction rétinienne globale et une dysfonction du nerf optique. Les évaluations de laboratoire n'ont révélé que la positivité de l'antigène leucocytaire humain (HLA)-A29. Le patient a été diagnostiqué comme souffrant d'une RCBS et a commencé un traitement par prednisone orale et a finalement été traité par infliximab.\n",
+        "synthetic_summary": {
+            "B1": "Un homme de 37 ans avait mal aux deux yeux. Il voyait un peu flou et voyait des petites taches qui bougent.\n\nLe docteur a regardé ses yeux. Il a vu que ses yeux étaient un peu gonflés et qu’il y avait des petites taches blanches.\n\nDes tests ont montré que ses yeux ne fonctionnaient pas très bien. Un test spécial a dit qu’il avait un signe appelé HLA-A29.\n\nLe docteur a dit qu’il avait une maladie des yeux appelée RCBS. Il a donné des médicaments pour aider ses yeux à aller mieux.",
+            "B2": "Un homme de 37 ans est venu consulter pour des douleurs aux deux yeux, une vision un peu floue et la présence de petites taches flottantes dans son champ de vision. Lors de l’examen, les médecins ont trouvé une inflammation dans le vitré (la partie gélatineuse à l’intérieur de l’œil), un gonflement du disque optique (la zone où le nerf optique entre dans l’œil) et des taches claires en forme d’œuf sur la couche de la choroïde, une partie importante de l’œil. Une technique spéciale d’imagerie appelée choroangiographie au vert d’indocyanine a montré plusieurs taches sombres dans ces zones, ce qui indique une inflammation active.\n\nDes tests électriques ont aussi été faits pour vérifier le fonctionnement de la rétine (la couche sensible à la lumière) et du nerf optique. Ces tests ont montré que la rétine et le nerf optique ne fonctionnaient pas normalement. Les analyses de sang ont révélé que le patient avait un marqueur génétique appelé HLA-A29, souvent lié à une maladie appelée rétinite à cellules en bouquet (RCBS), une inflammation chronique de l’œil.\n\nAvec ces résultats, les médecins ont diagnostiqué une RCBS. Pour traiter cette maladie, ils ont commencé par donner au patient des corticostéroïdes par voie orale (comme la prednisone) pour réduire l’inflammation. Ensuite, ils ont utilisé un médicament appelé infliximab, qui agit sur le système immunitaire pour calmer la réaction inflammatoire et protéger la vision.",
+            "B3": "Résumé structuré pour un public non spécialiste mais informé :\n\n**Contexte**  \nUn homme de 37 ans a consulté dans un centre spécialisé en uvéites (inflammations de l’œil) en raison d’un inconfort oculaire dans les deux yeux, d’une vision trouble et de la présence de corps flottants (petites taches ou filaments visibles dans le champ de vision). Il avait des antécédents de suspicion de maladie oculaire inflammatoire bilatérale depuis 2016, avec plusieurs traitements antérieurs sans succès durable.\n\n**Principales observations cliniques**  \nL’examen ophtalmologique a montré une inflammation du vitré (vitrite), un œdème (gonflement) du disque optique — la zone où le nerf optique entre dans l’œil — ainsi que des lésions spécifiques de la couche choroïdienne et rétinienne, caractérisées par des zones hypopigmentées (moins colorées) en forme d’ovale. Ces lésions ont été mises en évidence par une technique d’imagerie appelée coréoangiographie au vert d’indocyanine, qui a révélé de multiples taches sombres (hypocyanescentes) dans la phase intermédiaire de l’examen, indiquant une atteinte inflammatoire de la choroïde (couche vasculaire sous la rétine).\n\nLes tests électrophysiologiques, notamment l’électrorétinographie à champ complet (ffERG) et le potentiel évoqué visuel (PEV), ont montré une dysfonction globale de la rétine ainsi qu’une atteinte modérée du nerf optique, traduisant une altération de la transmission des signaux visuels.\n\nLes analyses sanguines n’ont révélé aucune infection ou autre maladie auto-immune, à l’exception de la présence d’un marqueur génétique appelé antigène leucocytaire humain HLA-A29, fortement associé à la maladie de Birdshot chorioretinopathy (BSCR), une forme rare d’uvéite chronique.\n\n**Interprétation clinique**  \nSur la base des signes cliniques, des résultats d’imagerie et de la positivité au HLA-A29, le diagnostic de Birdshot chorioretinopathy a été confirmé. Cette maladie auto-immune affecte principalement la choroïde et la rétine, entraînant une inflammation chronique pouvant compromettre la vision.\n\n**Prise en charge et évolution**  \nLe patient a débuté un traitement par corticostéroïdes oraux (prednisone) pour réduire l’inflammation. En raison de la persistance de la maladie active, un traitement immunosuppresseur par infliximab, un anticorps monoclonal ciblant l’inflammation, a été instauré. Ce traitement a permis une amélioration des signes inflammatoires oculaires, bien que la vision ait été partiellement affectée par la formation d’une cataracte sous-capsulaire postérieure, une complication fréquente des traitements corticostéroïdes prolongés.\n\nEn résumé, ce cas illustre la complexité du diagnostic et du traitement de la Birdshot chorioretinopathy, une maladie inflammatoire rare de l’œil nécessitant une prise en charge spécialisée et un suivi attentif."
+        }
+    },
+    {
+        "article": "Une fille est née à 34 semaines de grossesse avec un poids de naissance de 2 820 g. Un traitement complet de corticostéroïdes prénataux avait été administré et l'imagerie prénatale de routine a montré des polyhydramnios et un fœtus de grande taille pour la date. La mère avait des antécédents de diabète gestationnel et de pré-éclampsie.\n\nL'enfant est né par césarienne en bonne condition avec des scores APGAR de 61, 95 et 1 010, mais en raison de difficultés respiratoires, elle a reçu un surfactant par administration moins invasive 25 minutes après la naissance. Elle a ensuite été transférée à l'unité de soins intensifs néonataux sous ventilation assistée continue à 40 % d'oxygène. 4 heures après la naissance, en raison de difficultés respiratoires persistantes et d'une augmentation des besoins en oxygène jusqu'à 60 %, elle a été intubée et ventilée mécaniquement. Une radiographie thoracique a révélé des preuves d'une éventuelle éventration bilatérale des diaphragmes. Un examen échographique du diaphragme a confirmé ce soupçon. Un échocardiogramme (ECHO) effectué à ce moment-là a révélé une hypoplasie modérée de l'isthme, mais un ECHO répété a démontré un cœur normal sur le plan structurel. Après avoir subi un essai de respiration spontanée et une période d'évaluation non invasive de l'activité électrique du diaphragme, elle a été extubée avec succès après 36 heures de soutien ventilatoire invasif. En outre, elle n'a pas eu besoin d'un soutien respiratoire non invasif après extubation et elle a continué à se ventiler par l'air jusqu'à la sortie. Comme elle n'a pas eu besoin de périodes prolongées de soutien respiratoire invasif, elle n'a pas été considérée comme une candidate à une intervention chirurgicale dans la période néonatale aiguë.\n\nPendant sa période néonatale, elle a présenté une hypoglycémie à l'admission à l'unité néonatale avec une glycémie de 0,4 mmol/L et a nécessité une concentration maximale de glucose de 20 %. Elle a ensuite été diagnostiquée comme ayant un hyperinsulinisme et a commencé à recevoir du diazoxide. Elle avait une mauvaise alimentation malgré une vidéofluroscopie et un examen ORL normaux et a ensuite eu besoin d'une aide alimentaire par sonde nasogastrique. Au cours de l'évaluation neurologique, elle a présenté une hypotonie centrale avec des réflexes vifs et a été notée pour avoir de nombreux naevus mélanocytaires sur la face latérale des deux bras avec des taches supplémentaires sur le sacrum. L'examen histopathologique d'une biopsie par ponction a démontré des résultats compatibles avec une mélanocytose cutanée. Elle est née avec deux dents néonatales qui ont été enlevées après la naissance, mais elle a ensuite développé deux lésions fibreuses sur la crête alvéolaire antérieure qui étaient pédiculées et mobiles, elles ont ensuite été enlevées à 1 mois. Une enquête neurologique approfondie a été réalisée et a révélé une imagerie par résonance magnétique cérébrale normale, avec une électromyographie des membres supérieurs et inférieurs et des études de conduction nerveuse normales. Compte tenu du diagnostic différentiel de l'atrophie musculaire spinale, une analyse d'immunohistochimie a été réalisée, qui a donné des résultats normaux. Une évaluation ophtalmologique et une échographie rénale ont été réalisées, elles étaient normales. Les tests génétiques postnataux ont révélé une mutation du gène KMT2D, associée au syndrome de Kabuki.\n\nElle a été renvoyée chez elle le 64e jour après la naissance avec un soutien alimentaire nasogastrique et a continué à prendre des médicaments diazodix. Elle continue de recevoir une aide importante de la part d'ergothérapeutes, de logopèdes et d'équipes de physiothérapie.\n\nImagerie et mesures\nLa zone thoracique radiographique thoracique (CRTA) mesurée après extubation (trois jours après la naissance) était de 1 654 mm2, équivalant à celle d'un nourrisson à terme avec hernie diaphragmatique congénitale sévère. L'imagerie par ultrasons (USS) a montré une éventration diaphragmatique focale avec bombement du dôme du foie dans les hémithorax droit et gauche. Un essai de respiration spontanée (SBT) a été effectué avant l'exubation et l'électromyographie du diaphragme a été mesurée pendant cette période. L'amplitude moyenne de l'activité électrique diaphragmatique était de 2,47 μV, similaire en magnitude à celle des nourrissons ventilés du même âge gestationnel avec diaphragmes intacts. Elle a réussi le SBT et l'extubation ultérieure.\n\nLes parents ont donné leur consentement écrit éclairé pour ce rapport et l'approbation éthique a été donnée pour la mesure de l'EMG du diaphragme pendant la SBT avant l'extubation (référence REC : 20/SW/0,062).\n",
+        "gold_summary": "Une fille née à 34 semaines de gestation a nécessité une intubation et une ventilation à la naissance. L'imagerie radiographique thoracique a révélé une densité bilatérale à la base des deux champs pulmonaires avec des hémi-diaphragmes surélevés. L'imagerie par ultrasons a montré une éventration diaphragmatique focale avec bombement du dôme du foie dans les hémithorax droit et gauche. L'évaluation de l'activité électrique du diaphragme lors d'un essai de respiration spontanée a révélé une amplitude moyenne cohérente avec celle des nourrissons ventilés du même âge gestationnel avec des diaphragmes intacts. Elle a donc été extubée avec succès. La surface thoracique mesurée après extubation était de 1 654 mm2, équivalant à celle d'un nourrisson à terme présentant une hernie diaphragmatique congénitale sévère. L'activité électrique du diaphragme étant normale, cela suggère que le remplacement du tissu musculaire diaphragmatique par des bandes fibreuses était probablement seulement partiel, et explique pourquoi l'extubation a été réussie. Elle présentait d'autres anomalies au cours de la période néonatale, notamment une mélanocytose cutanée, une hypotonie centrale, un hyperinsulinisme et une mauvaise alimentation. L'enfant a fait l'objet d'une enquête approfondie qui a révélé une mutation du gène KMT2D associée au syndrome de Kabuki.\n",
+        "synthetic_summary": {
+            "B1": "Une petite fille est née un peu avant le temps. Elle a eu du mal à bien respirer. Les docteurs ont regardé ses poumons avec des images. Ils ont vu que son muscle sous les poumons était un peu différent. Son muscle avait une partie qui ne marchait pas comme d’habitude. Mais son muscle pouvait quand même aider à respirer. Alors, les docteurs ont enlevé le tube qui l’aidait à respirer. Elle a réussi à respirer toute seule après ça.\n\nLa petite fille avait aussi d’autres choses qui n’étaient pas tout à fait comme les autres enfants. Sa peau avait des taches spéciales. Elle avait du mal à manger et ses muscles étaient un peu mous. Les docteurs ont fait beaucoup de tests. Ils ont trouvé un petit changement dans un gène, qui s’appelle le syndrome de Kabuki.\n\nLes docteurs et les aides l’aident beaucoup pour qu’elle grandisse bien et devienne forte.",
+            "B2": "**Résumé adapté pour un adolescent de 14 ans**\n\nUne fille est née un peu avant terme, à 34 semaines de grossesse, et elle a eu besoin d’aide pour respirer dès sa naissance. Des radios ont montré que ses deux diaphragmes (les muscles sous les poumons qui aident à respirer) étaient un peu anormaux et remontés. Une échographie, qui est une sorte d’image par ultrasons, a confirmé qu’une partie de ses diaphragmes était affaiblie, ce qui a laissé le foie pousser un peu dans la poitrine des deux côtés.\n\nPour vérifier si ses diaphragmes fonctionnaient bien, les médecins ont mesuré l’activité électrique de ces muscles pendant qu’elle essayait de respirer toute seule. Les résultats étaient normaux, ce qui veut dire que ses diaphragmes pouvaient encore bien travailler malgré les anomalies. Grâce à cela, elle a pu être retirée du respirateur artificiel avec succès.\n\nLa taille de sa cage thoracique (la partie du corps qui protège les poumons et le cœur) était similaire à celle d’un bébé né à terme avec une grave malformation du diaphragme. Cela montre que même si ses muscles du diaphragme étaient partiellement remplacés par du tissu fibreux (moins souple), ce n’était pas complet, ce qui explique pourquoi elle a pu respirer seule.\n\nPendant son séjour à l’hôpital, elle a aussi présenté d’autres problèmes : une peau avec des taches spéciales appelées mélanocytose, un tonus musculaire faible au niveau du cerveau (hypotonie centrale), un excès d’insuline qui a fait baisser son sucre dans le sang (hyperinsulinisme), et des difficultés à s’alimenter. Après plusieurs examens, les médecins ont découvert qu’elle avait une mutation génétique dans un gène appelé KMT2D. Cette mutation est liée à une maladie rare appelée syndrome de Kabuki, qui peut causer plusieurs troubles comme ceux qu’elle a eus.\n\nEn résumé, cette petite fille a eu des problèmes respiratoires liés à une faiblesse partielle de ses diaphragmes, mais ses muscles fonctionnaient assez bien pour qu’elle puisse respirer seule rapidement. Elle a aussi d’autres signes qui ont aidé les médecins à poser un diagnostic génétique important pour mieux comprendre sa santé.",
+            "B3": "Résumé détaillé et structuré\n\nContexte  \nUne fille est née prématurément à 34 semaines de grossesse, pesant 2 820 grammes. Sa mère avait des antécédents de diabète gestationnel et de pré-éclampsie, et avait reçu un traitement complet par corticostéroïdes avant la naissance. L’imagerie prénatale avait révélé un excès de liquide amniotique (polyhydramnios) et un fœtus de grande taille pour son âge gestationnel.\n\nPrincipales observations  \nÀ la naissance, l’enfant a présenté des difficultés respiratoires nécessitant une assistance ventilatoire. Une radiographie thoracique a montré une densité anormale bilatérale à la base des deux poumons, avec des diaphragmes surélevés. Une échographie a confirmé la présence d’une éventration diaphragmatique focale, c’est-à-dire une zone où le diaphragme est affaibli ou déplacé, avec un bombement du dôme du foie dans les deux côtés de la cavité thoracique. Malgré ces anomalies, l’évaluation de l’activité électrique du diaphragme pendant un essai de respiration spontanée a montré une amplitude moyenne normale, comparable à celle d’autres nourrissons prématurés ventilés ayant un diaphragme intact. Cette observation a permis de procéder à une extubation réussie après 36 heures de ventilation mécanique.\n\nL’analyse radiographique de la surface thoracique après extubation a mesuré une zone de 1 654 mm², ce qui correspond à celle d’un nourrisson à terme atteint d’une hernie diaphragmatique congénitale sévère. Le fait que l’activité électrique diaphragmatique soit normale suggère que le remplacement du tissu musculaire du diaphragme par des bandes fibreuses (tissu cicatriciel) était partiel, ce qui explique la capacité de l’enfant à respirer sans assistance invasive prolongée.\n\nEn parallèle, l’enfant a présenté plusieurs autres anomalies cliniques : une hypoglycémie sévère à l’admission due à un hyperinsulinisme (production excessive d’insuline), une hypotonie centrale (tonus musculaire faible liée au système nerveux central), une mauvaise alimentation nécessitant une assistance par sonde nasogastrique, ainsi qu’une mélanocytose cutanée (présence de taches pigmentées sur la peau). Une évaluation neurologique approfondie, incluant une imagerie cérébrale et des tests neurophysiologiques, n’a pas révélé d’anomalies majeures. Enfin, des tests génétiques ont identifié une mutation du gène KMT2D, responsable du syndrome de Kabuki, une maladie génétique rare associée à divers troubles congénitaux.\n\nInterprétation clinique  \nLa combinaison d’une éventration diaphragmatique bilatérale partielle avec une activité électrique diaphragmatique conservée a permis une prise en charge respiratoire efficace sans recours à une intervention chirurgicale néonatale immédiate. Les autres manifestations cliniques, notamment l’hyperinsulinisme, l’hypotonie et la mélanocytose cutanée, ainsi que la mutation génétique identifiée, orientent vers un diagnostic global de syndrome de Kabuki, qui explique la complexité du tableau clinique.\n\nProchaines étapes  \nL’enfant a été suivie en milieu hospitalier pendant 64 jours, avec un soutien nutritionnel par sonde et un traitement médicamenteux par diazoxide pour contrôler l’hyperinsulinisme. Elle bénéficie d’un accompagnement multidisciplinaire comprenant ergothérapie, orthophonie et physiothérapie pour optimiser son développement moteur et fonctionnel. Un suivi médical régulier est nécessaire pour surveiller l’évolution de ses troubles respiratoires, métaboliques et neurologiques, ainsi que pour adapter les interventions thérapeutiques en fonction de ses besoins."
+        }
+    },
+    {
+        "article": "Patient de sexe masculin de 59 ans ayant des antécédents d'hémochromatose, d'accident ischémique transitoire et de glaucome. Il avait des antécédents familiaux de décès de deux oncles paternels à l'âge de 60 ans, suite à une maladie neurologique non spécifiée. Il présentait une histoire familiale de dysarthrie et de parésie faciale d'apparition soudaine, avec une amélioration en quelques jours. Après une semaine, il a présenté des mouvements involontaires du membre supérieur gauche (MSE), associés à une dysarthrie, une anomie légère (difficulté à nommer des personnes et des objets) et une dyscalculie (difficulté de calcul). Il ne présentait pas de fièvre ou d'autres symptômes. L'examen neurologique ne révélait pas de modification significative des fonctions nerveuses supérieures, avec une dysarthrie légère, une parésie faciale centrale droite, des mouvements myocloniques du MSE et une hémiface gauche. L'IRM-CE a montré une modification en T2 et en diffusion (DWI) dans le caudé droit et le putamen droit, sans implication du striatum contralatéral. En raison de la persistance de l'aggravation, il a répété l'IRM-CE cinq jours plus tard, ce qui a révélé une hyper-signe supplémentaire en diffusion du cortex fronto-pariéto-cingulaire médiale. L'enquête menée pour identifier les causes auto-immunes, infectieuses et paranéoplasiques a été négative. Le LCR présentait une augmentation de la protéine tau et de la protéine 14.3.3 normale. L'EEG a révélé une activité lente pariétale droite et frontotemporale bilatérale. Au cours des deux semaines suivantes, la dysarthrie s'est aggravée et une ataxie de la marche a fait son apparition. La possibilité d'une encéphalite auto-immune a été évoquée, et le patient a reçu une méthylprednisolone par voie intraveineuse (1 g pendant cinq jours), sans amélioration. Au cours des mois suivants, la détérioration neurologique s'est poursuivie, avec une évolution vers l'artérite (incapacité de la parole) et la dysphagie, l'hémiplégie gauche, l'incontinence urinaire et une détérioration cognitive avec altération de la mémoire récente, désorientation temporelle et dysfonction exécutive. Une nouvelle IRM-CE a été réalisée, qui a montré une restriction de la diffusion des ganglions de la base bilatérale et de multiples zones corticales, principalement le cortex frontal et pariétal. L'EEG a révélé une activité périodique de complexes de pointe-onde généralisée avec réactivité à la stimulation. Le patient est décédé quatre mois après le début de la maladie. L'analyse génétique effectuée par la suite a été positive pour la mutation c.598G > A (E200K).\n",
+        "gold_summary": "Nous présentons le cas d'un patient de 59 ans ayant présenté une parésie faciale centrale et une dysarthrie, suivies de myoclonies du côté gauche. L'IRM cérébrale initiale a montré une hyperintensité en T2 et une diffusion dans le caudé et le putamen droits et un liquide céphalorachidien hyperprotéinorachique. Les examens pour des causes auto-immunes, infectieuses et paranéoplasiques ont été négatifs. Au cours des mois suivants, il a progressivement présenté une hémiplégie gauche, une dysphagie, une incontinence urinaire et un mutisme acinétique. L'IRM cérébrale a montré une évolution vers une restriction de la diffusion des ganglions de la base bilatéralement et de multiples zones corticales ; l'électroencéphalographie a montré une activité périodique et une protéine Tau élevée dans le liquide céphalorachidien. L'analyse génétique a révélé une mutation c.598G > A. Le décès est survenu après quatre mois de maladie.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 59 ans est tombé très malade. D'abord, il avait du mal à parler et son visage bougeait moins bien d'un côté. Puis, son bras gauche bougeait tout seul.\n\nLe docteur a fait des images de sa tête. Elles montraient des choses qui n’allaient pas dans son cerveau. Il n’y avait pas d’infection ou d’autres maladies connues.\n\nAvec le temps, il a eu de plus en plus de difficultés. Il ne pouvait plus bouger son bras gauche. Il avait du mal à avaler et à contrôler sa vessie. Il ne parlait presque plus.\n\nLes images de sa tête ont montré que plusieurs parties de son cerveau étaient touchées. Le docteur a aussi fait d’autres tests qui ont montré que son cerveau ne fonctionnait pas bien.\n\nAprès quelques mois, le monsieur est malheureusement décédé. Les docteurs ont trouvé un petit changement dans ses gènes qui expliquait sa maladie.",
+            "B2": "**Ce qu'ils ont observé chez le patient**  \nUn homme de 59 ans a d'abord eu des problèmes pour parler clairement (dysarthrie) et une faiblesse d’un côté du visage (parésie faciale centrale). Ensuite, il a eu des mouvements involontaires rapides (myoclonies) du bras gauche. Une première IRM, qui est une sorte de photo détaillée du cerveau, a montré des anomalies dans certaines parties profondes du cerveau appelées caudé et putamen du côté droit. Le liquide autour du cerveau (liquide céphalorachidien) contenait plus de protéines que la normale, ce qui peut indiquer une maladie.  \n\n**Ce qu’ils ont cherché et ce qu’ils ont trouvé**  \nLes médecins ont cherché si la maladie venait d’une infection, d’un problème du système immunitaire ou d’un cancer, mais tous ces tests étaient négatifs.  \n\n**Comment la maladie a évolué**  \nAu fil des mois, sa santé a empiré : il a perdu la force dans tout le côté gauche de son corps (hémiplégie), a eu des difficultés à avaler (dysphagie), a perdu le contrôle de sa vessie (incontinence urinaire) et a finalement arrêté de parler (mutisme acinétique). Une nouvelle IRM a montré que les anomalies dans le cerveau s’étaient étendues, touchant plusieurs zones des deux côtés, notamment des parties importantes pour le mouvement et la pensée. Un examen appelé électroencéphalographie (EEG), qui mesure l’activité électrique du cerveau, a montré des signes anormaux réguliers.  \n\n**Ce que cela signifie**  \nLe liquide cérébral montrait aussi une augmentation d’une protéine appelée Tau, souvent liée à des maladies du cerveau qui détruisent les cellules nerveuses. Une analyse génétique a révélé une mutation spécifique (c.598G > A), qui est connue pour causer une maladie grave du cerveau appelée maladie de Creutzfeldt-Jakob.  \n\n**Conclusion**  \nMalheureusement, le patient est décédé quatre mois après le début de ses symptômes. Ce cas montre comment une maladie neurologique grave peut évoluer rapidement, avec des signes visibles à l’IRM et des tests qui aident à comprendre la cause génétique.",
+            "B3": "**Contexte**  \nNous rapportons le cas d’un homme de 59 ans présentant des troubles neurologiques progressifs. Ses antécédents médicaux incluaient une hémochromatose, un accident ischémique transitoire et un glaucome. Sur le plan familial, deux oncles paternels étaient décédés vers 60 ans d’une maladie neurologique non précisée, et des épisodes de dysarthrie (trouble de la parole) et de parésie faciale (faiblesse musculaire du visage) d’apparition soudaine avaient été notés dans la famille.\n\n**Principales Observations**  \nLe patient a initialement développé une parésie faciale centrale droite et une dysarthrie légère, suivies de mouvements involontaires (myoclonies) du membre supérieur gauche et de l’hémiface gauche. Une imagerie par résonance magnétique cérébrale avec injection de produit de contraste (IRM-CE) a montré des anomalies en hyperintensité sur les séquences pondérées en T2 et en diffusion dans le noyau caudé droit et le putamen droit, sans atteinte du côté opposé. Le liquide céphalorachidien (LCR) présentait une augmentation de la concentration en protéines, notamment une élévation de la protéine tau, un marqueur de dégénérescence neuronale, tandis que la protéine 14.3.3 était normale. Les investigations pour exclure une cause auto-immune, infectieuse ou paranéoplasique se sont révélées négatives. L’électroencéphalogramme (EEG) montrait une activité lente dans les régions pariétale droite et frontotemporale bilatérale.\n\nAu fil des semaines, les symptômes se sont aggravés : la dysarthrie s’est intensifiée, une ataxie de la marche (trouble de l’équilibre) est apparue, suivie d’une hémiplégie gauche (paralysie d’un côté du corps), d’une dysphagie (difficulté à avaler), d’une incontinence urinaire et d’une détérioration cognitive marquée par des troubles de la mémoire récente, une désorientation dans le temps et des difficultés dans les fonctions exécutives (planification, organisation). Une nouvelle IRM a révélé une extension des anomalies avec une restriction de la diffusion bilatérale des ganglions de la base et de multiples zones corticales, principalement frontales et pariétales. L’EEG a montré une activité périodique de complexes pointes-onde généralisés, caractéristique de certaines encéphalopathies dégénératives.\n\n**Interprétation Clinique**  \nL’évolution rapide et progressive des symptômes, associée aux résultats d’imagerie et aux analyses du LCR, a orienté vers une maladie neurodégénérative grave. L’absence de réponse à un traitement immunosuppresseur par méthylprednisolone a exclu une encéphalite auto-immune. L’analyse génétique a finalement identifié une mutation c.598G > A (E200K) dans le gène PRNP, responsable d’une forme héréditaire de maladie à prions, une affection neurodégénérative rare et mortelle.\n\n**Prochaines Étapes**  \nMalheureusement, le patient est décédé quatre mois après le début des symptômes, illustrant la rapidité et la gravité de cette maladie. Ce cas souligne l’importance d’une évaluation complète, incluant l’imagerie cérébrale, l’analyse du LCR, l’EEG et le dépistage génétique, dans le diagnostic des troubles neurologiques progressifs inexpliqués, notamment lorsqu’une maladie à prions héréditaire est suspectée."
+        }
+    },
+    {
+        "article": "Il s’agit d’un cas d’un homme de 23 ans ayant des antécédents médicaux sans particularité, qui a été référé pour une dyspnée inexpliquée. Avant sa maladie actuelle, il était en bonne santé et n’avait aucune difficulté à effectuer ses activités quotidiennes. Ses deux parents avaient le diabète, et son grand-père est décédé d’une crise cardiaque à l’âge de 74 ans. En outre, après avoir examiné de plus près les antécédents familiaux, nous avons découvert que l’oncle du patient avait des antécédents d’acromégalie.\n\nL’état du patient a commencé deux semaines avant son admission lorsqu’il a commencé à se plaindre de fièvre, de congestion nasale et de rhinorrhée. Trois jours plus tard, il a commencé à se plaindre de vomissements, de diarrhée et de douleurs abdominales. Après avoir été admis au service de médecine interne, nous avons été consultés pour des palpitations, une dyspnée et une orthopnée prononcées.\n\nPendant l'examen, sa température était légèrement élevée à 37,9 °C, sa tension artérielle était de 150/90 mmHg, sa fréquence cardiaque de 110/min et sa fréquence respiratoire de 22/min. L'auscultation a révélé de fines crépitations pulmonaires basales avec des ronflements expiratoires modérés bilatéraux. En outre, un souffle diastolique précoce a été détecté. Ses veines du cou étaient congestionnées, mais ne pulsaient pas, et il n'y avait pas d'œdème des membres inférieurs ou d'ascite.\n\nLes résultats de laboratoire étaient remarquables pour un niveau élevé de peptide natriurétique cérébral (BNP) (340 pg/mL). Les résultats complémentaires comprenaient un épanchement pleural bilatéral modéré et une cardiomégalie observée sur la radiographie thoracique. L'ECG a révélé une tachycardie sinusale avec des ondes T inversées dans les dérivations V3 et V4. L'échocardiographie transthoracique (TTE) a montré un ventricule gauche (VG) modérément dilaté et hypertrophié, une fonction systolique du VG légèrement altérée avec une fraction d'éjection de 48 % en mode M, une fonction diastolique altérée, une régurgitation mitrale modérée et une régurgitation aortique sévère. La racine aortique était nettement dilatée, avec des diamètres de 3,2 cm à l'annulus, 4,9 cm au sinus de Valsalva et 7,5 cm à la jonction sino-tubulaire (JST).\n\nEn conséquence, une aortographie a été réalisée, confirmant les mesures échocardiographiques des diamètres de la racine aortique. En outre, elle a révélé une dilatation de l'aorte ascendante d'un diamètre de 10 cm et de l'aorte descendante d'un diamètre de 2,5 cm. Le patient a commencé à prendre les médicaments suivants : Furosémide (20 mg toutes les 8 heures), Ramipril (1,25 mg une fois par jour) et Empagliflozin (10 mg une fois par jour). En 10 jours, le patient a connu une légère amélioration des symptômes, en particulier de la dyspnée, et a déclaré avoir mieux dormi. Une radiographie thoracique de suivi a montré une résolution partielle de l'épanchement pleural.\n\nAu début, nous avons considéré une maladie du tissu conjonctif comme le syndrome de Marfan ou d'Ehlers-Danlos. Cependant, le patient manquait les caractéristiques physiques typiques et les signes associés de ces conditions. En outre, son test de fonction pulmonaire était normal, ce qui serait probablement anormal dans un trouble multisystémique du tissu conjonctif. Les résultats de laboratoire ont montré des taux normaux de VS et de protéine C-réactive, ce qui réduit la probabilité d'une vascularite comme cause de la dilatation de la racine aortique. Le panel auto-immun, y compris les tests ANA et RF, était également négatif.\n\nL’acromégalie a ensuite été considérée comme la cause potentielle de l’hypertrophie de la LV et de la dilatation de la racine aortique, en particulier compte tenu des antécédents familiaux de la maladie. Par conséquent, le taux de facteur de croissance analogue à l’insuline 1 (IGF-1) a été mesuré et était élevé (320 ng/ml), et le taux de GH est resté supérieur à la normale (1,1 ng/ml) après un test de tolérance au glucose par voie orale confirmant le diagnostic d’acromégalie. Une image IRM du cerveau pondérée en T2 a montré une masse hyperintense de 7 × 4 mm dans la selle turcique, compatible avec un microadénome hypophysaire.\n\nPar la suite, la décision de procéder à l'opération a été prise après avoir obtenu le consentement du patient. Après une angiographie coronarienne normale, le patient a subi une procédure de remplacement de greffe composite, impliquant la valve aortique, la racine aortique et l'aorte ascendante (procédure de Bentall). Une valve mécanique a été utilisée, et le patient a commencé à prendre de la warfarine à une dose quotidienne de 3 mg, avec une surveillance étroite pour atteindre un taux de coagulation cible de 2 à 3.\n\nÀ la suite d'une consultation avec l'endocrinologue, le patient a commencé à recevoir des injections mensuelles d'acétate d'octréotide. Un plan de suivi complet a été établi, qui comprenait le contrôle du fonctionnement de la valve, l'évaluation de la fonction LV, la vérification de la conformité au traitement et la vérification des valeurs d'IGF-1 et d'INR. Mis à part une légère dyspnée d'effort, il est resté asymptomatique pendant 8 semaines après l'opération. Au cours de cette période, les échocardiogrammes de suivi ont montré que la valve aortique remplacée fonctionnait normalement sans aucune fuite ou dysfonctionnement. La racine aortique et l'aorte ascendante étaient également stables, sans aucun signe de dilatation, d'anévrisme ou d'autres complications. Il n'y a pas eu de progression de son hypertrophie LV non plus. Son niveau d'IGF-1 le plus récent était de 290 ng/ml, ce qui est légèrement inférieur au premier, et il a été maintenu sous Octreotide sans effets indésirables significatifs.\n",
+        "gold_summary": "Ce rapport présente le cas d'un homme de 23 ans sans antécédents médicaux significatifs, qui a présenté une dyspnée sévère après une infection thoracique. Il manquait des caractéristiques physiques distinctes de troubles génétiques ou endocriniens, mais son oncle souffrait d'acromégalie. L'échocardiographie a révélé une hypertrophie ventriculaire gauche et une dilatation massive de la racine aortique. L'augmentation du facteur de croissance analogue à l'insuline 1 (IGF-1) a confirmé le diagnostic d'acromégalie. Le patient a subi une procédure de Bentall, et son acromégalie a été gérée avec de l'octréotide et des suivis réguliers.\n",
+        "synthetic_summary": {
+            "B1": "Un jeune homme de 23 ans avait du mal à bien respirer.  \nIl avait eu un rhume avec de la fièvre avant.  \n\nLe docteur a regardé son cœur avec une machine spéciale.  \nLe cœur était un peu gros et une grosse veine était trop grande.  \n\nLe garçon avait une maladie appelée acromégalie.  \nC’est une maladie où le corps fabrique trop de certaines choses.  \n\nLe docteur a fait une opération pour réparer le cœur.  \nAprès, il a pris des médicaments pour aller mieux.  \n\nMaintenant, il va mieux et le docteur le surveille souvent.",
+            "B2": "Cas d’un jeune homme de 23 ans en bonne santé qui a commencé à avoir du mal à respirer après une infection des voies respiratoires. Il n’avait pas les signes habituels de maladies génétiques ou hormonales, mais son oncle avait une maladie appelée acromégalie, qui cause une production trop élevée d’une hormone de croissance.\n\nLors des examens, les médecins ont découvert que son cœur avait une partie appelée ventricule gauche un peu plus grosse que la normale, et que la base de son aorte (la grosse artère qui sort du cœur) était très dilatée, c’est-à-dire élargie. Pour comprendre la cause, ils ont mesuré un facteur appelé IGF-1, lié à l’hormone de croissance, et il était élevé. Cela a confirmé qu’il avait bien une acromégalie.\n\nPour traiter son problème cardiaque, il a subi une opération appelée procédure de Bentall. Cette intervention remplace la valve aortique, la racine aortique et une partie de l’aorte ascendante. Ensuite, son acromégalie a été traitée avec un médicament appelé octréotide, qui aide à réduire la production d’hormone de croissance. Le patient a été suivi régulièrement pour vérifier le bon fonctionnement de son cœur et l’évolution de sa maladie.",
+            "B3": "Résumé détaillé et structuré du cas clinique\n\nContexte  \nCe rapport décrit le cas d’un homme de 23 ans, auparavant en bonne santé, sans antécédents médicaux particuliers, qui a été admis pour une dyspnée (difficulté à respirer) progressive et inexpliquée. Ses antécédents familiaux incluaient un oncle atteint d’acromégalie (une maladie endocrinienne caractérisée par une production excessive d’hormone de croissance), ainsi que des parents diabétiques et un grand-père décédé d’une crise cardiaque.\n\nPrincipales observations  \nLes symptômes ont débuté deux semaines avant l’admission par des signes d’infection respiratoire (fièvre modérée, congestion nasale, écoulement nasal), suivis de troubles digestifs (vomissements, diarrhée, douleurs abdominales). À l’examen, le patient présentait une légère fièvre, une hypertension artérielle modérée, une tachycardie (rythme cardiaque rapide) et une respiration accélérée. L’auscultation pulmonaire a révélé des crépitements fins et des ronflements expiratoires, ainsi qu’un souffle cardiaque diastolique précoce, signe d’une atteinte valvulaire. Les veines du cou étaient congestionnées, témoignant d’une pression veineuse élevée, sans œdème périphérique.\n\nLes examens complémentaires ont montré :  \n- Un taux élevé de peptide natriurétique cérébral (BNP), indiquant une surcharge cardiaque.  \n- Une radiographie thoracique avec cardiomégalie (cœur agrandi) et épanchement pleural bilatéral modéré.  \n- Un électrocardiogramme (ECG) avec tachycardie sinusale et inversion des ondes T dans certaines dérivations, suggérant une souffrance myocardique.  \n- Une échocardiographie transthoracique révélant un ventricule gauche modérément dilaté et hypertrophié, une fonction systolique légèrement altérée (fraction d’éjection à 48 %), une fonction diastolique altérée, une régurgitation mitrale modérée et une régurgitation aortique sévère. La racine aortique était très dilatée, avec un diamètre maximal à la jonction sino-tubulaire de 7,5 cm (valeur nettement supérieure à la normale).  \n- Une aortographie confirmant ces dilatations et révélant une dilatation majeure de l’aorte ascendante (10 cm de diamètre).  \n\nLe patient a été traité initialement par des médicaments diurétiques (furosémide), un inhibiteur de l’enzyme de conversion (ramipril) et un inhibiteur du SGLT2 (empagliflozine), avec une amélioration partielle des symptômes et de l’épanchement pleural.\n\nInterprétation clinique  \nLes diagnostics initiaux ont envisagé des maladies du tissu conjonctif comme le syndrome de Marfan ou d’Ehlers-Danlos, mais l’absence de signes physiques caractéristiques, la fonction pulmonaire normale et des marqueurs inflammatoires normaux ont rendu ces hypothèses peu probables. De même, une vascularite a été exclue par l’absence d’inflammation et de marqueurs auto-immuns (ANA, facteur rhumatoïde négatifs).\n\nCompte tenu des antécédents familiaux et des anomalies cardiaques, une acromégalie a été suspectée. Cette maladie provoque une production excessive d’hormone de croissance (GH) et de facteur de croissance analogue à l’insuline 1 (IGF-1), entraînant une hypertrophie cardiaque et des anomalies vasculaires. Le diagnostic a été confirmé par un taux élevé d’IGF-1 (320 ng/ml) et un test de tolérance au glucose montrant une GH non supprimée. Une IRM cérébrale a révélé un microadénome hypophysaire (petite tumeur de la glande pituitaire) responsable de cette sécrétion hormonale excessive.\n\nProchaines étapes  \nLe patient a subi une intervention chirurgicale majeure, la procédure de Bentall, qui consiste à remplacer la valve aortique, la racine aortique et l’aorte ascendante par une greffe composite. Une valve mécanique a été implantée, nécessitant un traitement anticoagulant à base de warfarine pour prévenir les thromboses.  \n\nParallèlement, un traitement médical de l’acromégalie a été instauré avec des injections mensuelles d’acétate d’octréotide, un analogue de la somatostatine qui inhibe la sécrétion d’hormone de croissance. Un suivi régulier a été mis en place pour contrôler la fonction valvulaire, la fonction cardiaque, les niveaux d’IGF-1 et la coagulation sanguine (INR).  \n\nHuit semaines après l’opération, le patient présentait une bonne évolution clinique avec une fonction valvulaire normale, une stabilité de la racine aortique et de l’aorte ascendante, ainsi qu’une absence de progression de l’hypertrophie ventriculaire gauche. Son taux d’IGF-1 était légèrement diminué, témoignant d’un bon contrôle de l’acromégalie, sans effets secondaires notables liés au traitement.\n\nEn résumé, ce cas illustre l’importance de considérer l’acromégalie comme cause possible d’atteinte cardiaque sévère chez un jeune adulte présentant une dilatation aortique massive et une hypertrophie ventriculaire, surtout en présence d’antécédents familiaux évocateurs. Une prise en charge multidisciplinaire associant chirurgie cardiaque et traitement endocrinien permet une amélioration significative du pronostic."
+        }
+    },
+    {
+        "article": "Une fillette de 2 ans a été admise aux urgences avec une fièvre élevée de 5 jours, une toux et un gonflement bilatéral des paupières. Avant le début de cette maladie, elle souffrait d'un œdème et d'un furoncle au niveau de la peau du visage, au niveau du périné. Elle était auparavant en bonne santé.\n\nL'examen physique a révélé une fille très malade avec un œdème périorbitaire et facial, une fièvre élevée, une fréquence respiratoire accrue, une SpO2 diminuée et des crépitations thoraciques.\n\nUn examen oculaire a révélé un gonflement autour des yeux des deux côtés. Les deux globes ont montré une proptose axiale. Les examens ont également montré une injection, une décharge purulente dans les deux yeux avec des pupilles à réaction lente, une conjonctivite chimique sévère et une ophtalmoplegie externe affectant les troisième, quatrième et sixième nerfs crâniens.\n\nLe rapport de disque vertical de l'œil droit était de 0,3, tandis que celui de l'œil gauche était de 0,4. Il n'y avait aucune preuve de congestion des veines rétiniennes ou d'œdème du disque.\n\nLes examens de laboratoire ont révélé une numération leucocytaire significativement élevée (32 000 cellules/mm3), une faible hémoglobine (5,5 mg/dL) et une protéine C-réactive élevée (112 mg/L). La culture sanguine était négative.\n\nLa tomographie par ordinateur orbitale a révélé un épaississement important des tissus mous périorbitaux bilatéraux et un oedème sous-cutané facial. En outre, la tomographie par ordinateur avec contraste du thorax a révélé de multiples lésions cavitaires situées périphériquement dans les poumons bilatéraux (embolies septiques) et un pneumothorax modéré bilatéral associé avec des zones de consolidation avec bronchogramme aérien dans le poumon inférieur gauche.\n\nLe patient a été admis à l'unité de soins intensifs pédiatriques et un traitement a été initié avec de la ceftriaxone intraveineuse (IV) à 500 mg toutes les 12 heures, de la clindamycine IV à 100 mg toutes les 8 heures, des gouttes oculaires Voltaren toutes les 8 heures, des gouttes oculaires Lomefloxacin toutes les 12 heures après une dose de charge initiale d'une goutte toutes les 5 minutes pendant 25 minutes, de la pommade au chloramphénicol pour la nuit et du sirop d'ibuprofène oral toutes les 8 heures. Des tubes thoraciques bilatéraux ont été insérés pour la décompression du pneumothorax.\n\nSon nombre de globules blancs est revenu à la normale et sa radiographie thoracique s'est considérablement améliorée. Elle a quitté l'hôpital après 15 jours avec une antibiothérapie orale (co_amoxiclav syrup 400mg) à prendre pendant une semaine.\n",
+        "gold_summary": "Une fillette de 2 ans a présenté une fièvre élevée, une toux et un gonflement des paupières bilatérales pendant 5 jours, précédés d'un œdème et d'un furoncle de la peau du visage péranasal. L'examen a révélé une proptose axiale bilatérale et une cellulite orbitale et thoracique bilatérale, une embolie pulmonaire septique et un pneumothorax bilatéral.\n",
+        "synthetic_summary": {
+            "B1": "Une petite fille de 2 ans avait très chaud et toussait. Ses yeux étaient tout gonflés des deux côtés. Avant, elle avait un bouton gros sur le visage.\n\nLes docteurs ont vu que ses yeux étaient très gonflés et qu’elle avait mal dans la poitrine. Ses poumons avaient des petits problèmes. Ils ont donné des médicaments pour la soigner.\n\nAprès un moment, elle a commencé à aller mieux. Les docteurs ont dit qu’elle pouvait rentrer à la maison.",
+            "B2": "Une fillette de 2 ans est arrivée à l'hôpital avec une forte fièvre, une toux et un gonflement des paupières des deux yeux, qui duraient depuis cinq jours. Avant cela, elle avait un gonflement et un furoncle (une grosseur douloureuse avec du pus) sur la peau de son visage près du nez. Lors de l'examen, les médecins ont vu que ses yeux étaient poussés vers l'avant (on appelle cela une proptose) et qu'elle avait une infection grave autour des yeux (cellulite orbitale) ainsi qu'une infection des tissus du visage et de la poitrine. Des examens ont aussi montré qu'elle avait des caillots infectés dans ses poumons (embolies septiques) et de l'air dans la poitrine des deux côtés (pneumothorax), ce qui peut rendre la respiration difficile. Elle a reçu un traitement avec des antibiotiques et des soins pour ses yeux et ses poumons. Après deux semaines, elle s'est améliorée et a pu quitter l'hôpital avec des médicaments à prendre à la maison.",
+            "B3": "Résumé détaillé et structuré pour un public non-médecin :\n\n**Contexte**  \nUne fillette de 2 ans, auparavant en bonne santé, a été admise aux urgences après avoir présenté pendant cinq jours une fièvre élevée, une toux persistante et un gonflement important des paupières des deux yeux. Avant ces symptômes, elle avait développé un œdème (gonflement) et un furoncle (infection cutanée douloureuse) au niveau du visage, près du périnée.\n\n**Principales observations cliniques**  \nÀ l’examen, l’enfant était très malade avec un gonflement marqué autour des yeux et du visage. Ses yeux montraient une proptose axiale, c’est-à-dire que les globes oculaires étaient poussés vers l’avant des orbites. Elle présentait une inflammation sévère des tissus autour des yeux (cellulite orbitale) accompagnée d’une conjonctivite chimique sévère (inflammation de la membrane oculaire), une décharge purulente (pus) dans les deux yeux, ainsi qu’une paralysie des muscles oculaires contrôlés par les nerfs crâniens III, IV et VI, ce qui limitait ses mouvements oculaires. Ses pupilles réagissaient lentement à la lumière. Par ailleurs, elle avait une respiration rapide, une saturation en oxygène diminuée et des bruits anormaux dans les poumons.\n\nLes analyses sanguines ont montré une forte augmentation des globules blancs (32 000/mm³), signe d’une infection importante, une anémie sévère (hémoglobine à 5,5 mg/dL) et un taux élevé de protéine C-réactive, un marqueur d’inflammation. La culture sanguine n’a pas identifié de bactéries.\n\n**Imagerie et diagnostics complémentaires**  \nUne tomodensitométrie (scanner) des orbites a confirmé un épaississement important des tissus mous autour des yeux et un œdème sous-cutané du visage. Un scanner thoracique avec injection de produit de contraste a révélé la présence de multiples lésions cavitaires périphériques dans les deux poumons, correspondant à des embolies septiques (des caillots infectés bloquant les vaisseaux pulmonaires), ainsi qu’un pneumothorax modéré bilatéral (présence d’air dans la cavité pleurale, comprimant les poumons) et des zones de consolidation pulmonaire (zones de poumon remplies de liquide ou de cellules inflammatoires).\n\n**Interprétation clinique**  \nCette présentation correspond à une cellulite orbitale sévère bilatérale compliquée par une embolie pulmonaire septique et un pneumothorax bilatéral. L’origine initiale semble être une infection cutanée locale (furoncle) qui s’est propagée aux tissus orbitaires et a généré des complications pulmonaires graves.\n\n**Prise en charge et évolution**  \nLa fillette a été admise en unité de soins intensifs pédiatriques. Elle a reçu un traitement antibiotique intraveineux combinant la ceftriaxone et la clindamycine, ainsi que des soins oculaires spécifiques (gouttes anti-inflammatoires et antibiotiques). Un traitement symptomatique par ibuprofène a été administré pour la fièvre et la douleur. Des drains thoraciques ont été placés pour évacuer l’air accumulé dans la cavité pleurale (pneumothorax).\n\nSous ce traitement, son état s’est amélioré : le nombre de globules blancs est revenu à la normale et les images pulmonaires se sont nettement améliorées. Après 15 jours d’hospitalisation, elle a pu quitter l’hôpital avec une antibiothérapie orale à poursuivre pendant une semaine.\n\n**Prochaines étapes**  \nUn suivi médical régulier est nécessaire pour surveiller la résolution complète de l’infection et prévenir toute complication tardive, notamment au niveau oculaire et pulmonaire. Une attention particulière doit être portée à la fonction visuelle et à la récupération des mouvements oculaires."
+        }
+    },
+    {
+        "article": "Nous présentons le cas d'un Marocain blanc de 38 ans, sans facteurs de risque cardiovasculaire et ayant des antécédents de cécité bilatérale inexpliquée, qui s'est présenté au service des urgences avec un œdème chronique des membres et une dyspnée progressive.\n\nL'évaluation initiale a révélé un patient hémodynamiquement stable avec une tension artérielle normale de 105/76 mmHg, une fréquence cardiaque de 45 battements par minute et une saturation en oxygène de 93 % en air ambiant. L'examen physique a révélé une distension de la veine jugulaire externe, un œdème des jambes étendu et une ascite. L'auscultation cardiopulmonaire a révélé un murmure holosystolique 4/6 au foyer mitral avec des crépitations diffuses bilatérales symétriques. L'examen ophtalmologique a révélé une acuité visuelle réduite à la perception de la lumière.\n\nUn électrocardiogramme a montré une bradycardie sinusale avec une fréquence cardiaque de 45 battements par minute et un bloc de branche droit complet. La radiographie thoracique a révélé une cardiomégalie et une congestion périhiliale. Le taux de peptide natriurétique de type B était de 1230 pg/ml (pour une plage normale inférieure à 300 pg/ml), le taux de créatinine était de 9,6 mg/l (pour une plage normale comprise entre 6 et 12,5 mg/l), le taux d'albumine était légèrement bas à 36 g/l (pour une plage normale supérieure à 39 g/l), et il y avait une haute sensibilité de la troponine à 294 ng/l (pour une plage normale inférieure à 35 ng/l). Les autres résultats des tests de laboratoire étaient normaux, en particulier les taux de ferritine, de TSH et d'électrolyte.\n\nL'échocardiographie transthoracique (TTE) a montré un ventricule gauche dilaté (diamètre diastolique de base à la fin de 60 mm) avec une fraction d'éjection sévèrement réduite à 15 % (biplan Simpson), une régurgitation mitrale modérée et un thrombus apical mesurant 19 mm × 18 mm. Le ventricule droit était sévèrement dilaté (diamètre diastolique de base à la fin de 51 mm), avec une dysfonction systolique (excursion systolique du plan annulaire tricuspide (TAPSE) de 12 mm et onde S' du ventricule droit sur doppler tissulaire (S'VD) de 5 cm/s) et une régurgitation tricuspide sévère. La veine cave inférieure (VCI) était pléthorique avec un diamètre maximal de 37 mm.\n\nL’histoire détaillée a révélé que depuis ses 20 ans, le patient avait des problèmes de marche, une perte auditive et une anosmie et que sa cécité avait commencé avec une vision nocturne altérée, mais il n’avait jamais été évalué par un ophtalmologue avant cette présentation. Les examens neurologiques ont révélé une amyotrophie bilatérale des jambes avec une ataxie bilatérale. Un examen ophtalmologique a été effectué pour explorer sa cécité et a révélé une rétinite pigmentaire. L’image clinique du patient associant une cardiomyopathie dilatée aux signes neurologiques spécifiques était fortement suggestive de la maladie de Refsum. Nous avons effectué un dosage des concentrations plasmatiques d’acide phytique, qui a révélé un taux remarquablement élevé de 324 μmol/l, confirmant la maladie de Refsum. Initialement, le patient a été mis sous furosémide intraveineuse, qui a ensuite soulagé ses symptômes d’insuffisance cardiaque. Il a ensuite reçu un traitement par furosémide oral [40 mg deux fois par jour (b.i.d)], des inhibiteurs de l’enzyme de conversion de l’angiotensine (ramipril 2,5 mg b.i.d), de la spironolactone (25 mg une fois par jour (o.d)) et un inhibiteur de SGLT2 (empagliflozine 10 mg o.d.). Les bêta-bloquants n’ont pas été administrés en raison d’une bradycardie sinusale. En outre, le patient a reçu des antagonistes de la vitamine K pour le thrombus ventriculaire gauche.\n\nEn ce qui concerne le traitement spécifique de la maladie de Refsum, le patient a été conseillé de suivre un régime alimentaire restreint conçu pour éliminer les aliments contenant du phytol, avec un apport quotidien en acide phytanique inférieur à 10 mg. Cela impliquait d'éviter la consommation de viande ou de graisses provenant d'animaux ruminants (tels que l'agneau et le bœuf) et de produits de boulangerie contenant des graisses animales, ainsi que de produits laitiers tels que le beurre et le fromage.\n\nLe patient a récupéré et son état a été stabilisé avec des symptômes de l'insuffisance cardiaque chronique de classe NYHA 2 ; il a donc été renvoyé à domicile sous traitement médical pour insuffisance cardiaque, antagonistes de la vitamine K (VKA) et régime hyphatico-acide.",
+        "gold_summary": "Nous rapportons le cas d'un Marocain blanc de 38 ans admis dans notre service pour un épisode d'insuffisance cardiaque aiguë décompensée. L'échocardiographie transthoracique a révélé une cardiomyopathie dilatée avec une fraction d'éjection réduite à 15 %. Une évaluation plus approfondie a révélé des caractéristiques différentes de la maladie de Refsum. Un taux plasmatique élevé d'acide phytanique a confirmé le diagnostic. Les manifestations cardiaques sont fréquentes dans le cours tardif de la maladie de Refsum chez l'adulte et comprennent une cardiomyopathie, des anomalies électriques et une mort cardiaque subite. En outre, les arythmies restent l'une des principales causes de décès chez ces patients.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 38 ans avait un gros problème avec son cœur. Son cœur ne battait pas bien fort. \n\nLes docteurs ont fait des examens et ont trouvé une maladie qui s'appelle la maladie de Refsum. Cette maladie peut rendre le cœur très fatigué. \n\nCette maladie peut aussi faire que le cœur bat de travers. Cela peut être dangereux. \n\nLes docteurs ont aidé ce monsieur avec des médicaments et un régime spécial. Maintenant, il va mieux.",
+            "B2": "Cas d’un homme de 38 ans avec une maladie rare appelée maladie de Refsum\n\nNous racontons ici l’histoire d’un homme marocain de 38 ans qui est venu à l’hôpital parce qu’il avait une insuffisance cardiaque, c’est-à-dire que son cœur ne pompait pas bien le sang. Un examen spécial du cœur, appelé échocardiographie, a montré que son cœur était agrandi et que sa capacité à pomper le sang était très faible (seulement 15 % au lieu de 55-70 % normalement).\n\nEn cherchant la cause, les médecins ont découvert que cet homme avait une maladie rare appelée maladie de Refsum. Cette maladie se caractérise par un taux très élevé dans le sang d’une substance appelée acide phytanique. Cette substance s’accumule dans le corps et peut abîmer plusieurs organes, y compris le cœur.\n\nChez les adultes atteints de cette maladie, il est fréquent de voir des problèmes cardiaques comme une cardiomyopathie (maladie du muscle cardiaque), des troubles du rythme cardiaque (anomalies électriques) et un risque de mort subite à cause du cœur. Ces troubles du rythme sont l’une des principales causes de décès chez ces patients.\n\nCe cas montre l’importance de penser à cette maladie rare quand un patient a des signes cardiaques graves associés à des symptômes neurologiques ou visuels. Un diagnostic rapide permet de mieux gérer la maladie, notamment grâce à un régime alimentaire spécial et un traitement médical adapté.",
+            "B3": "Résumé détaillé et structuré pour un public adulte non spécialiste\n\n**Contexte**  \nNous présentons le cas d’un homme marocain de 38 ans, sans antécédents cardiovasculaires connus, qui s’est présenté aux urgences avec un œdème chronique des membres inférieurs et une difficulté progressive à respirer. Il avait également des antécédents de cécité bilatérale inexpliquée depuis plusieurs années.\n\n**Principales observations cliniques et paracliniques**  \nÀ l’examen, le patient était stable sur le plan hémodynamique, avec une tension artérielle normale, mais une fréquence cardiaque lente (bradycardie à 45 battements par minute). On notait une distension des veines du cou, un œdème important des jambes et la présence d’ascite (accumulation de liquide dans l’abdomen). L’auscultation cardiaque révélait un souffle important au niveau de la valve mitrale, et des crépitements dans les deux poumons. L’examen ophtalmologique confirmait une vision très réduite, limitée à la perception de la lumière.\n\nL’électrocardiogramme montrait une bradycardie sinusale associée à un bloc de branche droit complet, tandis que la radiographie thoracique révélait une augmentation de la taille du cœur et une congestion pulmonaire. Les analyses sanguines mettaient en évidence une élévation du peptide natriurétique de type B (marqueur d’insuffisance cardiaque), une légère augmentation de la troponine (indicateur de souffrance cardiaque), une fonction rénale normale et une albumine légèrement basse.\n\nL’échocardiographie transthoracique a montré une dilatation importante des ventricules gauche et droit, avec une fonction cardiaque sévèrement altérée (fraction d’éjection du ventricule gauche à seulement 15 %, alors que la normale est supérieure à 50 %). Une régurgitation (fuite) modérée de la valve mitrale et sévère de la valve tricuspide était présente. Un caillot (thrombus) important était visible dans l’apex (partie basse) du ventricule gauche.\n\nL’interrogatoire approfondi a révélé que depuis l’âge de 20 ans, le patient souffrait de troubles de la marche, de perte auditive, d’absence d’odorat (anosmie) et d’une cécité progressive débutant par une altération de la vision nocturne. Un examen neurologique a montré une fonte musculaire des jambes et une ataxie (trouble de la coordination). L’examen ophtalmologique a confirmé une rétinite pigmentaire, une maladie dégénérative de la rétine.\n\n**Interprétation clinique**  \nL’association d’une cardiomyopathie dilatée sévère avec des signes neurologiques spécifiques (troubles moteurs, sensoriels et oculaires) a orienté vers le diagnostic de la maladie de Refsum, une maladie métabolique rare caractérisée par une accumulation anormale d’acide phytanique dans le sang. Le dosage plasmatique a confirmé un taux très élevé d’acide phytanique, validant ce diagnostic.\n\nLes manifestations cardiaques, notamment la dilatation du cœur, la réduction de sa capacité à pomper le sang et les troubles du rythme, sont fréquentes dans les formes tardives de cette maladie chez l’adulte. Ces anomalies peuvent entraîner des complications graves, comme des arythmies cardiaques et un risque accru de mort subite.\n\n**Prise en charge et suivi**  \nLe patient a été traité initialement par des diurétiques pour soulager l’insuffisance cardiaque, puis par un traitement médicamenteux complet incluant des inhibiteurs de l’enzyme de conversion de l’angiotensine, un antagoniste des récepteurs minéralocorticoïdes, et un inhibiteur de SGLT2, tout en évitant les bêta-bloquants en raison de la bradycardie. Un traitement anticoagulant par antagonistes de la vitamine K a été instauré pour prévenir les complications liées au thrombus ventriculaire.\n\nParallèlement, un régime alimentaire strict a été recommandé afin de réduire l’apport en acide phytanique, en évitant notamment les viandes et graisses d’animaux ruminants, les produits laitiers riches en graisses animales, et certains produits de boulangerie.\n\nAprès stabilisation, le patient a présenté une amélioration clinique avec des symptômes d’insuffisance cardiaque modérés (classe fonctionnelle NYHA 2) et a pu être renvoyé à domicile sous traitement médical et régime adapté.\n\n**Conclusion**  \nCe cas illustre l’importance de considérer la maladie de Refsum dans le diagnostic différentiel d’une cardiomyopathie dilatée associée à des troubles neurologiques et sensoriels inexpliqués. La prise en charge repose sur un traitement symptomatique de l’insuffisance cardiaque, une anticoagulation adaptée et une restriction alimentaire ciblée pour limiter l’accumulation d’acide phytanique, ce qui peut améliorer le pronostic et la qualité de vie des patients."
+        }
+    },
+    {
+        "article": "En novembre 2019, un garçon âgé de 12 ans a été admis à l'hôpital pour enfants de Wuxi pour des vertiges intermittents, des maux de tête pendant plus d'un mois et une marche instable pendant une demi-mois. Il est à noter que le patient avait une toux modérée une semaine avant le début et qu'elle s'est résolue spontanément sans intervention. En outre, le garçon n'avait pas reçu de vaccinations depuis l'âge de 6 ans. Certains tests neurologiques, tels que le test d'Oppenheim, le signe de Brudzinski, le signe de Kernig et le signe de Babinski, ont donné des résultats négatifs, tandis que le test de marche en tandem et le test de doigt à nez ont donné des résultats positifs, en particulier dans la main droite. En outre, un spectre de maladies démyélinisantes du système nerveux central, tels que les anticorps contre l'aquaporine-4, la glycoprotéine oligodendrocytaire de myéline et la protéine acide fibrillaire gliale, était négatif. Les tests suivants pertinents pour l'encéphalite anti-NMDAR ont révélé que les récepteurs AMPA1/2 et GABABR dans le LCR étaient négatifs, mais que le tétramère NMDA IgG était positif avec un titre de 1:32. L'IRM du cerveau a révélé des signaux aberrants dans les deux hémisphères cérébelleux, indiquant une atrophie cérébelleuse significative. Finalement, le garçon a été diagnostiqué comme ayant une encéphalite anti-NMDAR. La détection de certains marqueurs tumoraux, notamment l'alpha-foetoprotéine, l'antigène carcino-embryonnaire, l'antigène glucidique (CA) 125 et le CA 19-9, a été effectuée pour exclure la possibilité de tumeurs, et tous étaient négatifs. Ce patient a ensuite été traité par une thérapie par impulsions de sodium succinate de méthylprednisolone (20 mg/kg, 3 jours) et a ensuite changé en comprimés de prednisolone (40 mg, po, qd). Finalement, les symptômes du garçon ont été soulagés et il a été sorti de l'hôpital. Les visites de suivi en janvier et en mai 2020 ont révélé que cet enfant était en bonne santé sans symptômes notables. Cependant, l'enfant a été réadmis à l'hôpital en août 2020 avec une dysgraphie pendant 6 jours. Les résultats de l'examen neurologique étaient comparables à la dernière fois, avec le test du doigt à nez restant positif, mais le Tandem Gait était négatif. Le titre de l'IgG NMDAR était de 1:10 dans le sérum et de 1:3.2 dans le LCR, et l'imagerie IRM a révélé une aggravation des lésions dans les hémisphères cérébelleux. En outre, le test de bande oligoclonale d'IgG dans le LCR a été effectué, et le résultat était positif. L'IgG anti-NMDAR combinée aux résultats d'imagerie a conduit au diagnostic d'encéphalite anti-NMDAR récurrente. Un protocole thérapeutique similaire a été appliqué, et le garçon a été renvoyé après l'amélioration de ses symptômes. Les visites de suivi ultérieures ont révélé que les symptômes du garçon avaient été atténués dans une certaine mesure, mais il y a eu une récidive. En outre, sa mémoire et ses capacités d'apprentissage étaient quelque peu altérées.\n\nLe séquençage du transcriptome du LCR a été effectué dans les deux épisodes pour aider à interpréter davantage l'étiologie de ce cas. Avant l'examen, le consentement éclairé a été obtenu auprès du garçon et de ses parents. En résumé, l'ARN total du LCR a été extrait à l'aide du kit RNeasy Micro (Qiagen) en suivant les instructions du fabricant, à partir duquel l'ARN ribosomique hôte a été retiré avant la construction de la bibliothèque de séquençage. La bibliothèque a ensuite été construite à l'aide du kit Trio RNA-seq (Nugen), et le séquençage méta-transcriptomique a été effectué sur la plateforme Illumina hiseq X-ten comme décrit précédemment. Les lectures brutes résultantes ont d'abord été ajustées pour supprimer celles de faible qualité et les adaptateurs à l'aide du logiciel Trimmomatic, et les lectures d'origine humaine ont été supprimées à l'aide du script interne. Les lectures propres générées ont ensuite été appliquées directement à l'analyse par blast contre la base de données nr dans NCBI pour analyser la composition taxonomique à l'aide de BLAST + 2.12.0. Après cela, les lectures d'intérêt ont été cartographiées aux séquences de référence pour résoudre la couverture à l'aide de bowie2, et ensuite assemblées de novo à l'aide du programme Megahit sous les paramètres par défaut. Les contigs assemblés ont ensuite été utilisés comme requêtes pour l'analyse par blast afin de confirmer leur statut taxonomique. En outre, le programme MEGA a été utilisé pour aligner et construire un arbre de probabilité maximale pour la relation phylogénétique avec d'autres souches de référence.\n\nPour le séquençage du premier épisode, il y avait 37 013 105 paires de lectures générées au total, dont la majorité était attribuée à l'Homo sapiens comme prévu. Sur la base de l'analyse de lecture par blast, celles qui appartenaient probablement aux eucaryotes, aux bactéries et aux virus représentaient respectivement 70,54 %, 17,04 % et 7,61 % des lectures non humaines. En outre, des résultats similaires ont été obtenus à partir de l'analyse de blast utilisant des contigs assemblés comme requêtes. Parmi ces lectures provenant d'agents exogènes présumés, un total de 2 459 peut être cartographié au hRSV de type B (souche SE01A-0135-V02) avec une couverture de 98,5 % de sa séquence génomique (numéro d'accès MZ516143). En particulier, la plupart des lectures étaient concentrées sur l'emplacement des gènes NS1, NS2 et L. La RT-PCR et le séquençage sanger ont été utilisés pour combler les lacunes des contigs assemblés et confirmer les séquences génomiques. Enfin, avec un total de 15 184 bases, la séquence de l'ensemble du génome a été récupérée, à l'exception d'une partie de la région 3' UTR. En outre, elle avait été déposée dans le Genbank (numéro d'accès ON630422). Sur la base de l'analyse de la séquence, la séquence génomique acquise partageait 99,69 % d'identité nucléotidique avec SE01A-0135-V02. Par la suite, en utilisant l'arbre ML basé sur le gène G, la relation phylogénétique de la souche Wuxi avec d'autres génotypes du groupe hRSV B a été démêlée. Les résultats ont indiqué que cette souche était groupée avec SE01A-0135-V02 dans B6, le génotype hRSV le plus répandu dans le groupe B dans le monde. Les autres lectures ont été dispersées dans d'autres groupes taxonomiques avec un faible nombre de lectures ou de contigs assemblés courts. La deuxième séquence a abouti à 34 609 924 paires de lectures, et à l'exception des lectures provenant d'êtres humains, aucune lecture associée à des agents n'a été confirmée comme étant pertinente pour les conditions de maladie humaine. En raison de l'absence de tests d'anticorps ou d'antigènes du hRSV au moment de l'apparition, nous avons effectué le test de l'IgG hRSV dans le sérum après le séquençage du LCR en utilisant le kit ELISA hRSV-IgG (SHUANGYING BIOLOGICAL), et le résultat a été positif.",
+        "gold_summary": "L'enfant a présenté une ataxie et des récepteurs anti-NMDA positifs dans le liquide céphalorachidien, diagnostiqués comme une encéphalite à récepteurs anti-NMDA en association avec des images IRM crâniales. Après une thérapie par impulsions hormonales à haute dose et des médicaments, la maladie s'est améliorée et il a été renvoyé. Cependant, une rechute a eu lieu presque un an plus tard, et l'imagerie IRM crâniale a montré une atrophie cérébelleuse progressive. Une souche hRSV du groupe B a été détectée dans son liquide céphalorachidien, et la séquence du génome entier a été récupérée en utilisant le séquençage du transcriptome.\n",
+        "synthetic_summary": {
+            "B1": "Un garçon avait du mal à marcher et avait mal à la tête. Les médecins ont trouvé que son cerveau était un peu malade. Ils ont donné des médicaments pour l’aider. Il est devenu mieux et est rentré à la maison.\n\nMais presque un an plus tard, il a eu encore des problèmes. Son cerveau était un peu fatigué. Les médecins ont trouvé un petit virus dans son corps. Ils ont regardé ce virus très attentivement pour mieux comprendre.",
+            "B2": "**Ce qu'ils ont trouvé chez le garçon**  \nUn garçon de 12 ans a eu des problèmes pour marcher droit et des maux de tête. Les médecins ont découvert qu’il avait une maladie appelée encéphalite anti-NMDA. Cette maladie attaque le cerveau à cause d’anticorps qui ciblent des récepteurs spéciaux appelés NMDA. Une IRM, qui est une sorte de photo détaillée du cerveau, montrait que certaines parties de son cerveau, surtout le cervelet (qui aide à contrôler les mouvements), étaient abîmées.\n\n**Comment ils l’ont soigné et ce qui s’est passé ensuite**  \nLe garçon a reçu un traitement avec des médicaments puissants appelés corticostéroïdes, qui aident à calmer l’inflammation dans le cerveau. Après ce traitement, ses symptômes se sont améliorés, et il est sorti de l’hôpital. Mais presque un an plus tard, ses problèmes sont revenus, avec une aggravation des lésions dans son cervelet. Les tests ont confirmé que la maladie était revenue.\n\n**Une infection virale liée à la maladie**  \nLes médecins ont cherché à comprendre pourquoi cette maladie était apparue. En analysant le liquide autour de son cerveau (le liquide céphalorachidien), ils ont trouvé un virus appelé virus respiratoire syncytial humain (hRSV), groupe B. Ce virus est habituellement connu pour causer des infections des voies respiratoires, mais ici, il a été détecté dans le cerveau. Les chercheurs ont même réussi à lire presque tout le génome de ce virus dans le liquide du garçon grâce à une technique appelée séquençage du transcriptome, qui permet d’étudier le matériel génétique.\n\n**Ce que cela signifie**  \nCette observation suggère que le virus hRSV pourrait avoir joué un rôle dans le déclenchement ou la récidive de l’encéphalite anti-NMDA chez ce garçon. Cela aide les médecins à mieux comprendre comment certaines infections peuvent provoquer des maladies du cerveau et à chercher des traitements adaptés.",
+            "B3": "### Contexte  \nUn garçon de 12 ans a été hospitalisé en novembre 2019 pour des symptômes neurologiques progressifs, notamment des vertiges intermittents, des maux de tête persistants et une démarche instable. Ces signes sont apparus peu après une toux modérée qui s’était résolue spontanément. L’enfant n’avait pas reçu de vaccinations depuis l’âge de 6 ans. Les examens neurologiques ont montré des troubles de la coordination, notamment un test doigt-nez positif à la main droite, tandis que certains réflexes pathologiques étaient absents. Les analyses immunologiques ont révélé la présence d’anticorps anti-récepteurs NMDA (N-méthyl-D-aspartate) dans le liquide céphalorachidien (LCR), confirmant le diagnostic d’encéphalite anti-NMDAR, une maladie auto-immune du système nerveux central. L’imagerie par résonance magnétique (IRM) cérébrale a montré des anomalies dans les deux hémisphères cérébelleux, avec une atrophie significative. Aucun marqueur tumoral n’a été détecté, excluant une cause tumorale associée.  \n\n### Principales Observations  \nLe traitement initial par des impulsions de méthylprednisolone à haute dose, suivi de corticostéroïdes oraux, a permis une amélioration notable des symptômes, et l’enfant a pu sortir de l’hôpital. Lors des suivis en janvier et mai 2020, il était en bonne santé sans symptômes apparents. Cependant, en août 2020, il a été réadmis pour une dysgraphie (difficulté à écrire), avec une aggravation des lésions cérébelleuses à l’IRM et une persistance des anticorps anti-NMDAR dans le LCR et le sérum, confirmant une récidive de l’encéphalite. Le test de bande oligoclonale d’IgG dans le LCR était également positif, témoignant d’une inflammation immunitaire persistante. Un traitement similaire a été administré, avec une amélioration partielle, mais des troubles de la mémoire et des capacités d’apprentissage ont été notés lors des suivis ultérieurs.  \n\n### Interprétation Clinique  \nL’encéphalite anti-NMDAR est une maladie auto-immune caractérisée par la production d’anticorps dirigés contre les récepteurs NMDA du cerveau, entraînant des symptômes neurologiques variés. Dans ce cas, la maladie a présenté une évolution récurrente avec une atteinte cérébelleuse progressive visible à l’IRM. L’absence de tumeur associée oriente vers une origine non paranéoplasique.  \n\nUn aspect important de ce cas est la détection d’une infection virale par le virus respiratoire syncytial humain (hRSV) de type B dans le LCR lors du premier épisode. Grâce au séquençage métatranscriptomique du LCR, une souche complète du génome viral a été identifiée, confirmant la présence active du virus dans le système nerveux central. Ce virus est habituellement responsable d’infections respiratoires, mais ici, il est associé à une encéphalite auto-immune, suggérant un rôle possible dans le déclenchement ou l’exacerbation de la maladie. Lors du second épisode, aucune autre infection virale n’a été détectée dans le LCR, mais des anticorps spécifiques au hRSV ont été retrouvés dans le sérum, témoignant d’une exposition antérieure.  \n\n### Prochaines Étapes  \nCe cas souligne l’importance de rechercher des infections virales dans les encéphalites auto-immunes, notamment par des techniques avancées comme le séquençage métatranscriptomique. Le suivi clinique et radiologique doit être rigoureux pour détecter les récidives et adapter le traitement immunomodulateur. Par ailleurs, la prise en charge doit inclure une surveillance des fonctions cognitives et motrices, car des séquelles peuvent persister malgré le traitement. Enfin, la relation entre infection virale et déclenchement de l’encéphalite anti-NMDAR mérite une exploration plus approfondie pour mieux comprendre les mécanismes pathogéniques et améliorer les stratégies thérapeutiques."
+        }
+    },
+    {
+        "article": "Une femme de huit ans d'origine indienne du sud a été présentée au service des urgences pour évaluation de maux de tête. Elle avait des maux de tête depuis plusieurs jours, qui ont été gérés avec de l'acétaminophène à la maison. Elle a nié des antécédents de vision floue, de vertiges, d'apnée du sommeil, de syncope et de traumatisme crânien. Il n'y avait pas d'antécédents de maux de gorge, d'infection cutanée, de vomissements et de diarrhée récents. Dans le passé, elle avait des maux de tête de nature similaire de manière intermittente pendant environ un an. Il n'y avait pas d'antécédents d'aggravation des maux de tête avec la lumière ou le son. La production d'urine était normale et il n'y avait pas d'antécédents de gonflement des pieds ou de l'abdomen ou de gonflement du visage. Il n'y avait pas d'autres problèmes médicaux passés importants connus, y compris une maladie cardiaque congénitale. Il n'y avait pas d'antécédents d'administration d'agents stimulant l'érythropoïétine ou de voyages récents en haute altitude. Elle est née à terme sans complications périnatales. Les antécédents familiaux étaient importants pour la consanguinité parentale, qui étaient les premiers cousins. Il n'y avait pas d'antécédents familiaux de migraines et d'érythrocytose.\n\nLors de l'examen, les signes vitaux ont montré un enfant apyrétique avec une fréquence cardiaque de 90 battements par minute, une fréquence respiratoire de 18 par minute et une pression artérielle manuelle de 190/100 mm Hg, qui est restée élevée de manière persistante lors des examens répétés. Sa saturation en oxygène était de 90 à 92 %, mais n'a pas nécessité de supplémentation en oxygène. La taille était au 75e centile et le poids au 55e centile. L'examen physique n'a été remarquable que pour le strabisme. Il n'y avait pas de poches pétéchiales, d'ascite ou d'œdème pédial. Elle a continué à avoir des maux de tête. Une tomographie par ordinateur non contrôlée du cerveau n'a pas révélé de signes d'hémorragie, d'infarctus ou de thrombose. L'hypertension a été gérée avec de l'hydralazine et du labetalol intraveineux. Elle a été admise pour une évaluation supplémentaire de l'hypertension. Les tests de la fonction rénale ont montré une urée sanguine de 14 mg/dL et une créatinine sérique de 1,6 mg/dL. L'albumine sérique était de 3,1 g/dL. Les autres électrolytes étaient normaux. Le compte sanguin complet a montré une hémoglobine de 17 g/dL, un hématocrite de 51 %, un nombre de globules blancs de 7,2 × 109/L et un nombre de plaquettes de 247 × 109/L (normal : 150-300 × 109/L). La saturation en fer était de 18 % (normal : 20-55 %), le fer était de 45 µg/dL (35-150 µg/dL), la transferrine était de 176 mg/dL (200-360 mg/dL), la capacité totale de liaison du fer (TIBC) était de 246 µg/dL (225-430 µg/dL), et la ferritine était de 98 ng/mL. Les taux de vitamine B12 et de folate étaient normaux. La biopsie de la moelle osseuse n'a pas été obtenue. L'analyse d'urine a montré une protéinurie de 4+ sans hématurie microscopique. Le rapport protéine/créatinine dans l'urine était de 14,6. Il y avait une hypercholestérolémie. Les compléments en fer étaient normaux. Les anticorps antinucléaires, antineutrophiles cytoplasmiques, anti-membranes basales glomérulaires et anti-ADN double brin étaient négatifs. Le panel de l'hépatite, le virus de l'immunodéficience humaine et le test de la tuberculine étaient tous négatifs. La fonction thyroïdienne, les catécholamines sériques, l'activité de la rénine plasmatique et la sécrétion de l'aldostérone étaient normales. L'étude duplex de l'artère rénale n'a révélé aucune sténose de l'artère rénale. La radiographie thoracique n'a révélé aucune preuve de consolidation, de pneumothorax ou d'épanchement. L'échographie abdominale était normale. Les swacnb nasopharyngés pour les virus respiratoires étaient négatifs. Sa saturation en oxygène est restée faible pendant quelques jours. L'échocardiogramme a montré des preuves d'hypertrophie ventriculaire gauche modérée, mais aucune autre anomalie. Le traitement consistait en une hydratation intraveineuse et l'initiation d'agents antihypertensifs, amlodipine et labetalol. Les pressions artérielles se sont stabilisées, mais la polycytémie était persistante (hémoglobine 15-16 g/dL). L'écho-cardiogramme a montré des preuves d'hypertrophie ventriculaire gauche modérée, mais aucune autre anomalie. Le traitement consistait en une hydratation intraveineuse et l'initiation d'agents antihypertensifs, amlodipine et labetalol. Les pressions artérielles étaient stables, mais la polycytémie était persistante (hémoglobine 15-16 g/dL). L'écho-cardiogramme a montré des preuves d'hypertrophie ventriculaire gauche modérée, mais aucune autre anomalie. Le traitement consistait en une hydratation intraveineuse et l'initiation d'agents antihypertensifs, amlodipine et labetalol. Les pressions artérielles étaient stables, mais la polycytémie était persistante (hémoglobine 15-16 g/dL). L'écho-cardiogramme a montré des preuves d'hypertrophie ventriculaire gauche modérée, mais aucune autre anomalie. Le traitement consistait en une hydratation intraveineuse et l'initiation d'agents antihypertensifs, amlodipine et labetalol. Les pressions artérielles étaient stables, mais la polycytémie était persistante (hémoglobine 15-16 g/dL).\n\nLa créatinine sérique a augmenté au cours des jours suivants pour atteindre 1,8 mg/dL (taux de filtration glomérulaire estimé de 32 ml/1,73 m2/min) par Schwartz. La concentration de parathyroïde intacte dans le sérum était de 217 pg/mL (normal : 12-88 pg/mL). La protéinurie néphrotique persistait, mais le rapport entre la protéine et la créatinine dans les urines a diminué pour atteindre des valeurs allant de 5 à 7 après l'ajout de lisinopril. Une biopsie rénale percutanée réalisée une semaine après la présentation initiale a montré des preuves de FSGS avec une atrophie tubulaire sévère et une fibrose interstitielle. Il y avait un effacement partiel du processus unguéal. Les tests génétiques pour la FSGS ont montré des mutations hétérozygotes dans ACTN4, INF2 et KANK1 et une mutation homozygote dans NUP93 par séquençage de nouvelle génération. En raison de mutations génétiques héréditaires et de la probabilité de résistance aux stéroïdes, elle n'a pas été traitée avec des stéroïdes ou des agents immunosuppresseurs. L'hypertension a été gérée avec lisinopril, amlodipine et labetalol avec une stabilisation de la pression artérielle. Un agent antiplaquettaire a été ajouté. La thérapie par fer a été initiée pour une anémie ferriprive modérée (IDA). Sa saturation en oxygène est revenue à la normale au moment de la sortie et la polycytémie a été résolue sans la nécessité d'une phlébotomie. Elle a ensuite progressé vers une maladie rénale en phase terminale dix mois après la présentation initiale et a été initialement traitée par hémodialyse chronique suivie d'une dialyse péritonéale. Elle a reçu un rein de donneur décédé quatre mois après avoir été en dialyse sans qu'il y ait eu de récurrence de FSGS lors de son dernier suivi deux mois après la transplantation. Sa maintenance immunosuppression consistait en tacrolimus, mycophenolate et prednisone.\n",
+        "gold_summary": "Nous décrivons ici une fille de 8 ans atteinte d'érythrocytose associée à une néphropathie et à une insuffisance rénale chronique avancée. L'érythrocytose a été découverte lors de l'évaluation pour une urgence hypertensive. Elle avait également une protéinurie de type néphrotique sans oedème. L'hémoglobine sérique et l'hématocrite étaient de 17 g/dL et de 51 %, respectivement, malgré une hydratation. Le test de la fonction rénale a montré un taux de filtration glomérulaire estimé de 30 ml/min/1,73 m2. Il y avait une anémie légère par carence en fer avec une saturation en fer sérique de 18 %. Le taux d'EPO sérique était normal. L'EPO urinaire n'a pas été mesuré. La biopsie rénale a montré des preuves de glomérulosclérose segmentaire focale. Les tests génétiques pour la néphropathie à IgA ont montré des mutations dans les gènes des podocytes : NUP93, INF2, KANK1 et ACTN4. L'analyse de la séquence des gènes associés à l'érythrocytose n'a montré aucune variante dans aucun de ces gènes. Dix mois plus tard, elle a eu besoin d'une dialyse chronique et, par la suite, d'une transplantation rénale 14 mois après la présentation initiale.\n",
+        "synthetic_summary": {
+            "B1": "Il y a une petite fille de 8 ans qui avait mal à la tête. Son corps faisait trop de sang. Cela a été découvert quand elle est venue à l'hôpital parce que son cœur battait très vite.\n\nSon corps avait aussi un problème avec ses reins. Les reins aidaient moins bien à nettoyer son sang. Elle avait du sang dans son pipi, mais elle n'avait pas de gros pieds ou de ventre gonflé.\n\nLes docteurs ont fait un petit test sur ses reins. Ils ont vu que ses reins étaient malades. Ils ont aussi cherché dans ses gènes, qui sont comme des petits livres dans son corps. Ils ont trouvé des changements qui expliquaient pourquoi ses reins ne marchaient pas bien.\n\nAprès un moment, ses reins ont été très fatigués. Elle a dû aller à l'hôpital souvent pour que des machines aident ses reins à faire leur travail. Puis, elle a reçu un nouveau rein pour l'aider à être en meilleure santé. Maintenant, elle va mieux avec ce nouveau rein.",
+            "B2": "**Ce qu'ils ont trouvé chez la fille de 8 ans**\n\nUne fille de 8 ans est venue à l'hôpital parce qu'elle avait de forts maux de tête. En la testant, les médecins ont découvert qu'elle avait une tension artérielle très élevée (hypertension) et un nombre de globules rouges anormalement élevé, appelé érythrocytose. Cela signifie que son sang contenait trop de globules rouges, ce qui peut rendre la circulation plus difficile. Elle avait aussi une grande quantité de protéines dans ses urines, ce qui montre que ses reins ne fonctionnaient pas bien. Malgré cela, elle n'avait pas de gonflements visibles.\n\n**Ce que cela signifie pour ses reins**\n\nLes examens ont montré que ses reins étaient en mauvais état, avec une fonction réduite. Une biopsie, c’est-à-dire un prélèvement d’un petit morceau de rein pour l’étudier, a révélé une maladie appelée glomérulosclérose segmentaire focale (FSGS). Cette maladie endommage certaines parties des reins, ce qui explique la perte de protéines dans l’urine et la baisse de la fonction rénale. Des tests génétiques ont trouvé des mutations dans plusieurs gènes importants pour les cellules des reins (appelées podocytes), notamment NUP93, INF2, KANK1 et ACTN4. Ces mutations peuvent expliquer pourquoi ses reins ne fonctionnent pas correctement.\n\n**Traitement et évolution**\n\nAu début, elle a reçu des médicaments pour contrôler sa tension artérielle et des traitements pour corriger une légère carence en fer. Malgré ces soins, sa maladie rénale a progressé rapidement. Dix mois après son arrivée à l’hôpital, ses reins ne fonctionnaient presque plus, et elle a dû commencer une dialyse, un traitement qui remplace temporairement la fonction des reins. Quatre mois plus tard, elle a reçu une greffe de rein. Deux mois après la transplantation, elle allait bien et la maladie des reins ne semblait pas être revenue.\n\n**En résumé**\n\nCette jeune fille souffrait d’une maladie rénale grave liée à des mutations génétiques qui ont causé une perte progressive de la fonction de ses reins. Son sang avait trop de globules rouges, ce qui est rare dans ce type de maladie. Grâce à un traitement adapté, elle a pu recevoir une greffe de rein, ce qui a amélioré sa santé.",
+            "B3": "Résumé détaillé pour un public non médical éduqué\n\n**Contexte**  \nUne fille de 8 ans originaire du sud de l’Inde a été admise en urgence pour des maux de tête persistants associés à une hypertension artérielle sévère (pression artérielle très élevée). Elle n’avait pas d’antécédents de troubles visuels, de vertiges ou d’autres symptômes neurologiques graves. Ses antécédents familiaux incluaient une consanguinité (ses parents étaient cousins), mais sans antécédents connus de migraines ou de troubles sanguins.  \n\n**Principales observations cliniques et biologiques**  \nÀ l’examen, sa pression artérielle était anormalement élevée (190/100 mm Hg), et sa saturation en oxygène était légèrement basse (90-92 %), sans nécessiter d’oxygène supplémentaire. Elle présentait un strabisme (déviation des yeux) mais aucun signe d’œdème ou d’infection. Les examens cérébraux (scanner) étaient normaux.  \n\nLes analyses sanguines ont révélé une polyglobulie (augmentation du nombre de globules rouges) avec une hémoglobine élevée à 17 g/dL et un hématocrite à 51 %, malgré une hydratation adéquate. Paradoxalement, elle avait une légère carence en fer, suggérée par une saturation en fer sérique basse (18 %). Sa fonction rénale était altérée, avec une créatinine élevée (1,6 puis 1,8 mg/dL) et un taux de filtration glomérulaire estimé à environ 30 ml/min/1,73 m², indiquant une insuffisance rénale modérée à sévère.  \n\nUne analyse d’urine a montré une protéinurie importante (présence élevée de protéines dans les urines), caractéristique d’une atteinte rénale dite « néphrotique », mais sans œdème. Les examens immunologiques et infectieux étaient négatifs, excluant des causes auto-immunes ou infectieuses. L’échographie abdominale et la radiographie thoracique étaient normales, tandis que l’échocardiogramme a montré une hypertrophie modérée du ventricule gauche, probablement liée à l’hypertension.  \n\n**Interprétation clinique et résultats complémentaires**  \nUne biopsie rénale a été réalisée et a confirmé la présence d’une glomérulosclérose segmentaire focale (FSGS), une maladie caractérisée par une cicatrisation partielle des glomérules, les unités filtrantes du rein. Cette pathologie explique la protéinurie et la progression vers l’insuffisance rénale.  \n\nDes analyses génétiques ont identifié des mutations dans plusieurs gènes codant pour des protéines des podocytes (cellules essentielles à la filtration rénale) : NUP93, INF2, KANK1 et ACTN4. Ces mutations sont associées à une forme héréditaire de FSGS, ce qui explique la résistance probable aux traitements immunosuppresseurs classiques (stéroïdes). Aucun gène lié à l’érythrocytose (augmentation anormale des globules rouges) n’a été trouvé, suggérant que la polyglobulie est secondaire à la maladie rénale.  \n\n**Prise en charge et évolution**  \nL’hypertension a été traitée efficacement par plusieurs médicaments (lisinopril, amlodipine, labetalol), et la saturation en oxygène est revenue à la normale. La polyglobulie s’est résorbée sans nécessiter de traitement spécifique comme la phlébotomie (saignée). Une anémie ferriprive modérée a été corrigée par une supplémentation en fer.  \n\nMalgré ces traitements, la fonction rénale a continué à se détériorer, conduisant à une insuffisance rénale terminale dix mois après le diagnostic initial. La patiente a alors débuté une dialyse chronique, d’abord par hémodialyse puis par dialyse péritonéale. Quatorze mois après sa présentation initiale, elle a reçu une transplantation rénale provenant d’un donneur décédé. Deux mois après la greffe, aucun signe de récidive de la maladie rénale n’a été observé. Elle est maintenue sous traitement immunosuppresseur associant tacrolimus, mycophénolate et prednisone pour prévenir le rejet du greffon.  \n\n**Conclusion**  \nCette jeune patiente présente une forme héréditaire de glomérulosclérose segmentaire focale associée à une polyglobulie secondaire et une hypertension sévère. La maladie rénale a évolué rapidement vers une insuffisance terminale nécessitant une dialyse puis une transplantation. Ce cas illustre l’importance d’une évaluation complète incluant des tests génétiques dans les néphropathies infantiles complexes, afin d’adapter au mieux la prise en charge thérapeutique."
+        }
+    },
+    {
+        "article": "Le patient, un homme de 61 ans, a été diagnostiqué avec une pancréatite aiguë neuf mois avant son admission et a reçu un traitement conservateur. Après sa sortie, il a éprouvé de manière intermittente une distension et une douleur abdominale supérieure, et une tomographie par ordinateur (CT) abdominale a montré la formation d'une pseudo-cyste pancréatique. Quatre jours avant son admission, le patient a développé une dyspnée sévère avec douleur thoracique et toux, suffisamment sévère pour l'empêcher de rester allongé. L'examen physique a indiqué un essoufflement, des sons respiratoires diminués bilatéraux, une tachycardie, et aucune anomalie abdominale. Le patient avait une longue histoire de consommation d'alcool et de tabac et de multiples interventions chirurgicales antérieures, y compris une chirurgie de fixation lombaire et une ablation de lipome de la paroi abdominale.\n\nLes tests de laboratoire ont montré une légère augmentation du marqueur tumoral du sérum, l’antigène du cancer 125, à 98,25 U/mL (intervalle normal 0–35 U/mL) et de l’amylase urinaire à 333 U/L (intervalle normal 32–641 U/L). L’imagerie (CT) a révélé une épanchement pleural bilatéral massif et la formation d’une pseudo-kystée pancréatique.\n\nDiagnostic et interventions\nLors de l'admission, une ponction thoracique a été effectuée, la culture bactérienne du liquide pleural était négative, aucune cellule tumorale n'a été trouvée, mais le niveau de l'antigène du cancer 125 dans le liquide pleural était significativement élevé à 1859 U/mL (intervalle normal 0-35 U/mL). Les niveaux d'amylase dans le liquide pleural étaient de 53 844 U/L à gauche et de 1365 U/L à droite. Le sixième jour, un diagnostic de PPF a été confirmé, et une ERCP a été effectuée avec la mise en place d'un conduit naso-pancréatique de 7Fr pour drainer la pseudo-cyste pancréatique.\n\nImmédiatement après l'admission, une ponction thoracique a été réalisée, drainant une grande quantité de liquide pleural teinté de sang pâle, ainsi qu'un soutien nutritionnel parentéral et un traitement par somatostatine, aidant progressivement le patient à effectuer des exercices de fonction pulmonaire. Le septième jour, un examen ERCP a révélé une communication entre le pseudocyste pancréatique et la cavité pleurale. Au cours de la canulation du canal pancréatique, le guide-fil a pu pénétrer dans le pseudocyste, de sorte qu'un canal naso-pancréatique de 7 Fr a été placé pour le drainage. La culture du liquide pancréatique du canal naso-pancréatique a révélé la présence d'Enterococcus faecium et de Klebsiella pneumoniae, mais le patient n'a pas développé de fièvre, et le nombre de globules blancs et de protéines C-réactives était normal, mais des antibiotiques ont été administrés. Le neuvième jour, aucun liquide n'a été drainé des drains thoraciques bilatéraux, et une autre ERCP a été réalisée. Le canal naso-pancréatique a été sectionné à la papille duodénale, laissant la partie interne comme stent du canal pancréatique.\n\nRésultats\nLe patient a reçu un total de 13 jours de traitement hospitalier, au cours duquel 4180 mL de liquide pleural a été drainé du côté gauche, 2470 mL du côté droit et 495 mL du conduit naso-pancréatique. Six mois après la sortie, le conduit naso-pancréatique restant a été enlevé. Il n’y a pas eu de récidive au cours d’un suivi de 5 ans, et l’état général du patient était bon\n",
+        "gold_summary": "Inquiétudes du patient : Un homme de 61 ans ayant des antécédents de consommation d'alcool et de tabac a présenté une dyspnée sévère, des douleurs thoraciques et une toux. Il avait été diagnostiqué avec une pancréatite aiguë 9 mois auparavant et avait éprouvé de manière intermittente des douleurs et une distension abdominale supérieures après le traitement.\n\nDiagnoses : PPF.\n\nInterventions : Le patient a subi un drain thoracique, un drain du conduit pancréato-nasal et un stent du conduit pancréatique, ainsi qu'une nutrition parentérale et une thérapie par la somatostatine.\n\nRésultats : Le traitement a entraîné la résolution de l'épanchement pleural et du pseudocyste. La patiente n'a pas eu de récidive au cours d'une période de suivi de 5 ans.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 61 ans avait mal au ventre et du mal à respirer. Il toussait beaucoup et avait mal à la poitrine. Avant, il avait eu un gros problème au ventre.\n\nLes docteurs ont trouvé un petit sac rempli de liquide près de son ventre. Ce sac faisait aussi du mal à ses poumons.\n\nIls ont mis des petits tuyaux pour enlever le liquide et aider le monsieur à mieux respirer. Ils lui ont aussi donné des médicaments et de la nourriture spéciale.\n\nAprès le traitement, le monsieur allait beaucoup mieux. Le sac a disparu et il n’a plus eu mal. Cinq ans après, il est toujours en bonne santé.",
+            "B2": "**Ce qu'ils ont trouvé chez le patient**  \nUn homme de 61 ans, qui avait déjà eu une inflammation du pancréas appelée pancréatite aiguë, a commencé à avoir du mal à respirer, des douleurs dans la poitrine et une toux. Avant cela, il avait souvent ressenti des douleurs et un gonflement dans le haut de son ventre. Il avait aussi une longue histoire de consommation d’alcool et de tabac.\n\n**Ce que cela signifiait**  \nLes médecins ont découvert qu’il avait une complication appelée fistule pancréatico-pleurale (PPF). Cela veut dire qu’un liquide du pancréas s’était échappé vers la cavité autour des poumons, provoquant une accumulation de liquide appelée épanchement pleural. En plus, il avait une pseudo-kyste pancréatique, c’est-à-dire une poche remplie de liquide près du pancréas.\n\n**Comment ils ont aidé le patient**  \nPour soigner cela, ils ont d’abord drainé le liquide autour des poumons avec des tubes. Ensuite, ils ont placé un drain spécial dans le canal du pancréas pour évacuer le liquide du pseudo-kyste. Le patient a aussi reçu une nutrition par voie veineuse (car il ne pouvait pas bien manger) et un médicament appelé somatostatine, qui aide à réduire la production de liquide par le pancréas. Des antibiotiques ont été donnés pour prévenir une infection.\n\n**Résultats et suivi**  \nAprès environ deux semaines à l’hôpital, le liquide accumulé a été complètement drainé et le problème s’est amélioré. Le drain dans le pancréas a été retiré six mois plus tard. Pendant les cinq années qui ont suivi, le patient n’a pas eu de retour de la maladie et sa santé est restée bonne.",
+            "B3": "Résumé détaillé et structuré pour un public non médical éduqué\n\n**Contexte**  \nUn homme de 61 ans, avec des antécédents importants de consommation d’alcool et de tabac, a été hospitalisé pour une difficulté respiratoire sévère (dyspnée), accompagnée de douleurs thoraciques et de toux. Neuf mois auparavant, il avait été diagnostiqué avec une pancréatite aiguë (inflammation soudaine du pancréas) traitée de manière conservatrice. Depuis, il souffrait de façon intermittente de douleurs et de distension dans la partie supérieure de l’abdomen. Une tomodensitométrie (scanner) avait révélé la formation d’une pseudo-kyste pancréatique, une cavité remplie de liquide liée à l’inflammation du pancréas.\n\n**Principales observations**  \nÀ son admission, le patient présentait un essoufflement marqué, une accélération du rythme cardiaque et des bruits respiratoires réduits dans les deux poumons, sans anomalie abdominale notable. Les analyses sanguines ont montré une légère augmentation d’un marqueur tumoral appelé antigène CA 125, ainsi qu’une élévation modérée de l’amylase urinaire, une enzyme liée au pancréas. L’imagerie a confirmé un important épanchement pleural bilatéral (accumulation de liquide dans les deux cavités entourant les poumons) et la présence d’un pseudo-kyste pancréatique.\n\nL’analyse du liquide prélevé dans la cavité pleurale a révélé une concentration très élevée d’amylase et d’antigène CA 125, sans infection bactérienne ni cellules tumorales. Ces résultats ont conduit au diagnostic d’une fistule pancréatico-pleurale (PPF), une communication anormale entre le pancréas et la cavité pleurale, permettant au liquide pancréatique de s’accumuler autour des poumons.\n\n**Interventions cliniques**  \nLe traitement a débuté par un drainage thoracique pour évacuer le liquide accumulé dans les poumons. Parallèlement, le patient a reçu une nutrition parentérale (alimentation par voie intraveineuse) et un traitement par somatostatine, une hormone qui réduit la sécrétion pancréatique, favorisant ainsi la guérison. Une cholangiopancréatographie rétrograde endoscopique (ERCP), une procédure utilisant une caméra et des rayons X pour visualiser les canaux pancréatiques, a permis de confirmer la communication entre le pseudo-kyste et la cavité pleurale. Un drain naso-pancréatique (un tube inséré par le nez jusqu’au pancréas) a été placé pour drainer le pseudo-kyste.\n\nLa culture du liquide pancréatique a détecté la présence de bactéries (Enterococcus faecium et Klebsiella pneumoniae), mais le patient n’a pas développé d’infection systémique, et un traitement antibiotique a été administré par précaution. Après stabilisation, le drain naso-pancréatique a été transformé en stent interne (un petit tube permanent) pour maintenir le canal pancréatique ouvert et faciliter le drainage.\n\n**Résultats et suivi**  \nAu total, plus de 6 litres de liquide ont été drainés des cavités pleurales et du pseudo-kyste pendant l’hospitalisation de 13 jours. Six mois après la sortie, le stent a été retiré sans complication. Le patient a été suivi pendant cinq ans sans récidive de la fistule ni d’autres complications, et son état général est resté satisfaisant.\n\n**Interprétation clinique**  \nCette observation illustre une complication rare mais grave de la pancréatite aiguë, la fistule pancréatico-pleurale, qui peut provoquer un important épanchement pleural et des symptômes respiratoires sévères. Le diagnostic repose sur la détection d’amylase élevée dans le liquide pleural et la confirmation par imagerie. Le traitement combiné de drainage, de réduction de la sécrétion pancréatique et d’intervention endoscopique permet une résolution efficace, évitant une chirurgie plus invasive.\n\n**Prochaines étapes**  \nLe suivi à long terme est essentiel pour surveiller la réapparition possible de la fistule ou du pseudo-kyste. En cas de récidive, des interventions similaires ou chirurgicales peuvent être envisagées. Par ailleurs, la gestion des facteurs de risque, notamment l’alcoolisme, est cruciale pour prévenir de nouvelles poussées de pancréatite."
+        }
+    },
+    {
+        "article": "Une femme de 65 ans a été admise avec un antécédent de myalgie, de faiblesse généralisée et de douleurs thoraciques non spécifiques intermittentes datant d'un mois.\n\nElle avait souffert d'un accident vasculaire cérébral deux ans auparavant, qui avait limité sa mobilité et pour lequel elle résidait dans une maison de retraite. Elle avait également connu un infarctus du myocarde sans élévation du segment ST (NSTEMI), avec intervention coronarienne percutanée sur l'artère descendante antérieure gauche cinq mois avant son admission actuelle. Ses autres antécédents comprenaient une maladie rénale chronique (MRC), une dyslipidémie, une hypertension résistante, une épilepsie, une insuffisance cardiaque, un diabète sucré de type 2 et un asthme. Elle était non-fumeuse et n'avait pas d'antécédents d'abus d'alcool.\n\nLes médicaments qu'elle prenait avant son admission comprenaient de nombreux médicaments anti-hypertensifs, de l'aspirine, du ticagrelor et de l'insuline. On lui a également prescrit de l'atorvastatine 80 mg, qu'elle prenait depuis près de deux décennies, bien que la dose ait été augmentée de 20 mg deux ans auparavant.\n\nLors de l'examen, elle avait une force globalement réduite, plus prononcée du côté droit, qui était le côté affecté par son accident vasculaire cérébral antérieur, et une sensibilité musculaire généralisée. Le reste de l'examen clinique était globalement insignifiant, avec un examen cardiovasculaire normal et aucune autre preuve d'un processus rhumatologique sous-jacent tel qu'une éruption cutanée ou un gonflement articulaire.\n\nLa découverte la plus notable issue de ses premières analyses en laboratoire fut un taux de troponine T cardiaque de haute sensibilité (hs-cTnT) nettement élevé de 3794 ng/l (normal < 12 ng/l), sans changement dynamique significatif entre les tests en série, et dont on a noté qu'il avait été relevé à un niveau similaire plusieurs mois auparavant suite à son NSTEMI. Une créatine kinase (CK) a ensuite été contrôlée, dont on a également constaté qu'elle était significativement élevée à 9416 U/l (normal 25-200 IU/l).\n\nSon ECG ne montrait aucune modification aiguë, et son échocardiogramme transthoracique (TTE) révélait une hypertrophie ventriculaire gauche (LVH), mais une fraction d'éjection ventriculaire gauche normale sans anomalies du mouvement de la paroi régionale, une fonction ventriculaire droite normale et aucune pathologie valvulaire significative.\n\nAu début, on ignorait si son CK représentait des dommages au muscle cardiaque ou squelettique. La signification de l'augmentation de hs-cTnT était également incertaine. On pensait que le syndrome coronarien aigu avait été exclu, car ses symptômes initiaux étaient incompatibles avec cela, il n'y avait pas de changements ECG ou TTE aigus, et les niveaux de hs-cTnT étaient relativement statiques. Le diagnostic différentiel était considéré comme étant entre la myocardite chronique, avec la faiblesse étant due à une myosite coexistante ou à un déconditionnement, et la myositis sans implication cardiaque et avec une fausse élévation de hs-cTnT.\n\nD’autres tests ont été demandés pour différencier ces deux possibilités. Une troponine cardiaque de haute sensibilité (hs-cTnI) a été réalisée et n’a été que légèrement élevée à 55 ng/l. Une hs-cTnT appariée prise au même moment est restée significativement élevée à 4532 ng/l. Une IRM cardiaque n’a montré aucune infiltration cardiaque ou inflammation. Une amélioration tardive du gadolinium dans une zone focale probablement due à son NSTEMI antérieur a été observée.\n\nSur la base des investigations ci-dessus, il a été estimé que les lésions cardiaques aiguës significatives avaient été exclues. La myosite avec fausse élévation de hs-cTnT était désormais considérée comme le diagnostic le plus probable et un avis de rhumatologie a été demandé. Ils ont conseillé un certain nombre de tests d'anticorps. Parmi ceux-ci, les anticorps anti-HMG-CoA réductase étaient positifs et les anticorps anti-PM/SCL75 étaient faiblement positifs. Les autres tests complémentaires recommandés à ce moment-là, y compris les tests ANA, ANCA et hépatite B/C, étaient négatifs, et une TDM du thorax, de l'abdomen et du bassin ne révélait aucune preuve de malignité sous-jacente. La constatation initiale d'une TSH élevée signifiait qu'une hypothyroïdie contribuant à la myosite devait être envisagée. Cependant, le fT4 s'est avéré normal, indiquant que le patient souffrait d'une hypothyroïdie infraclinique et excluant cette dernière comme facteur contributif significatif.\n\nUne IRM bilatérale des cuisses a également été conseillée, qui a révélé un changement de signal diffus élevé dans tous les muscles de la cuisse avec un œdème environnant correspondant à une myosite généralisée.\n\nSur la base des résultats cliniques, IRM et anticorps, un diagnostic de NMI induit par les statines a été posé. Pour confirmation, une biopsie musculaire du quadriceps a été réalisée. Les résultats n'étaient pas disponibles avant la sortie, mais lorsqu'ils ont été examinés, ils ont montré des changements compatibles avec la NMI.\n\nÀ la suite du diagnostic, l'atorvastatine a été arrêtée et la patiente a commencé à prendre de la prednisolone 40 mg OD. Cependant, elle a eu une réponse modeste, avec une réduction de ses taux de CK, mais peu de changement de ses symptômes. Par conséquent, après deux semaines de traitement par stéroïdes, elle a commencé à prendre une dose croissante de mycophenolate, à partir de 250 mg BD et d'immunoglobuline intraveineuse 2 g/kg sur cinq jours, parallèlement à un traitement IV de 500 mg de méthylprednisolone OD pendant trois jours, suivi d'une dose accrue de prednisolone orale à 60 mg OD. Il en a résulté une amélioration progressive des symptômes et une réduction continue de ses taux de CK. Sa cTnT a également diminué, mais est restée significativement élevée au-dessus de sa valeur initiale, même après plusieurs mois de traitement. Elle a été renvoyée chez elle avec du mycophenolate (1 g BD au moment du renvoi) et une dose de sevrage de prednisolone (30 mg OD au moment du renvoi). Elle devait être suivie par l'équipe de rhumatologie, mais malheureusement, elle n'a pas assisté à ses rendez-vous cliniques programmés.\n",
+        "gold_summary": "Nous présentons ici le cas d'une femme de 65 ans sous atorvastatine à long terme qui a présenté une faiblesse généralisée, des douleurs thoraciques non spécifiques et une troponine T cardiaque élevée de manière persistante. Après enquête, une lésion myocardique aiguë a été exclue et un diagnostic de myopathie nécrosante immuno-médiée induite par les statines (IMNM) a été posé. La patiente a présenté une amélioration après l'arrêt de l'atorvastatine et l'instauration d'une thérapie immunosuppressive avec mycophenolate, immunoglobuline intraveineuse et stéroïdes.\n",
+        "synthetic_summary": {
+            "B1": "Une dame de 65 ans se sentait très faible et avait mal à la poitrine. Elle prenait un médicament depuis longtemps pour son cœur. Les docteurs ont fait des examens et ont vu que son cœur allait bien. \n\nIls ont trouvé que ses muscles étaient malades à cause du médicament. Ils ont arrêté ce médicament. Puis, ils lui ont donné d’autres médicaments pour aider ses muscles à guérir. Petit à petit, elle a commencé à aller mieux.",
+            "B2": "**Présentation du cas**  \nUne femme de 65 ans, qui prenait depuis longtemps un médicament appelé atorvastatine (utilisé pour baisser le cholestérol), a commencé à ressentir une faiblesse musculaire générale et des douleurs au niveau de la poitrine. Lors des analyses, on a découvert que sa troponine T cardiaque, une substance qui peut indiquer un problème au cœur, était très élevée de façon constante.\n\n**Ce qu'ils ont cherché et trouvé**  \nLes médecins ont d'abord vérifié s'il y avait un problème aigu au cœur, comme une crise cardiaque, mais cela a été exclu grâce à plusieurs examens. Ensuite, ils ont pensé que la faiblesse musculaire pouvait venir d'une maladie appelée myopathie nécrosante immuno-médiée (IMNM), qui est une inflammation grave des muscles causée par une réaction du système immunitaire. Cette maladie peut être déclenchée par les statines, les médicaments pour le cholestérol.\n\nDes tests spécifiques ont confirmé la présence d’anticorps liés à cette maladie. Une IRM des cuisses a montré une inflammation des muscles, et une biopsie (prélèvement d’un petit morceau de muscle) a confirmé le diagnostic.\n\n**Traitement et évolution**  \nAprès avoir arrêté l’atorvastatine, la patiente a reçu des médicaments qui calment le système immunitaire : des stéroïdes, du mycophenolate et des immunoglobulines par perfusion. Ces traitements ont aidé à améliorer ses symptômes et à réduire les signes d’inflammation dans le sang. Cependant, la troponine est restée un peu élevée, ce qui peut arriver dans ce type de maladie.\n\n**Conclusion**  \nCe cas montre qu’une faiblesse musculaire et une troponine élevée chez une personne sous statines peuvent être dues à une maladie inflammatoire musculaire grave appelée IMNM. Il est important de reconnaître cette maladie rapidement pour arrêter le médicament responsable et commencer un traitement adapté.",
+            "B3": "Résumé détaillé et structuré\n\nContexte  \nUne femme de 65 ans, avec de multiples antécédents médicaux cardiovasculaires et métaboliques, notamment un infarctus du myocarde récent traité par angioplastie, était sous traitement par atorvastatine à haute dose depuis près de vingt ans. Elle a été admise pour une faiblesse musculaire généralisée, des douleurs thoraciques intermittentes non spécifiques et une myalgie évoluant depuis un mois.\n\nPrincipales observations  \nÀ l’examen clinique, la patiente présentait une faiblesse musculaire diffuse, plus marquée du côté droit, correspondant à son ancien accident vasculaire cérébral, ainsi qu’une sensibilité musculaire généralisée. Les examens cardiaques initiaux (ECG et échocardiogramme) ne montraient pas de signes d’ischémie ou d’inflammation aiguë. Les analyses sanguines révélaient une élévation très importante de la créatine kinase (CK), un marqueur de l’atteinte musculaire, ainsi qu’une troponine T cardiaque de haute sensibilité (hs-cTnT) très élevée et stable dans le temps, sans variation dynamique typique d’un infarctus aigu. Une troponine I cardiaque (hs-cTnI) était légèrement élevée, tandis que l’IRM cardiaque n’a montré aucune infiltration inflammatoire ni anomalie aiguë, seulement des séquelles d’infarctus ancien.\n\nCes résultats ont permis d’exclure une atteinte cardiaque aiguë et ont orienté vers une myosite (inflammation musculaire) avec élévation faussement élevée de la troponine T. Une IRM musculaire des cuisses a confirmé une inflammation diffuse des muscles (myosite généralisée). Des tests immunologiques ont mis en évidence la présence d’anticorps anti-HMG-CoA réductase, spécifiques d’une myopathie nécrosante immuno-médiée (NMI) induite par les statines. Une biopsie musculaire a confirmé ce diagnostic.\n\nInterprétation clinique  \nLa patiente souffrait d’une myopathie nécrosante immuno-médiée liée à la prise prolongée d’atorvastatine, une complication rare mais grave des statines caractérisée par une inflammation musculaire auto-immune persistante. Cette pathologie explique la faiblesse musculaire, les douleurs et l’élévation marquée de la CK. L’élévation persistante de la troponine T, malgré l’absence d’atteinte cardiaque aiguë, est attribuée à une libération musculaire non cardiaque de ce biomarqueur, phénomène documenté dans ce contexte.\n\nProchaines étapes et prise en charge  \nL’atorvastatine a été immédiatement arrêtée. La patiente a débuté un traitement immunosuppresseur associant corticostéroïdes (prednisolone puis méthylprednisolone), mycophenolate mofétil et immunoglobulines intraveineuses. Cette prise en charge a permis une amélioration progressive des symptômes et une diminution significative des taux de CK. La troponine T est restée élevée, mais à un niveau moindre. Un suivi spécialisé en rhumatologie a été prévu pour ajuster le traitement et surveiller l’évolution, bien que la patiente n’ait pas assisté aux consultations programmées.\n\nConclusion  \nCe cas illustre l’importance de considérer une myopathie nécrosante immuno-médiée induite par statines chez un patient présentant une faiblesse musculaire et une élévation persistante de la troponine T sans signes d’atteinte cardiaque aiguë. Le diagnostic repose sur la combinaison des examens cliniques, biologiques, d’imagerie et immunologiques. La prise en charge nécessite l’arrêt du traitement statinique et une immunosuppression adaptée pour contrôler l’inflammation musculaire."
+        }
+    },
+    {
+        "article": "Une patiente de 17 ans a été envoyée du service de pédiatrie au service de médecine buccale de l’hôpital Hasan Sadikin avec des plaintes de douleurs buccales, de sécheresse des lèvres et de difficultés à avaler. Cette condition a rendu difficile pour la patiente de manger et de boire, ce qui a entraîné une faiblesse et une débilité de la condition physique de la patiente. L’ulcère est présent depuis 3 jours, ne s’est pas amélioré et a tendance à saigner. Cependant, le saignement a cessé depuis la veille. Le service de pédiatrie a administré Kenalog en Orabase® en réponse à la condition orale de cette patiente.\n\nLe patient s'est plaint de douleurs corporelles, d'éruptions cutanées et de perte de cheveux il y a deux mois. Cette condition a été examinée à l'hôpital Kebon Jati, et le diagnostic de SLE a été confirmé. Il y a environ deux semaines, le patient s'est plaint de la même condition et a finalement décidé d'être traité à l'hôpital Hasan Sadikin. Des examens complets et multidisciplinaires ont établi qu'en plus du SLE, le patient a également été diagnostiqué avec une hépatosplénomégalie, au cours de la troisième semaine d'hospitalisation. L'élargissement du foie et de la rate a été constaté lors d'une tomographie par ordinateur abdominale.\n\nPendant cette période de deux semaines, le patient a suivi un régime médicamenteux diversifié administré par le service de pédiatrie, qui comprend le levofloxacin, l'amikacin, l'ampicillin-sulbactam et l'ethambutol pour les antibiotiques. Le fluconazole a été administré par voie intraveineuse. Des anti-inflammatoires stéroïdiens ont été administrés par voie intraveineuse, le méthylprednisolone et l'acétonide de triamcinolone par voie topique. L'oméprazole et le carbonate de calcium ont été administrés comme antiacides et inhibiteurs de la pompe à protons. Des compléments alimentaires tels que la vitamine D et le curcuma ainsi que du paracétamol ont également été administrés.\n\nL’examen extraoral a révélé une conjonctive anémique, une sécheresse et une exfoliation des lèvres qui tendent à saigner, ainsi que des croûtes hémorragiques séreuses et sanguinolentes. L’examen intraoral a révélé des lésions couvrant presque toutes les régions de la muqueuse buccale. Des ulcérations multiples sur la muqueuse labiale supérieure et inférieure. Une ulcération douloureuse sur la muqueuse buccale gauche mesurant 5 × 6 mm avec bord érythémateux. Un érythème palatal central a été observé sur le palais dur. Une pseudomembrane de candidose a également été observée sur le dos de la langue, accompagnée d’un allongement des papilles.\n\nGestion des cas\nNaCl 0,9 % a été administré et utilisé pour effectuer plusieurs instructions liées à l'état buccal de la patiente. Le nettoyage des dents à l'aide d'une gaze humidifiée au sérum physiologique était la chose la plus importante, car pendant les deux semaines d'hospitalisation, la patiente a négligé son hygiène buccale. Des croûtes hémorragiques sur les lèvres et la muqueuse labiale ont également été soignées à l'aide d'une gaze humidifiée (NaCl 0,9 %) aussi souvent que possible. Cela a été fait cinq fois par jour, dans le but d'humidifier les lèvres et d'enlever les croûtes.\n\nL'état de multiples ulcérations étendues sur la muqueuse labiale supérieure et inférieure, un mélange d'onguent stéroïdien topique, a été administré à la patiente. Un mélange contenant 0,5 mg de dexaméthasone mélangé à 2,5 mg de lanoline et à de la gelée de pétrole a été prescrit à la patiente pour l'utiliser trois fois par jour, après application d'un pansement salin. Compte tenu des autres ulcérations, dont une sur la muqueuse buccale gauche et d'autres ulcères difficiles à atteindre à la main, 0,025 % d'acide hyaluronique a été administré pour soulager l'inflammation localement.\n\nLors de la deuxième visite, le 22 novembre 2022, on a constaté que l'état général de la cavité buccale du patient s'était amélioré. La langue du patient présentait toujours une plaque blanchâtre, qui a finalement été traitée par une suspension orale de Nystatin®, mais a dû être arrêtée après 2 jours d'administration en raison de l'état d'hépatosplénomégalie. La pommade a été arrêtée et remplacée par de la gelée de pétrole. Les autres médicaments ont été poursuivis jusqu'à la prochaine évaluation, pendant les 6 jours suivants. Le 28 novembre 2022, le patient ne s'est plaint d'aucun problème de cavité buccale, mais il y avait toujours une présence clinique de chéilite exfoliative, de langue recouverte et d'ulcère dans la muqueuse buccale gauche, qui avait disparu.\n\nLe patient a été renvoyé à la maison 2 jours plus tard et a continué les soins ambulatoires. La dernière visite a eu lieu le 16 décembre 2022. Le patient n'avait aucune plainte, pouvait suivre les instructions d'hygiène buccale et a conseillé au patient d'extraire les racines des dents de lait 55 et 65.\n",
+        "gold_summary": "Une patiente de 17 ans a été référée par le service de pédiatrie avec des ulcères de la bouche accompagnés de lèvres sèches et une tendance à saigner. La lésion la plus préoccupante était située sur la muqueuse buccale gauche, une ulcération unique mesurant 5x6 mm. De multiples ulcérations se sont répandues sur la muqueuse labiale supérieure et inférieure, avec des croûtes hémorragiques sur les lèvres. Une ulcération douloureuse peut entraîner des difficultés à ouvrir la bouche et une altération de la fonction alimentaire et de la fonction de boire. Un érythème central a été observé sur le palais. Une candidose pseudomembraneuse a également été observée sur la langue de la patiente. L’hépatosplénomégalie a été confirmée par une tomodensitométrie, avec des valeurs enzymatiques de SGPT (386 U/L) et SGOT (504 U/L).\n\nGestion des cas\nL’administration de 0,9 % de NaCl a été indiquée au patient pour maintenir l’hygiène buccale et aider à hydrater les lèvres afin d’éliminer les croûtes hémorragiques. Administration de 0,025 % de solution buccale d’acide hyaluronique et de pommade stéroïde topique pour les conditions ulcérées et inflammatoires. Des ajustements de médicaments ont été faits en fonction des tests de laboratoire et l’état clinique du patient s’est amélioré.\n",
+        "synthetic_summary": {
+            "B1": "Une jeune fille avait mal dans la bouche. Ses lèvres étaient très sèches et un peu abîmées. Elle avait aussi une petite plaie qui faisait mal sur le côté de sa bouche.\n\nElle avait du mal à manger et à boire à cause de la douleur. Sa langue avait une couche blanche. Son ventre était un peu gros à cause de son foie et d’un autre organe.\n\nLes docteurs ont aidé en nettoyant bien sa bouche avec de l’eau spéciale. Ils ont mis une crème douce pour soigner les plaies. Petit à petit, elle a commencé à aller mieux.\n\nElle a bien suivi les conseils pour garder sa bouche propre. Après un moment, elle n’avait plus mal et pouvait manger normalement.",
+            "B2": "**Ce qu'ils ont trouvé chez la patiente**  \nUne jeune fille de 17 ans est venue à l’hôpital avec des plaies douloureuses dans la bouche, des lèvres très sèches qui saignaient facilement, et des difficultés pour manger et boire. La plaie la plus importante mesurait environ 5 mm sur 6 mm et se trouvait à l’intérieur de la joue gauche. Elle avait aussi plusieurs autres petites plaies sur les lèvres du haut et du bas, ainsi que des croûtes qui saignaient. Ces blessures rendaient la bouche très sensible et difficile à ouvrir. Sur le palais dur (le toit de la bouche), une zone rouge a été observée. De plus, la langue présentait une couche blanche, causée par une infection appelée candidose, qui est une prolifération de champignons. Par ailleurs, un examen spécial a montré que son foie et sa rate étaient plus gros que la normale, ce qu’on appelle une hépatosplénomégalie. Des analyses de sang ont révélé que ses enzymes hépatiques (SGPT et SGOT), qui montrent la santé du foie, étaient très élevées, indiquant un problème au foie.\n\n**Ce qu’ils ont fait pour la soigner**  \nPour aider la patiente, les médecins ont utilisé une solution saline (eau salée à 0,9 %) pour nettoyer sa bouche et hydrater ses lèvres. Cela a permis de retirer doucement les croûtes qui saignaient et de garder la bouche propre. Pour calmer l’inflammation et aider à guérir les plaies, ils ont appliqué une pommade contenant un médicament stéroïde (qui réduit l’inflammation) et une solution d’acide hyaluronique à faible concentration, qui aide à réparer les tissus. Les médicaments ont été ajustés selon les résultats des analyses et l’évolution de la patiente. Au fil du temps, son état s’est amélioré, avec moins de douleurs et une meilleure hygiène buccale.  \n\nEn résumé, cette jeune patiente souffrait de graves blessures dans la bouche liées à une maladie complexe, mais grâce à un traitement adapté et un bon suivi, elle a pu retrouver une meilleure santé buccale et générale.",
+            "B3": "Résumé détaillé et structuré pour un public non médical éduqué\n\n**Contexte**  \nUne jeune patiente de 17 ans, déjà diagnostiquée avec un lupus érythémateux disséminé (SLE, une maladie auto-immune chronique), a été adressée du service de pédiatrie au service de médecine buccale en raison de douleurs dans la bouche, de sécheresse des lèvres et de difficultés à avaler. Ces symptômes ont entraîné une incapacité à manger et à boire normalement, provoquant une faiblesse générale. Depuis trois jours, elle présentait des ulcérations (plaies ouvertes) dans la bouche, notamment une lésion douloureuse de 5 × 6 mm sur la muqueuse buccale gauche, ainsi que de nombreuses autres ulcérations sur les lèvres supérieures et inférieures, accompagnées de croûtes sanglantes. Un érythème (rougeur) a été observé au centre du palais dur, et une infection à levures (candidose pseudomembraneuse) recouvrait la langue. Par ailleurs, une hépatosplénomégalie (augmentation du volume du foie et de la rate) a été confirmée par une tomodensitométrie abdominale, avec des enzymes hépatiques élevées (SGPT à 386 U/L et SGOT à 504 U/L), indiquant une atteinte hépatique.\n\n**Principales observations**  \n- Ulcérations multiples et étendues sur la muqueuse buccale et labiale, avec croûtes hémorragiques sur les lèvres.  \n- Ulcération douloureuse significative sur la muqueuse buccale gauche, susceptible de gêner l’ouverture de la bouche et la prise alimentaire.  \n- Érythème central sur le palais dur.  \n- Candidose pseudomembraneuse sur la langue, caractérisée par une couche blanchâtre.  \n- Hépatosplénomégalie confirmée par imagerie et perturbation des enzymes hépatiques.  \n- Antécédents de lupus érythémateux disséminé, avec traitement antibiotique, antifongique, anti-inflammatoire stéroïdien et compléments nutritionnels.\n\n**Interprétation clinique**  \nLes ulcérations buccales étendues et la candidose sont probablement liées à l’état immunodéprimé de la patiente, aggravé par son lupus et les traitements médicamenteux. La sécheresse et les croûtes sur les lèvres compliquent la douleur et la fonction orale. L’hépatosplénomégalie et les anomalies enzymatiques suggèrent une atteinte systémique nécessitant une surveillance étroite. Le traitement local vise à réduire l’inflammation, favoriser la cicatrisation des ulcères et améliorer l’hygiène buccale, tandis que le traitement général prend en compte la maladie sous-jacente et ses complications.\n\n**Prochaines étapes et gestion**  \n- Nettoyage régulier de la bouche et des dents avec une gaze humidifiée au sérum physiologique (solution saline à 0,9 %) pour éliminer les croûtes et maintenir l’hydratation des lèvres, réalisé jusqu’à cinq fois par jour.  \n- Application d’un mélange topique contenant de la dexaméthasone (un corticostéroïde anti-inflammatoire) à faible dose, combinée à de la lanoline et de la gelée de pétrole, pour réduire l’inflammation des ulcérations labiales, trois fois par jour après nettoyage.  \n- Utilisation d’une solution buccale à 0,025 % d’acide hyaluronique pour apaiser l’inflammation des ulcérations difficiles d’accès.  \n- Traitement antifongique initial par suspension orale de Nystatin® pour la candidose, interrompu précocement en raison de l’atteinte hépatique.  \n- Surveillance continue de l’état général, avec ajustement des médicaments en fonction des résultats cliniques et biologiques.  \n- Conseils d’hygiène buccale stricts et suivi ambulatoire après la sortie de l’hôpital, incluant la recommandation d’extraction des racines résiduelles des dents de lait pour prévenir d’éventuelles infections.\n\nAu fil des visites, la patiente a montré une amélioration progressive de l’état buccal, avec disparition des douleurs et réduction des lésions, bien que certaines manifestations comme la chéilite (inflammation des lèvres) et la langue recouverte aient persisté temporairement. À la dernière consultation, elle ne présentait plus de plaintes et suivait correctement les soins recommandés."
+        }
+    },
+    {
+        "article": "Une fillette âgée d’un an a été adressée à notre hôpital avec un antécédent de 3 mois de diarrhée et de perte de poids. Elle était nourrie au sein et à l’aide de lait maternisé. À 6 mois, elle a commencé à manger du riz et du soja. À 8 mois, elle a commencé à manger du lait de vache et du blé. À 9 mois, elle a développé des vomissements, une diarrhée et une anorexie. Son diagnostic initial était une gastro-entérite infectieuse et un syndrome post-entérite. Un mois avant son admission à notre hôpital, elle a été admise à l’hôpital précédent parce que ses symptômes ne s’étaient pas améliorés en deux mois et que sa perte de poids progressait. Au cours des 2 mois précédant son admission, son régime alimentaire était illimité. Bien que ses vomissements aient été améliorés après quelques jours de jeûne, la prise orale de diètes élémentaires, de lait maternisé ou de porridge de riz a entraîné des diarrhées répétées. À son admission à notre hôpital, son examen physique a révélé ce qui suit : taille, 69,0 cm (écart-type [ES] : 2,2) ; poids, 6641 g (ES : 2,8) ; 999 g de moins que le poids mesuré 3 mois auparavant ; température corporelle, 37,1 °C ; fréquence cardiaque, 96 battements par minute ; et tension artérielle, 88/50 mmHg. Les résultats de ses tests sanguins étaient les suivants : nombre de globules blancs, 16 900/mL (ES : 7 000-15 000) ; pourcentage d’éosinophiles, 2,0 % (ES : < 5,6) ; hémoglobine, 9,9 g/dL (ES : 13,7-16,8) ; et nombre de plaquettes, 679 × 103 cellules/mL. Les résultats de ses tests de laboratoire étaient les suivants : protéines totales, 6,4 g/dL (ES : 6,8-8,1) ; albumine, 3,9 g/dL (ES : 4,1-5,1) ; aspartate aminotransférase, 35 IU/L (ES : 20-45) ; alanine aminotransférase, 17 IU/L (ES : 4-24) ; azote uréique sanguin, 7,4 mg/dL (ES : 8-20) ; protéine C-réactive, 0,47 mg/dL (ES : < 0,03) ; sodium, 135 mEq/L (ES : 137-147) ; potassium, 3,6 mEq/L (ES : 3,6-5,2) ; bicarbonate, 19,1 mmol/L (ES : 21,0-27,0) ; et acide lactique, 21 mg/dL (ES : 4-16) ; à ce moment, un nombre suffisant de calories, d’acides aminés et de graisses était administré par voie intraveineuse. Le taux d’IgE était de 1028 IU/mL (ES : < 30) et les tests radioallergosorbent étaient positifs pour le lait (63,7 UA/mL classe 5), la caséine (9,8 UA/mL classe 3), l’alpha-lactalbumine (51,6 UA/mL classe 5), le blanc d’œuf (58,8 UA/mL classe 5), le jaune d’œuf (10,8 UA/mL classe 3), l’ovomucoïde (13,2 UA/mL classe 3), le blé (14,5 UA/mL classe 3) et le soja (1,3 UA/mL classe 2). Les tests de piqûre cutanée n’ont pas été effectués pour confirmer les résultats des tests d’IgE spécifiques. Les taux d’Ig (IgG, 954 [NR 357-989] et IgM, 89 [NR 29-190]) et les ratios de sous-ensemble de lymphocytes étaient normaux. Les tests d’adénovirus fécaux, de rotavirus et de norovirus étaient négatifs.\n\nDes examens d'imagerie et d'endoscopie ont été réalisés pour déterminer la cause de la diarrhée prolongée. La tomodensitométrie abdominale et les examens par ultrasons n'ont révélé aucune anomalie dans l'intestin grêle ; l'intestin grêle était dilaté mais aucun épaississement de la paroi n'a été observé, ce qui suggère une entérite non spécifique. Une endoscopie digestive haute n'a révélé aucune anomalie macroscopique de l'œsophage au duodénum. Cependant, l'histopathologie de la muqueuse duodénale a révélé la perte de la structure villositaire muqueuse, une hyperplasie des cryptes, une apoptose des cryptes et une infiltration de lymphocytes et d'éosinophiles (<20 éos/hpf) dans la lamina propria, avec des abcès cryptes partiellement formés. Une coloscopie totale n'a révélé aucune anomalie macroscopique ; cependant, l'histopathologie de la muqueuse colique a révélé une érosion des muqueuses ; une cryptite avec une diminution des cellules caliciformes, une fibrose, des cellules plasmatiques et des lymphocytes ; et une infiltration de certains éosinophiles (<20 éos/hpf) dans la lamina propria. Ces résultats étaient similaires aux résultats de la muqueuse duodénale.\n\nL’auto-immunité intestinale et la maladie intestinale inflammatoire (MII) étaient suspectées ; des tests complémentaires ont donc été effectués. L’antigène de 75 kDa lié à l’auto-immunité intestinale et les anticorps anti-villosités étaient absents et aucune variante pathogène significative n’a été trouvée dans 25 gènes (couverts par l’assurance publique au Japon) liés aux MII monogéniques et à l’immunodéficience, polyendocrinopathie, syndrome lié à l’X de l’intestin (IPEX). L’EGID a été considérée dans le diagnostic différentiel, mais un diagnostic de FPE a finalement été suspecté sur la base des caractéristiques de la muqueuse intestinale, telles que l’atrophie des villosités de la muqueuse intestinale, l’hyperplasie des cryptes, l’infiltration d’éosinophiles en dessous des critères diagnostiques de l’EGID (<20 eos/hpf), et l’infiltration de lymphocytes. Le nombre d’éosinophiles dans le sang périphérique n’était pas élevé non plus. Une MII non IgE-GIFA atypique (7) a été suspectée (positive pour les IgE spécifiques) (7). Sa diarrhée a disparu après un traitement par prednisolone (PSL) (1 mg/kg) et l’élimination complète du lait maternisé, du lait de vache et des œufs de poule de son alimentation. Aucune rechute n’a eu lieu, même après l’arrêt du PSL un mois plus tard. Les effets indésirables dus au traitement à long terme par PSL, tels que l’hypertension, ne se sont pas produits. Cinq mois après l’arrêt du PSL oral et l’élimination complète du lait maternisé, du lait de vache et des œufs de poule de son alimentation, l’histopathologie du duodénum a révélé une structure villositaire normale et une disposition des conduits bien différenciée. Trois mois après la deuxième EGD, elle a recommencé à manger des œufs de poule sans éprouver de symptômes gastro-intestinaux tels que diarrhée et vomissements ; cependant, trois mois plus tard, ses symptômes, y compris les douleurs abdominales et la diarrhée, ont réapparu en quelques jours après la reprise de la consommation de lait de vache. Sur la base des résultats susmentionnés, la FPE a été diagnostiquée, et le lait de vache était soupçonné d’être la source de l’allergie. À 2 ans et 3 mois, sa taille était passée à 81,5 cm (SD −1,4) et son poids à 11,4 kg (SD +0,33) sans éprouver de symptômes gastro-intestinaux.\n",
+        "gold_summary": "Nous décrivons le cas d’une fille de 1 an atteinte d’une entéropathie induite par les protéines alimentaires (EIP) qui était difficile à diagnostiquer. Elle a été adressée à notre hôpital avec un historique de 3 mois de diarrhée, de vomissements et de perte de poids. Bien que sa diarrhée ait diminué après quelques jours de jeûne, la prise orale de régimes alimentaires élémentaires, de lait maternisé ou de porridge de riz a entraîné des rechutes répétées. Le taux d’IgE sérique était de 1028 IU/mL, et les tests radioallergosorbents étaient positifs pour le lait, la caséine, l’alpha-lactalbumine et d’autres allergènes. Une histopathologie de la muqueuse duodénale a révélé une perte de la structure villose de la muqueuse, une hyperplasie des cryptes, une apoptose des cryptes et une infiltration de lymphocytes et d’éosinophiles (<20 éos/hpf) dans la lamina propria. Après un traitement par prednisolone (PSL) et l’élimination complète du lait de vache et des œufs de poule de son régime alimentaire, la diarrhée de la patiente a disparu. Cinq mois après l’arrêt du PSL oral et l’élimination complète du lait de vache et des œufs de poule, le duodénum présentait une structure villose muqueuse normale et des conduits bien différenciés. Aucune anomalie n’a été observée lors d’une nouvelle exposition aux œufs ; toutefois, la diarrhée a réapparu après la nouvelle exposition au lait de vache.\n",
+        "synthetic_summary": {
+            "B1": "Il y a une petite fille qui avait mal au ventre et faisait beaucoup caca mou. Elle perdait du poids et ne se sentait pas bien. Quand elle ne mangeait rien, ça allait un peu mieux. Mais quand elle buvait du lait ou mangeait du riz, elle avait encore mal.\n\nLes docteurs ont fait des tests. Ils ont vu que son corps n’aimait pas le lait et les œufs. Son ventre était un peu malade à l’intérieur. \n\nLes docteurs lui ont donné un médicament doux et ont enlevé le lait et les œufs de sa nourriture. Alors, elle a commencé à aller mieux. \n\nAprès un moment, elle a pu manger des œufs sans problème. Mais quand elle a bu du lait encore, elle a eu mal au ventre et beaucoup de caca mou. \n\nLes docteurs ont compris que c’est le lait qui la rend malade. Maintenant, elle va mieux sans lait.",
+            "B2": "**Ce qu’ils ont observé chez la fillette**  \nUne petite fille d’un an avait depuis trois mois une diarrhée, des vomissements et elle perdait du poids. Même si sa diarrhée s’améliorait quand elle ne mangeait rien pendant quelques jours, elle revenait dès qu’elle reprenait certains aliments comme le lait maternisé, le porridge de riz ou des régimes spéciaux.  \n\nLes médecins ont fait des analyses de sang qui ont montré qu’elle avait beaucoup d’anticorps appelés IgE, qui sont souvent liés aux allergies. Ils ont aussi trouvé qu’elle était allergique à plusieurs aliments, notamment au lait de vache et aux œufs.  \n\n**Ce qu’ils ont trouvé dans son intestin**  \nEn regardant de près la muqueuse de son intestin (la couche qui absorbe les aliments), ils ont vu que les petites structures appelées villosités, qui aident à absorber les nutriments, étaient abîmées. Ils ont aussi vu des signes d’inflammation avec des cellules du système immunitaire appelées lymphocytes et éosinophiles, mais en nombre modéré.  \n\n**Le traitement et ce que cela signifie**  \nLa fillette a reçu un médicament anti-inflammatoire appelé prednisolone et on lui a enlevé complètement le lait de vache et les œufs de son alimentation. Après cela, sa diarrhée a disparu. Cinq mois après avoir arrêté le médicament et toujours sans lait ni œufs, son intestin avait retrouvé une apparence normale.  \n\nElle a pu recommencer à manger des œufs sans problème, mais quand elle a repris le lait de vache, la diarrhée est revenue rapidement.  \n\n**Conclusion**  \nLes médecins ont donc conclu que cette fillette souffrait d’une maladie appelée entéropathie induite par les protéines alimentaires (EIP). Cela signifie que son intestin réagissait mal à certaines protéines dans les aliments, surtout celles du lait de vache, ce qui causait ses symptômes. En évitant ces aliments et avec un traitement adapté, elle a pu guérir et grandir normalement.",
+            "B3": "**Contexte**  \nNous rapportons le cas d’une fillette d’un an présentant une entéropathie induite par les protéines alimentaires (EIP), une affection rare et difficile à diagnostiquer. Elle a été hospitalisée après trois mois de diarrhée persistante, de vomissements et de perte de poids progressive. Son alimentation comprenait initialement du lait maternel et du lait maternisé, puis des aliments solides comme le riz, le soja, le lait de vache et le blé. Les symptômes ont débuté à 9 mois, avec des épisodes répétés de diarrhée et de vomissements, initialement attribués à une gastro-entérite infectieuse.\n\n**Principales observations**  \nAprès un jeûne de quelques jours, la diarrhée s’est temporairement améliorée, mais la réintroduction de régimes oraux, incluant des diètes élémentaires, du lait maternisé ou du porridge de riz, a provoqué des rechutes. À l’admission, la patiente présentait un retard de croissance marqué avec une perte de près d’un kilogramme en trois mois. Les analyses sanguines ont montré une anémie modérée, une légère inflammation (protéine C-réactive élevée), une hypoalbuminémie (faible taux d’albumine) et une acidose métabolique légère (bicarbonates bas). Le taux d’immunoglobuline E (IgE), un marqueur d’allergie, était très élevé (1028 IU/mL, valeur normale <30), et des tests spécifiques ont révélé une sensibilisation importante à plusieurs allergènes alimentaires, notamment le lait de vache, ses protéines (caséine, alpha-lactalbumine), les œufs, le blé et le soja.\n\nLes examens d’imagerie abdominale n’ont pas montré d’anomalies structurelles majeures. L’endoscopie digestive haute a révélé une muqueuse duodénale sans anomalies visibles à l’œil nu, mais l’analyse microscopique a mis en évidence une atrophie des villosités (structures en forme de doigts qui augmentent la surface d’absorption dans l’intestin), une hyperplasie des cryptes (augmentation du nombre de cellules dans les glandes intestinales), une apoptose (mort cellulaire programmée) des cryptes, ainsi qu’une infiltration modérée de lymphocytes et d’éosinophiles (un type de globules blancs impliqués dans les réactions allergiques) dans la lamina propria (tissu de soutien de la muqueuse). La coloscopie a montré des lésions inflammatoires similaires au niveau du côlon, sans signes d’infection virale ni d’autres causes inflammatoires classiques.\n\nDes investigations complémentaires ont exclu une maladie inflammatoire chronique de l’intestin (MICI) et des troubles auto-immuns intestinaux, ainsi que des maladies génétiques associées à des déficits immunitaires ou à des syndromes auto-immuns. Le diagnostic différentiel a également considéré une gastro-entérite à éosinophiles (EGID), mais le faible nombre d’éosinophiles dans les tissus et dans le sang ne correspondait pas aux critères de cette maladie.\n\n**Interprétation clinique**  \nLe tableau clinique, biologique et histologique a conduit au diagnostic d’entéropathie protéino-induite (EIP), une forme d’allergie alimentaire non médiée uniquement par les IgE, caractérisée par une inflammation chronique de la muqueuse intestinale et une malabsorption. La forte élévation des IgE spécifiques au lait et aux œufs, ainsi que la réponse favorable au traitement, ont confirmé ce diagnostic. La patiente a reçu une corticothérapie par prednisolone à la dose de 1 mg/kg, associée à l’élimination complète du lait de vache, du lait maternisé et des œufs de son alimentation.\n\n**Prochaines étapes et évolution**  \nLa diarrhée a rapidement disparu sous traitement. Cinq mois après l’arrêt de la corticothérapie et le maintien de l’éviction alimentaire, une nouvelle endoscopie a montré une restauration complète de la structure villositaire duodénale. La réintroduction des œufs n’a pas provoqué de symptômes, tandis que la reprise du lait de vache a entraîné une récidive rapide des symptômes digestifs, confirmant que le lait était le principal allergène responsable. À l’âge de 2 ans et 3 mois, la croissance de la fillette s’était normalisée, avec un poids et une taille dans les normes, et sans symptômes gastro-intestinaux.\n\nCe cas illustre l’importance d’envisager une entéropathie induite par les protéines alimentaires chez les jeunes enfants présentant une diarrhée chronique et une malabsorption, surtout en présence d’une sensibilisation allergique confirmée. Le diagnostic repose sur l’association des données cliniques, biologiques, histologiques et la réponse au traitement d’éviction et corticostéroïde."
+        }
+    },
+    {
+        "article": "Un homme de 63 ans a été admis à notre service d'urgence avec des antécédents d'hématurie fréquente. L'examen physique n'a révélé aucun problème et son taux de créatinine sérique était normal, avec une créatinine sérique de 1,2 mg/dL. Une tomographie par ordinateur (CT) a révélé une croissance vésicale infiltrative étendue, principalement sur la paroi latérale droite et la voûte, avec une hydrourénonefrose gauche modérée et une insuffisance rénale droite due à une obstruction haute pression du côté gauche. Une tomographie par ordinateur (CT) a été programmée pour une cystoscopie diagnostique avec biopsie transurétrale. Cependant, il s'est présenté à l'urgence avant la date prévue d'admission avec une instabilité hémodynamique, une distension abdominale et une difficulté respiratoire, pour laquelle une assistance ventilatoire et inotrope était nécessaire. Son panel biochimique a montré une créatinine élevée (20 mg/dL), une hyperkaliémie (9 mEq/L) et une hyponatrémie (128 mEq/L), et sa gazométrie a montré une acidose métabolique sévère (pH 7,1). Après avoir interrogé les soignants du patient, un historique d'oligurie avec distension abdominale progressive au cours des 2 derniers jours a été obtenu, pour lequel il avait été soumis à une ponction de fluide « ascitique » dans un centre externe. Des mesures anti-hyperkaliémiques ont été initiées. Une échographie au chevet a montré une hydrourénonefrose gauche avec une hydrourénonefrose droite sévère et un fluide libre dans l'abdomen. Compte tenu de l'instabilité hémodynamique et de l'absence de dialyse dans nos installations, il a été décidé de procéder à une néphrostomie d'urgence au chevet, insérée dans le rein gauche fonctionnant seul. Sous guidage par ultrasons, une néphrostomie percutanée (NPC) a été insérée au chevet et l'état général du patient s'est amélioré. Il y a eu une diurèse initiale avec une chute du taux de créatinine à un nadir de 2 mg/dL. En raison des taux élevés de créatinine, la tomographie a été répétée après 4 jours de ponction de fluide et, à notre grande surprise, nous avons remarqué que la pointe du cathéter en forme de queue de cochon se trouvait dans l'espace péréphrénique gauche agissant comme un drain percutané avec résolution complète du fluide libre dans l'abdomen. La chronologie des événements d'une créatinine sérique initialement extrêmement élevée qui avait diminué de manière spectaculaire après le drainage du fluide extravasé, s'est ajustée à un tableau clinique de pseudo insuffisance rénale due à l'absorption d'urine extravasée. Nous avons émis l'hypothèse que la source de l'urine extravasée était très probablement une rupture du fornix rénal en raison d'une obstruction haute pression du côté gauche. Compte tenu de la créatinine sérique encore élevée et de la sortie graduellement décroissante du cathéter en forme de queue de cochon, un NPC a été inséré dans le système de collecte sous guidage fluoroscopique, suivi d'une normalisation de sa créatinine. Un néfrogramme par CT avec cystogram a été réalisé dans la suite et a montré une obstruction urétérale distale gauche et une vessie petite et intacte, excluant une perforation de la vessie. Une biopsie par cystoscopie de la croissance de la vessie a confirmé qu'il s'agissait d'un carcinome épidermoïde invasif musculaire. Nous avons expliqué le diagnostic et le pronostic au patient et avons effectué une laparotomie exploratoire 2 semaines après la biopsie. Au cours de l'opération, une réaction démoplastique dense a été observée autour de la vessie, qui a été rétrécie et collée aux parois latérales pelviennes et à l'os pubien. En raison de la nature inopérable de la maladie, le plan de cystectomie radicale a été abandonné et une dérivation palliative du conduit iléal a été réalisée sous guidage fluoroscopique, suivie d'une normalisation de sa créatinine. Le patient a bien récupéré après l'opération et a été libéré 5 jours plus tard. Cependant, il a développé de multiples métastases thoraciques au cours des mois suivants et son état général s'est détérioré de façon constante, ce qui a entraîné sa mort 3 mois après l'opération en raison d'une cachexie.\n",
+        "gold_summary": "Nous rapportons un cas de carcinome de la vessie qui a présenté des caractéristiques similaires à une insuffisance rénale aiguë, et qui s'est révélé plus tard être une pseudo-insuffisance rénale due à un écoulement urinaire intrapéritonéal d'une rupture du fornix rénal. Le patient a été traité en urgence avec un drainage percutané suivi d'une néphrostomie percutanée, ce qui a conduit à une normalisation de la créatinine. La cystoscopie a révélé une croissance de la vessie dans une vessie intacte de faible capacité, confirmée par biopsie comme étant un carcinome épidermoïde invasif musculaire. En raison de la nature avancée de sa malignité, il a été soumis à une dérivation de l'intestin grêle palliative, mais a ensuite développé des métastases thoraciques et a fini par succomber à la maladie.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur avait un gros problème avec sa vessie. Son corps faisait comme s’il avait un gros souci aux reins.  \n\nEn fait, de l’urine fuyait dans son ventre à cause d’un petit trou dans un rein. Cela faisait croire que ses reins ne marchaient plus bien.  \n\nLes docteurs ont mis un petit tuyau pour faire sortir l’urine et aider ses reins. Après, il allait un peu mieux.  \n\nIls ont regardé dans sa vessie et ont trouvé une grosseur qui n’était pas bonne. C’était un gros malade dans la vessie.  \n\nComme c’était très grave, ils ont fait une opération pour aider un peu, mais le monsieur est devenu très malade après.  \n\nIl est parti au ciel quelques mois plus tard. Les docteurs ont tout fait pour l’aider.",
+            "B2": "**Résumé simplifié pour un adolescent de 14 ans**\n\nUn homme de 63 ans avait du sang dans ses urines et des problèmes pour uriner. Des examens ont montré une grosseur dans sa vessie, mais aussi que ses reins ne fonctionnaient pas bien à cause d’un blocage. Il est arrivé à l’hôpital en très mauvais état, avec des reins presque arrêtés et un liquide qui s’était accumulé dans son ventre.\n\nLes médecins ont découvert que ce liquide était en fait de l’urine qui fuyait à cause d’une petite rupture dans un rein. Cette fuite a fait croire que ses reins étaient très malades, alors qu’en réalité, c’était une « fausse insuffisance rénale » causée par l’urine qui s’était répandue dans le ventre.\n\nPour l’aider, ils ont mis un drain dans son rein pour évacuer l’urine et cela a amélioré son état rapidement. Ensuite, ils ont confirmé que la grosseur dans sa vessie était un cancer appelé carcinome épidermoïde, un type agressif qui envahit les muscles de la vessie.\n\nComme le cancer était trop avancé pour être enlevé complètement, les médecins ont fait une opération pour créer un passage artificiel permettant à l’urine de sortir autrement, afin de soulager le patient. Malheureusement, malgré ces soins, le cancer s’est propagé aux poumons et l’homme est décédé trois mois plus tard.\n\nCe cas montre qu’un problème grave aux reins peut parfois cacher une fuite d’urine due à une rupture, et qu’un cancer de la vessie peut causer des complications très sérieuses.",
+            "B3": "Résumé structuré pour un public non médical éduqué\n\nContexte  \nUn homme de 63 ans a été admis à l’hôpital pour des épisodes répétés de sang dans les urines (hématurie). Initialement, ses examens sanguins montraient une fonction rénale normale. Une tomodensitométrie (scanner) a révélé une masse suspecte infiltrant la paroi de la vessie, ainsi qu’une obstruction des voies urinaires entraînant une accumulation d’urine dans les reins (hydrourénonefrose), particulièrement du côté gauche.\n\nPrincipales observations  \nAvant une procédure prévue pour biopsier la masse vésicale, le patient s’est présenté en urgence dans un état critique : instabilité circulatoire, abdomen distendu et difficultés respiratoires. Ses analyses sanguines montraient une insuffisance rénale sévère (créatinine très élevée), des troubles électrolytiques graves (hyperkaliémie et hyponatrémie) et une acidose métabolique. L’échographie a confirmé une obstruction bilatérale des reins avec présence de liquide libre dans l’abdomen. Une ponction de ce liquide avait été réalisée auparavant, mais sans diagnostic clair.  \n\nInterprétation clinique  \nL’état du patient s’est amélioré après la mise en place en urgence d’un drainage percutané du rein gauche (néphrostomie), qui a permis d’évacuer l’urine accumulée. La chute rapide de la créatinine suggérait que l’insuffisance rénale initiale était en réalité une « pseudo-insuffisance » causée par l’absorption d’urine s’étant échappée dans l’abdomen à la suite d’une rupture du fornix rénal (une partie du rein). Une nouvelle imagerie a confirmé que le cathéter de drainage avait également permis de drainer ce liquide abdominal. Par la suite, une obstruction de l’uretère gauche (le canal reliant le rein à la vessie) a été identifiée, ainsi qu’une vessie de petite taille mais intacte, excluant une perforation de la vessie. La biopsie de la masse vésicale a confirmé un carcinome épidermoïde invasif, une forme agressive de cancer de la vessie.\n\nProchaines étapes et évolution  \nEn raison de l’extension locale importante de la tumeur, une chirurgie radicale de la vessie n’a pas été possible. Une dérivation palliative par un conduit iléal (utilisation d’un segment d’intestin pour détourner l’urine) a été réalisée afin de restaurer l’écoulement urinaire. Le patient a initialement bien récupéré, mais a développé par la suite des métastases pulmonaires, témoignant de la dissémination du cancer. Son état s’est progressivement détérioré, conduisant à son décès trois mois après l’intervention, principalement en raison d’une cachexie (affaiblissement général sévère lié au cancer).  \n\nConclusion  \nCe cas illustre une présentation rare d’un cancer de la vessie compliqué par une pseudo-insuffisance rénale due à une fuite d’urine dans l’abdomen provoquée par la rupture du rein. La prise en charge d’urgence par drainage a permis une amélioration temporaire, mais la maladie cancéreuse avancée a conduit à une évolution défavorable."
+        }
+    },
+    {
+        "article": "La patiente, une femme de 56 ans, a été admise pour « 10 jours de ptosis du côté droit et 1 jour de ptosis du côté gauche ». Il y a 10 jours, la patiente n’avait pas de ptosis du côté droit évident et aucune restriction de mouvement du côté gauche, accompagnée de douleurs pariétales et occipitales, pas de nausées, pas de vomissements, pas de vertiges, pas de marche instable, pas de sensation de coton dans les pieds, pas de mots prononcés, pas de suffocation ou de toux en buvant de l’eau. La patiente a été traitée à l’extérieur de l’hôpital et a présenté des examens pertinents pour considérer le diagnostic d’« anévrisme cérébral ». Il y a 1 jour, la ptosis du côté droit de la patiente s’est aggravée, elle a donc été envoyée au service de neurochirurgie de notre hôpital. Antécédents médicaux : pas d’antécédents d’hypertension, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies 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vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de maladies vasculaires, pas d’antécédents de\n",
+        "gold_summary": "Une patiente de 56 ans a été admise à l'hôpital pour « 10 jours de chute de l'œil droit et 1 jour d'aggravation ». Après admission, l'examen physique a révélé que la patiente souffrait d'une scoliose sévère. La reconstruction 3D et le scanner CT amélioré des vaisseaux de la tête ont montré que les anévrismes de l'artère carotide interne droite C6 avaient été découpés sous anesthésie générale. Après l'opération, la patiente avait une pression artérielle élevée, avec un grand nombre de crachats en mousse rose attirés par le cathéter de la trachée, et les poumons étaient disséminés avec des râles humides lors de l'auscultation. Après le traitement de l'insuffisance cardiaque, la patiente est retournée à l'unité de soins intensifs par le cathéter de la trachée. Huit heures plus tard, le cathéter de la trachée a été retiré et la patiente a été libérée du ventilateur. Les symptômes ont été soulagés le cinquième jour après l'opération.\n",
+        "synthetic_summary": {
+            "B1": "Une dame avait un problème avec son œil qui tombait. Elle est allée à l’hôpital pour se faire soigner.\n\nLes docteurs ont regardé dans sa tête avec une machine spéciale. Ils ont trouvé un petit ballon dans un vaisseau. C’était dangereux, alors ils ont fait une opération pour le réparer.\n\nAprès l’opération, elle a eu un peu de mal à respirer. Les docteurs l’ont aidée à respirer avec un petit tuyau. Puis, elle a pu respirer toute seule.\n\nAu bout de quelques jours, elle allait mieux et son œil est redevenu normal. Les docteurs étaient contents car elle se sentait mieux.",
+            "B2": "Voici un résumé simple et clair de ce cas médical, adapté pour un élève de 14 ans en cours de biologie :\n\n**Ce qu’ils ont observé chez la patiente**  \nUne femme de 56 ans est venue à l’hôpital parce que ses paupières tombaient, surtout du côté droit, depuis 10 jours. Cela signifie qu’elle avait du mal à ouvrir ses yeux normalement. En plus, son état s’est un peu aggravé juste avant son arrivée à l’hôpital. Lors de l’examen, les médecins ont aussi remarqué qu’elle avait une scoliose, c’est-à-dire une courbure anormale de la colonne vertébrale.\n\n**Ce qu’ils ont découvert grâce aux examens**  \nLes médecins ont fait un scanner spécial en 3D pour regarder les vaisseaux sanguins dans sa tête. Ils ont trouvé des anévrismes sur une grosse artère appelée artère carotide interne droite. Un anévrisme est une sorte de « ballon » qui se forme sur un vaisseau sanguin et qui peut être dangereux s’il éclate.\n\n**Le traitement et ce qui s’est passé après**  \nLa patiente a subi une opération sous anesthésie générale pour réparer ces anévrismes. Après l’opération, elle a eu une pression artérielle élevée et des problèmes aux poumons, avec des crachats mousseux qui sortaient par un tube placé dans sa trachée (le tube qui permet de respirer). Les médecins ont diagnostiqué une insuffisance cardiaque, ce qui veut dire que son cœur avait du mal à bien fonctionner. Ils l’ont soignée pour cela et elle a été placée en soins intensifs avec un ventilateur pour l’aider à respirer.\n\n**L’évolution de la patiente**  \nHuit heures après, le tube dans sa trachée a été retiré et elle a pu respirer toute seule sans ventilateur. Cinq jours après l’opération, ses symptômes s’étaient beaucoup améliorés.\n\nEn résumé, cette patiente avait des problèmes sérieux avec ses vaisseaux sanguins dans la tête, ce qui a causé la chute de ses paupières. Grâce à une opération et des soins après, elle a pu se rétablir progressivement.",
+            "B3": "Résumé destiné à un adulte éduqué non-médecin\n\nContexte  \nUne femme de 56 ans a été admise en raison d’un ptosis (chute de la paupière) du côté droit depuis dix jours, avec une aggravation récente et une apparition d’un ptosis du côté gauche depuis un jour. Elle ne présentait pas d’autres symptômes neurologiques majeurs ni antécédents médicaux significatifs, notamment pas d’hypertension ni de maladies vasculaires. Des examens initiaux avaient été réalisés pour exclure un anévrisme cérébral.\n\nPrincipales observations  \nÀ l’hôpital, un examen physique a révélé une scoliose sévère (déformation de la colonne vertébrale). Des examens d’imagerie, incluant une reconstruction en 3D et un scanner avec injection de produit de contraste des vaisseaux cérébraux, ont permis d’identifier un anévrisme au niveau de l’artère carotide interne droite, segment C6. La patiente a été opérée sous anesthésie générale pour traiter cet anévrisme.  \n\nAprès l’intervention, la patiente a présenté une hypertension artérielle ainsi que des signes d’insuffisance cardiaque aiguë, notamment une expectoration abondante de mousse rose par le cathéter de la trachée, signe d’œdème pulmonaire. L’auscultation pulmonaire a révélé des râles humides diffus, témoignant d’une congestion pulmonaire. Un traitement adapté à l’insuffisance cardiaque a été instauré, et la patiente a été prise en charge en unité de soins intensifs avec ventilation mécanique via un cathéter trachéal.  \n\nInterprétation clinique  \nL’anévrisme de l’artère carotide interne était responsable des symptômes initiaux de ptosis, probablement par compression nerveuse ou complications vasculaires. La survenue d’une insuffisance cardiaque post-opératoire, avec œdème pulmonaire, a nécessité une prise en charge urgente en soins intensifs.  \n\nProchaines étapes et évolution  \nHuit heures après l’admission en soins intensifs, le cathéter trachéal a pu être retiré, et la patiente a été sevrée de la ventilation mécanique. Les symptômes neurologiques se sont améliorés progressivement, avec un soulagement notable dès le cinquième jour post-opératoire. La surveillance et la rééducation neurologique restent essentielles pour optimiser la récupération."
+        }
+    },
+    {
+        "article": "Femme de 69 ans, ayant des antécédents d'hypertension, de diabète sucré insulinodépendant, de céphalées chroniques et de tabagisme. Elle a rapporté une semaine plus tôt des maux de tête, des troubles de la conscience et des vomissements. L'examen en salle d'urgence a révélé un coma (échelle de coma de Glasgow à 5), une raideur de la nuque et une absence de réflexe pupillaire.\n\nLa tomographie par ordinateur (CT) a montré une HSA diffuse, une hémorragie intra-ventriculaire légère et une hydrocéphalie. L'angiographie par tomographie par ordinateur a montré un anévrisme de l'artère carotide interne supraclinoïde à droite. Une fois admise dans l'unité de soins intensifs (USI), elle a reçu un traitement avec ventilation mécanique invasive, acide tranexamique, nimodipine et VPA entérale (400 mg, trois fois par jour). Un drainage lombaire externe et une embolisation endovasculaire de l'anévrisme ont été effectués, sans preuve de vasospasme angiographique. La tomographie par ordinateur initiale a montré une hydrocéphalie, et un drainage ventriculaire externe a été effectué.\n\nEn guise de complication initiale, la patiente a développé une dysfonction neurocardiogénique, avec un électrocardiogramme montrant des modifications diffuses de la repolarisation et une troponine élevée (716 ng/mL). L'échocardiographie transthoracique a montré une dysfonction systolique (fraction d'éjection du ventricule gauche de 35 %) et des anomalies régionales de la contractilité parietale, qui ont été interprétées comme une cardiomyopathie de stress. Pendant son séjour en unité de soins intensifs, malgré le retrait de la sédation, la patiente est restée dans le coma (échelle de coma de Glasgow à 5 au sixième jour). Les tomographies ultérieures ont été négatives pour une hydrocéphalie, des lésions ischémiques ou d'autres complications.\n\nLes fonctions hépatique, rénale et thyroïdienne étaient normales, et elle ne présentait pas de troubles hydroélectrolytiques. Aucune complication extraneurologique n'a été trouvée. Le drainage ventriculaire externe a été retiré avec des cultures stériles. Le Doppler transcrânien était négatif pour le vasospasme et a montré un taux de pulsatilité normal. L'IRM n'a pas détecté d'anomalies. L'EEG standard a exclu les modèles ictal, mais a montré un modèle de DPG à prédominance frontale, caractérisé par un modèle de décharge périodique continue, une morphologie triphasée et une absence de fluctuation spontanée, comme on le voit dans les dysfonctions cérébrales toxiques et/ou métaboliques. (4) Compte tenu de ces résultats, la dose de VPA était de 65,3 µg/mL (plage thérapeutique de 50 - 100 µg/mL), et la dose d'ammoniac était de 160,2 µg/mL (plage normale de 18,7 - 86,0 µg/mL). Il n'y avait pas de défaillance hépatique ou de saignement gastro-intestinal. L'administration de VPA a ensuite été arrêtée, et un traitement pour hyperammonémie avec lactulose et une diète restreinte en protéines a été initié. Le taux d'ammoniac a diminué progressivement jusqu'à la normalisation (81,7 µg/mL), ce qui a été corrélé à une amélioration neurologique, comme en témoigne la réponse au commandement le jour 12.\n\nLes EEG suivants ont progressivement amélioré jusqu'à la normale. La patiente a eu besoin d'une trachéotomie pour retirer la ventilation mécanique et a présenté une fistule trachéo-œsophagienne comme complication. Elle a fini par décéder 85 jours après son admission.\n",
+        "gold_summary": "Nous rapportons le cas d'un patient ayant présenté une hémorragie sous-arachnoïdienne et ayant reçu une prophylaxie anticonvulsivante avec du valproate, qui a connu une aggravation neurologique associée à des taux plasmatiques élevés d'ammoniac et des décharges périodiques sur l'électroencéphalogramme, sans autre cause identifiable. L'arrêt du traitement par l'acide valproïque et la normalisation des taux plasmatiques d'ammoniac ont entraîné une amélioration du tableau neurologique et électroencéphalographique.\n",
+        "synthetic_summary": {
+            "B1": "Une dame très malade avait du sang dans sa tête. Elle a pris un médicament pour l’aider. Mais ce médicament a rendu son cerveau encore plus fatigué. \n\nLes docteurs ont arrêté ce médicament. Alors, elle a commencé à aller un peu mieux. Son cerveau a pu se reposer et se sentir mieux.",
+            "B2": "Cas d'une femme de 69 ans avec une hémorragie sous-arachnoïdienne (c’est-à-dire un saignement autour du cerveau). Elle a reçu un médicament appelé valproate (utilisé pour prévenir les crises d’épilepsie). Après ce traitement, son état neurologique s’est aggravé. Les médecins ont découvert que son sang contenait beaucoup trop d’ammoniac, une substance qui peut être toxique pour le cerveau. Son électroencéphalogramme (un examen qui mesure l’activité électrique du cerveau) montrait des anomalies appelées décharges périodiques.\n\nAucune autre cause n’a été trouvée pour expliquer cette détérioration. Quand les médecins ont arrêté le valproate et commencé un traitement pour faire baisser l’ammoniac, l’état de la patiente s’est amélioré. Son cerveau a retrouvé une activité électrique plus normale, et ses fonctions neurologiques ont progressé. Ce cas montre que le valproate peut parfois provoquer une accumulation d’ammoniac, ce qui peut aggraver la santé du cerveau. Il est donc important de surveiller ce risque chez les patients traités.",
+            "B3": "Résumé détaillé et structuré\n\nContexte  \nNous présentons le cas d’une femme de 69 ans, avec des antécédents médicaux importants incluant une hypertension artérielle, un diabète sucré insulinodépendant, des céphalées chroniques et un tabagisme. Elle a été admise en urgence dans un état de coma sévère, suite à une hémorragie sous-arachnoïdienne (HSA) diffuse associée à un anévrisme de l’artère carotide interne droite, confirmée par imagerie. La prise en charge initiale a inclus une ventilation mécanique, un traitement médicamenteux comprenant notamment du valproate de sodium (VPA) à visée prophylaxique anticonvulsivante, ainsi que des interventions neurochirurgicales pour drainer l’hydrocéphalie et emboliser l’anévrisme.\n\nPrincipales observations  \nAu cours de son séjour en unité de soins intensifs, la patiente a développé une dysfonction neurocardiogénique caractérisée par une altération de la fonction cardiaque, sans toutefois présenter d’autres complications neurologiques majeures visibles à l’imagerie. Malgré le sevrage de la sédation, elle est restée dans un coma profond. L’électroencéphalogramme (EEG) a révélé un pattern de décharges périodiques généralisées à prédominance frontale, avec une morphologie triphasée, typique des dysfonctions cérébrales toxiques ou métaboliques. Parallèlement, des analyses biologiques ont montré une hyperammoniémie importante (taux d’ammoniac plasmatique élevé) en l’absence de défaillance hépatique ou d’autres causes évidentes. La concentration plasmatique de valproate était dans la plage thérapeutique.\n\nInterprétation clinique  \nL’association d’un coma prolongé, d’un EEG anormal avec décharges périodiques triphasées, et d’une hyperammoniémie sans autre cause identifiée, suggère une encéphalopathie induite par le valproate. Ce médicament, utilisé ici pour prévenir les crises épileptiques, peut provoquer une élévation toxique de l’ammoniac, entraînant une altération neurologique sévère. L’absence d’autres complications hépatiques ou métaboliques renforce cette hypothèse.\n\nProchaines étapes  \nL’arrêt du valproate a été décidé, accompagné d’un traitement spécifique de l’hyperammoniémie par lactulose et d’une restriction protéique dans l’alimentation. Cette prise en charge a permis une diminution progressive du taux d’ammoniac sanguin, corrélée à une amélioration clinique notable, avec une reprise de la conscience partielle et une normalisation progressive des tracés EEG. Malgré ces améliorations, la patiente a présenté des complications liées à sa prise en charge prolongée, notamment une fistule trachéo-œsophagienne, et est décédée environ trois mois après son admission.\n\nConclusion  \nCe cas illustre l’importance de surveiller l’apparition d’une encéphalopathie hyperammoniémique chez les patients traités par valproate, même en l’absence d’insuffisance hépatique. La reconnaissance précoce de cette complication et l’arrêt rapide du médicament peuvent permettre une récupération neurologique partielle ou complète."
+        }
+    },
+    {
+        "article": "Un homme de 48 ans a été transféré dans notre hôpital depuis un établissement psychiatrique pour somnolence, ataxie cérébelleuse et dysarthrie de trois jours. Il n'avait pas eu de fièvre au cours du mois précédent. Il a déclaré avoir sniffé de l'escitalopram et du clonazépam dans les jours précédents, ainsi que du disulfirame par voie intranasale (1 à 2 g par jour avec une dose maximale de 10 g par jour dans les 48 heures précédentes) au cours des deux derniers mois à des fins récréatives.\n\nIl avait des antécédents de tension artérielle élevée non traitée et de schizophrénie paranoïde, qui avaient entraîné trois hospitalisations pour exacerbation en raison de l'absence de traitement. Il prenait de l'olanzapine 10 mg/8 heures et du paliperidone 100 mg par voie intramusculaire mensuelle pour la schizophrénie, ainsi que du clonazépam 0,5 mg/24 heures et de l'escitalopram 15 mg/24 heures. Il était également sous traitement par disulfiram 250 mg par voie orale par jour pour son alcoolisme chronique, malgré un mode de consommation actif.\n\nLors de l'arrivée aux urgences, la fréquence respiratoire était de 20 respirations/minute, la saturation en oxygène dans l'air ambiant était de 98 %, la fréquence cardiaque de 85 battements/minute, la pression artérielle de 177/100 mmHg et la température de 36,2 °C. Le patient était stupéfié et désorienté, avec une échelle de coma de Glasgow de 13/15. L'examen cardiovasculaire, respiratoire et abdominal était anodin. L'examen neurologique a mis en évidence des pupilles myotiques hyporéactives, un clignement abondant, une dysarthrie marquée et une démarche instable. Il n'y avait aucun signe clinique d'hypertension intracrânienne ou d'irritation méningée.\n\nL'analyse sanguine a révélé une acidose métabolique hyperchlorémique (pH : 7,28 ; bicarbonate réel : 16,4 mmol/L), une polyglobulie et une macrocytose. La fonction rénale et le profil hépatique étaient normaux. Aucune autre constatation d'intérêt n'a été trouvée. L'étude toxicologique a été négative pour l'éthanol, le méthanol et l'éthylène glycol. Le dépistage des toxines dans l'urine par immunodosage a été positif pour les benzodiazépines. La tomographie par ordinateur a révélé des hypodensités symétriques légères non spécifiques des noyaux pâles et des bras postérieurs des capsules internes, une atrophie cérébrale et des infarctus lacunaires chroniques.\n\nSoupçonnant que l’encéphalopathie du patient était liée à une intoxication médicamenteuse (probablement par des benzodiazépines), sans pouvoir exclure d’autres possibilités diagnostiques, il a été admis en salle d’hospitalisation. Cette première hypothèse reposait sur le fait qu’il s’agissait d’un syndrome hypnotique-sédatif chez un patient ayant déclaré avoir consommé des benzodiazépines et ayant présenté un résultat positif à un examen qualitatif des urines.\n\nLes taux plasmatiques de diazepam, de nordiazepam et de clonazépam ont été demandés, tous dans la plage thérapeutique ou infrathérapeutique (72 ng/mL, 412 ng/mL et négatif, respectivement). Un électroencéphalogramme a montré une activité lente diffuse, sans altérations focales ou épileptiformes. L'examen du liquide céphalorachidien a montré une hyperprotéinorachie légère et tous les tests microbiologiques ont été négatifs.\n\nL’interrogatoire du patient était difficile, car les informations fournies étaient souvent contradictoires. L’explication selon laquelle les taux de clonazépam étaient négatifs était que l’on ne pouvait pas garantir que le patient avait réellement pris du clonazépam. Sur la base de ces taux plasmatiques, il était très probable qu’il ne l’avait pas fait. D’autre part, le fait que les taux plasmatiques de diazepam et de nordiazepam étaient positifs était cohérent avec les informations fournies par le patient. Rétrospectivement, des ampoules de diazepam ont été trouvées chez le patient. Les taux plasmatiques dans la fourchette thérapeutique n’excluent pas la possibilité d’effets indésirables, mais rendent leur gravité et l’évolution clinique suivie par le patient moins probables. Les benzodiazépines ont probablement contribué au tableau, mais la causalité ne pouvait pas être attribuée en fonction de ces taux plasmatiques.\n\nD’autre part, l’acidémie hyperchlorémique avec des taux normaux de lactate dans le contexte clinique de ce patient nous a conduit à envisager un trouble métabolique, en particulier une acidémie organique, un trouble de la bêta-oxydation des acides gras ou un trouble du cycle de l’urée. L’étude systématique dans le plasma et l’urine des acides gras, acylcarnitines, acylglycines et carnitine était négative. En outre, les taux d’ammonium étaient normaux et une hypoglycémie hypocétotique n’a pas été retrouvée. L’acidémie s’est résolue en moins de 24 heures sans mesures spécifiques, ce qui rend très peu probable l’hypothèse d’un trouble métabolique. En outre, lors de la stabilisation initiale, le patient avait reçu une sédation intensive avec du NaCl à 0,9 %, ce qui aurait pu contribuer à l’acidémie.\n\nAu cours des 24 heures qui ont suivi, il a présenté une diminution progressive du niveau de conscience, avec un développement d'une insuffisance respiratoire rapidement progressive nécessitant une intubation endotrachéale et une ventilation mécanique, et un transfert vers l'unité de soins intensifs.\n\nL'examen respiratoire et la radiographie thoracique suggéraient une pneumonie par aspiration bronchique, et il a été traité en conséquence. Une IRM cérébrale a été réalisée pour rechercher l'étiologie de l'encéphalopathie. Elle a révélé un signal hyperintense hétérogène bilatéral et étendu dans les deux globes palléaux, le bras postérieur de la capsule interne et le putamen, sur les images FLAIR et T2. La séquence T1 renforcée a montré une hypointensité dans ces régions.\n\nSur la base de ces résultats, l'affaire a été réorientée vers une encéphalopathie induite par le disulfirame, étant donné que le schéma radiologique avait été décrit précédemment dans la littérature dans d'autres cas d'intoxication par le disulfirame, ainsi que dans des cas d'intoxication par le monoxyde de carbone (mais ce n'était pas le scénario clinique). Le diagnostic d'encéphalopathie par disulfirame a été fait par des critères d'exclusion. Selon l'algorithme de Naranjo et al [5], avec un score de 4 sur 10, il a été considéré possible d'attribuer la causalité au disulfirame dans ce cas. À son tour, les cas publiés d'encéphalopathie par disulfirame présentent d'importantes similitudes avec ce cas. Cependant, il n'y a pas de cas décrits de disulfirame inhalé, car ce n'est pas une voie d'administration approuvée. Malheureusement, il n'a pas été possible de mesurer les niveaux plasmatiques de disulfirame.\n\nAu cours des deux semaines suivantes, l'état respiratoire du patient s'est progressivement amélioré jusqu'à ce qu'il puisse être extubé. Après le retrait de la sédation, l'examen neurologique a révélé des difficultés de supination, un tremblement intentionnel et une dysmétrie de la manœuvre doigt-nez, ainsi qu'une faiblesse proximale des membres supérieurs et inférieurs. Par la suite, le patient a présenté une amélioration neurologique. La limitation de la motilité oculaire et la faiblesse ont disparu en quelques jours, mais un léger tremblement et une légère dysmétrie ont persisté. En raison de la myopathie du patient en état critique, la marche n'a pu être explorée avant deux semaines, moment où une résolution complète de l'ataxie a été observée.\n\nLe patient a été renvoyé avec un léger tremblement intentionnel résiduel. L'IRM cérébrale de contrôle à deux mois a montré une évolution des zones symétriques d'œdème cytotoxique vers une nécrose.\n",
+        "gold_summary": "Un patient de 48 ans souffrant d'alcoolisme chronique qui a déclaré avoir inhalé une dose très élevée de disulfiram sans avoir consommé d'alcool en même temps a développé une encéphalopathie aiguë avec une insuffisance respiratoire rapidement progressive. L'imagerie cérébrale a révélé une atteinte bilatérale symétrique étendue des deux noyaux gris centraux, un signe caractéristique de cette intoxication. La récupération neurologique a été lente. Deux mois après l'intoxication, le patient présentait un léger tremblement intentionnel résiduel et une IRM a montré une évolution des zones symétriques d'œdème cytotoxique vers la nécrose.\n",
+        "synthetic_summary": {
+            "B1": "Un homme très malade a pris un médicament de façon dangereuse. Ce médicament a fait que son cerveau a eu beaucoup de problèmes. Il a eu du mal à respirer et à bouger. \n\nLes médecins ont fait des images de son cerveau. Ils ont vu des parties qui étaient très abîmées. Petit à petit, il a commencé à aller un peu mieux. \n\nAprès deux mois, il avait encore un petit tremblement, mais il allait mieux. Les images montraient que certaines parties de son cerveau étaient encore un peu blessées.",
+            "B2": "Un homme de 48 ans, qui avait un problème d’alcoolisme, a inhalé une grande quantité de disulfirame, un médicament utilisé pour aider à arrêter de boire. Il n’avait pas bu d’alcool en même temps. Après cela, il a développé une maladie grave du cerveau appelée encéphalopathie, ce qui a aussi causé des difficultés à respirer rapidement. \n\nUne imagerie spéciale du cerveau, appelée IRM, a montré des zones endommagées des deux côtés dans une partie importante du cerveau appelée les noyaux gris centraux. Ce type de lésion est typique quand on est intoxiqué par le disulfirame. \n\nLa récupération de ses fonctions neurologiques, comme le mouvement et la coordination, a été lente. Deux mois plus tard, il avait encore un léger tremblement quand il bougeait volontairement. L’IRM de contrôle a montré que les zones touchées dans son cerveau avaient évolué d’un gonflement à une destruction plus permanente des cellules. \n\nCe cas montre que l’inhalation de disulfirame, même sans consommation d’alcool, peut causer des dommages graves au cerveau et une récupération longue.",
+            "B3": "**Contexte**  \nUn homme de 48 ans, avec des antécédents d’alcoolisme chronique et de schizophrénie paranoïde, a été admis pour somnolence, troubles de la coordination (ataxie cérébelleuse) et difficultés d’élocution (dysarthrie) évoluant depuis trois jours. Il avait récemment inhalé des doses élevées de disulfirame (médicament utilisé habituellement pour traiter l’alcoolisme), ainsi que de l’escitalopram et du clonazépam, à des fins récréatives. Son traitement habituel comprenait notamment de l’olanzapine, du palipéridone, du clonazépam, de l’escitalopram et du disulfirame oral.\n\n**Principales observations**  \nÀ son arrivée, le patient était désorienté et somnolent, avec une pression artérielle élevée mais sans fièvre ni signes d’infection initialement. L’examen neurologique montrait des pupilles petites et peu réactives, une dysarthrie marquée et une démarche instable. Les analyses sanguines révélaient une acidose métabolique hyperchlorémique (un déséquilibre du pH sanguin), mais sans anomalie hépatique ou rénale. Les tests toxicologiques ont confirmé la présence de benzodiazépines, mais les concentrations plasmatiques étaient dans les limites thérapeutiques, ce qui rendait leur rôle dans la gravité des symptômes incertain. Une imagerie cérébrale initiale par scanner montrait des anomalies non spécifiques, tandis que l’électroencéphalogramme indiquait une activité cérébrale ralentie sans foyer épileptique.\n\nDans les jours suivants, le patient a présenté une aggravation rapide de son état neurologique avec une insuffisance respiratoire nécessitant une intubation et une ventilation mécanique. Une pneumonie par aspiration a été diagnostiquée et traitée. Une imagerie par résonance magnétique (IRM) cérébrale a montré des lésions bilatérales symétriques étendues au niveau des noyaux gris centraux (globes palléaux, capsules internes, putamen), caractéristiques d’une encéphalopathie toxique.\n\n**Interprétation clinique**  \nL’ensemble des données a conduit à suspecter une encéphalopathie induite par le disulfirame inhalé, une voie d’administration non conventionnelle et non approuvée. Ce diagnostic a été retenu après exclusion d’autres causes métaboliques, infectieuses ou toxiques. Le schéma radiologique observé est cohérent avec des cas d’intoxication au disulfirame décrits dans la littérature, bien que la confirmation biologique par dosage plasmatique n’ait pas été possible. L’intoxication par benzodiazépines, bien que contributive, ne suffisait pas à expliquer la gravité clinique. L’acidose métabolique transitoire a été attribuée probablement à la réanimation initiale.\n\n**Prochaines étapes et évolution**  \nAprès deux semaines en soins intensifs, l’état respiratoire s’est amélioré, permettant le sevrage de la ventilation. La récupération neurologique a été progressive : des troubles moteurs tels que tremblement intentionnel, dysmétrie (manque de précision des mouvements) et faiblesse musculaire proximale ont persisté quelques jours, puis se sont atténués. La marche a pu être évaluée après deux semaines, montrant une résolution complète de l’ataxie. Deux mois plus tard, le patient présentait un léger tremblement résiduel, tandis que l’IRM de contrôle montrait une évolution des lésions cérébrales vers une nécrose, témoignant d’une lésion cérébrale permanente mais limitée.\n\n---\n\nCe cas illustre une forme rare et grave d’encéphalopathie toxique liée à l’inhalation abusive de disulfirame, avec une atteinte caractéristique des noyaux gris centraux et une récupération neurologique lente mais partielle. Il souligne également les risques associés à l’usage détourné de médicaments et la complexité du diagnostic dans un contexte de polypathologie et de consommation multiple."
+        }
+    },
+    {
+        "article": "Homme de 64 ans, sans antécédents pathologiques, qui vivait avec des animaux de compagnie (chiens). Il a consulté pour une céphalée holocraniale, une hémianopsie homonyme droite d'une semaine d'évolution associée à un épisode de crise convulsive tonique clonique généralisée, sans fièvre. Une TDM du cerveau a été réalisée, qui a mis en évidence une lésion au niveau cortico-sous-cortical frontal, accompagnée d'un œdème. Par la suite, une IRM du cerveau a été réalisée, dont le coefficient de diffusion a révélé une lésion hétérogène avec restriction dans cette séquence et corrélation dans ADC, avec un halo hypointense périphérique associé à un vaste œdème vasogénique qui a généré un effet de masse avec un effondrement partiel du ventricule latéral droit et du corps calleux et une déviation non significative de la ligne médiane vers la gauche, qui mesure 67x36x26 mm. Une excision complète d'une lésion encapsulée avec contenu purulent a été réalisée par accès transcortical, en commençant une thérapie antibiotique avec meropenem/vancomycin jusqu'à l'isolement en culture d'A. aphrophilus, en complétant le traitement avec ceftriaxone pendant 21 jours. Au cours de son séjour à l'hôpital, une échographie de l'abdomen total, du fond de l'œil et une échocardiographie transœsophagienne ont été réalisées, sans preuve d'autres sites d'infection. Il a évolué favorablement, ce qui a permis sa sortie de l'hôpital.\n",
+        "gold_summary": "Il s’agit d’un patient de 64 ans, sans antécédents significatifs, qui a été admis aux urgences pour un cas de céphalée, d’hémianopsie d’une semaine d’évolution et de crises toniques cloniques, et qui a ensuite été diagnostiqué d’un abcès cérébral dû à A. aphrophilus après des études d’imagerie et une culture de lésion cérébrale.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 64 ans avait très mal à la tête.  \nIl ne voyait pas bien d’un côté de ses yeux.  \nIl a eu un gros tremblement du corps.  \n\nLes docteurs ont fait des photos de sa tête.  \nIls ont trouvé une boule avec du pus dedans.  \nIls ont enlevé cette boule pour le soigner.  \n\nUn petit microbe a fait cette boule.  \nLes docteurs ont donné des médicaments pour le tuer.  \nLe monsieur a bien guéri et est rentré chez lui.",
+            "B2": "Voici un résumé adapté pour un adolescent de 14 ans en classe de biologie :\n\n**Ce qu'ils ont trouvé**  \nUn homme de 64 ans, en bonne santé avant, a eu de fortes douleurs à la tête, une perte partielle de la vision d’un côté de ses yeux pendant une semaine, et une crise d’épilepsie. Les médecins ont fait des examens d’imagerie du cerveau (scanner et IRM) qui ont montré une grosse masse avec un gonflement autour, ce qui a causé une pression sur certaines parties du cerveau.\n\n**Ce que cela signifie**  \nCette masse était un abcès cérébral, c’est-à-dire une poche de pus causée par une infection. Les médecins ont enlevé complètement cet abcès par chirurgie. Ils ont aussi fait une analyse du pus, appelée culture, pour trouver la bactérie responsable, qui s’appelait *Aggregatibacter aphrophilus* (une bactérie que l’on peut trouver chez les animaux). Ensuite, ils ont donné des antibiotiques puissants pendant 21 jours pour tuer cette bactérie.\n\n**Le suivi et l’évolution**  \nPendant son séjour à l’hôpital, ils ont vérifié s’il y avait d’autres infections dans le corps avec des examens comme une échographie et un contrôle des yeux, mais ils n’en ont pas trouvé. Grâce au traitement, l’homme s’est bien rétabli et a pu quitter l’hôpital.  \n\nEn résumé, cet homme a eu un abcès au cerveau causé par une infection rare, mais grâce à la chirurgie et aux antibiotiques, il a guéri.",
+            "B3": "Contexte  \nUn homme de 64 ans, sans antécédents médicaux notables, vivant avec des chiens, a consulté pour des maux de tête généralisés (céphalée holocraniale), une perte partielle de la vision dans la moitié droite du champ visuel (hémianopsie homonyme droite) évoluant depuis une semaine, ainsi qu’un épisode de crise convulsive généralisée de type tonico-clonique, sans fièvre associée.\n\nPrincipales Observations  \nUne tomodensitométrie (TDM) cérébrale a révélé une lésion cortico-sous-corticale dans la région frontale, accompagnée d’un œdème. Une imagerie par résonance magnétique (IRM) a précisé cette lésion, montrant une structure hétérogène avec une restriction de diffusion, un halo périphérique hypointense et un important œdème vasogénique. Cette masse, mesurant environ 67 x 36 x 26 mm, provoquait un effet de masse avec un effondrement partiel du ventricule latéral droit et du corps calleux, ainsi qu’un léger déplacement de la ligne médiane du cerveau.  \n\nUne intervention chirurgicale a permis l’excision complète d’une lésion encapsulée contenant du pus, confirmant la présence d’un abcès cérébral. Les cultures microbiologiques ont isolé la bactérie Aggregatibacter aphrophilus, un germe peu fréquent responsable d’infections cérébrales. Le patient a reçu un traitement antibiotique initial par meropenem et vancomycine, adapté ensuite à la ceftriaxone pendant 21 jours.  \n\nDes examens complémentaires, incluant une échographie abdominale, un examen du fond d’œil et une échocardiographie transœsophagienne, n’ont pas identifié d’autres foyers infectieux.  \n\nInterprétation Clinique  \nCe cas illustre une infection cérébrale rare chez un patient sans facteur de risque évident, probablement liée à une bactérie de la flore buccale ou associée aux animaux de compagnie. L’abcès cérébral a été diagnostiqué grâce à l’imagerie avancée et confirmé par la culture, ce qui a permis une prise en charge chirurgicale et antibiotique ciblée efficace.  \n\nProchaines Étapes  \nLe patient a présenté une évolution favorable sous traitement, permettant sa sortie de l’hôpital. Un suivi neurologique et infectiologique est recommandé pour surveiller la résolution complète de l’infection et prévenir toute récidive."
+        }
+    },
+    {
+        "article": "Il s’agit d’une patiente de 34 ans dont la maladie dure depuis quatre semaines. Deux mois auparavant, elle avait accouché par césarienne à la 37e semaine de grossesse et avait présenté des saignements persistants de la plaie opératoire. Dans ses antécédents personnels, elle a nié avoir présenté des antécédents de saignements pendant l’enfance ou l’adolescence. Trois ans auparavant, elle avait donné naissance à son premier enfant (également par césarienne), qui est mort à cause d’une chromosomopathie (selon la patiente). En outre, elle a déclaré être allergique au tramadol.\n\nLe tableau clinique a débuté par une lombalgie due à une lithiase rénale bilatérale. Par la suite, il a réussi à expulser un calcul et a ensuite présenté une hématurie pendant trois jours, pour laquelle il a reçu de l’acide tranexamique toutes les 12 heures. Trois semaines plus tard, il a présenté une douleur dans la région inférieure de la cuisse gauche qui a augmenté en intensité, avec un durcissement de la zone. En raison de la persistance des symptômes, on lui a prescrit du diclofenac par voie intramusculaire, qui a provoqué une ecchymose et un saignement dans la région des fesses et qui persiste malgré la compression avec des compresses.\n\nLa patiente a subi une échographie Doppler qui a révélé une thrombose veineuse profonde du membre inférieur gauche et s’est rendue à l’hôpital local avec ces résultats. Elle a été traitée par anticoagulant sous-cutané à l’énoxaparine 30 mg/24 h, ainsi que par de la morphine pour la gestion de la douleur et a été hospitalisée. Le jour suivant, elle a présenté une épigastralgie, une vision trouble, une fréquence cardiaque de 117 battements/min, une tension artérielle de 113/85 mmHg et une saturation de 93 %. Il a été décidé de suspendre l’énoxaparine. L’hémogramme a révélé une hémoglobine de 6,4 g/dl, ce qui représentait une différence de 4 g/dl par rapport au résultat un jour avant son admission, qui était de 10,4 g/dl. En conséquence, deux paquets globulaires ont été transfusés. En raison de la suspicion de vascularite, elle a été traitée par méthylprednisolone et a été référée à notre hôpital pour une étude plus approfondie.\n\nL'examen physique à l'admission a révélé une pâleur sévère, une écailleuse étendue sur la cuisse et la face latérale du genou gauche, ainsi qu'un hématome sur la cuisse droite. L'hémogramme a révélé une anémie modérée (Hb = 9,8 g/dl), normocytaire et normocromatique. L'examen biochimique a révélé des valeurs de glucose de 160 mg/dl. Les enzymes hépatiques AST et ALT étaient respectivement de 52 U/L et 86 U/L. Le profil de coagulation a montré une prolongation du temps de thromboplastine partielle activée (TTPa) de 91,2 s. Les autres composants de l'hémogramme, biochimique, électrolytique, hépatique et de coagulation étaient normaux. L'échographie des tissus mous de la région fessière droite a révélé une collection au niveau du tissu cellulaire sous-cutané (TCSC) et un œdème jusqu'au tiers supérieur de la cuisse. L'échographie Doppler du membre inférieur gauche a montré une bonne fluximétrie sans signe de thrombose dans la veine fémorale commune, superficielle et profonde.\n\nUn traitement symptomatique a été initié et une hémoculture et une uréoculture ont été demandées, qui ont été négatives. Les taux d'anticorps antinucléaires (ANA), de complément C3 et C4 et de ferritine étaient dans la plage de référence.\n\nDevant la suspicion d'hémophilie acquise, des études ont été demandées pour confirmation, où une correction partielle du TTPa a été trouvée dans le test de mélange. Le facteur VIII a été mesuré, son activité étant diminuée (<1,0 U/dl) et la présence d'un inhibiteur du facteur VIII a été démontrée : 8,64 unités Bethesda/ml. Ce qui a permis de confirmer le diagnostic d'hémophilie acquise, qui a été lié au post-partum par le début des symptômes.\n\nLa prednisone a été initiée à 50 mg po au petit déjeuner et 10 mg po au déjeuner, la cyclophosphamide à 50 mg 2 comprimés po q 24 h et le complexe coagulant anti-inhibiteur hémophilique (FEIBA). Cinq jours plus tard, ce dernier a été arrêté en raison de douleurs thoraciques oppressives, de dyspnée et de nausées (éventuelle réaction indésirable au médicament), et a été remplacé par le facteur VII recombinant activé (NovoSeven).\n\nL’évolution clinique de la patiente a été favorable, avec une diminution de l’ecchymose et l’absence de tout autre symptôme, et elle a pu quitter l’hôpital.\n",
+        "gold_summary": "Une patiente de 34 ans se présente avec des douleurs lombaires, une hématurie et un hématome dans la région fessière droite, sans antécédent de saignement. En raison de l'étendue des manifestations hémorragiques, elle est transférée au service des urgences. Les examens auxiliaires du profil de coagulation, le test de mélange et la mesure des titres d'inhibiteurs du facteur VIII ont confirmé le diagnostic.\n",
+        "synthetic_summary": {
+            "B1": "Une dame a eu mal au dos et du sang dans son pipi. Elle avait aussi un gros bleu sur sa fesse. Elle n'avait jamais eu de saignement avant. Les docteurs ont fait des tests pour comprendre. Ils ont trouvé un problème avec le sang qui ne s’arrête pas bien.",
+            "B2": "Une femme de 34 ans a eu plusieurs problèmes de santé après son accouchement par césarienne. Elle a d’abord eu des douleurs dans le bas du dos, puis du sang dans ses urines, et enfin un gros bleu (hématome) sur la fesse droite. Elle n’avait jamais eu de problèmes de saignement avant. À cause de ces symptômes graves, elle a été envoyée aux urgences pour faire des examens. Ces tests ont montré que son sang ne coagule pas bien à cause d’un problème avec une protéine appelée facteur VIII. Ce diagnostic s’appelle une hémophilie acquise, ce qui signifie que son corps produit des substances qui empêchent le facteur VIII de fonctionner normalement. Cette maladie est liée à sa récente grossesse. Grâce à un traitement adapté, elle a pu guérir et sortir de l’hôpital.",
+            "B3": "Résumé détaillé et structuré pour un public non médical éduqué\n\n**Contexte**  \nUne femme de 34 ans a développé des symptômes quatre semaines après un accouchement par césarienne survenu à la 37e semaine de grossesse. Initialement, elle a souffert de douleurs lombaires liées à des calculs rénaux, puis d’une hématurie (présence de sang dans les urines) pendant trois jours. Par la suite, elle a ressenti une douleur croissante et un durcissement au niveau de la cuisse gauche, suivi d’un hématome (accumulation de sang sous la peau) dans la région fessière droite, apparu après une injection de diclofénac (un anti-inflammatoire). Une échographie Doppler a révélé une thrombose veineuse profonde (caillot sanguin dans une veine) du membre inférieur gauche, et elle a été traitée par un anticoagulant (énoxaparine) et hospitalisée.\n\n**Principales observations**  \nLe lendemain de son hospitalisation, la patiente a présenté une aggravation de son état avec une anémie sévère (diminution importante du taux d’hémoglobine dans le sang), des douleurs abdominales, une vision trouble et une fréquence cardiaque élevée. L’énoxaparine a été arrêtée. À son admission dans un centre spécialisé, l’examen clinique a montré une pâleur importante, des ecchymoses étendues sur la cuisse gauche et un hématome sur la cuisse droite. Les analyses sanguines ont révélé une anémie modérée, une augmentation du temps de coagulation appelé temps de thromboplastine partielle activée (TTPa), et des enzymes hépatiques légèrement élevées. Une échographie a confirmé la présence d’une collection de liquide sous-cutanée (probablement un hématome) et un œdème (gonflement) au niveau de la cuisse droite. Les examens microbiologiques étaient négatifs, et les tests immunologiques (anticorps antinucléaires, complément, ferritine) étaient normaux.\n\n**Interprétation clinique**  \nDevant ce tableau de saignements inhabituels sans antécédents personnels de troubles hémorragiques, les médecins ont suspecté une hémophilie acquise, une maladie rare où le corps produit des anticorps qui inhibent le facteur VIII, une protéine essentielle à la coagulation du sang. Les tests spécifiques ont confirmé cette hypothèse : le test de mélange a montré une correction partielle du TTPa, l’activité du facteur VIII était très faible (<1 %), et un inhibiteur du facteur VIII a été détecté à un taux élevé (8,64 unités Bethesda/ml). Cette forme d’hémophilie est apparue dans le contexte post-partum, c’est-à-dire après l’accouchement.\n\n**Prise en charge et évolution**  \nLe traitement a combiné des corticostéroïdes (prednisone) et un immunosuppresseur (cyclophosphamide) pour réduire la production des anticorps inhibiteurs, ainsi que des agents de remplacement de la coagulation : initialement un complexe coagulant anti-inhibiteur hémophilique (FEIBA), remplacé ensuite par un facteur VII recombinant activé (NovoSeven) en raison d’effets secondaires. Sous ce traitement, la patiente a présenté une amélioration notable avec une diminution des ecchymoses et une stabilisation de son état général, ce qui lui a permis de quitter l’hôpital.\n\n**Prochaines étapes**  \nUn suivi médical régulier est nécessaire pour surveiller la disparition des inhibiteurs du facteur VIII, la normalisation de la coagulation et prévenir d’éventuelles rechutes. La prise en charge multidisciplinaire reste essentielle pour assurer une bonne récupération et éviter les complications liées à cette maladie rare et grave."
+        }
+    },
+    {
+        "article": "Un patient de 70 ans ayant des antécédents médicaux importants pour l’hépatite C, traité par une thérapie par interféron trois ans auparavant, et une hypertrophie de la prostate. Malgré des résultats virologiques négatifs persistants lors du suivi, le patient a été référé à notre service en raison d’une suspicion de carcinome hépatocellulaire (CHC). Notamment, le mode de vie du patient inclut la consommation quotidienne de 300 à 500 ml de whisky sans antécédents de tabagisme. Les tests sanguins étaient négatifs pour l’antigène HB et positifs pour les anticorps du VHC. La fonction hépatique était de grade A avec une classification de 5 points de Child-Pugh, et les dommages au foie étaient également de grade A. Le score ALBI était de -2,43, ALBI grade 2a, et ICG R15 19,1 %. Les marqueurs tumoraux étaient normaux avec CEA 2,5 ng/ml, mais AFP élevée 1984 ng/ml et CA19-9 3135 U/ml.\n\nTomographie par ordinateur (CT) avec contraste : une masse multinodulaire fusionnée d'une longueur maximale de 91 mm couvrant le segment postérieur et le lobe caudé a été observée. Le CHC a été détecté par une coloration foncée dans la phase précoce et par un lavage dans la phase d'équilibre. La limite de la branche primaire de la veine porte droite était masquée. Un hémangiome a été observé au S5 du foie et un petit kyste a été observé au S6 du foie.\n\nStratégie de traitement initial : Le diagnostic de CHC était cT3N0M0, cStage III. Il n'y avait pas de frontière avec la première branche de la veine porte, et la résection du lobe caudé droit du foie était considérée comme une résection radicale. Cependant, la limite de résection était de 44 % sur la base d'une ICG R15 résiduelle du foie de 40 % [4], et la résection a été jugée impossible en raison de la mauvaise fonction résiduelle du foie.\n\nThérapie ciblée : Le traitement initial consistait en une thérapie ciblée avec un agent ciblé moléculairement (lenvatinib, 8 mg) et une embolisation artérielle transcathéter (TAE). Une tomographie par ordinateur réalisée 4 semaines après le début du traitement a montré que la tumeur avait augmenté d'environ 120 % pour atteindre une longueur maximale de 110 mm. Nous avons changé pour une combinaison de thérapie ciblée atezolizumab (1200 mg) et bevacizumab (1000 mg), qui s'est avérée utile dans les cas négatifs au lenvatinib. Aucun événement indésirable n'est survenu avec les deux thérapies ciblées. Une tomographie par ordinateur réalisée après quatre cycles d'atézolizumab plus bevacizumab a montré que la tumeur avait rétréci à un diamètre maximal de 60 mm, l'effet de contraste avait disparu et la masse avait une absorption généralement faible.\n\nLes marqueurs tumoraux ont été normalisés à 3,4 ng/ml AFP et 18 U/ml CA19-9.\n\nConstatations chirurgicales : lobectomie post-hépatique. La perte de sang était de 293 ml. 6 h 23 min.\n\nConstatations histopathologiques : grossièrement, la tumeur était blanc jaunâtre avec d'autres fusions nodales. Histologiquement, la plupart des tumeurs étaient nécrotiques, et il n'y avait aucune preuve de HCC actif résiduel. La formation de granulome épithélioïde a été observée dans la région environnante, ce qui a été considéré comme un changement post-traitement.\n\nSure-après l'opération : La patiente ne présentait aucun signe de défaillance hépatique post-opératoire ; cependant, la TDM réalisée le jour 7 post-opératoire a révélé la formation d'un abcès du tronc. Un drainage percutané a rapidement soulagé l'inflammation, et la patiente a quitté l'hôpital le jour 22 post-opératoire sans que le drain n'ait été retiré. Le drain a été retiré le jour 38 post-opératoire. La patiente est actuellement en vie 16 mois après l'opération sans récidive. Il n'y a pas de traitement recommandé après résection, et aucun traitement supplémentaire n'a été fourni.\n",
+        "gold_summary": "Le patient, un homme d'une soixantaine d'années, a développé un CHC de 11,5 cm (T3N0M0 stade III) dans la zone hépatique postérieure après avoir été virologiquement négatif pour l'hépatite C. La tumeur était proche de la branche de la veine porte droite, rendant le lobe du foie non résécable en raison d'une mauvaise fonction hépatique. Après l'agrandissement de la tumeur, il a été traité avec atezolizumab et bevacizumab. Après 5 cycles, la tumeur a considérablement rétréci, permettant une résection complète avec élimination du segment postérieur. L'opération a révélé des tumeurs principalement nécrotiques sans cellules cancéreuses actives restantes.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur avait une grosse boule dans son foie. Cette boule était trop grande et près d’un gros vaisseau. Son foie ne pouvait pas être enlevé tout de suite. \n\nIl a pris des médicaments spéciaux pour faire diminuer la boule. Après un moment, la boule est devenue plus petite. \n\nAlors, les médecins ont pu enlever la partie du foie avec la boule. Dans la boule, il n’y avait presque plus de vilaines cellules. \n\nLe monsieur va mieux maintenant.",
+            "B2": "### Ce qu'ils ont trouvé\n\nUn homme d'environ 70 ans, qui avait déjà eu une hépatite C mais n'avait plus le virus dans son corps, a développé un cancer du foie appelé carcinome hépatocellulaire (CHC). Sa tumeur mesurait environ 11,5 cm et se trouvait dans une partie difficile du foie, près d'une grosse veine importante. À cause de la mauvaise santé de son foie, les médecins ne pouvaient pas enlever la tumeur par chirurgie au début.\n\n### Ce qu'ils ont fait\n\nLa tumeur a continué à grandir malgré un premier traitement. Alors, les médecins ont utilisé un nouveau traitement avec deux médicaments, atezolizumab et bevacizumab, qui ciblent spécifiquement les cellules cancéreuses. Après cinq cycles de ce traitement, la tumeur a beaucoup diminué, ce qui a permis aux chirurgiens de l’enlever complètement.\n\n### Ce que cela signifie\n\nLors de l’opération, ils ont vu que la tumeur était en grande partie morte (nécrotique) et qu’il ne restait plus de cellules cancéreuses actives. Cela montre que le traitement a bien fonctionné pour réduire la tumeur avant la chirurgie. Le patient a bien récupéré après l’opération et n’a pas eu de récidive du cancer pendant au moins 16 mois. Ce cas montre qu’une combinaison de médicaments ciblés peut aider à rendre possible une chirurgie même quand la tumeur semble trop grande ou trop proche des vaisseaux importants.",
+            "B3": "Résumé structuré destiné à un adulte éduqué non-médecin\n\nContexte  \nUn homme de 70 ans, avec des antécédents d’hépatite C traitée par interféron et une hypertrophie de la prostate, a été suivi pour une suspicion de cancer du foie appelé carcinome hépatocellulaire (CHC). Malgré l’absence de virus actif dans le sang, une masse tumorale importante a été détectée dans le foie, mesurant initialement 9,1 cm, puis augmentant à 11 cm. Le patient consommait régulièrement de l’alcool, ce qui peut aggraver les maladies du foie. Ses analyses sanguines montraient une fonction hépatique relativement préservée mais limitée, et des marqueurs tumoraux élevés, notamment l’alpha-foetoprotéine (AFP) et le CA19-9, suggérant une activité tumorale importante.\n\nPrincipales observations  \nL’imagerie par scanner a montré une masse tumorale multinodulaire dans la partie postérieure et le lobe caudé du foie, proche de la branche principale droite de la veine porte, ce qui rendait la chirurgie risquée en raison d’une fonction hépatique insuffisante pour supporter une résection large. Une première tentative de traitement par un médicament ciblé, le lenvatinib, associée à une embolisation artérielle (procédure visant à bloquer l’apport sanguin à la tumeur), n’a pas empêché la progression tumorale. Le traitement a donc été modifié pour une combinaison de deux médicaments immunothérapeutiques, l’atézolizumab et le bevacizumab, qui ont permis une réduction significative de la taille tumorale (de 11 cm à 6 cm) et une disparition des signes d’activité tumorale à l’imagerie. Les marqueurs tumoraux sont également revenus à des niveaux normaux.\n\nInterprétation clinique  \nCette réponse favorable a permis de réaliser une chirurgie visant à retirer la partie postérieure du foie contenant la tumeur. L’intervention s’est déroulée sans complications majeures, avec une perte de sang modérée. L’analyse microscopique de la tumeur retirée a montré que la majorité des cellules tumorales étaient mortes (nécrosées) et qu’aucune cellule cancéreuse active ne subsistait, indiquant un excellent effet du traitement préalable. Un changement inflammatoire local, appelé granulome épithélioïde, a été observé, ce qui est compatible avec une réaction post-traitement.\n\nProchaines étapes et suivi  \nAprès l’opération, le patient n’a pas présenté de défaillance hépatique, mais un abcès (collection infectieuse) s’est formé au niveau du foie, rapidement traité par drainage percutané. Le patient a pu quitter l’hôpital en bon état et le drain a été retiré environ un mois plus tard. Seize mois après la chirurgie, il est toujours en vie sans signe de récidive tumorale. Aucun traitement complémentaire n’a été nécessaire après la résection. Ce cas illustre l’efficacité possible de la combinaison atezolizumab-bevacizumab pour réduire une tumeur hépatique initialement non opérable, permettant une chirurgie curative."
+        }
+    },
+    {
+        "article": "Un homme de 39 ans s'est présenté dans un centre de soins tertiaires après avoir tenté de se pendre une heure auparavant. Selon le rapport du SMU, il a été trouvé sur le sol en train de tousser du sang à côté d'un arbre avec une corde de suspension. À la présentation, il était alerte et orienté. Il a rapporté avoir des difficultés à projeter sa voix, mais a nié avoir une dyspnée. L'examen physique a révélé une marque de ligature le long du cou antérieur au niveau du cartilage thyroïde. La saillie thyroïdienne pouvait être palpée, mais d'autres repères cervicaux étaient masqués par un emphysème sous-cutané.\n\nL'angiographie par TDM a révélé des lésions de l'intima avec thrombus (AAST grades III-V) des carotides communes bilatérales, de la carotide externe gauche et des artères vertébrales bilatérales. Une fracture de la vertèbre C4 a été constatée. Il y avait un emphysème sous-cutané étendu avec pneumomédiastinum. En y regardant de plus près, les muscles du bandeau infra-hyoïdien étaient rompus, avec une distension de l'os hyoïde et de l'épiglotte en supériorité et du cartilage thyroïde en infériorité. L'IRM a démontré une déchirure partielle du ligament nuchal, nécessitant une immobilisation continue de la colonne vertébrale.\n\nLe service OTO-HNS a été consulté pour évaluer les voies respiratoires du patient. La laryngoscopie souple a révélé des cordes mobiles bilatérales avec un léger oedème laryngé. L'épiglotte semblait être détachée du cartilage laryngé et la muqueuse des plis aryépiglottiques/fausses cordes était perturbée.\n\nPeu après l'évaluation initiale par l'OTO-HNS, le patient a été emmené en salle d'opération pour une intubation nasotrachéale consciente contrôlée. Il était stable du point de vue des voies respiratoires et, en raison de l'étendue de ses lacérations de la muqueuse laryngée, nous avons estimé que la meilleure option était de le transférer en salle d'opération pour une prise en charge définitive des voies respiratoires sous visualisation directe la nuit de son arrivée. Le deuxième jour de l'hospitalisation, le patient a subi une trachéotomie, une laryngoscopie, une oesophagoscopie et une réparation de la lésion hyolaryngée. Après avoir soulevé les lambeaux, un petit défaut a été constaté au-dessus de la pointe thyroïdienne dans la couche d'investissement du fascia cervical profond qui, lorsqu'il a été ouvert, a révélé un grand défaut des tissus mous s'étendant dans les voies respiratoires supraglótiques. Les muscles sterno-hyoïdien, thyro-hyoïdien et omo-hyoïdien avaient rompu 1 à 2 cm en dessous de leur insertion sur le hyoïde. La membrane thyro-hyoïdienne était complètement détruite, tout comme la muqueuse des fausses cordes et des plis aryépiglottiques. L'épiglotte a été détachée du cartilage thyroïde et a été déviée vers le haut par le hyoïde en raison des forces non opposées de la musculature supra-hyoïdienne.\n\nEn raison de lésions concomitantes de la colonne cervicale, le cou devait rester dans une position neutre. Une pince Allis a été utilisée pour rétracter l'hyoïde inférieure et une seule pince pour tirer le larynx/trachée vers le haut. La muqueuse laryngée a été réparée en premier avec une suture interrompue 4-0 en vicryl. Pour maintenir la tension hors de la plaie, une thyrohyoïdeopexie modifiée avec épiglotopexie a été réalisée. Une aiguille de calibre 20 a été passée à travers le cartilage thyroïde antérieur sous visualisation avec un bronchoscope flexible pour assurer une distance adéquate au-dessus de la commissure antérieure avant de passer la suture médiane. Du côté des voies respiratoires, la suture a ensuite été passée à travers le pétale de l'épiglotte. Le bras inférieur de quatre sutures supplémentaires 2-0 en vicryl a été passé à travers l'ala thyroïde supérieure (2 sutures de chaque côté). Le bras supérieur de chaque suture a ensuite été passé autour de l'hyoïde. Ces sutures de tension ont été sécurisées, en maintenant les hyoïdes et les cartilages thyroïdes en étroite proximité. Les extrémités rompues de la musculature de la ceinture ont été réapproximées, des drains de Penrose ont été placés et l'incision a été fermée en plusieurs couches.\n\nLe patient a eu une sonde de gastrostomie. Il a commencé à recevoir de l'héparine pour un thrombus carotidien et a continué une semaine de traitement intraveineux par Unasyn. Le premier changement de trachéotomie a été effectué le jour postopératoire (POD) 7 une fois que la résolution de l'œdème des voies respiratoires a été confirmée avec une laryngoscopie souple. Une étude de déglutition vidéo le jour postopératoire (POD) 14 a révélé une dysphagie oropharyngée modérée ou modérée qui a été minimisée avec des stratégies de déglutition. Il a été décannulé le jour postopératoire (POD) 17 et a été renvoyé le jour suivant.\n\nAu moment du suivi, le patient ne portait plus de collier cervical. Il tolérait une alimentation normale. Sa voix était légèrement enrouée, considérée comme un grade un pour la rugosité sur l'échelle GRBAS (grade, rugueux, respiratoire, asthénie, tension), mais il était capable de communiquer sans limitation. La laryngoscopie a démontré un larynx bien guéri avec des cordes vocales mobiles, un raccourcissement des plis aryépiglottiques gauches et un déplacement inférieur de l'épiglotte. La CTA du cou de suivi pour évaluer sa blessure carotidienne a démontré la résolution de l'air cervical avec une voie aérienne ouverte/intacte.\n",
+        "gold_summary": "Nous rapportons le cas d'un homme de 39 ans admis en unité de soins intensifs après une tentative de strangulation. Alerté et cliniquement stable, ses principaux symptômes étaient la douleur et des changements de voix. Son examen externe était remarquable seulement pour une marque de ligature cervicale et un emphysème sous-cutané à la palpation. L'imagerie par tomodensitométrie a révélé une rupture des muscles du col de l'hyoid et un déplacement de l'hyoid et de l'épiglotte vers le haut. Une laryngoscopie souple ultérieure par l'équipe d'Otorhinolaryngologie-Chirurgie de la Tête et du Cou (OTO-HNS) a révélé une avulsion de l'épiglotte du cartilage thyroïde et une rupture des plis aryépiglottiques/fausse corde muqueuse, entraînant une plaie ouverte dans les tissus mous du cou antérieur. La voie aérienne a été sécurisée en salle d'opération par intubation nasotrachéale fibreoptique. Une trachéotomie a été réalisée. L'exploration du cou a révélé une section des muscles du col antérieur et de la membrane thyro-hyoïde. La plaie a été réparée en couches par une thyro-hyoïdeopexie modifiée. Au mois suivant, le patient a été décanulé avec succès et tolérait une alimentation normale.\n",
+        "synthetic_summary": {
+            "B1": "Un homme a eu un gros accident au cou. Il a essayé de se faire du mal avec une corde. \n\nIl avait mal et sa voix était différente. Son cou avait une marque et un gonflement sous la peau. \n\nLes docteurs ont fait des images et ont vu que des muscles et des parties du cou étaient cassés. Une petite partie qui aide à parler et à respirer était déplacée. \n\nIls ont regardé dans sa gorge avec une petite caméra. Ils ont vu que des morceaux étaient cassés et ouverts. \n\nPour l’aider à respirer, ils ont mis un petit tuyau dans son nez jusqu’à sa gorge. Puis, ils ont fait une petite ouverture dans son cou pour qu’il puisse mieux respirer. \n\nLes docteurs ont réparé les muscles et les parties cassées doucement. \n\nAprès un mois, il a pu enlever le tuyau et manger normalement. Sa voix allait un peu mieux. Tout allait bien.",
+            "B2": "Voici un résumé adapté pour un adolescent de 14 ans en classe de biologie :\n\nUn homme de 39 ans a été amené à l’hôpital après avoir essayé de se pendre. Quand il est arrivé, il était conscient et stable, mais avait mal au cou et avait du mal à parler normalement. Les médecins ont vu une marque de corde sur son cou et ont senti de l’air sous la peau, ce qui montre qu’il y avait une blessure importante.\n\nDes examens d’imagerie, comme un scanner, ont montré que certains muscles du cou, autour d’un os appelé l’os hyoïde, étaient déchirés. Cet os et une partie appelée l’épiglotte, qui aide à protéger les voies respiratoires, avaient été déplacés vers le haut. Une caméra flexible a permis aux médecins de voir à l’intérieur de sa gorge : l’épiglotte s’était détachée d’un cartilage important et la muqueuse à l’intérieur de la gorge était déchirée, ce qui a créé une blessure ouverte.\n\nPour l’aider à respirer, les médecins ont placé un tube dans sa trachée pendant qu’il était éveillé, puis ils ont fait une ouverture dans sa trachée (une trachéotomie) pour mieux gérer sa respiration. En opérant, ils ont découvert que plusieurs muscles du cou et une membrane entre l’os hyoïde et le cartilage thyroïde étaient coupés. Ils ont réparé ces blessures en recousant les tissus en plusieurs couches pour que tout tienne bien en place.\n\nAprès environ un mois, le patient a pu retirer le tube de la trachéotomie et a recommencé à manger normalement. Sa voix était un peu enrouée, mais il pouvait parler sans problème. Les examens de contrôle ont montré que sa gorge avait bien guéri et que ses artères du cou étaient en bon état.",
+            "B3": "Résumé structuré du cas clinique d’un homme de 39 ans victime d’une tentative de strangulation\n\nContexte  \nUn homme de 39 ans a été admis en centre hospitalier tertiaire suite à une tentative de pendaison survenue une heure auparavant. À son arrivée, il était conscient, orienté, sans difficulté respiratoire majeure, mais se plaignait d’une voix faible. L’examen physique a mis en évidence une marque de ligature au niveau antérieur du cou, autour du cartilage thyroïde, ainsi qu’un emphysème sous-cutané étendu (présence d’air sous la peau) masquant certains repères anatomiques cervicaux.\n\nPrincipales observations  \nL’imagerie par tomodensitométrie (TDM) a révélé des lésions vasculaires graves, notamment des déchirures de la paroi interne (intima) des artères carotides bilatérales et des artères vertébrales, ainsi qu’une fracture de la vertèbre cervicale C4. Un emphysème sous-cutané étendu et un pneumomédiastin (air dans le médiastin, espace central du thorax) étaient également présents. L’analyse fine a montré une rupture des muscles infra-hyoïdiens (muscles situés sous l’os hyoïde dans le cou), avec un déplacement vers le haut de l’os hyoïde et de l’épiglotte (structure cartilagineuse qui protège les voies respiratoires lors de la déglutition), tandis que le cartilage thyroïde était déplacé vers le bas. Une IRM a confirmé une déchirure partielle du ligament nuchal (ligament à l’arrière du cou), justifiant une immobilisation cervicale stricte.\n\nL’examen endoscopique par laryngoscopie souple, réalisé par l’équipe d’oto-rhino-laryngologie (ORL), a montré que les cordes vocales étaient mobiles mais qu’il existait un œdème léger du larynx. L’épiglotte apparaissait détachée du cartilage thyroïde, et la muqueuse des plis aryépiglottiques et des fausses cordes vocales était déchirée, créant une plaie ouverte dans les tissus mous antérieurs du cou.\n\nIntervention et prise en charge  \nPour sécuriser les voies respiratoires, une intubation nasotrachéale consciente sous contrôle visuel a été réalisée en salle d’opération. Le lendemain, une trachéotomie a été pratiquée pour assurer une ventilation stable. Lors de l’exploration chirurgicale, les chirurgiens ont constaté une rupture complète des muscles sterno-hyoïdien, thyro-hyoïdien et omo-hyoïdien, ainsi qu’une destruction totale de la membrane thyro-hyoïdienne et des muqueuses des fausses cordes et plis aryépiglottiques. L’épiglotte était détachée et déplacée vers le haut par l’os hyoïde, en raison de la perte d’équilibre musculaire.\n\nLa réparation a consisté en une suture méticuleuse de la muqueuse laryngée, suivie d’une thyro-hyoïdeopexie modifiée associée à une épiglotopexie, techniques permettant de réaligner et stabiliser l’épiglotte et les cartilages thyroïde et hyoïde. Les muscles rompus ont été réapproximés, des drains ont été posés, et l’incision a été refermée en plusieurs couches. Par ailleurs, une sonde de gastrostomie a été mise en place pour l’alimentation, et un traitement anticoagulant a été initié pour prévenir les complications liées aux thromboses carotidiennes.\n\nÉvolution et suivi  \nLe patient a bénéficié d’un suivi attentif avec des contrôles endoscopiques réguliers. Le premier changement de canule de trachéotomie a eu lieu au septième jour postopératoire, après confirmation de la résolution de l’œdème laryngé. Une évaluation de la déglutition au quatorzième jour a révélé une dysphagie modérée, partiellement corrigée par des stratégies adaptées. La trachéotomie a été retirée au dix-septième jour, et le patient a pu être renvoyé à domicile le lendemain.\n\nAu suivi, il ne portait plus de collier cervical, mangeait normalement, et sa voix était légèrement enrouée mais fonctionnelle. L’examen endoscopique montrait un larynx bien cicatrisé avec des cordes vocales mobiles, malgré un raccourcissement des plis aryépiglottiques gauches et un déplacement inférieur de l’épiglotte. Une angiographie de contrôle a confirmé la résolution de l’air cervical et une voie aérienne intacte.\n\nConclusion  \nCe cas illustre la complexité des lésions cervicales après une tentative de strangulation, associant des traumatismes vasculaires, osseux, musculaires et muqueux. Une prise en charge multidisciplinaire rapide, incluant une sécurisation précoce des voies aériennes, une réparation chirurgicale précise des structures laryngées et une surveillance attentive des complications, a permis une récupération fonctionnelle satisfaisante chez ce patient."
+        }
+    },
+    {
+        "article": "Le patient était un garçon de 16 ans qui a été référé à notre hôpital en juillet 2022 en raison d'une insuffisance cardiaque sévère.\n\nÀ l'âge de 13 ans, il a été diagnostiqué d'une dystrophie musculaire de Becker portant la mutation causale dans le gène DMD (chrX:32841413-32862977, mutation hétérozygote) et le gène DSC2 (chr18:28659938, mutation hétérozygote). Il avait des antécédents de dyspnée légère et de détresse thoracique à l'effort et a reçu un traitement pour une dysfonction cardiaque ; cependant, la fonction cardiaque s'est détériorée et il a été référé à notre hôpital pour la première fois. L'examen physique lors de sa première consultation a révélé une taille de 173 cm, un poids de 78 kg, une tension artérielle de 110/90 mmHg, une fréquence cardiaque de 76 battements/minute, une fréquence respiratoire de 20 battements/minute, une température corporelle de 36,5 °C et une SpO2 de 100 % en air ambiant. Il n'y avait pas de dilatation de la veine jugulaire au niveau du cou. Ses sons d'auscultation cardiaque et pulmonaire étaient normaux. Son abdomen était plat. Il y avait un léger oedème au niveau du pied et de la cheville. Le patient ne présentait pas de lésions des omoplates ou de lordose. Une pseudo-hypertrophie des muscles gastrocnémiens bilatéraux a été observée. Le signe de Gower était négatif. Les tests de laboratoire ont montré que le taux de prohormone N-terminal du peptide natriurétique cérébral (NT-proBNP) était de 471,55 pg/ml, l'hémoglobine myocardique était de 272,61 ng/ml, la créatine kinase (CK) était de 5 493 U/L, la créatine kinase-MB (CK-MB) était de 115 U/L, la créatine kinase-MM (CK-MM) était de 5 378U/L. L'alanine aminotransférase (ALT) était de 138 U/L, l'aspartate aminotransférase (AST) était de 92 U/L, la lactate déshydrogénase (LDH) était de 393U/L. L'échocardiographie transthoracique a montré une fraction d'éjection ventriculaire gauche de 19 %, une dilatation de l'oreillette gauche, du ventricule gauche et de l'oreillette droite, une insuffisance mitrale modérée, une insuffisance ventriculaire systolique sévère, une diminution de la fonction diastolique du cœur entier. L'IRM des jambes a révélé des changements de dystrophie musculaire dans les cuisses bilatérales. Les traitements médicamenteux ont été commencés, y compris le sacubitril-valsartan, le carvedilol, l'ivabradine, le tolvaptan, la trimétazidine et ajustés en fonction des directives de traitement de l'insuffisance cardiaque dans les 3 prochaines années de suivi. La valeur de la LVEF lors de l'écho-cardiographie transthoracique a fluctué à 30-35 %.\n\nLe premier jour de cette consultation, le patient a présenté une détérioration de la douleur thoracique, des palpitations et un essoufflement au repos indiquant une insuffisance cardiaque progressive. Il a été envoyé à notre hôpital à 21 heures. À l'examen physique, tension artérielle de 106/63 mmHg, fréquence cardiaque de 120 battements/minute irréguliers, fréquence respiratoire de 20 battements/minute, température corporelle de 37℃ et SpO2 de 97 % en air ambiant. Un examen thoracique a révélé des crépitations humides dans les deux poumons. Ses bruits cardiaques étaient intacts mais irréguliers, et aucun murmure cardiaque n'a été observé. Sa force musculaire était de 5/5. Les tests de laboratoire ont montré les résultats suivants : numération des globules blancs, 10,56 × 109/L avec neutrophiles 60,5 % ; hémoglobine, 144 g/L ; numération plaquettaire, 177 × 109/L. La fonction de coagulation était légèrement anormale, comme suit : temps de prothrombine (PT), 14,8 s ; temps de thromboplastine partielle activée (APTT), 27,1 s ; D-Dimer, 0,27 mg/L. L'examen biochimique a montré une teneur en potassium de 3,9 mmol/L, une créatinine de 67µmol/L. Son taux total de bilirubine était normal, mais ses taux d'enzymes hépatiques étaient légèrement élevés, comme suit : ALT, 109 U/L ; AST, 87 U/L ; LDH, 376U/L. NT-proBNP était nettement élevé à 9 171pg/ml. Le niveau de cTnT était de 0,107 ng/ml. Les niveaux d'électrolytes étaient normaux. L'électrocardiogramme a montré une fibrillation auriculaire avec une fréquence ventriculaire rapide et un bloc cardiaque intra-ventriculaire.\n\nÀ 22 heures le premier jour, la détresse thoracique s'aggravait. 150 mg d'amiodaron par injection intraveineuse ont échoué à la cardioversion. La fréquence ventriculaire était de 120 bpm. Puis, 450 mg d'amiodaron ont été utilisés pour le contrôle de la fréquence et du rythme par goutte à goutte intraveineuse continue (6ug/Kg/min). Au même moment, nous avons fourni une perfusion continue de peptide natriurétique cérébral humain recombinant pour améliorer la fonction cardiaque clinique. Le moniteur ECG a montré une fibrillation auriculaire avec une fréquence ventriculaire de 90 bpm.\n\nÀ 13 heures le deuxième jour, la patiente est devenue pâle, a commencé à transpirer et a eu une orthopnée. La tension artérielle de la patiente a chuté à 75/50 mmHg, la fréquence cardiaque était de 74 bpm. L'amiodarone et la natriurèse cérébrale humaine recombinante ont donc été arrêtés et une perfusion intraveineuse de dopamine et de dobutamine a été administrée. Tous les médicaments oraux ont été arrêtés au même moment. L'ECG a montré un rythme sinusal normal de 84 bpm et un bloc auriculo-ventriculaire de deuxième degré. L'échocardiographie d'urgence au chevet de la patiente a montré une dilatation du cœur entier avec une fonction systolique réduite du ventricule gauche et droit (FEVG 25%), une hypertension artérielle pulmonaire modérée, un épanchement péricardique infime. L'examen physique a montré une tension artérielle de 89/60 mmHg, une fréquence cardiaque de 74 bpm régulièrement et une SpO2 de 99 % sous 3 L/minute d'oxygène. Des taches de peau étaient visibles sur les deux membres inférieurs. Le volume d'urine le deuxième jour était de 1000 ml.\n\nLe troisième jour, l'échographie abdominale a révélé des calculs biliaires et une cholécystite. Le meropénem (0,5 g q12h ivgtt) a été utilisé empiriquement pour contrôler l'infection. Le volume d'urine a diminué à 400 ml.\n\nLe 4e jour, le patient s'est plaint d'un soulagement de la gêne thoracique. Les tests de laboratoire ont montré les résultats suivants : ALT, 7 391 U/L ; AST, 5 671 U/L ; LDH, 8 089U/L ; CK, 2 875pg/ml, CK-MM, 28 522U/L ; CK-MB, 229U/L ; azote uréique, 29.8mmol/L ; acide urique, 859µmol/L ; créatinine, 305 µmol/L ; eGRF, < 30 ml/min/1.73m2 ; plaquette,104 × 109/L ; PTs, 29.3 s ; APTT, 29.9 s ; Fibrinogen, 163 mg/dl ; D-Dimer > 40 mg/L. Il a été envoyé en ICU pour un traitement supplémentaire.\n\nNous avons fourni un traitement de remplacement rénal continu au chevet du patient. Des administrations d'isoglycyrrhizate, de glutathion réduit et de phosphatidylcholine polyénique ont été administrées pour protéger la fonction hépatique. De la dopamine et de la dobutamine (1,3ug/kg/min) ont été administrées pour maintenir la tension artérielle et renforcer la contraction cardiaque. Des examens de laboratoire ont été effectués pour surveiller les paramètres associés du patient. Fonction de coagulation : le PT était de 22 s. Le D-dimère était supérieur à 40 mg/L. Les fonctions hépatiques étaient comme suit : taux total de bilirubine de 75,5 µmol/L, ALT de 5 060 U/L, AST de 1 952 U/L, LDH de 8 089U/L. Fonction rénale : azote uréique sanguin de 23,8 mmol/L, acide urique de 604 µmol/L, créatinine de 322 µmol/L, et eGRF de 23 ml/min/1,73m2. NT-proBNP était de 5701 pg/ml, CK était de 11476U/L, CK-MM de 11308U/L, CK-MB de 168U/L. L'ECG a montré un rythme sinusal normal de 62 bpm, un bloc cardiaque intra-ventriculaire, une hypertrophie de l'oreillette gauche et une déviation de l'axe gauche.\n\nÀ 22 heures, le 5e jour, la dopamine a été arrêtée. La tension artérielle a fluctué entre 90 et 112/50 et 70 mmHg. Nous avons administré du sacubitril-valsartan oral à 25 mg bid et de la trimétazidine orale à 35 mg bid le 10 juillet. L'ivabradine (5 mg bid p.o.) et le tolvaptan (10 mg qd p.o.) ont été administrés le 10e jour en raison d'une hémodynamique stable, d'une amélioration de la fonction rénale et d'une augmentation du volume quotidien d'urine. La dobutamine a été arrêtée le 11e jour. L'héparine de faible poids moléculaire a été démarrée le 12e jour.\n\nLe 15e jour, un réexamen des examens de laboratoire a suggéré une amélioration significative de la fonction hépatique. L'alanine aminotransférase était tombée à 255 U/L, l'aspartate aminotransférase à 35U/L. La quantité quotidienne de transfusion était de 2 106 ml avec une production quotidienne d'urine de 1 125 ml. Par conséquent, la polyen phosphatidylcholine a été arrêtée. Les cathéters d'hémodialyse ont été enlevés.",
+        "gold_summary": "Nous présentons le cas d’un garçon de 16 ans admis pour insuffisance cardiaque et fibrillation auriculaire. Il a été diagnostiqué comme souffrant d’une dystrophie musculaire de Becker et les tests génétiques ont révélé des mutations concomitantes dans les gènes DMD, ABCB4 et DSC2. L’amiodarone a été prescrit pour contrôler la fibrillation auriculaire paroxystique par voie intraveineuse. Cependant, les taux d’enzymes hépatiques étaient fortement élevés, ainsi que le choc cardiaque, l’insuffisance rénale et les troubles de la coagulation. Après une thérapie de remplacement rénal continue au chevet du patient, la fonction hépatique et l’état clinique du patient se sont rétablis.\n",
+        "synthetic_summary": {
+            "B1": "Il y a un garçon de 16 ans. Son cœur ne marche pas bien. Il a un muscle qui est un peu malade.\n\nSon cœur battait très vite et pas bien. Les docteurs lui ont donné un médicament pour aider son cœur.\n\nMais son foie est devenu très fatigué. Son corps était aussi très faible.\n\nLes docteurs ont aidé son corps avec une machine spéciale. Cette machine a aidé son sang et ses reins.\n\nAprès, il a commencé à aller mieux. Son foie et son cœur sont devenus plus forts. Les docteurs prennent bien soin de lui.",
+            "B2": "**Cas d’un garçon de 16 ans avec des problèmes cardiaques et musculaires**\n\nNous racontons l’histoire d’un garçon de 16 ans qui est venu à l’hôpital parce que son cœur ne fonctionnait pas bien. Il avait une maladie appelée dystrophie musculaire de Becker. Cette maladie affecte les muscles et est causée par des changements dans certains gènes, notamment le gène DMD, qui est important pour les muscles, ainsi que d’autres gènes liés au cœur.\n\n**Ce qu’ils ont découvert et fait**\n\nLe garçon avait aussi une fibrillation auriculaire, c’est-à-dire que son cœur battait de façon irrégulière et trop rapide. Pour essayer de contrôler ce problème, les médecins lui ont donné un médicament appelé amiodarone par perfusion. Mais ce traitement a causé des problèmes : ses enzymes du foie, qui montrent si le foie est en bonne santé, sont devenues très élevées, ce qui signifie que son foie était en danger. En plus, il a eu un choc cardiaque (son cœur ne pompait plus assez de sang), ses reins ont commencé à mal fonctionner, et sa coagulation sanguine était perturbée, ce qui peut causer des saignements ou des caillots.\n\n**Comment il a été soigné**\n\nPour l’aider, les médecins ont utilisé une méthode appelée thérapie de remplacement rénal continue. C’est un traitement qui remplace le travail des reins quand ils ne fonctionnent plus bien, en filtrant le sang. Grâce à ce soin et à d’autres médicaments pour protéger son foie et soutenir son cœur, la santé du garçon s’est améliorée. Sa fonction hépatique (du foie) et son état général sont revenus à la normale.\n\n**En résumé**\n\nCe cas montre qu’un garçon avec une maladie musculaire grave peut aussi avoir des problèmes importants au cœur et au foie. Les traitements doivent être adaptés et surveillés de près pour éviter des complications graves. La thérapie de remplacement rénal a été essentielle pour sauver sa vie et améliorer son état.",
+            "B3": "Résumé détaillé et structuré du cas clinique\n\nContexte  \nNous rapportons le cas d’un garçon de 16 ans atteint d’une dystrophie musculaire de Becker, une maladie génétique musculaire progressive liée à une mutation du gène DMD. Ce patient présentait également des mutations génétiques dans les gènes DSC2 et ABCB4, ce qui peut compliquer le tableau clinique. Il a été admis en juillet 2022 pour une insuffisance cardiaque sévère associée à une fibrillation auriculaire, une arythmie cardiaque caractérisée par un rythme cardiaque irrégulier et rapide.\n\nPrincipales observations  \nÀ l’admission, le patient souffrait de douleurs thoraciques, de palpitations et d’essoufflement au repos, signes d’une aggravation de son insuffisance cardiaque. L’examen clinique a révélé une fréquence cardiaque rapide et irrégulière, des crépitements pulmonaires humides indiquant une congestion pulmonaire, ainsi qu’un léger œdème des membres inférieurs. Les analyses sanguines ont montré une élévation importante du NT-proBNP, un marqueur de souffrance cardiaque, ainsi que des enzymes hépatiques (ALT, AST, LDH) fortement augmentées, témoignant d’une atteinte hépatique aiguë. Par ailleurs, des troubles de la coagulation et une insuffisance rénale aiguë se sont installés, avec une baisse de la fonction rénale évaluée par la créatinine et le débit de filtration glomérulaire estimé (eGFR). L’électrocardiogramme a confirmé la fibrillation auriculaire avec une fréquence ventriculaire rapide et un bloc cardiaque intra-ventriculaire.\n\nIntervention et évolution  \nLe traitement initial a inclus l’administration intraveineuse d’amiodarone pour tenter de contrôler la fibrillation auriculaire. Cependant, cette thérapie n’a pas permis de restaurer un rythme cardiaque normal et a été suivie d’une aggravation de l’état général, avec un choc cardiogénique (diminution sévère de la capacité du cœur à pomper le sang), une insuffisance rénale progressive et une défaillance hépatique. Face à cette situation critique, une thérapie de remplacement rénal continu a été mise en place au chevet du patient pour soutenir la fonction rénale. Parallèlement, des traitements visant à protéger le foie ont été administrés, ainsi que des médicaments pour soutenir la fonction cardiaque et maintenir la pression artérielle.\n\nAu cours du suivi, la fonction hépatique s’est progressivement améliorée, les enzymes hépatiques ont diminué de manière significative, et l’état clinique du patient s’est stabilisé. La fonction rénale s’est également partiellement rétablie, permettant l’arrêt progressif des traitements de soutien. Le rythme cardiaque est resté sous surveillance, avec une gestion adaptée des médicaments pour l’insuffisance cardiaque.\n\nProchaines étapes  \nCe cas illustre la complexité de la prise en charge d’un adolescent atteint de dystrophie musculaire de Becker avec complications cardiaques sévères et atteintes multiorganes. La surveillance étroite de la fonction cardiaque, hépatique et rénale est essentielle, ainsi qu’un ajustement rapide des traitements en fonction de l’évolution clinique. Un suivi multidisciplinaire associant cardiologie, néphrologie, hépatologie et génétique est recommandé pour optimiser la prise en charge à long terme et améliorer la qualité de vie du patient."
+        }
+    },
+    {
+        "article": "Informations du patient: il s´agit de Mr RL, âgé de 27 ans, soudeur de profession, célibataire, de bas niveau socioéconomique et sans antécédent pathologique particulier.\n\nRésultats cliniques: le patient était confus (Glasgow Coma Scale (GCS) 13/15-ème), agité pupilles en mydriase, avait des tremblements avec tachypnée et tachycardie, une hyperréfléxie associée à des myoclonies spontanées plus marquées au niveau des membres inférieurs avec une hypersudation et des frissons.\n\nChronologie: l´histoire de maladie remonte à une semaine avant sa consultation chez un médecin neurologue en secteur libéral, par l´installation des propos de persécution, des propos de négation de filiation, une bizarrerie de comportement et des attitudes hallucinatoires puis le tableau s´est compliqué par une agitation psychomotrice et un diagnostic initial d´un accès psychotique aigu a été retenu, et le patient a été mis sous halopéridone 5 mg par jour.\n\nDeux mois après, l´évolution a été marquée par une mauvaise observance thérapeutique avec persistance de la symptomatologie psychotique associée à des symptômes négatifs tel que la perte de plaisir, l´isolement et l´abolition avec un sommeil perturbé, motivant le malade à refaire une consultation chez le même médecin traitant qui lui a ajouté de la paroxétine 20 mg par jour et l´amitriptyline 25 mg par jour.\n\nQuelques heures (6 à 8h) après la prise des deux antidépresseurs, le malade présentait une perte de conscience et agitation psychomotrice motivant son hospitalisation aux unités des soins intensifs.\n\nDémarche diagnostique: le malade a bénéficié d´un bilan biologique complet, objectivant une perturbation des électrolytes avec une acidose métabolique et un taux de créatine phosphokinase (CPK) à 100 UL/L, l'examen cytobactériologique des urines (ECBU), l'étude du liquide céphalorachidien et les hémocultures se sont avérés négatifs. La concentration plasmatique de la C-reactive protein (CRP) et la numération formule sanguine étaient normales.\n\nL´électrocardiogramme (ECG) a objectivé une arythmie cardiaque par fibrillation auriculaire, et la radiographie thoracique et l'imagerie par résonance magnétique (IRM) cérébrale étaient sans particularités. Le diagnostic de syndrome sérotoninergique a été retenu après avoir éliminé une étiologie infectieuse, métabolique ou neurologique.\n\nIntervention thérapeutique: le patient a été mis sous ventilation mécanique, gavage 500cc/8H, réhydratation par eau plate 500cc/8H, ration de base SG 5% + 2g Nacl + 2g Kcl +1g ca 2+ / 8h , et SS 0,9% 500cc/4H, sédation par midazolam 8mg/H, IPP 40mg /j, avec un anticoagulant à visée préventive et insuline selon dextro.\n\nSuivi et résultats: l´état clinique hémodynamique et neurologique du patient s´est stabilisé après 24h, ensuite il a été transféré au service de psychiatrie où le médecin traitant a trouvé un patient calme sur le plan moteur, bien orienté dans le temps et l´espace, ayant eu un délire mystico religieux et de persécution, certaines réponses déplacées, un jugement perturbé sans présence d´un syndrome dépressif ni maniaque ou confusionnel. L´évolution de la symptomatologie psychiatrique a été marquée par une bonne amélioration avec un bon retour à l´état pré morbide, stabilisée sous neuroleptique atypique type olanzapine avec une posologie initiale de 5 mg par jour.",
+        "gold_summary": "Nous rapportons le cas clinique d´un patient qui a présenté un état de confusion avec une agitation psychomotrice et une hyperréfléxie et des myoclonies spontanées suite à la prise simultanée de la paroxétine et l´amitriptyline. Le diagnostic de syndrome sérotoninergique a été retenu après avoir éliminé les autres éventuels diagnostics, nécessitant une hospitalisation en unité de soins intensifs.",
+        "synthetic_summary": {
+            "B1": "Un monsieur a pris deux médicaments en même temps. Après, il était très confus et bougeait beaucoup sans pouvoir s’arrêter. Son corps faisait des mouvements tout seuls. Les docteurs ont dit que c’était à cause des médicaments. Ils l’ont mis à l’hôpital pour qu’il soit bien soigné et qu’il aille mieux.",
+            "B2": "### Ce qu'ils ont trouvé\n\nNous racontons l'histoire d'un homme de 27 ans, qui a commencé à avoir des troubles du comportement, comme des idées étranges et des hallucinations. Il a d'abord été traité pour un problème psychique avec un médicament appelé halopéridone. Mais après deux mois, ses symptômes n'ont pas disparu. Son médecin lui a alors donné deux autres médicaments, la paroxétine et l'amitriptyline, qui sont des antidépresseurs.\n\n### Ce qui s'est passé ensuite\n\nQuelques heures après avoir pris ces deux médicaments, le patient est devenu très agité, confus et a perdu connaissance. Il a été hospitalisé en soins intensifs. Les médecins ont fait plusieurs examens pour comprendre ce qui se passait. Ils ont éliminé des infections, des problèmes du cœur ou du cerveau. Finalement, ils ont diagnostiqué un syndrome sérotoninergique. C’est une réaction grave qui arrive quand il y a trop de sérotonine, une substance chimique du cerveau, souvent à cause de certains médicaments.\n\n### Comment ils l'ont soigné\n\nLe patient a été soigné avec des traitements pour l’aider à respirer, à se réhydrater et à calmer son agitation. Après un jour, son état s’est amélioré. Il a ensuite été transféré en psychiatrie où il est devenu plus calme et a retrouvé une bonne orientation dans le temps et l’espace. Son traitement a été changé pour un autre médicament appelé olanzapine, qui a bien aidé à stabiliser son état mental.\n\n### Ce que cela signifie\n\nCe cas montre qu’il faut faire attention quand on donne plusieurs médicaments qui agissent sur la sérotonine. Leur association peut provoquer un syndrome sérotoninergique, qui est dangereux et demande une prise en charge rapide en milieu hospitalier. Grâce à un diagnostic rapide et un traitement adapté, le patient a pu s’améliorer et retrouver son état normal.",
+            "B3": "Résumé détaillé du cas clinique de M. RL\n\nContexte  \nM. RL est un homme de 27 ans, soudeur de profession, sans antécédents médicaux notables, vivant dans un contexte socioéconomique modeste. Il a présenté une évolution psychiatrique initiale marquée par des idées de persécution, des comportements inhabituels et des hallucinations, conduisant à un diagnostic d’accès psychotique aigu. Il a été traité par halopéridone, un neuroleptique, mais son état s’est aggravé avec une mauvaise observance thérapeutique et l’apparition de symptômes négatifs tels que perte de plaisir, isolement social et troubles du sommeil. Deux mois plus tard, son traitement a été complété par deux antidépresseurs : la paroxétine et l’amitriptyline.\n\nPrincipales observations cliniques  \nQuelques heures après la prise simultanée de ces deux antidépresseurs, M. RL a développé une perte de conscience associée à une agitation psychomotrice, justifiant son hospitalisation en soins intensifs. À l’examen, il présentait un état de confusion (score de Glasgow 13/15), une agitation, des pupilles dilatées (mydriase), des tremblements, une respiration rapide (tachypnée), un rythme cardiaque accéléré (tachycardie), une hyperréflexie avec des myoclonies spontanées plus marquées aux membres inférieurs, ainsi qu’une hypersudation et des frissons.\n\nDémarche diagnostique  \nUn bilan biologique complet a révélé une perturbation des électrolytes, une acidose métabolique et une élévation modérée de la créatine phosphokinase (CPK), enzyme indiquant un possible stress musculaire. Les examens infectieux (analyse des urines, liquide céphalorachidien, hémocultures) étaient négatifs, tout comme la radiographie thoracique et l’imagerie cérébrale par IRM. L’électrocardiogramme a montré une fibrillation auriculaire, une arythmie cardiaque. Après avoir exclu les causes infectieuses, métaboliques et neurologiques, le diagnostic retenu a été celui d’un syndrome sérotoninergique, une réaction grave liée à un excès de sérotonine dans le système nerveux central, souvent provoquée par la prise simultanée de plusieurs médicaments augmentant la sérotonine.\n\nIntervention thérapeutique  \nLe patient a été pris en charge en unité de soins intensifs avec une ventilation mécanique, une alimentation par gavage, une réhydratation adaptée avec des solutions électrolytiques, une sédation par midazolam, un traitement préventif anticoagulant et un contrôle glycémique par insuline. Cette prise en charge a permis une stabilisation rapide de son état hémodynamique et neurologique en 24 heures.\n\nSuivi et évolution  \nAprès stabilisation, M. RL a été transféré en service de psychiatrie. À ce stade, il était calme, bien orienté dans le temps et l’espace, mais présentait encore des idées délirantes à contenu mystico-religieux et persécutoire, un jugement perturbé, sans signes dépressifs, maniaques ou confusionnels. Sous traitement neuroleptique atypique (olanzapine), son état psychiatrique s’est nettement amélioré, avec un retour progressif à son état antérieur.\n\nConclusion  \nCe cas illustre un syndrome sérotoninergique grave survenu chez un jeune patient à la suite de la prise concomitante de paroxétine et d’amitriptyline, deux antidépresseurs augmentant la concentration de sérotonine. Cette complication a nécessité une hospitalisation en soins intensifs et une prise en charge multidisciplinaire. Il souligne l’importance d’une surveillance attentive lors de l’association de médicaments sérotoninergiques, notamment chez les patients présentant des troubles psychiatriques complexes."
+        }
+    },
+    {
+        "article": "Un patient de 26 ans a été admis à notre hôpital avec des antécédents de jaunisse récurrente de la peau et des urines depuis plus d'un an. Le 1er juin 2022, le patient a présenté une jaunisse et des urines jaunes, sans déclencheur évident. Un examen échographique a révélé la présence de plusieurs calculs dans les voies biliaires communes et intrahépatiques, avec une légère dilatation des voies biliaires intrahépatiques (diamètre : 0,32 cm, référence : ≤ 0,2 cm) et des voies biliaires communes (diamètre : 1,04 cm, référence : 0,6-0,8 cm). Ces résultats ont confirmé l'impression initiale de jaunisse obstructive. Le 15 juin 2022, le patient a subi une cholédocholithotomie laparoscopique, une cholécystectomie et une lithotomie cholédoque. Cependant, il n'y a eu aucune amélioration de la fonction hépatique ni des symptômes de jaunisse après la chirurgie au cours de l'année écoulée. Afin de rechercher une assistance médicale supplémentaire, le patient a été admis à notre hôpital avec un ictère d'origine inconnue le 12 août 2023. Le patient a nié une histoire de tabagisme, d'abus d'alcool et d'utilisation à long terme de médicaments nocifs pour le foie, y compris des suppléments à base de plantes et des compléments alimentaires.\n\nL’examen physique a révélé la présence d’un jaunissement généralisé de la peau et de la sclère, ainsi qu’une rate palpable de 2 doigts sous la cage thoracique. En outre, l’indice de masse corporelle du sujet a été enregistré à 17,4 kg/m².\n\nLes résultats des examens de laboratoire vitaux ont été présentés dans le tableau 1. En outre, les anticorps antinucléaires (ANA) 1:100, les anticorps antineutrophiles cytoplasmiques (p-ANCA) positifs, le profil d'anticorps des maladies auto-immunes du foie étaient tous négatifs ; l'hépatite A à E, le virus d'Epstein-Barr, le cytomégalovirus, le virus Coxsackie, le virus de l'herpès zoster, le treponema pallidum et le virus de l'immunodéficience humaine étaient tous négatifs.\n\nLa cholangiopancréatographie par résonance magnétique (MRCP) a révélé l’existence d’un canal biliaire intrahépatique gauche et d’un canal biliaire commun dilatés, en l’absence de vésicule biliaire, d’une splénomégalie et de nombreux ganglions lymphatiques élargis dans la région hilaire. L’examen histologique du foie a révélé que la structure des lobules hépatiques et du réseau capillaire des voies biliaires n’était pas clairement discernable. Certains capillaires biliaires présentaient une dilatation, accompagnée de la formation d’un thrombus biliaire. Il existait également une fibrose de pontage des voies porteuses vers la veine centrale. La disparition des voies biliaires a été observée dans 10 des 12 voies porteuses. Ce phénomène est le plus souvent attribué au syndrome de la voie biliaire effacée (VBDS). Le score simplifié de Scheuer indiquait un grade 2 et un stade 3 à 4. Le séquençage de l’exome entier a révélé la présence d’une mutation hétérozygote dans PKLR (NM_000298.5:c.119G > A) et UGT1A1 (NM_000463.2:c.3275T > G).\n\nÀ la lumière des preuves susmentionnées, un diagnostic révisé a été rendu comme étant un VBDS avec PLKR et UGT1A1 mutation, cirrhose cholestatique. Une dose de 1000 mg/j d’acide ursodexycholique (UDCA) et 8 mg/j de méthylprednisolone a été administrée afin d’améliorer la cholestase et l’inflammation hépatique.\n\nAu fil du temps, une imagerie par résonance magnétique (IRM) à contraste amélioré, réalisée le 10 septembre 2023, a révélé la présence de calculs dans le canal biliaire commun, malgré l'absence de fièvre, de douleurs abdominales ou d'autres symptômes. La patiente a refusé de faire retirer les calculs du canal biliaire commun. Le 25 octobre 2023, un examen MRCP a révélé des changements dynamiques. Le système biliaire a présenté une sténose en bandes et un aspect d'arbre élagué, ce qui était cohérent avec l'aspect de la cholangite sclérosante observé par imagerie. Une nouvelle coloscopie a été réalisée avec une préparation intestinale adéquate, en respectant les directives pour les patients présentant des lésions muqueuses présumées, qui a révélé la présence d'une UC impliquant l'iléon terminal et le hémicolon droit. Ce résultat était cohérent avec les manifestations coloscopiques de la PSC-UC. En outre, la PSC-UC est un sous-type unique de UC, ce qui rend difficile l'application des critères de classification de Montréal pour décrire la topographie de la maladie. Par conséquent, le diagnostic a été révisé à PSC-UC avec des mutations PLKR et UGT1A1, cholédocholithiase.\n\nLe 25 novembre 2023, une cholangiopancréatographie rétrograde transduodénoscopique (ERCP) et une sphinctérotomie endoscopique (EST) ont été réalisées. Une pierre noire irrégulière de 4 mm × 5 mm et un grand nombre de pierres sédimentaires ont été enlevées avec succès en utilisant une dilatation papillaire duodénale endoscopique (EPBD). Après la résolution de l’obstruction, un régime à long terme de 1000 mg/d UDCA en association avec 10 mg/d d’acide obéticholique (OCA) a été prescrit pour améliorer la cholestase. En outre, 8 g/d de colestyramine a été prescrit pour faciliter l’adsorption des acides biliaires en excès, tandis que 1,2 g/d de rifaximine a été administré pour prévenir une infection des voies biliaires. En outre, étant donné que la UC du patient était limitée à l’iléon terminal et au droit hémicolon, il y avait peu de selles mucopurulentes et sanglantes, ainsi que de diarrhée. Les comprimés de mésalazine (2 g par jour) ont été administrés dans le but d’améliorer l’inflammation du côlon. Le 30 juillet 2024, la fonction hépatique du patient était la suivante : TB/DB 33/25,9 μmol/L, phosphatase alcaline (ALP)/GGT 183/112 U/L, IgG 17,19 g/L. L’état du patient est resté stable.\n",
+        "gold_summary": "Inquiétudes du patient : Un patient de sexe masculin âgé de 26 ans se plaint d'une histoire de peau et d'urine jaunes récurrentes depuis plus d'un an.\n\nDiagnostics : Après imagerie par cholangiopancréatographie par résonance magnétique dynamique, manifestation coloscopique, biopsie du foie et séquençage de l'exome entier, le patient a finalement été diagnostiqué avec une CSP - colite ulcéreuse avec mutation PLKR et UGT1A1.\n\nInterventions : Après résolution de l'obstruction, un régime à long terme de 1000 mg/j d'acide ursodexycholique en association avec 10 mg/j d'acide obéticholique pour améliorer la cholestase, 8 g/j de cholestyramine pour faciliter l'adsorption des acides biliaires en excès et 1,2 g/j de rifaximine pour prévenir l'infection des voies biliaires ont été prescrits.\n\nRésultats : Les paramètres biochimiques du foie du patient se sont considérablement améliorés. Son état est stable et il n'a pas subi de transplantation de foie à ce jour.\n",
+        "synthetic_summary": {
+            "B1": "Un jeune homme a eu la peau et l’urine jaunes depuis longtemps.  \n\nLes docteurs ont fait beaucoup de tests pour comprendre pourquoi.  \n\nIls ont trouvé que son foie et ses intestins ne marchaient pas bien.  \n\nIls lui ont donné des médicaments pour aider son foie à mieux travailler.  \n\nMaintenant, il va mieux et il est stable.  \n\nLes docteurs continuent de bien s’occuper de lui.",
+            "B2": "**Ce qu’il s’est passé avec le patient**  \nUn jeune homme de 26 ans avait la peau et les urines jaunes plusieurs fois depuis plus d’un an. Ce jaunissement, appelé jaunisse, est souvent lié à un problème dans le foie ou les voies biliaires, qui transportent la bile.\n\n**Ce qu’ils ont découvert**  \nDes examens d’imagerie ont montré que ses canaux biliaires étaient dilatés et contenaient des calculs (des petits cailloux). Une biopsie du foie, c’est-à-dire un prélèvement d’un petit morceau de foie pour l’étudier, a révélé que beaucoup de ses petits canaux biliaires avaient disparu, ce qui correspond à un syndrome appelé « voie biliaire effacée ». En plus, des analyses génétiques ont trouvé des mutations dans deux gènes, PKLR et UGT1A1, qui peuvent affecter le fonctionnement du foie.\n\nPlus tard, une coloscopie, un examen qui regarde l’intérieur du côlon, a montré qu’il avait une colite ulcéreuse, une maladie inflammatoire de l’intestin. Ces signes, avec les images des voies biliaires, ont conduit au diagnostic d’une maladie appelée cholangite sclérosante primitive (CSP) associée à la colite ulcéreuse.\n\n**Les traitements donnés**  \nAprès avoir enlevé les calculs dans les voies biliaires grâce à une procédure endoscopique (une technique utilisant un tube fin avec une caméra), le patient a reçu plusieurs médicaments :  \n- De l’acide ursodésoxycholique pour aider à améliorer le flux de bile et protéger le foie.  \n- De l’acide obéticholique pour réduire l’inflammation et la cholestase (l’arrêt du flux biliaire).  \n- De la cholestyramine pour éliminer l’excès d’acides biliaires qui peuvent irriter le corps.  \n- De la rifaximine pour prévenir les infections dans les voies biliaires.  \n- Et de la mésalazine pour calmer l’inflammation dans le côlon liée à la colite ulcéreuse.\n\n**Comment il va maintenant**  \nGrâce à ces traitements, les analyses de son foie se sont nettement améliorées et son état est stable. Jusqu’à présent, il n’a pas eu besoin de greffe du foie. Les médecins continuent de le suivre pour surveiller sa santé.",
+            "B3": "Résumé détaillé et structuré pour un public adulte non-médecin\n\n**Contexte**  \nUn homme de 26 ans a été suivi pendant plus d’un an pour des épisodes répétés de jaunisse, caractérisée par un jaunissement de la peau et des urines. Initialement, des calculs biliaires ont été détectés et retirés chirurgicalement, mais ses symptômes et la fonction hépatique ne se sont pas améliorés. À son admission en août 2023, il présentait un ictère persistant sans cause évidente, une perte de poids importante (indice de masse corporelle à 17,4 kg/m²) et une rate légèrement augmentée de volume.\n\n**Principales observations**  \nLes examens sanguins ont exclu les infections virales courantes du foie et les maladies auto-immunes classiques. L’imagerie par résonance magnétique (MRCP) a montré une dilatation des voies biliaires, l’absence de vésicule biliaire, une hypertrophie de la rate et des ganglions lymphatiques élargis. La biopsie hépatique a révélé une destruction quasi complète des petits canaux biliaires dans le foie, un phénomène appelé syndrome de la voie biliaire effacée (VBDS), associé à une fibrose avancée (cicatrisation du foie). Le séquençage génétique a identifié des mutations dans deux gènes, PKLR et UGT1A1, qui peuvent influencer le métabolisme du foie et la gestion des pigments biliaires.\n\nPar la suite, une nouvelle imagerie a montré des calculs persistants dans le canal biliaire commun. Une coloscopie a révélé une colite ulcéreuse (inflammation chronique du côlon) touchant spécifiquement l’iléon terminal et le côlon droit, une association fréquente avec une maladie appelée cholangite sclérosante primitive (CSP), une inflammation chronique des voies biliaires. Cette combinaison a conduit à un diagnostic révisé de CSP associée à une colite ulcéreuse (PSC-UC), avec les mutations génétiques identifiées.\n\n**Interventions**  \nLe patient a subi une intervention endoscopique pour retirer les calculs biliaires obstructifs. Ensuite, un traitement médicamenteux combiné a été instauré pour améliorer la circulation biliaire et réduire l’inflammation :  \n- Acide ursodésoxycholique (1000 mg/j) et acide obéticholique (10 mg/j) pour favoriser l’élimination de la bile et protéger les cellules hépatiques.  \n- Cholestyramine (8 g/j) pour adsorber les acides biliaires en excès et limiter leurs effets toxiques.  \n- Rifaximine (1,2 g/j) pour prévenir les infections des voies biliaires.  \n- Mésalazine (2 g/j) pour traiter l’inflammation intestinale liée à la colite ulcéreuse.\n\n**Résultats et suivi**  \nAprès plusieurs mois de traitement, les analyses sanguines montrent une amélioration notable des marqueurs de la fonction hépatique, bien que certains paramètres restent légèrement élevés, témoignant d’une maladie chronique stable. Le patient ne présente pas de complications majeures et n’a pas nécessité de transplantation hépatique à ce jour.\n\n**Conclusion**  \nCe cas illustre une forme complexe de maladie hépatobiliaire chronique associée à une inflammation intestinale, compliquée par des anomalies génétiques rares. Le diagnostic précis, combinant imagerie, biopsie et analyse génétique, a permis d’adapter un traitement ciblé qui stabilise la maladie et améliore la qualité de vie du patient. Un suivi régulier est indispensable pour surveiller l’évolution et prévenir les complications."
+        }
+    },
+    {
+        "article": "Le cas d'une femme de 43 ans, ayant des antécédents de cancer du sein, diagnostiqué avant la ménopause, est décrit. La patiente a présenté des symptômes gastro-intestinaux non spécifiques, tels que la plénitude postprandiale, l'augmentation du périmètre abdominal, des douleurs abdominales intermittentes, avec prédominance dans le méogastre, qui ont évolué pendant 12 mois. Par la suite, une dyspnée modérée a été ajoutée. La patiente s'est présentée à un médecin de premier contact, qui a établi le protocole d'étude et lui a demandé une échographie de l'abdomen et du bassin, qui a mis en évidence une tumeur qui couvrait l'ensemble de la cavité abdominale, et a complété l'étude par une tomographie par ordinateur avec contraste du thorax, de l'abdomen et du bassin, qui a montré une tumeur de 27,5 x 12,7 x 28,2 cm, hétérogène, à prédominance liquide, avec présence de septa.\n\nLes marqueurs tumoraux ont présenté Ca 125 à 84,16, ACE 10,07, AFP 1,83, B-HGC 0,1. La numération formule sanguine a montré des tests de fonction hépatique et des temps de coagulation dans les paramètres normaux. La patiente a été envoyée au Service des tumeurs gynécologiques de l’Hôpital d’oncologie du Centre médical national Siglo XXI, où nous avons proposé une laparotomie avec étude transopératoire. L’intervention chirurgicale a été effectuée et une salpingo-ovariectomie gauche a été réalisée et envoyée pour étude transopératoire.\n\nL'intervention chirurgicale a révélé une mucinose, avec un taux de carcinomatose de 16 points, avec des implants de mucine dans toute l'étendue du péritoine pariétal, la capsule de Gleason et la rate, ainsi qu'une tumeur ovarienne gauche rompue.\n\nL’ovaire gauche de 3450 g, mesurant 28 x 27 x 14 cm, a été reçu en étude transopératoire avec une capsule rompue, une surface interne multiloculaire avec un contenu mucineux et une zone kystique de 7 x 6,5 cm a été identifiée avec un contenu sébacé et des poils. Aux coupes histologiques, on a observé un tissu ectodermique composé d’épithélium squameux et de follicules pileux, ainsi qu’un tissu endodermique composé d’épithélium de type intestinal, qui dans plusieurs coupes a présenté une atypie marquée avec une disposition architecturale complexe jusqu’à ce que l’on trouve des cellules en anneau de sceau, correspondant à un adénocarcinome. Aucun élément immature n’a été identifié dans l’échantillon de la tumeur.\n\nLa chirurgie de stade et de réduction de la tumeur de l'ovaire a été poursuivie, avec une hystérectomie totale + salpingo-ovariectomie bilatérale + péritonectomie + appendicectomie. Des résultats positifs ont été obtenus en termes d'activité tumorale, et une cholécystectomie et une splénectomie ont été décidées. Une chimiothérapie hyperthermique intra-opératoire a été ajoutée avec 45 mg de cisplatine dans 1000 ml de solution saline physiologique à 0,9 % à 40 °C, et une réduction de la tumeur optimale a été obtenue, qui a été classée comme stade IIIC. Des implants de la tumeur (adénocarcinome) ont également été observés dans l'omentum, la capsule hépatique et la capsule splénique dans le rapport histopathologique.\n\nLa patiente a été envoyée au service d'oncologie médicale et a été considérée comme candidate à un traitement adjuvant par carboplatine et paclitaxel en six cycles, qui s'est terminé sans incident. Elle a actuellement de bons résultats oncologiques, avec une période sans maladie de sept mois ; elle est suivie par le service des tumeurs gynécologiques.\n",
+        "gold_summary": "Femme de 43 ans, atteinte d'un tératome mature malin à cellules en anneau de sceau. Une citoréduction primaire optimale a été réalisée ; hystérectomie totale, salpingo-ovariectomie bilatérale, péritonectomie, appendicectomie, cholécystectomie et splénectomie, ainsi qu'une chimiothérapie hyperthermique intra-opératoire (HIPEC).\n",
+        "synthetic_summary": {
+            "B1": "Une dame de 43 ans avait une grosse boule dans son ventre. Les docteurs ont enlevé cette boule avec une grande opération. Ils ont aussi enlevé quelques parties du corps pour que la dame aille mieux. Après, elle a reçu un médicament chaud pour tuer les petites choses mauvaises. Maintenant, elle va mieux et les docteurs la surveillent.",
+            "B2": "**Résumé simplifié pour un adolescent :**\n\nUne femme de 43 ans a été diagnostiquée avec un type rare de tumeur appelée tératome mature malin. Cette tumeur contenait des cellules spéciales appelées \"cellules en anneau de sceau\", qui sont un type de cellules cancéreuses.\n\nPour la soigner, les médecins ont fait une grande opération. Ils ont enlevé plusieurs organes : l’utérus (c’est l’organe où un bébé peut grandir), les deux ovaires, une partie de la membrane qui recouvre l’abdomen (le péritoine), l’appendice, la vésicule biliaire et la rate. Cette opération visait à retirer toute la tumeur possible, ce qu’on appelle une \"citoréduction optimale\".\n\nPendant la chirurgie, ils ont aussi utilisé une technique spéciale appelée chimiothérapie hyperthermique intra-opératoire (HIPEC). Cela signifie qu’ils ont chauffé un médicament anticancéreux (le cisplatine) et l’ont fait circuler directement dans l’abdomen pour tuer les cellules cancéreuses restantes.\n\nAprès cette opération et ce traitement, la patiente a reçu une chimiothérapie supplémentaire avec d’autres médicaments pour s’assurer que le cancer ne revienne pas. Sept mois après, elle va bien et ne montre pas de signes de maladie. Elle continue d’être suivie régulièrement par les médecins spécialistes.",
+            "B3": "Résumé détaillé et structuré pour un public adulte non spécialiste\n\n**Contexte**  \nUne femme de 43 ans, avec des antécédents de cancer du sein avant la ménopause, a présenté pendant un an des symptômes digestifs peu spécifiques, notamment une sensation de plénitude après les repas, une augmentation du volume abdominal et des douleurs intermittentes localisées surtout dans la région centrale de l’abdomen (mésogastre). Par la suite, elle a développé une difficulté modérée à respirer (dyspnée). Une échographie abdominale a révélé une masse tumorale occupant toute la cavité abdominale, confirmée par un scanner avec injection de produit de contraste qui a montré une tumeur volumineuse (environ 28 cm de grand axe), de nature hétérogène et contenant des zones liquides cloisonnées.\n\n**Principales observations**  \nLes analyses sanguines ont montré une élévation modérée du marqueur tumoral CA 125, souvent associé aux tumeurs ovariennes, tandis que d’autres marqueurs (ACE, AFP, B-HCG) étaient dans les limites normales. Les fonctions hépatiques et la coagulation étaient normales. La patiente a été prise en charge dans un centre spécialisé en oncologie gynécologique, où une intervention chirurgicale par laparotomie a été décidée.\n\nAu cours de l’opération, une tumeur mucineuse (produisant du mucus) a été découverte, avec une dissémination étendue de mucine dans le péritoine (membrane qui tapisse la cavité abdominale), la rate et la capsule de Gleason (une partie du péritoine). La tumeur ovarienne gauche, très volumineuse (plus de 3 kg), était rompue. L’examen rapide en cours d’opération a montré que cette tumeur contenait des tissus caractéristiques d’un tératome mature (une tumeur composée de plusieurs types de tissus, ici notamment des tissus cutanés et intestinaux), mais aussi des zones où des cellules cancéreuses en forme d’anneau de sceau (un type particulier d’adénocarcinome, c’est-à-dire un cancer des cellules glandulaires) étaient présentes, sans éléments immatures (plus agressifs).\n\nLa chirurgie a été étendue pour retirer l’utérus, les deux ovaires et trompes, le péritoine, l’appendice, la vésicule biliaire et la rate, afin d’éliminer au maximum la tumeur. Une chimiothérapie hyperthermique intra-opératoire (HIPEC) a été réalisée : il s’agit d’une technique qui consiste à appliquer localement un médicament anticancéreux chauffé (ici du cisplatine à 40 °C) dans la cavité abdominale pour détruire les cellules tumorales résiduelles. La réduction tumorale a été jugée optimale, et la maladie classée au stade IIIC, indiquant une atteinte étendue mais encore opérable.\n\nL’analyse histologique a confirmé la présence d’implants tumoraux sur plusieurs organes abdominaux, notamment l’épiploon (omentum), la capsule du foie et celle de la rate.\n\n**Interprétation clinique**  \nLe diagnostic principal est celui d’un tératome mature malin avec transformation carcinomateuse en adénocarcinome à cellules en anneau de sceau, une forme rare et agressive de tumeur ovarienne. La prise en charge a combiné une chirurgie étendue visant à retirer toute la masse tumorale visible, complétée par une chimiothérapie locale chauffée pour améliorer le contrôle de la maladie.\n\n**Prochaines étapes**  \nAprès la chirurgie, la patiente a reçu un traitement complémentaire par chimiothérapie systémique à base de carboplatine et paclitaxel, administrée en six cycles. Ce traitement a été bien toléré et a permis d’obtenir une rémission clinique, avec une absence de signes de maladie pendant au moins sept mois à ce jour. La patiente reste suivie régulièrement en oncologie gynécologique pour surveiller toute récidive éventuelle.\n\n---\n\nCe cas illustre l’importance d’une prise en charge multidisciplinaire combinant chirurgie radicale et traitements complémentaires adaptés pour les tumeurs ovariennes rares et complexes."
+        }
+    },
+    {
+        "article": "Femme de 60 ans, ancienne fumeuse, en surpoids et atteinte de polyarthrite rhumatoïde, traitée par méthotrexate et golimumab. Antécédent d'exérèse en bloc d'une tumeur pelvienne, avec résection du rectum, reconstruction par anastomose colorectale et sacrectomie distale au niveau de la quatrième vertèbre sacrée (S4). L'anatomie pathologique correspondait à une formation kystique multiloculaire de 22 x 8,5 cm. Les coupes histologiques ont révélé une paroi de tissu fibreux avec revêtement épithélial squameux ou pseudo-stratifié, et des infiltrats lympho-histiocytaires, des vaisseaux sanguins ectasiques et des structures glandulaires occasionnelles avec des modifications de type réactif. Ces résultats étaient compatibles avec un tératome kystique mature. Deux ans après l'exérèse, elle a présenté des symptômes au niveau sacré. Des tomodensitogrammes et des examens IRM ont été demandés, qui ont révélé, au niveau des dernières vertèbres sacrées, la présence d'une formation de parties molles hétérogènes d'environ 60 mm de diamètre, associée à une raréfaction des plans graisseux et à un liquide adjacente peu abondant. Une biopsie par aiguille fine a été réalisée, dont le résultat a confirmé la récidive d'un tératome mature. Après la stadification, qui n'a pas révélé de maladie systémique, elle a été évaluée par un comité multidisciplinaire de tumeurs et une conduite chirurgicale en bloc a été indiquée. Une approche postérieure a été réalisée en résécant la cicatrice pré-existante, une section partielle des muscles fessiers et pyramidaux, une section sacrée au niveau S2-S3, en respectant les deux racines S3, une libération de l'espace pré-sacré et une exérèse de la pièce. La patiente a évolué favorablement dans la période post-opératoire. L'examen anatomo-pathologique macroscopique a révélé une formation tumorale de 7,8 x 6 x 4,5 cm adhérente à l'os sacré. Au moment de la coupe, elle était principalement solide, de consistance hétérogène avec des secteurs d'aspect friable, des zones kystiques avec du liquide et du gel et des foyers de calcification. Les coupes histologiques ont montré l'atteinte osseuse par des structures glandulaires néoplasiques avec un pléomorphisme nucléaire modéré, la formation de structures micropapillaires, la production de mucine et des zones de nécrose. Dans certaines zones kystiques périphériques, on a reconnu un épithélium cilié colonnaire mature. Les marges chirurgicales de résection étaient libres de toute atteinte néoplasique. Les techniques d'immunomarquage ont été positives pour CK20, calretinine, p53 et, de manière focale, pour CDX2, et négatives pour CK7, WT-1, PAX8 et CA125. Ces résultats étaient compatibles avec une récidive de tératome mature avec transformation somatique maligne vers un adénocarcinome de type colorectal. Une vidéocolonoscopie normale a été réalisée, confirmant ainsi le diagnostic de transformation maligne de tératome sacré. Elle est restée sous contrôle multidisciplinaire. Après 24 mois sans maladie, elle a présenté une détérioration de l'état général et une augmentation rapide de CA 19.9, ce qui a conduit à une PET/CT qui a révélé de multiples images hyper-capteurs au niveau viscéral, des tissus mous et des os compatibles avec un secondaire. En raison de la détérioration fonctionnelle rapide, elle n'a pas pu recevoir un traitement systémique et est décédée deux mois plus tard.\n",
+        "gold_summary": "Le cas d'une femme de 60 ans ayant des antécédents de résection en bloc d'une tumeur pelviane présacrée dont l'anatomie pathologique a rapporté un tératome mature a été présenté. Après 2 ans, elle s'est présentée pour une douleur sacro-coccygienne. Les études d'imagerie ont révélé une tumeur de 6 cm avec une atteinte osseuse des dernières vertèbres sacrées. Une biopsie avec aiguille épaisse a été réalisée et a rapporté une récidive de tératome mature. Après cette stadification qui n'a pas mis en évidence de maladie systémique, elle a été évaluée par un comité multidisciplinaire et une conduite chirurgicale a été indiquée. Une résection en bloc a été réalisée avec une sacrectomie distale au niveau de S3 et des muscles environnants. L'étude anatomopathologique a rapporté la présence d'un tératome mature avec une transformation maligne, avec un composant d'adénocarcinome de type colorectal. Les marges de résection étaient exemptes de tumeur. Après une nouvelle évaluation multidisciplinaire, une stratégie de contrôle a été décidée. Elle est restée exempte de maladie pendant 24 mois, à partir desquels elle a présenté une détérioration générale associée à la progression de la maladie, et est morte 2 mois plus tard.\n",
+        "synthetic_summary": {
+            "B1": "Une dame de 60 ans avait une grosse boule près de ses os du bas du dos. Les docteurs l'ont enlevée. Cette boule n'était pas dangereuse.\n\nDeux ans plus tard, elle a eu mal au même endroit. Les docteurs ont vu qu'une autre boule avait poussé. Ils ont fait une petite opération pour prendre un bout.\n\nIls ont trouvé que la boule était revenue et qu'elle avait changé un peu. Ils ont fait une grande opération pour tout enlever. Après, elle est restée sans mal pendant deux ans.\n\nPuis, elle est devenue très fatiguée et malade. La maladie est revenue dans d'autres parties de son corps. Elle est partie au ciel deux mois après.",
+            "B2": "**Résumé adapté pour un adolescent de 14 ans**\n\nCette histoire parle d’une femme de 60 ans qui avait déjà eu une grosse tumeur près du bassin, appelée tératome mature. Un tératome mature est une sorte de tumeur qui contient différents types de tissus, comme de la peau ou des glandes, mais qui est généralement bénigne (pas cancéreuse). Elle avait subi une opération importante pour enlever cette tumeur.\n\nDeux ans plus tard, elle a commencé à avoir des douleurs dans le bas du dos, près du coccyx. Des examens d’imagerie, comme des scanners et des IRM, ont montré qu’une nouvelle masse d’environ 6 centimètres s’était formée au niveau des dernières vertèbres du sacrum (les os à la base de la colonne vertébrale). Une biopsie, c’est-à-dire un prélèvement d’un petit morceau de cette masse, a confirmé que la tumeur était revenue, toujours un tératome mature.\n\nAprès avoir vérifié qu’il n’y avait pas de maladie ailleurs dans le corps, une équipe de médecins spécialistes a décidé de refaire une opération pour enlever cette tumeur. L’opération a consisté à retirer la masse ainsi qu’une partie des os et des muscles autour. \n\nL’analyse de la tumeur en laboratoire a montré quelque chose d’important : la tumeur avait changé et était devenue en partie cancéreuse. En effet, une partie de la tumeur s’était transformée en un adénocarcinome, un type de cancer qui ressemble à celui que l’on trouve souvent dans le côlon (le gros intestin). Heureusement, les chirurgiens ont réussi à enlever toute la tumeur sans laisser de cellules cancéreuses autour.\n\nAprès cette opération, la femme a été suivie régulièrement. Pendant deux ans, elle n’a pas eu de problème. Puis, son état de santé s’est rapidement aggravé. Des examens ont montré que le cancer s’était propagé à plusieurs endroits dans son corps. Malheureusement, elle n’a pas pu recevoir de traitement et elle est décédée deux mois plus tard.\n\n**Ce qu’il faut retenir :**  \n- Un tératome mature est une tumeur souvent bénigne, mais qui peut parfois revenir et devenir cancéreuse.  \n- La surveillance après une opération est très importante pour détecter rapidement toute récidive.  \n- La transformation maligne d’un tératome est rare mais grave, car elle peut évoluer en cancer agressif.",
+            "B3": "Résumé structuré pour un public non médical éduqué\n\nContexte  \nUne femme de 60 ans, avec des antécédents médicaux comprenant une polyarthrite rhumatoïde et un surpoids, avait subi l’ablation complète d’une tumeur pelvienne située devant le sacrum (os à la base de la colonne vertébrale). Cette tumeur, identifiée comme un tératome mature (une tumeur bénigne composée de différents types de tissus), avait été retirée chirurgicalement avec une partie du rectum et une section du sacrum.\n\nPrincipales observations  \nDeux ans après cette opération, la patiente a ressenti des douleurs au niveau du sacrum. Des examens d’imagerie (scanner et IRM) ont montré une nouvelle masse d’environ 6 cm, envahissant les dernières vertèbres sacrées. Une biopsie a confirmé qu’il s’agissait d’une récidive du tératome mature. Aucun signe de propagation à distance n’a été détecté. Un comité multidisciplinaire a alors recommandé une nouvelle intervention chirurgicale, consistant en une résection en bloc (ablation complète) de la tumeur, incluant une partie du sacrum et des muscles environnants.\n\nInterprétation clinique  \nL’analyse détaillée de la pièce opératoire a révélé que la tumeur récidivante avait subi une transformation maligne, c’est-à-dire qu’une partie du tératome s’était transformée en un adénocarcinome de type colorectal, un cancer agressif ressemblant à celui du côlon. Les marges de la résection étaient saines, indiquant que la tumeur avait été complètement enlevée. Une coloscopie (examen du côlon) normale a confirmé que ce cancer ne provenait pas du côlon mais bien de la transformation du tératome sacré.\n\nProchaines étapes et évolution  \nAprès cette chirurgie, la patiente a été suivie régulièrement sans signe de maladie pendant 24 mois. Ensuite, son état général s’est rapidement dégradé, accompagné d’une augmentation importante d’un marqueur sanguin (CA 19-9) suggérant une récidive tumorale. Une imagerie par TEP/CT a montré une dissémination de la maladie dans plusieurs organes, tissus mous et os. En raison de son état général très affaibli, elle n’a pas pu bénéficier d’un traitement anticancéreux systémique et est décédée deux mois plus tard.\n\nCe cas illustre la possibilité rare mais grave de transformation maligne d’un tératome mature récidivant au niveau sacré, nécessitant une prise en charge chirurgicale complexe et un suivi attentif."
+        }
+    },
+    {
+        "article": "Les dossiers médicaux des patients atteints de myotonie congénitale, étudiés et suivis au sein du service de neurologie pédiatrique d’un hôpital de troisième niveau entre 2015 et 2020, ont été examinés. Les critères d’inclusion étaient un diagnostic clinique (myotonie, phénomène de réchauffement, patron électromyographique caractéristique et/ou antécédents familiaux) et/ou un diagnostic moléculaire (mutation dans le gène CLCN1). Les signes et symptômes cliniques, ainsi que les résultats des examens complémentaires et la mutation génétique trouvée, ont été recueillis au moyen d’un examen du dossier médical. Les variables démographiques (âge et sexe), l’évolution de la maladie (âge de début, symptômes et signes, temps écoulé jusqu’au diagnostic et évolution clinique), les antécédents familiaux et l’évaluation de la réponse au traitement ont été recueillis.\n\nCinq cas ont été identifiés avec un diagnostic clinique de myotonie congénitale (trois avec la maladie de Becker et deux avec la maladie de Thomsen). L'incidence par rapport au nombre de naissances est estimée à 1:15 000 nouveau-nés pour les cas avec le phénotype Becker et 1:21 000 nouveau-nés pour les phénotypes Thomsen.\n\nLa plupart de nos patients étaient des femmes, et le seul homme a commencé avant l'âge de six ans. La clinique initiale comprenait une myotonie des membres inférieurs chez quatre des cinq patients et des membres supérieurs également chez tous sauf un. L'âge au début variait de 22 mois à 12 ans, avec une médiane de 6 ans. Le diagnostic génétique a été effectué dans tous les cas environ deux ans après le début, et la famille d'une patiente a refusé de le faire. Tous ont présenté une aggravation par le froid, mais le phénomène de réchauffement, seulement ceux qui avaient le phénotype de Becker.\n\nLes patients atteints de myotonie congénitale récessive ont présenté une certaine progression. En ce qui concerne les antécédents familiaux, il convient de noter que les patientes 2 et 3 étaient sœurs, sans que les parents ne présentent aucun symptôme, et que la mère de la patiente 1 présentait des symptômes modérés et douteux au froid. La patiente qui a refusé l'étude avait des antécédents de myotonie du côté maternel.\n\nLes analyses sanguines n’ont révélé aucune augmentation de la créatine kinase chez aucun des patients. L’électromyogramme était pathologique chez tous les patients, sauf chez le premier patient âgé de 2,8/12 ans. Par la suite, le test n’a pas été répété car il n’était plus considéré comme nécessaire.\n\nLe traitement le plus utilisé initialement était l'oxcarbazépine (chez les patients atteints de la forme récessive), avec une bonne réponse en général. Dans le cas 2, il a perdu de l'efficacité avec le temps et le mexiletine a été initié. Le patient 4 a commencé à prendre plusieurs médicaments sans succès en raison d'une perte d'efficacité ou d'effets secondaires. Le patient 5 a refusé le traitement en raison d'une clinique légère.\n\nLe patient 1 présentait une mutation probablement pathogène non décrite précédemment (CLCN1 : c.824T>C), héritée de sa mère. Les cas 1 à 3 présentaient un phénotype Becker avec des mutations en hétérozygotie composée, et les cas 4 et 5 présentaient un phénotype Thomsen. Le cas 5 a refusé l'étude génétique.\n",
+        "gold_summary": "Les dossiers médicaux des patients atteints de myotonie congénitale, étudiés et suivis au sein du service de neurologie pédiatrique d'un hôpital de troisième niveau entre 2015 et 2020, ont été examinés. Les variables démographiques (âge et sexe), l'évolution de la maladie (âge de début, symptômes et signes, délai de diagnostic et évolution clinique), les antécédents familiaux et l'évaluation de la réponse au traitement ont été collectés. Cinq cas ont été identifiés avec un diagnostic clinique de myotonie congénitale (trois avec la maladie de Becker et deux avec la maladie de Thomsen). L'incidence par rapport au nombre de naissances a été estimée à 1:15 000 nouveau-nés pour les cas avec le phénotype Becker et à 1:21 000 nouveau-nés pour les phénotypes Thomsen. Nous avons trouvé une mutation probablement pathogénique non décrite précédemment (CLCN1 : c.824T>C).\n",
+        "synthetic_summary": {
+            "B1": "Il y a des enfants qui ont des muscles un peu raides. Cela s'appelle la myotonie. \n\nLes docteurs ont regardé cinq enfants avec cette raideur. Trois enfants avaient un type appelé Becker. Deux enfants avaient un autre type appelé Thomsen. \n\nCette raideur commence souvent quand les enfants ont entre 2 et 12 ans. Parfois, le froid rend les muscles encore plus raides. \n\nLes docteurs ont aussi trouvé un petit changement dans un gène, c’est comme un code dans le corps. Ce changement peut expliquer pourquoi les muscles sont raides. \n\nLes enfants peuvent prendre des médicaments pour aider leurs muscles à être moins raides. Les docteurs les surveillent pour voir si ça marche bien.",
+            "B2": "**Ce qu'ils ont étudié**  \nLes médecins ont examiné les dossiers de cinq enfants atteints d'une maladie appelée myotonie congénitale. Cette maladie affecte les muscles, qui ont du mal à se relâcher après une contraction. Ils ont regardé des informations comme l’âge, le sexe, les premiers signes de la maladie, le temps avant le diagnostic, les antécédents familiaux et la réponse aux traitements.\n\n**Ce qu'ils ont trouvé**  \nParmi ces cinq enfants, trois avaient une forme appelée maladie de Becker et deux une autre forme appelée maladie de Thomsen. Ces deux formes sont des types différents de myotonie congénitale. La maladie de Becker est un peu plus fréquente, touchant environ 1 bébé sur 15 000, tandis que la maladie de Thomsen touche environ 1 bébé sur 21 000.  \n\nLa plupart des patients étaient des filles, et les symptômes ont commencé entre 2 ans et 12 ans, en moyenne vers 6 ans. Les muscles des jambes étaient souvent touchés en premier, puis ceux des bras. Tous les patients avaient plus de difficultés quand il faisait froid, mais seulement ceux avec la maladie de Becker s’amélioraient un peu après avoir bougé un peu (on appelle ça le « phénomène de réchauffement »).  \n\n**Les analyses et traitements**  \nLes tests sanguins ne montraient pas de problème particulier, mais un examen des muscles appelé électromyogramme montrait des signes de la maladie chez presque tous les patients. Pour traiter la maladie, les médecins ont utilisé un médicament appelé oxcarbazépine, qui a bien aidé au début. Dans un cas, ce médicament est devenu moins efficace et un autre médicament, la mexilétine, a été essayé. Un patient a refusé de prendre un traitement parce que ses symptômes étaient légers.  \n\n**Découverte génétique importante**  \nChez un patient, ils ont trouvé une mutation (c’est-à-dire un changement dans un gène) qui n’avait jamais été décrite avant. Ce gène, appelé CLCN1, est important pour le fonctionnement des muscles. Cette découverte aide à mieux comprendre la maladie et pourrait aider à trouver de meilleurs traitements à l’avenir.  \n\nEn résumé, cette étude montre comment la myotonie congénitale peut commencer chez les enfants, comment elle se manifeste, et comment elle peut être traitée. Elle souligne aussi l’importance des tests génétiques pour mieux connaître cette maladie rare.",
+            "B3": "Résumé structuré sur la myotonie congénitale étudiée dans un service de neurologie pédiatrique\n\nContexte  \nCette étude a porté sur l’analyse des dossiers médicaux de cinq enfants diagnostiqués avec une myotonie congénitale, une maladie neuromusculaire rare caractérisée par une difficulté à relâcher les muscles après une contraction. Ces patients ont été suivis entre 2015 et 2020 dans un hôpital de troisième niveau spécialisé en neurologie pédiatrique. Le diagnostic reposait sur des critères cliniques (présence de myotonie, phénomène de réchauffement, résultats électromyographiques caractéristiques, et/ou antécédents familiaux) et/ou sur une confirmation génétique par la détection d’une mutation dans le gène CLCN1, responsable de la maladie.\n\nPrincipales observations  \nParmi les cinq cas identifiés, trois présentaient la forme dite « maladie de Becker » (forme récessive) et deux la forme « maladie de Thomsen » (forme dominante). L’incidence estimée était d’environ 1 cas pour 15 000 naissances pour la forme Becker, et 1 cas pour 21 000 naissances pour la forme Thomsen. La majorité des patients étaient des filles, avec un seul garçon dont les symptômes sont apparus avant l’âge de six ans. L’âge d’apparition des premiers signes variait de 22 mois à 12 ans, avec une médiane à 6 ans. La myotonie affectait principalement les membres inférieurs chez quatre patients, et les membres supérieurs chez tous sauf un. Tous les patients présentaient une aggravation des symptômes au froid, mais le phénomène de réchauffement (amélioration temporaire de la raideur musculaire après une contraction répétée) n’était observé que chez ceux atteints de la forme Becker.\n\nSur le plan familial, deux patientes étaient sœurs sans symptômes chez les parents, tandis que la mère d’une autre patiente présentait des signes modérés exacerbés par le froid. Une patiente avait des antécédents familiaux de myotonie maternelle mais a refusé l’étude génétique. Aucun patient ne présentait d’élévation de la créatine kinase (enzyme musculaire) dans le sang. L’électromyogramme, examen mesurant l’activité électrique des muscles, était anormal chez tous sauf le plus jeune patient, chez qui il n’a pas été répété.\n\nInterprétation clinique  \nLes patients atteints de la forme récessive (Becker) ont montré une certaine progression de la maladie. Le traitement initial le plus utilisé était l’oxcarbazépine, un médicament anticonvulsivant, qui a généralement bien amélioré les symptômes. Dans un cas, son efficacité a diminué avec le temps, nécessitant l’introduction de la mexilétine, un autre traitement spécifique. Un autre patient a essayé plusieurs médicaments sans succès à cause d’effets secondaires ou perte d’efficacité. Une patiente a refusé tout traitement en raison de symptômes légers.\n\nUne mutation génétique probablement pathogène, jamais décrite auparavant (mutation CLCN1 : c.824T>C), a été identifiée chez un patient et héritée de sa mère. Les patients avec la forme Becker présentaient des mutations en hétérozygotie composée (deux mutations différentes sur les deux copies du gène), tandis que ceux avec la forme Thomsen avaient des mutations dominantes. Une patiente n’a pas réalisé l’étude génétique.\n\nProchaines étapes  \nCes résultats soulignent l’importance d’un diagnostic clinique et génétique précis pour adapter le suivi et le traitement des patients atteints de myotonie congénitale. La découverte d’une nouvelle mutation pathogène enrichit la compréhension génétique de la maladie. Un suivi à long terme est nécessaire pour mieux évaluer l’évolution naturelle de ces formes cliniques et l’efficacité des traitements disponibles. Enfin, l’étude des antécédents familiaux reste essentielle pour identifier les porteurs asymptomatiques et conseiller les familles."
+        }
+    },
+    {
+        "article": "Homme de 68 ans, hypertension artérielle, maladie pulmonaire obstructive chronique et tabagisme actif, consulté aux urgences le 01/02/23 pour perte d'acuité visuelle progressive (3 mois d'évolution) associée à une hémiplégie brachio-crurale gauche, exacerbée les jours précédant la consultation.\n\nUn NIHSS de 5 points a été observé, avec une dysarthrie et une parésie minimale du côté gauche, une tension artérielle de 160/80 mm Hg, une fréquence cardiaque de 75 lpm et une oxymétrie de pouls de 94 % (FiO2 environnementale). Une angio-CT a révélé une sténose sévère de l'ACI droite et une IRM a mis en évidence des infarctus aigus dans l'hémisphère cérébral droit.\n\nL’écho Doppler a confirmé une sténose sévère (VPS 356 cm/s) de l’ACI droite. Après avoir été évalué minutieusement, confirmant une sténose carotidienne droite sévère symptomatique associée à une lésion morphologiquement haute (qui rend la CEA techniquement difficile) et un risque chirurgical élevé, nous avons décidé de procéder à un traitement endovasculaire par TCAR.\n\nLe 8 février 2003, sous anesthésie générale et héparinisation systémique (100 UI/kg d'héparine non fractionnée, pour un temps d'activation de la coagulation (ACT) > 250 s), la dissection de l'ACC et de la VYI a été réalisée. Une fois la fistule carotidio-jugulaire créée, l'ACC a été clampée, ce qui a entraîné une inversion dynamique du flux.\n\nAprès avoir traversé la lésion (avec la micro-guide-wire) et canalisé l’ACI distale, un stent carotidien (Casper® Mirovention, Terumo) de 8 × 30 mm a été déployé. Étant donné que la lésion était sévère et distale, un phénomène de migration proximale (vers l’ACC) s’est produit pendant le déploiement, nécessitant l’installation d’un deuxième stent (7 × 30 mm) pour traiter la lésion de manière satisfaisante.\n\nL'angiographie a montré une amélioration immédiate du lumen de l'ACI et une expansion adéquate des stents. L'ACC a été débloquée (rétablissement du flux cérébral antérograde), les éléments endovasculaires ont été retirés et l'incision a été fermée comme décrit précédemment.\n\nLe patient a récupéré de manière satisfaisante, n’a présenté aucune complication et a été libéré le deuxième jour postopératoire avec un double traitement antiplaquettaire.\n\nAu cours du suivi, il n'a présenté aucun événement neurologique et l'écho-doppler de contrôle (3, 6 et 12 mois) a montré que le stent était perméable et ne présentait aucun signe de ré-sténose.\n",
+        "gold_summary": "Homme de 68 ans souffrant d'hypertension et de maladie pulmonaire obstructive chronique, ayant développé un accident vasculaire cérébral secondaire à une sténose sévère de l'artère carotide interne droite. Une TCAR a été décidée en raison de sa localisation et du risque chirurgical. Au cours de la procédure, une fistule temporaire a été créée entre l'artère carotide et la veine jugulaire ipsilatérale pour inverser le flux et protéger le cerveau, permettant le déploiement sécurisé du stent. Le patient s'est rétabli sans complications et reste asymptomatique un an après le suivi.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 68 ans avait des problèmes pour voir et bouger son bras et sa jambe gauche. Son corps avait un tuyau important qui était très bouché. Les docteurs ont fait une petite réparation pour déboucher ce tuyau. Ils ont mis un petit tube dedans pour que le sang puisse mieux passer. Pendant l’opération, ils ont fait un petit chemin spécial pour protéger son cerveau. Après, le monsieur est allé mieux. Un an plus tard, il va toujours bien et peut bouger sans problème.",
+            "B2": "**Ce qu'ils ont trouvé**  \nUn homme de 68 ans, qui avait de l’hypertension (pression artérielle élevée) et une maladie pulmonaire, a perdu progressivement la vue et a eu une faiblesse d’un côté du corps. Après des examens, les médecins ont découvert qu’une de ses artères importantes du cou, appelée artère carotide interne droite, était très rétrécie. Ce rétrécissement avait causé un accident vasculaire cérébral (AVC) dans son cerveau.\n\n**Ce qu’ils ont fait**  \nComme l’endroit rétréci était difficile à opérer et que le risque d’une chirurgie classique était élevé, les médecins ont choisi une autre méthode appelée TCAR. Cette technique consiste à créer temporairement un petit passage entre l’artère carotide et une veine proche pour inverser le flux sanguin. Cela protège le cerveau pendant que les médecins placent un petit tube métallique appelé stent, qui sert à élargir l’artère rétrécie.\n\n**Ce que cela signifie**  \nLa procédure s’est bien passée sans problème. Le patient s’est bien remis et, un an plus tard, il n’a eu aucun nouveau symptôme. Les contrôles ont montré que le stent restait ouvert et fonctionnait bien, ce qui a permis d’éviter un autre AVC. Cette technique est donc une option sûre pour traiter ce type de problème quand la chirurgie est trop risquée.",
+            "B3": "Résumé détaillé et structuré\n\nContexte  \nUn homme de 68 ans, avec des antécédents d’hypertension artérielle, de maladie pulmonaire obstructive chronique et de tabagisme actif, a consulté aux urgences pour une perte progressive de la vision sur trois mois, associée à une faiblesse du bras et de la jambe gauches, aggravée dans les jours précédents. L’examen neurologique a révélé un score NIHSS de 5, indiquant une atteinte modérée avec dysarthrie et faiblesse légère à gauche. Les examens d’imagerie ont montré une sténose sévère de l’artère carotide interne droite et des infarctus aigus dans l’hémisphère cérébral droit.\n\nPrincipales observations  \nL’écho-Doppler a confirmé une sténose sévère de l’artère carotide interne droite, avec une vitesse de pointe systolique élevée (356 cm/s). La localisation haute de la lésion et le risque chirurgical important ont conduit à choisir une intervention endovasculaire par TCAR (TransCarotid Artery Revascularization), une technique moins invasive adaptée aux lésions difficiles d’accès chirurgical. Pendant la procédure réalisée sous anesthésie générale, une fistule temporaire a été créée entre l’artère carotide commune et la veine jugulaire interne du même côté, permettant d’inverser le flux sanguin cérébral pour éviter la migration de débris emboliques vers le cerveau. Un premier stent carotidien a été déployé, mais en raison d’une migration proximale du stent liée à la sévérité et à la localisation distale de la sténose, un second stent a été posé pour assurer une couverture complète de la lésion. L’angiographie finale a confirmé une bonne ouverture du vaisseau et une restauration du flux sanguin cérébral normal.\n\nInterprétation clinique  \nCette prise en charge par TCAR a permis de traiter efficacement une sténose carotidienne symptomatique complexe, évitant les risques liés à une chirurgie conventionnelle. La technique d’inversion du flux sanguin cérébral a joué un rôle clé dans la protection contre les complications emboliques. Le patient a présenté une récupération satisfaisante sans complication neurologique ni vasculaire immédiate.\n\nProchaines étapes  \nLe patient a été mis sous double traitement antiplaquettaire et a été suivi régulièrement. Les contrôles échographiques réalisés à 3, 6 et 12 mois ont montré une perméabilité durable des stents sans signe de rétrécissement. Aucun nouvel événement neurologique n’a été observé durant cette période, témoignant du succès à moyen terme de la procédure. Un suivi continu reste nécessaire pour surveiller la stabilité de la revascularisation."
+        }
+    },
+    {
+        "article": "Un patient de 72 ans s'est présenté avec des douleurs thoraciques irradiant vers son bras gauche et une dyspnée progressive au cours des dernières semaines. Il avait des antécédents de thrombose veineuse profonde du membre inférieur et d'hypertension artérielle contrôlée. Il n'y avait pas d'autres comorbidités pertinentes.\n\nL’examen physique a révélé un bon état général du patient, sans signe d’insuffisance cardiaque, une tension artérielle de 156/101 mmHg et une fréquence cardiaque de 73 bpm. L’eupnée était présente et la saturation en oxygène artériel était de 93 %. La fonction rénale était altérée, avec une créatinine sérique de 115 μmol/L et un taux de filtration glomérulaire estimé de 54 mL/min/1,73 m², la troponine T de haute sensibilité était légèrement élevée à 29 ng/L et le NT-proBNP significativement augmenté à 5463 ng/L. L’ECG a révélé un flutter auriculaire nouvellement diagnostiqué, avec un rythme cardiaque irrégulier de 93 bpm, ainsi que des troubles de la repolarisation antérieure et inférieure (inversion de l’onde T dans les dérivations II, III, aVF, V1-V4). Le score CHA2DS2-VASc était de 4 points.\n\n\nL’échocardiographie transthoracique a montré une fonction d’éjection ventriculaire gauche normale (LVEF 55%), une fonction ventriculaire droite légèrement altérée (TAPSE 18 mm), et une augmentation de la pression artérielle pulmonaire (sPAP 47 mm Hg). Un test de stress vélocipédique a été effectué et a montré une baisse significative de la pression artérielle de 138/74 mm Hg au repos à 118/76 mm Hg à 67% de la fréquence cardiaque maximale prévue par âge.\n\nSur la base de ces résultats, une maladie coronarienne pertinente était attendue, probablement avec une maladie de l'artère principale gauche (sur la base de la chute de la pression artérielle lors du test de stress).\n\nLa PE était un diagnostic différentiel possible (Wells Score de 4,5 points prévoyait un risque modéré avec une probabilité de PE de 16,2 %). L'anticoagulation était déjà indiquée en raison du flutter auriculaire.\n\nLe flutter auriculaire nouvellement documenté a été considéré comme associé à la maladie sous-jacente. Il n'y avait aucun signe d'anomalies neurologiques.\n\n\nEnquêtes\n\nL’angiographie coronarienne a révélé une maladie coronarienne à deux vaisseaux suivie d’une intervention coronarienne percutanée ad hoc avec revascularisation complète. La cathétérisation cardiaque droite, réalisée en raison de la légère augmentation de la pression artérielle pré-capillaire et post-capillaire, a révélé une pression artérielle moyenne élevée (mPAP) de 38 mmHg d’origine pré-capillaire et post-capillaire. L’angiographie pulmonaire a montré une occlusion thrombo-embolique de l’artère pulmonaire sous-segmentale du lobe inférieur droit. L’analyse des gaz du sang artériel a montré une alcalose respiratoire, partiellement compensée métaboliquement (pH 7,49, pCO23,4 kPa, pO211,7 kPa, HCO319,5 mmol/L, excès de base −3,8 mmol/L).\n\n\nTraitement\n\nLe patient a ensuite été admis à l'unité de soins coronariens (CCU) où une double antiagrégation plaquettaire (DAPT) avec aspirine et clopidogrel, ainsi qu'une anticoagulation orale avec apixaban ont été démarrés.\n\nLa surveillance hémodynamique à la CCU était acceptable avec une tension artérielle de 140/100 mmHg, une fréquence cardiaque de 85 bpm, une fréquence respiratoire de 17/min et un taux de SO2 de 94 % dans l'air ambiant. La TDM du thorax le jour suivant a confirmé la présence d'une EP avec des EP étendues, bilatérales, centrales et périphériques. Ces résultats étaient plus avancés que ceux de l'angiographie pulmonaire de la veille. Dans une évaluation ultérieure, le seul changement supplémentaire était un nouveau diagnostic de bloc de branche droit (BBR) et un changement de l'axe cardiaque sur l'ECG. La patiente ne ressentait toujours aucune gêne ni signe d'instabilité cardiopulmonaire et l'examen des gaz du sang artériel était inchangé.\n\nAu cours d'une chute après mobilisation indépendante sur le CCU, le patient a développé un arrêt circulatoire avec activité électrique sans pouls (PEA). Une réanimation cardiopulmonaire immédiate a été commencée. Au cours de la réanimation, une cathétérisation cardiaque droite a été effectuée, qui a montré un thrombus occlusif dans l'artère pulmonaire droite et s'est avérée impossible à mobiliser par des techniques interventionnelles.\n\n\nRésultat et suivi\n\nAprès 45 minutes de réanimation mécanique, le patient a développé une ligne plate sur l'ECG. Compte tenu des résultats récents de l'angiographie pulmonaire et de la réanimation mécanique déjà longue et infructueuse, la reprise de la circulation spontanée était très improbable et les efforts de réanimation ont été arrêtés, ce qui a entraîné la mort du patient.",
+        "gold_summary": "Nous présentons le cas d'un homme de 72 ans atteint d'un thromboembolisme pulmonaire aigu sous-massif. L'indice de gravité de l'embolie pulmonaire et la stratification du risque clinique commune recommandaient une anticoagulation systémique et un déroulement clinique sans complications était prévu. Une stratégie de reperfusion primaire n'était pas indiquée par les directives actuelles. Sous anticoagulation établie, le patient a été trouvé en arrêt cardiaque immédiatement après la mobilisation du lit le lendemain matin. La cathétérisation cardiaque droite sous réanimation en cours a révélé une obstruction complète de l'artère pulmonaire droite par un gros thrombus. L'intervention dirigée par cathéter pour contourner le thrombus avec des fils-guides interventionnels a échoué. En fin de compte, le patient est mort d'une insuffisance cardiaque droite aiguë.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 72 ans avait un gros caillot dans un vaisseau de ses poumons. Ce caillot empêchait le sang de bien passer. Les docteurs lui ont donné un médicament pour empêcher d’autres caillots. Ils pensaient qu’il allait aller mieux.\n\nMais un jour, quand il s’est levé de son lit, son cœur s’est arrêté. Les docteurs ont essayé de l’aider avec des soins très forts. Ils ont vu que le gros caillot bloquait toujours le vaisseau dans son poumon. Ils ont essayé de le déloger, mais ça n’a pas marché.\n\nÀ la fin, le cœur du monsieur n’a pas pu repartir. Il est mort à cause de ce gros caillot. Les docteurs étaient tristes, ils avaient fait tout leur possible pour l’aider.",
+            "B2": "Cas d’un homme de 72 ans avec une embolie pulmonaire grave\n\nNous racontons ici l’histoire d’un homme de 72 ans qui avait une embolie pulmonaire aiguë. Une embolie pulmonaire, c’est quand un caillot bloque une artère dans les poumons, ce qui peut empêcher le sang de circuler normalement. Dans ce cas, le caillot était assez important, mais pas au point de nécessiter un traitement très agressif selon les règles médicales actuelles.\n\nLes médecins avaient commencé un traitement avec des médicaments anticoagulants, qui empêchent la formation de nouveaux caillots et aident à dissoudre ceux déjà présents. Tout semblait bien se passer, et on s’attendait à ce que le patient ne rencontre pas de complications graves.\n\nCependant, le lendemain matin, juste après s’être levé, le patient a soudainement fait un arrêt cardiaque. Cela signifie que son cœur a cessé de battre correctement. Pendant la réanimation, les médecins ont réalisé un examen spécial appelé cathétérisation cardiaque droite. Cet examen a montré qu’une grosse partie de l’artère pulmonaire droite était complètement bouchée par un caillot.\n\nIls ont essayé d’enlever ce caillot avec des outils spécifiques, mais cela n’a pas fonctionné. Malheureusement, à cause de ce blocage, le cœur droit n’a plus pu pomper le sang correctement, ce qui a conduit à une insuffisance cardiaque aiguë. Malgré tous les efforts, le patient est décédé.\n\nCe cas montre que même avec un traitement adapté, une embolie pulmonaire peut évoluer rapidement et gravement. Il est important de surveiller de près les patients et de réagir vite en cas de complications.",
+            "B3": "Résumé détaillé et structuré du cas clinique\n\nContexte  \nNous rapportons le cas d’un homme de 72 ans présentant un thromboembolisme pulmonaire aigu sous-massif, c’est-à-dire une obstruction partielle des artères pulmonaires par un caillot sanguin, entraînant une augmentation de la pression dans les vaisseaux pulmonaires et une altération modérée de la fonction cardiaque droite. Ce patient avait des antécédents de thrombose veineuse profonde et d’hypertension artérielle, et s’était présenté avec des douleurs thoraciques irradiant au bras gauche ainsi qu’une dyspnée progressive.\n\nPrincipales observations  \nÀ l’admission, le patient affichait une tension artérielle élevée (156/101 mmHg), une fréquence cardiaque régulière à 73 bpm, et une saturation en oxygène légèrement diminuée à 93 %. L’électrocardiogramme (ECG) a révélé un flutter auriculaire nouvellement diagnostiqué avec un rythme irrégulier, ainsi que des anomalies de la repolarisation cardiaque. L’échocardiographie montrait une fonction ventriculaire gauche normale mais une fonction droite légèrement altérée, associée à une pression artérielle pulmonaire élevée (47 mmHg). Un test d’effort a mis en évidence une chute significative de la pression artérielle, suggérant une maladie coronarienne importante.\n\nLes examens complémentaires ont confirmé une maladie coronarienne à deux vaisseaux, traitée par angioplastie et revascularisation complète. La cathétérisation cardiaque droite a montré une hypertension pulmonaire mixte (pré- et post-capillaire). L’angiographie pulmonaire a identifié une occlusion thrombo-embolique dans une artère pulmonaire sous-segmentaire du lobe inférieur droit. Par ailleurs, une embolie pulmonaire étendue bilatérale a été confirmée par tomodensitométrie (TDM) thoracique.\n\nTraitement et évolution  \nLe patient a été placé en unité de soins coronariens et traité par double antiagrégation plaquettaire (aspirine et clopidogrel) associée à une anticoagulation orale par apixaban, conformément aux recommandations pour le flutter auriculaire et l’embolie pulmonaire. Malgré une surveillance hémodynamique stable et l’absence de signes d’instabilité cardiorespiratoire, le patient a présenté un arrêt circulatoire avec activité électrique sans pouls (PEA) au moment de sa mobilisation indépendante le lendemain.\n\nUne réanimation cardiopulmonaire immédiate a été initiée. Pendant la réanimation, une cathétérisation cardiaque droite a révélé une obstruction complète de l’artère pulmonaire droite par un thrombus volumineux. Les tentatives interventionnelles pour mobiliser ce caillot à l’aide de fils-guides ont échoué. Après 45 minutes de réanimation mécanique prolongée sans retour de circulation spontanée, les efforts ont été arrêtés, conduisant au décès du patient.\n\nInterprétation clinique  \nCe cas illustre une embolie pulmonaire aiguë sous-massive compliquée d’un arrêt cardiaque soudain malgré une anticoagulation adaptée et une prise en charge conforme aux recommandations actuelles. La stratification initiale du risque ne justifiait pas une thrombolyse ou une intervention de reperfusion primaire, ce qui souligne la difficulté à prédire certains événements catastrophiques. L’embolie massive, responsable d’une insuffisance cardiaque droite aiguë, a conduit à une obstruction vasculaire complète non réversible par les moyens interventionnels disponibles.\n\nProchaines étapes  \nCe cas met en lumière la nécessité d’une vigilance accrue chez les patients présentant une embolie pulmonaire sous-massive, même lorsque le traitement anticoagulant est en place et que la stabilité clinique semble assurée. Il suggère aussi que des stratégies supplémentaires, telles que la surveillance intensive ou des interventions plus agressives, pourraient être envisagées dans certains cas à risque élevé, bien que les recommandations actuelles ne les préconisent pas systématiquement. Enfin, il rappelle l’importance d’une prise en charge multidisciplinaire et d’une réévaluation continue du risque au cours de l’hospitalisation."
+        }
+    },
+    {
+        "article": "Un patient de 25 ans a consulté pour une consultation neurochirurgicale concernant sa santé. Ses antécédents comprenaient une chute dans une piscine pendant les vacances deux semaines auparavant. La chute avait entraîné une fracture de la colonne cervicale. Le patient a subi une intervention chirurgicale pendant ses vacances. Une stabilisation postérieure de la colonne cervicale a été réalisée. Le patient portait un collier cervical et la plaie chirurgicale n’avait pas encore cicatrisé, les sutures n’ayant pas encore été enlevées. Le patient ne présentait aucune parésie et pouvait se déplacer seul. Il n’avait pas de documentation médicale détaillée ni de rapports d’examen préopératoire et postopératoire. Au moment de la sortie, on lui a donné une imagerie post-opératoire de la colonne cervicale incomplète sous la forme de quelques vieilles radiographies qui montraient certaines vues, mais sans images numériques. Le résumé de la sortie ne contenait pas la description détaillée du traitement fourni, notamment les détails de l’instrumentation utilisée. Le personnel de l’hôpital ou les opérateurs ne pouvaient pas être contactés parce qu’ils ne répondaient pas au téléphone ou aux e-mails et aux SMS. Nous avons décidé qu’une nouvelle imagerie post-opératoire de la colonne cervicale devait être obtenue. Elle a révélé une fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et déplacement antérieur d’une partie du corps vertébral du C2. Le patient a été opéré par une approche postérieure. Une stabilisation postérieure de C2-C3 a été réalisée. Les vis ont été correctement positionnées dans les masses latérales du C3. Cependant, dans le C2 vertébral, les deux vis ont été initialement placées transpédi-culairement, mais leurs extrémités n’ont pas atteint le corps vertébral du C2 ou les masses latérales du C1 et se sont étendues dans l’espace articulaire antérieur du C1-C2. Les images d’imagerie post-opératoire ont révélé un état post-opératoire de fracture du col du fémur atypique de la colonne cervicale : une fracture du C2 pars interarticularis sur le côté gauche, une dislocation du C2 contre le C3, une fracture du corps vertébral du C2 avec détachement et\n",
+        "gold_summary": "Nous présentons un cas de fracture atypique du couteau du bourreau causée par une chute en avant dans une piscine et un choc contre le fond de la piscine. Le patient avait subi une opération dans un autre établissement, où une stabilisation postérieure des articulations C2-C3 avait été réalisée. En raison de la présence de vis dans les espaces articulaires C1-C2, le patient ne pouvait pas effectuer de mouvements de rotation de la tête. Une stabilisation antérieure pour prévenir une luxation de C2 contre C3 n'avait pas non plus été réalisée, et une stabilité rachidienne appropriée n'avait pas été assurée. Notre décision de réopérer a été motivée, entre autres facteurs, par notre intention de restaurer les mouvements de rotation de la tête. La chirurgie de révision a été réalisée à partir d'une approche antérieure et postérieure. Après la chirurgie, le patient a pu tourner la tête tout en maintenant la stabilité de la colonne cervicale. Le cas présenté ici représente non seulement un exemple unique de fracture atypique du couteau du bourreau, mais met également en évidence une technique de fixation qui a fourni la stabilité nécessaire pour une fusion réussie. La méthode utilisée a restauré le mouvement de rotation fonctionnel de la tête, préservant ainsi la qualité de vie du patient, ce qui est d'une importance primordiale compte tenu de l'âge du patient.\n",
+        "synthetic_summary": {
+            "B1": "Un jeune homme est tombé dans une piscine. Il s’est fait très mal au cou. Les docteurs l’ont opéré pour réparer son cou. Ils ont mis des petites vis pour tenir les os ensemble. Mais après, il ne pouvait plus tourner la tête. \n\nLes docteurs ont fait une autre opération. Cette fois, ils ont réparé le cou pour qu’il soit solide et qu’il puisse tourner la tête. Maintenant, il va mieux et peut bouger sa tête sans problème. \n\nC’est important parce que pouvoir tourner la tête aide beaucoup dans la vie. Les docteurs ont bien travaillé pour que le cou soit fort et que le jeune homme soit content.",
+            "B2": "**Ce qu’ils ont trouvé chez le patient**\n\nUn jeune homme de 25 ans est tombé dans une piscine et s’est blessé au cou, plus précisément à la colonne cervicale, qui est la partie haute de la colonne vertébrale dans le cou. Il avait une fracture compliquée au niveau de la deuxième vertèbre cervicale (appelée C2). Cette fracture était particulière et a été causée par un choc violent contre le fond de la piscine.\n\n**Ce qui avait été fait avant**\n\nLe patient avait déjà subi une opération dans un autre hôpital. Les chirurgiens avaient fixé les vertèbres C2 et C3 à l’arrière du cou pour stabiliser la colonne. Cependant, des vis avaient été placées dans une zone entre les vertèbres C1 et C2, ce qui empêchait le patient de tourner la tête normalement. De plus, aucune fixation n’avait été faite à l’avant du cou pour empêcher la vertèbre C2 de bouger trop par rapport à C3, ce qui aurait pu causer une instabilité.\n\n**Pourquoi ils ont décidé de refaire une opération**\n\nLes médecins ont choisi de réopérer le patient pour plusieurs raisons importantes. Ils voulaient d’abord assurer une meilleure stabilité de la colonne cervicale afin d’éviter tout risque de déplacement dangereux des vertèbres. Ensuite, ils souhaitaient permettre au patient de retrouver la capacité de tourner la tête, ce qui est essentiel pour la vie quotidienne.\n\n**Comment s’est passée la nouvelle opération**\n\nLa nouvelle chirurgie a été faite en deux étapes : par l’avant et par l’arrière du cou. Cette technique a permis de bien fixer les vertèbres et de stabiliser la colonne. Après l’opération, le patient a pu tourner la tête normalement tout en ayant une colonne cervicale stable.\n\n**Ce que cela signifie**\n\nCe cas est un exemple rare d’une fracture complexe de la colonne cervicale. Il montre aussi qu’avec une bonne technique chirurgicale, il est possible de stabiliser la colonne tout en gardant les mouvements importants de la tête. Cela est très important pour la qualité de vie du patient, surtout qu’il est jeune et a besoin de garder une bonne mobilité.",
+            "B3": "**Contexte**  \nUn homme de 25 ans a consulté en neurochirurgie suite à une fracture complexe de la colonne cervicale provoquée par une chute dans une piscine. Initialement, il avait subi une intervention chirurgicale dans un autre établissement, avec une stabilisation postérieure des vertèbres C2 et C3. Cependant, les documents médicaux étaient incomplets, et les images post-opératoires fournies étaient insuffisantes pour évaluer précisément l’état de la fixation.\n\n**Principales Observations**  \nUne nouvelle imagerie a révélé une fracture atypique du C2, incluant une fracture du pars interarticularis (une partie osseuse située entre les articulations vertébrales) gauche, une dislocation entre C2 et C3, ainsi qu’un déplacement antérieur d’une partie du corps vertébral de C2. Lors de la chirurgie initiale, des vis avaient été placées pour stabiliser C2-C3, mais celles insérées dans C2 n’avaient pas atteint les structures osseuses prévues et s’étaient étendues dans l’espace articulaire entre C1 et C2. Cette situation empêchait le patient de tourner la tête normalement, car les mouvements de rotation de la colonne cervicale haute (entre C1 et C2) étaient bloqués.\n\n**Interprétation Clinique**  \nLa fixation initiale n’avait pas assuré une stabilité suffisante de la colonne cervicale, notamment en ne prévenant pas la luxation (déplacement anormal) entre C2 et C3. De plus, la mauvaise position des vis avait compromis la mobilité fonctionnelle essentielle à la rotation de la tête. La situation nécessitait une réintervention chirurgicale pour corriger ces défauts, restaurer la stabilité rachidienne et préserver la mobilité cervicale.\n\n**Prochaines Étapes et Résultats**  \nUne chirurgie de révision a été réalisée en combinant une approche antérieure (par l’avant du cou) et postérieure (par l’arrière). Cette intervention a permis de repositionner correctement les vis et d’assurer une stabilisation efficace des vertèbres C2 et C3, tout en libérant l’espace articulaire C1-C2 pour permettre la rotation normale de la tête. Après la réopération, le patient a retrouvé la capacité de tourner la tête sans compromettre la stabilité de sa colonne cervicale.\n\n**Conclusion**  \nCe cas illustre une fracture atypique complexe de la colonne cervicale nécessitant une prise en charge chirurgicale précise. La technique de fixation employée lors de la révision a non seulement assuré une fusion solide des vertèbres concernées, mais a aussi permis de préserver la mobilité fonctionnelle de la tête, un élément crucial pour la qualité de vie, notamment chez un patient jeune. Cette expérience souligne l’importance d’un positionnement rigoureux des implants et d’une évaluation complète post-opératoire pour garantir à la fois stabilité et fonctionnalité."
+        }
+    },
+    {
+        "article": "Une femme de 29 ans, enceinte de 29 semaines, ayant eu 3 accouchements vaginaux spontanés et dont le dernier enfant avait été livré par césarienne suite à une induction de travail infructueuse 4 ans avant la grossesse en cours, est venue pour un suivi de l'ANC à un âge gestationnel de 32 semaines depuis son LNMP.\n\nAprès avoir examiné les antécédents médicaux, il a été découvert que tous ses enfants étaient en bonne santé, qu'ils allaient bien à l'école et qu'ils n'avaient pas d'antécédents connus de troubles génétiques ou convulsifs. Elle a été examinée au laboratoire de recherche sur les maladies vénériennes (VDRL), à l'antigène de surface de l'hépatite B (HBSag) et à l'analyse d'urine, qui ont tous été négatifs. Toutes les lignées cellulaires du CBC étaient normales, son groupe sanguin était A et son Rh était positif, selon le compte sanguin complet (CBC), le groupe sanguin et le Rh. Une échographie obstétrique a également été réalisée, montrant une échographie anatomique normale de toutes les parties du corps du fœtus, à l'exception du cœur. Une évaluation détaillée de l'échocardiographie fœtale a été réalisée avec les résultats suivants : les deux oreillettes ont une taille comparable et un situs normal. Les deux valves atrioventriculaires et semilunaire sont normalement positionnées avec ouverture et fermeture normales. Les deux ventricules sont comparables en taille et contractilité ; en 2D et en couleur, le ventricule gauche forme le sommet du cœur sans aucun défaut du septum ventriculaire. Mais sur les muscles papillaires du ventricule gauche, il y avait deux masses échogènes circonscrites, rondes, mesurant 18,2 mm par 8,3 mm et 13,5 mm par 8,3 mm. Après évaluation du tractus de sortie, les deux LVOT (ventricule gauche) et RVOT (ventricule droit) ont une anatomie et une fonction normales en utilisant l'évaluation par ultrasons 2D et CF. Selon les résultats de l'écho fœtal, un diagnostic de rhabdomyome cardiaque a été posé. Étant donné qu'il existe un risque élevé de sclérose tubéreuse dans le rhabdomyome cardiaque, une neurosonographie détaillée et d'autres examens systématiques ont été effectués pour rechercher d'autres signes de sclérose tubéreuse. Malgré la recherche d'autres signes de sclérose tubéreuse, aucun autre signe n'a été trouvé autre que la tumeur. Elle a eu un suivi régulier ANC de 32 semaines de gestation à 39 semaines sans aucune complication.\n\nÀ 39 semaines de grossesse plus 1 jour, elle a subi une césarienne pour l'indication d'une grossesse à terme plus une demande de césarienne répétée, avec un résultat de 3200 grammes pour la fille avec un score APGAR de 10 et 10 à la 1re et 5e minutes. La mère et le nouveau-né ont eu une période postopératoire sans problème et ont été libérés le troisième jour.\n\nAprès la naissance, le nouveau-né a été évalué les 1er, 7e et 30e jours pour toute régression ou augmentation de la masse, toute apparition de lésions cutanées ou de convulsions. Tous les résultats des examens physiques étaient normaux, et la taille de la masse était similaire à l'évaluation antepartum.\n\nAu septième mois, l'enfant a été évaluée à nouveau et, après interrogatoire, l'enfant avait un développement excellent pour son groupe d'âge. L'enfant a été examinée pour un retard de développement neurologique et elle grandissait de manière appropriée pour son âge. Une étude d'écholocographie par un cardiologue pédiatrique a révélé des masses hyperechoiques bien circonscrites sur les deux muscles papillaires du ventricule gauche, mesurant chacun 21,8 mm sur 9,2 mm et 14,7 mm sur 8,5 mm et ne créant aucune obstruction de l'écoulement vers le ventricule gauche.\n\nUne histoire familiale a été obtenue, et un examen physique avec mesures anthropométriques a été effectué pour évaluer son état de développement lors de son évaluation de première année. L'enfant se développait normalement, comme les autres enfants de son âge. À l'exception du cœur, tous les systèmes examinés étaient remarquables. Une étude d'échocardiographie a révélé des masses hyperechoiques bien circonscrites sur les deux muscles papillaires du ventricule gauche, sans augmentation de taille et sans obstruction de l'écoulement vers le ventricule gauche.\n",
+        "gold_summary": "Nous rapportons un cas isolé de masse intra-cardiaque fœtale asymptomatique (rhabdomyome) découverte à 32 semaines de gestation et suivie en ambulatoire jusqu'à 39 semaines et un jour, date à laquelle une césarienne a été pratiquée. Après l'accouchement, l'enfant a été évalué au 1er jour, au 7e jour, au 30e jour, au 7e mois et au 12e mois. Après un examen, la croissance anthropométrique et neurocomportementale de l'enfant était saine. À l'exception de la tumeur, qui n'a ni augmenté ni diminué de taille, aucun des critères de diagnostic cliniques du complexe de sclérose tubéreuse n'a été rencontré chez cet enfant jusqu'à l'âge d'un an.\n",
+        "synthetic_summary": {
+            "B1": "Un bébé avait une petite boule dans son cœur quand il était dans le ventre de sa maman. Cette boule ne faisait pas mal. \n\nLa maman a eu un bébé par une opération spéciale. Après la naissance, les docteurs ont regardé le bébé plusieurs fois. \n\nLe bébé grandissait bien et était en bonne santé. La petite boule dans son cœur ne changeait pas de taille. \n\nLe bébé n’avait pas d’autres problèmes. Tout allait bien jusqu’à ce qu’il ait un an.",
+            "B2": "**Ce qu'ils ont trouvé**  \nUne femme enceinte de 29 semaines a passé une échographie qui a montré une masse dans le cœur de son bébé. Cette masse s'appelle un rhabdomyome, c’est une tumeur bénigne (non cancéreuse) qui se forme dans le muscle du cœur. Elle ne causait pas de problème pour le bébé à ce moment-là. Les autres parties du corps du bébé semblaient normales.\n\n**Ce qu’ils ont fait**  \nLes médecins ont suivi la grossesse jusqu’à 39 semaines, puis la maman a eu une césarienne pour faire naître la petite fille. Après la naissance, le bébé a été examiné plusieurs fois : au premier, septième, trentième jour, puis à 7 mois et enfin à 1 an. À chaque fois, ils ont vérifié la taille de la tumeur, la santé générale, le développement du bébé et s’il y avait des signes d’une maladie appelée sclérose tubéreuse. Cette maladie peut être liée à ce type de tumeur, mais ils n’ont trouvé aucun autre signe chez l’enfant.\n\n**Ce que cela signifie**  \nLe bébé a grandi normalement, sans problème de développement ou neurologique. La tumeur dans le cœur est restée stable, ni plus grande ni plus petite, et elle ne bloquait pas le fonctionnement du cœur. Jusqu’à l’âge d’un an, l’enfant était en bonne santé et ne montrait aucun signe de maladie grave liée à cette tumeur. Ce cas montre qu’un rhabdomyome cardiaque peut être surveillé sans urgence si le bébé ne présente pas de symptômes.",
+            "B3": "Résumé détaillé et structuré :\n\nContexte  \nUne femme de 29 ans, enceinte de 32 semaines, a été suivie en consultation prénatale. Ses antécédents obstétricaux comprenaient trois accouchements par voie basse spontanée et une césarienne réalisée quatre ans auparavant. Aucun antécédent familial ou personnel de troubles génétiques ou neurologiques n’a été rapporté. Les examens prénataux standards, incluant les tests sérologiques (VDRL, antigène HBs) et l’analyse d’urine, étaient négatifs. Le groupe sanguin était A Rh positif, et le bilan sanguin complet était normal.\n\nPrincipales observations  \nL’échographie obstétricale a révélé un fœtus avec une anatomie normale, à l’exception du cœur. Une échocardiographie fœtale détaillée a mis en évidence deux masses échogènes bien délimitées, situées sur les muscles papillaires du ventricule gauche, mesurant respectivement 18,2 x 8,3 mm et 13,5 x 8,3 mm. Ces masses étaient compatibles avec un rhabdomyome cardiaque, une tumeur bénigne du muscle cardiaque fréquemment associée à la sclérose tubéreuse de Bourneville, une maladie génétique multisystémique. L’évaluation du reste du cœur, y compris les valves et les ventricules, était normale, sans obstruction du flux sanguin. Une neurosonographie et d’autres examens complémentaires n’ont pas révélé d’autres signes cliniques de sclérose tubéreuse.\n\nInterprétation clinique  \nLe diagnostic principal était celui d’un rhabdomyome cardiaque fœtal isolé, sans manifestation associée de sclérose tubéreuse à ce stade. Le suivi prénatal a été réalisé sans complication jusqu’à 39 semaines et un jour, moment où une césarienne a été pratiquée à la demande de la patiente. Le nouveau-né, une fille de 3200 grammes, a présenté un score APGAR optimal (10/10 aux 1re et 5e minutes) et une évolution postopératoire normale.\n\nProchaines étapes et suivi postnatal  \nAprès la naissance, l’enfant a été régulièrement examinée aux 1er, 7e et 30e jours, puis à 7 mois et 12 mois. Les masses cardiaques ont été surveillées par échocardiographie pédiatrique, montrant une légère augmentation de taille (21,8 x 9,2 mm et 14,7 x 8,5 mm), sans obstruction du flux sanguin ni complication. Aucun signe cutané, neurologique ou développemental évocateur de sclérose tubéreuse n’a été détecté. L’enfant a présenté un développement neurocomportemental et une croissance anthropométrique normaux, adaptés à son âge.\n\nConclusion  \nCe cas illustre la découverte fortuite d’un rhabdomyome cardiaque fœtal isolé, sans association clinique avec la sclérose tubéreuse au cours de la première année de vie. Le suivi régulier a permis de confirmer l’absence de progression tumorale significative ou de complications associées. Cette observation souligne l’importance d’un suivi multidisciplinaire rigoureux pour détecter précocement toute manifestation liée à cette pathologie génétique potentielle."
+        }
+    },
+    {
+        "article": "Un garçon de terme avec un poids à la naissance de 3 kg a été livré par césarienne en raison de la détresse fœtale. Il a pleuré immédiatement après la naissance. Des soins de routine ont été donnés et à 10 minutes de vie, il a été remarqué qu'il avait une faible lecture de SpO2 (saturation en oxygène) de 75-80%. Ainsi, il a été mis sous oxygène par boîte de tête à 5 L/min. Il a eu de bons efforts respiratoires avec une tachypnée modérée. Comme il continuait d'avoir une faible SpO2 même après un essai à la fois de 5 L/min d'oxygène de la boîte de tête et de PEEP (pression expiratoire positive) du réanimateur en pièce T avec 6 cm d'eau avec FiO2 (fraction d'oxygène inspirée) à 100%, il a été intubé et a commencé une ventilation à pression positive. Le bébé a été transféré à l'unité de soins intensifs néonatals pour une gestion ultérieure.\n\nMême après ventilation mécanique en mode synchronisée intermittent obligatoire (SIMV) avec des pressions stabilisatrices maximales de PEEP 6 cm et une pression de pointe de 20 cm d'eau et une sédation adéquate, la SpO2 maximale atteinte était de 80 %. Il avait une cyanose et des signes de mauvaise perfusion (tachycardie et temps de remplissage capillaire prolongé). Le bébé a donc été mis sous soutien inotrope après un bolus de solution saline normale. Les différentiels initiaux considérés étaient le choc septique, le pneumothorax, les malformations pulmonaires et la cyanose cardiaque. Une culture sanguine a été effectuée et le bébé a été mis sous antibiotiques de première ligne. La radiographie thoracique a montré une ombre cardiaque normale et des champs pulmonaires normaux. Un échocardiogramme a été effectué qui a exclu une hypertension pulmonaire persistante et une maladie cardiaque structurelle.\n\nLes gaz sanguins artériels réalisés après 1 h de ventilation (à 2 h de vie) ont montré un pH de 7,5, paCO2 de 19,1 mmHg, paO2 de 199 mmHg, lactate de 4 mmol/L, bicarbonate de 18,1 mmol/L et un excès de base de −3,6. Comme il y avait une hyperoxémie inexpliquée malgré une faible SpO2 et une cyanose persistante, une méthémoglobinémie a été suspectée, ce qui a été confirmé par un niveau élevé de metHb (méthémoglobine) (7,6 %). Les valeurs de gaz sanguins en série ont montré une hyperoxémie et des niveaux élevés de metHb. Il a reçu une dose unique de 3 mg de bleu de méthylène par voie intraveineuse et a commencé à prendre de l'acide ascorbique oral à 300 mg une fois par jour. Ses paramètres ventilatoires ont été progressivement sevré et il a été extubé après 16 h à l'air ambiant. Les inotropes ont également été réduits et arrêtés en 24 h. Comme sa culture sanguine n'avait pas de croissance, les antibiotiques ont été arrêtés après 2 jours. À partir du jour 2 de la vie, il a maintenu une saturation de 75 à 85 % en air ambiant.\n\nIl n'y avait pas de données pertinentes sur les antécédents périnataux et familiaux. Le taux de glucose-6-phosphate déshydrogénase et l'électrophorèse de l'hémoglobine étaient également normaux. Depuis le jour 3, il recevait des aliments orogastriques et était par ailleurs stable, à l'exception d'une cyanose persistante. Après l'envoi d'un test génétique (exome clinique), il a été renvoyé à la maison le jour 9, tout en recevant des aliments par voie orale, car il restait stable, à l'exception d'une cyanose et d'une faible lecture de SpO2 (80-85 %) en air ambiant avec un paO2 normal.\n\nAprès la décharge, le bébé a été suivi régulièrement et à 2 mois de vie, sa saturation en air ambiant était de 88 à 90 % et à 4 mois, sa SpO2 était > 92 % en air ambiant sans cyanose. L'exome clinique a montré une mutation dans la chaîne gamma de l'hémoglobine fœtale - substitution d'acides aminés de la tyrosine par l'histidine au codon 63 (p.His63Tyr) en raison d'une mutation de sens erroné dans le gène HBG2 (chr11:g.5275647G>A). Une fois que nous avons reçu le résultat du test génétique, l'acide ascorbique oral a été arrêté et les parents ont été conseillés sur l'excellent pronostic de cette maladie rare. À 5 mois de vie, il était bien, acyanotique et son niveau de metHb était normal.\n",
+        "gold_summary": "Nous rapportons un nouveau-né présenté avec cyanose et désaturation dès la naissance, qui a ensuite été trouvé métémoglobinémique et a commencé un traitement. L'évaluation génétique a révélé une mutation dans la chaîne gamma de l'hémoglobine fœtale (HbF) provoquant une hémoglobine anormale. Les mutations physiologiquement significatives dans les gènes de la gamma-globine provoquent des symptômes chez le fœtus et le nouveau-né qui disparaissent progressivement au cours des premiers mois de la vie.\n",
+        "synthetic_summary": {
+            "B1": "Un bébé est né avec la peau un peu bleue. Il avait du mal à avoir assez d'air. \n\nLes docteurs ont trouvé un problème dans son sang. Son sang ne gardait pas bien l’oxygène. \n\nIls ont donné un médicament pour l’aider. Petit à petit, ça allait mieux. \n\nLe bébé avait un petit changement dans son corps qui fait ça. Ce changement disparaît avec le temps. \n\nAprès quelques mois, le bébé était en bonne santé et sa peau était normale.",
+            "B2": "Un bébé est né par césarienne et a tout de suite eu du mal à bien respirer. Il avait une couleur bleutée de la peau, appelée cyanose, et un faible taux d’oxygène dans le sang. Malgré l’aide à la respiration avec de l’oxygène et un ventilateur, son taux d’oxygène restait bas. Les médecins ont alors cherché d’autres causes, comme une infection ou un problème au cœur, mais tout semblait normal.\n\nIls ont fait un test spécial du sang qui a montré un taux élevé de méthémoglobine. La méthémoglobine est une forme anormale de l’hémoglobine, la protéine qui transporte l’oxygène dans le sang. Cette forme ne peut pas bien transporter l’oxygène, ce qui explique la cyanose et la faible saturation en oxygène. Le bébé a reçu un médicament appelé bleu de méthylène pour traiter ce problème, ainsi qu’un complément de vitamine C.\n\nUn test génétique a révélé que le bébé avait une mutation dans un gène qui fabrique une partie de l’hémoglobine fœtale, appelée chaîne gamma. Cette mutation rend l’hémoglobine anormale, ce qui cause la méthémoglobinémie. Heureusement, cette maladie est rare et les symptômes s’améliorent avec le temps, car l’hémoglobine fœtale est remplacée par l’hémoglobine normale après quelques mois.\n\nLe bébé a été suivi régulièrement et a bien récupéré. Sa couleur est redevenue normale, et son taux d’oxygène dans le sang s’est amélioré sans traitement. Les médecins ont expliqué aux parents que cette maladie a un bon pronostic et que leur enfant allait bien évoluer.",
+            "B3": "Résumé destiné à un adulte éduqué non-médecin\n\nContexte  \nUn nouveau-né, né à terme par césarienne à cause d’une souffrance fœtale, a présenté immédiatement après la naissance une cyanose (coloration bleutée de la peau) et une saturation en oxygène (SpO2) anormalement basse, malgré des efforts respiratoires normaux. Malgré une assistance respiratoire mécanique et un apport élevé en oxygène, sa saturation restait faible, et il montrait des signes de mauvaise circulation sanguine.\n\nPrincipales observations  \nLes examens initiaux ont exclu des causes fréquentes telles que les infections sévères, un pneumothorax (air dans la cavité thoracique), ou une malformation cardiaque. Les gaz du sang ont montré une quantité élevée d’oxygène dissous, ce qui était paradoxal avec la faible saturation mesurée. Cette discordance a conduit à suspecter une méthémoglobinémie, une condition où une forme anormale de l’hémoglobine (la méthémoglobine) empêche le transport normal de l’oxygène. Ce diagnostic a été confirmé par un taux élevé de méthémoglobine dans le sang.\n\nLe nouveau-né a reçu un traitement par bleu de méthylène, un médicament qui aide à réduire la méthémoglobine, ainsi qu’un apport en vitamine C (acide ascorbique). Progressivement, sa saturation en oxygène s’est améliorée, il a pu être sevré de la ventilation mécanique et extubé, et les médicaments de soutien circulatoire ont été arrêtés.\n\nInterprétation clinique  \nUne analyse génétique approfondie a révélé une mutation spécifique dans le gène codant pour la chaîne gamma de l’hémoglobine fœtale (HbF), responsable d’une forme anormale d’hémoglobine. Cette mutation entraîne la formation d’une hémoglobine instable qui favorise la méthémoglobinémie, provoquant ainsi la cyanose et la désaturation observées dès la naissance. Heureusement, cette anomalie est transitoire car la production d’hémoglobine fœtale diminue naturellement au cours des premiers mois de la vie, remplacée par l’hémoglobine adulte normale.\n\nProchaines étapes et pronostic  \nLe bébé a été suivi régulièrement après sa sortie de l’hôpital. Sa saturation en oxygène s’est progressivement normalisée sans traitement supplémentaire, et il est devenu complètement asymptomatique à l’âge de 5 mois. L’arrêt de l’acide ascorbique a été possible après confirmation du diagnostic génétique. Les parents ont été informés que cette maladie rare a un excellent pronostic, avec une résolution naturelle des symptômes au fur et à mesure que l’hémoglobine fœtale est remplacée.\n\nEn résumé, ce cas illustre une cause génétique rare de cyanose néonatale liée à une mutation de l’hémoglobine fœtale, qui nécessite une prise en charge spécifique mais qui évolue favorablement avec le temps."
+        }
+    },
+    {
+        "article": "Homme de 35 ans ayant des antécédents de rupture totale du ligament croisé antérieur il y a 10 ans. Il a suivi un traitement conservateur avec immobilisation pendant quatre semaines, puis une physiothérapie pendant six mois avec une amélioration partielle des symptômes. À la fin du traitement conservateur, il a effectué des activités de la vie quotidienne sans limitation apparente jusqu'à un mois avant la nouvelle évaluation, avec une douleur de 6/10 sur l'échelle EVA du genou et une sensation d'instabilité en descendant les escaliers et un œdème intermittent, sans nouveau mécanisme de blessure. L'examen physique a révélé une douleur à la palpation sur la ligne articulaire latérale et la surface antérieure du genou ; arcs de mobilité du genou avec flexion active de 85° et flexion passive de 100°, extension complète. Force par groupes musculaires du genou 5/5 avec douleur référée à la face antérieure du genou. Les manœuvres spéciales pour évaluer cliniquement l'articulation du genou ont révélé : élévation antérieure, Lachman, Lelli : positive ; McMurray, Steinman et Apley latéral et médial : positive. Une résonance magnétique simple du genou droit a été demandée, elle a révélé : absence de LCA, arthrose grade III-IV du compartiment fémoro-tibial médial, arthrose grade II du compartiment fémoro-tibial latéral, amincissement de la corne postérieure et du corps du ménisque latéral avec une partie résiduelle minimale, déchirure horizontale de la corne postérieure et du corps du ménisque médial, oedème du ligament croisé postérieur (LCP) avec changement de la dégénérescence mucoïde. Des mesures radiographiques ont été prises pour l'intercondylé et l'angle alpha, en coupe axiale et sagittale, respectivement. Il a été décidé de procéder à une arthroscopie du genou. Avant la procédure chirurgicale et sous anesthésie générale, le test de pivot shift a été effectué, qui s'est révélé positif avec un degré III. Une arthroscopie a été effectuée, révélant : déchirure fermée et invétérée complète du LCA, pincement du LCP, rupture du corne postérieur et du corps du ménisque latéral, rupture chronique invétérée et extrudée du ménisque médial, pincement fémoro-tibial antérieur, corps libres intra-articulaires, lésion condrale de 1 cm2 sur le condyle fémoral latéral dans la zone de charge, arthrose grade IV du compartiment fémoro-tibial médial, synovite sous-quadricipitale. 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déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchirure de la déchir\nEn raison du degré d'arthrose, il a été décidé de ne pas effectuer de tunnels du LCA pour éviter de futures complications lors de la chirurgie définitive d'arthroplastie du genou. Après la chirurgie, l'utilisation d'un mobilisateur passif du genou de 0° d'extension à 100° de flexion ainsi que la marche assistée par des béquilles ont été indiqués.\nLe jour suivant l'opération, le patient a quitté l'hôpital sans complications et a commencé une physiothérapie pour renforcer et stabiliser les muscles. Au cours des visites de suivi à trois, six et neuf mois, le patient a déclaré ne présenter aucun symptôme, pouvoir effectuer ses activités quotidiennes sans aucune restriction et pratiquer des activités sportives à faible impact sans aucune entrave.\n",
+        "gold_summary": "Nous présentons le cas d'un patient de 35 ans avec rupture du LCA involuée de 10 ans. Avec une gestion conservatrice initiale qui évolue vers une instabilité du genou et une douleur dans la ligne articulaire médiale et latérale, ainsi qu'une augmentation du volume et une limitation fonctionnelle. Après des études diagnostiques, il est décidé de procéder à une arthroscopie diagnostique-thérapeutique et un suivi étroit est poursuivi pour la pathologie associée.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur a eu mal au genou depuis longtemps. Son genou était un peu cassé à l’intérieur. Il avait mal et son genou bougeait mal. Les docteurs ont regardé dedans avec une petite caméra. Ils ont aidé son genou à aller mieux. Après, il a fait des exercices pour que son genou soit fort. Maintenant, il peut marcher et jouer sans douleur.",
+            "B2": "Cas d’un homme de 35 ans avec une ancienne rupture du ligament croisé antérieur (LCA) datant de 10 ans. Au début, il a suivi un traitement sans chirurgie, avec une immobilisation puis des séances de physiothérapie. Cela a amélioré un peu ses symptômes, mais un mois avant la nouvelle consultation, il a ressenti une douleur importante au genou et une sensation d’instabilité, surtout en descendant les escaliers. \n\nL’examen médical a montré une douleur sur les côtés du genou, une mobilité réduite en pliant le genou, et des tests spéciaux ont confirmé que le ligament était toujours endommagé. Une IRM (une sorte d’image médicale) a révélé que le ligament croisé antérieur était complètement absent, avec aussi des signes d’arthrose, c’est-à-dire une usure du cartilage à l’intérieur de l’articulation. Des déchirures des ménisques, qui sont des petits coussinets dans le genou, ont aussi été trouvées.\n\nPour mieux comprendre et traiter ces problèmes, les médecins ont réalisé une arthroscopie, une opération où l’on regarde à l’intérieur du genou avec une petite caméra. Ils ont confirmé la rupture complète du LCA, des lésions des ménisques, une arthrose avancée et une inflammation de la membrane autour du genou. À cause de l’arthrose sévère, ils ont choisi de ne pas reconstruire le ligament pour éviter des complications futures.\n\nAprès l’opération, le patient a suivi une rééducation avec des exercices pour bouger le genou sans forcer et renforcer les muscles. Lors des contrôles à 3, 6 et 9 mois, il a rapporté ne plus avoir de douleur ni d’instabilité. Il a pu reprendre ses activités normales et faire du sport léger sans problème. Ce suivi montre que l’arthroscopie et la rééducation ont aidé à améliorer sa qualité de vie malgré les lésions anciennes.",
+            "B3": "Résumé détaillé et structuré du cas clinique\n\nContexte  \nNous rapportons le cas d’un homme de 35 ans présentant une rupture complète du ligament croisé antérieur (LCA) datant de dix ans, initialement prise en charge par un traitement conservateur comprenant une immobilisation suivie de physiothérapie. Après une amélioration partielle, le patient a pu reprendre ses activités quotidiennes sans limitation notable jusqu’à un mois avant la réévaluation récente, lorsqu’il a commencé à ressentir une douleur modérée (6/10 sur l’échelle visuelle analogique) et une sensation d’instabilité du genou, notamment en descendant les escaliers, accompagnées d’un œdème intermittent, sans nouveau traumatisme.\n\nPrincipales observations  \nL’examen clinique a mis en évidence une douleur à la palpation sur la ligne articulaire latérale et la surface antérieure du genou, une flexion active limitée à 85° (contre 100° en passif) avec extension complète, ainsi qu’une force musculaire conservée (5/5) mais douloureuse à la face antérieure. Les tests spécifiques du genou ont été positifs pour l’instabilité antérieure (tests de Lachman, Lelli et pivot shift de degré III), ainsi que pour des lésions méniscales (tests de McMurray, Steinman et Apley). L’imagerie par résonance magnétique a confirmé l’absence du LCA, une arthrose avancée (grade III-IV) du compartiment fémoro-tibial médial, une arthrose modérée du compartiment latéral, ainsi que des déchirures méniscales complexes et un œdème du ligament croisé postérieur (LCP) avec signes de dégénérescence.\n\nInterprétation clinique  \nL’arthroscopie diagnostique a révélé une rupture complète et ancienne du LCA, des lésions méniscales chroniques et invétérées des deux ménisques, un pincement du LCP, des corps libres intra-articulaires, une lésion condrale (atteinte du cartilage) de 1 cm² sur le condyle fémoral latéral, une arthrose sévère du compartiment médial et une synovite (inflammation de la membrane articulaire). En raison du stade avancé d’arthrose, il a été décidé de ne pas réaliser de reconstruction ligamentaire par tunnels osseux afin d’éviter des complications lors d’une éventuelle chirurgie future d’arthroplastie (remplacement articulaire) du genou.\n\nProchaines étapes et suivi  \nAprès l’intervention arthroscopique, le patient a bénéficié d’une mobilisation passive contrôlée du genou (de 0° à 100° de flexion) et d’une marche assistée par béquilles. Il a quitté l’hôpital sans complications dès le lendemain et a entamé un programme de physiothérapie visant à renforcer et stabiliser les muscles autour du genou. Lors des suivis à trois, six et neuf mois, le patient a rapporté une disparition complète des symptômes, une reprise normale de ses activités quotidiennes sans restriction, ainsi que la possibilité de pratiquer des sports à faible impact sans gêne.\n\nEn résumé, ce cas illustre la prise en charge d’une rupture ancienne du LCA associée à une arthrose sévère et des lésions méniscales chroniques, où la décision thérapeutique a été adaptée au stade évolutif de la maladie afin d’optimiser la fonction articulaire et de préparer une éventuelle intervention future plus lourde."
+        }
+    },
+    {
+        "article": "Notre patient est un homme hispanique de 37 ans en bonne santé qui a subi une rupture simultanée de ses tendons rotuliens bilatéraux après avoir sauté en tentant de faire un « panier de lay-up » en jouant au basket-ball. Les antécédents pertinents comprennent une reconstruction du ligament croisé antérieur (LCA) du genou droit en utilisant un autogreffe de tendon patellaire osseux ipsilatéral (BPTB) en 2002. Le patient était incapable de marcher et s’est présenté à notre clinique en fauteuil roulant. Le patient était incapable d’effectuer une élévation de la jambe droite et avait un défaut sensible au pôle inférieur de la patella bilatéralement. Les radiographies en plan ont démontré une patella alta bilatérale et les études d’IRM ont démontré des ruptures du tendon patellaire proximal bilatéral. La recommandation pour une réparation chirurgicale aiguë simultanée des deux genoux a été donnée au patient.\n\nTechnique opératoire\nL'examen intraopératoire a révélé une importante enflure des deux genoux, avec une extension et une flexion complètes à 140 degrés bilatéralement. Il y avait un défaut palpable et une patella alta bilatérale associée à une rupture du tendon rotulien.\n\nLe genou a été abordé par l'approche standard antérieure médiane. L'étendue de la déchirure a été élucidée, impliquant à la fois le réticulum médial et latéral. Un hématome a été évacué, et les tissus profonds et sous-cutanés ont été irrigués. Des sutures de traction ont été placées dans le tendon quadriceps pour aider à mobiliser la rotule distalement. Le tendon patellaire proximal et le moignon distal du tendon patellaire ont été élucidés.\n\nDeux ancrages de suture bio-composites SwiveLock de 4,75 mm (système d'implant SpeedBridge avec aiguille Scorpion-Multifire, Arthrex, Inc., n° AR-2600SBS-8) ont été placés dans le pôle inférieur de la rotule à l'origine du tendon rotulien. Une suture de verrouillage de Krackow a été réalisée avec chacun des ancrages de suture SwiveLock avec une suture de traction. Cette dernière a été amenée vers le haut et vers le bas du tendon rotulien dans une configuration de suture de verrouillage. Le genou a été placé en flexion à 30 degrés et la longueur du tendon rotulien a été fixée à 4,5 cm. Comme le patient ne disposait pas d'un tendon rotulien contra-latéral intact pour servir de base à la longueur du tendon rotulien, 4,5 cm a été choisi car il s'agit d'une longueur de tendon rotulien moyenne chez les hommes, récemment décrite dans la littérature. Une fluoroscopie intraopératoire en C-arm a été utilisée pour confirmer la hauteur du tendon rotulien. Cette dernière a été vérifiée par un double contrôle en tentant d'obtenir un indice de Caton-Deschamps d'environ 1:1. Les nœuds ont ensuite été noués à partir de la configuration de suture de verrouillage dans la réparation supérieure vers les ancrages de suture dans la rotule.\n\nLes mêmes ancrages avaient des sutures #2 FiberTape (Arthrex, Inc) chargées. Elles étaient croisées dans une configuration de pont de suture et placées dans des ancrages SwiveLock séparés dans le tubercule tibial avec le genou à 30 degrés de flexion. Le paratenon restant et les tissus mous ont été imbriqués pour aider à renforcer la réparation. Le rétaintec médiale et latérale ont ensuite été réparés avec une suture #2 FiberWire de verrouillage (Arthrex, Inc). Après une irrigation approfondie des tissus profonds et sous-cutanés, une fermeture standard en couches a ensuite été réalisée.\n\nLe genou gauche a été traité ensuite de la même manière. À la fin de cette procédure, chaque genou était capable d'obtenir une flexion de 0 à 30 degrés sans aucune tension excessive sur les réparations.\n\nSuivi des patients\nLe patient a été maintenu en position non portante, à l’exception des transferts, pendant 6 semaines après l’opération. Les deux genoux étaient initialement bloqués en pleine extension avec une attelle. Deux jours après l’opération, le patient a commencé une thérapie physique avec une machine de mouvement passif continu, augmentant d’environ 15° par semaine. Après 6 semaines, le patient a commencé à supporter tout son poids avec des attelles bloquées en extension avec un déambulateur. Son ROM était d’environ 0-110° sur les deux jambes, et il pouvait effectuer des élévations de la jambe droite sans difficulté.\n\nÀ 10 mois, il a démontré une force quadriceps de 5/5, une extension de -10° et une flexion de 140° bilatéralement. Le score IKDC (Knee Documentation Committee) était de 57 bilatéralement.\n\nÀ 12 mois, le patient avait un alignement normal avec une force quadriceps symétrique bilatérale. Sa ROM restait à −10 degrés d'extension passive non corrigée et 140 degrés de flexion bilatérale. Le score IKDC du genou droit et gauche du patient s'est amélioré à 69 et 72, respectivement. Son score Lysholm enregistré à 12 mois pour son genou droit et gauche était de 94 et 99, respectivement.\n",
+        "gold_summary": "Nous décrivons le cas d'un homme de 37 ans qui a présenté une rupture bilatérale simultanée du tendon rotulien sans aucun facteur de risque associé. En outre, il s'agit de la première utilisation rapportée de la technique de suture-pont avec des ancrages de suture rotuliens et tibiaux pour réparer une rupture bilatérale proximale du tendon rotulien. Au suivi à 12 mois, le patient avait un alignement normal, aucune épanchement et une force quadriceps symétrique.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur de 37 ans s’est fait très mal aux deux genoux en même temps. Ses tendons, qui aident à bouger ses jambes, se sont cassés. Les docteurs ont réparé ses tendons avec des fils spéciaux pour bien les tenir. Un an après l’opération, ses genoux allaient bien. Il pouvait bouger ses jambes normalement et ses muscles étaient forts. Tout est redevenu presque comme avant.",
+            "B2": "Voici un résumé adapté pour un élève de 14 ans en classe de biologie :\n\nUn homme de 37 ans s’est cassé en même temps les deux tendons rotuliens, qui sont les cordons solides reliant la rotule (l’os devant le genou) au tibia (l’os de la jambe). Cette blessure est très rare, surtout sans cause particulière. Pour réparer ces tendons, les médecins ont utilisé une nouvelle technique avec des petits implants appelés ancrages de suture. Ces ancrages permettent de bien fixer les fils qui tiennent le tendon à l’os, un peu comme un pont solide.\n\nAprès l’opération, le patient a suivi un programme de rééducation pour retrouver la force et le mouvement de ses genoux. Un an plus tard, ses genoux étaient bien alignés, sans gonflement, et ses muscles de la cuisse (les quadriceps) étaient aussi forts des deux côtés. Cela montre que la réparation a bien réussi et que cette méthode peut être efficace pour ce type de blessure.",
+            "B3": "Résumé réécrit pour un public adulte non spécialiste :\n\n**Contexte**  \nNous présentons le cas d’un homme hispanique de 37 ans, en bonne santé générale, qui a subi simultanément la rupture des deux tendons rotuliens (les tendons reliant la rotule au tibia) en jouant au basket-ball. Ce type de blessure bilatérale est extrêmement rare, surtout en l’absence de facteurs de risque connus. Le patient avait des antécédents de reconstruction du ligament croisé antérieur du genou droit, réalisée plus de 15 ans auparavant.\n\n**Principales Observations**  \nÀ son arrivée, le patient ne pouvait plus marcher ni relever ses jambes, avec une douleur et un défaut palpable sous chaque rotule. Les examens radiologiques ont confirmé que les tendons rotuliens étaient rompus près de leur insertion sur la rotule, avec une position anormalement haute des rotules (patella alta) des deux côtés. Une intervention chirurgicale urgente a été décidée pour réparer simultanément les deux tendons.\n\n**Technique chirurgicale**  \nL’opération a consisté à exposer les tendons rompus par une incision frontale sur chaque genou. Les chirurgiens ont utilisé une technique innovante appelée « suture-pont » qui emploie des ancrages spéciaux fixés à la rotule et au tibia pour renforcer la réparation. Des sutures solides ont été placées pour reconnecter précisément les tendons à leur point d’attache, en ajustant leur longueur à une mesure moyenne connue pour un homme. La position et la tension des tendons réparés ont été contrôlées par imagerie pendant l’opération. Les tissus environnants ont également été suturés pour renforcer la réparation. Les deux genoux ont été traités de manière identique, permettant une flexion initiale sans tension excessive.\n\n**Suivi et résultats**  \nAprès l’opération, le patient a été immobilisé et non porteur de poids pendant six semaines, avec un programme de rééducation progressive débutant dès le deuxième jour. À six semaines, il a pu commencer à marcher avec appui complet et une amplitude de mouvement des genoux allant jusqu’à 110 degrés. À dix mois, sa force musculaire des quadriceps était maximale, avec une flexion complète et une légère limitation d’extension. À un an, il présentait un alignement normal des genoux, une force musculaire symétrique et une amplitude de mouvement complète. Les scores fonctionnels évaluant la douleur et la capacité à utiliser ses genoux étaient très bons, témoignant d’une récupération satisfaisante.\n\n**Interprétation Clinique**  \nCe cas illustre une rupture bilatérale simultanée du tendon rotulien chez un patient sans facteurs de risque connus, ce qui est exceptionnel. La technique chirurgicale utilisée, combinant des ancrages rotuliens et tibiaux avec une configuration de suture-pont, est une première décrite dans la littérature pour ce type de blessure. Elle a permis une réparation solide et une récupération fonctionnelle favorable.\n\n**Prochaines Étapes**  \nLe suivi à long terme reste important pour surveiller la fonction des genoux et prévenir d’éventuelles complications. Ce cas ouvre la voie à l’utilisation de cette technique chirurgicale innovante dans des cas similaires de ruptures complexes du tendon rotulien."
+        }
+    },
+    {
+        "article": "Patient de 4 ans, sexe masculin, ayant des antécédents d'impétigo nasal deux semaines avant son admission (traité avec mupirocine topique et céfadroxil oral ; dose, durée et adhérence au traitement inconnus), sans autres antécédents morbides, qui a présenté une hématurie macroscopique glomérulaire associée à un œdème des membres inférieurs de 5 jours d'évolution, auxquels s'ajoutent les douze dernières heures avant la consultation, céphalée, nausées et vomissements. Il s'est rendu au service d'urgence (SU) en état convulsif, après 20 minutes de convulsion tonique-clonique généralisée.\n\nLors de son admission au SU, le patient était apyrétique, avec une pression artérielle non évaluable, un état de conscience quantitatif associé à une hypertonie généralisée et un œdème pré-palpébral et pré-tibial. L'intubation endotrachéale a été décidée et le phénobarbital (10 mg/kg) a été administré pour gérer le statut convulsif.\n\nLors de l'examen physique en unité de soins intensifs (USI), la tension artérielle était de 134/94 mmHg (PAM 110 mmHg) (p95 pour le patient 108/66 mmHg, p95+12 120/78 mmHg).\n\nLes paramètres de laboratoire initiaux comprenaient : urine complète avec hématurie (> 100 érythrocytes par champ), protéinurie 3+ et leucocyturie 10-25 par champ, créatinémie 0,3 mg/dL, anémie avec hématocrite (HTO) 21 %, hémoglobine (Hb) 7 g/dL, avec volume corpusculaire moyen (VCM) et concentration d'hémoglobine corpusculaire moyenne (CHCM) normaux, leucocytose de 23 900 cellules/mm3, thrombocytose de 756 000/mm3, sans élévation des réactifs de phase aiguë, hypocomplémentémie avec niveau de complément C3 à 25 mg/dL (valeur normale, VN : 80-150 mg/dL) et C4 normal. Le test rapide d'antigène pour Streptococcus beta-hémolytique groupe A (Streptococcus pyogenes) dans la gorge a été positif et l'Antiestreptolisine O (ASO) a été (+). La tomographie par ordinateur du cerveau sans contraste n'a pas montré de changements aigus. L'échographie rénale a conclu une néphromégalie bilatérale avec augmentation de l'échogénicité corticale et diminution de la différenciation corticomédullaire.\n\nLe patient a été diagnostiqué avec un syndrome néphrétique par GNAPE compliqué d'urgence hypertensive - état convulsif.\n\nAu cours des 24 premières heures de son séjour en USI, le patient a eu besoin d'une ventilation mécanique (VM) et d'une thérapie anticonvulsivante avec du phénobarbital. Il a évolué sans crise épileptique, avec un électroencéphalogramme (EEG) normal (au lendemain de son admission) et une étude du liquide céphalorachidien normale. Une thérapie antibiotique a été initiée pour éradiquer Streptococcus pyogenes avec du cefotaxime et une thérapie diurétique avec du furosémide.\n\nLe jour suivant, il a présenté une détérioration de la fonction rénale avec une augmentation de la créatinine à 0,99 mg/dL, une hypertension artérielle et une protéinurie de 24 heures de 36,6 mg/m2/h, sans oligurie. Il a commencé un traitement antihypertenseur avec amlodipine et labetalol intraveineux, avec un bon contrôle initial.\n\nÉtant donné l'évolution favorable, l'extubation a été réalisée au bout de 48 heures, et elle a été bien tolérée du point de vue ventilatoire. Néanmoins, après 24 heures d'extubation, le patient a vu sa conscience s'aggraver, avec une ouverture oculaire et un retrait des membres uniquement en réponse à une stimulation douloureuse et une faible réponse verbale (échelle de coma de Glasgow 8), et a développé une tension artérielle > p95+12 malgré une thérapie par labetalol en perfusion continue (jusqu'à 3 mg/kg/h), amlodipine (10 mg/jour) et furosémide, nécessitant à nouveau une VM et une perfusion de nitroprussiate de sodium (jusqu'à 3 mcg/kg/min), dans le but de réduire progressivement la tension artérielle (25 % par jour) pour prévenir des dommages neurologiques secondaires. Étant donné la présence de symptomatologie neurologique aiguë associée à l'hypertension artérielle chez un patient souffrant de glomérulonéphrite, le diagnostic de PRES a été suspecté, et a été confirmé par une IRM du cerveau (jour 5), qui a montré une augmentation du signal sous-cortical dans la région occipitale bilatérale et symétrique, sans restriction de la diffusion, compatible avec un oedème vasogénique (PRES). L'évaluation ophtalmologique était normale, et un nouvel EEG a révélé des épisodes occasionnels de dépression de tension généralisée.\n\nL'énalapril a été ajouté au traitement. Finalement, après 10 jours de sevrage pharmacologique lent, la tension artérielle a été normalisée. L'IRM de contrôle (jour 12) a révélé une régression des résultats précédents. L'extubation a été réussie après 5 jours.\n\nPendant son séjour à l’unité de soins intensifs, la concentration d’hémoglobine a chuté à 5 g/dL, avec un volume corpusculaire moyen et une concentration d’hémoglobine corpusculaire moyenne normaux, sans plaquétopénie, ce qui a fait suspecter une anémie hémolytique en raison d’un test de Coombs direct positif et d’une hémoglobinurie. Deux transfusions de globules rouges ont été nécessaires. Il a été décidé de commencer un traitement stéroïdien avec du méthylprednisolone (1 mg/kg/j) pendant 72 heures. Le coprocultures était négatif, tout comme l’antigène urinaire pour Streptococcus pneumoniae. Une sérologie pour virus Epstein-Barr et Parvovirus B19, un profil d’antigènes nucléaires extractibles (ENA), des anticorps anti-cytoplasme des neutrophiles (ANCA), des anticorps anti-ADN, des anticorps anti-B2 glycoprotéine 1, des anticorps anti-cardiolipines et un anticoagulant lupique, qui ont tous été négatifs. Toutes les cultures étaient négatives (cultures sanguines, urinaires, aspirats endotrachéaux et pharyngés). Seul ANA (anticorps antinucléaires) positif 1/160 a été noté.\n\nL’état du patient s’est amélioré, avec une tension artérielle plus basse, un taux de complément plus élevé et une urine sans protéinurie ni hématurie. Le test de Coombs direct est resté positif au neuvième jour de l’hospitalisation.\n\nLe patient a quitté l'hôpital le 31e jour, normotendu, sans anémie, avec une fonction rénale préservée, sans protéinurie ni hématurie, avec une normalisation des taux de C3 et asymptomatique du point de vue neurologique. Il a été libéré avec un traitement pharmacologique avec prednisone, amlodipine, enalapril et acide folique. Le patient n'a pas présenté de récidive et est resté asymptomatique 6 mois après la sortie.\n",
+        "gold_summary": "Patient de 4 ans, avec des antécédents de 5 jours d'hématurie et d'œdème, auxquels s'ajoutaient des céphalées, des nausées et des vomissements, a présenté un état convulsif et une crise hypertensive. Les résultats de laboratoire ont révélé une hypocomplémentémie C3 et des titres élevés d'anti-estréptolysine O, ce qui a été interprété comme une GNAPE. Il a évolué vers une encéphalopathie, ce qui a fait suspecter un PRES secondaire à une crise hypertensive, ce qui a finalement été confirmé par une IRM du cerveau. Il a également présenté une anémie hémolytique auto-immune, avec une hémoglobine allant jusqu'à 5 g/dL. Son traitement a été basé sur une thérapie antihypertensive, des mesures de neuroprotection et un traitement stéroïdien. Il a quitté l'hôpital 31 jours après son admission, asymptomatique 6 mois après sa sortie.\n",
+        "synthetic_summary": {
+            "B1": "Un petit garçon de 4 ans est tombé très malade. Il avait du sang dans son pipi et ses jambes étaient gonflées. Puis, il a eu très mal à la tête, il a vomi et s’est senti très mal.\n\nUn jour, il a eu une grosse crise où il a bougé tout son corps sans pouvoir s’arrêter. Les docteurs l’ont aidé à respirer avec une machine. Ils ont fait des examens et ont vu que son corps avait un problème avec ses reins et son sang.\n\nSon cerveau aussi était un peu malade à cause de sa tension qui était très haute. Les docteurs ont donné des médicaments pour faire baisser sa tension et pour protéger son cerveau. Ils lui ont aussi donné des médicaments pour son sang.\n\nAprès beaucoup de soins, le petit garçon est devenu mieux. Il est resté à l’hôpital un mois. Puis, il est rentré à la maison, en bonne santé, sans douleur, et il va très bien depuis six mois.",
+            "B2": "**Résumé simplifié pour un adolescent de 14 ans**\n\nUn garçon de 4 ans est arrivé à l’hôpital avec du sang dans les urines et des gonflements aux jambes depuis 5 jours. Il avait aussi mal à la tête, des nausées et des vomissements. Ensuite, il a fait une grosse crise de convulsions à cause d’une forte tension artérielle. \n\nLes médecins ont fait des analyses qui ont montré que son système immunitaire attaquait ses reins après une infection par une bactérie appelée streptocoque. Cette maladie s’appelle une glomérulonéphrite aiguë post-infectieuse (GNAPE), ce qui signifie que les petits filtres dans ses reins étaient enflammés.\n\nPendant son séjour, il a eu un problème au cerveau appelé PRES, qui arrive quand la tension artérielle est trop élevée et cause un gonflement temporaire du cerveau. Cela a été confirmé par une IRM, un examen spécial du cerveau. En plus, il a développé une anémie hémolytique auto-immune, c’est-à-dire que son corps détruisait ses propres globules rouges, ce qui a fait baisser son taux d’hémoglobine (la partie du sang qui transporte l’oxygène).\n\nPour le soigner, les médecins ont utilisé des médicaments pour faire baisser sa tension artérielle, des médicaments pour protéger son cerveau, et des corticoïdes (un type de médicament qui calme l’inflammation). Après 31 jours à l’hôpital, il est sorti en bonne santé, sans symptômes, avec ses reins et son cerveau en bon état. Six mois plus tard, il allait toujours bien, sans nouvelle crise.",
+            "B3": "Résumé détaillé et structuré pour un public non spécialiste\n\n**Contexte**  \nUn garçon de 4 ans, sans antécédents médicaux majeurs, a présenté une hématurie visible (sang dans les urines) et un œdème des jambes depuis cinq jours. Dans les dernières heures avant sa consultation, il a développé des maux de tête, des nausées et des vomissements. Il a ensuite fait une crise convulsive généralisée (convulsions affectant tout le corps) qui a duré environ 20 minutes, ce qui a motivé son admission en urgence.\n\n**Principales observations cliniques et paracliniques**  \nÀ son arrivée, le patient était conscient mais avec une hypertonie musculaire généralisée et un œdème autour des yeux et des jambes. Sa pression artérielle n’a pas pu être mesurée immédiatement, mais elle s’est révélée élevée par la suite (134/94 mmHg, supérieure au 95e percentile attendu pour son âge). Les analyses d’urine ont montré une hématurie importante, une protéinurie (présence de protéines dans les urines) et une leucocyturie (globules blancs dans les urines). Les examens sanguins ont révélé une anémie sévère (hémoglobine à 7 g/dL), une leucocytose (augmentation des globules blancs), une thrombocytose (augmentation des plaquettes), et surtout une hypocomplémentémie marquée avec un complément C3 très bas, signe d’une inflammation immunitaire. Le test rapide a confirmé la présence d’une infection récente par Streptococcus pyogenes (bactérie responsable d’infections de la gorge et de la peau). L’imagerie rénale a montré une augmentation du volume des reins et des modifications de leur structure, compatibles avec une inflammation glomérulaire.\n\n**Interprétation clinique**  \nLe diagnostic principal retenu est celui d’une glomérulonéphrite aiguë post-infectieuse (GNAPE), une inflammation des filtres rénaux (glomérules) survenant après une infection streptococcique. Cette maladie a provoqué un syndrome néphrétique, caractérisé par une hématurie, une protéinurie, un œdème et une hypertension artérielle. La crise hypertensive a conduit à un état convulsif et à une encéphalopathie hypertensive, compliquée par un syndrome de leucoencéphalopathie réversible postérieure (PRES), une atteinte cérébrale réversible liée à l’hypertension sévère, confirmée par une IRM cérébrale. Par ailleurs, le patient a développé une anémie hémolytique auto-immune (destruction des globules rouges par le système immunitaire), confirmée par un test de Coombs positif et une hémoglobinurie (présence d’hémoglobine dans les urines). Cette complication a nécessité des transfusions sanguines et un traitement par corticostéroïdes.\n\n**Traitement et évolution**  \nLe patient a reçu une prise en charge intensive comprenant une ventilation mécanique lors des crises convulsives, un traitement antihypertenseur combinant plusieurs médicaments (amlodipine, labetalol, nitroprussiate de sodium, énalapril) pour contrôler la pression artérielle, une antibiothérapie ciblée contre Streptococcus pyogenes, ainsi qu’un traitement stéroïdien pour l’anémie hémolytique auto-immune. La fonction rénale s’est initialement détériorée mais s’est progressivement améliorée. L’état neurologique s’est stabilisé après la réduction contrôlée de la pression artérielle et la résolution du PRES, confirmée par une IRM de contrôle. Le patient a été extubé avec succès après cinq jours de ventilation.\n\n**Prochaines étapes et suivi**  \nAprès 31 jours d’hospitalisation, le garçon est sorti de l’hôpital en bon état général, avec une pression artérielle normale, une fonction rénale préservée et sans signes d’anémie ni d’atteinte neurologique. Les analyses urinaires étaient normales, et les taux de complément C3 étaient revenus à la normale. Il a été maintenu sous traitement médicamenteux (prednisone, amlodipine, énalapril, acide folique) pour prévenir les récidives. Six mois après sa sortie, il restait asymptomatique, sans récidive de la maladie.\n\n---\n\nCe cas illustre la complexité d’une glomérulonéphrite post-infectieuse sévère chez un jeune enfant, avec des complications neurologiques graves liées à l’hypertension et une anémie auto-immune, nécessitant une prise en charge multidisciplinaire intensive et un suivi prolongé."
+        }
+    },
+    {
+        "article": "Un homme de 56 ans ayant des antécédents d’hypertension diagnostiquée à 46 ans était bien géré avec 40 mg de telmisartan et 5 mg d’amlodipine. Le patient consommait occasionnellement de l’alcool et ne fumait pas.\n\nUne TTE de 2011 a révélé une AR modérée dirigée vers l’AML, avec une vena contracta de 2,5 mm, une largeur de jet de 6,5 mm et un diamètre du tractus de sortie ventriculaire gauche (LVOT) de 29 mm. Le diamètre de l’aorte ascendante était de 38 mm. Une régurgitation mitrale modérée a également été observée, sans preuve de perforation ou de végétation.\n\nSix mois avant son admission, la patiente a ressenti une douleur dans la huitième dent supérieure gauche et des saignements récurrents lors du brossage. Durant les 3 mois précédant son admission, la patiente a eu des fièvres intermittentes supérieures à 40 °C sans essoufflement. N’ayant constaté aucune amélioration, la patiente s’est présentée à notre hôpital en avril 2016, a été admise le jour même pour une évaluation et un traitement complémentaires, et a été diagnostiquée avec une fièvre d’origine inconnue (FUO).\n\nLors de l’admission, la taille, le poids et l’indice de masse corporelle du patient étaient respectivement de 179 cm, 79,2 kg et 24,7 kg/m². Il était conscient et avait une température de 37,2°C, une tension artérielle de 124/77 mmHg, une fréquence cardiaque de 90 b.p.m. et une saturation en oxygène de 95 % (air ambiant). L’auscultation a révélé des bruits respiratoires clairs et un murmure systolique à la quatrième frontière sternale gauche, sans murmure diastolique. Il n’y avait pas de rougeurs cutanées, d’œdème, de lymphadénopathie pathologique ou de résultats neurologiques ou fondoscopiques anormaux.\n\nUn électrocardiogramme à 12 dérivations a montré un rythme sinusal normal avec une fréquence cardiaque de 82 b.p.m. et un axe normal. La radiographie thoracique a révélé un rapport cardiothoracique de 51 % sans congestion pulmonaire ou épanchement pleural. Les scanners de tomographie par ordinateur à contraste amélioré du thorax au bassin n’ont révélé aucune anomalie, source d’infection, lésion néoplasique ou source d’embolie. La scintigraphie au gallium réalisée pour étudier la fièvre de cause inconnue n’a révélé aucune accumulation anormale.\n\nBien que les lésions néoplasiques, la maladie du collagène et les maladies infectieuses aient été considérées comme des causes possibles de fièvre, ces résultats ont exclu les maladies néoplasiques et du collagène. Les cultures sanguines des jours 1 à 4 de l'hospitalisation (deux ensembles chacune) étaient positives pour S. oralis. La consultation avec le service de chirurgie dentaire et buccale a révélé une carie dans la huitième dent supérieure gauche, qui a nécessité un traitement et a été diagnostiquée comme une source possible de bactériémie.\n\nCes résultats suggéraient une IE, ce qui a entraîné une consultation en cardiologie. L’ECR a révélé les résultats suivants : fraction d’éjection ventriculaire gauche (FEVG) de 62 %, diamètre diastolique/systolique du ventricule gauche de 58/42 mm, diamètre de l’aorte ascendante de 38 mm, régurgitation mitrale modérée, régurgitation tricuspidale triviale (RT) et gradient de pression RT de 20 mmHg. L’AR, conforme aux résultats de 2011, avait dévié vers l’arrière, en collision avec l’AML. Une évaluation semi-quantitative a révélé un diamètre de la voie de sortie du ventricule gauche de 29 mm, une veine contractée de 4,2 mm et une largeur du jet de 6,5 mm, indiquant une AR modérée. Une végétation de 7,7 mm a été détectée au site de l’impact de l’AR sur l’AML, provoquant une perforation et un reflux.\n\nUn TEE le jour 5 de l'hospitalisation a confirmé des résultats similaires à ceux du TTE, montrant l'AR migrant empiétant sur l'AML avec végétation et perforation. Le TEE a également révélé une flexion partielle de la cuspide aortique droite (RCC) et un prolapsus, mais aucune végétation de la valve aortique (AV). Sur la base des critères de Duke, un diagnostic définitif d'IE a été établi. Aucune anomalie n'a été trouvée dans les examens du fond d'œil ou dermatologiques.\n\nLe traitement comprenait 8 g/jour d’AMPC (2 g q6) et 160 mg/jour de GM (80 mg q12). La patiente a présenté une défervescence, n’a pas eu de problèmes hémodynamiques et était dans un état stable sans insuffisance cardiaque ou symptômes neurologiques.\n\nLe septième jour, une IRM du cerveau a révélé de multiples signaux faibles dans les hémisphères cérébraux bilatéraux, le pons, les ganglions basaux bilatéraux, le thalamus gauche et le lobe frontal gauche sur l'image pondérée en fonction de la susceptibilité, qui étaient considérés comme étant dus à une hémorragie post-infarctus causée par un embolisme lié à l'IE.\n\nEn raison d'un dysfonctionnement valvulaire important, le traitement antibiotique a été poursuivi et une intervention chirurgicale a été planifiée pour le jour 19. Environ 7 mm de végétation ont été enlevés de l'AML au site du jet AR, suivis d'une réparation de la valve mitrale (résection de la végétation A2, patch péricardique autologue, Physio II, 32 mm) et d'une annuloplastie tricuspide (TAP) (procédure de De Vega). Une flexion partielle du RCC a été observée sans aucune végétation AV. Pour remédier à la RA résiduelle et prévenir une IE récurrente, une valvuloplastie aortique et un remplacement de l'aorte ascendante (annuloplastie CV-9 22 mm, triples 24 mm) ont été effectués simultanément. La patiente n'a présenté aucune complication postopératoire apparente. L'AMPC et le GM ont été administrés pendant 42 et 17 jours, respectivement. La patiente a été déchargée sans aucun résultat anormal.\n\nLe TTE à 6 mois postopératoirement n'a montré aucune récidive d'IE et aucune dysfonction de la valve mitrale. La patiente est restée stable pendant 3 ans et 10 mois postopératoirement.\n",
+        "gold_summary": "En 2011, un homme de 56 ans a présenté une AR modérée vers la LMA, révélée par un échocardiogramme transthoracique. En 2016, 3 mois avant son admission, le patient avait présenté des fièvres intermittentes de plus de 40 °C, qui ne s'amélioraient pas, et a été référé à notre hôpital. Un examen détaillé a révélé une végétation sur la LMA où la valve aortique était déplacée, et le site était perforé. L'AR était modérée. Les cultures sanguines étaient positives pour Streptococcus oralis. À partir de ces résultats, un diagnostic définitif d'endocardite infectieuse (EI) a été fait. Le patient a eu un infarctus cérébral et a subi une chirurgie semi-d'urgence.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur avait un petit problème au cœur depuis longtemps.  \n\nUn jour, il a eu très très chaud, comme une grosse fièvre.  \n\nLe docteur a regardé son cœur avec une machine spéciale.  \n\nIls ont vu un petit bout qui ne devait pas être là.  \n\nCe petit bout a fait un trou dans une partie du cœur.  \n\nDes petites bêtes dans son sang ont causé ce problème.  \n\nLe docteur a dit que c’était une maladie du cœur à soigner vite.  \n\nLe monsieur a eu un petit accident dans sa tête à cause du cœur.  \n\nAlors, les docteurs ont fait une opération pour réparer le cœur.  \n\nAprès, il est allé beaucoup mieux et est resté en bonne santé.",
+            "B2": "Voici un résumé simple et clair pour un élève de 14 ans :\n\nEn 2011, un homme de 56 ans avait un problème au cœur appelé régurgitation aortique modérée, ce qui signifie que la valve aortique ne fermait pas complètement et laissait un peu de sang revenir en arrière. En 2016, il a commencé à avoir des fièvres très élevées qui ne passaient pas. Lorsqu’il est venu à l’hôpital, les médecins ont fait plusieurs examens et ont trouvé une sorte de petite boule appelée végétation sur une autre valve du cœur, la valve mitrale, à l’endroit où le sang revenait. Cette zone était aussi abîmée, avec un trou (perforation). \n\nDes analyses de sang ont montré qu’il avait une infection causée par une bactérie appelée Streptococcus oralis. Cette infection s’appelle une endocardite infectieuse, c’est quand des microbes attaquent les valves du cœur. À cause de cette infection, il a eu un problème au cerveau appelé infarctus, qui est une sorte de blessure causée par un manque de sang. Pour soigner tout ça, il a dû avoir une opération importante pour réparer les valves du cœur. Après le traitement, il s’est bien remis.",
+            "B3": "Résumé détaillé et structuré destiné à un adulte éduqué non-médecin\n\n**Contexte**  \nUn homme de 56 ans, suivi pour une hypertension artérielle bien contrôlée depuis dix ans sous traitement médicamenteux, avait déjà été évalué en 2011 par échocardiographie transthoracique (TTE). À cette époque, il présentait une régurgitation aortique (RA) modérée, c’est-à-dire un reflux sanguin au niveau de la valve aortique, dirigée vers la valve mitrale antérieure (LMA). Cette régurgitation était stable et associée à une régurgitation mitrale modérée sans signes d’infection ou de lésion valvulaire.\n\n**Principales observations en 2016**  \nTrois mois avant son admission en 2016, le patient a développé des épisodes de fièvre élevée (supérieure à 40 °C) persistants, sans amélioration malgré l’absence d’essoufflement ou d’autres symptômes respiratoires. Il a également signalé une douleur dentaire avec saignements récurrents, suggérant une infection buccale. À son admission, les examens cliniques et paracliniques initiaux (radiographie thoracique, scanner, scintigraphie au gallium) n’ont pas identifié de foyer infectieux ou tumoral. Cependant, plusieurs hémocultures réalisées ont révélé la présence de Streptococcus oralis, une bactérie souvent liée aux infections dentaires.\n\nUne nouvelle échocardiographie transthoracique a montré une végétation (amas de bactéries et de cellules inflammatoires) de 7,7 mm sur la valve mitrale antérieure, précisément à l’endroit où le jet de régurgitation aortique impactait la valve. Cette végétation avait provoqué une perforation de la valve, aggravant le reflux sanguin. La régurgitation aortique était toujours modérée mais avait évolué, avec un déplacement du jet vers l’arrière. Une échocardiographie transœsophagienne (TEE), examen plus précis, a confirmé ces anomalies et a montré une flexion partielle d’une cuspide de la valve aortique sans végétation associée. Sur la base des critères diagnostiques internationaux (critères de Duke), un diagnostic définitif d’endocardite infectieuse (infection de la paroi interne du cœur et des valves) a été posé.\n\n**Interprétation clinique**  \nL’endocardite infectieuse était probablement liée à la bactérie Streptococcus oralis provenant d’une carie dentaire non traitée, qui avait provoqué une infection de la valve mitrale déjà fragilisée par le jet de régurgitation aortique. Cette infection a entraîné une perforation valvulaire et un risque accru de complications emboliques. En effet, une IRM cérébrale réalisée au septième jour d’hospitalisation a révélé plusieurs petites hémorragies cérébrales secondaires à des embolies (obstruction de petits vaisseaux par des fragments de végétation infectieuse), témoignant d’un infarctus cérébral lié à l’endocardite.\n\n**Traitement et évolution**  \nLe patient a reçu un traitement antibiotique intensif par ampicilline et gentamicine, entraînant une disparition progressive de la fièvre et une stabilisation de son état général. En raison de la gravité de la lésion valvulaire et du risque de complications, une intervention chirurgicale a été réalisée au 19e jour d’hospitalisation. Cette chirurgie a consisté en l’ablation de la végétation, la réparation de la valve mitrale (résection de la zone perforée et renforcement par un patch de péricarde, tissu du cœur), une annuloplastie tricuspide (réparation de la valve tricuspide), ainsi qu’une valvuloplastie aortique et un remplacement partiel de l’aorte ascendante pour corriger la régurgitation aortique résiduelle et prévenir une récidive d’infection. La chirurgie s’est déroulée sans complication majeure.\n\nAprès 42 jours d’antibiothérapie, le patient a été libéré de l’hôpital en bon état. Le suivi échocardiographique à six mois a montré une fonction valvulaire normale sans signe de récidive d’endocardite. Le patient est resté stable et asymptomatique pendant près de quatre ans après l’intervention.\n\n**Prochaines étapes**  \nCe cas illustre l’importance d’une prise en charge rapide et complète des infections dentaires chez les patients présentant des anomalies valvulaires cardiaques, afin de prévenir l’endocardite infectieuse. Le suivi régulier par échocardiographie et la vigilance face à toute fièvre prolongée sont essentiels pour détecter précocement cette complication grave. La collaboration multidisciplinaire entre cardiologie, chirurgie cardiaque et chirurgie dentaire a été déterminante dans la réussite du traitement."
+        }
+    },
+    {
+        "article": "Garçon de 11 ans présentant une céphalée occipitale et frontale bilatérale associée à des vomissements de 12 heures d'évolution après une chute banale sur la région sacro-coccygienne. Antécédent de SM dû à une mutation de type missense en hétérozygotie dans le gène FBN1 c.2243G>A.\n\nL'examen neurologique et l'examen par appareil étaient normaux, sauf en ce qui concerne l'habitude marfanoïde. Une analyse générale et une radiographie sacro-coccygienne ont été effectuées, sans anomalies. La céphalée s'est améliorée, jusqu'à disparaître en décubitus, mais elle réapparaissait en se levant et ne tolérait pas la position debout, raison pour laquelle elle a été admise.\n\nPendant l'admission, il a présenté une faible réponse à l'analgésie. Une tomographie axiale assistée par ordinateur (TAC) crânienne a été réalisée, qui a montré une augmentation de la densité des sinus transverses, probablement liée à un flux veineux lent. En raison du soupçon de SHI en relation avec une éventuelle fistule de LCR, une résonance magnétique (RM) crâniomédullaire a été demandée. La RM a montré une légère descente amygdale (5 mm) et un décollement de la dure-mère avec des collections liquides à l'extérieur de la dure-mère au niveau dorsal et lombo-sacré, compatible avec une fistule de LCR ; en outre, des kystes périneuraux de Tarlov ont été visualisés au niveau sacré. Cette image n'était pas compatible avec une ectasie dure, et le patient ne disposait pas de neuro-imagerie préalable.\n\nLe patient a été traité par hyperhydratation, analgésiques mineurs (dexkétoprofène et métamizole), hydrocortisone intraveineuse à la dose initiale de 8 mg/kg/jour, caféine par voie orale à la dose de 2,5 mg/kg/jour, et repos au lit en position de Trendelenburg. Cinq jours plus tard, le patient a commencé une mobilisation progressive, présentant une évolution favorable, avec une amélioration de la céphalée et tolérant la position debout. Il a pu quitter l'hôpital 12 jours plus tard.\n\nAprès quatre mois asymptomatiques, la clinique réapparut en même temps que le début de l'activité sportive à l'école. L'IRM de contrôle a montré la disparition de la collection dorsale avec persistance de collections sacrées. Il a de nouveau reçu le même schéma de traitement conservateur que lors de l'admission précédente.\n\nL’IRM de contrôle un an après a montré la résolution des collections sous-duraux ou extra-duraux dans le canal rachidien et a identifié comme nouvelle découverte une fine image d’hydromélie dorsale moyenne. Deux ans après la première admission, il a consulté de nouveau pour des céphalées orthostatiques, une IRM a été réalisée et a constaté une ré-fistulisation au niveau de L5-S1. Compte tenu de la récidive, un traitement par patch hématique épidural (PHE) lombaire (L4-L5) a été décidé par le service d’anesthésiologie. Un an après sa réalisation, et trois ans depuis le début de la clinique, le patient reste asymptomatique.\n",
+        "gold_summary": "Nous rapportons le cas d'un garçon de 11 ans avec céphalées orthostatiques et vomissements depuis 12 heures après une chute sur la région sacro-coccygienne ; antécédent de syndrome de Marfan. L'IRM crânio-médullaire a montré des collections liquides extra-durales au niveau dorsal et lombo-sacré compatibles avec une fistule de LCR. L'évolution a été favorable après traitement, mais deux nouveaux épisodes sont survenus pendant le suivi, ce qui a conduit à l'application d'un patch hématico-épidural deux ans après le début.\n",
+        "synthetic_summary": {
+            "B1": "Un garçon de 11 ans est tombé et a eu mal à la tête. Il avait aussi envie de vomir. \n\nLe docteur a fait des images de sa tête et de son dos. Ils ont vu un peu d'eau où il ne faut pas. Cela venait d’un petit trou qui laissait sortir cette eau. \n\nLe garçon a pris des médicaments et a beaucoup reposé. Il allait mieux. Mais après, il a eu encore mal à la tête deux fois. \n\nAlors, les docteurs ont fait un soin spécial pour boucher le trou. Maintenant, il va bien et n’a plus mal.",
+            "B2": "Cas d’un garçon de 11 ans avec des maux de tête qui s’aggravent en position debout et des vomissements, apparus après une chute sur le bas du dos. Il a un antécédent de syndrome de Marfan, une maladie génétique qui affecte le tissu conjonctif.\n\nLes examens d’imagerie, notamment une IRM, ont montré la présence de liquide anormal autour de la moelle épinière dans la région du dos et du bas du dos. Cela indiquait une fuite de liquide céphalorachidien (LCR), un liquide qui entoure normalement le cerveau et la moelle épinière pour les protéger. Cette fuite, appelée fistule, provoquait ses symptômes.\n\nLe garçon a reçu un traitement médical avec des médicaments pour la douleur, des corticoïdes, de la caféine, beaucoup de repos et une position spéciale allongée. Ses symptômes se sont améliorés, mais après quelques mois, les maux de tête sont revenus, surtout quand il a recommencé le sport à l’école.\n\nUne nouvelle IRM a montré que la fuite persistait dans une autre zone. Le même traitement a été donné à nouveau. Un an plus tard, l’IRM a montré que la fuite avait disparu, mais une autre anomalie appelée hydromélie (accumulation de liquide dans la moelle épinière) est apparue.\n\nDeux ans après le début, les maux de tête sont revenus. Une nouvelle fuite a été détectée au bas du dos. Cette fois, les médecins ont utilisé un patch hématico-épidural, une technique où l’on injecte du sang dans l’espace autour de la moelle épinière pour boucher la fuite.\n\nUn an après ce traitement, soit trois ans après le début des symptômes, le garçon ne présente plus de symptômes et se porte bien.",
+            "B3": "Résumé détaillé et structuré :\n\n**Contexte**  \nUn garçon de 11 ans, porteur d’un syndrome de Marfan dû à une mutation génétique spécifique (mutation missense hétérozygote dans le gène FBN1), a présenté des céphalées (maux de tête) bilatérales, localisées à l’arrière (occipitale) et au front, associées à des vomissements. Ces symptômes sont apparus 12 heures après une chute apparemment bénigne sur la région sacro-coccygienne (bas du dos). L’examen neurologique était normal, excepté des signes physiques évoquant une morphologie marfanoïde. Les examens radiographiques et biologiques initiaux n’ont pas révélé d’anomalies.\n\n**Principales Observations**  \nLa céphalée s’améliorait en position couchée mais réapparaissait dès que le patient se mettait debout, provoquant une intolérance à la station verticale. Une tomodensitométrie (TAC) cérébrale a montré une augmentation de la densité dans les sinus veineux transverses, suggérant un ralentissement du flux veineux. Une suspicion de syndrome d’hypotension intracrânienne (SHI), possiblement lié à une fuite de liquide céphalorachidien (LCR), a motivé la réalisation d’une imagerie par résonance magnétique (IRM) crânio-médullaire. Cette IRM a révélé une légère descente des amygdales cérébelleuses (5 mm), un décollement de la dure-mère (membrane entourant le cerveau et la moelle épinière) avec des collections liquides situées à l’extérieur de cette membrane au niveau dorsal et lombo-sacré, compatibles avec une fistule (fuite) de LCR. Des kystes périneuraux de Tarlov ont également été identifiés au niveau sacré. Ces images n’étaient pas compatibles avec une ectasie dure (dilatation anormale de la dure-mère). Le patient ne disposait pas d’imagerie antérieure pour comparaison.\n\n**Interprétation Clinique**  \nLe tableau clinique et l’imagerie étaient évocateurs d’un syndrome d’hypotension intracrânienne secondaire à une fuite de LCR au niveau rachidien, probablement provoquée par la chute. Cette condition explique les céphalées orthostatiques (qui s’aggravent en position debout) et les vomissements.\n\n**Prise en Charge et Évolution**  \nLe traitement initial a été conservateur : hyperhydratation, analgésiques mineurs (dexkétoprofène, métamizole), hydrocortisone intraveineuse, caféine orale et repos strict au lit en position de Trendelenburg (tête plus basse que les pieds). Après cinq jours, le patient a pu commencer une mobilisation progressive avec amélioration des symptômes, et il a quitté l’hôpital au bout de 12 jours.\n\nQuatre mois plus tard, après une période asymptomatique, les céphalées sont réapparues lors de la reprise d’activités sportives. L’IRM de contrôle a montré la disparition des collections dorsales mais la persistance de collections liquides sacrées. Le même traitement conservateur a été réappliqué avec succès.\n\nUn an après, l’IRM a montré la résolution complète des collections sous-durales et extra-durales, mais a mis en évidence une fine hydromélie dorsale moyenne (accumulation anormale de liquide dans la moelle épinière).\n\nDeux ans après la première hospitalisation, le patient a de nouveau consulté pour des céphalées orthostatiques. L’IRM a révélé une récidive de la fistule au niveau de L5-S1. En raison de cette récidive, un traitement par patch hématico-épidural lombaire (injection de sang autologue dans l’espace épidural pour colmater la fuite) a été réalisé. Un an après cette intervention, soit trois ans après le début des symptômes, le patient demeure asymptomatique.\n\n**Prochaines Étapes**  \nLe suivi clinique et radiologique doit se poursuivre pour surveiller toute récidive éventuelle. Le traitement conservateur reste la première approche, mais le patch hématico-épidural constitue une option efficace en cas de récidive ou d’échec du traitement médical. Une attention particulière est nécessaire chez les patients porteurs de syndrome de Marfan, qui peuvent présenter des fragilités tissulaires favorisant ce type de complications."
+        }
+    },
+    {
+        "article": "Un homme de 54 ans ayant des antécédents de syndrome de Wolff-Parkinson-White ayant entraîné un arrêt cardiaque dans la vingtaine a ensuite développé une cardiomyopathie non ischémique (New York Heart Association, classe IV, avec une fraction d'éjection de 15 %). Il a été admis pour insuffisance cardiaque et a suivi un traitement complexe en unité de soins cardiaques avec retrait de l'AICD/pacemaker en raison d'une endocardite et anticoagulation avec Coumadin pour thrombus auriculaire droit/fibrillation auriculaire. Il a été renvoyé, mais a dû être réadmis à plusieurs reprises pour insuffisance cardiaque, nécessitant finalement une oxygénation extracorporelle par membrane veino-artérielle par l'artère fémorale droite et la veine fémorale gauche en tant que réanimation cardiopulmonaire électronique en janvier 2020 et restera sous ECMO pendant 5 semaines. Il a subi une implantation de LVAD en utilisant les sites de canulation du ventricule gauche et de l'aorte ascendante 16 jours après la canulation ECMO et une trachéotomie ultérieure en février pour une insuffisance respiratoire persistante.\n\nDeux jours avant le retrait des canules ECMO, le patient a subi une amputation guillotine de l’extrémité inférieure droite en raison d’une gangrène sèche due à une dissection iliaque et à une embolisation distale. Cinq jours plus tard, le jour 25 après le LVAD, on a constaté une fuite de selles au niveau du site de sortie de la ligne de perfusion. L’équipe de chirurgie cardiothoracique a emmené le patient en salle d’opération et a procédé à une exploration limitée, constatant une blessure intestinale due à la ligne de perfusion. La blessure a été réparée avec une suture interrompue en soie et la ligne de perfusion a été laissée intacte. Trois jours après cette réparation, l’équipe de chirurgie des soins aigus a été consultée en raison d’une nouvelle fuite de selles au niveau du site de sortie de la ligne de perfusion. Le patient a été déclaré sévèrement septique. Il a été mis sous antibiotiques et emmené en salle d’opération pour une laparotomie exploratoire formelle et on a constaté que la ligne de perfusion LVAD traversait la cavité abdominale du quadrant supérieur droit au flanc gauche. La ligne de perfusion avait blessé le côlon transverse distal et la réparation antérieure avait fui. Il y avait une abondance de liquide fécal et de nombreux abcès intra-abdominaux qui ont été drainés. En raison de la septicémie du patient, le côlon a été agrafé proximal et distal au segment blessé et l’échantillon a été enlevé. Le patient a été laissé en discontinuité et un pansement abdominal temporaire a été placé pour une deuxième opération prévue. Il est revenu à l’unité de soins intensifs où il a reçu des antibiotiques, une ventilation mécanique et des vasopresseurs.\n\nTrois jours plus tard, lors de la deuxième opération prévue, l’abdomen paraissait propre. En raison de la nécessité du LVAD, la ligne de transmission ne pouvait pas être déconnectée. La première priorité était de mobiliser la ligne de transmission hors du péritoine. L’abdomen du patient a été ouvert du côté gauche de manière transversale pour permettre à la ligne de transmission de se rendre au milieu. Le péritoine a été enlevé du côté droit de l’abdomen du patient pour développer un plan rétro-rectal dans le but de repositionner la ligne de transmission à l’emplacement extra-péritonéal prévu. Une incision transversale plus petite a été faite du côté droit pour que la ligne de transmission se trouve dans ce plan rétro-rectal, loin de la ligne médiane. Ainsi, la ligne de transmission a été retirée avec succès du péritoine sans déconnexion. Une hémicolectomie droite a été réalisée, mais en raison de la ligne de transmission sortant près du quadrant inférieur droit, une iléostomie terminale a été réalisée dans le quadrant inférieur gauche. Sa fascie a été fermée et des sutures de rétention ont été placées en raison du mauvais état nutritionnel du patient et du degré de septicémie abdominale. Le patient s’est bien rétabli après l’opération et a pu reprendre une nutrition entérale le jour 3 post-opératoire, répondant à ses besoins caloriques le jour 7 post-opératoire. Il a subi une révision de son amputation guillotine 15 jours après sa dernière opération abdominale.\n\nL’évolution du patient a été compliquée par un abcès intra-abdominal nécessitant un drainage par radiologie interventionnelle 3 semaines après sa dernière chirurgie abdominale ainsi qu’un traitement antibiotique IV prolongé pour des organismes résistants, y compris VRE. Le patient a terminé son traitement antibiotique et a eu ses drains retirés. Au moment de ce rapport, le patient reste hospitalisé, tolère une nutrition entérale, est déconnecté de la ventilation mécanique et suit une thérapie physique.",
+        "gold_summary": "Un homme de 54 ans ayant des antécédents de syndrome de Wolff-Parkinson-White ayant entraîné de multiples réadmissions pour insuffisance cardiaque a finalement eu besoin d’un dispositif d’assistance ventriculaire gauche (LVAD). Plusieurs semaines plus tard, on a découvert qu’il y avait des selles qui s’écoulaient du site de la ligne de commande. Le patient a été emmené en salle d’opération pour une exploration limitée par l’équipe de chirurgie cardiothoracique et une blessure intestinale a été identifiée et réparée. Trois jours après cette réparation, des selles s’écoulaient à nouveau du site de la ligne de commande, ce qui a nécessité une nouvelle exploration par l’équipe de chirurgie d’urgence. En intra-opératoire, la réparation antérieure s’est avérée être une fuite et de multiples abcès intra-abdominaux ont été découverts. Le côlon transverse a été réséqué et laissé en discontinuité. Au cours d’une deuxième opération prévue, la ligne de commande LVAD a été relocalisée pour être extra-péritonéale et une colostomie a été formée.\n",
+        "synthetic_summary": {
+            "B1": "Un monsieur avait un gros problème avec son cœur. Il avait un appareil pour l’aider à battre.\n\nUn jour, il y avait du caca qui sortait d’un endroit où il ne devait pas. Les docteurs ont regardé dedans et ont trouvé un trou dans son ventre. Ils ont réparé ce trou.\n\nMais le caca est revenu à sortir. Les docteurs ont ouvert encore son ventre. Ils ont vu que le trou n’était pas bien fermé. Il y avait aussi du caca partout dans son ventre.\n\nIls ont enlevé une partie de son ventre qui était malade. Puis, ils ont fait un autre trou pour que le caca sorte ailleurs, où c’est plus sûr.\n\nAprès, ils ont bien aidé le monsieur à guérir. Il a commencé à manger et à bouger doucement. Les docteurs prennent bien soin de lui.",
+            "B2": "Un homme de 54 ans avait un problème cardiaque grave appelé syndrome de Wolff-Parkinson-White, qui avait déjà causé plusieurs arrêts du cœur et une insuffisance cardiaque sévère. Pour l’aider, les médecins lui ont implanté un dispositif appelé LVAD, qui aide le cœur à pomper le sang.\n\nQuelques semaines après cette opération, des selles ont commencé à sortir par un endroit où passe une ligne du LVAD sur son corps. Les chirurgiens ont alors fait une première opération pour regarder et réparer une blessure dans son intestin. Mais trois jours plus tard, les selles ont recommencé à fuir au même endroit. Le patient était très malade à cause d’une infection grave appelée septicémie.\n\nUne deuxième opération plus importante a été réalisée. Les chirurgiens ont découvert que la première réparation avait lâché et que des abcès (des poches de pus) s’étaient formés dans son ventre. Ils ont enlevé une partie de son côlon (le côlon transverse) et ont laissé l’intestin ouvert temporairement pour mieux soigner l’infection.\n\nLors d’une troisième opération programmée, ils ont déplacé la ligne du LVAD pour qu’elle ne traverse plus la cavité abdominale, afin d’éviter d’autres blessures. Ils ont aussi fait une colostomie, c’est-à-dire qu’ils ont créé une ouverture sur le ventre pour que les selles puissent sortir dans un sac, permettant à l’intestin de guérir.\n\nAprès ces opérations, le patient a reçu des antibiotiques puissants et a dû être soigné pour une infection persistante. Peu à peu, il a pu recommencer à manger par son tube digestif, respirer sans machine, et suivre une rééducation. Son état s’est amélioré, mais il reste encore hospitalisé pour continuer ses soins.",
+            "B3": "Résumé détaillé et structuré pour un public non médical éduqué\n\nContexte  \nUn homme de 54 ans souffrant d’une maladie cardiaque complexe, notamment un syndrome de Wolff-Parkinson-White ayant provoqué un arrêt cardiaque dans sa jeunesse, a développé une insuffisance cardiaque sévère due à une cardiomyopathie non ischémique (une maladie du muscle cardiaque non liée à une obstruction des artères). Sa fonction cardiaque était très réduite (fraction d’éjection à 15 %, indiquant une capacité de pompage très faible). Après plusieurs hospitalisations pour insuffisance cardiaque, il a reçu un dispositif d’assistance ventriculaire gauche (LVAD), un appareil mécanique qui aide le cœur à pomper le sang.\n\nPrincipales observations  \nPeu après l’implantation du LVAD, une complication grave est survenue : des selles s’écoulaient au niveau du site où la ligne de commande (câble externe contrôlant le LVAD) sortait du corps. Une première intervention chirurgicale limitée a révélé une blessure de l’intestin causée par cette ligne, qui a été réparée sans retirer la ligne. Cependant, trois jours plus tard, la fuite de selles a réapparu, accompagnée d’une infection sévère (septicémie). Une exploration chirurgicale plus approfondie a montré que la réparation initiale avait cédé, que la ligne de commande traversait la cavité abdominale en blessant le côlon transverse (partie du gros intestin), et qu’il y avait de nombreux abcès (poches de pus) dans l’abdomen.\n\nInterprétation clinique  \nFace à cette infection grave, les chirurgiens ont retiré la partie endommagée du côlon (résection) et ont laissé l’abdomen ouvert temporairement, avec un pansement spécial, en attendant une seconde intervention. Lors de cette deuxième opération, ils ont repositionné la ligne de commande du LVAD hors de la cavité abdominale, dans un espace situé derrière la paroi abdominale (extra-péritonéal), afin d’éviter de nouvelles blessures intestinales. Une colostomie (dérivation temporaire des selles vers une ouverture sur la peau) a été réalisée pour permettre à l’intestin de guérir. Le patient a ensuite bien récupéré, reprenant progressivement une alimentation par son tube digestif.\n\nProchaines étapes  \nMalgré une évolution favorable, le patient a présenté un abcès intra-abdominal nécessitant un drainage guidé par imagerie et un traitement antibiotique prolongé contre des bactéries résistantes, dont des entérocoques résistants à la vancomycine (VRE). À ce stade, il reste hospitalisé, ne dépend plus de la ventilation mécanique, tolère une alimentation entérale et suit une rééducation physique. Ce cas illustre la complexité des complications infectieuses liées aux dispositifs cardiaques implantés et l’importance d’une prise en charge chirurgicale adaptée pour préserver la fonction intestinale et la survie du patient."
+        }
+    },
+    {
+        "article": "Adolescent de 14 ans, auparavant en bonne santé, qui a consulté au Service des urgences primaires d'Osorno pour une toux irritative prédominante nocturne de 11 jours d'évolution. Traitement symptomatique indiqué, avec une évolution vers une dyspnée et une orthopnée. Il s'est rendu au Service des urgences de l'Hôpital de base d'Osorno (HBO), où il a été observé une insuffisance respiratoire sévère, une intolérance à la position couchée et une douleur abdominale. Il a été admis à l'unité de soins intensifs pédiatriques (UCIP), tachycardique, hypertendu, polypneique, saturant 96 % avec FiO2 35 %, rosé, hydraté et bien perfusé, avec des jugulaires plates, des adénopathies supraclaviculaires bilatérales de petite taille. Le thorax sans rétraction des parties molles, maintenu en position genou-poignet, avait un murmure pulmonaire diminué dans les deux bases, et l'auscultation cardiaque avait des sons étouffés, sans souffle. L'abdomen peu dépressible et sensible dans les deux hypocondres, des viscères de taille douteuse et des extrémités sans lésions. La radiographie thoracique a montré une masse médiastinale supérieure et une atélétose du lobe moyen droit associée à un épanchement pleural ipsilatéral. Aucune TDM avec contraste n'a été réalisée pour contre-indication anesthésique, comme indiqué dans le résumé du transfert de l'HBO. Il a été transféré en urgence à l'unité de soins intensifs pédiatriques (UCIP HBV), souffrant d'un syndrome de compression médiastinale, avec suspicion clinique de lymphome non hodgkinien. Il a été évalué par les équipes d'hémato-oncologie infantile, de chirurgie infantile, de soins intensifs pédiatriques, d'imagerie, de radiothérapie et, en raison du risque vital immédiat associé au diagnostic, il a été décidé d'offrir un traitement cytoréducteur, avec 6 mg/m2 de dexaméthasone et 100 mg/m2 de cyclophosphamide par jour pendant 5 jours, en plus d'une prophylaxie du syndrome de lyse tumorale (allopurinol 10 mg/kg/jour toutes les 8 heures), d'une surhydratation (3 000 ml/m2) et d'un traitement de l'insuffisance respiratoire. Physiopathologiquement, les masses médiastiniques rivalisent pour un espace avec des structures d'importance vitale. La pression intrathoracique négative, qui est la somme des forces anatomiques (y compris le tonus de la musculature intercostale) et physiologiques (respiration), tire effectivement la tumeur vers l'avant. La gravité exerce une force opposée, tirant la tumeur vers l'arrière sur des structures vulnérables, comme l'arbre trachéo-bronchique et le cœur droit (oreillette droite et artère pulmonaire). L'anesthésie, le bloc neuromusculaire et la ventilation à pression positive, pourraient exercer des effets profonds sur cet équilibre, tout comme l'effet net des pressions sur la tumeur, lorsque le patient adopte différentes positions. Ce qui permet de prévoir les changements d'effet d'anesthésie et de développer des stratégies pour prévenir et inverser l'effondrement cardiorespiratoire. Le patient a évolué vers un syndrome de lyse tumorale 24 heures après son admission, associé à une insuffisance rénale, avec une uricémie (14,6 mg/dl), LDH (2 177 U/L), un profil lipidique normal (cholestérol total, dans la plage normale élevée, HDL cholestérol dans la limite normale inférieure, triglycérides 159 mg/dl), fibrinogène 498 mg/dl et dimère D 1,61 ug/ml, phosphémie 8,8 mg/dL et créatinémie 0,82 mg/dL. Il a reçu de la rasburicase pour traiter le syndrome de lyse tumorale (0,2 mg/kg/jour), en suspendant l'allopurinol et en continuant la citoréduction avec dexaméthasone à la moitié de la dose initiale (3 mg/m2 par jour), sans cyclophosphamide.\n\nUne évaluation néphrologique a été réalisée, confirmant une insuffisance rénale secondaire à un syndrome de lyse tumorale, sans urgence diététique et tendance à l'hypertension, avec une créatininémie de 1,54 mg/dL, une phosphémie de 11 mg/dL, sans hypernatrémie. Elle a continué avec une hyperhydratation, un diurétique (furosémide) et un antihypertensif (amlodipine). Du point de vue respiratoire, elle a présenté une demande d'oxygène, avec une FIO2 de 35 % par masque de Venturi, l'apport étant suspendu le troisième jour de l'admission. Elle a évolué avec des épisodes d'agitation psychomotrice, associés au diagnostic en cours, qui ont été traités conformément au protocole institutionnel d'agitation psychomotrice, avec un soutien psychologique et psychiatrique, avec une évolution satisfaisante. Au troisième jour de l'admission et du traitement, une TDM thoracique, abdominale et pelvienne a été réalisée avec contraste, avec une augmentation de la taille du thymus, d'aspect homogène, probablement dans le contexte d'un processus lymphoprolifératif et de résultats suggérant une thrombose pulmonaire droite, avec une thrombose de la veine jugulaire gauche, un épanchement pleural bilatéral étendu associé à des atelectases dans les deux bases, avec des signes de néphropathie médicale bilatérale. Une anticoagulation a été indiquée avec de l'enoxaparine (1 mg/kg de dose, toutes les 12 heures) pendant vingt jours. Puis une TDM thoracique de contrôle a montré la résolution de la thrombose.Au quatrième jour de l'admission et du traitement, une étude diagnostique et d'extension a été réalisée, qui comprenait, entre autres, un profil biochimique complet, y compris un profil lipidique, une hyperplasie granulopoïétique de la moelle osseuse (myélogramme), une cytométrie de flux (moelle osseuse) dans laquelle aucune cellule prédominante clonale ou immunophénotype néoplasique n'a été observée, une cytométrie de flux dans le sang périphérique négatif pour les cellules néoplasiques, un cytologique de liquide pleural négatif pour les cellules néoplasiques, une cytométrie de flux de liquide pleural sans preuve de néoplasie hématologique. Elle a été présentée au comité oncologique pédiatrique, soulignant qu'il n'a pas été possible de prélever une biopsie de la tumeur étant donné que la masse médiastinale a disparu avec le traitement cytoréducteur, en assumant le diagnostic de lymphome lymphoblastique en raison du tableau clinique et de la réponse au traitement, selon le protocole PINDA 0516. Ce protocole prévoit une induction IA de huit doses de Lasp E. coli de 10 000 UI/m2. Après avoir reçu sept doses de L-asp et une dose cumulative de quatre-vingt-dix-mille unités internationales plus glucocorticoïdes (prednisone), elle a présenté un tableau de déclin, des vomissements, des douleurs abdominales et une déshydratation légère. Une suspicion de pancréatite a été suspectée, qui a été écartée par des valeurs normales d'amylase/lipase et des tests hépatiques normaux. À ce moment, elle avait un électrolyte plasmatique avec une hyponatrémie de 126 mOsm/kg, une hypertriglycéridémie de 1 115 mg/dL et un cholestérol total de 435 mg/dL). En raison de la persistance de l'hyponatrémie malgré un traitement de remplacement adéquat, elle a été évaluée par la néphrologie infantile, soulignant l'absence de modifications neurologiques, la normotension, les résultats d'osmolalité plasmatique 272 mOsm/kg et d'osmolalité urinaire 510 mOsm/kg, les deux valeurs normales. Avec l'hyponatrémie et l'hypertriglycéridémie, une suspicion de RAM de pseudo-hyponatrémie secondaire à une hypertriglycéridémie associée à L-asp a été évoquée. Elle a été évaluée par gastroentérologie et endocrinologie, indiquant un régime faible en sucres raffinés et riche en fibres, des fibrates (ciprofibrate 100 mg par voie orale par jour) et des oméga 3 (4 g par voie orale par jour), jusqu'à atteindre des valeurs de triglycérides de 300 mg/dL. Deux semaines plus tard, les triglycérides avaient une valeur de 79 mg/dL. Le ciprofibrate et les oméga 3 ont été suspendus, indiquant une utilisation prophylactique associée à un traitement corticoïde et L-asp. Elle a terminé douze doses de L-asp avec une dose cumulative de cent quatre-vingt-quatre mille unités internationales correspondant au protocole d'induction. La suspicion de RAM a été soumise à une évaluation de la causalité, avec l'algorithme de Karch et Lasagna modifié par l'OMS5, qui a abouti à une RAM « définitive » pour la combinaison L-asp et Prednisone\n",
+        "gold_summary": "Le tableau clinique d'un adolescent qui a présenté une pseudo-hyponatrémie et une hypertriglycéridémie au cours du traitement par lymphome non hodgkinien lymphoblastique (LNH) a été décrit. Une suspicion de réaction indésirable aux médicaments (RAM) a été évaluée selon l'algorithme de causalité modifié (Karch et Lasagna), ce qui a conduit à une RAM « définitive » pour l'association L-asp et corticoïdes. Il a été traité avec un régime hypogras et des médicaments modifiant les lipides. L-asp et prednisone n'ont pas été suspendus en raison de la fin de l'indication, conformément au protocole. L'hypertriglycéridémie a été récupérée sans complications après 14 jours de traitement.\n",
+        "synthetic_summary": {
+            "B1": "Un garçon malade a eu un problème avec son sang à cause des médicaments. Son sang avait trop de gras et pas assez de sel. Les docteurs ont donné une nourriture spéciale et des médicaments pour aider. Ils ont continué les médicaments importants pour sa maladie. Après deux semaines, il allait mieux et son sang est redevenu normal.",
+            "B2": "**Ce qu’ils ont observé chez l’adolescent**  \nUn garçon de 14 ans, traité pour un type de cancer appelé lymphome non hodgkinien lymphoblastique, a présenté deux problèmes pendant son traitement : une fausse baisse du sodium dans le sang (appelée pseudo-hyponatrémie) et un taux très élevé de graisses dans le sang (hypertriglycéridémie). Ces problèmes sont liés aux médicaments qu’il recevait, notamment la L-asparaginase (L-asp) et les corticoïdes (comme la prednisone).\n\n**Ce que cela signifie**  \nLes médecins ont utilisé une méthode spéciale pour vérifier si ces effets étaient bien causés par les médicaments. Cette méthode, appelée algorithme de Karch et Lasagna, a confirmé que la réaction était bien due à la combinaison de L-asp et de corticoïdes. Pour traiter l’hypertriglycéridémie, ils ont donné au patient un régime pauvre en graisses et des médicaments qui aident à réduire les lipides dans le sang.\n\n**Le suivi et l’évolution**  \nLes médecins n’ont pas arrêté les médicaments contre le cancer car le traitement devait être terminé selon le protocole prévu. Après 14 jours de soin, le taux de graisses dans le sang est revenu à la normale sans complications. Ainsi, même si ces effets secondaires étaient sérieux, ils ont pu être bien contrôlés tout en continuant le traitement contre le cancer.",
+            "B3": "Résumé détaillé et structuré pour un public non spécialiste\n\n**Contexte**  \nUn adolescent de 14 ans, auparavant en bonne santé, a été hospitalisé pour une toux persistante évoluant vers une insuffisance respiratoire sévère, associée à une masse médiastinale (zone située au centre du thorax) détectée à la radiographie. Cette masse comprimait des structures vitales, ce qui a conduit à la suspicion d’un lymphome non hodgkinien lymphoblastique, un type de cancer du système lymphatique fréquent chez l’enfant et l’adolescent. En raison du risque vital immédiat, un traitement cytoréducteur (destiné à réduire rapidement la taille de la tumeur) a été initié, comprenant des corticostéroïdes (dexaméthasone) et de la cyclophosphamide, ainsi qu’une prophylaxie contre le syndrome de lyse tumorale (complication liée à la destruction rapide des cellules cancéreuses).\n\n**Principales observations**  \nAu cours du traitement, le patient a développé un syndrome de lyse tumorale avec une insuffisance rénale, nécessitant une adaptation thérapeutique (administration de rasburicase, ajustement des médicaments et hydratation). Par la suite, une thrombose (formation de caillots sanguins) a été diagnostiquée au niveau pulmonaire et veineux jugulaire, traitée par anticoagulants. Les examens complémentaires n’ont pas permis de prélever une biopsie de la masse, qui a disparu sous traitement, ce qui a confirmé le diagnostic probable de lymphome lymphoblastique sur la base du tableau clinique et de la réponse au traitement.\n\nDurant la phase d’induction du protocole de chimiothérapie (traitement initial intensif), le patient a présenté un déclin général avec vomissements et douleurs abdominales. Une pancréatite a été suspectée mais exclue. Par ailleurs, une hyponatrémie (faible taux de sodium dans le sang) persistante et une hypertriglycéridémie (taux élevé de triglycérides, un type de lipides sanguins) très marquée ont été observées. L’évaluation néphrologique a montré que cette hyponatrémie n’était pas liée à un dysfonctionnement rénal ou neurologique.\n\n**Interprétation clinique**  \nL’association d’une hyponatrémie et d’une hypertriglycéridémie a conduit à suspecter une pseudo-hyponatrémie, un phénomène où le taux de sodium semble bas à cause d’une concentration élevée de lipides dans le sang, sans réelle carence en sodium. Cette situation a été attribuée à une réaction indésirable aux médicaments, en particulier à la combinaison de L-asparaginase (L-asp, un agent chimiothérapeutique utilisé dans le traitement du lymphome) et des corticostéroïdes (prednisone). Cette hypothèse a été confirmée par une évaluation rigoureuse de la causalité selon l’algorithme modifié de Karch et Lasagna, qui a classé cette réaction comme « définitive ».\n\n**Prise en charge et évolution**  \nLe patient a reçu un régime alimentaire pauvre en sucres raffinés et riche en fibres, ainsi que des médicaments hypolipémiants (ciprofibrate et oméga-3) pour réduire les triglycérides. Le traitement anticancéreux n’a pas été interrompu, conformément au protocole, car la chimiothérapie était proche de son terme. Après environ deux semaines, les taux de triglycérides sont revenus à des valeurs normales sans complications associées. Les médicaments hypolipémiants ont alors été arrêtés.\n\n**Prochaines étapes**  \nLe patient a terminé le protocole d’induction avec un bon contrôle de la maladie et sans récidive des troubles métaboliques. Cette observation souligne l’importance de surveiller les effets secondaires métaboliques rares mais significatifs liés à la chimiothérapie, notamment l’hypertriglycéridémie induite par L-asparaginase et corticostéroïdes, afin d’adapter la prise en charge nutritionnelle et médicamenteuse sans interrompre le traitement anticancéreux essentiel."
+        }
+    },
+    {
+        "article": "Femme de 34 ans. Antécédent de tumeur bénigne de la glande salivaire sous-maxillaire droite et de multiples fibroadénomes mammaires. Fumeuse modérée. Elle a consulté pour diplopie soudaine, altération de la coordination du membre supérieur droit, bradylalie et anomies isolées. À l'admission, l'examen neurologique a révélé une amélioration avec un examen normal. La tension artérielle et la glycémie étaient normales. Une IRM du cerveau a été réalisée, qui a révélé une image restrictive en séquence de diffusion au niveau de l'hippocampe gauche. L'admission à l'unité de soins cérébraux a été décidée pour la surveillance, les tests de dépistage et le traitement. Les résultats des analyses générales de laboratoire, de la vitesse de sédimentation des érythrocytes, de la protéine C réactive, de la sous-unité bêta de l'hCG, du VIH, du VDRL, du collagénogramme et de l'analyse toxicologique des urines étaient normaux. Les thrombophilies acquises et génétiques étaient négatives. L'angiotomographie des vaisseaux intra- et extra-crâniens, d'origine embryonnaire fœtale de l'artère cérébrale postérieure gauche, sans autre résultat important, a été réalisée. La télémétrie de 72 heures n'a pas révélé d'arythmie cardiaque. Considérant un éventuel embolus paradoxal, une échographie Doppler veineuse des quatre membres sans thrombose, une échographie transcrânienne Doppler avec contraste, avec passage spontané de bulles « rideau » dans les deux artères sylviennes et un échocardiogramme transthoracique avec contraste (ETT-c) a été réalisée, qui a indiqué un court-circuit droite-gauche avec passage modéré spontané avant le deuxième battement cardiaque. Il a été interprété comme un AVC associé à une FOP probable et un traitement a été initié avec double antiagrégation et statines. Au cours de la procédure préalable à la fermeture de la FOP, une échographie intracardiaque a été réalisée, sans preuve de communication interauriculaire ou de court-circuit intracardiaque droite-gauche. Il a été décidé de compléter l'évaluation avec une angiographie pulmonaire intra- et extra-crânienne, qui a révélé une MAV dans le segment postérieur du lobe pulmonaire inférieur droit. L'angiographie pulmonaire numérique a confirmé une MAV à haut débit. Une angiographie pulmonaire a été réalisée, avec occlusion complète du vaisseau par un dispositif endovasculaire, préservant les artères normales. Au cours du suivi, une évaluation clinique, gynécologique, oncologique et rhumatologique a été réalisée sans résultats pertinents. La patiente ne remplissait aucun des critères de Curaçao pour la télangiectasie hémorragique héréditaire (syndrome de Rendu-Osler-Weber), c'est-à-dire épistaxis récurrente, télangiectasies cutanées/muqueuses et atteinte viscérale multiple, ni n'avait d'antécédent de maladie chez un parent au premier degré. Il a également été décidé de procéder à un examen génétique avec un panel de télangiectasie hémorragique héréditaire (gènes : ACVRL1, ENG, EPHB4, GDF2, RASA1 et SMAD4), avec résultat négatif. La découverte a été interprétée comme une MAVP sporadique. La patiente est actuellement stable sur le plan clinique et neurologique. Le consentement éclairé de la patiente a été obtenu, autorisant la publication, la reproduction et la diffusion du cas clinique.\n",
+        "gold_summary": "Nous présentons le cas d’une femme de 34 ans ayant un AVC ischémique talamique gauche. Un passage de bulles « en rideau » dans les artères cérébrales a été détecté par Doppler transcrânien. L’échographie intracardiaque n’a pas révélé de foramen ovale perméable, ce qui a conduit à la réalisation d’une angiotomographie pulmonaire, qui a confirmé la présence d’une MAVP. La patiente a bénéficié d’un traitement endovasculaire réussi.\n",
+        "synthetic_summary": {
+            "B1": "Une dame de 34 ans a eu un problème dans son cerveau. Ce problème a fait que son corps ne bougeait pas bien. Les docteurs ont cherché d’où venait ce problème. Ils ont trouvé un petit trou dans ses poumons. Ce trou laissait passer des choses qui ne devraient pas passer. Les docteurs ont réparé ce trou avec un petit appareil. Maintenant, elle va mieux et son corps fonctionne bien.",
+            "B2": "Cas d’une femme de 34 ans avec un AVC au niveau du thalamus gauche (une partie du cerveau). Lors d’un examen spécial appelé Doppler transcrânien, les médecins ont vu des bulles passer dans les artères du cerveau, ce qui peut indiquer un passage anormal du sang. Une autre échographie du cœur n’a pas montré de trou habituel appelé foramen ovale perméable, souvent responsable de ce type de problème. Pour comprendre la cause, une angiographie des poumons a été faite et a révélé une malformation artério-veineuse pulmonaire (MAVP), c’est-à-dire un lien anormal entre une artère et une veine dans le poumon. Cette malformation a été traitée avec succès grâce à une procédure endovasculaire, qui consiste à bloquer la malformation depuis l’intérieur des vaisseaux sanguins. Aujourd’hui, la patiente va bien et son état neurologique est stable.",
+            "B3": "### Contexte  \nUne femme de 34 ans, avec des antécédents de tumeur bénigne de la glande salivaire sous-maxillaire droite et de multiples fibroadénomes mammaires, a consulté en raison d’une diplopie soudaine (vision double), d’une altération de la coordination du bras droit, d’une bradylalie (ralentissement de la parole) et d’anomalies isolées du langage. À son admission, son examen neurologique était redevenu normal. Les examens initiaux, incluant la tension artérielle, la glycémie et les analyses sanguines inflammatoires, étaient normaux. Une IRM cérébrale a montré une lésion restrictive au niveau de l’hippocampe gauche, suggérant un accident vasculaire cérébral (AVC) ischémique.\n\n### Principales Observations  \nLes investigations approfondies n’ont pas révélé de cause évidente : pas d’infection, pas de thrombophilie (trouble de la coagulation), ni d’arythmie cardiaque. Une échographie Doppler transcrânienne avec injection de bulles a mis en évidence un passage anormal de bulles d’air dans les artères cérébrales, ce qui suggère un court-circuit droite-gauche (passage de sang veineux vers la circulation artérielle sans passer par les poumons). Cependant, l’échographie intracardiaque n’a pas montré de foramen ovale perméable (FOP), une malformation cardiaque souvent responsable de ce type de court-circuit.\n\nFace à cette contradiction, une angiographie pulmonaire a été réalisée, révélant une malformation artério-veineuse pulmonaire (MAVP) dans le lobe inférieur droit. Cette malformation est une connexion anormale entre une artère et une veine pulmonaire qui permet au sang de contourner les capillaires pulmonaires, favorisant ainsi un passage direct de bulles ou d’emboles vers la circulation cérébrale.\n\n### Interprétation Clinique  \nLe diagnostic retenu est celui d’un AVC ischémique cérébral causé par un embolisme paradoxal secondaire à une MAVP sporadique, c’est-à-dire une malformation pulmonaire non liée à une maladie héréditaire. En effet, la patiente ne présentait pas les signes cliniques ni les antécédents familiaux du syndrome de Rendu-Osler-Weber (télangiectasie hémorragique héréditaire), et le test génétique spécifique était négatif.\n\n### Prochaines Étapes et Traitement  \nLa MAVP a été traitée avec succès par une procédure endovasculaire consistant à occlure la malformation à l’aide d’un dispositif inséré par voie vasculaire, ce qui a permis de préserver les artères pulmonaires normales. La patiente est actuellement stable sur le plan neurologique et clinique. Un suivi multidisciplinaire (neurologique, gynécologique, oncologique et rhumatologique) n’a pas révélé d’autres anomalies.\n\n### Conclusion  \nCe cas illustre l’importance d’une investigation approfondie devant un AVC ischémique chez un adulte jeune, notamment en recherchant des causes rares comme une malformation artério-veineuse pulmonaire, qui peut être responsable d’un passage paradoxal d’emboles vers le cerveau en l’absence de malformation cardiaque détectable. Le traitement endovasculaire est une option efficace pour prévenir la récidive."
+        }
+    }
+]
\ No newline at end of file
diff --git a/generating_data/tik_ache/pt_syntheticV1.json b/generating_data/tik_ache/pt_syntheticV1.json
new file mode 100644
index 0000000000000000000000000000000000000000..4798b57a7c7d32f44fb87d83a6e3b30257f57567
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@@ -0,0 +1,902 @@
+[
+    {
+        "article": "Um homem de 56 anos com histórico de hipertensão diagnosticada aos 46 anos de idade foi bem tratado com telmisartan 40 mg e amlodipina 5 mg. O paciente ocasionalmente consumia álcool e não fumava.\n\nUm TTE de 2011 revelou uma leve AR direcionada para a AML, com uma veia contracta de 2,5 mm, largura do jato de 6,5 mm e diâmetro do trato de saída do ventrículo esquerdo (LVOT) de 29 mm. O diâmetro da aorta ascendente foi de 38 mm. Uma leve regurgitação mitral também foi observada, sem evidência de perfuração ou vegetação.\n\nSeis meses antes da admissão, a paciente apresentou dor no oitavo dente superior esquerdo e sangramento recorrente enquanto escovava. Durante 3 meses antes da admissão, a paciente teve febres intermitentes acima de 40°C sem falta de ar. Sem melhora, a paciente apresentou-se ao nosso hospital em abril de 2016, foi internada no mesmo dia para avaliação e tratamento adicionais, e foi diagnosticada com febre de origem desconhecida (FUO).\n\nNa admissão, a altura, o peso e o índice de massa corporal do paciente foram de 179 cm, 79,2 kg e 24,7 kg/m², respetivamente. Ele estava consciente e tinha uma temperatura de 37,2 °C, pressão arterial de 124/77 mmHg, frequência cardíaca de 90 b.p.m. e saturação de oxigénio de 95% (ar ambiente). A auscultação revelou sons respiratórios claros e um murmúrio sistólico no quarto limite esternal esquerdo, sem murmúrio diastólico. Não havia erupções cutâneas, edema, linfadenopatia patológica ou achados neurológicos ou fundoscópicos anormais.\n\nUm eletrocardiograma de 12 derivações mostrou ritmo sinusal normal com uma frequência cardíaca de 82 b.p.m. e eixo normal. A radiografia de tórax revelou uma relação cardiotorácica de 51% sem congestão pulmonar ou derrame pleural. A tomografia computadorizada de contraste do tórax à pélvis não revelou anormalidades, fontes de infecção, lesões neoplásicas ou fontes embólicas. A cintilografia de gálio realizada para investigar a FUO não revelou qualquer acumulação anormal.\n\nEmbora lesões neoplásicas, doença do colágeno e doenças infecciosas tenham sido consideradas como possíveis causas de febre, esses resultados excluíram doenças neoplásicas e do colágeno. As culturas de sangue dos Dias 1 a 4 de hospitalização (dois conjuntos de cada) foram positivas para S. oralis. A consulta com o departamento de cirurgia dentária e oral revelou cáries no oitavo dente superior esquerdo, que requereu tratamento e foi diagnosticado como uma possível fonte de bacteriemia.\n\nEstes achados sugeriram IE, levando a uma consulta de cardiologia. O TTE revelou o seguinte: fração de ejeção ventricular esquerda (LV) de 62%, diâmetro diastólico/diâmetro sistólico do LV de 58/42 mm, diâmetro da aorta ascendente de 38 mm, regurgitação mitral leve, regurgitação tricúspide trivial (TR), e gradiente de pressão da TR de 20 mmHg. O AR, consistente com os achados de 2011, tinha deslocado-se posteriormente, colidindo com o AML. A avaliação semi-quantitativa mostrou um diâmetro do LVOT de 29 mm, veia contraída de 4,2 mm, e largura do jato de 6,5 mm, indicando AR leve a moderada. Uma vegetação de 7,7 mm foi detectada no local de impacto do AR no AML, causando perfuração e refluxo.\n\nUm TEE no Dia 5 de hospitalização confirmou achados semelhantes aos achados do TTE, mostrando a AR migrante a incidir sobre a LMA com vegetação e perfuração. O TEE também revelou flexão parcial da cúspide aórtica direita (RCC) e prolapso, mas sem vegetação da válvula aórtica (AV). Com base nos critérios de Duke, foi feito um diagnóstico definitivo de IE. Não foram encontradas anormalidades nos exames do fundo do olho ou dermatológicos.\n\nO tratamento incluiu 8 g/dia de AMPC (2 g q6) e 160 mg/dia de GM (80 mg q12). O paciente apresentou deferevescência, não teve problemas hemodinâmicos e estava em uma condição estável sem insuficiência cardíaca ou sintomas neurológicos.\n\nNo entanto, no Dia 7, uma ressonância magnética da cabeça revelou múltiplos sinais baixos nos hemisférios cerebelares bilaterais, pons, gânglios basais bilaterais, tálamo esquerdo e lobo frontal esquerdo na imagem ponderada em susceptibilidade, que se pensou ser devido a hemorragia pós-infarto causada por embolia relacionada com IE.\n\nDevido a uma disfunção valvar significativa, o tratamento antibiótico foi continuado e a cirurgia foi planeada para o Dia 19. Aproximadamente 7 mm de vegetação foi removida da AML no local do jato AR, seguida por reparação da válvula mitral (A2 ressecção da vegetação, patch pericárdico autólogo, Physio II, 32 mm) e anuloplastia tricúspide (TAP) (procedimento de De Vega). Foi observado um dobramento parcial do RCC sem vegetação AV. Para abordar o AR residual e prevenir a IE recorrente, a valvuloplastia aórtica e a substituição da aorta ascendente (anuloplastia CV-9 22 mm, triplos 24 mm) foram realizadas simultaneamente. O paciente não teve complicações pós-operatórias aparentes. O AMPC e o GM foram administrados durante 42 e 17 dias, respetivamente. O paciente foi dispensado sem quaisquer achados anormais.\n\nO TTE aos 6 meses pós-operatórios não mostrou nenhuma recorrência de IE e nenhuma disfunção da válvula mitral. O paciente permaneceu estável por 3 anos e 10 meses pós-operatórios.\n",
+        "gold_summary": "Em 2011, um homem de 56 anos apresentou-se com AR leve em direção à LMA, revelado num ecocardiograma transtorácico. Em 2016, 3 meses antes da admissão, o paciente tinha estado a experienciar febres intermitentes de mais de 40°C, que não melhoraram, e foi encaminhado para o nosso hospital. Um exame detalhado revelou uma vegetação na LMA onde a válvula aórtica estava deslocada, e o local estava perfurado. A AR era leve a moderada. As culturas de sangue foram positivas para Streptococcus oralis. A partir destes resultados, foi feito um diagnóstico definitivo de endocardite infeciosa (EI). O paciente teve um enfarte cerebral e foi submetido a uma cirurgia semi-emergência.\n",
+        "synthetic_summary": {
+            "B1": "Um homem estava com uma válvula do coração um pouco machucada. Ele teve febre alta por muitos dias. Os médicos acharam um bicho pequeno na válvula do coração dele. Esse bicho fez um furinho na válvula. O homem estava com um tipo de sujeira no sangue que veio da boca. Os médicos disseram que ele estava com uma infecção no coração. Ele também teve um problema no cérebro por causa disso. Então, ele fez uma cirurgia para arrumar o coração. Depois, ele ficou melhor.",
+            "B2": "**O que aconteceu com o paciente**\n\nUm homem de 56 anos já tinha um problema no coração chamado regurgitação aórtica (AR), que é quando a válvula do coração não fecha direito e o sangue volta para trás. Em 2011, esse problema era leve. Mas, em 2016, ele começou a ter febres muito altas, acima de 40°C, por três meses seguidos, sem melhorar.\n\n**O que os médicos descobriram**\n\nQuando ele veio ao hospital, os exames mostraram que a válvula do coração estava com uma vegetação, que é um tipo de “bichinho” ou acúmulo de bactérias e células que se formam na válvula. Essa vegetação estava causando uma perfuração, ou seja, um buraco na válvula mitral, que é outra parte do coração. A regurgitação aórtica tinha piorado para um nível leve a moderado. As culturas de sangue mostraram que ele estava com uma infecção causada por uma bactéria chamada Streptococcus oralis, que normalmente vive na boca.\n\n**O que isso significa**\n\nCom esses resultados, os médicos diagnosticaram o paciente com endocardite infecciosa, que é uma infecção grave nas válvulas do coração. Durante o tratamento, ele sofreu um pequeno derrame no cérebro, causado por pedaços da vegetação que se soltaram e bloquearam vasos sanguíneos.\n\n**Como foi o tratamento**\n\nO paciente passou por uma cirurgia urgente para remover a vegetação, consertar a válvula mitral e tratar a válvula aórtica e a aorta. Depois da cirurgia, ele recebeu antibióticos por várias semanas e se recuperou bem, sem novos problemas no coração até quase quatro anos depois.\n\n**Resumo final**\n\nEsse caso mostra como uma infecção na boca pode causar um problema sério no coração, especialmente se já houver uma válvula com defeito. É importante tratar infecções rapidamente para evitar complicações graves como a endocardite infecciosa.",
+            "B3": "**Contexto**  \nEm 2011, um homem de 56 anos foi diagnosticado com insuficiência aórtica (IA) leve direcionada para a válvula mitral anterior (LMA), identificada por ecocardiograma transtorácico (TTE). Ele tinha histórico de hipertensão controlada e não apresentava sintomas cardíacos significativos naquele momento.\n\n**Principais Achados Clínicos e Diagnósticos em 2016**  \nTrês meses antes da internação em 2016, o paciente passou a apresentar febres intermitentes superiores a 40°C, sem melhora com o tempo. Durante a avaliação hospitalar, foi detectada uma vegetação (uma massa infecciosa) na válvula mitral anterior, no local onde o jato da insuficiência aórtica atingia a válvula, causando perfuração e agravando o refluxo de sangue. A insuficiência aórtica, que inicialmente era leve, progrediu para um grau leve a moderado. Culturas sanguíneas repetidas confirmaram a presença da bactéria *Streptococcus oralis*, um microrganismo comum na boca, sugerindo que a origem da infecção poderia estar relacionada a uma cárie dentária previamente identificada.\n\n**Interpretação Clínica**  \nCom base nos critérios clínicos e laboratoriais (critérios de Duke), foi estabelecido o diagnóstico definitivo de endocardite infecciosa (EI), uma infecção grave das válvulas cardíacas. Durante a internação, o paciente sofreu um acidente vascular cerebral isquêmico com hemorragia secundária, provavelmente causado por embolias (fragmentos da vegetação que se desprenderam e viajaram para o cérebro).\n\n**Tratamento e Desfecho**  \nO paciente recebeu tratamento antibiótico intensivo com ampicilina e gentamicina, apresentando melhora clínica inicial. Devido à disfunção valvar significativa e risco de complicações, foi submetido a uma cirurgia semi-emergencial no 19º dia de internação. Durante o procedimento, a vegetação foi removida, a válvula mitral foi reparada, e foram realizadas intervenções na válvula aórtica e na aorta ascendente para corrigir a insuficiência e prevenir recidivas da infecção. O pós-operatório foi satisfatório, sem complicações aparentes. Após alta, o paciente manteve-se estável, sem sinais de recorrência da endocardite, durante quase quatro anos de acompanhamento.\n\n**Próximos Passos e Considerações**  \nEste caso destaca a importância da investigação detalhada em pacientes com febre persistente e histórico de valvulopatias, especialmente quando há sinais de infecção bacteriana. A associação entre infecções odontológicas e endocardite reforça a necessidade de cuidados dentários adequados para prevenção. O manejo multidisciplinar, envolvendo cardiologia, infectologia e cirurgia cardíaca, foi fundamental para o sucesso do tratamento e a recuperação do paciente."
+        }
+    },
+    {
+        "article": "Menino de 11 anos com cefaleia occipital e frontal bilateral associada a vômitos de 12 horas de evolução após queda banal na região sacro-coccígea. Antecedente de SM devido a mutação tipo missense em heterozigose no gene FBN1 c.2243G>A.\n\nA exploração neurológica e por aparelhos foi normal, salvo no que se refere ao hábito marfanoide. Realizou-se uma analítica geral e uma radiografia sacrocoxígea, ambas sem alterações. A cefaleia melhorou, chegando a desaparecer em decúbito, mas reaparecia ao incorporar-se e não tolerava a bipedestação, pelo que foi internado.\n\nDurante a internação, apresentou pouca resposta à analgesia. Foi realizada tomografia computadorizada (TAC) craniana que mostrou aumento de densidade dos seios transversais em provável relação com fluxo lento venoso. Ante a suspeita de SHI em relação com possível fístula de LCR, foi solicitada ressonância magnética (RM) crânio-medular. A RM mostrou leve descenso amigdalar (5 mm) e descolamento da dura-máter com coleções líquidas por fora da mesma a nível dorsal e lombo-sacro, compatível com fístula de LCR; além disso, foram visualizados cistos perineurais de Tarlov em localização sacra. Esta imagem não era compatível com ectasia dural, e o paciente não dispunha de neuroimagem prévia.\n\nFoi instituído tratamento com hiperhidratação, analgésicos menores (dexketoprofeno e metamizol), hidrocortisona intravenosa dose inicial 8 mg/kg/dia, cafeína via oral 2,5 mg/kg/dia, junto com repouso em cama na posição de Trendelemburg. Aos cinco dias o paciente iniciou mobilização progressiva, apresentando uma evolução favorável, com melhora da cefaleia e tolerando a bipedestação. Pôde ser dado de alta do hospital aos 12 dias.\n\nApós quatro meses assintomáticos, a clínica reapareceu coincidindo com o início da atividade esportiva na escola. A ressonância magnética de controle mostrou desaparecimento da coleção dorsal com persistência de coleções sacrais. Recebeu novamente a mesma pauta de tratamento conservador que no ingresso prévio.\n\nA ressonância magnética de controle após um ano mostrou resolução das coleções subdurais ou extradurais no canal raquídeo e identificou-se como novo achado uma fina imagem de hidromielia dorsal média. Dois anos após a primeira admissão, o paciente voltou a consultar por cefaleia ortostática, e foi realizada uma ressonância magnética constatando-se refistulização com origem a nível de L5-S1. Ante a recidiva, foi decidido tratamento com patch hemático epidural (PHE) lombar (L4-L5) por parte do serviço de Anestesiologia. Um ano após a sua realização, e três anos desde o início da clínica, o paciente permanece assintomático.\n",
+        "gold_summary": "Apresentamos o caso de um menino de 11 anos com cefaleia ortostática e vômitos de 12 horas de evolução após uma queda sobre região sacrocoxígena; antecedente de síndrome de Marfan. A ressonância craniomedular mostrou coleções líquidas extradurais a nível dorsal e lombo-sacral compatíveis com fístula de LCR. O quadro se resolveu após tratamento, mas houve dois novos episódios durante o seguimento, pelo que se aplicou um parche hemático epidural aos dois anos do início.\n",
+        "synthetic_summary": {
+            "B1": "Um menino de 11 anos caiu e ficou com dor de cabeça e vontade de vomitar. Ele tem uma doença que deixa os ossos e o corpo diferentes. Os médicos fizeram exames e viram que tinha um pouco de água no lugar errado perto da coluna dele. Isso fez a dor de cabeça aparecer. Ele tomou remédios e ficou de repouso, e melhorou. Depois, a dor voltou duas vezes. Então, os médicos fizeram um tratamento especial para ajudar. Agora, ele está bem e sem dor.",
+            "B2": "**O que aconteceu com o menino**\n\nUm menino de 11 anos, que tem uma condição chamada síndrome de Marfan (que afeta o corpo de várias formas), começou a sentir uma dor de cabeça que piorava quando ele ficava em pé. Ele também vomitou várias vezes durante 12 horas, depois de cair sentado na parte de baixo das costas.\n\n**O que os médicos encontraram**\n\nOs médicos fizeram exames de imagem, como a ressonância magnética, que mostraram que havia um vazamento de líquido ao redor da medula espinhal. Esse líquido, chamado líquor, normalmente fica protegido dentro do cérebro e da medula, mas nesse caso estava escapando por um buraco (fístula). Esse vazamento causava a dor de cabeça e os outros sintomas.\n\n**Como foi o tratamento**\n\nO menino recebeu tratamento com remédios para dor, descanso na cama em uma posição especial e outros cuidados para ajudar o corpo a se recuperar. Ele melhorou e teve alta do hospital. Porém, depois de alguns meses, os sintomas voltaram quando ele começou a fazer atividades físicas na escola. Os médicos repetiram o tratamento e, depois de um ano, ele estava bem, mas apareceu um novo problema chamado hidromielia, que é um acúmulo de líquido na medula.\n\nDois anos depois do primeiro problema, a dor de cabeça voltou de novo por causa do vazamento. Então, os médicos fizeram um procedimento chamado \"parche hemático epidural\". Nesse procedimento, eles colocam um pouco do próprio sangue do paciente perto da medula para fechar o vazamento. Depois disso, o menino ficou sem sintomas por pelo menos um ano.\n\n**O que isso significa**\n\nEsse caso mostra que, em pacientes com síndrome de Marfan, podem ocorrer vazamentos de líquor que causam dor de cabeça e outros sintomas. O tratamento pode ser difícil e exigir vários cuidados, incluindo procedimentos para fechar o vazamento. Com o tratamento certo, é possível melhorar e controlar os sintomas.",
+            "B3": "**Contexto**  \nEste relato descreve o caso de um menino de 11 anos que apresentou dor de cabeça intensa, localizada na parte de trás e na frente da cabeça, acompanhada de vômitos, com duração de 12 horas. Os sintomas surgiram após uma queda leve na região inferior das costas (sacro-coccígea). O paciente tem diagnóstico prévio de síndrome de Marfan, uma condição genética causada por uma mutação no gene FBN1, que afeta o tecido conjuntivo e pode levar a alterações no sistema esquelético, cardiovascular e outros órgãos.\n\n**Principais Achados**  \nDurante a avaliação inicial, o exame neurológico e geral não revelou alterações significativas, exceto pelo fenótipo marfanoide (características físicas típicas da síndrome de Marfan). Exames laboratoriais e radiografia da região sacrocoxígea foram normais. A dor de cabeça melhorava ao deitar, mas reaparecia ao ficar em pé, causando intolerância à posição ereta, o que levou à internação hospitalar.\n\nUma tomografia computadorizada do crânio evidenciou aumento da densidade dos seios venosos transversos, sugerindo fluxo sanguíneo lento. A ressonância magnética (RM) do crânio e da medula espinhal revelou um leve deslocamento para baixo das amígdalas cerebelares (parte do cérebro) e descolamento da dura-máter (membrana que envolve o cérebro e a medula), com acúmulo de líquido fora dessa membrana na região dorsal e lombar da coluna, indicando a presença de uma fístula de líquido cefalorraquidiano (LCR) — uma comunicação anormal que permite o vazamento desse líquido. Também foram identificados cistos perineurais de Tarlov na região sacral, que são pequenas bolsas cheias de líquido ao redor dos nervos espinhais. Não havia sinais de dilatação anormal da dura-máter (ectasia dural), e não existiam imagens anteriores para comparação.\n\n**Interpretação Clínica**  \nO diagnóstico principal foi de fístula de LCR, causando uma perda do líquido que envolve o sistema nervoso central, resultando em cefaleia ortostática (que piora ao ficar em pé) e vômitos. O tratamento inicial incluiu hidratação abundante, analgésicos leves, corticosteroide intravenoso, cafeína oral e repouso na posição de Trendelemburg (com a cabeça mais baixa que o corpo), visando reduzir o vazamento e aliviar os sintomas. Após cinco dias, o paciente começou a se movimentar gradualmente, com melhora progressiva da dor e tolerância à posição em pé, recebendo alta após 12 dias.\n\nDurante o acompanhamento, o paciente ficou assintomático por quatro meses, mas os sintomas retornaram com o início das atividades esportivas escolares. A ressonância de controle mostrou desaparecimento do acúmulo líquido dorsal, mas persistência das coleções na região sacral. O tratamento conservador foi reiniciado com sucesso.\n\nUm ano depois, a RM demonstrou resolução das coleções líquidas na coluna, mas revelou uma fina área de hidromielia (acúmulo anormal de líquido dentro da medula espinhal) na região dorsal média. Dois anos após o primeiro episódio, o paciente apresentou nova crise de cefaleia ortostática. A ressonância indicou recidiva da fístula, agora localizada entre as vértebras lombar 5 e sacral 1 (L5-S1). Diante da recidiva, foi realizado um procedimento chamado patch hemático epidural (injeção de sangue do próprio paciente no espaço epidural da coluna para selar a fístula), realizado pelo serviço de Anestesiologia.\n\n**Próximos Passos e Prognóstico**  \nUm ano após o procedimento com patch hemático epidural, e três anos desde o início dos sintomas, o paciente permanece sem sintomas, indicando sucesso do tratamento. Este caso ilustra a importância do diagnóstico precoce e manejo adequado da fístula de LCR em pacientes com síndrome de Marfan, que podem apresentar complicações relacionadas ao tecido conjuntivo, como vazamentos de líquido cefalorraquidiano. O acompanhamento contínuo é fundamental para detectar recidivas e garantir a qualidade de vida do paciente."
+        }
+    },
+    {
+        "article": "Um homem de 54 anos com histórico de síndrome de Wolff-Parkinson-White, que resultou em parada cardíaca quando tinha 20 anos, desenvolveu posteriormente cardiomiopatia não isquêmica (classe IV da New York Heart Association com fração de ejeção de 15%). Ele foi internado por insuficiência cardíaca e teve um curso complicado na unidade de cuidados cardíacos com remoção de AICD/Pacemaker devido a endocardite e anticoagulação com Coumadin para trombo atrial direito/fibrilhação atrial. Ele foi dispensado, mas precisou de múltiplas readmissões por insuficiência cardíaca, que acabou por requerer oxigenoterapia extracorpórea venosa-arterial através da artéria femoral direita e da veia femoral esquerda como eCPR em janeiro de 2020 e permaneceu em ECMO durante 5 semanas. Ele foi submetido a colocação de LVAD usando cânula no ventrículo esquerdo e na aorta ascendente 16 dias após a cânula ECMO e subsequente traqueostomia em fevereiro para insuficiência respiratória persistente.\n\nDois dias antes da remoção das cânulas ECMO, o paciente foi submetido a uma amputação guilhotina da extremidade inferior direita devido a gangrena seca, resultante de uma dissecção ilíaca e embolização distal. Cinco dias depois, no dia 25 pós-LVAD, observou-se vazamento de fezes no local de saída da linha de condução. A equipa de Cirurgia Cardiotorácica levou o paciente para a sala de operações e fez uma exploração limitada, encontrando uma lesão intestinal da linha de condução. A lesão foi reparada com sutura de seda interrompida e a linha de condução foi deixada intacta. Três dias depois desta reparação, a equipa de Cirurgia de Cuidados Agudos foi consultada devido a um novo vazamento de fezes no local de saída da linha de condução. O paciente foi encontrado em estado de sepsis profunda. Foi-lhe administrado antibióticos e foi levado para a sala de operações para uma laparotomia exploratória formal e foi encontrado a linha de condução LVAD a atravessar a cavidade abdominal do quadrante superior direito para o flanco médio esquerdo. A linha de condução tinha ferido o cólon transverso distal e a reparação anterior estava vazando. Havia um fluido fecal copioso e numerosos abscessos intra-abdominais que foram drenados. Devido à sepsia do paciente, o cólon foi grampeado proximal e distal ao segmento ferido e a amostra foi removida. O paciente foi deixado em discontinuidade e um curativo abdominal temporário foi colocado para uma segunda cirurgia de observação. Ele voltou para a UTI onde lhe foram administrados antibióticos, ventilação mecânica e vasopressores.\n\nTrês dias depois, durante a segunda cirurgia de revisão, o abdômen pareceu limpo. Devido à necessidade do LVAD, a linha de condução não pôde ser desconectada. A primeira prioridade foi a de mobilizar a linha de condução para fora do peritônio. O lado esquerdo do abdômen do paciente foi aberto de forma transversal para permitir que a linha de condução chegasse ao meio. O peritônio foi retirado do lado direito do abdômen do paciente para desenvolver um plano retrorreto numa tentativa de reposicionar a linha de condução para a localização extraperitoneal pretendida. Foi feita uma incisão transversal menor no lado direito para levar a linha de condução para este plano retrorreto, longe da linha média. Assim, a linha de condução foi removida com sucesso do peritônio sem desconexão. Foi realizada uma hemicolectomia direita, mas devido à linha de condução sair perto do quadrante inferior direito, foi feita uma ileostomia no quadrante inferior esquerdo. A sua fáscia foi fechada e foram colocadas suturas de retenção devido ao fraco estado nutricional do paciente e ao grau de sepse abdominal. O paciente foi bem após a operação e foi capaz de retomar a nutrição enteral no dia 3 pós-operatório, satisfazendo as suas necessidades calóricas no dia 7 pós-operatório. Ele foi submetido a uma revisão da sua amputação de guilhotina 15 dias após a sua última operação abdominal.\n\nO curso do paciente foi complicado por um abscesso intra-abdominal que exigiu intervenção radiológica de drenagem 3 semanas após sua última cirurgia abdominal, bem como tratamento prolongado com antibióticos IV para organismos resistentes, incluindo VRE. O paciente completou seu curso de antibióticos e teve seus drenos removidos. No momento deste relatório, o paciente permanece hospitalizado, tolerando nutrição enteral, sem ventilação mecânica e submetido a fisioterapia.",
+        "gold_summary": "Um homem de 54 anos com histórico de síndrome de Wolff-Parkinson-White, que resultou em múltiplas readmissões por insuficiência cardíaca, acabou por requerer a colocação de um dispositivo de assistência ventricular esquerda (LVAD). Várias semanas depois, foi encontrado um vazamento de fezes no local da linha de condução. O paciente foi levado para a sala de operações para uma exploração limitada pela equipa de Cirurgia Cardiotorácica e foi identificado e reparado um dano intestinal. Três dias após esta reparação, as fezes voltaram a vazar do local da linha de condução, o que obrigou a uma nova exploração pela equipa de Cirurgia de Cuidados Agudos. Durante a operação, verificou-se que a reparação anterior estava a vazar e foram descobertos múltiplos abcessos intra-abdominais. O cólon transverso foi ressecado e deixado em descontinuidade. Numa segunda operação planeada, a linha de condução do LVAD foi recolocada para ser extra-peritoneal e foi formada uma colostomia.\n",
+        "synthetic_summary": {
+            "B1": "Um homem ficou muito doente do coração. Ele precisou de uma máquina para ajudar o coração a bombear o sangue. Depois, ele teve um problema no intestino. Saiu cocô por um lugar que não devia. Os médicos fizeram uma cirurgia para arrumar. Mas o problema voltou. Eles fizeram outra cirurgia e tiraram uma parte do intestino que estava machucada. Também fizeram um novo caminho para o cocô sair do corpo. Agora ele está melhor e os médicos continuam cuidando dele com muito carinho.",
+            "B2": "**O que aconteceu com o paciente**\n\nUm homem de 54 anos tinha um problema no coração chamado síndrome de Wolff-Parkinson-White, que já tinha causado várias vezes insuficiência cardíaca — isso é quando o coração não consegue bombear sangue direito. Por isso, ele precisou colocar um aparelho chamado LVAD, que ajuda o coração a funcionar melhor.\n\n**Problemas após a cirurgia**\n\nAlgumas semanas depois da cirurgia, apareceu um vazamento de fezes (fezes são o cocô) perto do local onde passa um fio do aparelho LVAD. Isso indicava que havia um buraco no intestino. Os médicos fizeram uma cirurgia rápida e consertaram esse buraco.\n\nMas, três dias depois, o problema voltou: as fezes começaram a vazar de novo. O paciente estava muito doente, com uma infecção grave chamada sepse. Então, os médicos fizeram uma cirurgia maior para investigar melhor. Eles descobriram que o conserto anterior tinha falhado e que havia vários abscessos, que são acúmulos de pus, dentro da barriga.\n\n**O que os médicos fizeram para ajudar**\n\nPara controlar a infecção, os médicos precisaram retirar uma parte do intestino grosso chamada cólon transverso. Como o aparelho LVAD precisava continuar funcionando, eles não puderam tirar o fio que atravessava a barriga. Então, numa segunda cirurgia, eles mudaram o caminho desse fio para que ele ficasse fora da cavidade abdominal, diminuindo o risco de novos problemas.\n\nTambém fizeram uma colostomia, que é quando o intestino é ligado a uma abertura feita na barriga para o cocô sair por ali, evitando que passe pelo local machucado.\n\n**Como está o paciente agora**\n\nDepois dessas cirurgias, o paciente recebeu antibióticos para combater a infecção e passou por fisioterapia para se recuperar. Ele já consegue se alimentar pelo estômago e não precisa mais de ventilação mecânica (máquina para ajudar a respirar). Ainda está no hospital, mas está melhorando.",
+            "B3": "**Contexto**  \nUm homem de 54 anos com histórico de síndrome de Wolff-Parkinson-White, que causou uma parada cardíaca aos 20 anos, desenvolveu cardiomiopatia não isquêmica grave, com insuficiência cardíaca avançada (classe IV da New York Heart Association) e fração de ejeção do ventrículo esquerdo muito reduzida (15%). Após múltiplas internações por insuficiência cardíaca, ele necessitou de suporte circulatório avançado, incluindo oxigenoterapia extracorpórea venosa-arterial (ECMO) por cinco semanas e, posteriormente, a implantação de um dispositivo de assistência ventricular esquerda (LVAD) para ajudar o coração a bombear sangue. Durante o tratamento, o paciente sofreu complicações graves, como gangrena na perna direita que levou à amputação, e infecções associadas ao dispositivo.\n\n**Principais Achados**  \nCerca de 25 dias após a colocação do LVAD, foi identificado um vazamento de fezes no local onde a linha de condução do dispositivo atravessa a pele, indicando uma comunicação anormal entre o intestino e a superfície do corpo. Uma primeira cirurgia limitada realizada pela equipe de Cirurgia Cardiotorácica encontrou uma lesão intestinal na linha de condução, que foi reparada. No entanto, três dias depois, o vazamento retornou, acompanhado de sepse profunda (infecção generalizada grave). Uma segunda cirurgia exploratória realizada pela equipe de Cirurgia de Cuidados Agudos revelou que a sutura anterior estava falhando, com presença de grande quantidade de fezes e múltiplos abscessos (acúmulos de pus) dentro da cavidade abdominal. A linha de condução do LVAD estava perfurando o cólon transverso distal, causando a contaminação abdominal. Devido à gravidade da infecção, o segmento afetado do cólon foi removido e o abdômen foi deixado aberto temporariamente para controle da infecção.\n\nNa cirurgia de revisão realizada três dias depois, o abdômen estava limpo, mas a linha de condução do LVAD não podia ser desconectada. Para evitar nova contaminação, a equipe reposicionou a linha para fora da cavidade abdominal, criando um espaço extraperitoneal (fora da membrana que reveste o abdômen). Foi realizada uma hemicolectomia direita (remoção da parte direita do cólon) e, devido à localização da linha de condução, foi criada uma ileostomia (desvio do intestino delgado para a parede abdominal) para permitir a saída das fezes. O fechamento da parede abdominal foi reforçado com suturas especiais, considerando o estado debilitado e a infecção do paciente.\n\n**Interpretação Clínica**  \nEste caso ilustra uma complicação rara, porém grave, associada ao uso de dispositivos de assistência ventricular esquerda: a perfuração intestinal causada pela linha de condução do LVAD. A presença de uma comunicação entre o intestino e a pele levou a infecção abdominal grave e sepse, exigindo múltiplas cirurgias complexas para controlar a infecção, remover o segmento intestinal comprometido e reposicionar o dispositivo para evitar novos danos. O manejo multidisciplinar, envolvendo cirurgia cardíaca, cirurgia geral e cuidados intensivos, foi fundamental para a estabilização do paciente.\n\n**Próximos Passos e Prognóstico**  \nApós a última cirurgia, o paciente apresentou melhora clínica, retomando a alimentação por via enteral e sendo capaz de realizar fisioterapia. No entanto, o curso clínico continuou complicado por um abscesso intra-abdominal que necessitou drenagem guiada por imagem e tratamento prolongado com antibióticos, inclusive para bactérias resistentes. Atualmente, o paciente permanece hospitalizado, sem necessidade de ventilação mecânica, e em processo de recuperação funcional. O acompanhamento contínuo é essencial para monitorar possíveis complicações adicionais e otimizar a reabilitação."
+        }
+    },
+    {
+        "article": "Adolescente de 14 anos, previamente saudável, que consultou no Serviço de Atenção Primária de Urgência (SAPU) de Osorno, por tosse irritativa de predomínio noturno de 11 dias de evolução. Foi indicado tratamento sintomático, evoluindo com dispneia e ortopneia. Foi ao Serviço de Urgência do Hospital Base Osorno (HBO), observando-se dificuldade respiratória severa, intolerância ao decúbito e dor abdominal. Ingressou na UTI pediátrica (UCIP), taquicárdico, hipertenso, polineurotico, saturando 96% com FiO2 35%; rosado, hidratado e bem perfundido, euglicemia, adenopatia supraclavicular bilateral pequena. O tórax sem retração de partes moles, manteve posição genupectoral, tinha murmúrio pulmonar diminuído em ambas as bases, e a auscultação cardíaca tinha tons apagados, sem sopro. O abdômen mole pouco depressível e sensível em ambos os hipocondríos, duvidosas visceromegalias e extremidades sem lesões. A radiografia de tórax mostrou uma massa mediastinal superior e atelectasia do lóbulo médio direito associado a derrame pleural ipsilateral. Não se realizou TC de tórax com contraste por contraindicação anestésica, segundo se consignou em resumo de traslado desde HBO. Transladou-se grave a UTI pediátrica HBV, cursando com Síndrome de Compressão Mediastinal, com suspeita clínica de Linfoma não Hodgkin. Foi avaliado pelas equipes de Hemato-Oncologia infantil, Cirurgia infantil, Cuidados Intensivos pediátricos, Imagenologia, Radioterapia e perante o risco vital imediato associado ao diagnóstico, decidiu-se oferecer tratamento citoreductor, com dexametasona 6 mg/m2/dia e ciclofosfamida 100 mg/m2/dia por 5 dias, além de profilaxia de síndrome de lise tumoral (Alopurinol 10 mg/kg/dia a cada 8 horas), sobrehidratação (3.000 ml/m2) e tratamento da insuficiência respiratória. Fisiopatologicamente as massas mediastinais competem por um espaço com estruturas de significado vital. A pressão intratorácica negativa, que é a soma de forças anatômicas (incluindo o tônus da musculatura intercostal) e fisiológica (respiração), efetivamente traciona o tumor para frente. A gravidade torna-se uma força oposta, tracionando o tumor para trás sobre estruturas vulneráveis, como o árvore traqueobrônquico e o coração direito (átrio direito e artéria pulmonar). A anestesia, bloqueio neuromuscular e ventilação a pressão positiva, poderiam exercer efeitos profundos neste equilíbrio tanto como o efeito líquido das pressões sobre o tumor, quando o paciente assume diferentes posições. O anterior permite predizer as mudanças efeito de anestesia e desenvolver estratégias para prevenir e reverter o colapso cardiorrespiratório5.O paciente evoluiu com síndrome de lise tumoral às 24 horas desde o ingresso, associada a falha renal, com uricemia (14,6 mg/dl), LDH (2.177 U/L), perfil lipídico normal (colesterol total, em faixa normal alta, colesterol HDL em limite normal inferior, triglicérides 159 mg/dl), fibrinógeno 498 mg/dl e dímero D 1,61 ug/ml, fosfemia 8,8 mg/dL e creatinemia 0,82 mg/dL. Recebeu rasburicasa para tratar a síndrome de lise tumoral (0,2 mg/kg/d) suspendendo o alopurinol e continuando com a citorreducção com dexametasona a metade da dose inicial (3 mg/m2 ao dia), sem ciclofosfamida.\n\nAvaliação nefrológica foi realizada, confirmando falência renal secundária a síndrome de lise tumoral, sem urgência dialítica e tendência a hipertensão, com creatinina 1,54 mg/dL, fosfemia 11 mg/dL, sem hipernatremia. Continuou com hiperhidratação, diurético (furosemida) e anti-hipertensivo (amlodipina).Do ponto de vista respiratório, apresentou necessidade de oxigênio, com FIO2 35% por máscara de Venturi, suspendendo-se esta oferta no terceiro dia de admissão. Evolucionou com episódios de agitação psicomotora, associados ao diagnóstico em processo, que foi tratado de acordo com o protocolo institucional de agitação psicomotora, com apoio psicológico e psiquiátrico, com evolução satisfatória. No terceiro dia de admissão e tratamento foi realizado TC de tórax, abdômen e pelve com contraste, observando-se um aumento do tamanho do timo, de aspecto homogêneo, provavelmente no contexto de processo linfoproliferativo e achados sugestivos de tromboembolismo pulmonar basal direito. O angioTC de tórax mostrou trombose da veia jugular esquerda, extenso derrame pleural bilateral associado a fenômenos atelectásicos em ambas as bases, com sinais de nefropatia médica bilateral. Foi indicada anticoagulação com enoxaparina (1 mg/kg dose, cada 12 horas) por vinte dias. Então o angioTC de controle mostrou resolução da trombose.Ao quarto dia de admissão e tratamento, foi realizado estudo diagnóstico e de extensão, que contemplou, entre outros, perfil bioquímico completo incluindo perfil lipídico, hiperplasia granulopoiética da medula óssea (mielograma), citometria de fluxo (medula óssea) na qual não se observaram células com predomínio clonal ou imunofenótipo neoplásico de estirpe hematológica, citometria de fluxo em sangue periférico negativo para células neoplásicas, citológico de líquido pleural negativo para células neoplásicas, citometria de fluxo de líquido pleural sem evidência de neoplasia hematológica. Apresentou-se ao comitê oncológico pediátrico, destacando que não foi possível tomar biopsia do tumor dado que a massa mediastinal desapareceu com o tratamento citoreductor, assumindo-se o diagnóstico de Linfoma Linfoblástico pelo quadro clínico e a resposta ao tratamento, segundo protocolo PINDA 0516. Este protocolo contempla em Indução IA oito doses de Lasp E. coli de 10.000 UI/m2. Tendo recebido sete doses de L-asp e com uma dose cumulativa de noventa mil unidades internacionais mais glucocorticoide (prednisona), apresentou quadro de decaimento, vômitos, dor abdominal e desidratação leve. Suspeitou-se de pancreatite, que foi descartada por valores de amilase/lipase, normais e testes hepáticos normais. Naquele momento, tinha eletrolito plasma com hiponatremia de 126 meq/l, hipertrigliceridemia de 1.115 mg/dL e colesterol total de 435 mg/dL). Ante a persistência de hiponatremia apesar do tratamento de reposição adequado, foi avaliado por Nefrologia infantil, destacando ausência de alterações neurológicas, normotensão, resultados de osmolaridade plasmática 272 mOsm/kg e osmolaridade urinária 510 mOsm/kg, ambos valores normais. Com hiponatremia e hipertrigliceridemia, levantou-se a suspeita de RAM de pseudohiponatremia secundária a hipertrigliceridemia associada a L-asp. Foi avaliado por Gastroenterologia e Endocrinologia, indicando-se dieta baixa em açúcares refinados e rica em fibra, fibratos (ciprofibrato 100 mg oral ao dia) e ômega 3 (4 g oral ao dia), até alcançar valores de triglicérides de 300 mg/dL. Duas semanas depois os triglicérides tiveram um valor de 79 mg/dL. Ciprofibrato e ômega3 foram suspensos, indicando uso profilático associado a tratamento com corticoides e L-asp. Completaram-se doze doses de L-asp com uma dose acumulada de cento e oitenta e quatro mil unidades internacionais correspondente ao protocolo de indução.A suspeita de RAM foi submetida a avaliação de causalidade, com o algoritmo de Karch e Lasagna modificado pela OMS5, que resultou em RAM “Definitiva” para a associação L-asp e Prednisona\n",
+        "gold_summary": "Descreve-se o quadro clínico de um adolescente que, durante o tratamento para Linfoma Não Hodgkin Linfoblástico (LNH), apresentou pseudohiponatremia e hipertrigliceridemia, suspeitando-se de uma reação adversa a medicamentos (RAM). Esta suspeita de RAM foi avaliada de acordo com o algoritmo de causalidade modificado (Karch e Lasagna), resultando em RAM \"definitiva\" para a associação L-asp e corticoides. Recebeu tratamento com regime hipograso e medicamentos modificadores de lípidos. Não se suspenderam L-asp nem prednisona por termo da indicação, de acordo com o protocolo. A hipertrigliceridemia recuperou-se sem complicações após 14 dias de tratamento.\n",
+        "synthetic_summary": {
+            "B1": "Um menino estava doente e tomou remédios para ajudar. Esses remédios fizeram o sangue dele ficar diferente, com umas gordurinhas altas. Os médicos disseram que isso aconteceu por causa dos remédios. Eles deram um jeitinho com comida e outros remédios para ajudar. O menino continuou tomando os remédios para ficar melhor da doença. Depois de um tempo, as gordurinhas no sangue voltaram ao normal e ele ficou bem.",
+            "B2": "**O que aconteceu com o adolescente durante o tratamento**\n\nUm garoto de 14 anos estava sendo tratado para um tipo de câncer chamado Linfoma Não Hodgkin Linfoblástico, que afeta as células do sistema imunológico. Durante o tratamento, ele recebeu dois medicamentos importantes: L-asp (uma enzima usada para combater o câncer) e corticoides (como a prednisona, que ajuda a controlar a inflamação).\n\n**Problemas que surgiram**\n\nDurante o tratamento, o adolescente apresentou dois problemas no sangue: pseudohiponatremia e hipertrigliceridemia. A pseudohiponatremia é uma situação em que parece que o nível de sódio (um mineral importante) está baixo, mas na verdade isso é causado por um excesso de gorduras no sangue, chamado hipertrigliceridemia. Essa alta quantidade de gordura no sangue pode confundir os exames e parecer que o sódio está baixo.\n\n**Por que isso aconteceu?**\n\nOs médicos acreditam que esses problemas foram causados por uma reação adversa aos medicamentos L-asp e corticoides. Para ter certeza, eles usaram um método especial chamado algoritmo de causalidade, que ajuda a entender se um remédio está realmente causando um efeito ruim. O resultado mostrou que essa reação foi \"definitiva\", ou seja, muito provável que os medicamentos tenham causado esses efeitos.\n\n**Como foi o tratamento desses problemas?**\n\nPara ajudar o garoto, os médicos indicaram uma dieta com pouca gordura e deram remédios que ajudam a controlar os níveis de gordura no sangue. Mesmo com esses problemas, ele continuou tomando os medicamentos do câncer, porque eram essenciais para o tratamento. Depois de cerca de duas semanas, os níveis de gordura no sangue voltaram ao normal, e ele não teve outras complicações.\n\n**O que isso significa?**\n\nEsse caso mostra que alguns medicamentos usados para tratar câncer podem causar efeitos colaterais que precisam ser monitorados e tratados com cuidado. É importante que os médicos saibam identificar esses problemas para garantir que o tratamento seja seguro e eficaz.",
+            "B3": "**Contexto**  \nUm adolescente de 14 anos, previamente saudável, foi diagnosticado com Linfoma Não Hodgkin Linfoblástico (LNH) após apresentar sintomas respiratórios graves e uma massa mediastinal no tórax. Durante a internação, recebeu tratamento citoreductor com dexametasona e ciclofosfamida, seguido pelo protocolo de indução quimioterápica que inclui L-asparaginase (L-asp) e prednisona. O quadro inicial foi complicado por síndrome de lise tumoral, insuficiência renal e trombose venosa, que foram manejados adequadamente.\n\n**Principais Achados Clínicos e Diagnósticos**  \nDurante o tratamento, o paciente desenvolveu hiponatremia (nível baixo de sódio no sangue) persistente, associada a níveis muito elevados de triglicerídeos (hipertrigliceridemia), com valores superiores a 1.000 mg/dL. Apesar da hiponatremia, a avaliação da osmolaridade plasmática e urinária indicou que não havia alterações típicas de desidratação ou disfunção renal que justificassem o quadro. A ausência de sintomas neurológicos e a normalidade dos exames hepáticos e pancreáticos descartaram outras causas comuns.\n\n**Interpretação Clínica**  \nFoi levantada a hipótese de pseudohiponatremia, uma condição em que a concentração aparente de sódio no sangue está falsamente baixa devido à interferência dos níveis muito altos de lipídios (triglicerídeos) no exame laboratorial. Esta alteração foi atribuída a uma reação adversa aos medicamentos L-asparaginase e prednisona, usados no tratamento do linfoma. A associação entre esses fármacos e a hipertrigliceridemia é reconhecida, mas nem sempre evidente.\n\nA causalidade da reação adversa foi avaliada utilizando o algoritmo de Karch e Lasagna modificado pela Organização Mundial da Saúde, que classificou a reação como “definitiva” para a combinação de L-asp e corticoides.\n\n**Tratamento e Evolução**  \nO manejo incluiu uma dieta pobre em açúcares refinados e rica em fibras, além do uso de medicamentos para reduzir os lipídios no sangue, como ciprofibrato e ômega 3. O tratamento foi mantido até que os níveis de triglicerídeos caíssem para valores seguros (abaixo de 300 mg/dL). Após cerca de duas semanas, os triglicerídeos normalizaram-se (79 mg/dL), e os medicamentos foram suspensos, mantendo-se apenas a terapia oncológica conforme o protocolo.\n\nImportante destacar que o tratamento com L-asparaginase e prednisona não foi interrompido, pois a reação adversa foi controlada sem comprometer a continuidade do protocolo quimioterápico.\n\n**Conclusão e Relevância**  \nEste caso ilustra a importância de reconhecer a pseudohiponatremia induzida por hipertrigliceridemia como uma reação adversa potencialmente grave, porém reversível, associada ao uso de L-asparaginase e corticoides em pacientes com linfoma linfoblástico. O diagnóstico correto evita intervenções desnecessárias e permite a continuidade segura do tratamento oncológico, com monitoramento cuidadoso e suporte nutricional e farmacológico adequado."
+        }
+    },
+    {
+        "article": "Mulher de 34 anos. Antecedente de tumor benigno na glândula salivar submaxilar direita e múltiplos fibroadenomas mamários. Fumante leve. Consultada por causa de diplopia súbita, alteração na coordenação do membro superior direito, bradilalia e anomalias isoladas. No momento da admissão, constatou-se melhora do quadro neurológico com exame normal. Pressão arterial e glicemia normais. Realizou-se uma ressonância magnética do cérebro que evidenciou imagem restritiva na sequência de difusão ao nível do tálamo esquerdo. Decidiu-se internar a paciente na unidade de cerebrovasculares para monitorização, estudos de pesquisa e tratamento. Laboratório geral, eritrosedimentação, proteína C reativa, subunidade beta de hCG, HIV, VDRL, colagenograma e análise toxicológica na urina dentro da normalidade. Trombofilias adquiridas e genéticas negativas. Angiotomografia de vasos intra e extracranianos, com origem embrionária fetal de artéria cerebral posterior esquerda, sem outros achados de relevância. Telemetria de 72 horas sem evidência de arritmias cardíacas. Considerando possível embolia paradoxal, realizou-se Doppler venoso de quatro membros sem trombose, Doppler transcraniano com contraste com passagem espontânea de bolhas ''em cortina'' em ambas as artérias silvianas e um ecocardiograma transtorácico com contraste (ETT-c) que informou curtocircuito de direita esquerda com passagem moderada espontânea antes do segundo batimento cardíaco. Interpretou-se como AVC associado a provável FOP e iniciou-se tratamento com dupla antiagregação e estatinas. Durante o procedimento prévio ao encerramento de FOP, realizou-se ecocardiograma intracardíaco sem evidência de comunicação interauricular nem curtocircuito direita-esquerda intracardíaco. Decidiu-se completar a avaliação com angioTC pulmonar evidenciando MAV em segmento posterior do lóbulo pulmonar inferior direito. Na angiografia digital pulmonar confirmou-se MAV de alto fluxo. Realizou-se cateterismo seletivo da aferencia arterial e ocluiu-se em forma completa com um dispositivo endovascular, preservando as artérias normais. No seguimento realizou-se avaliação clínica, ginecológica, oncológica e reumatológica sem achados relevantes. A paciente não cumpria com nenhum dos critérios diagnósticos de Curaçao para telangiectasia hemorrágica hereditária (síndrome Rendu-Osler-Weber), ou seja, epistaxis recorrente, telangiectasias cutâneas/ mucosas e múltipla afetação visceral, nem contava com antecedente de familiar de primeiro grau com a doença. Igualmente, decidiu-se realizar estudo genético com painel de telangiectasia hemorrágica hereditária (genes: ACVRL1, ENG, EPHB4, GDF2, RASA1 e SMAD4), com resultado negativo. Interpretou-se o achado como MAVP esporádica. Atualmente a paciente evolui clínica e neurologicamente estável. Obteve-se a assinatura do consentimento informado por parte da paciente, autorizando a publicação, reprodução e divulgação do caso clínico.\n",
+        "gold_summary": "Apresentamos o caso de uma mulher de 34 anos com AVC isquêmico talâmico esquerdo. Foi detectado passagem de bolhas \"em cortina\" em artérias cerebrais mediante Doppler transcraniano. Em ecografia intracardíaca não se encontrou forame oval patente, motivo pelo qual se avançou com realização de angiotomografia pulmonar, a qual confirmou a presença de MAVP. A paciente recebeu tratamento endovascular bem sucedido.\n",
+        "synthetic_summary": {
+            "B1": "Uma mulher de 34 anos ficou com o lado do corpo meio estranho. Os médicos fizeram exames e viram que o sangue não estava chegando bem em uma parte do cérebro dela. Eles acharam que o sangue podia estar passando por um caminho errado no coração, mas não acharam esse caminho. Então, olharam os pulmões dela e acharam um lugar onde o sangue passava errado. Os médicos consertaram esse lugar com um tratamento especial. Agora, ela está melhor e se sentindo bem.",
+            "B2": "**O que aconteceu com a paciente**\n\nUma mulher de 34 anos teve um AVC, que é um problema no cérebro causado pela falta de sangue em uma parte dele. No caso dela, a área afetada foi o tálamo esquerdo, uma região importante para controlar movimentos e sensações.\n\n**Como descobriram o problema**\n\nOs médicos fizeram um exame chamado Doppler transcraniano, que usa ondas para ver o fluxo de sangue no cérebro. Eles viram que algumas bolhas passavam pelas artérias de forma anormal, o que pode indicar que o sangue estava passando por um caminho errado. Depois, fizeram um exame mais detalhado do coração e não encontraram uma abertura chamada forame oval patente, que às vezes permite que o sangue pule direto do lado direito para o esquerdo do coração.\n\nComo não acharam essa abertura no coração, os médicos fizeram uma tomografia dos pulmões e descobriram uma malformação arteriovenosa pulmonar (MAVP). Isso é um tipo de conexão errada entre artérias e veias nos pulmões, que pode deixar o sangue passar sem ser filtrado direito.\n\n**Tratamento e resultado**\n\nA paciente passou por um procedimento chamado tratamento endovascular, que é feito por dentro dos vasos sanguíneos para fechar essa conexão errada. O tratamento foi um sucesso, e ela está se recuperando bem, sem novos problemas.\n\n**Resumo final**\n\nEm resumo, a mulher teve um AVC causado por uma passagem anormal de sangue nos pulmões, que foi corrigida com um procedimento especial. Agora, ela está estável e em acompanhamento médico.",
+            "B3": "**Contexto**  \nEste relato descreve o caso de uma mulher de 34 anos que apresentou um acidente vascular cerebral (AVC) isquêmico localizado no tálamo esquerdo, uma região profunda do cérebro responsável por diversas funções sensoriais e motoras. A paciente tinha antecedentes de tumores benignos na glândula salivar e múltiplos fibroadenomas mamários, além de ser fumante leve. Os sintomas iniciais incluíram visão dupla (diplopia), dificuldade na coordenação do braço direito e fala lenta (bradilalia), mas melhoraram rapidamente ao ser avaliada.\n\n**Principais Achados Diagnósticos**  \nDurante a investigação, exames laboratoriais e de imagem não revelaram causas comuns para o AVC, como infecções, doenças autoimunes, distúrbios de coagulação ou problemas cardíacos evidentes. A ressonância magnética cerebral mostrou uma área de restrição ao nível do tálamo esquerdo, compatível com o AVC.\n\nUm exame chamado Doppler transcraniano com contraste detectou passagem anormal de bolhas de ar (\"em cortina\") pelas artérias cerebrais, sugerindo a existência de uma comunicação anormal entre a circulação venosa e arterial, que poderia permitir a passagem de êmbolos (coágulos ou bolhas) para o cérebro. Inicialmente, suspeitou-se de um forame oval patente (FOP), uma abertura entre as câmaras superiores do coração que pode causar esse tipo de passagem, mas o ecocardiograma intracardíaco não confirmou essa comunicação.\n\nDiante disso, foi realizada uma angiotomografia pulmonar, que revelou a presença de uma malformação arteriovenosa pulmonar (MAVP), uma conexão anormal entre artérias e veias nos pulmões que permite a passagem direta de sangue sem a filtragem normal, podendo causar embolias cerebrais. A confirmação da MAVP foi feita por angiografia digital pulmonar, que mostrou uma malformação de alto fluxo.\n\n**Interpretação Clínica**  \nA MAVP foi considerada a causa provável do AVC isquêmico da paciente, por permitir a passagem de êmbolos da circulação venosa para a arterial, atingindo o cérebro. A ausência de sinais clínicos e genéticos para a telangiectasia hemorrágica hereditária (síndrome Rendu-Osler-Weber), uma doença que frequentemente causa MAVs múltiplas, indicou que a MAVP era esporádica (isolada).\n\n**Tratamento e Evolução**  \nA paciente foi submetida a um procedimento endovascular, no qual um dispositivo foi inserido para ocluir (fechar) a malformação pulmonar, preservando as artérias normais. O tratamento foi bem-sucedido, e a paciente evoluiu de forma estável, sem novos sintomas neurológicos. Avaliações adicionais, incluindo ginecológica, oncológica e reumatológica, não identificaram outras causas ou complicações.\n\n**Próximos Passos**  \nO caso reforça a importância de investigar causas menos comuns de AVC em pacientes jovens, especialmente quando exames cardíacos não evidenciam comunicações intracardíacas. O acompanhamento clínico contínuo e a monitorização para possíveis complicações são essenciais para garantir a estabilidade da paciente. O consentimento informado para a divulgação do caso foi obtido, contribuindo para o conhecimento médico sobre essa condição rara."
+        }
+    },
+    {
+        "article": "Paciente de 4 anos, sexo masculino, com histórico de impetigo nasal duas semanas antes de sua admissão (tratado com mupirocina tópica e cefadroxilo oral; dose, duração e adesão ao tratamento desconhecidos), sem outros antecedentes mórbidos, que apresentou hematúria macroscópica glomerular associada a edema de extremidades inferiores de 5 dias de evolução, agregando-se nas últimas doze horas antes da consulta cefaleia, náuseas e vômitos. Acudiu ao serviço de urgência (SU) em estado convulsivo, após 20 minutos de convulsão tónico-clónica generalizada.\n\nNa admissão no SU, o paciente estava afebril, com pressão arterial não avaliável, com comprometimento quantitativo da consciência associado a hipertonia generalizada e edema pretibial e bipalpebral. A intubação endotraqueal foi decidida e o fenobarbital (10 mg/kg) foi administrado para controlar o status convulsivo.\n\nA pressão arterial no momento do exame físico na unidade de cuidados intensivos (UCI) foi de 134/94 mmHg (PAM 110 mmHg) (p95 para o paciente 108/66 mmHg, p95+12 120/78 mmHg).\n\nOs parâmetros laboratoriais iniciais incluíam: urina completa com hematúria (> 100 eritrócitos por campo), proteinúria 3+ e leucocitúria 10-25 por campo, creatinina 0,3 mg/dL, anemia com hematócrito (HTO) 21%, hemoglobina (Hb) 7 g/dL, com volume corpuscular médio (VCM) e concentração de hemoglobina corpuscular média (CHCM) normais, leucocitose de 23.900 cel/mm3, trombocitose de 756.000/mm3, sem elevação de reagentes de fase aguda, hipocomplementemia com nível de complemento C3 em 25 mg/dL (valor normal, VN: 80-150 mg/dL) e C4 normal. O teste rápido de antígeno para Estreptococo beta-hemolítico grupo A (Streptococcus pyogenes) na faringe resultou positivo e a Antiestreptolisina O (ASO) foi (+). A tomografia computadorizada cerebral sem contraste não mostrou mudanças agudas. A ecografia renal concluiu nefromegalia bilateral com aumento da ecogenicidade cortical e diminuição da diferenciação corticomedular.\n\nO paciente foi diagnosticado com síndrome nefrítica por GNAPE complicada com emergência hipertensiva - status convulsivo.\n\nNas primeiras 24 horas de internação na UTI, o paciente necessitou de ventilação mecânica (VM) e terapia anticonvulsivante com fenobarbital. Ele evoluiu sem crises epiléticas, com EEG normal (no dia seguinte à admissão) e estudo do fluido cerebrospinal normal. A terapia antibiótica foi iniciada para erradicar o Streptococcus pyogenes com cefotaxima e uso de terapia diurética com furosemida.\n\nNo dia seguinte, evoluiu com deterioração da função renal apresentando elevação da creatinina para 0,99 mg/dL, HTA e proteinúria de 24 horas de 36,6 mg/m2/h, sem oligúria. Iniciou-se a terapia anti-hipertensiva com amlodipina e labetalol intravenoso, com bom controle inicial.\n\nDada a evolução favorável, o paciente foi extubado após 48 horas, sendo bem tolerado do ponto de vista ventilatório. No entanto, após 24 horas de extubação, o paciente apresentou um agravamento do estado de consciência, com abertura ocular e retirada de extremidade apenas com estímulo doloroso e pouca resposta verbal (Escala de Coma de Glasgow 8) e desenvolveu valores de pressão arterial > p95+12, apesar de estar recebendo terapia com labetalol em infusão contínua (até 3 mg/kg/h), amlodipina (10 mg/dia) e furosemida, sendo necessário novamente iniciar VM e infusão de nitroprussiato de sódio (até 3 mcg/kg/min), com o objetivo de conseguir redução gradual dos valores de pressão arterial (25% diário) para prevenir dano neurológico secundário. Dada a presença de sintomatologia neurológica aguda associada a HTA em um paciente com glomerulonefrite, suspeitou-se o diagnóstico de PRES, que foi confirmado mediante ressonância magnética (RM) de cérebro (dia 5), que mostrou aumento do sinal subcortical na região occipital bilateral e simétrica, sem restrição na difusão, sendo compatível com edema vasogênico (PRES). A avaliação oftalmológica foi normal e um novo EEG evidenciou ocasionais episódios de depressão de voltagem generalizada.\n\nO enalapril foi adicionado ao tratamento. Finalmente, após 10 dias de retirada lenta da medicação, a pressão arterial voltou ao normal. A ressonância magnética de controle (dia 12) revelou a regressão dos achados previamente descritos. A extubação foi realizada com sucesso após 5 dias.\n\nDurante a sua estadia na UTI, o nível de hemoglobina diminuiu para 5 g/dL, com volume corpuscular médio e concentração de hemoglobina corpuscular média normais, sem plaquetopenia, pelo que se suspeitou de anemia hemolítica dado teste de Coombs direta positiva e hemoglobinuria. Requeru transfusões de glóbulos vermelhos em duas oportunidades. Decidiu-se iniciar terapia esteroidal com metilprednisolona (1 mg/kg/d) por 72 horas. O coprocultivo foi negativo, assim como o antígeno urinário para Streptococcus pneumoniae. Realizou-se serologia para vírus Epstein-Barr e Parvovirus B19, perfil de Antígenos Nucleares Extracteis (ENA), anticorpos anti-citoplasma de neutrófilos (ANCA), anticorpos anti-DNA, anticorpos anti B2 glicoproteína 1, anticorpos anti cardiolipinas e anticoagulante lúpico, os quais resultaram negativos. Todos os cultivos foram negativos (hemocultivos, urocultivo, cultivo de aspirado endotraqueal e cultivo faríngeo). Sólo destacou ANA (anticorpos antinucleares) positivo 1/160.\n\nO paciente evoluiu com melhora da pressão arterial, aumento do nível de complemento e exame de urina sem proteinúria ou hematúria. O teste de Coombs direto permaneceu positivo no nono dia de internação.\n\nNo dia 31, o paciente recebeu alta, normotenso, sem anemia, com função renal preservada, sem proteinúria ou hematúria, com níveis de C3 normalizados e sem sintomas neurológicos. Ele recebeu alta com terapia medicamentosa com prednisona, amlodipina, enalapril e ácido fólico. O paciente não apresentou recorrência e permaneceu assintomático 6 meses após a alta.\n",
+        "gold_summary": "Paciente do sexo masculino de 4 anos de idade, com histórico de 5 dias de hematúria e edema, com cefaleia, náuseas e vômitos, apresentou estado convulsivo e crise hipertensiva. O laboratório mostrou hipocomplementemia C3 e títulos elevados de antiestreptolisina O, o que foi interpretado como GNAPE. Ele evoluiu com encefalopatia, então se suspeitou de PRES secundário a emergência hipertensiva, o que foi finalmente confirmado por ressonância magnética do cérebro. Ele também apresentou anemia hemolítica autoimune, com hemoglobina de até 5 g/dL. Seu tratamento foi baseado em terapia anti-hipertensiva, medidas de neuroproteção e tratamento com esteróides. Ele recebeu alta após 31 dias de hospitalização, assintomático 6 meses após a alta.\n",
+        "synthetic_summary": {
+            "B1": "Um menino de 4 anos ficou doente. Ele tinha sangue na urina e os pés e as pernas inchados. Também sentia dor de cabeça, enjoo e vomitava.\n\nUm dia, ele teve uma convulsão, que é quando o corpo se mexe sozinho e a pessoa perde a consciência. Ele foi levado ao hospital.\n\nOs médicos fizeram exames e viram que ele estava com um problema nos rins por causa de uma infecção. Isso fez a pressão dele ficar muito alta.\n\nEle também ficou com o cérebro machucado por causa da pressão alta. Os médicos fizeram um exame especial para ver isso.\n\nO menino ficou com o sangue muito fraco e precisou de remédios e cuidados para melhorar.\n\nDepois de um tempo no hospital, ele ficou melhor. Saiu do hospital sem dor e sem problemas. Ele continuou bem depois disso.",
+            "B2": "**O que aconteceu com o paciente**\n\nUm menino de 4 anos ficou com sangue na urina (hematúria) e inchaço nas pernas por 5 dias. Depois, ele começou a ter dor de cabeça, náuseas e vômitos. Ele teve uma convulsão e pressão alta muito alta, o que levou ele a ser levado ao hospital.\n\n**O que os exames mostraram**\n\nOs exames de sangue e urina indicaram que ele tinha uma doença chamada glomerulonefrite pós-infecção por estreptococo (GNAPE). Isso acontece quando uma infecção na garganta ou pele causa inflamação nos rins. O exame mostrou que ele tinha pouca quantidade de uma proteína chamada complemento C3, que ajuda a defender o corpo, e também anticorpos contra a bactéria estreptococo.\n\nAlém disso, ele desenvolveu um problema no cérebro chamado PRES (Síndrome de Encefalopatia Posterior Reversível). Essa condição ocorre quando a pressão alta afeta o cérebro, causando inchaço e sintomas neurológicos. A ressonância magnética do cérebro confirmou esse diagnóstico.\n\nEle também teve anemia hemolítica autoimune, que é quando o corpo começa a destruir suas próprias células vermelhas do sangue, deixando a hemoglobina muito baixa (5 g/dL, quando o normal é bem maior).\n\n**Como foi o tratamento**\n\nO tratamento incluiu remédios para controlar a pressão alta, medicamentos para proteger o cérebro e o uso de esteróides para ajudar a controlar a anemia e a inflamação. Ele precisou de transfusões de sangue para aumentar a hemoglobina.\n\n**O que aconteceu depois**\n\nDepois de 31 dias no hospital, o menino melhorou bastante. A pressão arterial voltou ao normal, a função dos rins se recuperou, e ele não tinha mais sangue na urina nem anemia. Seis meses depois da alta, ele continuava sem sintomas e em boa saúde.\n\n**Resumo final**\n\nEsse caso mostra como uma infecção simples pode causar problemas sérios nos rins e no cérebro, mas com tratamento adequado, a recuperação é possível. É importante controlar a pressão alta e acompanhar os sintomas para evitar complicações.",
+            "B3": "**Contexto**  \nUm menino de 4 anos, previamente saudável, apresentou hematúria visível (sangue na urina) e inchaço nas pernas por cinco dias, acompanhado de cefaleia, náuseas e vômitos nas últimas horas. Ele foi admitido em estado convulsivo e com pressão arterial muito elevada, configurando uma crise hipertensiva. O histórico recente incluía um quadro de impetigo nasal (infecção bacteriana da pele) tratado com antibióticos.\n\n**Principais Achados Clínicos e Laboratoriais**  \nNa avaliação inicial, o paciente apresentava sinais de comprometimento neurológico, edema nas pernas e pálpebras, além de pressão arterial elevada (134/94 mmHg, acima do esperado para sua idade). Exames de urina revelaram grande quantidade de sangue e proteína, indicando inflamação dos rins. Os exames sanguíneos mostraram anemia grave (hemoglobina de 7 g/dL inicialmente, caindo para 5 g/dL), leucocitose (aumento de glóbulos brancos), trombocitose (aumento de plaquetas) e níveis muito baixos do complemento C3, uma proteína do sistema imunológico. O teste para Streptococcus pyogenes (bactéria causadora de infecções de garganta e pele) foi positivo, assim como os anticorpos antiestreptolisina O, sugerindo uma infecção recente por esse microrganismo. A tomografia cerebral inicial não mostrou alterações, mas a ultrassonografia dos rins indicou aumento e alterações compatíveis com inflamação glomerular.\n\n**Diagnóstico e Evolução Clínica**  \nO diagnóstico principal foi glomerulonefrite pós-infecciosa por Streptococcus (GNAPE), uma inflamação dos glomérulos renais que ocorre após infecção estreptocócica, levando à síndrome nefrítica (hematúria, edema, hipertensão e insuficiência renal). O paciente desenvolveu uma emergência hipertensiva complicada por convulsões e encefalopatia (disfunção cerebral). Após melhora inicial, houve piora do estado neurológico associada à pressão arterial persistentemente alta, levando à suspeita e confirmação por ressonância magnética do cérebro da Síndrome de Encefalopatia Posterior Reversível (PRES). Essa condição é caracterizada por edema (inchaço) cerebral, especialmente nas regiões posteriores do cérebro, causado por pressão arterial elevada e disfunção dos vasos sanguíneos cerebrais.\n\nAlém disso, o paciente apresentou anemia hemolítica autoimune, uma condição em que o sistema imunológico destrói os próprios glóbulos vermelhos, confirmada pelo teste de Coombs positivo e presença de hemoglobinúria (sangue na urina devido à destruição dos glóbulos vermelhos).\n\n**Tratamento**  \nO manejo incluiu controle rigoroso da pressão arterial com múltiplos medicamentos (amlodipina, labetalol, nitroprussiato de sódio e enalapril), suporte ventilatório com intubação e ventilação mecânica durante os episódios mais graves, terapia anticonvulsivante com fenobarbital, e tratamento antibiótico para erradicar a infecção estreptocócica. Para a anemia hemolítica, foi iniciada terapia com corticosteroides (metilprednisolona) e transfusões de sangue. A abordagem neuroprotetora visou reduzir gradualmente a pressão arterial para evitar danos cerebrais adicionais.\n\n**Desfecho e Prognóstico**  \nApós 31 dias de internação, o paciente apresentou recuperação completa da função renal, normalização da pressão arterial, resolução da anemia e regressão dos sinais de edema cerebral na ressonância magnética. Ele recebeu alta hospitalar em boas condições, mantendo o uso de prednisona, anti-hipertensivos e ácido fólico. Seis meses após a alta, o paciente permanecia assintomático, sem recidivas da doença ou complicações neurológicas.\n\n**Interpretação Clínica**  \nEste caso ilustra uma forma grave de glomerulonefrite pós-estreptocócica com complicações neurológicas severas, incluindo PRES, e anemia hemolítica autoimune. A associação dessas condições requer diagnóstico rápido e tratamento multidisciplinar para evitar sequelas permanentes. O controle rigoroso da pressão arterial e o suporte intensivo foram fundamentais para o desfecho favorável.\n\n**Próximos Passos**  \nO acompanhamento ambulatorial deve incluir monitoramento da função renal, pressão arterial, hemograma e avaliação neurológica para detectar precocemente possíveis recidivas ou sequelas. A manutenção da terapia medicamentosa e a observação clínica são essenciais para garantir a recuperação completa e prevenir complicações futuras."
+        }
+    },
+    {
+        "article": "Este é o caso de uma mulher de 36 anos da região de Oromia, zona de West Arsi, que apresentou uma história de 6 meses de ronco, disfonia e tosse, bem como perda de peso significativa, mas não quantificada, fadiga e febre baixa e intermitente, para a qual visitou várias instalações de saúde sem melhorias notáveis nos seus sintomas. Tem tido diabetes nos últimos 5 anos e está a tomar Metformin 500 mg duas vezes ao dia com controlo glicémico fraco. Os achados físicos na apresentação, incluindo o exame da garganta, foram insignificantes. O nível de açúcar no sangue aleatório foi de 300 mg/dl no momento da apresentação (elevado). A laringoscopia revelou um tumor irregular no terço anterior da corda vocal bilateralmente, envolvendo a comissura anterior. O resultado da biópsia revelou grânulos actinomicóticos com formação de abscesso. A paciente começou então a tomar Penicilina G (por 1 mês), com a resolução dos seus sintomas durante o acompanhamento, e depois Amoxicilina durante os 6 meses seguintes, que foi descontinuada quando se recuperou totalmente dos seus sintomas e a massa foi eliminada na laringoscopia de acompanhamento.\n\nApós investigação, a contagem completa de sangue, a taxa de sedimentação de eritrócitos, os testes de função renal e os testes de função hepática estavam dentro dos limites normais. Os testes de serologia para o Vírus da Imunodeficiência Humana (HIV), Antígeno de Superfície da Hepatite B (HbsAg) e RNA do Vírus da Hepatite C (RNA HCV) revelaram-se negativos. O nível de açúcar no sangue aleatório dela foi de 300 mg/dl, que é alto, e o seu controlo glicémico foi igualmente fraco no gráfico de acompanhamento.\n\nSeu exame de otorrinolaringologia foi normal, mas uma laringoscopia flexível revelou uma massa irregular no terço anterior do cordão vocal em ambos os lados, com envolvimento da comissura anterior.\n",
+        "gold_summary": "O nosso caso foi o de uma mulher de 36 anos da região de Oromia, zona de West Arsi, que apresentou uma história de 6 meses de ronco, disfonia e tosse, bem como uma perda de peso significativa, mas não quantificada, fadiga e febre baixa e intermitente, para a qual visitou várias instalações de saúde sem melhorias notáveis nos seus sintomas. Tem tido diabetes nos últimos 5 anos e está a tomar Metformin 500 mg duas vezes ao dia com um controlo glicémico fraco. Os achados físicos na apresentação, incluindo o exame da garganta, foram insignificantes. O nível de açúcar no sangue aleatório foi de 300 mg/dl no momento da apresentação (elevado). A laringoscopia revelou um tumor irregular no terço anterior da corda vocal bilateralmente, envolvendo a comissura anterior. O resultado da biópsia revelou grânulos actinomicóticos com formação de abscesso. A paciente começou então a tomar Penicilina G, e houve uma resolução dos seus sintomas durante o acompanhamento, e depois começou a tomar Amoxicilina durante os 6 meses seguintes, que foi descontinuada quando se recuperou totalmente dos seus sintomas e a massa foi eliminada na laringoscopia de acompanhamento.\n",
+        "synthetic_summary": {
+            "B1": "Uma mulher estava com tosse e febre por muito tempo. Ela também estava cansada e perdeu peso. Ela tinha diabetes e o açúcar no sangue estava alto. Os médicos olharam sua garganta e viram um caroço. Esse caroço era uma bolinha de pus que fazia mal. Ela tomou remédio para melhorar. Depois de um tempo, ela ficou bem e o caroço sumiu.",
+            "B2": "**O que aconteceu com a paciente**\n\nUma mulher de 36 anos, que mora na região de Oromia, apresentou vários sintomas durante seis meses. Ela começou a roncar, teve dificuldade para falar (disfonia) e tosse. Também perdeu muito peso, ficou cansada e teve febre baixa que aparecia e desaparecia. Mesmo depois de ir a vários médicos, seus sintomas não melhoraram.\n\n**Histórico de saúde e exames**\n\nEla tem diabetes há cinco anos e toma um remédio chamado Metformina para controlar o açúcar no sangue. No entanto, o controle do diabetes dela não estava bom, e o exame mostrou que o nível de açúcar estava muito alto (300 mg/dl). Quando os médicos examinaram sua garganta, não encontraram nada de anormal à primeira vista.\n\n**O que os exames mostraram**\n\nPara entender melhor, os médicos fizeram um exame chamado laringoscopia, que usa uma câmera para olhar as cordas vocais. Eles encontraram um tumor irregular (uma massa anormal) na parte da frente das cordas vocais dos dois lados. Para descobrir o que era, fizeram uma biópsia, que é quando se tira um pedacinho do tumor para analisar. A biópsia mostrou que o tumor era causado por uma infecção chamada actinomicose, que forma pequenos grânulos e abscessos (bolsas de pus).\n\n**Tratamento e recuperação**\n\nA paciente começou a tomar um antibiótico chamado Penicilina G por um mês. Com esse tratamento, seus sintomas começaram a melhorar. Depois, ela continuou o tratamento com outro antibiótico chamado Amoxicilina por seis meses. No final, ela se recuperou totalmente, e o tumor desapareceu, como confirmou a laringoscopia feita depois do tratamento.\n\n**Conclusão**\n\nEsse caso mostra que uma infecção pode causar um tumor nas cordas vocais, e que o tratamento com antibióticos pode curar o problema. Também destaca a importância de controlar bem o diabetes, pois o açúcar alto no sangue pode dificultar a recuperação.",
+            "B3": "Contexto  \nEste relato descreve o caso de uma mulher de 36 anos, residente na região de Oromia, zona de West Arsi, que apresentou sintomas persistentes ao longo de seis meses, incluindo ronco, alteração da voz (disfonia), tosse, perda significativa de peso (não quantificada), fadiga e febre baixa e intermitente. Durante esse período, ela procurou atendimento em várias unidades de saúde, porém sem melhora dos sintomas. A paciente tem histórico de diabetes mellitus há cinco anos, sendo tratada com Metformina 500 mg duas vezes ao dia, porém com controle inadequado da glicemia.\n\nPrincipais Achados  \nNo exame físico inicial, incluindo a avaliação da garganta, não foram observados achados relevantes. Contudo, a glicemia aleatória estava elevada, em 300 mg/dL, indicando descontrole glicêmico. A avaliação otorrinolaringológica com laringoscopia flexível revelou a presença de uma massa irregular localizada no terço anterior das cordas vocais bilateralmente, envolvendo também a comissura anterior (região que conecta as duas cordas vocais). A biópsia dessa lesão identificou grânulos actinomicóticos, característicos da infecção por Actinomyces, associada à formação de abscesso (acúmulo de pus).\n\nInterpretação Clínica  \nO diagnóstico estabelecido foi de actinomicose laríngea, uma infecção bacteriana rara que pode mimetizar tumores malignos devido à formação de massas. A presença de diabetes com controle glicêmico inadequado provavelmente contribuiu para a suscetibilidade da paciente à infecção. O tratamento inicial com Penicilina G por um mês resultou na melhora dos sintomas, seguido de terapia prolongada com Amoxicilina por seis meses. A abordagem antibiótica prolongada é fundamental para erradicar a infecção e evitar recidivas.\n\nPróximos Passos e Desfecho  \nDurante o acompanhamento, a paciente apresentou resolução completa dos sintomas e a massa laríngea desapareceu, conforme confirmado por laringoscopia de controle. Além disso, exames laboratoriais complementares, incluindo hemograma, taxa de sedimentação de eritrócitos, função renal e hepática, estavam dentro dos limites normais. Testes sorológicos para HIV, hepatite B e hepatite C foram negativos. O caso ressalta a importância de considerar infecções crônicas como a actinomicose no diagnóstico diferencial de massas laríngeas, especialmente em pacientes com fatores de risco como diabetes mal controlada. O manejo adequado com antibióticos pode levar à cura completa, evitando intervenções cirúrgicas desnecessárias."
+        }
+    },
+    {
+        "article": "O homem de 46 anos de idade apresentou-se com alteração visual de três anos de evolução, associada a cefaleias ocasionais, astenia, adinamia grave, disfunção erétil e perda de libido. Antecedentes pessoais de hipotireoidismo primário e NF1 com múltiplas lesões compatíveis com neurofibromas com diagnóstico confirmado em 2014. Os antecedentes familiares incluem uma filha com diagnóstico de NF1 operada de um astrocitoma cerebral aos 11 anos de idade. No exame físico apresentava múltiplas lesões compatíveis com neurofibromas, manchas cor café com leite no dorso e abdômen, funções mentais superiores conservadas, pupilas isocóricas e reativas, hemianopsia bitemporal, sem alterações de pares cranianos, nem déficit motor ou sensitivo. Em imagens de ressonância magnética (RM) de cérebro com contraste endovenoso observou-se uma lesão bilobulada selar com extensão supraselar, de 24x24x39mm de diâmetro, a qual gerava compressão do quiasma ótico, correspondendo a lesão tipo KNOSP II - Hardy C. Comportava-se hipointensa em T1 e ligeiramente hiperintensa em T2, com realce homogêneo após a administração de contraste, podendo corresponder a macroadenoma hipofisário.\n\nEle foi encaminhado ao Serviço de Endocrinologia, onde foram realizados exames laboratoriais e constatado panhipopituitarismo, hipovitaminose D com hiperparatireoidismo secundário e dislipidemia mista. O ionograma sérico e a densidade urinária foram normais, excluindo diabetes insipidus. A dosagem de catecolaminas urinárias e ácido vanilina mandélico foram normais. Foi decidida a realização de uma ressecção endoscópica transnasal clássica. Foi identificada uma lesão tumoral de coloração pálida, encapsulada, hipovascularizada e de consistência dura e elástica, ressecando-a em bloco. Às 12 horas da cirurgia, foi realizado um controle de imagem por tomografia com contraste endovenoso, onde foi constatada a excisão completa da lesão. O paciente apresentou diabetes insipidus nos primeiros dias pós-operatórios, respondendo à administração de desmopressina. Não apresentou sinais de fístula de líquido cefalorraquidiano. Foi dado alta com diagnóstico de diabetes insipidus parcial, com tratamento com carbamazepina 100 mg a cada 12 horas, hidrocortisona 30 mg por dia, levotiroxina 150 microgramos por dia, com boa resposta. Foi recebido o relatório de anatomia patológica que descreveu uma proliferação fusocelular compacta, disposta em um padrão estoriforme com muito estroma interposto. Os elementos celulares eram do tipo fusado com citoplasma eosinófilos e núcleos ligeiramente desiguais. Não foi observada atividade mitótica evidente, necrose nem remanescente do parênquima encefálico. O escasso estroma interposto destacava elementos vasculares CD34 positivos. A trama reticulínica foi preservada. Foi realizada imuno-histoquímica, resultando com positividade intensa e difusa para vimentina e nuclear para fator de transcrição tireoide 1 (TTF1), sendo focal para VCL2 e S100. Assim, foram negativos para sinaptofisina, EMA, GFAP e STAT6. KI67 6%. O diagnóstico final foi lesão fusocelular selar de baixo grau compatível com pitucitoma.\n",
+        "gold_summary": "Descreve-se o caso de um homem de 46 anos que apresentou defeitos do campo visual e sintomas de panhipopituitarismo de 3 anos de evolução. Como antecedentes pessoais apresentava neurofibromatose tipo 1, e a filha, com a mesma doença, operada de astrocitoma cerebral. No exame oftalmológico o paciente apresentava hemianopsia bitemporal e a avaliação hormonal confirmou hipopituitarismo. A ressonância magnética hipofisária evidenciou uma massa selar com extensão supraselar com realce homogêneo pós contraste, a qual gerava deslocamento do quiasma óptico. Realizou-se uma ressecção transnasal transesfenoidal. Posterior à cirurgia, desenvolveu diabetes insípida. A histopatologia mostrou padrões compatíveis com pituicitoma confirmado por imunohistoquímica. A ressecção total continua sendo o objetivo do tratamento.\n",
+        "synthetic_summary": {
+            "B1": "Um homem de 46 anos estava com problemas para enxergar há muito tempo. Ele também se sentia muito cansado e com pouca vontade de fazer coisas. Ele tinha uma doença chamada neurofibromatose, que faz pintinhas na pele.\n\nO médico fez um exame no olho dele e viu que ele não conseguia ver bem para os lados. Também fez um exame para ver os hormônios, que estavam baixos.\n\nO médico pediu uma imagem da cabeça e viu uma bolinha perto do osso da testa. Essa bolinha estava apertando os nervos dos olhos.\n\nO homem fez uma cirurgia pelo nariz para tirar essa bolinha. Depois da cirurgia, ele teve que tomar remédio para ajudar o corpo a guardar água.\n\nO médico viu que a bolinha era um tipo de tumor que cresce devagar e não é muito perigoso. Tirar tudo é o melhor para ele ficar bem.",
+            "B2": "**O que aconteceu com o paciente**\n\nUm homem de 46 anos teve problemas de visão por três anos, além de sentir muito cansaço, fraqueza, perda de desejo sexual e dificuldade para ter ereção. Ele já tinha uma doença chamada neurofibromatose tipo 1 (NF1), que causa manchas na pele e tumores benignos chamados neurofibromas. A filha dele também tem essa doença e já passou por cirurgia para um tumor no cérebro.\n\n**O que os médicos encontraram**\n\nNo exame dos olhos, foi detectada uma perda da visão nas partes laterais dos dois olhos, chamada hemianopsia bitemporal. Os exames de sangue mostraram que a glândula hipófise, que controla vários hormônios do corpo, estava funcionando mal, causando o que chamamos de panhipopituitarismo (quando a hipófise não produz hormônios suficientes). A ressonância magnética, que é um exame de imagem, mostrou um tumor na região da hipófise, que estava pressionando uma parte importante do cérebro chamada quiasma óptico, responsável pela visão.\n\n**O tratamento realizado**\n\nO paciente foi submetido a uma cirurgia feita pelo nariz, chamada ressecção transnasal transesfenoidal, para retirar o tumor. Após a cirurgia, ele teve um problema chamado diabetes insipidus, que faz o corpo perder muita água pela urina, mas isso foi controlado com remédios.\n\n**O que o exame do tumor mostrou**\n\nO tumor foi analisado em laboratório e identificado como um pituicitoma, que é um tipo raro de tumor de baixo grau (menos agressivo) que cresce na hipófise. Esse diagnóstico foi confirmado por testes especiais chamados imunohistoquímica, que mostram quais proteínas as células do tumor têm.\n\n**O que isso significa**\n\nA cirurgia para tirar todo o tumor é o melhor tratamento para esse tipo de lesão. O paciente está sendo acompanhado para controlar os hormônios e evitar complicações. Esse caso mostra como é importante investigar sintomas como problemas de visão e cansaço, pois podem estar ligados a tumores que afetam a hipófise.",
+            "B3": "**Contexto**  \nEste relato descreve o caso de um homem de 46 anos que apresentou, ao longo de três anos, alterações visuais associadas a sintomas indicativos de panhipopituitarismo (uma condição em que a hipófise, glândula responsável pela produção de vários hormônios, apresenta insuficiência generalizada). Ele possuía histórico pessoal de neurofibromatose tipo 1 (NF1), uma doença genética que causa o desenvolvimento de múltiplos tumores benignos nos nervos, e sua filha também tinha NF1, tendo sido submetida à cirurgia para remoção de um astrocitoma cerebral (um tipo de tumor no cérebro).\n\n**Principais Achados Clínicos e Exames**  \nNo exame oftalmológico, o paciente apresentava hemianopsia bitemporal, ou seja, perda da visão nos campos visuais laterais de ambos os olhos, sugerindo compressão do quiasma óptico — a região onde os nervos ópticos se cruzam. A avaliação hormonal confirmou o diagnóstico de panhipopituitarismo, indicando falha na produção dos hormônios hipofisários. A ressonância magnética da hipófise revelou uma massa tumoral localizada na região selar (área onde a hipófise está situada), com extensão para cima (supraselar), medindo aproximadamente 24x24x39 mm. A lesão apresentava características de realce homogêneo após a administração de contraste, compatível com um macroadenoma hipofisário ou outra lesão tumoral da hipófise, e causava deslocamento do quiasma óptico.\n\n**Intervenção e Evolução Pós-Operatória**  \nO paciente foi submetido a uma cirurgia endoscópica transnasal transesfenoidal, uma técnica minimamente invasiva que permite o acesso à hipófise através do nariz e seio esfenoidal para remoção da lesão. Durante o procedimento, a massa foi identificada como um tumor pálido, encapsulado, pouco vascularizado e de consistência dura e elástica, sendo removida completamente. Após a cirurgia, o paciente desenvolveu diabetes insipidus, uma condição caracterizada pela incapacidade dos rins de concentrar a urina, levando à perda excessiva de líquidos; essa complicação foi controlada com o uso de desmopressina, medicamento que substitui o hormônio antidiurético.\n\n**Diagnóstico Histopatológico e Imunohistoquímico**  \nA análise microscópica do tecido removido revelou uma proliferação de células fusiformes (em forma de fuso) organizadas em padrão estoriforme (semelhante a um tecido entrelaçado), sem sinais de atividade mitótica (divisão celular) ou necrose, o que indica uma lesão de baixo grau (menos agressiva). A imunohistoquímica, que utiliza marcadores específicos para identificar tipos celulares, mostrou positividade para vimentina e fator de transcrição tireoide 1 (TTF1), confirmando o diagnóstico de pituicitoma — um tumor raro e geralmente benigno da hipófise originado das células pituicíticas, que são células de suporte da glândula.\n\n**Interpretação Clínica e Próximos Passos**  \nEste caso ilustra a importância de considerar diagnósticos diferenciais além do adenoma hipofisário em pacientes com massas selar e sintomas de disfunção hipofisária, especialmente em indivíduos com histórico de doenças genéticas como a NF1. A ressecção cirúrgica completa permanece o tratamento de escolha para o pituicitoma, visando aliviar a compressão do quiasma óptico e restaurar, na medida do possível, a função hormonal. O acompanhamento clínico e radiológico é fundamental para monitorar possíveis recidivas e manejar complicações endócrinas, como o diabetes insipidus e o panhipopituitarismo, que requerem tratamento hormonal substitutivo contínuo."
+        }
+    },
+    {
+        "article": "Uma mulher japonesa de 71 anos com um histórico médico de diabetes tipo 1, doença renal em fase terminal, bloqueio atrioventricular completo e infarto do miocárdio prévio foi internada no serviço de Gastroenterologia do nosso hospital para avaliação e tratamento de perda de consciência aguda secundária a hipoglicemia. No momento da admissão, ela tinha um marcapasso permanente e estava em hemodiálise três vezes por semana. O serviço de Ortopedia foi contactado para avaliar inchaço, calor e vermelhidão da sua mão esquerda devido a uma ferida na ponta do dedo médio esquerdo que foi auto-infligida durante um episódio de demência. Um curso padrão de cefazolina intravenosa (1g por dia) foi prescrito para tratar a presunção de celulite. A infecção não respondeu e progrediu apesar de dois dias completos de tratamento com antibióticos. A cultura bacteriológica da lesão revelou Staphylococcus aureus resistente à meticilina (MRSA). Após o exame físico, a paciente apresentou todos os quatro sinais cardinais de Kanavel de tenossinovite flexora. A infusão de vancomicina (valor mínimo, 15-20 µg/mL) foi iniciada para tratar a infecção por MRSA, juntamente com desbridamento da ferida e uma amputação parcial na articulação interfalângica distal. A descompressão do nervo mediano foi realizada para aliviar a pressão resultante de um abcesso purulento. Embora a vermelhidão e o inchaço tenham persistido após este procedimento, a progressão da infecção pareceu ser um pouco reduzida. Enquanto o curso de antibióticos de vancomicina foi continuado, no dia 5 a paciente de repente se queixou de dor abdominal, sangue castanho escuro nas fezes, indicativo de uma hemorragia gastrointestinal, e desenvolveu sinais consistentes com choque sistêmico. A sua pressão arterial sistólica inicial foi de 60 mmHg, que respondeu a administração aguda de vasopressores. Os dados laboratoriais incluíam um aumento do número de glóbulos brancos (WBC) de 9890 por mm3, juntamente com níveis elevados de proteína C reativa (CRP; 259,7 mg/L) e creatinina (421,7 µmol/L) e níveis reduzidos de sódio (132 mEq/L), glicemia (2,6 mmol/L) e hemoglobina (8,2 g/dL). Os resultados de um estudo de tomografia computadorizada abdominal (CT) resultaram num diagnóstico de isquemia mesentérica não oclusiva; uma ressecção intestinal de emergência foi realizada. A alimentação por sonda foi iniciada e continuou durante uma semana. A norepinefrina foi adicionada ao seu regime para manter a pressão arterial a níveis necessários para sustentar a perfusão de órgãos com uma pressão arterial média alvo de 70.\n\nDurante a sua estadia no hospital, a paciente foi exposta ao SARS-CoV-2 após um contacto prolongado com um indivíduo infetado enquanto estava a fazer diálise. O teste de esfregaço nasal foi positivo para COVID-19 utilizando um ensaio de amplificação isotérmica mediada por loop. Quatro dias após o teste positivo, a paciente desenvolveu sinais de pneumonia aguda. Os resultados de uma radiografia de tórax e de uma TAC confirmaram este diagnóstico e revelaram consolidação dos pulmões, bem como derrames pleurais bilaterais. Foi iniciado um tratamento antiviral com favipiravir (200 mg por via oral duas vezes por dia) e a paciente foi transferida para a unidade de cuidados intensivos. Isto foi de acordo com as recomendações no momento da administração. A paciente estava hipervolémica com aumento da necessidade de oxigénio. Foi realizada uma hemodiafiltração contínua para evitar sobrecarga de fluidos.\n\nImediatamente antes da exposição ao COVID-19, a paciente desenvolveu sinais clínicos de fascite necrosante. A infeção estendeu-se à fáscia e à musculatura circundante da mão esquerda. Embora a amputação de emergência da mão fosse considerada necessária, a paciente desenvolveu choque séptico e precisou de respiração mecânica devido a um súbito aumento da necessidade de oxigénio. Foi administrado oxigénio de fluxo elevado de forma contínua através do tubo endotraqueal, e o seu regime antiviral foi alterado para remdesivir (100 mg intravenoso uma vez por dia) juntamente com hidrocortisona intravenosa (200 mg/dose). O remdesivir estava ainda em fase de utilização compassiva na altura. Enquanto estava a ser tratada para eventos agudos que ameaçavam a vida, a infeção progrediu para incluir as falanges do dedo médio esquerdo, com necrose óssea visível na radiografia. Foi prescrito vancomicina (500 mg) para gerir a osteomielite e prevenir a sua propagação. A paciente desenvolveu subsequentemente síndrome de dificuldade respiratória aguda (ARDS). Embora a infeção da paciente fosse controlada após duas semanas, esta desenvolveu coagulação intravascular disseminada (DIC; pontuação >4) que pode ter acelerado o crescimento bacteriano. Como a heparina era contraindicada neste caso, ART-123, uma forma recombinante e solúvel de trombomodulina alfa foi administrada intravenosamente (12,800 U uma vez por dia durante 3 dias) para dissolver os coágulos sistémicos. A infeção progrediu para incluir necrose de todo o terceiro dedo, bem como da pele, fáscia e musculatura até à articulação radio-carpal com sinais de invasão progressiva no antebraço. Infelizmente, as restrições e encerramentos hospitalares associados ao COVID impediram um tratamento cirúrgico adicional neste momento.\n\nA paciente acabou por recuperar da COVID-19. Duas semanas após o diagnóstico inicial, a paciente foi retirada da ventilação mecânica e o tubo endotraqueal foi retirado. Duas semanas após a extubação, a paciente completou o tratamento para a COVID-19 e teve um teste negativo para antígeno SARS-CoV-2. Foi então realizada uma grande amputação no terço distal do antebraço. Os tecidos foram completamente desbridados e lavados durante o procedimento e todo o tecido infectado foi removido. Como o local da amputação era proximal à sua derivação de hemodiálise, a sua substituição foi discutida com cirurgiões vasculares e nefrologistas. O procedimento revelou uma forte calcificação das artérias do seu antebraço esquerdo com tortuosidade e possíveis oclusões tanto proximais como distais à derivação. O ruído e o tremor detetados na derivação também sugeriram a possibilidade de síndrome isquémica de hipoperfusão distal. Foi alcançada uma cobertura adequada da pele e o coto foi fechado; um estudo radiográfico de acompanhamento não revelou complicações. O coto parecia estar a curar-se bem, um mês depois, a paciente sucumbiu a um choque séptico e a uma paragem cardiopulmonar.\n",
+        "gold_summary": "Uma mulher de 71 anos apresentou uma infecção descontrolada após uma ferida auto-infligida no dedo médio esquerdo. Uma cultura bacteriológica da lesão revelou Staphylococcus aureus meticilino-resistente (MRSA). A infecção não pôde ser controlada com antibióticos ou intervenções adicionais, incluindo desbridamento e amputação menor. Ela contraiu COVID-19 grave enquanto estava no hospital, o que limitou as opções de tratamento disponíveis. Numa tentativa de controlar a infecção, a paciente acabou por ser submetida a uma amputação maior do antebraço esquerdo distal. Enquanto se recuperava do procedimento, a paciente sucumbiu a um choque séptico e a uma paragem cardiopulmonar.\n",
+        "synthetic_summary": {
+            "B1": "Uma senhora de 71 anos machucou o dedo da mão esquerda. A ferida ficou muito feia e não melhorou com remédios. Ela ficou doente com uma infecção forte que não parava. No hospital, ela também pegou um vírus chamado COVID-19. Por causa disso, os médicos não puderam ajudar do jeito que queriam. Para tentar melhorar, os médicos tiraram uma parte maior do braço dela. Mesmo assim, ela ficou muito doente e não conseguiu melhorar.",
+            "B2": "**O que aconteceu com a paciente**\n\nUma mulher de 71 anos teve uma ferida no dedo médio da mão esquerda, que ela mesma causou durante um episódio de confusão mental. Essa ferida ficou infectada por uma bactéria chamada Staphylococcus aureus resistente à meticilina (MRSA), que é difícil de tratar com antibióticos comuns.\n\n**Tratamentos e complicações**\n\nApesar de receber antibióticos fortes, limpeza da ferida (desbridamento) e até uma pequena amputação no dedo, a infecção continuou piorando. Durante a internação, ela também contraiu COVID-19, o que dificultou ainda mais o tratamento da infecção.\n\nA infecção se espalhou para os ossos e tecidos ao redor da mão, e para tentar salvar a paciente, os médicos precisaram amputar uma parte maior do antebraço esquerdo. Mesmo assim, a paciente enfrentou várias complicações graves, como choque séptico, que é uma reação muito forte do corpo a uma infecção, e problemas respiratórios.\n\n**Desfecho**\n\nDepois da amputação maior, a paciente chegou a melhorar um pouco, mas infelizmente, algumas semanas depois, ela teve uma parada cardíaca causada pelo choque séptico e não resistiu.\n\n**O que isso significa**\n\nEsse caso mostra como infecções graves, especialmente por bactérias resistentes e em pessoas com outras doenças, podem ser muito difíceis de controlar. Além disso, a presença da COVID-19 complicou ainda mais o tratamento, limitando as opções médicas e piorando o quadro da paciente.",
+            "B3": "**Contexto**  \nUma mulher japonesa de 71 anos, com múltiplas condições médicas graves pré-existentes, incluindo diabetes tipo 1, insuficiência renal terminal em hemodiálise, bloqueio atrioventricular completo e histórico de infarto do miocárdio, foi internada após apresentar perda súbita de consciência causada por hipoglicemia. Durante a internação, desenvolveu uma ferida auto-infligida no dedo médio da mão esquerda, que evoluiu para uma infecção grave.\n\n**Principais Achados**  \nA ferida na mão esquerda revelou-se infectada por Staphylococcus aureus resistente à meticilina (MRSA), uma bactéria difícil de tratar devido à resistência a antibióticos comuns. Apesar do uso inicial de cefazolina e posterior vancomicina, além de procedimentos cirúrgicos como desbridamento (remoção do tecido infectado) e amputação parcial da ponta do dedo, a infecção progrediu, envolvendo tecidos profundos, como fáscia e músculos, caracterizando uma fascite necrosante — uma infecção agressiva e potencialmente fatal.\n\nDurante o tratamento, a paciente também desenvolveu complicações graves, como choque séptico (uma resposta inflamatória sistêmica que causa queda da pressão arterial e falência de órgãos), isquemia mesentérica não oclusiva (falta de fluxo sanguíneo adequada para o intestino), e hemorragia gastrointestinal. Foi necessária uma cirurgia de emergência para remoção de parte do intestino e suporte intensivo com vasopressores para manter a pressão arterial.\n\nAlém disso, a paciente contraiu COVID-19 durante a internação, o que agravou seu quadro clínico. A infecção viral evoluiu para pneumonia grave e síndrome do desconforto respiratório agudo (SDRA), exigindo ventilação mecânica e tratamento antiviral com remdesivir e corticosteroides. A sobrecarga hídrica foi controlada por hemodiafiltração contínua.\n\nA progressão da infecção na mão levou à necrose óssea (morte do tecido ósseo) e à necessidade de tratamento prolongado com vancomicina para osteomielite (infecção óssea). A coagulação intravascular disseminada (DIC), uma condição que provoca formação anormal de coágulos sanguíneos, complicou ainda mais o quadro, sendo tratada com trombomodulina alfa (ART-123).\n\n**Interpretação Clínica**  \nA combinação de múltiplas comorbidades, infecção por MRSA resistente, complicações sépticas, e infecção concomitante por COVID-19 criou um cenário clínico extremamente complexo e de alto risco. A fascite necrosante e a osteomielite progrediram rapidamente, limitando as opções cirúrgicas devido ao estado crítico da paciente e às restrições hospitalares impostas pela pandemia. A necessidade de amputação maior do antebraço distal foi uma medida extrema para controlar a infecção e preservar a vida.\n\n**Próximos Passos e Desfecho**  \nApós a recuperação da COVID-19 e a retirada da ventilação mecânica, a paciente foi submetida à amputação extensa do antebraço esquerdo, com remoção completa dos tecidos infectados. O procedimento considerou também a preservação da função da sua fístula para hemodiálise, apesar das dificuldades vasculares encontradas. Inicialmente, o coto cirúrgico evoluiu bem, sem complicações radiográficas evidentes.\n\nNo entanto, cerca de um mês após a amputação, a paciente desenvolveu choque séptico novamente, culminando em parada cardiopulmonar e óbito. Este caso ilustra a gravidade das infecções por MRSA em pacientes com múltiplas comorbidades e a complexidade do manejo durante a pandemia de COVID-19, quando limitações no tratamento cirúrgico e suporte clínico podem impactar negativamente o prognóstico."
+        }
+    },
+    {
+        "article": "Um lactente de seis meses, do sexo masculino, foi observado no serviço de urgência por febre (temperatura máxima 40ºC cada 6 horas), rinorreia, tosse e recusa alimentar com três dias de evolução.A gestação foi de termo, vigiada e decorreu sem intercorrências. No período neonatal foi internado por pneumonia congénita complicada com pneumotórax e recuperou com drenagem, antibioterapia e ventilação mecânica invasiva. Tinha imunizações atualizadas de acordo com o PNV e a incluir três doses da vacina Hib, duas doses da vacina MenB, duas doses de vacina MenACWY e duas doses da vacina contra o rotavírus. Frequentava infantário e os antecedentes familiares não eram relevantes.À admissão, apresentava-se febril, com temperatura timpânica de 40ºC, hemodinamicamente estável, corado e hidratado, com fontanela anterior normotensa e normopulsátil. Foi constatada ligeira hiperemia da orofaringe, sem outras particularidades no exame físico. Durante a permanência no serviço de urgência ficou prostrado e sonolento, com abaulamento da fontanela anterior.Por suspeita de meningite, realizou-se punção lombar. O líquido cefalorraquidiano (LCR) era claro, com contagem total de 3509 células/mm3 (0 - 5 células/mm3), com predomínio de polimorfonucleares, glicose 8 mg/dL (> 50% da glicemia), glicemia 93 mg/dL, proteínas 198 mg/dL (< 60 mg/dL), e pesquisa de antigénio capsular de Streptococcus pneumoniae por ensaio imunocromatográfico. As análises sanguíneas mostraram: hemoglobina 10 g/dL, leucócitos 6730/mL, neutrófilos 3870/mL, linfócitos 2790/mL, plaquetas 499 000/mL, proteína C reativa (PCR) 127 mg/L.Iniciou terapêutica com ceftriaxone via endovenosa em dose meníngea (100 mg/kg/dia) que completou durante 10 dias. A antibioticoterapia foi precedida de dexametasona, que manteve durante dois dias. Efetuou-se a quimioprofilaxia dos contactos com rifampicina e informou-se o delegado de saúde local. No exame cultural do LCR e sangue foi isolado H. influenzae, tendo sido notificado o Sistema de Informação Nacional de Vigilância Epidemiológica. A serotipagem da estirpe por PCR identificou um H. influenzae capsulado serotipo A. A determinação do teste de sensibilidade aos anti-microbianos por Etest evidenciou uma estirpe multissensível, nomeadamente às cefalosporinas de terceira geração. Verificou-se que a quimioprofilaxia instituída foi adequada. A pesquisa de vírus no LCR por PCR e no aspirado nasofaríngeo por imunofluorescência foram ambas positivas para adenovírus.A evolução clínica foi favorável, com apirexia a partir do quarto dia de terapêutica.No seguimento em consulta de pediatria, o doente apresentou sempre um desenvolvimento psicomotor adequado à idade. Foi seguido em consulta de otorrinolaringologia e imunodeficiências, que não reportaram alterações.",
+        "gold_summary": "Um lactente de seis meses deu entrada no serviço de urgência por quadro de febre, tosse e rinorreia. À admissão, encontrava-se vígil e hemodinamicamente estável, tendo ficado progressivamente letárgico e com abaulamento da fontanela. As análises sanguíneas mostraram contagem leucocitária normal e proteína C reativa elevada. A citologia e bioquímica do líquido céfalo-raquidiano foram compatíveis com meningite bacteriana, tendo iniciado terapêutica com ceftriaxone. A hemocultura e exame cultural do líquido céfalo-raquidiano foram positivos para Haemophilus influenzae. A serotipagem da estirpe identificou um Haemophilus influenzae serotipo A. As pesquisas de vírus no líquido céfalo-raquidiano e no aspirado nasofaríngeo foram positivas para adenovírus. Teve alta após 10 dias de antibiótico e recuperação clínica completa.",
+        "synthetic_summary": {
+            "B1": "Um bebê de seis meses estava com febre, tosse e nariz escorrendo. No hospital, ele ficou cansado e a cabeça dele estava um pouco inchada. Os médicos fizeram exames e viram que ele tinha uma infecção no cérebro. Eles deram remédio forte para ajudar. O remédio fez ele melhorar. Depois de 10 dias, o bebê ficou bom e voltou para casa.",
+            "B2": "**O que aconteceu com o bebê**\n\nUm bebê de seis meses foi levado ao hospital porque estava com febre alta, tosse e nariz escorrendo há três dias. No começo, ele estava acordado e com sinais vitais normais, mas depois ficou muito sonolento e a parte mole da cabeça dele, chamada fontanela, ficou inchada.\n\n**Exames feitos**\n\nOs médicos fizeram exames de sangue e encontraram uma proteína chamada proteína C reativa muito alta, que indica infecção. Também retiraram um pouco do líquido que envolve o cérebro e a medula espinhal, chamado líquido cefalorraquidiano, para analisar. Esse líquido mostrou sinais de uma infecção bacteriana, que é uma infecção causada por bactérias.\n\n**Diagnóstico e tratamento**\n\nOs exames mostraram que a infecção era causada por uma bactéria chamada Haemophilus influenzae, tipo A. Além disso, encontraram também um vírus chamado adenovírus no líquido do cérebro e no nariz do bebê. O bebê recebeu um remédio chamado ceftriaxona, que é um antibiótico forte para combater a bactéria, durante 10 dias. Ele também recebeu um medicamento para diminuir a inflamação.\n\n**Recuperação**\n\nDepois do tratamento, o bebê melhorou bastante e teve alta do hospital. Nos meses seguintes, ele continuou se desenvolvendo normalmente e não apresentou problemas de saúde relacionados à infecção.",
+            "B3": "**Contexto**  \nUm bebê do sexo masculino, com seis meses de idade, foi levado ao serviço de urgência devido a febre alta (até 40ºC a cada seis horas), coriza (rinorreia), tosse e recusa alimentar, sintomas que persistiam há três dias. O histórico prévio incluía uma pneumonia congênita complicada por pneumotórax no período neonatal, tratada com sucesso. O bebê estava com as vacinas em dia, incluindo imunizações contra Haemophilus influenzae tipo b (Hib) e meningococos, e frequentava creche. Não havia antecedentes familiares relevantes.\n\n**Principais Achados Clínicos e Laboratoriais**  \nNa admissão, o lactente apresentava-se febril, porém estável do ponto de vista cardiovascular, com boa coloração e hidratação. O exame físico inicial revelou apenas leve vermelhidão na garganta. Durante a observação, o bebê tornou-se progressivamente sonolento e apresentou abaulamento da fontanela anterior (uma protuberância na região mole do crânio), sinal sugestivo de aumento da pressão intracraniana. Diante da suspeita de meningite (infecção das membranas que envolvem o cérebro e a medula espinhal), foi realizada punção lombar para análise do líquido cefalorraquidiano (LCR).\n\nO exame do LCR mostrou-se claro, mas com uma contagem muito elevada de células (3509 células/mm³, sendo o normal até 5), predominantemente polimorfonucleares (um tipo de glóbulo branco associado a infecções bacterianas). A glicose no LCR estava muito baixa (8 mg/dL, sendo o esperado acima de 50% da glicemia), enquanto as proteínas estavam elevadas (198 mg/dL, valor normal abaixo de 60 mg/dL), características típicas de meningite bacteriana. Foi detectado o antígeno capsular de Streptococcus pneumoniae por um teste rápido, mas posteriormente as culturas do LCR e do sangue identificaram Haemophilus influenzae, especificamente o sorotipo A, uma forma encapsulada da bactéria que pode causar infecções invasivas. O teste de sensibilidade indicou que a bactéria era sensível a múltiplos antibióticos, incluindo cefalosporinas de terceira geração.\n\nAlém disso, testes moleculares (PCR) no LCR e exame do aspirado nasofaríngeo detectaram presença de adenovírus, sugerindo uma coinfecção viral.\n\nOs exames sanguíneos mostraram hemoglobina levemente baixa (10 g/dL), contagem normal de leucócitos (6730/mL) com predominância de neutrófilos, plaquetas elevadas (499.000/mL) e proteína C reativa (PCR) aumentada (127 mg/L), indicando inflamação.\n\n**Interpretação Clínica**  \nO quadro clínico e laboratorial foi compatível com meningite bacteriana causada por Haemophilus influenzae sorotipo A, uma forma menos comum atualmente devido à vacinação contra o sorotipo b, mas que pode causar doença invasiva em crianças pequenas. A presença simultânea de adenovírus sugere que uma infecção viral pode ter contribuído para a vulnerabilidade do paciente à infecção bacteriana.\n\nA evolução clínica foi favorável após o início imediato de antibioticoterapia endovenosa com ceftriaxona em dose adequada para meningite, associada a dexametasona (um corticosteroide usado para reduzir a inflamação). O bebê apresentou melhora progressiva, com desaparecimento da febre a partir do quarto dia de tratamento.\n\nFoi realizada quimioprofilaxia (medicação preventiva) com rifampicina para os contatos próximos, conforme protocolo, e as autoridades de saúde foram notificadas para vigilância epidemiológica.\n\n**Próximos Passos e Seguimento**  \nApós 10 dias de tratamento, o lactente recebeu alta hospitalar com recuperação completa. No acompanhamento ambulatorial, apresentou desenvolvimento psicomotor adequado para a idade, sem sequelas neurológicas aparentes. Consultas especializadas em otorrinolaringologia e imunologia não identificaram alterações ou imunodeficiências subjacentes.\n\nEste caso destaca a importância da vigilância contínua das infecções por Haemophilus influenzae, mesmo em crianças vacinadas, e a necessidade de diagnóstico rápido e tratamento eficaz para meningite bacteriana, garantindo um bom prognóstico."
+        }
+    },
+    {
+        "article": "Paciente de 15 anos de idade, previamente saudável, sem antecedentes patológicos a destacar, com vacinas completas para a idade. Oriundos de uma localidade rural da Província de Buenos Aires-Argentina. O pai trabalhava no campo. Em casa tinham cachorros e galinhas. Entre arvoredos de eucaliptos havia um galpão onde se guardavam sacos de sementes e geralmente havia pombos.\n\nO paciente consultou por tosse produtiva e dor no flanco de um mês de evolução, sem registros febris nem dificuldade respiratória associada. Inicialmente, foi realizada uma radiografia de tórax que evidenciou duas imagens de condensação na base pulmonar esquerda. Com estas imagens, foi decidido realizar uma Tomografia Computada de tórax, na qual foram encontradas imagens de consolidação nodular na base esquerda. Com suspeita de pneumonia, iniciou tratamento antibiótico com Amoxicilina. Foi encaminhado para nossa instituição.\n\nAs imagens da tomografia foram interpretadas como nódulos pulmonares e foi decidido realizar uma Tomografia por Emissão de Positrons (PET-TC) para medir a atividade metabólica da 18 Fluorodesoxiglucose e identificar a captação de glicose nos tecidos através do valor de captação estandardizado (SUV). As células neoplásicas, assim como os processos inflamatórios e infecciosos, evidenciam um metabolismo elevado neste estudo13. No exame, evidenciaram-se múltiplas lesões pulmonares no lóbulo inferior esquerdo com metabolismo aumentado por SUV num intervalo de 10,88-13,53. Não se encontraram lesões no sistema nervoso central, abdómen nem pélvis. As características tomográficas, poderiam corresponder a compromisso fúngico ou granulomatoso.\n\nOs exames laboratoriais completos estavam dentro da normalidade (hemograma, perfil hepático, função renal, painel eletrolítico, testes de coagulação), com reagentes de fase aguda negativos. Realizaram-se ecografias de abdômen, rim, testículo e tireoide sem achados patológicos. No contexto de estudo de nódulos pulmonares, realizou-se um cadastro para tuberculose, sem encontrar evidência de contatos próximos para esta doença; intradermorreação do derivado proteico purificado (PPD) com resultado negativo com valor de 0 mm; baciloscópias seriadas em escarro por tinção de Ziehl-Neelsen e cultura resultaram negativos.\n\nLevando em consideração as imagens e os fatores epidemiológicos de risco, como a origem rural e o contato com dejetos de aves, foi considerada a possibilidade de se tratar de uma micose. Foi decidido realizar uma lavagem broncoalveolar, na qual foram tomadas amostras para estudo microbiológico. A cultura foi negativa para bactérias, fungos e micobactérias. A determinação de serologias para Aspergillus na lavagem broncoalveolar foi negativa, assim como a reação em cadeia de polimerase para histoplasma.\n\nFoi realizada punção biopsia pulmonar guiada por tomografia. No estudo micológico direto, assim como na coloração de Giemsa, observaram-se leveduras. O resultado da cultura da biopsia foi positivo para Cryptococcus neoformans variedade grubii sensível a fluconazol (concentração inibitória mínima 4 ug/ml) e a itraconazol (concentração inibitória mínima 0,06 ug/ml). A anatomia patológica evidenciou um processo inflamatório pio granulomatoso com presença de células gigantes multinucleadas e estruturas esféricas positivas com a coloração de ácido periódico de Schiff (PAS), que poderiam corresponder a uma micose profunda, sem células neoplásicas.\n\nPor se tratar de um paciente sem antecedentes de imunocompromesse, foi solicitado um estudo imunológico com contagem de linfócitos B, CD3, CD4, CD8, NK que estava dentro dos limites normais, assim como a quantificação de imunoglobulinas (Ig) IgG, IgA, IgM e IgE e a determinação do complemento C3, C4 e CH-50. O teste de HIV por Elisa foi negativo.\n\nPor apresentar títulos elevados de antígeno criptocócico em seu soro (1:128) foi realizada uma tomografia do sistema nervoso central que resultou normal. A punção lombar, mostrou um resultado físico-químico normal, coloração de tinta chinesa negativa, pesquisa de antígeno criptocócico em líquido cefalorraquidiano (LCR) e cultura que resultaram negativos. A determinação para a análise de antígenos em soro e LCR foi realizada no Hospital de Infecciosas Francisco Javier Muñiz, CABA e a análise foi realizada por teste de aglutinação de látex.\n\nFoi tratado com 200 mg de itraconazol por dia durante 4 semanas, até que o diagnóstico fosse confirmado, e depois com 200 mg de fluconazol por dia durante 10 meses. Não houve efeitos adversos ao tratamento.\n\nAos 6 semanas de iniciado o tratamento, realizou-se uma reavaliação metabólica por PET-TC Corporal das lesões pulmonares evidenciando que as opacidades nodulares apresentavam menor tamanho e metabolismo com SUV de 3,01 a 5,19. Sem presença de novos focos. Apresentou remissão dos sintomas iniciais e permaneceu clinicamente assintomático.\n\nAo final dos 10 meses de tratamento, uma radiografia de tórax foi realizada sem achados patológicos relevantes e uma pesquisa de antígeno no sangue foi realizada com resultado negativo.\n",
+        "gold_summary": "Paciente de 15 anos, previamente saudável, oriundo de uma localidade rural, que consultou por tosse e dor no flanco de um mês de evolução, sem febre nem dificuldade respiratória, com duas imagens de condensação na base pulmonar esquerda em radiografia de tórax. A Tomografia Computadorizada mostrou que as imagens tinham aspecto nodular. Por suspeita de patologia neoplásica, completou-se o estudo com Tomografia por Emissão de Positrons que evidenciou lesões nodulares hipermetabólicas. As características tomográficas poderiam corresponder a um compromisso fúngico ou granulomatoso. Tendo em conta as imagens e os fatores epidemiológicos de risco, como a origem rural e o contacto com dejetos de aves, considerou-se a possibilidade de micose. Realizou-se punção biopsia pulmonar sob guia tomográfica. Identificou-se Cryptococcus neoformans na cultura microbiológica. Recebeu tratamento com itraconazol e fluconazol com boa resposta clínica e das imagens a 10 meses de terapia e seguimento.\n",
+        "synthetic_summary": {
+            "B1": "Um menino de 15 anos ficou com tosse e dor no peito por um mês. Ele não teve febre nem dificuldade para respirar. O médico fez uma foto do pulmão e viu umas manchas. Depois, fez outro exame que mostrou bolinhas no pulmão.\n\nO médico pensou que podia ser uma doença causada por um bicho pequeno chamado fungo. O menino morava no campo e tinha contato com animais, por isso isso era possível. Para saber melhor, o médico pegou um pedacinho do pulmão para ver.\n\nNo exame, acharam o fungo Cryptococcus. O menino tomou remédios para matar o fungo por muitos meses. Ele melhorou bastante e as manchas no pulmão sumiram. O médico ficou feliz porque ele ficou bem.",
+            "B2": "**O que aconteceu com o paciente**\n\nUm garoto de 15 anos, que sempre foi saudável, morava numa área rural e começou a ter tosse e dor no lado do peito por um mês. Ele não teve febre nem dificuldade para respirar. Quando fizeram um raio-x do seu pulmão, viram duas manchas estranhas na parte de baixo do pulmão esquerdo. Depois, fizeram uma tomografia, que é um exame que mostra imagens mais detalhadas, e essas manchas pareciam pequenos nódulos, que são como bolinhas ou caroços.\n\n**O que os médicos pensaram e fizeram**\n\nOs médicos ficaram preocupados que esses nódulos pudessem ser um tipo de tumor, então fizeram outro exame chamado PET-TC. Esse exame mostra onde as células estão mais ativas, usando uma substância que as células “comem” para produzir energia. Os nódulos estavam muito ativos, o que pode acontecer em tumores, infecções ou inflamações.\n\nComo o menino morava numa área rural e tinha contato com fezes de aves, os médicos pensaram que poderia ser uma infecção por fungos, que são organismos parecidos com bolores. Para descobrir, fizeram uma biópsia, que é quando retiram um pedacinho do pulmão para estudar melhor.\n\n**O que descobriram**\n\nNa biópsia, encontraram um fungo chamado Cryptococcus neoformans. Esse fungo pode causar uma infecção chamada criptococose, que afeta principalmente os pulmões. O garoto não tinha problemas no sistema imunológico, ou seja, seu corpo estava forte para lutar contra doenças.\n\n**Como foi o tratamento e o resultado**\n\nEle recebeu remédios antifúngicos chamados itraconazol e fluconazol durante 10 meses. Esses medicamentos ajudaram a eliminar a infecção. Depois de algumas semanas, os exames mostraram que os nódulos ficaram menores e menos ativos. No final do tratamento, o pulmão estava praticamente normal e ele não tinha mais sintomas.\n\n**Por que isso é importante**\n\nEsse caso mostra que, mesmo em pessoas saudáveis, infecções por fungos podem acontecer, especialmente em quem vive em áreas rurais e tem contato com animais. Por isso, é importante investigar bem quando aparecem manchas nos pulmões para dar o tratamento certo e evitar problemas maiores.",
+            "B3": "**Contexto**  \nUm adolescente de 15 anos, previamente saudável e residente em área rural da Província de Buenos Aires, apresentou tosse produtiva e dor no lado esquerdo do tórax por cerca de um mês. Não houve febre nem dificuldade para respirar. Na radiografia de tórax inicial, foram observadas duas áreas de consolidação (regiões onde o pulmão apresenta densidade aumentada) na base do pulmão esquerdo. A tomografia computadorizada (TC) revelou que essas áreas tinham aspecto nodular, o que levantou suspeita de uma possível doença neoplásica (tumoral).\n\n**Principais Achados Diagnósticos**  \nPara melhor avaliação, foi realizada uma Tomografia por Emissão de Pósitrons (PET-TC), exame que detecta atividade metabólica aumentada nas lesões por meio da captação de glicose marcada. As lesões pulmonares apresentaram alta captação, sugerindo metabolismo elevado, característica comum tanto em tumores quanto em processos inflamatórios ou infecciosos. A ausência de lesões em outras regiões do corpo reforçou o foco pulmonar. Considerando o histórico epidemiológico do paciente — vivendo em ambiente rural com exposição a dejetos de aves, o que é um fator de risco para infecções fúngicas —, levantou-se a hipótese de uma micose pulmonar.\n\nExames laboratoriais gerais, incluindo hemograma, função hepática e renal, e testes para tuberculose, foram normais ou negativos. Culturas iniciais de escarro e lavagem broncoalveolar não identificaram microrganismos. Por isso, foi realizada uma punção biopsia pulmonar guiada por tomografia, que permitiu a análise direta do tecido pulmonar. Nesse material, foram identificadas leveduras (fungos unicelulares) e a cultura confirmou a presença de Cryptococcus neoformans variedade grubii, um fungo capaz de causar infecção pulmonar, especialmente em pacientes imunocomprometidos, mas que pode afetar também pessoas saudáveis.\n\nA análise histopatológica da biopsia mostrou um processo inflamatório granulomatoso (formação de aglomerados de células de defesa) com células gigantes multinucleadas e estruturas fúngicas características, sem sinais de tumor. Testes imunológicos revelaram que o paciente não apresentava comprometimento do sistema imune, incluindo sorologia negativa para HIV.\n\nApesar da detecção de altos títulos de antígeno criptocócico no sangue, a avaliação do sistema nervoso central (por tomografia e punção lombar) não evidenciou envolvimento da infecção no cérebro ou na medula espinhal, o que é uma complicação grave comum nessa micose.\n\n**Interpretação Clínica**  \nO diagnóstico final foi de criptococose pulmonar, uma infecção fúngica profunda causada pelo Cryptococcus neoformans, em um paciente imunocompetente. A apresentação clínica atípica, sem febre e com sintomas leves, associada à imagem nodular pulmonar, exigiu investigação detalhada para excluir outras causas, como câncer ou tuberculose.\n\n**Tratamento e Evolução**  \nO paciente iniciou tratamento antifúngico com itraconazol por quatro semanas, seguido de fluconazol por dez meses. Durante o tratamento, não houve efeitos colaterais significativos. A reavaliação por PET-TC após seis semanas mostrou redução do tamanho e da atividade metabólica das lesões pulmonares. Ao final do tratamento, a radiografia de tórax não evidenciou alterações significativas e a pesquisa de antígeno criptocócico no sangue foi negativa, indicando resolução da infecção. O paciente permaneceu assintomático e sem sinais de recidiva.\n\n**Próximos Passos**  \nO acompanhamento clínico e radiológico deve continuar para monitorar possíveis recidivas ou complicações. A investigação imunológica inicial sugere que o paciente não apresenta fatores predisponentes para infecções oportunistas, mas a vigilância permanece importante. Este caso destaca a importância de considerar infecções fúngicas em pacientes jovens e imunocompetentes com lesões pulmonares nodulares, especialmente em contextos epidemiológicos de risco."
+        }
+    },
+    {
+        "article": "Um menino de 12 anos foi trazido ao nosso departamento apresentando sintomas de início súbito de dor de cabeça e síndrome de poliúria-polidipsia, que começou uma semana antes da sua visita inicial. A criança não tinha histórico médico significativo. Durante a primeira avaliação clínica, ele mediu 146,5 cm de altura (M) e pesava 30 kg (-1,4 SD). Não houve sinais observados de insuficiência adrenal ou hipotireoidismo. Ele estava no início da puberdade, com tamanhos de gônadas medindo 3,2 cm de cada lado e um comprimento do pênis de 6,2 cm (M). Notavelmente, o paciente apresentou síndrome de poliúria-polidipsia, com excreção de fluido atingindo até 113 ml/kg/dia, enurese noturna e uma ingestão excessiva de líquido de 3,8 litros/m². O exame oftalmológico produziu resultados esperados, sem deficiências visuais detectadas e achados normais de tomografia de coerência óptica (OCT).\n\nA avaliação biológica revelou DI, com um nível de sódio no soro de 140 mEq/l e uma osmolaridade plasmática de 287 mosm/kg, enquanto a osmolaridade da urina foi significativamente baixa a 179 mosm/kg. Além disso, os níveis séricos de fator de crescimento semelhante à insulina-1 (IGF1), prolactina (PRL), T4 livre, cortisol, hormônio folículo-estimulante (FSH) e hormônio luteinizante (LH) estavam dentro da faixa normal.\n\nAs imagens de ressonância magnética com e sem contraste destacaram a apoplexia num RCC, mostrando uma hiperintensidade espontânea nas sequências T1 e T2 de 15x6x11 mm. A glândula pituitária anterior apresentou uma absorção de contraste homogénea. No entanto, observámos uma perda da hiperintensidade típica da glândula pituitária posterior, sem indicações radiológicas de um craniopharyngioma. Por conseguinte, durante a avaliação hormonal inicial, a única deficiência hormonal identificada no nosso caso foi a DI, que apresentou uma melhoria significativa sob tratamento com vasopressina. O caso foi revogado numa reunião multidisciplinar, incluindo um endocrinologista, um neurocirurgião e um radiologista. Dada a ausência de sinais clínicos ou biológicos para além da DI e a estabilidade da apoplexia do RCC ao longo de nove meses de monitorização por ressonância magnética - com medidas de 12 × 11 × 10 mm - foi escolhido um método de gestão conservador com acompanhamento regular.\n\nA criança foi monitorada por três anos, durante os quais apresentou desenvolvimento normal da puberdade e manteve um perfil hormonal estável (Tabela 1). Avaliações visuais não revelaram anormalidades. No entanto, uma diminuição na velocidade de crescimento foi observada, caindo de -0.8 SD para -1.1 SD. Isso exigiu uma investigação para deficiência adquirida de hormônio do crescimento (GH). Aos 14 anos e nove meses, a criança foi readmitida para passar por dois testes de estimulação de GH: um teste de propranolol-glucagon e um teste de tolerância à insulina, que indicou uma deficiência parcial de GH com picos de 19.3 µUI/ml e 10.0 µUI/ml, respectivamente. Depois de receber tratamento com GH, o paciente apresentou um aumento notável na velocidade de crescimento, melhorando de -1.1 SD para 0.2 SD em um ano.\n\nSubsequentemente, o monitoramento por ressonância magnética mostrou uma aparência estável da apoplexia do CCR após dois anos (11 × 12 × 11 mm), com uma ligeira diminuição no tamanho observada no acompanhamento de três anos, medindo 7 × 10 × 6 mm. É importante notar que o acompanhamento radiológico foi consistentemente conduzido no mesmo centro de ressonância magnética, com o mesmo radiologista interpretando os achados de ressonância magnética recentes e anteriores durante reuniões multidisciplinares que incluíam um endocrinologista e um neurocirurgião.\n",
+        "gold_summary": "Apresentamos o caso de um menino de 12 anos admitido devido ao aparecimento recente de dores de cabeça e diabetes insipidus. A ressonância magnética revelou apoplexia do cisto de Rathke. Dada a ausência de sintomas de compressão num menino nas fases iniciais da puberdade e sem anomalias nos testes básicos de endócrino, foi empregue uma estratégia conservadora, que envolveu seguimentos clínicos, biológicos e radiológicos regulares. O menino teve uma puberdade normal sem quaisquer deficiências endócrinas exceto uma deficiência parcial da hormona de crescimento.\n",
+        "synthetic_summary": {
+            "B1": "Um menino de 12 anos começou a sentir dor de cabeça. Ele também precisava beber muita água e fazer xixi muito. O médico fez um exame especial chamado ressonância e viu um cisto no cérebro dele.\n\nO menino estava começando a crescer como os adultos, e ele estava bem. O médico não viu nada muito errado no corpo dele. Então, eles decidiram cuidar dele com calma, olhando ele sempre para ver se estava tudo bem.\n\nO menino cresceu normalmente, só precisou de um remédio para ajudar a crescer um pouco mais. Ele ficou bem e os médicos continuaram olhando para ele com cuidado.",
+            "B2": "**O que aconteceu com o menino**\n\nUm menino de 12 anos começou a sentir dores de cabeça fortes e a beber muita água, além de urinar muito. Esses sintomas indicaram uma condição chamada diabetes insipidus, que faz o corpo perder muita água. Para entender melhor o que estava acontecendo, os médicos fizeram uma ressonância magnética, que é um exame que tira fotos detalhadas do cérebro. Esse exame mostrou que ele tinha um cisto chamado cisto de Rathke, que sofreu uma apoplexia — isso significa que houve um sangramento ou uma lesão dentro do cisto.\n\n**Como os médicos cuidaram dele**\n\nComo o menino estava no começo da puberdade e não apresentava outros problemas hormonais ou sinais de que o cisto estava pressionando partes importantes do cérebro, os médicos decidiram não fazer cirurgia. Em vez disso, escolheram acompanhar o caso com exames regulares para ver se o cisto mudava e para controlar a saúde dele.\n\n**O que aconteceu depois**\n\nDurante o acompanhamento, o menino teve uma puberdade normal e não apresentou outras dificuldades hormonais, exceto por uma deficiência parcial do hormônio do crescimento. Esse hormônio é importante para o crescimento do corpo. Quando os médicos perceberam isso, ele começou a receber um tratamento com esse hormônio e, em pouco tempo, passou a crescer melhor.\n\n**Conclusão**\n\nEsse caso mostra que, mesmo com um cisto no cérebro que sofreu uma apoplexia, é possível cuidar do paciente de forma cuidadosa e sem cirurgia, desde que ele seja monitorado direitinho. O tratamento ajudou o menino a crescer normalmente e a ter uma vida saudável.",
+            "B3": "**Contexto**  \nEste relato descreve o caso de um menino de 12 anos que apresentou de forma súbita dores de cabeça associadas a sintomas de poliúria-polidipsia (urinar e beber líquidos em excesso), sinais típicos de diabetes insipidus (DI), uma condição em que os rins não conseguem concentrar a urina adequadamente. O paciente não tinha histórico médico relevante e encontrava-se no início da puberdade, com desenvolvimento físico compatível para a idade.\n\n**Principais Achados**  \nExames laboratoriais confirmaram o diagnóstico de diabetes insipidus, evidenciado por níveis normais de sódio e osmolaridade plasmática, porém com osmolaridade urinária muito baixa, indicando perda excessiva de água pela urina. Outros hormônios importantes para o crescimento e função endócrina — como IGF-1, prolactina, hormônios da tireoide, cortisol, FSH e LH — estavam dentro dos valores normais.  \n\nA ressonância magnética do cérebro revelou uma apoplexia (sangramento ou necrose súbita) em um cisto de Rathke (uma lesão benigna localizada na região da hipófise, glândula que regula vários hormônios). Essa apoplexia causou perda da característica normal da parte posterior da hipófise na imagem, mas não houve sinais de tumores malignos ou compressão de estruturas vizinhas.\n\n**Interpretação Clínica**  \nDiante da ausência de sintomas graves, como compressão de nervos ópticos ou outras deficiências hormonais além do diabetes insipidus, optou-se por um manejo conservador, com acompanhamento clínico, hormonal e por imagem ao longo do tempo. Durante três anos, o menino apresentou desenvolvimento puberal normal e estabilidade hormonal, exceto por uma redução na velocidade de crescimento que levou à investigação de deficiência parcial do hormônio do crescimento (GH). Testes específicos confirmaram essa deficiência, e o tratamento com GH resultou em melhora significativa da velocidade de crescimento.\n\nAs imagens de ressonância magnética mostraram estabilidade e até uma leve redução do tamanho do cisto com apoplexia ao longo do acompanhamento, reforçando a decisão pelo tratamento conservador.\n\n**Próximos Passos e Considerações**  \nEste caso destaca a importância do monitoramento multidisciplinar (endocrinologia, neurocirurgia e radiologia) em pacientes com apoplexia de cisto de Rathke e diabetes insipidus. A abordagem conservadora pode ser eficaz quando não há sinais de compressão ou múltiplas deficiências hormonais, permitindo o desenvolvimento puberal normal e o controle das complicações hormonais que possam surgir, como a deficiência de GH. O acompanhamento regular por exames clínicos, laboratoriais e de imagem é fundamental para detectar precocemente qualquer alteração que exija intervenção."
+        }
+    },
+    {
+        "article": "Homem de 60 anos com antecedentes de adenocarcinoma prostático Gleason 8 (4+4) que afetava ambos os lobos prostáticos, tratado com prostatectomia radical e linfadenectomia ilio-obturativa (pT3b-N0-Mx). Apresentou, após 2 anos de controle, recaída bioquímica (antígeno prostático específico de 1.9 ng/mL) e pequena adenopatia hipogástrica hipermetabólica subcentimétrica (S.U.V.: 3.8) visível em PET TC com Fluorocolina.\n\nFoi decidido, em um centro multidisciplinar, realizar uma linfadenectomia de resgate, com marcação pré-cirúrgica com carbono ativado guiada por imagem. Devido à profundidade do linfonodo, foi decidido realizar uma marcação pré-cirúrgica com anestesia local por tomografia computadorizada antes da cirurgia. A adenopatia estava rodeada pela artéria e veia hipogástrica para a frente e para o lado, respectivamente, e pela raiz nervosa de L5 para trás. A margem medial estava livre. Devido à disposição destas estruturas ao redor do objetivo, foi planejada uma marcação com abordagem contralateral, através de acesso trans-sacro com agulha T-Lok Bone Marrow Biopsy Standard de 4\", 11 Gauge (Argon Medical). Foi realizada uma anestesia, por planos, até alcançar o periósteo superficial do sacro, com lidocaína a 2% (10 cm3). No entanto, uma vez iniciado o procedimento, o peristaltismo intestinal mobilizou o cólon sigmoide no trajeto da agulha. Para evitar a transgressão de víscera oca, foi realizada uma hidrodissecção através de solução contrastada diluída para deslocá-la. Foi realizada uma progressão do instrumental sob supervisão tomográfica para garantir o deslocamento do cólon e, finalmente, a marcação foi realizada de forma coaxial com 1 ml de carbono ativado a 4% (Temis Lostaló) através de uma agulha tipo Chiba de 15 cm, 20 Gauge (Argon Medical).\n\nApós a marcação, as agulhas foram removidas e uma tomografia final foi realizada, sem complicações relacionadas ao procedimento. Após um breve período de observação no departamento de diagnóstico por imagem, o paciente foi transferido para a sala de cirurgia sem dor ou distúrbios hemodinâmicos. A cirurgia foi realizada sem complicações e o linfonodo marcado foi removido. A anatomia patológica confirmou linfonodo com infiltração por carcinoma.\n",
+        "gold_summary": "Homem de 60 anos com histórico de adenocarcinoma prostático em plano de ressecção de adenopatia hipogástrica. Foi indicada marcação pré-cirúrgica por guia de imagem.\n\nResultados: A marcação pré-cirúrgica foi realizada com anestesia local sob tomografia computadorizada com acesso transósseo e hidrodissecção.\n",
+        "synthetic_summary": {
+            "B1": "Um homem de 60 anos tinha um problema no osso perto da barriga. Os médicos precisavam encontrar um lugar pequeno para tirar. \n\nPara isso, eles usaram uma agulha fina e colocaram uma tinta preta para marcar o lugar. \n\nAntes de fazer isso, deram um remédio para não sentir dor. Usaram uma máquina para ver direitinho onde colocar a agulha. \n\nTudo correu bem e o homem não sentiu dor. Depois, os médicos conseguiram tirar o pedacinho marcado com segurança.",
+            "B2": "**Caso do Paciente e o Problema**\n\nUm homem de 60 anos teve um câncer na próstata chamado adenocarcinoma, que foi tratado com cirurgia para retirar a próstata e alguns gânglios linfáticos próximos. Depois de dois anos, exames mostraram que o câncer pode ter voltado, porque o nível de uma substância chamada antígeno prostático específico (PSA) aumentou. Um exame especial chamado PET TC identificou um pequeno gânglio linfático (adenopatia) que parecia estar afetado pelo câncer.\n\n**O Que Foi Feito Antes da Cirurgia**\n\nPara ajudar os médicos a encontrar exatamente esse gânglio durante a cirurgia, eles decidiram marcar ele antes da operação. Essa marcação foi feita usando imagens de tomografia computadorizada (uma espécie de raio-x detalhado) para guiar a colocação de um marcador especial chamado carbono ativado. O carbono ativado é uma tinta que ajuda a mostrar o gânglio para o cirurgião.\n\n**Como Foi Realizada a Marcação**\n\nA marcação foi feita com anestesia local, ou seja, o paciente ficou acordado, mas a área onde a agulha passou foi anestesiada para não sentir dor. A agulha foi inserida através do osso do sacro (uma parte da coluna perto do quadril), porque o gânglio estava em um lugar difícil de alcançar. Para evitar machucar o intestino, que estava perto do caminho da agulha, os médicos usaram uma técnica chamada hidrodissecção. Isso significa que eles injetaram um líquido para afastar o intestino e criar espaço seguro para a agulha passar.\n\n**O Resultado**\n\nA marcação foi feita com sucesso, sem causar dor ou problemas para o paciente. Depois, a cirurgia para remover o gânglio marcado foi realizada sem complicações. A análise do gânglio mostrou que ele realmente estava infiltrado pelo câncer, confirmando a necessidade da cirurgia.\n\n**Por Que Isso É Importante**\n\nMarcar o gânglio antes da cirurgia ajudou os médicos a encontrá-lo com precisão, mesmo estando em um lugar difícil e perto de órgãos importantes. Esse procedimento torna a cirurgia mais segura e eficaz para o paciente.",
+            "B3": "**Contexto**  \nTrata-se de um homem de 60 anos com diagnóstico prévio de adenocarcinoma prostático agressivo (Gleason 8, padrão 4+4), que acometia ambos os lobos da próstata. Após tratamento inicial com prostatectomia radical e remoção dos linfonodos ilio-obturatórios, o paciente apresentou, dois anos depois, uma elevação do antígeno prostático específico (PSA) para 1,9 ng/mL, indicando possível recidiva da doença. Um exame de PET-TC com Fluorocolina identificou uma pequena adenopatia (linfonodo aumentado) hipermetabólica na região hipogástrica, sugerindo atividade tumoral.\n\n**Principais Achados**  \nPara tratar essa recidiva localizada, foi planejada uma cirurgia de resgate para remoção do linfonodo suspeito. Devido à profundidade e à localização complexa do linfonodo, que estava rodeado por importantes vasos sanguíneos (artéria e veia hipogástrica) e pela raiz nervosa do nervo L5, optou-se por uma marcação pré-cirúrgica guiada por tomografia computadorizada (TC). Essa marcação foi realizada por via transóssea (através do osso do sacro), com anestesia local aplicada em camadas até o periósteo (membrana que reveste o osso). Durante o procedimento, o cólon sigmoide (parte do intestino) foi deslocado pelo movimento intestinal, o que poderia dificultar a passagem segura da agulha. Para evitar perfuração intestinal, foi realizada uma hidrodissecção: uma técnica que utiliza a injeção de solução líquida contrastada para afastar o intestino do trajeto da agulha. A marcação definitiva do linfonodo foi feita com injeção de carbono ativado, um material que facilita a identificação cirúrgica do tecido alvo.\n\n**Interpretação Clínica**  \nO procedimento de marcação pré-cirúrgica guiada por imagem, utilizando acesso transósseo e hidrodissecção para proteger estruturas adjacentes, foi realizado com sucesso e sem complicações. A técnica permitiu a localização precisa do linfonodo suspeito, facilitando sua remoção cirúrgica. A análise patológica confirmou a presença de infiltração por carcinoma no linfonodo, confirmando a recidiva tumoral.\n\n**Próximos Passos**  \nCom a remoção bem-sucedida do linfonodo comprometido, o paciente poderá ser avaliado para definir o tratamento adjuvante adequado, que pode incluir radioterapia ou terapia hormonal, dependendo da extensão da doença e dos níveis de PSA. O acompanhamento clínico e por imagem continuará essencial para monitorar possíveis novas recidivas."
+        }
+    },
+    {
+        "article": "Uma paciente de onze anos de idade com dor lombar por cinco anos associada a radiação bilateral para as extremidades inferiores, que é mais pronunciada no lado esquerdo. A dor foi insidiosa no início, piorando ao longo de um período de 2 meses. No exame neurológico, a força motora tornou-se 3/5 na flexão do quadril e extensão do joelho; a outra força muscular da extremidade inferior foi 5/5; o tônus foi normotônico; e os reflexos foram +2 em todos os tendões profundos. Ela foi encaminhada ao nosso centro para intervenção cirúrgica; caso contrário, não tinha histórico de trauma espinhal ou qualquer procedimento espinhal, incluindo um toque lombar.\n\nOs exames laboratoriais no dia da admissão incluíram um hemograma completo e estudos bioquímicos, que não mostraram anormalidades aparentes. A ressonância magnética lombo-sacral com contraste mostrou lesões hipocinéticas tipo 1 (T1) e hipercinéticas tipo 2, 6 cm caudo-cranial e 2 cm antero-posterior, lesões expansivas que se estendiam de L2 a L4 com envolvimento do cone e da cauda equina. Mostrou um aumento marginal após a administração de contraste. Na sala de operações, sob anestesia geral, foi feita uma posição propensa e uma incisão vertical na pele para expor a área operada. Uma laminectomia completa de L2 a L4 com laminectomia parcial de L1/L5 é feita, pois o tumor se estende em ambos os pólos, craniano e caudal, e a dura-máter é aberta na linha média. Durante a operação, a massa ancorou o cone intraduralmente, preenchendo o canal espinal e deslocando as raízes caudas anteriores e laterais, com aderência às raízes nervosas em ambos os lados de L2 a L4. O exame microscópico cirúrgico revelou um cisto de parede fina com conteúdo cinzento. Não tínhamos mais potencial motor evocado intraoperativo (MEP), potencial evocado sensorial (SEP), eletromiografia (EMG) ou aspirador cirúrgico ultrassônico (CUSA) para a redução da massa; por esta razão, não os utilizamos neste caso. A dissecção do tumor começou no sulco médio posterior. Poucas revisões defenderam o uso de ultrassom antes da mielotomia em casos difíceis. O conteúdo do cisto branco é expelido sem esforço, pois é sugável; a parede do cisto foi parcialmente excisada e a cápsula, que aderiu firmemente ao parênquima da medula espinal, foi deixada em algumas áreas para não sacrificar o tecido nervoso numa tentativa de realizar uma capsulectomia total. Cuidados foram tomados para evitar o derramamento do cisto na área subaracnóidea. Uma ressonância magnética lombo-sacral pós-operativa confirmou a excisão quase total. O conteúdo do cisto semelhante a gel e a sua parede foram enviados para exame histopatológico, que confirmou um cisto fibroso fragmentado revestido por células escamosas estratificadas maduras com manchas de queratina e fragmentos de músculo liso, que são típicos de cistos epidermóides. O percurso pós-operativo foi sem incidentes; a dor tinha sido resolvida, a função motora e sensorial estavam intactas e a paciente foi dada alta no terceiro dia pós-operativo. Ela foi seguida na nossa clínica de ambulatório durante os últimos 6 meses; durante o acompanhamento, a dor tinha sido resolvida, o exame neurológico não tinha tido incidentes.\n",
+        "gold_summary": "Uma paciente de 11 anos de idade apresentou dor nas costas com irradiação para ambas as extremidades inferiores, mas que piorou no lado esquerdo durante 5 anos. No exame neurológico, a força motora foi de 3/5 para flexão do quadril e extensão do joelho bilateralmente e 5/5 para outros grupos musculares importantes. A ressonância magnética lombo-sacral (MRI) com contraste revelou lesões hipointensas T1 e hiperintensas T2 no cone intramedular L2-L4 e cauda equina. A laminectomia e a ressecção quase total foram feitas, e o exame histopatológico revelou um cisto epidermóide. No terceiro dia pós-operatório, a paciente foi dispensada com a dor nas costas completamente resolvida e uma melhora na força motora das extremidades inferiores. Nas visitas de acompanhamento mensais por mais 6 meses, a dor nas costas e a fraqueza da paciente foram completamente resolvidas, e ela não apresentou déficits neurológicos. Uma ressonância magnética lombo-sacral pós-operatória foi feita e confirmou a excisão quase total do tumor.\n",
+        "synthetic_summary": {
+            "B1": "Uma menina de 11 anos sentia muita dor nas costas e nas pernas. A dor estava pior no lado esquerdo. Ela tinha dificuldade para mexer a perna e o joelho.\n\nOs médicos fizeram um exame para ver dentro das costas dela. Eles acharam um caroço que estava apertando os nervos.\n\nEla fez uma cirurgia para tirar quase todo o caroço. Depois da cirurgia, a dor sumiu. Ela conseguiu mexer melhor as pernas.\n\nDepois de seis meses, ela estava bem e sem dor. Os médicos fizeram outro exame e viram que o caroço quase não estava mais lá. Ela ficou saudável e feliz.",
+            "B2": "**O que aconteceu com a paciente**\n\nUma menina de 11 anos sentia dor nas costas há cinco anos. Essa dor também chegava até as pernas, principalmente do lado esquerdo. Com o tempo, a dor piorou e ela começou a ter dificuldade para mexer os quadris e os joelhos, ficando mais fraca nessas partes.\n\n**O que os exames mostraram**\n\nOs médicos fizeram uma ressonância magnética, que é um exame que usa imagens para ver dentro do corpo. Esse exame mostrou que havia uma lesão, que é como um caroço ou uma área diferente, na parte baixa da medula espinhal, entre as vértebras L2 e L4. Essa lesão estava pressionando os nervos que vão para as pernas.\n\n**Como foi o tratamento**\n\nPara ajudar a menina, os médicos fizeram uma cirurgia chamada laminectomia. Nessa cirurgia, eles abriram a coluna para tirar quase todo o cisto, que é uma bolha com líquido ou material dentro. Esse cisto era do tipo epidermóide, que é formado por células da pele que cresceram no lugar errado dentro da medula.\n\nDurante a cirurgia, os médicos tomaram cuidado para não machucar os nervos importantes. Eles conseguiram remover quase todo o cisto, deixando só um pouco que estava grudado para proteger a medula.\n\n**O que aconteceu depois da cirurgia**\n\nNo terceiro dia após a cirurgia, a dor da menina tinha desaparecido e a força nas pernas melhorou bastante. Ela recebeu alta do hospital e, durante os seis meses seguintes, continuou sem sentir dor ou fraqueza. Novos exames confirmaram que o cisto foi removido quase por completo.\n\n**Por que isso é importante**\n\nEsse caso mostra que, mesmo quando uma criança tem dor nas costas e fraqueza por muito tempo, é possível encontrar a causa e tratá-la com sucesso. A cirurgia ajudou a menina a voltar a se sentir bem e a usar as pernas normalmente.",
+            "B3": "**Contexto**  \nUma menina de 11 anos apresentou dor lombar persistente por cinco anos, irradiando para ambas as pernas, com maior intensidade no lado esquerdo. A dor começou de forma gradual e piorou progressivamente ao longo de dois meses. No exame neurológico, observou-se uma redução da força muscular para 3/5 na flexão do quadril e extensão do joelho em ambos os lados, enquanto os demais músculos das pernas mantinham força normal (5/5). Os reflexos estavam preservados e o tônus muscular era normal. Não havia histórico de trauma ou procedimentos na coluna.\n\n**Principais Achados Diagnósticos**  \nA ressonância magnética da região lombossacral com contraste revelou uma lesão expansiva intradural, estendendo-se das vértebras L2 a L4, envolvendo o cone medular (extremidade inferior da medula espinhal) e a cauda equina (conjunto de raízes nervosas). A lesão apresentava sinais típicos de cisto, com áreas hipointensas em T1 e hiperintensas em T2, além de realce marginal após contraste, sugerindo um processo expansivo benigno.\n\n**Intervenção Cirúrgica**  \nFoi realizada uma laminectomia (remoção parcial das lâminas vertebrais) de L2 a L4, com extensão parcial para L1 e L5, para acesso ao tumor. Durante a cirurgia, a massa foi encontrada aderida às raízes nervosas, preenchendo o canal espinhal e ancorando o cone medular. O conteúdo do cisto, de aspecto gelatinoso, foi cuidadosamente aspirado, e a parede do cisto foi parcialmente removida, preservando áreas aderidas ao tecido nervoso para evitar danos. A dura-máter (membrana que envolve a medula) foi aberta para permitir a remoção. Cuidados especiais foram tomados para evitar o vazamento do conteúdo do cisto na área subaracnóidea (espaço ao redor da medula).\n\n**Diagnóstico Histopatológico**  \nO exame microscópico confirmou tratar-se de um cisto epidermóide, caracterizado por uma parede fina revestida por células escamosas estratificadas maduras e presença de queratina, além de fragmentos de músculo liso, características típicas desse tipo de cisto benigno.\n\n**Evolução Pós-Operatória e Seguimento**  \nA paciente teve uma recuperação sem complicações, com resolução completa da dor lombar e melhora significativa da força muscular nas pernas. Ela recebeu alta hospitalar no terceiro dia após a cirurgia. Durante o acompanhamento ambulatorial de seis meses, não houve recidiva dos sintomas nem déficits neurológicos. A ressonância magnética realizada após a cirurgia confirmou a remoção quase total do cisto.\n\n**Conclusão**  \nEste caso ilustra a importância do diagnóstico preciso e da intervenção cirúrgica cuidadosa em cistos epidermóides intradurais da coluna lombar, que podem causar sintomas neurológicos progressivos em crianças. A abordagem cirúrgica adequada permitiu a resolução dos sintomas e a preservação da função neurológica da paciente."
+        }
+    },
+    {
+        "article": "Mulher de 31 anos, natural e proveniente de Lima, Peru, sem alergia a fármacos conhecidos, sem antecedentes de interesse nem hábitos nocivos. Ingressou no serviço de Emergência apresentando dor abdominal no flanco direito de vários dias de evolução, a qual se acompanhava de náuseas e vómitos, quatro dias antes do seu ingresso adicionou-se febre e depois constipação. O hemograma, amilase e lipase não mostraram alterações, e a determinação sérica de beta-HCG resultou negativa. A ecografia abdominal reportou litíase vesicular e abundante meteorismo intestinal. Em Emergência, perante a dor abdominal persistente, vómitos biliosos, distensão abdominal marcada e ausência de peristaltismo, foi-lhe realizada uma laparotomia exploratória, sem achados que explicassem o quadro, encontrando-se um tumor pequeno no íleo, que histopatologicamente correspondia a um quisto benigno de parede do intestino delgado sem atipia. A evolução pós-operatória foi favorável e, apesar da persistência da dor abdominal, que era de menor intensidade em comparação ao ingresso, foi dada de alta seis dias depois.\n\nTrês dias após a alta, a paciente apresentou convulsões tônico-clônicas generalizadas em casa, sendo reinternada. A tomografia cerebral e a punção lombar foram normais. O quadro apresentado resume os exames auxiliares solicitados. No terceiro dia de internação, apresentou alucinações visuais e convulsões, apesar da administração de antiepilépticos. No quinto dia, apresentou diminuição da força muscular em ambas as pernas, com arreflexia bilateral. No oitavo dia, apresentou taquicardia sinusal, paraparesia flácida e hipotonia, dificuldade respiratória e acidose respiratória grave, sendo internada em ventilação mecânica. O perfil tireoidiano, os anticorpos antinucleares e os complementos C3 e C4 foram encontrados em níveis normais.\n\nAs manifestações clínicas da paciente (dor abdominal, convulsões, alucinações visuais e diminuição da força muscular) e a mudança de cor da urina, fizeram suspeitar de uma crise aguda de porfiria, confirmando-se o diagnóstico com a determinação de níveis elevados do ácido delta aminolevulínico. Iniciou-se a administração de betabloqueadores e soluções de glicose. Por outro lado, também se considerou o uso de hemina, no entanto, o fármaco não se encontrava disponível no país.\n\nPor causa do comprometimento neuromuscular acentuado, e apesar de ter iniciado fisioterapia, foi difícil a retirada da ventilação mecânica, permanecendo em ventilação mecânica por seis semanas, com infecções nosocomiais sobrepostas.\n\nApós cinco semanas de hospitalização, o arginato de hemina foi administrado em doses de 4 mg/kg/dia. No segundo dia de administração, foi decidido suspender o tratamento devido à hipertransaminemia, para que, após 48 horas de normalização, fosse reiniciado o tratamento até completar quatro dias de tratamento. Uma semana depois, houve melhora da função muscular, com recuperação da mobilidade nos pés, iniciando-se a retirada progressiva da ventilação mecânica, levando quatro semanas para ser retirada definitivamente, após o que a paciente recebeu alta, com indicação de fisioterapia e terapia ocupacional.\n",
+        "gold_summary": "Paciente com PAI, que apresentava abdômen agudo, convulsões, posteriormente comprometimento neuro-psiquiátrico e neuropatia motora simétrica, sendo internado em ventilação mecânica. Devido à gravidade do comprometimento neurológico, recebeu arginato de hemina, apresentando hipertransaminemia transitória, evento adverso não relatado previamente. A evolução foi favorável, sendo retirada a ventilação mecânica e o paciente recebeu alta hospitalar.\n",
+        "synthetic_summary": {
+            "B1": "Uma mulher ficou com muita dor na barriga. Depois, ela teve convulsões e ficou com os músculos fracos. Ela precisou de uma máquina para ajudar a respirar. Os médicos deram um remédio especial para ajudar o corpo dela. Ela ficou um pouco doente por causa do remédio, mas melhorou. Depois, ela conseguiu sair da máquina e ir para casa.",
+            "B2": "**O que aconteceu com a paciente**\n\nUma mulher de 31 anos teve muita dor na barriga, vômitos e febre. Ela foi levada ao hospital, onde fizeram uma cirurgia para ver o que estava acontecendo. Encontraram um pequeno cisto (que é um tipo de bolha) no intestino, mas ele não era perigoso. Depois de alguns dias, ela teve convulsões (movimentos involuntários do corpo) e começou a ter problemas para andar e sentir fraqueza nas pernas.\n\n**Os sintomas e o diagnóstico**\n\nAlém das convulsões, ela teve alucinações (ver coisas que não existem) e dificuldade para respirar. Os médicos perceberam que esses sintomas, junto com a mudança na cor da urina, indicavam uma doença chamada porfiria. A porfiria é um problema que afeta a produção de uma substância importante para o corpo, causando vários sintomas no sistema nervoso e na pele.\n\n**O tratamento e a recuperação**\n\nPara tratar a porfiria, a paciente recebeu um remédio chamado arginato de hemina, que ajuda a controlar a doença. Durante o tratamento, ela teve um efeito colateral no fígado, mas isso melhorou depois de parar o remédio por um tempo. Ela ficou em ventilação mecânica (um aparelho que ajuda a respirar) por várias semanas, mas com o tratamento e a fisioterapia, conseguiu melhorar a força muscular e respirar sozinha novamente. Depois, teve alta do hospital e continuou a se recuperar com ajuda de terapias.",
+            "B3": "**Contexto**  \nTrata-se de uma mulher de 31 anos, sem antecedentes médicos relevantes, que inicialmente apresentou dor abdominal intensa no lado direito, acompanhada de náuseas, vômitos e febre. Exames iniciais não revelaram alterações significativas, e uma cirurgia exploratória identificou um pequeno cisto benigno no intestino delgado, sem explicar completamente os sintomas. Após alta hospitalar, a paciente desenvolveu convulsões generalizadas, alucinações visuais e fraqueza muscular progressiva nas pernas, evoluindo para insuficiência respiratória grave que exigiu ventilação mecânica.\n\n**Principais Achados**  \nDurante a internação, exames neurológicos e laboratoriais descartaram causas comuns para o quadro, mas a combinação de sintomas — dor abdominal, alterações neurológicas e mudança na cor da urina — levantou a suspeita de uma crise aguda de porfiria, uma doença metabólica rara que afeta a produção de heme (um componente essencial do sangue). O diagnóstico foi confirmado pela elevação do ácido delta-aminolevulínico no sangue. O tratamento inicial incluiu betabloqueadores e administração de glicose, mas a hemina, medicamento específico para a porfiria, não estava disponível no país.\n\nApós seis semanas em ventilação mecânica e complicações infecciosas, foi possível iniciar o tratamento com arginato de hemina. Durante a terapia, a paciente apresentou um aumento temporário das enzimas hepáticas (hipertransaminemia), um efeito colateral não descrito anteriormente para esse medicamento. O tratamento foi temporariamente suspenso e reiniciado após normalização dos exames, totalizando quatro dias de terapia.\n\n**Interpretação Clínica**  \nA paciente apresentou um quadro grave de porfiria aguda, manifestando-se inicialmente com sintomas abdominais e evoluindo para comprometimento neurológico severo, incluindo convulsões, alterações psiquiátricas e neuropatia motora simétrica. A necessidade prolongada de ventilação mecânica refletiu a gravidade do comprometimento neuromuscular. A introdução do arginato de hemina foi fundamental para a recuperação, apesar da ocorrência de uma toxicidade hepática transitória, que foi manejada com sucesso.\n\n**Próximos Passos**  \nApós a melhora da função muscular e a retirada gradual da ventilação mecânica, a paciente recebeu alta hospitalar com indicação de fisioterapia e terapia ocupacional para reabilitação motora. É importante o acompanhamento clínico contínuo para monitorar possíveis recidivas da porfiria e efeitos tardios do tratamento, além de orientações para evitar fatores desencadeantes da doença."
+        }
+    },
+    {
+        "article": "Apresentamos o caso de um homem de 51 anos que começou com pensamentos paranoides, alucinações auditivas e comportamento viciante aos 20 anos. Foi diagnosticado com esquizofrenia paranoide e tratado com antipsicóticos de primeira geração. Nos anos seguintes, o paciente teve várias internações hospitalares e em instituições psiquiátricas. Desde 2005, sua evolução foi parcialmente satisfatória. Ele mantinha uma relativa independência e fazia terapia ocupacional, com grande apoio familiar.\n\nNo final de 2014, o paciente desenvolveu uma síndrome rígida acinética. Ele estava sendo tratado com clozapina (200 mg/dia) e aripiprazol (15 mg/dia), além de triexifenidila (5 mg/dia), lorazepam e trazodona. A interferência dopaminérgica foi minimizada. Um DaTscan® foi realizado e foi patológico. Doses mínimas de levodopa foram testadas, mas os sintomas psicóticos se agravaram. Com apenas 150 mg de levodopa/dia, o paciente desenvolveu novamente ideias de dano e perseguição, e alucinações, e até mesmo precisou ser hospitalizado. Foi então decidido usar uma solução pediátrica de levodopa (5 mg/mL), embora o paciente não tolerasse doses acima de 4 mL, que só conseguiam um alívio mínimo.\n\nA doença progrediu significativamente. Em 2019, ele apresentava acentuada rigidez e acinesia bilateral, sendo incapaz de ficar em pé ou de dar alguns passos sem ajuda. Ele também apresentava disfagia e sialorreia. Ele perdeu muito peso e desenvolveu acentuada atrofia muscular devido à sua pouca mobilidade.\n\n\nNessa situação, o paciente foi avaliado para estimulação cerebral profunda subtalâmica (ECP-NST) por compaixão, como a única maneira de obter uma melhora motora em seu caso. Não foi feito teste de levodopa devido ao histórico dele, e ele também não conseguiu completar a avaliação neuropsicológica pré-cirúrgica. Finalmente, o paciente foi operado em fevereiro de 2020 com anestesia geral, sem complicações.\n\nSeis meses após a ECP-NST, a melhora foi muito evidente. O paciente foi capaz de ficar de pé sem ajuda e a marcha melhorou significativamente. Ele tinha acinesia bilateral moderada, predominantemente nas extremidades esquerdas. Além disso, a gravidade da disfagia e da sialorreia diminuiu significativamente. O tratamento com levodopa foi interrompido, enquanto o tratamento antipsicótico não foi alterado. Não identificamos piora nos sintomas psiquiátricos. A escala de sintomas positivos e negativos é um questionário de 30 perguntas com sete respostas possíveis, onde pontuações mais altas refletem um estado pior. Um ano após a intervenção, houve uma leve melhora na pontuação da escala, especialmente em relação aos sintomas negativos. Estes sintomas melhoraram em paralelo com a melhora na qualidade de vida. A família confirmou maior habilidade de comunicação, maior espontaneidade e maior velocidade de raciocínio. O estado cognitivo global, avaliado pela escala de demência de Mattis, não foi alterado após a intervenção.\n",
+        "gold_summary": "Apresentamos o caso de um paciente com doença de Parkinson idiopática e esquizofrenia, com má tolerância a doses mínimas de levodopa, que apresentou uma grande melhora após a estimulação cerebral profunda subtalâmica bilateral (ECP-NST). A ECP-NST foi considerada aqui, devido à gravidade deste caso particular, como a única possibilidade de conseguir uma melhora motora.\n",
+        "synthetic_summary": {
+            "B1": "Um homem estava muito doente. Ele tinha um problema que mexia com seu corpo e sua cabeça. Ele não podia tomar um remédio que ajudava outras pessoas, porque ficava pior.\n\nOs médicos fizeram uma cirurgia especial no cérebro dele. Depois da cirurgia, ele ficou muito melhor. Ele conseguiu mexer o corpo com mais facilidade. Isso deixou ele e a família muito felizes.",
+            "B2": "**O que aconteceu com o paciente**\n\nEste é o caso de um homem de 51 anos que tem duas doenças: esquizofrenia, que causa pensamentos e sensações estranhas, e doença de Parkinson, que dificulta os movimentos do corpo. Ele não conseguia tomar o remédio chamado levodopa, que ajuda a melhorar os sintomas do Parkinson, porque mesmo doses pequenas causavam piora nas alucinações e nos pensamentos ruins.\n\n**O que foi feito para ajudar**\n\nComo os remédios não funcionavam bem, os médicos decidiram tentar um tratamento chamado estimulação cerebral profunda subtalâmica (ECP-NST). Esse tratamento é uma cirurgia que coloca pequenos eletrodos no cérebro para ajudar a controlar os problemas de movimento.\n\n**O que mudou depois da cirurgia**\n\nSeis meses após a cirurgia, o paciente melhorou bastante. Ele conseguiu ficar em pé e andar melhor, sem precisar de ajuda. Também teve menos dificuldade para engolir e menos saliva escorrendo. Além disso, ele não teve piora nos sintomas da esquizofrenia. Um ano depois, a família percebeu que ele estava mais comunicativo, mais rápido para pensar e com melhor qualidade de vida.\n\n**Por que isso é importante**\n\nEste caso mostra que, mesmo quando os remédios não podem ser usados, a estimulação cerebral profunda pode ser uma opção para melhorar os sintomas do Parkinson. Também é importante que o tratamento não tenha piorado a esquizofrenia do paciente. Isso ajuda a entender como cuidar melhor de pessoas com doenças complexas.",
+            "B3": "**Contexto**  \nEste relato descreve o caso de um homem de 51 anos com diagnóstico prévio de esquizofrenia paranoide desde os 20 anos, que desenvolveu posteriormente sintomas motores graves compatíveis com doença de Parkinson. O paciente apresentava rigidez muscular intensa, dificuldade para se movimentar (acinesia), disfagia (dificuldade para engolir) e sialorreia (salivação excessiva), além de significativa perda de peso e atrofia muscular decorrente da imobilidade. O tratamento convencional com levodopa, medicamento padrão para Parkinson, foi limitado pela piora dos sintomas psicóticos mesmo em doses muito baixas.\n\n**Principais Achados**  \nDevido à intolerância à levodopa e à progressão severa dos sintomas motores, foi indicada a estimulação cerebral profunda subtalâmica bilateral (ECP-NST) como uma medida compassiva, ou seja, uma intervenção excepcional para tentar melhorar a qualidade de vida do paciente. A cirurgia foi realizada sem complicações em fevereiro de 2020. Após seis meses, o paciente apresentou melhora significativa na capacidade de ficar em pé e na marcha, com redução da rigidez e da acinesia, especialmente no lado esquerdo do corpo. Também houve melhora importante na disfagia e na sialorreia. O tratamento com levodopa foi suspenso, enquanto os antipsicóticos foram mantidos sem agravamento dos sintomas psiquiátricos.\n\nUm ano após a cirurgia, observou-se uma leve melhora nos sintomas negativos da esquizofrenia (como apatia e isolamento), acompanhada de melhor qualidade de vida, maior espontaneidade, comunicação mais eficaz e raciocínio mais rápido, conforme relatado pela família. A avaliação cognitiva global permaneceu estável, indicando que a intervenção não prejudicou as funções mentais do paciente.\n\n**Interpretação Clínica**  \nEste caso demonstra que a estimulação cerebral profunda subtalâmica pode ser uma alternativa viável e eficaz para pacientes com doença de Parkinson associada à esquizofrenia, especialmente quando o uso de levodopa é limitado pela piora dos sintomas psiquiátricos. A ECP-NST proporcionou melhora motora significativa sem exacerbar os sintomas psicóticos, o que é um resultado relevante dada a complexidade do quadro clínico.\n\n**Próximos Passos**  \nEmbora os resultados sejam promissores, é importante acompanhar o paciente a longo prazo para monitorar a estabilidade dos ganhos motores e psiquiátricos, além de avaliar possíveis efeitos adversos da estimulação cerebral profunda. Este caso também sugere a necessidade de estudos adicionais para entender melhor o papel da ECP-NST em pacientes com comorbidades psiquiátricas e distúrbios do movimento."
+        }
+    },
+    {
+        "article": "Um menino de 7 anos foi levado ao departamento de emergência pela mãe. A mãe se queixou de que o olho esquerdo da criança havia se desviado para cima. Cinco dias antes do desvio, o menino havia sofrido um trauma contuso de uma bola de futebol atingindo a órbita esquerda e o rosto. A mãe notou um desvio para cima, mas não procurou uma consulta médica imediata. A criança não tinha nenhuma dor, visão turva, diplopia, perda de consciência, náusea ou vômito, convulsões ou comportamento anormal na apresentação.\n\nA criança estava brincalhona durante o exame oftalmológico e não tinha uma posição anormal da cabeça. A sua visão era de 20/20 em ambos os olhos. Tinha uma ligeira limitação da depressão no olho esquerdo mas tinha uma motilidade extraocular total noutras direções cardinais. Na posição primária, foi observada uma hipertropia no olho esquerdo, e esta aumentou quando olhou para a esquerda com uma inclinação da cabeça para a direita, o que é consistente com uma paralisia do músculo reto inferior. Tinha uma pressão intraocular normal (IOP) no RE (17 mmHg) e no LE (16 mmHg) medida por um tonómetro (iCare, Vantaa, Finlândia). Não se sentiu qualquer massa à volta da órbita ao palpar, nem se observou qualquer deterioração da função do nervo ótico. O exame do fundo do olho mostrou uma cabeça do nervo ótico saudável e uma retina normal sem fratura. As medidas do exoftalmómetro na base (91 mm), RE (14 mm) e LE (15 mm) foram de tamanho normal.\n\nA tomografia computadorizada (TC) da cabeça revelou uma densidade de tecido mole envolvendo o seio maxilar esquerdo, estendendo-se para a cavidade nasal esquerda e para a órbita extraconal esquerda. Esta massa poderia ser atribuída a um hematoma organizador e foi relatado que estava correlacionado com os achados clínicos. A revisão do ouvido, nariz e garganta (ORL) não revelou descarga nasal ou obstrução. O corneto médio esquerdo estava congestionado com descarga purulenta aderente à membrana mucosa. A opacificação do seio maxilar foi atribuída secundariamente a trauma, mas uma ressonância magnética urgente com contraste foi recomendada para descartar outras causas.\n\nA ressonância magnética (MRI) mostrou uma lesão de 37,6 × 38,4 mm dentro do seio maxilar esquerdo, estendendo-se para a órbita, cavidade nasal, áreas pré-maxilares e retromaxilares com um sinal heterogêneo e leve aumento heterogêneo. Havia também um sinal de medula anormal subjacente no alvéolo maxilar posterior esquerdo com espessamento anormal e sinal na gengiva, que se suspeitava ser um processo neoplásico.\n\nUma biópsia do seio maxilar esquerdo e da cavidade nasal esquerda mostrou neoplasia de células redondas malignas positivas para desmina, miogenina e diferenciação miogênica 1. A hibridação in situ por fluorescência foi positiva para FOXO1.\n\nCom base nessas descobertas clínicas e de imagem, o paciente foi diagnosticado com RMS positivo para fusão alveolar. Um exame metastático completo incluiu análise do fluido cerebrospinal, aspiração e biópsia da medula óssea, tomografia computadorizada do tórax, ressonância magnética do cérebro, varredura óssea e tomografia por emissão de pósitrons. Não revelou nenhuma lesão metastática.\n\nUm mês após a apresentação, a criança desenvolveu conjuntivite química grave, pressão intraocular elevada e lagoftalmo. Foi-lhe dado dorzolamida 2% em gotas oculares três vezes ao dia para baixar a pressão intraocular.\n\nO Tumor Board classificou esta criança como tendo PM-RMS estádio III. De acordo com a classificação TNM, o tumor foi classificado como T2bNxM0, representando risco intermédio com base na Estratificação de Risco de Rabdomiosarcoma do Grupo de Oncologia Infantil.11 O plano de tratamento incluiu radioterapia e quimioterapia. A quimioterapia incluiu vincristina, actinomicina D e ciclofosfamida (VAC) em doses elevadas. A criança recebeu 45 Gy/25 fx utilizando a técnica rapidArc. Cinco ciclos foram dados, e o tratamento ainda está em curso. Três meses após o início do tratamento, houve uma diminuição acentuada no tamanho e extensão do tumor, com a imagem 3 meses depois a mostrar as órbitas e a bainha do nervo ótico livres de tumor. Seis meses após o início da terapia, a aparência do paciente melhorou, e a sua pressão intraocular normalizou-se. Por conseguinte, 2% de dorzolamide eye drops foram descontinuados. A criança continua a estar sob os cuidados de uma equipa multidisciplinar.\n",
+        "gold_summary": "Uma criança apresentou uma desviação para cima do olho esquerdo. Ele tinha um histórico de trauma contuso no rosto há 5 dias. A tomografia computadorizada (TC) da cabeça revelou uma densidade de tecido mole envolvendo o seio maxilar esquerdo. A ressonância magnética (MRI) mostrou uma lesão de 37,6 mm x 38,4 mm dentro do seio maxilar esquerdo estendendo-se para a órbita, cavidade nasal e áreas pré-maxilares e retromaxilares com um sinal heterogêneo e leve melhora heterogênea. Uma biópsia e histopatologia confirmaram RMS alveolar. A criança foi tratada com quimioterapia e radioterapia.\n",
+        "synthetic_summary": {
+            "B1": "Um menino teve o olho esquerdo olhando para cima. Isso aconteceu depois que ele levou uma bolada no rosto. Os médicos fizeram exames e acharam um caroço perto do olho e do nariz. Eles fizeram um teste para ver o que era. Descobriram que era um tipo de doença que precisa de remédios fortes. O menino está tomando remédios e fazendo tratamento para melhorar. Os médicos estão cuidando bem dele.",
+            "B2": "**O que aconteceu com a criança**\n\nUm menino de 7 anos teve o olho esquerdo desviado para cima, cinco dias depois de levar uma bola de futebol no rosto. Ele não sentia dor nem tinha problemas para enxergar. Quando os médicos examinaram, perceberam que o movimento do olho estava um pouco limitado para baixo, indicando que um músculo do olho não estava funcionando direito.\n\n**O que os exames mostraram**\n\nUma tomografia computadorizada, que é um tipo de raio-X detalhado, mostrou um tecido diferente dentro do osso perto do olho, chamado seio maxilar esquerdo. Depois, uma ressonância magnética, que usa ondas para criar imagens do corpo, revelou uma lesão grande que estava se espalhando para áreas próximas ao olho e ao nariz.\n\nPara entender melhor o que era essa lesão, os médicos fizeram uma biópsia. Isso significa que retiraram um pedacinho do tecido para analisar no laboratório. O resultado mostrou que a criança tinha um tipo de câncer chamado rabdomiossarcoma alveolar, que é um tumor maligno formado por células que normalmente virariam músculo.\n\n**Como foi o tratamento**\n\nO menino começou a receber quimioterapia, que são remédios fortes para matar as células do câncer, e radioterapia, que usa radiação para destruir o tumor. Após alguns meses, o tumor diminuiu bastante e o olho voltou a funcionar melhor. A pressão dentro do olho também voltou ao normal, e os médicos pararam de usar um colírio que ajudava nisso.\n\n**O que isso significa**\n\nEsse caso mostra como um trauma no rosto pode esconder um problema sério, como um tumor. Por isso, é importante procurar um médico se algo estranho acontecer, mesmo que não doa. O tratamento combinado de quimioterapia e radioterapia foi eficaz para controlar o câncer e melhorar a saúde da criança. Ela continua sendo acompanhada por uma equipe médica especializada para garantir sua recuperação.",
+            "B3": "**Contexto**  \nUm menino de 7 anos apresentou um desvio para cima do olho esquerdo cinco dias após sofrer um trauma contuso causado por uma bola de futebol atingindo o lado esquerdo do rosto. Apesar do desvio ocular, a criança não apresentava dor, visão turva, diplopia (visão dupla), nem sintomas neurológicos associados. O exame oftalmológico revelou uma leve limitação para olhar para baixo com o olho esquerdo, hipertropia (elevação do olho) e motilidade ocular preservada nas outras direções. A pressão intraocular estava normal e não havia sinais de fraturas ou comprometimento do nervo óptico.\n\n**Principais Achados Diagnósticos**  \nA tomografia computadorizada da cabeça identificou uma massa de tecido mole envolvendo o seio maxilar esquerdo, estendendo-se para a cavidade nasal e para a órbita extraconal (área ao redor do globo ocular). A ressonância magnética detalhou uma lesão de aproximadamente 38 mm que invadia o seio maxilar, a órbita, a cavidade nasal e regiões próximas ao maxilar, apresentando sinal heterogêneo, sugerindo uma composição complexa da massa. Além disso, houve alterações suspeitas na medula óssea do maxilar e na gengiva adjacente, levantando a hipótese de um processo tumoral.\n\nA biópsia da lesão confirmou o diagnóstico de rabdomiosarcoma alveolar (RMS), um tipo agressivo de câncer originado nas células musculares, caracterizado pela presença de células redondas malignas com marcadores específicos (desmina, miogenina, diferenciação miogênica 1) e a presença do gene de fusão FOXO1, típico dessa variante tumoral.\n\n**Interpretação Clínica**  \nO diagnóstico foi de rabdomiosarcoma alveolar positivo para fusão, classificado como estágio III segundo critérios oncológicos, indicando um tumor localmente avançado, mas sem metástases detectadas após exames completos, incluindo análise do líquido cerebrospinal, medula óssea, pulmões, cérebro e ossos. A doença foi considerada de risco intermediário.\n\nDurante o tratamento, a criança desenvolveu complicações oculares secundárias, como conjuntivite química, aumento da pressão intraocular e incapacidade de fechar completamente a pálpebra (lagoftalmo), que foram manejadas com colírios específicos para reduzir a pressão ocular.\n\n**Próximos Passos e Evolução**  \nO plano terapêutico incluiu radioterapia localizada com técnica avançada (rapidArc) e quimioterapia intensiva com vincristina, actinomicina D e ciclofosfamida. Após cinco ciclos de quimioterapia e 45 Gy de radiação, houve uma redução significativa do tumor, com imagens de acompanhamento mostrando ausência de lesões na órbita e ao redor do nervo óptico. Seis meses após o início do tratamento, a criança apresentou melhora clínica, normalização da pressão intraocular e suspensão dos colírios. Ela permanece em acompanhamento multidisciplinar para monitorar a resposta ao tratamento e prevenir possíveis recidivas.\n\n---\n\nEste caso ilustra a importância de uma avaliação cuidadosa após traumas faciais aparentemente leves, pois lesões ocultas podem revelar processos graves como tumores malignos. O diagnóstico precoce e o tratamento multidisciplinar são essenciais para o sucesso terapêutico e a preservação da função ocular e qualidade de vida da criança."
+        }
+    },
+    {
+        "article": "Uma mulher de 52 anos de idade foi encaminhada para a clínica de urologia com queixas urinárias. Os seus sintomas começaram há três anos atrás com frequência, disúria e gotejamento. Mencionou também a passagem frequente de substâncias semelhantes a fios vermelhos e negros na sua urina. Além disso, durante estas descargas, teve dor de cabeça, febre e calafrios. A coceira periuretral e genital intermitente foi outra queixa sua. Ela tinha sido tratada por vários especialistas com o diagnóstico de infecções recorrentes do trato urinário, sem melhoria clínica. A paciente negou viagens recentes, acampamento, caminhadas, agricultura, natação e picadas de insetos. Ela tinha histórico positivo de cirurgia de sinus pilonidal e histerectomia, 8 e 7 anos antes, respetivamente. Dois anos antes da visita atual, ela tinha sido hospitalizada para avaliação. No exame físico, ela estava bem com sinais vitais normais. Todos os seus testes laboratoriais, incluindo contagem de células sanguíneas, análise de urina e bioquímicas estavam dentro dos limites normais. A tomografia computadorizada (TC) abdominal e pélvica não revelou anormalidades. Por conseguinte, ela foi submetida a cistoscopia, que demonstrou eritema e hiperemia da mucosa da bexiga, detritos suspensos e dilatação do orifício ureteral esquerdo. Durante a consulta com um especialista em doenças infecciosas, suspeitou-se de esquistossomose. Por conseguinte, ela foi tratada com Praziquantel com a dose e duração apropriadas e foi dispensada do hospital.\n\nNo entanto, os seus sintomas não diminuíram. Foi novamente visitada por outro especialista em doenças infeciosas, que lhe prescreveu ivermectina devido a suspeita de miíase urinária. Não obstante, não se observou qualquer melhoria. Foi readmitida para submeter-se a irrigação da bexiga com polietileno glicol, mas o fluido de lavagem da bexiga não continha quaisquer larvas visíveis. Este procedimento foi seguido por uma hematuria de dois dias com cessação espontânea. Foi dispensada em casa e aconselhada a repetir a análise de urina um mês depois. A sua análise de urina aleatória foi normal, pelo que recolheu a sua urina de 24 horas e enviou-a para o laboratório para análise, onde uma larva viva foi demonstrada ao patologista ao microscópio de luz. A larva foi isolada e enviada a um entomologista para ser identificada morfologicamente. Finalmente, foi determinado que a larva pertencia à espécie Sarcophaga. A paciente foi aconselhada a tomar cuidados de higiene pessoal e a consumir pelo menos 3 L de água diariamente.\n",
+        "gold_summary": "Relatamos uma mulher de 52 anos com disúria persistente, apesar de múltiplos tratamentos para infecções suspeitas. A cistoscopia revelou eritema e detritos, mas as imagens e testes laboratoriais foram normais. Uma larva viva foi identificada na análise da urina, confirmando o diagnóstico. O tratamento envolveu uma melhor higiene e hidratação.\n",
+        "synthetic_summary": {
+            "B1": "Uma mulher estava com dor para fazer xixi por muito tempo. Os médicos olharam dentro da bexiga dela e viram que estava vermelha. Eles fizeram muitos exames, mas tudo parecia normal. Depois, acharam um bichinho na urina dela. Para melhorar, ela precisa tomar bastante água e cuidar bem da limpeza do corpo.",
+            "B2": "**O que aconteceu com a paciente**\n\nUma mulher de 52 anos sentia dor ao urinar (disúria) e outros sintomas urinários por três anos. Ela já havia recebido vários tratamentos para infecções, mas não melhorava. Exames como tomografia e análises de sangue e urina estavam normais. Um exame especial da bexiga (cistoscopia) mostrou inflamação e sujeira, mas não explicou o problema.\n\n**O que os médicos descobriram**\n\nDepois de muitos exames, os médicos encontraram uma larva viva na urina dela. Larva é a forma jovem de alguns insetos, parecida com uma pequena minhoca. Essa larva foi identificada como sendo da espécie Sarcophaga, um tipo de mosca. Isso explicou os sintomas que ela tinha.\n\n**O que foi feito para ajudar**\n\nO tratamento principal foi ensinar a paciente a cuidar melhor da higiene pessoal e beber bastante água, pelo menos 3 litros por dia. Isso ajuda a evitar que as larvas fiquem na bexiga e melhora os sintomas. Com essas medidas, a paciente pode se sentir melhor e evitar problemas futuros.",
+            "B3": "**Contexto**  \nUma mulher de 52 anos apresentou sintomas urinários persistentes há três anos, incluindo aumento da frequência urinária, dor ao urinar (disúria), gotejamento e passagem frequente de substâncias semelhantes a fios vermelhos e negros na urina. Durante esses episódios, ela também experimentava dor de cabeça, febre e calafrios, além de coceira intermitente na região genital e ao redor da uretra. Apesar de múltiplos tratamentos para infecções urinárias recorrentes, não houve melhora clínica. Exames laboratoriais e de imagem, incluindo tomografia computadorizada abdominal e pélvica, estavam normais. A cistoscopia mostrou inflamação da mucosa da bexiga e presença de detritos, mas não revelou causas definitivas.\n\n**Principais Achados**  \nA análise da urina de 24 horas revelou a presença de uma larva viva, que foi identificada por um entomologista como pertencente à espécie Sarcophaga, um tipo de mosca associada à miíase (infestação por larvas). Este achado confirmou que a paciente sofria de miíase urinária, uma condição rara em que larvas infestam o trato urinário.\n\n**Interpretação Clínica**  \nA persistência dos sintomas apesar de tratamentos convencionais para infecções urinárias, associada à identificação da larva na urina, indicou que a causa dos sintomas era uma infestação parasitária e não uma infecção bacteriana comum. A miíase urinária é uma condição incomum e pode ser facilmente confundida com infecções urinárias recorrentes, atrasando o diagnóstico correto.\n\n**Próximos Passos e Manejo**  \nO tratamento consistiu em orientações para melhorar a higiene pessoal e aumentar a ingestão de líquidos para pelo menos 3 litros por dia, visando facilitar a eliminação das larvas e prevenir novas infestações. A paciente foi monitorada para avaliar a resolução dos sintomas e evitar complicações. Este caso ressalta a importância de considerar causas parasitárias em pacientes com sintomas urinários persistentes e refratários a tratamentos convencionais."
+        }
+    },
+    {
+        "article": "Uma paciente de 2 anos de idade foi internada no Hospital Infantil de Shenzhen em julho de 2021 por causa de uma tosse, febre por 5 dias e agravamento da falta de ar por 1 dia. Cinco dias antes da admissão, a criança apresentou tosse produtiva paroxística, cianose e febre. A temperatura mais alta foi de 40,0℃. Quatro dias depois, a criança teve uma tosse pior e falta de ar significativa, então foi internada no hospital com suspeita de pneumonia.\n\nEla foi previamente diagnosticada com leucemia mieloide aguda (M5, CR1) e estava na fase de indução da quimioterapia. O regime de quimioterapia era de citarabina (Ara-c) 100 mg/m2 d1-7, etoposide (VP-16) 150 mg/m2 d3, cladribina (Cla) 5 mg/m2 d1-5, e fator estimulador de colônia de granulócitos (G-CSF) 200 µg/m2 d1-7. A paciente não tinha histórico de eczema ou sibilância. Não havia histórico de nascimento especial, histórico pessoal ou histórico familiar.\n\nO exame físico na admissão foi o seguinte: temperatura 38,9 °C, frequência cardíaca 138 batimentos/min, frequência respiratória 50 batimentos/min, pressão arterial 104/60 mmHg, peso 12 kg, e 94% de saturação de oxigênio arterial (com concentração de oxigênio suplementar de 65%). O paciente tinha um estado mental pobre, disforia, falta de ar, cianose, dilatação nasal, retração, sibilos, e estertores na auscultação. Os exames no coração, abdômen, e sistema nervoso foram sem observações. O tempo de preenchimento capilar foi de 2 s.\n\nOs testes laboratoriais foram os seguintes: contagem de glóbulos brancos 0.83*109/L, neutrófilos 0.21*109/L, linfócitos 0.62*109/L, hemoglobina 105 g/L, plaquetas 50*109/L, proteína C reativa hipersensível 22.71 mg/L; procalcitonina 2.95 ng/ml; análise de gases no sangue: pH 7.403, pressão parcial de dióxido de carbono 43.5 mmHg, pressão parcial de oxigénio 87.4 mmHg, e bicarbonato padrão 26.3 mmol/L. A base residual padrão foi de 2.2 mmol/L. A função hepática e renal, creatinase, péptido natriurético cerebral, eletrólito, e função de coagulação foram normais; a cultura de sangue e cultura de expectorado foram negativos. A cultura de garganta e fluido de lavagem alveolar para patógenos respiratórios (incluindo metapneumovírus, vírus influenza B, vírus influenza A H3N2, Chlamydia, Mycoplasma pneumonia, bocavírus, coronavírus, vírus respiratório sincicial (RSV), vírus influenza A H1N1, adenovírus, rinovírus, parainfluenza) indicou positivo apenas para RSV. A tomografia computadorizada de tórax sugeriu consolidação de ambos os pulmões com atelectasia segmentar.\n\nTratamento e acompanhamento: Durante a hospitalização, a criança estava na fase de indução da quimioterapia M5 com neutropenia e febre. Por isso, foi-lhe administrado o meropenem intravenoso (20 mg/kg q8 h), com oxigénio de alto fluxo por cateter nasal (HFNC), nebulização (com budesonida 2 ml, ipratropio 2 ml, salbutamol em aerossol 1,25 ml, uma vez/8 h), hidratação e antipirético. No 6º dia de hospitalização, a dificuldade respiratória e a retração estavam a agravar-se, e a saturação de oxigénio estava a 88% em HFNC, então foi transferida para a Unidade de Cuidados Intensivos Pediátricos (PICU). Por intubamento e ventilação mecânica, a saturação de oxigénio estava ainda abaixo de 90%, e ocorreram lesões pulmonares relacionadas com a ventilação mecânica, tais como enfisema subcutâneo e pneumatosis mediastinal. No 9º dia de hospitalização, foi-lhe dado o tratamento de oxigenoterapia extracorpórea (ECMO), pelo qual o volume respiratório estava ainda baixo, e o recrutamento manual do pulmão foi ineficaz. As radiografias de tórax repetidas indicaram sinais de “pulmão branco”. A obstrução das vias respiratórias foi considerada, a broncoscopia foi realizada no 10º, 13º, 15º e 19º dias de operação da ECMO, respetivamente, e muitos tampões de plástico foram aspirados durante os dois primeiros procedimentos. Depois disso, o volume respiratório aumentou. O fluido de lavagem alveolar foi enviado para um teste de etiologia de alto rendimento por sequenciação de próxima geração, que foi apenas positivo para RSV. A patologia dos tampões de plástico indicou secreções fibrinosas, bem como glóbulos vermelhos, linfócitos e neutrófilos. A ECMO foi retirada 35 dias depois. No momento da alta, estava a usar HFNC (FiO2 34%, fluxo 13 L/min) com uma saturação de oxigénio mantida acima de 95%.\n\nApós a alta, a criança teve tosse, intolerância ao exercício e rales úmidos persistentes na auscultação pulmonar. Uma tomografia computadorizada de tórax realizada seis meses após a alta (fevereiro de 2022) revelou inflação irregular, hiperinflação, opacidade em vidro fosco, atelectasia e espessamento do septo interlobular em ambos os pulmões. Consequentemente, foi diagnosticada bronquiolite obliterante (BO). montelukast sódico oral e azitromicina de baixa dose, bem como nebulização de budesonida, foram administrados. Uma tomografia computadorizada de acompanhamento realizada 19 meses após a alta (março de 2023) ainda indicou um padrão de atenuação em mosaico, atelectasia e espessamento do septo interlobular. Em outubro de 2022, pirfenidona oral foi iniciada para o tratamento de fibrose pulmonar. Atualmente, durante mais de dois anos de monitorização, não foi observada exacerbação de BO.",
+        "gold_summary": "Uma menina de 2 anos de idade, imunocomprometida, foi internada no hospital com tosse, febre por 5 dias e agravada com falta de ar por 1 dia. Com ventilação mecânica, sua insuficiência respiratória não foi aliviada e enfisema subcutâneo e pneumatosis mediastinal apareceram. Oxigenação extracorpórea da membrana (ECMO) foi administrada, mas o volume de respiração foi baixo. Portanto, uma broncoscopia foi realizada, pela qual secreções plásticas foram encontradas e removidas. A patologia das secreções plásticas confirmou o diagnóstico de PB tipo I. RSV foi o único patógeno positivo no fluido de lavagem alveolar pelo teste de sequenciamento de próxima geração. Após o procedimento broncoscópico, sua dispneia melhorou. A paciente foi dispensada com uma cânula nasal de alto fluxo, com saturação de oxigênio no pulso acima de 95%. Meio ano após a alta, ela desenvolveu sequelas de bronquite obliterante.\n",
+        "synthetic_summary": {
+            "B1": "Uma menininha de 2 anos ficou muito doente com tosse, febre e dificuldade para respirar. Ela foi para o hospital e precisou de ajuda para respirar com uma máquina. Mesmo assim, ela continuava com dificuldade para respirar e teve machucados no peito. Os médicos usaram uma máquina especial para ajudar o oxigênio a entrar no corpo dela.\n\nDepois, os médicos olharam dentro dos pulmões com um tubo e tiraram umas coisas que estavam bloqueando a respiração. Isso ajudou ela a respirar melhor. Eles acharam que um vírus chamado RSV foi o que deixou ela doente.\n\nDepois de sair do hospital, ela ainda teve um problema no pulmão chamado bronquite obliterante, que é uma doença que deixa a respiração difícil por um tempo. Os médicos continuam cuidando dela para ela melhorar.",
+            "B2": "**O que aconteceu com a criança**\n\nUma menina de 2 anos, que tinha o sistema imunológico fraco por causa de um tratamento contra leucemia, ficou doente com tosse, febre e dificuldade para respirar. Ela foi levada ao hospital porque a falta de ar piorou. Mesmo com a ajuda de um aparelho que ajuda a respirar (ventilação mecânica), a respiração dela não melhorou. Além disso, surgiram problemas nos pulmões, como enfisema subcutâneo (ar preso sob a pele) e pneumatosis mediastinal (ar em uma parte do peito onde não deveria ter).\n\n**Tratamento especial e o que encontraram**\n\nComo a respiração continuava difícil, os médicos usaram um tratamento chamado ECMO, que ajuda a oxigenar o sangue fora do corpo. Mesmo assim, o volume de ar que ela conseguia respirar era baixo. Por isso, fizeram um exame chamado broncoscopia, que é quando um tubo com uma câmera é colocado nos pulmões para ver o que está acontecendo. Nesse exame, eles encontraram e retiraram pedaços de secreção plástica, que são como tampões que bloqueiam as vias respiratórias.\n\nO exame dessas secreções mostrou que a menina tinha um problema chamado bronquiolite plástica tipo I, que é uma inflamação grave que bloqueia os pequenos tubos dos pulmões. O único vírus encontrado no exame do líquido dos pulmões foi o vírus sincicial respiratório (RSV), que pode causar infecções respiratórias sérias em crianças.\n\n**Melhora e consequências a longo prazo**\n\nDepois de retirar essas secreções, a respiração da menina melhorou. Ela recebeu alta do hospital usando um aparelho que ajuda a respirar com oxigênio pela narina (cânula nasal de alto fluxo) e conseguiu manter a oxigenação do sangue acima de 95%, o que é bom.\n\nNo entanto, seis meses depois, a menina desenvolveu uma doença chamada bronquiolite obliterante, que causa cicatrizes e bloqueios nos pulmões, dificultando a respiração. Para tratar essa condição, ela está recebendo medicamentos para ajudar a controlar a inflamação e melhorar a função pulmonar.\n\n**Resumo final**\n\nEssa história mostra como uma infecção respiratória grave, especialmente em uma criança com o sistema imunológico fraco, pode causar problemas sérios nos pulmões. O tratamento rápido, incluindo a remoção das secreções que bloqueavam as vias aéreas, foi essencial para a melhora dela. Mesmo assim, algumas sequelas podem aparecer depois, exigindo acompanhamento e cuidados médicos contínuos.",
+            "B3": "**Contexto**  \nUma menina de 2 anos, com o sistema imunológico comprometido devido a um tratamento recente para leucemia mieloide aguda, foi internada após apresentar tosse persistente, febre alta por cinco dias e piora da dificuldade para respirar no último dia. Ela estava em uso de quimioterapia intensiva, o que a deixava vulnerável a infecções graves.\n\n**Principais Achados Clínicos e Diagnósticos**  \nNa admissão, a paciente apresentava sinais de insuficiência respiratória, como cianose (coloração azulada da pele devido à falta de oxigênio), respiração acelerada e uso de oxigênio suplementar. Exames laboratoriais mostraram neutropenia (baixa contagem de neutrófilos, um tipo de glóbulo branco importante para combater infecções) e inflamação. A tomografia do tórax revelou consolidações pulmonares e áreas de colapso segmentar do pulmão. Testes para diversos vírus e bactérias respiratórias detectaram apenas o vírus sincicial respiratório (RSV), um agente comum de infecções respiratórias em crianças.\n\n**Tratamento e Evolução**  \nApesar do tratamento com antibióticos, oxigênio de alto fluxo e medicamentos para aliviar os sintomas respiratórios, a insuficiência respiratória da criança piorou, exigindo ventilação mecânica invasiva. Durante essa fase, surgiram complicações pulmonares relacionadas à ventilação, como enfisema subcutâneo (ar acumulado sob a pele) e pneumatosis mediastinal (ar no espaço entre os pulmões). Devido à gravidade, foi iniciada a oxigenação por membrana extracorpórea (ECMO), uma técnica avançada que substitui temporariamente a função dos pulmões.\n\nMesmo com ECMO, o volume respiratório permaneceu baixo, sugerindo obstrução das vias aéreas. Por isso, foi realizada broncoscopia — um exame que permite visualizar e limpar as vias respiratórias — durante a qual foram removidos numerosos tampões de secreções plásticas (formações densas de muco e células inflamatórias). A análise dessas secreções confirmou a presença de inflamação intensa compatível com broncopneumonia tipo I (PB tipo I). O sequenciamento genético do fluido pulmonar confirmou que o RSV era o único agente infeccioso presente.\n\nApós a remoção dessas obstruções, a respiração da paciente melhorou significativamente, permitindo a retirada gradual da ECMO e a alta hospitalar com suporte de oxigênio por cânula nasal de alto fluxo, mantendo níveis adequados de oxigenação.\n\n**Complicações a Longo Prazo e Seguimento**  \nSeis meses após a alta, a criança continuava apresentando tosse e dificuldade para se exercitar, além de ruídos pulmonares anormais. Uma nova tomografia mostrou alterações pulmonares típicas de bronquiolite obliterante (BO), uma condição crônica caracterizada por inflamação e cicatrização das pequenas vias aéreas, que pode causar obstrução persistente. O tratamento incluiu medicamentos anti-inflamatórios, antibióticos em baixas doses e nebulizações para controlar os sintomas e prevenir agravamentos.\n\nApós quase dois anos de acompanhamento, a paciente não apresentou novas crises significativas da bronquiolite obliterante, embora exames de imagem ainda mostrem alterações pulmonares residuais. Em outubro de 2022, foi iniciado o uso de pirfenidona, um medicamento que pode ajudar a reduzir a fibrose (cicatrização) pulmonar.\n\n**Interpretação Clínica**  \nEste caso ilustra a gravidade das infecções por RSV em crianças imunocomprometidas, que podem evoluir para insuficiência respiratória grave e complicações pulmonares complexas. A presença de tampões plásticos nas vias aéreas contribuiu para a dificuldade respiratória e exigiu intervenções invasivas para remoção. O desenvolvimento subsequente de bronquiolite obliterante destaca a importância do acompanhamento prolongado para identificar e tratar sequelas pulmonares crônicas.\n\n**Próximos Passos**  \nO manejo contínuo da paciente inclui monitoramento regular da função pulmonar, controle dos sintomas respiratórios e ajustes terapêuticos para minimizar a progressão da doença pulmonar crônica. A equipe médica deve permanecer atenta a possíveis exacerbações e complicações associadas à bronquiolite obliterante, garantindo suporte multidisciplinar para otimizar a qualidade de vida da criança."
+        }
+    },
+    {
+        "article": "Em fevereiro de 2013, uma mulher negra de 24 anos com anorexia nervosa, anemia crônica (hemoglobina basal, 9,5-11 g/dL), e depressão maior foi internada na unidade de cuidados cardíacos com sintomas de congestão e baixo débito cardíaco que necessitaram de suporte inotrópico. Ela não tinha histórico médico familiar notável. Três meses antes, ela foi internada por não ter se desenvolvido após vários meses de má ingestão oral que causaram uma perda de peso de 30 libras e anormalidades metabólicas. Os resultados laboratoriais iniciais incluíam níveis normais de tiamina, folato e selênio; no entanto, seus níveis de zinco eram baixos, com 23 μg/dL (intervalo normal, 70-120 μg/dL). Ela teve uma longa estadia no hospital enquanto estava em tubo de alimentação e recebeu terapia antidepressiva. Um ecocardiograma transtorácico (TTE), obtido para investigar a dispneia subjetiva, revelou uma fração de ejeção ventricular esquerda (LVEF) de 0,60 e nada incomum. Ela foi dispensada do hospital com planos para acompanhamento ambulatorial de saúde mental.\n\nDuas semanas antes da admissão atual, a paciente relatou dispneia progressiva e tosse, que foram atribuídas a uma infecção respiratória e foram tratadas sem sucesso com azitromicina. No dia da apresentação, sua mãe notou que ela tinha uma marcha instável, fraqueza no membro direito, queda de face e fala arrastada. O diagnóstico foi de acidente vascular cerebral agudo no lado direito da artéria cerebral média. A paciente recebeu ativador de plasminogênio tecidual intravenoso e recuperou gradualmente a função neurológica. Os resultados do estudo de hipercoagulabilidade não revelaram nada de notável, e não foram detectadas disritmias. No entanto, o exame físico e a auscultação revelaram pulsações venosas jugulares proeminentes, um aumento do ventrículo direito e um S3 do ventrículo esquerdo. Um TTE mostrou um LV dilatado com função globalmente reduzida, um LVEF de 0,10, uma dimensão final diastólica do LV de 4,6 cm, uma dimensão atrial esquerda de 4 cm e uma pressão sistólica estimada do ventrículo direito de 60 mmHg.\n\nOs resultados da cateterização cardíaca direita incluíram uma pressão atrial direita de 18 mmHg (normal, 2-6 mmHg), uma pressão sistólica da artéria pulmonar de 29 mmHg (normal, 15-30 mmHg), uma pressão capilar pulmonar de 16 mmHg (normal, 8-12 mmHg), um débito cardíaco de Fick de 2,59 L/min (normal, 4-8 L/min), e um índice cardíaco de 1,71 L/min/m2 (normal, 2,5-4 L/min/m2). A ressonância magnética cardíaca revelou espessuras e dimensões normais das câmaras, falência biventricular grave, e um derrame pericárdico de tamanho moderado. Não foram observados trombos frescos ou organizados nas câmaras cardíacas. As amostras de biópsia endomiocardica não apresentaram alterações inflamatórias ou infiltrativas agudas, inclusões virais, ou vírus adenovírus ou herpes simplex após coloração imunohistoquímica. Um ensaio de reação em cadeia da polimerase com transcriptase reversa foi negativo para a gripe A e B. De salientar, não foi obtida coloração para alterações associadas a cardiomiopatia secundária a deficiência de zinco, tais como níveis aumentados de superóxido dismutase ou a proteína LC3-II (um marcador de autofagia).\n\nA paciente iniciou um tratamento convencional para a insuficiência cardíaca avançada. A causa da cardiomiopatia de início recente nessa jovem mulher não era óbvia, então a equipe de tratamento procurou na literatura médica e, consequentemente, testou seus níveis de zinco. Estes estavam consistentemente baixos a 34 μg/dL. Ela iniciou um suplemento oral de zinco (220 mg/d) e foi encorajada a aumentar sua ingestão dietética. Quatro semanas depois, ela foi dispensada do hospital com um regime terapêutico de carvedilol (12,5 mg 2×/d), lisinopril (10 mg/d), espironolactona (50 mg/d), torsemida (10 mg/d), hidralazina (10 mg/d), isosorbide dinitrate (10 mg 3×/d), e zinco (220 mg/d).\n\nA LVEF da paciente melhorou para 0.25 após um mês e para 0.35 após 3 meses. A suplementação de zinco foi descontinuada aos 4 meses por um médico que não estava ciente das decisões terapêuticas anteriores, e a terapia restante continuou. Após 6 meses neste regime, os níveis de zinco da paciente recuperaram-se apenas parcialmente para 58 μg/dL, e a sua LVEF permaneceu em 0.35. Enquanto não estava a tomar zinco, teve outro período de má ingestão de alimentos; o seu nível de zinco diminuiu para 44 μg/dL, e a suplementação foi retomada. Um ano depois, período durante o qual continuou a terapia com zinco, os sintomas de HF da paciente resolveram-se, a sua LVEF melhorou para 0.60, e o seu nível de zinco aumentou para 62 μg/dL.",
+        "gold_summary": "Apresentamos o caso de uma mulher de 24 anos com anorexia nervosa e insuficiência cardíaca de início recente, cuja função sistólica ventricular esquerda deprimida melhorou após suplementação de zinco. Até onde sabemos, este é o primeiro relato de baixos níveis de zinco no plasma como a principal causa de cardiomiopatia que se resolveu após suplementação de zinco.32603465\n",
+        "synthetic_summary": {
+            "B1": "Uma moça jovem estava muito magrinha e seu coração estava fraco. Ela não comia direito e isso deixou seu corpo sem um mineral chamado zinco. O coração dela melhorou quando ela começou a tomar um remédio com zinco. Isso ajudou o coração a ficar forte de novo.",
+            "B2": "**O que aconteceu com a paciente**\n\nEsta é a história de uma jovem de 24 anos que tinha anorexia nervosa, uma doença em que a pessoa come muito pouco e perde muito peso. Ela também estava com o coração fraco, o que chamamos de insuficiência cardíaca. Isso significa que o coração dela não estava bombeando sangue direito.\n\n**O que os médicos descobriram**\n\nOs médicos fizeram vários exames e perceberam que o coração dela estava muito fraco, com a parte que bombeia o sangue (ventrículo esquerdo) funcionando mal. Eles também viram que ela tinha níveis muito baixos de zinco no sangue. O zinco é um mineral importante para o corpo funcionar bem.\n\n**O que foi feito para ajudar**\n\nComo não encontraram outra causa para o problema do coração, os médicos deram suplementos de zinco para ela tomar. Depois de alguns meses, a força do coração dela melhorou bastante. Quando ela parou de tomar o zinco, o coração voltou a ficar mais fraco, mas melhorou de novo quando voltou a tomar o suplemento.\n\n**Por que isso é importante**\n\nEste caso mostra que a falta de zinco pode causar problemas graves no coração, especialmente em pessoas que têm má alimentação, como na anorexia. É o primeiro relato que prova que dar zinco pode ajudar a melhorar a função do coração nesses casos. Por isso, é importante cuidar da alimentação e dos níveis de minerais no corpo para manter o coração saudável.",
+            "B3": "**Contexto**  \nEste relato descreve o caso de uma mulher jovem, de 24 anos, que sofria de anorexia nervosa — um transtorno alimentar caracterizado por restrição alimentar severa — e que desenvolveu insuficiência cardíaca recentemente. A insuficiência cardíaca é uma condição em que o coração não consegue bombear sangue adequadamente, levando a sintomas como falta de ar, fadiga e retenção de líquidos.\n\n**Principais Achados**  \nA paciente apresentou uma redução significativa da função do ventrículo esquerdo do coração, medida pela fração de ejeção ventricular esquerda (LVEF), que caiu para níveis muito baixos (10%), indicando uma falência grave do músculo cardíaco. Exames detalhados não identificaram causas comuns para essa cardiomiopatia (doença do músculo cardíaco), como inflamação, infecção viral, ou problemas estruturais. No entanto, foi detectada uma deficiência persistente de zinco no sangue, com níveis muito abaixo do normal.\n\nA equipe médica iniciou a suplementação oral de zinco, associada ao tratamento padrão para insuficiência cardíaca avançada. Após a introdução do zinco, a função cardíaca da paciente melhorou progressivamente, com a LVEF subindo para 25% em um mês, 35% em três meses e, finalmente, retornando a níveis normais (60%) após um ano de tratamento contínuo. Quando a suplementação foi interrompida, a deficiência de zinco e a função cardíaca pioraram novamente, reforçando a relação entre o baixo nível de zinco e a cardiomiopatia.\n\n**Interpretação Clínica**  \nEste caso sugere que a deficiência de zinco pode ser uma causa reversível de insuficiência cardíaca em pacientes com anorexia nervosa e má nutrição prolongada. O zinco é um mineral essencial para diversas funções celulares, incluindo a proteção contra o estresse oxidativo no músculo cardíaco. A melhora da função cardíaca após a reposição de zinco indica que a cardiomiopatia pode ter sido causada, pelo menos em parte, pela deficiência desse mineral.\n\n**Próximos Passos**  \nEste relato destaca a importância de avaliar os níveis de zinco em pacientes com insuficiência cardíaca de causa desconhecida, especialmente aqueles com histórico de desnutrição severa. A suplementação adequada pode representar uma intervenção terapêutica eficaz e potencialmente curativa para casos selecionados. Estudos adicionais são necessários para confirmar essa associação e entender melhor os mecanismos envolvidos.\n\n**Resumo Final**  \nApresentamos o primeiro caso conhecido em que baixos níveis de zinco no sangue foram identificados como a principal causa de uma cardiomiopatia grave, que se resolveu com a suplementação desse mineral. Essa descoberta reforça a necessidade de considerar deficiências nutricionais como causas tratáveis de doenças cardíacas em pacientes vulneráveis."
+        }
+    },
+    {
+        "article": "Homem de 40 anos, HIV positivo com adesão regular ao tratamento (carga viral de 4500/mm3 e CD4 de 70/mm3 no ano anterior), consultou por febre intermitente de dois anos de evolução que não respeitava o padrão de tempo e cedia transitoriamente com anti-inflamatórios não esteróides. Ele acrescentou, nos últimos dois meses, dor abdominal difusa e progressiva com predomínio no hemiabdomen superior, não relacionada à ingestão, e adenóma generalizado duro-elástico indolor. O laboratório de admissão evidenciou pancitopenia (hematócrito de 26%, leucócitos de 3100/mm3, plaquetas de 64 000/mm3), tempo de protrombina de 59% que se corrigia com adição de fatores de coagulação, albumina de 2,4 g/dl e reagentes de fase aguda francamente aumentados (eritrocitose superior a 160 mm/hora, proteína C reativa de 207 mg/dl, ferritina de 2166 ng/dl). A tomografia computadorizada (TC) de tórax, abdômen e pelve mostrou apenas hepato-esplenomegalia e adenóma generalizado, sem lesões pulmonares. A internação foi decidida e testes de autoimunidade, culturas séricas para germes comuns, Mycobacterium sp. e fungos, método Xpert MTB/RIF em escarro e sorologia para vírus hepatotrópicos foram realizados. O resultado desses estudos foi negativo, exceto pelo teste de reação em cadeia da polimerase em tempo real (RTPCR) para HHV-8, que foi positivo. A punção de medula óssea foi realizada com citometria de fluxo sem achados compatíveis com processo linfoproliferativo, e biopsia da mesma que apresentou plasmocitose reativa, sem evidência de hemofagocitose, com culturas negativas. A biopsia escisional de gânglio ilíaco esquerdo foi realizada, onde foram relatados setores com uma proliferação vascular, com vasos de paredes hialinizadas próximos ao centro folicular, sugerindo descartar doença de Castleman. Apesar de reiniciar TARV, persistiu com múltiplos registros febris diários e aumentou rapidamente a distensão e a dor abdominal. Continuou internado durante um mês, realizando ecografia abdominal, onde se destacava a crescente esplenomegalia (170 mm × 10 × 5 mm), Doppler esplenoportal sem evidência de hipertensão portal, vídeoendoscopia alta com presença de gastrite crônica não atrófica confirmada por biopsia, videocolonoscopia, fundo de olho e ecocardiograma Doppler que não apresentaram achados patológicos.  Após 3 semanas de internação, iniciou tratamento para ECM associada a HHV-8 com ganciclovir e corticoides, dada a contraindicação de rituximab por linfopenia grave. Evolucionou com falha multiorgânica e anasarca em um lapso menor a uma semana, contraindicando o tratamento iniciado. Neste contexto, foi realizada nova TC de tórax, abdômen e pelve, que apresentou a nível pulmonar infiltrados intersticiais, peribroncovasculares e septal bilateral com setores em lóbulos superiores direitos onde adquire configuração de árvore em broto e derrame pleural bilateral, e a nível abdominal, aumento marcado da hepato-esplenomegalia associada a ascite. Às 48 horas de sua suspensão, apresentou falha hepática fulminante e foi transferido para unidade de cuidados intensivos. Aspirado traqueal foi realizado e após suporte transfusional, foi obtida uma biopsia hepática por punção.  O paciente faleceu em poucas horas. Recebeu pós-mortem a cultura do aspirado traqueal positivo para Mycobacterium tuberculosis e a punção-biopsia de fígado com granulomas não necrotizantes e o resto do parênquima conservado. Este trabalho foi realizado em consonância com os princípios redigidos no código ético da OMS (Declaração de Helsinque).\n",
+        "gold_summary": "Apresentamos o caso de um homem de 40 anos, HIV positivo com regular adesão ao tratamento, que consultou por episódios febris intermitentes de dois anos de evolução, acrescentando nos últimos dois meses dor abdominal difusa progressiva e adenopatias generalizadas indolores. No laboratório apresentou pancitopenia, coagulopatia, hipoalbuminemia e reagentes de fase aguda aumentados. A tomografia computadorizada (TC) de tórax, abdômen e pelve apenas evidenciou hepato-esplenomegalia e adenopatias generalizadas. Realizaram-se múltiplos exames microbiológicos, incluindo culturas para Mycobacterium sp. de diferentes amostras, todos com resultados negativos, à exceção da RT-PCR para VHH-8. Realizou-se biopsia excisional de gânglio ilíaco esquerdo com achados compatíveis com doença de Castleman. Apesar de reiniciar terapia antirretroviral, a sintomatologia progrediu, iniciando tratamento com corticoides e ganciclovir. Após uma semana, desenvolveu falha mulitorgânica e anasarca, que contraindicaram os fármacos iniciados. Realizou-se nova TC de tórax que mostrou infiltrados com padrão em árvore em broto em lóbulo superior direito associado a derrame pleural bilateral, e a nível abdominal, progressão de hepato-esplenomegalia e ascite. Passou a unidade de cuidados intensivos 48 horas depois por falha hepática fulminante. O paciente faleceu em poucas horas. Recebeu postmortem o cultivo do aspirado traqueal positivo para Mycobacterium tuberculosis e a punção-biopsia hepática com granulomas não necrotizantes.\n",
+        "synthetic_summary": {
+            "B1": "Um homem estava doente há muito tempo. Ele tinha febre que ia e vinha. Também sentia dor na barriga e tinha caroços no corpo. \n\nOs médicos fizeram muitos exames. Eles viram que o fígado e o baço estavam grandes. Também acharam um vírus chamado HHV-8. \n\nEle tomou remédios, mas ficou pior. O corpo dele parou de funcionar direito. Ele foi para o hospital, mas não melhorou. \n\nNo final, os médicos descobriram que ele tinha uma doença chamada tuberculose. Ele morreu, mas os médicos tentaram ajudar muito.",
+            "B2": "**Resumo do Caso Médico para Jovens Estudantes**\n\n**Quem era o paciente e o que ele sentia?**  \nUm homem de 40 anos, que tinha HIV e tomava o remédio direitinho, começou a ter febre que aparecia e sumia durante dois anos. Nos últimos dois meses, ele também sentiu dor na barriga e notou que seus gânglios (pequenas bolinhas que ficam pelo corpo e ajudam a defender o organismo) estavam aumentados, mas sem doer.\n\n**O que os exames mostraram?**  \nOs exames de sangue mostraram que ele tinha poucos glóbulos vermelhos, brancos e plaquetas (chamamos isso de pancitopenia), além de problemas para o sangue coagular direito e níveis baixos de uma proteína chamada albumina. Outros exames mostraram que ele tinha o fígado e o baço maiores do que o normal, mas não havia sinais de infecção comum nos pulmões.\n\n**Quais testes foram feitos para descobrir a causa?**  \nForam feitos vários testes para procurar bactérias, fungos e vírus, mas só um vírus chamado HHV-8 apareceu positivo. Também foi feita uma biópsia, que é quando se tira um pedacinho de um gânglio para estudar, e os resultados indicaram uma doença chamada Doença de Castleman, que é um problema raro que afeta os gânglios.\n\n**Como foi o tratamento e o que aconteceu?**  \nMesmo tomando os remédios para HIV, os sintomas pioraram. Ele começou a tomar outros remédios, como corticoides (que diminuem a inflamação) e ganciclovir (um remédio para vírus). Mas, em menos de uma semana, ele teve falência de vários órgãos e inchaço pelo corpo, o que fez os médicos pararem esses remédios.\n\n**O que os exames finais mostraram?**  \nUma tomografia nova mostrou que os pulmões estavam com sinais de infecção grave e líquido acumulado. O fígado e o baço continuaram muito aumentados, e havia líquido na barriga. Pouco tempo depois, ele teve uma falência grave do fígado e precisou ir para a UTI (Unidade de Terapia Intensiva). Infelizmente, ele morreu algumas horas depois.\n\n**O que descobriram depois da morte?**  \nDepois que ele faleceu, os médicos receberam o resultado de um exame que mostrou que ele tinha tuberculose nos pulmões, causada pela bactéria Mycobacterium tuberculosis. Também encontraram no fígado sinais de inflamação típica dessa doença.\n\n**Por que esse caso é importante?**  \nEsse caso mostra como a tuberculose pode ser difícil de diagnosticar em pessoas com HIV, porque os sintomas e exames podem parecer com outras doenças. Também destaca a importância de investigar bem e tratar rápido para tentar evitar complicações graves.",
+            "B3": "**Contexto**  \nEste relato descreve o caso de um homem de 40 anos que vive com HIV e mantém adesão regular ao tratamento antirretroviral. Ele apresentou febre intermitente ao longo de dois anos, acompanhada nos últimos dois meses por dor abdominal difusa e progressiva, além de aumento generalizado dos gânglios linfáticos, que eram firmes e indolores.\n\n**Principais Achados Clínicos e Laboratoriais**  \nNa avaliação laboratorial inicial, o paciente apresentou pancitopenia (redução dos glóbulos vermelhos, brancos e plaquetas), distúrbios na coagulação sanguínea, baixa albumina (proteína importante para funções corporais) e marcadores inflamatórios elevados, indicando um processo inflamatório ativo. A tomografia computadorizada do tórax, abdômen e pelve revelou aumento do fígado e do baço (hepatoesplenomegalia) e linfonodos aumentados, sem lesões pulmonares evidentes.\n\nDiversos exames microbiológicos foram realizados para identificar infecções comuns em pacientes imunocomprometidos, incluindo culturas para bactérias, fungos e micobactérias (como a tuberculose), além de testes para vírus hepatotrópicos. Todos os resultados foram negativos, exceto a detecção do vírus HHV-8 (Herpesvírus humano tipo 8) por reação em cadeia da polimerase em tempo real (RT-PCR). A biópsia de um linfonodo ilíaco mostrou alterações compatíveis com a doença de Castleman, uma condição linfoproliferativa associada ao HHV-8.\n\n**Evolução Clínica e Tratamento**  \nApesar da retomada da terapia antirretroviral, o paciente continuou apresentando febres diárias e agravamento da dor e distensão abdominal. Foi iniciado tratamento com ganciclovir (antiviral) e corticosteroides para controlar a síndrome associada ao HHV-8, conhecida como síndrome de hiperinflamação ou síndrome de ativação macrofágica. O uso do rituximabe, um medicamento imunomodulador, foi contraindicado devido à linfopenia grave (baixa contagem de linfócitos).\n\nEm menos de uma semana, o paciente desenvolveu falência de múltiplos órgãos e edema generalizado (anasarca), o que levou à suspensão do tratamento antiviral e corticoide. Uma nova tomografia revelou infiltração pulmonar com padrão em “árvore em broto” — característico de infecção pulmonar ativa, associada a derrame pleural bilateral — e aumento significativo do fígado e baço, além de ascite (acúmulo de líquido na cavidade abdominal). O quadro evoluiu para insuficiência hepática fulminante, e o paciente foi transferido para a unidade de terapia intensiva.\n\n**Diagnóstico Definitivo e Desfecho**  \nApós o óbito, o cultivo do aspirado traqueal revelou infecção por Mycobacterium tuberculosis, a bactéria causadora da tuberculose. A biópsia hepática mostrou granulomas não necrotizantes (agregados de células inflamatórias típicos de infecções granulomatosas, como a tuberculose), com preservação do restante do tecido hepático.\n\n**Interpretação Clínica**  \nEste caso ilustra a complexidade do diagnóstico em pacientes com HIV avançado e sintomas sistêmicos prolongados. A presença do HHV-8 e a suspeita de doença de Castleman inicialmente direcionaram o tratamento, mas a tuberculose disseminada, não detectada nos exames iniciais, foi a causa fatal da falência orgânica. A tuberculose pode se manifestar de forma atípica em imunossuprimidos, dificultando sua identificação precoce.\n\n**Próximos Passos e Considerações**  \nCasos semelhantes ressaltam a importância de investigação minuciosa para tuberculose e outras infecções oportunistas em pacientes com HIV, mesmo quando exames iniciais são negativos. A abordagem multidisciplinar e o monitoramento rigoroso são essenciais para ajustar o tratamento conforme a evolução clínica. Além disso, a dificuldade em manejar síndromes inflamatórias associadas a vírus como o HHV-8 em contexto de imunossupressão grave destaca a necessidade de terapias individualizadas e vigilância constante para infecções secundárias."
+        }
+    },
+    {
+        "article": "Mulher de 75 anos, auto-suficiente, com antecedentes de hipertensão arterial em tratamento com losartan, apresenta quadro de um dia de evolução de mialgias generalizadas associadas a fraqueza nas extremidades inferiores (EEII) e cefaleia holocraniana. Vai a urgências em extra-sistema, é constatada hipertensa e é hospitalizada; são solicitados tomografia (TC) e ressonância magnética cerebral (RM), que descrevem meningioma não compressivo, sem sinais de encefalopatia posterior reversível. É prescrito tratamento sintomático e é dada alta às 48 horas. No entanto, a fraqueza progride comprometendo a bipedestação e afetando as extremidades superiores (EESS), juntamente com aumento da dor nas extremidades e recorrência de cefaleia. No quinto dia de evolução, consulta em urgências do Hospital Clínico da Universidade do Chile.\n\nEle refere retenção urinária e fecal há dois dias. Nega episódios de perda de consciência, tontura, palpitação, hiperidrose ou outros indicativos de disautonomia. Também não apresenta dificuldade respiratória, disfonia ou disfagia. Nega quadros infecciosos respiratórios ou digestivos recentes ou ter recebido vacinas no último mês.\n\nO exame físico do paciente foi descrito como alerta, orientado e acordado, com pressão arterial de 172/86 mmHg, frequência cardíaca de 90 bpm e outros sinais vitais normais. O exame neurológico por especialista descreveu:\n\nAgudeza e campos visuais preservados.\n\nPupilas isocóricas, reflexo fotomotor direto e consensual preservados, sem nistagmo.\n\nSulco nasogeniano direito apagado, comissura labial ipsilateral caída.\n\nReflexo de vômito bilateral diminuído, sem desvio da úvula ou paresia do palato mole.\n\nEsternocleidomastoide e trapézio com força M3.\n\nMobilidade lingual preservada, sem atrofia ou fasciculaciones.\n\nEESS: Direita: M2 global. Esquerda: força proximal M2 e distal M3.\n\nEEII: Direita: força global M2. Esquerda: força global M3.\n\nPares cranianos sem alterações; sem dor ou rigidez à mobilização cervical.\n\nSensibilidade preservada.\n\nReflexos osteotendinosos (ROT) diminuídos na EESS e abolidos na EEII.\n\nReflexo plantar extensor (-).\n\nSinais meníngeos (-).\n\nOs exames laboratoriais revelaram leucocitose (12.750/mL) e trombocitose (505.000/mL), proteína C reativa em níveis normais, hiponatremia e hipocloremia moderadas. A punção lombar revelou líquido incolor e transparente, com glicose de 80 mg/dL, proteínas de 232 mg/dL, sem eritrócitos nem leucócitos, coloração de Gram sem bactérias e cultura negativa.\n\nFoi diagnosticada tetraparesia flácida refratária progressiva com dissociação albumina/citológica no LCR compatível com SGB. Em um contexto de alto risco de insuficiência ventilatória devido a cefaloparesia precoce e uma pontuação EGRIS de 5 pontos, foi decidido que ele deveria ser internado na Unidade de Terapia Intensiva (UTI).\n\nAmplie-se o estudo com eletromiografia, revelando alteração poliradiculoneuropática mista com componentes desmielinizantes e axonais, além de elementos denervatórios ativos em EESS. Inicia-se tratamento com IgIV por 5 dias (0.4 g/kg/dia), monitorização e medidas de suporte (incluindo cateter urinário), além de assistência por kinesiologia e terapia ocupacional.\n\nA paciente apresenta choque séptico de origem urinária por E. coli MS na UTI, iniciando-se antibioterapia; posteriormente, sofre uma infecção por C. difficile sem comprometimento hemodinâmico, tratada com metronidazol via oral (VO).\n\nEvolução favorável, sem dificuldade respiratória, com recuperação gradual da força. No entanto, persiste com intensa dor urente e intermitente nas extremidades que aumenta com o movimento. Foi tratado inicialmente com bomba de infusão contínua de fentanil, que posteriormente foi trocada por SOS e foi adicionado paracetamol VO, pregabalina VO e metamizol endovenoso a cada hora. Durante a sua hospitalização, foram realizadas 2 tentativas falhadas de retirada do catéter urinário.\n\nDevido à estabilidade clínica, ela foi transferida para o serviço de medicina interna.\n\nEvolução e tratamento da dor\n\nDada a persistência da dor, paracetamol oral, pregabalina oral (150 mg), foi trocado por metamizol IV SOS e foi sugerido iniciar tramadol oral SOS, que a paciente rejeitou, indicando-se adesivo de fentanil (6,25 mcg/hora). Avaloraram-se possíveis interações farmacológicas entre fentanil e pregabalina (risco aumentado de deprimir o SNC), decidindo-se manter e monitorizar.\n\nEvolução favorável, com persistência de dor intermitente de menor intensidade, que aumenta com a mobilização ativa, pelo que se indica fentanil 25 mcg IV antes da reabilitação.\n\nFoi dada alta após 5 semanas de internação, com manutenção do uso de fentanil transdérmico na mesma dose a cada 72 horas e paracetamol 1 g VO SOS; a pregabalina foi suspensa.\n\nEvolução e tratamento da retenção urinária\n\nDevido à persistência da retenção urinária, a urologia sugeriu o início da administração de 0,4 mg/dia de tamsulosina para relaxamento do colo da bexiga antes da alta, e a retirada do cateter foi agendada para a semana após a alta, com sucesso.\n",
+        "gold_summary": "Apresentamos o caso de uma mulher de 75 anos com um quadro agudo de tetraparesia flácida arrefléctica compatível com SGB; recebe tratamento com imunoglobulina endovenosa (IgIV) com o que melhora o componente motor, mas associa dor refratária a antiinflamatórios não esteróides e pregabalina além de retenção urinária persistente com tentativas frustradas de retirada de catéter urinário. Indica-se fentanil transdérmico com boa resposta e tolerância, além de tamsulosina e cateterismo intermitente, conseguindo retirar o catéter ao cabo de seis semanas. Com base no caso, sugere-se a avaliação individualizada da dor e da retenção urinária em SGB, considerando o uso de opioides transdérmicos e medidas de esvaziamento vesical não invasivas respectivamente.\n",
+        "synthetic_summary": {
+            "B1": "Uma senhora de 75 anos ficou com os braços e as pernas muito fracos. Ela não conseguia mexer bem o corpo. Os médicos disseram que isso aconteceu por causa de uma doença que deixa os nervos cansados.\n\nEla tomou um remédio para ajudar os nervos a ficarem fortes de novo. Mas sentia muita dor nas pernas e nos braços. Também não conseguia fazer xixi direito e precisou usar um canudinho para isso.\n\nPara a dor, os médicos deram um remédio que cola na pele e ajuda a melhorar. Para o xixi, deram outro remédio que ajuda a bexiga a funcionar melhor. Depois de um tempo, ela conseguiu tirar o canudinho e ficou melhor.\n\nOs médicos dizem que cada pessoa pode sentir a dor e o problema para fazer xixi de um jeito diferente. Por isso, eles cuidam de cada um com remédios e jeitos diferentes para ajudar.",
+            "B2": "**O que aconteceu com a paciente**\n\nUma mulher de 75 anos ficou com fraqueza rápida e perda de força nos braços e pernas, chamada tetraparesia flácida. Isso aconteceu por causa de uma doença chamada Síndrome de Guillain-Barré (SGB), que faz o sistema de defesa do corpo atacar os nervos, dificultando o movimento.\n\n**Como foi o tratamento**\n\nEla recebeu um remédio chamado imunoglobulina endovenosa (IgIV), que ajuda o corpo a parar de atacar os nervos. Com isso, a força dos músculos melhorou. Porém, ela sentia muita dor que não melhorava com remédios comuns para dor, como anti-inflamatórios e pregabalina (um remédio para dor nos nervos).\n\nAlém disso, a paciente teve dificuldade para urinar, chamada retenção urinária, e precisou usar um cateter (um tubo para esvaziar a bexiga). Tentaram tirar o cateter várias vezes, mas não deu certo no começo.\n\n**O que ajudou na recuperação**\n\nPara controlar a dor, os médicos usaram um remédio forte chamado fentanil, que é aplicado na pele (transdérmico). Isso ajudou bastante e ela tolerou bem o remédio. Para ajudar a urinar, começou a usar um remédio chamado tamsulosina, que relaxa a parte da bexiga que controla a saída da urina. Também fizeram esvaziamento da bexiga de forma cuidadosa e sem cirurgia.\n\nDepois de seis semanas, a paciente conseguiu tirar o cateter com sucesso.\n\n**O que aprendemos com esse caso**\n\nEsse caso mostra que, em pacientes com Síndrome de Guillain-Barré, é importante cuidar da dor de forma personalizada, usando remédios fortes quando necessário, como opioides aplicados na pele. Também é fundamental prestar atenção na dificuldade para urinar, usando remédios e técnicas que ajudam a esvaziar a bexiga sem precisar de cirurgia. Cada paciente precisa de um cuidado especial para melhorar bem e evitar complicações.",
+            "B3": "**Contexto**  \nApresentamos o caso de uma mulher de 75 anos, previamente independente e hipertensa, que desenvolveu em poucos dias uma fraqueza progressiva nas quatro extremidades, acompanhada de dores musculares generalizadas e cefaleia. Após avaliação inicial e exames de imagem que descartaram causas compressivas ou encefalopatia, foi hospitalizada com diagnóstico de síndrome de Guillain-Barré (SGB), uma doença autoimune que afeta os nervos periféricos, levando à fraqueza muscular e alterações neurológicas.\n\n**Principais Achados Clínicos e Diagnósticos**  \nA paciente apresentou tetraparesia flácida (fraqueza muscular em braços e pernas sem rigidez) com diminuição ou ausência dos reflexos tendinosos, além de retenção urinária persistente. A punção lombar revelou uma dissociação albumina-citológica (aumento das proteínas no líquido cefalorraquidiano sem aumento de células), característica da SGB. A eletromiografia confirmou uma neuropatia mista com danos tanto na mielina (camada protetora dos nervos) quanto nos axônios (prolongamentos nervosos), com sinais de denervação ativa nos membros superiores.\n\n**Intervenções e Tratamento**  \nFoi iniciado tratamento com imunoglobulina endovenosa (IgIV) por cinco dias, que melhorou a força muscular. Devido à dor intensa e refratária a anti-inflamatórios e pregabalina (medicamento para dor neuropática), optou-se pelo uso de fentanil transdérmico (um opioide aplicado na pele), que proporcionou alívio eficaz e foi bem tolerado. A paciente também apresentou complicações infecciosas, como infecção urinária por Escherichia coli e infecção por Clostridium difficile, tratadas adequadamente com antibióticos.\n\nPara a retenção urinária, que dificultava a retirada do cateter vesical, foi iniciada tamsulosina, um medicamento que relaxa o colo da bexiga facilitando o esvaziamento urinário. Após seis semanas, foi possível remover o cateter com sucesso, evitando procedimentos invasivos.\n\n**Evolução Clínica**  \nDurante a internação de cinco semanas, a paciente apresentou melhora gradual da força muscular e controle da dor, com redução da intensidade das crises dolorosas, especialmente durante a reabilitação física. A combinação de fentanil transdérmico e paracetamol foi mantida para manejo da dor, enquanto a pregabalina foi suspensa devido à melhora clínica e para evitar interações medicamentosas.\n\n**Interpretação Clínica e Recomendações**  \nEste caso ilustra a complexidade do manejo da síndrome de Guillain-Barré, especialmente quando associada a dor neuropática intensa e disfunção autonômica, como a retenção urinária. Destaca-se a importância de uma avaliação individualizada da dor, considerando o uso de opioides transdérmicos quando os tratamentos convencionais não são eficazes ou bem tolerados. Além disso, a abordagem da retenção urinária com medicamentos relaxantes da musculatura vesical e cateterismo intermitente pode evitar complicações e promover a recuperação funcional.\n\n**Próximos Passos e Considerações Finais**  \nÉ fundamental o acompanhamento multidisciplinar, incluindo neurologia, urologia, fisioterapia e terapia ocupacional, para otimizar a reabilitação e a qualidade de vida do paciente com SGB. O manejo cuidadoso da dor e das complicações autonômicas deve ser parte integrante do tratamento, visando minimizar sequelas e promover a recuperação plena."
+        }
+    },
+    {
+        "article": "Um homem de 26 anos de idade, foi admitido no nosso hospital com febre e estado mental alterado. Ele relatou uma história de 12 dias de febre (38-39°C), dores de cabeça, foto sensibilidade, diplopia, e fadiga severa. Seus familiares declararam que ele era autônomo, um fumante leve, não bebia, e negou o uso de drogas. No departamento de emergência, ele estava sonolento, febril (temperatura de 38°C), e tinha uma frequência cardíaca de 110 batimentos por minuto. Ele negou ter desconforto torácico ou palpitações cardíacas. A pontuação da escala de coma de Glasgow do departamento de emergência foi de 13. Não havia evidência de erupção cutânea, contusão, ou petéquias. O exame dos sistemas respiratório, cardiovascular, e abdominal do paciente foi normal. O exame neurológico revelou rigidez leve do pescoço, mas sem sinal meníngeo.\n\nOs estudos no laboratório indicaram o seguinte: 5.8 x 109/L de glóbulos brancos, 11.2 g/L de hemoglobina, 243 x 109/L de plaquetas, 89.5% de neutrófilos, 3.1% de linfócitos, 126 mmol/L de sódio, 4 mmol/L de potássio, e 134 mg/dL de glicose. As culturas de sangue não detetaram qualquer crescimento. Uma radiografia de tórax não indicou qualquer patologia ou consolidação localizada, e a tomografia computorizada (TC) inicial do seu cérebro não foi notável. No terceiro dia, os resultados da sua punção lombar sugeriram meningite tuberculosa: aparência clara, aumento da contagem de glóbulos brancos (40/L) com predominância de linfócitos, glóbulos vermelhos (16/L), alta proteína (2.09 g/L), e baixa glicose (40 mg/dL). A relação fluido cerebral/glicose no soro foi inferior a 50%. Ambos foram negativos para citomegalovírus (CMV), toxoplasmose IgM, e serologia do vírus da imunodeficiência humana (HIV).\n\nO paciente foi internado no hospital com meningite e hiponatremia como diagnósticos clínicos. Inicialmente, foram administrados 2 gramas por dia de ceftriaxona, 10 miligramas por dia de injeção de dexametasona, solução salina hipertônica e paracetamol. A condição melhorou ligeiramente no segundo dia. Ele foi tratado por meningite tuberculosa com 10 miligramas por dia de injeção de dexametasona e uma combinação de 750 miligramas por dia de infusão de levofloxacina e medicamentos antituberculosos, incluindo 300 miligramas de isoniazida, 600 miligramas de rifampina, 1.100 miligramas de etambutol, 1.200 miligramas de pirazinamida e 50 miligramas de piridoxina, com base nos resultados da punção lombar. A condição do paciente melhorou ligeiramente, ele estava completamente consciente e continuou a sofrer de uma terrível dor de cabeça e paralisia do terceiro nervo. No entanto, a condição do paciente piorou consideravelmente no dia sete, manifestando-se como inconsciência e convulsões.\n\nOito dias após a admissão, uma tomografia computadorizada de contraste repetido do cérebro mostrou o desenvolvimento de ventriculomegalia sugestiva de hidrocefalia obstrutiva e aumento basilar. Houve um aumento dos ventrículos terceiro, quarto e lateral. Seus níveis de sódio no soro diminuíram (124 mmol/L) ao longo de vários dias. Com base em critérios de definição de caso bem estabelecidos de pesquisa de meningite tuberculosa, o paciente foi diagnosticado com provável meningite tuberculosa com uma pontuação total de 12, que inclui critérios clínicos (duração dos sintomas de mais de cinco dias (4), paralisia dos nervos cranianos (1)), critérios do fluido cerebrospinal (aparência clara (1), predominância linfocítica (1), concentração de proteínas superior a um g/L (1), concentração absoluta de glicose no fluido cerebrospinal inferior a 2.2 mmol/L (1)), critérios de imagem cerebral (hidrocefalia (1), aumento basilar meníngeo (2)). O paciente foi transferido para a unidade de cuidados intensivos (UCI) para a inserção de um shunt ventrículo-peritoneal de emergência. Observou-se a possibilidade de complicação após a inserção do shunt. Não identificamos complicações, tais como infecção, flebite, ou um shunt exposto no paciente. A condição do paciente piorou gradualmente, e ele morreu dez dias após a admissão hospitalar.\n\n",
+        "gold_summary": "Um homem de 26 anos sem histórico médico significativo, tuberculose ou indicações de comprometimento imunológico, foi internado no nosso hospital com febre e estado mental alterado. Ele estava sonolento, febril (temperatura de 38°C), tinha uma frequência cardíaca de 110 batimentos por minuto e apresentava uma ligeira rigidez no pescoço, mas sem sinal meníngeo. Uma punção lombar no terceiro dia de internamento sugeriu meningite tuberculosa. Ele foi tratado para meningite tuberculosa e a sua condição melhorou ligeiramente. No entanto, a condição do paciente de repente piorou e uma tomografia computadorizada de contraste repetido do cérebro mostrou o desenvolvimento de ventriculomegalia e aumento basilar. A inserção de um shunt ventriculoperitoneal de emergência foi realizada; no entanto, o paciente morreu dez dias após a admissão hospitalar.\n",
+        "synthetic_summary": {
+            "B1": "Um homem jovem ficou doente com febre e dor de cabeça. Ele ficou muito cansado e meio confuso. Os médicos fizeram um exame na cabeça dele e acharam que ele tinha uma doença no cérebro chamada meningite. Eles deram remédios para ajudar. No começo, ele melhorou um pouco. Mas depois, ele ficou pior e teve que fazer uma cirurgia para ajudar o líquido da cabeça a sair. Mesmo assim, ele não ficou bem e morreu depois de alguns dias no hospital. Os médicos tentaram cuidar dele com muito carinho.",
+            "B2": "**O que aconteceu com o paciente**\n\nUm homem de 26 anos chegou ao hospital com febre alta e confusão mental. Ele estava sonolento, com febre de 38°C e o coração batendo rápido. Durante o exame, os médicos perceberam que ele tinha o pescoço um pouco rígido, mas sem outros sinais típicos de infecção nas meninges (as membranas que envolvem o cérebro).\n\n**O que os exames mostraram**\n\nNo terceiro dia, os médicos fizeram uma punção lombar, que é quando retiram um pouco do líquido que envolve o cérebro e a medula para analisar. Esse exame indicou que ele tinha meningite tuberculosa, uma infecção grave causada pela bactéria da tuberculose que ataca as meninges.\n\n**Tratamento e evolução**\n\nO paciente começou a receber remédios específicos para combater a tuberculose e medicamentos para diminuir a inflamação. No começo, ele melhorou um pouco, ficando mais consciente, mas ainda sentia dores fortes de cabeça e tinha paralisia em um dos nervos do rosto.\n\nDepois de alguns dias, sua situação piorou muito. Ele ficou inconsciente e teve convulsões. Um novo exame de imagem do cérebro mostrou que os ventrículos, que são espaços cheios de líquido no cérebro, estavam aumentados, indicando um problema chamado hidrocefalia, que é o acúmulo excessivo de líquido no cérebro.\n\n**Intervenção e desfecho**\n\nPara tentar ajudar, os médicos colocaram um tubo chamado shunt ventriculoperitoneal, que serve para drenar o excesso de líquido do cérebro para outra parte do corpo. Apesar desse procedimento, o paciente não melhorou e, infelizmente, faleceu dez dias depois de ter sido internado.\n\n**O que isso significa**\n\nEsse caso mostra como a meningite tuberculosa pode ser muito grave e difícil de tratar, mesmo com remédios e cuidados intensivos. A inflamação pode causar complicações sérias, como o acúmulo de líquido no cérebro, que pode levar a danos irreversíveis. É importante diagnosticar e tratar essa doença o mais cedo possível para tentar evitar esses problemas.",
+            "B3": "**Contexto**  \nUm homem de 26 anos, sem antecedentes médicos relevantes, sem histórico de tuberculose ou sinais de imunodeficiência, foi admitido no hospital apresentando febre persistente e alteração do estado mental. Ele relatava sintomas há cerca de 12 dias, incluindo febre alta (38-39°C), dores de cabeça intensas, sensibilidade à luz, visão dupla (diplopia) e fadiga extrema. No momento da admissão, estava sonolento, com temperatura de 38°C, frequência cardíaca acelerada (110 bpm) e rigidez leve no pescoço, porém sem sinais típicos de irritação meníngea (como rigidez severa ou reflexos anormais).\n\n**Principais Achados**  \nExames laboratoriais iniciais mostraram um quadro inflamatório com predominância de neutrófilos, mas sem crescimento bacteriano nas culturas de sangue. A tomografia computadorizada (TC) cerebral inicial não revelou alterações. No terceiro dia, a análise do líquido cefalorraquidiano (punção lombar) indicou meningite tuberculosa, caracterizada por aumento de células brancas com predominância de linfócitos, proteína elevada e glicose baixa no líquido, além de ausência de infecções virais ou por toxoplasmose. O diagnóstico foi confirmado por critérios clínicos, laboratoriais e de imagem.\n\n**Interpretação Clínica**  \nO paciente recebeu tratamento específico para meningite tuberculosa, incluindo antibióticos antituberculosos (isoniazida, rifampicina, etambutol, pirazinamida), corticosteroides (dexametasona) e outros medicamentos de suporte. Inicialmente, houve uma melhora discreta do quadro clínico, com recuperação da consciência, mas persistência de dores de cabeça intensas e paralisia do terceiro nervo craniano (que controla movimentos oculares). No sétimo dia, sua condição piorou abruptamente, apresentando perda de consciência e convulsões.\n\nUma nova tomografia cerebral com contraste revelou ventriculomegalia (aumento dos ventrículos cerebrais) compatível com hidrocefalia obstrutiva, uma complicação grave que ocorre quando o fluxo do líquido cefalorraquidiano é bloqueado, causando aumento da pressão intracraniana. Além disso, foi observada inflamação das meninges na base do cérebro (aumento basilar meníngeo). O paciente também desenvolveu hiponatremia (níveis baixos de sódio no sangue), que pode agravar o quadro neurológico.\n\n**Próximos Passos e Desfecho**  \nDevido à hidrocefalia, foi necessária a colocação emergencial de um shunt ventriculoperitoneal, um dispositivo cirúrgico que drena o excesso de líquido do cérebro para o abdômen, aliviando a pressão intracraniana. Apesar da ausência de complicações relacionadas ao shunt, como infecção ou obstrução, o quadro clínico do paciente continuou a se deteriorar. Ele faleceu dez dias após a admissão hospitalar, evidenciando a gravidade e o rápido agravamento que a meningite tuberculosa pode causar, mesmo com tratamento adequado.\n\n---\n\nEste caso ilustra a complexidade do diagnóstico e manejo da meningite tuberculosa em adultos jovens, ressaltando a importância do monitoramento cuidadoso para complicações neurológicas graves, como a hidrocefalia, que podem levar a desfechos fatais."
+        }
+    },
+    {
+        "article": "Uma mulher de 20 anos foi acompanhada desde os oito anos por causa de uma NS idiopática, que se iniciou com uma trombose venosa cerebral, estendendo-se à veia jugular direita, com uma embolia pulmonar massiva. A paciente não teve sequelas. Não tinha outro histórico médico ou cirúrgico. Não foi relatado histórico familiar de trombose. A paciente não foi submetida a biópsia, porque não tinha insuficiência renal nem hematúria grave, nem hipertensão na primeira apresentação; além disso, não tinha outros sinais renais sugestivos de uma síndrome nefrótica secundária. Foi, por conseguinte, submetida a um tratamento anticoagulante (antagonista oral da vitamina K) e a um tratamento oral com corticosteroides, com uma boa evolução. Depois disso, a paciente recebeu vários tratamentos com corticosteroides de alta dose para as recaídas da NS dependentes de esteróides. Foi, por conseguinte, submetida a um tratamento com micofenolato de mofetil (MMF) como terapia de base para evitar os corticosteroides e assegurar um crescimento normal. Foi efetuada uma avaliação exaustiva da trombofilia, que não mostrou qualquer anormalidade. A taxa de homocisteína, a taxa de fibrinogénio no sangue, a proteína C, a proteína S, a antitrombina III, a mutação do factor V de Leiden, a mutação JAK-2, as crioglobulinas, os anticorpos anticardiolipina, o anticoagulante lúpico e os anticorpos beta-1-glicoproteína foram normais. O tratamento anticoagulante foi interrompido nove anos depois. A evolução foi marcada pela ocorrência de várias recaídas da doença, que foram controladas com um tratamento oral com corticosteroides. A remissão da NS foi observada desde 2017, pelo que o MMF foi gradualmente interrompido em 2019 e a paciente permaneceu assintomática e sem qualquer recaída.\n\nUm ano depois, o paciente veio ao nosso departamento de emergência por causa de uma dor abdominal intensa e difusa sem irradiação particular associada a vômitos pós-prandiais e edema bilateral dos membros inferiores nas últimas seis horas. O exame físico revelou uma intensa sensibilidade epigástrica com sinais vitais normais (pressão arterial de 120/70 mm Hg, frequência cardíaca de 83 bpm e saturação de oxigênio a 100% no ar ambiente). O paciente estava afebril com consciência normal. O resto do exame físico foi sem observações. A análise de urina com labstix revelou proteinúria. Os resultados da análise de gases no sangue mostraram acidose metabólica com compensação respiratória. Outros testes laboratoriais revelaram hipoalbuminemia, hipercolesterolemia, um tempo de protrombina de 90%, níveis elevados de D-dímero, lactato desidrogenase e creatina fosfocinase, bem como uma síndrome inflamatória biológica com CRP de 37 mg/L e leucocitose a 26.4 x 103/µL. As funções renais e hepáticas foram normais.\n\nO paciente foi hospitalizado numa unidade de cuidados intensivos com monitorização estreita dos sinais vitais e iniciação de medidas de ressuscitação. Um ultrassom abdominal foi realizado urgentemente mostrando um derrame intra-abdominal de baixa a moderada abundância. Um TAC abdominal revelou trombose aguda da artéria mesentérica superior com isquemia mesentérica aguda. O paciente foi imediatamente encaminhado para a sala de operações. A exploração intraoperativa confirmou isquemia mesentérica com extensa necrose de quase todo o intestino delgado, tornando as suas ressecções incompatíveis com a vida, como se mostra na Figura 3. O paciente morreu após 48 horas.\n",
+        "gold_summary": "Apresentamos o caso de uma mulher de 20 anos com uma história de 12 anos de NS idiopática, revelada por uma trombose venosa cerebral extensa com embolia pulmonar, tratada com terapia anticoagulante e terapia corticosteróide oral, seguida por micofenolato de mofetil (MMF). A avaliação da trombofilia não mostrou quaisquer anormalidades. A evolução foi marcada pela ocorrência de várias recidivas de NS, controladas por terapia corticosteróide oral, até 2017. Subsequentemente, a paciente não apresentou uma recidiva da sua doença. O tratamento anticoagulante e o MMF foram, portanto, interrompidos. Um ano depois, a paciente apresentou uma dor abdominal aguda difusa, associada a vómitos pós-prandiais e edema bilateral dos membros inferiores. Os resultados laboratoriais confirmaram uma recidiva de NS. Uma tomografia abdominal revelou uma trombose aguda da artéria mesentérica superior com isquemia mesentérica aguda. A exploração intraoperativa mostrou isquemia mesentérica com necrose extensa do intestino delgado, tornando as suas ressecções incompatíveis com a vida. A paciente morreu após 48 horas.\n",
+        "synthetic_summary": {
+            "B1": "Uma moça teve um problema no sangue desde pequena. Ela tomou remédios para ajudar o sangue a não ficar ruim. Ela melhorou e ficou sem dor por muito tempo.\n\nUm dia, ela sentiu uma dor forte na barriga. Também vomitou e seus pés ficaram inchados. Os médicos fizeram exames e viram que o sangue dela estava bloqueado em uma parte da barriga.\n\nEles tentaram ajudar no hospital, mas o problema no sangue fez o intestino dela ficar muito machucado. Infelizmente, ela ficou muito doente e morreu depois de dois dias.\n\nOs médicos ficaram tristes, mas tentaram cuidar dela com muito carinho.",
+            "B2": "**Histórico da Paciente e Doença Inicial**\n\nEsta é a história de uma jovem de 20 anos que desde os 8 anos tinha uma doença chamada síndrome nefrótica (NS) idiopática. A síndrome nefrótica é um problema nos rins que faz o corpo perder muita proteína pela urina. Quando ela tinha 8 anos, teve um problema sério: um coágulo de sangue no cérebro (trombose venosa cerebral) que se espalhou para uma veia do pescoço e causou um embolia pulmonar, que é quando um pedaço desse coágulo vai para os pulmões. Ela foi tratada com remédios que impedem a formação de coágulos (anticoagulantes) e com corticosteroides, que são remédios que ajudam a controlar a inflamação e a doença nos rins. Depois, para evitar os efeitos ruins dos corticosteroides, ela também tomou outro remédio chamado micofenolato de mofetil (MMF).\n\n**Tratamentos e Evolução**\n\nDurante muitos anos, a paciente teve várias recaídas da síndrome nefrótica, ou seja, a doença piorava de vez em quando, mas sempre melhorava com o tratamento com corticosteroides. Ela fez vários exames para ver se tinha alguma doença que causasse coágulos, mas todos os testes deram normais. Em 2017, a doença ficou controlada e ela não teve mais crises. Por isso, os médicos pararam os remédios anticoagulantes e o MMF em 2019. Ela ficou bem e sem sintomas por um ano.\n\n**O Problema Grave e o Desfecho**\n\nUm ano depois, a paciente chegou ao hospital com uma dor forte na barriga, vômitos e inchaço nas pernas. Os exames mostraram que a síndrome nefrótica tinha voltado, e que ela tinha um coágulo em uma artéria importante do intestino (artéria mesentérica superior). Esse coágulo bloqueou o sangue que chega ao intestino, causando uma falta de oxigênio chamada isquemia, o que levou à morte de uma grande parte do intestino (necrose). Os médicos tentaram operar, mas o dano era tão grande que não foi possível salvar a paciente, que morreu 48 horas depois.\n\n**O Que Isso Significa**\n\nEste caso mostra como a síndrome nefrótica pode causar problemas sérios, como coágulos no sangue, mesmo depois de muitos anos de tratamento. Embora a paciente tenha tido um bom controle da doença por um tempo, a volta da síndrome nefrótica pode levar a complicações graves e até fatais. Por isso, é importante acompanhar de perto pacientes com essa doença e tratar rapidamente qualquer sinal de problema.",
+            "B3": "**Contexto**  \nApresentamos o caso de uma mulher de 20 anos com um histórico de 12 anos de síndrome nefrótica (NS) idiopática, que inicialmente se manifestou aos 8 anos com uma trombose venosa cerebral extensa, estendendo-se à veia jugular direita, acompanhada de uma embolia pulmonar grave. Na época, a paciente foi tratada com anticoagulantes orais (medicamentos que impedem a formação de coágulos) e corticosteroides orais, apresentando boa resposta. Posteriormente, devido a múltiplas recaídas da síndrome nefrótica dependentes de corticosteroides, foi introduzido o micofenolato de mofetil (MMF), um imunossupressor usado para reduzir a necessidade de corticosteroides e permitir um crescimento normal. Uma avaliação detalhada para causas de trombose (trombofilia) não revelou nenhuma alteração. A paciente manteve várias recaídas controladas com corticosteroides até 2017, quando entrou em remissão prolongada. O tratamento anticoagulante e o MMF foram então suspensos.\n\n**Principais Achados**  \nUm ano após a suspensão dos tratamentos, a paciente procurou atendimento de emergência devido a dor abdominal intensa e difusa, acompanhada de vômitos após as refeições e inchaço (edema) nos dois membros inferiores, com início nas últimas seis horas. O exame físico mostrou sensibilidade marcada na região superior do abdômen (epigástrio), mas sinais vitais normais e ausência de febre. Exames laboratoriais indicaram uma recidiva da síndrome nefrótica, evidenciada pela presença de proteína na urina (proteinúria), baixos níveis de albumina no sangue (hipoalbuminemia) e colesterol elevado (hipercolesterolemia). Também foram detectados sinais de inflamação e coagulação aumentada, como níveis elevados de D-dímero e leucocitose (aumento dos glóbulos brancos). A função dos rins e do fígado estava preservada.\n\nUma tomografia computadorizada (TAC) abdominal revelou trombose aguda da artéria mesentérica superior, responsável por irrigar o intestino delgado, causando isquemia (falta de fluxo sanguíneo) e comprometimento grave do intestino. Durante a cirurgia de emergência, constatou-se necrose extensa de quase todo o intestino delgado, tornando a ressecção (remoção cirúrgica) inviável para a sobrevivência da paciente.\n\n**Interpretação Clínica**  \nEste caso ilustra uma complicação rara e grave da síndrome nefrótica: a trombose arterial mesentérica, que levou a uma isquemia intestinal extensa e fatal. Apesar do tratamento prévio anticoagulante e da ausência de fatores trombofílicos identificados, a paciente desenvolveu uma trombose arterial aguda, destacando a complexidade do risco trombótico em pacientes com síndrome nefrótica, mesmo após longo período de remissão. A recidiva da síndrome nefrótica provavelmente contribuiu para o estado pró-trombótico, facilitando a formação do coágulo arterial.\n\n**Próximos Passos e Considerações**  \nEste caso ressalta a importância do monitoramento contínuo em pacientes com síndrome nefrótica, mesmo após períodos prolongados de remissão, especialmente quanto ao risco de eventos trombóticos graves. Em situações de dor abdominal aguda em pacientes com histórico de síndrome nefrótica, deve-se considerar prontamente a possibilidade de trombose mesentérica para diagnóstico e intervenção precoce. Além disso, a decisão sobre a duração do tratamento anticoagulante em pacientes com síndrome nefrótica deve ser cuidadosamente avaliada, levando em conta os riscos e benefícios individuais. Infelizmente, neste caso, a extensão da isquemia intestinal tornou o tratamento cirúrgico inviável, culminando no óbito da paciente em 48 horas após a cirurgia."
+        }
+    },
+    {
+        "article": "Apresentação da paciente: trata-se de uma paciente de 37 anos que consultou por uma disfagia mista de instalação progressiva em um contexto de emagrecimento e de alteração do estado geral. Os antecedentes são sem particularidades. A evolução foi marcada por uma dispneia inspiratória de agravamento progressivo. A paciente apresentou-se com dispneia laríngea, o que levou a uma traqueotomia de urgência.\n\nResultados clínicos: o exame clínico geral encontrou uma paciente bem orientada no tempo e no espaço, com estado hemodinâmico estável. O exame ORL evidenciou uma massa parafaríngea direita preenchendo quase que totalmente a luz faríngea e obstruindo as vias aéreas superiores.\n\nCronologia: após o exame clínico, a paciente foi submetida a uma ressonância magnética cervical e, em seguida, a uma biópsia da massa parafaríngea sob anestesia local, cujo exame anatomopatológico motivou a realização de um exame de extensão com base em tomografia computadorizada (TC) toraco-abdomino-pélvica e cintilografia óssea.\n\nDiagnóstico: a ressonância magnética cervical mostrou um processo tumoral do espaço parafaríngeo direito, que se projeta para a faringe, com sinal T2 de alta intensidade, com restrição de difusão e que se eleva após a injeção de gadolínio. Tem 47 x 40 x 50 mm. O tumor ocupa quase toda a luz da faringe e invade o véu do palato superior. Este último é espesso, com áreas de necrose. A biópsia da massa, com exame anatomopatológico, evidenciou células tumorais redondas basófilas. O estudo imuno-histoquímico foi positivo para as proteínas CD99, anticorpos anti-S100 e Ki67. Além disso, foi realizado um estudo citogenético da amostra, com resultado positivo. O resultado final anatomopatológico concluiu que se tratava de um sarcoma de Ewing extraósseo do espaço parafaríngeo. O balanço de extensão foi negativo.\n\nIntervenção terapêutica: a paciente foi encaminhada para oncologia para quimioterapia de primeira linha com vincristina, ifosfamida, doxorrubicina e etoposide.\n\nSeguimento e resultados das intervenções terapêuticas: após 6 ciclos de quimioterapia, a progressão do tumor continuou e a paciente faleceu devido à extensão basicraniana da doença.\n",
+        "gold_summary": "Relatamos o caso clínico de uma paciente de 37 anos, admitida em urgência por dispneia inspiratória num quadro de astenia e anorexia. A ressonância magnética (RM) cervical objetivou um processo no espaço parafaríngeo direito, que obstruía quase toda a luz faríngea. O estudo anatomopatológico, imunohistoquímico e citogenético, concluiu por um sarcoma de Ewing extraesquelético. O balanço de extensão foi negativo. A paciente recebeu quimioterapia.\n",
+        "synthetic_summary": {
+            "B1": "Uma mulher estava com muita dificuldade para respirar. Ela também estava muito cansada e comendo pouco. Os médicos fizeram um exame para ver o que tinha na sua garganta. Eles acharam um caroço grande que estava quase fechando o caminho do ar. Os médicos fizeram um exame do caroço e descobriram que era um tipo de doença que cresce rápido. Ela fez um tratamento com remédios fortes para tentar melhorar.",
+            "B2": "**O que aconteceu com a paciente**\n\nUma mulher de 37 anos começou a sentir dificuldade para engolir e perdeu peso sem motivo aparente. Com o tempo, ela teve dificuldade para respirar, especialmente ao inspirar, o que piorou bastante. Por causa disso, precisou passar por uma traqueostomia, que é uma cirurgia para abrir um caminho na garganta e ajudar a respirar.\n\n**O que os exames mostraram**\n\nOs médicos fizeram uma ressonância magnética no pescoço e encontraram um tumor grande perto da faringe, que é a parte da garganta por onde passa o ar e a comida. Esse tumor estava quase bloqueando a passagem do ar. Para entender melhor o que era, fizeram uma biópsia, que é quando tiram um pedacinho do tumor para analisar.\n\nNo laboratório, os especialistas viram que as células do tumor eram do tipo sarcoma de Ewing extraósseo. Isso significa que o câncer veio dos tecidos moles, não dos ossos, e é um tipo raro e agressivo. Outros exames mostraram que o tumor ainda não tinha se espalhado para outras partes do corpo.\n\n**Como foi o tratamento**\n\nA paciente começou a receber quimioterapia, que é o uso de remédios fortes para tentar matar as células do câncer. Mesmo assim, depois de vários ciclos de tratamento, o tumor continuou crescendo e acabou se espalhando para áreas importantes da cabeça.\n\n**O que isso significa**\n\nInfelizmente, apesar do tratamento, o câncer avançou e a paciente não resistiu. Esse caso mostra como alguns tumores podem ser difíceis de tratar e a importância de um diagnóstico rápido para tentar melhorar as chances de cura.",
+            "B3": "**Contexto**  \nEste é o relato do caso de uma mulher de 37 anos que procurou atendimento médico devido a dificuldade para engolir (disfagia) que foi piorando progressivamente, acompanhada de perda de peso e piora do estado geral de saúde. Posteriormente, ela desenvolveu dificuldade para respirar ao inspirar (dispneia inspiratória), que se agravou a ponto de necessitar de uma traqueostomia de emergência (procedimento para abrir uma via aérea na traqueia).\n\n**Principais Achados**  \nNo exame clínico, a paciente estava consciente e orientada, com sinais vitais estáveis. A avaliação otorrinolaringológica revelou uma massa localizada no espaço parafaríngeo direito (região ao lado da faringe), que ocupava quase toda a passagem da garganta e bloqueava as vias aéreas superiores. A ressonância magnética do pescoço mostrou que essa massa tinha cerca de 4,7 x 4,0 x 5,0 cm, apresentava características típicas de tumor, incluindo áreas de necrose (morte celular) e invasão do véu do palato superior (parte da garganta).  \n\nA biópsia da massa, analisada ao microscópio, revelou células tumorais redondas com características específicas. Testes imunohistoquímicos indicaram a presença das proteínas CD99, S100 e Ki67, que são marcadores usados para identificar tipos específicos de tumores. Além disso, um estudo citogenético (análise dos cromossomos das células tumorais) confirmou o diagnóstico. Esses exames levaram à conclusão de que a paciente tinha um sarcoma de Ewing extraósseo, um tipo raro de tumor maligno que normalmente ocorre nos ossos, mas neste caso surgiu no tecido mole ao redor da faringe. Exames adicionais para verificar a extensão da doença (tomografia computadorizada do tórax, abdômen e pelve, além de cintilografia óssea) não mostraram metástases.\n\n**Interpretação Clínica**  \nO sarcoma de Ewing extraósseo é um tumor agressivo e raro, especialmente em localizações como o espaço parafaríngeo. A obstrução das vias aéreas superiores pela massa explica a dificuldade respiratória grave da paciente. O diagnóstico precoce e o tratamento multidisciplinar são essenciais, mas o prognóstico pode ser reservado devido à agressividade do tumor.\n\n**Próximos Passos e Evolução**  \nA paciente foi encaminhada para tratamento oncológico e iniciou quimioterapia combinada com os medicamentos vincristina, ifosfamida, doxorrubicina e etoposídeo, que são agentes usados para combater sarcomas agressivos. Apesar do tratamento, após seis ciclos de quimioterapia, o tumor continuou a progredir, invadindo a base do crânio, o que levou ao falecimento da paciente.\n\nEste caso destaca a importância do reconhecimento rápido de sintomas como disfagia e dispneia progressiva, a necessidade de exames de imagem e biópsia para diagnóstico preciso, e os desafios no tratamento de tumores raros e agressivos como o sarcoma de Ewing extraósseo."
+        }
+    },
+    {
+        "article": "Uma mulher grávida de 32 anos de idade, afetada pela síndrome de Holt-Oram, foi encaminhada à nossa instituição para uma ecografia de rotina de anatomia do segundo trimestre. Ela tinha um histórico familiar positivo da síndrome de Holt-Oram envolvendo a mãe e a irmã. Em todos os membros da família afetados, a única evidência clínica da síndrome diz respeito aos defeitos do membro superior, com uma malformação do osso carpal e agenesia do polegar. A ultrassonografia relatou uma aplasia bilateral do rádio, ulna ligeiramente curvada e mão torcida bilateral com quatro raios digitais. Um aumento significativo do átrio direito sem regurgitação tricúspide também foi detectado. A paciente recusou a amniocentese e decidiu continuar com a gravidez. No momento da ultrassonografia de acompanhamento às 30 semanas, o aumento do átrio direito foi confirmado sem insuficiência tricúspide ou outras malformações cardíacas. A paciente foi submetida a uma cesariana de emergência às 40 semanas de gestação devido a bradicardia fetal durante o trabalho de parto. Um recém-nascido do sexo masculino foi entregue com um peso ao nascer de 3.110 g e uma pontuação de APGAR de 9 e 9 aos 1′ e 5′ min. A avaliação pós-natal confirmou a hipoplasia grave do raio, ulna ligeiramente curvada e agenesia do primeiro raio. A ecocardiografia neonatal detetou o aumento do átrio direito, observando também defeitos atriais e dois pequenos defeitos do septo ventricular não detetados pré-natal. A análise genética também foi realizada, e a mutação TBX5 foi detetada.\n",
+        "gold_summary": "Apresentamos um caso de uma mulher grávida de 32 anos afetada pela síndrome de Holt-Oram, que foi encaminhada à nossa instituição para um exame de rotina de anatomia no segundo trimestre. O ultrassom relatou uma aplasia bilateral do rádio, ulna levemente curvada e mão bilateral torcida com quatro raios digitais. Um alargamento significativo do átrio direito sem regurgitação tricúspide também foi detectado. A paciente recusou a amniocentese e a avaliação pós-natal confirmou o diagnóstico da síndrome de Holt-Oram.\n",
+        "synthetic_summary": {
+            "B1": "Uma mamãe estava esperando um bebê. Ela tem uma doença que faz os braços crescerem diferente. No exame, o médico viu que os ossos dos braços do bebê estavam diferentes. O coração do bebê estava um pouco maior em um lado, mas estava batendo bem. Depois que o bebê nasceu, os médicos viram que ele tinha a mesma doença da mamãe. Tudo está bem cuidado e os médicos vão ajudar o bebê a crescer forte.",
+            "B2": "**O que aconteceu com a gestante**\n\nUma mulher de 32 anos, grávida, foi para um exame de ultrassom no segundo trimestre da gravidez. Ela tem uma condição chamada síndrome de Holt-Oram, que afeta os ossos dos braços e as partes do coração. Essa síndrome também está presente na mãe e na irmã dela.\n\n**O que o exame mostrou**\n\nNo ultrassom, os médicos viram que os ossos chamados rádio estavam faltando nos dois braços do bebê. Outros ossos, como a ulna, estavam um pouco curvados, e as mãos tinham uma forma diferente, com quatro dedos em vez de cinco. Também notaram que uma parte do coração do bebê, chamada átrio direito, estava maior do que o normal, mas sem problemas na válvula tricúspide, que ajuda o sangue a circular.\n\n**Decisões e resultados**\n\nA mãe decidiu não fazer um exame chamado amniocentese, que retira um pouco do líquido ao redor do bebê para verificar doenças. Ela continuou a gravidez normalmente. Quando o bebê nasceu, foi confirmado que ele tinha os mesmos problemas nos ossos dos braços e algumas pequenas alterações no coração que não tinham sido vistas antes. Um exame genético mostrou que o bebê tinha uma mudança no gene TBX5, que é a causa da síndrome de Holt-Oram.\n\n**Por que isso é importante**\n\nEsse caso mostra como a síndrome de Holt-Oram pode afetar os ossos e o coração do bebê. Os exames durante a gravidez ajudam a identificar essas mudanças, mas nem todos os problemas podem ser vistos antes do nascimento. Saber disso ajuda os médicos e as famílias a se prepararem para cuidar melhor do bebê.",
+            "B3": "**Contexto**  \nEste relato descreve o caso de uma mulher de 32 anos grávida, portadora da síndrome de Holt-Oram, uma condição genética que afeta principalmente os membros superiores e o coração. A paciente tinha histórico familiar positivo para a síndrome, com a mãe e a irmã também apresentando alterações nos ossos do punho e ausência do polegar, mas sem outras manifestações clínicas significativas.\n\n**Principais Achados**  \nDurante a ultrassonografia de rotina realizada no segundo trimestre da gestação, foram identificadas alterações ósseas características da síndrome: ausência bilateral do rádio (um dos ossos do antebraço), curvatura leve da ulna (outro osso do antebraço) e deformidade nas mãos, que apresentavam quatro dedos em vez de cinco. Além disso, foi detectado um aumento significativo do átrio direito do coração, sem evidência de regurgitação (retorno anormal de sangue) pela válvula tricúspide.\n\nA paciente optou por não realizar amniocentese (um exame invasivo para diagnóstico genético pré-natal) e decidiu continuar com a gestação. Na ultrassonografia de acompanhamento, realizada às 30 semanas, confirmou-se o aumento do átrio direito, sem outras alterações cardíacas aparentes.\n\nAo nascer, por meio de cesariana de emergência devido à bradicardia fetal (frequência cardíaca baixa do bebê) durante o trabalho de parto, o recém-nascido do sexo masculino apresentou peso adequado e boa adaptação inicial, com pontuações APGAR de 9 aos 1 e 5 minutos. A avaliação pós-natal confirmou as alterações ósseas graves no antebraço e a ausência do primeiro dedo da mão. A ecocardiografia neonatal revelou o aumento do átrio direito, além de identificar defeitos no septo atrial e dois pequenos defeitos no septo ventricular, que não foram detectados durante a gestação.\n\nA análise genética confirmou a presença de mutação no gene TBX5, responsável pela síndrome de Holt-Oram.\n\n**Interpretação Clínica**  \nEste caso ilustra a importância da avaliação detalhada dos membros superiores e do coração em gestantes com histórico familiar da síndrome de Holt-Oram. As alterações ósseas detectadas por ultrassonografia são marcadores importantes para o diagnóstico pré-natal, enquanto as anomalias cardíacas podem ser mais sutis e requerem acompanhamento cuidadoso. A mutação no gene TBX5 confirma o diagnóstico genético da síndrome.\n\n**Próximos Passos**  \nO acompanhamento multidisciplinar do recém-nascido é fundamental, incluindo avaliação ortopédica para manejo das deformidades dos membros superiores e cardiológica para monitoramento e tratamento dos defeitos cardíacos. O aconselhamento genético para a família também é recomendado, considerando o padrão hereditário da síndrome."
+        }
+    },
+    {
+        "article": "Os autores apresentam o caso de um paciente do sexo masculino com 49 anos de idade. Ele era até então assintomático e não tinha registro pessoal de uso de medicação crônica. Era atualmente tabagista, porém negava consumo de álcool ou tóxicos. O paciente foi admitido ao pronto-socorro em razão de dor torácica em opressão e dispneia com início meia hora antes. Cinco dias antes da admissão ao hospital, o paciente relatou episódio semelhante de dor torácica em opressão que começou durante caminhada e persistiu por cerca de 30 minutos após repouso.\n\nQuando da chegada ao pronto-socorro, o paciente estava prostrado e cianótico, com aumento da frequência respiratória e hipóxia, a despeito de máscara de oxigênio com alto débito. O paciente evoluiu rapidamente para parada cardiopulmonar, tendo sido iniciadas manobras de Suporte Avançado de Vida, e ele foi submetido à intubação orotraqueal e ventilação invasiva. A análise gasométrica do sangue revelou acidose metabólica grave, com hiperlactatemia (pH = 6,87, pressão parcial de gás carbônico - PaCO2 - de 105mmHg, pressão parcial de oxigênio - PaO2 - de 120mmHg, bicarbonato - HCO3 - de 13,9 e lactato de 13,5mmol/L). O eletrocardiograma mostrou taquicardia de complexos largos com R-R regular (170/minuto) com desvio do eixo para a direita, sugerindo taquicardia ventricular monomórfica. Como não se observou resposta às manobras de Suporte Avançado de Vida, com persistência de taquicardia ventricular sem pulso, e levando em conta a queixa de dor torácica, considerou-se a hipótese de infarto agudo do miocárdio e se realizou a ministração de alteplase para trombólise, tendo em vista que o hospital não dispunha de um laboratório de hemodinâmica. Após recuperação da circulação espontânea, um eletrocardiograma revelou ritmo sinusal (90/minuto) e T bifásico entre V3 e V5.\n\nO paciente foi transferido para a unidade de terapia intensiva. Uma ecocardiografia transtorácica revelou discreta hipocinesia do segmento apical da parede inferolateral. A análise do sangue mostrou leve anemia (hemoglobina 11,5g/dL), lesão renal aguda (creatinina 2,26mg/dL e ureia 76mg/dL) e leve hipocalemia (3,2mmol/L). Os marcadores de necrose miocárdica se encontravam ligeiramente aumentados: hs-troponina 84pg/mL (corte: 34,2pg/mL), creatinoquinase 510UI/L (corte: 200UI/L), creatinoquinase MB 6,8ng/mL (corte: 7,2ng/mL) e mioglobina 2914ng/mL (corte: 116ng/mL). O nível de dímero-D também estava elevado (1.678ng/mL; corte: 500ng/mL). Hs-troponina aumentou para 358,50pg/mL após 3 horas, e seu valor máximo foi de 832pg/mL, 24 horas após a admissão.\n\nA trombólise foi complicada por sangramento no ponto de inserção do cateter venoso central e hematêmese abundante. Realizou-se endoscopia digestiva alta, que mostrou sangramento da mucosa, sangue digerido e coágulos no estômago. Em razão do sangramento ativo, o caso foi discutido com o laboratório de hemodinâmica, e a angiografia foi adiada até a estabilização clínica e a cessação da hemorragia.\n\nTrês dias após a admissão, o paciente melhorou gradativamente, permitindo extubação orotraqueal. A tomografia computadorizada do crânio não mostrou alterações. Foi realizado um scan de ventilação-perfusão, excluindo embolia pulmonar. A angiografia coronária revelou artérias coronárias sem lesões relevantes e uma artéria coronária direita com origem anormal a partir do seio coronário esquerdo. Em seguida, uma ACTC confirmou a origem anormal da artéria coronária direita a partir do seio coronário esquerdo, com trajeto entre o tronco da artéria pulmonar e a aorta posteriormente - um percurso interarterial com extensão de 18mm; não se observaram evidências de um percurso intramural ou coronariopatia aterosclerótica, com escore de cálcio de zero. A ressonância magnética cardíaca não trouxe informações importantes e nem se detectou contraste tardio.",
+        "gold_summary": "Os autores relatam um raro caso de uso de Suporte Avançado de Vida no contexto de uma parada cardíaca ocorrida em razão de uma origem aórtica anômala da artéria coronária direita em um paciente de 49 anos de idade. O paciente foi admitido com dor torácica e dispneia, evoluindo rapidamente para taquicardia ventricular sem pulso e parada cardiopulmonar. Considerou-se um infarto agudo do miocárdio e, na ausência de um laboratório de hemodinâmica no hospital, realizou-se trombólise. Subsequentemente, uma angiografia coronária revelou ausência de lesões angiográficas nas artérias coronárias e origem anômala da artéria coronária direita do seio de Valsalva oposto. Uma angiografia coronária por tomografia computadorizada confirmou o achado e determinou um trajeto entre a artéria pulmonar e a aorta. O paciente foi submetido à cirurgia cardíaca com realização de ponte de mamária para a artéria coronária direita, sem qualquer novo episódio de arritmia.",
+        "synthetic_summary": {
+            "B1": "Um homem de 49 anos sentiu muita dor no peito e ficou com dificuldade para respirar. Ele ficou muito mal e o coração parou de bater direito. Os médicos fizeram um tratamento rápido para ajudar o coração a funcionar de novo.\n\nDepois, eles descobriram que um dos vasos do coração dele estava no lugar errado. Isso pode causar problemas no coração. Para ajudar, os médicos fizeram uma cirurgia para arrumar esse vaso. Depois da cirurgia, o homem ficou melhor e o coração dele ficou forte.",
+            "B2": "**O que aconteceu com o paciente**\n\nUm homem de 49 anos chegou ao hospital sentindo dor no peito e dificuldade para respirar. Pouco depois, ele teve uma parada cardíaca, que é quando o coração para de bater corretamente. Os médicos tentaram salvar sua vida usando técnicas especiais de emergência, chamadas Suporte Avançado de Vida. Como eles pensaram que ele poderia estar tendo um ataque cardíaco, deram um remédio para tentar dissolver um possível coágulo no coração.\n\n**O que os exames mostraram**\n\nDepois que o paciente melhorou, exames mostraram que suas artérias do coração não tinham bloqueios comuns, mas que a artéria coronária direita, que leva sangue ao coração, tinha uma origem diferente do normal. Em vez de sair do lugar esperado, ela saía de um ponto errado na aorta (a principal artéria do corpo) e passava entre duas grandes artérias importantes. Esse caminho anormal pode causar problemas no fluxo de sangue e aumentar o risco de parada cardíaca.\n\n**O que foi feito para ajudar**\n\nPara corrigir esse problema, o paciente passou por uma cirurgia no coração. Os médicos fizeram uma ponte, que é uma nova passagem para o sangue chegar ao coração, usando uma artéria do peito chamada mamária. Depois da cirurgia, o paciente não teve mais problemas com batimentos irregulares do coração.\n\n**Por que isso é importante**\n\nEsse caso é raro e mostra como uma artéria coronária com origem anormal pode causar uma parada cardíaca grave. Também destaca a importância de exames detalhados para descobrir essas anomalias e o papel da cirurgia para evitar novos problemas.",
+            "B3": "**Contexto**  \nEste relato descreve o caso incomum de um homem de 49 anos que sofreu uma parada cardíaca causada por uma anomalia na origem da artéria coronária direita, um dos vasos que irrigam o coração. O paciente, previamente saudável e fumante, apresentou dor no peito e dificuldade para respirar, sintomas que evoluíram rapidamente para uma arritmia grave chamada taquicardia ventricular sem pulso, seguida de parada cardiopulmonar.\n\n**Principais Achados**  \nAo chegar ao hospital, o paciente estava em estado crítico, com baixa oxigenação e acidose metabólica severa (um desequilíbrio no pH do sangue causado por falta de oxigênio). O eletrocardiograma indicou uma arritmia ventricular grave. Como o hospital não dispunha de um laboratório para procedimentos invasivos, foi administrada trombólise (medicamento para dissolver coágulos) sob a suspeita de infarto do miocárdio. Após recuperação da circulação, exames mostraram alterações leves na movimentação do músculo cardíaco e elevação moderada dos marcadores sanguíneos de lesão cardíaca, além de sinais de insuficiência renal aguda e anemia leve.\n\nO tratamento trombolítico causou complicações hemorrágicas, incluindo sangramento digestivo, o que atrasou a realização de exames invasivos. Após estabilização, exames avançados foram realizados: a angiografia coronária (exame que visualiza as artérias do coração) não identificou obstruções significativas, mas revelou que a artéria coronária direita tinha uma origem anômala, saindo do seio coronário esquerdo (uma estrutura próxima à aorta) e passando entre a artéria pulmonar e a aorta — um trajeto considerado de risco por poder comprimir o vaso. A tomografia computadorizada confirmou essa anomalia, sem sinais de aterosclerose (acúmulo de placas nas artérias). A ressonância magnética cardíaca não mostrou cicatrizes ou áreas de infarto.\n\n**Interpretação Clínica**  \nA origem anômala da artéria coronária direita com trajeto interarterial é uma condição rara, mas potencialmente fatal, pois pode causar compressão do vaso durante o esforço físico, levando a isquemia (falta de oxigênio no músculo cardíaco), arritmias graves e parada cardíaca, como ocorreu neste paciente. A ausência de obstruções arteriais e a elevação moderada dos marcadores cardíacos sugerem que o evento foi desencadeado pela anomalia anatômica e não por um infarto típico causado por placas.\n\n**Próximos Passos e Desfecho**  \nDiante do diagnóstico, o paciente foi submetido a cirurgia cardíaca para correção da anomalia, com a realização de uma ponte de mamária (cirurgia que cria um desvio para garantir o fluxo sanguíneo adequado à artéria coronária direita). Após o procedimento, não houve novos episódios de arritmia, indicando sucesso na prevenção de futuras complicações. O caso destaca a importância de considerar anomalias coronarianas em pacientes com parada cardíaca e dor torácica, especialmente quando exames convencionais não mostram obstruções arteriais."
+        }
+    },
+    {
+        "article": "Informação sobre o paciente\nUm homem de 24 anos, residente em Yopougon, uma cidade popular em Abidjan, solteiro, que abandonou os estudos no último ano, sem emprego, que sofre de problemas psiquiátricos não documentados, foi acompanhado pelos seus pais às urgências do nosso hospital, devido a dor e inchaço epigástrico, que se desenvolveu ao longo de 15 dias, após a ingestão voluntária de uma faca. Nenhum outro sinal (disfagia, vómito, problemas de trânsito, tosse, hemorragia digestiva) foi encontrado no interrogatório. Os pais informaram-nos da presença de um problema mental no paciente, diagnosticado e não tratado por psiquiatras ou terapeutas tradicionais.\n\nResultados clínicos\nO exame físico revelou uma massa inflamatória ulcerada de 3 x 4 cm, com a ponta de uma lâmina emergindo do centro. O restante do abdômen estava flexível e não distendido, sem umbigo e o toque retal era normal. A temperatura corporal do paciente era de 37,5 °C.\n\nAvaliação diagnóstica\nUma radiografia abdominal sem preparação mostra uma imagem linear, opaca à radiação, com a forma de uma lâmina de faca.\n\nOs exames laboratoriais revelaram uma taxa de hemoglobina de 10 g/dl, uma hiperleucocitose de 16 600/mm3.\n\nTratamento e acompanhamento\nFoi realizada uma intervenção cirúrgica sob anestesia geral.\n\nOs resultados intraoperatórios mostraram uma cavidade abdominal saudável, uma aderência da face anterior do corpo gástrico com a parede abdominal, cuja liberação mostra uma perfuração gástrica, com uma lâmina em seu interior, cuja ponta atravessa toda a parede abdominal anterior, com a alça permanecendo na luz gástrica.\n\nA extração do corpo estranho intragástrico foi realizada: tratava-se de uma faca inteira de fabricação local artesanal com uma lâmina pontiada em uma extremidade, de 6 cm de comprimento, 1,5 cm de largura na base, e um cabo redondo esculpido em madeira de 2 cm de diâmetro e 7 cm de comprimento. A faca media 13 cm. Para a perfuração gástrica, foi feita uma ressecção cuneiforme. Esta amostra não apresentou anomalias histológicas. Uma sutura gástrica foi então feita. A estadia no hospital durou oito dias, as consequências foram simples. O retorno a um ano é excelente, o paciente tem acompanhamento psiquiátrico.\n",
+        "gold_summary": "Apresentamos o relato de um caso de sucesso no tratamento das consequências da ingestão voluntária de uma faca por um homem de 24 anos com transtornos psiquiátricos não documentados. O paciente foi recebido na emergência com um abscesso cutâneo epigástrico fistulizado com a ponta de uma faca emergente. Tratou-se da migração extraordinária de uma faca ingerida que perfurou o estômago e se exteriorizou por um abscesso epigástrico. A extração cirúrgica do corpo estranho foi realizada.\n",
+        "synthetic_summary": {
+            "B1": "Um homem comeu uma faca de verdade. Isso machucou sua barriga. A faca ficou presa no estômago dele. Os médicos fizeram uma cirurgia para tirar a faca. Depois, ele ficou bem e está sendo cuidado por médicos para a cabeça dele.",
+            "B2": "Caso de um homem que engoliu uma faca e foi tratado com sucesso\n\nUm homem de 24 anos, que tinha problemas mentais não tratados, engoliu uma faca de propósito. Depois de 15 dias, ele sentiu dor e inchaço na parte superior da barriga e foi levado ao hospital pelos pais.\n\nO que os médicos encontraram\n\nNo exame, os médicos viram uma ferida inflamada na barriga, com a ponta da faca aparecendo. Um raio-X mostrou claramente a faca dentro do corpo. O paciente estava com uma leve febre e sinais de infecção no sangue.\n\nComo foi o tratamento\n\nO paciente passou por uma cirurgia para retirar a faca. Durante a operação, os médicos descobriram que a faca havia perfurado o estômago e atravessado a parede da barriga. Eles tiraram a faca inteira, que tinha cerca de 13 cm, e consertaram o buraco no estômago com pontos. O paciente ficou no hospital por oito dias e se recuperou bem.\n\nO que isso significa\n\nEsse caso mostra que, mesmo em situações graves como engolir uma faca, é possível salvar a pessoa com um tratamento rápido e adequado. Além disso, o paciente passou a receber acompanhamento psiquiátrico para cuidar da saúde mental.",
+            "B3": "**Contexto**  \nEste relato descreve o caso de um homem de 24 anos, residente em Yopougon (Abidjan), que apresentou um quadro clínico incomum após ingerir voluntariamente uma faca. O paciente, com histórico não documentado de transtornos psiquiátricos e sem tratamento psiquiátrico prévio, foi levado ao hospital pelos pais devido a dor e inchaço na região epigástrica (parte superior do abdômen), que se desenvolveram ao longo de 15 dias. Não havia outros sintomas associados, como dificuldade para engolir, vômitos ou sangramento digestivo.\n\n**Principais Achados Clínicos e Diagnósticos**  \nNo exame físico, foi identificada uma massa inflamatória ulcerada de aproximadamente 3 x 4 cm, da qual emergia a ponta de uma lâmina. O abdômen estava flexível e sem sinais de distensão, e a temperatura corporal estava levemente elevada (37,5 °C). A radiografia abdominal revelou uma imagem linear opaca, compatível com o formato de uma lâmina de faca. Exames laboratoriais mostraram anemia moderada (hemoglobina de 10 g/dl) e aumento do número de glóbulos brancos (leucocitose de 16.600/mm³), indicando resposta inflamatória.\n\n**Interpretação Clínica**  \nO quadro clínico indicava a presença de um corpo estranho metálico (a faca) que havia perfurado a parede do estômago e migrado até a parede abdominal anterior, formando um abscesso (acúmulo de pus) com fístula (comunicação anormal) externa, por onde a ponta da faca estava visível. Essa migração incomum da faca causou uma perfuração gástrica, mas sem comprometimento grave de outras estruturas abdominais.\n\n**Tratamento e Evolução**  \nO paciente foi submetido a cirurgia sob anestesia geral. Durante o procedimento, foi constatada a aderência da face anterior do estômago à parede abdominal, com perfuração gástrica causada pela lâmina, cuja ponta atravessava a parede abdominal. A faca, feita artesanalmente com lâmina pontiaguda de 6 cm e cabo de madeira esculpida, foi completamente removida. A perfuração gástrica foi tratada por ressecção cuneiforme (remoção de um segmento em forma de cunha) e sutura da parede do estômago. A análise histológica do tecido removido não revelou alterações patológicas. O paciente permaneceu internado por oito dias, com recuperação sem complicações. Após um ano, o acompanhamento psiquiátrico continuava, e o estado clínico do paciente era excelente.\n\n**Conclusão**  \nEste caso ilustra um exemplo raro e bem-sucedido de tratamento cirúrgico após a ingestão voluntária de um objeto cortante, destacando a importância da avaliação multidisciplinar, incluindo suporte psiquiátrico, para pacientes com transtornos mentais que apresentam comportamentos de risco. A remoção cirúrgica cuidadosa e o manejo adequado da perfuração gástrica foram fundamentais para a recuperação completa do paciente."
+        }
+    },
+    {
+        "article": "Paciente do sexo masculino de 48 anos de idade, que ingressa em nossa unidade hospitalar após apresentar lesão na mão esquerda posterior a carga axial, assim como compressão ao ser atropelado por veículo automotor; ao seu ingresso, se identifica incongruência articular nas linhas de Gilula. Além de apresentar fratura na metáfise proximal com extensão para a metáfise distal de F2 do terceiro dedo, amputação traumática com desarticulação de F1-F2 mais desnudação do quarto dedo, ferida sangrenta do quinto dedo mais lesão do extensor próprio do quinto dedo na zona V. Ao seu ingresso passa a cirurgia de controle de danos mais redução fechada de luxação peri-escafo-transtrapecio-transtrapezoidal.\n\nDurante a sua estadia, foi tratado com impregnação antibiótica e analgesia; após a impregnação antibiótica, passou por um procedimento definitivo onde foi realizada carpectomia do pulso esquerdo com artrodese da articulação interfalângica do terceiro dedo e dedo médio, e tenarrafia do extensor próprio do quinto dedo e retalho de ferida sangrenta no quinto dedo. Técnica cirúrgica. Foi realizada com via de abordagem longitudinal posterior (dado que apresenta melhor exposição e diminui o risco de lesões nervosas), usando como referência o tubérculo de Lister, liberando as bordas cutâneas do retináculo extensor, liberando entre o terceiro e quarto compartimento extensor posterior, observando a cápsula articular, identificamos o interósseo posterior do lado interno ao tubérculo de Lister, realizamos uma capsulotomia em T com incisão transversal a 2 mm da borda radial da inserção capsular e, paralela a ele, a incisão vertical no eixo do terceiro metacarpo; exploramos a integridade das fossas do semilunar e do escafóide para poder realizar a ressecção da primeira fila (realizando tração e flexão palmar), deste modo podemos realizar a retirada dos ossos da primeira fila do carpo (tendo cuidado para não lesionar a cartilagem do osso grande); iniciamos com a retirada do semilunar, posterior do piramidal e finalizamos com o escafóide; depois disso, é verificada a adequada flexo-extensão do pulso; continuamos com o fechamento da capsulotomia em T, assim como do ligamento anular, tecido celular subcutâneo e pele.\n",
+        "gold_summary": "Paciente do sexo masculino de 48 anos de idade, que ingressa em nossa unidade hospitalar após sofrer lesão na mão esquerda, após ser atropelado por um veículo automotor, com mecanismo de carga axial, apresentando deformidade na extremidade torácica esquerda, fratura de metáfise proximal da segunda falange do terceiro dedo, bem como luxação da articulação interfalângica proximal, com amputação traumática da segunda falange do quarto dedo, além de lesão extensora na zona V do quinto dedo, com perda de cobertura cutânea do quarto e quinto dedos. Ele veio a nossa unidade hospitalar 24 horas após a lesão.\n",
+        "synthetic_summary": {
+            "B1": "Um homem machucou muito a mão esquerda. Ele foi atropelado por um carro. A mão dele ficou machucada e doeu bastante. Alguns dedos ficaram machucados e um dedo perdeu uma parte. Ele veio para o hospital para receber ajuda. Os médicos cuidaram da mão para ela melhorar.",
+            "B2": "**O que aconteceu com o paciente**\n\nUm homem de 48 anos sofreu um acidente grave na mão esquerda depois de ser atropelado por um carro. A força do impacto machucou bastante sua mão. Ele teve uma fratura, que é quando um osso quebra, no terceiro dedo, perto da ponta. Além disso, uma das articulações desse dedo saiu do lugar, o que chamamos de luxação. No quarto dedo, ele perdeu uma parte importante, chamada segunda falange, que é um dos ossos do dedo, por causa da amputação traumática — isso significa que o dedo foi cortado ou arrancado pelo acidente. No quinto dedo, ele teve uma lesão no tendão extensor, que é o tecido que ajuda a esticar o dedo, e também perdeu parte da pele que cobre os dedos quatro e cinco.\n\n**Como foi o tratamento**\n\nO paciente chegou ao hospital um dia depois do acidente. Para tratar, os médicos fizeram uma cirurgia para controlar os danos e colocar os ossos e articulações no lugar. Depois, ele recebeu remédios para evitar infecção (antibióticos) e para aliviar a dor. Em uma cirurgia mais completa, os médicos retiraram alguns ossos do pulso para melhorar a função da mão e juntaram os ossos do terceiro dedo para que ele ficasse mais firme. Também consertaram o tendão do quinto dedo e fecharam as feridas com um retalho, que é um pedaço de pele usado para cobrir áreas machucadas.\n\n**Por que isso é importante**\n\nEsse tipo de acidente pode causar muitos problemas na mão, que é uma parte do corpo muito usada no dia a dia. O tratamento precisa ser rápido e bem feito para evitar infecções, dor e perda da função da mão. As cirurgias feitas ajudaram a recuperar o máximo possível da movimentação e da força dos dedos, mesmo com as lesões graves que ele teve.",
+            "B3": "**Contexto**  \nUm homem de 48 anos foi admitido em nosso hospital após sofrer um acidente em que foi atropelado por um veículo, resultando em uma lesão grave na mão esquerda. O trauma envolveu uma força axial (compressão direta ao longo do eixo da mão) e causou múltiplos danos complexos na região.\n\n**Principais Achados Clínicos e Radiológicos**  \nNa avaliação inicial, observou-se uma deformidade significativa na mão esquerda, com incongruência nas linhas de Gilula (que são referências usadas para avaliar o alinhamento dos ossos do carpo, ou punho). O paciente apresentava:  \n- Fratura na parte proximal (mais próxima do corpo) da segunda falange (osso do meio) do terceiro dedo, estendendo-se até a parte distal (mais afastada do corpo) dessa falange.  \n- Luxação (deslocamento) da articulação interfalângica proximal do terceiro dedo, que é a articulação entre a primeira e segunda falanges.  \n- Amputação traumática da segunda falange do quarto dedo, com desarticulação (separação da articulação) entre a primeira e segunda falanges desse dedo.  \n- Perda da cobertura da pele (desnudação) no quarto dedo, com ferida sangrante no quinto dedo.  \n- Lesão do tendão extensor próprio do quinto dedo na zona V (área específica da mão onde o tendão passa), comprometendo sua função.\n\nO paciente chegou ao hospital aproximadamente 24 horas após o acidente.\n\n**Intervenções Realizadas**  \nInicialmente, foi realizada uma cirurgia de controle de danos para estabilizar a mão, incluindo redução fechada da luxação peri-escafo-transtrapecio-transtrapezoidal (realinhamento dos ossos deslocados no punho, sem abrir a pele). Durante a internação, o paciente recebeu tratamento com antibióticos para prevenir infecção e analgesia para controle da dor.\n\nPosteriormente, foi realizada uma cirurgia definitiva que incluiu:  \n- Carpectomia do pulso esquerdo, que consiste na remoção dos ossos da primeira fila do carpo (semilunar, piramidal e escafóide), para melhorar a função e aliviar a dor.  \n- Artrodese (fusão cirúrgica) da articulação interfalângica do terceiro dedo, para estabilizar o dedo afetado.  \n- Tenarrafia do tendão extensor do quinto dedo, que é a sutura do tendão lesionado para restaurar sua função.  \n- Cobertura da ferida sangrante do quinto dedo por meio de retalho (movimentação de tecido saudável para cobrir a área exposta).\n\n**Detalhes Técnicos da Cirurgia**  \nA abordagem cirúrgica foi feita pela parte posterior da mão, com uma incisão longitudinal que permitiu melhor exposição e reduziu o risco de lesão nervosa. Como referência anatômica, foi utilizado o tubérculo de Lister, uma proeminência óssea no punho. Durante o procedimento, foram liberadas as bordas do retináculo extensor (estrutura que mantém os tendões no lugar), e realizada uma capsulotomia em “T” (incisão na cápsula articular para acesso ao interior da articulação), permitindo a remoção cuidadosa dos ossos da primeira fila do carpo. A retirada foi feita na sequência: semilunar, piramidal e escafóide, tomando cuidado para preservar a cartilagem do osso grande (capitato). Após a remoção, foi verificada a mobilidade adequada do pulso em flexão e extensão. Por fim, a cápsula articular, ligamentos, tecido subcutâneo e pele foram suturados para fechar a ferida.\n\n**Interpretação Clínica**  \nO paciente sofreu um trauma complexo na mão esquerda, com múltiplas fraturas, luxações, amputação parcial e lesão tendínea, que exigiram intervenções cirúrgicas em etapas para estabilizar, preservar função e evitar infecção. A carpectomia e artrodese visam restaurar a mobilidade e reduzir a dor a longo prazo, enquanto a reconstrução tendínea e cobertura cutânea são essenciais para a recuperação funcional dos dedos.\n\n**Próximos Passos**  \nO acompanhamento clínico incluirá monitoramento da cicatrização, controle da dor, fisioterapia para reabilitação da mão e avaliação contínua da função articular e tendínea. O objetivo é maximizar a recuperação funcional e minimizar complicações decorrentes do trauma e das cirurgias realizadas."
+        }
+    },
+    {
+        "article": "Uma menina de três anos de idade, acamada, apresentando quadro neurológico crônico (síndrome congênita do Zika vírus), foi internada para tratar um episódio de traqueíte. Ela havia sido submetida a traqueostomia e gastrostomia dois anos antes para tratamento de aspiração pulmonar crônica, episódios recorrentes de pneumonia e incoordenação da deglutição. Foi prescrita cânula plástica balonada continuamente inflada com baixa pressão, pois a criança necessitava de ventilação com pressão positiva intermitente.\n\nA paciente apresentou dois episódios de sangramento autolimitado à traqueostomia com intervalo de 48 horas, inicialmente atribuídos a trauma aspirativo. Novo episódio 48 horas após o relato inicial com sangue em projétil brilhante, sugestivo de sangramento arterial, foi então descrito pela mãe, necessitando de avaliação cirúrgica. A paciente não apresentava instabilidade fisiológica ou anemia grave.\n\nUm diagnóstico provisório de TIF foi dado pela equipe de cirurgia pediátrica. Uma angiotomografia imediata confirmou o diagnóstico e revelou TIF afetando a bifurcação da artéria inominada (AI) e a parede traqueal direita, com pequeno acúmulo de contraste próximo à fístula.\n\nA paciente foi tratada com a colocação endovascular de quatro stents de politetrafluoroetileno expandido (PTFE)/nitinol (Viabhan®) nas artérias carótida direita (5×50 e 6×100 mm) e subclávia direita (5×25 e 5×100 mm), cruzando a transição para a AI na configuração Y. Um stent (5×25 mm) migrou acidentalmente, ficando próximo à bifurcação ilíaca. Esse stent deslocado não foi recuperado, pois a equipe considerou que as tentativas de remoção implicariam uma relação risco-benefício desfavorável. Não foi detectada piora neurológica, isquemia de braço direito ou complicações relacionadas ao stent migrado após a cirurgia. O controle angiográfico, incluindo nova angiotomografia quatro meses após a cirurgia, mostrou fluxo sanguíneo normal nas artérias carótida e subclávia direita.\n\nForam prescritos anticoagulantes por dois meses (enoxaparina 20 mg bid por via subcutânea). Cinco meses após a cirurgia, a paciente permanece assintomática, sem novos episódios hemorrágicos ou complicações infecciosas, trombóticas ou isquêmicas relacionadas aos stents.",
+        "gold_summary": "Uma criança de 3 anos de idade, com encefalopatia, restrita ao leito e traqueostomizada havia dois anos foi internada para tratar um episódio de traqueíte. A criança usava uma cânula plástica balonada continuamente inflada com baixa pressão. A paciente apresentou dois episódios autolimitados de sangramento pela traqueostomia em um intervalo de 48 horas. Um novo episódio foi sugestivo de sangramento arterial e assumiu-se o diagnóstico provisório de TIF, confirmado através de angiotomografia, atingindo a bifurcação da artéria inominada e a parede direita da traqueia. A paciente foi imediatamente tratada pela inserção endovascular de um enxerto de politetrafluoroetileno (PTFE)/nitinol em “Y”. No seguimento, não foram encontradas recorrência de TIF, sequelas neurológicas ou isquemia do braço direito.",
+        "synthetic_summary": {
+            "B1": "Uma menininha de 3 anos estava doente e não podia sair da cama. Ela tinha um canudinho no pescoço para ajudar a respirar. Um dia, saiu um pouco de sangue desse canudinho. Depois, isso aconteceu mais duas vezes. Os médicos fizeram um exame e viram que um vasinho perto da traqueia estava machucado. Eles colocaram um pedacinho de tubo para ajudar o sangue a não sair mais. Depois disso, a menininha ficou bem, sem mais sangramentos ou problemas no braço.",
+            "B2": "**O que aconteceu com a criança**\n\nUma menina de 3 anos, que já tinha problemas no cérebro e precisava ficar na cama, usava um tubo chamado traqueostomia para ajudar a respirar. Ela também tinha um balãozinho pequeno no tubo para manter ele no lugar e evitar problemas. A menina ficou doente com uma inflamação na traqueia, que é o caminho do ar para os pulmões.\n\n**O problema do sangramento**\n\nEla teve dois episódios de sangramento pelo tubo, que pararam sozinhos. Depois, teve um sangramento mais forte, parecido com sangue vindo de uma artéria (um vaso que leva sangue do coração para o corpo). Os médicos suspeitaram de uma condição chamada fístula traqueoarterial, que é quando a traqueia e uma artéria ficam ligadas por um buraco, causando sangramento.\n\n**Como foi feito o diagnóstico**\n\nPara confirmar, os médicos fizeram um exame chamado angiotomografia, que é uma foto especial das artérias e da traqueia com contraste para ver melhor. O exame mostrou que a fístula estava na bifurcação da artéria inominada, que é um vaso importante perto da traqueia.\n\n**O tratamento**\n\nOs médicos trataram a menina colocando um tipo de tubo especial chamado stent, feito de um material chamado politetrafluoroetileno (PTFE) e nitinol, dentro das artérias para fechar o buraco. Eles usaram quatro stents em forma de “Y” para proteger as artérias e a traqueia. Um dos stents saiu do lugar, mas não causou problemas e não foi retirado para evitar riscos.\n\n**O que aconteceu depois**\n\nApós o tratamento, a menina recebeu remédios para evitar coágulos no sangue por dois meses. Cinco meses depois, ela estava bem, sem sangramentos, sem problemas no braço direito e sem complicações no cérebro. O sangue continuava a circular normalmente pelas artérias tratadas.\n\n**Resumo final**\n\nEssa menina teve um problema sério de sangramento causado por uma ligação anormal entre a traqueia e uma artéria. Os médicos conseguiram identificar e tratar o problema com um procedimento que colocou stents para fechar o buraco. O tratamento foi eficaz e ela está se recuperando bem.",
+            "B3": "**Contexto**  \nUma menina de três anos, com uma condição neurológica crônica causada pela síndrome congênita do vírus Zika, estava acamada e dependente de traqueostomia e gastrostomia realizadas dois anos antes devido a problemas respiratórios e dificuldade para engolir. Ela necessitava de ventilação mecânica com pressão positiva intermitente e usava uma cânula plástica balonada inflada com baixa pressão para manter a traqueostomia.\n\n**Principais Achados**  \nDurante a internação para tratar uma inflamação da traqueia (traqueíte), a criança apresentou três episódios de sangramento pela traqueostomia em um intervalo de cerca de quatro dias. Os dois primeiros episódios foram breves e cessaram espontaneamente, inicialmente atribuídos a trauma local. O terceiro episódio, no entanto, apresentou sangue brilhante e em jato, indicando possível sangramento arterial. Isso levou a equipe médica a suspeitar de uma fístula traqueoarterial (TIF), uma comunicação anormal entre a traqueia e a artéria inominada, que pode causar sangramento grave.\n\nA confirmação do diagnóstico foi feita por meio de uma angiotomografia, exame que mostrou a fístula na bifurcação da artéria inominada e na parede direita da traqueia, com pequeno acúmulo de contraste indicando o local do sangramento.\n\n**Interpretação Clínica**  \nDiante da gravidade do quadro, a equipe optou pelo tratamento endovascular, que consiste na colocação de stents (tubos metálicos revestidos) para fechar a fístula e restabelecer o fluxo normal nas artérias. Foram implantados quatro stents de politetrafluoroetileno (PTFE) e nitinol em formato de “Y” para cobrir a bifurcação da artéria inominada, envolvendo as artérias carótida e subclávia direita. Um dos stents migrou acidentalmente para a região da bifurcação da artéria ilíaca, mas não foi removido devido ao risco elevado da retirada. Felizmente, não houve complicações neurológicas, isquemia (falta de sangue) no braço direito ou outras intercorrências relacionadas ao stent deslocado.\n\n**Próximos Passos e Evolução**  \nApós o procedimento, a paciente recebeu anticoagulantes por dois meses para prevenir a formação de coágulos. O acompanhamento com exames de imagem realizados até quatro meses depois mostrou fluxo sanguíneo normal nas artérias tratadas. Cinco meses após a intervenção, a criança permanece sem novos episódios de sangramento, sem sinais de infecção, trombose ou problemas neurológicos, demonstrando boa resposta ao tratamento.\n\n**Resumo Final**  \nEste caso ilustra a importância do diagnóstico precoce da fístula traqueoarterial em crianças com traqueostomia e o sucesso do tratamento endovascular com stents para controlar sangramentos potencialmente fatais, garantindo a estabilidade clínica e a preservação das funções neurológicas e vasculares."
+        }
+    },
+    {
+        "article": "Uma paciente de 72 anos de idade, obesa, com hérnia de hiato por deslizamento, asmática e com histórico de câncer de pâncreas em tratamento quimioterápico, foi internada por 24 horas para realização de neurolise de nervos esplâncnicos.\n\nA intervenção foi realizada com orientação tomográfica, sob anestesia local (lidocaína a 2% sem epinefrina). O paciente foi posicionado em decúbito ventral. Foi utilizada a abordagem posterior unilateral esquerda, o acesso retrocrosal direito foi limitado por um osteófito vertebral. Após o planejamento da prática, uma agulha tipo PL 21 de calibre 21 foi introduzida de forma estéril, sob monitorização por imagem, no espaço retrocrosal entre as vértebras D11 e D12. Uma vez posicionada a agulha no espaço desejado, foi realizada a hidrodissecção com contraste intravenoso diluído. Após a confirmação da difusão adequada da solução de contraste no espaço pré-vertebral retrocrosal, foi infiltrado lentamente uma mistura (70%/30%) de etanol a 96% e ropivacaína 7,5 mg (volume total de álcool de aproximadamente 21 ml). O controle imediato pós-procedimento demonstrou ausência de complicações e difusão do contraste e do álcool para a cavidade torácica. A paciente tolerou o procedimento satisfatoriamente e foi transferida para o seu quarto para monitorização. No entanto, 50 minutos após a intervenção, foi constatada dessaturação a 85% de ar ambiente sem alterações na mecânica respiratória nem alterações na auscultação ou sinais de insuficiência cardíaca. A paciente não foi reanimada durante o estudo nem recebeu medicação que pudesse produzir depressão respiratória. Um estado ácido-base venoso não demonstrou hipercapnia. Um eletrocardiograma não revelou alterações. Foi realizada uma angiotomografia de tórax para detecção de tromboembolismo pulmonar, que foi negativa, observando-se um leve derrame pleural bilateral com derrame pericárdico laminar. Foram tomadas medidas de suporte vital com cânula de oxigênio suplementar a 2 litros/minuto com correção de saturação a 95%. Após 12 horas do início do quadro, a paciente corrigiu o seu transtorno de saturação sem intervenção terapêutica específica.\n\nA paciente recebeu alta 24 horas depois com correção da saturação, sem outros problemas e com boa gestão da dor. Não houve evidência de derrame pleural ou pericárdico no controle 10 dias após o procedimento.\n",
+        "gold_summary": "Apresentamos o caso de uma senhora de 72 anos com câncer no pâncreas e má gestão da dor apesar do uso de opioides. Foi indicada neurólise dos nervos esplâncnicos sob internação.\n\nResultados: Após o procedimento, apresentou bom controle da dor, mas evoluiu com hipoxemia, derrame pleural bilateral e pericárdico. Causas frequentes desses eventos foram descartadas. A paciente recebeu alta 24 horas depois com bom controle da dor.\n",
+        "synthetic_summary": {
+            "B1": "Uma senhora de 72 anos estava com muita dor no corpo. Ela tinha um problema no pâncreas e tomava remédios fortes, mas a dor não passava.\n\nOs médicos fizeram um cuidado especial para ajudar a dor dela. Depois, a dor ficou melhor.\n\nMas, ela teve um problema para respirar por um tempo. Os médicos cuidaram dela com oxigênio.\n\nDepois de um tempo, ela ficou bem e voltou para casa feliz, sem dor.",
+            "B2": "**O que aconteceu com a paciente**\n\nUma senhora de 72 anos, que tinha câncer no pâncreas e sentia muita dor mesmo usando remédios fortes chamados opioides, passou por um procedimento chamado neurólise dos nervos esplâncnicos. Esse procedimento ajuda a diminuir a dor ao bloquear sinais nervosos que vêm do abdômen.\n\n**Como foi o procedimento**\n\nEla ficou internada por um dia e o procedimento foi feito com anestesia local, ou seja, só a área onde a agulha foi colocada ficou anestesiada. Usaram uma máquina de imagem para guiar a agulha até o lugar certo perto das vértebras da coluna. Depois, aplicaram uma mistura de álcool e remédio para bloquear os nervos da dor.\n\n**O que aconteceu depois**\n\nLogo após o procedimento, a dor dela melhorou bastante. Mas, cerca de 50 minutos depois, ela teve uma queda no nível de oxigênio no sangue (hipoxemia), o que pode ser perigoso. Exames foram feitos para descobrir a causa, como verificar se havia coágulos nos pulmões, mas nada grave foi encontrado. Foi observado um pequeno acúmulo de líquido ao redor dos pulmões (derrame pleural) e do coração (derrame pericárdico), mas sem causar problemas sérios.\n\n**Recuperação**\n\nCom ajuda de oxigênio extra, o nível de oxigênio no sangue dela voltou ao normal em 12 horas, sem precisar de tratamentos especiais. A paciente recebeu alta no dia seguinte, com a dor controlada e sem complicações. Dez dias depois, exames mostraram que o líquido ao redor do pulmão e do coração havia desaparecido.\n\n**O que isso significa**\n\nEsse caso mostra que a neurólise dos nervos esplâncnicos pode ajudar a controlar a dor em pacientes com câncer, mas é importante acompanhar possíveis efeitos colaterais, como a queda de oxigênio no sangue e o acúmulo de líquidos no tórax. Felizmente, esses problemas foram temporários e a paciente se recuperou bem.",
+            "B3": "**Contexto**  \nEste relato descreve o caso de uma paciente de 72 anos, com histórico de câncer de pâncreas em tratamento quimioterápico, obesidade, hérnia de hiato por deslizamento e asma. Ela apresentava dor crônica difícil de controlar, mesmo com o uso de opioides, e foi internada para a realização de uma neurolise dos nervos esplâncnicos — um procedimento minimamente invasivo que visa aliviar a dor ao interromper os sinais nervosos que transmitem a sensação dolorosa.\n\n**Descrição do Procedimento**  \nA neurolise foi realizada sob anestesia local, com orientação por tomografia computadorizada para garantir a precisão da agulha introduzida entre as vértebras D11 e D12, no espaço retrocrosal. Após confirmação da posição correta por meio de contraste, foi administrada uma mistura de álcool (etanol a 96%) e anestésico local (ropivacaína) para destruir os nervos responsáveis pela dor. O procedimento foi bem tolerado, sem complicações imediatas.\n\n**Principais Achados Pós-Procedimento**  \nCinquenta minutos após a intervenção, a paciente apresentou uma queda significativa na saturação de oxigênio (hipoxemia), chegando a 85% em ar ambiente, sem sinais de dificuldade respiratória, alterações na ausculta pulmonar ou insuficiência cardíaca. Exames laboratoriais e eletrocardiograma não indicaram causas comuns de insuficiência respiratória ou cardíaca. Uma angiotomografia de tórax descartou tromboembolismo pulmonar, mas revelou um leve derrame pleural bilateral (acúmulo de líquido ao redor dos pulmões) e um derrame pericárdico laminar (pequena quantidade de líquido ao redor do coração). Com suporte de oxigênio suplementar, a saturação da paciente melhorou para 95% e, após 12 horas, normalizou-se sem necessidade de tratamentos adicionais.\n\n**Interpretação Clínica**  \nA hipoxemia e os derrames pleural e pericárdico observados após a neurolise dos nervos esplâncnicos são eventos incomuns, e as causas mais frequentes, como embolia pulmonar ou insuficiência cardíaca, foram excluídas. A presença desses derrames pode estar relacionada à reação inflamatória local ou à difusão do álcool para estruturas próximas, embora o mecanismo exato não tenha sido completamente esclarecido. A resolução espontânea dos sintomas sugere um quadro autolimitado.\n\n**Desfecho e Seguimento**  \nA paciente recebeu alta hospitalar 24 horas após o procedimento, com controle adequado da dor e sem outras complicações. Em acompanhamento realizado 10 dias depois, não foram detectados derrames pleural ou pericárdico, confirmando a resolução completa dos achados iniciais.\n\n**Conclusão**  \nEste caso ilustra que a neurolise dos nervos esplâncnicos pode ser eficaz no controle da dor em pacientes com câncer pancreático, mas pode estar associada a complicações respiratórias transitórias e derrames pleurais e pericárdicos leves. O reconhecimento precoce e o manejo adequado dessas alterações são essenciais para garantir a segurança do paciente."
+        }
+    },
+    {
+        "article": "Homem de 46 anos, haitiano, residente no Chile há um ano. Em seu país de origem, ele trabalhava com criação de animais de fazenda. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação de animais de fazenda no Haiti. Ele veio ao Chile há um ano atrás. Ele se dedicava à criação\n\nO paciente evoluiu favoravelmente, com regressão das lesões e sem evidência de recidivas até a data, ficando com uma leve hipopigmentação local, esperável em zonas de tratamento com crioterapia.\n",
+        "gold_summary": "O caso apresentado foi de um homem haitiano de 46 anos, residente no Chile, com placas verrucosas na região tibial anterior, com um ano de evolução. O diagnóstico de cromoblastomicose foi confirmado pela observação de células muriformes na histopatologia e colônias dematiáceas na cultura micológica; além disso, na microscopia direta, foram observados conídios compatíveis com Fonsecaea spp. Após seis meses de tratamento com antimicóticos sistêmicos e crioterapia, foi alcançada a remissão completa das lesões.\n",
+        "synthetic_summary": {
+            "B1": "Um homem tinha umas bolinhas na perna. Essas bolinhas ficaram lá por um ano. Os médicos olharam bem e viram que era uma coisinha que vem de um bichinho muito pequeno. Eles deram remédio e fizeram um tratamento com frio na pele. Depois de seis meses, as bolinhas sumiram. Ele ficou bem e a pele ficou um pouco mais clara onde o tratamento foi feito.",
+            "B2": "**Quem é o paciente e o que ele tinha?**  \nUm homem de 46 anos, que veio do Haiti e mora no Chile, tinha manchas grossas e com aspecto de verrugas na parte da frente da perna, perto da canela. Essas manchas estavam lá há um ano.\n\n**O que os médicos descobriram?**  \nPara entender o que ele tinha, os médicos fizeram exames em pedaços dessas manchas. Eles encontraram um tipo de célula chamada \"muriforme\", que é típica de uma doença chamada cromoblastomicose. Essa doença é uma infecção causada por fungos que crescem na pele. Também fizeram um teste para ver o fungo em um laboratório, e encontraram um fungo chamado Fonsecaea, que é um dos que causam essa doença.\n\n**Como foi o tratamento?**  \nO paciente recebeu remédios antifúngicos, que são medicamentos para matar o fungo, e também foi tratado com crioterapia. A crioterapia é um tratamento que usa frio intenso para destruir as lesões na pele.\n\n**Qual foi o resultado?**  \nDepois de seis meses de tratamento, as manchas desapareceram completamente. Só ficou uma área um pouco mais clara na pele, que é normal depois desse tipo de tratamento com frio.\n\n**O que isso significa?**  \nEsse caso mostra que, mesmo uma infecção de pele causada por fungos, que pode parecer difícil de tratar, pode melhorar muito com o tratamento certo. É importante procurar um médico para fazer os exames corretos e receber o tratamento adequado.",
+            "B3": "**Contexto**  \nTrata-se de um homem de 46 anos, natural do Haiti, que reside no Chile há um ano. No Haiti, ele trabalhava com criação de animais de fazenda, atividade que pode estar associada à exposição a fungos presentes no solo e matéria orgânica em decomposição.\n\n**Principais Achados**  \nO paciente apresentou placas verrucosas (com aspecto de verrugas) localizadas na região anterior da tíbia (parte frontal da perna), que evoluíram ao longo de um ano. Para esclarecer o diagnóstico, foram realizados exames laboratoriais específicos: a histopatologia (análise microscópica do tecido) revelou a presença de células muriformes, que são características da cromoblastomicose, uma infecção fúngica crônica da pele. A cultura micológica (crescimento do fungo em laboratório) identificou colônias dematiáceas, fungos pigmentados típicos dessa doença. Além disso, a microscopia direta mostrou conídios (estruturas reprodutivas do fungo) compatíveis com o gênero Fonsecaea, um dos agentes causadores mais comuns da cromoblastomicose.\n\n**Interpretação Clínica**  \nA cromoblastomicose é uma infecção fúngica crônica que afeta principalmente a pele e o tecido subcutâneo, geralmente em pessoas expostas ao ambiente rural, como criadores de animais e agricultores. O diagnóstico é confirmado pela identificação das células muriformes na pele e pela cultura do fungo. O tratamento é complexo e pode incluir medicamentos antifúngicos sistêmicos (administrados por via oral) e terapias locais, como a crioterapia (uso de frio intenso para destruir o tecido infectado).\n\n**Próximos Passos e Evolução**  \nO paciente foi tratado durante seis meses com antifúngicos orais combinados com sessões de crioterapia. Após esse período, houve remissão completa das lesões, ou seja, as placas verrucosas desapareceram. Como sequela, ficou uma leve hipopigmentação (áreas de pele com coloração mais clara), que é uma consequência esperada do tratamento com crioterapia.\n\nEste caso ilustra a importância do diagnóstico precoce e do tratamento combinado para o sucesso no manejo da cromoblastomicose, especialmente em pacientes com histórico de exposição ocupacional em áreas rurais."
+        }
+    },
+    {
+        "article": "Este é um caso de um homem de 23 anos com um histórico médico sem relevância que foi encaminhado com dispneia inexplicada. Antes da sua doença atual, ele estava com boa saúde e não tinha dificuldade em realizar atividades diárias. Ambos os seus pais tinham diabetes, e o seu avô faleceu de um ataque cardíaco aos 74 anos. Além disso, após uma revisão mais aprofundada do seu histórico familiar, descobrimos que o tio do paciente tem um histórico de acromegalia.\n\nA condição do paciente começou 2 semanas antes da admissão, quando ele começou a se queixar de febre, congestão nasal e rinorreia. Três dias depois, ele começou a se queixar de vômitos, diarreia e dor abdominal. Depois de ser admitido na enfermaria de medicina interna, fomos consultados por palpitações marcadas, dispneia e ortopneia.\n\nDurante o exame, a temperatura estava ligeiramente elevada a 37,9°C, a pressão arterial de 150/90 mmHg, a frequência cardíaca de 110/min, e a frequência respiratória de 22/min. A auscultação revelou crepitações pulmonares basais finas com roncos expiratórios bilaterais suaves. Além disso, foi detectado um murmúrio diastólico precoce. As veias do pescoço estavam congestionadas, mas não pulsantes, e não havia edema de membros inferiores ou ascite.\n\nOs resultados laboratoriais foram notáveis por um nível elevado de Peptídeo Natriurético do Cérebro (BNP) (340 pg/mL). Os resultados adicionais incluíram derrame pleural bilateral leve e cardiomegalia observados na radiografia do tórax. O ECG revelou taquicardia sinusal com ondas T invertidas nos leads V3 e V4. A ecocardiografia transtorácica (TTE) mostrou um ventrículo esquerdo (LV) levemente dilatado e hipertrofiado, função sistólica levemente prejudicada com uma fração de ejeção de 48% pelo modo M, função diastólica prejudicada, regurgitação mitral moderada e regurgitação aórtica grave. A raiz aórtica estava marcadamente dilatada, com diâmetros de 3,2 cm no anel, 4,9 cm no seio de Valsalva e 7,5 cm na junção sino-tubular (STJ).\n\nConsequentemente, foi realizada uma arteriografia de CT, confirmando as medições ecocardiográficas dos diâmetros da raiz da aorta. Além disso, revelou dilatação da aorta ascendente com um diâmetro de 10 cm e da aorta descendente com um diâmetro de 2,5 cm. O paciente iniciou o tratamento com os seguintes medicamentos: Furosemida (20 mg a cada 8 horas), Ramipril (1,25 mg uma vez ao dia) e Empagliflozin (10 mg uma vez ao dia). Em 10 dias, o paciente apresentou uma ligeira melhora nos sintomas, particularmente dispneia, e relatou melhor sono. Uma radiografia de tórax de acompanhamento mostrou resolução parcial do derrame pleural.\n\nInicialmente, consideramos doença do tecido conjuntivo como a síndrome de Marfan ou Ehlers-Danlos. No entanto, o paciente não apresentava as características físicas típicas e os sinais associados a estas condições. Além disso, o seu teste de função pulmonar era normal, o que seria provavelmente anormal num distúrbio do tecido conjuntivo multissistémico. Os resultados laboratoriais mostraram níveis normais de VHS e de proteína C-reativa, reduzindo a probabilidade de vasculite como causa da dilatação da raiz da aorta. O painel autoimune, incluindo os testes ANA e RF, também foi negativo.\n\nA acromegalia foi então considerada como a causa potencial da hipertrofia do VE e dilatação da raiz aórtica, especialmente considerando o histórico familiar da condição. Portanto, o nível do fator de crescimento semelhante à insulina 1 (IGF-1) foi ordenado e foi elevado (320 ng/ml), e o nível de GH permaneceu acima do normal (1,1 ng/ml) após um teste oral de tolerância à glicose, confirmando o diagnóstico de acromegalia. Uma imagem de ressonância magnética do cérebro ponderada em T2 mostrou uma massa hiperintensa de 7 × 4 mm na sela túrcica, consistente com um microadenoma da hipófise.\n\nSubsequentemente, a decisão da cirurgia foi tomada após obtenção do consentimento do paciente. Após uma angiografia coronária normal, o paciente foi submetido a um procedimento de substituição de enxerto composto, envolvendo a válvula aórtica, a raiz aórtica e a aorta ascendente (Procedimento Bentall). Foi utilizada uma válvula mecânica, e o paciente começou a tomar Warfarin numa dose diária de 3 mg, com monitorização estreita para alcançar um alvo INR de 2 a 3.\n\nApós consulta com o endocrinologista, o paciente começou a receber injeções mensais de acetato de octreótido. Foi estabelecido um plano de acompanhamento abrangente, que incluiu a monitorização do funcionamento da válvula, a avaliação da função LV, a garantia do cumprimento da medicação e a verificação dos valores de IGF-1 e INR. Para além da dispneia leve, ele permaneceu assintomático durante 8 semanas após a cirurgia. Durante este período, os ecocardiogramas de acompanhamento mostraram que a válvula aórtica substituída funcionava normalmente sem qualquer fuga ou disfunção. A raiz aórtica e a aorta ascendente também estavam estáveis, sem sinais de dilatação, aneurisma ou outras complicações. Não houve progressão da sua hipertrofia LV. O seu nível mais recente de IGF-1 foi de 290 ng/ml, que é ligeiramente reduzido do que o primeiro, e ele foi mantido com Octreótido sem efeitos adversos significativos.\n",
+        "gold_summary": "Este relatório apresenta um caso de um homem de 23 anos sem histórico médico significativo, que apresentou dispneia grave após uma infecção no peito. Ele não tinha características físicas distintas de distúrbios genéticos ou endócrinos, mas seu tio tinha acromegalia. A ecocardiografia revelou hipertrofia ventricular esquerda e dilatação maciça da raiz aórtica. O fator de crescimento semelhante à insulina 1 (IGF-1) elevado confirmou o diagnóstico de acromegalia. O paciente foi submetido a um procedimento de Bentall, e sua acromegalia foi tratada com octreotide e acompanhamento regular.\n",
+        "synthetic_summary": {
+            "B1": "Um homem jovem ficou com muita dificuldade para respirar depois de ficar doente. Ele não tinha sinais de doenças que mudam o corpo, mas seu tio tinha uma doença chamada acromegalia. O coração dele estava maior e uma parte importante do coração estava muito grande. Os médicos fizeram exames e descobriram que ele tinha acromegalia também. Ele fez uma cirurgia para consertar o coração e começou a tomar remédios para a doença. Os médicos vão cuidar dele para ele ficar bem.",
+            "B2": "**O que aconteceu com o paciente**\n\nUm homem de 23 anos, que antes estava saudável, começou a sentir falta de ar grave depois de uma infecção no peito. Ele não tinha sinais físicos que mostrassem doenças genéticas ou problemas hormonais, mas descobrimos que seu tio tinha uma doença chamada acromegalia.\n\n**O que os exames mostraram**\n\nUm exame do coração chamado ecocardiografia mostrou que a parte esquerda do coração dele estava maior e mais grossa do que o normal. Também foi encontrada uma grande dilatação na raiz da aorta, que é a principal artéria que sai do coração. Outro exame mediu um hormônio chamado IGF-1, que estava alto. Esse hormônio elevado confirmou que ele tinha acromegalia, uma condição em que o corpo produz muito hormônio do crescimento.\n\n**Como ele foi tratado**\n\nPara corrigir o problema no coração, ele passou por uma cirurgia chamada procedimento de Bentall, que substitui a válvula e a parte dilatada da aorta. Para tratar a acromegalia, ele começou a usar um remédio chamado octreotide, que ajuda a controlar a produção do hormônio do crescimento. Depois disso, ele passou a fazer acompanhamento médico regular para garantir que tudo estivesse indo bem.\n\n**Por que isso é importante**\n\nEsse caso mostra como uma doença hormonal pode afetar o coração de forma grave, mesmo em pessoas jovens e aparentemente saudáveis. O diagnóstico correto e o tratamento adequado foram essenciais para melhorar a saúde dele e evitar complicações maiores.",
+            "B3": "**Contexto**  \nEste é o relato de um homem jovem, de 23 anos, sem doenças prévias relevantes, que desenvolveu falta de ar intensa após um quadro inicial de infecção respiratória. Antes disso, ele gozava de boa saúde e não apresentava limitações para suas atividades diárias. Embora não apresentasse sinais físicos típicos de doenças genéticas do tecido conjuntivo ou distúrbios endócrinos, havia um histórico familiar importante: seu tio tinha acromegalia, uma condição causada pelo excesso do hormônio do crescimento.\n\n**Principais Achados Clínicos e Exames**  \nAo exame, o paciente apresentava sinais de insuficiência cardíaca, como crepitações nos pulmões, congestão venosa no pescoço e um sopro cardíaco diastólico precoce, sugerindo problemas valvulares. Os exames laboratoriais mostraram elevação do peptídeo natriurético cerebral (BNP), marcador de estresse cardíaco, e a radiografia evidenciou aumento do coração e derrame pleural leve. O eletrocardiograma indicou taquicardia e alterações isquêmicas.\n\nA ecocardiografia revelou um ventrículo esquerdo aumentado e hipertrofiado (com mais massa muscular), função cardíaca levemente reduzida, além de regurgitação (vazamento) moderada da válvula mitral e grave da válvula aórtica. A raiz da aorta estava muito dilatada, com medidas que indicavam risco elevado de complicações. A tomografia computadorizada confirmou essas dilatações, incluindo uma dilatação importante da aorta ascendente.\n\n**Diagnóstico Diferencial e Confirmação**  \nInicialmente, foram consideradas doenças do tecido conjuntivo, como síndrome de Marfan ou Ehlers-Danlos, que causam fragilidade e dilatação da aorta. No entanto, o paciente não apresentava os sinais físicos típicos dessas síndromes, e exames laboratoriais e imunológicos descartaram vasculites e outras causas inflamatórias.\n\nDiante do histórico familiar e das alterações cardíacas, a acromegalia foi investigada. Este distúrbio endócrino, causado por um tumor benigno na hipófise que produz excesso do hormônio do crescimento, pode levar à hipertrofia do coração e dilatação da aorta. Os níveis elevados do fator de crescimento semelhante à insulina 1 (IGF-1) e a falha na supressão do hormônio do crescimento após teste de tolerância à glicose confirmaram o diagnóstico. A ressonância magnética cerebral identificou um microadenoma na hipófise, responsável pela produção hormonal excessiva.\n\n**Tratamento e Evolução**  \nO paciente foi submetido a uma cirurgia complexa chamada procedimento de Bentall, que substitui a válvula aórtica, a raiz da aorta e a aorta ascendente, utilizando uma prótese mecânica. Após a cirurgia, iniciou anticoagulação com varfarina para prevenir tromboses na válvula mecânica.\n\nO tratamento da acromegalia foi iniciado com acetato de octreótido, um medicamento que reduz a produção do hormônio do crescimento. O acompanhamento clínico e por imagem mostrou boa recuperação, com melhora dos sintomas, função cardíaca estável e controle da dilatação aórtica. Os níveis de IGF-1 diminuíram, indicando resposta ao tratamento, e não foram observados efeitos colaterais significativos.\n\n**Interpretação Clínica e Próximos Passos**  \nEste caso ilustra a importância de considerar causas endócrinas raras, como a acromegalia, em pacientes jovens com dilatação significativa da raiz da aorta e hipertrofia ventricular esquerda, especialmente quando há histórico familiar sugestivo. O diagnóstico precoce e o tratamento adequado, incluindo cirurgia cardiovascular e controle hormonal, são essenciais para prevenir complicações graves, como insuficiência cardíaca avançada e ruptura da aorta.\n\nO plano de acompanhamento inclui monitorização regular da função cardíaca, avaliação da válvula mecânica, controle dos níveis hormonais e ajuste da anticoagulação, garantindo a melhor qualidade de vida possível para o paciente."
+        }
+    },
+    {
+        "article": "Uma menina de 2 anos de idade apresentou-se ao departamento de emergência com 5 dias de febre alta, tosse e inchaço bilateral das pálpebras. Antes do início desta doença, havia edema e um furúnculo perinasal na pele do rosto. Ela tinha sido previamente saudável.\n\nO exame físico revelou uma menina muito doente com edema periorbital e facial, febre de alto grau, aumento da taxa respiratória, diminuição da SpO2 e crepitações no peito.\n\nUm exame ocular revelou inchaço ao redor dos olhos em ambos os lados. Ambos os globos oculares mostraram proptose axial. Os exames também mostraram injeção, descarga purulenta em ambos os olhos com pupilas de reação lenta, conjuntivite química grave e oftalmoplegia externa que afeta os nervos cranianos terceiro, quarto e sexto.\n\nA relação do disco vertical do olho direito foi de 0,3, enquanto a do olho esquerdo foi de 0,4. Não houve evidência de veias retinais inchadas ou edema do disco.\n\nAs investigações laboratoriais mostraram uma contagem significativamente alta de glóbulos brancos (WBC = 32.000 células/mm3), baixa hemoglobina (5.5 mg/dL) e alta proteína C-reativa (112 mg/L). A cultura sanguínea foi negativa.\n\nA tomografia computadorizada orbital demonstrou espessamento extenso bilateral do tecido mole periorbital e edema subcutâneo facial. Além disso, a tomografia computadorizada de contraste do tórax revelou múltiplas lesões cavitárias localizadas periféricas nos pulmões bilaterais (embolia séptica) e pneumotórax moderado bilateral associado com áreas de consolidação com broncograma aéreo no pulmão inferior esquerdo.\n\nO paciente foi internado na UTI pediátrica e o tratamento foi iniciado com ceftriaxona intravenosa (IV) 500 mg a cada 12 horas, clindamicina IV 100 mg a cada 8 horas, Voltaren colírio 8 horas, Lomefloxacin colírio 12 horas após uma dose inicial de uma gota a cada 5 minutos durante 25 minutos, pomada de cloranfenicol e xarope de ibuprofeno oral 8 horas. Tubos de tórax bilaterais foram inseridos para a descompressão do pneumotórax.\n\nA contagem de glóbulos brancos normalizou-se e a radiografia de tórax melhorou significativamente. Ela recebeu alta do hospital após 15 dias com terapia antibiótica oral (co_amoxiclav xarope 400mg) a ser tomada por uma semana.\n",
+        "gold_summary": "Uma menina de 2 anos apresentou febre alta, tosse e inchaço bilateral das pálpebras por 5 dias, precedidos por edema e um furúnculo perinasal na pele facial. O exame revelou proptose axial bilateral e celulite orbital e torácica bilateral, embolia pulmonar séptica e pneumotórax bilateral.\n",
+        "synthetic_summary": {
+            "B1": "Uma menininha de 2 anos ficou com febre alta e tosse. Os olhos dela ficaram muito inchados dos dois lados. Antes disso, ela tinha uma bolinha vermelha no rosto. Os médicos viram que os olhos dela estavam muito inchados e que ela estava com problemas no peito. Ela ficou no hospital para melhorar.",
+            "B2": "**O que aconteceu com a menina**\n\nUma menina de 2 anos ficou com febre alta, tosse e inchaço em volta dos dois olhos durante 5 dias. Antes disso, ela teve um inchaço e um furúnculo perto do nariz, que é uma espécie de espinha grande e dolorida na pele do rosto.\n\n**O que os médicos encontraram**\n\nQuando os médicos examinaram a menina, viram que os olhos dela estavam muito inchados e saindo para frente, o que se chama proptose. Ela também tinha uma infecção chamada celulite orbital, que é quando os tecidos ao redor dos olhos ficam inflamados e infectados. Além disso, ela tinha problemas nos pulmões: uma embolia séptica, que é quando pedaços de infecção bloqueiam os vasos do pulmão, e pneumotórax, que é quando o ar escapa para o espaço ao redor dos pulmões, dificultando a respiração.\n\n**Como ela foi tratada**\n\nA menina foi levada para a UTI pediátrica e recebeu vários remédios para combater a infecção, incluindo antibióticos fortes por via intravenosa (direto na veia). Também foi necessário colocar tubos no peito para tirar o ar que estava fora do lugar e ajudar a respirar melhor. Depois de 15 dias, ela melhorou bastante e recebeu alta para continuar o tratamento em casa com remédios orais.\n\n**Por que isso é importante**\n\nEsse caso mostra como uma infecção na pele do rosto pode se espalhar para áreas importantes como os olhos e os pulmões, causando problemas graves. Por isso, é fundamental procurar ajuda médica rápido quando aparecem sinais de infecção e inchaço no rosto, para evitar complicações sérias.",
+            "B3": "**Contexto**  \nUma menina de 2 anos, previamente saudável, foi levada ao pronto-socorro após apresentar cinco dias de febre alta, tosse e inchaço em ambas as pálpebras. Antes do início desses sintomas, ela teve inchaço e um furúnculo (uma infecção cutânea com pus) próximo ao nariz.\n\n**Principais Achados Clínicos e Exames**  \nNo exame físico, a criança estava muito debilitada, com inchaço ao redor dos olhos e do rosto, febre alta, respiração acelerada, baixa saturação de oxigênio no sangue (SpO2) e sons anormais nos pulmões (crepitações). O exame dos olhos mostrou inchaço significativo ao redor das órbitas, com proptose axial bilateral (os olhos estavam projetados para frente), secreção purulenta (pus) em ambos os olhos, conjuntivite química grave (inflamação da conjuntiva) e paralisia dos músculos oculares externos, indicando comprometimento dos nervos cranianos III, IV e VI. Não houve sinais de aumento da pressão dentro dos olhos, como edema do disco óptico.\n\nOs exames laboratoriais indicaram uma infecção grave, com contagem muito alta de glóbulos brancos (32.000 células/mm³), anemia significativa (hemoglobina 5,5 mg/dL) e elevação da proteína C-reativa (112 mg/L), um marcador de inflamação. A cultura de sangue não identificou bactérias.\n\nA tomografia computadorizada (TC) das órbitas revelou um espessamento extenso dos tecidos moles ao redor dos olhos e edema facial. A TC do tórax com contraste mostrou múltiplas lesões cavitárias periféricas nos dois pulmões, compatíveis com embolia séptica (coágulos infectados que se alojaram nos pulmões), além de pneumotórax moderado bilateral (presença de ar na cavidade pleural) e áreas de consolidação pulmonar com broncograma aéreo, especialmente no pulmão inferior esquerdo.\n\n**Interpretação Clínica**  \nO quadro clínico e os exames indicam uma infecção grave que começou na pele do rosto (furúnculo perinasal), evoluindo para celulite orbital bilateral (infecção dos tecidos ao redor dos olhos) e complicações pulmonares graves, incluindo embolia séptica e pneumotórax bilateral. A paralisia dos nervos oculares sugere envolvimento neurológico devido à infecção.\n\n**Tratamento e Evolução**  \nA paciente foi internada na unidade de terapia intensiva pediátrica e recebeu tratamento com antibióticos intravenosos (ceftriaxona e clindamicina), medicamentos tópicos para os olhos (colírios e pomada antibiótica) e analgésicos. Para tratar o pneumotórax, foram inseridos tubos de drenagem em ambos os lados do tórax. Durante a internação, a contagem de glóbulos brancos voltou ao normal e a radiografia de tórax mostrou melhora significativa. Após 15 dias, a criança recebeu alta hospitalar com prescrição de antibióticos orais para continuidade do tratamento em casa.\n\n**Próximos Passos**  \nÉ fundamental o acompanhamento clínico para garantir a resolução completa da infecção e monitorar possíveis sequelas visuais ou respiratórias. A vigilância médica deve continuar para prevenir recidivas ou complicações tardias."
+        }
+    },
+    {
+        "article": "Apresentamos o caso de um homem branco marroquino de 38 anos sem fatores de risco cardiovascular e com histórico de cegueira bilateral não explorada, que se apresentou ao departamento de emergência com edema crônico dos membros e falta de ar progressiva.\n\nA avaliação inicial encontrou um paciente hemodinamicamente estável com uma pressão arterial normal de 105/76 mmHg, uma pulsação de 45 batimentos por minuto e saturação de oxigênio de 93% no ar ambiente. O exame físico mostrou uma distensão da veia jugular externa, edema extenso nas pernas e ascite. A auscultação cardiopulmonar foi notável por um murmúrio holosistólico 4/6 no foco mitral com crepitação difusa bilateral simétrica. A avaliação oftalmológica encontrou uma acuidade visual reduzida à percepção de luz.\n\nUm eletrocardiograma mostrou bradicardia sinusal com uma frequência cardíaca de 45 batimentos por minuto e bloqueio completo do ramo direito. A radiografia torácica foi notável por cardiomegalia e congestão perihilar. O nível de peptídeo natriurético tipo B foi de 1230 pg/ml (para um intervalo normal abaixo de 300 pg/ml), o nível de creatinina foi de 9,6 mg/l (para um intervalo normal entre 6 e 12,5 mg/l), o nível de albumina foi ligeiramente baixo a 36 g/l (para um intervalo normal superior a 39 g/l), e houve uma alta sensibilidade de troponina a 294 ng/l (para um intervalo normal abaixo de 35 ng/l). Outros resultados de testes laboratoriais foram normais, particularmente ferritina, TSH e níveis de eletrólitos.\n\nA ecocardiografia transtorácica (TTE) mostrou um ventrículo esquerdo dilatado (diâmetro basal diastólico final de 60 mm) com uma fração de ejeção severamente reduzida a 15% (biplano Simpson), regurgitação mitral leve e um trombo apical medindo 19 mm x 18 mm. O ventrículo direito estava severamente dilatado (diâmetro basal diastólico final de 51 mm), com disfunção sistólica (Excursão Sistólica do Plano Anular Tricúspide (TAPSE) de 12 mm e onda S' do ventrículo direito no Doppler de tecido (S'VD) de 5 cm/s) e regurgitação tricúspide severa. A veia cava inferior (IVC) estava pletórica com um diâmetro máximo de 37 mm.\n\nUma história detalhada revelou que, desde os seus vinte anos, o paciente tinha problemas de marcha, perda de audição e anosmia e que a sua cegueira começou com uma alteração da visão noturna, mas nunca tinha sido avaliado por um oftalmologista antes desta apresentação. Os exames neurológicos revelaram amiloidose bilateral das pernas com ataxia bilateral. Um exame fundoscópico foi realizado para explorar a sua cegueira e revelou retinite pigmentosa. O quadro clínico do paciente, que associava uma cardiomiopatia dilatada com os sinais neurológicos específicos, era fortemente sugestivo da doença de Refsum. Realizámos um ensaio das concentrações de ácido fitónico no plasma, que revelou um nível notavelmente elevado de 324 μmol/l, o que confirmou a doença de Refsum. Inicialmente, o paciente foi colocado em furosemida intravenosa, que proporcionou subsequente alívio dos seus sintomas de insuficiência cardíaca. Depois disso, recebeu tratamento com furosemida oral [40 mg duas vezes por dia (b.i.d)], inibidores da enzima conversora da angiotensina (ramipril 2,5 mg b.i.d), espironolactona (25 mg uma vez por dia (o.d)), e um inibidor do SGLT2 (empagliflozina 10 mg o.d.). Os bloqueadores beta não foram administrados devido a uma bradicardia sinusal. Além disso, o paciente recebeu antagonistas da vitamina K para o trombo ventricular esquerdo.\n\nEm termos do tratamento específico para a doença de Refsum, o paciente foi aconselhado a aderir a um regime de restrição alimentar projetado para eliminar alimentos contendo fitol, com uma ingestão diária de ácido fitânico abaixo de 10 mg. Isso envolveu evitar o consumo de carne ou gorduras de animais ruminantes (como cordeiro e carne) e produtos de panificação contendo gorduras animais, bem como produtos lácteos como manteiga e queijo.\n\nO paciente se recuperou e sua condição se estabilizou com sintomas de insuficiência cardíaca crônica de classe 2 da NYHA; portanto, ele recebeu alta com tratamento médico para insuficiência cardíaca, antagonistas da vitamina K (VKA) e um regime de baixo ácido fítico.",
+        "gold_summary": "Relatamos o caso de um homem branco marroquino de 38 anos que foi admitido no nosso departamento para um episódio de insuficiência cardíaca aguda descompensada. A ecocardiografia transtorácica encontrou uma cardiomiopatia dilatada com uma fração de ejeção reduzida a 15%. A avaliação posterior mostrou diferentes características da doença de Refsum. O nível elevado de ácido fítico no plasma confirmou o diagnóstico. As manifestações cardíacas são frequentes no curso tardio da doença de Refsum adulta e incluem cardiomiopatia, anomalias elétricas e morte súbita cardíaca. Além disso, as arritmias continuam a ser uma das principais causas de morte nestes pacientes.\n",
+        "synthetic_summary": {
+            "B1": "Um homem de 38 anos ficou muito cansado e com o coração fraco. O médico fez um exame do coração e viu que ele estava grande e não batia forte. O homem tinha uma doença chamada Refsum. Essa doença pode deixar o coração doente e fazer o coração bater errado. Por isso, o homem precisa de cuidados para o coração ficar melhor e para ele se sentir bem.",
+            "B2": "**O que aconteceu com o paciente**\n\nEste é o caso de um homem de 38 anos que chegou ao hospital com problemas no coração, chamados insuficiência cardíaca. Isso significa que o coração dele não estava bombeando sangue direito. Um exame chamado ecocardiografia mostrou que o coração dele estava maior do que o normal e funcionando muito mal, com uma fração de ejeção de apenas 15%. A fração de ejeção é a quantidade de sangue que o coração consegue enviar para o corpo a cada batida, e o valor normal é bem maior.\n\n**O que descobriram sobre a doença**\n\nDepois de mais exames, os médicos perceberam que ele tinha sinais de uma doença rara chamada doença de Refsum. Essa doença causa o acúmulo de uma substância chamada ácido fitânico no corpo, que pode prejudicar vários órgãos, incluindo o coração e o sistema nervoso. O exame do sangue confirmou que o nível de ácido fitânico estava muito alto, o que confirmou o diagnóstico.\n\n**Por que isso é importante**\n\nNa doença de Refsum, problemas no coração são comuns, especialmente em fases mais avançadas. Esses problemas podem incluir o aumento do coração, dificuldades no ritmo dos batimentos (chamadas arritmias) e até risco de morte súbita. Por isso, é muito importante identificar e tratar essa doença para evitar complicações graves.\n\n**Resumo final**\n\nEsse caso mostra como a doença de Refsum pode afetar o coração de forma grave. O diagnóstico foi feito por exames que mostraram o coração fraco e o alto nível de ácido fitânico no sangue. O tratamento e o acompanhamento são essenciais para controlar os sintomas e melhorar a qualidade de vida do paciente.",
+            "B3": "**Contexto**  \nApresentamos o caso de um homem marroquino de 38 anos, sem fatores de risco cardiovascular conhecidos, que deu entrada no hospital com sintomas de insuficiência cardíaca aguda descompensada, caracterizada por inchaço crônico nas pernas e falta de ar progressiva. Exames iniciais revelaram uma cardiomiopatia dilatada grave, com fração de ejeção do ventrículo esquerdo muito reduzida (15%), além de alterações elétricas no coração.\n\n**Principais Achados**  \nA ecocardiografia transtorácica mostrou um coração dilatado e com função comprometida, incluindo um trombo no ventrículo esquerdo. O paciente também apresentava bradicardia (batimentos cardíacos lentos) e bloqueio completo do ramo direito no eletrocardiograma. Além disso, exames neurológicos e oftalmológicos indicaram sintomas típicos da doença de Refsum, uma condição genética rara que afeta o metabolismo de ácidos graxos. O diagnóstico foi confirmado pela medição elevada de ácido fitânico (324 μmol/l) no plasma, substância que se acumula nessa doença.\n\n**Interpretação Clínica**  \nA doença de Refsum, embora rara, pode causar manifestações cardíacas graves, especialmente em fases avançadas. Essas incluem cardiomiopatia dilatada (dilatação e enfraquecimento do músculo cardíaco), distúrbios elétricos que podem levar a arritmias (alterações no ritmo do coração) e risco aumentado de morte súbita. As arritmias são uma das principais causas de mortalidade nesses pacientes. No caso apresentado, a associação entre os sintomas neurológicos, oftalmológicos e cardíacos foi fundamental para o diagnóstico.\n\n**Próximos Passos e Tratamento**  \nO tratamento inicial focou no controle da insuficiência cardíaca com diuréticos, inibidores da enzima conversora da angiotensina, espironolactona e um inibidor do SGLT2, além de anticoagulação para o trombo ventricular. Devido à bradicardia, bloqueadores beta foram evitados. Especificamente para a doença de Refsum, o paciente foi orientado a seguir uma dieta rigorosa com restrição de ácido fitânico, evitando alimentos como carnes e gorduras de animais ruminantes, produtos lácteos e certos produtos de panificação, para reduzir a carga tóxica dessa substância no organismo. Após o início do tratamento, o paciente apresentou melhora clínica e estabilização dos sintomas, sendo liberado para acompanhamento ambulatorial com tratamento contínuo para insuficiência cardíaca e dieta específica."
+        }
+    },
+    {
+        "article": "Em Novembro de 2019, um rapaz de 12 anos foi admitido no hospital infantil de Wuxi por causa de tonturas intermitentes, dores de cabeça durante mais de um mês e andar instável durante meio mês. É de salientar que o paciente teve uma tosse ligeira uma semana antes do início e que se resolveu espontaneamente sem intervenção. Além disso, o rapaz não recebeu quaisquer vacinas desde os 6 anos de idade. Alguns testes neurológicos, como o teste de Oppenheim, o sinal de Brudzinski, o sinal de Kernig e o sinal de Babinski, produziram resultados negativos, enquanto o teste de marcha em tandem e o teste de dedo-nariz produziram resultados positivos, particularmente na mão direita. Além disso, um espectro de doenças desmielinizantes no sistema nervoso central, como anticorpos contra aquaporin-4, glicoproteína oligodendrocítica da mielina e proteína ácida glial, foram negativos. Os seguintes testes relevantes de encefalite autoimune revelaram que os receptores AMPA1/2 e GABABR no LCR foram negativos, mas o NMDA-IgG foi positivo com um título de 1:32. A ressonância magnética do cérebro revelou sinais anormais em ambos os hemisférios cerebelares, indicando uma atrofia cerebelar significativa. Por fim, o rapaz foi diagnosticado com encefalite anti-NMDAR. A deteção de alguns marcadores tumorais, incluindo alfa-fetoproteína, antigénio carcinoembriónico, antigénio de hidratos de carbono (CA) 125 e CA 19-9, foi realizada para excluir a possibilidade de tumores, e todos foram negativos. Depois, este paciente foi tratado com terapia de pulso de sódio succinato de metilprednisolona (20 mg/kg, 3d) e depois mudou para comprimidos de prednisolona (40 mg, po, qd). Por fim, os sintomas do rapaz foram aliviados e ele foi dispensado do hospital. As visitas de acompanhamento em janeiro e maio de 2020 revelaram que esta criança estava em boa saúde sem sintomas visíveis. No entanto, a criança foi readmitida no hospital em agosto de 2020 com disgrafia durante 6 dias. Os resultados do exame neurológico foram comparáveis à última vez, com o teste dedo-nariz permanecendo positivo, mas o Tandem Gait foi negativo. O título de IgG NMDAR foi de 1:10 no soro e 1:3.2 no LCR, e a imagem de ressonância magnética revelou agravamento das lesões nos hemisférios cerebelares. Além disso, o teste de banda oligoclonal de IgG no LCR foi realizado, e o resultado foi positivo. A IgG anti-NMDAR combinada com os resultados da imagem levou ao diagnóstico de encefalite anti-NMDAR recorrente. Um esquema terapêutico semelhante foi aplicado, e o rapaz foi dispensado após a melhoria dos seus sintomas. Mais tarde, as visitas de acompanhamento revelaram que os sintomas do rapaz foram aliviados até certo ponto, mas houve uma recorrência. Além disso, a sua memória e capacidades de aprendizagem foram de alguma forma prejudicadas.\n\nA sequenciação do transcriptoma do LCR foi realizada em ambos os episódios para ajudar a interpretar a etiologia deste caso. Antes do exame, foi obtido o consentimento informado do rapaz e dos seus pais. Brevemente, o RNA total do LCR foi extraído utilizando o RNeasy Micro Kit (Qiagen) seguindo as instruções do fabricante, a partir do qual o rRNA do hospedeiro foi removido antes da construção da biblioteca de sequenciação. A biblioteca foi então construída utilizando o Trio RNA-seq Kit (Nugen), e a sequenciação meta-transcriptómica foi realizada na plataforma Illumina hiseq X-ten como descrito anteriormente. As leituras brutas resultantes foram primeiro recortadas para remover as de baixa qualidade e os adaptadores utilizando o software Trimmomatic, e as leituras de origem humana foram removidas utilizando o script interno. As leituras limpas geradas foram então aplicadas diretamente à análise blast contra a base de dados nr no NCBI para analisar a composição taxonómica utilizando o BLAST + 2.12.0. Depois disso, as leituras de interesse foram mapeadas para as sequências de referência para resolver a cobertura utilizando o bowie2, e depois montadas de novo utilizando o programa Megahit com os parâmetros predefinidos. Depois disso, os contigs montados foram usados como consultas para a análise blast para confirmar o seu estatuto taxonómico. Além disso, o programa MEGA foi usado para alinhar e construir uma árvore de máxima probabilidade para a relação filogenética com outras estirpes de referência.\n\nPara o sequenciamento no primeiro episódio, houve 37.013.105 leituras emparelhadas geradas no total, entre as quais a maioria foi atribuída a Homo sapiens, como esperado. Com base na análise de leitura de explosão, aqueles provavelmente pertencentes a eucariotas, bactérias e vírus representaram 70,54%, 17,04% e 7,61%, respectivamente, das leituras irrelevantes para humanos. Além disso, resultados semelhantes foram obtidos a partir da análise de explosão usando contigs montados como consultas. Entre essas leituras de agentes exógenos putativos, um total de 2459 pode ser mapeado para hRSV tipo B (estirpe SE01A-0135-V02) com cobertura de 98,5% da sua sequência genómica (acesso nº MZ516143). Em particular, a maioria das leituras concentrou-se na localização dos genes NS1, NS2 e L. A RT-PCR e a sequenciação sanger foram usadas para preencher as lacunas nos contigs montados e confirmar as sequências genómicas. Finalmente, com um total de 15.184 bases, a sequência de todo o genoma foi recuperada, exceto para parte da região 3' UTR. Além disso, foi depositada no Genbank (acesso nº ON630422). Com base na análise de sequência, a sequência genómica adquirida partilhou 99,69% de identidade de nucleótidos com SE01A-0135-V02. Depois disso, usando a árvore ML baseada no gene G, a relação filogenética da estirpe Wuxi com outros genótipos do grupo hRSV B foi desvendada. Os resultados indicaram que esta estirpe agrupou-se com SE01A-0135-V02 dentro de B6, o genótipo hRSV mais prevalente no grupo B em todo o mundo. As restantes leituras foram dispersas para outros grupos taxonómicos com números baixos de leituras ou contigs montados curtos. A segunda sequenciação resultou em 34.609.924 leituras emparelhadas, e exceto para leituras de seres humanos, não foram confirmadas leituras associadas a agentes relevantes para condições de doença humana. Devido à ausência de testes de anticorpos ou antigénios de hRSV no momento do aparecimento, realizámos o teste de IgG sérica para hRSV após a sequenciação do LCR utilizando o Kit de ELISA de IgG de RSV Humano (SHUANGYING BIOLOGICAL), e o resultado foi positivo.",
+        "gold_summary": "A criança foi diagnosticada com ataxia e receptores anti-NMDA positivos no fluido cerebrospinal, com encefalite de receptores anti-NMDA em combinação com imagens de MRI craniana. Após a terapia de pulso de hormônio de alta dose e medicação, a doença melhorou e ele foi dispensado. No entanto, uma recaída ocorreu quase um ano depois, e as imagens de MRI craniana mostraram atrofia cerebelar progressiva. Uma cepa de hRSV do grupo B foi detectada no seu fluido cerebrospinal, e a sequência do genoma completo foi recuperada usando sequenciamento de transcriptoma.\n",
+        "synthetic_summary": {
+            "B1": "Um menino ficou com o corpo meio bambo e com dor na cabeça. Os médicos acharam que ele tinha um problema no cérebro chamado encefalite. Eles fizeram um exame e viram que ele tinha umas coisas estranhas no líquido da cabeça. Ele tomou remédios fortes e melhorou. \n\nDepois de quase um ano, ele ficou doente de novo. O cérebro dele estava ficando menor em uma parte. Os médicos acharam um vírus no líquido da cabeça dele. Esse vírus é comum e pode deixar a gente doente. Eles estudaram o vírus para entender melhor. \n\nAgora, o menino está sendo cuidado para ficar bem.",
+            "B2": "**O que aconteceu com o garoto**\n\nUm menino de 12 anos ficou com problemas para andar direito, tonturas e dores de cabeça por mais de um mês. Os médicos fizeram exames e descobriram que ele tinha uma doença chamada encefalite anti-NMDAR. Essa doença acontece quando o sistema de defesa do corpo ataca partes do cérebro, causando sintomas como dificuldade para andar e problemas de coordenação.\n\n**Como foi o tratamento e o que aconteceu depois**\n\nEle recebeu um tratamento com remédios fortes para diminuir a inflamação no cérebro. Depois disso, melhorou bastante e pôde sair do hospital. Porém, quase um ano depois, os sintomas voltaram e exames mostraram que uma parte do cérebro chamada cerebelo estava ficando menor, o que pode afetar o equilíbrio e a coordenação.\n\n**O que os exames mostraram sobre a causa**\n\nOs médicos fizeram um exame especial no líquido que envolve o cérebro e a medula, chamado líquido cerebrospinal. Nesse exame, encontraram um vírus chamado vírus sincicial respiratório humano (hRSV), que normalmente causa problemas no pulmão, mas nesse caso estava no cérebro. Eles conseguiram ler quase todo o código genético desse vírus para entender melhor.\n\n**Por que isso é importante**\n\nEsse caso mostra que o vírus hRSV pode estar ligado a essa doença do cérebro, a encefalite anti-NMDAR, o que ajuda os médicos a entenderem melhor o que pode causar essa doença e como tratá-la. Além disso, o menino teve que passar por tratamento novamente por causa da recaída, e ainda teve algumas dificuldades na memória e no aprendizado depois disso.",
+            "B3": "**Contexto**  \nUm menino de 12 anos apresentou sintomas neurológicos progressivos, incluindo tonturas, dores de cabeça e dificuldade para caminhar, que evoluíram para ataxia (falta de coordenação dos movimentos). Exames laboratoriais revelaram a presença de anticorpos contra o receptor NMDA (um tipo de receptor cerebral) no líquido cefalorraquidiano (LCR), confirmando o diagnóstico de encefalite anti-NMDAR, uma doença autoimune em que o sistema imunológico ataca esses receptores no cérebro. A ressonância magnética (MRI) do cérebro mostrou alterações nos hemisférios cerebelares, indicando atrofia (redução do volume) do cerebelo.\n\n**Principais Achados**  \nO paciente foi inicialmente tratado com uma terapia intensiva de corticosteroides (metilprednisolona em pulsos seguidos de prednisolona oral), o que levou à melhora dos sintomas e alta hospitalar. Contudo, cerca de um ano depois, ele apresentou uma recaída com sintomas de disgrafia (dificuldade para escrever) e agravamento das lesões cerebelares observadas na MRI, confirmando a recorrência da encefalite anti-NMDAR. O teste de bandas oligoclonais no LCR, que indica inflamação crônica do sistema nervoso central, foi positivo nessa fase.\n\nPara investigar a causa subjacente da doença, foi realizado um sequenciamento do transcriptoma (análise do RNA presente) do LCR em ambos os episódios. No primeiro episódio, identificou-se a presença de uma cepa do vírus sincicial respiratório humano (hRSV) do grupo B, com quase todo o genoma viral sequenciado e confirmado por métodos adicionais. Esse vírus é conhecido por causar infecções respiratórias, mas sua detecção no LCR sugere uma possível associação com a encefalite. No segundo episódio, não foram encontrados agentes infecciosos relevantes no LCR. Posteriormente, testes sorológicos confirmaram exposição prévia ao hRSV.\n\n**Interpretação Clínica**  \nEste caso ilustra uma encefalite anti-NMDAR associada à presença do vírus sincicial respiratório no sistema nervoso central, sugerindo que a infecção viral pode ter desencadeado a resposta autoimune contra os receptores NMDA. A progressão para atrofia cerebelar e a recorrência dos sintomas indicam um curso clínico complexo e potencialmente crônico da doença, com impacto na função neurológica do paciente, incluindo memória e aprendizado.\n\n**Próximos Passos**  \nO manejo clínico deve incluir monitoramento cuidadoso da função neurológica e da atividade da doença autoimune, com possibilidade de tratamentos imunomoduladores adicionais para prevenir novas recaídas. A investigação da relação entre infecções virais como o hRSV e encefalites autoimunes pode ajudar a aprimorar o diagnóstico e a terapêutica dessas condições. Acompanhamento a longo prazo é fundamental para avaliar a recuperação funcional e o impacto cognitivo no paciente."
+        }
+    },
+    {
+        "article": "Uma menina de oito anos de descendência sul-indiana foi apresentada ao departamento de emergência para avaliação de dores de cabeça. Ela teve dores de cabeça por vários dias, que foram tratadas com acetaminofeno em casa. Ela negou histórico de visão turva, tontura, apneia do sono, síncope e trauma de cabeça. Não houve histórico de dor de garganta recente, infecção de pele, vômito e diarreia. No passado, ela teve dores de cabeça de natureza semelhante de forma intermitente por cerca de um ano. Não houve histórico de agravamento de dores de cabeça com luz ou som. A produção de urina foi normal e não houve histórico de inchaço dos pés ou abdômen ou inchaço facial. Não houve outros problemas médicos significativos conhecidos incluindo doença cardíaca congênita. Não houve histórico de administração de agentes estimulantes de eritropoietina ou viagens recentes a grande altitude. Ela nasceu a termo sem complicações perinatais. O histórico familiar foi significativo para consanguinidade parental, que foram os primeiros primos. Não houve histórico familiar de dores de cabeça de enxaqueca e eritrocitosis.\n\nApós o exame, os sinais vitais mostraram uma criança afebril com batimentos cardíacos de 90 batimentos por minuto, taxa respiratória de 18 por minuto e pressão arterial de 190/100 mmHg, que permaneceu persistentemente elevada após repetidos exames. A saturação de oxigênio no sangue mostrou-se baixa a 90-92% consistentemente, mas não exigiu suplementação de oxigênio. A altura estava no percentil 75 e o peso no percentil 55. O exame físico foi notável apenas pelo estrabismo. Não houve edema periorbital, ascite ou edema pedal. Ela continuou a ter dores de cabeça. Um exame de tomografia computadorizada sem contraste do cérebro não mostrou evidência de hemorragia, infarto ou trombose. A hipertensão foi controlada com hidralazina intravenosa e labetalol. Ela foi internada para avaliação adicional da hipertensão. O teste de função renal mostrou nitrogênio ureico no sangue de 14 mg/dL e creatinina sérica de 1,6 mg/dL. A albumina sérica foi de 3,1 gm/dL. O resto dos eletrólitos foi normal. A contagem completa de sangue mostrou hemoglobina de 17 gm/dL, hematócrito de 51%, contagem de glóbulos brancos de 7,2 × 109/L e contagem de plaquetas de 247 × 109/L (normal: 150-300 × 109/L). A saturação de ferro no soro foi de 18% (normal: 20-55%), ferro foi de 45 µg/dL (35-150 µg/dL), transferrina foi de 176 mg/dL (200-360 mg/dL), capacidade total de ligação de ferro (TIBC) foi de 246 µg/dL (225-430 µg/dL), e ferritina foi de 98 ng/mL. Os níveis de vitamina B12 e folato no soro foram normais. A biópsia da medula óssea não foi obtida. A análise de urina mostrou 4 + proteinúria sem hematuria microscópica. A razão proteína/creatinina na urina foi de 14.6. Houve hipercolesterolemia. Os complementos séricos foram normais. Os anticorpos antinucleares, citoplasmáticos antineutrofílicos, anti-membrana basal glomerular, e anti-DNA de cadeia dupla foram negativos. O painel de hepatite, vírus da imunodeficiência humana, e teste de tuberculina foram todos negativos. A função da tireóide, as catecolaminas séricas, a atividade da renina plasmática, e a aldosterona sérica foram normais. O estudo dúplex da artéria renal não mostrou evidência de estenose da artéria renal. A radiografia de tórax não mostrou evidência de consolidação, pneumotórax, ou efusão. A sonografia abdominal foi normal. A sonografia nasofaríngea para vírus respiratórios foi negativa. A saturação de oxigênio no sangue dela permaneceu baixa por alguns dias. O ecocardiograma mostrou evidência de hipertrofia ventricular esquerda leve, mas sem outras anormalidades. O tratamento consistiu em hidratação intravenosa e iniciação de agentes anti-hipertensivos, amlodipina, e labetalol. A pressão arterial estabilizou-se, mas a policitemia foi persistente (hemoglobina 15-16 gm/dL). A análise de sequência genética normal de nove variantes genéticas associadas à eritrocitose (genes testados: BPGM, EGLN1, EPAS1, EPOR, HBA1, HBA2, HBB, JAK2, e VHL) foi negativa.\n\nA creatinina sérica aumentou para 1,8 mg/dL (taxa de filtração glomerular estimada de Schwartz de 32 ml/1,73 m2/min) nos próximos dias. A concentração sérica de paratirina intacta foi de 217 pg/mL (normal: 12-88 pg/mL). A proteinúria nefrótica persistiu, mas a relação entre a proteína na urina e a creatinina diminuiu para valores que variam de 5 a 7 após a adição de lisinopril. Uma biópsia renal percutânea realizada uma semana após a apresentação inicial mostrou evidências de FSGS com atrofia tubular grave e fibrose intersticial. O processo de desbaste do pé foi parcial. O teste genético para FSGS mostrou mutações heterozigóticas em ACTN4, INF2 e KANK1 e uma mutação homozigótica em NUP93 por sequenciamento de próxima geração. Devido a mutações genéticas herdadas e à probabilidade de resistência a esteróides, ela não foi tratada com esteróides ou agentes imunossupressores. A hipertensão foi controlada com lisinopril, amlodipina e labetalol com estabilização da pressão arterial. Um agente antiplaquetário foi adicionado. A terapia com ferro foi iniciada para anemia por deficiência de ferro leve (IDA). A saturação de oxigênio voltou ao normal no momento da alta e a policitemia foi resolvida sem a necessidade de flebotomia. Ela progrediu subsequentemente para doença renal em estágio final (ESRD) dez meses após a apresentação inicial e foi inicialmente iniciada em hemodiálise crônica seguida por diálise peritoneal. Ela recebeu um transplante renal de doador falecido quatro meses depois de estar em diálise sem a ocorrência de FSGS recorrente durante o seu mais recente acompanhamento dois meses após o transplante. A sua manutenção com imunossupressão consistiu em tacrolimus, micofenolato e prednisona.\n",
+        "gold_summary": "Aqui, descrevemos uma menina de 8 anos com eritrocitosis em associação com NS e CKD avançada. A paciente foi encontrada com eritrocitosis durante a avaliação para urgência hipertensiva. Ela também tinha proteinúria sem edema. A hemoglobina sérica e o hematócrito foram de 17 g/dL e 51%, respectivamente, apesar da hidratação. O teste de função renal mostrou uma taxa de filtração glomerular estimada de 30 ml/min/1,73 m2. Havia uma anemia por deficiência de ferro leve com saturação de ferro sérico de 18%. O nível de EPO sérico foi normal. A EPO urinária não foi medida. A biópsia renal mostrou evidência de glomerulosclerose segmentar focal. O teste genético para NS mostrou mutações em genes de podócitos: NUP93, INF2, KANK1 e ACTN4. A análise da sequência genética de genes associados com eritrocitosis não mostrou variantes em nenhum desses genes. Ela precisou de diálise crônica dez meses depois e, posteriormente, um transplante renal 14 meses após a apresentação inicial.\n",
+        "synthetic_summary": {
+            "B1": "Uma menina de 8 anos estava com a pressão alta e dor de cabeça. Os médicos fizeram exames e viram que o sangue dela estava diferente. Ela tinha muito sangue, mas estava um pouco fraca por falta de ferro. O rim dela não estava funcionando bem. Os médicos fizeram um exame no rim e acharam um problema chamado FSGS. Eles também fizeram um teste para ver se ela tinha mudanças nos genes, e acharam algumas. A menina precisou de ajuda para limpar o sangue depois de um tempo. Depois, ela ganhou um novo rim para ficar melhor. Os médicos cuidam dela com muito carinho.",
+            "B2": "**O que aconteceu com a menina**\n\nUma menina de 8 anos foi levada ao hospital porque estava com dores de cabeça e pressão alta muito alta. Durante os exames, os médicos descobriram que ela tinha uma condição chamada eritrocitosis, que significa que ela tinha muitos glóbulos vermelhos no sangue. Esses glóbulos vermelhos são importantes porque carregam oxigênio, mas quando estão em excesso, podem causar problemas.\n\n**O que os exames mostraram**\n\nOs exames mostraram que a menina tinha proteína na urina, o que indica que os rins não estavam funcionando bem. Ela não tinha inchaço, o que é comum em algumas doenças renais. A quantidade de ferro no sangue dela estava um pouco baixa, o que causava anemia, um problema em que o corpo não tem glóbulos vermelhos suficientes ou eles não funcionam direito. A função dos rins estava bastante comprometida, com uma taxa de filtração glomerular baixa, que é uma medida de como os rins filtram o sangue.\n\n**O que a biópsia revelou**\n\nOs médicos fizeram uma biópsia, que é quando retiram um pedacinho do rim para analisar. Essa análise mostrou que ela tinha uma doença chamada glomerulosclerose segmentar focal (FSGS). Essa doença danifica partes dos rins chamadas glomérulos, que são responsáveis por filtrar o sangue.\n\n**O papel dos genes**\n\nTambém foi feito um exame genético que revelou mutações em alguns genes importantes para o funcionamento das células dos rins, chamadas podócitos. Esses genes são NUP93, INF2, KANK1 e ACTN4. Essas mutações podem explicar por que os rins dela estavam doentes. Por outro lado, os testes genéticos para a causa da eritrocitosis não mostraram alterações.\n\n**Tratamento e evolução**\n\nCom o tempo, a função dos rins piorou e a menina precisou fazer diálise, que é um tratamento que ajuda a limpar o sangue quando os rins não conseguem mais fazer isso sozinhos. Depois de cerca de um ano, ela recebeu um transplante de rim, que é quando um rim saudável de outra pessoa é colocado no corpo para substituir os rins doentes. Após o transplante, ela está sendo tratada com medicamentos para evitar que o corpo rejeite o novo rim.\n\n**Resumo final**\n\nEssa menina teve uma doença grave nos rins que causou muitos problemas, incluindo pressão alta, excesso de glóbulos vermelhos e perda da função renal. A combinação dos exames clínicos, biópsia e testes genéticos ajudou os médicos a entender a causa e a escolher o melhor tratamento para ela.",
+            "B3": "**Contexto**  \nEste relato descreve o caso de uma menina de 8 anos que apresentou eritrocitosis (aumento anormal do número de glóbulos vermelhos no sangue) associada a síndrome nefrótica (NS, uma condição caracterizada por perda significativa de proteínas na urina) e doença renal crônica (DRC) avançada. Ela foi inicialmente avaliada devido a uma urgência hipertensiva, ou seja, uma elevação grave e persistente da pressão arterial.\n\n**Principais Achados**  \nDurante a avaliação, a paciente apresentou níveis elevados de hemoglobina (17 g/dL) e hematócrito (51%), indicando eritrocitosis, mesmo após hidratação adequada. Ela também manifestou proteinúria significativa (perda de proteínas na urina) sem sinais de edema (inchaço). A função renal estava comprometida, com uma taxa de filtração glomerular estimada em cerca de 30 ml/min/1,73 m², evidenciando doença renal crônica em estágio avançado. Foi identificada anemia leve por deficiência de ferro, confirmada pela saturação de ferro sérico baixa (18%), enquanto o nível de eritropoietina (EPO, hormônio que estimula a produção de glóbulos vermelhos) no sangue estava dentro do esperado. A medição da EPO na urina não foi realizada.\n\nA biópsia renal revelou glomerulosclerose segmentar focal (FSGS), uma lesão renal caracterizada por cicatrizes em partes específicas dos glomérulos, que são as unidades filtrantes do rim. O exame genético identificou mutações heterozigóticas em genes relacionados à estrutura e função dos podócitos (células essenciais para a filtração renal): NUP93, INF2, KANK1 e ACTN4. Esses achados genéticos explicam a origem da síndrome nefrótica na paciente. Por outro lado, a análise genética para causas hereditárias de eritrocitosis não revelou alterações em genes conhecidos por provocar essa condição.\n\n**Interpretação Clínica**  \nA combinação de eritrocitosis com síndrome nefrótica e insuficiência renal avançada é incomum, especialmente em uma criança. A eritrocitosis persistente, apesar da ausência de mutações genéticas típicas para essa condição e da normalidade dos níveis séricos de EPO, sugere um mecanismo complexo possivelmente relacionado à doença renal crônica e à hipóxia crônica (baixa oxigenação do sangue), embora a saturação de oxigênio tenha normalizado antes da alta hospitalar. A presença de mutações em múltiplos genes de podócitos indica uma forma hereditária de FSGS, que é conhecida por ser resistente a tratamentos convencionais com corticosteroides e imunossupressores, o que influenciou as decisões terapêuticas.\n\n**Próximos Passos e Evolução**  \nA paciente evoluiu para insuficiência renal terminal dez meses após a apresentação inicial, necessitando de diálise crônica para substituir a função renal. Quatro meses após o início da diálise, ela recebeu um transplante renal de doador falecido. Até o último acompanhamento, dois meses após o transplante, não houve sinais de recorrência da FSGS no novo rim. O tratamento de manutenção incluiu imunossupressores como tacrolimus, micofenolato e prednisona para prevenir rejeição do órgão transplantado.\n\nEste caso ilustra a complexidade do diagnóstico e manejo de doenças renais hereditárias associadas a manifestações hematológicas incomuns, ressaltando a importância da avaliação genética detalhada e do acompanhamento multidisciplinar para otimizar o prognóstico em pacientes pediátricos com doenças renais crônicas graves."
+        }
+    },
+    {
+        "article": "Uma mulher de 31 anos da República do Zimbábue apresentou-se ao departamento de emergência do nosso hospital com uma história de 3 dias de febre, dor torácica, vômito e diarreia. A paciente não tinha histórico médico prévio de pneumonia, doenças contagiosas ou contatos conhecidos doentes e negou o uso de tabaco ou álcool. Além disso, ela não tinha histórico de hospitalização anterior. No Zimbábue, um subconjunto da população consome habitualmente argila vermelha, e a paciente estava entre esse grupo. Devido à indisponibilidade de argila vermelha, ela recorreu ao consumo de terra de jardim uma vez a cada dois meses, com a ingestão mais recente ocorrendo seis dias antes da apresentação. Ela desenvolveu uma febre com uma temperatura máxima de 38,8 ° C acompanhada de calafrios, tosse não produtiva e dor torácica do lado direito exacerbada pela respiração 3 dias após a ingestão de terra. Ela experimentou quatro episódios de vômito de fluido amarelo-verde e diarreia grave, com fezes amarelas aquosas ocorrendo 3-6 vezes por hora no seu pico. A paciente auto-administrou ibuprofeno, mas os seus sintomas persistiram, levando à sua referência ao nosso hospital devido ao agravamento da diarreia e fadiga.\nNa avaliação física, os sinais vitais do paciente foram os seguintes: temperatura corporal de 38°C, pressão arterial de 100/60 mmHg, pulso de 83 batimentos/min, taxa respiratória de 18 respirações/min, e saturação de oxigênio de 99% no ar ambiente. A auscultação revelou sons respiratórios ásperos bilateralmente. Os resultados laboratoriais indicaram uma contagem de glóbulos brancos de 28,65 × 109/L, com neutrófilos de 25,95 × 109/L e um percentual de neutrófilos de 90,6%. A proteína C reativa estava elevada a 198,76 mg/L. Além disso, o dímero D (22,62 mg/L), creatinina (276,0 μmol/L), nitrogênio ureico (14,27 mmol/L), bilirrubina total (61,0 μmol/L), bilirrubina direta (18,3 μmol/L), e bilirrubina indireta (42,7 μmol/L) estavam elevados. A tomografia computadorizada de tórax (TC) revelou duas lesões suspeitas no lobo inferior esquerdo, com cavitação observada na lesão maior.\nFoi iniciado um tratamento empírico com piperacilina-tazobactam e moxifloxacina. Para identificar o patógeno causador, foi realizada uma broncoscopia e a cultura do fluido de lavagem broncoalveolar (BALF) identificou P. aeruginosa e o teste de suscetibilidade antimicrobiana demonstrou que o isolado de P. aeruginosa era pan-sensível a cefoperazona-sulbactam, levofloxacina, ceftazidima, ceftazidima-avibactam, meropenem, piperacilina-tazobactam, ciprofloxacina, cefepima, aztreonam e imipenem. A cultura fecal indicou simultaneamente uma infecção com P. aeruginosa, enquanto a cultura microbiológica de sangue e urina não demonstrou anomalias significativas. Consequentemente, o regime antibacteriano foi ajustado para piperacilina-tazobactam e ciprofloxacina com base nos resultados de suscetibilidade. Foram administrados tratamentos sintomáticos, incluindo supressão de ácido, proteção gástrica, proteção hepática, agentes antidiarreicos e regulação da flora intestinal, resultando numa melhoria significativa dos sintomas gastrointestinais.\n\nApós 3 dias de terapia, a febre, o vômito e a diarreia da paciente se resolveram, restando apenas uma tosse leve. Uma tomografia computadorizada repetida, realizada após 11 dias, mostrou aumento e fusão das lesões no lobo inferior esquerdo com um pequeno derrame pleural do lado esquerdo. Apesar desses achados radiológicos, os marcadores de infecção da paciente tinham melhorado significativamente, levando à sua alta com instruções para continuar a terapia com moxifloxacina em regime ambulatorial. Um mês depois, uma tomografia computadorizada de acompanhamento demonstrou redução significativa nas lesões do lobo inferior esquerdo, e a paciente permaneceu assintomática.\n",
+        "gold_summary": "Apresentamos o caso de um paciente previamente saudável de 31 anos, professor do ensino médio, que desenvolveu CAP devido a P. aeruginosa após ingerir terra de jardim por três dias consecutivos. O paciente foi internado com sintomas incluindo febre, dor torácica, vômito e diarreia. A tomografia computadorizada (TC) do tórax revelou duas lesões suspeitas no lobo inferior esquerdo, com uma lesão apresentando cavitação. A cultura microbiológica do fluido de lavagem broncoalveolar (BALF) e das fezes confirmou a presença de infecção por P. aeruginosa. O teste subsequente de suscetibilidade antimicrobiana revelou que o isolado de P. aeruginosa era pan-sensível. Após 13 dias de terapia antimicrobiana direcionada, os sintomas e marcadores laboratoriais de infecção do paciente melhoraram significativamente. Uma tomografia computadorizada de acompanhamento um mês depois demonstrou resolução substancial das lesões do lobo inferior esquerdo, e o paciente permaneceu assintomático.\n",
+        "synthetic_summary": {
+            "B1": "Uma mulher ficou doente depois de comer terra do jardim. Ela teve febre, dor no peito, vômito e diarreia. O médico fez um exame do peito dela e viu umas manchas. O médico achou que tinha uma bactéria que fez ela ficar doente. Ela tomou remédio para melhorar. Depois de um tempo, ela ficou bem e as manchas no peito sumiram. Agora, ela está saudável e sem dor.",
+            "B2": "**O que aconteceu com a paciente**\n\nUma mulher de 31 anos, que estava saudável antes, ficou doente depois de comer terra de jardim por alguns dias. Ela teve febre, dor no peito, vômitos e diarreia. Esses sintomas a fizeram procurar o hospital.\n\n**O que os exames mostraram**\n\nNo hospital, fizeram uma tomografia do tórax, que é um exame que tira fotos detalhadas dos pulmões. Esse exame mostrou duas áreas estranhas no pulmão esquerdo, e uma delas tinha uma cavidade, que é como um buraco. Para descobrir o que estava causando a doença, os médicos coletaram um líquido dos pulmões para analisar. Também fizeram exames nas fezes. Esses testes mostraram que a bactéria chamada Pseudomonas aeruginosa estava causando a infecção.\n\n**Como foi o tratamento**\n\nOs médicos usaram remédios antibióticos que matam essa bactéria. Os testes mostraram que a bactéria era sensível a vários antibióticos, ou seja, os remédios funcionariam bem. Depois de 13 dias tomando o tratamento correto, a paciente melhorou bastante. A febre, os vômitos e a diarreia desapareceram, e os exames mostraram que a infecção estava controlada.\n\n**O que aconteceu depois**\n\nUm mês depois, outra tomografia mostrou que as lesões no pulmão tinham diminuído muito. A paciente estava sem sintomas e se sentindo bem. Isso mostra que o tratamento foi eficaz e que ela se recuperou da infecção causada pela bactéria.",
+            "B3": "**Contexto**  \nEste é o relato de uma mulher de 31 anos, previamente saudável, que desenvolveu uma pneumonia adquirida na comunidade (CAP) causada pela bactéria Pseudomonas aeruginosa após ingerir terra de jardim. A paciente apresentou-se ao hospital com sintomas de febre, dor no lado direito do tórax, vômitos e diarreia intensa, que surgiram poucos dias após a ingestão da terra.\n\n**Principais Achados Clínicos e Diagnósticos**  \nNa avaliação inicial, a paciente estava febril (38°C) e apresentava sons respiratórios ásperos em ambos os pulmões. Exames laboratoriais indicaram uma forte resposta inflamatória, com aumento significativo dos glóbulos brancos, especialmente neutrófilos, e níveis elevados de proteína C reativa, um marcador de inflamação. Outros exames mostraram alterações nos rins e no fígado, sugerindo algum grau de comprometimento orgânico. A tomografia computadorizada do tórax revelou duas lesões suspeitas no lobo inferior esquerdo do pulmão, sendo que a maior apresentava cavitação (uma área oca dentro da lesão, típica de infecção grave).\n\nPara identificar o agente causador, foi realizada uma broncoscopia com coleta do fluido dos pulmões (lavagem broncoalveolar), cuja cultura confirmou a presença de Pseudomonas aeruginosa. Essa mesma bactéria foi encontrada também na cultura das fezes da paciente, indicando uma possível origem gastrointestinal da infecção. Culturas de sangue e urina não mostraram infecção. Testes de suscetibilidade indicaram que a bactéria era sensível a múltiplos antibióticos, o que orientou o tratamento.\n\n**Interpretação Clínica**  \nA ingestão de terra contaminada provavelmente foi o fator desencadeante da infecção por P. aeruginosa, uma bactéria oportunista que pode causar pneumonia grave, especialmente em pessoas previamente saudáveis quando há exposição incomum. O quadro clínico da paciente, com sintomas respiratórios e gastrointestinais, além das alterações laboratoriais e radiológicas, confirmou a gravidade da infecção.\n\nO tratamento inicial com antibióticos de amplo espectro foi ajustado para medicamentos específicos aos quais a bactéria demonstrou sensibilidade, incluindo piperacilina-tazobactam e ciprofloxacina. Além disso, foram administrados medicamentos para controlar os sintomas gastrointestinais e proteger órgãos como o estômago e o fígado.\n\n**Evolução e Prognóstico**  \nApós três dias de tratamento, houve resolução da febre, vômitos e diarreia, restando apenas uma tosse leve. Embora a tomografia realizada após 11 dias tenha mostrado aumento e fusão das lesões pulmonares, os marcadores laboratoriais indicaram melhora significativa da infecção, permitindo a alta hospitalar com continuidade do tratamento em casa. Um mês após a alta, a tomografia de controle evidenciou redução substancial das lesões no pulmão, e a paciente permaneceu sem sintomas, indicando recuperação completa.\n\n**Próximos Passos**  \nO caso destaca a importância de considerar exposições ambientais incomuns, como a ingestão de terra, como possíveis fontes de infecção por bactérias oportunistas. O acompanhamento clínico e radiológico continuado é essencial para garantir a resolução completa da pneumonia e prevenir complicações. A educação sobre os riscos do consumo de substâncias não alimentares também é recomendada para evitar casos semelhantes."
+        }
+    },
+    {
+        "article": "Mulher de 76 anos de idade, com histórico de hipertensão arterial há 14 anos, em tratamento com candesartana, sem outros de interesse. Recorreu ao pronto-socorro, com histórico de AVC de 48 horas de evolução, com sinais de disartria e hemiparesia direita, que se resolveu em algumas horas, e voltou 24 horas depois. Ao chegar ao pronto-socorro, com 5 horas de evolução. Na exploração física, destacam-se sinais vitais normais, sonolência, desorientação em tempo e espaço, olhar preferencial para a esquerda, hemianopsia homônima direita, força muscular 0 de 5 no hemicorpo direito na escala de Daniels; hiperreflexia em membros inferiores 3/4 e hiporeflexia em membro superior direito 1/4, resposta plantar extensora bilateral, sem outros achados. Realizou-se de forma imediata tomografia computadorizada (TC) cerebral urgente, que evidenciou uma imagem hiperdensa extraaxial em relação à face lateral esquerda da medula oblonga que transcorre superiormente até a ponte, sendo possível observar nesse nível múltiplas densidades. O estudo urgente foi completado com angiotomografia cerebral, que evidenciou dolicoectasia basilar com 5.09 mm de diâmetro e aneurisma fusiforme a nível da artéria vertebral esquerda, de aproximadamente 20 x 9 mm, parcialmente obliterado com trombo mural e calcificado, com adequado passo do meio de contraste. A ressonância magnética cerebral nas horas posteriores evidenciou restrição à difusão em território de artéria coróidea anterior esquerda e em território basilar na protuberância.\n",
+        "gold_summary": "Mulher de 76 anos que foi ao pronto-socorro com um acidente vascular cerebral isquêmico que afetou o território da artéria basilar e da artéria coróidea anterior esquerda. Os exames de imagem mostraram uma dolicoectasia basilar associada a um aneurisma fusiforme com trombos no interior da artéria vertebral esquerda. As duas anomalias anatômicas estão associadas a um acidente vascular cerebral isquêmico.\n",
+        "synthetic_summary": {
+            "B1": "Uma senhora de 76 anos ficou com o lado direito do corpo fraco. Ela foi para o hospital porque o cérebro dela não estava funcionando bem. Os médicos fizeram fotos da cabeça dela. Eles viram que uma parte do sangue no cérebro estava diferente e com um buraquinho estranho. Isso fez o cérebro dela ficar doente. Os médicos vão cuidar dela para ela melhorar.",
+            "B2": "**O que aconteceu com a paciente**\n\nUma mulher de 76 anos foi ao hospital porque teve um derrame cerebral, que é quando o sangue não chega direito a uma parte do cérebro. Esse problema afetou duas áreas importantes do cérebro, chamadas artéria basilar e artéria coróidea anterior esquerda.\n\n**O que os exames mostraram**\n\nOs médicos fizeram exames de imagem, que são como fotos especiais do cérebro. Eles viram que a artéria basilar estava maior e torta, o que se chama dolicoectasia basilar. Também encontraram um aneurisma fusiforme na artéria vertebral esquerda. Um aneurisma é uma parte da artéria que está dilatada, como um balão, e dentro dele havia coágulos de sangue, chamados trombos.\n\n**O que isso significa**\n\nEssas duas alterações nas artérias podem ter causado o derrame cerebral, porque atrapalham o fluxo normal do sangue para o cérebro. Por isso, é importante entender esses problemas para ajudar a tratar e evitar novos derrames.",
+            "B3": "**Contexto**  \nTrata-se de uma mulher de 76 anos, com histórico de hipertensão arterial controlada há 14 anos, que apresentou um quadro de acidente vascular cerebral (AVC) isquêmico. Inicialmente, ela teve sintomas como dificuldade para falar (disartria) e fraqueza no lado direito do corpo (hemiparesia), que melhoraram temporariamente, mas retornaram 24 horas depois. Ao chegar ao pronto-socorro, cinco horas após o início dos sintomas, apresentava sonolência, desorientação, desvio do olhar para a esquerda, perda da visão no campo direito (hemianopsia homônima direita) e fraqueza total no lado direito do corpo, além de alterações nos reflexos.\n\n**Principais Achados**  \nOs exames de imagem realizados foram fundamentais para o diagnóstico. A tomografia computadorizada (TC) cerebral mostrou uma área anormal ao lado esquerdo da medula oblonga (parte do tronco cerebral), com múltiplas densidades que indicavam alterações estruturais. A angiotomografia, exame que avalia os vasos sanguíneos, revelou uma dolicoectasia basilar — que é um alargamento e alongamento anormal da artéria basilar, principal artéria do tronco cerebral — medindo 5,09 mm de diâmetro. Além disso, foi identificado um aneurisma fusiforme (dilatação em forma de fuso) na artéria vertebral esquerda, com dimensões aproximadas de 20 x 9 mm, contendo trombos (coágulos) e calcificações, mas ainda permitindo o fluxo sanguíneo. A ressonância magnética confirmou áreas de restrição à difusão, que indicam lesões recentes por falta de sangue, nas regiões irrigadas pela artéria coróidea anterior esquerda e pela artéria basilar na protuberância (outra parte do tronco cerebral).\n\n**Interpretação Clínica**  \nO quadro clínico da paciente está relacionado a um AVC isquêmico causado pela redução do fluxo sanguíneo em áreas do cérebro irrigadas pela artéria basilar e pela artéria coróidea anterior esquerda. A dolicoectasia basilar e o aneurisma fusiforme na artéria vertebral esquerda são alterações vasculares que provavelmente contribuíram para a formação de coágulos e obstrução do fluxo, levando ao AVC. Essas anomalias anatômicas, embora raras, são reconhecidas como fatores de risco para eventos isquêmicos no cérebro, especialmente no tronco cerebral, região vital para funções motoras e sensoriais.\n\n**Próximos Passos**  \nO manejo clínico deve focar na prevenção de novos eventos isquêmicos, controle rigoroso da pressão arterial e avaliação detalhada da possibilidade de intervenção vascular para tratar o aneurisma e a dolicoectasia, considerando os riscos e benefícios. A reabilitação neurológica será essencial para a recuperação funcional da paciente, dada a gravidade dos déficits apresentados. Monitoramento contínuo por equipe multidisciplinar especializada é recomendado para otimizar o prognóstico."
+        }
+    },
+    {
+        "article": "Um menino de 15 anos foi apresentado à nossa clínica com a principal queixa de hipertricose focal de cabelo branco por 4 meses. Ele tinha um histórico de vitiligo desde os 10 anos de idade. A lesão de vitiligo estava localizada no pescoço direito e foi tratada com tacrolimus tópico 0,1% pomada aproximadamente duas vezes ao dia e 308 nm excimer (500 mJ/cm2) e terapia com laser de CO2 fracionado (25 W, largura de pulso 2 ms, passo 1,3 mm) a cada 2 semanas durante os últimos anos, e ele notou o cabelo branco anormal há 4 meses atrás. O cabelo branco anormal na lesão de vitiligo cresce mais rápido do que os cabelos normais em outras partes do pescoço. Ele negou ter usado qualquer outra pomada na área. Depois que ele parou de usar tacrolimus por meio mês, os cabelos brancos em seu pescoço direito pararam de crescer. No acompanhamento de 2 meses, não foi observado mais crescimento de cabelos brancos. Durante este período, o paciente continuou a receber a terapia com laser de 308 nm excimer e CO2 fracionado a cada 2 semanas. Propomos que a hipertricose focal foi induzida por tacrolimus.\n",
+        "gold_summary": "Apresentamos um menino de 15 anos com hipertricose focal de cabelo branco por 4 meses, após tratamento com tacrolimus tópico 0,1% pomada. Ele negou ter usado qualquer outra pomada na área. Depois de ter parado de usar tacrolimus por meio mês, a hipertricose focal melhorou.\n",
+        "synthetic_summary": {
+            "B1": "Um menino de 15 anos tinha um pedaço de cabelo branco que crescia rápido no pescoço. Ele usava um creme para a pele chamada tacrolimus. Quando ele parou de usar o creme, o cabelo branco parou de crescer. O menino ficou melhor depois disso.",
+            "B2": "**O que aconteceu com o menino**\n\nUm menino de 15 anos tinha uma mancha de pele chamada vitiligo no pescoço. O vitiligo faz com que a pele perca a cor. Para tratar essa mancha, ele usava uma pomada chamada tacrolimus, que ajuda a pele a melhorar. Depois de algum tempo, ele percebeu que na área do vitiligo estava crescendo cabelo branco e mais grosso do que o normal. Esse crescimento diferente de cabelo é chamado de hipertricose focal.\n\n**O que os médicos fizeram e descobriram**\n\nQuando o menino parou de usar a pomada tacrolimus por cerca de 15 dias, o crescimento do cabelo branco parou. Mesmo assim, ele continuou recebendo outro tratamento com laser para ajudar a pele. Dois meses depois, não apareceu mais cabelo branco novo naquela área.\n\n**O que isso significa**\n\nOs médicos acreditam que a pomada tacrolimus pode ter causado o crescimento anormal do cabelo branco no local do vitiligo. Isso é importante para entender que alguns tratamentos podem ter efeitos inesperados, e é preciso observar o que acontece durante o uso dos remédios.",
+            "B3": "**Contexto**  \nUm menino de 15 anos, com histórico de vitiligo (uma condição que causa manchas claras na pele devido à perda de pigmentação) desde os 10 anos, apresentou uma área localizada de crescimento excessivo e acelerado de cabelos brancos (hipertricose focal) na região do pescoço direito, onde ele tinha uma lesão de vitiligo. Essa alteração capilar foi observada há aproximadamente quatro meses.\n\n**Principais Achados**  \nO paciente vinha sendo tratado na área afetada com tacrolimus tópico a 0,1% (um medicamento imunomodulador usado para tratar doenças inflamatórias da pele) aplicado duas vezes ao dia, além de sessões regulares de terapia com laser excimer de 308 nm e laser de CO2 fracionado a cada duas semanas. O cabelo branco na lesão crescia mais rápido do que os cabelos normais nas áreas vizinhas. Após interromper o uso do tacrolimus por cerca de 15 dias, o crescimento dos cabelos brancos cessou. Durante esse período, o tratamento com os lasers foi mantido, e no acompanhamento realizado dois meses depois, não houve retorno do crescimento anormal dos cabelos.\n\n**Interpretação Clínica**  \nOs dados sugerem que a hipertricose focal de cabelos brancos foi induzida pelo uso do tacrolimus tópico. A associação temporal entre o início do medicamento e o aparecimento do crescimento capilar anormal, bem como a melhora após a suspensão do medicamento, reforça essa hipótese. A continuidade da terapia com laser sem agravamento do quadro indica que o tacrolimus foi o fator mais provável responsável pela alteração.\n\n**Próximos Passos**  \nÉ importante monitorar pacientes com vitiligo que utilizam tacrolimus tópico para possíveis efeitos colaterais incomuns, como a hipertricose focal. Caso essa condição se manifeste, a interrupção do medicamento pode ser considerada, sempre sob supervisão médica. Além disso, estudos adicionais podem ajudar a esclarecer os mecanismos pelos quais o tacrolimus pode estimular o crescimento capilar em áreas específicas da pele."
+        }
+    },
+    {
+        "article": "Uma paciente de 17 anos de idade foi encaminhada do Departamento de Pediatria para o Departamento de Medicina Oral do Hospital Hasan Sadikin com queixas de úlceras bucais dolorosas, secura dos lábios e dificuldades em engolir. Esta condição tornou difícil para a paciente comer e beber, resultando na condição física da paciente ficando fraca e debilitada. A úlcera esteve presente durante 3 dias, não melhorou e tende a sangrar. No entanto, o sangramento parou desde o dia anterior. O Departamento de Pediatria administrou Kenalog em Orabase® em resposta à condição oral desta paciente.\n\nO paciente queixou-se de dores no corpo, erupções cutâneas e queda de cabelo há 2 meses atrás. Esta condição foi examinada no Hospital Kebon Jati, e o diagnóstico de LES foi confirmado. Cerca de 2 semanas atrás, o paciente queixou-se da mesma condição e finalmente decidiu ser tratado no Hospital Hasan Sadikin. Exames abrangentes e multidisciplinares estabeleceram que, além do LES, o paciente também foi diagnosticado com hepatoesplenomegalia, durante a terceira semana de hospitalização. Engrandecimento do fígado e do baço foram encontrados durante a tomografia computadorizada abdominal.\n\nDurante este período de duas semanas, o paciente tomou um regime de drogas diversificado que foi administrado pelo Departamento de Pediatria, que inclui Levofloxacin, Amikacin, Ampicillin-Sulbactam e Ethambutol para os antibióticos. Fluconazole foi dado intravenosamente. Drogas anti-inflamatórias esteróides foram dadas IV Methylprednisolone e Triamcinolone Acetonide topicamente. Omeprazole e Ca. Carbonate como antiácido e PPI. Vitamina D e Curcuma como suplementos dietéticos e Paracetamol também foram dados.\n\nEm exame extraoral, a conjuntiva do paciente estava anêmica, e havia secura e esfoliação dos lábios que tendem a sangrar, juntamente com crostas hemorrágicas com sangue seroso. Durante o exame intraoral, havia lesões que cobriam quase todas as áreas da mucosa oral. Múltiplas ulcerações na mucosa labial superior e inferior. Uma ulcera dolorosa na mucosa bucal esquerda, medindo 5 × 6 mm, com borda eritematosa. Erythema palatino central foi visto no palato duro. A pseudomembrana de candidíase também foi vista no dorso da língua, acompanhada por alongamento das papilas.\n\nGestão de Casos\nFoi administrado NaCl 0.9% e utilizado para realizar várias instruções relacionadas com a condição oral da paciente. A limpeza dos dentes utilizando uma gaze humedecida com solução salina foi a coisa mais importante, porque durante as 2 semanas de hospitalização, a paciente descuidou a sua higiene oral. Crostas hemorrágicas nos lábios e mucosa labial foram também instruídas para serem tratadas utilizando gaze húmida (NaCl 0.9%) o mais frequentemente possível. Isto foi feito cinco vezes por dia, com o objetivo de humedecer os lábios e remover as crostas.\n\nA condição de múltiplas e generalizadas ulcerações na mucosa labial superior e inferior, uma mistura de pomada de esteróide tópico, foi administrada ao paciente. Uma mistura contendo Dexametasona 0.5 mg misturada com Lanolina 2.5 mg e vaselina adicionada até 25 mg foi instruída para o paciente usar três vezes ao dia, após aplicar curativo salino. Considerando outras ulcerações, uma das quais estava na mucosa bucal esquerda e também outras úlceras que eram difíceis de alcançar com a mão, 0.025% de ácido hialurônico foi administrado para aliviar a inflamação localmente.\n\nDurante a segunda visita, a 22 de Novembro de 2022, verificou-se que o estado geral da cavidade oral do paciente tinha melhorado. A língua do paciente ainda apresentava uma placa esbranquiçada, que foi finalmente tratada com suspensão oral de Nystatin®, mas teve de ser interrompida após 2 dias de administração, devido à condição de hepatosplenomegalia. A pomada foi interrompida e substituída por vaselina. A outra medicação foi continuada até à próxima avaliação, durante os 6 dias seguintes. A 28 de Novembro de 2022, o paciente não apresentou queixas sobre a sua cavidade oral, mas clinicamente ainda havia uma presença de queilite esfoliativa, língua revestida e úlcera na mucosa bucal esquerda, que tinha diminuído.\n\nO paciente foi dispensado 2 dias depois e continuou o tratamento ambulatorial. A última visita foi realizada em 16 de dezembro de 2022. O paciente não tinha queixas, podia seguir as instruções de higiene oral e aconselhou o paciente a extrair a raiz dos dentes decíduos 55 e 65.\n",
+        "gold_summary": "Uma paciente de 17 anos foi encaminhada do Departamento de Pediatria com úlceras na boca acompanhadas por lábios secos e uma tendência a sangrar. A lesão mais preocupante foi localizada na mucosa bucal esquerda, uma única ulceração medindo 5x6 mm. Múltiplas ulcerações se espalharam pela mucosa labial superior e inferior, com crostas hemorrágicas nos lábios. A ulceração dolorosa pode levar a dificuldades na abertura da boca e função prejudicada ao comer e beber. O eritema central foi visto no palato. A candidíase pseudomembranosa também foi vista na língua da paciente. A hepatosplenomegalia foi confirmada por tomografia computadorizada, com valores enzimáticos de SGPT (386 U/L) e SGOT (504 U/L).\n\nGestão de Casos\nFoi dada a instrução de administração de 0.9% de NaCl ao paciente para manter a higiene oral e ajudar a hidratar os lábios, a fim de remover as crostas hemorrágicas. Administração de 0.025% de solução oral de ácido hialurónico e mistura de pomada de esteróides tópicos para condições ulceradas e inflamatórias. Foram feitos ajustes de medicamentos com base em testes laboratoriais e a condição clínica do paciente estava a melhorar.\n",
+        "synthetic_summary": {
+            "B1": "Uma menina de 17 anos tinha feridas doloridas na boca. Os lábios dela estavam secos e machucados. As feridas estavam em vários lugares da boca e do lado esquerdo era maior. Isso dificultava ela comer e beber.\n\nOs médicos usaram um remédio para limpar a boca dela e deixar os lábios molhados. Também passaram uma pomada para ajudar as feridas a melhorar. Com o tempo, a boca dela ficou melhor e ela conseguiu cuidar dela sozinha.",
+            "B2": "**O que aconteceu com a paciente**\n\nUma menina de 17 anos estava com feridas dolorosas na boca, lábios muito secos e sangrando. A maior ferida ficava na parte interna da bochecha esquerda e tinha cerca de 5 por 6 milímetros. Além disso, ela tinha várias outras feridas nos lábios de cima e de baixo, e crostas com sangue nos lábios. Essas feridas dificultavam que ela abrisse a boca e comesse ou bebesse direito. Também foi observado que o céu da boca estava vermelho no centro, e a língua tinha uma camada branca causada por uma infecção chamada candidíase, que é um tipo de fungo. Exames mostraram que o fígado e o baço dela estavam maiores do que o normal, uma condição chamada hepatosplenomegalia. Os exames de sangue indicaram que o fígado estava inflamado.\n\n**Como trataram a paciente**\n\nPara ajudar, os médicos ensinaram a paciente a limpar a boca e os lábios com uma solução de água salgada (soro fisiológico 0,9%) várias vezes por dia. Isso ajudava a hidratar os lábios e tirar as crostas com sangue. Para as feridas, ela usou uma pomada feita com remédios chamados esteróides, que ajudam a diminuir a inflamação e a dor. Também aplicaram uma solução com ácido hialurônico, que ajuda a curar e aliviar a inflamação na boca. Durante o tratamento, os médicos ajustaram os remédios conforme os exames e a melhora da paciente. Com o tempo, a condição dela foi melhorando, e ela conseguiu cuidar melhor da boca até ficar sem queixas.",
+            "B3": "**Contexto**  \nUma jovem de 17 anos, previamente diagnosticada com lúpus eritematoso sistêmico (LES), foi encaminhada do Departamento de Pediatria para o Departamento de Medicina Oral devido a úlceras dolorosas na boca, secura e sangramento nos lábios, além de dificuldade para engolir. Essas lesões orais afetavam significativamente sua alimentação e hidratação, contribuindo para seu estado geral de fraqueza. A paciente também apresentava hepatosplenomegalia (aumento do fígado e do baço), confirmada por tomografia computadorizada, e alterações laboratoriais indicativas de comprometimento hepático, com níveis elevados das enzimas SGPT (386 U/L) e SGOT (504 U/L).\n\n**Principais Achados Clínicos**  \nNo exame extraoral, observou-se palidez conjuntival (indicando anemia), lábios secos com descamação e crostas hemorrágicas. Intraoralmente, havia múltiplas úlceras distribuídas pela mucosa labial superior e inferior, sendo a mais significativa uma lesão dolorosa de 5 × 6 mm na mucosa bucal esquerda, com bordas avermelhadas (eritema). O palato duro apresentava eritema central, e a língua exibia uma pseudomembrana característica de candidíase (infecção fúngica), acompanhada de papilas alongadas.\n\n**Interpretação Clínica**  \nAs úlceras orais e as alterações mucosas são manifestações comuns em pacientes com LES, podendo ser agravadas por infecções oportunistas como a candidíase. A hepatosplenomegalia e os níveis elevados de enzimas hepáticas indicam envolvimento sistêmico da doença e possível comprometimento do fígado. A presença de crostas hemorrágicas e a secura labial sugerem fragilidade da mucosa e risco aumentado de sangramento, complicando a higiene oral e o conforto da paciente.\n\n**Gestão e Tratamento**  \nO manejo incluiu a higienização rigorosa da cavidade oral com solução salina a 0,9% para remover crostas e manter a hidratação dos tecidos, realizada várias vezes ao dia com gaze úmida. Para as úlceras, foi prescrita uma pomada tópica contendo dexametasona (um corticosteroide anti-inflamatório) misturada com lanolina e vaselina, aplicada três vezes ao dia após a limpeza salina. Para úlceras de difícil acesso, utilizou-se uma solução oral de ácido hialurônico a 0,025%, que ajuda a reduzir a inflamação e promove a cicatrização. A candidíase na língua foi inicialmente tratada com nistatina em suspensão oral, mas o tratamento foi suspenso devido à hepatosplenomegalia. Posteriormente, a pomada esteroide foi substituída por vaselina para proteção da mucosa.\n\nDurante o acompanhamento, a paciente apresentou melhora progressiva das lesões orais e do estado geral, com redução das úlceras e da queilite (inflamação dos lábios). A higiene oral foi reforçada e orientada para continuidade domiciliar. Foi também recomendada a extração das raízes dos dentes decíduos 55 e 65 para evitar possíveis focos infecciosos.\n\n**Próximos Passos**  \nApós alta hospitalar, a paciente continuou o tratamento ambulatorial com monitoramento regular da condição oral e sistêmica. A manutenção da higiene oral adequada e o acompanhamento multidisciplinar são essenciais para prevenir recidivas das lesões e controlar as complicações associadas ao LES e à hepatosplenomegalia. A extração dentária indicada visa reduzir riscos futuros de infecção e inflamação."
+        }
+    },
+    {
+        "article": "Uma menina de 1 ano de idade foi encaminhada ao nosso hospital com um histórico de 3 meses de diarreia e perda de peso. Ela foi alimentada com uma dieta mista (leite materno e fórmula infantil) desde o nascimento, começando com arroz e soja aos 6 meses e progredindo para leite de vaca, trigo e ovos (gema e clara) aos 8 meses. Ela não desenvolveu sintomas anafiláticos com a fórmula infantil e a ingestão de leite de vaca. Não houve sinais e sintomas acompanhantes relacionados a outros órgãos, como eczema leve, ressecamento da pele ou infecção respiratória superior frequente devido a alergia ao leite de vaca. Nem ela nem ninguém da família tinha doenças alérgicas, como dermatite atópica ou asma. Aos 9 meses de idade, ela desenvolveu vômitos, diarreia e anorexia; seu diagnóstico anterior foi de gastroenterite infecciosa e síndrome pós-enterite. Um mês antes de sua transferência para o nosso hospital, ela foi internada no hospital anterior porque seus sintomas não melhoraram por dois meses e sua perda de peso progrediu. Durante os 2 meses anteriores à sua admissão, sua dieta foi ilimitada. Embora seu vômito tenha melhorado após alguns dias de jejum, a ingestão oral de dietas elementares, fórmula infantil ou mingau de arroz resultou em diarreias repetidas. Após a admissão ao nosso hospital, seu exame físico revelou o seguinte: altura, 69,0 cm (desvio padrão [DP] −2,2); peso corporal, 6641 g (DP −2,8), 999 g menor que o peso medido 3 meses antes; temperatura corporal, 37,1 °C; frequência cardíaca, 96 batimentos por minuto; e pressão arterial, 88/50 mmHg. Seus resultados de exames de sangue foram os seguintes: contagem de glóbulos brancos, 16.900/mL (intervalo normal [IN] 7000–15.000); percentual de eosinófilos, 2,0% (IN < 5,6); hemoglobina, 9,9 g/dL (IN 13,7–16,8); e contagem de plaquetas, 679 × 103 células/mL. Seus resultados de testes laboratoriais foram os seguintes: proteína total, 6,4 g/dL (IN 6,8–8,1); albumina, 3,9 g/dL (IN 4,1–5,1); aminotransferase de aspartato, 35 IU/L (IN 20–45); aminotransferase de alanina, 17 IU/L (IN 4–24); nitrogênio ureico no sangue, 7,4 mg/dL (IN 8–20); proteína C reativa, 0,47 mg/dL (IN < 0,03); sódio, 135 mEq/L (IN 137–147); potássio, 3,6 mEq/L (IN 3,6–5,2); bicarbonato, 19,1 mmol/L (IN 21,0–27,0); e ácido láctico, 21 mg/dL (IN 4–16). Neste momento, um número suficiente de calorias, aminoácidos e gordura estava sendo administrado por via intravenosa. O nível de IgE foi de 1028 IU/mL (IN < 30), e os testes de radioalergosorvente foram positivos para leite (63,7 UA/mL classe 5), caseína (9,8 UA/mL classe 3), alfa-lactalbumina (51,6 UA/mL classe 5), clara de ovo (58,8 UA/mL classe 5), gema de ovo (10,8 UA/mL classe 3), ovomucoide (13,2 UA/mL classe 3), trigo (14,5 UA/mL classe 3), e soja (1,3 UA/mL classe 2). Os testes de picada na pele não foram realizados para confirmar os resultados dos testes de IgE específicos. Níveis de Ig (IgG, 954 [NR 357–989] e IgM, 89 [NR 29–190]) e proporções de subconjuntos de linfócitos foram normais. Os testes de eosinófilos fecais foram negativos, e não foi detectada infecção em testes de cultura de fezes. Adenovírus, rotavírus e norovírus fecais foram negativos.\n\nForam realizados exames de imagem e endoscopia para determinar a causa da diarreia prolongada. A tomografia computadorizada abdominal e os exames de ultrassom não revelaram anormalidades no intestino delgado; o intestino grosso estava dilatado, mas não foi observado espessamento da parede, sugerindo enterite não específica. Um EGD não revelou anormalidades macroscópicas do esôfago ao duodeno. No entanto, a histopatologia da mucosa do duodeno revelou a perda da estrutura das vilosidades mucosas, hiperplasia das criptas, apoptose das criptas e infiltração de linfócitos e eosinófilos (<20 eos/hpf) na lâmina própria, com abscessos das criptas parcialmente formados. A colonoscopia total não revelou achados macroscópicos anormais; no entanto, a histopatologia da mucosa do cólon revelou erosão das membranas mucosas; criptite com diminuição das células caliciformes, fibrose, células plasmáticas e linfócitos; e alguma infiltração de eosinófilos (<20 eos/hpf) na lâmina própria. Estes achados foram semelhantes aos achados na mucosa do duodeno.\n\nAutoimune enteropatia e doença intestinal inflamatória (IBD) foram suspeitadas; portanto, testes adicionais foram realizados. 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antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissimimun de antissim\n",
+        "gold_summary": "Descrevemos o caso de uma menina de 1 ano de idade com enteropatia induzida por proteínas alimentares (FPE) que foi difícil de diagnosticar. Ela foi encaminhada ao nosso hospital com um histórico de 3 meses de diarreia, vômitos e perda de peso. Embora a sua diarreia tenha melhorado após alguns dias de jejum, a ingestão oral de dietas elementares, leite de fórmula ou mingau de arroz resultou em repetidas recaídas. O nível de IgE no soro foi de 1028 IU/mL, e os testes de radioalergossorvente foram positivos para leite, caseína, alfa-lactalbumina e outros alérgenos. A histopatologia da mucosa duodenal revelou perda de estrutura de vilosidades da mucosa, hiperplasia de criptas, apoptose de criptas e infiltração de linfócitos e eosinófilos (<20 eos/hpf) na lâmina própria. Após a terapia com prednisolona (PSL) e a remoção completa de leite de vaca e ovos de galinha da sua dieta, a diarreia da paciente desapareceu. Cinco meses após a interrupção da PSL oral e a remoção completa de leite de vaca e ovos de galinha, o duodeno apresentou uma estrutura de vilosidades da mucosa normal e condutas bem diferenciadas. Não foram observadas anormalidades no desafio com ovo; no entanto, a diarreia voltou a ocorrer após o desafio com leite de vaca.\n",
+        "synthetic_summary": {
+            "B1": "Uma menininha de 1 ano estava com muita diarreia e vomitava. Ela também estava ficando muito magrinha. Quando ela parava de comer, a diarreia melhorava. Mas quando comia leite ou mingau, a diarreia voltava.\n\nOs médicos fizeram exames e viram que ela tinha alergia a leite e ovos. O intestino dela estava machucado e doendo. Eles deram um remédio para ajudar e tiraram o leite e os ovos da comida dela.\n\nDepois disso, a menininha melhorou muito. A diarreia parou e o intestino dela ficou bom de novo. Quando ela tentou comer ovo, não teve problema. Mas quando comeu leite, a diarreia voltou. Então, ela precisa continuar sem leite para ficar bem.",
+            "B2": "**O que aconteceu com a menina**\n\nUma menina de 1 ano teve diarreia, vômitos e perdeu peso por 3 meses. Quando ela parava de comer, a diarreia melhorava, mas voltava sempre que ela comia leite em fórmula, mingau de arroz ou outras comidas. Isso dificultou o diagnóstico do problema.\n\n**O que os exames mostraram**\n\nOs médicos fizeram vários exames. Encontraram que o nível de IgE no sangue dela estava muito alto. IgE é uma proteína que o corpo produz quando tem alergia. Ela também teve testes que mostraram alergia ao leite, a partes do leite (como caseína e alfa-lactalbumina) e a outros alimentos como ovos.\n\nQuando os médicos olharam o intestino dela com uma biópsia — que é quando tiram um pedacinho do tecido para estudar — viram que as vilosidades, que são pequenas estruturas que ajudam a absorver o alimento, estavam danificadas. Também havia sinais de inflamação, com células do sistema de defesa chamadas linfócitos e eosinófilos.\n\n**O tratamento e o que isso significa**\n\nA menina foi tratada com um remédio chamado prednisolona, que ajuda a diminuir a inflamação. Além disso, os médicos tiraram completamente o leite de vaca e os ovos da dieta dela. Depois disso, a diarreia desapareceu.\n\nCinco meses depois de parar o remédio e continuar sem leite e ovos, o intestino dela voltou ao normal, com as vilosidades restauradas. Quando ela comeu ovo de novo, não teve problema. Mas, ao comer leite de vaca, a diarreia voltou.\n\n**Conclusão**\n\nEssa menina tinha uma doença chamada enteropatia induzida por proteínas alimentares, que é uma reação ruim do intestino a certas proteínas do leite e dos ovos. O diagnóstico foi difícil, mas o tratamento correto e a dieta sem esses alimentos ajudaram muito na recuperação dela.",
+            "B3": "**Contexto**  \nApresentamos o caso de uma menina de 1 ano que enfrentou um quadro difícil de diagnosticar de enteropatia induzida por proteínas alimentares (FPE), uma condição em que o intestino reage de forma anormal a certas proteínas presentes nos alimentos, causando inflamação e sintomas gastrointestinais.\n\n**Principais Achados**  \nA criança foi levada ao hospital após três meses de diarreia persistente, vômitos e perda significativa de peso. Embora a diarreia tenha melhorado temporariamente com o jejum, a reintrodução de alimentos, incluindo fórmulas infantis, dietas elementares (alimentos compostos por nutrientes básicos) e mingau de arroz, provocou repetidas recaídas dos sintomas. Exames laboratoriais mostraram um nível elevado de IgE sérica (1028 IU/mL), um anticorpo relacionado a reações alérgicas, e testes específicos indicaram sensibilização a múltiplos alérgenos alimentares, como leite de vaca (incluindo caseína e alfa-lactalbumina) e ovos.\n\nA avaliação por endoscopia do duodeno (parte inicial do intestino delgado) não revelou alterações visíveis a olho nu, mas a análise microscópica da mucosa intestinal mostrou perda da estrutura normal das vilosidades (pequenas projeções que aumentam a absorção de nutrientes), aumento das criptas intestinais (áreas onde as células intestinais se renovam), morte celular programada (apoptose) nas criptas e infiltração de células inflamatórias, como linfócitos e eosinófilos (menos de 20 por campo de alta ampliação), indicando inflamação crônica.\n\n**Interpretação Clínica**  \nO diagnóstico de enteropatia induzida por proteínas alimentares foi confirmado pela resposta positiva ao tratamento com prednisolona (um corticosteroide que reduz a inflamação) e pela exclusão completa do leite de vaca e ovos da dieta da paciente, o que resultou na resolução da diarreia. Após cinco meses da suspensão da prednisolona e manutenção da dieta restrita, a estrutura das vilosidades duodenais voltou ao normal, demonstrando recuperação da mucosa intestinal.\n\nTestes de provocação alimentar mostraram que a criança tolerava o ovo sem apresentar sintomas, mas a reintrodução do leite de vaca desencadeou novamente a diarreia, confirmando a alergia alimentar específica ao leite.\n\n**Próximos Passos**  \nO manejo da paciente envolve a manutenção da exclusão do leite de vaca da dieta para evitar recorrência dos sintomas, além do acompanhamento clínico e nutricional para garantir crescimento adequado e monitorar a possível reintrodução futura de alimentos sob supervisão médica. Este caso ressalta a importância de considerar a enteropatia induzida por proteínas alimentares em crianças com diarreia crônica e perda de peso, especialmente quando há evidências laboratoriais e histológicas de reação alérgica intestinal."
+        }
+    },
+    {
+        "article": "A paciente, uma mulher de 56 anos, foi internada por “10 dias de queda do olho direito e 1 dia de agravamento”. Há 10 dias, a paciente não apresentava nenhuma evidência de queda do olho direito sem limitação de movimento, acompanhada por dor parietal e occipital direita, sem náusea, vômito, tontura, andar instável, sensação de algodão, sem palavras arrastadas, sem engasgos ou tosse ao beber água. A paciente foi tratada fora do hospital e apresentou exames relevantes para considerar o diagnóstico de “aneurisma cerebral”. Há +1 dia, a queda do olho direito da paciente foi agravada, então ela foi ao departamento de neurocirurgia do nosso hospital. História de doenças anteriores: Não há história de hipertensão, diabetes, história familiar de aneurismas, doenças respiratórias ou neurológicas. Exame físico após admissão: os sinais vitais da paciente estavam estáveis e sua mente estava clara. A pupila esquerda, com um diâmetro de cerca de 3 mm, era sensível à reflexão da luz; a pupila direita, com um diâmetro de cerca de 5 mm, era lenta à reflexão da luz; o olho direito tinha uma face caída; o olho direito tinha movimento ocular limitado; o olho direito tinha visão reduzida; o olho esquerdo não apresentava anormalidade óbvia na visão e no movimento ocular; os membros tinham força muscular normal e tensão muscular; os sinais patológicos bilaterais eram negativos; o sinal de estimulação meníngea era positivo; e a coluna vertebral estava dobrada. Após admissão, a reconstrução 3D e a varredura avançada dos vasos sanguíneos da cabeça mostraram que a extremidade do segmento C7 da artéria carótida interna direita estava inchada e dois processos saculares com um comprimento de cerca de 0,4 cm foram vistos, que eram aneurismas múltiplos com aneurismas filiais. Diagnóstico após admissão: 1. Aneurisma C6 da artéria carótida interna direita 2. Oftalmoplegia do lado direito 3. Anestesia e procedimento cirúrgico: sevoflurano foi dado para manter a respiração espontânea e após intubação traqueal bem sucedida com laringoscópio visual, a ventilação mecânica foi normal. Subsequentemente, a craniotomia de aneurisma foi realizada com sucesso. Durante as 3,6 horas de cirurgia, 3200 ml de líquido (1600 ml de cristal e 1300 ml de coloide) foram injetados, 1700 ml de urina foram urinados, e 200 ml de sangue foram sangrados. A última análise de gases no sangue (FiO2 50%) durante a operação mostrou que o pH era 7,45, PaCO2 era 40,3 mmHg, PaO2 era 212,7 mmHg, Na era 137,9 mmol/L, K era 3,24 mmol/L, e Ca era 1,0 mmol/L. Após a operação, a paciente foi transferida para a pequena sala de recuperação com um tubo. SpO2 99%, BP 100/50 mmHg, HR 68 bpm, EtCO2 32 mmHg no momento da admissão. Uma hora após entrar na sala de recuperação de anestesia, a paciente recuperou a respiração espontânea, mas o volume de respiração foi baixo, cerca de 90 ml. Meia hora depois, a paciente desenvolveu dispneia na fase inspiratória, sinal triplo côncavo grave, e expelia líquido espumoso rosa do tubo endotraqueal. SpO2 96%, BP 110/70 mmHg, HR 58 bpm, EtCO2 48 mmHg foram imediatamente aspirados para a traqueia, sugando uma grande quantidade de espuma rosa, com ventilação manual conduzida, e a resistência das vias aéreas foi alta (35 cm/H2O). O volume de respiração foi cerca de 60 ml. Confirmaram o cateter e retiraram o cateter traqueal para 16 cm, mas a resistência das vias aéreas não foi significativamente melhorada. O broncoscópio de fibra óptica mostrou que o edema dos principais brônquios esquerdo e direito basicamente desapareceu. Oito horas depois, eles retiraram o cateter traqueal e o separaram do ventilador. Os sintomas foram aliviados no quinto dia após a cirurgia e eles foram dispensados do hospital. Três meses após a alta, eles se recuperaram bem após o acompanhamento.\n",
+        "gold_summary": "Uma paciente de 56 anos de idade foi internada no hospital por \"10 dias de queda do olho direito e 1 dia de agravamento\". Após a admissão, o exame físico constatou que a paciente tinha escoliose grave. A reconstrução 3D e a tomografia computadorizada dos vasos da cabeça mostraram que os aneurismas C6 da artéria carótida interna direita foram cortados sob anestesia geral. Após a operação, a paciente teve aumento da pressão das vias aéreas, com um grande número de expectoração de espuma cor-de-rosa atraída pelo cateter da traqueia, e os pulmões estavam espalhados com rales úmidos durante a auscultação. Após o tratamento de anti-insuficiência cardíaca, a paciente voltou para a UTI através do cateter da traqueia. Oito horas depois, o cateter da traqueia foi retirado e a paciente foi liberada do ventilador. Os sintomas foram aliviados no quinto dia após a operação.\n",
+        "synthetic_summary": {
+            "B1": "Uma mulher de 56 anos teve o olho direito caído por muitos dias. Ela foi para o hospital para cuidar disso. Os médicos fizeram exames e viram que tinha um buraquinho no vaso do cérebro dela. Eles fizeram uma cirurgia para consertar isso.\n\nDepois da cirurgia, ela teve um problema para respirar. Saiu um líquido com espuma do tubo na garganta dela. Os médicos cuidaram dela com muito cuidado. Depois de um tempo, ela melhorou e conseguiu respirar sozinha. Cinco dias depois, ela estava melhor e saiu do hospital.",
+            "B2": "**O que aconteceu com a paciente**\n\nUma mulher de 56 anos ficou com o olho direito caído por 10 dias, e o problema piorou no último dia. Quando ela chegou ao hospital, os médicos fizeram vários exames e descobriram que ela tinha aneurismas na artéria carótida interna direita. Um aneurisma é como uma bolha que se forma na parede de um vaso sanguíneo e pode ser perigosa se estourar. Além disso, ela tinha escoliose, que é uma curvatura forte na coluna.\n\n**O tratamento realizado**\n\nA paciente passou por uma cirurgia para corrigir esses aneurismas. Durante a operação, ela recebeu anestesia geral, que faz a pessoa dormir profundamente para não sentir dor. A cirurgia foi feita com sucesso para cortar os aneurismas.\n\n**O que aconteceu depois da cirurgia**\n\nDepois da operação, a paciente teve problemas para respirar. Ela apresentou um aumento da pressão nas vias aéreas e soltou uma espuma rosa pelo tubo que ajudava na respiração. Isso indicava que havia líquido nos pulmões, o que pode causar dificuldade para respirar. Os médicos trataram esse problema com remédios para ajudar o coração e os pulmões a funcionarem melhor.\n\nEla foi levada para a Unidade de Terapia Intensiva (UTI) com o tubo na traqueia para ajudar na respiração. Oito horas depois, o tubo foi retirado e ela conseguiu respirar sozinha sem o ventilador. Cinco dias após a cirurgia, os sintomas dela melhoraram bastante.\n\n**Conclusão**\n\nA paciente teve um aneurisma que causou a queda do olho e precisou de uma cirurgia para corrigir. Apesar das complicações respiratórias após a operação, ela recebeu o tratamento adequado e se recuperou bem. Três meses depois, ela estava em boas condições de saúde.",
+            "B3": "**Contexto**  \nUma mulher de 56 anos foi internada após apresentar queda do olho direito por 10 dias, com piora significativa no último dia. Inicialmente, ela sentia dor na região parietal e occipital direita, sem outros sintomas neurológicos evidentes. Exames indicaram a presença de aneurismas (dilatações anormais) na artéria carótida interna direita, especificamente no segmento C6, confirmando o diagnóstico. A paciente não possuía histórico de hipertensão, diabetes ou doenças neurológicas prévias.\n\n**Principais Achados Clínicos e Diagnóstico**  \nNo exame físico, observou-se que o olho direito apresentava ptose (queda da pálpebra), movimento ocular limitado e pupila dilatada com resposta lenta à luz, enquanto o olho esquerdo estava normal. A paciente também tinha escoliose (curvatura anormal da coluna vertebral) e sinais de irritação meníngea (indicando possível inflamação das membranas que envolvem o cérebro). A força muscular dos membros estava preservada e não havia sinais patológicos nos reflexos.\n\nExames de imagem, incluindo reconstrução tridimensional e tomografia computadorizada dos vasos sanguíneos da cabeça, revelaram múltiplos aneurismas saculares na artéria carótida interna direita.\n\n**Intervenção e Curso Pós-Operatório**  \nA paciente foi submetida a uma craniotomia (abertura cirúrgica do crânio) para correção dos aneurismas sob anestesia geral, com intubação traqueal e ventilação mecânica. A cirurgia durou aproximadamente 3,6 horas, durante as quais foram administrados líquidos intravenosos e monitorados parâmetros sanguíneos importantes, que permaneceram estáveis.\n\nNo pós-operatório imediato, a paciente apresentou dificuldade respiratória caracterizada por dispneia (falta de ar) inspiratória, presença de espuma cor-de-rosa no tubo endotraqueal e aumento da pressão nas vias aéreas, sinais compatíveis com edema pulmonar (acúmulo de líquido nos pulmões). Foi realizada aspiração traqueal para remover a espuma, ventilação manual e monitoramento intensivo. O uso de broncoscópio descartou obstrução brônquica significativa.\n\nApós oito horas, o tubo traqueal foi removido e a paciente foi desmamada do ventilador mecânico. O quadro respiratório melhorou progressivamente, com alívio dos sintomas até o quinto dia pós-cirúrgico.\n\n**Desfecho e Seguimento**  \nA paciente teve recuperação satisfatória e recebeu alta hospitalar após estabilização clínica. No acompanhamento realizado três meses depois, ela apresentava boa recuperação funcional, sem sequelas aparentes relacionadas ao aneurisma ou à cirurgia.\n\n---\n\nEste caso ilustra a complexidade do manejo de aneurismas cerebrais com manifestações neurológicas focais, como a oftalmoplegia (paralisia dos músculos oculares), e destaca a importância do monitoramento cuidadoso das complicações respiratórias no pós-operatório neurocirúrgico."
+        }
+    },
+    {
+        "article": "Mulher de 69 anos, com história de hipertensão, diabetes mellitus insulinodependente, cefaleia crônica e tabagista. Referia há 1 semana dor de cabeça, confusão mental e vômitos. O exame no pronto-socorro revelou coma (escala de coma de Glasgow em 5), rigidez de nuca e ausência de alterações pupilares.\n\nA tomografia computadorizada (TC) mostrou HSA difusa, hemorragia intraventricular leve e hidrocefalia. A angiotomografia computadorizada demostrou aneurisma de artéria carótida interna supraclinoide à direita. Uma vez admitida na unidade de terapia intensiva (UTI), recebeu tratamento com ventilação mecânica invasiva, ácido tranexâmico, nimodipina e VPA enteral (400mg, três vezes ao dia). Foram realizadas drenagem lombar externa e embolização endovascular do aneurisma, sem evidência de vasoespasmo angiográfico. A TC inicial evidenciou hidrocefalia, sendo feita drenagem ventricular externa.\n\nComo complicação inicial, a paciente desenvolveu disfunção neurocardiogênica, com eletrocardiograma mostrando alterações difusas da repolarização e troponina elevada (716ng/mL). O ecocardiograma transtorácico demostrou disfunção sistólica (fração de ejeção do ventrículo esquerdo de 35%) e anormalidades regionais da contratilidade parietal, que foram interpretadas como miocardiopatia de estresse. Durante a permanência na UTI, apesar da retirada da sedação, a paciente permaneceu em coma (escala de coma de Glasgow em 5 no sexto dia). As tomografias subsequentes foram negativas para hidrocefalia, lesões isquêmicas ou outras complicações.\n\nAs funções hepática, renal e tireoidiana estavam normais, e ela não apresentava distúrbios hidroeletrolíticos. Não foram encontradas complicações extraneurológicas. A drenagem ventricular externa foi removida com culturas estéreis. O Doppler transcraniano foi negativo para vasoespasmo e mostrou índice de pulsatilidade normal. A ressonância magnética não detectou anormalidades. O EEG padrão descartou padrões ictais, mas demostrou um padrão de DPGs com predominância frontal, que se caracterizava como um padrão de descarga periódica contínua, com morfologia trifásica e sem flutuação espontânea, como visto em disfunções cerebrais tóxicas e/ou metabólicas.(4) Diante desses achados, a dosagem de VPA foi de 65,3µg/mL (faixa terapêutica de 50 - 100µg/mL), e a dosagem de amônia foi de 160,2µg/mL (faixa normal de 18,7 - 86,0µg/mL). Não se observaram insuficiência hepática ou sangramento gastrintestinal. Em seguida, a administração de VPA foi descontinuada, e foram iniciados o tratamento para hiperamonemia com lactulose e a dieta restrita em proteínas. O nível de amônia diminuiu progressivamente até a normalização (81,7ug/mL), o que foi correlacionado com uma melhora neurológica evidenciada por resposta ao comando no Dia 12.\n\nOs EEGs subsequentes melhoraram progressivamente até o normal. A paciente necessitou de traqueostomia para retirada da ventilação mecânica e apresentou fístula traqueoesofágica como complicação. Ela evoluiu para óbito 85 dias após a admissão.",
+        "gold_summary": "Apresentamos o caso de um paciente com hemorragia subaracnóidea que recebeu profilaxia anticonvulsivante com valproato e evoluiu com piora neurológica associada a níveis plasmáticos elevados de amônia e descargas periódicas no eletroencefalograma, sem outras causas identificáveis. A interrupção do tratamento com ácido valproico e a normalização dos níveis plasmáticos de amônia resultaram em melhora do quadro neurológico e eletroencefalográfico.",
+        "synthetic_summary": {
+            "B1": "Uma senhora ficou muito doente com uma machucadinha na cabeça. Ela tomou um remédio para ajudar o cérebro. Mas o remédio fez uma coisa ruim: deixou o corpo dela com uma coisa chamada amônia alta. Isso deixou ela mais confusa e cansada.\n\nOs médicos pararam o remédio. Eles deram outro tratamento para tirar a amônia do corpo dela. Depois disso, ela começou a melhorar e ficou um pouco mais acordada. Os médicos ficaram cuidando dela com muito carinho.",
+            "B2": "**O que aconteceu com a paciente**\n\nUma mulher de 69 anos teve um sangramento no cérebro chamado hemorragia subaracnóidea. Para evitar convulsões, ela recebeu um remédio chamado valproato, que ajuda a controlar crises. Porém, durante o tratamento, ela piorou e ficou com problemas no cérebro.\n\n**O que os médicos descobriram**\n\nOs exames mostraram que ela tinha níveis muito altos de amônia no sangue. A amônia é uma substância que, em excesso, pode prejudicar o cérebro. Além disso, o eletroencefalograma (EEG), que é um exame que mede a atividade elétrica do cérebro, mostrou padrões anormais chamados descargas periódicas. Não havia outras causas que explicassem esses problemas.\n\n**O que foi feito e o que isso significa**\n\nOs médicos pararam de dar o valproato para a paciente. Depois disso, os níveis de amônia no sangue voltaram ao normal e a atividade do cérebro melhorou, como mostrado nos exames. Isso ajudou a paciente a recuperar parte das funções neurológicas.\n\n**Resumo**\n\nEsse caso mostra que o remédio valproato pode causar aumento da amônia no sangue, o que piora o funcionamento do cérebro. Por isso, é importante monitorar esses níveis e considerar parar o remédio se isso acontecer.",
+            "B3": "**Contexto**  \nEste relato descreve o caso de uma mulher de 69 anos que sofreu uma hemorragia subaracnóidea (sangramento no espaço entre o cérebro e a membrana que o envolve), associada a um aneurisma cerebral. Ela apresentava múltiplas condições prévias, como hipertensão, diabetes insulinodependente, cefaleia crônica e era tabagista. Ao chegar ao hospital, encontrava-se em coma profundo, com rigidez no pescoço e sinais neurológicos graves. Exames de imagem confirmaram o sangramento cerebral, hidrocefalia (acúmulo de líquido no cérebro) e um aneurisma na artéria carótida interna direita.\n\n**Principais Achados**  \nDurante a internação na unidade de terapia intensiva, a paciente recebeu ventilação mecânica e tratamento medicamentoso, incluindo o ácido valproico (VPA), um anticonvulsivante usado para prevenir crises epilépticas. Procedimentos como drenagem do líquido cerebral e embolização do aneurisma foram realizados com sucesso, sem evidência de vasoespasmo (contração dos vasos sanguíneos cerebrais). Contudo, a paciente desenvolveu complicações cardíacas compatíveis com miocardiopatia de estresse, e permaneceu em coma mesmo após a suspensão da sedação.\n\nExames complementares mostraram ausência de outras causas estruturais para o coma persistente, como lesões isquêmicas ou hidrocefalia. O eletroencefalograma (EEG) revelou um padrão anormal de descargas periódicas contínuas, sugestivo de disfunção cerebral tóxico-metabólica. A dosagem do ácido valproico estava dentro da faixa terapêutica, mas a amônia plasmática estava significativamente elevada, indicando hiperamonemia (excesso de amônia no sangue), sem sinais de insuficiência hepática ou outras causas comuns.\n\n**Interpretação Clínica**  \nA associação entre o uso de ácido valproico e a elevação da amônia, que pode causar toxicidade cerebral, foi identificada como a provável causa da piora neurológica da paciente. A hiperamonemia induzida pelo valproato é uma complicação conhecida, embora rara, que pode levar a alterações no estado de consciência e padrões anormais no EEG, mesmo na ausência de disfunção hepática. A retirada do valproato e o tratamento específico para reduzir os níveis de amônia, com lactulose e dieta restrita em proteínas, resultaram na normalização dos níveis de amônia e na melhora progressiva do quadro neurológico e dos padrões eletroencefalográficos.\n\n**Próximos Passos e Desfecho**  \nApesar da melhora neurológica relacionada à correção da hiperamonemia, a paciente apresentou complicações adicionais, como fístula traqueoesofágica, e evoluiu para óbito após 85 dias de internação. Este caso destaca a importância de monitorar os níveis de amônia em pacientes tratados com ácido valproico, especialmente em contextos críticos, para identificar precocemente a toxicidade e ajustar o tratamento, visando melhorar o prognóstico neurológico."
+        }
+    },
+    {
+        "article": "Um homem de 48 anos foi transferido para o nosso hospital de um centro psiquiátrico com sonolência, ataxia cerebelar e disartria de três dias de evolução. Não apresentou febre no mês anterior. Ele relatou o uso de escitalopram e clonacepam nos dias anteriores, bem como disulfiram intranasal (1-2 g por dia com uma dose máxima de 10 g por dia nas 48 horas anteriores) durante os últimos dois meses para fins recreativos.\n\nEle tinha histórico de hipertensão arterial não tratada e esquizofrenia paranoide, que resultaram em três internações por exacerbações devido à falta de tratamento. Ele estava tomando 10 mg/8 horas de olanzapina e 100 mg de paliperidona intramuscular mensalmente para a esquizofrenia, além de 0,5 mg/24 horas de clonazepam e 15 mg/24 horas de escitalopram. Ele também estava sendo tratado com 250 mg de dissulfiram oral diariamente por causa de seu alcoolismo crônico, apesar de manter um padrão de consumo ativo.\n\nNa chegada ao pronto-socorro, a frequência respiratória era de 20 respirações/minuto, a saturação de oxigênio no ar ambiente era de 98%, a frequência cardíaca de 85 batimentos/minuto, a pressão arterial de 177/100 mmHg e a temperatura de 36,2 °C. O paciente estava estuporoso e desorientado, com uma escala de coma de Glasgow de 13/15. A exploração cardiovascular, respiratória e abdominal foi anódina. Na exploração neurológica, destacavam-se pupilas mióticas hiporreativas, um pestanejar profuso, uma marcada disartria e uma marcha instável. Não havia sinais clínicos de hipertensão intracraniana nem de irritação meníngea.\n\nO exame de sangue mostrou acidose metabólica hiperclorêmica (pH: 7,28; bicarbonato real: 16,4 mmol/L), poliglobúlia e macrocitoses. A função renal e o perfil hepático foram normais. Não foram encontrados outros achados de interesse. O estudo toxicológico foi negativo para etanol, metanol e etileno glicol. O rastreamento de tóxicos na urina por imunoensaio foi positivo para benzodiazepinas. A tomografia computadorizada revelou hipodensidades simétricas leves inespecíficas tanto dos núcleos pálidos como dos braços posteriores das cápsulas internas, atrofia cerebral e infartos lacunares crônicos.\n\nCom a suspeita de que a encefalopatia do paciente estava relacionada a uma intoxicação farmacológica (presumivelmente por benzodiazepinas), sem poder descartar outras possibilidades diagnósticas, ele foi internado na enfermaria. Esta primeira hipótese foi sustentada pelo fato de que se tratava de uma síndrome hipnótico-sedativa em um paciente que referia consumo de benzodiazepinas e que apresentava um estudo qualitativo positivo na urina.\n\nOs níveis plasmáticos de diazepam, nordiazepam e clonazepam foram solicitados, todos dentro da faixa terapêutica ou sub-terapêutica (72 ng/mL, 412 ng/mL e negativos, respectivamente). Um eletroencefalograma mostrou atividade lenta difusa, sem alterações focais ou epileptiformes. O exame do líquido cefalorraquidiano mostrou uma hiperproteinorraquia leve e todos os estudos microbiológicos foram negativos.\n\nA anamnese com o paciente foi difícil, pois a informação fornecida era muitas vezes contraditória. Neste sentido, a explicação para os níveis de clonacepam serem negativos foi que não se podia garantir que o paciente tivesse realmente tomado o clonacepam. Com base nestes níveis plasmáticos, é muito provável que não o tivesse tomado. Por outro lado, o facto dos níveis plasmáticos de diacepam e nordiacepam serem positivos foi consistente com a informação fornecida pelo paciente. Em retrospetiva, encontraram-se frascos de diacepam na casa do paciente. Os níveis plasmáticos no intervalo terapêutico não excluem a possibilidade de efeitos adversos, mas tornam a sua gravidade e a evolução clínica seguida pelo paciente menos provável. As benzodiazepinas provavelmente contribuíram para o quadro, mas não foi possível atribuir a causalidade tendo em conta estes níveis plasmáticos.\n\nPor outro lado, a acidemia hiperclorêmica com níveis normais de lactato no contexto clínico deste paciente nos levou a considerar o diagnóstico de um distúrbio metabólico, especialmente de uma acidemia orgânica, um distúrbio da beta-oxidação de ácidos graxos ou um distúrbio do ciclo da uréia. O estudo sistemático no plasma e na urina de ácidos graxos, acilcarnitinas, acilglicinas e carnitina foi negativo. Além disso, os níveis de amônio foram normais e não se encontrou uma hipoglicemia hipocetósica. A acidemia se resolveu em menos de 24 horas sem medidas específicas, o que tornava muito pouco provável a hipótese de um distúrbio metabólico. Além disso, durante a estabilização inicial, o paciente havia recebido suaeroterapia intensiva com NaCl a 0,9%, o que poderia ter contribuído para a acidemia.\n\nNas 24 horas seguintes, houve um declínio progressivo no nível de consciência, com o desenvolvimento de insuficiência respiratória rapidamente progressiva, que exigiu intubação endotraqueal e ventilação mecânica, e transferência para a unidade de terapia intensiva.\n\nO exame respiratório e a radiografia de tórax sugeriram uma pneumonia por broncoaspiração, que foi tratada em conformidade. Para investigar a etiologia da encefalopatia, foi realizada uma ressonância magnética cerebral. Esta revelou um sinal hiperintenso heterogêneo bilateral e extenso em ambos os globos pálidos, o braço posterior da cápsula interna e o putâmen, tanto em FLAIR como em T2. A sequência potenciada em T1 mostrou uma hipointensidade nas áreas mencionadas.\n\nCom base nessas descobertas, o caso foi reclassificado como encefalopatia induzida por dissulfiram, uma vez que o padrão radiológico foi previamente descrito na literatura em outros casos de intoxicação por dissulfiram, bem como em casos de intoxicação por monóxido de carbono (mas esse não era o cenário clínico). O diagnóstico de encefalopatia por dissulfiram foi feito por exclusão. De acordo com o algoritmo de Naranjo et al. [5], com uma pontuação de 4 em 10, a atribuição de causalidade ao dissulfiram neste caso foi considerada possível. Por sua vez, os casos publicados de encefalopatia por dissulfiram apresentam importantes semelhanças com este caso. No entanto, não há casos descritos de dissulfiram inalado, uma vez que não é uma via de administração aprovada. Infelizmente, não foi possível realizar níveis plasmáticos de dissulfiram.\n\nA condição respiratória do paciente melhorou gradualmente durante as duas semanas seguintes, até que ele pudesse ser extubado. Após a retirada da sedação, o exame neurológico revelou dificuldades na supinação, tremor intencional e dismetria dedo-nariz, bem como fraqueza proximal nos membros superiores e inferiores. O paciente apresentou subsequentemente uma melhora neurológica. A limitação da motilidade ocular e a fraqueza resolveram-se em poucos dias, mas persistiram com um leve tremor e uma leve dismetria. Devido à miopatia do paciente crítico, a marcha não pôde ser explorada até duas semanas depois, quando foi observada uma resolução completa da ataxia.\n\nO paciente recebeu alta com um leve tremor intencional residual. A ressonância magnética cerebral de controle após dois meses mostrou uma evolução das áreas simétricas de edema citotóxico para necrose.\n",
+        "gold_summary": "Paciente de 48 anos com enolismo crônico que relatou o uso de uma dose muito elevada de disulfiram por via intranasal sem ingestão simultânea de álcool, desenvolveu uma encefalopatia aguda com insuficiência respiratória rapidamente progressiva. A neuroimagem revelou uma extensa afetação simétrica bilateral de ambos os núcleos pálidos, um achado característico nesta intoxicação. A recuperação neurológica foi lenta. Dois meses após a intoxicação, o paciente apresentava um ligeiro tremor intencional residual e uma ressonância magnética mostrou uma evolução das áreas simétricas de edema citotóxico a necrose.\n",
+        "synthetic_summary": {
+            "B1": "Um homem tomou um remédio errado por um tempo. Isso deixou ele muito doente e com dificuldade para respirar. O médico fez um exame do cérebro dele e viu que algumas partes estavam machucadas dos dois lados. Ele melhorou devagar, mas ainda tremia um pouco. Depois de dois meses, o exame mostrou que o machucado no cérebro mudou, mas ele estava melhor.",
+            "B2": "**O que aconteceu com o paciente**\n\nUm homem de 48 anos, que tinha um problema sério com o álcool, usou uma grande quantidade de um remédio chamado dissulfiram, mas de um jeito diferente: ele inalava o pó pelo nariz, em vez de tomar pela boca. Ele não estava bebendo álcool ao mesmo tempo. Depois disso, ele ficou muito doente, com problemas no cérebro que causaram dificuldade para respirar.\n\n**O que os exames mostraram**\n\nOs médicos fizeram exames de imagem do cérebro e viram que uma parte chamada núcleos pálidos, que fica em ambos os lados do cérebro, estava muito afetada de forma parecida dos dois lados. Esse tipo de alteração é típico quando alguém tem intoxicação por dissulfiram.\n\n**Como foi a recuperação**\n\nA melhora do paciente foi lenta. Dois meses depois, ele ainda tinha um tremor leve quando tentava fazer movimentos precisos com as mãos. A ressonância magnética, que é um exame detalhado do cérebro, mostrou que as áreas que estavam inchadas e danificadas passaram a ter uma lesão mais grave chamada necrose, que é quando as células morrem.\n\n**O que isso significa**\n\nEsse caso mostra que usar dissulfiram de forma errada, especialmente inalando, pode causar um dano sério e rápido no cérebro. Mesmo sem beber álcool, a intoxicação pode ser grave e a recuperação demora bastante. É importante usar remédios só do jeito certo e sempre com acompanhamento médico.",
+            "B3": "**Contexto**  \nUm homem de 48 anos, com histórico de alcoolismo crônico e esquizofrenia, foi admitido no hospital apresentando sonolência, dificuldade de coordenação motora (ataxia cerebelar) e fala arrastada (disartria) que evoluíram ao longo de três dias. Ele relatou o uso recreativo recente de doses muito altas de dissulfiram administrado por via intranasal, além de medicamentos psiquiátricos, incluindo benzodiazepínicos. Não houve consumo de álcool nas últimas 48 horas.\n\n**Principais Achados Clínicos e Exames**  \nNa chegada, o paciente estava em estado de estupor e desorientação, com sinais neurológicos como pupilas contraídas e pouco reativas, tremores e marcha instável. Exames laboratoriais revelaram acidose metabólica (alteração no equilíbrio ácido-base do sangue), mas sem sinais de infecção ou intoxicação por álcool ou outros tóxicos comuns. A tomografia computadorizada do cérebro mostrou alterações leves e inespecíficas, enquanto a ressonância magnética revelou lesões simétricas extensas nos núcleos pálidos e outras estruturas profundas do cérebro, áreas típicas afetadas em intoxicações por dissulfiram.\n\nOs níveis sanguíneos de benzodiazepínicos estavam dentro ou abaixo da faixa terapêutica, sugerindo que esses medicamentos provavelmente não foram a causa principal do quadro. A acidose metabólica foi transitória e provavelmente relacionada à hidratação intravenosa inicial. O paciente desenvolveu insuficiência respiratória rapidamente, necessitando de ventilação mecânica, e apresentou pneumonia por aspiração.\n\n**Interpretação Clínica**  \nO diagnóstico final foi encefalopatia (disfunção cerebral) induzida por intoxicação por dissulfiram, uma substância usada para tratar alcoolismo, mas que em doses elevadas e por via não convencional (intranasal) pode causar danos cerebrais graves. A distribuição simétrica das lesões nos núcleos pálidos observada na ressonância magnética é característica dessa intoxicação e ajuda a diferenciá-la de outras causas, como intoxicação por monóxido de carbono, que foi descartada neste caso. A atribuição da causa ao dissulfiram foi feita por exclusão e com base em critérios clínicos, já que não foi possível medir seus níveis no sangue.\n\n**Evolução e Prognóstico**  \nApós tratamento intensivo e suporte respiratório, o paciente apresentou melhora gradual do estado neurológico. Ao final da internação, persistia um tremor leve e dificuldades motoras discretas, que melhoraram com o tempo. Dois meses após o episódio, a ressonância magnética mostrou que as áreas inicialmente afetadas evoluíram de edema cerebral (inchaço celular) para necrose (morte do tecido cerebral), indicando um dano permanente, embora limitado.\n\n**Próximos Passos e Considerações**  \nEste caso destaca os riscos graves associados ao uso inadequado e recreativo do dissulfiram, especialmente por vias não autorizadas como a intranasal. A monitorização neurológica e o suporte clínico são essenciais para a recuperação, que pode ser lenta e incompleta. Além disso, reforça a importância de investigar causas tóxicas em pacientes com encefalopatia aguda e histórico de uso de substâncias, mesmo quando exames iniciais são inconclusivos."
+        }
+    },
+    {
+        "article": "Homem de 64 anos de idade, sem antecedentes patológicos, que convivia com animais de estimação (cães). Consultaram por cefaleia holocraniana, hemianopsia homónima direita de uma semana de evolução associada a um episódio de crise convulsiva tónica clónica generalizada, sem febre. Realizou-se TAC de cérebro simples onde se evidenciou lesão a nível frontal cortico/subcortical acompanhada de edema. Posteriormente uma RMN de cérebro, no coeficienciente de difusão observou-se uma lesão heterogénea com restrição em dita sequência e correlato em ADC, com halo hipointenso periférico associado a extenso edema vasogénico que gerava efeito de massa com colapso parcial de ventrículo lateral direito e corpo caloso e desvio não significativo da linha média para a esquerda, a qual mede 67x36x26 mm. Mediante acesso transcortical realizou-se excisão completa de uma lesão encapsulada com conteúdo purulento, iniciando terapia antibiótica com meropenem/vancomicina até isolamento em cultura de A. aphrophilus completando tratamento com ceftriaxona por 21 dias. Durante a sua estadia hospitalar realizou-se, além disso, ecografia de abdome total, fundo de olho e ecocardiograma transesofágico sem evidência de outros locais de infecção. Evoluiu favoravelmente concedendo-lhe alta hospitalar.\n",
+        "gold_summary": "Apresenta-se o caso de um paciente do sexo masculino de 64 anos sem antecedentes de relevância que deu entrada no serviço de urgências com quadro de cefaleia, hemianopsias de uma semana de evolução e posteriormente crises tónico-clónicas, em quem posteriormente, em estudos de imagem e cultura de lesão cerebral, se chegou ao diagnóstico de abcesso cerebral por A. aphrophilus.\n",
+        "synthetic_summary": {
+            "B1": "Um homem de 64 anos ficou com dor de cabeça e dificuldade para ver de um lado. Depois, ele teve uma convulsão, que é quando o corpo mexe sozinho. Os médicos fizeram exames e acharam uma bolinha com pus no cérebro dele. Eles tiraram essa bolinha com uma cirurgia e deram remédios para matar o bicho que estava lá. Ele ficou melhor e foi para casa feliz.",
+            "B2": "**O que aconteceu com o paciente**\n\nUm homem de 64 anos, que não tinha doenças importantes antes, começou a sentir uma dor de cabeça forte e constante. Ele também perdeu parte da visão do lado direito e teve uma convulsão, que é quando o corpo se mexe de forma descontrolada. Esses sintomas duraram cerca de uma semana.\n\n**O que os médicos encontraram**\n\nOs médicos fizeram exames do cérebro usando máquinas especiais chamadas tomografia (TAC) e ressonância magnética (RMN). Eles viram uma área estranha no cérebro, perto da parte frontal, que estava inchada e parecia uma bolha com pus dentro. Isso indicava um abscesso cerebral, que é uma infecção com acúmulo de pus dentro do cérebro.\n\n**Como trataram**\n\nPara tratar, os médicos fizeram uma cirurgia para tirar todo o pus e a parte infectada. Depois, deram remédios fortes para matar as bactérias, chamados antibióticos. A bactéria que causou a infecção se chamou *Aggregatibacter aphrophilus*, que foi identificada em um exame de cultura, que é quando se tenta crescer a bactéria para saber qual é.\n\n**O que isso significa**\n\nEsse caso mostra que uma infecção no cérebro pode causar sintomas sérios como dor de cabeça, perda de visão e convulsões. É importante fazer exames rápidos para encontrar o problema e tratar com cirurgia e antibióticos para evitar complicações. O paciente melhorou bem e recebeu alta do hospital depois do tratamento.",
+            "B3": "**Contexto**  \nUm homem de 64 anos, sem doenças prévias conhecidas, procurou atendimento médico após apresentar dor de cabeça intensa que afetava toda a cabeça (cefaleia holocraniana), perda parcial da visão no lado direito (hemianopsia homônima direita) por uma semana e, em seguida, uma crise convulsiva generalizada do tipo tônico-clônica (movimentos musculares involuntários e perda de consciência). Ele não apresentou febre durante o quadro. O paciente convivia com cães, o que pode ser relevante para a origem da infecção.\n\n**Principais Achados**  \nA tomografia computadorizada (TAC) do cérebro revelou uma lesão localizada na região frontal, envolvendo tanto o córtex quanto a substância branca abaixo dele, acompanhada de edema (inchaço). A ressonância magnética (RMN) mostrou que essa lesão era heterogênea, apresentando restrição à difusão (sinal que indica áreas com células ou material inflamado), com um halo escuro ao redor e edema extenso que causava efeito de massa, comprimindo parcialmente o ventrículo lateral direito e o corpo caloso, estruturas importantes do cérebro. A lesão media aproximadamente 67x36x26 mm.  \n\nFoi realizada cirurgia para remover completamente a lesão, que estava encapsulada e continha pus, confirmando tratar-se de um abscesso cerebral (acúmulo de pus devido a infecção). O tratamento inicial com antibióticos de amplo espectro (meropenem e vancomicina) foi ajustado após o isolamento da bactéria Aggregatibacter aphrophilus na cultura do material purulento, passando a usar ceftriaxona por 21 dias.\n\nDurante a internação, exames adicionais, como ultrassonografia abdominal, exame do fundo do olho e ecocardiograma transesofágico (ultrassom do coração via esôfago), não mostraram outras fontes de infecção. O paciente evoluiu bem e recebeu alta hospitalar.\n\n**Interpretação Clínica**  \nEste caso ilustra um abscesso cerebral causado por Aggregatibacter aphrophilus, uma bactéria que faz parte da flora oral e pode causar infecções invasivas, especialmente em pessoas que convivem com animais ou apresentam fatores predisponentes. A apresentação clínica incluiu sintomas neurológicos progressivos e crise convulsiva, que, junto com os exames de imagem, orientaram para o diagnóstico. A remoção cirúrgica da lesão e o tratamento antibiótico direcionado foram fundamentais para a recuperação do paciente.\n\n**Próximos Passos**  \nO acompanhamento clínico e neurológico após a alta é essencial para monitorar possíveis sequelas e garantir a resolução completa da infecção. Além disso, é importante investigar e prevenir possíveis fontes de infecção futuras, especialmente em pacientes com contato frequente com animais ou outras condições de risco."
+        }
+    },
+    {
+        "article": "A paciente tinha 34 anos de idade e estava com quatro semanas de doença. Dois meses antes, ela havia feito uma cesariana na 37ª semana de gestação e apresentou sangramento persistente da incisão cirúrgica. Entre os antecedentes pessoais, ela negou ter apresentado histórico de sangramentos durante a infância ou adolescência. Três anos antes, ela havia dado à luz seu primeiro filho (também por cesariana), que faleceu devido a uma cromosomopatia (referida pela paciente). Além disso, ela afirmou ser alérgica ao tramadol.\n\nO quadro clínico iniciou com dor lombar por litíase renal bilateral. Posteriormente, conseguiu expulsar um cálculo e, depois disso, apresentou hematúria por três dias, motivo pelo qual recebeu ácido tranexâmico c/12 h. Três semanas depois, apresentou dor na região inferior da coxa esquerda que foi aumentando em intensidade, com endurecimento da zona. Por persistência dos sintomas, foi-lhe indicado diclofenaco por via intramuscular, que lhe provocou equimose e sangramento na zona do glúteo e que persiste apesar da compressão com gaze.\n\nA paciente realizou uma ultrassonografia Doppler que revelou trombose venosa profunda do membro inferior esquerdo e foi ao hospital da sua cidade com esses resultados. Foi-lhe administrado anticoagulação com enoxaparina 30 mg/24 h subcutânea, além de morfina para o tratamento da dor e foi hospitalizada. No dia seguinte, apresentou epigastralgia, visão turva, frequência cardíaca de 117 lat/min, pressão arterial de 113/85 mmHg e saturação de 93%. Decidiu-se suspender a enoxaparina. O hemograma revelou uma hemoglobina de 6,4 g/dl, que representava uma diferença de 4 g/dl em relação ao resultado um dia antes da sua admissão, que foi de 10,4 g/dl. Devido ao anterior, foram-lhe transfundidos dois pacotes globulares. Perante a suspeita de vasculite, foi-lhe indicado metilprednisolona e foi encaminhada para o nosso hospital para ampliar o estudo.\n\nNa exploração física ao ingresso, encontrou-se palidez severa, extensa equimosis na coxa e face lateral do joelho esquerdo; além de um hematoma na coxa direita. O hemograma revelou uma anemia moderada (Hb = 9,8 g/dl), normocítica e normocrômica. O exame bioquímico evidenciou valores de glicose de 160 mg/dl. As enzimas hepáticas AST e ALT encontravam-se em valores de 52 U/L e 86 U/L, respectivamente. O perfil de coagulação mostrou prolongamento do tempo de tromboplastina parcial ativada (TTPa) de 91,2 s. O resto de componentes do hemograma, bioquímico, eletrólitos, perfil hepático e perfil de coagulação encontravam-se em valores normais. A ecografia de partes moles da região glútea direita revelou uma coleção a nível do tecido celular subcutâneo (TCSC) e edema até ao terço superior da coxa. A ecografia Doppler em membro inferior esquerdo mostrou uma adequada flujometria sem sinais de trombose em veia femoral comum, superficial e profunda.\n\nFoi iniciado tratamento sintomático e solicitados hemocultura e urocultura, que foram negativos. Os valores de anticorpos antinucleares (ANA), complemento C3 e C4 e ferritina estavam dentro do intervalo de referência.\n\nDiante da suspeita de hemofilia adquirida, foram solicitados estudos para confirmação, onde foi encontrada uma correção parcial de TTPa no teste de mistura. O fator VIII foi medido, encontrando-se sua atividade diminuída (<1,0 U/dl) e foi demonstrada a presença de um inibidor do fator VIII: 8,64 unidades Bethesda/ml. O anterior permitiu confirmar o diagnóstico de HAA, que foi relacionado com o pós-parto pelo início dos sintomas.\n\nIniciou-se terapia com prednisona 50 mg VO no café da manhã e 10 mg VO no almoço, ciclofosfamida 50 mg 2 comprimidos VO c/24 h e complexo coagulante anti-inibidor hemofílico (FEIBA). Cinco dias depois, suspendeu-se o emprego deste último medicamento devido a dor torácica opressiva, dispnéia e náuseas (possível reação adversa medicamentosa), pelo qual se mudou para fator VII recombinante ativado (NovoSeven).\n\nA evolução clínica da paciente foi favorável, com diminuição da equimose e sem a presença de outros sintomas, por isso foi decidida a alta hospitalar.\n",
+        "gold_summary": "Apresenta-se o caso de uma paciente de 34 anos com dor lombar, hematúria e hematoma na região glútea direita, sem antecedentes prévios de sangramento. Por extensão das manifestações hemorrágicas, foi transferida para o serviço de emergência. Os exames auxiliares de perfil de coagulação, teste de misturas e medição dos títulos de inibidores do fator VIII permitiram confirmar o diagnóstico.\n",
+        "synthetic_summary": {
+            "B1": "Uma mulher de 34 anos estava com dor nas costas e machucados com sangue. Ela não tinha machucados assim antes. O médico fez exames para ver o sangue dela. Descobriram que o sangue dela estava diferente e isso causava os machucados. Por isso, ela foi para o hospital para cuidar melhor.",
+            "B2": "**O que aconteceu com a paciente**\n\nUma mulher de 34 anos começou a sentir dor nas costas e notou sangue na urina. Depois, apareceu um grande machucado roxo (hematoma) na parte de trás da coxa direita. Ela nunca tinha tido problemas de sangramento antes. Como os machucados e sangramentos estavam piorando, ela foi levada para o hospital.\n\n**Como descobriram o problema**\n\nNo hospital, os médicos fizeram vários exames para entender por que ela estava sangrando tanto. Eles testaram o sangue dela para ver como estava a coagulação, que é o processo que ajuda a parar o sangramento. Também fizeram um teste chamado “teste de mistura”, que ajuda a descobrir se o corpo está produzindo algo que impede a coagulação normal. Por fim, mediram a quantidade de um inibidor do fator VIII, que é uma proteína importante para a coagulação do sangue.\n\n**O que isso significa**\n\nCom esses exames, os médicos confirmaram que a paciente tinha uma doença chamada hemofilia adquirida. Isso acontece quando o corpo começa a produzir uma substância que atrapalha o fator VIII, dificultando a coagulação e causando sangramentos. No caso dela, isso aconteceu depois do parto, o que é uma causa conhecida dessa doença.\n\n**Tratamento e resultado**\n\nEla recebeu remédios para controlar o sangramento e o sistema imunológico que estava atacando o fator VIII. Depois de alguns dias, os machucados começaram a melhorar e ela não teve mais sintomas, então pôde deixar o hospital.",
+            "B3": "**Contexto**  \nTrata-se de uma mulher de 34 anos que, após uma cesariana realizada dois meses antes, apresentou sangramento persistente na cicatriz cirúrgica. Inicialmente, ela teve dor lombar relacionada a pedras nos rins e episódios de sangue na urina (hematúria). Posteriormente, desenvolveu dor e endurecimento na coxa esquerda, seguido por hematomas extensos após o uso de anti-inflamatórios. Uma ultrassonografia Doppler revelou trombose venosa profunda na perna esquerda, levando à hospitalização e início de anticoagulação. No entanto, a paciente evoluiu com anemia grave, aumento das equimoses (manchas roxas) e sangramento persistente, o que motivou a suspensão do anticoagulante e a investigação para causas de sangramento anormal.\n\n**Principais Achados**  \nNo exame físico, foram observadas palidez intensa e hematomas extensos nas coxas e joelho. Os exames laboratoriais mostraram anemia moderada, glicose elevada, elevação discreta das enzimas hepáticas e prolongamento significativo do tempo de tromboplastina parcial ativada (TTPa), que indica alteração na coagulação do sangue. A ultrassonografia da região glútea revelou acúmulo de líquido e edema, mas a trombose previamente detectada não foi confirmada no membro inferior esquerdo. Testes para infecções e autoimunidade foram negativos.\n\nPara esclarecer a causa do sangramento, foi realizado o teste de mistura, que mostrou correção parcial do TTPa, sugerindo a presença de um inibidor. A atividade do fator VIII (uma proteína essencial para a coagulação) estava muito baixa, e foi detectado um inibidor específico contra esse fator, confirmando o diagnóstico de hemofilia adquirida, uma condição rara em que o organismo produz anticorpos que bloqueiam o fator VIII. Neste caso, a doença foi associada ao período pós-parto.\n\n**Interpretação Clínica**  \nA hemofilia adquirida é uma doença hemorrágica grave que pode se manifestar com sangramentos espontâneos ou após procedimentos, mesmo em pessoas sem histórico prévio de distúrbios de coagulação. O diagnóstico baseia-se na presença de anemia, sangramentos extensos, prolongamento do TTPa que não corrige completamente com o teste de mistura, redução da atividade do fator VIII e detecção de inibidores contra ele. O quadro da paciente, iniciado após o parto, é característico dessa condição.\n\n**Próximos Passos e Tratamento**  \nO tratamento incluiu o uso de corticosteroides (prednisona) e ciclofosfamida para suprimir a produção dos anticorpos contra o fator VIII, além de medicamentos que auxiliam na coagulação, como o complexo coagulante anti-inibidor hemofílico (FEIBA). Devido a efeitos colaterais, houve troca para o fator VII recombinante ativado (NovoSeven). A paciente apresentou melhora clínica significativa, com redução dos hematomas e estabilização do quadro, permitindo a alta hospitalar.\n\nEste caso destaca a importância de considerar a hemofilia adquirida em pacientes com sangramentos inexplicáveis no pós-parto, para diagnóstico e tratamento precoces, evitando complicações graves."
+        }
+    },
+    {
+        "article": "Um homem de 63 anos deu entrada em nosso ambulatório com histórico de hematúria frequente. O exame físico não demonstrou problemas e seu exame de sangue era normal, com creatinina sérica de 1,2 mg/dL. Uma tomografia computadorizada contrastada (TC) do abdômen revelou um extenso crescimento vesical infiltrativo, mais na parede lateral direita e na cúpula com hidroureteronefrose esquerda moderada e rim direito com mau funcionamento devido a um cálculo obstrutivo da junção uretero-pélvica. Foi programada uma cistoscopia diagnóstica com biópsia transuretral. No entanto, ele compareceu à emergência antes da data prevista de admissão com instabilidade hemodinâmica, distensão abdominal e dificuldade de respiração, para os quais foi necessário suporte ventilatório e inotrópico. Seu painel bioquímico mostrou creatinina alta (20 mg/dL), hipercalemia (9 mEq/L) e hiponatremia (128 mEq/L), e sua gasometria mostrou acidose metabólica grave (pH 7,1). Ao questionar posteriormente os cuidadores do paciente, foi obtido um histórico de oligúria com distensão abdominal gradualmente crescente nos últimos 2 dias, para o qual ele havia sido submetido a uma punção de fluido “ascítico” em um centro externo. Foram iniciadas medidas anti-hipercalêmicas. Uma ultrassonografia à beira do leito mostrou hidroureteronefrose esquerda com hidroureteronefrose direita grave e fluido livre no abdômen. Em vista da instabilidade hemodinâmica e indisponibilidade de hemodiálise em nossas instalações, decidiu-se por uma nefrostomia de emergência à beira do leito, inserida no rim esquerdo em funcionamento solitário. Sob orientação de ultrassom, foi feita a inserção de nefrostomia percutânea (NPC) à beira do leito e o quadro geral do paciente melhorou. Houve uma diurese inicial com queda no nível de creatinina a um nadir de 2 mg/dL. Devido aos níveis persistentemente elevados de creatinina, a TC foi repetida após 4 dias de colocação da nefrostomia e, para nossa surpresa, notamos que a ponta do cateter pigtail encontrava-se no espaço perinefrício esquerdo atuando como um dreno percutâneo com resolução completa de fluido livre no abdômen. A cronologia dos eventos de uma creatinina sérica inicial extremamente elevada que havia diminuído drasticamente após a drenagem do fluido extravasado, ajustou-se a um quadro clínico de pseudo insuficiência renal devido à absorção de urina extravasada. Levantamos a hipótese de que a origem da urina extravasada se devia muito provavelmente a uma ruptura do fórnice renal devido a uma obstrução de alta pressão do lado esquerdo. Tendo em vista a creatinina sérica ainda elevada e a saída gradualmente decrescente do cateter pigtail, foi colocado um NPC dentro do sistema de coleta sob orientação fluoroscópica, seguido da normalização de sua creatinina. Um nefrograma por TC com cistograma foi realizado na sequência e mostrou uma obstrução ureteral distal esquerda e uma bexiga pequena e intacta, excluindo uma perfuração da bexiga. Uma biópsia por citoscopia do crescimento da bexiga confirmou-o como um carcinoma escamoso invasivo muscular. Explicamos o diagnóstico e o prognóstico ao paciente e procedemos a uma laparotomia exploratória 2 semanas após a biópsia. No intra-operatório observou-se uma densa reação desmoplástica ao redor da bexiga, que foi encolhida e colada nas paredes laterais pélvicas e no osso púbico. Devido à natureza inoperável da doença, abandonou-se o plano de cistectomia radical e foi feito um desvio paliativo do conduto ileal com nefrectomia lateral direita. O paciente evoluiu bem no pós-operatório e recebeu alta após 5 dias. No entanto, desenvolveu múltiplas metástases torácicas nos meses seguintes e seu quadro geral deteriorou-se de forma constante, resultando em sua morte 3 meses após a cirurgia devido à caquexia.",
+        "gold_summary": "Relatamos aqui um caso de carcinoma de bexiga que apresentou características semelhantes à insuficiência renal aguda, e mais tarde se revelou uma pseudo insuficiência renal devido a extravasamento urinário intraperitoneal de uma ruptura de fórnice renal. O paciente foi tratado com emergência com um dreno percutâneo seguido por uma nefrostomia percutânea, que levou à normalização da creatinina. A cistoscopia revelou o crescimento da bexiga em uma bexiga intacta, de pequena capacidade e que a biópsia confirmou como um carcinoma escamoso invasivo muscular. Devido à natureza avançada de sua malignidade, ele foi submetido a um desvio de conduto ileal paliativo, mas posteriormente desenvolveu metástase torácica e acabou sucumbindo à doença.",
+        "synthetic_summary": {
+            "B1": "Um homem estava com um problema na bexiga. Ele tinha sangue na urina e estava muito doente.\n\nOs médicos descobriram que ele tinha um caroço na bexiga. Esse caroço estava machucando os ossos e os rins.\n\nEle ficou muito mal e precisou de ajuda para fazer xixi. Colocaram um canudinho no rim para ajudar.\n\nDepois, fizeram um exame e viram que o caroço era um tipo de câncer. O câncer estava muito grande e difícil de tirar.\n\nOs médicos fizeram uma cirurgia para ajudar ele a ficar melhor. Mas o câncer estava muito forte.\n\nInfelizmente, o homem ficou mais doente e não conseguiu melhorar. Ele morreu depois de algum tempo.",
+            "B2": "**O que aconteceu com o paciente**\n\nUm homem de 63 anos teve sangue na urina várias vezes. Exames mostraram um crescimento grande na bexiga, que é o órgão que armazena a urina. Ele também tinha problemas nos rins, como um cálculo (pedra) que bloqueava a passagem da urina. Antes de fazer uma biópsia, ele ficou muito mal, com o corpo inchado e dificuldade para respirar. Seus rins pararam de funcionar direito, e ele tinha muita urina acumulada no abdômen, o que é perigoso.\n\n**Como os médicos ajudaram**\n\nOs médicos colocaram um dreno, que é um tubo para tirar o líquido acumulado, e depois fizeram uma nefrostomia, que é um procedimento para drenar a urina diretamente do rim. Isso ajudou a melhorar o funcionamento dos rins e a diminuir os problemas no corpo dele.\n\n**O que descobriram sobre o tumor**\n\nA biópsia, que é quando se tira um pedacinho do tecido para analisar, mostrou que o crescimento na bexiga era um tipo de câncer chamado carcinoma escamoso invasivo muscular. Esse tipo de câncer é agressivo e estava em um estágio avançado.\n\n**O tratamento e o desfecho**\n\nComo o câncer estava muito avançado e não podia ser removido completamente, os médicos fizeram uma cirurgia paliativa. Isso significa que o objetivo foi aliviar os sintomas, não curar a doença. Infelizmente, o câncer se espalhou para os pulmões e o paciente piorou, falecendo três meses depois da cirurgia.\n\n**Resumo final**\n\nEsse caso mostra como um câncer na bexiga pode causar problemas graves nos rins e no corpo, parecendo uma falha renal. O tratamento emergencial para drenar a urina acumulada foi essencial para melhorar o paciente temporariamente. Porém, o câncer avançado teve um desfecho triste, mostrando a importância de um diagnóstico e tratamento precoces.",
+            "B3": "**Contexto**  \nEste relato descreve o caso de um homem de 63 anos diagnosticado com câncer de bexiga que inicialmente apresentou sintomas e exames sugestivos de insuficiência renal aguda, mas cujo quadro clínico revelou-se mais complexo.\n\n**Principais Achados**  \nO paciente chegou ao hospital com hematúria (sangue na urina) frequente, mas sem alterações significativas no exame físico ou nos exames de sangue iniciais. Uma tomografia computadorizada mostrou um tumor extenso na bexiga, principalmente na parede lateral direita e na cúpula, além de obstrução e dilatação dos ureteres (hidroureteronefrose) e mau funcionamento do rim direito devido a um cálculo (pedra) na junção entre o ureter e a pelve renal. Antes da realização da biópsia, ele apresentou quadro grave de instabilidade hemodinâmica, distensão abdominal e insuficiência respiratória, com exames laboratoriais indicando insuficiência renal severa (creatinina muito elevada), desequilíbrios eletrolíticos e acidose metabólica.\n\nDurante a internação, foi detectado fluido livre no abdômen, que inicialmente foi interpretado como ascite (acúmulo de líquido na cavidade abdominal). O paciente foi submetido a uma drenagem de emergência por meio de nefrostomia percutânea (inserção de um cateter para drenar o rim) no rim esquerdo, que estava funcionando. Após o procedimento, houve melhora clínica e redução significativa da creatinina. Exames subsequentes mostraram que o cateter estava drenando urina extravasada no espaço ao redor do rim, indicando que a insuficiência renal aparente era, na verdade, uma “pseudo insuficiência renal” causada pela absorção de urina vazada para o abdômen, provavelmente devido à ruptura do fórnice renal (uma parte do rim) causada pela obstrução urinária.\n\nA investigação continuou com exames de imagem que confirmaram obstrução no ureter esquerdo e uma bexiga pequena, porém sem perfuração. A biópsia da lesão na bexiga revelou um carcinoma escamoso invasivo muscular, um tipo agressivo de câncer. Durante a cirurgia exploratória, constatou-se que o tumor estava muito avançado e aderido a estruturas pélvicas, tornando a remoção completa inviável. Assim, foi realizado um desvio urinário paliativo (conduto ileal) e remoção do rim direito comprometido.\n\n**Interpretação Clínica**  \nEste caso ilustra uma situação rara em que um câncer de bexiga avançado causou obstrução urinária grave, levando à ruptura do sistema coletor renal e extravasamento de urina para o abdômen. Essa condição simulou uma insuficiência renal aguda verdadeira, mas na realidade tratava-se de uma pseudo insuficiência causada pela absorção da urina extravasada. O manejo emergencial com drenagem percutânea foi fundamental para a estabilização do paciente e a normalização da função renal. O diagnóstico definitivo de carcinoma escamoso invasivo muscular indicou um prognóstico reservado devido à natureza agressiva e avançada da doença.\n\n**Próximos Passos e Desfecho**  \nApós o procedimento paliativo, o paciente teve alta hospitalar, mas evoluiu com disseminação metastática para os pulmões e deterioração progressiva do estado geral. Ele faleceu três meses após a cirurgia devido à caquexia (perda severa de peso e fraqueza associada ao câncer avançado).\n\nEste caso destaca a importância de considerar causas não convencionais de insuficiência renal aguda em pacientes com obstrução urinária e tumores avançados, bem como a relevância do diagnóstico precoce e manejo multidisciplinar em casos complexos de câncer de bexiga."
+        }
+    },
+    {
+        "article": "Descreve-se o caso de uma mulher de 43 anos de idade, com antecedente de ser mãe com câncer de mama, diagnosticado antes da menopausa. A paciente começou com sintomas gastrointestinais inespecíficos, como plenitude pós-prandial, aumento do perímetro abdominal, dor abdominal intermitente com predomínio no mesogástrio de 12 meses de evolução. Posteriormente, agregou-se dispneia de médios esforços. A paciente foi ao médico de primeiro contato, que estabeleceu o protocolo de estudo e lhe solicitou ultrassom de abdômen e pelvis, o qual evidenciou um tumor que abrangia a totalidade da cavidade abdominal, e complementou o estudo com tomografia computadorizada contrastada de tórax, abdômen e pelvis, a qual mostrou um tumor de 27,5 x 12,7 x 28,2 cm, heterogêneo, de predomínio líquido, com presença de septos.\n\nOs marcadores tumorais apresentaram Ca 125 em 84.16, ACE 10.07, AFP 1.83, B-HGC 0.1. A biometria hemática mostrou provas de função hepática e tempos de coagulação dentro de parâmetros normais. A paciente foi enviada ao Serviço de Tumores Ginecológicos do Hospital de Oncologia do Centro Médico Nacional Siglo XXI, onde propusemos a laparotomia com estudo transoperatório. Procedeu-se a intervenção cirúrgica em que se levou a cabo salpingooforectomia esquerda, a qual foi enviada para estudo transoperatório.\n\nA cirurgia encontrou mucinosis, com um índice de carcinomatose de 16 pontos, com implantes de mucina em toda a extensão do peritônio parietal, cápsula de Gleason e baço, além de um tumor de ovário esquerdo rompido.\n\nO ovário esquerdo de 3450 g foi recebido em estudo transoperatório, medindo 28 x 27 x 14 cm, com cápsula rompida, superfície interna multiloculada com conteúdo mucinoso e foi identificado uma área cística de 7 x 6,5 cm, com conteúdo sebáceo e pelos. Aos cortes histológicos, observou-se tecido de ectoderma composto por epitélio escamoso e folículos pilosos, bem como tecido de endoderma composto por epitélio de tipo intestinal, o qual em diversos cortes apresentou atipia marcada com disposição arquitetural complexa até chegar a encontrar células em anel de selo, correspondente a adenocarcinoma. Não se identificaram elementos imaturos na amostragem do tumor.\n\nA cirurgia de estadiamento e citorredução do ovário foi realizada com histerectomia total + salpingo-ooforectomia bilateral + peritonectomia + apendicectomia. Devido a achados de atividade tumoral, foi realizada uma colecistectomia e esplenectomia e foi adicionada quimioterapia intraoperatória com 45 mg de cisplatina em 1000 ml de solução salina fisiológica a 0,9% a 40°C, e foi alcançada uma citorredução ótima, que foi classificada como estágio IIIC. Além disso, foram observados implantes do tumor (adenocarcinoma) no omento, na cápsula hepática e na cápsula esplênica no relatório histopatológico.\n\nA paciente foi encaminhada para o Serviço de Oncologia Médica e foi considerada candidata a receber adjuvância com carboplatina e paclitaxel em seis ciclos, os quais finalizaram sem eventualidades. No momento, tem bons resultados oncológicos, com período livre de doença de sete meses; encontra-se em acompanhamento no Serviço de Tumores Ginecológicos.\n",
+        "gold_summary": "Mulher de 43 anos de idade, com diagnóstico de teratoma maduro maligno com células em anel de selo. Foi realizada cirurgia de citorredução primária ótima; histerectomia total, salpingooforectomia bilateral, peritonectomia, apendicectomia, colecistectomia e esplenectomia, além de quimioterapia hipertérmica intraoperatória (HIPEC).\n",
+        "synthetic_summary": {
+            "B1": "Uma mulher de 43 anos tinha um caroço grande na barriga. Os médicos fizeram uma cirurgia para tirar o caroço e outras partes do corpo para ajudar ela a ficar melhor. Também deram um remédio especial para matar as partes ruins do caroço. Agora, ela está sendo cuidada para melhorar cada dia mais.",
+            "B2": "**O que aconteceu com a paciente**\n\nUma mulher de 43 anos começou a sentir dores e desconforto na barriga, além de dificuldade para respirar. Depois de exames, os médicos descobriram que ela tinha um tumor muito grande dentro da barriga, que estava ligado ao ovário esquerdo.\n\n**O que é o tumor**\n\nO tumor foi identificado como um teratoma maduro maligno. Isso significa que ele era formado por vários tipos de tecidos diferentes, como pele, pelos e até tecido parecido com o intestino. Dentro desse tumor, os médicos encontraram células chamadas “em anel de selo”, que são um tipo de célula cancerígena.\n\n**Como foi o tratamento**\n\nPara tratar o tumor, a paciente passou por uma cirurgia grande. Os médicos retiraram o útero, os dois ovários, parte do revestimento da barriga (peritônio), o apêndice, a vesícula biliar e o baço. Também fizeram uma limpeza para tirar o máximo possível do tumor. Durante a cirurgia, aplicaram um tipo especial de quimioterapia quente diretamente na barriga, chamada quimioterapia hipertérmica intraoperatória (HIPEC). Essa técnica ajuda a matar as células cancerígenas que podem ter ficado.\n\n**O que isso significa**\n\nDepois da cirurgia e da quimioterapia, a paciente continuou o tratamento com mais quimioterapia por seis ciclos. Atualmente, ela está bem e sem sinais de câncer há sete meses. Ela continua sendo acompanhada pelos médicos para garantir que o tumor não volte.\n\nEsse caso mostra como é importante um diagnóstico cuidadoso e um tratamento completo para tumores complexos no ovário.",
+            "B3": "**Contexto**  \nTrata-se de uma mulher de 43 anos, com histórico familiar de câncer de mama, que apresentou sintomas gastrointestinais inespecíficos por cerca de um ano, incluindo sensação de plenitude após as refeições, aumento do volume abdominal e dor abdominal intermitente. Posteriormente, desenvolveu falta de ar ao realizar esforços moderados. Exames de imagem revelaram um grande tumor abdominal de aproximadamente 27 cm, com características heterogêneas e conteúdo predominantemente líquido, contendo septos internos.\n\n**Principais Achados**  \nOs marcadores tumorais mostraram elevação do CA 125, enquanto outros marcadores estavam dentro dos limites normais. Durante a cirurgia, foi identificado um tumor no ovário esquerdo, com ruptura da cápsula, e presença de mucinose (acúmulo de muco) espalhada pelo peritônio (membrana que reveste a cavidade abdominal) e órgãos adjacentes, como baço e cápsula hepática. O exame microscópico do tumor revelou um teratoma maduro (um tipo de tumor que contém diferentes tipos de tecidos) com áreas de adenocarcinoma, incluindo células em anel de selo (um tipo específico de célula cancerígena associada a tumores agressivos). Não foram encontradas células imaturas, o que sugere que o tumor não apresentava características de malignidade infantil.\n\n**Interpretação Clínica**  \nO diagnóstico final foi de teratoma maduro com transformação maligna, estágio IIIC, indicando disseminação significativa dentro da cavidade abdominal. A paciente foi submetida a uma cirurgia extensa para remoção do tumor e dos órgãos afetados, incluindo retirada do útero, ovários, peritônio, apêndice, vesícula biliar e baço, buscando eliminar o máximo possível da doença (citorredução ótima). Durante o procedimento, foi aplicada quimioterapia hipertérmica intraoperatória (HIPEC), que consiste na administração de quimioterápicos aquecidos diretamente na cavidade abdominal para aumentar a eficácia contra as células tumorais remanescentes.\n\n**Próximos Passos**  \nApós a cirurgia, a paciente recebeu tratamento complementar com seis ciclos de quimioterapia sistêmica à base de carboplatina e paclitaxel, que foram bem tolerados e concluídos sem complicações. Atualmente, ela encontra-se em acompanhamento regular, apresentando um período livre de doença de sete meses, o que indica uma resposta favorável ao tratamento até o momento. O seguimento contínuo é fundamental para monitorar possíveis recidivas e garantir a melhor qualidade de vida possível."
+        }
+    },
+    {
+        "article": "Um paciente do sexo masculino de 70 anos de idade, com histórico médico significativo para hepatite C, tratado com terapia de interferon três anos antes, e aumento da próstata. Apesar dos resultados virológicos negativos persistentes no acompanhamento, o paciente foi encaminhado ao nosso departamento devido a suspeita de carcinoma hepatocelular (HCC). Notavelmente, o estilo de vida do paciente inclui o consumo diário de 300-500 ml de uísque sem histórico de tabagismo. Os exames de sangue foram negativos para antígeno HB e positivos para anticorpos HCV. A função hepática foi grau A com uma classificação Child-Pugh de 5 pontos, e o dano hepático também foi grau A. A pontuação ALBI foi -2.43, grau ALBI 2a, e ICG R15 19.1%. Os marcadores tumorais foram normais com CEA 2.5 ng/ml, mas AFP alta 1984 ng/ml e CA19-9 3135 U/ml.\n\nTomografia computadorizada (TC) com realce de contraste: Observou-se uma massa fundida multinodular com um comprimento máximo de 91 mm que abrange o segmento posterior e o lobo caudado. O CHC foi detetado por coloração escura na fase inicial e por lavagem na fase de equilíbrio. A fronteira do ramo primário da veia porta direita foi obscurecida. Observou-se um hemangioma em S5 do fígado e um pequeno cisto em S6 do fígado.\n\nEstratégia de tratamento inicial: O diagnóstico de HCC foi cT3N0M0, cStage III. Não havia limite para o primeiro ramo da veia porta, e a ressecção do lobo caudado direito do fígado foi considerada uma ressecção radical. No entanto, o limite de ressecção foi de 44% com base em um ICG R15 residual do fígado de 40% [4], e a ressecção foi considerada impossível devido à fraca função hepática residual.\n\nTerapia alvo: O tratamento inicial consistiu numa terapia alvo com um agente molecular alvo (lenvatinib, 8 mg) e embolização arterial transcateter (TAE). Uma tomografia computadorizada realizada 4 semanas após o início do tratamento mostrou que o tumor tinha aumentado aproximadamente 120% para um comprimento máximo de 110 mm. Mudámos para uma combinação de atezolizumab (1200 mg) e bevacizumab (1000 mg) terapia alvo, que tem sido reportada como sendo útil em casos negativos para lenvatinib. Não ocorreram eventos adversos com ambas as terapias alvo. Uma tomografia computadorizada realizada após quatro cursos de atezolizumab mais bevacizumab mostrou que o tumor tinha encolhido para um diâmetro máximo de 60 mm, o efeito de contraste tinha desaparecido, e a massa tinha uma absorção geralmente baixa.\n\nOs marcadores tumorais foram normalizados para 3,4 ng/ml AFP e 18 U/ml CA19-9.\n\nDescobertas cirúrgicas: lobectomia pós-hepática. A perda de sangue foi de 293 ml. 6 h 23 min.\n\nDescobertas histopatológicas: A grosso modo, o tumor era branco-amarelado com outras fusões nodais. Histologicamente, a maioria dos tumores era necrótica, e não havia evidência de HCC ativo residual. A formação de granuloma epitelióide foi observada na área circundante, que foi considerada uma mudança pós-tratamento.\n\nCurso pós-operatório: O paciente não apresentou sinais de falência hepática pós-operatória; no entanto, a tomografia computadorizada realizada no dia pós-operatório 7 revelou a formação de um abscesso no tronco. A drenagem percutânea aliviou rapidamente a inflamação, e o paciente recebeu alta do hospital no dia pós-operatório 22 sem remoção do dreno. O dreno foi removido no dia pós-operatório 38. O paciente está vivo 16 meses após a operação sem recorrência. Não existe tratamento recomendado após a ressecção, e nenhum tratamento adicional foi fornecido.\n",
+        "gold_summary": "O paciente, um homem de 70 anos, desenvolveu um HCC de 11,5 cm (T3N0M0 Estágio III) na zona hepática posterior após ser virologicamente negativo para hepatite C. O tumor estava perto do ramo da veia porta direita, tornando o lobo hepático não ressecável devido à má função hepática. Após o aumento do tumor, ele foi tratado com atezolizumab e bevacizumab. Após 5 cursos, o tumor encolheu significativamente, permitindo a ressecção completa com remoção do segmento posterior. A cirurgia revelou tumores principalmente necróticos sem células cancerosas ativas remanescentes.\n",
+        "synthetic_summary": {
+            "B1": "Um senhor de 70 anos tinha um caroço grande no fígado. Ele já não tinha mais o vírus da hepatite C. O caroço estava perto de um vaso importante do fígado. O fígado dele não estava forte para tirar o caroço logo. O caroço cresceu mais um pouco. Então, ele tomou remédios especiais para diminuir o caroço. Depois de um tempo, o caroço ficou bem menor. Aí, os médicos fizeram uma cirurgia para tirar o caroço. Na cirurgia, viram que o caroço estava quase todo morto e não tinha mais células ruins. O senhor está bem depois da cirurgia.",
+            "B2": "**O que aconteceu com o paciente**\n\nUm homem de 70 anos, que já teve hepatite C, desenvolveu um tipo de câncer no fígado chamado carcinoma hepatocelular (HCC). O tumor era grande, com cerca de 11,5 cm, e estava localizado numa parte do fígado perto de um vaso importante chamado veia porta direita. Por causa disso, e porque o fígado dele não estava funcionando muito bem, os médicos não puderam fazer a cirurgia para tirar o tumor logo no começo.\n\n**Tratamento inicial e mudança na estratégia**\n\nO tumor cresceu ainda mais, então os médicos começaram a tratar o paciente com dois remédios chamados atezolizumab e bevacizumab. Esses medicamentos ajudam o sistema imunológico a combater o câncer e também bloqueiam o crescimento dos vasos que alimentam o tumor. Depois de cinco ciclos de tratamento, o tumor diminuiu bastante.\n\n**Cirurgia e resultados**\n\nCom o tumor menor, os médicos conseguiram fazer a cirurgia para remover a parte do fígado afetada. Durante a operação, eles viram que a maior parte do tumor estava morta (necrótica), e não havia sinais de células cancerosas vivas. Isso indica que o tratamento foi muito eficaz.\n\n**Recuperação**\n\nApós a cirurgia, o paciente teve uma infecção no fígado que foi tratada com drenagem e remédios, e ele se recuperou bem. Até 16 meses depois da operação, ele está vivo e sem sinais de que o câncer voltou.\n\n**Por que isso é importante**\n\nEsse caso mostra que, mesmo quando o câncer no fígado é grande e difícil de operar, tratamentos modernos com medicamentos que ajudam o corpo a combater o tumor podem reduzir o tamanho da doença. Isso pode permitir que os médicos façam a cirurgia com sucesso e melhorem a chance de cura.",
+            "B3": "**Contexto**  \nUm homem de 70 anos, com histórico de hepatite C tratada com interferon e sem sinais ativos da infecção, desenvolveu um carcinoma hepatocelular (HCC) de grande porte (11,5 cm) localizado no segmento posterior do fígado. O tumor estava próximo ao ramo principal direito da veia porta, o que, associado à função hepática comprometida, inicialmente impossibilitou a cirurgia para remoção do tumor.\n\n**Principais Achados**  \nO paciente apresentava um tumor avançado classificado como T3N0M0, Estágio III, com marcadores tumorais elevados (alfafetoproteína e CA19-9). A tomografia computadorizada mostrou uma massa multinodular que invadia áreas críticas do fígado. Devido à função hepática insuficiente para suportar a cirurgia, foi iniciada terapia medicamentosa com lenvatinibe, mas o tumor aumentou de tamanho. Posteriormente, o tratamento foi alterado para a combinação de atezolizumab (um anticorpo que estimula o sistema imune contra o câncer) e bevacizumab (um agente que bloqueia o crescimento dos vasos sanguíneos do tumor). Após quatro ciclos dessa terapia combinada, o tumor reduziu-se significativamente para 6 cm, com perda do realce típico na imagem, indicando redução da atividade tumoral.\n\n**Interpretação Clínica**  \nA resposta favorável ao tratamento com atezolizumab e bevacizumab tornou possível a cirurgia, que consistiu na remoção do segmento posterior do fígado afetado. A análise histopatológica do tecido removido revelou que a maior parte do tumor estava necrosada (morta) e não havia células cancerosas ativas restantes, sugerindo que a terapia pré-operatória foi eficaz em eliminar o tumor viável. A presença de granulomas epitelioides (agregados de células inflamatórias) ao redor do tumor indica uma reação do organismo ao tratamento.\n\n**Próximos Passos e Prognóstico**  \nO paciente apresentou uma complicação pós-operatória, um abscesso hepático, que foi tratado com drenagem e antibióticos, evoluindo bem. Ele recebeu alta hospitalar sem necessidade de tratamentos adicionais após a cirurgia. Até o momento, 16 meses após a operação, o paciente permanece vivo e sem sinais de recidiva do câncer. Não há recomendações para terapia complementar nesse caso, dada a resposta completa observada.\n\nEste caso ilustra a importância da terapia alvo combinada para reduzir tumores inicialmente inoperáveis em pacientes com função hepática limitada, possibilitando uma cirurgia curativa e melhorando o prognóstico."
+        }
+    },
+    {
+        "article": "Um homem de 39 anos apresentou-se num centro de cuidados terciários após ter tentado se enforcar uma hora antes. De acordo com o relatório do serviço de emergência, ele foi encontrado no chão a tossir sangue ao lado de uma árvore com um laço de arame suspenso. Na apresentação, ele estava alerta e orientado. Ele relatou dificuldade em projetar a voz, mas negou dispneia. O exame físico revelou uma marca de ligadura ao longo do pescoço anterior ao nível da cartilagem da tiróide. A marca da tiróide podia ser palpada, mas outros pontos de referência cervicais estavam obscurecidos por enfisema subcutâneo.\n\nA angiografia por TC revelou lesões da íntima com trombo (AAST Grades III-V) nas carótidas comuns bilateral, carótida externa esquerda e artérias vertebrais bilaterais. Notou-se uma fratura de processo transverso deslocado em C4. Havia um extenso enfisema subcutâneo com pneumomediastino. Numa inspeção mais detalhada, os músculos do cinto infra-hióide foram interrompidos, com distração do osso hióide e epiglote superior e da cartilagem da tiróide inferior. A ressonância magnética demonstrou uma ruptura parcial do ligamento nucal, que requer a imobilização da coluna vertebral.\n\nO serviço OTO-HNS foi consultado para avaliar a via aérea do paciente. A laringoscopia flexível demonstrou cordas móveis bilateralmente com leve edema laríngeo. A epiglote parecia estar separada da cartilagem laríngea e a mucosa das pregas aryepiglotticas/cordas falsas estava interrompida.\n\nPouco tempo depois da avaliação inicial pela OTO-HNS, o paciente foi levado para a sala de operações (OR) para uma intubação nasotracheal consciente controlada. Ele estava estável do ponto de vista das vias aéreas e, devido à extensão das suas lacerações da mucosa laríngea, sentimos que a opção mais segura era transferi-lo para a sala de operações para uma gestão definitiva das vias aéreas sob visualização direta na noite da sua chegada. No dia dois do hospital, o paciente foi submetido a traqueostomia, laringoscopia, esofagoscopia e reparação da lesão hyolaryngeal. Depois de levantar as abas, um pequeno defeito foi notado sobre a incisão da tireóide na camada de investimento da fáscia cervical profunda que, quando aberta, revelou um grande defeito de tecido mole que se estendia para a via aérea supraglótica. Os músculos esterno-hióide, tiro-hióide e omo-hióide romperam-se 1-2 cm abaixo da sua inserção no hióide. A membrana tiro-hióide foi completamente interrompida, assim como a mucosa das cordas falsas e pregas aryepiglotticas. A epiglote foi separada da cartilagem da tireóide e foi distraída superiormente com o hióide pelas forças não opostas da musculatura supra-hióide.\n\nDevido a lesões cervicais coexistentes, o pescoço teve que permanecer numa posição neutra. Foi usada uma pinça Allis para retrair o hióide inferiormente e um único gancho para puxar a laringe/traqueia superiormente. A mucosa laríngea foi reparada primeiro com sutura vicril 4-0 interrompida. Para manter a tensão fora da ferida, foi realizada uma tireo-hióideopexia modificada com epiglotopexia. Foi passada uma agulha de calibre 20 através da cartilagem tireóide anterior sob visualização com um broncoscópio flexível para assegurar uma distância adequada acima da comissura anterior antes de passar a sutura mediana. No lado das vias aéreas, a sutura foi então passada através do pecíolo da epiglote. O braço inferior de quatro suturas vicril 2-0 adicionais foi passado através da ala superior da tireóide (2 suturas de cada lado). O braço superior de cada sutura foi então passado ao redor do hióide. Estas suturas tensionais foram fixadas, mantendo as cartilagens hióide e tireóide em estreita aproximação. As extremidades rompidas da musculatura da cintura escapular foram reaproximadas, foram colocados drenos Penrose e a incisão foi fechada de forma estratificada.\n\nO paciente teve um tubo de gastrostomia colocado. Ele começou a tomar heparina para trombose da carótida e continuou com uma semana de Unasyn intravenoso. A primeira mudança na traqueostomia foi realizada no dia pós-operatório (POD) 7, assim que a resolução do edema das vias aéreas foi confirmada com laringoscopia flexível. Um estudo de deglutição por vídeo no POD 14 revelou disfagia orofaríngea leve a moderada, que foi minimizada com estratégias de deglutição. Ele foi decanulado no POD 17 e recebeu alta no dia seguinte.\n\nNo seguimento, o paciente já não usava o colar cervical. Estava a tolerar uma dieta regular. A sua voz estava ligeiramente rouca, considerada um grau um para a aspereza na escala GRBAS (grado, áspero, rouco, astenia, tensão), mas era capaz de comunicar sem limitação. A laringoscopia demonstrou uma laringe bem curada com cordas móveis, encurtamento das pregas aryepiglotticas esquerdas e deslocação inferior da epiglote. A CTA de seguimento do pescoço para avaliar a sua lesão da carótida demonstrou resolução do ar cervical com uma via aérea patente/intacta.\n",
+        "gold_summary": "Relatamos um caso de um homem de 39 anos de idade, admitido na Unidade de Cuidados Intensivos após tentativa de auto-estrangulamento. Alerta e clinicamente estável, os seus principais sintomas foram dor e alterações de voz. O seu exame externo foi notável apenas por uma marca de ligadura cervical e enfisema subcutâneo à palpação. A imagem de TAC demonstrou rutura dos músculos do cinto infra-hióide e deslocação do hióide e epiglote superiormente. A subsequente laringoscopia flexível pela equipa de Otorrinolaringologia-Cirurgia de Cabeça e Pescoço (OTO-HNS) revelou avulsão da epiglote da cartilagem da tiróide e rutura das pregas arrepigadas/mucosa do falso cordão, resultando numa ferida aberta nos tecidos moles do pescoço anterior. A via aérea foi assegurada na sala de operações através de intubação nasotracheal por fibra ótica. Foi realizada uma traqueostomia. A exploração do pescoço revelou transecção dos músculos do cinto anterior e da membrana tiroideia. A ferida foi reparada em camadas através de uma tiroideopexia modificada. No seguimento de um mês, o paciente foi decanulado com sucesso e tolerou uma dieta regular.\n",
+        "synthetic_summary": {
+            "B1": "Um homem de 39 anos tentou se machucar no pescoço. Ele foi levado ao hospital e estava acordado e calmo. Ele tinha uma marca no pescoço e um pouco de ar preso debaixo da pele.\n\nOs médicos olharam dentro da garganta com uma câmera pequena. Viram que algumas partes estavam machucadas e abertas. Para ajudar ele a respirar, colocaram um tubo na garganta com cuidado.\n\nDepois, fizeram uma cirurgia para consertar os músculos e partes machucadas no pescoço. Ele ficou com um tubo para respirar por um tempo.\n\nDepois de um mês, o homem conseguiu tirar o tubo e comer comida normal. Ele estava melhor e conseguia falar. Os médicos cuidaram muito bem dele.",
+            "B2": "**O que aconteceu com o paciente**\n\nUm homem de 39 anos tentou se enforcar e foi levado ao hospital. Quando chegou, ele estava acordado e estável, mas com dor no pescoço e a voz diferente do normal. No pescoço, os médicos viram uma marca do laço usado e sentiram um inchaço chamado enfisema subcutâneo, que é quando o ar fica preso debaixo da pele.\n\n**O que os exames mostraram**\n\nUm exame de imagem chamado tomografia computadorizada (TAC) mostrou que alguns músculos do pescoço estavam rompidos e que ossos importantes, como o hióide e a epiglote (uma parte que ajuda a proteger a garganta), estavam deslocados para cima. Depois, os médicos fizeram uma laringoscopia flexível, que é um exame com uma câmera para olhar dentro da garganta. Eles viram que a epiglote estava separada da cartilagem da tireoide e que havia cortes na mucosa, que é a camada que reveste os falsos cordões vocais, causando uma ferida aberta na frente do pescoço.\n\n**Como foi o tratamento**\n\nPara garantir que ele pudesse respirar bem, os médicos colocaram um tubo pela narina até a traqueia, usando uma fibra ótica para ajudar na passagem do tubo. Depois, fizeram uma traqueostomia, que é uma abertura cirúrgica na traqueia para ajudar na respiração. Durante a cirurgia, eles encontraram os músculos do pescoço cortados e a membrana tiroideia rompida. A ferida foi consertada em camadas, usando uma técnica chamada tiroideopexia modificada, que ajuda a manter as partes do pescoço unidas e firmes.\n\n**Como ele ficou depois**\n\nUm mês depois, o paciente conseguiu retirar o tubo da traqueostomia e voltou a se alimentar normalmente. A voz dele estava um pouco rouca, mas ele conseguia falar sem problemas. Os exames mostraram que o pescoço estava cicatrizando bem e que ele não tinha mais problemas para respirar.",
+            "B3": "**Contexto**  \nApresentamos o caso de um homem de 39 anos que tentou se enforcar, sendo admitido em uma unidade de terapia intensiva em estado alerta e clinicamente estável. Ele relatava dor no pescoço e alterações na voz, mas sem dificuldade respiratória significativa. O exame físico revelou uma marca de ligadura no pescoço anterior e enfisema subcutâneo (ar preso sob a pele) ao redor da região cervical.\n\n**Principais Achados**  \nAs imagens de tomografia computadorizada (TAC) mostraram ruptura dos músculos do cinto infra-hióide (músculos localizados abaixo do osso hióide no pescoço) e deslocamento superior do osso hióide e da epiglote (estrutura que protege as vias aéreas durante a deglutição). A avaliação endoscópica flexível da laringe, realizada pela equipe de Otorrinolaringologia e Cirurgia de Cabeça e Pescoço, revelou que a epiglote estava separada da cartilagem da tireoide, além de ruptura da mucosa e das pregas aryepiglóticas (dobras de tecido que ajudam a proteger as vias aéreas), resultando em uma ferida aberta nos tecidos moles do pescoço anterior.\n\n**Interpretação Clínica e Manejo**  \nPara garantir a segurança das vias aéreas, o paciente foi submetido a uma intubação nasotraqueal (introdução de tubo pela narina até a traqueia) guiada por fibra ótica na sala de operações. Posteriormente, foi realizada uma traqueostomia (abertura cirúrgica na traqueia para facilitar a respiração). Durante a cirurgia, constatou-se a transecção (corte completo) dos músculos do cinto anterior do pescoço e da membrana tiro-hióidea (tecido que conecta o osso hióide à cartilagem tireoide). A ferida foi reparada em camadas, utilizando uma técnica modificada de tireo-hióideopexia, que consiste em suturar e aproximar as estruturas para restaurar a anatomia e a função laríngea.\n\n**Próximos Passos e Evolução**  \nNo acompanhamento de um mês, o paciente apresentou boa recuperação, sendo decanulado (remoção do tubo traqueal) com sucesso e capaz de manter uma dieta regular. Sua voz estava levemente rouca, mas funcional, e a laringoscopia de controle mostrou cicatrização adequada com preservação do movimento das cordas vocais. A avaliação por imagem confirmou a resolução do enfisema cervical e a manutenção de uma via aérea aberta e estável.\n\nEste caso ilustra a complexidade do manejo das lesões cervicais por autoestrangulamento, destacando a importância da avaliação detalhada das vias aéreas, o uso de técnicas cirúrgicas específicas para reparação das estruturas laríngeas e o acompanhamento multidisciplinar para garantir a recuperação funcional do paciente."
+        }
+    },
+    {
+        "article": "O paciente era um menino de 16 anos que foi encaminhado ao nosso hospital em julho de 2022 por causa de uma insuficiência cardíaca grave.\n\nCom 13 anos, foi-lhe diagnosticada distrofia muscular de Becker, com a mutação causadora no gene DMD (chrX:32,841,413–32,862,977, mutação heterozigótica), e testes genéticos mostraram as mutações comórbidas de ABCB4 (chr7:87041219, mutação heterozigótica) e DSC2 (chr18:28659938, mutação heterozigótica). Ele tinha um histórico de falta de ar leve e desconforto torácico ao esforço e recebeu tratamento para disfunção cardíaca; no entanto, a função cardíaca piorou e ele foi encaminhado ao nosso hospital pela primeira vez. O exame físico na primeira consulta mostrou uma altura de 173 cm, peso corporal de 78 kg, pressão arterial de 110/90 mmHg, frequência cardíaca de 76 batimentos/minuto, frequência respiratória de 20 batimentos/minuto, temperatura corporal de 36,5 °C e SpO2 de 100% com ar ambiente. Não houve dilatação da veia jugular no pescoço. Seus sons de auscultação pulmonar e cardíaca foram normais. Seu abdômen estava plano. Havia um leve edema no tornozelo e no pé. O paciente não apresentou ombros em forma de asas ou lordose. A pseudohipertrofia do músculo gastrocnêmio bilateral foi observada. O sinal de Gower foi negativo. O teste laboratorial mostrou que o nível de N-terminal pró-hormona do peptídeo natriurético cerebral (NT-proBNP) foi de 471,55pg/ml, mioglobina foi de 272,61ng/ml, creatina quinase (CK) foi de 5.493 U/L, creatina quinase-MB (CK-MB) foi de 115 U/L, creatina quinase-MM (CK-MM) foi de 5.378U/L. A alanina aminotransferase (ALT) foi de 138 U/L, a aspartato aminotransferase (AST) foi de 92 U/L, lactato desidrogenase (LDH) foi de 393U/L. A ecocardiografia transtorácica mostrou uma fração de ejeção ventricular esquerda de 19% (LVEF), dilatação do átrio esquerdo, ventrículo esquerdo e átrio direito, regurgitação mitral grave, disfunção sistólica ventricular esquerda grave, diminuição da função diastólica de todo o coração. A ressonância magnética do membro inferior revelou alterações de distrofia muscular bilateral. O tratamento medicamentoso foi iniciado incluindo sacubitril-valsartan, carvedilol, ivabradina, tolvaptano, trimetazidina e ajustado de acordo com as diretrizes de tratamento da insuficiência cardíaca nos próximos 3 anos de acompanhamento. O valor da LVEF na ecocardiografia de acompanhamento flutuou entre 30-35%.\n\nNo primeiro dia desta referência, o paciente sofreu deterioração da angústia torácica, palpitação e falta de ar em repouso, indicando insuficiência cardíaca progressiva. Ele foi encaminhado ao nosso hospital às 21:00. No exame físico, a pressão arterial de 106/63 mmHg, a frequência cardíaca de 120 batimentos/minuto irregularmente, a frequência respiratória de 20 vezes/minuto, a temperatura corporal de 37℃ e a SpO2 de 97% no ar ambiente. Um exame torácico revelou crepitações úmidas em ambos os pulmões. Seus sons cardíacos estavam intactos, mas irregulares, e não foi observado murmúrio cardíaco. A sua força muscular era de 5/5. Os testes laboratoriais mostraram os seguintes resultados: contagem de glóbulos brancos, 10,56 × 109/L com neutrófilos 60,5%; hemoglobina, 144 g/L; contagem de plaquetas, 177 × 109/L. A função de coagulação foi ligeiramente anormal, como segue: tempo de protrombina (PT), 14,8 s; tempo de tromboplastina parcial ativada (APTT), 27,1 s; D-Dimer, 0,27 mg/L. O exame bioquímico mostrou potássio de 3,9 mmol/L, creatinina de 67µmol/L. O nível total de bilirrubina do paciente era normal, mas os níveis de enzimas hepáticas estavam ligeiramente elevados, como segue: ALT, 109 U/L; AST, 87 U/L; LDH, 376U/L. NT-proBNP foi significativamente elevado para 9,171pg/ml. O nível de cTnT foi de 0,107ng/ml. Os níveis de eletrólitos estavam normais. O eletrocardiograma mostrou fibrilação atrial com taxa ventricular rápida e bloqueio cardíaco intraventricular.\n\nÀs 22:00 do primeiro dia, a angústia torácica estava se agravando. 150 mg de amiodaron através de injeção intravenosa falhou na cardioversão. A taxa ventricular era de 120 bpm. Então, 450 mg de amiodaron foi usado para controlar a taxa e o ritmo através de gotejamento intravenoso contínuo (6ug/Kg/min). Ao mesmo tempo, fornecemos infusão contínua de peptídeo natriurético cerebral humano recombinante para melhorar a função cardíaca clínica. O monitor ECG mostrou fibrilação atrial com taxa ventricular de 90 bpm.\n\nÀs 13:00 do segundo dia, o paciente ficou pálido, suando e com ortopneia. A pressão arterial do paciente caiu para 75/50 mmHg, a frequência cardíaca foi de 74 bpm. Portanto, a amiodarona e o peptídeo natriurético cerebral humano recombinante foram descontinuados e a infusão intravenosa de dopamina e dobutamina foi administrada. Todos os medicamentos orais foram interrompidos ao mesmo tempo. O ECG mostrou um ritmo sinusal normal de 84 bpm e um bloqueio atrioventricular tipo II de segundo grau. A ecocardiografia de emergência ao lado da cama mostrou que a dilatação de todo o coração com função sistólica reduzida do ventrículo esquerdo e direito (LVEF 25%), hipertensão pulmonar leve, efusão pericárdica infinitesimal. O exame físico mostrou pressão arterial de 89/60 mmHg, frequência cardíaca de 74 bpm regularmente e SpO2 de 99% com 3 L/minuto de oxigênio. A pele manchada foi visível em ambos os membros inferiores. O volume de urina no segundo dia foi de 1.000 ml.\n\nNo terceiro dia, a ultrassonografia abdominal revelou cálculos biliares e colecistite. Meropenem (0,5 g q12h ivgtt) foi usado empiricamente para controlar a infecção. O volume de urina diminuiu para 400 ml.\n\nNo 4º dia, o paciente queixou-se de alívio do desconforto torácico. Os testes laboratoriais mostraram os seguintes resultados: ALT, 7.391 U/L; AST, 5.671 U/L; LDH, 8.089U/L; CK, 2.875pg/ml, CK-MM, 28.522U/L; CK-MB, 229U/L; nitrogênio ureico, 29.8mmol/L; ácido úrico, 859µmol/L; creatinina, 305 µmol/L; eGRF, < 30 ml/min/1.73m2; plaqueta,104 × 109/L; PTs, 29.3 s; APTT, 29.9 s; Fibrinogen, 163 mg/dl; D-Dimer > 40 mg/L. Ele foi encaminhado para a UTI para tratamento adicional.\n\nFornecemos terapia de substituição renal contínua ao lado da cama. As administrações de isoglicirrinato, glutationa reduzida e fosfatidilcolina poliénica foram dadas para proteger a função hepática. A dopamina e dobutamina (1.3ug/kg/min) foram administradas para sustentar a pressão arterial e fortalecer a contração cardíaca. Os exames laboratoriais foram realizados para monitorizar os índices relacionados com o paciente. Função de coagulação: PTs foi de 22 s. D-Dimer foi superior a 40 mg/L. A função hepática foi a seguinte: nível total de bilirrubina de 75.5µmol/L, ALT de 5,060 U/L, AST de 1,952 U/L, LDH de 8,089U/L. Função renal: nitrogénio ureico no sangue de 23.8mmol/L, ácido úrico de 604 µmol/L, creatinina de 322 µmol/L, e eGRF 23 ml/min/1.73m2. NT-proBNP foi de 5701 pg/ml, CK foi de 11476U/L, CK-MM 11308U/L, CK-MB 168U/L. O ECG mostrou um ritmo sinusal normal de 62 bpm, bloqueio cardíaco intraventricular, hipertrofia atrial esquerda e desvio do eixo esquerdo.\n\nÀs 22:00 do 5º dia, a dopamina foi descontinuada. A pressão arterial oscilou entre 90-112/50-70 mmHg. Administrámos sacubitril-valsartan oral 25 mg bid e trimetazidina 35 mg bid no dia 10 de julho. Ivabradina (5 mg bid p.o.) e tolvaptano (10 mg qd p.o.) foram administrados no dia 10 devido a uma hemodinâmica estável, melhoria da função renal e aumento do volume diário de urina. A dobutamina foi interrompida no dia 11. A heparina de baixo peso molecular foi iniciada no dia 12.\n\nNo 15º dia, a reavaliação dos exames laboratoriais sugeriu uma melhora significativa da função hepática. A alanina aminotransferase estava em 255 U/L, a aspartato aminotransferase em 35U/L. A quantidade diária de transfusão era de 2.106 ml com uma produção diária de urina de 1.125 ml. Portanto, a fosfatidilcolina polienada foi interrompida. Os cateteres de hemodiálise foram removidos.",
+        "gold_summary": "Apresentamos um caso de um rapaz de 16 anos admitido com insuficiência cardíaca e fibrilhação atrial (FA). Foi-lhe diagnosticada distrofia muscular de Becker (BMD) e o teste genético mostrou comorbidades em mutações no gene DMD, ABCB4 e DSC2. Amiodarone foi prescrito para controlar a fibrilhação atrial paroxística intravenosa. No entanto, os níveis das enzimas hepáticas estavam acentuadamente elevados, juntamente com choque cardíaco, falência renal e distúrbios de coagulação. Após a terapia de substituição renal contínua ao lado da cama, a função hepática e o estado clínico do paciente foram reabilitados.\n",
+        "synthetic_summary": {
+            "B1": "Um menino de 16 anos estava com o coração muito fraco. Ele tem uma doença que deixa os músculos muito cansados. O médico deu um remédio para ajudar o coração a bater melhor. Mas o menino ficou com o fígado doendo e os rins pararam de trabalhar direito. Ele ficou muito doente. Os médicos fizeram um tratamento especial para ajudar os rins e o fígado. Com esse cuidado, ele começou a melhorar e ficou mais forte.",
+            "B2": "**O que aconteceu com o paciente**\n\nEste é o caso de um garoto de 16 anos que foi internado no hospital porque seu coração estava muito fraco, uma condição chamada insuficiência cardíaca. Ele também tinha um problema chamado fibrilação atrial, que é quando o coração bate de forma irregular e rápida. Esse garoto já sabia que tinha uma doença chamada distrofia muscular de Becker, que afeta os músculos e é causada por uma mudança no gene DMD. Além disso, ele tinha outras mudanças genéticas em dois genes chamados ABCB4 e DSC2, que podem influenciar sua saúde.\n\n**Como o tratamento foi feito**\n\nPara tentar controlar o ritmo irregular do coração, os médicos deram um remédio chamado amiodarona por via intravenosa, ou seja, direto na veia. Porém, durante o tratamento, o garoto começou a apresentar problemas no fígado, que é o órgão que ajuda a limpar o corpo, e os exames mostraram que suas enzimas hepáticas estavam muito altas, indicando que o fígado estava machucado. Além disso, ele teve choque cardíaco (quando o coração não consegue bombear sangue suficiente), falência dos rins (que filtram o sangue) e problemas na coagulação do sangue, que é o processo que ajuda a parar sangramentos.\n\n**O que os médicos fizeram para ajudar**\n\nDiante dessa situação grave, os médicos começaram um tratamento chamado terapia de substituição renal contínua, que é uma espécie de \"rim artificial\" para ajudar a limpar o sangue quando os rins não funcionam bem. Esse tratamento foi feito ao lado da cama do paciente, para que ele recebesse cuidados constantes. Com essa ajuda, o fígado dele melhorou e seu estado geral de saúde também foi recuperado.\n\n**Por que isso é importante**\n\nEste caso mostra como uma doença muscular pode afetar o coração e outros órgãos importantes do corpo. Também destaca a importância de um tratamento rápido e adequado para evitar que problemas graves piorem ainda mais a saúde do paciente.",
+            "B3": "**Contexto**  \nEste relato descreve o caso de um jovem de 16 anos com diagnóstico prévio de distrofia muscular de Becker (uma doença genética que afeta os músculos) e mutações genéticas adicionais nos genes DMD, ABCB4 e DSC2, que podem influenciar a função muscular e cardíaca. Ele foi admitido no hospital com insuficiência cardíaca grave e fibrilação atrial (um tipo de arritmia cardíaca caracterizada por batimentos irregulares e rápidos).\n\n**Principais Achados Clínicos e Diagnósticos**  \nO paciente apresentava sintomas progressivos de insuficiência cardíaca, incluindo falta de ar, palpitações e desconforto torácico. Exames mostraram uma função cardíaca muito comprometida, com fração de ejeção do ventrículo esquerdo (medida da capacidade do coração de bombear sangue) reduzida para cerca de 19-35%, dilatação das câmaras cardíacas e regurgitação mitral grave (vazamento da válvula do coração). Durante a internação, desenvolveu fibrilação atrial com ritmo ventricular rápido e bloqueio cardíaco intraventricular, evidenciado pelo eletrocardiograma.\n\nLaboratoriais revelaram elevações marcantes das enzimas hepáticas (ALT, AST, LDH), indicando lesão no fígado, além de insuficiência renal aguda (evidenciada por aumento da creatinina e diminuição da taxa de filtração glomerular estimada) e distúrbios na coagulação sanguínea (prolongamento do tempo de protrombina e níveis elevados de D-dímero). A insuficiência cardíaca avançada levou a um quadro de choque cardiogênico, caracterizado por pressão arterial baixa e má perfusão dos órgãos.\n\n**Intervenções e Tratamento**  \nPara controlar a fibrilação atrial paroxística (episódios intermitentes da arritmia), foi administrado amiodarona por via intravenosa, porém sem sucesso inicial na reversão do ritmo irregular. Posteriormente, o paciente recebeu infusão contínua do medicamento para tentar controlar a frequência cardíaca. Com a piora do quadro clínico, incluindo hipotensão (pressão baixa) e insuficiência renal, foi necessária a suspensão da amiodarona e o início de suporte inotrópico com dopamina e dobutamina para melhorar a função cardíaca e manter a pressão arterial.\n\nDevido à falência renal, foi iniciada terapia de substituição renal contínua (um tipo de diálise realizada à beira do leito) para remover toxinas e equilibrar os líquidos e eletrólitos do corpo. Paralelamente, foram administrados medicamentos para proteger o fígado, como isoglicirrinato, glutationa reduzida e fosfatidilcolina poliénica.\n\nCom o tratamento intensivo, o paciente apresentou melhora progressiva da função hepática e renal, estabilização hemodinâmica e controle da arritmia. Medicamentos orais para insuficiência cardíaca, incluindo sacubitril-valsartan, trimetazidina, ivabradina e tolvaptano, foram introduzidos conforme a condição clínica permitiu.\n\n**Interpretação Clínica**  \nEste caso ilustra a complexidade do manejo de um adolescente com distrofia muscular de Becker e múltiplas mutações genéticas que afetam o coração, levando a insuficiência cardíaca avançada e arritmias graves. A combinação de choque cardiogênico, insuficiência renal e lesão hepática aguda representa um quadro crítico que requer intervenção multidisciplinar e suporte intensivo. A falha inicial no controle da fibrilação atrial com amiodarona e a necessidade de suporte inotrópico evidenciam a gravidade da disfunção cardíaca.\n\n**Próximos Passos e Considerações**  \nO acompanhamento contínuo da função cardíaca, hepática e renal é essencial para ajustar o tratamento e prevenir complicações futuras. A reabilitação clínica após a fase aguda deve incluir suporte nutricional, fisioterapia e monitoramento genético para avaliar o impacto das mutações associadas. Este caso destaca a importância do manejo integrado em pacientes com doenças musculares genéticas e complicações cardíacas severas, bem como a necessidade de intervenções precoces para evitar a progressão para falência múltipla de órgãos."
+        }
+    },
+    {
+        "article": "Informações do paciente: Trata-se do Sr. RL, 27 anos, soldador de profissão, solteiro, de baixo nível socioeconômico e sem histórico patológico particular.\n\nResultados clínicos: o paciente estava confuso (Escala de Coma de Glasgow (GCS) 13/15), pupilas agitadas em midríase, tinha tremores com taquipneia e taquicardia, uma hiperreflexia associada a mioclonias espontâneas mais marcadas nos membros inferiores com uma hipersudoração e calafrios.\n\nCronologia: a história da doença remonta a uma semana antes da consulta com um médico neurologista no setor privado, pela instalação de proposições de perseguição, proposições de negação de filiação, uma bizarrice de comportamento e atitudes alucinatórias, e o quadro se complicou com uma agitação psicomotora e um diagnóstico inicial de um acesso psicótico agudo foi retido, e o paciente foi colocado sob haloperidona 5 mg por dia.\n\nDois meses depois, a evolução foi marcada por uma má adesão terapêutica com persistência da sintomatologia psicótica associada a sintomas negativos, como a perda de prazer, o isolamento e a abolição com um sono perturbado, motivando o doente a refazer uma consulta com o mesmo médico que lhe adicionou paroxetina 20 mg por dia e amitriptilina 25 mg por dia.\n\nAlgumas horas (6 a 8 horas) após a ingestão dos dois antidepressivos, o paciente apresentou perda de consciência e agitação psicomotora, o que motivou sua internação na unidade de terapia intensiva.\n\nDiagnóstico: o paciente foi submetido a um exame biológico completo, que objetivou uma perturbação dos eletrólitos com uma acidose metabólica e um nível de creatina fosfocinase (CPK) de 100 UL/L, o exame citobacteriológico da urina (ECBU), o estudo do líquido cefalorraquidiano e as hemoculturas foram negativos. A concentração plasmática da proteína C-reativa (CRP) e a contagem da fórmula sanguínea foram normais.\n\nO eletrocardiograma (ECG) objetivou uma arritmia cardíaca por fibrilação atrial, e a radiografia torácica e a ressonância magnética (MRI) cerebral foram sem particularidades. O diagnóstico de síndrome serotoninérgica foi retido após ter eliminado uma etiologia infecciosa, metabólica ou neurológica.\n\nIntervenção terapêutica: o paciente foi colocado sob ventilação mecânica, gavagem 500cc/8H, reidratação por água 500cc/8H, ração de base SG 5% + 2g Nacl + 2g Kcl +1g ca 2+ / 8h, e SS 0,9% 500cc/4H, sedação por midazolam 8mg/H, IPP 40mg /j, com um anticoagulante com objetivo preventivo e insulina de acordo com a dextrose.\n\nSeguimento e resultados: o estado clínico hemodinâmico e neurológico do paciente estabilizou-se após 24h, em seguida foi transferido para o serviço de psiquiatria onde o médico tratante encontrou um paciente calmo no plano motor, bem orientado no tempo e no espaço, tendo tido um delírio místico religioso e de perseguição, algumas respostas deslocadas, um julgamento perturbado sem presença de um síndrome depressivo nem maníaco ou confusional. A evolução da sintomatologia psiquiátrica foi marcada por uma boa melhoria com um bom retorno ao estado pré mórbido, estabilizada sob neuroléptico atípico tipo olanzapina com uma posologia inicial de 5 mg por dia.\n",
+        "gold_summary": "Relatamos o caso clínico de um paciente que apresentou um estado de confusão com agitação psicomotora e hiperreflexia e mioclonias espontâneas após a ingestão simultânea de paroxetina e amitriptilina. O diagnóstico de síndrome serotoninérgica foi feito após a exclusão de outros diagnósticos possíveis, necessitando de internação em unidade de terapia intensiva.\n",
+        "synthetic_summary": {
+            "B1": "Um homem ficou muito confuso e agitado. Ele tremia e seu corpo mexia sozinho. Isso aconteceu depois que ele tomou dois remédios juntos. Os médicos cuidaram dele no hospital para ele melhorar.",
+            "B2": "**O que aconteceu com o paciente**\n\nUm homem de 27 anos começou a apresentar confusão, agitação e movimentos involuntários chamados mioclonias, que são como pequenos tremores. Esses sintomas surgiram depois que ele tomou dois remédios antidepressivos ao mesmo tempo: paroxetina e amitriptilina.\n\n**O que é síndrome serotoninérgica**\n\nEssa combinação de sintomas fez os médicos suspeitarem de uma doença chamada síndrome serotoninérgica. Essa síndrome acontece quando há muita serotonina, uma substância química do cérebro, causando problemas como agitação, tremores e reflexos exagerados.\n\n**Como foi o tratamento**\n\nO paciente precisou ser internado na unidade de terapia intensiva para receber cuidados especiais, como ajuda para respirar e medicamentos para controlar os sintomas. Depois de um tempo, ele melhorou e foi transferido para o setor de psiquiatria, onde continuou o tratamento com outro remédio que ajudou a controlar os sintomas sem causar problemas graves.\n\n**Por que isso é importante**\n\nEsse caso mostra que tomar certos antidepressivos juntos pode causar efeitos perigosos. Por isso, os médicos precisam cuidar muito bem das combinações de remédios para evitar problemas sérios como a síndrome serotoninérgica.",
+            "B3": "**Contexto**  \nApresentamos o caso do Sr. RL, um homem de 27 anos, soldador, sem antecedentes médicos relevantes, que inicialmente procurou atendimento por sintomas psiquiátricos agudos, incluindo delírios de perseguição e comportamento alterado. Após um diagnóstico inicial de episódio psicótico agudo, foi tratado com haloperidol, mas apresentou má adesão ao tratamento e persistência dos sintomas, incluindo isolamento social e distúrbios do sono. Posteriormente, foram adicionados dois antidepressivos, paroxetina e amitriptilina.\n\n**Principais Achados Clínicos**  \nCerca de 6 a 8 horas após a introdução dos antidepressivos, o paciente desenvolveu um quadro grave caracterizado por confusão mental, agitação psicomotora, midríase (dilatação anormal das pupilas), tremores, taquicardia (batimentos cardíacos acelerados), taquipneia (respiração rápida), hiperreflexia (reflexos exagerados) e mioclonias espontâneas (movimentos involuntários musculares), acompanhados de sudorese excessiva e calafrios. Esses sinais indicaram uma alteração neurológica e autonômica significativa.\n\n**Diagnóstico Clínico e Exames Complementares**  \nApós a internação em unidade de terapia intensiva, foram realizados diversos exames para excluir causas infecciosas, metabólicas e neurológicas, incluindo análises laboratoriais, exames de imagem cerebral e cardíaca, que não revelaram anormalidades específicas. Destacou-se uma arritmia cardíaca por fibrilação atrial e uma acidose metabólica leve, além de níveis normais de marcadores inflamatórios. Com base no quadro clínico e na exclusão de outras causas, foi estabelecido o diagnóstico de síndrome serotoninérgica, uma condição causada pelo excesso de serotonina no sistema nervoso central, frequentemente associada à combinação de medicamentos que aumentam a serotonina.\n\n**Intervenção Terapêutica**  \nO tratamento incluiu suporte intensivo com ventilação mecânica, sedação, hidratação cuidadosa com reposição eletrolítica, prevenção de complicações tromboembólicas e controle metabólico. O manejo foi realizado em ambiente de terapia intensiva para garantir a estabilidade hemodinâmica e neurológica do paciente.\n\n**Evolução e Seguimento**  \nApós 24 horas, o paciente apresentou estabilização do quadro clínico e neurológico, permitindo sua transferência para o serviço de psiquiatria. No acompanhamento, observou-se melhora significativa dos sintomas psiquiátricos, com retorno ao estado mental prévio, sem sinais de depressão, mania ou confusão. O tratamento psiquiátrico foi ajustado para o uso de um neuroléptico atípico, olanzapina, com boa resposta clínica.\n\n**Interpretação Clínica**  \nEste caso ilustra a importância de reconhecer a síndrome serotoninérgica como uma complicação potencialmente grave da associação de antidepressivos que atuam sobre o sistema serotoninérgico. O diagnóstico precoce e a exclusão de outras causas são essenciais para o manejo adequado e a prevenção de complicações fatais. A monitorização cuidadosa e a adesão ao tratamento psiquiátrico são fundamentais para a recuperação do paciente.\n\n**Próximos Passos**  \nRecomenda-se acompanhamento psiquiátrico contínuo, com atenção especial à escolha e ajuste das medicações antidepressivas para evitar recidivas da síndrome serotoninérgica. Além disso, é importante orientar o paciente sobre os riscos da automedicação e a necessidade de comunicação clara com os profissionais de saúde sobre todos os medicamentos em uso."
+        }
+    },
+    {
+        "article": "Um paciente do sexo masculino de 26 anos de idade foi admitido no nosso hospital com um histórico de pele e urina amarelas recorrentes por mais de um ano. A 1 de Junho de 2022, o paciente apresentou pele e urina amarelas, sem quaisquer desencadeadores óbvios. Um exame de ultrassom revelou a presença de múltiplas pedras no ducto biliar comum e intra-hepático, com ligeira dilatação do ducto biliar intra-hepático (diâmetro: 0.32 cm, referência: ≤ 0.2 cm) e comum (diâmetro: 1.04 cm, referência: 0.6-0.8 cm). Estes achados apoiaram a impressão inicial de icterícia obstrutiva. A 15 de Junho de 2022, o paciente foi submetido a coledocolitotomia laparoscópica, colecistectomia e litotomia coledocoscópica. No entanto, não houve melhoria na função hepática nem nos sintomas de icterícia após a cirurgia no último ano. A fim de procurar assistência médica adicional, o paciente foi admitido no nosso hospital com icterícia de origem desconhecida a 12 de Agosto de 2023. O paciente negou um histórico de tabagismo, abuso de álcool e uso a longo prazo de medicação prejudicial ao fígado, incluindo suplementos de ervas e dietéticos.\n\nO exame físico revelou a presença de amarelecimento generalizado da pele e da esclera, bem como um baço palpável com 2 dedos abaixo da caixa torácica. Além disso, o índice de massa corporal do sujeito foi registado em 17,4 kg/m².\n\nOs resultados dos exames laboratoriais vitais foram apresentados na Tabela 1. Além disso, anticorpo antinuclear (ANA) 1:100, anticorpos citoplasmáticos antineutrófilos (p-ANCA) positivos, perfil de anticorpos de doenças autoimunes do fígado foram todos negativos; hepatite A a E, vírus Epstein-Barr, citomegalovírus, vírus Coxsackie, vírus herpes zoster, treponema pallidum e vírus da imunodeficiência humana foram todos negativos.\n\nA colangiopancreatografia por ressonância magnética (MRCP) demonstrou a existência de dilatação do ducto biliar intra-hepático esquerdo e comum, na ausência de uma vesícula biliar, esplenomegalia e múltiplos linfonodos alargados na região hilar. O exame histológico do fígado revelou que a estrutura dos lobos hepáticos e a rede capilar do ducto biliar não eram claramente discerníveis. Alguns ductos biliares capilares apresentavam dilatação, acompanhada pela formação de trombos biliares. Também se observou fibrose de ponte dos tratos porta para a veia central. Observou-se desaparecimento dos ductos biliares em 10 dos 12 tratos porta. Este fenómeno é mais comumente atribuído à síndrome do ducto biliar em desaparecimento (VBDS). A pontuação simplificada de Scheuer indicou um grau 2 e estágio 3 a 4. A sequenciação do exome completo revelou a presença de uma mutação heterozigótica em PKLR (NM_000298.5:c.119G > A) e UGT1A1 (NM_000463.2:c.–3275T > G).\n\nÀ luz da evidência acima mencionada, um diagnóstico revisado foi apresentado como VBDS com PLKR e mutação UGT1A1, cirrose colestática. Uma dose de 1000 mg/d de ácido ursodeoxicólico (UDCA) e 8 mg/d de metilprednisolona foi administrada a fim de melhorar a colestase e a inflamação hepática.\n\nCom o tempo, uma ressonância magnética com contraste realizada a 10 de setembro de 2023 revelou a presença de cálculos no ducto biliar comum, apesar da ausência de febre, dor abdominal ou outras queixas. O paciente recusou-se a remover os cálculos do ducto biliar comum. A 25 de outubro de 2023, um exame MRCP mostrou alterações dinâmicas. O sistema biliar mostrou estenose em banda e uma aparência de árvore podada, que estava em conformidade com a aparência de imagem da colangite esclerosante. Foi realizada uma colonoscopia adicional com preparação intestinal adequada, aderindo às diretrizes para pacientes com suspeita de danos na mucosa, que revelou a presença de UC envolvendo o íleo terminal e o hemicólon direito. Esta descoberta foi consistente com as manifestações colonoscópicas de PSC-UC. Além disso, PSC-UC é um subtipo único de UC, o que torna difícil a aplicação dos critérios de classificação de Montreal para descrever a topografia da doença. Consequentemente, o diagnóstico foi revogado para PSC-UC com PLKR e mutações UGT1A1, coledocolitíase.\n\nEm 25 de Novembro de 2023, foram realizadas colangiopancreatografia retrógrada endoscópica (CPRE) e esfincterotomia endoscópica (EST). Uma pedra preta irregular de 4 mm x 5 mm e um grande número de pedras sedimentares foram removidas com sucesso utilizando dilatação do esfíncter papilar duodenal endoscópico (DPPE). Após a resolução da obstrução, foi prescrito um regime de longa duração de 1000 mg/d UDCA em combinação com 10 mg/d de ácido obeticólico (OCA) para melhorar a colestase. Além disso, foi prescrito 8 g/d de colestiramina para facilitar a adsorção do excesso de ácidos biliares, enquanto 1,2 g/d de rifaximina foi administrado para prevenir a infecção do trato biliar. Além disso, dado o facto de a UC do paciente se limitar ao íleo terminal e ao hemicolo direito, houve uma escassez de fezes mucopurulentas e sanguinolentas, bem como diarreia. Com comprimidos de mesalazina (2 g por dia) foi medicado com o objetivo de melhorar a inflamação do cólon. Em 30 de Julho de 2024, a função hepática do paciente foi a seguinte: TB/DB 33/25.9 μmol/L, fosfatase alcalina (ALP)/GGT 183/112 U/L, IgG 17.19 g/L. A condição do paciente permaneceu estável.\n",
+        "gold_summary": "Preocupações do paciente: Um paciente do sexo masculino de 26 anos de idade queixa-se de uma história de pele e urina amarelas recorrentes por mais de um ano.\n\nDiagnósticos: Após a realização de uma colangiopancreatografia por ressonância magnética, uma colonoscopia, uma biópsia hepática e um sequenciamento do exoma completo, o paciente foi finalmente diagnosticado com PSC - colite ulcerativa com mutação PLKR e UGT1A1.\n\nIntervenções: Após a resolução da obstrução, foi prescrito um regime de longo prazo de 1000 mg/d de ácido ursodeoxicólico em combinação com 10 mg/d de ácido obetichólico para melhorar a colestase, 8 g/d de colestiramina para facilitar a adsorção de excesso de ácidos biliares e 1.2 g/d de rifaximina para prevenir a infecção do trato biliar.\n\nResultados: Os parâmetros bioquímicos do fígado do paciente melhoraram significativamente. A sua condição é estável e não foi submetido a transplante de fígado neste momento.\n",
+        "synthetic_summary": {
+            "B1": "Um homem jovem ficou com a pele e a xixi amarelos por muito tempo. \n\nOs médicos fizeram muitos exames para entender o que ele tinha. Eles descobriram que ele tinha um problema no fígado e no intestino. \n\nEle tomou remédios para ajudar o fígado a ficar melhor e para evitar que ele ficasse doente. \n\nCom o tempo, ele melhorou e está bem agora. Os médicos continuam cuidando dele com muito carinho.",
+            "B2": "**O que o paciente sentia**  \nUm homem de 26 anos teve a pele e a urina amareladas várias vezes durante mais de um ano. Isso é um sinal de que algo não estava funcionando bem no fígado ou nas vias biliares, que são os canais por onde a bile, um líquido importante para a digestão, passa.\n\n**Como descobriram o problema**  \nOs médicos fizeram vários exames para entender o que estava acontecendo. Usaram uma ressonância magnética para olhar os canais da bile, fizeram uma colonoscopia para examinar o intestino, retiraram um pedaço do fígado para analisar (biópsia) e também estudaram o DNA do paciente (sequenciamento do exoma). Com esses exames, descobriram que ele tinha uma doença chamada colangite esclerosante primária (PSC), que causa inflamação e cicatrizes nos canais da bile, junto com colite ulcerativa (uma inflamação no intestino). Além disso, ele tinha mutações em dois genes chamados PKLR e UGT1A1, que podem afetar o funcionamento do fígado.\n\n**Tratamento dado**  \nDepois de remover pedras que bloqueavam os canais da bile, os médicos deram remédios para ajudar o fígado a funcionar melhor. Ele tomou ácido ursodeoxicólico e ácido obetichólico para melhorar o fluxo da bile, colestiramina para ajudar a eliminar o excesso de ácidos biliares, e rifaximina para evitar infecções no sistema biliar.\n\n**Como ele está agora**  \nCom o tratamento, os exames do fígado melhoraram bastante e a saúde dele está estável. Até agora, ele não precisou passar por um transplante de fígado. Os médicos continuam acompanhando para garantir que ele fique bem.",
+            "B3": "**Contexto Clínico**  \nUm homem de 26 anos apresentou um quadro persistente de pele e urina amareladas (icterícia) por mais de um ano, sem fatores desencadeantes claros. Inicialmente, exames de imagem identificaram múltiplas pedras nos ductos biliares, levando à cirurgia para remoção dessas pedras e da vesícula biliar. Contudo, os sintomas e a função hepática não melhoraram após o procedimento, motivando investigação mais aprofundada.\n\n**Principais Achados Diagnósticos**  \nExames avançados, incluindo colangiopancreatografia por ressonância magnética (MRCP), colonoscopia, biópsia hepática e sequenciamento genético do exoma completo, revelaram:  \n- Dilatação e estreitamento dos ductos biliares, com características compatíveis com colangite esclerosante primária (PSC), uma doença inflamatória crônica dos ductos biliares.  \n- Presença de colite ulcerativa (UC), uma inflamação crônica do cólon, localizada no íleo terminal e no hemicólon direito, associada à PSC (subtipo PSC-UC).  \n- Alterações histológicas no fígado indicativas de síndrome do ducto biliar em desaparecimento (VBDS), com fibrose (cicatrização) e perda significativa dos ductos biliares.  \n- Mutações genéticas heterozigóticas nos genes PKLR (relacionado ao metabolismo energético das células) e UGT1A1 (envolvido no processamento da bilirrubina), que podem contribuir para a doença hepática e colestase (retenção de bile).\n\n**Intervenções Terapêuticas**  \nApós a remoção endoscópica das pedras biliares, o paciente iniciou tratamento medicamentoso para controlar a colestase e a inflamação hepática:  \n- Ácido ursodeoxicólico (1000 mg/dia) e ácido obetichólico (10 mg/dia), que ajudam a melhorar o fluxo biliar e reduzir a inflamação.  \n- Colestiramina (8 g/dia), para adsorver o excesso de ácidos biliares e aliviar sintomas relacionados.  \n- Rifaximina (1,2 g/dia), um antibiótico que previne infecções no trato biliar.  \n- Mesalazina (2 g/dia), para controlar a inflamação intestinal causada pela colite ulcerativa.\n\n**Evolução e Prognóstico**  \nApós o início do tratamento, os exames laboratoriais mostraram melhora significativa nos parâmetros de função hepática, incluindo níveis de bilirrubina e enzimas hepáticas. A condição clínica do paciente permaneceu estável até o último acompanhamento, sem necessidade de transplante hepático até o momento. O manejo multidisciplinar e o monitoramento contínuo são essenciais para controlar a progressão da doença e prevenir complicações futuras."
+        }
+    },
+    {
+        "article": "Mulher de 60 anos, ex-fumante, com sobrepeso e artrite reumatoide em tratamento com metotrexato e golimumab. Ela tinha um histórico de remoção em bloco de um tumor pélvico, com ressecção do reto, reconstrução com anastomose colorretal e sacrectomia distal ao nível da quarta vértebra sacral (S4). A anatomia patológica correspondeu a uma formação quística multilocular de 22 x 8,5 cm. Os cortes histológicos evidenciaram uma parede de tecido fibroso com revestimento epitelial escamoso maduro ou colunar pseudoestratificado e infiltrados linfo-histiocíticos, vasos sanguíneos ectásicos e ocasionais estruturas glandulares com alterações de tipo reativo. Estes achados foram compatíveis com um teratoma quístico maduro.  Aos dois anos da remoção, apresentou desconforto a nível sacral. Solicitaram-se tomografia computadorizada e ressonância magnética que evidenciaram, ao nível das últimas vértebras sacrais, a presença de uma formação de partes moles heterogénea perto dos 60 mm de diâmetro, associada a rarefacção de planos gordos e escasso líquido adjacente. Realizou-se uma biopsia percutânea com agulha grossa, cujo resultado confirmou a recorrência de teratoma maduro. Após a estadificação, que não evidenciou doença sistémica, foi avaliada num comité multidisciplinar de tumores e foi indicada conduta cirúrgica com remoção em bloco. Realizou-se abordagem posterior, ressecando a cicatriz prévia, secção parcial de músculos glúteos e piramidais, secção sacral ao nível S2-S3, respeitando ambas as raízes S3, libertação do espaço pré-sacral e remoção da peça. A paciente evoluiu favoravelmente no pós-operatório. O estudo anatomopatológico macroscópico evidenciou uma formação tumoral de 7,8 x 6 x 4,5 cm aderida ao osso sacro. Ao corte, era predominantemente sólida, de consistência heterogénea com setores de aspeto friável, zonas quísticas com conteúdo líquido e gelatinoso e múltiplos focos de consistência cálcica. Os cortes histológicos mostraram o compromisso ósseo por estruturas glandulares neoplásicas com moderado pleomorfismo nuclear, formação de estruturas micropapilares, produção de mucina e zonas de necrose. Em alguns espaços quísticos da periferia reconheceu-se um epitélio colunar ciliado maduro. As margens cirúrgicas de remoção encontravam-se livres de compromisso neoplásico. As técnicas de imunomarcação foram positivas para CK20, calretinina, p53 e focalmente para CDX2, e negativas para CK7, WT-1, PAX8 e CA125. Estes achados foram compatíveis com recidiva de teratoma maduro com transformação somática maligna para um adenocarcinoma de tipo colorretal. Realizou-se uma videocolonoscopia que foi normal, confirmando assim o diagnóstico de transformação maligna de teratoma sacro. Permaneceu em controlo multidisciplinar. Após 24 meses livre de doença, apresentou deterioração do estado geral e rápida elevação de CA 19.9, pelo que se realizou PET/TC que evidenciou múltiplas imagens hipercaptantes a nível visceral, em partes moles e ósseas compatíveis com secundarismo. Por rápido deterioração funcional não pôde realizar tratamento sistémico e faleceu dois meses depois.\n",
+        "gold_summary": "O caso de uma mulher de 60 anos com histórico de ressecção em bloco de tumor pélvico pré-sacral, cuja anatomia patológica relatou teratoma maduro, foi apresentado. Após 2 anos, ela consultou por dor sacro-coccígea. Os estudos de imagem revelaram um tumor de 6 cm com comprometimento ósseo das últimas vértebras sacrais. Foi realizada uma biopsia com agulha grossa que relatou recorrência de teratoma maduro. Após estadiamento que não evidenciou doença sistêmica, foi avaliada em comitê multidisciplinar e foi indicada conduta cirúrgica. Foi realizada uma ressecção em bloco com sacrectomia distal ao nível de S3 e músculos circundantes. O estudo anatomopatológico relatou a presença de um teratoma maduro com transformação maligna, com componente de adenocarcinoma de tipo colorretal. As margens de ressecção estavam livres de tumor. Após uma nova avaliação multidisciplinar, foi decidida uma estratégia de controle. Ela permaneceu livre de doença por 24 meses, a partir dos quais apresentou deterioração geral associada à progressão da doença, falecendo 2 meses depois.\n",
+        "synthetic_summary": {
+            "B1": "Uma senhora de 60 anos teve um caroço grande na parte de baixo das costas. Os médicos tiraram esse caroço e viram que ele era um tipo que não faz mal. Dois anos depois, ela sentiu dor no mesmo lugar. Os exames mostraram que o caroço voltou e estava perto dos ossos. Os médicos fizeram uma cirurgia para tirar tudo de novo. Quando olharam o caroço tirado, viram que uma parte tinha ficado ruim. Depois da cirurgia, ela ficou bem por dois anos. Depois disso, ela ficou doente de novo e não conseguiu melhorar.",
+            "B2": "**O que aconteceu com a paciente**\n\nUma mulher de 60 anos teve um tumor grande na região pélvica, perto do osso sacro, que foi retirado por cirurgia. Esse tumor era um teratoma maduro, que é um tipo de tumor formado por vários tipos de células, geralmente benigno. Dois anos depois da cirurgia, ela sentiu dor na parte baixa das costas, perto do osso sacro.\n\n**O que os exames mostraram**\n\nExames de imagem, como tomografia e ressonância magnética, mostraram que o tumor voltou, com cerca de 6 centímetros, e estava afetando os ossos das últimas vértebras sacrais (ossos na base da coluna). Uma biópsia, que é quando retiram um pedaço do tumor para analisar, confirmou que o teratoma havia retornado.\n\n**O tratamento realizado**\n\nComo não havia sinais de que o tumor tinha se espalhado para outras partes do corpo, uma equipe de médicos de diferentes áreas decidiu que a melhor opção era uma nova cirurgia para retirar o tumor de uma vez só. Na operação, eles removeram parte do osso sacro e músculos ao redor para garantir que tirassem todo o tumor.\n\n**O que mostraram os exames após a cirurgia**\n\nO exame do tumor retirado revelou que parte dele havia se transformado em um câncer chamado adenocarcinoma, parecido com o câncer que pode aparecer no intestino. Felizmente, os médicos conseguiram remover todo o tumor, sem deixar células doentes nas bordas da cirurgia.\n\n**O que aconteceu depois**\n\nA paciente ficou bem e sem sinais de tumor por dois anos. Depois desse período, ela começou a piorar rapidamente, e exames mostraram que o câncer tinha se espalhado para outros órgãos e ossos. Infelizmente, devido à rápida piora, ela não pôde receber tratamentos para controlar a doença e faleceu dois meses depois.\n\n**Resumo final**\n\nEsse caso mostra que, mesmo um tumor geralmente benigno como o teratoma maduro pode voltar e, em alguns casos, se transformar em um câncer mais agressivo. Por isso, é importante o acompanhamento cuidadoso e o tratamento adequado para tentar controlar a doença.",
+            "B3": "**Contexto**  \nTrata-se de uma mulher de 60 anos, ex-fumante e com sobrepeso, portadora de artrite reumatoide em tratamento imunossupressor, que inicialmente foi submetida à remoção cirúrgica em bloco de um tumor pélvico pré-sacral. A cirurgia incluiu ressecção do reto, reconstrução colorretal e sacrectomia distal ao nível da quarta vértebra sacral (S4). A análise do tecido removido revelou um teratoma quístico maduro, um tipo de tumor benigno composto por diferentes tipos de tecido, como epitélio escamoso e colunar, com sinais inflamatórios e vasos sanguíneos dilatados.\n\n**Principais Achados**  \nDois anos após a cirurgia, a paciente apresentou desconforto na região sacral. Exames de imagem, incluindo tomografia computadorizada e ressonância magnética, identificaram uma lesão heterogênea de aproximadamente 6 cm nas últimas vértebras sacrais, com sinais de comprometimento ósseo e alterações nos tecidos adjacentes. A biópsia por agulha grossa confirmou a recorrência do teratoma maduro. Após a exclusão de doença em outras partes do corpo (estadiamento negativo para doença sistêmica), a paciente foi discutida em um comitê multidisciplinar, que indicou nova cirurgia.\n\nNa intervenção cirúrgica, foi realizada ressecção em bloco da lesão, incluindo sacrectomia ao nível das vértebras S2-S3 e retirada parcial dos músculos glúteos e piramidais. O exame macroscópico da peça revelou um tumor sólido e heterogêneo, com áreas quísticas e focos calcificados aderidos ao osso sacro. A análise microscópica identificou, além do teratoma maduro, transformação maligna em adenocarcinoma com características semelhantes ao câncer colorretal, incluindo produção de mucina, pleomorfismo celular (variação no tamanho e forma das células) e necrose. As margens cirúrgicas estavam livres de tumor, indicando remoção completa da lesão. Imunohistoquímica (técnica que detecta proteínas específicas) confirmou o diagnóstico, com marcadores típicos do adenocarcinoma colorretal positivos e outros negativos. Colonoscopia posterior não revelou tumor primário no intestino, reforçando que a malignização ocorreu dentro do teratoma sacral.\n\n**Interpretação Clínica**  \nEste caso ilustra a rara transformação maligna de um teratoma maduro pré-sacral em adenocarcinoma, um tipo de câncer agressivo. A paciente teve inicialmente um bom controle da doença após a segunda cirurgia, permanecendo sem sinais de tumor por dois anos. No entanto, posteriormente, apresentou piora clínica rápida associada a elevação do marcador tumoral CA 19-9, indicando progressão da doença. Exames de PET/CT mostraram múltiplas metástases em órgãos internos, tecidos moles e ossos.\n\n**Próximos Passos e Desfecho**  \nDevido à rápida deterioração do estado geral, a paciente não pôde receber tratamento sistêmico (como quimioterapia) e faleceu dois meses após a detecção da recidiva metastática. Este caso destaca a importância do acompanhamento rigoroso após ressecção de teratomas maduros, especialmente quando há transformação maligna, e a complexidade do manejo multidisciplinar em tumores raros com comportamento agressivo."
+        }
+    },
+    {
+        "article": "Os prontuários de pacientes diagnosticados com miotonia congênita, estudados e acompanhados na consulta de neurologia pediátrica em um hospital de terceiro nível entre os anos de 2015 e 2020, foram revisados. Os critérios de inclusão foram apresentar um diagnóstico clínico – miotonia, fenômeno de aquecimento (warm-up), padrão eletromiográfico característico e/ou histórico familiar – e/ou um diagnóstico molecular (mutação no gene CLCN1). Os sinais e sintomas clínicos, bem como os resultados das explorações complementares e a mutação genética encontrada, foram recolhidos mediante a revisão da história clínica. Recolheram-se variáveis demográficas (idade e sexo), curso da doença (idade de início, sintomas e sinais, tempo transcorrido até o diagnóstico e evolução clínica), antecedentes familiares e avaliação da resposta ao tratamento.\n\nCinco casos foram identificados com diagnóstico clínico de miotonia congênita (três com doença de Becker e dois com doença de Thomsen). A incidência em relação ao número de nascimentos foi estimada em 1:15.000 recém-nascidos para os casos com fenótipo Becker e 1:21.000 recém-nascidos para os fenótipos Thomsen.\n\nA maioria dos nossos pacientes era do sexo feminino, e o sexo masculino foi o único a começar antes dos seis anos. A clínica inicial incluiu miotonia nos membros inferiores em quatro dos cinco pacientes e nos membros superiores também em todos, exceto um. A idade no início variou de 22 meses a 12 anos, com uma mediana de 6 anos. O diagnóstico genético foi realizado em todos os casos aproximadamente dois anos após o início, e a família de uma paciente se recusou a fazê-lo. Todos apresentaram piora com o frio, mas o fenômeno de aquecimento, apenas aqueles com o fenótipo de Becker.\n\nOs pacientes afetados por miotonia congênita recessiva apresentaram alguma progressão. Como antecedentes familiares, destaca-se que as pacientes 2 e 3 eram irmãs, sem que os pais apresentassem qualquer clínica, e que a mãe da paciente 1 apresentava uma clínica leve duvidosa com o frio. A paciente que rejeitou o estudo tinha antecedentes de miotonia no ramo materno.\n\nOs exames de sangue não mostraram aumento da creatina quinase em nenhum dos pacientes. O eletromiograma foi anormal em todos os pacientes, exceto no primeiro, com 2,8/12 anos de idade. O teste não foi repetido, pois não foi considerado necessário.\n\nO tratamento mais usado inicialmente foi a oxcarbacepina (nos pacientes afetados pela forma recessiva), com boa resposta em geral. No caso 2, perdeu eficácia com o tempo e iniciou-se mexiletina. O paciente 4 iniciou vários fármacos sem sucesso por perda de eficácia ou por efeitos secundários. O paciente 5 rejeitou tratamento por apresentar uma clínica leve.\n\nO paciente 1 apresentou uma mutação provavelmente patogênica não descrita previamente (CLCN1: c.824T>C), herdada de sua mãe. Os casos 1 a 3 apresentaram fenótipo Becker, com mutações em heterozigose composta, e os casos 4 e 5 apresentaram fenótipo Thomsen. O caso 5 recusou o estudo genético.\n",
+        "gold_summary": "Os prontuários de pacientes diagnosticados com miotonia congênita e estudados e acompanhados na consulta de neurologia pediátrica em um hospital de terceiro nível entre os anos de 2015 e 2020 foram revisados. Variáveis demográficas (idade e sexo), curso da doença (idade de início, sintomas e sinais, tempo transcorrido até o diagnóstico e evolução clínica), antecedentes familiares e avaliação da resposta ao tratamento foram coletados. Cinco casos foram identificados com diagnóstico clínico de miotonia congênita (três com doença de Becker e dois com doença de Thomsen). A incidência em relação ao número de nascimentos foi estimada em 1:15.000 recém-nascidos para os casos com fenótipo Becker e em 1:21.000 recém-nascidos para os fenótipos Thomsen. Encontramos uma mutação provavelmente patogênica não descrita previamente (CLCN1: c.824T>C).\n",
+        "synthetic_summary": {
+            "B1": "Cinco crianças tinham um problema que fazia os músculos ficarem durinhos. Esse problema é muito raro e aparece em poucas crianças. Algumas crianças tinham um tipo e outras tinham outro tipo. Os médicos estudaram o que aconteceu com elas e como elas melhoraram com remédios. Eles também acharam uma mudança no corpo que nunca tinham visto antes. Tudo isso ajuda os médicos a entender melhor essa doença.",
+            "B2": "**O que foi estudado**\n\nOs médicos revisaram os casos de cinco crianças que tinham uma doença chamada miotonia congênita. Essa doença afeta os músculos, fazendo com que eles fiquem rígidos e difíceis de mexer. Os pacientes foram acompanhados entre 2015 e 2020 em um hospital especializado em neurologia pediátrica.\n\n**Quem foram os pacientes**\n\nEntre os cinco casos, três tinham um tipo chamado doença de Becker e dois tinham outro tipo chamado doença de Thomsen. Essas duas formas são parecidas, mas têm algumas diferenças nos sintomas e na genética. A doença de Becker apareceu em cerca de 1 a cada 15.000 recém-nascidos, e a de Thomsen em 1 a cada 21.000.\n\n**Principais descobertas**\n\nA maioria dos pacientes era menina, mas os meninos começaram a apresentar sintomas mais cedo, antes dos seis anos. Os sintomas começaram entre 22 meses e 12 anos de idade, com uma média de 6 anos. Todos os pacientes pioravam quando estavam com frio, e só os que tinham a doença de Becker melhoravam um pouco ao se aquecerem.\n\nOs exames mostraram que todos tinham alterações nos músculos, confirmadas por um teste chamado eletromiograma, que mede a atividade elétrica dos músculos. Nenhum deles teve aumento de uma substância chamada creatina quinase, que normalmente indica dano muscular.\n\n**Genética e tratamento**\n\nOs médicos encontraram uma mutação genética nova, que pode causar a doença, em um dos pacientes. Essa mutação nunca tinha sido descrita antes. Os pacientes com a doença de Becker tinham mutações diferentes, chamadas heterozigose composta, e os com a doença de Thomsen tinham outras mutações.\n\nO tratamento mais usado foi um remédio chamado oxcarbazepina, que ajudou a maioria dos pacientes. Em um caso, esse remédio parou de funcionar e foi trocado por outro chamado mexiletina. Um paciente tentou vários remédios, mas não teve sucesso por causa dos efeitos colaterais. Outro paciente com sintomas leves preferiu não fazer tratamento.\n\n**O que isso significa**\n\nEste estudo ajuda a entender melhor a miotonia congênita, mostrando como os sintomas aparecem, como a doença evolui e como os tratamentos funcionam. Também descobriu uma mutação genética nova, que pode ajudar no diagnóstico e no desenvolvimento de tratamentos no futuro.",
+            "B3": "**Contexto**  \nEste estudo revisou os prontuários de pacientes diagnosticados com miotonia congênita, uma doença neuromuscular rara que causa dificuldade no relaxamento dos músculos após a contração. Os pacientes foram acompanhados em uma consulta de neurologia pediátrica de um hospital de alta complexidade entre 2015 e 2020. Para fazer parte do estudo, os pacientes precisavam apresentar sinais clínicos típicos, como miotonia (rigidez muscular), o fenômeno de aquecimento (melhora da rigidez após repetição do movimento), padrões específicos no exame eletromiográfico (que avalia a atividade elétrica dos músculos) e/ou histórico familiar, além de confirmação genética por mutação no gene CLCN1, responsável pela doença.\n\n**Principais Achados**  \nForam identificados cinco casos de miotonia congênita: três com a forma conhecida como doença de Becker (forma recessiva) e dois com a doença de Thomsen (forma dominante). A incidência estimada foi de aproximadamente 1 caso para cada 15.000 nascimentos na forma de Becker, e 1 para cada 21.000 nascimentos na forma de Thomsen. A maioria dos pacientes era do sexo feminino, embora os meninos tenham apresentado início dos sintomas antes dos seis anos de idade. Os sintomas iniciais mais comuns foram rigidez muscular nos membros inferiores e superiores, com idade de início variando entre 22 meses e 12 anos (mediana de 6 anos). Todos os pacientes relataram piora da rigidez com o frio, mas apenas aqueles com a forma de Becker apresentaram melhora com o fenômeno de aquecimento.\n\nDo ponto de vista genético, todos os pacientes realizaram o exame aproximadamente dois anos após o início dos sintomas, exceto uma paciente que recusou o estudo. Foi identificada uma mutação no gene CLCN1 (c.824T>C) que provavelmente é patogênica e ainda não havia sido descrita na literatura. Os pacientes com fenótipo Becker apresentaram mutações em heterozigose composta (duas mutações diferentes em cada cópia do gene), enquanto os pacientes com fenótipo Thomsen apresentaram mutações dominantes. Em um caso, a mutação foi herdada da mãe, que apresentava sintomas leves relacionados ao frio.\n\nOs exames laboratoriais, como a dosagem de creatina quinase (enzima muscular), estavam normais em todos os pacientes. O eletromiograma mostrou alterações típicas da doença em quase todos os casos, exceto em um paciente muito jovem, no qual o exame não foi repetido por não ser considerado necessário.\n\n**Interpretação Clínica**  \nA miotonia congênita apresenta variações clínicas e genéticas que influenciam o início, a progressão e a resposta ao tratamento. A forma de Becker tende a apresentar piora progressiva dos sintomas, enquanto a forma de Thomsen pode ter manifestações mais leves. O fenômeno de aquecimento é um sinal importante para diferenciar os tipos. A resposta ao tratamento medicamentoso, principalmente com oxcarbacepina, foi geralmente boa nos pacientes com forma recessiva, embora em alguns casos tenha sido necessária a troca para outros medicamentos, como a mexiletina, devido à perda de eficácia ou efeitos colaterais. Um paciente com sintomas leves optou por não iniciar tratamento.\n\n**Próximos Passos**  \nEste estudo reforça a importância do diagnóstico clínico e genético na miotonia congênita para orientar o manejo adequado. A identificação de mutações novas, como a variante c.824T>C no gene CLCN1, amplia o conhecimento sobre a doença e pode contribuir para futuros avanços no diagnóstico molecular. O acompanhamento contínuo dos pacientes é fundamental para monitorar a evolução dos sintomas e ajustar o tratamento conforme necessário. Além disso, o estudo dos antecedentes familiares ajuda a compreender a herança genética e a orientar aconselhamento genético para as famílias afetadas."
+        }
+    },
+    {
+        "article": "Descrevemos uma mulher de 25 anos de idade diagnosticada com AD desde a infância e subsequente início de vitiligo lentamente progressivo aos 16 anos. No exame inicial, a paciente apresentou xerosis cutânea difusa, pápulas excoriadas e placas nas costas, e lesões eritematosas liquenificadas nos membros superiores e dorso das mãos com um Eczema Area and Severity Index (EASI) de 18. A paciente relatou coceira intensa (Número Rating Scale [NRS] = 10). Maculas acromáticas confluentes sugestivas de vitiligo também estavam presentes nos cotovelos e no rosto, predominantemente na região da pálpebra, bilateralmente. A paciente também apresentou múltiplas maculas acromáticas de forma irregular no pescoço, tronco e dorso das mãos, e manifestações hipopigmentadas iniciais na região axilar esquerda e joelho esquerdo com um Vitiligo Area Scoring Index (VASI) de 0.45. Ambas as condições da pele tiveram um impacto na sua qualidade de vida, resultando num Dermatology Life Quality Index (DLQI) de 17.\n\nOs tratamentos anteriores para AD incluíram corticosteroides tópicos e sistémicos, inibidores tópicos de calcineurina, anti-histamínicos e um curto período de ciclosporina, que foi descontinuado devido a intolerância. O tratamento anterior para vitiligo incluiu tratamento de curto prazo com corticosteroides tópicos e sistémicos no início da doença e, durante os primeiros 2 anos, sem resultados. Posteriormente, tacrolimus, um inibidor tópico de calcineurina, foi usado durante vários anos após um regime de manutenção por impulsos pró-ativos após um período de indução inicial, produzindo benefícios terapêuticos mínimos. Antioxidantes e produtos à base de vitaminas foram também usados como terapias adjuvantes. Por razões logísticas, o paciente recusou a fototerapia.\n\nDada a coexistência de AD e vitiligo, e considerando os potenciais benefícios adicionais, a terapia sistémica com upadacitinib 15 mg diariamente foi iniciada após avaliações médicas e laboratoriais para excluir a gravidez e outras contraindicações. Com base na indicação aprovada de upadacitinib para AD, optamos por iniciar o tratamento com vista a alcançar a menor dose eficaz.\n\nFoi observada uma melhora progressiva da AD após as primeiras semanas de tratamento com remissão clínica na semana 16 (EASI 0; NRS 0) associada a uma melhora da qualidade de vida (DLQI 0). Ao mesmo tempo, foi observada uma melhora clara do vitiligo com repigmentação completa das áreas acromáticas no pescoço, tronco, costas das mãos e cotovelos (Fig. 1b), e repigmentação parcial mas significativa das manchas acromáticas da região das pálpebras (Fig. 2b) (VASI = 0.25). Foi alcançada uma remissão quase completa do vitiligo na semana 28 de tratamento e foi mantida até 1 ano de acompanhamento, sem efeitos colaterais exceto um ligeiro agravamento da acne, facilmente controlado com terapias tópicas.\n",
+        "gold_summary": "Descrevemos uma mulher de 25 anos de idade, diagnosticada com DA desde a infância e subsequente aparecimento de vitiligo lentamente progressivo aos 16 anos de idade. Iniciou-se uma terapia sistémica com o inibidor de JAK1, upadacitinib 15 mg diariamente, após uma avaliação médica e laboratorial para excluir a gravidez e outras contraindicações. Observou-se uma melhoria progressiva da DA após as primeiras semanas de tratamento com remissão clínica na semana 16. Ao mesmo tempo, observou-se uma clara melhoria do vitiligo com uma remissão quase completa alcançada na semana 28 de tratamento.\n",
+        "synthetic_summary": {
+            "B1": "Uma mulher jovem tinha dois problemas na pele desde pequena. Um problema fazia a pele ficar muito seca e coçar. O outro problema fazia algumas partes da pele perderem a cor.\n\nEla começou a tomar um remédio novo, uma vez por dia. Antes, os médicos fizeram exames para ter certeza que o remédio era seguro para ela.\n\nDepois de algumas semanas, a pele seca e a coceira melhoraram muito. Depois de alguns meses, as manchas sem cor também melhoraram bastante.\n\nEla ficou muito melhor e não teve problemas graves com o remédio.",
+            "B2": "**Caso de uma jovem com problemas de pele**\n\nEsta é a história de uma mulher de 25 anos que tem dois problemas de pele: dermatite atópica (DA) e vitiligo. A dermatite atópica é uma doença que causa coceira e manchas vermelhas na pele, e ela teve isso desde criança. O vitiligo apareceu quando ela tinha 16 anos e faz com que algumas áreas da pele percam a cor, ficando brancas.\n\n**Tratamento com um remédio novo**\n\nPara ajudar, os médicos começaram a dar a ela um remédio chamado upadacitinibe, que é um tipo de medicamento que age dentro das células para controlar a inflamação. Antes de começar, fizeram exames para garantir que ela poderia usar o remédio com segurança.\n\n**Resultados do tratamento**\n\nDepois de algumas semanas usando o remédio, a dermatite atópica melhorou bastante, e em 16 semanas ela não sentia mais coceira nem tinha manchas vermelhas. Ao mesmo tempo, o vitiligo também começou a melhorar, com as manchas brancas ficando menores e algumas áreas voltando a ter cor. Após 28 semanas, a maioria das manchas de vitiligo quase desapareceu.\n\n**O que isso significa**\n\nEsse caso mostra que o upadacitinibe pode ajudar não só na dermatite atópica, mas também no vitiligo, melhorando a pele e a qualidade de vida da paciente. O tratamento foi seguro, com poucos efeitos colaterais leves que foram fáceis de controlar.",
+            "B3": "**Contexto**  \nEste relato descreve o caso de uma mulher de 25 anos que convive desde a infância com dermatite atópica (DA), uma condição inflamatória crônica da pele caracterizada por coceira intensa e lesões cutâneas. Aos 16 anos, ela desenvolveu vitiligo, uma doença autoimune que causa a perda progressiva da pigmentação da pele, resultando em manchas claras. Ambas as condições afetavam significativamente sua qualidade de vida.\n\n**Principais Achados**  \nNo início do acompanhamento, a paciente apresentava lesões típicas de dermatite atópica, incluindo pele seca e placas inflamadas, com um índice de gravidade (Eczema Area and Severity Index - EASI) de 18, indicando doença moderada a grave. O vitiligo manifestava-se por manchas acromáticas (sem pigmento) em várias áreas do corpo, incluindo rosto, cotovelos, pescoço e mãos, com um índice de extensão da doença (Vitiligo Area Scoring Index - VASI) de 0,45. A coceira era intensa, e o impacto na qualidade de vida, medido pelo Dermatology Life Quality Index (DLQI), era alto (17 pontos).\n\nTratamentos prévios para a dermatite atópica incluíram corticosteroides tópicos e sistêmicos, inibidores tópicos de calcineurina, anti-histamínicos e ciclosporina, esta última suspensa por intolerância. Para o vitiligo, foram utilizados corticosteroides e tacrolimus tópicos, além de antioxidantes e vitaminas, porém com resultados limitados. A paciente recusou fototerapia por questões logísticas.\n\n**Interpretação Clínica**  \nDiante da coexistência das duas doenças e da necessidade de um tratamento eficaz, foi iniciada a terapia sistêmica com upadacitinib, um inibidor seletivo da enzima JAK1 (Janus quinase 1), na dose diária de 15 mg. Este medicamento é aprovado para o tratamento da dermatite atópica e atua modulando a resposta inflamatória do sistema imunológico.\n\nApós as primeiras semanas de tratamento, houve uma melhora progressiva da dermatite atópica, com remissão completa dos sintomas na semana 16 (EASI 0; coceira ausente; DLQI 0). Paralelamente, observou-se uma melhora significativa do vitiligo, com repigmentação total das manchas em pescoço, tronco, mãos e cotovelos, e repigmentação parcial, porém importante, nas pálpebras. Na semana 28, a remissão do vitiligo era quase completa, e os resultados foram mantidos até um ano de acompanhamento. O tratamento foi bem tolerado, com apenas um leve agravamento da acne, controlado com terapias tópicas.\n\n**Próximos Passos**  \nEste caso sugere que o upadacitinib pode ser uma opção terapêutica promissora para pacientes com dermatite atópica e vitiligo coexistentes, especialmente quando outras terapias convencionais falharam ou foram mal toleradas. A resposta favorável tanto da inflamação da pele quanto da repigmentação indica que a modulação da via JAK1 pode atuar em mecanismos comuns a ambas as doenças autoimunes. Estudos clínicos adicionais são necessários para confirmar a eficácia e segurança do upadacitinib no tratamento do vitiligo."
+        }
+    },
+    {
+        "article": "O paciente era um homem japonês de 59 anos de idade com um histórico de 28 anos de diabetes tipo 1. Ele visitou nosso hospital mensalmente para o tratamento da diabetes com terapia intensiva empregando injeções de insulina de múltiplas doses. Sua altura e peso corporal foram de 168 cm e 52 kg (índice de massa corporal: 18,4 kg/m2), respectivamente. Ele apresentou depleção da secreção de insulina (nível de peptídeo C no soro abaixo do limite de detecção), de modo que seus níveis de glicose no sangue flutuaram severamente, e seu nível de hemoglobina A1c (HbA1c) foi de cerca de 9,0%, apesar da terapia intensiva com insulina. Ele foi diagnosticado com regurgitação aórtica crônica grave (grau III) assintomática 16 anos antes da apresentação atual, mas recusou o acompanhamento para a AR. Ele nunca foi submetido a cirurgia nem ao implante de qualquer dispositivo protético.\n\nOito dias após a sua visita regular ao hospital, ele visitou uma clínica de emergência a queixar-se de dificuldade respiratória e tinha uma febre acima de 38℃. Até esse dia, ele não tinha notado qualquer febre, calafrios, fraqueza, ou quaisquer outros sintomas. A sua pressão arterial e pulsação eram de 192/82 mmHg e 118/min, respetivamente. Ele apresentou ortopneia, e a sua saturação de oxigénio (SpO2) era de 80%. Ele foi transportado para o departamento de emergência do nosso hospital. Um exame físico revelou um murmúrio sistólico de Levine 3/6, embora o seu murmúrio cardíaco não tivesse sido verificado em visitas regulares ao hospital. Não foram reconhecidos achados físicos sugestivos de IE, tais como nódulos de Osler, lesões de Janeway, ou petéquias conjuntivais. A sua contagem de glóbulos brancos (WBC) estava significativamente aumentada para 20,800 /μL, e a sua proteína C-reativa (CRP) estava elevada para 6.06 mg/dL. A creatina fosfocinase MB sérica estava dentro do intervalo normal, a 6.0 IU/L, e a troponina T era negativa. A radiografia de tórax mostrou congestão pulmonar com dilatação cardíaca (relação cardiotorácica: 55%). A eletrocardiografia revelou elevação do ST em V1-V4, mas a ecocardiografia de emergência não revelou disfunção da contractilidade cardíaca. Ele foi diagnosticado com insuficiência cardíaca aguda devido a doença valvular, e foi iniciado o tratamento com ventilação positiva não invasiva e nitratos.\n\nApós a admissão hospitalar, um exame detalhado por ecocardiografia transtorácica mostrou regurgitação aórtica grave, regurgitação mitral grave e uma vegetação móvel na válvula mitral. A ecocardiografia transesofágica revelou uma vegetação móvel de 16,5 x 6 mm na folha anterior da válvula mitral e uma vegetação não móvel de 11,2 x 5 mm na cúspide não coronária da válvula aórtica. Estes achados levantaram fortes suspeitas de NVC. Neste caso, a tomografia computadorizada (TC) e a ressonância magnética da cabeça não revelaram infarto cerebral ou hemorragia, embora tenha sido detetada uma vegetação móvel.\n\nAo rever o curso clínico até à hospitalização, notamos que na visita quatro meses antes da admissão, a contagem de glóbulos brancos (GB) tinha sido ligeiramente elevada. No mês seguinte, o nível de albumina (Alb) tinha diminuído para 3,0 g/dL, e o nível de hemoglobina (Hb) tinha mostrado um declínio gradual ao longo dos 2 meses anteriores à admissão. Durante este período, ele tinha perdido 4 kg. Foi realizada uma esofagogastroduodenoscopia e uma TAC de corpo inteiro, mas não foram detetadas anomalias. Um mês depois, ele tinha recuperado algum peso, e os resultados laboratoriais tinham quase normalizado, exceto por um nível de CRP ligeiramente elevado (0,54 mg/dL). Na última visita (8 dias antes da admissão), a contagem de glóbulos brancos (GB) tinha novamente aumentado para 9300/μL, enquanto o nível de Hb e Alb tinha novamente diminuído para 13,1 g/dL e 3,0 g/dL, respetivamente. Além disso, o nível de CRP tinha aumentado para 4,18 mg/dL. Nessa altura, a sua pressão arterial diastólica tinha mostrado um declínio óbvio. Até então, ele não tinha tido febre ou quaisquer sintomas além da perda de peso. Suspeitamos de doenças de origem infecciosa e/ou maligna e iniciámos exames abrangentes para identificar a origem dos seus achados clínicos.\n\nApós o tratamento da insuficiência cardíaca ter sido iniciado, os seus sintomas clínicos mostraram uma rápida melhoria, e a sua estabilidade hemodinâmica foi mantida durante as primeiras seis horas. Inicialmente, recebeu uma terapia antibiótica intravenosa empírica consistindo em 12 g/dia de sulbactam de ampicilina (ABPC/S) e 120 mg/dia de gentamicina (GM). Três conjuntos de cultura de sangue foram obtidos na admissão, e todos foram positivos para S. warneri [concentração inibitória mínima (MIC) para ABPC/S ≤8 μg/mL; MIC para GM ≤1 μg/mL; MIC para cefazolin (CEZ) ≤2 μg/mL]. Assim, IE causada por este organismo foi diagnosticada.\n\nDe acordo com a diretriz clínica estabelecida pela Sociedade de Circulatório Japonesa, a cirurgia de emergência é geralmente recomendada para insuficiência cardíaca de NYHA III a IV ou cirurgia urgente para vegetação móvel de NVE superior a 10 mm e disfunção grave da válvula. Neste caso, no entanto, a sua insuficiência cardíaca foi melhorada com sucesso. Com base na diretriz, o risco de embolia foi considerado como tendo sido reduzido pela administração de uma terapia antibiótica apropriada. Além disso, o paciente tinha diabetes tipo 1, e o seu controlo glicémico foi tão pobre que estávamos preocupados que a cirurgia de válvula dupla fosse um procedimento de alto risco. Por conseguinte, planeámos uma cirurgia eletiva após um controlo suficiente tanto da infeção como da diabetes.\n\nCom base nos resultados da cultura de sangue, o regime de antibióticos foi mudado para 6 g/dia de CEZ. Um exame dentário detalhado não revelou anormalidades, como periodontite. Após quatro semanas de terapia antibiótica, ele foi submetido a terapia cirúrgica. A sua válvula aórtica foi encontrada a ser bicúspide, e os anéis aórticos e mitrais estavam intactos sem formação de abscesso. Grandes vegetações foram exentradas, e as válvulas aórticas e mitrais foram ambas substituídas por válvulas mecânicas. Ele não teve complicações pós-operatórias e foi dispensado no 22º dia após a operação sem embolia aparente. Ele não teve qualquer recorrência em mais de dois anos desde a operação.",
+        "gold_summary": "Um homem de 59 anos com diabetes tipo 1 apresentou insuficiência cardíaca. A ecocardiografia mostrou grandes vegetações nas válvulas mitral e aórtica. A cultura bacteriológica do sangue foi positiva para Staphylococcus warneri, um membro da família de estafilococos coagulase-negativos (CoNS). Ele foi diagnosticado com endocardite valvular nativa (NVE) induzida pelas bactérias residentes e, finalmente, foi submetido a substituição de válvula dupla. Retrospectivamente, ligeiras anormalidades laboratoriais e perda de peso que começaram quatro meses antes podem ter sido sinais de NVE. Ele não tinha histórico de terapias imunossupressoras ou de implante de dispositivo médico.\n",
+        "synthetic_summary": {
+            "B1": "Um homem de 59 anos estava doente no coração. Ele tinha diabetes, que é quando o corpo não controla bem o açúcar no sangue. O médico viu que duas partes do coração dele estavam com sujeira que não deveria estar lá. Essa sujeira era feita por bichinhos chamados bactérias.\n\nOs médicos fizeram um exame do sangue e acharam esses bichinhos. Eles disseram que o homem tinha uma doença no coração causada por esses bichinhos. Para ajudar, os médicos deram remédios e depois fizeram uma cirurgia para trocar as partes do coração que estavam doentes.\n\nAntes de ficar muito doente, o homem perdeu peso e teve alguns exames diferentes. Isso pode ter sido um sinal de que o coração dele estava começando a ter problema. Depois da cirurgia, ele ficou melhor e está bem até agora.",
+            "B2": "**O que aconteceu com o paciente**\n\nUm homem de 59 anos, que tinha diabetes tipo 1 há muito tempo, começou a sentir problemas no coração chamados insuficiência cardíaca. Isso significa que o coração dele não estava funcionando direito para bombear o sangue. Quando os médicos fizeram um exame chamado ecocardiografia, que usa ondas de som para ver o coração, eles encontraram grandes \"vegetações\". Vegetações são como pedaços de tecido infectado que ficam grudados nas válvulas do coração, que são as portas que controlam o fluxo do sangue. Essas vegetações estavam nas válvulas mitral e aórtica.\n\n**O que causou a infecção**\n\nOs médicos fizeram um exame do sangue para procurar germes e encontraram uma bactéria chamada Staphylococcus warneri. Essa bactéria faz parte de um grupo chamado estafilococos coagulase-negativos, que normalmente vivem no corpo, mas podem causar infecções quando entram no coração. Com isso, o paciente foi diagnosticado com uma doença chamada endocardite valvular nativa (NVE). Essa doença acontece quando as válvulas do coração, que são naturais do corpo (não artificiais), ficam infectadas.\n\n**Como foi o tratamento**\n\nO paciente recebeu remédios para combater a infecção e, depois de controlar a infecção e a diabetes, os médicos fizeram uma cirurgia para substituir as duas válvulas do coração que estavam doentes. A cirurgia foi bem-sucedida, e ele se recuperou sem problemas graves.\n\n**O que podemos aprender**\n\nAnalisando o caso, os médicos perceberam que, meses antes da internação, o paciente já apresentava sinais leves de problema, como perda de peso e mudanças em exames de sangue. Esses sinais podem ter sido os primeiros indícios da infecção no coração. É importante lembrar que ele não tinha passado por tratamentos que enfraquecem o sistema imunológico nem tinha dispositivos médicos implantados, o que mostra que a infecção aconteceu mesmo sem esses fatores de risco.",
+            "B3": "**Contexto**  \nUm homem japonês de 59 anos, com histórico de 28 anos de diabetes tipo 1 mal controlada, foi admitido com insuficiência cardíaca aguda. Ele apresentava regurgitação aórtica crônica grave diagnosticada 16 anos antes, mas sem acompanhamento regular para essa condição valvular. Nos meses anteriores à hospitalização, o paciente apresentou perda de peso, elevações discretas na contagem de glóbulos brancos, redução dos níveis de albumina e hemoglobina, além de aumento da proteína C-reativa (CRP), sugerindo um processo inflamatório ou infeccioso silencioso.\n\n**Principais Achados**  \nNa admissão, o paciente apresentava febre, dificuldade respiratória, pressão arterial elevada e saturação de oxigênio baixa. Exames laboratoriais indicaram leucocitose (aumento dos glóbulos brancos) e elevação significativa da CRP, marcadores de inflamação. Radiografia de tórax mostrou congestão pulmonar e dilatação cardíaca. A ecocardiografia transtorácica e transesofágica identificaram vegetações móveis grandes nas válvulas mitral e aórtica, confirmando a suspeita de endocardite valvular nativa (NVE). Culturas sanguíneas foram positivas para Staphylococcus warneri, uma bactéria da família dos estafilococos coagulase-negativos (CoNS), geralmente parte da flora normal da pele, mas capaz de causar infecção em condições específicas.\n\n**Interpretação Clínica**  \nO diagnóstico foi de endocardite infecciosa envolvendo as válvulas cardíacas nativas, causada por S. warneri. Essa infecção bacteriana das válvulas cardíacas levou à insuficiência cardíaca aguda. Os sinais laboratoriais e a perda de peso observados meses antes da hospitalização provavelmente representaram manifestações iniciais da infecção, que evoluiu de forma silenciosa e progressiva. O paciente não tinha histórico de uso de medicamentos imunossupressores nem de implantes de dispositivos cardíacos, fatores que geralmente aumentam o risco para esse tipo de infecção, o que torna o caso incomum.\n\n**Próximos Passos e Desfecho**  \nO paciente recebeu tratamento inicial com antibióticos intravenosos adequados, que controlaram a infecção e melhoraram a insuficiência cardíaca. Após quatro semanas de terapia antibiótica, foi realizada cirurgia para substituição das válvulas mitral e aórtica, que apresentavam vegetações extensas. Durante o procedimento, as válvulas foram removidas e substituídas por próteses mecânicas, sem complicações cirúrgicas ou pós-operatórias. O paciente teve alta hospitalar no 22º dia após a cirurgia e não apresentou recorrência da infecção em mais de dois anos de acompanhamento.\n\n**Resumo Final**  \nEste caso destaca a importância de considerar a endocardite valvular nativa como causa de sintomas inespecíficos, como perda de peso e alterações laboratoriais discretas, especialmente em pacientes com doenças cardíacas pré-existentes e diabetes. A identificação precoce e o tratamento adequado, incluindo terapia antibiótica e cirurgia valvular, são essenciais para o sucesso clínico e a prevenção de complicações graves."
+        }
+    },
+    {
+        "article": "Paciente e observação\nInformações relativas ao paciente (apresentação do paciente): trata-se de um jovem de 28 anos, solteiro, sem filhos, militar em atividade. Há 5 semanas, apresentava dores abdominais de instalação progressiva, mais acentuadas no epigástrio e hipocôndrio direito, seguidas, pouco tempo depois, por febre não quantificada, calafrios, suores profusos num contexto de anorexia e emagrecimento quantificado em 6 quilos. Note-se que o paciente não é alcoólico-tabagista, vacinado com BCG, não apresentando nenhum outro antecedente pessoal ou familiar contributivo.\n\nResultados clínicos: na admissão, o exame físico encontrou o paciente em estado geral alterado, asténico com um emagrecimento de 6 kg num mês. Um síndrome inflamatório com resposta sistémica clínica estava presente com os seguintes elementos: uma febre a 39,1°C, uma taquicardia (124 batimentos/min), uma polipneia (22 ciclos/min). O exame pulmonar e a exploração das áreas ganglionares superficiais estavam sem particularidades. A nível abdominal, uma sensibilidade moderada no hipocôndrio direito com uma hepatomegalia foi encontrada.\n\nCronologia: remonta a fevereiro de 2022 pela instalação de uma dor abdominal difusa com transtorno do trânsito intestinal com diarreia e constipação, tudo num contexto de conservação do estado geral com febre predominantemente noturna. Um tratamento sintomático foi instaurado sem sucesso. A evolução é marcada pela persistência da febre associada a uma anorexia e um emagrecimento progressivo de 12 quilos em três meses. Perante este transtorno do trânsito intestinal com febre inexplicável e a degradação do estado geral, o paciente foi admitido nas urgências para melhor investigação.\n\nDiagnóstico: desde a sua admissão, foram realizados exames que relataram uma síndrome infecciosa biológica, uma hiperleucocitose (17800 células/mm3) com predomínio neutrofílico (14000 células/mm3) e uma proteína C-reativa elevada a 323 mg/L.\n\nDiante de sua dor abdominal, a lipase e a troponina realizadas voltaram normais, respectivamente, 38 UI/L (VN: <3 78 UI/L) e 4 ng/L (VN: 2 a 16 ng/L). O balanço hepático estável com ALT (alanina amino-transferase) a 22 UI/L (VN: < 40UI/L), AST (aspartato amino-transferase) a 17 UI/L (VN: < 35UI/L), GGT (gama glutamil transferase) a 42 UI/L (VN: < 50UI/L), PAL (fosfatase alcalina) a 115 UI/L (VN: 40- 150 UI/L) e uma bilirrubinemia normal. A função hepática era normal com um nível de protrombina a 78% e uma albuminemia a 39 g/L. O ionograma sanguíneo e a função renal voltaram normais. A radiografia do tórax e a ecografia abdominal realizadas sem particularidades.\n\nCom uma procalcitonina positiva a 4,1 ng/L, um balanço infeccioso à procura do foco infeccioso foi iniciado, incluindo um exame citobacteriológico das urinas e das hemoculturas durante os picos febris a 39°C, que foram negativos. As serologias de hepatites virais B, C e VIH, bem como a serologia da sífilis realizada em hospitalização, foram todas negativas. A lactato desidrogenase (LDH) e a beta-2 microglobulina foram normais, respetivamente 231 UI/L e 2,28 mg/L. O GeneXpert à procura do Mycobactérium nestas peças biopsiadas foi negativo. O quantiféron voltou negativo. A pesquisa do Mycobactérium nas expectorações matinais de 3 dias consecutivos foi negativa.\n\nNo plano morfológico, um scanner toraco-abdomino-pélvico mostrou, ao nível do estádio abdominal, um fígado aumentado de tamanho (flecha hepática a 17 cm), sede de múltiplas lesões hipodensas tecidulares, arredondadas bem limitadas, não realçadas após injeção do produto de contraste, cujas mais volumosas se encontram no segmento I (21 x 16 mm) e no segmento V (36 x 27 mm). Ao nível dos estágios torácico e pélvico, não foi evidenciada qualquer lesão suspeita. As primeiras biopsias hepáticas obtidas por punção eco-guiada revelaram, ao exame histológico, lesões hepáticas fibro-inflamatórias subagudas, sem índice histológico de especificidade ou de malignidade.\n\nUma ressonância magnética hepática após a tomografia computadorizada objetivou um fígado dismórfico, sede de lesões em sinal heterogêneo T2, rodeado por uma parede em hipersinal T2, realçado na periferia após injeção do produto de contraste, cujas maiores dimensões se situam no segmento I (20 x 22 mm) e no segmento V (33 x 31 mm). Nenhuma adenoidite profunda foi objetivada, tanto na tomografia computadorizada como na ressonância magnética. Uma laparoscopia diagnóstica realizada nos nódulos hepáticos, o exame histológico encontrou granulomas epitelioides e gigantes, de tamanho variável, com necrose calcificada, a favor de uma tuberculose hepática.\n\nIntervenção terapêutica: o paciente foi submetido a tratamento antituberculoso de acordo com o protocolo padrão durante meses, a saber: Fase 1: quádrupla (Isoniazida + Rifampicina + Pirazinamida + Etambutol) em uma única tomada oral todas as manhãs em jejum durante 2 meses. Fase 2: biterapia (Isoniazida + Rifampicina) em uma única tomada oral todas as manhãs em jejum durante 4 meses\n\nSeguimento e resultados das intervenções terapêuticas: desde os primeiros dias do tratamento, uma boa resposta foi obtida com desaparecimento da síndrome inflamatória de resposta sistémica tanto a nível clínico como biológico. Ao fim de três meses de tratamento, um scanner hepático de controlo mostrou uma diminuição do número e do volume das lesões hepáticas.\n",
+        "gold_summary": "Este caso clínico relatado em um jovem marroquino, apresentando-se em um quadro de cólica hepática evoluindo há um mês associado a sinais frustres de imersão tuberculosa. Lesões nodulares hepáticas não específicas foram reveladas no scanner e na imagem por ressonância magnética (IRM) hepática. O diagnóstico de tuberculose hepática focal foi confirmado após análise anatomopatológica em biopsias dos nódulos hepáticos obtidos após uma laparoscopia. Após início do tratamento antibacteriano bem conduzido, uma boa melhora clínico-biológica foi obtida.\n",
+        "synthetic_summary": {
+            "B1": "Um jovem homem ficou com dor na barriga por um mês. Ele também teve febre e perdeu peso. Os médicos fizeram exames e viram que o fígado dele tinha algumas bolinhas estranhas.\n\nPara saber o que era, eles pegaram um pedacinho do fígado para olhar melhor. Descobriram que ele tinha uma doença chamada tuberculose no fígado. \n\nEle tomou remédios para essa doença e logo começou a melhorar. A dor e a febre sumiram, e o fígado ficou melhor também.",
+            "B2": "**O que aconteceu com o paciente**\n\nUm jovem de 28 anos começou a sentir dores na barriga, principalmente na parte superior direita, junto com febre, suor e perda de apetite. Ele também perdeu bastante peso em pouco tempo. Quando foi ao hospital, os médicos perceberam que ele estava muito fraco e com sinais de infecção no corpo, como febre alta e batimentos cardíacos acelerados.\n\n**O que os exames mostraram**\n\nOs exames de sangue indicaram uma infecção, mas não mostraram problemas comuns no fígado ou no pâncreas. A radiografia do tórax e o ultrassom da barriga não mostraram nada estranho. Porém, uma tomografia computadorizada (um exame que tira fotos detalhadas do corpo) mostrou que o fígado estava maior e tinha várias manchas que pareciam lesões. A ressonância magnética, outro exame de imagem, confirmou essas lesões no fígado.\n\nPara entender melhor o que era, os médicos fizeram uma laparoscopia, que é uma cirurgia pequena para olhar dentro do corpo e tirar pedaços dessas lesões para análise. O exame do tecido mostrou que o fígado tinha granulomas, que são grupos de células que aparecem quando o corpo tenta combater uma infecção, e indicaram que a causa era tuberculose no fígado.\n\n**O que isso significa**\n\nA tuberculose é uma doença causada por uma bactéria que normalmente ataca os pulmões, mas neste caso, ela afetou o fígado. Essa forma de tuberculose é rara e pode ser difícil de diagnosticar porque os sintomas são parecidos com outras doenças.\n\n**Como foi o tratamento**\n\nO paciente começou um tratamento com remédios específicos para tuberculose, que ele tomou por seis meses. Desde os primeiros dias, ele melhorou bastante, com a febre e os outros sintomas desaparecendo. Depois de três meses, exames mostraram que as lesões no fígado estavam menores.\n\n**Resumo final**\n\nEste caso mostra que a tuberculose pode afetar órgãos além dos pulmões, como o fígado. É importante fazer exames detalhados e, às vezes, uma pequena cirurgia para confirmar o diagnóstico. Com o tratamento correto, a recuperação é possível e rápida.",
+            "B3": "Contexto  \nEste relato descreve o caso de um jovem militar de 28 anos que apresentou, ao longo de cinco semanas, dores abdominais progressivas localizadas principalmente na região superior direita do abdômen, acompanhadas de febre alta, calafrios, suor intenso, perda de apetite e emagrecimento significativo (6 kg em um mês). O paciente não tinha antecedentes de álcool ou tabagismo, nem histórico familiar relevante, e estava vacinado contra tuberculose (vacina BCG).\n\nPrincipais Achados Clínicos e Exames  \nNa admissão hospitalar, o paciente encontrava-se debilitado, com febre de 39,1°C, frequência cardíaca acelerada (taquicardia) e respiração rápida (polipneia). O exame físico revelou sensibilidade moderada no hipocôndrio direito e aumento do fígado (hepatomegalia). Exames laboratoriais mostraram um quadro inflamatório intenso, com aumento dos glóbulos brancos, especialmente neutrófilos, e elevação marcante da proteína C-reativa, um marcador de inflamação. Outros exames, como enzimas pancreáticas, função hepática, radiografia de tórax e ultrassonografia abdominal, estavam normais ou sem alterações significativas.\n\nInvestigação Diagnóstica  \nDiante da febre persistente sem foco infeccioso claro, foram realizados exames específicos para tuberculose, incluindo testes sanguíneos (Quantiferon), pesquisa do bacilo em escarro e GeneXpert em amostras biopsiadas, todos negativos. A tomografia computadorizada (TC) do tórax, abdômen e pelve revelou um fígado aumentado com múltiplas lesões nodulares arredondadas, que não captavam contraste, sugerindo áreas de alteração tecidual. A ressonância magnética hepática confirmou essas lesões, mostrando características compatíveis com processos inflamatórios ou infecciosos.\n\nPara esclarecer o diagnóstico, foi realizada uma laparoscopia com biópsia dos nódulos hepáticos. O exame histológico revelou granulomas epitelioides e gigantes, estruturas formadas por células do sistema imunológico em resposta a infecções, com áreas de necrose calcificada, características típicas da tuberculose hepática focal.\n\nIntervenção e Evolução  \nO paciente iniciou tratamento antituberculoso padrão, que consiste em uma fase inicial de quatro medicamentos (Isoniazida, Rifampicina, Pirazinamida e Etambutol) por dois meses, seguida por dois medicamentos (Isoniazida e Rifampicina) por mais quatro meses. Desde os primeiros dias de terapia, houve melhora clínica significativa, com desaparecimento dos sinais inflamatórios e febre. Após três meses, exames de imagem mostraram redução no número e tamanho das lesões hepáticas.\n\nInterpretação Clínica  \nEste caso ilustra uma forma rara e localizada de tuberculose, afetando especificamente o fígado, sem envolvimento pulmonar ou outros órgãos. A apresentação clínica inespecífica, com dor abdominal e febre persistente, associada a lesões nodulares hepáticas, pode dificultar o diagnóstico. A confirmação por biópsia é fundamental para diferenciar a tuberculose de outras causas infecciosas ou neoplásicas. O tratamento adequado e precoce leva a uma recuperação satisfatória, como observado neste paciente.\n\nPróximos Passos  \nÉ importante manter acompanhamento clínico e radiológico para garantir a resolução completa das lesões e prevenir recidivas. Além disso, a investigação de possíveis focos tuberculosos em outros órgãos deve ser considerada, mesmo que inicialmente negativos, para um manejo integral do paciente. A conscientização sobre formas extrapulmonares de tuberculose é essencial para o diagnóstico precoce e tratamento eficaz."
+        }
+    },
+    {
+        "article": "Um paciente de 25 anos apresentou-se para uma consulta neurocirúrgica preocupado com a sua saúde. O seu histórico incluía um mergulho de cabeça numa piscina durante as férias, duas semanas antes. O mergulho resultou numa fratura da coluna cervical. O paciente foi submetido a uma cirurgia durante as férias. Estabilizou-se a coluna cervical por trás. O paciente usava um colar cervical e a ferida cirúrgica ainda não tinha sarado, com as suturas ainda não removidas. O paciente não demonstrou paresias e foi capaz de se mover por conta própria. Ele não tinha documentação médica detalhada ou relatórios de exames pré-operativos e pós-operativos. Na alta, foi-lhe dado um TAC pós-operativo incompleto da coluna cervical na forma de alguns filmes antigos que mostravam algumas das vistas, mas sem imagens digitais. O resumo da alta não continha a descrição detalhada necessária do tratamento fornecido, incluindo detalhes sobre o instrumento utilizado. Não foi possível contactar o pessoal do hospital ou os operadores, porque não responderam ao telefone ou aos e-mails e às mensagens de texto. Decidimos que deveria ser obtido um novo TAC da coluna cervical. Este revelou uma fratura atípica de enforcamento da coluna cervical: uma fratura da pars interarticularis C2 do lado esquerdo, deslocação da C2 contra a C3, fratura do corpo vertebral C2 com separação e deslocação anterior de uma parte do corpo vertebral C2. O paciente foi operado por abordagem posterior. Estabilizou-se a coluna cervical por trás. Os parafusos foram colocados corretamente nas massas laterais da C3. No entanto, dentro da vértebra C2, ambos os parafusos foram inicialmente colocados transpedicularmente, mas as suas extremidades não atingiram o corpo vertebral C2 ou as massas laterais da C1 e estenderam-se para a articulação C1-C2 esquerda e direita. As imagens de TAC do estado pós-cirúrgico inicial, realizadas noutro centro, revelaram que o paciente não podia realizar movimentos de rotação da cabeça, uma vez que os parafusos foram colocados dentro das articulações C1-C2. A estabilização anterior para evitar a deslocação da C2 contra a C3 também não foi realizada, e a estabilidade da coluna vertebral não foi assegurada. Após a análise das imagens de TAC da coluna vertebral, decidimos reoperar. A nossa intenção era restaurar os movimentos de rotação da cabeça, assegurando a estabilidade da coluna vertebral. Decidimos usar uma abordagem anterior e posterior. A primeira fase do procedimento, de uma abordagem posterior, consistiu na remoção dos parafusos de C2 bilateralmente, com as extremidades dos parafusos dentro das articulações C1-C2, seguida pela colocação, a partir da mesma abordagem, de parafusos mais curtos que terminaram dentro de C2, não atingindo assim as articulações C1-C2 e não bloqueando a rotação da cabeça. Antes do procedimento, não sabíamos que tipo de parafusos (fabricante) tinham sido usados originalmente. Foi revelado intraoperativamente que os parafusos eram de um tipo que também estava disponível no nosso hospital. Não mudámos a localização dos parafusos dentro das massas laterais C3, uma vez que foram implantados de forma adequada. Os parafusos C2-C3 foram então unidos bilateralmente com hastes longitudinais. Na segunda fase do procedimento, de uma abordagem anterior, realizámos uma discectomia C2/C3 e colocámos uma gaiola no espaço C2/C3, seguida pela colocação de um parafuso de pressão ao longo do corpo de C2 e do processo odontoide. Por fim, usamos uma placa cervical fixada com 4 parafusos para a estabilização C2-C3. O período pós-operativo decorreu sem quaisquer complicações. Para além da dor associada à ferida cirúrgica, não foram observados sintomas preocupantes, tais como disfagia ou rouquidão. Uma TAC de seguimento revelou aparências pós-operativas normais correspondentes às suposições pré-operativas. O paciente foi dispensado em casa num estado neurológico e geral bom. Uma TAC de seguimento funcional da coluna cervical, 8 semanas após o procedimento, também revelou aparências pós-operativas normais. Atualmente, o paciente tem aparências pós-operativas normais de flexão/extensão e de rotação da cabeça e a estabilidade da coluna cervical também foi preservada.\n",
+        "gold_summary": "Apresentamos um caso de fratura atípica de enforcamento causada por uma queda de cabeça em uma piscina e atingindo o fundo da piscina. O paciente havia sido submetido a uma cirurgia em outro centro, onde a estabilização posterior C2-C3 foi realizada. Devido à presença de parafusos nos espaços articulares C1-C2, o paciente não podia realizar movimentos rotacionais da cabeça. A estabilização anterior para evitar a luxação C2 contra C3 também não foi realizada, e a estabilidade espinal apropriada não foi assegurada. A nossa decisão de reoperar foi motivada, entre outros fatores, pela nossa intenção de restaurar os movimentos rotacionais da cabeça. A cirurgia de revisão foi realizada tanto por abordagem anterior como posterior. Após a cirurgia, o paciente foi capaz de rodar a cabeça enquanto mantinha a estabilidade da coluna cervical. O caso apresentado aqui representa não só um exemplo único de fratura atípica de C2, mas também destaca uma técnica de estabilização que forneceu a estabilidade necessária para uma fusão bem-sucedida. O método utilizado restaurou o movimento rotacional funcional da cabeça, preservando assim a qualidade de vida do paciente, que é de suma importância considerando a idade do paciente.\n",
+        "synthetic_summary": {
+            "B1": "Um homem machucou o pescoço ao mergulhar numa piscina. Ele fez uma cirurgia para consertar o pescoço. Mas os parafusos foram colocados de um jeito que ele não podia mexer a cabeça para os lados. Então, os médicos fizeram outra cirurgia. Eles tiraram os parafusos que atrapalhavam e colocaram outros no lugar certo. Depois disso, ele conseguiu mexer a cabeça e o pescoço ficou firme e seguro. Agora, ele pode viver bem e se mexer sem dor.",
+            "B2": "**O que aconteceu com o paciente**\n\nUm jovem de 25 anos sofreu uma fratura na parte superior do pescoço (coluna cervical) depois de mergulhar de cabeça numa piscina. Ele fez uma cirurgia num hospital diferente para tentar estabilizar essa parte do pescoço, colocando parafusos para segurar os ossos. Porém, os parafusos foram colocados de um jeito que bloqueou o movimento de rotação da cabeça, ou seja, ele não conseguia virar a cabeça para os lados como antes. Além disso, a cirurgia não garantiu que a coluna estivesse bem estável, o que poderia causar problemas.\n\n**O que os médicos fizeram depois**\n\nOs médicos decidiram fazer uma nova cirurgia para corrigir isso. Eles usaram duas abordagens: uma por trás do pescoço (posterior) e outra pela frente (anterior). Primeiro, retiraram os parafusos que estavam bloqueando a articulação entre as vértebras C1 e C2, que são as que permitem girar a cabeça. Depois, colocaram parafusos menores que não atrapalhassem esse movimento. Também reforçaram a estabilidade entre as vértebras C2 e C3 com hastes e parafusos. Na parte da frente do pescoço, removeram o disco entre C2 e C3 e colocaram uma espécie de \"gaiola\" para ajudar na fixação, além de uma placa com parafusos para manter tudo firme.\n\n**O que isso significa**\n\nDepois da segunda cirurgia, o paciente conseguiu mover a cabeça normalmente para os lados e a coluna ficou estável. Isso é muito importante para a qualidade de vida dele, especialmente porque é jovem. Esse caso mostra um tipo raro de fratura na vértebra C2 e também apresenta uma técnica cirúrgica que consegue estabilizar a coluna sem perder os movimentos naturais da cabeça. Assim, o paciente pode ter uma recuperação melhor e voltar a fazer suas atividades com mais conforto e segurança.",
+            "B3": "**Contexto**  \nEste relato descreve o caso de um paciente jovem de 25 anos que sofreu uma fratura incomum na segunda vértebra cervical (C2), conhecida como fratura atípica de enforcamento, após um mergulho de cabeça numa piscina. Inicialmente, o paciente foi submetido a uma cirurgia em outro hospital para estabilizar a coluna cervical pela parte de trás (abordagem posterior). No entanto, essa cirurgia não conseguiu garantir a estabilidade adequada da coluna nem preservar os movimentos normais da cabeça.\n\n**Principais Achados**  \nNa cirurgia inicial, os parafusos usados para fixar as vértebras foram colocados dentro das articulações entre a primeira e a segunda vértebra cervical (articulações C1-C2). Essa posição bloqueou os movimentos de rotação da cabeça, limitando significativamente a mobilidade do paciente. Além disso, não foi realizada a estabilização pela frente da coluna (abordagem anterior), o que permitiu que a segunda vértebra (C2) permanecesse deslocada em relação à terceira (C3), comprometendo a estabilidade da coluna cervical.\n\n**Interpretação Clínica**  \nA ausência de uma fixação adequada e a colocação incorreta dos parafusos resultaram em uma limitação funcional importante, com risco potencial para a segurança e qualidade de vida do paciente. A fratura atípica de C2, por sua complexidade e localização, exige uma abordagem cirúrgica cuidadosa para restaurar tanto a estabilidade da coluna quanto a mobilidade da cabeça, especialmente em pacientes jovens, para preservar sua funcionalidade a longo prazo.\n\n**Próximos Passos e Tratamento Realizado**  \nDiante dessas limitações, optou-se por uma reoperação combinando abordagens posterior e anterior. Na primeira etapa, pela parte de trás, os parafusos mal posicionados foram removidos e substituídos por parafusos mais curtos, que ficaram dentro da vértebra C2, evitando as articulações C1-C2 e, assim, permitindo a rotação da cabeça. Os parafusos já corretamente posicionados na vértebra C3 foram mantidos e conectados por hastes para garantir a fixação. Na segunda etapa, pela parte da frente da coluna, foi realizada a remoção do disco entre C2 e C3 (discectomia), seguida da colocação de uma estrutura de suporte (gaiola intervertebral) e de uma placa com parafusos para estabilizar firmemente essas vértebras.\n\n**Resultados e Prognóstico**  \nO pós-operatório transcorreu sem complicações significativas, com o paciente apresentando boa recuperação neurológica e geral. Exames de imagem realizados após a cirurgia confirmaram a estabilidade da coluna cervical e a preservação dos movimentos de flexão, extensão e rotação da cabeça. O paciente conseguiu recuperar a mobilidade funcional da cabeça, mantendo a estabilidade da coluna, o que é fundamental para sua qualidade de vida, especialmente considerando sua idade jovem.\n\n**Conclusão**  \nEste caso ilustra uma fratura rara e complexa da vértebra C2 e destaca a importância de uma técnica cirúrgica adequada para garantir tanto a estabilidade da coluna cervical quanto a preservação dos movimentos da cabeça. A abordagem combinada utilizada demonstrou ser eficaz para restaurar a função e proporcionar uma fusão vertebral segura, contribuindo para a recuperação e bem-estar do paciente."
+        }
+    },
+    {
+        "article": "Uma grávida de 29 anos de idade, V par IV (todas vivas, 3 partos vaginais espontâneos, e a última criança nasceu por cesariana devido a uma indução falhada 4 anos antes da gravidez atual) veio para um seguimento de ANC com uma idade gestacional de 32 semanas do seu LNMP.\n\nApós a recolha do histórico médico, descobriu-se que todos os seus filhos estavam saudáveis, com bom desempenho escolar e sem historial conhecido de distúrbios genéticos ou convulsões. Foi-lhe feito um exame com o Laboratório de Investigação de Doenças Venéreas (VDRL), antígeno de superfície da hepatite B (HBSag) e análise de urina, que foram todos negativos. Todas as linhas celulares no hemograma completo (CBC) eram normais, o seu grupo sanguíneo é A e o RH é positivo, de acordo com o hemograma completo (CBC), grupo sanguíneo e RH. Foi também realizado um exame de ultrassom obstétrico que mostrou uma análise anatómica normal de todas as partes do corpo do feto, exceto o coração. Foi feita uma avaliação ecocardiográfica fetal detalhada com os seguintes resultados: ambas as aurículas têm tamanho comparável e situs normal. Ambas as válvulas atrioventriculares e semilunares estão normalmente posicionadas com abertura e fecho normais. Ambos os ventrículos têm tamanho e contractilidade comparáveis; em 2D e fluxo de cor, o ventrículo esquerdo forma o ápice do coração sem qualquer defeito no septo ventricular. Mas nos músculos papilares do ventrículo esquerdo havia duas massas ecogênicas circunscritas, redondas, medindo 18,2 mm por 8,3 mm e 13,5 mm por 8,3 mm. Após a avaliação do trato de saída, tanto o LVOT (trato de saída do ventrículo esquerdo) como o RVOT (trato de saída do ventrículo direito) têm anatomia e função normais, utilizando a avaliação por ultrassom 2D e CF. De acordo com o achado do eco fetal, foi feito um diagnóstico de rabdomioma cardíaco. Como existe uma grande probabilidade de esclerose tuberosa no rabdomioma cardíaco, foram feitos exames neurológicos detalhados e outros exames do sistema para procurar outros sinais de esclerose tuberosa. Apesar de procurar outros sinais de esclerose tuberosa, não foi encontrado nenhum outro sinal para além do tumor. Teve um acompanhamento regular de ANC a partir das 32 semanas de gestação até às 39 semanas sem quaisquer complicações.\n\nNa idade gestacional de 39 semanas e 1 dia, foi submetida a uma cesariana por indicação de gravidez a termo e por pedido de repetição da cesariana, com o resultado de uma menina de 3200 gramas com uma pontuação APGAR de 10 e 10 nos minutos 1 e 5. Tanto a mãe como o recém-nascido tiveram um período pós-operatório tranquilo e foram dispensados no terceiro dia.\n\nApós o parto, o recém-nascido foi avaliado no 1º, 7º e 30º dias para qualquer regressão ou aumento da massa, aparecimento de lesões cutâneas ou convulsões. Todos os resultados dos exames físicos foram normais, e o tamanho da massa foi semelhante à avaliação antepartal.\n\nNo sétimo mês, a criança foi novamente avaliada e, após questionamento sobre o histórico, a criança estava desenvolvendo-se muito bem para a sua faixa etária. A criança foi examinada quanto a atraso no desenvolvimento neurológico e estava crescendo adequadamente para a sua idade. Um estudo de ecocardiografia realizado por um cardiologista pediátrico revelou massas hiperecóicas bem circunscritas em ambos os músculos papilares do ventrículo esquerdo, cada uma medindo 21,8 mm por 9,2 mm e 14,7 mm por 8,5 mm e não criando obstrução ao fluxo de entrada do ventrículo esquerdo.\n\nFoi obtido um histórico da família e foi realizado um exame físico com medidas antropométricas para avaliar a condição de desenvolvimento durante a avaliação do primeiro ano. A criança estava se desenvolvendo normalmente, como as outras crianças da mesma idade. Exceto pelo coração, todos os sistemas examinados foram notáveis. Um estudo de ecocardiografia revelou massas hiperecóicas bem circunscritas em ambos os músculos papilares do ventrículo esquerdo, sem aumento de tamanho e sem criar obstrução do fluxo de entrada do ventrículo esquerdo.\n",
+        "gold_summary": "Estamos relatando uma massa intracardíaca fetal isolada e assintomática (rabdomioma) que foi descoberta na 32ª semana de gestação e foi acompanhada como paciente ambulatorial até a 39ª semana mais um dia, quando foi realizada uma cesariana. Após o parto, a criança foi avaliada no 1º dia, 7º dia, 30º dia, 7º mês e 12º mês de idade. Após um check-up, o crescimento antropométrico e neurocomportamental da criança foi saudável. Exceto pelo tumor, que não estava crescendo nem diminuindo de tamanho, nenhum dos critérios de diagnóstico clínico para o complexo de esclerose tuberosa foram atendidos para esta criança até a idade de um ano.\n",
+        "synthetic_summary": {
+            "B1": "Um bebê tinha uma bolinha no coração quando estava na barriga da mãe. A bolinha não doía nem atrapalhava. A mamãe foi ao médico muitas vezes para ver como o bebê estava. O bebê nasceu de cesariana, bem forte e saudável. Depois do nascimento, os médicos olharam o bebê várias vezes. O bebê cresceu bem e brincou como outras crianças. A bolinha no coração ficou do mesmo tamanho e não cresceu. O bebê não teve outros problemas de saúde até fazer um ano. Tudo está bem com o bebê e a mamãe.",
+            "B2": "**O que foi encontrado no bebê antes do nascimento**\n\nDurante a gravidez, aos 32 semanas, os médicos fizeram um exame especial do coração do bebê e descobriram duas massas pequenas dentro do ventrículo esquerdo do coração. Essas massas são chamadas de rabdomiomas, que são tumores benignos, ou seja, não cancerosos. Eles não estavam causando problemas no funcionamento do coração. Como esses tumores podem estar ligados a uma doença chamada esclerose tuberosa, que afeta vários órgãos, os médicos fizeram vários exames para procurar sinais dessa doença, mas não encontraram nada.\n\n**O acompanhamento após o nascimento**\n\nA bebê nasceu de cesariana na 39ª semana, saudável e com boa pontuação no teste APGAR, que avalia a saúde do recém-nascido. Depois do nascimento, os médicos acompanharam a criança várias vezes: no 1º, 7º e 30º dia, depois no 7º e no 12º mês. Em todas essas avaliações, o tumor no coração não cresceu nem diminuiu, e a bebê estava se desenvolvendo normalmente, tanto no crescimento do corpo quanto no desenvolvimento do cérebro e das habilidades.\n\n**O que isso significa**\n\nAté o primeiro ano de vida, a criança não apresentou sinais da doença esclerose tuberosa, que poderia causar problemas mais sérios. O tumor no coração, apesar de estar presente, não atrapalhou o funcionamento do órgão nem o crescimento da criança. Por isso, os médicos continuam acompanhando para garantir que tudo continue bem. Esse caso mostra como é importante fazer exames detalhados durante a gravidez e o acompanhamento cuidadoso após o nascimento para cuidar da saúde do bebê.",
+            "B3": "Resumo Detalhado e Estruturado sobre Caso de Rabdomioma Cardíaco Fetal\n\nContexto  \nEste relato descreve o acompanhamento de uma gestante de 29 anos, com histórico obstétrico de quatro filhos vivos, que durante a 32ª semana de gravidez foi identificada uma massa no coração do feto por meio de ultrassonografia detalhada. A massa foi diagnosticada como rabdomioma cardíaco, um tumor benigno do músculo cardíaco frequentemente associado à esclerose tuberosa, uma doença genética que pode afetar múltiplos órgãos.\n\nPrincipais Achados  \n- O exame ecocardiográfico fetal revelou duas massas ecogênicas (visíveis ao ultrassom por refletirem ondas sonoras) bem delimitadas localizadas nos músculos papilares do ventrículo esquerdo, medindo aproximadamente 18,2 x 8,3 mm e 13,5 x 8,3 mm.  \n- A anatomia e função das demais estruturas cardíacas estavam normais, sem sinais de obstrução do fluxo sanguíneo.  \n- Exames laboratoriais maternos foram normais, sem sinais de infecções ou outras complicações.  \n- Considerando a associação frequente entre rabdomiomas cardíacos e esclerose tuberosa, foram realizados exames neurológicos e avaliações de outros sistemas para identificar possíveis manifestações da doença, mas nenhum outro sinal foi detectado durante a gestação.  \n- A gestação transcorreu sem complicações até a realização de cesariana eletiva na 39ª semana, resultando no nascimento de uma menina saudável, com peso adequado e boa adaptação neonatal (pontuação APGAR 10/10).  \n- Após o nascimento, o bebê foi acompanhado em consultas regulares no 1º, 7º, 30º dia, 7º e 12º meses de vida, com avaliações clínicas, neurológicas e ecocardiográficas.  \n- As massas cardíacas permaneceram estáveis em tamanho, sem crescimento ou regressão, e não causaram obstrução ao fluxo sanguíneo ou sintomas clínicos.  \n- O desenvolvimento neuropsicomotor e o crescimento físico da criança foram normais para a idade, sem sinais de atraso ou complicações relacionadas à esclerose tuberosa.\n\nInterpretação Clínica  \nEste caso ilustra a importância do diagnóstico pré-natal de rabdomioma cardíaco e do acompanhamento multidisciplinar para monitorar possíveis complicações e manifestações associadas, especialmente a esclerose tuberosa. Apesar da alta probabilidade de associação, a ausência de outros sinais clínicos até o primeiro ano de vida sugere uma apresentação isolada do tumor, o que é menos comum, mas possível. A estabilidade das massas e o desenvolvimento saudável da criança indicam um prognóstico favorável até o momento.\n\nPróximos Passos  \nRecomenda-se a continuidade do acompanhamento clínico e ecocardiográfico regular para monitorar possíveis alterações no tamanho das massas ou surgimento de sintomas cardíacos. Além disso, o seguimento neurológico e dermatológico deve ser mantido para detectar precocemente quaisquer manifestações tardias da esclerose tuberosa, que podem se desenvolver após o primeiro ano de vida. A família deve ser orientada sobre os sinais de alerta e a importância do acompanhamento especializado contínuo."
+        }
+    },
+    {
+        "article": "Um menino com peso ao nascer de 3 kg foi entregue por cesariana em vista do sofrimento fetal. Ele chorou imediatamente após o nascimento. Cuidados de rotina foram dados e aos 10 minutos de vida, foi notado que ele tinha uma leitura de SpO2 (saturação de oxigênio) baixa de 75-80%. Assim, ele começou a receber oxigênio por caixa de cabeça a 5 L/min. Ele teve bons esforços respiratórios com taquipneia leve. Como ele continuou a ter SpO2 baixa mesmo após uma tentativa de ambos os 5 L/min de oxigênio de caixa de cabeça e PEEP (pressão expiratória final positiva) com 6 cm de água com FiO2 (fração de oxigênio inspirado) 100%, ele foi intubado e começou a respiração com pressão positiva. O bebê foi transferido para a Unidade de Terapia Intensiva Neonatal para gestão adicional.\n\nMesmo após ventilação mecânica em modo de ventilação intermitente sincronizada (SIMV) com pressões estabilizadoras máximas de PEEP 6 cm e pressão máxima de 20 cm de água e sedação adequada, a SpO2 máxima atingida foi de 80%. Ele tinha cianose e características de má perfusão (taquicardia e tempo de preenchimento capilar prolongado). Assim, o bebê começou com suporte inotrópico após um bolus de solução salina normal. Os diferenciais iniciais considerados foram choque séptico, pneumotórax, malformações pulmonares e doença cardíaca cianótica. Foi feito um hemocultivo e o bebê começou com antibióticos de primeira linha. A radiografia de tórax mostrou uma sombra cardíaca normal e campos pulmonares normais. Foi feito um ecocardiograma que descartou hipertensão pulmonar persistente e doença cardíaca estrutural.\n\nO gás arterial feito após 1 h de ventilação (2 h de vida) mostrou pH de 7.5, paCO2 19.1 mmHg, paO2 de 199 mmHg, lactato 4 mmol/L, bicarbonato 18.1 mmol/L e base excessiva de −3.6. Como houve hiperóxia inexplicada apesar da baixa SpO2 e cianose persistente, suspeitou-se de metemoglobinemia que foi confirmada por alto nível de metHb (metemoglobin) (7.6%). Os valores de gases sanguíneos em série mostraram hiperóxia e níveis elevados de metHb. Ele recebeu 3 mg intravenosos de dose única de azul de metileno e começou a tomar ácido ascórbico oral 300 mg uma vez ao dia. As suas definições de ventilador foram lentamente retiradas e ele foi extubado após 16 h para ar ambiente. Os inotrópicos foram também reduzidos e parados dentro de 24 h. Como a sua cultura sanguínea não tinha crescimento, os antibióticos foram parados após 2 dias. A partir do dia 2 de vida, ele manteve uma saturação de 75-85% em ar ambiente.\n\nNão houve história familiar ou perinatal relevante. O nível de glicose-6-fosfato desidrogenase e eletroforese de hemoglobina também foram normais. Desde o dia 3, ele estava em alimentação orogástrica e estava estável, exceto pela cianose persistente. Depois de enviar o teste genético (exoma clínico), ele foi dispensado no dia 9 enquanto estava em alimentação direta ao peito, pois ele continuou estável, exceto pela cianose e baixa leitura de SpO2 (80-85%) em ar ambiente com paO2 normal.\n\nApós a alta, o bebé foi seguido regularmente e, aos 2 meses de vida, a sua saturação no ar ambiente era de 88-90% e, aos 4 meses, a SpO2 era superior a 92% no ar ambiente sem cianose. O exoma clínico mostrou uma mutação na cadeia gama da hemoglobina fetal – substituição do aminoácido tirosina por histidina no códon 63 (p.His63Tyr) devido a uma mutação sem sentido no gene HBG2 (chr11:g.5275647G>A). Assim que recebemos o resultado do teste genético, o ácido ascórbico oral foi interrompido e os pais foram aconselhados sobre o excelente prognóstico desta condição de doença rara. Aos 5 meses de vida, ele estava bem, não tinha cianose e o seu nível de metHb era normal.\n",
+        "gold_summary": "Relatamos um recém-nascido que apresentou cianose e dessaturação logo após o nascimento, que mais tarde foi diagnosticado com metemoglobinemia e iniciou a medicação. A avaliação genética revelou uma mutação na cadeia gama da hemoglobina fetal (HbF) causando hemoglobina anormal. Mutações fisiologicamente significativas em genes de gama-globina causam sintomas no feto e no recém-nascido que gradualmente diminuem nos primeiros meses de vida.\n",
+        "synthetic_summary": {
+            "B1": "Um bebê nasceu e estava com a pele meio azulada. Ele não conseguia respirar direito e o oxigênio no sangue estava baixo. Os médicos deram remédio e ajudaram ele a respirar melhor.\n\nDepois, eles fizeram um exame especial e viram que o sangue do bebê era diferente. Isso aconteceu por causa de um problema no sangue que ele nasceu com. Esse problema faz o bebê ficar azul, mas vai melhorando com o tempo.\n\nCom o passar dos meses, o bebê ficou cada vez melhor e não ficou mais azul. Os médicos disseram que ele vai ficar bem.",
+            "B2": "**O que aconteceu com o bebê**\n\nUm recém-nascido apresentou cianose, que é quando a pele fica azulada por falta de oxigênio, e níveis baixos de oxigênio no sangue logo após nascer. Mesmo com ajuda de oxigênio e ventilação, ele continuava com esses sintomas. Os médicos suspeitaram de um problema chamado metemoglobinemia, que acontece quando a hemoglobina, a proteína que carrega oxigênio no sangue, não funciona direito.\n\n**O que descobriram**\n\nExames mostraram que o bebê tinha uma forma anormal de hemoglobina fetal, que é a hemoglobina que os bebês têm antes de nascer. Essa alteração foi causada por uma mutação genética, ou seja, uma mudança no DNA que afeta a produção da hemoglobina. Essa mutação fez com que o oxigênio não fosse transportado bem, causando a cianose e a baixa saturação de oxigênio.\n\n**O que isso significa**\n\nEsse problema genético afeta principalmente os recém-nascidos e os sintomas melhoram com o tempo, conforme a hemoglobina fetal vai sendo substituída pela hemoglobina normal do adulto. O bebê recebeu tratamento com medicamentos que ajudaram a melhorar a situação e, com o passar dos meses, ele ficou completamente bem, sem mais cianose e com níveis normais de oxigênio no sangue.\n\n**Resumo final**\n\nEm resumo, o bebê teve um problema raro causado por uma mutação na hemoglobina fetal, que dificultava o transporte de oxigênio. Com o diagnóstico correto e o tratamento adequado, ele melhorou e está saudável hoje. Essa condição costuma melhorar sozinha nos primeiros meses de vida.",
+            "B3": "**Contexto**  \nEste relato descreve o caso de um recém-nascido que apresentou cianose (coloração azulada da pele devido à baixa oxigenação) e níveis baixos de saturação de oxigênio (SpO2) logo após o nascimento, apesar de receber suporte respiratório adequado. Inicialmente, foram considerados diagnósticos comuns como infecção, problemas pulmonares ou cardíacos, mas esses foram descartados após exames detalhados.\n\n**Principais Achados**  \nO bebê manteve uma saturação de oxigênio persistentemente baixa (75-85%) mesmo com ventilação mecânica e suporte inotrópico, apresentando cianose e sinais de má perfusão. Exames laboratoriais revelaram níveis elevados de metemoglobina (metHb), uma forma anormal de hemoglobina que não transporta oxigênio eficientemente, confirmando o diagnóstico de metemoglobinemia. O tratamento inicial incluiu administração intravenosa de azul de metileno e ácido ascórbico oral, que ajudaram a melhorar seu quadro clínico.\n\nA investigação genética por sequenciamento do exoma clínico identificou uma mutação específica no gene HBG2, responsável pela cadeia gama da hemoglobina fetal (HbF). Essa mutação provoca a substituição do aminoácido tirosina por histidina na posição 63 da cadeia gama (p.His63Tyr), resultando em uma hemoglobina anormal que causa a metemoglobinemia. Essa alteração genética explica a persistência da cianose e da baixa saturação, apesar da oxigenação adequada do sangue arterial.\n\n**Interpretação Clínica**  \nMutações fisiologicamente relevantes nos genes da gama-globina, como a encontrada neste paciente, afetam principalmente o feto e o recém-nascido, pois a hemoglobina fetal é predominante nessa fase da vida. Com o tempo, à medida que a produção de hemoglobina fetal diminui e a hemoglobina adulta aumenta, os sintomas tendem a melhorar gradualmente. No caso relatado, a saturação de oxigênio e a cianose melhoraram progressivamente nos primeiros meses de vida, até a normalização completa aos cinco meses.\n\n**Próximos Passos e Prognóstico**  \nApós a confirmação do diagnóstico genético, o tratamento com ácido ascórbico foi suspenso, e os pais receberam orientações sobre o excelente prognóstico da condição, que é rara, mas benigna e autolimitada. O acompanhamento regular mostrou melhora contínua, com resolução da cianose e normalização dos níveis de metemoglobina. Esse caso destaca a importância de considerar causas genéticas raras em recém-nascidos com cianose persistente e baixa saturação, especialmente quando exames convencionais são normais."
+        }
+    },
+    {
+        "article": "Homem de 35 anos de idade com histórico de ruptura total do ligamento cruzado anterior há 10 anos. Teve tratamento conservador com imobilização por quatro semanas e, posteriormente, fisioterapia por seis meses com melhora parcial da sintomatologia. Ao finalizar o tratamento conservador, realizou atividades da vida diária sem limitação aparente até um mês antes da nova avaliação, começando com dor de 6/10 na escala EVA de joelho, bem como sensação de instabilidade ao descer escadas e edema intermitente, sem novo mecanismo de lesão. Na exploração física, evidencia-se dor à palpação sobre a linha articular lateral e superfície anterior do joelho; arcos de mobilidade de joelho com flexão ativa de 85° e flexão passiva de 100°, extensão completa. Força por grupos musculares de joelho 5/5 com dor referida à face anterior do joelho. Nas manobras especiais para avaliar clinicamente a articulação do joelho, evidencia-se caixão anterior, Lachman, Lelli's: positivos; McMurray, Steinman e Apley lateral e medial: positivos. Solicita-se ressonância magnética simples do joelho direito, onde se encontra: ausência de LCA, osteoartrose grau III-IV do compartimento femorotibial medial, osteoartrose grau II do compartimento femorotibial lateral, afinamento da haste posterior e corpo de menisco lateral com mínima porção residual, rasgo horizontal da haste posterior e corpo de menisco medial, edema de ligamento cruzado posterior (LCP) com mudança da degeneração mucoide. Realizaram-se medições radiográficas para notch intercondíleo e ângulo alfa, em corte axial e sagital, respectivamente. Decidiu-se realizar manejo diagnóstico-terapêutico mediante artroscopia de joelho. Previamente ao procedimento cirúrgico e com o paciente sob anestesia geral, realizou-se o teste de pivot shift, que foi positivo com grau III. Procedeu-se a realizar artroscopia, onde se evidencia: escotadura fechada, ruptura completa inveterada de LCA, pinçamento de LCP, ruptura do corno posterior e corpo de menisco lateral, ruptura crônica inveterada e extrudada de menisco medial, pinçamento femorotibial anterior, corpos livres intraarticulares, lesão condral de 1 cm2 em côndilo femoral lateral em zona de carga, osteoartrose grau IV de compartimento medial de joelho, sinovite subquadricipital. Durante a artroscopia, realizou-se escotadura, liberação de LCP, desbridamento de osteófito em espinha tibial anterior, meniscectomia parcial de flap inferior do corno posterior e corpo de menisco lateral, meniscectomia parcial de raiz meniscal remanente de menisco medial, extração de corpos livres osteocondrais posteromedial, medial e subquadricipital, remodelamento de lesão condral em côndilo femoral lateral em zona de carga, desbridamento condral na periferia de côndilo femoral medial (periartrose), sinovite subquadricipital.\nDevido ao grau de artrose, foi decidido não realizar o túnel do LCA para evitar futuras complicações na cirurgia definitiva de artroplastia do joelho. Após a cirurgia, foi indicado o uso de mobilizador passivo do joelho de 0° de extensão a 100° de flexão, bem como deambulação assistida por muletas.\nO paciente recebeu alta do hospital no dia seguinte à cirurgia, sem complicações, e iniciou fisioterapia para fortalecimento e estabilidade muscular. Em visitas de acompanhamento, três, seis e nove meses depois, o paciente relatou estar assintomático, realizando suas atividades diárias sem limitação, bem como atividades esportivas de baixo impacto sem impedimentos.\n",
+        "gold_summary": "Apresentamos o caso de um paciente de 35 anos com ruptura inveterada do LCA de 10 anos de evolução. Com manejo conservador inicialmente que progride para instabilidade de joelho e dor na linha articular medial e lateral, assim como aumento de volume e limitação funcional. Após estudos diagnósticos, decide-se realizar artroscopia diagnóstica-terapêutica e continua-se com acompanhamento estreito por patologia associada.\n",
+        "synthetic_summary": {
+            "B1": "Um homem machucou o joelho há muito tempo. Ele sentia dor e o joelho ficava meio bambo. O médico olhou com cuidado e fez uma cirurgia pequena para ajudar. Depois, ele fez exercícios para o joelho ficar forte. Agora, ele está melhor e consegue fazer suas coisas sem dor.",
+            "B2": "**O que aconteceu com o paciente**\n\nUm homem de 35 anos sofreu uma lesão no joelho há 10 anos, quando rompeu completamente o ligamento cruzado anterior (LCA). O LCA é um ligamento importante que ajuda a manter o joelho estável. Ele fez um tratamento sem cirurgia, usando imobilização e fisioterapia, e melhorou um pouco. Porém, depois de um tempo, começou a sentir dor no joelho, inchaço e uma sensação de que o joelho “falha”, principalmente ao descer escadas.\n\n**O que os exames mostraram**\n\nOs médicos fizeram vários exames, incluindo uma ressonância magnética, que é uma imagem detalhada do joelho. Eles viram que o LCA estava totalmente rompido e que havia desgaste na cartilagem do joelho, chamado de osteoartrose, que causa dor e dificuldade para movimentar a articulação. Também encontraram lesões nos meniscos, que são como “amortecedores” dentro do joelho, e sinais de inflamação.\n\n**O que foi feito para ajudar**\n\nPara entender melhor o problema e tentar melhorar, os médicos fizeram uma artroscopia, que é uma cirurgia pequena onde colocam uma câmera dentro do joelho para ver tudo de perto. Durante o procedimento, eles limparam as áreas danificadas, retiraram pedaços soltos e trataram as lesões nos meniscos e na cartilagem. Como o desgaste do joelho estava avançado, decidiram não fazer a cirurgia para reconstruir o LCA naquele momento, para evitar problemas futuros.\n\n**Como foi a recuperação**\n\nDepois da cirurgia, o paciente usou um aparelho para ajudar a movimentar o joelho e caminhou com muletas. Ele começou fisioterapia para fortalecer os músculos e melhorar a estabilidade do joelho. Nas consultas de acompanhamento, três, seis e nove meses depois, ele relatou que não sentia mais dor e conseguia fazer suas atividades diárias e esportes leves sem dificuldade.\n\n**O que isso significa**\n\nEsse caso mostra que, mesmo com uma lesão antiga e desgaste no joelho, é possível melhorar a qualidade de vida com o tratamento adequado. A artroscopia ajudou a aliviar os sintomas e a fisioterapia foi importante para recuperar a força e o movimento. É fundamental acompanhar o joelho para evitar que o problema piore e para planejar tratamentos futuros, se necessário.",
+            "B3": "**Contexto**  \nEste é o caso de um homem de 35 anos que sofreu uma ruptura completa do ligamento cruzado anterior (LCA) do joelho direito há 10 anos. Inicialmente, ele foi tratado sem cirurgia, com imobilização e fisioterapia, o que trouxe melhora parcial. Durante quase uma década, ele conseguiu realizar suas atividades diárias normalmente. Porém, cerca de um mês antes da nova avaliação, começou a sentir dor intensa no joelho (nota 6 em uma escala de 0 a 10), sensação de instabilidade ao descer escadas e episódios de inchaço, mesmo sem ter sofrido uma nova lesão.\n\n**Principais Achados Clínicos e Exames**  \nNo exame físico, o paciente apresentava dor ao toque nas áreas lateral e anterior do joelho, com mobilidade reduzida na flexão (dobrar o joelho) e força muscular preservada, embora com dor referida. Testes específicos para avaliar a estabilidade do joelho indicaram instabilidade significativa, confirmando a lesão antiga do LCA. A ressonância magnética mostrou ausência do ligamento cruzado anterior, desgaste avançado da cartilagem (osteoartrose grau III-IV) no compartimento medial do joelho, lesões nos meniscos (estruturas que amortecem o joelho) e sinais de inflamação no ligamento cruzado posterior.\n\nDurante a artroscopia (procedimento minimamente invasivo para visualizar e tratar o interior da articulação), foram encontradas várias alterações: escotadura óssea estreita, ruptura crônica do LCA, lesões nos meniscos medial e lateral, corpos soltos dentro da articulação, lesão na cartilagem do côndilo femoral lateral e sinovite (inflamação da membrana que reveste a articulação). Procedeu-se a limpeza das áreas lesionadas, remoção parcial dos meniscos danificados, extração dos corpos soltos e tratamento das lesões da cartilagem. Devido ao grau avançado de artrose, optou-se por não reconstruir o LCA naquele momento para evitar complicações futuras, especialmente considerando a possibilidade de uma cirurgia de prótese do joelho.\n\n**Interpretação Clínica**  \nO paciente apresentava uma lesão antiga do LCA que evoluiu para instabilidade crônica do joelho, associada a desgaste articular significativo e lesões meniscais crônicas. A artroscopia teve papel diagnóstico e terapêutico, permitindo tratar as complicações associadas e aliviar os sintomas. A decisão de não reconstruir o ligamento cruzado anterior foi baseada no risco aumentado de complicações devido à artrose avançada, priorizando o manejo dos sintomas e a preservação da função.\n\n**Próximos Passos e Evolução**  \nApós a cirurgia, o paciente iniciou reabilitação com uso de aparelho para mobilização passiva do joelho e apoio com muletas para caminhar. Ele recebeu alta hospitalar no dia seguinte, sem complicações. Nas consultas de acompanhamento aos três, seis e nove meses, relatou estar sem dor, com estabilidade adequada do joelho e capacidade para realizar suas atividades diárias e exercícios físicos de baixo impacto, demonstrando boa resposta ao tratamento conservador pós-artroscopia. O acompanhamento contínuo é importante para monitorar a evolução da osteoartrose e avaliar a necessidade futura de intervenções adicionais, como a artroplastia (substituição da articulação)."
+        }
+    },
+    {
+        "article": "O nosso paciente é um homem hispânico de 37 anos de idade, que sofreu uma ruptura simultânea dos tendões patelares bilaterais após saltar enquanto tentava fazer um cesto, enquanto jogava basquetebol. A história relevante inclui a reconstrução do ligamento cruzado anterior (ACL) do joelho direito, utilizando um autoenxerto de tendão patelar ósseo ipsilateral (BPTB) em 2002. O paciente não conseguia andar e apresentou-se na nossa clínica numa cadeira de rodas. O paciente não conseguia realizar um levantamento da perna reta e tinha um defeito sensível no pólo inferior da patela bilateralmente. As radiografias de plano demonstraram patela alta bilateral e os estudos de MRI demonstraram rupturas do tendão patelar proximal bilateral. A recomendação para reparação cirúrgica simultânea aguda de ambos os joelhos foi dada ao paciente.\n\nTécnica Operativa\nO exame intraoperatório mostrou inchaço significativo em ambos os joelhos, com extensão e flexão completas de 140 graus bilateralmente. Havia um defeito palpável e patela alta bilateralmente associada à ruptura do tendão patelar.\n\nO joelho foi abordado através da abordagem padrão da linha média anterior. A extensão da lesão foi elucidada, envolvendo tanto o retinaculo medial como o lateral. Um hematoma foi evacuado e os tecidos profundos e subcutâneos foram irrigados. Suturas de tração foram colocadas no tendão do quadríceps para ajudar a mobilizar a patela distalmente. O tendão proximal da patela e o coto distal do tendão da patela foram elucidados.\n\nDuas âncoras de sutura SwiveLock bio-compósitas de 4,75 mm (Sistema de Implante SpeedBridge com Agulha Scorpion-Multifire, Arthrex, Inc., No. AR-2600SBS-8) foram colocadas dentro do pólo inferior da patela na origem do tendão patelar. Um ponto de sutura de bloqueio Krackow foi realizado com cada uma das âncoras de sutura SwiveLock com uma sutura de puxar. Isso foi trazido para cima e para baixo do tendão patelar em uma configuração de ponto de bloqueio. O joelho foi colocado em 30 graus de flexão, e o comprimento patelar foi feito para ser de 4,5 cm. Como o paciente não tinha um tendão patelar contralateral intacto para basear o comprimento do tendão patelar, 4,5 cm foi escolhido, pois este tem sido um comprimento patelar médio masculino recentemente descrito na literatura. A fluoroscopia intraoperativa em C-arm foi utilizada para confirmar a altura patelar apropriada. Isso foi verificado duas vezes, tentando obter um índice de Caton-Deschamps de aproximadamente 1:1. Os nós foram então amarrados a partir da configuração de ponto de bloqueio na reparação superior de volta para as âncoras de sutura na patela.\n\nOs mesmos ancoradores tinham suturas #2 FiberTape (Arthrex, Inc) carregadas. Estas foram cruzadas em uma configuração de ponte de sutura e colocadas em ancoradores SwiveLock separados no tubérculo tibial com o joelho em 30 graus de flexão. A paratenon remanescente e o tecido mole foram imbricados para ajudar a reforçar o reparo. O retinaculo medial e lateral foram então reparados com uma sutura #2 FiberWire de bloqueio (Arthrex, Inc). Depois de uma extensa irrigação dos tecidos profundos e subcutâneos, um fechamento padrão em camadas foi então realizado.\n\nO joelho esquerdo foi tratado em seguida de forma idêntica. No final deste caso, cada joelho foi capaz de obter de 0 a 30 graus de flexão sem qualquer tensão indevida nas reparações.\n\nSeguimento do paciente\nO paciente permaneceu sem suportar peso exceto para transferências por 6 semanas após a operação. Ambos os joelhos foram inicialmente bloqueados em extensão total com uma cinta. Dois dias após a cirurgia, o paciente iniciou fisioterapia com uma máquina de movimento passivo contínuo, aumentando ∼15° por semana. Após 6 semanas, o paciente começou a suportar peso total com as cintas bloqueadas em extensão com um andador. A sua ROM foi aproximadamente 0-110° em ambas as pernas, e ele podia realizar elevações de perna reta sem dificuldade.\n\nAos 10 meses, ele demonstrou 5/5 de força do quadríceps, −10° de extensão e 140° de flexão bilateralmente. A pontuação do IKDC (Knee Documentation Committee) foi de 57 bilateralmente.\n\nAos 12 meses, o paciente tinha alinhamento normal com força quadríceps simétrica bilateralmente. A sua ROM permaneceu a −10 graus de extensão passiva incorrigível e 140 graus de flexão bilateralmente. A pontuação IKDC do joelho direito e esquerdo do paciente melhorou para 69 e 72, respetivamente. A sua pontuação Lysholm registada aos 12 meses para o joelho direito e esquerdo foi de 94 e 99, respetivamente.\n",
+        "gold_summary": "Descrevemos o caso de um homem de 37 anos que apresentou ruptura bilateral simultânea do tendão patelar sem quaisquer fatores de risco associados. Além disso, este é o primeiro uso relatado da técnica de ponte de sutura com âncoras de sutura patelar e tibial na reparação de ruptura bilateral proximal do tendão patelar. Após 12 meses de acompanhamento, o paciente apresentou alinhamento normal, sem efusão e força quadríceps simétrica.\n",
+        "synthetic_summary": {
+            "B1": "Um homem de 37 anos machucou os dois joelhos ao pular. Os fios que seguram os ossos do joelho se romperam dos dois lados. Os médicos fizeram uma cirurgia para consertar os fios. Depois de um ano, os joelhos dele ficaram bons. Ele consegue mexer as pernas e está forte.",
+            "B2": "**O que aconteceu com o paciente**\n\nUm homem de 37 anos quebrou os tendões patelares dos dois joelhos ao mesmo tempo. O tendão patelar é uma faixa forte que liga a patela (osso do joelho) à tíbia (osso da perna). Ele não tinha nenhum problema de saúde que pudesse explicar essa lesão.\n\n**Como foi o tratamento**\n\nOs médicos usaram uma técnica nova para consertar os tendões rompidos. Eles colocaram pequenas âncoras com fios especiais na patela e na tíbia para segurar o tendão no lugar, formando uma espécie de \"ponte\" que ajuda a reparar a lesão. A cirurgia foi feita nos dois joelhos ao mesmo tempo.\n\n**Como foi a recuperação**\n\nDepois da operação, o paciente ficou sem apoiar o peso nas pernas por 6 semanas e usou aparelhos para ajudar na movimentação. Com o tempo, ele começou a fazer fisioterapia para recuperar a força e o movimento dos joelhos.\n\n**Resultado após 12 meses**\n\nUm ano depois, o paciente estava com os joelhos alinhados normalmente e sem inchaço. A força dos músculos da frente da coxa (quadríceps) estava igual nos dois lados, mostrando que a recuperação foi boa. Essa técnica mostrou ser eficaz para casos difíceis como o dele.",
+            "B3": "**Contexto**  \nApresentamos o caso de um homem hispânico de 37 anos que sofreu uma ruptura simultânea dos tendões patelares em ambos os joelhos após um salto durante uma partida de basquetebol. O paciente não possuía fatores de risco conhecidos para esse tipo de lesão e tinha histórico prévio de reconstrução do ligamento cruzado anterior (LCA) do joelho direito, realizada com enxerto do próprio tendão patelar em 2002. No momento da avaliação, ele não conseguia caminhar, apresentava incapacidade para elevar as pernas estendidas e tinha dor e defeito palpável na região inferior das patelas bilateralmente. Exames de imagem confirmaram a presença de patela alta (posição elevada da patela) e rupturas proximais dos tendões patelares em ambos os joelhos.\n\n**Procedimento Cirúrgico**  \nFoi realizada uma reparação cirúrgica simultânea e aguda dos dois tendões patelares. Durante a cirurgia, constatou-se inchaço significativo e patela alta em ambos os joelhos, com rupturas que afetavam também as estruturas laterais (retináculos medial e lateral). A técnica utilizada envolveu a fixação dos tendões à patela por meio de âncoras de sutura bio-compatíveis (SwiveLock), com pontos de sutura especiais (bloqueio Krackow) para garantir firmeza na reparação. Para restaurar a altura correta da patela, foi adotado um comprimento padrão de tendão patelar (4,5 cm), confirmado por imagens intraoperatórias. Além disso, foi empregada uma configuração em “ponte de sutura” cruzada para reforçar a fixação entre a patela e a tíbia (osso da perna), utilizando fios de alta resistência (FiberTape). Os tecidos moles remanescentes foram cuidadosamente suturados para fortalecer o reparo. O procedimento foi repetido de forma idêntica no joelho esquerdo.\n\n**Recuperação e Seguimento**  \nApós a cirurgia, o paciente permaneceu sem apoio de peso nos membros inferiores por seis semanas, com os joelhos imobilizados em extensão total. Iniciou fisioterapia precoce com movimento passivo contínuo, aumentando gradualmente a flexão dos joelhos. Após seis semanas, começou a apoiar peso total com auxílio de andador e cintas ortopédicas. Aos 10 meses, o paciente apresentava força muscular completa no quadríceps, amplitude de movimento ampla (0 a 140 graus de flexão) e leve déficit na extensão (−10 graus). Aos 12 meses, manteve alinhamento normal dos joelhos, força simétrica e ausência de inchaço. As avaliações funcionais (pontuações IKDC e Lysholm, que medem sintomas e capacidade funcional do joelho) indicaram melhora significativa, com resultados próximos ao normal.\n\n**Interpretação Clínica**  \nEste caso é notável por relatar uma ruptura bilateral simultânea do tendão patelar em um paciente sem fatores predisponentes, uma situação rara. Além disso, representa o primeiro relato do uso da técnica de ponte de sutura com âncoras tanto na patela quanto na tíbia para reparar rupturas proximais bilaterais do tendão patelar. A abordagem cirúrgica combinada com reabilitação precoce proporcionou recuperação funcional satisfatória, com restauração da força muscular e amplitude de movimento adequada após um ano.\n\n**Próximos Passos**  \nO acompanhamento contínuo é importante para monitorar a manutenção da função do joelho e prevenir complicações a longo prazo, como rigidez articular ou recidiva da lesão. Este caso também sugere que a técnica descrita pode ser uma opção eficaz para lesões similares, mas estudos adicionais são necessários para confirmar sua aplicabilidade em populações maiores."
+        }
+    },
+    {
+        "article": "Paciente do sexo feminino, caucasiana, 73 anos de idade que procurou um serviço de distúrbios mamários com queixa de alteração rósea na pele da mama direita há cerca de 30 dias. A mamografia bilateral 5 meses antes da consulta mostrou alterações benignas ( Breast Imaging Reporting and Data System – BI-RADS™ 2). A paciente apresentou histórico de carcinoma ductal invasivo na mama direita G3 sem tipo especial, que fora tratado com ressecção segmental e dissecção de linfonodos axilares níveis I e II em dezembro de 2011. No momento da cirurgia, observaram-se tumor medindo 3,0cm e três linfonodos axilares apresentando metástase (3/10). A imuno-histoquímica relevou que o tumor era positivo para receptor de estrógeno (90%), positivo para receptor de progesterona (2%), HER-2 negativo, Ki-67 positivo (60%) e do subtipo luminal B. A terapia adjuvante da paciente incluiu seis ciclos de doxorrubicina, ciclofosfamida e terapia com paclitaxel, seguida de radioterapia (25 sessões com dose de 50Gy na mama direita e fossa supraclavicular, além de boost de 10Gy). Atualmente, a paciente está em tratamento endocrinológico com letrozole (6 anos de tratamento). Em exame físico, ela apresentou duas lesões róseas na mama direita, sendo uma eritematosa leve e quase imperceptível, na junção do quadrante superior (JQS), e a outra uma lesão violácea mais intensa, na junção do quadrante inferior (JQI) medindo 0,5cm.\n\nRealizou-se biópsia incisional da lesão no JQI, que demostrou lesão vascular atípica em coloração de hematoxilina-eosina. Um estudo imuno-histoquímico complementar do angiossarcoma foi sugerido para conclusão do diagnóstico. Após o resultado desse estudo, a paciente foi submetida à ressecção de ambas as lesões cutâneas. O relato patológico anatômico do espécime ressecado mostrou angiossarcoma bem diferenciado (G1), tratando-se de neoplasia caracterizada por anastomoses vasculares alinhadas por células endoteliais atípicas caracterizada pela presença de hipercromatismo e anisocariose e, em alguns casos, contendo eritrócitos, organizados no padrão de crescimento infiltrado, permeando o parênquima mamário e a derme na JQS, medindo 1,9x1,4cm, e na JQI, constituindo neoplasia restrita à derme, medindo 1,1x0,5cm. O exame imuno-histoquímico relevou positividade para expressão do grupamento de diferenciação 31 (CD31) e oncogene C-MYC, confirmando a malignidade secundária à terapia por radiação. A tomografia computadorizada do tórax e abdômen e a cintilografia óssea não mostraram sinais de metástase distante. O paciente realizou mastectomia simples do lado direito, sem reconstrução como tratamento complementar. O relato final histopatológico mostrou angiossarcoma bem diferenciado (G1) e mais três focos microscópicos foram encontrados no parênquima mamário, sendo que o maior deles mediu 2mm. Dois anos após a cirurgia, a paciente não desenvolveu recidiva.",
+        "gold_summary": "Relatamos o caso de uma mulher de 73 anos, com história prévia de tratamento conservador de câncer de mama direita, apresentando alteração rósea discreta em pele da mama homolateral. A mamografia demostrou resultado compatível com alterações benignas (BI-RADS 2). No material de biópsia incisional, a hematoxilina-eosina demonstrou lesão vascular atípica e sugeriu imuno-histoquímica para elucidação diagnóstica. A paciente foi submetida à ressecção de lesões, e a histologia demonstrou angiossarcoma radiogênico. Em seguida, mastectomia simples foi realizada. A imuno-histoquímica demonstrou positividade para os antígenos relacionados a CD31 e CD34, e a amplificação do oncogene C-MYC confirmou o diagnóstico de angiossarcoma induzido por radiação mamária. O atraso no diagnóstico constitui questão importante. Considerando que as alterações iniciais da pele do angiossarcoma radiogênico são sutis e podem ser confundidas com outras condições benignas da pele, como telangiectasias, neste relato destacamos os aspectos clínicos, no intuito de alertar sobre a possibilidade de angiossarcoma de mama em pacientes com história prévia de radioterapia adjuvante para tratamento de câncer de mama. A paciente permaneceu assintomática 16 meses após a cirurgia.",
+        "synthetic_summary": {
+            "B1": "Uma senhora de 73 anos teve um machucado diferente na pele da mama direita. Ela já teve um problema sério na mama antes e fez tratamento. O exame de imagem mostrou que parecia ser algo que não fazia mal. Mas o machucado não sumiu, então os médicos fizeram um teste para ver o que era. Eles acharam um tipo de machucado que pode crescer e precisa ser tirado. A senhora fez uma cirurgia para tirar esse machucado. Depois, ela ficou bem e não teve mais problemas por muito tempo. É importante cuidar bem de machucados na pele, especialmente se a pessoa já teve tratamento na mama antes.",
+            "B2": "**O que aconteceu com a paciente**\n\nEsta é a história de uma mulher de 73 anos que já havia sido tratada de um câncer na mama direita. Ela percebeu uma pequena mancha rosada na pele dessa mesma mama. Mesmo que a mamografia (um exame de raio-X das mamas) feita meses antes mostrasse que estava tudo bem, essa mancha chamou atenção.\n\n**O que os médicos fizeram**\n\nPara entender melhor, os médicos retiraram um pedacinho da mancha para analisar, chamado biópsia. Esse exame mostrou que havia um tipo diferente de crescimento de vasos sanguíneos, algo estranho que precisava ser investigado mais a fundo. Depois, eles retiraram as duas manchas da pele para estudar melhor.\n\n**O que descobriram**\n\nA análise mostrou que a paciente tinha um angiossarcoma, que é um tipo de tumor maligno (câncer) que nasce das células dos vasos sanguíneos. Esse tumor apareceu por causa do tratamento com radiação que ela recebeu no passado para o câncer de mama. A radiação, apesar de ajudar a tratar o câncer, às vezes pode causar esse tipo de problema depois de um tempo.\n\n**Por que isso é importante**\n\nO angiossarcoma causado pela radiação pode começar com sinais muito leves na pele, parecendo apenas manchas ou vermelhidão, que podem ser confundidas com coisas menos graves. Por isso, é importante que médicos e pacientes fiquem atentos a qualquer mudança na pele, especialmente em quem já fez radioterapia.\n\n**O que aconteceu depois**\n\nDepois de confirmar o diagnóstico, a paciente passou por uma cirurgia para retirar toda a mama direita. Dois anos após essa cirurgia, ela não apresentou sinais de que o tumor voltou. Esse caso mostra como é importante investigar bem qualquer alteração na pele em pacientes que já tiveram câncer e tratamento com radiação.",
+            "B3": "**Contexto**  \nEste relato descreve o caso de uma mulher de 73 anos que apresentou uma alteração discreta na coloração da pele da mama direita, local onde havia sido tratada anteriormente para câncer de mama. Cinco meses antes, uma mamografia bilateral indicou apenas alterações benignas (classificação BI-RADS 2). A paciente tinha histórico de carcinoma ductal invasivo grau 3 na mama direita, tratado em 2011 com cirurgia conservadora (ressecção segmentar) e remoção de linfonodos axilares, seguido de quimioterapia e radioterapia. Atualmente, ela fazia uso de terapia hormonal com letrozole.\n\n**Principais Achados**  \nDurante o exame físico, foram identificadas duas pequenas lesões róseas na mama direita: uma discreta, quase imperceptível, no quadrante superior, e outra violácea, mais evidente, no quadrante inferior. A biópsia incisional da lesão violácea revelou uma lesão vascular atípica, sugerindo a necessidade de exames imuno-histoquímicos para esclarecer o diagnóstico. Após a remoção cirúrgica das lesões, a análise histopatológica confirmou a presença de angiossarcoma bem diferenciado (G1), um tipo raro de tumor maligno originado das células que revestem os vasos sanguíneos. O tumor apresentou características típicas, como vasos anastomosados (conectados) revestidos por células endoteliais com alterações atípicas, e infiltrava tanto a derme quanto o tecido mamário.\n\nO exame imuno-histoquímico mostrou positividade para CD31 (um marcador específico de células endoteliais) e para o oncogene C-MYC, cuja amplificação é indicativa de angiossarcoma secundário à radioterapia. Exames de imagem do tórax, abdômen e ossos não identificaram metástases à distância. Como tratamento complementar, a paciente foi submetida a mastectomia simples do lado direito, sem reconstrução mamária. O exame final do tecido removido revelou focos microscópicos adicionais do tumor no parênquima mamário, todos muito pequenos (até 2 mm). Dois anos após a cirurgia, a paciente permanece sem sinais de recidiva.\n\n**Interpretação Clínica**  \nO angiossarcoma radiogênico da mama é uma complicação rara, porém grave, que pode surgir anos após radioterapia para câncer de mama. Suas manifestações iniciais na pele costumam ser sutis e facilmente confundidas com alterações benignas, como telangiectasias (pequenos vasos dilatados). O diagnóstico precoce é desafiador, mas fundamental para o manejo adequado, pois o tumor é agressivo e pode se espalhar rapidamente.\n\n**Próximos Passos e Recomendações**  \nEste caso destaca a importância de vigilância cuidadosa em pacientes com histórico de radioterapia mamária, especialmente quando surgem alterações cutâneas incomuns na região tratada. Qualquer lesão vascular atípica deve ser investigada com biópsia e estudos imuno-histoquímicos para excluir angiossarcoma. O tratamento envolve cirurgia ampla, podendo incluir mastectomia, e acompanhamento rigoroso para detecção precoce de recidivas ou metástases. A conscientização clínica sobre essa possibilidade pode contribuir para diagnósticos mais rápidos e melhores desfechos."
+        }
+    },
+    {
+        "article": "Homem de 40 anos que foi ao pronto-socorro por dor precordial. Entre seus antecedentes, destacavam-se sobrepeso, esteatose hepática não alcoólica, síndrome de apneia hipopneia do sono sem requerimentos de pressão positiva contínua na via aérea e coronariopatia em seu avô. Começou 6 dias antes da consulta com dor precordial na classe funcional II (1000 metros), intensidade 5/10, ardência, sem irradiação, de 15 a 20 minutos de duração, melhorou com o repouso e sem associação a dispneia, palpitações ou sudorese. Repetiu episódios similares nos dias seguintes antes da consulta, na mesma classe funcional, 2 horas antes do internamento, iniciou a dor na classe funcional IV, pós-prandial, de maior intensidade, 8/10, associada a dispneia, pelo que decidiu consultar.Ao internamento, apresentou os seguintes sinais vitais: TA 150/80 mmHg, FC 85 LPM, FR 16 RPM, saturação 98% (0.21), afebril. Dor torácica residual de intensidade 4/10, sem sinais de insuficiência cardíaca. Realizou eletrocardiograma onde se visualizaram ondas T negativas, simétricas em derivações precoriais e supradesnivelamento de ST de < 1 mm com ondas T bifásica em V3, sem ondas Q e boa progressão de R em precoriais (não visto em eletrocardiograma prévio). Laboratório: Hto 43%, Cr 0.8 mg/dl, troponina ultrassensível de 132 pg/ml com posterior elevação a 172 pg/ ml. Interpretou-se infarto agudo de miocárdio sem elevação do ST, TIMI score de 3 pontos, GRACE score 66 pontos. Administrou-se carga de aspirina, estatinas de alta intensidade e anticoagulação com heparina de baixo peso molecular. Iniciou tratamento com nitroglicerina endovenosa, com melhora da dor. Em um novo eletrocardiograma objetivou-se reversão de ondas T negativas em precoriais, mas persistência do supradesnivelamento com onda T bifásica em V2-V3. No ecocardiograma evidenciou-se boa função ventricular e hipocinesia anteroseptal, basal e medial. Na coronariografia visualizou-se lesões graves em terço proximal, meio da artéria descendente anterior e lesão grave em terço médio da primeira diagonal, pelo que se colocou três stents liberadores de drogas em tais lesões. Realizou-se um novo eletrocardiograma após a colocação dos stents onde se objetivou ausência de alterações antes descritas. O paciente foi dado de alta sem complicações.\n",
+        "gold_summary": "O caso apresentado foi de um homem de 40 anos sem antecedentes cardiovasculares, que foi internado no nosso centro por dor precordial. No eletrocardiograma, evidenciou-se um padrão típico, já descrito, conhecido como síndrome de Wellens tipo 1 ou A, caracterizado por supradesnivelamento do ST < 1 mm e onda T bifásica na derivação V3. Foi diagnosticado infarto agudo do miocárdio sem elevação do ST, TIMI 3 e GRACE score 66 pontos. Este padrão eletrocardiográfico é de alto risco, para além dos pontuações estratificadores, dado que se correlaciona com lesão grave na artéria descendente anterior a nível proximal e requer intervenção percutânea sem demoras. Na coronariografia, evidenciaram-se 3 lesões graves: terço proximal e médio da artéria descendente anterior e primeira diagonal.\n",
+        "synthetic_summary": {
+            "B1": "Um homem de 40 anos sentiu dor no peito. A dor apareceu e sumiu, mas depois ficou mais forte. Ele foi ao hospital para cuidar disso.\n\nOs médicos fizeram um exame do coração chamado eletrocardiograma. Esse exame mostrou que o coração dele estava com um problema sério.\n\nEles fizeram outro exame para olhar as veias do coração. Viram que três partes estavam muito machucadas.\n\nOs médicos colocaram umas pecinhas chamadas stents para ajudar o coração a ficar melhor.\n\nDepois do tratamento, o homem ficou bem e saiu do hospital sem problemas.",
+            "B2": "**O que aconteceu com o paciente**\n\nUm homem de 40 anos foi ao hospital porque sentia dor no peito, que é chamada de dor precordial. Ele não tinha problemas sérios no coração antes. Durante os exames, os médicos fizeram um eletrocardiograma, que é um teste que mostra como o coração está funcionando. Nesse exame, eles viram um padrão chamado síndrome de Wellens tipo 1, que tem sinais específicos no eletrocardiograma, como uma pequena elevação no segmento ST (menos de 1 mm) e uma onda T com duas fases na parte chamada V3.\n\n**O que isso significa**\n\nEsse padrão no eletrocardiograma indica que o paciente teve um tipo de ataque cardíaco chamado infarto agudo do miocárdio sem elevação do ST. Esse tipo de infarto pode ser perigoso porque está ligado a um bloqueio grave em uma artéria importante do coração, chamada artéria descendente anterior, especialmente na parte próxima ao começo dela (proximal). Por isso, o paciente precisava de um tratamento rápido.\n\n**O que os médicos fizeram**\n\nOs médicos fizeram um exame chamado coronariografia, que mostra as artérias do coração para ver onde estão os bloqueios. Eles encontraram três bloqueios sérios: dois na artéria descendente anterior (no terço proximal e no terço médio) e um na primeira artéria diagonal, que é uma ramificação importante. Para tratar esses bloqueios, os médicos colocaram três stents, que são pequenos tubos que ajudam a manter as artérias abertas para o sangue passar melhor.\n\n**Conclusão**\n\nEsse caso mostra como é importante reconhecer sinais no eletrocardiograma que indicam problemas graves no coração. O paciente recebeu o tratamento correto a tempo e teve uma boa recuperação, saindo do hospital sem complicações.",
+            "B3": "**Contexto**  \nEste relato descreve o caso de um homem de 40 anos, sem histórico prévio conhecido de doenças cardíacas, que procurou atendimento médico devido a dor no peito (dor precordial). Ele apresentava fatores de risco como sobrepeso, esteatose hepática não alcoólica (acúmulo de gordura no fígado), apneia do sono leve e histórico familiar de doença coronariana (problemas nas artérias do coração) em seu avô.\n\n**Principais Achados Clínicos e Exames**  \nO paciente iniciou sintomas seis dias antes da internação, com episódios de dor no peito de intensidade moderada (5 em 10), que duravam cerca de 15 a 20 minutos e melhoravam com repouso. Nos dias seguintes, as dores se repetiram, tornando-se mais intensas (8 em 10) e associadas a falta de ar, o que motivou a busca por atendimento hospitalar.\n\nNo exame inicial, seus sinais vitais estavam estáveis, mas o eletrocardiograma (ECG) mostrou alterações importantes: ondas T negativas e bifásicas (com duas fases) na região anterior do coração (derivações precoriais, especialmente V3), além de um leve aumento do segmento ST (menos de 1 mm). Essas alterações são características da chamada síndrome de Wellens tipo 1, um padrão eletrocardiográfico que indica risco elevado de obstrução grave na artéria descendente anterior do coração.\n\nOs exames laboratoriais revelaram elevação da troponina ultrassensível, um marcador de lesão do músculo cardíaco, confirmando o diagnóstico de infarto agudo do miocárdio sem elevação do segmento ST (IAMSSST). As pontuações de risco TIMI (3 pontos) e GRACE (66 pontos) indicaram risco moderado para eventos cardíacos adversos.\n\n**Interpretação Clínica**  \nA síndrome de Wellens tipo 1, identificada no ECG, é um sinal precoce e de alto risco de obstrução crítica na artéria descendente anterior, que pode levar a um infarto extenso se não tratada rapidamente. Apesar das pontuações de risco moderado, a presença desse padrão eletrocardiográfico justifica intervenção urgente.\n\nO ecocardiograma mostrou boa função do ventrículo esquerdo (a principal câmara de bombeamento do coração), mas com áreas de movimento reduzido (hipocinesia) na parede anteroseptal, confirmando o comprometimento regional do músculo cardíaco.\n\nA coronariografia (exame invasivo que visualiza as artérias do coração) revelou três lesões graves: no terço proximal e médio da artéria descendente anterior e na primeira artéria diagonal (um ramo importante). Essas obstruções foram tratadas com a colocação de três stents liberadores de drogas, que são pequenos dispositivos metálicos que mantêm as artérias abertas e liberam medicamentos para evitar nova obstrução.\n\n**Próximos Passos e Desfecho**  \nApós o procedimento, o ECG voltou ao normal, sem as alterações iniciais, e o paciente apresentou melhora clínica significativa. Ele recebeu tratamento medicamentoso com aspirina, estatinas (para controle do colesterol) e anticoagulantes, além de nitroglicerina para alívio da dor. O paciente teve alta hospitalar sem complicações.\n\n**Resumo Final**  \nEste caso ilustra a importância de reconhecer padrões específicos no eletrocardiograma, como a síndrome de Wellens tipo 1, que indicam lesões graves nas artérias coronárias mesmo na ausência de elevação clássica do segmento ST. O diagnóstico precoce e a intervenção rápida são essenciais para prevenir danos maiores ao músculo cardíaco e garantir um bom prognóstico."
+        }
+    },
+    {
+        "article": "Um paciente iraniano de 38 anos apresentou-se ao departamento de emergência do Hospital Kowsar, em Semnan, no dia 2 de outubro de 2021, com queixas principais de dor abdominal intensa e edema das extremidades inferiores. A dor, originada na região umbilical e que se espalhou por todo o abdômen, motivou a visita. Os sinais vitais foram registados da seguinte forma: pressão arterial (PA) = 130/90 mmHg, frequência cardíaca (FC) = 80 bpm e temperatura (T) = 37 °C. O exame abdominal revelou sons intestinais normais, ligeira sensibilidade na região inguinal e sons tímpanos. Também se observou que ele tinha SBS congénita com um comprimento total do intestino delgado medido de aproximadamente 185 cm, significativamente mais curto do que o intervalo normal, e ausência de omento.\n\nA 10 de agosto de 2021, o paciente foi submetido a uma hemicolectomia direita e a uma ileostomia devido a dor abdominal associada a um diagnóstico de obstrução intestinal. Posteriormente, a 21 de setembro de 2021, o paciente teve uma colostomia removida e foi hospitalizado durante 6 dias (incluindo 3 dias na unidade de cuidados intensivos [UCI]). Após a alta, o paciente teve dor abdominal e edema, com uma escalada de sintomas a 1 de outubro de 2021. Foi relatada náusea aquando da admissão, mas sem vómitos, e não houve queixas relacionadas com a micção. Devido à dor pós-prandial e ao mau apetite, a ingestão nutricional do paciente foi comprometida. Não foi relatada febre, calafrios ou dispneia. Foi observado edema das extremidades inferiores (2+), sem clubbing ou cianose. Outros sinais vitais estavam dentro dos limites normais (pulsação de 82 batimentos/minuto, pressão arterial de 110/70 mmHg, taxa respiratória de 18 respirações/minuto, temperatura de 37 °C). A dor abdominal dificultou um exame completo devido a dor severa. O exame da cabeça, pescoço e tórax não revelou achados específicos.\n\nA contagem sanguínea completa indicou leucocitose (hemoglobina 11.7 g/dL, contagem de glóbulos brancos 19.23 × 103/µL, plaquetas 406 × 103/µL, RBC 4.30 × 106/µL, e hematócrito [HTC] 34.3%), enquanto a análise de gases arteriais mostrou alcalose metabólica (pH 7.56, pressão parcial de oxigênio [PO2] 204.5 mmHg, pressão parcial de dióxido de carbono [PCO2] 31.9 mmHg, excesso de base [BE] 7.0 mmol/L, e bicarbonato [HCO3] 29.1 mmol/L).\n\nRaio-X abdominal e torácico do homem de 38 anos com síndrome do intestino curto congênita e ausência do omento. Raio-X abdominal deitado de costas demonstrava alças intestinais dilatadas e ausência do omento, sem evidência de níveis de ar-fluido. Além disso, o raio-X torácico não mostrou anormalidades significativas, confirmando os achados cardiopulmonares normais. O raio-X abdominal deitado de pé revelou evidências de distensão gasosa e alças consistentes com o diagnóstico do paciente.\n\nFoi recomendada uma tomografia computadorizada (TC) de contraste do abdômen e da pelve. A secreção fecal das suturas do paciente levantou preocupações sobre peritonite pós-operatória devido a vazamento anastomótico, levando a uma intervenção cirúrgica imediata. O paciente foi submetido a laparotomia de emergência, drenagem e jejunostomia de duplo barril.\n\nA recuperação da paciente foi sem intercorrências, com ingestão oral de líquidos transparentes permitida no dia 2 pós-operatório e líquidos completos no dia 4 pós-operatório.\n\nPara a ausência congénita de omento e síndrome do intestino curto, as opções de tratamento incluem apoio nutricional, como nutrição total parenteral ou enteral. Casos graves podem necessitar de intervenção cirúrgica para alongar o intestino restante ou realizar um transplante intestinal. Estratégias para a síndrome do intestino curto resultante da ausência congénita de omento podem envolver apoio nutricional, juntamente com o aumento da expressão de proteínas de transporte (como cotransportadores de Na+/glucose, permutadores de Na+/H+) para facilitar a adaptação intestinal. As intervenções humanas incluem tratamento com glutamina e hormônio do crescimento ou administração de peptídeos semelhantes ao glucagon, embora sejam necessários estudos multicêntricos para obter provas conclusivas.\n",
+        "gold_summary": "Este caso apresenta uma confluência única destas condições raras num homem iraniano de 38 anos com um histórico de obstrução intestinal que requereu uma hemicolectomia direita e uma ileostomia. Subsequentemente, apresentou-se ao departamento de emergência com dor abdominal intensa e inchaço nas extremidades inferiores. Investigações laboratoriais revelaram um elevado número de glóbulos brancos e alcalose metabólica. Durante a exploração cirúrgica solicitada pela sua apresentação aguda, foram confirmadas a ausência congénita do omento e a síndrome do intestino curto. Foi realizada uma jejunostomia, mas, infelizmente, esta intervenção resultou numa má absorção grave e subsequente caquexia. Este caso lança luz sobre a ocorrência rara de fuga anastomótica e subsequente peritonite após uma hemicolectomia direita e uma ileostomia num paciente com as condições combinadas de intestino curto congénito e ausência congénita do omento.\n",
+        "synthetic_summary": {
+            "B1": "Um homem de 38 anos estava com muita dor na barriga e os pés e pernas inchados. Ele tinha um problema no intestino desde que nasceu. O intestino dele era muito curto e faltava uma parte que ajuda a proteger a barriga.\n\nEle já tinha feito uma cirurgia para tirar uma parte do intestino porque estava doendo muito. Depois, a dor voltou e ele ficou muito inchado. Os médicos fizeram exames e viram que ele estava com uma infecção.\n\nEntão, fizeram outra cirurgia para ajudar ele a melhorar. Depois, ele ficou tomando cuidado para comer e beber direitinho. Esse caso é muito raro e mostra que às vezes o intestino pode ter problemas difíceis, mas os médicos tentam ajudar com cirurgias e cuidados especiais.",
+            "B2": "**O que aconteceu com o paciente**\n\nUm homem de 38 anos do Irã teve problemas sérios no intestino. Ele já tinha uma condição rara chamada síndrome do intestino curto, que significa que seu intestino delgado é muito menor do que o normal. Além disso, ele nasceu sem omento, que é uma camada de tecido que ajuda a proteger os órgãos dentro da barriga. Por causa de uma obstrução intestinal, ele precisou passar por uma cirurgia para remover parte do intestino e criar uma ileostomia, que é quando o intestino é ligado a uma abertura no abdômen para eliminar fezes.\n\n**Os sintomas e o que os exames mostraram**\n\nDepois da cirurgia, ele voltou ao hospital com muita dor na barriga e inchaço nas pernas. Os exames de sangue mostraram que ele tinha muitos glóbulos brancos, o que indica que o corpo estava lutando contra uma infecção. Também foi detectada uma alteração no equilíbrio do sangue chamada alcalose metabólica, que pode acontecer quando o corpo está tentando se ajustar a problemas internos.\n\n**O que os médicos fizeram**\n\nDevido à gravidade dos sintomas, os médicos fizeram uma nova cirurgia para investigar e tratar o problema. Eles confirmaram que o paciente realmente não tinha omento e que seu intestino era muito curto. Durante a operação, foi feita uma jejunostomia, que é uma abertura no jejuno (parte do intestino delgado) para ajudar na alimentação e drenagem.\n\n**O que isso significa**\n\nInfelizmente, essa cirurgia causou dificuldades na absorção dos nutrientes, levando o paciente a um estado chamado caquexia, que é quando o corpo fica muito fraco e emagrece demais. Esse caso é importante porque mostra como é raro e complicado tratar pacientes que têm tanto a síndrome do intestino curto quanto a ausência do omento. Também alerta para um problema grave que pode acontecer depois de cirurgias intestinais, chamado fuga anastomótica, quando a conexão feita entre partes do intestino começa a vazar, causando uma infecção perigosa chamada peritonite.\n\n**Conclusão**\n\nEsse caso ajuda os médicos a entenderem melhor como cuidar de pessoas com essas condições raras. O tratamento envolve muito cuidado, apoio nutricional especial e, às vezes, mais cirurgias para tentar melhorar a qualidade de vida do paciente.",
+            "B3": "**Contexto**  \nEste relato descreve o caso de um homem iraniano de 38 anos que possui duas condições congênitas raras: síndrome do intestino curto (uma situação em que o intestino delgado é significativamente mais curto do que o normal, comprometendo a absorção de nutrientes) e ausência congênita do omento (uma estrutura de tecido gorduroso que normalmente cobre e protege os órgãos abdominais). O paciente havia sido submetido previamente a uma hemicolectomia direita (remoção parcial do cólon) e ileostomia (desvio do intestino delgado para uma abertura abdominal) devido a uma obstrução intestinal.\n\n**Principais Achados Clínicos e Diagnósticos**  \nApós a cirurgia inicial, o paciente apresentou dor abdominal intensa e edema (inchaço) nas pernas, sintomas que o levaram a buscar atendimento de emergência. Exames laboratoriais mostraram leucocitose (aumento dos glóbulos brancos, indicando inflamação ou infecção) e alcalose metabólica (alteração do equilíbrio ácido-base do sangue, com pH elevado). Radiografias revelaram alças intestinais dilatadas e ausência do omento, sem sinais claros de níveis de ar-fluido que normalmente indicam obstrução. A tomografia computadorizada foi solicitada para melhor avaliação.\n\nDevido à presença de secreção fecal nas suturas cirúrgicas, suspeitou-se de vazamento anastomótico (fuga na conexão feita entre segmentos intestinais durante a cirurgia), o que pode causar peritonite — uma inflamação grave da membrana que reveste a cavidade abdominal. Isso levou à realização de uma laparotomia de emergência (abertura cirúrgica do abdômen), drenagem do conteúdo infectado e criação de uma jejunostomia de duplo barril (uma abertura no jejuno, parte do intestino delgado, para desviar o trânsito intestinal).\n\n**Interpretação Clínica**  \nEste caso é notável pela combinação rara de síndrome do intestino curto congênito e ausência do omento, que complicaram o quadro clínico e o manejo cirúrgico. A ausência do omento reduz a capacidade natural do corpo de conter infecções e proteger os órgãos abdominais, aumentando o risco de complicações pós-operatórias como a peritonite causada pelo vazamento anastomótico. A jejunostomia, embora necessária para controlar a infecção, resultou em má absorção severa dos nutrientes, levando à caquexia (perda extrema de peso e massa muscular).\n\n**Próximos Passos e Considerações Terapêuticas**  \nO tratamento dessas condições envolve suporte nutricional intensivo, frequentemente por meio de nutrição parenteral total (alimentação intravenosa) ou enteral (via tubo alimentar), para compensar a absorção insuficiente causada pelo intestino curto. Em casos graves, podem ser consideradas cirurgias para aumentar o comprimento intestinal remanescente ou até transplante intestinal. Além disso, terapias que promovem a adaptação intestinal, como o uso de glutamina, hormônio do crescimento ou peptídeos semelhantes ao glucagon, podem ser úteis, embora ainda careçam de evidências conclusivas em estudos amplos.\n\nEste caso destaca a complexidade do manejo clínico e cirúrgico em pacientes com anomalias congênitas raras do trato gastrointestinal, reforçando a importância de um acompanhamento multidisciplinar para otimizar a recuperação e a qualidade de vida."
+        }
+    },
+    {
+        "article": "Um homem de 20 anos de idade, trabalhando como fazendeiro, sem histórico médico e cirúrgico, foi internado no departamento de emergência, queixando-se de dor cólica severa na região do flanco direito, irradiando para a área circundante e virilha. A dor está associada a febre de alto grau e vômitos recorrentes. Ele relatou hematúria indolor, febre e sintomas semelhantes a gripe 2 semanas antes da admissão no hospital. A febre e os sintomas semelhantes a gripe foram tratados com o uso de analgesia. Ele não tinha histórico anterior de doença de cálculos urinários ou infecções do trato urinário. O exame físico mostrou sensibilidade na virilha direita e sensibilidade positiva no ângulo costovertebral direito, caso contrário, era normal. Um hemograma completo, urinálise, análise de fezes e ultrassom abdominal foram realizados. A análise laboratorial mostrou leucocitose moderada de 20 000/mm3 (intervalo normal: 4,5-11 × 103/mm3), neutrofilia relativa e linfopenia relativa. A creatinina sérica estava normal. A urinálise mostrou +3 hematúria e cristais de oxalato de cálcio. A análise de fezes mostrou Entamoeba histolytica presente, sem ovos ou vermes detectados, e o resto da análise de fezes era normal. O ultrassom abdominal mostrou uma estrutura cilíndrica hiperechoica de 6 mm de diâmetro e 6 cm de comprimento na parte distal do ureter direito envolvendo a junção ureterovesical (UVJ) associada a hidronefrose direita mínima e um leve aumento na ecogenicidade do rim direito. Não há pedra renal definida; caso contrário, ambos os rins são normais em tamanho, local e forma. A imagem Doppler não foi realizada.\n\nEle foi hospitalizado no departamento de urologia; tratamento conservador foi inicialmente seguido. Foi feito um contraste de tomografia computadorizada, que mostrou uma estrutura tubular de 6 cm (um corpo estranho) localizada no ureter distal cerca de 2,5 cm dentro da bexiga. A estrutura mostra a densidade do tecido mole na parede e a densidade do fluido no aspecto interior, causando uma hidroureteronefrose do lado direito mínima. Uma imagem axial ao nível da parte distal do ureter direito mostra um ureter dilatado e um defeito de enchimento arredondado que representa o parasita obstrutivo. Imagem axial de tomografia computadorizada ao nível da junção vesicoureteral com 10 minutos de fase de atraso que mostra o parasita a passar parcialmente através da junção vesicoureteral. Caso contrário, o rim direito é normal em tamanho, ecotextura e espessura cortical sem pedras ou massas. Não há evidência de uma fístula entre o trato gastrointestinal e o urinário.\n\nFoi realizada uma ureteroscopia no hospital. Durante o procedimento, foi descoberta uma estrutura semelhante a cera de 6 mm no terço distal do ureter direito, acompanhada por uma quantidade significativa de pus. Além disso, foi observada uma projeção semelhante a um pólipo dentro da vista do ureteroscópio. O objeto extraído media 6 cm de comprimento, tinha uma coloração castanha, não era uma estrutura móvel e apresentava uma consistência elástica firme. Para facilitar a drenagem do pus, foi inserido um stent ureteral duplo J. Posteriormente, o espécime morto foi submetido a revisão patológica, sendo identificado como A lumbricoides. O paciente recebeu um comprimido de 400 mg de albendazol uma vez por dia durante 3 dias e recuperou sem incidentes.\n",
+        "gold_summary": "Neste relatório, apresentamos um caso de um homem de 20 anos que chegou à sala de emergência com dor no flanco direito, febre de alto grau e vômitos recorrentes. Avaliações diagnósticas foram realizadas, incluindo um hemograma completo, urinálise, análise de fezes, ultrassom abdominal e tomografia computadorizada. O diagnóstico final foi A lumbricoides encontrado na parte distal do ureter. Um procedimento de ureteroscopia confirmou o diagnóstico e extraiu o verme, que media 6 cm de comprimento, tinha cor marrom e apresentava uma consistência elástica firme.\n",
+        "synthetic_summary": {
+            "B1": "Um homem jovem estava com muita dor na barriga e febre. Ele foi ao hospital para ajudar. Os médicos fizeram exames para saber o que estava errado. Eles acharam um bichinho dentro do tubo que leva o xixi. Esse bichinho era um verme. Os médicos tiraram o verme com cuidado. Depois, ele tomou remédio e ficou bem.",
+            "B2": "**O que aconteceu com o paciente**\n\nUm homem de 20 anos sentiu uma dor forte na parte direita das costas, perto da barriga, junto com febre alta e vômitos. Ele foi ao hospital para descobrir o que estava causando esses sintomas.\n\n**Os exames feitos**\n\nOs médicos fizeram vários exames, como sangue, urina, fezes, ultrassom do abdômen e uma tomografia computadorizada, que é um tipo de raio-X detalhado. Esses exames mostraram que havia algo estranho no tubo que leva a urina do rim até a bexiga, chamado ureter.\n\n**O que eles encontraram**\n\nDurante um exame especial chamado ureteroscopia, que usa uma câmera para olhar dentro do ureter, os médicos acharam um verme chamado *Ascaris lumbricoides*. Esse verme tinha cerca de 6 centímetros, era marrom e firme. Ele estava bloqueando o ureter e causando a dor e a infecção.\n\n**Como trataram**\n\nOs médicos retiraram o verme com o exame e colocaram um pequeno tubo para ajudar a urina a sair. Depois, deram um remédio chamado albendazol, que mata os vermes. O paciente melhorou e se recuperou bem.\n\n**Por que isso é importante**\n\nEsse caso mostra que, às vezes, vermes podem causar problemas no sistema urinário, o que é raro. Por isso, é importante fazer exames detalhados quando alguém tem dor forte e febre, para encontrar a causa certa e tratar rápido.",
+            "B3": "**Contexto**  \nUm homem de 20 anos, trabalhador rural sem antecedentes médicos relevantes, foi admitido no pronto-socorro com dor intensa em cólica no flanco direito, irradiando para a região da virilha, acompanhada de febre alta e episódios repetidos de vômito. Ele relatou também presença de sangue na urina (hematúria) sem dor, além de sintomas gripais e febre ocorridos duas semanas antes da internação, tratados apenas com analgésicos. Não havia histórico prévio de cálculos renais ou infecções urinárias.\n\n**Principais Achados Clínicos e Exames**  \nNo exame físico, destacaram-se sensibilidade dolorosa na virilha direita e dor à palpação no ângulo costovertebral direito, indicando possível envolvimento renal ou ureteral. Os exames laboratoriais revelaram leucocitose moderada (aumento dos glóbulos brancos, 20.000/mm³), com predominância de neutrófilos e redução relativa de linfócitos, sugerindo infecção bacteriana. A função renal estava preservada, com creatinina sérica normal. A urinálise mostrou sangue em quantidade significativa (+3 hematúria) e presença de cristais de oxalato de cálcio, comuns em cálculos renais. A análise de fezes detectou o parasita Entamoeba histolytica, mas sem ovos ou vermes, e o restante estava normal.\n\nO ultrassom abdominal identificou uma estrutura cilíndrica hiperecogênica (com maior reflexão do som, indicando densidade aumentada) de 6 mm de diâmetro e 6 cm de comprimento na parte distal do ureter direito, próximo à junção entre ureter e bexiga (junção ureterovesical), associada a um leve aumento do volume do rim direito (hidronefrose mínima) e alteração na ecogenicidade renal, sugerindo obstrução parcial. Não foram visualizadas pedras renais definidas.\n\nA tomografia computadorizada com contraste confirmou a presença de uma estrutura tubular de 6 cm no ureter distal, estendendo-se parcialmente para dentro da bexiga, com densidade compatível com tecido mole na parede e conteúdo líquido no interior. Essa estrutura causava obstrução parcial do ureter, levando à hidroureteronefrose (dilatação do ureter e do rim). Não havia evidência de comunicação anormal entre o trato urinário e o sistema gastrointestinal.\n\n**Interpretação Clínica e Procedimento**  \nDiante desses achados, foi realizada uma ureteroscopia, procedimento endoscópico para visualização direta do ureter. Durante o exame, foi encontrada uma estrutura marrom, firme e elástica, com 6 cm de comprimento, obstruindo o terço distal do ureter direito, acompanhada por pus, indicando infecção local. Também foi observada uma projeção semelhante a um pólipo na parede ureteral. O parasita foi removido com sucesso e um stent ureteral duplo J foi colocado para garantir a drenagem adequada da urina e do pus.\n\nA análise patológica do material extraído confirmou que se tratava do verme Ascaris lumbricoides, um parasita intestinal que, neste caso raro, migrou para o trato urinário e causou obstrução e infecção.\n\n**Tratamento e Desfecho**  \nO paciente recebeu tratamento antiparasitário com albendazol, 400 mg por dia durante três dias, e evoluiu sem complicações, recuperando-se completamente.\n\n**Resumo Final**  \nEste caso ilustra uma apresentação incomum de Ascaris lumbricoides obstruindo o ureter distal, causando dor intensa, febre e infecção urinária. O diagnóstico foi estabelecido por exames de imagem e confirmado por ureteroscopia com remoção do parasita. O tratamento combinou intervenção endoscópica para desobstrução e terapia antiparasitária, resultando em recuperação satisfatória."
+        }
+    },
+    {
+        "article": "Uma paciente de 27 anos apresentou vermelhidão, coceira e ardência no olho direito quatro horas após receber a terceira dose total da vacina de reforço de mRNA contra a COVID-19. Ela usou lágrimas artificiais, mas seus sintomas permaneceram inalterados no dia seguinte, o que a levou a procurar um exame oftalmológico. Ela negou fotofobia, visão turva, visão dupla, sensação de corpo estranho, epífora, flashes visuais ou flutuadores visuais. Não houve episódios semelhantes anteriores com a mesma vacina antes das duas doses. O olho esquerdo foi assintomático e não foi afetado. O histórico médico passado da paciente foi significativo para astigmatismo míope de ambos os olhos, conjuntivite alérgica bilateral, rinite alérgica, doença de Crohn e asma leve intermitente.\n\nNo exame oftalmológico, a acuidade visual melhor corrigida permaneceu 20/20 bilateralmente. As pressões intraoculares foram medidas em 15 mmHg no olho direito e 16 mmHg no olho esquerdo. A conjuntiva direita tinha 2+ injeção que branqueou com gotas de fenilefrina. Não houve injeção escleral, nem sensibilidade escleral, nem irritação física adjacente à área da episclerite (por exemplo, sem triquiase). A câmara anterior do olho direito pareceu profunda e calma. A episclerite associada foi descrita. O restante do exame clínico dos segmentos anterior e posterior foi sem observações. O paciente continuou com lágrimas artificiais e começou a tomar ibuprofeno 200 mg três vezes ao dia durante uma semana. O paciente aderiu e tolerou o regime descrito e uma semana depois, todos os sintomas oculares e sinais foram resolvidos.\n\nA paciente ficou satisfeita com o cuidado que recebeu. Ela ficou aliviada que os seus sintomas se resolveram e que a sua visão final não foi afetada. Ela planeia verificar com o seu reumatologista antes de futuras doses de reforço da vacina contra a COVID-19. Consentimento informado por escrito foi obtido da paciente para publicação e para uso de dados e imagens.\n",
+        "gold_summary": "Uma mulher de 27 anos apresentou vermelhidão, coceira e ardência no olho direito, com um histórico de 1 dia. A paciente relatou o desenvolvimento desses sintomas dentro de 3-4 horas após a vacinação. O histórico médico passado foi relevante para a doença de Crohn. O exame oftalmológico revelou uma injeção conjuntival direita 2+ que branqueou com gotas de fenilefrina. Caso contrário, o exame oftalmológico foi normal. A paciente começou a usar lágrimas artificiais e ibuprofeno 200 mg três vezes ao dia durante uma semana. Depois de uma semana, todos os sintomas foram resolvidos e o exame oftalmológico voltou ao nível inicial.\n",
+        "synthetic_summary": {
+            "B1": "Uma moça tomou uma vacina no olho direito. Logo depois, o olho ficou vermelho, coçando e ardendo. Ela ficou assim por um dia. \n\nO médico olhou no olho dela. O olho estava vermelho, mas não doía muito. O resto estava normal. \n\nEla usou colírio e tomou remédio para dor. Depois de uma semana, o olho ficou bom de novo. Tudo voltou ao normal.",
+            "B2": "**O que aconteceu com a paciente**\n\nUma mulher de 27 anos teve vermelhidão, coceira e ardência no olho direito, começando cerca de 3 a 4 horas depois de tomar a terceira dose da vacina contra a COVID-19. Esses sintomas duraram um dia e a deixaram preocupada. Ela já tinha uma doença chamada Crohn, que afeta o intestino, mas não tinha problemas graves nos olhos antes.\n\n**O que os médicos encontraram**\n\nQuando os médicos examinaram seu olho, viram que a parte branca do olho direito estava vermelha, o que chamamos de \"injeção conjuntival\". Eles usaram um colírio chamado fenilefrina, que ajudou a diminuir essa vermelhidão. Fora isso, o exame dos olhos estava normal, sem sinais de problemas mais sérios.\n\n**O tratamento e o resultado**\n\nA paciente começou a usar lágrimas artificiais para ajudar a aliviar o desconforto e tomou ibuprofeno, um remédio para dor e inflamação, três vezes ao dia por uma semana. Depois desse tempo, todos os sintomas desapareceram e o exame do olho voltou ao normal.\n\n**O que isso significa**\n\nEsse caso mostra que, em algumas pessoas, a vacina pode causar uma inflamação leve e temporária no olho, chamada episclerite, que melhora com tratamento simples. A paciente ficou satisfeita porque sua visão não foi afetada e pretende conversar com seu médico antes de tomar futuras doses da vacina.",
+            "B3": "**Contexto**  \nUma mulher de 27 anos apresentou vermelhidão, coceira e sensação de ardência no olho direito, iniciando-se aproximadamente quatro horas após receber a terceira dose da vacina de reforço contra a COVID-19, baseada em tecnologia de mRNA. Ela não apresentou sintomas como sensibilidade à luz (fotofobia), visão embaçada, visão dupla, sensação de corpo estranho, lacrimejamento excessivo ou alterações visuais como flashes ou manchas. Seu histórico médico incluía astigmatismo míope, conjuntivite alérgica bilateral, rinite alérgica, doença de Crohn e asma leve intermitente. Não houve episódios semelhantes após as doses anteriores da vacina.\n\n**Principais Achados**  \nNo exame oftalmológico, a acuidade visual corrigida permaneceu normal (20/20) em ambos os olhos. A pressão intraocular estava dentro dos limites normais (15 mmHg no olho direito e 16 mmHg no esquerdo). Observou-se uma vermelhidão moderada (classificada como 2+) na conjuntiva do olho direito, que desapareceu temporariamente após a aplicação de gotas de fenilefrina (um vasoconstritor que reduz a vermelhidão). Não foram encontradas alterações na esclera (a parte branca do olho), nem sinais de irritação física ou inflamação mais profunda. A câmara anterior do olho direito estava com aparência normal, sem sinais de inflamação. O restante do exame dos segmentos anterior e posterior do olho não revelou anormalidades.\n\n**Interpretação Clínica**  \nO quadro clínico foi compatível com episclerite, uma inflamação superficial e benigna da camada que cobre a esclera, geralmente autolimitada e sem risco para a visão. A episclerite pode ser associada a doenças autoimunes, como a doença de Crohn, que a paciente possui. A relação temporal entre a vacinação e o início dos sintomas sugere uma possível reação inflamatória desencadeada pela vacina, embora não tenha ocorrido após as doses anteriores.\n\n**Próximos Passos e Desfecho**  \nO tratamento consistiu no uso de lágrimas artificiais para aliviar o desconforto e ibuprofeno 200 mg, um anti-inflamatório não esteroidal, administrado três vezes ao dia durante uma semana. A paciente aderiu ao tratamento e apresentou resolução completa dos sintomas e sinais clínicos após esse período, mantendo a visão preservada. Ela expressou satisfação com o atendimento recebido e pretende consultar seu reumatologista antes de futuras doses de reforço da vacina contra a COVID-19 para avaliar riscos e orientações específicas.\n\nO caso foi documentado com consentimento informado da paciente para publicação e uso dos dados clínicos e imagens."
+        }
+    },
+    {
+        "article": "Este é um paciente de 8 meses de idade, nascido de uma mãe para 3. A mãe fez acompanhamento de ANC, mas era irregular, e estava num centro de saúde rural com uma instalação precária, onde não conseguiu fazer ultrassom obstétrico. O parto foi em casa com um assistente de parto tradicional. Após o parto, os pais notaram um inchaço na parte occipital da cabeça. Ele aumentou de tamanho progressivamente até atingir o tamanho atual. Os pais foram ao centro de saúde, onde foram encaminhados ao hospital primário, que os encaminhou ao nosso centro. O inchaço não tinha secreção, e o paciente não tinha febre, vômito, incapacidade de sucção, choro agudo, movimento corporal anormal ou letargia. Após o exame do paciente, havia um cisto gigante de 40 cm por 35 cm, transiluminado com luz, macio, massa occipital na área do torcula dos seios. Havia um defeito ósseo palpável na base do saco. As fontanelas anterior e posterior não estavam abertas. O bebê era brincalhão, alerta, movendo todas as extremidades, sugando bem, e tinha sinais vitais estáveis. O paciente foi então examinado com um CBC, grupo sanguíneo, função renal e hepática, que estavam dentro da faixa normal, e a ressonância magnética do cérebro revelou um grande saco occipital hipointenso e T2 hiperintenso com múltiplos fluxos de vazio mostrando torcula, superior sagital sinus, e transverso sinus, e uma parte do lobo occipital direito do cérebro com defeito ósseo na base do saco. Depois de obter o consentimento informado por escrito, o paciente foi colocado na mesa de operação com a cabeça pendurada além da borda da mesa de operação ao lado da máquina de anestesia, com um anestesista segurando a cabeça e o saco pendurado além da mesa, e foi intubado com a primeira tentativa. Após a intubação, o paciente foi colocado em posição prona com a ajuda de uma ferradura de Mayfield. O cabelo foi raspado e limpo com sabão e água, e um assistente segurando a massa com a mão estéril, a pele foi então limpa e drapeada. Inicialmente, fizemos uma incisão transversal na pele, drenamos o LCR, e o saco colapsou. Então, o tecido cerebral displásico foi ressecado, e o seio venoso, tumor, torcula e outro tecido cerebral de aparência viável foram gentilmente reduzidos ao crânio. A dura foi dissecada, aparada, aparada e fechada como uma primária estanque. Não recomendamos cranioplastia em um encefalocele occipital gigante com alto risco de hidrocefalia pós-operativa; portanto, não fechamos o defeito ósseo. Depois disso, a pele foi aparada e fechada em duas camadas. Após a operação, o paciente ficou no departamento de neurocirurgia por sete dias sem hidrocefalia e sem déficit neurológico. O paciente é então seguido em uma clínica ambulatorial a cada duas semanas sem complicações neurológicas ou relacionadas à cirurgia.\n",
+        "gold_summary": "Este é um caso de um menino de 8 meses de idade, filho de uma mãe que não teve cuidados pré-natais regulares. Depois do bebé apresentar uma massa cefálica posterior progressiva, cística, transiluminada, sensível e com um tamanho de 40 cm x 35 cm, a imagem demonstrou um tecido cerebral pequeno, principalmente parte do lóbulo occipital direito, com a maior parte do saco ocupado por fluido cerebrospinal. A reparação foi feita e o tecido cerebral displásico foi ressecado, depois o tecido cerebral de aparência saudável e os seios dural foram reduzidos ao crânio, depois o paciente ficou no hospital e foi seguido de perto por hidrocefalia durante sete dias e foi dispensado sem hidrocefalia e sem déficit neurológico.\n",
+        "synthetic_summary": {
+            "B1": "Um bebê de 8 meses tinha uma bolinha grande na cabeça. A bolinha era cheia de água e um pedacinho do cérebro estava dentro dela. Os médicos fizeram uma cirurgia para tirar o pedacinho que não estava bom. Eles colocaram o resto do cérebro no lugar certo. O bebê ficou no hospital para os médicos verem se estava tudo bem. Depois, ele foi para casa feliz e sem problemas.",
+            "B2": "**O que aconteceu com o bebê**\n\nUm menino de 8 meses nasceu numa região rural, onde a mãe não fez todos os exames de gravidez necessários. Depois do nascimento, os pais perceberam que ele tinha um grande inchaço na parte de trás da cabeça. Esse inchaço foi crescendo até ficar com cerca de 40 cm por 35 cm. Quando o bebê foi examinado, os médicos viram que esse inchaço era uma bolsa cheia de líquido, chamada de encefalocele, que continha parte do cérebro e líquido que normalmente fica dentro da cabeça.\n\n**O que os médicos fizeram**\n\nOs médicos fizeram uma cirurgia para corrigir esse problema. Primeiro, eles retiraram o líquido da bolsa para que ela murchasse. Depois, tiraram uma parte do tecido cerebral que não estava normal (chamado tecido displásico) e colocaram o tecido cerebral saudável e as veias importantes de volta para dentro do crânio. Eles fecharam a pele, mas deixaram o buraco no osso aberto, porque fechar poderia causar outro problema chamado hidrocefalia, que é quando o líquido dentro do cérebro acumula demais.\n\n**Como o bebê ficou depois**\n\nDepois da cirurgia, o bebê ficou no hospital por uma semana. Durante esse tempo, os médicos observaram para ver se ele teria hidrocefalia ou algum problema no cérebro, mas ele não teve nenhum desses problemas. O bebê estava alerta, se mexendo bem e sugando o leite normalmente. Depois, ele continuou sendo acompanhado em consultas regulares e não apresentou complicações relacionadas à cirurgia ou ao cérebro.\n\n**Por que isso é importante**\n\nEsse caso mostra que, mesmo com um problema grande e raro como uma encefalocele gigante, é possível fazer uma cirurgia segura e ajudar o bebê a ter uma boa recuperação. Também destaca a importância do acompanhamento durante a gravidez para tentar evitar ou preparar melhor para situações como essa.",
+            "B3": "**Contexto**  \nEste relato descreve o caso de um menino de 8 meses, filho de uma mãe que teve acompanhamento pré-natal irregular em uma área rural com recursos limitados. O parto ocorreu em casa, assistido por uma parteira tradicional. Após o nascimento, os pais notaram um inchaço progressivo na parte posterior da cabeça do bebê, que cresceu até atingir 40 cm por 35 cm. O bebê não apresentava sinais de infecção, como febre ou secreção, nem sintomas neurológicos como vômitos, irritabilidade intensa, movimentos anormais ou sonolência excessiva.\n\n**Principais Achados Clínicos e Exames**  \nNo exame físico, foi identificada uma grande massa macia e translúcida na região occipital (parte de trás da cabeça), com um defeito ósseo palpável na base dessa massa. As fontanelas (moleiras) anterior e posterior estavam fechadas, e o bebê apresentava bom estado geral: alerta, ativo, com movimentos normais e boa sucção. Exames laboratoriais básicos, incluindo hemograma completo e funções renal e hepática, estavam normais.\n\nA ressonância magnética do cérebro revelou um grande saco occipital contendo principalmente líquido cerebrospinal (líquido que envolve o cérebro e a medula), com uma pequena porção de tecido cerebral displásico (tecido cerebral anormal) proveniente do lobo occipital direito. O saco envolvia estruturas vasculares importantes, como a torcula (junção dos seios venosos cerebrais) e outros seios venosos principais.\n\n**Intervenção Cirúrgica**  \nApós consentimento informado, o paciente foi submetido à cirurgia para correção da encefalocele (uma protrusão do tecido cerebral e das membranas cerebrais através de um defeito no crânio). Durante o procedimento, o líquido cerebrospinal foi drenado para colapsar o saco, o tecido cerebral displásico foi removido, e o tecido cerebral saudável, junto com os seios venosos, foi cuidadosamente recolocado dentro do crânio. A dura-máter (membrana que envolve o cérebro) foi fechada de forma estanque (sem vazamentos), mas o defeito ósseo não foi reparado para evitar complicações, como hidrocefalia (acúmulo de líquido no cérebro) pós-operatória. A pele foi fechada em duas camadas.\n\n**Desfecho e Seguimento**  \nO bebê permaneceu internado por sete dias no setor de neurocirurgia, sem apresentar sinais de hidrocefalia ou déficits neurológicos. Após a alta hospitalar, ele foi acompanhado regularmente em ambulatório a cada duas semanas, sem complicações relacionadas à cirurgia ou ao quadro neurológico.\n\n**Resumo Final**  \nEste caso ilustra o manejo bem-sucedido de uma encefalocele occipital gigante em um bebê, com remoção do tecido cerebral anormal e preservação do tecido saudável e das estruturas vasculares, seguido de fechamento cuidadoso das membranas cerebrais. O acompanhamento rigoroso permitiu a identificação precoce de possíveis complicações, garantindo um resultado favorável sem déficits neurológicos."
+        }
+    },
+    {
+        "article": "Este homem de 53 anos apresentou inicialmente desconforto agudo no peito como um sintoma isolado. Ele era anteriormente um não-fumante ativo, em forma e bem, sem histórico médico ou familiar.\n\nAo exame, ele tinha sons cardíacos normais sem murmúrios. A pressão venosa jugular não estava elevada. O tórax estava limpo e não havia edema de tornozelo.\n\nA pressão arterial dele era de 98/78 mm Hg e o seu ritmo cardíaco de 62 batimentos por minuto. A saturação de oxigénio era de 100% com ar ambiente e o seu ritmo respiratório era de 16 respirações por minuto. Ele estava apirexial com uma temperatura de 37.1°C.\n\n\nInvestigações\n\nECG mostrou LVH e inversões de onda T generalizadas. Os níveis séricos de troponina I cardíaca de alta sensibilidade (hs-cTnI) aumentaram de 28 ng/L (0 horas) para 77 ng/L (6 horas) (limite superior de referência para este teste em homens: 34 ng/L). Foi tratado com dupla terapia antiplaquetária para um diagnóstico funcional de infarto do miocárdio sem elevação do segmento ST.\n\nA angiografia coronária por TC mostrou placa calcificada em duas artérias coronárias. A angiografia convencional não confirmou a limitação do fluxo. A ecocardiografia transtorácica mostrou LVH moderado com obstrução significativa do trato de saída. Houve um leve comprometimento sistólico com acinesia localizada da parede inferior. Foi solicitada uma ressonância magnética cardíaca como investigação ambulatorial.\n\nUm mês depois, o paciente foi readmitido com mais desconforto no peito. Quatro dias de telemetria não revelaram disritmia durante esses episódios de desconforto. O ECG não mostrou alterações dinâmicas. Houve um aumento estático de baixo nível de hs-cTnI em 37 ng/L, 30 ng/L e 33 ng/L, respectivamente, tomado diariamente devido a múltiplos episódios intermitentes de dor no peito ao longo de vários dias. O nível de proteína reativa C foi inferior a 3 mg/L e ele estava afebril.\n\nA ressonância magnética cardíaca mostrou LVH concêntrico, uma área de edema basal inferolateral provável e um padrão incomum de aumento tardio de gadolínio (LGE) predominantemente endocárdico com aumento da parede média septal e aumento subendocárdico difuso. Ele tinha volumes normais do LV e fração de ejeção (61%), mas uma massa elevada de 221 g (101 g/m2) consistente com a hipertrofia. Como a pressão arterial permaneceu normal, estávamos relutantes em atribuir o LVH a doença cardíaca hipertensiva.\n\n\nDiagnóstico diferencial\n\nDevido à natureza incomum do caso, foi discutido na reunião da equipa multidisciplinar regional. A ressonância magnética não foi considerada como sendo clássica de miocardite ou amiloide, mas o resultado da reunião sugeriu a triagem para cardiomiopatia amiloide e doença de Anderson-Fabry.\n\nO nível de alfa galactosidase foi normal, excluindo efetivamente a doença de Fabry.\n\nA cadeia leve livre de soro (SF) apresentou aumento de SF Kappa para 253,20 mg/L (intervalo de referência: 3,3-19,4) com normal de SF Lambda 9,6 mg/L (intervalo de referência: 5,7-26,3). A razão kappa/lambda foi de 26,375 (intervalo de referência: 0,26-1,65).\n\nA aspiração da medula óssea mostrou partículas em grande parte obscurecidas por depósitos extracelulares proteicos azuis, nublados e amorfos. Estes depósitos apresentaram-se cor-de-rosa salmão com coloração vermelha Congo. Quando visualizados sob microscopia de luz polarizada, apresentaram uma birrefringência verde-maçã característica - consistente com a deposição amiloide. Houve um ligeiro excesso de células plasmáticas, que foi insuficiente para diagnosticar uma discrasia de células plasmáticas.\n\nA coloração de amostras de gordura aspiradas com vermelho Congo não demonstrou evidências convincentes de deposição amilóide.\n\nUm TAC do abdómen e da pélvis não mostrou mais nada que explicasse a sua amiloidose. Os testes de hepatite B, hepatite C e HIV foram negativos. A eletroforese do soro não mostrou nenhuma banda monoclonal anormal e as imunoglobulinas estavam normais.\n\n\nTratamento\n\nO paciente foi encaminhado ao Centro Nacional de Amiloidose em Londres, onde o diagnóstico foi confirmado. Por recomendação deles, a equipa de hematologia local supervisionou a administração de quimioterapia para amiloidose primária AL com envolvimento cardíaco. Ele recebeu um ciclo de 21 dias de VCD (bortezomib, ciclofosfamida e dexametasona).\n\nForam fornecidos medicamentos de apoio adicionais, incluindo doxiciclina, aciclovir e alopurinol para os primeiros 2 ciclos de quimioterapia.\n\n\nResultado e acompanhamento\n\nO acompanhamento após um ano do diagnóstico mostrou que o paciente permaneceu estável, a dor no peito havia se resolvido completamente e ele ainda não apresentava nenhum sintoma de insuficiência cardíaca.\n\nNo entanto, quando a pandemia de COVID-19 atingiu o país, a sua quimioterapia foi interrompida pelos seus médicos no Centro Nacional de Amiloidose, dado o seu bom progresso com o tratamento e os riscos associados de COVID-19.\n\nDois meses depois, ele apresentou outro episódio de dor torácica e aumento de hs-cTnI de baixo nível. A quimioterapia foi, portanto, reintroduzida, e a dor torácica foi resolvida posteriormente.",
+        "gold_summary": "Um homem de 53 anos apresentou-se num hospital geral distrital com dor torácica, alterações no ECG e um pequeno aumento da troponina I cardíaca de alta sensibilidade. Não houve sintomas de insuficiência cardíaca. A angiografia coronária por TAC revelou uma doença calcificante moderada e a angiografia convencional não confirmou qualquer limitação do fluxo. A ecocardiografia mostrou uma hipertrofia ventricular esquerda (HVE). A sua pressão arterial permaneceu normal durante toda a sua admissão. O centro terciário rotulou este evento como um evento de “ruptura de placa”, mas a HVE permaneceu inexplicada. A ressonância magnética cardíaca apresentou um padrão invulgar de realce tardio de gadolínio, que não era clássico de amilóide. No entanto, uma cadeia leve kappa livre sérica elevada, juntamente com a deposição de amilóide no seu aspirado de medula óssea, confirmou o diagnóstico de amiloidose AL primária com envolvimento cardíaco. O paciente passou a fazer quimioterapia e permaneceu estável no seguimento de 1 ano.\n",
+        "synthetic_summary": {
+            "B1": "Um homem de 53 anos sentiu dor no peito e foi ao hospital. Ele fez exames no coração. O coração dele estava maior do que o normal. O médico achou estranho porque a pressão dele estava boa.\n\nUm exame especial mostrou que tinha um problema diferente no coração. Outro exame mostrou que tinha um tipo de sujeira chamada amiloide no corpo dele.\n\nOs médicos deram remédios fortes para limpar essa sujeira. Depois de um ano, ele ficou bem e a dor no peito passou. Os médicos continuam cuidando dele com muito carinho.",
+            "B2": "**O que aconteceu com o paciente**\n\nUm homem de 53 anos foi ao hospital porque sentia dor no peito. Os exames mostraram algumas mudanças no coração, como no eletrocardiograma (ECG), e um pequeno aumento de uma proteína chamada troponina, que aparece quando o coração está machucado. Ele não tinha sinais de que o coração estivesse falhando.\n\n**O que os exames mostraram**\n\nUm exame chamado angiografia por tomografia computadorizada (TAC) mostrou que ele tinha placas duras (calcificadas) em algumas artérias do coração, mas o sangue ainda passava normalmente. Outro exame, o ecocardiograma, mostrou que o músculo do lado esquerdo do coração estava mais grosso do que o normal, o que se chama hipertrofia ventricular esquerda (HVE). A pressão arterial dele estava normal o tempo todo.\n\n**O que os médicos pensaram**\n\nNo começo, os médicos acharam que ele teve um problema chamado “ruptura de placa”, que pode causar dor no peito. Mas a causa do músculo do coração estar mais grosso não estava clara. Um exame mais detalhado, a ressonância magnética do coração, mostrou um padrão diferente do que é comum em algumas doenças do coração, como a amiloidose.\n\n**Como foi feito o diagnóstico**\n\nOs médicos fizeram exames de sangue e encontraram uma proteína chamada cadeia leve kappa muito alta. Também fizeram uma biópsia da medula óssea, que é quando retiram um pouquinho do osso para analisar, e viram que havia depósitos de uma substância chamada amiloide. Isso confirmou que ele tinha amiloidose AL primária, uma doença rara onde proteínas anormais se acumulam no coração, prejudicando seu funcionamento.\n\n**O tratamento e o que aconteceu depois**\n\nO paciente começou a fazer quimioterapia, que é um tratamento com remédios para tentar controlar a doença. Depois de um ano, ele estava estável, sem dor no peito e sem sinais de piora no coração.\n\n---\n\nEste caso mostra como é importante investigar direitinho quando o coração apresenta sinais estranhos, para encontrar doenças raras e tratar a tempo.",
+            "B3": "**Contexto**  \nUm homem de 53 anos, previamente saudável e sem fatores de risco evidentes, apresentou-se inicialmente com dor torácica aguda isolada. Durante a avaliação hospitalar, não foram observados sinais de insuficiência cardíaca, como inchaço nas pernas ou pressão venosa jugular elevada. Seus sinais vitais estavam estáveis, com pressão arterial normal e ritmo cardíaco regular.\n\n**Principais Achados Diagnósticos**  \nO eletrocardiograma (ECG) revelou hipertrofia ventricular esquerda (HVE) e inversões generalizadas da onda T, indicando alterações no músculo cardíaco. Os níveis de troponina I cardíaca de alta sensibilidade, um marcador de lesão cardíaca, estavam elevados, sugerindo dano ao coração, embora sem evidência de infarto clássico com elevação do segmento ST. A angiografia coronária por tomografia computadorizada mostrou placas calcificadas em duas artérias, mas a angiografia convencional não demonstrou obstrução significativa do fluxo sanguíneo. A ecocardiografia confirmou hipertrofia moderada do ventrículo esquerdo com obstrução importante no trato de saída do ventrículo, além de uma área com movimento anormal na parede inferior do coração.\n\nPosteriormente, a ressonância magnética cardíaca evidenciou hipertrofia concêntrica do ventrículo esquerdo e um padrão incomum de realce tardio de gadolínio (LGE), que não correspondia aos padrões típicos de miocardite (inflamação do músculo cardíaco) ou amiloidose clássica. A massa cardíaca estava aumentada, mas a função de ejeção do ventrículo esquerdo permanecia normal, e a pressão arterial do paciente continuava dentro dos limites normais, o que dificultava atribuir a hipertrofia a hipertensão arterial.\n\n**Diagnóstico Diferencial e Confirmação**  \nDiante da apresentação atípica, o caso foi discutido em uma equipe multidisciplinar especializada. Foram descartadas doenças como a cardiomiopatia de Anderson-Fabry, por níveis normais da enzima alfa-galactosidase. No entanto, exames laboratoriais mostraram um aumento significativo da cadeia leve kappa livre no soro, com uma razão kappa/lambda muito elevada, sugerindo uma produção anormal dessas proteínas. A biópsia da medula óssea revelou depósitos extracelulares que, após coloração específica com vermelho Congo, apresentaram birrefringência verde-maçã sob luz polarizada — característica típica da amiloidose, uma condição em que proteínas anormais se acumulam nos tecidos. Embora não houvesse evidência clara de uma doença das células plasmáticas, esses achados confirmaram o diagnóstico de amiloidose primária do tipo AL com envolvimento cardíaco.\n\n**Tratamento e Evolução**  \nO paciente foi encaminhado a um centro especializado em amiloidose, onde iniciou quimioterapia combinada com bortezomib, ciclofosfamida e dexametasona, visando reduzir a produção das proteínas amiloides. Medicamentos de suporte, como doxiciclina, aciclovir e alopurinol, foram administrados para prevenir complicações durante o tratamento. Após um ano de acompanhamento, o paciente manteve-se estável, sem sintomas de insuficiência cardíaca e com resolução completa da dor torácica.\n\nDurante a pandemia de COVID-19, a quimioterapia foi temporariamente suspensa devido ao bom progresso e aos riscos associados à infecção. Contudo, após novo episódio de dor no peito e aumento dos níveis de troponina, o tratamento foi retomado, resultando em melhora dos sintomas.\n\n**Interpretação Clínica**  \nEste caso ilustra a complexidade do diagnóstico de amiloidose cardíaca, especialmente quando os sinais clínicos e exames de imagem não apresentam padrões típicos. A hipertrofia ventricular esquerda com dor torácica e elevação discreta da troponina, em ausência de obstrução coronariana significativa, deve levantar suspeita para doenças infiltrativas como a amiloidose AL. A confirmação depende da combinação de exames laboratoriais, imagem especializada e biópsia tecidual.\n\n**Próximos Passos**  \nO manejo da amiloidose cardíaca AL requer acompanhamento multidisciplinar contínuo, com monitoramento rigoroso da função cardíaca e resposta ao tratamento quimioterápico. A reintrodução da quimioterapia diante de sinais de atividade da doença é essencial para controlar a progressão e melhorar a qualidade de vida do paciente. Além disso, a vigilância para possíveis complicações infecciosas, especialmente em contextos como a pandemia, deve ser cuidadosamente considerada."
+        }
+    },
+    {
+        "article": "Um paciente de 72 anos apresentou-se com dor no peito irradiando para o braço esquerdo e dispneia progressiva nas últimas semanas. Ele tinha um histórico de trombose venosa profunda do membro inferior e hipertensão arterial controlada. Não havia outras comorbidades relevantes.\n\nNa avaliação física, o paciente apresentou-se em bom estado geral sem sinais de insuficiência cardíaca, com pressão arterial de 156/101 mmHg e frequência cardíaca de 73 bpm. Ele estava eupneico e a saturação de oxigênio arterial foi de 93%. A função renal foi prejudicada com uma creatinina sérica de 115 μmol/L e uma taxa de filtração glomerular estimada de 54 mL/min/1.73 m², a troponina T de alta sensibilidade foi ligeiramente elevada a 29 ng/L e NT-proBNP significativamente aumentado a 5463 ng/L. O ECG mostrou flutter atrial recém-diagnosticado com uma frequência cardíaca irregular de 93 bpm, bem como distúrbios de repolarização anterior e inferior (inversão da onda T em II, III, aVF, V1-V4). A pontuação CHA2DS2-VASc foi de 4 pontos.\n\n\nA ecocardiografia transtorácica mostrou função de ejeção ventricular esquerda normal (LVEF 55%), uma função ventricular direita ligeiramente prejudicada (TAPSE 18 mm) e aumento da pressão arterial pulmonar (sPAP 47 mm Hg). Um teste de esforço em bicicleta foi realizado e mostrou uma queda relevante da pressão arterial de 138/74 mm Hg em repouso para 118/76 mm Hg a 67% da frequência cardíaca máxima prevista para a idade.\n\nCom base nessas descobertas, era esperada uma doença coronária relevante, provavelmente com doença coronária esquerda (com base na queda da pressão arterial no teste de estresse).\n\nA EP foi um possível diagnóstico diferencial (Escore de Wells de 4,5 pontos previu um risco moderado com uma chance de 16,2% de EP). A anticoagulação já foi indicada devido ao flutter atrial.\n\nO flutter atrial recém-documentado foi visto como associado à doença subjacente. Não houve sinais de anormalidades neurológicas.\n\n\nInvestigações\n\nO angiograma coronário revelou uma doença coronária de dois vasos seguida de intervenção coronária percutânea ad hoc com revascularização completa. O cateterismo cardíaco direito, realizado devido ao ligeiro aumento da sPAP, revelou uma PAP média elevada (mPAP) de 38 mmHg de origem precapilar e pós-capilar. O angiograma pulmonar mostrou oclusão tromboembólica da artéria pulmonar subsegmentar do lobo inferior direito. A análise do gás arterial mostrou alcalose respiratória, parcialmente compensada metabolicamente (pH 7,49, pCO23,4 kPa, pO211,7 kPa, HCO319,5 mmol/L, excesso de base -3,8 mmol/L).\n\n\nTratamento\n\nO paciente foi então admitido na unidade de cuidados coronários (CCU), onde iniciou-se a terapia antiplaquetária dupla (DAPT) com aspirina e clopidogrel, bem como a anticoagulação oral com apixaban.\n\nA monitorização hemodinâmica na UTI foi aceitável com uma pressão arterial de 140/100 mmHg, uma frequência cardíaca de 85 bpm, uma frequência respiratória de 17/min e um SO2 de 94% no ar ambiente. A TC do tórax no dia seguinte confirmou a EP com EP extensivas, bilaterais, centrais e periféricas. Estes achados foram progressivos em comparação com os resultados da angiografia pulmonar do dia anterior. Numa avaliação posterior, a única alteração adicional foi um novo diagnóstico de bloqueio do ramo direito (BRD) e uma alteração do eixo cardíaco no ECG. O paciente ainda não apresentava qualquer desconforto ou sinais de instabilidade cardiopulmonar e o exame de gases arteriais no sangue não se alterou.\n\nDurante uma queda após mobilização independente na CCU, o paciente desenvolveu parada circulatória com atividade elétrica sem pulso (PEA). A ressuscitação cardiopulmonar imediata foi iniciada. Durante a ressuscitação, foi realizado um cateterismo cardíaco direito, que mostrou um trombo oclusivo na artéria pulmonar direita e foi considerado impossível de mobilizar por técnicas intervencionistas.\n\n\nResultado e acompanhamento\n\nApós 45 minutos de ressuscitação mecânica, o paciente desenvolveu uma linha plana no ECG. Com base na descoberta recente no angiograma pulmonar e na ressuscitação mecânica já prolongada e sem sucesso, o retorno da circulação espontânea era muito improvável e os esforços de ressuscitação foram interrompidos, após o que o paciente morreu.",
+        "gold_summary": "Apresentamos um caso de um homem de 72 anos com tromboembolismo pulmonar agudo submassivo. O índice de gravidade da embolia pulmonar e a estratificação de risco clínico comum recomendaram a anticoagulação sistémica e um curso clínico sem complicações. Uma estratégia de reperfusão primária não foi indicada pelas diretrizes atuais. Sob anticoagulação estabelecida, o paciente foi encontrado em paragem cardíaca imediatamente após a mobilização da cama na manhã seguinte. A cateterização cardíaca direita sob ressuscitação em curso revelou uma obstrução completa da artéria pulmonar direita por um grande trombo. A intervenção dirigida por cateter, tentando contornar o trombo com fios guia intervencionais, falhou. Por fim, o paciente morreu de insuficiência cardíaca direita aguda.\n",
+        "synthetic_summary": {
+            "B1": "Um senhor de 72 anos estava com um problema no pulmão. Ele tinha um pedaço de sangue que não devia estar lá. Os médicos deram remédios para o sangue não piorar. Eles acharam que ele ficaria bem assim.\n\nNo dia seguinte, quando ele tentou levantar da cama, seu coração parou. Os médicos tentaram ajudar, mas o pedaço de sangue estava bloqueando o pulmão. Eles tentaram tirar, mas não conseguiram.\n\nInfelizmente, o coração dele não voltou a funcionar. Ele morreu por causa disso.",
+            "B2": "**Resumo do Caso Médico Explicado**\n\nEste é o relato de um homem de 72 anos que teve um problema sério chamado tromboembolismo pulmonar agudo submassivo. Isso significa que um coágulo (um pedaço de sangue endurecido) bloqueou uma parte importante da artéria que leva sangue aos pulmões, dificultando a passagem do sangue.\n\nOs médicos usaram métodos para avaliar o risco do paciente e decidiram que o melhor tratamento era usar remédios anticoagulantes. Esses remédios ajudam a evitar que novos coágulos se formem e que os já existentes cresçam. Segundo as regras médicas atuais, não era indicado fazer um tratamento mais agressivo para tentar remover o coágulo logo de início.\n\nMesmo com o tratamento correto, no dia seguinte, quando o paciente tentou se levantar da cama, ele teve uma parada cardíaca, que é quando o coração para de funcionar direito. Durante a tentativa de reanimá-lo, os médicos fizeram um exame especial para olhar o coração e os vasos do pulmão. Eles descobriram que a artéria pulmonar direita estava completamente bloqueada por um grande coágulo.\n\nOs médicos tentaram usar fios e cateteres para desobstruir essa artéria, mas não conseguiram. Infelizmente, o paciente acabou morrendo por causa da falha do coração direito, que não conseguiu bombear o sangue para os pulmões devido ao bloqueio.\n\n**O que isso significa**\n\nEsse caso mostra como o tromboembolismo pulmonar pode ser perigoso, mesmo quando tratado corretamente com remédios. Às vezes, o coágulo pode causar uma parada cardíaca súbita e ser difícil de remover. Por isso, é importante que pacientes com esse problema sejam monitorados de perto e tratados rapidamente para evitar complicações graves.",
+            "B3": "**Contexto**  \nEste relato descreve o caso de um homem de 72 anos que apresentou um quadro complexo envolvendo tromboembolismo pulmonar (TEP) agudo submassivo, uma condição na qual coágulos sanguíneos bloqueiam parcialmente as artérias dos pulmões, comprometendo a circulação e a função cardíaca.\n\n**Principais Achados**  \nO paciente chegou ao hospital com dor no peito irradiando para o braço esquerdo e falta de ar progressiva. Exames iniciais indicaram uma arritmia cardíaca chamada flutter atrial, elevação de marcadores cardíacos (troponina e NT-proBNP) e sinais de pressão arterial pulmonar aumentada. O teste de esforço revelou uma queda significativa da pressão arterial, sugerindo doença coronária, confirmada posteriormente por angiografia que mostrou obstruções em duas artérias coronárias, tratadas com sucesso por intervenção percutânea.\n\nAlém disso, o cateterismo cardíaco direito revelou pressão arterial pulmonar média elevada, indicando hipertensão pulmonar de origem mista (pré e pós-capilar). A angiografia pulmonar identificou oclusão tromboembólica em ramos subsegmentares da artéria pulmonar direita, confirmando o diagnóstico de embolia pulmonar. A tomografia computadorizada do tórax evidenciou embolias extensas, bilaterais, tanto centrais quanto periféricas.\n\n**Interpretação Clínica**  \nO paciente foi tratado com anticoagulação oral (apixabana) e terapia antiplaquetária dupla devido à doença coronária e ao flutter atrial. Apesar da anticoagulação e da ausência de instabilidade clínica inicial, ele sofreu uma parada cardíaca do tipo atividade elétrica sem pulso (PEA) logo após mobilização na unidade coronariana. Durante a ressuscitação, um cateterismo cardíaco direito revelou um trombo grande e oclusivo na artéria pulmonar direita, que não pôde ser removido por técnicas intervencionistas. A falha na reperfusão e a obstrução persistente levaram à insuficiência cardíaca direita aguda e ao óbito do paciente.\n\n**Próximos Passos e Considerações**  \nEste caso ilustra a complexidade do manejo do tromboembolismo pulmonar submassivo, especialmente quando coexistem outras doenças cardíacas, como doença coronária e arritmias. Embora as diretrizes recomendem anticoagulação como tratamento padrão para pacientes estáveis, a possibilidade de progressão rápida para parada cardíaca destaca a importância da monitorização rigorosa e da avaliação contínua do risco. A falha da intervenção dirigida por cateter evidencia os desafios terapêuticos em casos graves de embolia pulmonar, sugerindo que estratégias adicionais ou alternativas podem ser necessárias em situações semelhantes."
+        }
+    },
+    {
+        "article": "Homem de 68 anos com hipertensão arterial, doença pulmonar obstrutiva crônica e tabagismo ativo, consultou no Pronto-Socorro em 01/02/23 por perda de acuidade visual progressiva (3 meses de evolução) associada a hemiparesia braquio-crural esquerda, exacerbada nos dias anteriores à consulta.\n\nFoi evidenciado um NIHSS de 5 pontos, com disartria e paresia mínima do hemicórpio esquerdo, pressão arterial de 160/80 mmHg, frequência cardíaca de 75 bpm e oximetria de pulso de 94% (FiO2 ambiental). Foi realizado um Angio-TC evidenciando uma estenose severa alta da ACI direita e uma Ressonância Magnética objetivou infartos agudos no hemisfério cerebral direito.\n\nO eco Doppler confirmou uma estenose severa (VPS 356 cm/s) da ACI direita. Após ser avaliado minuciosamente, confirmando uma estenose carotídea direita severa sintomática associado a uma lesão morfológica alta (que dificulta tecnicamente a CEA) e alto risco cirúrgico, decidimos realizar tratamento endovascular mediante TCAR.\n\nA dissecção da ACC e da VYI foi realizada em 23/02/2008, sob anestesia geral e heparinização sistêmica (100 UI/kg de heparina não fracionada, para um Tempo de Ativação da Coagulação [ACT] >250 s). Uma vez criada a fístula carótido-jugulária, a ACC foi clampeada, instaurando a reversão dinâmica do fluxo.\n\nCruzando a lesão (com a micro-guia de trabalho) e canalizando a ACI distal, procedeu-se a implantação de um stent carotídeo (Casper®. Mirovention, Terumo) de 8x30 mm. Por ser uma lesão severa e distal, durante a implantação ocorreu um fenômeno de migração proximal (para a ACC), sendo necessário instalar um segundo stent (7x30 mm) para tratar satisfatoriamente a lesão.\n\nO angiograma mostrou melhora imediata do lúmen da ACI e expansão adequada dos stents. A ACC foi desobstruída (restaurando o fluxo cerebral anterógrado), os stents foram removidos e a incisão foi fechada como descrito anteriormente.\n\nO paciente se recuperou satisfatoriamente, sem complicações, e recebeu alta no segundo dia pós-operatório com dupla terapia antiplaquetária.\n\nDurante o acompanhamento, não houve eventos neurológicos e no eco Doppler de controle (3, 6 e 12 meses), o stent foi encontrado permeável e sem sinais de reestenose.\n",
+        "gold_summary": "Homem de 68 anos com hipertensão e doença pulmonar obstrutiva crônica que desenvolveu um acidente vascular cerebral secundário a uma estenose severa alta na artéria carótida interna direita. Foi decidido realizar TCAR devido à sua localização e risco cirúrgico. Durante o procedimento, foi criada uma fístula transitória entre a artéria carótida e a veia jugular ipsilateral para inverter o fluxo e proteger o cérebro, permitindo a implantação segura do stent. O paciente recuperou-se sem complicações e permanece assintomático após um ano de acompanhamento.\n",
+        "synthetic_summary": {
+            "B1": "Um homem de 68 anos ficou com o lado esquerdo do corpo fraquinho e a visão ruim. Isso aconteceu porque um caninho do sangue no pescoço estava muito apertado. Os médicos fizeram uma operação para abrir esse caninho. Eles usaram um tubo pequeno para ajudar o sangue a passar melhor. Durante a operação, eles fizeram um caminho especial para proteger o cérebro. O homem ficou bem e, depois de um ano, está saudável e sem problemas.",
+            "B2": "**O que aconteceu com o paciente**\n\nUm homem de 68 anos, que tinha pressão alta e problemas nos pulmões, começou a perder a visão e teve fraqueza no lado esquerdo do corpo. Ele sofreu um acidente vascular cerebral (AVC), que é quando o sangue não chega direito ao cérebro, por causa de um entupimento grave em uma artéria importante do pescoço chamada artéria carótida interna direita.\n\n**Como foi o tratamento**\n\nOs médicos decidiram fazer um procedimento chamado TCAR, que é uma forma de tratar esse entupimento sem precisar de uma cirurgia muito complicada. Durante o procedimento, eles criaram uma conexão temporária entre a artéria carótida e uma veia próxima para mudar o fluxo do sangue. Isso protegeu o cérebro enquanto eles colocavam um tubo pequeno chamado stent para abrir a artéria entupida.\n\n**O que aconteceu depois**\n\nO paciente se recuperou bem, sem problemas, e recebeu alta do hospital dois dias depois. Durante um ano de acompanhamento, ele não teve mais sintomas e os exames mostraram que o stent continuou funcionando bem, mantendo a artéria aberta.",
+            "B3": "**Contexto**  \nUm homem de 68 anos, com histórico de hipertensão arterial, doença pulmonar obstrutiva crônica e tabagismo ativo, apresentou perda progressiva da visão ao longo de três meses, associada a fraqueza no lado esquerdo do corpo (hemiparesia braquio-crural). Nos dias que antecederam a consulta, esses sintomas pioraram, levando-o a buscar atendimento no pronto-socorro. A avaliação neurológica indicou um escore NIHSS de 5 pontos, com dificuldades na fala (disartria) e fraqueza leve no lado esquerdo, além de pressão arterial elevada (160/80 mmHg) e saturação de oxigênio de 94% em ar ambiente.\n\n**Principais Achados**  \nExames de imagem mostraram uma estenose (estreitamento) severa na porção alta da artéria carótida interna direita, confirmada por Angio-Tomografia Computadorizada (Angio-TC) e eco Doppler, que indicou uma velocidade máxima de fluxo de 356 cm/s, evidenciando a gravidade da obstrução. A ressonância magnética cerebral revelou infartos recentes no hemisfério direito do cérebro, explicando os sintomas neurológicos do paciente.\n\n**Interpretação Clínica**  \nDevido à localização alta da estenose carotídea e ao risco elevado para cirurgia convencional (endarterectomia carotídea), optou-se por realizar um procedimento endovascular chamado TCAR (TransCarotid Artery Revascularization). Este método envolve a criação temporária de uma conexão (fístula) entre a artéria carótida e a veia jugular do mesmo lado, permitindo a inversão do fluxo sanguíneo para proteger o cérebro contra possíveis embolias (fragmentos que poderiam causar novos acidentes vasculares) durante a colocação do stent.\n\nDurante o procedimento, sob anestesia geral e anticoagulação adequada, foi implantado um stent carotídeo para desobstruir a artéria. Como houve migração do primeiro stent para uma posição proximal, foi necessário implantar um segundo stent para garantir o tratamento completo da lesão. O fluxo sanguíneo cerebral foi restaurado com sucesso, e o procedimento transcorreu sem complicações.\n\n**Próximos Passos e Evolução**  \nO paciente teve recuperação satisfatória, recebeu alta hospitalar no segundo dia após o procedimento e iniciou terapia antiplaquetária dupla para prevenir a formação de coágulos. Durante o acompanhamento clínico e por meio de exames de eco Doppler realizados aos 3, 6 e 12 meses, o stent permaneceu aberto (permeável) e sem sinais de reestenose (novo estreitamento). Não houve ocorrência de novos eventos neurológicos, mantendo o paciente assintomático após um ano do tratamento.\n\nEste caso ilustra uma abordagem inovadora e segura para tratar estenoses carotídeas complexas em pacientes com alto risco cirúrgico, garantindo proteção cerebral eficaz e boa recuperação funcional."
+        }
+    },
+    {
+        "article": "O paciente é um homem de 27 anos, nascido e residente na Cidade do México, com pais e três irmãos aparentemente saudáveis. Ele recebeu a vacina BCG no nascimento, mas apresentou uma reação adversa dois meses depois, com adenite em ambas as axilas e falta de cicatrização no local da aplicação da vacina; ele melhorou com a administração de rifampicina por oito meses, mas ficou com uma cicatriz queloide. Aos nove meses, ele desenvolveu candidíase oral e na área da fralda. Embora ambos tenham se resolvido com o tratamento, eles foram recorrentes. A candidíase oral persiste até hoje, afetando a língua e as gengivas. Aos sete anos, ele desenvolveu tinea capitis, que foi resolvido com um tratamento não especificado. Desde os dez anos, ele tem rosácea facial, inicialmente com pápulas e eritema na pele das bochechas e nariz, e agora com alterações crônicas. Aos 15 anos, ele desenvolveu onicomicose, recebeu múltiplos tratamentos antifúngicos, sem melhora e com persistência até hoje. Ele tem rosácea ocular desde a infância, e também tem asma e rinite alérgica.\n\nOs testes cutâneos foram positivos para ácaros, epitélios de animais e pólen. Foram administrados esteróides tópicos e broncodilatadores inalados.Devido à natureza crônica da candidíase, foi considerada uma alteração do sistema imunológico, a infecção por HIV foi descartada e foi informado que ele sofria de uma doença granulomatosa crônica (não se sabe em que se baseou o diagnóstico). Aos 26 anos, apresentou febre, perda de peso, astenia, adinamia, hiporexia, tosse, hemoptise, dispnéia e um abscesso glúteo. No serviço de urgência, o paciente estava em mau estado geral, com desnutrição, palidez da pele e mucosas, dificuldade respiratória, saturação de oxigênio de 87%, rosácea no rosto, língua e mucosa oral com placas brancas, eritema nas gengivas, cicatriz da vacina BCG de 5 cm de diâmetro, hipoventilação pulmonar e onicomicose nas mãos e pés.\n\nA tomografia de tórax mostrou imagem compatível com derrame pleural direito e pneumonia multifocal. O ultrassom do glúteo mostrou um abscesso profundo. Os resultados laboratoriais evidenciaram anemia, leucocitose com neutrofilia e elevação da proteína C reativa. O teste de diidrorrodamina foi normal, o que descartou o diagnóstico previamente estabelecido de doença granulomatosa crônica. A cultura da amostra tomada da cavidade oral e a cultura de sangue, tiveram crescimento de Candida albicans; na cultura de escarro, obteve-se C. albicans e C. krusei; a cultura de líquido broncoalveolar foi negativa.\n\nFoi iniciado o tratamento com vancomicina para o abcesso, com o qual apresentou melhora. O paciente recebeu ceftriaxona, claritromicina e fluconazol, mas a febre persistiu. Foi realizada uma biopsia pleural, na qual foi detectado M. tuberculosis por PCR. Foi iniciada a fase intensiva do esquema antituberculoso, ou antifímico, com isoniacida, rifampicina, pirazinamida e etambutol, obtendo-se uma adequada melhora. Durante esta hospitalização, também desenvolveu herpes zóster que remitiu com 10 dias de valaciclovir. Atualmente, o paciente se encontra completando seu tratamento antituberculoso.Revaluando o caso, pelos antecedentes de infecção pelo bacilo de Calmette-Guérin, tuberculose, herpes zóster, candidíase mucocutânea e rosácea, o diagnóstico se orientou para um aumento da função do STAT1 (figura 4). Foi solicitado um painel de genes de erros inatos da imunidade, por sequenciamento de nova geração, e foi encontrada a variante patogênica c.961A>G (p.Arg321Gly) no gene STAT1, associada com aumento da função do STAT1. Seus pais e três irmãos não carregam a mutação (WT/WT) gen STAT1.\n",
+        "gold_summary": "Este relatório é sobre um paciente que apresentou aumento da função do fator STAT1 no primeiro ano de vida. Ele tem 27 anos de idade, apresentou infecção por bacilo de Calmette-Guérin e Mycobacterium tuberculosis, candidíase mucocutânea crônica, tinea capitis e rosácea facial e ocular. A infecção por HIV foi descartada. Com base nas manifestações clínicas, suspeitou-se de um defeito imunológico inato, especificamente, com aumento da função ou atividade do STAT1. O diagnóstico foi corroborado com o sequenciamento de múltiplos genes associados a defeitos imunológicos inatos. Neste paciente, a variante patogênica c.961A>G (p.Arg321Gly) no gene STAT1 foi encontrada, previamente relatada como uma mutação de aumento da função.\n",
+        "synthetic_summary": {
+            "B1": "Este é um menino que tem 27 anos. Quando ele era bebê, ficou doente com uma vacina e com um tipo de bactéria. Ele também teve fungos na boca e na pele muitas vezes. Ele tem uma pele vermelha no rosto e nos olhos.\n\nOs médicos fizeram muitos exames para ver o que estava acontecendo. Eles descobriram que o corpo dele tem uma parte que funciona diferente, chamada STAT1. Isso faz ele ficar doente mais fácil.\n\nOs médicos acharam isso com um exame que olha os genes, que são como as instruções do corpo. A família dele não tem esse problema. Agora, os médicos cuidam bem dele para ele ficar melhor.",
+            "B2": "**O que aconteceu com o paciente**\n\nEste é o caso de um homem de 27 anos que teve problemas de saúde desde bebê. Ele recebeu uma vacina chamada BCG, usada para prevenir tuberculose, mas logo depois teve uma reação ruim, com inchaço nas axilas e ferida que não cicatrizava. Com o tempo, ele teve várias infecções, como candidíase — que é uma infecção causada por um fungo, aparecendo na boca e na pele — e também uma infecção no couro cabeludo chamada tinea capitis. Além disso, ele desenvolveu rosácea, que causa vermelhidão no rosto e nos olhos, e teve problemas nas unhas por fungos.\n\n**O que os médicos descobriram**\n\nOs médicos perceberam que ele tinha muitas infecções que não melhoravam direito, o que indicava que seu sistema imunológico, que é a defesa do corpo contra doenças, não estava funcionando bem. Testes mostraram que ele não tinha HIV, uma doença que também afeta a imunidade. Mais tarde, ele teve uma infecção grave nos pulmões e um abscesso, que é uma bolsa de pus, no glúteo. Durante o tratamento, descobriram que ele tinha tuberculose ativa, uma doença causada pela bactéria Mycobacterium tuberculosis.\n\n**O diagnóstico genético**\n\nPara entender melhor o problema, os médicos fizeram um exame especial chamado sequenciamento genético, que analisa os genes relacionados ao sistema imunológico. Eles encontraram uma mudança no gene chamado STAT1, que faz parte do sistema que ajuda o corpo a combater infecções. Essa mudança faz com que o STAT1 funcione demais, o que pode atrapalhar a defesa do corpo e causar as infecções constantes que ele teve. Essa mutação não foi encontrada nos pais e irmãos dele, o que significa que foi uma alteração nova nesse paciente.\n\n**O que isso significa**\n\nEssa alteração no gene STAT1 explica por que o paciente teve tantas infecções difíceis de tratar desde pequeno. Saber disso ajuda os médicos a escolherem o melhor tratamento e a entenderem melhor como cuidar dele no futuro. Além disso, esse caso mostra como problemas genéticos podem afetar o sistema imunológico e causar doenças que parecem difíceis de explicar.",
+            "B3": "**Contexto**  \nEste relatório descreve o caso de um homem de 27 anos que apresenta uma condição rara relacionada ao sistema imunológico, identificada desde o primeiro ano de vida. O paciente nasceu e reside na Cidade do México, com histórico familiar sem doenças aparentes. Desde a infância, ele manifestou diversas infecções e alterações cutâneas persistentes, incluindo uma reação adversa à vacina BCG (vacina contra tuberculose), candidíase mucocutânea crônica (infecção fúngica na boca e pele), tinea capitis (infecção fúngica no couro cabeludo) e rosácea facial e ocular (inflamação crônica da pele e dos olhos). A infecção pelo vírus HIV foi descartada, eliminando essa causa para sua imunodeficiência.\n\n**Principais Achados Clínicos e Diagnósticos**  \nO paciente apresentou inicialmente adenite (inflamação dos gânglios linfáticos) após a vacinação BCG, seguida por episódios recorrentes de candidíase oral e na região da fralda ainda na infância. Ao longo dos anos, desenvolveu outras condições como onicomicose (infecção fúngica das unhas), rosácea crônica e infecções pulmonares graves, incluindo tuberculose ativa confirmada por PCR (uma técnica molecular) em uma biópsia pleural. Durante a internação, também apresentou herpes zóster, uma reativação do vírus da catapora, indicando fragilidade imunológica. Exames laboratoriais mostraram anemia, inflamação e infecções fúngicas persistentes, enquanto testes específicos descartaram a doença granulomatosa crônica, uma condição imunológica previamente suspeitada.\n\n**Interpretação Clínica**  \nDiante do quadro clínico complexo e da história de infecções recorrentes e atípicas, os médicos levantaram a hipótese de um defeito imunológico inato, ou seja, uma alteração genética que afeta a resposta do sistema imune desde o nascimento. Foi realizado um painel genético por sequenciamento de nova geração, que identificou uma mutação patogênica no gene STAT1, especificamente a variante c.961A>G (p.Arg321Gly). Essa mutação está associada ao aumento da função do STAT1, uma proteína que regula a resposta imunológica. O aumento da atividade do STAT1 pode levar a uma resposta imune desregulada, explicando a susceptibilidade do paciente a infecções fúngicas crônicas, tuberculose e outras manifestações inflamatórias.\n\n**Próximos Passos e Considerações**  \nO paciente está atualmente em tratamento antituberculoso, com melhora clínica significativa após a fase intensiva do esquema medicamentoso. O diagnóstico genético permite um melhor entendimento da doença e pode orientar estratégias terapêuticas futuras, incluindo monitoramento rigoroso para infecções oportunistas e possíveis intervenções imunomoduladoras. Além disso, o fato de seus familiares próximos não apresentarem a mutação sugere que a alteração genética ocorreu de forma espontânea neste paciente. Este caso reforça a importância da investigação genética em pacientes com infecções recorrentes e manifestações clínicas incomuns, para um diagnóstico preciso e manejo adequado."
+        }
+    },
+    {
+        "article": "A paciente é uma menina de 6 anos de idade, de uma família de agricultores, em uma área não de alta altitude. Ela foi apresentada com cianose leve dos lábios ao nascer e foi inicialmente diagnosticada com doença cardíaca congênita. Por causa da cianose progressiva e dispneia, a paciente veio à nossa clínica ambulatorial para diagnóstico e tratamento adicionais. Ela teve crescimento e desenvolvimento normais sem atrasos físicos ou intelectuais significativos. A família relatou que ela era propensa a pneumonia e tossia frequentemente desde o nascimento. O exame físico revelou sopros cardíacos significativos, dedão do pé em garra e cianose dos lábios. A eletrocardiografia mostrou ritmo sinusal com hipertrofia biventricular e desvio do eixo direito. A ecocardiografia transtorácica revelou hipertrofia significativa de ambos os ventrículos e do átrio esquerdo, com ausência de eco entre a parede esquerda da aorta ascendente e a parede direita da artéria pulmonar principal (MPA), que media aproximadamente 18 mm. Havia um segmento estreito no istmo do arco da aorta, medindo aproximadamente 4 mm, e interrupção do arco da aorta distal à artéria subclávia esquerda (LSA). A artéria pulmonar direita (RPA) surgiu da aorta ascendente, enquanto a artéria pulmonar esquerda (LPA) originou-se do tronco pulmonar. Entre a aorta descendente e a artéria pulmonar esquerda, havia um PDA proeminente com um diâmetro de aproximadamente 6 mm. Os septos atrial e ventricular estavam intactos, a função da válvula era normal, e as origens das artérias coronárias eram normais. A hipertensão pulmonar era de 50 mm Hg. A paciente não tomou tratamento anti-hipertensivo pulmonar antes da cirurgia. Subsequentemente, a paciente foi submetida a angiografia por TC, que confirmou os achados da ecocardiografia. A reconstrução tridimensional mostrou claramente um APW tipo I, tipo A IAA, e PDA. Quatro ramos foram também visualizados, nomeadamente a artéria carótida comum direita (RCCA), a artéria carótida comum esquerda (LCCA), a artéria subclávia direita anormal (ARSA), e a artéria subclávia esquerda (LSA), que surgiram todas do final proximal do arco aórtico interrompido.\n\nCom base no histórico médico e nos exames do paciente, foi estabelecido um diagnóstico definitivo de síndrome de Berry, e foi indicada a intervenção cirúrgica. A família do paciente solicitou a cirurgia. Foi realizado um procedimento padrão de mid-sternotomia, revelando abundantes vasos colaterais da artéria pulmonar principal. Durante o reparo do arco aórtico interrompido, foram empregadas a parada circulatória convencional hipotermica profunda e a perfusão cerebral seletiva. Primeiramente, o ducto arterioso foi dissecado distalmente e ligado, seguido pela excisão do tecido ductal. O arco aórtico e a aorta descendente foram cuidadosamente mobilizados, e foi realizada uma anastomose final entre a aorta descendente e o arco aórtico. A parede anterior foi reforçada com um patch pericárdico. Após a correção da IAA, o RPA foi desconectado. A APW foi observada, e o defeito foi aproximadamente 1 cm do anel da válvula aórtica. A origem das artérias coronárias foi normal. Ao longo da borda da APW, a aorta e a MPA foram separadas, enquanto o RPA foi anastomosado final para a MPA. Um patch pericárdico bovino foi usado, e a incisão na aorta foi fechada com suturas 6-0 prolene de maneira contínua. A ecocardiografia transesofágica intraoperativa confirmou o fluxo contunho através do arco aórtico e não houve desvio entre a MPA e a aorta. O paciente recebeu tratamento adicional na UTI pós-operativamente e foi transferido para uma enfermaria regular após 5 dias. A hipertensão pulmonar reduziu para 26 mmHg após a cirurgia e não foi necessário medicamento para a hipertensão pulmonar. O paciente não precisou de suporte hemodinâmico após a cirurgia. Uma avaliação bem-sucedida foi realizada, e o paciente foi dispensado 7 dias depois.\n",
+        "gold_summary": "Preocupações do paciente: Neste artigo, relatamos um caso de uma menina de 6 anos com síndrome de Berry que apresentou sintomas significativos de isquemia e hipóxia.\n\nDiagnósticos: Com base no histórico médico e nos exames do paciente, foi estabelecido um diagnóstico definitivo da síndrome de Berry.\n\nIntervenções: Ela foi submetida a um tratamento cirúrgico de 1 estágio e teve alta com sucesso. O processo cirúrgico teve como objetivo preservar o potencial de crescimento da aorta e das artérias pulmonares, ao mesmo tempo em que se alcançava um fluxo de saída do ventrículo esquerdo desobstruído e a continuidade do arco aórtico, sem garantir qualquer derivação entre as principais artérias pulmonares.\n\nResultados: A ecocardiografia transesofágica intraoperatória confirmou fluxo contínuo através do arco aórtico e sem desvio entre o MPA e a aorta.\n",
+        "synthetic_summary": {
+            "B1": "Esta é a história de uma menina de 6 anos. Ela tinha os lábios meio azuis quando nasceu. Isso aconteceu porque o coração dela não estava funcionando bem.\n\nOs médicos fizeram muitos exames e descobriram que ela tinha um problema no coração chamado síndrome de Berry. Esse problema fazia o sangue não andar direito.\n\nPara ajudar, ela fez uma cirurgia. Os médicos consertaram o coração dela para o sangue poder passar direitinho. Eles cuidaram para que o coração e os vasos crescessem bem.\n\nDepois da cirurgia, o coração dela ficou melhor. O sangue passou sem dificuldade. A menina ficou bem e pôde ir para casa feliz.",
+            "B2": "**O que aconteceu com a paciente**  \nEste é o caso de uma menina de 6 anos que nasceu com um problema no coração chamado síndrome de Berry. Ela tinha dificuldade para respirar e os lábios dela ficavam com uma cor azulada, o que indica que o sangue não estava recebendo oxigênio suficiente (isso se chama hipóxia). Esses sintomas mostravam que o coração dela não estava funcionando direito.\n\n**Como foi feito o diagnóstico**  \nOs médicos usaram vários exames para entender o problema, como ultrassom do coração (ecocardiografia) e tomografia computadorizada. Eles descobriram que a menina tinha várias alterações nas artérias do coração, incluindo um arco da aorta interrompido (uma parte importante da principal artéria do corpo estava bloqueada) e uma comunicação anormal entre a aorta e a artéria pulmonar. Com esses exames e o histórico dela, os médicos confirmaram que ela tinha a síndrome de Berry.\n\n**O tratamento realizado**  \nPara ajudar a menina, os médicos fizeram uma cirurgia complexa para corrigir esses defeitos no coração. Durante a operação, eles consertaram a parte bloqueada da aorta e separaram corretamente as artérias que estavam ligadas de forma errada. Também usaram um pedaço de tecido especial para reforçar as paredes do coração. O objetivo da cirurgia foi garantir que o sangue pudesse sair do coração e circular pelo corpo normalmente, sem misturar sangue com pouco oxigênio com sangue rico em oxigênio.\n\n**Resultados após a cirurgia**  \nDepois da cirurgia, os exames mostraram que o sangue estava fluindo bem pela aorta, sem problemas. A pressão alta nos pulmões da menina diminuiu bastante, e ela não precisou de remédios para isso. Ela se recuperou bem, ficou alguns dias no hospital e depois teve alta para continuar a recuperação em casa.\n\n**O que isso significa**  \nEsse caso mostra que, mesmo com problemas graves no coração desde o nascimento, é possível fazer uma cirurgia que corrige essas alterações e melhora muito a saúde da criança. O acompanhamento médico é importante para garantir que ela continue crescendo e se desenvolvendo bem.",
+            "B3": "**Contexto**  \nEste relato descreve o caso de uma menina de 6 anos diagnosticada com a síndrome de Berry, uma condição cardíaca congênita rara caracterizada por anomalias complexas nas grandes artérias do coração. Desde o nascimento, a paciente apresentava cianose leve (coloração azulada dos lábios devido à baixa oxigenação do sangue) e sintomas respiratórios frequentes, como tosse e pneumonia, além de sopros cardíacos detectados ao exame físico. Exames detalhados, incluindo ecocardiografia e angiografia por tomografia computadorizada, revelaram múltiplas malformações cardíacas: hipertrofia dos ventrículos e átrio esquerdo, interrupção do arco aórtico (uma interrupção na continuidade da principal artéria que sai do coração), comunicação anormal entre a aorta e a artéria pulmonar (defeito do septo aortopulmonar), além de alterações nas origens das artérias pulmonares e presença de um ducto arterioso patente (conexão persistente entre a aorta e a artéria pulmonar).\n\n**Principais Achados e Diagnóstico**  \nO diagnóstico definitivo foi a síndrome de Berry, caracterizada pela associação dessas anomalias cardíacas complexas. A paciente apresentava hipertensão pulmonar moderada (pressão elevada nas artérias dos pulmões), mas sem comprometimento significativo da função cardíaca ou atraso no desenvolvimento físico e intelectual.\n\n**Intervenção Cirúrgica**  \nFoi indicada e realizada uma cirurgia corretiva em um único procedimento, com o objetivo de restaurar a continuidade da aorta e corrigir as conexões anormais entre as artérias pulmonares e a aorta, preservando o potencial de crescimento das estruturas vasculares. A cirurgia envolveu a remoção do tecido anormal, reconstrução do arco aórtico interrompido por meio de anastomose (conexão cirúrgica) entre a aorta descendente e o arco aórtico, e fechamento do defeito entre a aorta e a artéria pulmonar com um enxerto de pericárdio bovino (tecido que reveste o coração). Técnicas avançadas, como parada circulatória hipotérmica profunda (redução da temperatura corporal para proteger órgãos durante a interrupção do fluxo sanguíneo) e perfusão cerebral seletiva (manutenção do fluxo sanguíneo ao cérebro), foram utilizadas para garantir a segurança do procedimento.\n\n**Resultados Pós-Operatórios**  \nA avaliação intraoperatória por ecocardiografia transesofágica confirmou que o fluxo sanguíneo pelo arco aórtico estava normal e contínuo, sem comunicação anormal entre a artéria pulmonar principal e a aorta. Após a cirurgia, a paciente apresentou redução significativa da hipertensão pulmonar, não necessitando de medicamentos específicos para essa condição. Ela teve recuperação estável, sem necessidade de suporte hemodinâmico (como medicamentos para manter a pressão arterial), e recebeu alta hospitalar sete dias após o procedimento.\n\n**Interpretação Clínica e Prognóstico**  \nEste caso demonstra que a correção cirúrgica precoce e adequada da síndrome de Berry pode resultar em boa recuperação e melhora dos sintomas, preservando a função cardíaca e o crescimento das grandes artérias. O sucesso do tratamento reforça a importância do diagnóstico detalhado e da abordagem cirúrgica especializada para condições cardíacas congênitas complexas em crianças. A paciente deverá ser acompanhada regularmente para monitorar o desenvolvimento cardiovascular e prevenir possíveis complicações futuras."
+        }
+    },
+    {
+        "article": "Em Dezembro de 2020, um homem de 43 anos com um histórico de 9 anos de hepatite B foi submetido a uma ecografia durante um exame médico de rotina no Hospital Popular de Ruian, que revelou várias lesões hipoecóicas no seu fígado.\n\nOs testes laboratoriais mostraram uma ligeira elevação nos níveis de alfa-fetoproteína (AFP) (AFP: 32,9 ng/ml), enquanto outros marcadores tumorais, como antígenos de carboidratos 19-9, 125 e 153, e antígeno carcinoembrionário, estavam dentro dos limites normais. As lesões apareceram como de baixa densidade com margens pouco claras na tomografia computadorizada (TC) e mostraram realce centrípeto da fase arterial para a fase portal na tomografia computadorizada com contraste dinâmico. Os tamanhos das lesões variaram, sendo a maior uma lesão de forma irregular com 4,1 × 4,3 cm de diâmetro.\n\nNa ressonância magnética com contraste dinâmico (MRI), a maior lesão exibiu um realce periférico imediato em forma de anel, seguido por um realce contínuo e progressivo e uma cicatriz central. Enquanto isso, lesões menores exibiam um realce em forma de anel com realce centrípeto gradual durante as fases portal venosa e retardada. Para um exame mais aprofundado, o paciente foi encaminhado para o Hospital Huashan de Xangai em 30 de dezembro de 2020.\n\nO paciente foi prontamente submetido a uma tomografia por emissão de pósitrons (PET) com [18F]-FDG, que não revelou nenhuma absorção óbvia. No entanto, a tomografia por emissão de pósitrons/tomografia computadorizada (PET/CT) com [11C]-acetato indicou uma absorção ligeira apenas para a maior lesão localizada no lobo VII (valor máximo de captação padronizada [SUVmax] = 4.21, relação tumor-fundo [TBR] = 1.45), enquanto outras menores não apresentaram absorção. É interessante notar que a tomografia por emissão de pósitrons/tomografia computadorizada (PET/CT) com [68Ga] Ga-FAPI-04 não só mostrou uma absorção forte e elevada para a maior lesão (SUVmax = 1.94, TBR = 3.08), mas também para as menores lesões intra-hepáticas (SUVmax = 1.47, TBR = 2.33).\n\nCom base nas avaliações existentes, foi feito um diagnóstico preliminar de carcinoma hepatocelular (HCC). O paciente recebeu então uma hepatectomia parcial em 6 dias, e o diagnóstico foi confirmado por análise patológica. A maior lesão localizada no segmento VII foi identificada como um HCC solitário, enquanto as outras lesões menores foram diagnosticadas como epitelioma hemangioendotelioma hepático (HEHE).\n\nMicroscopicamente, lesões menores apareceram como ninhos e cordões de células epiteliais endoteliais, com luz intracitoplasmática espalhada por todo o estroma mixóide. A coloração de CD31 e ERG1 foi fortemente positiva, confirmando o diagnóstico de HEHE (Fig. 4A-E). A lesão hepática do segmento VII exibiu positividade de Hep1 em imuno-histoquímica, confirmando o diagnóstico de HCC.\n\nO paciente recebeu alta no dia 9 pós-operatório e não foi detectado nenhum caso de recorrência durante o seu acompanhamento até agora.\n",
+        "gold_summary": "Apresentamos um caso de carcinoma hepatocelular (HCC) e HEHE num paciente masculino chinês de 43 anos de idade. Foram apresentadas múltiplas lesões hepáticas hipoecóicas, mas não foram detetados achados específicos de imagem na tomografia computorizada (TC) ou na ressonância magnética (MRI) com contraste. O paciente foi então submetido a PET/CT com [18F]-FDG, PET/CT com [11C]-acetato e PET/CT com [68Ga]Ga-FAPI-04. As lesões HEHE não apresentaram captação na tomografia computorizada com [18F]-FDG e com [11C]-acetato, mas apresentaram uma visualização clara na PET/CT com [68Ga]Ga-FAPI-04. A maior lesão localizada no segmento VII foi finalmente diagnosticada como HCC, enquanto as outras menores foram diagnosticadas como HEHE, o que foi confirmado por coloração imuno-histoquímica para CD31. Tanto quanto sabemos, apenas 2 casos foram relatados na literatura mundial, e o primeiro caso realizou PET/CT com [11C]-acetato e [68Ga]Ga-FAPI-04 em vez de PET/CT com [18F]-FDG.\n",
+        "synthetic_summary": {
+            "B1": "Um homem estava com o fígado doente. Os médicos fizeram vários exames para ver o que tinha. Eles viram que ele tinha uma parte grande do fígado com um problema que pode virar câncer. Também tinham partes pequenas que eram outro tipo de problema, mas que não faziam tanto mal.\n\nPara entender melhor, os médicos usaram máquinas especiais que tiram fotos do corpo. Uma dessas máquinas mostrou bem as partes pequenas e a parte grande do fígado. Depois, os médicos fizeram uma cirurgia para tirar a parte doente. Eles olharam bem de perto e confirmaram o que cada parte tinha.\n\nO homem ficou bem e os médicos continuam cuidando dele para que ele fique saudável.",
+            "B2": "**O que aconteceu com o paciente**\n\nUm homem de 43 anos, que tinha hepatite B há 9 anos, fez um exame de rotina e descobriram várias manchas estranhas no fígado dele. Essas manchas foram vistas em exames de imagem, como ultrassom, tomografia computadorizada (TC) e ressonância magnética (MRI). Mas as imagens não mostraram claramente o que eram essas manchas.\n\n**Os exames especiais feitos**\n\nPara entender melhor, os médicos usaram três tipos diferentes de PET/CT, que são exames que mostram como as células do corpo usam certas substâncias. Um deles usou uma substância chamada [18F]-FDG, outro usou [11C]-acetato, e o terceiro usou [68Ga]Ga-FAPI-04. As manchas menores, chamadas HEHE (um tipo raro de tumor no fígado), não apareceram nos dois primeiros exames, mas ficaram bem visíveis no exame com [68Ga]Ga-FAPI-04. Já a maior mancha, que era um câncer chamado carcinoma hepatocelular (HCC), apareceu em todos os exames, mas com destaque diferente.\n\n**O que os médicos descobriram**\n\nDepois de retirar parte do fígado, os médicos confirmaram que a maior mancha era um câncer chamado HCC, e as manchas menores eram outro tipo raro de tumor chamado HEHE. Eles usaram um teste chamado coloração imuno-histoquímica, que ajuda a identificar o tipo de células, para confirmar o diagnóstico.\n\n**Por que isso é importante**\n\nEsse caso é muito raro. Até agora, só existem dois casos assim no mundo. Além disso, foi a primeira vez que usaram os exames PET/CT com [11C]-acetato e [68Ga]Ga-FAPI-04 para ajudar no diagnóstico, em vez do exame mais comum com [18F]-FDG. Isso pode ajudar médicos a identificar melhor esses tumores no futuro.\n\n**Resumo final**\n\nUm homem com hepatite B teve dois tipos diferentes de tumores no fígado. Exames comuns não mostraram tudo, mas um exame especial com [68Ga]Ga-FAPI-04 ajudou a ver melhor as manchas menores. A cirurgia confirmou os diagnósticos, e o paciente está bem até agora. Esse caso pode ajudar a melhorar o diagnóstico de tumores no fígado.",
+            "B3": "**Contexto**  \nEste relato descreve o caso de um homem chinês de 43 anos com histórico de hepatite B, que apresentou múltiplas lesões no fígado detectadas durante um exame de rotina. As imagens iniciais por ultrassonografia, tomografia computadorizada (TC) e ressonância magnética (MRI) com contraste mostraram lesões hipoecóicas (áreas que refletem menos o ultrassom) e de baixa densidade, mas sem características específicas que permitissem um diagnóstico definitivo.  \n\n**Principais Achados Diagnósticos**  \nPara investigar melhor as lesões, o paciente foi submetido a diferentes exames de tomografia por emissão de pósitrons (PET/CT) com três tipos de marcadores:  \n- [18F]-FDG, que não mostrou captação significativa nas lesões menores;  \n- [11C]-acetato, que indicou leve captação apenas na maior lesão;  \n- [68Ga]Ga-FAPI-04, que evidenciou captação forte e clara tanto na maior lesão quanto nas menores.  \n\nApós a cirurgia de remoção parcial do fígado, a análise microscópica confirmou que a maior lesão no segmento VII era um carcinoma hepatocelular (HCC), um tipo comum de câncer de fígado. As lesões menores foram diagnosticadas como epitelioma hemangioendotelioma hepático (HEHE), um tumor raro que afeta os vasos sanguíneos do fígado. A confirmação do HEHE foi feita por meio da coloração imuno-histoquímica para CD31, um marcador específico de células endoteliais (que revestem vasos sanguíneos).  \n\n**Interpretação Clínica**  \nEste caso é excepcional porque combina dois tipos distintos de tumores hepáticos no mesmo paciente: HCC e HEHE. Além disso, destaca a utilidade do PET/CT com o marcador [68Ga]Ga-FAPI-04, que demonstrou maior sensibilidade para detectar as lesões de HEHE em comparação com os marcadores tradicionais [18F]-FDG e [11C]-acetato. Isso sugere que o [68Ga]Ga-FAPI-04 pode ser uma ferramenta valiosa para o diagnóstico e avaliação de tumores hepáticos raros, especialmente quando os métodos convencionais não são conclusivos.  \n\n**Próximos Passos e Considerações**  \nO paciente teve alta hospitalar sem complicações e não apresentou sinais de recidiva até o momento do acompanhamento. Este relato contribui para a literatura médica ao ser um dos poucos casos documentados que utilizam PET/CT com [68Ga]Ga-FAPI-04 para diferenciar múltiplas lesões hepáticas de natureza distinta. Estudos futuros poderão explorar o papel desse método na detecção precoce e no manejo clínico de tumores hepáticos raros, melhorando o diagnóstico diferencial e o planejamento terapêutico."
+        }
+    },
+    {
+        "article": "Um homem de 65 anos apresentou inchaço e deformidade boutonniere no dedo médio direito seis meses após um acidente de motocicleta em 1 de janeiro de 2023. Inicialmente, ele administrou a lesão com analgésicos e não procurou atenção médica. Após seis meses de sintomas persistentes, incluindo uma incapacidade de estender totalmente o dedo e edema notável, ele procurou tratamento.\n\nDescobertas clínicas\nA inspeção da mão direita mostrou a presença de deformidade com edema. A amplitude ativa de movimento (ROM) foi prejudicada na articulação PIP do dedo III da mão direita. A amplitude ativa de movimento (ROM) da articulação PIP do dedo III da mão direita foi de 45 a 110 graus. A amplitude passiva de movimento (ROM) da articulação PIP do dedo III da mão direita foi dentro do normal.\n\nAvaliação diagnóstica\nFizemos um raio-X da mão direita AP/Lateral que mostrou que não havia anormalidade no osso e diagnosticamos a deformidade de tecido mole que é uma lesão central por escorregamento.\n\nTécnica cirúrgica\nFoi realizada uma reconstrução de defeito de deslizamento central utilizando o lado ulnar do tendão flexor digitorum superficial. Sob anestesia, o paciente foi posicionado deitado de costas com um torniquete aplicado no braço superior. Foi feita uma incisão midlateral no aspecto ulnar da falange média direita, centrada na articulação PIP. A incisão estendeu-se dorsaalmente de forma oblíqua. Foi feita uma incisão transversal sobre a prega de flexão da articulação MCP, imediatamente proximal à polia A1. O procedimento envolve a identificação e proteção do feixe neurovascular digital ulnar, expondo o deslizamento central e o tendão extensor para a PIPJ, e eleva-se a prega dorsal de espessura total. O tecido cicatricial e o tecido pseudotendinoso são identificados e excisados. O deslizamento central não pode ser reparado em primeiro lugar, pelo que o deslizamento ulnar do tendão FDS é utilizado para reconstrução. O feixe neurovascular ulnar é mobilizado para visualizar a inserção periosteal da polia A3.\n\nO tendão extensor é mobilizado e tenolizado, seguido por incisão da cápsula dorsal da articulação PIP e remoção do tecido interposto. A inserção periosteal da polia A3 é incisada longitudinalmente, e a cápsula volátil da articulação PIP é incisada longitudinalmente. O deslizamento ulnar do tendão FDS é identificado e uma sutura monofilamento não absorvível 2-0 é colocada ao redor dele. Uma incisão transversal é feita na dobra flexora da articulação MCP, proximal à polia A1, revelando a bainha do tendão flexor. A bainha do tendão e a polia A1 são incisadas longitudinalmente. O tendão FDS é identificado. O deslizamento ulnar do tendão FDS é isolado e seccionado para liberar o deslizamento ulnar, evitando o aprisionamento ou captura do deslizamento radial. A sutura 2-0 que foi colocada ao redor do deslizamento ulnar ao nível da articulação PIP é usada para liberar o deslizamento distal do tendão FDS e entregar o deslizamento ulnar do tendão FDS distalmente.\n\nUma broca de 2,8 mm é usada para criar um túnel ósseo orientado verticalmente dorsal a volar. Um elevador é colocado entre o tendão flexor digitorum profundus, a placa volar e o aspecto volar da base da falange média, protegendo as estruturas anatômicas volar. O deslizamento do tendão FDS passa pelo túnel, mantendo a articulação PIP em extensão e posição reduzida. O deslizamento do tendão FDS passou pela seção proximal intacta do deslizamento central e do tendão extensor. Um tecelão de tendão completa um tecido de Pulvertaft, confirmando a tensão apropriada com a PIPJ na posição reduzida, de extensão total. Uma sutura não absorvível 3-0 segura o tecido de Pulvertaft. As margens da reconstrução da cápsula e do deslizamento central são aproximadas através da articulação PIP, e as aderências são liberadas e as bandas laterais são mobilizadas.\n\nA postura geral, estabilidade e movimento com tenodesis são avaliados. Todas as incisões são abundantemente irrigadas. O torniquete é desinflado e a hemostasia é obtida. O preenchimento capilar de todos os dedos é avaliado. A pele é fechada usando pontos horizontais. Um curativo estéril é aplicado com uma tala de extensão da articulação PIP adequadamente acolchoada para permitir o movimento precoce da articulação DIP e da articulação MCP.\n\nSeguimento e resultados\nO primeiro acompanhamento foi feito 4 dias depois para tratamento da ferida. O paciente recebeu meloxicam oral 7,5 mg duas vezes ao dia e doxiciclina 100 mg duas vezes ao dia durante 3 dias. O segundo acompanhamento foi feito 3 dias depois para tratamento da ferida. Após 2 semanas, removemos a placa de apoio, removemos a sutura externa e começamos o exercício de ROM ativo e passivo. Após 3 semanas, a ferida foi curada, e encontramos a ROM da articulação do IPP de 0 a 90 graus. E após um mês, o paciente veio com ROM melhorada da articulação do IPP de 0 a 100 graus, e resultado funcional melhorado. Após 7 semanas de reabilitação física, os pacientes já voltaram ao trabalho com ROM melhorada da articulação do IPP de 0 a 110 graus. A função da mão direita do paciente é avaliada com a pontuação DASH, que melhora significativamente de 50 para 4.2.\n",
+        "gold_summary": "Um paciente do sexo masculino de 65 anos apresentou inchaço e deformidade boutonnière no dedo III da mão direita. O paciente havia caído anteriormente de uma motocicleta, e o dedo médio direito do paciente foi atingido por uma motocicleta seis meses atrás. Após o incidente, o dedo médio direito do paciente não pode ser totalmente estendido. A mão direita do paciente apresentou edema com flexão da articulação interfalangeal (PIP) e hiperextensão da articulação interfalangeal distal (DIP). A amplitude de movimento (ROM) do dedo médio direito da articulação PIP foi de 45 a 110 graus. A radiografia da mão direita AP/oblíqua não mostrou envolvimento ósseo na deformidade. O paciente passou por uma reconstrução do defeito de deslizamento central utilizando o lado ulnar parcial do tendão superficial flexor digitorum. Uma tala de extensão da articulação PIP foi aplicada por 2 semanas. O exercício ativo e passivo da amplitude de movimento da articulação PIP começou após 2 semanas de aplicação da tala de extensão da articulação PIP. A amplitude de movimento da articulação PIP do paciente (0 a 90 graus) melhorou significativamente 1 mês após a cirurgia. A amplitude de movimento da articulação PIP do paciente voltou ao normal após 2 meses após a cirurgia. A função da mão direita do paciente foi avaliada com a pontuação DASH, que melhorou significativamente de 50 para 4.2.\n",
+        "synthetic_summary": {
+            "B1": "Um homem machucou o dedo da mão direita. Ele caiu da moto e o dedo ficou inchado e torto. O dedo não conseguia abrir direito.\n\nO médico fez uma cirurgia para arrumar o dedo. Depois, colocou uma tala para ajudar o dedo a ficar reto.\n\nDepois de duas semanas, ele começou a mexer o dedo devagarinho. Com o tempo, o dedo melhorou muito.\n\nDepois de dois meses, o dedo voltou quase ao normal. Agora ele consegue usar a mão melhor e sem dor.",
+            "B2": "**O que aconteceu com o paciente**\n\nUm homem de 65 anos sofreu um acidente de motocicleta e machucou o dedo do meio da mão direita. Depois do acidente, ele não conseguiu esticar totalmente esse dedo e ele ficou inchado e deformado, com uma posição chamada \"deformidade boutonnière\". Isso significa que a articulação do meio do dedo (chamada PIP) ficou dobrada para dentro, enquanto a ponta do dedo (articulação DIP) ficou esticada demais.\n\n**Exames e diagnóstico**\n\nOs médicos fizeram um raio-X da mão e viram que os ossos estavam normais, ou seja, não tinham quebrado. O problema estava nos tecidos moles, como os tendões, que são estruturas parecidas com cordas que ajudam a mover os dedos. Eles descobriram que o tendão extensor, que ajuda a esticar o dedo, estava lesionado no meio do dedo.\n\n**Tratamento e cirurgia**\n\nPara consertar o tendão, os médicos fizeram uma cirurgia usando uma parte do tendão flexor superficial, que é um tendão que ajuda a dobrar o dedo. Eles usaram esse pedaço para substituir o tendão lesionado e reconstruir a articulação do dedo. Depois da cirurgia, o paciente usou uma tala que mantinha o dedo esticado por duas semanas para ajudar na recuperação.\n\n**Recuperação e resultados**\n\nApós duas semanas, o paciente começou a fazer exercícios para mexer o dedo, tanto sozinho (ativo) quanto com ajuda (passivo). Um mês depois da cirurgia, ele já conseguia mover a articulação do dedo quase normalmente, de 0 a 90 graus. Depois de dois meses, a movimentação voltou ao normal, de 0 a 110 graus. A função da mão melhorou muito, medida por um teste chamado pontuação DASH, que caiu de 50 (muito ruim) para 4,2 (quase normal).\n\n**Conclusão**\n\nEsse caso mostra que, mesmo com uma lesão grave no tendão do dedo, é possível recuperar a função da mão com uma cirurgia adequada e reabilitação correta. É importante procurar ajuda médica logo após um acidente para evitar problemas que podem piorar com o tempo.",
+            "B3": "**Contexto**  \nUm homem de 65 anos sofreu um acidente de motocicleta em janeiro de 2023, que resultou em uma lesão no dedo médio da mão direita. Após o trauma, ele apresentou inchaço e uma deformidade conhecida como boutonnière, caracterizada pela incapacidade de estender completamente a articulação interfalangeana proximal (PIP) do dedo afetado. Inicialmente, o paciente não buscou atendimento médico, mas após seis meses com sintomas persistentes, incluindo edema (inchaço) e limitação funcional, procurou tratamento especializado.\n\n**Principais Achados Clínicos e Diagnósticos**  \nNa avaliação, observou-se edema e deformidade no dedo médio direito, com flexão limitada da articulação PIP (amplitude de movimento ativa entre 45 e 110 graus) e hiperextensão da articulação interfalangeana distal (DIP). A amplitude de movimento passiva da articulação PIP estava preservada, indicando que a limitação era funcional e não causada por rigidez articular fixa. Radiografias da mão direita não revelaram alterações ósseas, confirmando que a deformidade era decorrente de uma lesão nos tecidos moles, especificamente um defeito no deslizamento central do tendão extensor, que é responsável pela extensão do dedo.\n\n**Intervenção Cirúrgica**  \nFoi realizada uma cirurgia para reconstrução do deslizamento central do tendão extensor utilizando uma parte do tendão flexor digitorum superficialis (FDS) do lado ulnar (lado do dedo mínimo) do dedo médio. O procedimento envolveu uma incisão cuidadosa para expor e remover tecido cicatricial e pseudotendinoso (tecido fibroso que substitui o tendão lesionado), seguido pela criação de um túnel ósseo na falange média para passagem e fixação do tendão FDS, restaurando a função do deslizamento central. Durante a cirurgia, estruturas neurovasculares foram protegidas para evitar danos. Após a reconstrução, a articulação PIP foi estabilizada com uma tala em extensão para permitir a cicatrização adequada.\n\n**Pós-Operatório e Reabilitação**  \nNos primeiros dias após a cirurgia, o paciente foi acompanhado para controle da ferida e recebeu medicação anti-inflamatória e antibiótica para prevenir infecções e controlar a dor. Após duas semanas, a tala foi removida e iniciaram-se exercícios ativos e passivos de amplitude de movimento para a articulação PIP, visando restaurar a mobilidade sem comprometer a reconstrução cirúrgica. Um mês após a cirurgia, a amplitude de movimento da articulação PIP melhorou significativamente, alcançando 0 a 90 graus, e após sete semanas, o paciente recuperou a amplitude normal de movimento (0 a 110 graus) e retornou às suas atividades laborais.\n\n**Avaliação Funcional e Resultados**  \nA função da mão direita foi avaliada utilizando a escala DASH (Disabilities of the Arm, Shoulder and Hand), que mede a incapacidade e sintomas relacionados ao membro superior. A pontuação do paciente melhorou drasticamente, de 50 (indicando incapacidade moderada a grave) para 4,2 (quase ausência de sintomas e limitações), demonstrando uma recuperação funcional excelente após a cirurgia e reabilitação.\n\n**Conclusão**  \nEste caso ilustra a importância do diagnóstico e tratamento adequados de lesões tendíneas complexas, como a deformidade boutonnière causada por defeito no deslizamento central do tendão extensor. A reconstrução cirúrgica utilizando o tendão flexor digitorum superficialis, associada a um protocolo rigoroso de reabilitação, pode restaurar a função e a mobilidade do dedo afetado, permitindo o retorno às atividades diárias e laborais com resultados funcionais satisfatórios."
+        }
+    },
+    {
+        "article": "Uma mulher de 26 anos foi encaminhada por um neurologista por perda de visão progressiva, sequencial e bilateral e visão turva ao longo de um mês, começando pelo olho direito e tornando-se mais proeminente, sem quaisquer movimentos oculares dolorosos. Ela tinha um histórico médico de síndrome clinicamente isolada envolvendo a medula espinal. Seus sintomas sensoriais começaram 7 anos antes da apresentação, envolvendo o pé esquerdo e migrando ao longo de um período de semanas para alcançar um nível distal à cintura. A ressonância magnética (MRI) do cérebro e da coluna vertebral revelou uma lesão na região infratentorial e outra na coluna vertebral torácica. A ressonância magnética de acompanhamento identificou novas lesões de realce temporalmente distintas nos níveis C4, C6-C7, T2 e T7-T8. A análise adicional revelou resultados negativos para anticorpos aquaporin-4 e proteína oligodendrocítica da mielina (MOG). Ela não estava recebendo quaisquer medicamentos no momento da apresentação e seu histórico de tabagismo e consumo de álcool não foi notável. O histórico familiar foi insignificante para causas hereditárias de perda de visão, incluindo LHON.\n\nO exame neuro-oftalmológico revelou uma acuidade visual (AV) corrigida de 20/100 OD e 20/30-2 OS. A sua AV demonstrou melhorias graduais durante os subsequentes exames de acompanhamento. As placas de cores de Ishihara revelaram que era capaz de ler apenas 1 de 17 placas de cores no olho direito e 14 de 17 placas de cores no olho esquerdo. Não havia nenhum defeito pupilar aferente relativo. A tomografia de coerência ótica (OCT) demonstrou uma espessura média da camada de fibras nervosas da retina de 83 microns OD e 93 microns OS com ligeiro afinamento temporal. O exame do fundo dilatado mostrou palidez de ambos os nervos óticos com uma relação copo/disco de 0.2.\n\nO diagnóstico diferencial para os seus sintomas visuais incluiu neuropatias ópticas bilaterais, tais como neurite ótica ou LHON. As deficiências nutricionais foram excluídas devido à contagem sanguínea completa normal, B12, folato. Ela prosseguiu com prednisona 1250 mg PO diariamente durante 3 dias, seguida por 60 mg e uma redução gradual de 10 mg a cada 5 dias; no entanto, na visita de acompanhamento, ela não relatou quaisquer melhorias nos seus sintomas. Exames adicionais revelaram hiperintensidades T2 suaves no lado direito do quiasma ótico e três novas lesões de matéria branca cerebral (esplenoma; 2 lesões de matéria branca periventricular parietal esquerda) na ressonância magnética. Os achados de MRI e as bandas oligoclonais detetadas com punção lombar confirmaram o diagnóstico de MS. Nas visitas de acompanhamento subsequentes, os seus testes de campo visual mostraram escotomas centrais bilaterais em ambos os olhos. A natureza lentamente progressiva, o envolvimento sequencial dos olhos, escotomas centrais simétricos, sintomas que não respondem a esteróides e hiperintensidades no quiasma ótico detetadas por MRI foram sugestivos de LHON. O exame do fundo dilatado revelou palidez temporal. Os testes genéticos para três mutações primárias foram negativos; no entanto, ela era heterozigótica para a variante c.152A>G do gene DNAJC30 associado a arLHON. Ela também foi testada positiva para a variante c.1239C>T no gene UQCRC1 com padrão de herança autossómica dominante. Ela foi diagnosticada com síndrome de Harding e começou a tomar idebenona 300 mg PO TDS diariamente, o que levou a melhorias nos seus sintomas. O seu campo visual demonstrou melhorias graduais ao longo dos anos de acompanhamento (o seu último campo visual corrigido foi de 20/40-2 OD e 20/20-2 OS) e as métricas e exames de OCT permaneceram estáveis com palidez temporal bilateral. Os campos visuais e os OCTs 4 anos após o acompanhamento são mostrados.\n",
+        "gold_summary": "Apresentamos uma mulher de 26 anos com perda visual bilateral progressiva, sequencial e indolor, que não respondia a esteróides, e dois episódios temporais distintos de distúrbios neurológicos sugestivos de desmielinização do sistema nervoso central. Investigações exaustivas, incluindo testes serológicos, excluíram outras causas, incluindo neuromielite óptica negativa e anticorpos da proteína oligodendrocítica da mielina (MOG) e deficiências nutricionais. A ressonância magnética detetou áreas de desmielinização dentro da medula espinal e do cérebro (áreas infratentorial e periventricular). Após análise genética que revelou a mutação c.152A>G (p.Tyr51Cys) no gene DNAJC30, foi sugerida a LHON. Foi-lhe receitado idebenona e a sua acuidade visual resolveu-se para normal após 4 anos de acompanhamento.\n",
+        "synthetic_summary": {
+            "B1": "Uma moça de 26 anos começou a ver cada vez pior nos dois olhos. A visão dela foi ficando ruim devagar, sem dor. Os remédios que ela tomou não ajudaram.\n\nOs médicos fizeram muitos exames para entender o que estava acontecendo. Eles viram no cérebro e na coluna dela algumas partes que estavam diferentes. Também fizeram um exame do sangue e outros testes, mas não acharam nada errado ali.\n\nDepois, os médicos fizeram um exame especial do DNA dela. Eles acharam uma mudança que pode causar problemas na visão. Então, ela começou a tomar um remédio chamado idebenona.\n\nCom esse remédio, a visão dela melhorou muito. Depois de quatro anos, ela quase voltou a ver normal. Os médicos ficaram felizes porque ela está melhor.",
+            "B2": "**O que aconteceu com a paciente**\n\nUma mulher de 26 anos começou a perder a visão nos dois olhos, primeiro no direito e depois no esquerdo. Essa perda foi lenta, sem dor, e não melhorou com o uso de remédios chamados esteróides. Ela também teve problemas no sistema nervoso, que pareciam ser causados por uma perda da proteção das células nervosas, chamada desmielinização.\n\n**O que os médicos fizeram para entender o problema**\n\nOs médicos fizeram vários exames para descobrir a causa da perda de visão. Eles descartaram outras doenças, como a neuromielite óptica, que é uma inflamação dos nervos dos olhos, e também verificaram se ela tinha falta de vitaminas, o que não aconteceu. A ressonância magnética mostrou áreas com danos no cérebro e na medula espinhal, que são partes importantes do sistema nervoso.\n\n**O que descobriram com os exames genéticos**\n\nDepois, os médicos fizeram um exame genético e encontraram uma alteração no gene chamado DNAJC30. Essa alteração está ligada a uma doença chamada LHON, que é uma condição que afeta os nervos dos olhos e pode causar perda de visão.\n\n**Como ela foi tratada e o que aconteceu depois**\n\nEla começou a tomar um remédio chamado idebenona, que ajuda as células dos olhos a funcionarem melhor. Com o tratamento, a visão dela melhorou bastante e, depois de quatro anos, voltou quase ao normal.\n\n**Resumo final**\n\nEssa paciente teve uma perda de visão causada por uma doença genética que afeta os nervos dos olhos. O diagnóstico foi feito com exames de imagem e testes genéticos. O tratamento com idebenona ajudou a recuperar a visão ao longo do tempo.",
+            "B3": "**Contexto**  \nApresentamos o caso de uma mulher de 26 anos que desenvolveu perda progressiva e sequencial da visão em ambos os olhos, sem dor associada, ao longo de um mês. Ela já possuía um histórico neurológico de episódios anteriores compatíveis com desmielinização (perda da camada protetora dos nervos) na medula espinal, diagnosticada como síndrome clinicamente isolada. Exames de imagem (ressonância magnética) mostraram lesões características no cérebro e na medula, sugerindo um processo inflamatório desmielinizante.\n\n**Principais Achados**  \nDurante a avaliação, foram descartadas causas comuns de neuropatias ópticas, como neuromielite óptica (doença autoimune que afeta os nervos ópticos e a medula) e deficiências nutricionais (vitamina B12 e folato normais). A paciente não respondeu ao tratamento com corticosteroides, que normalmente melhora a neurite óptica inflamatória. A ressonância magnética revelou novas lesões no quiasma óptico (região onde os nervos ópticos se cruzam) e em áreas típicas do cérebro afetadas pela esclerose múltipla (EM). A análise do líquor (líquido cefalorraquidiano) mostrou bandas oligoclonais, reforçando o diagnóstico de EM.\n\nContudo, a progressão lenta da perda visual, o envolvimento sequencial dos olhos, os escotomas centrais (áreas de perda de visão no centro do campo visual) e a falta de resposta aos esteróides indicaram uma causa diferente: a neuropatia óptica hereditária de Leber (LHON), uma doença genética que afeta as mitocôndrias (as “usinas” das células). Testes genéticos para as mutações mais comuns de LHON foram negativos, mas a paciente apresentou uma variante heterozigótica no gene DNAJC30, associada a uma forma autossômica recessiva de LHON (arLHON). Também foi identificada uma variante no gene UQCRC1, relacionada a padrões hereditários dominantes.\n\n**Interpretação Clínica**  \nO diagnóstico final foi síndrome de Harding, uma forma de LHON que pode se manifestar com sintomas semelhantes aos da esclerose múltipla, dificultando o diagnóstico inicial. A presença da mutação no DNAJC30 confirmou a origem genética da neuropatia óptica. A palidez temporal dos nervos ópticos observada no exame de fundo de olho é típica da LHON e indica perda das fibras nervosas.\n\n**Próximos Passos e Evolução**  \nA paciente iniciou tratamento com idebenona, um medicamento que atua como antioxidante e melhora a função mitocondrial, na dose de 300 mg três vezes ao dia. Ao longo de quatro anos de acompanhamento, sua acuidade visual melhorou progressivamente, chegando a níveis quase normais (20/40 no olho direito e 20/20 no esquerdo). Os exames de campo visual e tomografia de coerência óptica (OCT), que avalia a camada de fibras nervosas da retina, permaneceram estáveis, embora a palidez dos nervos ópticos tenha persistido.\n\nEste caso destaca a importância de considerar causas genéticas em neuropatias ópticas bilaterais progressivas, especialmente quando há associação com lesões desmielinizantes e resposta inadequada a tratamentos convencionais para esclerose múltipla. A identificação precisa permite a escolha do tratamento mais adequado e melhora o prognóstico visual a longo prazo."
+        }
+    },
+    {
+        "article": "Uma mulher de 58 anos apresentou-se ao Serviço de Urgência com um histórico de 6 meses de agravamento da dispneia. Nos 10 dias anteriores, os seus sintomas tinham-se agravado, acompanhados por um leve desconforto torácico e inchaço bilateral das pernas. O seu histórico médico incluía asma e hipertensão. À chegada, foi encontrada hipoxémica com uma saturação de oxigénio de 74%, que melhorou para 94% com 5 litros de oxigénio suplementar. O exame físico revelou crepitantes inspiratórios bilaterais e edema de pitting nas extremidades inferiores.\n\nAs investigações laboratoriais demonstraram um nível elevado de NT-proBNP (péptido natriurético cerebral) de 2110 ng/mL (intervalo <125 ng/mL) e níveis normais de troponina. A angiografia torácica por tomografia computorizada (TC) revelou infiltrados de vidro fosco parciais, moderados e bilaterais, um tronco da artéria pulmonar (AP) alargado e dilatação do átrio direito (AD) e do ventrículo direito (VD) sem evidência de embolia pulmonar. A ecocardiografia transtorácica (ETT) mostrou uma fração de ejeção ventricular esquerda (FEVE) de 75% a 80%, dilatação moderada da AP e do VD, achatamento sistólico e diastólico do septo interventricular, função sistólica reduzida do VD e uma pressão sistólica estimada da AP de 55 a 60 mmHg. Não foi identificado um desvio intracardíaco no Doppler colorido ou na injeção de contraste agitado em solução salina.\n\nO paciente foi iniciado com furosemida intravenosa. O cateterismo cardíaco direito (RHC) foi realizado no dia seguinte, enquanto o paciente recebia 3 litros de oxigênio suplementar via cânula nasal. O procedimento confirmou a PH, com uma pressão arterial pulmonar média (mPAP) de 41 mmHg e um débito cardíaco elevado de 8,46 L/min pelo método de Fick. Um teste de vasoreatividade utilizando o protocolo padrão de adenosina confirmou que o paciente não era vasoreativo, indicando que a terapia com bloqueadores dos canais de cálcio não seria benéfica. Investigações adicionais, incluindo hemograma completo, hormônio estimulador da tireóide, triagem para HIV, triagem para anticorpos antinucleares, fator reumatoide e níveis de tiamina, foram sem observações. Estudos de imagem, incluindo angiografia por TC do tórax e abdômen e ultrassom Doppler do fígado, descartaram shunts sistêmicos, malformações arteriovenosas pulmonares e esplenomegalia. No momento da alta, a hipoxemia do paciente havia se resolvido com diurese.\n\nA avaliação ambulatorial incluiu um teste de função pulmonar que mostrou um leve defeito ventilatório obstrutivo. O estudo do sono e o estudo de ventilação-perfusão foram notáveis. Como o RHC demonstrou uma pressão de oclusão da artéria pulmonar (pressão de cunha) de 11 mmHg (<15 mmHg) e um gradiente transpulmonar alto de 26 mmHg (>12 mmHg), o Grupo II de PH devido a doença cardíaca esquerda foi excluído. Foi-lhe prescrito um inalador de corticosteroide, e o furosemide oral (20 mg diariamente) foi continuado. A terapia específica para a hipertensão pulmonar não foi iniciada, dado que o seu PH foi categorizado como grupo III, atribuído a doença pulmonar obstrutiva. Durante as consultas de acompanhamento, a paciente relatou uma melhoria inicial na sua dispneia percebida, que depois se estabilizou. Ela permaneceu consistentemente na categoria de risco intermediário-baixo de acordo com a ferramenta de avaliação de risco de 4 níveis para acompanhamento de PH.\n\nDois anos depois, ela voltou com piora da dispneia e inchaço nas pernas após a interrupção do uso de furosemida. A angiografia pulmonar por tomografia computadorizada repetida revelou achados semelhantes aos da imagem inicial, mas identificou adicionalmente uma veia pulmonar esquerda anormal que drenava para o tronco braquiocefálico esquerdo. Uma revisão retrospectiva da imagem inicial por tomografia computadorizada confirmou a anomalia não detectada. A ecocardiografia transesofágica mostrou EFV de 60%, dilatação moderada da RA e do VE, função sistólica reduzida do VE e uma pressão sistólica estimada da artéria pulmonar de 50 a 55 mmHg. Em contraste com a RHC anterior, a avaliação da derivação dessa vez demonstrou um aumento de 6% na saturação de oxigênio entre a veia cava superior (VCS) e a RA, confirmando uma derivação de esquerda para direita. Essa discrepância foi devida à medição da saturação da VCS que foi apropriadamente obtida acima da drenagem do tronco braquiocefálico esquerdo, agora guiada pelo conhecimento da PAPVR a partir dos achados da tomografia computadorizada. A fração da derivação (Qp/Qs) foi calculada como sendo 1,52. Consequentemente, sua PH foi reclassificada como grupo I devido a doença cardíaca congênita adulta.\n\nA paciente recebeu tratamento com diuréticos intravenosos. Devido ao seu PH leve e classificação de risco intermediário-baixo com base na ferramenta de avaliação de risco de 4 níveis (WHO-FC III, NT-proBNP 81 pg/mL, e uma distância de caminhada de 6 minutos de 460 m), a terapia específica para PH não foi aconselhada. Ela recusou avaliações adicionais, incluindo ressonância magnética cardíaca (MRI) e encaminhamento para um centro de cardiologia congênita adulta, optando por continuar com monitoramento ambulatorial próximo.\n",
+        "gold_summary": "Relatamos o caso de uma mulher de 58 anos que inicialmente apresentou dispneia progressiva e foi diagnosticada com hipertensão pulmonar do grupo III atribuída a doença pulmonar obstrutiva. Dois anos depois, ela voltou com sintomas semelhantes após a interrupção da terapia diurética. A avaliação posterior revelou uma anomalia previamente não detectada da veia pulmonar esquerda que drenava para a veia innominada esquerda.\n",
+        "synthetic_summary": {
+            "B1": "Uma senhora de 58 anos estava com dificuldade para respirar. No começo, pensaram que era por causa dos seus pulmões. Dois anos depois, ela ficou com os mesmos problemas. Descobriram que uma veia do seu pulmão estava diferente. Essa veia levava o sangue para um lugar errado. Agora, ela está sendo cuidada com muito cuidado.",
+            "B2": "**O que aconteceu com a paciente**\n\nUma mulher de 58 anos começou a sentir falta de ar que piorava com o tempo. Ela também teve inchaço nas pernas e um leve desconforto no peito. No hospital, os médicos descobriram que ela tinha pressão alta nos vasos dos pulmões, chamada hipertensão pulmonar. No começo, eles acharam que isso aconteceu por causa de um problema nos pulmões dela.\n\n**O que os médicos descobriram depois**\n\nDois anos depois, a mulher voltou a sentir falta de ar e inchaço porque parou de tomar um remédio que ajuda a eliminar o excesso de líquido do corpo. Novos exames mostraram que ela tinha uma veia do pulmão esquerdo que estava ligada no lugar errado, drenando para uma veia grande do peito. Essa veia anormal não tinha sido percebida nos exames anteriores.\n\n**O que isso significa**\n\nEssa veia ligada no lugar errado causa um desvio de sangue que aumenta a pressão nos pulmões, explicando a hipertensão pulmonar dela. Por isso, o diagnóstico mudou para um tipo diferente de hipertensão, causada por uma doença do coração que a pessoa já nasce com, chamada doença cardíaca congênita. A paciente recebeu tratamento para controlar os sintomas e está sendo acompanhada para evitar que o problema piore.",
+            "B3": "**Contexto**  \nEste relato descreve o caso de uma mulher de 58 anos que procurou atendimento médico devido a um quadro progressivo de dificuldade para respirar (dispneia) ao longo de seis meses, com piora recente acompanhada de inchaço nas pernas e desconforto no peito. Inicialmente, ela foi diagnosticada com hipertensão pulmonar (pressão arterial elevada nas artérias dos pulmões) do grupo III, relacionada a uma doença pulmonar obstrutiva leve.\n\n**Principais Achados**  \nNa primeira avaliação, exames mostraram pressão elevada nas artérias pulmonares, dilatação das câmaras cardíacas direitas e sinais de sobrecarga do ventrículo direito, mas sem evidência de coágulos ou desvio anormal de sangue entre os lados do coração. Testes laboratoriais e de imagem descartaram outras causas comuns de hipertensão pulmonar, como doenças autoimunes, infecções ou malformações vasculares. O tratamento inicial com diuréticos (medicamentos que ajudam a eliminar o excesso de líquido) melhorou os sintomas e a oxigenação.\n\nDois anos depois, após a paciente interromper o uso dos diuréticos, os sintomas retornaram. Uma nova tomografia computadorizada revelou uma anomalia vascular não detectada anteriormente: uma veia pulmonar esquerda que drenava erroneamente para a veia braquiocefálica esquerda (também chamada de veia innominada esquerda), em vez de se conectar ao átrio esquerdo do coração, como ocorre normalmente. Essa condição é conhecida como drenagem venosa pulmonar anômala parcial (PAPVR, na sigla em inglês). A presença dessa anomalia causava um desvio de sangue da esquerda para a direita no coração, contribuindo para a hipertensão pulmonar.\n\n**Interpretação Clínica**  \nA descoberta da drenagem venosa pulmonar anômala levou à reclassificação da hipertensão pulmonar da paciente para o grupo I, que inclui doenças cardíacas congênitas (defeitos estruturais do coração presentes desde o nascimento). Essa alteração no diagnóstico é importante porque muda a abordagem terapêutica e o prognóstico. Apesar da reclassificação, a paciente apresentava uma forma leve da doença e um risco intermediário-baixo, o que justificou a manutenção do tratamento conservador com diuréticos e monitoramento regular, sem a introdução de terapias específicas para hipertensão pulmonar.\n\n**Próximos Passos**  \nFoi recomendada a continuidade do acompanhamento ambulatorial próximo, com monitoramento dos sintomas e da função cardíaca. A paciente optou por não realizar exames adicionais, como ressonância magnética cardíaca, nem buscar avaliação em centro especializado em cardiologia congênita adulta, preferindo manter o tratamento atual. O caso destaca a importância de reavaliar diagnósticos quando os sintomas persistem ou retornam, e de considerar causas menos comuns de hipertensão pulmonar, como malformações vasculares congênitas."
+        }
+    },
+    {
+        "article": "Um homem sírio de 61 anos com histórico de alcoolismo e tabagismo intenso apresentou-se ao departamento de dermatologia com queixas de lesões pigmentadas pruriginosas sem telangiectasias, descamação ou atrofia no lado direito do tronco e na coxa direita. O paciente negou histórico prévio de exposição a produtos químicos ou solventes, e não havia histórico familiar de câncer de pele, doenças de pele ou condições sistêmicas relevantes. Essas lesões persistiram por 3 anos, e o paciente recebeu previamente uma pomada tópica de hidrocortisona 0,1% de um dermatologista local para aliviar a coceira; o paciente usou a pomada de forma intermitente e apenas quando a coceira era intensa. Após o exame clínico, foram evidentes manchas hiperpigmentadas no lado direito do tronco e na superfície lateral da coxa direita, sem outras características clínicas. Os exames de sangue do paciente estavam dentro dos limites normais, exceto por um ligeiro aumento na contagem de glóbulos brancos. Dadas as características não específicas, foi realizada uma biópsia de pele para avaliação adicional, e o exame histopatológico da biópsia revelou epiderme hiperqueratósica parakeratósica com ligeira espongiose. A derme papilar foi infiltrada moderadamente por linfócitos atípicos com leve deposição de melanófagos. O infiltrado linfocítico foi localizado em grupos e em distribuição basilaris linear ao longo da junção dermo-epidermal. A imunologia dos linfócitos atípicos foi CD3+, CD8+, CD4−, CD20−. Foi realizado um exame de tomografia computadorizada (TC) de tórax e abdômen, mas os resultados foram normais, sem linfadenopatia ou organomegalia. O paciente foi diagnosticado com HPMF em estágio inicial e foi encaminhado a um hospital especializado para receber o tratamento. O nosso paciente foi submetido a psoraleno e luz ultravioleta A (PUVA), com 8-metoxipsoraleno oral duas vezes por semana, e foi prescrito um dipropionato de betametasona tópico 0,1%. Após 12 semanas de tratamento, a coceira foi aliviada, e a hiperpigmentação regrediu, mas não desapareceu. O prognóstico a longo prazo do nosso paciente é excelente, e ele foi instruído a aplicar hidratante e evitar a exposição ao sol, e é avaliado a cada 6 meses para detectar qualquer recidiva ou novas lesões noutras áreas do corpo.\n\n",
+        "gold_summary": "Um homem sírio de 61 anos apresentou-se na clínica de dermatologia a queixar-se de uma lesão pruriginosa pigmentada persistente no lado direito do tronco e na coxa direita. O exame histológico da biópsia cutânea mostrou epiderme hiperqueratósica paraqueratósica com espongiose e deposição de melanófagos, a imuno-histoquímica mostrou CD3+, CD4-, CD8+ e CD20-, e o nosso paciente foi diagnosticado com micose fungóide hiperpigmentada, e subsequentemente tratado com psoraleno e terapia ultravioleta A, observou-se uma melhoria muito boa, e o prognóstico foi excelente.\n",
+        "synthetic_summary": {
+            "B1": "Um homem de 61 anos tinha manchas escuras que coçavam na pele. Essas manchas estavam no lado do corpo e na perna dele. O médico fez um exame com um pedacinho da pele. O exame mostrou que ele tinha uma doença na pele que precisa de cuidado. O homem tomou um remédio e ficou melhor. A coceira parou e as manchas ficaram menores. O médico disse que ele vai ficar bem e deve cuidar da pele, usando creme e evitando o sol forte.",
+            "B2": "**O que aconteceu com o paciente**\n\nUm homem de 61 anos, que já fumou muito e bebeu álcool, foi ao médico por causa de manchas escuras e que coçavam no lado direito do corpo e na coxa. Essas manchas estavam lá há 3 anos e não melhoravam com pomadas comuns para coceira.\n\n**O que os médicos fizeram**\n\nPara entender melhor o problema, os médicos retiraram um pedacinho da pele (isso se chama biópsia) para olhar no microscópio. Eles viram que a pele tinha algumas mudanças nas células e que havia um tipo especial de células do sistema de defesa (linfócitos) em um padrão diferente do normal. Esses resultados ajudaram a descobrir que o paciente tinha uma doença chamada micose fungoide hiperpigmentada, que é um tipo raro de câncer de pele que começa nas células do sistema imunológico da pele.\n\n**Como foi o tratamento**\n\nO paciente recebeu um tratamento que combina um remédio chamado psoraleno com luz ultravioleta A (PUVA). Esse tratamento ajuda a controlar as células doentes na pele. Além disso, ele usou uma pomada com corticoide para diminuir a inflamação. Depois de 12 semanas, a coceira melhorou bastante e as manchas escuras ficaram menos visíveis, embora não tenham desaparecido completamente.\n\n**O que isso significa**\n\nO prognóstico, que é a previsão de como o paciente vai ficar, é muito bom. Ele deve continuar cuidando da pele, usando hidratante e evitando o sol forte. O médico vai acompanhar ele a cada seis meses para garantir que a doença não volte ou que não apareçam novas manchas. Assim, o paciente pode ter uma boa qualidade de vida com o tratamento adequado.",
+            "B3": "**Contexto**  \nUm homem sírio de 61 anos, com histórico significativo de alcoolismo e tabagismo, apresentou-se ao serviço de dermatologia queixando-se de lesões pigmentadas e pruriginosas (com coceira) localizadas no lado direito do tronco e na coxa direita. Essas lesões estavam presentes há cerca de três anos e não apresentavam sinais típicos de outras condições, como telangiectasias (vasos sanguíneos dilatados visíveis), descamação ou atrofia da pele. O paciente não relatou exposição prévia a produtos químicos nem histórico familiar de doenças dermatológicas ou câncer de pele.\n\n**Principais Achados**  \nO exame clínico revelou manchas hiperpigmentadas (áreas de pele com coloração mais escura) nas regiões mencionadas, sem outras alterações visíveis. Os exames laboratoriais mostraram resultados dentro dos limites normais, exceto por um leve aumento na contagem de glóbulos brancos, sugerindo uma possível reação inflamatória. Para esclarecer o diagnóstico, foi realizada uma biópsia da pele afetada. O exame microscópico revelou alterações na epiderme, incluindo hiperqueratose (espessamento da camada externa da pele) com paraqueratose (presença anormal de células na camada córnea) e espongiose (acúmulo de líquido entre as células epidérmicas). Na derme papilar (camada superficial da derme), observou-se um infiltrado moderado de linfócitos atípicos (células do sistema imunológico com características anormais), acompanhados por melanófagos (células que fagocitam pigmentos de melanina). A distribuição desses linfócitos foi agrupada e linear ao longo da junção entre a epiderme e a derme. A análise imunohistoquímica indicou que essas células eram CD3 positivas (marcador de linfócitos T), CD8 positivas (subtipo de linfócitos T citotóxicos), CD4 negativas (não apresentavam marcador de linfócitos T auxiliares) e CD20 negativas (não eram células B).\n\nExames de imagem, incluindo tomografia computadorizada do tórax e abdômen, não revelaram linfadenopatia (aumento dos gânglios linfáticos) nem aumento de órgãos, sugerindo ausência de disseminação sistêmica da doença.\n\n**Interpretação Clínica**  \nCom base nos achados clínicos, histopatológicos e imunológicos, o paciente foi diagnosticado com micose fungóide hiperpigmentada (MFH), uma variante rara do linfoma cutâneo de células T, caracterizada por manchas pigmentadas e infiltrado linfocitário atípico na pele. Essa condição é considerada um tipo de câncer de pele de origem linfocitária, geralmente de evolução lenta e com bom prognóstico quando diagnosticada precocemente.\n\n**Tratamento e Evolução**  \nO paciente iniciou tratamento com psoraleno oral (um medicamento que sensibiliza a pele à luz) associado à terapia com luz ultravioleta A (PUVA), administrados duas vezes por semana. Além disso, foi prescrito o uso tópico de dipropionato de betametasona 0,1%, um corticosteroide para reduzir a inflamação e a coceira. Após 12 semanas, houve melhora significativa dos sintomas, com alívio da coceira e regressão parcial das manchas hiperpigmentadas, embora estas não tenham desaparecido completamente.\n\n**Prognóstico e Acompanhamento**  \nO prognóstico a longo prazo para esse paciente é excelente, considerando a resposta positiva ao tratamento e a ausência de sinais de disseminação. Ele foi orientado a manter a pele hidratada, evitar exposição solar excessiva para prevenir agravamento das lesões e realizar avaliações dermatológicas semestrais para monitorar possíveis recidivas ou aparecimento de novas lesões em outras áreas do corpo."
+        }
+    },
+    {
+        "article": "Descrevemos um caso de um paciente de 18 anos de idade, afetado por DMD e em cadeira de rodas desde os 11 anos de idade, que sempre foi seguido por uma equipa multidisciplinar na nossa Instituição. Desde os 6 anos de idade, foi tratado com deflazacort por via oral. Durante estes anos, o paciente foi regularmente seguido por pneumologistas, utilizando espirometria e por neurologistas, que monitorizaram a evolução da doença neuromuscular em termos de função toraco-abdominal e escoliose. A capacidade vital forçada (CVF), o volume expiratório forçado em 1 s (VEF1) e o fluxo expiratório máximo (PEF) foram, respetivamente, de 60%, 70% e 70% dos valores previstos (CVF, 2,24 L; VEF1, 2,09 L; PEF, 4,07 L). O paciente foi também submetido a cateterização cardíaca direita para monitorizar as resistências vasculares pulmonares, com evidência de valores dentro do intervalo normal. Quando desenvolveu progressivamente cardiomiopatia dilatada em 2016, aos 14 anos de idade, foi submetido a implante de LVAD HeartWare, devido a insuficiência cardíaca refratária aguda. A opção de transplante de coração não foi considerada pelos cirurgiões cardíacos pediátricos, (i) devido à emergência em que o paciente se encontrava e (ii) devido ao ceticismo comum em relação ao transplante de coração nestes pacientes com DMD. A retirada da ventilação mecânica ocorreu de forma rotineira, e não foram encontradas complicações pós-operatórias.\n\nDurante os 47 meses seguintes, o paciente foi seguido regularmente e só reportamos uma infecção no local de saída do LVAD, tratada com antibióticos e limpeza cirúrgica, 30 meses após a implantação do LVAD. A limpeza da linha de condução consistiu numa incisão da pele no local da passagem do cabo, exteriorização do cabo mais proximalmente, limpeza do trajeto fistuloso e re‐suturação da pele. Embora a recuperação tenha sido excelente, visto que a saída da linha de condução estava muito próxima da ferida esternal, o paciente ficou psicologicamente estressado o suficiente para pedir espontaneamente uma solução radical para o problema. A FVC, a FEV1 e o PEF foram, respetivamente, de 1,66 l, 1,62 l e 4,41 l. Com base nas boas condições gerais do paciente e na motivação pessoal do paciente, a nossa equipa multidisciplinar começou a considerar o transplante de coração como uma opção. Assim, a 12 de fevereiro de 2020, com 18 anos, o paciente foi submetido a um transplante de coração sem complicações pós‐operativas. A retirada da ventilação mecânica ocorreu como de costume. No primeiro dia pós‐transplante, foi possível extubar o paciente. A alta da UTI foi possível no terceiro dia pós‐operativo. No que diz respeito à mobilização, na nossa unidade, os pacientes são acompanhados por uma equipa especializada de fisioterapeutas. O paciente foi treinado por eles desde os primeiros dias; e assim que foi transferido da UTI para a enfermaria, a mobilização foi iniciada o mais rapidamente possível. No que diz respeito à estabilização esternal, como é habitual, sugerimos a utilização de uma banda esternal. A mobilização numa cadeira de rodas foi possível no quinto dia pós‐operativo. A estadia total no hospital foi de 3 semanas, o tempo necessário para realizar as três biopsias canónicas para a avaliação de qualquer rejeição miocárdica. Foi administrada uma terapia imunossupressora padrão com três agentes (ciclosporina, micofenolato de mofetil e esteróides). Aos 3 meses, a FVC, a FEV1 e o PEF foram inalterados em relação ao pré‐transplante.",
+        "gold_summary": "Descrevemos o caso de um paciente de 18 anos, afetado por DMD e em cadeira de rodas desde os 11 anos. Ele desenvolveu progressivamente cardiomiopatia dilatada e, em 2016, aos 14 anos, foi submetido a implante de LVAD HeartWare, como terapia de destino, sem complicações pós-operatórias. Ele foi seguido por 47 meses consecutivos; e 30 meses após o implante LVAD, ele desenvolveu uma infecção no local de saída, tratada com antibióticos e lavagem cirúrgica. Após este evento, com base nas boas condições gerais do paciente e na sua vontade, começámos a considerar o transplante de coração como uma opção. Antes do paciente ser inscrito, ele foi submetido a um trabalho de investigação exaustivo, e encontrámos valores mais elevados de capacidade vital forçada, volume expiratório forçado em 1 s, e fluxo expiratório de pico, comparados com os valores previstos para pacientes DMD da mesma idade. O paciente não tem escoliose nem necessita de ventilação mecânica não invasiva, e finalmente, foi sempre tratado com esteróides com função toraco-abdominal estável ao longo dos anos. De acordo com estas considerações, o paciente foi inscrito para transplante de coração. A 12 de fevereiro de 2020, aos 18 anos, o paciente foi submetido a transplante de coração sem complicações pós-operatórias. O transplante cardíaco não é considerado uma opção válida para pacientes DMD, devido à escassez de disponibilidade de dadores e à natureza sistémica da doença DMD. Tendo em consideração que este paciente já tinha tido uma complicação relacionada com LVAD e que tinha um melhor estado geral do que os seus pares com DMD, inscrevemo-lo para transplante de coração. Descrevemos o caso de um paciente com DMD que foi submetido a transplante cardíaco bem sucedido após 47 meses de assistência com LVAD HeartWare. O acompanhamento de três meses foi sem incidentes.\n",
+        "synthetic_summary": {
+            "B1": "Este é um menino de 18 anos que tem uma doença que deixa os músculos fracos. Ele usa cadeira de rodas desde os 11 anos. Quando tinha 14 anos, o coração dele ficou muito cansado. Então, os médicos colocaram uma máquina para ajudar o coração a trabalhar.\n\nDepois de algum tempo, ele teve uma machucadinha onde a máquina sai do corpo. Os médicos cuidaram bem disso com remédios e limpeza. O menino ficou bem e queria tentar um novo coração.\n\nOs médicos viram que ele estava forte para fazer a cirurgia. Então, quando ele tinha 18 anos, ele ganhou um coração novo. A cirurgia foi boa e ele ficou bem depois.\n\nAgora, ele está se cuidando e os médicos estão felizes porque ele está melhor.",
+            "B2": "**Caso de um jovem com DMD e transplante de coração**\n\nEste é o relato de um paciente de 18 anos que tem DMD, uma doença que enfraquece os músculos. Ele está em cadeira de rodas desde os 11 anos. Aos 14 anos, seu coração começou a funcionar mal por causa da doença, e ele recebeu um aparelho chamado LVAD HeartWare. Esse aparelho ajuda o coração a bombear sangue. A cirurgia para colocar o LVAD foi feita sem problemas.\n\nDurante quase quatro anos, os médicos acompanharam o paciente de perto. Trinta meses depois da cirurgia, ele teve uma infecção no local onde o aparelho saía do corpo. Essa infecção foi tratada com remédios e limpeza cirúrgica, e ele se recuperou bem.\n\nComo ele estava em boa forma geral e muito motivado, os médicos começaram a pensar em fazer um transplante de coração, que é quando o coração doente é substituído por um saudável de um doador. Antes disso, eles fizeram muitos exames para garantir que ele estava bem para a cirurgia. O paciente tinha uma boa capacidade de respirar e não precisava de ajuda para respirar com máquinas. Além disso, ele não tinha escoliose, que é uma curvatura da coluna comum em pessoas com DMD.\n\nNo dia 12 de fevereiro de 2020, ele recebeu o transplante de coração. A cirurgia foi um sucesso e não houve complicações depois. Ele saiu da unidade de terapia intensiva em poucos dias e começou a se movimentar com a ajuda de fisioterapeutas. Em três semanas, ele teve alta do hospital.\n\nO transplante de coração geralmente não é feito em pacientes com DMD, porque a doença afeta todo o corpo e há poucos corações disponíveis para doação. Mas, neste caso, como o paciente estava melhor do que outros jovens com DMD e já tinha tido o LVAD, os médicos decidiram fazer o transplante.\n\nApós três meses do transplante, o paciente estava bem, sem problemas novos. Este caso mostra que, em situações especiais, o transplante de coração pode ser uma opção para pacientes com DMD.",
+            "B3": "**Contexto**  \nEste relato descreve o caso de um jovem de 18 anos diagnosticado com distrofia muscular de Duchenne (DMD), uma doença genética que causa fraqueza muscular progressiva. Ele está em cadeira de rodas desde os 11 anos e tem sido acompanhado por uma equipe multidisciplinar desde a infância. Aos 14 anos, desenvolveu uma complicação cardíaca grave chamada cardiomiopatia dilatada, que compromete a função do coração. Para tratar essa insuficiência cardíaca aguda, foi implantado um dispositivo chamado LVAD HeartWare, que auxilia o bombeamento do coração.\n\n**Principais Achados**  \nDurante os quase quatro anos seguintes ao implante do LVAD, o paciente teve acompanhamento regular e apresentou apenas uma infecção localizada no ponto onde o dispositivo sai do corpo, tratada com antibióticos e limpeza cirúrgica. Apesar dessa complicação, o paciente manteve uma boa condição geral, com função pulmonar relativamente preservada para alguém com DMD, sem escoliose (curvatura anormal da coluna) e sem necessidade de ventilação mecânica não invasiva. Ele também recebeu tratamento contínuo com corticosteroides, que ajudaram a manter a função muscular toraco-abdominal estável.\n\n**Interpretação Clínica**  \nEmbora o transplante de coração raramente seja considerado em pacientes com DMD devido à natureza sistêmica da doença e à escassez de doadores, neste caso, a equipe médica avaliou que o paciente apresentava condições físicas favoráveis e motivação pessoal para o procedimento. Além disso, ele já havia passado por uma complicação relacionada ao LVAD, o que reforçou a necessidade de buscar uma solução definitiva. Após uma avaliação detalhada, que incluiu testes de função pulmonar mostrando valores superiores aos esperados para pacientes com DMD da mesma idade, o paciente foi inscrito para transplante cardíaco.\n\n**Próximos Passos e Desfecho**  \nEm 12 de fevereiro de 2020, o paciente foi submetido ao transplante de coração sem complicações durante ou após a cirurgia. A retirada da ventilação mecânica ocorreu rapidamente, e ele recebeu acompanhamento fisioterapêutico intensivo para mobilização precoce. A alta hospitalar ocorreu após três semanas, período em que foram realizadas biópsias para monitorar possíveis rejeições do órgão transplantado. A terapia imunossupressora padrão foi administrada para evitar rejeição. Três meses após o transplante, a função pulmonar do paciente permaneceu estável, sem intercorrências. Este caso demonstra que, em situações selecionadas, o transplante cardíaco pode ser uma opção viável e bem-sucedida para pacientes com DMD, especialmente quando suportados por dispositivos como o LVAD e acompanhados por uma equipe multidisciplinar."
+        }
+    },
+    {
+        "article": "O Sr. S. era um paciente de 88 anos, aposentado, trabalhador da construção civil, viúvo, que morava sozinho num apartamento no primeiro andar com escadas. Ele tinha apenas uma filha, sua cuidadora principal. Ele não tinha ajuda em casa antes de sua hospitalização.\n\nO seu histórico clínico foi marcado por repetidas artrites descritas como gota, insuficiência cardíaca numa estenose da válvula aórtica que subsequentemente beneficiou de TAVI, insuficiência renal crónica moderada (depuração 45 ml/min/1,73 m2), stenting bi-femoral aorto-bi-femoral, pressão arterial elevada, acidente vascular isquémico transitório, tremor essencial e uma trombose venosa sural direita. Não tinha hábitos tóxicos ou alergias.\n\nA 7 de Novembro, este paciente foi admitido no departamento de emergência para descompensação cardio-renal consecutiva a uma pneumopatia. O paciente recuperou com antibiótico associado a terapia diurética. Depois de cinco dias, foi transferido para uma ala geriátrica para uma avaliação geriátrica padronizada e para reabilitação face ao descondicionamento do exercício.\n\nAs amostras de sangue iniciais de 13 de Novembro, encontraram um nível de cálcio de 2.55 mmol/L, corrigido para 2.84 mmol/L. Havia desnutrição grave com uma dose de albumina medida em 28.3 mmol/L. Um PTH aumentado para 94 ng/L e um 25-hidroxi-vitamina D colapsada em 15 nmol/L foram encontrados. Clinicamente, ele não apresentou sinais clínicos sugestivos de hipercalcemia. A radiografia de tórax não apresentou anomalias. Em Dezembro, dada a suspeita de hiperparatiroidismo secundário devido a hipovitaminose D e não em linha com as recomendações padrão, um ultra-som paratireóide não revelou nódulos suspeitos. A suplementação de colecalciferol foi introduzida. Além disso, iniciou-se a gestão nutricional. M. S apresentou ao mesmo tempo uma artrite dolorosa nos joelhos com derrame articular associado a síndrome inflamatória biológica. Suspeitou-se de condrocalcinose mas o nível de ácido úrico foi elevado 478 µmol/L. Foi realizada uma punção: 920 células nucleadas por mm3 e cristais de urato de sódio foram encontrados no fluido articular. O tratamento com colchicina e depois a adição de alopurinol melhoraram os sintomas. O estado cardíaco e as melhorias físicas permitiram ao paciente voltar a casa no dia 2 de Janeiro.\n\nInfelizmente, uma nova descompensação cardíaca requereu uma re-hospitalização a 23 de janeiro. Durante esta subsequente hospitalização, os níveis de cálcio no sangue permaneceram ligeiramente aumentados (2.64 mmol/L) e a PTH foi significativamente aumentada (191 ng/L) apesar da suplementação de vitamina D. Em março, uma amostra de urina de 24 horas foi recolhida para medição de calciúria, que revelou uma diminuição da concentração de cálcio urinário de 1.23 mmol/L. A fração de excreção de cálcio foi de 1.2%. Devido a estes resultados não característicos, uma MIBI paratireoideia cintigrafia não revelou anomalias a favor de um adenoma ou hiperplasia paratireoideia. Em abril, uma análise genética para detetar a mutação inibitória do gene CASR que codifica para o recetor sensível ao cálcio (gene 3q21.1) revelou uma variante patogénica classificada como FHH tipo 1 de acordo com as orientações ACMG. A família do paciente foi informada e foi organizado um rastreio genético para evitar testes adicionais desnecessários. O paciente foi finalmente capaz de ir para casa. O paciente e a sua família deram o seu consentimento informado para este caso clínico. Não foi necessária a aprovação ética para este manuscrito. Foi obtido o consentimento para publicação da filha do paciente.",
+        "gold_summary": "Relatamos o diagnóstico de FHH num paciente de 88 anos com múltiplas patologias e com hipercalcemia descoberta durante um check-up para descompensação cardíaca. Apesar de uma apresentação clínica confusa com sintomas de gota, incluindo episódios repetidos de artrite do joelho, a hipercalcemia persistente levou a investigações adicionais. Os testes biológicos excluíram o hiperparatiroidismo primário ou hiperparatiroidismo relacionado com malignidade, confirmando o diagnóstico de FHH através da deteção de uma mutação inibitória no gene do recetor sensível ao cálcio.\n",
+        "synthetic_summary": {
+            "B1": "O senhor S. tem 88 anos e estava doente com o coração e os ossos. Os médicos viram que ele tinha muito cálcio no sangue. Isso pode ser estranho, mas não era um problema grave para ele. \n\nEle também tinha dores nos joelhos, que eram por causa de um problema chamado gota. Os médicos fizeram muitos exames para entender o que estava acontecendo. \n\nNo fim, eles descobriram que o corpo dele tem um jeito diferente de cuidar do cálcio. Isso é algo que ele já nasceu assim. Não precisa de remédio forte para isso. \n\nOs médicos explicaram para a família e cuidaram dele com muito carinho. Agora, ele pode ficar em casa e descansar melhor.",
+            "B2": "**O que aconteceu com o paciente**\n\nUm homem de 88 anos, que já tinha vários problemas de saúde, foi internado no hospital por causa de dificuldades no coração e nos rins. Durante os exames, os médicos descobriram que ele tinha o nível de cálcio no sangue mais alto do que o normal, algo chamado hipercalcemia. Isso chamou a atenção porque ele também estava com dores e inchaço nos joelhos, sintomas parecidos com os da gota, uma doença que causa inflamação nas articulações.\n\n**O que os médicos investigaram**\n\nPara entender por que o cálcio estava alto, os médicos fizeram vários exames. Eles queriam saber se o problema vinha das glândulas paratireoides, que ajudam a controlar o cálcio no corpo, ou se havia algum câncer causando isso. Os testes mostraram que não era nenhum desses casos. Então, eles fizeram um exame genético, que é um teste para ver se havia alguma mudança no DNA do paciente.\n\n**O que descobriram e o que isso significa**\n\nO exame genético revelou que o paciente tinha uma mutação no gene que controla um receptor sensível ao cálcio. Essa mutação causa uma condição chamada Hipercalcemia Familiar Benigna (FHH), que é uma doença hereditária. Na FHH, o corpo mantém o cálcio no sangue um pouco alto, mas isso geralmente não causa problemas graves e não precisa de tratamento agressivo.\n\n**Por que isso é importante**\n\nSaber que o paciente tem FHH ajuda os médicos a evitar tratamentos desnecessários e a informar a família, já que essa condição pode ser passada para os parentes. Também explica por que o cálcio dele estava alto, mesmo sem sinais de outras doenças mais graves. Assim, o paciente pode receber cuidados mais adequados e a família pode fazer exames para entender se alguém mais tem essa condição.",
+            "B3": "**Contexto**  \nEste relato descreve o caso do Sr. S., um homem de 88 anos com múltiplas doenças crônicas, que foi internado inicialmente por uma descompensação cardíaca e renal associada a uma infecção pulmonar. Durante sua avaliação hospitalar, foi detectada uma hipercalcemia (nível elevado de cálcio no sangue), o que motivou uma investigação detalhada para identificar a causa desse desequilíbrio metabólico.\n\n**Principais Achados**  \nO paciente apresentava um quadro clínico complexo, incluindo artrite dolorosa nos joelhos, inicialmente suspeita de condrocalcinose (depósito de cristais de cálcio nas articulações) ou gota, confirmada pela presença de cristais de urato no líquido articular. Apesar do tratamento para gota e da suplementação de vitamina D para corrigir uma deficiência, os níveis de cálcio no sangue permaneceram elevados, assim como os níveis do hormônio paratireoideano (PTH), que regula o metabolismo do cálcio.\n\nExames complementares, como ultrassonografia das paratireoides e cintilografia com MIBI (um exame que detecta adenomas ou hiperplasia das glândulas paratireoides), não mostraram alterações que justificassem o aumento do PTH. Além disso, a análise da calciúria (quantidade de cálcio excretada na urina) revelou valores baixos, o que não é típico do hiperparatiroidismo primário.\n\nDiante desses resultados atípicos, foi realizada uma análise genética que identificou uma mutação patogênica no gene CASR, responsável pelo receptor sensível ao cálcio. Essa mutação causa a condição conhecida como hipercalcemia familiar benigna (FHH, do inglês “Familial Hypocalciuric Hypercalcemia”), caracterizada por níveis elevados de cálcio no sangue, níveis altos ou normais de PTH e baixa excreção urinária de cálcio, sem necessidade de tratamento específico.\n\n**Interpretação Clínica**  \nO diagnóstico de FHH explica a hipercalcemia persistente do paciente, que não se enquadrava nas causas mais comuns, como o hiperparatiroidismo primário ou doenças malignas. Essa condição é benigna e geralmente não causa sintomas graves, embora possa ser confundida com outras doenças que elevam o cálcio sanguíneo. O reconhecimento correto da FHH evita tratamentos desnecessários e intervenções invasivas.\n\n**Próximos Passos**  \nApós a confirmação genética do diagnóstico, a família do paciente foi orientada e submetida a um rastreamento genético para identificar outros possíveis portadores da mutação, prevenindo exames e tratamentos inadequados. O paciente recebeu alta com acompanhamento clínico, sem necessidade de intervenções específicas para a hipercalcemia. O caso reforça a importância de uma investigação cuidadosa em pacientes idosos com hipercalcemia persistente e múltiplas comorbidades, para garantir um diagnóstico preciso e um manejo adequado."
+        }
+    },
+    {
+        "article": "Uma mulher japonesa de 65 anos de idade, que apresentou dispneia, visitou um hospital próximo e foi hospitalizada por insuficiência cardíaca e pneumonia em outubro de 2017. A imunofisopatologia revelou a presença de proteína Bence Jones tipo λ. A imunofisopatologia direta mostrou uma imunoglobulina G de 1325 mg/dL; imunoglobulina A de 712 mg/dL; e imunoglobulina M de 46 mg/dL. Os fatores complementares 3 e 4, e a atividade hemolítica do complemento foram normais. Os anticorpos antinucleares, o fator reumatóide e os anticorpos citoplasmáticos antineutrófilos foram negativos. A sua análise de urina revelou proteinúria de 1,29 g/gramo de creatinina urinária e < 1 glóbulo vermelho/campo de alta potência. A tomografia computadorizada mostrou derrames pleurais bilaterais e infiltrações que indicavam pneumonia em ambos os pulmões. A ecocardiografia após admissão mostrou os seguintes achados: diâmetro final diastólico do ventrículo esquerdo, 41,8 mm; diâmetro final sistólico do ventrículo esquerdo, 28,7 mm; fração de ejeção, 59,6%; espessura do septo interventricular, 14,8 mm; espessura da parede posterior do ventrículo esquerdo, 14,5 mm; E/A ratio, 1,14; e E/e' 14,75. O espessamento extenso do ventrículo esquerdo e do septo interventricular, e a diástole disfuncional (padrão restritivo) foram observados, e, assim, foi diagnosticada insuficiência cardíaca com fração de ejeção preservada (ICFp). Ela foi classificada como classe IV da New York Heart Association (NYHA) e grupo C (Wet-Cold) da classificação de Nohria-Stevenson. Ela também foi diagnosticada com amiloidose cardíaca avançada após consulta cardiológica. Iniciamos o tratamento com antimicrobianos, noradrenalina, dobutamina, e diálise contínua por hemodiafiltração (CHDF). As configurações de CHDF foram as seguintes: fluxo de sangue de 60-80 ml/min, fluxo de dialisato de 100-300 ml/h, e taxa de filtração de 100-300 ml/h. O seu estado geral estabilizou-se gradualmente, e foi mudada para diálise peritoneal intermitente (DPI). A DPI foi realizada durante 4 horas com um fluxo de sangue de 100-120 ml/min, utilizando um dialisador de polietersulfona (PES-15Eαeco, Nipro Corporation, Osaka, Japão). No entanto, desenvolveu trombocitopenia, e os anticorpos anti-heparina-fator 4 (PF4) tornaram-se positivos (1,1 U/mL; valor negativo foi abaixo de 0,9 U/mL) no 14º dia após admissão. Interrompemos a heparina devido a suspeita de heparina-induzida trombocitopenia (HIT), e administramos um regime de diálise livre de heparina e argatroban. Além disso, desenvolveu hipotensão intradiálise (IDH). Sob estas circunstâncias, foi difícil continuar a DPI, e mudámos a RRT para PD. Um cateter de PD foi inserido sob anestesia local no 16º dia após admissão. A partir do 2º dia pós-operatório, a PD contínua ambulatória foi iniciada, e ajustámos o regime de PD com base no volume do paciente. O regime de PD foi finalmente fixado para a diálise peritoneal automatizada utilizando 4 L de tampão neutro 1.35% de glucose peritoneal (Midpeliq 135L, Terumo Corporation, Tóquio, Japão) e 1 L de 7.5% de icodextrina peritoneal (Nicopeliq, Terumo Corporation, Tóquio, Japão) por dia. A remoção de fluido por PD foi de aproximadamente 500 ml/dia, e conseguimos gerir o volume do paciente com sucesso com este regime. O volume de urina foi de aproximadamente 1000 ml/dia com a administração de furosemida 160 mg/dia, espironolactona 50 mg/dia, e tolvaptan 15 mg/dia e não mudou durante a hospitalização, indicando uma boa função renal residual. Ela foi dispensada em casa no 44º dia após admissão. Os níveis de BNP e NT-proBNP melhoraram para 195.1 pg/mL e 12,922.0 pg/mL na descarga, respetivamente. Desde então, foi seguida como um paciente ambulatório, e continua a fazer a PD durante 2 anos sem quaisquer sintomas ou complicações graves. Tem uma boa qualidade de vida e gosta de viajar pelo Japão. Os resultados da ecocardiografia após descarga foram os seguintes: diâmetro final diastólico do ventrículo esquerdo, 42.9 mm; diâmetro final sistólico do ventrículo esquerdo, 31.0 mm; fração de ejeção, 54.1%; espessura do septo interventricular, 16.4 mm; espessura da parede posterior do ventrículo esquerdo, 11.4 mm; E/A ratio, 0.71; e E/e' 8.57. Estes achados foram semelhantes aos da hospitalização, embora a diástole disfuncional tenha sido ligeiramente melhorada.",
+        "gold_summary": "Uma mulher de 65 anos foi hospitalizada por insuficiência cardíaca e pneumonia num hospital próximo. Ela tinha sido previamente diagnosticada com amiloidose de cadeia leve (AL) e tratada com melfalano mais dexametasona (Mel-Dex), e lenalidomida mais dexametasona (Len-Dex). Ela começou o tratamento incluindo antimicrobianos e diuréticos, mas a sua função renal piorou progressivamente, e foi transferida para o nosso hospital para cuidados nefrológicos. Ela foi tratada com antimicrobianos, noradrenalina, dobutamina, e hemodiafiltração contínua. O seu estado geral estabilizou-se gradualmente, e foi transferida para hemodiálise intermitente (HD). No entanto, a HD foi descontinuada devido a hipotensão intradiálise e ao desenvolvimento de trombocitopenia induzida por heparina. A sua terapia de substituição renal foi transferida para diálise peritoneal (DP), que permitiu um bom controlo do volume e uma função cardíaca estável. Ela foi dispensada e encontra-se ainda em boas condições, sem complicações graves e com um prognóstico consideravelmente melhor do que o previsto.\n",
+        "synthetic_summary": {
+            "B1": "Uma senhora de 65 anos ficou doente com o coração e os pulmões. Ela foi para o hospital para receber cuidados. Os médicos deram remédios para ajudar seu corpo a ficar melhor. \n\nEla precisou de uma máquina para limpar o sangue porque os rins dela não estavam bem. Primeiro, usaram uma máquina que funciona o tempo todo. Depois, tentaram outra que funciona só às vezes. Mas essa segunda máquina fez ela se sentir mal. \n\nEntão, os médicos mudaram para um jeito diferente de limpar o sangue, chamado diálise peritoneal. Esse jeito ajudou ela a ficar melhor e o coração dela ficou forte. \n\nEla saiu do hospital e está bem até hoje. Ela não tem problemas grandes e pode fazer coisas que gosta.",
+            "B2": "**O que aconteceu com a paciente**\n\nUma mulher de 65 anos foi levada ao hospital porque estava com dificuldade para respirar e tinha pneumonia, uma infecção nos pulmões. Ela também sofria de uma doença chamada amiloidose de cadeia leve (AL), que faz com que uma proteína estranha se acumule no corpo e prejudique órgãos importantes, como o coração e os rins.\n\n**Tratamentos realizados**\n\nNo começo, ela recebeu remédios para combater a infecção e ajudar o coração a funcionar melhor. Porém, os rins dela começaram a piorar, e ela precisou ser transferida para outro hospital especializado em problemas renais. Lá, ela recebeu tratamentos como hemodiafiltração contínua, que é um tipo de limpeza do sangue feita o tempo todo para substituir a função dos rins.\n\nDepois que seu estado melhorou um pouco, ela passou para a hemodiálise intermitente, que é uma limpeza do sangue feita algumas vezes por semana. Mas esse tratamento teve que ser parado porque ela teve uma queda no número de plaquetas, que são células do sangue importantes para a coagulação, causada por uma reação à heparina, um remédio usado na hemodiálise. Além disso, ela apresentava pressão baixa durante as sessões.\n\n**Mudança para diálise peritoneal e resultados**\n\nPor causa desses problemas, os médicos mudaram o tratamento para a diálise peritoneal. Essa técnica usa o próprio abdômen da paciente para filtrar o sangue, o que é mais suave para o corpo. Com essa diálise, foi possível controlar bem o excesso de líquidos e manter o coração funcionando de forma estável.\n\n**Situação atual**\n\nA paciente recebeu alta do hospital e continua fazendo a diálise peritoneal em casa há dois anos. Ela está bem, sem complicações graves, e sua qualidade de vida melhorou bastante. Ela até gosta de viajar pelo Japão, mostrando que o tratamento ajudou muito no seu dia a dia.\n\n**O que isso significa**\n\nEsse caso mostra que, mesmo com doenças graves como a amiloidose e problemas no coração e nos rins, é possível encontrar tratamentos que ajudam a pessoa a viver melhor. A diálise peritoneal foi uma opção importante para essa paciente, porque evitou complicações e permitiu que ela tivesse uma vida mais ativa.",
+            "B3": "**Contexto**  \nUma mulher japonesa de 65 anos foi inicialmente hospitalizada devido a insuficiência cardíaca e pneumonia. Ela possuía diagnóstico prévio de amiloidose de cadeia leve (AL), uma condição causada pelo acúmulo anormal de proteínas amiloides no organismo, que já estava sendo tratada com combinações de medicamentos quimioterápicos (melfalano com dexametasona e lenalidomida com dexametasona). Durante a internação, seu quadro clínico agravou-se com piora progressiva da função renal, o que motivou sua transferência para um hospital especializado em nefrologia.\n\n**Principais Achados e Tratamento Inicial**  \nNo novo hospital, a paciente recebeu tratamento com antimicrobianos para a pneumonia, além de suporte hemodinâmico com noradrenalina e dobutamina para insuficiência cardíaca. Para a insuficiência renal, foi iniciada hemodiafiltração contínua, uma modalidade de diálise que permite a remoção gradual de fluidos e toxinas. Com a estabilização do quadro geral, a terapia renal foi modificada para hemodiálise intermitente, procedimento mais convencional e realizado em sessões.\n\n**Complicações e Ajustes no Tratamento**  \nDurante a hemodiálise intermitente, a paciente desenvolveu hipotensão intradiálise (queda significativa da pressão arterial durante o procedimento) e trombocitopenia (redução do número de plaquetas no sangue). A investigação revelou a presença de anticorpos anti-heparina-fator 4, confirmando o diagnóstico de trombocitopenia induzida por heparina (HIT), uma reação imunológica grave que contraindica o uso de heparina, um anticoagulante comum em diálise. Devido a essas complicações, a hemodiálise foi suspensa.\n\n**Transição para Diálise Peritoneal e Evolução Clínica**  \nA terapia renal foi então convertida para diálise peritoneal (DP), que utiliza a membrana do peritônio (revestimento interno do abdômen) para filtrar o sangue. A DP permitiu um controle eficaz do volume de líquidos no organismo e manteve a estabilidade da função cardíaca, sem provocar hipotensão ou outras complicações associadas à hemodiálise. A paciente manteve uma boa produção urinária residual, indicando preservação da função renal remanescente.\n\n**Desfecho e Prognóstico**  \nApós 44 dias de internação, a paciente recebeu alta hospitalar em condições estáveis. Ela continuou a realizar diálise peritoneal de forma ambulatorial por pelo menos dois anos, sem apresentar sintomas ou complicações graves. A qualidade de vida foi preservada, permitindo-lhe inclusive viajar pelo Japão. Exames de imagem cardíacos realizados após a alta mostraram manutenção da função cardíaca com leve melhora da diástole (fase de relaxamento do coração).\n\n**Interpretação Clínica**  \nEste caso ilustra a complexidade do manejo de uma paciente com amiloidose cardíaca avançada associada à insuficiência renal e complicações infecciosas. A adaptação da terapia renal substitutiva, especialmente a transição da hemodiálise para a diálise peritoneal, foi fundamental para evitar efeitos adversos graves e garantir a estabilidade clínica. A abordagem multidisciplinar e o monitoramento cuidadoso permitiram um prognóstico melhor do que o inicialmente esperado para pacientes com amiloidose cardíaca avançada e insuficiência renal."
+        }
+    },
+    {
+        "article": "Um homem de 60 anos desmaiou na sauna de um hotel cápsula, um alojamento económico com pequenas unidades de dormida, onde ele residia há dois anos. O paciente relatou uma história de uma semana de falta de apetite, diarreia e febre baixa, acompanhada por uma progressivamente piora da dispneia nos três dias anteriores à admissão. A sua história médica e medicamentos eram desconhecidos devido a uma falta de contactos familiares e a uma grave dispneia que impediu um historial detalhado.\n\nNa admissão, o paciente apresentou taquicardia, taquipneia e hipoxemia. Seus sinais vitais foram os seguintes: pressão arterial 128/85 mmHg, frequência cardíaca 120 batimentos por minuto, frequência respiratória 40 respirações por minuto, saturação de oxigênio 88% em uma máscara de não-rebreather de 15L, e temperatura corporal 37.8°C, consistente com febre de baixo grau. O exame físico revelou respiração rápida e superficial usando músculos respiratórios acessórios. A sua pontuação na Escala de Coma de Glasgow foi E4V5M6.\n\nAs investigações laboratoriais iniciais revelaram acidose metabólica grave com compensação respiratória, como evidenciado por uma análise de gases arteriais que mostrava um pH de 7,067, pressão parcial de dióxido de carbono (pCO₂) de 63,1 mmHg, pressão parcial de oxigénio (pO₂) de 126 mmHg, bicarbonato (HCO₃⁻) de 17,3 mmol/L, e lactato de 11 mmol/L. Os resultados laboratoriais também indicaram disfunção renal grave com uma ureia no sangue (BUN) de 147,2 mg/dL e creatinina de 8,82 mg/dL. A aspartato aminotransferase (AST) estava elevada para 268 U/L e alanina aminotransferase (ALT) para 108 U/L, juntamente com lactato desidrogenase (LDH) a 1910 U/L e creatina quinase (CK) a 1552 U/L. A inflamação foi evidente, com uma contagem de glóbulos brancos (WBC) de 64 × 10⁹/L e uma proteína C-reativa (CRP) de 17,13 mg/dL. O paciente também tinha trombocitopenia, com uma contagem de plaquetas (PLT) de 8,6 × 10⁹/L (ver Tabela 1 para os resultados laboratoriais completos). Os testes para HIV, COVID-19, e antígeno de legionela na urina foram negativos. Uma tomografia computadorizada do tórax revelou consolidações bilaterais com lesões cavitárias, predominantemente no pulmão esquerdo.\n\nAmostras de escarro obtidas por lavagem broncoalveolar revelaram cocci Gram-positivos e bacilos Gram-negativos. O paciente foi diagnosticado com pneumonia grave e abscesso pulmonar causado por uma infecção polimicrobiana. Ele foi entubado após a admissão na UTI. Antibióticos empíricos, incluindo vancomicina, piperacilina-tazobactam e azitromicina, foram iniciados. A hidrocortisona 200 mg/dia também foi administrada. A relação PaO₂/FiO₂ inicial foi de 110 em ventilação mecânica, consistente com SDRA moderado. Devido ao agravamento da hipóxia, o bloqueio neuromuscular foi iniciado e continuado por 48 horas, e a posição prona foi iniciada. Devido ao agravamento da disfunção renal, a terapia de substituição renal foi iniciada. Uma estratégia de hipercapnia permissiva permitiu um pH tão baixo como 7.15.\n\nAo terceiro dia, a sua relação PaO₂/FiO₂ tinha diminuído rapidamente para 65, mostrando uma deterioração adicional. A terapia com óxido nítrico inalado foi iniciada mas não resultou numa melhoria significativa. Consequentemente, a oxigenoterapia por membrana extracorpórea venovenosa (VV-ECMO) foi iniciada na noite do terceiro dia.\n\nAs culturas de expectoração revelaram apenas Moraxella catarrhalis, que foi discordante com a coloração Gram inicial, sugerindo uma infecção polimicrobiana. Os resultados da cultura foram inconsistentes com os achados iniciais da coloração Gram. Tendo em conta esta discrepância e a residência do paciente num hotel cápsula, suspeitou-se de tuberculose como a causa subjacente da sua pneumonia refratária e ARDS. No dia quatro de admissão, o teste de bacilos acidorresistentes foi fortemente positivo (>10 bacilos acidorresistentes por campo de imersão em óleo), e a reação em cadeia da polimerase detetou Mycobacterium tuberculosis, confirmando o diagnóstico de tuberculose pulmonar. Iniciou-se a terapêutica anti-tuberculose com isoniazida, rifampicina, pirazinamida e etambutol. Administrou-se 1 g de metilprednisolona durante três dias para tratar a ARDS associada à tuberculose. Foi realizada uma broncoscopia diária para gerir a depuração do expectorado.\n\nEntre os dias 9 e 11, a condição clínica do paciente melhorou, como evidenciado pela resolução radiográfica de infiltrados pulmonares e um aumento na conformidade do sistema respiratório para 40 ml/cmH₂O, permitindo o desmame bem sucedido da VV-ECMO. Subsequentemente, uma traqueostomia foi realizada cinco dias depois para facilitar o suporte ventilatório prolongado.\n\nDois dias após a traqueostomia, a lesão hepática induzida por drogas necessitou de ajuste da terapia anti-TB para etambutol, estreptomicina e levofloxacina. A cicloserina foi adicionada três dias depois. O paciente permaneceu dependente de ventilação e foi transferido para um hospital designado para TB 29 dias após a admissão. Como vários profissionais de saúde foram expostos à TB antes da confirmação, foi implementado um programa de triagem de exposição. Isso incluiu avaliação médica, radiografia de tórax e teste de liberação de interferon-gama sem identificação de infecções de TB ativas ou latentes entre os funcionários.\n",
+        "gold_summary": "Relatamos um caso de um homem de 60 anos que desenvolveu insuficiência respiratória grave após colapsar numa sauna. Inicialmente diagnosticado com pneumonia comunitária grave e síndrome de angústia respiratória aguda (ARDS), a sua condição deteriorou-se apesar do tratamento padrão, necessitando de oxigenoterapia por membrana extracorpórea venovenosa (VV-ECMO). O teste de bacilos acidorresistentes confirmou tuberculose pulmonar (TB) no dia 4, levando ao início da terapia anti-TB. Após a melhoria clínica, o paciente foi desmontado com sucesso da VV-ECMO e transferido para um hospital especializado em TB para cuidados contínuos.\n",
+        "synthetic_summary": {
+            "B1": "Um homem de 60 anos ficou muito doente depois de desmaiar numa sauna. Ele teve muita dificuldade para respirar. Os médicos pensaram que ele tinha uma infecção no pulmão. Eles deram remédios para ajudar, mas ele piorou. Então, usaram uma máquina para ajudar ele a respirar melhor. Depois, descobriram que ele tinha uma doença chamada tuberculose no pulmão. Começaram um tratamento especial para essa doença. Com o tempo, ele melhorou e não precisou mais da máquina. Depois, ele foi para outro hospital para continuar o tratamento com cuidado.",
+            "B2": "**O que aconteceu com o paciente**\n\nUm homem de 60 anos desmaiou numa sauna e foi levado ao hospital com dificuldade grave para respirar. Ele tinha febre baixa, diarreia e perda de apetite durante uma semana antes disso. Quando chegou, estava muito cansado e com sinais de infecção no corpo.\n\n**O que os médicos encontraram**\n\nOs exames mostraram que ele tinha uma pneumonia muito grave, que é uma infecção nos pulmões, e também uma condição chamada síndrome do desconforto respiratório agudo (SDRA), que dificulta muito a respiração. Mesmo com os tratamentos iniciais, incluindo vários antibióticos e suporte para respirar, o estado dele piorou. Foi necessário usar uma máquina especial chamada oxigenoterapia por membrana extracorpórea (VV-ECMO), que ajuda a oxigenar o sangue quando os pulmões não conseguem.\n\n**O diagnóstico importante**\n\nNo quarto dia, os médicos descobriram que a causa da pneumonia era a tuberculose pulmonar, uma doença causada por uma bactéria chamada Mycobacterium tuberculosis. Essa bactéria pode causar infecções sérias nos pulmões. Eles confirmaram isso com um exame que detecta os bacilos acidorresistentes, que são as bactérias da tuberculose.\n\n**O tratamento e a recuperação**\n\nApós o diagnóstico, o paciente começou um tratamento específico para tuberculose com vários remédios. Ele também recebeu medicamentos para ajudar a controlar a inflamação nos pulmões. Aos poucos, seu estado melhorou, e ele conseguiu sair da máquina VV-ECMO. Depois, foi transferido para um hospital especializado em tuberculose para continuar o tratamento.\n\n**Por que este caso é importante**\n\nEste caso mostra que a tuberculose pode causar problemas muito graves nos pulmões, que às vezes são difíceis de identificar no começo. Também destaca a importância de pensar em tuberculose quando uma pneumonia não melhora com os tratamentos comuns, especialmente em pessoas que vivem em lugares com condições de vida mais simples, como hotéis cápsula.",
+            "B3": "**Contexto**  \nEste relato descreve o caso de um homem de 60 anos que apresentou insuficiência respiratória grave após desmaiar numa sauna de um alojamento económico onde residia. Ele tinha sintomas prévios de uma semana, incluindo falta de apetite, diarreia, febre baixa e piora progressiva da dificuldade para respirar. Na admissão hospitalar, o paciente estava em estado crítico, com sinais de insuficiência respiratória severa, acidose metabólica, disfunção renal grave e evidências de inflamação intensa.\n\n**Principais Achados**  \nExames laboratoriais iniciais mostraram acidose metabólica grave com compensação respiratória, níveis elevados de marcadores de lesão hepática e muscular, além de uma contagem muito alta de glóbulos brancos e plaquetas muito baixas. A tomografia do tórax revelou consolidações pulmonares bilaterais com áreas de cavitação, sugerindo infecção pulmonar grave. Amostras de escarro indicaram infecção polimicrobiana, e o paciente foi tratado inicialmente com antibióticos de amplo espectro e corticosteroides. Apesar disso, a insuficiência respiratória piorou, evoluindo para síndrome do desconforto respiratório agudo (SDRA) moderado a grave, o que levou à necessidade de ventilação mecânica avançada, bloqueio neuromuscular, posição prona e, finalmente, oxigenoterapia por membrana extracorpórea venovenosa (VV-ECMO).\n\nNo quarto dia, a suspeita de tuberculose pulmonar foi confirmada pelo teste de bacilos acidorresistentes e pela reação em cadeia da polimerase para Mycobacterium tuberculosis. A partir daí, iniciou-se a terapia específica para tuberculose com um esquema padrão de quatro medicamentos. Para tratar a inflamação pulmonar associada, foi administrada metilprednisolona. A broncoscopia diária auxiliou na remoção do excesso de secreções pulmonares.\n\n**Interpretação Clínica**  \nEste caso ilustra uma apresentação atípica e grave de tuberculose pulmonar, inicialmente confundida com pneumonia bacteriana polimicrobiana. A rápida deterioração respiratória, apesar do tratamento empírico, evidenciou a necessidade de considerar tuberculose como diagnóstico diferencial, especialmente em pacientes com fatores de risco como residência em alojamentos coletivos. A confirmação tardia da tuberculose permitiu o início da terapia específica, que foi fundamental para a melhora clínica e a retirada da VV-ECMO.\n\n**Próximos Passos e Desfecho**  \nApós a estabilização pulmonar e melhora dos parâmetros respiratórios, o paciente foi desmamado da VV-ECMO e submetido a traqueostomia para suporte ventilatório prolongado. Devido a efeitos colaterais hepáticos relacionados à medicação anti-tuberculose, o esquema terapêutico foi ajustado com a introdução de outros fármacos. O paciente permaneceu dependente de ventilação mecânica e foi transferido para um hospital especializado em tuberculose para continuidade do tratamento. Além disso, foi implementado um programa de triagem para profissionais de saúde expostos, sem identificação de casos ativos ou latentes de tuberculose entre eles.\n\nEste caso destaca a importância de considerar tuberculose em pacientes com pneumonia grave e falência respiratória progressiva, especialmente em contextos de vulnerabilidade social, e demonstra a complexidade do manejo clínico em situações de insuficiência respiratória aguda grave associada à tuberculose."
+        }
+    },
+    {
+        "article": "Um menino de 4 anos de idade, diagnosticado pré-natal com dilatação pelocalicial direita, foi confirmado com múltiplos microquistos hiperecóicos no grupo pelocalicial superior direito após o nascimento. Consultas regulares não mostraram anormalidades físicas, embora ultrassons de acompanhamento tenham indicado um aumento progressivo de três cistos polares superiores.\n\nAo nascer, um ultrassom renal revelou dilatação moderada do sistema calíce superior e múltiplos microcistos hiperecóicos no rim superior direito. O rim esquerdo mostrou dilatação leve das cavidades pelocaliciais (7 mm de diâmetro anteroposterior).\n\nAos 2 meses, a criança desenvolveu uma infecção urinária febril (UTI). O ultra-som mostrou o rim direito medindo 58 mm, com uma lesão cística de 24 mm e uma formação hiperechoica (18 × 8 mm), que era móvel. O rim esquerdo media 54 mm, com dilatação calcífera global moderada (10 mm de diâmetro anteroposterior). Uma cistouretrografia de micção (VCUG) aos 5 meses confirmou o refluxo vesicoureteral bilateral (VUR), grau 2. A cintigrafia renal DMSA mostrou função renal simétrica sem cicatrizes. O tratamento anti-séptico urinário profilático foi iniciado com monitorização clínica e radiológica regular.\n\nAos 7 meses, uma uro-CT identificou cistos corticais simples, sendo o maior de 37 mm, e revelou cavidades ureteropielocaliciais bilaterais finamente delineadas. Aos 11 meses, o rim direito media 75 mm, com três cistos (39 × 29 × 25 mm, 17 × 14 × 11 mm, e 10 × 6 × 5 mm). O rim esquerdo permaneceu normal, e não houve recorrência de UTIs, permitindo a descontinuação de antibióticos profiláticos aos 1,5 anos.\n\nAos 2 anos, o rim direito media 100 mm, com dois cistos polares superiores (60 × 50 × 53 mm e 15 × 12 × 2 mm). O rim esquerdo permaneceu normal. Aos 3,5 anos, um ultrassom de acompanhamento mostrou um cisto polar superior exofítico medindo 70 × 47 mm, com paredes finas e septos incompletos. O rim esquerdo continuou a parecer normal.\n\nUma aspiração percutânea de cisto guiada por TC produziu fluido seroso. A análise citológica confirmou um fluido paucicelular desprovido de características anaplásicas. No entanto, o ultrassom pós-aspiração revelou um cisto no seio polar superior do rim direito (81 × 78 × 64 mm). À luz destes achados, a intervenção cirúrgica foi recomendada.\n\nFoi realizada uma nefrectomia direita superior por abordagem aberta através de uma incisão anterolateral lombar. No exame anatomopatológico, a amostra da hemi-nefrectomia foi ocupada por um cisto com uma parede de consistência esclerótica de cor esbranquiçada. Este cisto foi coberto por um crescente de tecido renal com 0,6 cm de espessura. A secção em série da parede deste cisto revelou um segundo cisto com um lúmen preenchido com uma substância pastosa de cor branco-amarelada. O maior cisto tinha uma superfície interna revestida por um epitélio multicamadas, muitas vezes do tipo transicional e com células escamosas queratinizadas focais. A restante parede do cisto era composta por tecido fibroso rico em células musculares lisas. O menor cisto apresentava características de um cisto dermoide, com um lúmen preenchido com queratina e células escamosas descamadas. A sua parede estava revestida por um epitélio epidérmico e continha folículos pilosos e glândulas sebáceas. Em torno destes cistos, observou-se tecido conjuntivo e adiposo, contendo outro cisto revestido por epitélio escamoso e túbulos circundados por tecido conjuntivo celular semelhante a uma displasia renal. Além disso, o tecido renal identificado macroscopicamente não apresentava lesões.\n\nO acompanhamento pós-operatório ao longo de três anos não revelou infecções urinárias. O monitoramento por ultrassom demonstrou um rim direito reduzido a 50 mm e um rim esquerdo normal, sem lesões císticas ou sólidas e sem dilatação das cavidades excretórias.\n",
+        "gold_summary": "Relatamos o caso de um menino de 4 anos de idade diagnosticado com dilatação pelocalicial direita no útero, confirmada após o nascimento como MCDK. Ultrassons de acompanhamento revelaram um rápido crescimento de três cistos do polo superior, atingindo 8 cm. Foi realizada uma nefrentomia do polo superior direito, e a histopatologia revelou um cisto dermoide renal dentro de uma displasia renal multicística segmentada.\n",
+        "synthetic_summary": {
+            "B1": "Um menino pequeno tinha um problema no rim direito desde que estava na barriga da mamãe. Depois que ele nasceu, os médicos viram que ele tinha bolinhas cheias de água no rim. Essas bolinhas cresceram rápido e ficaram bem grandes.\n\nOs médicos fizeram uma cirurgia para tirar a parte do rim com as bolinhas. Quando olharam essa parte no microscópio, viram que tinha um tipo especial de bolinha chamada cisto dermoide. Isso é uma coisa que não faz mal, mas que precisava ser tirada para o menino ficar bem.\n\nAgora, o menino está bem e os médicos continuam cuidando dele com muito carinho.",
+            "B2": "**O que aconteceu com o menino**\n\nUm menino de 4 anos foi diagnosticado antes de nascer com um problema nos rins chamado dilatação pelocalicial direita. Isso significa que algumas partes do rim direito estavam maiores do que o normal. Depois que ele nasceu, exames mostraram que ele tinha vários pequenos cistos — que são bolsinhas cheias de líquido — no topo do rim direito. Com o tempo, esses cistos cresceram rápido, chegando a cerca de 8 centímetros.\n\n**O que os médicos fizeram**\n\nPor causa do tamanho e do crescimento desses cistos, os médicos decidiram fazer uma cirurgia para remover a parte superior do rim direito. Essa cirurgia é chamada de nefrectomia parcial, que significa tirar só uma parte do rim.\n\n**O que os exames mostraram**\n\nQuando os médicos analisaram o tecido removido, encontraram um tipo especial de cisto chamado cisto dermoide. Esse cisto é diferente porque pode conter células da pele, pelos e glândulas, como se fosse uma pequena \"bolsa\" com partes do corpo que normalmente não ficam no rim. Além disso, o rim tinha uma condição chamada displasia renal multicística segmentada, que é quando algumas partes do rim se formam de maneira anormal, com muitos cistos e tecido diferente do normal.\n\n**O que isso significa**\n\nEsse caso é importante porque mostra que, mesmo em crianças pequenas, cistos nos rins podem crescer rápido e precisar de cirurgia. Também ajuda os médicos a entender melhor essas condições raras, para cuidar melhor dos pacientes no futuro.\n\n**Como está o menino agora**\n\nDepois da cirurgia, o menino foi acompanhado por três anos. Ele não teve mais infecções no rim e o rim esquerdo está funcionando bem, sem problemas. Isso indica que a cirurgia foi um sucesso e que ele está se recuperando bem.",
+            "B3": "**Contexto**  \nEste é o relato de um menino de 4 anos que, ainda durante a gestação, foi diagnosticado com dilatação da parte superior do sistema coletor do rim direito (dilatação pelocalicial). Após o nascimento, exames de ultrassom confirmaram a presença de múltiplos microcistos (pequenas bolsas cheias de líquido) no polo superior do rim direito, caracterizando uma condição chamada displasia renal multicística (MCDK), que é uma malformação renal com múltiplos cistos e tecido renal anormal.\n\n**Principais Achados**  \nDurante o acompanhamento, os ultrassons mostraram que três cistos localizados no polo superior do rim direito cresceram rapidamente, chegando a cerca de 8 centímetros. O rim esquerdo permaneceu normal, sem alterações significativas. O paciente apresentou uma infecção urinária febril aos 2 meses, e exames complementares identificaram refluxo vesicoureteral bilateral grau 2 (um fluxo anormal de urina da bexiga para os rins), que foi tratado profilaticamente com antibióticos até a idade de 1,5 anos.\n\nA partir dos 3,5 anos, devido ao aumento do tamanho dos cistos e à persistência de uma lesão volumosa, foi indicada a remoção cirúrgica do polo superior do rim direito (nefrectomia parcial). A análise microscópica do tecido removido revelou que, além da displasia renal multicística segmentada, havia um cisto dermoide renal — um tipo raro de cisto benigno que contém estruturas semelhantes à pele, como células escamosas, queratina, folículos pilosos e glândulas sebáceas.\n\n**Interpretação Clínica**  \nA presença simultânea de displasia renal multicística segmentada e um cisto dermoide é uma associação incomum. A displasia multicística indica uma formação anormal do rim com múltiplos cistos e tecido renal mal desenvolvido, enquanto o cisto dermoide representa uma lesão benigna derivada de células embrionárias que formam tecidos semelhantes à pele. O crescimento rápido dos cistos e o risco potencial de complicações justificaram a intervenção cirúrgica.\n\n**Próximos Passos e Prognóstico**  \nApós a cirurgia, o paciente foi acompanhado por três anos, sem episódios de infecção urinária ou outras complicações. O rim direito remanescente apresentou redução de tamanho, enquanto o rim esquerdo manteve-se normal, sem sinais de cistos ou dilatação. O acompanhamento clínico e por imagem continua sendo fundamental para monitorar a função renal e prevenir possíveis complicações futuras.\n\nEste caso destaca a importância do monitoramento cuidadoso em crianças com malformações renais detectadas precocemente, permitindo intervenções oportunas e preservação da função renal sempre que possível."
+        }
+    },
+    {
+        "article": "Uma mulher de 65 anos foi internada com um histórico de um mês de mialgia, fraqueza generalizada e dor torácica não específica intermitente.\n\nEla tinha sofrido um AVC dois anos antes, o que limitou a sua mobilidade e para o qual ela residia numa casa de repouso. Ela também tinha sofrido um enfarte agudo do miocárdio sem elevação do segmento ST (NSTEMI), com intervenção coronária percutânea na artéria descendente anterior esquerda cinco meses antes da sua admissão atual. O seu outro histórico incluía doença renal crónica (CKD), dislipidemia, hipertensão resistente, epilepsia, insuficiência cardíaca, diabetes mellitus tipo 2 e asma. Ela não era fumadora e não tinha histórico de consumo excessivo de álcool.\n\nA medicação pré-admissão incluiu múltiplos medicamentos anti-hipertensivos, aspirina, ticagrelor e insulina. Também lhe foi receitado atorvastatin 80 mg ON, que tomou durante quase duas décadas, embora a dose tivesse sido aumentada de 20 mg ON dois anos antes.\n\nAo exame, ela apresentava uma diminuição global da força, mais proeminente no lado direito, que foi o lado afetado pelo seu AVC anterior, e uma sensibilidade muscular generalizada. O resto do exame clínico foi, em geral, sem relevância, com um exame cardiovascular normal e sem outras evidências de um processo reumático subjacente, como uma erupção cutânea ou inchaço das articulações.\n\nA descoberta mais notável de suas investigações laboratoriais iniciais foi um nível de troponina T cardíaca de alta sensibilidade (hs-cTnT) notavelmente elevado de 3794 ng/l (normal < 12 ng/l), sem mudança dinâmica significativa entre testes em série, e que foi observado ter sido elevado a um nível similar vários meses antes, após seu NSTEMI. Uma creatina quinase (CK) foi subsequentemente verificada, que também foi encontrada significativamente elevada a 9416 U/l (normal 25-200 IU/l).\n\nO seu ECG não mostrou alterações agudas, e o seu ecocardiograma transtorácico (TTE) mostrou hipertrofia ventricular esquerda (LVH), mas uma fração de ejeção ventricular esquerda normal sem anormalidades do movimento da parede regional, função ventricular direita normal, e sem patologia valvular significativa.\n\nInicialmente, não ficou claro se o CK representava danos no músculo cardíaco ou esquelético. A importância do hs-cTnT elevado também era incerta. Pensou-se que a síndrome coronária aguda foi excluída, pois os seus sintomas iniciais foram inconsistentes com esta, não houve alterações agudas no ECG ou TTE, e os níveis de hs-cTnT foram relativamente estáticos. O diagnóstico diferencial foi considerado entre a miocardite crónica, com a fraqueza sendo devida a miosite coexistente ou descondicionamento, e a miocardite sem envolvimento cardíaco e com uma falsa elevação de hs-cTnT.\n\nForam solicitados testes adicionais para diferenciar entre estas duas possibilidades. Foi realizado um teste de troponina I cardíaca de alta sensibilidade (hs-cTnI) que apresentou um aumento ligeiro de 55 ng/l. Um hs-cTnT emparelhado, realizado ao mesmo tempo, permaneceu significativamente elevado a 4532 ng/l. Uma ressonância magnética cardíaca não apresentou evidências de infiltração ou inflamação cardíaca. Foi observado um aumento tardio de gadolínio numa área focal, provavelmente devido ao seu anterior NSTEMI.\n\nCom base nas investigações acima, considerou-se que a lesão cardíaca aguda significativa tinha sido excluída. A miosite com falsa elevação de hs-cTnT foi agora considerada o diagnóstico mais provável e foi solicitada uma opinião de reumatologia. Eles aconselharam uma série de testes de anticorpos. Destes, os anticorpos HMG-CoA Reductase foram positivos e os anticorpos PM/SCL75 foram fracamente positivos. Outros testes adicionais recomendados feitos nessa altura, incluindo ANA, ANCA e hepatite B/C, foram negativos, e uma TAC do tórax, abdómen e pélvis não mostrou evidência de malignidade subjacente. A descoberta inicial de um TSH elevado significou que o hipotiroidismo que contribuiu para a miosite teve de ser considerado. No entanto, o fT4 foi encontrado normal, indicando que o paciente tinha hipotiroidismo subclínico e excluindo-o como um factor significativo que contribuiu.\n\nUma ressonância magnética bilateral das coxas também foi recomendada, que revelou uma mudança de sinal difusa e alta em todos os músculos das coxas com edema circundante, em conformidade com uma miosite generalizada.\n\nCom base nas descobertas clínicas, de ressonância magnética e de anticorpos, foi feito um diagnóstico de IMNM induzido por estatina. Para confirmação, foi feita uma biópsia muscular do quadríceps. Os resultados não estavam disponíveis até depois da alta, mas quando examinados, mostraram alterações consistentes com IMNM.\n\nApós o diagnóstico, a atorvastatina foi interrompida e a paciente começou a tomar prednisolona 40 mg OD. No entanto, teve uma resposta modesta, com uma redução dos níveis de CK, mas pouca mudança nos seus sintomas. Por isso, após duas semanas de tratamento com esteróides, começou a tomar uma dose crescente de micofenolato, começando com 250 mg BD e imunoglobulina intravenosa 2 g/kg durante cinco dias, juntamente com um curso de três dias de metilprednisolona IV 500 mg OD, seguido por uma dose aumentada de prednisolona oral a 60 mg OD. Isto resultou numa melhoria progressiva dos sintomas e numa redução contínua dos níveis de CK. A sua cTnT também diminuiu, mas permaneceu significativamente elevada acima da sua linha de base anterior, mesmo após vários meses de tratamento. Foi dada alta em casa com micofenolato (1 g BD no momento da alta) e uma dose de desmame de prednisolona (30 mg OD no momento da alta). Estava prevista para acompanhamento pela equipa de reumatologia, mas, infelizmente, não compareceu repetidamente às suas consultas clínicas agendadas.\n",
+        "gold_summary": "Apresentaremos um caso de uma mulher de 65 anos de idade, em tratamento prolongado com atorvastatina, que apresentou fraqueza generalizada, dor torácica não específica e troponina T cardíaca de alta sensibilidade persistentemente elevada. Após investigação adicional, excluiu-se a possibilidade de lesão miocárdica aguda e fez-se o diagnóstico de miopatia necrotizante imunomediada induzida por estatina (IMNM). A paciente apresentou melhora com a suspensão da atorvastatina e o início de terapia imunossupressora com micofenolato, imunoglobulina intravenosa e esteróides.\n",
+        "synthetic_summary": {
+            "B1": "Uma senhora de 65 anos estava muito fraca e sentia dor no peito. Ela tomava um remédio chamado atorvastatina há muito tempo. Os médicos fizeram exames e viram que o coração dela estava bem. Eles descobriram que o remédio estava deixando os músculos dela doentes. Pararam o remédio e deram outros remédios para ajudar os músculos. Com isso, ela começou a melhorar devagarinho.",
+            "B2": "**O que aconteceu com a paciente**\n\nUma mulher de 65 anos, que tomava um remédio chamado atorvastatina há muito tempo para controlar o colesterol, começou a sentir fraqueza no corpo todo e dores no peito que não eram muito claras. Quando os médicos fizeram exames, viram que um marcador no sangue chamado troponina T, que normalmente indica problemas no coração, estava muito alto, mas sem sinais de um ataque cardíaco recente.\n\n**O que os médicos descobriram**\n\nDepois de vários exames, eles perceberam que o coração dela não estava com uma lesão aguda, ou seja, não havia um problema cardíaco novo acontecendo. Em vez disso, a fraqueza e os exames indicaram que ela tinha uma inflamação nos músculos, chamada miopatia necrotizante imunomediada (IMNM). Essa doença faz com que o sistema de defesa do corpo ataque os músculos, e nesse caso, foi causada pelo uso da estatina (atorvastatina).\n\n**Como foi o tratamento**\n\nOs médicos pararam o remédio atorvastatina e começaram a tratar a paciente com remédios que diminuem a reação do sistema imunológico, como prednisolona (um tipo de esteróide), micofenolato e imunoglobulina intravenosa. Com esse tratamento, a paciente melhorou, a fraqueza diminuiu e os exames de sangue mostraram redução da inflamação muscular.\n\n**Por que isso é importante**\n\nEsse caso mostra que, embora as estatinas sejam muito usadas para proteger o coração, elas podem, em casos raros, causar problemas sérios nos músculos. Por isso, é importante que os médicos fiquem atentos a sintomas como fraqueza e dor muscular em pacientes que usam esses remédios, para poderem agir rápido e evitar complicações.",
+            "B3": "**Contexto**  \nEste relato descreve o caso de uma mulher de 65 anos que, após uso prolongado da medicação atorvastatina (uma estatina usada para controlar o colesterol), desenvolveu sintomas de fraqueza muscular generalizada, dor torácica inespecífica e níveis persistentemente elevados de troponina T cardíaca de alta sensibilidade — um marcador geralmente associado a lesão do músculo cardíaco.\n\n**Principais Achados**  \nAo ser internada, a paciente apresentava fraqueza muscular difusa, especialmente no lado direito, que já havia sido afetado por um acidente vascular cerebral (AVC) prévio. Exames laboratoriais revelaram níveis extremamente elevados de creatina quinase (CK), uma enzima que indica dano muscular, e troponina T cardíaca muito acima do normal, porém sem sinais de infarto agudo do miocárdio ou inflamação cardíaca ativa, confirmados por eletrocardiograma, ecocardiograma e ressonância magnética do coração. Testes adicionais identificaram anticorpos específicos contra a HMG-CoA redutase, uma enzima-alvo das estatinas, sugerindo uma reação imunológica contra os músculos.\n\nA ressonância magnética das coxas mostrou inflamação muscular difusa compatível com miosite (inflamação dos músculos). A biópsia muscular confirmou o diagnóstico de miopatia necrotizante imunomediada induzida por estatina (IMNM), uma condição rara em que o sistema imunológico ataca os músculos devido ao uso prolongado de estatinas.\n\n**Interpretação Clínica**  \nEmbora a troponina T elevada inicialmente sugerisse dano cardíaco, a ausência de alterações cardíacas agudas e a presença de níveis elevados de creatina quinase indicaram que o problema principal estava nos músculos esqueléticos, não no coração. A identificação de anticorpos contra a HMG-CoA redutase reforçou a hipótese de que a estatina havia desencadeado uma resposta autoimune muscular. O diagnóstico de IMNM é importante porque exige tratamento específico com imunossupressores, além da suspensão da estatina.\n\n**Próximos Passos e Tratamento**  \nA atorvastatina foi interrompida imediatamente, e a paciente iniciou tratamento com prednisolona (um corticosteroide). Como a resposta inicial foi limitada, foram adicionados micofenolato (um imunossupressor) e imunoglobulina intravenosa, além de um reforço com metilprednisolona intravenosa. Esse regime combinado levou a uma melhora progressiva dos sintomas e redução dos níveis de creatina quinase, indicando controle da inflamação muscular. Apesar da melhora, a troponina T permaneceu elevada, sugerindo que alguns marcadores podem continuar alterados mesmo com o tratamento eficaz.\n\nA paciente recebeu alta com acompanhamento reumatológico planejado para monitorar a evolução e ajustar a terapia imunossupressora. Infelizmente, houve dificuldades no seguimento clínico devido a faltas nas consultas agendadas.\n\n---\n\nEste caso ilustra a importância de considerar causas musculares para elevações persistentes de troponina em pacientes em uso de estatinas, especialmente quando exames cardíacos não indicam lesão aguda. O reconhecimento precoce da IMNM e o início do tratamento imunossupressor são fundamentais para melhorar o prognóstico e a qualidade de vida do paciente."
+        }
+    },
+    {
+        "article": "O paciente, um homem de 61 anos, foi diagnosticado com pancreatite aguda 9 meses antes da admissão e recebeu tratamento conservador. Após a alta, ele experimentou distensão abdominal superior e dor de forma intermitente, e uma tomografia computadorizada abdominal (TC) mostrou a formação de uma pseudocisto pancreático. Quatro dias antes da admissão, o paciente desenvolveu dispneia grave com dor torácica e tosse, grave o suficiente para impedir que ele ficasse deitado. O exame físico indicou falta de ar, sons respiratórios diminuídos bilaterais, taquicardia, e sem anormalidades abdominais. O paciente tinha um longo histórico de uso de álcool e tabaco e múltiplas cirurgias anteriores, incluindo cirurgia de fixação lombar e remoção de lipoma da parede abdominal.\n\nOs testes laboratoriais mostraram um ligeiro aumento do antígeno do cancro do marcador do tumor do soro 125 a 98.25 U/mL (intervalo normal 0-35 U/mL) e amilase na urina a 333 U/L (intervalo normal 32-641 U/L). A imagem (CT) revelou um derrame pleural bilateral maciço e a formação de um pseudocisto pancreático.\n\nDiagnóstico e intervenções\nAo ser admitido, foi realizada uma punção torácica, a cultura bacteriológica do fluido pleural foi negativa, não foram encontradas células tumorais, mas o nível do antígeno do cancro 125 no fluido pleural foi significativamente elevado a 1859 U/mL (intervalo normal 0–35 U/mL). Os níveis de amilase no fluido pleural foram 53,844 U/L no lado esquerdo e 1365 U/L no lado direito. No sexto dia, foi confirmado um diagnóstico de PPF, e foi realizada uma ERCP com a colocação de um ducto nasopancreático 7Fr para drenar o pseudocisto pancreático.\n\nImediatamente após a admissão, foi realizada uma punção torácica, drenando uma grande quantidade de fluido pleural tingido de sangue pálido, juntamente com suporte de nutrição parenteral e tratamento com somatostatina, que gradualmente ajudou o paciente nos exercícios de função pulmonar. No sétimo dia, um exame ERCP revelou comunicação entre o pseudocisto pancreático e a cavidade pleural. Durante a canulação do ducto pancreático, o fio guia poderia entrar no pseudocisto, então um ducto nasopancreático de 7Fr foi colocado para drenagem. A cultura do fluido pancreático do ducto nasopancreático cresceu Enterococcus faecium e Klebsiella pneumoniae, mas o paciente não desenvolveu febre, e a contagem de leucócitos e a proteína C-reativa foram normais, mas os antibióticos foram administrados. No nono dia, nenhum fluido foi drenado dos drenos torácicos bilaterais, e outra ERCP foi realizada. O ducto nasopancreático foi cortado na papila duodenal, deixando a parte interna como um stent do ducto pancreático.\n\nResultados\nO paciente recebeu um total de 13 dias de tratamento hospitalar, durante o qual 4180 mL de fluido pleural foi drenado do lado esquerdo, 2470 mL do lado direito e 495 mL do ducto nasopancreático. Seis meses após a alta, o ducto nasopancreático remanescente foi removido. Não houve recorrência durante um acompanhamento de 5 anos, e a condição geral do paciente foi boa\n",
+        "gold_summary": "Preocupações do paciente: Um homem de 61 anos de idade com histórico de uso de álcool e tabaco apresentou dispneia grave, dor torácica e tosse. Ele foi diagnosticado com pancreatite aguda 9 meses antes e experimentou intermitentemente dor abdominal superior e distensão após o tratamento.\n\nDiagnósticos: PPF.\n\nIntervenções: O paciente foi submetido a drenagem torácica, drenagem do ducto nasopancreático e colocação de stent no ducto pancreático, juntamente com nutrição parenteral e terapia com somatostatina.\n\nResultados: O tratamento resultou na resolução do derrame pleural e da pseudocisto. O paciente não teve recorrência durante um período de acompanhamento de 5 anos.\n",
+        "synthetic_summary": {
+            "B1": "Um homem de 61 anos ficou com muita dificuldade para respirar. Ele também sentia dor no peito e tosse. Antes, ele teve um problema no seu estômago chamado pancreatite.\n\nOs médicos acharam que ele tinha um problema com um líquido no peito. Eles tiraram esse líquido com uma agulha. Também colocaram um canudinho no lugar do problema para o líquido sair.\n\nEle recebeu remédios e comida pela veia para ajudar a melhorar. Depois do tratamento, ele ficou bem e não teve mais o problema por muito tempo.",
+            "B2": "**O que aconteceu com o paciente**  \nUm homem de 61 anos, que já tinha problemas no pâncreas causados pelo álcool e pelo tabaco, começou a sentir falta de ar forte, dor no peito e tosse. Ele tinha sido tratado antes por uma inflamação no pâncreas chamada pancreatite aguda, e depois disso sentia dor e inchaço na barriga de vez em quando.\n\n**O que os médicos descobriram**  \nOs exames mostraram que ele tinha um pseudocisto pancreático, que é como uma bolsa cheia de líquido perto do pâncreas. Além disso, havia muito líquido acumulado nos pulmões, chamado derrame pleural. Esse líquido tinha níveis muito altos de uma substância chamada amilase, que vem do pâncreas, indicando que o líquido do pseudocisto estava vazando para os pulmões. Essa condição é chamada de fístula pancreática pleural (PPF), que é quando o líquido do pâncreas passa para a área dos pulmões.\n\n**Como foi o tratamento**  \nOs médicos drenaram o líquido dos pulmões para ajudar a respirar melhor. Também colocaram um tubo especial chamado stent no ducto pancreático, que é o canal por onde o suco do pâncreas passa, para ajudar a drenar o pseudocisto e evitar que o líquido vazasse. O paciente recebeu alimentação pela veia (nutrição parenteral) e um remédio chamado somatostatina, que ajuda a diminuir a produção de suco pancreático.\n\n**O que aconteceu depois**  \nCom esse tratamento, o líquido nos pulmões desapareceu e o pseudocisto foi resolvido. O paciente ficou internado por 13 dias e, depois de seis meses, o stent foi retirado. Durante cinco anos de acompanhamento, ele não teve mais problemas, e sua saúde ficou boa.\n\n**Por que isso é importante**  \nEsse caso mostra como uma complicação rara da pancreatite pode causar problemas nos pulmões e como o tratamento correto, com drenagem e stent, pode ajudar o paciente a se recuperar completamente.",
+            "B3": "**Contexto**  \nUm homem de 61 anos, com histórico significativo de consumo de álcool e tabaco, foi inicialmente diagnosticado com pancreatite aguda há nove meses e tratado de forma conservadora. Após a alta hospitalar, ele apresentou episódios intermitentes de dor e distensão na parte superior do abdômen. Quatro dias antes da nova internação, desenvolveu falta de ar intensa, dor no peito e tosse, sintomas que o impediam até mesmo de deitar-se confortavelmente.\n\n**Principais Achados Clínicos e Diagnósticos**  \nNa avaliação inicial, o exame físico revelou dificuldade respiratória, sons pulmonares reduzidos em ambos os lados, e taquicardia, sem alterações significativas no abdômen. Exames laboratoriais mostraram elevação moderada do marcador tumoral CA 125 no sangue e níveis elevados de amilase na urina, indicando atividade pancreática. A tomografia computadorizada evidenciou um grande acúmulo de líquido nos pulmões (derrame pleural bilateral) e a presença de um pseudocisto pancreático, que é uma coleção de líquido encapsulada que se forma após inflamações no pâncreas.\n\nA análise do líquido retirado dos pulmões revelou níveis extremamente elevados de amilase e CA 125, sugerindo comunicação entre o pseudocisto pancreático e a cavidade pleural, caracterizando uma fístula pancreática pleural (PPF). A cultura do líquido pancreático identificou bactérias, mas o paciente não apresentou sinais de infecção sistêmica.\n\n**Intervenções Realizadas**  \nImediatamente após a admissão, foi realizada a drenagem do líquido acumulado nos pulmões para aliviar a falta de ar, além de suporte nutricional por via intravenosa (nutrição parenteral) e administração de somatostatina, uma medicação que reduz a produção de enzimas pancreáticas. No sexto dia, uma colangiopancreatografia retrógrada endoscópica (ERCP) confirmou a comunicação entre o pseudocisto e a cavidade pleural. Durante esse procedimento, foi inserido um cateter (stent) no ducto pancreático para permitir a drenagem contínua do pseudocisto e promover a cicatrização da fístula.\n\n**Resultados e Prognóstico**  \nDurante o período hospitalar de 13 dias, foram drenados mais de 7 litros de líquido pleural e quase meio litro pelo stent pancreático. Após a alta, o stent foi removido seis meses depois, sem que houvesse recorrência dos sintomas ou do derrame pleural. O paciente manteve-se em boas condições clínicas durante um acompanhamento de cinco anos, demonstrando que o tratamento combinado de drenagem, suporte nutricional e terapia medicamentosa foi eficaz para a resolução da fístula pancreática pleural e do pseudocisto associado.\n\n**Considerações Finais**  \nEste caso ilustra a importância do diagnóstico precoce da fístula pancreática pleural, uma complicação rara da pancreatite, e destaca o papel fundamental da drenagem endoscópica e do manejo multidisciplinar para o sucesso terapêutico e a recuperação prolongada do paciente."
+        }
+    },
+    {
+        "article": "Apresentamos o caso de um homem de 82 anos com diagnóstico de adenocarcinoma de cólon ascendente, confirmado por biopsia endoscópica. Nos estudos de estadiamento pré-operatório não se observavam sinais de doença a distância e tinha um CEA de 2,8 ng/mL. Foi-lhe realizada uma hemicolectomia direita laparoscópica, evoluindo favoravelmente no pós-operatório. A anatomia patológica informou um adenocarcinoma moderadamente diferenciado, estágio 1, T1 N0, pelo que não requereu tratamento adjuvante.\n\nNo acompanhamento oncológico, foi identificado por tomografia, uma imagem de aspecto nodular na cadeia ilíaca primitiva esquerda que media 22 mm em seu eixo menor. Devido a este achado, foi realizado um PET-TC com 18F-FDG no qual foi evidenciada uma lesão ovoide, única, a nível retroperitoneal, adjacente à bifurcação aórtica de aproximadamente 34 mm de diâmetro maior com escasso realce pós administração de contraste iodado.\n\nEsta imagem provou ser hipermetabólica (SUV: 6.7). Não foram encontradas outras imagens relacionadas com a patologia em estudo. Tendo em conta os antecedentes do paciente, foi programada uma biopsia percutânea guiada por imagem com anestesia local. O procedimento foi bem tolerado e não se associou a complicações. Este estudo provou que o achado se tratava de um schwannoma. Após um ano de acompanhamento, constatou-se aumento de tamanho da lesão biopsiada (44 mm de diâmetro maior), no entanto, sem manifestações clínicas. Por sua vez, não houve evidência de progressão de doença oncológica.\n",
+        "gold_summary": "Apresentamos o caso de um paciente do sexo masculino de 82 anos com diagnóstico recente de adenocarcinoma de cólon moderadamente diferenciado e com um nódulo periaórtico hipermetabólico como achado incidental.\n\nResultados: A biopsia percutânea do nódulo periaórtico confirmou o diagnóstico de schwannoma. Após um ano de acompanhamento, o crescimento do schwannoma foi demonstrado. Não há sinais de progressão da doença oncológica.\n",
+        "synthetic_summary": {
+            "B1": "Um senhor de 82 anos estava com um caroço no intestino. Ele fez uma cirurgia para tirar esse caroço. Depois, os médicos acharam outro caroço perto do coração.\n\nEles fizeram um exame para ver o que era esse caroço. Descobriram que era um caroço que não faz mal, chamado schwannoma. Depois de um ano, esse caroço cresceu um pouco, mas o senhor está bem e o câncer não voltou.",
+            "B2": "Caso de um homem de 82 anos com câncer no cólon\n\nUm homem de 82 anos foi diagnosticado com um tipo de câncer chamado adenocarcinoma no cólon, que é a parte do intestino grosso. Esse câncer estava em um estágio inicial e não tinha se espalhado para outras partes do corpo. Ele passou por uma cirurgia para retirar a parte do cólon com o tumor e se recuperou bem.\n\nO que encontraram depois da cirurgia\n\nDurante os exames de acompanhamento, os médicos viram uma imagem diferente perto da aorta, que é uma grande artéria do corpo. Essa imagem parecia um nódulo, que é como um caroço, e estava \"hipermetabólica\", o que significa que usava muita energia, algo que pode indicar um problema.\n\nO que fizeram para entender melhor\n\nPara saber o que era esse nódulo, os médicos fizeram uma biópsia, que é quando retiram um pedacinho do tecido para analisar. A biópsia mostrou que o nódulo era um schwannoma, que é um tumor benigno (não canceroso) que cresce nos nervos.\n\nO que aconteceu depois\n\nDepois de um ano, o schwannoma cresceu um pouco, mas o paciente não teve sintomas ou problemas por causa disso. Além disso, não houve sinais de que o câncer no cólon tivesse voltado ou se espalhado.\n\nResumo final\n\nEsse caso mostra a importância de investigar qualquer alteração encontrada em exames, mesmo que o paciente já tenha um câncer. Nem tudo que aparece é câncer, como nesse caso, em que o nódulo era um tumor benigno chamado schwannoma. O acompanhamento cuidadoso ajudou a garantir que o paciente estivesse bem.",
+            "B3": "**Contexto**  \nEste relato descreve o caso de um homem de 82 anos diagnosticado com adenocarcinoma moderadamente diferenciado do cólon ascendente, confirmado por biópsia endoscópica. Inicialmente, não foram identificadas metástases (disseminação da doença para outras partes do corpo) e o marcador tumoral CEA estava dentro do normal (2,8 ng/mL). O paciente foi submetido a uma hemicolectomia direita por via laparoscópica, com boa recuperação pós-operatória. A análise do tecido removido indicou um tumor em estágio inicial (T1 N0, estágio 1), o que dispensou a necessidade de tratamento complementar.\n\n**Principais Achados**  \nDurante o acompanhamento oncológico, uma tomografia computadorizada revelou um nódulo com aspecto nodular na região da cadeia ilíaca primitiva esquerda, medindo 22 mm no seu menor eixo. Para melhor avaliação, foi realizada uma tomografia por emissão de pósitrons (PET-TC) com 18F-FDG, que mostrou uma lesão única, ovalada, localizada retroperitonealmente (atrás do peritônio, a membrana que reveste a cavidade abdominal), próxima à bifurcação da aorta, medindo cerca de 34 mm no seu maior diâmetro. Essa lesão apresentou captação aumentada do marcador radioativo (hipermetabólica) com valor de SUV (Standardized Uptake Value, um índice de atividade metabólica) de 6,7, sugerindo atividade celular elevada.\n\nDiante desses achados, foi realizada uma biópsia percutânea guiada por imagem, com anestesia local, para determinar a natureza do nódulo. O procedimento foi bem tolerado e sem complicações. O exame histopatológico confirmou que a lesão era um schwannoma, um tumor benigno originado das células da bainha nervosa.\n\n**Interpretação Clínica**  \nApós um ano de acompanhamento, observou-se que o schwannoma havia aumentado de tamanho, passando a medir 44 mm no maior diâmetro. Apesar desse crescimento, o paciente permaneceu assintomático, sem apresentar sintomas relacionados à lesão. Além disso, não houve evidência de progressão ou recidiva do adenocarcinoma de cólon.\n\n**Próximos Passos**  \nO caso destaca a importância do acompanhamento cuidadoso de lesões incidentais em pacientes oncológicos, especialmente quando apresentam características hipermetabólicas em exames de imagem. O crescimento do schwannoma, embora benigno, deve ser monitorado para avaliar a necessidade de intervenção futura, considerando o estado clínico do paciente e a ausência de sintomas. Paralelamente, o controle rigoroso da doença oncológica permanece essencial para garantir a detecção precoce de possíveis recidivas ou metástases."
+        }
+    },
+    {
+        "article": "Um homem de 71 anos de idade, hospitalizado em outro hospital por insuficiência cardíaca com histórico de várias internações por insuficiência cardíaca, foi transferido para o nosso hospital para avaliação e tratamento adicionais de insuficiência cardíaca refratária. Embora ele fosse suspeito de ter amiloidose cardíaca no hospital anterior, não foi feito um diagnóstico.\n\nNa admissão no nosso hospital, recebeu medicamentos orais incluindo muitos tipos de diuréticos, mas ainda tinha dispneia com uma classe funcional IV da NYHA. A sua pressão arterial era de 106/70 mmHg, e o terceiro som cardíaco era audível no ápice. Observou-se congestão das veias jugulares, mas não se encontrou edema periférico. A radiografia do tórax mostrou uma relação cardiotorácica elevada de 61% com derrame pleural bilateral. Os achados eletrocardiográficos foram uma frequência cardíaca de 65/min com fibrilhação atrial, atraso da condução intraventricular e desvio do eixo esquerdo. A ecocardiografia transtorácica revelou uma hipertrofia difusa do ventrículo esquerdo (VE) com aumento da espessura da parede de 12 mm, movimento da parede do VE hipocinético leve (fração de ejeção = 43%), aumento da espessura da parede do ventrículo direito de 7 mm com uma função sistólica do VD reduzida, e dilatação biatrial. A ecocardiografia de rastreamento de manchas mostrou um padrão de “poupança apical” de deformação longitudinal. Ele tinha resultados anormais de testes laboratoriais que mostravam um nível elevado de peptídeo natriurético cerebral (BNP) (1.186 pg/mL) e um nível elevado de troponina T cardíaca de alta sensibilidade (0.057 ng/mL). A cintilografia com pirofosfato de 99mTechnetium (99mTc-PYP) revelou uma captação cardíaca de grau 3 na imagem de fusão SPECT/CT. A proteína de Bence-Jones não foi detectável, e a relação de cadeia leve livre κ/λ foi normal. Mais tarde, realizámos uma biópsia endomiocardica e análise genética, e finalmente fizemos um diagnóstico de ATTRwt.\n\nNo que diz respeito à gestão da insuficiência cardíaca, tentámos controlar a sua insuficiência cardíaca com oxigenoterapia e gestão médica incluindo injeção intravenosa de furosemida, mas ele ainda tinha dispneia com fadiga geral persistente, e o seu nível de bilirrubina aumentou. O cateterismo cardíaco direito (RHC) mostrou uma alta pressão de cunha da artéria pulmonar e hipertensão pulmonar e um baixo índice cardíaco de 1.37 L/min/m2 (termodiluição) com uma pressão média atrial direita de 8 mmHg.\n\nCom base nestes resultados, iniciámos a infusão de dobutamina a 2 μg/kg/min para o seu baixo débito cardíaco. Os seus sintomas melhoraram significativamente com a melhoria dos níveis de creatinina e bilirrubina. Seis dias depois, administramos pimobendan para reduzir a infusão de dobutamina. Durante o curso do tratamento, ele estava basicamente estável, exceto por uma deterioração temporária da insuficiência cardíaca devido à gripe. Após um mês de terapia médica e reabilitação cardíaca enquanto estava internado, a infusão de dobutamina foi terminada, e o RHC mostrou uma melhoria dramática no seu estado hemodinâmico. Desde a alta hospitalar, a sua condição permaneceu estável sem deterioração da insuficiência cardíaca ou arritmias durante seis meses.",
+        "gold_summary": "Tratámos um homem de 71 anos com insuficiência cardíaca refratária devido a ATTRwt. Esperava-se que ele dependesse de infusão de dobutamina. Administrámos pimobendan e melhorámos com sucesso os seus sintomas e estado hemodinâmico para permitir a sua alta do hospital. Uma investigação retrospectiva adicional observou que havia oito pacientes com amiloidose ATTR que foram administrados pimobendan. Embora todos os pacientes no momento da administração de pimobendan fossem classe III ou IV da NYHA com hospitalização repetida por insuficiência cardíaca, o pimobendan pareceu ser eficaz para melhorar os sintomas e permitir que os pacientes fossem dispensados e recebessem cuidados médicos ambulatórios. Além disso, focando-se nas alterações em alguns biomarcadores, descobrimos que o peptídeo natriurético cerebral e os valores estimados da taxa de filtração glomerular melhoraram após a administração de pimobendan em 5 pacientes consecutivos para os quais os dados estavam disponíveis sem tratamento adicional (p = 0,018 e 0,051, respetivamente).\n",
+        "synthetic_summary": {
+            "B1": "Um homem de 71 anos estava com o coração muito cansado. Ele tinha um problema chamado ATTRwt, que faz o coração ficar duro. Ele precisava de um remédio que ajudava o coração a bater melhor, chamado dobutamina.\n\nDepois, os médicos deram outro remédio chamado pimobendan. Esse remédio ajudou ele a se sentir melhor. Ele conseguiu sair do hospital e ficar em casa.\n\nOs médicos também viram que outras pessoas com o mesmo problema melhoraram com esse remédio. Elas ficaram menos cansadas e puderam cuidar da saúde sem ficar no hospital. Os remédios ajudaram o coração e os rins a ficarem mais fortes. Tudo isso deixou os médicos felizes.",
+            "B2": "**O que aconteceu com o paciente**\n\nUm homem de 71 anos tinha um problema sério no coração chamado insuficiência cardíaca, que não melhorava com os tratamentos comuns. Ele foi diagnosticado com uma doença chamada ATTRwt, que é um tipo de amiloidose. Amiloidose é quando uma proteína anormal se acumula no coração, dificultando seu funcionamento.\n\n**Como trataram o paciente**\n\nPara ajudar seu coração a funcionar melhor, os médicos usaram um remédio chamado dobutamina, que é dado pela veia para ajudar o coração a bombear sangue. Depois, eles começaram a usar outro remédio chamado pimobendan, que ajuda o coração a bater com mais força e relaxar melhor. Com esse tratamento, os sintomas dele melhoraram bastante, e ele pôde deixar o hospital.\n\n**O que os médicos descobriram com outros pacientes**\n\nOs médicos também olharam para outros oito pacientes com a mesma doença (amiloidose ATTR) que receberam pimobendan. Todos esses pacientes estavam muito doentes, com sintomas graves e precisavam ir ao hospital várias vezes. O pimobendan ajudou a melhorar os sintomas deles, permitindo que ficassem em casa e continuassem o tratamento sem precisar ficar internados.\n\n**Mudanças nos exames importantes**\n\nAlém disso, os médicos notaram que, após o uso do pimobendan, alguns exames mostraram melhora. Um deles é o peptídeo natriurético cerebral (BNP), que indica como o coração está sobrecarregado. Outro exame mede como os rins estão funcionando. Esses resultados sugerem que o remédio ajudou não só o coração, mas também os rins, sem precisar de outros tratamentos extras.\n\n**Resumo final**\n\nEm resumo, o pimobendan pode ser um remédio útil para ajudar pacientes com insuficiência cardíaca causada pela amiloidose ATTR, melhorando seus sintomas e qualidade de vida, e ajudando a evitar internações no hospital.",
+            "B3": "**Contexto**  \nApresentamos o caso de um homem de 71 anos com insuficiência cardíaca grave e refratária, causada por amiloidose cardíaca do tipo ATTRwt (amiloidose por transtirretina de forma selvagem, uma doença em que proteínas anormais se acumulam no coração, comprometendo sua função). Ele havia sido hospitalizado várias vezes anteriormente e foi transferido para nosso hospital para avaliação e tratamento mais avançados. Apesar da suspeita prévia de amiloidose, o diagnóstico só foi confirmado após exames detalhados, incluindo biópsia cardíaca e testes genéticos.\n\n**Principais Achados Clínicos e Diagnósticos**  \nNa admissão, o paciente apresentava dispneia severa (dificuldade para respirar), sinais de congestão venosa e alterações cardíacas evidenciadas por exames de imagem e laboratoriais. A ecocardiografia mostrou aumento da espessura das paredes do coração e função ventricular reduzida, além de dilatação das câmaras cardíacas. A cintilografia com 99mTc-PYP revelou captação intensa compatível com amiloidose ATTRwt. Testes laboratoriais indicaram níveis elevados de peptídeo natriurético cerebral (BNP), marcador de estresse cardíaco, e troponina T, indicador de lesão cardíaca. O cateterismo cardíaco confirmou baixa capacidade de bombeamento do coração e hipertensão pulmonar.\n\n**Intervenção e Evolução Clínica**  \nInicialmente, o paciente recebeu oxigenoterapia e diuréticos intravenosos, mas continuou com sintomas graves e piora de marcadores laboratoriais. Foi então iniciada infusão contínua de dobutamina, um medicamento que melhora a força de contração do coração, o que levou a uma melhora significativa dos sintomas e dos parâmetros laboratoriais. Para reduzir a dependência da dobutamina, introduzimos o pimobendan, um fármaco que combina ação inotrópica (aumenta a força de contração cardíaca) e vasodilatadora (dilata os vasos sanguíneos), facilitando o trabalho do coração. Com essa combinação, o paciente estabilizou-se, conseguiu realizar reabilitação cardíaca e teve alta hospitalar após um mês, mantendo-se estável por pelo menos seis meses.\n\n**Análise Retrospectiva e Resultados em Outros Pacientes**  \nAlém deste caso, revisamos retrospectivamente oito pacientes com amiloidose ATTR tratados com pimobendan. Todos estavam em estágios avançados da insuficiência cardíaca (classe III ou IV da NYHA) e haviam sido hospitalizados repetidamente. O uso do pimobendan foi associado a melhora dos sintomas, permitindo que esses pacientes fossem liberados para cuidados ambulatoriais. Em cinco pacientes com dados disponíveis, observamos melhora significativa nos níveis de peptídeo natriurético cerebral e na função renal estimada (medida pela taxa de filtração glomerular) após o início do pimobendan, sem necessidade de outros tratamentos adicionais.\n\n**Conclusão e Implicações Clínicas**  \nEste relato sugere que o pimobendan pode ser uma opção terapêutica eficaz para pacientes com insuficiência cardíaca avançada causada por amiloidose ATTRwt, especialmente para aqueles que dependem de suporte inotrópico contínuo como a dobutamina. O medicamento não apenas melhora os sintomas e a função cardíaca, mas também pode contribuir para a estabilização clínica e a possibilidade de alta hospitalar, melhorando a qualidade de vida desses pacientes. Estudos adicionais são necessários para confirmar esses achados e definir protocolos de tratamento mais precisos."
+        }
+    },
+    {
+        "article": "Uma mulher afro-americana de 48 anos de idade, com histórico médico significativo apenas para hipertensão essencial descontrolada, apresentou-se ao departamento de emergência com uma queixa principal de palpitações. Ela também relatou fadiga associada e falta de ar. No mês passado, ela descreveu uma sensação intermitente de um batimento cardíaco irregular sem quaisquer gatilhos específicos. Seus sintomas progrediram para desconforto torácico do lado esquerdo com formigamento associado no membro superior esquerdo. Além disso, ela relatou pontos negros em sua visão, bem como disfagia principalmente para sólidos, que também havia piorado nas últimas semanas. Ela não tinha histórico de sintomas semelhantes no passado. Ela não estava tomando nenhum medicamento.\n\nNa admissão, os sinais vitais foram significativos para uma pressão arterial de 166/92 mmHg e uma frequência cardíaca de 109 batimentos/minuto. Um exame físico foi significativo para uma palidez conjuntival, sem evidência de glossite ou koilonychia. No Departamento de Emergência, um painel metabólico completo foi normal, incluindo uma creatinina sérica de 0,56 mg/dL [0,60-1,20 mg/dL]. Um eletrocardiograma mostrou taquicardia sinusal com complexos ventriculares prematuros ocasionais. As troponinas estavam dentro dos limites normais. A hemoglobina na admissão foi de 5,7 g/dL [11,9-15,1 g/dL] com um volume corpuscular médio de 65,3 fL [80,0-96,0 fL]. O ferro sérico na admissão foi de 12 ug/dL [50-212 ug/dL], a saturação de ferro foi de 3% [20-50%], e a ferritina foi de 3,1 ng/mL [11,0-306,8 ng/mL]. O resultado do teste imunocemico fecal (FIT) foi negativo. Após questionamento adicional, a paciente afirmou que ainda menstruava, mas não descreveu menorragia. Ela negou hematemese, hematochezia, ou melena. Ela foi transfundida com 2 unidades de glóbulos vermelhos concentrados no Departamento de Emergência e começou com 1400 mg de infusões complexas de ferro intravenoso.\n\nA paciente não conseguiu se sentar para um esofagograma para avaliar a disfagia secundária a náuseas e vômitos enquanto tentava beber o agente de contraste. A gastroenterologia foi consultada, e a paciente passou por esofagogastroduodenoscopia (EGD) e colonoscopia no dia 6 de sua hospitalização. Os resultados da colonoscopia estavam dentro dos limites normais. A EGD revelou algumas estenoses intrínsecas no esôfago superior, com a mais estreita medindo 9 milímetros. Biopsias foram obtidas do esôfago proximal e distal com pinças a frio para suspeita de esofagite eosinófila versus síndrome de Plummer-Vinson, com base na aparência bruta. Um exame de patologia do esôfago mostrou mucosa apenas escamosa, com inflamação crônica leve inativa. Não foi observada eosinofilia. Dadas as descobertas clínicas, laboratoriais e endoscópicas, foi feito um diagnóstico de síndrome de Plummer-Vinson. A sua disfagia melhorou ao longo dos próximos 9 dias no hospital após infusões de ferro e transfusões de sangue, e ela foi capaz de tolerar uma dieta regular comendo devagar com pequenas mordidas.\n\nEla foi submetida a um exame cardíaco para avaliar as palpitações, incluindo um ecocardiograma, que revelou uma fração de ejeção de 30-34%, com hipocinesia global e sem patologia valvular ou hipertensão pulmonar. Um teste de estresse nuclear foi negativo para isquemia miocárdica. Um novo diagnóstico de insuficiência cardíaca congestiva com fração de ejeção reduzida foi feito. A cardiologia foi consultada e ela começou a tomar carvedilol, lisinopril, espironolactona e hidralazina. Ela recebeu um colete salva-vidas no hospital na alta.\n\nAproximadamente 6 meses após a alta, foi feito um telefonema de acompanhamento para a paciente. Ela afirmou que estava tomando todos os medicamentos e que a disfagia havia se resolvido. No momento do telefonema, ela estava tolerando uma dieta regular sem restrições alimentares.",
+        "gold_summary": "Paciente: Feminino, 48\n\nDiagnóstico Final: Síndrome de Plummer-Vinson\n\nSintomas: Dor no peito • fadiga • palpitação\n\nMedicação: —\n\nProcedimento Clínico: Esofagogastroduodenoscopia (EGD) • colonoscopia\n\nEspecialidade: Medicina Geral e Interna\n\nApresentamos o caso de uma mulher afro-americana de 48 anos com anemia sintomática e insuficiência cardíaca congestiva de início recente, secundária a hipertensão, que apresentou os sintomas clássicos de PVS.\n",
+        "synthetic_summary": {
+            "B1": "Uma mulher de 48 anos estava muito cansada e com o coração batendo rápido. Ela sentia dor no peito e dificuldade para engolir comida. Os médicos fizeram exames para olhar dentro da barriga e o esôfago, que é o tubo da comida. Eles descobriram que ela tinha um problema chamado síndrome de Plummer-Vinson. \n\nEla recebeu remédios e tomou um tratamento com ferro para melhorar o sangue. Depois, ela ficou melhor e conseguiu comer direitinho. Os médicos também cuidaram do coração dela para que ele ficasse forte de novo. Agora, ela está se sentindo bem e comendo sem problemas.",
+            "B2": "**Caso de uma mulher de 48 anos com sintomas no coração e dificuldade para engolir**\n\nUma mulher de 48 anos, que tinha pressão alta não controlada, foi ao hospital porque sentia palpitações, que são batimentos cardíacos acelerados ou irregulares. Ela também estava cansada e com falta de ar. Além disso, ela sentia dor no lado esquerdo do peito e formigamento no braço esquerdo. Ela percebeu pontos escuros na visão e dificuldade para engolir alimentos sólidos, que pioraram nas últimas semanas.\n\nNo hospital, os médicos perceberam que ela estava com a pressão alta e o coração acelerado. Um exame de sangue mostrou que ela estava com anemia, que é quando o sangue tem poucos glóbulos vermelhos, o que pode causar cansaço e palidez. Os níveis de ferro no sangue estavam muito baixos, o que ajuda a explicar a anemia. Para investigar a dificuldade para engolir, os médicos fizeram exames do estômago e intestinos. No esôfago, que é o tubo que leva a comida da boca para o estômago, eles encontraram estreitamentos que dificultavam a passagem dos alimentos.\n\nCom base nos sintomas, exames e biópsias (que são pedaços pequenos de tecido retirados para análise), os médicos diagnosticaram a paciente com Síndrome de Plummer-Vinson. Essa síndrome é uma condição rara que causa anemia por falta de ferro e estreitamento no esôfago, levando à dificuldade para engolir.\n\nAlém disso, ela foi diagnosticada com insuficiência cardíaca, que é quando o coração não consegue bombear sangue direito. Ela começou a tomar remédios para ajudar o coração a funcionar melhor e recebeu transfusões de sangue e ferro para tratar a anemia.\n\nDurante a internação, a dificuldade para engolir melhorou bastante com o tratamento. Seis meses depois, a paciente estava bem, conseguia comer normalmente e seguia tomando os remédios para o coração.\n\n**O que aprendemos com esse caso?**\n\nA Síndrome de Plummer-Vinson pode causar anemia grave e problemas para engolir. É importante tratar a anemia com ferro e cuidar do coração, especialmente quando há pressão alta envolvida. O acompanhamento médico é fundamental para a recuperação completa.",
+            "B3": "Resumo Detalhado do Caso Clínico\n\nContexto  \nUma mulher afro-americana de 48 anos, com histórico de hipertensão arterial essencial não controlada, procurou atendimento médico devido a palpitações cardíacas, acompanhadas de fadiga e falta de ar. Nos dias anteriores, ela percebeu episódios intermitentes de batimentos cardíacos irregulares, que evoluíram para dor no lado esquerdo do peito, formigamento no braço esquerdo, visão com pontos escuros e dificuldade para engolir alimentos sólidos (disfagia), que piorou nas últimas semanas. Ela não fazia uso de medicamentos regularmente e não apresentava sintomas semelhantes anteriormente.\n\nPrincipais Achados Clínicos e Exames  \nNa admissão, a paciente apresentava pressão arterial elevada (166/92 mmHg) e frequência cardíaca acelerada (109 batimentos por minuto). O exame físico revelou palidez nas mucosas oculares, sugerindo anemia, sem sinais de inflamação na língua ou alterações nas unhas. Exames laboratoriais mostraram anemia severa, com hemoglobina muito baixa (5,7 g/dL) e glóbulos vermelhos menores que o normal (volume corpuscular médio de 65,3 fL), além de níveis muito reduzidos de ferro sérico, ferritina e saturação de ferro, indicando deficiência de ferro. O teste para sangue oculto nas fezes foi negativo, e a paciente negou sangramentos digestivos evidentes ou menstruação excessiva.\n\nDurante a internação, ela recebeu transfusões de sangue e tratamento com ferro intravenoso. A avaliação da disfagia foi dificultada inicialmente por náuseas e vômitos. Após estabilização, foram realizadas uma endoscopia digestiva alta (esofagogastroduodenoscopia - EGD) e colonoscopia. A colonoscopia não mostrou alterações, enquanto a EGD revelou estreitamentos no esôfago superior, com a área mais estreita medindo 9 milímetros. As biópsias do esôfago demonstraram inflamação leve e crônica, sem presença de eosinófilos (células associadas a alergias e inflamação específica). Esses achados, junto com o quadro clínico e laboratorial, levaram ao diagnóstico de síndrome de Plummer-Vinson (PVS), uma condição rara caracterizada por anemia ferropriva, disfagia e estreitamento esofágico.\n\nAlém disso, a paciente foi submetida a avaliação cardíaca devido às palpitações. O ecocardiograma revelou uma fração de ejeção reduzida (30-34%), indicando insuficiência cardíaca congestiva com diminuição da capacidade do coração de bombear sangue, associada a movimento reduzido do músculo cardíaco (hipocinesia global). Um teste de estresse cardíaco não evidenciou isquemia (falta de suprimento sanguíneo ao coração). Com base nisso, foi iniciado tratamento medicamentoso com betabloqueador (carvedilol), inibidor da enzima conversora de angiotensina (lisinopril), diurético poupador de potássio (espironolactona) e vasodilatador (hidralazina). A paciente recebeu um dispositivo de proteção cardíaca (colete salva-vidas) antes da alta hospitalar.\n\nInterpretação Clínica  \nEste caso ilustra a apresentação clássica da síndrome de Plummer-Vinson, que envolve anemia ferropriva grave associada a disfagia causada por estreitamento do esôfago. A anemia provavelmente contribuiu para os sintomas cardíacos e a insuficiência cardíaca congestiva, especialmente em um contexto de hipertensão descontrolada. O tratamento com reposição de ferro e suporte cardíaco resultou em melhora significativa dos sintomas, incluindo a resolução da dificuldade para engolir.\n\nPróximos Passos e Seguimento  \nSeis meses após a alta, a paciente relatou boa adesão ao tratamento medicamentoso e completa resolução da disfagia, com retorno à alimentação normal sem restrições. O acompanhamento contínuo para controle da insuficiência cardíaca e monitoramento da anemia é fundamental para prevenir recidivas e complicações futuras."
+        }
+    },
+    {
+        "article": "A paciente era uma senhora de 81 anos de idade com um histórico médico de hipertensão e hiperlipidemia. A paciente foi trazida ao nosso hospital com uma hemiparesia direita grave e afasia total, e a pontuação do National Institutes of Health Stroke Scale (NIHSS) no momento da admissão foi de 16. O último conhecido (LKW) para o tempo de chegada foi de 12 horas. Em nossa unidade, seguimos um protocolo de imagem baseado no tempo para casos agudos de AVC: casos dentro de 4,5 horas do início do tratamento passam por CTA primeiro, enquanto casos além de 4,5 horas são avaliados com MRI primeiro. A MRI demonstrou infarto cerebral na área da artéria cerebral média esquerda, e a pontuação do Alberta Stroke Program Early CT Score (DWI ASPECTS) foi de 7. A MRA revelou oclusão do segmento M2 esquerdo. No entanto, os achados do raio-X do tórax indicaram uma possível anomalia no arco da aorta, levando-nos a realizar uma CTA adicional para avaliar a via de acesso para trombectomia. A CTA revelou RAA com ramificação espelhada. A paciente não recebeu um ativador de plasminogênio tecidual recombinante intravenoso. Embora existam evidências limitadas que apoiam a MT em tais cenários, avaliamos cuidadosamente a condição da paciente com base em vários fatores: a escala modificada de Rankin pré-AVC (mRS) foi de 0, a pontuação DWI ASPECTS foi de 7, e a apresentação foi um AVC despertador com um desajuste DWI-FLAIR, sugerindo que o tempo real desde o início pode não ser tão prolongado como indicado pelo LKW. Além disso, a paciente apresentou sintomas graves com uma pontuação NIHSS de 16. Com base nesses fatores, julgamos que a MT foi apropriada, pois proporcionou uma chance de melhorar o resultado da paciente.\n\nEscolhemos o sistema de orientação habitual. Uma bainha de 9 Fr foi inserida na artéria femoral comum direita. Um fio guia (Radifocus; Terumo, Tóquio, Japão) e um cateter JB2 de 6 Fr (Medikit, Tóquio, Japão) foram avançados usando um cateter guia de balão OPTIMO de 9 Fr (Tokai Medical Products, Aichi, Japão).\n\nO guia cateter foi avançado da aorta abdominal no meio da coluna vertebral para a aorta torácica no lado direito da coluna vertebral e foi facilmente colocado na artéria carótida interna esquerda da maneira habitual com referência à CTA. A angiografia carótida interna esquerda revelou uma oclusão do tronco inferior M2 esquerdo. A trombólise na reperfusão do infarto cerebral 2B foi alcançada usando Trevo NXT 3 × 32 mm (Stryker, Fremont, CA, EUA) e Catalyst 6 (Stryker) após 3 passagens. O tempo da punção para recanalização foi de 61 minutos (10 minutos, da punção para a colocação do guia cateter na artéria carótida interna esquerda; 51 minutos, da colocação do guia cateter para a recanalização). A TC pós-procedimento revelou uma pequena hemorragia subaracnóide.\n\nA fibrilação atrial não foi detectada, e foi realizada uma tomografia computadorizada de contraste de corpo inteiro para procurar a fonte da embolia. A trombose venosa profunda (TVP) e a embolia pulmonar (EP) foram observadas na veia femoral profunda direita e nas duas artérias pulmonares, respetivamente. A ecocardiografia transesofágica demonstrou um forame oval patente (FOP). Apesar dos anticorpos antinucleares e da coagulabilidade serem examinados através de testes sanguíneos, estes não foram as causas do enfarte cerebral. A patogénese do enfarte cerebral foi determinada como uma embolia paradoxal, e o apixaban foi administrado após a TVP e a EP serem reveladas. O trombo na veia femoral e na artéria pulmonar quase desapareceu, e o enfarte cerebral não recorreu. A hemiparesia direita e a afasia persistiram, e na alta, a pontuação mRS foi de 5.\n",
+        "gold_summary": "Uma senhora de 81 anos apresentou hemiparesia direita grave e afasia. A pontuação da Escala de Acidente Vascular Cerebral dos Institutos Nacionais de Saúde foi de 16, a ressonância magnética demonstrou uma pontuação de 7 na imagem ponderada por difusão do Programa de Ressonância Magnética de Alberta para Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância 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Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética de Ressonância Magnética\n",
+        "synthetic_summary": {
+            "B1": "Uma senhora de 81 anos ficou com o lado direito do corpo muito fraco. Ela também não conseguia falar. Os médicos fizeram um exame para ver o que estava acontecendo no cérebro dela. Eles viram que uma parte do cérebro estava machucada porque o sangue não estava chegando direito.\n\nOs médicos fizeram um tratamento para ajudar o sangue a voltar a passar. Eles usaram um tubo para tirar o bloqueio dentro do corpo dela. Depois do tratamento, ela ficou melhor, mas ainda tinha dificuldade para mexer o corpo e falar. Os médicos cuidaram dela com muito carinho para ela melhorar.",
+            "B2": "**O que aconteceu com a paciente**\n\nUma senhora de 81 anos teve um AVC, que é quando o sangue para de chegar a uma parte do cérebro. Ela ficou com fraqueza forte no lado direito do corpo (chamado hemiparesia) e não conseguia falar (afasia). Os médicos usaram uma escala chamada NIHSS para medir a gravidade do AVC, e ela marcou 16, o que é bastante grave.\n\n**Como os médicos examinaram o cérebro**\n\nEles fizeram uma ressonância magnética, que é um exame que mostra imagens detalhadas do cérebro. Nesse exame, usaram uma pontuação chamada ASPECTS para ver o quanto do cérebro estava afetado. A paciente teve nota 7, o que indica que parte do cérebro ainda estava saudável. Também descobriram que uma artéria importante estava bloqueada.\n\n**O que foi diferente no corpo dela**\n\nDurante os exames, os médicos perceberam que a paciente tinha uma anomalia na aorta, que é a principal artéria do corpo. Essa anomalia se chama arco aórtico direito com ramificação espelhada, ou seja, os vasos sanguíneos estavam em uma posição diferente do normal.\n\n**O tratamento feito**\n\nComo o AVC dela era grave e havia chance de melhorar, os médicos decidiram fazer uma trombectomia. Esse é um procedimento para retirar o coágulo que está bloqueando a artéria no cérebro. Eles usaram cateteres, que são tubos finos, para chegar até o local do bloqueio e remover o coágulo. A cirurgia demorou pouco mais de uma hora e foi bem-sucedida.\n\n**O que descobriram depois**\n\nDepois do procedimento, a paciente teve uma pequena hemorragia, que é um sangramento no cérebro, mas isso foi controlado. Os médicos também fizeram exames para entender por que ela teve o AVC. Encontraram coágulos nas veias da perna e nos pulmões, e um orifício no coração chamado forame oval patente, que pode permitir que coágulos passem do sangue venoso para o arterial, causando o AVC. Isso é chamado de embolia paradoxal.\n\n**O que aconteceu depois do tratamento**\n\nA paciente recebeu um remédio chamado apixaban para evitar novos coágulos. Os coágulos nas veias e pulmões diminuíram bastante, e ela não teve outro AVC. Porém, a fraqueza e a dificuldade para falar continuaram, e na alta hospitalar ela ainda precisava de ajuda para as atividades diárias.\n\n**Resumo final**\n\nEssa senhora teve um AVC grave causado por um coágulo que veio das veias, passou pelo coração e foi para o cérebro. Apesar de uma anomalia nas artérias, os médicos conseguiram retirar o coágulo com um procedimento especial. Ela recebeu tratamento para evitar novos coágulos, mas ainda ficou com sequelas do AVC. Esse caso mostra como é importante investigar a causa do AVC para escolher o melhor tratamento.",
+            "B3": "**Contexto**  \nUma paciente de 81 anos, com histórico de hipertensão e níveis elevados de colesterol (hiperlipidemia), foi admitida no hospital apresentando fraqueza intensa no lado direito do corpo (hemiparesia direita grave) e perda total da capacidade de falar (afasia total). A avaliação inicial pelo National Institutes of Health Stroke Scale (NIHSS), que mede a gravidade do AVC, indicou um escore de 16, sugerindo um AVC grave. O tempo desde o último momento em que a paciente foi vista sem sintomas (Last Known Well, LKW) até a chegada ao hospital foi de 12 horas.\n\n**Principais Achados**  \nDe acordo com o protocolo do hospital para AVCs agudos, pacientes com mais de 4,5 horas do início dos sintomas são avaliados inicialmente por ressonância magnética (MRI). A MRI mostrou um infarto cerebral na região da artéria cerebral média esquerda, com uma pontuação de 7 no Alberta Stroke Program Early CT Score (ASPECTS) baseado em imagens ponderadas por difusão (DWI), indicando uma área moderada de dano cerebral. A angiografia por ressonância magnética (MRA) revelou oclusão do segmento M2 da artéria cerebral média esquerda.  \n\nAlém disso, um raio-X do tórax sugeriu uma anomalia no arco da aorta, que foi confirmada pela tomografia computadorizada angiográfica (CTA) como uma aorta com ramificação espelhada (uma variação anatômica rara). A paciente não recebeu tratamento trombolítico intravenoso com ativador de plasminogênio tecidual recombinante (rt-PA), devido ao tempo prolongado desde o início dos sintomas.\n\n**Interpretação Clínica**  \nApesar do tempo prolongado desde o início do AVC, a equipe médica considerou a realização da trombectomia mecânica (MT), um procedimento para remover o coágulo que bloqueia o fluxo sanguíneo cerebral. Essa decisão foi baseada em vários fatores favoráveis: a paciente tinha boa funcionalidade antes do AVC (escala modificada de Rankin pré-AVC igual a 0), a área de dano cerebral ainda era moderada (DWI ASPECTS de 7), e a apresentação do AVC foi do tipo “despertar” (sintomas percebidos ao acordar), com um desajuste entre as imagens DWI e FLAIR que sugeria que o AVC poderia ter ocorrido mais próximo do horário da chegada do que o LKW indicava. Além disso, a gravidade dos sintomas (NIHSS 16) reforçou a necessidade de intervenção para tentar melhorar o prognóstico.\n\nDurante o procedimento, a equipe utilizou a via femoral comum direita para inserir os cateteres e guias, navegando pela aorta com ramificação espelhada até alcançar a artéria carótida interna esquerda. A angiografia confirmou a oclusão do segmento M2 esquerdo, e após três tentativas com dispositivos específicos (Trevo NXT e Catalyst 6), a recanalização foi alcançada em 61 minutos desde a punção inicial. Após o procedimento, uma tomografia computadorizada mostrou uma pequena hemorragia subaracnóide, uma complicação possível, mas controlada.\n\n**Diagnóstico da Causa do AVC e Tratamento Posterior**  \nA investigação para a origem do coágulo não revelou fibrilação atrial, uma causa comum de AVC embólico. No entanto, exames adicionais identificaram trombose venosa profunda (TVP) na veia femoral profunda direita e embolia pulmonar (EP) nas artérias pulmonares, além de um forame oval patente (FOP) detectado por ecocardiografia transesofágica. O FOP é uma comunicação anormal entre as câmaras do coração que pode permitir que coágulos venosos passem para a circulação arterial, causando uma embolia paradoxal, que foi considerada a causa do AVC nesta paciente. Testes para doenças autoimunes e distúrbios de coagulação foram negativos.\n\nCom base nesse diagnóstico, a paciente foi tratada com apixabana, um anticoagulante oral, para prevenir novos eventos tromboembólicos. O tratamento resultou na quase completa resolução da trombose venosa e da embolia pulmonar, e não houve recorrência do AVC.\n\n**Prognóstico e Desfecho**  \nApesar da intervenção e do tratamento anticoagulante, a paciente apresentou persistência da hemiparesia direita e da afasia. No momento da alta hospitalar, sua pontuação na escala modificada de Rankin era 5, indicando dependência severa para as atividades diárias.\n\n**Próximos Passos**  \nO caso destaca a importância da avaliação individualizada em pacientes idosos com AVC, especialmente quando há variações anatômicas e apresentações atípicas, como o AVC despertador. A trombectomia mecânica pode ser considerada mesmo em janelas de tempo prolongadas, desde que haja evidências de tecido cerebral viável e potencial benefício clínico. O diagnóstico e tratamento da causa subjacente do AVC, neste caso a embolia paradoxal associada a TVP, EP e FOP, são essenciais para prevenir novos eventos e otimizar a recuperação funcional."
+        }
+    },
+    {
+        "article": "Um homem de 37 anos apresentou-se na nossa unidade terciária de uveíte em janeiro de 2020, por encaminhamento para uma avaliação vitreorretiniana adicional. Os seus sintomas eram flashes e fotopsias predominantemente no olho direito. Ele tinha sido previamente diagnosticado com uma presumida BSCR bilateral no verão de 2016. As avaliações laboratoriais iniciais, incluindo hemograma completo, painel metabólico completo, hemoglobina A1c e estudos de absorção de anticorpos fluorescentes, foram todas sem observações. As avaliações laboratoriais para etiologias infecciosas, incluindo QuantiFERON-TB Gold (QFT), reagina plasmática rápida (RPR) e absorção de anticorpos fluorescentes (FTA-ABS), foram todas negativas ou não reativas. A ressonância magnética do cérebro em setembro de 2016 foi sem observações. Em novembro de 2016, o paciente foi tratado com corticosteroide tópico e bevacizumab intravitreal no olho direito (OD), bem como 60 mg de prednisona oral diária. Em dezembro de 2016, ele foi iniciado em terapia imunomoduladora (IMT) com ciclosporina e metotrexato, que foram ambos interrompidos em 2017 devido a uma possível falta de eficácia. O paciente foi então iniciado em adalimumab, durante o qual os seus sintomas (flashes e flutuadores) melhoraram. Após cerca de 1 ano de terapia, o adalimumab foi interrompido devido a níveis reduzidos de ferro no soro no início de 2019. Em outubro de 2019, recebeu uma injeção intravitreal de acetónido de fluocinolona de 0,18 mg no olho direito, mas não notou subsequente melhoria dos sintomas visuais.\n\nNa avaliação inicial, em janeiro de 2020, o paciente apresentou desconforto ocular moderado (OD > OS), visão turva (OD > OS) e moscas volantes (OU). A acuidade visual foi de 20/20 OU. Na avaliação inicial, a revisão dos sistemas foi negativa do ponto de vista sistêmico. As pressões intraoculares foram de 13 mmHg OD e 12 mmHg OS. O exame do segmento anterior foi notável por um brilho bilateral 1+, com catarata posterior subcapsular leve OD, mas, de outra forma, não foi notável. O exame do fundo dilatado foi notável por edema do disco óptico (OD > OS) e lesões corretinas periféricas e periféricas hipopigmentadas (OU). O olho direito também apresentou atrofia temporal peripapilar, 1+ células vítreas, alterações pigmentadas do epitélio do pigmento da retina macular e pequena hemorragia retinal na periferia do quadrante supertemporal. A tomografia de coerência óptica no domínio espectral (SD-OCT) mostrou elevação do disco óptico no fluido intra-retinal peripapilar com membrana epirretinal leve (ERM) OD > OS. A angiografia de fluorescência de grande angular (FA) (OPTOS Plc, Dunfermline, Reino Unido) mostrou meios turvos, vazamento do disco e coloração peripapilar OD, e vazamento difuso do disco óptico com coloração segmentar leve de vênulas ao longo da arcada temporal inferior OS. Houve hiperfluorescência de várias lesões na região peripapilar e ao longo da arcada temporal inferior sem qualquer sinal de vazamento OU.\n\nDuas semanas depois, a eletroretinografia de campo total (ffERG) mostrou disfunção retinal global leve a moderada, com regiões geográficas claras de depressão macular (OD > OS). Os tempos de cintilação implícitos de 30 Hz revelaram um atraso significativo em ambos os olhos (OS > OD). O potencial visual evocado mostrou um atraso relativamente simétrico para ambos os estímulos pequenos e grandes, sugerindo uma disfunção do nervo ótico leve. Os campos visuais de Goldmann (GVF) e os campos visuais de Humphrey (HVF) mostraram um alargamento do ponto cego OD e um ponto cego normal sem constrição generalizada OS. As avaliações laboratoriais foram notáveis apenas para a positividade do antígeno leucocitário humano (HLA) A29. Os resultados dos testes da enzima conversora da angiotensina, da lisozima e do teste QFT repetido estavam dentro dos limites normais.\n\nNa visita de acompanhamento de 1 mês em fevereiro de 2020, o paciente notou acuidade visual estável, alguma melhora em flutuadores em ambos os olhos, e nebulosidade persistente predominantemente OD. A acuidade visual permaneceu 20/20 OU. A pressão intraocular foi de 15 mm Hg OD e 8 mm Hg OS. O exame do segmento anterior foi notável por um brilho OU de 1+. O exame do fundo dilatado foi notável por 0,5+ células e 0,5+ nebulosidade no vítreo OU. Os achados gerais do exame do pólo posterior foram estáveis. Os achados no SD-OCT e na FA de grande angular foram relativamente inalterados desde a primeira visita. A corioangiografia de indocyanina verde de grande angular (ICG) mostrou meios claros, múltiplos pontos hipocianescentes no pólo posterior e na periferia média na fase intermédia, e os pontos hipocianescentes desvaneceram-se na fase tardia OU. A autofluorescência do fundo mostrou hipofluorescência em torno do disco ótico e da retina.\n\nO paciente foi diagnosticado com BSCR com base na positividade de HLA-A29, aparência típica do fundo do olho e avaliação negativa para outras etiologias autoimunes e infecciosas. Dada a doença ativa do paciente, como evidenciada pelo edema do disco óptico associado a células vítreas em ambos os olhos, juntamente com achados de FA e ICG altamente sugestivos, o paciente iniciou a terapia com infliximab numa dose de 7,5 mg/kg mensalmente. Ele também recebeu 3 dias de metilprednisolona intravenosa (IV) numa dose de 1000 mg/dia, seguida por um curso de redução gradual de prednisona oral.\n\nO paciente não veio para a visita de acompanhamento até abril de 2021 e recebeu oito ciclos de infusões de 7,5 mg/kg de infliximab juntamente com 1000 mg de prednisona durante 3 dias nesse período. A AV diminuiu para 20/40 OD devido à formação de catarata subcapsular posterior (PSC) e foi 20/20 OS. Não houve células AC e flare presentes em ambos os olhos. O vítreo estava nebuloso OD devido à PSC e o OS claro. O SD-OCT do disco óptico não mostrou alterações significativas. Na FA, o meio estava nebuloso no centro OD devido à formação de catarata. A coloração parcial do disco óptico estava presente em OU. Não houve coloração vascular retiniana e vazamento capilar em OU. A coloração das lesões corio-retinianas periféricas nos quadros iniciais e tardios da FA permaneceu a mesma em OU. Quatro meses depois, o paciente recebeu mais quatro ciclos de infusões de IFX juntamente com 1 dia de 1000 mg de metilprednisolona. A AV diminuiu para 20/70 OD devido à progressão da PSC e foi 20/20 OS. O exame oftalmológico, SD-OCT e FA permaneceram inalterados. ICG foi realizado e os pontos hipocyanescentes mostraram uma melhora acentuada com poucos pontos hipocyanescentes espalhados no pólo posterior (OS>OD) em ambos os olhos no ICG. O teste eletrofisiológico incluindo ffERG, mfERG, e VEP e o teste do campo visual, incluindo GVF e HVF, permaneceram os mesmos desde a visita inicial. Embora tenha havido uma melhora significativa nas descobertas oculares no exame e tanto na FA quanto na ICG, o tratamento com 2000 mg diários de micofenolato de mofetil foi adicionado ao seu regime de tratamento devido à presença de edema do disco óptico e permaneceram alguns pontos hipocyanescentes no pólo posterior no ICG.\n",
+        "gold_summary": "Um homem de 37 anos apresentou-se no nosso serviço de uveíte terciária com desconforto ocular bilateral, visão turva e flutuadores. O exame ocular foi notável por vitrite, edema do disco óptico e lesões corio-retinais hipopigmentadas, visíveis na corioangiografia com verde indocyanina como múltiplos pontos hipocyanescentes na fase intermédia. A eletroretinografia de campo total e o potencial visual evocado mostraram disfunção retinal global e disfunção do nervo ótico. As avaliações laboratoriais foram notáveis apenas pela positividade do antígeno leucocitário humano (HLA)-A29. O paciente foi diagnosticado com BSCR e começou a tomar prednisona oral e, eventualmente, foi tratado com infliximab.\n",
+        "synthetic_summary": {
+            "B1": "Um homem de 37 anos estava com os olhos doendo e vendo coisas estranhas. Ele via umas manchas que se mexiam e tudo estava meio embaçado. Os médicos olharam bem os olhos dele e viram que estavam um pouco inchados e com algumas pintinhas diferentes.\n\nEles fizeram alguns exames e viram que os olhos dele não estavam funcionando direito. Também acharam que o nervo que ajuda a ver estava um pouco cansado. Os exames de sangue mostraram uma coisa chamada HLA-A29, que ajuda a entender o que ele tem.\n\nOs médicos disseram que ele tem uma doença que deixa os olhos doentes, chamada BSCR. Para ajudar, ele começou a tomar um remédio que é como um corticoide e depois outro remédio para melhorar os olhos. Eles vão cuidar dele para que ele fique melhor.",
+            "B2": "**O que aconteceu com o paciente**\n\nUm homem de 37 anos chegou ao nosso serviço especializado com desconforto nos dois olhos, visão embaçada e pontos que pareciam flutuar na frente dos olhos, chamados de \"flutuadores\". Durante o exame, notamos que ele tinha inflamação no vítreo (uma parte gelatinosa dentro do olho), inchaço na cabeça do nervo óptico (que conecta o olho ao cérebro) e algumas manchas claras na parte de trás do olho, chamadas lesões corio-retinais hipopigmentadas.\n\n**Como foi feito o diagnóstico**\n\nPara entender melhor o problema, fizemos um exame chamado corioangiografia com verde indocianina, que mostrou vários pontos escuros no olho, indicando áreas afetadas pela doença. Outros testes que medem a função da retina e do nervo óptico mostraram que ambos estavam funcionando de forma ruim. Nos exames de sangue, encontramos que ele tinha um marcador chamado HLA-A29, que está ligado a uma doença chamada Síndrome de Birdshot (BSCR), que afeta os olhos.\n\n**O tratamento e o que isso significa**\n\nCom base nesses resultados, diagnosticamos o paciente com BSCR. Ele começou a tomar um remédio chamado prednisona, que é um tipo de corticoide para diminuir a inflamação. Depois, passou a receber um tratamento com infliximab, que é um medicamento que ajuda a controlar o sistema imunológico para evitar que ele ataque os olhos. Esse tratamento é importante para proteger a visão e reduzir os sintomas.",
+            "B3": "**Contexto**  \nUm homem de 37 anos procurou atendimento especializado em uveíte devido a sintomas oculares persistentes, incluindo desconforto em ambos os olhos, visão turva e presença de flutuadores (pequenas manchas móveis no campo visual). Ele já havia sido diagnosticado anteriormente com Birdshot Chorioretinopathy (BSCR), uma doença inflamatória rara que afeta a retina e o nervo óptico, associada ao antígeno HLA-A29.\n\n**Principais Achados Clínicos e Exames**  \nNo exame oftalmológico, foram identificados sinais de inflamação no vítreo (vitrite), edema do disco óptico (inchaço na região onde o nervo óptico entra no olho) e múltiplas lesões hipopigmentadas na retina, especialmente na região periférica. A corioangiografia com verde de indocianina, exame que avalia a circulação da camada vascular da retina, revelou vários pontos hipocianescentes (áreas que aparecem mais escuras, indicando possível comprometimento vascular ou inflamatório) durante a fase intermediária do exame.\n\nTestes eletrofisiológicos, como a eletroretinografia de campo total (ffERG) e o potencial visual evocado (VEP), demonstraram uma disfunção global da retina e também uma leve disfunção do nervo óptico, confirmando o impacto da doença na função visual. As análises laboratoriais não revelaram sinais de infecções ou outras causas autoimunes, exceto pela presença do antígeno leucocitário humano HLA-A29, fortemente associado à BSCR.\n\n**Interpretação Clínica**  \nCom base nos sintomas, nos achados clínicos característicos e na positividade para HLA-A29, o diagnóstico de Birdshot Chorioretinopathy foi confirmado. Esta condição inflamatória pode levar a perda progressiva da visão se não for adequadamente tratada, devido à inflamação contínua da retina e do nervo óptico.\n\n**Tratamento e Evolução**  \nInicialmente, o paciente recebeu corticosteroides orais (prednisona) para controlar a inflamação. Posteriormente, devido à atividade persistente da doença, foi iniciado tratamento com infliximab, um medicamento imunossupressor que atua bloqueando a inflamação mediada por certas proteínas do sistema imunológico. Durante o acompanhamento, apesar de algumas complicações como o desenvolvimento de catarata subcapsular posterior (um tipo de opacificação do cristalino que pode afetar a visão), o tratamento com infliximab resultou em melhora significativa dos sinais inflamatórios observados nos exames de imagem e estabilização da função visual.\n\n**Próximos Passos**  \nDevido à persistência de edema do disco óptico e alguns pontos hipocianescentes na corioangiografia, foi acrescentado ao tratamento o micofenolato de mofetil, outro imunossupressor, para intensificar o controle da inflamação e prevenir danos adicionais à retina e ao nervo óptico. O acompanhamento contínuo com exames oftalmológicos detalhados e testes funcionais é essencial para monitorar a resposta ao tratamento e ajustar as terapias conforme necessário."
+        }
+    },
+    {
+        "article": "Uma criança do sexo feminino nasceu com 34 semanas de gestação completa e um peso de 2820 g. Foi-lhe dado um curso completo de corticosteroides pré-natais e a imagem pré-natal de rotina mostrou polidrâmnio e um feto grande para a data. A mãe tinha antecedentes de diabetes gestacional e pré-eclâmpsia.\n\nA criança nasceu por cesariana em boas condições com pontuações APGAR de 61, 95 e 1010, mas devido a dificuldades respiratórias, foi-lhe administrado surfactante por via menos invasiva 25 minutos após o nascimento. Foi então transferida para a unidade de cuidados intensivos neonatais com pressão positiva contínua nas vias respiratórias (CPAP) a 40% de oxigénio. 4 horas após o nascimento, devido a dificuldades respiratórias em curso e a um aumento da necessidade de oxigénio até 60%, foi intubada e ventilada mecanicamente. Uma radiografia de tórax revelou evidências de possível dilatação bilateral dos diafragmas. Um exame de ultrassom do diafragma confirmou esta suspeita. Um ecocardiograma (ECHO) realizado nessa altura revelou uma hipoplasia leve do istmo, mas um ECHO repetido demonstrou um coração estruturalmente normal. Depois de ter sido submetida a um teste de respiração espontânea e a um período de avaliação não invasiva da atividade elétrica do diafragma, foi extubada com sucesso após 36 horas de suporte ventilatório invasivo. Além disso, não precisou de suporte respiratório não invasivo pós-extubação e continuou a respirar por si mesma no ar até à alta. Como não precisou de períodos prolongados de suporte respiratório invasivo, não foi considerada candidata a intervenção cirúrgica no período neonatal agudo.\n\nDurante o período neonatal, a paciente apresentou hipoglicemia com glicose no sangue de 0,4 mmol/L e precisou de uma concentração máxima de glicose de 20%. Foi então diagnosticada com hiperinsulinismo e começou a tomar diazóxido. A paciente não se alimentava bem, apesar de uma videofluoroscopia normal e um exame de ouvido, nariz e garganta (ENT) e precisou de apoio nutricional através de um tubo nasogástrico. Durante a avaliação neurológica, a paciente apresentou hipotonia central com reflexos rápidos e foi observada uma grande quantidade de nevos melanocíticos na parte lateral de ambos os braços, com manchas adicionais no sacro. O exame histopatológico de uma biópsia por punção demonstrou resultados consistentes com a melanocitose dérmica. A paciente nasceu com dois dentes neonatais que foram removidos após o nascimento, mas posteriormente desenvolveu duas lesões fibrosas na crista alveolar anterior, que foram pedunculadas e móveis, sendo que estas foram removidas um mês depois. Foi realizada uma investigação neurológica exaustiva, que revelou uma ressonância magnética cerebral normal, com eletromiografia normal dos membros superiores e inferiores e estudos de condução nervosa. Considerando o diagnóstico diferencial de atrofia muscular espinal, foi realizada uma análise de imuno-histoquímica, que apresentou resultados normais. Foi realizada uma avaliação oftalmológica e uma ecografia renal, que foram normais. Os testes genéticos pós-natais revelaram uma mutação no gene KMT2D, associado à síndrome de Kabuki.\n\nEla foi dispensada em casa no dia 64 após o nascimento com apoio de alimentação nasogástrica e continuou com medicação diazóide. Ela continua a ter uma grande participação de terapeutas ocupacionais, terapeutas de fala e linguagem e equipes de fisioterapia.\n\nImagens e medições\nA área torácica radiográfica do tórax (CRTA) medida após a extubação (dia três após o nascimento) foi de 1.654 mm2, equivalente a um recém-nascido a termo com hérnia diafragmática congénita grave. A imagem por ultrassom (USS) mostrou uma eventração diafragmática focal com abaulamento da cúpula do fígado para o hemitórax direito e esquerdo. Um teste de respiração espontânea (SBT) foi realizado antes da extubação e a eletromiografia do diafragma foi medida durante este período. A amplitude média da atividade elétrica diafragmática foi de 2.47 μV, semelhante em magnitude àquela de recém-nascidos ventilados da mesma idade gestacional com diafragmas intactos. Ela passou com sucesso o SBT e a subsequente extubação.\n\nOs pais deram consentimento informado por escrito para este relatório e foi dada aprovação ética para medir o EMG do diafragma durante o SBT antes da extubação (referência REC: 20/SW/0,062).\n",
+        "gold_summary": "Uma criança do sexo feminino nascida com 34 semanas de gestação necessitou de intubação e ventilação ao nascer. A radiografia do tórax revelou uma densidade bilateral nas bases de ambos os campos pulmonares com hemi-diafragmas elevados. A ecografia revelou uma eventração diafragmática focal com abaulamento da cúpula do fígado para o hemitórax direito e esquerdo. A avaliação da atividade elétrica do diafragma durante um teste de respiração espontânea demonstrou uma amplitude média consistente com a de crianças ventiladas da mesma idade gestacional com diafragmas intactos. Por conseguinte, foi extubada com sucesso. A área torácica radiográfica do tórax medida após a extubação foi de 1654 mm2, equivalente à de uma criança a termo com hérnia diafragmática congénita grave. Como a atividade elétrica do diafragma foi normal, isto sugere que a substituição do tecido muscular diafragmático com bandas fibrosas foi provavelmente apenas parcial, e por isso a extubação foi bem-sucedida. A criança apresentou outras anomalias no período neonatal incluindo melanocitose dérmica, hipotonia central, hiperinsulinismo e má alimentação. A criança foi submetida a uma investigação exaustiva que revelou uma mutação do gene KMT2D associada à síndrome de Kabuki.\n",
+        "synthetic_summary": {
+            "B1": "Uma menina nasceu um pouco antes do tempo. Ela teve dificuldade para respirar e precisou de ajuda para respirar com um tubo. O médico fez fotos do peito dela e viu que o músculo que ajuda a respirar estava um pouco diferente. Mas o músculo ainda funcionava bem.\n\nDepois, os médicos tiraram o tubo e ela conseguiu respirar sozinha. Ela também teve algumas outras coisas diferentes no corpo, como manchas na pele e dificuldade para comer. Os médicos fizeram muitos exames e descobriram que ela tem uma coisa chamada síndrome de Kabuki, que é algo que a faz ser diferente, mas os médicos vão ajudar ela a ficar melhor.",
+            "B2": "**O que aconteceu com a criança ao nascer**\n\nUma menina nasceu um pouco antes do tempo, com 34 semanas de gestação, e teve problemas para respirar logo após o nascimento. Por isso, os médicos precisaram colocar um tubo para ajudá-la a respirar com uma máquina (intubação e ventilação). Um exame de raio-X do peito mostrou que a parte inferior dos pulmões dela estava mais densa do que o normal, e que os músculos chamados diafragmas, que ajudam na respiração, estavam mais altos do que deveriam.\n\n**O que os exames mostraram sobre o diafragma**\n\nUm exame de ultrassom, que usa ondas de som para ver dentro do corpo, mostrou que o diafragma dela tinha uma área enfraquecida, chamada eventração diafragmática, onde parte do fígado empurrou para cima dentro do peito. Para entender se o diafragma ainda funcionava bem, os médicos mediram a atividade elétrica dele enquanto a menina tentava respirar sozinha. Essa atividade estava parecida com a de outros bebês da mesma idade que também estavam usando ventilação, o que indicou que o diafragma ainda trabalhava normalmente.\n\n**Como foi o desmame da ventilação**\n\nPor causa dessa boa atividade do diafragma, os médicos conseguiram retirar o tubo de respiração com sucesso, e a menina passou a respirar sozinha. A área do tórax dela, medida no raio-X, era parecida com a de bebês que têm uma condição chamada hérnia diafragmática congênita grave, que é quando há um problema no diafragma desde o nascimento. Mas como o músculo do diafragma dela ainda funcionava bem, isso ajudou na recuperação.\n\n**Outros problemas que a menina teve**\n\nAlém dos problemas respiratórios, a menina teve outras dificuldades no começo da vida. Ela apresentou melanocitose dérmica, que são manchas escuras na pele causadas por um aumento de células chamadas melanócitos. Também teve hipotonia central, que é quando os músculos ficam mais fracos por causa do sistema nervoso, e hiperinsulinismo, que é quando o corpo produz muita insulina e pode causar queda no açúcar do sangue. Ela também teve dificuldade para se alimentar.\n\n**O que os exames genéticos mostraram**\n\nDepois de muitos exames, os médicos descobriram que a menina tem uma mutação no gene chamado KMT2D. Essa alteração está ligada à síndrome de Kabuki, uma condição genética que pode causar vários problemas de saúde e desenvolvimento.\n\n**Resumo final**\n\nEssa menina nasceu com um problema no diafragma que afetou a respiração, mas seu músculo ainda funcionava bem o suficiente para ela conseguir respirar sozinha depois de um tempo. Ela também teve outras condições médicas que precisaram de cuidados especiais. O diagnóstico genético ajudou a entender que ela tem a síndrome de Kabuki, o que explica vários dos sintomas que ela apresentou.",
+            "B3": "**Contexto**  \nUma menina nasceu prematuramente, com 34 semanas de gestação, apresentando dificuldades respiratórias logo após o nascimento que exigiram intubação e ventilação mecânica. Exames de imagem indicaram alterações no diafragma, órgão fundamental para a respiração, e outras complicações neonatais foram identificadas durante sua avaliação clínica.\n\n**Principais Achados**  \nA radiografia do tórax mostrou aumento da densidade nas bases pulmonares de ambos os lados, acompanhada de elevação dos hemi-diafragmas (as metades do diafragma). A ultrassonografia confirmou uma eventração diafragmática focal, ou seja, uma área localizada onde o diafragma estava enfraquecido e o fígado projetava-se para dentro do tórax, tanto do lado direito quanto do esquerdo.  \n\nDurante um teste de respiração espontânea, que avalia a capacidade do bebê de respirar sem ajuda, a atividade elétrica do diafragma foi medida por eletromiografia (um exame que registra a função muscular). A amplitude dessa atividade foi semelhante à observada em recém-nascidos da mesma idade gestacional com diafragmas normais, indicando que o músculo diafragmático ainda mantinha boa função.  \n\nA área radiográfica do tórax após a extubação foi de 1654 mm², valor comparável ao de recém-nascidos a termo com hérnia diafragmática congênita grave, uma condição em que há defeito no diafragma permitindo que órgãos abdominais invadam o tórax.  \n\nAlém das alterações respiratórias, a criança apresentou outras condições clínicas importantes: melanocitose dérmica (um aumento de células pigmentares na pele), hipotonia central (diminuição do tônus muscular devido a alterações no sistema nervoso central), hiperinsulinismo (produção excessiva de insulina causando baixos níveis de açúcar no sangue) e dificuldades na alimentação.  \n\nUma investigação genética detalhada revelou uma mutação no gene KMT2D, que é conhecido por estar associado à síndrome de Kabuki, uma doença rara que causa múltiplas anomalias congênitas e atraso no desenvolvimento.\n\n**Interpretação Clínica**  \nA presença de atividade elétrica diafragmática normal sugere que a substituição do tecido muscular do diafragma por tecido fibroso (bandas fibrosas) foi parcial, permitindo que o músculo mantivesse função suficiente para a respiração espontânea. Isso explica o sucesso na extubação precoce da criança, apesar das alterações estruturais detectadas.  \n\nAs múltiplas manifestações clínicas, incluindo a melanocitose dérmica, hipotonia e hiperinsulinismo, juntamente com a mutação genética identificada, indicam um quadro complexo que requer acompanhamento multidisciplinar.\n\n**Próximos Passos**  \nA criança recebeu alta hospitalar com suporte nutricional via sonda nasogástrica e medicação para controlar o hiperinsulinismo. Ela continua sob acompanhamento intensivo por equipes de fisioterapia, terapia ocupacional e fonoaudiologia para apoiar seu desenvolvimento motor, alimentar e neurológico. O diagnóstico da síndrome de Kabuki orienta a necessidade de monitoramento contínuo para possíveis complicações associadas e intervenções especializadas conforme o crescimento."
+        }
+    },
+    {
+        "article": "Doente do sexo masculino de 59 anos com antecedentes de hemocromatose, acidente isquémico transitório e glaucoma. Apresentava história familiar em dois tios paternos de morte aos 60 anos por doença neurológica não especificada. Apresentou-se com disartria e parésia facial de instalação súbita, com melhoria em poucos dias. Após uma semana iniciou movimentos involuntários do membro superior esquerdo (MSE), associados a disartria, ligeira anomia (dificuldade na nomeação de pessoas e objetos) e discalculia (dificuldade no cálculo) Não apresentava febre ou outra sintomatologia. Ao exame neurológico não apresentava alteração significativa das funções nervosas superiores, com disartria ligeira, parésia facial central direita, movimentos mioclónicos do MSE e hemiface esquerda. A RM-CE mostrou alteração em T2 e difusão (DWI) no caudado e putamen direitos, sem envolvimento do estriado contralateral. Por manter agravamento, repetiu RM-CE após cinco dias, tendo-se verificado adi cional hipersinal em difusão do córtex fronto-parieto-cingular medial. A investigação realizada para identificação de causas autoimunes, infecciosas e paraneoplásica resultou negativa, LCR apresentava aumento da proteína tau e proteína 14.3.3 normal. O EEG revelou atividade lenta parietal direita e frontotemporal bilateral. Nas duas semanas seguintes, verificou-se agravamento da disartria e surgimento de ataxia da marcha. Colocou-se a possibilidade de encefalite autoimune, tendo sido administradametilprednisolona endovenosa (1 g durante cinco dias), sem melhoria. Nos meses seguintes a deterioração neurológica mantevese progressiva, com evolução para anartria (incapacidade de articulação verbal) e disfagia, hemiparesia esquerda, incontinência urinária e agravamento cognitivo com alteração da memória recente, desorientação temporal e disfunção executiva. Foi realizada nova RM-CE, que mostrou restrição à difusão dos gânglios da base bilateralmente e múltiplas áreas corticais, predominantemente córtex frontal e parietal. O EEG identificou atividade periódica de complexos pontaonda generalizadas com reatividade à estimulação. O doente viria a falecer aos quatro meses de doença. A análise genética efetuada posteriormente resultou positiva para a mutação c.598G > A (E200K).",
+        "gold_summary": "Apresentamos um caso de um doente de 59 anos com quadro súbito de parésia facial central e disartria, seguindo-se mioclonias no hemicorpo esquerdo. A ressonância magnética crânio-encefálica inicial mostrava hipersinal T2 e difusão no caudado e putamen direitos e líquido cérebro-raquidiano com hiperproteinorraquia. A investigação para causas autoimunes, infecciosas e paraneoplásicas foi negativa. Verificou-se um agravamento progressivo nos meses seguintes para hemiplegia esquerda, disfagia, incontinência urinaria e posterior mutismo acinético. A ressonância magnética crânio-encefálica mostrou evolução para restrição à difusão dos gânglios da base bilateralmente e múltiplas áreas corticais; A eletroencefalografia mostrou atividade periódica e proteína Tau no líquido cérebro-raquidiano elevada. A análise genética revelou mutação c.598G > A. O falecimento ocorreu após quatro meses de doença.",
+        "synthetic_summary": {
+            "B1": "Um homem de 59 anos começou a ter problemas para falar e mexer o lado direito do rosto. Depois, seu braço esquerdo começou a se mexer sozinho. O médico fez um exame do cérebro e viu algumas partes diferentes. Eles fizeram muitos exames, mas não acharam nenhuma doença comum. Com o tempo, ele foi ficando pior. Ele não conseguia andar direito, nem engolir bem. Também perdeu o controle da urina e parou de falar. O exame do cérebro mostrou que mais partes estavam doentes. O médico fez um exame especial e achou uma mudança no seu corpo que explica a doença. Infelizmente, ele ficou muito doente e morreu depois de quatro meses.",
+            "B2": "**O que aconteceu com o paciente**\n\nUm homem de 59 anos começou a apresentar problemas de fala (disartria) e fraqueza em um lado do rosto (parésia facial). Depois, ele teve movimentos involuntários em um braço. Esses sintomas apareceram de forma rápida e foram piorando com o tempo.\n\n**O que os exames mostraram**\n\nUma ressonância magnética, que é um exame que tira fotos do cérebro, mostrou alterações em áreas chamadas caudado e putamen, que ficam dentro do cérebro e ajudam a controlar os movimentos. O líquido que envolve o cérebro e a medula espinhal (líquido cérebro-raquidiano) tinha uma proteína em quantidade maior do que o normal, o que pode indicar dano no cérebro. Outros exames para descartar doenças causadas por infecções ou problemas do sistema imunológico deram negativos.\n\nCom o passar dos meses, o paciente piorou bastante. Ele perdeu o movimento do lado esquerdo do corpo (hemiplegia), teve dificuldade para engolir (disfagia), perdeu o controle da bexiga (incontinência urinária) e parou de falar (mutismo acinético). Novas imagens do cérebro mostraram que as alterações se espalharam para outras áreas importantes do cérebro. Um exame chamado eletroencefalograma (EEG), que mede a atividade elétrica do cérebro, mostrou um padrão anormal.\n\n**O que isso significa**\n\nDepois de fazer um exame genético, descobriram que ele tinha uma mutação chamada c.598G > A, que está ligada a uma doença neurológica grave chamada doença de Creutzfeldt-Jakob, que causa a morte rápida das células do cérebro. Infelizmente, o paciente faleceu quatro meses depois do início dos sintomas.\n\n**Resumo final**\n\nEsse caso mostra como uma doença do cérebro pode começar com sintomas simples e evoluir rapidamente para problemas graves de movimento, fala e cognição. A combinação dos exames de imagem, do líquido cerebral, do EEG e do teste genético ajudou a entender o que estava acontecendo, mesmo que não tenha sido possível salvar o paciente.",
+            "B3": "**Contexto**  \nEste relato descreve o caso de um homem de 59 anos com antecedentes médicos relevantes, incluindo hemocromatose (uma condição que causa acúmulo excessivo de ferro no organismo), um episódio prévio de acidente isquêmico transitório (uma espécie de “mini-derrame”) e glaucoma. Havia também histórico familiar sugestivo de doença neurológica grave, com dois tios paternos falecidos aos 60 anos por causas neurológicas não especificadas.\n\n**Principais Achados Clínicos e Exames**  \nO paciente apresentou, de forma súbita, fraqueza central na face (parésia facial central) e dificuldade para articular palavras (disartria). Poucos dias depois, surgiram movimentos involuntários rápidos e breves (mioclonias) no lado esquerdo do corpo. A ressonância magnética do cérebro evidenciou alterações específicas nos núcleos da base do lado direito (caudado e putamen), com sinais de edema e restrição à difusão, indicando lesão ativa nessas áreas. O exame do líquido cérebro-raquidiano (LCR) revelou aumento da proteína total, sugerindo dano neurológico, embora a proteína 14.3.3, frequentemente associada à doença de Creutzfeldt-Jakob, estivesse normal. Testes para causas autoimunes, infecciosas e paraneoplásicas foram negativos.\n\nNos dias seguintes, a condição do paciente piorou, com agravamento da fala, surgimento de dificuldades na coordenação da marcha (ataxia) e comprometimento cognitivo leve, incluindo dificuldades para nomear objetos e realizar cálculos simples. O eletroencefalograma (EEG) mostrou atividade elétrica cerebral anormal, com ondas lentas e, posteriormente, padrões periódicos característicos.\n\n**Evolução Clínica e Diagnóstico**  \nApesar do tratamento com corticosteroides intravenosos (metilprednisolona), não houve melhora. O quadro evoluiu para perda quase total da fala (anartria), dificuldade para engolir (disfagia), fraqueza intensa no lado esquerdo do corpo (hemiparesia), incontinência urinária e declínio cognitivo progressivo, com perda da memória recente, desorientação no tempo e comprometimento das funções executivas (planejamento, organização).\n\nNovas imagens por ressonância magnética mostraram que as lesões nos gânglios da base tornaram-se bilaterais e que múltiplas áreas do córtex cerebral, especialmente nas regiões frontal e parietal, também estavam afetadas. O EEG passou a evidenciar complexos periódicos generalizados, um achado típico em doenças neurodegenerativas rápidas. A proteína Tau, marcador de dano neuronal, estava elevada no LCR.\n\nA análise genética confirmou a presença da mutação c.598G > A no gene PRNP, conhecida por estar associada à forma genética da doença de Creutzfeldt-Jakob, uma enfermidade neurodegenerativa fatal causada por príons (proteínas malformadas que provocam destruição cerebral rápida).\n\n**Interpretação Clínica**  \nEste caso ilustra a apresentação e evolução típicas da doença de Creutzfeldt-Jakob genética, caracterizada por início súbito de sintomas neurológicos focais, rápida progressão para comprometimento motor e cognitivo severo, e alterações específicas em exames de imagem e eletrofisiologia. A ausência de resposta a imunossupressores e os achados laboratoriais reforçam o diagnóstico.\n\n**Desfecho e Considerações Finais**  \nO paciente faleceu quatro meses após o início dos sintomas, refletindo a natureza agressiva e fatal da doença. Este caso destaca a importância da investigação genética em pacientes com quadro neurodegenerativo progressivo e história familiar sugestiva, além da necessidade de considerar diagnósticos raros em casos de deterioração neurológica rápida e inexplicada."
+        }
+    },
+    {
+        "article": "Em fevereiro de 2020, um homem de 36 anos sem histórico médico significativo apresentou uma massa penoscrotal no lado esquerdo com 5 anos de evolução. Ele não tem sintomas do trato urinário inferior. Não tem histórico de trauma ou infecções e negou qualquer histórico de perda de peso, anorexia ou febre. No exame, há uma superfície lisa, lesão cística sensível de cerca de 20 mm * 20 mm ligada ao lado esquerdo da uretra bulbar na junção penoscrotal, era profunda sem qualquer ligação à pele e não relacionada com o cordão espermático esquerdo e era parcialmente móvel.\n\nA ultrassonografia Doppler mostrou uma massa hipoecoica bem definida medindo 2,7 ∗ 3,1 ∗ 2,0 cm com vascularidade significativamente aumentada à esquerda da junção penoscrotal. A ressonância magnética da pélvis revelou uma massa no lado inferior esquerdo da base do pênis com um plano de gordura claro, que é isointense para os testículos na ressonância ponderada em T2, na ressonância ponderada em T1 e na ressonância ponderada em difusão e estava ligada ao ducto deferente, sem linfadenopatia. Os níveis de alfa-fetoproteína e beta-gonadotrofina humana estavam todos dentro da faixa normal. Dados os resultados do tratamento e a dor experimentada pelo paciente, foi tomada a decisão de proceder com a remoção cirúrgica da massa para fins diagnósticos e terapêuticos. Durante a cirurgia, uma massa foi vista no lado inferior esquerdo do escroto e foi completamente ressecada e enviada para histopatologia.\n\nA histopatologia da massa mostrou um tumor de células fusiformes dispostas em fascículos interligados, as células têm núcleos vesiculares fusiformes com cromatina uniformemente dispersa e nucléolos discretos. O tumor mostrou uma alta atividade mitótica, atingindo até 3/Campo de Alta Potência. A análise de imuno-histoquímica foi consistente com um sarcoma sinovial, revelando um TLE-1 positivo, CD99, linfoma de células B 2 (BLC2), citoqueratina focal e antígeno epitelial focal (EMA). O material foi enviado para uma hibridação in situ por fluorescência (FISH) e relatou um rearranjo do gene SS18 em 18q11.2, que foi observado em sarcomas sinoviais. As margens da massa foram difíceis de serem avaliadas por histopatologia, pois a amostra tinha margens fragmentadas.\n\nO paciente apresentou-se na clínica após 2 semanas e, dado o relatório de histopatologia, uma re-ressecção com margem mais ampla foi discutida com o paciente e ele concordou. Tomografia por emissão de pósitrons - tomografia computadorizada (PET/CT) foi feita para Cabeça e Pescoço, Tórax, Abdome, Pelve e estruturas musculoesqueléticas. Apenas um nódulo da tireóide de 29 * 27 mm no pólo inferior do lobo esquerdo da tireóide com hipermetabolismo moderado em valores de captação padronizados (SUVs) de 4.9. A US da tireóide mostrou um nódulo sólido, isoecoico, bem definido no pólo inferior do lobo esquerdo da tireóide sem focos ecogênicos, o Relatório de Imagem da Tireóide e Sistema de Dados (TIRADS) foi TR3.\n\nUma segunda ressecção foi feita 3 semanas após a primeira. O espécime total foi ressecado de ambos os cordões, bilateralmente, o que foi aprofundado até ao corpo esponjoso, que foi raspado superiormente até à uretra. O espécime foi enviado para histopatologia. A massa ressecada tinha 6,0 x 6,0 x 3,0 cm de dimensão e foi negativa para qualquer patologia. O paciente passou então para vigilância ativa e, após 16 meses de vigilância ativa, foi encontrado com lesões metastáticas no sexto segmento do fígado e no corpo vertebral L1. A equipa de oncologia iniciou um regime de quimioterapia com Ifosfamida e Doxorubicina durante 6 ciclos, sem melhoria da lesão hepática. Foi feita ressecção cirúrgica para as secções do quinto e sexto fígado com colecistectomia. O paciente desenvolveu então uma nova lesão pulmonar e foi iniciado com Pazopanib e Radioterapia Estereotáxica Corporal SBRT. O paciente passou então por vigilância durante 6 meses, desenvolveu novas lesões hepáticas e pulmonares, iniciou um regime de quimioterapia com Gemcitabina e Docetaxel durante 3 ciclos e progrediu, então, iniciou 2 ciclos de Dacarbazina e progrediu, então, 2 ciclos de Pembrolizumab e progrediu. O paciente passou então para cuidados paliativos e deixou de ser seguido.\n",
+        "gold_summary": "Um homem de 36 anos apresentou uma massa escrotal mole durante 5 anos. O paciente foi submetido a ressecção cirúrgica da massa. A histopatologia revelou um tumor de células fusiformes, organizado em fascículos entrelaçados. A análise de imuno-histoquímica revelou um TLE-1 positivo, CD99, linfoma de células B 2 (BLC2), citoqueratina focal e antígeno epitelial focal (EMA). No nosso caso, o paciente foi tratado de forma agressiva com duas ressecções cirúrgicas e ainda assim progrediu e metastatizou, continuando a progredir mesmo após diferentes regimes de quimioterapia.\n",
+        "synthetic_summary": {
+            "B1": "Um homem tinha um caroço mole no saco que segura os testículos. Ele sentiu isso por muitos anos. Os médicos fizeram uma cirurgia para tirar o caroço. Depois, olharam o caroço com um microscópio e viram que era um tipo de tumor. \n\nMesmo tirando o caroço duas vezes e usando remédios fortes, o tumor cresceu e apareceu em outras partes do corpo. Os médicos tentaram muitos tratamentos, mas o tumor continuou crescendo. Eles cuidaram dele com muito carinho até o fim.",
+            "B2": "**O que aconteceu com o paciente**\n\nUm homem de 36 anos percebeu que tinha uma massa mole no escroto, que é a pele que segura os testículos. Essa massa estava lá há 5 anos, mas ele não sentia dor ou outros sintomas no trato urinário.\n\n**O que os médicos fizeram**\n\nOs médicos decidiram tirar essa massa por cirurgia para descobrir o que era. Quando analisaram a massa no laboratório, viram que era um tumor feito de células fusiformes — células que têm formato parecido com um fuso, alongadas. Essas células estavam organizadas em grupos chamados fascículos, que se entrelaçavam.\n\nPara entender melhor o tumor, os médicos fizeram um exame chamado imuno-histoquímica. Esse exame usa marcadores para identificar tipos específicos de células. No caso dele, o tumor mostrou sinais positivos para algumas proteínas chamadas TLE-1, CD99, BLC2, citoqueratina e EMA. Esses resultados indicam que o tumor é um sarcoma sinovial, um tipo raro de câncer que pode crescer perto das articulações ou tecidos moles.\n\n**O que aconteceu depois**\n\nMesmo depois de duas cirurgias para tentar tirar todo o tumor, o câncer continuou crescendo e se espalhou para outras partes do corpo, como o fígado e os pulmões. O paciente recebeu vários tratamentos com quimioterapia, que são remédios fortes para tentar matar as células do câncer, mas o tumor não parou de crescer.\n\n**O que isso significa**\n\nEsse caso mostra que alguns tumores, como o sarcoma sinovial, podem ser difíceis de tratar. Mesmo com cirurgias e quimioterapia, eles podem continuar crescendo e se espalhando. Por isso, é importante que os médicos acompanhem esses pacientes de perto e tentem diferentes tratamentos para controlar a doença.",
+            "B3": "**Contexto**  \nUm homem de 36 anos apresentou uma massa indolor e mole na região penoscrotal esquerda, que vinha crescendo lentamente há cerca de cinco anos. Ele não apresentava sintomas urinários, histórico de trauma, infecções ou sinais sistêmicos como febre, perda de peso ou falta de apetite. O exame físico revelou uma lesão cística sensível, profunda, de aproximadamente 2 cm, localizada na junção penoscrotal, sem conexão com a pele ou estruturas como o cordão espermático.\n\n**Principais Achados Diagnósticos**  \nExames de imagem, incluindo ultrassonografia Doppler e ressonância magnética, mostraram uma massa bem delimitada, com aumento significativo da vascularização, localizada próxima ao ducto deferente, sem sinais de linfonodos aumentados. Marcadores tumorais sanguíneos (alfa-fetoproteína e beta-gonadotrofina humana) estavam normais. A decisão foi pela remoção cirúrgica da massa para diagnóstico e tratamento.\n\nA análise microscópica da peça cirúrgica revelou um tumor composto por células fusiformes (em forma de fuso) organizadas em feixes entrelaçados, com alta atividade de divisão celular (mitoses). A imuno-histoquímica — exame que identifica proteínas específicas nas células — demonstrou positividade para TLE-1, CD99, BCL2, citoqueratina focal e antígeno epitelial de membrana (EMA), características típicas do sarcoma sinovial, um tipo raro de tumor maligno originado em tecidos moles. A confirmação genética foi feita por um teste chamado hibridação in situ por fluorescência (FISH), que identificou o rearranjo do gene SS18, marcador específico desse tumor.\n\n**Interpretação Clínica e Tratamento**  \nDevido à dificuldade em avaliar as margens cirúrgicas na primeira cirurgia, foi realizada uma segunda ressecção mais ampla para tentar garantir a remoção completa do tumor. Exames de imagem adicionais não mostraram metástases iniciais, exceto por um nódulo na tireoide classificado como de risco intermediário, que não foi relacionado ao tumor principal.\n\nApesar das duas cirurgias e do acompanhamento inicial, o paciente desenvolveu metástases no fígado e na coluna vertebral após 16 meses. Foram administrados vários regimes quimioterápicos, incluindo Ifosfamida, Doxorrubicina, Gemcitabina, Docetaxel, Dacarbazina e imunoterapia com Pembrolizumab, além de tratamentos locais como radioterapia estereotáxica e ressecção cirúrgica das lesões hepáticas. Infelizmente, o tumor continuou a progredir, com aparecimento de novas lesões pulmonares e hepáticas.\n\n**Conclusão e Prognóstico**  \nEste caso ilustra a agressividade do sarcoma sinovial, mesmo em um paciente jovem e inicialmente assintomático. Apesar do tratamento cirúrgico agressivo e múltiplas linhas de quimioterapia e radioterapia, a doença evoluiu com metástases e resistência às terapias convencionais. O paciente acabou sendo encaminhado para cuidados paliativos, ressaltando a necessidade de novas abordagens terapêuticas para esse tipo de tumor raro e agressivo."
+        }
+    },
+    {
+        "article": "Uma mulher chinesa de 30 anos apresentou uma massa ovariana esquerda durante um exame físico de rotina. Ela era assintomática e não tinha histórico médico prévio de tumores cerebrais ou distúrbios neurológicos. A paciente sofria de ovários policísticos aos 19 anos sem qualquer tratamento. Os níveis séricos de CEA, CA125 e CA19-9 estavam dentro dos limites normais.\n\nUma ressonância magnética revelou uma lesão hipointensa ponderada em T1 e hiperintensa ponderada em T2, com 6,3 × 4,8 cm na área anexial esquerda, com um nódulo de fixação mural de sinal ligeiramente mais baixo. Além disso, a imagem ponderada em difusão (DWI) mostrou um sinal isointense dos nódulos murais. Portanto, foi considerado como um tumor benigno ou limítrofe.\n\nA paciente foi submetida a ressecção laparoscópica do ovário esquerdo e trompa de Falópio. Durante os 12 meses de acompanhamento, foi submetida a exames de ultrassom pélvico e abdominal a cada três meses, e não foram detectadas anormalidades. Ela permaneceu em boas condições após a cirurgia sem quimiorradioterapia.\n\nDescobertas patológicas\nEm exame macroscópico, uma massa cística de 5 × 3,5 × 1 cm foi encontrada no ovário esquerdo. Dois nódulos murais com diâmetros de 0,8 cm e 1,2 cm foram observados, que eram cinza-vermelhos e de textura macia. Histologicamente, formou um nódulo bem definido com baixa ampliação. Os componentes do teratoma incluíam epiderme, apêndices cutâneos eram visíveis no nódulo mural circundante e no tecido da parede do cisto. Sob alta ampliação, revelou células gliais desordenadas e gangliões proliferados no nódulo mural. Gangliões anormais foram agregados, com núcleo grande e irregular, que também exibia núcleos óbvios, e células binucleadas foram vistas. As figuras mitóticas foram dificilmente identificadas.\n\nImmuno-histoquimicamente, as células gliais foram positivas para GFAP e Olig2. As células ganglionares foram positivas para Neu-N, CgA, Nestin e CR. Além disso, as células ganglionares expressaram CD34 e destacaram as células tumorais ramificadas. Foi observada fraca expressão de NSE e expressão de tipo selvagem de P53 em algumas células tumorais. Além disso, as células tumorais foram negativas para IDH1 e BRAF V600E. O índice Ki67 foi aproximadamente 5%. Com base nestes achados, foi feito um diagnóstico de ganglioglioma resultante de um teratoma cístico maduro ovariano.\n",
+        "gold_summary": "A paciente, uma mulher de 30 anos sem histórico médico anterior de tumores cerebrais ou distúrbios neurológicos, foi encontrada com uma massa cística no ovário esquerdo, acompanhada por dois nódulos murais. Histologicamente, o nódulo mural no teratoma exibiu uma combinação de células neoplásicas ganglionares e gliais. Notavelmente, as células ganglionares exibiam binucleação e distribuição focal, com a presença ocasional de corpos de Nissl. Imuno-histoquimicamente, GFAP e Olig2 foram positivos em células gliais, cromogranina A (CgA), Nestin, CD34, Neu-N e Calretinin (CR) foram positivos em células ganglionares. As células tumorais demonstraram um baixo índice Ki67, abrigaram uma expressão P53 de tipo selvagem e foram negativas para IDH1 e BRAF V600E. A paciente foi submetida a ressecção laparoscópica do ovário esquerdo e trompa de Falópio e estava em boas condições 12 meses após o acompanhamento.\n",
+        "synthetic_summary": {
+            "B1": "Uma mulher tinha uma bolinha no seu lado do corpo, perto da barriga. Os médicos tiraram essa bolinha com uma cirurgia pequena. Eles olharam a bolinha com um microscópio e viram que tinha dois tipos de células diferentes dentro dela. Essas células não eram perigosas. Depois da cirurgia, a mulher ficou bem e não teve mais problemas. Os médicos cuidaram dela e ela está saudável até agora.",
+            "B2": "**O que foi encontrado na paciente**\n\nUma mulher de 30 anos, que não tinha problemas de saúde relacionados ao cérebro ou nervos, descobriu durante um exame de rotina que tinha uma massa no ovário esquerdo. Essa massa era uma espécie de cisto, que é uma bolsa cheia de líquido, e dentro dela havia dois pequenos nódulos, que são como bolinhas sólidas.\n\n**O que mostraram os exames do tecido**\n\nQuando os médicos analisaram o tecido retirado do ovário, viram que esses nódulos tinham dois tipos de células diferentes: células gliais e células ganglionares. As células gliais são células que dão suporte aos neurônios no cérebro, e as células ganglionares são um tipo de neurônio, que é uma célula nervosa. Algumas dessas células nervosas tinham duas núcleos, o que é um sinal de que elas estavam se comportando de forma diferente do normal.\n\nPara entender melhor, os médicos usaram testes especiais que mostram se certas proteínas estão presentes nas células. Eles encontraram proteínas típicas das células gliais e das células nervosas, confirmando que o tumor tinha essas duas partes. Além disso, o tumor tinha poucas células se dividindo, o que indica que ele crescia lentamente. Também não havia sinais de mutações genéticas comuns em tumores mais agressivos.\n\n**O que foi feito e o que aconteceu depois**\n\nA paciente passou por uma cirurgia feita com pequenas incisões, chamada laparoscopia, para remover o ovário esquerdo e a trompa de Falópio. Após a cirurgia, ela foi acompanhada por um ano com exames regulares e não apresentou problemas. Ela não precisou de tratamentos como quimioterapia ou radioterapia e continuou bem.\n\n**O que isso significa**\n\nO tumor encontrado é chamado ganglioglioma, que é um tipo raro de tumor feito de células nervosas e células de suporte, e neste caso, ele surgiu dentro de um teratoma maduro, que é um tipo de tumor benigno que pode conter diferentes tipos de tecidos. A boa notícia é que, após a remoção, a paciente teve uma recuperação tranquila e sem sinais de retorno do tumor até o momento.",
+            "B3": "Resumo Reescrito para Público Adulto Não Médico\n\n**Contexto**  \nUma mulher de 30 anos, sem histórico prévio de tumores cerebrais ou problemas neurológicos, foi diagnosticada com uma massa cística no ovário esquerdo durante um exame de rotina. Essa massa continha dois pequenos nódulos na parede (chamados de nódulos murais). Ela não apresentava sintomas e seus exames de sangue para marcadores tumorais estavam normais.\n\n**Principais Achados Patológicos**  \nA análise microscópica da massa revelou que os nódulos continham dois tipos principais de células: células gliais (que normalmente compõem o tecido de suporte do sistema nervoso) e células ganglionares (células nervosas especializadas). As células ganglionares apresentavam características atípicas, como núcleos grandes e irregulares, algumas com dois núcleos, e a presença ocasional de estruturas chamadas corpos de Nissl, típicas de neurônios. A combinação dessas células indicou a presença de um ganglioglioma, que é um tumor raro formado por células gliais e neurais.\n\n**Resultados dos Testes Imunohistoquímicos**  \nPara confirmar o diagnóstico, foram realizados testes que detectam proteínas específicas nas células tumorais:  \n- As células gliais reagiram positivamente para GFAP e Olig2, marcadores típicos desse tipo celular.  \n- As células ganglionares expressaram proteínas como cromogranina A (CgA), Nestina, CD34, Neu-N e Calretinina (CR), que são indicativas de células nervosas diferenciadas.  \n- O índice de proliferação celular (Ki67) foi baixo, sugerindo que o tumor não estava crescendo rapidamente.  \n- A proteína P53, associada a mutações em muitos cânceres, apresentou expressão normal (“tipo selvagem”).  \n- As células tumorais não apresentaram mutações comuns em genes como IDH1 e BRAF V600E, que são frequentemente encontradas em outros tipos de tumores cerebrais.\n\n**Interpretação Clínica e Tratamento**  \nCom base nesses achados, o diagnóstico final foi de um ganglioglioma originado dentro de um teratoma cístico maduro do ovário, um tumor benigno raro que contém diferentes tipos de tecidos. A paciente foi tratada com a remoção cirúrgica laparoscópica do ovário esquerdo e da trompa de Falópio. Durante um acompanhamento de 12 meses, com exames regulares por ultrassom, ela permaneceu sem sinais de recidiva ou complicações, sem necessidade de quimioterapia ou radioterapia.\n\n**Próximos Passos**  \nO acompanhamento contínuo é importante para monitorar possíveis recidivas, embora o prognóstico seja favorável devido à natureza benigna do tumor e ao tratamento cirúrgico completo realizado."
+        }
+    },
+    {
+        "article": "Mulher de 76 anos, paraguaia, residente na Cidade Autônoma de Buenos Aires, sem histórico de viagens recentes, com histórico de estenose aórtica e hipertensão arterial, medicação habitual: bisoprolol. Começou 5 dias antes da admissão com febre, tosse com expectoração mucopurulenta e dispneia que progrediu para classe funcional III-IV, dor abdominal e cefaleia. Foi medicada de forma ambulatorial 48 horas antes da admissão com amoxicilina-ácido clavulânico; foram realizados testes de SARS-CoV-2, vírus influenza A e B e vírus sincicial respiratório por reação em cadeia da polimerase, que foram negativos. Consultada no hospital por dispneia classe funcional IV, náuseas e dor abdominal, foi realizada tomografia axial computadorizada (TAC) que evidenciou infiltrado intersticial bilateral. Admitida na Unidade de Terapia Intensiva em 30 de março de 2023, com choque séptico secundário a foco respiratório, febre 38 °C, 120 batimentos por minuto e acidose, os escores de gravidade SOFA (Sepsis Related Organ Failures Assesment) somaram 7 pontos e APACHE II (Acute Physiology and Cronic Health Classification System II) 21 pontos. Iniciou-se reanimação com fluidos, foram realizados exames clínicos, que evidenciaram aumento do hematócrito, foi interpretada a hemoconcentração, leucocitose e insuficiência renal aguda, foram tomadas amostras para hemocultura, urocultura e cultura respiratória. As amostras foram enviadas para laboratório de virologia de sangue para vírus dengue e CHIKV. Foi realizado ecocardiograma modalidade point of care ultrasound (POCUS) que evidenciou estenose aórtica moderada, com velocidade pico de 3.4 m/segundos, função sistólica do ventrículo esquerdo conservada, sem alterações da mobilidade segmentares, sem sinais de falha cardíaca aguda, não foram objetivadas vegetações em válvulas por essa abordagem. Iniciou-se tratamento com antibióticos de amplo espectro: ceftriaxona e vancomicina. Evolucionou com progressão de falhas respiratórias, hemodinâmica e renal. Requeru ventilação mecânica, vasopressores em altas doses, infusão de furosemida por oligúria, choque refratário, falecendo em 31 de março de 2023. Postmorten, os cultivos bacteriológicos de sangue, urina e secreções traqueais concluíram sem desenvolvimento bacteriano, reação em cadeia da polimerase em tempo real e antígeno NS1 não detectado para vírus dengue, e reação em cadeia da polimerase em tempo real para CHIKV detectado em soro.\n",
+        "gold_summary": "Foi apresentado o caso de uma senhora de 76 anos, com antecedentes de hipertensão arterial e estenose aórtica, admitida em terapia intensiva por choque séptico com foco respiratório, com padrão de pneumonia intersticial, evolução tórpida e óbito dentro de 24 horas do ingresso. Foi recebido postmorten o resultado detectável de vírus Chikungunya por reação em cadeia da polimerase em tempo real.\n",
+        "synthetic_summary": {
+            "B1": "Uma senhora de 76 anos ficou muito doente. Ela tinha pressão alta e um problema no coração. Ela foi para o hospital porque estava com muita dificuldade para respirar. Os médicos cuidaram dela, mas ela ficou pior e morreu no dia seguinte. Depois, os médicos acharam um vírus chamado Chikungunya no sangue dela. Esse vírus deixou ela muito doente.",
+            "B2": "**O que aconteceu com a paciente**\n\nUma senhora de 76 anos, que tinha pressão alta e um problema no coração chamado estenose aórtica (quando a válvula do coração está apertada), ficou muito doente. Ela foi levada para a Unidade de Terapia Intensiva porque estava com choque séptico, que é uma infecção grave que afeta o corpo todo, e tinha uma infecção no pulmão parecida com pneumonia.\n\n**Como foi a doença**\n\nEla teve febre, tosse com catarro, dificuldade para respirar, dor na barriga e dor de cabeça. Mesmo tomando um remédio para infecção, piorou rápido e precisou de ajuda para respirar com aparelhos. O exame de imagem mostrou que os pulmões estavam inflamados dos dois lados.\n\n**O que descobriram depois**\n\nInfelizmente, ela morreu em menos de um dia após a internação. Depois da morte, os médicos fizeram exames no sangue e encontraram o vírus Chikungunya, que é transmitido por mosquitos e pode causar febre e dores no corpo. Esse vírus foi detectado usando um exame chamado reação em cadeia da polimerase, que procura o material genético do vírus.\n\n**Por que isso é importante**\n\nEsse caso mostra que o vírus Chikungunya pode causar uma doença muito grave, especialmente em pessoas idosas com problemas de saúde. É importante ficar atento aos sintomas e procurar ajuda médica rapidamente.",
+            "B3": "**Contexto**  \nTrata-se de uma mulher de 76 anos, residente em Buenos Aires, com histórico prévio de hipertensão arterial e estenose aórtica moderada. Ela não havia viajado recentemente. Cinco dias antes da internação, apresentou febre, tosse com expectoração mucopurulenta, dificuldade respiratória progressiva (classificada como classe funcional III-IV), dor abdominal e cefaleia. Foi inicialmente tratada em ambulatório com amoxicilina-ácido clavulânico, mas os sintomas pioraram. Testes para infecções respiratórias comuns, incluindo SARS-CoV-2, influenza A e B, e vírus sincicial respiratório, foram negativos.\n\n**Principais Achados**  \nAo ser admitida no hospital, a paciente encontrava-se com dispneia grave (classe funcional IV), náuseas e dor abdominal. A tomografia computadorizada revelou infiltrados intersticiais bilaterais nos pulmões, sugerindo pneumonia de padrão intersticial. Na Unidade de Terapia Intensiva (UTI), foi diagnosticada com choque séptico de origem respiratória, apresentando febre de 38 °C, taquicardia (120 batimentos por minuto) e acidose metabólica. Os escores de gravidade indicaram comprometimento significativo dos órgãos (SOFA 7 e APACHE II 21). Exames laboratoriais mostraram hemoconcentração (aumento do hematócrito), leucocitose (aumento dos glóbulos brancos) e insuficiência renal aguda. Amostras para culturas bacterianas e exames virais foram coletadas.\n\nUm ecocardiograma realizado à beira do leito confirmou a estenose aórtica moderada, mas sem sinais de insuficiência cardíaca aguda ou infecção valvular. O tratamento inicial incluiu antibióticos de amplo espectro (ceftriaxona e vancomicina).\n\n**Interpretação Clínica**  \nApesar do tratamento intensivo, a paciente evoluiu com piora progressiva da função respiratória, circulatória e renal, necessitando ventilação mecânica, uso de vasopressores em doses elevadas e diuréticos devido à baixa produção urinária. O choque séptico tornou-se refratário, culminando em óbito menos de 24 horas após a admissão.\n\nOs exames pós-morte não identificaram infecção bacteriana nas culturas de sangue, urina e secreções respiratórias. Testes específicos para vírus dengue foram negativos, porém a reação em cadeia da polimerase (PCR) em tempo real detectou a presença do vírus Chikungunya no soro da paciente.\n\n**Próximos Passos**  \nEste caso evidencia a possibilidade de infecção grave por vírus Chikungunya, que pode evoluir para choque séptico e falência múltipla de órgãos, mesmo em pacientes sem histórico de viagens recentes para áreas endêmicas. Ressalta-se a importância de considerar agentes virais emergentes no diagnóstico diferencial de síndromes febris graves com comprometimento respiratório e choque, especialmente em regiões onde o vírus está presente. A detecção precoce e o manejo adequado dessas infecções são essenciais para melhorar o prognóstico. Estudos adicionais são necessários para compreender melhor os mecanismos de gravidade e definir protocolos terapêuticos eficazes para casos semelhantes."
+        }
+    },
+    {
+        "article": "É um rapaz de 16 anos que, nos meses anteriores à consulta, sofria de paralisia do sono ocasionalmente, após alguns minutos de início da sesta pós-prandial, o que lhe gerava muita ansiedade, motivo principal pelo qual veio a consulta. Ocasionalmente, estas paralisia do sono eram acompanhadas de alucinações hipnopómpicas (que ele relacionava com sonhos ou com não estar acordado completamente). Tem um horário de sono noturno de cerca de sete horas, mais duas horas de sesta que lhe são muito refrescantes. Tem um bom rendimento escolar. Ao fazer anamnese dirigida refere que, após meses a sofrer estas paralisia do sono, apareceram episódios de sacudidas de braços e pernas, sobretudo quando ria, que em alguma ocasião quase o fizeram cair (‘pensava que isso acontecia a toda a gente’). Posteriormente, a estes sintomas juntaram-se uns três despertares noturnos de breve duração, com conciliação posterior imediata e ocasionais ataques de sono pela manhã, que relaciona com as aulas de matemática (‘o professor é muito aborrecido’). Após a suspeita clínica, solicitamos estudo de teste de latências múltiplas de sono e um estudo de polisomnográfico noturno, que são conclusivos com o diagnóstico de narcolepsia (latência de sono muito curta, latência de sono REM adiantada, sono algo fragmentado, média no teste de latências múltiplas do sono de 2,1 minutos e presença de quatro sleep onset REM). Já que os episódios de sonolência lhe ocorrem todos os dias à mesma hora, é-lhe prescrita uma sesta breve matutina que, a princípio, o refresca muito e refere poder continuar com a sua atividade escolar. Posteriormente, foi preciso acrescentar à mesma hora modafinilo (200 mg). Recomendamos-lhe venlafaxina para as cataplejías ou mesmo iniciar tratamento com oxibato sódico (este último não o quer tomar por incomodidade da segunda dose, e a venlafaxina também a rejeita por medo dos efeitos secundários). Acordámos que cumprirá com boa higiene de sono, tomará o modafinilo e seguirá com as sestas pautadas (a vespertina que já realizava e a matutina) e, se piorar, acrescentaremos outros tratamentos. Mantém-se bem com esta pauta, não percebe muita fragmentação do sono noturno (um ou dois despertares muito breves após os quais volta a conciliar sem problema); de facto, acorda descansado, as cataplejías são ocasionais e não o incomodam no desenvolvimento da sua vida diária, e os ataques de sono estão muito controlados. Refere-se sentir melhor e sem grandes limitações na sua vida diária (bom rendimento académico, não bebe álcool, mas também não o afeta, já que nunca bebeu, mantém horários de sono regulares e realiza atividade física regular).\n",
+        "gold_summary": "Um rapaz de 16 anos que veio consultar-nos depois de consultar vários especialistas por causa de paralisia do sono durante as sestas, que lhe causavam medo e ocasionalmente faziam com que objetos caíssem das suas mãos (diagnosticados como possíveis mioclonias). Na anamnese, ficámos surpreendidos com a presença de paralisia do sono imediatamente após o início das sestas e, na anamnese dirigida, esses movimentos bruscos provocados por emoções eram compatíveis com cataplexias, pelo que realizámos um estudo polisomnográfico noturno e um teste de latências múltiplas do sono. Com a evolução, apareceram alucinações hipnopómpicas e sono fragmentado noturno, assim como ocasional sonolência diurna (completou-se assim a tétrada sintomatológica típica da narcolepsia com cataplexia de tipo 1).\n",
+        "synthetic_summary": {
+            "B1": "Um menino de 16 anos tinha medo de dormir a sesta. Às vezes, ele ficava paralisado e deixava cair coisas das mãos. Também mexia os braços e as pernas quando ria muito.\n\nEle tinha sonhos estranhos e acordava várias vezes à noite. Ficava com muito sono durante o dia, principalmente na escola.\n\nOs médicos fizeram exames para ver como ele dormia. Eles descobriram que ele tem uma doença chamada narcolepsia. Isso faz ele dormir de um jeito diferente e sentir sono forte durante o dia.\n\nAgora, ele faz sestas curtas e toma remédios para ajudar. Ele está melhor e consegue estudar e brincar sem problemas.",
+            "B2": "**O que aconteceu com o rapaz**\n\nUm garoto de 16 anos veio ao médico porque, durante as sestas (pequenos cochilos após o almoço), ele sentia paralisia do sono. Isso significa que, por alguns minutos, ele não conseguia mexer o corpo, o que o deixava com medo. Às vezes, objetos caíam das suas mãos por causa de movimentos involuntários chamados mioclonias, que são como pequenos tremores. Ele também teve episódios de alucinações hipnopómpicas, que são imagens ou sensações estranhas que aparecem quando a pessoa está acordando, mas ainda meio sonolenta.\n\n**O que os médicos descobriram**\n\nAo conversar com ele, os médicos perceberam que esses sintomas apareciam logo no começo das sestas e que ele tinha movimentos bruscos nos braços e pernas quando ria, que são chamados de cataplexias. Cataplexia é quando os músculos ficam fracos ou paralisados por causa de emoções fortes, como rir muito. Para entender melhor, fizeram dois exames do sono: um estudo durante a noite para ver como ele dormia (polissonografia) e um teste que mede quanto tempo ele demora para pegar no sono e entrar na fase do sono REM, que é quando sonhamos.\n\nOs exames mostraram que ele dormia muito rápido e tinha sono fragmentado, ou seja, acordava várias vezes durante a noite. Ele também tinha episódios de sonolência durante o dia. Esses sinais juntos formam a chamada \"tétrade da narcolepsia tipo 1\", que é uma doença do sono que causa sono excessivo, paralisia do sono, cataplexia e alucinações ao acordar.\n\n**Como ele está sendo tratado**\n\nPara ajudar, os médicos recomendaram que ele faça sestas curtas pela manhã e à tarde, o que o ajuda a se sentir mais descansado. Também começou a tomar um remédio chamado modafinilo, que ajuda a controlar a sonolência durante o dia. Para as cataplexias, sugeriram outros remédios, mas ele não quis tomar por medo dos efeitos colaterais. Por enquanto, ele está seguindo as orientações, dormindo bem, e consegue manter suas atividades escolares sem grandes problemas. Ele não bebe álcool, tem horários regulares para dormir e faz exercícios, o que também ajuda a controlar os sintomas.",
+            "B3": "**Contexto**  \nTrata-se de um jovem de 16 anos que procurou avaliação médica devido a episódios recorrentes de paralisia do sono que ocorriam durante as sestas após as refeições. Esses episódios geravam-lhe ansiedade significativa e, em algumas ocasiões, causavam a queda de objetos que segurava, sintomas inicialmente interpretados como possíveis mioclonias (movimentos involuntários bruscos). Além disso, ele relatava alucinações hipnopómpicas, ou seja, percepções visuais ou auditivas ao despertar, que associava a sonhos ou à sensação de não estar completamente acordado.\n\n**Principais Achados**  \nDurante a anamnese detalhada, observou-se que a paralisia do sono ocorria logo no início das sestas, o que é incomum. Também foram identificados episódios de movimentos bruscos nos braços e pernas desencadeados por emoções, especialmente ao rir, característicos de cataplexia — uma perda súbita e temporária do tônus muscular associada à narcolepsia. Posteriormente, surgiram despertares noturnos breves e sonolência diurna, especialmente pela manhã, completando assim os quatro sintomas clássicos da narcolepsia tipo 1: sonolência excessiva, cataplexia, paralisia do sono e alucinações hipnagógicas ou hipnopómpicas.\n\nPara confirmar o diagnóstico, foram realizados dois exames do sono: a polissonografia noturna e o teste de latências múltiplas do sono. Os resultados mostraram latência muito curta para o início do sono, entrada precoce no sono REM (fase do sono associada aos sonhos), sono fragmentado e múltiplos episódios de início de sono REM durante o teste, confirmando a narcolepsia tipo 1.\n\n**Interpretação Clínica**  \nO quadro clínico e os exames são compatíveis com narcolepsia com cataplexia, uma condição neurológica crônica que afeta o controle do sono e da vigília. A cataplexia, desencadeada por emoções, é um sintoma distintivo dessa forma da doença. A fragmentação do sono noturno e os episódios de sonolência diurna interferem na qualidade de vida, mas, no caso deste paciente, o impacto tem sido moderado, permitindo bom desempenho escolar e manutenção de hábitos saudáveis.\n\n**Próximos Passos e Tratamento**  \nInicialmente, foi recomendada a realização de uma sesta breve matutina, que proporcionou melhora significativa na sonolência diurna. Posteriormente, foi introduzido o modafinilo, um medicamento estimulante que ajuda a manter a vigília, na dose de 200 mg pela manhã. Para o controle das cataplexias, foram sugeridos tratamentos com venlafaxina (um antidepressivo que pode reduzir esses episódios) ou oxibato de sódio (um medicamento específico para narcolepsia), porém o paciente recusou ambos devido a preocupações com efeitos colaterais e inconvenientes na administração.\n\nFoi acordado que ele manteria uma boa higiene do sono, continuaria com as sestas programadas (matutina e vespertina) e o uso do modafinilo. Até o momento, o paciente apresenta melhora significativa, com sonolência diurna controlada, cataplexias ocasionais que não interferem em suas atividades diárias e sono noturno relativamente preservado, com apenas breves despertares que não comprometem o descanso. Ele relata sentir-se melhor, com poucas limitações, mantendo bom rendimento acadêmico, abstendo-se do consumo de álcool e praticando atividade física regularmente.\n\nEste acompanhamento contínuo visa ajustar o tratamento conforme a evolução dos sintomas, garantindo qualidade de vida e funcionalidade adequadas para o jovem."
+        }
+    },
+    {
+        "article": "Um recém-nascido de termo de 3050 g nasceu após uma gravidez sem complicações de uma mulher primípara de 20 anos de idade com 39 semanas de gestação. A gravidez foi sem complicações. O trabalho de parto não foi prolongado com uma evolução espontânea normal por via vaginal. As pontuações de Apgar foram de 8 e 9 ao 1 minuto e ao 5 minuto, respetivamente, com uma pontuação de 2 para a expressão facial de dor. A sua Apgar manteve-se a 9 ao 10 e 20 minutos. Ele estava alerta com um bom choro, cor rosada, uma pulsação de 134 e uma taxa respiratória de 56. Foi-lhe dada vitamina K ao nascer. Ele apresentou-se no nosso hospital com uma incapacidade de mamar durante três dias com 29 dias de idade. A família afirmou também que ele tinha vomitado de forma intermitente desde o nascimento. Não houve história de diátese hemorrágica, febre, rigidez do pescoço ou convulsões. Na apresentação, ele tinha uma fontanela anterior saliente. Moro era incompleto; a sucção não foi sustentada mas foi observado um bom tónus muscular em todas as extremidades. A sua contagem total de sangue (CBC) e o perfil de coagulação foram normais. A ressonância magnética cerebral mostrou uma convexidade cerebelar bilateral T1WI e T2WI, um hematoma hiperintenso de 2 cm com extensão supracerebral e periaquedutal. Além disso, a dilatação do quarto ventrículo e a dilatação do terceiro e lateral ventrículos também foram observados. Sob anestesia geral, o paciente foi colocado numa posição de decúbito ventral utilizando uma incisão na linha média da pele, foi feita uma craniotomia bilateral. Depois de a dura ser aberta numa incisão cruciforme, uma membrana espessa bem definida; com sangue hemolizado escuro saiu com pressão. Durante a operação, o paciente teve uma paragem cardíaca para a qual foi feito um ciclo de ressuscitação cardiopulmonar (CPR) e foi alcançado um retorno da circulação espontânea. Depois disso, a pele foi fechada, um dreno subdural foi colocado e o paciente foi extubado e transferido para a unidade de cuidados intensivos (ICU). A tomografia computadorizada de controlo feita no 3º dia pós-op mostrou a evacuação completa do hematoma e a melhoria da hidrocefalia. O paciente foi dado de alta no 7º dia pós-op com melhoria. O primeiro mês de acompanhamento pós-op foi sem incidentes com marcos de desenvolvimento normais alcançados para a sua idade.\n",
+        "gold_summary": "Um recém-nascido do sexo masculino de vinte e nove dias de idade apresentou falha de sucção por três dias associada a vômitos. A imagem mostrou hematoma subdural crônico bilateral posterior da fossa e hidrocefalia obstrutiva. Foi realizada craniotomia bilateral e a evacuação do hematoma resultou em um excelente resultado.\n",
+        "synthetic_summary": {
+            "B1": "Um bebê de 29 dias não conseguia mamar direito por três dias. Ele também vomitava às vezes. O médico viu que tinha um machucado com sangue na cabeça dele. O sangue estava apertando o cérebro e fazendo a cabeça ficar maior. Os médicos fizeram uma cirurgia para tirar o sangue. Depois da cirurgia, o bebê melhorou muito e ficou bem.",
+            "B2": "**O que aconteceu com o bebê**\n\nUm bebê de 29 dias teve dificuldade para mamar durante três dias e também vomitava de vez em quando. Os médicos fizeram exames e descobriram que ele tinha um acúmulo de sangue chamado hematoma, que estava pressionando o cérebro na parte de trás da cabeça. Esse problema causou um aumento do líquido dentro do cérebro, chamado hidrocefalia, que pode ser perigoso.\n\n**Como os médicos ajudaram**\n\nPara resolver isso, os médicos fizeram uma cirurgia chamada craniotomia, que consiste em abrir o crânio para tirar o sangue acumulado. Durante a cirurgia, o bebê teve uma parada cardíaca, mas os médicos conseguiram reanimá-lo com sucesso. Depois da operação, o hematoma foi completamente removido e o excesso de líquido no cérebro diminuiu.\n\n**O que isso significa**\n\nO bebê melhorou bastante depois da cirurgia e recebeu alta do hospital em poucos dias. No primeiro mês após a operação, ele se desenvolveu normalmente, alcançando as fases esperadas para a sua idade. Isso mostra que, com o tratamento certo, problemas sérios no cérebro de bebês podem ser tratados com sucesso.",
+            "B3": "**Contexto**  \nUm bebê do sexo masculino, nascido a termo com peso de 3050 gramas após uma gravidez e parto normais, apresentou dificuldade para mamar durante três dias aos 29 dias de vida. A família também relatou episódios intermitentes de vômito desde o nascimento. Não houve sinais de infecção, sangramento anormal, convulsões ou rigidez no pescoço. No exame físico, o bebê estava alerta, com boa cor e tônus muscular, porém apresentava uma fontanela anterior saliente (área mole no topo da cabeça) e reflexos incompletos relacionados à sucção.\n\n**Principais Achados**  \nOs exames laboratoriais, incluindo hemograma e testes de coagulação, estavam normais. A ressonância magnética do cérebro revelou a presença de um hematoma subdural crônico (acúmulo de sangue antigo) bilateral na região posterior da fossa craniana (área próxima ao cerebelo), com sinais de sangue hemolizado (degradado) e extensão para áreas próximas ao aqueduto cerebral. Além disso, foi identificada hidrocefalia obstrutiva, caracterizada pela dilatação dos ventrículos cerebrais (cavidades que contêm líquido cefalorraquidiano), indicando acúmulo anormal de líquido devido à obstrução do fluxo.\n\n**Interpretação Clínica**  \nO hematoma subdural crônico estava causando compressão cerebral e bloqueio do fluxo normal do líquido cefalorraquidiano, resultando em hidrocefalia. Esses fatores explicam a dificuldade do bebê em mamar e os vômitos persistentes, sintomas indicativos de pressão intracraniana aumentada e comprometimento neurológico.\n\n**Procedimento e Evolução**  \nFoi realizada uma craniotomia bilateral (abertura cirúrgica dos ossos do crânio em ambos os lados) para evacuar o hematoma. Durante a cirurgia, foi observada uma membrana espessa contendo sangue hemolizado, que foi removida sob anestesia geral. O procedimento foi complicado por uma parada cardíaca intraoperatória, que foi revertida com sucesso após ressuscitação cardiopulmonar. Após a cirurgia, um dreno subdural foi colocado para evitar o acúmulo de líquido. A tomografia computadorizada realizada três dias depois mostrou a remoção completa do hematoma e melhora significativa da hidrocefalia.\n\n**Prognóstico e Seguimento**  \nO bebê teve alta hospitalar no sétimo dia pós-operatório com melhora clínica evidente. No acompanhamento durante o primeiro mês após a cirurgia, ele apresentou desenvolvimento neurológico adequado para a idade, sem complicações adicionais. Este caso destaca a importância do diagnóstico precoce e tratamento cirúrgico eficaz em hematomas subdurais crônicos associados à hidrocefalia em recém-nascidos."
+        }
+    },
+    {
+        "article": "Uma senhora de 80 anos, que estava sendo avaliada por uma significativa perda de peso involuntária, foi admitida no departamento de emergência devido a vômitos e ao súbito aparecimento de dor aguda na coxa direita. A dor era constante e piorava com o movimento. O exame clínico revelou um ponto de grande sensibilidade na região proximal da coxa direita. Não havia indicação de trauma.\n\nA paciente foi encaminhada para um raio-X do quadril direito para investigar uma possível fratura patológica. Não foi observada fratura ou desalinhamento, e ela foi admitida no departamento de ortopedia para tratamento da dor e mobilização. Ela foi dispensada no dia seguinte, apesar da dor persistente e do vômito. No terceiro dia, a paciente foi readmitida no departamento de emergência com os mesmos sintomas. Ela estava afebril, mas devido a marcadores de infecção levemente elevados, leucócitos a 13,5 × 109/L (intervalo de referência 4,1–9,8 × 109/L) e CRP a 60 mg/L (< 5 mg/L), um raio-X do tórax foi realizado, revelando consolidações confluentes basais no pulmão direito, levantando a suspeita de um infiltrado pneumônico. A paciente foi transferida para a enfermaria médica para observação. Antibióticos não foram iniciados devido a sintomas respiratórios mínimos.\n\nNo dia quatro, o estado da mulher deteriorou-se, apresentando taquicardia (frequência cardíaca de 119 bpm), uma taxa respiratória de 28 respirações por minuto (intervalo normal: 12-16), e uma febre de 38.1°C. O seu nível de CRP também aumentou de 50 para 250 mg/L. A piperacilina-tazobactam foi iniciada intravenosamente numa dose ajustada ao peso de 2 g x 4, e foi encaminhada para uma tomografia computorizada do tórax/abdómen/pelve devido a suspeita de sepsis de um foco abdominal. A tomografia computorizada revelou um laço encarcerado de intestino delgado que se projetava através do canal obturador direito e dilatação do intestino delgado pré-obstrutiva, consistente com uma hérnia obturadora aguda, irredutível. O cirurgião de plantão foi prontamente consultado, e a paciente foi agendada para cirurgia de emergência.\n\nDurante a laparoscopia sob anestesia geral, um pequeno intestino encarcerado foi encontrado no canal do obturador, consistente com os achados do CT. O intestino foi cuidadosamente reduzido, sem sinais de necrose ou perfuração. Depois que a hérnia foi reduzida, o paciente apresentou hipotensão, com pressão arterial de 98/37 mmHg. A análise arterial gasosa intraoperativa mostrou pH 7.22 (7.36–7.44), PCO2 (a) 7.0 (4.7–6.0 kPa), PO2 (a) 15.0 (> 8.7 kPa), HCO3 19 (22–26 mmol/L), excesso de base -6.6 (-1.9–4.5 mmol/L), Cl 104 (98–107 mmol/L), e lactato 1.0 (0.4–1.3 mmol/L), consistente com a acidose respiratória e metabólica mista. A hipercapnia foi presumida como sendo causada pela absorção perioperativa de CO2 insuflado do peritoneu para a rede capilar. A infusão de norepinefrina foi iniciada a 0.04 mcg/kg/min, e a ventilação por minuto foi aumentada para corrigir a acidose. O segmento do intestino delgado reduzido foi reavaliado e foi considerado ainda viável, sem necessidade de ressecção. O defeito da hérnia foi fechado com suturas primárias usando sutura de barbear monofilamento não absorvível, sem nós (V-Loc) para minimizar o tempo da cirurgia devido à deterioração da condição do paciente.\n\nA paciente foi extubada imediatamente após a cirurgia e observada na unidade de cuidados intensivos até ao dia seguinte. Os vasopressores e um tubo de descompressão nasogástrico foram removidos no primeiro dia pós-operatório. Foi então transferida para a enfermaria cirúrgica. A função intestinal foi retomada no segundo dia pós-operatório. Os antibióticos foram descontinuados no terceiro dia pós-operatório. No mesmo dia, foi também transferida de volta para a enfermaria médica para uma avaliação mais aprofundada da sua perda de peso.",
+        "gold_summary": "Uma senhora de 80 anos com história de perda de peso involuntária apresentou-se ao departamento de emergência devido a dor aguda na coxa direita, náuseas e vómitos. No exame, a paciente apresentou sensibilidade à palpação no aspeto proximal e medial da coxa direita. A tomografia computorizada abdominal revelou um laço de intestino delgado que se projetava através do canal obturador direito, consistente com uma hérnia obturadora encarcerada. Foi realizada uma laparoscopia de emergência, revelando que o segmento de intestino delgado afetado era viável após a redução da hérnia. Devido ao desenvolvimento de acidose respiratória e hipotensão, o defeito obturador foi primeiramente suturado para reduzir o tempo de operação. A paciente fez uma boa recuperação e foi transferida para a enfermaria médica para posterior avaliação da sua perda de peso.\n",
+        "synthetic_summary": {
+            "B1": "Uma senhora muito velha sentiu uma dor forte na perna. Ela também estava com vontade de vomitar. Os médicos fizeram um exame e viram que um pedacinho do intestino estava preso dentro da perna dela. \n\nEles fizeram uma cirurgia para tirar o intestino de lá. O intestino estava bem e não estava machucado. Depois da cirurgia, a senhora ficou melhor e foi para o quarto para descansar e cuidar da saúde.",
+            "B2": "**O que aconteceu com a paciente**\n\nUma senhora de 80 anos, que estava perdendo peso sem querer, foi ao hospital porque sentia uma dor forte na parte superior da coxa direita, além de sentir náuseas e vomitar. Quando os médicos examinaram, ela sentia muita dor ao tocar essa região da coxa.\n\n**O que os exames mostraram**\n\nUm exame chamado tomografia computadorizada, que é como uma foto detalhada do corpo, mostrou que um pedaço do intestino delgado estava preso em um lugar chamado canal obturador, que fica perto da coxa. Isso é chamado de hérnia obturadora encarcerada, que acontece quando o intestino fica preso e não pode voltar ao lugar normal.\n\n**O que os médicos fizeram**\n\nOs médicos fizeram uma cirurgia chamada laparoscopia, que usa pequenas câmeras para olhar e consertar o problema. Eles conseguiram tirar o intestino do lugar onde estava preso e viram que ele ainda estava saudável, sem sinais de morte ou ferimentos. Durante a cirurgia, a paciente teve alguns problemas de pressão baixa e dificuldade para respirar direito, então os médicos fecharam o local da hérnia rapidamente para terminar a operação logo e cuidar dela melhor.\n\n**Como foi a recuperação**\n\nDepois da cirurgia, a paciente melhorou bem. Ela foi para a unidade de cuidados intensivos para ser observada e, em poucos dias, voltou para o setor médico para continuar investigando por que estava perdendo peso. A cirurgia ajudou a resolver a dor e o problema no intestino, e ela recebeu os cuidados necessários para se recuperar.",
+            "B3": "**Contexto**  \nUma mulher de 80 anos, com histórico de perda de peso involuntária significativa, procurou atendimento de emergência devido ao surgimento súbito de dor intensa na região proximal da coxa direita, acompanhada de náuseas e vômitos. A dor era constante e aumentava com o movimento, sem relato de trauma prévio. No exame físico, foi identificada sensibilidade localizada na parte superior e interna da coxa direita.\n\n**Principais Achados Diagnósticos**  \nInicialmente, radiografias do quadril direito não mostraram fraturas ou desalinhamentos ósseos. Posteriormente, exames laboratoriais indicaram sinais leves de infecção, com aumento dos leucócitos e da proteína C reativa (PCR). Uma tomografia computadorizada (TC) do abdômen revelou a presença de um segmento do intestino delgado preso (encarcerado) no canal obturador direito, caracterizando uma hérnia obturadora aguda irredutível. Essa condição é rara e ocorre quando uma parte do intestino fica aprisionada em um canal pélvico, causando obstrução e risco de comprometimento da circulação intestinal.\n\n**Interpretação Clínica e Conduta**  \nDiante do diagnóstico, a paciente foi submetida a cirurgia de emergência por via laparoscópica para reduzir (libertar) o intestino preso. Durante o procedimento, o segmento intestinal foi considerado viável, sem sinais de necrose ou perfuração, o que evitou a necessidade de ressecção intestinal. No entanto, durante a cirurgia, a paciente apresentou hipotensão e acidose respiratória e metabólica, provavelmente relacionada à absorção do dióxido de carbono insuflado no abdômen para a realização da laparoscopia. Para minimizar o tempo cirúrgico e estabilizar a paciente, o defeito da hérnia foi fechado rapidamente com suturas especiais que dispensam nós, reduzindo o risco de complicações.\n\n**Desfecho e Próximos Passos**  \nA paciente foi extubada logo após a cirurgia e monitorada na unidade de terapia intensiva, onde recebeu suporte hemodinâmico e ventilatório até sua estabilização. A função intestinal retornou ao normal no segundo dia pós-operatório, e os antibióticos foram suspensos no terceiro dia. Posteriormente, ela foi transferida para a enfermaria médica para investigação detalhada da causa da perda de peso involuntária que motivou sua avaliação inicial.\n\nEste caso destaca a importância do diagnóstico precoce da hérnia obturadora, uma condição rara que pode se manifestar com dor na coxa e sintomas abdominais inespecíficos, e a necessidade de intervenção cirúrgica rápida para evitar complicações graves. A recuperação favorável da paciente reflete o manejo adequado e a atenção multidisciplinar durante todo o processo."
+        }
+    }
+]
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